Manual of

Critical Care
Nursing
Nursing Interventions and
Collaborative Management

SEVENTH EDITION

MARIANNE SAUNORUS BAIRD,

MN, RN, ACNS-BC
Corporate Director, Magnet Recognition Program, Magnet Program
Director, Clinical Nurse Specialist, Emory Healthcare, Nursing
Administration, Atlanta, Georgia

2
3
Table of Contents
Cover image

Title page

Copyright

Contributors

Preface

1. General concepts in caring for the critically ill

Acid-base imbalances

Altered mental status

Fluid and electrolyte disturbances

Hemodynamic monitoring

Mechanical ventilation

Nutrition support

Pain

Prolonged immobility

4
 Sedation and neuromuscular blockade

Wound and skin care

Selected references

2. Managing the critical care environment

Bioterrorism

Emerging infections

Emotional and spiritual support of the patient and significant others

Ethical considerations in critical care

Patient safety

Selected references

3. Trauma
Major trauma

Abdominal trauma

Acute cardiac tamponade

Acute spinal cord injury

Burns

Compartment syndrome/ischemic myositis

Drowning

Pelvic fractures

Renal and lower urinary tract trauma

Thoracic trauma

Traumatic brain injury

Selected references

5
4. Respiratory disorders
Respiratory assessment: General

Acute asthma exacerbation

Acute respiratory distress syndrome

Acute pneumonia

Acute respiratory failure

Pneumothorax

Pulmonary embolism

Pulmonary hypertension

Selected references

5. Cardiac and vascular disorders

Cardiovascular assessment: General

Heart failure

Acute coronary syndrome

Acute infective endocarditis

Acute pericarditis

Aortic aneurysm/dissection

Cardiogenic shock

Cardiomyopathy

Dysrhythmias and conduction disturbances

Hypertensive emergencies

Peripheral vascular disease

Valvular heart disease

6
 Selected references

6. Kidney injury
Genitourinary assessment: General

Acute kidney injury

Continuous renal replacement therapies

Selected references

7. Neurologic disorders
General neurologic assessment

Brain death

Cerebral aneurysm and subarachnoid hemorrhage

Care of the patient after intracranial surgery

Meningitis

Neurodegenerative and neuromuscular disorders

Status epilepticus

Stroke: Acute ischemic and hemorrhagic

Selected references

8. Endocrinologic disorders
Endocrine assessment

Acute adrenal insufficiency (adrenal crisis)

Diabetes insipidus

Hyperglycemia

Myxedema coma

7
 Syndrome of inappropriate antidiuretic hormone

Thyrotoxicosis crisis (thyroid storm)

Selected references

9. Gastrointestinal disorders
Gastrointestinal assessment: General

Acute gastrointestinal bleeding

Acute pancreatitis

Enterocutaneous fistula

Hepatic failure

Peritonitis

Selected references

10. Hematologic/immunologic disorders

General hematology assessment

Anaphylactic shock

Profound anemia and hemolytic crisis

Bleeding and thrombotic disorders

Selected references

11. Complex special situations

Abdominal hypertension and abdominal compartment syndrome

Drug overdose

Stimulants

High-risk obstetrics: Hypertension in pregnancy

8
 Oncologic emergencies

Organ transplantation

Sepsis, septic shock, systemic inflammatory response syndrome, and

multiple organ dysfunction syndrome

Selected references

Heart and breath sounds

Glasgow coma scale

Cranial nerves Assessment and dysfunctions

Major deep tendon muscle stretch reflexes

Major superficial cutaneous reflexes

Inotropic and vasoactive medication infusions

Sample relaxation technique

Abbreviations used in this manual

Index

Ibc

9
Copyright

3251 Riverport Lane

St. Louis, Missouri 63043
MANUAL OF CRITICAL CARE NURSING: NURSING
INTERVENTIONS AND COLLABORATIVE MANAGEMENT,
SEVENTH EDITION
ISBN: 978-0-323-18779-4
Copyright © 2016 by Elsevier, Inc. All rights reserved.

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mechanical, including photocopying, recording, or any information
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Notices
Knowledge and best practice in this field are constantly changing.
As new research and experience broaden our understanding,
changes in research methods, professional practices, or medical
treatment may become necessary. Practitioners and researchers
must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or
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With respect to any drug or pharmaceutical products identified,
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11
NANDA International, Inc. Nursing Diagnoses: Definitions &
Classifications 2015-2017, Tenth Edition. Edited by T. Heather
Herdman and Shigemi Kamitsuru. 2014 NANDA International, Inc.
Published 2014 by John Wiley & Sons, Ltd. Companion website:
www.wiley.com/go/nursingdiagnoses.

Previous editions copyrighted 2011, 2005, 2001, 1998, 1995, 1991.

International Standard Book Number: 978-0-323-18779-4

Executive Content Strategist: Lee Henderson

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Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1

12
Contributors
Patrice C. Al-Saden, BS, RN, CCRC, Senior Clinical Research
Associate, Comprehensive Transplant Center, Feinberg School of
Medicine, Chicago, Illinois

Sonia Astle, RN, MS, CCNS, CCRN, CNRN, Clinical Nurse

Specialist, Critical Care, Inova Fairfax Medical Campus, Falls
Church, Virginia

Carol Ann Batchelder, MSN, RN, CCRN, ACCNS-AG BC,

Clinical Nurse Specialist, Intensive Care Units, Tri-campus,
Northside Hospital System, Atlanta, Georgia

Risa Benoit, DNP, CNS-BC, Advanced Practice Nurse,

Perioperative Services, Sarasota Memorial Healthcare System,
Sarasota, Florida

Cheryl L. Bittel, MSN, APRN, CCNS, NP-C, CCRN, Clinical

Nurse Specialist, Emory Saint Joseph’s Hospital, Atlanta, Georgia

Carolyn Blayney, BSN, RN, Clinical Operation Manager,

Pediatrics, Harborview Medical Center, Seattle, Washington

13
Madalina Boitor, BScN, RN, PhD Student, Ingram School of
Nursing, McGill University, Montreal, Canada

Jemma Brown, MSN-ED, RN, CCRN, CCM-BC, Stroke Program

Coordinator, Emory University Hospital Midtown, Atlanta,
Georgia

Susan B. Cali, MSN, RN, MHA, Infection Control Coordinator,

Emory University Hospital Midtown, Atlanta, Georgia

Mimi Callanan, MSN, RN, Epilepsy Clinical Nurse Specialist,

Stanford Comprehensive Epilepsy Center, Stanford Health Care,
Stanford, California

Gretchen J. Carrougher, MN, RN, Research Nurse Supervisor,

Department of Surgery, Harborview Medical, Center, Seattle,
Washington

Cynthia Rebik Christensen, MSN, CVN, ARNP-BC, Nurse

Practitioner, Family Practice, Certified Vascular Nurse, Mobile
Medical Professionals, Ankeny, Iowa

Janice C. Colwell, MS, RN, CWOCN, FAAN, Advanced Practice

Nurse, University of Chicago Medicine, Chicago, Illinois

Alice E. Davis, PhD, GNP-BC, ACNP-BC, FNP-BC, Associate

Professor, School of Nursing, University of Hawaii at Hilo, Hilo,
Hawaii

Joni L. Dirks, MS RN-BC, CCRN-K, Manager Clinical Educators

& ICU Educator, Providence Health Care, Spokane, Washington

14
Beverly George Gay, MSN, RN, Assistant Professor, Department
of Nurse Anesthesia, School of Allied Health Professions, Virginia
Commonwealth University, Richmond, Virginia

Céline Gélinas, PhD, RN

Associate Professor, Ingram School of Nursing, McGill University
Researcher, Center for Nursing Research and Lady Davis, Institute
for Medical Research, Jewish General Hospital, Montreal, Quebec,
Canada

Patricia R. Gilman, APRN, MSN, ACNS-BC

Adult Health Clinical Nurse Specialist, Cardiac ICU, Emory
University Hospital (2012–2014), Atlanta, Georgia
Robert Wood Johnson Nursing & Health, Policy Collaborative
Fellow, University of New Mexico College of Nursing,
Albuquerque, New Mexico

Vicki S. Good, RN, MSN, CENP, CPSS, System Director

Quality/Safety, CoxHealth, Springfield, Missouri

Phyllis Gordon, MSN, APRN, ACNS-BC

Clinical Nurse Specialist, Vascular Surgery, Division
Clinical Assistant Professor, School of Nursing, University of Texas
Health Science Center, San Antonio, San Antonio, Texas

Kimberly Graham, MSN, APRN, ACNS-BC, Clinical Nurse

Specialist, General Medical, Emory University Hospital Midtown,
Atlanta, Georgia

Vinay Paul Singh Grewal, B.Sc., Medical Student, Windsor

University School of Medicine, St. Kitts

15
Kiersten Henry, MSN, ACNP-BC, CCNS, CCRN-CMC, Acute
Care Nurse Practitioner, Chief Advanced Practice Provider,
MedStar Montgomery Medical Center, Olney, Maryland

Adina Hirsch, PharmD, BCNSP

Clinical Specialist–Nutrition Support, Critical Care, Saint Joseph’s
Hospital of Atlanta;
Assistant Professor of Pharmacy Practice, School of Pharmacy,
Philadelphia College of Osteopathic Medicine, Atlanta, Georgia

Beth Hundt, MS, APRN, NP-C, ACNS-BC

Clinical Nurse Specialist, Marcus Stroke & Neuroscience Center,
Grady, Health System, Atlanta, GA (2012–2014);
Clinical Nurse Specialist, Neuroscience Center of Excellence,
University, of Virginia Health System, Charlottesville, Virginia
(current)

Susie Hutchins, DNP, RN, Associate Clinical Professor,

Coordinator, Simulation and Standardized Patient Lab for, MEPN,
University of San Diego, Hahn School of Nursing, San Diego,
California

Anne E. Hysong, MSN, APRN, CCNS, Clinical Nurse Specialist,

Critical Care, Gwinnett Medical Center–Duluth, Duluth, Georgia

Jonathan Wesley Kandiah, B.Sc., Medical Student, All Saints

University, St. Vincents and the Grenadines

Roberta Kaplow, PhD, APRN-CCNS, AOCNS, CCRN,

Oncology Clinical Nurse Specialist, Emory University Hospital,
Atlanta, Georgia

16
Alice S. Kerber, MN, APRN, ACNS-BC, AOCN, APNG, Clinical
Nurse Specialist, Oncology, Advanced Practice Nurse in Genetics,
Georgia Center for Oncology Research and, Education (Georgia
CORE), Atlanta, Georgia

Kathleen Kerber, MSN, RN, ACNS-BC, CCRN, Clinical Nurse

Specialist, Medical Intensive Care Unit/Critical Care, Step Down
Unit, MetroHealth Medical Center, Cleveland, Ohio

Barbara McLean, MN, RN, CCNS-BC, NP-BC, CCRN, FCCM,

Critical Care Clinical Specialist, Critical Care Division, Grady
Health Systems, Atlanta, Georgia

James P. McMurtry, MSN, APRN, CNS-BC, CCRN, Clinical

Nurse Specialist, MICU; Pulmonary Critical Care, Emory
University Hospital Midtown, Atlanta, Georgia

Maria Paulsen, BSN, RN, Critical Care Nurse, Coordinator,

Trauma Outreach Education, Program, Harborview Medical
Center, Seattle, Washington

Lisa Reif, MSN, RN, APRN-CCNS, CCRN, Clinical Nurse

Specialist, Neuroscience ICU, Emory University Hospital, Atlanta,
Georgia

Alan Sanders, PhD, Director, Ethics, Trinity Health, Newtown

Square Office, Pennsylvania

Paul E. Schmidt, RPh, BCPS, Clinical Pharmacist, Critical Care,

Northside Forsyth Hospital, Cumming, Georgia

Elizabeth Scruth, PhD, RN, MPH, FCCM, CCNS, CCRN

17
Clinical Practice Consultant, Clinical Effectiveness Team, Kaiser
Permanente Northern California, Regional Quality and Regulatory
Services, Oakland, California
Critical Care Transport RN, Bayshore Ambulance, Foster City,
California

Maureen A. Seckel, MSN, RN, APN, ACNS-BC, CCNS, CCRN,

FCCM, Clinical Nurse Specialist, Medical Pulmonary Critical
Care, Christiana Care Health System, Newark, Delaware

Kara A. Snyder, MS, RN, CCRN, CCNS, Director, Quality

Improvement and Outcomes, Management, Banner University
Medical Center, Tucson, and South Campuses, Tucson, Arizona

Monica Tennant, MSN, APRN, CCNS, Critical Care Clinical

Nurse Specialist, Emory Saint Joseph’s Hospital, Atlanta, Georgia

Daryl Todd, MS, APRN-CNS, CCCC, ACNS-BC, Certified

Cardiovascular Care Coordinator, Clinical Nurse Specialist,
Coordinator Bariatrics and Chest Pain, Centers of Excellence,
Clinical Support for, Hospice and Observation Units, Emory
University Hospital Midtown, Atlanta, Georgia

Sharon Vanairsdale, MS, APRN, ACNS-BC, NP-C, CEN,

Clinical Nurse Specialist, Emergency Department and Serious
Communicable Disease Unit, Emory University Hospital, Atlanta,
Georgia

Colleen Walsh-Irwin, DNP, RN, ANP, CCRN

Cardiology Nurse Practitioner, Northport VAMC, Northport, New
York;
Cardiovascular Clinical Nurse Advisor, Department of Veterans
Affairs, Washington, DC;

18
Clinical Assistant Professor, Stony Brook University, Stony Brook,
New York

Joyce Warner, MN, RN, CCRN, Nurse Clinician, Surgical

Intensive Care Unit, Emory Healthcare, Atlanta, Georgia

Karen E. Zorn, MSN, RN, ONC, Enterprise Solution Architect,

Acute Care Integration, Emory Healthcare, Atlanta, Georgia

Reviewers
Bimbola Fola Akintade, PhD, ACNP-BC, MBA, MHA, Co-
Specialty Director and Assistant Professor, Adult Gerontological
Acute Care Nurse, Practitioner/Clinical Nurse Specialist, Program,
University of Maryland Baltimore, School of Nursing, Baltimore,
Maryland

David Allen, MSN, RN, CCRN, CCNS-BC, Deputy Chief,

Center for Nursing Science and, Clinical Inquiry, Brooke Army
Medical Center, Fort Sam Houston, TX 78109

Penelope S. Benedik, PhD, CRNA, RRT, Associate Professor of

Clinical Nursing, University of Texas Health Science Center at,
Houston, Houston, TX

Marcia Bixby, RN, MS, CCRN, APRN-BC, Critical Care Clinical

Nurse Specialist, Consultant, Randolph, Massachusetts

Marylee Bressie, DNP, RN, CCRN, CCNS, CEN, Assistant

Professor, University of Arkansas Fort Smith and, Capella
University, Ft Smith, Arkansas and Minneapolis, Minnesota

19
Diane Dressler, MSN, RN, CCRN, Clinical Assistant Professor,
Marquette University College of Nursing, Milwaukee, WI

Jennifer L. Embree, DNP, RN, NE-BC, CCNS, Clinical Assistant

Professor and Consultant, Indiana University School of Nursing -
Indiana, University Purdue University Indianapolis, Indianapolis,
Indiana

Joyce Foresman-Capuzzi, MSN, RN, CCNS, CEN, CPN, CPEN,

CCRN, CTRN, SANE-A, AFN-BC, EMT-P, FAEN, Clinical
Nurse Educator, Lankenau Medical Center, Wynnewood, PA

David Goede, DNP, ACNP-BC, Assistant Professor of Nursing,

Hospitalist, Nurse Practitioner, University of Rochester School of
Nursing, Rochester New York

Vinay Paul Singh Grewal, B.Sc., Medical Student, Windsor

University School of Medicine, Basseterre, Saint Kitts & Nevis

Elizabeth A. Henneman, PhD, RN, CCNS, FAAN, Associate

Professor of Nursing, University of Massachusetts Amherst,
Amherst, Massachusetts

Jennifer M. Joiner, MSN, RN, AGPCNP-BC, CCRN-CSC,

Clinical Nurse Educator, CTICU, and CCU Robert Wood Johnson
University Hospital, New Brunswick, NJ

Irena L. Kenneley, PhD, APHRN-BC, CIC, Assistant

Professor/Faculty Development Coordinator, Case Western Reserve
University, Cleveland, Ohio

20
Julene B. Kruithof, MSN, RN, CCRN, Nurse Educator, Spectrum
Health, Grand Rapids, Michigan

Elaine Larson, PhD, RN, FAAN, Anna C. Maxwell Professor of

Nursing, Research, School of Nursing and Professor, of
Epidemiology, Mailman School of Public, Health, Columbia
University, Columbia University, NY, NY

Rosemary K. Lee, DNP, ARNP-BC, CCNS, CCRN, Clinical

Nurse Specialist, Homestead Hospital, Homestead, FL

Justin Milici, MSN, RN, CEN, CPEN, CFRN, CCRN, TNS, RN

III Emergency Department, Parkland Health and Hospital System,
Dallas, Texas

Fadi B. Nahab, MD
Associate Professor, Department of Necrology and Pediatrics,
Emory University
Medical Director, Stroke Program, Emory University Hospitals,
Atlanta, Georgia

Michaelynn Paul, MS, RN, CCRN, Assistant Professor, Walla

Walla University, College Place, Washington

Julia Retelski, MSN, RN, CNRN, CCRN, CCNS, Clinical Nurse

Specialist Neurosurgical Intensive Care Unit, Carolinas Health Care
System, Charlotte, NC

Johnnie Robbins, MSN, RN, CCRN, CCNS, Critical Care

Clinical Nurse Specialist, US Army Institute of Surgical Research,
Fort Sam Houston, Texas

21
Tara L. Sacco, MS, RN, CCRN, ACNS-BC, ACCNS-AG, Visiting
Assistant Professor, St. John Fisher College Wegmans School of,
Nursing, Rochester, New York

Diane Vail Skojec, MS, DNP, CRNP, Nurse Practitioner,

Department of Surgery, The Johns Hopkins Hospital, Baltimore,
Maryland

Scott C. Thigpen, DNP, RN, CCRN, CEN, Dean and Professor of

Nursing, South Georgia State College, Douglas, Georgia

Judith A. Young, DNP, RN, CCRN, Clinical Assistant Professor,

Indiana University School of Nursing, Indianapolis, Indiana

22
Preface
Manual of Critical Care Nursing is a clinical reference for both
practicing nurses and students in critical care, progressive care, and
complex medical-surgical units. It is the most comprehensive of the
critical care handbooks available, yet is a concise and easy reference
with an abbreviated outline format and a portable, trim size. This
handbook provides quick information for more than 75 clinical
phenomena seen in critical care and other high acuity care
environments, which promotes evidence-based practice in planning
goal-driven care.

Who will benefit from this book?

Nurses from novice to expert will have access to key information
used to perform appropriate assessments, plan and implement care,
and evaluate the outcomes of interventions provided to critically ill
and acutely ill patients. The textual information and numerous
tables will serve as a focused review for the practicing nurse and
advanced practice providers. Academicians may find the book
helpful in teaching students to apply didactic classroom
information to clinical practice. Students will have an excellent tool
for assessing the patient systematically, and setting priorities for
nursing interventions.

Why is this book important?

The book provides information concisely, with emphasis on
evidence-based practice and outcomes achievement. Goal-directed
care is vital to patient safety, and promoting interdisciplinary

23
collaboration. Both a collaborative plan of care, and specific nursing
care plans are presented. Given the increasing acuity of
hospitalized patients, problems previously managed in critical care
such as using arterial blood gas interpretation to correct acid-base
imbalances, medically managing dysrhythmias with medication
infusions, or controlling blood pressure with vasoactive drugs can
be part of daily care of patients in progressive care units, telemetry,
stepdown units, and high-acuity medical-surgical units.
Accordingly, the care plans presented are applicable across the
spectrum of high-acuity care, from complex medical-surgical to
critical care. The book addresses the highly technical life-support
equipment as part of the care options for each condition, and in
detail for those who are actively using the technology in separate,
detailed sections.

Benefits of using this book

The primary goal of this reference is to present the information
necessary to provide patient- and family-centered care in a
technologically advanced environment in a concise, easy-to-use
format. The whole patient is addressed with care recommendations
for physical, emotional, mental, and spiritual distress involved in
illness. The prevention of potentially life-threatening complications
is crucial to patient safety and addressed through collaborative,
evidence-based care planning. The intent is to offer a thorough
selection of prioritized actions that can be chosen as needed in
planning individualized care.

How to use this book

Manual of Critical Care Nursing is organized for easy access and
logical presentation. Information regarding general concepts of
patient care, including those unique to the critical care
environment, is presented in the first two chapters, General
Concepts in Caring for the Critically Ill and Managing the Critical
Care Environment. Following is a chapter on Trauma and related
disorders. Chapters 4 through 10 cover disorders classified by body
systems, and Chapter 11 addresses Complex Special Situations,
such as high-risk obstetrics and organ transplantation.

24
 Each body system–specific chapter includes a general physical
assessment, and several chapters include generic plans of care
applicable to patients with all disease processes affecting that body
system. Each disorder includes a brief review of pathophysiology,
physical assessment, diagnostic testing, collaborative management,
NANDA-approved nursing diagnoses and nursing interventions,
patient/significant other teaching, desired outcomes, and disease-
specific discharge planning considerations. Gerontologic icons
highlight material relevant to the care of older adults, bariatric icons
have been added for care specific to people of size, and safety alerts
highlight key information needed to prevent complications. Desired
nursing care outcomes and interventions are based on the
University of Iowa’s Nursing Intervention Classification (NIC) and
Nursing Outcomes Classification (NOC) systems and are
highlighted throughout the text. Nursing interventions are linked to
nursing diagnoses, and suggested outcomes include specific
measurement criteria for physical parameters and time frames for
attainment of expected outcomes. The suggested time frames for
outcomes achievement are guidelines. Each patient’s response to
the illness and interventions is unique.
For clarity and consistency throughout the book, normal values
are given for hemodynamic monitoring and other measurements.
All values should be individualized to each patient’s baseline
health status.

New to this edition

The seventh edition has been revised to further emphasize
evidence-based practices and patient safety and mirrors a practicing
nurse’s approach to patient care. Changes include:

• Enhanced patient safety information, including new patient safety

alerts.

• Updated evidence-based guidelines, including evolving strategies

for management of heart and respiratory failure, and advances in
technology associated with mechanical ventilation, cardiac
mechanical assist devices, and hemodynamic monitoring.

25
• Information to help assess and plan care for bariatric patients.

• Enhanced medical and nursing management information for

correction of acid-base imbalances, management acute asthma,
brain injury, burns, sepsis, organ transplantation, obstetric
emergencies, cardiogenic shock, heart and respiratory failure,
and the management of altered mental status including delirium.

• Appropriate resuscitation interventions within the section on

Dysrhythmias and Conduction Disturbances.

I hope that critical care and high-acuity acute care providers,

students, and academicians will find that the new edition of Manual
of Critical Care Nursing provides a wealth of updated, concisely
comprehensive, easy-to-access knowledge applicable to clinical
practice as well as the classroom.

Acknowledgments
I want to thank many individuals who supported the development
of this manuscript. In particular, I am grateful for the time and
efforts of the Elsevier Science staff, including Melissa Rawe,
Content Development Specialist, and Marquita Parker, Senior
Project Manager, Book Production. I appreciate the guidance of Lee
Henderson, Executive Content Strategist. I thank all the
contributors for their work, as well as all the reviewers whose
comments helped guide our revisions. All are recognized as shining
stars in their own right. Both perseverance and patience are the
fundamental characteristics inherent in all participants.
Marianne Saunorus Baird
I acknowledge the support of my daughter Rachel, my best
cheerleader, and my husband Thom for his patience. I also cannot
thank the authors enough for your attention to detail; particularly
all the new authors who “filled the gaps” from Emory Healthcare,
Atlanta, Georgia. I would also like to acknowledge Savannah Davis,
who helped the team begin our process with Elsevier Science.
MSB

26
CHAPTER 1

General concepts in
caring for the
critically ill
Acid-base imbalances
Cells must transport ions, metabolites, and gases to function
appropriately in their respective roles in the body. For this to occur,
the chemical environment of the bloodstream must be electrically
stable. The stability of the environment is measured by the arterial
pH and must be chemically neutral (pH 7.40) for all systems to
function properly. The arterial blood gas (ABG) is the most
commonly used analysis to measure acid-base balance and to assess
the efficacy of oxygenation. Respiratory (CO2) and metabolic acids
(H+) are generated as cells work and must be buffered or eliminated
to maintain a neutral chemical environment. When the chemical
environment is no longer neutral, the patient has an acid-base
imbalance. Ineffective metabolism (tissue level), renal dysfunction,
and/or problems with ventilation (breathing gasses effectively) are
often the cause of acid-base imbalance.
There are two main types of acid-base imbalance: acidosis and
alkalosis. The kidneys and lungs work in tandem to maintain
chemical neutrality, but it is actually cellular function that produces
acid. When either the kidneys or lungs are overfunctioning or
underfunctioning, the other system is designed to have the opposite
response to compensate and bring the pH back to a normal range.

27
When the kidneys fail to regulate metabolic acids (H+), the lungs
must compensate. When the lungs fail to regulate respiratory acid
(CO2), the kidneys must compensate. Additional buffering
mechanisms are also available to help regulate the accumulation of
acids. Control of alkaline states, resulting from accumulation of
bases or loss of acids, is maintained in a similar manner between
the lungs and kidneys.

Pathophysiology of acid-base regulation

Arterial pH is an indirect measurement of CO2 and H+
concentration, which reflects the overall level of acid and
effectiveness of maintaining the balance. The normal acid-base ratio
is 1:20—1 part acid (the H+ and CO2 component of H2CO3) to 20
parts base (HCO3−). If the ratio is altered through an increase or a
decrease in either acid H+, or CO2, or the base, HCO3−, the pH
changes. Chemically, the CO2 does not contain H+, but when
dissolved in water (plasma), CO2 + H2O yields H2CO3 (carbonic
acid). CO2, when combined with H2O, becomes the largest
contributor of H+ (acids), which must be eliminated or buffered to
maintain normal pH. Too many H+ ions in the plasma create
acidemia (pH less than 7.35), whereas too few H+ ions create
alkalemia (pH greater than 7.45).
Maintaining the 1:20 ratio (“the balance”) depends on the ability
of the lungs and kidneys to help normalize concentrations of
carbonic acid (H2CO3), a product of hydrogen ion (H+) plus
bicarbonate buffer (HCO3−). Both the kidneys and lungs are
designed to eliminate carbonic acid effectively, and therefore
without the presence of lung or kidney disease, the pH should
always be in the normal range. A pH change is a symptom that
there is a significant problem with one or both of the systems.

• Acidosis: Extra acids are present or base is lost, with a pH less

than 7.35.

1. Cellular acidosis: When cells are hypoxic or

28
 processing proteins to yield glucose, there is an
increase in lactic acid or ketoacid.

2. Respiratory acidosis: If lung function is

inadequate, such as in chronic obstructive
pulmonary disease (COPD), the failure to
effectively ventilate results in the inability to
excrete CO2, and that failure causes carbonic acid
to increase (more acid) and pH to decrease.

3. Renal acidosis: When the kidney function is

inadequate, the ability to break down carbonic
acid into H+ and HCO3− is impaired. When this
failure occurs, carbonic acid increases (more acid)
and pH decreases.
• Buffering of acid or compensation for acidosis occurs in three
primary ways:

1. Plasma and cellular buffering: Using bicarbonate,

proteins, intracellular electrolytes, and chloride to
buffer H+, the most common is the marriage of H+
and HCO3−, which yields carbonic acid (H2CO3).

2. Hyperventilation (lungs): The presence of

increased carbonic acid stimulates a
hyperventilation response. This allows for
exhaling (“blow off”) more of the CO2 component
of carbonic acid. This compensatory response for
metabolic acidosis occurs within minutes and
should bring the pH to a normal range.

29
 3. Acid excretion (kidneys): A functional kidney
will use increased carbonic acid by breaking
H2CO3 into bicarbonate and H+, excreting H+ and
retaining bicarbonate. This should compensate
for the increased respiratory acidosis but is very
slow, taking 4 to 48 hours for compensation to
occur.
• Alkalosis: Extra base is present or there is loss of acid, with a pH
greater than 7.45.

1. Respiratory alkalosis: When hyperventilation is

the primary problem, there is a very rapid
removal of CO2, causing carbonic acid to decrease
(less acid) and pH to increase.

2. Renal alkalosis: If kidney function is

overstimulated (e.g., with aggressive diuresis),
there may be excessive loss of hydrogen ions
(H+), causing carbonic acid to decrease (less acid)
and pH to increase.

3. Other contributors: Gastric and intestinal removal

of acids may occur when patients have diarrhea,
vomiting, or when excessive gastric drainage
influences the acid-base balance.

• Compensation for alkalosis occurs in two ways:

1. Hypoventilation: The respiratory system

responds by slowing ventilation and retaining
CO2 (acid) to help compensate for metabolic

30
 alkalosis from any cause. This response occurs
within minutes.

2. Renal response: The kidneys respond by

retaining more acid (H+) and excreting more
bicarbonate to help correct respiratory alkalosis.
This response occurs within 4 to 48 hours.

Example of compensation (pH regulation)

When metabolic acids accumulate, they are drawn to bicarbonate.
The binding of H+ and HCO3− buffers the acid. This yields an
increase in carbonic acid (H2CO3) and causes the pH to decrease.
Chemoreceptors are stimulated by the presence of this acid and the
hypothalamus, if not damaged, triggers a hyperventilation
response. Because H+ is not measured directly, the indirect
calculation of bicarbonate or the base is used to evaluate the
presence or absence of metabolic acid. As H+ increases, the
bicarbonate or base decreases. When evaluating the acid-base
balance, it is simplest to look at bicarbonate but to think of it in
terms of how bicarbonate level also reflects the acid level. These
values travel in completely opposite directions (when bicarbonate
decreases, H+ increases and vice versa).
The lungs increase buffering to compensate for a failure of the
kidneys or a cellular excess acid production to keep the pH
balanced. The lungs do this by effectively exhaling more CO2 than
usual, breaking down carbonic acid and therefore bringing the pH
back toward normal.
When CO2 is retained or increased because of respiratory failure,
the kidneys should, in turn, respond by processing the increased
H2CO3. The kidneys separate the carbonic acid into H+ and HCO3−
and excrete the H+ while retaining HCO3− bicarbonate. If either the
kidneys or lungs do not respond to a pH change (no compensation)
or they provide an ineffective response (partial compensation), the

31
patient will remain in acid-base imbalance. If the pH is outside the
normal range, then there is a primary problem and compensation is
inadequate or has failed. Patients may have a pure acidosis or
alkalosis and the overall problem may be masked by compensation
or two problems presenting at the same time.
Unless the patient has ingested acid (aspirin, ethanol, etc.), all
acid in the bloodstream has been produced at the cellular level
(Table 1-1). When evaluating patients, care providers must have a
basic understanding of the acid-base balancing system. The main
formula for maintenance of acid-base balance is:

Table 1-1
PRODUCERS AND REGULATORS OF ACID

Acid
Cause Measure
Pathways
Cells Hypermetabolic states, such as pain, hyperthermia, or HCO3−
produce inflammation. The respiratory and heart rates
acid (acid increase, and bicarbonate is initially consumed by
production buffering.
increases). Tissues are hypoxic; anaerobic metabolism ensues Lactate level ↑
resulting in lactic acidosis.
Absolute insulin deficiency results in failure of Blood glucose level ↑
glucose to be transported into cells. Ketoacids ↑
Cells When acid production (H+) increases, pH decreases, pH ↓
regulate bicarbonate is initially consumed by buffering, and HCO3↓
acids. CO2 is exhaled in larger amounts, and H+ exchanges K+↑
for K+ as cells buffer acid. Total serum CO2↓
Lungs When acid increases as a result of hypermetabolic Paco2↓
regulate states such as pain, hyperthermia, or inflammation,
acid. carbonic acid (H2CO3) increases and rapidly converts
to CO2 and H2O. The respiratory rate increases to
blow off CO2.
Kidneys When acid increases, tubules are affected by low HCO3↑
regulate blood pH, and work to neutralize increased carbonic Kidney function is
acid. acid (H2CO3) by separating it into H+ and bicarbonate assessed by serum blood
HCO3. Kidneys excrete what is necessary to sustain urea nitrogen and
normal pH if renal function is normal. If abnormal, creatinine; elevated
kidneys may not perform this task. blood urea nitrogen and
creatinine indicate
abnormal kidney
function.

32
 The most important component identified is H2CO3 or carbonic
acid. As carbonic acid increases (“goes up”), the pH decreases
(“goes down”), reflecting the presence of acid. If carbonic acid
decreases (“goes down”), the pH increases (“goes up”), reflecting
the absence of acid. The equation is constantly shifting from left to
right and right to left to maintain a normal H2CO3 and therefore a
normal pH. Whatever causes the change of carbonic acid
concentration (may be related to a regulation failure by either the
lungs or kidneys or a metabolic acid production state) is the
“primary culprit.” Identifying the origin or cause of the change in
pH direction identifies the problem. Therefore, if the problem is too
much acid (either increased CO2 or H+), carbonic acid increases and
pH decreases. The primary problem is acidosis. Further evaluation
is needed to determine whether failure to regulate the acid was
ineffective regulation by the lungs, the kidneys, or an increase in
cellular acid production (ketoacidosis or lactic acidosis).

Changes in pH are associated with changes in the potassium

level. As the plasma level of nonvolatile or metabolic acid (H+)
increases, H+ moves into the cells to reduce the acidemia. In this
case, H+ “exchanges places” with the intracellular potassium (K+),
resulting in a measured serum hyperkalemia but is actually an
intracellular hypokalemia. The positively charged intracellular
potassium ions are replaced by positively charged hydrogen ions.
During an alkalotic state, K+ may shift into cells as H+ is released
into the serum, creating a transient hypokalemia. As pH changes,
it is imperative for the care providers to observe the corresponding
changes in the K+ level, and manage K+ carefully. When the pH
normalizes, the K+ will shift back to its original location. If a
transient K+ change is managed too aggressively, the patient may
experience dangerous hypokalemia or hyperkalemia when pH
normalizes.

Understanding the arterial blood gas (ABG)

33
The ABG is the most commonly used measurement to help assess
the origin of problems with acid-base imbalance and to guide
treatment designed to restore pH balance and effective
oxygenation. “Perfect” values reflect chemical neutrality. There are
normal variations or a range for each value.

Arterial blood gas values

Blood gas analysis is usually based on sampling of arterial blood.
Mixed venous blood sampling from a pulmonary artery (PA)
catheter (SVO2) and central venous sampling from a central
intravenous (IV) line (ScVO2) may also be performed for patients
who are very critically ill. Venous values are given for reference
only.
Normal Arterial Values Normal Venous Values
pH: 7.35–7.45 pH: 7.32–7.38
Paco2: 35–45 mm Hg Pvco2: 42–50 mm Hg
Pao2: 80–100 mm Hg Pvo2: 40 mm Hg
Sao2: 95%–100% Svo2: 60%–80%
Base excess (BE): –2 to +2 BE: –2 to +2 (only calculated on ABG analyzer)
HCO3−: 22–26 mEq/L Total serum CO2−: 23–27 mEq/L

pH (perfect 7.40, normal range 7.35 to 7.45): This reflects the level
of respiratory and metabolic acids found in the blood during the
continuous “balancing act” that regulates the acid environment. If
this balance is altered, derangements in pH occur. Any alteration in
pH should be evaluated. If the pH has changed from perfect, it can
only be one of two reasons: normal variation or abnormality with
compensation. When pH is less than 7.35 or greater than 7.45, it is
considered an acute change that is uncompensated. When full
compensation is attained for an acid-base imbalance, the pH
normalizes. Failure to bring the pH into normal range means there
is failure to compensate, despite the body attempting to mount a
response. Traditionally, if the body made an attempt to
compensate, this was known as partial compensation. This term is
no longer advocated.
PaCO2 (perfect 40, normal range 35 to 45 mm Hg): This is a
measure of pressure (partial pressure designated by the P) that the
dissolved CO2 exerts in the arterial blood. The dissolved gas exerts

34
the pressure of CO2, enabling it to diffuse across the capillary and
alveolar cell wall.
CO2 is released during aerobic metabolism and is the main
contributor to serum acid. CO2 is controlled through ventilation. In
the normal lung, CO2 is regulated by changes in the rate and depth
of alveolar ventilation. CO2 is carried both bound to hemoglobin
and dissolved in the blood. The measured CO2 is termed PaCO2.
PaCO2 is directly measured (not calculated) and is a reliable
indicator of respiratory acid-base regulation. The correlation
between PaCO2 and respiratory-based pH changes is direct,
consistent, and linear. In other words, if PaCO2 is up and pH is
down, the cause is respiratory deregulation. If the issue is
metabolic, and respiratory compensation has occurred, the PaCO2
will decrease to bring pH back to normal levels. Respiratory
compensation typically occurs rapidly in metabolic acid-base
disturbances as long as respiratory function is not impaired. When
a patient hyperventilates, PaCO2 decreases as it is “blown off” by
rapid exhalations. During hypoventilation (slow and/or shallow
breathing), PaCO2 increases. Although the only way to evaluate true
lung function is by the gas exchange, the capacity of the lungs (CO2
regulation response) is measured via the minute ventilation (VE or
MV). This measures the amount of volume exhaled per minute (VE)
calculated as respiratory rate (RR) multiplied by tidal volume (VT).
Normal MV is approximately 8 to 10 L/min.
PaO2 (perfect 95 to 100 mm Hg, normal range 80 to 100 mm Hg):
The partial pressure of oxygen (O2), or PaO2, is a measure of the
dissolved (usable) gas in the arteries. The dissolved gas exerts the
pressure of O2, enabling it to diffuse across the capillary and cell
wall to oxygenate cells. PaO2 normally declines in the older adult.

• Hypoxemia (PaO2 less than 80 mm Hg): Low partial pressure of

O2 affects the cellular levels of oxygen available and may result in
cellular metabolic dysfunction reflected by lactic acid production
and metabolic acidosis.

35
• FIO2: Fraction of inspired O2 or the percentage of the atmospheric
pressure that is oxygenated. Room air is 21% or 0.21 O2. O2
delivery devices can increase the FIO2 to 100% or 1.00.

P/F ratio (greater than 300): PaO2 is evaluated in relationship to

FIO2, that is, the higher the percent O2 pressure that is delivered to
the lungs, the higher the O2 in the blood should be.

SaO2 (perfect 100% or 1.0, normal range 95% to 100% or 0.95 to

1.0): O2 saturation (SaO2) reflects the loading of O2 onto hemoglobin
(Hgb) in the lungs. When Hgb is loaded with O2, it is termed
oxyhemoglobin. Hgb is the primary transporter of O2 and supplies
a reservoir (reserve) of O2 for cellular use. Each Hgb molecule
carries 1.34 to 1.36 mL of O2. O2 must be released from the Hgb,
dissolve in blood (PaO2), and exert pressure to diffuse across the cell
wall. The uptake/use of O2 by the tissues is measured by SVO2
and/or ScVO2 (mixed venous and/or central venous saturation of
Hgb, respectively). Cellular metabolism and O2 use are affected by
changes in stress level, temperature, pH, blood flow, and PaCO2.
When the PaO2 falls to less than 60 mm Hg, there is a large drop in
saturation, reflected in the oxyhemoglobin dissociation curve.

• Pulse oximetry (SpO2): This can be used to noninvasively trend

the arterial O2 saturation and determine ventilation status using a
probe fastened to the patient’s finger, earlobe, or forehead. This
monitoring technique is frequently used in critical care areas for
patients at high risk of ventilation problems, in operating rooms,
and in emergency departments. SpO2 should be correlated with
SaO2 (or oxyhemoglobin) via blood gas analysis when pulse

36
 oximetry is initiated, to assess accuracy of SpO2 readings. Pulse
oximetry is a close correlate to SaO2 under normal physiologic
conditions, but if perfusion decreases, the pulse needed for
accurate measurement by the SpO2 probe is decreased, prompting
inaccurate readings. Patients with anemia should have
consistently high readings, thus what is usually considered a
normal SpO2 reading may be too low in a patient with anemia.
The measure of true oxyhemoglobin (Hgb saturated with O2)
requires an ABG analysis. Many centers do not perform a
correlation analysis when oximetry is initiated.

• BE (perfect 0, normal range –2 to +2): Base excess or base deficit

uses a calculation to reflect the presence (excess) or absence
(deficit) of buffers. The calculation reflects the tissue and renal
tubular presence (or absence) of acid. As the proportion of acid
rises, the relative amount of base decreases (and vice versa).
Abnormally high values (greater than +2) reflect alkalosis, or an
excess of base; low values (less than –2) reflect acidosis, or a
deficit of base (base deficit).

• All buffers: Absorb acids (H+), but do so with a

varying affinity. Buffers are present in all body
fluids and cells and act within 1 second after acid
accumulation begins. They combine with excess
acid to form substances that may not greatly affect
pH. Some buffers have a strong affinity to acid,
others are weak. The three primary plasma buffers
are bicarbonate (HCO3−), intracellular proteins, and
chloride (Cl−). All are negatively charged to
facilitate attraction to positively charged hydrogen
ions (H+). Combining positively charged with
negatively charged ions yields a neutral substance.

• Proteins: Serum and intracellular proteins offer a

37
 significant contribution to buffering acids. Hgb not
only transports O2 but also provides a very strong
buffer for hydrogen ions (H+). Albumin is also a
significant buffer, and hypoalbuminemia must be
considered when performing anion gap
calculations.

• HCO3− (perfect 24, normal range 22 to 26 mEq/L):

Serum bicarbonate (HCO3−) is one of the major
components of acid-base regulation by the kidney.
Bicarbonate is generated and/or excreted by
normally functioning kidneys in direct proportion
to the amount of circulating acid to maintain acid-
base balance. Because bicarbonate is affected by
both the respiratory and metabolic components of
the acid-base system, the relationship between
metabolic acidosis and bicarbonate is not
particularly linear or predictable. When the
bicarbonate level changes, the acid level changes in
the opposite direction. To determine the cause of
bicarbonate changes (as the source of a pH problem
versus compensation), the relationship to pH must
be evaluated. The pH changes in the presence or
absence of acid, and the directional relationship
reflects what caused the pH alteration. The kidney
is responsible for the regeneration of bicarbonate
ions as well as excretion of the hydrogen ions.
Although serum bicarbonate is a buffer, it is usually
reported in the standard electrolyte panel from a
venous blood sample as “CO2 content” or “total

38
 CO2” rather than as bicarbonate (HCO3−). The
serum HCO3− concentration is usually calculated
and reported separately with ABG analysis. Either
value may be used as part of the assessment of acid-
base balance (Table 1-2).

• Chloride (Cl−): The number of positive and negative

ions in the plasma must balance at all times. Aside
from the plasma proteins, bicarbonate and chloride
are the two most abundant negative ions (anions) in
the plasma. To maintain electrical neutrality, any
change in chloride must be accompanied by the
opposite change in bicarbonate concentration. If
chloride increases, bicarbonate decreases
(hyperchloremic acidosis) and vice versa. However,
the combination of H+ and chloride actually creates
hydrochloric acid (HCl). Chloride concentration
may influence acid-base balance (see Anion gap).
Chloride concentration should be observed closely
when large amounts of normal saline are
administered to patients.

• Other buffers: Other buffers, including phosphate

and ammonium, are present in very limited
quantities and have a lesser impact on acid
regulation.

• Cellular electrolytes: The cells also offer protection in the

metabolic acid environment. H+ may exchange across the cell
wall, attracted by negatively charged intracellular proteins in a
cellular buffering process. When this happens, K+ is released from
the proteins and shifts out of the cell, causing an excess of K+ in

39
 the blood.

• Anion gap: Anion gap is an estimate of the differences between

measured and unmeasured cations (positively charged particles,
such as Na and H+, respectively) and measured and unmeasured
anions (negatively charged particles, such as HCO3− and Cl−).
Normally, cations and anions are equally balanced in live
humans (in vivo), but when measured in the laboratory (in vitro),
the difference may be between 10 and 14 mmol/L. This difference
is termed a normal gap (between number of + and – ions).
Particles that possess charges tend to have high affinity to bind to
other particles that possess charges that are opposite their own
(hence the term “opposites attract”). Anion gap is used to
determine if a metabolic acidosis is attributable to an
accumulation of nonvolatile acids, such as lactic acid or
ketoacids. Both contribute a positive charge as a result of excess
H+ or from net loss of bicarbonate (e.g., diarrhea). The gap is not
affected when a patient has metabolic acidosis purely from
kidney failure. The formula for the calculation of anion gap (AG)
is:

Unmeasured cations: Calcium, magnesium, gamma

globulins, potassium, hydrogen ions (bind to
negative-charged particles).

Unmeasured anions: Albumin, phosphate, sulfate,

lactate (bind to positive-charged particles).

Table 1-2
DIAGNOSTIC TESTS FOR ACID-BASE BALANCE

40
 Role of ABG Measures Normals
Evaluation of arterial oxygen Arterial oxygen saturation Sao2: 0.95 to 1.0 or 95%
(dissolved oxygen and oxygen (oxygen bound to hemoglobin) to 100%
bound to hemoglobin)
Partial pressure of arterial Pao2: 80 to 100 mm Hg
oxygen (dissolved oxygen) (decreased over the age
of 70 years)
Calculation of alveolar-arterial (A- Alveolar-arterial gradient A-a Do2: <20 mm Hg
a) oxygen gradient Pao2/Fio2 ratio PF ratio: 300
Evaluation of cellular environment pH (reflects H2CO3) i.e., ↑ H2CO3 pH
then pH ↓ Perfect: 7.40
Normal range: 7.35 to
7.45
Evaluation of ventilation Paco2 Paco2 Normal range: 35
to 45 mm Hg
Evaluation of tissue metabolism H+ inversely (indirectly) pH
reflected by buffers: Perfect: 7.40
bicarbonate (HCO3−) Total Normal range: 7.35 to
CO2 7.45
−
+
i.e., ↑ H then buffers ↑ HCO 3 : 22 to 26 mEq/L

Total CO2: 20 to 26
Base
Normal range: −2 to +2
Anion gap: 12 ±2
Additional measures of tissue Both contribute H+ to blood Lactic acid: 1 to 2
metabolism Lactic acid mmol/L
Ketoacids Lactic acid: 1 to 2
mmol/L
Ketoacids
Blood: 0.27 to 0.5
mmol/L
Urine levels
Small: ≤20 mg/dL
Moderate: 30 to 40
mg/dL
Large: >50 mg/dL
Evaluation of renal clearance Appropriate clearance of pH
excessive components: Perfect: 7.40
H+ or (HCO3−) Range: 7.35 to 7.45
Appropriate clearance of BUN: 0 to 20 mg/dL
excessive components: BUN Creatinine: <2.0 mEq/L
and creatinine
ABG, Arterial blood gas; BUN, blood urea nitrogen.

Step-by-step guide to arterial blood gas analysis

A systematic analysis is critical to the accurate interpretation of
ABG values to determine the origin of acid-base imbalance and
level of compensation (see Table 1-2).

Step 1: Check the pH: Determine if pH is perfect (7.40)

41
When there is a perfect balance of acid and buffer (base), the pH is
termed neutral or perfect. If it is not perfect, determine if the
direction of the difference is above or below 7.40. Next, determine if
it is in the normal range (7.35 to 7.45). If it is abnormal, identify
whether it is on the acidotic (less than 7.35) or alkalotic (greater
than 7.45) side of normal. “Perfect pH” occurs when the system
preserves neutrality (pH 6.8) inside the cells, where most chemistry
occurs, and maintains the serum pH at 7.40. For the purposes of
learning, the perfect pH is where all measurement begins. When the
system contains too many acid ions (in the form of ↑CO2 or ↑H+),
this causes acidemia. When the system contains too few acid ions
(in the form of ↓CO2 or ↓H+), this causes alkalemia, and the pH will
reflect the change. Any variation in the pH in relationship to perfect
(7.40) must be noted by the provider. If the pH is in the range of
7.35 to 7.45, there are only two possibilities. First, the deviation is a
normal variation, wherein no abnormalities exist on either the
respiratory side (PaCO2) or the metabolic side (HCO3−) of the pH
equation. Second, there is a problem with ventilation (respiratory),
cellular acid production (metabolic), or the ability of the kidneys
(metabolic) to balance the pH. Diagnosis of a problem with
metabolic acid-base balance is more complex, because many
conditions generate metabolic acids and renal failure creates an acid
clearance deficit.
pH less than 7.35, Acidosis: Extra acids are present or base is lost.
If pH is 7.35 to 7.39, the pH is normal but not perfect (7.40); the pH
is considered “on the acidotic side.”

• Acidosis: Extra acids are present or base is lost, with a pH less

than 7.35.

1. Cellular acidosis: When cells are hypoxic or

processing proteins to yield glucose, there is an
increase in lactic acid or ketoacid.

2. Respiratory acidosis: If lung function is

inadequate, such as in COPD, the failure to

42
 effectively ventilate results in the inability to
exhale CO2, and that failure causes carbonic acid
to increase (more acid) and pH to decrease.

3. Renal acidosis: If kidney function is inadequate,

the ability to break carbonic acid from H2CO3 into
hydrogen ions (H+) and HCO3− is reduced or lost.
When this failure occurs, carbonic acid increases
(more acid) and pH decreases.

pH greater than 7.45, Alkalosis: Extra base is present or there is

loss of acid. If pH is 7.41 to 7.45, the pH is normal but not perfect
(7.40); the pH is considered “on the alkalotic side.”

• Alkalosis: Extra base is present or there is loss of acid, with a pH

greater than 7.45.

1. Respiratory alkalosis: When hyperventilation is

the primary problem, there is a very rapid
removal of CO2, causing carbonic acid to decrease
(less acid) and pH to increase.

2. Renal alkalosis: If kidney function is

overstimulated (e.g., with aggressive diuresis),
there may be excessive loss of hydrogen ions
(H+), causing carbonic acid to decrease (less acid )
and pH to increase.

3. Other contributors: Gastric and intestinal removal

of acids may occur when patients have diarrhea,
vomiting, or when excessive gastric drainage

43
 removes acidic secretions and influences the acid-
base balance.

Step 2: Check the PaCO2

Check PaCO2 for perfect levels (40 mm Hg). If not perfect, determine
if the direction of change is above or below 40 mm Hg. Next,
determine if CO2 is in the normal range (35 to 45 mm Hg). If
abnormal, identify whether it is on the acidotic (> 45 mm Hg) or
alkalotic (< 35 mm Hg) side of normal. If PaCO2 has been retained as
a result of hypoventilation or overly removed through
hyperventilation, the change in pH will be in the opposite direction
of the PaCO2. Elevated CO2 lowers pH, whereas decreased CO2
increases pH. If the change in pH is in the normal range but not
perfect, or is out of range, with a PaCO2 value that has traveled in
the opposite direction, respiratory acid retentions caused the
imbalance. Using this technique helps determine whether the
primary problem is respiratory (involving PaCO2) or metabolic
(reflected by HCO3−). The PaCO2 has to be outside the normal range
for there to be a problem.

Step 3: Check for base (deficit or excess)

Check bicarbonate (HCO3−) (24 mEq/L) and base (0) for perfect
levels. If not perfect, determine if the direction of change is above or
below perfect. Next, determine if HCO3− (22 to 26 mEq/L) and/or
base (–2 to +2) is in the normal range. If the values are abnormal,
relate the two values to metabolic acid (H+). If bicarbonate and base
are decreased (a deficit), metabolic acid is increased. If bicarbonate
and base are increased (in excess), metabolic acid is decreased. If
the change in pH is in the normal range but not perfect, or out of
range and the assumed H+ is in the opposite direction (meaning that
the HCO3− and/or base are in the same direction as the pH),
metabolic issues caused the imbalance. Using this technique helps
determine whether the primary problem is respiratory (involving

44
PaCO2) or metabolic (reflected by HCO3−), or both.

Step 4: Evaluate both PaCO2 and HCO3−

Correlating the direction of the pH change with the direction of
change in PaCO2 and H+ (HCO3−) is essential. The value that deviates
in the opposite direction from the pH suggests that the primary
disturbance is responsible for the altered pH. Assess pH for acidosis
or alkalosis, and then evaluate whether the change in CO2 or H+
(HCO3−) is most reflective of the “direction” of the pH change.
A mixed metabolic-respiratory acid-base imbalance or
compensation may be responsible for the values reflected by the
ABG.

Step 5: Check PaO2 and SaO2

Check PaO2 and O2 saturation to determine whether they are
decreased, normal, or increased. Decreased PaO2 and O2 saturation
may signal the need for increased concentrations of O2 or alveolar
recruitment strategies. Conversely, high PaO2 may indicate the need
to decrease delivered concentrations of O2. Oxygen evaluation is the
same for all ABG values, although in the presence of metabolic
acidosis, a more in-depth investigation will require evaluation of
tissue metabolic functions.

Respiratory acidosis
Pathophysiology

Evaluation of an abnormal arterial blood gas resulting in a

decreased pH attributable to hypoventilation
Example: pH 7.28, PaCO2 55, HCO3− 24, PaO2 92 mm Hg, SaO2 91%.

Step 1: pH is 7.28, not perfect or neutral (7.40) and outside

the normal range of 7.35 to 7.45
Ideally the pH should always be perfect (7.40), but a small variation
is acceptable (range of 7.35 to 7.45). One must remember that pH

45
changes are a symptom of a problem. Thus, the first issue is to
identify the problem.
pH: The primary problem with pH regulation is identified by the
direction of the pH change with regard to perfect: Is it on the acid
side (less than 7.40) or the alkaline side (greater than 7.40)?

1. pH 7.28: Acid side, outside the normal range.

2. Question: Is there a problem? YES, acidosis (identified by the

pH).

3. Where is the acid being generated? Are the acids respiratory or

metabolic?

4. PaCO2: 55 (elevated outside the normal range) ↑ respiratory acid is

accumulating.

5. (HCO3−)−: 24 (perfect) ↑ metabolic acid is not present, perfect

HCO3.

Step 2: PaCO2 is 55 mm Hg, not perfect (40 mm Hg) and

above the normal range of 35 to 45 mm Hg, indicating an
excess of respiratory acid

Investigation begins

1. Hypercapnia/elevated PaCO2 (PaCO2 greater than 45 mm Hg):

Signals alveolar hypoventilation. This problem occurs when alveoli
are not recruited, there is poor blood flow, the RR rate or tidal
volume is inadequate, or there is fluid or an increase in the space
between the alveoli and blood vessel. These conditions may be
chronic or acute.

2. If this is the causative problem, the pH has to be below 7.40,

reflecting excess acid (CO2) or an increase in carbonic acid (H2CO3),
which is a primary acidosis. Therefore, one must now investigate
what caused the increase in carbonic acid (H2CO3). For every 10 mm
Hg increase in CO2, the pH will acutely decrease 0.08 (on the acid

46
side).

3. Problem: Respiratory acidosis

Respiratory acidosis (hypercapnia, hypoventilation) is always

related to a ventilation problem caused by inadequate therapeutic
interventions or lung pathophysiology, resulting in retention of
PaCO2. PaCO2 derangements are direct reflections of the degree of
ventilatory function or dysfunction. The degree to which the
increased PaCO2 alters the pH depends on the rapidity of onset and
the ability of the blood and kidney to compensate via the blood
buffer and renal regulation systems. The pH may be profoundly
affected initially because of the time required (hours to days) for
kidney compensation to occur. The most common cause of
inadequate CO2 excretion (CO2 retention) is inadequate alveolar
ventilation or alveolar hypoventilation. Alveolar hypoventilation
can occur when there is airway obstruction, loss of alveolar recoil,
or inadequate time for exhalation affecting the ability to express
carbon gas into the environment. For CO2 to be removed from the
blood, the partial pressure of CO2 in the alveoli must be less than
that in the blood. In air-trapping syndrome (loss of alveolar recoil
or elasticity or airway obstructive disease) or profound
hypoventilation states, the alveolar concentration of CO2 increases,
which then limits the removal of CO2 from the blood. If the problem
is not properly managed, the patient may deteriorate into acute
respiratory failure.

Step 3: The HCO3− in the example is perfect at 24 mEq/L

The normal range of bicarbonate is 22 to 26 mEq/L.

Investigation begins

1. Normal HCO3− indicates that there is not a metabolic problem,

although compensation should begin within 4 to 48 hours, as
opposed to respiratory compensation for metabolic pH imbalances,
which happens in minutes.

47
2. Problem: No apparent kidney or metabolic problems.

Is there compensation for the respiratory acidosis? 

For compensation to occur, the carbonic acid must be presented to
the kidney and separated into H+ and HCO3−. In other words, the
excess CO2 will be processed into carbonic acid and ultimately into
H+ (which will be excreted in a functional kidney state) and HCO3−.
Kidney or renal compensation for accumulation of respiratory acids
is a slow process. After 48 hours if there continues to be an acidotic
pH, one must assume that the kidneys have lost the ability to
eliminate H+ or retain HCO3−.

Step 4: Diagnosis begins

1. Only the CO2 is elevated, without a change in the HCO3−.

2. pH is down and outside the range reflecting the presence of acid

in the blood.

3. Problem: The patient has acute respiratory failure, causing an

accumulation of respiratory acid (CO2). There is no compensation,
but no evidence is available at this time.

Diagnosis: Acute Respiratory Acidosis

Step 5: PaO2 92 mm Hg (not perfect 98 to 100 mm Hg but

within normal range 80 to 100 mm Hg), SaO2 91% (not
perfect 100% and below normal range of 95% to 100%)

Investigation begins: Slight decrease is apparent in PaO2 and

SaO2

1. Use of O2: If O2 is not in use on a patient with reduced PaO2 and

SaO2, applying O2 often corrects the readings. If O2 is in use,
changing to a device that delivers a higher concentration of O2, such
as changing from a nasal cannula to a face mask, may be sufficient
to correct the alveolar levels of O2. If the PaO2 and SaO2 do not

48
respond to the first device change or values further deteriorate, a
100% nonrebreather mask may be applied to provide close to 100%
O2. Note: All ABG readings must be recorded with consideration of
the mode of O2 delivery recorded, as well as the FIO2 or
concentration of O2. Otherwise, evaluation of the PaO2 and SaO2
values is meaningless. If the values are NOT recorded, the
assumption is made that the readings are done on room air, without
O2 in place.

2. Evaluating risk for poor tissue oxygenation: Thus far, ventilation

has been evaluated using the ABG, but both ventilation and
perfusion must be evaluated as part of O2 delivery to the cell level.
To objectively and proactively identify the patient at risk for tissue
hypoxia, early signs of the perfusion changes that precede increases
in serum lactate and the widening anion gap associated with lactic
acidosis may be noted. Changes in heart rate (HR), blood pressure
(BP), respiratory rate (RR), urine output, saturation of continuous
central or mixed venous Hgb, and serum creatinine are common. In
the shock setting, normal or near normal PaO2 and SaO2 readings are
possible on an ABG while capillary bed dysfunction ensues.
Normal readings indicate that O2 is being provided in adequate
amounts to saturate Hgb effectively, but the ABG is unable to assess
whether all tissue beds are receiving O2 or whether the cells are able
to use the O2. Until metabolic acidosis ensues resulting from
accumulation of lactic acid byproducts of anaerobic metabolism
caused by hypoperfusion, the ABG and SpO2 readings may be
misleading.

Collaborative management: Acute

respiratory acidosis
Care priorities

1. Restore effective alveolar ventilation

• Symmetrical lung expansion: Always check for symmetrical lung

49
 expansion, particularly if the patient was recently admitted for
trauma, has recently had central line placement, or has recently
been intubated or extubated. A pneumothorax may be present,
which may cause ineffective ventilation.

• Support ventilation: If PaCO2 is greater than 50 to 60 mm Hg,

there may be a need to intubate and place the patient on
mechanical ventilation, or if already ventilated, there may be a
need to reevaluate the ventilation settings. The primary
mechanism to treat respiratory acidosis is to increase the tidal
volume (VT) and/or the respiratory rate (F), to increase minute
ventilation (VT × F). Care must be taken to ensure the adequate
minute ventilation; therefore, if low tidal volumes are applied,
the respiratory rate may need to be increased. If lung compliance
allows, the flow rate (how rapidly the volume is delivered) may
also be increased. This will prolong exhalation time and allow
adequate time for CO2 excretion.

• Bronchodilation: Consider the use of inhaled beta-agonists to

maintain open airways.

2. Normalize the pH

• Although a life-threatening pH must be corrected to an acceptable

level promptly, a normal pH is not the immediate goal.
Generally, the use of bicarbonate is avoided because of the risk of
alkalosis when the respiratory disturbance has been corrected
and the secondary effect of blocking the signal to the hemoglobin
to release the oxygen (shift to the left). Note: If lactic acidosis is
present, the patient has metabolic acidosis, which has resulted
from ineffective tissue oxygenation. Supporting ventilation will
not resolve lactic acidosis. Further, bicarbonate may temporarily
neutralize the pH, but may actually worsen tissue hypoxia.

3. Evaluate compensation (occurs in the presence of normal

renal function)

• Although the response of the kidneys to an abnormal pH level is

50
 slow (4 to 48 hours), they are able to facilitate a nearly normal pH
level by excreting or retaining large quantities of HCO3− or H+
from the body. Note that the level of available HCO3− is always
opposite the level of H+ present in the plasma. HCO3 is partnered
as it buffers H+ which yields carbonic acid.

Compensatory response for acute respiratory acidosis

When the respiratory acid level (CO2) increases, carbonic acid
increases and the pH decreases. The increased H2CO3 (carbonic
acid) is presented to the kidney, where the H+ is separated from the
bond, yielding HCO3−. The “free” bicarbonate (HCO3−) provides
additional buffer. In addition, the kidneys excrete the “free” H+
(hydrogen ions) in the urine to reduce the acid level. When the
kidneys are functional, the pH decrease seen from increased
respiratory acid is less dramatic. The decrease in pH is modified to
a small degree by intracellular buffering. To compensate for the
acidosis created by increased CO2, K+ ions are released from cellular
proteins and H+ ions take their place, bound to the proteins. The
result is frequently serum hyperkalemia (reflective of intracellular
hypokalemia). This is much more common and dangerous in the
presence of metabolic acidosis (particularly diabetic ketoacidosis
[DKA]).
Renal or kidney compensation via synthesis and retention of
HCO3 regulates much of the acid; however, the pH will not be
returned to perfect. When carbonic acid is converted into HCO3−
(bicarbonate buffer), the pH will be decreased only by
approximately 0.03 for every 10 mm Hg increase in CO2.

1. Uncompensated respiratory acidosis: pH 7.28, PaCO2 55, HCO3−

24 [PaO2 92 mm Hg, SaO2 91%]

Compensation for respiratory acidosis

51
Over time, if ventilation is not effectively managed, the HCO3− will
increase to 32, which will correct the pH to 7.35 if kidneys are
functioning normally. The CO2 remains 55. O2 provided at 4 L/min
by nasal cannula increases the PaO2 to 100% and the SaO2 to 100%.
With the same PaCO2, the pH is corrected, primarily by the
kidneys, to 7.35: on the acid side of the normal range. Whenever the
pH is less than 7.40, it reflects either a normal variation OR
abnormality with compensation.

2. Respiratory acidosis with kidney compensation: pH 7.35, PaCO2

55, HCO3− 32 (PaO2 100 mm Hg, SaO2 100%)

pH 7.35: Acid side but in normal range.

PaCO2 55 mm Hg: Acid and outside normal range.

Problem: Respiratory acidosis, but pH is in normal range.

HCO3− 32 mEq/L: The kidneys took the H2CO3, separated it into

HCO3− and H+, and then excreted the H+ and retained the end
product, the bicarbonate (made from the CO2).
Ultimately, the increase in PaCO2, which created an increase in
carbonic acid, made the pH decrease. When the increased carbonic
acid was presented to the kidney, it was separated into
↑bicarbonate (H+↓) and yielded the end diagnosis: compensated
respiratory acidosis. The kidneys must be functional for
compensation to occur in the presence of respiratory acidosis.

Chronic respiratory acidosis

The compensated scenario just described is what is often seen with
chronic hypercapnia, which occurs with chronic obstructive
pulmonary disorders (e.g., chronic emphysema and bronchitis,
cystic fibrosis), restrictive disorders (e.g., pneumothorax,

52
hemothorax, Pickwickian syndrome), neuromuscular abnormalities
(e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic
lateral sclerosis), respiratory center depression (e.g., brain tumor,
stroke, bleed, head injury), and poor ventilation management. In
patients with a chronic lung disease, a near-normal pH is the result
of kidney compensatory mechanisms, as discussed earlier.
Patients with chronic lung disease can experience acute increases
in PaCO2 or lose their metabolic compensation (increased
production of metabolic acid or loss of renal function) secondary to
superimposed disease states, such as pneumonia, hypermetabolic
cellular hypoxia, or renal dysfunction. If the chronic compensatory
mechanisms in place (e.g., elevated) are inadequate to meet the
sudden increase in PaCO2 or if the circulation of metabolic acids
increases, pH may change rapidly. In fact, these patients frequently
have normal HCO3− measures upward of 30. As an acute (on top of
chronic) process begins, the pH decreases, but the bicarbonate may
be slower to reflect the real problem. Care must be taken when
evaluating patients with chronic respiratory acidosis who have
secondary issues.

Clinical presentation
Patients may have possible increased work of breathing, anxiety,
pallor, sweating, reflective of respiratory distress. In advanced
respiratory acidosis, somnolence and inability to awaken the
patient are common. CO2-based acidosis has a sedative-like effect
on patients. Sleep may ensue following distress, giving the false
impression that the problem has resolved, when in reality, the
problem has resulted in sufficient CO2 accumulation for the patient
to lose consciousness from the sedative effect of severe
hypercapnia. Patients with obstructive sleep apnea are at risk for
developing respiratory acidosis.

Physical assessment
Patients have decreased depth of respirations with an initially
increased rate or decreased rate and depth of respirations in severe
respiratory acidosis. With obstructive lung disease or acute asthma
exacerbation, audible wheezing may be present. With severe

53
asthma, the chest can become silent, indicative gas exchange is
extremely impaired, and the patient is close to respiratory arrest.

Monitoring parameters
Use pulse oximetry to assess if hypoxemia ensues because of
ineffective ventilation. The patient needs close observation for
deterioration, so appropriate steps can be taken to provide
noninvasive positive-pressure ventilation (NPPV), such as bilevel
positive airway pressure (BiPAP) or endotracheal (ET) intubation
with mechanical ventilation.

Care plan: Respiratory acidosis

Impaired gas exchange 
related to alveolar-capillary membrane changes secondary to pulmonary
tissue destruction
Goals/Outcomes: Within 24 hours of initiation of treatment, the
patient improves and is reevaluated. The ultimate goal of adequate
gas exchange is evidenced by PaCO2, pH, and SaO2 that are normal
or within 10% of the patient’s baseline.
Respiratory Status Ventilation, Vital Signs Status, Respiratory
Status: Gas Exchange, Symptom Control Behavior, Comfort Level,
Endurance, Acid-Base Management: Respiratory Acidosis.

Respiratory monitoring

1. Monitor serial ABG results to assess the patient’s response to

therapy. Consult the provider for significant findings: Increasing
PaCO2 with decreasing pH, PaO2, and SaO2 values.

2. Monitor O2 saturation via pulse oximetry (SpO2). Compare SpO2

with SaO2 values to assess reliability. Watch SpO2 closely, especially
when changing FIO2, and evaluate the patient’s response to
activities (e.g., repositioning, chest physiotherapy).

3. Assess and report on the respiratory response to exertion and

treatments: Respiratory rate and rhythm, work of breathing, and

54
breath sounds. Compare findings before and after (e.g., O2 therapy,
physiotherapy, medications) for improvement.

4. Assess and report on changes in the patient’s level of

consciousness (LOC). If PaCO2 increases, be alert to subtle,
progressive changes in mental status. A common progression is
agitation → insomnia → somnolence → coma. To avoid creating a
comatose state caused by increasing CO2 levels, regularly awaken
patients with elevated PaCO2. Consult the advanced practice
provider if the patient is difficult to awaken.

Oxygen therapy

1. Carefully monitor the patient’s response to prescribed O2

therapy. Assess respiratory status after every change in FIO2.
Patients with chronic CO2 retention may be very sensitive to
increases in FIO2, resulting in respiratory depression. If the patient is
no longer able to breathe effectively enough to exhale an adequate
amount of CO2, mechanical ventilation may be needed. Be
aware of the importance of maintaining the compensated acid-base
status. If the PaCO2 is rapidly decreased by excessive mechanical
ventilation (dropping PaCO2, but a remaining excess of bicarbonate),
a severe metabolic alkalosis (posthypercapnic metabolic alkalosis)
could develop. The sudden onset of metabolic alkalosis may cause
hypocalcemia, which can result in tetany (see Hypocalcemia), or
hypokalemia, which coupled with severe alkalosis may precipitate
cardiac dysrhythmias.

Ventilation assistance

1. Assess for presence of bowel sounds and monitor for

gastrointestinal (GI) distention, which can impede movement of the
diaphragm and further restrict ventilatory effort.

2. Assess for presence of symmetrical lung expansion and normal

resonance of lung fields. Hyperresonance and asymmetry indicate
pneumothorax; dullness and asymmetry indicate solid tissue or

55
fluid occupation of lung or pleural space (e.g., hemothorax, pleural
effusion, and hyperplasia).

3. In patients who have obstructive lung disease and are not

intubated, encourage use of pursed-lip breathing (inhalation
through nose, with slow exhalation through pursed lips), which
helps airways to remain open and allows for better air excursion.
Optimally, this technique will diminish air entrapment in the lungs
and make respiratory effort more efficient.

Cough Enhancement, Acid-Base Management, Respiratory

Acidosis, Mechanical Ventilation, Artificial Airway Management,
Oral Health Maintenance.

Additional nursing diagnoses and

interventions
Nursing diagnoses and interventions are specific to the
pathophysiologic process. See Acute Pneumonia (Chapter 4), Acute
Lung Injury and Acute Respiratory Distress Syndrome (Chapter 4),
and Acute Respiratory Failure (Chapter 4), along with Mechanical
Ventilation later in this chapter.

Respiratory alkalosis
Pathophysiology
The problem is alveolar hyperventilation, which results in an
increased pH.
Example: pH 7.48, PaCO2 30, HCO3 23.

Step 1: The pH is not perfect

The problem is named by the direction of the pH with regard to
perfect: Is the pH on the alkaline side greater than 7.40 or the acid
side less than 7.40? The pH of 7.48 is on the alkaline side.

Step 2: The PaCO2 has decreased to 30 mm Hg, reflecting

hypocapnia (PaCO2 less than 35 mm Hg)

56
This signals alveolar hyperventilation (decreased respiratory acid
causing an alkaline pH). When minute ventilation is increased, CO2
decreases, which causes H2CO3 to also decrease (production of
carbonic acid decreases) and the pH becomes alkalotic. Question: Is
there a problem? The CO2 has decreased and the pH has increased.
The problem is respiratory alkalosis.

Step 3: The HCO3− is 23, which is less than perfect but still
in the normal range
It must be determined if there is a metabolic contribution to the
alkalosis or if there is compensation provided by the kidney
retaining acid and excreting bicarbonate. The BE is –1, within the
normal range.

Step 4: The Pco2 is low, the pH is high, and the HCO3 is

normal
The patient is exhibiting a rapid respiratory rate, with deep breaths.

Step 5: The SpO2 may be normal because the patient is

breathing very rapidly but effectively
However, when the respiratory rate is very rapid, there is less time
for oxygen diffusion, thus it is possible that the patient’s oxygen
levels may decrease.
Problem: ↓CO2 +H2O → ↓H2CO3 → HCO3− + H+

Acute respiratory alkalosis

Respiratory alkalosis occurs as a result of an increase in the minute
ventilation (alveolar hyperventilation). Defined as PaCO2 less than
35 mm Hg, acute alveolar hyperventilation results most frequently
from anxiety and is commonly referred to as hyperventilation
syndrome. Caution must be applied to evaluate whether
hyperventilation is actually a compensatory mechanism for primary
metabolic acidosis. Although it may become necessary to control
the patient’s minute ventilation, in the presence of metabolic
acidosis, loss of the hyperventilation compensation may create a
life-threatening acidotic pH and profound refractory hypotension

57
and asystole.
In the alkalotic environment, cells release H+ and K+. The result is
frequently serum hypokalemia (low serum K+ with intracellular
hyperkalemia). Kidney compensation for the respiratory alkalosis is
not clinically apparent for 4 to 48 hours. Acute respiratory alkalosis
progresses to chronic respiratory alkalosis if it persists for longer
than 6 hours and/or renal compensation occurs.

Compensatory response to respiratory alkalosis

The kidneys, within 4 to 48 hours, should excrete bicarbonate and
retain additional H+ in an attempt to compensate for the lack of
respiratory acid.

• Acute respiratory alkalosis: First 4 to 48 hours HCO3− (and

therefore the increase in H+) will decrease 2 mEq/L for every 10
mm Hg decrease in Pco2.

• Chronic respiratory alkalosis: After approximately 48 hours, the

amount of bicarbonate should decrease 4 mEq/L of HCO3 for
every 10 mm Hg decrease in Pco2.

1. Uncompensated respiratory alkalosis: pH 7.48,

PaCO2 30, HCO3− 23

2. Compensated respiratory alkalosis: pH 7.44,

PaCO2 30, HCO3− 19

If there is only one problem contributing to the pH abnormalities,

the pH should function as expected. In other words, a removal of
acid by the problem system should be compensated by acid

58
retention by the opposing system.

Chronic respiratory alkalosis

Chronic respiratory alkalosis is a state of chronic hypocapnia
caused by stimulation of the respiratory center. The decreased
PaCO2 stimulates the renal compensatory response and results in a
proportionate decrease in plasma bicarbonate (and retention of H+)
until a new, steady state is reached. Maximal renal compensatory
response requires several days to occur and can result in a normal
or near-normal pH. Chronic respiratory alkalosis is not commonly
observed in patients who are acutely ill but, when present, it can
signal a poor prognosis.

In alkalotic environments

• Sodium and potassium: May be decreased slightly to profoundly

(potassium will shift from the extracellular space to the
intracellular space in exchange for H+).

• Serum calcium: May be decreased because of increased calcium

and bicarbonate binding. Signs of hypocalcemia include muscle
cramps, hyperactive reflexes, carpal spasm, tetany, and
convulsions.

• Serum phosphorus: May decrease (less than 2.5 mg/dL),

especially with salicylate intoxication and sepsis, because the
alkalosis causes increased uptake of phosphorus by the cells. No
symptoms occur, and treatment usually is not required unless a
preexisting phosphorus deficit is present.

Clinical presentation
Presentation includes lightheadedness, anxiety, paresthesias
(especially of the fingers), and circumoral numbness. In extreme
alkalosis, confusion, tetany, syncope, and seizures may occur.

59
Physical assessment
Increased rate and depth of respirations (hyperventilation) are
present.

Monitoring parameters
Cardiac dysrhythmias are present.

Care plan: Respiratory alkalosis

Ineffective breathing pattern 
related to anxiety, tissue hypoxia, or work of breathing.
Goals/Outcomes: If the respiratory alkalosis is primary, within 4
hours of initiating treatment the patient has improved. Final
outcome is that the patient’s breathing pattern is effective, as
evidenced by PaCO2 ≥35 mm Hg and pH 7.45.
Respiratory Status: Ventilation, Vital Signs Status,
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance; Electrolyte and Acid-Base Balance.

Ventilation assistance

1. Manage anxiety: Reassure the patient that a staff member will

remain in the room.

Encourage slower, deeper breathing. Have the patient

mimic your own breathing pattern. Administer
sedatives or tranquilizers if prescribed. Report the
patient’s response to the advanced practice
provider.
2. Monitor for and manage dysrhythmias: Consult the advanced
practice provider for new or increased dysrhythmias. Slight
alkalosis can sometimes cause dysrhythmias in those with
preexisting heart disease requiring inotropic drugs (see Appendix
6). Hypokalemia associated with alkalosis increases the probability
of dysrhythmias.

60
3. Manage fatigue: Provide uninterrupted rest after the breathing
pattern has stabilized. Hyperventilation can result in fatigue.

Hyperventilation may lead to hypocalcemic tetany despite a

normal or near-normal calcium level because of increased binding
of calcium. For chronic respiratory alkalosis, nursing diagnoses
and interventions are specific to the pathophysiologic process.

Additional nursing diagnoses and

interventions
Nursing diagnoses and interventions are specific to the
pathophysiologic process.

Metabolic acidosis
Pathophysiology
Accumulation of metabolic acids, reflected by decreased HCO3−
(less than 22 mEq/L) with a pH decreased below 7.40. Metabolic
acids are circulating acids that cannot be exhaled. These acids
should be neutralized by buffers, excreted by the kidneys, or
metabolized.
Example: pH 7.28, PaCO2 39, HCO3− 16, PaO2 98 mm Hg, SaO2 99%.

Step 1: The pH is not perfect

The problem is named by the direction of the pH with regard to
perfect: Is the pH on the alkaline side greater than 7.40 or the acid
side less than 7.40? The pH of 7.28 is on the acid side.

• Increased acid production: Excessive lactate and ketones cause

acidosis and contribute more unmeasured positives (H+) into
circulation. When an increase in H+ occurs, HCO3− decreases

61
 because the role of bicarbonate is to buffer H+. The conjugation of
H+ and HCO3− yields an increase in carbonic acid. As carbonic
acid (H2CO3) increases, the pH decreases.

• Decreased renal tubular function (acute tubular necrosis [ATN] or

chronic failure): If the kidney is unable to excrete H+, or if the
load is beyond tubular transport capabilities, an increase in H+
occurs. HCO3− decreases because the role of bicarbonate is to
buffer H+ and the kidney has lost the capability to regulate and
create appropriate bicarbonate. The conjugation of H+ and
available HCO3− yields an increase in carbonic acid. As carbonic
acid (H2CO3) increases, the pH decreases.

• Ingestion of exogenous acids: Certain medications can cause an

increase in circulating acids. Alcohols and other ingested acids
can facilitate a wide anion gap.

Step 2: The PaCO2 is slightly decreased to 39 but within the

normal range
The patient does not have respiratory alkalosis or acidosis. The
lungs are not retaining CO2 and are not exhaling excessive amounts
of CO2.

Step 3: The HCO3− is 16, which is less than perfect and

below the normal range
This means that the metabolic acid (H+) is increased. The BE is –6,
below the normal range. It must be determined if the acidosis is the
problem or a compensatory mechanism for respiratory alkalosis.
We have determined respiratory alkalosis is not present.
Problem: Metabolic acidosis is caused by any/or any combination
thereof:

• Failure of the kidneys to regulate and excrete acid appropriately

(acute or chronic kidney failure).

• Cellular production of acid increases beyond normal regulatory

capacity resulting from metabolic alterations (lactic acidosis or

62
 ketosis).

• Ingestion of acids (aspirin, methanol).

Metabolic acidosis is much more difficult to diagnose than

the simple presence or absence of acid. One must first diagnose the
cause of the acid-base imbalance.

Step 4: The Pco2 is normal, whereas the HCO3− is decreased

The patient is exhibiting a normal respiratory rate, with normal
depth. With a decreased HCO3− and normal PaCO2, the patient is not
compensating for a respiratory alkalosis. The PaCO2 would be
decreased with respiratory alkalosis if the decreased HCO3− was a
compensatory response. The decreased HCO3− is the primary
problem; an acute metabolic acidosis. Question: What is the
problem? The HCO3− has decreased and no compensation is
apparent by the lungs. The respiratory rate and depth have not
increased.

Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has normal oxygenation.

Step 6: Performed only in metabolic acidosis: Evaluate

glucose, ketones, lactate, chloride level, anion gap and
tissue oxygenation (if necessary)
Example: pH 7.28, PaCO2 39, HCO3− 16, PaO2 98 mm Hg, SaO2 99%.
One must investigate why H+ is increased and bicarbonate is
decreased.

• Is it a compensatory response? If so, the H2CO3↑ (H+↑) and the

patient would have a pH on the alkaline side, indicating

63
 compensatory response for respiratory alkalosis.

• Is it a kidney problem? In this case, blood urea nitrogen (BUN)

and/or creatinine would be elevated.

• Is it a high chloride (inadequate buffer) problem? If so, the

chloride would have to be high.

• Did the patient ingest acids?

• Is it a tissue metabolism issue? In this case, the patient will have

high ketones and/or lactic acidosis.

If the answer to the first four questions is no, or those problems

do not seem significant enough for the pH change, a further
investigation must be performed.
Evaluation of glucose and ketones may be reviewed (see Diabetic
Ketoacidosis, Chapter 8). If glucose is elevated, a serum ketone level
should also be drawn to evaluate for ketoacidosis. If the patient is
not found to be in hyperglycemic crisis, lactic acidosis may be
present. Evaluation of tissue perfusion and oxygenation requires
more testing. Consideration must be allowed for glucose and
ketones.
If lactic acid is elevated, it may become necessary to find the
cause by using measures to evaluate tissue oxygenation.
Glucose 120, Ketones negative, Lactate 6.8.
This then points to acute metabolic (lactic) acidosis.

Metabolic lactic acidosis (lactate level > 4

MMOL/L)
Assessing perfusion and oxygen consumption at the
cellular level
Since the early work of Dr. William Shoemaker, it has been well
identified that global tissue hypoxia accompanies all categories of
shock, including both O2 delivery and O2 use shock. The work of
the Surviving Sepsis Campaign to establish early goal-directed
therapy validated the role of lactate measurement as a guide to

64
therapy. When cells are in a shock state, O2 delivery shock is
present. Shock effects the mechanics of delivery, whereas systemic
inflammatory response or severe sepsis, with the secondary effects
of endothelial dysfunction, vasodilation, inflammatory mediation,
and unopposed procoagulation, interfere with the use of O2 at a
microcirculatory and cellular level. Large areas of the capillary beds
may be hypoperfused, resulting in cells resorting to anaerobic
metabolism to survive.
Anaerobic metabolism results in the production of lactic acid, a
metabolic acid that can create acidosis if compensation fails. The
ABG reflects a decreased pH but does NOT always reflect a
markedly decreased PaO2 and SaO2. Persistent tissue-level hypoxia
further exacerbates the systemic inflammatory response and may
lead to multi-organ dysfunction syndrome (MODS) and eventually
death.
Arterial lactate concentration is dependent on the balance
between its production and consumption. In the critically ill septic
population, increased glucose metabolism, increased energy
expenditures, and profound catabolism are the norm. The
corresponding lactic acidosis signals physiologic stress but may not
necessarily be evidence of tissue hypoxia. The concomitant energy
expenditures, along with metabolic dysfunction, will increase
lactate production, but high levels of clearance may mask this
disturbing trend.
These conditions, coupled with an out-of-control inflammatory
response and increasing oxygenation dysfunction at the tissue level,
combine to produce a profound tissue acidosis. The lactate
production is further increased via other abnormal pathways that
are specifically related to metabolic dysfunction, even in the
absence of tissue hypoxia (type B lactic acidosis).
The main cause of the significantly increased lactate is still a
puzzle. One factor is the failure of adenosine triphosphate (ATP)
production, which clearly occurs in the presence of a profound O2
supply/demand imbalance (type A lactic acidosis). This in turn
affects the mitochondrial ability to use pyruvate, and the increased
pyruvate is indicative of a profound metabolic hyperlactatemia, an
elevated lactate/pyruvate ratio, increased glucose, and low energy
production. Ultimately, as severe sepsis progresses, it evolves into a

65
mediator-induced cardiac failure state, with profound intraarterial
hypovolemia.

Special considerations for patients with lactic acidosis

In 2004, Nguyen et al., in their work related to early goal-directed
therapy when treating sepsis, validated that the higher the
clearance of lactate in the first 6 hours after resuscitation, the lower
the mortality. In those first hours of evaluation and resuscitation,
achieving a normal ScVO2 along with an increasing lactate clearance
is the desired therapeutic end point, reducing the potential for
MODS.

Measuring lactic acids

In any patient whose condition arouses suspicion (e.g., with
tachycardia, tachypnea, hyperventilation, and/or hypotension), it is
essential to directly measure acid.

1. Lactate level: All patients who run the risk of cellular hypoxia
must have a sample drawn for a lactate level to evaluate for lactic
acidosis. An arterial lactate sample should be placed on ice and
taken as soon as possible to the laboratory. Any lactate greater than
4 mmol/L needs to be investigated for severe tissue hypoxia and
hypoperfusion. Lactates greater than 2 mmol/L should be observed
along with the clinical conditions of the patient. Serial lactates
should be performed to evaluate therapy effectiveness and follow
the clearance level. A lactate clearance greater than 10% in 24 hours
is considered a successful measure of therapeutic intervention for
severe sepsis.

a. Limitations to lactate level: The value of lactate is

obviously limited as a result of lactate
concentrations that are affected by both
production and elimination. Liver dysfunction,
ketosis, and many medications administered in
the critical care unit may affect the measured
lactate levels. Therefore, lactate levels by

66
 themselves will not give as much beneficial
information as those in the presence of wide
anion gap and low or normal ScVO2.

Collaborative management: Metabolic lactic

acidosis
Care priorities
Key concepts to keep in mind when managing the patient with
lactic acidosis, including specific additional monitoring used in
refining the plan of care.

1. Manage perfusion first

Lactic acidosis IS NOT respiratory acidosis! Respiratory acidosis is
primarily a ventilation problem, whereas lactic acidosis is primarily
a perfusion-, metabolic stress–, or cellular O2 consumption or
extraction–related problem.

2. Do not rely on SaO2 to assess oxygenation

Reflects reservoir bound O2 and very indirectly reflects oxygen
delivery. Normal SaO2 is 0.95 to 1.00.

3. Implement additional monitoring for tissue hypoxia

Supplemental measures may be used in patients who are critically
ill for evaluation of tissue hypoxia. Mixed venous and/or central
venous saturation of Hgb evaluates the amount of O2 being used by
the cells. The comparison of arterial (precellular) saturation to
central or mixed venous (postcellular) is most commonly used to
evaluate the tissue O2 consumption compared with O2 delivery.

• Mixed venous (Svo2) or central venous oxygen saturation (Scvo2):

This value is measured by an indwelling O2 probe/sensor on the

67
 tip of a catheter placed in the central vein (CV catheter) or PA
(PA catheter). Measurement may provide an early indication of
perfusion failure or increased tissue demands for O2, reflected by
a decreased mixed venous saturation of Hgb. If this saturation is
normal or high, but the patient has an increased lactate level, the
cells may be unable to extract or use O2, which frequently occurs
in the later stages of severe sepsis.

• Mixed venous saturation values (Svo2): This value should always

be correlated with other tissue indicators of hypoxia, base deficit,
widening anion gap, serum bicarbonate, and lactate levels. The
difference between arterial and venous blood gases is reflective of
global O2 consumption. The following standard parameters are
based on mixed venous blood gas and have not yet been
standardized for central venous gases; however, the basic
principles are the same.

• Svo2 or Scvo2: Reflect unused O2 or remaining reservoir after

release of needed O2 has occurred. Normal SVO2 is 0.60 to 0.80 OR
ScVO2 of 0.65 to 0.85.

• Oxygen consumption: SaO2 minus ScVO2 reflects O2 consumption.

Example: SaO2 1.00 – SVO2 0.70 = 0.30, approximately

30% consumption.

• O2 extraction ratio: SaO2 minus SVO2 divided by SaO2 reflects O2

extraction ratio: Example: (SaO2 1.00 – SVO2 0.70) ÷1.00 = 30%
oxygen extraction ratio.

Normal oxygen extraction ratio is 20% to 30%: In other words, the

patient should normally use between 20% and 30% of their total
available O2. O2 extraction is a mathematical formula that assists in
evaluating the compensatory mechanisms. The first line of
compensation is to increase the delivery of O2 (increase the cardiac
output [CO], amount of Hgb, and O2 saturation), and the second

68
line is to release O2 from Hgb to provide more dissolved O2 at the
cell level, resulting in a shift to the right in the dissociation curve
(Figure 1-1).

FIGURE 1-1 The oxyhemoglobin dissociation

curve. Source: (From Stillwell SB: Mosby’s critical care nursing reference,
ed 4, St Louis, 2006, Mosby).

4. Recognize unusual findings, such as persistent lactic

acidosis with normal SVO2
Patients presenting with a normal SVO2 and persistent lactic acidosis
are NOT normal. Patients who are using more than 20% to 30% are
signaling inadequate O2 delivery, dipping into second-line
compensation by removing abnormally high levels of oxygen from
the hemoglobin. Second line compensation may be short lived,
resulting in acute celluar hypoxia when desaturation of
oxyhemoglobin fails.

Acute metabolic acidosis

Example: pH 7.28, PaCO2 39, HCO3− 16, PaO2 98 mm Hg, SaO2 99%.
Bicarbonate is decreased, which always means that H+ is

69
elevated. If H+ is elevated, resulting in increased carbonic acid, and
the pH is decreased even slightly, the problem is acid accumulation.
In this case, it is acute metabolic acidosis, without compensation.

As the nonvolatile acid H+ increases, it will displace the

intracellular potassium, resulting in a serum hyperkalemia but an
intracellular hypokalemia. The lungs should increase the rate and
depth of respirations to exhale CO2, to compensate for the excess
metabolic acid, so that the pH can return to normal range.

Compensatory response to acute metabolic

acidosis
When H+ (acid) increases, pH decreases in the plasma. The central
respiratory center in the brain responds by increasing the rate and
depth of ventilation to four to five times the normal level to exhale
significant amounts of CO2 and returning the carbonic acid;
therefore, the pH is back to normal (but never perfect if there is a
problem). The decrease in pH (high presence of H+) stimulates
respirations. Attempts to compensate occur rapidly, as manifested
by lowering of the PaCO2, which may be reduced to as little as 10 to
15 mm Hg. The most important mechanism for ridding the body of
excess H+ is the increase in acid excretion through ventilation. In
addition, if the kidney is functional, acid will be excreted and
bicarbonate reabsorbed. Nonvolatile acids, however, may
accumulate more rapidly than the body’s buffers can neutralize
them, compensated for by the respiratory system, or excreted by the
kidneys.

1. Uncompensated acute metabolic acidosis: pH 7.28, PaCO2 39,

HCO3− 16.

70
2. Compensated metabolic acidosis: pH 7.36, PaCO2 30, HCO3− 16,
SaO2 99%, PaO2 100%.

Step 1: pH 7.36: Acid side but in normal range

• Question: Is there a problem? Normal variation in pH from

perfect, OR a compensated acid-base imbalance?

• Answer: Yes, there is a problem. The pH decrease is not a normal

variation because the PaCO2 and HCO3 are out of range.

Step 2: PaCO2 30 mm Hg
Level is decreased, which should reflect toward the alkaline side,
which does not coincide with the direction of the pH change.

Step 3: HCO3− 16 mEq/L

Level is decreased and beyond the low normal range, which means
the metabolic acid (H+) is increased. Here is the cause of the
problem that decreased the HCO3−.

Step 4: The PaCO2 is decreased in the presence of a

decreased HCO3−
Acid reduced the pH, and the lungs compensated by separating the
H2CO3 into CO2 and H2O and, with the help of the respiratory
center, exhaled the CO2. The problem is compensated metabolic
acidosis.

Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has normal oxygenation.

71
Collaborative management: Acute metabolic
acidosis
Care priorities

1. It is most important to treat the underlying disorder, if

possible

• Diabetic ketoacidosis: Insulin and fluids. If acidosis is severe

(with a pH of less than 7.15 or HCO3− 6 to 8 mEq/L), judicious
administration of NaHCO3 may be necessary.

• Alcoholism-related ketoacidosis: Glucose and saline.

• Diarrhea: Usually occurs in association with other fluid and

electrolyte disturbances; correction addresses concurrent
imbalances.

• Acute renal failure: Hemodialysis or peritoneal dialysis to

maintain an adequate level of plasma HCO3−.

• Renal tubular acidosis: May require modest amounts (less than

100 mEq/day) of bicarbonate.

• Poisoning and drug toxicity: Treatment depends on drug

ingested or infused. Hemodialysis or peritoneal dialysis may be
necessary.

• Lactic acidosis: Correction of underlying disorder related to

hypoxia and/or hypoperfusion. Mortality associated with lactic
acidosis is high. Unless pH is life threatening, treatment with
NaHCO3 is generally not indicated and may actually be harmful.

2. Measure anion gap

Anion gap is an estimate of the differences between measured and
unmeasured cations (positively [+] charged particles, such as Na
and H+, respectively) and measured and unmeasured anions
(negatively [–] charged particles, such as HCO3− and Cl−). A

72
thorough discussion was provided earlier in this chapter. The gap is
not affected when a patient has metabolic acidosis purely from
kidney failure. The formula for calculation of anion gap (AG) is:

3. Treat the pH
Treat the pH only if the patient’s life is threatened. Sodium
bicarbonate (NaHCO3) may be indicated when arterial pH is ≤7.15.
The usual mode of delivery is IV drip: 2 or 3 ampules (44.5
mEq/ampule) in 1000 mL D5W, although NaHCO3 may be given by
IV push in emergencies. Deficit should be calculated and replaced
accordingly. Concentration depends on severity of the acidosis and
presence of any serum sodium disorders. NaHCO3 must be given
very cautiously to avoid metabolic alkalosis and pulmonary edema
as a result of the sodium load. Dose (mmol) = BE × weight/10 to
replace half of the loss. Usual dose for full replacement is 1
mmol/kg IV (repeated as required).

4. Manage hyperkalemia
Usually serum hyperkalemia is present, but an intracellular
potassium deficit may be present. If a potassium deficit exists (K+
less than 3.5), it must be corrected before NaHCO3 is administered,
because when the acidosis is corrected, the potassium shifts back to
intracellular spaces. This shift in K+ could result in a profound
serum hypokalemia with serious consequences, such as cardiac
irritability with fatal dysrhythmias and generalized muscle
weakness. See Hypokalemia for more information.

5. Support ventilation
If mechanical ventilation is required on the basis of ABG results and
clinical signs, it is important that the patient’s compensatory
hyperventilation be allowed to continue to prevent acidosis from
becoming more severe. Therefore, the respiratory rate on the
ventilator should not be set lower than the rate at which the patient
has been breathing spontaneously, and the tidal volume should be

73
large enough to maintain compensatory hyperventilation until the
underlying disorder can be resolved.

Nursing diagnoses and interventions

Nursing diagnoses and interventions are specific to the
pathophysiologic process. See nursing diagnoses and interventions
in the section on Mechanical Ventilation, Acute Respiratory Failure
(Chapter 4), Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2), Acute Renal Failure/Acute Kidney
Injury (Chapter 6), and Diabetic Ketoacidosis (Chapter 8).

Chronic metabolic acidosis

Assessment

History and risk factors

Affected patients generally include those with chronic renal failure,
renal tubular acidosis, loss of alkaline fluid (e.g., with diarrhea or
pancreatic or biliary drainage) for greater than 3 to 5 days.

Clinical presentation
Usually the process leading to chronic metabolic acidosis is gradual
and the patient is symptom-free until serum HCO3− is ≤15 mEq/L.
Fatigue, malaise, and anorexia may be present in relation to the
underlying disease. Findings vary, depending on underlying
disease states and the severity of the acid-base disturbance and the
speed with which it developed. There may be changes in LOC that
range from fatigue and confusion to stupor and coma.

Physical assessment
Tachycardia (until pH is less than 7.0, then bradycardia), decreased
BP, tachypnea leading to alveolar hyperventilation (may be
Kussmaul respirations), dysrhythmias, and shock state. Depending
on the type of shock and the vascular response, skin temperature
and color will be affected. Mild metabolic acidosis (HCO3− 15 to 18
mEq/L) may result in no symptoms, whereas symptoms will

74
develop with a pH less than 7.2.

Monitoring parameters
A waveform suggestive of hyperkalemia (prolonged PR interval,
widened QRS, and peaked T waves) may occur. Persistent
tachycardia may indicate tissue hypoperfusion.
Electrocardiography (ECG): Detects dysrhythmias, which may
be caused by metabolic acidosis or hyperkalemia. Changes seen
with hyperkalemia include peaked T waves, depressed ST segment,
decreased size of R waves, decreased or absent P waves, and
widened QRS complex. Ventricular fibrillation may occur.

Collaborative management: Chronic

metabolic acidosis
Care priorities

1. Normalize the pH with alkalizing agents

• For serum HCO3− levels less than 15 mEq/L, oral alkalis may be
administered (NaHCO3 tablets or sodium citrate and citric acid
oral solution [Shohl solution]). They are used cautiously to
prevent fluid overload and tetany caused by hypocalcemia.

• Caution: Be alert to the possibility of pulmonary edema if

bicarbonate is administered parenterally to patients with renal
insufficiency or cardiovascular disorders.

2. Manage hypophosphatemia with oral phosphates

• These are given if hypophosphatemia is present; it is not common

with chronic renal failure but may result from overuse of
phosphate binders given to treat hyperphosphatemia (very
common with chronic renal failure).

3. Provide renal replacement therapies

• Hemodialysis, citrated blood and renal replacement therapy

75
 (CRRT), or peritoneal dialysis may be indicated for chronic renal
failure or other disease processes (see Acute Renal Failure,
Chapter 6).

Nursing diagnoses and interventions for

chronic metabolic acidosis
Nursing diagnoses and interventions are specific to the underlying
pathophysiologic process.

Metabolic alkalosis
Pathophysiology
Elevated HCO3− levels (greater than 26 mEq/L) reflect decreasing
circulating metabolic acids (H+). Caution must be applied to
differentiate compensatory alterations in response to respiratory
acidosis versus primary disorder. The diagnosis is made by the
presence of elevated serum HCO3− (up to 45 to 50 mEq/L). Acute
metabolic alkalosis most commonly reflects:

• Excessive loss of hydrogen ions: Loss of gastric acid from

vomiting or gastric suction, diuretic therapy.

• Excessive resorption of bicarbonate: Posthypercapnic alkalosis

(which occurs when chronic CO2 retention is corrected rapidly).

• Ingestion or administration of alkaline: Excessive NaHCO3

administration (i.e., overcorrection of a metabolic acidosis) or
ingestion of over-the-counter antacids.

Even when the causative factors have been removed, the alkalosis
will be sustained until volume and electrolyte disturbances that are
contributing to the alkalosis have been corrected. Severe alkalosis
(pH greater than 7.6) is associated with high morbidity and
mortality. Acidosis is better tolerated than alkalosis. SpO2 will be
used for Step 5, because a discussion of PaO2 and SaO2 does not add
to knowledge of metabolic alkalosis.

76
Example: pH 7.58, PaCO2 40 mm Hg, HCO3− 35, SaO2 99%, PaO2 99
mm Hg.

Problem: CO2 + H2O ← H2CO3↓← ↑HCO3− + H+↓

Step 1: The pH is not perfect

The problem is named by the direction of the pH with regard to
perfect: on the acid side less than 7.40 or the alkaline side greater
than 7.40.

Example: pH 7.58 on alkaline side, outside normal range.

Question: Is there a problem? YES.

Step 2: The PaCO2 is 40 mm Hg, which is perfect

This indicates PaCO2 is not driving the increase in pH.

Step 3: HCO3− has increased to 35 mEq/L, indicating that

the kidneys are retaining bicarbonate (H+ is decreased)
Here is the cause of the problem: acute metabolic alkalosis.
HCO3− is 35 (up and out of range), which means that the
metabolic acid and H+ is decreased.

Step 4: The PaCO2 has not increased in an attempt to help

correct or compensate for the increased HCO3−
The patient is exhibiting a normal respiratory rate, with normal
depth. With an increased HCO3−, and normal PaCO2, the patient is
not compensating for a metabolic alkalosis.

Step 5: The PaO2 and SaO2 are normal because the patient
is breathing normally
The patient has a normal oxygenation, but has an abnormal
response to alkalosis. The respiratory rate and depth should
decrease to promote CO2 retention to compensate.

Compensatory response to metabolic alkalosis

77
When H+ (acid) decreases, pH increases. The central respiratory
center in the brain responds by decreasing the rate and depth of
ventilation (in the normal lung) to 50% to 75% of the normal level.
This method of compensation is very poorly tolerated, because
patients will almost stop breathing.
Uncompensated metabolic alkalosis: pH 7.58, PaCO2 40 mm Hg,
HCO3− 35.

Compensated metabolic alkalosis: pH 7.45, PaCO2 59 mm Hg,

HCO3− 35.

In this example: pH 7.45, PaCO2 59 mm Hg, HCO3− 35, SaO2 99%,

PaO2 99 mm Hg.

Step 1: pH 7.45

Alkaline side, inside the normal range.

• Question: Is there a problem, despite the normal pH? Yes! Other

values are abnormal.

Step 2: PaCO2 59 mm Hg
Increased level, which reflects toward the acid side; change is
opposite the pH, which is toward the alkaline side. The PaCO2 is not
the problem but rather a compensation. The increased PaCO2 would
not increase the pH to alkaline. This measure is in the wrong
direction to be the cause.

Step 3: HCO3− 35 mEq/L

Increased and out of range. Here is the cause of the problem.
Metabolic alkalosis is present because the metabolic acid (H+) is

78
decreased.

Step 4: The PaCO2 is elevated at 59 mm Hg

The PaCO2 has increased response to an increased HCO3− level.
When HCO3− increases, the pH increases, indicating that less H+ is
present in the body. The pH has normalized on the alkaline side,
thus the patient has fully compensated metabolic alkalosis.

Step 5: The SaO2 is normal

The patient has a normal rate and depth of respirations.

Collaborative management: Acute metabolic

alkalosis
Management will depend on the underlying disorder. Mild or
moderate metabolic alkalosis usually does not require specific
therapeutic interventions. Correction of chloride deficits is a
priority for treatment with many underlying disorders.

Care priorities

1. Manage chloride deficit

Normal saline infusion may correct volume (chloride) deficit in
patients with gastric alkalosis because of gastric losses. Metabolic
alkalosis is difficult to correct if hypovolemia and chloride deficit
are not corrected.

2. Correct hypokalemia
Potassium chloride (KCl) is indicated for patients with low
potassium levels. KCl is preferred over other potassium salts
because chloride losses can be replaced simultaneously.

3. Sodium and potassium chloride

Effective for posthypercapnic alkalosis, which occurs when chronic
CO2 retention is corrected rapidly (e.g., via mechanical ventilation).
If adequate amounts of chloride and potassium are not available,

79
renal excretion of excess HCO3− is impaired and metabolic alkalosis
continues.

4. Cautious IV administration of isotonic hydrochloride

solution, ammonium chloride, or arginine hydrochloride
May be warranted if severe metabolic alkalosis (pH greater than 7.6
and HCO3− greater than 40 to 45 mEq/L) exists, especially if chloride
or potassium salts are contraindicated. The medication is delivered
via continuous IV infusion at a slow rate, with frequent monitoring
of IV insertion site for signs of infiltration. Ammonium chloride and
arginine hydrochloride may be dangerous to patients with renal or
hepatic failure.

Nursing diagnoses and interventions for

acute metabolic alkalosis
Nursing diagnoses and interventions are specific to the underlying
pathophysiologic process.

Chronic metabolic alkalosis

Pathophysiology
Chronic metabolic alkalosis results in a pH greater than 7.45 and
HCO3− greater than 26 mEq/L. PaCO2 will be elevated (greater than
45 mm Hg) to compensate for the loss of H+ or excess serum HCO3−.
The three clinical situations in which this can occur are:

1. Abnormalities in the excretion of HCO3− of the kidneys related to

a mineralocorticoid effect.

2. Loss of H+ through the GI tract.

3. Long-term diuretic therapy, especially with the thiazides and

furosemide. A compensatory increase in PaCO2 (up to 50 to 60 mm
Hg) may be seen. Respiratory compensation is very limited because
of hypoxemia, which develops as a result of decreased alveolar

80
ventilation.

Compensatory response to chronic alkalosis

When extracellular fluid is alkalotic, the kidneys conserve H+ and
eliminate HCO3−, resulting in excretion of alkalotic urine. Renal
excretion of acid load and increase in circulating buffer represent
the major compensation for respiratory deficits and require a
normally functioning kidney. Although the response of the kidneys
to an abnormal pH level is slow (4 to 48 hours), they are able to
facilitate a nearly normal pH level by excreting or retaining large
quantities of HCO3− or H+ from the body. Acid-base balance is
regulated by increasing or decreasing H+ and bicarbonate (HCO3−)
concentration in body fluids. A series of complex reactions with H+
secretion, sodium ion (Na2+) resorption, HCO3− retention, and
ammonia synthesis (excretes H+ in the urine) occurs.

Clinical presentation
Muscular weakness, neuromuscular instability, and hyporeflexia
because of accompanying hypokalemia are present. Decrease in GI
tract motility may result in an ileus. Severe alkalosis can result in
apathy, confusion, and stupor. Seizures may occur.

Physical assessment
Decreased respiratory rate and depth, periods of apnea, and
tachycardia (atrial or ventricular) are present.

Monitoring parameters
Atrial and ventricular dysrhythmias as a result of cardiac irritability
secondary to hypokalemia; prolonged QT intervals are present (see
Hypokalemia).

• Urinalysis: Urine chloride levels can help identify the cause of the
metabolic alkalosis. Urine chloride level will be less than 15
mEq/L if hypovolemia and hypochloremia are present, and
greater than 20 mEq/L with excess retained HCO3−. This test is
not reliable if diuretics have been used within the previous 12

81
 hours.

• ECG findings: To assess for dysrhythmias, especially if profound

hypokalemia or alkalosis is present.

Collaborative management: Chronic

metabolic alkalosis
The goal is to correct the underlying acid-base disorder via the
following interventions.

Care priorities

1. Fluid management
If volume depletion exists, normal saline infusions are given.

2. Potassium replacement
If a chloride deficit is also present, KCl is the drug of choice. If a
chloride deficit does not exist, other potassium salts are acceptable.

• IV potassium: If the patient is undergoing cardiac monitoring, up

to 20 mEq/h of KCl is given for serious hypokalemia.
Concentrated doses of KCl (greater than 40 mEq/L) require
administration through a central venous line because of blood
vessel irritation.

• Oral potassium: Unpleasant flavor if mixed as a liquid; 15

mEq/glass is the most patients can tolerate, with a maximum
daily dose of 60 to 80 mEq. Slow-release potassium tablets are an
acceptable form of KCl. All forms of KCl may be irritating to
gastric mucosa.

3. Dietary
The normal diet contains 3 g or 75 mEq potassium but not in the
form of KCl. Dietary supplementation of potassium is not effective
if a concurrent chloride deficit is also present.

4. Potassium-sparing diuretics

82
These may be added to treatment if thiazide diuretics are the cause
of hypokalemia and metabolic alkalosis.

Clinical presentation
The patient may be symptom-free. With severe potassium depletion
and profound alkalosis, the patient may experience weakness,
neuromuscular instability, and a decrease in GI tract motility,
which can result in ileus.

Physical assessment
Decreased respiratory rate and depth, and tachycardia (atrial or
ventricular) are present.

Monitoring parameters
Frequent premature ventricular contractions (PVCs) or U waves with
hypokalemia and alkalosis are present.

Nursing diagnoses and interventions for

chronic metabolic alkalosis
Nursing diagnoses and interventions are specific to the underlying
pathophysiologic process.

Altered mental status

Pathophysiology
Consciousness is a state of awareness of the self and environment
composed of three aspects: arousal (ability to awaken), ability to
perceive internal and external stimuli, and ability to perform goal-
directed behavior. Alterations are noted when a person has
difficulty focusing, sustaining, or shifting attention. Mental status is
the salient feature of consciousness and a direct measure of brain
function. Mental status encompasses orientation, thought
processing, memory and learning, attention, and judgment.
Changes in mental status occur as a result of direct injury to brain

83
tissue resulting from perfusion defects (ischemia), brain injury, and
tumors. Mental status change also occurs as a result of systemic
problems, including infection, metabolic, or endocrine problems. A
change in mental status is also associated with dementia, delirium,
coma, encephalopathy, and psychiatric disorders. Mental status
change may be as subtle as a variation in behavior or as profound
as loss of consciousness. Whatever the cause, confusion, memory
loss, change in alertness, disorientation, lack of judgment or insight,
emotional dysregulation, anxiety, agitation, restlessness, and
change in psychomotor skills or behavior are critical clues to a
changing condition.
Factors precipitating various alterations in consciousness or
mental status are listed in Table 1-3. These precipitating factors
arise from intrinsic causes (medical condition and associated
problems) and extrinsic causes (environmentally produced).
Impaired consciousness or change in mental status, regardless of
etiology, results in higher complication rates, puts the patient’s
safety at risk, causes longer hospital stays, and is linked to higher
morbidity and mortality. Three states of mental status change or
impaired consciousness, coma, delirium, and cognitive dysfunction,
can be recognized in emergency department and hospitalized
patients. Although each of these conditions may arise from distinct
medical problems, the clinical features are often similar and may be
superimposed on each other, making diagnosis and treatment more
complex. Change in mental status or change in behavior are often
the early warning signs of a medical emergency. The differential
diagnosis is crucial to the proper treatment of these mental status
changes. The following are descriptions of common mental status
variants that require further evaluation.

Table 1-3
FACTORS PRECIPITATING ALTERATIONS IN CONSCIOUSNESS
OR CHANGE IN MENTAL STATUS

84
CNS, Central nervous system; DKA, diabetic ketoacidosis; ICU, intensive care unit.

Abnormal behavior
Often a precursor to alterations in consciousness, acute change in
behavior is a frequent predictor of an underlying medical or
psychiatric problem. Abnormal behavior described as an objective
change in a person’s normal activity pattern is often associated with
confusion. Although there are no specific medical definitions of
abnormal behavior or confusion, subtle changes in normal routine
are identified by family members and caregivers. Reported
behavioral changes may be simply a variation in daily pattern,
inability to articulate a common word or do a familiar task, failure
to recognize danger, fear, euphoria, somnolence, or change in
interaction with a known person (friend, family member, caregiver,
or authority figure). Individuals do not have insight into their
change in behavior, thus the reports of others must be recognized
as valid. Although the causes of abnormal behavior and associated
confusion are varied, the first step in the evaluation of abnormal
behavior is to identify life-threatening causes. Screening for vital
sign changes (BP, HR, RR, and temperature), hypoxia, and
hypoglycemia provide initial data to differentiate acute medical
conditions such as sepsis, DKA, and respiratory compromise that

85
require immediate attention or hypovolemia caused by
dehydration. For elderly persons and persons with existing chronic
conditions, behavior change may be the single indicator of
declining medical status. The second step in evaluation of a patient
with change in behavior is determining if the problem is
disorientation and memory (linked to medical or neurologic
problems) or changes in thought content (linked to psychiatric
problems). In addition to the history of the present illness, taking a
thorough medical and substance abuse history is imperative. Quick
bedside tests such as the Six-Item Screen, Quick Confusion Scale, or
Vigilance A Test provide reliable information for cognitive
function, attention, and confusion.

Delirium
This is a state of disordered attention that reflects an underlying
acute or subacute process. It is usually a transient condition (may be
prolonged) that develops along a continuum including a clouding
of consciousness, confusion, attention deficit, global cognitive
impairment, and psychosis. Symptoms include disorientation to
time, place, and person; disorganized thinking; fear; irritability;
misinterpretation of sensory stimuli (e.g., pulling at tubes and
dressings); appearance of being distracted; altered psychomotor
activity; altered sleep-wake cycles; memory impairment;
hallucinations; inappropriate communication (e.g., yelling,
swearing, nonsensical speech); and dreamlike delusions. Lucid
intervals alternate with episodes of delirium. Patients may have
difficulty following commands. Daytime drowsiness is contrasted
with nighttime agitation. Clinical variants of delirium include the
hyperactive-hyperalert form, the quiet form, and a combination
form that combines the hyperactive-hyperalert and quiet forms to
produce both lethargy and agitation (Figure 1-2).

86
 FIGURE 1-2 Linking sedation and delirium monitoring;
a two-step approach to assess
consciousness. Source: (Copyright © E. Wesley Ely, MD, MPH, and
Vanderbilt University, 2002.)

Coma
Coma is an alteration in arousal and diminished awareness of self
and environment. No understandable response to external stimuli
or inner need is elicited. No language is spoken. There are no covert
or overt attempts at communication or eye opening. Spontaneous
purposeful movement and/or localizing movements are absent.
Motor responses to noxious stimuli are reflexive and do not result
in recognizable defensive movements. Sleep-wake cycles are absent
on the electroencephalogram (EEG). The extent of coma is difficult
to quantify because limits of consciousness are difficult to define.
Self-awareness can only be inferred from appearance and actions.
Coma occurs when normal central nervous system (CNS) function
is disrupted by alteration in the cerebral structure (brain injury),
cerebrovascular impairment (hemorrhage, ischemia, or edema), or
metabolic conditions (hepatic encephalopathy). If coma persists for
longer than 4 weeks, it is defined as transitioning to a vegetative

87
state.

Differential diagnosis of coma

The characteristics of syndromes or mental states described as
follows are useful in determining the differential diagnosis because
many have similar presentations.

• Stupor: Deep sleep with responsiveness only to vigorous and

repeated stimuli with return to unresponsiveness when the
stimulus is removed. Stupor usually is related to diffuse organic
cerebral dysfunction but may be confused with the catatonic
behavior of schizophrenia or the behavior associated with a
severe depressive reaction.

• Minimally conscious state (MCS): Describes patients who

demonstrate inconsistent but reproducible behavior indicating
awareness of self and environment. Generally, they cannot
reliably follow commands or communicate but show visual
fixation and tracking and have emotional and/or behavioral
responses to external stimuli. Once the patient consistently
follows commands, can reliably communicate, and uses objects in
a functional way, the minimal conscious state ends. Although the
etiology is uncertain, MCS seems to be related to diffuse,
bilateral, subcortical, and hemispheric damage.

• Akinetic mutism (AM): Subcategory of MCS in which a decrease

in spontaneity and initiation of actions, thoughts, speech, or
emotion is present. Sensory motor function is normal. Visual
tracking and eye movements are intact, and there is occasional
speech and movement to commands. However, internally guided
behavior is absent because cortical activation is inadequate. AM
is associated with orbitomedial frontal cortex, limbic system, and
reticular formation lesions.

• Vegetative state (VS): VS is a subacute or chronic condition that

may follow coma from brain injury or occur independently of
coma (e.g., dementia). Transition from coma to VS occurs if coma
without detectable awareness of environment persists for longer
than 4 weeks. Onset of VS is signaled by a return of wakefulness

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 (eyes are open and sleep patterns may be observed) with return
of spontaneous control of autonomic function but without
observable signs of cognitive function. The patient cannot follow
commands, offers no comprehensible sounds, and displays no
localization to stimuli. There is complete loss of meaningful
interaction with the environment. When the VS continues for
weeks or months, it is considered persistent vegetative state
(PVS). PVS may exist for many years because the autonomic and
vegetative functions necessary for life have been preserved. PVS
generally resolves more quickly in patients with a traumatic brain
injury than in patients with no trauma.

• Locked-in syndrome (LIS): Characterized by paralysis of all four

extremities and the lower cranial nerves but with preservation of
cognition. Associated with deafferentation (disruption of the
pathways of the brainstem motor neurons), this condition
prevents the patient from communicating with a full range of
language and body movement. Generally, consciousness, vertical
eye movement, and eyelid blinking are intact and provide a
mechanism for communication. LIS is classified by the degree of
voluntary speech and motor function preservation. In complete
LIS, there is total immobility and anarthria (inability to speak). In
incomplete LIS, there is vertical eye movement and blinking
function. LIS can be distinguished from a VS because patients
give appropriate signs of being aware of themselves and their
environment. Often, sleep patterns are disrupted (see Spinal Cord
Injury).

Cognitive dysfunction
This is an alteration in thought process involving many of the
following brain functions: memory, learning, language, attention,
judgment, reasoning, reading, and writing. Aphasia, or difficulty
understanding language or with responding with the proper
words, may also be present. Dysphagia, or difficulty swallowing,
occurs because of attention deficits or muscle weakness. These
cognitive impairments, whether permanent or transitory, if
overlooked, underdiagnosed or incorrectly diagnosed may result in
failure to correct a new acute illness or an exacerbation of a chronic

89
illness. See Table 1-3 for factors contributing to cognitive
dysfunction in acute, critical, or chronic illnesses. Acute changes in
behavior or mental status superimposed on chronic cognitive
dysfunction (dementia) is a harbinger of an underlying condition
that needs immediate attention.

Assessment: Mental status or alteration in

consciousness
Goal of assessment
• Identify changes in behavior, including ability to both understand
and comply with directions.

• Determine if different or altered behaviors have occurred in the

past or occur regularly; new-onset changes in mental status
should be evaluated very closely. Considerations of cause may
include withdrawal from abused substances, a reaction to a new
medication, hypoxia, and hypoglycemia.

• Determine the severity of the change in behavior from baseline;

acute changes require prompt action.

• An acute or unexpected change in mental status that occurs

should be investigated immediately and requires an extensive
medical evaluation with laboratory analysis, physical
examination, and neuroimaging. These patients may need
immediate transfer to a higher level of care. Change in mental
status is often the earliest warning sign of a medical emergency!

• Resist the temptation to sedate an agitated patient before

completing a full assessment, to ensure the patient is not hypoxic
or hypoglycemic. Assessment for hypoxia should include both a
ventilation and perfusion assessment. The ABG includes an
estimated Hgb level, which can prove to be invaluable to
determine if the patient may have internal bleeding or an
unrecognized anemia.

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History and risk factors

• Age : Older adults (age 60 years and older) are more prone to
alterations in consciousness, especially with changes in the
environment, subclinical response to infection or other medical
conditions including myocardial infarction (MI), and prescription
drug toxicity.

• Brain injury: Lesions of the cortex, subcortex, and brainstem

caused by global or focal ischemia, stroke, or traumatic brain
injury (see Traumatic Brain Injury, Chapter 3).

• Cerebral disorders: Deteriorating brain conditions, such as

expanding lesions, hydrocephalus, Parkinson disease, dementia,
or mental health disorders (bipolar, depression, schizophrenia).

• Cardiovascular status: Disorders that lower CO (heart failure, MI,

shock states), procedures that cause postcardiotomy delirium,
intraaortic balloon pump sequelae, and hypoperfusion states
(altered cerebral perfusion pressure and dysrhythmias).

• Pulmonary disorders: Those causing hypoxia and hypoxemia

such as pneumonia, acute respiratory distress syndrome (ARDS),
and pulmonary emboli.

• Drug therapy: Sedation, analgesia, drug toxicity, drug

interactions, drug withdrawal, or drug sensitivity.

• Medication review

• Full review of all prescription medications currently

being taken.

• When prescribed (new or old) dose, last time taken,

reason for taking.

• Be alert to the following medication classifications

that may cause behavioral change or alterations in

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 consciousness: Sympathomimetics, anticholinergics,
hallucinogens, opioid, sedative-hypnotic,
cholinergic, and serotonin uptake inhibitors.
• Surgical factors: Nature (hip, cardiac, neurosurgery patients at
increased risk) and extent of surgery and anesthesia time.

• Infection: Bacteremia, urinary tract infections, pneumonia, or

sepsis.

• Perceptual/sensory factors: Sleep deprivation, sensory overload,

sensory deprivation, impaired sensation (hypesthesia, decreased
hearing or vision), impaired perception (inability to identify
environmental stimuli), and impaired integration (inability to
integrate environmental stimuli).

• Metabolic factors: Changes in glucose level, hypermetabolism,

hypometabolism, renal insufficiency, and endocrine crises
(diabetic coma, ketoacidosis, pituitary dysfunction or injury,
myxedema).

• Fluid and electrolyte disturbances: Sodium and potassium

imbalances, hypovolemia, or dehydration.

Vital signs
All of the following vital sign changes may be associated with an
alteration in consciousness:

• Fever may indicate possible sepsis and/or bacteremia. Subnormal

or absence of fever may also indicate sepsis.

• Tachycardia may indicate hypovolemia, resulting from

dehydration or bleeding. If the patient has undergone a recent
invasive procedure, evaluation for internal bleeding is warranted.
Tachycardia is also present with fever and hypoglycemia.

• Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV).

Any change in SV will increase HR to maintain CO and decrease

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 CO will cause a change in HR initially.

• Tachypnea, if coinciding with tachycardia, may reflect the same

findings but is also a compensatory mechanism to help control
acidosis. Tachypnea is also present during a panic attack, as well
as hypoxia.

• Bradypnea may be associated with high doses of narcotics used

for pain control.

• Patients with a head injury may exhibit signs of increased

intracranial pressure (ICP), which vary depending on the degree
of pressure elevation (see Traumatic Brain Injury, Chapter 3).
Often changes in behavior including restlessness and agitation or
a decrease in agitation (increasing somnolence) herald worsening
injury and require immediate attention.

• Hypotension may indicate a later sign of shock or may be

associated with higher doses of antihypertensive medications,
narcotics, or other medications that can slow the HR or reduce
the BP.

Observation and neurologic evaluation

• The patient’s normal baseline neurologic status must be
documented and used for comparison. This evaluation may begin
with simple scales, such as the Six-Item Screen or Quick
Confusion Scale, often used in the emergency department.

• Baseline neurologic findings elicited from each component of the

examination must be documented.

• Requires a thorough evaluation of mental/emotional status,

cranial nerve function, motor function, sensory function, and
reflex activity. When changes in mental status are noted, the
mental/emotional component of the examination is of particular
importance. Is there a behavioral change without other focal
signs or symptoms?

93
• In patients who are unconscious or demonstrate low-level
function, assessment techniques are used that do not require
patient participation, such as coma and cognitive functioning
scales. The purpose of assessment is to determine the extent of
wakefulness and cognition through observed responses, such as
eye opening, movement of the head and body, verbalization, and
ability to follow commands. These observations alone will not
fully discriminate the subtle differences in altered states of
arousal.

• Assessment should be accompanied by an in-depth history

focusing on the possible etiology of the change in mental status.
Extensive cognitive testing including attention, concentration,
memory, and learning assessments is performed when the
patient is arousable and aware.

Screening labwork
• ABGs evaluate ventilation, perfusion, estimated Hgb, and acid-
base status.

• Point-of-care blood glucose readings evaluate for hypoglycemia

or extreme hyperglycemia.

• Biochemical panel analysis evaluates for electrolyte imbalances,

such as hyponatremia, which are associated with alterations in
behavior.

• Urine analysis and urine drug screen for detection of renal

function and drug use.

• Serum lactate levels if systemic inflammatory response syndrome

(SIRS) or sepsis is suspected.

Neurologic evaluation
• Mental status testing: Subjective assessment requiring patient
cooperation for best results (Box 1-1).

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• Quick Confusion Scale: Consists of six items and is used for
screening impaired mental status in the emergency department.
Total points are 15 with a total score of 11 suggesting the need for
further evaluation and a score of ≤7 confirming impairment (Box
1-2).

• Mini-Mental Status Examination (MMSE): Objective

neuropsychological tool used to measure orientation, recall,
attention, calculation, and language. Scores less than 23 (total 25)
indicate cognitive dysfunction. Patient participation is necessary
for this examination (Box 1-3).

• Six-Item Screen: Used for assessing cognitive function, attention,

and confusion, and was developed from the MMSE. Six items
related to cognition, attention, and short-term memory are scored
using a nine-point scale. Scores less than 5 indicate cognitive
impairment (Box 1-4).

• Vigilance A Test: This is a quick bedside test for attention and

concentration. Given a series of 60 random letters, patients are
asked to identify all the A’s in the sequence. Omission of more
than two A’s is suggestive of attention deficit (Box 1-5).

• Glasgow Coma Scale: Quantitative, three-part scale that assesses

the patient’s ability to open his or her eyes, to move, and to
speak/communicate. Scores range from 3 to 15, with 3 being
unresponsive to all stimuli and 15 being awake, alert, and
oriented. Patients who are unable to cooperate can be evaluated
using this scale (see Appendix 1).

• Coma Recovery Scale: Quantitative 35-item scale used to assess

brain function at four levels (generalized, localized, emergent,
cognitively mediated). Seven responses are evaluated: arousal
and attention, auditory perception, visual perception, motor
function, oromotor ability, communication, and initiative.
Patients who are unable to cooperate can be evaluated using this
scale.

• Confusion Assessment Method (CAM, CAM-Intensive Care

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 Unit): Four-part scale used to evaluate confusion. Onset and
course, inattention, disorganized thinking, and LOC are assessed
(Box 1-6).

• Intensive Care Delirium Screening Checklist (ICDSC): Eight-

item scale that rates behavioral responses exhibited by patients in
intensive care; delirium is indicated with scores greater than 4 to 8
(Table 1-4).

• Richmond Agitation-Sedation Scale (RASS): Scores sedation

and agitation with a 10-point scale using verbal and physical
stimulation to determine the patient’s response, and used to
titrate medications (Table 1-5).

• Rancho Los Amigos (RLA) Cognitive Functioning Scale: Seven-

level scale that describes levels of cognitive functioning. Levels
range from unresponsive to sensory stimuli to
purposeful/appropriate actions. Patients who cannot cooperate
can be evaluated using this scale (Table 1-6).

Table 1-4
INTENSIVE CARE DELIRIUM SCREENING CHECKLIST

Symptom Checklist (total 0 to

Level of Consciousness Scoring
8)
Level of Consciousness Level of Consciousness
Inattentiveness
Disorientation A: No response: none
Hallucination, delusion, B: Response to intense, repeated stimuli (loud voice or pain):
psychosis none
Agitation C: Response to mild or moderate stimulation: 1
Inappropriate speech or mood D : normal wakefulness: 0
Sleep/wake cycle disturbance E : exaggerated response to normal stimulation: 1
Symptom fluctuation (if A or B above do not complete evaluation for the day)
Adapted from Bergeron N, Dubois M-J, Dumont M, et al: Intensive care delirium
screening checklist: evaluation of a new screening tool. Intensive Care Med
27(5):859-864, 2001.

Table 1-5
RICHMOND AGITATION-SEDATION SCALE (RASS)

+4 Combative Overtly combative or violent, immediate danger to staff

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+3 Very agitated Pulls on or removes tubes or catheters, aggressive behavior toward staff
+2 Agitated Frequent nonpurposeful movement or patient-ventilator dyssynchrony
+1 Restless Anxious or apprehensive but movements not aggressive or vigorous

0 Alert and calm

−1 Drowsy Not fully alert, sustained (≥10 seconds) awakening, eye contact to voice
−2 Light sedation Briefly (<10 seconds) awakens with eye contact to voice
−3 Moderate Any movement (but no eye contact) to voice
sedation
−4 Deep sedation No response to voice, any movement to physical stimulation
−5 Unarousable No response to voice or physical stimulation
Procedure
1. Observe the patient. Is patient alert and calm (score 0)?
Does the patient have behavior that is consistent with restlessness or agitation?
Assign score +1 to +4 using the criteria listed above.

2. If the patient is not alert, in a loud-speaking voice state the patient’s name and direct the
patient to open his or her eyes and look at the speaker. Repeat once if necessary. Can prompt
the patient to continue looking at the speaker.
The patient has eye opening and eye contact, which is sustained for more than 10 seconds
(score −1).
The patient has eye opening and eye contact, but this is not sustained for 10 seconds (score −2).
The patient has any movement in response to voice, excluding eye contact (score −3).

3. If the patient does not respond to voice, physically stimulate the patient by shaking shoulder
and then rubbing sternum if there is no response.
The patient has any movement to physical stimulation (score −4).
The patient has no response to voice or physical stimulation (score −5).

Score Term Description

+4 Combative Overtly combative, violent, immediate danger to staff
+3 Very agitated Pulls or removes tube(s) or catheter(s); aggressive
+2 Agitated Frequent nonpurposeful movement, fights ventilator
+1 Restless Anxious but movements not aggressive or vigorous
0 Alert and calm
−1 Drowsy Not fully alert, but has sustained awakening (eye opening/eye contact) to
voice (≥10 seconds)
−2 Light sedation Briefly awakens with eye contact to voice (<10 seconds)
−3 Moderate Movement or eye opening to voice (but no eye contact)
sedation
−4 Deep sedation No response to voice, but movement or eye opening to physical stimulation
−5 Unarousable No response to voice or physical stimulation
Procedure for RASS Assessment
1. Observe the patient
• The patient is alert, restless, or agitated (score 0 to +4).

2. If not alert, state the patient’s name and say to open eyes and look at the speaker.
• The patient awakens with sustained eye opening and eye contact (score −1).
• The patient awakens with eye opening and eye contact, but not sustained (score −2).
• The patient has any movement in response to voice but no eye contact (score −3).

3. When no response to verbal stimulation, physically stimulate the patient by shaking shoulder
and/or rubbing sternum.
• The patient has any movement to physical stimulation (score −4).
• The patient has no response to any stimulation (score −5).

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Reproduced, with permission, from Sessler CN, Gosnell M, Grap MJ, et al: The
Richmond Agitation-Sedation scale: validity and reliability in adult intensive care unit
patients. Am J Respir Crit Care Med 166(10):1338-1344, 2002. Copyright © 2002
American Thoracic Society. From Ely EW, Truman B, Shintani A, et al: Monitoring
sedation status over time in ICU patients: the reliability and validity of the Richmond
Agitation-Sedation Scale (RASS). JAMA 289(22):2983-2991, 2003.

Table 1-6
COGNITIVE REHABILITATION GOALS

Level Response Goal/Intervention

I None Goal: Provide sensory input to elicit responses of increased quality,
II Generalized frequency, duration, and variety.
III Localized Intervention: Give brief but frequent stimulation sessions, and present
stimuli in an organized manner, focusing on one sensory channel at a
time; for example:
Visual: Intermittent television, family pictures, bright objects.
Auditory: Tape recordings of family or favorite song, talking to the
patient, intermittent television or radio.
Olfactory: Favorite perfume, shaving lotion, coffee, lemon, orange
Cutaneous: Touch or rub skin with different textures, such as velvet, ice
bag, warm cloth.
Movement: Turn, range-of-motion exercises, up in chair.
Oral: Oral care, lemon swabs, ice, sugar on tongue, peppermint,
chocolate.
IV Confused, Goal: Decrease agitation and increase awareness of environment. This
agitated stage usually lasts 2 to 4 weeks.
Intervention: Remove offending devices (e.g., nasogastric tube,
restraints), if possible.
Do not demand the patient to follow through with task.
Provide human contact unless this increases agitation.
Provide a quiet, controlled environment.
Use a calm, soft voice and manner around the patient.
V Confused, Goal: Decrease confusion and incorporate improved cognitive abilities
inappropriate into functional activity.
VI Confused, Intervention: Begin each interaction with introduction, orientation, and
appropriate interaction purpose.
List and number daily activity in the sequence in which it will be done
throughout the day.
Maintain a consistent environment.
Provide memory aids (e.g., calendar, clock).
Use gentle repetition, which aids learning.
Provide supervision and structure. Reorient as needed.
VII Automatic, Goal: Integrate increased cognitive function into functional community
appropriate activities with minimal structuring.
Intervention: Enable practicing of activities.
Reduce supervision and environmental structure.
Help the patient plan adaptation of activities of daily living and home
living skills to home environment.
Modified from the Rancho Los Amigos Levels of Cognitive Functioning Scale (scale
based on behavioral descriptions or responses to stimuli). From Swift CM:
Neurologic disorders. In Swearingen PL, editor: Manual of medical-surgical nursing

98
care, ed 4, St Louis, 1999, Mosby.

Box 1-1
MENTAL STATUS COMPONENT OF THE
NEUROLOGIC EXAMINATION
1. General appearance

2. Behavior (with and without stimulation)

3. Language and speech characteristics (organization, coherence,

and relevance)

4. Mood and affect

5. Judgment

6. Abstract thinking

7. Orientation (time, place, person)

8. Attention and concentration

9. Memory (recent, remote)

10. Cognition (following commands, fund of knowledge,

interpretation of information, problem solving)

Box 1-2
QUICK CONFUSION SCALE

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Adapted from Huff J, Farace E, Brady W, et al: The Quick Confusion Scale in the
emergency department: comparison with the Mini-Mental State Examination. Am J
Emerg Med 19:461-464, 2001.

Box 1-3
MINI-MENTAL STATUS EXAMINATION
1. What is the year, season, date, day, month? (5 points)

2. Where are we: state, county, town, hospital, room? (5 points)

3. Name three objects. (3 points)

4. Count backward by sevens (e.g., 100, 93, 86, 79, 72). (5 points)

5. Repeat same three objects from item number 3 above. (3 points)

6. Name a pencil and watch. (2 points)

7. Follow a three-step command. (3 points)

8. Write a sentence. (1 point)

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9. Follow the command “close your eyes.” (1 point)

10. Copy a design (e.g., two hexagons). (1 point)

Box 1-4
SIX-ITEM SCREEN
Six-item screen (used to detect problems with cognition,
attention, short-term memory, and orientation; subset of
the mmse, the blessed dementia rating scale (bdrs), and
the word list recall)
1. Examiner names three items and asks patient to repeat each item.
(3)

2. Examiner asks what year, what month, what day of the week? (3)

3. Examiner asks patient to recall the three items (3) in number 1

above.

Total score is 9. If score <5, then patient has cognitive

impairment
Adapted from Callahan C, Unverzagt F, Hui S, et al: Six-item screener to identify cognitive
impairment among potential subjects for clinical research. Med Care 40(9):771-781, 2002.

Box 1-5
VIGILANCE A TEST
Vigilance A Test Scoring
Random list of 60 letters with the letter A appearing greater Count number of omissions or
than random frequency. The patient is asked to tap or commission of the target letter (A).
indicate when the target letter (A) is spoken by the Greater than two missed is
examiner. abnormal

Box 1-6
CONFUSION ASSESSMENT METHOD-

101
INTENSIVE CARE UNIT (CAM-ICU)
WORKSHEET
Feature 1: Acute onset or fluctuating course
Positive if you answer “yes” to either 1A or 1B.
Positive or Negative
1A: Is the patient different than his/her baseline mental status?
Or
1B: Has the patient had any fluctuation in mental status in the
past 24 hours as evidenced by fluctuation on a sedation scale (e.g.,
RASS), GCS, or previous delirium assessment?
Yes or No
Feature 2: Inattention
Positive if either score for 2A or 2B is less than 8.
Attempt the ASE Letters first. If the patient is able to perform
this test and the score is clear, record this score and move to
Feature 3. If the patient is unable to perform this test or the score is
unclear, then perform the ASE Pictures. If you perform both tests,
use the results of the ASE Pictures to score the feature.
Positive or Negative
2A: ASE Letters: Record score (enter NT for not tested)
Directions: Say to the patient, “I am going to read you a series of 10
letters. Whenever you hear the letter ‘A,’ indicate by squeezing my hand.”
Read letters from the following letter list in a normal tone.
SAVEAHAART
Scoring: Errors are counted when patient fails to squeeze on the
letter “A” and when the patient squeezes on any letter other than
“A.”
Score (out of 10): ______
2B: ASE Pictures: record score (enter NT for not tested)
Directions are included on the picture packets.
Score (out of 10): ______
Feature 3: Disorganized thinking
Positive if the combined score is less than 4
Positive or Negative
3A: Yes/No Questions

102
 (Use either Set A or Set B, alternate on consecutive days if
necessary):
Set A Set B
1. Will a stone float on water? 1. Will a leaf float on water?
2. Are there fish in the sea? 2. Are there elephants in the sea?
3. Does one pound weigh more than two 3. Do two pounds weigh more than one
pounds? pound?
4. Can you use a hammer to pound a nail? 4. Can you use a hammer to cut wood?

Score ___ (Patient earns 1 point for each correct answer out of 4)
3B: Command
Say to patient: “Hold up this many fingers” (Examiner holds two
fingers in front of patient). “Now do the same thing with the other
hand” (Not repeating the number of fingers). (If patient is unable
to move both arms, for the second part of the command ask patient
“Add one more finger”). Score___ (Patient earns 1 point if able to
successfully complete the entire command)
Combined Score (3A + 3B):_____ (out of 5)
Feature 4: Altered level of consciousness
Positive if the Actual RASS score is anything other than “0”
(zero)
Positive Negative
Overall CAM-ICU (Features 1 and 2 and either Feature 3 or 4):
Positive Negative
Copyright © 2002, E. Wesley Ely, MD, MPH and Vanderbilt University, all rights reserved.

Diagnostic tests
Neurodiagnostic testing
See the section on Traumatic Brain Injury in Chapter 3.

Neuropsychological testing
Although not a routine part of critical care, neuropsychological
testing should be planned and implemented for patients with brain
injury or altered consciousness when they enter the recovery phase.
This testing provides a comprehensive baseline for rehabilitation by
evaluating higher cortical functions, such as memory, learning, and

103
language.

Laboratory studies
If there is an acute or unexpected mental status change, laboratory
studies include complete blood count (CBC), electrolytes, cardiac
profile, blood and sputum cultures, urinalysis and culture, ABG,
chest radiograph, ECG, and other tests as determined by signs and
symptoms.

Collaborative management
Care priorities
When evaluating alteration in consciousness or a change in mental
status, there are two primary targets: (1) recognize that the disorder
is present and (2) uncover the underlying cause. Acute and/or life-
threatening problems must be ruled out before proceeding.
Therefore, signs and symptoms such as lethargy, somnolence,
fatigue, anxiety, or sleeplessness should not be normalized as part
of illness behavior but as signs and symptoms prompting further
investigation. Although severe agitation is difficult to manage, it is
imperative that physiologic causes of agitation are ruled out before
sedating the patient. Once acute causes of the problem are ruled
out, the following measures may be implemented for other causes
of behavioral changes:

1. Delirium

• Determine and correct physiologic imbalances and drug

interactions.

• Correct sensory/perceptual deficits (e.g., provide hearing aid,

eyeglasses).

• Reorient the patient to self and environment.

• Implement appropriate medications to help control behavior.

• Consider consultation with a geriatrician.

104
• Manage pain and assess effectiveness.

• Minimize sedative medications; benzodiazepines are not

recommended.

• Check bowel and bladder function.

• Establish sleep-wake cycle.

• Treat agitation.

• Perform neuropsychological testing.

• See Sedation and Neuromuscular Blockade, Chapter 2.

For mild confusion, good outcomes have been reported with

the use of reorientation techniques and observation (use of
“sitters”), especially by family members. Prophylactic low-dose
haloperidol did not prevent delirium but was noted to reduce the
severity of delirium in one study. Newer atypical antipsychotic
medications, those with fewer extrapyramidal side effects such as
quetiapine, olanzapine, and risperidone, have been shown to have
an efficacy similar to haloperidol.

2. Coma

• Assess cognitive function using the RLA score or Coma Recovery

Scale.

• Initiate a sensory stimulation program for patients with low-level

cognition.

• Minimize stimulation for patients who are confused or agitated.

• Plan care to prevent or minimize problems related to the injury

105
 (e.g., spasticity, swallowing disorders) and complications of
immobility (e.g., disuse syndrome, contractures, and pressure
ulcers).

• Consult with rehabilitation services including physical,

occupational, and speech therapy.

3. Locked-in syndrome

• Provide a normal day/night routine to help minimize sleep-wake

cycle disturbances.

• Establish a communication system/pattern.

• Consult a mental health professional to assess the psychological

impact of this syndrome.

• Consult with rehabilitation (see preceding section on Coma).

4. Vegetative state

• Perform neurodiagnostic and neuropsychological testing to

confirm the diagnosis.

• Provide essential supportive care to minimize complications such

as pressure ulcers and aspiration.

• Initiate a sensory stimulation program for low-level cognitive

function, including visual, auditory, tactile, gustatory, and
vestibular stimuli (Figure 1-3).

106
 FIGURE 1-3 Sensory stimulation (SS) programs as an
intervention technique in the critically ill. Source: (From Kater
K: Response of head-injured patients to sensory stimulation. West J Nurs
Res 11[1]:20-33, 1989; Lewinn E, Dimancescu M: Environmental
deprivation and enrichment in coma. Lancet 2[8081]:156-157, 1978; Mackay
L, Bernstein BA, Chapman PE, et al: Early intervention in severe head
injury: long-term benefits of a formalized program. Arch Phys Med Rehabil
73[7]:635-641, 1992; Mitchell S, Bradley VA, Welch JL, et al: Coma arousal
procedure: a therapeutic intervention in the treatment of head injury. Brain
Inj 4[3]: 273-279, 1990; Schinner K, Chisholm AH, Grap MJ, et al: Effects of
auditory stimuli on intracranial pressure and cerebral perfusion pressure in
traumatic brain injury. J Neurosci Nurs 27[6]:336-341, 1994; and Wilson S,
Powell GE, Brock D, et al: Vegetative state and response to sensory
stimulation: an analysis of 24 cases. Brain Inj 10[11]:807-818, 1996.)

Research has demonstrated positive outcomes from two

107
interventions designed to reduce delirium in the intensive care unit
—one was to reduce delirium in postoperative patients by
controlling disturbances in the sleep-wake cycle. The second
involved the daily visit of a geriatric consult service, which
provided targeted recommendations using a 10-item protocol. The
protocol included (1) maintenance of central nervous system O2
delivery, (2) fluid and electrolyte corrections, (3) pain management,
(4) removal of unnecessary medications, (5) bowel/bladder
regulation, (6) establishing adequate nutrition, (7) mobilization
and rehabilitation, (8) detection/prevention and treatment of
surgical complications, (9) sensory stimulation, and (10) treatment
of agitational variant of delirium.

Care plans: Alteration in consciousness

Acute confusion 
related to physiologic changes; psychological changes; environmental
changes; sensory deprivation; sensory overload; drug interactions.
Goals/Outcomes: If the cause of alteration in consciousness is an
extracerebral event, within 72 hours of this diagnosis, the patient’s
level of arousal and cognition improves and the patient responds
consistently and appropriately to stimuli. If the cause is cerebral,
increased arousal and improvement in cognition may take days to
weeks.
Cognitive Orientation, Distorted Thought Self-Control,
Information Processing.

Neurologic status: Consciousness

Cognitive ability: Ability to execute complex mental processes;
ability to identify person, place, and time.
Information Processing: Ability to acquire, organize, and use
information.

1. Priority care is to identify the cause of the change in mental

status. Perform laboratory and diagnostics tests to identify the

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cause of the problem and correct it. This may include limiting
sedation or pain medication, monitoring for withdrawal
syndromes, drug interactions, or impending sepsis (SIRS, see
Chapter 11).

2. Eliminate environmental causes of sensory/perceptual deficit.

• Assess patient for potential causes of

sensory/perceptual deficits. For the hearing-
impaired or vision-impaired patient, wearing
eyeglasses or hearing aids will decrease
misinterpretation of visual and auditory stimuli.

• Assess environment for potential causes of

disorientation and confusion. Maintain day/night
environment as much as possible. Keep clocks and
calendars within the patient’s field of vision.
3. Develop a plan of care consistent with sensory/perceptual deficit.

4. Assess the patient for sensory deprivation and sensory overload.

Decrease or increase stimulation based on RLA assessment (see
Figure 1-3) and the patient’s needs. For example, individuals who
are agitated and confused require structure and reorientation
interventions, whereas those who are comatose or stuporous
require stimulation techniques.

• Orient the patient to time, place, and person during

all interactions. Explain procedures in terms the
patient can understand.

• Teach significant others reorientation and sensory

stimulation strategies, and provide liberal visitation
to facilitate their assistance.

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• Assess underlying cause of confusion or delirium
before using sedation, anxiolytic, analgesic, or
antipsychotic drug therapy (see Sedation and
Neuromuscular Blockade).

Cognitive Restructuring; Cognitive Stimulation;

Environmental Management; Reality Orientation; Dementia
Management; Electrolyte Management; Delirium Management.

Impaired verbal communication 

related to neurologic deficits
Goals/Outcomes: If the cause of alteration in consciousness is an
extracerebral event, within 72 hours of this diagnosis, the patient
communicates needs and feelings and exhibits decreased
frustration and fear related to communication barriers. If the cause
is cerebral, improvement in communication may take days to
weeks.
Communication: Expressive; Communication;
Communication: Receptive.

Communication enhancement

1. Determine the underlying cause of impaired communication,

including physiologic (cortical, brainstem, or cranial nerve injury)
or psychological (depression, fear, or anger).

2. When communicating with patients, use their name, face them,

use eye contact if they are awake, speak clearly, and use a normal
tone of voice.

3. Be alert to nonverbal messages, especially eye movement,

blinking, facial expressions, and head and hand movements.
Attempt to validate these signals with the patient.

4. Assure the patient that you are attempting to find methods that
promote communication if the patient’s needs cannot always be
understood.

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5. For the patient who does not respond to or acknowledge verbal
stimulation, continue communication attempts.

6. Teach significant others methods of communication and

encourage them to continue attempts at communication.

7. Brainstem-evoked potentials and audiometry (hearing test) can

provide useful information related to the patient’s ability to receive
and process auditory stimuli. Detection and treatment of otitis
media in patients who have ET tubes will improve hearing.

8. Obtain a speech therapy consultation to assess nature and

severity of communication impairment and assist in developing a
communication plan. Special attention is required for individuals
with locked-in syndrome.

9. Obtain a mental health consultation to assist with a patient who

is angry, frustrated, and fearful because of the communication
impairment.

Communication Enhancement: Speech Deficit; Support

System Enhancement.

Impaired physical mobility 

related to perceptual or cognitive impairment; imposed restrictions of
movement
Goals/Outcomes: By the time of discharge from the critical care
unit, the patient demonstrates range of motion (ROM) and muscle
strength within 10% of maximal normal function.
Mobility, Ambulation.

Exercise therapy: Joint mobility

1. Assess muscle strength and tone to determine type of

interventions required. Consult physical therapy and occupational
therapy for evaluation and treatment plan.

2. Manage decreased muscle tone (flaccidity):

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• Maintain body alignment and positioning.

• Perform passive ROM and stretching exercises.

• Avoid prolonged periods of limb flexion.

• Apply splints and other adaptive devices to

maintain functional position of the extremities.

• Turn patient every 2 hours.

• Consider chair sitting as the patient stabilizes.

3. Manage increased muscle tone (spasticity):

• Avoid supine position; use side-lying, semiprone,

prone, and high Fowler positions.

• Position limbs opposite flexion posture.

• Use skeletal muscle relaxant, such as baclofen

(Lioresal), as prescribed for decreasing tone.

4. Monitor calcium and alkaline phosphatase levels. Increased

levels can lead to the development of heterogeneous ossification,
which is often seen with states of impaired mobility, such as spinal
cord injury. See Fluid and Electrolyte Disturbances.

5. Maintain the patient’s skin integrity. See Wound and Skin Care.

6. Prevent pulmonary complications in the following ways:

• Encourage deep breathing if the patient is able, or

suction as needed. Coughing is warranted only if

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 sputum is present.

• Assess swallowing ability before initiating oral

feedings. Obtain dysphagia consultation (usually
from a speech therapist) if swallowing reflexes are
impaired.

• Initiate enteral feeding protocol for patients with

feeding tubes to prevent aspiration. See Nutritional
Support.

Bed Rest Care; Positioning; Exercise Promotion; Self-Care

Assistance.

Additional nursing diagnoses

Also see nursing diagnoses and interventions under Nutritional
Support, Sedation and Neuromuscular Blockade, Prolonged
Immobility, and Risk for Disuse Syndrome, in Traumatic Brain
Injury, Acute Spinal Cord Injury, and SIRS, Sepsis, and MODS.

Fluid and electrolyte disturbances

The volume and composition of body fluids and electrolytes are
affected by hormonal, renal, vascular, and exogenous factors. An
understanding of the complexity of chemical currents, cellular
function, and distribution of water between the cells and vessels
provides the information used to facilitate the best patient outcome.
Water is the major constituent of the human body, comprising
55% to 72% of body mass. Body water decreases with both age and
increasing body fat. The average male adult is approximately 60%
water by weight, whereas the average female adult is 55% water by
weight. Two thirds of body fluid is within the intracellular fluid
compartment (ICF) accounting for approximately 40% of body
weight. ICF contains a high concentration of potassium (K+),

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magnesium (Mg+), phosphates (PO4−), proteins, and sulfates. The
extracellular fluid compartment (ECF) is composed of interstitial
fluid, which surrounds the cells (14% of body weight), intravascular
fluid, contained within blood vessels (5% of body weight), and
transcellular fluid, which includes cerebral spinal fluid and fluid
contained in other body spaces such as joint spaces, pleural,
peritoneal, and pericardial spaces (1% to 2% of total body weight.)
ECF contains the remaining one third of body fluid and has a high
concentration of the plasma ions sodium (Na+), chloride (Cl−), and
bicarbonate (HCO3−).
The composition and concentration of ECF are primarily
regulated by the concentration of Na+, which defines the relative
relationship of sodium and water. Although ECF is altered and
then modified as the body reacts with its surrounding environment,
ICF remains relatively stable. Intracellular stability is important for
maintaining normal cellular function.
In addition to water, body fluids contain two types of dissolved
substances: electrolytes and nonelectrolytes. Electrolytes are
substances that carry an electrical current and can dissociate into
ions, which have either a positive or a negative charge. They are
measured by their capacity to combine (milliequivalents/liter
[mEq/L]) or by the molecular weight in milligrams (millimoles/liter
[mmol/L]). Nonelectrolytes are substances such as glucose and urea
that do not dissociate in solution and are measured by weight
(milligrams per 100 milliliters, or mg/dL) and mmol/L. The
intravascular and extravascular components of the ECF are
separated by a semipermeable or porous capillary membrane,
which allows movement of dissolved substance/particles between
compartments, and slow passage of albumin (5% per hour), which
is returned to the circulation via the lymphatic system at the same
rate. The unique composition of each compartment is maintained
(Table 1-7) in a state of equilibrium. Whereas the hydrostatic
pressure within the circulation tends to drive fluid out, the oncotic
pressure of the plasma proteins (e.g., albumin) draws fluid in and
maintains the relative constancy of the plasma volume.

Table 1-7
PRIMARY CONSTITUENTS OF BODY WATER COMPARTMENTS*

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*
This is a partial list. Other constituents include calcium (Ca2+), magnesium (Mg2+),
and proteins.
Cl−, Chloride; HCO3−, bicarbonate; HPO4−, phosphate; K+, potassium; Na+, sodium.

Osmolality
Osmolality is the number of particles in solution. This concentration
of particles determines the relationship of fluid between the ICF
and ECF. Normal osmolality is regulated by a wide variety of
mechanisms, which include arterial BP, sympathetic stimulation,
renal regulation, and hormonal outflow.
Osmolality = 2(Na+) + Glucose/18 + BUN/2.8 (normal value: 265 to
285 mOsm/L)

Hormonal influence
Three hormones are responsible for fluid volume regulation:

• Antidiuretic hormone (ADH) or vasopressin: Released by the

posterior pituitary in response to a reduction in intravascular
volume (hypovolemia) or an increase in extracellular osmolality,
which acts on the kidney at both the glomerulus and the tubules
to conserve water by increasing urine concentration. The
hormone regulates the electrolyte and fluid balance to keep
serum in “perfect” concentration (osmolality). Thirst is
stimulated by hypovolemia and increased osmolality.

• Aldosterone: Released by the adrenal cortex in response to an

increased plasma renin level, acts on the kidney to conserve

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 sodium (along with water), and increases potassium and
hydrogen excretion.

• Atrial natriuretic peptide (ANP): Released by the cardiac atria in

response to increased atrial pressure (e.g., acute volume
expansion). ANP reduces BP and vascular volume by increasing
excretion of sodium and water by the kidneys, decreasing release
of aldosterone and ADH, and by direct vasodilation.

Fluid disturbances
Fluid changes affect the volume status, regulation, and the
composition of body fluids. Fluid loss or gain changes the
concentration of particles in fluid compartments.

Hypovolemia
Pathophysiology
ECF volume depletion or hypovolemia may be caused by abnormal
skin losses, GI losses, polyuria/diuresis, bleeding, decreased intake,
and movement of fluid into a third space (e.g., pleura, peritoneum,
interstitium). Depending on the type of fluid lost or “third-spaced,”
hypovolemia may be accompanied by acid-base, osmolar, or
electrolyte imbalances. Severe ECF volume depletion can lead to
hypovolemic shock and cellular dehydration, which causes
alterations in electric potentials (the ability to conduct impulse)
throughout the body.
Compensatory mechanisms in hypovolemia include increased
sympathetic nervous system stimulation: increased HR, increased
force of cardiac contraction (positive inotropic effect),
vasoconstriction to maintain perfusion to O2-dependent organs (i.e.,
heart, lungs, brain), increased thirst, and increased release of
aldosterone and ADH (vasopressin). Reduced perfusion to high-
flow, low O2–consuming organs (i.e., kidney, mesenteric bed,
skeletal muscles) may lead to acute renal failure, ischemic bowel,
and skeletal muscle cell rupture.
Hypovolemic shock develops when the intravascular volume

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decreases to the point where compensatory mechanisms can no
longer maintain the perfusion needed for normal, aerobic cellular
function. Without normal levels of O2, cellular metabolism becomes
anaerobic, resulting in acidosis, cardiac depression, intravascular
coagulation, increased capillary permeability, and release of toxins.
If shock is not adequately treated, it may become irreversible,
leading to death.

Hypovolemia assessment
Goal of assessment
Identify the signs and symptoms of hypovolemia.

History and risk factors

The following list of factors may be associated with loss of
intravascular fluids or overall blood volume:

• Abnormal GI losses: Vomiting, nasogastric suctioning, diarrhea,

intestinal drainage.

• Abnormal skin losses: Excessive diaphoresis secondary to fever or

exercise, burns.

• Abnormal renal losses: Diuretic therapy, polyuria/osmotic

diuresis seen with DKA, hyperglycemic hyperosmolar nonketotic
syndrome (HHNS), nephrotoxicity, rhabdomyolysis, diabetes
insipidus, diuretic phase of acute renal failure/acute kidney
injury, adrenal insufficiency.

• Third-spacing or plasma-to-interstitial fluid shift: Peritonitis,

intestinal obstruction, burns, ascites, severe sepsis.

• Hemorrhage: Major trauma, GI bleeding, obstetric complications,

postoperative bleeding, high dosage of anticoagulants or
antiplatelet medications.

• Altered intake: Coma, fluid deprivation.

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Vital signs
Evaluate BP, HR, temperature, weight, central venous pressure
(CVP), pulmonary artery wedge pressure (PAWP), and urine
output to determine the extent of volume depletion.

• Check BP lying, sitting, and standing to determine presence of

orthostasis.

• HR will be increased (tachycardia).

• Narrowed pulse pressure.

• Low CVP (less than 2 mm Hg).

• Low PAWP (less than 3 mm Hg).

• Urine output decreased and may be less than 0.5 mL/kg/h.

• Increased temperature.

• Acute weight loss unless third spacing is occurring (Table 1-8).

Table 1-8
WEIGHT LOSS AS AN INDICATOR OF EXTRACELLULAR FLUID
DEFICIT IN THE ADULT

Acute Weight Loss Severity of Deficit

2% to 5% Mild
5% to 10% Moderate
10% to 15% Severe
15% to 20% Fatal

Observation
Evaluate the skin, mucous membranes, and clinical presentation for
signs of dehydration including furrowed tongue, dry mucous
membranes, sunken eyeballs, flat neck veins, clinical pallor,
dizziness, weakness, fatigue, syncope, anorexia, nausea, vomiting,
thirst, confusion, and constipation.

Palpation

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Chest and abdominal palpation are performed to elicit pain in the
abdomen or chest.

Screening labwork
Blood studies can reveal the extent of hypovolemia, because the
blood becomes more concentrated as fluid is lost. If bleeding is
present, studies will reveal blood loss.

• Hematocrit levels are elevated with dehydration and decreased

with bleeding.

• BUN values may be elevated, with a BUN/creatinine ratio of

greater than 20:1 suggesting hypovolemia.

• Electrolyte levels will vary depending on the type of fluid lost.

• ABG values depend on the type of fluid lost.

• Serum and urine osmolality depend on the type of fluid lost and a
comparison assists in the diagnosis of renal insufficiency.

Early hypovolemic shock is often missed. Blood pressure

(BP) may be compensated and remain normal or slightly elevated.
Narrowing of pulse pressure (systolic BP − diastolic BP = pulse
pressure) is a more accurate tool in early shock.
A narrow pulse pressure in a patient with hypovolemic shock
indicates a decreasing cardiac output and an increasing peripheral
vascular resistance. Reduced venous blood volume from blood or
fluid loss stimulates the sympathetic nervous system to increase or
maintain the falling BP through systemic vasoconstriction.
Stimulation of beta receptors increases heart rate and myocardial
contractility, which temporarily correct the rate of decline in
systolic BP. Vasoconstriction increases diastolic BP and thus pulse
pressure can be reduced. A BP of 104/88 mm Hg appears “normal,”
but perfusion requires further assessment.

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 As shock progresses, pulse pressure may widen as the
compensatory response fails. Heart rate decreases, ventricular
compliance is reduced, and with impaired ventricular relaxation
during diastole, ventricular filling time is reduced, resulting in
decreased central venous pressure and pulmonary artery pressure.
Volume status may be underestimated. If the difference in systolic
and diastolic blood pressure is less than 25% of the systolic blood
pressure, the pulse pressure is considered to be narrow. A wide
pulse pressure is considered to be greater than 50% of the systolic
blood pressure.

Collaborative management
Care priorities
Identification of patients at risk for volume loss and prevention of
continued losses and fluid replacement guide the care plan for these
patients.

1. Restore tissue perfusion with fluid volume replacement and

correct electrolyte disturbances: Administer and monitor fluid
replacement with crystalloids, colloids, or blood.

2. Document response to fluid administration.

3. Maintain a safe environment for patients with neurologic

symptoms.

4. Monitor for signs and symptoms of dehydration.

• Monitor urine output.

• Moisten mucous membranes.

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5. Protect skin with lotions and egg crate or alternating pressure
mattress.
Management of Hypovolemia
1. Restore Normal Fluid Volume and Correct Acid-Base and Electrolyte Disturbances
The type of fluid replacement depends on the type of fluid lost and the severity of the deficit and on serum
electrolytes, serum osmolality, and acid-base status. Intravenous (IV) fluids are provided to expand
intravascular volume or to correct an underlying imbalance in fluids or electrolytes. Fluids should be
infused at a rate resulting in a positive fluid balance (e.g., 50 to 100 mL in excess of all hourly losses).
Replacement fluids
• Isotonic solutions (normal saline 0.9%): Expand the extracellular fluid compartment (ECF)
only; do not enter the intracellular fluid compartment (ICF). Appropriate for rapid volume
replacement.
• Hypotonic saline solutions (0.45% saline): Expand the ECF and provide some free water to
the cells. Used in the management of the patient who is both volume-depleted and
hyperosmolar (e.g., in cases of hypernatremia or hyperglycemia).
• Dextrose and water (5% dextrose in water): Provide free water only that will be distributed
evenly through both the ICF and ECF; used to treat water deficit.
• Mixed isotonic saline/electrolyte solutions: Provide additional electrolytes (e.g., potassium
and calcium) and a buffer (e.g., lactate or acetate). Example: Lactated Ringer solution (Ringer
lactate): Isotonic solution containing a small amount of K+ and lactate, which metabolizes to
bicarbonate in the liver to assist blood buffering.
• Blood and albumin: Expand only the intravascular portion of the ECF. Both packed red
blood cells and fresh-frozen plasma expand the intravascular volume.
• Dextran or hetastarch, hypertonic saline, hextend: Synthetic colloidal solutions used to
expand the intravascular volume.
2. Restore Tissue Perfusion (Hypovolemic Shock)
• Rapid volume replacement with crystalloids: Fluids may be given rapidly as long as cardiac
filling pressures and blood pressure remain low. Overaggressive fluid resuscitation in
uncontrolled hemorrhage can increase the risk of secondary hemorrhage as the intravascular
hydrostatic pressure increases.
• Volume replacement with colloids: Use of volume replacement with colloids to prevent the
development of pulmonary edema secondary to rapid volume replacement remains
controversial. Solutions include albumin and synthetics such as hetastarch.
• Blood: Administered only if necessary to maintain oxygen-carrying capacity. Hematocrit
should not be raised greater than 35%.
• Vasopressors: Used to reduce the size of blood vessels while volume infusions continue to
increase blood pressure. Effective for false hypovolemia induced by vasogenic (septic,
anaphylactic, neurogenic) shock to control severe vasodilation.

Care plans for hypovolemia

Deficient fluid volume 
related to loss of body fluid or blood
Goals/Outcomes: Within 24 hours of starting fluid therapy, the
patient becomes normovolemic, as evidenced by urine output ≥0.5
mL/kg/h, specific gravity 1.010 to 1.030, stable weight, no clinical
evidence of hypovolemia (e.g., furrowed tongue), BP within the
patient’s normal range, HR and pulse pressure normalized, CVP 2

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to 6 mm Hg, pulmonary artery pressure (PAP) 20 to 30/8 to 15 mm
Hg, CO 4 to 7 L/min, mean airway pressure (MAP) 70 to 105 mm
Hg, HR 60 to 100 beats per minute (bpm), and systemic vascular
resistance (SVR) 900 to 1200 dynes/s/cm5.
Fluid Balance, Hydration, Kidney Function.

Fluid monitoring

1. Monitor input and output (I&O) hourly: During initial therapy,

intake should exceed output. Consult the advanced practice
provider for urine output less than 0.5 mL/kg/h for 2 consecutive
hours. Measure urine specific gravity every 4 hours as available.
Normal range is 1.010 to 1.030. Expect it to decrease with therapy.

2. Monitor vital signs and hemodynamic pressures for continued

hypovolemia: Be alert to decreased BP, CVP, PAP, CO, and MAP
and to increased HR and SVR.

3. Weigh the patient daily: Daily weight measurements are the

single most important indicator of fluid status, because acute
weight changes usually indicate fluid changes. A decrease in daily
weight of 1 kg is equal to the loss of 1 L of fluid. The adult who is
not eating or receiving enteral nutrition or parenteral nutrition (PN)
may lose 0.25 kg of nonfluid weight daily because body tissues are
used for glucose production. Weigh patient at the same time of day
(preferably before breakfast) on a balanced scale, with the patient
wearing approximately the same clothing. Document type of scale
used (i.e., standing, bed, chair).

4. Monitor for signs of fluid overload or too-rapid fluid

administration: Crackles (rales), decreased O2 saturation (pulse
oximetry/SpO2), shortness of breath (SOB), tachypnea, tachycardia,
increased CVP, increased PA pressures, neck vein distention, and
edema.

5. Monitor the patient for hidden fluid losses: Measure/record

abdominal girth or limb size if indicated.

6. Monitor for signs of abdominal compartment syndrome: Acute

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increase in ventilator pressures and a decrease in SpO2.

7. Monitor for signs of bleeding: Decreased hematocrit (Hct), Hgb,

tachycardia. Note that Hct, serum Na+, and BUN may decrease in
dehydrated patients as rehydration progresses.

8. Monitor for hypocalcemia: May develop in patients who are

rapidly transfused as a result of the citrate used in banked blood
(citrate binds calcium, making it unavailable for cellular uptake).
Sudden symptoms may include refractory hypotension (see
Hypocalcemia. Calcium chloride or gluconate may be prescribed.

Fluid management

1. Place hypotensive patients in supine position with legs elevated

to 45 degrees to increase venous return. Avoid the Trendelenburg
position, which causes abdominal organs to lean on the diaphragm,
thereby impairing ventilation.

2. Administer oral (per os, PO) and IV fluids as prescribed. Ensure

adequate intake, especially in older adults, a population at higher
risk for volume depletion. Give water with enteral feedings and
supplements.

3. Ensure a patent IV access and availability of blood products if

needed.

Fluid Monitoring; Hypovolemia Management; Fluid

Resuscitation; Intravenous (IV) Therapy; Invasive Hemodynamic
Monitoring; Shock Management; Volume.

Ineffective peripheral tissue perfusion 

related to lack of blood volume
Goals/Outcomes: Within 12 hours after initiation of volume
resuscitation, the patient has adequate perfusion, as evidenced by
alertness, warm and dry skin, BP within the patient’s normal range,
HR ≤100 bpm, urinary output ≥0.5 mL/kg/h, and capillary refill less
than 2 seconds.
Circulation Status, Tissue Integrity: Skin and Mucous

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Membranes.

Circulatory care: Arterial insufficiency

1. Monitor for signs of decreased cerebral perfusion: vertigo,

syncope, confusion, restlessness, anxiety, agitation, excitability,
weakness, nausea, and cool and clammy skin. Consult the
physician or midlevel practitioner for worsening symptoms.

2. To avoid unnecessary vasodilation, treat fevers promptly.

3. Cover the patient with a light blanket to maintain body

temperature.

4. Palpate peripheral pulses bilaterally in arms and legs (radial,

brachial, dorsalis pedis, posterior tibial). Use a Doppler ultrasonic
device if unable to palpate pulses. Rate pulses (0 to 4+ scale).
Consult the physician for weak/absent pulses.

Abnormal pulses may also be caused by a local vascular

disorder.

5. Consult the advanced practice provider for urinary output less

than 0.5 mL/kg/h for 2 consecutive hours.

Positioning

1. Protect patients who are at high risk for falling: those who are
confused, dizzy, or weak. Keep side rails up and bed in lowest
position with wheels locked. Assist with ambulation. Raise the
patient to sitting or standing positions slowly.

2. Monitor for orthostatic hypotension: decreased BP, increased HR,

dizziness, and diaphoresis. If symptoms occur, return the patient to
supine position.

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 Neurologic Monitoring

Additional nursing diagnoses

For additional nursing diagnoses, see specific medical disorder,
electrolyte imbalance, or acid-base disturbance.

Hypervolemia
Pathophysiology
Hypervolemia is a state of higher-than-normal intravascular
volume that occurs in four situations: (1) excessive retention of
sodium and water caused by a chronic renal stimulus to conserve
sodium and water; (2) abnormal renal functioning causing reduced
excretion of sodium and water; (3) excessive administration of IV
fluids; and (4) interstitial-to-plasma fluid shifting. Hypervolemia
may lead to heart failure and pulmonary edema, especially in the
patient with cardiovascular dysfunction.

Hypervolemia assessment
Goal of assessment
• Evaluate the potential causes and sequelae of hypervolemia.

History and risk factors

• Retention of sodium and/or water: Heart failure, hepatic failure,
nephrotic syndrome, excessive administration of
glucocorticosteroids, and syndrome of inappropriate antidiuretic
hormone (SIADH).

• Abnormal renal function: Acute or chronic renal failure, oliguria,

anuria, and excessive administration of IV fluids.

• Interstitial-to-plasma fluid shifting: Remobilization of fluid after

burn treatment, excessive administration of hypertonic solutions
(i.e., mannitol, hypertonic saline), and excessive administration of

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 colloid oncotic solutions (i.e., albumin).

Observation
• Evaluate for the clinical signs of volume overload: SOB,
orthopnea, peripheral edema, distended neck veins, and moist
skin.

Vital signs
• HR, BP, and hemodynamic measurements to evaluate volume
status.

• Increased BP.

• BP: will decrease as the heart fails.

• HR: tachycardia.

• Respirations: tachypnea.

• O2 saturation decreased.

• Increased CVP, PAP, PAWP.

• MAP: increased unless heart failure is present.

• Pulse pressure: may be narrow early in development of

cardiogenic shock.

Palpation
• Pulse assessment to evaluate tissue perfusion: Bounding pulses,
ascites, and peripheral and sacral edema.

Auscultation
• Heart and lung assessment to evaluate signs of volume overload:
Tachycardia, gallop rhythm, crackles, rhonchi, and wheezes.

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Screening labwork
• Blood studies are variable and nonspecific: Hematocrit, BUN and
creatinine, ABGs, serum sodium and osmolality, urinary sodium,
and urine specific gravity.

Radiology
• Chest radiograph may reveal signs of pulmonary vascular
congestion.

Diagnostic Tests for Hypervolemia

Test Purpose Abnormal Findings

Hematocrit Assess for Decreased: As a result of hemodilution by excess fluids in the
anemia vasculature
Blood urea Evaluate for Decreased: In pure hypervolemia. Increased: With renal failure
nitrogen presence of
renal
dysfunction
Arterial Assess for Hypoxemia with alkalosis: May be present as a result of tachypnea
blood hypoxemia associated with early pulmonary edema.
gases and acid- Respiratory acidosis: May be present in severe pulmonary edema.
base Diffusion of oxygen is difficult across the edematous alveolar-
imbalance capillary membrane
(acidosis or
alkalosis)
Serum Assess for Decreased: If hypervolemia is from water retention (i.e., chronic
sodium water renal failure)
and serum retention
osmolality
Urinary Evaluate Elevated: Results from kidneys excreting excess sodium. Sodium
sodium efficacy of excretion prompts fluid excretion. Note: Urinary sodium is not
renal elevated with secondary hyperaldosteronism (e.g., heart failure,
handling of cirrhosis, nephrotic syndrome) because hypervolemia occurs
sodium secondary to a chronic renal stimulus; the aldosterone increases
resorption of Na+
Urine Evaluate the Decreased: If the kidney is excreting excess volume. May be fixed at
specific solute 1.010 in acute renal failure
gravity concentrating
ability of the
kidney
Chest Assess for May reveal signs of pulmonary vascular congestion (“whiter”
radiograph pulmonary appearance)
edema

Collaborative management

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Care priorities
The priorities include prevention of further volume overload and
returning the patient to a euvolemic state.

1. Restrict intake of sodium and water: Monitor intake of oral,

enteral, and parenteral fluids. Prevent the intake of high sodium
foods. Box 1-7 lists foods high in sodium.

2. Administer diuretics: May be given IV or PO. Loop diuretics (i.e.,

furosemide) are indicated for severe hypervolemia or heart failure.
Diuresis may prompt profound electrolyte loss.

3. Monitor weight and output: Assess the response to diuretics.

Monitor for electrolyte loss.

4. Renal replacement therapy: Used in renal failure or life-

threatening fluid overload (see Acute Renal Failure/Acute Kidney
Injury, Chapter 6).

5. Patient education: Signs and symptoms of volume overload.

Information provided regarding high sodium-containing foods.

6. Vital signs: Monitor for changes in BP and CO with diuresis.

Box 1-7
FOODS HIGH IN SODIUM
Bouillon

Celery

Cheeses

Dried fruits

Frozen, canned, or packaged foods

Monosodium glutamate (MSG)

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Mustard

Olives

Pickles

Preserved meat

Salad dressings and prepared sauces

Sauerkraut

Snack foods (e.g., crackers, chips, pretzels)

Soy sauce

Also see specific discussions under Burns (Chapter 3), Acute

Lung Injury and Acute Respiratory Distress Syndrome (Chapter 4),
and Acute Renal Failure/Acute Kidney Injury (Chapter 6).

Care plans for hypervolemia

Excess fluid volume 
related to the patient’s disease state(s), medications, and/or other therapies
Goals/Outcomes: Within 24 hours of starting treatment, the
patient is improved, as evidenced by reduced edema, BP
approaching the patient’s normal range, HR 60 to 100 bpm, CVP 2
to 6 mm Hg, PAP 20 to 30 mm HG systolic, 8 to 15 mm Hg diastolic,
MAP 70 to 105 mm Hg, and CO 4 to 7 L/min.
Electrolyte and Acid-Base Balance, Fluid Balance, Fluid
Overload Severity.

Fluid/electrolyte management

129
1. Monitor intake and output hourly. Urine output should be ≥0.5
mL/kg/h unless the patient is in oliguric renal failure.

2. Measure urine specific gravity or urine osmolality if available,

every 4 hours. If the patient is receiving diuretic therapy, specific
gravity should be 1.010 to 1.020 with osmolality less than 500
mOsm/L.

3. Monitor and manage edema (pretibial, sacral, periorbital), using a

0 to 4+ rating scale.

4. Weigh patient daily. Daily weight measurements are the single

most important indicator of fluid status.

5. Limit oral, enteral, and parenteral sodium intake as prescribed.

Be aware that medications may contain sodium (e.g., penicillin,
bicarbonate). See Box 1-7 for some foods high in sodium.

6. Limit fluids as prescribed. Offer a portion of allotted fluids as ice

chips to minimize the patient’s thirst. Teach the patient and
significant others the importance of fluid restriction and how to
measure fluid volume.

7. Provide oral hygiene at frequent intervals to keep oral mucous

membranes moist and intact.

8. Document response to diuretic therapy (e.g., increased urine

output, decreased CVP/PAP, decreased adventitious breath sounds,
decreased edema). Many diuretics (e.g., furosemide, thiazides)
cause hypokalemia. Observe for indicators of hypokalemia: muscle
weakness, dysrhythmias (especially PVCs and ECG changes such
as flattened T wave, presence of U waves). (See Hypokalemia)
Potassium-sparing diuretics (e.g., spironolactone, triamterene) may
cause hyperkalemia: signs include weakness, ECG changes (e.g.,
peaked T wave, prolonged PR interval, widened QRS complex).
(See Hyperkalemia) Consult the advanced practice provider for
significant findings.

9. Observe for indicators of overcorrection and dangerous volume

depletion. Vertigo, weakness, syncope, thirst, confusion, poor skin

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turgor, flat neck veins, and acute weight loss.

10. Monitor vital signs and hemodynamic parameters for volume

depletion occurring with therapy. Decreased BP, CVP, PAP, MAP,
and CO; increased HR. Consult the advanced practice provider for
significant changes or findings.

11. Monitor appropriate laboratory tests (e.g., BUN and creatinine

in renal failure). Consult with the advanced practice provider for
abnormal trends.

Fluid Monitoring; Hypervolemia Management;

Fluid/Electrolyte Management; Invasive Hemodynamic
Monitoring; Hemodialysis Therapy.

Impaired gas exchange 

related to fluid volume overload
Goals/Outcomes: Within 12 hours of initiating treatment, the
patient has improved gas exchange, as evidenced by RR <20
breaths/min with normal depth and pattern (eupnea), HR <100
bpm, PaO2 >80 mm Hg; pH 7.35 to 7.45, PaCO2 35 to 45 mm Hg, and
SpO2 >92%. The patient exhibits reduction in or absence of crackles,
gallops, or other clinical indicators of pulmonary edema. PAP is
≤30/15 mm Hg and PAWP is 6 to 12 mm Hg.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation.

Respiratory monitoring

1. Monitor the patient for signs of acute pulmonary edema, a

potentially life-threatening complication of hypervolemia: air
hunger, decreased pulse oximetry, anxiety, cough with production
of frothy sputum, crackles, rhonchi, tachypnea, increasing
ventilator pressures, tachycardia, gallop rhythm, and elevation of
PAP and PAWP. Administer diuretics and other medications to
reduce venous return to the heart, as prescribed.

2. Monitor ABG values for hypoxemia and respiratory alkalosis.

Monitor O2 saturation. Administer O2 to maintain SpO2 >92%.

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Increased O2 requirements may signal increased pulmonary
vascular congestion.

3. Keep the patient in semi-Fowler position or position of comfort to

minimize dyspnea.

Ventilation Assistance, Positioning.

Impaired skin integrity 

related to edematous, possibly friable tissue

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 Goals/Outcomes: The patient’s skin and tissue remain intact.
Tissue Integrity: Skin and Mucous Membranes.

Pressure management

1. Assess and document circulation to extremities at least each shift.

Note color, temperature, capillary refill, and peripheral pulses.
Consult the physician or midlevel practitioner if capillary refill is
delayed or if pulses are diminished or absent.

2. Turn and reposition the patient at least every 2 hours to minimize

tissue pressure.

3. Check tissue areas at risk with each position change (e.g., heels,
sacrum, areas over bony prominences).

4. Use pressure-relief mattress as indicated.

5. Support arms and hands on pillows and elevate legs to decrease

dependent edema. Do not elevate legs in the presence of pulmonary
congestion.

6. Treat pressure ulcers per unit protocol. Consult the advanced

practice provider if sores, ulcers, or areas of tissue breakdown are
present, especially with patients who are at high risk for infection
(i.e., those with diabetes mellitus or renal failure or who are
immunosuppressed).

7. Consult a skin/wound care nurse specialist for advanced tissue

breakdown or any alteration in tissue integrity in high-risk patients.

Circulatory Care; Skin Surveillance.

Hyponatremia (serum sodium less than 135

mEq/L)
Pathophysiology
Hyponatremia occurs from a net gain of water or a loss of sodium-
rich fluids that have been replaced by water (net gain fluid > net

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gain Na2+). The most common cause of hyponatremia is water gain
from renal dysfunction. The kidneys should increase output if
intake increases. As serum osmolality decreases, fluid shifts into
cells, causing swelling and sometimes compartment syndromes.
There are three types of hyponatremia: hypovolemic,
hypervolemic, and euvolemic. Dilutional states are the most
frequent cause of hyponatremia in the critically ill. Clinical
indicators and treatments depend on the cause of hyponatremia
and whether it is associated with normal, decreased, or increased
ECF volume. For more information, see Burns (Chapter 3), Heart
Failure (Chapter 5), Acute Renal Failure/Acute Kidney Injury
(Chapter 6), and Syndrome of Inappropriate Antidiuretic Hormone
(Chapter 8).

Hyperlipidemia, hyperproteinemia, and hyperglycemia may

cause a pseudohyponatremia. Pseudohyponatremia reduces the
Na2+ content but also causes a reduction in volume. Actual
osmolality may be normal or high. If blood glucose, lipids, or
proteins are elevated, an osmolality calculation or laboratory
determination should be performed. Hyperlipidemia and
hyperproteinemia reduce the percentage of plasma water. With
hyperglycemia, the osmotic action of elevated glucose causes
water to shift out of the cells into the extracellular fluid
compartment, thus diluting the serum sodium. For every 100 mg/dL
that glucose is elevated, sodium is diluted by 1.6 mEq/L. The
sodium-to-water ratio of plasma is unchanged, but the amount of
sodium in the plasma is reduced.

Hyponatremia assessment
Goal of assessment
• Evaluate for the signs and symptoms of hyponatremia.

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History and risk factors
• Decreased ECF volume. GI losses: diarrhea, vomiting, fistulas,
and nasogastric suction; renal losses: diuretics, salt-wasting
kidney disease, and adrenal insufficiency; skin losses: burns,
wound drainage, and excessive diaphoresis.

• Normal/increased ECF volume. Hypothyroidism, SIADH,

edematous states: heart failure, cirrhosis, and nephrotic
syndrome; vigorous administration of hypotonic IV fluids; very
dilute enteral feedings; oliguric renal failure; primary polydipsia;
any patient with impaired ability to excrete free water (e.g., those
being treated with thiazide diuretics) is at risk if given hypotonic
fluids.

Vital sign assessment

• BP and HR will vary based on the state of ECF volume.

• Postural hypotension with decreased ECF volume.

• Elevated BP with normal or increased ECF volume.

• Weight gain with normal or increased ECF volume.

• Hemodynamic measurements.

• Decreased ECF volume: decreased CVP, PAP, CO,

MAP; increased SVR.

• Increased ECF volume: increased CVP, PAP, MAP.

Observation
• Hyponatremia with decreased ECF volume: Irritability,

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 apprehension, dizziness, personality changes, poor skin turgor,
dry mucous membranes, tremors, seizures, and coma.

• Hyponatremia with normal or increased ECF volume: Headache,

lassitude, apathy, confusion, weakness, edema, convulsions, and
coma.

Palpation
• Cold clammy skin with decreased ECF volume.

• Hyperreflexia and muscle spasms with normal on increased ECF

volume.

Screening labwork
• Serum sodium.

• Serum osmolality.

• Urine specific osmolality.

• Urine sodium.

Diagnostic Tests for Hyponatremia

Test Purpose Abnormal Findings

Serum Evaluate sodium Decreased: Less than 135 mEq/L.
sodium level
Serum Assess hydration Decreased: Except in cases of pseudohyponatremia.
osmolality status
Urine Assess renal Elevated: Usually greater than 100 mOsm/kg, but less than the
specific concentrating plasma level.
osmolality ability SIADH: The urine will be inappropriately concentrated.
Urine Assess renal Decreased: Usually less than 20 mEq/L EXCEPT with SIADH,
sodium ability to salt-wasting kidney disease, adrenal insufficiency, or excessive
conserve sodium diuretic therapy.
SIADH, Syndrome of inappropriate antidiuretic hormone.

Collaborative management

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Care priorities

1. Replace sodium and fluid losses with reduced ECF

volume
Adequate replacement of fluid volume is essential to stop the
physiologic stimulus to ADH release and enable the kidneys to
restore sodium and water balance. Administer IV fluids while
monitoring for further signs and symptoms of hyponatremia and
I&O.

2. Replace other electrolyte losses

Other electrolytes include potassium and bicarbonate.

3. Administer IV hypertonic saline (3% NaCl)

Use if serum sodium is dangerously low or the patient has extreme
symptoms. The therapeutic goal is to slowly shrink the cerebral
cells. The dose is based on the patient’s response. Therapy is
sufficient when symptoms resolve and may be discontinued.
Therapy MUST BE administered carefully, because too rapid
correction can result in a life-threatening demyelination syndrome.

4. Monitor rate of sodium replacement to prevent too rapid

correction of hyponatremia
Mild symptoms/no symptoms of hyponatremia: Strive to increase
serum sodium 0.5 to 1 mEq/L/h. Severe symptoms, including
seizures: Increase serum sodium no more than 1 to 2 mEq/L/h for 3
to 4 hours. Sodium should not increase more than 10 mEq/L in any
24-hour period, and no more than 6 mEq/L during the first 3 to 4
hours.

5. For hyponatremia with expanded ECF volume

• Remove or treat the underlying cause.

• Administer diuretics.

• Restrict fluid intake to 1000 mL/day to establish a negative water

balance and increase sodium levels.

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6. Assess for resolution of the signs and symptoms of
neurologic changes.

7. For dilutional hyponatremia

Administer diuretics and restrict water intake.
See Syndrome of Inappropriate Antidiuretic Hormone, Chapter 8,
for specific treatment of hyponatremia.

HIGH ALERT!
Osmotic Demyelination Syndrome
Overly aggressive or inappropriate treatment of hyponatremia can also
cause permanent neurologic damage secondary to osmotic demyelination
syndrome. Osmotic demyelination is poorly understood but should
always be suspected after hypertonic resuscitation when patients
display bilateral neurologic deficits, flaccidity, and quadriparesis.
Initially, sodium levels should not increase at a level greater than
0.5 to 1.0 mEq/L/h in patients being treated for symptomatic
hyponatremia with hypertonic NaCl. For those symptomatic with
severe hyponatremia (less than 120 mEq/L), the rate of correction
should be 1 to 2 mEq/h for 3 to 4 hours. After an initial 6 to 8
mEq/L increase in the serum sodium level, the rate of increase
should not be greater than 0.5 mEq/L/h. Levels should not increase
at an average rate of greater than 0.5 mEq/L/h in patients without
symptoms. The total increase in the first 24 hours of treatment
should not exceed 12 mEq/L.

Care plans for hyponatremia

Readiness for enhanced fluid balance 
related to the dynamic fluid and electrolyte changes that prompt sodium
imbalance
Goals/Outcomes: Within 24 hours of initiating treatment, the
patient’s volume status is improving, as evidenced by
normalization of the heart and respiratory rates (HR 60 to 100 bpm,

138
RR 12 to 20 breaths/min), BP within the patient’s normal range,
CVP 2 to 6 mm Hg, and PAP 20 to 30 mm HG systolic, 8 to 15 mm
Hg diastolic or within the patient’s normal range.
Fluid Balance, Kidney Function, Hydration.

Fluid monitoring
If the patient is receiving hypertonic saline, assess carefully for
signs of intravascular fluid overload: tachypnea, tachycardia, acute
SOB, crackles (rales), rhonchi, increased CVP and PAP, gallop
rhythm, and increased BP. For other interventions, see
Hypovolemia or Hypervolemia.
Electrolyte Management: Hyponatremia; Fluid/Electrolyte
Management; Intravenous (IV) Therapy; Invasive Hemodynamic
Monitoring.

Acute confusion 
related to hyponatremia
Goals/Outcomes: Within 48 hours of treatment, the patient more
consistently verbalizes orientation to time, place, and person and
has not sustained physical injury related to altered sensorium.
Serum sodium level should ideally increase to greater than 125
mEq/L in the first 48 hours after treatment.
Cognitive Orientation; Distorted Thought Self-Control;
Information Processing; Neurologic Status: Consciousness.

Neurologic monitoring

1. Assess and document LOC, orientation, and neurologic status

with each vital sign check. Reorient the patient as necessary.
Consult the advanced practice provider for significant changes.

2. If seizures are expected, pad side rails and keep an appropriate-

size airway at the bedside.

3. Inform the patient and significant others that altered sensorium is

temporary and will improve with treatment.

4. Keep side rails up and bed in lowest position with wheels locked.

139
5. Use reality therapy such as clocks, calendars, and familiar objects;
keep these items at the bedside within the patient’s visual field.

6. Monitor serum sodium levels closely. Permanent neurologic

damage may occur with untreated, severely symptomatic
hyponatremia secondary to cerebral edema.

HIGH ALERT!
Overly rapid correction of chronic hyponatremia may result in
permanent neurologic damage.

Electrolyte Management: Hyponatremia; Seizure

Precautions, Reality Orientation, Fall Prevention.

Hypernatremia (serum sodium greater than

145 mEq/L)
Pathophysiology
Hypernatremia may occur with either free water loss or sodium
gain. Hypernatremia always causes hypertonicity because sodium
is the major determinant of ECF osmolality. Hypertonicity causes a
shift of water out of the cells, which leads to intracellular
dehydration. Hypernatremia usually results from volume depletion
(hypovolemia) and is rarely caused by increased sodium intake.

Hypernatremia assessment
Goal of assessment
Evaluate the risk factors and clinical symptoms of hypernatremia.

History and risk factors

• Water (volume) loss: Increased diaphoresis, respiratory infection,
mechanical ventilation, diabetes insipidus, osmotic diuresis (e.g.,

140
 hyperglycemia), and osmotic diarrhea.

• Sodium gains: IV administration of hypertonic saline or sodium

bicarbonate, increased oral intake, primary aldosteronism, and
drugs such as sodium polystyrene sulfonate (Kayexalate).

Observation
• Symptoms related to hypertonicity, intracellular dehydration, and
electrolyte imbalance: Intense thirst, fatigue, restlessness,
agitation, coma, flushed skin, and peripheral edema.

Vital signs
• Low-grade fever.

• Postural hypotension.

• Increased CVP and PAP: with sodium excess.

• Decreased CVP and PAP with water loss: may be minimized by

the extracellular shift of fluid that occurs with hypernatremia.

• Tachycardia may be present.

Symptoms of hypernatremia occur only in individuals who

do not have access to water or who have an altered thirst
mechanism (e.g., infants, older adults, those who are comatose).

Symptoms are most likely to develop with a sudden increase

in plasma sodium. After 24 hours, brain cells adjust to
extracellular fluid hypertonicity by increasing intracellular
osmolality. The mechanism of action is unclear, but the increased

141
osmolality helps to rehydrate the cells. Individuals with chronic
hypernatremia exhibit few symptoms. This adaptive mechanism
plays a key role in the treatment of hypernatremia.

HIGH ALERT!
Overly aggressive water administration may cause rapid movement of
water into the cells, which can result in dangerous cerebral edema caused
by a too-rapid reduction of sodium.

Diagnostic Tests for Hypernatremia

Test Purpose Abnormal Findings

Serum Assess level of Increased: Greater than 145 mEq/L.
sodium sodium
Serum Determine Increased: As a result of elevated serum sodium; greater than
osmolality concentration of 300 mOsm/kg.
solutes
Urine Assess the ability of Increased: Greater than 1.030. Lower than expected in
specific the kidneys to retain diabetes insipidus and too dilute in early osmotic diuresis
gravity water (e.g., hyperglycemia).

Collaborative management
Care priorities
1. Assess the patient for fluid losses or gains.

2. Administer IV or PO water replacement: Used for water loss. If

sodium is greater than 160 mEq/L, IV 5% dextrose or hypotonic
(0.45%) saline is given to replace pure water deficit (see Diabetes
Insipidus, Chapter 8).

3. Monitor intake to prevent too rapid correction of water loss.

4. Administer diuretics with water replacement: Use for sodium

142
gain.

5. Provide information to the patient to help decrease sodium

intake.

Hypernatremia is corrected slowly, over approximately 2

days, to avoid too great a shift of water into brain cells.

Care plans for hypernatremia

Acute confusion 
related to hypernatremia
Goals/Outcomes: Within 48 hours after treatment, the patient
more consistently verbalizes orientation to time, place, and person
and has not sustained an injury caused by altered sensorium or
seizures. Serum sodium level has decreased and is approaching
high normal (145 mEq/L).
Cognitive Orientation; Distorted Thought Self-Control;
Information Processing; Neurologic Status: Consciousness.

Fluid/electrolyte management

1. Monitor serial serum sodium levels (sodium should not decrease

at a rate greater than 0.5 to 1.0 mEq/L/h); consult the physician for
rapid decreases. Cerebral edema may occur if hypernatremia is
corrected too rapidly.

2. Assess the patient for signs of cerebral edema: lethargy,

headache, nausea, vomiting, increased BP, widening pulse
pressure, decreased HR, altered sensorium, and seizures.

3. Assess and document LOC, orientation, and neurologic status

with each vital sign check. Reorient the patient as necessary.
Consult the advanced practice provider for deterioration.

143
4. Inform the patient and significant others that altered sensorium is
temporary and will improve with treatment.

5. Keep side rails up and bed in lowest position with wheels locked.

6. Use reality therapy such as clocks, calendars, and familiar objects;

keep these items at the bedside within the patient’s visual field.

7. If seizures are anticipated, pad side rails and keep an

appropriate-size airway at the bedside.

8. Provide comfort measures to decrease thirst.

Neurologic Monitoring; Electrolyte Management:

Hypernatremia; Seizure Precautions; Surveillance: Safety.

Additional nursing diagnoses

See Hypovolemia for Fluid Volume Deficit and Hypervolemia for
Fluid Volume Excess.

Potassium imbalance (normal serum K+ level

3.5 to 5 mEq/L)
Potassium is the primary intracellular cation (+ or positive ion), with
normal levels inside cells of 150 mEq/dL. Of total potassium, 98% is
inside the cell and markedly affects cell metabolism. Abnormal
serum K+ levels may adversely affect neuromuscular and cardiac
function, because they affect resting membrane potential and
conduction velocity of nerve and cardiac cells. A relatively small
amount of potassium is present in the ECF, and concentrations are
maintained within a narrow range. Potassium is constantly moving
into and out of the cell. Distribution of potassium between the ECF
and ICF is maintained by the sodium-potassium pump located in
the membrane of all body cells and is affected by ECF pH, glucose
and protein metabolism, insulin levels, and stimulation of beta2-
adrenergic receptors. Acute changes in serum pH are accompanied
by reciprocal changes in serum potassium concentration as the
exchange of K+ and H+ takes place.

144
 The body gains potassium through foods (primarily meats, fruits,
and vegetables) and medications. The ECF also gains potassium
from breakdown or death of cells, when a large amount of
intracellular K+ is released from the cell contents. Potassium is
eliminated from the body through the kidneys, the GI tract, and the
skin. The potassium level may decrease in the serum (ECF) when K+
shifts inside the cells. The serum potassium level increases when
renal function decreases, when circulation is reduced to a large
amount of cells causing cell death, with cellular lysis, and with
rhabdomyolysis. Changes in insulin production, insulin and other
receptor activity, and catecholamine level affect the movement of K+
across the cell wall. The kidneys are the primary regulators of
potassium balance.

Disorders of potassium balance are potentially life

threatening because of the effects of altered potassium levels on
neuromuscular and cardiac function. Suspected alterations in
potassium balance require prompt consultation with the advanced
practice provider.

Hypokalemia (serum potassium level less

than 3.5 mEq/L)
Pathophysiology
Hypokalemia occurs because of a loss of potassium from the body
or a movement of potassium into the cells. Acid-base imbalances
are associated with changes in serum potassium level. Management
of shifts in the K+ level must be done judiciously if an acid-base
imbalance is present. Hypokalemia is sometimes associated with
alkalosis (see Acid-Base Imbalances). Serum K+ levels are an
inadequate measure of intracellular K+, but intracellular
measurement is not clinically available.

145
 Changes in serum potassium levels reflect changes in
extracellular fluid potassium—not necessarily changes in total
body levels.

Hypokalemia assessment
Goal of assessment
Evaluate for the risk factors and signs and symptoms of
hypokalemia and use the information to manage the symptoms.
The patient is at risk for torsades de pointes and ventricular
tachycardia.

History and risk factors

• Reduction in total body potassium: Hyperaldosteronism, diuretic
therapy or abnormal urinary losses, increased GI losses,
increased loss through diaphoresis, decreased intake, and
dialysis.

• Intracellular shift: Increased insulin (e.g., from total parenteral

nutrition [TPN] or aggressive IV insulin), acute alkalosis: K+
moves into the cells in exchange for H+ to electrically and pH
balance the serum; stress causing a loss of potassium in the urine
secondary to increased release of aldosterone; intracellular shift
of potassium secondary to increased stimulation of beta2-
adrenergic receptors.

Vital signs
• Postural hypotension.

• Irregular respiratory pattern resulting from respiratory muscle

weakness.

146
Auscultation
• Decreased bowel sounds.

Palpation
• Weak and irregular pulse.

• Decreased reflexes.

• Decreased muscle tone.

• Paresthesias.

Screening
12-Lead ECG: Evaluate changes typically seen with hypokalemia,
including ST segment depression, flattened T waves, presence of U
waves; with severe hypokalemia, P wave amplitude is increased,
PR interval is prolonged, QRS and QT complexes widen, and
patient is at risk for torsades de pointes.

An inadequate diet may contribute to but will rarely cause

hypokalemia. Large amounts of potassium are contained in many
common foods. Hypokalemia sometimes develops when patients
are maintained on parenteral fluid therapy with inadequate
replacement of potassium or when increased losses occur when
oral intake is poor.

Diagnostic Tests for Hypokalemia

Test Purpose Abnormal Findings

Serum Determine if Decreased: Less than 3.5 mEq/L.
potassium hypokalemia is present
Arterial Evaluate for the Increased pH and bicarbonate. Hypokalemia is
blood gases presence of alkalosis associated with metabolic alkalosis.

147
 Hypokalemia potentiates the effect of digitalis.
Electrocardiography may reveal signs of digitalis toxicity despite
a normal serum digitalis level.

Collaborative management
Care priorities

1. Replace potassium (K+)

Administer IV potassium as an infusion if less than 3.0 mEq/L. IV
infusion is 40 to 80 mEq/L given in divided doses. Generally, 10
mEq of K+ is diluted in 50 mL IV solution and given over 30
minutes. The process is repeated until the K+ is normalized. If K+
level is 3.0 to 3.5 mEq/L, increase dietary intake and use oral
supplements (see Box 1-8 for high-potassium foods).

Never give potassium IV push to avoid lethal

dysrhythmias.

Box 1-8
FOODS HIGH IN POTASSIUM
Apricots

Artichokes

Avocados

Bananas

Cantaloupes

148
Carrots

Cauliflower

Chocolate

Dried beans, peas

Dried fruit

Mushrooms

Nuts

Oranges, orange juice

Peanuts

Potatoes

Prune juice

Pumpkins

Spinach

Swiss chard

Sweet potatoes

Tomatoes, tomato juice, tomato sauce

2. Document dietary intake of potassium

3. Administer potassium-sparing diuretics

This is done in place of thiazide or loop diuretics, which promote
potassium loss. Diuretics are often associated with hypokalemia.

149
4. Monitor for signs of hyperkalemia
When replacing K+ monitor for signs of hyperkalemia.

HIGH ALERT!
Patients receiving 10 to 20 mEq/h should be on a continuous
cardiac monitor.
If potassium is administered via a peripheral line, the rate of
administration may need to be decreased to prevent irritation of
vessels. The development of tall, peaked T waves suggests the
presence of hyperkalemia and should be reported to the advanced
practice provider. Intravenous potassium may be administered as
potassium chloride or potassium phosphate.

Care plans for hypokalemia

Decreased cardiac output 
related to dysrhythmias caused by hypokalemia
Goals/Outcomes: Within 2 hours of treatment, the patient is
normalizing cardiac conduction, as evidenced by normal T wave
configuration and normal sinus rhythm without ectopy on ECG.
Cardiac Pump Effectiveness, Circulation Status.

Electrolyte management

1. Administer potassium supplement as prescribed. Avoid giving

IV potassium chloride at a rate faster than recommended, because
this can lead to life-threatening hyperkalemia. K+ supplements for
symptomatic hypokalemia may be given in isotonic saline, as
sometimes D5W increases the insulin-induced intracellular shift of
potassium. Concentrated solutions of potassium may be
administered in limited volumes (i.e., 20 mEq in 100 mL of isotonic
NaCl), administered at less than 20 mEq/h. Concentrated solutions
are used only with severe hypokalemia.

150
 Potassium chloride should not be added to intravenous (IV)
bags while they are hanging on a pole, to avoid accumulation of K+
at the bottom of the IV bag. The solution container should be
inverted before adding the medication and mixed well.

2. Be aware that IV potassium chloride (KCl) can cause local

irritation of veins and chemical phlebitis. Assess IV insertion site for
erythema, heat, or pain. Irritation may be relieved by applying an
ice bag, giving mild sedation, or numbing insertion site with a small
amount of local anesthetic. Phlebitis may necessitate changing of IV
site.

3. Oral supplements may cause GI irritation. Administer with a full

glass of water or fruit juice; encourage the patient to sip slowly.
Consult the advanced practice provider for symptoms of abdominal
pain, distention, nausea, or vomiting. Do not switch potassium
supplements without consulting with the advanced practice
provider.

4. Monitor I&O hourly. Report urine output less than 0.5 mL/kg/h.
Unless severe symptoms of hypokalemia are present, potassium
supplements should not be given to patients with low urine output;
hyperkalemia may develop in patients with oliguria (output less
than 15 to 20 mL/h). High urine output (diuresis or polyuria)
increases the risk of hypokalemia.

5. Monitor ECG for signs of continuing hypokalemia (i.e., ST

segment depression, flattened T wave, presence of U wave,
ventricular dysrhythmias) or hyperkalemia during potassium
replacement (i.e., tall, thin T waves; prolonged PR interval; ST
depression; widened QRS complex; loss of P wave).

6. Monitor serum potassium levels in patients at risk for

hypokalemia, such as patients taking diuretics or undergoing

151
gastric suction.

7. Administer potassium cautiously in patients at risk for

hyperkalemia, such as patients receiving potassium-sparing
diuretics (e.g., spironolactone or triamterene) or angiotensin-
converting enzyme (ACE) inhibitors (e.g., captopril).

8. Monitor patients on digitalis, because hypokalemia potentiates

the effects. Signs of increased digitalis effect include multifocal or
bigeminal PVCs, paroxysmal atrial tachycardia with
atrioventricular block, and other heart blocks.

Electrolyte Management: Hypokalemia; Medication

Administration; Dysrhythmia Management.

Ineffective breathing pattern 

related to respiratory muscle weakness associated with severe hypokalemia
Goals/Outcomes: Within 2 hours of treatment, the patient has an
effective breathing pattern, as evidenced by normal respiratory
depth and pattern and rate of 12 to 20 breaths/min.
Respiratory Status: Ventilation; Vital Signs.

Respiratory monitoring

1. If the patient has worsening hypokalemia, if respirations become

rapid and shallow, notify the advanced practice provider. Severe
hypokalemia causes respiratory muscle weakness. Shallow
respirations, apnea, and respiratory arrest may occur.

2. Keep manual resuscitator (Ambu bag) at the patient’s bedside

when severe hypokalemia is present. Reposition the patient every 2
hours to prevent stasis of secretions; suction airway as needed.

3. Encourage deep breathing (and coughing if indicated) every 2

hours.

Ventilation Assistance.

Hyperkalemia (serum potassium level

152
greater than 5 mEq/L)
Pathophysiology
Hyperkalemia results from increased intake of potassium,
decreased urinary excretion of K+, or sudden movement of K+ out of
cells. The rate of change in serum K+ is as important as the level.
Rapid increases do not allow time to compensate. Hyperkalemia is
often associated with acidosis.

Changes in serum potassium levels reflect changes in

extracellular fluid potassium—not necessarily changes in total
body levels of potassium.

Hyperkalemia assessment
Goal of assessment
Evaluate for the risk factors and signs and symptoms of
hyperkalemia. Information should be used immediately to manage
potentially life-threatening dysrhythmias. Hyperkalemia is often
associated with acidosis.

History and risk factors

• Inappropriately high intake of potassium: IV potassium delivery,
aggressive red blood cell administration, and symptomatic
hyperkalemia may develop when doses of IV potassium are
administered too rapidly.

• Decreased excretion of potassium: Renal disease both acute and

chronic, potassium-sparing diuretics and ACE inhibitors, and
Addison disease (hypoaldosteronism).

• Movement of potassium out of the cells: Acidosis, insulin

deficiency particularly in patients on dialysis, and tissue

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 catabolism (e.g., fever, sepsis, trauma, surgery).

Observation
• Irritability.

• Abdominal distention.

• Diarrhea.

• Ascending weakness.

• Parethesias.

Vital signs
• Irregular pulse.

• Cardiac arrest at levels greater than 8.5 mEq/L.

• Hypotension.

Screening
• 12-Lead ECG: Tall, thin T waves, prolonged PR interval, ST
depression, widened QRS complex with progression to cardiac
arrest, loss of P wave; eventually, QRS widens further and
cardiac arrest occurs.

Diagnostic Tests for Hyperkalemia

Test Purpose Abnormal Findings

Serum Evaluate potassium Elevated: Greater than 5 mEq/L.
potassium level
Arterial blood Evaluate acid-base Decreased pH and bicarbonate. Hyperkalemia associated
gases status with acidosis.

Pseudohyperkalemia may occur with mechanical trauma

during venipuncture or incorrect handling of the laboratory

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specimen. If red blood cells hemolyze (are injured), potassium is
released from damaged cells while or after specimen has been
drawn.

Collaborative management
Care priorities

1. Administer calcium gluconate to decrease myocardial

irritability for severe hyperkalemia
IV calcium gluconate is given to counteract the neuromuscular and
cardiac effects of hyperkalemia. Serum K+ may remain elevated.

2. Administer insulin and IV glucose and bicarbonate to

move potassium into the cell for severe hyperkalemia
This strategy provides a temporary reduction in serum potassium.
Sodium bicarbonate shifts K+ into the cells.

3. Administer beta2-adrenergic agonists (albuterol) to shift

K+ back into the cells
This provides a temporary reduction in K+ level.

4. Take precautions when drawing blood to prevent

hemolysis.
Damaged cells release intracellular contents into the blood sample,
which elevates the K+ level of the sample. Most laboratories can
provide information about whether the sample was hemolyzed.

5. Administer cation exchange resin orally or rectally

Cation exchange resin (e.g., Kayexalate) is given orally, or as a
retention enema to exchange sodium for potassium in the gut. The
oral form is combined with sorbitol to promote rapid transit
through the gut and to induce diarrhea. Recommended rectal dose
is 30 to 60 g every 6 hours.

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6. Provide hemodialysis to lower K+ level if rapid removal
for K+ is needed

7. Monitor for signs of hypokalemia

Hypokalemia may result from aggressive management of
hyperkalemia.

The effects of calcium, glucose and insulin, sodium

bicarbonate, and beta2-adrenergic agonists are temporary, lasting
only a few hours. These medications should be followed by therapy
to remove potassium from the body (i.e., hemodialysis or
administration of cation exchange resins).

Care plans for hyperkalemia

Decreased cardiac output 
related to dysrhythmias induced by hyperkalemia
Goals/Outcomes: Within 6 hours after initiation of treatment, the
patient’s CO is adequate, as evidenced by PAP 20 to 30/8 to 15 mm
Hg, CVP ≤6 mm Hg, CO 4 to 7 L/min, HR ≤100 bpm, BP within the
patient’s normal range, and absence of the clinical signs of heart
failure or pulmonary edema (e.g., crackles, SOB). ECG shows
normal sinus rhythm without ectopy or other electrical
disturbances. Serum K+ levels normalize.
Cardiac Pump Effectiveness, Circulation Status.

Fluid/electrolyte management

1. Monitor I&O: Consult the advanced practice provider for urine

output less than 0.5 mL/kg/h. Oliguria increases the risk for
development of hyperkalemia.

2. Monitor for signs of hyperkalemia: Irritability, anxiety,

abdominal cramping, diarrhea, ascending weakness, paresthesias,

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and irregular pulse. Assess for hidden sources of potassium:
medications (e.g., potassium penicillin G), banked blood, salt
substitute, GI bleeding, or catabolic conditions (i.e., infection or
trauma).

3. Monitor for signs of hypokalemia after treatment: Muscle

weakness, cramps, nausea, vomiting, decreased bowel sounds,
paresthesias, and weak and irregular pulse.

4. Monitor serum potassium levels, especially in high-risk patients

(i.e., those with renal failure): Monitor other laboratory values
associated with conditions that alter potassium levels (e.g., BUN,
creatinine, ABGs, glucose). Consult the advanced practice provider
for abnormal values.

5. Monitor ECG for signs of hypokalemia (i.e., ST segment

depression, flattened T waves, presence of U wave, ventricular
dysrhythmias) or continuing hyperkalemia (i.e., tall, thin T waves,
prolonged PR interval, ST depression, widened QRS complex, loss
of P wave): Report changes to the advanced practice provider as
soon as possible.

6. Administer insulin and glucose in the order prescribed.

7. Administer calcium gluconate as prescribed: Use caution in

patients receiving digitalis. Monitor for digitalis toxicity. Do not
add calcium gluconate to solutions containing sodium bicarbonate,
because precipitates may form. For more information about calcium
administration, see Hypocalcemia.

8. If administering cation exchange resins by enema, encourage the

patient to retain the solution for at least 30 to 60 minutes to ensure
therapeutic effects: Administer Kayexalate (without sorbitol) via a
Foley catheter inserted into the rectum. The balloon is filled with
sterile water to keep the catheter in place, and the catheter is
clamped. Cleansing enemas may be done before administering
Kayexalate to enhance absorption, and after to reduce the risk of
bowel complications.

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 Electrolyte Management: Hyperkalemia; Dysrhythmia
Management; Hemodialysis Therapy.

Calcium imbalance (normal serum Ca2+ level:

8.5 to 10.5 mg/dL, ionized 4.5 to 5.5 mg/dL)
Calcium, one of the body’s most abundant ions, combines with
phosphorus to form the mineral salts of the bones and teeth.
Calcium exerts a sedative effect on nerve cells and has important
intracellular functions, including development of the cardiac action
potential and contraction of muscles. Only 1% of the body’s calcium
is contained within the ECF, yet this concentration is regulated
carefully by the hormones parathyroid hormone (PTH) and
calcitonin.
Slightly less than half of the calcium in the plasma is free or
ionized calcium. The percentage of ionized calcium is affected by
plasma pH and the albumin level. Approximately 40% of calcium is
bound to protein, primarily albumin. Calcium bound to albumin is
not ionized and cannot be used. Albumin releases calcium to the
ionized state when needed. Only the ionized calcium exerts
physiologic effects and combines with nonprotein anions such as
phosphate, citrate, and carbonate. Patients with alkalosis may show
signs of hypocalcemia because of increased calcium binding.
Changes in the plasma albumin level will affect the total serum
calcium level without changing the level of ionized calcium.

To determine the “true calcium level” or calcium correction

factor: For every gram of albumin less than 4, add 0.8 to the serum
calcium value.

PTH is released by the parathyroid gland in response to low

serum Ca2+ levels to increase movement of Ca2+ and phosphorus out
of the bone (resorption of bone); to activate vitamin D (increases the
absorption of calcium from the GI tract); and to stimulate the
kidneys to conserve calcium and excrete phosphorus. Calcitonin is

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produced by the thyroid gland when serum Ca2+ increases to inhibit
bone resorption.
Calcium regulates skeletal and cardiac muscle contractions, is
part of the clotting cascade, and has other essential functions. It is
imperative to maintain the Ca2+ balance.

Hypocalcemia (serum calcium less than 8.5

mg/dL, ionized less than 4.5 mg/dL)
Pathophysiology
Symptoms of hypocalcemia result from decreased total body
calcium or a decreased percentage of ionized calcium. Low total
calcium levels may be caused by increased calcium loss, reduced
intake secondary to altered intestinal absorption, altered regulation
(i.e., hypoparathyroidism), and aggressive infusion of citrated
blood or CRRT if citrate is used for anticoagulation. Elevated
phosphorus levels and decreased magnesium levels may precipitate
hypocalcemia.

Hypocalcemia assessment
Goal of assessment
Evaluate the signs and symptoms of hypocalcemia.

History and risk factors

• Decreased ionized calcium.

• Alkalosis.

• Rapid administration of citrated blood. Citrate

added to the blood to prevent clotting may bind
with calcium, causing hypocalcemia.

• Hemodilution (e.g., occurring with volume

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 replacement with normal saline after massive
hemorrhage).
• Increased calcium loss in body fluids.

• Large volume diuresis from loop diuretics.

• Decreased intestinal absorption: Decreased intake, impaired

vitamin D metabolism, chronic diarrhea, and postoperatively
following a gastrectomy.

• Other causes: Acute and chronic renal failure,

hypoparathyroidism, hyperphosphatemia, hypomagnesemia,
acute pancreatitis, chemotherapy, and treatment with
bisphosphonates.

Observation
• Numbness with tingling of fingers and circumoral region.

• Tetany.

• Convulsions.

• Alteration in mental status (anxiety, depression, frank psychosis).

Vital signs
• Hypotension secondary to vasodilation.

• Heart failure secondary to decreased myocardial contractility.

Percussion
• Positive Trousseau sign: Ischemia-induced carpopedal spasms.
Elicited by applying a BP cuff to the upper arm and inflating it
past systolic BP for 2 minutes.

• Positive Chvostek sign: Unilateral contraction of facial and eyelid

160
 muscles. Elicited by stimulating the facial nerve during
percussion of the face just in front of the ear.

Screening
• 12-Lead ECG: Prolonged QT interval caused by elongation and
elevation of ST segment.

Diagnostic Tests for Hypocalcemia

Test Purpose Abnormal Findings

Total serum Evaluate total Decreased: Less than 8.5 mg/dL. Evaluate with serum
calcium calcium level albumin. For every 1 g/dL drop in the serum albumin level
level there is a 0.8 to 1 mg/dL drop in the total calcium level.
Ionized Evaluate the free Decreased: Less than 4.5 mg/dL.
calcium calcium level
level
ParathyroidEvaluate for Hypoparathyroidism: Less than 150 pg/mL.
hormone hyperparathyroidism Hyperparathyroidism: Greater than 70 pg/mL.
level or Varies among laboratories.
hypoparathyroidism
Magnesium Evaluate for Decreased: Less than 1.5 mEq/L.
level hypomagnesemia
Phosphorus Evaluate for Increased: More than 4.5 mg/dL.
level hyperphosphatemia

Collaborative management
Care priorities

1. Administer IV calcium by continuous infusion over 4 to 6

hours
May give PO or IV calcium. Tetany is treated with 10 to 20 mL of
10% calcium gluconate administered IV or by continuous infusion
of 100 mL of 10% calcium gluconate diluted in 1000 mL D5W over at
least 4 to 6 hours.

2. Administer vitamin D therapy

Provide additional vitamin D (e.g., dihydrotachysterol, calcitriol) to
increase vitamin D absorption from the GI tract. Use of oral vitamin
D3 (activated vitamin D, available over the counter) is helpful to

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maintain calcium levels over time.

3. Administer magnesium replacement

Used for magnesium depletion; hypomagnesemia-induced
hypocalcemia is often refractory to calcium therapy alone.

4. Administer phosphate binders if needed

Used to reduce elevated phosphorous before treating hypocalcemia.
Used primarily in renal failure.

5. Monitor for signs of hypercalcemia during calcium

replacement therapy
Lethargy, weakness, anorexia, nausea, vomiting, constipation,
itching, polyuria, confusion, personality changes, stupor, and coma.

Care plans for hypocalcemia

Ineffective protection 
related to the potential complications of hypocalcemia
Goals/Outcomes: The patient is not permanently harmed by
severe hypocalcemia.
Electrolyte and Acid-Base Balance; Nutritional Status: Food
and Fluid Intake; Kidney Function; Fluid Balance.

Electrolyte management: Hypocalcemia

1. Monitor the patient for worsening hypocalcemia and consult the

advanced practice provider promptly for symptoms that occur
before overt tetany: Numbness and tingling of fingers and
circumoral region, hyperactive reflexes, and muscle cramps.
Positive Trousseau or Chvostek sign also signals latent tetany.
Monitor total and ionized calcium levels as available.

HIGH ALERT!
Administer intravenous (IV) calcium slowly. Undiluted IV 10%
calcium should not be given faster than 0.5 to 1 mL/min. Diluted

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calcium given in an infusion is preferred. Rapid administration can
cause hypotension. Observe IV insertion site for infiltration; calcium
will slough tissue. Concentrated calcium solutions (calcium chloride)
should be administered through a central line. Do not add calcium to
solutions containing sodium bicarbonate or sodium phosphate to
avoid dangerous precipitates. Digitalis toxicity may develop,
because calcium potentiates digitalis. Monitor for hypercalcemia:
lethargy, confusion, irritability, nausea, and vomiting.

Always clarify the type of intravenous (IV) calcium to be

given. Both calcium chloride and calcium gluconate come in 10-mL
ampules. One ampule of calcium chloride contains 13.6 mEq of
calcium, whereas one ampule of calcium gluconate contains 4.5
mEq of calcium.

2. For patients with chronic hypocalcemia, administer oral calcium

supplements and vitamin D preparations as prescribed. Administer
oral calcium 30 minutes before meals or at bedtime for maximal
absorption. Administer phosphorus-binding antacids with meals. If
calcium carbonate is being administered primarily to bind
phosphorus, administer with food.

3. Consult the advanced practice provider if response to calcium

therapy is ineffective. Tetany that does not respond to IV calcium
may be caused by hypomagnesemia.

4. Maintain seizure precautions for affected patients.

5. Avoid hyperventilation if hypocalcemia is suspected. Respiratory

alkalosis may cause tetany if pH increases when ionized calcium is
low.

6. Monitor for calcium loss (e.g., with loop diuretics, renal tubular

163
dysfunction) or conditions that place the patient at risk for it (e.g.,
acute pancreatitis).

7. Inform the patient and significant others that the

neuropsychiatric symptoms of hypocalcemia will improve with
treatment.

Neurologic Monitoring; Seizure Precautions; Medication

Administration.

Decreased cardiac output 

related to abnormal action of calcium in myocardial contractile tissues
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient’s CO is improving, as evidenced by readings approaching
normal baseline or PAP 20 to 30/8 to 15 mm Hg, CVP less than 6
mm Hg, CO 4 to 7 L/min, HR 100 bpm, BP within the patient’s
normal range, and diminishing clinical signs of heart failure or
pulmonary edema (e.g., crackles, SOB). ECG shows a sinus rhythm
without ectopy or other electrical disturbances.
Cardiac Pump Effectiveness.

Cardiac care: Acute hemodynamic regulation

1. Monitor ECG for signs of worsening hypocalcemia (e.g.,

prolonged QT interval) or of digitalis toxicity with calcium
replacement: multifocal or bigeminal PVCs, paroxysmal atrial
tachycardia with AV block, and other heart blocks.

2. Hypocalcemia may decrease cardiac contractility. Monitor patient

for signs of heart failure or pulmonary edema: crackles, rhonchi,
SOB, decreased BP, increased HR, increased PAP, or increased
CVP.

Dysrhythmia Management; Cardiac Care.

Ineffective breathing pattern 

related to abnormal rigidity of upper airway and respiratory muscles
Goals/Outcomes: Within 1 hour of initiation of treatment, the
patient is regaining an effective breathing pattern, as evidenced by

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more comfortable work of breathing with RR 12 to 20 breaths/min
and absence of the indicators of laryngeal spasm: laryngeal stridor,
dyspnea, or crowing.
Respiratory Status: Ventilation; Respiratory Status: Airway
Patency.

Respiratory monitoring

1. Assess the patient’s respiratory rate, character, and rhythm. Be

alert to laryngeal stridor, dyspnea, and crowing, which occur with
laryngeal spasm, a life-threatening complication of hypocalcemia.

2. Keep an emergency tracheostomy tray at the bedside of all

patients with symptoms of hypocalcemia.

Airway Management; Ventilation Assistance.

Hypercalcemia (serum calcium level greater

than 10.5 mEq/L, ionized greater than 5.5
mg/dL)
Pathophysiology
Hypercalcemia is caused by increased total serum calcium or
increased percentage of free, ionized calcium. If hypercalcemia is
accompanied by a normal or elevated serum phosphorus level,
calcium phosphate crystals may precipitate in the serum and
deposit throughout the body. Soft tissue calcifications usually occur
when the product of the serum calcium and serum phosphorus (i.e.,
calcium level × phosphorus level) exceeds 70 mg/dL.

Hypercalcemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for hypercalcemia.

History and risk factors

165
• Hyperparathyroidism: May be stress-related in critical illness.

• Lymphoproliferative disorders: Which prompt parathyroid

protein production.

• Increased intake of calcium: Excessive administration during

cardiopulmonary arrest; milk-alkali syndrome.

• Increased intestinal absorption: Vitamin D overdose or

hyperparathyroidism. Increased release of calcium from bone:
hyperparathyroidism, malignancies, prolonged immobilization;
Paget disease.

• Decreased urinary excretion: Renal failure, thiazide diuretics, and

hyperparathyroidism.

• Increased ionized calcium: Acidosis.

Observation
• Symptoms absent unless serum calcium is greater than 11 mg/dL.

• Behavioral changes: Personality changes and depression.

• Neurologic changes: Lethargy, weakness, confusion, paresthesias,

stupor, and coma.

• GI/digestive changes: Anorexia, nausea, vomiting, and

constipation.

• Other: Polyuria, itching, and bone pain.

Vital signs
• Hypertension.

• Heart block.

• Cardiac arrest.

166
12-Lead ECG
• Shortening ST segment and QT interval.

• PR interval is sometimes prolonged.

• Ventricular dysrhythmias.

Diagnostic Tests for Hypercalcemia

Test Purpose Abnormal Findings

Total serum Evaluate total calcium level; calcium Elevated: More than 10.5 mg/dL.
calcium is bound to albumin; if albumin is Evaluate with serum albumin level
low, calcium is low. to avoid false lows.
Ionized calcium Evaluate free calcium level. Elevated: More than 5.5 mg/dL.
Parathyroid Assess for hyperparathyroidism or Elevated: More than 70 pg/mL.
hormone hypoparathyroidism.
Radiographs Evaluate for bone changes or urinary Osteoporosis, bone cavitations, or
(bone scan, calculi. urinary calculi.
DEXA scan,
KUB)
DEXA, Dual energy x-ray absorptiometry; KUB, kidney, ureter, and bladder.

Collaborative management
Care priorities

1. Administer loop diuretics and isotonic saline

Administered rapidly to increase urinary calcium excretion.
Concomitant administration of furosemide prevents the
development of fluid volume excess and further increases urinary
calcium excretion.

2. Discontinue vitamin supplements and thiazide diuretics

If the patient has been taking vitamin supplements and thiazide
diuretics, then discontinue them.

3. Treat the underlying cause

May include antitumor chemotherapy for malignancy, partial

167
parathyroidectomy for hyperparathyroidism, discontinuation of
calcium supplements, vitamins A and D, and thiazide diuretics.

4. Facilitate rebuilding of bone

• Increase activity level: Weight-bearing stimulates bone

deposition; increased activity decreases bone resorption.

• Administer bisphosphonates (etidronate and pamidronate): Act

directly on bone to reduce decalcification; used primarily to treat
hypercalcemia associated with neoplastic disease. May take
several days to work but the effects last for days to weeks.

• Mithramycin: Is a cytotoxic antibiotic that decreases bone

resorption.

• Calcitonin: Reduces bone resorption and increases bone

deposition of calcium and phosphorus; increases urinary calcium
and phosphate excretion.

• Gallium nitrate: Inhibits osteoclasts and increased bone calcium.

Used in the treatment of malignancy-induced hypercalcemia.

5. Reduce calcium intake and intestinal absorption

Administer steroids to compete with vitamin D, thereby reducing
intestinal absorption of calcium.

6. Monitor for signs of hypocalcemia

May result from hypercalcemia therapies.

Care plans for hypercalcemia

Ineffective protection 
related to the inability to guard self from internal and external threats
attributable to acute confusion.
Goals/Outcomes: Within 24 to 48 hours of initiating treatment,
the patient more consistently verbalizes orientation to time, place,
and person. The patient does not exhibit evidence of injury caused

168
by neurosensory changes.
Cognitive Orientation; Distorted Thought Self-Control;
Neurologic Status.

Neurologic monitoring

1. Monitor the patient for worsening hypercalcemia: disorientation

to time, place, and person; and deterioration in neurologic status.

2. Note personality changes, hallucinations, paranoia, and memory

loss. Inform the patient and significant others that altered
sensorium is temporary and will improve with treatment. Use
reality therapy: clocks, calendars, and familiar objects; keep them at
the bedside within the patient’s visual field.

Electrolyte monitoring: Hypercalcemia

1. Administer fluids and diuretics as prescribed. Evaluate response

to therapy. Monitor serum calcium levels and albumin levels.
Observe for signs of fluid volume excess that develop with
treatment.

2. Hypercalcemia causes neuromuscular depression with poor

coordination, weakness, and altered gait. Provide a safe
environment. Keep side rails up and bed in lowest position with
wheels locked. Assist with ambulation.

3. Monitor for signs of digitalis toxicity (hypercalcemia potentiates

digitalis): multifocal or bigeminal PVCs, paroxysmal atrial
tachycardia with AV block, and other heart blocks.

4. Monitor serum electrolytes: calcium, potassium, and phosphorus

(normal range is 2.5 to 4.5 mg/dL). Note changes that result from
therapy. Consult the advanced practice provider for abnormal
values.

5. Encourage increased mobility to reduce bone resorption. Ideally,

the patient should be out of bed and up in a chair for at least 6
hours a day.

169
 Fluid Monitoring; Dysrhythmia Management; Fluid
Management.

Impaired urinary elimination 

related to hypercalcemia decreasing the ability of the kidneys to
concentrate urine, which can lead to polyuria and possible fluid volume
deficit. Hypercalcemia can impair renal function.
Goals/Outcomes: Within 24 hours of initiation of treatment, the
patient exhibits a voiding pattern and urine characteristics that are
moving toward normal for the patient.
Urinary Elimination.

Fluid management

1. Monitor I&O hourly. Consult the advanced practice provider for

unusual changes in urine volume (e.g., oliguria alternating with
polyuria, which may signal urinary tract obstruction, or continuous
polyuria). This is a type of nephrogenic diabetes insipidus (see
Diabetes Insipidus, Chapter 8). Monitor for signs of volume
depletion when giving diuretics: decreased BP, CVP, PAP, and
increased HR.

2. Monitor the patient’s renal function carefully: urine output, BUN,

and creatinine values (see Acute Renal Failure/Acute Kidney Injury,
Chapter 6).

3. Provide the patient with a low-calcium diet and avoid use of

calcium-containing medications (e.g., antacids such as Tums).
Encourage intake of fruits (e.g., cranberries, prunes, plums) that
leave an acid ash in the urine. Acidic urine reduces the risk of
calcium stone formation. Also increase fluid intake (at least 3 L in
nonrestricted patients) to reduce the risk of renal stone formation.

4. Assess the patient for indicators of kidney stone formation:

intermittent pain, nausea, vomiting, and hematuria.

Fluid Monitoring; Urinary Elimination Management;

Electrolyte Management: Hypercalcemia.

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Phosphorus imbalance (normal serum level
2.5 to 4.5 mg/dL or 1.7 to 2.6 mEq/L)
Phosphorus, the primary anion (− or negative ion) of the ICF, has a
wide variety of vital functions: formation of energy-storing
substances (e.g., ATP); formation of red blood cell 2,3-
diphosphoglycerate (2,3-DPG) (facilitates the release of O2 from the
Hgb to be used by the cells); metabolism of carbohydrates, protein,
and fat; and maintenance of acid-base balance. In addition,
phosphorus is critical to normal nerve and muscle function and
provides structural support to bones and teeth.
Plasma phosphorus levels vary with diet and acid-base balance.
Glucose, insulin, or sugar-containing foods cause a temporary drop
in phosphorus because of a shift of serum phosphorus into the cells.
Phosphorous and calcium have an interdependent effect on each
other and share many of the common causes of abnormalities.
Alkalosis, particularly respiratory alkalosis, may cause
hypophosphatemia as a result of an intracellular shift of
phosphorus. Although the exact mechanism for this shift is not
fully understood, it may be related to an alkalosis-induced cellular
glycolysis, with increased formation of phosphorus-containing
metabolic intermediates. Respiratory acidosis may cause a shift of
phosphorus out of the cells and contribute to hyperphosphatemia.
Although the level of ECF phosphate is affected by a combination
of factors, including dietary intake, intestinal absorption, and
hormonally regulated bone resorption and deposition, phosphorus
balance depends largely on renal excretion.

Hypophosphatemia (serum phosphate level

less than 2.5 mg/dL or less than 1.7 mEq/L)
Pathophysiology
Hypophosphatemia (serum phosphorus less than 2.5 mg/dL) may
occur because of transient intracellular shifts, increased urinary
losses (most common), decreased intestinal absorption, or increased
use (see History and Risk Factors that follow). Severe phosphorus
deficiency may also develop because of a combination of factors in

171
conditions such as chronic alcohol abuse and DKA.

Hypophosphatemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for
hypophosphatemia. Acute, severe hypophosphatemia can be a life-
threatening condition. Symptoms can be so profound that care
providers focus on extensive workups while sometimes
overlooking the hypophosphatemia.

History and risk factors

• Intracellular shifts: Carbohydrate load, respiratory alkalosis, and
treatment of DKA.

• Increased use because of increased tissue repair: TPN with

inadequate phosphorus content; recovery from protein-calorie
malnutrition. Hypophosphatemia is common in the critical care
patient largely because of nutritional deficiency.

• Increased urinary losses: Hypomagnesemia, ECF volume

expansion, hyperparathyroidism, use of thiazide diuretics,
diuretic phase of ATN, and glucosuria.

• Reduced intestinal absorption or increased intestinal loss: Use of

phosphorus-binding medications; vomiting and diarrhea;
malabsorption disorders such as vitamin D deficiency; and
prolonged gastric suction.

• Other conditions: Chronic alcohol abuse, DKA, severe burns, and

sepsis.

• Resulting from interventions: Postoperative patients, patients on

mechanical ventilation, and postoperative renal transplant
patients.

Observation

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Symptoms may be caused by sudden decreases in serum
phosphorus, or they may develop gradually because of chronic
deficiency. The majority of symptoms are secondary to decreases in
ATP and 2,3-DPG; therefore, the patient will become acutely
hypoxic at the cellular level, producing a high lactate and metabolic
acid load, resulting in poor coordination, confusion, seizures, and
coma. Other acute symptoms include:

• Chest pain as a result of poor oxygenation of the myocardium.

• Muscle pain and weakness.

• Increased susceptibility to infection.

• Numbness and tingling of the fingers.

• Numbness of the circumoral region.

• Respiratory alkalosis from hyperventilation.

• Difficulty speaking as a result of decreased strength.

• Bruising and bleeding because of platelet dysfunction.

• Rhabdomyolysis, hemolysis.

Chronic symptoms include memory loss, lethargy, weakness,

bone pain, joint stiffness, arthralgia, cyanosis, osteomalacia, and
possible pseudofractures.

Vital signs
• Decreased respiratory rate.

• Increased PAWP.

• Decreased CO.

• Decreased BP with decreased response to pressor agents.

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 Respiratory alkalosis causes phosphorus to move
intracellularly, aggravating the existing hypophosphatemia.

Diagnostic Tests for Hypophosphatemia

Test Purpose Abnormal Findings

Serum Determine the severity of Decreased: Less than 2.5 mg/dL (1.7 mEq/L).
phosphate hypophosphatemia Mild: 1 to 2.5 mg/dL.
level Severe: Less than 1 mg/dL.
Parathyroid Evaluate for Elevated: In hyperparathyroidism, to greater than 70
hormone hyperparathyroidism pg/mL.
Serum Evaluate loss of Decreased because of increased urinary excretion of
magnesium magnesium magnesium in hypophosphatemia.
Skeletal Evaluate bone changes Skeletal changes of osteomalacia.
radiographs

Collaborative management
Care priorities

1. Discontinue use of phosphate binders

Phosphate binders include aluminum, magnesium, or calcium gels
of antacids.

2. Correct respiratory alkalosis if present

See Acid-Base Balance.

3. Increase phosphorus intake

Mild hypophosphatemia may respond to increased intake of foods
high in phosphorus, such as milk (Box 1-9).

Box 1-9
FOODS HIGH IN PHOSPHORUS

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Dried beans and peas

Eggs and egg products (e.g., eggnog, soufflés)

Fish

Meats, especially organ meats (e.g., brain, liver, kidney)

Milk and milk products (e.g., cheese, ice cream, cottage cheese)

Nuts (e.g., Brazil nuts, peanuts)

Poultry

Seeds (e.g., pumpkin, sesame, sunflower)

Whole grains (e.g., oatmeal, bran, barley)

4. Administer oral phosphate supplements

Moderate hypophosphatemia is treated with phosphate
supplements including Neutra-Phos (sodium and potassium
phosphate) or Phospho-Soda (sodium phosphate).

5. Administer IV sodium phosphate or potassium phosphate

Severe hypophosphatemia is treated with sodium phosphate or
potassium phosphate. IV infusions are also used for patients with a
nonfunctional GI tract.

6. Monitor for resolution or progression of neurologic and

hematologic signs and symptoms

Care plans for hypophosphatemia

Ineffective protection 
related to inability to guard self from internal and external threats
attributable to impaired decision-making resulting from acute confusion

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 Goals/Outcomes: Within 24 hours of initiation of treatment the
patient exhibits improvement of acute confusion and normalization
of associated electrolyte imbalances.
Cognitive Orientation; Distorted Thought Self-Control;
Neurologic Status.

Neurologic monitoring

1. Monitor the patient for worsening hypophosphatemia:

disorientation to time, place, and person; and deterioration in
neurologic status.

2. Note personality changes, hallucinations, paranoia, and memory

loss. Inform the patient and significant others that altered
sensorium is temporary and will improve with treatment.

3. Apprehension, confusion, and paresthesias are signals of

developing hypophosphatemia. Assess and document LOC,
orientation, and neurologic status with each vital sign check.
Reorient the patient as necessary. Alert the advanced practice
provider to significant changes.

4. Inform the patient and significant others that altered sensorium is

temporary and will improve with treatment.

5. Keep the side rails up and the bed in its lowest position with
wheels locked.

6. Use reality therapy: clocks, calendars, and familiar objects. Keep

these articles at the bedside within the patient’s visual field.

7. If the patient is at risk for seizures, pad the side rails and keep an
appropriate-size airway at the bedside.

Electrolyte management: Hypophosphatemia

1. Monitor serum phosphorus levels in patients at increased risk.

Consult the advanced practice provider for decreased levels.
Monitor for signs of associated electrolyte and acid-base
imbalances: hypokalemia, hypomagnesemia, respiratory alkalosis,

176
and metabolic acidosis.

2. When IV phosphorus is administered as potassium phosphate,

the infusion rate should not exceed 10 mEq/h. Monitor IV site for
signs of infiltration, because potassium phosphate can cause
necrosis and sloughing of tissue.

HIGH ALERT!
Do not administer intravenous (IV) phosphate at a rate greater than that
recommended by the manufacturer. Potential complications of IV
phosphorus administration include tetany as a result of
hypocalcemia (serum calcium levels may drop suddenly if serum
phosphorus levels increase suddenly; see Hypocalcemia, for
additional information); soft tissue calcification (if
hyperphosphatemia develops, the calcium and phosphorus in the
extracellular fluid compartment may combine and form deposits in
tissue); and hypotension, caused by a too-rapid delivery.

3. Encourage intake of foods high in phosphorus (see Box 1-9).

Teach the patient and significant others the importance of using
phosphorus-binding antacids only as prescribed.

Medication Administration.

Impaired gas exchange 

related to respiratory muscle weakness, coupled with the inability of red
blood cells to off-load O2 at the cellular level resulting from decreased 2,3-
dpg levels
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient has increasingly normal gas exchange, as evidenced by RR
12 to 20 breaths/min with normal depth and pattern; orientation to
time, place, and person; SpO2 at least 92%; and absence of the
indicators of hypoxia (e.g., restlessness, somnolence).
Respiratory Status: Gas Exchange.

177
 With decreased 2,3-diphosphoglycerate levels, the
oxyhemoglobin dissociation curve will shift to the left. At a given
PaO2 level, more O2 will be bound to hemoglobin and less will be
available to the tissues.

Respiratory monitoring

1. Assess the patient for signs of hypoxia: restlessness, confusion,

increased respirations, complaints of chest pain, and cyanosis (a late
sign).

2. Monitor SpO2 as available. Administer O2 as prescribed to

maintain SpO2 at ≥92%.

3. Monitor rate and depth of respirations in patients with severe

hypophosphatemia. Assess for decreased tidal volume or decreased
minute ventilation. Consult the advanced practice provider for
changes.

4. Monitor ABG values for evidence of hypoxemia or hypercapnia.

Consult the advanced practice provider for significant changes.

5. Monitor serum phosphate levels in patients who are

mechanically ventilated; they exhibit a high incidence of
hypophosphatemia. Hypophosphatemia may contribute to
difficulty in weaning patients from ventilators.

Oxygen Therapy. Impaired physical mobility related to

muscle weakness resulting from hypophosphatemia
Goals/Outcomes: Within 24 hours of initiation of therapy, the
patient is able to move purposefully and has full or baseline ROM
and muscle strength.
Mobility; Transfer Performance.

Exercise promotion: Strength training

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1. Monitor all patients with suspected hypophosphatemia for
decreasing muscle strength. Perform serial assessments of hand
grasp strength and clarity of speech. Consult the advanced practice
provider for changes.

2. Monitor serum phosphorus levels if mobility or strength

decreases. Consult the advanced practice provider for changes.

3. Assist the patient with ambulation and activities of daily living

(ADLs).

4. Medicate for pain as prescribed.

Energy Management; Pain Management.

Decreased cardiac output 

related to cardiac muscle weakness related to hypophosphatemia
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient’s CO is increasingly adequate, as evidenced by CO at least 4
L/min, cardiac index (CI) at least 2.5 L/min/m2, CVP 4 to 6 mm Hg,
PAP 20 to 30 mm Hg systolic, 8 to 15 mm Hg diastolic, HR <100
bpm, BP within the patient’s normal range, and absence of the
clinical signs of heart failure or pulmonary edema.
Cardiac Pump Effectiveness.

Cardiac care

1. Monitor the patient for signs of heart failure or pulmonary

edema: crackles, rhonchi, SOB, decreased BP, increased HR,
increased PAP, or increased CVP.

2. Prevent the patient from hyperventilating. Metabolic alkalosis

causes increased movement of phosphorus into cells, which will
reduce CO.

3. For additional interventions if decreased CO develops, see Heart

Failure.

Cardiac Care: Acute Hemodynamic Regulation; Vital Signs

Monitoring.

179
Ineffective protection 
related to compromised immunity resulting from hypophosphatemia
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia and absence of erythema, swelling, warmth, and
purulent drainage at invasive sites.
Immune Status.

Infection protection

1. Monitor temperature every 4 hours for evidence of infection.

Obtain cultures of wounds and drainage as prescribed if infection is
suspected.

2. Use meticulous aseptic technique when changing dressings or

manipulating indwelling lines (e.g., TPN catheters, IV needles).

3. Provide oral hygiene and skin care at regular intervals. Intact

skin and membranes are the body’s first line of defense against
infection.

Risk Identification.

Hyperphosphatemia (serum phosphate level

greater than 4.5 mg/dL or greater than 2.6
mEq/L)
Pathophysiology
Hyperphosphatemia is common in patients with renal
insufficiency/failure whose kidneys are unable to effectively excrete
excess phosphorus. Other causes of hyperphosphatemia include
increased intake of phosphates, extracellular shifts (i.e., movement
of phosphorus out of the cell and into the ECF), cellular destruction
with concomitant release of intracellular phosphorus, and
decreased urinary losses that are unrelated to decreased renal
function. As serum phosphorus levels increase, serum calcium
levels often decrease, leading to hypocalcemia. Hypocalcemia is
most likely to occur in sudden, severe hyperphosphatemia (e.g.,

180
after IV administration of phosphates) or in patients prone to
hypocalcemia (e.g., those with chronic renal failure).
The primary complication of hyperphosphatemia is metastatic
calcification (i.e., the precipitation of calcium phosphate in the soft
tissue, joints, and arteries). Chronic hyperphosphatemia in the
patient with chronic renal failure may contribute to the
development of renal osteodystrophy.
Precipitation of calcium phosphate occurs when the product of
the serum calcium and serum phosphorus (i.e., calcium ×
phosphorus) exceeds 70 mg/dL.

Hyperphosphatemia assessment
Goal of assessment
Evaluate the signs, symptoms, history, and risk factors for
hyperphosphatemia.

History and risk factors

• Renal failure: Acute and chronic; may signal declining glomerular
filtration rate.

• Increased intake

• Excessive administration of phosphorus

supplements.

• Vitamin D excess with increased GI absorption.

• Excessive use of phosphorus-containing laxatives or

enemas.

• Massive transfusion.

• Extracellular shift: Respiratory acidosis, DKA (before treatment).

181
• Cellular destruction

• Neoplastic disease (e.g., leukemia, lymphoma)

treated with cytotoxic agents.

• Increased tissue catabolism.

• Rhabdomyolysis.
• Decreased urinary losses: Hypoparathyroidism, volume
depletion.

Observation
• GI symptoms: Anorexia, nausea, and vomiting.

• Neuromuscular symptoms: Muscle weakness, hyperreflexia, and

tetany.

Vital signs
• Hypotension secondary to vasodilation.

• Heart failure secondary to decreased myocardial contractility.

• Tachycardia.

Percussion
• Positive Trousseau sign: Ischemia-induced carpopedal spasms.
Elicited by applying a BP cuff to the upper arm and inflating it
past systolic BP for 2 minutes.

• Positive Chvostek sign: Unilateral contraction of facial and eyelid

muscles. Elicited by stimulating the facial nerve during
percussion of the face just in front of the ear.

182
 Usually patients experience few symptoms with
hyperphosphatemia. The majority of symptoms relate to
development of hypocalcemia or soft tissue (metastatic)
calcifications. Indicators of metastatic calcification include
oliguria, corneal haziness, conjunctivitis, irregular heart rate, and
popular eruptions.

Screening
• 12-Lead ECG: Deposition of calcium phosphate in the heart may
lead to dysrhythmias and conduction disturbance; prolonged QT
interval caused by elongation and elevation of ST segment.

Diagnostic Tests for Hyperphosphatemia

Test Purpose Abnormal Findings

Serum phosphate Determine severity of Elevated: Greater than 4.5 mg/dL (2.6
level hyperphosphatemia mEq/L)
Parathyroid Evaluate for hypoparathyroidism Decreased: In hypoparathyroidism
hormone
Skeletal Assess for bony changes May show skeletal changes of
radiographs osteodystrophy

Collaborative management
Care priorities

1. Reduce severely elevated phosphate level

Hemodialysis may be used for acute, severe hyperphosphatemia
accompanied by symptoms of hypocalcemia.

2. Administer phosphate binders

Aluminum, magnesium, or calcium antacids.

3. Monitor for symptoms of hypocalcemia

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Positive Chvostek and/or positive Trousseau sign.

Calcium carbonate and calcium acetate are the preferred

preparations for the patient with chronic renal failure. Magnesium
antacids are avoided in renal failure because of the risk of
hypermagnesemia. Aluminum-containing antacids are
contraindicated because they may lead to aluminum accumulation
and contribute to the development of bone disease.

Care plans for hyperphosphatemia

Deficient knowledge 
related to medications that may induce hyperphosphatemia
Goals/Outcomes: Within the 24-hour period before discharge
from the intensive care unit (ICU), the patient describes the
potential complications of uncontrolled hyperphosphatemia and
preventive measures.
Health Promoting Behavior; Health Promoting Behavior
Medication.

Prevention of long-term complications relies primarily on

adequate patient education, because symptoms of
hyperphosphatemia may be minimal.

Teaching: Prescribed medication

1. Teach patients the purpose of phosphate binders. Stress the need

to take binders as prescribed with or after meals to maximize
effectiveness.

2. Educate patients about possible constipation from phosphate

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binders. Encourage use of bulk-building supplements or stool
softener if constipation occurs. Phosphate-containing laxatives and
enemas must be avoided (i.e., Fleet’s Phospho-Soda products).

3. Phosphate binders are available in liquid, tablet, or capsule form.

Confer with the physician or midlevel practitioner regarding an
alternate form or brand for individuals who find binders
unpalatable or difficult to take. Phosphate binders vary in
aluminum, magnesium, or calcium content. One may not be
exchanged for another without first ensuring that the patient is
receiving the same amount of elemental aluminum, magnesium, or
calcium.

4. Discuss avoiding or limiting foods high in phosphorus (see Box

1-9).

5. Review the importance of avoiding phosphorus-containing over-

the-counter medications: certain laxatives, enemas, and mixed
vitamin-mineral supplements. Instruct the patient and significant
others to read the label for the words “phosphorus” and
“phosphate.”

Teaching: Prescribed Medication; Electrolyte Management:

Hyperphosphatemia.

Ineffective protection 
related to the inability to avoid internal complications associated with
hyperphosphatemia
Goals/Outcomes: The patient does not develop symptoms of
physical injury caused by precipitation of calcium phosphate in the
soft tissue or joints, or by hypocalcemic tetany.
Activity Tolerance; Mobility; Energy Conservation.

Electrolyte management: Hyperphosphatemia

1. Monitor serum phosphorus and calcium levels. Calculate the

calcium-phosphorus product (calcium × phosphorus). Values
greater than 70 mg/dL are associated with precipitation of calcium
phosphate in the soft tissue. Consult the advanced practice provider

185
for abnormal values. Phosphorus values may be kept slightly
higher (4 to 6 mg/dL) to ensure adequate levels of 2,3-DPG in
patients with chronic renal failure, to minimize effects of chronic
anemia on O2 delivery to the tissues.

2. Vitamin D products and calcium supplements (taken between

meals) may be limited until serum phosphorus approaches a
normal level.

3. Consult the advanced practice provider if the patient develops

indicators of metastatic calcification: oliguria, corneal haziness,
conjunctivitis, irregular HR, and papular eruptions.

4. Monitor the patient for symptoms of increasing hypocalcemia

that may precede overt tetany: numbness and tingling of the fingers
and circumoral region, hyperactive reflexes, and muscle cramps.
Positive Trousseau or Chvostek sign may signal latent tetany.
Consult the advanced practice provider promptly if these
symptoms develop (See Hypocalcemia.)

5. Because hyperphosphatemia can impair renal function, monitor

renal function carefully: urine output, BUN, and creatinine values.

Neurologic Monitoring; Energy Management.

Magnesium imbalance (normal serum

magnesium level 1.5 to 2.5 mEq/L)
Approximately 60% of the body’s magnesium is located in the
bone, and approximately 1% is located in the ECF. The remaining
magnesium is contained within cells. Mg2+ is the second most
abundant intracellular cation (+ or positive ion) after potassium.
Magnesium is regulated by a combination of factors, including
vitamin D–regulated GI absorption and renal excretion.
Because magnesium is a major intracellular ion, it plays a vital
role in normal cellular function. Specifically, it activates enzymes
involved in the metabolism of carbohydrates and protein, and it
triggers the sodium-potassium pump, thus affecting intracellular
potassium levels. Magnesium is also important in the transmission

186
of neuromuscular activity, neural transmission within the CNS, and
myocardial functioning.

Hypomagnesemia (serum magnesium level

less than 1.5 mEq/L)
Pathophysiology
Hypomagnesemia usually results from decreased GI absorption,
increased urinary loss, or excessive GI loss (e.g., vomiting,
diarrhea), and with prolonged administration of magnesium-free
parenteral fluids. Chronic alcohol abusers (see History and Risk
Factors that follow) and patients who are critically ill most
commonly experience low magnesium. Hypomagnesemia is
associated with increased mortality in the critical care setting.
Dysrhythmias and sudden death increase when decreased
magnesium levels occur in combination with MI, heart failure, or
digitalis toxicity. Hypomagnesemia is usually associated with
hypocalcemia and hypokalemia (see Hypokalemia and
Hypocalcemia for additional information). Symptoms of
hypomagnesemia tend to develop once the serum magnesium level
drops below 1 mEq/L. Decreased magnesium intake has been
identified as a risk factor for hypertension, cardiac dysrhythmias,
ischemic heart disease, and sudden cardiac death.

Hypomagnesemia assessment
Goal of assessment
Evaluate for the signs, symptoms, and risk factors for
hypomagnesemia and investigate further whether the patient may
also have hypokalemia and/or hypocalcemia.

History and risk factors

• Chronic alcoholism: Poor dietary intake, decreased GI absorption,
and increased urinary excretion.

187
• Decreased GI absorption: Cancer, colitis, pancreatic insufficiency,
surgical resection in the GI tract, use of laxatives, and diarrhea.

• Increased GI losses: From prolonged vomiting or gastric suction.

• Administration of low-magnesium or magnesium-free parenteral

solutions: Especially with refeeding after starvation.

• Poorly controlled diabetes including DKA: A result of movement

of magnesium out of the cell and loss in the urine because of
osmotic diuresis.

• Increased urinary excretion: Use of diuretics, diuretic phase of

ATN.

• Medications: Amphotericin, tobramycin, gentamicin, cisplatin,

cyclosporine, or digoxin.

• Protein-calorie malnutrition.

• Cardiopulmonary bypass.

Observation
• Behavioral changes: Mood changes, lethargy, hallucinations, and
confusion.

• Neuromuscular symptoms: Weakness, fatigue, paresthesias,

tremors, convulsions, and tetany.

• GI symptoms: Anorexia, nausea, and vomiting.

Vital signs
• Hypotension.

• Tachycardia.

• Shallow respirations with respiratory muscle weakness.

188
• Laryngeal stridor.

Percussion
• Increased reflexes.

• Positive Chvostek sign.

• Positive Trousseau sign.

• Skeletal muscle weakness.

Screening
• 12-Lead ECG: PVCs, possible torsades de pointes, prolonged PR
interval, widened QRS complex, prolonged QT interval,
depressed ST segment, flattened T wave, prominent U wave,
atrial fibrillation, paroxysmal atrial tachycardia with variable
block, or other heart blocks related to digitalis effect (in those
taking digitalis derivatives).

Diagnostic Tests for Hypomagnesemia

Test Purpose Abnormal Findings

Serum Evaluate for Decreased: Less than 1.5 mEq/L
magnesium low
level magnesium
Magnesium Identify those Results based on the amount of magnesium retained after an
tolerance with or at infusion of magnesium
test risk
Serum Evaluate the Possibly decreased: Possible failure of the cellular sodium
potassium sodium potassium pump to move potassium into the cell and the
level potassium accompanying loss of potassium in the urine. This hypokalemia
pump may be resistant to replacement until the magnesium deficit has
been corrected
Serum Assess for Possibly decreased: Magnesium deficit may lead to hypocalcemia
calcium hypocalcemia because of a reduction in the release and action of parathyroid
level hormone

Collaborative management
Care priorities

189
1. Increase magnesium level

• Administer IV or intramuscular (IM) magnesium: To manage

severe hypomagnesemia and related symptoms.

• Administer magnesium supplements: Chronic loss is treated with

magnesium oxide or chloride. Magnesium-containing antacids
(e.g., Mylanta, Maalox, Milk of Magnesia, Gelusil) may be used.

• Encourage food high in magnesium: See Box 1-10.

Box 1-10
FOODS HIGH IN MAGNESIUM
Bananas

Chocolate

Coconuts

Grapefruits

Green, leafy vegetables (e.g., beet greens, collard greens)

Kelp

Legumes

Molasses

Nuts and seeds

Oranges

Refined sugar

Seafood

Soy flour

190
Wheat bran

2. Monitor for ECG changes and manage changes with IV

magnesium
Check for hypokalemia and manage hypomagnesemia before
treating hypokalemia.

3. Monitor for hypotension, shallow respirations, and

laryngeal stridor

Care plans for hypomagnesemia

Ineffective protection 
related to the inability to control the internal effects of hypomagnesemia
Goals/Outcomes: Within 8 hours of initiation of treatment, the
patient verbalizes orientation to time, place, and person. The patient
does not exhibit evidence of cardiac or brain injury caused by
complications of severe hypomagnesemia.
Neurologic Status: Consciousness; Neurologic Status.

Electrolyte management: Hypomagnesemia

1. Monitor serum magnesium levels in patients at risk for

hypomagnesemia and its deleterious effects (e.g., those who are
alcohol abusers or experiencing heart failure, cases of recent MI or
digitalis toxicity). Normal range for serum magnesium is 1.5 to 2.5
mEq/L. Consult the physician or midlevel practitioner for abnormal
values.

Symptoms of hypomagnesemia may be mistakenly attributed

to delirium tremens of chronic alcoholism. Be alert to indicators of
magnesium deficit in these patients.

191
2. Administer IV MgSO4 slowly. Refer to the manufacturer’s
guidelines. Too-rapid administration may lead to dangerous
hypermagnesemia, with cardiac or respiratory arrest. Patients
receiving IV magnesium should be monitored for decreasing BP,
labored respirations, and diminished patellar reflex (knee jerk). An
absent patellar reflex signals hyporeflexia (seen with dangerous
hypermagnesemia). Should any of these changes occur, stop the
infusion and consult the physician or midlevel practitioner
immediately (see Hypermagnesemia). Keep calcium gluconate at
the bedside in the event of hypocalcemic tetany or sudden
hypermagnesemia.

3. For patients with chronic hypomagnesemia, administer oral

magnesium supplements as prescribed. All magnesium
supplements should be given with caution in patients with reduced
renal function because of an increased risk of the development of
hypermagnesemia. Caution the patient that oral magnesium
supplements may cause diarrhea. Administer antidiarrheal
medications as needed.

4. When it is appropriate, encourage intake of foods high in

magnesium (see Box 1-10). For most patients, a normal diet is
usually adequate.

5. Maintain seizure precautions for patients with symptoms (i.e.,

those who have hyperreflexia). Decrease environmental stimuli
(e.g., keep the room quiet; use subdued lighting).

6. For patients in whom hypocalcemia is suspected, caution against

hyperventilation. Metabolic alkalosis may precipitate tetany as a
result of increased calcium binding.

7. Dysphagia may occur in hypomagnesemia. Test the patient’s

ability to swallow water before giving food or medications.

8. Assess and document LOC, orientation, and neurologic status

with each vital sign check. Reorient the patient as necessary. Notify

192
the physician or midlevel practitioner for significant changes.
Inform the patient and significant others that altered mood and
sensorium are temporary and will improve with treatment.

9. See Hypokalemia, Hypocalcemia, and Hypophosphatemia for

nursing care of patients with these disorders.

Because magnesium is necessary for the movement of

potassium into the cell, intracellular potassium deficits cannot be
corrected until hypomagnesemia has been treated.

Neurologic Monitoring; Electrolyte Management:

Hypomagnesemia; Electrolyte Management: Hypokalemia;
Electrolyte Management: Hypocalcemia; Seizure Precautions;
Medication Administration.

Decreased cardiac output 

related to abnormal contraction of myocardial tissues resulting in heart
failure
Goals/Outcomes: Within 24 hours of initiating treatment, the
patient’s CO is adequate, as evidenced by CO at least 4 L/min, CI at
least 2.5 L/min/m2, normal configurations on ECG, and HR within
the patient’s normal range. The patient has urinary output of at
least 0.5 mL/kg/h.
Cardiac Pump Effectiveness; Circulation Status.

Cardiac care

1. Monitor HR and regularity with each vital sign check. Consult

the advanced practice provider for changes. Be alert to decreased
CO and CI.

2. Assess ECG for evidence of hypomagnesemia. Consider

hypomagnesemia as a possible cause if the patient develops sudden
ventricular dysrhythmias.

193
3. Because hypomagnesemia (and hypokalemia) potentiate the
cardiac effects of digitalis, monitor for digitalis-induced
dysrhythmias. ECG changes may include multifocal or bigeminal
PVCs, paroxysmal atrial tachycardia with varying AV block, and
other heart blocks.

4. Monitor for and report decreased urinary output and delayed

capillary refill.

Dysrhythmia Management.

Imbalanced nutrition: Less than body requirements 

related to a diet lacking in magnesium or poor overall food intake
Goals/Outcomes: Within 24 hours of resumption of oral feeding,
the patient receives a diet adequate in magnesium.
Knowledge: Diet; Nutritional Status: Nutrient Intake.

Teaching: Prescribed diet

1. Encourage intake of small, frequent meals.

2. Teach the patient about foods high in magnesium content (see

Box 1-10) and encourage intake of these foods during meals.

3. Include the patient, significant others, and the dietitian in meal

planning as appropriate.

4. Provide oral hygiene before meals to enhance appetite.

5. As with the other major intracellular electrolyte levels,

magnesium depletion may develop with refeeding after starvation.
Anticipate hypomagnesemia with refeeding and ensure increased
dietary intake or supplementation.

6. Consult the physician or midlevel practitioner for patients

receiving magnesium-free solutions (e.g., TPN) for prolonged
periods.

Nutritional Monitoring; Nutrition Management; Nutrition

Therapy; Nutritional Counseling.

194
Hypermagnesemia (serum magnesium level
greater than 2.5 mEq/L)
Pathophysiology
Hypermagnesemia occurs almost exclusively in individuals with
renal failure who have an increased intake of magnesium (e.g.,
those who use magnesium-containing medications). It may also
occur in acute cases of adrenocortical insufficiency (Addison
disease) or in obstetric patients treated with parenteral magnesium
for pregnancy-induced hypertension. In rare cases
hypermagnesemia occurs because of excessive use of magnesium-
containing medications (e.g., antacids, laxatives, enemas). The
primary symptoms of hypermagnesemia are the result of depressed
peripheral and central neuromuscular transmission. Symptoms
usually do not occur until the magnesium level exceeds 4 mEq/L.

Hypermagnesemia assessment
Goal of assessment
Evaluate the signs, symptoms, and risk factors for the development
of hypermagnesemia.

History and risk factors

• Decreased magnesium excretion: Renal failure or adrenocortical
insufficiency.

• Increased intake of magnesium: Excessive use of magnesium-

containing antacids, enemas, or laxatives.

• Excessive administration of magnesium sulfate: In the treatment

of hypomagnesemia or pregnancy-induced hypertension.

Observation
• Neurologic/neuromuscular symptoms: Altered mental status,
drowsiness, coma, muscular weakness or paralysis, sensation of

195
 warmth, diaphoresis, flushing, and thirst.

• Paralysis of respiratory muscles: When magnesium level exceeds

10 mEq/L.

• Nausea and vomiting.

Vital signs
• Hypotension.

• Bradycardia.

• Decreased arterial pressure caused by peripheral vasodilation.

Palpation
• Soft tissue calcification (metastatic).

• Decreased deep tendon reflexes.

• Loss of patellar reflex when level exceeds 8 mEq/L.

Screening
• 12-Lead ECG: Prolonged PR interval, prolonged QRS and QT
intervals with levels greater than 5 mEq/L, complete heart block,
cardiac arrest in severe hypermagnesemia.

Diagnostic Tests for Hypermagnesemia

Test Purpose Abnormal Findings

Serum Evaluate severity Elevated: Greater than 2.5 mEq/L
magnesium level
Electrocardiogram Assess for presence of Magnesium levels greater than 5 mEq/L: Prolonged
abnormalities PR, QRS, and QT intervals
Magnesium levels greater than 15 mEq/L:
Complete heart block and cardiac arrest

Collaborative management

196
Care priorities

1. Discontinue magnesium-containing medications

Especially in patients with renal failure (see Box 1-10).

2. Administer diuretics and IV fluids

Use loop diuretics and 0.45% NaCl solution to promote magnesium
excretion in patients with adequate renal function.

3. Administer IV calcium gluconate

Use 10 mL of 10% solution to antagonize the neuromuscular effects
of magnesium for patients with potentially lethal
hypermagnesemia.

4. Consider use of hemodialysis

A magnesium-free dialysate may be used for patients with severely
decreased renal function, who may not respond as readily to other
magnesium-lowering strategies. Patients must be very closely
monitored for other electrolyte changes during treatment.

5. Monitor ECG for changes and manage dysrhythmias

Manage according to Advanced Cardiac Life Support (ACLS)
guidelines, bearing in mind the special considerations related to
correcting the hypermagnesemia while using additional
recommended strategies.

6. Monitor hypotension and bradycardia

Manage according to ACLS guidelines, bearing in mind the special
considerations related to correcting the hypermagnesemia while
using additional recommended strategies.

7. Monitor for neurologic and neuromuscular status

changes
To help gauge efficacy of treatment.

Care plans for hypermagnesemia

197
Ineffective protection 
related to inability to control internal changes caused by hypermagnesemia
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient verbalizes orientation to time, place, and person. The patient
does not exhibit evidence of injury as a result of complications of
hypermagnesemia, including no symptoms of soft tissue
(metastatic) calcifications: oliguria, corneal haziness, conjunctivitis,
irregular HR, and papular eruptions.
Neurologic Status.

Neurologic monitoring

1. Monitor serum magnesium levels in the patient at risk for

hypermagnesemia (e.g., those with chronic renal failure). Normal
range for serum magnesium levels is 1.5 to 2.5 mEq/L.

2. Assess and document LOC, orientation, and neurologic status

(e.g., hand grasp) with each vital sign check. Assess patellar (knee
jerk) reflex in patients with a moderately elevated magnesium level
(greater than 5 mEq/L). With the patient lying flat, support the knee
in a moderately fixed position and tap the patellar tendon firmly
just below the patella. Normally the knee will extend. An absent
reflex suggests a magnesium level of greater than 7 mEq/L. Consult
the advanced practice provider for significant changes.

3. Reassure the patient and significant others that altered mental

functioning and muscle strength will improve with treatment.

4. Keep side rails up and the bed in its lowest position with the
wheels locked.

5. Assess the patient for the development of soft tissue calcification.

Consult the advanced practice provider for significant findings.

6. Monitor for cardiopulmonary effects of hypermagnesemia:

hypotension, flushing, bradycardia, and respiratory depression.

Electrolyte Management: Hypermagnesemia.

198
Deficient knowledge 
related to magnesium-containing medications
Goals/Outcomes: Within the 24-hour period before discharge
from ICU, the patient verbalizes the importance of avoiding
unusual magnesium intake and identifies potential sources of
unwanted magnesium.
Knowledge: Medication.

Teaching: Individual

1. Caution patients with chronic renal failure to review all over-the-

counter medications with the physician or midlevel practitioner
before use.

2. Provide a list of common magnesium-containing medications

(Table 1-9).

3. Caution patients to avoid combination vitamin-mineral

supplements because they usually contain magnesium.

Table 1-9
MAGNESIUM-CONTAINING MEDICATIONS

Brand Name Antacids Laxatives

Aludrox Magnesium citrate
Camalox Magnesium hydroxide (Milk of Magnesia, Haley M-O)
Di-Gel Magnesium sulfate (Epsom salts)
Gaviscon Magnesium-containing mineral supplements
Gelusil and Gelusil II
Maalox and Maalox Plus
Mylanta and Mylanta-II
Riopan
Simeco
Tempo

Teaching: Prescribed Diet; Teaching: Prescribed Medication.

Hemodynamic monitoring
Hemodynamic monitoring is continuous monitoring of the
pressures being exerted on or within the veins, arteries, and heart.
Hemodynamic monitoring is a diagnostic tool, not a treatment or

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therapy. The information gained from hemodynamic monitoring is
used to evaluate cardiovascular performance, which includes
information about the cardiac output (CO), tissue perfusion, blood
volume, tissue oxygenation, and vascular tone. Hemodynamic
monitoring readings encompass a broad array of measurements,
depending on the technology used. Understanding hemodynamic
values and the trends of the information provided is important in
determining actions used to improve cardiac function, oxygenation,
oxygen use, overall circulation, and tissue perfusion. Accurately
determined hemodynamic values are used to guide fluid and
occasionally blood administration and cardiovascular drug–based
and device-based therapies provided to patients who are critically
ill.
The three overarching assessment parameters provided by
hemodynamic monitoring are calculation of preload (end-diastolic
volume and pressure in both ventricles before contraction),
afterload (pressure created by blood volume and arterial tone,
which the heart must overcome to open the aortic and pulmonic
heart valves), and contractility (ability of the heart muscle to
pump/contract effectively). Preload, afterload, contractility, and HR
ultimately determine stroke volume (SV), CO, and BP. Changes in
any of the four determinants of CO (preload, afterload, contractility,
or HR) may produce significant adverse effects on BP with resulting
adverse changes in cellular function and energy production as a
result of altered tissue perfusion. Hemodynamic monitoring helps
to assess these parameters in the patient who is critically ill so that
appropriate treatment with medications or devices can be provided.
Usage guidelines were developed to outline when use of
hemodynamic monitoring provides the most benefit (Box 1-11).

Box 1-11
OPTIMAL USE OF PULMONARY ARTERY
CATHETERS
Rajaram et al., in 2013, published a review of studies of pulmonary
artery catheter (PA catheter) use in adult patients in intensive care
units (ICUs). The total number of patients included in the review
was 5686. The authors concluded that there was no difference in

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ICU or hospital length of stay, mortality, or cost between patients
who had a PA catheter and those that did not. The evidence does
not support the argument that the PA catheter is costly and
unnecessary. However, the authors remind their readers that
hemodynamic monitoring is a diagnostic tool not a treatment.
A 2013 guideline for the management of heart failure from the
American College of Cardiology Foundation and the American
Heart Association (ACCF/AHA) gave a Class I recommendation
for use of a PA catheter. The report indicated that the PA catheter
should be used to guide therapy in patients who have respiratory
distress or clinical evidence of impaired perfusion such that cardiac
filling pressures could not be determined via clinical assessment.
The ACCF/AHA 2011 guideline for coronary bypass surgery
included placement of a PA catheter as a Class I recommendation
for patients in cardiogenic shock undergoing coronary bypass
surgery.
In 2007, the ACCF/AHA produced guidelines on perioperative
cardiovascular evaluation and care for patients undergoing
noncardiac surgery. The following excerpts concern their
recommendations on the use of hemodynamic monitoring.
The use of a PA catheter may be helpful in the surgical patient at
risk for hemodynamic disturbances detectable using a PA catheter.
The guideline suggests that three parameters should be assessed
before use: patient disease (incidence of fluid shifts), surgical
procedure (anticipate fluid shifts), and practice setting (presence of
skilled personnel to maintain the PA catheter and interpret data).
Routine use of a PA catheter perioperatively, especially in patients
at low risk of developing hemodynamic disturbances, is not
recommended.
In 2003, Practice Guidelines for Pulmonary Artery Catheterization:
An Updated Report by the American Society of Anesthesiologists Task
Force on Pulmonary Artery Catheterization was published.
The task force recommended looking at the patient, surgery, and
setting before making a clinical decision to use hemodynamic
monitoring. “Patients at increased risk for hemodynamic
disturbances are those with clinical evidence of significant
cardiovascular disease, pulmonary dysfunction, hypoxia, renal
insufficiency, or other conditions associated with hemodynamic

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instability (e.g., advanced age, endocrine disorders, sepsis, trauma,
burns).
Low-risk patients: Include those with an American Society of
Anesthesiologists (ASA) physical status score of 1 or 2, with
hemodynamic disturbances unlikely to cause organ dysfunction.
Moderate-risk patients: Category ASA 3 who have hemodynamic
disturbances that occasionally cause organ dysfunction. High-risk
patients: Category ASA 4 or 5 who have hemodynamic
disturbances with a great chance of causing organ dysfunction or
death. “The assessment of risk should be based on a thorough
analysis of the medical history and physical examination findings,
rather than on exclusive consideration of specific laboratory results
or other quantitative criteria. Surgical procedures associated with
an increased risk of complications from hemodynamic changes,
including damage to the heart, vascular tree, kidneys, liver, lungs,
or brain, may increase the chance of benefiting from PA
catheterization.”

Pathophysiology
Determinants of cardiac output and blood pressure
The most powerful determinant of CO is tissue oxygen (O2)
demand. The primary function of circulation is to provide a
medium for exchange of oxygen, nutrients, and waste products
between the blood and tissues. The flow of blood throughout the
microcirculation, where the exchange occurs, is dependent on
arterioles (regulate blood flow through changing level of
resistance), capillaries (primary exchange vessels), and venules
(collect and exchange vessels). As metabolism and O2 consumption
increase or decrease, the heart responds, and CO increases or
decreases in direct response to increased or decreased need. The
heart works as a two-sided pump, with the right side pumping
deoxygenated blood into the lower pressure pulmonary circulation
(reflected by PA pressure) and the left side pumping oxygenated
blood into the higher pressure systemic circulation (reflected by

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BP). Evaluation of CO requires an assessment of the components
that determine SV (preload, afterload, and contractility) for both
sides of the heart and factors affecting the HR.
In the absence of underlying pathology, such as intracardiac
right-to-left or left-to-right shunting, the output of the ventricles
should be the same. If the output of one of the ventricles changes,
the other ventricle should adjust its output to compensate for the
difference. The right and left sides of the heart are connected by the
pulmonary arteries and veins. Many specialized types of central
vessel and arterial catheters are available to measure the pressures
within the cardiopulmonary circulation and provide a means to
calculate CO. The original PA catheter was known as the Swan-
Ganz catheter named after the physicians who developed it. All PA
catheters provide information about the right side and left side of
the heart, as well as systemic circulation. Options for measurements
vary with each uniquely configured catheter. Once the
hemodynamic data are evaluated, strategies may be implemented
to manipulate preload, afterload, contractility, and HR.

Preload
Understanding Frank Starling’s law is fundamental to
understanding preload. Starling’s law of the heart states, “The
greater the ability of the myocardial muscle to stretch at the end of
diastole, the greater is the force of myocardial contraction.”
However, if the stretch becomes consistently excessive, the force of
contraction will diminish. Preload is determined by the compliance
(ability to stretch) of the ventricles during diastole as the blood
volume fills the ventricles. As the blood volume increases, the heart
must “stretch” with each heartbeat to accommodate it. As the blood
volume decreases, the heart stretches much less but must still
generate the force needed to propel the blood volume forward
during systole. This mechanism enables the heart to adjust
ventricular size to varying blood volumes. Preload coupled with
the electrical conduction system of the heart coordinates the output
of the right and left ventricles.
Factors that affect ventricular blood volume include venous
return, circulating blood volume, condition of the heart valves, and
atrial contractility. Ventricular compliance is affected by stiffness

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and thickness of the cardiac muscle. Any stressor that influences
one of these factors will result in a change in preload, with a
concomitant change in CO. Heart disease affects preload. Patients
with biventricular heart failure and/or “stiff ventricles” are not able
to handle increased intravascular volume. Their preload is always
high because the heart cannot stretch normally to accommodate
more volume. The diseased heart has little ability to compensate for
volume changes. Patients with a right ventricular (RV) infarction
are in a difficult position, as they require a higher preload to
maintain a normal CO because the infarct zone cannot stretch. Extra
ventricular blood volume, or higher preload, creates more stretch in
the normal RV tissues to promote better RV output but can result in
excessive work for the left ventricle. All patients with heart disease
may develop heart failure, thus expert monitoring by the clinician is
required to optimize CO (see Heart Failure, Chapter 5).
Clinically, preload is measured as ventricular end-diastolic
pressure (VEDP), because pressure in the ventricles correlates
closely with volume. For the right side of the heart, RV end-
diastolic (filling) pressure (RVEDP) is reflected by right atrial (RA)
pressure (RAP) or CVP. Left ventricular (LV) end-diastolic (filling)
pressure (LVEDP) is reflected by left atrial (LA), PA diastolic
(PAD), or PA occlusive (PAOP) or wedge (PAWP) pressure
measurements. If preload begins to increase in a patient with heart
disease, appropriate medications, including diuretics, may be given
to help decrease CVP and PAOP. Vasodilating drugs with strong
venodilating properties may also be used to decrease venous return
so that a heart with limited ability to stretch can accommodate and
pump the lesser blood volume. An increase in preload signals that
the ventricles may be unable to eject enough of the end-diastolic
volume, causing more blood to be retained in the ventricles. As a
result, venous congestion and fluid overload occurs, leading to the
clinical signs of congestive heart failure. Conversely, decreased
preload is seen with hypovolemia and certain types of shock where
vasomotor tone is affected causing vasodilation. Decreased preload
can lead to a decrease in CO related to the decrease in SV.
Hypovolemia may be difficult to assess, because the patient may
have pitting edema but is deficient of fluid volume within the blood
vessels. The CVP may not always provide a complete picture of

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volume status. Stroke volume variability (SVV) can assist the
clinician in assessment of the need for fluid replacement and the
adequacy of the volume delivered. SVV is determined using the
arterial waveform to calculate the change in SV from beat to beat of
the heart (see Septic Shock).

Afterload
Afterload refers to the pressure or force that must be generated
within the right and left ventricles/ventricular myocardium during
systole to overcome the vascular resistance to ejection. The
pressures created by the blood volume and vascular tone within the
pulmonary, aortic, and systemic circulation create resistance against
the aortic and pulmonic valves, which can impede ventricular
ejection. Other resistant forces include increased blood viscosity,
reduced distensibility of the vascular system (created by
atherosclerosis or “hardening of the arteries”), and diseased heart
valves. The clinician should be aware that diseased ventricles are
extremely sensitive to abrupt changes in afterload because the
diseased tissue cannot readily generate additional force to
overcome additional resistance to ejection. Paying close attention to
PA pressures, as well as systemic arterial pressure, is of paramount
importance. If blood volume starts to be retained in the ventricles,
rather than being normally ejected, VEDP increases, followed by
increases in PA pressure. When these changes are observed,
measures such as administration of diuretics or vasodilating drugs
with strong arterial dilating properties may be initiated to decrease
afterload and help improve ventricular ejection. Medications used
for management of hypertension are administered to reduce
afterload.
Because vascular resistance plays a major role in determining
pressures throughout the heart and lungs, RV afterload is evaluated
by calculating pulmonary vascular resistance (PVR), whereas LV
afterload is reflected by SVR. The higher the afterload, the greater
the myocardial wall tension/pressure must be to open the aortic
and/or pulmonic valves, and the greater is the work of the heart to
overcome resistance to flow. This explains why hypertension is
called “the silent killer,” because the constantly increased afterload
strains the heart. Increased cardiac work requires increased

205
myocardial blood flow to deliver additional O2. When blood
flowing through the coronary arteries is diminished by
atherosclerosis, the demand for the increased blood flow required
to manage energy needs created by increased afterload may not be
met, resulting in myocardial ischemia, injury, and possibly
infarction.

Contractility
This is the inherent capacity of the myocardium to contract during
systole. This mechanism functions independently of variations in
preload and afterload. Changes in ventricular contractility have a
significant effect on tissue perfusion and the shape/slope of the
ventricular function curves generated during CO measurement.
Although contractility is not measured directly, a change in
contractility can be inferred when CO is decreased and other
variables that affect CO (i.e., preload, SV, afterload, HR) remain the
same. Changes in ventricular function curves infer changes in
contractility. Several factors positively influence contractility:
sympathetic stimulation, calcium, and positive inotropic agents,
such as digitalis, dobutamine, milrinone, and beta-adrenergic
drugs. Factors such as acidemia, hypoxia, myocardial ischemia,
myocardial infarct, cardiomyopathies, beta-blocker drugs, and
antidysrhythmic drugs can decrease contractility.

Heart rate
Changes in HR affect myocardial functioning significantly. Slight
increases in HR with a constant SV result in increased CO. Very
rapid HRs are associated with a reduction in CO as the duration of
diastole is shortened, resulting in decreased coronary perfusion and
reduced ventricular filling time. Patients who are critically ill often
manifest sinus tachycardia to maintain a CO that meets the demand
for O2 and nutrients at the cellular level. The heart requires more O2
when the HR increases, and as long as coronary artery perfusion is
adequate, HR increases provide compensation needed for increased
metabolic demands. Tachycardia can, however, reach a critical
point where the heart is receiving less O2 if filling time becomes too
brief to provide appropriate coronary artery perfusion. Bradycardia

206
often results in decreased CO unless there are increases in SV
during the longer ventricular filling times. Athletes are able to
maintain excellent CO with slower HRs, but the patient who is
critically ill may not be as fortunate when HR decreases.
Algorithms have been created for advanced cardiac life support,
which include both pharmacologic and electrical therapies to
manage HR.

Hemodynamic assessment
The goal of hemodynamic monitoring is to obtain accurate
measurements and to observe trends in values that are used in
combination with physical assessment findings to provide
appropriate, effective therapies to maintain adequate BP, CO, and
tissue perfusion. The hemodynamic measurements listed in Table 1-
10 are considered the values needed in a complete hemodynamic
profile.

Table 1-10
HEMODYNAMIC NORMAL VALUES AND DERIVED VALUES

Parameter Formula Normal Values

Arterial blood pressure (BP) systolic 90 to 130/50 to 80 mm Hg
(SBP)/diastolic
Mean arterial pressure (MAP) SBP + (D × 70 to 100 mm Hg
2)/3
Central venous pressure (CVP)* 2 to 6 mm Hg
Right atrial pressure (RAP)* 2 to 6 mm Hg
Left atrial pressure (LAP) 8 to 12 mm Hg
Right ventricular pressure (RVP) 15 to 25/0 to 8 mm Hg
Pulmonary artery systolic (PAS) pressure 15 to 25 mm Hg
Pulmonary artery diastolic (PAD) pressure 8 to 15 mm Hg
Pulmonary artery occlusive pressure (PAOP) 6 to 12 mm Hg
Same as wedge (pulmonary capillary wedge
pressure [PCWP] or pulmonary wedge pressure
[PWP])
Mean pulmonary artery pressure (MPAP, PAM) PAS + (PAD 10 to 20 mm Hg
× 2)/3
Cardiac output (CO) HR × SV 4 to 8 L/min
Cardiac index (CI) 2.5 to 4 L/min/m2
Systemic vascular resistance (SVR) MAP − 800 to 1200 dynes/s/cm5
RAP/CO × 80
Pulmonary vascular resistance (PVR) MPAP − 150 to 250 dynes/s/cm5
PAOP/CO ×
80
Coronary perfusion pressure (CPP) Diastolic BP 50 to 70 mm Hg

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 − PAOP
Stroke volume (SV) CO/HR × 55 to 100 mL/beat
1000
Stroke volume index (SVI) SV/BSA 30 to 60 mL/beat/m2
Right ventricular stroke work index (RVSWI) SVI (PAM − 4 to 8 g/m2/beat
RAP) ×
0.0136

Left ventricular stroke work index (LVSWI) SVI (MAP − 40 to 75 g/m2/beat

PAOP) ×
0.0136
Arterial oxygen content (Cao2) (Hgb × 1.34) 18 to 20 mL/vol%
× Sao2
Venous oxygen content (Cvo2) (Hgb × 1.34 × 15.5 mL/vol%
Svo2)
Oxygen delivery (Do2) Cao2 × CO × 800 to 1000 mL/min
10
Oxygen delivery index (Do2I) Cao2 × CI × 500 to 600 mL/min/m2
10
Arteriovenous oxygen content difference (C[a − Cao2 × Cvo2 4 to 6 mL/vol%
v]o2)
Oxygen consumption (Vo2) CO × 10 × 200 to 250 mL/min
C(a − v)o2
Oxygen consumption index (Vo2I) CI × 10 × C(a 115 to 165 mL/min/m2
− v)o2
Arterial oxygen saturation (Sao2) 95% to 98%
Mixed venous oxygen saturation (Svo2) (CO × Cao2 × 60% to 80%
(Global venous return) 10) − Vo2 Values should be trended
for optimal clinical
assessment
Mixed venous oxygen saturation-regional (Scvo2) 65% to 85%
(Head and neck venous return) Values should be trended
for optimal clinical
assessment
Stroke volume variation (SVV) 10% to 15%
*
CVP and RAP are used interchangeably at times.
BSA, Body surface area; Hgb, hemoglobin; HR, heart rate.

Systemic arterial pressure or blood pressure may be

measured indirectly and/or directly
• Indirect measurement: A “spot check” or “snapshot” of the BP in
a moment of time, performed with a manually inflated BP cuff
and manometer. Arterial pressure is auscultated over a pulse
point using a stethoscope or Doppler ultrasound device. A
noninvasive automatic BP cuff (NIBP or NBP) may be used, in
lieu of manually inflating the cuff and auscultating the pressure

208
 using a stethoscope and manometer. Manual or auscultatory BP
readings are wrought with pitfalls that cause false-high and false-
low readings. Proper cuff size, proper cuff position, arm position
being level with the heart, and skill in determining the onset of
the first Korotkoff sound are imperative components for accurate
readings.

• Bariatric consideration: Proper cuff size may

require a special large and/or long cuff for proper
fit. Alternate BP measurement sites may be required
such as the forearm or lower leg, and the site used
must be documented with the BP reading. Alternate
sites also require correct cuff size for accurate
readings (refer to the manufacturer’s instruction for
proper fit and placement). Regardless of the site
used, the cuff should be at the level of the patient’s
heart. If using a lower extremity, the patient should
be in a supine position.

• Geriatric consideration: Comparison of BP

readings from each arm on initial encounter is best
practice, because it may provide information about
the vascular status of the individual. Both BP
measurements are recorded with the site noted, and
it is recommended that the site with the higher
pressure be used and documented. This practice is
not limited to the elderly. Measurement of BP with
the individual lying or sitting rather than taken
when standing is used to determine if the
individual has orthostatic hypotension (sometimes
called postural hypotension). Orthostatic
hypotension is indicated when the systolic BP drops

209
 20 mm Hg and/or the diastolic BP falls by 10 mm
Hg, or greater change when in the standing
position. Clinically the patient may be dizzy or
light-headed. Prepare to safely assist the patient
back to a sitting or lying position to prevent a fall.

• Direct measurement: Continuous monitoring of BP that requires

insertion of a hollow, semirigid catheter into an artery to create
an arterial line (A-line). When an arterial line is used to measure
BP, it is labeled ABP to distinguish this from a noninvasive
measurement. BP is a dynamic or ever-changing event and the
continuous monitoring of ABP reflects the beat-to-beat changes
that occur. Cardiovascular dynamics are assessed through a
review of pressure waveforms and analysis of trends in arterial
pressure readings. Arterial lines are used to obtain arterial blood
samples for labwork, including blood gas determinations,
without repeated arterial punctures.

Arterial oxygen saturation

• The percentage of oxyhemoglobin (Hgb bound with O2)
compared with the total amount of Hgb can be measured directly
using blood samples from the arterial line or approximated
indirectly by photoelectric technology using an external pulse
oximetry probe placed on the patient’s finger, ear, or forehead.

Central venous pressure or right atrial pressure

• CVP can be monitored continuously or “spot checked” using a
central line.

• CVP and RAP may be used interchangeably to assess

intravascular fluid volume, efficacy of venous return to the right
side of the heart, and RVEDP or preload.

• RAP is obtained using the RA port of a PA catheter.

210
• Specialized CV catheters allow continuous venous oximetry
(ScVO2) monitoring that provides information on oxygen use.

Pulmonary artery pressures

• PAPs are measured continuously using a flow-directed,
multilumen catheter placed in the PA. PA catheters vary in
technology. More sophisticated catheters provide information
about O2 delivery and O2 consumption (SVO2) and may provide
continuous cardiac output (CCO) measurements. Basic PA
catheters provide measurement of RAP, PAP, PAOP or “wedge
pressures,” and CO.

• The RAP, PAP, PAOP, and CO provide information that helps in

calculating preload, afterload, and contractility. Waveform
analysis helps to identify any pathology or abnormality of the
heart valves and other cardiac disorders.

• The hemodynamic measurements paired with the data gathered

about oxygen delivery and oxygen use give the clinician
information about tissue perfusion.

Cardiac output
CO can be calculated using several methods.

• Fick oxygen consumption method: The original, or “gold

standard,” mathematical method used to calculate CO. The
formula for CO uses arteriovenous O2 content difference to
calculate the value. A number of technical problems can interfere
with obtaining accurate results, and because of the cumbersome
nature of the procedure, the formula is generally used in research
laboratories, rather than routinely in clinical practice.

• Thermodilution (TD) method: Measurement method using a PA

211
 catheter to determine the flow rate of a room temperature IV
solution (injectate) passing through the heart. The temperature of
the injectate is lower than the temperature of the blood in the
central circulation. IV solution is injected into a more proximally
located port in the PA catheter and travels through the heart to a
more distally located port. A temperature sensor is used to track
the flow rate of the injectate. The speed of the flow from the
proximal to the distal port is used to calculate CO. It is
considered accurate and reliable. The TD method of CO
determination is now used as the standard for comparing other
methods of CO determination.

• Continuous cardiac output measurement: Performed using a

specialized PA catheter using thermal technology that allows the
user to obtain readings that are averaged over 3-minute periods
and updated every 30 to 60 seconds.

• Arterial pressure–based cardiac output measurement (APCO):

This method of CO calculation assesses the aortic pulse pressure
using the arterial waveform to calculate the SV and is a beat-to-
beat measurement.

• Impedance cardiography (ICG) method of CO measurement:

ICG is a noninvasive measurement that uses transthoracic
bioimpedance to determine CO. Currently, BioZ and Task Force
monitoring have proven to accurately determine CO compared
with the TD method in medical cardiac patients. ICG
measurements are less reliable in patients with valvular disease,
aortic vessel disease, cardiac shunts, or states with fluid
accumulation in the thorax. Therefore, this method is not
recommended for use in cardiac surgery patients.

• Transthoracic echocardiograms (TTE) and transesophageal

echocardiograms (TEE): Can determine CO as a calculation of
SV. TTE is noninvasive and is used for short-term diagnostics.
TEE is minimally invasive and is often used in the surgical
setting.

Tissue oxygenation

212
Adequate tissue oxygenation is the goal of therapy for patients in
critical care. The regulation of oxygenation is dependent on
regulation of blood flow. The cardiovascular system controls blood
flow by maintaining the appropriate perfusion pressure throughout
the arterial system supplying blood to each organ, and by allowing
each organ to regulate vascular resistance based on the needs of the
organ. CO can be redistributed at the organ or tissue level based on
need. Vasoregulation occurs at the local level by the arterioles or
resistance vessels. Vasoactive medications used to support
perfusion pressure require careful titration based on an analysis of
meaningful data. To assist the clinician in meeting this goal, oxygen
use is measured via specialized catheters.

• The SVO2 PA catheter not only gives a CCO but also measures the
venous O2 saturation (SVO2) via a fiber optic tip in the PA, and is
used for determination of the balance between O2 delivery and O2
use. O2 delivery is the result of CO multiplied by the arterial O2
content (CaO2). The arterial O2 content is determined by Hgb and
arterial O2 saturation (SaO2). The balance between oxygen
delivery (DO2) and oxygen use (VO2) is reflected by the SVO2.

• The ScVO2 is measured via a specialized CV catheter, usually

placed in the subclavian vein. The ScVO2 reflects the mixed
venous oxygen use as does the SVO2. However, the ScVO2
measurement is taken from the superior vena cava and does not
include the inferior vena cava contribution. The ScVO2 trends
with the SVO2 and the same factors influence the findings. The
factors that affect tissue oxygenation include CO, SaO2, Hgb,
oxygen delivery (DO2), and oxygen use (VO2). Oxygen use is
dynamic and SVO2 and ScVO2 can normally change 5%. Therefore,
the clinician should act on changes of greater than 5% to 10% that
are sustained greater than 5 minutes. Both SVO2 and ScVO2 should
be used with CO, Hgb, and SaO2 monitoring to give the clinician
a complete picture of oxygen use (see Table 1-10).

Promoting accuracy of hemodynamic values: Setting

213
up equipment
Ensuring proper setup and maintenance of the pressure monitoring
system will prevent most inaccuracies. Normal waveform
configurations must be understood for all readings so that
abnormal waveforms can be readily identified. Abnormal
waveforms can sometimes reflect a problem with the system setup
or maintenance.

General considerations related to the hemodynamic

monitoring setup

1. Use rigid pressure tubing from the transducer to the patient.

Most monitoring kits have the proper setup prepackaged with
disposable transducers to assure proper use. Flexible tubing may be
used from the flush bag to the transducer.

2. During the initial setup, flush or prime the monitoring system (all
tubing and the transducer[s]) without pressure applied to the flush
bag to help prevent formation of air bubbles from turbulent flow
within the empty tubing. Slower priming allows for more even
fluid dispersion throughout the system.

3. Remove excess air from the flush bag before flushing to help
prevent an air embolus from entering the patient’s vasculature. The
excess air can be accidentally introduced into the patient.

4. Flush all stopcocks and apply sterile dead-end caps to seal the
system. Vented caps are not recommended, because the venting
offers an entry point for organisms and could create a leak in the
system.

5. Maintain a minimum of 100 mL in the flush bag and change the

bag according to institutional guidelines. Many institutions focus
on maintaining a closed system to minimize the chance of
contamination. The Centers for Disease Control and Prevention
(CDC) recommends that the tubing be changed every 96 hours.

6. Apply and maintain 300 mm Hg of pressure to the pressure bag

enclosing the flush bag.

214
7. Maintain electrical safety guidelines to avoid microshocks
entering the heart via the fluid column created by the monitoring
system.

8. Normal saline is the recognized flush solution of choice for

hemodynamic monitoring systems. Heparinized saline is no longer
recommended for routine use, to avoid the risk of inducing
heparin-induced thrombocytopenia (HIT positive).

Leveling and zeroing the system

1. All monitoring systems must be leveled before use. To level the

system, the transducers are positioned at the phlebostatic axis to
provide the most accurate pressure readings. Transducers must
remain leveled to provide accurate pressure readings. The
phlebostatic axis is located at the intersection of the fourth
intercostal space and the line that denotes half the anteroposterior
diameter of the chest. Readings are accurate with the head of the
bed (HOB) elevated from 0 to 60 degrees. Higher HOB elevation
will result in false-low readings.

2. Transducers must be “zeroed” before using the monitoring

system. Newer computerized bedside monitors remind the nurse to
zero the system. Zeroing the transducer requires opening the
transducer to air while possibly pressing a button on the bedside
monitor to establish a referenced atmospheric pressure of zero.

3. Leveling and zeroing should be done at least once a shift, for any
change in patient position, when the system has been opened to air,
and/or if there is a question of accuracy in values or waveforms
obtained.

Square wave testing (also called fast flush or dynamic

response test)

1. This is done to test the compliance of the monitoring system to

provide a common measure of accuracy. Hemodynamic systems
are constructed differently in each monitoring setting, but,
minimally, each should have a flush system pressurized at 300 mm

215
Hg and a continuous fluid column contained within rigid tubing
between the transducer and the patient. The number of transducers,
and type and length of tubing may vary. Flaws within the system
directly affect the accuracy of pressure readings. The test indicates
if the system is normal, overdamped, or underdamped.

2. Overdamping causes the systolic pressure to be falsely low and

the diastolic pressure to be falsely high. Large air bubbles, loose
connections, no or low amount of flush solution in the system, low
pressure on the flush bag, or a kinked catheter causes overdamping.

3. Underdamping causes the systolic pressure to be falsely high and

the diastolic pressure to be falsely low. Small air bubbles, a
defective transducer, or pressure tubing that is too long causes
underdamping.

4. Testing should be done when the system is set up, once every
shift, when the system is opened to air for any reason (including
blood sampling), and when waves appear distorted from the usual
appearance.

5. To perform the square wave test:

• Fast flush the monitoring system by pulling the

pigtail or pressing the appropriate button for each
transducer. The flush should be pressurized to 300
mm Hg.

• When the system is being flushed, a large, square

wave appears on the monitor. Stop flushing
abruptly (snap the flush mechanism) and observe
the shape of the square wave, and wait for the
pressure waveform to normalize.

• An acceptable response is the waveform

normalizing and returning to baseline following 1.5

216
 to 2 oscillations (Figure 1-4, A). If the resulting
waveform is abnormally shaped, lacks shape, lacks
amplitude, or does not return to baseline, the
response is abnormal.

• In optimally damped systems, one small

undershoot (negative deflection) and one small
overshoot (exaggerated positive deflection or
bounce) are seen, followed by a return of the
normal waveform.

• Overdamped systems (Figure 1-4, B) demonstrate

less than 1.5 oscillations or bounces, and a slurring
of the square wave upstroke. Waves are blunted,
sluggish, and falsely wide.

• Underdamped systems (Figure 1-4, C) have greater

than 2 oscillations, sharp bounces with waves that
are exaggerated, narrow, and falsely peaked.

• If overdamping or underdamping is present,

troubleshoot the monitoring system. If
troubleshooting is ineffective, the monitoring
system should be checked by the biomedical
engineer or technician. If these problems cannot be
resolved, another monitor may be needed to obtain
accurate readings. Also see Troubleshooting (Table
1-11).

217
 FIGURE 1-4 Dynamic response testing (square wave,
frequency response testing) using the fast-flush
system. A, Optimally damped system. B, Overdamped
system. C, Underdamped system.

Hemodynamic monitoring: Considerations during

setup, line insertion, and placement

218
Arterial pressure monitoring

• The most common sites used for intraarterial catheter insertion

are the radial, brachial, or femoral arteries. Arterial catheters are
inserted via the radial artery, because this artery is readily
accessible and collateral blood flow is usually adequate. The
arterial catheter may also be inserted in the femoral or brachial
artery. The arterial pressure waveform is displayed on a bedside
monitor to provide continuous observation of systolic, diastolic,
and mean arterial pressures (Figure 1-5). The appearance of the
arterial waveform is influenced by variations in BP,
dysrhythmias, hypovolemia, vasoconstriction, and mechanical
factors. Mechanical factors that influence the waveform include
overdamping, catheter whip, and inaccurate calibration/zeroing
(Table 1-12).

• Potential complications include decreased perfusion distal to the

insertion site, which can cause limb ischemia. Slower blood flow
can lead to thrombus formation. If air inadvertently enters the
system during line insertion, through a crack or other flaw in the
closed system, an air embolus may result, which, if lodged in the
hand, can render distal tissues anoxic. Rarely, patients have
needed to have fingers amputated because of prolonged lack of
perfusion. If the closed system is cracked or becomes
disconnected, exsanguination may occur. With any invasive
procedure the risk of infection is present. Follow strict adherence
to invasive line insertion procedures to decrease the risk of
infection.

FIGURE 1-5 Arterial pressure waveform. Source: (Redrawn

219
 from Daily E, Schroeder J: Techniques in bedside hemodynamic monitoring,
ed 4, St Louis, 1989, Mosby.)

Table 1-12
ABNORMAL PULMONARY ARTERY PRESSURES

Hemodynamic Normal
Clinical Conditions
Pressure Range
Pulmonary artery 20 to 30 Increased: Right ventricular failure, chronic left ventricular failure,
systolic (PAS) mm Hg constrictive pericarditis, cardiac tamponade, pulmonary
pressure hypertension (primary or related to lung disease).
Decreased: Hypovolemia, preload reduction.
Pulmonary artery 8 to 15 Increased: Left ventricular failure, mitral stenosis, left-to-right
diastolic (PAD) mm Hg shunts, pulmonary hypertension (primary or related to lung
pressure* disease).
Decreased: Hypovolemia, preload reduction.
Pulmonary artery 6 to 12 Increased: Left ventricular failure, cardiac tamponade, mitral valve
occlusive mm Hg regurgitation, mitral valve stenosis, acute ventricular septal
pressure (PAOP)† defect, fluid volume overload.
Decreased: Hypovolemia, afterload reduction.
*
PAD may exceed PAOP by ≥5 mm Hg in patients with pulmonary hypertension,
hypoxemia, acidosis, pulmonary emboli, and other lung disease.
†
PAOP > PAD signals a mechanical problem (i.e., overwedging or improper
identification of PAD).

Pulmonary artery pressure monitoring

• The most common sites used for PA catheter insertion are the
internal jugular or subclavian veins. Femoral and brachial veins
may also be used. The most common PA catheter placement
technique is percutaneous insertion of the catheter
introducer/introducing needle using the Seldinger technique for
insertion, in combination with waveform analysis provided by
the hemodynamic monitoring system as the catheter passes
through the heart. Waveform analysis and pressure readings
provide the practitioner with the information needed to know the
position of the catheter. Insertion may also be done using a
cutdown to expose the vessel but is rarely needed. Catheter
placement is occasionally done under fluoroscopy for patients
with abnormal cardiac or vasculature structures.

• Potential complications include decreased perfusion distal to end

220
 of the PA catheter if the catheter is inserted too far or migrates
out of position. This can cause pulmonary tissue ischemia or
infarction, if it is severe. Slower blood flow can lead to thrombus
formation. If air inadvertently enters the system during line
insertion, through a crack or other flaw in the closed system, an
air embolus may result. If the closed system is cracked or
becomes disconnected, exsanguination may occur. The cardiac
chambers can be perforated during insertion, resulting in
hemorrhage into the mediastinum and cardiac tamponade. The
vasculature can be perforated during insertion, resulting in the
extravascular catheter tip causing fluid or blood accumulation in
the pleural space or the mediastinum and/or a pneumothorax.
Dysrhythmias may occur, particularly when the catheter passes
through the right ventricle.

Diagnostic Tests Associated with Pulmonary Artery Catheter

Placement for Hemodynamic Monitoring

Diagnostic tests

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Factors affecting hemodynamic measurements

Systolic blood pressure

This is determined by (1) the amount of blood ejected by the
ventricle per beat (SV), (2) wall compliance of the arterial system,
and (3) peripheral resistance. Elevations in systolic pressure
produce large, steep waveforms, often reflective of changes in
vascular compliance, such as the hypertension seen in patients with
atherosclerosis. A decrease in systolic pressure producing smaller,
slightly wider waveforms is seen in connection with heart disorders
that result in decreased SV. The use of arterial vasodilators such as
nitroprusside, hydralazine, and nifedipine will cause a rapid
upstroke and steep decline with a drop in diastolic pressure related
to the potent arterial dilation.

Diastolic blood pressure

This is determined by (1) volume of blood within the arterial
system, (2) compliance of the arterial wall, and (3) peripheral
resistance. Coronary artery blood flow occurs during diastole, and a
drop in diastolic pressure may result in myocardial ischemia as
flow is reduced with lower diastolic pressure. Monitoring of
diastolic BP is critical, especially when vasodilating drugs are
administered, because diastolic BP generally decreases from the
effect of these medications.

Caution must be used in managing hypertension or

decreasing afterload with sodium nitroprusside (e.g., Nipride),
because this medication causes both venous and arterial
vasodilation and can rapidly decrease the blood pressure (BP),
causing hypotension with rapid decrease in delivery of O2 and
nutrients to the cells. Nitroprusside may also induce deterioration
in arterial O2 saturation if ventilation cannot increase enough to
“match” the increased blood in the lungs caused by pulmonary
vasodilation. If the BP is extremely labile, the patient may be
intravascularly volume-depleted or hypovolemic. Replacing fluid
volume or blood (if hemorrhage is the cause) will help stabilize the

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BP.

Mean arterial pressure (MAP)

The normal MAP value is 70 to 100 mm Hg. MAP is the average
pressure within the arterial tree throughout the cardiac cycle,
reflecting the average force that pushes blood through the systemic
circulation to the tissues. MAP is the product of CO × SVR. An
increase in CO or SVR will increase MAP. A decrease in either
value will decrease MAP. MAP is the most accurate noninvasive
measurement of central aortic pressure. The intraaortic balloon
provides the most accurate invasive measurement as it is taken
from the catheter tip located just after the aortic arch in the
descending aorta. MAP can be calculated by the following formula:
MAP = SBP + (DBP × 2)/3.

Central venous pressure (CVP)

The normal CVP value is 2 to 6 mm Hg. CVP is the measurement of
systemic venous pressure at the level of the superior vena cava just
before it enters the right atrium. CVP can be measured by a catheter
threaded into the jugular, subclavian, or other large vein, by the use
of a CV catheter; often, these are multilumen catheters. RAP
correlates with CVP because the normal values and waveforms
(Figure 1-6) are the same and the terms are used interchangeably in
practice. Using a PA catheter, RAP is measured through the
proximal port, which lies in the right atrium. Because 60% of total
blood volume resides in the venous system, CVP is valuable in
assessing for fluid volume excess or deficit and venous tone. CVP
also provides indirect information regarding RV function. RV
failure, cardiac tamponade, fluid volume overload, pulmonary
hypertension, tricuspid valve disease, and chronic LV failure may
increase CVP. Decreased CVP is most often caused by
hypovolemia. Venous dilation caused by sepsis, drugs, or
neurogenic dysfunction may also decrease CVP. Complications of
CV catheters include venous air embolism, dysrhythmias,
hemorrhage, infection, vascular erosion, perforation of cardiac
chambers, pneumothorax, and thromboembolic problems.

223
 FIGURE 1-6 Right atrial pressure waveform with
electrocardiography (ECG). Source: (Redrawn from Daily E,
Schroeder J: Techniques in bedside hemodynamic monitoring, ed 4, St
Louis, 1989, Mosby.)

Be alert for air embolism during central catheter insertion

and maintenance of the central venous pressure monitoring system.
This is an uncommon but potentially fatal event. As little as 20 mL
of air may cause a problem for patients who are critically ill.
Entry of 200 to 300 mL of air into the vessel over a short period of
time (seconds) has a 50% mortality rate. Prevention is the key.
During insertion, ensure the practitioner inserting the catheter does
not allow ports to be uncapped or uncovered (open to air) once
inside the vessel. Air can be entrained down the port by the blood
flow during inspiration (when intrathoracic pressure is negative),
resulting in embolization. If air embolism is suspected, place the
patient with head of the bed down (Trendelenburg position) in the
left lateral decubitus position immediately (see Suspected Air
Embolism in the Collaborative Management section).

Right atrial pressure (RAP)

The normal mean RAP is 2 to 6 mm Hg. RAP is measured via the
proximal catheter port and is essentially the same as CVP. With the
PA catheter, RAP can be monitored continuously and displayed on
a bedside screen (see Figure 1-6). In addition, the catheter lumen
can be used for fluid or drug administration.

224
Right ventricular pressure (RVP)
The normal RVP is 15 to 25 mm Hg systolic, 0 to 8 mm Hg diastolic.
RVP is measured only during catheter insertion and provides
information about the function of the right ventricle and the
tricuspid and pulmonic valves. Elevation of RV systolic pressure
may be seen in pulmonic stenosis, pulmonary hypertension, or
ventricular septal defect (VSD) with left-to-right shunt. Elevation of
RV diastolic pressure may occur with RV failure, cardiac
tamponade, or constrictive pericarditis.

It is important for the nurse to identify the normal right

ventricular waveform (Figure 1-7), because a complication of the
pulmonary artery (PA) catheter is potential displacement of the
catheter tip into the right ventricle, causing ventricular ectopy.
Immediate action to reposition the PA catheter should be
performed. Some institutions may allow nurses to reposition the
patient and inflate the PA catheter balloon so blood flow into the
PA carries the catheter back into position, whereas others may be
required to immediately pull the PA catheter back into the right
atrium.

225
 FIGURE 1-7 Location of catheter tip and waveforms
obtained during insertion of pulmonary artery catheter.
PAOP, Pulmonary artery occlusion
pressure. Source: (From Urden LD, Stacy KM, Lough ME: Priorities in
critical care nursing, ed 5, St Louis, 2008, Mosby.)

Pulmonary artery (PA) pressures

Multiple values are measured via the use of a PA catheter (see
Table 1-10). PAP monitoring is used to evaluate heart function and
pulmonary vascular status. PA catheters (e.g., Swan-Ganz,
Opticath, and others) provide valuable information used to assess
and treat life-threatening illness or injury. Blood volume, heart
function, and tissue oxygenation can be assessed using various
available pressures. PA catheters are inserted via the jugular,
subclavian, brachial, or femoral vein and passed through the right
side of the heart into the PA, where the tip of the catheter is
positioned in the distal PA. The PA catheter should be positioned in
zone 3 of the lung field, below the level of the left atrium to
promote maximal accuracy of readings, given the effects of gravity
on blood flow through the lungs.
PA pressures are normally one fifth of systemic BP. PA systolic
(PAS), PA mean (PAM), and PA diastolic (PAD) pressures are
monitored continuously by the distal port of the PA catheter, after
the catheter is passed out of the right side of the heart, through the
pulmonic valve, and into the PA. PAOP can be assessed after
inflating the balloon on the distal end of the catheter, which allows
it to float and “wedge” into a smaller branch of the PA. Once the
artery is occluded by the balloon, the filling pressures of the left
side of the heart can be indirectly measured. PAOP is often referred
to as the PA wedge (PAW) pressure or occasionally the pulmonary
capillary wedge pressure (PCWP) or, in general conversation, as the
“wedge.”
If a more sophisticated SVO2 PA catheter is used, mixed venous
O2 saturation levels are also continuously monitored. CO can be
measured intermittently using TD or, with some PA/SVO2 catheters,
is measured continuously. A full hemodynamic profile can also be
calculated for the patient, including SV, stroke work, PVR, and SVR

226
(see Table 1-10). All values are helpful in determining how to
manage the patient’s fluid balance, heart function, and vascular
tone and can be individualized to the patient’s body size (index
values). There is ongoing research on the usefulness of indexing
hemodynamic values to body weight in the morbidly obese
population; no consensus has been formed. Abnormal PA pressures
are discussed in Table 1-12. Complications of PA catheters include
ventricular or atrial dysrhythmias, pulmonary ischemia or
infarction, valvular damage (tricuspid, pulmonic), PA rupture,
infection, emboli (thrombotic, air, balloon), and pneumothorax. The
incidence of PA catheter complications ranges from less than 1% to
3% and most are related to insertion.

PA systolic (PAS), diastolic (PAD), and mean pressures

(PAM)
Normal PA pressures are 15 to 25/8 to 15 mm Hg (PAS/PAD) with
PAM 10 to 20 mm Hg (Figure 1-8). The PA pressures are used to
evaluate heart function and pulmonary vascular disease. In patients
with healthy pulmonary vasculature, the PAD pressure
corresponds closely to the PAOP and reflects the LVEDP. A
significant difference (i.e., greater than 5 mm Hg) between the PAD
and PAOP is seen with pulmonary disease or a pulmonary
embolus. When this occurs, PA systolic and diastolic pressures are
elevated, whereas the PAOP remains normal. Specific disease states
that result in elevated PA pressures include pulmonary
hypertension, pulmonary embolism, hypoxia, and LV failure
resulting from valve disease, MI, cardiomyopathy, and left-to-right
intracardiac shunt. Decreased PA pressures are seen with
hypovolemia and pharmacologic preload reduction.

227
 FIGURE 1-8 Pulmonary artery pressure
waveform. Source: (Redrawn from Daily E, Schroeder J: Techniques in
bedside hemodynamic monitoring, ed 4, St Louis, 1989, Mosby.)

Pulmonary artery occlusive pressure (PAOP)

Normal mean PAOP is 6 to 12 mm Hg (Figure 1-9). The PAOP
(“wedge pressure”) reflects the LVEDP and is used to evaluate
cardiac performance. PAOP does not accurately reflect LVEDP in
patients with severe pulmonary hypertension. An elevated PAOP
may be seen with LV failure, acute mitral regurgitation, acute VSD,
and acute cardiac tamponade. A decreased PAOP is seen with
hypovolemia and afterload reduction. On patients who are
mechanically ventilated, positive end-expiratory pressure (PEEP) or
continuous positive airway pressure (CPAP) settings of greater than
10 cm H2O may result in falsely elevated PA pressures and PAOP.
Regardless of the inaccuracy, patients should not be disconnected
from the ventilator to measure PA pressures, because significant
hypoxemia and inaccurate measurements can result. Correlation of
measured pressures with the respiratory cycle improves the
accuracy of these measurements.

228
 FIGURE 1-9 Pulmonary artery occlusive pressure
waveform. Source: (From American Association of Critical-Care Nurses
(AACN): AACN procedure manual for critical care, ed 5, Philadelphia, 2005,
Saunders.)

Cardiac output (CO) and cardiac index (CI)

The normal CO value is 4 to 8 L/min. CO is the volume of blood in
liters ejected by the heart each minute and is calculated as the
product of the SV and the HR (CO = SV × HR). SV is the volume of
blood ejected by the heart per beat. Normal SV is 55 to 100 mL/beat.
The CO is commonly individualized in relation to body size by
dividing the CO by the body surface area (BSA) to obtain the value
known as the CI. The normal CI is 2.5 to 4 L/min/m2. If continuous
CO monitoring is done, the machine obtains an average CO that is
recorded over 3-minute intervals and updated every 30 to 60
seconds. CCO monitoring closely and accurately monitors the
patient’s hemodynamic profile. Benefits of CCO monitoring may
improve response to changes in output, resulting in improved
outcomes for patients who are severely ill (e.g., cardiomyopathy,
ejection fractions less than 20%). CO reflects the overall

229
management of preload, afterload, contractility, and HR. The
presence of intracardiac shunts renders CO measurements invalid,
because pulmonary and systemic blood flows are erratic and
unequal.

Left atrial pressure (LAP)

The normal value for LAP is 8 to 12 mm Hg. LAP is the most direct
measure of the volume within the left ventricle at the end of
diastole (LVEDP). LAP monitoring is not commonly used. A small,
semirigid catheter is inserted into the left atrium during cardiac
surgery and brought through the chest wall or epigastric area.
Continuous monitoring of LVEDP may be indicated for the cardiac
surgery patient with significant pulmonary hypertension. PAOP is
no longer reflective of left-side heart function when severe
pulmonary hypertension is present. Because the catheter enters
directly into the left atrium, the patient is at high risk for air or
tissue emboli. An in-line air filter should be added to the flush
system to reduce the risk of air emboli. If the waveform pattern
dampens, the catheter should be aspirated until blood is seen. If
there is no blood return, consult the physician. It is not advisable to
flush the LA catheter because of the risk of inducing arterial air
embolism.

Calculated or derived measurements

All hemodynamic readings can be adjusted to body size by
dividing the direct reading by the BSA. It is sometimes beneficial to
use indexed values to gain a clearer idea of the normalcy of the
hemodynamic profile. On first glance, a profile may appear
relatively normal, but when indexed, numerous values are found
out of normal range (see Table 1-10).
In addition to indexed values, various other calculations are done
to help guide therapies (as follows).

Systemic vascular resistance (SVR)

The normal value for SVR is 800 to 1200 dynes/s/cm5. SVR is the
major factor that determines LV afterload or resistance that must be
overcome before LV ejection. The formula for SVR is: SVR = (MAP −
CVP)/CO × 80.

230
 Any factor that increases SVR will increase the workload of the
heart and may reduce CO. Vasodilator therapy is used to reduce
SVR to normal limits. A low SVR can indicate systemic
vasodilation, commonly seen with septic, anaphylactic, and
neurogenic shocks, and seen immediately postoperatively when
recovering vascular tone. Vasopressors and IV fluids are
administered to manage vasodilatation along with medications
directed at the cause. Patients with low SVR often have high CO as
a result of low resistance to ventricular ejection. Medications may
affect SVR: norepinephrine, vasopressin, and phenylephrine (Neo-
Synephrine) increase it, whereas isoproterenol, nifedipine,
prostaglandins, sodium nitroprusside, and acetylcholine decrease
it.

Pulmonary vascular resistance (PVR)

The normal value is 150 to 250 dynes/s/cm5. PVR measures RV
afterload or the resistance the right ventricle must overcome to eject
into the pulmonary circulation. The formula for PVR is: PVR =
(PAM − PAOP)/CO × 80.
PVR may be elevated as a result of primary pulmonary
hypertension or secondary pulmonary hypertension resulting from
mitral or aortic valve disease, congenital heart disease, long-
standing LV heart failure, hypoxia, COPD, or pulmonary embolus.
Medications may affect PVR: norepinephrine, vasopressin, and
phenylephrine increase it, whereas isoproterenol, nifedipine,
prostaglandins, sodium nitroprusside, and acetylcholine decrease
it.

Mixed venous oxygen saturation

The normal range for SVO2 is 60% to 80%. SVO2 is defined as the
average percentage of Hgb bound with O2 in the venous blood,
which infers the balance of O2 supply and demand at the tissue
level. SVO2 reflects the global mixed venous oxygen saturation.
Other specialized catheters can measure the venous oxygen
saturation regionally. SVO2 measures the mixed venous oxygen
saturation from blood returned from the head and neck. This
regional measurement correlates with SVO2 and all of the

231
considerations discussed with SVO2 also apply to ScVO2. Traditional
belief was that hemodynamic stability and normal ABG levels
meant O2 delivery (DO2) to tissues was adequate to meet and
address cellular O2 needs. As technology developed, it became clear
that conventional methods were unable to measure cellular O2
needs (O2 demand) or use (O2 consumption) by assessing O2
delivery alone. With the development of monitors displaying SVO2
continuously, the onset of O2 supply/demand/consumption
imbalance can be more readily identified. SVO2 can be measured
intermittently using mixed venous blood samples from the distal
port of the PA catheter or continuously using a specialized fiber
optic SVO2 PA catheter. CO, Hgb level, and arterial O2 saturation
impact O2 delivery. SVO2 is reflective of O2 delivery and
consumption. If O2 delivery is inadequate, or O2 demand is high,
more O2 will be extracted from Hgb. If the patient is anemic, there
are fewer red blood cells carrying oxyhemoglobin, thus more O2 is
extracted. If the patient has pulmonary disease, such as ARDS, O2
saturation is less, thus less O2 is delivered. Normal O2 delivery is
600 mL O2/min/m2 if CO, Hgb level, and O2 saturation (SaO2 or
SpO2) are normal. Normal O2 consumption ( O2), which should
mirror demand, is 150 mL/min/m2, which means 450 mL/min/m2 of
O2 should be left in the red blood cells returning to the heart. In
other words, approximately 25% of O2 is used, leaving behind
approximately 75%. The textbook normal value for SVO2 is 0.75, or
75%. Very low levels (less than 30%) indicate poor perfusion and
are often associated with lactic acidosis (see Acid-Base Balance). If
the SVO2 value changes by more than 10% for longer than 10
minutes, the nurse should evaluate SaO2, CO, Hgb, and O2. SVO2
monitoring can be used to evaluate the effects of medical and
nursing interventions on tissue O2 use. By examining the variables
involved in tissue oxygenation, the nurse can help determine which
parameters may need to be better managed to meet the current
metabolic demands (Table 1-13).

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Table 1-13
FACTORS AFFECTING MIXED VENOUS OXYGEN SATURATION

Svo2 is a sensitive indicator of oxygen supply/demand balance. Scvo2 will respond in the same
manner as Svo2. If Svo2 decreases to less than 50%, the patient should be rapidly assessed for
the cause of an increased oxygen demand, or decrease in supply. Anemia, hypoxemia, and
decreased CO may result in markedly reduced oxygen delivery. In the presence of the high
metabolic demands imposed by critical illness, a reduction in O2 delivery or further increase in
O2 demand can produce profound instability in the patient. Changes in Svo2 often precede
overt changes reflective of physiologic instability.
Factor Effect Clinical Examples
on
Svo2
Arterial Oxygen Saturation
↑ Sao2 ↑ Supplemental oxygen
Svo2
↓ Sao2
↓Svo2 Reduced oxygen supply (e.g., ARDS, ET suctioning, removal of
supplemental oxygen, pulmonary disease, asthma, respiratory failure,
obstructive sleep apnea)
Cardiac Output
↑ CO ↑ Administration of inotropes to increase contractility
Svo2
↓ CO ↓ Dysrhythmias, increased SVR, MI, hypovolemia, ↑HR, or ↓HR
Svo2
Hemoglobin
↓ Hgb ↓ Hemorrhage, hemolysis, severe anemia in patients with cardiovascular
Svo2 disease
Oxygen Consumption
↑ Vo2 ↓ States in which metabolic demand exceeds oxygen supply (e.g., shivering,
Svo2 seizures, hyperthermia, hyperdynamic states)
↓ Vo2 ↑ States in which there is failure of peripheral tissue to extract or use oxygen.
Svo2 Significant peripheral arteriovenous shunting: cirrhosis, renal failure.
Redistribution of blood away from beds where oxygen extraction occurs:
sepsis, acute pancreatitis, major burns.
Blockage of oxygen uptake or use: cyanide poisoning (including
nitroprusside toxicity), carbon monoxide poisoning.
Mechanical ↑ Wedged PA catheter creates falsely elevated Svo2
problems Svo2

ARDS, Acute respiratory distress syndrome; CO, cardiac output; ET, endotracheal;
Hgb, hemoglobin; HR, heart rate; MI, myocardial infarction; PA, pulmonary artery;
SVR, systemic vascular resistance.

Stroke volume variability (SVV)

SVV is determined using the arterial waveform to calculate the
change in SV from beat to beat of the heart. SVV can assist the
clinician in assessment of the need for fluid replacement and the

233
adequacy of the volume delivered. The normal range for SVV is
10% to 15% with the goal of therapy 13% or less.

The accuracy of stroke volume variability (SVV) has only

been studied on patients with mechanically controlled ventilation.
The SVV is not an accurate measurement when the patient is
having dysrhythmias.

Collaborative management
The need for accuracy of hemodynamic values cannot be stressed
enough. Making clinical decisions based on these values and the
calculations derived from them is the reason for using
hemodynamic monitoring in patients who are critically ill.
Continuous monitoring of hemodynamic and oxygen use values
allow the clinical team to see trends so that they can intervene
earlier and accurately monitor response to treatment.

Care priorities

1. Promote patient safety by meticulously managing the

monitoring system, assessing the pressure
readings/waveforms, and assessing the patient (see table 1-
11).

• Ensure proper setup and maintenance of the pressure monitoring

system. Assessment of PAOP provides information about the
blood being pumped from the left side of the heart, as does the
CO. In combination with BP readings, the values frame the
treatment plan. Configuration of normal waveforms must be
understood so that abnormalities can be recognized, analyzed,
and managed.

• Assess for proper system compliance. Before initiating

monitoring, and any time overdamping or underdamping is

234
 suspected, square wave testing is done to assess proper
compliance within the system, which is essential for accurate
readings.

• Prevent pulmonary infarction. A continuous PAOP waveform

with the balloon deflated indicates that the catheter has migrated
distally and is lodged in a small pulmonary vessel. The chest
radiograph may reveal that the catheter is visible beyond the
mediastinal structures, which indicates that the catheter has
passed too far into the distal pulmonary circulation. The catheter
should be repositioned immediately according to institutional
protocol to avoid damage to the surrounding lung tissues.

• Prevent limb ischemia. Before radial artery catheter insertion, the

practitioner should perform the Allen test to ensure that the ulnar
artery is pulsatile. Maintaining all arterial lines should include a
neurovascular assessment distal to the catheter.

• Prevent RV irritation by the catheter. RV waveform instead of the

PA wave indicates improper positioning. The catheter should be
repositioned according to institutional protocol to avoid
ventricular dysrhythmias.

2. Recognize and manage the complications associated

with hemodynamic monitoring equipment.

• Complications of arterial catheters: Arterial thrombosis with

ischemia, infection, infiltration, and blood loss caused by
disconnection. Continuous observation of the arterial line
insertion site for infection and leakage is an essential nursing
responsibility. Monitor and document pulses distal to the
catheter site every 1 to 2 hours. It is important to note the
patient’s baseline BP and to compare left and right cuff BPs with
arterial BPs. Meticulous care should be taken with setup and
maintenance of the arterial pressure monitoring system. If air
enters a peripheral arterial catheter, the distal structures (e.g.,
hand, leg) are at highest risk for ischemic complications caused
by air bubbles lodging in smaller arterial vessels.

235
• Suspected air embolus: Complications are seen more frequently
from venous air emboli, which may happen during any central
catheter insertion, including PA catheters. Symptoms include
acute respiratory distress, apnea, possible wheezing, sudden
hypotension, syncope, hypoxia, cyanosis, possible murmur,
elevated CVP, neurologic deficits, cardiac arrest with asystole,
pulseless electrical activity (PEA), or ventricular fibrillation.
Arterial monitoring systems connected to intraaortic balloon
catheters can cause life-threatening air embolism in the central
circulation, including the aorta, but this is rarely seen in clinical
practice.

HIGH ALERT!
Suspected Air Embolus
The patient should immediately be placed in left lateral
Trendelenburg (head down) position and 100% O2 administered.
Have the patient try to perform a Valsalva maneuver. Aspirate air
from the system: intravenous tubing, arterial line tubing, or the
catheter itself. If severe complications ensue, hyperbaric O2
treatment using the Diving Accident Protocol may be used if
available. Perform cardiopulmonary resuscitation if necessary. Air
can cause stroke or death in the patient.

3. Recognize the characteristics of normal waveforms and

pressure readings.

• Arterial pressure waveform: The upstroke on arterial pressure

waveform represents the rapid ejection phase of ventricular
systole. The anacrotic shoulder (rounded peak) is where the
systolic pressure is measured. The descent represents slowed
ventricular ejection followed by aortic valve closure represented
by the dicrotic notch, followed by runoff of flow systemically
during diastole. Diastolic pressure is measured as the end-
diastolic pressure just before the next systole (see Figure 1-5).

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• PA waveform: Has the same waveform components as arterial
pressure, except that the dicrotic notch represents pulmonic valve
closure, followed by runoff flow in the pulmonary vasculature
during diastole. The PA pressure measurements are taken at the
peak systolic and end-diastolic pressures (see Figure 1-8).

• End-expiratory pressures: Care must be taken to measure and

record all end-expiratory pressures. With positive-pressure
ventilation, these will be at the low point of the wave. With
spontaneous ventilation, end-expiratory pressures are higher
than pressure during inspiration. One must be careful not to
import or just assume that the digital average is an accurate
reading. Readings must be done at end expiration; as with
respiratory fluctuations, values can be off 10 to 20 mm Hg. To
assure accuracy, measurements should be obtained from a
graphic tracing with simultaneous ECG tracing for proper
waveform identification.

• RAP, CVP, and PAOP waveforms: Are composed of an a-wave,

followed by an x descent; a c-wave may look like a notch on the a-
wave or may be a separate wave, followed by a v-wave, and this is
followed by the y descent (see Figure 1-6). The a-wave represents
atrial systole, the c-wave if present represents valvular closure, the
x descent is atrial relaxation, and the v-wave is produced by atrial
filling during ventricular systole as the atrioventricular valve
bulges toward the atrium when the ventricle contracts. The c-
wave is not commonly seen in the PAOP waveform as a result of
the time of retrograde transmission (see Figure 1-9).

• Timing waveforms with the ECG: The a-wave and v-wave are
distinguished by their timing with the ECG. The electrical
conduction of the heart occurs before mechanical contraction.
This is why the RAP/CVP a-wave is found just before the QRS
and the v-wave is found at the T wave. The PAOP wave has
farther to travel to be transmitted; therefore, the a-wave follows
the QRS and the v-wave is found after the T wave and before the
next P wave (see Figure 1-6).

• Cannon waves and large v-waves: ECG correlations are

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 important diagnostic adjuncts, because a-waves are absent in an
atrioventricular junctional or idioventricular rhythm. Large,
abnormal a-waves called cannon waves are caused by the atria
trying to contract against a closed AV valve, which may occur
during atrial fibrillation and complete heart block. PAOP with a
large v-wave is an indication of mitral insufficiency.

• Inflating the PAOP balloon: When obtaining the PAOP, the PA

catheter balloon should be inflated slowly with no more than 1.5
mL of air. The PA waveform should be observed changing to a
smaller PAOP/wedge waveform. No additional air should be
used once the change has begun. Once the PAOP has been
obtained, the balloon should be deflated passively; the syringe is
removed and emptied of air, and then reattached to prevent
accidental balloon inflation (see Figures 1-7 and 1-9).

HIGH ALERT!
Pulmonary Artery Rupture and Occlusion
Overwedging or rapid balloon inflation can cause pulmonary
artery (PA) rupture. Prolonged balloon inflation or PA catheter
migration can lead to balloon rupture, as well as clot formation and
pulmonary infarction. Pulmonary artery occlusive pressure
(PAOP) may be assessed less frequently if a strong correlation is
established between the PAOP and the PA diastolic to avoid
repeated trauma to the pulmonary vessels and to prolong the life
of the balloon. The PA waveform must be continually monitored to
observe for distal migration of the catheter, or proximal
displacement resulting from pulling on the catheter or movement
of the external monitoring system during patient care procedures
(see Table 1-11).

Table 1-11
MECHANICAL PROBLEMS AFFECTING HEMODYNAMIC
MEASUREMENTS

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*
Whenever the amplitude of an arterial or PA waveform decreases, the patient should
first be assessed for hypovolemia or shock.
†
If line has become disconnected or a portion open to air, the patient must be
assessed for any potential air embolus; then, the line should be changed to prevent
sepsis. PA catheters must always be transduced, as it is necessary to assess
catheter migration through waveform analysis. Catheter migration may result in
pulmonary infarction if not identified and managed.
CPR, Cardiopulmonary resuscitation; PA, pulmonary artery; PAOP, pulmonary artery
occlusive pressure; PEA, pulseless electrical activity; RV, right ventricular.

Care plans for hemodynamic monitoring

Deficient knowledge 
related to the rationale for hemodynamic monitoring and procedure for
catheter insertion
Goals/Outcomes: Before and during catheter placement, the
patient or significant other states that they are comfortable with the
rationale for hemodynamic monitoring, procedure for insertion of
lines, and sensations that are experienced during and after the
procedure.
Knowledge: Treatment Regimen.

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Teaching: Procedure/treatment

1. Assess the patient’s knowledge about hemodynamic monitoring.

As indicated, explain to the patient/family that hemodynamic
monitoring measures BP within the body and BP within the heart
and lungs, and gives information about the pumping action of the
heart, which is useful in guiding therapy.

2. Teach the patient about the insertion procedure, emphasizing

that a local anesthetic agent will be used, he or she will not be able
to move during the procedure, and, following the procedure, a
dressing will be applied to the insertion site. For radial arterial
lines, explain that an arm board or other device may be used to
immobilize the wrist. For PA and central lines, explain that a large
drape is placed over the body and face during insertion and a chest
radiograph will be obtained following the procedure.

3. Explain that unusual sensations may be felt during the procedure

and that a nurse will be present to hold his or her hand, offer
support should they have questions, and be able to administer
supplemental medications to promote their comfort. Depending on
the situation, a clue to the next sensation anticipated is best
rendered during the procedure, such as, “You may feel coolness
from the cleansing solution” or, “You may feel a ‘bee sting’ from
injection of the local anesthetic” or, “You may feel pressure as the
catheter advances.”

Risk for ineffective cardiac tissue perfusion 

related to complications from PA catheter presence in the pulmonary
circulation
This includes circulatory impairment from migration of PA
catheter into a wedged position, “overwedging” of the catheter
balloon, PA rupture, pulmonary vascular thrombosis, or other
patient safety hazards associated with the monitoring system.
Goals/Outcomes: Within 15 minutes of recognizing a
complication with the hemodynamic monitoring system, the
problem is addressed and resolved.
Tissue Perfusion: Cardiac; Tissue Perfusion: Peripheral;
Tissue Perfusion: Pulmonary.

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Hemodynamic regulation

1. Monitor the PA waveform continuously. Report any change in

configuration, particularly if the waveform becomes decreased in
amplitude and flattened in appearance (see Table 1-11).

2. Assess the patient for decreased pulmonary arterial blood flow,

as evidenced by acute onset of pleuritic chest pain, SOB, tachypnea,
and hemoptysis.

3. Evaluate the position of the catheter via chest radiograph

according to institutional protocol. Never push the PA catheter
forward in the PA to avoid possibility of PA rupture or lodging the
catheter in a small vessel.

4. Record the position of the PA catheter when inserted. Assess and

record this level every shift. If there is a change in the waveform,
catheter position should be reassessed. The advanced practice
provider should be notified for catheters that are out of position or
fail to wedge.

5. Exercise care in taking PAOP measurements. Prolonged and

repeated readings can cause trauma to the vessel wall. The catheter
can also be “overwedged.” Proper wedging entails slow injection of
enough air to obtain a wedge configuration, but no more than the
amount recommended by the catheter manufacturer. Never pull
back on the plunger of a balloon syringe to remove air; rather,
disconnect the syringe and allow passive deflation of the balloon.

6. Verify and document PAD and PAOP* every 4 to 8 hours. PAD

may exceed PAOP by ≥5 mm Hg in patients with acidosis,
hypoxemia, pulmonary emboli, lung disease, and pulmonary
hypertension. If the PAD approximates the PAOP, the frequency of
PAOP readings may be able to be reduced in some practice settings,
to preserve the catheter balloon and reduce the possibility of vessel
erosion. *Note: In some institutions routine PAOP readings are not
performed and in certain settings the nurse may not perform this
function. Please refer to the institutional policy concerning
hemodynamic monitoring.

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7. Consult the advanced practice provider if the PA waveform
remains in wedged position after balloon deflation. This may
indicate that the catheter has lodged in the vessel, which can lead to
pulmonary infarction resulting from lack of perfusion distal to the
lodged catheter.

8. Pay special attention to the PA waveform when the patient is

moved (e.g., when being taken to the radiology department; getting
into a chair, when position is changed or bed is made). The
monitoring system may no longer be appropriately leveled with the
patient’s phlebostatic axis (RA level) after the patient has changed
position. Assess the catheter position to ensure that the catheter has
not moved. Also ensure the catheter is not pulled on when moving
the patient.

Ineffective protection 
related to inability to control internal responses and external threats posed
by the presence of invasive hemodynamic catheters
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, white blood cell (WBC) count <11,000/mm3,
negative culture results, and absence of erythema, heat, swelling, or
purulent drainage at the insertion site.
Immune Status Uncompromised.

Infection protection

1. Before insertion, full barrier precautions should be in place

according to institution protocol. Central line catheter insertion and
dressing changes are to be done with strict adherence to sterile
technique. Following a central line bundle checklist is
recommended.

2. On a daily basis, monitor for temperature elevations >37.7° C

(100° F) and WBC count elevation.

3. Monitor the catheter insertion site for erythema, tenderness to the

touch, local warmth, and purulent drainage.

4. Use normal saline rather than D5W for hemodynamic flush

242
solution, because dextrose solutions better support bacterial
growth.

5. Change hemodynamic tubing, transducer, and flush solution

according to hospital protocol.

6. Maintain a closed system from the transducer to the flush

solution and the patient. Keep all external openings and stopcocks
securely capped at all times.

7. Use a closed system for CO injection fluid.

8. Maintain an occlusive, dry sterile dressing over the insertion site.

As prescribed, obtain a culture of any suspicious drainage and
report positive findings.

9. Change the central/PA line dressing according to hospital

protocol, using aseptic technique.

10. Record the date of catheter insertion: Ensure that the catheter is
changed according to agency protocol.

11. If the line becomes infected, notify the advanced practice

provider. The catheter should be removed and the catheter tip cut
off and then sent in a sterile container for a culture and sensitivity
test.

Central venous pressure monitoring is the recommended

monitoring strategy during early goal-directed therapy
recommended by the Society of Critical Care Medicine, for patients
with sepsis. Line sepsis may be masked as a potential cause of
current infection. The lines should be changed only as needed
unless reddened, white blood cells are increasing, or the patient is
febrile. Most central lines are able to remain in place for 7 days;
but should be removed as soon as possible when central access or
monitoring is no longer needed.

243
Ineffective peripheral tissue perfusion (involved extremity) 
related to interrupted blood flow secondary to presence of arterial catheter
or thrombosis caused by the catheter.

244
 Goals/Outcomes: Within 15 minutes of this diagnosis, the patient
has adequate perfusion to affected extremity, as evidenced by brisk
capillary refill (less than 2 seconds), natural color, warm skin,
normal sensation, and the ability to move the fingers.
Circulation Status.

Circulatory precautions

1. Continuously monitor capillary refill, color, temperature,

sensation, pulses, and movement. Be alert to indicators of ischemia
and teach them to the patient, stressing the importance of notifying
staff members promptly if they occur.

2. Maintain arterial line on continuous flush at 3 mL/h with normal

saline with the pressure bag inflated to 300 mm Hg. Heparinized
saline is infrequently used, as it has not been shown to be
significantly more effective at maintaining patency, when all other
measures of pressure monitoring are done.

3. Ensure tight connections of tubing throughout the system.

4. Support the patient’s wrist or appropriate extremity with an arm

board or other supportive device to prevent flexion and movement
of the catheter.

Ineffective protection 
related to potential for insertion complications secondary to ventricular
irritability, patient movement during insertion procedure, or difficult
anatomy.
Goals/Outcomes: The patient has no complications from PA or
CVP catheter insertion, as evidenced by normal sinus rhythm on
ECG, BP within the patient’s normal range, HR <100 bpm, RR <20
breaths/min with normal pattern and depth, normal breath sounds,
and absence of adventitious breath sounds or muffled heart sounds.
Circulation Status.

Risk identification

1. Use patient safety precautions used for any invasive procedures

245
to conduct a preprocedure verification process; mark the correct site
and use of “Time Out” to assure patient safety.

2. During preprocedure teaching, caution the patient about the

importance of remaining still during insertion of the catheter.
Provide sedation and analgesics as prescribed.

3. Perform a baseline assessment, monitoring BP, HR, RR, breath

sounds, heart sounds, and ECG.

4. Be alert to decreased BP, pulsus paradoxus, increased HR or RR,

diminished or absent breath sounds, and muffled heart sounds, as
well as dysrhythmias on ECG. Report any significant findings to the
physician or midlevel practitioner.

5. Perform a postprocedure assessment, comparing it with baseline

findings. After the procedure, obtain a chest radiograph as
prescribed.

6. Monitor for catheter-related complications (see Table 1-11).

7. Keep amiodarone or lidocaine at bedside for immediate IV

injection if the patient has sustained ventricular dysrhythmias. This
precaution should be rarely required.

Mechanical ventilation
Mechanical ventilation provides assistance with movement of gases
in and out of the lungs to facilitate blood-alveolar clearance of CO2
and uptake of O2 into the blood. For ventilation to be effective, the
nervous system must be intact, the diaphragm and respiratory
muscle groups must contract, the rib cage must be intact, the
external fibrous level of the pleural sac must be attached to the rib
cage, and intrapleural or intraalveolar pressures should be normal.
This combination of conditions decreases the alveolar resting
pressures, promoting a pressure gradient that facilitates gas
movement into the conducting tubes that ultimately distends
(recruits) the alveoli.
Spontaneous ventilation (whether or not supported) depends on

246
the ability to generate alveolar distention, or negative pressure, and
therefore increases compliance. This is referred to as increasing
alveolar compliance (static compliance), a decreasing alveolar
pressure (pPlat), or negative pressure breathing. There are other
conditions required for patients to generate negative pressure and
breathe spontaneously (Box 1-12). When patients are too weak to
generate adequate force (negative pressure), too weak to maintain
their airway, too sick or sedated to stimulate and contract the
diaphragm, or when the conducting airways or the alveolar units
are constricted, collapsed, or congested (Box 1-13), ventilator
support may be unavoidable. To ensure optimal care of the patient
who requires mechanical ventilation, the practitioner must have
adequate knowledge of the equipment and processes involved in
mechanical ventilation. An exhaustive review of mechanical
ventilation is not possible in this chapter; however, basic concepts
must be addressed.

Box 1-12
FACTORS AFFECTING NORMAL
SPONTANEOUS VENTILATION
1. Having intact phrenic nerve innervation of the diaphragm

2. Ability of the diaphragm and external intercostals to maintain the

appropriate contractile force

3. Ability to maintain a patent airway

4. Diameter of the airway

5. Ability of the alveoli to open during inspiration

Box 1-13
CONDITIONS THAT MAY REQUIRE
VENTILATOR SUPPORT

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Acute obstructive disease: acute severe asthma; airway mucosal
edema

Altered ventilatory drive: hypothyroidism; intracranial

hemorrhage; dyspnea-related anxiety

Atelectasis: acute respiratory distress syndrome; pneumonia

Burns and smoke inhalation: inhalation injury, surface burns

Cancer: malnutrition; infections

Cardiopulmonary problems: congestive heart failure; pulmonary

hemorrhage

Chest trauma: blunt injury; flail chest; penetrating injuries

Chronic obstructive pulmonary disease: emphysema, chronic

bronchitis, asthma; cystic fibrosis; bronchiectasis

Fatigue/atrophy: muscle overuse; disuse

Head/spinal cord injury: medullary brainstem injury; Cheyne-

Stokes breathing; neurogenic pulmonary edema

Neuromuscular disease: amyotrophic lateral sclerosis; Guillain-

Barré syndrome; myasthenia gravis

Postoperative conditions: cardiac and thoracic surgeries

Pharmacologic agents/drug overdose: muscle relaxants;

barbiturates; Ca2+ channel blockers; long-term
adrenocorticosteroids; aminoglycoside antibiotics

Review of basic ventilation terms

Respiratory rate (RR or f [frequency of breathing])

248
• Charted as breaths per minute.

• The frequency of breaths enabled by the patient and/or delivered

by the ventilator may range from 10 to 50 bpm depending on
ventilation strategies, except during weaning, when the
frequency of breaths may be less than 10 to augment, rather than
fully support, breathing.

Tidal volume (VT)

• Volume (amount) of gas delivered with each preset breath.

Controversy exists regarding use of lung protective tidal volumes
on all patients, versus those solely with noncompliant lung
conditions. Predicted body weight (PBW) is often used to
calculate Vt, rather than ideal body weight (IBW). The formula is
as follows: Males: PBW (kg) = 50 + 2.3 (height [in] – 60); Females:
PBW (kg) = 45.5 + 2.3 (height [in] – 60). PBW and IBW are similar
values.

• In patients who are mechanically ventilated, VT is usually set at 8

mL/kg PBW according to the National Heart, Lung, and Blood
Institute ARDS Network (www.ardsnet.org).

• VT decreases to 6 mL/kg IDBW or PBW if the patient has a

noncompliant lung condition.

• Many clinicians have successfully used strategies to

treat ARDS by reducing the delivered tidal volume
(from 8 to 10 mL/kg IBW to 4 to 6 mL/kg IBW)
balanced with an RR (12 to 35) necessary to
maintain adequate minute ventilation. Lung-
protective ventilator strategies are considered
standard practice in the care of patients with ARDS.
Level of positive end expiratory pressure (PEEP)
and fraction of inspired oxygen (FIO2) are adjusted
in tandem with Vt to provide the most effective gas

249
 exchange, while helping to reduce the incidence of
ventilator induced lung injury.
• Charted as: VT or tidal volume (i.e., 375 mL/breath).

Minute ventilation (Ve VTE or M )

• The amount of volume exhaled per minute (VE or VTE).

• Measured as: Respirations × VTE (MV).

• Normal is 8 to 10 L/min.

Fraction of inspired oxygen (Fio2)

• Percent of atmospheric pressure (760 mm Hg) that is O2.

• For example, 0.21 or 21% is calculated as: 0.21 × 760 mm Hg = 159

mm Hg Patmos O2.

• For simplicity, documented as Fio2, use the decimal (0.21) in P/F

calculations or the calculated pressure in A-aDO2 calculations.

Peak inspiratory pressure (PIP)

• Peak pressure measured when the tidal volume is pushed into the
airways. The value is also called peak airway pressure (PAP).

• Value used to set high-pressure and low-pressure alarm limits.

• In normal lungs (resistance and compliance normal) less than 35

cm H2O.

• In any condition that increases resistance or decreases

compliance, may be greater than 35 cm H2O.

Mean airway pressure

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• Average proximal airway pressure during the entire respiratory
cycle; a major determinate for oxygenation and a focus for the
settings of alternative ventilation.

Pressure measured during inspiratory hold (Pplateau or

Pplat)

• Airway pressure measured during an inspiratory hold after a

volume-controlled breath.

• Used to determine the patient’s static lung compliance.

• Normally less than 25 cm H2O.

Flow rate ( )
• The delivery method and rate of speed for the tidal volume
breath (also affects time spent in inspiration versus exhalation, as
well as pressure reached).

• Normally 40 to 60 L/min.

All airway pressures, including peak inspiratory pressure,

pulmonary artery wedge pressure, and pPlateau, are measured by
changing the tidal volume, airway resistance, and peak inspiratory
flow rate. Pressures are also significantly affected by alterations
in lung compliance.

Trigger: What starts a breath? Inspiratory flow begins

• Elapsed time: How many breaths per minute?

• Patient effort: Negative inspiratory force: The patient’s effort can

be “sensed” as a change in pressure or a change in flow (in the

251
 circuit).

Sensitivity
• A setting on the ventilator that adjusts how much negative
inspiratory pressure the patient must generate (see Patient effort)
before the ventilator delivers a breath. Is activated only in assist-
control ventilation (ACMV) or synchronized intermittent
mandatory ventilation (SIMV).

Cycle: What stops a breath? Inspiratory flow ends

1. Pressure cycle: A predetermined and preset pressure terminates
inspiration. Pressure is constant/volume is variable. Used for
pressure control ventilation.

2. Volume cycle: A predetermined and preset volume when

delivered terminates the inspiration. Volume is constant/pressure is
variable. Used for volume control ventilation.

3. Time cycle: Delivers air/gas over a set time after which the
inspiration ends (affects the I:E)—inspiratory time/exhalation time
(I:E).

• Directly related to how rapidly or slowly the flow of

tidal volume occurs.

• Directly related to the pressure achieved when

volume is delivered at a certain rate of speed.

4. I:E time examples.

• If an assumed tidal volume of 400 mL/breath is

delivered at a flow rate (rate of speed) of 80 L/min,
either volume or pressure control limits will be
reached rapidly and “inspiratory (I) time” will be

252
 shorter and “exhalation (E) time” will be longer.
This strategy is used in compliant lungs when CO2
retention or ventilator dyssynchrony is evaluated.

• If an assumed tidal volume of 400 mL/breath is

delivered at a flow rate (rate of speed) of 40 L/min,
either volume or pressure control limits will be
reached over a longer period of time and “I time”
will be longer and “E time” will be shorter. This
strategy may be used to recruit alveoli when lungs
are noncompliant and hypoxemia is the problem,
that is, low oxygen and high pressures are an issue.
The expectation is that the pressure generated when
the tidal volume flows will be lower.

• If an assumed tidal volume of 400 mL/breath is

delivered at a flow rate (rate of speed) of 100 L/min,
either volume or pressure control limits will be
reached over a shorter period of time and “I time”
will be shorter and “E time” will be longer. This
strategy may be used to allow for more time to
exhale and is generally used if the expectation is
that the pressure generated when the tidal volume
flows will be lower, but that the patient’s major
problem is alveolar recoil (i.e., COPD disease).

Negative pressure ventilation

Normal intrapleural pressure ranges from −2 (rest) to −10 cm H2O
(inspiration). Negative pressure ventilators generate

253
subatmospheric pressure to the thorax and trunk (similar to
applying an external vacuum) to initiate respiration and do not
require intubation for use. The iron lung, chest cuirass shell, and
poncho chest shell are examples. Because these devices are
noninvasive and do not require intensive monitoring, there has
been a resurgence of interest in their use for long-term home
therapy. They are not discussed here.

Positive-pressure ventilation
All methods of mechanical ventilation require a means of
administering positive pressure for delivery of a predetermined
volume of gas. Positive-pressure ventilation creates a super
atmospheric pressure (greater than 760 mm Hg), which is generated
at the upper airway. The resultant pressure gradient between the
upper airway and the alveoli then allows for the “pushing” gas
volume. This delivery system may be administered via a mask
system (noninvasive) or invasively via an ET tube or tracheostomy.
The concept, put very simply, is to decrease the need for the
development of a significant negative pressure or force,
supplanting that requirement with the super atmospheric pressure.

Noninvasive positive-pressure ventilation

(NiPPV or NPPV)
Positive-pressure support may be administered via a face mask,
nasal mask, helmet, or mouth seal. This may also be presented as
CPAP or BiPAP. The early application of NPPV or noninvasive
mechanical ventilation (NIMV) may enhance respiratory rescue and
may be applied by trained providers outside of ICU. Indications
include airway obstruction disorders, chest wall disease,
neuromuscular weakness, and sleep-related breathing disorders.
Currently, NPPV is contraindicated in patients who cannot protect
their airway or clear secretions and those with severe agitation or
shock. NPPV may allow patients to maintain normal functions,
such as speaking and eating, and assists in the avoidance of the
risks and complications of intubation and sedation. Patients who
are severely distressed may be dependent on the system, and may

254
be unable to remove the system to eat or drink without
deterioration. Consideration for additional support is needed when
patients cannot remove the system for short periods of time.

1. CPAP: A mode of assistance with positive pressure via

application of a constant pressure to the airways. This method does
not supply any volume breath, but rather maintains airway and
alveolar opening to facilitate inspiration and decrease collapse
during exhalation. Very similar in concept and design to methods
applied for sleep apnea.

2. BiPAP: A mode of ventilatory assistance that uses alternating

inspiratory positive pressures (IPAP) and expiratory positive
pressures (EPAP) to enhance variable spontaneous tidal volumes.
The resistance and compliance of the airways will determine the
IPAP “driving pressure” necessary to produce a desired tidal
volume. The level of EPAP needed is based on the oxygenation
status of the patient. The physician determines a tidal volume goal
(usually 8 to 12 mL/kg) and an oxygenation goal the clinician will
use to determine the titration range for IPAP, EPAP, and Fio2.
BiPAP (may be referred to as BiLevel) mode can be found on many
conventional ventilators and on freestanding units used for NPPV.

Invasive mechanical ventilation

When endotracheal intubation is required (Box 1-14), the oral route
is generally preferred to nasal, to reduce incidence of sinusitis. After
intubation, the nurse or respiratory therapist should do the
following:

1. Confirm the placement of the ET tube using a CO2 detector and

then auscultate for bilateral breath sounds.

2. Mark and chart the centimeter mark on the tube using the teeth
as a reference point.

3. Secure the tube to the face and head.

4. Cut/shorten the tube to reduce dead space, taking care not to cut

255
the pilot balloon, so only 4 cm protrudes from the teeth.

5. Over the next 4 hours, monitor for the development of a life-

threatening tension pneumothorax, by assessing for hypoxia,
bradycardia, tachycardia, and moderate to life-threatening
hypotension.

Box 1-14
REASONS TO CONSIDER INTUBATION
Severe acidosis or hypoxemia

Severe dyspnea

Respiratory arrest

Cardiovascular instability

Aspiration risk

Copious/viscous secretions

Recent facial trauma

Extreme obesity

Basic ventilation modes

Assist-control ventilation (A/C or ACV)
This mode can be used with either volume of gas or pressure within
the patient/ventilation system as the limit used to end inspiration,
or breath limit. In assist-control (often labeled “volume control,” or
“pressure control”), patients may receive either ventilator-
controlled or ventilator-assisted breaths. The set rate will deliver
breaths in a time line (i.e., rate of 12 ventilator delivers breaths 12
times per minute). In addition, when the patient generates a natural

256
breath, the machine senses the negative-pressure event (sensitivity
set on the ventilator), which triggers the ventilator to deliver a
breath of identical duration and magnitude as the mandatory
breath. The patient receives a breath each time a spontaneous
breath is initiated, regardless of actual minute ventilation
requirement. The “interactive” feature of this mode is that the
patient receives a breath when he or she generates enough negative
pressure to turn the ventilator on. The advantage of this mode is
that patients breathe spontaneously with small amounts of work.
Conventional assist-control (A/C) delivers a preset breath based on
time intervals (defined by frequency). The inspiratory flow rate is
measured in liters per minute, and it determines how quickly the
breath is delivered. The time required to complete inspiration is
determined by the tidal volume delivered and the flow rate: Ti =
VT/Flow rate. The breath is limited by reaching either the preset
volume (volume control [VC]) or pressure (when volume is
delivered reaching a predetermined pressure [pressure control,
PC]). Every breath is controlled (either pressure or volume), but the
patient may take more breaths than the mandatory rate determines
(Table 1-14).

Table 1-14
VOLUME-CONTROLLED VERSUS PRESSURE-CONTROLLED
MECHANICAL VENTILATION

Volume Control Pressure Control

Volume delivery constant Volume delivery varies
Inspiratory pressure varies Inspiratory pressure constant
Inspiratory flow constant Inspiratory flow varies
Inspiratory time determined by set flow and VT Inspiratory time set by clinician

ALL breaths in ACMV are ventilator-assisted: Set rate plus

patient-generated request (effort).

Every breath, whether ventilator-determined or patient-

requested, is a ventilator breath and predetermined for either

257
pressure or volume control.

Control mode should never be deliberately set because

ventilators should never be insensitive to a patient’s inspiratory
effort. New ventilators do not incorporate a pure “control”
method, although the rate predetermined by the provider in
conjunction with sedation and analgesic management will
essentially “control” the patient. Controlling ventilation is related
to the context and must be attributable to the loss of sympathetic
and parasympathetic drive (i.e., spinal cord injury) or
pharmacologic control.

Synchronized intermittent mandatory ventilation

(SIMV)
Delivers a preset mandatory volume-controlled or pressure-
controlled breath at a preset rate. The patient can also breathe
spontaneously (at his or her own rate with a variable tidal volume
and pressure) between mandatory ventilator breaths from a flow-
by circuit. The difference between ACMV and SIMV is that in SIMV
the patient may take spontaneous nonventilated breaths between
the required ventilator breaths. In addition, the ventilator is
synchronized to deliver the mandatory breath (controlled volume
or pressure) when the patient initiates inspiration; however, if time
is reached when mandatory breath must be administered, it will be
done even if the patient has not initiated his or her own negative
inspiratory effort. SIMV is generally administered in conjunction
with pressure support, which is applied on spontaneous flow-by
breaths.
Only set rate breaths in SIMV are ventilator-assisted: Set rate plus
patient-generated request (effort).

258
 Only set breath is a ventilator breath and predetermined for
either pressure or volume control. All patient breaths are
volume/pressure variable.

All providers should analyze the methods and modes of

ventilation support and consider the use of synchronized
intermittent mandatory ventilation and the flow rate before
administration of sedatives to control the patient and/or reduce
their efforts. Frequently, agitation will be present if the flow rate
of the gas is too low or if the patient feels like he or she cannot
control his or her own breathing. After consideration of flow and
mode, sedation may be used to decrease respiratory drive, and
machine sensitivity should be adjusted to prevent hyperventilation
in patients whose respiratory rate increases because of mild
anxiety or neurologic factors. Assist-control ventilation has
effectively replaced controlled ventilation, because the control of
respiratory efforts must be performed pharmacologically and not
mechanically.

Pressure support ventilation (PSV)

PSV augments or supports the patient’s spontaneous inspiration
with a preselected pressure level. Pressure is applied (via flow of
gas) at the initiation of inspiration and ends when a minimum
inspiratory flow rate is reached. The patient retains control over
inspiratory and expiratory time, frequency, tidal volume, and
spontaneous minute ventilation. PSV creates less patient discomfort
and diaphragmatic stress than assist-control or SIMV alone.
Compensating for resistance created by the demand valve or ET
tube size decreases inspiratory work. PSV MUST be combined with
SIMV to improve patient tolerance of mechanical ventilation, to
overcome the resistance offered by the ET tube (tube
compensation), and to decrease the work of breathing through the
ET tube. PSV is often used to facilitate weaning from mechanical
ventilation.

259
 These two methods are flow-triggered/limited and (pressure) and
volume-controlled. In ACMV when the patient takes a breath, the
controlled method (volume) turns on. In SIMV when the patient
takes a breath, the breath may either be a synchronized ventilator
breath or a spontaneous volume breath.
Mode and method of ventilation should be determined by
patient need and provider expertise rather than by individual
bias.

Breath limit
• Time limited or cycled: Relates to time that inspiratory flow is
administered and is determined by a preset time or percent of
cycle that relates to inspiration. Inspiratory time is increased to
deliver a volume-controlled or pressure-controlled breath over a
longer time of the breath cycle. Depending on the manufacturer,
inspiratory (I) and expiratory (E) times or flow rate may be the
direct setting to adjust. In either case, the provider may maintain
the tidal volume, minute ventilation, and frequency when
adjusting the E time. I time is increased to deliver a volume-
controlled or pressure-controlled breath over a longer time of the
breath cycle. This will affect the frequency and therefore the tidal
volume delivered. This may be used for noncompliant lungs and
alveolar recruitment to promote better oxygenation and is
referred to as inverse I to E.

• Pressure controlled (PC): The peak inspiratory pressure (PIP) is

preset based on the estimated tidal volume requirements. A
smaller tidal volume may be given if the preset pressure is
reached too soon, such as in a state of low compliance or high
airway resistance.

• Volume control (VC): Volume is preset and the pressure is

variable to deliver the preset volume. The PIP seen at the end of
inspiration is higher under conditions of low compliance and/or
high airway resistance.

A comparison of ventilator strategies and variables is available in

Table 1-15.

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Table 1-15
MODES OF MECHANICAL VENTILATION

PCV, Pressure-controlled ventilation; PSV, pressure support ventilation; SIMV,

synchronized intermittent mandatory ventilation; VCV, volume-controlled ventilation.

Airway pressure and lung volumes have a DIRECT impact

on the intrathoracic pressure, which then may decrease blood flow
and blood pressure and INDIRECTLY affect different organ
systems.

Basic ventilation adjuncts

Positive end-expiratory pressure (PEEP) and alveolar
mechanics
The application of trapping of fresh gas (flow) is known as PEEP.
PEEP increases functional residual capacity (FRC) and compliance
while decreasing dead space ventilation, shunt fraction, and is very
effective for recruitment of atelectatic alveoli, as well as for
equalizing opening pressures in alveoli that are filled with fluid.
PEEP does not improve lung function as a result of poor perfusion
and may affect the perfusion of lung capillaries. As the alveolar
pressure rises, the vessels are compressed and pulmonary blood
flow is reduced. There may be a decrease in RA filling, which also
affects overall perfusion. In hemodynamically unstable patients,

261
application of or increase in PEEP may prompt a decrease in BP.
Generally, PEEP pressures range from 2.5 to 20 cm H2O. Higher
pressures (greater than 24 cm H2O) may be used if the patient can
tolerate the increase and if the condition is warranted. Tolerance is
primarily determined by monitoring BP and regularly assessing for
a pneumothorax.
The role of PEEP in lung ventilation is to stabilize alveoli,
decreasing alveolar collapse, and promoting better gas exchange.
PEEP is applied when the exhalation valve in the circuit closes,
promoting lung trapping of gas (refreshed), which is then measured
as pressure sustained at the end of expiration. When PEEP is
increased, the valve closes earlier. In lung-protective ventilation,
PEEP allows for better distribution of gas over a larger open lung
surface, while preventing alveolar over distention. Gattinoni et al.
showed that injured lungs have less lung surface, which
participates in ventilation, and the application of PEEP in this
diagnosis can open collapsed alveoli and prevent the shear stresses
caused by alveolar recruitment/derecruitment. In the open lung
approach, alveoli and small airways are stented open with a
constant airway pressure. This allows the breath to reach more
functional surface area early in inspiration, as alveolar opening is
maintained by the application. PEEP promotes better gas exchange,
increases the P/F ratio, and allows for reduction of Fio2, and is
frequently used in conjunction with mechanical ventilation to
improve oxygenation. Clinical improvements are reflected by
increased partial pressure of O2 in arterial blood (PaO2) and the
ability to decrease Fio2.
Application of PEEP increases intrathoracic pressure and can
compromise the patient’s hemodynamic status by compressing the
heart and great vessels. Increased intrathoracic pressure decreases
venous return, RV-filling pressures, and CO, which may cause or
potentiate hypotension and shock. Patients with intravascular
volume depletion are at higher risk for associated hemodynamic
instability. High levels of PEEP can cause pneumothorax,
particularly if lung compliance is diminished. The understanding
gained through the study of alveolar mechanics would suggest that
an open lung approach might minimize shear stress and improve

262
oxygenation. Multiple modes of ventilation will allow for open lung
ventilation: high-frequency oscillatory ventilation (HFOV), airway
pressure-release ventilation (APRV), and alveolar recruitment
maneuvers (high levels of PEEP applied for short times to open
collapsed alveoli), followed by the application of PEEP. The
decision-making strategies for patient management are discussed in
Table 1-16.

Table 1-16
FACTORS CONSIDERED WHEN CHOOSING MODES OF
VENTILATION

Gas Exchange Ventilation Effect Airway Compliance

Fio2 >0.35 Vital capacity >10 to 15 mL/kg body weight Tidal volume >325 mL
Pao2 >60 mm Hg Maximal negative inspiratory pressure Tidal volume/body
weight >4 mL/kg
A-a Pao2 gradient <−30 cm H2O Dynamic compliance
<350 mm Hg >22 mL/cm H2O
Pao2/Fio2 ratio >200 Minute ventilation <10 L/min Static compliance >33
mL/cm H2O
Maximal voluntary ventilation more than twice
resting minute ventilation

Clinicians should be prepared for a narrowing pulse

pressure, decreasing stroke volume, blood pressure, and cardiac
output when positive end-expiratory pressure levels are increased.
Hemodynamic changes may include volume resuscitation and/or
inotropic support to correct the decrease in blood pressure and
cardiac output.

Low tidal volume/protective lung

ventilation/permissive hypercapnia
The strongest evidence-based methods for mechanically supported
ventilation are reflected in the work of the ARDS Network. Low
tidal volumes used with PEEP levels high enough to open a
possibly recruitable lung may allow the most injured portions of the

263
lung to “rest” until the resolution of the underlying lung injury.

A methodolog approach to low tidal volume, Fio2, and PEEP can be

accessed at
http://www.ardsnet.org/system/files/Ventilator+Protocol+Card.pdf

Calculation of predicted or ideal body weight (PBW or IBW) can be

performed with the automatic calculator at ARDSnet:
http://www.ardsnet.org/node/77460.

Formulas:

1-1
RESEARCH BRIEF BOX
Higher positive end-expiratory pressure (PEEP) should be used for
moderate and severe acute respiratory distress syndrome (ARDS),
whereas lower PEEP may be more appropriate in patients with
mild ARDS. PEEP should be set to maximize alveolar recruitment
while avoiding overdistention. Volume and pressure limitation
during mechanical ventilation can be described in terms of stress
and strain. Fraction of inspired oxygen and PEEP are typically
titrated to maintain arterial oxygen saturation (SpO2) of 88% to 95%
(PaO2 55 to 80 mm Hg).

From Biehl M, Kashiouris MG, Gajic O: Ventilator-induced lung injury: minimizing its
impact in patients with or at risk for ARDS. Respir Care 58(6):927-937, 2013.

Additional modes of mechanical ventilation to promote

alveolar recruitment
This discussion is designed to introduce alternative ventilatory
methods. It is beyond the scope of this book to perform a
substantive manual of alternative techniques.

264
 When Fio2 is at a toxic level (levels of oxygen that promote radical
byproducts, which may actually cause alveolar lining destruction),
it may be of vital importance to consider alternative strategies
designed to increase the functional lung surface available for gas
exchange. The following list is a small sample of current and
experimental ventilator modes designed to optimize MAP and
alveolar recruitment.

Inverse ratio ventilation (IRV)

During IRV, the inspiratory phase is prolonged (as the flow rate is
low for a given volume or pressure) and the expiratory phase is
shortened. Normal inspiration/expiration (I/E) ratio is 1:2 to 1:4.
During IRV, the inspiratory phase of the I:E ratio is increased to
greater than 1:1 (e.g., 2:1), thereby promoting alveolar recruitment
through achieving a more constant MAP (at the level required for
alveolar opening), which improves oxygenation by keeping alveoli
open for longer periods of time. The patient will require
administration of sedation, analgesia, and possibly a paralyzing
agent to minimize the discomfort and anxiety associated with this
unusual breathing pattern.

Airway pressure-release ventilation (APRV or BiVent)

APRV is basically a set level of CPAP that intermittently releases
(valve open) to a lower level using a time-controlled release valve.
High CPAP and lung volumes are reestablished when the release
valve closes. The principle of reducing lung volume distinguishes
this technique from other modes of ventilation. APRV always
implies a reverse I:E ratio because it uses a very short low-pressure
time (for removal of CO2) for pressure release. APRV is a mode
with two basic methods applied: PC/IRV (via a BiPAP method) and
SIMV. First, it appears similar to PC/IRV as it uses a high-pressure
time that may be relatively long and a low-pressure time that is
profoundly short. The inverse times promote a constant airway
pressure and an intrinsic PEEP (auto-PEEP) to optimize
oxygenation. An inspiratory time (T HIGH) and an expiratory time
(T LOW) are set, as well as inspiratory pressure (P HIGH) and
expiratory pressure (P LOW). During the high time, the patient may
breathe spontaneously as well as receive ventilator breaths, which

265
will be synchronized whenever possible (SIMV). Spontaneous
breathing is not required, but facilitated. No breathing occurs
during low time until weaning begins.

Bilevel ventilation
BiLevel is a method of switching between low-pressure and high-
pressure limits based on the patient’s inspiration and exhalation. In
BiPAP, the circuit switches between a high-airway and low-airway
pressure in an adjustable time sequence. If the patient is not
breathing spontaneously, the I:E ratio and the ventilatory frequency
can be adjusted to optimize ventilation and oxygenation. If the I:E
ratio is reversed, then APRV has to be set up, and mandatory
breaths can be applied. Breathing is allowed during both high-
pressure and low-pressure times. Airway pressure is not as well
controlled. BiLevel can be used initially as pressure-controlled
ventilation, can be weaned to BiPAP, and then weaned to CPAP
before extubation.

High-frequency oscillatory ventilation (HFOV)

Recently, this mode of ventilation has received much more
attention for use in the adult population. HFOV uses very small
tidal volumes (not really tidal volume, but rather amplitude,
termed Delta P:P) usually equal to, or less than, the dead space (150
mL) to maintain a continuously high alveolar opening pressure.
“Breaths” are administered at a very fast rate (Hertz [Hz] set at 4 to
5 breaths per second). Given that large tidal volumes in ARDS
cause alveolar stress (via continuously opening and closing alveoli),
in theory, very small, rapid tidal volumes used in HFOV should be
protective because alveoli are no longer fully closing, and are
continuously recruited by the higher constant airway pressure.

Adjuncts to mechanical ventilation

Autoflow is an advance in volume-controlled modes of mechanical
ventilation. The ventilator automatically regulates inspiratory
flow. This autoregulation works in conjunction with the set tidal
volume and the patient’s lung compliance.

266
Mandatory minute ventilation or minimum minute ventilation
(MMV) provides a predetermined minute ventilation to augment
the patient’s spontaneous minute ventilation (breathing efforts).
It is used to prevent hypoventilation and respiratory acidosis
during ventilator weaning when SIMV is supporting the patient.

In proportional-assist ventilation (PAV), the ventilator

automatically adjusts airway pressure in response to the patient’s
ventilatory patterns. The ventilator frequently adjusts needed
support based on the patient’s inspiratory flow rate, exhaled tidal
volume, compliance, and resistance.

Other methods such as tracheal gas insufflation, extracorporeal

membrane oxygenation, and methods that may be used for
patients with refractory hypoxemia are currently used in less
than 5% of institutions and therefore will not be discussed further
here.

Diagnostic Evaluation of Appropriate Ventilation

267
ALI, Acute lung injury; ARDS, acute respiratory distress syndrome; IBW, ideal body
weight; PEEP, positive end-expiratory pressure; PAWP, pulmonary artery wedge
pressure; PIP, peak inspiratory pressure.

Complications related to mechanical

ventilation
Barotrauma, volutrauma, and pneumothorax
Barotrauma can occur when ventilatory pressures increase
intrathoracic and intrapleural pressures, causing damage to the
lungs, the major vessels, and possibly all organs in the thorax, with
referred damage to the abdomen. If severe, barotrauma can lead to
pneumothorax: a partially or totally collapsed lung. Symptoms vary
depending on the amount of lung collapsed.

Tension pneumothorax
This develops when pressurized air escapes from the lungs and
enters and collects in the thoracic cavity, causing one or both lungs
to collapse. High pressure from mechanical positive-pressure
ventilation may tear diseased or fragile lung tissue, leading to this
life-threatening complication. Symptoms include respiratory
distress, fluctuations in BP, shifting of the trachea toward the
unaffected side, and sudden and sustained increases in PIP.

HIGH ALERT!
If tension pneumothorax is suspected, the patient should be
disconnected from the ventilator immediately and ventilated using
a bag/valve/tube device (Ambu bag). While the primary
nurse/therapist is using tube/mask ventilation, others will facilitate
an emergency physician call and set up the patient for immediate
chest tube insertion/placement.

Gastrointestinal complications

268
Peptic ulcers with profound hemorrhage may develop as a result of
physiologic pressures and stress. Histamine H2-receptor antagonists
(e.g., ranitidine) or proton-pump inhibitors (e.g., omeprazole
[Prilosec], lansoprazole [Prevacid], rabeprazole [Aciphex],
pantoprazole [Protonix], esomeprazole [Nexium], and Zegerid), or
sucralfate (Carafate) may be administered to prevent these ulcers
from developing. A great deal of controversy surrounds the best
strategy for peptic ulcer prevention and the evidence is evolving. In
addition, gastric dilation can occur as a result of the large amounts
of air swallowed in the presence of an artificial airway. If gastric
dilation is left untreated, paralytic ileus, vomiting, and aspiration
may develop. Extreme dilation can compromise respiratory effort
because of the restriction of diaphragmatic movement. Treatment
includes insertion of a gastric tube orally or nasally (oral placement
may be preferred) connected to low intermittent suction to remove
air from the GI tract.

Hypotension with decreased cardiac output

This develops as a result of decreased venous return secondary to
increased intrathoracic pressure caused by positive-pressure
ventilation. Unless associated with tension pneumothorax, this
phenomenon is transient and is seen immediately after the patient
has been placed on mechanical ventilation. This may require
aggressive volume resuscitation.

Sustained hypotension with decreased cardiac output

PEEP, especially at levels greater than 20 cm H2O, and MAP
strategies to open the alveoli (lung) may increase the incidence and
severity of the phenomena resulting from compression of the heart
and large blood vessels from increased intrathoracic pressure. This
produces an arterial hypovolemic state. Aggressive IV fluid therapy
and occasionally inotropic support may be used with PEEP to
maintain adequate intravascular volume for sufficient CO to
perfuse vital organs. HR and BP should be monitored frequently if
the patient is unstable.

Increased intracranial pressure (ICP)

269
Increased ICP occurs as a result of decreased cerebral venous return
to the heart resulting from compression of intrathoracic blood
vessels when using PEEP greater than 5 cm H2O or mean airway
pressure management strategies. This may limit cerebral venous
outflow, therefore increasing the ICP. See the section on Traumatic
Brain Injury in Chapter 3 for additional information.

Fluid imbalance
Increased production of ADH occurs as a result of increased
pressure on baroreceptors in the thoracic aorta, which causes the
system to react as if the body were volume-depleted. ADH
stimulates the renal system to retain water. Patients may need
diuretics if signs of hypervolemia are present. Be alert to new
symptoms of dependent edema or adventitious breath sounds.

Ventilator-associated event (VAE)

Patients with mechanical ventilation are at high risk for developing
healthcare-associated pneumonia or ventilator associated
pneumonia (VAP). In 2012, the National Healthcare Safety Network
facilities reported greater than 3957 VAP cases. The incidence for
various hospital units ranged from 0.0 to 4.4 per 1000 ventilator
days. Providers continually disagreed on criteria for VAP,
prompting the reportable benchmark to be changed to VAE. Studies
indicate that 70% to 90% of patients who are mechanically
ventilated colonize hospital-acquired bacteria in the oropharynx,
trachea, or digestive tract. Aspiration of bacteria from the
oropharynx is a leading cause of VAP. The onset of infection may
have several mechanisms:

• Presence of an ET/tracheostomy tube creates a bypass of upper

respiratory tract defense mechanisms of cough and mucociliary
clearance action.

• Contaminated secretions pool above the ET/tracheostomy tube

cuff promoting colonization of bacteria and ultimately leak into
the lower respiratory tract.

• Use of endotracheal tubes with subglottic secretion drainage is

270
 effective for the prevention of VAP and may be associated with
reduced duration of mechanical ventilation.

• Supine positioning, the presence of a nasogastric tube, or reflux of

bacteria from the stomach contribute to oropharyngeal
colonization. The medications that patients who are mechanically
ventilated may receive to prevent GI bleeding also alter the
gastric pH. Use of sucralfate, which does not increase gastric pH,
decreases the incidence of pneumonia compared with antacids
alone or in combination with hydrogen ion antagonists.

• Use of contaminated equipment/supplies, inadequate hand

washing, or poor infection control practices may directly
inoculate the tracheobronchial tree with pathogens.

Anxiety
Many individuals experience anxiety related to the discomfort
associated with loss of control over their ventilatory process and the
perception that their health status is threatened. Hypoxemia and air
hunger, if present, contribute to anxiety and prompt rapid, shallow,
and often irregular respiratory efforts. The first approach is always
to evaluate mode and method of ventilation to insure appropriate
ventilatory support. The flow rate of the volume must be
considered, and can best be evaluated with a volume-pressure loop.
Coordinated and effective ventilation may not be possible with
severe anxiety and agitation. Diligent administration of anxiolytic
drugs and analgesics, along with close monitoring of the patient’s
response to potent medications, may be necessary to reduce the
work of breathing and facilitate effective mechanical ventilation.
The use of an approved sedation scale is also recommended (see
Sedation and Neuromuscular Blockade). In extreme cases, if the
patient is unable to tolerate the ventilator mode most appropriate
for his or her condition and cannot be managed using high-dose
anxiolytic agents, sedatives, and analgesics, the advanced practice
provider may consider use of neuromuscular blockade (induced
paralysis) to facilitate more effective ventilation. Neuromuscular
blockade should be reserved for only the most extreme situations,
wherein the patient’s life is threatened by the overall energy

271
expenditure related to fear, anxiety, or inability to attain control
over his or her breathing pattern despite other efforts (see Sedation
and Neuromuscular Blockade).

Weaning the patient from mechanical

ventilation
Weaning patients from mechanical support requires skill,
knowledge, and patience. This goal may take many forms ranging
from abrupt cessation to gradual withdrawal from ventilatory
support. Successful weaning depends primarily on the patient’s
overall condition as well as the techniques used. Patients for whom
attempts at weaning fail constitute a unique problem in critical care.
Physiologic factors (cardiovascular status, fluids and electrolyte
balance, acid-base balance, nutritional status, comfort, and sleep
pattern) and emotional factors (fear, anxiety, coping skills, general
emotional state, ability to cooperate) are important and must be
evaluated both before and during the weaning process. Adequate
pulmonary function parameters must be attained before the
weaning process is begun (Table 1-17). To begin the weaning
process, patients must be hemodynamically stable and able to
initiate a spontaneous breath. A weaning assessment tool that is
chosen for use in patients who are critically ill should be well
designed and supported by evidence, and thus strategies have a
better opportunity for success. The most well evaluated and
internationally used is the Burns Wean Assessment Program
(BWAP). A series of predictors for weaning success is listed in Table
1-17, and a listing of ventilator adjustments during weaning is
included in Table 1-18.

Table 1-17
PARAMETERS FOR WEANING FROM MECHANICAL VENTILATION

Optimal
Pulmonary Function Definition
Parameters
Minute ventilation >10 L/min Tidal volume × respiratory rate; if adequate, it indicates that
the patient is breathing at a stable rate with adequate tidal
volume
Negative inspiratory >−20 cm Measures respiratory muscle strength; maximum negative
force H2O pressure indicates that the patient is able to generate and

272
 initiate spontaneous respirations; indicative of the patient’s
ability to initiate inspiration independently
Maximum voluntary 2 × resting Measures respiratory muscle endurance; indicates the
ventilation minute patient’s ability to sustain maximal respiratory effort
ventilation
Tidal volume 5 to 10 Indicates the patient’s ability to ventilate lungs adequately
mL/kg
Arterial blood gases Pao2 >60
Fractional mm Hg
concentration of Pao2 <45
inspired oxygen mm Hg
(Fio2) 0.40 pH 7.35 to
7.45
or
patient’s
baseline

Table 1-18
COMMON ADJUSTMENTS DURING WEANING TO IMPROVE GAS
EXCHANGE

Ventilation Strategies Oxygenation Strategies

When CO2 retention is the problem When refractory oxygenation is the problem
Increase minute ventilation Increase f (RR) Increase Fio2
Increase VT When Fio2 is >0.40 (40%), consider PEEP
Increase flow rate When PEEP is >12 to 15, consider MAWP strategies
MAWP, Mean airway pressure; PEEP, positive end-expiratory pressure; RR,
respiratory rate; VT, tidal volume.

Traditional weaning methods

Two weaning protocols are generally used: incremental reduction
of ventilator support or progressively longer periods of
spontaneous breathing trials. Physical rehabilitation is an important
component of weaning protocols. Success depends on
comorbidities, hospital culture, level of knowledge of the care
providers, availability of physical therapy, use of weaning
protocols, and patient autonomy. Methods for incremental
reduction of ventilator support include:

1. SIMV mode: The patient is switched to SIMV from assist-control

mode, or respiratory rate and pressure support are decreased if the
patient is already on SIMV.

273
Patients with nonchronic pulmonary disease decrease
rate every 30-minute interval. After 2 hours at a
mandatory rate of zero with CPAP, if the patient is
clinically stable, he or she may be extubated.

Patients with chronic pulmonary disease begin with

an RR of 8 breaths per minute and decrease SIMV
rate by 2 breaths per hour unless the patient
experiences clinical deterioration. If stable after at
least 1 hour of a mandatory rate zero with CPAP,
the patient may be extubated.
2. Pressure support ventilation (PSV): Start with 25 cm of pressure
support and no mandatory breaths.

Patients with Nonchronic Pulmonary Disease

decrease pressure support every 30 minutes; if the
patient is able to tolerate PSV of zero for 2 hours, he
or she can be extubated.

Patients with Chronic Pulmonary Disease decrease

pressure support by 2 to 4 cm H2O every hour as
long as the patient is stable.

When PSV is zero for at least 1 hour, fit the patient

with a T-piece or initiate CPAP and observe.

3. T-piece method: A T-shaped adapter is placed on the end of the

ET tube. The patient is taken off the ventilator and allowed to
initiate spontaneous breaths for increasingly longer periods of time.
The T-piece method may be used by starting with 1 to 2 minutes off
the ventilator, followed by 58 to 59 minutes on, with a gradual
reversal of this ratio until the patient breathes independently. In

274
this manner, the patient builds strength and endurance for
independent respiratory effort.

Spontaneous breathing trials

The patient is closely monitored for a period of time while
disconnected from the ventilator. Respiratory pattern, gas
exchange, hemodynamic stability, and patient comfort should be
monitored closely. If the patient tolerates the spontaneous
breathing trial for 30 to 120 minutes, extubation should be
considered.

HIGH ALERT!
Apnea
Frequent patient assessments with vigilant monitoring must be
done, because there may not be ventilator backup or an apnea
program to support the patient if the patient fails to breathe.

Failure to wean
Patients who need prolonged mechanical ventilation are increasing
in numbers. These complex patients require high resource use and
achieve suboptimal outcomes, especially if elderly. Patients who fail
the transition from ventilator support to sustained spontaneous
breathing do so primarily because of weakness of the respiratory
muscles, including the diaphragm. Considerations regarding the
following parameters should be evaluated before attempting
weaning. The following parameters should be evaluated when
patients are unable to be weaned from the ventilator.

• Nutrition and metabolic deficiencies: K, Mg, Ca, phosphate, and

thyroid hormone.

• Complications related to use of corticosteroids or need for

corticosteroids.

275
• Left ventricular dysfunction, cardiomyopathy, and
myocardial ischemia.
• Chronic renal failure, which alters capacity for compensation.

• Systemic diseases that affect protein synthesis, degradation, and

glycogen stores.

• Hypoxemia and hypercapnia.

• Critical illness–related neuromuscular

abnormalities.

Troubleshooting mechanical ventilator

problems
The most important assessment factor in troubleshooting a
mechanical ventilator is the effect on the patient. Regardless of
which alarm sounds, always assess the patient first to evaluate his
or her physiologic response to the problem. (See Table 1-19 and Box
1-15 for processes that contribute to high-pressure and low-pressure
alarm situations.) If at any time the patient is not receiving the
proper volumes or the nurse is unable to properly assess and
manage the alarm situation, take the patient off the ventilator,
ventilate with a bag-valve tube system, and ask someone to contact
the respiratory therapist immediately.

Table 1-19
CAUSES OF HIGH-PRESSURE ALARMS DURING MECHANICAL
VENTILATION

Increased airway resistance Decreased lung compliance

Patient requires suctioning Pneumothorax
Kinks in ventilator circuitry Pulmonary edema
Water or expectorated secretions in circuitry Atelectasis
Patient coughs or exhales against ventilatory breaths Worsening of underlying disease
process

276
 Patient biting ET tube ARDS
Bronchospasm

Herniation of airway cuff over end of artificial airway

Change in patient position that restricts chest wall
movement
Breath stacking
ARDS, Acute respiratory distress syndrome; ET, endotracheal.

Box 1-15
CAUSES OF LOW-PRESSURE ALARMS
Patient disconnected from machine

Leak in airway cuff

Insufficient air in cuff

Hole or tear in cuff

Leak in one-way valve of inflation port

Leak in circuitry

Poor fittings on water reservoirs

Dislodged temperature-sensing device

Hole or tear in tubing

Poor seal in circuitry connections

Displacement of airway above vocal cords

Loss of compressed air source

277
Care plans for mechanical ventilation
Impaired gas exchange 
related to altered oxygen supply resulting from an abnormal tidal volume
distribution associated with mechanical ventilation.
Goals/Outcomes: The patient has adequate gas exchange, as
evidenced by PaO2 greater than 60 mm Hg, Paco2 35 to 45 mm Hg,
SpO2 greater than 92%, SvO2 greater than 60%, and RR 12 to 20
breaths/min.
Respiratory Status: Gas Exchange.

Mechanical ventilation

1. Observe for, document, and report any changes in the patient’s

condition consistent with increasing respiratory distress (see Acute
Respiratory Failure, Chapter 4).

2. Position the patient to allow for maximal alveolar ventilation and

comfort. Remember that the dependent lung usually receives more
ventilation and more blood flow than the nondependent lung;
however, during mechanical ventilation the dependent portion of
the lung receives less distribution of tidal volume than the
nondependent areas.

• Analyze SpO2, SVO2, and ABG results with the

patient in different positions to determine adequacy
of ventilation.

• Use postural drainage principles where appropriate.

• In unilateral lung disease, position the patient with

the healthy lung down.

• In bilateral lung disease, position the patient in the

right lateral decubitus position, inasmuch as the

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 right lung has more surface area. If ABG results
show that the patient tolerates left lateral decubitus
position, alternate between the two positions.
Rotational therapy (rotating the patient and/or use
of a chest percussion bed) may be effective.

3. Turn the patient at least every 2 hours if signs of deteriorating

pulmonary status occur.

4. Auscultate the upper chest over the artificial airway to assess for
leaks.

5. Assess the ventilator for proper functioning and parameter

settings, including Fio2, tidal volume, rate, mode, PIP, and
temperature of inspired gases. In addition, ensure that connections
are tight and alarms are set. A thorough ventilator check is
generally done every 2 hours in best practice settings. Ventilator
checks should be systematically documented in the medical record
by the respiratory care practitioner. Assessing the ventilator for
proper function and the patient’s response to therapy is most often
a collaborative effort between the nurse and the respiratory
therapist.

6. Keep the ventilator circuitry free of condensed water and

expectorated secretions. Not all ventilators have a problem with
condensation. Fluids present in the circuit may obstruct the flow of
gases to and from the patient. Water is a warm, moist environment
that is ideal for the growth of microorganisms. Gloves should be
worn any time the ventilator circuit is manipulated.

7. Monitor serial ABG results. Be alert for hypoxemia (decreases in

PaO2 ) or hypercapnia (increases in Paco2) with concomitant
decrease in pH (less than 7.35), which can signal hypoventilation
and/or inadequate oxygenation. Also observe for decreased Paco2
(less than 35 mm Hg) with increased pH (greater than 7.45), which
may signal mechanical hyperventilation.

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8. Notify the advanced practice provider of dysrhythmias, which
can occur even with modest alkalosis if the patient has heart disease
or is receiving inotropic medications (see Appendix 6).

9. If changes in patient status are noted, note the SpO2 reading and
end-tidal CO2, if used, or follow institutional protocol for
addressing deterioration in the status of a patient receiving
mechanical ventilation. An ABG analysis may be warranted.

10. Keep manual resuscitator or bag-valve device at the bedside for

ventilation in case of malfunctioning equipment.

Ineffective airway clearance (or risk for same) 

related to altered anatomic structure secondary to the presence of ET or
tracheostomy tube.
Goals/Outcomes: The patient maintains a patent airway, as
evidenced by the absence of adventitious breath sounds or signs of
respiratory distress, such as restlessness and anxiety.
Respiratory Status: Airway Patency.

Airway management

1. Assess and document breath sounds in all lung fields at least

every 2 hours. Note quality and presence or absence of adventitious
sounds.

2. Monitor the patient for restlessness and anxiety, which can signal
early airway obstruction and hypoxia.

3. Avoid routine or scheduled suctioning. Use aseptic technique

(including use of sterile gloves) for suctioning based on the needs of
the patient. The decision to suction is based on assessment findings,
and is done to maintain a patent airway when the patient is unable
to cough out secretions. Document the amount, color, and
consistency of tracheobronchial secretions and the patient’s
tolerance of the procedure. Collaborate with the respiratory care
practitioner and report significant changes (e.g., increase in
production of secretions, tenacious secretions, bloody sputum) to
the physician or midlevel practitioner. Maintain the artificial airway

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in a secure and proper alignment.

4. Maintain the correct temperature (32° C to 36° C [89.6° F to 96.8°

F]) of inspired gas. Cold air irritates the airways, and hot air may
burn fragile lung tissue.

5. Maintain humidification of inspired gas either using the

ventilator or an alternative device, to prevent drying of tracheal
mucosa. Without humidification, tracheobronchial secretions may
become thick and tenacious, creating mucous plugs that place the
patient at risk for development of atelectasis and infection.

Ineffective breathing pattern 

related to anxiety resulting from the need for mechanical ventilation.
Goals/Outcomes: The patient exhibits a stable respiratory rate of
12 to 20 breaths/min (synchronized with ventilator) without
restlessness, anxiety, lethargy, or sounding of the high-pressure
ventilator alarm.
Mechanical Ventilation Response: Adult.

Ventilation assistance

1. Monitor for evidence of ventilator dyssynchrony: Frequent

sounding of high-pressure alarm when the patient breathes against
mechanical inspiration or mismatch of the patient’s respiratory rate
and ventilatory cycle.

2. Monitor the respiratory rate and quality, and for early signs of
respiratory distress (e.g., tachypnea, hyperventilation, anxiety,
restlessness, lethargy). Cyanosis is a late sign of respiratory
insufficiency.

3. Teach the patient the technique for progressive muscle relaxation

(see Appendix 7). When the patient becomes anxious, remain at the
bedside until the respirations are under control. Reassure the
patient that they have the best opportunity to synchronize
respirations with the ventilator if he/she relaxes.

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HIGH ALERT!
Restlessness Management
Administer prescribed medication for restlessness only after any
physiologic causes, including hypoxia and hypoglycemia, have
been ruled out. Restlessness, if attributable to a nonphysiologic
cause such as anxiety or unrelieved pain, should be managed with
either sedation or analgesia, because it increases O2 demand and
consumption and can interfere with adequate ventilation.

Ineffective protection 
related to increased environmental exposure (contaminated respiratory
equipment); tissue destruction (during intubation or suctioning); invasive
procedures (intubation, suctioning, presence of ET tube);
immunocompromised state; and/or the physiologic stress resulting from a
critical illness.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, WBC count ≤11,000/mm3, clear sputum, and
negative sputum culture results.
Immune Status.

Infection protection

1. Assess the patient for signs and symptoms of infection, including

temperature greater than 38° C (100.4° F), tachycardia (HR greater
than 100 bpm), erythema of tracheostomy, and foul-smelling
sputum. Document all significant findings.

2. To minimize the risk of cross-contamination, wash hands before

and after contact with the respiratory secretions of any patient
(even though gloves were worn) and before and after contact with
the patient who is undergoing intubation.

3. Maintain appropriate seal on artificial airway cuff to prevent

aspiration of oral secretions.

4. Implement the Institute for Healthcare Improvement Ventilator

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bundle:

• Keep the HOB elevated 30 to 45 degrees.

• Perform daily sedation vacations (interruption of

sedation) and assessment for readiness to extubate.

• Implement peptic ulcer disease prophylaxis.

• Provide daily oral care with chlorhexidine.

• Implement venous thromboembolism (VTE)

prophylaxis.

5. Monitor the patient for reflux of feedings, as well as for signs of

intolerance to feedings (absence of bowel sounds, abdominal
distention, residual feedings of greater than 100 mL), which can
precipitate vomiting and result in pulmonary aspiration of gastric
contents.

6. Consider the use of a postpyloric feeding tube if the patient is at

high risk for aspiration or is intolerant of conventional feeding
strategies.

7. Recognize that bacteria and spores can be introduced easily

during suctioning. Follow standard techniques:

• Use aseptic technique during suctioning process,

including use of sterile catheter and gloves. Use of
lavage solutions is not recommended.

• Suction the tracheobronchial tree before suctioning

the oropharynx if using the same suction catheter,
to avoid introducing oral pathogens into the
tracheobronchial tree. Ideally, a separate tonsil

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 suction device is dedicated to use exclusively in the
oropharynx.

• Never store or reuse a single-use suction catheter.

Consider use of closed system for suctioning.

• Change suction canisters and tubing within the time

frame established by the agency and/or always
when filled. Change canisters and tubing between
patients.
8. Wash hands and use sterile gloves when performing
tracheostomy care to prevent colonization of stoma with bacteria
from the practitioner’s hands.

9. Provide oral hygiene at least every 4 hours to prevent

overgrowth of normal flora and aerobic gram-negative bacilli.
Suction the oropharynx and posterior pharynx to prevent pooling
of secretions. Endotracheal tubes with subglottic secretion drainage
are available to provide continuous suctioning of the posterior
pharynx. Oral rinse products with chlorhexidine have been used to
help control bacteria. Specialized suctioning toothbrushes may be
used to brush the teeth and tongue every 12 hours.

• Change the entire ventilator circuit (ventilator

tubing) within the time frame established by policy,
or sooner if soiled with secretions or blood.

• When disconnecting the patient from ventilatory

circuits, keep ends of connectors clean. Avoid
unnecessary disconnection.

• Keep connectors on manual resuscitator bags clean

and free of secretions between uses. Although no

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 data suggest that disposable bags be changed with
any frequency, reusable bags should not be used
between patients without sterilization.
10. Be aware of special risk factors for patients with tracheostomy
tubes, and intervene accordingly:

• Maintain the tracheostomy tube in a secure and

proper alignment to avoid irritation of stoma from
too much movement.

• Change the tracheostomy ties daily, or more

frequently if heavily soiled with secretions or
wound exudate.

• Perform stoma care at least every 8 hours, using

aseptic technique until the stoma is completely
healed. Keep the area around the stoma dry at all
times to prevent maceration and infection. Change
the stoma dressing as needed to keep it dry.

• Avoid use of cotton-filled gauze or other material

that may shed small fibers. The patient may
aspirate fibers, which in turn can lead to infection.

• Use aseptic technique (including use of sterile

gloves and drapes) when changing the
tracheostomy tube.

• Culture secretions or wound drainage; administer

antibiotics as prescribed.

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Anxiety 
related to actual or perceived threat to health status as a result of the need
for or the presence of mechanical ventilation.
Goals/Outcomes: During the interval of mechanical ventilation,
the patient relates the presence of emotional comfort and exhibits a
decrease in irritability, with an HR within the patient’s normal
range.
Anxiety Level.

Anxiety reduction

1. Reassure the patient and significant others that ventilatory

support may be a temporary measure until the underlying
pathophysiologic process has resolved. The patient may be weaned
from the ventilator at that time. Some in the general public equate
ventilator placement with a hopelessly chronic, vegetative state. Set
time lines for reevaluation of the patient’s progress.

2. Reassure the patient that he or she will not be left alone.

3. Explain all procedures before they are initiated to the patient and
significant others. Inform the patient of his or her progress.

4. Describe and point out the alarm system, explaining that it will
alert staff in the event of any problem with the ventilator, including
an accidental disconnection.

5. Provide the patient with a mechanism for communication (e.g.,

picture board, erasable marker board, pen and paper).

6. If aggressive sedation is used, perform a “sedation vacation” at

least every 24 hours to assess if the patient can tolerate mechanical
ventilation without sedation. Weaning the patient from sedation is
an important step in the weaning from mechanical ventilation
process. Sedatives can also mask symptoms of pain.

7. Evaluate the patient’s need for pain control, particularly during

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the daily sedation vacation. Analgesics should be administered to
control pain.

Impaired gas exchange 

related to decreasing support or ventilation during weaning from
mechanical ventilation.
Goals/Outcomes: The patient has adequate gas exchange, as
evidenced by PaO2 less than 60 mm Hg, Paco2 less than 45 mm Hg,
SpO2 greater than 92%, SVO2 greater than 60%, and pH 7.35 to 7.45
(or values within 10% of the patient’s baseline).
Mechanical Ventilation Weaning Response: Adult.

Mechanical ventilatory weaning

1. Maintain the patient in a comfortable position to enhance

ventilation. Many patients find that a semi-Fowler position, with
the HOB elevated 30 to 45 degrees, promotes more effective
ventilation. Studies support these findings and recommend that the
HOB remains elevated throughout mechanical ventilation, to
reduce the risk of aspiration.

2. Observe for indicators of hypoxia, including tachycardia,

tachypnea, cardiac dysrhythmias, pain, anxiety, and restlessness.

3. Assess and record vital signs every 15 minutes for the first hour
of weaning, then hourly if the patient is stable. Report significant
findings to the advanced practice provider such as increased
respiratory effort, hyperventilation, anxiety, lethargy, and cyanosis.

4. Check the patient’s tidal volume after the first 15 minutes of

weaning and as needed. Optimally, it will be within 5 to 10 mL/kg.

5. Obtain a specimen for ABG analysis during weaning as indicated

and per hospital protocol. Monitor SpO2 continuously and, as
available, SVO2 for values outside the normal range.

Anxiety 
related to perceived threat to health status secondary to the weaning

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process
Goals/Outcomes: During the weaning process, the patient
expresses the attainment of emotional comfort and is free of the
signs of harmful anxiety, as evidenced by HR less than 100 bpm, RR
less than 20 breaths/min, and BP within the patient’s normal range.
Anxiety Self-Control.

Anxiety reduction

1. Before the weaning process is initiated, discuss plans for weaning

with the patient and significant others. Explain that the patient’s
condition will be assessed at frequent intervals during the weaning
procedure. Provide time for questions and answers about the
procedure.

2. Stay with the patient during the initial phase of weaning, keeping
the patient informed of progress being made. Provide positive
feedback for positive efforts.

3. Teach the patient progressive muscle relaxation technique, which

may reduce anxiety and fear, and thus relax chest muscles (see
Appendix 7).

4. Instruct the patient to take deep breaths if he or she is capable of

doing so. This may provide the confidence of knowing that he or
she can initiate and sustain respirations independently.

5. Encourage the patient to sit in the chair or to move about in the

bed as much as possible.

6. Leave call light within the patient’s reach before leaving bedside.
Reassure the patient that help is nearby.

Acid-Base Management; Acid-Base Monitoring; Airway

Management; Airway Suctioning; Anxiety Reduction; Aspiration
Precautions; Bedside Laboratory Testing; Infection Control;
Laboratory Data Interpretation; Mechanical Ventilation; Mechanical
Ventilatory Weaning; Oxygen Therapy; Positioning; Respiratory
Monitoring; Vital Signs Monitoring.

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Additional nursing diagnoses
Also see nursing diagnoses and interventions under Prolonged
Immobility and Emotional and Spiritual Support of the Patient and
Significant Others, Chapter 2.

Nutrition support
Malnutrition in patients who are hospitalized is common, with an
incidence ranging from 24% to over 50% in different studies. The
impact of malnutrition on patient outcomes is significant, including
decreased wound healing, immune dysfunction, increased
infection, and increased mortality. Length of stay and costs can be
as much as three times higher in patients with a diagnosis of
malnutrition than in patients who are well nourished. The patient
who is critically ill is at high risk for malnutrition and its negative
sequelae. The metabolic response to critical illness includes
increased energy expenditure, protein catabolism, oxidation of
stored lipids, and altered carbohydrate metabolism. Because the
body has no protein stores, protein is transported from the
periphery (muscle mass) to the liver during critical illness for
production of acute phase proteins and gluconeogenesis and to the
gut for preservation of the GI lining and gut-associated lymphoid
tissue. The resting energy expenditure in patients who are critically
ill can be elevated by up to 120% to 160% and remains elevated for
up to 21 days in patients with sepsis or trauma, even when these
conditions are being adequately managed. In patients with sepsis
and trauma, 13% of total body protein stores are lost in the first 21
days of illness despite the provision of adequate nutrition support.
In the patient who is unfed, stressed, and critically ill, up to 250 g
(∼0.5 lb) of lean body mass can be broken down daily. Patients
who are critically ill are often admitted to ICU with some degree of
malnutrition. Those who were not previously suffering from
malnutrition have poor volitional intake in ICU. The role of
nutrition support in the management of patients who are critically
ill cannot be overestimated.
Nutrition support is defined as the administration of parenteral
or enteral nutrition. The goals of nutrition support therapy in the

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patient who is critically ill are to preserve lean body mass, maintain
immune function, prevent metabolic complications, and in certain
instances to attenuate the disease process. Since the publication of
the last edition of this handbook, the American Society of
Parenteral and Enteral Nutrition (ASPEN) and the Society of
Critical Care Medicine (SCCM) have published joint guidelines for
the provision of nutrition support in the adult patient who is
critically ill. The Canadian Critical Care Nutrition (CCCN)
guidelines were updated in 2013 to include additional
recommendations for the administration of nutrition support in
patients who are critically ill. The revised guidelines underscore the
importance of nutrition support in improving patient outcomes.
The recommendations will be discussed throughout this chapter.

Nutrition assessment
Multiple sources of information are used for the assessment of
nutritional status in the hospitalized patient who is critically ill
including medical and nutrition history, anthropometric data (body
measurements), biochemical analysis of blood and urine, and type
and duration of the disease process. With an individual who is
critically ill, the medical and nutrition history may be obtained from
significant others. Although clinical dietitians in ICU are
responsible for a complete nutrition assessment during the patient’s
stay, according to The Joint Commission, screening for nutrition
risk should be done within 48 hours of admission and is usually
performed by the nurse.

Medical/diet history
A diet history identifies individuals who are or may be at risk for
malnutrition resulting from inadequate intake or an imbalance in
food intake. It should describe the adequacy of both usual and
recent food intake, as well as focus on factors that may have
impaired adequate selection, preparation, ingestion, digestion,
absorption, and excretion of nutrients. The medical history is
included to assess diseases or conditions affecting nutritional status.
The following should be included in the medical and diet history
assessment:

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• Comprehensive review of usual dietary intake, including food
allergies, food aversions, use of nutritional supplements
including vitamins, supplements, and alternative/complementary
therapies.

• Recent weight loss or gain; intentional or unintentional.

• Chewing or swallowing difficulties.

• Nausea, vomiting, or pain with eating.

• Altered pattern of elimination (e.g., constipation, diarrhea).

• Diseases/conditions increasing energy needs (e.g., burns,

extensive wounds, decubitus ulcers, sepsis, surgery, trauma).

• Chronic disease affecting use of nutrients (e.g., malabsorption,

pancreatitis, diabetes mellitus).

• Use of medications (e.g., laxatives, antacids, antibiotics,

antineoplastic drugs).

• How food is obtained and meals are prepared (and by whom).

• Cultural preferences restricting specific nutrient intake or causing

excessive intake.

• Alcohol or drug use.

• Recent fad or vegetarian diets.

• Other influences on nutritional status, such as living

environment, functional status, dependency on caregivers, and
financial resources.

Risk factors for malnutrition

The following factors may place a patient at risk of or indicate the
presence of nutritional deficiencies:

• Age younger than 18 years or older than 65 years (increased risk

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 at older than 75 years).

• Recent unintentional weight loss of more than 5% in 1 month or

more than 10% in 6 months. Weight loss is calculated as follows:

Percent weight loss = (UBW − CBW)/UBW, where

UBW is usual body weight and CBW is current
body weight.
• Excessive alcohol intake or other substance abuse.

• Living conditions: Homelessness or living with limited access to

food.

• Limited capacity for oral intake resulting from physical problems,

such as dysphagia, odynophagia, stomatitis, or mucositis.

• NPO (nil per os [nothing by mouth]) status for more than 3 days.

• Increased metabolic demands induced by extensive burns, major

surgery, trauma, fever, infection, draining abscesses or wounds,
fistulas, pregnancy.

• Protracted nutrient losses associated with malabsorption

syndromes, short gut syndrome, draining abscesses, wounds, or
fistulas; effusions, renal dialysis.

• Requires intake of catabolic drugs including corticosteroids,

immunosuppressants, and antineoplastic agents.

• Protracted emesis from conditions such as anorexia nervosa,

bulimia, hyperemesis gravidarum, radiation, or oncologic
chemotherapy.

• Presence of chronic disease such as acquired immune deficiency

syndrome (AIDS), diabetes, cystic fibrosis, or cancer.

• Patients with obesity who are critically ill experience more

complications than patients with normal body mass index (BMI),

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 including length of stay, infectious morbidity, mortality, and
attainment of nutritional goals.

Physical assessment
Most physical findings are not conclusive for particular nutritional
deficiencies. It is important to compare current assessment findings
with past assessments, especially related to the following:

• Loss of muscle and adipose tissue.

• Work and muscle endurance, neuromuscular function.

• Changes in hair and nails and the presence of skin lesions.

Anthropometric data
Anthropometrics is the measurement of the body or its parts.
Pounds and inches are converted to metric measurements using the
following formulas:

Divide pounds by 2.2 to convert to kilograms (kg).

Multiply inches by 2.54 to convert to centimeters (cm).

• Height: Used to determine ideal weight and BMI; if unavailable,

obtain estimate from family or significant others.

• Weight: A readily available and practical indicator of nutritional

status that can be compared with previous weight and ideal
weight or used to calculate BMI. Large changes may reflect fluid
retention (edema, third spacing), diuresis, dehydration, surgical
resections, traumatic amputations, or weight of dressings or
equipment. Note: 1 liter (L) of fluid equals approximately 2
pounds (lb). Frequent monitoring of patient weight is essential to
detect significant weight loss and weight gain in patients who are
critically ill.

• Body mass index (BMI): Used to evaluate adult weight. One

calculation and one set of standards apply to both men and

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 women:

• BMI ≤ 15: Severely underweight

• BMI < 18.5: Underweight

• BMI 18.5 to 24.9: Normal

• BMI 25 to 29.9: Overweight

• BMI 30 to 34.9: Obesity Class I

• BMI 35 to 39.9: Obesity Class II

• BMI > 40: Obesity Class III (morbid obesity)

Although obesity is usually associated with poor health

outcomes, several metaanalyses of the effects of obesity on patient
outcomes in the critical care setting have actually shown no
difference in mortality between patients who are obese and their
counterparts who are not obese. This phenomenon has been given
the term “the ICU conundrum.” However, BMI values less than
18.5 and greater than 40 are associated with an increase in
morbidity and are associated with longer ICU stay, increased
postoperative complications, and higher readmission rates.

• Midarm muscle circumference (MAMC): Measures muscle mass

of the mid-upper arm using a formula.

• Triceps skinfold thickness (TSF): Measured at the midpoint of the

upper arm by taking half the distance between the olecranon and
the acromion process and grasping the skin and subcutaneous
tissue at the back of the arm approximately 1 cm from the
midpoint. Surgical calipers are used to measure the skinfold. A
TSF measurement of less than 3 mm signals severely depleted fat

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 stores.

Specially trained clinicians and dietitians should perform this

assessment for more accurate and consistent results. The skill level
and technique used vary among clinicians.
See Table 1-20 for height and weight determinations in men and
women.

Table 1-20
HEIGHT AND WEIGHT GUIDELINES FOR MEN AND WOMEN

Diagnostic tests
No laboratory test specifically measures nutritional status. Status
can be estimated, however, using the following parameters.

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Visceral protein status
Normal values may vary with different laboratory procedures and
standards. If the hydration status is normal and anemia is absent,
albumin and transferrin levels may be the initial parameters used
for a general assessment of nutritional status. The following are all
visceral proteins:

• Serum albumin (3.5 to 5.5 g/dL): An indicator associated with

increased morbidity in critical illness if the level is less than 3.5
g/dL. It has a long half-life (14 to 21 days) and changes slowly in
response to nutrition support when protein-calorie malnutrition
is present.

• Prealbumin (20 to 30 mg/dL): A reliable indicator of response to

nutritional therapy. It has a short half-life (2 to 3 days) and may
not be reliable if the patient is severely stressed or ill, has an
elevated C-reactive protein (CRP) level, is on steroid therapy, or
has renal failure.

• Retinol-binding protein (4 to 5 mg/dL): The indicator with the

shortest half-life (12 hours) used to assess the response to
nutritional therapy. It is not as reliable in patients who are
severely stressed or those with inflammation, vitamin A
deficiency, and renal failure.

• Transferrin (180 to 260 mg/dL): The indicator with a longer half-

life (8 to 10 days), used as a baseline indicator of protein intake
and synthesis. Similar to prealbumin, it may not be reliable when
the patient is severely stressed and is also affected by changes in
iron status.

It is important to note that none of these markers of nutritional

status are validated in the patient who is critically ill because they
are all affected by the acute phase response.
The Academy of Nutrition and Dietetics (AND) in conjunction
with the American Society of Parenteral and Enteral Nutrition
recently published recommended clinical characteristics for
identifying patients with moderate to severe malnutrition. These
characteristics include energy intake, weight loss, body fat and

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muscle loss, edema, and reduced grip strength, as well as the
presence or absence of acute illness or injury, chronic illness, or
social or environmental circumstances that would predispose
patients to malnutrition. Regarding interpretation of weight loss,
percent of weight change over time is used to differentiate between
moderate and severe malnutrition. Of note, both the AND-ASPEN
guidelines and the ASPEN-SCCM guidelines do not recommend
using visceral protein markers to identify malnutrition.

Nitrogen balance
Nitrogen balance is used in the clinical setting to measure protein
metabolism and protein status. Nitrogen balance is calculated as
follows: Nitrogen balance = Nitrogen in (calculated from total
protein intake) − Nitrogen out (the sum of nitrogen lost in urine,
stool, and body fluids). Most nitrogen loss occurs through the urine,
with a small, constant amount lost via the skin and feces. Nitrogen
balance studies should be performed by nutrition support
specialists, because accurate calculation is important to determine
the patient’s protein status and protein requirements. Nitrogen
balance studies require a 24-hour urine collection and accurate
measurement of protein intake. Heavy losses of protein in the
presence of ascites, large wounds, malabsorption, and excessive
chest tube drainage are difficult to measure but are considered by
the nutrition support specialist when calculating the nitrogen
balance. A positive or neutral nitrogen balance is optimal, but is
sometimes difficult to attain during critical illness because of the
catabolic nature of the disease.

Estimating nutrition requirements

Energy needs
The primary goals of nutrition support are to preserve lean body
mass, preserve immune functioning, and to prevent metabolic
complications while also preventing worsening of malnutrition in
the patient who is critically ill. The nutrition support plan should
avoid overfeeding and underfeeding and the complications
associated with both. Energy needs can be estimated using the

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following options.

Calculation based on patient weight

Estimated energy requirements are 25 to 35 kcal/kg daily for the
patient who is not stressed. Patients who are highly stressed or
malnourished may require up to 40 kcal/kg daily. Patients who are
obese may require 11 to 14 kcal/kg daily or 22 to 25 kcal/kg of IBW.
Although this is not a preferred method for determining energy
needs in patients who are critically ill, calculation based on weight
is often used because of its simplicity.

Indirect calorimetry
Indirect calorimetry is the “gold standard” for calculating energy
needs in the patient who is critically ill and mechanically ventilated.
This test measures O2 consumption and CO2 production as a
byproduct of metabolism and gives the resting metabolic rate
(RMR) and the respiratory quotient (RQ). The RMR is slightly
higher than the basal metabolic rate (BMR). The RQ is the ratio of
carbon dioxide produced relative to oxygen consumption, and can
determine if the patient is being adequately fed (RQ 0.85), underfed
(RQ < 0.82), or overfed (RQ > 1). Indirect calorimetry accuracy can
be affected by many factors including Fio2 ≥ 60, leaking chest tubes,
bronchopleural fistulas, and renal replacement therapy. Specialized
personnel and access to a metabolic cart are required to provide
accurate results.

Predictive equations
Many predictive equations have been validated over the years. The
Harris Benedict Equation was formerly the most common and
accepted formula used to determine RMR. Published originally in
1919, it was widely accepted until 2003 when the American Dietetic
Association recommended other more reliable equations.
Currently, there are many available equations for estimating
energy needs. We will focus on the two equations that are
commonly endorsed and are validated for use for patients who are
critically ill, including the patient with obesity who is critically ill.

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Mifflin St Jeor (MSJ)
The MSJ formula is based on patient age, height, weight, and
gender. The MSJ formula has been shown to be one of the most
accurate formulas for predicting RMR in both obese and nonobese
patients. It has been endorsed by the American Dietetic Association
and by the American Society of Parenteral and Enteral Nutrition.
The MSJ formula is appropriate for most healthy patients. For
critically ill hospital patients who are not mechanically ventilated,
adding a stress factor of 1.2 to 1.3 × MSJ is recommended.

Modified Penn state formula

The Modified Penn State Formula is intended for patients who are
mechanically ventilated. It is based on the MSJ formula (it was
formerly based on the Harris Benedict Equation) and includes
additional measures including temperature and minute ventilation
(a function of tidal volume and respiratory rate). If it is not possible
to perform indirect calorimetry or to calculate the Modified Penn
State Formula, then the MSJ formula can be used.

where VE = minute ventilation (Tidal volume [L] × Rate) and Tm =

Tmax (centigrade)

Provision of macronutrients (carbohydrate, fat, and

protein)
• Carbohydrate: Carbohydrates should comprise 45% to 65% of the
total caloric intake. Dextrose is the carbohydrate source in PN.
Increased dextrose loads can lead to hyperglycemia, excessive
CO2 production, hypophosphatemia, fat deposits in the liver, and
transient elevated liver enzymes. A minimum of 50 g of

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 carbohydrate daily is required to prevent ketosis.

• Protein: Protein requirements are generally calculated based on

g/kg of IBW unless the patient’s actual weight is less than his/her
IBW, when actual body weight is used. ASPEN-SCCM guidelines
recommend using actual body weight for patients whose BMI is
less than 30. For BMI > 30, IBW should be used to calculate
protein needs. Protein requirements for maintenance therapy are
0.8 to 1.2 g/kg/day. Patients who are critically ill, as well as
patients with fever, infection, and wounds, may need an
estimated 1.5 to 2 g/kg/day. Patients on hemodialysis or
continuous renal replacement therapy have even higher protein
requirements, up to 2 g/kg/day. Whereas in the past, protein has
been restricted for patients with advanced liver disease, currently
higher protein is recommended for such patients (1 to 1.5 g/kg)
unless the patient has refractory hepatic encephalopathy in which
case protein restriction is recommended until resolution of
hepatic encephalopathy. Severe stress or burns may increase
protein requirements up to 4 g/kg/day.

• Fat requirements: Fat requirements range from 25% to 55% of

total calories. Fat should not exceed 60% of total caloric intake.
Fat can be administered in minimal quantities to satisfy needs for
essential fatty acids, or it can be provided in larger quantities, as
tolerated, to meet energy needs. In patients receiving PN, the
maximum recommended amount of IV fat emulsion in patients
who are critically ill is 1 g/kg/day. A minimum of 100 g IV fat
emulsion per week is necessary to prevent essential fatty acid
deficiency (EFAD). Signs and symptoms of EFAD include dry,
scaly skin and rash, impaired wound healing, and rarely
neurologic symptoms.

Vitamin and essential trace mineral requirements

In general, the recommended dietary allowances (RDAs) for
vitamins, minerals, and trace elements should be followed to
provide minimum quantities of vitamins and minerals. For specific
patients, supplements of specific vitamins or minerals are needed in
increased amounts for existing disease states (e.g., zinc and

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vitamins A and C for burns; thiamine, folate, and vitamin B12 for
chronic alcohol ingestion). Patients who are malnourished and who
are at increased risk of refeeding syndrome should receive
additional thiamine (B1). Enteral formulas contain the RDA for most
vitamins and minerals. However, it is not uncommon for patients
who are tube fed to receive additional multivitamin preparations.
Parenteral multivitamin infusion (MVI) is added to TPN. Trace
elements include zinc, copper, manganese, chromium, and
selenium. Trace elements are usually included in enteral or oral
multivitamin preparations. They are available as a separate
multitrace element preparation for IV administration in TPN. For a
list of common signs and symptoms of vitamin and mineral
deficiency and toxicity, see Table 1-21. For a list of common signs
and symptoms of trace element deficiencies, see Table 1-22.

Table 1-21
SIGNS AND SYMPTOMS OF VITAMIN DEFICIENCY AND TOXICITY

From Clark SF. Vitamins and Trace Elements. The A.S.P.E.N. Adult Nutrition
Support Core Curriculum, 2nd Edition. Charles M. Mueller, Editor. 2012.

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Fluid requirements
Many factors affect fluid balance. All sources of intake (oral, enteral,
intravenous, and medications), as well as output (urine, stool,
drainage, emesis, fluid shifts, and respiratory and evaporative
losses), must be considered. Fluid intake is closely associated with
energy provided. Approximately 1 mL fluid per calorie is one
method to calculate fluid requirements; however, this often
underestimates fluid needs. Another method to determine fluid
requirements is according to patient weight. Most patients require
between 30 and 40 mL/kg of fluid daily. For patients with fluid
restriction, use less than 25 mL/kg or 1.4 to 1.9 L daily. It is
important to remember to calculate fluid received from enteral
nutrition and PN to avoid fluid overload. Fever increases fluid
needs, and fluid intake should be closely monitored in renal and
cardiac dysfunction.

Nutrition support modalities

Enteral nutrition
Enteral feedings (tube feedings) are the preferred strategy for
nutrition support in the critically ill. Studies indicate that enteral
feedings prevent the passage of bacteria from the GI tract into the
lymphatic system (bacterial translocation) and other organs,
reducing a major source of sepsis and possible organ failure. Cost,
safety, and convenience considerations have been the rationale for
using enteral over parenteral support, because the potential
physiologic benefits justify that every effort be made to use enteral
feeds. Enteral feedings promote wound healing and immune
competence and preserve gut function. Current ASPEN-SCCM
guidelines for nutrition support in the patient who is critically ill
recommend enteral nutrition as the preferred route of therapy.
According to these guidelines, enteral nutrition should be initiated
as soon as possible in the patient who is critically ill: within 24 to 48
hours after admission once the patient is fully resuscitated and the
patient is hemodynamically stable. The guidelines further
recommend that enteral feedings be advanced to the goal rate over
the next 48 to 72 hours. Despite these recommendations and the

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benefits of enteral nutrition, patients in the ICU setting frequently
receive only up to 50% of their goal calories. This is as a result of
unnecessary holding of enteral feeds around procedures, ordering
inadequate calories, or tube feeding intolerance. It is also
attributable to a common misconception that enteral feeding cannot
be started until bowel sounds are present. According to the ASPEN-
SCCM 2009 guidelines, as well as the CCCN guidelines, neither the
presence of bowel sounds nor the presence of flatus or stool is
necessary to initiate tube feeding in the patient who is critically ill.
The rationale for this is that bowel sounds are indicators of gut
contractility and do not necessarily correlate with gut function or
absorptive capacity. The reasons for patient intolerance of enteral
feeds in the critical care setting are multifactorial and can be
attributed to inappropriate enteral formula selection, enteral access,
mode of enteral feeding (e.g., bolus versus continuous tube
feeding), medications, or the patient’s underlying disease process.
A dedicated interdisciplinary nutrition support team can address
these issues and prevent tube feeding intolerance in many if not
most circumstances.

1-2
RESEARCH BRIEF BOX
Early enteral nutrition in patients who are critically ill
Another recent trial, by Elke et al., was a secondary analysis of
pooled data that were collected prospectively from nutrition
studies. This trial looked at clinical outcomes of critically ill
mechanically ventilated patients with sepsis and/or pneumonia (N
= 2207) who were enterally fed at either close to goal calories or
hypocaloric or trophic feeding. The study results showed that an
increase of 1000 kcal daily was associated with a statistically
significant reduction in 60-day mortality (odds ratio 0.61, 95%
confidence interval 0.53 to 5.08, P = 0.02) and a statistically
significant increase in ventilator-free days (2.81 days, 95%
confidence interval 0.48 to 0.77, P <0.001). Similar results were
found regarding an increase of 30 g daily of protein
From Elke G, Wang M, Weiler N, et al: Close to recommended caloric and protein intake

303
by enteral nutrition is associated with better clinical outcome of critically ill septic patients:
secondary analysis of a large international nutrition database. Crit Care 18(1):R29, 2014.

Whether one chooses to base clinical practice on the EDEN trial

or the trial by Elke et al., it is important to note that both trials
implemented early enteral nutrition in patients who were critically
ill.

Enteral formulas
Enteral formulas are composed of a wide variety of standard and
modular formulas. See Table 1-23 for a more detailed discussion of
currently available enteral formulas.

• Standard: Consist of intact proteins and a caloric source; most are

lactose-free; all are sterile, and suitable for small-bore feeding
tubes and have a fixed nutrient composition. Vitamins and trace
elements and minerals are included.

• Modular: Consist of a single nutrient that may be combined with

other modules (nutrients) for a formula tailor-made for an
individual’s specific deficits (e.g., carbohydrate, fat, protein,
specific amino acids). The most common modular product is
protein powder.

• Specialty: Enteral formulas that are disease-specific, as described

in the following section on special diets for organ-specific
pathology and in Table 1-23.

Table 1-23
TYPES OF ENTERAL FORMULATIONS

Enteral Formula Description

Blenderized Diet
Compleat, Compleat Modified Nutritionally complete, requiring complete digestive
capabilities; composed of natural foods, including meat,
vegetables, milk, and fruit
Standard Lactose-Free Formulas
Nutren, Isosource, Osmolite Nutritionally adequate, liquid preparation; used for non–
disease-specific nutrition support; standard isotonic; low
residue formulas
Specialty Formulas
Hepatic failure

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Nutrihep Nutritionally complete; has a greater ratio of branched chain
to aromatic amino acids while restricting total amino acid
concentrations and adding nonprotein calories. Calorie-
dense to prevent fluid overload.
Renal failure
Suplena Low-protein, calorie-dense, low-electrolyte (no electrolytes
Renalcal in Renalcal) formulas designed for patients with reduced
kidney function but not yet on dialysis; restricted total
protein content may reduce or postpone need for dialysis.
High in vitamin B6 and folic acid.

Nepro Calorie-dense, high-protein, low-electrolyte formulas

Novasource Renal designed for patients on dialysis. High in vitamin B6 and
folic acid.

Respiratory Insufficiency
Pulmocare Nutritionally complete; contains a higher proportion of fat to
Novasource Pulmonary carbohydrates; may help prevent an increase in CO2
production. Helpful in patients with COPD, cystic fibrosis,
or respiratory failure.
Oxepa Specialized formula with unique blend of patented oils (EPA
and GLA) to help modulate the inflammatory response in
patients who are critically ill and ventilated, especially those
with ALI, ARDS, and sepsis.
Hypermetabolic and Trauma States
Impact Peptide 1.5, Pivot 1.5 Very-high protein, calorie-dense, immune-enhancing
formulas with added arginine for the patient who is
metabolically stressed and immunosuppressed.
Impact, Impact with fiber, Impact Specialized nutrition for surgical and trauma patients.
glutamine, Pivot 1.5
Peptamen bariatric Very-high protein, low-calorie to meet the needs of patients
who are critically ill and obese.
Oxepa Specialized formula with unique blend of patented oils (EPA
and GLA) to help modulate the inflammatory response in
patients who are critically ill and ventilated, especially those
with ALI, ARDS, and sepsis.
Diabetes or Hyperglycemia
Diabetisource AC, Glucerna Reduced carbohydrate, fiber-containing formulas to help
products, Glytrol minimize glycemic response. Lactose-free.
Fiber-Enhanced
Compleat, FiberSource Replete Fiber blends help to support digestive health and normal
fiber, Promote with Fiber Jevity, bowel function. Products contain soluble or insoluble fiber
Nutren Fiber, Impact with Fiber, or a blend of both. Insoluble fiber is NOT recommended in
Peptamen 1.5 with Prebio, critically ill patients in the ICU setting.
Glucerna products, Diabetisource
AC, Glytrol
Calorie-Dense Products
TwoCal HN, Nutren 2.0 Calorie content is 2 calories/mL to provide adequate
nutrients in lower volume for volume-restricted patients;
some standard products also come in 1.5 calories/mL
concentration.
High-Protein Formulas
Promote, Replete Increased protein to help support wound healing. Meets or
exceeds 100% of recommended daily intake for vitamins and
minerals.
Soy-Based Products

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 FiberSource HN, Isosource HN Soy protein isolate and soy fiber for patients who cannot
tolerate milk protein. Not suitable for patients with
galactosemia.
Elemental or Semielemental
Vivonex, Optimental, Peptamen Designed for easy absorption for the patient who has
products, Perative, Impact malabsorption or intestinal atrophy; protein source is free
Peptide 1.5, Vital products amino acids or protein hydrolysates (peptides) or both; fat
sources are oils easily absorbed: MCT, soybean, canola,
safflower; some formulas contain fiber; some have flavor
packets for oral use.

ALI, Acute lung injury; ARDS, acute respiratory distress syndrome; COPD, chronic
obstructive pulmonary disease; EPA, eicosapentaenoic acid; GLA, gamma linolenic
acid; MCT, medium chain triglycerides.

Nutritional composition of enteral formulas

• Carbohydrates are the most abundant macronutrient and energy

source, comprising between 40% and 90%, in enteral formulas.
Carbohydrates are broken down and absorbed as
monosaccharides (glucose, galactose, and fructose) in the small
intestine. Nearly all enteral formulas are lactose-free to avoid
problems in individuals with lactase deficiencies. However, these
formulas are not appropriate for patients with galactosemia.

• Fiber is a polysaccharide that is found in plant foods and is not

digested in the human GI tract. There are two types of fiber:
soluble and insoluble. Soluble fiber is fermented by gut bacteria
to produce short-chain fatty acids, which help maintain gut
integrity and promote water and sodium absorption. Insoluble
fiber is not fermented in the gut. Both soluble and insoluble fiber
are included in many enteral formulas to decrease incidence of
diarrhea by increasing water and sodium absorption, decreasing
transit time, and increasing fecal weight. Fiber may also help
with glucose control in patients with diabetes mellitus.

Some enteral formulas contain prebiotics (such as FOS

[fructooligosaccharides]). Prebiotics promote the growth of
beneficial bacteria in the gut (such as bifidobacteria and
lactobacillus).
Care should be used when administering high-fiber (especially
insoluble fiber) formulas to patients who are critically ill, because
this can lead to bowel ischemia. Current ASPEN-SCCM guidelines

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recommend avoiding insoluble fiber in patients who are critically ill
and at high risk for gut dysmotility and ischemia. Adverse side
effects of fiber and prebiotics include bloating, abdominal pain, and
flatulence.

• Protein: Enteral formulas contain either intact protein,

hydrolyzed protein, or free amino acids.

• Intact protein: Most standard enteral formulas

contain intact protein, which is the protein found in
complete and original form (e.g., commercial and
blenderized whole food diets). The most common
types of intact protein in enteral formulas are casein
and whey (derived from milk) and soy.

• Hydrolyzed protein: Formulas that contain

hydrolyzed proteins are called semielemental or
elemental formulas. Hydrolyzed protein has been
broken down to smaller peptides to aid absorption.
It is better absorbed in patients with GI dysfunction
or pancreatic insufficiency.

• Free amino acids (FAAs) have been broken down

completely to single amino acids and, therefore,
require no additional digestion before absorption.
Similar to elemental and semielemental formulas,
FAAs are intended for use in patients with GI
dysfunction or pancreatic insufficiency.

• Fat generally comprises between 30% and 50% of enteral

formulas. Fat provides energy, essential fatty acids, and is a
source of fat-soluble vitamins (A, D, E, and K). Most enteral
formulas contain both long-chain triglycerides (LCTs) and
medium-chain triglycerides (MCTs). LCTs are a source of

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 essential fatty acids and calories. MCTs are more easily absorbed
and digested because they do not require pancreatic enzymes for
digestion and are absorbed immediately into the GI tract without
having to be absorbed via the lymph system. However, MCTs do
not contain essential fatty acids and are therefore not a sole fat
source in enteral formulas. Some enteral formulas contain
“structured” lipids. Structured lipids have been chemically
modified to contain both LCTs and MCTs on the same lipid
backbone.

Specialized enteral formulas for organ-specific pathology

These formulas are costly, and the metabolic advantages of some of
these products remain unproved.

• Hepatic failure: Branched-chain amino acids (BCAAs) in

combination with reduced aromatic amino acid concentrations
may help alleviate encephalopathy associated with hepatic
failure. However, data with regard to the efficacy of BCAAs are
very limited, and these formulas are not currently routinely
recommended for patients with liver failure. These formulas
should be reserved for patients with hepatic encephalopathy that
is refractory to lactulose and antibiotics.

• Renal disease: Predialysis formulas contain lower protein content

and are low in phosphorus and potassium. These formulas are
calorie dense (fluid restricted). Some formulas have no
electrolytes. Dialysis formulas are higher in protein, are
calorically dense, are lower in phosphorus and potassium, and
have vitamin and mineral profiles that are designed for patients
on hemodialysis.

• Respiratory disease: It was previously thought that high-

carbohydrate load exacerbated pulmonary dysfunction in
patients with chronic pulmonary diseases. It is now accepted that
avoidance of overfeeding any substrate (fat, carbohydrate, or
protein) in this patient population prevents an increase in CO2
production and, consequently, prevents an increase in the work
of breathing. Pulmonary formulas are lower in carbohydrate and

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 are higher in fat. The high-fat content can lead to intolerance in
some patients. Although these formulas are still available, they
are not widely used, and nutrition support clinicians prefer to use
standard formulas and to avoid overfeeding. There are specific
formulas for ARDS and acute lung injury (ALI) that have an
antiinflammatory lipid profile (borage oil and omega-3 fatty
acids) and high amounts of antioxidants. The ASPEN-SCCM
guidelines for nutrition support in the patient who is critically ill
recommend these formulas for ICU patients with ALI/ARDS,
with a high level of recommendation. However, recent
randomized, controlled trials failed to show any benefit of these
products in patients with ALI, thus these recommendations may
be downgraded in updated guidelines. The recently updated
CCCN guidelines did downgrade the recommendation for use of
these formulas in patients with ALI/ARDS from “recommended”
to “should be considered.”

• Diabetes: Diabetic formulas, designed to maintain good glycemic

control, contain reduced carbohydrates, higher fat content, and
higher fiber content. Some of these products contain high
amounts of insoluble fiber and should be avoided in patients who
are critically ill and at high risk for GI dysmotility and bowel
ischemia (ASPEN-SCCM guidelines). According to the AND,
there is insufficient evidence to determine whether diabetes-
specific formulas have an impact on mortality in the patient with
diabetes who is critically ill. Current guidelines for nutrition
support in the adult ICU patient with hyperglycemia do not
make specific recommendations regarding use of diabetes-
specific formulas for patients who are critically ill. Current
practice is to use a standard formula with insulin coverage for
hyperglycemia, reserving the diabetic formulas for patients who
have problems maintaining good glucose control despite insulin.

Enteral access
There are many different options for enteral access based on length
of therapy desired (short term versus long term), site of entry (nasal
versus enterostomy), and terminal site (stomach, duodenum,
jejunum).

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 Site of delivery

Stomach: The stomach is the easiest site for enteral tube placement;
gastric feeding simulates normal GI function, and may be used
for bolus, intermittent, cyclic, or continuous feedings. Entry site
into the stomach is nasal (NG), oral (OG), percutaneous (PEG),
laparoscopic, or surgical (open gastrostomy).

Postpyloric: Postpyloric placement includes anywhere distal to the

pylorus but before the ligament of Treitz. The most common site
of entry for postpyloric feeding tubes is the nose, and these tubes
can be placed at the bedside, endoscopically, or under
fluoroscopy.

Jejunal: Jejunal tubes are placed distal to the ligament of Treitz.

These tubes are more difficult to place at the bedside, although
specially trained personnel can place nasojejunal (NJ) tubes at the
bedside. Generally, NJ placement is done endoscopically or
under fluoroscopy. Direct jejunal feeding tubes can be placed
either percutaneously, under fluoroscopy, laparoscopically, or
surgically.

Site of Entry

Nasoenteric feeding tubes: Nasoenteric tubes are indicated for

short-term enteral nutrition. Nasoenteric tubes are measured by
their external diameter, but flow through these tubes is
determined by their internal diameter. Therefore, a tube with a
small internal diameter will be more prone to clogging even if its
external diameter is larger. Nasoenteric tubes are available in
different lengths, depending on the desired site of delivery of
enteral nutrition. Nasogastric tubes are the shortest, whereas
nasoenteric tubes are longer for placement into the duodenum or
jejunum. Nasoenteric feeding tubes are most commonly used in
the ICU setting. It is vital that feeding tube placement be verified
either by x-ray, fluoroscopy, or electromagnetic imaging before
initiation of enteral feeding.

Complications of nasoenteric feeding tube placement

310
Procedure-related: The most common procedure-related
complications are epistaxis, aspiration, and circulatory or
respiratory arrest. The most serious complication is misplacement
into the bronchi. For this reason, verification of feeding tube
placement is imperative when placing a nasoenteric feeding tube.

Postprocedure-related: The most common postprocedural

complication of nasal feeding tubes is feeding tube clogging. One
of the most effective methods to prevent feeding tubes from
clogging is to flush the feeding tube regularly with water (at least
30 mL every 6 hours). Other complications include dislodgment
of the feeding tube or feeding tube malfunction (kinking or
breaking of the tube).

Enterostomy tubes: Enterostomy tubes are indicated for long-term

enteral nutrition support (usually defined as greater than 4
weeks) and include gastrostomy tubes, gastrojejunostomy tubes,
and jejunostomy tubes. Gastrojejunostomy tubes are intended for
patients with GI dysmotility who require simultaneous gastric
decompression and jejunal feeding. As stated earlier, gastrostomy
and jejunostomy tubes can be placed percutaneously, under
fluoroscopy, laparoscopically, or surgically (open G or J tube).

Enterostomy tube placement complications

Procedure-related: Procedure-related complications of enterostomy

tubes are less common than those associated with nasoenteric
tubes. Complications include perforation of the GI lumen,
hemorrhage, aspiration, and ileus.

Postprocedure-related: Minor postprocedural complications include

infection and leakage around the site of the feeding tube. Major
complications include necrotizing fasciitis and buried bumper
syndrome. This syndrome occurs when gastric mucosa grows
over the internal bumper of the enterostomy tube. Risk factors for
buried bumper syndrome include poor wound healing and
significant weight gain. Another complication is feeding tube
dislodgement. Dislodged feeding tubes must be replaced
immediately to prevent closure of the entry site.

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Methods of administration of enteral nutrition
Enteral nutrition can be delivered either as continuous infusion,
cyclic infusion, intermittent feeding, or bolus or gravity drip
feeding. For patients with feeding tubes terminating in the jejunum,
only continuous or cyclic infusion is appropriate because the
jejunum cannot tolerate large boluses of fluid.
Continuous, pump-assisted, tube feeding is the most common
and preferred method of enteral nutrition delivery in ICU patients.
Other indications for continuous infusion are patients at risk for
refeeding syndrome, patients receiving feeding via a jejunostomy
tube, patients with poor glycemic control, or those who have not
tolerated bolus or intermittent feeding. Continuous tube feeding is
usually started at a low rate (10 to 25 mL/h) and is advanced slowly
every 4 to 6 hours to the goal rate. The goal rate can be calculated
by determining the total daily volume to be infused and dividing
by 24 hours.
Cyclic tube feeding is almost the same as continuous tube
feeding, but the total volume is infused over a shorter amount of
time, usually 12 to 16 hours, but sometimes as little as 8 hours. This
method is also used to infuse tube feeds at night (nocturnal tube
feeding) as a method to help the patient transition to an oral diet.
Intermittent tube feeding can be delivered via a pump or by the
gravity drip method. Larger volumes of formula (240 to 720 mL or 1
to 3 cans) are infused over a shorter period of time (usually from 20
to 60 minutes) several times a day, depending on the volume
needed to meet the patient’s caloric needs.
Bolus or gravity drip feedings are similar to intermittent tube
feeding, but the volume of enteral formula is given over a shorter
period of time (5 to 10 minutes) several times a day instead of being
allowed to infuse over a longer period of time. Bolus feeding is
most similar to normal feeding, and is the least expensive and
cumbersome method of tube feeding. It is generally not used in
patients who are critically ill and who cannot tolerate such rapid
infusion of large amounts of volume (Table 1-24).

Table 1-24
METHODS OF ADMINISTRATION FOR ENTERAL PRODUCTS

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Type Typical Rate of Administration Comments
Bolus 250 to 400 mL four to six times daily. Recommended for stable,
Administer using an open-ended, 60-mL ambulating patients. May cause
catheter-tipped syringe allowing infusion by cramping, bloating, nausea,
gravity. Do not push until feeding tolerance diarrhea, aspiration; not
is well established. recommended for unstable
critically ill patients. Higher risk for
aspiration.
Intermittent Bolus feeding infused by pump: Begin with Starting regimen
120 mL formula (half a can) over 1 hour, Should not exceed 30 mL/hr; may
with 30 to 50 mL water flush before and cause cramping, nausea,
after feeding. bloating, diarrhea, aspiration;
Advancement: Increase formula by 60 mL may need to reduce infusion rate
every 8 to 12 hours if residual is less than to decrease discomfort and
half the volume of the previous feeding to increase tolerance.
a maximum of 450 mL of feeding.
Cyclic Continuous tube feeding generally infused Recommended for patients who
over 12 to 20 hours daily. Rate to be cannot tolerate bolus or
determined by formula and caloric needs. intermittent feeding and patients
Full-strength formula should be used to with J-tubes. Allows more time for
afford the patient the best opportunity to absorption of nutrients while also
receive maximal support from the feeding. allowing time for gut rest and
allowing time for patient to
ambulate freely.
Continuous Rate to be determined by formula and Allows more time for absorption of
caloric needs. Full-strength formula should nutrients. Less risk of aspiration.
be used. If not well tolerated, reducing the Recommended for patients who are
infusion rate may be warranted. Be mindful critically ill and patients with J-
of the number of interruptions in feedings, tubes.
as each interruption reduces the amount of
nutrition support the patient receives.

Monitoring tolerance of enteral feeding

Tolerance of enteral feedings should be monitored based on
physical assessment, measurement of gastric residuals, and by
radiographic confirmation (abdominal x-ray) if ileus or obstruction
is suspected.
Gastric residual volumes should be checked approximately every
4 hours in continuously enterally fed patients. According to the
current ASPEN-SCCM guidelines (2009), holding tube feeding for
gastric residuals less than 500 mL in the absence of other signs of
intolerance should be minimized. Recently published Canadian
Nutrition Support guidelines (2013) for patients who are critically
ill recommend holding enteral feeding for gastric residuals of
greater than 250 mL (approximately 8 oz or one cup). It is important
to monitor physical symptoms, such as abdominal pain or
distension, and by passage of stool or flatus.

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 For patients receiving bolus or intermittent bolus enteral feeding,
gastric residuals should be checked before initiation of the bolus
feeding.
To minimize aspiration, the following factors should be
considered:

1. Keep the HOB elevated at 30 to 45 degrees.

2. For patients at high risk of aspiration, use continuous infusion.

3. Use prokinetic agents (metoclopramide, erythromycin,

alvimopan for opiate-induced dysmotility).

4. Consider postpyloric placement of the feeding tube.

5. Maintain good oral hygiene.

Management of feeding tube complications

For management of feeding tube complications, see Table 1-25.

Table 1-25
MANAGEMENT OF COMPLICATIONS IN THE TUBE-FED PATIENT

Complication/Possible
Suggested Management Strategy
Causes
Nausea and Vomiting
Fast rate Decrease rate
Fat intolerance Change to a low-fat formula
Fiber content Change to a low-fiber formula
Delayed gastric Change from bolus to continuous or cyclic tube feeding
emptying Decrease rate or hold tube feeding, consult the physician to rule out
Gastrointestinal ileus, gut ischemia
intolerance (high
residuals, abdominal
pain and distension)
Clogged Tube
Inadequate flushing Flush tube with at least 30 mL water after each feeding and before and
after medication administration. Flush every 4 hours with a
minimum of 30 mL water as ordered. For clogged feeding tubes,
flush with warm water (60 to 100 mL), repeat as necessary. If feeding
tube is still clogged, consider an enzyme solution to unclog feeding
tube, such as Viokace or Clog-Zapper.
Do not use Coca-Cola or pineapple juice to unclog feeding tube
because this can further denature the protein and exacerbate the
clog.
Instillation of crushed Do not instill crushed medications in small-bore tubes. Substitute

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medications liquid preparations after consulting the pharmacist and prescriber.
Some medications may be crushed into a fine powder and dissolved.
Check with the pharmacist, because crushing can alter medication
characteristics. Never crush time-released medications.
Incompatibilities between drugs and feeding formulas are possible.
Some medications that require that tube feeding be held around
administration include phenytoin, warfarin, fluoroquinolone, and
tetracyclines.
Viscous medications Dilute viscous medications with water before administering.
Dislodged feeding If a standard tube for replacement is not immediately available, insert
tube (enterostomy a Foley catheter of suitable size to keep the entry site open until a
tube) feeding tube is available.

Medication administration via feeding tubes

Medication administration via feeding tubes is a very complex
issue. Administration of medications via feeding tubes can change
the effectiveness of the drug (either decreasing efficacy or
increasing toxicity), can be incompatible with enteral feeding, can
cause diarrhea, or can cause drug interactions by administering
multiple medications at the same time. In addition, there is always
the concern that medications administered via syringe can be
accidentally administered via an IV line causing catastrophic
consequences.
In 2003, a case report was published of a 38-year-old woman who
received both extended-release nifedipine and labetalol via a
feeding tube. The nifedipine caused a profound decrease in her BP
and the labetalol prevented a compensatory increase in her HR. The
patient went into cardiac arrest (asystole) and was resuscitated.
However, the underlying reason for her arrest was not clarified.
The next day, she received the same medications via her feeding
tube, again went into cardiac arrest, and died.
To ensure safe administration of medications via feeding
tubes, the following steps are recommended.

1. Use oral route when possible (if the patient is taking some PO,
PO administration is preferred).

2. Liquid preparations (solutions, suspensions, elixirs) are the

preferred dosage form via feeding tubes. Dilute thick liquid
preparations with water (1:1) before administration to prevent
clogging of feeding tube.

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3. Check osmolality and sorbitol content if the patient experiences
diarrhea. If medication has high osmolality, dilute before
administration.

4. If solid dosage form is used, make sure tablets can be crushed or

capsules can be opened. Not all immediate-release tablets and
capsules can be administered via feeding tubes.

5. In general, sustained-release tablets and capsules cannot be

administered via feeding tubes. Sustained-release preparations will
usually have the following acronyms: CD, CR, ER, LA, SA, SR, TD,
TR, XL, XR.

6. Flush feeding tube BEFORE AND AFTER drug delivery with at

least 15 mL (preferably 30 mL) of water.

7. Administer medications ONE AT A TIME via feeding tube to

prevent drug-drug interactions.

8. Do NOT mix medications directly into feeding formulas.

9. Certain medications require that tube feeding be held around

administration to prevent decreased efficacy. A list of common
specific drug-nutrient interactions is provided in the following
section.

10. Consult pharmacy to review medications for all patients who

are tube fed, to determine if they can be safely administered via
feeding tubes.

11. DO NOT use Luer-Lock syringes to administer medications or

flush feeding tubes to prevent inadvertent IV administration.

Specific drug-nutrient interactions

1. Phenytoin: Hold tube feeding for 2 hours before and after drug
administration.

2. Fluoroquinolones (levofloxacin, ciprofloxacin, moxifloxacin) and

tetracyclines (doxycycline, minocycline, tetracycline): Hold tube

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feeding 1 hour before and 2 hours after drug administration.

3. Warfarin: QUICKLY administer warfarin dose OR hold tube

feedings 1 hour before and after warfarin administration.

For a noncomprehensive list of medications that cannot be

crushed, see Table 1-26.

Table 1-26
SELECTED “DO NOT CRUSH” MEDICATIONS AND MEDICATIONS
THAT REQUIRE CAUTION WITH CRUSHING

“Do Not Crush” Comments

Aggrenox Sustained release
Alendronate Mucous membrane irritant, use solution
Benzonatate Local anesthesia of mucosa
Bisacodyl Sustained release
Diltiazem (sustained action and Immediate-release formulation has coating that releases
immediate release) the drug over 3 hours
Pancreatic enzymes (Creon, Zenpep, Sustained release – Viokace is an immediate-release
Pancrelipase) alternative
Dabigatran Increased toxicity
KCl tablet Use liquid formulation
Lopinavir/ritonavir tablet Use liquid formulation
Mycophenolate mofetil capsule Use suspension
Nifedipine (immediate release and DO NOT administer via feeding tube!
sustained release) Request alternative calcium-channel blocker
Ritonavir tablet/capsule Use liquid formulation
Sevelamer carbonate Tablets expand and can clog feeding tubes; use liquid
formulation
Sirolimus Pharmacokinetic, nanocrystal technology may be
affected
Tamsulosin Request alternative selective or nonselective alpha-
blocker
Caution when crushing Comments
Dutasteride, finasteride Women who are or may become pregnant should NOT
handle this drug
Hydroxyurea Skin toxicities can occur with exposure; wear gloves
when handling

For a list of common medications that can cause or exacerbate

diarrhea, see Table 1-27.

Table 1-27
SELECTED MEDICATIONS THAT CAN CAUSE OR EXACERBATE
DIARRHEA

317
Common Medications with High Osmolality Common Medications with High
Sorbitol Content
Acetaminophen liquid Hydroxyzine HCl Acetaminophen liquid
syrup
Acetaminophen with codeine Lithium citrate Guaifenesin/dextromethorphan
elixir syrup syrup
Dexamethasone solution Metoclopramide Lithium citrate syrup
HCl syrup

Diphenoxylate HCl-atropine Multivitamin Metoclopramide HCl syrup

sulfate suspension infusion liquid
Docusate sodium syrup KCl liquid, Pseudoephedrine syrup

Ferrous sulfate liquid Promethazine HCl Pseudoephedrine/triprolidine syrup

syrup
Theophylline oral solution

Parenteral nutrition
Parenteral (IV) nutrition provides some or all of the patient’s
required nutrients using either a peripheral venous catheter (PIV)
or central venous catheter (CVC). TPN or hyperalimentation (HAL)
are interchangeable terms referring to the administration of IV
nutrition. TPN that is administered via a peripheral vein is called
peripheral parenteral nutrition (PPN). TPN administered via a
central line is called central parenteral nutrition (CPN). CPN can
meet total nutritional needs in patients who cannot be given enteral
support safely or whose GI tract cannot be accessed. Parenteral
nutrition is also used when the GI tract is unable to function, such
as in the case of motility disorders, for example, postoperative ileus
or small bowel obstruction. PPN, by contrast, usually does not meet
the nutritional needs of the patient and is generally reserved for
short-term IV nutrition.
Parenteral nutrition solutions are compounded from a
combination of dextrose, amino acids, electrolytes, vitamins, trace
elements, sterile water for injection (SWFI), and IV fat emulsion (IV
lipids). Total nutrient admixtures (TNAs) are formulated by
combining dextrose, fat, and amino acids together in one container.
2-in-1 TPN admixtures combine dextrose and amino acids, and are
combined with electrolytes, vitamins, and minerals, and IV fat
emulsion is given separately. A 0.22-micron in-line filter must be
used with 2-in-1 TPN formulas (amino acids and dextrose
solutions). The 0.22-micron filter cannot be used for TNA solutions
because it can disrupt the lipid emulsion. Instead, a 1.2-micron filter

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should be used with TNA. A 1.2 micron filter should be used for IV
fat emulsions hung separately. TPN can be infused as a continuous
infusion or as a cyclic TPN. Cyclic TPN is usually infused over 8 to
16 hours and is beneficial in long-term TPN patients to increase
patient mobility and to allow for organ rest.

Components of TPN

• Carbohydrates: Dextrose solutions are used to meet the majority

of the patient’s energy needs. Dextrose provides 3.4 kcal/g in
contrast to dietary carbohydrate that provides 4 kcal/g. PPN
contains less than 10% dextrose, but CPN can contain up to 25%
dextrose. Administration of excess dextrose can lead to
hyperglycemia, hyperlipidemia, increased liver function tests,
steatosis, and refeeding syndrome. Refeeding syndrome occurs in
previously malnourished patients who receive a significant
amount of dextrose. This is manifested by significant electrolyte
shifts (hypophosphatemia, hypokalemia, and hypomagnesemia)
and fluid shifts that can be life threatening if not treated. If high
dextrose containing TPN is stopped abruptly, this can lead to
rebound hypoglycemia; therefore, CPN should always be tapered
by 50% for 1 to 2 hours before discontinuing the infusion.

• Protein: Protein in TPN is provided by crystalline amino acid

solutions. They provide 4 kcal/g similar to dietary protein. Amino
acid stock solutions are available in different concentrations
(from 3% to 20%) and are available as standard amino acid
solutions or disease-specific (hepatic failure, metabolic stress,
renal failure, pediatric). Excessive protein administration without
adequate nonprotein calories and/or fluid can lead to prerenal
azotemia.

• Fat: IV fat emulsion (lipids) are available as 10%, 20%, and 30%
emulsions. The 10% and 20% emulsions can be administered as
part of TPN or separately; 30% fat emulsion can only be used to
compound TNA and cannot be administered separately. IV fat
emulsions (IVFEs) are isotonic solutions that provide essential
fatty acids and a source of concentrated calories. IVFEs in the
United States have traditionally consisted of polyunsaturated

319
 LCTs only. Recently, a new IVFE has been approved by the U.S.
Food and Drug Administration (FDA) that also contains olive oil
(a monounsaturated LCT). Outside of the United States, IVFEs
containing MCTs and fish oil are also available. As stated earlier,
an IVFE that is administered separately can be infused without
an in-line filter. As stated earlier, an IVFE that is administered
separately should be infused a 1.2 micron in-line filter.
Additionally, for TNA a 1.2 micron filter (not a 0.22-micron filter)
should be used.

• When IVFEs are administered separately,

infusion should not exceed 12 hours and should not
be infused too quickly to avoid adverse reactions.
Symptoms of adverse reactions include febrile
response, hypertriglyceridemia, chills and
shivering, and pain in the chest and back. A
delayed type of adverse reaction occurs with
prolonged use of IVFEs and may result in a
transient increase in liver enzyme levels,
eosinophilia, and hypertriglyceridemia. IVFE
should be held in patients with triglyceride levels
greater than 400 mg/dL. In addition, IV lipids are
contraindicated in patients with egg, soy, and
peanut allergies, because the emulsion contains egg
phospholipids, soy, and peanuts (in some
formulations). CDC guidelines for the prevention of
fungemia recommend that when IV lipids are given
as a separate infusion, the IV lipids should be
infused over 12 hours (as opposed to a 24-hour
infusion). In addition, any unused portion of the
IVFE infusion should be discarded immediately.
When in a TNA, the admixture may infuse over 24

320
 hours. Patients receiving propofol (Diprivan),
which is lipid-based, should receive fat emulsion
with caution, not to exceed 60% of total calories
from fat. Current recommendations for patients
who are critically ill recommend no more than 1
g/kg of IVFE daily.
• Multivitamins: Multivitamins for TPN are available as MVI-12
and MVI-13. The IV MVI contain fat-soluble vitamins (A, E, D,
and K) and water-soluble vitamins (B complex and C). The only
difference between the two formulations is that MVI-12 does not
contain vitamin K. Usually 10 mL of MVI is added to the TPN
daily.

• Trace elements: Trace elements include zinc, copper, manganese,

chromium, and selenium. Parenteral trace elements are available
as MTE-4 or MTE-5 in the United States. MTE-4 does not contain
selenium. There is currently a severe shortage of parenteral trace
elements in the United States, and many hospitals are unable to
obtain parenteral trace elements. The FDA has temporarily
allowed for the importation of trace elements from Europe. These
trace elements differ from commercially available trace elements
in the United States in that they contain the following additional
trace elements: iodine, fluoride, iron, and molybdenum. Some
recommendations for managing the current shortage include:

1. Use oral formulations of trace elements whenever

possible if patients can tolerate PO.

2. Give individual trace elements separately if

available.

3. Administer parenteral trace elements three times

weekly instead of daily.

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 4. Use imported products if use is approved by the
specific institution.

5. Increase awareness of signs and symptoms of

specific trace element deficiencies (see Table 1-
22).

Parenteral feeding: Selection of catheter insertion site

Types of catheters: See Table 1-28.

Table 1-28
CATHETERS USED IN PARENTERAL NUTRITION

Catheter Description
Temporary/Short-Term Use
Peripherally May be inserted into a peripheral vein and threaded into a central vein at
inserted bedside by a physician or specially trained infusion therapy nurse. May be a
central single or double lumen.
catheter May be used for total parenteral nutrition (TPN) administration at home.
(PICC) Catheter may remain in place for several months. Multiple uses of a single
lumen for blood sampling, nutrition support, and medication administration
increase the risk of infection, especially in patients who are
immunocompromised. Note: A midline PICC is NOT a central catheter and
only peripheral parenteral nutrition should be infused via this type of line.
Multilumen Inserted at bedside. May have up to four lumens. Subclavian or jugular vein
central accessed. Dedicate one lumen, preferably the most distal, for administration of
venous TPN. Other lumen(s) are used for medication administration and drawing of
catheter blood samples.
(CVC)
Permanent/Long-Term Use
Right atrial Generally placed surgically by a physician into the subclavian or jugular vein
catheter (e.g., with the catheter tunneled and exiting from the skin. The catheter usually
Hickman, includes a Dacron cuff from which the catheter exits the vessel. This type of
Broviac) catheter is associated with the lowest infection rates of all central lines.
Implantable May be placed by a radiologist or surgeon. Designed for repeated access,
venous making the need for repeated venipuncture unnecessary.
access device
(IVAD, such
as Infuse-a-
Port, or Port-
a-Cath)
Modified from Eisenberg P. In Swearingen PL, editor: Manual of medical-surgical
nursing care, ed 6, St Louis, 2007, Mosby Elsevier.

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 Central venous IV catheter (CVC): Used for infusion of large
amounts of nutrients or electrolytes with smaller fluid volumes
(hypertonic solutions) than those in PPN. The solution is usually
delivered through a large-diameter vein (e.g., superior vena cava
via the subclavian vein). The volume of blood flow rapidly dilutes
the hypertonic solutions and decreases irritation of vein walls.
Nontunneled catheters are usually placed in the ICU for short-term
infusion of medications and TPN. Tunneled catheters are more
difficult to insert, but are better suited for long-term TPN. For a list
of complications associated with central lines, refer to Table 1-29.

Table 1-29
LINE COMPLICATIONS IN PATIENTS RECEIVING PARENTERAL
NUTRITION

Potential
Management Strategy
Complications
Upon Central Line Insertion
Pneumothorax Position a rolled towel under the patient’s back, parallel to the spine before the
temporary catheter is inserted. Ensure that x-ray is done immediately after
insertion to determine placement of catheter before initiating total parenteral
nutrition (TPN). Monitor for diminished or unequal breath sounds, tachypnea,
dyspnea, and labored breathing. The greater the number of catheter attempts,
the greater the chance for pneumothorax.
Accidental If pulsatile, bright red blood returns into the syringe during central catheter
subclavian insertion into the subclavian vein, assist with immediate removal of the needle
artery and apply pressure for 10 minutes anteriorly and posteriorly at the point of
penetration penetration. If internal bleeding is unable to be controlled, the patient will
leading to develop a hemothorax and hemorrhagic shock.
hemothorax
During Catheter Maintenance
Catheter If solution is infusing sluggishly, flush line using positive pressure with saline.
occlusion Check to see if line or tubing is kinked. If line is occluded, try to aspirate clot
and contact the physician or midlevel practitioner who may prescribe a
thrombolytic agent, such as Cathflo TPA, TPA (tissue plasminogen activator),
or urokinase, according to agency protocol.
Leakage or Do not insert needles into central line port lumen caps to avoid damaging the
catheter catheter. If the lumen is accidentally punctured and begins leaking, notify the
puncture physician or midlevel practitioner immediately for further action.
Air embolism If signs of air embolism occur, examine the catheter to determine whether an
(a medical open port enabled air to enter the infusion system. Clamp the catheter distal to
emergency) any opening discovered. Turn the patient onto their left side and place in the
Trendelenburg position (head down, feet up) and notify the physician or
midlevel practitioner immediately while administering oxygen.
Central line– Assess for swelling of the upper extremities and perform a neurovascular
related assessment. If limb is swollen, is cool, and has reduced or absent pulses, the
thrombosis physician or midlevel practitioner should be notified and consideration given
leading to to removing the central venous catheter. The extremity should be elevated and
upper the thrombosis managed as ordered to address anticoagulation.

323
extremity deep
vein
thrombosis

Peripheral venous access: Peripheral IV (PIV) lines are generally

not as effective for TPN infusion as central venous administration.
The need for low osmolality of solutions (less than 900 mOsm/L)
means that PPN will not meet the caloric and protein requirements
of most patients. PPN is usually prepared in a higher volume of
fluid because of the necessity of low osmolality, which can be
problematic with patients who require fluid restriction. PPN can be
infused either as a TNA or a 2-in-1 TPN with IV lipids infused
separately. PPN is usually reserved for individuals who need
partial or total nutrition support for short periods (5 to 7 days, no
more than 2 weeks) when CVC access is unavailable or not
warranted. Adverse reactions to PPN include phlebitis and burning
at the infusion site. Because PPN solutions are hyperosmolar and
can irritate peripheral veins, PIV sites should be changed every 48
to 72 hours.
TPN Administration: Continuous TPN is infused at a constant
rate using an infusion pump. When initiating cyclic TPN, the
infusion rate is gradually increased to avoid hyperglycemia. Then
when stopping TPN, the rate is similarly gradually decreased
(usually by 50%) to prevent rebound hypoglycemia.
Discontinuation of CPN should never be done abruptly, but is
accomplished by tapering the CPN by reducing the rate by half for
2 hours, then stopping the CPN. PPN usually has a low
concentration of dextrose and can, therefore, be stopped without
tapering the infusion.

Indications for TPN

Parenteral nutrition is indicated for patients who are unable to meet
their nutrition requirements with enteral or oral nutrition and who
are at risk for malnutrition. PPN can be used when patients require
nutrition support for up to 2 weeks. CPN should be used when
patients require more than 2 weeks of nutrition support. Specific
indications for TPN include paralytic ileus, small bowel
obstruction, mesenteric ischemia, and high-output fistula when
enteral feeding cannot be administered distal to the fistula. Other
indications include failure of enteral nutrition despite trials of

324
postpyloric placement and elemental feedings, and other GI
dysfunction that precludes oral or enteral intake.
Although the initiation of enteral nutrition support in the patient
who is critically ill is highly recommended within the first 24 hours
of admission to ICU, early initiation of TPN in the patient who is
critically ill and who cannot maintain volitional oral intake or who
is not a candidate for enteral nutrition is no longer routinely
recommended. In general, it is recommended to wait at least 5 days
before initiating TPN in patients who are critically ill. These
recommendations were based on studies that found a decreased
risk of infectious morbidity and complications in patients who were
NPO compared with those who received TPN.
Early initiation of TPN in patients who are critically ill is
recommended for patients who are already malnourished on
admission (10% to 15% recent weight loss or a patient weighing less
than 90% of his or her IBW), especially those who are going to
undergo major GI surgery. Some clinicians will recommend
holding IVFE for the first week of PN therapy in patients who are
critically ill because fat metabolism is impaired in critical illness and
soy-based IVFE may have immunosuppressive properties. It is
important to note that TPN therapy that is provided for a very short
time period (less than 5 to 7 days) is not recommended because it
will not improve the patient’s nutritional status and only puts the
patient at risk for complications. It is also important that patients
who are receiving TPN be reassessed frequently for the possibility
of transitioning to either enteral or oral nutrition.

TPN complications
Complications with TPN can be divided into two categories: early
complications and late complications. Early complications from
TPN include hyperglycemia, hyperlipidemia, line infections,
phlebitis, azotemia, refeeding syndrome, and electrolyte
abnormalities. Late complications include trace element
deficiencies, hepatobiliary disorders (hepatic steatosis, PNALD
(PN-associated liver disease), metabolic bone disease, and central
line infections.
For information regarding managing macronutrient-related and
micronutrient-related complications, see Table 1-30.

325
Table 1-30
MACRONUTRIENT AND MICRONUTRIENT COMPLICATIONS IN
PATIENTS ON TOTAL PARENTERAL NUTRITION

Complication Management Strategy

Macronutrient-Related

Hyperglycemia Consider insulin therapy (exogenous insulin or insulin added to total

parenteral nutrition [TPN]). Monitor blood glucose every 4 to 6 hours
initially.
Patients with diabetes or at risk for hyperglycemia should start with
lower dextrose concentrations in TPN.

Hypoglycemia Avoid stopping TPN abruptly (rebound hypoglycemia).

May be related to excessive insulin in TPN.
Ensure that all physicians and midlevel practitioners are aware about
insulin being added to TPN so that excess insulin is not prescribed.

Hypertriglyceridemia Can result from either excessive intravenous (IV) fat emulsion or by
infusing IV fat emulsion too quickly.
Hypertriglyceridemia can also result from excessive dextrose
administration.
Monitor triglycerides weekly. Hold IV fats for triglycerides >400 mg/dL.
Essential fatty acid Usually seen in patients who are not receiving IV fat emulsion with
deficiency (EFAD) TPN.
Can occur within 1 to 3 weeks of IV fat emulsion-free TPN.
Minimum IV fat emulsion necessary to prevent EFAD is 100 g weekly
(500 mL of 20% IV fat emulsion)
Azotemia Usually occurs because the patient is either receiving excessive protein,
inadequate fluid, or both.
Monitor input and output for signs of dehydration. Ensure adequate
fluid intake.
Micronutrient and Fluid and Electrolyte Disturbances: See Tables 1-21, 1-22
Refeeding syndrome Usually attributable to carbohydrate administration in patients who are
malnourished or prolonged NPO (nil per os) status. Initiate TPN slowly
(lower % dextrose). Monitor electrolytes (especially phosphorus,
potassium, and magnesium). Consider the addition of thiamine in TPN
to prevent thiamine deficiency and subsequent lactic acidosis, beriberi,
and Wernicke encephalopathy.
From Kumpf VJ, Gervasio J. Complications of Parenteral Nutrition. The A.S.P.E.N.
Adult Nutrition Support Core Curriculum, 2nd Edition. Charles M. Mueller, Editor.
2012.

For information regarding signs and symptoms of vitamin,

mineral, and trace element deficiencies, see Tables 1-21 and 1-22.

Table 1-22
SIGNS AND SYMPTOMS OF TRACE ELEMENT DEFICIENCY AND
TOXICITY

326
 Trace
Signs of Deficiency Toxicity
Element
Chromium Glucose intolerance, hyperlipidemia, Renal failure, anemia,
peripheral neuropathy, encephalopathy thrombocytopenia, liver failure
Copper Common: hypochromic, microcytic anemia Gastrointestinal symptoms, hepatic
and neutropenia (similar to signs and failure
symptoms of vitamin B12 deficiency) Biliary excretion – caution in liver
Central nervous system dysfunction, failure
hypotonia

Manganese Weight loss, transient dermatitis Parkinson-like motor dysfunction,

Rare: nausea and vomiting neurologic and psychiatric
symptoms (irritability,
hallucinations)

Selenium Cardiomyopathy, myalgia, myositis, Chronic: nail and hair changes, N/V,
hemolysis, and impaired cellular immunity weight loss, paresthesias, fatigue,
garlic odor on breath, ↑ incidence
of diabetes
Acute (rare): cardiac abnormalities,
hypotension

Zinc Dermatitis, alopecia, anorexia, growth Gastrointestinal symptoms, copper

failure, reduced taste sensitivity, poor night deficiency, renal failure, neuropathy,
vision, immune compromise, impaired metallic taste
wound healing

From Vanek VW, Borum P, Buchman A, et al. A.S.P.E.N. position paper

recommendations for changes in commercially available parenteral multivitamin and
multi-trace element products. Nutr Clin Pract. 2012;27:440-491. Jensen GL and
Binkley J. Clinical manifestations of nutrient deficiency. JPEN J Parenter Enteral
Nutr. 2002;26:S29-S33

Electrolyte imbalances
Electrolyte imbalances can occur during the administration of both
enteral nutrition and PN (Table 1-31).

Table 1-31
POSSIBLE ELECTROLYTE IMBALANCES OCCURRING IN
ENTERAL AND PARENTERAL NUTRITION

Sodium: Daily requirement is 1 to 2 mEq/kg. Sodium is the primary extracellular cation in

maintaining concentration and volume of extracellular fluid.
Complication Pathophysiology and Management
Hypernatremia May result from free water deficit, overdiuresis, excessive water loss,
hypertonic total parenteral nutrition (TPN) solutions, inadequate
volume of TPN solutions, or inadequate water flushes via feeding tube.
May be attributable to nephrogenic or central diabetes insipidus,
uncontrolled diabetes mellitus, or use of sodium penicillin, heparin
sodium, or corticosteroids.
Management

327
 Parenteral: Increase free water, decrease sodium in TPN, increase volume
of TPN.
Enteral: All enteral formulas are low sodium. Change tube feeding
formula to less concentrated formula and increase water flushes.
Hyponatremia Most common cause in patients receiving TPN is administration of
hypotonic fluids or volume overload. In patients who are tube-fed,
hyponatremia may be caused by excessive fluid administration or
excessive water flushes. Other causes of hyponatremia include adrenal
insufficiency, renal insufficiency, SIADH (syndrome of inappropriate
antidiuretic hormone), cirrhosis, and chronic heart failure.
Management
Parenteral: Decrease fluid and/or increase sodium in TPN.
Enteral: Switch to calorie-dense, fluid-restricted tube-feeding formula,
decrease water flushes via feeding tube or flush with normal saline as
directed.

Potassium: Daily requirement is 1 to 2 mEq/kg. Potassium is the major intracellular cation

required for neurotransmission, protein synthesis, cardiac and renal function, and carbohydrate
metabolism.
Complication Pathophysiology and Management
Hyperkalemia May be caused by excessive parenteral or enteral potassium
supplementation, metabolic acidosis, increased tissue catabolism, and
renal insufficiency. Medications that can cause elevated potassium
levels include angiotensin-converting enzyme inhibitors, angiotensin
receptor blockers, heparin, cyclosporine, and potassium-sparing
diuretics.
Management
Parenteral and Enteral: Decrease potassium in TPN or switch to low
electrolyte tube-feeding formula. Decrease other sources of exogenous
potassium (in intravenous [IV] fluids, potassium supplementation).
Consider stopping or reducing dose of potassium-sparing medications.
Correct metabolic acidosis with sodium bicarbonate if present. May
require administration of glucose with insulin, IV calcium gluconate (if
electrocardiography changes are present), beta2-adrenergic agents (e.g.,
albuterol), or hemodialysis in severe cases.

Hypokalemia May occur during anabolism (tissue synthesis) in patients or in refeeding

syndrome causing potassium to shift into the intracellular space. Other
causes include excessive gastrointestinal (GI) losses, diuretic use, or
inadequate potassium intake. In metabolic alkalosis, potassium is also
decreased (potassium is decreased by 0.4 to 1.5 mEq/L for every 0.1
increase in pH).
Management
Parenteral: Increase potassium in TPN, provide potassium
supplementation in patients receiving tube feeding. Potassium given
via a peripheral line can be irritating to the peripheral vein.
Administration via a peripheral line should not exceed 10 mEq/h.
Enteral: PO (per os) potassium supplementation can be irritating to GI
mucosa and may cause diarrhea. If hypomagnesemia is present, it
should be corrected before potassium supplementation.
Both: Initiate tube feeding or TPN slowly to avoid refeeding syndrome.
Correct metabolic alkalosis if present.
Phosphorus: Daily requirement is approximately 20 to 40 mmol/day. Phosphorus is required
for release of oxygen from hemoglobin in the form of 2,3-diphosphoglycerate and for bone
deposition, calcium regulation, and synthesis of carbohydrates, fats, and protein.
Complication Pathophysiology and Management
Hyperphosphatemia Occurs in catabolic stress, renal failure, and hypocalcemia or excessive

328
 exogenous administration of phosphorus. Medications that can cause
hyperphosphatemia include phosphorus-rich solutions, antacids,
diuretic agents, and steroids. Associated with metabolic acidosis.
Management
Parenteral: Decrease phosphate in TPN or other exogenous phosphate
administration.
Enteral: May require treatment with phosphate binders such as
sevelamer (Renvela) and calcium acetate (PhosLo). Change to a renal
tube-feeding formula.
Hypophosphatemia A complication with a high mortality, often found in malnourished
patients with refeeding syndrome. As the patient receives fluids
containing dextrose, phosphorus shifts rapidly into the intracellular
space, causing hypophosphatemia. Refeeding syndrome also affects
other intracellular electrolytes, particularly potassium and magnesium.
Associated with metabolic alkalosis.
Management
Parenteral and Enteral: Initiate tube feeding or TPN slowly to avoid
refeeding syndrome.
Parenteral: Increase phosphorus in TPN or provide other sources of
phosphorus (sodium phosphate, potassium phosphate) in patients
with low phosphorus levels.

Magnesium: Daily requirement is 18 to 30 mEq/day. Magnesium is required for carbohydrate

and protein metabolism and enzymatic reactions.

Complication Pathophysiology and Management

Hypermagnesemia Generally seen with excessive magnesium supplementation including

magnesium-containing antacids or renal failure. Medications include
Milk of Magnesia and magnesium citrate.
Management
Parenteral: Decrease magnesium in TPN or IV fluids.
Parenteral and Enteral: Discontinue any medications that contain
magnesium. May require diuresis or hemodialysis in severe cases.
Hypomagnesemia Low levels commonly occur in patients with severe malnutrition,
patients with refeeding syndrome, or in patients with lower GI losses,
prolonged nasogastric suctioning, and diabetic ketoacidosis. Often
occurs in alcoholics, malabsorption syndromes, and the critical care
population. Medications that can cause hypomagnesemia include
diuretics, insulin, and cyclosporine.
Management
Parenteral: Increase magnesium in TPN, give supplemental magnesium.
Parenteral magnesium should be used to treat moderate to severe
hypomagnesemia in patients receiving parenteral and enteral nutrition.
Enteral: Give oral magnesium supplements. Monitor for diarrhea.
Calcium: Daily requirement is 1000 to 1500 mg (10 to 15 mEq/day) of elemental calcium.
Calcium is a necessary ingredient of the cells that plays a major role in neurotransmission and
bone formation.
Complication Pathophysiology and Management
Hypercalcemia Occurs in prolonged immobilization, malignancy, hyperparathyroidism,
tumor lysis syndrome, adrenal insufficiency, and renal failure.
Medications that can cause hypercalcemia include thiazide diuretics,
lithium, calcium supplements, and aluminum-containing and
magnesium-containing antacids.
Management
Parenteral and Enteral: Volume expansion with normal saline, which
disrupts the stimulus for calcium reabsorption in the kidney. Loop
diuretics are calcium wasting and may be used in cases of severe

329
 hypercalcemia. Bisphosphonates can be used to treat chronic
hypercalcemia.
Parenteral: Decrease calcium in TPN.
Hypocalcemia Occurs with reduced vitamin D intake, hypoparathyroidism, and
hypomagnesemia. Medications that can cause hypocalcemia include
loop diuretics, bisphosphonates, calcitonin, phenobarbital, and
phenytoin.
Management
Parenteral and Enteral: Calcium supplementation (parenteral or oral).
Ionized calcium level should be used as a guide to replacement,
because serum calcium is bound to albumin. If albumin level is low,
calcium level will appear falsely low.

Transitional feeding
A period of adjustment is needed before discontinuing nutrition
support. It is good practice to taper enteral nutrition and PN as oral
intake increases instead of discontinuing nutrition support as soon
as the patient is able to take a PO diet. Often, parenteral or enteral
nutrition can be cycled over a period of hours as a means of
tapering. For example, the nutrition support clinician may cycle the
enteral or parenteral feeding at night to allow the patient to increase
PO intake during the day. If nutrition support is not tapered when
the patient begins an oral diet, this can interfere with the patient’s
appetite and minimize his or her PO intake, keeping him or her on
nutrition support for longer than necessary.

Care plans: Patients receiving enteral and

parenteral nutrition
Imbalanced nutrition: Less than body requirements 
related to the inability to ingest, digest, or absorb nutrients.
Goals/Outcomes: Within 7 days of initiating parenteral/enteral
nutrition, the patient’s nutritional status is improving, as evidenced
by stable weight or steady weight gain (weight gain is not often
seen in the acute care setting); malnutrition is improved, as
indicated by increasing or normal measures of protein stores
(serum albumin, transferrin, prealbumin, and retinol-binding
protein)—usually not seen in the critical care setting; positive
nitrogen balance; presence of wound granulation; and absence of

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infection (see Risk for Infection).
Nutritional Status: Nutrient Intake.

Nutrition monitoring

1. Ensure nutrition screening and assessment of the patient within

24 to 48 hours of admission by nursing staff and within 72 hours by
a dietitian; document nutrition assessment. See Nutrition
Assessment. Reassess weekly.

2. Monitor electrolytes and blood glucose levels daily until

stabilized. Ensure that serum albumin, transferrin, or prealbumin
are monitored weekly. Ensure that trace elements are monitored
periodically (quarterly).

3. Monitor hemoglobin and hematocrit, as the patient may have an

iron-deficiency anemia or a macrocytic anemia (B12 or folate
deficiency).

4. Weigh the patient daily.

5. Monitor for dry, flaky skin with depigmentation (sign of

vitamin/trace element deficiency or EFAD).

6. Monitor for pale, reddened, and dry conjunctival tissue (sign of

vitamin/trace element deficiency).

7. Evaluate energy level for malaise, weakness, and fatigue

indicative that the patient is not receiving adequate nutrition to
promote strength and mobility.

8. Monitor for spoon-shaped, brittle, ridged nails (sign of vitamin

deficiency).

9. Record I&O carefully, tracking fluid balance trends. Check

volume enteral nutrition or PN infused and rate of infusion hourly.

10. Ensure that the patient receives the prescribed amount of

nutrients.

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11. Be aware that residual volumes of gastric feedings include not
only feeding but also gastric secretions. The amount of residual
feeding is NOT purely feeding. More recent studies indicate that
caregivers may not need to be concerned about residual volumes of
less than 250 to 500 mL. Patient positioning also effects the amount
of residual volume that may be found by the caregiver.

Ineffective protection resulting in risk for aspiration 

related to GI bleeding, delayed gastric emptying, or location/type of
feeding tube.
Goals/Outcomes: The patient is not aspirating, as evidenced by
auscultation of clear breath sounds; vital signs within the patient’s
baseline; and absence of signs of respiratory distress.
Immune Status, Respiratory Status.

Enteral tube feeding

1. Check the radiograph to assess the position of the feeding tube

before the first feeding (Note: Radiographic confirmation is not
required for PEG tubes or surgically placed feeding tubes). Mark
and secure the tube for future reference. Insufflation with air and
aspiration of stomach contents are commonly used to confirm
position thereafter but do not guarantee correct position and are no
longer recommended by the American Association of Critical Care
(AACN) guidelines.

2. Assess the respiratory status at least every 4 hours, observing

respiratory rate and effort, and presence of adventitious breath
sounds.

3. Monitor temperature at least every 4 hours.

4. Auscultate for bowel sounds, and assess abdominal contour and

girth every 8 hours. Consult the advanced practice provider if the
abdomen becomes distended, or nausea and vomiting occur.

5. Elevate the HOB at least 30 degrees during and for 1 hour after
feeding. If the patient is receiving continuous enteral nutrition, the
HOB should always be elevated at least 30 degrees.

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6. Notify the advanced practice provider if gastric residual is
greater than 250 to 500 mL (per institution protocol) or if the patient
is having any signs of abdominal pain or distention. The patient
should be positioned on their right side for 20 minutes before
aspirating the enteral tube for residual volume to ensure that
feeding is being directed toward the small bowel. False high
volumes may be reported if feeding has pooled in the body of the
stomach in a supine patient. If the caregiver is certain that the
residual volume was properly obtained, hold feeding for 1 hour,
and then recheck residuals.

7. Stop the enteral feeding 0.5 to 1 hour before chest physical

therapy or lowering the HOB when the patient is supine.

8. Discuss with the advanced practice provider the possibility of

placing the feeding tube beyond the pylorus to help minimize the
risk for aspiration in patients at higher risk for aspiration.

9. As prescribed for delayed gastric emptying, administer

prokinetic agents such as metoclopramide HCl, erythromycin, or
other agents that promote gastric motility.

Diarrhea 
related to adjustment to formula, method of administration, and volume of
enteral feeding.
Goals/Outcomes: The patient has begun to form normal stools
within 24 to 48 hours of intervention.
Bowel Elimination, Electrolyte and Acid-Base Balance;
Nutritional Status: Food and Fluid Intake

Diarrhea management

1. Assess abdomen and GI status, including bowel sounds,

distention, consistency and frequency of bowel movements,
characteristics of stools, cramping, skin turgor, and indicators of
hydration such as skin turgor, thirst, and presence or absence of
sunken eyes.

2. Obtain daily weights and monitor I&O status carefully to prevent

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dehydration.

3. Cramping or diarrhea associated with bolus feeding: Evaluate

whether proper technique is used for bolus feeding, including a
slow infusion of a room temperature feeding. If proper technique is
used and cramping results, switch to an intermittent, cyclic, or
continuous feeding method.

4. Evaluate the patient for presence of Clostridium difficile if diarrhea

is present with any patient who is critically ill. Diarrhea is often
blamed on tube feeding intolerance, when the actual cause is
inappropriate use of antibiotics resulting in antibiotic-associated
diarrhea or C. difficile-associated diarrhea.

5. Avoid lactose-containing products. Most enteral products are

lactose-free.

6. Bacterial contamination:

• Use clean technique in handling feeding tube,

enteral products, and feeding sets.

• Wear disposable gloves when administering enteral

nutrition.

• Change administration sets every 24 hours.

• Hang time for reconstituted formula, enteral

nutrition with additives, or mother’s milk is 4
hours.

• Use sterile water for reconstitution of powdered

formula.

• Hang time for sterile decanted formula is 8 hours.

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• Hang time for closed-system enteral formulas is 24
to 48 hours per manufacturer’s guidelines.

• Refrigerate all opened products but discard them

after 24 hours.

• A feeding pump with a drip chamber is

recommended because it can prevent retrograde
contamination of the enteral formula from the
feeding tube.
7. Osmolality intolerance:

• Determine osmolality of feeding formula. Most are

isotonic (plasma osmolality 300 mOsm). If
hypertonic, change to an isotonic formula.

• Determine the osmolality of medications

administered via feeding tube. If hyperosmolar,
dilute the medications before administration.

8. Medications:

• Monitor use of antibiotics, antacids, potassium

chloride, and sorbitol in liquid medications. Dilute
liquid medications with water. Use sterile water for
dilution of medication.

• The use of probiotics to restore GI flora is

controversial and should only be given as
prescribed by the physician or midlevel
practitioner. ASPEN-SCCM guidelines do not have

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 a recommendation for administration of probiotics
in patients in ICU. The 2013 CCCN guidelines
currently recommend that probiotics be considered
in patients who are critically ill. There have been
reports of gut ischemia with probiotic use in
patients with acute pancreatitis (PROPATRIA trial)
and there have been several cases of fungemia
associated with the use of Saccharomyces boulardii
(Florastor). Therefore, it would be prudent to avoid
use of probiotics in patients with acute pancreatitis
and to avoid the use of Florastor in patients in ICU
or those with CV catheters.

Impaired tissue integrity 

related to mechanical irritant presence of enteral tube, intolerance of tube
feeding, diarrhea, or hyperglycemia.
Goals/Outcomes: At time of discharge from critical care, the
patient’s tissue is intact with absence of erosion around orifices,
excoriation, skin rash, or mucous membrane breakdown.
Bowel Elimination, Nutritional Status: Food and Fluid Intake,
Tissue Integrity: Skin and Mucous Membranes.

Skin surveillance

1. Initiate appropriate strategies to manage diarrhea, control blood

glucose, and assess tolerance of tube feeding. Changing the site of
feeding/feeding tube insertion and type of feeding may assist with
tolerance of feedings and diarrhea, which will facilitate
improvement of skin integrity.

2. Maintain blood glucose goal ranges of 140 to 180 mg/dL in

patients who are critically ill to enhance wound healing.

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Nasoenteric tube/postpyloric feeding tube

3. Assess nares for irritation or tenderness every 8 hours and alter

position to avoid pressure. Use hypoallergenic tape to anchor tube.

4. Use a small-bore tube if possible.

5. Provide frequent oral care to maintain integrity of teeth and oral

mucosa.

6. If long-term support is needed (> 4 weeks), discuss using

gastrostomy or jejunostomy tube with the physician or midlevel
practitioner.

7. Give ice chips, chewing gum, or hard candies PRN (pro re nata
[when necessary]) if permitted.

8. Apply petroleum jelly to lips every 2 hours.

9. Brush teeth and tongue every 8 hours.

Gastrostomy tube/PEG

10. Assess site for erythema, drainage, tenderness, and odor every 4
hours.

11. Monitor placement of tube every 8 hours.

12. Secure tube so that there is no tension on the patient’s tissue and
skin.

13. After insertion, clean skin with mild soap and water. Rinse and
dry the area thoroughly. Routine use of antibiotic ointment and
hydrogen peroxide is no longer recommended.

Jejunostomy tube/PEJ

14. Assess site for erythema, drainage, tenderness, and odor every 4
hours.

15. Secure tube to avoid tension. Coil tube on top of dressing if

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necessary.

16. Provide frequent oral care to maintain integrity of teeth and oral
mucosa.

17. Skin care for a PEG tube is the same as for gastrostomy tube.

18. Avoid large-volume water flushes (greater than 120 mL) as this
may cause small bowel necrosis.

19. Avoid bolus feeding via a jejunal feeding tube as this can cause
abdominal pain and can lead to small bowel necrosis.

Risk for infection 

related to the presence of central line for TPN
Goals/Outcomes: The patient does not acquire a bloodstream
infection, as evidenced by temperature and vital signs within
normal limits, total lymphocytes 25% to 40% (1500 to 4500 mL),
WBC count less than 11,000/mm3, and absence of clinical signs of
sepsis, including erythema and swelling at insertion site, chills,
fever, and hyperglycemia.
Immune Status, Respiratory Status.

Infection protection

1. When the central line is inserted, ensure that the CDC central line
insertion guidelines are followed, including use of full barrier
precautions.

2. Twice weekly and PRN, monitor CBC and differential for values
outside the normal range.

3. Check blood glucose at least every 6 hours initially or using the

facility’s guidelines for values outside the normal range.

4. Examine catheter insertion site(s) every 8 hours for erythema,

swelling, or purulent drainage.

5. Use sterile technique when changing central line dressing,

containers, or lines.

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6. Avoid using the nutrition support port on the central IV or PIV
catheter for blood drawing, pressure monitoring, or administration
of medications or other fluids.

7. Change all IV administration sets and rotate insertion site within

the time frame per institutional protocol.

8. Do not allow parenteral solutions to hang longer than 24 hours.

9. If infection or sepsis is suspected, take blood specimens for

culture and administer antibiotics as prescribed. Remove catheter
and culture catheter tip if prescribed.

10. Routine use of antibiotic ointments at catheter insertion site is

not recommended.

Risk for injury 

related to central line insertion.
Goals/Outcomes: The patient has adequate gas exchange, as
evidenced by stable vital signs, stable ABG values, normal bilateral
chest excursion, and arterial oximetry within normal limits, and
absence of dyspnea, tachypnea, cyanosis, chest pain, tachycardia,
and hypotension.
Neurological Status: Consciousness, Respiratory Status.

IV insertion

1. When central line is inserted, place the patient in the

Trendelenburg position.

2. Observe central line insertion procedure and remind the

practitioner inserting the line to avoid leaving the catheter open to
air once blood vessel has been entered.

3. If the patient experiences SOB, tachypnea, chest pain,

hypotension, or cyanosis during line insertion, place on his or her
left side in the head down position to facilitate trapping any air
introduced in the right ventricle, and administer high-flow O2 by
face mask.

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4. Check chest radiograph film to determine catheter position
following insertion.

IV therapy

1. Use the Trendelenburg position when changing tubing or when

CV catheters are inserted or removed.

2. Teach the patient the Valsalva maneuver (if possible) for

implementation during tubing changes.

3. Use Luer-Lock connectors on all connections.

4. Use occlusive dressing over insertion site for 24 hours after the
catheter is removed to prevent air entry via catheter-sinus tract.

5. Monitor the patient for chest pain, tachycardia, tachypnea,

cyanosis, and hypotension.

6. If air embolus is suspected, clamp the catheter and turn the

patient to left side-lying Trendelenburg position to trap air in the
right ventricle. Administer high-flow O2 and contact the physician
immediately.

Risk for imbalanced fluid volume 

related to overhydration or underhydration.
Goals/Outcomes: The patient’s hydration status is adequate, as
evidenced by baseline vital signs, glucose less than 300 mg/dL,
balanced I&O, urine specific gravity 1.010 to 1.025, and electrolytes
within normal limits.
Fluid Balance, Electrolyte and Acid-Base Balance; Nutritional
Status: Food and Fluid Intake, Hydration

Fluid monitoring

1. Weigh the patient daily; monitor I&O hourly.

2. Consult advanced practice provider for urine output less than 0.5
mL/kg/h.

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3. Check urine specific gravity; consult the physician or midlevel
practitioner for elevated specific gravity according to institutional
guidelines.

4. Monitor serum osmolality and electrolytes daily and PRN;

consult the physician or midlevel practitioner for abnormalities.

5. Monitor for circulatory overload during fluid replacement.

Ensure that IV fluids are adjusted when TPN or enteral nutrition is
initiated to prevent volume overload.

6. Monitor for indicators of hyperglycemia and manage

appropriately to avoid osmotic diuresis. Perform point-of-care
blood glucose reading at least every 6 hours or using institutional
guidelines until blood glucose is stable. Administer insulin
according to institutional guidelines to control blood glucose.
Targets for blood glucose during critical illness may range from 140
to 180 mg/dL.

7. Assess rate and volume of nutrition support hourly. For HHNS,

discontinue infusion until blood glucose and fluid balance is
normalized. Reset to prescribed rate as indicated (see
Hyperglycemia, Ch 8).

8. Provide 1 to 2 mL water for each calorie of enteral formula

provided (or 30 to 40 mL/kg body weight). For patients with fluid
restriction, provide either less than 25 mL/kg water or 1.4 to 1.9 L
daily. Make sure to include the free water provided by the enteral
formula to prevent fluid overload.

Additional nutrition-related nursing

diagnoses
For other nursing diagnoses and interventions, see Fluid and
Electrolyte Disturbances, which includes a discussion of electrolyte
abnormalities listed in Table 1-31.

Pain
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Advances in pharmacologic and complementary therapies, ongoing
research in pain management and numerous guidelines, position
statements, and practice recommendations have flourished over the
past decades. Despite these innovations and national and
international efforts, pain remains a common phenomenon in ICU.
Patients who are critically ill experience moderate to severe pain at
rest and during procedures such as turning, drain removal,
coughing, and endotracheal suctioning. Removal of endotracheal
tubes, a common procedure in ICU, is a substantial trigger of severe
pain in patients in ICU, and the majority of patients who are
mechanically ventilated experience moderate to severe pain despite
an unrestricted use of fentanyl and morphine. In addition to
procedure-induced pain, pathologic conditions, tissue damage, and
immobility are common sources of pain. The acuity and care
requirements of patients admitted in ICU expose them to multiple
sources of pain. These are presently addressed with pharmacologic
and nonpharmacologic treatments, yet pain remains undertreated
in most of these patients.
Advances in medical technology and an aging population have
resulted in an increased demand for intensive care services
including the use of invasive procedures such as endotracheal
intubation. Ultimately, the need for better pain relief of patients in
ICU will only continue to grow.
Unrelieved pain is not benign but affects every aspect of the
patient’s experience with critical care. It is a significant stressor for
patients who are critically ill and contributes to and potentiates
other problems such as confusion, inadequate ventilation,
immobility, sleep deprivation, depression, and
immunosuppression, which can lead to extended healing times. The
cardiovascular effects of unrelieved pain are increased HR, BP,
SVR; increased myocardial O2 consumption; altered regional blood
flow; and deep vein thrombosis (DVT). The pulmonary effects
noted of uncontrolled pain are decreased lung volumes, atelectasis,
decreased cough effort, increased sputum retention, and
hypoxemia. GI and genitourinary effects are decreased gastric and
bowel motility and urinary retention. The neuroendocrine response
to uncontrolled pain is to release more of the stress hormones such
as catecholamines, cortisol, and glucagon. Psychological effects are

342
anxiety, fear, and sleeplessness.
Unrelieved pain can also lead to multisystem complications,
anatomic changes, and physiologic changes in the nervous system
contributing to the development of chronic disabling pain and
posttraumatic stress disorder, which in turn may seriously impact
the patient’s functioning, quality of life, and well-being. The
negative impacts of pain are not only experienced by the patient
admitted in ICU but they also extend to family members and
significant others. Admission of a relative who is critically ill to ICU
causes both stress and anxiety to family members. They are
exposed to a number of potential stressors including deterioration
in the patient’s condition, uncertain prognosis, an unfamiliar
environment loaded with mechanical equipment, and pain and
suffering experienced by the patient. Posttraumatic stress disorder,
anxiety, guilt, frustration, and depression are some of the emotional
reactions of families to such stressors.

Pathophysiology
Pain is a warning signal to which the body responds to prevent
further injury. Nociception represents the neural processes of
encoding and processing noxious stimuli that can be perceived as
painful. Four processes are involved in nociception: (1)
transduction, (2), transmission, (3) perception, and (4) modulation.
In summary, transduction refers to the mechanical (e.g., surgical
incision), thermal (e.g., burn), or chemical (e.g., toxic substance)
noxious stimuli that damage tissues. These noxious stimuli lead to
the release of excitatory neurotransmitters that stimulate
nociceptors and thus serve to initiate transmission. Afferent nerve
fibers such as A delta (Aδ) and C fibers respond to pain stimuli
peripherally and relay this information to the spinal cord entering
through the dorsal horn. Aδ fibers are small, myelinated, fast-
conducting fibers that transmit pain sensation that is well localized.
C fibers are small, unmyelinated, slow-conducting fibers that
transmit poorly localized, dull, aching pain sensations. In the dorsal
horn, neurotransmitters such as substance P are released in
response to the nociceptive input that activates the second-order
dorsal horn neurons. The activation of the second-order neurons

343
results in (1) spinal reflex responses such as muscle spasm, and
increased sensitization; and (2) activation of the ascending tracts,
which transmits the nociceptive input to several regions within the
brain. This is where several responses to pain occur, including the
perception of pain and the emotional and behavioral responses.
Modulation refers to the release of endogenous opioids, which
inhibit, through the descending pathways, the transmission of the
nociceptive signal in the spinal cord and produce analgesia.

Assessment
Definition and types of pain
Pain is described as an unpleasant sensory and emotional
experience associated with actual or potential tissue damage. Such a
definition highlights the subjectivity of a complex multidimensional
pain experience. Indeed, the “gold standard” measure for pain is
the patient’s self-report. However, in the critical care setting, many
patients are unable to self-report their pain. In such a situation,
behavioral changes caused by pain are valuable forms of self-report
and should be considered as alternative measures of pain. The
inability to self-report does not negate the possibility that an
individual is experiencing pain and is in need of appropriate pain-
relieving treatment, and pain assessment methods must be adapted
to the patient’s cognitive capacity and condition.
Pain can be classified as acute or chronic, and nociceptive or
neuropathic. Acute pain implies tissue damage that is usually from
an identifiable cause that lasts for the healing process, which is
approximately 30 days. Chronic pain persists for more than 3 to 6
months following the healing process. Pain can be nociceptive or
neuropathic. Nociceptive pain arises from the activation of
nociceptors and can be of somatic or visceral origin. Somatic pain
involves peripheral tissues such as the skin, muscles, joints, and
bones. Visceral pain involves organs such as the heart, stomach,
and liver. Neuropathic pain arises as a direct consequence of an
injury or disease affecting the somatosensory system. It can
originate from the peripheral (e.g., neuropathy) or central (e.g.,
phantom pain, stroke) somatosensory system.

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Goal of assessment
Pain assessment is an integral part of nursing care and is a
prerequisite for adequate pain management. Pain is a subjective
and multidimensional concept that requires complex assessment.
Many factors may alter verbal communication in patients who are
critically ill, making pain assessment more difficult. The American
Society for Pain Management Nursing has described a stepwise
approach for pain assessment in vulnerable patients including the
critically ill:

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1. Attempt to obtain the patient’s self-report of pain: A
comprehensive initial assessment of pain, whenever possible, is
important in accurately evaluating and managing pain. Regular
follow-up pain assessments are necessary postoperatively and
during ICU stay until the pain is well controlled. A simple yes or no
for presence or absence of pain communicated verbally or using
signs (e.g., head nodding, hand grasping) should be considered as a
valid self-report.

2. Identify potential causes of pain: Pathologic conditions requiring

admission to ICU and care procedures (e.g., turning, endotracheal
suctioning, drain/tube removal, wound care) known to be painful
in patients who are critically ill should trigger an intervention. If
there is reason to suspect pain, the critical care nurse may assume
that pain is present and attempt an analgesic trial (according to the
2008 American Pain Society guidelines). Other problems that may
be causing pain or discomfort should be identified and adequately
treated (e.g., infection, constipation).

3. Observe changes in the patient’s behaviors: When it is not

possible to obtain the patient’s self-report of pain, behavior
observation is an alternative and valid approach to pain
assessment. Although behaviors are useful in detecting if pain is
present or not, it is not an accurate reflection of pain intensity.
Indeed, a behavioral pain score of 5/10 is not equal to a patient’s
self-report of pain intensity of 5/10 as these two measures assess
different aspect of the pain experience. Awareness of the patient’s
baseline and changes that occur during care procedures are useful
in differentiating pain from other causes.

4. Use of proxy reporting: Relevant information can be obtained

from a family member or relative who knows the patient well. Their
familiarity with the patient and knowledge of their behaviors can
assist the critical care nurse in identifying changes in behaviors that
may be indicative of pain. Discrepancies exist between the patient’s
self-report and the external observer’s evaluations of pain intensity.

346
1-3
RESEARCH BRIEF BOX
Puntillo et al. compared patient, family member, nurse reports, and
physician reports of the perceived intensity and distressing aspects
of pain in patients in the intensive care unit. Family members’
reports of both the intensity and distress of the patient’s pain was
positively moderately correlated with the patient’s self-report.
Interestingly, these family members were more accurate at
determining the intensity and distress of their loved one’s pain
than that of the physicians and nurses currently in charge of the
patient’s care. Proxy pain assessments should be combined with
other evidence such as direct observation using validated
behavioral pain scales, and the patient’s diagnosis, health history
and physical examination, and evaluation of treatment response.
Derived from Puntillo KA, White C, Morris AB, et al: Patients’ perceptions and responses
to procedural pain: results from Thunder Project II. Am J Crit Care 10(4):238-251, 2001.

History and risk factors

Origins for undertreated pain in the intensive care unit

Interferences with optimal pain management persist and are often
attributed to the patient, the healthcare team, and the healthcare
system. In the critical care context, clinician-related barriers such as
knowledge deficits regarding pain assessment and management
principles, personal and cultural bias, and communication
difficulties between the patient and the healthcare team have been
the main contributors to suboptimal pain management. Specific
professional and patient-related barriers include (1) societal
expectations concerning pain (e.g., unrelieved pain is expected and
accepted in certain situations such as during surgical or invasive
procedures, treatment for malignant conditions, or as a normal part
of aging); (2) professionals’ knowledge deficits regarding the
pharmacokinetics and equianalgesic dosing; (3) patients’ lack of
knowledge concerning the side effects of unrelieved pain and the
lack of knowledge of pain management in general; (4) inadequate
pain assessment techniques by healthcare professionals (failure to
assess and acknowledge the existence of pain); (5) inappropriate

347
professional attitudes and beliefs (e.g., certain patients do not have
pain [e.g., neonates], pain management is low priority); (6)
inappropriate patients’ attitudes and beliefs (e.g., pain builds
character, pain is a part of procedures); (7) cultural norms that
frame the expected response to pain (e.g., succumbing to pain is a
sign of weakness); (8) views of the spiritual significance of enduring
suffering (e.g., suffering on earth will entitle the person to more
rewards in the afterlife); and (9) fear of tolerance, addiction, and
analgesic side effects by both professionals and patients.

Assessment

Vital signs to use with caution in pain assessment

Vital signs such as BP, HR, and RR are easily accessible through
continuous monitoring and are widely used by critical care nurses
for pain assessment. However, their validity for this purpose is not
supported because vital signs have been found to increase,
decrease, or remain stable in patients in ICU. Fluctuations in vital
signs may also occur with physiologic or emotional distress, or may
be a medication effect (e.g., vasodilation and decreased BP
following the administration of morphine). No vital signs have
been found to predict the presence of pain. Considering that vital
sign use for pain assessment remains poor, they are not considered
valid pain indicators and should only be used as cues to begin
further assessment of pain.

Self-report pain assessment tools

Whenever possible, the patient’s self-report of pain should be
obtained. Mechanical ventilation should not be a barrier for critical
care nurses to document patients’ self-reports of pain. Indeed,
many patients who are intubated can use pain scales by pointing to
them. Attempts should be made before concluding that a patient is
unable to self-report. Sufficient time must be allowed for the patient
to respond with each attempt. Various self-report pain scales exist
such as 0 to 10 Numeric Rating Scale (NRS; where 0 refers to “no
pain” and 10 to “worst possible pain”), 100 mm Visual Analog
Scale, Verbal Descriptor Scale (VDS; no pain, mild, moderate,
severe), and Faces Scales (Figure 1-10). The use of a tool must take

348
into account the patient’s preference. A vertical pain intensity scale
seems to be easier to use for patients who are elderly because it
reminds them of a thermometer. Also, in a recent study, an
enlarged, readable horizontal 0 to 10 NRS-Visual was the most
feasible scale in patients in ICU. Once the nurse determines which
scale the patient can use, the same scale should be used for the
duration of clinical care so that accurate comparisons can be made
regarding the patient’s pain intensity, effectiveness of pain
management strategies, and to guide further alterations in pain
relief efforts.

FIGURE 1-10 Pain intensity scales. A, 0 to 10 Numeric

Scale. B, Visual Analog Scale. C, Descriptive Scale. D,
Faces Pain Scale–Revised Source: (From Hicks et al., 2001;
www.painsourcebook.ca). E, Faces Pain Thermometer (From Hicks et al.,
The Faces Pain Scale-Revised: toward a common metric in pediatric pain
measurement. Pain. 2001 Aug;93(2):173-83) (From Gelinas C:
Management of pain in cardiac surgery intensive care unit patients: have we

349
 improved over time? Intensive Crit Care Nurs 23(5):298-303, 2007).

Behavioral pain scales

Several behavioral pain assessment tools have been developed in
recent years. The Behavioral Pain Scale (BPS) and the Critical-Care
Pain Observation Tool (CPOT) are the two suggested scales for
clinical use in patients in ICU in the recent practice guidelines of the
SCCM. A cut-off score is useful to identify the presence of
significant pain and can help to evaluate the effectiveness of pain
management interventions. The cut-off of the 3 to 12 BPS is greater
than 5, and greater than 2 for the 0 to 8 CPOT. Following
appropriate training, the use of these scales has led to increased
frequency of pain assessments, a better use of analgesic and
sedative agents, and better patient outcomes.

Collaborative management

1. Ethical obligation: Nurses’ role in pain management

Nurses have an ethical obligation to relieve pain and reduce
associated physiologic and psychological risks of untreated pain,
which may be poorly understood by the patient. In line with the
ethical principles of beneficence and nonmaleficence, healthcare
professionals are held responsible to provide pain management and
comfort to all patients, including those vulnerable individuals who
are unable to speak for themselves. Ensuring that adequate pain
management is also provided to patients unable to self-report, their
pain is directed by the principle of justice that demands the
provision of quality and comparable care to all individuals. The
American Society for Pain Management Nursing insists that all
persons with pain deserve prompt recognition and treatment such
that pain is routinely assessed, reassessed, and documented to
facilitate treatment and communication among healthcare
clinicians. A standard for pain assessment using valid and reliable
pain assessment tools is identified to be essential for the recognition
and prompt treatment of pain. Moreover, the use of pain
assessment tools is needed to reassess pain relief and guide
analgesia readjustments that may include upward titration of

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treatment as well as tapering of the analgesics and implementation
of adjuvant therapies. In the recent clinical guidelines of the SCCM,
the use of nonpharmacologic interventions is recommended for the
management of pain in adults who are critically ill, and nurses
should attempt to employ these interventions in their efforts to
promote optimal pain relief.

• There are many sources of pain in ICU and unrelieved pain can
have multiple negative impacts on the patient’s recovery.

• Nurses have an ethical responsibility to provide comfort to all

their patients by systematically assessing for the presence of pain,
administering the appropriate pharmacologic and
nonpharmacologic treatments, and reassessing if optimal pain
relief was achieved.

• In assessing pain, patient self-report should be attempted first.

However, when self-report is not available, the use of behavioral
indicators is considered a valid approach to pain assessment.

• Pain assessment findings are to be communicated with the

multidisciplinary team to ensure an optimal care plan for pain
management.

2. Pharmacologic therapies
The pharmacologic management of pain is widely used in the
critical care setting. Pain pharmacology can be divided into three
main categories of action: opioids, nonopioids, and adjuvants. The
mechanism of action of these different agents in association with
nociception, their administration routes, therapeutic uses, and side
effects are described in Table 1-32. Pain can be managed using a
combination of the available agents, and must consider the type of
pain and the patient response to treatment.

Table 1-32
EQUIANALGESIC DOSES OF NARCOTIC ANALGESICS

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*
Recommended starting dose; actual dose must be titrated to patient response.
†
Starting doses lower (codeine 30 mg, oxycodone 5 mg, meperidine 50 mg,
propoxyphene 65 to 130 mg, pentazocine 50 mg).
‡
Respiratory depressant effects persist longer than analgesic effects.
Modified from Hazard V, Hopfer DJ: Davis’ drug guide for nurses, ed 5, Philadelphia,
1997, Davis; Macintyre PE, Ready LBN: Acute pain management: a practical guide,
London, 1996, Saunders; and Salerno E: Pharmacologic approaches. In Salerno E,
Willens JS, editors: Pain management handbook: an interdisciplinary approach, St
Louis, 1996, Mosby.
IM, Intramuscular; IV, intravenous; PO, oral; SC, subcutaneous.

Opioids: The opioids most commonly used are agonists, and

their IV administration is recommended as first-line analgesics to
treat acute nonneuropathic pain in patients who are critically ill.
The agonist opioids bind to mu (µ) receptors (transmission
process), which appear to be responsible for pain relief. They are
used to manage moderate to severe acute pain. For the most
effective therapy, titrate in small increments to produce the desired

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analgesia with minimal side effects. “As needed” dosing provides
poor pain management because of delays in administration and
fluctuations in the patient’s analgesic blood levels. Patient-
controlled analgesia (PCA) pumps, continuous peripheral or
epidural infusions, and small, frequent IV bolus dosing are effective
methods used for patients in critical care settings. Opioid tolerance,
physiologic or psychological dependence, and addiction are
unusual when opioids are used to manage acute pain in patients
without a history of chemical dependency. Parenteral opioids may
cause hypotension in patients with hypovolemia. Restore fluid
volume before or concurrently with administration. Some patients
are at a greater risk for respiratory depression such as the opioid
naïve, those with compromised pulmonary status or
neuromuscular disease, the extremely young (neonates), and older
adults. Opioid-induced respiratory depression can be prevented
with careful titration and monitoring.

• Morphine: Most frequently used opioid for the treatment of

moderate to severe acute pain. With its vasodilatory effects and
little effect on CO and HR, morphine is beneficial for patients
with LV failure, pulmonary hypertension, or pulmonary edema.
Rapid IV injection may trigger histamine release with related
vasodilation, decreased preload, and decreased BP. Continuous
opioid infusion minimizes hemodynamic changes that can occur
with bolus dosing. Epidural administration may result in reduced
responsiveness of the respiratory center in the brainstem to CO2.
This results in gradual decrease in the depth and rate of
respiration, increase in Paco2, increase in sedation level, and
respiratory acidosis.

• Hydromorphone (Dilaudid): Highly effective opioid; substitute

analgesic for patients with morphine allergy or intolerance. Care
must be taken to modify the dose of hydromorphone in
comparison to morphine, because hydromorphone is
approximately 5 to 7 times stronger than morphine (see Table 1-
32).

• Meperidine (Demerol): Not suggested for routine analgesia use in

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 the critical care unit, it may be indicated for brief courses (i.e., <
48 hours, < 600 mg/24 h) in patients with allergy or intolerance to
morphine, hydromorphone, or other opioids, and for the
treatment of postoperative shivering. Morphine is approximately
7 to 10 times stronger than meperidine, thus meperidine doses
are much higher (see Table 1-32). The drug is not well tolerated
by older adults . Its toxic metabolite, normeperidine, is a
cerebral irritant and may cause seizures, which has decreased
its usage in both older adults and the critically ill. Some patients
report little pain relief from meperidine, despite stating a strong
feeling of intoxication.

Use of naloxone on patients receiving chronic or high-dose

therapy may result in seizures caused by predominance of
convulsant activity from normeperidine overriding the central
nervous system depressant effects of meperidine.

• Fentanyl: Potent synthetic opioid. IV preparation is especially

useful in critical care because of minimal cardiovascular effects,
short duration of action, and rapid onset of action. Duration of
action increases with repeated doses. Caution must be taken if
large doses of fentanyl are given rapidly. This may cause chest
wall muscle rigidity requiring ventilatory support and rapid-
acting muscle relaxants. Other forms for chronic pain are
available such as a transdermal patch.

HIGH ALERT!
A fentanyl patch may be used for continuous analgesia, usually
with supplemental doses of morphine or another opiate titrated to
produce analgesia for breakthrough pain but should be used only
for patients with opiate tolerance. A fentanyl patch is not
recommended for mild pain, acute postoperative pain, or

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intermittent pain because of its slow onset (12 to 16 hours) and
long duration, and because it is difficult to reverse its side effects
and adverse effects. Respiratory depression with hypoventilation
occurs, as with morphine. Transdermal fentanyl absorption can be
increased in patients with elevated temperatures.

Nonopioids: Nonopioids can be used to treat mild pain, and as

coanalgesics for the treatment of moderate to severe pain. Their use
can help decrease the amount of opioids administered and to
decrease opioid-related side effects.

• Acetaminophen: Acetaminophen is a safe nonopioid agent, and

side effects are rare at therapeutic doses. The critical care nurse
must consider the other products containing acetaminophen that
the patient may receive when calculating the total daily dose of
acetaminophen. Total daily dose of acetaminophen should be
reduced to not exceed 2 g in patients with liver dysfunction,
malnutrition, or a history of excess alcohol consumption.

• Nonsteroidal antiinflammatory drugs (NSAIDs): The use of

NSAIDs is indicated in the patient with acute musculoskeletal
and soft tissue inflammation. NSAIDs can be grouped as first-
generation (COX-1 and COX-2 inhibitors, such as aspirin,
ibuprofen, naproxen, and ketorolac) or second-generation (COX-
2 inhibitors, such as celecoxib) agents. The inhibition of COX-1 is
thought to be responsible for many of the side effects, such as
gastric ulceration, bleeding as a result of platelet inhibition, and
acute renal failure. In contrast, the inhibition of COX-2 is
responsible for the suppression of pain and inflammation.
Second-generation NSAIDs are associated with minimal risks of
serious adverse effects, but their role in patients who are critically
ill remains unknown. Most NSAIDs are given orally (e.g.,
ibuprofen, aspirin), but injectable NSAIDs such as ketorolac are
available.

• Ketorolac (Toradol): Effective for short-term use in relieving mild

to moderate pain. The effect on ventilation is minimal, and the

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 drug has been effective when given on an alternate schedule with
morphine or another opioid analgesic during ventilator weaning
of postoperative patients. Renal toxicity is possible, which limits
use to patients with normal renal function. Bleeding
complications are more likely with high-dose therapy and in
older adults.

Adjuvants: According to Barr et al. (2013), anticonvulsants, either

enterally administered gabapentin or carbamazepine, should be
considered for the treatment of neuropathic pain. Antidepressants
administered at lower doses are also considered as adjuvant
analgesics in a variety of chronic pain syndromes, such as
headache, fibromyalgia, low back pain, neuropathy, central pain,
and cancer pain. They are usually divided into two main groups:
tricyclic antidepressants (e.g., amitriptyline, imipramine,
desipramine), and biogenic amine reuptake inhibitors (e.g.,
venlafaxine, paroxetine, sertraline).
Other agents: Ketamine: Ketamine is a dissociative anesthetic
agent that has analgesic properties, and is commonly used for
specific procedural pain. In comparison to opioids, ketamine has
the benefit of sparing the respiratory drive. However, it has many
side effects related to the release of catecholamines and delirium.
Before administering the drug, the dissociative state should be
explained to the patient. Dissociative state refers to the feelings of
separateness from the environment, loss of control, hallucinations,
and vivid dreams. The use of benzodiazepines (e.g., midazolam)
can help reduce the incidence of this unpleasant effect.
Dexmedetomidine (Precedex): Dexmedetomidine is a short-
acting alpha2-agonist used for sedation in patients who are critically
ill and mechanically ventilated or not. This drug has sedative,
analgesic, and anxiolytic effects. It is ideal for mild to moderate
sedation, often referred to as conscious sedation. The analgesic
effect of dexmedetomidine is attributable to spinal antinociception
via binding to nonnoradrenergic receptors located on the dorsal
horn neurons of the spinal cord. It can help reduce opioid
requirements and spares the respiratory drive. Its main side effects
are hypotension and bradycardia.

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Older adults
Older adults are more sensitive to the therapeutic and toxic
effects of analgesics. The distribution of medications is altered by
age. With aging, lean body mass decreases and body fat increases.
Also, muscle and soft tissue mass decrease, and body water
declines. This results in water-soluble opioid analgesics such as
morphine having a lower volume of distribution. This causes an
increased rate of the onset of action and raises the peak
concentration, which is associated with increased toxicity. Lipid-
soluble opioid analgesics (e.g., fentanyl) may be more widely
distributed, resulting in a delayed onset of action and accumulation
with repeated doses. Because of age-related changes in metabolism
and elimination, older adults are also at risk for drug-accumulation
toxicity.
In treating older adults, it is best to start at lower doses (50%
to 75% of recommended younger adult doses). The interval
between doses can be increased, using opioids with shorter half-
lives (morphine, hydromorphone, oxycodone). All older adults
should be monitored for signs of opioid toxicity, including
increased sedative effects, inability to awaken the patient easily,
and respiratory depression. With careful assessment, proper dosing
and titration, knowledge of analgesic onset and peak times, and
careful monitoring, the risk for respiratory depression is low.
However, naloxone (Narcan), an opioid antagonist, should be
immediately available to reverse respiratory depression.

Naloxone reduces respiratory depression but also reverses

analgesia—dilute 0.4 mg ampule in 10 mL 0.9% normal saline and
administer 0.5 mL (0.02 mg) by direct intravenous push every 2
minutes; titrate to effect patient response to avoid withdrawal,
seizures, and severe pain; onset occurs within 1 to 2 minutes with a
duration of approximately 45 minutes. Patients can sometimes
exhibit aggressive and sometimes violent behavior when the
naloxone takes effect. See Table 1-32 for equianalgesic doses of
narcotic analgesics.

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Nonpharmacologic interventions
In light of the recognition of the high prevalence of pain in the
critically ill despite the administration of standard pharmacologic
treatments, a multimodal approach to pain management in patients
in ICU is recommended. A multimodal approach supports the
combination of nonopioid with opioid analgesics for optimal pain
relief versus an increase in the dosage of opioids administered to
prevent the adverse effects of high opioid doses on patients.
Moreover, the recent clinical practice guidelines of the SCCM for
the management of pain in ICUs suggest the use of complementary,
nonpharmacologic interventions for pain management (massage,
music therapy, relaxation techniques) in addition to a multimodal
approach.
The general belief of ICU nurses is that pain is primarily
managed with pharmacologic treatments such as indicated in most
ICU pain management protocols, but when this type of treatment is
not sufficient, they try different nonpharmacologic approaches.
Several nonpharmacologic interventions such as deep breathing
exercises, massage, and positioning were reported to be already
used by nurses for the management of pain in ICU.
These nonpharmacologic interventions are intended to
supplement pharmacologic treatments to maximize pain relief.
Even though they are commonly used in clinical practice, there is
still limited evidence to support their effectiveness in critical care
settings. These interventions include sensory, emotional, and
cognitive interventions, such as massage, relaxation, distraction,
guided imagery, repositioning, and transcutaneous electrical nerve
stimulation, and are used for mild pain and anxiety and as adjuncts
to pharmacologic management of moderate to severe pain.

Physical techniques

• Massage: Massage has been identified to be advantageous in its

opioid-sparing and analgesia-enhancing properties, but also
because it is recognized to be low cost, easy to provide, and safe
to administer. Several therapeutic benefits have already been

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 documented for the administration of massage in various clinical
settings. It has been shown to reduce fatigue and improve sleep
quality, to promote relaxation and decrease muscle tension, and
to impact vital signs by decreasing systolic and diastolic BP,
cardiac, and respiratory rates.

Patients and family members with a previous

experience of ICU hospitalization and ICU nurses
identified massage as a nonpharmacologic
intervention to be useful, relevant, and feasible for
pain management in ICU. Feasibility results of a
randomized controlled trial and a pilot study
revealed that hand-massage and hand-holding by
an interventionist were feasible in ICU, especially if
clinicians (i.e., nurses and physicians) supported its
administration. Also, participants receiving
massage reported enjoying the experience and
further recommended its delivery to other patients.
Thus, massage is viewed favorably by both patients
and clinicians, and has gained more consideration
in its regular delivery in ICU.
• Cold Application: This therapy is used to alter the pain threshold,
reduce muscle spasm, and decrease vascular congestion,
particularly in the area of injury. Ice is believed to relieve pain by
inducing local anesthesia around the treatment area. Ice therapy
was found to reduce pain in the critically ill after chest tube
removal when ice packets were placed around the site for 10
minutes before removal. Cold is also known to decrease initial
tissue injury response.

Cognitive-behavioral techniques

• Relaxation: This nonpharmacologic technique is defined as the

absence of physical, mental, and emotional tension, and can

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 impact pain levels both physiologically and psychologically. At
the physiologic level, it can reduce the sympathetic response to
pain with subsequent decreases in oxygen consumption, BP, HR,
and respiration. Psychologically, through distraction, this
technique decreases the cognitive awareness of pain by
encouraging the patient to focus on something unrelated to the
pain. Examples include conversing, reading, watching television
or videos, and listening to music.

• Guided imagery: Using this nonpharmacologic treatment, the

patient employs a mental process that uses images to alter a
physical or emotional state. This technique promotes relaxation
and decreases pain sensations. Several barriers might interfere
with the patient’s ability to direct attention away from pain in the
critical care environment, yet the successful use of guided
imagery may be beneficial to maximize pain relief.

1-4
RESEARCH BRIEF BOX
Owens and Flom indicate that family members of patients in the
intensive care unit are able to predict when their loved one is in
pain approximately 75% of the time, but the severity is usually
underestimated
From Owens D, Flom J: Integrating palliative and neurological critical care. AACN Clin
Issues 16(4):542-550, 2005.

Care plans for pain management

Pain 
related to biophysical injury secondary to pathology: surgical, diagnostic,
treatment or intervention; or related to trauma.
Goals/Outcomes: Within 1 hour of initiating therapy, the
patient’s pain levels improve. Those able to self-report will express

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a decrease in pain, and the use of valid and reliable scales for pain
assessment in patients who are noncommunicative will indicate
lower pain scores.
Pain Control.

Pain management

1. Develop a systematic approach to pain management for each

patient. The primary nurse should collaborate with the physician
and patient for optimal management of pain.

2. Monitor the patient at frequent intervals for the presence of

discomfort. Use a formal, patient-specific method of assessing pain.
One method is to have the patient rate discomfort on a scale of 0 (no
discomfort) to 10 (worst pain imaginable). Other methods may be
used, but the method selected should be used consistently and the
patient’s report should be respected and documented as reported.

3. Evaluate patients with acute and chronic pain for nonverbal

indicators of discomfort.

4. Evaluate health history for evidence of alcohol and drug

(prescribed and nonprescribed) use. Individuals with a history of
chemical dependence may require a higher dose for effective
analgesia. Persons with evidence of chronic or acute hepatic
insufficiency may require a reduced dose and careful selection of
appropriate analgesics. Consult pain control team if available. All
care providers must be consistent in setting limits while providing
effective pain control through pharmacologic and
nonpharmacologic methods. Psychiatric consultation may be
warranted. Be aware that some opioid agonist–antagonist
analgesics (e.g., butorphanol, buprenorphine, pentazocine) have
strong narcotic antagonist activity and may trigger withdrawal
symptoms in individuals with opiate dependency.

Analgesic administration

1. Administer opioid and related mixed agonist–antagonist

analgesics as prescribed. Monitor for side effects, such as excessive

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sedation, respiratory depression, nausea, vomiting, and
constipation.

Opioid-induced sedation precedes respiratory depression,

thus frequent assessment is warranted to determine patient
arousability, especially in patients who are opioid-naive or
receiving opioids by intravenous or epidural routes. Opioids
should be stopped if the patient is difficult to arouse. Be aware
that meperidine (Demerol) may produce excitation, muscle
twitching, and seizures, especially in conjunction with
phenothiazines. Do not administer mixed agonist-antagonist
analgesics concurrently with morphine or other pure agonists,
because reversal of analgesic effects may occur. Meperidine is
poorly tolerated by older adults.

2. Assess patients receiving opioid analgesics at frequent intervals

for evidence of excessive sedation when awake or respiratory
depression (i.e., RR less than 10 breaths/min or SaO2 less than 92%).
In the presence of respiratory depression, reduce the amount or
frequency of the dose as prescribed. Have naloxone (Narcan)
readily available to reverse severe respiratory depression.

3. If the patient is receiving an epidural or intrathecal opioid,

monitor closely for side effects and complications.

4. Check the patient’s analgesia record for the last dose and amount
of medication given during surgery and in the postanesthesia care
unit. Be careful to coordinate timing and dose of postoperative
analgesics with previously administered medication.

Medication management

1. Administer nonnarcotics and NSAIDs as prescribed for relief of

mild-to-moderate pain or on alternating schedule with opiate

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analgesics for moderate-to-severe pain.

Long-term use of acetaminophen is associated with

hepatotoxicity and nephrotoxicity. Daily dose restrictions are
recommended: 4000 mg/day for short-term use in normal, healthy
adults, up to 3600 mg/day for chronic, long-term use, and no more
than 2000 mg for older adults. Total daily doses should be
calculated on a running 24-hour clock and include all combination
products such as hydrocodone (e.g., Lortab, Vicodin) and
propoxyphene (e.g., Darvocet). Patient teaching should include
attention to products containing acetaminophen and cumulative
daily doses (e.g., maximum total number of pills taken per day).
Nonsteroidal antiinflammatory drugs are especially effective when
pain is associated with inflammation and soft tissue injury.
Ketorolac (Toradol) may be given intramuscularly or
intravenously when oral agents are contraindicated. Monitor for
excessive bleeding, gastric irritation, and renal compromise in
patients receiving all nonsteroidal antiinflammatory drugs,
including all products containing ibuprofen and naproxen.

2. Administer PRN analgesics before pain becomes severe. Assess

pain and offer the patient PRN pain medication around-the-clock
based on the PRN schedule to achieve better and more even pain
relief. Prolonged stimulation of pain receptors results in increased
sensitivity to painful stimuli and will increase the amount of drug
required to relieve pain.

3. Administer intermittently scheduled or supplemental analgesics

before painful procedures (e.g., suctioning, chest tube removal) and
ambulation and at bedtime, scheduling them so that their peak
effect is achieved at the inception of the activity or procedure.

4. Augment analgesic therapy with sedatives and tranquilizers to

prolong and enhance analgesia. Avoid substituting sedatives and

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tranquilizers for analgesics.

5. Wean the patient from opioid analgesics by decreasing dosage or

frequency of the drug. When changing route of administration or
medication, be certain to use equianalgesic doses of the new drug
(see Table 1-32). Remember doses listed on the table are ratios of
one drug to another and one route to another; these ratios should be
used as estimates for a new starting dose along with pain intensity,
patient pain assessment, and patient response to the drug. The
current total 24-hour dosage will need to be calculated first; include
scheduled and rescue doses.

Self-responsibility facilitation

1. Augment action of medication by using nonpharmacologic

methods of pain control. Many of these techniques may be taught to
and implemented by the patient and significant others.

2. Sudden or unexpected changes in pain intensity can signal

complications such as internal bleeding or leakage of visceral
contents. Carefully evaluate the patient’s report of pain, compare to
previous pain reports, and consult the surgeon immediately.

3. Educate patients about their medications, including asking for

medications when in pain and declining them if offered when not
in pain.

Environmental management: Comfort

1. Maintain a quiet environment to promote rest. Plan nursing

activities to enable long periods of uninterrupted rest at night.

2. Evaluate for and correct nonoperative sources of discomfort (e.g.,

position, full bladder, infiltrated IV site).

3. Position the patient comfortably, and reposition at frequent

intervals to relieve discomfort caused by pressure and to improve
circulation.

4. Document efficacy of analgesics and other pain control

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interventions, using the pain scale or other formalized method.

Analgesic Administration; Analgesic Administration:

Intraspinal; Patient-Controlled Analgesia (PCA) Assistance.

Ineffective breathing pattern 

related to neuromuscular impairment secondary to central respiratory
depression; pain-induced splinting.
Goals/Outcomes: The patient exhibits effective ventilation within
30 minutes of this diagnosis, as evidenced by relaxed breathing, RR
12 to 20 breaths/min with normal depth and pattern (eupnea), clear
breath sounds, normal color, PaO2 ≥80 mm Hg, pH 7.35 to 7.45,
Paco2 35 to 45 mm Hg, HCO3− 22 to 26 mEq/L, and SpO2 ≥92%.
Respiratory Status: Ventilation.

Respiratory monitoring

1. Assess and document respiratory rate and depth hourly. Note

signs of respiratory compromise, including RR less than 10 or
greater than 26; shallow or grunting respirations; use of accessory
muscles of respiration; prolonged I:E ratio; pallor or cyanosis;
decreased vital capacity; and increased residual volume. Consult
the physician for evidence of respiratory compromise.

2. Monitor SpO2 and ABG values. Consult the physician for

decreased SpO2 (less than 92%) or increased Paco2 (greater than 45
mm Hg).

3. Assess and document LOC every 1 to 2 hours.

4. Use apnea monitor as indicated.

5. Keep naloxone (Narcan) at the patient’s bedside during and for

24 hours after epidural or intrathecal administration.

6. Maintain IV access for immediate administration of naloxone to

reverse respiratory depression.

7. Respiratory depression may persist for as long as 24 hours after

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the last dose of epidural morphine. Monitor for respiratory
depression during and for 24 hours after the patient has received
epidural or intrathecal opioids.

Airway Management; Oxygen Therapy; Aspiration

Precautions.

Urinary retention 
related to inhibition of reflex arc secondary to opioid action
Goals/Outcomes: Within 4 hours of this diagnosis, complete
bladder emptying is achieved. Overflow incontinence is absent.
Urinary Elimination.

Urinary retention care

1. Monitor for symptoms of urinary retention: bladder distention,

frequent voiding of small amounts of urine, sensation of bladder
fullness, residual urine, dysuria, and overflow incontinence.

2. Monitor I&O precisely.

3. Catheterize bladder intermittently or insert indwelling catheter as

prescribed.

4. Administer IV naloxone as prescribed.

Urinary Catheterization.

Risk for impaired skin integrity 

related to itching secondary to alteration in sensory modulation from
opioid effects.
Goals/Outcomes: The patient’s skin remains intact.
Tissue Integrity: Skin and Mucous Membranes.

Medication management

1. Decrease the opioid dose via epidural or PCA infusion.

2. Administer diphenhydramine or hydroxyzine as prescribed.

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Monitor sedation when antihistamine is added.

3. Maintain comfortably cool environment.

4. Apply cool, moist compresses.

5. If relief from the above measures is inadequate, administer small

amounts of IV naloxone as prescribed and until RR is at least 8/min,
continue to assess patient closely and frequently because naloxone
may need to be repeated as effect of opioid is of longer duration
than the effect of naloxone.

See also Prolonged Immobility in the following section.

Skin Surveillance; Positioning; Pressure Ulcer Prevention.

Prolonged immobility
Prolonged immobility is a common consequence of prolonged
hospitalization for severe and critical illness. Morbidity related to
prolonged immobility is often profoundly impacted by nursing
care. Nurses attend to patients continuously, providing ongoing,
expert assessments and interventions. Significant adverse outcomes
of prolonged immobility have been demonstrated to be preventable
(Box 1-16).

Box 1-16
PHYSIOLOGIC EFFECTS AND
COMPLICATIONS OF BED REST
(DECONDITIONING)
Cardiovascular
• Increased heart rate and blood pressure for submaximal
workload

• Decrease in functional capacity

• Decrease in circulating volume

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• Orthostatic hypotension

• Reflex tachycardia

• Deep vein thrombosis

Pulmonary
• Modest decrease in pulmonary function

• Atelectasis

• Pneumonia

• Pulmonary embolus

Gastrointestinal
• Ileus

• Deficient protein state

• Negative nitrogen state

Musculoskeletal
• Loss of muscle mass

• Loss of muscle contractile strength

• Bone demineralization

• Joint contractures

Skin
• Decubitus ulcers

Illnesses or diseases that may necessitate prolonged bed rest

368
include:

• Neurologic disorders such as stroke/cerebrovascular accident and

Guillain-Barré syndrome.

• Cardiovascular disorders such as severe heart failure and

cardiomyopathy.

• Pulmonary disorders such as chronic obstructive lung disease

and pneumonia.

• Musculoskeletal disorders such as postmotor vehicle accident and

joint contractures.

• Others:

• Complications from surgery.

• Severe sepsis.

• Failure to thrive.

Safe patient handling

Healthcare workers are needlessly injured on the job. During 2011,
workers in the healthcare sector suffered a higher rate of
musculoskeletal injuries and disorders than construction, mining,
or manufacturing workers. Also, “in 2011, registered nurses ranked
fifth among all occupations for the number of cases of
musculoskeletal disorders resulting in days away from work, with
11,880 total cases. Nursing assistants reported 25,010 cases, the
highest for any occupation.”
The following are the Interprofessional Standards of Safe Patient
Handling and Mobility (SPHM) as established by the American
Nurses Association (ANA).

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Standard 1. Establish a culture of safety
The employer and healthcare workers partner to establish a culture
of safety that encompasses the core values and behaviors resulting
from a collective and sustained commitment by organizational
leadership, managers, healthcare workers, and ancillary/support
staff to emphasize safety over competing goals.

1.1 Employer

1.1.1 Establish a statement of commitment to a culture of

safety 
Organizational policy will include a written commitment to a
culture of safety that will be used to guide the organization’s
priorities, resource allocation, policies, and procedures. The written
statement regarding SPHM will describe layers of accountability
across sectors and settings.

1.1.2 Establish a nonpunitive environment 

Organizational policy will support a system to encourage
healthcare workers to report hazards, errors, incidents, and
accidents, so that the precursors to SPHM errors can be better
understood and organizational issues can be changed to prevent
future incidents and injuries. Healthcare workers know that they
are accountable for their actions, but will not be held accountable
for problems within the system or environment that are beyond
their control.

1.1.3 Provide a system for right of refusal 

Organizational policy will provide the healthcare worker the right
to accept, reject, or object to any healthcare recipient transfer,
repositioning, or mobility assignment that puts the healthcare
recipient or the healthcare worker at risk for injury. The refusal
shall be made in writing, without fear of retribution. The policy will
describe steps for resolving the hazard.

1.1.4 Provide safe levels of staffing 

An evidence-based system will be used to determine safe and
appropriate caseloads. Adequate staffing levels will support safe

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patient handling and mobility, including allocated time for training
and education.

1.1.5 Establish a system for communication and collaboration 

Collaboration among all sectors and settings is critical. The
organization will use a variety of communication systems to inform
and engage the healthcare workers and healthcare recipients about
SPHM.

1.2 Healthcare worker

1.2.1 Participate in creating and maintaining a culture of

safety 
The healthcare worker will actively participate in creating and
maintaining a culture of safety.

1.2.2 Notify the employer of hazards, incidents, near misses,

and accidents 
The healthcare worker will notify the employer of hazards, near
misses, incidents, and accidents related to SPHM as soon as
possible, using the reporting procedures defined by the employer.

1.2.3 Use the system to communicate and collaborate 

The healthcare worker will engage, verbally and in writing, with
others about SPHM.
The Patient’s Ability to Assist with Transfer (U.S. Department
of Veterans Affairs):

1. Assess the patient’s height and weight. Weight alone may be the
determining factor in deciding how much assistance is needed or if
an assistive device is needed.

2. Assess the patient’s level of independence with turning and

transferring.

• Independent: Can the patient independently

perform turning or transferring (e.g., bed to
stretcher, bed to chair) safely, with or without

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 assistive devices (e.g., cane or walker), without staff
assistance?

• Some Assistance Required: Can the patient partially

assist with transfer, needing one caregiver to
observe or assist? Remember to assess upper and
lower extremity strength, mobility, and ability to
cooperate and comprehend instructions.

• Total Dependence: Is the patient unable to assist

with turning or transfer?

Assistive devices 
Assistive devices are very helpful in preventing injury and
decreasing the number of staff needed to assist. There are many
assistive devises on the market, usually in the form of slings. Some
types of slings may be independent, roll on wheels, and be able to
be moved from one patient to another. Another type of sling, which
is not portable, may be attached to the ceiling and slide.
It is important to know how to use the sling properly and to have
enough staff to assist with the use safely. Read the instructions
before using any new device that is not familiar.
The following set of nursing care plans frames the care of those
who require prolonged periods of bed rest and/or those who are
immobile.

Care plans for prolonged immobility

Activity intolerance 
related to prolonged bed rest; generalized weakness; and imbalance
between O2 supply and demand.
Goals/Outcomes: Within 48 hours of discontinuing bed rest, the
patient exhibits cardiac tolerance to low-intensity exercise (defined

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later), as evidenced by:

• HR ≤20 bpm over resting HR.

• Systolic BP ≤20 mm Hg over or under resting systolic BP.

• SaO2 greater than 90%.

• SVO2 ≥60%.

• RR ≤20 breaths/min.

• Normal sinus rhythm.

• Skin warm and dry.

• Absence of crackles, murmurs, and chest pain.

Activity Tolerance; Endurance.

Exercise promotion: Strength training

1. Perform low-intensity exercise 2, 3, or 4 times daily: ROM

exercises on each extremity. Individualize the exercise plan on the
basis of the following guidelines. Depending on the degree of
debility of the patient, it may be necessary to begin with passive
exercises, moving the joints through the motions of abduction,
adduction, flexion, and extension.

2. Progress to active-assisted exercises, in which the nurse supports

the joints while the patient initiates muscle contraction. When the
patient is able, supervise him or her in active exercises and then
isotonic exercises, during which the patient contracts a selected
muscle group, moves the extremity at a slow pace, and then relaxes
the muscle group. Have the patient repeat each exercise 3 to 10
times.

HIGH ALERT!

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Avoid isometric exercises in patients with cardiac disease. Stop any
exercise that causes muscular or skeletal pain. Consult with a
physical therapist for necessary modifications to allow for exercise
without causing muscular or skeletal pain.

3. Assess exercise tolerance:

• Be alert to signs and symptoms that the

cardiovascular and respiratory systems cannot meet
the demands of the low-level ROM exercises.
Excessive SOB may occur if:

• Transient pulmonary congestion occurs secondary

to ischemia or LV dysfunction.

• Lung volumes are decreased.

• O2-carrying capacity of the blood is reduced.

• There is shunting of blood from the right to the left

side of the heart without adequate oxygenation.

• If CO does not increase to meet the body’s needs

during modest levels of exercise, look for:

• A fall in the systolic BP.

• Dysrhythmias.

• Crackles that can be auscultated.

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• A new S3 or a systolic murmur indicating mitral
regurgitation that may occur.

• If the patient tolerates the exercise, increase the

intensity or number of repetitions each day.

• Ask the patient to rate perceived exertion (RPE)

using the scale shown in Table 1-33. The patient
should not experience an RPE greater than 3 while
performing ROM exercises. Reduce the intensity of
the exercise and increase the frequency until an RPE
of ≤3 is attained.

4 Monitor the intensity of the activity:

• Begin with 3 to 5 repetitions, as tolerated by the

patient.

• Assess exercise tolerance by measuring HR and BP

at rest, peak exercise, and 5 minutes after exercise.

• If HR or systolic BP increases more than 20 bpm or

more than 20 mm Hg over the resting level,
decrease the number of repetitions.

• If HR or systolic BP decreases more than 10 bpm or

more than 10 mm Hg at peak exercise, this could be
a sign of LV failure, denoting that the heart cannot
meet this workload.

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• Plan to increase duration:

• Begin with 5 minutes or less of exercise.

• Gradually increase the exercise to 15 minutes as

tolerated.

• Plan to increase frequency:

• Begin exercises 2 to 4 times daily.

• As the duration increases, the frequency can be

reduced.

5. Increase activity as the patient’s condition improves:

• Progress to sitting in a chair as soon as possible.

• Assess for orthostatic hypotension, which can occur

as a result of decreased plasma volume and
difficulty in adjusting immediately to postural
change.

• Prepare the patient by increasing the amount of

time spent in a high-Fowler position and moving
the patient slowly and in stages as follows:

• Level I/bed rest: Allow flexion and extension of

extremities 4 times daily with 15 repetitions per
extremity. Deep breathing should occur 4 times
daily, 15 breaths each time. Reposition the patient

376
 every 2 hours.

• Level II/out of bed to chair: The patient sits in the

chair 2 or 3 times daily for 20 to 30 minutes as
tolerated. ROM exercises may be performed 2 times
daily while sitting in the chair.

• Level III/ambulate in room: The patient ambulates

for 3 to 5 minutes, 3 times daily as tolerated.

• Level IV/ambulate in the hall: The patient initially

walks 50 to 200 feet 2 times daily, and progresses to
600 feet 4 times daily. Slow stair climbing may be
incorporated in preparation for hospital discharge.

• If the patient is able, have him or her independently

perform self-care activities, such as eating, mouth
care, and bathing, as tolerated.

6. Teach and involve significant others in interventions for

preventing deconditioning.

7. Provide emotional support to help allay fears of failure, pain, or

medical setbacks.

Table 1-33
RATING PERCEIVED EXERTION

Rating Perceived Exertion

0 Nothing at all
1 Very weak effort
2 Weak (light) effort
3 Moderate
4 Somewhat stronger effort

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 5 Strong effort
6
7 Very strong effort
8
9 Very, very strong effort
10 Maximal effort
From Borg G: Psychophysical bases of perceived exertion. Med Sci Sports Exerc
14(5):377-381, 1982.

Exercise Therapy: Ambulation; Energy Management; Cardiac

Care: Rehabilitative.

Risk for disuse syndrome 

related to mechanical or prescribed immobilization; severe pain;
altered LOC.
Goals/Outcomes: The patient displays full ROM without verbal
or nonverbal indicators of pain.
Mobility.

Exercise promotion

1. Prevent joint contractures by performing ROM exercises. The

following areas are at high risk for joint contractures:

• Shoulders can become “frozen,” which would limit

abduction and extension.

• Wrists can “drop,” prohibiting extension.

• Fingers can develop flexion contractures that limit

extension.

• Hips can develop flexion contractures that affect the

gait by shortening the limb or can develop external
rotation or adduction deformities that affect the
gait.

• Knees can develop flexion contractures that limit

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 extension and alter the gait.

• Feet can “drop” as a result of plantar flexion, which

limits dorsiflexion and alters the gait.
2. Change the patient’s position at least every 2 hours. Post a
turning schedule at the patient’s bedside. Position changes will:

• Maintain all joints in a neutral position.

• Reduce strain on the joints.

• Prevent contractures.

• Minimize pressure on bony prominences.

• Promote maximal chest expansion.

3. Position to achieve proper standing alignment and maintain with
pillows, towels, or other positioning aids.

• Head neutral or slightly flexed on neck.

• Hips extended.

• Knees extended or minimally flexed.

• Feet at right angles to the legs.

• HOB elevated 30 degrees.

• The patient’s shoulders and arms extended using

pillows for support.

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• Fingertips to extend over the edge of the pillows to
maintain normal arching of hands.

• Hip flexion contracture prevention. Ensure that

when the patient is in the side-lying position, the
hips are extended for the same amount of time the
patient is in the supine position.

HIGH ALERT!
Because elevating the head of the bed promotes hip flexion, ensure
that the patient spends equal time with the hips in extension. When
the patient is in the side-lying position, extend the lower leg from
the hip to help prevent hip flexion contracture.

4. Maintain the joints in neutral position by using:

• Pillows, rolled towels, blankets, sandbags,

antirotation boots, splints, and orthotics.

• When using adjunctive devices, monitor the

involved skin at frequent intervals for alterations in
integrity. Implement measures to prevent skin
breakdown.
5. Prevent foot drop.

• Foot posture is naturally in plantar flexion, thus be

alert to the patient’s inability to pull the toes up.
Document this assessment daily.

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• Foam boots or “high top” tennis shoes may be used
to support the feet.

• Teach the patient the rationale and procedure for

ROM exercises, and have the patient return the
demonstrations, if able.

6. Ensure that the patient does not exceed his or her tolerance by
performing constant assessment of activity tolerance. Provide
passive exercises for patients unable to perform active or active-
assistive exercises. Incorporate exercising all joints with ADLs, such
as changing position, giving bed baths, using bedpan, and changing
the patient’s gown.

7. Assess the patient’s existing muscle mass, strength, and joint

motion.

• Perform and document limb girth measurements.

• Use dynamography, hand-grip device to measure

muscle strength.

• Establish exercise baseline limits.

• Perform ROM.

8. Educate the patient. Maintaining or increasing muscle strength

and tissue elasticity surrounding joints is imperative. Consult with
the physician about the form and extent of the exercise. Muscle
atrophy occurs from disuse leading to decrease in muscle mass,
decrease in blood supply, loss of tissue elasticity surrounding joints,
pain, and further difficulty moving.

9. Reinforce progress.

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• Post the exercise regimen at the patient’s bedside to
ensure consistency by all healthcare personnel.

• Provide a chart to show the patient’s progress.

• Provide large amounts of positive reinforcement.

10. Balance rest and activity. Provide periods of uninterrupted rest

between exercises/activities to enable the patient to replenish
energy stores.

11. Consult rehabilitation services. Seek a referral to a physical

therapist or occupational therapist as appropriate.

Positioning; Pressure Management; Exercise Therapy: Joint

Mobility; Exercise Therapy: Muscle Control.

Impaired skin integrity of the oral mucous membrane 

related to ineffective oral hygiene
Goals/Outcomes: The patient’s oral mucosa, lips, and tongue are
intact within 24 hours before discharge from ICU.
Tissue Integrity: Skin and Mucous Membranes.

Oral health maintenance

1. Assess the patient’s oral mucous membrane, lips, and tongue at

least every 4 hours, noting the presence of dryness, exudate,
swelling, blisters, and ulcers.

2. Perform oral care every 2 to 4 hours.

• Use a soft-bristle toothbrush (premade mouth care

kits are available) to cleanse the teeth. This is
particularly important for patients who are
intubated because evidence shows that pneumonia
can be reduced or prevented. Suction mouth

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 continuously during oral hygiene to remove fluid
and debris.

• Use a moistened cloth or sponge-tip applicator to

moisten and help remove crusty areas or exudate
on tongue and oral mucosa.

3. Offer sips of water or ice chips to prevent dryness if the patient is

alert and able to take oral fluids.

4. Apply lip balm every 2 hours and as needed to prevent cracking

of lips.

5. Consider using an artificial saliva preparation to assist in keeping

mucous membrane moist.

6. Have the patient wear dentures as possible, to improve

communication and enhance comfort.

7. Teach family the proper oral hygiene techniques and encourage

them to perform oral hygiene.

Self-Care Assistance: Bathing, Hygiene.

Self-care deficit 
related to cognitive, neuromuscular, or musculoskeletal impairment;
activity intolerance secondary to prolonged bed rest.
Goals/Outcomes: The patient’s physical needs are met by the
patient, nursing staff, and/or significant others while the patient is
being encouraged to participate as much as possible.
Self-Care: Activities of Daily Living.

Self-care assistance: Bathing/hygiene, feeding, and toileting

1. Assess the patient’s ability to perform self-care on the basis of

functional status (e.g., comatose state, hemiplegia, sensory or motor
deficit, alterations in vision).

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• Use assessment criteria for activity tolerance: If the
patient experiences a decrease in BP of more than
20 mm Hg, an increase in HR of more than 20 bpm
above resting HR, or a HR above 120 bpm in a
patient receiving beta-adrenergic drugs, the patient
is not fully tolerating the activity.
2. If the patient is comatose, meet all the patient’s physical needs:
bathing, oral hygiene, feeding, and elimination.

3. Explain all procedures to the patient and significant others before

performing them.

• Involve significant others in the plan of care.

• Invite family and/or significant other in care as

feasible.

• Collaborate with the patient and/or significant other

to develop the plan of care.

4. For the patient who is not comatose:

• Promote as much self-care as the patient is capable

of providing.

• Schedule care activities around the periods of time

the patient has the most energy.

• Question the patient about activity intolerance

when assessment findings reveal the activity may
exceed the patient’s tolerance.

384
5. If the patient is alert, keep toiletries and other necessary items
within reach.

6. Do not rush the patient; allow adequate time for performance of

self-care activities and try to schedule activities at a point in the
work shift to allow the patient to have the time needed.

7. Encourage the patient; reinforce the value of progress that is

made.

8. Provide assistive devices. Consult with the occupational therapy

department regarding use of devices such as large handle utensils
for eating.

9. If visual impairment exists, place all objects within the patient’s

field of vision. If diplopia is present, apply an eye patch and
alternate it between the patient’s eyes every 2 to 3 hours as
prescribed.

Energy Management; Self-Care Assistance:

Dressing/Grooming.

Ineffective peripheral tissue perfusion 

related to interrupted arterial and venous flow secondary to prolonged
immobility.
Goals/Outcomes: By discharge from ICU, the patient has
adequate peripheral circulation, as evidenced by normal skin color
and temperature, and adequate distal pulses (more than 21 on a 0 to
41 scale) in peripheral extremities. (Distal pulse scales may vary
with facility.)
Circulation Status.

Circulatory care: Venous insufficiency

1. Identify patients at highest risk for tissue impairment including

those with altered LOC, extreme immobility/inability to assist with
ADLs, hypothermia, hyperthermia, cachexia, hypoalbuminemia, and
advanced age.

385
2. Identify patients at risk for DVT: chronic infection, malignancy,
peripheral vascular disease, history of smoking, obesity, anemia,
prolonged bed rest, and advanced age.

3. DVT/VTE prophylaxis should be initiated according to

institutional guidelines (see Pulmonary Embolus, Chapter 4).

Note: All patients who are in bed greater than 50% of the
time, including at night, should have deep vein thrombosis
prophylaxis, either medical (heparin, enoxaparin) or mechanical.

Embolus precautions
The following measures are generally a part of a DVT prevention
program.

1. Assess for a positive Homan sign. The Homan sign is not very
sensitive or specific for DVT but can be elicited by flexing the knee
30 degrees and dorsiflexing the foot. Pain elicited with the
dorsiflexion may indicate DVT and may warrant further evaluation
by the physician.

2. Assess laboratory values and vital signs for risk of DVT.

• Fever.

• Tachycardia.

• Elevated sedimentation rate.

• CRP is a nonspecific marker of inflammation and

may be elevated with DVT.

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• Patients who are “hypercoagulable” are at higher
risk for DVT.

• In patients prone to DVT:

• Acquire bilateral baseline measurements of the

midcalf, knee, and midthigh.

• Record these measurements on the patient’s initial

assessment.

• Monitor these measurements daily.

• Compare measurements with the baseline

measurements to rule out extremity enlargement
that could be caused by DVT.

3. Teach the patient and family the signs of DVT.

• Pain.

• Swelling and warmth in the involved area.

• Coolness, unnatural color or pallor in involved area.

• Superficial venous dilation distal to the involved

area.

• Report signs to a staff member, physician, or

midlevel practitioner promptly if they occur.

387
4. Advise the patient and family to perform only the exercises
prescribed by the healthcare team. Discourage practices such as
massaging the legs when swelling and discomfort are noted.

5. Exercises for DVT prevention.

• Teach patient calf-pumping (ankle dorsiflexion-

plantar flexion).

• Teach patient ankle-circling exercises.

• Unless symptomatic, instruct the patient to repeat

each movement 10 times hourly during extended
periods of immobility.

• Help promote circulation by performing passive

ROM or encouraging active ROM exercises.

• Encourage deep breathing, which increases negative

pressure in the lungs and thorax to promote
emptying of large veins.
6. Provide mechanical venous compression for patients on bed rest.

• When not contraindicated by peripheral vascular

disease, ensure that the patient wears antiembolic
hose or pneumatic sequential compression
stockings.

• Remove mechanical venous compression device for

10 to 20 minutes every 8 hours.

• Inspect underlying skin for evidence of irritation or

388
 breakdown.

• Reapply hose after elevating the patient’s legs at

least 10 degrees for 10 minutes.
7. Position for maximal venous circulation. Instruct the patient not
to cross the feet at the ankles or knees while in bed because doing
so may cause venous stasis. If the patient is at risk for DVT, elevate
the foot of the bed 10 degrees to increase venous return.

8. Reduce the potential for thrombus formation and embolization.

• Medications that inhibit blood clotting:

• Heparin

• Low-molecular-weight heparin

• Aspirin

• Platelet inhibitors

• Sodium warfarin

9. Administer medication as prescribed, and monitor appropriate

laboratory values:

• Prothrombin time

• International normalized ratio

• Partial thromboplastin time

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• Heparin level

10. Educate patient to self-monitor for and report bleeding:

• Epistaxis

• Bleeding gums

• Hematemesis

• Hemoptysis

• Melena

• Hematuria

• Ecchymoses

Note: High-risk patients may have an inferior vena cava

filter placed to protect against pulmonary embolism.

Circulatory Precautions.

Altered cerebral tissue perfusion (orthostatic hypotension) 

related to interrupted arterial flow to the brain secondary to prolonged bed
rest.
Goals/Outcomes: When getting out of bed, the patient has
adequate cerebral perfusion, as evidenced by HR less than 120 bpm
and BP ≥90/60 mm Hg immediately after position change (or within
20 mm Hg of the patient’s normal range), nondiaphoretic skin,
normal skin color, denial of vertigo, no syncope, and HR and BP to
resting levels within 3 minutes of position change.

390
 Neurologic Status; Neurologic Status: Consciousness.

Cerebral perfusion promotion

1. Assess the patient for factors that increase the risk of orthostatic
hypotension.

• Fluid volume changes

• Recent diuresis

• Diaphoresis

• Change in vasodilator therapy

• Altered autonomic control

• Diabetic cardiac neuropathy

• Denervation after heart transplant

• Advanced age

• Severe LV dysfunction

2. Educate the patient. Explain cause of orthostatic hypotension and

measures for prevention.

3. Apply elastic stockings to help prevent orthostatic hypotension.

For patients who continue to have difficulty with orthostatic
hypotension, it may be necessary to supplement the hose with
elastic wraps to the groin when the patient is out of bed. Ensure
that these wraps encompass the entire surface of the legs.

391
4. Prepare the patient for getting out of bed. Encourage position
changes within necessary confines. Consider using a tilt table to
reacclimate the patient to upright positions.

5. Follow these guidelines for mobilization:

• Closely monitor the BP of any high-risk patient for

whom this will be the first time out of bed.

• Dangle the patient’s legs at the bedside. Be alert to

indicators of orthostatic hypotension:

• Diaphoresis

• Pallor

• Tachycardia

• Hypotension

• Syncope

• Feeling of lightheadedness or dizziness

• Check vital signs for indicators of orthostatic

hypotension and return the patient to a supine
position with:

• Drop in systolic BP of 20 mm Hg

• Increased pulse rate

• Feeling of vertigo

392
• Impending syncope

• Stand at bedside if leg dangling is tolerated. Have at

least two staff members assisting the patient.
Progress to ambulation if no adverse signs or
symptoms occur.

Energy Management; Surveillance.

Constipation 
related to less-than-adequate fluid or dietary intake and bulk; immobility;
lack of privacy; positional restrictions; use of opioid analgesics.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
verbalizes knowledge of measures that promote bowel elimination.
The patient relates the return of his or her normal pattern and
character of bowel elimination within 3 to 5 days of this diagnosis.
Older adults often experience constipation.
Bowel Elimination.

Bowel management

1. Assess the patient’s bowel history. Determine normal bowel

habits and interventions that are used successfully at home.

2. Monitor and document the patient’s bowel movements, diet, and

I&O. Be alert to the following indications of constipation:

• Fewer than patient’s usual number of bowel

movements.

• Abdominal discomfort or distention.

• Straining at stool.

• Patient complaints of rectal pressure or fullness.

393
• Fecal impaction, which may be manifested by
oozing of liquid stool and confirmed via digital
examination.
3. Auscultate each abdominal quadrant for at least 1 minute to
determine the presence of bowel sounds. Normal sounds are clicks
or gurgles occurring at a rate of 5 to 34 per minute.

Bowel sounds are decreased or absent with paralytic ileus.

High-pitched rushing sounds may be heard during abdominal
cramping, indicating an intestinal obstruction.

4. Remove rectal fecal impaction. Use a gloved, lubricated finger to

remove stool from the rectum. Digital stimulation alone may
prompt a bowel movement. Oil-retention enemas may soften
impacted stool.

5. Encourage a high-fiber/high-fluid diet. Unless contraindicated, a

high-roughage diet and a fluid intake of at least 2 to 3 L/day help to
promote regular bowel movements. Individualize fluid intake
according to physiologic state for patients with renal, hepatic, or
cardiac disorders.

6. Promote bowel regularity.

• Offer the bedpan at intervals and allow for use of

bedside commode when safe.

• Ensure privacy.

• Time laxatives, enemas, or suppositories to take

effect at the time of day the patient normally has a

394
 bowel movement.

• Provide warm fluids before breakfast.

• Encourage toileting to gain advantage of gastrocolic

or duodenocolic reflexes.

7. Promote peristalsis. Encourage as much activity as tolerated.

8. Consult the physician for pharmacologic interventions as

necessary. To help prevent rebound constipation, make a priority
list of interventions to ensure minimal disruption of the patient’s
normal bowel habits. The following is a suggested hierarchy of
interventions:

• Bulk-building additives (e.g., psyllium)

• Mild laxatives (e.g., apple or prune juice, Milk of

Magnesia)

• Stool softeners (e.g., docusate sodium or docusate

calcium)

• Potent laxatives and cathartics (e.g., bisacodyl,

cascara sagrada)

• Medicated suppositories

• Enemas

9. Discuss, with the patient, the role narcotics and other medications
have in constipation. Consider alternative methods of pain control
(see Box 1-15) in an attempt to reduce narcotic dosage.

Constipation/Impaction Management.

395
Deficient diversional activity 
related to prolonged illness and hospitalization
Goals/Outcomes: Within 24 hours of intervention, the patient
engages in diversional activities and relates the absence of
boredom.
Motivation.

Self-responsibility facilitation

1. Prevent boredom. Provide the patient with something to read or

do. Explore activities the patient enjoys. Assess the patient’s activity
tolerance using the criteria listed in the Activity Intolerance nursing
diagnosis on the first care plan in this section.

2. Personalize the patient’s environment with favorite objects and

photographs. Suggest that significant others bring in a radio or a
television, if not part of the standard room furnishings.

3. Tailor activities to attention span. Initiate activities that require

little concentration, and proceed to more complicated tasks as the
patient’s condition allows. For example, if reading requires more
energy or concentration than the patient is capable of, suggest that
significant others read to the patient or bring in audiotapes of
books, such as those marketed for the visually impaired.

4. Remember the pleasant past. Encourage discussion of past

activities or reminiscence as a substitute for performing favorite
activities during convalescence.

5. Progress activities as the patient’s endurance improves. Move

from reading to other diversions, such as puzzles, model kits,
handicrafts, and computerized games and activities.

6. Encourage visitation by significant others within limits of the

patient’s endurance. Involve significant others in patient activities,
such as playing cards or backgammon. Encourage significant others
to stagger their visits throughout the day.

7. Provide social interaction time. Spend time talking with the

396
patient. Arrange for hospital volunteers to visit, play cards, read
books, or play board games as appropriate. Consider relocation to a
room in an area of high traffic if the patient desires more social
interaction.

8. Remember the outdoors to promote normalcy. As the patient’s

condition improves, assist him or her with sitting in a chair near a
window. When able, provide opportunities to sit in a solarium so
that patients can interact together. If physical condition and
weather permit, take the patient outside for brief periods. Natural
sunlight helps to promote a more normal sleep-wake cycle.

9. Support spiritual, mental, and emotional health. Request

consultation for interventions as appropriate from social services,
occupational therapy, pastoral services, and psychiatric nursing.

Energy Management; Activity Therapy; Art Therapy;

Recreation Therapy; Spiritual Support; Family Support; Emotional
Support.

Risk of injury 
related to falls
Goals/Outcomes: The patient will remain free from falls
throughout stay in ICU.
Cognitive Orientation, Distorted Thought Self-Control,
Information Processing.

NIC: Self responsibility facilitation

1. Identify those patients at moderate or high risk for falls:

• History of falls.

• Needs assistance with ambulation.

• Sensory impairment.

• Confused or disoriented.

397
• Needs assistance with elimination (bowel or
bladder).

• Vital signs are unstable (bradycardia, tachycardia,

hypotension, fever, etc.).

• Receiving cardiovascular or neurologic medications.

2. Use any or all of the following to notify those coming in contact
with the patient that this patient is at risk for falls:

• Place an armband on the patient’s wrist.

• Place hospital identification on door.

• Place hospital identification on chart.

• Share with the patient’s family or significant others

education related to the hospital’s fall prevention
program.

3. Universal fall prevention:

• Instruct the patient to call for help before getting out

of bed.

• Provide the patient with non-skid footwear.

• Familiarize the patient and family with the

environment.

• Keep the call light within the patient’s reach.

398
• Have the patient demonstrate use of the call light.

• Have the patient’s personal belongings within

reach.

• Maintain bed in the low position and wheels locked

and turn on the bed alarm if needed.

• Keep side rails up.

• Use subdued lighting at night.

• Maintain uncluttered environment at bedside.

• Keep the floor clean and dry.

• Have handrails in the patient’s room, bathroom,

and halls.

• Consult pharmacy for medication review.

4. Hourly rounds by nursing staff (registered nurses, nurse

assistants, nurse technicians [using the 5 Ps]): Hourly rounds
proactively address the patient’s needs and potentially prevent
falls. Before leaving the room ask, “Is there anything I can help you
with before I leave the room?” Remind the patient that a member of
the nursing staff will return in 1 hour.

• Pain: Assess the patient’s pain level and offer pain

medication.

• Position: Assess the patient comfort and assist the

patient to a more comfortable position as requested.

399
 For patients who are immobile, turn patients every
2 hours.

• Personal needs: Assess and assist the patient to the

toilet, offer snack or fluids.

• Placement: Place the call light or button, phone,

magazines or books, TV control, etc. within easy
reach of the patient.

Footwear.

Additional nursing diagnoses

Also see nursing diagnoses and interventions under Nutritional
Support, Sedation and Neuromuscular Blockade, and Risk for
Disuse Syndrome, in Traumatic Brain Injury (Ch 3).

Sedation and neuromuscular

blockade
With the 2013 update of the SCCM guidelines for pain, agitation,
and delirium, practice changes evolved. The term analgosedation
refers to the use of analgesic medications, most commonly opiates,
as first-line therapy for agitation, when another definitive treatable
source of the agitation is not apparent (Box 1-17). Agitation is
defined as nonpurposeful movement or motor restlessness.
Inadequate pain control may manifest as agitation, and can result in
decreased participation in ICU care (slower vent weaning and
mobilization), chronic pain, and posttraumatic stress disorder.
Clinically, undertreated or untreated pain can lead to serious
consequences including hyperglycemia, embolic events,
hemodynamic abnormalities, muscle breakdown, persistent
catabolism, and impaired wound healing.

400
Box 1-17
PATHOLOGIC CONDITIONS
CONTRIBUTING TO AGITATION
Addisonian crisis

Alzheimer disease

Anxiety disorder

Delirium

Delirium tremens

Developmental disability

Diabetes

Drugs

Subtherapeutic

Supratherapeutic (toxic)

Withdrawal syndromes

Idiosyncratic reactions

Drug interactions

Steroids

Encephalopathy

Hepatic

401
Metabolic

Uremic

Fear

Fluid/electrolyte abnormalities

Hypercarbia

Hyperthyroidism

Hypoglycemia

Hyponatremia

Hypophosphatemia

Hypoxemia

Impaired cerebral perfusion

Cerebral thrombosis

Subarachnoid hemorrhage

Intracranial bleeding

Cerebral vasospasm

Cerebral edema
Increased intracranial pressure

Tumor

Cerebrovascular accident

402
Hydrocephalus

Infection

Meningitis

Encephalitis

Brain abscess

Sepsis syndrome
Pain, inadequately controlled

Sleep deprivation

Stress

Tachyphylaxis to drugs (drug resistance)

Thyroid disease

Many patients who are critically ill also experience anxiety,

restlessness, and/or agitation, which may require the use of
sedation. Unrelieved stress, manifested in the form of anxiety or
agitation, retards healing and can increase mortality. Optimally,
causes of agitation are identified and managed using
nonpharmacologic methods (see Emotional and Spiritual Support
of the Patient and Significant Others, Chapter 2). When
nonpharmacologic methods fail, analgosedation is the
recommended first-line drug therapy. Pain control is discussed in
this chapter.
Following optimizing the analgesic agents, sedating or anxiolytic
agents can be added to promote comfort and decrease anxiety.
Anxiety and agitation in patients who are severely ill may be
prompted by emotional factors, including fear, loss of physical

403
control, life-threatening illness, inability to communicate (e.g.,
mechanical ventilation), and feelings of helplessness.
Environmental factors such as noise, temperature extremes, and
sleep deprivation add to anxiety and agitation. The influence of
environmental factors is sometimes more pronounced in those with
altered LOC (see Alterations in Consciousness). Common
pathophysiologic factors that contribute to agitation include
hypoxemia, impaired cerebral perfusion, infection, alcohol
withdrawal, and encephalopathy (Box 1-17). These causes must be
ruled out before initiating sedation because the use of sedative
medications may mask a treatable problem. Litigation resulting
from patient harm induced by use of sedation to manage hypoxia-
induced agitation is not rare in the United States.

Delirium
Consideration of the possibility of delirium is imperative when
beginning the management of agitation. Many of the clinical factors
associated with agitation (see Box 1-17) are also causative for
delirium, occurring in up to 50% of patients in ICU and up to 80%
of patients who are mechanically ventilated. Causes are
multifactorial and include the presence of invasive devices, use of
benzodiazepines, sleep deprivation, and prolonged immobility.
Following ruling out of other causes for agitation, the
recommendation of the SCCM is to deliver light sedation to the
patient using a validated agitation assessment scale, either the
RASS or the Sedation-Agitation Scale (SAS) (see Appendices 1 and
2). A fluctuation in the patient’s RASS or SAS score can be the first
indication that delirium may be present. It is recommended that
assessments be done on all patients in ICU every 12 hours, given
that fluctuation in mental status is common. The diagnosis is made
using one of two validated scales: the Confusion Assessment
Method for the ICU (CAM-ICU) or the Intensive Care Delirium
Screening Checklist (ICDSC). Delirium can be hyperactive
(previously known as ICU-psychosis), but is much more commonly
hypoactive or a mixture between the two. Hypoactive delirium may
be manifested as a flat affect, withdrawal, lethargy, apathy, or an
otherwise relatively unremarkable change in mental status. The
unfortunate term “pleasantly confused” is sometimes used for these

404
patients, but the outcome is often worse than for the hyperactive
patient because it is so easy to ignore or undertreat. Delirium is
associated with increased ICU and hospital length of stay, increased
ventilator time, increased mortality, and some degree of permanent
cognitive impairment in up to one third of patients. Studies have
calculated that delirium may increase hospital costs by an average
of almost $15,000. Treatment involves discontinuing medications
that can be deliriogenic, identifying and modifying preexisting or
precipitating risk factors if possible, nondrug treatment strategies
(Box 1-18), and finally haloperidol or atypical antipsychotic
medications. There is insufficient evidence to support the use of
antipsychotics for prophylaxis in patients who are at high risk for
delirium.

Box 1-18
NONDRUG TREATMENT STRATEGIES
FOR DELIRIUM AND CONFUSION
Repeated reorientation of the patient

Repeated provision of cognitively stimulating activities

Nonpharmacologic sleep protocols; minimizing unnecessary noise

and stimulation

Early mobilization/range-of-motion exercises

Timely removal of catheters and other invasive devices

Timely removal of physical restraints

Use of eyeglasses/magnifying lenses/hearing aids. Earwax

disimpaction

Adequate hydration

Adequate pain control

405
Administering sedation
Assuming that pain and delirium are addressed, the goal of further
pharmacologic sedation is to reduce anxiety and produce a calm
but communicative state, if possible. This is best accomplished by
administering frequent, incremental doses of sedatives only until
the desired effects are achieved. For a majority of patients, the goal
of therapy is light sedation, or 0 to −1 on the RASS, 3 to 4 on the
SAS. Light sedation, as opposed to deeper levels, has been
associated with decreased time on the ventilator, decreased hospital
and ICU length of stay, and decreased incidence of delirium.
Deeper levels of sedation may be appropriate for certain clinical
conditions including elevated intracranial pressures, alcohol or
other drug withdrawal, seizures, ARDS, hemodynamic instability,
ventilator dyssynchrony, concomitant therapy with neuromuscular
blocking agents (NMBAs), or comfort care.
If intermittent boluses of sedatives fail, it may be necessary to use
a continuous infusion. SCCM guidelines recommend fentanyl as the
initial infusion, followed by propofol or dexmedetomidine. If large
amounts of medication are necessary, careful consideration should
be given for consultation with a physician or midlevel practitioner
who specializes in the management of patients who are critically ill
using sedation, analgesia, and, if necessary, neuromuscular
blockade. Major organ dysfunction, multiple medications, tissue
catabolism, and other factors render patients who are critically ill
especially vulnerable to the toxic effects of many sedatives.
Oversedation and toxicity should be carefully avoided through
close monitoring, individualized dosing, and titration to desired
effect. Excessive sedation has been associated with delayed
recognition of neurologic events, muscle wasting, and nosocomial
complications such as DVT, compression injury, and pneumonia.
The literature supports performing daily wake up assessments on
patients with continuous drips to assure that there has been no
underlying neurologic changes and that the drips are at the lowest
effective dose, if indeed they are still required at all.
When providing sedation, if anxiolytic or other adjunctive agents
fail to help stabilize ventilation and perfusion in patients who are

406
mechanically ventilated, NMBAs may need to be added.
Neuromuscular blockade results in total paralysis of the striated
muscle at the neuromuscular junction. Neither the nondepolarizing
paralytic agents (see Table 1-36) nor succinylcholine possess
anxiolytic nor analgesic properties. The patient may be terrified,
given that they are fully aware that they have no ability to move,
communicate, or breathe. Paralysis is always done in conjunction
with sedation and analgesia to ensure that the patient is not
overwhelmed with fear. If not done, the patient undergoes extreme
stress, which can be further exacerbated if they also have
unrelieved pain. The pain should be addressed with either
scheduled (not PRN) opiates or a continuous opiate drip, usually
fentanyl, and potential anxiety with a sedative drip such as
propofol.
Patients may not tolerate or may inadvertently “fight” necessary
treatments. Those with severe respiratory dysfunction may require
use of specialized ventilator settings (ventilator dyssynchrony) such
as reversing the inspiration to expiration time (reverse I:E ratios), or
the use of oscillatory ventilation. Successful ventilation may not be
possible without use of NMBAs to stop the patient from tensing in
response to the treatment. Tensing reduces tidal volume and
requires increased energy expenditure. Care providers must create
an anticipatory plan for pain management and anxiolysis when the
patient is no longer able to voice his or her needs.

1-5
RESEARCH BRIEF BOX
Delirium evaluation in patients in the intensive care unit (ICU)
requires the use of an arousal/sedation assessment tool before
assessing consciousness. The Richmond Agitation-Sedation Scale
(RASS) and the Riker Sedation-Agitation Scale (SAS) are well-
validated arousal/sedation tools. The concordance of RASS and
SAS assessments in determining eligibility of patients in ICU for
delirium screening using the confusion assessment method for ICU
(CAM-ICU) was assessed. A prospective cohort study was
performed in the adult medical, surgical, and progressive (step-
down) ICUs of a tertiary care, university-affiliated, urban hospital

407
in Indianapolis, Indiana. The cohort included 975 admissions to
ICU between January and October 2009. In total, 2469 RASS and
SAS paired screens were performed and the conclusion was that
both SAS and RASS led to similar rates of delirium assessment
using CAM-ICU.
From Khan BA: Comparison and agreement between the Richmond Agitation-Sedation
Scale and the Riker Sedation-Agitation Scale in evaluating patients’ eligibility for delirium
assessment in the ICU. Chest 142(1):48-54, 2012.

Neuromuscular blockade
Monitoring paralytic agents: When a patient is paralyzed using
NMBA therapy, it is of paramount importance to be able to
evaluate whether the levels of sedation, analgesia, and paralysis are
appropriate. The previously mentioned means of monitoring pain
and agitation do not apply in the patient who is paralyzed, hence
the need for continuous infusions or around-the-clock boluses of
each for the duration of paralysis, without decreasing the doses.
The “gold standard” for monitoring paralytics is the use of a
peripheral nerve stimulator to deliver four (train of four or TO4)
tiny, sequential stimulating shocks to nerves on the wrist, foot, or
face. The muscle response is measured to evaluate how many of the
four signals are blocked by the NMBA compared with the number
perceived. In the absence of neuromuscular blockade, the muscle
should move four times equally in response to four signals. As
receptors are saturated with NMBAs, fewer muscle contractions are
seen (Table 1-34). Nerve stimulators are the best monitoring option,
with bispectral index (BIS) monitoring and drug holidays largely
falling from favor, but can be uncomfortable for the patient being
evaluated on an hourly basis. To avoid this, a baseline setting
should be established before the paralytic is started. Termed the
“supramaximal stimulation point,” it is the electrical setting on the
nerve stimulator after which no increased muscle movement is
noted. Once the drip is started, under no circumstances should this
electrical setting be increased. Also, it is very important to
recognize that the purpose of the nerve stimulator is to avoid
overexposure to these exceptionally dangerous drugs, in other
words the nurse should attempt to decrease the drip rate if one or
fewer twitches are present. Increasing the drip should only be done

408
based on clinical necessity, never TO4 results, even if all four
twitches are present.

Table 1-34
NERVE STIMULATION IN RELATIONSHIP TO PERCENT
BLOCKAGE

Number of Twitches Percent Blockage

4 0-50
3 60-70
2 70-80
1 80-90
None >90

Collaborative management
Care priorities

1. Ensure agitation is not caused by pathophysiology

All agitated patients should be evaluated for the presence of
hypoxia, impending shock, hypoglycemia, sepsis, electrolyte
imbalance, acid-base imbalance, drug reactions, and other common
causes of abnormal behavior. History of mental illness and
substance abuse should be evaluated, as psychiatric disorders and
substance withdrawal often manifest with agitation. Ensure those
with psychopathology are receiving appropriate prehospitalization
medications, and those withdrawing from substances are placed on
the appropriate management plan.

2. Attempt to manage pain and anxiety simultaneously, using

an opiate analgesic with sedative effects
Opiates reliably relieve pain, are easily titrated, and have significant
sedative effects. Morphine is widely administered using intermittent
bolus dosing and as a continuous infusion. Morphine may be
helpful in relieving hypoxia as it acts as a venodilator to reduce
preload to help promote better circulation in patients with heart
failure, as well as dilating the pulmonary vasculature to assist with
gas exchange. In renal failure, dosing should be reduced by 50% as
a result of the accumulation of an active metabolite of morphine.

409
Other opiates commonly used include hydromorphone (Dilaudid)
and fentanyl citrate (Sublimaze). Fentanyl and hydromorphone are
rapidly absorbed by the CNS and therefore are more potent than
morphine. Fentanyl is the shortest acting opiate and is best used as
a continuous infusion. The SCCM recommends that fentanyl be
used for rapid onset of analgesia and in patients who are
hemodynamically unstable. Meperidine (Demerol) is not
recommended as a primary analgesic, particularly in older adults
and those with renal failure. Patients often report inadequate pain
control, while experiencing euphoria. Meperidine accumulates with
repeated doses and causes an increased risk of neurotoxicity (see
Table 1-32).

3. Sedatives and antipsychotics options

After analgosedation is maximized, generally propofol or
dexmedetomidine can be added for further sedation of ongoing
agitation, followed by a benzodiazepine. Antipsychotics can be
used if delirium is present. Patients who experience adverse
reactions are sometimes given larger doses to correct the agitation
associated with what is actually drug intolerance. Constant
assessment of the patient’s response to sedation is needed so that
appropriate revisions can be made to drug dosage and selection.
When patients are placed on sedation, the care team must keep in
mind that the goal is not solely effective sedation but rather to
manage the problem causing the agitation so that the patient can be
weaned off the sedation.

Propofol (Diprivan): A lipid-based emulsion administered as a

titratable, continuous infusion for short-term (several hours to 5
days) sedation for patients who are mechanically ventilated.
Propofol contains significant fat calories, 1.1 kcal/mL, and this
should be taken into account when patients are receiving TPN in
addition to propofol. When discontinued, patients usually
awaken readily with prompt return to baseline mental function.
Downward titration by 5 µg/kg/min increments every 10 minutes
is preferable to abrupt discontinuation, in that rebound agitation
may occur. Hemodynamic changes (e.g., vasodilation, decreased
MAP) can be minimized by adequate hydration and similarly

410
 slow increases in the infusion rate. Propofol is particularly useful
for patients with neurologic impairment, because the short action
facilitates daily awakening during the sedation vacation to
evaluate underlying mental status. The drug is not an analgesic,
thus pain medication should be prescribed. Effectiveness of pain
management should be assessed during daily awakening.
Scheduled doses or a continuous infusion of opiate analgesics
provide effective pain control when used in combination with
propofol. Doses in ventilated ICU patients should rarely exceed
50 µg/kg/min (or 3 mg/kg/h) because the agent is considered an
anesthetic at higher doses. It is metabolized and eliminated
largely independent of renal and hepatic function. The lipophilic
drug accumulates more readily in patients who are obese, and
dosing should be based on either IBW or adjusted body weight
(ABW), (ABW − IBW) × 0.4 + IBW, in patients who are obese.
These patients may also be at increased risk for a more prolonged
recovery time after the infusion is discontinued. Prolonged
recovery time may occur with any patient when the infusion is
continued for more than 3 days at high doses.

• Propofol-related infusion syndrome: Propofol-

related infusion syndrome (PRIS) is a rare, often
fatal syndrome observed in patients who are
critically ill receiving propofol for sedation. PRIS is
characterized by acute bradycardia that progresses
to asystole, associated with severe unexplained
metabolic acidosis, acute renal failure,
rhabdomyolysis, hyperkalemia, and cardiovascular
collapse. The exact pathophysiology of PRIS has not
been determined. Impaired tissue metabolism
caused by propofol infusion has emerged as an
important mechanism leading to complete
cardiovascular collapse. Known risk factors include
sepsis, severe cerebral injury, and high propofol

411
 doses. Early recognition is the key to successful
management. If symptoms of PRIS are noted,
propofol should be discontinued and an alternative
sedative agent initiated. Measures to support
cardiac and renal function should be promptly
initiated.
Dexmedetomidine (Precedex): A novel agent with a mechanism of
action similar to clonidine. The drug blocks sympathetic outflow
through a central alpha stimulation to produce sedation when
used as a continuous infusion. Although not an analgesic,
dexmedetomidine has been shown to have opiate-sparing
properties. Level of awareness may be assessed without
downward titration of the drip. The drug is effective in managing
alcohol withdrawal syndrome, delirium, and failed extubation.
Dexmedetomidine is not associated with respiratory depression
but can cause hypotension and bradycardia. The drug should be
initiated in well-hydrated patients to avoid hypotension. The
recommended initial bolus dose may be omitted in borderline
hypovolemic patients. The SCCM has positioned the drug, as
well as propofol, ahead of benzodiazepines in the treatment of
agitation after analgosedation has been adequately attempted.
Although the labeling gives a maximum duration of 24 hours,
there are sufficient data that support extended use of the drug,
up to 72 hours or more. The maximum dose is 1 µg/kg/h,
although safety has been established at up to 1.5 µg/kg/h. It can
also be used in nonintubated patients, unlike propofol.

Benzodiazepines: Benzodiazepines may be used to relieve anxiety,

promote sleep, and produce sedation via nonspecific CNS
depression or via a specific depressant effect on gamma-
aminobutyric acid (GABA). Benzodiazepines produce muscle
relaxation, which facilitates using a lesser dose of NMBAs if the
patient requires paralysis. Dose-related effects on mental status
range from relief of anxiety to sedation and coma. All
benzodiazepines promote amnesia, an effect that is particularly
useful in patients undergoing unpleasant procedures. Midazolam

412
 (Versed) is considered superior to other benzodiazepines in
preventing recall. Ease of use, a general lack of paradoxic
agitation, and lack of recall are advantages of benzodiazepines,
but these are offset by a higher incidence of delirium and some
pharmacokinetic disadvantages (see later). They are the primary
drugs used to alleviate symptoms of acute alcohol withdrawal,
which commonly contribute to agitation in the critically ill.
However, benzodiazepines do not have analgesic properties
present in opiates, thus pain should always be ruled out as a
cause of agitation before using benzodiazepines solely. If present,
pain should be treated with analgesics before these drugs are
initiated. Table 1-35 describes specific characteristics of the
widely used benzodiazepines.

• Lorazepam (Ativan): Commonly given as an

intermittent IV or IM bolus and is sometimes used
as a continuous infusion, particularly with alcohol
withdrawal syndrome. Lorazepam has the slowest
onset and the longest duration of action of all
benzodiazepines. An advantage of lorazepam is
that it is metabolized by glucuronidation, as
opposed to oxidation as with the other
benzodiazepines, thus liver impairment does not
significantly affect drug metabolism. Lorazepam
has no active metabolites, thus it is safer for use in
patients who are renally impaired. However, at
high doses for prolonged periods of time,
hyperosmolality, acidosis, and ATN can occur
resulting from the propylene glycol diluent in
which the drug is delivered. Caution should be
used when administering lorazepam to older
adults, those who are severely ill, and those with
limited pulmonary reserve. Despite possible

413
 complications, it is the benzodiazepine of choice for
prolonged sedation. Patients who are lightly
sedated should awaken within 30 minutes during
the daily wake up assessment (sedation vacation).
When patients have difficulty awakening during
these assessments, the dosage should be decreased.

• Diazepam (Valium): An older benzodiazepine with

a long half-life, which may result in prolonged
sedation attributable to an active metabolite (up to
200 hours after a given dose). Diazepam should be
avoided in patients with liver dysfunction or severe
heart failure because of reduced hepatic clearance.
Limited solubility in water restricts use of standard
formulation to intermittent IV bolus injections.

• Midazolam (Versed): Short-acting and rapidly

metabolized, the drug is particularly useful for
short invasive procedures (e.g., bronchoscopy or
endoscopy). Because of its short half-life,
continuous infusions are required to maintain
sedation for longer periods. Delayed drug
metabolism in some patients who are critically ill
may lead to extended sedation, particularly with
sepsis or hepatic impairment. Midazolam is used
with caution in patients with renal failure, because
some of the active metabolites are renally secreted.
Antipsychotics: These agents can be used to reduce agitation in
disoriented and delirious or CAM-ICU positive patients. A
component of delirium or psychosis should be identified before
use of these agents is initiated. Patients should be well hydrated

414
 to avoid hypotension if given parenterally. Antipsychotics may
be used as part of management of alcohol withdrawal syndrome.

• Haloperidol lactate (Haldol): A butyrophenone

antipsychotic that is especially helpful in managing
psychosis and during withdrawal of sedatives.
Incremental IV or IM bolus doses are used,
although the IV route is unlabeled on the package
insert. The IV route has been widely used in
patients who are critically ill because onset of action
is rapid and extrapyramidal side effects occur less
frequently than with the IM route. Haldol should be
given cautiously to patients with severe
cardiovascular disorders because of the possibility
of transient hypotension and QT prolongation.
There is a general lack of evidence proving the drug
is useful in the treatment of delirium, although the
benefit probably outweighs the risk of low-dose
(less than 8 mg/day) PRN therapy.

Atypical Antipsychotics: The newer generation of antipsychotics

used to reduce agitation when delirium has been established.
These medications are associated with fewer extrapyramidal side
effects than haloperidol.

• Aripiprazole (Abilify): Provides sedation via partial

agonist activity at dopamine and serotonin (5-HT1A)
receptors and antagonist activity at serotonin (5-
HT1B) receptors. Also used to manage patients with
schizophrenia and bipolar disorders. It is given in a
dose of 9.75 mg IM at most every 2 hours to a
maximum of 30 mg/day. Although it has the

415
 cleanest side effect profile of the injectable atypical
antipsychotics, it is also less sedating, which can be
a disadvantage.

• Ziprasidone (Geodon): A piperazine derivative that

antagonizes alpha-adrenergic, dopamine,
histamine, and serotonin receptors and inhibits
reuptake of serotonin and norepinephrine. It is
given as 10 mg IM every 2 hours or 20 mg every 4
hours to a maximum of 40 mg/day to diminish
delirium, mania associated with bipolar disorders,
and the symptoms associated with schizophrenia. It
can have significant QT interval prolongation and
should be monitored for this.

• Olanzapine (Zyprexa): A thienobenzodiazepine

derivative that antagonizes alpha1-adrenergic,
dopamine, histamine, muscarinic, and serotonin
receptors. It is given as 10 mg IM every 2 to 4 hours
to a maximum of 30 mg/day to prompt CNS
sedation and to decrease symptoms associated with
delirium, schizophrenia, and bipolar mania. It
generally has more anticholinergic side effects than
the previously mentioned agents.

• Quetiapine (Seroquel): Although not available as a

parenteral dosage form, this is a good option for PO
or NG administration when that route is available.
It has a mechanism of action similar to previous
agents, with a fairly predictable sedative effect
when used in patients who are delirious. It can be

416
 started at 25 mg every 8 to 12 hours and increased
to 300 mg or more daily if needed. QT prolongation
and orthostatic hypotension can occur with
quetiapine.

• Risperidone (Risperdal): Another option for PO or

NG administration, given as 1 to 2 mg every 12 to
24 hours for agitation associated with delirium, up
to 6 mg/day. Its side effect profile is similar to
quetiapine, with possibly more extrapyramidal side
effects.
Neuromuscular Blocking Agents: NMBAs are used when longer
periods of complete paralysis are necessary in patients who are
mechanically ventilated. All possible causes of agitation (e.g.,
pain, fear, suctioning, hypoxemia) must be investigated
thoroughly before neuromuscular blockade is initiated. Outside
the operating room and other invasive procedural areas,
paralysis should be used as “a last resort” to control energy
expenditure in patients who are unstable, only when all methods
of sedation have failed. NMBAs generally are used in the
following situations: (1) to decrease O2 consumption in patients
who otherwise cannot obtain satisfactory O2 saturation; (2) to
alleviate specific medical conditions (e.g., status asthmaticus,
tetanus, malignant hyperthermia, status epilepticus, ARDS); (3)
to immobilize patients for surgical and invasive procedures; and
(4) to manage increased ICP. NMBA therapy also provides
effective management of shivering when deleterious effects occur
during therapeutic hypothermia, a therapy used to facilitate
neurologic recovery in patients postcardiac arrest.

• Depolarizing NMBAs: Succinylcholine (Anectine) is

the only depolarizing NMBA with widespread
clinical use. It is used to produce rapid, brief

417
 paralysis, most often during emergent intubation.
Long-term blockade is not practical because of
rapid tachyphylaxis and desensitization of
receptors to blocking effects.

• Nondepolarizing NMBAs: The class of NMBAs

most commonly used for paralysis in patients who
are critically ill. The most common agents used are
pancuronium (Pavulon), vecuronium (Norcuron),
rocuronium (Zemuron), and cisatracurium
(Nimbex). Pharmacokinetic and pharmacodynamic
properties of the three agents are listed in Table 1-
36. Cisatracurium is the most expensive of the three
agents, but its cost is justified by decreased
incidence of prolonged paralysis and weakness in
patients with severe hepatic and/or renal
impairment. The drug is beneficial in patients who
require steroids, because it lacks the steroidal
structure of other nondepolarizing agents. Steroid-
induced myopathy associated with concomitant use
of NMBAs and steroids is considered less likely
with cisatracurium and will be less severe if it
occurs. Numerous medications and several disease
states augment or antagonize neuromuscular
blockade (Box 1-19). The patient should be
monitored throughout therapy for conditions
affecting neuromuscular blockade.

Table 1-35

418
BENZODIAZEPINE CHARACTERISTICS

Table 1-36
NEUROMUSCULAR BLOCKING AGENT CHARACTERISTICS

BP, Blood pressure; CO, cardiac output; HR, heart rate; MAP, mean airway
pressure; PRN, pro re nata (when necessary).

Box 1-19
DRUGS AND PHYSIOLOGIC CONDITIONS
THAT AFFECT NEUROMUSCULAR
BLOCKADE
Drugs that augment neuromuscular blockade
Aminoglycoside antibiotics

Bacitracin

419
Calcium channel blockers

Clindamycin

Colistimethate

Cyclosporine

Inhaled anesthetics

Lidocaine

Piperacillin

Procainamide

Propranolol

Quinidine

Vancomycin

Drugs that antagonize neuromuscular blockade

Anticholinesterase agents

Azathioprine

Carbamazepine

Corticosteroids

Phenytoin

Ranitidine

Theophylline

Physiologic conditions that increase neuromuscular

blockade

420
Acidosis

Dehydration

Hypercalcemia

Hypermagnesemia

Hypocalcemia

Hypokalemia

Hyponatremia

Hypothermia

Myasthenia gravis

Physiologic conditions that decrease neuromuscular

blockade
Alkalosis

Decreased peripheral perfusion

Hyperkalemia

Hypernatremia

Clinicians should determine a therapeutic end point or goal for

paralysis and titrate neuromuscular blockade to achieve that goal.
Examples of therapeutic end points are decreases in PIP or
decreases in O2 consumption. Negative end points include
development of extreme weakness or inability to move. Monitoring
the degree of neuromuscular blockade is essential. It cannot be
overemphasized that NMBAs provide no analgesia or anxiolysis.
All patients receiving NMBAs must also have therapy with
continuously dosed opiates and anxiolytics.

421
Care plans for sedation and neuromuscular
blockade
Anxiety 
related to actual or perceived threat of death; change in health status;
threat to self-concept or role; unfamiliar people or environment; the
unknown.
Goals/Outcomes: Within 4 to 6 hours of initiating therapy, the
patient’s anxiety is diminished, as evidenced by verbalization of
same, HR less than 100 bpm, RR less than 20 breaths/min, and
decrease in restlessness and extraneous motor movement.
Anxiety Self-Control.

Anxiety reduction

1. Carefully assess for and correct factors contributing to anxiety

(see Box 1-17).

2. Ensure pathophysiology is not overlooked as the cause of anxiety

or agitation.

3. Provide emotional and spiritual support for the patient and

family, especially if the patient requires neuromuscular blockade
(see Emotional and Spiritual Support of the Patient and Significant
Others, Chapter 2).

4. Evaluate adequacy of pain control. Administer opiate or other

analgesics in appropriate doses on a schedule or through a
continuous infusion (see Pain).

5. Initiate nonpharmacologic measures to reduce anxiety (see Box 1-

15).

6. Assess the patient using a recognized agitation assessment tool

(see Alterations in Consciousness).

7. If administering a short-acting benzodiazepine in small doses at

frequent intervals, monitor carefully for excessive sedation and
respiratory depression. Have flumazenil (Romazicon) immediately

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available for reversal of drug effects.

8. If anxiety is profound and associated with sensory/perceptual

alterations (e.g., hallucinations), consider use of an antipsychotic
agent. Perform a valid delirium assessment before using
antipsychotics. Ensure adequate hydration before use and monitor
closely for hypotension.

9. For patients undergoing neuromuscular blockade, provide

careful monitoring of level of blockade with a peripheral nerve
stimulator on the train of four settings, coupled with fixed, effective
dosing of sedatives and analgesics.

Risk for injury 

related to impaired gas exchange resulting from hypoventilation associated
with sedative induced respiratory depression.
Goals/Outcomes: Within 1 hour of intervention, the patient has
adequate gas exchange, as evidenced by orientation to time, place,
and person; PaO2 greater than 80 mm Hg; Paco2 24 to 30 mm Hg;
SpO2 greater than 90; and RR 12 to 20 breaths/min with normal
depth and pattern. Achieving the patient’s “healthy” baseline is
generally the goal for improvement. Decreased O2 supply
secondary to decreased ventilatory drive occurring with sedative
use and CNS depression or secondary to decreased chest wall
movement occurring with residual neuromuscular blockade are
resolved.
Respiratory Status: Gas Exchange.

Ventilation assistance

1. Assess the patient’s respiratory rate, depth, and rhythm at least

hourly when heavily sedated. Patients who are fully sedated
require continuous direct monitoring until vital signs are stable and
protective reflexes (e.g., gag reflexes) are present.

2. Propofol should only be used as part of sedation on patients who

are mechanically ventilated to avoid the risk of apnea.

3. Provide appropriate care related to mechanical ventilation (see

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Mechanical Ventilation).

4. If NMBAs are used, assess depth of paralysis using peripheral

nerve stimulator. Titrate dose to maintain desired level of paralysis
(see Table 1-34). Only increase paralytic drip for clinical reasons,
not in response to train of four results.

5. Provide a daily sedation vacation and/or drug holiday to assess

LOC, ability to initiate spontaneous breaths, and ability to remain
stable off sedation and/or neuromuscular blockade.

6. Continuously monitor SpO2 via pulse oximetry and end tidal CO2.

7. Alternatively, monitor chest wall movement via apnea monitor.

8. Have appropriate antidote (e.g., naloxone for opiates, flumazenil

for benzodiazepines) and airway management equipment
immediately available.

9. Position the patient to promote full lung expansion, and turn the
patient to mobilize sputum.

Deficient knowledge 
related to lack of recall, related to interrupted memory consolidation
secondary to benzodiazepine use.
Goals/Outcomes: Within 12 hours of cessation of benzodiazepine
therapy, the patient recalls information essential to self-protection
and self-care.
Knowledge: Treatment Procedures.

Teaching: Procedure/treatment

1. Remind the patient and family that recall of unpleasant

procedures (e.g., cardioversion, endoscopy) will be diminished and
that this is a desired effect of the medication.

2. Reinforce necessary information (e.g., NPO instructions, need to

call for assistance when changing positions, need for deep
breathing) with the patient and family at frequent intervals until

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comprehension is demonstrated.

3. Review outcome or findings of procedure with the patient as

necessary until the patient expresses satisfactory understanding.

Additional nursing diagnosis

Additional nursing care plans are available in sections on
Alterations in Consciousness, Pain, and Emotional and Spiritual
Support of the Patient and Significant Others, Chapter 2).

Wound and skin care

A wound is a disruption of tissue integrity caused by trauma,
surgery, or an underlying medical disorder. Wound management is
designed to promote healing, prevent infection, and/or reduce
deterioration in wound status. Principles of wound management
are used to move a wound toward healing and should be integrated
into the plan of care for the patient with a wound.
Renewed emphasis on the role of nurses in the prevention of
pressure ulcers is evident in the Centers for Medicare and Medicaid
Services (CMS) standards of care.
Noting that hospital-acquired conditions could be reasonably
prevented with evidence-based guidelines, CMS discontinued
additional payment to hospitals for pressure ulcers that were not
present on admission. CMS will no longer pay for the treatment of
hospital-acquired stage 3 and stage 4 pressure ulcers. Pressure
ulcers are considered by some to be “avoidable” problems within
the healthcare system. If a pressure ulcer is “present on admission”
documented by a clinician who diagnoses and treats, the hospital
will be entitled to reimbursement of treatment for stage 3 and stage
4 pressure ulcers. Pressure ulcer prevention programs should be in
every healthcare facility and address issues such as skin and risk
assessment, the use of products to both reduce risk and treat wound
and skin issues, as well as patient and family education.
There are reliable and valid risk assessment tools to be used to
identify risk factors that contribute to the development of pressure
ulcers. The Braden Scale and Norton Scale have been extensively

425
studied and found to be valid for the prediction of pressure ulcer
risk. As a result of the emphasis on prevention of avoidable
pressure ulcers and the accompanying economic impact of fiscal
restraints, more effort is being placed on prevention. Norton scores
of 14 are indicative of mild risk; a score of 12 indicates “high risk.”
Braden scores of 18 to 15 indicate mild risk, and 12 is high risk. A
risk assessment tool should be used in acute care on admission and
reassessment should be done at least every 24 to 48 hours or when
the patient’s condition changes or deteriorates.

Wounds closed by primary intention

Clean surgical or traumatic wounds with edges that are closed with
sutures, staples, sterile tape strips, or wound glue are referred to as
wounds closed by primary intention. Impairment of healing most
frequently manifests as dehiscence, evisceration, infection, or
delayed healing. Individuals at high risk for disruption of wound
healing include those who are obese, diabetic, older, malnourished,
receiving steroids, immunosuppressed, undergoing chemotherapy
or radiation therapy, or receiving vasopressors. Coexistent
infections at another body site and colonization with
microorganisms such as methicillin-resistant Staphylococcus aureus
(MRSA) are factors that may contribute to the development of
infection. The continuum of contamination of wounds ranges from
colonized to critically colonized to infection. Once microorganisms
adhere to the surface of the wound, a biofilm develops. Biofilms on
the base of the wound inhibit efficacy of antibiotics and are
suspected to delay wound healing. Proper wound management will
decrease the risk of biofilm development, wound infections, and
facilitate wound healing.

Assessment
Optimal wound healing
Immediately after a surgical injury, the incision is warm, red,
indurated, and tender. Inflammation normally subsides in 3 to 5
days. A healing ridge can be palpated just under the intact suture
line by days 5 to 9. It is produced by the newly formed connective

426
tissue (see Table 1-37).

Impaired healing
Impaired healing is recognized by the lack of an adequate
inflammatory response surrounding a wound, continued drainage
from an incision line 2 days after injury (when no drain is present),
absence of a healing ridge by day 9 after injury, and/or presence of
purulent drainage (see Table 1-37). A chronic wound is one that
fails to proceed to healing within a reasonable time, to progress
through a normal repair process, and is usually associated with
pathology (i.e., diabetes or pressure damage). Wound assessment
should be done on an ongoing basis to determine the progress or
deterioration of the wound. Assessment includes anatomic location,
dimensions (length, width depth), percent of tissue type
(granulation, slough, necrotic), exudate (amount, color, odor), and
condition of the periwound skin. The wound should be cleansed
before assessment to allow for visualization of the wound base.

Diagnostic Tests During Wound Healing

Test Rationale Abnormal Findings

Complete Assess for discrepancies in red Low red blood cells and hemoglobin may
blood count blood cells, white blood cells, and impair oxygen delivery. Platelet count:
(CBC) with hemoglobin, platelet count High will increase risk of clot.
differential Low platelets will add to the risk of
abnormal bleeding.
An increase in the white blood cell count
can indicate infection.
Low white blood cells will reduce the
body’s ability to fight microorganisms.
Plasma protein Protein levels assist with the Transferrin less than 100 mg/dL, albumin
levels: regulation of fluid in the body and less than 3.5 g/dL, and/or prealbumin less
transferrin, are necessary to make collagen, than 19.5 mg/dL indicate malnutrition.
albumin, and which is essential for wound Request a nutrition consultation.
prealbumin healing
Wound culture Determine the presence of Culture will identify the specific aerobic
and sensitivity microbes and susceptibility and anaerobic organisms and their
infection susceptibility to antibiotics. Preliminary
culture results in 24 hours, final in 48
hours.

Table 1-37
ASSESSMENT OF HEALING OF WOUNDS CLOSED BY PRIMARY

427
INTENTION

Expected Findings Abnormal Findings

Edges well approximated Edges not well approximated
Inflammatory response (redness, Decreased inflammatory response or inflammatory
warmth, induration, pain) lasting 3 to 5 response that lasts more than 5 days after injury
days
No drainage (without drain present) 2 Drainage continues more than 2 days after injury
days after closure
Healing ridge present by postsurgical Absence of healing ridge by day 9
days 5 to 9
Hypertrophic scar or keloid present

Collaborative management
Care priorities for surgical wounds healing by primary
intention
1. Application of a sterile dressing in surgery or at the time of
injury: Protects wound from external contamination, trauma, or
pressure injury. Usually, the surgeon or advanced practice nurse
changes the initial dressing.

2. Nutrition (oral diet, enteral nutrition, PN): Provides sufficient

nutrients for wound healing. Wounds require specific nutrients and
adequate nutrition is key to meet healing needs.

3. Multivitamins (all but especially vitamin C) and minerals

(especially zinc and iron): Corrects any deficits and supports
healing.

4. Pain control: Maximizes subcutaneous blood flow to the wound

to support healing.

5. Insulin: Necessary to control glucose levels in individuals with

diabetes mellitus or hyperglycemia from other causes (e.g., steroid
therapy, TPN, enteral nutrition). Hyperglycemia is associated with
abnormal and prolonged inflammation, reduced collagen synthesis,
and impaired epithelial migration. Patients who are critically ill
often develop insulin resistance, resulting in hyperglycemia.
Evidence-based hyperglycemia management protocols are available

428
from many sources, including the SCCM and the American
Association of Critical-Care Nurses. Choice of protocol is based on
the ability of each nurse to comply with the recommended insulin
dosage regime and associated monitoring. Protocols vary with
number of steps, frequency of monitoring blood glucose, and need
for available technology, such as access to computers, the Internet,
point-of-care blood glucose meters, and other variables. Control of
blood glucose has been consistently associated with more timely
and effective would healing. Glucose stabilization must be done
with a protocol that given the available resources, nurses are able to
appropriately monitor blood glucose and manage hypoglycemia to
maintain patient safety.

6. Topical or systemic antibiotics: Given when infection is present

and can be used prophylactically for a limited period of time. CMS
recommend that prophylactic antibiotics are discontinued within 24
hours after surgery is complete to decrease the occurrence of
resistant microbes. Specific orders must be written for continuation
to comply with the recommendation.

7. Antiseptics: Dakin solution at 0.25% may be used for a limited

time to clean slough from a wound bed. Dressings that provide an
antimicrobial affect against bacteria may have an active ingredient,
that is, silver or cadexomer iodine, and can be used in treating a
wound infection.

8. Incision and drainage: Removes wound exudate when infection

is present and localized. Healing occurs by secondary intention. The
wound may be irrigated to flush out organisms.

Care plans for wound healing by primary

intention
Impaired tissue integrity: Wound 
related to altered circulation; metabolic disorders (e.g., diabetes mellitus);
alterations in fluid volume and nutrition; and medical therapy
(chemotherapy, radiation therapy, steroid administration).
Goals/Outcomes: The patient exhibits the following signs of

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wound healing: well-approximated wound edges, good initial
postinjury inflammatory response (erythema, warmth, induration,
pain), no inflammatory response after the fifth day postinjury, no
drainage (without drain present) 48 hours after closure, and healing
ridge present by postoperative days 5 to 9. Tissue integrity is
restored.
Tissue Integrity: Skin and Mucous Membranes.

Wound care

1. Assess, document, and report impaired wound healing,

including absence of a healing ridge, presence of drainage or
purulent exudate, and delayed or prolonged inflammatory
response. Monitor vital signs and laboratory work for signs of
infection, including elevated temperature, HR, and WBCs.

2. Use standard (universal) precautions and follow proper

infection-control techniques when changing dressings. If a drain is
present, assess patency and handle gently to prevent the drain from
moving out of position, or being accidentally removed.

3. Provide wound care teaching and need for continued

postdischarge care. Demonstrate care for the patient or caregiver
and provide “teach back” time to validate knowledge and skills.
Coordinate care with home healthcare agency, if appropriate.

• For persons with hyperglycemia, maintain blood

glucose within ordered range.

• Explain to the patient that deep breathing promotes

oxygenation, which enhances wound healing. Stress
the importance of position changes and activity as
tolerated to promote ventilation. Use an incentive
spirometer to promote deep inspiration and
expiration. Evaluate the patient for smoking, and if
present, encourage smoking cessation because

430
 smoking increases vasoconstriction, which
compromises perfusion impacting negatively on
wound healing.

• For nonrestricted patients, ensure a fluid intake of at

least 1.5 L/24 h.

• Provide nutrients for healing: a diet with adequate

protein, calories, vitamins, and minerals. Encourage
between-meal supplements and give frequent small
feedings as needed/tolerated. (See Nutritional
Support.)

Surgical or traumatic wounds healing by

secondary intention
Wounds healing by secondary intention are those with tissue loss
or heavy contamination, not closed at the surface, and left open to
fill with granulation tissue, contract, and reepithelize. Impaired
healing is frequently caused by heavy contamination and impaired
perfusion, oxygenation, and/or nutrition, which delays the healing
process. Individuals at risk for impaired healing include those who
are obese, diabetic, malnourished, older, receiving steroids,
immunosuppressed, undergoing radiation therapy or
chemotherapy, or receiving vasopressors.

Assessment
Optimal healing
Initially, the wound edges are inflamed, indurated, and tender. Pale
granulation tissue on the wound floor and wound wall proliferates
and progresses to a deeper pink and then red; the tissue should be

431
moist. As the wound fills with granulation tissue, epithelial cells
from the surrounding tissue migrate across the granulation tissue,
fill the defect, and contraction occurs simultaneously to close the
wound. As healing continues, the wound edges approximate and
the newly resurfaced epithelium is pink and dry. If present, a
wound tract or sinus gradually decreases in size. The time frame for
healing depends on the size and location of the wound, as well as
the patient’s physical and psychological status (Table 1-38).

Table 1-38
ASSESSMENT OF HEALING OF WOUNDS CLOSING BY
SECONDARY INTENTION

Expected Findings Abnormal Findings

Granulation tissue initially pale and moist and then Granulation tissue remains pale or is
becomes pink and red over time excessively dry
No odor Abnormal odor
No slough (moist yellow avascular tissue) or Slough or necrotic tissue
necrotic (dead) tissue

No tunneling (dead space caused by tissue Tunneling or undermining that is not

destruction) or undermining, or decrease in size of decreasing in size or length
tunnels or undermining areas
Pain
Wound increases in size, tissue type
changes from granulation tissue and
becomes slough or necrotic

Impaired healing
Exudate, slough, and necrotic material appear on the base and walls
of the wound, indicating that healing has not progressed. The
percentage of nonviable tissue in the wound must be assessed for
distribution, color, presence of odor, and presence of wound
exudate (color, amount, and consistency). Assess the periwound
skin for signs of tissue damage, including disruption, moisture-
related skin damage, discoloration, and increasing pain. Volume,
color, and odor of drainage are assessed and measured if possible
(see Table 1-38).

Diagnostic tests
See discussion on Wounds Closed by Primary Intention.

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Test Purpose Abnormal Findings
Culture Test for the presence Culture will identify the specific aerobic and anaerobic
of infection organisms and their susceptibility to antibiotics. Preliminary
culture results in 24 hours, final in 48 hours.
Biopsy To rule out the Consult appropriate treating specialty as needed (e.g.,
presence of cancer or oncology or dermatology). Incorrect diagnosis of wound
dermatologic etiology can have untoward delay in treatment.
diagnosis

Collaborative management
Care priorities
1. Débride slough and necrotic tissue: To remove nonviable tissue,
use surgical or sharp débridement (done by provider certified to
perform débridement) for rapid removal and enzymatic (e.g.,
Santyl) or autolytic (e.g., hydrocolloid dressing) for slower removal.

2. Infection: Use systemic antibiotics specific to the pathogen. Each

time wound care is provided, wound cleansing should be
performed. This is to remove waste products and to dislodge and
remove bacteria, necrotic tissue, foreign bodies, and exudate.

3. Moisture: Wound healing must take place in a moist

environment. Dressing choices need to meet this need; excessive or
inadequate moisture will delay wound healing.

4. Edges: Wound edges that are thickened and rolled downward

may indicate premature closure of a chronic wound called epibole;
cautery using silver nitrate may be needed to open the wound
edges to move toward healing.

5. Fluids (oral/IV): Ensure adequate intravascular volume to

support healing.

6. Topical or systemic vitamin A: When indicated, used to reverse

adverse effects of steroids on healing.

7. Drain(s): Removes excess tissue fluid or purulent drainage.

Closed drains are preferable to open drains because of infection
control.

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8. Negative pressure wound therapy: Reduces edema and wound
exudate, promotes wound contraction, reduces bacterial bioburden,
and stimulates granulation tissue formation.

9. Skin graft/cultured keratinocytes/cultured skin substitute:

Provides coverage of wound if necessary.

10. Tissue flap: Fills tissue defect and provides wound closure with
its own blood supply. Requires pressure redistribution bed surface
to minimize pressure on operative flap.

11. Growth factors: These are naturally occurring proteins that

stimulate new cell formation and have been approved for use in the
treatment of diabetic foot ulcers. (e.g., platelet-derived growth
factor).

12. Hyperbaric O2: Used with difficult wounds to improve oxygen-

carrying capacity and improve local tissue oxygenation.

13. Diet: Designed to maintain weight at optimal BMI with

controlled blood glucose, includes multivitamins and minerals. See
discussion on Wounds Closed by Primary Intention.

Care plans for wounds healing by secondary

intention
Impaired tissue integrity: 
wound, related to presence of contaminants; metabolic disorders; medical
therapy; altered perfusion; immunosuppression; and malnutrition.
Goals/Outcomes: The patient’s wound exhibits the following
signs of healing: initially, postsurgical wound edges are inflamed,
indurated, and tender; epithelialization begins, granulation tissue
develops, and there is no odor or necrotic tissue. Exudate is
minimal. The wound begins to contract and the base starts to fill
with granulation tissue.
Wound Healing: Secondary Intention.

Wound care

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1. Impaired wound healing: Assess and document wound condition
daily. Report and manage decreased inflammatory response or
inflammatory response lasting more than 5 days; epithelialization
slowed or mechanically disrupted; granulation tissue remains pale
or becomes dry; presence of odor, exudate, necrotic tissue, pain,
wound breakdown, or if the wound edges close prematurely
(epibole).

2. Pack wounds lightly: Apply prescribed dressings (Table 1-39).

Lightly pack dressing into all tracts to promote gradual closure. Do
not overpack wounds with dressings; fill wound without pressure.
Thoroughly wash hands before and after dressing changes. Use
clean gloves; dispose of contaminated dressings appropriately.

3. Manage wound drains: Maintain patency, prevent kinking, and

secure drain/tubing to prevent accidentally moving or removing the
drain. Medical device related pressure ulcers occur beneath drains;
report and manage edema under drains.

4. Prevent contamination: Cleanse the skin surrounding the wound

with normal saline. Use minimal friction if skin is friable.

5. Wound cleansing: Provide pressure irrigation using a 35-mL

syringe with a 19-gauge Angiocath attached to provide a powerful
irrigation stream. Commercial wound cleansers have the necessary
pressure between 4 and 15 psi built into the spray nozzle. If the
tissue is friable or the wound is over a major organ or blood vessel,
use extreme caution with irrigation pressure. To remove
contaminants effectively, use a large volume of irrigant (e.g., 100 to
150 mL).

6. Topical enzymes: If prescribed to assist in debridement, follow

package directions carefully to help ensure efficacy. Certain other
topical agents, such as povidone-iodine, deactivate enzymes.
Protect undamaged skin with zinc oxide or liquid skin barrier.

7. Wound care teaching: Demonstrate, then have the patient or

caregiver “teach back” to validate understanding and skills.

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Table 1-39
DRESSINGS USED FOR WOUND CARE

Dressing Advantages Disadvantages

Transparent Provides moist environment and protects Cannot absorb excessive
dressing wound base. Transparent so can view wound; moisture, may result in
(e.g., Op-Site, prevents loss of wound fluid; protects from maceration of periwound
Tegaderm, friction and shear. Can use as secondary tissue.
Bioclusive) dressing and for securement.
Hydrocolloid Maintains moist wound environment; Do not use with heavily
(e.g., facilitates autolytic debridement; easy to apply, draining wounds; opaque;
DuoDerm, reduces pain. exudate present on removal
Restore, may be confused with infection;
Exuderm) dressing can roll.
Hydrogel Nonadherent; provides moisture to wound, Cannot be used with heavily
(e.g., minimizes pain; can be used with infected draining wounds; may
Skintegrity, wounds. macerate periwound skin.
Elasto-gel,
Replicare)
Foam (e.g., Absorptive; nontraumatic; easy to apply and Not intended for dry wounds;
Biatain, remove. may require tape or secondary
PolyMem) dressing to secure.

Calcium Dressing is seaweed and is highly absorptive, Cannot be used for dry
Alginate used for heavily exudative wounds, wounds; requires secondary
(e.g., appearance is gel-like upon removal. dressing; may have foul odor
SeaSorb, when removed.
Algisite)

Gauze (e.g., 2 Inexpensive; easy to use; ideal for packing May result in tissue maceration
× 2, 4 × 4, wound. if inserted too moist; may result
rolled gauze) in tissue disruption if allowed
to dry.
Composites Use for partial- to full-thickness wounds. Adhesive borders may disrupt
(e.g., surrounding skin. Composite
Alldress, dressings come in a variety of
Covaderm sizes, may be difficult to carry a
Plus) large supply.
Silver Antiseptic capability while in the wound. Silver sensitivity or allergy.
dressings: Different manufacturers will identify the length Rare cases of issues of tattooing
foam, of time their dressing has in continuing to shed have been noted. Silver ions
alginates, silver. will be deactivated by some
gels solutions.

Pressure ulcers
The National Pressure Ulcer Advisory Panel (NPUAP) defines a
pressure ulcer as localized injury to the skin and/or underlying
tissue usually over a bony prominence, as a result of pressure, or
pressure in combination with shear. High-risk patients include

436
patients with impaired sensory perception, advanced age, skin
moisture (incontinence, excessive sweating), decreased activity and
mobility levels, poor nutritional intake, and exposure to friction and
shear.

Assessment: Pressure ulcer risk and staging

ulcers
High-risk individuals should be assessed for risk on admission,
with daily assessments during hospitalization, using a standard
pressure ulcer assessment tool. Daily (or in some cases more often
according to facility policy) use of the Braden Scale or Norton Scale
will assist in identifying patients at risk for skin breakdown and
help the nurse make decisions on when to use preventative
interventions. A daily skin assessment should be done to assess for
any alterations in skin integrity.
When pressure ulcers are present, staging of the tissue layers is
an important evaluation of the level of tissue damage. A pressure
ulcer can be staged on a scale of 1 to 4 if the base of the wound can
be visualized. If the wound base cannot be seen, the wound is
considered “unstageable.” The following staging criteria are
endorsed by the NPUAP and are widely used in healthcare settings.

Stage I: Nonblanchable erythema

Intact skin with nonblanchable redness of a localized area usually
over a bony prominence. Darkly pigmented skin may not have
visible blanching; its color may differ from the surrounding area.
The area may be painful, firm, soft, warmer, or cooler compared
with adjacent tissue. Stage I may be difficult to detect in individuals
with dark skin tones. When seen under normal pressure conditions,
may indicate “at-risk” persons.

Stage II: Partial thickness

A partial thickness loss of dermis, presents as a shallow, open ulcer
with a red pink wound bed, without slough; can present as closed
or a ruptured serum-filled or serosanguineous fluid-filled blister;
may also be a shiny or dry shallow ulcer without slough or
bruising*. This stage should not be used to describe nonpressure-

437
related skin tears, tape burns, incontinence-associated dermatitis,
maceration, or excoriation.
*Note: Bruising indicates deep tissue injury.

Stage III: Full thickness skin loss

Full thickness tissue loss. Subcutaneous fat may be visible. Bone,
tendon, or muscle is not exposed nor directly palpable. Slough may
be present, but does not obscure the depth of tissue loss. Wound
undermining and tunneling may be present. The depth of a stage III
pressure ulcer varies by anatomic location. The bridge of the nose,
ear, occiput, and malleolus do not have (adipose) subcutaneous
tissue and stage III ulcers can be shallow. Areas of significant
adiposity can develop extremely deep stage III pressure ulcers.

Stage IV: Full thickness tissue loss

Full thickness tissue loss with exposed and/or directly palpable
bone, tendon, or muscle. Slough or eschar may be present. Often
includes undermining and tunneling. The depth of a stage IV
pressure ulcer varies by anatomic location. The bridge of the nose,
ear, occiput, and malleolus do not have (adipose) subcutaneous
tissue and these ulcers can be shallow. Stage IV ulcers can extend
into muscle and/or supporting structures (e.g., fascia, tendon, or
joint capsule) making osteomyelitis or osteitis likely to occur.

Unstageable: Full thickness skin or tissue loss, depth

unknown
Full thickness tissue loss in which actual depth of the ulcer is
completely obscured by slough (yellow, tan, gray, green, or brown)
and/or eschar (tan, brown, or black) in the wound bed. Until
enough slough and/or eschar are removed to expose the base of the
wound, the true depth cannot be determined. These wounds are
either stage III or stage IV. Stable (dry, adherent, intact without
erythema or fluctuance) eschar on the heels serves as “the body’s
natural (biological) cover” and should not be removed.

Suspected deep tissue injury, depth unknown

Purple or maroon localized area of discolored intact skin or blood-
filled blister resulting from damage of underlying soft tissue from

438
pressure and/or shear. The area may be preceded by tissue that is
painful, firm, mushy, boggy, warmer, or cooler compared with
adjacent tissue. Deep tissue injury may be difficult to detect in
individuals with dark skin tones. Evolution may include a thin
blister over a dark wound bed. The wound may further evolve and
become covered by thin eschar. Evolution may be rapid exposing
additional layers of tissue even with optimal treatment.

Diagnostic tests
See Diagnostic Tests.

Collaborative management
See Collaborative Management in Surgical Wounds Healing by
Primary Intention and Collaborative Management in Surgical or
Traumatic Wounds Healing by Secondary Intention.

Care plans for prevention and management

of pressure ulcers
Risk for impaired tissue integrity 
related to excessive tissue pressure, shearing forces, friction, and altered
circulation. Presence of pressure ulcer with increased risk for breakdown,
related to altered circulation; presence of contaminants or irritants
(chemical, thermal, mechanical).
Goals/Outcomes: High risk: skin integrity of the patient remains
intact. After intervention/instructions, the patient/caregiver
verbalizes causes and preventive measures for pressure ulcers and
successfully participates in the plan of care to promote healing and
prevent further breakdown if a pressure ulcer is present. Ulcers
present have granulation tissue and are moving toward healing.
There is a reduction in or no slough or necrotic tissue, or odor
present.
Tissue Integrity: Skin and Mucous Membranes.

Pressure ulcer prevention

439
1. Risk assessment: Identify individuals at risk daily with a
reliable/valid risk assessment tool; systematically document skin
condition from head to toe according to institutional policy.

2. Turning/Positioning: Turn or reposition the patient on a turning

schedule.

• Assist the patient with turning every 1 to 2 hours or

as the patient’s condition allows. Use pillows or
foam wedges to prevent direct pressure on bony
prominences.

• Patients with a history of previous tissue injury will

require pressure redistribution measures more
frequently.

• A high-Fowler position results in increased

shearing. Use a low-Fowler position and alternate
supine position with prone and 30-degree elevated
side-lying positions.

The Centers for Medicare and Medicaid Services has

addressed the problem of ventilator-acquired pneumonia as an
avoidable condition. The plan of care to avoid pneumonia
incorporates the positioning of the patient with elevation of the
head of the bed at 30 degrees or above. The clinician must perform
a risk/benefit analysis for the individual patient regarding height
of the head of the bed, weighing pressure ulcer prevention against
ventilator-acquired pneumonia prevention.

3. Heels: Float the heels using pillows placed under the length of

440
the calf.

4. Sacrum: Consider the use of soft silicone border foam dressings

over the sacrococcygeal area to prevent skin breakdown in high-
risk patients. Several studies have provided evidence that pressure
ulcer incidence is reduced when used.

5. Medical devices: To prevent medical device–related pressure

ulcer, cushion skin with dressings in high-risk areas such as the
nose; confirm that devices are not placed directly under a patient
who has reduced sensation or is immobile.

6. Minimize friction on tissue during activity: Lift rather than drag

the patient during position changes and transferring; use a draw
sheet to facilitate patient movement. Ideally, the patient should be
moved using lift equipment to prevent injury from friction and
shearing as friable skin “drags” over the sheets. Do not massage
bony prominences.

7. Minimize skin exposure to moisture: Cleanse at the time of

soiling and at routine intervals. Use moisture barriers and moisture
wicking underpads with minimization of disposable briefs.
Consider use of bowel management systems if the patient has
intractable fecal incontinence.

8. Pressure redistribution surfaces: Use an overlay or mattress that

redistributes pressure, such as low air loss, alternating air, or gel.
Choice of the most appropriate surface is based on the weight of the
patient, ability to be turned, stage and location of the ulcer(s), and
the overall goals of care for the patient.

Pressure ulcer care

1. Staging: Evaluate stage of pressure ulcer. See Assessment.

2. Maintain vigilant skin care: Research supports use of

commercially available skin care products. Keep the patient’s skin
clean with regular bathing, and be especially conscientious about
washing urine and feces from the skin. Commercial no-rinse

441
cleansers are available. If soap must be used, then thoroughly rinse
from the skin.

3. Moisture management: If the patient has excessive perspiration,

ensure frequent cleansing and change bedding as needed.

4. Information sharing: Teach the patient and caregivers the

importance of and measures for preventing and redistributing
pressure as a means of treating pressure ulcers.

Skin Surveillance; Incision Site Care; Wound Care; Pressure

Ulcer Care; Pressure Ulcer Prevention; Wound Irrigation.

Additional nursing diagnoses

For additional information on specific conditions, refer to the
following:

Impaired Tissue Integrity under Surgical or Traumatic Wounds

Healing by Secondary Intention.

Pain management; Pain decreasing with cutaneous stimulation.

Deficient knowledge related to care of wound/pressure ulcer.

Imbalanced Nutrition, less than body requirements for wound

healing.

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CHAPTER 2

Managing the critical

care environment
Bioterrorism
Bioterrorism is the intentional release of a biological agent,
generally aimed at causing as great a number of people as possible
to suffer illness and death. A bioterrorism event should be
suspected when there is an unusual and unexplained increase in an
illness.
The Centers for Disease Control and Prevention (CDC) identified
six biological agents as Category A, of highest concern for use in
terrorism: anthrax, botulism, hemorrhagic fever viruses, plague,
smallpox, and tularemia. Several factors explain why these agents
are more likely to be used:

1. Most people are susceptible to these organisms.

2. Most can be aerosolized, but not all are transmitted in the air.

3. They are fairly stable in aerosolized form.

4. Because of reason 3, agents transmitted through the air can cause

disease in a large group of individuals without direct contact.
Agents recognized as Category A transmitted by contact are
exceptionally virulent and, when not recognized early, can spread
rapidly and become an epidemic.

5. Resultant diseases are difficult to diagnose and treat.

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6. They have high morbidity and/or mortality rates.

7. Despite prevention and surveillance efforts to date, the

international community remains underprepared to fully address
the threat. As of 2012, more than 80% of nations failed to meet the
international requirements of the World Health Organization
(WHO) to ensure they are prepared to manage pandemics or
bioterrorism.

Bioterrorism assessment: Surveillance

Goal of surveillance
The goal is to detect a biological event as early as possible to limit
the spread of the infection.

Key signs
Bioterrorism should be suspected when the following situations are
seen:

• An outbreak of an illness within a short period of time, similar to

one that happens in a healthy population, without a link to
explain the transmission such as a similar food source.

• An outbreak of an illness that occurs at an unusual time of year.

• An outbreak with an unusual age distribution.

• A large cluster of patients are affected by an uncommon disease,

which results in a higher than expected death rate.

• The severity of the disease is increased with patients having

unusual routes of exposure.

• Strains of organisms seen have unusual antibiotic resistance.

• Those indoors are not as affected as or “as are those” who have
been outdoors.

• With some strains, an increased number of dead animals is noted.

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• Those presenting within 48 to 72 hours of exposure have likely
been exposed to a biological agent, as opposed to those exposed
to a toxin, who present within a few hours.

In 2003, the U.S. Department of Homeland Security introduced

BioWatch; a federally supported environmental monitoring system
designed to speed detection of specific bioterrorism agents released
in aerosolized form during an attack. BioWatch air sampling
devices have been deployed primarily outdoors, in more than 30
major urban areas. Samples are screened in designated laboratories
every 24 hours for genetic material from specified pathogens.
In 2007, Homeland Security Presidential Directive 21 “Public
Health and Medical Preparedness” (HSPD-21) recognized the
health-related security threats to the nation. HSPD-21 was
established a as federal advisory committee including
“representatives from state and local government, public health
authorities, and appropriate private sector health care entities, to
ensure that the federal government is meeting the goal of enabling
state and local government public health surveillance capabilities.”
The U.S. Department of Health and Human Services received and
subsequently delegated implementation of the mandate to the
CDC. On May 1, 2008, the CDC established the National
Biosurveillance Advisory Subcommittee (NBAS), a group of well-
recognized experts from public health, health care providers,
academics, the U.S. Department of Homeland Security, the U.S.
Department of Defense, and the private sector to advise the federal
government. The Advisory Committee of the Director is informed
by the NBAS of issues that impact development and
implementation of a nationwide biosurveillance strategy to
promote human health.

Monitor
• Observe for an unusual or unexplained increase in an illness,
especially with the characteristics listed in Key Signs.

U.S. President Barack Obama developed a Global Health Security

Agenda in 2014. The United States and several international
partners are leading the global community to ensure appropriate

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steps are taken to increase worldwide security against infectious
diseases.
The proposed strategy for international security against
bioterrorism is as follows:

1. Prevent outbreaks by mitigating risks. Well-developed laboratory

systems are needed in all countries to identify pathogens and
facilitate “right care at the right time”: right drug and right dosage
at the right time. Protocols to protect and defend key laboratories
from terrorists attempting to acquire biological weapons are
needed, along with routine, universal immunizations for the
worldwide population.

2. Detect disease threats immediately in all countries. Improved

specialized biosurveillance systems require trained participants to
monitor incidence of diseases, identify cases, determine the cause,
and contain outbreaks before they become epidemics.

3. Respond more quickly to occurrences. All nations require well-

developed emergency management systems with a unified
response. Improved strategies are needed to mobilize international
resources, including strengthening the ability of global health
organizations to respond more quickly and comprehensively to
crises.

As part of the 2014 Global Health Security Agenda, the United

States pledged to assist more than 30 countries to meet these targets
and has challenged the international community to assist in
dedicating the resources needed to implement the proposed
strategies.

Report
• All occurrences of the six Category A diseases must be reported
to the CDC.

• The CDC also monitors Category B organisms (includes

Brucellosis [Brucella sp.], epsilon toxin of Clostridium perfringens,
food safety threats [e.g., Salmonella sp., Escherichia coli O157:H7,

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 Shigella], glanders [Burkholderia mallei], melioidosis [Burkholderia
pseudomallei], psittacosis [Chlamydia psittaci], Q fever [Coxiella
burnetii], ricin toxin from Ricinus communis [castor beans],
staphylococcal enterotoxin B, typhus fever [Rickettsia prowazekii],
viral encephalitis [alphaviruses, e.g., Venezuelan equine
encephalitis, Eastern equine encephalitis, Western equine
encephalitis], and water safety threats [e.g., Vibrio cholerae,
Cryptosporidium parvum]). These organisms are the second highest
priority.

• Category C organisms are the third highest priority

agents and include emerging pathogens that could
be engineered for mass dissemination in the future
because of availability, ease of production and
dissemination, and potential for high morbidity and
mortality rates, and major health impact. The agents
include emerging infectious diseases such as Nipah
virus and hantavirus.

Contain (prevent the spread of the disease)

• Appropriate personal protective equipment (PPE) and isolation
precautions need to be taken to inhibit the spread of the
infectious agent.

Labwork
• Appropriate laboratory studies should be done to confirm the
presence of the suspected biological agent. Many of these
diseases require testing at specialty laboratories because these are
uncommon bacteria and most hospital laboratories are not set up
to test for these agents.

Anthrax

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Pathophysiology
Anthrax is a serious disease caused by Bacillus anthracis, a spore-
forming bacterium. A spore is a dormant (inactive) cell that
activates under the right conditions. Anthrax spores, once inside
the human body, are able to germinate. Once germinated, the
replicating bacteria release endotoxins leading to hemorrhage,
edema, and necrosis.
There are three types of anthrax: skin (cutaneous), lung
(inhalation), and digestive (gastrointestinal). Hemorrhagic
mediastinitis is present with the inhalation form, and bloody
diarrhea is seen with the intestinal form. When enough endotoxin is
released into the bloodstream, the disease can be fatal even if
antibiotics eradicate the bacteria. Anthrax infections are usually
very rare because it takes thousands of spores to cause an infection.
Inhalation anthrax is usually fatal even with treatment.
Gastrointestinal anthrax has a mortality rate of 25% to 60%,
whereas 20% of those with untreated cutaneous anthrax die.
Cutaneous anthrax is rarely fatal unless untreated.

Transmission
Anthrax has not been known to spread from one person to another.
Humans may acquire anthrax by handling products from infected
animals or inhaling anthrax spores from infected animal products
(e.g., wool). People acquire gastrointestinal anthrax by eating
undercooked meat from infected animals. Anthrax in soil may enter
the body through open skin. The organism is easy to obtain,
produce, and store.

Assessment
The symptoms (warning signs) of anthrax differ depending on the
type of disease:

• Inhalation: The most serious form with the highest mortality rate,
this begins 1 to 6 days after exposure with cold or influenza (flu)-
like symptoms, with sore throat, mild fever, and muscle aches.
Later symptoms include cough, chest discomfort, shortness of

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 breath, fatigue, and muscle aches. Inhalation anthrax quickly
progresses to respiratory failure and shock. Chest radiograph
reveals a widened mediastinum and pleural effusions.

• Cutaneous: The first symptom is a raised, itchy bump that

develops into a blister, seen 1 to 7 days after exposure. The blister
progresses to a skin ulcer with a blackened center. The sore, the
blister, and the ulcer are painless. Fever, headache, and swollen
glands may occur.

• Gastrointestinal: At 2 to 5 days after exposure, the person exhibits

nausea, loss of appetite, bloody diarrhea, and fever, followed by
severe stomach pain. If untreated, it can progress to generalized
toxemia and sepsis.

Diagnostic tests
Diagnostic tests to isolate anthrax antigen are not widely available.
Confirmation of the diagnosis is made by sending a specimen to a
national reference laboratory after the treatment begins. Clinicians
should begin treatment based on clinical signs and symptoms,
because early treatment is imperative to enhance chances of
survival from inhalation anthrax. Standard blood culture may be
useful if the laboratory is told to look for bacillus species. A Gram
stain, enzyme-linked immunosorbent assay (ELISA), and nasal
swab check for spores may also be useful.

Collaborative management
Care priorities

1. Antibiotics
Used to treat all three types of anthrax. Ideally, the antibiotic should
be based on culture and sensitivity results. If those are not
available, the antibiotics of choice are doxycycline and
ciprofloxacin. Additionally, levofloxacin is recommended for
adults. Occasionally, rifampin may also be used. Early
identification and treatment are crucial to minimize the amount of

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endotoxin released.

2. Intubation and mechanical ventilation (inhalation)

To support gas exchange and help maintain acid-base balance.

3. Intravenous fluids (inhalation and gastrointestinal)

To prevent dehydration and maintain adequate circulatory volume.

4. Prevention after exposure

Treatment differs when a person exposed to anthrax is not yet
having symptoms. Health care providers use antibiotics (e.g.,
ciprofloxacin, doxycycline, penicillin) combined with anthrax
vaccine to prevent anthrax infection and, for contact anthrax,
instruct the exposed person to immediately scrub hands and arms
or take a shower (if available) and remove and place their clothes in
a plastic bag when apprised of an exposure.

5. Treatment after infection

Treatment is usually a 60-day course of antibiotics. Success depends
on the type of anthrax, the general health of the individual, and
how early treatment begins. A 60-day course is necessary so that
the antibiotic is in the person’s system when the spores activate.
Inactive spores are not susceptible to antibiotics.

6. Vaccination
A vaccine to prevent anthrax exists, but it is not yet available to the
general public. Anyone at risk for anthrax exposure, including
certain members of the U.S. Armed Forces, laboratory workers, and
workers who may enter or reenter contaminated areas, may be
vaccinated. If anthrax is used as a weapon, a vaccination program
will be initiated to vaccinate as many exposed people as possible.

Care plans: Anthrax

Gas exchange, impaired 
related to respiratory insufficiency from respiratory tract infection
secondary to inhalation of anthrax.

469
 Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate gas exchange, as evidenced by PaO2 at least 80 mm
Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal
breath sounds, and absence of adventitious breath sounds. The
respiratory rate (RR) is 12 to 20 breaths/min with normal pattern
and depth.
Respiratory Status: Gas Exchange.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs

of increased work of breathing such as use of accessory muscles or
retraction of intercostal or supraclavicular muscles.

3. Monitor for diaphragmatic muscle fatigue.

4. Ensure airway is not obstructed by tongue (snoring or choking-

type respirations) and monitor breathing patterns. New patterns
that impair ventilation should be managed as appropriate for
setting.

5. Auscultate breath sounds noting areas of decrease/absent

ventilation and presence of adventitious sounds.

6. Note changes in oxygen saturation from arterial blood gases

(SaO2), pulse oximetry (SpO2), and end-tidal CO2 (etco2) as
appropriate.

7. Monitor for increased restlessness or anxiety.

8. If increased restlessness or unusual somnolence occurs, evaluate

the patient for hypoxemia and hypercapnia as appropriate.

9. Monitor chest x-ray reports as new films become available.

Oxygen therapy

1. Administer supplemental oxygen using liter flow and device as

470
ordered. Add humidity as appropriate.

2. Restrict the patient and visitors from smoking while oxygen is in

use.

3. Document pulse oximetry with oxygen liter flow in place at time

of reading as ordered. Oxygen is a drug; the dose of the drug must
be associated with the oxygen saturation reading or the reading is
meaningless.

4. Obtain arterial blood gases (ABGs) if the patient experiences

behavioral changes or respiratory distress, to check for hypoxemia
or hypercapnia.

5. Monitor for changes in chest radiograph and breath sounds

indicative of oxygen toxicity and absorption atelectasis in patients
receiving higher concentrations of oxygen (greater than Fio2 45%)
for longer than 24 hours. The higher the oxygen concentration, the
greater the chance of toxicity.

6. Monitor for skin breakdown where oxygen devices are in contact

with skin, such as nares and around edges of mask devices.

7. Provide oxygen therapy during transportation and when the

patient gets out of bed.

Mechanical ventilation

1. Monitor for conditions indicating a need for ventilation support.

2. Monitor for impending respiratory failure.

3. Consult with other health care providers to select the ventilatory

mode.

4. Administer muscle-paralyzing agents, sedatives, and narcotic

analgesics as appropriate.

5. Monitor the effectiveness of mechanical ventilation on the

physiologic and psychological status of the patient.

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6. Provide the patient with means of communication.

7. Monitor adverse effects of mechanical ventilation.

8. Perform routine mouth care.

9. Elevate the head of the bed (HOB) up to 45 degrees as tolerated.

Botulism
Pathophysiology
Botulism is a muscle-paralyzing disease associated with respiratory
dysfunction caused by a toxin produced from Clostridium botulinum
bacteria. The toxin is the most potent lethal substance known to
humans. Man-made inhalational botulism is brought into being
when aerosolized botulinum toxin is inhaled. The bacterium
naturally lives for weeks in nonmoving water and food. There are
three naturally acquired types of botulism:

• Foodborne: A person ingests toxin that leads to illness in a few

hours to days.

• Infant: Occurs in a small number of susceptible infants each year

who harbor C. botulinum in their intestinal tracts.

• Wound: Occurs when a wound is infected with C. botulinum.

Botulinum toxin, once absorbed into the bloodstream, is

transported to the peripheral cholinergic synapses, where it binds
irreversibly. The toxin then blocks the release of acetylcholine in the
neuromuscular junctions, causing paralysis of the muscles.

Transmission
Botulism is not spread from person to person. Botulinum toxin is
absorbed through lung or intestinal mucosa and nonintact skin.
Foodborne botulism occurs in all age groups.

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Assessment
• Foodborne: Double vision, drooping eyelids, slurred speech,
dysphagia, dry mouth, and descending muscle weakness are
symptoms. Weakness starts in the shoulders and upper arms,
descends to the lower arms and upper thighs, and eventually
spreads down to the lower legs and feet. Paralysis of the
respiratory muscles leads to respiratory failure unless ventilation
is supported with mechanical ventilation. Patients are generally
afebrile and alert.

• Respiratory assessment: Patients who are not intubated should

have their respiratory status monitored closely to detect
deterioration in respiratory muscle strength. One of the best
assessment tools is periodic measurement of negative inspiratory
force (NIF). If the NIF falls below 20 cm H2O, the patient is likely
to require intubation and mechanical ventilation.

Diagnostic tests
Currently, the CDC and fewer than 25 public health laboratories
perform the diagnostic test for botulism. Diagnosis is made
clinically, after ruling out other causes of paralysis. Classic botulism
paralysis is descending in nature and involves the cranial nerves.

Collaborative management
Care priorities

1. Antitoxin
Botulinum antitoxin is available in two forms from the CDC.
Because both are equine derivatives, it is important to perform a
skin test as directed in the package insert to check for
hypersensitivity before administering. Antitoxin helps prevent
further nerve damage from the botulinum toxin but cannot reverse
the existing paralysis. It is most effective if given within the first 24
hours. The antitoxin is not effective in infant botulism. For infant
botulism, botulism immune globulin-intravenous (BIG-IV) is

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administered.

2. Antibiotic
Antibiotics are given to treat wounds infected with C. botulinum
and secondary infections. Antibiotics have no effect on botulinum
toxin.

3. Supportive care
Includes mechanical ventilation, nutrition support, care for
immobility, and treatment for secondary infections.

Care plans: Botulism

Breathing pattern, ineffective 
related to respiratory tract infection
Goals/Outcomes: The patient demonstrates effective air
exchange, as evidenced by RR 12 to 20 breaths/min, PaO2 ≥80 mm
Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, SaO2 greater than 95%,
SVO2 greater than 60%, and ecto2 5% to 6% (35 to 45 mm Hg).
Respiratory Status: Ventilation.

Respiratory monitoring

1. Monitor rate, rhythm, depth, and effort of respirations.

2. Monitor for diaphragmatic muscle fatigue.

3. Auscultate breath sounds, noting areas of decreased/absent

ventilation, and presence of adventitious sounds.

4. Assess for breathing effectiveness by monitoring SaO2, SVO2, ecto2,

and changes in ABG values, as appropriate.

5. Insert oral or nasopharyngeal airway if the patient cannot

maintain patent airway; if severely distressed, the patient may
require endotracheal intubation.

Ventilation assistance

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1. Position the patient to alleviate dyspnea and insure maximal
ventilation, generally in a sitting upright position unless severe
hypotension is present.

2. Assist with incentive spirometer, as appropriate.

3. Clear secretions from airway by having the patient cough, or

provide nasotracheal, oropharyngeal, or endotracheal tube
suctioning as needed.

4. Have the patient breathe slowly or manually ventilate with an

Ambu (manual resuscitation) bag slowly and deeply between
coughing or suctioning attempts.

5. Turn the patient every 2 hours if immobile. Encourage the patient

to turn self or get out of bed as much as tolerated if able to do so.

Hemorrhagic fever viruses

Pathophysiology
Hemorrhagic fever viruses (HFVs) include many diseases separated
into four families of viruses; not all are viewed as risks for
bioterrorism. Those thought to or that have posed a significant risk
include Ebola virus disease, Marburg virus disease, Lassa fever,
New World Arenaviridae, Rift Valley fever, yellow fever, Omsk
hemorrhagic fever, and Kyasanur forest disease. In 2014, the
largest, most devastating outbreak of Ebola virus occurred in West
Africa, affecting thousands of African people and international aid
workers including health care professionals. The pathophysiology
of these diseases is not well understood. Outbreaks are sporadic
and have occurred in areas with very limited health care. Infection
with these viruses leads to thrombocytopenia and possibly platelet
dysfunction. The effects of these viruses vary, but all lead to
coagulation problems, hemorrhage, and shock. Mortality ranges
from less than 1% with Rift Valley fever to 50% to 90% with Ebola
virus. Only one of the Arenaviridae viruses has been identified in
the United States. Other HFVs have not emerged.

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Transmission
HFVs reside in many animal hosts and arthropod vectors. Humans
become infected when bitten by an infected arthropod, by inhaling
aerosolized virus from infected rodent excreta, from direct contact
with infected animal carcasses, and from other human beings.
Humans infected with Ebola, Marburg, Lassa fever, and
arenaviruses can spread the disease through contact with body
fluids.

Isolation
Strict droplet and contact precautions are required if a patient is
suspected of infection. The recommendations for management of
Ebola patients has evolved worldwide. It was recognized that a
large number of secondary infections from Ebola virus disease
during the 2014 outbreak occurred in health care workers exposed
during care of infected patients. Leading U.S. special contagious
disease centers have used full-body Tyvek suits and powered air
purifying respirator (PAPR) hoods as part of the contact and
droplet precautions protocol.

Assessment
Clinical scenarios vary depending on the virus. The most common
symptom is a fever.

• Ebola and Marburg: Maculopapular rash, bleeding, disseminated

intravascular coagulation (DIC), jaundice, nausea, vomiting,
diarrhea, and headache.

• Lassa fever and New World arenaviruses: Gradual onset of fever,

nausea, abdominal pain, conjunctivitis, and jaundice. Severe
exudative pharyngitis in Lassa fever.

• Rift Valley fever: Fever, headache, photophobia, and jaundice.

Diagnostic tests
Only the CDC and U.S. Army Research Institute of Infectious

476
Diseases laboratories have testing available.

Collaborative management
Care priorities

1. Supportive care
Maintain fluid and electrolyte balances, and treat hypotension with
early use of vasopressors if fluid therapy is not effective,
mechanical ventilation, renal dialysis, and anticonvulsive therapy.
Administration of clotting factor concentrates, platelets, fresh-
frozen plasma, and heparin in patients with DIC.

2. Antivirals
These agents are not effective against these diseases.

3. Ribavirin
Institute a 10-day course if Lassa fever or New World arenavirus is
confirmed.

4. Control risk for bleeding

Intramuscular injections, aspirin, nonsteroidal antiinflammatory
drugs, steroids, and anticoagulant therapies are contraindicated.

5. Vaccine
A vaccine is available for yellow fever, which is only recommended
for travelers going to South America or Africa where yellow fever is
endemic and for laboratory personnel who are exposed to yellow
fever samples. The vaccine is not helpful postexposure because the
short incubation period does not allow immunity to develop if the
vaccine is administered following exposure.

Plague
Pathophysiology
Plague is an infectious disease caused by the bacterium Yersinia

477
pestis that is found in rodents and their fleas. Several forms of
plague can occur individually or in combination: bubonic,
pneumonic, and septicemic plague. Bubonic plague is the most
common, occurring when an infected flea bites a human or when
infectious materials enter through a break in the skin. Pneumonic
plague occurs when Y. pestis infects the lungs through direct or
close contact with a person who has pneumonic plague or in
untreated patients with bubonic or septicemic plague, allowing
bacterial spread to the lungs. Septicemic plague can occur as a
complication of either of the previous types of plague or alone. The
bacteria enter the bloodstream and multiply, prompting the
systemic effects of sepsis.
The Y. pestis bacteria travel to lymph nodes, where they resist
defense mechanisms and rapidly multiply, causing destruction of
lymph nodes. Bacteria enter the bloodstream and prompt sepsis,
septic shock, DIC, and coma. Without treatment, mortality
approaches 100%; with treatment, the mortality can be as low as
5%.

Transmission
Pneumonic plague is spread through direct contact with an infected
person. Neither bubonic nor septicemic plagues are transmitted by
person-to-person contact.

• Pneumonic plague: Droplet precautions until the patient receives

antibiotics for 72 hours.

• Bubonic or septicemic plague: Standard precautions.

Assessment
• Pneumonic plague: Fever, headache, weakness, and rapidly
developing pneumonia with shortness of breath, chest pain,
cough, and sometimes bloody or watery sputum. The pneumonia
progresses and in 2 to 4 days can cause respiratory failure and
shock. Without treatment, patients with pneumonic plague will
die.

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• Bubonic plague: Swollen, tender lymph glands (called buboes),
fever, headache, chills, and weakness.

• Septicemic plague: Fever and chills, abdominal pain, and shock

with bleeding (caused by DIC).

Diagnostic tests
• Gram stain of sputum or blood: Reveals gram-negative bacilli. A
laboratory may misidentify the bacteria unless notified that Y.
pestis is suspected.

Collaborative management
Care priorities

1. Antibiotics
Given within the first 24 hours of symptoms. Streptomycin,
gentamicin, tetracyclines, and chloramphenicol are all effective in
treating pneumonic plague. The preferred choice in adults is
streptomycin 1 g intramuscularly (IM) twice a day for 10 days or
gentamicin 5 mg/kg either IM or IV once a day or 2 mg/kg loading
dose followed by 1.7 mg/kg administered IM or IV three times a
day for 10 days. In children, the drug of choice is streptomycin 15
mg/kg IM twice a day with maximum dose of 2 g or gentamicin 2.5
mg/kg IM or IV three times a day for 10 days.

2. Vaccine
There currently is no vaccine available in the United States. Work is
currently under way to develop a vaccine.

3. Supportive care
Ventilatory support, pain management, and treatment for shock,
DIC, and multiorgan dysfunction syndrome, as appropriate.

Smallpox (variola)

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Pathophysiology
Smallpox is a serious, contagious, and sometimes fatal infectious
disease. It is a member of the orthopoxvirus family, along with
monkeypox, vaccinia, and cowpox. Although all of these can cause
skin lesions, only smallpox is readily transmitted from person to
person. There are two main clinical forms of smallpox: Variola
major and Variola minor, with several additional strains. Variola
major is the severe and most common form of smallpox, with a
more extensive rash and higher fever. Historically, Variola major
had a 30% mortality rate. Variola minor was less common and
much less severe. Smallpox was eradicated after a successful
worldwide vaccination program. The last case of smallpox in the
United States was in 1949. The last naturally occurring case in the
world was in Somalia in 1977. There is currently questionable
access to the virus since the separation of the Soviet Union, because
Moscow and the United States housed the only two storage
laboratories at that time.
Smallpox virus enters the body through the mucosa in the
oropharyngeal and respiratory tracts. The virus multiplies in the
lymph nodes, the spleen, and the bone marrow. Eventually the
virus, contained in lymphocytes, localizes in small blood vessels of
the dermis and infects adjacent cells, causing the pustules to form.
Smallpox is an excellent agent for bioterrorism because it is easy
to both transport and store, and because it is very stable and
markedly virulent when aerosolized.

Transmission
Smallpox is transmitted via droplet nuclei or aerosols expelled from
the oropharynx of an infected person. Usually direct and fairly
prolonged face-to-face contact was required to spread smallpox
from person to person. Smallpox can be spread through direct
contact with infected bodily fluids or contaminated objects (e.g.,
bedding or clothing). Rarely, the virus spreads through the air in
enclosed settings (e.g., buildings, buses, trains). Humans are the
only natural hosts of variola (there is no recorded transmissions
from animals or insects).
A person with smallpox is sometimes contagious with onset of

480
fever (prodrome phase). Most infected persons become contagious
with the onset of rash. At this stage, the person is usually very sick,
unable to move around in the community. The person remains
contagious until the last smallpox scab falls off.

Assessment
• Clinical case definition: An illness with acute onset of fever ≥101°
F (38.3° C), followed by a rash characterized by firm, deep-seated
vesicles or pustules in the same stage of development without
any other apparent cause. These characteristics help differentiate
the smallpox from chickenpox. Smallpox may be easily missed in
the early stage by health care providers.

• Incubation period: Usually 12 to 14 days but can range from 7 to

17 days. During this time, the patient feels fine and is not
contagious.

• Prodromal period: Begins with a high fever (101° F to 104° F),

malaise, headache, and backache. The patient may exhibit severe
abdominal pains, vomiting, and delirium. This period lasts for 2
to 4 days before a rash develops. The rash begins with small red
spots on the tongue and mouth. During this phase, the person is
most contagious.

• Rash development: Progresses in the mouth and develops on the

skin, starting on the face and moving to the arms and legs and
then to the feet and hands. It usually spreads to all parts within
24 hours. When the rash appears, the patient’s fever subsides and
the patient starts to feel better. On day 3, the rash consists of
raised bumps. On day 4, the bumps fill with thick, cloudy fluid
with a possible indent in the center. Indentation is the classic sign
of smallpox rash. The bumps become pustules and eventually
scab over. During the pustule stage, the patient is again febrile.
After 2 weeks, most of the sores have scabs, which begin to fall
off, leaving marks that will become pitted scars on the skin.

Diagnostic tests

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Laboratory diagnostic testing for variola should be done by a CDC
Laboratory Response Network (LRN) laboratory using LRN-
approved polymerase chain reaction (PCR) tests and protocols for
variola virus. Laboratory testing should be reserved for cases that
meet the clinical case definition, thus classified as being a potential
high risk for smallpox.

Initial confirmation of a smallpox outbreak requires

additional testing at the Centers for Disease Control and
Prevention.

Laboratory criteria for confirmation of smallpox

• PCR identification of variola DNA in a clinical specimen.

• Isolation of smallpox (variola) virus from a clinical specimen

(WHO Smallpox Reference Laboratory or laboratory with
appropriate reference capabilities) with variola PCR
confirmation.

Collaborative management
There are no approved treatments for smallpox. Currently,
treatment consists of supportive care. However, cidofovir, an
antiviral, is currently being studied to see if it is effective against the
smallpox virus.

Care priorities

1. Vaccine
A key is to identify smallpox exposure and administer vaccine
within 3 days, to prevent or significantly lessen the severity of the
disease process. Vaccine administered within 4 to 7 days after
exposure may provide some protection and lessen the disease
severity.

482
2. Isolation
Patients presenting with symptoms should be isolated immediately
in a negative-pressure room. The door should be kept closed at all
times. All health care workers entering the room should wear an N-
95 respirator mask. Because smallpox is also transmitted via body
fluids (contaminating the bedding), health care workers should use
contact precautions (i.e., gown, gloves, and shoe covers) when
entering the room. Other infection control practices, such as
limiting patient transport, designating patient care equipment, and
so forth, should follow the institution’s policies. Linen should be
autoclaved and corpses cremated.

3. Supportive management

• Provide hydration: Intravenous fluids to prevent dehydration.

• Provide nutrition: To help strengthen the immune system.

• Initiate mechanical ventilation: If the patient experiences

respiratory failure.

• Hemodynamic monitoring: If management of fluid balance and

blood pressure is difficult.

• Control fever: Antipyretics to reduce body temperature if greater

than 103° F.

• Reduce pain and anxiety: Analgesics and sedatives as indicated.

Care plans: Smallpox

Body image, disturbed 
related to numerous skin lesions resulting from infection with smallpox.
Goals/Outcomes: The patient will acknowledge change in
physical appearance and express a positive self-worth.
Body Image, Self-Esteem.

Body image enhancement

483
1. Use anticipatory guidance to prepare the patient for predictable
changes in body image.

2. Assist the patient to discuss changes caused by illness.

3. Assist the patient to separate physical appearance from feelings

of personal self-worth.

4. Identify the effects of the patient’s culture, religion, race, sex, and
age in terms of body image.

Emotional support

1. Discuss with the patient the emotional experience.

2. Make supportive or empathetic statements.

3. Support the use of appropriate defense mechanisms.

4. Encourage the patient to express feelings of anxiety, anger, or

sadness.

5. Listen to and encourage expressions of feelings and beliefs.

6. Refer for counseling as appropriate.

Tularemia
Pathophysiology
Tularemia is caused by a bacterial zoonosis called Francisella
tularensis. One of the most infectious pathogenic bacteria known, it
is found in infected water, soil, vegetation, small mammals, ticks,
fleas, and mosquitoes. F. tularensis is a small, nonmotile, aerobic,
gram-negative coccobacillus that targets the lymph nodes, lungs,
pleura, spleen, liver, and kidneys. Bacteria enter through skin,
mucous membranes, gastrointestinal tract, and lungs to invade
cells, causing inflammation and permanent damage if untreated.

Transmission

484
Tularemia is transmitted by bites from infected arthropods;
handling infectious animal tissues or fluids; direct contact with or
ingestion of contaminated water, food, or soil; and inhaling infected
aerosols. There is no evidence of person-to-person transmission.
Patients should be placed on standard precautions.

Assessment
• Disease presentation: May vary depending on the infecting
organism, dose, and site of inoculation. It usually starts abruptly
with a fever of 100.1° F to 104° F (38° C to 40° C), headache, chills,
generalized body aches, rhinitis, and a sore throat. Some patients
have a dry cough, substernal pain, skin or mouth ulcers, swollen
painful lymph glands, and swollen and painful eyes.

• Illness progression: Progressive weakness, malaise, anorexia, and

weight loss. If untreated, symptoms may persist for several
weeks to months. Secondary sepsis, pleuropneumonia, and,
rarely, meningitis may develop.

Diagnostic tests
Rapid diagnostic testing for F. tularensis is not widely available. If
tularemia is suspected, specimens of respiratory secretions and
blood should be collected and sent to a designated laboratory for
microscopic identification using fluorescent-labeled antibodies.

Collaborative management
Care priorities

1. Antibiotics
Several types of antibiotics have been effective. Oral tetracyclines
(i.e., doxycycline) or fluoroquinolones (i.e., ciprofloxacin) can be
used. IV streptomycin and gentamicin are effective. Bacterial
cultures and sensitivity data are used to determine the most
appropriate treatment. The patient may be placed on a 10-day

485
course.

Emerging infections
Infectious diseases pose a serious health care threat. Although
medicine has been able to develop strategies to successfully prevent
and treat infections, both familiar and lesser known organisms
continue to present treatment challenges. Emerging infections are
complex, and their evolution has been challenging for health care
personnel to recognize, understand, and treat. Many infections,
such as H1N1, H5N1, hantavirus, and “mad cow” disease, originate
from different species of animals and spread to humans. Other
infectious diseases are acquired from exposure to specific
environments such as health care settings, or are transmitted from
person to person. Regardless of how infections and infectious
diseases are transmitted, prevention and control are challenging.

Infection prevention and infection control

For several decades, infection prevention and control programs
have focused on breaking the chain or cycle of infection. The single
most important way to prevent the spread of infection is through
the use of appropriate hand hygiene. Hand hygiene should be used
before and after all contact with a patient or the patient’s
environment. The WHO identifies “Five Moments of Hand
Hygiene.” These include (1) before touching a patient, (2) before
clean or aseptic procedures, (3) after body fluid exposure or risk, (4)
after touching a patient, and (5) after touching patient
surroundings. The use of hand hygiene is crucial in infection
prevention and control.
Standard precautions are infection prevention practices that are
designed to prevent and control the spread of infections. Standard
precautions include the use of barriers or PPE (e.g., gloves, masks,
and gowns) to interrupt transmission of organisms between
patients and health care providers. Health care personnel should
use and be familiar with the appropriate PPE depending on the risk
of transmission during the activity being performed.
A tiered subset of standard precautions is transmission-based

486
precautions. Universal precautions and other infection prevention
methods are the long-standing strategies used in hospitals
commonly referred to as isolation precautions. The most recent
revision (2007) by the CDC and the Healthcare Infection Control
Practices Advisory Committee reflects evidence-based practices and
the knowledge base of 2007. These techniques and procedures are
transmission-based, interrupting the transmission of infectious
agents and adhere to five basic principles:

1. To provide infection control recommendations for the entire

health care system, including hospitals, long-term care facilities,
ambulatory care, home care, and hospices.

2. To reaffirm standard precautions as the foundation for

preventing transmission of organism during patient care in all
settings.

3. To reaffirm the importance of implementing transmission-based

precautions based on the clinical presentation of the syndrome and
likely pathogens until the infectious etiology is known.

4. To provide epidemiologically sound and, whenever possible,

evidence-based recommendations.

5. To provide a unified infection control approach to multidrug-

resistant organisms (MDROs).

The 2007 guideline contains two tiers of precautions:

1. Standard precautions: Designed for the care of all patients in the

health care setting, regardless of diagnosis or infection status.

2. Transmission-based precautions: Used for patients known to be

infected or colonized with epidemiologically important pathogens
that can be transmitted by airborne or droplet or contact with dry
skin or contaminated surfaces. Isolation techniques that prevent
transmission are the following:

a. Airborne infection isolation: For patients known

487
 or suspected to be infected with microorganisms
transmitted person to person by airborne droplet
nuclei that remain suspended in the air and that
can be dispersed widely by air currents.

b. Droplet: For patients known or suspected to be

infected with microorganisms transmitted by
respiratory droplets (more than 5 µm in size),
generated by the patient coughing, sneezing, or
talking or during performance of cough-inducing
procedures.

c. Contact: For patients with known or suspected

infections or evidence of syndromes that
represent increased risk for contact transmission,
including colonization or infection with MDROs
according to recommendations in the CDC
guidelines (2007).

d. Protective environment: To minimize fungal

spore counts in the air for patients undergoing
allogeneic, hematopoietic stem cell
transplantation. Specific requirements for the
protective environment were defined by the CDC
in 2000.

Humans can be vulnerable, with inadequate natural defenses to

control all possible infections. Our inborn defenses must be
augmented to enhance infection protection. Researchers are hard
pressed to develop vaccines, medications, and treatments.
Regardless of sex, age, socioeconomic status, or ethnic background,

488
infectious disease can strike at any time and may lead to significant
morbidity and mortality.

Multidrug-resistant organisms
MDROs pose a serious health risk to the patient who is
hospitalized. These organisms are resistant to one or more classes of
antimicrobial agents and thus are difficult to successfully manage.
Prolonged treatment leads to increased length of stay, increased
health care costs, and increased morbidity and mortality.
Methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-
resistant Enterococci (VRE) are the most common MDROs. Several
gram-negative bacilli, including Carbapenem-resistant
Enterobacteriaceae (CRE), are developing increased resistance to
treatment. MDROs are spread by person-to-person contact and by
contact with contaminated environmental surfaces. Treatment is
prescribed based on the sensitivity of the causative organism to the
available antimicrobial agents.
Many individuals are colonized with MDROs rather than having
active infections. The organism is present within the body without
signs or symptoms of infection. These patients are carriers. Patients
are placed on contact precautions to prevent the spread of the
MDRO to others. Hand hygiene remains the most important
infection control measure for the prevention of MDROs.

Methicillin-resistant Staphylococcus aureus (MRSA)

MRSA is the most common organism seen in community and
health care settings. MRSA most commonly occurs in skin
infections but can also occur as a bloodstream infection or
pneumonia where it can become life threatening. The CDC reports
that invasive MRSA infections have decreased 54% from 2006 to
2011 but still pose a serious health care risk in patients who are
hospitalized. Vancomycin-intermediate Staphylococcus aureus
(VISA) and vancomycin-resistant Staphylococcus aureus (VRSA) are
also resistant strains of Staphylococcus aureus. These organisms pose
treatment challenges, given their resistance to the commonly
appropriate antimicrobial agents.

489
Vancomycin-resistant Enterococcus (VRE)
VRE developed from the enterococci normally present in the
intestines, female genitalia, and the environment, which most often
cause urinary tract, bloodstream, and surgical wound infections.
Enterococcal infections have often been treated with vancomycin.
After many years of managing these infections with vancomycin,
various strains of enterococci developed resistance to eradication by
vancomycin. Patients most likely to develop VRE infections include
those previously treated with a prolonged regimen of vancomycin
or other antibiotics; patients who are hospitalized and receiving
antibiotics for an extended period of time; patients who are
immunosuppressed, including critically ill, oncology, and patients
who have had a transplant procedure; patients who have
undergone abdominal and chest surgical procedures; those with the
need for prolonged management using a urinary catheter or central
IV catheter; and those already colonized with VRE.

Carbapenem-resistant Enterobacteriaceae (CRE)

CRE is a serious health threat with a high mortality rate. CRE is not
only resistant to the carbapenem class of antibiotics but is also
resistant to most other classes of antimicrobials, thus leaving very
limited treatment options. The most commonly seen
Enterobacteriaceae are E. coli and Klebsiella pneumoniae. Others include
KPC (K. pneumoniae carbapenemase) and NDM (New Delhi
metallo-beta-lactamase). News agencies have shared disturbing
comments from the CDC about new “dangerous bacteria,” also
called “superbug 2013,” and “nightmare bacteria.” The number of
outbreaks of CRE remains small, is confined to hospitals and long-
term care facilities, but has the potential to increase. When infected,
the death rate is 50%, despite aggressive antibiotic treatment and
supportive measures. With few drug companies developing new
antibiotics, survival advantage may be in favor of the resistant
organisms, rather than those who acquired the infection.

Ebola virus disease

Ebola virus disease (EVD) or Ebola hemorrhagic fever is a rare and
most often fatal disease caused by a virus from the family

490
Filoviridae, genus Ebolavirus. There are five Ebolavirus species but
only four are known to cause disease in humans, Zaire ebolavirus,
Sudan ebolavirus, Tai Forest ebolavirus, and Bundibugyo ebolavirus.
EVD was first identified in 1976 near the Ebola River in the
Democratic Republic of the Congo. Since first identified, there have
been sporadic outbreaks in Africa.
The 2014 Ebola outbreak is the largest in world history. The first
cases reported occurred in Guinea in March of 2014 and is the first
outbreak in West Africa. The 2014 West Africa outbreak has
affected several countries with the majority of the cases occurring in
Sierra Leone, Liberia, Guinea, and more recently, Mali. As of March
2015, there have been over 25,000 cases reported with over 10,000
confirmed deaths.
The natural reservoir remains unknown; however, researchers
believe the virus is animal-borne with bats being the most likely
reservoir. Ebola is also considered an agent of bioterrorism. Of the
five subtypes listed earlier, four occur in an animal host that is
native to Africa.

Transmission
Ebola is spread through direct contact to mucous membranes or
broken skin with blood and body fluids, including but not limited
to blood, sweat, vomit, feces, saliva, breast milk, and semen. It is
not spread through the air or by water.
Screening tools should be used in all health care settings to
establish risk factors for EVD. These include recent travel to areas
that have active EVD and a fever of greater than 38.6° C or 101.5° F.
Additional symptoms are severe headache, muscle pain, vomiting,
diarrhea, unexplained hemorrhage, or abdominal pain. Health care
providers should also include malaria as a working diagnosis
because it is also the most common febrile illness in people who
have recently travelled to the affected countries.

Case definitions
Early recognition and detection is crucial, and health care providers
need to be alert and evaluate any patients suspected with EVD. The
following categories have been defined by the CDC.

491
 Person Under Investigation (PUI): A person who has both risk
factors and symptoms as follows:

• Clinical criteria: Fever greater than 38.6° C or 101.5° F with severe

headache, muscle pain, vomiting, diarrhea, abdominal pain, or
unexplained hemorrhage;

AND

• Risk factors within the past 21 days: Contact with blood/body

fluids or human remains of a person with known or suspected
EVD, residence in or travel to and area where there is active EVD,
or direct handling of bats or nonhuman primates in areas with
active EVD.

Probable Case: A PUI with risk factors of low-risk or high-risk

exposure.
Low-risk exposure includes:

• Household contact with a person who has EVD.

• Close contact with a person who has EVD, such as being within 3
feet of a patient with EVD, in the room or in the care area of the
person who is ill for a prolonged period of time.

• Direct contact without PPE.

High-risk exposure includes:

• Percutaneous or mucous membrane exposure to blood or body

fluids of a patient with EVD.

• Direct unprotected skin contact with blood or body fluids of a

patient with EVD.

• Direct contact with a dead body in a country with an EVD

outbreak with PPE.

Confirmed Case: A person with a confirmed laboratory test for

EVD.

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 No Known Exposure: A person who has been in a country where
there is an EVD outbreak in the past 21 days but does not report a
high-risk or low-risk exposure.

Signs and symptoms

Symptoms of EVD usually appear from 2 to 21 days after an
exposure and averages from 8 to 10 days. Symptoms include: fever
greater than 38.6° C or 101.5° F, severe headache, muscle pain,
weakness, diarrhea, vomiting, abdominal pain, and unexplained
hemorrhage, which includes bleeding or bruising.

Prevention and infection control

All health care workers who enter rooms with patients who are PUI
(probable, or known) should wear PPE including masks, gloves,
gowns, and eye protection. Shoe covers and leg covers should be
used as needed. It has been recognized that a large number of
secondary infections from Ebola Virus Disease during the 2014
outbreak occurred in health care workers exposed during care of
infected patients. Leading U.S centers addressing serious
contagious diseases have used full-body Tyvek suits and powered
air purifying respirator (PAPR) hoods as part of the contact and
droplet precautions protocol when caring for patients with
confirmed EVD. Patients should be isolated in private rooms with
private bathrooms if possible or cohort patients with EVD in the
same ward. Health care workers who handle dead bodies should
also wear appropriate PPE.
Restrict visitors with the exception of individuals who may be
essential to the well-being of the patient. This should be determined
on a case-by-case basis. A logbook should be kept to document all
persons entering the patient’s room, including health care
personnel.As of March, 2015, U.S centers managing patients with a
confirmed diagnosis of EVD have not allowed visitors, outside of
essential health care providers, into the room.
Aerosol-generating procedures should be avoided. If the patient’s
condition warrants these procedures, PPE including respiratory
protection such as N-95 respirators or a higher level of respiratory
protection should be used along with a negative-pressure

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environment or airborne isolation room. Powered air purifying
respirator (PAPR) hoods have been used to provide additional
protection with enhanced comfort.
Diligent environmental cleaning and disinfection measures
should be used along with safe handling of potentially
contaminated materials. Use of Environmental Protection Agency-
registered hospital disinfectants with a label claim for
nonenveloped viruses should be used to disinfect environmental
surfaces in the patient’s room with suspected or confirmed EVD.
Patients with EVD should not be placed in rooms with carpet,
upholstered furniture, or curtains. Mattresses or pillows should
have a nonporous covering that fluids cannot penetrate. Any cloth
products or textiles should not be laundered. These items should be
disposed of into the waste stream. Any disposable single-use items
should be placed in leak-proof containment. Any plastic waste bags
should be placed in a rigid waste receptacle. U.S. centers have used
more extensive environmental protection measures including
autoclaving trash prior to placing it in rigid waste receptacles,
treating toilet water with disinfectants when waste is deposited,
and extensive terminal cleaning measures, based on lessons learned
from care providers managing the EVD outbreak in West Africa.

Diagnosis
Diagnosis is made by recent travel to areas where EVD is endemic
and by symptoms. This can be difficult in the early stages but
health care providers can follow the case definitions previously
listed.
Laboratory tests include:
Timeline of Infection Diagnostic Tests Available
Within a few days after Antigen-capture enzyme-linked immunosorbent assay
symptoms begin (ELISA) testing
• Immunoglobulin M (IgM) ELISA
• Polymerase chain reaction (PCR)
• Virus isolation
Later in disease course or after • IgM and IgG antibodies
recovery
Retrospectively in deceased • Immunohistochemistry testing
patients • PCR
• Virus isolation

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Treatment
Treatment is dependent on symptoms and patients are provided
supportive care. Early treatment and interventions increase the
chance of survival. Managing fluid and electrolytes by providing IV
fluids, maintaining oxygen levels and blood pressure are all
essential to survival. Patients may produce 10 liters of diarrhea
daily.
There are currently no U.S. Food and Drug Administration
(FDA)-approved vaccines or medications available for EVD. There
have been some experimental vaccines and treatments but they
have not been fully tested for effectiveness and safety.
Recovery depends on good supportive care and the patient’s
immune response. Patients who recover develop antibodies that
last for at least 10 years. At present, it is not known if they are
immune for life or can become infected with different species of
EVD. Long-term complications have occurred in patients who have
recovered from EVD, such as joint and vision problems.

Severe acute respiratory syndrome

Severe acute respiratory syndrome (SARS) is a febrile lower
respiratory tract infection that mimics many other respiratory
illnesses. To date, there are no specific clinical or laboratory
findings that distinguish with certainty SARS-associated
coronavirus (CoV) disease from other respiratory illnesses rapidly
enough to facilitate management decisions that must be made soon
after the patient presents to the health care system. Therefore, early
recognition of this disease still relies on a combination of clinical
and epidemiologic features.
The virus may have originated from animals and spread to
humans. SARS first emerged in the Guangdong Province in China
during November 2002 through June 2003, where approximately
15,000 probable cases were identified. A worldwide epidemic
occurred when a SARS-infected physician contaminated several
guests at a hotel in Hong Kong.
A novel CoV has been identified as the cause of SARS and is now
labeled SARS-CoV. Research in China has detected several CoVs
closely related to SARS-CoV in two animal species (masked palm

495
civet cat and raccoon dog). Both are considered delicacies in China
and are consumed by humans. One theory states that this CoV had
mutated and was transmitted to humans through handling of these
animals or contact with their saliva and feces.

Pathophysiology
SARS begins much like the common flu, progressing to pneumonia,
and potentially to acute respiratory distress syndrome (ARDS) and
death. Lymphopenia, thrombocytopenia, and leucopenia are noted.
SARS-CoV may infect blood cells and/or induce autoantibodies to
damage these cells, leading to immunologic dysregulation in
response to SARS-CoV.

Transmission
The most common mode of transmission for SARS is close person-
to-person contact: kissing, sharing eating or drinking utensils, close
conversation (less than 3 feet), physical examination, and any other
direct physical contact. Respiratory droplets are expelled by the
infected person by a cough or sneeze into the air. Droplets then
reach the mucosal membrane of the nose, mouth, or eyes of a
nearby person, infecting him or her.
Surfaces contaminated with SARS droplets may serve as a
reservoir for the virus. SARS droplets can remain viable up to
several days depending on the type of surface.

Assessment
Goal of assessment
Evaluate for early clinical and epidemiologic features of SARS.

History and risk factors

Evaluation of SARS-CoV among persons presenting with

community-acquired illness
The CDC recommends the following approach for the evaluation of

496
SARS-CoV disease among persons presenting with community-
acquired illness. The suspicion of SARS-CoV disease is raised if,
within 10 days of symptom onset, the patient:

• Has a history of recent travel to mainland China, Hong Kong, or

Taiwan or close contact with ill persons with a history of recent
travel to such areas,

OR

• Is employed in an occupation at particular risk for SARS-CoV

exposure, including a health care worker with direct patient
contact or a worker in a laboratory that contains live SARS-CoV,

OR

• Is part of a cluster of cases of atypical pneumonia without an

alternative diagnosis.

• In addition, all patients with fever or lower respiratory symptoms

(e.g., cough, shortness of breath, difficulty breathing) should be
questioned about whether within 10 days of symptom onset they
have had:

• Close contact with someone suspected of having

SARS-CoV disease,

OR

• A history of foreign travel (or close contact with an

ill person with a history of travel) to a location with
documented or suspected SARS-CoV,

OR

• Exposure to a domestic location with documented

or suspected SARS-CoV (including a laboratory that

497
 contains live SARS-CoV) or close contact with an ill
person with such an exposure history.

Signs and symptoms

The initial presentation of SARS is similar to that of other lower
respiratory tract infections. No specific clinical or laboratory
findings are available to rapidly distinguish SARS from any other
respiratory illness. Early recognition of SARS requires assessment
of clinical and epidemiologic features. The incubation period is 2 to
10 days. Early clinical manifestations include fever, myalgia,
headache, and rhinorrhea. Fever is a key component. On the second
day of the fever, a dry, nonproductive cough may develop,
progressing to shortness of breath, hypoxemia, and ARDS. The
CDC has delineated three different levels of how patients may
clinically present with SARS:

Early illness

• Presence of two or more of the following: fever, chills, rigors,

myalgia, headache, diarrhea, sore throat, rhinorrhea.

Mild-to-moderate respiratory illness

• Temperature of greater than 100.4° F (38° C), and

• One or more of the clinical findings of lower respiratory illness

(e.g., cough, shortness of breath, difficulty breathing).

Severe respiratory illness

• Meets clinical criteria for mild-to-moderate respiratory illness

including one or more of the following:

• Chest radiograph illustrating pneumonia,

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• ARDS (see Acute Lung Injury and Acute
Respiratory Distress Syndrome, Chapter 4), or

• Autopsy findings of pneumonia or ARDS without

an identifiable cause.

Screening labwork
Laboratory studies such as bacterial cultures and respiratory viral
panels can be used to rule out other potential causes of respiratory
tract infection. SARS-CoV reverse transcription (RT)-PCR and
enzyme immunoassay (EIA) tests are not typically ordered until
after a high index of suspicion by the physician and notification of
public health officials.

Diagnostic Tests for Severe Acute Respiratory Syndrome

Coronavirus (SARS-CoV)

499
Collaborative management

500
Care priorities for SARS-CoV
(see Care Priorities for MERS-CoV)

Middle eastern respiratory syndrome

coronavirus (MERS-CoV)
Middle Eastern respiratory syndrome (MERS-CoV) is a viral
respiratory illness caused by a coronavirus. It was first reported in
Saudi Arabia in September 2012. Camels have been found to be the
primary source of the virus. As of April 2014, there have been 536
laboratory-confirmed cases of MERS-CoV reported primarily in the
Middle East; however, with international travel MERS-CoV has
been seen in Europe, Asia, and the United States. All documented
cases have had recent travel to the Middle East or are in close
contact with individuals who are ill. Close contact is identified as
those individuals who live or care for the ill, and there has been no
evidence to support widespread spreading of MERS-CoV in the
community setting.

Pathophysiology
The clinical signs and symptoms of MERS-CoV include fever,
cough, dyspnea, chills, rigor, headache, myalgia, and malaise.
Other reported symptoms included nausea, vomiting, diarrhea,
abdominal pain, and sore throat. Patients present with acute
respiratory illness and can rapidly progress to pneumonitis,
respiratory failure, septic shock, and multiorgan failure, which may
result in death.
The incubation period ranges from 2 to 13 days with a median
incubation period of 5 days. Most patients present to the hospital on
day 4. The median time of onset of illness to death in the patient
who is critically ill is 12 days.

Transmission
MERS-CoV can spread from a person who is ill to others through
close contact. Close contact means individuals who care for the
individual who is ill or those living with the person who is infected.

501
There has been transmission to health care providers by patients
who are infected. There have been no reported community
outbreaks at this time, although this is being closely monitored. All
cases that have been reported have been linked to countries in or
near the Arabian Peninsula, and most people who have become ill
have lived or recently traveled to the area.

Assessment
Goal of assessment
Evaluate for early clinical and epidemiologic features of MERS-
CoV.

History and risk factors

Health care providers should consider MERS-CoV for any patient
who has traveled to the Arabian Peninsula in the past 14 days and
developed symptoms of acute respiratory illness such as fever,
cough, or shortness of breath. Others at risk include individuals
who have had close contact with anyone who has traveled to the
Arabian Peninsula, anyone who has had close contact with
someone with suspected or confirmed MERS-CoV, and any health
care worker exposed to MERS-CoV and has not used the
appropriate infection control measures. Individuals with other
comorbidities appear to be at a higher risk as well as individuals
who are immunosuppressed.

Signs and symptoms

Most individuals come to the health care setting with symptoms of
a severe acute respiratory illness. These symptoms include a fever,
cough, and shortness of breath. There have also been reports of
gastrointestinal symptoms that include nausea, vomiting, and
diarrhea. MERS-CoV rapidly progresses to pneumonitis, severe
respiratory distress syndrome, sepsis, and multisystem organ
failure.

Diagnostic Tests for Middle Eastern Respiratory Syndrome

Coronavirus (MERS-CoV)

502
Care priorities for MERS-CoV and SARS-CoV

1. Treating the patient with supportive measures

As outlined earlier, this is recommended. There are no vaccines or
specific management for MERS-CoV or SARS-CoV.

2. Infection control
Patients are to be placed in a negative-pressure room under
airborne, contact, and standard precautions. Anyone who enters the
patient’s room must wear gowns, gloves, an N-95 respirator, and
eye protection. Hand hygiene should be performed after contact
with a patient on precaution. If there is a lack of negative-pressure
rooms and/or there is a need to concentrate infection control efforts
and resources, patients may be cohorted on a floor or nursing unit
designated for the care of patients with MERS only if air-handling
systems can be modified to allow these areas to operate under
negative pressure relative to surrounding areas.

• Designate “clean” and “dirty” areas for isolation materials.

503
 Maintain a stock of clean patient care and PPE supplies outside
the patient’s room. Decide where contaminated linen and waste
will be placed. Locate receptacles close to the point of use and
separate from clean supplies.

• Limit the amount of patient-care equipment brought into the

room to that which is medically necessary. Provide each patient
with patient-dedicated equipment (e.g., blood pressure cuff,
thermometer).

• Limit patient movement and transport out of the negative-

pressure room. Whenever possible, use portable equipment to
perform radiographs and other procedures in the patient room.
Limit visits to patients to persons who are necessary for the
patient’s emotional well-being and care.

• Health care workers who perform aerosol-generating procedures

should be alert to the fact that there may be an increased risk of
SARS-CoV and MERS-CoV transmission when these procedures
are performed. PPE should fit properly and protect all skin
surfaces and clothing. A fluid-repellant gown or full-body suit,
eye protection, N-95 respirator, and gloves that fit snuggly over
the gown cuff should be worn. After an aerosol-generating
procedure (e.g., intubation, bronchoscopy), clean and disinfect
horizontal surfaces around the patient as soon as possible.

Additional nursing diagnoses for MERS-CoV

and SARS-CoV
See nursing diagnoses for Acute Lung Injury and Acute Respiratory
Distress Syndrome (Chapter 4), Acute Pneumonia (Chapter 4),
Acute Respiratory Failure (Chapter 4), Mechanical Ventilation
(Chapter 1), Fluid and Electrolyte Disturbances (Chapter 1), and
Emotional and Spiritual Support of the Patient and Significant
Others (Chapter 2).

Creutzfeldt-Jakob disease

504
Pathophysiology
Creutzfeldt-Jakob disease (CJD) is a rare, fatal, neurodegenerative
disorder, believed to be caused by an abnormal isoform of a
glycoprotein known as a prion, a proteinaceous infectious particle.
The most common disorder is bovine spongiform encephalopathy,
or “mad cow” disease. A new form of CJD has emerged, called new
variant CJD (vCJD or nvCJD). This form of CJD is linked to
consumption of cattle with “mad cow” disease. Clinical and
epidemiologic evidence supporting this link between “mad cow”
disease and vCJD has become stronger. vCJD generally affects
younger people with a mean age of 29 years, whereas CJD occurs in
those aged 65 to 69 years.
CJD is classified as a transmissible spongiform encephalopathy.
Prion disease occurs in animals, particularly cattle, sheep, and goats.
CJD is endemic around the world and its estimated incidence report
is 1 case per 1 million population. Three forms of “classic” CJD
have been identified. Sporadic CJD affects older adults with rapid-
onset dementia and neurologic symptoms of unknown cause.
Familial CJD is an inherited disease and generally strikes younger
individuals. It has a longer course in comparison to sporadic CJD.
Iatrogenic CJD occurs through contact with infected tissue via
medical procedures or treatments.
Prion proteins are normal proteins in the body and brain. In CJD,
these proteins become abnormally shaped, as a result either of
genetics or of contamination from an outside source. This leads to
surrounding normal prion proteins taking on the abnormal shape.
Central nervous system (CNS) function is disrupted, leading to
cognitive impairment and cerebellar dysfunction. As the process
continues, the abnormal prions accumulate in the brain, causing
neuronal dysfunction, neuron death, gliosis (proliferation of
neuroglial tissue in the CNS), and ultimately death.

Transmission
CJD can spread via infectious or hereditary means. Prion infections
are transmitted via the peripheral route, either orally or
transcutaneously. They may be introduced to lymphatic organs,
particularly the spleen and lymph nodes, where initial replication

505
of the infected prions occurs. Infections can either enter the
circulatory system and be hematogenously spread to the brain, or
infected prions may travel via the vagus nerve to the brain. Genetic
mutation of the human prion gene PrP on chromosome 20 leads to
the dysfunction of the prion protein. More than 20 reported
mutations of this chromosome have been reported. All mutations
influence the onset and duration of CJD. vCJD is theorized to be
caused by the consumption of meat from cattle that is infected.
Once ingested, the infected prions follow the same neuroinvasion
route of CJD.

Assessment: Creutzfeldt-Jakob disease

Goal of assessment
Evaluate for clinical signs of CJD.

Risk factors and history

• Family history of CJD.

• Exposure to contaminated tissue. People who have received

human growth hormone derived from human pituitary glands or
who have had dura mater grafts.

Sporadic CJD

• Reported as having “come out of the blue.”

• Early symptoms are memory loss, loss of interest, and mood

changes that progress quickly (within a few weeks) to confusion
and memory problems. Complaints of clumsiness, with jerky and
stiff limbs, are also seen.

• Median age at death is 68 years in patients who are initially seen

with dementia and neurologic deterioration.

• Course of illness is often 4 months.

• Blurred eyesight and incontinence follow.

506
• At end stage, patients are unable to move or speak and need 24-
hour care.

• Death occurs approximately 6 months after the onset of the

disease.

Familial CJD

• Symptoms vary between different people, depending in part on

the type of gene mutation responsible.

• In some cases, the illness is similar to sporadic CJD in type,

duration, and progression, whereas in others, it is a more slowly
developing dementia that progresses over a few years.

vCJD

• The incubation period is unknown and may take up to several

years before manifesting.

• vCJD affects younger people, with a mean age of 29 years.

• Initial symptoms are more psychiatric than neurologic.

• Patients are anxious and depressed and display withdrawal or

other behavioral changes.

• Persistent pain and odd sensations in the face and extremities are
common. As disease progresses, the patient develops ataxia,
sudden erratic movements, and progressive dementia with
marked memory loss.

• Ultimately, the patient will lose the ability to move or speak and
will require 24-hour care. Death soon follows.

Diagnostic tests
CJD is diagnosed based on typical signs, symptoms, and
progression of disease.

507
Diagnostic Tests for Creutzfeldt-Jakob Disease (CJD)

Collaborative management
There is no known treatment or cure for CJD. Management of these
patients is supportive and palliative in nature. There is no vaccine
for CJD.

Care priorities

1. Supportive care
Ventilatory support, pain management, patient safety, intensive
skin care, assessment, nutrition support, care for immobility, and
treatment for secondary infections.

2. Infection control
Standard precautions are used to care for patients with CJD. If a
brain biopsy or other procedure is performed on a patient with CJD
or suspected CJD, inform the central sterile department so that
stringent chemical and autoclave sterilization methods can be used
to reprocess instruments.

Additional nursing diagnoses

See nursing diagnoses and interventions in Nutrition Support,

508
Mechanical Ventilation, Alterations in Consciousness, Wound and
Skin Care, Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support for the Patient and Significant Others, and Ethical
Considerations in Critical Care (Chapter 2).

West nile virus

Pathophysiology
West Nile virus (WNV) is a single-stranded positive RNA virus
from the Japanese encephalitis virus serogroup of the genus
Flavivirus, family Flaviviridae, which is known for Japanese
encephalitis and St. Louis encephalitis. In rare cases, WNV may
lead to encephalitis or meningitis and death. WNV has an
incubation period of 2 to 14 days. It can also be divided into two
lineages. Lineage I strains are more widely distributed and linked
to human infections.

Transmission
WNV is a disease that has spread worldwide. Initially, WNV was a
disease that only occurred in bird species. Approximately 146
different species of birds have been reported to acquire this disease.
This disease is spread among the bird population by 29 different
species of mosquitoes (vectors). The natural cycle is from bird 1 to
mosquito 1 to bird 2 to mosquito 2, and so forth. Because of a
complex intensification of this natural cycle, bridge vectors
(mosquitoes that bite both birds and humans) became infected with
the WNV and spread the disease to humans. Only birds and
humans in the United States and Israel have been known to die
from WNV.

Assessment: West nile virus

Goal of assessment
Evaluate for signs and symptoms of WNV.

History and risk factors

509
Exposure to mosquitoes where WNV exists increases risk. WNV is
common in areas such as Africa, West Asia, and the Middle East. It
first appeared in the United States in the summer of 1999 and since
then has been found in all 48 contiguous states. Older age is
associated with a higher risk for developing more serious CNS
disease.

Incubation period
• Generally 2 to 14 days, although longer incubation periods have
been documented in persons who are immunosuppressed.

Mild infection/west nile fever

• Symptoms last 3 to 6 days.

• Sudden onset of a fever with malaise, anorexia, nausea, vomiting,

eye pain, headache, myalgia, rash, and lymphadenopathy.

Severe infection/WNV meningitis, WNV encephalitis,

and WNV poliomyelitis
• When the CNS is affected, clinical syndromes ranging from
febrile headache to aseptic meningitis to encephalitis may occur,
and these are usually indistinguishable from similar syndromes
caused by other viruses.

• WNV encephalitis or meningoencephalitis is characterized by

altered mental status or focal neurologic findings.

• WNV meningitis involves fever, headache, and nuchal rigidity

(stiff neck). Pleocytosis (abnormal increase in white blood cell
[WBC] count in cerebrospinal fluid [CSF]) is present. Changes in
consciousness are not usually seen and are mild when present.

• WNV encephalitis also involves fever and headache and more

global symptoms. There is typically an alteration of
consciousness, which may be mild and result in lethargy but may
progress to confusion or coma. Focal neurologic deficits,

510
 including limb paralysis and cranial nerve palsies, may be
observed. Tremor and movement disorders have also been
identified.

• WNV poliomyelitis is characterized by the acute onset of

asymmetric limb weakness or paralysis in the absence of sensory
loss. Pain sometimes precedes the paralysis. The paralysis can
occur in the absence of fever, headache, or other common
symptoms associated with WNV infections. Involvement of the
respiratory muscles, leading to acute respiratory failure, can
occur.

Clinical features

• Fever

• Gastrointestinal (GI) disturbances

• Change in mental status

• Development of a maculopapular or morbilliform rash

(infrequent) involving the neck, trunk, arms, or legs

• Seizures

• Myelitis

• Polyradiculitis

• Optic neuritis

• Cranial nerve abnormalities

• Severe weakness

• Flaccid paralysis sometimes

• Ataxia/extrapyramidal signs

• Myocarditis, pancreatitis, and fulminant hepatitis have been

noted in outbreaks before 1990.

511
Labwork
Certain findings are seen in patients with severe disease.

• Total leukocyte count is mostly normal but can be elevated with

lymphocytopenia and anemia.

• Hyponatremia is sometimes present, particularly among patients

with encephalitis.

• CSF examination shows pleocytosis, usually with a predominance

of lymphocytes. Protein is universally elevated. Glucose is
normal.

Diagnostic Tests for West Nile Virus (WNV)

Testing for WNV can be obtained through local or state health

departments. WNV is on the list of designated nationally notifiable
arboviral encephalitides, and the proper authorities should be
informed. Check your local or state health department for guidance.

Collaborative management
Treatment of WNV infection is supportive. High-dose ribavirin and
interferon alfa-2b have some activity against WNV in vitro. There is
no specific antibiotic or antidote for the viral infection. Also, there is
no vaccine.

Care priorities

512
Supportive care
Includes IV fluids to prevent dehydration, antipyretics for fever
management, oxygen therapy and ventilatory support, patient
safety, nutrition support, and treatment for secondary infections.
Standard precautions should be taken at all times; follow
organization’s policy for appropriate personal protection category.

Additional nursing diagnoses

See nursing diagnoses and interventions in Nutrition Support
(Chapter 1), Mechanical Ventilation (Chapter 1), Altered Mental
Status/Alterations in Consciousness (Chapter 1), Wound and Skin
Care (Chapter 1), Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support for the Patient and Significant Others (Chapter 2),
and Ethical Considerations in Critical Care (Chapter 2).

Pandemic flu
An epidemic occurs when there are an unusually high number of
people affected by a disease. A pandemic is an international
epidemic. An influenza pandemic may occur when a new influenza
virus is detected and the human population has no immunity. With
the increase in global travel and transportation, and urban
development with areas of overcrowding, epidemics that result
from a new influenza virus are likely to be disseminated around the
world and rapidly become a pandemic. The WHO has defined the
phases of a pandemic to create a global framework to aid countries
in pandemic preparedness and response planning. Pandemics can
be either mild or severe in the illness and death they cause. The
severity of a pandemic can change during the time the illness
continues to spread.
The WHO has developed a global influenza preparedness plan
that outlines the responsibilities of WHO and national authorities in
the event of an influenza pandemic. The WHO also offers guidance
tools and training to assist in the development of national pandemic
preparedness plans (www.who.int/csr/disease/influenza/A58_13-
en.pdf).

513
Avian influenza (“bird flu”)
Pathophysiology
Avian influenza is an infection caused by avian (bird) flu viruses,
type A strains. These viruses occur naturally among birds. Wild
birds carry the viruses in their intestines but usually do not get sick
from them. However, domesticated birds such as poultry can
become very ill and die from avian influenza viruses.
It is theorized that certain subgroups of avian influenza mutated,
crossed species, and infected humans. The subgroups of avian
influenza linked to human infections include but are not limited to
H5N1, H7N7, H9N2, H7N3, and H7N9. The H5N1 subgroup is of
particular concern to humans because of its ability to mutate and its
tendency to acquire genes from viruses from other animal species.
It has demonstrated high pathogenicity and causes severe disease
in humans. The H7N9 is a new subgroup first reported in March
2013, characterized by rapid development of serious pneumonia,
which leads to sepsis, ARDS, and multisystem organ failure.

Transmission
Avian influenza is most commonly spread from infected birds to
humans. The virus is harbored in birds (in the intestine), which
shed the virus through their saliva, nasal secretions, and feces. The
most common means of transmission among birds is fecal to oral.
Humans who come in direct contact with infected poultry are
susceptible to infection. Avian influenza survives on inanimate
objects. Items contaminated with secretions/excretions of infected
birds can be a vector for transmission to humans. The spread of
avian influenza from one person who is ill to another has been
reported very rarely, and transmission has not been observed to
continue beyond one person.

Assessment
History and risk factors

514
• Direct or close contact with infected poultry or contaminated
surfaces. In outbreaks, most cases have occurred in previously
healthy children and young adults.

• A Health Safety Alert will be sent out by the CDC to all hospitals
if there are avian influenza outbreaks that lead this federal
organization to recommend heightened surveillance and
diagnostic testing of targeted patients. In this situation, the CDC
will outline triage guidelines, which will likely include travel to
the outbreak location within the past 10 days and hospitalization
with a severe respiratory illness.

Signs and symptoms

• Similar to the “common flu”: fever, cough, sore throat, muscle
aches, and eye infections.

• In more severe cases of avian influenza, when assessed, the

patient may display signs and symptoms of viral pneumonia (see
Acute Pneumonia, p. 373) and ARDS (see Acute Lung Injury and
Acute Respiratory Distress Syndrome, p. 365).

• These symptoms can be accompanied by nausea, diarrhea,

vomiting, and neurologic changes.

Diagnostic tests
Diagnostic Tests for Avian Influenza

Abnormal
Test Purpose
Findings
Laboratory Studies
Complete blood count Assess for changes Elevated white
suggestive of other blood cell count
bacterial infections.
Influenza A/H5 (Asian lineage) virus real-time To identify causative Positive
reverse transcription–polymerase chain reaction agent.
(RT-PCR) assay:
Must consult with and have authorization from
local or state health departments. Test is
conducted only in designated laboratories.
Rapid bedside tests: Conduct for rapid Positive.

515
 Available but results are not confirmatory. screening for virus. Confirmatory
tests should
be
performed.
Viral culture: Identify causative agent. Positive for
Must be conducted in biosafety Level 3 laboratory. pathogen
Radiology
Chest radiograph Identify progression of Infiltrates,
lung disease and atelectasis
anatomic involvement.
Respiratory Tests
Arterial blood gas (if patient is in respiratory Determination of Acidosis,
distress) oxygen saturation and alkalosis
blood gases.
Pulse oximetry Measure oxygen <90%
saturation.

Collaborative management
At present, the primary medication therapy option is oseltamivir
(Tamiflu) and zanamivir (Relenza); however, there is concern that
viruses may become resistant to both of these drugs. Treatment is
supportive in accordance to the clinical status of the patient.

Care priorities

1. Supportive management
Includes IV fluids to prevent dehydration, antipyretics for fever
management, oxygen therapy and ventilatory support, patient
safety, nutrition support, and treatment for secondary infections.

2. Infection control
Place patients in a negative-pressure room under airborne, contact,
and standard precautions. An N-95 respirator should be worn by
everyone who enters the room. Gowns and gloves are to be worn
for all patient contact, and eye protection should be worn when
within 3 feet of the patient. Good hand hygiene should be practiced.
Precautions should be continued for 14 days after onset of
symptoms or until either an alternative diagnosis is established or
diagnostic test results indicate that the patient is not infected.
Restricted visitation should be implemented and an ongoing log
kept of all people entering the patient’s room. Minimize the number

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of health care personnel caring for the patient. All equipment and
other items should remain in the patient’s room and should not be
used with other patients or outside the isolation room.

3. Vaccination of health care workers

Health care workers caring for patients with documented or
suspected avian influenza should be vaccinated with the most
recent seasonal influenza vaccine. This allows for protection against
the predominant circulating strain and reduces the likelihood of
health care workers becoming coinfected with human and avian
strains, which could lead to the emergence of a pandemic strain. At
present, there is no vaccine for avian influenza.

Additional nursing diagnoses

See nursing diagnoses for Acute Lung Injury and Acute Respiratory
Distress Syndrome, Acute Pneumonia, Acute Respiratory Failure
(Chapter 4), Mechanical Ventilation (Chapter 1), and Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2).

Emotional and spiritual support of the

patient and significant others
Similar to all health care professionals, nurses must remain mindful
of the need to remain objective and nonjudgmental; therefore,
imposing one’s own personal views upon others must be avoided.
Instead, a patient’s significant others may feel that they are in the
best position to assign significance to an event, or to decide the
most appropriate response. To facilitate therapeutic interactions
when faced with challenging situations, nurses must assess both the
patient’s and significant others’ understanding and perception of
the situation before implementing a plan of care. Assessment of
patient and significant others’ needs requires that nurses employ
active listening, are fully present during interactions, and invest as
much high-quality time as possible during the process. An
interdisciplinary team may be employed to assist with assessment
and subsequent problem-solving. Given resource limitations,

517
possible inconsistency of nurse assignment, and the amount of
coverage available by other disciplines, time constraints may lead to
dysfunctional situations that are not handled in the best manner to
produce a sustainable solution or, in worst-case scenarios, to not
being noticed at all.
It is of paramount importance that nurses are familiar with how
to provide both emotional and spiritual support to patients and
significant others, and to help guide them through the challenges
posed by critical illness and hospitalization. Complex support
system issues may include identification of high-risk dependent
relationships among older adults, family members, domestic
partners, children, or religious leaders. Actions required may
include steps to prevent infliction of physical, emotional, or sexual
harm, exploitation, or neglect of basic life necessities.
Effective exchange of information is foundational for
collaboration among the health care team, patients, and their
significant others. Accurate and timely information should be
shared throughout the hospitalization to ensure the delivery of
holistic patient care. In our current fast-paced, dynamic health care
environment, relationships among health care professionals and
their clients vary, and can evolve over time.
With less opportunity to establish relationships, trusting the
clinical knowledge, decisions, and judgment of unknown providers
may be difficult. In large teaching hospitals, the problem is
compounded as the monthly rotation of multiple levels of physician
house staff ensues. Nursing care is often delivered on a dynamic
schedule and includes increasing numbers of contract and per diem
clinical staff. Therefore, stabilizing the team and taking the time
needed to provide effective communication can be challenging. The
larger the number of health care team members or
family/significant others involved, the greater the challenge of
adequate communication. In addition, emotionally charged events
are common in the critical care environment. To help provide care
of the whole patient and family system, emotional support can be
of assistance to promote healthy coping.
Occasionally, however, providers are also in need of emotional
support to cope with difficult situations. Emotional support is
defined as support for emotions that will help provide the best

518
outcomes. Key elements of holistic care include providing
encouragement, reassurance, and acceptance during times of stress.
Mental, emotional, and spiritual interventions are often needed to
help with coping and decision-making during critical illness.
Emotional responses may be closely associated with mental
processes; in other words, thoughts or perceptions drive feelings
about life events. Knowledge affects perception, so keeping patients
and families informed and up to date is of paramount importance
to their emotional well-being. Knowledge will promote them
having more perceived control of the situation. Frequent, repetitive,
simple explanations are often needed. During emotional upset, the
ability to recall and retain information is often impaired.
Nurses can facilitate adaptation to perceived stressors, changes,
or threats that interfere with meeting the demands present in the
lives of patients and their significant others. Coping techniques that
are used vary with individuals, including health care providers,
and are often affected by culture. Counseling or family-centered
care team conferences may be provided, using an interactive,
helpful approach, and may focus on the needs, problems, or
feelings of the patient, significant others, and health care team
members. Actions are designed to enhance or support coping, crisis
management, problem-solving, and interpersonal relationships.
Emotionally charged ethical issues frequently arise in the critical
care environment. Care providers are prompted to address end-of-
life decision-making, including “Do Not Resuscitate” issues,
withdrawal of care, and whether or not the family desires to be
present if resuscitation is needed. Involvement of the
interdisciplinary team (which may include members such as
pastoral care, mental health professionals, social work, palliative
care, and an ethics professional) may be warranted on admission to
the critical care unit and throughout the stay if complex end-of-life
issues arise.

2-1
RESEARCH BRIEF
A large percentage of the U.S. general public has stated they would
like to have loved ones present during resuscitation. Despite the

519
countless benefits reported, family presence during resuscitation is
still a controversial, highly debated issue among health
professionals in adult critical care units. Baumhover and Hughes
(2009) designed an exploratory, descriptive, and correlational
study to determine the relationship between the spirituality of
health care professionals and support for family presence during
invasive procedures and resuscitation. The holistic Spirituality
Assessment Scale (SAS) developed by Howden (1992) was used to
obtain information regarding a more comprehensive meaning of
spirituality; not focused exclusively on religious beliefs and
feelings of patients but also including the feelings of health care
providers. Data were collected from 73 nurses, 31 physicians, and 4
physician assistants. Results suggested a link between a holistic
perspective and support for family presence. The higher the scores
of spirituality for health care providers, the greater the likelihood
that they supported family presence as a patient’s right and
essential part of holistic care. This study helps to fill the gap in the
current literature regarding certain demographic characteristics
affecting whether or not health care providers are willing to allow
families to be present during invasive procedures and
resuscitation. Further analysis of extraneous variables is needed
before the results of this study can be generalized.
From Baumhover N, Hughes L: Spirituality and support for family presence during
invasive procedures and resuscitations in adults. Am J Crit Care 18:357-367, 2009.

Promoting psychological peace in the final phase of life is of

paramount importance to the patient and their significant others
and involves exploration of the spiritual beliefs of all those involved
in making decisions. Disagreement on the appropriate course of
action stems from many factors. For example, confusion among
significant others regarding the wishes of the patient, their own
views on death and dying, or vacillating patient views may create a
dysfunctional care environment. The problem is compounded
when various subgroups of decision-makers share perspectives in
isolation, rather than discussing them openly in a group composed
of all key decision-makers.
In extreme cases, anger and confusion may result in violent
behavior, and the lines of communication may deteriorate if

520
appropriate avenues are not initiated to repair damages. The
American College of Critical Care Medicine has developed patient
and family guidelines that help widen perspectives, open new
options, and suggest different ideas for health care providers to
help abate situations before they escalate to the point of physical
violence.
Spiritual support is regarded as a part of providing holistic care.
Spirituality is not to be confused with religion. Although the vast
majority of nurses believe spiritual care is a part of providing
patient-centered, holistic care, over half feel inadequate to perform
spiritual care interventions. Spirituality has been described as the
values, beliefs, and behaviors of an individual related to purpose
and meaning in life; connectedness to self, others, and life and
universal dimensions; innerness or inner resources and capacity for
transcendence. Using these characteristics, Howden developed the
Spirituality Assessment Scale or SAS (Box 2-1). The 28 items on the
SAS provide a strong operational framework for evaluating the
ability of all involved with patient care and decision-making to
connect or to be sensitive to the spiritual dimensions of others, and
possibly frame the approach on addressing the emotional needs of
others. If a health care provider has not developed the capacity to
connect with others, providing care that requires embracing a
viewpoint outside of his or her personal sphere of perception is
extremely difficult. Behavior modification of the patient, significant
others, or health care team members may be necessary as part of
facilitating adaptation to life changes for the patient and significant
others resulting from hospitalization. Values may collide, based on
past experiences of all involved; therefore, staying focused on the
present can assist all involved in remaining objective when
approaching the situation.

Box 2-1
ELEMENTS OF THE HOWDEN SPIRITUAL
ASSESSMENT SCALE (SAS)*
Has a sense of belongingness Feels part of the community lived in
Has capacity to forgive Feels reconciling relationships is important
Can rise above or go beyond mental and Can rise above or go beyond body changes or

521
 physical problems body losses
Is concerned about environmental Feels responsible for preserving the planet
destruction
Can find peace during a devastating event Has inner resources for dealing with uncertainty

Has a sense of kinship to others Has found inner strength during past struggles
Has a connection to all of life Possesses life goals and aims
Relies on inner strength when struggling Possesses inner strength
Enjoys serving others Feels a sense of fulfillment in life
Has a sense of inner spiritual guidance Trusts life is good despite discouraging events
Perceives ability for self-healing Feels good about themselves
Perceives meaning of life provides peace Has the sense life has meaning and purpose
Feels a sense of balance within life Feels inner harmony and peace
Boundaries of personal universe extend Inner strength is related to belief in a higher
beyond space and time power or supreme being

*
Items are rated 1 (Strongly disagree) through 6 (Strongly agree) on a Likert scale after
reading statements about the elements listed here.
From Howden JW: Development and psychometric characteristics of the Spirituality
Assessment Scale. Dissert Abstr Int 54:166B, 1992. Abstract reproduced with permission
from ProQuest LLC. © 2007 ProQuest LLC; all rights reserved. Further reproduction is
prohibited without permission.

Assessment of need for emotional and

spiritual support
Goal of assessment
The goal of assessment is to determine the ability of the patient and
significant others to demonstrate a healthy response to changes
brought forth by critical illness. In addition, a comprehensive
assessment can ensure that appropriate emotional and spiritual
support can be provided to facilitate appropriate decision-making
as part of patient and family-centered care. True family-centered
care requires the creation of mutually beneficial partnerships
among patients, families, and health care providers. A concerted
effort may be required to create one unified voice for the right
course of action in every situation that arises.

History and risk factors

Innumerable variables can affect coping and decision-making

522
abilities. The factors listed in Box 2-1 have been demonstrated by
various studies to affect how decisions are made and how they may
adversely affect coping because of a difference in beliefs related to
spirituality. The following characteristics in any member of a
decision-making team may be associated with ineffective coping:
poor self-image, a lack of fulfillment, significant financial problems,
existing unhealthy and/or unrepaired relationships, resistance to
change, a lack of meaning or purpose in life, difficulty in learning, a
poor sense of belonging or connectedness, a lack of inner peace or
strength, the inability to forgive others, difficulty relating to others,
and/or unclear life goals.

Care plans: Emotional and spiritual support

of the patient, family, and significant others
Anxiety 
related to actual or perceived threat of death; change in health status;
threat to self-concept or role; unfamiliar people and environment; the
unknown.
Goals/Outcomes: After intervention, anxiety is absent or
reduced, as evidenced by the patient’s verbalization of same, vital
signs at the patient’s baseline, and an absence of or decrease in
irritability and restlessness. Family members appear calmer.
Anxiety Level, Anxiety: Self-Control, Concentration, Coping.

Anxiety reduction

1. Engage in honest communication with the patient and family;

empathize. Actively listen and establish an atmosphere that enables
free expression. Express to the patient that you care about his or her
health.

2. Assess level of anxiety with the patient and family. Be alert to

verbal and nonverbal cues:

a. Mild: Restless.

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 b. Moderate: Inattentive, expresses concern,
narrowed perceptions, disturbed sleep pattern,
altered vital signs.

c. Severe: Expressing feelings of doom; rapid

speech; tremors; poor eye contact; preoccupation
with the past; inability to understand the present;
possible presence of tachycardia, palpitations,
nausea, and hyperventilation.

d. Panic: Cannot concentrate or communicate,

distorting reality, increased motor activity,
vomiting, tachypnea.
3. For severe anxiety or panic state, refer to appropriate psychiatric
health care team member.

4. If hyperventilation occurs, encourage slow, deep breaths and

have the patient or significant other mimic your own breathing
pattern.

5. Validate the nursing assessment of anxiety with the patient or

significant other. (“You seem distressed; are you feeling anxious or
overwhelmed?”)

6. After an episode of anxiety, review and discuss the thoughts and

feelings that led to the episode.

7. Identify coping behaviors currently being used (e.g., denial,

anger, repression, withdrawal, daydreaming, drug or alcohol
dependence). Review coping behaviors used in the past. Assist in
using adaptive coping to manage anxiety.

8. Encourage expression of fears, concerns, and questions. (“This

room may look like a maze of wires and tubes; please let me know
when you have any questions.”)

524
9. Reduce sensory overload by providing an organized, quiet
environment. (See Alterations in Consciousness, Chapter 1).

10. Introduce one self and other health care team members; explain
each individual’s role as it relates to the plan of care or care map.

11. Teach relaxation and imagery techniques. See Sample

Relaxation Technique in Appendix 7.

12. Enable significant others to be in attendance whenever possible.

13. Consult palliative care services if available and appropriate.

14. Engage in and promote awareness of touch to significant others

when appropriate. Types of touch are described in Box 2-2.

Box 2-2
TYPES OF TOUCH
Instrumental touch
• Task- or procedure-related

• May be negatively perceived but accepted as impersonal

Affective touch
• Expressive, personal

• Caring

• Comforting

• May be positively or negatively perceived

• Influenced by cultural patterns

Therapeutic touch
• Deliberate intervention to accomplish a purpose

525
• Acupressure

• Use of space around the individual to mobilize energy fields

Coping Enhancement; Calming Technique, Active Listening,

Presence.

Social isolation 
related to altered health status; inability to engage in satisfying personal
relationships; altered mental status; altered physical appearance.
Goals/Outcomes: Within 24 hours after diagnosis, the patient
demonstrates interaction and communication with others.
Loneliness Severity, Mood Equilibrium, Personal Well-Being.

Socialization enhancement

1. Assess factors contributing to social isolation.

• Restricted visiting hours.

• Absence of or inadequate support system.

• Inability to communicate (e.g., presence of

endotracheal tube/tracheostomy).

• Physical changes that affect self-concept.

• Denial or withdrawal.

• Critical care environment.

2. Recognize patients at higher risk for social isolation: the older

adult, disabled, chronically ill, socioeconomically disadvantaged.

3. Assist the patient with identification of feelings associated with

526
loneliness and isolation. (“You seem very sad when your family
leaves the room. Can you tell me more about your feelings?”)

4. Determine the need for socialization and identify available and

potential support systems. Explore methods for increasing social
contact (e.g., recordings of loved ones, more frequent
visitations/hospital volunteers, scheduled interaction with nurse or
support staff).

5. Provide positive reinforcement for socialization that lessens

feelings of isolation and loneliness. (“Please continue to call me
when you need to talk to someone. Talking will help both of us to
better understand your feelings.”)

6. Facilitate the patient’s ability to communicate with others (see

Alterations in Consciousness, Chapter 1).

Support System Enhancement, Mood Management.

Compromised family coping 

related to situational crisis (patient’s illness)
Goals/Outcomes: After intervention, family/significant others
demonstrate effective adaptation to change/traumatic situation, as
evidenced by seeking external support when necessary and sharing
concerns.
Family Coping, Family Normalization.

Coping enhancement

1. Assess character of family/significant others: social,

environmental, ethnic, and cultural factors; relationships; and role
patterns. Identify developmental stage. Be aware that other
situational or maturational crises may be ongoing, such as an older
parent or teenager with a learning disability.

2. Assess previous adaptive behaviors. (“How do you deal with

stressful situations?”) Discuss observed conflicts and
communication breakdown. (“I noticed that your brother has not
visited your mother today. Has there been a problem we should be

527
aware of? Knowing about it may help us better care for your
mother.”)

3. Acknowledge the family’s or significant others’ involvement in

patient care and promote strengths. (“You were able to encourage
your wife to turn and cough. That is very important to her
recovery.”) Encourage participation in patient care conferences.
Promote frequent, regular patient visits as appropriate for the
patient’s situation.

4. Provide information and guidance related to the patient. Discuss

the stresses of hospitalization and encourage discussions of
feelings, such as anger, guilt, hostility, depression, fear, or sorrow.
(“You seem to be upset since having been told that your husband is
not leaving the hospital today.”) Refer to clergy, case manager,
clinical nurse specialist, social services, or palliative care specialist
as appropriate.

5. Evaluate interactions among patient and family/significant

others. Encourage reorganization of roles and priority setting as
appropriate. (“It appears as though your husband is concerned
about his insurance policy and seems to expect you to investigate it.
I’ll ask the financial counselor to talk with you.”)

6. Encourage family/significant others to schedule periods of rest

and activity and to seek support when necessary. (“Your neighbor
volunteered to stay in the waiting room this afternoon. Would you
like to rest at home? I’ll call you if anything changes.”)

Family Support; Family Process Maintenance; Normalization

Promotion, Financial Resource Assistance.

Fear 
related to patient’s life-threatening condition; lack of information
Goals/Outcomes: After the intervention, the patient and
family/significant others relate that fear has been lessened or is
manageable.
Fear Level, Fear Self-Control.

528
Security enhancement

1. Assess fears and understanding related to the patient’s clinical

situation. Evaluate verbal and nonverbal responses.

2. Acknowledge the fears. (“I understand these tubes may frighten

you, but they are necessary to help nourish your son.”)

3. Assess history of coping behavior. (“How do you cope with

difficult situations?”) Determine resources and significant others
available for support. (“Who/what usually helps during stressful
times?”)

4. Provide opportunities for expression of fears and concerns, while

setting boundaries of appropriate behavior. Recognize that anger,
denial, withdrawal, and demanding behavior may be adaptive
coping responses during the initial period of crisis.

5. Provide information at frequent intervals about the patient’s

status, and the therapies and equipment used. Demonstrate a caring
attitude.

6. Encourage use of positive coping behaviors by identifying fear(s),

developing goals, identifying supportive resources, facilitating
realistic perceptions, and promoting problem-solving.

7. Be alert to maladaptive responses to fear: potential for violence,

withdrawal, severe depression, hostility, and unrealistic
expectations of staff or of patient’s recovery. Provide referrals to
psychiatric service or palliative care specialist as appropriate (see
Box 2-3 for ways to reduce the risk of violence).

8. Assess your own feelings about the patient’s life-threatening

illness. Acknowledge that your attitude and fear may be reflected to
the family/significant others.

Box 2-3
SAFETY PRECAUTIONS IN THE EVENT OF
VIOLENT BEHAVIOR

529
Patient safety
• Remove harmful objects from the environment, such as heavy
objects, scissors, tubing.

• Apply padding to side rails according to agency protocol if the

patient is acting out.

• If available, use bed alarms. Ensure all unit staff members are
aware of potential for violence.

• Use physical or chemical restraints as necessary and prescribed.

Monitor the patient’s neurovascular status at frequent intervals.

• Set limits on the patient’s behavior, using clear and simple

commands.

• As prescribed, consider chemical sedation when unable to control

the patient’s behavior with other means.

• Explain safety precautions to the patient and family/significant

others.

Caregiver safety
• Place the patient in bed closest to nursing station. Maintain
visibility at all times by keeping door open.

• Alert hospital security department when risk of violence is

present from the patient or family.

• Do not approach a violent patient or family member without

adequate assistance from others.

• Never turn your back on a violent patient or family member.

• Maintain a calm, matter-of-fact tone of voice. Set limits on

family’s behavior.

• Monitor security measures at frequent intervals.

530
• Remain alert.

From Bureau of Labor Statistics (BLS), U.S. Department of Labor, for the National Institute
for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention:
Survey of workplace violence prevention, Washington, 2005, U.S. Department of Labor.
Retrieved from www.bls.gov/iif/osh_wpvs.htm.

Coping Enhancement; Calming Technique; Support System

Enhancement.

Grieving 
related to perceived potential loss of physiologic well-being (e.g., expected
loss of body function or body part, changes in self-concept or body image,
terminal illness).
Goals/Outcomes: After interventions, patient and significant
others/family express grief, participate in decisions about the
future, and communicate concerns to health care team members
and to one another.
Adaptation to Physical Disability, Body Image Enhancement.

Acceptance health status

1. Assess the source of perception of loss.

2. Assess factors contributing to anticipated loss.

3. Assess patient and family’s behavioral response. Expect reactions

such as disbelief, denial, guilt, anger, and depression. Determine
stage of grieving as described in Table 2-1.

4. Assess spiritual, religious, and sociocultural expectations related

to loss. (“Is religion/spirituality an important part of your life? How
do you and your family/significant others usually deal with serious
health problems?”) Refer to the clergy or community support
groups as appropriate.

Table 2-1
STAGES OF GRIEVING

Protest stage Denial: “No, not me”

531
 Disbelief: “But I just saw her this morning”
Anger
Hostility
Resentment
Bargaining to postpone loss
Appeal for help to recover loss
Loud complaints
Altered sleep and appetite
Disorganization Depression
Withdrawal
Social isolation
Psychomotor retardation
Silence
Reorganization Acceptance of loss
Development of new interests and attachments
Restructuring of lifestyle
Return to preloss level of functioning

Emotional support

1. Encourage the patient and family/significant others to share their

concerns. (“Is there anything you’d like to talk about today?”) Also,
respect their desire not to speak or actively listen.

2. Demonstrate empathy. (“This must be a very difficult time for

you and your family.”) Touch when appropriate (see Box 2-2).

3. In selected circumstances, provide an explanation of the grieving

process. This approach may assist in better understanding and
acknowledging feelings.

4. Assess grief reactions of the patient and family/significant others,

and identify a potential for dysfunctional grieving reactions (e.g.,
absence of emotion, hostility, avoidance). If the potential for
dysfunctional grieving is present, refer to case manager, psychiatric
service, clergy, or palliative care specialist as appropriate.

5. When appropriate, recruit tissue donation professionals to

discuss donation. Assess the patient’s wishes about tissue donation.

Active Listening; Dying Care; Grief Work Facilitation.

Spiritual distress 
related to separation from spiritual/religious/cultural supports; challenged

532
belief and value system.
Goals/Outcomes: After diagnosis, the patient and family
verbalize spiritual or religious beliefs and express hope for the
future, the attainment of spiritual or religious support, and the
availability of what is required to resolve conflicts.
Spiritual Health, Dignified Life Closure.

Spiritual support

1. Assess spiritual or religious beliefs, values, and practices. (“Do

you have a religious preference? How important is it to you? Are
there any religious or spiritual practices you wish to participate in
while in the hospital?”)

2. Inform the patient and family/significant others of the availability

of spiritual aids, such as a chapel, religious services, or pastoral care
service. Discuss advance directives.

3. Present a nonjudgmental attitude toward religious or spiritual

beliefs and values. Create an environment conducive to free
expression and invite sharing of beliefs. Identify available support
systems that may assist in meeting the patient’s religious or
spiritual needs (e.g., clergy, the patient’s fellow church members,
support groups).

4. Be sensitive to comments related to spiritual concerns or conflicts.

(“I don’t know why God is doing this to me.” “I’m being punished
for my sins.”)

5. Use active listening and open-ended questioning to assist in

resolving conflicts related to spiritual issues. (“I understand that
you want to be baptized. We can arrange to do that here.”)

6. Provide privacy and opportunities for religious practices, such as

prayer and meditation.

7. If spiritual beliefs and therapeutic regimens are in conflict,

provide honest, concrete information to encourage informed
decision-making. (“I understand that your religion discourages
receiving blood transfusions. Have the implications of not receiving

533
blood transfusions been discussed with you?”)

Coping Enhancement, Conflict Mediation, Presence.

Ineffective individual coping and ineffective denial 

related to health crisis; sense of vulnerability; inadequate support systems.
Goals/Outcomes: After diagnosis, the patient verbalizes feelings,
identifies strengths, and begins using positive coping behaviors.
Coping, Acceptance Health Status, Personal Well-Being,
Adaptation to Physical Disability.

Coping enhancement

1. Assess the patient’s perceptions and ability to understand current

health status.

2. Establish honest communication. (“Please tell me what I can do to

help you.”) Assist with identifying strengths, stressors,
inappropriate behaviors, and personal needs.

3. Support positive coping behaviors. (“I see that easy listening

music seems to help you relax.”)

4. Provide opportunities for expression of concerns; gather

information from nurses and other support systems. Provide
explanations about prescribed routine, therapies, and equipment.
Acknowledge feelings and assessment of current health status and
environment.

5. Identify factors that inhibit the ability to cope (e.g., unsatisfactory

support system, knowledge deficit, grief, fear).

6. Recognize defensive and maladaptive coping behaviors (e.g.,

severe depression, drug or alcohol dependence, hostility, violence,
suicidal ideations). Address these behaviors. (“You seem to be
requiring more pain medication. How does the pain medication
help you?”) Refer the patient to case manager, psychiatric liaison,
clergy, or palliative care specialist as appropriate (see Box 2-3 for
ways to reduce the risk of violence).

534
Support system enhancement

1. Encourage regular visits by significant others as appropriate.

Encourage them to engage in conversation with the patient to help
minimize the patient’s emotional and social isolation.

2. Assess significant others’ interactions with the patient. Attempt

to mobilize support systems by involving them in patient care
whenever possible.

3. As appropriate, explain to significant others that increased

dependency, anger, and denial may be adaptive coping behaviors
used by the patient in early stages of crisis until effective coping
behaviors are learned.

Socialization Enhancement; Resiliency Promotion, Self-

Awareness Enhancement.

Disabled family coping 

related to inadequate or incorrect information or misunderstanding;
temporary family disorganization and role change; exhausted support
systems; unrealistic expectations; fear; anxiety.
Goals/Outcomes: After interventions, family/significant others
verbalize feelings, identify ineffective coping patterns, identify
strengths and positive coping behaviors, and seek information and
support from the nurse or other support systems.
Caregiver-Patient Relationship, Caregiver Performance:
Direct Care, Caregiver Performance: Indirect Care.

Caregiver support

1. Have the family designate one member as the primary point of

contact. Explain how this will allow the nurse to spend more time
taking care of the patient and less time on the telephone explaining
the patient’s status to each family member separately.

2. Establish open, honest communication. Assist in identifying

strengths, stressors, inappropriate behaviors, and personal needs.
(“I understand your mother was very ill last year. How did you

535
manage the situation?” “I hear that your loved one is very ill. How
can I help you?”)

3. Assess for ineffective coping (e.g., depression, substance abuse,

violence, withdrawal) and identify factors that inhibit effective
coping (e.g., inadequate support system, grief, fear of disapproval
by others, knowledge deficit). (“You seem to be unable to talk about
your husband’s illness. Is there anyone with whom you can talk
about it?”) (See Box 2-3 for ways to reduce the risk of violence.)

4. Assess knowledge regarding the patient’s current health status

and therapies. Provide information frequently, and allow sufficient
time for questions. Reassess understanding at frequent intervals.

5. Provide opportunities in a private setting for both patients and

significant others to talk and share concerns with nurses or other
health care providers. If appropriate, refer to psychiatric clinical
nurse specialist for therapy.

6. Offer realistic hope. Help family/significant others develop

realistic expectations for the future and identify support systems
that will assist them with planning for the future.

7. Reduce anxiety in significant others by encouraging diversionary

activities (e.g., period of time outside of hospital) and interaction
with outside support systems. (“I know you want to be near your
son, but if you would like to go home to rest, I will call you if any
changes occur.”)

8. Establish open, honest communication and rapport. (“I am here

to care for your mother and to help you, as well.”)

9. Identify ineffective coping behaviors (e.g., violence, depression,

substance abuse, withdrawal). (“You seem to be angry. Would you
like to talk to me about your feelings?”) Refer to psychiatric liaison,
clergy, or support group as appropriate.

10. Identify perceived or actual conflicts. (“Are you able to talk

openly among yourselves?” “Are your brothers and sisters able to
help and support you during this time?”)

536
11. Encourage healthy functioning. For example, facilitate open
communication and encourage behaviors that support
cohesiveness. (“Your mother seemed to enjoy your last visit. Would
you like to see her now?”)

12. Assess knowledge about the patient’s current health status.

Provide opportunities for questions; reassess understanding at
frequent intervals.

13. Assist with developing realistic goals, plans, and actions. Refer
to clergy, case manager, psychiatric nurse, social services, financial
counseling, and family therapy as appropriate.

14. Encourage family/significant others to spend time outside of the

hospital and to interact with/support individuals.

15. Include the family/significant others in the patient’s plan of care.

Offer them opportunities to become involved in patient care, for
example, range-of-motion (ROM) exercises, patient hygiene, and
comfort measures (e.g., backrub).

Family Involvement Promotion; Family Mobilization; Family

Support.

Powerlessness 
related to health care environment; treatment regimen
Goals/Outcomes: After diagnosis, assess the patient’s and
family’s preferences, needs, values, and attitudes. The patient
makes decisions about self-care and therapies and relates an
attitude of realistic hope and a sense of self-control and the family
accepts decisions.
Depression Self-Control, Family Participation in Professional
Care, Health Beliefs: Perceived Control.

Self-responsibility facilitation

1. Explain the Patient and Family Rights and Responsibilities

information the hospital provides. Help the patient and significant
others understand their rights and responsibilities, and

537
responsibilities of the hospital with regard to patient care.

2. Ensure the patient and family know who is taking care of the
patient. Tell the patient and family if a staff member does not have
an identification badge visible, it is alright to ask for their name and
their role in patient care.

3. Before providing information, ensure the patient’s privacy is

maintained, and assess the patient’s and family’s understanding of
health condition, prognosis, and plan of care.

4. Recognize expressions of fear, lack of response to events, and lack

of interest in information, any of which may signal a sense of
powerlessness.

5. Evaluate medical and nursing interventions, and adjust them, as

appropriate, to support the patient’s and/or caregiver’s sense of
control. For example, if the patient always bathes in the evening to
promote relaxation before bedtime, modify the care plan or map to
include an evening bath rather than follow the hospital routine of
giving a morning bath.

6. Assist the patient to identify and demonstrate activities that can

be performed independently.

7. Encourage the patient and/or family to keep a notebook with

them at all times, which can serve as a helpful tool to remember
questions or write down information that will be shared with other
family members during this stressful time.

8. Whenever possible, offer alternatives related to routine hygiene,

diet, diversion activities, visiting hours, or treatment times.

9. Encourage the patient and family to ask to speak with the charge
nurse, nurse manager, nurse supervisor, or patient advocate/patient
representative if there is a problem with any member of the health
care team.

10. Ensure privacy and preserve territorial rights whenever

possible. For example, when distant relatives and casual

538
acquaintances request information about the patient’s status, refer
them to the patient or a family member who can provide acceptable
amounts of information.

11. Avoid paternal or parental behaviors with patients and families.

12. Assess support systems; enable significant others to be involved

in care whenever possible.

13. Offer realistic hope for the future. If appropriate, encourage

direction of thoughts beyond the present.

14. Provide referrals to clergy, palliative care specialists, and other

support systems as appropriate.

Emotional Support; Family Involvement Promotion, Support

Group.

Sleep pattern, disturbed 

related to environmental changes; illness; therapeutic regimen; pain;
immobility; psychological stress.
Goals/Outcomes: After discussion, the patient identifies factors
that promote sleep. Within 8 hours of intervention, the patient
attains adequate periods of uninterrupted sleep and verbalizes
satisfaction with the ability to rest.
Personal Well-Being, Sleep.

Sleep enhancement

1. Assess usual sleeping patterns (e.g., bedtime routine, hours of

sleep per night, sleeping position, use of pillows and blankets,
napping during the day, nocturia).

2. Explore relaxation techniques that promote rest/sleep (e.g.,

imagining relaxing scenes, listening to soothing music or taped
stories, using muscle relaxation exercises).

3. Identify causative factors and activities that contribute to sleep

pattern disturbance, adversely affect sleep patterns, or awaken the
patient. Examples include pain, anxiety, depression, hallucinations,

539
medications, underlying illness, sleep apnea, respiratory disorder,
caffeine, fear, and medical and nursing interventions.

4. Organize procedures and activities to allow for 90-minute

periods of uninterrupted rest/sleep. Limit visiting during these
periods.

5. Whenever possible, maintain a quiet environment by providing

ear plugs or decreasing alarm levels. The use of “white noise” (e.g.,
low-pitched, monotonous sounds; electric fan; soft music) may
facilitate sleep. Dim the lights for a period of time every 24 hours by
drawing the drapes (if safe to do so) or providing blindfolds.

6. If appropriate, limit daytime sleeping. Attempt to establish

regularly scheduled daytime activity (e.g., ambulation, sitting in
chair, active ROM), which may promote nighttime sleep.

7. Investigate and provide nonpharmacologic comfort measures

that are known to promote sleep (Table 2-2).

Table 2-2
NONPHARMACOLOGIC MEASURES TO PROMOTE SLEEP

Activity Example(s)
Mask or eliminate Use eye shields, ear plugs
environmental stimuli Play soothing music
Dim lights at bedtime
Mask odors from dressings/drainage; change dressing or
drainage container as indicated
Promote muscle relaxation Encourage ambulation as tolerated throughout the day
Teach and encourage in-bed exercises and position change
Perform back massage at bedtime
If not contraindicated, use a heating pad
Reduce anxiety Ensure adequate pain control
Keep the patient informed of his or her progress and treatment
measures
Avoid overstimulation by visitors or other activities
immediately before bedtime
Avoid stimulant drugs (e.g., caffeine)
Promote comfort Encourage the patient to use own pillows, bedclothes if not
contraindicated
Adjust bed; rearrange linens
Regulate room temperature
Promote usual presleep Offer oral hygiene at bedtime
routine Provide warm beverage at bedtime
Encourage reading or other quiet activity

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Minimize sleep disruption Maintain quiet environment throughout the night
Plan nursing activities to allow long periods (at least 90
minutes) of undisturbed sleep
Use dim lights when checking on the patient during the night

Environmental Management; Environmental Management:

Comfort.

Body image disturbance 

related to loss of or change in body parts or function; physical trauma.
Goals/Outcomes: Before hospital discharge, the patient
acknowledges body changes and demonstrates movement toward
incorporating changes into self-concept. Maladaptive responses,
such as severe depression, are absent.
Body Image, Adaptation to Physical Disability, Self-Esteem,
Psychosocial Adjustment: Life Change.

Body image enhancement

1. Establish open, honest communication. Promote an environment

that is conducive to free expression. (“Please feel free to talk to me
whenever you have any questions.”) Assess indicators suggesting
body image disturbance, as listed in Box 2-4.

2. When planning care, be aware of interventions that may

influence body image (e.g., medications, procedures, monitoring).

3. Assess knowledge of the patient’s pathophysiologic process and

current health status. Clarify any misconceptions.

4. Discuss the loss or change with the patient. Recognize that what
may seem to be a small change may be of great significance to the
patient (e.g., arm immobilizer, catheter, hair loss, ecchymoses, facial
abrasions).

5. Explore expressions of concern, fear, and guilt. (“I understand

that you are frightened.” “What is your understanding of how your
condition will change over time?”)

6. Encourage the patient and family/significant others to interact

with one another. Help family/significant others to support the

541
patient’s feelings related to the changed body part or function. (“It
seems as though your son looks very different to you now, but it
would help if you speak to him and touch him as you would
normally.”)

7. Encourage gradual participation in self-care activities as the

patient becomes physically and emotionally able. Allow for some
initial withdrawal and denial behaviors. For example, when
changing dressings over traumatized part, explain what you are
doing but do not expect the patient to watch or participate initially.

8. Discuss the potential for reconstruction of the loss or change (i.e.,

surgery, prosthesis, grafting, physical therapy, cosmetic therapies,
organ transplant). (“What is your understanding of the potential for
reconstruction?”)

9. Recognize manifestations of severe depression (e.g., sleep

disturbances, change in affect, change in communication pattern).
As appropriate, refer to case manager, psychiatric liaison, clergy, or
support group.

10. Help the patient attain a sense of autonomy and control by

offering choices and alternatives whenever possible. Emphasize
strengths and encourage activities that interest the patient.

11. Offer realistic hope for the future.

Box 2-4
INDICATORS SUGGESTING BODY IMAGE
DISTURBANCE
Nonverbal indicators
• Missing body part: internal or external (e.g., splenectomy,
amputated extremity)

• Change in structure (e.g., open, draining wound)

• Change in function (e.g., colostomy)

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• Avoiding looking at or touching body part

• Hiding or exposing body part

Verbal indicators
• Expression of negative feelings about body

• Expression of feelings of helplessness, hopelessness, or

powerlessness

• Personalization or depersonalization of missing or mutilated part

• Refusal to acknowledge change in structure or function of body

part

Self-Esteem Enhancement; Emotional Support; Grief Work

Facilitation, Suicide Prevention.

Complicated grieving 
related to loss of physiologic well-being; fatal illness.
Goals/Outcomes: After diagnosis, the patient and family express
grief, explain the meaning of the loss, and talk with each other. The
patient assumes necessary self-care activities.
Mood Equilibrium, Grief Resolution, Depression Self-
Control.

Grief work facilitation

1. Assess grief stage (see Table 2-1) and previous coping abilities.
Discuss feelings of the patient and family, the meaning of loss, and
goals. (“How do you feel about your condition/illness or your loved
one’s condition? What do you hope to accomplish in these next few
days/weeks? Are you afraid your family will not be taken care of if
you pass away?”)

2. Acknowledge and permit anger; set limits on the expression of

anger to discourage destructive behavior. (“I understand that you

543
must feel very angry, but for the safety of others, you may not
throw equipment.”)

3. Identify suicidal behavior (e.g., severe depression, statements of

intent, suicide plan, previous history of suicide attempt). Ensure
safety and refer to case manager, psychiatric service, psychiatrist,
clergy, or palliative care specialist.

4. Encourage the patient and family/significant others to participate

in activities of daily living and diversion activities. Identify
physiologic problems related to loss (e.g., eating or sleeping
disorders) and intervene accordingly.

5. Collaborate with the care team about a visit by another

individual with the same disorder, if appropriate.

Hope instillation

1. Provide opportunities for the patient to feel cared for, needed,

and valued by others. For example, emphasize the importance of
relationships. (“Tell me about your grandchildren.” “It seems that
your family loves you very much.”)

2. Support significant others who seem to spark or maintain the

patient’s feelings of hope. (“Your husband’s mood seemed to
improve after your visit.”)

3. Recognize factors that promote sense of hope (e.g., discussions

about family members, reminiscing about better times).

4. Promote anticipation of positive events (e.g., mealtime,

grandchildren’s visits, bathtime, extubation, removal of traction).

5. Help the patient recognize that although there may be no hope

for returning to original lifestyle, there is hope for a new but
different life.

6. Avoid insisting that the patient assume a positive attitude.

Encourage hope for the future, even if it is the hope for a peaceful
death.

544
7. Set realistic, attainable goals, and reward achievement.

Suicide Prevention, Family Integrity Promotion.

Risk for self-directed violence or risk for other-directed

violence by patient or family 
related to sensory overload; suicidal behavior; rage reactions; neurologic
disease; perceived threats; toxic reaction to medications; substance
withdrawal.
Goals/Outcomes: The patient or family does not harm themselves
or others.
Aggression Self-Control, Abusive Behavior Self-Restraint,
Abuse Cessation.

Environmental management: Violence prevention

1. Assess factors that may contribute to or precipitate violent

behavior (e.g., medication reactions, inability to cope, suicidal
behavior, confusion, hypoxia, substance withdrawal, preictal and
postictal states), or dysfunctional family behaviors such as arguing,
pushing, and shoving.

2. Attempt to eliminate or treat causative factors. For example,

provide patient teaching, assess the family for homicidal behavior,
reorient the patient, and reduce sensory overload (see Alterations in
Consciousness, p. 24). Facilitate mental health consults as
appropriate.

3. Approach the patient and family in a positive manner, and

encourage verbalization of feelings and concerns. (“You appear
upset and frightened. I will be here from 3 pm to 11 pm to care for
you, or for your family member.”)

4. Help the patient distinguish reality from altered perceptions,

including hallucinations, delusions, and illusions. Orient to time,
place, and person. Alter the environment to promote reality-based
thought processes (e.g., provide clocks, calendars, pictures of loved
ones, familiar objects).

545
5. For acute confusion that becomes aggressive, do not attempt to
reorient patient and avoid arguing. Instead, provide support by
stating, “I believe that you (see, hear) that; however, I do not (see,
hear) that.” Use nonthreatening mannerisms, facial expressions,
and tone of voice.

6. Initiate measures that prevent or reduce excessive agitation for

the patient or family:

• Reduce environmental stimuli (e.g., alarms, loud or

unnecessary talking).

• Before touching the patient/family, ask for

permission. Provide concise explanations.

• Speak quietly (but firmly, as necessary), and project

a caring attitude. (“We are very concerned for your
comfort and safety. Can we do anything to help you
feel more relaxed?”)

• Avoid crowding (e.g., of equipment, visitors, health

care personnel) in the patient’s personal
environment.

• Avoid direct confrontation.

7. Explain and discuss the patient’s behavior with family/significant

others. Acknowledge frustration, concerns, fears, and questions.
Review safety precautions with family/significant others (see Box 2-
3).

Abuse protection support

1. Assess for history of physical aggression, family violence,

extreme dependence in relationships (including religious leaders),

546
and substance abuse as maladaptive coping behaviors (see Box 2-3).

2. Discuss the need for Adult Protective Services involvement to

protect the patient or family caregiver(s) with the medical team,
case manager, and social worker if pathologic relationships are
identified.

3. Monitor for early signs of increasing anxiety and agitation (e.g.,

restlessness, verbal aggressiveness, inability to concentrate). Assess
for body language that is indicative of violent behavior: clenched
fists, rigid posture, increased motor activity.

Delusion Management, Anger Control Assistance, Anxiety

Reduction, Surveillance: Safety, Crisis Intervention.

Readiness for enhanced family coping: Potential for

growth 
related to use of support systems and referrals; choosing experiences that
optimize wellness.
Goals/Outcomes: At the time of the patient’s diagnosis,
family/significant others express their intent to use support systems
and resources and identify alternative behaviors that promote
communication and strengths. Family/significant others express
realistic expectations and decrease use of ineffective coping
behaviors.
Family Functioning, Family Normalization, Respite Care.

Normalization promotion

1. Assess relationships, interactions, support systems, and

individual coping behaviors. Permit movement through stages of
adaptation. Encourage further positive coping.

2. Acknowledge expressions of hope, future plans, and growth

among family members/significant others.

3. Encourage development of open, honest communication. Provide

opportunities in a private setting for interactions, discussions, and
questions. (“I know the waiting room is very crowded. Would you

547
like some private time together?”)

4. Refer the family/significant others to community or support

groups (e.g., ostomy support group, head injury rehabilitation
group).

5. Encourage exploration of outlets that foster positive feelings for

significant others, for example, periods of time outside the hospital
area, meaningful communication with the patient or support
individuals, and relaxing activities (e.g., showering, eating,
exercising).

Support Group, Resiliency Promotion, Anticipatory

Guidance.

Deficient knowledge 
related to disease process, diet, medication, prescribed activity, fall
prevention, infection control, health resources, treatment procedures,
treatment regimen, substance use control, personal safety.
Goals/Outcomes: The patient and family/significant others
verbalize understanding of current diet, disease process, health
resources, medication, prescribed activity, treatment procedures,
and treatment regimen before discharge from the critical care unit.
Knowledge: Disease Process, Diet, Fall Prevention, Health
Behavior, Illness Care, Infection Control, Medication, Personal
Safety, Substance Use Control.

Teaching individual and family support

1. Assess current level of knowledge about all aspects of disease

process and illness management, including health resources,
medication, prescribed activity, treatment procedures, and
treatment regimen.

2. Assess cognitive and emotional readiness to learn.

3. Recognize barriers to learning, such as impaired verbal

communication, altered thought processes, confusion, impaired
memory, sensory alterations, fear, anxiety, and lack of motivation.

548
4. Assess learning needs and establish short- and long-term goals.

5. Use individualized verbal or written information to promote

learning and enhance understanding. Give simple, direct
instructions. If indicated, use audiovisual tools to supplement
information.

6. Encourage significant others to reinforce correct information

rendered by health care providers.

7. Encourage interest about health care information by involving

the patient in planning care. Explain rationale for care.

8. Interact frequently with the patient to evaluate comprehension of

information given. Ask the patient and family to repeat what has
been explained. Individuals in crisis often need repeated
explanations before information can be understood. Also be aware
that many individuals may not understand seemingly simple
medical terms (e.g., “terminal,” “malignant,” “constipation”).

9. As appropriate, assess understanding of informed consent. Assist

the patient to use information received to make informed health
care decisions (e.g., about invasive procedures, surgery,
resuscitation).

10. Assess understanding of right to self-determination; provide

information as indicated. If requested, assist the patient with
mechanism for executing an advance directive for health care.

11. At frequent intervals, inform the family/significant others about

the patient’s current health status, therapies, and prognosis. Use
individualized verbal, written, and audiovisual strategies to
promote understanding.

12. Evaluate the family/significant others at frequent intervals for

understanding of information that has been provided. Adjust
teaching as appropriate. Some individuals in crisis need repeated
explanations before comprehension can be assured. (“I have
explained many things to you today. Would you mind
summarizing what I’ve told you so that I can be sure you

549
understand your husband’s status and what we are doing to care
for him?”)

13. Encourage the family/significant others to relay correct

information to the patient. This also reinforces comprehension for
the family/significant others and the patient.

14. Ask if needs for information are being met. (“Do you have any
questions about the care your mother is receiving or about her
condition?”)

15. Help the family/significant others use the information they

receive to guide health care decisions (e.g., regarding the patient’s
surgery, resuscitation, organ donation).

16. Promote active participation in patient care when appropriate.

Encourage the family/significant others to seek information and
express feelings, concerns, and questions.

Teaching: Disease Process, Prescribed Medication,

Procedure/Treatment, Health System Guidance, Fall Prevention;
Health Education; Patient Rights Protection; Infection Protection,
Learning Facilitation; Learning Readiness Enhancement.

Impaired verbal communication 

related to neurologic or anatomic deficit (e.g., hearing impairment, visual
impairment); psychological or physical barriers (e.g., tracheostomy,
intubation); cultural or developmental differences.
Goals/Outcomes: At the time of intervention, the patient
communicates needs and feelings, and relates decrease in or
absence of frustration over communication barriers.
Communication: Expressive, Communication: Receptive,
Information Processing.

Communication enhancement: Speech, hearing, and/or visual

deficit

1. Assess etiology of impaired communication (e.g., tracheostomy,

stroke, cerebral tumor, Guillain-Barré syndrome).

550
2. With the patient and significant others, assess the patient’s ability
to hear, see, speak, read, write, and comprehend English. If the
patient speaks a language other than English, collaborate with an
English-speaking family member or interpreter to establish effective
communication.

3. When communicating, use eye contact; speak in a clear, normal

tone of voice; and face the patient.

4. If the patient cannot speak because of a physical barrier (e.g.,

tracheostomy, wired mandibles), provide reassurance and
acknowledge frustration. (“This may be frustrating for you, but
please do not give up. I want to understand you.”)

5. Provide slate, word cards, pencil and paper, alphabet board,

pictures, or other communication device to assist the patient. Adapt
the call system to meet the patient’s needs. Document the meaning
of the patient’s signals in response to questions.

6. Explain to significant others the source of the communication

impairment; demonstrate effective communication alternatives (see
preceding intervention).

7. Be alert to nonverbal messages, such as facial expressions, hand

movements, and nodding of the head. Validate meanings of
nonverbal cues with the patient.

8. Recognize that the inability to speak may foster maladaptive

behaviors. Encourage the patient to communicate needs; reinforce
independent behaviors.

9. Be honest; do not relate understanding if you cannot interpret the

patient’s communication.

Active Listening; Communication Enhancement: Hearing

Deficit, Speech Deficit, Visual Deficit.

Disturbed sensory perception 

related to therapeutically or socially restricted environment; psychological

551
stress; altered sensory reception, transmission, or integration; chemical
alteration.
Goals/Outcomes: At the time of intervention, the patient
verbalizes orientation to time, place, and person; relates the ability
to concentrate; and expresses satisfaction with the degree and type
of sensory stimulation being received.
Distorted Thought Self-Control, Neurologic Status:
Cranial/Sensory Motor Function, Vision Compensation Behavior.

Environmental management

1. Assess factors contributing to the sensory/perceptual alteration.

• Environmental: Excessive noise in the environment;

constant, monotonous noise; restricted environment
(immobility, traction, isolation); social isolation
(restricted visitors, impaired communication);
therapies.

• Physiologic: Altered organ function; sleep or rest

pattern disturbance; medication; history of altered
sensory perception.

2. Determine the appropriate sensory stimulation needed; plan care

accordingly.

3. Control factors that contribute to environmental overload. For

example, avoid constant lighting (maintain day/night patterns);
reduce noise whenever possible (e.g., set alarms appropriately,
avoid loud talking, keep room door closed [if safe for the patient],
provide ear plugs).

4. Provide meaningful sensory stimulation:

• Display clocks, large calendars, and meaningful

photographs and objects from home.

552
• Depending on the patient’s preferences, provide a
radio, music, reading materials, and tape recordings
of family and significant others. Earphones help
block out external stimuli.

• Position the patient toward window when possible.

• Discuss current events, time of day, holidays, and

topics of interest during patient care activities.

• As needed, orient the patient to surroundings.

Direct the patient to reality as necessary.

• Establish personal contact by touch to help promote

and maintain contact with the real environment.

• Encourage significant others to communicate with

the patient frequently, using a normal tone of voice.

• Convey concern and respect. Introduce yourself,

and call the patient by name.

• Stimulate vision with mirrors, colored decorations,

and pictures.

• Stimulate sense of taste with sweet, salty, and sour

substances if appropriate.

• Encourage use of appropriate eyeglasses and

hearing aids.
5. Inform the patient before initiating interventions and using
equipment.

553
6. Encourage participation in health care planning and decision-
making whenever possible by asking the patient first.

7. Provide patient with choices when possible.

8. Assess sleep-rest pattern to evaluate its contribution to the

sensory/perceptual disorder. Ensure that the patient attains at least
90 minutes of uninterrupted sleep as frequently as possible.

Environmental Management; Cognitive Restructuring;

Cognitive Stimulation.

Ethical considerations in critical care

Perhaps more attention is paid to health care decisions in critical
care than in any other health care area. Because of the sudden onset
of life and death scenarios, interprofessional team members in
intensive care areas seem to discuss and notice ethical dilemmas
more frequently than other areas of the hospital. These decisions
have been debated vigorously in the literature, and although some
of these issues have had reasonable and workable solutions, others
continue to be argued. A brief overview of common ethical
considerations in critical care will be presented.
Health care providers must develop a clear understanding of
ethical issues to ensure that the care provided is morally and legally
acceptable. Ethical reasoning enables the health care professional to
examine the moral principles involved in decision-making and
identify appropriate options. Although there are many ethical
principles, the following four principles are probably the most
widely referenced: (1) respect for autonomy (recognizing that each
patient has a right to make decisions for himself/herself), (2)
nonmaleficence (not harming a patient), (3) beneficence (helping a
patient), and (4) justice (treating patients equally).

Informed consent
Without adequate knowledge, patients and their significant others
cannot make good decisions. Part of a nurse’s obligation is to
inform patients and families, in a caring manner, what is to be

554
expected from different treatment options. Informed consent serves
not only to protect the health care provider from liability but its
primary purpose is to support the ethical principle of respect for
autonomy. Informed consent is instrumental to a patient’s right to
accept, continue, or reject all or part of health care interventions.
The elements of informed consent should be used as a guide but are
not absolutely necessary for all nursing or medical interventions
(Box 2-5).

Box 2-5
ELEMENTS OF INFORMED CONSENT
Threshold elements (preconditions)
1. Competence (to understand and decide)

2. Voluntaries (in deciding)

Information elements
3. Disclosure (of material information)

4. Recommendation (of a plan)

5. Understanding (of items 3 and 4)

Consent elements
6. Decision (in favor of a plan)

7. Authorization (of the chosen plan)

From Beauchamp TL, Childress JF: Principles of biomedical ethics, ed 6, New York, 2009,
Oxford University Press.

If a patient is unsure, does not understand, or feels pressured

about consenting to the treatment plan, nurses are responsible for
advocating for the patient and communicating this to the physician,
other health care professionals, and administration if necessary.

555
Decision-making capacity
A patient’s ability to make a decision is fundamental to informed
consent. The four components of decision-making capacity are the
ability to: (1) express a choice, either verbally or via another means,
(2) understand the relevant information, (3) appreciate the
importance of the information to one’s own situation, including
risks and benefits of options, and (4) reason about options
consistently with one’s beliefs, values, etc.
Patients are presumed to have decision-making capacity. Lack of
orientation to person and place, medications, psychological
disorders, and cognitive decline may be reasons to question a
patient’s capacity, but they are not sufficient reasons to declare that
a patient cannot make a decision. Health care professionals should
try to maximize the patients’ capacity, such as removing or adding
medications, having discussions during a certain part of the day, or
discussing in the presence of family members.
Decision-making capacity is decision-specific. The more critical
and complex the decision, the higher level of decision-making
capacity required. Capacity should be assessed on an ongoing basis
as decisions need to be made. All health care providers must be
familiar with individual state laws regarding who can legally assess
a patient’s capacity and how it should be documented.

Advance directives
Advance directives refer to a patient’s directions on how to provide
care in the event that the patient becomes unable to make decisions
or verbalize them on his or her own behalf. An advance directive
can be written or verbal and can be in the form of a living will or a
durable power of attorney for health care (DPAHC).
A living will specifies what treatment a patient wants or does not
want in the event that the condition is terminal and the patient
cannot make health care decisions. A DPAHC appoints a person to
make decisions for a patient when the patient cannot make
decisions.
A surrogate decision-maker is someone named in the DPAHC.
When no DPAHC exists, the legal next of kin becomes the surrogate
decision-maker for the patient. If the patient does not have family

556
or a DPAHC, a court-appointed guardian becomes the surrogate
decision-maker. This person is obligated to make choices that the
patient would make if able. If those choices are unknown, the
surrogate decision-maker must try to determine, based on the
patient’s values, what the patient would want.
Interpretation of advance directives can be problematic.
Although many patients express a desire for no “extraordinary
measures,” the meaning of this term can vary. For example, a
ventilator can be considered “extraordinary,” but it is also part of
very common temporary treatments regularly used in critical care.
Despite problems with interpretation, caregivers must responsibly
deal with these ambiguities and seek to honor the patient’s wishes.
Many states are adopting Physician Orders for Life Sustaining
Treatment (POLST, also known as MOST and POST) to clarify
patient choices. POLST forms differ from a living will insofar as the
form becomes a physician order as soon as it is signed. Therefore,
there should be careful deliberation regarding when it is
appropriate for a patient to complete a POLST form.

Confidentiality
Confidentiality in a relationship between a health care provider and
a patient means that one does not identify or expose information
that is not relevant to care. Also, one does not communicate
information gained from a patient except with providers and
decision-maker identified by the patient. Health care provider
codes of ethics generally include provisions for keeping all
information about a patient confidential. Any disclosure of patient
information should be considered very carefully.
The Health Insurance Portability and Accountability Act of 1996
(HIPAA) was mandated by the U.S. Congress to establish a federal
standard regarding confidentiality of specific electronic medical
information. Individual states may have stricter privacy laws.
HIPAA sets the lowest acceptable standard for privacy. State laws
apply over HIPAA.
There are situations in which one is legally obligated to breach
patient confidentiality. These situations include public welfare
risks, sexually transmitted diseases, gunshot wounds, and

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suspected abuse and/or neglect of children, older adults, or
developmentally disabled individuals. HIPAA supports the
disclosure of protected health information when required by law.

Quality of life
A person’s quality of life is based on physical, intellectual,
emotional, and social components. Although improving quality of
life is a primary focus of health care, assessing quality of life is
difficult at best. Numerous studies have demonstrated that health
care providers consistently rate patients’ quality of life lower than
the patients do themselves. Studies also reveal that such judgments
by health care providers do affect care. A life of dependence on
medications, treatments, and care rendered by others is generally
viewed as “not desirable” by many people, including health care
providers, until they are actually faced with the choice between a
dependent life versus death involving a family member or
themselves. Nurses and care team members in critical care should
be aware of all the dynamics underlying choices of patients and
families, because hospitalization reflects a minuscule part of a
patient’s entire life.
A patient’s assessment of quality of life may be compromised
when that patient becomes depressed or newly disabled (e.g.,
stroke, paraplegia, quadriplegia). Although critical care nurses care
for many patients in such situations, it is usually the first time that
this patient or family has faced such life-altering circumstances. The
stress of the situation makes evaluation of quality of life difficult for
them. It is important to provide the patient and family with support
and time before making critical decisions.
Studies indicate that health care providers not only base quality
of life on the patient’s medical condition but also have social
prejudices that affect care. These include biases against older adults,
people with alternative lifestyles, those with alcohol and/or other
substance abuse, and patients with a history of criminal activity.
Comments about perceived flawed decision-making by patients
and families may be passed on to others during nursing reports and
hand-off communications between other team members. Rather
than viewing care with objectivity, the team is at risk of developing

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the plan of care with biases shared in conversation. The team must
regularly evaluate the plan of care and patterns of communication
with the patient and family. Poor communication may undermine
the relationship between the health care team with
patients/significant others and overall success of the
interdisciplinary plan of care.

Truth telling
Respect for patient autonomy and the principles of informed
consent require that patients are told the truth about their medical
condition. There are times when family members or treating
professionals believe that telling patients the truth about their
condition may negatively affect their outcomes. Sometimes called
the therapeutic exception to truth telling, it should be used very
rarely, and only with confirming evidence that telling the truth
would truly harm the patient. Sometimes requests from family
members to withhold medical information from a patient entail
religious and/or cultural considerations. These requests should be
addressed on a case-by-case basis.

Withholding and withdrawing treatment

The acts of withholding (not starting) and withdrawing (stopping)
treatment are considered to have no moral or legal difference.
However, health care providers and patients’ family members often
feel more comfortable withholding than withdrawing treatment.
Once a treatment has been started and is determined to be of no
benefit to the patient, the reasons used to justify withholding
treatment can be used when stopping or withdrawing supportive
measures. One question to ask about withdrawing treatment is, “If
the patient was not already receiving the treatment, would it be
morally acceptable not to initiate it?”
It has been noted that when decisions to withhold resuscitation
(do not resuscitate [DNR] or allow natural death [AND]) have been
made, it seems unclear what other care should be provided. DNR
and AND should not be interpreted as “do not treat.” Many
patients with DNR orders receive critical care interventions,
surgery, and other treatments and then survive to discharge. Once a

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decision has been made to withhold resuscitation, it is important to
clearly define treatments to be withheld or provided.

Assisted suicide and euthanasia

Euthanasia refers to one person killing another person for a
“compassionate” reason, and without causing pain. Assisted
suicide occurs when someone provides a means for a patient to
commit suicide (such as deliberately providing enough medicine
for an overdose) but the patient actually performs the act that
results in death. Although controversy surrounds assisted suicide,
the American Nurses Association (ANA), the American Association
of Critical-Care Nurses (AACN), the American Medical Association
(AMA), and the National Hospice Organization (NHO) explicitly
oppose it. As of 2014, assisted suicide is legal in the states of
Oregon, Montana, Vermont, Washington, and New Mexico, and is
being debated in New Jersey. A ballot that explored legalizing
physician-assisted suicide failed to be accepted by voters in
Massachusetts in 2012. A Gallup Poll conducted in May 2013
revealed that 70% of respondents agreed that when patients and
their families requested assisted suicide, physicians should be
allowed to “end the patient’s life by some painless means.”

Comfort care
Patients who are chronically ill, debilitated, or dying are generally
isolated from and by society, as well as by health care providers.
Health care providers now recognize that pain and depression may
be undertreated in the routine care of patients and while caring for
those who are chronically ill or dying. Health care professionals
express fears of causing dependence, unresponsiveness, and even
death resulting from use of sedatives and narcotic analgesics. When
faced with a patient who is dying, it is unreasonable to worry about
potential dependence on medication. The benefits of analgesics far
outweigh the risks of dependence. Health care providers should try
to provide the maximal pain relief possible while preserving
responsiveness. When that is not possible, many patients and
families choose to accept a decreased responsiveness to ensure that
adequate pain relief is provided for the patient who is dying.

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 Many health care providers voice concerns that giving potent
opioids or opiates to a patient who is dying may actually kill the
patient. This concern is magnified when decisions to withdraw and
withhold treatments have been made simultaneously. Opioid and
opiate analgesics afford a broad therapeutic index and have a long
history of safe use in patients who are medically frail. Many
patients can tolerate increasing doses of these drugs without
adverse respiratory or cardiovascular effects. Doses must be
individualized or titrated based on pain relief using a pain scale. It
is nearly impossible to predict a “perfect dose” of medication, given
that not everyone responds to opioid analgesics the same way.
Even though it is very difficult to determine what amount of
opioid or opiate will cause a person’s death, such medicines can
still be given by applying the principle of double effect. Simplified,
this principle explains that giving narcotics to relieve pain is
morally acceptable, even while knowing that it may also cause the
patient to die sooner. However, growing evidence suggests that
opiates, even at high doses, when given according to the latest
palliative care guidelines, do not hasten death while meeting the
patient’s needs for comfort. The principle of double effect rarely
needs to be used to justify the administration of opioids.

Ethical reasoning
When nurses find themselves in a situation in which they think
something is “wrong,” they should first consider the situation
logically and systematically. By doing this, nurses can defend their
positions rationally and provide ethically as well as medically
sound care.

1. Determine the relevant facts of the case: These facts include the
patient’s medical, mental, and emotional condition, as well as the
current plan of care.

2. Evaluate personal biases: The nurse must consider his or her

personal values and ethical position regarding the situation as it
may affect care. Nurses should consider the values and ethical
positions of all the decision-makers involved.

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3. Identify the problem: Do the facts support your view of the
problem? Would others view the problem differently? If so, how?

4. Consider what ethical values and principles are at stake: Think

about patient autonomy, patient harm (maleficence and
beneficence), justice, and other considerations.

5. Explore options and their consequences: Consider identified

values and principles; explore all plausible options for resolving the
dilemma.

If direct communication with those involved does not resolve the

issue, the bedside nurse should then involve the charge nurse or
unit manager. The medical director’s involvement may also be
beneficial. If assistance is still needed in resolving the dilemma, The
Joint Commission (TJC) requires that health care providers have
access to institutional means for resolving ethical dilemmas (such as
an ethics consultant or committee).

Preventive ethics
Just as it is easier to prevent heart disease than it is to cure it, it is
easier to prevent an ethical conflict than it is to resolve one. When
evaluating actions taken to resolve a dilemma, nurses should
consider how those actions can provide guidance in future
situations. When the bedside nurse first detects a problem,
strategies used in previous, similar situations can be employed to
prevent this situation from developing into a conflict. Many
problems may be resolved after the first few steps of an ethical
inquiry; gathering information and coordinating a patient care
conference involving all relevant people. The interdisciplinary team
should refrain from speculation or gossip and instead openly
communicate with the patient, family, and other members of the
care team about the plan of care. The nurse should promote
discussions regarding the possible patient outcomes, ensuring that
significant others have considered that they could be facing the
patient’s lifelong debility, the possibility of death, and are aware of
the extent of time that may be needed to achieve a reasonable
recovery. Lastly and most importantly, nurses should respect each

562
patient as a person and treat that patient accordingly. The local
ethics committee or team may be consulted for assistance with any
ethical questions or concerns.

Care plans for ethical considerations

Deficient knowledge 
related to medical/nursing interventions related to end-of-life care.
Goals/Outcomes: Before any medical or nursing intervention, the
patient and significant others will verbalize understanding of
explanations and agree to or refuse the intervention.
Knowledge: Treatment Procedure(s).

Teaching: Procedure/treatment

1. Have the patient identify appropriate decision-maker. If the

patient has not executed an advance directive before becoming
unable to speak for themselves, state law dictates the appropriate
chain of decision-makers within the support system.

2. Assess decision-making capacity.

3. Determine that the patient has not been coerced into making
decisions that are not in harmony with their wishes.

4. Accept the patient’s/significant others’ permission for or refusal

of the intervention.

Teaching: Procedure/Treatment; Teaching: Disease Process;

Learning Facilitation.

Deficient knowledge 
related to end-of-life decisions related to available documents.
Goals/Outcomes: The patient will verbalize understanding of the
options available regarding advance directives (living wills and
DPAHC).
Knowledge: Disease Process

Decision-making support

563
1. Provide the patient with information regarding living wills and
DPAHC.

2. Assess understanding of living wills/DPAHC; provide

information as indicated.

3. Identify who is legally empowered as a surrogate decision-

maker.

Health System Guidance; Patient Rights Protection.

Grieving 
related to withholding/withdrawal of treatment; anticipation of loss.
Goals/Outcomes: After intervention, the patient and significant
others communicate feelings and participate in decisions regarding
death and dying.
Grief Resolution.

Anticipatory guidance

1. Assess the patient’s/significant others’ understanding of medical

prognosis and planned interventions.

2. Provide specific information regarding what to expect, what

care/interventions will be given, and what will be
withheld/discontinued; answer questions openly.

3. Allow for significant others to be with the patient during the

dying process if they desire to be present.

4. Provide comfort measures for the patient/significant others.

Grief Work Facilitation; Support System Enhancement;

Active Listening; Family Support; Environmental Management:
Comfort; Spiritual Support; Decision-Making Support.

Patient safety
In 1999, the Institute of Medicine (IOM) released the report, To Err

564
Is Human: Building a Safer Health Care System, which focused
national attention on patient safety. The IOM estimated that
between 44,000 and 98,000 persons die annually as a result of health
care errors and that more than 1 million patients sustain injury as a
result of health care errors. Since its release over 10 years ago,
regulatory agencies, health care facilities, and consumers have
joined together to enhance patient safety with minimal
improvement. The report emphasized that individual clinicians’
competency, hard work, and good intentions were not the cause of
these errors but that the complex health care system with
complicated processes were leading to these errors.
Shifting the goal from eliminating individual errors to reducing
or eliminating the potential for patients to be harmed is significant.
A proactive approach generally yields more globally successful
outcomes. Nurses can contribute significantly to keeping patients
safe by focusing on system-wide improvements, rather than
reacting to adverse events. Nurses spend extensive periods of time
with patients and are placed in roles that require interdisciplinary
care coordination. The coordinative role prompts familiarity with a
variety of hospital processes that may place the patient at risk for
harm. Although it is not an easy journey, health care facilities now
focus attention on designing systems where errors are prevented,
and when they occur, practitioners can easily recognize and recover
from actual and potential errors.

Patient safety standards

Patient safety standards are set by a variety of organizations,
including The Joint Commision (TJC), Centers for Medicare and
Medicaid Services (CMS), Agency for Health care Research and
Quality (AHRQ), National Quality Forum (NQF), Institute for
Healthcare Improvement (IHI), and National Patient Safety
Foundation (NPSF). All agencies have completed extensive research
related to health care quality and provide extensive materials to
support health care providers in performance improvement efforts
to improve patient safety. The descriptions for these agencies are as
follows:

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AHRQ
The mission of the AHRQ (www.AHRQ.gov) is to improve the
quality, safety, efficiency, and effectiveness of health care for all
Americans. The agency’s research assists both consumers and
professionals in making more informed decisions about health care
and facilitate quality improvement in health care services. The
AHRQ was formerly known as the Agency for Health Care Policy
and Research.

CMS
The Medicare and Medicaid programs were signed into law on July
30, 1965. The CMS (www.cms.gov) administers the Medicare
program and jointly with state governments administers the
Medicaid program. The CMS activities are focused to ensure access
to safe and quality health care for beneficiaries.

IHI
The IHI (www.ihi.org) is an independent, nonprofit organization
that strives to lead the improvement of worldwide health care. The
IHI facilitates improvement by augmenting the desire or will for
change, developing concepts for improving patient care, and
helping health care systems put those ideas into action.

• Transforming Care at the Bedside (TCAB) was a national

initiative developed by the Robert Wood Johnson Foundation
(RWJF) in partnership with the IHI to improve hospital patient
care and the hospital work environment by empowering front-
line nurses to implement innovative new practices on their units.

• TCAB emphasized a “bottom-up” approach to

change; unlike the majority of quality programs,
which use a “top-down” strategy.

• The goal was to make the hospital experience safer

and more pleasant for patients and to create time
for nurses to spend more time in direct patient care.

566
• Nurse job satisfaction, retention, and quality of care
were all expected to improve.

• TCAB was a three-phase program lasting from 2003

to 2008. The initial two phases were targeted at
development and pilot testing of the TCAB
approach in 13 select hospitals; the third phase
continued the pilot projects and more broadly
disseminated the model.

NQF
The NQF (www.qualityforum.org) is a not-for-profit organization
focused on improving the quality of health care for all Americans.
Their three-part mission includes setting priorities for performance
improvement, supporting national consensus standards for
performance measurement and public reporting of this information,
and facilitating attainment of national goals by offering education
and outreach programs.

NPSF
The NPSF (www.npsf.org) is an independent, not-for-profit
organization founded in 1997, with a mission to improve safety of
patients and families within the health care system. The NPSF is
committed to a collaborative, interprofessional approach including
key stakeholders. The goal of the group is to unite professional
disciplines with organizational leaders across the continuum of
care.

TJC
The mission of TJC (www.jointcommission.org) is to continuously
improve the safety and quality of care provided to patients through
the provision of health care accreditation. The organization has set
standards that include National Patient Safety Goals and Sentinel

567
Event Alerts. The 2007 Joint Commission Annual Report on Quality
and Safety revealed inadequate communication between health
care providers, or between providers and the patient and family
members, as the main or root cause of at least half the serious
adverse events in hospitals. Other causes included inadequate
assessment of the patient’s condition and poor leadership or
training. TJC has launched several patient safety initiatives
including the “Do Not Use Abbreviation” list, Infection Control,
“Speak Up,” and Universal Protocol (“Time Out”). Many of these
initiatives have risen as a result of sentinel events that have
occurred across the United States. TJC was formerly known as the
Joint Commission on Accreditation of Health care Organizations
(JCAHO).
Websites for additional resources are listed in Table 2-3.

Table 2-3
RESOURCES ON PATIENT SAFETY

Agency for Healthcare Research and Quality www.ahrq.gov

American Hospital Association www.aha.org
Centers for Medicare and Medicaid Services www.cms.hhs.gov
Emergency Care Research Institute www.ecri.org
Institute for Safe Medication Practices www.ismp.org
National Patient Safety Foundation www.npsf.org
National Priorities Partnership www.nationalprioritiespartnership.org
The Institute for Health Care Improvement www.ihi.org
The Joint Commission www.jointcommission.org
Outcome Engenuity Just Culture Community www.justculture.org
WHO Collaborating Centre for Patient Safety Solutions www.ccforpatientsafety.org

Sentinel event alerts

In 1996, TJC established the sentinel event policy, which called for
the identification, reporting, evaluation, and prevention of sentinel
events, defined as any unexpected occurrence involving death or
serious physical or psychological injury or risk thereof (Boxes 2-6
and 2-7). One of the fundamental aspects of the sentinel event
policy is the publication of sentinel event alerts by TJC. Sentinel
event alerts consolidate experiences and “lessons learned” by
accredited health care organizations with the goal of preventing
health care errors in the future. Accredited organizations are
expected to analyze current practices in order to recommend

568
practices outlined by sentinel event alerts and close any
inconsistencies that may exist in practice.

Box 2-6
SENTINEL EVENT POLICY
A sentinel event is an unexpected occurrence involving death or
serious physical or psychological injury, or the risk thereof. The
terms “Sentinel Event” and “Health Care Error” are not
synonymous. Not all sentinel events are caused by a health care
error, nor do all health care errors result in a sentinel event. All
accredited organizations are required to define “sentinel event” for
its own purpose and establish how all sentinel events will be
identified and managed. Accredited organizations’ response to a
“sentinel event” includes conducting a timely, thorough, and
credible root cause analysis, and development of an action plan.
From The Joint Commission. Retrieved from www.jointcommission.org.

Box 2-7
OCCURRENCES THAT ARE SUBJECT TO
REVIEW BY THE JOINT COMMISSION
UNDER THE SENTINEL EVENT POLICY
• Event has resulted in an unanticipated death or major permanent
loss of function, not related to the natural course of the patient’s
illness or underlying condition

OR

• Suicide of any patient receiving care, treatment, and services in a

staffed around-the-clock care setting or within 72 hours of
discharge

• Unanticipated death of a full-term infant

• Abduction of any patient receiving care, treatment, and services

569
• Discharge of an infant to the wrong family

• Rape, assault (leading to death or permanent loss of function), or

homicide of any patient receiving care, treatment, and services

• Rape, assault (leading to death or permanent loss of function), or

homicide of a staff member, licensed independent practitioner,
visitor, or vendor while on site at the health care organization

• Hemolytic transfusion reaction involving administration of blood

or blood products having major blood group incompatibilities

• Invasive procedure, including surgery, on the wrong patient,

wrong site, or wrong procedure

• Unintended retention of a foreign object in a patient after surgery

or other procedure

• Severe neonatal hyperbilirubinemia (bilirubin >30 mg/dL)

• Prolonged fluoroscopy with cumulative dose >1500 rad to a single

field or any delivery of radiotherapy to the wrong body region or
>25% above the planned radiotherapy dose

National patient safety goals

In July 2002, TJC launched the National Patient Safety Goal (NPSG)
program in all accredited facilities. NPSGs are identified and
prioritized by the Patient Safety Advisory Group, which consists of
physicians, nurses, pharmacists, and other clinicians with expertise
in patient safety for all accredited bodies (i.e., acute care facilities,
ambulatory health care, behavioral health, etc.). The Patient Safety
Advisory Group uses data from sentinel events and other
authoritative sources to define NPSGs from year to year. NPSGs are
evaluated each year, and a decision is made to continue current
goals, add to the goal, delete the goal, move the goal to the
accreditations standards, and/or add additional goals (Box 2-8).
Some of the patient safety goals may be moved from the NPSG

570
chapter to the main body of standards in the TJC standards manual
over time. Patient safety goals evolve into the standard of care.

Box 2-8
THE 2014 JOINT COMMISSION NATIONAL
PATIENT SAFETY GOALS
For acute care hospitals
• Identify patients correctly

• Improve staff communication

• Use medicines safely

• Use alarms safely

• Prevent infections

• Identify patient safety risks

• Prevent mistakes in surgery

“Serious reportable events” (SRE) or “never events”

In 2001, Ken Kizer, MD, the former CEO of the NQF, introduced a
list of 21 adverse events that were serious and should never occur.
Over the years, the list has expanded and as of 2011 encompasses 29
events in 7 categories (Box 2-9). Effective October 2008, health care
facilities no longer receive payment from the CMS for any patient
who suffers a “Never Event” while in the care of the facility. The
condition lists included on the CMS “Never Events” and the NQF
“Never Events” overlap but are not identical. Refer to the CMS
website (www.cms.hhs.gov) for current regulations surrounding
payment structure for “Never Events.”

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Box 2-9
“SERIOUS REPORTABLE EVENTS”
(previously known as “Never Events”)
Seven categories
1. Surgical or invasive procedure events

2. Product or device events

3. Patient protections events

4. Care management events

5. Environmental events

6. Radiologic events

7. Potential criminal events

“Patient safety organizations”

Recognizing the need to capture information from adverse events,
Congress passed the Patient Safety and Quality Improvement Act
of 2005 (Patient Safety Act). The act authorized the creation of
Patient Safety Organizations (PSOs) to collect and analyze data
from patient safety events. PSOs include public and private entities
demonstrating the goal to collect, aggregate, and analyze data for
the improvement of patient safety.

Culture of safety
Health care organizations have identified that 95% of health care
errors are directly related to system flaws, whereas only 5% of
health care errors are caused by incompetent or poorly intended
care (Sexton and Thomas, 2004). System flaws are largely related to
flawed communication, which may lead to disjointed or

572
uncoordinated care. Not all members of the team are consistently
aware of key information that, if omitted, may cause harm to the
patient. Therefore, to improve patient safety and address health
care errors, health care organizational culture must value
communication and team collaboration. Focus on these two factors
will result in improved clinical effectiveness and job satisfaction
among health care professionals (Box 2-10).

Box 2-10
COMPONENTS OF SUCCESSFUL
TEAMWORK
• Trust

• Respect

• Collaboration

• Open communication

• Nonpunitive environment

• Clear direction

• Methods to evaluate outcomes and amend processes as needed

• Defined roles and responsibilities of team members

• Atmosphere of respect

• Flattening of caregiver hierarchy

• Methodologies to resolve conflict

• Defined decision-making procedures

From O’Daniel M, Rosenstein AH: Professional communication and team collaboration. In

Hughes RG, editor: Patient safety and quality: an evidence-based handbook for nurses, Rockville,
2008, Agency for Health care Research and Quality.

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Communication
Despite years of training, coaching, and experience, communication
among health care professionals remains a challenge and a leading
root cause of sentinel events in many facilities. In a metaanalysis of
research studies, Seago (2008) found that the evidence remains
mixed on a preferred format for communication strategies. In the
AACN Standards for Establishing and Sustaining a Healthy Work
Environment, Skilled Communication is the first standard
addressed and is the one standard that weaves its way into the five
other standards. The emphasis by the AACN on healthy work
environment standards is a testimony to the importance of excellent
communication skills in acute and critical care (Table 2-4).

Table 2-4
AMERICAN ASSOCIATION OF CRITICAL-CARE NURSES
STANDARDS FOR ESTABLISHING AND SUSTAINING HEALTHY
WORK ENVIRONMENTS

Skilled Nurses must be as proficient in communication skills as they are in clinical

communication skills
True Nurses must be relentless in pursuing and fostering true collaboration
collaboration
Effective Nurses must be valued and committed partners in making policy, directing
decision- and evaluating clinical care, and leading organizational operations
making
Appropriate Staffing must ensure effective match between patient needs and nurse
staffing competencies
Meaningful Nurses must be recognized and must recognize others for the value each
recognition brings to the work of the organization
Authentic Nurse leaders must fully embrace the imperative of a healthy work
leadership environment, authentically live it, and engage others in its achievement
From American Association of Critical-Care Nurses: AACN Advanced critical care
nursing, Aliso Viejo, 2008, American Association of Critical-Care Nurses, p 7.

Nurses and physicians are trained to deliver and receive

communication using different strategies that often lead to a
communication gap between these highly skilled health care
professionals. Nurses tend to communicate in a lengthier manner,
unfolding patient conditions in a narrative and highly descriptive
style (e.g., a patient has an alteration in comfort versus a patient is
in pain). Physicians are taught in medical school to present
“highlights” to their attending physician, giving them only the
needed data to make a clinical decision. Therefore, when a nurse

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communicates with a physician or midlevel practitioner and does
not provide a focused report, key patient care data may not be
communicated effectively.
The power of structured communication methods has been
successfully used in many industries including the airline industry,
nuclear power, and the U.S. Department of Defense. One such
method of structured communications is the Situation-Background-
Assessment-Recommendation (SBAR) documentation format.
Using SBAR is helpful to those who have difficulty with focused,
concise communications. The AHRQ and others across the United
States have advocated for SBAR as a form of standardized
communication among complex health care teams (Table 2-5).

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Table 2-5
STRUCTURED COMMUNICATION: SITUATION-BACKGROUND-
ASSESSMENT-RECOMMENDATION (SBAR)

Before initiating an SBAR conversation, nurses should assess the patient; review the health care
record for appropriate physician or other care provider to call; know the patient’s diagnoses,
procedures, and medical history; read all recent physician progress notes (especially from the
past 12 hours); have available the following clinical data (chart, allergies, medications recently
given, recent diagnostic tests, and patient code status); and, last, take a moment to organize all
data, thoughts, and requests.
S Situation Give your name and unit “Dr. James, I’m Susie, a critical care RN. Mr.
you are calling from, Smith is a 42-year-old currently in radiology for
the patient’s full name, a computed tomography (CT) of the head after a
room number, and motor vehicle crash (MVC). I am the rapid
attending physician response nurse and was called to see him for
name if calling the on- anxiety and shortness of breath.”
call physician.
If the problem is urgent,
please notify the
provider at the
beginning of the call.
The patient’s code status
if appropriate.
B Background The patient’s admission “Mr. Smith was the driver and sustained blunt
diagnosis, admission chest trauma during the MVC approximately 3
date, and pertinent hours ago. There is no significant medical
medical history. history.”
Provide a brief synopsis
of the treatments and
plan of care thus far.
A Assessment Provide a brief “I think Mr. Smith has a pneumothorax on the
description of the right. Breath sounds are absent in the right
problem or primary middle and lower lobes. He is short of breath,
concern. anxious, and tachypneic with an oxygen
If uncertain of the saturation of 88% on 4 liters of oxygen.”
problem, acknowledge
the uncertainty.
Provide clinical data such
as most recent vital
signs, physical
assessment findings,
and clinical changes
specific to the problem
you are calling about.
Provide update of all
pertinent therapies (IVs,
O2, etc.).
R Express what you think “I think Mr. Smith needs more oxygen and a
Recommendation the patient needs to chest tube right away. I have asked the
address the problem. radiology technician to obtain the supplies for
If unclear on what chest tube placement. Can you come to
interventions are radiology to assess the patient for chest tube
needed, acknowledge placement, or is there someone else we should

576
 uncertainty. call?”
If requesting the
practitioner to come
and assess the patient,
clarify with the
practitioner the exact
time frame to expect
their arrival.

TJC recognizes the importance of communication and has woven

communication throughout many of the NPSGs. In particular, TJC
calls for each accredited facility to define a methodology for which
staff communicates information about patient care in a consistent
manner when moving a patient from one practitioner to the care of
a different practitioner. A report at the time of transition of
caregivers is called “hand-off communication” (Box 2-11).

Box 2-11
HAND-OFF COMMUNICATION
Elements of hand-off communication
• Standardized to the situation to which it applies

• When to use certain techniques (i.e., read-back or repeat-back)

• Interactive: Allow for questioning between giver and receiver of

the patient information.

• Contain the most recent information regarding patient care,

treatment, services, condition, and any recent or anticipated
changes.

• Interruptions during hand-offs are limited.

Strategies to improve hand-off communication

• Use clear language and avoid all abbreviations or terms that can
be misinterpreted.

• Use effective communication techniques.

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• Limit interruptions and distractions.

• Provide adequate time for interaction.

• Standardize use of tools to facilitate the interaction, especially

during high-volume, high-distraction times, such as shift-to-shift,
unit-to-unit.

• Use technology to enhance communications—electronic health

care records, portable computers, handheld devices, etc.

Several national programs have been developed to enhance both

intradisciplinary and interdisciplinary communication among
health care providers:

TeamSTEPPS
The AHRQ and the U.S. Department of Defense have partnered
together to develop an evidence-based curriculum and training
program with the goal of promoting patient safety through
improving communication and teamwork skills among health care
professionals (Table 2-6).

Table 2-6
THREE PHASES OF THE TeamSTEPPS IMPLEMENTATION

Phase 1 Determine the organizational readiness for undertaking a TeamSTEPPS-

Assess the based initiative.
Need • Establish an organizational change team.
• Conduct a site assessment.
• Define the problem, challenge, or opportunity for improvement.
• Define the goal of the intervention.
Phase 2 TeamSTEPPS is designed to be customized to the organization.
Planning, Implementation options include use of all tools and strategies across the
Training, and entire organization or a phased-in approach that targets specific units or
Implementation departments, or selected individual tools can be introduced at specific
intervals.
• Define the intervention.
• Develop a plan for determining the interventions and effectiveness.
• Develop an implementation plan.
• Gain leadership commitment to the plan.
• Develop a communication plan.
• Prepare the facility.
• Implement training.

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 Phase 3 Sustain and spread improvements in teamwork performance, clinical
Sustainment processes, and outcomes.
Continual learning and reinforcement of skills on the unit or within the
facility:
• Provide opportunities for clinicians to practice skills.
• Ensure leaders emphasize new skills.
• Provide regular feedback and coaching.
• Celebrate and measure successes.
• Update the plan.

The focus of TeamSTEPPS is to develop competency in four

primary trainable teamwork skills. These skills are leadership,
communication, situation monitoring, and mutual support. When
all individuals of a team possess competency in these skills,
research has demonstrated that the team can enhance three types of
teamwork outcomes: performance, knowledge, and attitudes.

“Just culture”
The creation of a “Just Culture” has been advocated as a means to
enhance the patient safety culture of an organization. A culture of
learning must exist that encourages the reporting of adverse events
and near misses without the fear of retribution. The practitioner
must be offered protection from disciplinary action when they
report injuries, errors, and near misses when personally involved.
This implies that errors are most often not intentional, nor are they
caused by human failures alone. Most are often a series of system
failures that come together at an intersection involving the patient.
The creation of a “Just Culture” does acknowledge that there are
exceptions where health care workers do not have protection.
Protection should not be granted for risky and/or criminal behavior,
for active malfeasance, or in cases in which an injury is not reported
in a timely manner (Box 2-12).

Box 2-12
“JUST CULTURE”
Creation of a culture where clinicians are willing to report errors so
that the process can be analyzed and solutions found, but clinician
responsibility for events is maintained. The culture is not “blame-
free” but blame-appropriate.
From Marx D: Patient safety and the “just culture”: a primer for health care executives, New

579
York, 2001, Columbia University. Retrieved from www.psnet.ah rq.gov/resource.aspx?
resourceID-1582.

Patient/family involvement
Patient and family involvement in the plan of care can be a crucial
element of patient safety, because both are familiar with key
information that, if known, may prevent harm. Understanding of
medications, the health history, and proposed plan of care is vital to
a safe patient care experience. Patients and families may feel
reluctant to challenge, remind, or question their health care
providers. There has been a recent shift within all patient safety
organizations as well as professional organizations to include the
patient in daily rounds, to provide time for daily goal setting, and
to ensure all parts of the treatment plan have been communicated
and are understood. Several national programs have been
developed and promoted to facilitate the involvement of patients
and families in the plan of care (Box 2-13).

Box 2-13
STEPS TO INVOLVING PATIENTS IN
PATIENT SAFETY
Obtain patient feedback through a variety of sources such as
patient satisfaction, focus groups, community groups, hotlines, etc.
Review patient plan of care and daily goals with patients and
their families.
Never separate a patient from their family unless that is desired;
allow patient access 24 hours per day.
Never deny a patient information; a variety of tools can be used
to enhance communication and sharing of information such as
reviewing the health care record; orientation to the unit,
equipment, and team members; wipe boards; sharing clinical
pathways; patient conferences with interdisciplinary team; and
customized discharge instructions.
Encourage patient’s and family’s involvement in care by inviting
them to participate through creative campaigns; staff wearing
buttons asking “Ask me if I’ve washed my hands”; tent cards in

580
patient rooms; brochures and pamphlets educating patients on
how to be involved in their care.
From Roizen M, Oz M, The Joint Commission: You: the smart patient, New York, 2006,
Simon & Schuster Inc. Retrieved from
www.jointcommission.org/GeneralPublic/smart_patient.htm.

Speak up
TJC supports a national campaign urging patients to partner with
their health care provider to prevent health care errors by becoming
involved in their care. The campaign offers a variety of tools
(videos, brochures, artwork, etc.) to educate patients on steps they
can take to partner with health care workers to enhance safe care
delivery. Topics include but are not limited to “Help Avoid
Mistakes with Your Medication,” “Five Things You Can Do to
Prevent Infection,” and “What You Should Know about Pain
Management” (Box 2-14).

Box 2-14
SPEAK UP
Speak up if you have questions or concerns. If you still do not
understand, ask again. It is your body and you have a right to
know.
Pay attention to the care you get. Always make sure you are
getting the right treatments and medicines by the right health care
professionals. Do not assume anything.
Educate yourself about your illness. Learn about the medical
tests you get and your treatment plan.
Ask a trusted family member or friend to be your advocate
(advisor or supporter).
Know what medicines you take and why you take them. Health
care errors are the most common health care mistakes.
Use a hospital, clinic, surgery center, or other type of health care
organization that has been carefully checked out. For example, The
Joint Commission visits hospitals to see if they are meeting The
Joint Commission’s quality standards.
Participate in all decisions about your treatment. You are the
center of the health care team.

581
 From The Joint Commission: Speak Up: help prevent errors in your
care, and speak up: know your rights. Retrieved from
www.jointcommission.org/assets/1/18/speakup_hc.pdf.

Nothing about me, without me

In 2001, the NPSF established a Patient and Family Advisory
Council to provide guidance and expertise on all NSPF’s activities.
One of the fundamental principles advocated by this council is the
philosophy of “Nothing about Me, without Me.” This phrase was
suggested in 1998 by an English midwife at a seminar advocating
that patients should be involved in every step of their health care.
This phrase has now been quoted by key patient safety leaders such
as but not limited to Delbanco, Berwick, Tye, and IOM’s Crossing
the Quality Chasm report and is the title of a consumer book on
health care safety. (Table 2-7 outlines the NPSF recommendations.)

Table 2-7
NATIONAL AGENDA FOR ACTION: PATIENTS AND FAMILIES IN
PATIENT SAFETY: ROAD MAP FOR ACTION

Education and Awareness • Raise public awareness on the definition and frequency
of health care error and patient safety.
• Educate the public on how to aid in safeguarding their
own care.
• Educate health care professionals and leadership about
the importance of the patient/family perspective.
• Raise health care providers’ awareness of the experiences
of patients and their families.
• Raise awareness in the behavioral health community on
health care errors.
• Educate the media.
• Build patient safety and health care error prevention into
all health care professional education curricula.
• Build interactive, interdisciplinary education programs.
• Develop a central clearinghouse and interactive resource
center.
Build a Culture of Patient- and • Teach and encourage effective communication skills.
Family-Centered Patient Safety • Engage leadership in promoting and training providers
in open communication about health care error.
• Empower hospital patient representatives to effectively
advocate.
• Establish patient and family advisory councils.
• Represent patients’ interests on boards and trustees.

582
 • Establish patient safety task forces.
• Create a national forum for state coalitions.
Research • “Bridging the gap.”
• Disclosure.
• Short- and long-term effects of incorporating patients
and families into the system.
• Current patient safety information and resource
landscape for patients and families.
• Posttraumatic stress specific to health care error.
• Team relationships.

Support Services • National resource center and information line.

• Emergency hotline.
• Peer resource counseling.
• Support groups for families and individuals who have
suffered as a result of a health care error.
• Disclosure and communication programs.
• National training programs for hospitals implementing
any of the above programs.
From National Patient Safety Foundation: National agenda for action: patients and
families in patient safety: Nothing about Me, without Me, 2003. Retrieved from
www.npsf.org/pdf/paf/AgendaFamilies.pdf.

High-reliability organizations
High-reliability organizations (HROs) are those that are known to
be complex and risky yet maintain safety and effectiveness. Key
characteristics of HROs include preoccupation with failure and
safety, deference to expertise, sensitivity to operations, commitment
to resilience, and reluctance to simplify. HROs are continually
analyzing and asking questions to prevent failures within the
systems and analyzing how to minimize effects from failures when
and if they occur. The use of the prospective tool of a failure mode
and effects analysis (FMEA) and the use of a retrospective tool such
as a root cause analysis (RCA) have proven valuable to health care
organizations (Table 2-8).

Table 2-8
FAILURE MODE AND EFFECTS ANALYSIS VERSUS ROOT CAUSE
ANALYSIS

Failure Mode and Effects Analysis (FMEA) Root Cause Analysis (RCA)
Proactive analysis of a process or equipment to Retrospective analysis of an event that has
anticipate any potential process or product already occurred; actual failure
failure
Looks forward through a process to identify any Looks back chronologically after a process

583
potential failure points has failed
Multidisciplinary team involvement is key to Multidisciplinary team involvement by all
success who were involved in the failure is key to
success
Three key questions are addressed: Three key questions are addressed:
• How likely is the equipment or process to • What happened?
fail? • Why did it happen?
• What is the significance of the failure? • What can be done to prevent it from
• How likely it is that someone will be able to happening again?
detect this failure?
Analytical tools used: Analytical tools used:
• Flow diagrams of all main and subprocesses • Timeline
• Brainstorm • Cause-and-effect diagrams
• Cause-and-effect diagrams • Frequency plots
• Scatterplots

Patient safety is an ever-changing specialty within health care;

new resources and knowledge are constantly being defined as
research is completed. The provision of safe care delivery is
demanded by regulators, payers, health care providers, and, most
important, the patient. Therefore, it is crucial that every clinician
accept accountability for the provision of a health care environment
that both supports and provides a culture of safe care delivery.

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CHAPTER 3

Trauma
Major trauma
Pathophysiology
Traumatic injuries account for over 5 million deaths worldwide. In
the United States, traumatic injuries are the leading cause of death
for patients between the ages of 1 and 44 years. Traumatic injuries
also account for over 2.6 million hospitalizations each year. Major
trauma occurs when energy is applied to body tissues in excess of
what the tissues are able to absorb. The energy can be in the form of
kinetic, thermal, chemical, electrical, and radiant energy. Trauma
can also occur when the body is deprived of an essential element
such as oxygen or heat. Kinetic energy is the most common cause of
trauma and includes mechanisms such as motor vehicle collisions
(MVCs), falls, and gunshot wounds. Thermal, chemical, electrical,
and radiation energy cause burns. Lack of oxygen occurs in
drowning and hanging injuries. The amount of damage to the tissue
will depend on the amount of force applied, the length of time the
force is applied, and the resiliency of the tissue. Hollow organs tend
to absorb more energy and are injured less frequently than are solid
organs because the organ tissue has more flexibility to withstand
the forces.
The primary pathophysiologic process that occurs with major
trauma is shock. Patients with major trauma are at risk for all types
of shock, but the most common type is hypovolemic shock resulting
from hemorrhage. Hypovolemic shock is usually broken into four
stages that are used to describe the physiologic response to

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hemorrhage and are useful in estimating the amount of blood loss.
All body systems require both oxygen and glucose for cellular
energy production. The classic signs of hypovolemic shock occur
from activation of the central nervous system (CNS). Following
major injury, the CNS triggers a series of reactions to increase
delivery of oxygen and glucose to the cells. Catecholamines
(epinephrine and norepinephrine) and glucocorticoids are released
from the adrenal glands to preserve perfusion to vital organs,
mobilize glycogen stores, increase available glucose and oxygen,
suppress pancreatic insulin secretion, and enhance glucose uptake.
Hyperglycemia is common following major trauma. Glycogen
stores are rapidly depleted (within 24 hours). Without nutrition,
energy is generated from the breakdown of the body or catabolism.
Breakdown of muscle tissue, fat, and viscera creates a negative
nitrogen balance. Subclinical adrenal insufficiency may become
clinically apparent after severe injury.
The posterior pituitary release of antidiuretic hormone promotes
water absorption in the distal renal tubules. Intravascular volume
increases as urinary output decreases. Blood pressure (BP) is
increased by the renin-angiotensin-aldosterone system. Aldosterone
promotes sodium and water reabsorption to increase intravascular
volume, and angiotensin II causes vasoconstriction.
Several factors can alter the patient’s response to blood loss and
must be considered in the resuscitation of these patients. These
factors include the patient’s age, location of injury, type and
severity of the injury, the amount of time that has elapsed since the
injury, prehospital interventions to address blood loss, and
medications taken for chronic conditions, especially anticoagulants
and beta-blockers. Because the patient has many other injuries, the
classic signs of shock may be altered.
The source of the bleeding must be identified and stopped as
soon as possible. The patient must be adequately resuscitated or the
patient is at risk of developing acidosis, coagulopathy, and
hypothermia, which are considered the deadly triad of trauma.
Once these conditions occur, they tend to stimulate each other and
become a vicious cycle that is difficult to break.
Acidosis occurs when the number of red blood cells is reduced
from blood loss and cellular oxygen supply is reduced, resulting in

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end-organ hypoxia caused by inadequate tissue perfusion.
Anaerobic metabolism may ensue if blood and volume replacement
is inadequate to maintain perfusion. While anaerobic metabolism
continues, lactic acid builds up, leading to an increase in the base
deficit and decrease in the pH.
After initial restoration of circulating fluid volume, the body may
develop a hyperdynamic circulatory state to help compensate for
the cellular oxygen debt incurred. This phase should peak at 48 to
72 hours and diminish within 7 to 10 days. The hyperdynamic state
is evidenced by an increased cardiac index (CI), oxygen delivery
(DO2), and oxygen consumption ( O2). Inability to achieve and
maintain a hyperdynamic state is associated with higher mortality
and shock-related organ failure.
Coagulopathy develops from both the consumption of clotting
factors as the body forms clots in an attempt to stop the bleeding of
injured tissues and the dilution of the blood from infusion of
crystalloids and massive transfusion of packed red blood cells
when clotting factors are not replaced. If coagulopathy is not
reversed, disseminated intravascular coagulopathy (DIC) can occur.
Factors contributing to development of DIC include hypotension,
impaired tissue perfusion, and capillary dysfunction leading to
stasis, hypoxemia, and hypothermia.
Multiple factors increase the likelihood of hypothermia in major
trauma. Exposed body surface area or viscera may occur at the
scene of injury or during the initial resuscitation. If blood and
resuscitation fluids are infused without warming, the core body
temperature can drop. Prolonged exposure to cool temperatures in
resuscitation or operative areas can also lower the body
temperature. When present, central thermoregulatory failure
caused by CNS injury, intoxication, or hypoperfusion contributes to
hypothermia. Mild hypothermia can help preserve the function and
viability of major organs, particularly when tissue perfusion is
diminished as a result of injury, shock, or surgical clamping of
arteries. Severe hypothermia creates significant physiologic
alterations, including CNS depression, dysrhythmias, acidosis, and
substantial electrolyte imbalances. Catecholamine infusions are
often ineffective until body temperature approaches 33.9 °C (93
°F).

594
 In patients who sustain major trauma, a widespread
inflammatory response known as systemic inflammatory response
syndrome (SIRS) may be triggered by massive tissue injury and the
presence of foreign bodies such as road dirt, shrapnel, and invasive
medical devices. Inflammatory mediators activate the coagulation
cascade, increased catecholamines stimulate the production and
release of white blood cells, and endothelial dysfunction ensues.
The hemodynamic response and clinical findings are similar to
those with sepsis. (See Chapter 11 for information on SIRS.)
The overwhelming inflammation associated with SIRS may lead
to multiple organ dysfunction syndrome (MODS). MODS is a
leading cause of late mortality in patients with multitrauma,
accounting for approximately 10% of trauma deaths. Inadequate
initial resuscitation or inability to achieve and maintain a
compensatory hyperdynamic state contributes to the development
of organ failure in patients with trauma. Presence of endotoxin,
tumor necrosis factor, interleukin-1, and other inflammatory
mediators cause vasodilation, leading to hypotension. Capillary
dysfunction results in poor cellular circulation and subsequent
tissue destruction. Acidosis, pulmonary compromise, and
circulatory collapse may result. Clinical trials are under way for
therapies to help control inflammatory mediators.

Psychological response
Victims of major trauma sustain life-threatening injuries. The
patient often is aware of the situation and fears death. Even after
the physical condition stabilizes, the patient may have a prolonged
and severe psychological reaction triggered by the trauma called
posttraumatic stress disorder.

Major trauma assessment: Primary

Goal of system assessment
Evaluate and treat life-threatening injuries.

Airway assessment
Determine airway patency.

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• Is the airway open?

• Can the patient maintain the open airway?

• Is there potential for airway obstruction?

• Inspect the face and neck for signs of trauma.

• Look in the mouth for secretions, blood, vomitus, or loose teeth.

• Palpate the neck for crepitus.

Breathing assessment
• Is there adequate air exchange?

• Inspect the chest for signs of trauma that could interfere with
chest excursion.

• Inspect the neck for tracheal deviation and jugular vein distention
(JVD).

• Palpate the chest for crepitus, tenderness over the ribs or sternum.

• Auscultate breath sounds.

• What is the oxygen saturation?

Circulatory assessment
• Observe skin color.

• Is there any obvious bleeding?

• Palpate for pulses, and note strength and rate.

• Palpate skin for temperature.

• Auscultate heart sounds and BP.

Disability assessment

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• Observe the patient’s responsiveness.

• If not alert, does the patient respond to shout or pain?

• Determine the patient’s Glasgow Coma Scale (GCS) score.

• Assess pupils for size, equality, and responsiveness.

Exposure
• Expose the patient to observe for signs of trauma.

• Institute measures to keep the patient warm.

Major trauma assessment: Secondary

Goal of system assessment
Identify all the injuries the patient has incurred.

Vital signs
• Pulse rate may be elevated if the patient has experienced
blood loss or stimulation of the sympathetic nervous system
(SNS) or be decreased in response to elevated intracranial
pressure (ICP) from a severe head injury.

• Respiratory rate (RR) may also be increased as a result of SNS

stimulation or hypoxia, or may be decreased secondary to
decreased level of consciousness (LOC).

• BP will be elevated with SNS stimulation or increased ICP, or

decreased as a result of hemorrhage.

• Temperature may be decreased from exposure to cold

environment and development of hemorrhagic shock.

History
• AMPLE (Allergies, Medications, Past surgeries and pertinent

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 medical conditions, Last meal, Events leading up to incident).

• Last menstrual period for women of child-bearing age.

• Determine the mechanism of the trauma.

• Determine any injury modifiers.

• Identify safety devices used.

• Determine the use of intoxicants.

• Tetanus status.

Head-to-toe assessment
• Observe each area for signs of trauma including bruising,
abrasions, lacerations, and contusions.

• Auscultate for lung sounds, heart sounds, bowel signs, and bruits.

• Palpate each area to feel for crepitus and swelling.

Head and neck

• Observe head for Battle signs (temporal bruising indicating a

basilar skull fracture [BSF]) and raccoon eyes (periorbital
bruising).

• Observe the neck for tracheal alignment, JVD, and expanding

hematomas.

Chest

• Observe for symmetrical chest wall movement.

• Percuss chest for dullness or hyperresonance.

• Palpate over ribs and sternum for tenderness.

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• Listen to breath sounds, noting equality and for any abnormal
breath sounds.

Abdomen and pelvis

• Observe the abdomen for distention.

• Auscultate for bowel sounds.

• Palpate for tenderness and guarding.

Extremities

• Observe for deformities.

• Palpate for crepitus.

• Check neurovascular status of all four extremities.

Posterior surface

• Inspect the posterior surface; if the patient’s spine has not been
cleared, the patient must be logrolled, maintaining spinal
precautions.

• Palpate along the vertebral column, accessing for tenderness,

deformity, or crepitus.

Laboratory work
Blood studies can reveal indications of hypoxia and/or continued
bleeding and developing shock, as well as identify special
circumstances such as pregnancy and intoxication.

• Blood typing and screening or cross-matching.

• Complete blood counts: hemoglobin (Hgb), increased white blood

cell (WBC) count.

• Coagulation studies including platelets, prothrombin time (PT),

partial thromboplastin time (PTT), and international normalized

599
 ratio (INR).

• Serial arterial blood gases (ABGs).

• Electrolytes.

• Urine or serum beta human chorionic gonadotropin for

pregnancy.

• Blood alcohol levels and toxicology screens.

Diagnostic Tests for Major Trauma

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Collaborative management
The primary goals of initial assessment in major trauma are to
identify life-threatening injuries, stop bleeding, and restore
adequate oxygenation to the tissues. Once life-threatening injuries
have been addressed, a secondary assessment is performed to
identify all injuries the patient may have sustained; perform a
thorough organized head-to-toe assessment to minimize the chance
of missing injuries. The following treatments may be required.

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Care priorities

1. Secure a patent airway

A patent airway must be secured when a GCS score of 8 or less
or potential for airway compromise is possible and/or the patient
has respiratory failure requiring mechanical ventilation. The airway
is secured by intubation using a rapid sequence intubation protocol
to prevent patient movement and aspiration during the procedure.
If the patient is unable to be intubated, a surgical airway must be
performed. The surgical airway of choice in an emergency situation
is a cricothyroidotomy. If the cervical spine has not been cleared,
the spine must be stabilized during the procedure by maintaining
constant in-line positioning with gentle traction.

2. Support ventilation
If the patient is not adequately ventilating to maintain oxygen
saturations greater than 93%, the patient should be placed on
supplemental oxygen. Most patients with major trauma will require
supplemental oxygen. Blood loss creates reduced oxygen-carrying
capacity, and tissue demand for oxygen is greatly increased during
the hypermetabolic phase. High-flow oxygen by mask is indicated
initially. Oxygen therapy can be titrated according to ABG and
pulse oximetry values. Mechanical ventilation may be required if
the patient is not ventilating well enough to remove CO2. If the
patient does not have equal breath sounds, a pneumothorax or
hemothorax may have occurred and a tube thoracotomy may be
indicated. Capnography should be considered for patients who are
mechanically ventilated, because it is an early marker of
hypoventilation and apnea.

3. Manage hemorrhage and hypovolemia

Stopping blood loss and restoring adequate circulating blood
volume are imperative. Lack of resuscitation will lead to increasing
oxygen debt and eventually to MODS and death. The goal of
resuscitation in any patient with trauma should be to restore
adequate tissue perfusion. Two or more large-bore (≥16-gauge)
short catheters should be placed to maximize delivery of fluids and
blood. Use of intravenous (IV) tubing with an exceptionally large

602
internal diameter (trauma tubing), absence of stopcocks, and use of
external pressure are techniques used to promote rapid fluid
volume therapy when indicated. In some cases, the patient may
require large central venous access, such as an 8.5 Fr introducer.
When rapid infusion of large amounts of fluid is required, all fluid
should be warmed to body temperature to prevent hypothermia.
Rapid warmer/infuser devices are available to facilitate rapid
administration of blood products. Fluid resuscitation should be
used more judiciously in pediatric and older patients, as well as
patients with significant craniocerebral trauma, who have precise
fluid requirements (see Traumatic Brain Injury).

• Crystalloids: Initial IV fluid used for resuscitation should be an

isotonic electrolyte solution such as 0.9% normal saline (NS) or
lactated Ringer (LR). Other balanced electrolyte solutions such as
Normosol-R pH 7.4 (Hospira) or Plasmalyte-A 7.4 (Baxter) may
be used after initial fluid resuscitation has been completed.

• Rapid bolus: Between 1 and 2 L of rapid IV fluid infusion for

adults and 20 mL/kg for pediatric patients should be initiated in
the prehospital setting. If the patient continues to show signs of
shock after the bolus is complete, blood transfusions should be
considered.

• Packed red blood cells (PRBCs): Typed and cross-matched blood

is ideal, but in the immediate resuscitation period, if cross-
matched blood is not available, type O blood may be used. Once
the patient has been typed, type-specific blood can be used.
Those patients requiring continuous blood transfusions need
reassessment to identify the source of bleeding and definitive
treatment to stop ongoing blood loss. A massive transfusion
protocol may also need to be initiated.

• Massive transfusion is defined as replacement of one half of the

patient’s blood volume at one time or complete replacement of
the patient’s blood volume over 24 hours. A massive transfusion
protocol ensures that the patient receives plasma, platelets, and
cryoprecipitate in addition to PRBCs to prevent the complications
related to coagulopathy. Another concern with massive

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 transfusion is hypocalcemia caused by calcium binding with
citrate in stored PRBCs, resulting in depressed myocardial
contractility, particularly in patients with hypothermia or in those
with impaired liver function. One ampule of 10% calcium
chloride should be considered for administration after every 4
units of PRBCs.

Only O-negative packed cells should be transfused into

prepubescent females and women in childbearing status to prevent
sensitization and future complications during pregnancy.

• Autotransfusion: Shed blood from the patient can be collected,

filtered, and reinfused. Shed blood is captured from chest tube
drainage or the operative field and reinfused immediately.
Various techniques are used to capture and reinfuse the blood.
Advantages of autotransfusion include reduced risk of disease
transmission, absence of incompatibility problems, and
availability. Disadvantages include risk of blood contamination
and presence of naturally occurring factors that promote
anticoagulation.

• Colloids: Resuscitation with colloids has not been shown to

reduce mortality and is not used in the initial resuscitation of
patients with trauma.

• Recombinant factor VIIa (rFVIIa): The standard use of rFVIIa in

the resuscitation of patients with trauma is still controversial.
Some studies have shown a decrease in the number of units of
PRBCs required for patients in hemorrhagic shock but have not
shown a decrease in mortality. More studies are needed to
determine the appropriate indications, contraindications, dosage,
and timing of rFVIIa administration in patients with trauma who
experience hemorrhagic shock.

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4. Identify, prevent, and/or manage hypothermia
Warmed blankets, forced warm air blankets, and warmers for
IV fluids and blood should be used to prevent hypothermia. If the
patient is already hypothermic, more aggressive measures to
rewarm the patient may be necessary. Warming lights are useful for
pediatric patients. Core rewarming measures can include irrigation
of the peritoneal and/or thoracic cavities with warmed saline, use of
heated humidified oxygen, and extracorporeal blood rewarming.

5. Provide gastric decompression

Gastric intubation permits gastric decompression, aids in removal
of gastric contents, and helps to prevent vomiting or possible
aspiration. The nasal route is contraindicated in patients with
basilar skull fractures because of the need to prevent tubes entering
the cranial vault via abnormal openings in the fractured skull. In
patients with facial trauma or suspected or known BSF, gastric
tubes should be placed orally.

6. Ensure urinary drainage

An indwelling catheter is inserted to obtain a specimen for
urinalysis and to monitor hourly urine output. See Renal and
Lower Urinary Tract Trauma for precautions.

7. Prevent infection with antibiotics

Broad-spectrum antibiotics are used initially to prevent infections if
there are open wounds or compound fractures. More specific
antimicrobial agents are used when results from culture and
sensitivity tests are available.

8. Control pain and anxiety with analgesics and anxiolytics

Relief of pain and anxiety are accomplished using IV opiates and
anxiolytics. All IV agents should be carefully titrated to desired
effect, while avoiding respiratory depression, masking injury, or
disguising changes in physiologic variables. Use of the World
Health Organization ladder for pain management and a pain-rating
scale are essential for the trauma population.

9. Provide tetanus prophylaxis

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Tetanus immunoglobulin (TIG) and tetanus-toxoid (Tt) are
considered on the basis of the Centers for Disease Control and
Prevention recommendations (Table 3-1).

Table 3-1
GUIDE TO TETANUS PROPHYLAXIS IN ROUTINE WOUND
MANAGEMENT

*
Such as (but not limited to) wounds contaminated with dirt, feces, soil, and saliva;
puncture wounds; avulsions; and wounds resulting from missiles, crushing, burns,
and frostbite.
†
For children younger than 7 years, DTaP (Diphtheria, Tetanus, and Pertussis) is
recommended; if pertussis vaccine is contraindicated, DT is given. For individuals 7
to 9 years of age or 65 years or older, Td is recommended. For individuals 10 to 64
years, Tdap is preferred to Td if the patient has never received Tdap and has no
contraindication to pertussis vaccine. For individuals 7 years of age or older, if Tdap
is not available or not indicated because of age, Td is preferred to TT.
‡
TIG is human tetanus immunoglobulin. Equine tetanus antitoxin should be used
when TIG is not available.
§
If only three doses of fluid toxoid have been received, a fourth dose of toxoid,
preferably an adsorbed toxoid, should be given. Although licensed, fluid tetanus
toxoid is rarely used.
||
Yes, if it has been 10 years or longer since the last dose.
¶
Yes, if it has been 5 years or longer since the last dose. More frequent boosters are
not needed and can accentuate side effects.
From Centers for Disease Control and Prevention: Manual for the surveillance of
vaccine-preventable diseases, Atlanta, 2008, Centers for Disease Control and
Prevention.

10. Initiate nutrition support therapy

Infection and sepsis contribute to the negative nitrogen state and
increased metabolic needs. Prompt initiation of nutrition therapy is
essential for rapid healing and prevention of complications.

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Parenteral nutrition or postpyloric (jejunal) feedings may be used if
postoperative ileus or injury to the gastrointestinal (GI) tract is
present. For more information, see Nutrition Support.

11. Facilitate evaluation for surgery

Need for surgery depends on the type and extent of injuries. The
surgical team is coordinated by the trauma surgeon. When several
specialty surgeons are required for various injuries, the order of
surgeries is coordinated carefully to preserve life and limit the
potential for disability.

Care plans: Major trauma

Ineffective tissue perfusion, cardiopulmonary 
related to substantial loss of blood volume.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
exhibits adequate tissue perfusion, as evidenced by BP within
normal limits for the patient, heart rate (HR) 60 to 100 beats per
minute (bpm), normal sinus rhythm on electrocardiogram (ECG),
peripheral pulses greater than 2+ on a 0-to-4+ scale, warm and dry
skin, hourly urine output ≥0.5 mL/kg, base deficit between −2 and
+2 mmol/L, serum lactate less than 2.2 mmol/L, measured cardiac
output (CO) 4 to 7 L/min, central venous pressure (CVP) or
pulmonary artery wedge pressure (PAWP) 6 to 12 mm Hg, and
patient awake, alert, and oriented.
Blood Loss Severity.

Shock management: Volume

1. Monitor for sudden blood loss or persistent bleeding.

2. Prevent blood volume loss (e.g., apply pressure to site of

bleeding).

3. Monitor for fall in systolic BP to less than 90 mm Hg or a fall of 30

mm Hg in patients who are hypertensive.

4. Monitor for signs/symptoms of hypovolemic shock (e.g.,

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increased thirst, increased HR, increased systemic vascular
resistance [SVR], decreased urinary output [urine output],
decreased bowel sounds, decreased peripheral perfusion, altered
mental status, or altered respirations).

5. Position the patient for optimal perfusion.

6. Insert and maintain large-bore IV access.

7. Administer warmed IV fluids, such as isotonic crystalloids, as

indicated.

8. Administer blood products (e.g., PRBCs, platelets, plasma, and

cryoprecipitate), as appropriate.

9. Administer oxygen and/or mechanical ventilation, as

appropriate.

10. Draw ABGs and monitor tissue oxygenation.

11. Monitor Hgb/hematocrit (Hct) level.

12. Monitor coagulation studies, including INR, PT, PTT,

fibrinogen, fibrin degradation/split products, and platelets.

13. Monitor laboratory studies (e.g., serum lactate, acid-base

balance, metabolic profiles, and electrolytes).

14. Monitor fluid status, including intake and output, as

appropriate.

15. Monitor for clinical signs and symptoms of overhydration/fluid

excess.

Vital signs monitoring

1. Monitor BP, pulse, temperature, and respiratory status, as

appropriate.

2. Note trends and wide fluctuations in BP.

608
3. Auscultate BPs in both arms and compare, as appropriate.

4. Initiate and maintain a continuous temperature monitoring

device, as appropriate.

5. Monitor for and report signs and symptoms of hypothermia and

hyperthermia.

6. Monitor the presence and quality of pulses.

7. Monitor cardiac rate and rhythm.

Acid-base monitoring

1. Examine the pH level in conjunction with the Paco2 and HCO3

levels to determine whether the acidosis/alkalosis is compensated
or uncompensated.

2. Monitor for an increase in the anion gap (greater than 14 mEq/L),

signaling an increased production or decreased excretion of acid
products.

3. Monitor base excess/base deficit levels.

4. Monitor arterial lactate levels.

5. Monitor for elevated chloride levels with large volumes of NS.

Impaired gas exchange 

related to airway obstruction, inadequate oxygenation
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate gas exchange, as evidenced by PaO2 ≥80 mm Hg, Paco2
35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal breath sounds,
and absence of adventitious breath sounds. RR is 12 to 20
breaths/min with normal pattern and depth.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation.

Airway management

609
1. Assess for patent airway; if snoring, crowing, or strained
respirations are present, indicative of partial or full airway
obstruction, open airway using chin-lift or jaw-thrust technique and
maintain cervical spine alignment.

2. Insert oral or nasopharyngeal airway if the patient cannot

maintain patent airway; if severely distressed, the patient may
require endotracheal intubation.

3. When the spine is cleared, position the patient to alleviate

dyspnea and ensure maximal ventilation, generally in a sitting
inclined position unless severe hypotension is present.

4. Clear secretions from airway by having the patient cough

vigorously, or provide nasotracheal, oropharyngeal, or
endotracheal tube suctioning as needed.

5. Have the patient breathe slowly or manually ventilate with bag-

valve-mask device slowly and deeply between coughing or
suctioning attempts.

6. Assist with use of incentive spirometer, as appropriate.

7. Turn the patient every 2 hours if immobile. Encourage the patient

to turn self, or get out of bed as much as tolerated if the patient is
able.

8. Provide chest physical therapy as appropriate, if other methods

of secretion removal are ineffective.

Oxygen therapy

1. Provide humidity in oxygen.

2. Administer supplemental oxygen using liter flow and device as

ordered.

3. Restrict the patient and visitors from smoking while oxygen is in

use.

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4. Document pulse oximetry with oxygen liter flow in place at time
of reading as ordered. Oxygen is a drug; the dose of the drug must
be associated with the oxygen saturation reading or the reading is
meaningless.

5. Obtain ABGs if the patient experiences behavioral changes or

respiratory distress to check for hypoxemia or hypercapnia.

6. Monitor for changes in chest radiograph and breath sounds

indicative of oxygen toxicity and absorption atelectasis in patients
receiving higher concentrations of oxygen (Fio2 greater than 45%)
for longer than 24 hours. The higher the oxygen concentration, the
greater the chance of toxicity.

7. Monitor for skin breakdown where oxygen devices are in contact

with skin, such as nares and around edges of mask devices.

8. Provide oxygen therapy during transportation and when the

patient gets out of bed.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs

of increased work of breathing such as use of accessory muscles or
retraction of intercostal or supraclavicular muscles.

3. Ensure airway is not obstructed by tongue (snoring or choking-

type respirations) and monitor breathing patterns. New patterns
that impair ventilation should be managed as appropriate for
setting.

4. Note that trachea remains midline, because deviation may

indicate that the patient has a tension pneumothorax.

5. Auscultate breath sounds following administration of respiratory

medications to assess for improvement.

6. Note changes in oxygen saturation (SaO2), pulse oximetry (SpO2),

611
end-tidal CO2 (etco2), and ABGs as appropriate.

7. Monitor for dyspnea and note causative activities/events.

8. If increased restlessness or unusual somnolence occurs, evaluate

the patient for hypoxemia and hypercapnia as appropriate.

9. Monitor chest x-ray reports as new films become available.

Acute pain 
related to physical injury
Goals/Outcomes: Within 30 minutes of intervention, the patient’s
subjective evaluation of discomfort improves, as documented by a
pain scale. Nonverbal indicators, such as grimacing, are absent.
Vital signs return to baseline. ECG changes present during event
resolve.
Comfort Status: Physical, Pain Level.

Pain management

1. Assess and document the location and intensity of the pain.

Devise a pain scale with the patient, rating discomfort from 0 (no
pain) to 10 or any system that assists in objectively reporting pain
level. If intubated, use a physiologic scale such as adult nonverbal
pain scale or the FLACC (Face, Legs, Activity, Cry, Consolability)
scale.

2. Determine the needed frequency of making an assessment of

patient comfort and implement monitoring plan.

3. Provide the patient with optimal pain relief with prescribed

analgesics.

4. Ensure pretreatment analgesia and/or nonpharmacologic

strategies before painful procedures.

5. Evaluate the effectiveness of the pain control measures used

through ongoing assessment of the pain experience.

612
Hypothermia 
related to altered temperature regulation
Goals/Outcomes: The patient will maintain a normal body
temperature greater than 36° C (96.8° F).
Thermoregulation.

Temperature regulation

1. Monitor temperature at least every 2 hours, as appropriate.

2. Institute a continuous core temperature monitoring device, as

appropriate.

3. Monitor BP, pulse, and respirations, as appropriate.

4. Monitor skin color and temperature.

Treatment for hypothermia

1. Cover with warmed blankets, as appropriate.

2. Administer warmed (37° C to 40° C) IV fluids, as appropriate.

3. Administer heated oxygen, as appropriate.

4. Infuse all whole blood and PRBCs through a warmer.

5. Institute active core rewarming techniques (e.g., colonic lavage,

hemodialysis, peritoneal dialysis, and extracorporeal blood
rewarming), as appropriate.

6. Minimize exposure of the patient.

7. Keep the room temperature comfortable for the patient.

Posttrauma syndrome 
related to inadequate coping ability resulting from major physical and
emotional stress.
Goals/Outcomes: The patient exhibits appropriate coping
mechanism and reduced anxiety, as evidenced by decreased

613
restlessness, pulse rate 60 to 100 bpm, RR 12 to 20 breaths per
minute, and decrease in the amount of pain medication requested.
Anxiety Level; Coping.

Anxiety reduction

1. Explain all procedures, including sensations likely to be

experienced during the procedure.

2. Provide factual information concerning diagnosis, treatment, and

prognosis.

3. Encourage the family to stay with the patient, as appropriate.

4. Create an atmosphere to facilitate trust.

5. Control stimuli, as appropriate for patient needs.

6. Determine the patient’s decision-making ability.

7. Administer medications to reduce anxiety, as appropriate.

8. Assess for verbal and nonverbal signs of anxiety.

9. Support the use of appropriate defense mechanisms.

Coping enhancement

1. Provide an atmosphere of acceptance.

2. Provide the patient with realistic choices about certain aspects of

care.

3. Acknowledge the patient’s spiritual/cultural background.

4. Encourage the use of spiritual resources, if desired.

5. Encourage verbalization of feelings, perceptions, and fears.

6. Assist the patient to identify available social supports.

614
7. Encourage family involvement, as appropriate.

Emotional support

1. Make supportive and empathetic statements.

2. Encourage the patient to express feelings of anxiety, anger, or

sadness.

3. Refer for counseling, as appropriate.

Additional nursing diagnoses

Also see nursing diagnoses and interventions as appropriate in
Nutrition Support, Mechanical Ventilation, Hemodynamic
Monitoring, Prolonged Immobility, and Emotional and Spiritual
Support of the Patient and Significant Others (Chapters 1 and 2).

Abdominal trauma
Pathophysiology
The patient with abdominal injury can be the most challenging and
difficult to manage. Forces may be blunt or penetrating and the
organs are either solid (pancreas, kidneys, adrenal glands, liver,
and spleen) or hollow (stomach, small bowel, and colon).This
patient may have subtle signs of internal hemorrhage, which can be
a major contributor to the increase in mortality and morbidity noted
after the initial injury has been managed. The severity of abdominal
injury is related to the type of force applied to the organs
suspended inside the peritoneum. Motor vehicle collision (MVC),
either auto-auto or auto-pedestrian, is the most common cause of
blunt abdominal trauma worldwide.

Blunt trauma
There are three mechanisms of action with blunt trauma.

1. Rapid deceleration: On impact, the different organs that reside

615
inside the abdominal cavity move at different speeds depending on
their density. This creates what is known as shear force, that is, two
different directions applied to the organ, usually at the point of
attachment, causing injury to other organs such as the aorta.

2. Crush of contents between the walls: Solid viscera are

exceptionally affected when compression occurs from the anterior
abdominal wall and the spine or posterior cage.

3. External compression force: The force of external traumatic

impact may increase the organ and abdominal pressures to such a
degree that the hollow organs rupture.

Mechanisms of action with penetrating injury

External penetration to the abdominal cavity can be caused by any
missile or object that intrudes into the abdominal cavity.
Penetrating forces injure the organ(s) in the direct path of the
instrument or missile, and shock waves from high-velocity
weapons (e.g., high-powered rifles) may also injure adjacent
organs. Stab wounds are generally easier to manage than gunshot
wounds but may be fatal if a major blood vessel (aorta) or highly
vascular organ (liver) is penetrated. The three most common
injuries associated with penetrating abdominal trauma are those to
the small bowel, liver, and colon. With blunt trauma, injuries to the
liver, spleen, and kidney are more common. Undetected mesenteric
damage may cause compromised blood flow, with eventual bowel
infarction. Perforations or contusions result in release of bacteria
and intestinal contents into the abdominal cavity, causing serious
infection.
The abdomen can be divided into four areas: (1) intrathoracic
abdomen, (2) pelvic abdomen, (3) retroperitoneal abdomen, and (4)
true abdomen.

Intrathoracic abdomen
The upper abdomen resides beneath the rib cage and includes the
diaphragm, liver, spleen, and stomach.

• Diaphragm: Commonly injured at the left posterior portion after

616
 blunt trauma, the tear is best visualized by chest radiograph,
which reveals an elevation of the left hemidiaphragm and air
under the diaphragm.

• Spleen: The organ most frequently injured after blunt trauma.

Massive hemorrhage from splenic injury is common. Damage to
the spleen may occur with the most trivial of injuries, thus index
of suspicion should be high. Splenic injury is often associated
with hepatic or pancreatic injury because of the close proximity
of these organs. Splenectomy is the treatment of choice for major
spleen injuries. Minor splenic injuries may be managed with
direct suture techniques.

• Liver: Most frequently involved in penetrating trauma (80%)

because of its large size and location, the liver is less often
affected by blunt injury (20%). Control of bleeding and bile
drainage is the priority with hepatic injury. Mortality from liver
injuries is approximately 10%. In most patients, bleeding from a
liver injury can be controlled, such as with perihepatic packing.
Approximately 5% of injuries require packing for bleeds. Major
arterial bleeding from the liver parenchyma will require further
attention. Biliary tree injuries may require surgical repair and are
associated with liver injury. The patient may be asymptomatic or
have mild to moderate abdominal discomfort with biliary tree
injury.

Pelvic abdomen
As defined by bony pelvis, this includes the urinary bladder,
urethra, rectum, small intestine, and, in females, the ovaries,
fallopian tubes, and uterus. Diagnosis is difficult because many of
these injuries are extraperitoneal (outside the peritoneal cavity).

Retroperitoneal abdomen
This includes the kidneys, ureters, pancreas, aorta, and vena cava.
Evaluation may require a computed tomography (CT) scan,
angiography, and an IV pyelogram (IVP).

• Retroperitoneal vessels: Tears in retroperitoneal vessels

617
 associated with pelvic fractures or damage to retroperitoneal
organs (pancreas, duodenum, and kidney) can cause bleeding
into the retroperitoneum.

• Although the retroperitoneal space can accommodate up to 4 L of

blood, detection of retroperitoneal hematomas is difficult and
sophisticated diagnostic techniques may be required.

True abdomen
This includes the small and large intestines, uterus (when
enlarged), and bladder (when distended). Perforation usually
presents with peritonitis such as pain and tenderness.

• Colon: Injury is most frequently caused by penetrating forces,

although lap belts, direct blows, and other blunt forces cause a
small percentage of colonic injuries. Because of the high bacterial
content, infection is even more a concern than it is with small
bowel injury. Most patients with significant colon injuries require
a temporary colostomy.

• Undetected mesenteric damage: May cause compromised

blood flow, with eventual bowel infarction. Perforations or
contusions result in release of bacteria and intestinal contents into
the abdominal cavity, causing serious infection.

• Pelvis: See Renal and Lower Urinary Tract Trauma (Chapter 3).

Occasionally the lower portion of the esophagus is involved in

penetrating trauma. The stomach is usually not injured with blunt
trauma because it is flexible and readily displaced, but it may be
injured by direct penetration. Injury to either the esophagus or
stomach results in the escape of irritating gastric fluids as a result of
gastric perforation and the release of free air below the level of the
diaphragm. Esophageal injuries are often associated with thoracic
injuries. Once hemorrhage has been controlled, attention is turned
to prevention of further contamination by controlling spillage of gut
contents.
Traumatic pancreatic or duodenal injury is uncommon but is
associated with high morbidity and mortality. These injuries are

618
difficult to detect and may be associated with massive injury to
nearby organs, prompting spillage of irritating fluids, activated
enzymes, and bile, which augments the inflammatory response.
Pancreatic injury is rare; however, the pancreas can be contused or
lacerated. Clinical indicators of injury to these retroperitoneal
organs may not be obvious for several hours.
Injuries to major vessels such as the abdominal aorta and inferior
vena cava most often are caused by penetrating trauma but also
occur with deceleration injury. Hepatic vein injuries are frequently
associated with juxtahepatic vena cava injury and result in rapid
hemorrhage. Blood loss after major vascular injury is massive.
Survival depends on rapid transport to a trauma center and
immediate surgical intervention.

Assessment: Abdominal trauma

Goal of system assessment
Rapidly evaluate for significant primary and secondary injuries (for
all systems) while performing basic and advanced trauma life
support. Airway, breathing, circulation, disability, and exposure are
the structural components of all trauma assessment.

In a patient who is unstable, immediate identification of free

intraabdominal fluid by Focused Assessment with Sonography for
Trauma (FAST) examination or a diagnostic peritoneal lavage
(DPL) is imperative and supports decisions to move straight to the
operating room.

In the traditional perspective of the “Golden Hour of

Trauma” (period of time immediately after traumatic injury in
which rapid intervention may prevent death), the American College
of Surgeons guideline recommends that rapid assessment of
hemorrhage includes aggressive volume resuscitation.

History and risk factors

619
First and foremost, it is essential to establish how the injury
occurred (Box 3-1). Details regarding circumstances of the accident
and mechanism of injury are invaluable in detecting the presence of
specific injuries. Second, allergies, medications, and last meal eaten
will play an important role in the maintenance of good
resuscitation. Other information, previous abdominal surgeries,
and use of safety restraints (if appropriate) should be noted. Hollow
viscous injury is often missed but is more likely to be present when
a contusion is seen on the abdomen. Medical information including
current medications and last Tt immunization should be obtained.
The history is sometimes difficult to obtain because of alcohol or
drug intoxication, head injury, breathing difficulties, or impaired
cerebral perfusion. Family members and emergency personnel may
be valuable sources of information.

Vital signs
Assess for impending hemorrhagic shock: Pulse greater than
100 bpm, decreased pulse pressure, oliguria: blood loss 750 to 1500
mL; pulse greater than 120 bpm, hypotension, oliguria, confusion:
blood loss 1500 to 2000 mL; pulse greater than 140 bpm, severe
oliguria, lethargy: blood loss greater than 2000 mL.

HIGH ALERT!
Persistent Tachycardia
Persistent tachycardia: Should always be considered a clue to
tissue hypoxia. While the neuroendocrine response ensues,
persistent tachycardia indicates a response to tissue
hypermetabolism and inadequate resuscitation.

• Hypotension: Presence of hypotension is a sign of impending

doom, but the absence of hypotension does not always accurately
reflect an absence of hemorrhage. After an injury, a profound
neuroendocrine response ensues to activate the beta receptors
(sinus node and ventricular contractile tissue), the alpha
receptors (smooth muscle in the arteries), and the renal tubules

620
 (promoting preservation of fluid), resulting in significant
tachycardia, profound vasoconstriction, and progressive oliguria.
These responses may mask the severity of hemorrhage. Patients
on alpha- or beta-antagonists or those with acute spinal cord
injuries (above C5) will not manifest these responses and
therefore will have few compensatory mechanisms.

• Pulse pressure: This measure may be effectively used to

determine the amount of volume in the arteries (systolic minus
diastolic BP, normal greater than 40 mm Hg). Pulse pressure
generally correlates with the volume ejected by the left ventricle
and therefore is a valuable tool to evaluate the volume in the
vascular bed. Presence of pulsus paradoxus (Box 3-2) may be
visualized with either the invasive arterial pressure trace or the
plethysmograph of the pulse oximeter and is an invaluable tool
in evaluating arterial volume.

Box 3-2
MEASURING PARADOXICAL PULSE
• After placing blood pressure (BP) cuff on the patient, inflate it
above the known systolic BP. Instruct the patient to breathe
normally.

• While slowly deflating the cuff, auscultate BP.

• Listen for the first Korotkoff sound, which will occur during
expiration with cardiac tamponade.

• Note the manometer reading when the first sound occurs, and
continue to deflate the cuff slowly until Korotkoff sounds are
audible throughout inspiration and expiration.

• Record the difference in millimeters of mercury between the first

and second sounds. This is the pulsus paradoxus.

621
Observation and subjective/objective symptoms
• Inspection of all surfaces of trunk, head, neck, and extremities,
including anterior lateral and posterior exposure, with notation
of all penetrating wounds, contusions, tenderness, ecchymosis, or
other marks and indicators. Multiple wounds may represent
entrance or exit wounds but do not eliminate the possibility of
objects that may remain internally.

• Kehr sign (left shoulder pain caused by splenic bleeding) may

also be noted, especially when the patient is recumbent.

• Nausea and vomiting may occur, and the conscious patient who
has sustained blood loss often complains of thirst; an early sign of
hemorrhagic shock.

• Preoperative pain is anticipated and is a vital diagnostic aid. The

nature of postoperative pain can also be important. Incisional and
some visceral pain can be anticipated, but intense or prolonged
pain, especially when accompanied by other peritoneal signs, can
signal bleeding, bowel infarction, infection, or other
complications.

It is important to note that damage to retroperitoneal

organs such as the pancreas and duodenum may not cause
significant signs and symptoms for 6 to 12 hours or longer.
Relatively slow bleeding from abdominal viscera may not be
clinically apparent for 12 hours or longer after the initial injury. In
addition, the nurse should be aware that complications such as
bowel obstruction caused by adhesions or narrowing of the bowel
wall from localized ischemia, inflammation, or hematoma may
develop days or weeks after the traumatic event. The need for
vigilant observation in the care of these patients cannot be
overemphasized.

622
Inspection
• Abrasions and ecchymoses may indicate underlying injury. The
absence of ecchymosis does not exclude major abdominal trauma
and massive internal bleeding. In the event of gunshot wounds,
entrance and exit (if present) wounds should be identified.

• Ecchymosis over the left upper quadrant suggests splenic

rupture, and erythema and ecchymosis across the lower portion
of the abdomen suggest intestinal injury caused by lap belts.

• Grey-Turner sign, a bluish discoloration of the flank, may indicate

retroperitoneal bleeding from the pancreas, duodenum, vena
cava, aorta, or kidneys.

• Cullen sign, a bluish discoloration around the umbilicus, may be

present with intraperitoneal bleeding from the liver or spleen.
Ecchymosis may take hours to days to develop, depending on the
rate of blood loss.

Auscultation
It is important to auscultate before palpation and percussion,
because these maneuvers can stimulate the bowel and confound
assessment findings.

• Bowel sounds: These are likely to be decreased or absent with

abdominal organ injury or intraperitoneal bleeding. The presence
of bowel sounds, however, does not exclude substantial
abdominal injury. Immediately after injury, bowel sounds may be
present, even with major organ injury. Bowel sounds should be
auscultated in each quadrant every 1 to 2 hours in patients with
suspected abdominal injury. Absence of bowel sounds is
expected immediately after surgery. Failure to auscultate bowel
sounds within 24 to 48 hours after surgery suggests ileus,
possibly caused by continued bleeding, peritonitis, or bowel
infarction.

Palpation

623
• Tenderness to light palpation suggests pain from superficial or
abdominal wall lesions, such as that occurring with seat belt
contusions.

• Deep palpation may reveal a mass, which may indicate a

hematoma. Internal injury with bleeding or release of GI contents
into the peritoneum results in peritoneal irritation and certain
assessment findings. Box 3-3 describes signs and symptoms that
suggest peritoneal irritation.

• Subcutaneous emphysema of the abdominal wall is usually

caused by thoracic injury but also may be produced by bowel
rupture.

• Measurements of abdominal girth may be helpful in identifying

increases in girth attributable to gas, blood, or fluid. Visual
evaluation of abdominal distention is a late and unreliable sign of
bleeding.

• Peritoneal signs (pain, guarding, rebound tenderness) or

abdominal distention in a patient who is unconscious
requires immediate evaluation in either case.

HIGH ALERT!
Flank (Grey-Turner sign) or umbilical (Cullen sign) ecchymosis
may be delayed several hours to days in patients with
retroperitoneal hemorrhage. Based on the index of suspicion,
persistent hypotension is always investigated with ultrasound or
radiography.

Box 3-3
SIGNS AND SYMPTOMS THAT SUGGEST
PERITONEAL IRRITATION
• Generalized abdominal pain and tenderness.

624
• Involuntary guarding of the abdomen.

• Abdominal wall rigidity.

• Rebound tenderness.

• Abdominal pain with movement or coughing.

• Decreased or absent bowel sounds.

• Mild tenderness to severe abdominal pain may be present, with

the pain either localized to the site of injury or diffuse.

• Blood or fluid collection within the peritoneum causes irritation

that results in involuntary guarding, rigidity, and rebound
tenderness.

• Fluid or air under the diaphragm may cause referred shoulder

pain.

Percussion
• Unusually large areas of dullness may be percussed over
ruptured blood-filled organs. For example, a fixed area of
dullness in the left upper quadrant suggests a ruptured spleen.
An absence (or decrease in the size) of liver dullness may be
caused by free air below the diaphragm, a consequence of hollow
viscous perforation, or, in unusual cases, displacement of the
liver through a ruptured diaphragm.

• The presence of tympany suggests gas; dullness suggests that the

enlargement is caused by blood or fluid.

HIGH ALERT!
Massive intestinal edema is common following laparotomy
and prolonged shock. Inflammatory response, neuroendocrine
stimulation, aggressive crystalloid resuscitation, bowel handling,
intraabdominal packing, and retroperitoneal hematomas may

625
cause a delay in abdominal closure. If the abdomen is closed, the
intraabdominal volume may compress arteries, capillaries, the
bladder, and the ureters. This compartment hypertension
(abdominal compartment syndrome) may cause significant
hypotension, oliguria, and base deficit that will be difficult to
combat. (See Abdominal Hypertension and Abdominal
Compartment Syndrome, Chapter 10).

Diagnostic Evaluation of Abdominal Trauma

Collaborative management
The initial focus should be stabilization and supporting
hemodynamics, but the highest priority is to diagnose and repair

626
causes of hemorrhage. Timely provision of needed surgery,
preferably in a trauma center, is the crucial factor impacting
survival. Prolonged hypovolemia and shock result in organ
ischemia and ultimately failure. See Major Trauma (Chapter 3)
Acute Respiratory Distress Syndrome (Chapter 4) Cardiogenic
Shock (Chapter 5), Acute Renal Failure (Chapter 6), and Hepatic
Failure (Chapter 9).

Care priorities

1. Identify and manage hypothermia

Patients with trauma are often profoundly hypothermic on arrival
in the emergency department as a result of inadequate protection,
IV fluid administration, ongoing blood loss, and environmental
exposure. Hemorrhagic shock leads to decreased cellular perfusion
and oxygenation and impoverished heat production. Hypothermia
interferes with coagulation and platelet aggregation, and therefore
exacerbates hemorrhage.

• Remove all wet clothing and make sure the patient is dry. The
patient should be actively warmed with blankets, air-warming
devices, or possibly continuous arteriovenous warming
techniques. A simple method is to cover all extremities and the
abdomen with plastic (e.g., blue side of underpads or trash bags)
to trap all heat produced.

2. Provide oxygen therapy to manage hypoxia

Abdominal injury may result in poor ventilatory efforts caused by
pain or compression of thoracic structures. High-flow supplemental
oxygen is indicated initially and then titrated according to ABG
values. Mechanical ventilation may be necessary.

3. Manage hypovolemia and anemia

Because massive blood loss is associated with most abdominal
injuries, immediate volume resuscitation is crucial. Initially, LR
or a similar balanced salt solution is given. Colloid solutions may be
helpful in the postoperative period if there are low filling pressures
and evidence of decreased plasma oncotic pressure. Typed and

627
cross-matched fresh blood is the optimal fluid for replacement of
large blood losses. However, because fresh whole blood is rarely
available, a combination of packed cells and fresh-frozen plasma is
often used. Overaggressive use of colloids and PRBCs may increase
third spacing and SIRS. (See Major Trauma for more information.)

• Indication for immediate blood transfusion: Ongoing blood loss

indicates hemodynamic instability despite the administration of 2
L of fluid to adult patients.

• Acidosis: Hemorrhagic shock reduces perfusion, resulting in

hypoxemia, anaerobic metabolism, and lactic acidosis. The
compensatory vasoconstrictive response shunts blood to the
heart, lungs, and brain from the skin, muscles, and abdominal
organs. Base deficit or lactate levels should be used to guide fluid
resuscitation, ventilation, and BP support.

• Coagulopathy: Hypothermia, acidosis, and massive blood

transfusion all lead to coagulopathy. The top priority is to stop
the bleeding. Coagulopathy is treated by the administration of
fresh-frozen plasma, factor VII, cryoprecipitate, and platelets, and
correcting hypothermia and acidosis. If bleeding persists,
consider vasopressin infusion, which causes vasoconstriction and
calcium chloride.

4. Consider surgery for penetrating abdominal injuries

• Indication for emergency laparotomy:

• Signs of peritonitis.

• Uncontrolled shock or hemorrhage.

• Clinical deterioration during observation.

• Positive hemoperitoneum findings with FAST

(Focused Assessment with Sonography for Trauma)

628
 or DPL (diagnostic peritoneal lavage) examinations.

• Removing penetrating objects can result in additional injury; thus,

attempts at removal should be made only under controlled
situations with a surgeon and operating room immediately
available.

• If evisceration occurs initially or develops later, do not reinsert

tissue or organs. Place a saline-soaked gauze over the
evisceration, and cover with a sterile towel until the evisceration
can be evaluated by the surgeon.

• The issue of mandatory surgical exploration versus observation

and selective surgery, especially with stab wounds, remains
controversial. There is a trend toward observation of patients
without obvious injury or peritoneal signs.

• Indications for laparotomy include one or more of the following:

(1) penetrating injury indicative of invading the peritoneum (e.g.,
abdominal gunshot wound or abdominal stab wound with
evisceration, hypotension, or peritonitis); (2) positive peritoneal
signs (e.g., tenderness, rebound tenderness, involuntary
guarding); (3) shock; (4) GI hemorrhage; (5) free air in the
peritoneal cavity as seen on x-ray film; (6) evisceration; (7)
massive hematuria; and (8) positive findings on DPL.

The patient should be evaluated for peritoneal signs at least

hourly by the same examiner. Consult the surgeon immediately if
the patient shows peritoneal signs, evidence of shock, gastric or
rectal bleeding, or gross hematuria.

5. Consider an appropriate surgical intervention based on

type of injury

629
• Blunt, nonpenetrating abdominal injuries: Physical examination is
important in determining the necessity for surgery in patients
who are alert, cooperative, and nonintoxicated. Additional
diagnostic tests such as abdominal ultrasound, DPL, or CT are
necessary to evaluate the need for surgery in the patient who is
intoxicated or unconscious or who has sustained head or spinal
cord trauma.

• Nonoperative management: In blunt abdominal

trauma, including severe solid organ injuries,
selective nonoperative management (closely
monitoring vital signs and frequently repeating the
physical examination) is considered the standard of
care, and based on CT scan diagnosis and
hemodynamic stability of the patient.

• Pediatric patients can generally be resuscitated and

treated without surgery; some pediatric surgeons
often transfuse up to 40 mL/kg of blood products to
stabilize a pediatric patient.

• Hemodynamically stable adults with solid organ

injuries, primarily liver and spleen, may be
candidates.

• Splenic artery embolotherapy may be used for adult

blunt splenic injury.

• These patients should be evaluated in the same

manner as that described in the section Surgical
Considerations for Penetrating Abdominal Injuries.

• Immediate laparotomy for blunt abdominal

630
 trauma is indicated under the following
circumstances: (1) clear signs of peritoneal irritation
(see Box 3-3); (2) free air in the peritoneum; (3)
hypotension caused by suspected abdominal injury,
or persistent and unexplained hypotension; (4)
positive DPL findings; (5) GI aspirate or rectal
smear-positive result for blood; and (6) other
positive findings in diagnostic tests such as CT or
arteriogram.
• Need for immediate surgery versus triad of failure: Once in the
operating room, it may become apparent that the patient cannot
survive a long procedure, or that the triad of failure (acidosis,
hypothermia, and coagulopathy) may cause death. At this point
the surgeon may do limited repair and packing, choosing to
delay major surgical repair.

• Transfer the patient to the intensive care unit (ICU),

where the triad may be corrected. Survival from
abdominal trauma and surgery requires an
integrated team effort.

• Focus is to limit the effects of hemorrhage, acidosis,

and coagulopathy and to promote perfusion of all
organs.

6. Considerations regarding closure of the abdominal

surgical incision
During closure after surgery, if the bowel (intestines) can be
visualized with an abdominal horizontal view, the abdomen fascia
should not be closed. If the abdomen has been closed, it may
become necessary to open it again either in the ICU or the operating

631
room. There are multiple methods discussed in the literature to
supplement closure.

1. Silo bag closure: A 3-L sterile plastic irrigation bag is emptied and
cut to lie flat. The edges are trimmed and sutured to the skin.

2. Vacuum pack: A 3-L sterile plastic irrigation bag is emptied and

cut to lie flat, then placed into the abdomen, and the edges are
placed under the sheath. Two suction drains are placed on top of
the bag, and a large adherent Steri-Drape is then placed over the
whole abdomen. The catheters are placed to suction, providing
continuous drainage.

3. Vacuum-assisted closure: This consists of a sterile sponge

dressing with an adherent dressing and a continuous negative
pressure; it promotes closure, blood flow, and collagen formation.

HIGH ALERT!
Sudden release of abdominal pressure may lead to further
injuries such as ischemia-reperfusion, acute vasodilatation, and
cardiac dysfunction and arrest. The nurse should hydrate the
patient with at least 2 L of intravenous fluids and vasopressors
should be immediately available in case severe hypotension occurs.

7. Provide nutrition support

Patients with abdominal trauma have complex nutritional needs
because of the hypermetabolic state associated with major trauma
and traumatic or surgical disruption of normal GI function. Often,
infection and sepsis contribute to a negative nitrogen state and
increased metabolic needs. Prompt initiation of parenteral or
postpyloric feedings, as appropriate, in patients unable to accept
conventional enteric feedings and the administration of
supplemental calories, proteins, vitamins, and minerals are
essential for healing. For additional information, see Nutrition
Support (Chapter 1).

632
8. Prevent infection with antibiotics
Abdominal trauma is associated with a high incidence of
intraabdominal abscess, sepsis, and wound infection, particularly
with injury to the terminal ileum and colon. Patients with
penetrating or blunt trauma and suspected intestinal injury are
started on parenteral antibiotic therapy immediately. Broad-
spectrum antibiotics are continued postoperatively and stopped
after approximately 72 hours unless there is evidence of infection.

9. Manage pain using analgesics

Because opiates alter the sensorium, frequent assessment of LOC is
important. Analgesics are used in the immediate postoperative
period to relieve pain and promote ventilatory excursion.
Nonsteroidal antiinflammatory drugs (NSAIDs) can increase risk of
bleeding and should be used cautiously.

Care plans: Abdominal trauma

Deficient fluid volume 
related to active loss of blood volumes or secondary to management of
fluids.
Goals/Outcomes: Within 12 hours of this diagnosis, the patient
becomes normovolemic, as evidenced by mean arterial pressure
(MAP) greater than 70 mm Hg, HR 60 to 100 bpm, normal sinus
rhythm on ECG, CVP 2 to 6 mm Hg, PAWP 6 to 12 mm Hg, CI
greater than 2.5 L/min/m2, SVR 900 to 1200 dynes/s/cm−5, urinary
output greater than 0.5 mL/kg/h, warm extremities, brisk capillary
refill (less than 2 seconds), and distal pulses greater than 2+ on a 0-
to-4+ scale. Although hemodynamic measurements are helpful to
determine adequacy of resuscitation, serum lactate and base deficit
are essential to evaluate cellular perfusion.
Fluid Balance; Electrolyte and Acid-Base Balance.

Fluid management

1. Monitor BP every 15 minutes, or more frequently in the presence

of obvious bleeding or unstable vital signs. Be alert to changes in
MAP of greater than 10 mm Hg.

633
 Even a small but sudden decrease in blood pressure signals
the need to consult the advanced practice provider and/or surgeon,
especially for the patient with trauma in whom the extent of injury
is unknown.

2. Monitor HR, ECG, and cardiovascular status every 15 minutes

until volume is restored and vital signs are stable. Check ECG to
note HR elevations and myocardial ischemic changes (i.e.,
ventricular dysrhythmias, ST segment changes), which can occur
because of dilutional anemia in susceptible individuals.

3. In the patient with evidence of volume depletion or active blood

loss, administer pressurized fluids rapidly through several large-
caliber (16-gauge or larger) catheters. Use short, large-bore IV
tubing (trauma tubing) to maximize flow rate. Avoid use of
stopcocks, because they slow the infusion rate.

4. Fluids should be warmed to prevent hypothermia.

HIGH ALERT!
Evaluate patency of intravenous catheters continuously during
rapid volume resuscitation.

5. Measure central pressures and thermodilution CO every 1 to 2

hours or more frequently if blood loss is ongoing. Calculate SVR
and pulmonary vascular resistance every 4 to 8 hours or more often
in patients who are unstable. Be alert to low or decreasing CVP and
PAWP.

634
HIGH ALERT!
An elevated heart rate (HR), along with decreased pulmonary
artery wedge pressure, decreased cardiac output/cardiac index
(CO/CI), and increased systemic vascular resistance suggest
hypovolemia (see Table 5-10 for hemodynamic profile of
hypovolemic shock). Anticipate slightly elevated HR and CO
caused by hyperdynamic cardiovascular state in some patients
who have undergone volume resuscitation, particularly during the
preoperative phase. Also anticipate mild to moderate pulmonary
hypertension, especially in patients with concurrent thoracic
injury, such as pulmonary contusion, smoke inhalation, or early
acute respiratory distress syndrome. Acute respiratory distress
syndrome is a concern in patients who have sustained major
abdominal injury, considering that there are many potential
sources of infection and sepsis that make the development of acute
respiratory distress syndrome more likely (see Acute Respiratory
Distress Syndrome).

6. Measure urinary output every 1 to 2 hours. Be alert to output of

less than 0.5 mL/kg/h for 2 consecutive hours. Low urine output
usually reflects inadequate intravascular volume in the patient with
abdominal trauma.

7. Monitor for physical indicators of arterial hypovolemia: (1) cool

extremities, (2) capillary refill greater than 2 seconds, (3) absent or
decreased amplitude of distal pulses, (4) elevated serum lactate,
and (5) base deficit.

8. Estimate ongoing blood loss. Measure all bloody drainage from

tubes or catheters, noting drainage color (e.g., coffee grounds,
burgundy, bright red; Table 3-2). Note the frequency of dressing
changes as a result of saturation with blood to estimate amount of
blood loss by way of the wound site.

Table 3-2
CHARACTERISTICS OF GASTROINTESTINAL DRAINAGE*

635
 Source Composition and Usual Characteristics

Mouth and Saliva; thin, clear, watery; pH 7

oropharynx
Stomach Hydrochloric acid, gastrin, pepsin, mucus; thin, brown to green, acidic
Pancreas Enzymes and bicarbonate; thin, watery, yellowish brown; alkaline
Biliary tract Bile, including bile salts and electrolytes; bright yellow to brownish green
Duodenum Digestive enzymes, mucus, products of digestion; thin, bright yellow to light
brown, may be green, alkaline
Jejunum Enzymes, mucus, products of digestion; brown, watery with particles
Ileum Enzymes, mucus, digestive products, greater amounts of bacteria; brown,
liquid, feculent
Colon Digestive products, mucus, large amounts of bacteria; brown to dark brown,
semiformed to firm stool
Postoperative Initially, drainage expected to contain small amounts of fresh blood
(gastrointestinal appearing bright to dark; later, drainage mixed with old blood appearing
surgery) dark brown (“coffee grounds”), and then approaches normal composition
Infection Drainage cloudy, may be thicker than usual; strong or unusual odor, drain
present site often erythematous and warm
*
It is important to know the normal to recognize the abnormal.

Electrolyte Management; Fluid Monitoring; Hypovolemia

Management.

Acute pain 
related to physical injury secondary to trauma or surgical intervention.
Goals/Outcomes: The patient’s subjective evaluation of
discomfort improves, as assessed by use of a pain scale and/or
assessed by nonverbal indicators of discomfort, such as grimacing,
restlessness, and/or physiologic indicators.
Pain Control; Comfort Level.

Pain management

1. Medicate appropriately for pain relief. It is important to note that

opiate analgesics can decrease GI motility, causing nausea,
vomiting, and delay of bowel activity. These factors are especially
important if the patient has had a recent laparotomy.

2. Provide comfort measures, maintain proper positioning of

affected extremities while turning the patient and supporting
incisional areas.

3. Explain procedures to the patient and include education

636
regarding pain relief measures.

Risk for infection 

related to inadequate primary infection defenses secondary to physical
trauma or surgery; inadequate secondary defenses caused by decreased
Hgb or inadequate immune response; tissue destruction and
environmental exposure (especially to intestinal contents); multiple
invasive procedures.
Goals/Outcomes: The patient is free of infection, as evidenced by
core or rectal temperature less than 37.7° C (100° F); HR less than
100 bpm; CI less than 4 L/min/m2; SVR greater than 900 dynes/s/cm–
5
; orientation to time, place, and person; and absence of unusual
redness, warmth, or drainage at surgical incisions and drain sites.
Risk Control.

Infection protection

1. Note color, character, and odor of all drainage from any surgical
site, orifice, drain, or site of invasive catheters.

2. Report the presence of foul-smelling or abnormal drainage. See

Table 3-2 for a description of the usual characteristics of GI
drainage.

3. Monitor temperature, hemodynamics, and vital signs closely.

Administer pneumococcal vaccine to patients with total

splenectomy to minimize the risk of postsplenectomy sepsis.

4. For more interventions, see this diagnosis in the section on Major

Trauma.

Infection Control; Infection Protection.

Ineffective tissue perfusion: GI 

637
related to interruption of arterial or venous blood flow or episodes of
hypovolemia resulting in decreased perfusion to GI organs.
Goals/Outcomes: The patient has adequate GI tract tissue
perfusion, as evidenced by normoactive bowel sounds; soft,
nondistended abdomen; and return of bowel elimination.
Tissue Perfusion: Abdominal Organs.

Circulatory precautions

1. Auscultate for bowel sounds hourly during the acute phase of

abdominal trauma and every 4 to 8 hours during the recovery
phase. Report prolonged or sudden absence of bowel sounds
during the postoperative period, because these signs may signal
bowel ischemia or mesenteric infarction.

2. Evaluate the patient for peritoneal signs (see Box 3-3), which may
occur initially as a result of injury or may not develop until days or
weeks later, if complications caused by slow bleeding or other
mechanisms occur.

3. Ensure adequate intravascular volume (see Deficient Fluid

Volume).

4. Evaluate laboratory data for evidence of bleeding (e.g., serial Hct)

or organ ischemia (e.g., aspartate aminotransferase [AST], alanine
aminotransferase [ALT], lactic dehydrogenase [LDH]). Desired
values are as follows: Hct greater than 28% to 30%, AST 5 to 40
International Unit/L, ALT 5 to 35 International Unit/L, and LDH 90
to 200 U/L.

5. Document amount and characteristics of GI secretions, drainage,

and excretions.

6. Assess and report any indicators of infection or bowel obstruction

(e.g., fever, severe or unusual abdominal pain, nausea and
vomiting, unusual drainage from wounds or incisions, change in
bowel habits).

638
HIGH ALERT!
Note changes that suggest bleeding (presence of frank or occult
blood), infection (e.g., increased or purulent drainage), or
obstruction (e.g., failure to eliminate flatus or stool within 3 to 4
days after surgery).

Circulatory Care: Arterial Insufficiency; Bowel Management.

Impaired skin integrity 

related to mechanical factors (including physical injury); increased
metabolic needs secondary to trauma/stress response; altered circulation
secondary to hemorrhage or direct vascular injury; exposure to irritants
(gastric secretions).
Goals/Outcomes: The patient has adequate tissue integrity by the
time of hospital discharge, as evidenced by wound healing within
an acceptable time frame (according to extent of injury) and absence
of skin breakdown caused by GI drainage.
Tissue Integrity: Skin and Mucous Membranes.

Skin surveillance

1. Protect the skin surrounding tubes, drains, or fistulas, keeping

the areas clean and free from drainage. Gastric and intestinal
secretions and drainage are highly irritating and can lead to skin
excoriation. If necessary, apply ointments, skin barriers, or drainage
pouches to protect the surrounding skin. If available, consult the
ostomy nurse for complex or involved cases.

2. For other interventions, see this diagnosis in the section on Major

Trauma.

Wound Care; Tube Care.

Imbalanced nutrition: Less than body requirements 

related to decreased intake secondary to disruption of GI tract integrity
(traumatic or surgical); increased need secondary to hypermetabolic
posttrauma state.

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 Goals/Outcomes: The patient has adequate nutrition, as
evidenced by maintenance of baseline body weight and state of
nitrogen balance on nitrogen studies.
Nutritional Status: Food and Fluid Intake; Nutritional Status.

Nutrition management

1. Collaborate with advanced practice providers, dietician, and

pharmacist to estimate the patient’s metabolic needs on the basis of
type of injury, activity level, and nutritional status before injury.

2. Consider the patient’s specific injuries when planning nutrition.

For example, expect patients with hepatic or pancreatic injury to
have difficulty with blood glucose regulation.

3. Patients with trauma to the upper GI tract may be fed enterally,

but feeding tube must be placed distal to the injury. Disruption of
the GI tract may require a feeding gastrostomy or jejunostomy.
Patients with major hepatic trauma may have difficulty with
protein tolerance.

4. Ensure patency of gastric or intestinal tubes to maintain

decompression and encourage healing and return of bowel
function. Avoid occlusion of the vent side of sump suction tubes,
because this may result in vacuum occlusion of the tube.

Use caution when irrigating gastric or other tubes that have

been placed in or near recently sutured organs.

• For additional information, see sections on

Nutrition Support (Chapter 1) and Major Trauma.

Electrolyte Management; Feeding; Nutrition Therapy; Tube

640
Feeding.

Disturbed body image 

related to creation of stoma (often without the patient’s previous
knowledge); as part of management of penetrating physical injury to
internal organs.
Goals/Outcomes: The patient is able to acknowledge body
changes, views and touches affected body part, and demonstrates
movement toward incorporating changes into self-concept and is
able to verbalize some level of coping.
Body Image; Self-Esteem.

Body image enhancement

1. Evaluate the patient’s reaction to the stoma or missing/mutilated

body part by observing and noting evidence of body image
disturbance (see Box 2-4).

2. Anticipate feelings of shock and disbelief initially. Be aware that

patients with trauma usually do not receive the emotional
preparation for ostomy, amputation, and other disfiguring surgery
that the patient undergoing elective surgery receives.

3. Anticipate and acknowledge normalcy of feelings of rejection and

isolation (and uncleanliness in the case of fecal diversion).

4. Offer the patient an opportunity to view the stoma/altered body

part. Use mirrors if necessary.

5. Encourage the patient and significant others to verbalize feelings

regarding altered/missing body part.

6. Offer the patient an opportunity to participate in the care of the

ostomy, wound, or incision.

7. Confer with the surgeon regarding advisability of a visit by an

ostomate or a patient with similar alteration in body part.

8. Be aware that most colostomies are temporary in patients with

colonic trauma. This fact can be reassuring to the patient, but it is

641
important to verify the type of colostomy with the surgeon before
explaining this to the patient.

Box 3-4
HOROWITZ CLASSIFICATION OF
PERICARDIAL EFFUSIONS
Grade 1: Small: Echo-free space in diastole less than 10 mm.

Grade 2: Moderate: Echo-free space at least greater than 10 mm

posteriorly.

Grade 3: Large: Echo-free space greater than 20 mm.

Grade 4: Very Large: Echo-free space greater than 20 mm and

compression of heart is present.

Ostomy Care.

Additional nursing diagnoses

Also see Major Trauma for Hypothermia (Chapter 2) and
Posttrauma Syndrome. For additional information, see other
diagnoses under Major Trauma, as well as nursing diagnoses and
interventions in the following sections, as appropriate:
Hemodynamic Monitoring (Chapter 1), Prolonged Immobility
(Chapter 1), Emotional and Spiritual Support of the Patient and
Significant Others, Peritonitis (Chapter 9), Enterocutaneous Fistula
(Chapter 9), SIRS, Sepsis, and MODS (Chapter 10), and Acid-Base
Imbalances (Chapter 1).

Acute cardiac tamponade

Pathophysiology
Cardiac tamponade is a condition that results in a low CO state

642
caused by decreased filling of the chambers of the heart from
pressure exerted by fluid, blood, purulent liquid, or gas in the
pericardial space surrounding the heart. Cardiac tamponade is
classified as acute, subacute, occult, or regional. Acute cardiac
tamponade occurs when there is a rapid accumulation of fluid in
the pericardial space that compresses the heart, resulting in sudden
hemodynamic instability that can be life threatening.
Potential causes of cardiac tamponade include the following:

• Trauma: Blunt or penetrating cardiac trauma.

• Iatrogenic: Cardiac surgery, cardiac catheterization, pacemaker

implant.

• Nontraumatic hemorrhage: Dissecting aortic aneurysm,

anticoagulation therapy.

• Left ventricular rupture: Following extensive myocardial

infarction.

• Infection: Viral, bacterial, or fungal.

• Neoplasms/carcinoma: Most commonly breast and lung.

• Other: Connective tissue disease, pleural effusions, radiation

therapy, uremic states.

Acute cardiac tamponade is usually a result of trauma, iatrogenic

causes, and hemorrhage resulting in inadequate CO, decreased
tissue perfusion, and possibly death. Subacute tamponade causes are
related to the slower accumulation of fluids seen with infections,
neoplasms, and tissue disease. Occult or low pressure tamponade is
seen in hypovolemic settings. Regional tamponade can occur with
large pleural effusions or with fluid localized or loculated within
one part of the pericardial space. Pericardial effusions can be
described using the Horowitz classification system based on the
echo-free space seen with echocardiograms (Box 3-4). Any nonacute
tamponade may become acute when rapid deterioration in patient
condition causes shock related to low CO.
Acute cardiac tamponade manifests when the heart is

643
compressed within the pericardial sac to the point where the
chambers of the heart cannot fill. The pressure within the sac must
be relieved. The rapid detection and treatment of acute tamponade
are key to patient survival. The pericardial sac contains 20 to 50 mL
of fluid to protect and provide a friction-free surface for the beating
heart. The pericardial sac has a fibroelastic quality, which allows
limited stretching ability. A sudden addition of 50 to 100 mL of
fluid can markedly increase intrapericardial pressure. Conversely, a
slowly accumulating tamponade can result in 2000 mL of fluid
collection without life-threatening cardiac compromise because the
pericardial sac has an opportunity to stretch slowly, expanding to
accommodate the slow accumulation of fluid volume within the
pericardial sac.
When there is a rapid increase in intrapericardial pressure, the
heart is compressed causing a decrease in intraventricular filling.
The compliance of the right side of the heart is limited, because it is
competing for the fixed volume within the pericardium. The right
atrium (RA), as a low pressure heart chamber is the most
susceptible to collapse, which decreases filling of the right ventricle.
This decreased filling results in JVD. While the pressure continues
to increase, the right ventricle has partial collapse during early
diastole. The decreased right ventricle free wall compliance causes a
right-to-left shift of the septum, which is pronounced during
inspiration, causing the pulsus paradoxus seen with cardiac
tamponade. An unresolved tamponade puts pressure on all
chambers of the heart, pulmonary vessels, and coronary arteries,
causing hemodynamic instability. Hemodynamically, while
pulmonary artery pressures (PAPs) increase, an equalization of
pressures of the right and left atria are seen, and decreased
ventricular filling occurs. This hemodynamic compromise results in
decreased CO and hypotension with decreased tissue perfusion.

Assessment: Acute cardiac tamponade

Goal of system assessment
Determine rapid diagnosis and treatment of acute cardiac
tamponade to prevent cardiac collapse and irreversible shock.

644
HIGH ALERT!
Pulseless electrical activity may be the presenting sign of cardiac
tamponade. Have a high suspicion of tamponade if presenting
rhythm is narrow-complex tachycardia without a pulse.
Cardiopulmonary resuscitation must be initiated immediately.

• IV insertion and advanced airway placement as soon as possible.

• Epinephrine 1 mg IVP or vasopressin 40 units IVP with ongoing

cardiopulmonary resuscitation.

• Fluid administration: LR or NS bolus.

• Emergent pericardiocentesis.

• Prepare for emergent thoracotomy if qualified surgeon is present.

Observation
• Early signs and symptoms: Beck triad consisting of muffled or
distant heart tones, distended neck veins, and hypotension; an
unwillingness to lay flat/supine, high anxiety, dyspnea, a change
in mental status and pulsus paradoxus. Pulsus paradoxus is a
decrease of greater than 10 mm Hg in systolic BP that occurs
during inspiration in the setting of increased intrathoracic
pressure. Stroke volume is reduced by the increased intrathoracic
pressure compressing the heart and blood vessels. The decrease
in systolic BP during inspiration is heard when slowly
auscultating the BP.

• Important bariatric considerations: Distended neck veins may

be difficult or impossible to assess related to neck size and
adipose distribution. Additionally, proper BP cuff size is essential
to accurately assess for pulsus paradoxus in the absence of
invasive arterial pressure monitoring. Without a large enough

645
 cuff, the subtle drop in the systolic BP heard during inspiration
when auscultating the BP is almost impossible to recognize.

• Early hemodynamic changes: Decreased BP, increase in RA

pressure (RAP) or CVP. Pulsus paradoxus of greater than 10 mm
Hg (see Box 3-2); low CO.

• Late signs and symptoms: Signs of cardiogenic shock including

decreased BP, weak or thready pulse, confusion, restlessness,
cold clammy skin, pallor.

• Late-stage hemodynamic changes: Continued hypotension, low

CO, right and left atrial pressures equalize, and PAP increases.

Vital signs
• Sinus tachycardia, commonly seen as compensatory response to
decreased stroke volume.

• Monitor BP; assess for significant hypotension, narrow pulse

pressure, systolic BP less than 90 mm Hg, and pulsus paradoxus.

• Exertional dyspnea early, progressing to dyspnea and orthopnea.

• Hoarseness and hiccups may be present resulting from laryngeal

and phrenic nerve involvement.

• Low urine output is a result of low CO, and taken with other
signs should be viewed as a signal for intervention in the absence
of hemodynamic monitoring.

Auscultation
• Beck triad, although described as classic, is seen in 10% to
33% of patients. Muffled heart tones may not be apparent with
the patient sitting upright, depending on the volume of
tamponade, and may be difficult to hear in a busy, noisy
environment. JVD is not always present in acute tamponade, but
is commonly seen in constrictive pericarditis. Differentiating

646
 constrictive pericarditis from cardiac tamponade is important. In
the presence of hypovolemia, blood flowing toward the RA
during inspiration makes the finding of JVD less likely with
tamponade. Pericardial friction rub may be heard with
pericarditis.

Percussion
• Dullness to percussion under the left scapula posteriorly,
related to compression of the left lower lobe. The Bamberger-
Pins-Ewart sign is a localized pulmonary auscultation and
percussion finding noted in the setting of large pericardial
effusions. There is dullness to percussion, increased fremitus, and
bronchial breathing between the vertebral column and the
scapula. A blowing sound can be heard, generally on the left side,
resulting from atelectasis caused by the enlarged pericardial sac.

Hemodynamic monitoring
If hemodynamic monitoring is not already in progress, do not delay
other treatments, but prepare for appropriate monitoring, according
to the hemodynamic system used. This may include insertion and
monitoring of an arterial line and pulmonary artery catheter or
another system capable of CO measurement.

• Decreased BP: Systolic BP less than 90 mm Hg requires

intervention.

• Increased CVP: Greater than 12 mm Hg or increasing above base

line. The CVP may also be decreased if significant hypovolemia is
present.

• Pulsus paradoxus: Systolic arterial pressure decreases greater

than 10 mm Hg during inspiration; easily seen in arterial
waveform with lower systolic BP during inspiration. This may be
less apparent with severe shock.

• Absence of Kussmaul sign: Kussmaul sign is a paradoxical

increase in jugular venous (JV) pressure with noticeable external
JV distention during inspiration seen with constrictive

647
 pericarditis, but rarely with cardiac tamponade. The right
ventricle can accommodate increased volume with inspiration in
the setting of tamponade, and thus a decline in JV pressure can
be seen on the CVP waveform. With cardiac tamponade, jugular
veins are distended with a prominent x descent and an absent y
descent on the CVP waveform. The right atrial y descent is lost
because no blood can enter the atrium. Patients with constrictive
pericarditis have a prominent x and y descent. This is important
in differentiating tamponade from constrictive pericarditis.

• Low CO: CI less than 2.2.

• PAP: Increased.

• Stroke volume variation (SVV): Increased. May be less apparent

with severe shock, but is inaccurate in setting of dysrhythmias.

• CVP equalizes with left atrial pressure or pulmonary artery

occlusive pressure.

• BP, CO, and CI continue to decrease, requiring fluid and

vasopressor and inotropic support until definitive treatment is
provided.

• If untreated, tamponade can lead to pulseless electrical activity

(PEA) or total cardiac arrest.

Abnormally elevated central venous pressure, pulmonary

artery pressure, and pulsus paradoxus may not be seen with the
patient who is hypovolemic until fluid administration is begun.

• Pulsus paradoxus related to hypovolemia will resolve with fluid

administration.

• Pulsus paradoxus will not resolve in acute cardiac tamponade

648
 with fluid administration alone.

Screening diagnostic tests

• Echocardiogram is indicated as a quick diagnostic tool for
assessment.

Diagnostic Tests for Acute Cardiac Tamponade

Collaborative management
From www.acc.org/qualityandscience/clinical/statements.htm.

Guidelines on the Diagnosis and Management of Pericardial

Disease from the Task Force on the Diagnosis and Management of
Pericardial Diseases of the European Society of Cardiology

649
 Pericardiocentesis should be avoided when cardiac
tamponade is associated with aortic dissection; immediate
surgical intervention is indicated.
The American College of Cardiology Foundation
(ACCF)/American Heart Association (AHA)/American Association
for Thoracic Surgery (AATS)/American College of
Radiology(ACR)/Society of Cardiovascular Anesthesiologists
(SCA)/Society for Cardiovascular Angiography and Interventions
(SCAI)/Society of Interventional Radiology (SIR)/Society of
Thoracic Surgeons (STS)/Society for Vascular Medicine (SVM)
issued Guidelines for the Diagnosis and Management of Patients
With Thoracic Aortic Disease in 2010. This safety alert information
was derived from that report.

Care priorities

1. Stabilize ventilation with oxygen, intubation, and

mechanical ventilation
Oxygen is administered using the equipment that most effectively
corrects each patient’s hypoxia. Devices used range from nasal
cannula to 100% nonrebreather masks to mechanical ventilators. If
the patient presented in cardiac arrest, chest compressions should
be in progress while ventilation is being stabilized.

650
2. Facilitate providing pericardiocentesis
Needle aspiration of the pericardium can be performed using a
subxiphoid or left parasternal approach to drain excess fluid from
the pericardial space. The blood removed often will not clot,
because the heart action can cause clotting factors within the
pericardial sac to break down (defibrination). Pericardiocentesis
alone may not suffice to manage acute pericardial tamponade.
Surgical exploration with pericardial window is recommended
because of the high incidence of recurrent bleeding if surgery is not
performed. A drain may stay in place until fluid output decreases
or ceases.

3. Anticipate the need to provide a surgical procedure

Subxiphoid pericardiostomy is a resection of the xiphoid process to
drain the pericardial sac. It is performed using either local or
general anesthesia. Other, more extensive surgical procedures,
including a pericardiectomy, can be used for cardiac
decompression. An immediate thoracotomy can be done in the ICU
or emergency department if the patient becomes suddenly
bradycardic (HR less than 50 bpm) or severely hypotensive (systolic
BP less than 70 mm Hg) or has PEA or cardiac arrest. Thoracotomy
allows for pericardial sac evacuation, hemorrhage control, and
internal cardiac massage if needed.

4. Provide fluid resuscitation

IV fluid infusion is used to increase ventricular filling pressures
during diastole and may result in increased CO and BP. Blood
products, colloids, or crystalloids may be used.

5. Administer vasoconstrictors
Medications used to increase BP by stimulating vasoconstriction in
the peripheral vasculature include neosynephrine or
norepinephrine. These medications are less effective in a setting of
hypovolemia.

6. Administer inotropic agents

Medications used to increase myocardial contractility and CO

651
include dopamine, dobutamine, and milrinone (see Appendix 6).

7. Stabilize BP with ongoing titration of medications and

fluids
This must be done with hemodynamic monitoring and goal-
directed therapy derived at by the entire critical care team.

Care plans: Acute cardiac tamponade

Decreased CO
related to decreased preload secondary to compression of ventricles by fluid
in the pericardial sac.
Goals/Outcomes: Within 4 to 6 hours after fluid resuscitation or
evacuation of tamponade, the patient has adequate CO, as
evidenced by CVP 4 to 6 mm Hg, CO 4 to 7 L/min, CI ≥2.5 L/min,
systolic BP at least 90 mm Hg (or within the patient’s normal
range), HR 60 to 100 bpm, normal sinus rhythm on ECG, SVV 13%
or lower, and absence of new murmurs or gallops, distended neck
veins, and pulsus paradoxus.
Cardiac Pump Effectiveness.

Cardiac care: Acute hemodynamic regulation

1. Assess cardiovascular function by evaluating heart sounds and

neck veins hourly. Consult provider for muffled heart sounds, new
murmurs, new gallops, irregularities in rate and rhythm, and
distended neck veins.

2. Monitor all patients with blunt or penetrating trauma to the chest

and abdomen for physical signs of acute cardiac tamponade,
persistent hemodynamic instability, and shock symptoms more
severe than expected for the blood loss.

3. Evaluate the patient for pulsus paradoxus (see Box 3-2).

4. Measure and record hemodynamic measurements. Consult the

advanced practice provider for sudden abnormalities or changes in
trend. Early signs of tamponade include elevated CVP with normal

652
BP SVV greater than 13% and pulsus paradoxus. Later signs include
equalization of CVP and left atrial pressure (pulmonary artery
occlusive pressure) and elevated PAP in the presence of
hypotension, SVV greater than 13% and not fluid responsive, low
CO and CI (see Box 3-4).

5. Evaluate ECG for ST segment changes, T wave changes, rate, and

rhythm. The optimum is sinus rhythm or sinus tachycardia.
Maintain continuous cardiac monitoring.

6. For patients presenting with PEA and narrow complex

tachycardia on ECG, suggest acute cardiac tamponade and follow
ACLS (Advanced Cardiac Life Support) guidelines to treat and
relieve cardiac tamponade.

7. Administer blood products, colloids, or crystalloids as

prescribed. For patients with trauma, use large-bore IV lines in the
periphery, if possible. Use pressure infusers and rapid
volume/warmer infusers for patients who require massive fluid
resuscitation.

8. Be prepared to administer vasoconstrictor agents (e.g.,

norepinephrine, phenylephrine, dopamine) if fluid resuscitation
does not support the patient’s BP. Positive inotropic agents (e.g.,
milrinone) may be used to support CO in short-term management.
The underlying problem is decreased ventricular filling, thus these
are temporizing measures for hemodynamic support until
correction of the tamponade occurs.

9. Have emergency equipment available for immediate pulmonary

artery catheterization, central line insertion, arterial line insertion,
pericardiocentesis, or thoracotomy.

10. Assess heart rate and monitor ECG: sinus tachycardia,

commonly seen as compensatory response to decreased stroke
volume.

Cardiac Care; Cardiac Care: Acute; Emergency Care;

Hemodynamic Regulation; Invasive Hemodynamic Monitoring;

653
Fluid Monitoring; Fluid Management; Blood Product
Administration; Medication Administration; Oxygen Therapy;
Resuscitation; Shock Management: Cardiac; Vital Signs Monitoring;
Dysrhythmia Management.

Ineffective tissue perfusion: Pulmonary, peripheral, and

cerebral 
related to interruption of arterial and venous flow secondary to
compression of the myocardium, by the collection of fluid within the
pericardial sac.
Goals/Outcomes: Within 4 to 6 hours after management with
fluids or evacuation of tamponade, the patient has adequate
perfusion, as evidenced by orientation to time, place, and person;
systolic BP at least 90 mm Hg (or within the patient’s normal
range); RR 12 to 20 breaths/min with normal depth and pattern
(eupnea) and ease of respirations; SaO2 at least 95%; peripheral
pulses at least 2+ on a 0-to-4+ scale; equal and normoreactive pupils;
warm and dry skin; brisk capillary refill (less than 2 seconds); and
urine output at least 0.5 mL/kg/h.
Circulation Status.

Shock management: Cardiac

1. Assess tissue perfusion by evaluating the following at least

hourly: LOC, BP, pulses, pupillary response, skin temperature,
capillary refill, and hemodynamic monitoring measurements if
available.

2. Evaluate urine output hourly to ensure that it is at least 0.5

mL/kg/h for patients with nonrenal failure.

3. Maintain tissue perfusion by delivering prescribed blood

products, colloids, crystalloids, vasopressors, and positive
inotropes.

4. If hypotension occurs, ensure that hypovolemia is treated, with

fluid administration, before or simultaneously with vasopressors
for treatment of hypotension. Administer vasopressors via the
central line whenever possible. Frequently assess peripheral IV

654
lines for evidence of infiltration. If vasopressor agents infiltrate
subcutaneous tissues, necrosis occurs. Follow appropriate
management protocol for your institution.

5. Have emergency oxygen and intubation and mechanical

ventilation equipment available.

6. Anticipate and prepare for pericardiocentesis and/or emergent

cardiac surgery (pericardial window, possible pericardiostomy or
pericardiectomy). If needle aspiration of the pericardium is
ineffective, surgical evacuation of the pericardium is immediately
required if the patient is in shock.

7. Prepare for emergency open chest procedure in the postcardiac

surgery patient exhibiting signs of tamponade.

Vasoconstrictors (e.g., norepinephrine, phenylephrine,

dopamine) should be infused through a central line.

Cardiac Care: Acute; Circulatory Care; Emergency Care;

Invasive Hemodynamic Monitoring; Respiratory Monitoring; Shock
Management; Vital Signs Monitoring; Cerebral Perfusion
Promotion; Neurologic Monitoring; Medication Administration;
Medication Management; Oxygen Therapy; IV Therapy;
Fluid/Electrolyte Management.

Additional nursing diagnoses

For other nursing diagnoses and interventions, see also Major
Trauma, Chest Trauma, Hemodynamic Monitoring (Chapter 9),
and Emotional and Spiritual Support of the Patient and Significant
Others (Chapter 2).

Acute spinal cord injury

655
Pathophysiology
Injury to the spinal cord can be a devastating event initiating a
cascade of physical and psychological changes that may last a
lifetime. Spinal cord injury (SCI) affects approximately 12,000
people each year; this number depicts a continuing trend in injuries
associated with motor vehicle crashes (39.2%), falls (28.3%), and
violent acts, primarily gunshot wounds (14.6%) but a decreasing
trend in sports injuries (8.2%) with 9.7% classified as other. The
average age at injury is increasing and is now 41.6 years; the rising
trend may reflect referral patterns survival of older adults at the
scene, or an increase in the number of injuries in those who are 60
years and older. Young white males continue to be injured most
frequently but a mixed racial/ethnicity pattern has emerged since
2005 that may reflect the U.S. population trend; a decrease in white
populations with an increase in African-American and Hispanic
populations being injured. Cervical injuries occur most frequently
at a rate of 56% over lumbar and thoracic injuries. There are
estimated to be between 250,000 and 400,000 people living with an
SCI, and approximately 85% of patients with SCI who survive the
initial 24 hours live at least 10 years. Less than 1% of patients
experience complete recovery at the time of discharge from the
hospital.
The spinal cord is approximately 18 inches in length running
from the base of the brain to the lumbar (L) spine area between L1
and L2 where the cord tapers to form the conus medullaris, a
bulbous end that terminates into a collection of nerve roots known
as the cauda equina (horse’s tail). The spinal nerve roots exit the
spinal cord at corresponding levels below the vertebral body of the
spinal column and are the anatomic connection between the central
and peripheral nervous system. Because the spinal cord ends at L1
and L2, the nerves descending from the conus medullaris making
up the cauda equina are considered peripheral nerves. The brain
and spinal cord communicate sensory and motor information along
a complex system of tracts, some descending from the brain (motor)
and others ascending from the periphery (sensory). Damage to
pathways along this communication system results in unique but
very distinguishable syndromes that include upper motor neurons
(UMNs), which carry messages between the brain and the

656
periphery along the spinal cord, and lower motor neurons (LMNs),
those nerves that branch out from the vertebrae (peripheral nerves).
Damage to UMNs results in muscle spasticity and hyperreflexia,
whereas damage to LMNs results in muscle flaccidity and areflexia.
Mechanisms of injury to the spinal cord can be traumatic or
nontraumatic. Traumatic injuries include MVCs, falls, sports
injuries, or acts of violence (e.g., gunshot wounds or stabbings).
These mechanical force injuries result in sudden flexion,
hyperextension, vertebral fracture, compression of the cord,
rotation of the cord, or direct injury to the cord such as in a stabbing
or gunshot wound. Nontraumatic injuries may be a result of
vascular injury (aortic disruption or spinal artery occlusion),
degenerative diseases (spondylosis), inflammatory events,
neoplasms, or autoimmune diseases (multiple sclerosis). Injuries to
the spinal cord regardless of mechanism of injury include
concussion, contusion, laceration, transsection, hemorrhage,
ischemia, and avascularization. See SCI classifications and
terminology in Table 3-3.

Table 3-3
SPINAL CORD INJURY CLASSIFICATIONS AND TERMINOLOGY

Type Closed (blunt)

Open (gunshot wound or stabbing)
Cause Motor vehicle collisions, falls, sports-related injury, acts of violence
Site Level of injury involved (cervical thoracic, lumbar, sacral)
Mechanism Flexion (deceleration injury, backward fall, diving injury)
Extension (whiplash or fall with hyperextension of neck)
Stability Integrity of supporting anatomy including vertebral bodies, ligaments, articulating
processes, and facet joints
Complete Tetraplegia (quadriplegia) or paraplegia (absence of motor, sensory, and
vasomotor function below the level of injury)
More frequently seen in cervical injuries
Incomplete Sparing of some motor and sensory function below the level of the lesion
More frequently seen in lumbar injuries

Fractures involving the vertebral bodies

Vertebral column fractures may or may not cause SCI. Severe SCI
can occur without damage to the vertebrae but rather result from
ischemia. With severe fractures, such as the “burst” fracture
(fragmentation of a vertebral body with penetration of the spinal

657
cord), paralysis almost always occurs. Penetration of the spinal cord
with bony fragments may cause hemorrhage, infection, and leakage
of cerebrospinal fluid (CSF).

Spinal shock
Spinal shock occurs following both complete and partial
transsection of the cord. It is a temporary loss of reflex and
sensorimotor function in all segments below the level of injury.
Spinal shock does not involve the classic shock symptoms,
including hypotension, tachycardia, and cardiovascular
compensation to help support the BP. The “shock” manifests as
temporarily “stunning” the function of the spinal cord. Spinal shock
occurs immediately after SCI, lasting several hours to weeks and is
a separate phenomenon from neurogenic shock. Sensorimotor
function of the disrupted portion of the spinal cord can return once
spinal shock resolves.

Neurogenic shock
Neurogenic shock occurs in patients who injure the cervical or
upper thoracic cord, disrupting sympathetic innervation to the
vasculature and the heart. Cardiovascular compensatory
mechanisms controlled by sympathetic nerves in the upper thoracic
cord are lost. The loss of sympathetic innervation causes
widespread vasodilation and venous pooling in the extremities and
splanchnic vasculature. Loss of sympathetic innervation to the heart
leads to bradycardia. The ensuing hypotension and bradycardia
reduce CO as a result of decreased preload (decreased venous
return) and inability to increase heart rate, putting patients at risk
for secondary injury related to ischemia.

Spinal shock with neurogenic shock

Patients who injure the cervical or upper thoracic cord may
experience neurogenic shock and spinal shock simultaneously.

Although spinal shock is seen in spinal cord injuries (SCIs)

at any level, the loss of central control of peripheral vascular tone

658
(neurogenic shock) occurs most dramatically in high cervical spine
injuries, with interruption of the sympathetic nervous system.
Profound bradycardia and hypotension are possible. With SCIs
lower than the midthoracic area, the patient will experience a
phase of neurogenic shock, with loss of sympathetic innervation to
vasculature below the level of the lesion; however, the effects of
that loss are not as dramatic.

Septic shock
Septic shock (see Septic Shock) may occur in patients with SCI as a
result of infections related to pneumonia, urinary tract infections
(UTIs), pressure sores, overuse of corticosteroids, and other causes.

HIGH ALERT!
Autonomic Dysreflexia
A life-threatening condition affecting victims with lesions at or
above T6, stemming from stimulation of the SNS by relatively
minor events. The resultant uncompensated cardiovascular
response may cause seizures, subarachnoid hemorrhage, fatal
cerebrovascular accident, and myocardial infarction if not
immediately recognized and treated.
Once spinal shock resolves, autonomic dysreflexia may occur at
any time from the acute phase to several years following the injury.

Causes
Most commonly, stimuli to the bladder, including distention,
infection, calculi, cystoscopy; or from the bowel with fecal
impaction, rectal examination, suppository insertion; or from the
skin, such as tight clothing or sheets, temperature extremes, sores,
or areas of broken skin. Initiating a regular toileting program is of
paramount importance as the patient recovers.

659
Acute phase assessment
Goal of assessment
There are two goals for spinal cord assessment: (1) identify and
initiate management of fractures, spinal shock, and cord
syndromes; and (2) prevent further injury.

Clinical assessment
The clinical assessment of the patient with SCI begins with the
trauma primary survey at the time of arrival to the emergency
department (see sections on Major and Abdominal Trauma
discussed earlier). Once stabilized the secondary trauma survey can
be completed and an extensive neurologic and functional
assessment can be performed.
Neurologic examination: Use of the American Spinal Injury
Association Scale (ASIA) documents the motor and sensory
impairment related to the injury (Table 3-4).

Table 3-4
AMERICAN SPINAL INJURY ASSOCIATION SCALE

Level Description of Impairment

A No motor or sensory function preserved below the level through the sacral segments
(S4-S5). Complete injury.
B Sensory but no motor function preserved below the level through the sacral segments
(S4-S5).
C Motor function is preserved below the level but the majority of muscle groups has
muscle grade strength level of less than 3 (has no antigravity movement).
D Motor function is preserved below the level but the majority of muscle groups has
muscle grade strength level of 3 (has antigravity movement).
E Normal motor and sensory functions (no cord injury).

Functional Assessment: The Functional Independence Measure

(FIM, an 18-item scale) provides measurement of disability based
on the International Classification of Impairment, Disabilities, and
Handicaps. The scale is useful in determining the ability of the
patient with SCI to carry out activities of daily living.

Interpretation of physical assessment findings

Interpretation of physical assessment findings begins with vital

660
signs, respiratory status, including oxygen saturation (pulse
oximetry), vital capacity, and monitoring for ascending edema.
Consideration for cardiac monitoring, placement of nasogastric
(NG) tubes, or Foley catheters occurs as a result of cardiac, GI, and
genitourinary assessment. Interpretation of laboratory values and
diagnostic studies assist in the development of the plan of care.

Types of injury
Complete SCI is total loss of motor and sensory function below the
level of the lesion. Symptoms are a result of physiologic
transsection of the cord either from bruising or compression of cord
and blood vessels. Both sides of the body are affected equally.
Approximately 50% of injuries are complete.
Incomplete SCI has preservation of some motor or sensory
function below the level of the lesion. The pattern of injury may not
be symmetrical. Several cord syndromes (anterior cord syndrome,
central cord syndrome, lateral cord/Brown-Séquard syndrome,
posterior cord syndrome, conus medullaris syndrome, and cauda
equina syndrome) have been identified and will be discussed under
Acute Phase Assessment.

Levels of injury
Tetraplegia (quadriplegia): Injury to the cervical cord resulting in
motor loss in all four extremities.
Paraplegia: Injury to the thoracic and lumbar cord resulting in
motor loss in the lower trunk and extremities.
The patient should be evaluated for the following SCI specific
conditions:
Spinal shock initial symptoms:

• Flaccid paralysis below the level of injury of all skeletal muscles

with absence of deep tendon reflexes.

• Loss of cutaneous sensation.

• Loss of temperature control with development of anhidrosis

(absence of sweating).

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• Loss of vasomotor tone.

• Loss of proprioception (position sense).

• Loss of visceral and somatic sensation, and loss of the penile

reflex.

• GI shutdown resulting in paralytic ileus.

• Bowel and bladder paralysis resulting in urinary retention and

fecal retention.

Recovery phase of spinal shock: As spinal shock subsides, the

patient may experience:

• Flexor spasms evoked by cutaneous stimulation.

• Reflex emptying of the bowel and bladder.

• Extensor or flexor rigidity.

• Hyperreflexic deep tendon reflexes, and reflex priapism or

ejaculation in the male, evoked by cutaneous stimulation.

Neurogenic shock symptoms include:

• Vasodilation.

• Hypotension.

• Bradycardia.

Septic shock symptoms include:

• Vasodilation.

• Hypotension.

• See Chapter 11.

Autonomic dysreflexia symptoms include:

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• Pounding headache.

• Paroxysmal hypertension (up to 300 mm Hg systolic).

• Flushing of the skin with sweating above the level of the lesion.

• Nasal congestion.

• Blurred vision.

• Nausea.

• Bradycardia (30 to 40 bpm).

• Chest pain.

• Below the level of the lesion, pilomotor erection (goose bumps),

pallor, chills, and vasoconstriction will be present (Table 3-5).

Table 3-5
LEVELS OF CORD INJURY

Level
of Manifestation
Injury
C4 Loss of muscle function, including respiratory function; fatal outcome unless
and ventilation is provided immediately.
above
C4-C5 Same as above; phrenic nerve may be spared; assisted ventilation;
quadriplegia/tetraplegia.
C6-C8 Diaphragm and accessory muscles or respiration retained; movement of neck,
shoulders, chest, and upper arms; quadriplegia.
T1-T3 Neck, chest, shoulder, arm, hand, and respiratory function retained; difficulty
maintaining a sitting position; paraplegia.
T4- More stability of trunk muscles; paraplegia.
T10
T11- Use of upper extremities, neck, and shoulders; some function of upper thigh; reflex
L2 emptying of bowel; males may have difficulty achieving and maintaining an erection;
decreased seminal emission.
L3-S1 Reflex emptying of bowel/bladder; decreased/lack of ability to have an erection;
decreased seminal emission; all muscle groups in upper body function; most muscles of
lower extremities function.
S2-S4 Flaccid bowel and bladder; lower extremity weakness; all muscle groups function; no
ability to have a reflex erection.

Cord syndromes

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Anterior cord syndrome: Injury to the anterior two thirds of the
spinal cord supplied by the anterior spinal artery caused by an
acute burst fracture, herniation of an intervertebral disk, a vascular
injury or occlusion resulting from trauma, clot, or surgical
procedure, such as aortic aneurysm repair.
The prognosis varies with each patient and depends on the
degree of structural damage and edema.
Symptoms include:

• Loss of varying degrees of motor function below the level of

injury.

• Loss of pain and temperature sensation below the level of injury.

• Position, pressure, and vibration sensations remain intact.

Central cord syndrome: Most common SCI affecting the central

gray matter of the spinal cord. Primary causes of injury include
compression of the cord, low-velocity injuries, fractures and
dislocations, and interruption of blood supply to the central spinal
cord. In older persons with underlying conditions such as cervical
spondylosis, a hyperextension injury related to a fall may result in
central cord injury. Vertebral injury may be noted on the
radiograph. Motor and sensory deficits are less severe in the lower
extremities than in the upper extremities because of the central
arrangement of cervical fibers in the spinal cord. Incomplete
injuries carry a relatively good prognosis. Many patients can
ambulate with an assistive device and may regain bowel and
bladder function. There is a less favorable prognosis regarding
regaining useful function in the hands.
Symptoms include the following:

• Motor and sensory deficits are usually severe in the upper

extremities and profound in the hands and fingers.

• Sacral and some lumbar fibers are spared, therefore motor and
sensory function in the perineum, genitalia, and lower
extremities is present.

664
• Bladder dysfunction varies with each patient.

Lateral cord (Brown-Séquard) syndrome: Results from a

horizontal hemisection of the spinal cord (e.g., from a gunshot or
stab wound). Patients usually have bilateral motor and sensory
impairment, with a relative difference in function from one side to
the other. Prognosis is usually good for recovery of upper and
lower extremity function.
Symptoms include:

• Ipsilateral weakness.

• Decrease in light touch, vibratory and position senses.

• Contralateral pain (hypalgesia) and temperature loss.

• Usually there are bilateral motor and sensory deficits, but motor
activity will be better on the contralateral side and sensory
activity will be better on the ipsilateral side.

Posterior cord syndrome: Although rare, posterior cord

syndrome represents an incomplete injury to the posterior columns
of the spinal cord.
Symptoms include:

• Loss of proprioception.

• Preserved motor function, pain, and light touch.

Conus medullaris syndrome: The conus medullaris is the

tapered end of the spinal cord between the first and second lumbar
disks. The conus medullaris consist of sacral spinal cord segments.
Injury at this level is considered an UMN lesion. Injury is as a result
of a lumbar burst fracture, lateral disk herniation, lumbar stenosis
(multilevel), ankylosing spondylitis, neoplasm, infection (abscess),
spinal anesthesia, congenital anomalies (tethered cord,
arteriovenous malformations), spinal hemorrhage, and multiple
sclerosis. Because the injury is at the junction of the conus
medullaris and the cauda equina, the lower cord as well as
individual peripheral nerves of the cauda equina may be injured,

665
presenting a mixed clinical picture of UMN and LMN lesions.
Symptoms include:

• Motor strength: mixed UMN (symmetrical) and LMN paralysis

(asymmetrical).

• Sensation (numbness) varies but tends to be symmetrical,

bilateral, and in the perianal area.

• Bladder function is either preserved (UMN) or areflexic (LMN).

• Erectile dysfunction and impotence (UMN) or anesthesia to sacral

dermatomes (LMN).

• May exhibit increased muscle tone (spasticity), especially if the

lesion is isolated and primarily UMN.

• Deep tendon reflexes demonstrate hyperreflexia (UMN).

Differentiation from cauda equina may be difficult. Signs and

symptoms are very similar except for the bilateral presentation in
conus medullaris, sacral sparing with preservation of the
bulbocavernosus reflex, and normal sphincter tone.
Cauda equina syndrome: The cauda equina (horse’s tail) is a
bundle of nerve roots at the end of the spinal cord representing the
lumbar and sacral nerve roots. Injury at this level is an LMN. Injury
to the cauda equina is associated with a central disk fracture or
lumbar disk below the level of the conus medullaris.
Symptoms include:

• Pattern of LMN responses (flaccid paralysis, areflexia, and loss of

muscle tone with muscle fasciculation).

• Diminished muscle strength in the lower extremities consistent

with the involved nerve root.

• Greater involvement in the lower lumbar and sacral roots based

on the muscle group distribution innervated by the spinal nerve
involved.

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• Sensation is diminished or lost to pinprick and light touch
along the dermatome pattern of the nerve; often there is saddle
anesthesia with diminished or absent sensation to the glans penis
or clitoris.

HIGH ALERT!
Requires immediate attention (decompression) to prevent
permanent injury.

• Anal sphincter tone may or may not be present.

• There may be a history of urinary retention or loss of bladder tone

and incontinence.

• Diminished or absent muscle strength in the muscles listed as

follows assists in localizing the injury:

• L2 iliopsoas (hip flexion).

• L3 quadriceps (knee extension).

• L4 tibialis anterior (ankle dorsiflexion).

• L5 extensor hallucis longus (big toe extension).

• S1 gastrocnemius/soleus (ankle plantar flexion).

HIGH ALERT!
Vertebral artery injury (VAI): Recognizing the potential for
VAI in patients with cervical spine injuries is important. These are

667
occult injuries but may account for changes in mental status in a
patient without a history of brain injury. Patients may be
asymptomatic or complain of headache. Some go on to have
posterior fossa infarcts. Magnetic resonance imaging should be
part of the diagnostic workup for early detection of VAI. Patients
with VAI may be placed on anticoagulants.

Diagnostic tests
Following trauma, the commonly used radiologic investigations do
not rule out injury to the spinal cord, especially for children,
particularly resulting from the elasticity of the cervical spine. There
is a possibility of SCI without radiologic abnormality (SCIWORA).
The changes may be identified using magnetic resonance imaging
(MRI). SCIWORA may be present in patients who have experienced
blunt trauma who report immediate or transient symptoms of
neurologic deficit or who exhibit symptoms upon initial
assessment. Treatment within 6 hours with high-dose
methylprednisolone improves the outcome. It is possible to reduce
the incidence of neurologic complications by increasing awareness
and initiating early treatment with steroids and immobilization of
the affected area, most often, the cervical spine.

Spinal radiograph
Plain radiographs provide information on the bony anatomy of the
spine, thereby delineating fractures, dislocations, and subluxations
of the vertebral bodies, as well as demonstrating narrowing of the
spinal canal and level of hematomas, neoplasms, or abscesses.
Additional views such as open mouth, bilateral oblique, or flexion-
extension films also aid in diagnosis.
Cervical spine x-rays taken to rule out fracture on patients with
traumatic brain injury or SCI include three views: anterior posterior
(AP), lateral, and odontoid. Visualization from C1 to T1 is
imperative but may be difficult in patients with large necks and
shoulder muscles. If visualization is clear, CT or MRI must be done
before removing cervical spine collars.

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HIGH ALERT!
Films must be obtained with extreme caution in the evaluation
of the patient with a possible spinal cord injury because any
sudden or incorrect movement of the injured area could cause
further trauma to the spinal cord or cause injury in a patient who is
neurologically intact. Flexion-extension films should only be
obtained when a patient is alert and able to describe pain on
manipulation or under the supervision of a radiologist using
fluoroscopy techniques.

CT scans
The CT scan provides detailed information on the bony structures
of the vertebral bodies, especially related to encroachment on the
spinal canal by bone fragments or vertebral body displacement. CT
images are especially useful for evaluation of the cervical thoracic
junction. Helical or spiral CT scans are used to reconstruct the
sagittal and coronal planes. The entire spine should be imaged
if there is an SCI to identify injuries at other levels.

Spinal MRI scans

MRI identifies the extent of cord injury and provides information
on the cause of cord compression, degree of compression, extent of
contusion, degree of ligament involvement, and other related soft
tissue injuries. MRI is also the best method to differentiate between
swelling/edema and ischemia.

Collaborative management
Care priorities

1. Immobilize the injured site

Additional injury to the spinal cord as a result of inadequate
stabilization after injury is sustained by 10% to 25% of patients with

669
SCI. Immobilization continues until the spine is stable either by
traction or surgical decompression and fixation. Remove the patient
from the spine board as soon as possible to prevent skin
breakdown. This is usually done after the primary survey is
completed. There is new evidence to suggest that use of spine
boards should be reserved only for those with obvious SCI during
prehospital care.

Cervical spine injury

Cervical collar and/or head blocks and backboard: The initial

treatment for a suspected cervical spine injury.

Cervical traction: Once the injury has been diagnosed, cervical

traction to immobilize and reduce the fracture or dislocation can
be achieved in several ways including application of a
cervicothoracic orthotic, a halo device with a vest, or a traction
system using Gardner-Wells, Vinke, or Crutchfield tongs. In
traction therapy, the tongs are inserted through the outer table of
the skull and attached to ropes and pulleys with weights to
achieve bony reduction and proper alignment. Guidelines
recommend 3 to 5 lb for each vertebral body fractured but not to
exceed 70 lb total weight for all involved vertebrae. Use of muscle
relaxants is also recommended. Cross-table lateral radiographs
should be obtained until desired realignment of the vertebral
bodies is achieved (this may take several hours and several trials
with weights). Another alternative is special frames or beds (e.g.,
kinetic treatment table). The use of the cervicothoracic orthotic or
halo device for skeletal fixation of the head and neck allows for
earliest mobilization and rehabilitation if no surgery is needed.
Closed reduction should be done with use of MRI if the patient
has brain injury or has an altered LOC from other causes (alcohol
intoxication).

Surgical intervention: During the immediate postinjury phase,

surgery is controversial, and immediate or early surgery
postinjury may have little effect on the neurologic outcome and
the benefit-to-harm ratio is uncertain. Surgery may be performed
(1) if the neurologic deficit is progressing—for example, if cord

670
 compression is imminent, in the presence of an expanding
hematoma or neoplasm; (2) in the presence of compound
fractures; (3) if there is a penetrating wound of the spine; (4) if
bone fragments are localized in the spinal canal; or (5) if there is
acute anterior spinal cord trauma. Surgeries may include
decompression laminectomy, closed or open reduction of the
fracture, or spinal fusion for stabilization. Anterior cervical
decompression is advocated for significant disk herniation. Once
stabilization of the spine occurs, the patient can be mobilized
unless contraindicated for other reasons.

Thoracic and lumbar spine injuries: May require surgical

stabilization with laminectomy with or without fusion. Bone
grafts, pedicle screws, and rods are used for fusions. If the injury
is stable, it may be treated with closed reduction using a
thoracolumbosacral orthotic (turtle shell–like immobilizer). If the
fracture is unstable and the patient is unable to go to surgery for
repair because of medical instability, bed rest with the use of the
thoracolumbosacral orthotic should be a priority.

2. Prevent secondary injury

Although administration of methylprednisolone within 8 hours of
injury may still be used in some trauma centers, the use of steroids
in the treatment of acute SCI is under scrutiny. As a result of
methodological flaws in the original study that demonstrated
improved neurologic outcomes with methylprednisolone and the
increasing evidence of complications associated with steroid use,
the standard of acute care for SCI management is changing and
high-dose methylprednisolone is now one of several treatment
options, not a standard of care. More recent studies are
emphasizing arterial oxygenation and spinal cord perfusion.
Modulating postinjury inflammation may arrest the secondary
injury cascade. The more common secondary injuries include
spasticity, pain, respiratory insufficiency leading to pneumonia,
genitourinary problems that may prompt infection, pressure ulcers,
and autonomic dysreflexia. Other promising therapies emerging
include thyrotropin-releasing hormone, neuroprotection with
minocycline (a semisynthetic second-generation tetracycline

671
derivative), use of calcium channel blockers to aid in axonal
conduction, use of Cethrin (a Rho antagonist) for neuroregeneration
and neuroprotection, and the use of anti-Nogo monoclonal
antibodies to augment plasticity and regeneration. Cell-mediated
repair is being investigated using stem cells and bone marrow
stromal cells. The use of GM1 gangliosides to improve spinal cord
outcomes has not been supported.
Methylprednisolone protocol is as follows: Within 8 hours of
injury, a loading dose (30 mg/kg) is administered by IV bolus over a
15-minute period. After a 45-minute wait, 5.4 mg/kg/h is then
administered in a continuous IV infusion over a 23-hour period and
then stopped. If the infusion is interrupted for any reason, it must
be recalibrated so that the entire dose can be completed within the
original 23-hour time frame.

HIGH ALERT!
Use of this protocol and the 48-hour protocol is no longer the
standard of care and is used only if benefit outweighs the risk.

3. Maintain hemodynamic stability

Hypotension: Maintain MAP between 85 and 90 mm Hg for the

first 7 days after injury to reduce secondary SCI (e.g., ischemia
and cord injury) and maximize recovery.

Orthostatic hypotension: This is a lifelong problem, especially

in patients with cervical and high thoracic injuries. Caregivers
should move the patient slowly into the upright position (slow
elevation of the head of the bed before 90 degrees) to avoid a
sudden drop in BP, prompting cerebral hypoxia and loss of
consciousness. Abdominal binders and Ace bandages or thigh-
high antiembolic stockings may also help prevent orthostatic
hypotension. These interventions should be applied before
mobilizing the patient.

Vasopressors (e.g., vasopressin, norepinephrine): To treat the

672
 hypotension during the immediate postinjury stage caused by
loss of vasomotor control below the level of injury, with resultant
vasodilation and a relative hypovolemia (see Appendix 6).

HIGH ALERT!
Vasopressor support should be initiated only after fluid
resuscitation has been done or in cases of refractory hypotension or
low systemic vascular resistance.

Antihypertensives (e.g., hydralazine hydrochloride, methyldopa,

nitroprusside sodium): To treat the severe hypertension that
occurs in autonomic dysreflexia. There is some support for the
use of enteral theophylline to treat bradycardia in cervical cord
injury in an effort to avoid use of the long-term infusions of
inotropic or chronotropic agents.

4. Manage vasodilation-induced hypovolemia

In patients with neurogenic or septic shock, blood volume is
normal but the vascular space is enlarged, causing peripheral
pooling, decreased venous return, and decreased CO. Careful fluid
repletion, usually with crystalloids, is indicated. Vasopressor
therapy is initiated for patients unresponsive to fluid volume
replacement. (For fluid management in patients with multisystem
trauma, see Major Trauma).

5. Support ventilation
Respiratory insufficiency is a hallmark in SCI, and the higher the
level of injury, the more likely the injury will affect ventilation. The
need for assisted ventilation is based on the level of injury, ABG
values, pulse oximetry, capnography, and the results of pulmonary
function tests, pulmonary fluoroscopy, and physical assessment
data. The need for mechanical ventilation is likely with injuries at
C4 and above, patients older than 40 years, smokers, and patients
with associated chest trauma and immersion injuries. Initially, the

673
patient may require intubation and, later, tracheotomy. Patients
with low cervical or high thoracic injuries whose respiratory status
is stable initially may need temporary intubation later if ascending
edema develops. Patients with high cervical injury who survive the
initial injury but have paralysis of the muscles of respiration may
require permanent tracheotomy and mechanical ventilation.

6. Provide aggressive pulmonary care

Respiratory complications are the most common cause of
morbidity and mortality in patients with cervical SCI accounting for
up to 80% of deaths, with pneumonia accounting for 50% of deaths.
Prevention, detection, and treatment of atelectasis, pulmonary
infection, and respiratory failure must be priorities. Recognition of
signs and symptoms of pulmonary embolism (PE) are crucial in
patients with SCI who may have no complaints of chest pain. Chest
physiotherapy and noninvasive positive-pressure ventilation using
bilevel continuous positive airway pressure may provide support,
but intubation with mechanical ventilation is sometimes required.
Bronchodilators (e.g., beta-2-agonists, methylxanthines): To dilate
bronchioles and facilitate removal of secretions. Consider early
treatment especially in patients who have a history of chronic
obstructive pulmonary disease (COPD) or smoking and who show
evidence of difficulty moving secretions.
Mucolytic agents (e.g., guaifenesin, acetylcysteine): To reduce
tenacity and viscosity of purulent and nonpurulent secretions.
Antibiotics: As prescribed to treat pulmonary infections related to
aspiration or ventilator-acquired pneumonia.

7. Prevent aspiration using gastric decompression

Gastric tube placement to decompress the stomach, prevent
aspiration of gastric contents, and manage paralytic ileus is
necessary (often seen within 72 hours of injury in patients with
lesions higher than T6). Placement of an NG tube may be necessary
before surgery to prevent development of ileus, which commonly
occurs postoperatively.

8. Gastric ulcer prevention

Proton-pump inhibitors (PPIs; e.g., pantoprazole, omeprazole): PPIs

674
are recommended over histamine blockers for stress ulcer (a
Cushing ulcer) prophylaxis. Cushing ulcers are related to CNS
trauma and occur more often in the stomach than the duodenum,
and occasionally affect the esophagus. PPIs reduce the production
of acid in the stomach by blocking gastric parietal cell hydrogen-
potassium ATPase. Recommended therapy for PPIs is 4 weeks.

9. Relieve pain and anxiety

Analgesics (e.g., acetaminophen, NSAIDs, or opioids): Use of

analgesics is necessary to minimize pain associated with injury or
surgery in patients who are alert and unconscious. Sensory loss
may be incomplete giving rise to pain in areas below the level of
the lesion.

Sedatives (e.g., midazolam, lorazepam): Sedation should be

used cautiously in patients with SCI who are not intubated.
Thorough assessment of respiratory status should be performed
if the patient is anxious, restless, or agitated. Rule out
hypercapnia and hypoxia in these patients first. Capnography
can provide information about declining effectiveness of
respiration before pulse oximetry detects a change in oxygen
saturation. If the respiratory status is stable, anxiolytics or
benzodiazepines can be used to decrease anxiety caused by the
injury, hospitalization, or fear of the prognosis. These agents may
also be useful when the patient is being mechanically ventilated.

10. Prevent deep venous thrombosis and thromboembolism

Patients with SCI are at high risk for development of vascular
complications because of immobility, loss of vasoconstriction
capabilities below the level of injury, and loss of muscle innervation
in the lower extremities that facilitates venous flow. Interventions
to prevent or treat vascular complication should be put in place
at the time of admission.

Early stabilization and mobilization: Once spinal stability is

achieved either through orthotic devices or surgery, patients
should be out of bed. A rehabilitation plan that includes physical
and occupational therapy should be initiated.

675
Early detection of vascular complications: Use of Doppler
ultrasonography or plethysmography for detection of deep
venous thrombosis (DVT) is recommended. CT angiography has
a greater specificity to diagnose PE than D dimer and ventilation-
perfusion scan.

Anticoagulants (heparin or low–molecular-weight heparins such as

dalteparin [Fragmin] or enoxaparin [Lovenox]): To prevent
thrombophlebitis, DVT, and PE.

HIGH ALERT!
Patients who are not candidates for anticoagulation therapy
may have an inferior vena cava filter inserted to trap emboli
traveling from the lower extremities to the lungs.

11. Nutrition support

As a result of the massive catabolic demand associated with CNS
injuries, nutrition therapy should be started as early as possible. If
the patient is not able to take oral nutrients, enteral feeding should
be started. If there is a coexisting problem with the GI tract from
injury, ileus, or surgery, total parenteral nutrition should be
considered.

12. Skin care

Prevent pressure sores: Remove from spinal board as soon as
possible after admission to the emergency department. Begin turn
schedule either manually or using specialty beds. Monitor bony
prominences (occiput of head, heels, elbows, sacrum, iliac rests)
every shift for signs of pressure. Check beneath cervical spine collar
if still in place. Early consult to wound therapy if the patient is
vulnerable (prolonged hemodynamic instability, nutrition
problems, ventilator dependence, inability to mobilize) for
prevention strategies including specialty beds.

676
13. Bladder program
Once the stability of the patient is ensured, a bladder program
using an intermittent straight catheterization procedure is
recommended.

HIGH ALERT!
Early bladder decompression and drainage using a Foley
catheter is necessary during the acute phase (3 to 4 days after
injury). To prevent bladder infections, begin bladder training and
remove the Foley catheter once the patient is stable. Bladder
distention can be a trigger for onset of autonomic dysreflexia.

Bladder training: Begin intermittent straight catheterizations on a

q3-4h (every 3 to 4 hours) schedule and advance to q6h. If urine
output is greater than 300 mL, increase frequency of intermittent
catheterizations; if less than 300 mL, increase time between
catheterizations. Once oral feeding is initiated, monitor fluid
intake to match catheterization output to prevent overdistension
of the bladder. The goal is to maintain detrusor stretch and
relaxation until spinal shock dissipates and reflexive bladder can
be trained.

Prevent spinal shock by decompressing the bladder: Insert an

indwelling or intermittent catheter to decompress an atonic
bladder in the immediate postinjury phase (spinal shock). With
the return of the reflex arc after spinal shock subsides, a reflex
neurogenic bladder that fills and empties automatically will
develop in patients with lesions above T12. Patients with lesions
at or below T12 generally have an atonic, areflexic neurogenic
bladder that overfills, distending the bladder, and causing
overflow incontinence. Intermittent catheterization may be
necessary.

14. Bowel management

Initiation of a bowel regimen at the time of admission assures GI

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function and prevents constipation and impaction. Liquid or oral
stool softeners (e.g., docusate sodium), suppositories, and small-
volume enemas are used.

Bowel training: Part of the rehabilitation plan commences with the

return of spinal reflexes. Medication along with digital
stimulation of the external sphincter is a common bowel training
protocol. The aim is to begin training for bowel independence
and to prevent fecal impaction and distention of the bowel,
which could stimulate an episode of autonomic dysreflexia.

Hyperosmolar laxatives (e.g., glycerin suppository): To facilitate

movement of the bowels on a regular basis and prevent fecal
impaction.

Irritant or stimulant laxatives (e.g., senna bisacodyl): To stimulate

bowel movements as part of a bowel training program.

15. Prevent infections

Pneumonia: Aggressive pulmonary hygiene.

UTI: Remove Foley catheter as soon as the patient is stable.

Skin: Avoid pressure sores and wound infections.

Care plans: Acute spinal cord injury

Impaired gas exchange 
related to altered oxygen supply associated with hypoventilation secondary
to paresis or paralysis of the muscles of respiration (diaphragm, intercostal
muscles) and/or inability to maintain clear airway occurring with high
cervical spine injury or ascending cord edema.
Goals/Outcomes: The patient has adequate gas exchange, as
evidenced by orientation to time, place, and person; PaO2 ≥80 mm
Hg; and Paco2 ≤45 mm Hg. RR 12 to 20 breaths/min with normal
depth and pattern, HR 60 to 100 bpm, BP stable and within the
patient’s normal range, and vital capacity (depth or volume of

678
inspiration) is ≥1 L. Motor and sensory losses remain at the same
spinal cord level as the initial findings.

HIGH ALERT!
Patients with cervical injuries usually arrive in the intensive
care unit (ICU) already intubated. However, with some high
thoracic or low cervical lesions, patients who ventilate
independently in the emergency department may arrive in the ICU
without assisted ventilation. This patient is at risk for an
increasingly higher level of cord damage because of hemorrhage
and edema, which can result in a higher level of dysfunction and a
change in respiratory status that requires assisted ventilation.
Before attempting oral intubation with neck flexion, ensure that
cervical x-ray studies have confirmed the absence of cervical
involvement. Use either nasal intubation or orotracheal intubation
with manual cervical spine immobilization if cervical spine injury
is not ruled out. Fiber optic intubation may also be considered.

Respiratory Status: Ventilation.

Respiratory monitoring

1. Assess for signs of respiratory dysfunction: shallow, slow, or

rapid respirations; poor cough; vital capacity; changes in
sensorium; anxiety; restlessness; tachycardia; pallor; adventitious
breath sounds (i.e., crackles, rhonchi); decreased or absent breath
sounds (bronchial, bronchovesicular, vesicular); decreased tidal
volume (less than 75% to 85% of predicted value); or vital capacity
(less than 1 L). Capnography can be used for early detection of
elevations in pCO2 levels, which may signal early respiratory
insufficiency, which can lead to hypoxia if not promptly addressed.

2. Monitor ABG tests; report abnormalities. Be particularly alert to

PaO2 less than 60 mm Hg, Paco2 greater than 50 mm Hg, and
decreasing pH, considering that these findings indicate the need for
assisted ventilation possibly caused by atelectasis, pneumonia, or

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respiratory fatigue.

3. Monitor vital capacity at least q8h. If it is less than 1 L, PaO2/PaO2

ratio is ≤0.75, or copious secretions are present, intubation is
recommended.

4. Monitor for signs and symptoms of pulmonary embolism (PE).

The patient may not have sensory symptoms (chest pain or
tightness) based on the level of the lesions.

5. If the patient does not require intubation with mechanical

ventilation, implement the following measures to improve airway
clearance:

• Place the patient in a semi-Fowler position unless it

is contraindicated (e.g., the patient is in cervical
tongs with traction or has unstable thoracic or
lumbar fractures).

• Turn the patient from side to side at least every 2

hours to help mobilize secretions.

• Keep the room humidified to help loosen secretions.

• Unless contraindicated, keep the patient hydrated

with at least 2 to 3 L fluid/day.

• Teach deep-breathing and coughing exercises,

which should be performed at least every 2 hours.

6. Suction secretions as needed and hyperoxygenate before

suctioning.

HIGH ALERT!

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 Be alert for bradycardia associated with tracheal suctioning. If
the patient’s cough is ineffective, implement the following method,
known as quad coughing: place palm of hand under the patient’s
diaphragm, and push up on the abdominal muscles as the patient
exhales. Be aware that using the quad cough maneuver in patients
with intracaval filters to prevent pulmonary emboli has been
reported to have significant complications, including bowel
perforation and filter migration and deformation.

7. Monitor the patient for evidence of ascending cord edema:

increasing difficulty with swallowing secretions or coughing,
presence of respiratory stridor with retraction of accessory muscles
of respiration, bradycardia, fluctuating BP, and increased motor
and sensory loss at a higher level than the initial findings.

8. If the patient has cranial tongs or traction with a halo apparatus

in place, monitor the patient’s respiratory status every 1 to 2 hours
for the first 24 to 48 hours and then every 4 hours if patient’s
condition is stable. Be alert to absent or adventitious breath sounds,
and inspect chest movement to ensure that the vest is not restricting
diaphragmatic movement.

HIGH ALERT!
Have a plan to remove the vest if cardiopulmonary
resuscitation is needed.

9. If intubation via endotracheal tube or tracheotomy becomes

necessary, explain the procedure to the patient and significant
others.

Airway Management; Oxygen Therapy; Respiratory

Monitoring; Mechanical Ventilation.

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Autonomic dysreflexia (or risk for same) 
related to abnormal response of the autonomic nervous system to a
stimulus.
Goals/Outcomes: The patient has no symptoms of autonomic
dysreflexia, as evidenced by dry skin above the level of injury, BP
within the patient’s normal range, HR ≥60 bpm, and absence of
headache and other clinical indicators of autonomic dysreflexia.
ECG demonstrates normal sinus rhythm.
Risk Detection.

Dysreflexia management

1. Assess for the classic triad of autonomic dysreflexia:

throbbing headache, cutaneous vasodilation, and sweating above
the level of injury. In addition, extremely elevated BP (e.g., ≥250 to
300/150 mm Hg), nasal stuffiness, flushed skin (above the level of
injury), blurred vision, nausea, bradycardia, and chest pain can
occur. Be alert to the following signs of autonomic dysreflexia that
occur below the level of injury: pilomotor erection, pallor, chills,
and vasoconstriction.

2. Assess for cardiac dysrhythmias, via cardiac monitor during

initial postinjury stage (2 weeks).

3. Implement measures to prevent factors that may precipitate

autonomic dysreflexia: bladder stimuli (i.e., distention, calculi,
infection, cystoscopy); bowel stimuli (i.e., fecal impaction, rectal
examination, suppository insertion); and skin stimuli (i.e., pressure
from tight clothing or sheets, temperature extremes, sores, areas of
broken skin).

4. If indicators of autonomic dysreflexia are present, implement the

following measures:

• Elevate the head of the bed or place the patient in a

sitting position. This will decrease BP by promoting
cerebral venous return.

682
• Monitor BP and HR every 3 to 5 minutes until the
patient stabilizes.

• Identify and remove offending stimulus. If the

patient’s bladder is distended, catheterize
cautiously, using sufficient lubricant containing a
local anesthetic. If the patient has an indwelling
urinary catheter, check for obstruction, such as
granulation in catheter or kinking of tubing; as
indicated, irrigate catheter, using no more than 30
mL NS. If UTI is suspected, obtain a urine specimen
for culture and sensitivity once the crisis stage has
passed. Check for fecal impaction; perform the
rectal examination gently, using an ointment
containing a local anesthetic (e.g., Nupercainal).
Check for sensory stimuli and loosen clothing, bed
covers, or other constricting fabric as indicated.

5. Consult the physician for severe or prolonged hypertension or

other symptoms that do not abate. Severe or prolonged elevations
of BP may result in life-threatening consequences: seizures,
subarachnoid or intracerebral hemorrhage, and fatal
cerebrovascular accident.

6. As prescribed, administer an antihypertensive agent and monitor

its effectiveness.

7. Remain calm and supportive of the patient and significant others

during these episodes.

8. Upon resolution of the immediate crisis, answer the patient’s and

significant others’ questions regarding the cause of autonomic
dysreflexia. Provide the patient and family education regarding
signs and symptoms and methods of treatment of autonomic
dysreflexia. This is particularly crucial for the patient with SCI who

683
has sustained injury above T6, because these patients are at risk for
autonomic dysreflexia for life.

Dysreflexia Management.

Decreased CO
related to relative hypovolemia secondary to enlarged vascular space
occurring with neurogenic shock.
Goals/Outcomes: The patient has adequate CO, as evidenced by
orientation to time, place, and person; systolic BP ≥90 mm Hg (or
within the patient’s normal range); HR 60 to 100 bpm; RAP 4 to 6
mm Hg; PAP 20 to 30/8 to 15 mm Hg; PAWP 6 to 12 mm Hg; SVR
900 to 1200 dynes/s/cm−5; normal amplitude of peripheral pulses
(greater than 2+ on a 0-to-4+ scale); urinary output ≥0.5 mL/kg/h;
and normal sinus rhythm on ECG.
Circulation Status.

Hemodynamic regulation

1. Monitor the patient for indicators of decreased CO: drop in

systolic BP less than 20 mm Hg, systolic BP greater than 90 mm Hg,
or a continuous drop of 5 to 10 mm Hg with each assessment; HR
greater than 100 bpm, irregular HR, lightheadedness, fainting,
confusion, dizziness, flushed skin; diminished amplitude of
peripheral pulses; change in BP, HR, mental status, and color
associated with a change in position. Monitor input and output;
urine output less than 0.5 mL/kg/h for 2 consecutive hours should
be reported. Assess hemodynamic measurements. In the presence
of neurogenic shock, anticipate decreased RAP, PAP, PAWP, and
SVR (see Table 1-13).

2. Continuously assess cardiac rate and rhythm; report changes in

rate and rhythm.

3. Prevent episodes of decreased CO caused by orthostatic

hypotension:

• Change the patient’s position slowly.

684
• Perform range-of-motion (ROM) exercises every 2
hours to prevent venous pooling.

• Apply elastic antiembolic hose as prescribed to

promote venous return.

• Avoid placing pillows under the patient’s knees,

“gatching” the bed, or allowing the patient to cross
the legs or sit with legs in a dependent position.

• Collaborate with physical therapy personnel in

progressing the patient from a supine to upright
position, using a tilt table.

4. As prescribed, administer fluids to control mild hypotension.

5. Administer and monitor therapeutic effects of vasopressor

therapy (see Appendix 6).

6. Ensure adequate volume repletion before or concurrently with

vasopressor therapy.

Cardiac Care; Fluid Management.

Risk for injury: Gastric 

related to risk of development of gastric ulcer (a Cushing ulcer) or gastritis
secondary to increased gastric acid production.
Goals/Outcomes: The result of the patient’s gastric pH test is
greater than 5, and the patient has no symptoms of gastric ulcer, as
evidenced by gastric aspirate and stool culture that are negative for
blood; BP within the patient’s normal range; HR ≤100 bpm; and
absence of midepigastric or referred shoulder pain.

HIGH ALERT!
Patients sustaining major trauma are at high risk for

685
development of gastritis/gastric ulcers caused by increased
production of gastric acid. Although ulceration can occur at any
time in the patient with spinal cord injury, it is most likely to occur
within 3 weeks of the injury. Cushing ulcers develop in the
stomach, duodenum, and rarely the esophagus in the setting of
central nervous system trauma, whereas Curling ulcers are stress
ulcers related to burns and other trauma that occur almost
exclusively in the duodenum.

Risk Control.

Bleeding precautions

1. Assess for indicators of GI ulceration or hemorrhage:

midepigastric pain (dull, gnawing, burning ache) if the patient has
sensation; and hematemesis, melena, constipation, anemia, pallor,
decreased BP, increased HR, and complaints of shoulder pain.

2. Test gastric aspirate and stools for blood q8h. Promptly consult
the physician if blood is present.

3. Monitor complete blood count (CBC) for signs of anemia:

decreases in Hct, Hgb, and red blood cells (RBCs). Monitor clotting
factors PTT, PT/INR, and platelets.

4. As prescribed, implement measures to treat or prevent ulceration

and hemorrhage:

• Administer PPIs to suppress secretion of gastric

acids, decrease irritating effects of gastric secretions,
and facilitate healing.

• Insert gastric tube and attach to low, intermittent

suction to remove gastric contents.

• Prepare the patient for surgery as indicated.

686
5. For the patient with GI ulceration and hemorrhage, bowel
perforation is an added risk. Be alert to the following indicators:
pallor, shock state, abdominal distention, may or may not have
voluntary or involuntary guarding, vomiting of material that
resembles coffee grounds, absent bowel sounds, elevated WBC
count (greater than 11,000/mm3), and presence of air on abdominal
x-ray view. In some cases the only indicators are tachycardia and
shoulder pain. Lack of pain is not a reliable indicator of bowel
perforation in the patient with SCI. Bowel perforation is an
emergency situation, requiring immediate surgical intervention.

Surveillance; Medication Administration; Bleeding

Precautions; Risk Identification.

Ineffective tissue perfusion (or risk for same): Peripheral

and cardiopulmonary 
related to interruption of blood flow associated with thrombophlebitis,
DVT, and PE secondary to venous stasis, vascular intimal injury, and
hypercoagulability occurring as a result of decreased vasomotor tone and
immobility.
Goals/Outcomes: The patient is free of symptoms of
thrombophlebitis, DVT, and PE, as evidenced by absence of heat,
swelling, discomfort, and erythema in the calves and thighs; HR
≤100 bpm; RR ≤20 breaths/min with normal pattern and depth; BP
within the patient’s normal range; PaO2 ≥80 mm Hg; oxygen
saturation greater than 90%; and absence of chest or shoulder pain.
Tissue Perfusion: Pulmonary.

Cardiac care: Acute

1. The high-risk interval for this diagnosis is the 6- to 12-week

period after injury. Assess for indicators of thrombophlebitis and
DVT: unusual heat and erythema of calf or thigh, increased
circumference of calf or thigh, unilateral tenderness or pain in
extremity (depending on the patient’s level of injury and whether
injury is complete or incomplete). Pain in the calf area with
dorsiflexion (positive reaction for Homan sign) is not a reliable sign
and should be avoided. Recommend Doppler ultrasonography for

687
definitive diagnosis of DVT.

2. Assess for indicators of PE: sudden chest or shoulder pain,

tachycardia, dyspnea, tachypnea, hypotension, pallor, cyanosis,
cough with hemoptysis, restlessness, increasing anxiety, and low
PaO2.

3. Implement measures to prevent development of

thrombophlebitis, DVT, and PE:

• Change the patient’s position at least every 2 hours

to prevent venous pooling.

• Perform ROM exercises on all extremities every 1 to

2 hours to promote venous return and prevent
stasis.

• Avoid use of knee gatch or pillows under the knees,

which can compromise circulation.

• If the patient is out of bed and in a chair, do not

allow the patient to cross legs at the knee or sit with
legs dependent for longer than 0.5 to 1 hour. For the
patient experiencing some return of spinal reflexes
below the lesion with spasticity of lower
extremities, instruct the patient to alert the nurse
should legs become crossed.

• Apply sequential compression devices or

antiembolic hose as prescribed.

• Maintain adequate hydration of at least 2 to 3 L/day,

unless contraindicated, to prevent dehydration and

688
 concomitant increase in blood viscosity, which can
promote thrombus formation.

• Administer prophylactic low-dose, low–molecular-

weight heparin as prescribed.

• Begin transition from low–molecular-weight

heparin to warfarin following PT/INR.

HIGH ALERT!
Patients with spinal cord injury who are not candidates for
anticoagulation because comorbidities may require surgical
intervention (insertion of intracaval filter) to prevent pulmonary
emboli as a result of thrombophlebitis or deep venous thrombosis.

Circulatory Care: Arterial Insufficiency; Circulatory Care:

Venous Insufficiency; Peripheral Sensation Management; Cardiac
Care: Acute; Respiratory Monitoring; Shock Management: Cardiac.

Risk for impaired skin integrity 

related to prolonged immobility secondary to immobilization device or
paralysis.
Goals/Outcomes: The patient’s skin remains intact without areas
of breakdown or irritation.
Tissue Integrity: Skin and Mucous Membranes.

Pressure management

1. Perform a complete skin assessment at least every 8 hours. Pay

close attention to skin that is particularly susceptible to breakdown
(i.e., skin over bony prominences and around halo vest edges,
occiput of head, edges of C spine collar). Be alert to erythema,

689
warmth, open or macerated tissue, and foul odors (indicative of
infection with tissue necrosis).

2. Turn and reposition the patient and massage susceptible skin at

least every 2 hours. Post a turning schedule and include the patient
in the planning and initiating of the schedule.

HIGH ALERT!
Do not turn the patient until the injury has been stabilized or a
turning protocol has been ordered. If turning is allowed before
immobilization with tongs, halo, or surgery, use the logrolling
technique only, using at least three people to turn the patient: one
to support the head and neck and keep them in alignment during
the procedure, and two to turn the patient.

3. Keep skin clean and dry.

4. Pad halo vest edges (e.g., with sheepskin) to minimize irritation

and friction.

5. Provide pressure relief mattress most appropriate for the

patient’s injury.

6. For more information related to the maintenance of skin and

tissue integrity, see Wound and Skin Care, Chapter 1.

Pressure Management; Pressure Ulcer Prevention; Skin

Surveillance.

Imbalanced nutrition: Less than body requirements 

related to decreased oral intake secondary to anorexia, difficulty eating in
prone position, fear of choking and aspiration, and inability to feed self
because of paralysis of upper extremities; decreased GI motility secondary
to autonomic nervous system dysfunction.
Goals/Outcomes: The patient has adequate nutrition, as

690
evidenced by balanced nitrogen state per nitrogen balance studies,
serum albumin 3.5 to 5.5 g/dL, thyroxine-binding prealbumin 20 to
30 mg/dL, and retinol-binding protein 4 to 5 mg/dL.
Nutritional Status.

Nutrition management

1. Perform a complete baseline assessment of nutritional status.

2. Assess the patient’s readiness for oral intake: presence of bowel

sounds, passing of flatus, or bowel movement.

3. If unable to receive proper oral nutrition, prepare to insert a

postpyloric enteral feeding tube or a peripherally inserted central
catheter line for total parenteral nutrition.

4. When the patient begins an oral diet, progress slowly from

liquids to solids as tolerated.

5. Monitor and record percentage of each meal eaten by the patient.

6. Implement measures to maintain or improve the patient’s intake.

• Obtain dietary consultation to provide the patient

with his or her favorite foods, as well as those that
are highly nutritious.

• Provide oral hygiene before and after meals, and

decrease external stimuli (which will also help the
patient concentrate on chewing and swallowing
and thus minimize the risk of aspiration).

• Provide small, frequent feedings; feed the patient

slowly, providing small, bite-size pieces, which
facilitate digestion and help prevent choking; also
less likely to cause abdominal distention, which

691
 may compromise respiratory movement; and less
fatiguing.

• Feed the patient in a position to minimize aspiration

risk, and if the patient is in a halo device or has
been stabilized, feed in high-Fowler position or get
out of bed to chair.

7. Once the patient’s condition has been stabilized, consult with

occupational therapy personnel for selection of assistive devices
that will enable the patient to learn independent feeding
techniques.

Fluid/Electrolyte Management; Swallowing Therapy; Self-

Care Assistance: Feeding.

Urinary retention or reflex urinary incontinence 

related to inhibition of the spinal reflex arc secondary to spinal shock after
SCI or related to loss of reflex activity for micturition and bladder
flaccidity secondary to cord lesion at or below T12.
Goals/Outcomes: The patient has urinary output without
incontinence.

HIGH ALERT!
Urinary retention with stretching of the bladder muscle may
trigger autonomic dysreflexia. Therefore, it is crucial to assess for
retention and to treat it promptly.

Urinary Elimination.

Urinary retention care

1. Assess for indicators of urinary retention: suprapubic distention

and intake greater than output.

692
2. Assess for effects of medications that can cause urinary retention
such as tricyclic antidepressants and anticholinergics.

3. Catheterize the patient as prescribed. Patients usually have an

indwelling catheter for the first 3 to 4 days after injury. Then,
intermittent catheterization is used to try to retrain the bladder. If
intermittent catheterization is used and episodes of urinary
incontinence occur, catheterize more frequently. If greater than 300
mL of urine is obtained, catheterize more often and space fluids to
match output.

4. Measure the amount of residual urine and attempt to increase the

length of time between catheterizations, as indicated by decreased
amounts (i.e., less than 50 to 100 mL of urine).

5. Ensure continuous patency of the drainage system to prevent

reflux of urine into the bladder or blockage of flow, which could
lead to urinary retention or UTI, which may cause autonomic
dysreflexia. Tape the catheter over the pubis to prevent traction on
the catheter, which can lead to ulcer formation in the urethra and
erosion of the urethral meatus.

6. Maintain a fluid intake of at least 2.5 to 3 L/day to prevent early

stone formation caused by mobilization of calcium. Do not reduce
fluids to accommodate bladder training; increase frequency of
intermittent catheterization instead.

7. Teach the patient and significant others the procedure for

intermittent catheterization. Alert them to the indicators of UTI
(restlessness, incontinence, malaise, anorexia, fever, and cloudy or
foul-smelling urine) and the importance of adequate fluid intake,
regular urine cultures, good handwashing technique, and cleansing
of the urinary catheter before catheterization.

HIGH ALERT!
Urinary tract infection (UTI) is one of the leading causes of
morbidity and mortality in the patient with spinal cord injury. This

693
patient may not be aware of the presence of UTI until he or she is
severely ill as a result of pyelonephritis (calculi, infection,
septicemia).

8. Monitor and record input and output. Distribute fluids evenly

throughout the day to prevent overdistention, which can cause
incontinence and increase the risk for autonomic dysreflexia.

9. Decrease fluid intake before bedtime to prevent nighttime

incontinence.

10. For other treatment interventions, see Autonomic Dysreflexia

(or risk for same).

Urinary Catheterization; Urinary Retention Care.

Ineffective thermoregulation 
related to inability of the body to adapt to environmental temperature
changes secondary to poikilothermic reaction occurring with SCI.
Goals/Outcome: Within 2 to 4 hours of this diagnosis, the patient
becomes normothermic.

HIGH ALERT!
With spinal cord injury the patient is poikilothermic, that is, the
patient has a decreased ability to regulate temperature below the
level of the lesion through vasodilation or vasoconstriction
(sweating and shivering). Because there is no autonomic control of
core body temperature, the patient is susceptible to temperature
variations in the environment. Attention to room temperature and
use of external cooling or warming devices may be necessary.

Thermoregulation.

Temperature regulation

694
1. Monitor the patient’s temperature at least every 4 hours and
assess the patient for signs of ineffective thermoregulation:
complaints of being too warm, excessive diaphoresis, warmth of
skin above the level of injury, complaints of being too cold,
pilomotor erection (goose bumps), or cool skin above the level of
injury.

2. Implement measures to attain normothermia: regulate room

temperature, provide extra blankets to prevent chills, protect the
patient from drafts, provide warm food and drink if the patient is
chilled; provide cool drinks if the patient is warm, remove excess
bedding to facilitate heat loss, provide a tepid bath or cooling
blanket to facilitate cooling.

Temperature Regulation; Environmental Management.

Constipation 
related to atonic bowel, paralytic ileus with concomitant autonomic
dysreflexia or loss of anal sphincter control.
Goals/Outcomes: The patient remains free of symptoms of
constipation and/or paralytic ileus, as evidenced by auscultation of
normal bowel sounds, and free of symptoms of autonomic
dysreflexia, and the patient has bowel elimination of soft and
formed stools.

HIGH ALERT!
Paralytic ileus occurs most often in patients with spinal cord
injury at T6 and above and usually within the first 72 hours after
injury.

Bowel Elimination.

Constipation/impaction management

1. Obtain history of the patient’s preinjury bowel elimination

pattern.

695
2. Assess for indicators of paralytic ileus: decreased or absent bowel
sounds, abdominal distention, anorexia, vomiting, and altered
respirations as a result of pressure on the diaphragm. Report
significant findings promptly.

3. Keep the patient NPO (nil per os) until evidence of return of
bowel function (flatus or bowel movements are the most reliable
signs).

4. If indicators of paralytic ileus appear, implement the following,

as prescribed:

• Discontinue oral or enteral intake.

• Insert NG tube to decompress the stomach; attach to

low intermittent suction.

• Monitor NG tube output as large amount may result

in dehydration or metabolic alkalosis.

• Insert a rectal tube if prescribed.

5. Perform a gentle digital examination for fecal impaction and
check for rectal reflexes. Before the return of rectal reflexes, manual
removal of feces may be needed. If a fecal impaction is present in an
atonic bowel, administration of a small-volume enema may be
necessary.

6. Observe closely for signs of autonomic dysreflexia, which can be

triggered by distention of the abdomen (for assessment and
treatment of autonomic dysreflexia, see interventions with
Autonomic Dysreflexia or risk for same).

7. Monitor the patient for indicators of constipation (nausea,

abdominal distention, and malaise) and fecal impaction (nausea,
vomiting, increasing abdominal distention, palpable colonic mass,
or presence of hard fecal mass on digital examination).

696
HIGH ALERT!
Be aware that overdistention of the bowel or stimulation of the
anal sphincter caused by impaction, rectal tube, rectal examination,
or enema may precipitate autonomic dysreflexia. Use generous
amounts of anesthetic lubricant when performing a rectal
examination or administering an enema.

8. Monitor skin at rectal tube site for breakdown. Sensation to

rectum may be spared in incomplete injuries and thus the patient
may have complaints of discomfort with the rectal tube. Remove
the tube as soon as possible to prevent injury to rectal mucosa and
damage to the rectal sphincter.

9. Administer stool softeners (e.g., docusate sodium) daily.

10. If possible, avoid enemas for long-term bowel management,

because the patient with SCI cannot retain the enema solution.
However, if impaction occurs, a gentle, small-volume cleansing
enema may be necessary, followed by manual removal of fecal
material.

11. Assess the patient’s readiness for a bowel retraining program,

including neurologic status and current bowel patterns, noting
frequency, amount, and consistency. Bowel retraining is initiated
when the patient is neurologically stable.

12. Patients with upper extremity function should be engaged in

learning how to perform digital rectal stimulation, insert
suppository, and massage abdomen to facilitate bowel movements.

Surveillance: Bowel Management; Dysreflexia Management;

Tube Care; Constipation/Impaction Management.

Risk for infection 

related to inadequate primary defenses (broken skin) secondary to presence

697
of invasive immobilization devices.
Goals/Outcomes: The patient is free of infection at insertion site
for tongs or halo device, as evidenced by normothermia; negative
culture results; and absence of erythema, swelling, warmth,
purulent drainage, or tenderness at insertion site.
Risk Control.

Infection protection

1. Assess insertion sites every 8 hours for indicators of infection:

erythema, swelling, warmth, purulent drainage, and increased or
new tenderness. Note pin migration. If the pin appears to be loose,
consult the advanced practice provider and instruct the patient to
remain still until the pin can be secured.

2. Perform pin care as prescribed. Cleanse the site with soap and
water or NS; the area may be left open to air. Monitor for drainage
or infection.

Infection Control; Infection Protection; Skin Surveillance.

Disturbed sensory perception visual 

related to presence of immobilization device; use of therapeutic bed.
Goals/Outcome: After intervention(s), the patient expresses
satisfaction with visual capabilities.
Vision Compensation Behavior.

Environmental management

1. Assess for factors that limit the patient’s visual capabilities:

presence of tongs, cervical traction, halo device, and use of specialty
beds.

2. Provide for increased visualization of the patient’s surroundings:

• Obtain prism glasses or hand mirror for patients

who are supine or have restricted head movement
because of halo traction devices.

698
• Position mirrors to increase the amount of area that
can be visualized from the patient’s position.

• Approach the patient and converse within the

patient’s visual field.

• Keep clocks, calendars, and other personal objects

within the patient’s visual field.

Positioning.

Sexual dysfunction or ineffective sexuality patterns 

related to trauma-associated SCI.
Goals/Outcomes: The patient verbalizes sexual concerns before
discharge from ICU.
Sexual Functioning.

Sexual counseling

1. Assess the patient’s level of sexual function or loss from a

neurologic and psychological perspective. The general rule for men
is that the higher the lesion, the greater is the chance of maintaining
the ability to have an erection, but with less chance for ejaculation.
For women, ovulation may stop for several months because of
stress after the injury. Ovulation usually returns, however, and the
woman can become pregnant and have a normal pregnancy. Both
men and women with high lesions may experience feelings of
excitement similar to a preinjury orgasm.

2. Allow the patient to speak about sexual concerns or consult with

a counselor.

3. Check level of patient’s knowledge, questions, and concerns

about sexual function after the SCI.

4. It is normal for men to experience a reflex erection upon

699
resolution of the spinal shock, particularly for individuals with
lesions in the cervical and thoracic areas. Reassure the patient that
this is normal and minimize embarrassment by providing coping
skills.

5. Expect acting-out behavior related to the patient’s sexuality. This

is a normal response to the patient’s concern regarding his or her
sexual prognosis.

6. Provide accurate information regarding expected sexual function

in an open, interested manner, based on your assessment of the
patient’s readiness for information.

7. Facilitate communication between the patient and his or her

partner.

8. Refer the patient and partner for sexual counseling by a sex

therapist, psychologist, or other knowledgeable rehabilitation
professional upon resolution of the critical stages of SCI.

9. Provide the patient with information on the following

organizations that can be accessed through the internet: National
Spinal Cord Injury Association and Spinal Cord Injury Network
International.

Sexual Counseling; Anxiety Reduction; Body Image.

Additional nursing diagnoses

Also see nursing diagnoses and interventions as appropriate under
sections on Nutrition Support, Mechanical Ventilation, and
Prolonged Immobility in Chapter 1, and Emotional and Spiritual
Support of the Patient and Significant Others in Chapter 2.

Burns
Pathophysiology
Burn injuries involve damage to the skin and underlying tissues,

700
but other organ systems may be affected, especially with extensive
(greater than 20% total body surface area [TBSA]) burn injuries. The
cause of injury may be thermal (flame/flash; contact with hot
liquids, semiliquids, hot objects), electrical, chemical, or radiation.
Relative risk of injury differs by age, gender, occupation, and
recreational activities. Estimates for the number of burn injuries in
the United States range from 1.4 to 2 million injuries annually, and
of those, approximately 450,000 seek medical treatment. Of these, it
is estimated that 40,000, including 30,000 at hospital burn centers,
require hospitalization. For those who survive their injury, the
average hospital length of stay is slightly greater than 1 day per 1%
TBSA burn. The number of deaths as a result of fire, burns, and/or
smoke inhalation each year is approximately 3400. In the United
States, the two most common reported etiologies are fire/flame
(43%) and scalds (34%); electrical burn injuries account for 4% of all
admissions to burn centers each year. The burning agent, intensity,
and duration of exposure, location, and depth of burn, and the
extent or size of injury, determine overall injury severity.
Burn injuries are categorized based on depth of injury. The longer
and more intense the exposure to the burning agent, the greater is
the depth of injury. A burn injury is described as either a partial-
thickness or full-thickness injury, relative to the layer(s) of skin and
tissues injured. A superficial injury, commonly referred to as “first-
degree” burn (e.g., sunburn), damages only the epidermis. These
burns typically heal within 3 to 5 days and without permanent
scarring. Partial-thickness injury, called a “second-degree” burn,
involves varying levels of the dermis, which contain structures
essential to skin function (e.g., sweat and sebaceous glands, hair
follicles, sensory nerves, capillary network). These burns typically
heal within 14 to 21 days, depending on the depth. Full-thickness
injury, a “third-degree” burn, destroys the epidermis and dermis
and exposes the less vascularized fat layer, which contains adipose
tissue, roots of sweat glands, and hair follicles. These wounds
require surgical excision of the dead tissue and skin grafting to
provide the best functional and cosmetic outcomes. In very small
full-thickness wounds (e.g., size of a quarter or smaller), healing
may occur by granulation and migration of healthy epithelium
from the wound margins. When full-thickness injuries include

701
destruction of tendon and bone, clinicians often describe these
injuries as “fourth-degree” burns. These injuries are the deepest
and require excision, possibly amputation of extremities, and skin
grafting to heal. Refer to Table 3-6 for detailed burn wound
classification and descriptions.
In patients admitted to burn centers, approximately 10% to 20%
have an associated inhalation injury. Inhalation injury commonly
occurs with flame injuries, particularly if the victim is trapped in an
enclosed, smoke-filled space, and is an important determinant of
survival (60% to 70% of patients who die in burn centers have
inhalation injuries). The associated pathophysiology can be divided
into three types of injury as follows.

• Inhalation of carbon monoxide and other noxious gases: Most

fatalities occurring at the scene of a fire are as a result of
asphyxiation and/or carbon monoxide inhalation (poisoning).
Carbon monoxide binds to Hgb with an affinity that is 200 times
greater than oxygen, resulting in tissue hypoxia.

702
• Injury above the glottis: Injury above the glottis (nasopharynx,
oropharynx, and larynx) can be thermal or chemical in nature.
The heat exchange capability of the respiratory tract is very
efficient such that tissue damage from breathing in heated air
occurs most often above the vocal cords. Heat damage to the
pharynx can be severe enough to cause upper airway edema
resulting in obstruction.

• Injury below the glottis: Injury below the glottis is almost always
chemical in nature, causing direct damage to airway epithelium
from inhalation of the noxious chemicals (e.g., aldehyde, sulfur
oxide, phosgene) of smoke.

Overall, the age of the patient, concomitant injury, and preinjury

health—in combination with injury severity—impact mortality,
length of hospitalization, and ultimately rehabilitation outcomes in
the patient with burn injuries.
Care for the patient with a major burn injury is based on the
patient’s stage of recovery from the pathophysiologic changes
resulting from the cutaneous burn and inhalation injury. The initial
resuscitative period lasts from the time of injury until capillary
membrane integrity is restored, typically 48 to 72 hours after the
burn occurs. Following resuscitation, the acute phase may last for
days to months. It begins with resolution of the fluid shifts and
continues until all or nearly all wounds are healed. The last stage,
or rehabilitative stage, can continue for many months to years and
is seldom a focus for critical care nurses. However, early
rehabilitative efforts such as patient positioning, splinting, exercise,
and patient and family education begin on admission to the
hospital.

Injury severity assessment

The American Burn Association (ABA) has developed an injury
severity classification system that categorizes burn injuries as
minor, moderate, and major. The ABA advocates that patients with
major burns be treated in a burn center or a facility with expertise in
burn care. Moderate burns usually require hospitalization, although

703
not necessarily in a burn center, and minor burns are often treated
on an outpatient basis. Box 3-5 outlines the ABA criteria for patients
who should be referred to a recognized burn center.

Box 3-5
AMERICAN BURN ASSOCIATION BURN
CENTER REFERRAL GUIDELINES
• Partial-thickness burns greater than 10% total body surface area
(TBSA) burn in patients younger than 10 years or older than 50
years.

• Partial-thickness burns greater than 20% TBSA burn in patients 11

to 50 years of age.

• Burns that involve the face, hands, feet, genitalia, perineum, or

major joints.

• Full-thickness burns in any age group.

• Electrical burns (to include lightning injuries).

• Chemical burns.

• Burn injuries with associated inhalation injury.

• Burn injury in patients with preexisting medical disorders that

could complicate management, prolong recovery, or affect
mortality.

• Any patient with burns and concomitant trauma in which the

burn injury poses the greatest risk of morbidity/mortality.

• Burn injury in children at hospitals without qualified personnel or

equipment for the care of children.

• Burn injury in patients who will require special social, emotional,

or long-term rehabilitative interventions.

704
 Excerpted from American Burn Association/American College of
Surgeons Committee on Trauma: Guidelines for the operation of burn
centers. Resources for optimal care of the injured patient 2006, Chicago,
2006, American Burn Association, pp. 79-86.

History and risk factors for a major burn

Several factors affect survival after a major burn injury. The
patient’s age is a determining factor with those at the extremes of
age (less than 2 years and greater than 65 years of age) being at
highest risk of death. Preexisting cardiac or lung disease (e.g.,
COPD) or history of smoking increases susceptibility to respiratory
distress. Patients who sustain a thermal injury in a confined area
may have a concomitant inhalation injury and are also at increased
risk. Patients with preexisting cardiac, vascular, renal, or
respiratory conditions may not tolerate aggressive fluid
resuscitation therapy and may experience complications.
Conditions such as immunosuppression, diabetes, collagen vascular
disease, history of cardiopulmonary or vascular disease, and
invasive procedures contribute to the likelihood of infection, sepsis,
and prolonged healing. Those patients with a history of drug
and/or alcohol abuse have an increased mortality risk and often
have longer hospital stays. Burn injury can be associated with a
concomitant traumatic injury from a blast, motor vehicle crash, or
fall. Careful evaluation for secondary injury is essential.

Initial assessment
In the prehospital setting or emergency department, patients with a
burn injury should be evaluated using a primary survey followed
by a more thorough, secondary survey; the principles of which are
taught in the Advanced Burn Life Support (ABLS) course. The
primary patient survey includes the basic ABCs, with the addition
of D and E: A: airway and cervical spine immobilization (based on
mechanism of injury); B: breathing; C: circulation; D: disability or
neurologic deficit; and E: exposure and evaluation. Once the
primary survey is complete, a secondary survey should be

705
performed and includes a detailed head-to-toe assessment,
exploration of the circumstances of the injury, and the patient’s
medical history. Injury severity is assessed according to patient’s
age, potential for inhalation injury, TBSA burn, depth and location,
past medical history, and concomitant trauma.

Initial system assessment

• Assess airway for obstruction.

• Assess breathing for distress.

• Assess for decreased tissue perfusion.

• Assess for TBSA burn and depth of burn injury.

• Trauma assessment to identify concomitant injury.

• Assess for pain and anxiety.

Airway/breathing
• Observe for foreign objects in mouth, including a large tongue
that may obstruct the airway.

• Observe for signs of accessory muscle use for respirations.

• If intubated, verify tube placement, work of breathing, and

appropriate ventilator settings.

Heart rate, heart rhythm, BP to evaluate CO and

perfusion
• Assess HR and rhythm, especially if the TBSA burn is greater
than 20% because patients tend to be tachycardic (pain will also
increase HR).

• Central line monitoring for hemodynamic status (e.g., CVP, PAP,

PAWP, CO) is not commonly used unless the patient exhibits
signs of hemodynamic instability.

706
• Take BP on uninjured extremity if possible. Arterial line may be
necessary for BP monitoring if burn injury to bilateral extremities
is extensive and/or patient exhibits hemodynamic instability.
Compare cuff BP to arterial line BP if arterial line is in place;
decide which pressure is deemed the most accurate.

• Evaluate for distal tissue perfusion, appearance of uninjured skin,

color of nail beds, capillary refill, and temperature of extremities.
Assess for the six “Ps”:

• Pain out of proportion to the injury.

• Pallor.

• Pulselessness.

• Paresthesias.

• Paralysis.

• Poikilothermia (or “polar”/cold to touch).

Burn wound extent (calculation of TBSA burn)

The extent of the burn wound is reported as a percent of the TBSA
injured. In adults, this is easily estimated by using the rule of nines
(Figure 3-1). In children, this rule is altered slightly, reflecting the
different body proportion in infants and children. The rule of nines
technique is used in prehospital settings and emergency
departments when a quick assessment is necessary. For very small
and/or irregularly shaped or scattered burns, it helps to remember
that the surface area of the patient’s palm (palm plus fingers) equals
1% of the patient’s TBSA. A more accurate assessment tool is the
Lund-Browder chart (Figure 3-2), which is more detailed and
accounts for changes in body areas according to age. This chart may

707
be used for both children and adults and is frequently used in
critical and acute care settings. More recent studies have called into
question the use of these measures in the morbidly obese
population and suggest that as the body mass index increases, the
size of the palmer surface in relation to the percent TBSA burn
decreases.

FIGURE 3-1 Estimation of adult burn injury: rule of

nines. A, Anterior view. B, Posterior view. Source: (From
Thompson M, McFarland GK, Hirsch JE, et al: Mosby’s clinical nursing, ed
4, St Louis, 1997, Mosby.)

708
 FIGURE 3-2 Estimation of burn injury: Lund and
Browder chart. Areas represent percentages of body
surface area that vary according to age. The
accompanying table indicates the relative percentages
of these areas in various stages of life. Source: (From
Sabeston DC Jr, editor: Textbook of surgery: the biographical basis of
modern surgical practice, ed. 11, Philadelphia, 1977, Saunders.)

Electrical burn injuries may reveal only cutaneous

injuries on initial inspection, but extensive damage can occur to
deep and underlying tissues, nerves, blood vessels, and muscles
along the conduction path and at the electrical current contact
sites.

709
• Estimate wound size (percent TBSA burn) and assess depth
(partial- or full-thickness burn injury).

Palpation
• Pulse assessment to evaluate for decreased tissue perfusion of all
extremities:

• Pulse quality and regularity bilaterally (0-to 4+

scale);

• Edema (0-to-4+ scale): unburned tissue of

extremities.
• Turgor assessment of unburned extremities.

• Temperature of extremities (cool extremities may be indicative of

poor distal perfusion of extremities).

Auscultation
• Respiratory sounds to assess for adventitious breath sounds;
confirm for bilateral breath sounds.

• Heart sounds to evaluate for contributors to decreased CO (note

changes with body positioning and respirations):

• S1 and S2: quality, intensity, pitch;

• Extra sounds: S3 (after S2), S4 (before S1) indicative

of heart failure.

• Bowel sounds: presence or absence; location.

Respiratory system

710
 Respiratory compromise may occur as a result of upper airway
swelling, inhalation injury, carbon monoxide poisoning, or
respiratory tract infection. The upper airway is injured when hot air
causes heat injury to the respiratory mucosa. The lower respiratory
tract can be damaged by contact with products of combustion and
inhalation of vaporized caustic substances, such as sulfur, hydrogen
cyanide, ammonia, acrolein, aldehydes, and hydrochloric acid.
These noxious gases are produced from the combustion of common
household items, such as carpeting, furniture, and decorations.
Airway injury, obstruction, or respiratory distress may not occur
immediately following injury.

• Secure and protect airway; check for any cervical injuries and
need to stabilize neck area for appropriate airway protection
positioning.

• Progressive swelling of the upper airway (above the glottis) may

lead to airway obstruction. Check for airway obstruction as a
result of swelling caused by heat, smoke, or chemical injury to
nasopharyngeal mucosa or by constriction around the neck or
chest caused by eschar (burned, devitalized tissue) formation.

• Assess for singed nasal hairs, perioral burns, change in voice, or

coughing, especially if productive for soot (mucus will have gray
or black particles).

• Carbon monoxide, a byproduct of combustion, displaces oxygen

from Hgb, resulting in hypoxia. Headache, decreased visual
acuity, tinnitus, vertigo, confusion, unresponsiveness, and
convulsions are signs of carbon monoxide poisoning. Refer to
Table 3-7 for signs and symptoms of carbon monoxide poisoning.

Unresponsiveness is not normally associated with burn

injuries; patients who are difficult to arouse at the scene or in the
emergency department should be evaluated for carbon monoxide
exposure or other potential causes (i.e., traumatic brain injury,
drugs/alcohol).

711
Table 3-7
CARBON MONOXIDE POISONING

Carboxyhemoglobin Saturation (%) Signs and Symptoms

≤10 Impaired vision
11-20 Headache, facial flushing
21-30 Nausea, trouble with dexterity
31-40 Nausea, vomiting, dizziness, syncope
41-50 Tachypnea, tachycardia, loss of consciousness
>50 Coma, death

• Epithelial or mucosal sloughing with bronchitis and respiratory

distress may occur 6 to 72 hours after the burn occurs and may
further contribute to airway obstruction. The top layer of the
mucosal lining of the airway “peels” away; similar to the skin
peeling after a sunburn.

• Stridor, severe hoarseness, hacking cough, labored breathing,

dyspnea, tachypnea, and possible altered LOC caused by
hypoxia.

Physical and radiographic evidence of respiratory

compromise may be absent initially, despite pulmonary injury.
Progression to airway obstruction and acute respiratory distress
can occur rapidly, especially in the presence of injury above the
glottis or secondary to large fluid volume resuscitation for burns
greater than 40% total body surface area.

• Pulmonary excursion is limited by circumferential full-thickness

wounds of the neck and torso. Circumferential full-thickness
burns of the torso often cause inadequate pulmonary excursion,
leading to inadequate ventilation. When pronounced, a chest wall
escharotomy may need to be performed.

• Assess for low blood oxygen content, respiratory distress,

impaired chest wall excursion, increased peak pressures,

712
 decreased compliance, and abnormal ABG values.

• Patients with inhalation injury are at risk for pneumonia. On

average, 50% of all burn patients with inhalation injury who
require mechanical ventilation will develop pneumonia.

• Assess for bronchial breath sounds over areas of consolidation,

crackles.

Cardiovascular system
Circulatory compromise results from the fluid shifts that occur
following a significant (typically greater than 20% TBSA) burn
injury. Increased capillary permeability caused by the inflammatory
response results in a shift of intravascular fluid into the interstitial
spaces in the first 72 hours postburn. This causes a decrease in
circulating volume and increased blood viscosity. Other systemic
responses include increases in catecholamines, cortisol, renin-
angiotensin, antidiuretic hormone, and aldosterone production as
the body attempts to retain sodium and water to replenish
intravascular fluid. Rapid fluid shifts can result in massive edema
in unburned and burned areas, hemoconcentration, and thrombus
formation.

• Signs of hypovolemic shock, such as thirst, pallor, dry

mucous membranes, decreased LOC, and cool skin temperature;
tachycardia, hypotension, and decreased filling pressures (CVP,
PAP, PAWP); decreased or absent peripheral pulses and delayed
capillary refill; and impaired peripheral perfusion with possible
obstruction caused by vascular compression with circumferential
full-thickness burns or thrombus formation.

• Cardiac dysrhythmias caused by direct cardiac damage (electrical

burns).

• Electrolyte imbalance (e.g., hyperkalemia caused by cellular

hemolysis).

• Peripheral edema as a result of fluid shifts and hypoproteinemia.

713
Gastrointestinal system
Initially, blood flow is shunted away from the GI tract and
peristalsis is slowed or stopped completely, causing a gastric ileus
(usually resolves within 72 hours after burn injury).

• Before the initiation of early enteral feedings, life-threatening

stomach and intestinal ulcerations (Curling ulcers) and
hemorrhage (associated with low gastric pH) often occur.
Prophylaxis should be initiated with the use of PPIs or H2-
receptor antagonists and/or early enteral feeding.

• Large fluid resuscitation volumes pose a significant risk for

abdominal compartment syndrome.

• Assess for diminished or absent bowel sounds; presence of

nausea and vomiting; abdominal distention.

Renal system
Hemoconcentration and reduced circulatory volumes result in
decreased renal blood flow and low urinary output. Dark
concentrated urine in the presence of muscle injury implies
myoglobinuria or hemoglobinuria. Continued poor renal perfusion
results in acute tubular necrosis and renal failure. Urine output
guides fluid resuscitation measures and recognition of renal
compromise or poor CO is essential.

Target urinary output is 30 to 50 mL/h for adults (up to 100

mL/h with hemoglobinuria or myoglobinuria) during the initial 24
to 48 hours of resuscitation.
Target urinary output for children (weighing less than 30 kg) is 1
mL/kg/h.

• Urine output less than 30 mL/h in adults and 0.5 mL/kg/h in

children less than 30 kg; dark-colored, concentrated urine.

714
 Bladder pressures exceeding 20 mm Hg may constitute an
emergency as it may indicate abdominal compartment syndrome.
Thus it is important for the nurse to monitor any increases in
trending of bladder pressures.

• Consider bladder pressure monitoring every 4 hours during

excessive fluid administration. During the resuscitation period,
excessive fluid administration is usually defined as greater than
1.5 to 2 times the calculated fluid resuscitation estimates (see
Collaborative Management).

Integumentary system
Loss of skin integrity results in increased fluid loss through
evaporation, hypothermia, pain, and increased risk of infection.
Evaporative fluid losses can be substantial, especially in patients
with large surface area burns and in pediatric patients with burn
injuries who have larger surface area per kilogram of body weight.
Significant hypothermia can result in patients with large surface
area burns, long transports to the hospital, and long surgeries and
in those who require prolonged wound care.
Patients with burn injuries can experience three types of pain:

• Procedural pain is experienced during painful procedures (e.g.,

wound debridement, dressing changes, staple removal, active
physical therapy) and is often described as pain that is of short
duration and high intensity.

• Background pain, which is experienced at rest or while doing

minimal physical activities, and is often described as constant
and of low intensity.

• Breakthrough pain is experienced during activities or painful

procedures despite the administration of procedural pain
medication and is intense and of short duration.

715
 Circumferential full-thickness burns can cause constriction of
underlying tissue, blood vessels, and muscles with circulatory
compromise to underlying muscles and distal extremities. Healed
skin may result in some scar formation, which can lead to
contractures that limit joint ROM.
See Table 3-6 for a complete description of partial-thickness and
full-thickness burn wound injuries.

Wound infection
Loss of skin integrity means that the body’s first line of defense
against infection is compromised. Ongoing evaluation for burn
wound infection is imperative because a significant infection may
lead to delayed healing, tissue loss, and sepsis. Typically, the larger
the wound or delay in complete healing, the greater is the risk for
wound infection. Early signs of wound infection include fever,
increase or decrease in WBC count, erythema surrounding the burn
wound, increased wound pain, change in exudate or wound
appearance, and loss of previously healed skin grafts. Invasive
wound infection is indicated by rapid eschar separation (invasive
fungal infections); focal, dark red, brown, or black discolorations in
the eschar; rapid conversion of an area of partial- to full-thickness
injury; and hemorrhagic fat necrosis.

Systemic inflammatory response syndrome/septic

shock
All patients who are severely burned display signs and symptoms
of SIRS; therefore, this term is not used to describe the
inflammatory processes in the patient with burn injuries. However,
if more than three signs and symptoms of SIRS (modified
slightly for the patient with burn injuries) are present along with a
documented source of infection, sepsis is present.
Signs of burn sepsis include:

• Tachycardia: HR greater than 110 bpm (depending on baseline,

age, and comorbidity).

• Tachypnea: RR greater than 25 breaths/min (age-dependent).

716
• Decreased BP with low SVR.

• Labile core body temperature (may fluctuate by more than 3° C,

as low as 36.5° C).

• Low platelet count (thrombocytopenia).

• Changes in LOC (confusion, disorientation, agitation).

• Hyperglycemia or increasing insulin requirements.

• Feeding intolerance; increased enteral feeding residuals; loss of

appetite.

• Gastric distention or gastric ileus.

Diagnostic Tests for Major Burn Injury

717
Diagnostic tests
Bronchoscopy
The ABA Consensus Conference on Burn Sepsis and Infection
Group has determined that bronchoscopy is the best and most
reliable test for diagnosis of smoke inhalation injury below the
glottis. Signs of injury below the glottis that can be observed with
bronchoscopy include carbonaceous material, edema, and
ulceration. Therapeutic bronchoscopy facilitates removal of
carbonaceous material and nonviable tissue.

718
Fluorescein examination
This procedure uses orange dye (fluorescein) and an ultraviolet
light (Wood lamp) to detect foreign bodies in the eye and/or
damage to the cornea. This examination should occur in all patients
with possible eye injury and should be performed early (first 24
hours after burn injury), before swelling prevents a thorough
examination.

Culture and sensitivity studies

This diagnostic test evaluates sputum (pneumonia), blood
(bacteremia or septicemia), urine (UTI), and wound tissue for
evidence of colonization and infection.
Burn wound infection is defined as more than 105
microorganisms/g of burn wound tissue with active invasion of
adjacent, viable, unburned skin. Gram-negative organisms include
Pseudomonas aeruginosa, Klebsiella, Serratia, Acinetobacter, Escherichia
coli, and Enterobacter cloacae. Gram-positive organisms
(Staphylococcus and Streptococcus) and fungal pathogens (Candida
and Aspergillus) may also be present. Colonization of burn wounds
is common and not treated with systemic antimicrobial therapy.
Topical agents are used to reduce microbes. Surveillance cultures
may be collected on admission for screening of multidrug-resistant
organisms and methicillin-resistant Staphylococcus aureus. An
epidemiologic investigation may be needed to evaluate infection
trends.

Urine collections
Perform urinalysis and culture and sensitivity early to detect UTI. A
24-hour urine collection to measure total nitrogen, urea nitrogen,
creatinine, and amino acid nitrogen values may indicate return of
capillary integrity (3 to 5 days after burn occurrence) and
mobilization of third-spaced fluids, the degree of catabolism
present, and the onset or resolution of acute renal failure.
Myoglobinuria can result from muscle injury sustained from an
electrical injury or deep full-thickness burn.

Hematology

719
Elevated Hct resulting from hemoconcentration during initial
resuscitation. Hgb will be decreased secondary to dilution, surgical
burn wound excision, hemolysis, or multiple laboratory draws.
During the first 24 hours postburn, neither the Hgb level nor the
Hct is a reliable guide to fluid resuscitation. WBCs may be
elevated resulting from systemic inflammatory response or sepsis.
Patients with burn injuries will typically be leukopenic initially
because WBCs migrate to areas of burned tissue.

Electrolyte panel
Hyperglycemia is common in patients related to the normal stress
response of injury. Hyperglycemia may also be seen in patients
with sepsis and multiple organ failure. Sodium shifts occur during
resuscitation; carefully monitor and adjust type of resuscitation
fluid 24 hours postinjury. Vigilant monitoring of the ECG for T
wave elevation indicative of hyperkalemia is of paramount
importance. Early identification of hyperkalemia facilitates prompt
treatment. Potassium may be elevated as a result of cell lysis, fluid
shifts, or renal insufficiency. Blood urea nitrogen (BUN) is elevated
because of hypovolemic state, increased protein catabolism, or
possible acute renal failure. Persistent elevation of BUN and
creatinine signals inadequate fluid intake or acute renal failure.
Total protein and albumin are decreased secondary to leakage of
plasma proteins into interstitial spaces. Creatine kinase (CK) is
sometimes used as an index of muscle damage, but a burn injury
that damages even a small quantity of muscle tissue will result in
markedly elevated CK levels in the first 24 hours. Troponin levels
are more indicative of cardiac damage. Increase in lactate may
indicate inadequate fluid resuscitation (first 12 to 24 hours
postburn), infection, or shock state from decreased tissue perfusion
or sepsis.

ECG
Evaluate for tachycardia secondary to hypovolemia or pain.
Tachycardia of 100 to 120 bpm is common in the adult patient who
appears adequately resuscitated. Myocardial damage secondary to
high-voltage electrical burn injury may be evident (e.g.,
dysrhythmias, prolonged QT interval). Dysrhythmias related to

720
electrolyte imbalance may occur. Hyperkalemia is relatively
common and, if extreme, requires immediate care to avoid a lethal
dysrhythmia.

Collaborative management
Care priorities

1. Manage hypoxemia and protect the upper airways by

using humidified oxygen therapy
Treats hypoxemia and prevents drying and sloughing of the
mucosal lining of the tracheobronchial tree. If the patient is awake,
oxygen administration by nonrebreather face mask may be
sufficient; intubation may be required if the patient is stuporous,
unconscious, or with significant burn injuries to the face or upper
airway area. Any patient with suspected carbon monoxide
poisoning/inhalation injury should receive humidified 100%
oxygen by nonrebreather face mask until the carboxyhemoglobin
level falls below 10%. Hyperbaric oxygen therapy (HBOT) is a
treatment sometimes used to accelerate resolution of carbon
monoxide poisoning in patients with burn injuries, as well as
healing of gangrene, wounds, and infections in which tissues are
unable to receive adequate oxygen. The purpose of HBOT in carbon
monoxide poisoning is to reduce the amount of carbon monoxide in
the blood by displacing carbon monoxide molecules bound to
hemoglobin (carboxyhemoglobin), and replacing them with oxygen
(O2) molecules (oxyhemoglobin) to restore the oxygen level to
normal quickly. The high pressure within the chamber increases
blood oxygen level 10- to 15-fold. HBOT can break the cycle of
swelling, tissue hypoxia, and tissue necrosis. HBOT is used
consistently to resolve carbon monoxide poisoning, but on a case-
by-case basis to manage tissue damage associated with thermal
burn injuries.

2. Support ventilation by providing intubation and

mechanical ventilation:
Endotracheal intubation is indicated if respiratory distress or

721
failure is present, airway obstruction from laryngeal edema
associated with the superheated gases is imminent (e.g.,
progressive hoarseness and/or stridor), or the patient cannot protect
their airway (impaired LOC). Large burn injury (more than 40%
TBSA) may result in generalized tissue edema even in the absence
of inhalation injury, requiring prophylactic intubation for airway
protection. Because laryngeal edema typically resolves in 3 to 5
days after the burn injury, tracheostomy is avoided for upper
airway distress unless there is acute obstruction or prolonged need
for ventilatory support.
For patients requiring intubation and mechanical ventilation,
implementation of measures (e.g., Ventilator Bundle) to prevent
ventilator-associated pneumonia are instituted. Ventilator-
associated events are identified by using a combination of objective
criteria: deterioration in respiratory status after a period of stability
or improvement on the ventilator, evidence of infection or
inflammation, and laboratory evidence of respiratory tract infection
(www.cdc.gov/nhsn/pdfs/pscManual/10-VAE_FINAL.pdf).
Ventilator-associated pneumonia is the leading cause of death
among patients with hospital-acquired infections; it prolongs time
spent on the ventilator, in the ICU, and the total hospital length of
stay.
The key components of the Institute for Healthcare Improvement
(IHI) Ventilator Bundle are noted as follows (*); other key
preventative interventions are also suggested:

• Hand hygiene.

• Elevation of the head of the bed 30 to 45 degrees.*

• Mouth care and endotracheal tube care.

• Daily “sedative interruptions” and assessment of readiness for

extubation.*

• Peptic ulcer disease prophylaxis.*

• DVT prophylaxis* (unless contraindicated).

722
• Lung protective ventilator strategies.

• Early mobilization.

The Institute for Healthcare Improvement (IHI) Ventilator

Bundle is a set of key evidence-based interventions related to
mechanical ventilator care that when implemented collectively
and consistently lead to better patient outcomes.

3. Thin secretions with bronchodilators and mucolytic

agents
Aid in promoting gas exchange and in loosening of pulmonary
secretions.

4. Relieve constriction of circumferential burns with

escharotomy
An incision through eschar to relieve constriction caused by
circumferential, full-thickness burns. Escharotomies of the chest
wall relieve respiratory distress secondary to circumferential, full-
thickness burns of the trunk. Escharotomies of the extremities
lessen pressure created by underlying edema to restore adequate
tissue perfusion. Escharotomies of the torso and/or extremities may
be performed at the bedside or in the emergency department by
trained personnel. Indicated when patients have burns of thorax,
when respiratory excursion is restricted or exhibit cyanosis and
cold temperature of distal unburned skin, prolonged capillary
filling, decreased sensation and movement, or weak or absent
peripheral pulses (mimics compartment syndrome).

5. Hydrate using large-bore IV access

Peripheral veins should be used to establish IV access using two
large-bore IV catheters. Veins underlying unburned skin are
preferred; however, veins beneath burned skin can be used if

723
necessary. If peripheral IV access is not possible, obtain central
venous line access (preferably through nonburned skin) for IV
administration. Intraosseous infusion may be necessary if
peripheral or central venous access is not possible.

Patients with less than 20% total body surface area burns
may be candidates for oral fluid resuscitation. Oral resuscitation
should be considered when the patient is able to tolerate oral
intake (intact gastrointestinal tract) or when resources are limited
(e.g., mass casualty situation).

6. Fluid resuscitation
The goal of fluid resuscitation is to maintain tissue perfusion
and organ function while avoiding the complications of inadequate
or excessive fluid therapy (Advanced Burn Life Support). Fluid
replacement protocols are based on body weight and percent of
TBSA burned and provide an estimate for resuscitation. The ABA
Consensus formula recommends administration of 2 to 4 mL fluid
per kilogram body weight per percent TBSA burned (adult) and 3
to 4 mL fluid per kilogram body weight per percent TBSA burned
(infants and young children weighing less than 30 kg) to provide
the total estimate of fluids to be administered in the first 24 hours
following the time the burn occurred. Give half in the first 8 hours
and then the second half over the next 16 hours. The initial infusion
rate is calculated using the Consensus formula and subsequent
hourly titration is guided by urinary output (30 to 50 mL/h for
adults and 1 mL/kg/h in children weighing less than 30 kg). LR
solution is used in the first 24 hours, with small amounts of colloid
fluids added during the second 24 hours after injury. Colloids are
generally avoided during the first 12 to 24 hours after injury
because increased capillary permeability allows leakage of protein
into the interstitial tissues. The greater surface area–to–body mass
ratio of children necessitates the administration of relatively greater
amounts of resuscitation fluid. In addition, infants and young

724
children should receive fluid with 5% dextrose (e.g., D51⁄4 NS or D51⁄2
NS) at a maintenance rate in addition to the LR resuscitation fluid.
Maintenance fluids are provided at a constant rate and are based on
the child’s dry weight. A child weighing up to 10 kg should receive
4 mL/kg/h; those 11 to 20 kg should receive 2 mL/kg/h, and those 21
to 30 kg should receive 1 mL/kg/h during the first 24 hours
following injury. Patients who are particularly sensitive to excessive
fluid resuscitation include children, older adults, and those with
preexisting cardiac disease.

Calculate fluid infusion from the time of injury, not the time
of hospital admission. Fluid resuscitation and maintenance
formulas should be modified based on individual patient responses
and needs. Hourly urine output serves to guide infusion rates.
Patients with electrical injuries, very deep burns, inhalation
injury, prior dehydration, ethanol intoxication, and concomitant
trauma (e.g., crushing injuries) may have greater fluid needs than
suggested by their cutaneous burn injury alone.

7. Maintain an accurate record of the fluid balance

Insertion of an indwelling urinary catheter may be essential for
accurate hourly measurement of urine output and evaluation of
renal status in patients with a major burn injury.

8. Facilitate core body temperature regulation

For patients with extensive burn injuries, the body’s response to
injury is to increase core and skin temperatures by 2° C above
normal. Increasing the ambient room temperature to 33° C (91.4° F)
helps to attenuate the hypermetabolic response. Limit body
exposure during wound care and dressing changes.

9. Prevent aspiration of gastric contents by ng intubation

Permits gastric decompression, reducing risk of aspiration. Aids in
the removal of gastric contents, which may be necessary during the

725
resuscitative phase because of the potential for gastric ileus in
patients with greater than 20% TBSA burn and in patients with
intubated airway.

10. Provide proper patient positioning to decrease the

potential for further injury
Burn injured extremities should be elevated to reduce dependent
edema formation. Patients with burns of the head or ears should be
positioned without a pillow (to prevent the incidence of neck
flexion contractures and ear chondritis [can develop from pressure
on injured, fragile ear cartilage]). Patients should be routinely
positioned to reduce contracture formation with frequent position
changes to reduce the incidence of pressure sores.

11. Provide aggressive nutrition support

High metabolic activity and increased protein catabolism related to
burn injury result in dramatic increases in energy requirements and
nutritional needs. Additional injury (e.g., long bone fractures) or
poor nutritional status before the burn injury may further increase
nutritional needs. This hypermetabolic response to injury typically
continues beyond the acute phase of recovery and may last up to 1
year for those with extensive burn injuries (i.e., >40% TBSA burn).
Energy requirements are estimated using one of several predictive
formulas based on body size and extent of burn, with adjustment
for age, and are calculated by nutritionists. Indirect calorimetry is
also used to measure energy expenditure, thus providing a measure
of calories needed. However, the equipment required for indirect
calorimetry is expensive and requires trained personnel to
administer the test.
Although nutrition practices vary, nutrition support should be
initiated early in the recovery process. The appropriate mix of
protein, fat, and carbohydrates to be provided is not standardized,
but a positive nitrogen state can be achieved with patients who are
administered high-protein, moderate-carbohydrate, and low-fat
diets.
Oral, enteral, or parenteral methods of delivery are used, based
on patient tolerance. Many critically ill patients with burn injuries
are unable to meet their increased nutrition requirements with oral

726
intake alone. Enteral feedings are preferred in these patients and
have the added benefit of decreasing GI acidity and ulcer
formation. Either gastric or postpyloric jejunal feedings may be
used. Elemental jejunal feedings may be tolerated when
conventional feedings are not. Total parenteral nutrition may be
initiated for the patient with gastric ileus or inability to tolerate an
adequate amount of enteral feedings.
For patients who are difficult to wean from the ventilator, it has
been suggested that the use of higher-fat, lower-carbohydrate diets
may be beneficial because excess carbohydrate increases CO2
production.

• Support nutrition status with multivitamin and mineral

supplements: Many vitamins and minerals affect immune
function, protein synthesis, and wound healing. Vitamins A and
C and zinc are especially important for promoting wound
healing. Multivitamins are commonly prescribed for patients
with burn injuries.

12. Perform wound care

Wound cleansing is accomplished with use of mild soap and water.
Burns are débrided using manual, enzymatic, or surgical
techniques. Topical antimicrobial agents, such as silver sulfadiazine
and mafenide acetate, are used to control bacterial proliferation.
Burn wounds may be covered and ultimately closed with various
temporary and permanent coverings as in the following list. Care of
the patient with these coverings depends on the type of wound
closure technique used.
Wound coverage and closure techniques:

• Cutaneous autograft: includes split-thickness skin graft and

cultured epithelial autograft; provides permanent wound
coverage.

• Cutaneous allograft: fresh or preserved donated adult cadaver

skin; provides temporary wound coverage until the wound bed is
ready for autografting.

• Cutaneous xenograft: harvested adult porcine epidermis

727
 (pigskin); provides temporary wound coverage until the wound
bed beneath is healed or is ready for permanent autografting.

• Biosynthetic coverings: artificial dermis (e.g., Integra); provides a

permanent dermal tissue layer that requires a thin autograft for
permanent coverage.

• Synthetic coverings: various dressings often used to cover partial-

thickness burns and/or donor sites; provide temporary wound
coverage until the wound bed beneath is healed or is ready for
permanent autografting; often include an antimicrobial agent
(e.g., silver) that is released over time. Use and care of wounds
when treated using these specialized dressings are specific to the
type of product used; follow directions by manufacturer for use
based on burn depth (some dressings may only be appropriate
for use in partial-thickness burn injuries), length of use (this is of
particular importance in dressings providing time release of
silver), and dressing removal procedure.

13. Prepare for surgery as needed

Need for surgery depends on the depth and extent of the burn
injury. The burn surgeon coordinates the surgical team.

Pharmacotherapy

1. Provide tetanus prophylaxis

Tetanus immunoglobulin (TIG) or tetanus-toxoid (Tt) should be
provided based on the patient’s previous immunization for tetanus
prophylaxis. Obtain a history of tetanus immunization from the
patient or medical records so that appropriate tetanus prophylaxis
can be accomplished. Individuals with risk factors for inadequate
tetanus immunization status should be treated as tetanus
immunization—unknown. The tetanus prophylaxis administered
should be consistent with the recommendations of the American
College of Surgeons (see
www.facs.org/trauma/publications/tetanus.pdf). Burn injuries are
considered “tetanus-prone wounds.” Tetanus prophylaxis is given
intramuscularly.

728
2. Manage pain with IV analgesics and anxiolytics
Morphine sulfate and fentanyl are common agents used for pain
management. They are administered in small, frequent IV doses, as
needed for comfort and before painful procedures. Consider
adjunctive treatment using benzodiazepines (e.g., lorazepam,
diazepam, midazolam) to decrease anxiety. Anxiety increases the
perception of pain.

During the resuscitative phase of care, all medications,

except tetanus immunoglobulin or tetanus-toxoid, are
administered intravenously to avoid sequestration of medication,
which then would “flood” the vascular system with the return of
capillary integrity and the diuresis of third-spaced (interstitial)
fluids.

3. Consider gastric acid suppression therapy

Maintain gastric pH greater than 5.0 to prevent development of
gastric ulcers. Early initiation of enteral tube feedings or use of IV
PPIs and an H2-blocking agent assist with maintenance of gastric
pH and the prevention of ulcers.

4. Administer antibiotics for known infections

Antibiotics are not routinely prescribed unless a known or
suspected infection exists. Broad-spectrum antibiotics may be used
initially to treat a suspected infection. More specific antimicrobial
agents are used when results from culture and sensitivity tests are
available. Burn wound colonization is treated with topical
antimicrobial agents only.

5. Provide DVT prophylaxis

Prophylactic measures may include the selective use of sequential
compression devices on unburned extremities, subcutaneous
heparin, low–molecular-weight heparin, or IV heparin drip. The
incidence of DVT in the burn population is unknown; however, it is

729
logical to assume that this patient population is at high risk because
of hypercoagulability, altered vascular integrity from the burn
injury, imposed immobilization, and multiple operative
procedures.

Care plans: Burns

Ineffective airway clearance (or risk for same) 
related to increased pulmonary secretions and inflammation, swelling of
nasopharyngeal mucous membranes secondary to smoke irritation or
impaired cough; potential of constricting neck and thorax burns and
decreased expansion of alveoli secondary to circumferential thorax burns,
or pneumonia.
Goals/Outcomes: The patient maintains a clear airway, as
evidenced by auscultation of normal breath sounds over the lung
fields and a state of eupnea.
Respiratory Status: Airway Patency.

Airway management

1. Assess and document respiratory status, noting breath sounds

and rate and depth of respirations. Identify deteriorating
respiratory status, as evidenced by crackles, rhonchi, stridor,
labored breathing, dyspnea, tachypnea, restlessness, and decreasing
LOC. Consult physician promptly for all significant findings.

2. Assess and document characteristics and amount of secretions

after each deep-breathing and coughing exercise.

3. Reposition the patient from side to side every 1 to 2 hours to help

mobilize secretions; position the head of the bed at a 30 degree
elevation. Consider the use of a specialized rotation bed.

4. As prescribed, administer percussion and postural drainage to

facilitate airway clearance (this is contraindicated with fresh skin
grafts over thorax). Perform oropharyngeal or endotracheal
suctioning, as indicated by the presence of adventitious breath
sounds and the patient’s inability to clear the airway effectively by

730
coughing.

5. Administer bronchodilating medications, if prescribed.

Airway Management; Airway Suctioning; Artificial Airway

Management; Aspiration Precautions; Cough Enhancement;
Mechanical Ventilation.

Impaired gas exchange (or risk for same) 

related to inhalation injury with tracheobronchial swelling and
carbonaceous debris; competition of carbon monoxide with oxygen for Hgb;
hypoventilation associated with constricting circumferential burns to the
thorax or large fluid volume resuscitation.
Goals/Outcomes: The patient exhibits adequate gas exchange, as
evidenced by PaO2 ≥80 mm Hg, oxygen saturation ≥95%, Paco2 35 to
45 mm Hg, age-appropriate RR with a normal pattern and depth,
and absence of adventitious breath sounds and other signs of
respiratory dysfunction. These outcomes should be adjusted for
patients with preinjury respiratory disease (e.g., COPD).
Respiratory Status: Gas Exchange.

Respiratory monitoring

1. Assess and document respiratory status, noting rate and depth,

breath sounds, and LOC. Identify deteriorating respiratory status,
as evidenced by indicators of upper airway distress (e.g., severe
hoarseness, stridor, dyspnea) and lower airway distress (e.g.,
crackles, rhonchi, hacking cough, labored or rapid breathing).
Consult the physician promptly for all significant findings.

Infants and young children have relatively smaller

airways, thus placing them at greater risk for airway occlusion.
In the obese adult, common alterations in lung function
include restrictive lung pattern (resulting from abnormally high
diaphragmatic position and increase in chest wall mass) and
obstructive sleep apnea. This combination results in increased

731
work of breathing and predisposes patients to apneic episodes
and/or oxygen desaturations.

2. Administer humidified oxygen therapy, mechanical ventilation,

or bronchodilator treatment, as prescribed.

3. Unless contraindicated, place the patient at a minimum of 30

degrees head elevation to limit upper airway edema formation and
to enhance respiratory excursion and prevent aspiration.

4. Monitor for hypoxemia and hypercapnia. Serial ABG values,

pulse oximetry, and end-tidal CO2 monitoring provide crucial
information concerning arterial oxygen and CO2 levels. Declining
vital capacity, tidal volume, and/or inspiratory force indicates
respiratory insufficiency (patients who are mechanically ventilated
only).

5. Teach the patient who is not intubated the necessity of deep-

breathing and coughing exercises every 2 hours, including use of
incentive spirometry while awake.

6. Prepare equipment and the patient for intubation and mechanical

ventilation, if needed. Note that the position of the patient’s head is
crucial for successful intubation.

Airway Management; Respiratory Monitoring; Oxygen

Therapy; Bedside Laboratory Testing; Cough Enhancement:
Laboratory Data Interpretation.

Deficient fluid volume 

related to active loss through the burn wound and leakage of fluid, plasma
proteins, and other cellular elements into the interstitial space.
Goals/Outcomes: The patient fluid volume status stabilizes, as
evidenced by MAP greater than 60 mm Hg, peripheral pulses
greater than 2+ on a 0-to-4+ scale, and urine output 30 to 50 mL/h
(adult) or 1 mL/kg/h (child less than 30 kg dry body weight).

732
Outcomes for urine output should be adjusted for those patients
with preexisting renal failure/compromise. In the presence of
myoglobinuria (red-pigmented urine indicative of myoglobin or
red blood cells in the urine), a urinary output of 1 to 1.5 mL/kg/h
(approximately 75 to 100 mL/h in the adult) is the desired outcome
until the heme pigments clear from the urine (urine color returns to
normal).
Fluid Balance.

Fluid management

1. Monitor the patient for evidence of fluid volume deficit,

including tachycardia, decreased MAP, decreased amplitude of
peripheral pulses, urine output less than 30 mL/h (adult), urine
output less than 1 mL/kg/h (child weighing less than 30 kg), thirst,
and dry mucous membranes.

2. Establish two large-bore peripheral IV lines, preferably through

nonburned skin. Establish central line if necessary.

Consider placement of intraosseous device if unable to

achieve peripheral or central venous access.

3. Monitor intake and output; administer fluid therapy using the

ABA Consensus formula or as prescribed. Adjust infusion to
maintain desired urine output at the desired resuscitation hourly
rate. Do not exceed 50 mL/h urine output (adults) or 1 mL/kg/h in
children during initial 48 hours of resuscitation (unless heme
pigments are present in the urine). Avoid colloids during first 12 to
24 hours following the burn injury, if possible.

Evaluate patency of intravenous catheters continuously

733
during rapid volume resuscitation.

4. Monitor weight daily during fluid resuscitation; report significant

gains or losses. A significant weight gain will occur with large
volume fluid resuscitation. A significant weight loss may also occur
as a result of catabolism, an increased metabolic rate, and with
extensive removal of burn tissue (e.g., large body fascial excisions).

5. Monitor serial Hct and Hgb values. During the first 24 hours
postburn, neither the Hct nor Hgb levels are reliable guides to fluid
resuscitation. While the circulating volume is restored,
hemoconcentration is no longer present and Hct returns to within
normal limits. Consult the physician for significant anemia.

6. Monitor the patient for signs and symptoms of large volume fluid
administration (shortness of breath, tachypnea, excessive urine
output). Central hemodynamic monitoring is recommended for
patients who have preexisting heart or lung disease.

7. In the presence of myoglobinuria (associated with high-voltage

electrical injuries or significant soft tissue injury from mechanical
trauma), confer with the physician regarding the need to increase
the rate of fluid administration and to consider urine alkalinization.
On occasion, the use of mannitol to promote osmotic diuresis and
prevent renal tubular sludging is considered. Other diuretics are
avoided because they further deplete an already compromised
intravascular volume. Administration of a diuretic precludes the
subsequent use of hourly urine output as a guide to fluid
resuscitation.

8. With the onset of spontaneous diuresis (48 to 72 hours postburn),

decrease infusion rates as prescribed. Continue to reduce rates
gradually according to intake/output ratio and clinical status.

Fluid/Electrolyte Management; Fluid Monitoring;

Hypovolemia Management; Shock Prevention; Venous Access
Devices Maintenance.

734
Ineffective tissue perfusion: Peripheral 
related to thermal injury, circumferential burns, edema, hypovolemia.
Goals/Outcomes: The patient maintains adequate tissue
perfusion.
Note: Tissue perfusion in burned extremities is adequate when
peripheral pulses are greater than 2+ on a 0-to-4+ scale, capillary
refill is brisk (less than 2 seconds), and uninjured and healing skin
is warm to the touch.
Tissue Perfusion: Peripheral; Circulation Status.

Circulatory precautions

1. Monitor tissue perfusion hourly in burned extremities during the

resuscitation phase of care. Note capillary refill, temperature, and
peripheral pulses. Report signs of impaired tissue perfusion to the
advanced practice provider immediately, including coolness of the
extremity, weak or absent peripheral pulses, pain or paresthesias,
and delayed capillary refill.

2. Elevate burned extremities at or above heart level to promote

venous return, prevent excessive dependent edema formation, and
reduce risk for compartment syndrome of the extremities.

Hypothermia 
related to exposure at the scene of injury; large body surface area burns,
administration of large volumes of unwarmed fluid.
Goals/Outcomes: The patient’s temperature returns to normal
(smaller burn injuries) or is slightly elevated (38.5° C; extensive
burn injuries) within 24 hours of this diagnosis. Complications of
hypothermia have been avoided.
Thermoregulation.

Temperature management

1. Warm fluids administered during the initial resuscitation phase

and until the patient approaches desired core temperature. Keep
room temperature as warm as possible. Goal is 33° C (91.4° F)
ambient room temperature.

735
2. Avoid unnecessary exposure of the body. Keep the patient
covered with warmed or warming blanket.

3. Monitor core temperature via rectal or esophageal probe, urinary

catheter attachment, or pulmonary artery catheter.

4. Be aware that vasodilation during rewarming can result in

further intravascular fluid volume deficit.

5. Monitor for and promptly report serious dysrhythmias (i.e., atrial

fibrillation with rapid ventricular response, ventricular
dysrhythmias, atrial ventricular conduction block) associated with
severe or prolonged hypothermia.

6. Monitor ABG values for evidence of hypoxemia. Hypothermia

causes a shift to the left in the oxyhemoglobin dissociation curve
and may impair oxygen unloading to peripheral tissue.

Risk for infection 

related to inadequate primary and secondary defenses secondary to
traumatized tissue, bacterial proliferation in burn wounds, presence of
invasive IV lines or urinary catheter, and immunocompromised status.
Goals/Outcomes: The patient is free of infection, as evidenced by
core temperatures of 38.5° C (101.3° F) for those with extensive burn
injuries, WBC count less than 11,000/mm3, negative culture results,
and absence of purulent matter and other clinical indicators of burn
wound infection.
Risk Control.

Infection prevention

1. Practice universal precautions to reduce the risk of transmission

of microorganisms. Contact isolation measures as appropriate.

2. Recommend sequestration of patients with methicillin-resistant

Staphylococcus aureus, vancomycin-resistant enterococci, or other
multidrug-resistant organisms.

3. Administer TIG or Tt, as prescribed.

736
4. Assess burn wound daily for signs of infection.

5. Report to the physician if:

• fever is greater than 39° C (102.2° F), or temperature

is less than 35° C (95° F),

• elevated or decreased WBC count,

• change in color or odor of wound exudate and

purulent material, and

• signs of wound deterioration: loss of previously

healed wounds, disappearance of a well-defined
burn margin with edema formation, and
hemorrhagic discoloration.

6. Wash burn wound with a mild soap and rinse thoroughly with
water.

7. Except for eyebrows, shave all hair within burn wound to

prevent wound contamination on a daily basis. Eyebrows are left in
place because if shaved, may not grow back, or the new growth
may appear distorted. This practice continues until wound closure.

8. Administer antipyretic and antimicrobial agents, as prescribed.

Ensure aseptic technique when administering care to burned areas
and performing invasive techniques.

9. Assess appearance of graft sites, including adherence to recipient

bed, appearance, color, and odor. Be alert to erythema,
hyperthermia, increasing tenderness, purulent drainage, and
swelling around the grafted site.

10. Assess all invasive lines and devices (e.g., urinary catheters)
daily. Review necessity with prompt removal of unnecessary lines
and devices.

737
11. For patients with a central line, implement the IHI central line
bundle:

• Hand hygiene.

• Maximal barrier precautions upon insertion.

• Chlorhexidine skin antisepsis.

• Optimal catheter site selection, with avoidance of

the femoral vein in adult patients.

• Daily review of line necessity with prompt removal

of unnecessary lines.

12. Observe for clinical indicators of sepsis: tachypnea,

hypothermia, hyperthermia, ileus, subtle disorientation,
unexplained metabolic acidosis, low platelet count, feeding
intolerance, and glucose intolerance. If sepsis is suspected, obtain
wound, blood, sputum, and urine culture specimens as prescribed.

Environmental Management; Infection Control; Infection

Protection; Surveillance; Wound Care; Shock Management.

Acute pain 
related to burn injury and treatment
Goals/Outcomes: Within 30 minutes of treatment/intervention,
the patient’s subjective evaluation of discomfort improves and/or
nonverbal indicators of discomfort are absent or diminished.
Pain Control.

Pain assessment and management

1. Assess the patient’s level of discomfort at frequent intervals.

Patients with partial-thickness burns may experience severe pain
because of damage and exposure of sensory nerve endings. Pain
tolerance often decreases with prolonged hospitalization, multiple

738
painful procedures, and sleep deprivation.

2. Monitor the patient for clinical indicators of pain: increased

BP/MAP, tachypnea, shivering, rigid muscle tone, or guarded
position. Pain assessment using observational tools may be
required for preverbal children or those requiring intubation and
sedation.

3. For verbal children (generally children older than 3 years),

adolescents, and adults, use age-appropriate self-reporting pain
assessment tools.

4. Assess preinjury coping abilities.

5. Administer opioid analgesia and anxiolytics, as prescribed. Time

dosage for optimal effectiveness before painful procedures.

6. Provide simple explanations of all procedures.

7. Employ adjunctive nonpharmacologic interventions, as indicated

(relaxation breathing, guided imagery, distraction, and music
therapy).

8. If possible, avoid wound care procedures during sleeping hours.

9. Ensure that the patient receives periods of uninterrupted sleep by

grouping care procedures when possible.

Analgesic Administration; Anxiety Reduction;

Environmental Management: Comfort; Pain Assessment and
Management.

Impaired tissue integrity 

related to burn injury; edema
Goals/Outcomes: The patient’s wound exhibits evidence of
healing. Wound healing occurs without hypertrophic scarring (late
outcome finding).
Note: Healing time varies with the extent and depth of injury.
Tissue Integrity: Skin and Mucous Membranes.

739
Healing

1. Assess and document extent and depth of burn wound (see Table
3-6).

2. Cleanse and débride the wound, as prescribed.

3. Apply topical antimicrobial treatments, as prescribed, using

aseptic technique.

4. Elevate burned extremities at or above heart level to facilitate

venous return and reduce edema formation and risk for
compartment syndrome.

Table 3-6
BURN WOUND DESCRIPTION AND CHARACTERISTICS

Modified from Carrougher GJ, editor: Burn care and therapy, St Louis, 1998, Mosby.

For patients with skin grafts:

5. Help prevent graft loss if fluid collection beneath graft occurs.

Notify the burn surgeon. Small fluid collections should be removed;
if caught early and removed, will allow for graft readherence.

6. Monitor type and amount of drainage from wounds. Promptly

740
report the presence of bright red bleeding, which would inhibit
graft take, or purulent exudate, which indicates infection.

7. Maintain immobility of grafted site for 3 to 5 days or as

prescribed. This is achieved with a combination of positioning,
splinting, or light pressure and sedation. In some instances, bulky
or occlusive dressings may be required to maintain immobilization
and promote hemostasis of graft.

8. Apply elastic wraps, as prescribed, to legs that have grafts and/or

donor sites to promote venous return and to promote graft
adherence when out of bed.

9. Provide donor site care, as prescribed, and be alert to signs of

donor site infection.

10. Teach the patient about need for compression to prevent

bleeding and to promote graft adherence.

Infection Protection; Positioning; Wound Care.

Ineffective tissue perfusion: Gastrointestinal 

related to hypovolemia and interruption in blood flow associated with
splanchnic vasoconstriction secondary to fluid shifts and catecholamine
release.
Goals/Outcomes: The patient has adequate GI tissue perfusion,
as evidenced by auscultation of bowel sounds within 48 to 72 hours
after burn injury; bowel elimination and appetite within the
patient’s normal pattern; and absence of nausea and vomiting.

Be aware that prolonged impaired perfusion to

gastrointestinal organs increases the likelihood of complications
such as impaired gastric motility, adynamic ileus, gastritis, and
gastric ulcer development.

Tissue Perfusion: Abdominal Organs.

741
Gastrointestinal intubation

1. Assess bowel function every 2 to 4 hours. Identify abdominal

distention and decreasing or absent bowel sounds, which occur
with adynamic ileus or abdominal compartment syndrome.
Consider bladder pressure monitoring; notify the physician if
pressures reach 20 mm Hg.

2. During period of absent bowel sounds, maintain gastric tube to

intermittent low suction as prescribed. Check at intervals to ensure
patency and position of the tube. Before removing tube, clamp for
several hours to be certain that the patient has sufficient GI motility.
Abdominal distention, nausea, vomiting, or return of a large
volume of gastric contents when tube is reconnected indicates
insufficient motility to tolerate tube removal.

3. Maintain NPO status until return of bowel sounds. Provide

mouth care for comfort and hygiene.

4. Administer PPIs, H2-receptor antagonists, and other agents

prescribed to reduce formation of gastric acids. If prescribed, start
enteral feedings.

5. Test gastric aspirate for occult blood, as indicated, and report to

the physician.

Gastrointestinal Intubation; Hemodynamic Regulation;

Nutrition Management; Tube Care: Gastrointestinal.

Imbalanced nutrition: Less than body requirements of

protein, vitamins, and calories 
related to hypermetabolic state.
Goals/Outcomes: The patient has adequate nutrition, as
evidenced by stable weight (following resuscitation period),
balanced nitrogen state per nitrogen tests, serum albumin 3.5 g/dL,
thyroxine-binding prealbumin 20 to 30 mg/dL, retinol-binding
protein 4 to 5 mg/dL, and evidence of continued burn wound
healing and graft take.
Nutritional Status.

742
Nutrition management

1. Collaborate with the physician and dietitian to estimate the

patient’s metabolic needs on the basis of injury extent, dry weight,
and nutritional status before injury.

2. Consider the patient’s specific injuries, ability to consume diet,

and preexisting medical condition when planning nutrition.

3. Provide diet as prescribed. When the patient can take foods

orally, promote supplemental feedings/snacks between meals.

4. Consider placement of a soft Silastic feeding tube for provision of

enteral tube feedings for those who are unable to meet their caloric
and protein requirements orally.

5. Recognize that opioids decrease GI motility and may cause

nausea and vomiting.

6. Administer medications to prevent/treat opioid-associated GI

complications (constipation, decrease in GI motility).

7. Recognize that patients with an ileus that persists for longer than
4 days or those unable to meet caloric needs enterally may require
total parenteral nutrition.

8. Record all intake for daily calorie counts.

9. Monitor the patient’s weight. Minimize error by weighing the

patient without dressings or splints, if possible.

10. Monitor markers of nutritional status: serum albumin,

thyroxine-binding prealbumin, retinol-binding protein, and urine
nitrogen measurements. Long periods of catabolism cause these
serum values to decrease. Be alert to measures of protein
deficiencies, weight loss, and poor wound healing, all of which are
signals that nutritional needs are not being met.

Nutrition Management; Nutrition Therapy; Nutrition

Monitoring.

743
Fear 
related to potentially threatening situation (e.g., serious injury,
hospitalization) and supported by presence of pain, unfamiliarity, and
noxious environmental stimuli present in critical care area;
communication barrier (e.g., intubation); sensory impairment from direct
injuries.
Goals/Outcomes: The patient exhibits decreased symptoms of
fear: apprehension, tension, nervousness, tachycardia,
aggressiveness, and withdrawal.
Fear Control.

Anxiety reduction

1. Assess level of fear and understanding of present condition.

2. Plan care to provide as restful an environment as possible.

3. Provide information regarding nursing care, treatment plan, and

progress. It is often necessary to repeat information because injury,
stress, and fear can interfere with comprehension.

4. Promote visits by family members and significant others.

5. Offer to consult hospital spiritual care or the patient’s clergy as

desired by the patient.

6. Assess and promote the patient’s usual coping strategies. Consult

with a psychologist for assistance.

7. Provide referral to burn survivor support groups.

Coping Enhancement; Security Enhancement; Support

System Enhancement.

Disturbed sensory perception: Tactile and visual 

related to altered reception secondary to medications, sleep pattern
disturbance, pain, swollen eyelids, and full-thickness burn wound.
Goals/Outcomes: The patient verbalizes orientation to time,
place, and person and describes rationale (age-appropriate

744
understanding) for necessary treatments.
Vision Compensation Behavior: Cognitive Orientation.

Sensory perception management

1. Assess the patient’s orientation to time, place, and person using

age-appropriate questions.

2. Answer the patient’s questions simply and succinctly, providing

information regarding immediate surroundings, procedures, and
treatments. Anticipate the necessity of having to repeat information
at frequent intervals.

3. For the patient with cutaneous burn injury, explain why tactile
sensation is decreased or absent. If the patient’s eyelids are swollen
shut because of facial edema, reassure the patient that he or she is
not blind and that swelling will resolve within 3 to 5 days. Apply
eye lubricant, as prescribed, for those patients with excessive
swelling and/or inhibited blink.

4. Touch the patient on unburned skin to provide nonpainful tactile

stimulation.

5. Explain that alterations in perception can be related to opioids

and other medications commonly prescribed during the acute
phase of burn recovery.

Peripheral Sensation Management; Surveillance: Safety;

Communication Enhancement: Visual Deficit; Environmental
Management.

Risk for disuse syndrome 

related to immobilization from pain, splints, or scar formation.
Goals/Outcomes: The patient displays complete ROM without
verbal or nonverbal indicators of discomfort.
Risk Control.

Positioning

1. Provide ROM exercises every 4 hours while awake. When

745
possible, combine when medicated with analgesics for other
procedures and during activities of daily living.

2. Apply splints, as prescribed, to maintain extremities in functional

position and to prevent contracture formation.

3. For the patient with grafts, institute ROM exercises and

ambulation on prescribed postgrafting day (often 3 to 7 days
postgrafting). Premedicate with analgesic to aid in mobility and
reduce discomfort.

Exercise Therapy: Ambulation; Exercise Therapy: Joint

Mobility; Exercise Promotion; Nutrition Management.

Disturbed body image 

related to biophysical changes secondary to burn injury.
Goals/Outcomes: The patient begins to acknowledge body
changes and demonstrates movement toward incorporating
changes into self-concept.
Body Image.

Body image enhancement

1. Assess the patient’s perceptions and feelings about the burn

injury and changes in lifestyle and relationships, especially those
with significant others.

2. Involve significant others in as much care as possible to maintain

bond with the patient.

3. Respect the patient’s need to express anger over body changes.

4. Consider consultation with a rehabilitation psychologist and/or

child life therapy.

5. Provide information concerning eventual appearance of grafts

and donor sites.

6. Provide names and telephone numbers of local and national

support groups for burn survivors: the American Burn Association,

746
National Headquarters Office, website: www.ameriburn.org,
phone: (312) 642-9260; the Phoenix Society for Burn Survivors, Inc.,
National Headquarters Office, website: www.phoenix-society.org,
phone: (800) 888-2876.

Anxiety Reduction; Coping Enhancement; Grief Work

Facilitation; Self-Esteem Enhancement; Support System
Enhancement.

Deficient knowledge 
related to lack of knowledge regarding ability for self-care management
and/or use of resources for supportive care.
Goals/Outcomes: Within 24 hours of initiation of acute care, the
patient and significant others verbalize knowledge about prescribed
medications and techniques that facilitate continued wound healing
and limb mobility.
Knowledge: Medication; Knowledge: Treatment Regimen.

Teaching: Disease process

1. Review the splinting and exercise program for contracture

prevention, as directed by the physical therapist.

2. Teach the patient and significant others to monitor for pain or

pressure caused by improperly applied splint and to assess splinted
extremity for coolness, pallor, cyanosis, decreased pulses, and
impaired function.

3. Discuss current skin and wound care plan.

4. Explain indicators of wound infection.

5. Review nutritional needs.

6. Review current pain and anxiolytic medications.

Learning Facilitation; Learning Readiness Enhancement;

Teaching: Individual.

747
Additional nursing diagnoses
For other nursing diagnoses and interventions, see the following, as
appropriate: Nutrition Support, (Chapter 1); Mechanical
Ventilation, (Chapter 1); Prolonged Immobility, (Chapter 1);
Compartment Syndrome/Ischemic Myositis, (Chapter 3); Emotional
and Spiritual Support of the Patient and Significant Others,
(Chapter 2).

Compartment syndrome/ischemic
myositis
Pathophysiology
Compartment syndrome is caused by pathologic elevation of
intercompartmental pressures within nonexpansible tissue
envelopes. The pressure increase may come from either an increase
in volume within a tissue compartment or externally applied
pressure compressing a tissue compartment. While pressure within
the anatomic space increases, local perfusion is compromised,
leading, if untreated, to irreversible damage of the tissues within
the compartment. Compartment syndrome is a surgical emergency
that requires rapid intervention to prevent permanent cosmetic or
functional deformity or loss of limb. Compartment syndrome may
be acute or chronic (exercise-related forms); this section focuses on
the acute peripheral type.
Most compartment syndromes are associated with trauma, but
the condition may also occur from multiple other etiologies
including reperfusion injuries, ischemia, burns, prolonged limb
compression, drug abuse, or poor positioning during prolonged
surgical procedures (Table 3-8). The incidence of compartment
syndrome in those younger than 35 years is increased probably
secondary to the larger muscle mass contained within the
osteofascial space.
Any muscle may be affected as long as the pressure within a
muscle is sustained for a prolonged period of time. Most often the
muscles affected are those that are contained within an osteofascial

748
space in the upper or lower extremity. The most common site in the
upper arm is the forearm. The forearm contains two compartments:
the volar and dorsal. The volar compartment contains the flexors of
the wrist and fingers and the dorsal compartment contains the
extensors. The lower extremity contains a total of seven
compartments: three in the thigh and four in the calf. The three
compartments of the thigh are the anterior, posterior, and medial.
The calf compartments are the anterior, lateral/peroneal, deep
posterior, and superficial posterior. The tibial nerve lies within the
posterior compartment and provides sensation to the plantar
surface of the foot and flexion of the toes. The anterior
compartment contains the peroneal nerve providing sensation to
the first web space and motor function of the extensors of the calf
and foot. The anterior compartment of the calf is the most common
site of compartment syndrome.
Increased and sustained pressure within a muscle compartment
can develop because of increased volume in the compartment from
a hematoma or edema. A second etiology is prolonged ischemia,
which may be as a result of external compression or arterial
compromise. Finally, compartment syndrome may be caused by
decreased overall size of the muscle compartment from scar
formation, especially following circumferential burns (see Table 3-
8).
Regardless of the etiology or location, ischemia begins when the
metabolic demands of the tissues cannot be met. The normal
pressure in muscle compartments is less than 10 to 12 mm Hg.
Whitesides’ theory states that the development of compartment
syndrome depends on both the intracompartmental pressure and
the systemic BP. The diastolic BP minus the compartmental
pressure should be greater than 30 mm Hg to avoid ischemia in the
tissues. Thus, increasing the compartmental pressure or decreasing
the perfusion pressure can each lead to a compartment syndrome.
When injury occurs, the depletion of intracellular energy stores
causes cellular swelling and increasing venous pressures, allowing
edema to develop and local blood flow to decrease. Lymphatic
drainage initially increases and then decreases as a result of
congestion from the growing tissue edema. Compartmental tissue
pressure increases, compromising capillary blood flow. Histamine

749
is released, producing vasodilation and increased capillary
permeability. Rising compartmental pressure further increases
venous congestion and results in reduction in the arteriovenous
pressure gradient, reducing local tissue perfusion and further
increasing capillary pressure. Fluids and proteins escape from the
capillaries and contribute to even higher tissue pressures. The
higher tissue pressures eventually exceed both capillary and venous
pressures, stopping nutrient blood flow and promoting further
ischemia. Local blood flow to muscles is severely compromised
when the interstitial tissue pressure equals or exceeds the diastolic
pressure. As a result of impaired venous return, anaerobic
metabolism creates more lactic acid, which stimulates vasodilation
further, decreasing BP and elevating tissue pressure. The pressure
within the compartment continues to increase, equaling or
exceeding the capillary pressure and leading to arteriolar
compression, causing further ischemia of the muscle and nerves.
Sustained hypotension and shock are associated with greater
incidence of compartment syndrome resulting from the lowered
pressure gradient. Less compartmental pressure is needed to result
in arteriolar spasm and ischemic changes in the muscles.
The earliest signs of compartment syndrome are often subtle but
are primarily neurologic as a result of the susceptibility to hypoxia
of the nonmyelinated sensory fibers. Sensory changes in the
extremity begin with paresthesias or hyperesthesias within 30
minutes of the onset of ischemia and may become functionally
irreversible after 12 to 24 hours. The average interval between the
initial injury to the compartment and the beginning symptoms of
compartment syndrome is 2 hours. Compartmental tissue ischemia
that lasts longer than 6 hours results in muscle necrosis and
irreversible tissue changes.
Late-onset compartment syndrome is seen in patients who are
comatose or confused and who are unable to communicate
symptoms. Late-onset compartment syndrome is often more
difficult to recognize and manage, sometimes worsening following
treatment with fasciotomy. The late syndrome may occur in
compartments already treated with fasciotomy. Healthy
granulation tissue may cover necrotic muscle within partially
opened compartments. With sufficient muscle tissue injury (e.g.,

750
after crush injuries) or undiagnosed compartment syndrome,
rhabdomyolysis may develop with the release of metabolic toxin
and intracellular components, especially myoglobin. The release of
toxins can result in secondary myoglobinemia, leading to acute
tubular necrosis, which may progress to acute kidney injury and
multisystem failure.

Compartment syndrome assessment

Goal of assessment
The goals are to prevent ischemia and reduce long-term sequelae by
earlier diagnosis and treatment through reduction in internal or
external pressure.

History and risk factors

• Any patient with a peripheral injury listed in Table 3-8 is at risk
for compartment syndrome.

• Patients admitted for acute renal failure after treatment for crush
injuries or compartment syndrome should be suspected of having
late-onset or continuing compartment syndrome.

• Patients with profound shock who receive aggressive fluid

resuscitation are at risk for acute compartment syndrome.

Table 3-8
CAUSES OF COMPARTMENT SYNDROME

Modified from Callahan J: Compartment syndrome. Orthop Nurs 4:11-15, 1985.

751
Vital signs
• Hypotension potentiates compartment syndrome.

Observation and subjective symptoms

Early indicators

• Unusually severe pain for an injury is a cardinal symptom.

Passive stretch of an involved muscle group significantly
increases the pain.

Late-onset syndrome indicators

• Persistent peripheral edema or continued elevation of tissue

pressures even after fasciotomy.

• If compartment syndrome is not treated, the necrosing muscles

become fibrotic and contract and can no longer function (e.g.,
Volkmann ischemic contracture).

• Late decompression fasciotomy seldom restores lost myoneural

function. Early recognition is the key to successful management
and preservation of function.

• Extreme pain is out of proportion to the injury.

• Increased pain occurs on passive ROM (stretch) of the affected

extremity.

Late findings

• Paresthesias (early loss of vibratory sensation).

• Pallor of the extremity.

• Paralysis.

Palpation

752
• Feel for temperature of affected area; polar (coolness) of affected
area is a late sign.

• Palpation of the compartment reveals tension and slowed

capillary refill.

• Assess pulses in all extremities; pulselessness is a late sign.

Diagnostic Tests for Compartment Syndrome

Test Purpose Abnormal Findings

Blood Chemistry: Elevation is caused by the release of the Continued elevation in
Creatine enzyme by the injured muscle tissue. the course of treatment
phosphokinase may indicate late-onset
compartment syndrome.
Extensive muscle
necrosis may lead to
myoglobinemia and
myoglobinuria, and may
lead to rhabdomyolysis.
Blood urea nitrogen and
creatinine levels will be
elevated if acute renal
failure results from
rhabdomyolysis.
Serum creatine CK-MM isoenzyme is most specific for skeletal In compartment
kinase (CK)-MM muscle damage. Serum CK levels begin syndrome, CK levels
increasing 2 to 12 hours after the onset of may rise as high as
muscle injury. They peak within 1 to 3 days 100,000 units/L. Levels
and decrease 3 to 5 days after muscle injury greater than 2000 units/L
ceases. raise the possibility of
muscle damage. CK
values greater than 2000
units/L after surgery can
be a warning sign of
acute compartment
syndrome in patients
who are ventilated and
sedated.
Intracompartmental Compartment pressure and associated critical Delta pressures of ≤30
pressure values may be monitored intermittently by mm Hg for 6 hours or
monitoring inserting needles (pressure within 10 to 30 mm ≤40 mm Hg for 8 hours
Hg of diastolic blood pressure), which get require prompt
obstructed by muscle tissue. Continuous consultation with the
infusion catheters (pressure >45 mm Hg) and physician. Pressures
wick or slit catheters (>30 to 35 mm Hg) warranting fasciotomy
monitor continuously via fluid-filled catheters vary with clinical
and pressure monitors. In patients who are indicators, the patient’s
hypotensive and at higher risk for systemic condition, and
compartment syndrome, the delta pressure measurement technique.
should be calculated. Delta pressure equals
mean arterial pressure minus compartmental

753
 pressure.
Near-infrared Based on the different light absorption More studies are needed,
spectroscopy properties, NIRS can measure the local but NIRS may provide
(NIRS) changes in concentration of oxygenated and the benefit of a rapid,
deoxygenated hemoglobin and perfusion in continuous, noninvasive,
different tissues including muscle. sensitive, and specific
tool for early detection of
acute compartment
syndrome.

Ultrasound: pulsed More investigation is needed to determine Increased

phase–locked loop effectiveness. intracompartmental
(PPLL) The PPLL ultrasound locks on to a pressure during
characteristic reflection that comes from a compartment syndrome
specific tissue and can detect the very subtle causes a reduction in
movements of fascia that correspond to local normal fascial
arterial pulsation. displacements in
response to arterial
pulsation.
Scintigraphy Radionuclide imaging that shows the Can study all
physiologic function of the system being compartments of an
investigated as opposed to its anatomy. extremity at once but
limited usefulness
because of inability to
study over time.
Pulse oximetry Assesses perfusion of distal tissues. Decreased perfusion will
Readings should be compared with readings result in lower pulse
from a contralateral, uninvolved extremity. oximetry measurements
but may not be
decreased until
significant time and
injury has occurred.
Pulse oximetry cannot
measure
intracompartmental
tissue oxygen saturation
and requires adequate
pulsatile flow.
Magnetic resonance MRI is useful in detecting soft tissue edema on MRI cannot differentiate
imaging (MRI) T1 images. the edema from trauma
with edema from a
compartment syndrome
in the acute phases and
thus is of limited value
in diagnosis in the acute
phase. MRI is useful in
identifying the tissue
changes in an
established compartment
syndrome in a very late
stage.
Arteriograms and Radiologic examination of blood vessels may
venograms be performed when embolus, thrombus, or
other vascular injury is indicated.

Compartmental pressure monitoring

754
Compartmental pressure monitoring continues to be the preferred
method of definitive diagnosis of acute compartment syndrome.
Several methods of direct compartment measurement exist
including the needle manometer, the wick catheter, and the slit
catheter. Continuous readings are not possible with the needle
manometer method and may result in falsely high levels caused by
the injection of saline into the muscle. Pressures within
compartments may be continuously monitored with either the wick
method or the slit catheter method by attaching a pressure
transducer to an implanted catheter within a muscle compartment.
Indications for continuous or intermittent pressure monitoring are
in the patient who is unconscious, children or other patients
difficult to assess, patients with nerve injury, and those with
multiple orthopedic traumas. Regardless of technique,
compartmental pressures greater than 30 mm Hg above the
systemic diastolic pressure indicate the need for a compartment
fasciotomy.

Early indicators

• Palpation of the compartment reveals tension and slowed

capillary refill.

• Tissue pressures vary with the method of measurement.

Generally, normal tissue pressures vary from 10 to 12 mm Hg,
and sustained pressures greater than 30 mm Hg above the
systemic diastolic pressure result in tissue necrosis.

• The thin-walled lower extremity veins may collapse at lower

pressures, further contributing to the pathogenesis.

Collaborative management
Care priorities

1. Eliminate external pressure on the affected

compartment
Identify and relieve circumferential constriction: Loosen or remove

755
circumferential casts and padding or dressings; escharotomy for
circumferential burns or frostbite.

2. Manage pain
Analgesia: Parenteral opiates often with sedative adjuncts.

3. Reduce internal compartmental pressure

IV hypertonic mannitol: Used as a preventive measure to reduce
compartmental pressure via systemic diuresis and to help the
kidneys excrete the large molecules of myoglobin if extensive tissue
necrosis is present. This diuresis may potentiate more ischemia if
the patient is hypovolemic.

4. Provide surgical intervention

Fasciotomy of myofascial compartment: The goal of treatment of
acute compartment syndrome is to decrease tissue pressure, restore
blood flow, and minimize tissue damage.

• Treatment of choice to accomplish these goals is a surgical

fasciotomy to allow unrestricted swelling. The affected
compartment alone may be opened but, more commonly,
adjacent or all tissue compartments in the area are
prophylactically incised. In the forearm, a volar aspect fasciotomy
is most common. In the thigh, a lateral incision can decompress at
three compartments, and in the calf, a lateral fasciotomy
expansible to release all compartments or medial and lateral
incisions is generally adequate.

• Persistent peripheral edema with elevated creatine

phosphokinase, or the presence of acute renal failure, may justify
reexploration and wide excision of all necrotic muscle in involved
and adjacent compartments.

• Complications of fasciotomy include wound infection, the

potential for osteomyelitis, and large scars.

• Secondary wound closure may be accomplished after 3 to 4 days

once the compartmental pressure has returned to normal.

756
 Multiple methods of wound closure have been used, including
mechanical closure devices, dynamic skin sutures, vacuum-
assisted closure, and healing by secondary intention.

• Skin grafting may be needed to ensure complete coverage of the

exposed compartments.

5. Provide vascular surgical intervention if blood vessel

injury caused the compartment syndrome
Treat vascular injury: The involved blood vessel is explored and
treated.

• Papaverine, a vasodilating drug that relaxes smooth muscle, can

be injected in a bolus of fluid to reestablish normal internal artery
dynamics.

• Blood vessel lacerations can be repaired or severely damaged

vessels can be resected.

6. Renal protection

• Ischemia that persists for at least 4 hours causes significant

myoglobinuria, which peaks approximately 3 hours following
restoration of the circulation. Myoglobinuria can persist for up to
12 hours. When rhabdomyolysis is apparent, aggressive IV fluid
administration and, possibly, bicarbonate may be administered to
maintain urine output at 1 to 2 mL/kg/h.

• A combination of myoglobinemia, hypovolemia, and acidemia

may lead to acute renal failure. Alkalization of the urine coupled
with diuresis may be renal protective because hemoglobin and
myoglobin are more soluble in an alkaline solution. Patients with
trauma who generally survive recover renal function, including
patients who require extended support using hemodialysis.
Current recommendations include:

• Manage hypovolemia with crystalloid solution.

757
• Administer 500 mL/h IV crystalloid solution and
22.4 mEq bicarbonate (total 12 L/day, prompting
diuresis of approximately 8 L/day).

• If urine output is less than 300 mL/h, one dose of

mannitol 1 g/kg IV is given.

• For a pH greater than 7.45, acetazolamide, 250 mg,

is administered IV.

• Vital signs, urine pH level, and volume are

monitored hourly.

• Osmolarity, electrolytes, and ABG values are

evaluated every 6 hours.

Care plans: Compartment syndrome

Ineffective tissue perfusion (or risk for same): Peripheral
(compartment) 
related to interruption of capillary blood flow secondary to increased
pressure within the anatomic compartment.
Goals/Outcomes: Throughout the hospitalization, the patient has
adequate perfusion to compartment tissues, as evidenced by brisk
(less than 2 seconds) capillary refill, peripheral pulses greater than
2+ on a 0-to-4+ scale, normal tissue pressures (0 to 10 mm Hg), and
absence of edema or tautness. Within 2 hours of admission, the
patient verbalizes understanding of reporting symptoms of
impaired neurovascular status.
Circulation Status.

Circulatory precautions

758
1. Monitor neurovascular status of injured extremity at least every 2
hours.

2. Assess for increased pain on passive extension or flexion of the

digits.

3. Monitor for sluggish capillary refill, decrease in or loss of two-

point discrimination, increasing limb edema, and tautness over
individual compartments.

4. Use pulse oximetry to help assess distal tissue perfusion and

report significant differences from oximetry readings taken from
the uninvolved contralateral extremity.

5. Assess for the six “Ps”:

• Pain (especially on passive digital movement and

with pressure over the compartment).

• Pallor.

• Polar (coolness).

• Pulselessness.

• Paresthesia.

• Paralysis.

6. Report deficits in neurovascular status promptly.

7. Loosen circumferential dressings as indicated.

8. Educate the patient about the symptoms to be promptly reported:

severe, unrelieved pain; paresthesias (diminished sensation,
hyperesthesia, or anesthesia); paralysis; coolness; or pulselessness.

759
9. Monitor tissue pressures continuously, with an
intracompartmental pressure device if needed.

10. Consult the advanced practice provider if pressures exceed

normal or preestablished levels or if the patient manifests brown
urine indicative of myoglobinuria.

HIGH ALERT!
Pressures greater than 10 mm Hg may reflect significant
elevation. Myoglobinuria may indicate that rhabdomyolysis has
ensued, which if not immediately managed may lead to acute renal
failure.

11. Monitor closely for additional tissue injury if the patient

becomes hypotensive.

Cast Care: Maintenance; Heat/Cold Application; Peripheral

Sensation Management; Shock Management; Skin Surveillance;
Teaching: Disease Process.

Acute pain 
related to physical factors (tissue ischemia) secondary to compartment
syndrome.
Goals/Outcomes: Throughout the hospitalization, the patient’s
pain is controlled, as reflected by a pain scale. Nonverbal indicators
of discomfort (e.g., grimacing) are reduced or absent. Within 2
hours of admission, the patient verbalizes understanding of the
need to report uncontrolled or increasing pain.
Pain Control; Comfort Level.

Pain management

1. Assess for pain: onset, duration, progression, and intensity.

Devise a pain scale with the patient, rating discomfort “0” for no
pain to “10” for unbearable pain. Patients who are

760
noncommunicative or of low-level intellect may require a simpler
or different pain scale.

2. Determine if passive stretching of digits and pressure over limb

compartments increases the pain. Both may indicate early
compartment syndrome.

3. Adjust the medication regimen to the patient’s needs; document

medication effectiveness.

4. Promptly report uncontrolled pain.

5. Prevent pressure from being applied on involved compartment

and neurovascular structures.

6. Following a fasciotomy, pain that remains unrelieved may

indicate that the fasciotomy is incomplete.

7. Pain that increases several days after a fasciotomy may signal

compartmental infection.

8. Continue to monitor neurovascular function with each vital sign

check to assess for recurring compartment syndrome or infection.

Analgesic Administration; Anxiety Reduction; Coping

Enhancement; Progressive Muscle Relaxation; Simple Guided
Imagery.

Risk for infection 

related to inadequate primary defenses secondary to necrotic tissue, wide
excision fasciotomy, and open wound.
Goals/Outcomes: Throughout the hospitalization the patient is
free of infection, as evidenced by normothermia, WBC count less
than 11,000/mm3, and absence of wound erythema and other
clinical indicators of infection. Within 24 hours of admission, the
patient verbalizes understanding of the need to promptly report
any indicators of infection.
Risk Control; Wound Healing: Primary Intention.

Infection protection

761
1. Monitor the patient for fever, increasing pain, and laboratory
data indicative of infection (e.g., increased WBC count or
erythrocyte sedimentation rate).

2. Assess exposed wounds for erythema, increasing wound

drainage, purulent wound drainage, increasing wound
circumference, edema, and localized tenderness.

3. Assess neurovascular deficits, which may signal infection or

pressure in adjacent inflamed tissues.

4. After primary closure or grafting of wound, assess for signs of

infection beneath the closure.

5. Assess for chronic infection and osteomyelitis; key complications

of compartment syndrome.

6. Instruct the patient to report the following indicators of infection:

fever, localized warmth, increasing pain, increasing wound
drainage (especially if purulent), swelling, and redness.

7. Consult with the advanced practice provider promptly regarding

significant findings.

Environmental Management; Medication Management;

Surveillance; Vital Signs Monitoring; Wound Care; Wound Care:
Closed Drainage.

Disturbed body image 

related to physical changes secondary to large, irregular fasciotomy wound
and skin-grafted scar; loss of function in or change in appearance of an
extremity; or amputation.
Goals/Outcomes: Within the 24-hour period before discharge
from ICU, the patient acknowledges body changes and
demonstrates movement toward incorporating changes into self-
concept. The patient does not exhibit maladaptive response (e.g.,
severe depression) to wound or functional loss.
Body Image; Self-Esteem.

762
Body image enhancement

1. Discuss compartment syndrome, therapeutic interventions, and

long-term effects.

2. Provide time for the patient to share feelings about his or her
changed appearance and function. Encourage questions and
discussion of these feelings with the patient’s significant others.

3. Help the patient set realistic goals for recovery.

4. Facilitate progression through the grieving process, as

appropriate.

5. Recognize when patient is ready to view or discuss the injury.

Adjustment time varies.

6. Encourage self-care. Provide necessary adjunctive aids (e.g.,

built-up utensils, button hooks, orthotics) to facilitate independence
in activities of daily living.

7. Collaborate with the advanced practice provider for patients with

functional loss or amputation, introduce use of orthotics and
adjunctive devices to facilitate self-care.

Active Listening; Amputation Care; Anxiety Reduction;

Coping Enhancement; Emotional Support; Self-Care Assistance;
Wound Care.

Drowning
Incidence
Drowning accounts for over 4000 deaths annually in the United
States according to the Centers for Disease Control and Prevention
and 388,000 deaths worldwide according to the World Health
Organization, making drowning the third leading cause of
unintentional deaths worldwide. The highest mortality rates are in
children younger than 5 years of age; drowning occurs more

763
frequently among males than females.

Pathophysiology
Drowning is defined as a process of experiencing respiratory
impairment from submersion/immersion in a liquid by the World
Health Organization. The terms drowning and near-drowning are
often used to distinguish between individuals who die within 24
hours of the drowning incident and those who live 24 hours or
longer following the incident (termed “near-drowning”).
Individuals classified as “near-drowning” may eventually die from
the submersion/immersion. Healthcare providers cannot always
determine who will die within the first 24 hours. Both populations
receive the same treatment. The 2010 American Heart Association
guidelines support these definitions to maintain consistency in the
reporting of data related to drowning. A current term used to
describe patients who survive a submersion is nonfatal drowning.
The main effects of drowning are decreased lung compliance,
ventilator-perfusion mismatch, and intrapulmonary shunting
leading to hypoxemia and decreased oxygen delivery to the tissues,
which can lead to failure of multiple organs, most importantly, the
CNS. Hypotension, pulmonary edema, hypothermia, and
respiratory and metabolic acidosis occur after nonfatal drowning,
compounding the detrimental effects of the hypoxemia. In addition
to the neurologic deficits from cerebral anoxia, acute lung injury or
acute respiratory distress syndrome, pneumonia, acute renal failure
secondary to acute tubular necrosis, and DIC can occur. Cervical
SCI is not common in nonfatal drowning. Any aspirated
contaminants (e.g., algae, chemicals, sand) may cause or contribute
to obstruction and lead to asphyxiation. Bacterial pneumonia can
develop, depending on the type of contaminant in the aspirant, and
chemical pneumonitis can occur if gastric contents were aspirated.
Drowning was formerly categorized by the type of water
(freshwater versus saltwater) and whether the person aspirated
fluid into the lungs (wet versus dry drowning). These distinctions
are thought to be irrelevant in providing care to patients following
nonfatal drowning.

764
Wet versus dry drowning
An individual experiencing the drowning process will initially
attempt to hold their breath. During breath holding there is some
degree of laryngospasm that is followed by falling oxygen levels
and increasing carbon dioxide levels in the blood. Eventually, the
drive to breathe takes over and the individual begins to aspirate
fluid into the lung (wet drowning). In individuals with prolonged
laryngospasms, oxygen tension drops and the laryngospasm
eventually subsides, prompting aspiration of water before cardiac
arrest. Other causes of cardiac arrest are possible in individuals
found in water without water in their lungs (dry drowning).

Freshwater versus saltwater drowning

Literature previously reported a difference in freshwater drowning
versus saltwater drowning. The prevailing thought was that the
hypertonic nature of saltwater would cause water to be pulled into
the lungs leading to massive pulmonary edema, whereas the
hypotonic freshwater entering the lungs would be rapidly absorbed
into the circulatory system, causing dilution of electrolytes and
volume overload. An individual must aspirate over 11 mL/kg
before these effects occur and most victims of drowning aspirate far
less. Given how rarely massive aspiration occurs, this distinction is
now thought to be unimportant. Both types of drowning result in
loss of surfactant leading to noncardiogenic pulmonary edema.
Hypothermia, defined as a drop in core temperature to 33° C
(91.4° F) or below, may also occur. Its progression can cause muscle
activity and vital functions to cease, resulting in ventricular
fibrillation (occurs at approximately 28° C [82.4° F]). These patients
must be handled carefully to avoid prompting ventricular
dysrhythmias. Hypothermia may protect the brain from permanent
anoxic damage by decreasing cerebral metabolism by as much as
50%. The hypothermic protection is dependent on the temperature
dropping to the point of slowing cerebral metabolism before the
ischemic injury occurring in the brain. This occurs most often with
drowning in icy waters or where the victim has been able to stay
afloat for a period of time while the temperature drops before being
submersed. Because these factors are not often known about the
victim, all victims of drowning should receive aggressive initial

765
resuscitation. Resuscitation should be continued until the victim is
rewarmed to at least 32° C (89.6° F), because the heart may start
beating at that temperature. The adage, “a patient is not dead until
warm and dead,” describes the need to ensure that proper
rewarming has occurred in all patients who are hypothermic before
pronouncing them dead. Many medications used during
resuscitation are ineffective until the patient is warmed.
Resuscitation remains possible after 30 minutes of submersion.
Resuscitation efforts frequently should be continued for at least 1
hour.

Assessment: Drowning
Goal of system assessment
Evaluate for respiratory and neurologic functioning, as well as
determining if concurrent injuries were sustained such as head
and/or spinal trauma.

History and risk factors

Age of the victim, inability to swim, submersion time, temperature
of the water, degree of water contamination, use of alcohol and/or
drugs, associated injuries such as head and spine injuries,
underlying medical conditions, and prehospital resuscitation
received should all be considered.

Vital signs
• Temperature may be low if drowning occurred in cold water.

• RR may be elevated or absent if the patient is in arrest.

• Hypotension.

• HR may be increased or decreased depending on the temperature

and respiratory status. The patient may also have presenting
symptoms including atrial fibrillation, asystole, or ventricular
tachycardia/fibrillation.

766
• RR may be increased with dyspnea or may be absent if arrest has
occurred. Absent respiratory effort may indicate a high cervical
spinal cord injury (SCI).

Observation
Evaluate for signs of trauma to head and neck, skin coloring as an
indication of hypoxia, signs of neurologic functioning including
pupil size and equality and response to stimuli.

• Pink, frothy sputum may indicate pulmonary edema.

Palpation
• Evaluate skin for temperature, neck for deformities, and head for
signs of trauma including swelling.

Auscultation
Evaluate lung fields to identify abnormal breath sounds.

• Decreased breath sounds may indicate a pneumothorax or

hemothorax.

• Sucking sound on inspiration may indicate an open

pneumothorax.

• Crackles, rhonchi, wheezing.

Diagnostic Tests for Drowning

767
Collaborative management
Care priorities
The primary goal of treatment is to restore ventilation and correct
hypoxemia and acidosis. Once ventilation is normal, hypoxemia
and acidosis may resolve without further treatment; however,
many patients, especially those submerged for more than a few
minutes may require additional measures. The following
treatments may be required:

1. Provide oxygen therapy

Oxygen (100%) is initiated immediately to treat hypoxia and is
continued. All patients, including those who are alert with
spontaneous ventilation, are at risk for hypoxia and acidosis.
Warmed oxygen 40° C to 43° C (104° F to 109.4° F) may be used as
part of the rewarming process for patients with hypothermia.

2. Correct hypothermia with rewarming

Warm, moist oxygen 40° C to 43° C (104° F to 109.4° F) may be used
to elevate core temperature. Peritoneal and gastric lavage are used
for rewarming. Fluid for lavage is warmed to 37° C (98.6° F). The

768
goal is to rewarm as safely and quickly as possible to achieve a
normal core temperature. Care must be taken not to rewarm too
quickly because blood can pool in the extremities, especially with
external rewarming strategies, prompting hypotension. IV fluids
should also be warmed to prevent further exacerbation of the
hypothermia. Rewarming cannot be safely accomplished as quickly
as cooling.

3. Manage ventilation and acid-base balance

Profound metabolic acidosis is treated with sodium bicarbonate,
aggressive ventilation, and careful monitoring of arterial pH. If
bronchospasm is present, aerosolized bronchodilators such as
epinephrine, albuterol, or isoproterenol HCl may be used.

4. Assess for need for endotracheal intubation and

mechanical ventilation
Intubation provides a patent airway for patients who are unable to
manage secretions. Mechanical ventilation is used to manage
respiratory failure resulting from reduced lung compliance, or
if for any reason the patient is unable to maintain effective
respiratory effort. Patients may require 1.5 to 2 times normal tidal
volume at slower rates to allow optimal lung expansion and
ventilation of alveoli.

5. Initiate positive end-expiratory pressure

If the patient is unresponsive to high levels of oxygen (Fio2 ≥0.50
to maintain a PaO2 ≥60 mm Hg), positive end-expiratory pressure
improves oxygenation by preventing the collapse of alveoli during
expiration. The pressure keeps alveoli open despite inadequate
surfactant. Positive end-expiratory pressure should be removed
cautiously, because levels of surfactant can remain low for 48 to 72
hours after a nonfatal drowning.

6. Consider bronchoscopy
To remove aspirated contaminants, if necessary.

7. Assess for the need of extracorporeal membrane

769
oxygenation
Extracorporeal membrane oxygenation (ECMO), if available,
may be useful when the patient is unable to maintain good
oxygenation despite intubation and mechanical ventilation.

8. Promote neurologic/brain recovery

Depends on the severity of the neurologic impairment. Severe
impairment may require ICP monitoring, steroids, osmotic diuretics
(e.g., mannitol), and mechanical ventilation. Recent studies have
not supported the use of barbiturate coma or therapeutic
hypothermia. Avoid hyperthermia resulting from the increase
in metabolic demand and potential of further neurologic damage.

9. Manage fluid and electrolyte imbalance

Although uncommon, fluid and electrolyte abnormalities may
occur. Usually, no specific therapy is required for minor
disturbances. Fluid volume may be replaced with crystalloid
solutions (LR or NS).

10. Prevent and/or control infection

Temperature elevation up to 38° C (100.4° F) during the first 24
hours can be a normal response to injury. Antibiotics may be
prescribed if fever greater than 38° C (100.4° F) persists for longer
than 24 hours after the submersion or the patient develops
pneumonia. Use of steroids and prophylactic antibiotics is not
recommended.

11. Identify and manage the event that precipitated the

drowning
Conditions such as substance abuse, seizure, myocardial infarction,
or cervical spine fracture. Cervical spine injuries are uncommon in
the victim of nonfatal drowning. Unless the mechanism of injury
suggests the possibility of a cervical spine injury, routine cervical
spine immobilization is not recommended because of the chance of
interfering with airway management.

Care plans: Drowning

770
Impaired gas exchange 
related to asphyxiation and aspiration
Goals/Outcomes: Within 12 hours of initiation of treatment, the
patient has adequate gas exchange, as evidenced by the following
ABG values: PaO2 greater than 80 mm Hg and Paco2 less than 45 mm
Hg. Within 3 days of treatment, RR is less than 20 breaths/min with
normal depth and pattern; breath sounds are clear and bilaterally
equal; and the patient is oriented to time, place, and person
(depending on degree of permanent neurologic impairment).
Respiratory Status: Gas Exchange.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs

of increased work of breathing such as use of accessory muscles or
retraction of intercostal or supraclavicular muscles.

3. Auscultate breath sounds, noting areas of decrease/absent

ventilation and presence of adventitious sounds.

4. Determine the need for suctioning by auscultating for crackles

and rhonchi over major airways.

5. Monitor the patient’s respiratory secretions.

6. Note changes in oxygen saturation (SaO2), pulse oximetry (SpO2),

end-tidal CO2 (etco2), and ABGs as appropriate.

7. Monitor for increased restlessness or anxiety.

8. If the patient is restless or has unusual somnolence, evaluate for

hypoxemia and hypercapnia as appropriate.

9. Monitor chest x-ray results while new films become available.

Oxygen therapy

771
1. Administer supplemental oxygen using liter flow and device as
ordered.

2. Add humidity as appropriate.

3. Restrict the patient and visitors from smoking while oxygen is in

use.

4. Document pulse oximetry with oxygen liter flow in place at time

of reading as ordered. Oxygen is a drug; the dose of the drug must
be associated with the oxygen saturation reading or the reading is
meaningless.

5. Obtain ABGs if the patient experiences behavioral changes or

respiratory distress to check for hypoxemia or hypercapnia.

6. Monitor for changes in chest radiograph and breath sounds

indicative of oxygen toxicity and absorption atelectasis in patients
receiving higher concentrations of oxygen (greater than Fio2 45%)
for longer than 24 hours. The higher the oxygen concentration, the
greater is the chance of toxicity. The rapid movement of oxygen
molecules across the alveolar capillary membranes can damage the
membranes, prompting a syndrome that mimics acute lung injury.

7. Monitor for skin breakdown where oxygen devices are in contact

with skin, such as nares and around edges of mask devices.

8. Provide oxygen therapy during transportation and when the

patient gets out of bed.

Mechanical ventilation

1. Monitor for conditions indicating a need for ventilation

support.

2. Monitor for impending respiratory failure or signs of pneumonia.

3. Consult with other healthcare personnel in selection of the

ventilatory mode.

772
4. Administer muscle paralyzing agents, sedatives, and narcotics
analgesics as appropriate.

5. Monitor for activities that increase oxygen consumption (fever,

shivering, seizures, pain, or basic nursing activities) that; may
supersede ventilator support settings and cause O2 desaturation.

6. Monitor the effectiveness of mechanical ventilation on the

patient’s physiologic and psychological status.

7. Provide the patient with means of communication, if he or she is

alert.

8. Monitor adverse effects of mechanical ventilation.

9. Perform routine mouth care.

10. Elevate the head of the bed minimally at 30 degrees.

Hypothermia 
related to immersion in cold water
Goals/Outcomes: Within 24 hours of initiating therapy, the
patient’s core temperature increases to 35° C to 37° C (95° F to 98.6°
F). BP, RR, and HR are normalizing for the patient.
Thermoregulation.

Hypothermia treatment

1. Monitor the patient’s temperature using a low-recording

thermometer, if necessary.

2. Institute a continuous core temperature–monitoring device, as

appropriate.

3. Monitor for and treat ventricular fibrillation.

4. Minimize stimulation of the patient to avoid precipitating

ventricular fibrillation.

5. Institute active external rewarming measures (e.g., warming

773
lights, warmed baths, warmed blankets, forced air warming
blankets), as appropriate. Do not attempt surface or external
warming until core temperature is within acceptable limits (i.e., 35°
C to 37° C [95° F to 98.6° F]). Premature surface rewarming can lead
to the return of cold blood to the heart and precipitate an “after
drop” in core temperature.

6. Institute active core rewarming techniques (e.g., colonic lavage,

hemodialysis, peritoneal dialysis, and extracorporeal blood
rewarming), as appropriate.

7. Monitor for rewarming shock.

Risk for infection 

related to aspiration
Goals/Outcomes: The patient is free of infection, as evidenced by
body temperature less than 37.5° C (99.5° F) after the first 24 hours,
WBC count within normal limits for the patient, clear sputum, and
negative culture results.
Infection Severity.

Infection protection

1. Monitor for signs and symptoms of infection (fever, changes in

sputum).

2. Monitor absolute granulocyte count, WBC, and differential

results.

3. Obtain cultures, as needed.

4. Encourage deep breathing and coughing, as appropriate.

5. Use aseptic technique when suctioning the secretions.

Additional nursing diagnoses

Also see Posttrauma Syndrome in Major Trauma, see other nursing
diagnoses and interventions and Emotional and Spiritual Support
of the Patient and Significant Others, Chapter 2.

774
Pelvic fractures
Pathophysiology
The pelvis is composed of three bones: two innominate bones and
the sacrum. The innominate bones are each composed of three
bones (ilium, pubis, and ischium) that fuse after childhood. The two
innominate bones are joined by the symphysis pubis, a fibrous
cartilage joint that connects the two pubic bones anteriorly; they are
attached posteriorly to a third bone, the sacrum, by a system of
ligaments termed the posterior osseous ligamentous structures. Many
blood vessels run through the pelvis and join to form the large
venous plexus.
MVCs and auto-pedestrian trauma cause approximately two
thirds of all pelvic fractures, which have a mortality rate of up to
50% in some studies. A large force is needed for a pelvic fracture to
occur, because these bones are stabilized by a strong network of
ligaments. Pelvic fractures have been classified by several systems,
but perhaps the most helpful are the systems that classify fractures
by their stability and the mechanism of injury (Table 3-9). Pelvic
fractures are considered stable fractures when the posterior osseous
ligamentous structures are intact. An unstable pelvic fracture occurs
when the osseous ligamentous structures are disrupted posteriorly
and portions of the pelvis can move in any direction.

Table 3-9
CLASSIFICATION OF PELVIC FRACTURES

Pelvic fractures are most commonly classified using one of two systems: the Tile Classification
System and the Young Classification System.
1. Tile Classification System: Focuses on whether the posterior sacroiliac complex is intact:
• Type A Injuries: The sacroiliac complex is intact with a pelvic ring stable fracture that can be
managed without surgery.
• Type B Injuries: The posterior sacroiliac complex is partially disrupted, are often unstable,
and result from internal rotational forces.
• Type C Injuries: The posterior sacroiliac complex is completely disrupted, have both
rotational and vertical instability, and result from motor vehicle collisions, a fall from great
heights, or severe compression.

2. Young Classification System: Focuses on mechanism of injury including lateral

compression, anteroposterior compression, vertical shear, or a combination of forces. Lateral
compression fractures include transverse fractures of the pubic rami, located ipsilateral or

775
 contralateral to a posterior injury.
• Grade I: Associated sacral compression on side of impact.
• Grade II: Associated posterior iliac (“crescent”) fracture on side of impact.
• Grade III: Associated contralateral sacroiliac joint injury.

Classification Mechanism of Injury Description

of Injury
Anteroposterior External rotation is caused “Open book injury”; the force causes the
compression by a crushing force on the symphysis pubis to spring open. Rupture of
posterior superior iliac anterior sacroiliac and sacrospinous ligaments
spines. occurs, but posterior ligaments are intact. Stable
vertically but can rotate externally. May be
associated with ruptured bladder
(intraperitoneal) if injury occurs when bladder
is full.
Lateral Internal rotation from a Most common type of injury. Often does not
compression high-energy injury that affect posterior ligamentous complex. Partially
causes direct pressure to unstable fracture that is rotationally unstable
crush anterior sacrum. but vertically stable. May have extensive soft
Pressure on the greater tissue injury. May be associated with ruptured
trochanter causes the bladder (extraperitoneal).
femoral head to displace the
anterior pubic rami.
Vertical shear Excessive force from trauma Most severe injury with the highest mortality
(Malgaigne such as falls and crush rates. Very unstable. Complete disruption of the
fracture) injuries in a vertical plane posterior osseous ligamentous system. Often
leads to unstable disruption accompanied by injuries of the skin and
of the anterior and posteriorsubcutaneous tissues or injuries to the
ring. gastrointestinal, genitourinary, vascular, and
neurologic systems.
Complex Excessive and powerful Pelvic ring disruptions resulting in bizarre
fracture forces from many directions. fractures or dislocations in a combination of
injury patterns. Usually very unstable.

The most serious complications from a pelvic fracture are

hemorrhage and exsanguination, which cause up to 60% of deaths.
The pelvis receives a rich supply of blood from a complex system of
interconnected collateral arteries and the venous plexus of the iliac
system, often called the vascular sink. The aorta and internal iliac
artery are close to the pelvis. This vascular network can easily be
damaged or disrupted by the same forces that injure the pelvis.
Pelvic fragments can damage vascular structures. The
retroperitoneal space can hold as much as 4 L of blood before
spontaneous tamponade occurs. Acute blood loss is difficult to
identify until systemic symptoms, such as those occurring with
shock, appear. In addition, damage to the sciatic and sacral nerves
may occur with sacral and sacroiliac disruption.
The most common cause of pelvic fractures in older adults is
falls, as opposed to MVCs in younger people. Older adults with

776
a pelvic fracture have a 20% mortality rate. Older adults have more
problems related to preexisting conditions. Cardiovascular disease
often causes insufficient compensatory function to manage the
stress of injury. Despite a less severe mechanism of injury, rates of
sepsis and death are higher in older adults than in patients with
trauma who are younger than 65 years with similar injuries.

Assessment: Pelvic fractures

Goal of system assessment
Evaluate for stability of the pelvis and the probability of substantial
blood loss.

History and risk factors

The most common mechanisms of injuries are MVCs, motorcycle
collisions, pedestrians struck by motor vehicles, and falls. Up to
15% of patients with a pelvic fracture have associated renal and
lower urinary tract (LUT) injuries. Fifty percent of patients with
both pelvic fractures and urologic injuries also have abdominal
injuries.
Risk factors include:

• Age.

• Smoking.

• History of bone disease including osteoporosis.

• Previous hysterectomy.

• Use of anticoagulants.

• Concomitant injuries including intraabdominal organ injuries and

bladder and urethral injuries.

Stable pelvic fracture

• Can withstand normal physiologic forces without abnormal

777
 deformation.

Unstable pelvic fracture

• Fracture of the pelvic ring in more than one place that results in
displacement.

Vital signs
• Temperature may be low if the patient is developing shock.

• RR may be elevated as a compensatory mechanism in

hypovolemic shock.

• BP may be decreased in response to substantial blood loss.

• HR will be increased with substantial blood loss.

Observation
Evaluate for signs of trauma to the abdominal and pelvic regions.

• Lower extremity shortening and abnormal external rotation of the

leg.

• Pelvic instability and/or pain with palpation.

• Lacerations of the vagina, peritoneum, groin, or anus may

indicate an open pelvic fracture.

• Groin, genitalia, and suprapubic swelling may be present.

• Blood at the meatus, signifying urethral trauma, which often

accompanies pelvic fractures.

• Evidence of hypovolemic shock.

Palpation
The pelvis is palpated by placing inward and posterior compression
on the iliac crests.

778
• Assess for pain with palpation.

• Feeling of movement of the pelvic bones upon palpation.

• Neurovascular status of the lower extremities should be checked.

• Palpate for pulses in lower extremities, femoral.

• Check for sensation bilaterally.

Diagnostic Tests for Pelvic Fractures

Test Purpose Abnormal Findings

Blood Studies
Complete blood Assess for blood loss. Decreased Hgb and Hct
count indicate blood loss.
Hemoglobin Often Hgb and Hct are within
(Hgb) normal range initially,
Hematocrit (Hct) especially if the patient has
not received a significant
amount of fluid to replace
the blood loss. Hgb and Hct
testing should be repeated
after the patient has a fluid
challenge if there is any
indication of significant
bleeding.
Coagulation Assess for causes of bleeding, clotting, and Decreased PT with low INR
profile disseminated intravascular coagulation promotes clotting; elevation
Prothrombin indicative of abnormal clotting present in promotes bleeding; elevated
time (PT) with shock or ensuing shock. fibrinogen and D dimer reflect
international abnormal clotting.
normalized
ratio (INR)
Partial
thromboplastin
time
Fibrinogen
D dimer
Radiology
Pelvic Assess bony integrity of the pelvis. Fractures that disrupt the
radiograph pelvic ring.
Pelvic computed Assess bony integrity of the pelvis and Fractures within the pelvic
tomography (CT) presence of retroperitoneal hemorrhage. ring, retroperitoneal bleeding.
scan
Interventional
Radiology
Angiography Indicated when the patient has evidence of Extravasation of dye from torn
hemodynamic instability with an ongoing blood vessels.
need for blood transfusion where there is no
evidence of any other bleeding source

779
 besides the pelvic fracture. If contrast
extravasation or a false aneurysm is
identified, then embolization can be done.
Angiography is currently the gold standard
for diagnosis of arterial bleeding secondary
to pelvic fracture.

Collaborative management
Care priorities

1. Stabilize the pelvis

External immobilization: Defined as any device that is applied to
immobilize the pelvis either externally or percutaneously through
the skin into the bone. Noninvasive external fixation can be
accomplished in several ways and can be applied at the scene of
injury to preserve function and prevent further orthopedic and
neurovascular injury. When an unstable pelvis is identified, the
pelvis should be stabilized. Stabilization can be achieved with
several methods including:

• A sheet wrapped around the pelvis and secured with towel clips.

• Commercially available devices such as the T-POD, SAM Sling,

and Pelvic Binder.

• Internal rotation and taping the lower extremities, which is

referred to as IRTOTLE.

With external immobilization, care should be taken to limit the

amount of pressure and time the pressure is applied to prevent skin
damage. Most of these devices/techniques should not be used for
longer than 24 hours. These are temporary measures to limit the
amount of hemorrhaging until more definite treatment can be
initiated.
An invasive emergency external fixation device, consisting of one
pin in each iliac wing connected by a bar, can be inserted to provide
pelvic stability. If an emergency laparotomy is performed, more
complex fixation devices may be applied.

780
 If abnormal shortening or rotation has occurred with the injury,
the lower extremities should be supported and stabilized in the
position in which they were found. A backboard supported by
pillows, towels, or blankets taped in place with cloth tape are used
until a traction splint can be applied.

Use of an external fixation device is not sufficient for

maintaining reduction in the posterior pelvis or for stabilizing the
pelvic posterior elements. As long as the patient is on bed rest or in
traction, however, it can be used to manage the acute phase of the
fracture.

Internal immobilization: Surgical open reduction and

immobilization of unstable pelvic ring disruptions with surgically
implanted plates, screws, or other devices. Permanent fixation
requires closed reduction for final pelvic stabilization.

2. Initiate surgical exploration

Done to identify blood vessels in need of ligation or repair for
ongoing hemorrhage. Inflow of blood to the pelvic circulation can
be limited by ligation of the internal iliac artery to control bleeding.
Because many collateral vessels exist in the pelvic circulation,
infarction rarely occurs with this procedure. Surgical exploration is
not always recommended. When the peritoneal space is entered,
the tamponade is released and bleeding can increase. The extensive
vascular sink makes identification of bleeding vessels difficult.
Some patients may undergo angiography and selective
embolization of bleeding points with either an autologous blood
clot or particulate gel foam instead of surgery.

3. Replace blood loss with massive transfusion

Patients who continue to exhibit signs of shock after receiving 2 L of
crystalloid IV fluid should receive blood transfusions. Blood
replacement is best given according to established massive
transfusion protocols, which have been shown to decrease mortality

781
by eliminating the deadly triad of acidosis, hypothermia, and
coagulopathy. See Major Trauma for further discussion of massive
transfusion protocols. Some studies have supported withholding
aggressive fluid resuscitation until after operative or embolic repair
because an increase in MAP will increase intravascular hydrostatic
pressure and may increase bleeding from torn vessels.

4. Initiate pharmacotherapy for the following

Manage pain with analgesics: IV morphine sulfate usually relieves

pain and can be readily reversed with naloxone if hypotension or
respiratory insufficiency is noted.

Control BP with vasopressors: For hypotension only after sufficient

volume replacement has occurred (see Appendix 6).

Provide protection from disease with tetanus immunization:

Booster is given if history is unknown or if a booster is needed
(see Table 3-1).

Manage infection with antibiotics: Initial use for prophylaxis

against infection is controversial in patients with open fractures.
Used later for positive cultures of wounds, blood, or urine.

Care plans: Pelvic fractures

Decreased CO
related to blood loss from severity of fracture(s) and/or concomitant
injuries.
Goals/Outcomes: Within 24 hours of injury, the patient
demonstrates adequate perfusion, as evidenced by the following
ABG values: pH between 7.35 and 7.45 and base deficit level greater
than 2.0 mmol/L, regular HR ≤100 bpm, bilaterally strong and equal
peripheral pulses, warm and dry extremities, brisk (less than 2
seconds) capillary refill, systolic BP ≥90 mm Hg (or within 10% of
patient’s normal range), and urine output ≥0.5 mL/kg/h. If
hemodynamic monitoring is present, PAWP is ≥6 mm Hg and CI is
≥2.5 L/min/m2. The patient is awake, alert, and oriented to time,

782
place, and person without restlessness or confusion.
Tissue Perfusion: Peripheral; Blood Loss Severity.

Hemorrhage control

1. Apply compression device or sheet to pelvic area or tape feet in

an internal rotation position to align broken pelvis and decrease
bleeding.

2. Note Hgb/Hct levels before and after blood loss.

3. Monitor trends in BP and hemodynamic measurements, if

available (e.g., CVP and pulmonary capillary/artery wedge
pressure).

Hypovolemia management

1. Monitor the patient for evidence of fluid volume deficit,

including tachycardia, decreased MAP, decreased amplitude of
peripheral pulses, urine output less than 30 mL/hr (adult), urine
output less than 1 mL/kg/hr (child weighing less than 30 kg), thirst,
and dry mucous membranes.

2. Establish two large-bore peripheral IV lines. Establish central line

if necessary.

3. Monitor intake and output; administer fluid therapy as

prescribed. Adjust infusion to maintain desired urine output at the
desired resuscitation hourly rate. Do not exceed 50 mL/hr urine
output.

4. Monitor weight daily during fluid resuscitation; report significant

gains or losses. A significant weight gain will occur with large-
volume fluid resuscitation.

5. Monitor serial Hct and Hgb values. While the circulating volume
is restored, hemoconcentration is no longer present and Hct returns
to within normal limits (WNL).

6. Monitor the patient for signs and symptoms of large-volume

783
fluid administration (shortness of breath, tachypnea, excessive
urine output).

Risk for infection 

related to impaired wound healing
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, WBC count 11,000/mm3, negative culture results,
HR 100 bpm, BP within the patient’s normal range, and absence of
agitation, purulent drainage, and other clinical indicators of
infection.
Risk Identification.

Incision site care

1. Inspect the incision for redness, swelling, or signs of dehiscence.

2. Note the characteristics of any drainage.

3. Monitor the healing process at the incision site.

4. Change the dressing at appropriate intervals.

5. Perform pin care as prescribed. Current evidence does not

support any one method of pin care.

Infection prevention

1. Monitor for systemic and localized signs and symptoms of

infection.

2. Monitor vulnerability to infection.

3. Monitor absolute granulocyte count, WBC, and differential

results.

4. Promote sufficient nutrition intake.

5. Encourage rest.

6. Obtain cultures as needed.

784
Impaired physical mobility 
related to limitation in movement of pelvis needed to stabilize fracture
with fixation device and other loss of joint movement or ability to ambulate
independently.
Goals/Outcomes: The patient will not develop complications of
impaired mobility such as skin breakdown on any dependent areas
or areas involved with fracture stabilization; venous
thromboembolism; or constipation.
Immobility Consequences: Physiologic.

Bed rest care

1. Place on appropriate therapeutic mattress/bed.

2. Keep bed linen clean, dry, and wrinkle-free.

3. Apply devices to prevent foot drop, as needed.

4. Attach a trapeze bar to the bed, as appropriate.

5. Turn immobilized patients every 2 hours, according to a specific

schedule.

6. Perform passive and active ROM exercises.

7. Apply antiembolism devices (e.g., stocking, sequential

compression devices, foot pump).

8. Monitor for constipation, urinary function, and pulmonary

status.

Positioning

1. Premedicate the patient before turning as appropriate.

2. Position in proper body alignment.

3. Support the legs during turning to minimize movement of the

pelvis.

785
4. Monitor fixation/traction devices for proper setup, and maintain
position and integrity of traction when repositioning the patient.

5. Minimize friction and shearing forces when positioning and

turning the patient.

6. Place call light within reach.

7. Place frequently used items within reach.

Renal and lower urinary tract trauma

Pathophysiology
Injuries to the genitourinary tract represent a small proportion of
patients severe enough for admission to a trauma service. The
majority of patients experience blunt trauma caused by MVCs, falls
from heights, and blows to the torso or external genitalia.
Genitourinary tract injury is rarely life threatening. However,
shattered kidney, major renal vascular laceration with hemorrhage,
renal artery dissection, or pedicle avulsion can be a result of a
significant deceleration injury that may be life threatening or a
threat to the kidney itself. These can be seen as a result of a high-
speed MVC or a fall from a substantial height.
Pelvic fractures are most commonly associated with injury to the
female genital tract. Injuries to the external genitalia, urethra, and
bladder are often overlooked in the initial trauma assessment
because they frequently accompany life-threatening injuries that
require aggressive and immediate management. Urethral
disruption is seen with pelvic fracture in approximately 5% of
women and 25% of men. In males, penile injury results from
rupture of the tunica albuginea, with concomitant urethral injury in
approximately 20% of patients.
The genitourinary tract is divided into upper and lower tracts.
The upper tract consists of the kidney and the ureters, and the LUT
involves the external genitalia, urethra, and bladder. Renal and
LUT trauma can also occur with penetrating injuries (stab and
gunshot wounds). Other mechanisms of injury include physical or

786
sexual assault and rough consensual sexual intercourse. Injury to
the vulva or penis is uncommon and should alert one for prompt
screening for interpersonal violence. Pathophysiology for renal and
LUT trauma is shown in Table 3-10.

Table 3-10
PATHOPHYSIOLOGY FOR RENAL AND LOWER URINARY TRACT
TRAUMA

Urethral injury may cause males long-term problems with sexual

intercourse and voiding. Sexual dysfunction may be a result of
damage to neural and vascular structures. Incontinence may result
from damage to the sphincters or their innervations. In patients
with complete urethral disruption, approximately 20% have
voiding dysfunction and 25% have sexual dysfunction.

Renal and lower urinary tract assessment

787
Goal of system assessment
Identify specific location of physical injuries and presence of signs
and symptoms indicating injury to organs affected by the renal
system or surrounding organs.

History and risk factors

• Ask about allergies, current medications, preexisting medical
conditions, and factors surrounding the injury.

• Patients with preexisting renal diseases such as polycystic kidney

disease and pyelonephritis are at higher risk for renal injury.

• Ask about any suprapubic tenderness.

• Ask about inability to void spontaneously or any past bloody

urine.

• Ask about flank pain, pain at the costovertebral angle, back

tenderness, and colicky pain with the passage of blood clots.

Observation and subjective symptoms

• Renal trauma: Abdominal or flank pain, back tenderness, colicky
pain with passage of blood clots, pallor, diaphoresis, gross
hematuria, restlessness, confusion, obvious wounds, contusions,
or abrasions in the flank or abdomen; abdominal distention; Grey
Turner sign (bruising over the lower portion of the back and the
flank caused by a retroperitoneal hemorrhage); pain at the
costovertebral angle.

HIGH ALERT!
Gross hematuria is present in only slightly more than half of
patients with renal trauma and is considered an unreliable
diagnostic sign.

788
• Ureter trauma: Gross hematuria may be present; if the ureter is
transected, normal urine from the unaffected kidney may still be
voided. Late signs may include fever and flank or abdominal
discomfort. Urine may be found at the entrance or exit sites of
penetrating abdominal wounds or wounds of the middle to lower
back areas.

• Bladder trauma: Inability to void spontaneously, gross hematuria

(present in approximately 95% of patients), and abdominal
discomfort. Perineal or scrotal edema and hematoma, abnormal
position of prostate, abdominal distention, palpable suprapubic
mass, and palpable and overdistended bladder.

• Urethral trauma: Blood at the meatus, inability to void

spontaneously, urethral bleeding, prostate tenderness,
microscopic or gross hematuria, pain and tenderness of genitalia,
and perineal hematoma. Tracking of urine into tissues of the
thighs or abdominal wall, bruised to discolored genitalia.

HIGH ALERT!
Physical signs may be masked because the kidneys are located
beneath abdominal organs, back muscles, and bony structures.

Vital signs
• Hypotension.

• Tachycardia.

• Flank or abdominal mass.

• Bladder trauma: Late signs may include fever.

Palpation

789
• Bladder trauma: Suprapubic tenderness.

• Renal trauma: Hematoma over the flank of the eleventh or twelfth

ribs.

• Ureter trauma: Enlarging retroperitoneal mass.

Inspection
• Digital rectal examination to check for rectal tone, gross blood,
and the position of the prostate. Posterior urethral disruption
may result in a “high riding” prostate in males, which moves
away from the examiner during the procedure. The finding
indicates rupture of the urethra, which requires surgical repair or
“railroading” as soon as the patient’s general condition permits.
Diminished rectal tone may indicate SCI or imply that the patient
engages in anal intercourse.

• A meticulous vaginal examination should be performed in all

women with pelvic fractures to assess for bone fragments or
lacerations that could result in hemorrhage and infection.

Diagnostic Tests for Renal and Lower Urinary Tract Trauma

Collaborative management
Care priorities

1. Identify and manage bleeding complications,

including hypovolemic or hemorrhagic shock

• Hemorrhagic shock: Volume resuscitation with crystalloids,

colloids, or blood products as indicated.

2. Manage pain

• Analgesics: IV narcotics may be used as a first line to relieve pain.

790
• Phenazopyridine (Pyridium) is a urinary antispasmodic agent
that helps to relieve burning and frequency.

• Both of these strategies provide symptom relief only. Managing

the cause of the pain treats the injury.

3. Prevent and/or manage infection

• Source control: Avoid urinary catheterization when possible to

prevent catheter-associated UTI. Remove the catheter when no
longer needed, according to the Centers for Disease Control and
Prevention guidelines for prevention of catheter-associated UTI
and/or nurse-driven Foley catheter removal protocol.

• Infections: As indicated, obtain blood and urine cultures and

initiate appropriate antibiotics and other infection control
measures.

• Antibiotics: Consider initiating for positive urine culture results,

penetrating injuries, or peritonitis.

4. Support renal function

• Renal dysfunction: Fluids need to be carefully managed with

goal-directed therapy; fluids may be administered or restricted
depending on the phase of renal dysfunction; renal replacement
therapies may be indicated for fluid and electrolyte management
if the degree of dysfunction is severe enough. See Acute Renal
Failure, Chapter 5, for more information.

If renal function is impaired, may need to adjust dosages

of medications metabolized through the renal system.

5. Manage urinary elimination without causing further injury

791
Catheterization

• If the patient is unable to void: Catheter should be passed

only as far as it will progress without undue force. If any
resistance is met during catheterization, a urethrogram is
indicated.

• If blood is present at the urethral meatus: The patient should not

be catheterized until diagnostic tests are completed, because the
blood may signal urethral injury. In the presence of urethral
injury, an improperly placed catheter can result in an incomplete
injury progressing to a complete disruption.

• Urethral trauma: A suprapubic catheter may be used to manage

severe urethral lacerations and urethral disruption.

• Renal trauma: In addition to direct surgical intervention,

diversion of urine may be required by nephrostomy tube,
depending on location of injury or in cases of coexisting
pancreatic and duodenal injury.

• Ureteral trauma: Internal ureteral catheters (ureteral stents) may

be indicated for ureteral trauma, particularly for gunshot
wounds, to maintain ureteral alignment, ensure urinary drainage,
and provide support during anastomosis.

6. Facilitate a timely surgical intervention

• Surgical intervention is required in a minority of patients who

sustain renal trauma. The majority of patients who undergo
surgical intervention have sustained penetrating trauma.

• Surgical correction: Surgical correction may be performed open or

with minimally invasive technology, such as in interventional
radiology. Surgical correction may be indicated for transected
ureter, partial ureteral tears of more than one third of the
circumference of the ureter, bladder perforation with associated
abdominal injuries or intraperitoneal rupture, and injuries
accompanied by rapidly expanding, pulsating hematomas. See

792
 Table 3-11 for examples of procedures for the various types of
renal and LUT injuries.

• In the incidence of multiple trauma: The collaboration of the

trauma surgeon and the urologist is paramount in the effort to
decrease morbidity and mortality.

• Organ Injury Scale: The American Association for the Surgery of

Trauma Organ Injury has developed an Organ Injury Scale of
solid organs including the kidney. This scale was designed to
provide a system to describe injuries by a common nomenclature
and severity of injury. The severity score for the kidney is
described in Table 3-12.

Table 3-11
SURGICAL PROCEDURES FOR RENAL AND LOWER URINARY
TRACT TRAUMA

Type of
Surgical Indications/Surgical Management
Injury
Minor renal Conservative management. Rest and observation with careful follow-up to
trauma prevent progressive deformity and to evaluate blood pressure.
Major renal Surgical intervention if hypotension and hemodynamic instability occur.
trauma
Critical renal Immediate surgical exploration; low rates of renal salvage.
trauma
Proximal Primary ureterostomy with end-to-end anastomosis.
ureteral
injury
Distal Ureteral stenting or percutaneous nephrostomy, depending on location and
ureteral extent of injury.
injury
Bladder Use of urinary or suprapubic drainage. Surgical repair may be indicated.
injury
Urethral Urinary or suprapubic catheterization is used for long-term management.
injury

Table 3-12
AMERICAN ASSOCIATION FOR THE SURGERY OF TRAUMA
ORGAN INJURY SEVERITY SCORE FOR THE KIDNEY

Grade Type Injury Definition

1 Parenchyma Subcapsular hematoma and/or contusion
Collecting No injury
system

793
 2 Parenchyma Laceration less than 2 cm in depth and into the cortex, small hematoma
contained within Gerota fascia
Collecting No injury
system
3 Parenchyma Laceration greater than 1 cm in depth and into the medulla, hematoma
contained within Gerota fascia
Collecting No injury
system
4 Parenchyma Laceration through the parenchyma into the urinary collecting system
Collecting Vascular segmental vein or artery injury
system Laceration, one or more in the collecting system with urinary
extravasation
Renal pelvis laceration and/or complete ureteral pelvic disruption
5 Vascular Main renal artery or vein laceration or avulsion main renal artery or vein
thrombosis
From Buckley JC, McAninch JW: Revision of the current American Association for
the Surgery of Trauma Renal Injury Grading System. J Trauma 70:35-37, 2011.

Care plans: Renal and lower urinary tract

trauma
Impaired urinary elimination 
related to mechanical trauma secondary to injury to the kidney and LUT
structures.
Goals/Outcomes: Within 6 hours after immediate trauma
management, the patient has a urinary output of ≥0.5 mL/kg/h with
no evidence of bladder distention.
Urinary Elimination.

Urinary elimination management

1. Monitor urinary outflow. Encourage the patient to void. If patient

is unable to void, assess for full bladder. Urinary catheterization or
suprapubic drainage may be needed. Report findings to the
physician. Monitor for the following signs of kidney or LUT
trauma:

• Urge but inability to void spontaneously despite

adequate volume replacement.

• Blood at the urethral meatus.

794
• Difficult or unsuccessful urinary catheterization.

• Anuria after urinary catheterization.

• Hematuria.

2. Do not catheterize the patient if there is blood at the urethral

meatus. Call the advanced practice provider for consultation for a
possible urethral injury.

3. Monitor serum BUN and creatinine.

4. Document input and output hourly. Consult the advanced

practice provider if urine output is less than 0.5 mL/kg/h.

5. Assess whether clots may be occluding the drainage system. If

indicated, obtain order for catheter irrigation or call the advanced
practice provider to irrigate the catheter. Sudden cessation of urine
flow through the collection system (particularly if past output was
greater than 50 mL/h) indicates possible catheter obstruction. If
catheter irrigation does not resume urine drainage, consider
changing the urinary catheter after discussion with the physician.

6. Ensure that nephrostomy tubes are not occluded by the patient’s

weight or external pressure. Irrigate the nephrostomy tube only if
prescribed with ≤5 mL of fluid. The renal pelvis holds less than 10
mL of fluid.

7. Assess entrance site of the nephrostomy tube for bleeding or

leakage of urine. Catheter blockage or dislodging causes a sudden
decrease in urine output. Inspect urine color and for blood clots.
Hematuria is normal for 24 to 48 hours after nephrostomy tube
insertion. Consult the physician if gross bleeding (with or without
clots) occurs.

8. Hydrate to allow for clearing of contrast material from the

patient’s system after diagnostic testing.

795
 Urinary Catheterization; Fluid Management; Fluid
Monitoring; Tube Care: Urinary.

Risk for infection 

related to inadequate primary defenses and tissue destruction secondary to
bacterial contamination of the urinary tract system occurring with
penetrating trauma, rupture of the bladder into the perineum, or
instrumentation.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, WBC count ≤11,000/mm3, and negative results of
urine and wound drainage testing for infective organisms.
Immune Status; Risk Control.

Infection protection

1. Use aseptic technique when caring for drainage systems. Keep

catheters and collection container at a level lower than the bladder
to prevent reflux; ensure that drainage tubing is not kinked.

2. Record the color and odor of urine each shift. Culture urine
specimen when signs or symptoms of infection are present.

3. Monitor the patient’s WBC count daily and temperature every 4

hours for elevations.

4. Assess for signs of peritonitis: abdominal pain, abdominal

distention with rigidity, nausea, vomiting, fever, malaise, and
weakness.

5. Assess catheter exit site each shift for the presence of erythema,
swelling, or drainage.

6. Assess thigh, groin, and lower portion of abdomen for indicators

of urinary extravasation: swelling, pain, mass(es), erythema, and
tracking of urine along fascial planes.

7. Assess surgical incision for approximation of suture line and

evidence of wound healing, noting presence of erythema, swelling,
and drainage. Note color, odor, and consistency of drainage. Notify

796
the physician of purulent or foul-smelling drainage. Consider
obtaining a culture.

8. Assess skin at invasive sites for indicators of irritation: erythema,

drainage, and swelling.

9. Cleanse catheter insertion sites with antimicrobial solution or per

hospital policy. Manage catheter exit sites per protocol.

10. Consider dressing changes every 24 hours or as soon as noted

they are wet. If skin is irritated from contact with urine, consider
use of a pectin wafer skin barrier for extra protection.

Incision Site Care; Wound Care; Infection Control;

Surveillance; Tube Care: Urinary.

Acute pain (acute tenderness in lower abdomen) 

related to physical injury associated with LUT structural injury,
procedures for urinary diversion, or surgical incisions.
Goals/Outcomes: Within 2 hours after giving analgesic agent, the
patient’s subjective evaluation of discomfort improves, as
documented by an approved pain scale. Nonverbal indicators of
discomfort, such as grimacing, are absent.
Pain Control; Comfort Level.

Pain management

1. Assess the patient for pain at least every 4 hours.

2. Be alert to shallow breathing in the presence of abdominal pain,

which can cause inadequate pulmonary excursion. Medicate
promptly, and document the patient’s response to analgesic agent,
using the appropriate pain scale. IV narcotics may be indicated if
the injury is severe.

3. Explain the cause of the pain to the patient.

4. Assist the patient into a position of comfort. Often knee flexion

will relax lower abdominal muscles and help reduce discomfort.

797
5. Implement nonpharmacologic measures for coping with pain:
diversion, touch, and conversation.

Analgesic Administration; Positioning; Presence.

Thoracic trauma
Pathophysiology
Thoracic trauma may be caused by blunt or penetrating injuries to
the chest, back, flanks, and upper abdomen region. Thoracic trauma
accounts for up to 60% of all trauma-related deaths in the United
States. Careful assessment is needed to quickly identify life-
threatening injuries to the heart, lungs, and great vessels. Close
monitoring is required to prevent complications secondary to
injuries that develop over the first 24 hours, such as pulmonary
contusions.
Thoracic injuries can result from both direct and indirect forces.
Direct force such as direct impact involving an object can result in
bony fractures, tissue bruising, and ruptured organs. Indirect forces
can cause tissues to stretch beyond their limits and can result in
tears leading to rupture of blood vessels and disruption of organs,
such as the bronchus and esophagus. Thoracic injuries often lead to
problems with ventilation, oxygenation, and perfusion, causing a
decrease in the delivery of oxygen and nutrients to the tissues.
The lungs are often affected by space-occupying injuries, such as
hemothoraces, pneumothoraces, and hemopneumothoraces, which
compress lung tissue, interfering with lung expansion, thereby
limiting the amount of ventilation and decreasing oxygen exchange
at the alveoli level. The most serious of these injuries is a tension
pneumothorax where the pressure in the chest is so high that not
only is oxygenation impaired but also venous return to the heart is
diminished, leading to decreased CO and shock.
One of the most common thoracic injuries is contusions to the
lungs. When the lung tissue is bruised, alveolar hemorrhage and
parenchymal destruction occur, leading to both local and systemic
consequences. The reduced compliance impairs ventilation and
causes an increase in shunting with decreased pulmonary blood

798
flow. Hypoxemia and hypercarbia develop and usually worsen
over the following 72 hours.
Blunt thoracic trauma can cause injury to the heart muscle by one
or more of the following four mechanisms: compression of the heart
between the sternum and vertebrae, bruising of heart tissue by
bony structures, rupture or compression of coronary arteries by the
blow, or cardiac rupture caused by intrathoracic or intraabdominal
pressure. Causes of blunt cardiac injury are MVCs, direct blows to
the chest, falls from great heights, sporting and industrial injuries,
and kicks from animals. There are no reliable diagnostic tests to
identify blunt cardiac injury. Cardiac injury is considered
significant when the patient has new findings, such as new
dysrhythmias, abnormal cardiac wall motion, or injury to the heart.
Penetrating thoracic trauma is caused by gunshot wounds, stab
wounds, or foreign bodies entering the chest or upper abdomen.
Open chest injuries can result in an open pneumothorax or
lacerations to the lung tissue or the airways, heart, great vessels,
and/or the esophagus. Penetrating injuries to the heart are the most
common cause of intrapericardial hemorrhage.

Assessment: Thoracic trauma

Goal of system assessment
Evaluate for traumatic injuries of the heart, lung, great vessels, and
bony thorax.

History and risk factors

Age, smoking history, mechanism of injury, chronic lung disease.

Vital signs
• RR may be increased if hypoxia is present.

• BP may be decreased.

• HR may increase as a result of hypoxia or hemorrhage.

799
Observation
Check chest for signs of trauma and chest excursion.

• Bruising, abrasions, contusions, and lacerations indicate that the

thoracic area of the body received some of the force.

• Carefully observe chest wall for signs of penetrating injuries

because the skin may close up, masking the entry, especially with
low-velocity injuries such as stabbings.

• Logroll the patient to inspect the back of the chest.

• Observe position of the trachea.

• Observe for neck vein distention.

Percussion
• Percuss over the lung fields to identify areas of hyperresonance,
indicating a collection of air in the pleural space. Dullness may
indicate atelectasis or a collection of blood in the pleural space.

Palpation
• Over the ribs, sternum, and scapula to identify areas of
tenderness and step-offs.

• Feel chest for crepitus or subcutaneous emphysema.

Auscultation
• Lung fields to identify abnormal breath sounds.

• Decreased breath sounds may indicate a pneumothorax or

hemothorax.

• Sucking sound on inspiration may indicate an open

pneumothorax.

• Heart to identify abnormal heart sounds.

800
• Muffled heart sounds may indicate a pericardial tamponade.

Assessment
The nurse and interdisciplinary team assess for the following
common injuries.

Pneumothorax/tension pneumothorax

• Chest pain.

• Respiratory distress.

• Decreased chest wall excursion.

• Hypoxia.

• Decreased breath sounds on the affected side.

• Tachycardia.

• Additionally, with a tension pneumothorax, tracheal deviation,

JVD, hypotension, and cyanosis (late sign) may be present.

Hemothorax

• Chest pain.

• Respiratory distress.

• Decreased breath sounds on the affected side.

• Signs/symptoms of blood loss up to and including shock.

Flail chest

• Paradoxical chest wall movement.

• Pain over affected chest wall on palpation.

• Hypoxia.

801
• Decreased chest excursion resulting from pain.

• Decreased breath sounds.

Pulmonary contusion

• Hypoxia.

• Respiratory distress.

Blunt cardiac injury

• Arrhythmias.

• Chest wall contusions.

• Chest pain.

Aortic trauma

• Hypotension/hypertension.

• Tachycardia.

• Unequal pulses, absent pulses below the level of injury.

• Mottling below the level of injury.

Diagnostic Tests for Thoracic Trauma

802
803
Collaborative management
Collaborative management should start with addressing the ABCs
as outlined in the section on Major Trauma, including oxygen, IV
fluids, and blood as indicated. During the initial assessment, several
conditions involving injuries to the thoracic organs may warrant
immediate intervention. These include the following:

• Open pneumothorax.

• Tension pneumothorax.

• Massive hemothorax.

• Flail chest.

• Cardiac tamponade.

• Torn aorta or great vessels.

Care priorities
With pulmonary injuries, interventions are directed toward
managing acute respiratory compromise while correcting the
underlying injuries that may cause deterioration in the patient’s
condition. Intervention should be aimed at correcting and
preventing hypoxia. With cardiac and great vessel injuries, the care
priorities are focused on stopping hemorrhage, restoring perfusion,
and supporting cardiac function.

1. Ensure patent airway

• When the patient is unable to maintain a patent airway either as a

result of trauma or a decreased LOC, an artificial airway is
inserted through oral intubation or via emergent tracheostomy.

• Intubation: Maintains patent airway, decreases airway resistance

and respiratory effort, provides route for easy removal of airway
secretions, and allows for manual or mechanical ventilation, as
necessary.

804
2. Restore intrathoracic negative pressure

• Interventions are aimed at restoring the negative pressure in the

thoracic cavity to allow for adequate ventilation.

• Pleural decompression: Relieves life-threatening tension

pneumothorax. A 14-gauge needle or IV catheter is inserted into
the second intercostal space at the midclavicular line to relieve
the pressure in the chest cavity.

If a tension pneumothorax is suspected, pleural

decompression should not be delayed for a confirmation chest
radiograph.

• Tube thoracostomy: Chest tubes are used to remove fluid or

trapped air from the chest cavity as in a hemothorax or
pneumothorax. A thoracic catheter is inserted, usually through
the second intercostal space, the midclavicular line, or the fifth
lateral intercostal space, midaxillary line. Placement depends on
the location and extent of the hemothorax, effusion, or
pneumothorax. The catheter can be connected to a one-way
flutter valve (for air evacuation only) or to a closed chest drainage
system. Tension pneumothorax is a life-threatening emergency
requiring pleural decompression.

3. Enhance oxygenation and ventilation

• Oxygen therapy: Device is determined by the patient’s response

to therapy and may range from nasal cannula to 100%
nonrebreathing mask, depending on extent of hypoxemia.

• Pulmonary toileting: Use of incentive spirometer, chest

percussion, and suctioning to prevent atelectasis.

• Analgesia: Manages pain to minimize splinting and improve

805
 breathing. Opioid analgesics are used cautiously to avoid
respiratory depression. An epidural patient-controlled analgesia
pump or an intercostal nerve block may help to relieve local rib
pain.

• Mechanical ventilation: Must be implemented for extreme

respiratory distress or ventilatory collapse.

• Stabilization and fixation of flail chest: Most flail chest injuries

stabilize within 10 to 14 days without surgical intervention.
Stabilization of fractures is achieved using a volume-cycled
ventilator. During surgery, a flail segment can be externally
fixated by wiring or otherwise attaching the segment to the intact
bony structures.

4. Restore perfusion and oxygen-carrying capacity

• Volume replacement: A high priority in the victim of trauma.

Blood loss is replaced with PRBCs or whole fresh blood, if
available. Blood replacement via autotransfusion may also be
used. Use of colloid versus crystalloid fluids for volume
replacement remains controversial. Volume is more often
replaced with crystalloid fluids (e.g., NS, LR) rather than
colloidal IV fluids (e.g., plasma, albumin). Colloids increase the
risk of developing acute respiratory distress syndrome and acute
renal failure, and are more expensive; furthermore, research has
failed to demonstrate a significant benefit.

• Thoracotomy: Consider in patients with penetrating injuries to

the chest who arrive in PEA or develop PEA shortly after arrival.
This procedure should only be performed if a qualified surgeon
is present. Opening the chest allows the surgeon to gain control
over bleeding and restore intravascular volume to get the patient
to the operating room for more definitive care.

• Repair of thoracic aortic injuries: If the patient is stable, repair

should be delayed until the other injuries have been addressed
and the patient is over the critical period. Repair may even occur
on an elective basis after the patient is discharged from the

806
 hospital. Repair using endovascular stenting has been shown to
decrease patient morbidity.

5. Support cardiac function

• Monitoring of hemodynamic status: If there is major cardiac or

pulmonary involvement, use pulmonary artery monitoring and
CO determinations with direct arterial pressure monitoring if
indicated.

• Treatment of dysrhythmias: Use the ACLS protocols of the

American Heart Association. If rhythm disturbances do not
appear in the first 5 days after trauma, they rarely occur later.

• Immediate corrective surgical repair: Indicated for ruptured

valve, torn papillary muscle, or torn intraventricular septum
accompanied by hemodynamic instability.

• Treatment of shock: Initially, shock should be treated with fluid

resuscitation to ensure adequate intravascular volume. Once
intravascular volume has been restored and the patient remains
hypotensive, vasopressor drugs (i.e., norepinephrine,
epinephrine, vasopressin) may be necessary to enhance BP.

• Treatment of myocardial failure: Oxygen, diuretics, positive

inotropic agents, and monitoring with a pulmonary artery
catheter for right-sided and left-sided heart pressures.

Because of the potential for hemorrhage, never remove a

penetrating object until the surgeon is present and studies have
been completed to determine what the object has penetrated.

Care plans: Thoracic trauma

807
Ineffective breathing pattern 
related to pulmonary and/or cardiac injury
Goals/Outcomes: Within 24 hours of this diagnosis, RR stabilizes
to 12 to 20 breaths/min with normal work of breathing; lung injuries
are managed to provide expanded lungs with minimal fluid and/or
blood accumulation in the thoracic cavity; sources of bleeding are
identified and managed to provide adequate Hgb level for
adequate oxygenation; lost intravascular volume is replaced to
reflect a CVP of 6 to 12 mm Hg; oxygen saturation is at least 95%,
with PaO2 at least 80 mm Hg with oxygen and Paco2 less than 45 mm
Hg with (or without) mechanical ventilation; and HR is 60 to 100
bpm with BP stable (at least 100 mm Hg systolic and 60 mm Hg
diastolic).
Respiratory Status: Ventilation.

Airway management

1. Monitor for sudden blood loss or persistent bleeding.

2. Prevent blood volume loss (e.g., apply pressure to site of

bleeding).

3. Administer oxygen and/or mechanical ventilation, as

appropriate.

4. Draw ABGs and monitor tissue oxygenation.

Ventilation assistance

1. Monitor fluid status, including intake and output, as appropriate.

2. Maintain patent IV access.

Respiratory monitoring

1. Monitor BP, pulse, temperature, and respiratory status.

2. Note trends and wide fluctuations in BP and auscultate BPs in

both arms and compare.

808
3. Initiate and maintain a continuous temperature-monitoring
device.

Decreased CO
related to cardiac injury or ineffective cardiac compensatory response to
oxygenation or perfusion deficits.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
exhibits adequate CO, as evidenced by BP within normal limits for
the patient; HR 60 to 100 bpm; normal sinus rhythm on ECG;
peripheral pulses at least 2+ on a 0-to-4+ scale; warm and dry skin;
hourly urine output at least 0.5 mL/kg; measured CO 4 to 7 L/min;
CVP 2 to 6 mm Hg; PAP 20 to 30/8 to 15 mm Hg; PAWP 6 to 12 mm
Hg; and patient awake, alert, oriented, and free from angina pain.
Blood Loss Severity, Cardiac Pump Effectiveness.

Hemorrhage control

1. Apply manual pressure and/or pressure dressing as indicated.

2. Identify the cause of the bleeding.

3. Monitor the amount and nature of the blood loss.

4. Monitor Hgb and Hct levels.

5. Monitor clotting status via PT/PTT and INR values.

Shock management

1. Monitor vital signs, mental status, and urinary output.

2. Use arterial line monitoring to improve accuracy of BP readings,

as appropriate.

3. Monitor ABG results and tissue oxygenation.

4. Monitor trends in hemodynamic measurements (e.g., CVP, MAP,

pulmonary capillary/artery wedge pressure).

5. Monitor determinants of tissue oxygen delivery (e.g., PaO2, SaO2,

809
Hgb levels, CO), if available.

6. Insert and maintain large-bore IV access.

7. Administer crystalloids, as appropriate.

8. Administer blood and blood products, as appropriate.

9. Monitor fluid status, including daily weights and hourly urine

output.

10. Administer inotropes, as appropriate.

11. Administer DVT and stress ulcer prophylaxis, as appropriate.

Additional nursing diagnoses

For other nursing diagnoses and interventions, see sections on
Major Trauma (Chapter 3), Acute Cardiac Tamponade (Chapter 1),
Pain (Chapter 3), and Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2).

Traumatic brain injury

Pathophysiology
Traumatic brain injury (TBI), also known as acquired brain injury,
occurs as a result of either blunt or penetrating forces to the head.
Approximately 1.5 million TBIs occur each year with 52,000
resulting in death. Males are twice as likely to suffer a TBI as are
females. Peak ages in the very young (until 1 year of age), young
adults (15 to 24 years), and older adults (older than 65 years). Blunt
injuries to the head are caused by acceleration, deceleration, and
rotational forces (e.g., vehicular collisions, falls, high-impact sports).
Penetrating injuries occur from piercing forces that traverse the
skull and damage underlying brain tissue and support structures.
The initial impact (force) results in widespread injury resulting
from tissue stresses and strain, which activate biomolecular
processes within the cells. Injury results from structural and

810
neuronal damage, vascular insufficiency, and inflammation. The
cerebral vasculature and skull are often damaged. Tissue stresses
result in contusions, diffuse axonal injuries, and compression
injuries. Biomolecular processes cause neuroexcitation and
deafferentation of the neurons. The neuroexcitatory injury activates
excitatory neurotransmitters (glutamate and aspartate), which
depolarize neurons. This neurotransmitter surge causes aberrant
cell signaling, leading to long-lasting or permanent neuronal
dysfunction. Deafferentation destroys the neurofilament of the
axon, and the axon swells and retracts. Reduced blood flow,
through cerebral edema or vasoconstrictive mechanisms, causes
ischemia and augments cell death.
Outcome after TBI can be predicted to some extent based on the
type of lesion, severity of injury, and length of coma. Age, preinjury
medical status, mechanism of injury, ICP, and brainstem integrity
are important factors influencing outcome.

Changes in intracranial pressure dynamics

Intracranial pressure dynamics is based on the volume-pressure
relationship within the cranium (Monro-Kellie hypothesis). Three
volumes exist within the fixed, rigid cranial vault: the brain, the
blood, and the cerebrospinal fluid (CSF). Under normal conditions
these volumes exert a pressure that is less than 15 mm Hg. The
brain requires a constant blood supply to maintain normal function
and when volume increases, pressure increases and compensatory
mechanisms (shunting of CSF into the intrathecal space or
vasoconstriction to reduce blood volume) are activated to reduce
the volume. In brain injury, when the intrinsic compensatory
mechanisms are damaged or overwhelmed, the functions that serve
to maintain cerebral perfusion are compromised. Extrinsic
measures are necessary to maintain the normal pressure-volume
relationship and preserve cerebral perfusion pressure (CPP). Box 7-
1 lists indicators of increased ICP (IICP). Treatment of
derangements in ICP dynamics is based on the relationship
between ICP and CPP and is stated simply: CPP = MAP − ICP.

Box 3-1

811
INITIAL HISTORY TAKING OF PATIENTS
IN MOTOR VEHICLE COLLISIONS
(BYSTANDERS, PASSENGERS, AND
RESCUE PERSONNEL)
• Extent of damage to the vehicle

• Approximate speed

• Did the airbag deploy?

• Were they wearing a seat belt?

• Were they ejected?

• Was prolonged extrication required?

• Was there a “T-bone” type of occurrence (intrusion into the

passenger/or driver side)?

• Alcohol or drugs?

• Possible psychiatric problems/suicide attempts?

All patients in motor vehicle collisions are suspected as having

dual diagnosis of head and spine until cleared.

MAP is calculated using the following equation:

The goal of treatment is to maintain CPP greater than 50 to 70

mm Hg and reduce ICP to less than 20 mm Hg.

Primary brain injuries

When the skull and brain are subjected to mechanical forces, a host

812
of injuries in the cerebral cortex, brainstem, or cerebellum may
change CPP. Severity of brain injuries is classified using the GCS:
mild (GCS score = 13 to 15), moderate (GCS score = 9 to 12), and
severe (GCS score ≤8). The FOUR score (Full Outline of
UnResponsiveness) has been used with increasing frequency as a
predictor of outcomes in patients with TBI. Verbal assessment is not
possible with intubated patients using the GCS, which also lacks
testing of brainstem reflexes. The FOUR score features four
elements: eye, motor, brainstem, and respiration with a maximum
score of 4 points for each element. The FOUR score provides
additional details lacking in the GCS, can recognize locked-in
syndrome, assesses brainstem reflexes, breathing patterns, and can
recognize the different stages of herniation. Specific injuries arising
from the mechanical forces are as follows:

• Contusion: Bruising that occurs as a result of mechanical forces to

the head typically from the brain striking the skull or the dural
folds. Cerebral contusions are seen as scattered areas of bleeding
on the surface of the brain or the undersurface of the frontal and
temporal poles. Coup (brain injury is directly beneath the site of
impact) or contrecoup (brain injury is opposite the site of impact)
injuries, herniation contusions (parahippocampal structures and
cerebellar tonsils forced against the tentorium), and gliding
contusions (from rotational forces in the parasagittal areas) can
result in focal hemorrhage of the cortex and adjacent white
matter. Surface (scalp) contusions are focal bruises, lacerations,
and capillary hemorrhages found with contact forces. Surface or
brain contusions may or may not be associated with fractures.

• Diffuse axonal injuries: Mild to severe injuries that occur when

diffuse areas of white matter have been torn or sheared or when
axons have been stretched. Injury evolves and generally worsens
over time. The initial CT scan may not demonstrate a pathologic
condition and does not reflect the severity that will manifest over
time.

• Concussion: Neuroexcitatory injury sometimes associated with

diffuse, axonal brain injuries. Classified as mild (no loss of
consciousness, possible brief episodes of confusion or

813
 disorientation); moderate (brief loss of consciousness, transient
focal neurologic deficits); or severe (prolonged loss of
consciousness with sustained neurologic deficits lasting less than
24 hours). No changes are seen on CT scan, but patients with
neurologic deficits require observation.

• Extra axial: Injuries are located outside the brain and are
attributable to forces that disrupt the superficial layers of the
brain resulting in bleeding (see Hematomas discussed later).

Secondary brain injuries

Secondary injuries such as inflammation, edema, and changes in
blood flow occur after the primary processes and further contribute
to brain damage. They may be intrinsic or extrinsic. Secondary
injury, despite the underlying cause, compromises the supply-
demand ratio for cerebral oxygenation. Failure to manage
secondary injury can result in irreversible neuronal damage
superimposed on the already compromised injured brain.

• Intrinsic: Injuries that result from primary brain injury including

intracranial hypertension, hypotension, hypovolemia, impaired
autoregulation (causes reduced cerebral blood flow), reperfusion
injury, brain edema, hemorrhage, herniation, cerebral vasospasm,
hypoxia, inflammation, seizures, shivering, agitation, electrolyte
imbalances, and hyperthermia.

• Extrinsic: Injuries unrelated to primary brain injury resulting

from inadequate resuscitation, poor oxygenation, extreme
hyperventilation, substance abuse, or hospital-acquired factors
such as infections (meningitis), pneumonia, atelectasis,
pulmonary edema, respiratory insufficiency, ventilatory-
associated lung injury, or anesthetic agents used for surgical
repair of injuries (see Meningitis, Chapter 7).

Associated skull fractures

Skull fractures occur as a result of blunt or penetrating impact force.
Primary and secondary brain injuries are usually present.

814
• Linear skull fractures: Nondisplaced, associated with low-velocity
impact.

• Basilar skull fractures: Linear fracture, involving the base of the

anterior, middle, and posterior fossae of the cranium.

• Depressed skull fractures: Depression of the skull over the point

of impact; may be comminuted (usually closed without direct
brain penetration), compressed, or compound (open).

Vascular injuries
Vascular injuries are intrinsic brain injuries resulting from impact
force that causes bleeding of cerebral arteries or veins. These
injuries usually accompany moderate and severe primary injuries.

• Epidural hematomas: Commonly occur after a temporal

linear skull fracture that lacerates the middle meningeal artery
below it or from fractures of the sagittal and transverse sinuses.
The hematoma develops rapidly in the space between the skull
and dura and represents a life-threatening emergency.

• Subdural hematomas: Bleeding from veins between the dura and

the arachnoid spaces; may be acute, subacute, or chronic. With
the increased use of therapeutic anticoagulation for cardiac,
stroke, and vascular problems, an increase in spontaneous and
injury (falls) related subdural hematomas are being seen in
the older population and alcoholics.

• Subarachnoid hemorrhage: Bleeding in the subarachnoid space

seen over convexities of the brain or in the basal cisterns.

• Intracranial hematomas: Blood collection from injury to the small

arteries and veins within the subcortical white matter of the
temporal and frontal lobes; usually associated with petechiae,
contusions, and edema.

Neurologic complications

Herniation syndromes

815
Displacement of a portion of the brain through openings within the
intracranial cavity that result from increased ICP. Herniation occurs
when there is a pressure difference between the supratentorial
and infratentorial compartments within the skull. When herniation
occurs, significant portions of the cerebral vasculature are
compressed, destroyed, or lacerated, resulting in ischemia, necrosis,
and ultimately death.

• Cingulate herniation: Occurs with IICP or swelling in one brain

hemisphere (left shift or right shift on CT). The affected high-
pressure side shifts toward the low-pressure side causing
compression of the anterior cerebral artery and internal cerebral
vein. Reduced blood flow results in development of cerebral
ischemia, edema, and IICP. Neurologic deficits include decreased
LOC, with unilateral or bilateral lower extremity weakness or
paralysis.

• Uncal herniation: Life-threatening, emergent situation that occurs

when an expanding lesion (blood, edema, tumor) of the middle
or temporal fossa forces the tip (uncus) of the temporal lobe
toward the midline. The uncus protrudes over the edge of the
tentorium cerebelli and compresses the oculomotor (third cranial)
nerve and posterior cerebral artery. The uncus may be lacerated
in the process and the midbrain is compressed against the
tentorial edge. The patient manifests with an irregularly shaped
pupil that may become fixed and dilated on the side of
herniation, a change in respiratory pattern, marked deterioration
in LOC, further elevation in ICP or decrease in ICP as the
herniation progresses.

• Central (transtentorial) herniation: Life-threatening, emergent

situation that occurs with expanding lesions of the frontal,
parietal, or occipital lobes or with severe, generalized cerebral
edema. Often, cingulate and uncal herniation precede this life-
threatening process. Table 3-13 describes the clinical features of
uncal and central herniation syndromes. Subcortical structures,
including the basal ganglia and diencephalon (thalamus and
hypothalamus), herniate through the tentorium cerebelli, causing
compression of the midbrain and posterior cerebral arteries

816
 bilaterally. Symptoms of increased ICP often occur too rapidly to
be observed. Changes in respiratory patterns may not be seen in
patients who are critically ill and mechanically ventilated,
depending on mode of ventilation (e.g., controlled or intermittent
mandatory ventilation).

• Transcranial (extracranial) herniation: Occurs when intracranial

contents under pressure are forced through an open wound,
surgical site, or cranial vault fracture. Although the resultant loss
of brain volume lowers ICP and may prevent intracranial
herniation, this is an ominous sign and the patient is at risk for
infection, further brain injury, and death.

Assessment: Traumatic brain injury

Neuroimaging is performed on all patients indicative of brain
injury (see list as follows). CT scans demonstrate fractures,
hematomas, and cerebral edema. Baseline physical examination
data should include assessment of:

• Mental status

• Cranial nerves

• Motor status

• Sensory status

• Reflexes

Thereafter, ongoing neurologic assessment should be based on

the clinical status of the patient. Ideally, a complete neurologic
assessment should be performed. However, many components of
the examination require patients to follow commands. For patients
unable to follow commands, the neurologic assessment should be
tailored individually to the patient’s abilities and redesigned as
necessary. The Glasgow Coma Scale (see Appendix 2) is applicable
for use in the acute phase, and the Rancho Los Amigos Cognitive
Functioning Scale (see Cognitive Rehabilitation Goals, Table 1-6)
can be used for recovery/rehabilitation assessment and should be

817
part of the neurologic assessment.
The following are assessment findings related to specific types of
brain injuries.

Epidural hematoma/linear skull fracture

• Scalp lacerations, swelling, tenderness, and ecchymosis of the
head and scalp are associated injuries.

• Classic epidural signs are loss of consciousness, followed by a

lucid interval and then rapid deterioration.

• Ipsilateral pupil dilation and contralateral weakness, followed by

brainstem compression, occur if treatment is not initiated
emergently.

Basilar skull fracture

• Dural tears resulting in rhinorrhea and otorrhea are common.

• Anterior fossa injuries are associated with periorbital ecchymosis

(raccoon eyes), epistaxis, damage to cranial nerves I and II, and
meningitis.

• Middle and posterior fossa injuries may damage cranial nerves

VII and VIII and are associated with tinnitus, hemotympanum,
and destruction of the cochlear vestibular apparatus.

• Ecchymosis of the mastoid process (Battle sign) is common.

Compound depressed skull fracture

• Changes in LOC, pupillary changes

• Headache

• Increased ICP (if measured invasively)

• CSF leaks if the dura has been torn, tympanum rupture

818
• Comminuted fractures are open wounds with or without dural
tears, CSF leak, and transcalvarial herniation.

Concussion
• Headache, although there are no overt signs of injury

• Dizziness

• Vomiting

• Memory loss

• Decreased attention and concentration skills

HIGH ALERT!
Moderate and severe injuries require close observation because
cerebral edema and increased intracranial pressure can develop.
Changes in behavior, level of consciousness, or refractory
intracranial pressure require an immediate computed tomography
scan.

Contusion
• Loss of consciousness is common. May have surface bruising of
face or scalp along with hematoma.

• Neurologic deficits may be generalized or focal, depending on the

site and severity of injury.

Diffuse axonal injury

• May occur with other injuries and is characterized by an
immediate loss of consciousness. Duration of coma varies,
depending on the severity of the injury, but often coma is

819
 prolonged and recovery of function is minimal to moderate.

• Edema and unstable ICP dynamics are common.

Subdural hematoma
• With acute subdural hematoma, neurologic deterioration is seen
within 24 to 72 hours (or earlier), changing LOC, ipsilateral
dilated pupil, and contralateral extremity weakness.

• Subacute hematoma may present within 48 hours to days after

injury and manifests initially as a headache as LOC begins to
deteriorate and focal neurologic deficits ensue.

• Chronic subdural are associated with progression of elusive,

fluctuating deficits, such as personality changes, memory loss,
headache, extremity weakness, and incontinence, especially in
high-risk groups such as older adults and chronic alcohol users.
The insidious nature of the bleed and hematoma formation
delays critical signs and symptoms weeks to months after the
injury occurs.

HIGH ALERT!
Neurologic signs associated with a chronic subdural hematoma
may occur weeks or months after injury.

Subarachnoid hemorrhage
• Severe headache often reported as “the worst headache of my
life.”

• Changes in LOC.

• Meningeal signs: nuchal rigidity, elevated temperature, and

positive Kernig sign and Brudzinski sign (loss of ability to extend

820
 leg when thigh is flexed on abdomen).

• Noncommunicating hydrocephalus is a delayed complication that

requires placement of an external ventricular shunt to drain CSF.

Intracranial hematoma
• Neurologic deficits are based on the site and severity of injury.

Diagnostic Tests for Traumatic Brain Injury

Test Purpose Abnormal Findings

Skull radiograph Detect structural deficits. Skull fractures, facial bone
destruction, air-fluid level in
sinuses, unusual intracranial
calcification, pineal gland
location (normally midline), and
radiopaque foreign bodies.
Cervical spine Evaluate for structural deficits of Cervical spine injuries, including
radiograph the spine. fractures, dislocations, and
Cervical spine immobilization is subluxations.
mandated in all patients with
trauma until the cervical spine
(C1-T1) is visualized completely
and fractures are ruled out.
Computed Fast diagnostic tool to evaluate for Gray and white matter, blood,
tomography (CT) primary and secondary brain and cerebrospinal fluid (CSF) are
without contrast injuries and structural changes identified by their different
Spiral CT can be used secondary to injury. radiologic densities. CT is used
for angiographic to diagnose cerebral hemorrhage,
imaging infarction, hydrocephalus,
cerebral edema, and structural
changes.
Magnetic resonance Identify type, location, and extent Spatial resolution can follow
imaging (MRI) of injury. metabolic processes and detect
tissue and structural changes.
Cerebral angiography Examine the cerebral vasculature. Abnormalities in cerebral
circulation, filling defects,
diminished blood flow.
Electroencephalography Measure spontaneous brain Abnormal brain activity
(EEG) electrical activity via surface (irritability) associated with
electrodes. seizures and generalized brain
Drug therapy, especially with activity related to drug overdose,
narcotics, sedatives, and coma, or suspected brain death.
anticonvulsants, alters brain
activity. Use of these drugs
should be documented if the
drug cannot be withheld 24 to 48
hours before performing EEG.
Evoked responses Evaluates the electrical potentials Abnormal or delayed expected
(responses) of the brain to an response levels indicating lesions

821
 external stimulus (i.e., auditory, of the cortex or ascending
visual, somatosensory). Evoked pathways of the spinal cord,
potentials are used to determine brainstem, or thalamus
the extent of injury in patients who
are uncooperative, confused, or
comatose.
CSF analysis Evaluate for infection and bleeding Abnormal color,
turbidity/cloudiness, red blood
cell (RBC) and white blood cell
(WBC) counts, protein, glucose,
electrolytes, gram stain, culture,
and sensitivity.

Laboratory work Evaluate for metabolic imbalances, Can indicate infection, anemia,
WBCs infection, coagulation status, nutritional deficiencies,
Hemoglobin bleeding, and drug use. electrolyte imbalances, and drug
Hematocrit use. All need to be monitored
Partial thromboplastin closely during emergency and
time, prothrombin acute phases.
time/international
normalized ratio
Electrolyte panel
Glucose
Osmolality
Alcohol and urine drug
screen (admission)

Collaborative management
Care priorities

1. Surgical intervention

• Performed to evacuate mass lesions (epidural, subdural, and

intracranial hematomas), place an ICP monitoring system (often
placed in the emergency department or at the bedside), elevate
depressed skull fractures, debride open wounds and brain tissue,
and repair dural tears or scalp lacerations. Decompressive
craniectomies and frontal and/or temporal lobectomies may be
necessary to control severe increases in ICP.

2. Preoperative and postoperative management of

coagulopathies

• Home medication history is imperative along with preoperative

PT/INR and PTT evaluation in all patients with TBI.

822
• Subdural hematomas or intracerebral hemorrhage are more
common in patients on clopidogrel (Plavix), aspirin, warfarin, or
other anticoagulants.

Stop all anticoagulation medication including heparin.

If the patient is to have an emergent craniotomy for evacuation of
a subdural hematoma or other injury, prothrombin
time/international normalized ratio, partial thromboplastin time,
and platelets must be normalized.

• For patients on warfarin with INR greater than 1.2, infuse fresh-
frozen plasma, or factor VII, and administer vitamin K until INR
is in nontherapeutic range (less than 1.2). Monitor PT/INR daily
and continue infusion of fresh-frozen plasma and administration
of vitamin K based on results.

• For patients on Plavix (clopidogrel) or other antiplatelet

medications, infuse platelets to achieve homeostasis. Platelet
counts will appear normal, but their coagulation function has
been altered by the clopidogrel or aspirin. Daily regimen of
platelet replacement should continue for up to 5 postoperative
days.

HIGH ALERT!
There are no evidence-based studies for reversing
coagulopathies because patients’ response to medication is very
individual. These strategies are aimed at monitoring the
coagulopathy while they wax and wane over the postoperative
course.

823
3. Management of ICP dynamics

• ICP monitoring is performed by a variety of techniques (Table 3-

14). All monitoring systems provide a digital display of ICP, but
CPP must be calculated (see Chapter 3).

Table 3-14
TYPES OF INTRACRANIAL MONITORING

CSF, Cerebrospinal fluid.

• The goal is to maintain CPP greater than 50 to 70 mm Hg.

Intraventricular catheters and parenchymal catheters are
recommended for monitoring ICP over subarachnoid and
epidural monitoring systems.

3-1
RESEARCH BRIEF
Intracranial pressure (ICP) monitoring is indicated for patients
with a Glasgow Coma Scale (GCS) score ≤8 after resuscitation and
an abnormal admission computed tomography (CT) scan.
Placement of an ICP monitor is also suggested in patients who
have a GCS ≤8 with a normal CT scan and if two or more of the

824
following are noted on admission: (1) the patient is older than 40
years, (2) the patient has unilateral or bilateral abnormal posturing,
or (3) the patient’s systolic blood pressure is less than 90 mm Hg.
Physician discretion may also determine the use of ICP monitoring.
Adapted from Brain Trauma Foundation: Guidelines for the management of severe head
injury. J Neurotrauma 24(Suppl 1):S1-S106, 2007.

4. Reduction of ICP by CSF drainage

• Performed using intraventricular or ventriculostomy systems.

• To prevent overdraining, the drainage collection bags must be

maintained at the level of the tragus of the ear or higher, thereby
preventing excessive CSF flow caused by a higher-to-lower
pressure gradient.

5. Hyperventilation via mechanical ventilation

Hyperventilation is no longer recommended as a first-

line treatment and should be used only with cerebral oxygen
monitoring to reduce intracranial pressure. Hyperventilation
should be avoided during the first 24 hours after injury.

• Prophylactic hyperventilation (Paco2 greater than 25 Hg) is

recommended for short periods until more definitive therapies
are initiated or increased ICP is reduced to avoid herniation.
Maintaining Paco2 within a normal range is now considered
optimal ventilation. Recent evidence suggests that
hyperventilation may cause neurologic dysfunction as a result of
decreased cerebral perfusion.

6. Monitoring jugular venous oxygen saturation (SjO2)

825
• Used to measure cerebral oxygenation by determining oxygen
content of cerebral venous blood as a global measurement of
oxygen supply and demand. Three types of blood flow can be
discriminated:

• Normal (SjO2 = 55% to 70%).

• Oligemic (SjO2 less than 55%).

• Hyperemia (SjO2 greater than 70%).

• Treatment should be aimed at maintaining normal

range.

7. Monitoring brain tissue oxygenation (PbTO2)

• Used to monitor the partial pressure of regional brain tissue

oxygenation at catheter tip to detect cerebral ischemia and
hypoxia. Cerebral hypoxia, a secondary brain injury event, has
been associated with poor patient outcomes.

• PbTO2 levels greater than 20 are recommended.

HIGH ALERT!
Optimal management of a severe traumatic brain injury should
include monitoring of cerebral perfusion pressure (CPP),
intracranial pressure (ICP), and PbTO2, as well as ventilation
management. ICP threshold should be less than 20 mm Hg,
optimal CPP is 50 to 70 mm Hg, and optimal PbTO2 is greater than
20 mm Hg. While ICP rises and PbTO2 falls, it may be necessary to
adjust the Fio2 to keep PbTO2 greater than 20. It is not uncommon
for Fio2 to be 0.1 or 100% to maintain adequate cerebral

826
oxygenation. PaO2 less than 60 mm Hg should be avoided.

• Other ways to improve PbTO2 include raising BP, treating

anemia, and adjusting pCO2.

8. Hyperosmolar therapy

• Reduces cerebral brain volume by removing fluid from the

extracellular compartment of the brain.

• Mannitol, an osmotic diuretic, and hypertonic saline are generally

used. Mannitol may be given in 0.25 to 1.0 g/kg body weight
doses as needed to reduce ICP or may be given as a scheduled
dose every 4 to 6 hours. Although there is no level 1 evidence
supporting the use of hypertonic saline, patients with TBI who
received hypertonic saline in a small study of patients with
polytrauma had improved survival and restoration of
hemodynamic stability. It may be useful as an adjunct therapy in
refractory IICP.

• Dehydration is a major complication with the continued use of

hyperosmolar therapies. Serum electrolyte and osmolality values
should be closely monitored.

• Fluid balance is maintained with fluid therapy (75 to 100 mL/h).

Replacement of urine losses may be prescribed based on the
volume of urine collected 1 hour after giving hyperosmolar
agents. Given either milliliter for milliliter or 0.5 mL for milliliter
over a 3- to 4-hour period.

9. Mintenance of blood pressure to maintain CPP

• Hypotension and hypertension both contribute to cerebral edema,

which compresses blood vessels. Hypotension can result in
decreased oxygen delivery to brain cells. Elevated Paco2 reduces
pH causing cerebral vessels to vasodilate. Hypotension reduces

827
 MAP and thus CPP. Glucose solutions are not used for fluid
resuscitation in TBI.

• Vasoconstrictive medications (phenylephrine, norepinephrine) or

inotropic medications (dobutamine) may be used. The aim is to
avoid systolic BP less than 90 mm Hg.

• Effects of hypertension (elevated CPP and increased cerebral

edema) are unclear, but increased capillary permeability and
petechial hemorrhage are seen. Antihypertensive medications,
such as labetalol HCl (Normodyne) or nitroprusside sodium
(Nipride), may be required.

10. Reduction of metabolic demand

• Important strategy when treating ICP problems, because cerebral

blood supply must match demand to maintain cerebral function.

• Sedating agents: Use of individual or combined continuous

infusions of sedatives, analgesics, and paralytic drugs to reduce
metabolic demand. Midazolam HCl (Versed), opiate analgesics
such as fentanyl citrate (Sublimaze), sufentanil, or morphine
sulfate, and anesthetic agents such as propofol (Diprivan) are
used. Propofol may be preferred for its short half-life. Watch for
“propofol infusion syndrome” (metabolic acidosis,
rhabdomyolysis, hyperkalemia, and renal failure).
Recommendations of doses are given in Table 3-15.
Nondepolarizing neuromuscular blocking agents, including
vecuronium bromide (Norcuron) or atracurium, are used but
must be used with sedation and can mask seizure activity. (See
also Sedation and Neuromuscular Blockade, Chapter 1.)

• Seizure control: Seizure activity increases the metabolic demand

of the brain. Anticonvulsants are recommended to prevent early
posttraumatic seizures (7-day course) despite the fact that early
posttraumatic seizure is not associated with worse outcomes.
Posttraumatic seizure may occur with all TBIs but there is a
higher incidence in patients with focal brain injuries such as
depressed, comminuted, or compound skull fractures,

828
 contusions, lacerations, and penetrating injuries.

• Seizure prophylaxis with anticonvulsant agents such as

phenytoin sodium (Dilantin) or, less often, levetiracetam
(Keppra) or valproic acid is often prescribed. When using
phenytoin, a weight-based loading dose of 15 to 20 mg/kg is
given slowly at 50 mg/min, followed by a daily dose of 100 mg
three times daily. Phenytoin cannot be administered with a
dextrose solution because it will precipitate. Therapeutic levels
are reported to be between 10 and 20 mg/mL. Doses should be
scheduled to maintain free Dilantin levels between 1 and 2
mg/mL. Doses should be patient-specific (higher levels may be
necessary to prevent breakthrough seizures, whereas lower levels
may be acceptable if seizures are controlled).

Table 3-15
ANALGESICS AND SEDATIVES RECOMMENDATIONS FOR USE IN
TRAUMATIC BRAIN INJURY

Agent Dose Comments

Morphine 4 mg/h continuous infusion Titrate PRN
sulfate Reverse with Narcan
Midazolam 2 mg test dose; then 2 to 4 mg/h continuous Reverse with flumazenil
infusion
Fentanyl 2 µg/kg test dose; then 2 to 5 µg/kg/h continuous
infusion
Sufentanil 10 to 30 µg test dose; then 0.05 to 2 µg/kg
continuous bolus
Propofol 0.5 mg/kg test bolus; then 20 to 75 µg/kg/min Do not exceed 5 mg/kg/h
continuous infusion Monitor closely, especially
young adults
From Brain Trauma Foundation: Guidelines for the management of severe brain
trauma. J Neurotrauma 24(Suppl 1):S1-S73, 2007.

In a patient with normal albumin levels, the free level

correlates closely with the therapeutic level, but in patients who
are hypoalbuminemic, such as patients with acute traumatic brain
injury, the free level can be significantly higher and more
accurately represents the patient’s “true” phenytoin (Dilantin)
level.

829
• Barbiturate coma: A less-often used method of reducing
metabolic demand, barbiturate administration, is recommended
to control ICP refractory to standard medical and surgical
treatment.

• High doses of barbiturates should not be used

without continuous ICP and hemodynamic
monitoring and controlled mechanical ventilation.
Barbiturates may induce profound cardiac and
cerebral depression. Pentobarbital sodium
(Nembutal) is the drug of choice.

• A loading dose between 5 and 10 mg/kg is given

(discontinue if MAP falls to less than 70 mm Hg),
followed by a maintenance dose of 1 to 3 mg/kg/h.

• Clinically significant hypotension is usually seen

with barbiturate coma. It is not responsive to fluid
resuscitation and requires the use of vasopressors
such as dopamine or phenylephrine.

• Barbiturates are withdrawn gradually while the

patient improves. Patients with barbiturate coma
require intensive physical care and physiologic
monitoring.

• Assessment of brain death criteria, if appropriate,

cannot be initiated until barbiturate levels return to
zero.

• Maintaining body temperature: For every 1° C in temperature

elevation, there is a 10% to 13% increase in metabolic rate. Body
temperature should be normal to control metabolic demand.

830
HIGH ALERT!
Normal temperatures range from 35.8° C to 37.5° C (96.4° F to
99.5° F) with a diurnal variation of 1° C. Rectal temperatures are
0.2° C to 0.6° C higher than oral and can be 0.8° C higher than right
atrial, esophageal, and oral temperatures. Evaluation of the
etiology of fever is important with brain injury, because it
influences treatment choice.

• Fever may be caused by brain injury (central fever), an infectious

process (peripheral fever), or drugs (drug fever). Central fever
reflects disturbance in the hypothalamic thermoregulatory
mechanism. It is characterized by lack of sweating, no diurnal
variation, plateau-like elevation patterns, elevations up to 41° C
(105.8° F), absence of tachycardia, persistence for days or weeks,
and temperature reduction with external cooling rather than with
antipyretic agents.

• Peripheral fever is associated with wound infections, meningitis,

sepsis, pneumonia, and other bacterial invasion. Sweating,
diurnal variation, response to antipyretic agents, and tachycardia
are present.

• Drug fever occurs in response to certain medications including

antibiotics.

External cooling with a hypothermia blanket may cause

shivering, the body’s mechanism to increase heat production.

HIGH ALERT!
Shivering increases metabolic demand and may increase
intracranial pressure. Shivering may be controlled by wrapping
distal extremities in bath towels before initiating hypothermia or
using chlorpromazine (Thorazine), which, must be used with
caution because it may cause hypotension. Research on use of

831
hypothermia in treatment of acute brain injury is evolving. If used,
follow a strict hypothermia protocol. Currently, there is no support
for prophylactic hypothermia.

11. Modifying nursing care activities that raise ICP

• Transient brief and rapid elevations in ICP, which cannot always

be avoided, are commonly seen during position changes or other
nursing care activities. Generally, ICP returns to resting baseline
within a few minutes.

HIGH ALERT!
All nursing care activities that increase intracranial pressure
(ICP) should be spaced to enable a return of ICP to baseline and
maximizing of cerebral perfusion pressure. Clustering nursing care
such as bathing, turning, and suctioning creates a stair-step rise in
ICP. Sustained increases (longer than 5 minutes) should be
avoided.

• Suctioning: Causes a significant rise in ICP. To minimize adverse

effects associated with suctioning, implement the guidelines
outlined in Box 3-6.

• Neck positioning: Flexion, extension, and lateral movements of

the neck can significantly raise ICP. Maintaining the neck in a
neutral position at all times is important. In patients with poor
neck control, stabilize the neck with towel rolls or sandbags.

• Elevating head of bed: Although head of bed elevation at 30

degrees is believed to improve venous drainage and contribute to
ICP reduction, ICP may be improved at higher or lower
elevations. Adjust head of bed elevation to optimize the patient’s
CPP and PbTO2 and minimize ICP.

832
• Turning: Turning is necessary to prevent pressure ulcer formation
and is not contraindicated. Individual patient responses to
turning should be evaluated. Initially, turning from side to side
will elevate pressure, but ICP should return to resting baseline
after a few minutes. If ICP does not return to resting baseline
within 5 minutes, CPP may be compromised and the patient
should be returned to a position that reduces ICP and maximizes
CPP. Hip flexion also increases ICP. If independent nursing
activities do not decrease ICP, then medical protocols must be
used.

• Bathing: Although bathing itself has not been documented as

raising ICP, the rapid turning from side to side associated with
linen changes raises ICP. These “turn procedures” are actually
clustered activities because the length of the procedure does not
allow sufficient time for ICP to return to baseline. Evaluation of
the patient’s response may necessitate performing the linen
change in stages or allowing adequate time for ICP to return to
resting baseline.

• Sensory stimulation: A sensory stimulation program may be

implemented safely in patients who are comatose early after
injury when ICP is stable. This rehabilitative technique may be an
important adjunct to traditional care and improve admission to
an active rehabilitation program (Table 3-16).

Table 3-16
MANAGEMENT OF SEVERE BRAIN INJURY

Level of
Treatment Recommendation
Evidence*
Blood pressure Level II† Avoid early postinjury episodes of hypotension <90 mm Hg.
Oxygenation Level III Avoid Pao2<60 mm Hg and O2 saturation <90%.
ICP treatment Level II Treatment to lower ICP should be initiated at 20 mm Hg.
threshold
CPP treatment Level III CPP should be maintained at ≥50 mm Hg. Maintain MAP >90
mm Hg.
Cerebral Level III Keep PbTO2>20.
oxygenation
Hyperventilation Level II Avoid prophylactic hyperventilation; hyperventilate for short
duration for refractory increased ICP >25 mm Hg.
Level III Avoid hyperventilation in the first 24 hours postinjury.

833
 Hyperosmolar Level II Mannitol: use intermittent boluses of 0.25 to 1 mg/kg.
therapy
Option Hypertonic saline (3%). No recommended dose.
Barbiturates Level II May be considered in patients with hemodynamic stability
refractory to other methods to reduce ICP.
Propofol Level II Use for control of ICP.
Glucocorticoids Standard Use is not recommended.
Nutrition Level II Full caloric replacement by postinjury day 7
Seizure Level II Anticonvulsants can be considered an option for high-risk
prophylaxis patients early after injury.

Not recommended for preventing late posttraumatic seizures.

*
Level of evidence denotes the degree that the recommendation represents clinical
certainty.
†
Level II, Moderate clinical certainty; Level III/Option, unclear clinical certainty;
Standard, high level of certainty. Level of evidence is based on scientific literature
where the highest degree of certainty is drawn from prospective randomized clinical
trials.
Data from Brain Trauma Foundation: Guidelines for the management of severe head
injury. J Neurotrauma 24(Suppl 1):S1-S106, 2007.
CCP, Cerebral perfusion pressure; ICP, intracranial pressure; MAP, mean arterial
pressure.

Box 3-6
GUIDELINES FOR SUCTIONING
SECRETIONS FROM PATIENTS AT RISK
FOR INCREASED INTRACRANIAL
PRESSURE
• Suction only if the clinical status of the patient warrants.

• Precede suctioning with preoxygenation using 100% oxygen.

• Limit each suctioning pass to ≤10 seconds.

• Limit suction passes to two.

• Follow each pass with 60 seconds of hyperventilation using 100%

oxygen.

• Use negative suction pressure less than 120 mm Hg.

• Keep the patient’s head in a neutral position.

834
• Use a suction catheter with an outer-to-inner diameter ratio of 2:1.

12. Nutrition support: Feeding should be initiated as early

as possible to achieve full caloric replacement within 7 days
of injury

• Enteral nutrition helps to maintain the integrity of the gut mucosa

and should be initiated as early as possible after injury.

• When postpyloric (duodenum or jejunum) feeding tubes are

used, enteral feedings can be initiated before bowel sounds
return to normal.

• In some cases, gastric tubes for decompression are used

simultaneously with the postpyloric tubes. See Nutrition Support
(Chapter 1) for documentation of proper placement and checking
of residual volumes. If enteral feedings are contraindicated or not
tolerated by the patient, total parenteral nutrition must be started.

13. Prevention of aspiration

• Prevalent complication after brain injury.

• Aspiration may occur at the time of injury or as an iatrogenic

complication of intubation, enteral feedings, or prolonged use of
artificial airways.

• Tracheobronchial secretions should be checked for glucose (a sign

that tube feedings have been aspirated).

• Follow enteral feeding protocols initiated.

• Initial and ongoing swallowing assessments can be done at the

bedside or under fluoroscopy.

14. DVT prophylaxis

• Patients with TBI are at risk for developing DVT as well as PE as a

835
 result of prolonged bed rest. There is concern for the use of
anticoagulation therapies because there is risk for expansion of
intracranial hemorrhage. There is level III support for the
prophylactic use of low–molecular-weight heparin or
unfractionated heparin along with mechanical measures to
prevent DVT (sequential compression devices); however, there is
no evidence to support optimum doses or time when to begin
therapy. Clinical practice guidelines for TBI also support the use
of graduated compression stockings, unless the lower extremity
injuries prevent their use. However, there are no
recommendations for the therapeutic treatment of DVT or PE.
DVT management is determined by the attending physician
based on risk-benefit ratios.

15. Management of cardiac dysrhythmias

• Commonly seen in patients with brain injuries and probably

related to autonomic (sympathetic and parasympathetic)
derangement or compression of midbrain and brainstem
structures.

• ECG changes seen with elevated ICP are prominent U waves, ST

segment changes, notched T waves, and prolongation of the QT
interval.

• Bradycardia, supraventricular, tachycardia, and ventricular

dysrhythmias are common.

16. Glucose management

• Keep serum glucose ranges within normal limits. Avoid levels

greater than 170 mg/dL and less than 50 mg/dL to avoid
worsening the brain injury. Insulin therapy may be required to
control hyperglycemia.

17. Glucocorticoid

• Use of glucocorticoids (dexamethasone) is not indicated for brain

injury and may result in worse outcomes.

836
18. Rehabilitation

• Brain injury often results in physical (paralysis, spasticity, and

contractures) and cognitive impairments.

• Consult with physical, occupational, and speech therapists early

to minimize deficits and prepare the patient for an acute
rehabilitative program.

• National Institutes of Health (NIH) Consensus Development

Conference Recommendations on Rehabilitation of Persons with
Brain Injury are available. Support also is available through the
Brain Injury Association of America (www.biausa.org).

19. Neuroprotective strategies

• Ongoing brain injury research is targeting neuroprotective

strategies that include hypothermia, IV progesterone, and use of
magnesium, cyclosporine, erythropoietin, and hyperbaric
therapies.

Care plans: Traumatic brain injury

Impaired gas exchange 
related to decreased oxygen supply and increased CO2 production
secondary to decreased ventilatory drive occurring with pressure on
respiratory center, imposed inactivity, pneumonia, acute respiratory
distress syndrome, and possible neurologic pulmonary edema.
Goals/Outcomes: Keep Paco2 values in normal range greater than
35 mm Hg and PaO2 greater than 60 mm Hg. By the time of
discharge from ICU or transfer to rehabilitation unit, the patient has
adequate gas exchange, as evidenced by appropriate mental status
and orientation; PaO2≥60 mm Hg; RR 12 to 20 breaths/min with
normal depth and pattern; and absence of adventitious breath
sounds.
Respiratory Status: Gas Exchange.

Respiratory monitoring

837
1. Assess the patient’s RR, depth, and rhythm. Auscultate lung
fields for breath sounds every 1 to 2 hours and as needed. Monitor
for respiratory patterns described in Table 3-13. Be alert to IICP (see
Box 7-1).

2. Assess the patient for signs of hypoxia, including confusion,

agitation, restlessness, and irritability. Remember that cyanosis is a
late indicator of hypoxia.

3. Ensure a patent airway via proper positioning of neck and

frequent assessment of the need for suctioning. Ensure
hyperoxygenation of the patient before and after each suction
attempt to prevent dangerous, suction-induced hypoxia or PbTO2
less than 20. Do not overventilate. Keep Paco2 between 35 and 45
mm Hg.

4. Monitor ABG values; consult the physician for significant

findings or changes. Be alert to levels indicative of hypoxemia (PaO2
less than 80 mm Hg) and to Paco2 less than 35 mm Hg, considering
that levels higher than this range may increase cerebral blood flow
and thus increase ICP.

5. Ensure that oxygen is delivered within prescribed limits.

6. Assist with turning every 2 hours, within limits of the patient’s

injury, to promote lung drainage and expansion and alveolar
perfusion. Unless contraindicated, raise the head of the bed 30
degrees to enhance gas exchange.

7. Encourage deep breathing at frequent intervals to promote

oxygenation. Avoid coughing exercises for patients at risk for IICP.

8. Evaluate the need for an artificial airway in patients unable to

maintain airway patency or adequate ventilatory effort.

Table 3-13
ASSESSMENT OF CENTRAL AND UNCAL HERNIATIONS

838
Modified from Plum F, Posner J: Diagnostic of stupor and coma, ed 3, Philadelphia,
1980, Davis.

Airway Management; Oxygen Therapy; Respiratory

Monitoring.

Risk for infection: CNS 

related to inadequate primary defenses secondary to direct access to the
brain in the presence of skull fracture, penetrating wounds, craniotomy,
intracranial monitoring, or bacterial invasion caused by pneumonia or
iatrogenic causes.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, WBC count ≤11,000/mm3, negative culture results,
HR ≤100 bpm, BP within the patient’s normal range, and absence of
agitation, purulent drainage, and other clinical indicators of
infection.
Risk Identification.

Infection protection

1. Assess vital signs at frequent intervals for indicators of CNS

839
infection. Be alert to elevated temperature and increased HR and
BP.

2. Monitor the patient for signs of systemic infection, including

discomfort, malaise, agitation, and restlessness.

3. Inspect cranial wounds for the presence of erythema, tenderness,

swelling, and purulent drainage. Obtain prescription for culture as
indicated.

4. Monitor CSF from intraventricular catheter for cloudy

appearance or blood. Analysis of CSF should be done on a routine
basis.

5. Other infection sites: Monitor for signs of UTI if the patient has
an indwelling Foley catheter. Monitor other injury and surgical
sites.

6. Apply a loose sterile dressing (sling) to collect CSF drainage from

nose. Do not pack the nose or ears if there is CSF drainage. Record
amount, color, and characteristics of drainage.

7. Caution the patient against coughing, sneezing, nose blowing, or

Valsalva or similar maneuvers, because these activities can further
damage the dura. Use orogastric tubes if BSFs or severe frontal
sinus fractures are present.

8. Ensure timely administration of prescribed antibiotics.

9. Apply basic principles for care of any invasive device used with
ICP monitoring:

• Use good handwashing technique before caring for

the patient.

• Discourage the patient from touching devices if

awake; apply restraints only if necessary to keep the
patient from harm. Restraints can increase ICP by

840
 causing straining and agitation.

• Maintain aseptic technique during care of device,

following agency protocol for infection control.

Decreased intracranial adaptive capacity 

related to decreased CPP or infections that can occur with secondary head
injury.
Goals/Outcomes: Within 12 to 24 hours of
treatment/interventions, the patient has adequate intracranial
adaptive capacity, as evidenced by equal and normoreactive pupils;
RR 12 to 20 breaths/min with normal depth and pattern (eupnea);
HR 60 to 100 bpm; ICP up to 15 mm Hg; CPP greater than 50 mm
Hg; and absence of headache, vomiting, and other clinical
indicators of IICP. Optimally, by the time of discharge from ICU or
transfer to rehabilitation unit, the patient is oriented to time, place,
and person and has bilaterally equal strength and tone in the
extremities.
Neurologic Status.

Neurologic monitoring

1. Assess neurologic status at least hourly (GCS and FOUR score are
commonly used). Monitor pupils, LOC, and motor activity; also
perform cranial nerve assessments (see Appendix 3). A decrease in
LOC is an early indicator of IICP. Changes in the size and reaction
of the pupils, a decrease in motor function (e.g., hemiplegia,
abnormal flexion posturing), and cranial nerve palsies.

2. Monitor vital signs at frequent intervals. Be alert to changes in

respiratory pattern, fluctuations in BP and pulse, widening pulse
pressure, and slow HR.

3. Monitor the patient for indicators of IICP (see Box 7-1).

4. Monitor hemodynamic status to evaluate CPP and ensure that it

841
is greater than 50 mm Hg. Be alert to decreases in mean systolic
arterial BP (less than 80 mm Hg) or increases in MAP. Perform
ongoing assessment of ICP, CPP, and PbTO2 recording levels
hourly until stable. Consult the physician if pressure changes
significantly (e.g., ICP greater than 20 mm Hg; PbTO2 less than 20
or other preestablished ranges for PbTO2). Perform ongoing
calibration and zeroing of transducer to ensure accuracy of
readings.

5. Maintain a patent airway and ensure precise delivery of oxygen

to promote optimal cerebral perfusion.

6. Facilitate cerebral venous drainage by maintaining the neck in a

neutral position avoiding hyperflexion.

7. To help prevent fluid volume excess, which could add to cerebral

edema, ensure precise delivery of IV fluids at consistent rates.

8. Ensure timely administration of medications that are prescribed

for the prevention of sudden increase or decrease in BP, HR, or RR.

9. Treat elevations in ICP immediately (Box 3-7).

Box 3-7
NURSING INTERVENTIONS FOR
PATIENTS WITH INCREASED
INTRACRANIAL PRESSURE
• Maintain head of bed elevation at level that keeps intracranial
pressure (ICP) less than 20 mm Hg and cerebral perfusion
pressure (CPP) greater than 50 mm Hg.

• Loosen constrictive objects around the neck to facilitate venous

blood flow from the head.

• With position changes, ensure ICP and CPP return to baseline or

stay within acceptable measurements within 5 minutes of turn.

842
• Maintain head in neutral position.

• Correct factors that may increase ICP such as hypoxia, pain,

anxiety, fear, and abdominal or bladder distention.

• Evaluate activities that increase ICP (e.g., suctioning, bathing,

dressing changes) and reorganize care to minimize elevations
and hip flexion.

Cerebral Edema Management; Cerebral Perfusion

Management; Intracranial Pressure Monitoring; Neurologic
Monitoring.

Ineffective thermoregulation 
related to trauma associated with injury to or pressure on the
hypothalamus.
Goals/Outcomes: The patient becomes normothermic within 24
hours of the diagnosis.
Thermoregulation.

Temperature regulation

1. Monitor for signs of hyperthermia: temperature greater than

38.3° C (101° F), pallor, absence of perspiration, torso that is warm
to the touch.

2. As prescribed, obtain blood, urine, and sputum specimens for

culture to rule out underlying infection.

3. Be alert to signs of meningitis: fever, chills, nuchal rigidity,

Kernig sign, Brudzinski sign (see Meningitis, Chapter 7).

4. Assess wounds for evidence of infection, including erythema,

tenderness, and purulent drainage.

5. If the patient has hyperthermia, remove excess clothing and

administer tepid baths, hypothermic blanket, or ice bags to axilla or
groin, but avoid inducing shivering.

843
6. As prescribed, administer antipyretics such as acetaminophen.

7. As prescribed, administer chlorpromazine to treat or prevent

shivering, which can cause further increases in ICP.

8. Keep environmental temperature at optimal range.

9. Assess for possible drug fever reaction, which can occur with
antimicrobial therapy.

Fever Treatment.

Risk for disuse syndrome 

related to immobilization and prolonged inactivity secondary to brain
injury, spasticity, or altered LOC.
Goals/Outcomes: The patient has baseline/optimal ROM without
verbal or nonverbal indicators of pain.
Mobility Level: Muscle Function.

Positioning

1. Begin performing passive ROM exercises every 4 hours on all

extremities as soon as the patient’s acute condition stabilizes.
Monitor ICP during exercise, being alert to dangerous elevations
outside of the established measurements. Consult with the physical
therapist accordingly.

2. Teach passive ROM exercises to significant others. Encourage

their participation in patient exercise as often as they are able.

3. Reposition the patient every 2 hours within restrictions of the

head and other injuries, using the logrolling technique as indicated.

4. Ensure proper anatomic position and alignment. Support

alignment with pillows, trochanter rolls, and wrapped sandbags.

5. For the patient with spasticity, use foot cradles to keep linens off
the feet. To maintain dorsiflexion, provide the patient with shoes
that are cut off at the toes, with the shoes ending just proximal to
the head of the patient’s metatarsal joints. Because there is no

844
contact of the balls of the feet with a hard surface, the risk of
spasticity will be minimized. Consult the occupational therapist for
use of splints or other supportive device.

6. For the patient without spasticity, use foot supports to prevent

plantar flexion and avoid external hip rotation.

7. To maintain anatomic position of the hands, provide the patient

with spasticity with a splint or a cone that is secured with an elastic
band. Either device will limit spasticity by pressing on the muscles,
whereas the elastic band will stimulate the extensor muscles,
thereby promoting finger extension.

Exercise Therapy: Joint Mobility.

Impaired tissue integrity: Corneal (or risk for same) 

related to irritation associated with corneal drying and reduced lacrimal
production secondary to altered consciousness or cranial nerve damage.
Goals/Outcomes: The patient’s corneas are moist and intact.
Tissue Integrity: Skin and Mucous Membranes.

Risk identification

1. Assess for indicators of corneal irritation: red and itching eyes,

ocular pain, sensation of a foreign object in the eye, scleral edema,
and blurred vision.

2. Avoid exposing the patient’s eyes to irritants such as baby

powder or talc.

3. Lubricate the patient’s eyes every 2 hours with isotonic eye drops
or ointment.

4. Facilitate an ophthalmology consultation as indicated.

Medication Administration: Eye.

Additional nursing diagnoses

Also see Decreased Adaptive Capacity: Intracranial in Cerebral

845
Aneurysm and Subarachnoid Hemorrhage (Chapter 7). As
appropriate, see nursing diagnoses and interventions under
Alterations in Consciousness (Chapter 1), Care of the Patient after
Intracranial Surgery (Chapter 7), and Meningitis (Chapter 7). See
Risk for Trauma in Status Epilepticus (Chapter 7). Also see nursing
diagnoses and interventions under Nutrition Support (Chapter 1),
Mechanical Ventilation (Chapter 1), Hemodynamic Monitoring
(Chapter 1), Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2).
The patient with craniocerebral trauma is at risk for diabetes
insipidus and syndrome of inappropriate antidiuretic hormone. See
Diabetes Insipidus (Chapter 8) and Syndrome of Inappropriate
Antidiuretic Hormone (Chapter 8).

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CHAPTER 4

Respiratory disorders
Respiratory assessment: General
Goal of system assessment
Evaluate for ineffective breathing patterns, impaired gas exchange,
and airway obstruction.

• Considerations for the bariatric patient: The majority of

bariatric patients admitted for diagnoses other than weight loss
surgery are women 20 to 30 years of age with respiratory
diagnoses.

Vital sign assessment

• Respiratory rate (RR) and depth to evaluate for tachypnea,
bradypnea, and work of breathing.

• Pulse oximetry to help identify low readings reflective of

impaired gas exchange.

• Heart rate (HR) to evaluate for tachycardia or bradycardia;

generally associated with RR changes.

• Considerations for the bariatric patient: Tachypnea is more

common with this population.

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Continuous pulse oximetry (SpO2
monitoring)
• Evaluate for changes over time and/or since the last recorded
reading. Results should be correlated with the arterial oxygen
saturation (SaO2) readings derived from arterial blood gases
(ABGs).

• Pulse oximetry accuracy is dependent on the presence of an

adequate pulse in the area in which the measurement probe has
been applied.

• Ensure readings are done using an appropriate probe placed on

the anatomic location with the best pulse and least interference.
Probes are available for the finger, forehead, and ear lobe.

• Readings must be correlated with physical assessment findings

and can remain normal despite signs of impending deterioration.
Physical assessment findings such as use of accessory muscles or
presence of tachypnea are indicative of respiratory distress but
may not be reflected in a change in SpO2. If an increasing amount
of oxygen (O2) is needed to maintain SpO2, this is also indicative
of impending deterioration of the patient.

Considerations for the bariatric patient: Patients who are

extremely obese are at higher risk of hypoxemia than people of
average size, which, combined with problems positioning patients
for intubation and difficult anatomy, makes securing an airway
challenging.

Observation
• Evaluate for use of accessory muscles, shortness of breath, and air
hunger.

• Ensure that the patient is evaluated for the presence of chronic

obstructive pulmonary disease (COPD) before applying O2

859
 therapy so that appropriate liter flow is determined to prevent
respiratory impairment.

• Evaluate facial and lip color for pallor or cyanosis indicative of

hypoxemia.

Considerations for the bariatric patient

• Persons of size have an increased probability of lung

derecruitment resulting from the increased weight of the chest
wall, protuberant abdomen encroaching on the diaphragm in the
recumbent position, and provider reticence to extubate an
extremely obese patient at high risk for having a difficult airway.

• Assess for obstructive sleep apnea (OSA), which is very

common in the bariatric population.

Auscultation
• Listen to breath sounds to evaluate for presence of adventitious
sounds that reflect factors contributing to respiratory distress,
including those related to both airway obstruction and impaired
gas exchange.

• Adventitious sounds: Crackles (rales) indicative of fluid in

alveoli, bubbles (rhonchi) indicative of secretions in bronchioles,
wheezing (inflammation), inspiratory stridor (narrowing of
airways as a result of massive inflammation or obstruction by
secretions or foreign body), or pleural friction rub
(inflammation).

• Lungs must be auscultated anteriorly and posteriorly in all three

lobes of the right lung, the two lobes of the left lung, over the
right and left main bronchi, and over the trachea.

• Considerations for the bariatric patient: Breath sounds may be

distant resulting from the layers of adipose tissue between the
skin and chest wall.

860
Screening labwork
• ABG analysis can reveal increases or decreases in pH; levels of O2,
O2 saturation, CO2, and bicarbonate; base excess or base deficit
indicative of impending respiratory failure;
hyperpnea/tachypnea; and metabolic derangements affecting
breathing patterns. Blood gas analysis may be done using either
arterial blood or mixed venous blood samples. Mixed venous
blood samples are available only using a pulmonary artery
catheter and can be used to calculate efficacy of both O2 delivery
and O2 consumption. ABGs cannot be used to calculate O2
consumption.

Considerations for the bariatric patient: Obesity creates

values similar to those seen in restrictive lung disease. Increased
pulmonary blood volume and increased chest wall mass from
adipose tissue restrict normal chest wall movements. Abnormal
diaphragm position, upper airway resistance, and increased daily
CO2 production further increase the work of breathing. The
restrictive pattern results in decreased functional residual capacity,
vital capacity, total lung capacity, inspiratory capacity, minute
ventilator volume, and expiratory reserve volume.

Care plans: General approaches to

respiratory disorders
Impaired spontaneous ventilation with or without impaired
gas exchange
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate gas exchange, reflected by PaO2 greater than 80 mm
Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal
breath sounds, and absence of adventitious breath sounds. RR is 12
to 20 breaths/min with normal pattern and depth or back to normal
baseline.
Respiratory Status: Ventilation, Vital Signs Status,

861
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.

Ventilation assistance

1. Assess for patent airway; if snoring, crowing, stridor, or

strained respirations are present, indicative of partial or full airway
obstruction, open airway using chin lift or jaw thrust.

2. Insert an oral airway if the patient becomes unconscious and

cannot maintain patent airway; use a nasopharyngeal airway if the
patient is conscious to avoid provoking vomiting. If severely
distressed, the patient may require endotracheal intubation.

3. Position the patient to alleviate dyspnea and ensure maximal

ventilation; generally, sitting in an upright position unless severe
hypotension is present.

4. Monitor changes in oxygenation following position change: SpO2,

S VO 2, ScVO2, end-tidal CO2 (ETCO2), A-aDO2 levels, and ABGs.

5. Clear secretions from airway by having the patient cough

vigorously, or provide nasotracheal, oropharyngeal, or
endotracheal tube suctioning, as needed.

6. Have the patient breathe slowly or manually ventilate with

manual resuscitator or bag-valve-mask device slowly and deeply
between coughing or suctioning attempts.

7. Assist with use of incentive spirometer as appropriate.

8. Turn the patient every 2 hours if immobile. Encourage the patient

to turn self, or get out of bed as much as tolerated if he or she is
able.

9. Provide mucolytic and bronchodilating medications orally,

intravenously, or by inhaler, aerosol, or nebulizer as ordered to
assist with thinning secretions and relaxing muscles in lower
airways.

862
10. Provide chest physical therapy as appropriate, if other methods
of secretion removal are ineffective.

11. Considerations for the bariatric patient: The prevalence of

OSA syndrome in bariatric surgical patients is 39% to 71%. Sleep
studies (polysomnography) are recommended as part of
preoperative evaluation. Continuous positive airway pressure
(CPAP) via mask (10 cm H2O) is begun if patients are unable to
complete sleep studies before surgery. OSA is characterized by
repetitive, partial, or complete obstruction of the upper airway,
which prompts arterial blood oxygen desaturations and
awakenings from sleep. Frequent decreases in RR with periods of
apnea occur, resulting in instances of severe hypoxia. Patients
manifest snoring, systemic and pulmonary hypertension, nocturnal
angina, sleep-related cardiac dysrhythmias, gastroesophageal reflux
disease (GERD), insomnia, polycythemia, and daytime somnolence.

Oxygen therapy

1. Ensure humidity is provided when using O2 or bilevel positive

airway pressure (BiPAP) device for more than 12 hours to help thin
secretions.

2. Administer supplemental O2 using liter flow and device as

ordered.

3. Restrict the patient and visitors from smoking while O2 is in use.

4. Document pulse oximetry with O2 liter flow in place at time of

reading as ordered. Oxygen is a drug; the dose of the drug must be
associated with the O2 saturation or the reading is meaningless.

5. Obtain ABGs if the patient experiences behavioral changes or

respiratory distress to check for hypoxia or hypercapnia.

6. Monitor for hypoventilation, especially in patients with COPD.

7. Monitor for changes indicative of O2 toxicity in patients receiving

863
higher concentrations of O2 (greater than 45% Fio2) for longer than
24 hours. Changes will be apparent in chest radiograph and breath
sounds. Absorption atelectasis may be present. The higher the O2
concentration, the greater is the chance of toxicity.

8. Monitor for skin breakdown where O2 devices are in contact with

the skin, such as nares, around the ears, and around edges of mask
devices.

9. Provide O2 therapy during transportation and when the patient

gets out of bed.

10. If the patient is unable to maintain SpO2 reading of more than

88% off O2, consult with the respiratory care practitioner/therapist
and the physician about the need for home O2 therapy.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs

of increased work of breathing such as use of accessory muscles or
retraction of intercostal or supraclavicular muscles. Consider use of
noninvasive positive-pressure ventilation (NPPV or NiPPV) for
impending respiratory failure.

3. Monitor for snoring, coughing, and possibly choking-type

respirations when patient has a decreased level of consciousness to
assess if airway is obstructed by tongue.

4. Monitor for new breathing patterns that impair ventilation,

which may need aggressive management in a specialized, highly
skilled setting.

5. Note that trachea remains midline, because deviation may

indicate that the patient has a tension pneumothorax.

6. Auscultate breath sounds before and after administration of

respiratory medications to assess for improvement.

864
7. Evaluate changes in SaO2, SpO2, ETco2, ScVO2, and ABGs as
appropriate.

8. Monitor for dyspnea and note causative activities/events.

9. If increased restlessness or unusual somnolence occurs, evaluate

the patient for hypoxemia and hypercapnia as appropriate.

10. Monitor chest radiograph reports when new images become

available.

11. Considerations for the bariatric patient: Mechanical ventilation

for the obese patient with respiratory failure is challenging.
Delivered tidal volume should be calculated based on ideal body
weight (IBW) rather than actual body weight to avoid high airway
pressures and barotrauma. End-tidal CO2 monitors are unreliable
because of widened alveolar-arterial gradients present in most
obese patients. The reverse Trendelenburg position at 45 degrees
facilitates liberation from the ventilator 24 hours of mechanical
ventilation postoperatively.

Cough Enhancement; Acid-Base Management; Mechanical

Ventilation; Artificial Airway Management; Oral Health
Maintenance.

Acute asthma exacerbation

Pathophysiology
The incidence of asthma is growing steadily by 2.9% each year in
the United States. The number of people with asthma has increased
from 20.3 million in 2001 to 25.7 million in 2010. Asthma manifests
variable, recurrent symptoms related to airflow limitation
stemming from chronic airway inflammation. Bronchiolar smooth
muscles manifest overactive bronchoconstriction and are
hyperresponsive to internal and environmental stimuli. Airflow
obstruction is fully or partially reversible, but as the disease
progresses, chronic airway inflammation creates edema, mucus,

865
and eventually mucus plugging, which further decreases airflow.
Eventually, irreversible changes in airway structure occur,
including fibrosis, smooth muscle hypertrophy, mucus
hypersecretion, injury to epithelial cells, and angiogenesis. Persons
with asthma eventually develop air trapping, increased functional
residual capacity, and decreased forced vital capacity. Several types
of cells and cellular elements are affected including mast cells,
epithelial cells, T lymphocytes, macrophages, eosinophils, and
neutrophils, which when triggered can sometimes prompt sudden,
fatal exacerbations of coughing, wheezing, chest tightness, and
breathlessness.
Life-threatening asthma exacerbation results from bronchial
smooth muscle contraction (bronchospasm), bronchial
inflammation leading to airway edema, and mucus plugging. When
an episode of bronchospasm (critical airway narrowing) is not
reversed after 24 hours of maximal doses of traditional inhaled
short-acting beta2-adrenergic agonists (SABAs) such as albuterol or
levalbuterol, injected systemic beta2-agonists such as epinephrine,
inhaled anticholinergics such as ipratropium, and systemic steroid
therapy with prednisone, prednisolone, or methylprednisolone, the
refractory patient may be diagnosed with status asthmaticus.
Common triggers for asthma exacerbations include respiratory tract
infections, allergens (airborne or ingested), air pollutants, smoke,
and physical irritants (e.g., cold air, exercise). Anxiety or “panic”
attacks and use of beta-adrenergic blocking agents and nonsteroidal
antiinflammatory drugs (NSAIDs) may predispose patients to
development or exacerbation of severe asthma. Activities that
prompt deeper inhalation, such as vigorous laugher or physical
exertion, can trigger an episode. Exercise-induced asthma or
exercise-induced bronchospasms are well recognized in the
literature.
Several clinical patterns for development of an asthma
exacerbation are recognized. An “attack” can happen suddenly
(over several hours) or it may take several days to reach critical
airway obstruction. The more common gradual presentation
manifests with increasing symptoms of sputum production,
coughing, wheezing, and dyspnea. As air trapping increases, lung
hyperinflation prompts increased work of breathing. Rapid

866
exhalations increase insensible water loss through exhaled water
vapor and diaphoresis. Oral intake may be decreased, contributing
to hypovolemia. Without adequate oral intake to promote
hydration, mucus becomes thick and begins to plug the airways.
Terminal bronchioles can become occluded completely from
mucosal edema and tenacious secretions. Ventilation-perfusion
mismatch or shunting occurs as poorly ventilated alveoli continue
to be perfused, which leads to hypoxemia. Tachycardia is an early
compensatory mechanism to increase O2 delivery to the body cells,
but it increases myocardial O2 demand. Oxygen requirements and
work of breathing increase, leading to respiratory failure,
hypercapnia, and respiratory arrest if not managed promptly and
appropriately.

Assessment
Goal of system assessment
• Evaluate for ineffective breathing patterns, impaired gas
exchange, and airway obstruction.

• Determine the patient’s previous treatment regimen; classify

which “step” of treatment has been needed to control symptoms;
the patient may need to move to the next step of treatment to
maintain control.

• Classify severity of exacerbation: should be determined following

initial assessment and diagnostic testing.

History and risk factors

For asthma

• Asthma symptoms: Cough (especially if worse at night),

wheezing, recurrent difficulty breathing, and recurrent chest
tightness.

• Family history: Patients with either family history or atopic

867
 disease are at higher risk of asthma.

• Common triggers: Symptoms worsen with viral respiratory

infections, environmental airborne allergens, irritants in the home
(mold, mildew, wood-burning stove, cockroaches, dust mites,
animal dander, carpeting laid over concrete), recent emotional
upset, aggressive exercise or physical exertion, fear, anxiety,
frustration, food, new medications, changes in weather
(especially exposure to cold air), occupational chemicals or
allergens, and hormonal changes (menstrual cycle).

• Comorbid conditions: Sinusitis, rhinitis, GERD, OSA, and allergic

bronchopulmonary aspergillosis.

For asthma exacerbation

• Classify asthma severity: Intermittent (step 1 treatment) or

persistent: mild, moderate, severe (steps 2, 3, 4, 5, and 6
treatments); steps differ for children younger than 5 years old,
children between 5 and 12 years old, and adults.

• Classify severity of exacerbation: Mild to severe or life

threatening.

• Assess control: Determine if pattern of previous exacerbations is

inherent to the current episode.

• Compliance/ability to control: Assess the patient’s knowledge and

skills for self-management.

• Identify precipitating factors: Situation: exposure at home, work,

daycare, or school to inhalant allergens or irritants; time of day,
season or time of year, relationship of symptoms to meals,
deterioration in other health conditions, or menses.

• Identify comorbid conditions that may impair asthma

management (e.g., sinusitis, rhinitis, GERD, OSA, obesity, stress,
or depression).

• Surgery: Patients with asthma are at high risk for exacerbations

868
 following endotracheal intubation, general anesthesia, and
ventilation provided during surgical or other invasive
procedures. Impaired cough, hypoxemia, and hypercapnia may
trigger exacerbation.

Spirometry or peak expiratory flow

• Peak expiratory flow (PEF): Measurement of rate or force of
exhalation; those with easier breathing will have higher values
than those in distress. A peak flow meter is used by patients at
home to assess asthma control. Those with more severe asthma
may have difficulty discerning worsening of symptoms and may
use PEF several times daily to assess for declining rate of
exhalation.

• Assesses degree of obstruction and reversibility in patients older

than 5 years.

• Spirometry is essential for establishing the diagnosis of asthma.

Patients’ perceptions of airflow obstruction are highly variable.
Spirometry or PEF provides an objective measurement to help
classify severity of exacerbation.

• Decreased to less than 40% of predicted value indicates severe

exacerbation; less than 25% of predicted value for life
threatening.

Vital signs (severe to life-threatening asthma

exacerbation)
• Presence of fever: Temperature elevation helps discern whether
the patient’s condition is related to a microbe (fever) versus an
allergen (afebrile).

• Pulse oximetry: Oxygen saturation is decreased from the patient’s

baseline value.

• Tachycardia (HR greater than 140 beats/min [bpm]) and

tachypnea (RR greater than 40 breaths/min).

869
• Hypotension may be present; hypotension is exacerbated by
underlying dehydration often present in patients with severe
asthma.

Observation
• Severe attacks render patients unable to speak resulting from
breathlessness.

• Use of accessory muscles; fatigued, with or without diaphoresis.

• Ashen, pale, or gray/blue facial color, lip color, or nail beds.

• Chest expansion may be decreased or restricted.

• Altered level of consciousness (confusion, disorientation,

agitation).

• Agitation is more commonly associated with hypoxemia, whereas

somnolence is associated with hypercapnia (elevated CO2 level).

• Frequent nonproductive coughing unless associated with

superimposed infection.

• Increased nasal secretions, mucosal swelling, and nasal polyps.

• Prolonged phase of forced expiration.

Auscultation
• Wheezing bronchial breath sounds; wheezing on inspiration is
more indicative of acute airway narrowing, versus wheezing on
expiration, which is more common.

• Wheezing during normal breathing is common.

• Chest may be nearly silent if airflow is severely obstructed.

During an asthma attack, if wheezing stops, the patient may
either have resolution of symptoms or complete airway
occlusion.

870
Palpation
• Palpate to assess for chest expansion; chest may be hyperinflated
or may be asymmetrical; chest expansion during inspiration may
be decreased.

• Decreased tactile fremitus may be present.

Percussion
• May reveal hyperresonance (pneumothorax), a complication of
asthma.

Screening labwork
• Complete blood count (CBC) with white blood cell (WBC)
differential: Evaluates for elevated WBCs indicative of chronic
inflammation as a result of allergic response and infection
including presence of eosinophils, neutrophils, and mononuclear
cells.

• ABG analysis: Evaluates for hypoxemia and hypercapnia.

4-1
RESEARCH BRIEF
Important changes in prescribing practices resulting from recent
studies are occurring in primary care. The Asthma Clinical
Research Network is reporting evidence that improvement in FEV1
(forced expiratory volume in 1 second) in response to albuterol is a
reliable predictor of improved asthma control using tiotropium, a
long-acting muscarinic antagonist. This holds particular promise
for long-term control in patients with severe asthma. There is
evidence supporting improvement in lung function with
tiotropium as an add-on therapy to inhaled corticosteroids and
long-acting beta-agonists. These practical studies are examples of
what is commonly referred to as real-world research, an effort to
investigate the patient’s disease course at the interface of their daily

871
life and activities. Patient-reported outcome measures (PROMs) are
guiding investigators toward a better appreciation of the relevance
of investigational end points. Improvements in PROMs include
morning peak expiratory flow and asthma control days among
other outcomes.
From Peter SP, Bleecker ER, Kunselman SJ, et al: Predictors of response to tiotropium
versus salmeterol in asthmatic adults. J Allergy Clin Immunol 132:1068-1074, 2013.

Diagnostic Tests for Acute Asthma Exacerbation

Test Purpose Abnormal Findings

Arterial blood gas Assess for abnormal gas exchange or pH changes: Acidosis may
(ABG) analysis compensation for metabolic derangements. reflect respiratory failure;
Initially Pao2 is normal and then decreases alkalosis may reflect
as the ventilation-perfusion mismatch tachypnea.
becomes more severe. A normal PCO2 in a Carbon dioxide: Elevated CO2
distressed patient with asthma receiving reflects respiratory failure;
aggressive treatment may indicate decreased CO2 reflects
respiratory fatigue, which causes a tachypnea; rising PCO2 is
progressively ineffective breathing pattern, ominous, because it
which can also lead to respiratory arrest. signals severe
Oxygenation assessment differs from acid- hypoventilation, which
base balance assessment, wherein the PCO2 can lead to respiratory
value is used as the hallmark sign for arrest. Hypoxemia:
respiratory failure induced acidosis. Pao2 less than 80 mm Hg.
Oxygen saturation: Sao2 less
than 92%.
Bicarbonate: HCO3 less than
22 mEq/L.
Base deficit: less than −2.
Complete blood WBC differential evaluates the strength of Eosinophils: Increased in
count (CBC) with the response of the immune system to the patients not receiving
white blood cell trigger of exacerbation and for the presence corticosteroids; indicative
(WBC) differential of infection. of magnitude of
inflammatory response.
Increased WBC count: More
than 11,000/mm3 is seen
with bacterial
pneumonias. WBCs may
be increased by asthma in
the absence of infection.
Hematocrit (Hct): May be
increased from
hypovolemia and
hemoconcentration.
Pulmonary The hallmark sign of asthma is a decreased Forced expiratory volume
function (FEV): Decreased during

872
tests/spirometry FEV1 (forced expiratory volume in 1 acute episodes; if less than
second)/FVC (forced vital capacity). If peak 0.7, narrowed airways
expiratory flow (PEF) rate does not improve prevent forceful exhalation
with initial aggressive inhaled of inspired volume (Table 4-
bronchodilator treatments, morbidity 1).
increases. PEF rate: Less than 100 to
125 L/min in a normal-sized
adult indicates severe
obstruction to air flow.
Pulse oximetry Noninvasive technology that measures the Normal Spo2: Greater than
(SpO2) oxygen saturation of arterial blood 95%. Correlation of Spo2
intermittently or continuously using a probe with Sao (arterial
2
placed on the patient’s finger or ear. When
using pulse oximetry, it is helpful to obtain saturation) is within 2%
when Sao2 is greater than
ABG values to compare the oxygen
saturation and evaluate the Pao2, Paco2, and 50%. Temperature, pH,
Paco2, anemia, and
pH.
hemodynamic status may
reduce the accuracy of pulse
oximetry measurements.
Presence of other forms of
hemoglobin in the blood
(carboxyhemoglobin or
methemoglobin) can
produce falsely high
readings.
Serologic studies Acute and convalescent titers are drawn to Increased antibody titers: A
diagnose a viral infection. positive sign for viral
infection.
Chest radiograph Evaluates the severity of air trapping; also Lung hyperinflation: Caused
useful in ruling out other causes of by air trapping
respiratory failure (e.g., foreign body Flat diaphragm: Related to
aspiration, pulmonary edema, pulmonary increased intrathoracic
embolism, pneumonia). volume.
12-Lead ECG Evaluates for dysrhythmias associated with Sinus tachycardia: Important
(electrocardiogram) stress response and asthma medications. baseline indicator; use of
some bronchodilators (e.g.,
metaproterenol) may
produce cardiac stimulant
effects and dysrhythmias.
Sputum Gram Culture and sensitivity may show Gross examination may
stain, culture, and microorganisms if infection is the show increased viscosity
sensitivity precipitating event. or actual mucous plugs.
The most reliable specimens are obtained Gram stain positive: Indicates
via bronchoalveolar lavage (BAL) during organism is present.
bronchoscopy, or using a protected Culture: Identifies organism.
telescoping catheter (mini-BAL or using Sensitivity: Reflects
BAL) to decrease the risk of effectiveness of drugs on
contamination from oral flora. identified organism.
Diagnostic fiber Obtains specimens during simple Gram stain positive: Indicates
optic bronchoscopy bronchoscopy without contaminating the organism is present.
using a PSB aspirate; modified technique (mini-BAL) is Culture: Identifies organism.
(protected also effective without the need of full Sensitivity: Reflects
specimen brush) bronchoscopy. effectiveness of drugs on
and BAL identified organism.
Serum theophylline Important baseline indicator for patients Acceptable therapeutic
level who take theophylline regularly; range is 10 to 20 µg/mL.

873
 therapeutic level is close to toxic level. If There is little evidence to
additional theophylline is given, serial support clinical benefit for
levels should be measured within the first adding theophylline to
12 to 24 hours of treatment and daily inhaled beta-adrenergic
thereafter. Patients are monitored for side blocking agents and steroids
effects (e.g., nausea, nervousness, for patients with acute,
dysrhythmias). severe asthma who were not
already using theophylline
regularly.

Collaborative management
Care priorities
The goal of asthma management is to control the disease using a
stepwise approach to therapies. Ideal control is attained when
patients are free of daytime symptoms, do not awaken breathless or
coughing at night, have few or no limitations on activities, do not
regularly use rescue medications, have no exacerbations, and
maintain a forced expiratory volume in 1 second (FEV1) and/or
peak expiratory flow rate (PEFR) greater than 80% of the predicted
value. When prevention fails, the potential for life-threatening
respiratory failure is high during exacerbations unresponsive to
treatment within the first hour. Management is directed toward
decreasing bronchospasm and increasing ventilation. Other
interventions are directed toward treatment of complications (Table
4-1).

Table 4-1
PULMONARY FUNCTION TESTS IN ASTHMA EXACERBATION

874
1. Determine severity of asthma exacerbation

a. Acute severe: PEFR is less than 40% of predicted or personal best

in a patient who is unable to speak a complete sentence in one
breath, with RR greater than 25 breaths/min and HR greater than
110 bpm.

b. Life threatening: In a patient with severe asthma, the PEFR is less

than 25% of predicted or personal best, SpO2 less than 90%, PaO2
less than 80 mm Hg; PCO2 35 to 45 mm Hg, silent chest, weak
respiratory effort, exhaustion, cyanosis, bradycardia, hypotension,
dysrhythmias, confusion, and coma.

c. Near fatal: PCO2 greater than 45 mm Hg and/or requiring

mechanical ventilation using increased positive pressure to
overcome inspiratory pressures; the patient also has other findings
of life-threatening exacerbation.

2. Oxygen therapy
Patients have profound hypoxia and can tolerate high doses of O2
(Fio2) unless they retain CO2 and breathe by hypoxic drive. Most
patients with asthma are able to tolerate high flow O2, versus those
with other obstructive lung disease who cannot. Oxygen dosage
must be limited in nonintubated, mechanically ventilated patients
who breathe via hypoxic drive to avoid hypoventilation and
respiratory arrest. Humidified O2 therapy is begun immediately to
correct hypoxemia and thin secretions. PaO2 is maintained slightly
above normal unless the patient retains CO2 to compensate for the
increased O2 demands imposed by the increased work of breathing.
The degree of hypoxemia and patient response determines the
method of O2 delivery. A high-flow device (e.g., 100%
nonrebreather mask) delivers more precise and higher Fio2.
Management of anxiety must be considered, especially if the patient
will not wear a mask because of feelings of suffocation.

3. Heliox therapy

875
A blended mixture of helium and O2, available in mixtures of 60:40,
70:30, and 80:20, which is delivered either through a tight-fitting
face mask or through a mechanical ventilator circuit. Heliox
reduces the turbulent flow of air in narrowed airways. Helium is
not as dense as nitrogen, which accounts for the decreased
turbulence, therefore reducing the work of breathing and
improving gas exchange. Findings of upper airway sounds in the
bronchopulmonary system are inconsistent with the diagnosis of
asthma. The advanced practice provider should be consulted for
further actions should auscultation reveal this finding.

4. Intubation and mechanical ventilation

Strongly considered when the patient has severe hypoxemia or
hypercapnia indicative of impending respiratory failure: confusion,
somnolence, agitation, or central cyanosis; or if the patient
experiences intolerable respiratory distress. There are varying
practices and no consensus guideline regarding the criteria for
intubation and mechanical ventilation for the patient with asthma.
These interventions can create significant complications for the
patient related to intubation and concomitant bronchial reactivity.
Intubation and mechanical ventilation should be considered
cautiously. Hypoventilation with low minute ventilation, low tidal
volume (6 mL/kg), and long exhalation time are necessary to
prevent barotrauma, increased intrathoracic pressures, and cardiac
compromise. Plateau pressure should not exceed 30 cm H2O and
auto-positive end-expiratory pressure (auto-PEEP) should be
maintained at less than 10 cm H2O. In exceptionally severe cases,
neuromuscular blockade may be warranted in addition to sedation
and analgesia.

5. Pharmacotherapy to manage acute asthma exacerbation

Vigorous therapy is initiated to decrease bronchospasms, help
reduce airway inflammation, and help remove secretions.
Treatment is continued until wheezing is eliminated and
pulmonary function tests return to baseline (Table 4-2).

• Bronchodilators: Dilate smooth muscles of the airways to help

relieve bronchospasms, resulting in increased diameter of

876
 functional airways. SABAs are the mainstay of asthma
exacerbation management, whereas long-acting beta-adrenergic
agonists (LABAs) are used for long-term control of asthma.
Theophylline and aminophylline are no longer recommended for
management of acute bronchospasms.

• Corticosteroids: Given intravenously during the acute phase of

the exacerbation to decrease the inflammatory response, which
causes edema in upper airways. Administration should decrease
reactivity and swelling of the airways. Dosage varies according to
severity of episode and whether or not the patient is currently
taking steroids. The patient may be converted to inhaled
corticosteroids once the acute phase has been resolved. Acute
adrenal insufficiency can develop in patients who take steroids
routinely at home, if these drugs are not given to the patient
during hospitalization.

• Anticholinergics: Inhaled medications used to reduce vagal tone

of the airways, thus helping to reduce bronchospasms.
Ipratropium (Atrovent) is used in combination with inhaled
SABAs for severe, acute asthma.

• Magnesium sulfate: Magnesium sulfate has been shown to

inhibit smooth muscle contraction, inhibit acetylcholine release,
and decrease histamine release from mast cells. The American
Thoracic Society asthma management guidelines (2008)
recommend consideration of a single dose of magnesium sulfate
1.2 to 2 g over 20 minutes for patients with severe, life-
threatening, or fatal exacerbation who have an inadequate or
ineffective response to inhaled bronchodilators. Recent
metaanalyses and high-quality random control trials have
identified intravenous (IV) magnesium sulfate as an effective
adjunct to standard therapy in the context of severe or life-
threatening exacerbation. However, the use of nebulized MgSO4
is not supported by adequate evidence.

• Sedatives and analgesics: Used in more limited doses in patients

who are not intubated or mechanically ventilated, unless the
patient is extremely anxious, agitated, and unable to cooperate

877
 with therapy. These agents depress the central nervous system
(CNS) response to hypoxia and hypercapnia. Once mechanical
ventilation is in place, the dosage is titrated until the patient is
comfortable and/or hypoxemia or hypercapnia begins to resolve.

• Buffers: Sodium bicarbonate may be given to correct severe

acidosis not corrected by intubation and mechanical ventilation.
Generally, this is only a temporizing measure to help relieve
lactic acidosis. The physiologic response to bronchodilators
improves with correction of metabolic acidosis.

• Antibiotics: Given if a respiratory infection is indicated, as

evidenced by fever, purulent sputum, or leukocytosis.

Table 4-2
MEDICATIONS USED FOR ASTHMA EXACERBATION*

*
Recommendations originate from the National Institutes of Health (NIH) Expert
Panel on the Diagnosis and Management of Asthma (2007). Intravenous
theophylline and magnesium are not recommended for general use in a hospitalized
patient with acute asthma by the NIH guidelines. A 20-minute intravenous
magnesium sulfate infusion for poorly responding patients is recommended by the
British Thoracic Society guidelines. All patients receiving theophylline before
hospitalization should have a theophylline level determined before a loading dose is
given.

878
6. Fluid replacement
To liquefy secretions and replace insensible losses. Generally,
crystalloid fluids (e.g., 5% dextrose in water [D5W], 5% dextrose in
normal saline [D5NS]) are used.

7. Chest physiotherapy
Generally contraindicated in acute phases of exacerbation because
of acute respiratory decompensation and hyperreactive airways.
Once the crisis is over, the patient may benefit from percussion and
postural drainage every 2 to 4 hours to help mobilize secretions.

Care plans: Acute asthma exacerbation

Impaired gas exchange 
related to ineffective breathing patterns secondary to narrowed airways.
Goals/Outcomes: Within 2 to 4 hours of initiation of treatment,
the patient has adequate gas exchange reflected by PaO2 greater
than 80 mm Hg, Paco2 35 to 45 mm Hg, and pH 7.35 to 7.45 (or ABG
values within 10% of the patient’s baseline), with mechanical
ventilation, if necessary. Within 24 to 48 hours of initiation of
treatment, the patient is weaning or weaned from mechanical
ventilation, and RR is approaching baseline rate, depth, and
pattern.
Respiratory Status: Ventilation, Vital Signs Status;
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.

Ventilation assistance

1. Monitor for signs of increasing hypoxia at frequent intervals:

Restlessness, agitation, and personality changes are indicative of
severe exacerbation. Cyanosis of the lips (central) and of the nail
beds (peripheral) are late indicators of hypoxia.

2. Monitor for signs of hypercapnia at frequent intervals:

Confusion, listlessness, and somnolence are indicative of

879
respiratory failure and near-fatal asthma exacerbation.

3. Monitor ABGs when continuous pulse oximetry values or patient

assessment reflects progressive hypoxemia: ABGs will also identify
the pH and level of CO2, alerting the provider to impending
hypoxemic and/or hypercapnic respiratory failure. Be alert to
decreasing PaO2 and increasing Paco2 or decreasing O2 saturation
levels, indicative of impending respiratory failure.

4. Monitor for decreased breath sounds or changes in wheezing at

frequent intervals: Absent breath sounds in a distressed patient
with asthma may indicate impending respiratory arrest.

5. Position the patient for comfort and to promote optimal gas

exchange: High-Fowler position, with the patient leaning forward
and elbows propped on the over-the-bed table to promote maximal
chest excursion, may reduce use of accessory muscles and
diaphoresis resulting from work of breathing. The use of a portable
electric fan is sometimes reported by the patient as greatly
improving comfort and stamina.

6. Monitor Fio2 to ensure that O2 is within prescribed concentrations:

If the patient does not retain CO2, a 100% nonrebreather mask may
be used to provide maximal O2 support. If the patient retains CO2
and is unrelieved by positioning, lower-dose O2, bronchodilators,
steroids, intubation, and mechanical ventilation may be necessary
sooner than in patients who are able to receive higher doses of O2
by mask.

Mechanical ventilation

1. Monitor patients who are intubated and mechanically

ventilated for increased intrathoracic pressure (auto-PEEP) as a
result of “breath stacking,” wherein the next breath is delivered
before complete emptying of the first breath. Each subsequent
breath failing to completely empty increases lung volume and
predisposes the patient to barotrauma, pneumothorax, and
decreased cardiac output resulting from dynamic hyperinflation

880
(DHI) causing pressure increases inside the thorax, which impede
venous return to the heart.

2. Monitor for hypotension: Decreased venous return can lead

to hypotension. DHI should be suspected in an intubated patient
with asthma who is hypotensive following intubation and initiation
of mechanical ventilation, when there is no other obvious cause
(e.g., tension pneumothorax). Current evidence and outcome data
support judicious fluid administration in response to hypotension
in patients who are mechanically ventilated. Fluid boluses should
be done cautiously, based on objective indicators including an
assessment of stroke volume variation. A fluid bolus may be
attempted for differential diagnosis of ventilation versus
intravascular volume changes affecting the blood pressure (BP). If
DHI is suspected, consult with the respiratory therapist and the
advanced practice provider to modify ventilator settings.

Ineffective airway clearance 

related to increased tracheobronchial secretions and bronchoconstriction;
decreased ability to expectorate secretions secondary to fatigue.
Goals/Outcomes: Within 24 hours of initiating treatment, the
patient’s airway has reduced secretions, as evidenced by return to
baseline RR (12 to 20 breaths/min) and absence of excessive
coughing. Within 24 to 48 hours of resolution of severe, refractory
asthma, the patient reports an increased energy level with
decreased fatigue and associated symptoms.
Respiratory Status: Airway Patency.

Cough enhancement

1. Monitor the patient’s ability to clear tracheobronchial secretions

frequently. Set up suction equipment at the bedside.

2. Encourage oral fluid intake or administer IV fluids within the

patient’s prescribed limits to help decrease viscosity of the
secretions.

3. Encourage coughing to clear secretions and deep breathing

unless the patient is already coughing uncontrollably or going into

881
respiratory failure. If the patient can manage to take deep breaths,
respiratory failure is manageable.

4. Provide humidified O2 to help liquefy tracheobronchial

secretions.

5. Evaluate whether or not the patient may benefit from chest

physiotherapy, after crisis phase of exacerbation has been resolved.
Discuss with the advanced practice provider. If appropriate, teach
significant others to perform chest physiotherapy.

6. Teach the patient proper coughing technique for effective

management of secretions.

7. Instruct the patient to take several deep breaths. Instruct

significant others in coaching this technique.

8. After the last inhalation, teach the patient to perform a succession

of coughs (usually three or four) on the same exhalation until most
of the air has been expelled.

9. Explain that the patient may need to repeat this technique several
times before the cough becomes productive.

Asthma management

1. Determine the patient’s previous asthma control status, including

which “step” of therapy was implemented (Table 4-3).

2. Compare current status to past exacerbation responses to

determine respiratory status.

3. Ensure spirometry measurements (FEV1, FVC, FEV1/FVC ratio) or

PEFR readings are obtained before and after use of a short-acting
bronchodilator.

4. Educate the patient about use of a PEFR meter at home.

5. Determine the patient’s compliance with treatments.

882
6. Note onset, frequency, and duration of coughing and advise the
patient to avoid triggers of coughing if identified.

7. Coach in breathing or relaxation exercises.

8. Encourage the patient to breathe slowly and deeply. Teach

pursed-lip breathing technique to assist the patient with controlling
respirations as appropriate:

• Inhale through the nose.

• Form lips in an O shape as if whistling.

• Exhale slowly through pursed lips.

• Record the patient’s response to the breathing

technique. Educate significant others in coaching.

9. Teach the patient and family how to decrease metabolic demands

for O2 by limiting or pacing the patient’s activities and procedures.

10. Schedule rest times after meals to avoid competition for O2

supply during digestion.

11. Monitor SpO2 by pulse oximetry during activity to evaluate

limits of activity, set future activity goals, and recommend optimal
positions for oxygenation.

12. Assess for fever every 2 to 4 hours. Consult the advanced

practice provider and provide treatment as prescribed to decrease
temperature and thus O2 demands.

Table 4-3
STEPPED MEDICATION MANAGEMENT FOR ASTHMA CONTROL

883
*
Information based on National Institutes of Health Asthma Management Guidelines
(2007). Retrieved from www.nhlbi.nih.gov/health-pro/guidelines/current/asthma-
guidelines. Accessed February 6, 2014.
CNS, Central nervous system; DPI, dry powder inhaler; HFA, hydrofluoroalkanes
(ozone-benign propellant for inhalation); ICS, inhaled corticosteroid; IgE,
immunoglobulin E; LABA, long-acting beta2-agonist; LTRA, leukotriene receptor
antagonist; MDI, metered dose inhaler; PUD, peptic ulcer disease; SABA, short-
acting beta2-agonist; SVT, supraventricular tachycardia.

Anxiety reduction

1. Ascertain and alleviate the cause of restlessness to decrease

metabolic demands (e.g., if restlessness is related to anxiety, help
reduce anxiety by providing reassurance, enabling family members
to stay with the patient, and offering distractions such as soft music
or television).

• Restlessness may be an early sign of hypoxemia.

2. Explain all procedures and offer support to minimize fear and

884
anxiety, which can increase O2 demands.

Acid-Base Management; Acid-Base Monitoring; Airway

Management; Bedside Laboratory Testing; Cough Enhancement;
Emotional Support; Energy Management; Fluid Management; Fluid
Monitoring; Laboratory Data Interpretation; Mechanical
Ventilation; Oxygen Therapy; Positioning; Respiratory Monitoring;
Vital Signs Monitoring.

Additional nursing diagnoses

Also see the section on Acute Respiratory Failure for information
about support of breathing. For other nursing diagnoses and
interventions, see Emotional and Spiritual Support of the Patient
and Significant Others (Chapter 2).

Acute respiratory distress syndrome

Pathophysiology
The primary goal of the pulmonary system is to promote an
appropriate and reasonable gas exchange at the alveolar-capillary
surface, generally measured by pulse oximetry and ABGs. Acute
respiratory failure is a general term that identifies a primary lung
dysfunction. Mild to severe symptoms of acute respiratory distress
syndrome (ARDS) are potentially lethal complications of critical
illness that are unfortunately common in some intensive care units
(ICUs). This dysfunction ultimately results in failure to promote
appropriate and proportionate O2 uptake at the alveolar-capillary
interface. Type I (hypoxemic) is oxygenation failure, whereas type
II (hypercapnic) is ventilation failure. Many patients manifest
respiratory failure of types I and II simultaneously. Clinically, type I
failure exists when PaO2 is less than 50 mm Hg with the patient at
rest and breathing room air (Fio2 = 0.21 or 21% of the atmospheric
pressure, which is 760 mm Hg at sea level). Ultimately there will
also be failure to remove CO2 (known as hypoventilation), and/or
Paco2 greater than 50 mm Hg (type II) is significant for acute

885
ventilation failure or hypercapnia. A wide variety of disease states
create a single or mixed respiratory failure. One of the simplest
methods of evaluating patients relates to the understanding of basic
gas exchange. Oxygenation occurs primarily during inspiration and
the removal of CO2 occurs during exhalation. The basic concepts
applied here include compliance and recoil. Lung compliance is the
measure of expansion of the alveoli (the gas-exchanging surface),
which occurs on inspiration, whereas elasticity refers to the ability
of the alveoli to recoil, as they do on exhalation. Restrictive airway
diseases generally present with significant hypoxemia, whereas
obstructive disorders are more likely to develop a persistent and
chronic hypercapnia. See Box 4-1 for a description of some of the
disease processes that can lead to acute respiratory failure.

Box 4-1
DISEASE PROCESSES LEADING TO THE
DEVELOPMENT OF RESPIRATORY
FAILURE
Obstructive disease states, impaired exhalation, impaired
minute ventilation, CO2 retention

• Chronic obstructive pulmonary disease (emphysema, bronchitis,

asthma, cystic fibrosis)

• Neuromuscular defects (Guillain-Barré syndrome, myasthenia

gravis, multiple sclerosis, muscular dystrophy, polio, brain/spinal
injury)

• Depression of respiratory control centers (drug-induced cerebral

infarction, inappropriate use of high-dose oxygen therapy,
drug/toxic agents)

Restrictive disease states, impaired inspiration, impaired

alveolar recruitment: Hypoxemia, refractory hypoxemia
• Restrictive pulmonary disease (interstitial fibrosis, pleural

886
 effusion, pneumothorax, kyphoscoliosis, obesity, diaphragmatic
paralysis)

• Pulmonary emboli

• Atelectasis

• Pneumonia

• Bronchiolitis

• Acute respiratory distress syndrome

• Chest trauma (rib fractures)

• Chest wall issues

Diffusion disturbances
• Pulmonary/interstitial fibrosis

• Pulmonary edema

• Acute respiratory distress syndrome

• Anatomic loss of functioning lung tissue (pneumonectomy)

The terms acute lung injury (ALI) and ARDS were historically
used to differentiate and describe a continuum of lung dysfunction.
ARDS was defined in 1994 by the American-European Consensus
Conference. Many concerns regarding the evaluation methods and
categorization of lung dysfunction and interventions have evolved
since that time. In 2011, the Berlin definition equalized the
diagnosis and divided the disorder by levels of hypoxemia, as well
as Fio2 and PEEP requirements (Table 4-4).

Table 4-4
STAGING ACUTE RESPIRATORY DISTRESS SYNDROME BASED
ON BERLIN DEFINITIONS

887
 Mild Pao2/Fio2 < 200 mm Hg Pao2/Fio2 < 300 mm Hg with PEEP or
CPAP ≥5 cm H2O
Moderate Pao2/Fio2 < 100 mm Hg Pao2/Fio2 < 200 mm Hg with PEEP or
CPAP ≥5 cm H2O
Severe Pao2/Fio2 < 100 mm Hg with PEEP or
CPAP ≥5 cm H2O

CPAP, Continuous positive airway pressure; PEEP, positive end-expiratory pressure.

The term ALI no longer exists. Under the Berlin definition,

patients with PaO2/Fio2 200 to 300 are diagnosed with “mild ARDS.”
The onset of ARDS (diagnosis) must be acute, defined as occurring
within 7 days of a particular event, such as sepsis, pneumonia, or
simply a patient’s recognition of worsening respiratory symptoms.
Bilateral opacities consistent with pulmonary edema must be
present and can be detected on computed tomography or chest x-
ray. Heart failure is not excluded from the current definition
because patients with high pulmonary capillary wedge pressures or
known congestive heart failure with left atrial hypertension can still
have ARDS.
There may be a primary (intrapulmonary) or secondary
(extrapulmonary) insult to both the lung endothelium and the
epithelium. The associated release of mediators, increasing vascular
and alveolar permeability (leak), eventually perpetuates alveolar
collapse and supports the accumulation of fluids in the pulmonary
interstitium. While the capillary permeability and alveolar
epithelial damage continue to worsen, surfactant activity is
reduced, protein production increases, and therefore gas exchange
decreases as a result of widened diffusion distance and
intrapulmonary shunting. The alveoli tend to collapse,
communicating the loss of opening pressure to other alveoli in the
sac. All resist reexpansion in the absence of surfactant and the
presence of significant infiltration and collapsing fluid pressure.
Initially, acute hypoxemia develops, worsens, and ultimately
progresses into hypercapnic respiratory failure. The shunt fraction
(blood flow past derecruited alveoli rejoins in the pulmonary
venous circulation without adequate O2 exposure) as well as
alveolar (physiologic) dead space (overventilation of the unaffected
alveolar sacs) increase, ultimately progressing to a profoundly

888
noncompliant, derecruited, and gas dysfunctional state.
The evaluation of respiratory failure includes the understanding
of the following:

Match
This general term refers to the relationship of gas distribution ( )
to the amount of blood ( ), which passes the total alveolar
surface in 1 minute of time. Normal alveolar ventilation occurs at a
rate of 4 L/min, and normal pulmonary vascular blood flow occurs
at a rate of 5 L/min. The normal ratio is therefore 4 L/min
divided by 5 L/min, or a ratio of 0.8, almost in a 1:1 ratio. Any
disease process that interferes with either side of the equation
upsets the physiologic balance, causing a mismatch.

Components of an abnormal ratio

Alveolar dead space ventilation: This is a primary problem with
pulmonary perfusion. Alveoli may be compliant and elastic, but in
a condition where the alveoli are normal or hyperventilated, and
the perfusion is proportionately lower than the ventilation, there is
a primary gas exchange problem. This is measured or evaluated as
a high mismatch, wherein ventilation is proportionately
greater than perfusion. This is frequently seen with low cardiac
output states, or pulmonary embolus, and in overventilation of the
independent lung surface.
Diffusion distance: O2 and CO2 must cross the barrier created by
the alveolar epithelium, the interstitial space, and the capillary
endothelium. That space between is typically fluid free and product
free, allowing gas to move rapidly across. Diffusion is affected
when an increase in anatomic distance and/or product (fluid,
proteins, and neutrophils) alters the ability of gas exchange
between alveoli and the capillary bed. Pulmonary edema is a major
problem that interferes with diffusion.

Carbon dioxide production

The volume of CO2 produced by the body tissues varies with
metabolic rate (fever, pain, agitation, sepsis, and so forth). The Paco2

889
must be interpreted in conjunction with the volume exhaled,
especially in patients who are mechanically ventilated. Many
vagaries of CO2 flux can be eliminated by controlling ventilation
and muscular activity. Current evidence supports that the
overdistension and shear force of opening-closing also profoundly
affect the healthy lung.
Intrapulmonary right-to-left shunt: Large amounts of blood pass
from the right side of the heart to the left side of the heart and out
into the general circulation without adequate oxygenation. This
process occurs when alveoli are not recruited on inspiration
resulting from atelectasis or the alveoli are flooded. Primary causes
of intrapulmonary shunt are atelectasis and ARDS.
ARDS is primarily defined once the injury creates a hypoxemia
requiring intubation and mechanical ventilation. The presence of
refractory hypoxemia in conjunction with diffuse pulmonary
infiltrates in the absence of left atrial hypertension is considered to
be the primary indicator of the continuum of acute respiratory
failure. Despite advances in the treatment of the primary
inflammatory process and progress in the method of ventilatory
support, the continuum of ALI/ARDS continues to be associated
with high morbidity and mortality, reaching greater than 60%.
Since 1964, when the continuum was first described, the
understanding of the etiology, pathophysiology, and epidemiology,
as well as the relationship of genetic prodrome and ventilator-
induced lung injury process, has significantly increased (Table 4-5).

Table 4-5
RISK FACTORS FOR ACUTE RESPIRATORY DISTRESS
SYNDROME

Direct Injury Indirect Injury

Pneumonia Severe sepsis
Aspiration Trauma
Lung contusions Pancreatitis
Inhalation/burn injury Transfusion-related lung injury
Severe acute respiratory syndrome Ventilation-associated lung injury

Assessment

890
Goal of system assessment
Evaluate for decreasing PaO2/Fio2 and increasing requirements for
pressure control and PEEP. (See Acid-Base Imbalances, Chapter 1).

History and risk factors

Shock: Trauma, hemorrhagic shock, sepsis, massive blood
transfusion, and aggressive fluid replacement creating an extra
vascular lung water excess.

Respiratory: Inhalation of toxic substances, pneumonia, severe

pneumonitis, aspiration of gastric contents, drowning, air or fat
embolus, O2 toxicity, ventilator-induced lung injury.

Other: Acute pancreatitis, postperfusion cardiopulmonary bypass,

drug overdose, neurologic injury, immunosuppression, and
malaria.

Vital signs
• If breathing spontaneously (with or without ventilation support),
RR may be rapid and compensatory for metabolic acidosis.

• Rapid HR if not receiving beta-antagonist therapy.

• Spo2 is lower than expected when reviewing the ventilation

settings or O2 support.

Observation: Oxygenation failure

• Nasal flaring and expiratory grunt may be present.

• Use of accessory muscles indicates respiratory distress.

• May appear fatigued, with or without diaphoresis.

• May present with ashen, pale, or gray/blue facial color, lip color,
or nail beds.

891
• Chest expansion may be decreased, restricted, or asymmetrical
with severe changes in one lung manifesting severe atelectasis or
pleuritic pain.

• Altered level of consciousness (confusion, disorientation, and

agitation) is more common with older adults but is a very
significant sign in any age group.

• Agitation is more commonly associated with hypoxemia, whereas

somnolence is associated with hypercarbia (elevated CO2 level).

Hypoxemic hypoxia in mild ARDS

• Initially: Dyspnea, restlessness, hyperventilation, cough,
increased work of breathing; chest may appear to be clear on
auscultation or there may be late inspiratory crackles. The patient
may be significantly agitated and if intubated may appear
combative.

• Ventilator pressures: As most of these patients will already be

ventilated, increasing peak airway pressure (pulmonary arterial
wedge pressure [PawP] or peak inspiratory pressure [PIP]) and a
validation of increased pressure measured during inspiratory
hold (Pplateau) when administering a volume-controlled breath
should be evaluated and documented. The rising pressure
(Pplateau) indicates a loss of functional alveolar surface; and while
the compliance of the lung decreases, the pressure measured
when a volume breath is delivered will rise.

• The patient with a loss of lung function will have a decreased P/F
ratio (defined later). Initially, there may be a shift from volume
control ventilation to pressure control as well as an increase in
PEEP (see Table 4-1).

Hypoxemic hypoxia in moderate to severe ARDS

• Initially: Respiratory failure including cyanosis, pallor, grunting
respirations, mid to late inspiratory rales, rapid and shallow
breathing, intercostal-suprasternal retractions, tachypnea,

892
 tachycardia, diaphoresis, and mental obtundation.

• Ventilator pressures: The increasing peak and plateau pressures

will be measured when the patient is given a volume control
breath (cannot be measured during a pressure-controlled breath).

• The O2 (P/F) ratio will decline further and generally requires a

change in ventilation support to a mean airway pressure strategy.

Auscultation
• Decreased or bronchial breath sounds.

• High-pitched inspiratory crackles heard best after the patient

coughs.

• Low-pitched inspiratory crackles caused by airway secretions.

Palpation
• Palpate chest wall for tenderness indicative of inflammation.

• Palpate to assess for symmetry of chest expansion.

Percussion
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).

Screening labwork
• CBC: Evaluates for elevated WBCs indicative of infection.
Bandemia (immature neutrophils) of greater than 10% is
especially concerning.

• Sputum Gram stain, culture, and sensitivity: Identifies infecting

organism.

• Blood culture and sensitivity: If result is positive, it may indicate

that the organism has migrated into the bloodstream to cause a

893
 systemic infection.

• ABG analysis: Evaluates for hypoxemia and eventually

hypercapnia.

A-a gradient/A-aDO2/P(A-a)o2

• The A-a gradient for hypoxemia and eventually tension

difference is a clinically useful calculation. The calculation is
based on a model as though the lung were one large alveolus and
the entire blood flow of the right side of the heart passed around
it. Using the rules of partial pressure as well as the laws of CO2
production at the cell and the content of CO2 exerting alveolar
pressure, the theoretical alveolar Po2 (PaO2) is calculated. Once
the theoretical PaO2 has been calculated, the gradient is achieved
by subtracting the measured arterial PaO2. The gradient is the
difference between the calculated alveolar oxygen (PaO2) and the
measured arterial oxygen (PaO2).

• When the Fio2 is above 0.21, the arterial oxygen (PaO2) is a

measurement of proportional gas exchange, although the
difference between alveolar and arterial values should always be
less than 150 mm Hg.

• Extrapulmonary failure: The A-a gradient generally remains

normal or narrow. With shunt or mismatch, the gradient is
usually wider than normal.

• P/F ratio: The PaO2 divided by the Fio2 (PaO2/Fio2 ratio known as
the P/F ratio) can be used to more simply assess the severity of
the gas exchange defect. The normal value for the ratio of the
partial pressure of arterial blood O2 to Fio2 {PaO2/Fio2} (Fio2 is
expressed as a decimal ranging from 0.21 to 1.00) is 300 to 500. A
value of less than 300 indicates gas exchange derangement, and a
value below 200 or greater than 40% Fio2 is indicative of severe
impairment and is a major component of the diagnostic criteria
for ARDS. The inverse relationship of the P/F and the A to a

894
 difference is important to consider when discussing the level of
gas exchange failure.

• QS/QT: The shunt fraction compares the nonoxygenated

(shunted: QS) blood exiting the pulmonary bed to the total blood
flow (cardiac output: QT). This mathematical calculation, which
requires mixed venous blood gas and pulmonary blood gas,
evaluates total intrapulmonary shunting. Normal physiologic
shunt is 3% to 4% and may increase to 15% to 20% or more in
ARDS. Shunt may be present when the ecto2-Paco2 ratio is greater
than 10 mm Hg. The routine measurements of ABGs, chest
radiograph, A greater than 10 mm Hg ratio, as well as the
presence of refractory hypoxemia are much more routinely used
to diagnose intrapulmonary shunting, a core feature of ARDS.

Diagnostic tests
Diagnostic Tests for Acute Respiratory Distress Syndrome

895
Collaborative management
Maintaining adequate arterial oxygenation while protecting the
functional lung is the highest priority in both traditional and more
recent approaches to ventilator management for ARDS. Careful
consideration should be given to evaluate neurologic conditions
and OSA because these are commonly overlooked causes of
respiratory failure. In addition, the primary goal is to determine

896
and treat the underlying pathophysiologic condition.

Care priorities

1. Augment oxygen content with oxygen therapy

The goal is to provide acceptable PaO2 levels (greater than 60 mm
Hg) with Fio2 less than 0.50, but Fio2 up to 1.00 may be necessary for
a short time while other adjustments are made. If an increase in Fio2
exceeds 50%, clinicians should consider increasing PEEP (by
increments of 2 to 5 cm H2O every 1 to 2 hours, until 15 or 20 cm
H2O of PEEP is reached) to reduce the right-to-left shunt and
promote oxygenation. For those on mechanical ventilation PEEP
improves arterial oxygenation, primarily by recruiting collapsed
and partially fluid-filled alveoli, therefore increasing the functional
residual capacity at end-expiration, which decreases the effort and
sheer stress (which may damage the alveoli) of opening the alveoli
again during the next inspiration. This strategy is referred to as a
mean airway pressure or open lung strategy, that is, by increasing
the mean airway pressure, the lung will be constantly maintained in
an open state.

2. Facilitate ventilation and gas exchange

Mechanical ventilation: Provide mechanical ventilation with

moderate to high levels of PEEP (to prevent tidal collapse) and
low tidal volumes of approximately 6 mL/kg IBW, to protect the
functional lung from overdistension. This lung-protective
ventilatory strategy has been shown to ensure adequate gas
exchange, decrease the levels of intraalveolar and systemic
mediators, and improve outcomes in patients with ALI and
ARDS. Many clinicians have successfully used strategies to treat
ARDS by reducing the delivered tidal volume (from 8 to 10
mL/kg IBW to 4 to 6 mL/kg IBW) balanced with an RR (12 to 40
breaths/min) necessary to maintain adequate minute ventilation.
This decrease of volume in the noncompliant lung reduces both
peak inspiratory and plateau pressures. At the same time, the use
of a lower tidal volume protects the functional lung surface from

897
 volutrauma and pressure trauma, both of which cause
overdistension and stimulation of inflammation. Lung-
protective ventilator strategies are considered standard practice
in the care of patients with ARDS. To minimize ventilator-
induced lung injury, attention is directed at avoidance of alveolar
overdistension and cyclical opening and closing. The lowest
possible plateau pressure and tidal volume should be selected. A
reasonable target tidal volume in patients who are mechanically
ventilated is 6 mL/kg. A topic of much controversy is the optimal
setting of PEEP.

4-2
RESEARCH BRIEF
Evidence suggests that higher positive end-expiratory pressure
(PEEP) should be used for moderate and severe acute respiratory
distress syndrome (ARDS), whereas lower PEEP may be more
appropriate in patients with mild ARDS. PEEP should be set to
maximize alveolar recruitment while avoiding overdistension.
Volume and pressure limitation during mechanical ventilation can
be described in terms of stress and strain. Fraction of inspired
oxygen and PEEP are typically titrated to maintain arterial oxygen
saturation (SpO2) of 88% to 95% (PaO2 55 to 80’ mm Hg).
From Biehl M, Kashiouris MG, Gajic O: Ventilator-induced lung
injury: minimizing its impact in patients with or at risk for ARDS.
Respir Care 58:927-937, 2013.

If PEEP trials fail, other strategies designed to open and maintain

opening of the alveoli may be considered. These methods such as
airway pressure release ventilation, inverse ratio (I greater than
E), and high-frequency oscillation are also mean airway pressure
strategies, but the discussion of this type of advanced ventilation
is beyond the scope of this book.

Patient positioning: Primary lung edema occurs most aggressively

898
 in the dependent areas of the lung. Repositioning the patient at
least every 2 hours is indicated in patients with hypoxemia;
however, if staffing allows and the patient can tolerate it, more
frequent (every 30 minutes) turning could be beneficial.
Continuous lateral motion therapy beds may also be used to
continuously turn the patient. Motion therapy assists in the
redistribution of interstitial edema and may improve
oxygenation.

4-3
RESEARCH BRIEF
Successful early mobilization of patients who are critically ill can
reduce several complications including atelectasis and ventilator-
associated pneumonia and shorten ventilator time. In addition,
evidence shows that cognitive and functional limitations may last 1
to 5 years after discharge from the intensive care unit (ICU).
A schedule of repositioning every 2 hours was not superior to
every 4 hours to prevent pressure ulcers in ICU patients under
mechanical ventilation and on modern support surfaces. These
position changes require a higher nursing workload and increases
the likelihood of an adverse effect.
From Manzano F, Colmenero M, Perez-Perez AM, et al:
Comparison of two repositioning schedules for the prevention of
pressure ulcers in patients on mechanical ventilation with
alternating pressure air mattresses. Intensive Care Med 40:1679-1687,
2014.

Prone patient positioning: Prone positioning of the patient may

improve the oxygenation of many patients with ARDS. There are
various methods to turn the patient prone: staff generated with
pillows, foam wedges, the Vollman prone positioner, or
mechanically with the Roto-Prone bed.

3. Maintain adequate cardiac output with fluid therapy

899
Usually, the patient’s cardiac output is supported with fluid
therapy. The balance between dehydration and euvolemia is a
difficult one to achieve. New measures of total blood volume and
arterial stroke volume may assist the provider in achieving
adequate fluid without causing volume overload. The use of
crystalloid versus colloid fluids has been and remains controversial,
but the SAFE Study Investigators (2004) validated that the use of
colloids in the general population of patients did not improve
outcomes but significantly increased cost. More recently, concerns
have been studied regarding the presence of extravascular lung
water.

4-4
RESEARCH BRIEF
Managing thirst in the patient who is mechanically ventilated can
be challenging. Thirst is a prevalent, intense, and distressing
symptom in patients in the intensive care unit. Simple bundled
therapies including ice water spray, mouth hygiene, and lip
wetting reduced the perception and memory of severe thirst.
Integrating this practice with routine thirst assessment can relieve
one of the most distressing symptoms experienced by patients who
are critically ill.
From Rose L, Nokoyama N, Rezai S, et al: Psychological
wellbeing, health related quality of life and memories of intensive
care and a specialised weaning centre reported by survivors of
prolonged mechanical ventilation. Intensive Crit Care Nurs 30:145-
151, 2013; Puntillo K, Arai SR, Cooper BA, et al: A randomized
clinical trial of an intervention to relieve thirst and dry mouth in
intensive care unit patients. Intensive Care Med 40:1295-1302, 2014.

4. Reduce anxiety
Before any medication is administered, the provider must ascertain
that the ventilation is tailored to the patient. This can best be
evaluated by analyzing the volume-pressure loop and the flow/time
graph. The respiratory therapist is an invaluable resource for this

900
method of evaluation. After ensuring adequate ventilation, many
patients will require anxiety reduction with medication such as
fentanyl and anxiolytics. Those patients who cannot be adequately
oxygenated and ventilated with mechanical ventilation may be
given anxiety-reducing agents such as propofol and
dexmedetomidine. A sedation scale and protocol should be used to
standardize this practice. The use of sedating agents has been
linked to ICU delirium and post-ICU syndrome. In addition, the
bedside nurse must ascertain if the patient is in pain and administer
analgesics appropriately. A wide variety of pain scales can be used
effectively.
Patients who are unable to achieve appropriate ventilation as a
result of agitation and dyssynchrony or are hemodynamically
unstable may require heavy sedation with agents such as propofol
(Diprivan) or, in extreme cases, the diaphragm may need to be
paralyzed with a neuromuscular blocking agent such as
vecuronium bromide (Norcuron) or cisatracurium (Nimbex).
Although very user-dependent, train of four should be performed
when evaluating level of pharmacologic paralysis. The caregiver
must recognize that, although the patient who is pharmacologically
paralyzed may appear to be resting quietly or may even be
comatose, he or she may be alert and extremely anxious because of
the total lack of muscle control. These patients must receive
appropriate sedation (e.g., lorazepam [Ativan]) and analgesia (e.g.,
morphine), and they will require expert psychosocial nursing
interventions. (See Sedating and Neuromuscular Blockade, Chapter
1.) When patients appear agitated, ventilation should be evaluated
first (as long as the patient is not in danger of extubation or self-
harm) followed by pain evaluation and analgesia, followed by
anxiety-relieving medications. Neuromuscular paralysis should be
performed as a last resort and only when necessary to control
ventilation.

5. Provide nutrition support

Energy outlay with respiratory failure is high, in part because of the
increased work of breathing. If the patient is unable to consume
adequate calories with enteral feedings, total parenteral nutrition is
added. It is important to perform an occasional evaluation of the

901
patient’s caloric and metabolic needs to make certain that the
patient is being adequately nourished but not overfed. All efforts
should be made to feed enterally so that the gut is used. Newer
elemental feedings require no digestion and can be used in the
stomach, duodenum, or jejunum. (See Nutrition Support, Chapter
1.)

4-5
RESEARCH BRIEF
Risk Factors for Physical Impairment After Acute Lung Injury in a
National Multicenter Study
The investigators of this study set out to determine what risk
factors could be found that predicted physical impairment after
acute lung injury/acute respiratory distress syndrome (ALI/ARDS).
They evaluated patients enrolled from the ARDS Network studies
around the United States using the physical measures from the
Short Form-36 (SF-36). At 6 and 12 months, strength was 92% and
93% of maximal strength, 6-minute walk distance was 64% and
67% of predicted values, and SF-36 Physical Function Score was
61% and 67% of predicted values.
When adjusted for risk and acuity, corticosteroid dosage and
intensive care unit length of stay were highly associated with poor
or reduced physical outcomes.
From Needham DM, Wozniak AW, Hough CL, et al: National Institutes of Health NHLBI
ARDS Network. Am J Respir Crit Care Med 189:1214-1224, 2014.

Care plans for ards

Impaired gas exchange 

related to alveolar-capillary membrane changes secondary to increased
permeability with alveolar injury and collapse.
Goals/Outcomes: On initiation of therapy, and the titration of
ventilatory support, the patient has adequate gas exchange, as
evidenced by the following ABG values: PaO2 greater than 60 mm
Hg, Paco2 less than 45 mm Hg, pH 7.35 to 7.45. Success is achieved
when the patient can maintain his or her PaO2 even with Fio2

902
decreases.
Respiratory Status: Ventilation, Vital Signs Status;
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.

Respiratory monitoring

1. Assess and document characteristics of respiratory effort: rate,

depth, rhythm, and use of accessory muscles of respiration.

2. Assess the patient for signs and symptoms of respiratory distress:

restlessness, anxiety, confusion, tachypnea (RR greater than 20
breaths/min), and use of accessory muscles.

3. Assess breath sounds with each vital signs check. Adventitious

sounds, which are usually present in the later stages of ARDS, are
not as likely to occur during the early stage.

4. Monitor serial ABG values and consult the advanced practice

provider for significant changes. Explain the need for frequent
analysis to the patient and significant others.

5. Compare ABG saturation with pulse oximetry saturation for

accuracy. Consult the Change to advanced practice provider for
pulse oximetry values less than 90%.

6. Administer O2 and monitor Fio2 as prescribed.

7. Measure and compare ecto2 and arterial CO2.

8. Monitor and record pulmonary function tests as prescribed,

especially tidal volume and minute ventilation. Expect decreased
tidal volume and increased minute ventilation with respiratory
distress.

9. Position the patient for comfort and to promote adequate gas

exchange: usually semi-Fowler position.

10. Keep oral airway and self-inflating manual ventilating bag at

the bedside for emergency use. Keep emergency intubation

903
equipment at the bedside.

Risk for injury 

related to dislodging of life-sustaining equipment during positioning or
repositioning.
Goals/Outcomes: The patient can be turned, placed prone, or
repositioned without dislodging life-sustaining equipment or
devices.
Personal Safety Behavior; Risk Control.

Environmental management: Safety

1. Secure the endotracheal (ET) tube/other devices to prevent

accidental movement or dislodging.

2. Provide the appropriate length ventilator tubing to facilitate

positioning of the patient without risk of pulling on the ET tube.

3. Facilitate tolerance of rotational therapy by managing anxiety

and promoting sleep with medications.

4. When proning, assess oxygenation. Typical responders will

demonstrate at least 10 mm Hg increase in PaO2 within 10 minutes
of being placed prone.

5. Collaborate with the respiratory care practitioner to decrease the

delivered O2 while the patient improves.

Acid-Base Management; Airway Management; Bedside

Laboratory Testing; Laboratory Data Interpretation; Mechanical
Ventilation; Oxygen Therapy; Positioning; Respiratory Monitoring;
Ventilation Assistance; Vital Signs Monitoring.

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Nutrition Support,
Mechanical Ventilation, Prolonged Immobility, Acid-Base
Imbalances, and Emotional and Spiritual Support of the Patient and
Significant Others (Chapters 1 and 2).

904
Acute pneumonia
Pathophysiology
Pneumonia is the ninth leading cause of death in the United States
and the leading cause of death as a result of infectious disease
(www.cdc.gov/Features/Pneumonia/). The hallmark
pathophysiology of pneumonia is inflammation of the lung
parenchyma, which include the alveolar spaces, respiratory
bronchioles, and interstitial tissue. Pneumonia can be classified as
community-acquired pneumonia (CAP) or hospital-acquired
pneumonia (HAP).
Predisposing factors in the development of pneumonia are
immunosuppression and neutropenia. The microorganisms
involved include bacteria, protozoa, fungi (Candida, Aspergillus),
and viruses (cytomegalovirus). Patients who have a severely
compromised immune system, that is, acquired immune deficiency
syndrome, are most often infected by Pneumocystis jirovecii, a
fungus.
Sepsis, septic shock, respiratory failure, ARDS, emphysema,
or lung abscesses are complications of pneumonia that may require
intensive critical care. Those with the highest risk are older adults,
the very young, and those with chronic medical conditions.
Common disorders include COPD, cardiac disease, diabetes
mellitus, liver disease, renal disease, or cerebrovascular disease,
malignancy, or an immunocompromised state.

Community-acquired pneumonia
Pneumonia that occurs outside of the inpatient or “in facility”
healthcare environment is associated with high mortality and
morbidity rates. The most common pathogen is Streptococcus
pneumoniae. Approximately 4 million patients develop CAP
annually, resulting in 600,000 hospitalizations at a cost of
approximately $23 billion. Mortality rates range from 5.1% for
patients who are hospitalized and ambulatory to 36.5% for patients
requiring critical care. The disease occurs in all age groups but is
most common in those from the mid-50s to the late 60s.

905
Nosocomial pneumonia
Nosocomial pneumonia is the second most common cause of
hospital infections and has proven to be a fatal complication for
many patients, especially the critically ill. The three types of
nosocomial pneumonia are hospital acquired pneumonia (HAP),
which transpires 48 hours or more after hospital admission noting
that the infection was not incubating at the time of admission.
Healthcare-associated pneumonia includes patients with recent
hospitalization within 90 days of infection, exposure to healthcare
environments such as nursing homes, long-term care facilities, and
chronic hemodialysis; and receiving IV antimicrobial therapy,
chemotherapy, or wound care with 30 days of pneumonia. The final
type is ventilator-associated pneumonia (VAP), which develops 48 or
more hours after ET intubation. VAP has been very difficult to
define, resulting in inconsistent tracking and reporting of the
hospital-acquired condition. VAP is now part of a broader
classification of conditions associated with mechanical ventilation
termed ventilator-associated events (VAEs). For practical purposes,
HAP is the term used in this chapter to cover all the
aforementioned types.
A diagnosis of HAP requires new or advanced infectious
infiltrate on chest imaging and the presence of two of the following:
fever, leukopenia and leukocytosis (which is WBC count less than
5000 cells/mm3 or 10,000 cells/mm3), or purulent-appearing sputum
or ET aspirate. Other clinical manifestations used by the Centers for
Disease Control and Prevention (CDC) include change in mental
status, increase in respiratory secretions, new onset of dyspnea or
cough, rales, and adventitious bronchial lungs sounds. Another
criterion by the CDC is at least one positive result from a blood
culture or pleural fluid, or bronchoalveolar culture. The risk factors
for HAP are multifactorial from severe illness related to
comorbidities, hemodynamic compromise, and depressed immune
system. The use of conventional treatment modalities such as
antibiotics, corticosteroids, sedatives, and acid-relieving
medications (proton pump inhibitors and histamine blockers),
which increase gram-negative colonization of the aerodigestive
tract, artificial airway in the trachea, and respiratory therapy
equipment (e.g., mechanical ventilation where bacteria can be

906
inhaled from aerosols) also increase the risk of HAP.

Aspiration pneumonia
Aspiration pneumonia occurs when oropharyngeal flora or gastric
material are aspirated into the lower respiratory tract resulting
from dysphagia or impaired coughing mechanisms. Aspiration
pneumonia can lead to ALI, ARDS, empyema, or lung abscess. The
patient population at highest risk is the older adult population.
Other predictors of aspiration pneumonia in older adults include
COPD, congestive heart failure, tube feeding, delirium, immobility,
cerebrovascular accident, GERD, and obesity. Pathogens
associated with aspiration pneumonia are gram-negative bacilli,
given gastric pH-altering medications, anaerobes, and
Staphylococcus aureus.

Ventilator-associated pneumonia
A patient who acquires pneumonia more than 48 hours following
ET intubation and initiation of mechanical ventilation may be
classified as having VAP. VAP is associated with increased
duration of ET intubation, mechanical ventilation, intensive care
stay, and hospital cost (approximately $99,600 per case). Hospital
mortality of mechanically ventilated patients who develop VAP is
46% compared with 32% for those without VAP, with 4.4% of
deaths occurring at day 30 and 5.9% on day 60 in 2011. In 2010, the
National Healthcare Safety Network (NHSN) facilities reported
more than 3525 VAP cases. VAP incidence for hospital units ranged
from 0.0 to 5.8 per 1000 ventilator days; a very broad range,
indicative of a problem with consistency of reporting. Currently,
there is no valid, reliable definition for VAP. The most widely used
VAP definitions and criteria were evaluated and were found to be
neither sensitive nor specific.

Ventilator-associated events
Surveillance for VAEs by the NHSN was limited to VAP until 2013.
In 2011, the Centers for Disease Control and Prevention composed a
Working Group of key stakeholder organizations to evaluate the
limitations of the NHSN pneumonia definitions and to develop a

907
more reliable approach to VAE surveillance by the NHSN. A VAE
surveillance algorithm was developed by the Working Group and
implemented by the NHSN in January 2013. The approach is based
on measurable, simplified, and “automation-friendly” criteria
designed to identify a comprehensive list of conditions and
complications associated with adult patients who are mechanically
ventilated. The three tiers of the VAE algorithm include: ventilator-
associated condition, infection-related ventilator-associated
complication, and possible and probable VAP. The Centers for
Medicare and Medicaid Services has recognized VAP as a
preventable illness when appropriate patient care is provided. The
key components for improvement in outcomes of patients who are
mechanically ventilated are defined within the “ventilator bundle”
developed by the Institute for Healthcare Improvement. The
evidence-based practices include elevation of the head of the bed,
daily sedation vacation and assessment of readiness to extubate,
peptic ulcer disease prophylaxis, daily oral care with chlorhexidine,
and deep venous thrombosis (DVT) prophylaxis.

Assessment
Goal of system assessment
Identify ineffective breathing patterns, impaired gas exchange, and
airway obstruction. Findings are influenced by the patient’s age,
extent of the disease process, underlying medical condition, and
pathogen involved. Severity of pneumonia should be determined
following initial assessment and diagnostic testing.

History and risk factors

In addition to the risk factors listed in Table 4-5, any factor that
alters the integrity of the lower airways, thereby inhibiting ciliary
activity, increases the likelihood of pneumonia. Impairment of the
“mucociliary elevator” system impairs the ability of the patient to
move secretions from the airways to the oral cavity for
expectoration. These factors include hypoventilation, hyperoxia
(increased Fio2), hypoxia, airway irritants such as smoke, and the
presence of an artificial airway.

908
Cough
• Can be unrelenting and severe; may induce vomiting in some
patients.

• May be productive, weak, strong, or dry (nonproductive).

• Sputum varies in color depending on pathogen and degree of

inflammation (yellow, green, rust, brown; blood-tinged with
severe inflammation).

• May be associated with pleuritic chest pain.

Chest radiograph
• Determines presence of pneumonia, but initial radiograph finding
is often negative if the patient is dehydrated.

• Reflects infiltrates (abnormal “white” areas) in various patterns,

reflective of abnormal fluid distribution in the lungs; can be
mistaken for heart failure.

Vital signs
• Fever occurs in response to infection; some patients are not
febrile, especially if being cooled or on continuous renal
replacement therapy.

• Pulse oximetry: Oxygen saturation is decreased from the patient’s

normal baseline value.

• P/F ratio (ratio of arterial O2 tension to fractional inspired O2) is

decreased when O2 therapy is applied.

• Tachycardia and tachypnea are present if pneumonia is moderate

to severe.

• Hypotension may be present if sepsis is ensuing; hypotension is

exacerbated by underlying dehydration often present in patients
with pneumonia.

909
• Hypovolemia alone may prompt tachycardia.

Observation
• Nasal flaring and expiratory grunt may be present.

• Use of accessory chest and abdominal muscles indicates

respiratory distress.

• May appear fatigued, with or without diaphoresis if coughing has

been relentless.

• Ashen, pale, or gray/blue facial color, lip color, or nail beds.

• Chest expansion may be decreased, restricted, or asymmetrical

with severe pneumonia in one lung manifesting severe atelectasis
or pleuritic pain.

• Altered level of consciousness (confusion, disorientation, and

agitation) is more common with older adults.

• Agitation is more commonly associated with hypoxemia, whereas

somnolence is associated with hypercarbia (elevated CO2 level).

Auscultation
• Decreased or bronchial breath sounds.

• High-pitched inspiratory crackles heard best after the patient

coughs.

• Low-pitched inspiratory crackles caused by airway secretions.

Palpation
• Palpate chest wall for tenderness indicative of inflammation.

• Palpate to assess for symmetry of chest expansion.

Percussion

910
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).

Screening labwork
• CBC: Evaluates for elevated WBCs indicative of infection.

• Sputum Gram stain, culture, and sensitivity: Identifies infecting

organism.

• Blood culture and sensitivity: If result is positive, it indicates that

the pneumonia organism has migrated into the bloodstream to
cause a systemic infection.

• ABG analysis: Evaluates for hypoxemia and hypercapnia.

Diagnostic Tests for Acute Pneumonia

Abnormal
Test Purpose
Findings
Arterial Oxygenation status and acid-base balance are evaluated pH changes:
blood gas with ABGs. Acidosis may
(ABG) reflect
analysis respiratory
failure; alkalosis
may reflect
tachypnea.
Carbon
dioxide:Elevated
CO2 reflects
respiratory
failure;
decreased CO2
reflects
tachypnea.
Hypoxemia: Pao2
less than 80 mm
Hg.
Oxygen saturation:
Sao2 less than
92%.
Bicarbonate: HCO3
less than 22
mEq/L.
Base deficit: less
than −2.
Complete Evaluates for presence of infection. Increased white

911
blood count blood cell (WBC)
(CBC) count: less than
11,000/mm3 is
seen with
bacterial
pneumonias.
Normal or low
WBC count: Seen
with viral or
mycoplasma
pneumonias.
Sputum Identifies infecting organism. Gram stain
Gram stain, A sputum culture should be obtained from the lower positive:
culture, and respiratory tract before initiation of antimicrobial Indicates
sensitivity therapy. The most reliable specimens are obtained via organism is
bronchoalveolar lavage (BAL) during bronchoscopy, present.
suctioning with a protected telescoping catheter (mini- Culture: Identifies
BAL), or open-lung biopsy (used occasionally to reduce organism.
contamination of specimen with oral flora). Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.
Blood culture Identifies whether pneumonia organism has become Secondary
and systemic; blood cultures help to identify the causative bacteremia: A
sensitivity organism. frequent finding;
patients with
bacteremia are at
higher risk for
developing
respiratory failure.
Serologic Acute and convalescent titers are drawn to diagnose viral Increased antibody
studies pneumonia. Both serologic and urine tests are available for titers: A positive
Legionnaires’ pneumonia. sign for viral
infection.
Acid-fast To rule out mycobacterial infection (e.g., tuberculosis). Positive:
stain Mycobacterial
infection is
present.
Chest Identifies anatomic involvement, extent of disease, presence Lobar: Entire lobe
radiograph of consolidation, pleural effusions, or cavitation. involved.
Segmental
(lobular): Only
parts of a lobe
involved.
Bronchopneumonia:
Affects alveoli
contiguous to
the involved
bronchi.
Diagnostic Obtains specimens during simple bronchoscopy without Gram stain
fiber optic contaminating the aspirate; modified technique (mini-BAL) positive:
bronchoscopy is also effective without the need of full bronchoscopy. Indicates
using a PSB organism is
(protected present.
specimen Culture: Identifies

912
 brush) and organism.
BAL Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.
Thoracentesis Removal of pleural effusion fluid from the pleural space Gram stain
using a needle to drain the chest cavity. Pleural effusion positive:
fluid may be cultured following thoracentesis to identify Indicates
the causative organism. organism is
present.
Culture: Identifies
organism.
Sensitivity:
Reflects
effectiveness of
drugs on
identified
organism.

Pneumonia management strategies are based on the

recommendations of the Infectious Disease Society of America
(IDSA), the American Thoracic Society (ATS), the American Society
of Emergency Room Physicians, The Joint Commission as part of
the Core Measures (revised July 25, 2014), and are endorsed by the
Centers for Medicare and Medicaid Services.

PNEUMONIA MEASURES*

Indicators Measure
Appropriate PN-6: Initial antibiotic is appropriate for community-acquired pneumonia in
antibiotic immunocompetent patients
selection
Appropriate PN-6A: Initial antibiotic selection for community-acquired pneumonia in an
antibiotic immunocompetent patient-intensive care unit patient
selection
Appropriate PN-6B: Initial antibiotic selection for community-acquired pneumonia in an
antibiotic immunocompetent patient-non–intensive care unit patient
selection
Blood PN-3A: Blood cultures performed within 24 hours before or 24 hours after
cultures hospital arrival for patients who were transferred or admitted to the intensive
drawn care unit within 24 hours of hospital arrival
*
Criteria to include vaccinations PN-2 (pneumococcal vaccination) and PN-7
(influenza vaccination) were retired effective 1 January 2012. These measures have
been replaced with the two immunization measures from The Joint Commission that
are applicable to all patients regardless of diagnosis, rather than restricting the need
for the vaccinations to patients with community-acquired pneumonia.
Retrieved from www.jointcommission.org/pneumonia/

913
Collaborative management

Care priorities

1. Relieve hypoxemia

• Oxygen therapy: Administered when the patient has an SpO2 less

than 92% or exhibits symptoms of air hunger or respiratory
distress. Hypoxic drive, which contributes to the compensatory
mechanisms needed for effective breathing in patients with
COPD who retain CO2, can be lost with aggressive oxygen
therapy. For patients with chronic CO2 retention, O2 is delivered
in low concentrations while O2 saturation (SpO2) is closely
monitored. Once the patient’s SpO2 exceeds the 88% to 92%
range, the contributions of both hypoxic drive and hypoxic
pulmonary vasoconstriction to maintaining stability are lost.
Carbon dioxide dilates the pulmonary vasculature, while
pulmonary arteries constrict in the presence of hypoxia.
Identifying and maintaining the individual patient’s balance
between ventilation and perfusion optimizes gas exchange. The
healthcare provider should be consulted for measurements of
“acceptable” O2 saturation values in any patient with CO2
retention. Patients in need of higher-level O2 may be considered
for noninvasive, positive-pressure ventilation to help reduce
work of breathing. Increased work of breathing indicates that the
patient is having difficulty supporting ventilation.

• Intubation and mechanical ventilation: Intubation may be

necessary if a patient experiences progressive respiratory distress
despite treatments or if the patient becomes severely hypercapnic
(CO2 level greater than 50 mm Hg in normal patients; CO2 level
possibly greater than 70 mm Hg in patients who retain CO2).
Mechanical ventilation is indicated if the patient in respiratory
distress is unable to maintain an adequate PaO2 (PaO2 greater than
60 mm Hg) with supplemental O2. High concentrations of O2 and
PEEP may be necessary in severe cases of pneumonia that lead to
acute respiratory failure. (See the section on Acute Respiratory

914
 Failure.)

2. Determine severity of pneumonia

Mortality rates for severe pneumonia range from 20% to 53%. The
IDSA/ATS criteria for severe CAP are the presence of any single
measurement as follows:

• RR greater than 30 breaths/min.

• Systolic BP less than 90 mm Hg.

• Diastolic BP less than 60 mm Hg.

• Bilateral or multilobar involvement on chest radiograph.

• P/F ratio (ratio of PaO2 to Fio2) less than 250.

• Confusion/disorientation.

• Urine output less than 20 mL/h or a total output of less than 80

mL/h over 4 hours.

• Acute renal failure.

• A 50% increase in size of the pulmonary infiltrate during the first

48 hours following diagnosis.

• Thrombocytopenia.

• The patient requires ET intubation and mechanical ventilation.

• Septic shock.

• Leukopenia.

• Hypothermia (core temperature less than 36° C).

3. Control infection

• Antibiotics or antiinfectives: Prescribed empirically on the basis of

presenting signs and symptoms, clinical findings, and chest

915
 radiograph results until sputum or blood culture results are
available. Pneumococcus is the most common pathogen associated
with CAP, whereas enteric gram-negative bacteria are the most
common pathogens identified with HAP. Pseudomonas aeruginosa
and methicillin-resistant Staphylococcus aureus are the most
common organisms seen in patients on long-term mechanical
ventilation. Antimicrobial therapy in patients who are critically ill
is usually parenteral and guided by sensitivity of the causative
organism. Many of the organisms responsible for nosocomial
pneumonias are resistant to multiple antibiotics or antimicrobials.
Proper identification of the organism, determination of sensitivity
to the medication, and attainment of therapeutic drug levels are
crucial for effective therapy.

• Isolation: Some patients with pneumonia may require isolation

and transmission-based precautions.

4. Control cough
Antitussives are used to relieve coughing. Occasionally, narcotics
such as codeine are required if coughing is unrelieved by other
agents. Patients receiving narcotics for pleuritic or other pain
control may experience a reduction in coughing as a beneficial side
effect of the narcotics. If cough is productive, adding an expectorant
to help manage thicker secretions may assist the patient. Additional
IV or enteral fluids may also help thin secretions by augmenting
overall hydration. Coughing should be controlled to a reasonable
level, but not at the expense of expectorating sputum.

5. Provide hydration
IV fluids may be necessary to replace insensible fluid loss and help
thin secretions (e.g., tachypnea, diaphoresis with fever), in addition
to providing enteral fluids. Volume resuscitation for dehydration
must be done carefully to avoid volume overload in patients with
multiple comorbidities. Dehydration causes secretions to become
thick, tenacious, and difficult to expectorate.

6. Reduce fever
Analgesic antipyretics such as acetaminophen are used to reduce

916
body temperature. Aspirin is generally not used for temperature
control.

7. Provide pain relief

Analgesics are used to relieve pleuritic pain. Patients with
pneumonia may have substantial pleuritic pain that requires
administration of narcotic analgesics for relief. When opiates (e.g.,
codeine, morphine sulfate, and meperidine) are given, varying
degrees of respiratory depression occur, but these agents are also
generally effective in controlling severe coughing, which
contributes to pain and discomfort. Careful and frequent
monitoring of the patient’s RR and depth, as well as O2 saturation
via pulse oximetry, is necessary.

8. Support nutritional status

Malnutrition is a causative factor in the development of infections.
In patients who are severely ill, enteral nutrition may provide the
best protection against the development of sepsis, owing to
probable prevention of bacterial translocation from the gut. A
nutritional therapy consultation is warranted for all patients who
have developed an infection and those at high risk of infection.

9. Relieve congestion
Percussion and postural drainage are indicated if deep breathing,
coughing, hydration (either enteral or parenteral fluids), and
moving about in bed or ambulation are found to be ineffective in
raising and expectorating sputum. Consult with the respiratory care
provider as indicated.

INSTITUTE FOR HEALTHCARE IMPROVEMENT (IHI) VENTILATOR-

ASSOCIATED PNEUMONIA (VAP) BUNDLE

917
Retrieved from www.jsicm.org/pdf/VAPbundle2010kaitei_ENGLISH.pdf.

Care plans for acute pneumonia

Risk for injury 
related to respiratory compromise present with pneumonia
Goals/Outcomes: The patient is free of infection reflected by
normothermia and negative culture results; WBC count is within
normal limits for the patient; and sputum is clear to white in color.
Infection Severity, Infection Protection.

Infection control

1. Implement standard precautions for infection prevention.

2. Provide additional infection control measures if infecting

organism requires isolation.

3. Maintain a closed or in-line suction system or an aseptic

environment when suctioning the secretions from the patient.

4. Inform visitors of effective precautions or pertinent isolation

procedures.

5. Encourage and help provide turning, coughing, deep breathing,

and use of incentive spirometer. Educate significant others to assist

918
with these activities.

6. Encourage and assist with ambulation as soon as possible.

Infection risk

1. Identify presurgical patients at increased risk for nosocomial

pneumonia.

2. Provide presurgical patients and significant others with verbal

and written instructions and demonstrations of turning, coughing,
and deep-breathing exercises performed after surgery to prevent
atelectasis, which may lead to pneumonia.

3. Postoperatively encourage lung expansion: turning and

repositioning in bed, deep breathing, and coughing at frequent
intervals. Mobilization of secretions is facilitated by movement.

4. Encourage and assist with ambulation as soon as possible.

5. Recognize the following ways in which nebulizer reservoirs can

contaminate the patient: introduction of nonsterile fluids or air;
manipulation of nebulizer cup; or backflow of condensation into
reservoir or into the patient when delivery tubing is manipulated.

6. Use only sterile fluids and dispense them aseptically.

7. Recognize and manage risk factors for patients with

tracheostomy or ET tubes and patients who are mechanically
ventilated:

• Presence of underlying lung disease or other serious

illness.

• Colonization of oropharynx or trachea by aerobic

gram-negative bacteria.

• Greater access of bacteria to lower respiratory tract.

919
• Cross-contamination is more likely with
manipulation of these tubes.

• Change breathing circuits when visibly dirty or

damaged; frequent changes to circuits is not
advisable.

• Use “no-touch” technique, or use sterile gloves on

both hands until a new tracheostomy wound has
healed or formed granulation tissue around the
tube.

• Suction on an “as needed” rather than a routine

basis. Frequent suctioning increases the risk of
trauma and cross-contamination.
8. For patients who cannot remove secretions effectively by
coughing, perform procedures that stimulate coughing such as
chest physiotherapy, which includes breathing exercises, postural
drainage, and percussion.

9. If pain interferes with lung expansion, control it by administering

as-needed analgesics approximately 30 minutes before deep-
breathing exercises, and provide splint support of wound areas
with hands or pillows placed firmly across site of incision.

10. Identify patients at risk for aspiration, such as those with a

decreased level of consciousness or dysphagia or who have a
nasogastric or gastric tube in place.

11. For patients with decreased level of consciousness who are

unable to eat normally, consult with the physician regarding the
need for a method of enteral feeding in which risk of aspiration is
minimal such as postpyloric feeding (e.g., weighted small-bore
feeding tube that imports enteral feeding to the duodenum) or
percutaneous endoscopic gastrostomy (PEG tube).

920
12. Elevate the head of the bed to at least 30 degrees during
feedings and for 1 hour after any feeding or medication to reduce
the risk of aspiration.

Deficient fluid volume 

related to insensible fluid losses associated with pneumonia
Goals/Outcomes: The patient is normovolemic reflected by no
clinical evidence of hypovolemia (e.g., furrowed tongue), stable
weight, BP within the patient’s normal range, if available central
venous pressure (CVP) 2 to 6 mm Hg, pulmonary artery pressure
(PAP) 15 to 30/8 to 15 mm Hg, cardiac output 4 to 8 L/min, mean
arterial pressure 70 to 105 mm Hg, HR 60 to 100 bpm, and systemic
vascular resistance (SVR) 800 to 1200 dynes/s/cm−5.
Fluid Balance; Electrolyte; Acid-Base Balance.

Fluid management

1. Identify patients at risk for dehydration, including those with

poor nutritional status, reduced fluid intake, history of severe
coughing (may be associated with inability to eat and/or vomiting),
increased insensible loss secondary to hyperventilation, fever, and
use of supplemental O2.

2. Monitor input and output hourly. Initially, intake should exceed

output during volume replacement therapy. Consult appropriate
provider for urine output less than 0.5 mL/kg/h for 2 consecutive
hours.

3. Monitor vital signs and hemodynamic pressures for signs of

continued hypovolemia. Be alert to decreased values in BP, CVP,
PAP, cardiac output, and mean arterial pressure, as well as
increased HR and SVR.

4. Weigh the patient daily, at the same time of day (preferably

before breakfast), on a balanced scale, with the patient wearing the
same type of clothing. Use the same number of linens and
equipment in place for bed weights.

5. Administer fluids by mouth (PO) and IV as prescribed.

921
Document the patient’s response to fluid replacement therapy.

6. Monitor for signs and symptoms of fluid overload or too-rapid

fluid administration: crackles (rales), shortness of breath,
tachypnea, tachycardia, increased CVP, increased PAPs, jugular
vein distention, and edema.

Aspiration Precautions; Chest Physiotherapy; Cough

Enhancement; Environmental Management; Fluid/Electrolyte
Management; Fluid Monitoring; Hypovolemia Management;
Infection Control; Intravenous Therapy; Mechanical Ventilation;
Nutrition Management; Positioning; Surveillance; Respiratory
Monitoring; Vital Signs Monitoring.

Additional nursing diagnoses

Also see Drowning (Chapter 3), and Acute Asthma Exacerbation
(Chapter 4). As appropriate, see nursing diagnoses and
interventions in Nutrition Support (Chapter 1), Acute Respiratory
Failure (Chapter 4), Mechanical Ventilation (Chapter 1), Prolonged
Immobility (Chapter 1), and Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2).

Acute respiratory failure

Pathophysiology
The primary goal of the pulmonary system is to promote
appropriate and reasonable gas exchange at the alveolar-capillary
surface, which is most often measured by pulse oximetry and
ABGs. Acute respiratory failure is a general term that identifies a
primary lung dysfunction, resulting in failure to remove CO2
(known as hypoventilation) and/or failure to promote appropriate,
proportionate O2 uptake at the alveolar-capillary interface.
Ventilation and perfusion must “match” to ensure the oxygen is
able to appropriately diffuse across an intact alveolar-capillary
membrane and attach to the hemoglobin carried on red blood cells.
Saturation of hemoglobin with oxygen (oxyhemoglobin) in the

922
lungs is the first step to oxygen delivery to the tissues. Carbon
dioxide must also diffuse from the bloodstream into the alveoli to
be exhaled. Type I respiratory failure (hypoxemic) is oxygenation
failure, whereas type II (hypercapnic) is ventilation failure. Many
patients manifest respiratory failure of types I and II
simultaneously. Clinically, type I failure exists when PaO2 is less
than 50 mm Hg with the patient at rest and breathing room air (Fio2
0.21 or 21% of the atmospheric pressure, which is 760 mm Hg at sea
level). Paco2 greater than 50 mm Hg is significant for acute
ventilation failure or hypercapnia. The PaO2 provides the “driving
pressure” for the saturation of hemoglobin. Without adequate
pressure (PaO2), the hemoglobin is inadequately saturated.
Approximately 98% of the oxygen delivered to tissues is provided
by oxyhemoglobin. The amount of oxygen combined with
hemoglobin depends on the PaO2. The relationship is articulated
within the oxyhemoglobin dissociation curve.
Carbon dioxide is transported in three main forms: (1) in simple
solution, (2) as bicarbonate, and (3) combined with protein of
hemoglobin as a carbamino compound. Under healthy conditions,
the amount of carbon dioxide produced by the tissues is constant
and equals the amount of carbon dioxide eliminated by the lung. A
wide variety of disease states creates a single or mixed respiratory
failure; some affecting ventilation, others, perfusion. One of the
simplest methods of evaluating patients relates to the
understanding of basic gas exchange. Oxygenation occurs primarily
during inspiration and the removal of CO2 occurs during
exhalation. The basic concepts applied here include compliance and
recoil. Lung compliance is the measure of expansion of the alveoli
(the gas-exchanging surface), which occurs on inspiration, whereas
elasticity refers to the ability of the alveoli to recoil, as they do on
exhalation. Restrictive airway diseases [generally] present with
significant hypoxemia, whereas obstructive disorders are more
likely to develop a persistent and chronic hypercapnia. See Box 4-1
for a description of some of the disease processes that can lead to
acute respiratory failure.
The evaluation of respiratory failure includes the understanding
of the following:

923
Ventilation and perfusion matching ( match)
This general term refers to the relationship of gas distribution ( )
to the amount of blood ( ), which passes the total alveolar
surface in 1 minute of time. Normal alveolar ventilation occurs at a
rate of 4 L/min, and normal pulmonary vascular blood flow occurs
at a rate of 5 L/min. The normal ratio is therefore 4 L/min
divided by 5 L/min, or a ratio of 0.8, almost in a 1:1 ratio. Any
disease process that interferes with either side of the equation
upsets the physiologic balance, causing a mismatch.

Components of an abnormal ratio

Alveolar dead space ventilation: This is a primary problem with

pulmonary perfusion. Areas where alveoli expand, but have less
than normal blood surrounding the alveoli are called “dead
spaces” because gas exchange is impaired rendering the area
functionally “dead.” Alveoli may be compliant and elastic,
normal or hyperventilated, with perfusion proportionately lower
than the ventilation. The imbalance is measured or evaluated as a
high mismatch, wherein ventilation is proportionately
greater than perfusion. Because perfusion is the problem,
underlying causes are often low cardiac output states resulting
from pump impairment, or vascular occlusion impairing blood
flow, such as seen with pulmonary embolus. Ventilatory causes
involve overventilation of the independent lung surface.

Diffusion distance: Governed by the “thickness” of the alveolar-

capillary membrane. O2 and CO2 must cross the barrier created
by the alveolar epithelium, the interstitial space, and the capillary
endothelium. That space between is typically fluid-free and
product-free, allowing gas to move rapidly across. Diffusion is
affected when an increase in anatomic distance and/or product
(fluid, proteins, and neutrophils) alters the ability of gas exchange
between alveoli and the capillary bed. Pulmonary edema is a
major problem that interferes with diffusion, because it increases
the “diameter” or thickness of the alveolar-capillary membrane.

924
Volume of CO2: The volume of CO2 produced by the body tissues
varies with metabolic rate (fever, pain, agitation, sepsis, and so
forth). The Paco2 must be interpreted in conjunction with the
volume exhaled, especially in patients who are mechanically
ventilated. Many of the variables impacting CO2 flux can be
eliminated by controlling ventilation and muscular activity.
Current evidence supports that the overdistension and shear
force of opening-closing also profoundly affect the healthy lung.

Intrapulmonary right-to-left shunt: Large amounts of blood pass

from the right side of the heart (receives the deoxygenated
venous blood) to the left side of the heart without adequate
saturation of hemoglobin with oxygen in the lungs. Poorly
oxygenated blood passes in and out of the general circulation,
impacting the amount of oxygen available to the cells. This
process occurs when alveoli are not recruited on inspiration
resulting from atelectasis or the alveoli are flooded with fluid.
Primary causes of intrapulmonary shunt are atelectasis and
ARDS.

Assessment
Goal of system assessment
To evaluate for poor gas exchange and increased ventilatory
support requirements (see sections on Acid-Base Balance and
Mechanical Ventilation, Chapter 1).

History and risk factors

Indicators of acute respiratory failure vary according to the
underlying disease process and severity of the failure. Acute
respiratory failure is one of the most common causes of altered
mental status and agitation. Respiratory failure is often associated
with heart failure, pneumonia, or stroke. Sometimes, the onset of
acute respiratory failure is so insidious it is missed or
misinterpreted, similar to the insidious onset of shock in some
patients. A patient may be somnolent attributable to hypercapnia
(CO2 retention causing elevated CO2) from ventilatory failure, or

925
agitated and combative as a result of hypoxia. Patients with COPD
have reduced airway diameter as well as chronic inflammation and
airway remodeling, and when the underlying chronic condition is
exacerbated, mucus hypersecretion and airway edema compound
the initial condition. Increased effort is needed to mobilize gas in
and out of the lungs, particularly during exhalation. The failure to
exhale leads to air trapping and hyperinflation, which further
compromise inspiratory effort and contribute to increasing hypoxia
and hypercapnia. Patients with impending shock are at high risk
for respiratory failure. Inhalation of toxic substances, pneumonia,
severe pneumonitis, aspiration of gastric contents, drowning, and
air or fat embolus may prompt respiratory failure. Other causes
include acute pancreatitis, drug overdose, neurologic injury,
hemorrhage, sepsis, extreme obesity, or any condition that has
enlarged the abdomen to the point of exerting upward pressure on
the diaphragm.

Vital signs
• Early indicators: Dyspnea, restlessness, anxiety, headache,
fatigue, cool and dry skin, increased BP, tachycardia, and
persistent rapid RR, which indicate hypoxia. Hypercapnia results
in slurred speech and headache.

• Intermediate indicators: Confusion, profound lethargy,

tachypnea, hypotension and somnolence (if pH is less than 7.25),
and cardiac dysrhythmias.

• Late indicators: Cyanosis, diaphoresis, coma, and respiratory

arrest.

A patient with a history of chronic obstructive pulmonary

disease may increasingly or excessively use inhaled beta2-agonists.
If this is the case, evaluation of tachycardia may be indicative of
recent medication use.

926
Vital signs
• RR is rapid. If the patient is experiencing impending shock, RR is
compensatory for metabolic acidosis.

• Rapid HR if not receiving beta-antagonist therapy (beta-blockers).

• Spo2 is lower than expected when reviewing O2 support. Analysis

of the PaO2/Fio2 ratio may reveal a value of less than 300.

A-a gradient/A-aDO2/P(A-a)o2

• The A-a gradient or alveolar-arterial O2 tension difference is a

clinically useful calculation. The calculation is based on a model
as though the lung were one large alveolus and the entire blood
flow of the right side of the heart passed around it. Using the
rules of partial pressure as well as the laws of CO2 production at
the cell and the content of CO2 exerting alveolar pressure, the
theoretical alveolar Po2 (PaO2) is calculated. Once the theoretical
PaO2 has been calculated, the gradient is achieved by subtracting
the measured arterial PaO2. The calculated “gradient” represents
the difference between the calculated alveolar oxygen (PaO2) and
the measured arterial oxygen (PaO2).

• When the Fio2 is greater than 0.21, the A-a gradient becomes less
accurate as in the measurement of proportional gas exchange,
although the difference should always be less than 150 mm Hg.

• Extrapulmonary failure: The A-a gradient generally remains

normal or narrow.

• With shunt or mismatch, the gradient is usually wider than

normal. The A-a gradient also measures the severity of gas
exchange impairment. At any age, an A-a gradient greater than
20 mm Hg on room air or greater than 100 mm Hg on increased

927
 Fio2 should be considered abnormal and indicative of pulmonary
dysfunction.

Observation
• Nasal flaring and expiratory grunt may be present.

• Use of accessory muscles indicates respiratory distress.

• May appear fatigued, with or without diaphoresis.

• May present with ashen, pale, or gray/blue facial color, lip color,
or nail beds.

• Chest expansion may be decreased, restricted, or asymmetrical

with severe changes in one lung manifesting severe atelectasis or
pleuritic pain.

• Altered level of consciousness (confusion, disorientation, and

agitation) is more common with older adults but is a very
significant sign in any age group.

• Agitation is more commonly associated with hypoxemia, whereas

somnolence is associated with hypercarbia (elevated CO2 level).

Auscultation
Evaluate the presence of normal breath sounds and synchronous
lung expansion. Auscultate for the presence of:

1. Late inspiratory rales (crackles): Anterior, lateral, and posterior:

alveolar fluid or late opening.

2. Midinspiratory rales (crackles): Anterior, lateral, and posterior

alveolar consolidation.

3. Early loud, coarse rales (bubbles or rhonchi): Anterior, lateral,

and posterior: conducting airway inflammation and mucus
secretion.

928
4. Inspiratory wheezes: Anterior, lateral, and posterior: early airway
narrowing.

5. Expiratory wheezes: Anterior, lateral, and posterior: late airway

narrowing.

Palpation
• Palpate chest wall for tenderness indicative of inflammation.

• Palpate to assess for symmetry of chest expansion.

Percussion
• May reveal presence of consolidation or fluid (dullness) or
hyperresonance (pneumothorax).

Screening labwork
• Blood gas evaluation can determine primary and secondary
problems, or primary problems with compensation (see Acid-
Base Balance, Chapter 1).

• Pulse oximetry is used for continuous monitoring of O2

saturation.

• Sputum Gram stain, culture, and sensitivity: Identifies infecting

organism.

• Blood culture and sensitivity: If result is positive, it may indicate

that the organism has migrated into the bloodstream to cause a
systemic infection.

• ABG analysis: Evaluates for hypoxemia and eventually

hypercapnia.

Diagnostic Tests for Acute Respiratory Failure

929
Collaborative management
Careful consideration should be given to evaluate neurologic
conditions and OSA because these are commonly overlooked
causes of respiratory failure. In addition, the primary goal is to
determine and treat the underlying pathophysiologic condition.

Care priorities

1. Correction of hypoxemia: First treatment priority

PaO2 levels less than 30 mm Hg for longer than 5 minutes may
cause permanent brain damage or death. High-concentration O2
therapy, in conjunction with pharmacotherapy (e.g.,
bronchodilators, steroids, antibiotics), often improves ABG levels
sufficiently to remove the patient from danger, but increasing Fio2 is
a temporary solution and does not actually treat the problem.
Adding additional molecules of oxygen improves the diffusion
gradient from the alveolus into the capillary, and provides “driving
pressure” for the saturation of hemoglobin with oxygen. Patients
with COPD who chronically retain CO2 (chronic hypercapnia) are
unable to receive high concentrations of O2 unless ventilation is
highly supported with an underlying rate control strategy such as

930
NPPV or NiPPV, CPAP or BiPAP, or invasive mechanical
ventilation.

2. Correction of respiratory acidosis (hypercapnia)

May be corrected using NPPV such as BiPAP, or invasive
mechanical ventilation following ET intubation. Exhalation time
should be increased and particular attention to that time must be
applied when altering tidal volume or RR. Because CO2 is removed
during exhalation time in the respiratory cycle, any patient with
CO2 retention must be provided with a longer E time.

• Noninvasive (NPPV): Ventilator support that is given without ET

intubation or tracheotomy. Administered via a face or nasal
mask. Requires skilled management but not necessarily intensive
care admission. NPPV or invasive mechanical support is used as
a continuous replacement for normal lung function until the
underlying cause of the failure can be corrected and the patient
can resume ventilatory efforts independently.

• Invasive: Mechanical ventilation delivered using an ET tube or

tracheotomy; requires intensive or high-acuity care. The purposes
of intubation and mechanical ventilation are to restore alveolar
ventilation and systemic oxygenation, provide compensation in
metabolic acidosis/alkalosis, and decrease work of breathing.
Early intubation can prevent further airway collapse and tissue
injury. In most cases of respiratory failure, the patient will require
intubation and mechanical ventilation to support adequate
respiratory function and stabilize ABG levels. (See Mechanical
Ventilation, Chapter 1.)

3. Correction of acidotic ph as a result of hypercapnia

(hypoventilation)
Adequate cellular and metabolic functioning are hindered when pH
level remains outside the normal range of 7.35 to 7.45. When the pH
is less than 7.20, evaluate for signs of systemic compromise such as
failure to maintain vascular tone and therefore BP. After efforts to
correct ventilation have failed or if the patient presents with clinical
symptoms such as hypotension refractory to volume and

931
vasopressors, IV sodium bicarbonate may be used conservatively to
return the pH to a level higher than 7.25. The use of sodium
bicarbonate is a short-term solution for most acid-base disturbances
and its use may actually make the overall situation worse.

4. Correction of alkalotic pH as a result of hypocapnia

(hyperventilation)
A pH greater than 7.45 may indicate primary hyperventilation with
a high minute ventilation (F or VT). If possible, assess the patient for
anxiety and rapid RR. If the patient is intubated, assess the settings
on the ventilator to assure that an appropriate method is being
used.
If the minute ventilation is not the causative problem or cannot
be adjusted, evaluate for a primary metabolic alkalosis. Causative
factors of primary metabolic alkalosis may be overdiuresis,
diarrhea, or aggressive nasogastric drainage. The pH may be
managed by compensation with CO2 retention via a rebreathing
mask, decreasing minute ventilation, or by increasing dead space
on mechanical ventilator circuitry.

5. Provide nutrition support

Energy outlay with respiratory failure is high, in part because of the
increased work of breathing. If the patient is unable to consume
adequate calories with enteral feedings, total parenteral nutrition is
added. It is important to perform an occasional evaluation of the
patient’s caloric and metabolic needs to make certain that the
patient is being adequately nourished but not overfed. All efforts
should be made to feed enterally so the gut is used. Newer
elemental feedings require no digestion and can be used in the
stomach, duodenum, or jejunum. (See Nutrition Support, Chapter
1.)

4-6
RESEARCH BRIEF
Clinical research to evaluate the effectiveness of life support
systems in acute fatal illness has unique problems of logistics,

932
ethics, and consent. There have been 10 prospective comparative
trials of extracorporeal membrane oxygenation in acute fatal
respiratory failure, using different study designs. The trial designs
were prospective controlled randomized, prospective adaptive
randomized, sequential, and matched pairs. The trials were
reviewed with regard to logistics, ethics, consent, statistical
methods, economics, and impact. The matched pairs method is the
best study design for evaluation of life support systems in acute
fatal illness.
From Bartlett RH: Clinical research in acute fatal illness: lessons from extracorporeal
membrane oxygenation. J Intensive Care Med Sep 15;pii: 0885066614550278 [Epub ahead of
print], 2014.

Care plans for acute respiratory failure

Impaired gas exchange 
related to disease process underlying impending respiratory failure.
Goals/Outcomes: Within 2 to 4 hours of initiation of treatment,
the patient has adequate gas exchange reflected by PaO2 greater
than 80 mm Hg, Paco2 35 to 45 mm Hg, and pH 7.35 to 7.45 (or ABG
values within 10% of the patient’s baseline), with mechanical
ventilation, if necessary. Within 24 to 48 hours of initiation of
treatment, the patient is weaning or weaned from mechanical
ventilation, and RR is 12 to 20 breaths/min with normal baseline
depth and pattern.
Respiratory Status: Ventilation, Vital Signs Status;
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.

Respiratory monitoring

1. Monitor for signs of increasing hypoxia at frequent intervals:

restlessness, agitation, and personality changes are indicative of
severe exacerbation. Cyanosis of the nail beds (peripheral) and/or
lips (central) is an early and late indicator of hypoxia, respectively.

2. Monitor for signs of hypercapnia at frequent intervals: confusion,

listlessness, and somnolence may indicate respiratory failure or

933
near-fatal asthma exacerbation.

3. Monitor ABGs when continuous pulse oximetry values or patient

assessment reflects progressive hypoxemia or development of
hypercapnia. Be alert to decreasing PaO2 and increasing Paco2 or
decreasing O2 saturation levels, indicative of impending respiratory
collapse.

4. Monitor for synchronous, bilateral lung expansion, decreased

breath sounds, or changes in wheezing at frequent intervals. Absent
breath sounds in a distressed patient with asthma may indicate
impending respiratory arrest.

Anxiety reduction

1. Ascertain and alleviate the cause of restlessness to decrease

metabolic demands (e.g., if restlessness is related to anxiety, help
reduce anxiety by providing reassurance, enabling family members
to stay with the patient, and offering distractions such as soft music
or television).

2. Be aware that restlessness may be an early sign of hypoxemia.

3. Explain all procedures and offer support to minimize fear and

anxiety, which can increase O2 demands.

Oxygen therapy

1. Provide humidity in O2 if used for more than 12 hours to help

thin secretions.

2. Administer supplemental O2 using liter flow device as ordered.

3. Document pulse oximetry with O2 liter flow in place at time of

reading as ordered. Oxygen is a drug; the dose of the drug must be
associated with the O2 saturation or the reading is meaningless.

4. Monitor for skin breakdown where O2 devices are in contact with

934
the skin, such as nares, and around edges of mask devices.

5. Monitor Fio2 to ensure that O2 is within prescribed concentrations.

If the patient does not retain CO2, a 100% nonrebreather mask may
be used to provide maximal O2 support. If the patient retains CO2
and is unrelieved by positioning, lower-dose O2, bronchodilators,
steroids, intubation, and mechanical ventilation may be necessary
sooner than in patients who are able to receive higher doses of O2
by mask.

Ventilation assistance

1. Obtain ABGs if the patient experiences behavioral changes or

respiratory distress to check for hypoxia or hypercapnia.

2. Monitor for induced hypoventilation, especially in patients with

COPD.

3. Monitor for changes in chest radiograph and breath sounds

indicative of O2 toxicity and absorption atelectasis in patients
receiving higher concentrations of O2 (greater than 45% Fio2) for
longer than 24 hours. The higher the O2 concentration, the greater is
the chance of toxicity.

4. Position the patient for comfort and to promote optimal gas

exchange. High-Fowler’s position, with the patient leaning forward
and elbows propped on the over-the-bed table to promote maximal
chest excursion, may reduce use of accessory muscles and
diaphoresis resulting from work of breathing.

5. Consider use of NPPV before ET intubation and mechanical

ventilation.

Acid-Base Management; Acid-Base Monitoring; Airway

Management; Bedside Laboratory Testing; Cough Enhancement;
Emotional Support; Energy Management; Fluid Management; Fluid
Monitoring; Laboratory Data Interpretation; Mechanical
Ventilation; Oxygen Therapy; Positioning; Respiratory Monitoring;

935
Vital Signs Monitoring.

Additional nursing diagnosis

See sections relating to underlying pathologic condition of patients.
Refer to Mechanical Ventilation, Chapter 1, for further information.

Pneumothorax
Pathophysiology
Pneumothorax is an accumulation of air between the parietal and
visceral pleura with secondary lung collapse. There are three types
of pneumothorax: spontaneous, traumatic, and tension.

Spontaneous
A portion of the lung may spontaneously collapse, while the chest
wall remains intact with no leak to the atmosphere. Both primary
and secondary spontaneous pneumothoraces may result from the
rupture of a bleb or bullae on the visceral pleural surface, usually
near the apex, resulting in air entering the thorax. A primary
spontaneous pneumothorax is rarely life threatening and generally
occurs in healthy, 20- to 40-year-old lean, thin men who smoke. The
cause of the bleb/bullae rupture is unknown, although it may result
from a weakness related to a respiratory infection. Symptoms most
often occur at rest rather than with vigorous exercise or coughing.
There is a high probability for recurrence within 2 to 3 years.
A secondary spontaneous pneumothorax may occur in all age
groups resulting from an underlying lung disease (COPD, cystic
fibrosis, tuberculosis, malignant neoplasm). Symptoms are
more likely to be life threatening than with a primary spontaneous
pneumothorax, and recurrence rates are high in this population.
The rate of reabsorption of spontaneous pneumothoraces is 1.25%
to 1.8% of the volume of the hemithorax every 24 hours. A 15%
pneumothorax requires 8 to 12 days to fully resolve without
treatment.

936
Traumatic
The integrity of the chest wall may or may not be disrupted before
lung collapse in a pneumothorax resulting from trauma. An open
pneumothorax occurs when air enters the pleural space from the
atmosphere through an opening in the chest wall, such as with a
penetrating injury (includes stabbing, gunshot wound to the chest)
or an invasive medical procedure (e.g., lung biopsy, thoracentesis,
placement of a central line into a subclavian vein). A closed
pneumothorax occurs when the visceral pleura is penetrated but
the chest wall remains intact, with no atmospheric leak. Closed
chest wall lung collapse occurs with blunt trauma, including
cardiopulmonary resuscitation, when an external impact on the
chest fractures and dislocates the ribs (i.e., motor vehicle crash with
the chest hitting the steering wheel). It may also occur from the use
of high-level PEEP therapy. For more information about blunt chest
injuries, see Chest Trauma, Chapter 3.

Tension
Tension pneumothorax is a life-threatening medical emergency
most often associated with trauma or infection. Tension can ensue
with a spontaneous pneumothorax or during positive-pressure
mechanical ventilation. The integrity of the chest wall may or may
not be disrupted before lung collapse. Air enters the pleural space
during inspiration through a pleural tear and continues to
accumulate inside the pleural cavity. The air cannot escape during
expiration because the intrapleural pressure is greater than alveolar
pressure, which creates a one-way or flap-valve effect. The
increasing intrathoracic pressure is transmitted to the mediastinum,
resulting in a mediastinal shift toward the unaffected side. The
encroachment of the enlarging affected side makes it impossible for
the unaffected side to fully expand. The increased pressure also
compresses the vena cava, which impedes venous return, and
reduces preload/end-diastolic volume. Cardiac output is
progressively reduced while intrathoracic pressure and
compression of the vena cava increases, leading to circulatory
collapse if not promptly diagnosed and managed. Bilateral tension
pneumothoraces may occur and generally result in cardiac arrest
shortly after the lungs collapse.

937
Assessment
Goal of system assessment
Identify ineffective breathing patterns and impaired gas exchange.
The clinical presentation will vary in degree, depending on the type
and size of the pneumothorax. With tension pneumothorax,
evaluate for decreased cardiac output and decreased tissue
perfusion. See the section on Respiratory Assessment General:
(earlier in Chapter 4), and Cardiac Assessment: General (Chapter 5).

History and risk factors

Trauma, pulmonary infection, high-level positive-pressure
mechanical ventilation: Nearly 46% of patients with primary
pneumothoraces do not seek medical advice for more than 2 days.
Assessing for delay is important because the occurrence of
reexpansion pulmonary edema after reinflation may be related to
the length of time the lung has been collapsed.

Chest radiograph
• Determines presence of pneumothorax, usually estimated in
percentages depending on the size of the lung collapsed.

• Reflects absence of lung markers; includes absence of “white”

blood vessels.

• No circulation is present in collapsed area filled with air (black).

Vital signs
• Tachycardia, tachypnea.

• Possible fever.

• BP may increase or decrease, depending on response to any

changes in cardiac output, which are profound with tension
pneumothorax.

938
• Small pneumothoraces may not affect vital signs at all.

Observation/inspection

Spontaneous or traumatic pneumothorax

• Sudden onset of sharp, stabbing chest pain on the affected side,

radiating to the shoulder if pneumothorax is large enough
(greater than 20% collapse).

• The British Thoracic Society 2010 guidelines define “small” as a

pneumothorax of less than 2 cm and “large” as a pneumothorax
of greater than 2 cm between the lung margin and the chest wall
(at the level of the hilum). Percentages of lung that have
collapsed are also used to quantify the extent of lung collapse in
clinical practice.

• Moderate to severe dyspnea and anxiety may be present if

pneumothorax is large enough (greater than 30% collapse).

• Decreased chest wall movement on the affected side if the

pneumothorax is large enough (greater than 40% collapse).

• Pale appearance is likely with a larger pneumothorax (greater

than 50% collapse).

• With a small pneumothorax (10% to 20% collapse), the patient

may have no pain and no abnormality in chest wall movement
and be unaware that lung collapse has occurred.

Tension pneumothorax

• Severe dyspnea.

• Chest pain on affected side.

• Pale progressing to gray/blue, cool, clammy, mottled skin.

• Anxiety and restlessness resulting from progressive hypoxemia.

939
• Decreased chest wall movement on affected side.

• Expansion of affected side throughout respiratory cycle, rather

than expansion and relaxation.

• Progressively increasing jugular vein distention as vena cava is

compressed.

• Cardiac arrest is possible with bilateral tension pneumothoraces.

Palpation

Spontaneous or traumatic pneumothorax

• Subcutaneous emphysema (crepitus).

• Tactile and vocal fremitus decreased or absent on affected side.

Tension pneumothorax

• Tracheal shift toward unaffected side.

• Subcutaneous emphysema in neck and chest.

Percussion

Spontaneous or traumatic pneumothorax

• Hyperresonance on affected side.

Tension pneumothorax

• Hyperresonance on affected side.

Auscultation

Spontaneous or traumatic pneumothorax

• Absent or decreased breath sounds on affected side.

940
• Increased RR.

• Moderate tachycardia (HR greater than 140 bpm) may be present.

Tension pneumothorax

• Absent or decreased breath sounds on affected side.

• Distant heart sounds.

• Tachypnea/increased RR (greater than 30 breaths/min).

• Hypotension/decreased BP (more than a 20% drop from previous

BP).

• Tachycardia/increased HR (greater than 140 bpm).

Tension pneumothorax is life threatening. Immediate

medical intervention is crucial.

Diagnostic Tests for Pneumothorax

Test Purpose Abnormal Findings

Chest radiograph Reveals the size of the Affected side: Air is present in the
A lateral chest or lateral pneumothorax and pleural space (black); lung markings are
decubitus radiograph presence of tracheal absent in area of collapse (black);
should be done if the shift. abnormal expansion of the chest wall
clinical suspicion of with tension pneumothorax with
pneumothorax is high, lowering/flattening of the diaphragm.
but a posterior-anterior
radiograph is normal.
Expiratory chest
radiographs are not
recommended for the
routine diagnosis of
pneumothorax.
Chest computed CT scanning is The presence of blackened areas is
tomography (CT) scan recommended when indicative of air, with the absence of
differentiating a white areas indicative of blood
pneumothorax from circulating in tissues, which may have
bullous lung disease, been obliterated or unclear on the chest
when incorrect tube radiograph.

941
 placement may be
present, and when the
chest radiograph is
obscured by surgical
emphysema.

Arterial blood gas (ABG) Assesses for Hypoxemia (Pao2 <80 mm Hg on room
analysis hypoxemia and air) is generally present with a 20% or
acidosis. greater lung collapse. Mild hypoxemia is
present with smaller pneumothoraces.
Tension pneumothoraces may cause
both respiratory and lactic acidosis (pH
<7.35) from impending respiratory
failure and circulatory collapse. Elevated
carbon dioxide and lactate lower the
blood pH.
12-Lead ECG Rules out acute Vena cava compression from tension
(electrocardiogram) coronary syndrome as pneumothorax affects perfusion of the
a cause for chest pain coronary arteries if pneumothorax is not
with vital sign changes diagnosed and managed promptly. ST
indicative of segment depression, indicative of
deterioration. myocardial ischemia, may be present,
along with decreased QRS
amplitude/decreased R waves,
rightward axis deviation.
Pulmonary function tests Pulmonary function Not recommended.
tests provide
minimally sensitive
data to validate
presence or size of
pneumothorax.

Collaborative management
Care priorities
Patients with shortness of breath should not be left without
intervention regardless of the size of the pneumothorax seen on the
chest radiograph.

1. Relieve hypoxemia

• Oxygen therapy/adjustment in mechanical ventilation: Oxygen is

administered when ABG values demonstrate the presence of
hypoxemia. If the patient is already receiving mechanical
ventilation, Fio2 is increased while evaluation is done regarding
amount of positive pressure used during inspiratory and
expiratory phases of ventilation. If positive pressure is a

942
 suspected cause of the pneumothorax, positive pressure is
reduced if possible.

• High-flow O2: If a patient with a pneumothorax is admitted for

observation, high-flow (10 L/min) O2 should be administered,
with appropriate caution in patients with COPD with sensitivity
to high concentrations of O2. Use of high-flow O2 has resulted in a
fourfold increase in the rate of pneumothorax reabsorption while
the therapy is in progress.

2. Reexpand the collapsed lung

• Observation: No treatment may be required for small, closed

pneumothoraces without significant dyspnea or breathlessness.

• Simple aspiration: Recommended as first line of treatment for all

primary pneumothoraces in need of intervention. Performed
immediately in tension pneumothorax to remove air from the
chest cavity. A large-bore needle is inserted into the second
intercostal space, midclavicular line, which correlates with the
superior portion of the anterior axillary lobe. A sudden rushing
out of air confirms the diagnosis of tension pneumothorax. To
decrease the risk of further pleural laceration while the chest
reexpands, a stylet introducer needle with a plastic sheath may be
used. The needle is removed after penetration, and the plastic
catheter sheath is left in place to allow decompression of the chest
cavity. Simple aspiration is less likely to succeed in secondary
pneumothoraces and is recommended as an initial treatment in
small (less than 2 cm) pneumothoraces in patients younger than
50 years with mild shortness of breath. Large secondary
pneumothoraces (larger than 2 cm), especially in patients older
than 50 years, are generally not successfully managed using
simple aspiration and are at high risk for recurrence.
Intercostal/chest tube drainage is recommended as appropriate
initial treatment. Once air is removed from the pleural space, the
lung is able to reexpand.

• Catheter aspiration: Catheter aspiration of the trapped air in a

943
 simple pneumothorax is done by passing a small (approximately
8 Fr) catheter over a guide wire into the pleural space. A three-
way stopcock is attached and air may be aspirated via a 50-mL
syringe. Addition of a Heimlich valve and suction may improve
success rates to over 60%. If simple aspiration or catheter
aspiration drainage is unsuccessful, a chest/intercostal tube
should be inserted.

• Chest tube placement/tube thoracostomy: Recommended in

secondary pneumothorax except in patients who are
symptomatic with a very small (less than 1 cm or apical)
pneumothorax. Chest tubes cause inflammation, ultimately
scarring the pleura to help prevent recurrent spontaneous
pneumothoraces. Patients with recurrent lung collapse or
extensive lung disease generally require chest tubes rather than
needle decompression because their visceral pleura does not seal
promptly. Chest tubes are inserted in the second or third lateral
intercostal space, midclavicular line, or near the fifth intercostal
space at the midaxillary line to promote fluid evacuation.
Abdominal viscera may be punctured with placement below the
fifth intercostal space. During insertion, the patient should be in
an upright position so that the lung falls away from the chest
wall. A small (1 to 2 cm) incision is made, and the chest tube is
placed, sutured in place, and connected to an underwater-seal
drainage system. Usually simple underwater-seal drainage is all
that is necessary for 6 to 24 hours. A one-way flutter valve may
be placed on the chest tube instead of the underwater-seal
drainage system, to allow air to escape while preventing reentry.
After chest tube insertion and removal of air from the pleural
space, the lung begins to reexpand. There is no evidence that
large tubes (20 to 24 Fr) are more effective than small tubes (10 to
14 Fr). The initial use of large (20 to 24 Fr) intercostal tubes is not
recommended. If a persistent air leak is present, it may be
necessary to replace a small chest tube with a larger one. Suction
may be used, depending on the size of the pneumothorax, the
patient’s condition, and the amount of drainage. Suction can be
applied with a flutter valve in place.

• Chest tube suction: Suction should not be applied directly after

944
 tube insertion, but rather added after 48 hours if persistent air
leak is present or the pneumothorax fails to reexpand. High-
volume, low-pressure (greater than 10 to less than 20 cm H2O)
suction systems are recommended. Patients requiring suction
should be managed by physicians and nurses who have
experience managing complex pneumothoraces. There is no
evidence to support routine use of immediate suction with chest
drain systems in the treatment of spontaneous pneumothorax.

• Chemical pleurodesis: The instillation of caustic substances into

the pleural space, resulting in aseptic inflammation with
formation of dense adhesions, which can seal persistent air leaks.
Pleurodesis is associated with a high recurrence rate of primary
and secondary pneumothoraces, despite use of various
sclerosants to reduce these rates. The chemicals are instilled
either through chest tubes or during surgery. Doxycycline and
talc slurry are the preferred sclerosing agents. Few usage
guidelines are available for physicians. Prevention of additional
recurrent pneumothoraces should be managed surgically in most
cases.

3. Relieve pain

• Analgesic: Provides relief of pain of pneumothorax or its

treatment. A chest tube may cause pleuritic pain, slight
temperature elevation, and pleuritic friction rub. The nurse
should administer analgesics and monitor the patient’s response
to the analgesics administered during the procedure.

4. Remove chest drainage device

• Stepped/staged approach: Remove chest tube using a

stepped/stage approach to ensure that the air leak has resolved. A
chest radiograph demonstrating complete resolution of the
pneumothorax with no clinical evidence of air leak should be
done first. Secondly, chest tube suction is discontinued.
Clamping before discontinuation of the chest tube is
controversial and performed by only half of trained practitioners.

945
• Chest radiograph before tube removal: Chest radiographs are
obtained following the last evidence of air leak but before chest
tube removal at intervals ranging from less than 4 to 24 hours
after the last air leak assessment. Nearly two thirds of
practitioners wait 5 to 12 hours after last evidence of air leak
before obtaining the preremoval radiograph. Practices range from
less than 4 to 24 hours.

5. Manage persistent air leak

• Continued observation: Patients should be observed for 4 days to

assess for spontaneous closure of a pneumothorax caused by
bronchopleural fistula. If the air leak persists longer than 4 days,
patients should be evaluated for surgery to close the air leak with
additional pleurodesis procedure to prevent recurrence.
Thoracoscopy is the preferred management procedure.

• Additional closure techniques: Use of an additional chest tube or

bronchoscopy in an attempt to seal endobronchial sites of air
leakage is not indicated. Except in special circumstances where
surgery is contraindicated or a patient refuses surgery, chemical
pleurodesis should not be used.

6. Provide surgical intervention for recurrent

pneumothoraces

• Thoracoscopy: Can be performed with or without video

assistance. Intraoperative bullectomy should be performed by
staple bullectomy in patients with apical bullae visualized at
surgery.

• Thoracotomy: May be indicated when a patient is at high risk for

repeated recurrence and is not successfully managed by
thoracoscopy. High-risk status is present when at least two
spontaneous pneumothoraces occurred in the same lung or if
resolution of the pneumothorax has not occurred within 7 days.
Thoracotomy may involve mechanical abrasion or decortication
of the pleural surfaces with a dry, sterile sponge or chemical
abrasion via an agent such as tetracycline (e.g., doxycycline)

946
 solution or talc, both of which result in pleural adhesions to
prevent recurrence. A partial pleurectomy may be performed
instead of mechanical or chemical abrasion.

Care plans for pneumothorax

Impaired spontaneous ventilation and impaired gas
exchange 
related to collapsed lung
Goals/Outcomes: Within 2 to 6 hours of initiation of treatment,
the patient exhibits adequate gas exchange, as evidenced by PaO2
≥60 mm Hg and Paco2 ≤45 mm Hg (or values within 10% of the
patient’s baseline values, which depend on the underlying
pathophysiology), RR less than 20 breaths/min with normal depth
and pattern, and orientation to time, place, and person.
Respiratory Status: Ventilation, Vital Signs Status;
Respiratory Status: Gas Exchange, Symptom Control Behavior,
Comfort Level, Endurance.

Ventilation assistance

1. Position the patient to allow for full expansion of unaffected lung.

Semi-Fowler position usually provides comfort and allows
adequate expansion of chest wall. The patient can also be turned
unaffected side-down with the head of the bed elevated to ensure a
better match.

2. Change the patient’s position every 2 hours to promote drainage

and lung reexpansion and to facilitate alveolar perfusion.

3. Encourage the patient to take deep breaths, providing necessary

analgesia to decrease discomfort during deep-breathing exercises.
Deep breathing will promote full lung expansion and may decrease
the risk of atelectasis.

4. Ensure delivery of prescribed concentrations of O2.

Environmental management: Safety

947
1. Assist the advanced practice provider with chest tube insertion
according to institutional guidelines.

2. Assess and maintain closed chest drainage system:

• Closed chest drainage systems are typically a single

disposable “dry” suction, plastic unit. They have
one, two, or three collection chambers to
accommodate large amounts of drainage. The
amount of fluid evacuated is easily measured by
graduated measurements on the collection
chambers.

• While fluid accumulates in the chambers,

hydrostatic resistance increases while air also leaves
the pleural space. Air passing through the water
seal provides a flutter valve, thus minimizing
resistance to pressure changes in the pleural space
and reducing the resistance to the flow of drainage.

• Avoid all kinks in the tubing, and ensure that the

bed and equipment are not compressing any
component of the system.

• Closed systems must remain intact/airtight to

maintain negative pressure and avoid air
entrapment in the pleural space.

• Stabilize the chest drainage system with appropriate

device/holder on the floor to prevent tipping or
other disruption, which may open the system to air.

948
• Ensure that the system is appropriately vented at all
times to help prevent the possibility of tension
pneumothorax should the system be disrupted. Air
should be released if the system is vented.

• The drainage system should be kept below the level

of the chest to maintain appropriate pressure
dynamics.

• Maintain fluid in underwater-seal chamber, and

suction chamber at appropriate levels. Check the
water level in “wet” suction controlled units at least
every shift, because the water evaporates.

• Be aware that the suction apparatus does not

regulate the amount of suction applied to the closed
drainage system. The amount of suction is
determined by the water level in the suction control
chamber. Minimal bubbling is optimal. Excessive
bubbling causes rapid evaporative loss.

• Suction aids in the reexpansion of the lung.

Removing suction for short periods of time will not
be detrimental to the patient as long as the system is
appropriately vented to allow for the escape of air.

• Fluctuations in the underwater-seal chamber

indicate the tube is patent. Fluctuations stop when
either the lung has reexpanded or there is a kink or
obstruction in the chest tube.

949
• Bubbling in the underwater-seal chamber occurs
only during expiration and reflects air is leaving the
pleural space through the drainage system.

• Continuous bubbling on both inspiration and

expiration in the underwater-seal chamber is a
signal that air is leaking into the drainage system.
Locate and seal the system’s air leak, if possible.

A bubbling chest tube should never be clamped. Chest tubes

should generally remain unclamped. Clamping a chest tube
inserted for pneumothorax should be done under the supervision of
a respiratory physician or thoracic surgeon if required. If a patient
with a clamped drain experiences shortness of breath or develops
subcutaneous emphysema, the tube must be unclamped
immediately.

3. Keep necessary emergency supplies at the bedside: (1) petroleum

gauze pad to apply over insertion site if the chest tube becomes
dislodged and (2) sterile water in which to submerge the chest tube
if it becomes disconnected from the underwater-seal system. Never
clamp a chest tube without a specific directive from the physician:
clamping may lead to tension pneumothorax because the air can no
longer escape.

4. Assist with chest tube removal in accordance with institutional

guidelines.

Oxygen therapy

1. Provide humidity in O2 if used for more than 12 hours to help

thin secretions.

950
2. Administer supplemental O2 using liter flow device as ordered.

3. Document pulse oximetry with O2 liter flow in place at time of

reading as ordered. Oxygen is a drug; the dose of the drug must be
associated with the O2 saturation or the reading is meaningless.

4. Monitor for skin breakdown where O2 devices are in contact with

the skin, such as nares, and around edges of mask devices.

Cough Enhancement; Oral Health Maintenance.

Respiratory monitoring

1. Obtain ABGs if the patient experiences behavioral changes or

respiratory distress to check for hypoxia or hypercapnia.

2. Monitor for induced hypoventilation, especially in patients with

COPD.

3. Monitor for changes in chest radiograph and breath sounds

indicative of O2 toxicity and absorption atelectasis in patients
receiving higher concentrations of O2 (greater than 45% Fio2) for
longer than 24 hours. The higher the O2 concentration, the greater
the chance of toxicity.

Acid-Base Management.

Acute pain 
related to chest tube placement and pleural irritation
Goals/Outcomes: Within 1 to 2 hours of initiating analgesic
therapy, the patient’s subjective evaluation of discomfort improves
as documented by a pain scale. Nonverbal indicators of discomfort,
such as grimacing and splinting on inspiration, are absent.
Comfort Level; Pain Control Behavior; Pain Level.

Pain management

1. At frequent intervals, assess the patient’s degree of discomfort,

using the patient’s verbal and nonverbal cues. Devise a pain scale

951
with the patient, rating discomfort on a scale of 0 (no pain) to 10
(worst pain). Medicate with analgesics as prescribed, evaluating
and documenting the effectiveness of the medication on the basis of
the pain scale.

2. Position the patient on unaffected side to minimize discomfort

from chest tube insertion site. Administer medication 30 minutes
before initiating movement.

3. Teach the patient to splint affected side during coughing,

moving, or repositioning. Move the patient as a unit to enhance
stability and comfort.

4. Schedule activities to provide for periods of rest, because fatigue

may lower the patient’s pain threshold.

5. Stabilize the chest tube to reduce pull or drag on latex connector

tubing. Tape the chest tube securely to thorax, and loop latex tubing
on the bed beside the patient.

Self-responsibility facilitation

1. Teach the patient to maintain active range of motion on the

involved side to prevent development of a stiff shoulder from the
immobility.

2. Give the patient and significant others appropriate information

regarding chest tube placement and maintenance.

Acid-Base Management; Acid-Base Monitoring; Analgesic

Administration; Environmental Management: Comfort; Exercise
Promotion; Laboratory Data Interpretation; Medication
Administration; Medication Management; Oxygen Therapy; Pain
Management; Positioning; Respiratory Monitoring; Vital Signs
Monitoring.

Additional nursing diagnoses

Also see the section on Activity Intolerance in Acute Asthma
Exacerbation. See appropriate nursing diagnoses and interventions

952
in Chapter 2 on Emotional and Spiritual Support of the Patient and
Significant Others.

4-7
RESEARCH BRIEF
A faster and more efficient method for assessing pneumothorax
progression in patients receiving positive-pressure mechanical
ventilation would certainly lead to earlier intervention and
improved patient safety. Ultrasonography is a common bedside
tool that can offer clinicians a less expensive and more accessible
alternative to computed tomography scanning in the assessment of
pneumothorax. Research using animal models has provided
reliable evidence that could possibly contribute to the development
of best practice. Pneumothorax progression is known as the best
indicator for the need for chest tube placement.
From Oveland NP, Lossius HM, Wemmelund K, et al: Using thoracic ultrasonography to
accurately assess pneumothorax progression during positive pressure ventilation: a
comparison with CT scanning. Chest 143:415-422, 2013.

Pulmonary embolism
Pathophysiology
Pulmonary embolism (PE) is a blockage in the pulmonary
circulation created by a lodged blood clot, vasculitis from fatty
acids, or presence of air or other endogenous substances.
Pulmonary emboli resulting from DVT affect from 300,000 to
600,000 patients (1 to 2 per 1000 patients; and in those older than 80
years, 1 per 100 patients) annually in the United States. It is
estimated that from 60,000 to 10,000 people die of DVT/PE, with
10% to 30% dying in the first 30 days. Sudden death is the first
symptom of a problem in approximately 25% of patients. PE occurs
in nearly 70% of patients with venous thrombosis in veins proximal
to the knee and is less common with more distal thrombosis. PE is
associated with recurrent embolic events (within 10 years) in over
33% of affected patients. Venous thromboembolism (VTE)

953
prevention augments both public health and patient safety. Despite
efforts to prevent hospital-acquired VTE, the number of secondary
diagnoses has increased. During 2007 to 2009, the data from each
year revealed that approximately 550,000 adult hospital stays had a
discharge diagnosis of VTE. Prevention of VTE has recently been
the focus of attention from both researchers and quality
improvement organizations as a leading strategy to help reduce
morbidity and mortality in patients who are hospitalized. Acute
right ventricular failure with resultant low cardiac output is the
leading cause of death related to PE. Despite strong evidence,
recommended evidence-based practices are inconsistently
implemented. VTE rates are increasing as the U.S. population ages,
is progressively obese, and is living longer with chronic
diseases, which may promote thrombus formation. Venous
thrombosis is the most common cause of PE, followed by fat
emboli. Emboli related to venous air, foreign bodies, and other
sources (amniotic fluid, sepsis/infection, and tumors) occur more
rarely.

Venous thromboembolism
A formed blood clot from a large vein dislodges and travels to the
pulmonary circulation, where it may obstruct one (massive PE) or
both branches (saddle emboli) of the pulmonary artery or a smaller,
distal vessel. Blood clots typically originate in the deep veins of the
legs, the iliofemoral system, or pelvis. Many patients with VTEs
have no symptoms of DVT. Thrombus formation can result from
blood stasis, alterations in clotting factors, and injury to vessel
walls. Emboli are classified by size and location and include
submassive, massive, and saddle emboli. Total obstruction of blood
flow leading to pulmonary infarction is rare. Prevention, early
diagnosis, and appropriate treatment may reduce development of
DVT and PE by 68% and mortality to less than 10%. Although most
thrombotic emboli resolve completely, leaving no residual deficits,
some patients may be left with chronic pulmonary hypertension
(Table 4-6).

Table 4-6

954
INCIDENCE OF VENOUS THROMBOEMBOLISM IN HOSPITALIZED
PATIENTS

Incidence Patient Type

10% to 26% Medical/nonsurgical
11% to 75% Stroke
15% to 40% Major surgery: general, gynecologic, urologic
15% to 40% Neurosurgery
15% to 80% Critically ill patients admitted to intensive care units
40% to 60% Hip or knee surgery/orthopedic surgical patients
40% to 60% Major trauma
60% to 80% Spinal cord injury
Composite of statistics from the British Thoracic Society (2003), American College of
Chest Physicians (2008), European Society of Cardiology (2008), and IMPROVE
(2007) registry data on prevention of venous thromboembolism.

Fat embolism/fat embolism syndrome

The most common nonthrombotic cause of PEs is fat emboli, which
occur in less than 1% of patients. Fat emboli can result from trauma
(fracture of long bones, accidents, or soft tissue injury) or
nontrauma (burns or fatty liver). The event and subsequent
syndrome most often occurs within 12 to 36 hours after skeletal
trauma or major orthopedic surgery, but may be fulminant, with
rapid embolization of fat into the pulmonary and systemic
circulation, followed by right ventricular failure and cardiovascular
collapse. Fat emboli most often result from the release of free fatty
acids during a surgical procedure, prompting toxic vasculitis
followed by thrombosis and obstruction of small pulmonary
arteries by fat. More recently, fat embolism has been reported
following liposuction, with lipid and propofol infusions, fatty liver,
and hepatic necrosis.

Venous air embolism

Venous air embolism is almost always an iatrogenic complication
caused by a large volume of air that enters the venous circulation
and travels to the pulmonary circulation. The incidence of venous
air embolism can range between 10% (penetrating chest trauma,
during invasive monitoring catheter placement) and 80% (during
laparoscopic surgical procedures). Smaller amounts of air may be
completely unproductive of symptoms, because air can be rapidly

955
resorbed. Surgical procedures, insertion of pulmonary artery
catheters, central venous catheters, hemodialysis, endoscopy, and
use of automatic injectors such as those used for contrast media can
prompt symptomatic air emboli. A larger bolus of air into the right
ventricle may completely obstruct pulmonary blood flow, leading
to cardiac arrest. In severe cases, venous air embolus has a
mortality rate greater than 50%. Rapid diagnosis and treatment are
essential. Case reports describe the adult lethal volume of air as
approximately 200 to 300 mL delivered rapidly. Air occludes the
right ventricular pulmonary outflow tract, or the smaller
pulmonary arteriole with a mixture of air and fibrin clots, which
results in right ventricular failure and cardiogenic shock.

Intravascular foreign bodies

Most foreign bodies in the central circulation are parts of
intravascular catheters, a guide wire, or an inferior vena cava (IVC)
filter that has accumulated a clot and migrated. More recently, coils
for embolization and endovascular stenting have also migrated
from their desired position. Most foreign bodies travel to the
pulmonary arteries, with the right side of the heart and vena cava
being the secondary locations.

Other types of pulmonary embolism

Amniotic fluid embolism occurs in less than 1:8000 to 80,000
women as a result of amniotic fluid being forced into the central
circulation through tears in the uterine veins that may occur during
normal labor. Death of both the mother and fetus may result during
the delivery. Septic pulmonary emboli are infected clots dislodged
from either the peripheral or abdominal vein, or septic
thrombophlebitis, or right-sided endocarditis. Prognosis is
dependent on the overall patient condition and severity of the
sepsis. Tumor embolism occurs with many types or carcinoma and
sarcoma but causes significant respiratory symptoms in less than
3% of affected patients. Talc embolism results from drug users
grinding up and injecting oral medications that are made with talc
particles, which lodge in the small vessels of the pulmonary system.

956
Assessment
Goal of system assessment
Evaluate for ineffective breathing patterns and impaired gas
exchange. The clinical presentation will vary in degree, depending
on the type and size of the embolus. With a submassive or massive
embolism, evaluate for decreased cardiac output and decreased
tissue perfusion. Massive embolism may prompt cardiogenic shock.
For saddle emboli, identifying pulmonary embolus as the cause for
acute cardiopulmonary decompensation is of paramount
importance so that life-saving treatments can be provided. (See the
section on Respiratory Assessment: General, and Cardiac
Assessment: General in Chapter 5.)

History and risk factors for venous thromboembolism

The American College of Chest Physicians, American Thoracic
Society, American College of Physicians, American Academy of
Family Physicians, European Society of Cardiology, British
Thoracic Society, and an array of medical and surgical specialty
organizations have created guidelines for VTE prophylaxis and
management. VTE prophylaxis protocols should be initiated when
patients are admitted to the hospital, to help prevent development
of DVT (Tables 4-7 and 4-8).

Table 4-8
RISK FACTORS FOR VENOUS THROMBOEMBOLISM

Strong Risk Factors Moderate Risk Factors Weak Risk Factors

Fracture (hip or leg) Arthroscopic knee surgery Prolonged bed rest
Hip or knee replacement Central venous lines Immobility
Major general surgery Chemotherapy/cancer Age >40 years
Major trauma Congestive heart or respiratory failure Laparoscopic surgery
Spinal cord injury Estrogen Obesity
Age >65 years Pregnancy
Paralytic stroke Varicose veins
Postpartum period
Previous venous thromboembolism
Thrombophilia
From Anderson FA Jr, Spencer FA: Risk factors for venous thromboembolism.
Circulation 107(23 Suppl 1): 9-16, 2003.

957
Determine probability based on risk factors
• Helps determine presence of pulmonary embolus: More than six
factors is considered high, two to six is moderate, and less than
two is considered low probability.

• Diagnostic tests chosen are dependent on the probability that a

DVT or VTE is present; a scoring system may be developed based
on number of risks present. Reveals the presence of the infiltrates.

Vital signs
• Severity of all findings varies with size of the embolus; patients
with small emboli may be asymptomatic.

• Tachycardia (HR greater than 100 bpm), tachypnea (RR greater

than 20 breaths/min), fever (greater than 99.5° F or 37.5° C).

• Massive embolus: Hypotension (BP decreases by greater than

20%).

• Saddle embolus: May result in immediate cardiopulmonary

arrest.

Observation/inspection
• Dyspnea, nonproductive cough, and nausea.

• Syncope, pallor, and palpitations.

• Restlessness and anxiety.

• Diaphoresis, cool and clammy skin.

• Pleuritic chest pain and hemoptysis.

• Signs of lower limb DVT: Leg/calf tenderness, swelling, and/or

edema.

• Submassive embolus: Any combination of the symptoms listed

958
above.

959
• Massive embolus: Severe chest pain, cyanosis, and acute
respiratory distress.

• Saddle embolus: Sudden-onset acute respiratory distress with

cyanosis, which may progress to cardiopulmonary arrest.

Palpation
• Possible reduced chest excursion on affected side attributable to
splinting for pain.

Percussion
• Unchanged.

Auscultation
• Crackles.

• S3 and S4 gallop rhythms.

• Transient pleural friction rub may be present.

HIGH ALERT!
Saddle pulmonary embolus is life threatening. Immediate medical
or surgical intervention is crucial. Thrombolysis directed at the
pulmonary embolus will also prompt lysis of other clots and may
lead to other bleeding complications. If thrombolysis is
contraindicated, surgical or percutaneous catheter-mediated
embolectomy is performed immediately.

Fat embolism

History and risk factors

960
• Multiple long bone fractures, particularly the femur and pelvis.

• Lower limb amputation.

• Trauma to adipose tissue or liver.

• Burns, see Chapter 3.

• Hemolytic crisis, see Chapter 10.

• Osteomyelitis.

Observation/inspection
Patients are often asymptomatic for 12 to 24 hours after the
embolization occurs. This period ends with a sudden deterioration
in cardiopulmonary and neurologic status.

• Dyspnea and acute respiratory distress.

• Restlessness, confusion, delirium, and coma.

• Petechial rash may appear especially over the upper torso and
axillae, secondary to thrombocytopenia. The platelets aggregate
in the presence of circulating fats.

Vital signs

• RR greater than 20 breaths/min and HR greater than 100 bpm.

• Increased BP and elevated temperature.

Auscultation

• Inspiratory crowing and expiratory wheezes.

Venous air embolism

History and risk factors

• Recent surgical procedure.

961
• Pulmonary artery/central venous catheter insertion.

• Misuse of closed-wound suction unit.

• Cardiopulmonary bypass.

• Hemodialysis.

• Endoscopy.

Clinical presentation
Depends on severity of the bolus.

Observation/inspection
Agitation, confusion, cough, dyspnea, and chest pain.

Vital signs
RR greater than 20 breaths/min, HR greater than 100 bpm, and
hypotension.

Auscultation
Wheezing, “mill wheel heart murmur,” which can be defined as a
temporary loud, machinery-like sound resulting from right
ventricular blood mixing with air.

Foreign bodies

History and risk factors

• Advanced practice provider accidentally lets go of the guide wire

during central line insertion.

• Vena cava filter has not been retrieved within recommended time
frame.

• Intravascular catheter breaks during insertion.

• Coils or stent components are accidentally released or not

properly secured during insertion.

962
Diagnostic Tests for Venous Thrombotic Pulmonary Embolism

Test Purpose Abnormal Findings

D-dimer Predicts likelihood that a Positive: A thrombus is present.
Several assays are thrombus is present in low-risk Scales range from 250 to 1000
available with variable or intermediate-risk patients. ng/mL; the most common cutoff
levels of sensitivity and When the value exceeds the value is 500 ng/mL.
specificity. This test cutoff, the test is positive. A Low-risk and intermediate-risk
may not be needed in negative D-dimer test reliably patients do not require imaging
high-risk or high- excludes pulmonary embolism for venous thromboembolism
probability patients. (PE) in patients with low or (VTE) if the [D-dimer] is
Hospitals should intermediate clinical negative.
provide information on probability.
specificity and
sensitivity of test used.
Lower extremity duplex Reveals slow or obstructed Positive: Reduced or obstructed
ultrasound imaging flow in the venous system. blood flow is detected.
A single normal test Test is done on patients at high
cannot be used to rule or moderate risk of DVT.
to subclinical deep
venous thrombosis
(DVT).
Chest radiograph: Reveals abnormal lung Affected side: Initially the chest
posterior-anterior and markings and fluid shifts that radiograph shows normal findings
lateral chest radiograph occur during flow obstruction or an elevated hemidiaphragm.
Cannot be used alone to and pulmonary infarction. A After 24 hours, small infiltrates
diagnose pulmonary baseline chest radiograph is secondary to atelectasis from
embolus helpful for comparison with decrease in surfactant may
subsequent films to identify develop. If pulmonary infarction is
changes. present, infiltrates and pleural
effusions may be seen within 12 to
36 hours.
Spiral CT angiography Reveals flow obstruction in Generally reveals right ventricular
with contrast pulmonary circulation. dilatation. Patients with
Current technology is Recommended for patients intermediate or high pretest
nearly 100% accurate. with intermediate-to-high probability of PE require
Older technology may probability of lower extremity diagnostic imaging studies.
be insufficient to rule DVT.
out PE.
Ventilation-perfusion Assesses for or If there is a mismatch of ventilation
lung scan ventilation/perfusion and perfusion (e.g., normal
The patient inhales mismatching; a good ventilation with decreased
radioactive-tagged alternative for patients who perfusion), vascular obstruction is
gases, and radioactive cannot receive contrast needed likely. Results may not be
particles are injected for spiral CT angiography. definitive. False-positive results
peripherally. are more common than false-
negative results.
Arterial blood gas (ABG) Assesses for hypoxemia and Initially, hypoxemia (Pao2 <80 mm
analysis acidosis. Saddle embolus may Hg), hypocapnia (Paco2 <35 mm
Pulse oximetry may be cause both respiratory and Hg), and respiratory alkalosis (pH
used to monitor O2 lactic acidosis (pH <7.35) from >7.45). A normal Pao2 does not rule
saturation changes. CO2 impending respiratory failure
and circulatory collapse. out the presence of VTE. Mild
increases and pH hypoxemia may be present with
changes require ABG smaller emboli.
analysis.

963
 12-Lead ECG Rules out acute coronary If VTE is extensive, signs of acute
(electrocardiogram) syndrome as a cause for chest pulmonary hypertension may be
Vitally important because pain with vital sign changes present: right-shift QRS axes, tall
chest pain can mimic indicative of deterioration. and peaked P waves, ST segment
severe angina or acute changes, and T wave inversion in
myocardial infarction leads V1 to V4.

Echocardiogram Diagnoses the presence of May reveal right ventricular

right ventricular impairment hypokinesis, dilatation, or elevated
or failure as part of risk pressures. Right ventricular
stratification. dilatation is found in >25% of
patients with PE.
Pulmonary angiography A definitive study for VTE. An abrupt vessel “cutoff” may be
The Miller (European) The right ventricle is seen at the site of embolization.
and Walsh (United catheterized and dye is Usually, filling defects are seen.
States) scores were used injected into the pulmonary Used when other tests are
to define the amount of artery to visualize pulmonary inconclusive, because the
luminal obstruction. vessels. Formerly, the gold procedure has a 0.2% mortality
Improved accuracy standard for definitive rate.
with current CT diagnosis.
angiography has
markedly reduced the
need for this invasive
procedure.
Hemodynamic studies To determine if obstruction of PA pressures increase (>20 mm
blood flow is significant Hg) if 30% to 50% of the
enough to cause pulmonary pulmonary arterial tree is affected.
hypertension or right Massive VTEs cause pressure
ventricular failure. increases to >40 mm Hg, resulting
in right ventricular failure,
decreased cardiac output, and
hypotension.

Fat embolism
• ABG values: Hypoxemia (PaO2 less than 80 mm Hg) and
hypercapnia (Paco2 greater than 45 mm Hg) will be present with
respiratory acidosis (pH less than 7.35).

• Chest radiograph: A pattern similar to ARDS is seen: diffuse,

extensive, bilateral interstitial, and alveolar infiltrates.

• CBC with WBC differential: May reveal decreased hemoglobin

and hematocrit secondary to hemorrhage into the lung,
thrombocytopenia, and possibly mild leukocytosis.

Venous air emboli

964
• ABG values: Hypoxemia (PaO2 less than 80 mm Hg), hypercapnia
(Paco2 greater than 45 mm Hg), and respiratory acidosis (pH less
than 7.35) are generally present in severe cases.

• Chest radiograph: Reveals changes consistent with pulmonary

edema or air-fluid levels in the main pulmonary artery system.

• Pulmonary artery pressure: Systolic, diastolic, and mean

pressures are acutely elevated, but slight elevation of pulmonary
artery wedge pressure remains within normal limits.

Foreign bodies
• Chest radiograph: All devices are radiopaque for easy
identification using radiographs. The “lost” device should be
easily visible using a chest radiograph.

Collaborative management
Care priorities: Venous thromboembolism
Patients with shortness of breath should not be left without
intervention regardless of the probability that VTE is present.

1. Relieve hypoxemia
Patent foramen ovale (or atrial septal defect) may augment
hypoxemia if right atrial pressure exceeds left atrial pressure,
causing deoxygenated blood to shunt from the right to the left
atrium.

• Oxygen therapy/adjustment in mechanical ventilation: Oxygen is

administered when ABG values demonstrate the presence of
hypoxemia. If the patient is already receiving mechanical
ventilation, Fio2 is increased while evaluation is done regarding
amount of positive pressure needed during inspiratory and
expiratory phases of ventilation.

2. Manage right ventricular failure in patients with

965
hypotension or shock
Hemodynamic stabilization is achieved using a combination of
fluid therapy to increase the end-diastolic volume in the right
ventricle and positive inotropic agents to increase the force of right
ventricular contraction. Management of right ventricular failure is
complex. Efforts should be directed at restoring patency of
pulmonary circulation in patients with VTE. When the obstruction
is relieved, the patient generally improves rapidly. See the sections
on Heart Failure and Cardiogenic Shock in Chapter 5.

• Initiate cardiopulmonary resuscitation if the patient arrests with

saddle embolus. Generally, these patients require pulmonary
embolectomy because VTE has resulted in lethal cardiogenic
shock. Sophisticated centers can use extracorporeal devices as a
bridge to clot removal.

3. In patients who are less severely ill, or those in need of

vte prophylaxis, prevent clot development or clot extension
Pharmacologic therapy: All patients at risk of developing VTE
should be screened for bleeding risk before implementing
prophylaxis using medications, because all agents have the
potential to cause bleeding. Thromboprophylaxis medications
include low–molecular-weight heparin (enoxaparin [Lovenox],
dalteparin [Fragmin]), low-dose unfractionated heparin,
fondaparinux (Arixtra), direct thrombin inhibitors (argatroban,
lepirudin, bivalirudin), and warfarin (Coumadin). Warfarin
requires 3 and 5 days of oral therapy to attain therapeutic effect,
during which time the patient requires an injectable medication as a
“bridge” to warfarin. Ongoing therapy may include low-dose or
regular-dose aspirin.

VENOUS THROMBOEMBOLISM PROPHYLAXIS:

CONSIDERATIONS FOR CONTRAINDICATIONS/COMPLICATIONS

Absolute Contraindications Relative Other Conditions That May

Contraindications Complicate Therapy
Active hemorrhage Intracranial Immune-mediated heparin-
Allergy hemorrhage induced thrombocytopenia
within the past

966
 year
Severe head or spinal cord trauma within Craniotomy within Epidural analgesia; catheter
4 weeks 2 weeks present, or will be present in the
spine

Note: Absolute contraindication means Intraocular Note: Unfractionated heparin

that therapy should not be administered surgery within 2 and low–molecular-weight
to the affected patients under any weeks heparins can stimulate
circumstances, because the risk of Active intracranial heparin-induced
bleeding outweighs the benefits of clot lesions or thrombocytopenia, an
prevention. neoplasms immune response that
Thrombocytopenia destroys platelets. Non–
(platelets <50,000) heparin anticoagulants:
Coagulopathy Argatroban (Argatroban)
(prothrombin time Bivalirudin (Angiomax)
>18 seconds) Fondaparinux (Arixtra)
End-stage liver Lepirudin (Refludan)
disease Danaparoid (Orgaran)
Gastrointestinal, (unavailable in the United
genitourinary States)
hemorrhage
within 1 month
Current
hypertensive
urgency or
emergency
Current
postoperative
bleeding

• Risk stratification: Provide appropriate therapy based on

evaluation for level of risk of development of VTE and risk of
bleeding.

VENOUS THROMBOEMBOLISM PROPHYLAXIS BASED ON LEVEL

OF RISK (SELECT ONE DRUG/ONE DOSAGE REGIMEN)

Low Risk Intermediate Risk High Risk

Early aggressive ambulation Heparin 5000 units Enoxaparin 30 mg SC
Short-term mechanical subcutaneously (SC) every 12 hours
thromboprophylaxis may be every 8 hours Enoxaparin 40 mg SC
Heparin 7500 units SC daily
recommended for “borderline”-risk every 12 hours Dalteparin 5000 units
patients Heparin 5000 units SC SC daily
every 12 hours (if <50 kg Fondaparinux 2.5 mg
or >75 years old) SC daily
Enoxaparin 40 mg SC Warfarin until
daily international
Dalteparin 2500 units normalized ratio is
daily for low or 2 to 3
intermediate risk Add sequential
Consider adding compression

967
 sequential compression devices
devices

• Mechanical prophylaxis: Sequential compression devices may be

used as the sole preventive strategy in patients at low risk and in
patients at moderate to high risk who are not able to receive
thromboprophylaxis drugs because of risk for bleeding.
Plexipulse and elastic compression stockings are not considered
sufficient as a sole VTE prophylaxis strategy for patients who are
hospitalized. Compression stockings with a pressure of 30 to 40
mm Hg at the ankle may be implemented before discharge and
used posthospitalization.

4. Prevent clot extension or migration in patients with DVT

or VTE

• Pharmacologic therapy: To inhibit thrombus growth, promote

resolution of the formed thrombus, and prevent further embolus
formation. The goals are achieved by keeping the activated
partial thromboplastin time (aPTT) at 1.5 to 2.5 times the normal.
Platelet counts should be obtained every 3 days, to monitor for
thrombocytopenia and paradoxical arterial thrombosis associated
with heparin therapy in predisposed patients. (See Bleeding and
Thrombotic Disorders, p. 837.)

• Weight-based IV heparin (unfractionated) therapy: Treatment of

choice; started immediately in patients without bleeding or
clotting disorders and in whom signs and symptoms of VTE are
present. Initial dose: 80 units/kg IV bolus. Dosage should be
given based on the patient’s weight.

• Maintenance dose: Following initial dose, a

continuous IV infusion is usually begun at 18
units/kg/h and titrated by serial aPTT values to
determine level of anticoagulation. Titration is done
according to institutional protocol (see Table 4-9).

968
• Heparin requirements are the largest in the initial
72 hours of therapy. Maintenance continues for 7 to
14 days, during which time the patient is placed on
bed rest to ensure that the thrombus is firmly
attached to the vessel wall before ambulation.
Platelets should be monitored, because patients
sometimes experience heparin-induced
thrombocytopenia (HIT) or low platelets. Protamine
sulfate is a heparin antidote, which should be
readily available during heparin therapy. Fatal
hemorrhage occurs in 1% to 2% of patients
undergoing heparin therapy. Risk of bleeding is
greatest in women older than 60 years.
• Subcutaneous low–molecular-weight heparin (dalteparin,
enoxaparin): An alternative to unfractionated heparin with
longer half-life, greater bioavailability, and more predictable
anticoagulant activity. Enoxaparin is given 1 mg/kg
subcutaneously (SC) every 12 hours or 1.5 mg/kg SC daily.
Dalteparin is given 200 units (international units)/kg SC daily to a
maximum daily dose of 18,000 international units, while the
patient is being bridged to warfarin.

• SC Tinzaparin: A heparin alternative given 175 units

SC daily.

• SC Fondaparinux: Dose is given based on three

body sizes.

• 5 mg SC daily: Weight less than 50 kg.

• 7.5 mg SC daily: Weight 50 to 100 kg.

969
• 10 mg SC daily: Weight greater than 100 kg.

Table 4-9
UNFRACTIONATED HEPARIN INTRAVENOUS INFUSION DOSAGE
TITRATION

Activated Partial Thromboplastin Dosage Titration

Time (aPTT; in Seconds)
Less than 35 (<1.2 times the control) 80 units/kg bolus; begin infusion at 18 units/kg/h; increase
infusion rate by 4 unit/kg/h
35 to 45 (1.2 to 1.5 times the 40 units/kg bolus; increase infusion rate by 2 units/kg/h
control)
46 to 70 (1.6 to 2.3 times the No change; this is the desirable range
control)
71 to 90 (2.4 to 3 times the control) Decrease infusion rate by 2 units/kg/h
>90 (>3 times the control) Hold/stop infusion for 1 hour; then restart at 3 units/kg/h
less than when stopped
Active hemorrhage Vitamin K, fresh-frozen plasma, and protamine sulfate
may be used to help reverse heparin effects.

Inferior vena cava (IVC) filter: Also known as a “Greenfield

filter,” the devices are designed to trap emboli before they enter the
heart and pulmonary arteries. Various types of IVC filters are
available, with different recommendations governing the
removal/retrieval of each device. The filter is inserted through an
introducer sheath into the femoral vein, threaded through the
venous system, and deployed below the level of the renal veins in
the IVC. The American College of Chest Physicians recommends
that most retrievable devices are removed approximately 2 weeks
following insertion. Many devices are left in place for longer
periods, with associated complications of device thrombosis and
migration in 10% of patients. Permanent IVC filters are associated
with recurrent DVT (in 20% of patients) and postthrombotic
syndrome (in 40% of patients). Routine use is not recommended for
management of VTE.

5. Dissolve clot using thrombolytic drugs in patients with

massive or saddle embolus
These “clot buster” drugs lyse clots via conversion of plasminogen
to plasma and may be given within 72 hours of VTE to speed the

970
process of clot lysis. These medications are not often used but can
be used immediately when severe cardiopulmonary compromise or
arrest has occurred. Heparin therapy is used following
thrombolytic infusion. As many as 33% of patients who receive
thrombolytic therapy have hemorrhagic complications. The drug
should be discontinued and fresh-frozen plasma infusion may be
initiated for severe bleeding complications.

• Streptokinase: Loading dose of 250,000 international units in

normal saline or D5W given IV over a 30-minute period.
Maintenance dose is 100,000 international units per hour given IV
for 12 to 24 hours.

• Tissue plasminogen activator (Alteplase, rTPA): 100 mg IV

infusion over 2 hours, or 0.6 mg/kg over 15 minutes (maximum
dose 50 mg).

• Urokinase: 4400 international units/kg as a loading dose over 10

minutes, followed by an infusion of 4400 international units/kg/h
for 12 to 14 hours.

6. Remove thrombus with an invasive procedure

• Surgical pulmonary embolectomy: Often reserved for patients in

cardiopulmonary arrest; can also be used for patients with
contraindications to thrombolytic therapy, those with patent
foramen ovale, and those with intracardiac thrombi. Anesthesia
is rapidly induced, a median sternotomy performed, and the
pulmonary artery incised to remove the clot. Cardiopulmonary
bypass should be avoided in patients with patent foramen ovale
or intracardiac thrombi.

• Percutaneous catheter embolectomy with fragmentation: A

possibly life-saving measure wherein a Greenfield suction
embolectomy catheter (or other Roto-Blade cardiac catheter) is
inserted through an introducer sheath, threaded through the
pulmonary valve into the pulmonary artery, wherein the clot is
macerated and fragmented, with the fragments immediately
suctioned from the vessel to avoid distal embolization.

971
• Endovascular ultrasound delivered thrombolysis: Intended for
controlled and selective infusion of thrombolytics in the
peripheral vasculature for treatment of DVTs and PE including
“saddle emboli.” This therapy may be used in veins, arteries,
behind valves, and through IVC filters. Ultrasonic energy
prepares the clot by thinning fibrin, which increases permeability
of the clot and creates a pressure gradient to transport clot-
dissolving drugs inside the thrombus. This form is used in
difficult-to-reach areas such as behind valves, reduces the risk of
thrombus breakages and emboli, and uses less drug as the
thrombus is directly exposed to the lytic, preventing hemolysis.

7. Long-term anticoagulation to prevent recurrence of VTE

Active cancer places a patient at high risk of recurrence of PE, with
20% of patients having another VTE within the first year. Other
patient populations have lower, variable rates of recurrence based
on whether the precipitating event was attributable to a modifiable
risk factor or isolated event such as trauma or surgery. Patients
with idiopathic PE are more difficult to stratify for risk of
recurrence. Risk of bleeding must be considered when prescribing
the duration of therapy.

• Low–molecular-weight heparin: SC injections may be indicated

for a period of 6 months following hospitalization when a patient
is at high risk for repeated recurrence.

• Vitamin K antagonists (VKAs): Oral warfarin (Coumadin) is

prescribed at doses to keep the international normalized ratio
(INR) at 2 to 3. It is started within 24 hours of initiation of heparin
therapy. An average initial dose is 5 to 10 mg. Both agents are
given simultaneously for 4 to 6 days to allow time for warfarin to
inhibit vitamin K–dependent clotting factors before heparin is
discontinued. Daily warfarin dose is adjusted according to INR,
and correct dosage is individualized per patient based on
frequent INR determinations.

• Prothrombin time (PT): Monitored daily, with a

goal of 1 to 1.5 times normal. Once the patient’s

972
 condition has stabilized and the heparin is
discontinued, weekly monitoring of INR is
acceptable. After hospital discharge the PT should
be monitored every 2 weeks for as long as the
patient continues to take warfarin.

• Maintenance: May be approximately 10 mg/day,

but dosage varies greatly depending on the
patient’s age, weight, other medications taken, diet,
and other factors. Warfarin is continued for 3 to 6
months and based on the continued presence of risk
factors.

• Vitamin K administration: For bleeding

emergencies, reverses the effects of warfarin in 24 to
36 hours. Fresh-frozen plasma may be required in
cases of serious bleeding.

• Caution: Warfarin crosses the placental barrier

and can cause spontaneous abortion and birth
defects.

8. Special considerations during pregnancy

Getting an accurate diagnosis is of paramount importance,
because a prolonged course of heparin or low–molecular-weight
heparin therapy is needed to resolve the emboli. Neither drug
crosses the placental barrier or is found in breast milk in significant
amounts. All diagnostic modalities, including computed
tomography scanning, may be used without putting the fetus at
significant risk for harm. Use of SC low–molecular-weight heparin
has been increasingly recommended while evidence evolves.

973
Warfarin or another VKA is not recommended during the first and
third trimesters and is used with caution during the second
trimester. Anticoagulant therapy should be continued for 3 months
postpartum.

Care priorities: Fat emboli

1. Manage hypoxemia
Concentration of O2 is based on clinical presentation, ABG results,
and the patient’s previous respiratory status. Intubation and
mechanical ventilation may be required.

2. Control toxic vasculitis

Corticosteroids including cortisone and methylprednisolone have
been used to decrease local injury to pulmonary tissue and
pulmonary edema.

3. Manage pulmonary edema

Pulmonary edema develops in approximately 30% of patients with
fat emboli, necessitating use of diuretics to remove fluid from the
vascular system.

4. Manage right ventricular failure and cardiogenic shock

Although rare, fulminant, sudden onset cases of cardiovascular
collapse have been reported. See the sections on Heart Failure and
Cardiogenic Shock in Chapter 5.

Care priorities: Venous air emboli

Emphasis is on prevention. Ensure that the central venous

catheter is inserted with the patient in the Trendelenburg position.
Use Luer-Lok connectors on all intravenous tubing to prevent a
disconnection. Should venous air embolus occur despite
precautions, the following measures are anticipated.

974
1. Prevent further air entry
If central line is being inserted, catheter hub should be occluded
using a clamp, or the inserter’s gloved finger.

2. Manage hypoxemia
Oxygen using 100% Fio2 is initiated immediately.

3. Minimize dispersion of air bolus into central circulation

Place the patient in the Trendelenburg position with a left decubitus
tilt (turned to left side, bed in “head-down” position) to minimize
further movement of air bolus through the heart and into the
pulmonary vasculature and beyond.

4. Remove air, if possible

If a central venous catheter is in place near the right atrium, an
attempt is made to aspirate the air using a syringe.

5. Hyperbaric oxygen therapy

Case reports reveal the therapy to be beneficial with all types of air
embolization. Impressive results have been gleaned with cerebral
air embolization.

Care priorities: Intravascular foreign bodies

1. Remove the foreign body

The advanced practice provider retrieves the migrated device or
part of a device using a snare.

Care plans for pulmonary embolism

Risk for ineffective cardiopulmonary tissue perfusion 
related to partial to complete obstruction of the lumen of one/both
pulmonary arteries or smaller pulmonary vessels: the nurse will identify
and provide preventive measures and appropriate treatments for patients

975
at risk of DVT and/or VTE and other pulmonary emboli.
Goals/Outcomes: The patient is free of hemodynamic instability
and shortness of breath reflected by normal (return to the patient’s
stable baseline) vital signs and normal work of breathing. Within 12
hours of initiation of therapy, the patient has adequate gas
exchange reflected by the following ABG values: PaO2 greater than
60 mm Hg, Paco2 35 to 45 mm Hg, and pH 7.35 to 7.45. Within 2 to 4
days of initiating anticoagulant therapy, the patient’s RR is 12 to 20
breaths/min with normal depth and pattern. Unobstructed,
unidirectional blood flow at an appropriate pressure is restored
through large vessels of the pulmonary and systemic circuits.
Circulation Status; Cardiac Pump Effectiveness; Respiratory
Status: Gas Exchange.

Embolus precautions

1. Assess the patient for risk factors associated with VTE (see Table
4-7).

2. Implement VTE precautions appropriate for the patient’s risk

level.

3. Instruct the patient not to cross legs, either when in bed or sitting
in a chair.

4. Apply sequential compression hose for patients who are

bedridden. If the patient is aggressively ambulating, use of
sequential compression hose is not necessary.

5. Aggressively ambulate all appropriate patients following surgical

procedures.

6. Administer SC anticoagulants as ordered or according to VTE

prophylaxis protocol/guidelines.

Table 4-7
RISK FACTORS FOR VENOUS THROMBOEMBOLISM IN
HOSPITALIZED PATIENTS*

976
 Age >50 years Previous history of venous Myocardial infarction
thromboembolism (VTE)
Myeloproliferative Impaired mobility, paresis, or Acute or chronic lung disease
disease paralysis
Dehydration Recently bedridden >3 days Obesity
Congestive heart Inflammatory bowel disease Known thrombophilic stroke
failure
Active Active rheumatic disease Varicose veins or chronic
malignancy/cancer venous stasis
Moderate to major Nephrotic syndrome Pregnancy
surgery
Hormone replacement Sickle cell disease Recently postpartum with
therapy immobility
Central venous Estrogen therapy or estrogen
catheter in place contraceptives
*
Patients who have more than a single condition are at increased risk of developing
venous thromboembolism. The more conditions present, the higher the risk.

Embolus care: Pulmonary

1. Evaluate chest pain for intensity, location, and precipitating and

relieving factors.

2. Auscultate breath sounds to assess for presence of crackles or

other changes that may account for shortness of breath.

3. Monitor respiratory pattern for increased work of breathing.

4. Monitor the determinants of tissue O2 delivery as possible

(cardiac output, hemoglobin level, O2 saturation/pulse
oximetry/ABGs).

5. Evaluate ABGs for decreased PaO2 (hypoxemia), increased level

of CO2 (hypercapnia), and decreased pH (acidosis).

6. Assess for symptoms of respiratory failure and inadequate tissue

oxygenation including altered mental status, anxiety, restlessness,
increased work of breathing, pallor, cyanosis, and inability to
maintain O2 saturation without repeated increases in amount of
supplemental O2.

7. Instruct the patient/family/support system regarding diagnostic

977
tests needed as part of differential diagnosis.

8. Screen the patient for risk of bleeding (see the VTE prophylaxis
chart) in preparation for anticoagulant and possibly thrombolytic
drug administration.

9. Administer anticoagulants as ordered and monitor for bleeding

complications. If unfractionated or low–molecular-weight heparin
is used, monitor for decreased platelet count, which may signal
development of heparin-induced thrombocytopenia.

10. Administer thrombolytic agents as ordered and monitor for

bleeding complications.

11. Consult with the dietician to ensure that the patient maintains a
diet with consistent intake of vitamin K if VKAs, such as warfarin
(Coumadin) are initiated. Varying vitamin K intake may have a
marked effect on the ability to regulate the appropriate dose of
medication to avoid bleeding and clotting complications.

12. Consult with the pharmacist about use of IV protamine sulfate,

if the patient has the need for heparin reversal as a result of severe
bleeding.

13. To avoid negative interactions with anticoagulants or

thrombolytic therapy, establish compatibility of all drugs before
administering them:

• Heparin: Digitalis, tetracyclines, nicotine, and

antihistamines decrease the effect of heparin
therapy. Establish compatibility before infusing
other IV drugs through heparin IV line.

• Warfarin sodium: Numerous drugs result in a

decrease or an increase in response to treatment
with warfarin. Consult with the pharmacist to
obtain specific information about the patient’s

978
 medication profile.

• Thrombolytic therapy: Do not infuse other

medications through the same IV line.
14. Monitor PT with INR when using warfarin and aPTT when
using heparin. Adhere carefully to drug titration and/or dosage
guidelines.

15. Monitor neurologic status for deterioration because recurrent

embolism, shock attributable to bleeding, cardiogenic shock, and
intracranial bleeding are possible. Neurologic changes are the first
subtle sign that shock may be ensuing.

16. Medicate for pain as needed.

Hemodynamic regulation

1. Recognize presence of BP alterations.

2. Auscultate heart and breath sounds.

3. Monitor SVR and pulmonary vasculature resistance (PVR). PVR

will be elevated with massive or saddle embolus, and can prompt
right ventricular failure. SVR changes with the stages of shock.
Initially, SVR is high while the body attempts to raise BP in the
presence of cardiogenic shock if right ventricular failure has
ensued.

4. Implement recommendations for managing right ventricular

failure as ordered.

• Systemic hypotension should be managed to avoid

progression of right ventricular failure.

• Regulate vasoactive drugs. Vasopressor drugs such

as dopamine or Levophed will increase afterload

979
 and may worsen heart failure. Inodilator drugs
such as milrinone, amrinone, and, to a lesser extent,
dobutamine may not work well, because all
decrease venous return, which may also worsen
right ventricular failure.

• Aggressive fluid challenge is not recommended,

despite some evidence of efficacy in right
ventricular failure. Hemodynamics of right
ventricular failure differs in the scenario of acute
PE, because heart disease is not the root cause of the
problem.
5. Monitor for hypovolemic shock resulting from excessive bleeding
when using thrombolytics or anticoagulants. Patients may develop
either hypovolemic or cardiogenic shock in the setting of PE.
Differential diagnosis of shock states may be assisted by examining
PAPs and cardiac output.

• Cardiogenic shock/right ventricular failure related

to PE: Elevated CVP, elevated PVR, and decreased
cardiac output.

• Hypovolemic shock related to hemorrhage:

Decreased CVP, decreased PVR, and decreased
cardiac output.

• Combined right ventricular failure and bleeding:

Because CVP and PVR effects are opposite,
hemodynamic readings may be difficult to
interpret.

980
Bleeding precautions

1. Maintain bed rest during active bleeding.

2. Administer blood products (fresh-frozen plasma, platelets,

cryoprecipitate) as ordered.

3. Protect the patient from trauma, which may cause bleeding.

4. Avoid taking rectal temperatures.

5. Avoid puncturing the skin for injections, blood samples, and

starting IV lines as much as possible.

6. The patient should wear shoes when ambulating, to avoid

injuring the feet.

7. The patient should use a soft toothbrush for oral care.

8. The patient should use an electric razor for shaving.

9. Coordinate timing of invasive procedures with administration of

fresh-frozen plasma and platelets as much possible to lessen the
chance of bleeding.

10. Refrain from inserting devices into bleeding orifices.

Bleeding reduction

1. Identify the cause of bleeding.

2. Note hemoglobin/hematocrit levels before and after blood loss.

3. Maintain patent IV access so that transfusions can occur quickly

if needed.

4. Arrange for the availability of blood products, possibly using

blood typing, screening, and holding the sample until products are
needed.

981
5. Administer blood products if needed and monitor for transfusion
reaction.

6. Instruct the patient and family regarding signs of bleeding

(bruising, nosebleeds, bleeding gums) and to notify the nurse if
bleeding ensues.

7. Instruct the patient on activity restrictions and how to apply

direct pressure if bleeding ensues before the nurse arrives.

8. Discuss severity of bleeding and measures being provided to

manage the situation.

9. Avoid use of drugs containing aspirin and NSAIDs (e.g.,

ibuprofen), which are platelet-aggregation inhibitors that prolong
episodes of bleeding.

10. Monitor serial coagulation or thrombin times. Report values

outside the desired therapeutic ranges. Optimal range for aPTT is
1.5 to 2.5 times control value. A therapeutic INR is 2 to 3. Optimal
range for thrombin time is 2 to 5 times normal.

11. Ensure easy access to antidotes for prescribed treatment:

• Protamine sulfate: 1 mg counteracts 100 units of

heparin. Usually, the initial dose is 50 mg.

• Vitamin K: 20 mg given SC.

• Epsilon-aminocaproic acid (e.g., Amicar): Reverses

the fibrinolytic condition related to thrombolytic
therapy.

Teaching: Oral anticoagulant therapy

1. Determine the patient’s knowledge of oral anticoagulant therapy.

982
2. Discuss the drug name, purpose, dosage, schedule, potential side
effects, and complications of therapy.

3. Inform the patient of the potential side effects and complications

of anticoagulant therapy: easy bruising, prolonged bleeding from
cuts, spontaneous nosebleeds, black and tarry stools, and blood in
urine and sputum.

4. Teach the rationale and application procedure for antiembolism

stockings. Explain that the patient should put them on in the
morning before getting out of bed.

5. Stress the importance of preventing impairment of venous return

from the lower extremities by avoiding prolonged sitting, crossing
the legs, and wearing constrictive clothing.

6. Teach the patient about foods high in vitamin K (e.g., fish,

bananas, dark-green vegetables, tomatoes, cauliflower), which can
interfere with anticoagulation. The patient must understand the
importance of a consistent intake of foods high in vitamin K to
avoid bleeding or clotting complications.

7. Caution the patient that a soft-bristle toothbrush, rather than a

hard-bristle one, and an electric razor, rather than a safety razor,
should be used during anticoagulant therapy while at home.

8. Instruct the patient to consult with the advanced practice

provider before taking any new over-the-counter or prescribed
drugs. The following are among many drugs that enhance the
response to warfarin: aspirin, ibuprofen, cimetidine, and
trimethoprim. Drugs that decrease the response include antacids,
diuretics, oral contraceptives, and barbiturates, among others.

Acid-Base Management; Acid-Base Monitoring; Bedside

Laboratory Testing; Health Education; Oxygen Therapy;
Respiratory Monitoring; Surveillance; Teaching: Individual;
Teaching: Prescribed Medication; Respiratory Monitoring; Vital
Signs Monitoring.

983
Pulmonary hypertension
Pathophysiology
Pulmonary hypertension and pulmonary arterial hypertension
(PAH) are complex, progressive, often fatal diseases caused by
elevated pulmonary pressures. PAH is defined as a mean
pulmonary artery pressure (MPAP) greater than 25 mm Hg,
pulmonary capillary wedge pressure (PCWP) or left atrial pressure
or left ventricular end-diastolic pressure less than 15 mm Hg, and
PVR greater than 3 Wood units. Wood units are a calculated PVR
that is obtained by subtracting the PCWP from the PAP systolic and
dividing by the cardiac output. The pulmonary vasculature is
normally a highly distensible, low-resistance system. All types of
pulmonary hypertension or PAH may result in right ventricular
failure, because the right ventricle is under constant strain to pump
into the highly resistant pulmonary vasculature. (See Table 4-10 for
World Health Organization classifications.) Each classification of
pulmonary hypertension has a different cause and different
approach to therapy.
Idiopathic pulmonary arterial hypertension (IPAH) is rare, has a
poor prognosis, and affects primarily middle-aged and young
women. Causes of IPAH are unclear. Heritable PAH is thought to
be familial with a link to germline mutations, such as bone
morphogenetic receptor 2 (BMPR2) or other causes. Associated
pulmonary arterial hypertension (APAH) is attributable to
secondary causes such as scleroderma or portopulmonary
hypertension. Other causes of pulmonary hypertension are more
common, with management directed at treating the underlying
cause and lowering PAPs using vasodilator drugs. IPAH and
APAH are often unresponsive to conventional treatments and may
require specialty therapies.
In PAH, there is dysfunction and imbalance between vasodilation
and vasoconstriction of the pulmonary vasculature from the right
side of the heart to the lungs resulting in chronic vasoconstriction.
The vessel walls thicken and hypertrophy causing vascular
remodeling from a non–muscular low-pressure system to a high-
pressure, low-flow system. The endogenous vasodilators, nitric

984
oxide and prostacyclin production, are impaired. In addition,
endothelin-1, a potent endogenous vasoconstrictor, is increased.
This increase in PVR and impedance to flow causes right
ventricular strain, impaired filling, and increased right ventricular
dilatation. This then leads to right ventricular ischemia. Eventually,
the right side of the heart weakens and is unable to accommodate
venous blood returning to the heart. PAH is generally a primary
disease of the right side of the heart.
The pathophysiology of pulmonary hypertension differs from
PAH in that it is generally attributable to primary disease of the left
side of the heart such as left ventricular diastolic dysfunction or
valvular heart disease. See the section on Heart Failure (Chapter 5)
for further discussion of left-sided to right-sided heart failure.
Pulmonary hypertension may also be caused by chronic
pulmonary diseases such as COPD or PE leading to cor pulmonale.
The pulmonary vasculature responds to alveolar hypoxia by
vasoconstriction, a beneficial mechanism that shunts blood away
from underventilated areas to better ventilated areas in the lungs,
thereby improving oxygenation. The resulting rise in PAP and
increase in PVR from acute hypoxia are completely reversible once
the hypoxia has been resolved. However, in the presence of chronic
hypoxia, the pulmonary vasculature undergoes permanent changes
similar to the changes in PAH, causing vascular remodeling. The
right ventricle dilates and hypertrophies under the constant strain
and workload. Eventually, the right side of the heart weakens and
is unable to accommodate venous blood returning to the heart. As a
result, pressure in the systemic venous circulation increases,
causing cor pulmonale, or right-sided heart failure.

Assessment
Goal of assessment
Because the low-resistance pulmonary vascular bed is clinically
silent until late in the disease process, onset is insidious.
Assessment before late stages of the disease should focus on
discerning the cause of early indicators and classifying functional
status (Box 4-2) so that an appropriate plan of care is created.

985
Box 4-2
WORLD HEALTH ORGANIZATION
CLASSIFICATION: FUNCTIONAL STATUS
OF PATIENTS WITH PULMONARY
HYPERTENSION
Class I: Patients with pulmonary hypertension (PH) but without
resulting limitation of physical activity. Ordinary physical
activity does not cause undue dyspnea or fatigue, chest pain, or
near syncope.

Class II: Patients with PH resulting in slight limitation of physical

activity. They are comfortable at rest. Ordinary physical activity
causes undue dyspnea or fatigue, chest pain, or near syncope.

Class III: Patients with PH resulting in marked limitation of

physical activity. They are comfortable at rest. Less than ordinary
activity causes undue dyspnea or fatigue, chest pain, or near
syncope.

Class IV: Patients with PH with inability to carry out any physical
activity without symptoms. These patients manifest signs of
right-sided heart failure. Dyspnea and/or fatigue may even be
present at rest. Discomfort is increased by any physical activity.

History and risk factors

Factors associated with PAH and pulmonary hypertension include
familial, exposure to amphetamines, connective tissue diseases,
congenital anomalies (patent foramen ovale or ventricular septal
defect) by which additional blood is shunted from the left side of
the heart to the right side of the heart, left ventricular failure,
acidemia, COPD, sleep apnea, interstitial lung disease or
pulmonary fibrosis, massive PE, ARDS resulting in noncardiogenic

986
pulmonary edema, and an array of other causes. See Table 4-10 for
etiologic factors.

Table 4-10
WORLD HEALTH ORGANIZATION CLINICAL CLASSIFICATION OF
PULMONARY HYPERTENSION

World Health
Organization Subsets/Examples of Causes
Class/Group
1. Pulmonary 1.1 Idiopathic PAH (IPAH): Occurs at random. Also known as primary
arterial pulmonary hypertension.
hypertension 1.2 Heritable: Formerly familial PAH; includes two types of PAH.
(PAH) 1.3 Drug- and toxin-induced: Includes antiobesity drugs such as [fen-phen]
(fenfluramine + phentermine), methamphetamine, and cocaine.
1.4 Associated with other disorders: Diseases include connective tissue
diseases, human immunodeficiency virus (HIV), portal hypertension,
congenital heart disease, schistosomiasis, chronic hemolytic anemia, and
persistent pulmonary hypertension of the newborn.
2. Pulmonary 2.1 Systolic dysfunction
hypertension 2.2 Diastolic dysfunction
(PH) with left- 2.3 Valvular disease
sided heart
disease
3. PH associated 3.1 Chronic obstructive pulmonary disease
with lung 3.2 Interstitial lung disease
diseases and/or3.3 Other pulmonary diseases with mixed restrictive and obstructive
hypoxemia pattern
3.4 Sleep-disordered breathing
3.5 Alveolar hypoventilation disorders
3.6 Chronic exposure to high altitude
3.7 Developmental abnormalities
4. Chronic Pulmonary thromboembolism or embolism attributable to fat, tumor,
thromboembolic parasites, and foreign material.
pulmonary
hypertension
5. Unclear 5.1 Hematologic disorders
multifactorial 5.2 Systemic disorders: sarcoidosis, pulmonary Langerhans’ cell
mechanisms histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, and
vasculitis.
5.3 Metabolic disorders: glycogen storage disease, Gaucher disease, and
thyroid disorders.
5.4 Others: tumoral obstruction, fibrosing mediastinitis, and chronic renal
failure on dialysis.
From Simonneau G, Robbins IM, Beghetti M, et al: Updated clinical classification of
pulmonary hypertension. J Am Coll Cardiol 54 S43-S54, 2009.

Clinical presentation

Early indicators

987
Exertional dyspnea, fatigue, and weakness.

Late indicators
Chest pain, dizziness, syncope, palpitations, and lower extremity
edema.

Vital signs
• Tachycardia and tachypnea.

• BP may increase or decrease, depending on response to any

changes in cardiac output, which may be significant with
markedly elevated PAPs.

Observation/inspection
• Cyanosis of the lips and nail beds.

• Peripheral edema.

• Hepatic enlargement and ascites.

• Anasarca (generalized, massive edema).

• Distended jugular veins.

Palpation
• Right ventricular heave (visible left parasternal systolic lift).

Auscultation
• Accentuated pulmonary component of the second heart sound.

• Right ventricular heave at the left parasternal area.

• Systolic murmur of tricuspid regurgitation.

• S3 or S4.

988
• Distant breath sounds.

• Clear or basilar crackles in lung fields.

Screening diagnostic tests

• Chest radiograph: Validates presence of underlying pathology,
which may have prompted development of pulmonary
hypertension.

• 12-Lead electrocardiogram (ECG): Assesses if the patient has an

acute myocardial infarction associated with heart failure. May
show right ventricular hypertrophy or strain, right-axis
deviation, right bundle branch block, and enlarged P waves.

Diagnostic Tests for Pulmonary Hypertension

Test Purpose Abnormal Findings

Arterial blood gas Important to the differential Values vary: Generally Pao2 will be less
(ABG) values diagnosis of the cause of than 60 mm Hg. Paco2 will be within
pulmonary hypertension. normal limits (35 to 45 mm Hg) unless
chronic obstructive pulmonary disease
is the cause of the pulmonary
hypertension, in which case Paco2 is
usually elevated.
Chest radiograph Will confirm anatomic Right ventricular dilation or
abnormalities associated with hypertrophy, enlarged pulmonary
chronic right ventricular failure. artery secondary to increased pressure,
and diminished diaphragmatic
excursion.
Computed Helps to identify specific Will confirm the presence of interstitial
tomography scan pathology. lung disease.
Hemodynamic Helps to confirm the presence of Cardiac output can be a better measure
measurements elevated pulmonary artery of disease severity than the pulmonary
pressures and monitor treatment artery pressures. Used for definitive
effectiveness. Pressures in the diagnosis of pulmonary hypertension.
pulmonary vasculature are
measured by a pulmonary artery
(e.g., Swan-Ganz) catheter.
Right heart Gold standard for definitive Data will differentiate or quantify the
catheterization diagnosis. contribution of the left or right
ventricular failure and measure the
response to pharmacotherapy.
Echocardiography Assesses for elevated pulmonary May reveal enlarged right atrium and
artery systolic pressure, but not right ventricle, diminished wall
the mean pulmonary artery motion, and pulmonic valve
pressure. Hemodynamic malfunction (midsystolic closure or
monitoring is used for definitive delayed opening). Unfortunately, false-

989
 diagnosis. positive results are common with
echocardiography.
Pulmonary Important for differential Will vary according to cause.
function tests diagnosis of the underlying
pathologic condition.

Pulmonary To rule out an embolic event as the Will not be positive if the cause is
angiography and underlying cause. pulmonary hypertension.
perfusion scans

Red blood Screens for polycythemia May be increased above normal.

cell/hematocrit associated with chronic hypoxia.
values

Type B natriuretic Monitors the progress of any Will be progressively elevated as heart
peptide level associated heart failure. failure worsens.
Other blood tests Used to rule out other possible Various values will be positive for
diagnoses, such as liver disease, specific pathologies.
human immunodeficiency virus
(HIV), and autoimmune disease.

Collaborative management
The goal of interdisciplinary management is to diagnose and treat
the underlying disorder or process causing the pulmonary
hypertension and improve the patient’s symptoms, functional
status, quality of life, and survival. Treatment is directed primarily
toward preventing progression of the disease, preventing thrombi
in situ, and reducing pulmonary artery vasoconstriction.

Care priorities

1. Relieve hypoxemia and improve gas exchange

• Oxygen therapy: To eliminate hypoxia, a cause of pulmonary

vascular vasoconstriction, and the resulting right ventricular
afterload.

2. Promote dilation of the pulmonary vasculature to

promote blood flow and better gas exchange

• Nitric oxide therapy: Nitric oxide gas is administered through

either a face mask or artificial airway to promote pulmonary
vasodilation. The vasodilation reduces BP in the pulmonary
circulation. Owing to the short half-life of nitric oxide, chronic

990
 therapy is not available. It is currently under research as a
portable device.

• Vasodilators:

• Calcium channel blockers: Are used to reverse

pulmonary vasoconstriction, reduce right
ventricular afterload, and enhance pulmonary
blood flow in a small subset of patients who show a
positive vasoreactive response during cardiac
catheterization.

• Endothelin blockers: Medications such as bosentan

(Tracleer), ambrisentan (Letairis), and macitentan
(Opsumit) block endothelin, which contributes to
vasoconstriction and vascular remodeling. Liver
function tests must be performed monthly. Note:
Endothelin blockers are contraindicated for use in
pregnancy as a result of teratogenic effects.

• Prostacyclin (PGI2) analogues: Produced in

endothelial cells from prostaglandin H2, PGI2
vasodilates the pulmonary vessels. Prostacyclin also
prevents formation of platelet plugs. Synthetic
prostacyclin analogues (epoprostenol [Flolan],
epoprostenol room temperature stable [Veletri],
iloprost [Ventavis], treprostinil [Remodulin,
Tyvaso]) are given IV, SC, or by inhalation. These
medications require specialized infusion or
inhalation devices. The first PO prostacyclin
medication has recently been approved, treprostinil
(Orenitram). Note: Prostacyclin is inhibited by

991
 NSAIDs, so the patient must be educated to avoid
them.
• Phosphodiesterase-5 (PDE-5) inhibitors: Vasodilates the
pulmonary vessels. Sildenafil (Revatio) and tadalafil (Adcirca)
while used for pulmonary hypertension are also marketed under
the trade names of Viagra and Cialis at much lower doses for
erectile dysfunction.

• Guanylate cyclase stimulator: New classification of medication

that is specifically for use in chronic thromboembolic pulmonary
hypertension. Riociguat (Adempas) is an oral medication and
works by stimulation of the enzyme, which is responsible for the
production of nitric oxide.

3. Reduce circulating blood volume to reduce strain on the

right side of the heart

• Diuretics: Reduce circulating volume via loss of sodium and

water, which may decrease PAP and right ventricular workload.
In turn, this reduces leftward septal bulging seen with right
ventricular overload. Carefully evaluate response; if the patient’s
condition declines, a volume infusion may be needed if the
patient is in right ventricular failure. Higher right ventricular
pressure may be needed to overcome the elevated PAP to
promote right ventricular ejection.

4. Enhance myocardial contractility to improve blood flow

through the pulmonary and systemic circulation:

• Digitalis: Generally used only with biventricular failure when

other therapies have not been sufficient. The inotropic effects of
digitalis can increase cardiac output and pulmonary resistance,
which are deleterious in the presence of right ventricular failure.

5. Prevent pulmonary thromboembolism:

• Anticoagulants: Warfarin is used for ongoing prevention of

992
 pulmonary emboli (blood clots in the lungs).

HIGH ALERT!
Complex Parenteral Therapy
Epoprostenol and treprostinil are the only intravenous
medications delivered in nanogram per kilogram per minute
(1,000,000 [1 million] nanograms = 1 milligram). Because of the
high risk of dose errors, verification of correct dose and dose
weight should occur with the patient and family, specialty
pharmacy, inpatient pharmacy, pulmonary arterial hypertension
team if the institution has one, and provider team. Parenteral
therapy should not be stopped, flushed, or diluted for any reason,
and must be infused in a dedicated line without any flush bag.
Owing to the short half-life of the medication epoprostenol, there
must be an immediate backup bag available at all times. Any
interruption or error in calculation can lead to rebound pulmonary
hypertension and risk of death.

Care plans for pulmonary hypertension

Risk for ineffective cardiopulmonary tissue perfusion 
related to blood flow anomalies stemming from pulmonary hypertension
and right ventricular strain.
Goals/Outcomes: Within 24 hours of initiating vasodilator
medications, diuretics, and inotropic agents, PAPs are reduced by
at least 10%, CVP or right atrial pressure is maintained at a level
that facilitates forward flow of blood if the patient has right
ventricular failure, PVR is reduced below 3 Wood units or below
300 dynes/s/cm−5, and cardiac index is at least 2 L/min/m2. Systemic
BP is maintained at no less than 90 mm Hg systolic, with diastolic
pressure at least 50 mm Hg.
Tissue Perfusion: Pulmonary; Tissue Perfusion: Cardiac;
Cardiac Pump Effectiveness; Respiratory Status: Gas Exchange;

993
Circulation Status.

Hemodynamic regulation

1. If present, monitor PAPs and cardiac output in response to

vasodilator medications, diuretics, and inotropic medications.

2. Monitor invasive or noninvasive BP for improvement. Owing to

the vasodilatory effects of acute and chronic PAH therapies, the
patient may be normally hypotensive and the normal BP for the
patient must be established. Medications and intravascular volume
regulation may help improve cardiac output and systemic
circulation. Those with right ventricular failure require a delicate
balance between medication administration and volume regulation.

3. Auscultate breath sounds to assess for crackles at least every 2

hours.

4. Monitor for decreased urine output every 2 hours. Improvement

in urine output is reflective of improved systemic circulation,
resulting in improved renal blood flow.

5. If available, judiciously monitor CVP or right atrial pressure if the

patient has right ventricular failure. Preload must be maintained at
a sufficient level to be able to overcome the increased resistance to
ejection (right ventricular afterload) created by pulmonary
hypertension. The patient may require a CVP that is considerably
higher than normal to facilitate forward flow of blood. If diuretics
worsen hemodynamics, a volume infusion may be attempted to see
if the cardiac output improves.

Impaired gas exchange 

related to altered blood flow secondary to pulmonary capillary constriction
and fluid, which may be present in the alveoli secondary to heart failure.
Goals/Outcomes: Gas exchange improves within 12 hours of
initiating therapies, toward a goal of at least 90%. Those who are
O2-dependent must be assessed using their baseline value coupled
with their activity tolerance, because both are lower than expected
for the general population.

994
 Respiratory Status: Gas Exchange.

Oxygen therapy

1. Administer O2 as prescribed. Advance O2 delivery devices as

needed. If the patient requires consistent increases in Fio2 to
maintain the same O2 saturation, notify the advanced practice
provider, because this is a sign of deteriorating gas exchange.

2. Assess respiratory pattern, rate, and depth; chest excursion and

use of accessory muscles.

3. Monitor ABG results for hypoventilation, a sign of impending

respiratory failure. (See Acute Respiratory Failure).

Ventilation assistance

1. Monitor for changes in O2 saturation and work of breathing in

response to pulmonary vasodilator medications. If the patient fails
to improve and respiratory distress increases, the patient must be
intubated and placed on mechanical ventilation. (See Mechanical
Ventilation for detailed information.)

2. Provide emotional and spiritual support for the patient and his or
her support system. (See Emotional and Spiritual Support of the
Patient and Significant Others, Chapter 2.)

3. Once the patient is on mechanical ventilation, strategies such as

nitric oxide therapy can be initiated for patients who are severely ill
and unresponsive to other vasodilator medications. Patients
receiving nitric oxide should improve their O2 saturation within 24
hours of initiating treatment. In addition, optimal ventilation
management in the patient with right ventricular failure may
include low tidal ventilation and low PEEP. Hyperinflation and
increased PEEP can lead to excessive PVR and fatal drop in cardiac
output.

4. If the patient is unable to sustain an improved O2 saturation on

995
nitric oxide, the advanced practice provider may need to approach
the patient (if aware and oriented) and support system about
extracorporeal membrane oxygenation if they are a candidate for
heart-lung transplantation. If there are no further options available,
discontinuation of life support may need to be addressed (see
Ethical Considerations in Critical Care, Chapter 2).

Deficient knowledge 
related to disease process and treatment of pulmonary hypertension and
associated underlying diseases if present.
Goals/Outcomes: Throughout the hospitalization, the patient and
support system voice understanding of the plan of care; within 24
hours of hospital discharge, the patient and support system
verbalize sufficient knowledge of management of the disease
process(es) and treatments to sustain the patient outside the
hospital.
Knowledge: Disease Process; Knowledge: Treatment and
Procedure(s).

Teaching: Treatments and procedures

1. Explain all steps in the process of providing various O2 delivery

and ventilatory support strategies.

2. Discuss the selection of various modalities of vasodilator

therapies. Inhaled medications and SC and IV infusions that will be
continued outside the hospital require more extensive education
and patient demonstration of independence before discharge.
Owing to the high cost of medications and long-term care
restrictions, patients may not be discharged to rehabilitation or
skilled nursing facilities.

3. Involve case manager who is specialized in PAH if available and

discharge planner in discussions of medications, so that all resource
options are clarified. Many of the medications used are obtained
from specialty pharmacies only and must be preapproved
financially and clinically before administration and/or discharge.

996
4. If the patient requires mechanical ventilation, ensure that the
patient understands how to communicate with care providers (see
Mechanical Ventilation care plans for further details).

5. When preparing for discharge home, discuss the purpose of

medications designed to reduce the workload on the heart
(vasodilators), relax the heart (calcium channel blocking agents),
and prevent fluid accumulation (diuretics). Include teaching and
discussion of two forms of birth control for all women of child-
bearing years because of the high maternal mortality between (30%
and 50%), along with teratogenic effects of warfarin and endothelin
blockers.

6. Ensure that the patient is familiar with the home health providers
who will provide O2 therapy and other ventilation strategies, such
as a nebulizer or aerosol, if needed.

Teaching: Disease process

1. Assess the patient’s level and key support system members’ level
of understanding of the disease process.

2. If the cause of pulmonary hypertension has been identified,

discuss appropriate management strategies of the associated
disease process.

3. Discuss lifestyle changes that could prevent further

complications.

4. Explain the value of learning relaxation therapy, including

various breathing and visualization exercises, listening to music,
meditation, and biofeedback.

5. Explain how smoking and second-hand smoke increase the

workload of the heart by causing vasoconstriction. The patient
should be encouraged to live in a smoke-free environment. Support
system members who smoke should be given the opportunity to
understand this vital information. Smoking cessation information
should be provided.

997
6. If activity has been progressively impaired, consult with a
physical therapist and respiratory therapist regarding an
appropriate exercise program.

7. Have a dietician visit the patient to offer assistance with meal

planning.

Activity Therapy; Airway Management; Acid-Base

Monitoring; Anxiety Reduction; Cardiac Care: Acute; Coping
Enhancement; Invasive Hemodynamic Monitoring; Medication
Administration: Intravenous; Medication Administration:
Inhalation; Medication Administration: Oral; Self-Care Assistance;
Sleep Enhancement; Support Group.

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CHAPTER 5

Cardiac and vascular

disorders
Cardiovascular assessment: General
Goal of system assessment
Evaluate for decreased cardiac output (CO) and decreased tissue
perfusion.

Vital sign assessment

Measure heart rate (HR), heart rhythm, and blood pressure (BP) to
evaluate CO and perfusion.

• Measure BP on both arms using an appropriate sized cuff. Use the

higher reading to monitor BP.

• Compare cuff BP to arterial line BP if arterial line is in place;

decide which pressure is the most accurate; treat BP using that
value.

• Note pulse pressure.

• Considerations for the bariatric patient: Use

appropriate BP cuff. Avoid using thigh cuff on the
bicep or forearm.

1009
12-lead electrocardiogram
Evaluate for changes from last electrocardiogram (ECG) to assess
for worsened heart disease (myocardial damage) or for electrolyte
imbalances, which may decrease CO; this should be done on every
patient to use for comparison.

• Heart rate: diagnose type of tachycardia, bradycardia, or irregular

rhythm

• PR, QRS, and QT intervals

• ST segment and T wave changes such as depression or elevation

• Pacing and conduction: Regular, normal rate and velocity

Considerations for the bariatric patient: Low

voltage may be noted on the ECG tracing.

Observation
• Evaluate for facial and lip color, appearance of skin and nails, and
patterns of edema (especially dependent areas) to evaluate for
decreased tissue perfusion.

Considerations for the bariatric patient: The

bariatric patient may have excess tissue and
“stretch marks” because of increased body surface
area.

• Inquire about the presence of chest, arm, and jaw discomfort.

• Inquire about compliance with taking cardiac medications as

1010
 prescribed.

Considerations for the bariatric surgery patient:

For those patients who have bariatric bypass
surgery, note that pills must be crushed. Find
alternatives to sustained-release tabs/capsules as
they will not be absorbed.

Palpation
Pulse assessment to evaluate for decreased tissue perfusion:

• Pulse quality and regularity bilaterally (scale 0 to 4+)

• Edema (scale 0 to 4+: Extremities, back, and sacrum)

• Capillary refill

• Evaluate all peripheral pulses to assess for vascular disease.

Auscultation
• Heart sounds to evaluate for contributors to decreased CO (note
changes with body positioning and respirations):

Considerations for the bariatric patient: Heart

sounds may be distant because of large body
habitus
• Aortic, pulmonic, Erb point, tricuspid, mitral

• S1 (lub) and S2 (dub): Quality, intensity, pitch

• Extra sounds: S3 (after S2), S4 (before S1) indicative of heart failure

(HF)

1011
• Extra sounds: Murmurs, clicks (may indicate valve disease)

• Extra sounds: Friction rub indicative of pericarditis

Labwork
Blood studies can reveal causes of dysrhythmias or changes in
pacing/conduction or HR changes:

• Electrolyte levels: ↑ or ↓ potassium, magnesium, sodium, chloride,

and calcium

• Complete blood counts: Anemia, ↑ white blood cells (WBCs)

• Coagulation studies

• Lipid profile

• Cardiac enzymes/isoenzymes/troponin

• B-type natriuretic peptide (BNP)

• Levels of cardiac medications

Care plans for generalized cardiovascular

dysfunctions
Activity intolerance 
related to decreased cardiac output (CO)
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the critical care unit (CCU), the patient exhibits
cardiac tolerance to increasing levels of activity as evidenced by
respiratory rate (RR) less than 24 breaths per minute (breaths/min),
normal sinus rhythm (NSR) on ECG, BP within 20 mm Hg of the
patient’s normal range, HR less than 120 beats per minute (bpm) (or
within 20 bpm of resting HR for patients on beta-blocker therapy),
and absence of chest pain.
Endurance

1012
Energy management

1. Determine patient’s physical limitations.

Considerations for the bariatric patient: Assess the

previous level of functioning before hospitalization.
Fatigue can be common in a bariatric patient.

2. Determine causes of fatigue and perceived causes of fatigue.

3. Monitor cardiorespiratory response to activity (tachycardia, other

dysrhythmias, tachypnea, dyspnea, diaphoresis, pallor) and
hemodynamic response (elevated pulmonary artery pressures
[PAPs], central venous pressure [CVP], or no change/little increase
in CO) if a pulmonary artery catheter or bioimpedance device is in
place.

4. Monitor for chest discomfort during activity.

5. Reduce all causes of discomfort, including those induced by the

patient’s environment, such as uncomfortable room temperature or
position, thirst/dry mouth, and wrinkled or damp bedding.

6. Provide alternating periods of rest and activity.

Self-care assistance: Instrumental activities of daily living

1. Determine need for assistance with Instrumental Activities of

Daily Living (IADLs) including walking, cooking, shopping,
housekeeping, transportation, and money management.

2. Provide for methods of contacting support/assistance (such as

lifeline services and emergency response services including readily
accessible telephone numbers if the patient’s area is not 911
accessible).

3. Determine financial resources and personal preferences for

modifying the home to accommodate any disabilities.

1013
Decreased cardiac output 
related to altered cardiac pump function.
Goals/Outcome: Within 24 hours of this diagnosis, the patient
exhibits adequate CO, as evidenced by BP within normal limits for
the patient, HR 60 to 100 bpm, NSR on ECG, peripheral pulses
greater than 2+ on a 0 to 4+ scale, warm and dry skin, hourly urine
output greater than 0.5 mL/kg, measured CO 4 to 7 L/min, CVP 4 to
6 mm Hg, PAP 20 to 30/8 to 15 mm Hg, pulmonary artery wedge
pressure (PAWP) 6 to 12 mm Hg, and patient awake, alert, oriented,
and free from anginal pain.
Considerations for the bariatric patient: Preload and after
load may be increased because of increased blood volume.
Circulation Status

Cardiac care: Acute

1. Palpate and evaluate quality of peripheral pulses, for presence of

edema, capillary refill, and skin color and temperature of
extremities.

2. Monitor ECG continuously, noting HR and rhythm. Select the

most diagnostic lead(s) for monitoring patient. Consider use of ST-
segment monitoring if available.

3. Compare current ECG readings with past readings and report

abnormal findings that create instability or have the potential to
create instability.

4. Use a 12- or 15-lead ECG to diagnose heart rhythm changes,

because one or two leads are often insufficient to fully diagnose
ECG changes.

5. Provide antidysrhythmic medications as appropriate to abate

heart rhythms that prompt hypotension, chest discomfort, or
fatigue. Consult with advanced practice provider for symptomatic
ECG rhythm changes.

6. Provide positive inotropic drugs as appropriate to help increase

CO to maintain stable BP.

1014
7. Monitor effects of negative inotropic medications (e.g., beta
blockers) carefully, as the decreased myocardial workload may
prompt hypotension.

8. Evaluate chest pain for location, radiation, intensity, duration,

and precipitating factors. Emphasize to the patient the importance
of reporting all instances of chest pain and pressure and arm, neck,
and jaw pain.

9. Apply oxygen when chest pain is present, according to Advanced

Cardiac Life Support (ACLS) guidelines.

10. Monitor pacemaker function as appropriate to insure device is

sensing, pacing, and capturing appropriately.

11. Auscultate heart tones; be alert for development of new S3 and

S4, new “split” sounds, or pericardial friction rubs.

12. Auscultate lungs for rales, crackles, wheezes, rhonchi, pleural

friction rubs, or other adventitious sounds indicative of fluid
retention.

13. Monitor for diminished level of consciousness or altered mental

status, which may signal cerebral perfusion is compromised
secondary to decreased CO.

14. Auscultate abdomen and monitor for decreased bowel sounds

and/or abdominal distention, which may indicate abdominal
perfusion is compromised.

15. Record intake and output (I&O), urine output, and daily weight
and evaluate for fluid retention, which may indicate compromised
renal perfusion.

16. Note electrolyte values at least daily, monitoring closely for

changes in potassium, magnesium, sodium, chloride, and calcium,
which may prompt dysrhythmias; increased blood urea nitrogen
(BUN) or increased creatinine, which may indicate low CO is
causing renal insufficiency; and hyperglycemia, which may indicate
patient has underlying diabetes.

1015
17. Monitor for increasing activity intolerance, dyspnea, excessive
fatigue, and orthopnea, which may all indicate CO is lessening.

18. Keep head of the bed (HOB) elevated if the patient is unable to
breathe comfortably when flat in bed.

19. Insert urinary catheter if the patient is unable to void without

markedly increasing activity level, or anuria is noted, as
appropriate.

Hemodynamic regulation

1. Monitor values generated by pulmonary artery catheter to

directly assess CO. Considerations for the bariatric patient: CO
is increased because of oxygen demands of an increased body mass
index. Monitor the bariatric patient responses to cardiac-altering
medications carefully.

2. Assess for further decreases in CO reflected by elevated

pulmonary artery occlusive/wedge pressure, elevated CVP, and
elevated pulmonary vascular resistance (PVR), which may signal
right- and/or left-sided HF.

3. Monitor for fluid overload by assessing for elevated systemic

vascular resistance (SVR).

4. Monitor the effects of all medications on hemodynamic readings,

including effects of positive or negative inotropic agents,
antidysrhythmics, and vasodilating or vasoconstricting
medications.

Impaired gas exchange 

related to decreased lung perfusion
Goals/Outcome: Within 12 to 24 hours of treatment, the patient
has adequate gas exchange as evidenced by PaO2 greater than 80
mm Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, presence of normal
breath sounds, and absence of adventitious breath sounds. RR is 12
to 20 breaths/min with normal pattern and depth.

1016
 Respiratory Status: Ventilation

Airway management

1. Assess for patent airway; if snoring, crowing, or strained

respirations are present, indicative of partial or full airway
obstruction, open airway using chin-lift or jaw-thrust.
Considerations for the bariatric patient: Sleep apnea is very
common. Patients who are not intubated may require noninvasive
positive pressure ventilation (NIPPV: CPAP or BiPAP) when
sleeping.

2. Insert oral or nasopharyngeal airway if the patient cannot

maintain patent airway; if severely distressed, the patient may
require endotracheal intubation.

3. Position the patient to alleviate dyspnea and ensure maximal

ventilation—generally in a sitting upright position unless severe
hypotension is present.

4. Clear secretions from airway by having patient cough vigorously,

or provide nasotracheal, oropharyngeal, or endotracheal tube
suctioning as needed.

5. Have patient breathe slowly or manually ventilate with Ambu

bag slowly and deeply between coughing or suctioning attempts.

6. Assist with use of incentive spirometer as appropriate.

7. Turn patient every 2 hours if immobile. Encourage patient to turn

self or get out of bed as much as tolerated if able.

8. Provide mucolytic and bronchodilating medications orally,

intravenously (IV), or by inhaler, aerosol, or nebulizer as ordered to
assist with thinning secretions and relaxing muscles in lower
airways.

9. Provide chest physical therapy as appropriate, if other methods

of secretion removal are ineffective.

1017
Oxygen therapy

1. Provide humidity in oxygen or bilevel positive airway pressure

(BiPAP) device if used for longer than 12 hours to help thin
secretions.

2. Administer supplemental oxygen using liter flow and device as

ordered.

3. Prohibit patient and visitors from smoking while oxygen is in

use.

4. Document pulse oximetry with oxygen liter flow in place at time

of reading as ordered. Oxygen is a drug; the dose must be
associated with the oxygen saturation reading or the reading is
meaningless.

5. Obtain arterial blood gases (ABGs) if the patient experiences

behavioral changes or respiratory distress to check for hypoxemia
or hypercapnia.

Considerations for the bariatric patient: There may

be increased CO2 levels, which may be the normal
state because of abnormal diaphragm position
and upper airway obstruction caused by the
structure of the neck.
6. Monitor for oxygen-induced hypoventilation, especially in
patients with chronic obstructive pulmonary disease (COPD).

Considerations for the bariatric patient: ABGs may

be similar to those of a COPD patient, without ever
using tobacco.

7. Monitor for changes in chest radiograph and breath sounds

indicative of oxygen toxicity and absorption atelectasis in patients

1018
receiving higher concentrations of oxygen (greater than Fio2 45%)
for longer than 24 hours. The higher the oxygen concentration, the
greater the chance of toxicity.

8. Monitor for skin breakdown where oxygen devices are in contact

with skin, such as nares and around edges of mask devices.

9. Provide oxygen therapy during transportation and when patient

gets out of bed.

10. If the patient is unable to maintain an SpO2 of greater than 88%

off oxygen, consult with respiratory care practitioner and physician
about the need for home oxygen therapy.

Respiratory monitoring

1. Monitor rate, rhythm, and depth of respirations.

2. Note chest movement for symmetry of chest expansion and signs

of increased work of breathing such as use of accessory muscles or
retraction of intercostal or supraclavicular muscles. Consider use of
BiPAP for impending respiratory failure.

3. Note that trachea remains midline, as deviation may indicate the

patient has a tension pneumothorax.

4. Auscultate breath sounds following administration of respiratory

medications to assess for improvement.

5. Note changes in oxygen saturation (SaO2), pulse oximetry (SpO2),

end-tidal CO2, and ABGs as appropriate. Obtain arterial blood
gas if validity of noninvasive monitoring of O2 and CO2 is
questionable.

6. Monitor for dyspnea and note causative activities or events.

7. If increased restlessness or unusual somnolence occur, evaluate

patient for hypoxemia and hypercapnia. Consult with advanced
practice provider about escalating current therapies from simple

1019
oxygen therapy (if present) to either NiPPV or endotracheal
intubation with mechanical ventilation to help support the work of
breathing.

8. Monitor chest radiograph reports as new films become available.

Heart failure
Pathophysiology
Heart failure (HF) is the inability of the heart to adequately fill with
blood or pump blood through the body. Effective pumping of the
heart is determined by the components of CO: preload (end-
diastolic volume in the ventricles, which stretches the myocardial
fibers); afterload (resistance to ejection); and contractility of the
myocardium. Myocardial contractility depends heavily on the
delivery of oxygen and nutrients to the heart.
Functional and structural factors that affect any component of CO
can lead to impaired cardiac function and eventual HF. Preload
may be impacted by valvular disorders, cardiac tamponade,
pericarditis, or cardiac arrhythmias such as atrial fibrillation.
Conditions that may increase afterload include aortic stenosis and
hypertension. Contractility may be reduced by direct damage to the
cardiac muscle during myocardial infarction, myocarditis,
cardiomyopathy, or during times of increased metabolic demand
such as thyroid storm. Damaged areas of myocardium can become
hypokinetic (weakly contractile), akinetic (noncontractile), or
dyskinetic (moving opposite from the normal cardiac muscle).

Systolic and diastolic dysfunction

HF may be described as systolic or diastolic dysfunction. Systolic
failure results from reduced cardiac contractility, commonly
described as ejection fraction (EF), or the percent of blood ejected by
the left ventricle with each beat. Normal EF is 55% to 70%, with a
value of 40% or less considered to be diagnostic of HF. Common
causes of systolic dysfunction include coronary artery disease
(CAD), ischemic cardiomyopathy, hypertension, idiopathic

1020
cardiomyopathy, and valvular heart disease. Less common causes
include alcohol- and substance-induced cardiomyopathy, viral
cardiomyopathy, and peripartum cardiomyopathy.
In diastolic failure, cardiac relaxation and ventricular filling are
impaired but EF is preserved. Common causes of diastolic
dysfunction include CAD, ischemic cardiomyopathy, hypertension,
arrhythmias, and aging. Some patients manifest the symptoms of
HF without evidence of systolic or diastolic dysfunction .
Obesity, chronic lung disease, pulmonary embolism, or acute
coronary ischemia can be alternate causes of these symptoms.

Left- versus right-sided heart failure

Heart failure is described as left-sided or right-sided depending on
which ventricle is impacted. Left ventricular (LV) failure may be
caused by ischemic heart disease, systemic hypertension, mitral or
aortic valve disease, arrhythmias, myocarditis, or substance abuse.
Causes of right ventricular (RV) failure include pulmonary
hypertension, obstructive sleep apnea, tricuspid or pulmonic valve
disease, atrial or ventricular septal defect, and RV infarction. Right-
sided HF can also develop in patients with left-sided HF, as
increased pressure in the left ventricle backs up into the lungs and
increases RV afterload.

Heart failure progression

HF is a progressive condition that results from prolonged
neurohormonal activation. Stress induced by underlying causes
leads to activation of the renin-angiotensin-aldosterone system
(RAAS). Catecholamines cause peripheral vasoconstriction,
increased resistance to ventricular ejection, increased HR, and
increased myocardial oxygen consumption, and may precipitate
myocardial ischemia and ventricular arrhythmias. Prolonged
activation of the RAAS leads to sodium retention, vasoconstriction,
hypertension, and eventual ventricular remodeling. In remodeling,
the affected ventricle dilates, hypertrophies, and becomes more
spherical. The remodeling process itself increases wall stress,
causing further remodeling. Early identification of HF and
evidence-based medications to reduce remodeling are key

1021
components of effective HF management. The progression of HF
symptoms varies with each patient.
Death results from HF-related complications (such as lethal
dysrhythmias) before some patients develop symptoms, while
others are managed for years with an effective medical regimen.
Patients with EF less than 35% are at significantly increased risk of
sudden cardiac death. Advanced HF is classified by severity of
symptoms, cardiac dysfunction, frequency of hospitalization, and
reduction in functional status. Patients with advanced or end-stage
HF may require advanced intervention such as implanted
defibrillator, cardiac resynchronization therapy, inotropic therapy,
ventricular assist device, or cardiac transplantation.

Cardiovascular assessment: Heart failure

Goal of system assessment
• Patients should be assessed for signs and symptoms of left- and
right-sided HF as outlined in Table 5-1. Table 5-2 outlines the
American Heart Association/American College of Cardiology HF
classes. These classes group patients by disease state and
symptoms.

• Evaluate for decreased CO and decreased tissue perfusion

initially with General Assessment, (Chapter 4).

• If a patient has developed HF secondary to ACS, see Assessment

in Acute Coronary Syndromes (Chapter 4).

Table 5-2
AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART
ASSOCIATION HEART FAILURE CLASSES

Heart Failure Class Defining Characteristics

A Patients at high risk for heart failure without heart disease or symptoms
B Structural heart disease without prior or current symptoms of heart failure
C Structural heart disease with prior or current symptoms of heart failure
D Refractory heart failure requiring specialized interventions

1022
History and risk factors
• History of HF, CAD, myocardial infarction (MI), hypertension,
hypercholesterolemia, obstructive sleep apnea, diabetes,
arrhythmias, and recent viral illness.

• Familial history of CAD and MI

• Age older than 65 years

• Obesity

• History of HF symptoms including fatigue, weight gain,

decreased exercise tolerance, dyspnea, or peripheral edema

• In patients with previously diagnosed HF, compliance with low-

sodium diet, weight monitoring, fluid restriction, medications,
and exercise recommendations

Diagnostic Tests for Acute Heart Failure

See diagnostic tests in Acute Coronary Syndromes.

1023
1024
Collaborative management
Care priorities

1. Treat the underlying cause and precipitating factors

Initial therapy focuses on stabilizing the hemodynamic and
respiratory status and searching for reversible causes of HF.
Ischemic heart disease should always be considered in a patient
with newly diagnosed heart failure. Use diagnostic tools including
laboratory values and echocardiography to determine cardiac
function and possible etiology (Table 5-3). The goals of long-term
therapy focus on improvement of the quality of the patient’s life
and management of the compensatory mechanisms causing the
patient’s symptoms. Angiotensin converting enzyme inhibitors
(ACEIs)/angiotensin receptor blockers (ARBs), and beta blockers
have been shown to improve mortality and morbidity and are now
the standard of care in patients with systolic HF.

1025
2. Provide oxygen therapy and support ventilation
Supplemental oxygen is required to optimize the patient’s oxygen
saturation.

Pulse oximetry is done in combination with respiratory

assessment, as use of pulse oximetry alone is an inaccurate
reflection of efficacy of oxygenation at the cellular level. If patient
is tachypneic with increased work of breathing, noninvasive
positive pressure ventilation (NiPPV or NPPV; bilevel positive
airway pressure [BiPAP]) may be used to reduce the work of
breathing, and thus relieve additional stress associated with heart
failure (see Acute Respiratory Failure, p. 383, for additional
information regarding NiPPV, mechanical ventilation, and oxygen
therapy).

• Pulse oximetry (SpO2): External monitoring of patient’s

hemoglobin saturation. SpO2 does not provide information about
ventilation and CO2 retention

3. Provide evidence-based pharmacotherapy to help

improve long-term prognosis, relieve symptoms, and
promote stabilization during acute episodes
Medications help reduce intravascular volume, promote
vasodilation to reduce resistance to ventricular ejection, and
promote enhanced myocardial contractility. HF patients should
have their medication regimen reviewed during hospitalization to
ensure optimal medical therapy.

• Evidence-Based Therapy to Improve Morbidity and Mortality

in Systolic Dysfunction

• Beta-adrenergic blocking agents: The HF clinical

guidelines specify the use of three beta blockers that

1026
 have been shown to improve survival (carvedilol,
metoprolol succinate, and bisoprolol). All stable
patients with current or prior symptoms of HF and
reduced EF should receive a beta blocker unless
contraindicated. These drugs block the pathologic
effects of circulating catecholamines (epinephrine
and norepinephrine) in patients with HF. Beta
blockers reduce contractility and HR, resulting in
decreased myocardial oxygen consumption and
demand. While a reduction in HR and CO seems
counterintuitive for a patient with HF, allowing the
heart more time to fill and pump with each beat
leads to more effective function. COPD is not a
contraindication to beta-blocker therapy in patients
without significant active wheezing. A
cardioselective beta blocker such as metoprolol
succinate or bisoprolol would be preferable in
patients with a history of COPD. The combination
of ACEI, diuretics, and beta blockers administered
together may cause hypotension. Spacing
medication administration and indicating clear
“hold” parameters for BP in hospitalized patients
can help to reduce this effect.

• ACEIs (benazepril, captopril, enalapril, fosinopril,

lisinopril, perindopril, quinapril, ramipril,
trandolapril): ACEIs affect the renin-angiotensin
system by inhibiting the conversion of circulating
angiotensin I into angiotensin II. They reduce
remodeling, preload, and afterload to decrease the
work of the ventricles. This results in increased CO

1027
 and systemic tissue perfusion. Treatment with an
ACEI has been shown to reduce mortality and HF
symptoms while improving exercise tolerance and
LVEF. All patients with an EF ≤ 40% should be
treated with an ACEI unless they have a
contraindication or intolerance. ACEIs are
considered reasonable therapy and likely beneficial
in all other patients with HF, regardless of EF. They
help prevent HF in patients at high risk with
atherosclerosis, diabetes mellitus, or hypertension
with other cardiovascular risk factors. ACEI dose
should be titrated to the maximum tolerated;
however, 10% to 20% of patients are ACEI
intolerant. The most troubling side effect from
ACEIs is cough, which may prompt a change to an
ARB or a combination of hydralazine and a nitrate.
Most patients who cough on ACEIs are doing so
because of HF rather than intolerance to the ACEI.
Cough may disappear with increased diuresis.
Development of either angioedema or acute renal
failure requires that the drug be stopped
immediately.

• ARBs (candesartan, eprosartan, irbesartan,

olmesartan, losartan, telmisartan): ARBs have been
shown in clinical trials to be noninferior to ACE
inhibitors for patients with HF. The clinical
guidelines indicate that patients who are ACEI
intolerant can be placed on ARB therapy. ARBs do
not cause the side effects of cough or angioedema,
but they do have similar contraindications in renal

1028
 failure and hyperkalemia.

• Aldosterone antagonists (spironolactone,

eplerenone): Aldosterone inhibition reduces sodium
and water retention, endothelial dysfunction, and
myocardial fibrosis. Hyperkalemia is a significant
potential side effect of aldosterone blockade. Serum
potassium levels must be closely monitored, and
the medications should not be used in patients with
impaired renal function. When added to baseline
therapy of a beta blocker and ACEI/ARB,
aldosterone antagonists have been shown to
improve HF morbidity and mortality in patients
with moderately severe to severe symptoms of HF.
The newest clinical guidelines outline the role of
aldosterone antagonists in HF. These agents should
not be used in patients who will not undergo close
monitoring of renal function and potassium levels
as part of outpatient management, or those with
creatinine greater than 2.5 mg/dL.

• Hydralazine and isosorbide dinitrate: The

combination of hydralazine and isosorbide dinitrate
is shown to reduce morbidity and mortality in
specific patient populations. Patients who self-
identify as African American benefit from the
addition of hydralazine and isosorbide dinitrate to
beta blocker and ACEI/ARB therapy. In patients
who are unable to take ACEI/ARB medications
caused by renal insufficiency or hyperkalemia,
hydralazine with isosorbide dinitrate is an

1029
 alternative therapy.

• Symptom Management in Heart Failure:

• Diuretics: Reduce blood volume and decrease

preload. Diuretics effectively manage respiratory
distress caused by pulmonary edema, but have not
been shown to improve survival in HF patients.
Diuretics are the only medications used in HF
therapy that can control the retention of fluid.
Diuretic therapy should be used in conjunction with
evidence-based HF therapy (including beta blocker
and ACEI/ARB.) A loop diuretic is first-line for
patients with volume overload, while thiazide
diuretics may be beneficial in patients with
significant hypertension (Table 5-1). Diuretics may
cause azotemia, hypokalemia, metabolic alkalosis,
hypotension, and elevation of neurohormone (e.g.,
BNP) levels. See Table 5-3 for diuretic dosing.

• Digoxin: Slows HR, giving the ventricles more time

to fill, strengthens contractions, and improves CO.
Digoxin may be prescribed for patients with LV
end-systolic dimension who remain symptomatic
on standard therapy, especially if they develop
atrial fibrillation. Digoxin controls ventricular
response in atrial fibrillation without decreasing BP.
Digoxin is excreted by the kidneys, and so is used
cautiously in patients with impaired renal function.
Bradycardia and heart block are contraindications
to digoxin therapy.

1030
• Inodilators (milrinone and inamrinone):
Phosphodiesterase-inhibiting drugs increase
myocardial contractility and lower SVR through
vasodilation. This allows the failing heart to pump
against less pressure (reduced afterload), resulting
in increased CO. Milrinone is used for hypotensive
patients with low-CO HF and pulmonary
hypertension. It is a more potent pulmonary
vasodilator than dobutamine. Milrinone is superior
to dobutamine for patients on chronic oral beta-
blocker therapy who develop acute hypotensive
HF.

• Morphine: Used to reduce anxiety and relieve

distress in patients with pulmonary edema.
Morphine has been associated with poorer
outcomes in patients with acute decompensated
HF. Morphine is used in end-stage HF to relieve the
symptoms of severe pulmonary edema.

• Vasodilators: Used for the management of dyspnea

and volume overload in patients with stable BP.
Vasodilators do not improve morbidity or mortality
in HF.

• Intravenous nitroglycerin (NTG) is beneficial in

patients with hypertension, coronary ischemia, or
severe mitral regurgitation. Nitroprusside reduces
preload and afterload, and is beneficial in patients
with severe hypertension or mitral regurgitation.

1031
• Nitroprusside can induce significant hypotension
and must be titrated carefully. Nitroprusside is
ideally used only for a short time in patients with
advanced renal disease to avoid thiocyanate
toxicity, resulting from an accumulation of this
byproduct of the hepatic metabolism of
nitroprusside. Nitroprusside should also be
avoided in patients with ACS because it may cause
coronary steal syndrome, which shunts blood away
from the ischemic myocardium to better-perfused
muscle.

• Nesiritide is a vasodilator that has demonstrated no

impact on hospitalizations, mortality, or renal
failure. The longer half-life of nesiritide increases
the chance for prolonged hypotension.

Table 5-1
HEART FAILURE ASSESSMENT

Left-Sided Heart Failure Pulmonary Edema and Right-Sided Heart Failure Cor Pulmonale
Congestion and Systemic Congestion
Symptoms
• Decreased exercise tolerance • Decreased exercise tolerance
• Fatigue • Fatigue
• Weakness • Peripheral edema (legs, hands,
• Anxiety abdomen, sacrum)
• Dyspnea • Weight gain
At rest • Decreased urination
On exertion • Abdominal tenderness
Orthopnea (inability to lie flat) • Nausea, vomiting, constipation, and
Paroxysmal anorexia
nocturnal dyspnea (awakening from sleep with
significant dyspnea)
• Cough (possibly moist with frothy sputum)
• Diaphoresis
• Palpitations
Physical Assessment

1032
 • Tachypnea • Dependent pitting edema
• Rales (most often dependent, in lung bases) • Jugular venous distention
• Unilateral or bilateral diminished lung sounds at • Hepatomegaly
the base (pleural effusion) • Splenomegaly
• Hypertension or hypotension • Ascites
• Orthostasis (drop in BP ≥20 mm Hg with sitting • Positive hepatojugular reflex
or standing) • Cardiogenic shock in acutely ill patients
• Tachycardia (significant hypotension, tachycardia,
• Atrial or ventricular arrhythmia altered mental status)
• S3
• Cyanosis or pallor
• Cardiogenic shock in acutely ill patients
(significant hypotension, tachycardia, altered
mental status, significant dyspnea)
• The combination of skin and pulmonary
assessment can provide information about
perfusion and volume status:
• Warm and dry
• Well-perfused and euvolemic
• Warm and wet
• Well-perfused with volume overload
• Cold and dry
• Hypoperfused without volume overload
• Cold and wet
• Hypoperfused with volume overload

Monitoring
Daily weight Daily weight
Arrhythmias Arrhythmias
SpO2 less than 90% In patients with advanced hemodynamic
Signs of decreased cardiac output: monitoring:
Hypotension Elevated right atrial pressure and central
Tachycardia venous pressure
Decreased urine output Decrease in Svo2 with minimal activity
Weak peripheral pulses Possible decrease in CO/CI caused by
In patients with advanced hemodynamic right ventricular failure causing reduced
monitoring: left ventricular preload
• Decreased CO/CI
• Decreased Svo2
• Elevated pulmonary artery pressures and
pulmonary artery wedge pressure
• Elevated systemic vascular resistance

CI, Cardiac index; CO, cardiac output; Svo2, venous O2 saturation.

Table 5-3
DIURETIC DOSING IN HEART FAILURE

Generic (Trade
Type of
Name) and Initial Usage Information
Diuretic
Dose
Loop Furosemide (Lasix) 20 Given per os (PO) or intravenously (IV); PO dosage is
mg doubled for the equivalent effect of IV dosing.

1033
 Bumetanide (Bumex) PO and IV administrations result in the same effects from the
0.5 mg same dosage.
Torsemide Given PO or IV. Has the strongest PO effects of all loop
(Demadex) 10 to 20 diuretics.
mg
Ethacrynic acid Given IV to patients who are allergic to furosemide or other
(Edecrin) 50 mg loop diuretics.
Thiazide Hydrochlorothiazide Given PO mainly to manage hypertension; can easily lead to
12.5 mg hypokalemia, hyponatremia, and dehydration.
Metolazone Given PO; should be given 30 minutes before furosemide if
(Zaroxolyn) 2.5 mg used together; has high incidence of hypokalemia.

4. Manage acute pulmonary edema; include the

following immediate interventions

• Monitor for signs and symptoms of acute respiratory failure

• Titrate supplemental oxygen to maintain adequate oxygenation

• Provide NiPPV for patients with increased work of breathing

• Elevate head of bed (HOB) as needed to promote oxygenation

• If NiPPV is unsuccessful, consider endotracheal (ET) intubation

with mechanical ventilation (see Acute Respiratory Failure,
Chapter 4).

• Diuretic therapy: In severely ill patients, furosemide or

bumetanide may be used as continuous IV infusion to assist with
constant fluid removal. Patients with renal impairment/failure
may require infusions of appropriate diuretics.

• In patients refractory to diuretic therapy, ultrafiltration may be

utilized for isotonic fluid removal.

• Pharmacologic therapy, including continuous IV infusions of

inotropic agents, vasodilators, beta blockers, and IV morphine. If
CS ensues, vasopressors and intra-aortic balloon pumping (IABP)
may also be necessary. Adjustment or discontinuation of
medications that affect renal function (such as ACEI/ARB) should
be considered in patients with worsening BUN/creatinine.

1034
5. Initiate a low-cholesterol and low-sodium diet

• Extra salt and water are held in the circulatory system, causing
increased strain on the heart. Limiting sodium (Table 5-4) will
reduce the amount of fluid retained by the body. In addition,
fluids may be limited to 1500 to 2000 mL/day in patients who are
hyponatremic.

Table 5-4
REDUCING DIETARY SODIUM

Foods High in Sodium* Foods Low in Sodium

Beans and frankfurters Bread
Bouillon cubes Cereal (dry or hot); read labels
Canned or packaged soups Fresh fish, chicken, turkey, veal, beef, and lamb
Canned, smoked, or salted meats;
salted fish
Dill pickles Fresh fruits and vegetables
Fried chicken dinners and other fast Fresh or dried herbs
foods
Monosodium glutamate (e.g., Accent) Gelatin desserts
Olives Oil, salt-free margarine
Packaged snack foods Peanut butter
Pancake or waffle mix Tabasco sauce
Processed cheese Low-salt tuna packed in water
Seasoned salts (e.g., celery, onion,
garlic)
Sauerkraut
Soy sauce
Vegetables in brine or cans
Additional suggestions
Do not add table salt to foods. Do not buy convenience foods; remember that fresh is
best.
Season with fresh or dried herbs. Read all labels for salt, sodium, and sodium chloride
content.
Avoid salts or powders that contain
salt.
*
Many of these foods now are available in low-salt or salt-free versions

6. Consider an implanted cardiac device

• Implanted cardioverter defibrillator (ICD): Systolic dysfunction

places patients at increased risk of sudden cardiac death.
Implantation of an ICD is indicated for patients with LVEF ≤35%
and HF symptoms. Patients must be on optimal medical therapy
and at least 40 days post-MI before implantation. (In some

1035
 instances, LVEF will improve with medical therapy and/or
treatment of CAD.) ICD therapy has been shown to significantly
reduce mortality in patients with reduced LVEF. Patients should
have a life expectancy of at least 1 year before implantation. In
patients with end-stage HF symptoms who have an ICD in place,
the decision can be made to deactivate the defibrillator to avoid
unnecessary discomfort at end of life.

• Cardiac resynchronization therapy (CRT): Approximately one

third of HF patients develop a widened QRS complex, indicating
asynchronous ventricular function. Implantation of biventricular
pacing allows coordination of the right and left ventricles. CRT is
indicated for patients with LVEF ≤35%, and a QRS duration of
150 ms or greater with HF symptoms. CRT can improve
contractility and EF, and decrease cardiac remodeling. CRT can
be combined with an ICD as a single device if the patient meets
the requirements for both therapies.

7. Initiate advanced heart failure therapy

• Patients with advanced HF are defined as those with refractory

symptoms despite optimal goal-directed medical therapy.
Indicators of advanced HF include two or more hospitalizations
for HF in the past year, progressive renal dysfunction, and
intolerance of evidence-based medical therapy caused by
hypotension or renal failure.

• Inotropic agents: Dopamine, dobutamine, and milrinone are

inotropic agents used to treat advanced HF. Inotropes may be
used acutely in the patient with CS or as a bridge to transplant or
other advanced therapy. Inotropic therapy may also be used as a
palliative measure in patients with end-stage HF for symptom
relief. Although hemodynamic status may be improved with
inotropes, there is no demonstrated improvement in patient
outcomes with their use. Inotropic therapy should only be used
in patients with severe hemodynamic compromise and evidence
of systemic hypoperfusion. Medications should be titrated to the
lowest dose needed to obtain clinical improvement.

1036
• LV assist devices (LVADs): Some patients with CS unresponsive
to intraaortic balloon counterpulsation and IV inotrope therapy
may be referred for mechanical circulatory support. LVADs may
be used as a bridge to cardiac transplantation or as a destination
therapy for those ineligible for transplant. The inflow cannula of
an LVAD is connected to the apex of the left ventricle. Blood is
pumped by the device via the outflow cannula to the aorta.
Complications include stroke, infection, coagulopathy with
bleeding, multiple organ dysfunction syndrome (MODS), and
prosthetic valve insufficiency. Most modern LVADs have
continuous flow, leaving the patient without a palpable pulse
despite adequate perfusion.

• Cardiac transplantation: Indicated for end-stage HF patients with

symptoms refractory to guideline-based medical therapy. Cardiac
transplantation has been shown to improve symptoms and
quality of life. Patients are not transplant candidates if they have
significant comorbidities including pulmonary hypertension,
active infection, significant psychosocial issues, or history of
medical noncompliance. Following cardiac transplantation,
patients must maintain lifelong immunosuppression to prevent
rejection, which places them at high risk for opportunistic
infections and malignancies.

8. Patient education and psychosocial support

• Self-care: HF patients should be educated on self-care of their HF.

This education includes daily weight monitoring, symptom
management, follow-up care, and dietary and medication
compliance.

• Advance directives: Patients with advanced HF should have a

discussion about plan of care, including resuscitation status.

• Palliative care: Care to manage physical and psychosocial

symptoms of HF should be incorporated in conjunction with
goal-directed medical therapy. In patients with advanced HF
who enter palliative or hospice care, evidence-based therapy such
as beta blockers, ACEIs, and symptom management should be

1037
 continued to prevent abrupt worsening of clinical condition.

Care plans for heart failure

Excess fluid volume 
related to compromised regulatory mechanism secondary to decreased
cardiac output.
Goals/Outcomes: Within 24 hours of treatment, the patient
becomes normovolemic as evidenced by absence of adventitious
lung sounds, decreased peripheral edema, increased urine output,
and weight loss. In patients with advanced hemodynamic
monitoring, goals include PAWP less than 18 mm Hg, SVR less
than 1200 dynes/sec/cm-5, and CO greater than 4 L/min.
Fluid Overload Severity; Fluid Balance; Electrolyte and Acid-
Base Balance

Fluid/electrolyte management

1. Pulmonary edema: Auscultate lung fields for presence of crackles

and rhonchi or other adventitious sounds.

2. Decreased renal perfusion: Monitor I&O closely. Report positive

fluid state or decrease in urine output to less than 0.5 mL/kg/h.

3. Third spaced fluid: Weigh patient daily; report increases in

weight. An acute gain in weight of 1 kg can signal a 1 L gain in
fluid.

4. Note changes from baseline assessment to detect worsening of

HF, such as increased pedal edema, increased jugular venous
distention, development of S3 heart sound or new murmur, and
dysrhythmias.

5. Monitor hemodynamic status every 1 to 2 hours and on an as-

needed basis. Note response to drug therapy as well as indicators of
the need for more aggressive therapy, including increasing PAWP
and SVR and decreasing CO.

1038
6. Administer medications as prescribed.

7. Fluid restriction as prescribed, particularly for patients with

hyponatremia

Invasive Hemodynamic Monitoring; Medication

Management; Nutrition Counseling; Surveillance; Teaching:
Disease Process; Hemodialysis Therapy

Decreased CO 
related to disease process that has resulted in decreased ability of the heart
to provide adequate pumping to maintain effective oxygenation and
nutrition of body systems.
Goals/Outcomes: Within 24 hours of initiating treatment, the
patient has attained a cardiac index (CI) of at least 2.0, PAP is
reduced to within 10% of patient’s normal baseline, BP has
stabilized to within 10% of baseline, and HR is controlled to within
10% of normal baseline.
Cardiac Pump Effectiveness; Circulation Status

Cardiac care: Acute hemodynamic regulation

1. Manage CO: Monitor cardiac rhythm and rate continuously.

Control tachycardia as soon as possible with beta blockers or other
appropriate measures as determined by the physician and ACLS
guidelines.

2. Obtain 12/15/18-lead ECG to assess new dysrhythmias or

profound instability.

3. Monitor CO, CI, pulmonary and systemic vascular pressures, and

other hemodynamic values at least hourly, as appropriate.
Implement continuous CO and SVO2 monitoring if available.

4. Decreased cerebral perfusion: Monitor neurologic status to assess

for adequate cerebral perfusion.

5. Decreased renal perfusion: During periods of instability, monitor

renal function (BUN and creatinine) daily.

1039
6. Hepatic congestion: Monitor liver function (SGOT/AST,
SGPT/ALT, and/or bilirubin), as appropriate.

7. Oxygen delivery: Monitor the other determinants of oxygen

delivery, including level of hemoglobin (Hgb) and oxygen
saturation.

8. IABP may be necessary; prepare needed equipment for insertion

of the balloon catheter and implementation of pumping.

9. If the patient has atrial fibrillation, ensure that appropriate

anticoagulants or antiplatelet agents to prevent thrombus formation
are given.

Cardiac Care: Acute; Circulatory Care: Mechanical Assist

Device; Hemodynamic Regulation; Shock Management: Cardiac;
Neurologic Monitoring; Medication Management; Dysrhythmia
Management

Impaired gas exchange 

related to alveolar-capillary membrane changes secondary to fluid
collection in the alveoli and interstitial spaces.
Goals/Outcomes: Within 24 hours of initiation of treatment, the
patient has improved gas exchange as evidenced by PaO2 at least 80
mm Hg, RR 12 to 20 breaths/min with normal pattern and depth,
and absence of adventitious breath sounds.
Respiratory Status: Gas Exchange; Mechanical Ventilation
Response: Adult

Respiratory monitoring

1. Monitor respiratory rate, rhythm, and character every 1 to 2

hours. Be alert to RR greater than 20 breaths/min, irregular rhythm,
use of accessory muscles of respiration, or cough.

2. Auscultate breath sounds, noting presence of crackles, wheezes,

and other adventitious sounds.

3. Provide supplemental oxygen as prescribed and titrate to SpO2 of

1040
90% or greater.

4. Monitor SpO2 for decreases to less than 90%.

5. Assess ABG findings; note changes in response to oxygen

supplementation or treatment of altered hemodynamics.

6. Suction patient’s secretions as needed.

7. Establish a protocol for deep breathing, coughing, and turning

every 2 hours.

8. Place patient in semi-Fowler or high-Fowler position to maximize

chest excursion.

9. If mechanical ventilation is necessary, monitor ventilator settings,

endotracheal tube function and position, and respiratory status.

Airway Management; Anxiety Reduction; Cardiac Care:

Acute; Medication Management; Oxygen Therapy; Respiratory
Monitoring

Activity intolerance 
related to imbalance between oxygen supply and demand secondary to
decreased functioning of the myocardium.
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the critical care unit, the patient exhibits cardiac
tolerance to increasing levels of activity as evidenced by RR less
than 24 breaths/min, NSR on ECG, and HR 120 bpm or less (or
within 20 bpm of resting HR).
Activity Tolerance; Energy Conservation

Energy management

1. Balance rest and activity: Maintain prescribed activity level, and

teach the patient the rationale for activity limitation. Organize
nursing care so that periods of activity are interspersed with
extended periods of uninterrupted rest.

2. To help prevent complications of immobility, assist patient with

1041
active/passive range-of-motion exercises, as appropriate. Encourage
the patient to do as much as possible within prescribed activity
allowances.

3. Activity intolerance: Note patient’s physiologic response to

activity, including BP, HR, RR, and heart rhythm. Signs of activity
intolerance include chest pain, increasing shortness of breath (SOB),
excessive fatigue, increased dysrhythmias, palpitations, HR
response greater than 120 bpm, systolic BP greater than 20 mm Hg
from baseline or greater than 160 mm Hg, and ST-segment changes.
If activity intolerance is noted, instruct patient to stop the activity
and rest.

4. Blood pressure: Administer medications as prescribed, and note

their effect on patient’s activity tolerance.

5. Physical therapy: As needed to help prevent muscle loss and

wasting, refer patient to physical therapy department.

Activity Therapy; Energy Management; Teaching: Prescribed

Activity/Exercise; Dysrhythmia Management; Pain Management;
Medication Management

Deficient knowledge 
related to disease process with HF; need to stop smoking, if applicable;
activity requirements and limitations; need for daily weight log; symptoms
to report; prescribed diet and fluid restriction and medications.
Goals/Outcomes: Within the 24-hour period before discharge
from the critical care unit, the patient and significant others
verbalize understanding of the disease, as well as the prescribed
diet and medication regimens.
Knowledge: Cardiac Disease Management

Teaching: Disease process

1. Pathophysiology: Using appropriate language, teach the patient

the physiologic process of HF and how fluid volume increases
because of poor heart function.

1042
2. Smoking cessation: Teach the patient about the adverse effects of
smoking and how smoking cessation may benefit him or her.
Provide information about smoking cessation classes and nicotine
patches and medications prescribed to help people stop smoking,
such as varenicline and bupropion.

3. Restrict sodium: Teach the patient about the importance of a low-

sodium diet to help reduce volume overload. Provide him with a
list of foods that are high and low in sodium. Teach patient how to
read and evaluate food labels.

4. Fluid volume excess: Teach the patient the signs and symptoms
of fluid volume excess that necessitate medical attention: irregular
or slow pulse, increased SOB, orthopnea, decreased exercise
tolerance, and steady weight gain (≥1 kg/day for 2 successive days).
The importance of daily weights should be stressed.

5. Daily weight: Advise the patient about the need to keep a journal
of daily weight. Explain that an increase of ≥1 kg/day on 2
successive days of normal eating necessitates notification of
advanced practice provider.

6. Device management: Teach the patient how to manage any

advanced therapy that may be used, e.g., biventricular pacemaker
or internal cardiac defibrillator, ventricular assist device (VAD), or
heart transplant.

7. Activity tolerance: Instruct the patient regarding the prescribed

activity progression after hospital discharge, signs of activity
intolerance that signal the need for rest, and the need to report
worsening symptoms with activity to their physician. General
activity guidelines are as follows:

• Get up and get dressed every morning.

• Weigh yourself before breakfast.

• Space your meals and activities to allow time for

1043
 rest and relaxation.

• Perform activities at a comfortable, moderate pace.

If you get tired during any activity, stop to rest for
15 minutes before resuming.

• Avoid activities that require straining or lifting.

• Plan at least 30 minutes of exercise on most days of

the week

• Warning signals to stop your activity and rest: chest

pain, SOB, dizziness or faintness, unusual
weakness.

Cardiac Care: Rehabilitation; Exercise Promotion; Smoking

Cessation Assistance; Teaching: Prescribed Activity/Exercise;
Emotional Support; Progressive Muscle Relaxation; Weight
Management; Mutual Goal Setting; Teaching: Prescribed Diet;
Teaching: Prescribed Medication

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Hemodynamic
Monitoring (Chapter 1), Prolonged Immobility (Chapter 1), and
Emotional and Spiritual Support of the Patient and Significant
Others (Chapter 2).

Acute coronary syndrome

Pathophysiology
Acute coronary syndrome (ACS) consists of diagnoses related to
myocardial ischemia, a decrease in blood flow through the coronary

1044
arteries that results in insufficient perfusion of the myocardium.
ACS includes unstable angina (UA), non-ST-elevation myocardial
infarction (NSTEMI), and ST-segment elevation myocardial
infarction (STEMI). Angina pectoris, or angina as it is commonly
called, is chest discomfort or pain associated with myocardial
ischemia. Angina may be caused by reduced coronary blood flow
as a result of vessel lumen narrowing by plaque or vasospasm. It
can also occur when perfusion pressure is low, as in sudden
hypotension, or when there is increased myocardial workload, as in
aortic stenosis caused by the tremendous resistance to ejection
created by the narrowed aortic valve. Dysrhythmias may also cause
chest discomfort caused by either increased workload (e.g., with
tachycardias) or coronary perfusion deficit (e.g., with bradycardias).
If the chest pain has a predictable pattern, such as being triggered
by increased demand as in exertion (e.g., exercise), it is considered
stable. Those with chest pain or chest discomfort that occurs at rest
or with normal activity, as well as with exertion, have UA. There is
also a variant form of angina, called Prinzmetal angina, which is
caused by vasospasm of the coronary arteries.
Acute myocardial infarction (AMI), either ST elevation or non-ST
elevation, results from necrosis of myocardial tissue caused by
relative or absolute lack of blood supply to the myocardium. Most
AMIs are caused by atherosclerosis, which results in plaque
formation within the coronary arteries. Plaque deposition results in
endothelial changes, which over time cause narrowing of the lumen
of the coronary artery. If an unstable plaque ruptures, the immune
system responds with localized inflammation: platelets aggregate at
the site of the injured plaque, and a thrombus forms. If the lesion is
large enough to fill the vessel lumen, this process results in total
occlusion of blood flow. Occlusion can also be caused by coronary
artery vasospasm. The site of the MI is determined by the location
of the arterial occlusion. In addition to known biomarkers that are
used to diagnose MI, novel biomarkers to help predict plaque
instability that can lead to ACS are being researched.
American Heart Association (AHA)/American College of
Cardiology (ACC) standards recommend treatment protocols for
three types of ACSs: UA, MI with ST-segment elevation (STEMI),
and MI without ST-segment elevation (NSTEMI or non-STEMI).

1045
Patients with STEMI evolve to an ECG with Q waves. Infarcts with
Q waves are larger, although Q waves resolve in 15% of STEMIs.
ECGs in patients with NSTEMIs do not show Q waves. The type of
clot present in the coronary artery may determine the type of event
that evolves. Platelet-rich clots often result in UA or NSTEMI, but
as the rupture of the plaque leads to thrombus formation, it may
result in a STEMI.
The cause of acute chest pain may not be related to myocardial
ischemia. Differential diagnosis of cardiac pain versus other origins
is critical and can challenge the most experienced clinician.
Extracardiac causes of chest pain include pulmonary embolus,
pneumonia, bronchitis, pneumothorax, pleurisy, aortic arch or high
thoracic aortic aneurysm, esophagitis, esophageal motility
disorders, hiatal hernia, cholecystitis, cholelithiasis,
gastroesophageal reflux disease, costochondritis, musculoskeletal
strain, anemia, hypoglycemia, fractured ribs or sternum, thyroid
disease, anxiety disorder, obstipation, and bowel obstruction.
Cardiac causes of chest pain not directly related to ischemia include
valvular disease, aortic dissection, cardiac trauma, cardiac
tamponade, pericarditis, and endocarditis.
The diagnostic process should initially focus on ruling out MI. It
is the most common cause of severe, unrelieved chest pain and
requires immediate intervention to minimize loss of myocardium.
Left unchecked, patients with large areas of necrosis can progress to
cardiogenic shock (CS) quickly. The patient’s history and physical
examination provide the initial framework for treatment decisions,
coupled with the initial diagnostic ECG and assessment of serum
biomarkers. If MI does not appear likely from these findings,
differential diagnosis of chest pain should then focus on
identification of other life-threatening events such as dissecting
thoracic or aortic arch aneurysms, large pulmonary embolism, or
cardiac tamponade.

Cardiovascular assessment: Acute coronary

syndrome
Goal of system assessment

1046
• Evaluate for decreased CO and decreased tissue perfusion
initially with General Assessment, (Chapter 4).

History and risk factors

• Family history of CAD, age older than 70 years, male sex,

postmenopausal females, cigarette smoking, dyslipidemia,
hypertension, hyperglycemia, increased waist circumference,
diabetes, obesity, increased stress, sedentary lifestyle.

Chest pain: Angina

• May result from exertion or emotional stress

• Onset can be abrupt or gradual

• Stable angina: Gradually increases in severity during episodes

over several months; does not occur with rest; subsides gradually
with rest

• Lasts for 1 to 4 minutes; can last up to 30 minutes

• Should be relieved by NTG in 45 to 90 seconds

• Unstable angina: Pain that has changed significantly from past

patterns and can occur at rest; includes Wellens syndrome (left
anterior descending coronary artery lesion), rest angina,
preinfarction (crescendo) angina (may cause slight ST elevation
and increased troponin level), Prinzmetal angina (from coronary
artery vasospasms at rest), and new-onset angina

• Most common feelings: Substernal pressure, chest tightness,

heaviness or squeezing in the chest

• Extreme pain: Crushing substernal chest pain radiating down the

left arm, or up to the jaw with shortness of breath

• Variations: Jaw or arm pain only, shoulder pain, right- or left-

1047
 sided chest discomfort, pain in the teeth, nausea, epigastric pain,
syncope, extreme sudden fatigue, or SOB

• No pain: Does not rule out ischemia; common in elders,

women, and diabetics

Chest pain: Acute myocardial infarction

• Onset can be abrupt or gradual

• Does not subside with rest

• Lasts for longer than 30 minutes

• NOT relieved by sublingual NTG

• Most common feelings: Continuous substernal pressure, chest

tightness, heaviness, or squeezing in the chest

• Extreme pain: Continuous crushing substernal chest pain

radiating down the left arm or up to the jaw, nausea, vomiting,
SOB, orthopnea, anxiety, apprehension, diaphoresis, cyanosis,
syncope, stroke-like symptoms

• Variations: Jaw or arm pain only, shoulder pain, right- or left-

sided chest discomfort, pain in the teeth, epigastric pain

• No pain: Does not rule out infarction; 25% of MIs are “silent”
or without pain; common in older adults, women, and diabetic
persons who may feel extreme, sudden-onset fatigue rather than
pain

12-lead electrocardiogram: Angina and acute

myocardial infarction
• Compare current ECG with past ECG

• Angina: Review for ST-segment depression in at least two

contiguous leads, which indicates myocardial ischemia

1048
• AMI: Review for ST-segment elevation in at least two contiguous
leads, which indicates active myocardial damage (acute
infarction); Q waves may or may not form

• Evaluate pacing and conduction: Rhythm regularity, rate, and

conduction velocity (PR, QRS, QT intervals)

• Dysrhythmias: New bundle branch block (especially left) is

diagnostic for MI; sinus bradycardia, atrioventricular (AV) heart
blocks, and ventricular ectopy may also be present

Vital signs
• Possible fever in patients with AMI

• BP may increase or decrease, depending on sympathetic nervous

system (SNS) response to change in CO

• HR may increase or decrease depending on SNS response and

ensuing damage to the conduction pathway, hypoxia; SNS
response is blunted by beta-adrenergic blocking agents

Observation
Evaluate for facial and lip pallor, ashen or diaphoretic appearance
of skin, ashen or cyanotic nail beds, and edema (especially in
dependent areas) to determine decreased tissue perfusion

• Instruct patient to report any discomfort immediately

• Evaluate telemetry for dysrhythmias

Palpation
Pulse amplitude may be increased or decreased, depending on SNS
response; evaluate for:

• Pulse quality and regularity bilaterally (scale 0 to 4+)

• Edema (scale 0 to 4+): extremities and sacrum

1049
• Slow capillary refill (longer than 2 seconds)

Auscultation
Heart sounds to evaluate for contributors to decreased CO (note
changes with body positioning and respirations):

• S1 and/or S2 split indicative of altered conduction

• S3 indicative of HF (systolic)

• S4 indicative of HF (diastolic)

• Murmurs, clicks indicative of valve disease

• Friction rub indicative of pericarditis

Labwork
Blood studies can indicate MI and reveal causes of dysrhythmias or
changes in pacing/conduction or HR changes:

• Cardiac enzymes/isoenzymes: Elevated troponin, CPK-MB if MI

has occurred

• Complete blood counts: Possible anemia, ↑WBCs

• Electrolyte levels: ↑ or ↓ potassium or magnesium

• BNP: Elevated if HF is present

• Levels of cardiac medications (digoxin): Low levels may reveal

noncompliance with ordered medications

Diagnostic Tests for Acute Coronary Syndrome

1050
1051
Electrocardiographic monitoring and interpretation

First ECG
The first ECG is done immediately upon complaint of chest pain
and is used as part of the process to differentiate STEMI from
NSTEMI/UA or other causes of chest pain and to help determine
diagnosis. It is also helpful in determining the possible need for
thrombolytic therapy or percutaneous coronary intervention (PCI)
for STEMI or antiplatelet medications for patients with
NSTEMI/UA. Reperfusion strategies should be implemented

1052
immediately for STEMI patients.

Standard 12-lead ECG

The standard 12-lead ECG is designed for evaluation of the
anterior, inferior, and lateral walls of the left ventricle. Infarcts that
extend to the right ventricle and/or the posterior wall of the left
ventricle cannot be clearly detected by the 12-lead ECG.

15- to 18-lead ECG

Indications for performing additional ECG evaluation with 15 or 18
leads include ST-segment elevation suggestive of an inferior wall
MI (II, III, AVF); isolated ST-segment elevation in V1 or ST-segment
elevation in V1 greater than in V2; borderline ST-segment elevation
in V5 and V6 or in V1 through V3; and ST-segment depression or
suspicious isoelectric ST segments in V1 through V3.

Serial ECGS
ECGs are then done in a series (initially and then every 30 minutes
for the first 2 hours). Characteristic changes in certain lead groups
identify the area and evolution of infarct. After the initial evaluation
phase, ECGs may be done every 8 to 24 hours and as needed for
complaints of chest pain.

Significant electrocardiogram changes

ST-segment changes and new bundle branch block

The presence or absence of ST-segment elevation is used to stratify
risk and determine the best treatment plan. ST segments are
elevated in the leads “over” or facing the infarcted area. Reciprocal
changes (ST-segment depressions) will be found in leads 180
degrees from the area of infarction. New left bundle branch block,
coupled with other findings, may also indicate that MI is present.
Patients with STEMI are candidates for emergency reperfusion
strategy. PCI within 90 minutes of arrival to a PCI-capable hospital
is the ideal therapy. Patients who are admitted to a non-PCI-
capable hospital should receive fibrinolytic therapy (unless
contraindicated) as the primary reperfusion therapy within 30

1053
minutes of arrival.
Not all patients experience STEMI. The 2012 ACCF/AHA practice
guidelines outline treatment options for UA/NSTEMI patients. They
include treatment with P2Y12 receptor inhibitors such as
clopidogrel, prasugrel, or ticagrelor.

Geriatric alert: Prasugrel is not recommended in patients

older than 75 years. Also contraindicated in patients who weigh
less than 60 kg or have a history of stroke/transient ischemic
attack (TIA).

Q waves
Q waves are a later ECG change and may or may not be present in
patients presenting with an MI. Q waves are indicative of MI and
are “pathologic” if they meet the following criteria: wider than 0.03
seconds, ≥ 1 mm in depth, and present in 2 contiguous leads. Q
waves may develop later, or the tissue necrosis may extend itself if
a reperfusion strategy is withheld.

ST segment elevation myocardial infarction accounts for

25% to 40% of hospital presentations for acute myocardial
infarction (AMI). Left bundle branch block (and, to a lesser extent,
right bundle branch block) can distort the 12-lead ECG, making
recognition of ST segment elevation difficult to impossible. Rarely,
hyperacute T wave changes can occur before ST elevation.

Twelve-lead ECG diagnosis of posterior wall myocardial

infarction (MI) can only be made by noting that the reciprocal
change is the anterior leads (V1 to V3). Lead V1 is the only lead that
may indicate an isolated right ventricle (RV) MI. Use of 15- or 18-
lead ECGs that provide a more direct view of the posterior and RV
walls of the heart is recommended for more accurate diagnosis of
both posterior wall and RV MI.

1054
T-wave changes
Within the initial hour of infarction, tall, peaked, “hyperacute”
upright T waves may be seen in leads over the infarct. Within
several hours to days, the T wave becomes inverted. Gradually over
time, the ST segment becomes isoelectric and the T wave may
remain inverted. T-wave changes may last for weeks and return to
normal or remain inverted for the rest of the patient’s life. T-wave
changes reflective of posterior and RV MI are not clearly seen on
the 12-lead ECG. Use of 15- or 18-lead ECGs should provide better
information about these areas (Table 5-5).

Table 5-5
12- TO 18-LEAD ECG LOCATION OF MYOCARDIAL INFARCTION
(MI)

*
Leads must be added to normal 12-lead ECG.
LAD, Left anterior descending artery; LV, left ventricle.

Collaborative management
ACUTE MYOCARDIAL INFARCTION HOSPITAL QUALITY
ALLIANCE INDICATORS

1055
Care priorities for all acute coronary syndromes
Prevention of initial or further coronary thrombus formation may
include administration of anticoagulant/antithrombin medications
(i.e., unfractionated or low-molecular-weight heparin [LMWH])
and antiplatelet drugs (e.g., aspirin, clopidogrel, or glycoprotein
[GP] IIb/IIIa inhibitors such as abciximab, eptifibatide, or tirofiban).
In patients evolving toward AMI, these agents are thought to abate
complete closure of the coronary arteries or to prevent more
extensive clot formation. Cardiac catheterization is often performed
to assess the size and location of coronary lesions. If significant
lesions are found, PCI can immediately follow catheterization in
facilities that offer PCI.

1. Relief of acute ischemic pain

Drugs are administered and titrated to reduce or eliminate chest
pain. Morphine, oxygen, nitrates, and aspirin (MONA) are
considered primary treatment modalities. The preferred order of
these basic interventions is oxygen, aspirin (if not already given),
nitrates, and morphine.

• Oxygen: Usually 2 to 4 L/min by nasal cannula, or mode and rate

as directed by ABG values, to promote both myocardial and
generalized increases in oxygenation. As oxygen delivery to the

1056
 heart is enhanced, pain can be relieved. If the patient deteriorates,
other methods of oxygen delivery may be implemented (e.g.,
nonrebreather mask with reservoir and mechanical ventilation
for those who deteriorate markedly).

• Aspirin: 162 to 325 mg ideally chewed should be given

immediately if the patient has not been given aspirin before
arrival at the hospital.

• Oral, sublingual, and other forms of nitrates/NTG: Can be used

for short-term therapy or longer-lasting prophylactic effects.
These non-IV medications are used for management of
myocardial ischemia or angina pectoris rather than for MI.

• IV nitrates/NTG: For UA or evolving MI, titrated until relief is

obtained, generally up to 200 µg/min as long as the patient
maintains a systolic BP of at least 80 mm Hg.

• IV or oral immediate-release morphine sulfate: Given in small

increments (e.g., 2 mg) until relief is obtained. This medication is
usually not necessary unless an MI is occurring. Low BP may
contraindicate administration.

2. Prevention of coronary artery clot formation

• Antiplatelet therapy: Aspirin is the initial treatment as indicated

above. P2Y12 inhibitors such as clopidogrel, prasugrel, or
ticagrelor are recommended as soon as possible. Infusion of GP
IIb/IIIa inhibitors (e.g., abciximab, eptifibatide, tirofiban) is used
in patients undergoing angiography.

• Antithrombin therapy: Unfractionated heparin (UFH) or LMWH

is sometimes implemented to prevent clot extension and/or
formation, particularly during PCI. UFH should be weight-based
and follow a titration protocol based on ongoing studies of partial
thromboplastin time/activated partial thromboplastin time
(PTT/aPTT). LMWH, such as enoxaparin, can be administered
subcutaneously or IV and does not require monitoring of
PTT/aPTT. Fondaparinux, an LMWH, cannot be administered as

1057
 the only anticoagulant during PCI because of the increased risk of
catheter thrombosis.

• Direct thrombin inhibitors (DTIs): An anticoagulant that binds

directly to thrombin and blocks its interaction with its substrates.
DTIs act independently of antithrombin, so they can inhibit
thrombin bound to fibrin or fibrin degradation products.
Bivalirudin is commonly used during PCI because its duration of
action is short. Coagulation times return to baseline
approximately 1 hour following cessation of administration.

3. Reduction of myocardial workload and myocardial

oxygen consumption

• Limit activities: Restrictions are based on patient’s activity

tolerance. Bed rest with bedside commode privileges generally is
recommended for patients with AMI for up to 12 hours after
symptom onset although there is no good data to support this.
Longer periods of bed rest can promote development of
orthostatic intolerance, which is prevented by elevation of the
HOB, dangling the lower extremities, and other low-exertion
activities. Patients should be instructed to avoid the Valsalva
maneuver when toileting, because it may predispose them to
ventricular dysrhythmias.

• Administer medications:

• Beta-adrenergic blocking agents (e.g., metoprolol,

carvedilol, propranolol): To decrease HR, BP, and
myocardial contractility. Recommended as part of
primary pharmacologic therapy for AMI patients.

• ACEIs (e.g., enalapril, ramipril, quinapril): To

decrease BP and thus reduce the resistance to
ventricular ejection. Used to reduce LV remodeling
and if long-term BP control is needed. Effective in

1058
 prevention and treatment of HF. Should be used for
patients with diabetes, chronic kidney disease,
and/or reduced EF unless contraindicated.

• ARBs (candesartan, eprosartan, irbesartan,

olmesartan, losartan, telmisartan): Have similar
effects to ACEIs but have not been proved to reduce
mortality. ARBs are used in patients who are ACEI
intolerant.

• CCBs (e.g., nifedipine, diltiazem): No longer

recommended for management of patients with
ACS unless coronary artery spasms are strongly
suspected.

4. Prevention, recognition, and treatment of dysrhythmias

Beta blockers should be prescribed within the first 24 hours unless

contraindicated.

ACLS algorithms should be used.

HIGH ALERT!
Caution should be exercised in the use of antiarrhythmic agents in
patients with acute myocardial infarction (AMI), especially to
manage reperfusion dysrhythmias, because instability of the
conduction system with AMI is sometimes aggravated by use of
antiarrhythmic agents. Electrical therapies such as synchronized
cardioversion, defibrillation, external/transthoracic pacing, or
transvenous pacing may provide a safer management strategy for
these patients.

1059
5. Prevention of contrast-induced nephropathy related
to use of contrast during coronary angiography/PCI

• Hydration using IV and oral fluids is paramount.

Additional treatments

1. Management of unstable AMI with ST-segment elevation

(STEMI)

• Hemodynamic monitoring: Used in a patient with a complicated

MI resulting in ventricular failure with threat of CS. Pulmonary
artery (PA) and capillary pressures are measured, along with CO
and SVR. Unstable patients may manifest increased PAP,
increased PAWP, decreased CO, and increased SVR.

2. Acute STEMI: PCI procedures

• Primary PCI: A balloon-tipped catheter is inserted into the

coronary arterial lesion, and the balloon is inflated to compress
the plaque material against the vessel wall, thereby opening the
narrowed lumen. Primary PCI is performed on individuals with
STEMI. Elective PCI may be performed on patients with
postinfarction angina, postcoronary angina, and UA. The ideal
candidate for primary PCI has single-vessel disease with a
discrete, proximal, noncalcified lesion. While PCI may be done on
noninfarct arteries electively, primary PCI should target only the
infarct artery. During the procedure, the patient is sedated lightly
and is given a local anesthetic at the insertion site, either the
radial or femoral artery. ECG electrodes are placed on the chest.
An introducer sheath is inserted into the femoral or radial artery,
a guidewire is passed into the aorta and coronary artery, and the
balloon catheter is passed over the guidewire to the stenotic site.
The patient may be asked to take deep breaths and cough to
facilitate passage of the catheter. Heparin, GP IIb/IIIa inhibitor,
and/or a direct thrombin inhibitor, such as bivalirudin, is
administered to prevent clot formation. The balloon is inflated
repeatedly for 60 to 90 seconds at a pressure of 4 to 15
atmospheres. Subsequently, radiopaque dye is injected to

1060
 determine whether the stenosis has been reduced to less than
50% of the vessel diameter, which is the goal of the procedure.
The femoral artery site may be closed using a device, or the
introducer sheath is left in the femoral artery until the effect of
anticoagulant medications has diminished. In the case of radial
access, a radial artery band is applied.

• Complications after PCI: These include acute

coronary artery occlusion, coronary artery
dissection, reocclusion in AMI patients, AMI,
coronary artery spasm, bleeding, circulatory
insufficiency, pseudoaneurysm, allergic or renal
hypersensitivity to contrast material, hypokalemia,
vasovagal reaction, dysrhythmias, and
hypotension. Restenosis can occur 6 weeks to 6
months after PCI, although the patient may not
experience angina.
• Intracoronary stent procedure: A PCI wherein endovascular
stents (metal-mesh tubes) are used to keep arteries open. Can be
done during primary PCI or electively. A variety of designs,
materials, and deployment procedures are available. Bare metal
stents were the first stents developed, have an increased risk of
restenosis, and are used in patients who cannot tolerate dual
antiplatelet therapy. Drug-eluting stents are coated with
antiproliferative drugs that elute into the coronary artery wall to
reduce scar tissue formation and restenosis.

• Aspiration thrombectomy: This may be done during primary PCI.

Catheter is advanced with guidewire that has a distal lumen
attached to a suction device to vacuum thrombus out.

• Coronary artery atherectomy: A PCI that removes atherosclerotic

plaque from coronary arteries using a special catheter equipped
with a cutting device that shaves the lesion. Three types are
directional, rotational, and laser.

1061
3. Surgical revascularization

• Surgical revascularization procedures are rarely used as the

primary management strategy for AMI unless primary PCI has
failed, there is persistent ischemia causing hemodynamic
instability, and the anatomy is amenable to CABG. CABG is
usually done electively. Several approaches are available for
myocardial revascularization, including CABG via median
sternotomy or minimally invasive technique. Patients with
multivessel or diffuse CAD are the most appropriate candidates
for these procedures. Surgical indications include (1) stable
angina with 50% stenosis of the left main coronary artery, (2)
stable angina with three-vessel CAD, (3) UA with three-vessel
disease or severe two-vessel disease, (4) recent MI, (5) ischemic
HF with CS, and (6) signs of ischemia or impending MI after
angiography. Robotics can be used to assist the surgeon with the
procedure. Cardiac surgery should be readily available for
patients who experience complications undergoing any
diagnostic or treatment procedures in the cardiac catheterization
laboratory.

4. Acute STEMI: Thrombolytic therapy

• Thrombolytic therapy (lysis of coronary arterial clot): Used for

reperfusion of the occluded coronary vessel(s) causing the AMI.
Streptokinase and anisoylated plasminogen streptokinase
activator complex (APSAC) are first-generation, nonfibrin-
specific agents. They are no longer available in the United States.
Second-generation drugs that are fibrin specific include
tenecteplase, alteplase, and reteplase (Box 5-1 and Table 5-6).
Thrombolytic therapy is an AHA/ACC class I intervention for
patients with ST-segment elevation in two or more contiguous
leads, new left bundle branch block (obscuring ST-segment
analysis), and history suggestive of AMI who present within 12
hours of symptom onset and are younger than 75 years of age.
Patients must be carefully screened for risk of bleeding before
administration of these IV medications (Box 5-2). Time from the
patient’s entry into the emergency department to treatment with
thrombolytics should be within 30 minutes.

1062
Box 5-1
THROMBOLYTICS
First-generation (nonselective) thrombolytics
Streptokinase: An enzyme derived from group C beta-hemolytic
streptococci. Because it is an antigen, patients who have had
previous exposure to streptococcal organisms may have
antibodies against streptokinase. Therefore steroids or
antihistamines are administered before streptokinase therapy to
prevent a hypersensitivity reaction.

Anistreplase: A plasminogen activator that induces clot lysis with

fewer systemic lytic effects than streptokinase. Allergic and
anaphylactic reactions are possible.

Second-generation (fibrin-selective) thrombolytics

These fibrin-specific agents decrease the systemic activation of
plasminogen and the resulting degradation of circulating
fibrinogen compared with first-generation thrombolytics. They are
also nonantigenic.

Alteplase: A recombinant tissue plasminogen activator (rtPA) with

the same amino acid sequence as endogenous tissue plasminogen
activator (tPA). Has a shorter half-life, 4 to 6 minutes, than other
agents. Several dosage regimens are approved for coronary
thrombolysis.

Reteplase: A recombinant deletion mutein of tPA, reteplase

catalyzes cleavage of endogenous plasminogen to generate
plasmin. It is not clot-specific, so fibrinogen levels fall to lower
levels than those seen with rtPA (alteplase), with a return to
baseline value within 48 hours after infusion. The half-life is 13 to
16 minutes, and the drug is cleared by the liver and kidneys. It is
given as two boluses 30 minutes apart, each over 2 minutes.

Tenecteplase: A modified form of human tPA that binds to fibrin

and converts plasminogen to plasmin. In the presence of fibrin,

1063
 conversion of plasminogen to plasmin is increased relative to its
conversion in the absence of fibrin. Following administration of
tenecteplase, there are decreases in circulating fibrinogen and
plasminogen. It has a half-life of up to 130 minutes for final
clearance and is mostly metabolized through the liver. There are
less bleeding complications than with alteplase. Tenecteplase is
given as a single 5-second bolus and is dosed by weight.

Box 5-2
CONTRAINDICATIONS AND WARNINGS
FOR THROMBOLYTIC THERAPY
Absolute contraindications
• Known hypersensitivity to thrombolytic agents

• Suspected aortic dissection

• Active internal bleeding

• History of stroke (except ischemic stroke within 4.5 hours)

• Recent intracranial or intraspinal surgery or trauma

• Known bleeding diathesis

• Severe, uncontrolled hypertension

Warnings (risks may be increased and should be

weighed against anticipated benefits)
• Recent major surgery (e.g., coronary artery bypass graft, obstetric
delivery, organ biopsy)

• Previous puncture of noncompressible vessels

• Cerebrovascular disease

1064
• Recent internal bleeding (within 2 to 4 weeks)

• Recent trauma

• Hypertension (systolic blood pressure >180 mm Hg and/or

diastolic blood pressure >110 mm Hg)

• History of chronic, severe, poorly controlled hypertension

• Dementia

• Hemostatic defects including those secondary to severe hepatic or

renal disease

• Severe hepatic or renal dysfunction

• Pregnancy

• Diabetic hemorrhagic retinopathy or other hemorrhagic

ophthalmic conditions

• Active peptic ulcer

• Advanced age

• Currently receiving anticoagulants (e.g., warfarin)

• Any other condition in which bleeding constitutes a significant

hazard or would be particularly difficult to manage because of its
location

Care plans for acute coronary syndromes

Activity intolerance 
related to imbalance between oxygen supply and demand secondary to
decreased cardiac output associated with coronary artery disease.
Goals/Outcomes: Within the 12- to 24-hour period before

1065
discharge from the CCU, the patient exhibits cardiac tolerance to
increasing levels of activity as evidenced by RR less than 24
breaths/min, NSR on ECG, BP within 20 mm Hg of patient’s normal
range, HR less than 120 bpm (or within 20 bpm of resting HR for
patients on beta-blocker therapy), and absence of chest pain.
Energy Conservation, Instrumental Activities of Daily Living
(IADL)

Energy management

1. Assist patient with identifying activities that precipitate chest

pain, and teach patient to use NTG prophylactically before the
activity.

2. Assist patient as needed in a progressive activity program,

beginning with level I and progressing to level IV, as tolerated
(Table 5-7).

3. Assess patient’s response to activity progression. Be alert to

presence of chest pain, SOB, excessive fatigue, and dysrhythmias.
Monitor for a decrease in BP greater than 20 mm Hg and an
increase in HR to greater than 120 bpm (greater than 20 bpm above
resting HR in patients receiving beta-blocker therapy).

4. Teach the patient about measures that prevent complications of

decreased mobility, such as active ROM exercises. (For additional
details, see Prolonged Immobility, Chapter 1).

Energy Management, Self-Care Assistance: IADL

Risk for deficient fluid volume 

related to increased risk of bleeding
Goals/Outcomes: The patient will not experience bleeding or a
decrease in Hgb or hematocrit (Hct).
Fluid Balance

Bleeding precautions

1. Monitor dosing of all drugs known to increase bleeding,

1066
including aspirin and other antiplatelet drugs, GP IIb/IIIa
inhibitors, direct thrombin inhibitors, and thrombolytics.

2. Monitor Hgb and Hct closely. Report Hgb drop greater than 2 g
to physician immediately.

3. Monitor vital signs closely. Drop in BP and increase in HR may

indicate developing shock, which may be cardiogenic or indicate
hidden bleeding.

4. After PCI via femoral sheath, keep HOB less than 30 degrees and
affected leg straight as ordered.

5. After PCI, monitor vital signs, sheath site, and distal pulses every
15 minutes until sheath is removed, then every 15 minutes x2, then
every 30 minutes x2, then every 4 hours.

6. Carefully follow provider’s orders for sheath removal after PCI.

7. If bleeding occurs at the insertion site, position the patient flat

and apply pressure until hemostasis is achieved and obtain stat
CBC. Notify provider of drop in Hgb.

8. Instruct the patient to report any discomfort. Groin pain may

indicate pseudoaneurysm; back pain may indicate retroperitoneal
bleed.

Bleeding Reduction; Surveillance; Hemorrhage Control;

Neurologic Monitoring

Decreased CO (or risk for same) 

related to alterations in rate, rhythm, and conduction secondary to
increased irritability of ischemic tissue during reperfusion (usually occurs
within 1 to 2 hours after initiation of therapy); reocclusion of thrombolysed
vessels; negative inotropic changes secondary to cardiac disease;
hypotension secondary to blood loss.
Goals/Outcomes: Within 12 hours of initiation of thrombolytic
therapy or PCI, the patient has adequate CO as evidenced by
normal HR (60 to 100 bpm), peripheral pulses greater than 2+ on a 0

1067
to 4+ scale, warm and dry skin, and hourly urine output >0.5
mL/kg/h. Patient is awake, alert, and oriented without palpitations,
chest pain, or dizziness. Within 48 hours, the patient maintains
stability as just described.

Reocclusion occurs in as many as 16% of patients within 24

to 48 hours after thrombolysis.

Circulation Status

Cardiac care

1. Monitor ECG continuously for evidence of dysrhythmias.

Consult provider for significant dysrhythmias or new or worsening
ST-segment elevation.

2. With any dysrhythmia, check vital signs and note accompanying

signs and symptoms such as dizziness, lightheadedness, syncope,
and palpitations.

3. Ensure availability of emergency drugs and equipment: atropine,

isoproterenol, epinephrine, amiodarone, adenosine, vasopressin,
procainamide, sotalol, lidocaine (use cautiously with AMI),
defibrillator-cardioverter, and external and transvenous pacemaker.

4. Evaluate patient’s response to medications and emergency

treatment.

5. Monitor patient for signs of reocclusion: chest pain, nausea,

diaphoresis, and dysrhythmias.

6. Consult provider for any signs of reocclusion.

7. Obtain 12/15/18-lead ECG if reocclusion is suspected.

8. Anticipate and prepare patient for cardiac catheterization, PCI

with stent, or repeated thrombolytic therapy.

1068
9. Monitor for signs of bleeding and bleeding complications:
bleeding at sheath site or at IV sites, back pain (may indicate
retroperitoneal bleed), signs and symptoms of cerebrovascular
accident (CVA)/stroke (see Stroke: Acute Ischemic and
Hemorrhagic, Chapter 7).

Hemodynamic Regulation; Circulatory Care; Dysrhythmia

Management; Cardiac Care: Acute

Risk for injury 

related to potential for allergic or anaphylactic reaction to streptokinase or
anistreplase secondary to antigen/antibody response.
Goals/Outcomes: Patient has no symptoms of allergic response as
evidenced by normothermia, RR 12 to 20 breaths/min with normal
pattern and depth, HR less than 100 bpm, BP at baseline or within
normal limits, natural skin color, and absence of itching, urticaria,
headache, muscular and abdominal pain, and nausea.
Risk Control

Risk identification

1. Before treatment, question the patient about history of previous

streptokinase therapy or streptococcal infection. Consult provider
for positive findings.

2. Administer prophylactic hydrocortisone as prescribed.

3. Monitor patient during and for 48 to 72 hours after infusion for

indicators of allergy: hypotension (brief or sustained), urticaria,
fever, itching, flushing, nausea, headache, muscular pain,
bronchospasm, abdominal pain, dyspnea, or tachycardia. These
indicators can appear immediately after or as long as several days
after streptokinase therapy.

4. If hypotension develops, increase rate of IV infusion/administer

volume replacement as prescribed. Prepare for vasopressor
administration if there is no response to volume replacement.

5. Treat allergic response with diphenhydramine or other

1069
antihistamine as prescribed.

Shock Management: Vasogenic; Shock Management

Decreased cardiac output 

related to cardiac dysfunction following acute coronary event.
Goals/Outcomes: Within 24 hours of this diagnosis, the patient
exhibits adequate CO, as evidenced by BP within normal limits for
patient, HR 60 to 100 bpm, peripheral pulses greater than 2+ on a 0
to 4+ scale, warm and dry skin, hourly urine output greater than 0.5
mL/kg, measured CO 4 to 7 L/min, right atrial pressure (RAP) 4 to 6
mm Hg, PAP 20 to 30/8 to 15 mm Hg, PAWP 6 to 12 mm Hg, and
the patient awake, alert, oriented, and free from anginal pain.
Tissue Perfusion: Cardiac

Cardiac care, acute

1. See Care Plans for Generalized Cardiovascular Dysfunctions,

(Chapter 5).

2. Monitor for ST-segment elevation indicative of myocardial injury,

ST depression indicative of myocardial ischemia, new left bundle
branch block, and Q waves indicative of MI. All ECG changes must
be present in at least two contiguous leads.

3. Collaborate with provider if decreased CO does not respond to

acute cardiac care interventions.

4. Maintain fluid balance carefully, with close assessment for need

for fluids versus diuretics. Patients with right-sided HF may require
support with IV fluids, while those with left-sided HF may respond
better to diuretics.

5. Provide patient with platelet-inhibiting (e.g., clopidogrel, aspirin,

abciximab) and thrombin-inhibiting medications (e.g., heparin,
enoxaparin, fondaparinux, bivalirudin) as appropriate, according to
AHA guidelines for STEMI or NSTEMI.

Hemodynamic regulation

1070
1. Monitor for unstable BP and use hemodynamic readings to help
assess need for titration of vasoactive, inotropic, and antiarrhythmic
medications.

2. Collaborate with provider to assess if the patients with severe

bundle branch block might benefit from biventricular cardiac
pacing to improve synchrony of ventricular contraction.

3. Assess effects of fluid challenges on CVP and pulmonary artery

occlusive pressure (PAOP), especially in patients with RV
infarction.

4. Elevate legs rather than placing patients in Trendelenburg

position to help augment venous return to increase BP.

Circulatory care: Mechanical assist device

1. Assess peripheral circulation meticulously when intra-aortic

balloon catheter is in place.

2. Evaluate impact of changes in balloon counterpulsation settings

on CO, CI, all hemodynamic pressures, and BP.

3. Examine all cannulas for kinking or disconnection if the patient

becomes suddenly unstable without other notable cause.

4. Use strict aseptic technique when changing device-related

dressings.

5. Administer anticoagulants or thrombolytics as appropriate.

6. Collaborate with provider regarding need for further

interventions if the patient remains unstable despite mechanical
assist device and vasoactive, inotropic, and antiarrhythmic
medications.

Deficient knowledge: Coronary artery disease process and

its lifestyle implications 
related to the need to help prevent further incidence of heart
disease.

1071
 Goals/Outcomes: Within the 24-hour period before discharge
from the step-down unit, the patient verbalizes understanding of
his or her disease, as well as the necessary lifestyle changes that
may modify risk factors.
Knowledge: Disease Process; Knowledge: Medication;
Knowledge: Diet; Knowledge: Energy Conservation; Sexual
Identity: Acceptance; Knowledge: Sexual Functioning

Teaching: Cardiac disease process

1. Teach the patient about ischemia and its resultant chest pain,
referred to as angina pectoris.

2. Discuss the pathophysiologic process underlying patient’s

angina, using drawings or heart models as indicated.

3. Assist the patient in identifying his or her own risk factors (e.g.,
cigarette smoking, high-stress lifestyle, hyperglycemia, high-fat
diet).

4. Teach the patient about risk factor modification:

• Smoking cessation: Teach the patient that smoking

causes the coronary arteries to constrict, thus
decreasing blood flow to the heart.

• Stress management: Discuss the role that stress

plays in angina. Explain that stress increases
sympathetic tone, which can cause the BP and HR
to increase, resulting in increased oxygen demand.
By using relaxation techniques such as imagery,
meditation, or biofeedback, one can decrease the
effects of stress on the heart. For a sample relaxation
technique, see Appendix 7.

1072
 Teaching: Individual; Teaching: Disease Process,
Thrombolysis

Altered protection 
related to risk of bleeding/hemorrhage secondary to nonspecific
thrombolytic effects of therapy.
Goals/Outcomes: Symptoms of bleeding complications are absent
as evidenced by BP within patient’s normal range, HR less than 100
bpm, blood-free secretions and excretions, natural skin color,
baseline or normal level of consciousness (LOC), and absence of
back and abdominal pain, hematoma, headache, dizziness, and
vomiting.
Risk Control

Risk identification

1. When patient is admitted, obtain a thorough history, assessing

for the following:

• Risk factors for intracranial hemorrhage:

uncontrolled hypertension, cerebrovascular
pathology, central nervous system (CNS) surgery
within previous 6 months

• Bleeding risks: recent or active gastrointestinal (GI)

bleeding, recent trauma, recent surgery, bleeding
diathesis, advanced liver or kidney disease

• Risk of systemic embolization: suspected left-sided

heart thrombus

• History of streptococcal infection or previous

streptokinase therapy

2. Monitor clotting studies per hospital protocol. Regulate heparin

1073
drip to maintain PTT at 1.5 to 2 times control levels or according to
protocol. Never discontinue heparin without consulting with the
provider.

3. Apply pressure dressing over puncture sites. If cardiac

catheterization was performed, inspect site at frequent intervals for
evidence of hematoma formation. Immobilize extremity for 6 to 8
hours after catheterization procedure.

4. Avoid unnecessary venipunctures, IM injections, or arterial

puncture. Obtain laboratory specimens from heparin-lock device.

5. Monitor patient for indicators of internal bleeding: back pain,

abdominal pain, decreased BP, pallor, and bloody stool or urine.
Report significant findings to provider.

6. Monitor patient for signs of intracranial bleeding every 2 hours:

change in LOC, headache, dizziness, vomiting, and confusion.

7. Test all stools, urine, and emesis for occult blood.

8. Use care with oral hygiene and when shaving patient. For more
information about safety precautions, see Pulmonary Embolus,
(Chapter 4).

Teaching: Diet and prescribed medications

1. Diet low in cholesterol and saturated fat: Provide sample diet

plan for meals that are low in cholesterol and saturated fat. Teach
the patient about foods that are high or low in cholesterol and
saturated fat. Stress the importance of reading food labels.

2. BP control: If the patient was found to have hypertension

associated with MI, the patient should be taught the importance of
taking appropriate medications to control BP and to follow
recommended dietary guidelines to minimize sodium intake.
Sodium promotes water retention, which can increase BP. Higher
systemic BP increases the workload of the heart, demanding that
more myocardial oxygen be consumed.

1074
• Teach the patient about the prescribed medications,
including name, purpose, dosage, action, schedule,
precautions, and potential side effects.

• Teach the patient the actions that should be taken if

chest pain is unrelieved or increases in intensity.

Teaching: Activity/exercise
If chest pain occurs:

1. Stop and rest.

2. Take 1 tablet of NTG; wait 5 minutes. If pain is not relieved, take

a second NTG; wait 5 minutes. If pain is not relieved, take a third
NTG and call 911 or local emergency number.

3. Lie down if headache occurs. The vasodilation effect of NTG

causes a decrease in BP, which may result in orthostatic
hypotension and transient headache.

4. Explain to the patient that it is no more beneficial to be in the

emergency department than it is to be at home during episodes of
chest pain caused by angina and therefore traveling to a hospital at
the first sign of chest pain usually is unnecessary.

5. Review activity limitations and prescribed progressions (see

Tables 5-3 and 5-6). Provide the following information:

• When you are discharged from the hospital, it is

important that you continue your walking program.
Do not overestimate your ability; rather, start off
slowly and build up. Depending on how you feel,
you may only be able to stay at one level or you
may progress to 2 miles quickly. Remember to

1075
 warm up and cool down with stretches for 5 to 7
minutes and to walk 3 to 5 times each week.

• Avoid sudden energetic activities.

• Plan for regular rest periods in the afternoon.

• Let your body guide you regarding whether to

increase or decrease activity.

• Inform your provider of any changes in activity

tolerance, such as the development of new
symptoms with the same activity.
6. Avoid exercising outdoors in very cold, hot, or humid weather.
Extreme weather places an additional stress on the heart. If you do
exercise in extremes of weather, decrease the pace and monitor
your response carefully.

7. Pulse monitoring: Teach the patient how to take pulse, including

parameters for target HRs and limits.

Table 5-6
THROMBOLYTIC DOSAGE REGIMENS

1076
Teaching: Sexuality
Sexual activity guidelines: Because sexual activity is a physical
activity, certain guidelines can help the patient and his or her
partner enjoy a satisfying sexual relationship while minimizing the
workload of the heart:

1. Rest is beneficial before engaging in intercourse.

2. Find a position that is comfortable for you and your partner.

Assuming a different position that is uncomfortable to both may
increase the workload of the heart.

3. Medications such as NTG may be taken prophylactically by the

patient before intercourse to prevent chest pain.

4. Postpone intercourse for 1 to 2 hours after eating a heavy meal.

5. Report the following symptoms to your physician if they are

experienced after sexual relations: SOB, increased HR that persists
for longer than 15 minutes, unrelieved chest pain.

1077
6. Do not take phosphodiesterase type-5 (PDE-5) inhibitors
(sildenafil, vardenafil) if taking nitrates.

Teaching: Disease Process; Teaching: Prescribed

Activity/Exercise; Teaching: Prescribed Medication; Teaching:
Sexuality

Acute pain (chest) 

related to biophysiologic injury related to decreased oxygen supply to the
myocardium.
Goals/Outcomes: Within 30 minutes of intervention, the patient’s
subjective evaluation of discomfort improves, as documented by a
pain scale. Nonverbal indicators, such as grimacing, are absent.
Vital signs return to baseline. ECG changes present during the
event resolve.
Pain Control

Pain management

1. Assess and document the character of the patient’s chest pain,

including location, duration, quality, intensity, precipitating and
alleviating factors, presence or absence of radiation, and associated
symptoms. Devise a pain scale with the patient, rating discomfort
from 0 (no pain) to 10 or using a system that assists in objectively
reporting pain level.

2. Measure BP and HR with each episode of chest pain. BP and HR

may increase because of sympathetic stimulation as a result of pain.
If the chest pain is caused by ischemia, the heart muscle may not be
functioning normally and CO may decrease, resulting in a low BP.
In addition, dysrhythmias such as bradycardia and ventricular
ectopy may be noted with ischemia. If BP is low, it may not be
advisable to administer nitrates and morphine, which can further
reduce BP, adding to myocardial ischemia.

3. After each titration of IV NTG, evaluate patient’s BP and the

effects of therapy in relieving patient’s chest pain. If slight
hypotension occurs (80 to 90 mm Hg systolic), reduce the flow rate
to one-half or less of the infusing dose. If severe hypotension (less

1078
than 80 mm Hg systolic BP) occurs, stop the infusion and contact
the provider for further directions.

Cardiogenic shock occurs in 5% to 10% of acute

myocardial infarctions.

4. Monitor for side effects of NTG, including headache,

hypotension, syncope, facial flushing, and nausea. If side effects
occur, place the patient in a supine position and consult physician
for further interventions.

5. Administer heparin, GP IIb/IIIa inhibitors (abciximab, tirofiban,

eptifibatide), and aspirin as prescribed. Heparin infusion usually
should be administered using a weight-based protocol, which is
titrated according to PTT results. These patients are predisposed to
bleeding and may need to be given bleeding precautions.

6. Maintain a quiet environment and group patient care activities to

allow for periods of uninterrupted rest. Consider healing touch
therapy, relaxation exercises, or music therapy.

7. Position patient according to his or her comfort level.

8. Provide care calmly and efficiently; reassure patient during chest

pain episodes.

9. Ensure that activity restrictions and bed rest are maintained;

teach patient about activity limitation and its rationale; to minimize
oxygen requirements and thus decrease chest pain. Reassure
patient that activities are allowed based on individual response.
Often, patients may be afraid to engage in activities for fear of
further deterioration.

10. Instruct the patient to report any further episodes of chest pain.

Dysrhythmia management

1079
1. Obtain a 12/15/18-lead ECG during patient’s episode of chest
pain. During angina, ischemia usually is demonstrated on the ECG
by ST-segment depression and T-wave inversion.

2. Administer nitrates as prescribed, titrating IV NTG so that chest

pain is relieved yet systolic BP remains greater than 90 mm Hg.
NTG drip is usually 50 mg NTG in 250-mL D5W. Begin with 6
mL/h, which is 5 µg/min. Titrate by increments of 10 to 20 mL every
5 minutes (or 10 to 20 µg/min every 5 minutes) up to a maximum
dosage determined by agency protocol, physician, or midlevel
practitioner.

3. As prescribed, administer beta blockers and possibly calcium

channel blockers (CCBs), which relieve chest pain by (1)
diminishing coronary artery spasm, causing coronary and
peripheral vasodilation, and (2) decreasing myocardial contractility
and oxygen demand. Monitor for side effects, including
bradycardia and hypotension. Be alert to indicators of HF,
including fatigue, SOB, weight gain, and edema, and to indicators
of heart block, such as syncope and dizziness.

4. Administer oxygen per nasal cannula at 2 to 4 L/min, as

prescribed.

Analgesic Administration; Cardiac Care: Acute;

Hemodynamic Regulation

Care plans for patients undergoing

percutaneous coronary intervention
Deficient knowledge 
related to angioplasty procedure and postprocedure care
Goals/Outcomes: Within the 24-hour period before the
procedure, the patient describes the rationale for the procedure,
how it is performed, and postprocedure care. Patient relates
discharge instructions within the 24-hour period before discharge
from the CCU.
Knowledge: Treatment Procedure(s); Knowledge:

1080
Medications; Knowledge: Disease Process

Teaching: Cardiac disease process

1. Assess patient’s understanding of CAD and the purpose of

angioplasty. Evaluate patient’s style of coping and degree of
information desired.

2. As appropriate for coping style and using a heart drawing,

discuss the location of the patient’s CAD with the patient and
significant others.

Teaching: Procedure/treatment

1. Use of local anesthesia and sedation during procedure

2. Insertion site of catheter: groin or arm

3. Sensations that may occur: mild chest discomfort, a feeling of

heat as the dye is injected

4. Use of fluoroscopy during procedure. Determine patient’s history

of sensitivity to contrast material or allergy to iodine/shellfish

5. Ongoing observations made by nurse after procedure: BP, HR,

ECG, leg or arm pulses, and lab work

6. Importance of lying flat in bed for 6 to 12 hours after procedure if

a femoral approach is used, unless a vascular closure device is used.
Patients are able to get out of bed sooner when a closure strategy is
used

7. Necessity for nursing assistance with eating, drinking, and

toileting needs after procedure

8. Need for increased fluid intake after procedure to flush contrast

from system

9. If the patient and significant others express or exhibit evidence of

anxiety regarding the procedure, try to arrange for them to meet

1081
with another patient who has had a successful intervention.

Teaching: Prescribed medication

Discharge instructions:

1. Importance of taking antiplatelet drugs to prevent restenosis

2. Importance of taking statins and other antilipid drugs to prevent

progression of CAD

3. Avoidance of strenuous activity during first few weeks at home

4. Follow-up visit with cardiology 1 week after hospital discharge

5. Signs and symptoms to report to healthcare professional (e.g., GI

upset, repeat of angina, fainting)

Teaching: Procedure/Treatment; Anxiety Reduction; Support

Group

Additional nursing diagnoses

Also see nursing diagnoses and interventions as appropriate in
Nutritional Support (Chapter 1), Mechanical Ventilation (Chapter
1), Hemodynamic Monitoring (Chapter 1), Prolonged Immobility
(Chapter 1), Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2), Acute Cardiac Tamponade (Chapter
5), Heart Failure (Chapter 5), and Dysrhythmias and Conduction
Disturbances (Chapter 5).

Acute infective endocarditis

Pathophysiology
Infective endocarditis (IE) is infection of the endocardium (the
innermost layer of the heart), often involving the natural or
prosthetic valve; Staphylococcus aureus is considered the primary
pathogen; others are Staphylococcus epidermis, Streptococcus species:
Group A, B, C, G and D, Viridans, Bovis. Enterococci: alpha-

1082
hemolytic, Intermedius, Lugdunensis, Enterococcal gram-negative
bacilli, Legionella, Haemophilus, Aphrophilus, Actinobacilus,
Actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens,
Kingella kingae, Bartonella, Candida, Aspergillus, and Pseudomonas
aeruginosa. Forty percent of patients with IE have no underlying
heart disease. Despite diagnosis and treatment strategies, the
fatality rate has not decreased since the 1970s. The age of a patient,
proliferation of implanted biomechanical devices, rise in resistant
organisms, and the incidence of hospital-associated infection may
have influenced that. Antibiotic prophylaxis has had little effect on
decreasing the incidence.
Portals of entry for the infecting organism include the mouth and
GI tract, upper airway, skin, and external genitourinary (GU) tract.
All heart valves are at risk for infection, but the aortic and mitral
valves are more commonly affected than the right-sided pulmonic
and tricuspid valves. IV drug abuse, along with right-side insertion
of invasive lines increases the possibility of tricuspid IE. Once the
infection process begins, valvular dysfunction, manifested by
insufficiency with regurgitant blood flow, can occur, ultimately
resulting in a decrease in CO. The vegetation may enlarge and
obstruct the valve orifice, further reducing CO. The vegetation may
break apart and embolize to vital organs. In severe cases, the
affected valve may necrose, develop an aneurysm, and rupture; or
the infection may extend through the myocardium and epicardium
to cause a pericarditis (see Acute Pericarditis, Chapter 5). If the
conduction system is affected by the spreading infection, bundle
branch block may occur. The chordae tendineae can become
infected and rupture, resulting in severe acute mitral or tricuspid
regurgitation. Complications of IE occur suddenly, with a dramatic
change in the clinical picture. Mortality rates between 20% and 50%
have been reported. The infection recurrence rate is 10% to 20%.
The incidence of IE is higher in patients older than 50 years of age,
is more common in men than in women, and is uncommon in
children.
Types of IE include:

• Native valve endocarditis, acute and subacute

1083
• Prosthetic valve endocarditis, early and late: 10% to 20%

• IV drug abuse

• Pacemaker

• Nosocomial

Assessment
Goal of assessment
The goal is to identify the severity of symptoms. The severity of
symptoms varies depending on the infective organism. (For
example, Staphylococcus aureus infection is more severe than that
with Streptococcus viridans.) Acute presentation is defined as onset
within 1 week of infection, while subacute infections may take up to
4 weeks to present.

History and risk factors

Patients at higher risk for bacteremia leading to IE include those
with valvular disease undergoing invasive procedures and
insertion of devices including temporary pacemakers, PA catheters,
and central IV catheters or ports; those undergoing endoscopy,
surgery, or dental work; and immunosuppressed patients (e.g.,
with organ transplants, carcinoma, burns, or diabetes mellitus).
Users of illicit IV drugs are at risk of tricuspid valve disease.

Vital signs
• Fever, tachycardia, possible dysrhythmias, possible hypotension,
fatigue, and valvular dysfunction

Hemodynamic measurements
Invasive monitoring devices are used cautiously with these
patients, as they may cause further valvular dysfunction,
embolization, and infection.

• PA catheters are used to assess hemodynamic function if

1084
 necessary.

• Elevations of PAP and CVP, with reduced CO, are expected in

most patients with IE.

Observation
• The skin is often pale.

• If right-sided HF is present, skin and sclera may be jaundiced and

edematous, with neck vein distention, a positive hepatojugular
reflex, and ascites.

• Late assessment findings include anemia, petechiae, and clubbing

of the fingers.

• Splenomegaly occurs by 10 days because of the activation of the

reticuloendothelial system. If marked, a splenic infarct may have
occurred.

• Acute infective stage: Diaphoresis, fatigue, anorexia, joint pain,

weight loss, abdominal pain, flulike symptoms, pleuritic pain,
headache.

• Splinter hemorrhages: Small red streaks on the distal third of the

fingernails or toenails

• Janeway lesions: Painless, small, hemorrhagic lesions found on

the fingers, toes, nose, or earlobes, probably occurring as the
result of immune complex deposition with inflammation

• Osler nodes: Painful, red, subcutaneous nodules found on the

pads of the fingers or on the feet, probably occurring as a result of
emboli producing small areas of gangrene or vasculitis

• Roth spots: Retinal hemorrhages with pale centers seen on

funduscopic examination

1085
 If emboli of the vegetations occur in other areas, signs and
symptoms of stroke or peripheral, myocardial, renal, or mesenteric
arterial insufficiency, occlusion, or infarct will be seen.

Auscultation
• A new or changed murmur may be heard as a result of the
valvular dysfunction.

• If HF is present, fine crackles may be auscultated at the lung

bases, and an S3 or S4 heart sound may be audible.

Screening labwork
Blood studies can reveal presence of infection or further and
progressive worsening heart status, such as HF, conduction
problems, or ischemia.

• Cardiac enzymes/isoenzymes: To rule out MI as a cause of chest

discomfort or SOB

• BNP: Elevated if HF is present

• Levels of cardiac medications: Low levels may reveal

noncompliance with ordered medications.

12-lead electrocardiogram
Evaluates for changes from last ECG to assess for worsening of
heart disease (myocardial damage). ECG changes resulting from
electrolyte imbalances may also decrease CO. An initial 12-lead
ECG should be done on every patient and used for comparison
over the course of hospitalization.

• Heart rate: Diagnose type of tachycardia, bradycardia, or

irregular rhythm. During acute episodes, atrial dysrhythmias
such as paroxysmal atrial tachycardia, premature atrial

1086
 contractions, atrial flutter, or atrial fibrillation may occur.

• PR, QRS, QT intervals: May increase, but may be regular with a

normal rate and conduction velocity.

• ST-segment and T-wave changes: Depression or elevation

Diagnostic Tests for Infective Endocarditis

1087
Collaborative management
Care priorities

1. Prevent infective endocarditis in patients undergoing

invasive procedures

• The AHA recommends prophylactic antibiotics for high-risk

patients only: Those with a prosthetic heart valve or who have
had a heart valve repaired with prosthetic material.

• A history of endocarditis

• A heart transplant with abnormal heart valve function

1088
• Certain congenital heart defects including:

• Cyanotic congenital heart disease (birth defects with oxygen

levels lower than normal), that has not been fully repaired,
including children who have had a surgical shunts and conduits.

• A congenital heart defect that has been completely repaired with

prosthetic material or a device for the first 6 months after the
repair procedure.

• Repaired congenital heart disease with residual defects, such as

persisting leaks or abnormal flow at or adjacent to a prosthetic
patch or prosthetic device.

• Prophylaxis treatment: Amoxicillin 2 g in a single dose before the

procedure. If penicillin-allergic, use clindamycin 600 mg orally in
a single dose or azithromycin 500 mg orally in a single dose.

• Treatment with confirmation: Patients may be treated IV for at

least 2 weeks in the hospital and observed for cardiac and
noncardiac complications. The patient may be a candidate for
outpatient and home parenteral antibiotic therapy.

Table 5-9
ECG CHANGES FREQUENTLY FOUND WITH VENTRICULAR AND
ATRIAL HYPERTROPHY

Chamber ECG Change

Left “R” voltage increases in V4 to 6; “S” voltage increases (deeper inflection) in V1 to 2;
ventricular the sum of “S” in V1 or V2 and “R” in V5 or V6 will be more than 35 mm, or “R” in
enlargement any V lead will be more than 25 mm.
Left atrial “P mitral” in leads II, III, aVF, and V1; P wave is m-shaped with a duration more
enlargement than 0.1 second.
Right “R” voltage increases in V1 or V2; “S” voltage increases in V5, V6; sum of “R” in V1
ventricular or V2 and “S” in V5 or V6 will be more than 35 mm.
enlargement
Right atrial “P pulmonale” in leads II, III, aVF, and V1; P wave is 2.5 mm voltage and 0.1
enlargement second duration.

Table 5-8
ASSESSMENT FINDINGS WITH VALVULAR HEART DISEASE

1089
BP, Blood pressure; CO, cardiac output; CVP, central venous pressure; ICS,
intercostal space; LSB, left sternal border; LV, left ventricle/ventricular; LVEDP, left
ventricular end-diastolic pressure; MCL, midclavicular line; PA, pulmonary artery;
PAEDP, pulmonary artery end-diastolic pressure; PAP, pulmonary artery pressure;
RA, right atrium; RAP, right atrial pressure; RSB, right sternal border; RV, right
ventricle/ventricular.

2. Treat infection and prevent further complications,

such as septic emboli, HF, or cardiogenic shock

• Antibiotics: Treatment of the infection: prompt and accurate

treatment has an important effect on outcomes. It is initially
empiric in nature and then modified based on blood cultures;
penicillin G and gentamicin are given for streptococci coverage.
With recent history of antibiotics and possible resistance to
antibiotics (methicillin-resistant Staphylococcus aureus and
penicillin-resistant streptococci), empiric treatment strongly leans
toward vancomycin over penicillin for initial therapy. Patients
usually require 4 to 8 weeks of IV antibiotics. The first 2 weeks
may be initiated during hospitalization and the remaining
therapy given on an outpatient basis. The vegetation must be
sterilized, abscesses treated, and spread of infection prevented.
Initial antibiotic selection is empiric followed by therapy based
on the results of the blood/tissue culture and sensitivity studies.

• Fluid and sodium restriction: Used for optimal fluid balance with

1090
 reduced heart function or HF. Specific restrictions must be
individualized and based on severity of symptoms.

• Bed rest: May be used initially, with activity as tolerated for the
remainder of treatment

• Diet: High in protein and calories to prevent cardiac cachexia and

support the immune system

• Watch for signs of embolization during the first 3 months of

treatment: Monitor renal status, vital signs, and oxygenation.

3. Pharmacotherapy

• Oxygen therapy with pulse oximetry (SpO2): Oxygen (Fio2) to

maintain PaO2 at 80 mm Hg or higher and pulse oximetry to
monitor oxygen saturation continuously or intermittently to keep
SpO2 at 95% or higher

• Diuretics: May be used to decrease symptoms of HF by reducing

intravascular volume

• Positive inotropic agents (e.g., digoxin, dobutamine, milrinone):

Used to increase contractility and CO

• Vasodilators (nitroprusside, NTG): Reduce cardiac work and

improve coronary arterial perfusion. Both preload and afterload
(end-diastolic ventricular volume and pressure) may be reduced
to help relieve symptoms of HF. Aggressive vasodilation is not
well tolerated by all patients.

• Sedation: May be necessary to allay anxiety and to reduce

myocardial oxygen consumption

4. Manage HF and/or cardiogenic shock

See Heart Failure (Chapter 5) and Cardiogenic Shock (Chapter 5).

5. Consider surgical valve replacement

Required when HF worsens or if the infection fails to respond to

1091
antibiotics (see Valvular Heart Disease, Chapter 5). An abscess or
infected tissue may be surgically removed if there is no response to
long-term antibiotics. If the patient is hemodynamically stable,
surgery may not be needed. A surgeon is usually consulted in case
of an HF emergency. Early surgical intervention with severe
valvular damage may decrease hospital mortality.

• Indications for urgent native valve replacement include:

• Heart failure: Caused by acute aortic or mitral

regurgitation

• Persistent fever and bacteremia: For longer than 8

days despite adequate antimicrobial therapy

• Local spread of infection: Includes abscesses,

pseudoaneurysms, abnormal communications (i.e.,
fistulas) or rupture of one or more valves,
conduction disturbances, and myocarditis

• Virulent organisms: Antibiotic-resistant

microorganisms (e.g., fungi, Brucella and Coxiella
spp.) or microorganisms with a high potential for
rapid destruction of cardiac structures (e.g.,
Staphylococcus lugdunensis)

• Indications for replacement of prosthetic valves: Complications

that may prompt the need to replace a prosthetic valve include
primary valve failure, prosthetic valve endocarditis, prosthetic
valve thrombosis, thromboembolism, and mechanical hemolytic
anemia.

• Prosthetic valve endocarditis (PVE): The hallmark

sign of PVE in mechanical valves is ring abscesses.

1092
 Ring abscess may lead to valve dehiscence,
perivalvular leakage, and formation of myocardial
abscesses. Extension to the conduction system may
prompt a new atrioventricular block. Valve stenosis
and purulent pericarditis are seen less often. Valve
stenosis is more common with bioprosthetic valves
than mechanical valves. Bioprosthetic valve PVE
results in leaflet tears or perforations. Ring
abscesses, purulent pericarditis, and myocardial
abscesses are seen less often in bioprosthetic valve
PVE.
• Early PVE: Occurs within 60 days of valve insertion and is usually
the result of perioperative contamination

• Late PVE: Occurs 60 days or later after insertion and is usually the
result of transient bacteremia from dental or GU sources, GI
manipulation, or IV drug abuse

Care plans for acute infective endocarditis

Decreased cardiac output 
related to altered preload, afterload, or contractility secondary to valvular
dysfunction.
Goals/Outcomes: Within 72 hours after initiation of therapy, the
patient has adequate hemodynamic function with NSR or
controlled atrial fibrillation as evidenced by the following: HR less
than 100 bpm, BP greater than 90/60 mm Hg, stable weight, intake
equal to output plus insensible losses, RR less than 20 breaths/min
with normal depth and pattern, and absence of S3 or S4 heart
sounds, crackles, distended neck veins, and other clinical signs of
HF. Optimally, the following normal parameters will be achieved:
CO 4 to 7 L/min, CVP 4 to 12 mm Hg, and MAP 60 to 105 mm Hg.
Cardiac Pump Effectiveness; Circulation Status

1093
Cardiac care

1. Monitor for valvular dysfunction: Assess heart sounds every 2 to

4 hours. A change in the characteristics of a heart murmur may
signal progression of valvular dysfunction, which can occur with
insufficiency, stenosis, dislodgment of vegetation, or unseating of a
prosthetic valve. A new S3 or S4 sound may signal HF.

2. Monitor for new dysrhythmias that may contribute to HF: Report

new dysrhythmias, which may indicate the spread of infection to
the conduction system or atrial volume overload. Correlate
dysrhythmias with changes in BP and CO.

3. Monitor for signs of left-sided HF: Crackles, S3 or S4 sounds,

dyspnea, tachypnea, digital clubbing, decreased BP, increased pulse
pressure, increased serum BNP levels, increased LVEDP, and
decreased CO.

4. Monitor for signs of right-sided HF: Increased CVP, distended

neck veins, positive hepatojugular reflex, edema, jaundice,
increased serum BNP levels, and ascites.

5. Monitor for renal dysfunction, fluid volume overload, and third

spaced fluids: Measure I&O hourly, and weigh at a consistent time
each day, with the same scale and amount of clothing for accuracy.
Consult physician or advanced practice provider if patient’s weight
increases by more than 1 kg per day.

• Optimize ventricular filling pressures: If the

patient’s CVP or PAWP is elevated and CO
decreases, decrease preload (filling pressures) by
limiting fluid and sodium intake and administer
diuretics and venous dilators (e.g., NTG) as
prescribed. Filling pressures may need to be higher
to optimize CO.

• Reduce resistance to ventricular ejection: If the

1094
 patient’s MAP is high, decrease afterload with
prescribed arterial dilators (e.g., nitroprusside).

• Optimize volume status: For low CVP or BP, consult

with advanced practice provider. Vasopressors may
be prescribed. Patient may be developing sepsis, so
monitor carefully.

• Optimize coronary artery perfusion: If diastolic BP

is low, coronary artery perfusion may be reduced.
Prevent further reductions by avoiding
administration of morphine sulfate or rapid
warming of hypothermic patients. Increase
contractility with inotropic drugs, as prescribed.
6. Balance rest and activities: Intolerance indicates ineffective
oxygenation.

7. Manage stress: Help the patient reduce stress and myocardial

oxygen consumption by teaching stress-reduction techniques such
as imagery, meditation, or progressive muscle relaxation. For
description of a relaxation technique, see Appendix 7.

• Provide sedation as needed for anxiety and/or

agitation after ruling out the patient is NOT
hypoxic.
8. Prevent orthostatic hypotension: Change patient’s position from
lying to sitting to standing slowly.

See Cardiogenic Shock, Chapter 5, for a discussion of preload and

afterload medications.
Energy Management

Impaired gas exchange 

1095
related to alveolar-capillary membrane changes with decreased diffusion of
oxygen secondary to pulmonary congestion.
Goals/Outcomes: Within 24 hours of initiation of oxygen therapy
and during the weaning process, the patient has adequate gas
exchange as evidenced by RR less than 20 breaths/min with normal
pattern and depth, SVO2 60% to 80%, PaO2 greater than 80 mm Hg,
SaO2 greater than 95%, and natural skin color.
Respiratory Status: Gas Exchange; Tissue Perfusion:
Pulmonary

Ventilation assistance

1. Monitor for and manage pulmonary congestion: Assess rate,

effort, and depth of respirations. RR increases in response to
inadequate oxygenation. Assess color of skin and mucous
membranes. Pallor signals impaired oxygenation. Auscultate lungs
every 2 hours. Report crackles, rhonchi, and wheezing.

2. Monitor for signs of impending instability: If hemodynamic

monitoring with oximetry is used, monitor for decreased SVO2
prompted by increased metabolic demands or from increased
extraction as a result of reduced perfusion/oxygen delivery. SVO2
values may fall before the patient is symptomatic; the values
correlate with CO.

3. Monitor for and manage hypoxemia: Monitor ABG values for

PaO2 less than 80 mm Hg, respiratory acidosis (Paco2 greater than 45
mm Hg, pH less than 7.35) indicative of respiratory insufficiency or
respiratory alkalosis (Paco2 less than 35 mm Hg, pH greater than
7.45) from tachypnea.

• Deliver oxygen as prescribed. COPD patients may

require NiPPV or intubation and mechanical
ventilation to tolerate aggressive oxygen therapy.
Oxygen alone may prompt hypoventilation and/or
respiratory arrest.

1096
• Assess arterial oxygen saturation with pulse
oximetry. Normal oxygen saturation is 95% to 99%.
Levels of 90% to 95% necessitate frequent
assessment. Oxygen levels that trend down to less
than 90% require aggressive interventions to
increase oxygen saturation. Consider increasing
FIO2, decreasing preload, and taking measures to
improve ventilation.

• Place patient in high Fowler position to facilitate gas

exchange as tolerated.

• Have patient cough, deep breathe, and use incentive

spirometry to prevent atelectasis.

Invasive Hemodynamic Monitoring; Oxygen Therapy;

Respiratory Monitoring

Risk for infection (systemic) 

related to presence of invasive catheters and lines; inadequate secondary
defenses secondary to prolonged antibiotic use.
Goals/Outcomes: The patient is free of secondary infection as
evidenced by clear urine with normal odor, wound healing within
acceptable time frame, and absence of erythema, warmth, and
purulent drainage at insertion sites for IV lines. On resolution of
acute stage of IE, the patient remains normothermic with WBC
count less than 11,000/mm3, negative culture results, and HR less
than 100 bpm. CO is less than 7 L/min, and SVO2 is 60% to 80%. No
yeast overgrowth infections are present. Patient and significant
others verbalize rationale for antibiotic therapy and identify where
and how to obtain guidelines.
Infection Severity

Infection protection

1097
1. Prevent central line-associated bloodstream infection: Use strict
aseptic technique to care for all invasive monitoring device
insertion sites and IV lines. Rotate central lines per hospital
protocol. Discuss feasibility of a tunneled catheter or peripherally
inserted central catheter (PICC) line with advanced practice
provider.

• Change tubing, containers, and peripheral insertion

sites per agency protocol. Inspect all catheter
insertion sites daily for redness, drainage, or other
evidence of infection. Rotate site immediately if
infection is suspected.
2. Control secondary fungal infections: Provide oral care at least
every 4 hours to minimize fungal and other infections. Women may
require antifungal medications to manage vaginal yeast infections.

3. Prevent catheter-associated urinary tract infections (CAUTI):

Implement the CAUTI prevention bundle. Assess ongoing need for
a urinary catheter. Remove if possible. Provide perineal care with
soap and water for patients with indwelling urinary catheters.
Inspect urine for evidence of infection, such as casts, cloudiness, or
foul odor. Be alert to patient complaints of burning with urination
after catheter is removed.

4. Monitor temperature, WBC count, and HR. Increases may

indicate signs of infection.

5. Monitor for signs of sepsis: Calculate SVR with CO

measurements. Symptoms of sepsis include increased CO,
decreased SVR, and increased SVO2 during the early stages.

6. Teach patient and significant others the importance of reporting

signs and symptoms of recurring infections (e.g., fever, malaise,
flushing, anorexia) or HF (e.g., dyspnea, tachypnea, tachycardia,
weight gain, peripheral edema).

7. Stress the importance of prophylactic antibiotics before invasive

1098
procedures such as dental examinations or surgery. The AHA
publishes general guidelines for prophylactic antibiotic treatment to
prevent IE.

Fever Treatment; Surveillance; Infection Control

Unlike peripheral venous emboli, these emboli are caused by

the vegetations; therefore, prevention is difficult. Interventions are
aimed at early detection of embolization and supportive therapies.

Ineffective tissue perfusion (or risk for same) renal,

gastrointestinal, peripheral, cardiopulmonary, and cerebral 
related to interrupted arterial blood flow secondary to septic emboli caused
by valvular vegetations.
Goals/Outcomes: The patient has adequate perfusion as
evidenced by urine output at least 0.5 mL/kg/h, at least 5 bowel
sounds/min, peripheral pulses at least 2+ on a 0 to 4+ scale, warm
and dry skin, BP at least 90/60 mm Hg, RR 12 to 20 breaths/min
with normal pattern and depth, NSR on ECG, and orientation to
time, place, and person.
Circulation Status

Hemodynamic regulation

1. Monitor I&O at frequent intervals. Be alert to urinary output less

than 0.5 mL/kg/h for 2 consecutive hours. Report oliguria, as it may
signal impending acute renal failure.

2. Monitor bowel sounds every 2 hours. Report hypoactive or

absent bowel sounds. Patients are at risk for decreased mesenteric
perfusion and mesenteric or bowel infarction.

3. Assess peripheral pulses, color, and temperature of extremities.

Weak pulses (2+ or less on a 0 to 4+ scale) with pale, cool
limbs/hands/feet may denote peripheral embolization.

1099
4. Monitor patient for confusion and changes in sensorimotor
capabilities or cognition, which may signal cerebral emboli.

5. Assess for chest pain, decreased BP, SOB, ischemic or injury

pattern on 12-lead ECG, or elevated cardiac enzyme levels
indicative of MI caused by vegetation emboli that have migrated to
the coronary arteries (see Acute Coronary Syndromes, Chapter 5).

6. Assess for and report appearance of splinter hemorrhages, Osler

nodes, Janeway lesions, and Roth spots (see Endocarditis
Observation, Chapter 5).

Circulatory Care; Cardiac Care: Acute

Additional nursing diagnoses

As appropriate, also see nursing diagnoses and interventions in
Nutritional Support (Chapter 1), Hemodynamic Monitoring
(Chapter 5), Prolonged Immobility (Chapter 1), Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2),
Acute Cardiac Tamponade (Chapter 5), Heart Failure (Chapter 5),
and Cardiogenic Shock (Chapter 5).

Acute pericarditis
Pathophysiology
Pericarditis is the general term for an inflammatory process
involving the pericardium and the epicardial surface of the heart.
Inflammation can occur as the result of an AMI, an infection,
chronic renal failure, or an immunologic, chemical, or mechanical
event (Box 5-3). Often, early pericarditis manifests as a dry
irritation, whereas late pericarditis (after 6 weeks) involves
pericardial effusions that can lead to cardiac tamponade if severe.
Pericarditis is often seen in the CCU as a secondary finding
following coronary revascularization surgery or valve replacement
or associated with chronic renal failure. A thorough assessment and
recognition are essential for appropriate treatment, as symptoms

1100
can be masked by the primary condition. For example, patients are
sometimes transferred into a CCU with acute cardiac
decompensation resembling ACS, when in reality, the condition is
caused by pericardial effusions.

Box 5-3
CAUSES OF PERICARDITIS
• Autoimmune cardiac injury

• Dressler syndrome (post acute myocardial infarction)

• Drug induced (e.g., hydralazine, phenytoin)

• Hypothyroidism

• Idiopathic

• Infection (bacterial or viral)

• Myocardial infarction

• Metabolic disorders

• Neoplasms

• Postpericardiotomy syndrome

• Radiation injury

• Rheumatologic disease

• Rheumatic fever

• Rheumatoid arthritis

• Systemic lupus erythematosus

• Sarcoidosis

1101
• Trauma

• Uremia

The initial pathophysiologic findings of pericarditis include

infiltration of polymorphonuclear leukocytes, increased vascularity,
and fibrin deposition. Inflammation may spread from the
pericardium to the epicardium or pleura. The visceral pericardium
may develop exudates or adhesions. Large effusions can lead to
cardiac tamponade. The excess fluid compresses the heart within
the pericardial sac, which impairs filling of the chambers and
ventricular ejection.

Assessment
Goal of assessment
The goal is to assess severity of the symptoms and to rule out ACS
as the cause of ECG changes (ST-segment elevation and/or
depression) and chest pain. Acute pericarditis is characterized by
chest pain, pericardial friction rub, and serial electrocardiographic
changes. Severe pericardial effusions can cause cardiac tamponade.

History and risk factors

Assess for AMI, recent bacterial or viral infection, chronic renal
failure, autoimmune disease including rheumatoid arthritis and
systemic lupus erythematosus, radiation therapy, cardiac surgery,
or chest trauma. Viral infection is the more common cause (1% to
10%) of acute pericarditis, followed by bacterial infection, which
can lead to purulent pericarditis (1% to 8%). Tuberculosis causes 1%
to 4% of cases.

Observation
The patient presents with chest pain, but the location and quality
can vary. Pain can be knifelike and stabbing and may radiate to the
neck or shoulder. Usually the pain is aggravated by a supine
position, coughing, deep inspiration, and swallowing. Pain may be

1102
lessened when leaning forward. Dyspnea develops because of
shallow breathing to prevent pain.

Early indicators of pericarditis

Fatigue, pallor, fever, and anorexia

Late indicators and evidence of effusions

Increased dyspnea, crackles, and neck vein distention. Joint pain
may be present when inflammation is generalized. Evaluate for
signs of pain, distress, and tamponade.

• Dyspnea level and oxygen need

• Neck vein distention assessment

• Use of pain scale to determine progress of treatment

Vital sign assessment

HR, heart rhythm, and BP are used to evaluate CO and perfusion.

• BP elevated on right arm: When BP is taken on both arms, if

cardiac tamponade is ensuing, blood cannot flow into and
through the constricted heart.

• Narrowing pulse pressure: May indicate effusion is exerting

pressure around the heart

• Pulsus paradoxus: BP should be checked for a paradoxic pressure

greater than 10 mm Hg. Normally the systolic pressure is slightly
higher during the expiration and lower during inspiration. When
effusions are present, this difference in systolic pressure across
the respiratory cycle will be greater than 10 mm Hg.

• Tachycardia: Heart rate is usually rapid and regular.

• Beck triad: Hypotension, elevated venous pressure with jugular

venous distention, and muffled heart sounds may occur in
patients with cardiac tamponade, especially if sudden
intrapericardial hemorrhage occurs.

1103
Hemodynamic measurements
If used, the PA catheter reveals elevated CVP, PAP, and PAWP.

• As effusions increase: CO will decrease. If adhesions are present,

the filling of the chambers may be restricted, resulting in reduced
end-diastolic volumes and pressures.

• If cardiac tamponade is developing: Pressures in all heart

chambers eventually equalize and the patient has a cardiac arrest.

Auscultation
Heart sounds may reveal an intermittent pericardial friction rub.
The pericardial friction rub has three components; one systolic and
two diastolic: one early in diastole when the heart begins to stretch
during ventricular filling and the other during late diastole when
the ventricles are fully stretched. The first and second heart sounds
are obscured by the rubbing sounds, which are sometimes
described as the sound of squeaky leather shoes. S1 and S2 are no
longer crisp and clear. If all three components of the rub are
audible, S2 may sound split.
Pericardial friction rub: The rub is heard best with the diaphragm
of the stethoscope positioned at the left lower sternal border. The
rub is often positional, so auscultation should be done with the
patient in several positions (i.e., supine, sitting and leaning forward,
lying on the left lateral side). A friction rub may not be heard, even
in the presence of pericarditis.

Screening labwork
• CBC: May reveal elevated WBCs and anemia

• Cardiac enzymes: Isoenzymes may be elevated if the epicardium

is inflamed.

12-lead electrocardiogram
Evaluates for changes from last ECG; assesses for worsened heart
disease (myocardial damage) or electrolyte imbalances that may
decrease CO; should be done on every patient to use for

1104
comparison.

• HR: Diagnose type of tachycardia, bradycardia, or irregular

rhythm. During acute episodes, atrial dysrhythmias such as PAT,
PACs, atrial flutter, or atrial fibrillation may occur.

• PR, QRS, QT intervals: May lengthen or shorten

• ST-segment and T-wave changes: Depression or elevation

• Pacing and conduction: Regular, normal rate and velocity

• Late dysrhythmias: Include ventricular ectopy or bundle branch

blocks if the inflammatory process involves the ventricles.
Pericardial effusion may decrease the voltage of the QRS complex
on the ECG. Diffuse ST-segment elevation can be documented as
described in Table 5-10.

Diagnostic Tests for Acute Pericarditis

1105
1106
Table 5-10
ECG CHANGES WITH PERICARDITIS

Time of
Stage Pattern
Change
1 Onset of pain ST segments have a concave elevation in all leads except AVL and V1; T
waves are upright
2 1 to 7 days Return of ST segments to baseline with T wave flattening and invert
3 1 to 2 weeks Inversion of T waves without R or Q changes
4 Weeks to ECG returns to prepericarditis state
months

Collaborative management
Care priorities

1. Relieve acute pain

May experience retrosternal or left precordial chest pain,
nonproductive cough, and SOB. Pleural effusion may be present.

• Oxygen: Usually 2 to 4 L/min by nasal cannula, or mode and rate

as directed by ABG values or pulse oximetry. Used to promote
both myocardial and generalized increases in oxygenation. As
oxygen (O2) delivery to the heart is enhanced, pain can be
relieved. If the patient deteriorates, other methods of O2 delivery
may be implemented (e.g., nonrebreather mask with reservoir
and mechanical ventilation for those who deteriorate markedly).

• Aspirin: 160 to 320 mg ideally chewed. Should be given

immediately if the patient has not been given aspirin before
admission to the hospital.

• Nonsteroidal anti-inflammatory drugs (NSAIDs): Preferred for

reducing inflammation, particularly if the patient has had an MI
or cardiac surgery, since these drugs do not delay healing as do
corticosteroids. NSAIDs have fewer side effects than steroids.
Examples include aspirin, indomethacin, and ibuprofen. NSAIDs
can increase fluid retention and may cause renal insufficiency
and worsen HF, as well as pose a risk for GI bleeding.

1107
• Colchicine: Reduces inflammation in the body; may be prescribed
as a first-line treatment for pericarditis or for recurrent
symptoms. Colchicine can reduce the length of pericarditis
symptoms and decrease the risk that the condition will recur.
However, the drug is not safe for people with certain preexisting
health problems, such as liver or kidney disease. Carefully check
the patient’s health history before prescribing colchicine.

• Prednisone: Given at 20 to 80 mg daily for 5 to 7 days if there is

no response to NSAIDs. Corticosteroids are contraindicated if
pericarditis occurs secondary to an AMI because they can cause
thinning of the scar formation and increase risk of rupture.

• Medications to manage the cause: Antibiotics, immunoglobulin,

antifungals, chemotherapy

2. Prevent cardiac damage and manage pericardial

effusions to prevent cardiac tamponade

• Subxiphoid pericardiocentesis: Performed if effusions persist and

cardiac status decompensates. A needle (used in a tamponade
emergency) or catheter is used to remove the fluid compressing
the heart. Echocardiography is used to guide the catheter tip and
assess the amount of effusion remaining. The pericardial catheter
may be removed after the fluid has been withdrawn or may be
left in place for several days to allow for gradual removal of fluid.
Usually 100 mL or more is withdrawn every 4 to 6 hours. The
catheter is flushed with saline every 4 to 6 hours after withdrawal
of the effusion to prevent clotting. Strict aseptic technique is
essential for preventing infection.

• Pericardiectomy: A surgical procedure to prevent cardiac

compression or relieve the restriction. It may be necessary in
chronic pericarditis for patients with recurrent effusions or
adhesions. This procedure is often required in severe and
recurrent pericarditis associated with uremia.

Care plans for acute pericarditis

1108
Ineffective breathing pattern 
related to guarding as a result of chest pain
Goals/Outcomes: Within 48 hours of this diagnosis, the patient
demonstrates RR 12 to 20 breaths/min with normal depth and
pattern and reports that chest pain is controlled.
Respiratory Status: Ventilation

Respiratory monitoring

1. Assess rate and depth of respirations along with the character

and intensity of the chest pain. Provide prescribed pain medication
as needed.

2. Teach the patient to avoid aggravating factors such as a supine

position. Encourage patient to alter his or her position to minimize
the chest pain. The following positions may be helpful: side-lying,
high Fowler, or sitting and leaning forward.

3. Assess lung sounds every 4 hours. If breath sounds are

decreased, encourage patient to perform incentive spirometry
exercises every 2 to 4 hours along with coughing and deep-
breathing exercises.

4. To facilitate coughing and deep breathing, teach the patient to

support the chest by splinting with pillows or by holding the arms
around the chest.

Positioning; Pain Management

Activity intolerance 
related to bed rest, weakness, and fatigue secondary to impaired cardiac
function, ineffective breathing pattern, or deconditioning.
Goals/Outcomes: Within 72 hours of this diagnosis, the patient
exhibits cardiac tolerance to increasing levels of exercise as
evidenced by peak HR less than 20 bpm over patient’s resting HR,
peak systolic BP less than 20 mm Hg over patient’s resting systolic
BP, SVO2 at least 60%, RR less than 24 breaths/min, NSR on ECG,
warm and dry skin, and absence of crackles, murmurs, and chest
pain during or immediately after activity.

1109
 Energy Conservation; Endurance; Activity Tolerance

Energy management

Steroid myopathy may develop in patients who receive high-

dose or long-term steroid treatment. Muscle weakness occurs in
the large proximal muscles. Patients experience difficulty lifting
objects and moving from a sitting position to a standing position.
Steroids also increase the risk of developing osteoporosis and bone
fracture; therefore, when on long-term therapy, the patient should
take recommended daily intake of calcium and vitamin D.

1. Assess the patient for evidence of muscle weakness; assist with

activities as needed.

2. Modify the activity plan for the patient with post-MI pericarditis
who is receiving steroids. A lower activity level may help prevent
thinning of the ventricular wall and reduce the risk of an aneurysm
or rupture of the ventricle.

3. Teach the patient to resume activities as tolerated, resting

between activities.

4. For other interventions, see this nursing diagnosis in Prolonged

Immobility, Chapter 1.

Cardiac Care: Rehabilitative; Teaching: Prescribed

Activity/Exercise

Additional nursing diagnoses

Also see Decreased Cardiac Output in Acute Cardiac Tamponade
(Chapter 3). For other nursing diagnoses and interventions, see
Prolonged Immobility (Chapter 1).

1110
Aortic aneurysm/dissection
Pathophysiology
The aorta is exposed to high pulsatile pressure, making it
susceptible to injury and disease from mechanical trauma.
Conditions that weaken the medial layer or increase stress on the
vessel wall can lead to dilation, aneurysmal formation, and
eventually rupture or dissection of the aorta. Pathologies related to
the aorta can be life-threatening because of the potential for
disruption of blood flow to a large portion of the body, including
vital organs such as the brain, heart, kidneys, and GI tract.
Symptoms may mimic other conditions, and survival depends
largely on timely diagnosis and rapid intervention to preserve end-
organ function.
An aortic aneurysm is an abnormal dilation of the vessel, with an
increase of at least 50% its normal diameter. Aneurysms are usually
described based on their location along the aorta (thoracic,
abdominal) and their morphology. A true aneurysm involves all
three layers of the arterial wall (intima, media, adventitia). The two
forms of a true aneurysm are fusiform (symmetrical dilation of the
entire circumference of the aorta) and saccular (eccentric ballooning
of only a portion of the aortic wall). A false aneurysm or
“pseudoaneurysm” is a hematoma caused by injury to the aortic
wall, resulting in blood contained by the adventitia or surrounding
tissue.
Most often aneurysms develop at the site of an atherosclerotic
lesion, which precipitates degeneration of the tissue and allows the
arterial wall to dilate. With advancing age, the elastin in the aorta is
decreased, which further weakens the vessel wall. Hypertension
increases mechanical stress on the vessel, promoting further
expansion of the aneurysm. Smoking has been linked to accelerated
expansion of both thoracic and abdominal aneurysms. The rate at
which the aneurysm increases is not predictable; however, the
likelihood of rupture or dissection increases dramatically when the
size exceeds 6 cm. Aortic aneurysms result in approximately 17,000
deaths per year, the majority because of rupture.
An aortic dissection is a longitudinal tear in the intimal layer of

1111
the aortic wall. Dissection can occur without the presence of an
aneurysm. As blood enters the tear, pulsatile pressure creates a
false channel between the intimal and medial layers. The force of
pressure generated by ventricular contraction and systemic BP can
cause the dissection to extend either distally or proximally—
compromising flow to structures perfused by that segment of the
aorta. Precipitating factors for aortic dissection include medial
degeneration from inherited (e.g., connective tissue diseases,
congenital defects) or acquired (e.g., hypertension, inflammation)
disorders, trauma, pregnancy, and cocaine abuse (see Hypertensive
Emergencies, Chapter 5).
Aortic dissection is classified by location, using two different
systems. The DeBakey classification defines a dissection as type I if
it involves the entire aorta, type II if it is confined to the ascending
aorta only, and type III if the dissection originates in the descending
aorta, distal to the left subclavian artery. The Stanford system
classifies dissections into two groups: type A, which involves both
the ascending and descending aorta (DeBakey types I and II), and
type B, which affects only the descending aorta (DeBakey type III).
Ascending dissections occur much more frequently (65%) than
descending dissections and are considered more lethal.
The morbidity and mortality associated with aortic dissection are
greatest near the time of the initial injury. Patients who present for
medical evaluation within 2 weeks or less of symptom onset are
characterized as “acute,” while a dissection diagnosed after this
time is considered “chronic.” Approximately 2000 episodes of acute
aortic dissection occur annually, with mortality approaching 75% if
left untreated.

Assessment
Goal of the assessment
Gather information that can assist in making the differential
diagnosis so appropriate management can be initiated immediately.

History and risk factors

Assess for hypertension, atherosclerosis, and related risk factors

1112
(e.g., smoking, CAD, hyperlipidemia), connective tissue disorders
(e.g., Marfan syndrome, Ehlers-Danlos syndrome), congenital
defects (e.g., coarctation of the aorta, bicuspid aortic valve), family
history of aneurysm or dissection, blunt chest trauma, pregnancy,
cocaine use, advanced age (older than 60 years), and male sex.

Vital signs
• Hypertension may be preexisting or an SNS response to pain;
more common in descending dissections.

• Hypotension secondary to hemorrhage or complications is

associated with ascending dissection (aortic regurgitation, MI,
tamponade).

• BP differences between extremities reflect involvement of brachial

arteries; variation of 20 mm Hg is considered significant.

Observation

Pain

• Intense pain of abrupt onset, often described as tearing, ripping,

or sharp

• Midline, anterior pain is typical of type A dissection, while

posterior (intrascapular), back, or abdominal pain is more
common in type B dissection.

• With rupture of an abdominal aneurysm, pain will occur along

the flank or lumbar back.

• Pain may radiate, following the path of the dissection.

• Vasovagal responses to intense pain: Diaphoresis, apprehension,

nausea, vomiting, faintness may occur.

• Up to 10% of patients may have no pain

Impaired organ perfusion

1113
• Symptoms vary based on location of the dissection and resultant
compromise in tissue perfusion.

• Acute LV failure (SOB, chest pain): Results from involvement of

coronary arteries or the aortic valve.

• Neurologic deficits: Syncope, confusion, sensorimotor changes,

and lethargy result from involvement of branches of the
ascending aorta.

• Paraplegia, paresthesia, or focal deficits: Result from involvement

of spinal arteries.

• Decreased urine output: If dissection extends to renal arteries, it

can cause impaired perfusion and decreased kidney function.

Palpation
• Pulse deficits (difference in pulse volume or absent pulses) are
considered a classic finding; they occur in only 30% of patients.

• Sudden loss of pulses indicates extension of dissection.

• Slow capillary refill and cool skin reflect diminished perfusion.

Auscultation
• Diastolic murmur: With aortic regurgitation

• Muffled heart tones: With cardiac tamponade

• Development or progression of bruits: With turbulent flow

through carotid, brachial, or femoral vessels

• Hyperactive bowel sounds: With mesenteric artery ischemia

Diagnostic tests

1114
HIGH ALERT!
Rapid diagnostic imaging is essential, because mortality from
aortic dissection increases by the hour. Transesophageal
echocardiography, CT angiography, and magnetic resonance
imaging are all highly accurate in identifying the presence and
extent of dissection. The choice of study is usually determined by
the patient’s clinical stability and the facility’s resources. Although
the definitive diagnosis is made by imaging studies, additional
diagnostic tests may be helpful in ruling out other potential causes
of chest pain (pulmonary embolism, MI, pericarditis) or evaluating
the extent of end-organ involvement (see Diagnostic Tests Table).

Diagnostic Tests for Acute Aortic Dissection

Collaborative management

1115
Because of the emergent nature of this disorder, limited
randomized controlled trials are available to guide the treatment of
patients with aortic dissection or rupture. The establishment of the
International Registry of Acute Aortic Dissection has provided
valuable information regarding presentation, management, and
outcomes for this patient population. This information was
combined with an appraisal of available cohort studies and
retrospective reviews to develop the practice guidelines described
in the following table.

ACUTE AORTIC DISSECTION GUIDELINES

In 2010 the American College of Cardiology, American Heart Association, and a number of other
professional groups issued guidelines for diagnosis and management of patients with thoracic aortic
disease. Some of the class I recommendations for managing acute and chronic dissection are listed below:
Initial Management of Acute Dissection
1. Initial management of thoracic aortic dissection should be directed at decreasing aortic wall
stress by controlling heart rate and blood pressure as follows:
• In the absence of contraindications, intravenous beta blockade should be initiated and
titrated to a target heart rate of 60 beats per minute (bpm) or less.
• In patients with clear contraindications to beta blockade, nondihydropyridine calcium
channel-blocking agents should be used as an alternative for rate control.
• If systolic blood pressure remains greater than 120 mm Hg after adequate heart rate control
has been obtained, then ACEIs and/or other vasodilators should be administered
intravenously to further reduce blood pressure to a level that maintains adequate end-organ
perfusion.
• Beta blockers should be used cautiously in the setting of acute aortic regurgitation because
they will block compensatory tachycardia.

Definitive Management of Acute Dissection

1. Urgent surgical consultation should be obtained for all patients diagnosed with thoracic
aortic dissection regardless of the anatomic location (ascending versus descending) as soon as
the diagnosis is made or highly suspected.
2. Acute thoracic aortic dissection involving the ascending aorta should be urgently evaluated
for emergent surgical repair because of the high risk of associated life-threatening
complications such as rupture.
3. Acute thoracic aortic dissection involving the descending aorta should be managed medically
unless life-threatening complications develop (e.g., malperfusion syndrome, progression of
dissection, enlarging aneurysm, inability to control blood pressure or symptoms).
Management of Asymptomatic Descending and Thoracoabdominal Aneurysms
1. In patients with chronic dissection, especially those with connective tissue disorders, open
repair is recommended for aneurysms measuring more than 5.5 cm.
2. In patients with degenerative or traumatic aneurysms of the ascending aorta measuring more
than 5.5 cm, endovascular stent grafting should be considered when feasible.
3. In patients with thoracoabdominal aneurysms at high risk for surgery and limited stent
options, open repair is recommended when the aneurysm is more than 6.0 cm.
Medical Treatment of Patients with Thoracic Aortic Diseases
• Stringent control of hypertension, with a goal of ≤140/90 mm Hg in patients without
diabetes, or <130/80 mm Hg in patients with diabetes or chronic renal disease.
• Optimization of lipid profiles, smoking cessation, and other measures to reduce the risk of

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 atherosclerosis.
From: Hiratzka LF, Bakris GL, Beckman JA, et al: 2010 ACCF/AHA/AATS/ACR/ASA/
SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients
with thoracic aortic disease: executive summary. J Am Coll Cardiol 55:1509-1544,
2010.

Care priorities
The immediate goal of therapy for aortic dissection or rupture is to
limit propagation of the dissection by reducing the shearing forces
created by myocardial contractility and BP.

1. Preserve the tissue integrity of the aorta with beta-

blocker therapy (e.g., metoprolol, esmolol)
To reduce the velocity of LV ejection, slow HR, and reduce BP.
Usually administered intravenously, titrating to achieve an HR of
60 bpm or less. In patients unable to tolerate beta-blockers (because
of asthma, bradycardia, or signs of HF), CCBs (diltiazem,
verapamil) may be used as an alternative.

• Antihypertensive therapy: Initiated if the patient remains

hypertensive after beta blockers. Usually nitroprusside or
nicardipine is started, as described in Hypertensive Emergencies,
Chapter 5. Labetalol is another option, with the added advantage
of providing beta blockade. A systolic BP of less than 120 mm Hg
is desired.

Initiation of a vasodilator before beta blockade can cause a

reflexive increase in heart rate and contractility. This sympathetic
nervous system-mediated response can lead to further dissection.

2. Control pain
Usually achieved with IV morphine sulfate, 2 to 10 mg, since
morphine helps diminish sympathetic outflow. If additional
sedation is required, midazolam may be used.

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3. Evaluate for and facilitate surgical or endovascular
treatment
Urgent intervention is recommended for type A (ascending)
dissection and type B (descending) dissection when impending
rupture, significant organ ischemia, or refractory hypertension
occurs. Surgery involves removal of the affected section of the aorta
and replacement with a prosthetic graft. Repair or replacement of
the aortic valve may also be needed. For patients who meet clinical
and anatomic criteria, endovascular repair is increasingly an option.
This involves placement of a stent graft to occlude the false lumen,
thus restoring flow in the true lumen. Fenestration, a technique in
which holes are created either in the dissection flap or in the graft to
reestablish flow from the aorta into branching arteries, may also be
used.

4. Continue medical management

Patients with stable type B dissections are generally managed
medically. After control of BP is achieved with IV agents, oral
antihypertensive therapy is initiated, along with gradual weaning
from the IV infusion. The goal of chronic therapy is to maintain a
systolic BP less than 130 mm Hg to prevent further dissection.
Long-term management includes beta blockade, lipid control,
smoking cessation, and serial imaging to evaluate for further
changes in the aorta. This strategy may be evolving, however, since
a recent study showed improved 5-year survival when thoracic
endovascular repair was added to standard medical therapy.

Care plans for aortic aneurysm/dissection

Ineffective tissue perfusion: Peripheral, cardiopulmonary,
renal, and cerebral 
related to interruption of arterial blood flow secondary to narrowed aortic
lumen.
Goals/Outcomes: Within 48 hours of this diagnosis, the patient
has adequate tissue perfusion as evidenced by distal pulses
bilaterally equal and greater than 2+ on a 0 to 4+ scale, brisk
capillary refill (less than 2 seconds), warm skin, bilaterally equal

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sensations in the extremities, bilaterally equal systolic BP less than
120 mm Hg, HR less than or equal to 60 bpm, NSR on ECG, urine
output greater than 0.5 mL/kg/h, equal and normoreactive pupils,
and orientation to time, place, and person.
Circulation Status

Shock prevention

1. Myocardial infarction: Assess cardiovascular status by

monitoring HR and rhythm, ECG, and cardiac enzyme levels. A
dissection along the coronary arteries will result in an MI.

2. Perfusion changes: Perform bilateral assessment of BP and distal

pulses (particularly radial, femoral, and dorsalis pedis) hourly
during initial phase of dissection and then every 4 hours as the
patient’s condition stabilizes. Report changes in strength or
symmetry of distal pulses. Be alert to any change in color, capillary
refill, and temperature of each extremity.

3. Emerging dissection: If the difference in systolic BP between the

extremities exceeds 10 mm Hg, consult advanced practice provider
immediately. Titrate vasodilators based on the highest arm BP.

4. Manage intravascular volume: Monitor hemodynamic

parameters (BP, CVP, PAP) for signs of decreased intravascular
volume. Establish separate IV lines for volume and medications.

5. Spinal perfusion pressure: Monitor for paresthesias of the

extremities—a sign of diminished perfusion to the spinal arteries.
Implement drainage of cerebral spinal fluid if available to improve
spinal perfusion pressure.

6. Pericardial tamponade: Assess for signs of pericardial

tamponade, e.g., distended neck veins, muffled heart sounds,
decreased systolic BP (less than 90 mm Hg or greater than 20 mm
Hg drop in systolic trend), and pulsus paradoxus.

7. Aortic regurgitation: Assess for signs of acute aortic

regurgitation: diastolic murmur, dyspnea, decreased CO.

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8. Decreased renal perfusion: Monitor urine output hourly. Consult
advanced practice provider if urine output is less than 0.5 mL/kg/h
for 2 consecutive hours.

9. Decreased cerebral perfusion: Assess neurologic status hourly.

Report restlessness and changes in level of consciousness (LOC),
pupil size, or reaction to light.

Hemodynamic Regulation; Cardiac Care: Acute; Circulatory

Care; Surveillance

Acute pain 
related to biophysical injury secondary to necrosis at the aortic media and
distal tissue hypoperfusion.
Goals/Outcomes: Within 24 to 48 hours of this diagnosis,
patient’s subjective evaluation of pain improves, as documented by
a pain scale. Nonverbal indicators, such as grimacing, are decreased
or absent.
Pain Control

Pain management

1. Monitor patient at frequent intervals for the presence of

discomfort. Devise a pain scale with the patient, rating discomfort
from 0 (no pain) to 10 (severe pain). Medicate with analgesics as
prescribed, and rate relief obtained using the pain scale.

2. During episodes of pain, assess for a change in peripheral pulses

or altered hemodynamics (i.e., BP, PAP, PAWP, CO, SVR), because
such changes often are associated with extension of the aortic
dissection.

3. Control BP during episodes of pain by titrating vasodilator or use

a beta blocker to maintain specified parameters.

4. Immediately consult advanced practice provider for any increase

in the severity of pain, because it may indicate the need for
emergency surgery.

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Additional nursing diagnoses
For other nursing diagnoses and interventions, also see the
following as appropriate: Hemodynamic Monitoring (Chapter 1),
Prolonged Immobility (Chapter 1), Emotional and Spiritual Support
of the Patient and Significant Others (Chapter 2), and Chest Trauma
(Chapter 3).

Cardiogenic shock
Pathophysiology
Cardiogenic shock (CS) represents the final pathway of a large
number of pathologic conditions, which lead to severe impairment
of CO (cardiac function) and result in significant impaired end-
organ perfusion. Initial perfusion changes resulting from CS are
associated with a cycle of inflammation, ischemia, and progressive
myocardial dysfunction. Morbidity and mortality are the end result
of severe LV failure. CS may be caused by several conditions:
primary LV failure, RV failure, severe valvular regurgitation, or
ventricular septal rupture, which may occur alone or in
combination. Because of the wide spectrum of causes of CS, the true
incidence is unknown; however, the most common cause of CS is
AMI. CS occurs in 5% to 8% of patients experiencing an AMI, most
commonly in patients with STEMI. Although uncommon, NSTEMI
can result in CS. There are few studies characterizing the
differences in shock in patients presenting with STEMI versus
NSTEMI. Despite high mortality rates in all patients with shock, no
definitive guideline recommendations exist for the management of
shock in patients with NSTEMI.
CS is initiated by a severe impairment in CO leading to decreased
perfusion of the coronary arteries. The result is ischemia, which
further reduces myocardial performance, commonly known as
“pump failure.” Myocardial necrosis or stunning of the
myocardium can occur from reperfusion injury during invasive
intervention such as primary PCI or reocclusion of the infarcted
artery. Next in the cascade of events is the compensatory
neurohumoral response to reduced blood flow. Activation of the

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SNS and renin-angiotensin-aldosterone system result in
vasoconstriction and salt and water retention. As resistance to
ventricular ejection increases, the result is worsening myocardial
ischemia and end-organ hypoperfusion, with an increased
incidence of ventricular dysrhythmias. Catecholamine release from
the SNS also induces tachycardia, which further increases
myocardial oxygen demand and worsens pump failure. As
perfusion continues to decrease, compensation fails and vascular
beds begin dilating, resulting in anaerobic metabolism and lactic
acidosis, which further decreases myocardial contractility.
Inflammatory mediators including interleukin-6 and tumor necrosis
factor-alpha are elevated, which adds to the negative inotropic
effects. Nitric oxide level increases are the result of high levels of
cytokines. Vasodilatation progressively increases, which results in
hypotension and worsening of lactic acidosis.
Despite decades of studies, the mortality rate from CS remains
high. In the future, improved outcomes for patients with CS will
result from an improved understanding of the pathophysiology
and advances in pharmacologic and mechanical therapies.

Assessment
Goals of assessment
The goals are to identify the severity of symptoms and the stage of
shock and provide the patient’s clinical and laboratory data to assist
with the differential diagnosis of the cause.
The diagnosis of CS is dependent on several findings.

• Hypotension: Noninvasive assessment or invasive assessment of

BP

• Decreased CO: Tachycardia, low pulse pressure, weak pulses,

distant heart sounds, displaced apical impulse, and S3 or S4.
Systolic murmur may indicate mitral regurgitation or ventricular
septal defect. LV or RV dysfunction can be detected through the
use of angiography or electrocardiography

• Hypoperfusion: Cool clammy or cyanotic extremities, oliguria

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 from renal hypoperfusion, disorientation, lethargy, elevated lactic
acid indicating visceral hypoperfusion

• Pulmonary congestion: Elevated jugular venous pressure, rales,

and/ or chest X-ray indicating pulmonary edema

Observation
As shock progresses from the low CO state, there is evidence of
vital organ hypoperfusion: disorientation (altered mental status),
oliguria, and acidosis. Skin is cool to cold (mottling may be present)
and diaphoretic caused by decreased peripheral perfusion.

Vital signs and diagnostic criteria for cs

1) Systolic BP less than 90 mm Hg for at least 30 minutes or the
need for supportive measures to maintain systolic BP above 90 mm
Hg

2) Cool extremities or a urine output ≤ 30 mL/hour

3) HR ≥ 60 bpm

4) Cardiac index ≤ 2.2 L/min/m2 of body surface area

5) Capillary refill greater than 3 seconds (jugular venous distention)

6) Pulmonary capillary occlusion pressure ≥15 mm Hg

Auscultation
• S3 or S4 heart sounds may be present resulting from an
overdistended, noncompliant ventricle.

• Pulmonary congestion and tachypnea result in rales throughout

lung fields.

• Mitral regurgitation if present will result in a murmur that is high

pitched, holosystolic, and radiates to the axilla. The intensity of
the murmur may not correlate with the severity of the

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 regurgitation. Electrocardiographic changes in mitral
regurgitation are nonspecific and are primary changes of LV
hypertrophy and strain.

Hemodynamic measurements

Hemodynamic monitoring
An arterial line is used to guide initial therapy. The role of invasive
hemodynamic monitoring with a pulmonary artery catheter in
patients with CS is uncertain. Although no clinical trial has
established a clinical benefit from its use, it is still being
recommended for use in this patient population. Currently less
invasive methods are also being used including:

• Transpulmonary thermodilution

• Pulse contour analysis

• Thoracic electrical bioimpedance

• Bedside Doppler echocardiography

The pulmonary artery catheter may serve to assist with the

following in CS patients:

• Diagnostic accuracy

• Help distinguish between LV failure and RV failure:

• LV failure: high PAOP, low CO, high SVR

• RV failure: high RA pressure and ratio of right

atrial/PAOP greater than 0.8

• Large V wave in PAOP tracing indicates mitral regurgitation.

• Assisting in guiding fluid therapy and inotropic therapy

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• Measuring mixed venous oxygen, SVO2, which is an indicator of
how well oxygen supply meets tissue demand for energy
production

Measuring tissue perfusion

The major focus for the treatment of CS is the improvement and
preservation of tissue perfusion. Adequate tissue perfusion
depends on an adequate supply of oxygen being transported to the
tissues and the cell’s ability to use it. Oxygen transport is influenced
by pulmonary gas exchange, CO, and Hgb levels. Oxygen use is
influenced by the internal metabolic environment.

Improving cellular oxygen transport

Part of the management of CS focuses on improving oxygen
transport to the tissues. SVO2 falls below the normal range of 60% to
80% when oxygen supply is decreased or tissue demand in
increased. SVO2 has a positive correlation with CO. Continuous
monitoring of SVO2 provides an indirect but continuous assessment
of CO and perfusion.

Diagnostic tests
See Diagnostic Tests for Heart Failure page and Acute Coronary
Syndromes (Chapter 5).

Collaborative management
Care priorities
Patients in CS have high mortality rates. Early and rapid relief of
ischemia when the cause of CS is AMI is essential to avoid
refractory multiorgan dysfunction and death. Treatment of CS is
aimed at improving symptoms and stabilizing the hemodynamics.
The goals are to:

• Maximize oxygen delivery at the cellular level

• Reduce causes of increased stress or workload, which increases

1125
 oxygen demand.

Normalization of ventricular filling pressures and optimization of

CO are critical for patient stabilization. The challenge is to augment
ventricular filling pressures (preload) without increasing afterload
(systemic BP/SVR and PAP) in the process. All measures aim to
increase the CO, which is the primary cause of the hypotension
associated with severe HF/CS.

Initial therapy
Limited fluid resuscitation is reasonable unless there is pulmonary
edema upon presentation. The maintenance of adequate
oxygenation and airway protection is required, along with
mechanical intubation if needed. Excessive levels of positive end-
expiratory pressure should be avoided to prevent oxygen toxicity.
Hypokalemia and hypomagnesemia contribute to ventricular
arrhythmias and should be treated immediately. Amiodarone can
be used to prevent arrhythmia recurrence. Bradycardia caused by
heart block or drug effects should be corrected. Anxiety and pain
can be treated with narcotic analgesics as they will also reduce
preload, afterload, and sympathetic activity.

Pharmacologic support of the failing heart

The major goals of pharmacologic therapy in CS are to maintain
adequate arterial pressure and CO. Both inotropes and
vasopressors are frequently required. These therapies in high doses
are associated with worse outcomes; therefore the lowest possible
doses should be used.
The following vasoactive drugs are used in CS:

Dobutamine: Dobutamine is a beta1-agonist agent and is used to

increase CO in an unstable patient when systolic BP is above 100
mm Hg.

Milrinone: Milrinone is a phosphodiesterase-3 inhibitor agent and

is used to increase CO in a patient who is not critically unstable,
and when the systolic BP is above 90 mm Hg.

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Dopamine: Dopamine is used to increase CO and BP when the HR
is below 110 bpm Dopamine is used in both low and high doses:

• Low dose: Dopamine receptor agonist–beta1 agonist

• High dose: Alpha agonist

Norepinephrine: Norepinephrine is an alpha agonist and limited

beta1 agonist. It is used to increase BP and CO when the systolic
BP is less than 90 mm Hg and/or the HR is more than 110 bpm.

Epinephrine: Epinephrine is an alpha agonist and a beta1 agonist. It

is used to increase HR, contractility, and systolic BP when the
patient is critical.

Isoproterenol: Isoproterenol is a beta1 and beta2 agonist and is used

to increase HR when the systolic BP is not ≥ 120 mm Hg. Other
agents are ideally used before isoproterenol, as the drug can
significantly increase myocardial oxygen demand. Isoproterenol
may be used more often in patients with a denervated heart
following cardiac transplantation to increase HR.

Levosimendan: Levosimendan is an inodilator indicated for the

short-term treatment of acutely decompensated severe chronic
HF and in situations where conventional therapy is not adequate.
Data describing the use of levosimendan in CS are scarce;
however, the drug appears to be safe and improve some
hemodynamic and ventricular indices.

The principle pharmacological effects of

levosimendan are:

• Increased cardiac contractility by calcium

sensitization of troponin C

• Vasodilation

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• Cardioprotection

The vasodilation and cardioprotection are related to the opening

of sarcolemma and mitochondrial potassium–ATP channels.
Levosimendan improves hemodynamics in the HF patient with no
significant increase in cardiac oxygen consumption and relieves
symptoms of acute HF. It also has favorable effects on
neurohormone levels in HF patients. Patients who are under beta
blockade can also be treated with levosimendan as it does not lose
effect in these patients. Hemodynamic effects are maintained up to
7 to 9 days after stopping levosimendan because of the formation of
an active metabolite. Compared to dobutamine, it produces a
slightly greater increase in CO and a greater decrease in PAOP.
Severe renal failure is a contraindication for levosimendan because
of the absence of studies based on this risk element.

Vasopressin: In high doses vasopressin activates vascular smooth

muscle and oxytocin receptors causing vasoconstriction. It is
considered to be a reasonable drug in CS from RV failure. It also
reverses hypotension when vasoplegia complicates LVAD
surgery.

The American College of Cardiology Foundation/American Heart

Association (ACCF/AHA) guidelines no longer recommend the use
of any particular agent, although they do report that dopamine may
be associated with more harm than other agents. Treatment
decisions are therefore based on clinical experiences and the
patient’s presenting hemodynamic profile.
Table 5-11 provides a summary of the hemodynamic effects of
drugs used in CS.

Table 5-11
HEMODYNAMIC EFFECTS OF DRUGS USED IN CARDIOGENIC
SHOCK

1128
BP, Blood pressure; CO, cardiac output; D, decrease; HR, heart rate; I, increase; O,
no effect; SVR, systemic vascular resistance.

Intravascular volume optimization

Optimization of the filling pressures enhances hemodynamic
improvement in CS. Hypovolemia should be treated with
crystalloids, colloids, and blood products. As CS is more often
associated with hypervolemia in the HF population, diuretics are
sometimes used to decrease resistance to ventricular ejection or
extremely high filling pressures. The concept of managing
hypotension because of hypervolemia is difficult for those
inexperienced with CS and HF. Balancing use of diuretics to
support reduction of resistance to ejection while maintaining
functional filling pressures can be challenging.

Loop diuretics
Furosemide is a loop diuretic that blocks the sodium potassium
chloride transporter and increases urinary excretion of sodium and
chloride. LV filling pressures are reduced because of the ability of
furosemide to increase the systemic venous capacitance.
Other loop diuretics that can be used are bumetanide and
torsemide.

Mechanical support of the failing heart

Reduce left ventricular afterload and increase coronary

arterial perfusion using balloon counterpulsation
therapy/IABP

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IABP is the most widely used form of mechanical hemodynamic
support in patients with CS. The IABP is a balloon inserted into the
descending aorta between the arch vessels and renal arteries. The
balloon inflates after cardiac ejection and deflates before the onset
of the following systole. The balloon displaces blood proximally,
increasing coronary perfusion pressure and raising diastolic aortic
pressure. Deflation of the balloon during systole reduces end-
diastolic pressure and LV afterload. The main aims of the use of
IABP are to improve hemodynamics, increase perfusion of vital
organs, and reduce myocardial oxygen consumption. Results of
recent studies have resulted in the ACCF/AHA downgrading the
use of the IABP to class IIa (can be useful) in the guidelines for the
management of STEMI.

Advanced mechanical circulatory support

Percutaneous Left Ventricular Assist Devices

There are currently two devices that can be used in CS

patients who are refractory to standard therapy.

TandemHeart

The TandemHeart consists of an external centrifugal

blood pump, a 21-French inflow cannula placed in
the left atrium via transseptal puncture, and a 17-
French outflow cannula inserted into the femoral
artery. The system supports the failing LV by
providing a 4 to 5 L/min flow. The improved
hemodynamics from the Tandem Heart include
increased CI, decreased PAOP, and increased MAP.
Risks include leg ischemia and displacement of the
inflow cannula into the right atrium.

Impella recover 2.5

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The Impella device is minimally invasive and the least
invasive of the LVADs. It consists of a catheter-
based 12-French pump motor inserted via a femoral
artery and positioned across the aortic valve. The
pump pulls blood from the LV through an inlet area
and expels blood into the proximal ascending aorta.
The Impella can generate up to 2.5 L/min of
forward flow into the systemic circulation. After the
pump is inserted and positioned, an activated
clotting time (ACT) between 160 and 180 seconds is
required to prevent clot formation in the motor. The
current ACCF/AHA guidelines provide a IIb
recommendation (may be considered) for the use of
alternative LVADs for patients with refractory CS.

Extracorporeal membrane oxygenation

Veno-arterial (V-A) extracorporeal membrane

oxygenation (ECMO) can also be used to support
the CS patient. The ECMO circuit consists of a
centrifugal blood pump, a heater, and a membrane
oxygenator. ECMO is deployed into the patient via
a sternotomy or percutaneously inserted cannula
placed in the right atrium (via the femoral vein) and
the descending aorta (via the femoral artery). The
maximum flow rate is 4 L/min. The use of V-A
ECMO provides hemodynamic stabilization and
resolution of organ dysfunction from
hypoperfusion. The literature to date on the efficacy
of ECMO in CS is limited.

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Provide other treatments for cardiogenic shock after the
cause of pump failure has been identified

1. Emergency CABG or surgical reperfusion

2. Emergency PCI with stent placement in the occluded artery

3. Heart transplantation

Care plans for cardiogenic shock

Decreased CO 
related to increased afterload, increased preload, or decreased contractility
secondary to loss of 40% or more of myocardial functional mass.
Goals/Outcomes: The patient’s hemodynamic function is
optimized as evidenced by CO of at least 4 L/min, BP greater than
90/60 mm Hg, SVR less than 1200 dynes/sec/cm-5, and PAOP less
than 18 mm Hg, before weaning from assist device or
pharmacologic agents. PAOP may need to be higher in some
patients to maintain the BP.
Tissue Perfusion: Cardiac; Hemodynamic Regulation:
Circulatory Care;

Shock management: Cardiac

1. Monitor arterial vital signs and hemodynamics continuously.

2. Customize alarm parameters on patient monitoring systems to

the parameters ordered by the advanced practice provider and the
ICU’s policy and procedures to decrease unnecessary and
nonactionable alarms and noise for patient and family.

3. Titrate vasoactive drugs to achieve a CO between 4 and 7 L/min,

arterial BP at least 90/60 mm Hg, and PAOP less than 18 mm Hg. If
reduction of filling pressures results in worsening hypotension,
filling pressures are generally maintained at the level that optimizes

1132
the BP.

4. Assess CO/CI and SVR every 1 to 4 hours and after titration of

pharmacologic therapy. If SVR increases to greater than 1200
dynes/sec/cm-5, notify physician.

5. Auscultate lung sounds every 2 hours, and monitor urine output

hourly. Report any change that is significantly different from
previous assessment.

6. Keep HOB elevated at least 30 to 45 degrees if not

contraindicated and if IABP not in place.

7. Ventricular dysrhythmias are treated only if compromising

CO/CI.

8. Temporary cardiac pacing may be indicated for symptomatic

bradycardia.

9. If medical management fails to improve hemodynamic profile,

prepare patient and family for insertion of IABP or LVAD.

Ineffective tissue perfusion: Altered cardiopulmonary,

cerebral, peripheral, and or renal tissue perfusion 
related to interrupted arterial blood flow to vital organs secondary to
inadequate arterial pressure.
Goals/Outcomes: Within 96 hours of initial diagnosis of CS, the
patient will have adequate tissue perfusion as evidenced by
orientation time, place and person, equal and normoreactive pupils;
normal deep tendon reflexes; urine output at least 0.5 mL/kg/h;
warm and dry skin; peripheral pulses at least 2+ on a 0 to 4 scale;
brisk refill; BP at least 90/60 mm Hg; and SVO2 greater than 65% or
within patient’s normal range.
Circulation status

Cardiac care: Acute hemodynamic regulation

1. Check neurologic status every 2 hours to assess cerebral

perfusion. Changes in LOC, orientation, perception, motor activity,

1133
reflexes, and pupillary response to light should be reported to the
physician.

2. Monitor I&O hourly to assess renal perfusion; report urine

output less than 0.5 mL/kg/h for 2 consecutive hours. Assess
extremities every 2 hours for any changes in skin color,
temperature, capillary refill, and distal pulses.

3. Titrate vasoactive drugs to maintain systolic BP at 90 mm Hg or

above.

Impaired gas exchange 

related to alveolar-capillary membrane changes secondary to pulmonary
congestion; altered oxygen-carrying capacity of the blood secondary to
acidosis occurring with anaerobic metabolism.
Goals/Outcomes: Before weaning from supplemental oxygen or
ventilator assistance is attempted, the patient will have adequate
gas exchange as evidenced by PaO2 of at least 80 mm Hg, RR 12 to
20 breaths/min with normal depth and pattern, oxygen saturation
at least 95%, SVO2 60% to 80%, and ScVO2 at least 80%.
Tissue Perfusion: Pulmonary; Respiratory Status: Gas
Exchange

Ventilation assistance

1. Every hour assess rate, depth, and effort of patient’s respirations.

Note tachypnea or labored breaths. Inspect skin and mucous
membranes for pallor or cyanosis, which indicates hypoxia. Consult
advanced practice provider if any changes occur.

2. Auscultate lung fields every 1 to 2 hours.

3. Monitor ABG values for hypoxemia (PaO2 less than 80 mm Hg) or

metabolic acidosis (pH less than 7.35 and HCO3− less than 22 mEq/L
may indicate lactic acidosis).

4. Administer oxygen as ordered.

5. Monitor oxygen saturation with a pulse oximeter. If less than

1134
90%, notify physician.

6. Monitor and manage SVO2 by supporting CO. When CO

decreases, perfusion decreases and oxygen extraction increases,
lowering SVO2.

7. If the patient deteriorates, prepare for intubation and

mechanical ventilation.

For patients undergoing IABP procedure

Decreased cardiac output 

related to negative inotropic changes and rates, rhythm and conduction
alterations secondary to ischemia or injury.
Goals/Outcomes: Within 24 hours of diagnosis of CS, patient’s
CO is effectively supported as evidenced by MAP at least 60 mm
Hg to support peripheral perfusion, improved ECG rhythm, HR
above 60 and less than 100 bpm or at a higher rate that optimizes
the BP without prompting angina, peripheral pulses audible with
Doppler or palpable, hourly urine output at least 0.5 mL/kg/h or
renal support strategy in place, CI greater than 2.5 L/min/m2, SVR
less than 1200 dynes/sec/cm-5, SVO2 60% to 80%, ScVO2 at least 80%,
and patient is able to awaken and maintain periods of alertness, is
oriented or responds to reorientation, and has chest pain controlled.
Hemodynamic Regulation: Circulatory Care; Cardiac Pump
Effectiveness

Circulatory care: Mechanical assist device

1. Monitor BP, CVP, PAP, RAP, SVO2, and HR continuously.

Monitor PAOP, SVR, and CO/CI hourly. Report increased PAOP,
decreased CO, new ST-segment elevation or depression,
deterioration in heart rhythm, decreased SVO2, or elevated SVR to
advanced practice provider.

2. Monitor hourly urine output. Report output less than 0.5

mL/kg/h for 2 consecutive hours. Monitor BUN and creatinine
values daily. Report increased BUN (greater than 20 mg/dL) and

1135
serum creatinine (greater than 1.5 mg/dL) indicative of acute renal
failure.

3. Monitor bilateral peripheral pulses along with color and

temperature of extremities every 2 hours.

4. Maintain ventilator support or oxygen delivery as ordered.

5. Titrate inotropic agents to maintain CI at least 2.5 to 4 L/min/m2.

Monitor for drug side effects, including changes in heart rhythm.

6. Regulate afterload-reducing agents to maintain SVR less than

1200 dynes/sec/cm-5. Monitor for side effects including hypotension,
dizziness, headache, nausea and vomiting, and cutaneous flushing.

7. Administer diuretic agents as ordered for elevated PAOP (greater

than 14 mm Hg). Monitor for signs and symptoms of hypokalemia
caused by the diuretics.

8. Provide a quiet environment for the patient and family.

9. Administer pain medications as ordered and assess effectiveness

using pain assessment tools/scales.

10. Monitor Hgb and Hct values daily as loss of blood reduces
oxygen delivery to the cells, resulting in tachycardia and tachypnea.

Ineffective tissue perfusion: peripheral: Involved leg 

related to interrupted arterial blood flow secondary to arterial wall
dissection by sheath or thrombus formation.
Goals/Outcomes: Throughout hospitalization, the patient has
adequate perfusion in the involved leg as evidenced by Doppler or
palpable peripheral pulses, normal color and sensation, warmth,
full motor function, and absence of bleeding, abdominal pain, and
tingling in the involved leg.
Tissue Perfusion: Peripheral; Circulation Status

Circulatory care: Arterial insufficiency

1. Monitor circulation in affected leg every 30 minutes for 2 hours

1136
and every 2 hours thereafter if assessment is within normal limits.
Assess pulses, temperature, color and sensation, and mobility of the
toes in the involved leg. Consult physician or midlevel provider
immediately if any changes occur.

2. Instruct patient to notify RN if pain, numbness, or tingling occurs

in the involved leg.

3. Provide protection to heel of involved leg to prevent pressure

ulcer and place protective material such as sheepskin between toes.

4. Have patient perform passive foot exercises at least 4 times daily

without bending leg at the hip.

5. Administer IV medications as ordered to prevent clots from

forming on the balloon. Monitor patient for signs of bleeding,
including decreased Hct, abdominal pain, hematuria, oral bleeding,
or blood-tinged mucus.

6. Keep HOB at least 30 degrees or less to prevent migration of the

balloon catheter.

7. Assess the following for balloon migration: decreased left radial

pulse, sudden decrease in urine output, flank pain, and dizziness.
Notify advanced practice provider if changes are noted.

Impaired tissue integrity 

related to external factors (pressure and immobilization); internal factors
(altered circulation, possible insulin resistance, and decreased nutritional
intake).
Goals/Outcomes: Throughout hospitalization, patient’s tissues
remain intact.
Tissue Integrity: Skin and Mucous Membranes.

Pressure ulcer prevention:

1. Position patient on low-pressure protective bed to enhance blood

flow to dependent areas and allow air circulation across the skin,
promoting evaporation of moisture.

1137
2. Reposition patient every 2 hours keeping involved leg extended
and log-roll patient onto side.

3. Provide care to keep skin dry and clean, inspect pressure areas at
the beginning of each shift.

4. Patient’s diet should be high in protein and calories.

5. Keep glucose within recommended range (the American

Association of Clinical Endocrinologists and American Diabetes
Association consensus statement recommends a target glucose
range of 140 to 180 mg/dL in critically ill patients).

6. Encourage ambulation after assessing patient utilizing an

evidence-based mobility protocol if available or consulting with
physician (if not on IABP or LVAD).

Ineffective breathing pattern 

related to fatigue and decreased energy secondary to HF; decreased lung
expansion secondary to medically imposed position (HOB at 30 degrees).
Goals/Outcomes: Within 4 hours after diagnosis of HF, the
patient has an effective breathing pattern as evidenced by PaO2 at
least 80 mm Hg, SpO2 at least 90%, absence of adventitious breath
sounds, and RR 12 to 20 breaths/min with normal pattern and
depth.
Respiratory Status: Ventilation; Respiratory Status: Gas
Exchange

Respiratory monitoring

1. Monitor breath sounds every 2 hours. Assess anterior and

posterior lung fields for adventitious or absent sounds.

2. Monitor oxygen saturation continuously and maintain greater

than 90%.

3. Monitor RR, rhythm, and breathing pattern hourly.

4. Assess for atelectasis and respiratory infection (increased

1138
temperature, SOB, increased sputum production or coughing, and
altered color of sputum).

5. Monitor temperature every 4 hours and WBC daily for signs of

infection.

6. Encourage patient to breathe deeply, cough, and use incentive

spirometer every hour.

7. Reposition patient every 2 hours to minimize status of lung

secretions.

8. Monitor I&O.

9. Elevate HOB 30 degrees or more as tolerated.

10. Prepare for intubation and mechanical ventilation if the patient’s

respiratory status deteriorates.

Ineffective protection 
related to risk of bleeding secondary to coagulopathy or IV
anticoagulants needed to maintain therapeutic equipment (left
ventricular assist devices).
Goals/Outcomes: Throughout hospitalization, patient’s bleeding
is controlled as evidenced by secretions and excretions negative for
blood, chest tube drainage within acceptable amounts, and absence
of abdominal pain or ecchymosis.
Blood Coagulation

Bleeding precautions

1. Monitor PTT, ACT (or other blood clotting labwork), and platelet
levels daily.

2. Monitor Hct and Hgb daily.

3. Protect patient from injury and suction oral cavity carefully.

4. Administer gastric acid-neutralizing drugs as ordered.

1139
 Bleeding Reduction

Patients with ventricular assist devices

Risk for complications from immobility 

related to imposed restrictions against movement secondary to presence of
assist device or debilitated state.
Goals/Outcomes: Patient is able to retain baseline range of
motion of joints affected by immobilization.
Mobility.

Exercise therapy: Joint immobility

1. Turn patient every 2 hours with assist device in place if care is

taken during turning.

2. Provide passive range of movement to extremities 4 times daily

and encourage family to assist.

Energy Management

Decreased cardiac output 

related to altered preload and negative inotropic changes secondary to
reduced right ventricular contraction occurring with left- sided heart
assist device.

This is a complication of left-sided heart assist devices,

particularly when the outflow cannula is located in the left
ventricle. When the left ventricle is decompressed, septal wall
motion is diminished, reducing right ventricle contraction.

Goals/Outcomes: Within 24 of diagnosis of HF patient’s CO will

be adequate as evidenced by measured CO 4 to 7L/min, RAP 4 to 6
mm Hg, PVR 60 to 100 dynes/sec/cm-5, and LAP at least 10 mm Hg.
Circulation Status; Cardiac Pump Effectiveness

1140
Circulatory care: Mechanical assist device

1. Monitor patient for decrease in CO with associated increases in

RAP and PVR.

2. An adequate preload is necessary to prevent a vacuum effect

from the device, thereby decreasing CO.

Risk for infection 

related to inadequate primary defenses secondary to presence of multiple
invasive lines, movement restrictions, and stasis of body fluids.
Goals/Outcomes: Patient is free of infection as evidenced by
normothermia, WBC count 11,000/mm3 or less, negative culture
results, and absence of swelling, warmth, tenderness, and purulent
drainage at incision or cannulation sites.
Immune Status

Infection protection

1. Every day monitor vital signs temperature, WBC count, and

observe incisions and cannulation sites for evidence of infection.

2. Culture any drainage that is purulent, and report positive

findings.

3. Change IV tubing every 72 hours (or per protocol) using aseptic

technique.

4. Change all dressings over catheter insertion sites as per protocol.

5. Administer antibiotics as ordered.

6. Attain nitrogen balance by providing adequate nutrition.

7. Monitor breath sounds every 2 hours; after extubation have

patient perform coughing and deep breathing exercises and have
him or her mobilize as soon as possible.

8. Provide gentle chest physiotherapy as ordered.

1141
Imbalanced nutrition less than body requirements 
related to decreased intake secondary to oral intubation; increased
nutrition needs secondary to debilitated state and impaired tissue
perfusion with concomitant nitrogen malabsorption.
Goals/Outcomes: Within the 24- to 48-hour period before
discharge from the ICU, the patient will have adequate nutrition as
evidenced by a balanced nitrogen state and stable weight.
(Optimal nutrition in the ICU patient is still being debated in the
literature.)
Nutritional Status: Nutrient Intake

Nutritional management

1. Provide via tube feedings or total parental nutrition, to ensure

minimum 1 to 5 g protein/kg/day. (In patients with body mass
index [BMI] less than 30, protein requirements should be in the
range of 1.2 to 2.0 g/kg actual body weight.) In the critically ill obese
patient, permissive underfeeding or hypocaloric feeding is
recommended. In obesity where BMI is greater than 30, the goal of
the enteral feeding regimen should not exceed 60% to 70% of target
energy requirements or 11 to 14 kcal/kg actual body weight/day (or
22 to 25 kcal/kg ideal body weight/day). Protein should be provided
in a range of ≥ 2.0 g/kg ideal body weight/day for patients with BMI
30 to 40 and ≥ 2.5 g/kg ideal body weight/day for BMI ≥ 40.

2. A dietician should be monitoring the patient daily.

3. Weigh patient daily for trend.

4. Monitor I&O hourly.

Cardiomyopathy
Pathophysiology
Cardiomyopathy (CM) refers to a heterogeneous group of
myocardial diseases that are often genetic and associated with
mechanical and electrical dysfunction. Most types of CM result in

1142
inappropriate ventricular hypertrophy or dilation. The AHA 2006
Expert Panel on Contemporary Definitions and Classification of
Cardiomyopathy categorized CM into two major groups: primary
and secondary CM. Primary CMs are caused by pathology confined
to the heart muscle alone; whereas secondary CMs are caused by
pathology from a variety of generalized systemic (multiorgan)
disorders (Table 5-12). Some common disease entities involving the
heart muscle have been excluded from the present contemporary
CM classification. These include pathologic myocardial processes
and cardiac dysfunction caused by another cardiovascular
abnormality, such as valvular heart disease, systemic hypertension,
congenital heart disease, and atherosclerotic CAD. Other conditions
not included in this CM classification are cardiac tumors, diseases
affecting the endocardium with little or no myocardial
involvement, and hypertensive hypertrophic CM. Primary and
secondary CMs included in the 2006 AHA definition of CM are
further classified into the following: hypertrophic CM (HCM),
dilated CM (DCM), arrhythmogenic RV CM/dysplasia (ARVC/D),
and LV noncompaction (LVNC). Be aware that one disease, be it
primary or secondary CM, may fall into more than one CM
classification, causing confusion if there is an overlap between
categories. For example, some genetic primary CMs are known to
cause both DCM and HCM. Furthermore, a CM may evolve as a
consequence of remodeling from one category to another as the
disease progresses. CMs, whether confined to the heart (primary
CM) or part of a generalized systemic disorder (secondary CM),
often lead to cardiovascular death or progressive HF-related
disability.

Table 5-12
TYPES AND CAUSES OF CARDIOMYOPATHY

Primary Types of
Secondary Causes of Cardiomyopathy
Cardiomyopathy
Genetic Autoimmune/Collagen
Hypertrophic Systemic lupus erythematosus, dermatomyositis, rheumatoid
cardiomyopathy arthritis, scleroderma, polyarteritis, nodosa
Arrhythmogenic right
ventricular Storage
cardiomyopathy/dysplasia Hemochromatosis, Fabry disease, glycogen storage disease (type
Left ventricular II, Pompe), Niemann-Pick disease

1143
 noncompaction Friedreich ataxia, Duchenne-Becker muscular dystrophy,
Mixed Type (Genetic and Emery-Dreifuss muscular dystrophy, myotonic dystrophy,
Nongenetic) neurofibromatosis, tuberous sclerosis
Dilated cardiomyopathy
Infiltrative
Restrictive cardiomyopathy
(nonhypertrophied and Amyloidosis, Gaucher disease, Hurler disease, Hunter disease
nondilated) Inflammatory (Granulomatous)
Acquired Type Sarcoidosis
Inflammatory (myocarditis) Endocrine
Stress-induced (“tako- Diabetes mellitus, hyperthyroidism, hypothyroidism,
tsubo” or “broken heart hyperparathyroidism, pheochromocytoma, acromegaly
syndrome”) Cardiofacial
Peripartum Noonan syndrome, lentiginosis
Tachycardia induced Endomyocardial
Endomyocardial fibrosis, hypereosinophilic syndrome (Löeffler
endocarditis)
Nutritional Deficiencies
Beriberi (thiamine), pellagra, scurvy, selenium, carnitine,
kwashiorkor
Toxicity
Drugs, heavy metals, chemical agents
Electrolyte Imbalance
Consequence of Cancer Therapy
Anthracyclines: doxorubicin (Adriamycin), daunorubicin,
cyclophosphamide, radiation
Infectious
HIV, Lyme disease, Chagas, coxsackie, influenza
Note: This table lists common diseases associated with primary and secondary CM
and is not intended to represent an exhaustive and complete list of conditions
associated with CM. Some disagreement exists in the scientific community regarding
the classification, definition, and nomenclature of CM; therefore, discrepancies and
contradictions may occur among various scientific resources.

Functional classifications of cardiomyopathy

Dilated cardiomyopathy
Dilated cardiomyopathy (DCM) is characterized by marked,
progressive dilation of the ventricles, resulting in decreased
myocardial contractility and a reduced systolic ejection fraction
(less than 40%). DCM is the most common cause of
cardiomyopathy. Infectious agents (particularly viruses producing
myocarditis), cocaine, chronic excessive alcohol consumption, and
chemotherapeutic agents are common causes of DCM, along with
other autoimmune, neurologic, metabolic, endocrine, nutritional,
and other systemic disorders. About 20% to 35% of DCM cases have
been reported as familial, and they are frequently associated with
skeletal muscle or neuromuscular disorders. In patients with severe

1144
dilation, the increase in total cardiac mass may lead to ventricular
hypertrophy. Alternatively, DCM may occur as a late manifestation
of hypertrophic heart disease. DCM may ultimately lead to a
decline in LV contractile function, ventricular and supraventricular
arrhythmias, conduction system abnormalities, thromboembolism,
progressive HF, and sudden or HF-related death.

Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is characterized by
inappropriate hypertrophy of the ventricular muscle, leading to LV
stiffness and diastolic dysfunction. HCM is most often a genetically
acquired illness and is the most common inherited heart defect.
Approximately 60% to 70% of patients with HCM have familial
HCM, an inherited autosomal dominant condition. Other
cardiovascular diseases, including hypertension and aortic stenosis,
are capable of producing the same magnitude of wall thickening
seen with HCM. HCM is the most common cause of sudden cardiac
death in the young, especially in athletes, but may lead to HF and
disability at any age. Obstructive HCM (also called hypertrophic
obstructive cardiomyopathy or HOCM) occurs when the enlarged
heart muscle, usually the ventricular septum, obstructs the
ventricular outflow channel. HOCM may result in angina, HF, and
sudden death.

Restrictive cardiomyopathy
Restrictive cardiomyopathy (RCM) is less common than HCM or
DCM and is characterized by nondilated ventricles with impaired
ventricular filling from rigid or fibrotic ventricular walls. LV
diastolic dysfunction occurs, often associated with very high end-
diastolic pressures and moderate to marked biatrial enlargement
secondary to elevated atrial pressures. Hypertrophy is typically
absent, although the infiltrative and storage diseases (such as
amyloid and hemochromatosis) may cause an increase in LV wall
thickness. Systolic function usually remains normal, at least early in
the disease. Treatment is difficult and prognosis is poor.
Differentiating RCM from constrictive pericarditis is important
since the two clinical pictures are similar, while management is
markedly different.

1145
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
(ARVC/D) is an uncommon genetic disease characterized by
progressive replacement of normal myocardial cells with fatty or
fibrofatty tissue. Initially thought to be a disease isolated to the
right ventricle, more recent evidence shows that the left ventricle is
also involved in as many as 75% of cases. Clinical manifestations
include ventricular arrhythmias and HF. In young adults, ARVC/D
often presents with sudden death.

Left ventricular noncompaction

Left ventricular noncompaction (LVNC) is an anatomic abnormality
of LV myocardial development characterized by a “spongy” and
“noncompacted” morphologic appearance of the LV myocardium.
Noncompaction predominantly involves the apical portion of the
LV chamber with deep intertrabecular recesses, or channels, in
communication with the ventricular cavity and filled with blood
from the ventricular cavity. LVNC has been associated with a high
incidence of HF, thromboembolism, and ventricular arrhythmias in
adults.

Assessment
Goal of assessment
The physical assessment of patients with CM attempts to
characterize the etiology and severity of cardiac dysfunction, the
level of functional impairment, and the optimal therapeutic
approach. Furthermore, the physical assessment should identify
factors that precipitated clinical decompensation, for example,
exercise or exacerbation of autoimmune disease. A good physical
assessment will help differentiate heart and circulatory failure from
entities that cause similar complaints and findings. During the
course of treatment, the physical assessment will also provide
feedback about the patient’s response to therapies (Table 5-13).

Table 5-13
SIGNS AND SYMPTOMS OF CARDIOMYOPATHY

1146
AV, atrioventricular; CHF, congestive heart failure; CM, cardiomyopathy; CO, cardiac
output; HCM, hypertrophic cardiomyopathy; HF, heart failure; JVD, jugular venous
distention; LV, left ventricular; LVH, left ventricular hypertrophy; PMI, point of
maximal impulse; PND, paroxysmal nocturnal dyspnea; RCM, restrictive
cardiomyopathy; RV, right ventricular.

Observation
A patient’s clinical presentation will vary according to the type and
extent of the CM and whether the patient has progressed to overt
HF. The clinical presentation will reflect both the hemodynamic
abnormalities caused by cardiac dysfunction and the degree of
secondary compensatory mechanisms. Patients’ presenting
symptoms may range from asymptomatic to, unfortunately,
symptoms continuous with cardiogenic shock (CS) or sudden
death. Most commonly, patients will present with symptoms of HF
or arrhythmias. Diagnostic tests used in patients with suspected
cardiomyopathy are outlined in the following table.

Diagnostic Tests for Cardiomyopathy

1147
1148
Collaborative management
Care priorities

1. Reduce activity level to decrease oxygen demand during

periods of activity intolerance because of instability
When the patient stabilizes, increase activity gradually, as tolerated,
to prevent complications of immobility. Document activity
tolerance (including position in bed) to help reflect if treatments are
effective.

1149
2. Initiate pharmacotherapy to maintain or reestablish
hemodynamic stability, control symptoms, and prevent
cardiac remodeling, all of which aid in halting further
disease progression
Medications commonly used in the treatment of CM and their
nursing implications (also see Heart Failure, Chapter 5, and
Cardiogenic Shock, Chapter 5):

• HCM: Beta blockers reduce myocardial oxygen demand and

increase diastolic filling time by slowing the HR, relaxing cardiac
muscle, and increasing CO. Also, beta blockers help decrease
cardiac outflow obstruction during exercise and reduce
sympathetic cardiac stimulation in patients with HCM.

• DCM: Beta blockers block the compensatory response of the

adrenergic system to HF and increase CO/CI. Vital signs should
be monitored to ensure patients do not develop symptomatic
bradycardia or hypotension. Note: These effects are not
immediate and may take days to weeks to occur. Initiating or
increasing beta-blocker doses while a patient is experiencing
signs and symptoms of HF may worsen dyspnea, edema,
bradycardia, and vasodilation . Beta-blocker therapy should
be started at a low dose and titrated up slowly to avoid
exacerbation of acute HF symptoms. Not all patients with CM
tolerate target doses of beta blockers and should be titrated
individually while monitoring BP, HR, and signs and symptoms
of worsening HF.

ACEIs/ARBs: Used in DCM to decrease preload and afterload and

block the compensatory response of the renin-angiotensin system
to HF. Goal systolic BP is greater than 90 mm Hg. Monitor
patients for postural hypotension, hyperkalemia, and worsening
renal function.

Diuretics: Diuretics reduce preload and pulmonary congestion. If a

patient is hemodynamically monitored, diuretics will result in a
decreased PAWP and help to achieve a negative fluid balance
and ultimately a euvolemic state. Use diuretics cautiously for
HCM since they are contraindicated in some patients with

1150
 obstructive HCM. Monitor the patient for weakness, postural
hypotension, hypokalemia (see Hypokalemia, Chapter 1),
hypomagnesemia, dehydration, and worsening renal function.

Aldosterone antagonists: Aldosterone is a neurohormone shown to

contribute to the development of LV hypertrophy and fibrosis
involved in cardiac remodeling. Aldosterone antagonists are
weak diuretic drugs that block the action of aldosterone. These
drugs inhibit sodium reabsorption in the distal convoluted tubule
of the kidney and cause retention of potassium and magnesium.
Potassium levels must be closely monitored to avoid
hyperkalemia or worsening renal function. Other side effects
include postural hypotension and gynecomastia if taking
spironolactone.

Potassium supplements: Potassium lost in the urine as a result of

diuresis may necessitate replacement with potassium
supplements. Maintain serum levels in the high normal range (4.2
to 5 mEq/L).

Vasodilators (hydralazine and nitrates): These drugs decrease

preload and afterload in DCM, resulting in improved CO and
enhanced nitric oxide availability. It is important to maintain a
stable BP (keep MAP at 65 mm Hg or higher). Nitrates are not
typically used in HCM. Side effects of vasodilators include
postural hypotension, dizziness, headache, nausea, and vomiting.

Inotropic therapy (digoxin, dobutamine, milrinone): Inotropes

enhance contractility. If a patient has hemodynamic monitoring,
the goal of milrinone and dobutamine is to increase CO/CI and
maintain a stable BP for adequate perfusion. Monitor for rhythm
disturbances. Other potential side effects include headache and
angina.

Digoxin is contraindicated in the treatment of obstructive

hypertrophic cardiomyopathy, as it may be ineffective or worsen
the condition. Digoxin is also contraindicated in patients with a

1151
diagnosis of amyloidosis.

Antiarrhythmic agents: Medications used to control atrial and

ventricular arrhythmias are common for patients diagnosed with
DCM and HCM.

Anticoagulants: Anticoagulants are important to prevent thrombus

formation related to atrial fibrillation or decreased ventricular
contraction and emptying. INRs must be monitored with extra
caution because of the potential for medication interactions that
affect the INR (such as antibiotic use).

Calcium channel blockers (CCBs): Nonhydropyridine CCBs, such

as verapamil or diltiazem, may be used to treat HCM by
improving diastolic filling time, heart muscle relaxation, and
exercise capacity. Most CCBs are contraindicated in DCM, except
for hydropyridine CCBs (such as amlodipine), which are
occasionally used to treat hypertension in patients with DCM.

4. Initiate electrical/device-based therapy to maintain or

reestablish hemodynamic stability, control symptoms, and
prevent cardiac remodeling
(For further information, also see Heart Failure, Chapter 5, and
Cardiogenic Shock, Chapter 5.)

• Dual-chamber pacemaker: Implantation of a dual-chamber

pacemaker may be performed to treat symptomatic bradycardia
(including sick sinus syndrome or heart block).

• Implanted cardioverter defibrillator (ICD): Implantation of an

ICD is indicated for patients with LVEF 35% or less and HF
symptoms. Patients must be on optimal medical therapy and at
least 40 days post-MI before implantation. (In some instances,
LVEF will improve with medical therapy and/or treatment of
CAD.) ICD therapy has been shown to significantly reduce
mortality in patients with reduced LVEF. Patients should have a

1152
 life expectancy of at least 1 year before implantation. In patients
with end-stage HF symptoms who have an ICD in place, the
decision can be made to deactivate the defibrillator to avoid
unnecessary discomfort at end of life.

• Cardiac resynchronization therapy (CRT): Approximately one

third of HF patients develop a widened QRS complex, indicating
asynchronous ventricular function. Implantation of biventricular
pacing allows coordination of the right and left ventricles. CRT is
indicated for patients with LVEF 35% or less, and a QRS duration
of 150 ms or greater with HF symptoms. CRT can improve
contractility and EF and decrease cardiac remodeling. CRT can be
combined with an ICD as a single device if the patient meets the
requirements for both therapies.

5. Initiate hemodynamic monitoring to help evaluate

intracardiac pressures during therapeutic interventions
Routine hemodynamic monitoring is not recommended for all
patients with cardiomyopathy or decompensated HF.
Hemodynamic monitoring should be considered in patients with
persistent symptoms in whom renal function is worsening with
therapy and inotropic or vasoactive agents are required, and those
who are being considered for advanced therapies such as LVAD
implantation or cardiac transplantation.

6. Initiate advanced therapies for symptom management

and stabilization

Alcohol ablation: During a cardiac catheterization, ethanol is

injected into the septal branches of the LAD. This purposeful
reduction of myocardial tissue through a limited, therapeutic
septal infarction will reduce outflow obstruction in HCM.

Ultrafiltration: Ultrafiltration, used to treat acute decompensated

HF with volume overload, is the mechanical removal of excess
body fluid by the generation of a convective gradient across the
hemofilter membrane. The electrolyte concentration of the
ultrafiltrate is equal to that of the plasma and avoids the
stimulation of the renin-angiotensin-aldosterone axis.

1153
Intraaortic balloon pump (IABP): In the presence of a failing
myocardium, an IABP helps to decrease afterload and increase
coronary artery perfusion

• Left ventricular assist devices (LVADs): Some

patients with CS unresponsive to intra-aortic
balloon counterpulsation and IV inotrope therapy
may be referred for mechanical circulatory support.
LVADs may be used as a bridge to cardiac
transplantation or as a destination therapy for those
ineligible for transplant. The inflow cannula of an
LVAD is connected to the apex of the left ventricle.
Blood is pumped by the device via the outflow
cannula to the aorta. Complications include stroke,
infection, coagulopathy with bleeding, multiple
organ dysfunction syndrome (MODS), and
prosthetic valve insufficiency. Most modern LVADs
have continuous flow, leaving the patient without a
palpable pulse despite adequate perfusion.

7. Provide surgical interventions to maintain or reestablish

hemodynamic stability, control symptoms, and prevent
cardiac remodeling
(For further information, also see Heart Failure, Chapter 5, and
Cardiogenic Shock, Chapter 5.)

Ventricular septal myotomy-myectomy: During this procedure, the

hypertrophied ventricular septum of obstructive HCM is
removed.

Heart transplantation: Open heart transplantation is pursued for

patients with advanced CM refractory to optimal medical

1154
 therapy. Each institution has criteria that must be met before
transplantation is considered a treatment option (see Organ
Transplantation, Chapter 11).

Care plans for cardiomyopathy

Nursing care must be based on the type of CM, its associated
pathology, and the patient’s clinical manifestations. Acute
decompensated HF is a gradual or rapid change in HF signs and
symptoms resulting in a need for urgent therapy because of
elevated LV filling pressures and/or low CO. The primary aspects
of care related to acute decompensated HF are outlined since this is
the most common presenting problem, for this patient population,
in the acute care setting.

Decreased cardiac output 

related to disease process that has resulted in decreased ability of the heart
to provide adequate pumping to maintain effective oxygenation and
nutrition of body systems.
Goals/Outcomes: Within the 24-hour period before discharge
from the CCU, the patient has adequate CO as evidenced by:

NORMAL VALUES FOR HEMODYNAMIC MEASUREMENTS

Assessment Measure Goal

SBP At least 90 mm Hg
MAP At least 65 mm Hg
CI 2.5 to 4 L/min/m2
CO 4 to 7 L/min
PAWP Less than 18 mm Hg
Right atrial pressure 4 to 6 mm Hg
(RAP)/CVP
RR 12 to 20 breaths/min
HR Less than 100 bpm
Urinary output More than 0.5 mL/kg/hr
Skin assessment Warm and dry
Peripheral pulses At least 2+ on a 0 to 4+ scale
Mental status Orientation to time, place, and person (assuming baseline
orientation ×3)

SBP, Systolic blood pressure; MAP, Mean arterial pressure; CI, Cardiac Index; CO,
Cardiac Output; PAWP, Pulmonary artery wedge pressure; CVP, Central venous
pressure; RR, Respiratory Rate; HR, Heart rate.

1155
 Cardiac Pump Effectiveness; Circulation Status

Cardiac care: Acute hemodynamic regulation

1. Pulmonary artery pressures: Evaluate hemodynamic readings at

least every 1 to 2 hours. Manage PAWP greater than 18 mm Hg and
RAP/CVP greater than 6 mm Hg. Although normal PAWP is 6 to 12
mm Hg, these patients may need increased filling pressures for
adequate preload, with wedge pressure at 15 to 18 mm Hg. Those
with right-sided HF may need an RAP/CVP 8 to 12 mm Hg.
Measure CO/CI every 2 to 4 hours and on an as-needed basis.
Optimally, CO should be 4 to 7 L/min and CI should be 2.5 to 4
L/min/m2; for some patients, the best CO/CI will be below expected
normal values.

2. Electrolytes and renal function: Monitor I&O records and weigh

the patient daily at the same time every day, noting trends and goal
weight. Individuals with CM may be on a strict fluid-restricted
(e.g., 1000 to 2000 mL/day) and sodium-restricted (e.g., less than
2000 mg/day) diet. Notify the advanced practice provider if urinary
output is less than 0.5 mL/kg/h, or if urine output does not increase
after diuretic therapy.

3. Dysrhythmias: Monitor ECG continuously for sinus or atrial

tachycardias, atrial fibrillation, or ventricular ectopy, which may
further decrease CO.

4. Mobility: Assist patients with activities of daily living (ADLs) and

report worsening exercise tolerance. To prevent complications of
immobility, perform or teach patients and significant others active,
passive, and assistive ROM exercises. For a discussion of an in-bed
exercise program, see Table 5-7 and interventions in Prolonged
Immobility, Chapter 1.

5. Medication management: Administer prescribed medications in

accordance with possible food and medication interactions.
Administer the HF medications throughout the day rather than
administering them all at once. Provide ongoing patient education
regarding the purpose and common side effects for each

1156
medication.

Table 5-7
ACTIVITY LEVEL PROGRESSION FOR HOSPITALIZED PATIENTS*

Level Activity
I Bed rest Flexion and extension of extremities 4 times daily, 15 times each extremity;
deep breathing 4 times daily, 15 breaths; position change from side to side
every 2 hours
II Out of As tolerated, 3 times daily for 20 to 30 minutes
bed to
chair
III Ambulate As tolerated, 3 times daily for 20 to 30 minutes
in room
IV Ambulate Initially, 50 to 200 ft twice daily; progressing to 50 to 200 ft 4 times daily
in hall
*
Signs of activity intolerance: Decrease in blood pressure less than 20 mm Hg;
increase in heart rate to greater than 120 bpm (or more than 20 bpm above resting
heart rate in patients receiving beta-blocker therapy).

Cardiac Care: Acute; Circulatory Care: Mechanical Assist

Device; Hemodynamic Regulation; Shock Management: Cardiac;
Neurologic Monitoring; Medication Management; Dysrhythmia
Management

Activity intolerance 
related to imbalance between oxygen supply and demand secondary to
decreased functioning of the myocardium.
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the CCU, patients should exhibit cardiac tolerance
to increasing levels of activity as evidenced by respiratory rate less
than 24 breaths/min, BP within 20 mm Hg of patient’s normal
range, HR within 20 bpm of patient’s normal resting HR, return to a
stable baseline ECG rhythm, and activity tolerance to a level
without presence of angina/chest pain or worsening dyspnea.
Activity Tolerance; Energy Conservation

Energy management

1. Monitor the patient’s physiologic response to activity, reporting

any symptoms of chest pain, new or increasing SOB, increases in
HR greater than 20 bpm above resting HR, and increase or decrease

1157
in systolic BP greater than 20 mm Hg.

2. Assess for and manage decreased CO, e.g., changes in mentation,

cool-clammy skin, or tachycardia.

3. Plan nursing care so that the patient is assured of extended

periods of rest (at least 90 minutes). Consult the advanced practice
provider to ensure that exercises are within the patient’s prescribed
limitations.

Activity Therapy; Energy Management; Teaching: Prescribed

Activity/Exercise; Dysrhythmia Management; Pain Management;
Medication Management

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Hemodynamic
Monitoring (Chapter 1), Heart Failure (Chapter 5), Prolonged
Immobility (Chapter 1), Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2), and Cardiogenic Shock
(Chapter 5).

Dysrhythmias and conduction

disturbances
Pathophysiology
Cardiac dysrhythmias reflect abnormal function of the heart’s
electrical system. Cardiac electrical cells closely interface with the
mechanical cells, which contain the contractile muscle filaments.
Dysrhythmias may originate in any part of the electrical system,
from the pacing cells (sinoatrial [SA] node, atrioventricular [AV]
junction) to any portion of the conduction system (atria, His–
Purkinje system, bundle branches, and ventricles). Sympathetic and
parasympathetic nerve fibers influence the rate of discharge of the
SA node, conduction through the AV node, and force of both atrial
and ventricular contraction. The main parasympathetic influence is

1158
the vagus nerve, which slows the rate of pacing by the SA node and
AV junction, and decreases force of contraction. Sympathetic nerve
fibers originate from T1 to T5 and, when stimulated, produce the
neurotransmitter norepinephrine, which increases HR during the
stress response. Sympathetic stimulation also promotes production
of catecholamines by the adrenal glands, and the hormones are
received by catecholamine receptors (alpha receptors, beta
receptors, dopaminergic receptors), which increase HR, force of
contraction, BP, and CO. Electrical dysfunction can markedly
change the CO and cause prompt deterioration in the patient’s
hemodynamic status (Figure 5-1).

FIGURE 5-1 Electrical conduction system. Source: (From

Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)

Cardiac electrophysiology involves studying the electrical

impulses and their conduction across the atria and throughout the
ventricles to provide power and coordination for the cardiac cycle.
Electrical impulses are created by ion exchange. Exchange of ions in
the mechanical or muscle cells generates electrical activity. At rest,
the muscle has slightly more positive ions (Na+and Ca2+) on the
outside of the cells and more negative ions inside the cells (resting
membrane potential or polarization). K+ is the most prevalent

1159
intracellular ion. The resting cells have a threshold for activation,
based on the difference in the ion concentrations (action potential).
Stimulation of a cardiac muscle cell, or depolarization, is created by
a rapid influx of Na+ followed by a slower influx of Ca2+ into the
cell. Normally, the influx is followed by muscle contraction. The cell
responds to the influx by K+ diffusing out of the cell to help
rebalance the positive ions (early repolarization and plateau phase)
on both sides of the cell membrane. A slower efflux is followed by a
rapid efflux of K+ (rapid repolarization). Finally, the sodium-
potassium pump must activate to fully rebalance the electrical
potential of the cell, restore the ions to their original position, and
achieve resting membrane potential or polarization.
Normal electrical activity of the heart produces waves or
deflections on the ECG (Figure 5-2). The waves and intervals that
comprise the components of the ECG make up one electrical cardiac
cycle (Figure 5-3).

• P wave: Electrical impulse originating in the SA node, the heart’s

primary pacemaker, which prompts atrial depolarization or the
spread of the impulse across the right and left atria. It is the first
positive deflection from the isoelectric baseline in most ECG
leads but may be positive, negative, or biphasic in leads III, aVL,
and V1. The atria contract following the appearance of the P
wave. The wave should be rounded, less than 0.11 second in
duration (width), and no greater than 2.5 mm in height (voltage).

• PR interval: The P wave plus the isoelectric line extending to the

beginning of the QRS complex, wherein the impulse spreads
through the AV node, the bundle of His, the right and left bundle
branches, and Purkinje fibers. The interval measures 0.12 to 0.2
second in normal adults.

• QRS complex: A set of three combined waves (Q, R, and S) that

represents ventricular depolarization, which stimulates
ventricular contraction. The wave of atrial repolarization is
hidden within this larger, dominant complex. The QRS complex
should be 0.06 to 0.1 second in normal adults and varies in
direction depending on the ECG lead but is most recognized as
positive deflection (which represents the R wave, a positive

1160
 deflection from the baseline). Some normal positive complexes
are “missing” a distinct Q or S wave. The complex is
predominantly negative in leads aVR, V1, and V2 and biphasic in
leads V3, V4, and, occasionally, lead III (which represents stronger
Q- and S-wave activity, which are the negative deflections that
precede and follow the R wave).

• ST segment: The isoelectric line between the end of the QRS

complex and the T wave, which represents early ventricular
repolarization. The segment changes in response to myocardial
ischemia, injury, hypokalemia, pericarditis, and other ventricular
tissue abnormalities. The “J” point is where the ST segment
begins and the QRS complex terminates.

• T wave: Represents ventricular repolarization, wherein during

the first part of the wave, the tissue is refractory to further
stimulation (absolute refractory period). At the peak of the T
wave, the tissue becomes sensitive to stronger electrical stimuli
(relative refractory period), and ventricular dysrhythmias may
occur.

• QT interval: Represents the depolarization and repolarization of

the ventricle, measured from the beginning of the QRS complex
to the end of the T wave. If no Q wave is present, the interval is
measured from the beginning of the R wave to the end of the T
wave. As the HR increases, the QT interval should decrease
proportionately. There are tables available to reflect the duration
of a normal QT interval for various HRs. When the duration of
the QT interval is adjusted or corrected for HR, the interval is
termed the QTc interval. A QT interval that is greater than half
the RR interval (distance between two R waves) is considered
prolonged.

• U wave: A small positive waveform that sometimes follows the T

wave. The significance is unknown, but it is theorized to be a
wave of Purkinje fiber repolarization.

• TP segment: A segment rarely used clinically when discussing

the ECG. It is the isoelectric segment on the ECG between the end

1161
of the T wave and beginning of the P wave. It reflects the time the
cardiac cells are electrically silent or neutral.

1162
 FIGURE 5-2 Electrical basis of the ECG. Source: (From
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)

1163
 FIGURE 5-3 Components of the ECG. Source: (From Huszar
RJ: Basic dysrhythmias: interpretation and management, ed 3, St. Louis,
2002, Mosby.)

Abnormal electrocardiographic tracings

Myocardial ischemia, electrolyte or other chemical imbalance, and
an abnormally configured electrical system are factors likely to
stimulate dysrhythmias. The normal flow of impulses depends on
properly nourished, well-oxygenated electrical tissues with an
anatomically correct pacing and conduction system. The cardiac
cycle depends on a balance of basic regulatory substances including
sodium, potassium, calcium, and glucose and appropriate amounts

1164
of catecholamines. Imbalance of these regulators can cause a
disturbance in automaticity, conduction/conductivity, or
myocardial contractility.

• Automaticity: The ability of cardiac cells to initiate an electrical

impulse spontaneously, without stimulation by a nerve or other
source. Hypokalemia and hypocalcemia increase automaticity.
The SA node, AV junction, and Purkinje fibers possess
automaticity. All cardiac muscle is electrically “irritable” or
excitable because of the concentration of ions on both sides of the
cell membranes, but not all cells possess automaticity. All cardiac
cells are able to respond to external stimuli, including electrical
and mechanical sources.

• Conduction/conductivity: All cardiac cells can receive electrical

stimuli and transmit or conduct impulses to an adjacent cell.
Intercalated disks in the cell membranes facilitate the
transmission of impulses throughout the heart muscle. When
impulses reach muscle cells, they stimulate muscle contraction.

• Myocardial contractility: Cardiac muscle cells “shorten” in

response to electrical impulses, which manifests as a muscle
contraction.

Causes of abnormal rhythms

Disturbances in automaticity
May involve an acceleration or deceleration in pacing or
automaticity of the SA node, such as sinus tachycardia (HR greater
than 100 bpm) or sinus bradycardia (HR less than 60 bpm).
Premature beats or possibly an escape or compensatory heart
rhythm may arise from the atria, junction, or ventricles if the SA
node is dysfunctional or arrests. Without additional catecholamines
prompted by the stress response, escape rhythms generated from
the AV junction or the ventricles are usually bradycardic (HR less
than 60 bpm). Abnormal rhythms, such as atrial or ventricular
tachycardia, may also result from excessive sympathetic stimulation
or electrolyte imbalance.

1165
Disturbances in conduction
Conduction may be too rapid, as in conditions that induce the stress
response (e.g., severe/critical illness, certain endocrine diseases,
profound emotional stress) or in the presence of an accessory
pathway (e.g., Wolff-Parkinson-White [WPW] syndrome).
Accessory pathways are extraconduction fibers that provide a
direct connection between the atria and the ventricles,
circumventing the AV node. Rhythms generated from these
anatomically incorrect conduction systems are called AV
reciprocating tachycardias and may have rates greater than 250
bpm. Reentry is a situation in which a misdirected electrical
impulse reexcites a conduction pathway through which it has
already passed. Once started, this impulse may circulate through
the same area repeatedly, prompting an AV reentrant tachycardia.
The trapped impulse becomes the pacemaker in this circumstance.
Impulse conduction may be delayed or too slow (e.g., first- and
second-degree AV block), or become totally blocked from
continuing down the pathway by abnormal electrical tissues (e.g.,
third-degree or complete heart block) (Figure 5-4).

1166
 FIGURE 5-4 Anomalous AV conduction. Source: (From
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)

1167
Combinations of disturbed automaticity and conduction
Several dysrhythmias may occur simultaneously (e.g., first-degree
AV block [disturbance in conductivity], premature atrial complexes
[PACs] [disturbance in automaticity]).

Assessment
Goal of assessment
To diagnose the type of dysrhythmia, the cause of the rhythm
(electrolyte or acid-base imbalance, structural abnormality, heart
and/or renal disease, nervous system or neuroendocrine
dysfunction), the impact of the dysrhythmia on the CO
(BP)/coronary artery perfusion (may prompt chest discomfort), and
to determine the urgency and type of treatment. Lethal
dysrhythmias result in cardiac arrest.

History and risk factors

Assess for acidosis or alkalosis, ACS (CAD, angina, MI), or other
heart disease or acute conditions (pericarditis, presence of accessory
conduction pathways, cardiomyopathy, HF, valvular disease,
cardiac tamponade), anemia, current use of antidysrhythmic or
bronchodilating drugs, recreational drug abuse, drug overdose, use
of catecholamines (epinephrine, dopamine, dobutamine,
norepinephrine), use of tricyclic antidepressants, diuretics,
exposure to other environmental toxins, electrolyte disturbances
(especially hypokalemia, hypoglycemia, or hypomagnesemia),
endocrine disease (posterior pituitary, thyroid, parathyroid,
adrenal, or pancreas), hypothermia, hypoxia, hypotension,
hypovolemia, hypervolemia, increased intracranial pressure,
infection pneumothorax or tension pneumothorax, pulmonary
disease including pulmonary embolism, peripheral vascular or
peripheral arterial disease (PAD), respiratory failure, renal failure,
and sepsis.

Observation
The patient’s appearance varies from absence of symptoms to
complete cardiopulmonary arrest. Common symptoms include

1168
activity intolerance, weakness, pallor, hypotension, dizziness, SOB,
dyspnea, palpitations, chest discomfort or pressure, and sensation
of “racing heart” or “skipped beats.” More serious symptoms
include altered mental status, anxiety, respiratory insufficiency,
syncope, and seizures, which may lead to HF and cardiopulmonary
arrest. Pulseless ventricular tachycardia, ventricular fibrillation,
asystole, and pulseless electrical activity (PEA) result in immediate
cardiac arrest.

Vital signs
Vary with type of dysrhythmia. Vital signs may be unaffected or
affected slightly. Accelerated or decelerated HR may cause
hypotension, result in HF, or deteriorate into pulselessness.
Symptomatic dysrhythmias most often result in a very rapid, slow,
or irregular pulse, changed pulse quality, hypotension, pallor,
possibly a variable HR (fast, then slow), and tachypnea. If the CO is
markedly decreased, shocklike symptoms ensue including cold,
clammy skin, dusky or cyanotic appearance, decreased urine
output, and feeling of impending doom or imminent death.

Electrocardiographic and hemodynamic

measurements
Hemodynamic measurements will vary, depending on the effect of
the dysrhythmia on the CO. If the patient has HF, CO is decreased
and PAP may be elevated. Right- and left-sided HF manifest
differently (see Heart Failure, Chapter 5). Tachycardias usually
increase CO initially, unless the rate is too fast to allow adequate
ventricular filling, in which case CO decreases and may lead to HF.
ECG findings seen with various dysrhythmias include
abnormalities in rate such as sinus bradycardia or sinus
tachycardia, irregular rhythm such as atrial fibrillation, extra beats
such as PACs and premature junctional complexes, wide and
bizarre-looking beats such as premature ventricular complexes
(PVCs) and ventricular tachycardia (VT), a fibrillating baseline such
as ventricular fibrillation (VF), and a straight line as with asystole.
Figures 5-5 through 5-30 give an overview of common rhythms,
dysrhythmias, conduction disturbances, and pacemaker rhythms

1169
and their treatment. Occasionally, patients have an electrical
rhythm without corresponding mechanical pumping. This
condition is known as PEA. Initially, the rhythm may appear nearly
normal but rapidly deteriorates as the conduction pathway
becomes hypoxic.

FIGURE 5-5 Normal sinus rhythm. Source: (From Huszar RJ:

Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1170
FIGURE 5-6 Sinus tachycardia. Source: (From Huszar RJ: Basic
dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1171
FIGURE 5-7 Sinus bradycardia. Source: (From Huszar RJ: Basic
dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1172
 FIGURE 5-8 Sinus dysrhythmia. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

FIGURE 5-9 Normal sinus rhythm with sinus

arrest. Source: (From Aehlert B: ECGs made easy: pocket reference, ed
2, St. Louis, 2002, Mosby.)

1173
FIGURE 5-10 Sinus tachycardia with premature atrial
complexes (PACs). Source: (Top, from Emergency Nurses
Association: Sheehy’s manual of emergency care, ed 6, St. Louis, 2005,
Mosby. Bottom, from Aehlert B: ECGs made easy: pocket reference, ed 2,
St. Louis, 2002, Mosby.)

1174
 FIGURE 5-11 Atrial tachycardia. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1175
FIGURE 5-12 Atrial flutter (type I). Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1176
FIGURE 5-13 Atrial fibrillation (AF). Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1177
FIGURE 5-14 AV junctional rhythm or junctional escape
rhythm. Source: (From Huszar RJ: Basic dysrhythmias: interpretation and
management, ed 3, St. Louis, 2002, Mosby.)

FIGURE 5-15 Accelerated junctional rhythm. Source: (From

Aehlert B: ECGs made easy: pocket reference, ed 2, St. Louis, 2002,
Mosby.)

1178
 FIGURE 5-16 Premature junctional
complexes. Source: (Top, from Emergency Nurses Association:
Sheehy’s manual of emergency care, ed 6, St. Louis, 2005, Mosby. Bottom,
from Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3,
St. Louis, 2002, Mosby.)

FIGURE 5-17 Junctional tachycardia (JT). Source: (From

1179
 Aehlert B: ECGs made easy: pocket reference, ed 2, St. Louis, 2002,
Mosby.)

FIGURE 5-18 Ventricular tachycardia. Source: (Top, from

Emergency Nurses Association: Sheehy’s manual of emergency care, ed 6,

1180
St. Louis, 2005, Mosby. Bottom, from Huszar RJ: Basic dysrhythmias:
interpretation and management, ed 3, St. Louis, 2002, Mosby.)

FIGURE 5-19 Torsade de pointes. Source: (From Aehlert B:

ECGs made easy: pocket reference, ed 2, St. Louis, 2002, Mosby.)

1181
FIGURE 5-20 Ventricular fibrillation. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1182
FIGURE 5-21 Idioventricular rhythm. Source: (From Aehlert B:
ACLS Study Guide, ed 3, St. Louis, 2007, Mosby.)

FIGURE 5-22 Asystole. Source: (From Huszar RJ: Basic

dysrhythmias: interpretation and management, ed 3, St. Louis, 2002,
Mosby.)

1183
FIGURE 5-23 First-degree AV block. Source: (From Huszar RJ:
Basic dysrhythmias: interpretation and management, ed 3, St Louis, 2002,
Mosby.)

1184
 FIGURE 5-24 Second-degree AV block (type I)
(Wenckebach). Source: (From Huszar RJ: Basic dysrhythmias:
interpretation and management, ed 3, St. Louis, 2002, Mosby.)

1185
 FIGURE 5-25 Second-degree AV block (type
II). Source: (From Huszar RJ: Basic dysrhythmias: interpretation and
management, ed 3, St. Louis, 2002, Mosby.)

1186
 FIGURE 5-26 Complete (third-degree) AV
block. Source: (Top, from Emergency Nurses Association: Sheehy’s
manual of emergency care, ed 6, St. Louis, 2005, Mosby. Bottom, from
Huszar RJ: Basic dysrhythmias: interpretation and management, ed 3, St.
Louis, 2002, Mosby.)

FIGURE 5-27 Ventricular demand pacemaker

(VVI). Source: (From Aehlert B: ECGs made easy: pocket reference, ed 2,
St. Louis, 2002, Mosby.)

1187
 FIGURE 5-28 Dual-chambered pacemaker. Source: (From
Aehlert B: ECGs made easy: pocket reference, ed 2, St. Louis, 2002,
Mosby.)

FIGURE 5-29 VVI pacemaker with failure to

capture. Source: (From Aehlert B: ECGs made easy: pocket reference,
ed 2, St. Louis, 2002, Mosby.)

FIGURE 5-30 VVI pacemaker with failure to

sense. Source: (From Aehlert B: ECGs made easy: pocket reference, ed
2, St. Louis, 2002, Mosby.)

Auscultation
If HF is present, heart sounds may include S3 and S4; basilar crackles
or rales are audible with lung auscultation; and a wet cough with
frothy sputum may be present. If atrial fibrillation or other

1188
dysrhythmias that prompt an irregular ventricular response are
present, the irregularity is audible with auscultation.

Palpation
With HF, jugular veins are distended and peripheral edema is
present. ECG rhythms reflecting an irregular ventricular response
will prompt an irregular pulse upon palpation. Electrical complexes
that resulted in decreased stroke volume will be reflected as a lesser
or absent pulse beat.

Diagnostic Tests: Cause(s) of Dysrhythmias

1189
Collaborative management
Care priorities

1. Identify the dysrhythmia and assess for symptoms

Diagnose the type of dysrhythmia and the effect of the rhythm on
the patient’s hemodynamic status. Rhythms resulting in
hypotension, respiratory distress, chest discomfort, or pulselessness
are considered unstable and require immediate management. When
evaluating rhythms, the following basic assessments can be made
before diagnosing the exact dysrhythmia:

Consciousness: Is the patient responsive or unconscious? If

unconscious, is he or she breathing? If not breathing, open the
airway and check the pulse. If still not breathing, and pulse is not
present, the patient is in cardiac arrest (regardless of rhythm) and
cardiopulmonary resuscitation (CPR) must be initiated while
another person obtains the cardiac monitor, defibrillator, or
automated external defibrillator (AED). An ECG rhythm is
sometimes present without a pulse (PEA).

1190
HR and rhythm: Too fast or too slow? Regular or irregular? When
the HR exceeds 150 or is less than 50 bpm, patients are more
likely to experience adverse effects. Fast rhythms include sinus
tachycardia, atrial tachycardia, atrial flutter, atrial fibrillation,
junctional tachycardia, and VT with a pulse. Slow rhythms
include sinus bradycardia, junctional rhythms, ventricular or
idioventricular rhythms, and second- and third-degree heart
blocks.

Appearance of QRS complexes: Wide or narrow? Tachycardias with

QRS that exceed 0.10 second in duration are more likely to
originate from the ventricles, unless the patient has reason to
have aberrant conduction or has a history of bundle branch block.

Presence of P waves/PR interval: Is there one P wave preceding

each QRS complex? Is the P wave normal in appearance? Is the
PR interval short, normal, or prolonged?

Stable or unstable vital signs and assessment: Unstable patients

require immediate management. Symptomatic bradycardia
resulting in hypotension may be best managed with
transcutaneous cardiac pacing if atropine is ineffective.
Symptomatic tachycardias may be best managed using
synchronized cardioversion. Pulseless patients with tachycardia
are managed with unsynchronized cardioversion/defibrillation.

Cardiopulmonary arrest: All patients receive CPR and IV or

intraosseous (epinephrine 1 mg immediately, and every 3 to 5
minutes throughout resuscitation). Vasopressin 40 mg may be
given instead of the first or second dose of epinephrine. Atropine
1 mg may be given to patients with slow-rate PEA or asystole
every 3 to 5 minutes up to 3 mg total dose. Patients with pulseless
VT or VF require immediate defibrillation.

1191
 FIGURE 5-31 Placement of the left and right chest
leads. Source: (From Aehlert B: ACLS study guide, ed 3, St. Louis, 2007,
Mosby.)

1192
 FIGURE 5-32 Posterior chest lead
placement. Source: (From Aehlert B: ACLS study guide, ed 3, St. Louis,
2007, Mosby.)

2. Determine the urgency of correcting the dysrhythmia

and whether drugs or electrical therapy is the most
appropriate approach for the patient
The more unstable the patient, the more aggressive the treatment.
There are situations wherein dysrhythmias do not readily respond
to treatment, requiring further evaluation. Some lethal
dysrhythmias may be resistant to correction, resulting in death.
Generally, electrical therapies provide almost immediate correction
of the instability associated with dysrhythmias, if the patient is able
to respond to treatment. Boluses of medications such as atropine,
adenosine, and ibutilide work quickly. Loading doses of
medications that are followed by infusions such as amiodarone or
diltiazem sometimes result in correction of rhythms but generally
require the medication infusion to attain full correction and
stability. Each patient’s situation must be managed using a

1193
thorough evaluation of his or her history and under the guidance of
the AHA guidelines for ACLS. A handbook of emergency cardiac
care for health providers is updated regularly to reflect current
research. The resource includes information reviewed by AHA
Committee on Emergency Cardiovascular Care, and Subcommittees
on Basic Life Support, Pediatric Resuscitation, and Advanced
Cardiac Life Support.

3. Provide pharmacologic management to correct

dysrhythmias if recommended as the first strategy by ACLS
guidelines
Management of dysrhythmias is based on providing and/or
balancing electrolytes, catecholamines, and other regulators of the
cardiac cycle. Provision of antidysrhythmic drugs is done using an
antidysrhythmic drug classification system, which has evolved
from the original Vaughan Williams classification system. Toxic
levels of any antidysrhythmic medication can prompt
development of different and sometimes lethal dysrhythmias. All
antidysrhythmic agents have the potential for proarrhythmic effects
(Box 5-4).

Box 5-4
ANTIDYSRHYTHMIC DRUGS
Class I (sodium channel blockers)
Block the rapid, inward sodium current. Local anesthetics and
other drugs that decrease automaticity of ventricular conduction,
delay ventricular repolarization, decrease conduction velocity,
increase conduction via AV node, and suppress ventricular
automaticity. Class IA decreases depolarization moderately and
prolongs repolarization. May prolong the QT interval. Class IB
decreases depolarization and shortens repolarization. Class IC
significantly decreases depolarization with minimal effect on
repolarization.
Class IA Class IB Class IC
Disopyramide (PO) Lidocaine (IV, IM) Encainide (PO)
Procainamide (PO, IV, IM) Mexiletine (PO) Flecainide (PO)

1194
Quinidine (PO, IV) Phenytoin (PO) Propafenone (PO)
Tocainide (PO)

Moricizine (PO)

Class II (beta-adrenergic blockers)

Block stimulation of beta1 and beta2 receptors by catecholamines.
Slow sinus node automaticity and conduction via AV node, control
ventricular response to supraventricular tachycardias, and shorten
the action potential of Purkinje fibers.
Acebutolol (PO) Carvedilol (PO) Oxyprenolol (PO)*
Atenolol (PO) Esmolol (IV) Penbutolol (PO)
Betaxolol (PO) Labetalol (PO, IV) Pindolol (PO)
Bisoprolol (PO) Metoprolol (PO,IV) Propranolol (PO, IV)
Carteolol (PO) Nadolol (PO, IV) Timolol (PO, IV)

Class III (potassium channel/1K1 blockers)

Block the outward current of potassium. Increase the action
potential and refractory period of Purkinje fibers, increase
ventricular fibrillation threshold, restore injured myocardial cell
electrophysiology toward normal, and suppress reentrant
dysrhythmias. May prolong the QT interval.
Amiodarone (PO, IV) Bretylium (IV, IM) Ibutilide (IV)
Azimilide (PO) Dofetilide (PO) Sotalol (PO, IV)

Class IV (calcium channel blockers)

Depress automaticity in the SA and AV nodes, block the slow
calcium current in the AV junctional tissue, reduce conduction via
the AV node, and are useful in treating tachydysrhythmias caused
by AV junctional reentry.

Diltiazem (PO, IV)

Verapamil (PO, IV)

Unclassified
Depress activity of the AV node.

Adenosine (IV)

1195
* Available in Great Britain.
AV, Atrioventricular; IV, intravenous; IM, intramuscular; PO, by mouth; SA, sinoatrial.

4. Provide therapy for rapid hrs using current ACLS

guidelines to manage ventricular tachycardias
(monomorphic and polymorphic), ventricular fibrillation,
and supraventricular tachycardias (atrial tachycardia,
junctional tachycardia, atrial flutter, or atrial fibrillation)
Defibrillation and cardioversion: Delivery of electrical shocks to
the heart through the chest wall via use of an external defibrillator
used to convert symptomatic, rapid atrial, or ventricular rhythms to
sinus rhythm. Shocks may be synchronized (cardioversion) with the
patient’s R waves (QRS complexes) or may be given as
random/unsynchronized (defibrillation) countershocks. The
operator must set the desired amount of electricity, apply the
defibrillator paddles with conductive gel or hands-free gel patches
to the patient’s chest, and discharge the device. Defibrillators also
provide the ability to provide electrical therapy “hands free.” A
special cable and multifunction/defibrillator pads are used instead
of the conventional paddles.

• The placement of the pads or paddles is critical to deliver the

electrical therapy to the heart muscle. The two pads are placed
either on the anterior chest with one beneath the right clavicle
and one on the left chest near the lower aspect of the heart, or
with one pad over the heart anteriorly, and the other on the
patient’s back over the posterior side of the heart. Pads/paddles
should not be placed over the larger bones (sternum and clavicle
anteriorly, scapula and spinal column posteriorly), medication
patches, or implanted electrical devices, including pacemakers
and ICDs. Medication patches should be removed and residual
medication wiped off. Defibrillators may use monophasic or
biphasic technology. Biphasic defibrillation requires lower energy
settings than recommended for monophasic defibrillation.
Synchronized cardioversion also requires the additional step of

1196
 synchronizing the patient’s R waves with the cardioverter; lower
energy is also required to convert the rhythm to NSR.

• Defibrillation: Used for ventricular tachycardias

without a pulse and ventricular fibrillation. Patients
are in full cardiopulmonary arrest when
defibrillation is used. Recommendations change for
how electrical therapy should be performed. The
energy sequence for biphasic defibrillators is
initially 120 to 200 joules (manufacturer guidelines
provide recommendations) followed by 2 minutes
of CPR, then 300 joules followed by 2 minutes of
CPR, then 360 joules (AHA, Advanced Cardiac Life
Support guidelines, 2011). Torsades de Pointes is
generally paroxysmal. Defibrillation should be used
as a last resort, after managing the cause of
prolonged QT syndrome.

• Cardioversion: Used for all types of tachycardia

with a pulse present, when patients have unstable
vital signs or a high risk of developing unstable
vital signs. Can be scheduled in advance for
patients with a high risk of developing unstable
vital signs. Short-acting sedation is used before
discharging the energy, to render the patient
unaware of the pain produced by the electrical
shock received. The energy sequence may vary
slightly for various tachycardias and
recommendations change but, in general, it begins
with 50 to 100 joules, followed by 200 joules, then
300 joules, then 360 joules. Energy is always

1197
 increased with subsequent shocks (AHA Advanced
Cardiac Life Support Guidelines, 2011.

Defibrillation (Unsynchronized Cardioversion)

Providers must clear the area by shouting “clear” before pressing
the button to discharge the defibrillator. Ensure no one else is
touching the patient/bed as shock is delivered. Anyone in contact
with the bed is at risk of receiving the electrical shock. All fluids in
contact with the patient should be considered electrical conductors.
Every attempt must be made to wipe or dry fluids from the area
surrounding the patient. It is unsafe to defibrillate or cardiovert a
patient who is in a pool of liquid (water, therapeutic fluids, or body
fluids) unless the care providers are NOT in contact with the fluids.

Synchronized cardioversion
The defibrillator will not discharge the energy until R wave
synchronization is achieved, which sometimes takes several
seconds. Providers need to exercise extreme caution to remain
“clear” and not touch the patient, bed, or anything connected to the
patient until the energy is delivered.

• AED: Defibrillation technique designed to provide ECG

interpretation needed for the device to determine the need for
electrical therapy. The device will give a series of voice prompts
instructing the operator on how to connect the cable and apply
defibrillator pads, assess the patient, and clear the area when the
device analyzes the rhythm. When finished analyzing, the device
will either automatically discharge if appropriate (fully
automatic) or ask the provider to press a button to discharge if
appropriate (semiautomatic). When providing basic life support,
the sequence of actions includes defibrillation as the fourth step,

1198
 after ensuring a patent airway, providing manual ventilation if
breathing is absent, and providing cardiac compressions if the
pulse is absent. The operator must be able to assess for
pulselessness and apnea, along with applying hands-free
defibrillator pads in the proper position at the right sternal
border and anterior axillary line, fifth intercostal space. If
healthcare providers are using the AED, the anterior-posterior
pad position may also be used.

AEDs
Not all automated external defibrillators are programmed per
current ACLS guidelines. Some still deliver three stacked shocks
(per older ACLS guidelines) when it is time to defibrillate, rather
than the currently recommended one shock. If a healthcare
provider comes across this type of defibrillator, the provider is
generally advised to follow the instructions and not interrupt the
cycle. Interruption may cause the device to malfunction, resulting
in the patient not receiving any further electrical therapy, or the
device ceasing to give associated instructions regarding the proper
steps of resuscitation.

• Life vest “wearable” cardioverter-defibrillator: The first

defibrillator worn outside the body rather than implanted in the
chest with continuous cardiac monitoring to detect life-
threatening dysrhythmias, including VT and VF. The device uses
nonadhesive sensing electrodes. If a life-threatening rhythm is
detected, the device alerts the patient before delivering the shock,
which allows time for a conscious patient to disarm the device
before the shock. If the patient is conscious, the shock may not be
necessary. If the patient is unconscious, the device releases a gel
over the therapy electrodes and delivers the shock. The device is
designed for home use, rather than as part of hospital
management. The device may be used as a “bridge” to ICD
implantation while patients are evaluated for appropriateness of
the therapy.

1199
• ICD: A battery-powered pulse generator (electrical device)
implanted into the pectoral area, with a lead system and shocking
coil positioned inside the heart and superior vena cava, which
can recognize and terminate potentially lethal dysrhythmias.
Risks and complications of thoracotomy versus nonthoracotomy
implantation are outlined in Table 5-14. Newer, third-generation
devices do not require thoracotomy for insertion. The devices are
smaller and lighter, allowing prepectoral implantation. These
devices may also provide antitachycardia pacing (ATP), low-
energy cardioversion, high-energy cardioversion,
antibradycardia pacing, and high-energy defibrillation along
with the ability to score performance data. Algorithms for
treatment of recognized dysrhythmias are programmed into the
device. Maximal energy output is 30 to 40 joules, which can
defibrillate malignant or lethal rhythms such as pulseless
ventricular tachycardia and ventricular fibrillation. Magnets may
be used for emergency deactivation/activation or suppression of
all or part of programmed therapies in newer devices. If the
patient has a combination ICD/pacemaker, the magnet will
deactivate the ICD and change from demand (discharges
electrical impulses or “fires” as needed to maintain the selected
HR) pacing to fixed mode (discharges the selected number of
impulses per minute, regardless of the patient’s underlying heart
rhythm). When the device discharges or fires, the patient’s status
should be documented in the medical record.

Table 5-14
IMPLICATIONS FOR PATIENT CARE AND COSTS: IMPLANTABLE
CARDIOVERTER-DEFIBRILLATORS (ICDs)

1200
 Immediate intervention is required for a device that is not
delivering appropriate therapy. If the device does not deliver
therapy, external cardioversion can be used. A patient with an
implantable cardioverter defibrillator (ICD) who has a sustained
hemodynamically unstable ventricular rhythm should be treated
exactly as one who does not have an ICD. The placement of the
external pads should not be over the ICD generator. When
inappropriate firing occurs in the absence of a treatable
dysrhythmia, there is a high probability that an ICD lead has
become dislodged, a connection has become loose, or the device
sensitivity setting is too “low,” which causes the device to respond
“too soon” to certain rhythm changes.

• Catheter ablation: Before ablation, an electrophysiology study is

done to evaluate the electrical activity of the heart. The “electrical
map” guides the placement of the ablation catheters, which are
placed in the heart during cardiac catheterization. The energy
stimulus is then applied to the area in which the dysrhythmia
originates or where an accessory pathway (bypassing AV node
during conduction) is located. The energy causes controlled,
localized necrosis of the area and may be applied via
radiofrequency, thermal (heat), or cryo (cold) catheters. Bypass
tracts (WPW) that produce AV reciprocating tachycardias and
reentrant pathways that produce AV nodal reentrant
tachycardias can be ablated to modify the heart tissue and stop

1201
 abnormal rapid conduction in these areas, which produces
supraventricular tachycardia. Ablation can be done as adjunctive
therapy for management of monomorphic VT, following
placement of an ICD to enhance rhythm control. Postablation
assessment of the patient involves careful monitoring of the
cardiac rhythm, vital signs, catheter insertion sites, LOC, and
peripheral pulses. Complications include cardiac perforation,
cardiac tamponade, coronary artery spasm, cerebral or
pulmonary embolus, bleeding, thrombosis, and dysrhythmias
including AV blocks.

• Specific tachycardias:

• Sustained monomorphic VT: The VT ECG tracing

has a regular rhythm, the QRS shape is wide and
uniform, and the ventricular rate ranges from 130 to
250 bpm. The impulse is generated either from a
single site of increased automaticity on one of the
ventricles or is because of reentry. Scarring from
prior MI often provides the setup for reentry, as the
impulse attempts to travel around the infarcted
tissue. Patients may be hemodynamically stable or
may be pulseless, so proper assessment is crucial in
deciding on therapy. Options for treatment include
antidysrhythmic medication (amiodarone 150 mg
IV over 10 minutes, repeated once if needed and
followed by a continuous IV infusion at 0.5 mg/min;
total dose should not exceed 2.2 g in 24 hours).
Synchronized cardioversion is used for unstable
tachycardia (hypotension or chest discomfort
accompanies the rapid HR). Defibrillation is used if
the patient is unconscious, apneic, and pulseless
(cardiac arrest), with 120 to 200 joules using a

1202
 biphasic defibrillator (or 360 joules using a
monophasic device), along with CPR and advanced
life support measures. See ACLS guidelines for
tachycardia with pulses or pulseless arrest for
specific management algorithms.

• Sustained polymorphic VT includes Torsades de

Pointes: Appears as a series of somewhat irregular,
multishaped wide QRS “twisting” around the
isoelectric line as seen on the ECG. It is important to
try to determine if the patient’s QT interval was
normal or prolonged just before the tachycardia
ensued. If the QT interval was normal before onset
of the tachycardia, the rhythm is simply called
polymorphic VT. If polymorphic VT is sustained
and the patient is symptomatic because of the
tachycardia, treat any ischemia, correct electrolyte
imbalances, and manage using guidelines for
monomorphic VT. If the QT interval was
prolonged, the patient has a particular type of
polymorphic VT called torsade de pointes (TdP).
Abnormal levels of potassium, magnesium, and
calcium may contribute. Acquired TdP is usually
related to drug toxicity or electrolyte abnormalities,
or myocardial ischemia. Many patients with TdP
experience cardiac arrest immediately. Regardless,
when TdP is sustained and the patient is
symptomatic, discontinue any medications
(particularly continuous infusions) that may
prolong the QT interval; correct electrolyte
abnormalities; initially give magnesium sulfate IV if

1203
 the patient is stable; if the patient is unstable,
attempt defibrillation as for VF. These patients may
be resistant to defibrillation. If the patient continues
to experience TdP, an agent such as isoproterenol
may be infused to increase the HR, thereby
shortening the QT interval. This may be especially
necessary if TdP is caused by medications with a
long half-life. Antidysrhythmic drugs including
class 3 amiodarone and sotalol prolong the QT
interval and, like class 1 agents (e.g., quinidine,
disopyramide), are proarrhythmic. Initiate a
magnesium infusion if not done initially. Other
drugs, including certain antibiotics and
antihistamines, may promote polymorphic VT,
particularly when used in combination. Congenital
causes include long-QT syndrome, Brugada
syndrome (possibly congenital), and
catecholaminergic polymorphic VT.

• Atrial fibrillation: Atrial fibrillation with rapid

ventricular response may result in progressive
ventricular dysfunction and decreased CO. The
“quivering” atria are not contracting, so the atrial
contribution to ventricular filling is lost. Blood
stagnates in the atria, often resulting in clot
formation. Platelet activation occurs, making
thromboembolic complications possible when the
atria once again contract. The goal of therapy is to
convert the rhythm to NSR as soon as possible
unless the atrial fibrillation is chronic. Those with
sustained, new-onset atrial fibrillation who become

1204
unstable (signs of decreased CO, congestive HF, or
ACS) or become hemodynamically unstable are
generally managed with synchronized
cardioversion. Atrial fibrillation may occur post-
CABG, producing CO compromise and danger of
stroke. Rate control to slow the rapid ventricular
response can be achieved by diltiazem. Loading
dose is 0.75 mg/kg IV followed by a continuous
infusion at 5 mg/h. If atrial fibrillation reoccurs or
persists over a 24-hour period, warfarin
anticoagulation for 4 weeks will be needed. For
patients with normal QTc interval, immediate
chemical conversion might be attained using
ibutilide, 1 mg diluted in 10-mL IV solution given
over 10 minutes, and repeated once if atrial
fibrillation has been present for less than 48 hours.
Ibutilide is reserved for patients with a normal QTc
interval to avoid lethal ventricular dysrhythmias
following administration. An alternative is
amiodarone in a loading dose of 150 mg IV over 10
minutes followed by 1 mg/min drip for 6 hours and
then 0.5 mg/min drip for 18 hours. For chronic atrial
fibrillation patients, conversion to NSR without
anticoagulation is not a goal because of the risk of
atrial thrombus formation and possible
embolization. If synchronized cardioversion is
needed during the immediate postoperative period
and anticoagulation is not an option, Doppler or
transesophageal echocardiography may be used to
check for atrial thrombus formation. In addition to

1205
 cardioversion, other nonpharmaceutical treatments
for atrial fibrillation include AV node and focal
ablation, surgical correction such as the Maze
procedure, and implanted permanent pacing with
atrial fibrillation suppression algorithms.

5. Provide electrical therapy (cardiac pacing) to support

unstable patients with slow HRs, and some rapid HRs if
recommended as the most appropriate strategy by current
ACLS guidelines
Management of symptomatic bradycardias includes heart blocks,
slow junctional rhythms, and idioventricular rhythms or certain
tachycardias (antitachycardia pacing) including atrial flutter, atrial
tachycardia, reentrant tachycardias, and WPW. Cardiac pacing can
be provided temporarily or permanently.

• Permanent cardiac pacing: A battery-powered device is

implanted to provide an artificial pacing or electrical pacing
stimulus for the heart. It is used for problems with either
automaticity or conduction to either generate an appropriate
number of pacing impulses or facilitate conduction of the
impulses to all areas of the heart in a coordinated fashion to
facilitate increased CO. Although most often used for
management of symptomatic bradycardias including second- and
third-degree heart block, it may also be used for patients with
ventricular asynchrony (RV and LV contraction is
uncoordinated). Specialized devices may also be used to correct
rapid atrial and ventricular rhythms via ATP. Third-generation
ICDs may also be programmed for cardiac pacing. Pacemakers
are named or coded based on the functions they are able to
perform (Table 5-15). If CO is disturbed by ventricular
asynchrony, biventricular pacing or cardiac resynchronization
therapy (CRT) may be used. CRT is recommended for patients
with LVEF ≤ 35%, a QRS duration ≥ 0.12 second, and a sinus
rhythm. CRT may also have an ICD added for treatment of

1206
 patients with New York Heart Association (NYHA) functional
class III or ambulatory class IV HF symptoms.

• Temporary cardiac pacing: Temporary pacing can be done using

transthoracic, transcutaneous pacing pads applied to the skin on
the chest (may be a dual pad used for either pacing or
cardioversion [synchronized and unsynchronized]), via
transvenous catheter insertion with positioning of leads into the
endocardium, via a specialized pulmonary artery catheter with
the capacity for transvenous cardiac pacing, or via surgically
inserting epicardial wires with leads during open heart surgery.

Patients in critical care often have electrolyte disturbances,

are receiving antidysrhythmic medications, and are in acute
coronary syndrome, acid-base imbalance, or hypotension/shock
states. All of these conditions may alter the ability of the cardiac
muscle to respond to a pacing stimulus and loss of capture may
occur. Vigilance in watching for proper pacemaker function
(pacing, capture, and sensing) is warranted in both temporary and
permanent pacing.

Table 5-15
NBG PACEMAKER CODES

NASPE, North American Society of Pacing and Electrophysiology.

1207
’• Temporary epicardial pacing: Placement of temporary pacing
wires on the epicardial surface of the heart while the chest is open
during cardiac surgery so that cardiac pacing can be used in the
postoperative period. Usually two atrial and two ventricular
wires (pacing and ground wires) are attached to the outside
surface of the heart and exit through the skin incision allowing
attachment to a temporary pacing generator. The exposed pacing
wires may be capped and later connected to a generator if pacing
is needed. The end of the leads, connection points, and pacing
generator terminals should be protected and insulated from
electrical microshock. The temporary pacing wires are removed
when no longer needed by slowly and gently pulling them out
through the skin. The patient is monitored carefully after the
pacing wires are removed for dysrhythmias, cardiac tamponade,
hemorrhage, hematoma, and hemodynamic changes. If left in for
a prolonged period of time, tissue may adhere to the wires and
the provider may elect to cut the external wires at the level of the
skin. The skin will then grow over the entry points and heal.

• Atrial overdrive pacing: ATP is used to control or terminate

supraventricular dysrhythmias including atrial flutter, atrial
tachycardia, reentrant tachycardias, and WPW. Atrial flutter and
reentrant supraventricular tachycardias often result from
electrical pathways or circuits set up around scarred or infarcted
tissue. Using atrial pacing wires (transvenous or epicardial)
connected to a pulse generator (pacemaker), the atria are rapidly
paced by rapid bursts of electrical impulses during a 10- to 30-
second period. The pacing rate selected is usually 20% to 30%
faster than the rate of the tachydysrhythmia being treated.
Successive bursts are performed at gradually increasing rates
until termination of the tachycardia is achieved. The short bursts
of rapid pacing create refractory cardiac tissue that interrupts the
reentry circuit.

Special care is given to proper connection of the atrial wires

and to ensure against microshock. Rapid pacing of the atria can

1208
result in ventricular tachycardia or ventricular fibrillation.

• Transcutaneous, transthoracic cardiac pacing: Cardiac pacing

performed with a device that delivers electrical stimulation to the
heart via two conductive pads applied to the skin of the chest,
positioned either anteriorly or over the anterior and posterior
walls of the heart. Certain defibrillators include a capability for
transcutaneous cardiac pacing. One pad is near the left sternal
border and the other is near the left paraspinal line beneath the
scapula for anterior-posterior position or in the same areas used
for hands-free defibrillator pads in the proper position at the
right sternal border and anterior axillary line, fifth intercostal
space. Resistance of all muscles and bones of the chest wall must
be overcome for impulses to reach the heart, requiring a higher
milliampere to be used. Transcutaneous pacing will cause the
muscles of the chest and back to contract, which can be quite
uncomfortable for the patient, and sedation may be required.

The pads cannot both sense and pace; therefore, the device
includes an electrocardiogram (ECG) monitor so that efficacy
(capture) of pacing can be assessed. Leads should be applied to the
chest in addition to the pads to assess capture. Capture should
reflect that the level of electrical stimulation (mA) provided was
able to prompt ventricular contraction. The ECG tracing generally
becomes larger and wider when capture is achieved. When pacing
is effective, the patient’s vital signs should improve. If the level of
energy needed to achieve capture is high, sedation may be
necessary for the patient to tolerate transcutaneous cardiac
pacing.

6. Provide surgical procedures to help control dysrhythmias

1209
• LV aneurysmectomy and infarctectomy: Excision of possible focal
spots of ventricular dysrhythmias.

• Myocardial revascularization: Performed alone or in conjunction

with electrophysiologic mapping, with excision or cryoablation of
the dysrhythmia focus. Newer surgical techniques are less
invasive than the standard median sternotomy approach.

• Maze procedure: Surgically placed incisions arranged in a pattern

resembling a Maze in the atria to eliminate atrial fibrillation.
Some Maze procedure variations use both surgical incisions and
ablation of cardiac tissue in the electrophysiology laboratory
(convergence procedure).

• Stellate ganglionectomy and block: Alters the electrical stability of

the myocardium. Surgical option to treat inherited long-QT
interval and predisposition to ventricular dysrhythmias.

7. Initiate anticoagulation for patients at higher risk for

development of blood clots within the heart secondary to
dysrhythmias that decrease either atrial or ventricular wall
motion
Use of warfarin and/or platelet inhibitors (e.g., ticlopidine,
clopidogrel) may be recommended.

8. Explain the content of dietary guidelines designed to help

reduce stimulants normally consumed
Patients with recurrent dysrhythmias are usually placed on a diet
that restricts or reduces caffeine and sodium and is low in fat and
cholesterol (see Tables 5-5, 5-16, and 5-17). Dietary guidelines for
patients at risk for or with heart disease require constant vigilance
to stay informed of current recommendations. The DASH diet and
the AHA diets (Mediterranean diet) outline other options that have
proven successful in managing patients.

Care plans for dysrhythmias and conduction

disturbances

1210
Decreased cardiac output 
related to altered rate, rhythm, or conduction or negative inotropic
changes secondary to cardiac disease.
Goals/Outcomes: Within 15 minutes of development of serious
dysrhythmias, the patient has adequate CO as evidenced by BP at
least 90/60 mm Hg or baseline, HR 60 to 100 bpm, and NSR on
ECG. CVP is less than 7 mm Hg, and CO is 4 to 7 L/min.
Circulation Status

Cardiac care

1. Monitor the patient’s heart rhythm continuously; note BP and

symptoms if dysrhythmias occur or increase in occurrence.

2. If a PA catheter is present, note PAP, PAWP, and RAP; monitor

for reduced CO in response to dysrhythmias.

3. Document dysrhythmias with a rhythm strip. Use a 12/15/18-lead

ECG as necessary to identify the dysrhythmia.

4. Monitor patient’s laboratory data, particularly K+, Mg2+, glucose,

and digoxin levels.

5. Administer antidysrhythmic agents as prescribed; note patient’s

response to therapy.

6. Provide oxygen as prescribed. Oxygen may be beneficial if

dysrhythmias are related to ischemia.

7. Maintain a quiet environment, and administer pain medications

promptly. Both stress and pain can increase sympathetic tone and
cause dysrhythmias.

8. If life-threatening dysrhythmias occur, initiate immediate

unit protocols or standing orders for treatment, as well as CPR and
ACLS algorithms as necessary.

9. When dysrhythmias occur, stay with patient; provide support

and reassurance while performing assessments and administering

1211
treatment.

10. Administer inotropic agents (see Appendix 6) as prescribed to

support patient’s BP and CO.

Hemodynamic Regulation; Medication Management; Oxygen

Therapy; Respiratory Monitoring; Vital Signs Monitoring

Risk for activity intolerance 

related to imbalance between oxygen supply and demand secondary to
dysrhythmias that reduce cardiac output.
Goals/Outcomes: During activity, the patient rates exertion less
than 3 on a scale of 0 to 10 and exhibits tolerance of the
dysrhythmia by an RR less than 20 breaths/min, systolic BP within
20 mm Hg of baseline, HR within 20 bpm of resting HR, and
absence of chest discomfort and/or new dysrhythmias.
Activity Tolerance; Endurance; Energy Conservation

Energy management

1. Monitor patient’s response to activity. Instruct patient to report

chest discomfort and SOB. Note new dysrhythmias associated with
activity or other stressors.

2. Administer medications as prescribed.

3. Observe and report signs of acute decreased CO, including

oliguria, decreasing BP, altered mentation, and dizziness.

4. Monitor BP and other vital signs frequently, and as soon as

possible report to the advanced practice provider changes such as
irregular HR, HR greater than 120 bpm, or decreasing BP.

5. Assess integrity of peripheral perfusion by monitoring peripheral

pulses, distal extremity skin color, and urinary output. Report
changes such as decreased pulse amplitude, pallor or cyanosis, and
decreased urine output.

Activity Therapy; Cardiac Care; Surveillance

1212
Deficient knowledge of disease process or other
mechanisms by which dysrhythmias occur 
related to lifestyle implications.
Goals/Outcomes: Within the 24-hour period before discharge
from critical care, the patient and significant others verbalize
knowledge about causes of dysrhythmias and the implications for
modification of patient’s lifestyle.
Knowledge: Disease Process; Knowledge: Health Promotion;
Knowledge: Medication

Teaching: Individual

1. Discuss causal mechanisms for dysrhythmias, including resulting

symptoms. Use a heart model or diagrams as necessary.

2. Teach the signs and symptoms of dysrhythmias that necessitate

medical attention: unrelieved and prolonged palpitations, chest
pain, SOB, rapid pulse (greater than 150 bpm), dizziness, and
syncope.

3. Teach the patient and significant others how to check pulse rate
for 1 full minute.

4. Teach the patient and significant others about medications that

will be taken after hospital discharge, including drug name,
purpose, dosage, schedule, precautions, and potential side effects.
Stress that the patient will be maintained on long-term
antidysrhythmic therapy and that it could be life-threatening to
stop or skip these medications without physician approval, because
doing so may decrease blood levels required for dysrhythmia
suppression.

5. Advise the patient and significant others about the availability of

support groups and counseling; provide appropriate community
referrals. Patients who survive sudden cardiac arrest may
experience nightmares or other sleep disturbances at home. Explain
that anxiety and fear, along with periodic feelings of denial,
depression, anger, and confusion, are normal following this
experience.

1213
6. Stress the importance of leading a normal and productive life,
even though the patient may fear breakthrough of life-threatening
dysrhythmias. If the patient is going on vacation, advise him or her
to take along sufficient medication and to be aware of healthcare
facilities in the vacation area.

7. Advise the patient and significant others to take CPR classes;

provide addresses of community programs.

8. Teach the importance of follow-up care; confirm date and time of

next appointment, if known. Explain that outpatient Holter
monitoring is performed periodically.

9. Explain that individuals with recurrent dysrhythmias should

follow a general low-fat, low-sodium, and low-cholesterol diet (see
Tables 5-5, 5-16, and 5-17) and reduce intake of products containing
caffeine, including coffee, tea, chocolate, and colas. Dietary
guidelines are dynamic. New recommendations frequently emerge.
Patients may benefit from knowing changes in the
recommendations, and more than one diet may be successful in
preventing cardiovascular disease.

10. As indicated, teach patient relaxation techniques or guided

imagery, which will reduce stress and enable patient to decrease
sympathetic tone (see Appendix 7).

Surveillance; Teaching: Prescribed Medication; Vital Signs

Monitoring

Ineffective health maintenance 

related to ineffective stress management and inability to relax.
Goals/Outcomes: Within the 24-hour period after instruction, the
patient verbalizes and demonstrates the following relaxation
technique.
Health Promoting Behavior; Health-Seeking Behavior

Anxiety reduction

1. Explain that to decrease sympathetic tone, some patients with

1214
dysrhythmias may benefit from practicing a relaxation response.
Many different techniques can be used, including use of breathing
alone or in conjunction with muscle group contraction and
relaxation. Other techniques incorporate use of imagery.

2. Teach the patient a relaxation technique effective for stress

reduction and facilitation of ability to take deep breaths slowly to
relax. See Appendix 7 for a sample relaxation technique.

Calming Technique; Meditation; Music Therapy; Simple

Guided Imagery; Simple Relaxation Therapy; Teaching: Prescribed
Activity/Exercise

For patients with an ICD and/or permanent pacemaker

Deficient knowledge: 
ICD or related to pacemaker insertion procedure and follow-up
care.
Goals/Outcomes: Within the 24-hour period before the
procedure, the patient and significant others describe rationale for
the procedure and method of insertion. Within the 24-hour period
before discharge from ICU, the patient and significant others
describe postinsertion care and need for continued advanced
practice provider follow-up.
Knowledge: Illness Care

Teaching: Procedure/treatment

1. Assess patient’s understanding of his or her medical condition

(dysrhythmias) and the amount of detailed information desired.

2. Discuss the following with the patient and significant others:

• Type of dysrhythmia the patient has, using rhythm

strip and heart model or
drawings/illustrations/charts to promote
understanding.

1215
• Possible need for temporary transvenous pacemaker
insertion before ICD or permanent pacemaker
procedure.

• Use of appropriate anesthesia throughout

procedure.

• Testing of the ability of the device to control lethal

dysrhythmias, which will occur in the operating
room/catheterization laboratory after implantation
and before the incision is closed.

• Reassurance that should the mechanism fail to

control the dysrhythmia, the device can be adjusted
or reprogrammed to do so.

• Continuous observation of patient in a CCU for

about 24 hours, with ongoing monitoring of BP,
HR, and RR.

• Importance of deep breathing, coughing (as

necessary), and incentive spirometry exercises as
appropriate. Explain that patient is at increased risk
for respiratory tract and incisional infection if
thoracic surgery was done, which tends to cause
patient to avoid deep breathing and coughing to
guard against pain. Have patient return
demonstrations of breathing exercises. Reassure
patient that analgesics can be administered before
pulmonary toilet exercises, if needed.

1216
• No lifting of arm above level of shoulder for at least
4 weeks; may resume showering at 72 hours.

• Discharge instructions: Follow-up visit within 10 to

14 days, need for obtaining an AED/home
defibrillator, and importance of CPR/defibrillator
classes for significant others.

3. Describe the procedure should ICD device deliver a shock. If the

patient is aware of the shocks, the advanced practice provider
should be notified as soon as possible that the device is firing. With
newer devices, patients may be unaware of shocks but may become
symptomatic (e.g., become intolerant of activity or dizzy, have chest
discomfort) with prolonged or serious dysrhythmias. Teach the
patient to record the number of shocks experienced.

4. Explain use of the AED/home defibrillator. These devices, which

are available commercially from several companies, are designed to
allow the nonmedical person or care providers untrained in
dysrhythmia interpretation to effect defibrillation and to convert
lethal dysrhythmias should the ICD fail. Provide information on
Life Vest (as appropriate.).

5. Explain that shocks during sinus rhythm may indicate a lead

fracture in the ICD system. Usually this is detected while the
patient is being monitored (e.g., by ECG in physician’s office, by
hospital monitor, or by Holter monitor).

Learning Facilitation; Learning Readiness Enhancement; Risk

Identification; Teaching: Disease Process; Teaching: Prescribed
Medication; Teaching: Psychomotor Skill

Risk for infection 

related to invasive procedure into thorax
Goals/Outcomes: Patient is free of infection as evidenced by
normothermia, WBC count 11,000/mm3 or less, negative culture
results, and absence of the clinical indicators of infection at the

1217
incision site and in the respiratory tract.
Infection Severity

Infection protection

1. Encourage and assist with deep breathing, coughing (if needed),

and incentive spirometry exercises every 2 hours, and encourage
early ambulation to the chair. As indicated, assist patient with
splinting the incision site with hands or pillow to promote pain
control. Administer prescribed analgesics 20 minutes before
scheduled breathing exercises. For more information, see this
nursing diagnosis in Acute Pneumonia, p. 373.

2. Assess incision site every 2 hours for warmth, erythema,

swelling, and drainage. The presence of a seroma, which has the
same symptoms as incision site infection, is confirmed by decubitus
chest radiograph studies or CT.

3. Monitor patient’s temperature every 2 to 4 hours, being alert to

elevation greater than 38.6° C (101.5° F).

4. Monitor CBC for elevation of WBCs.

5. Consult advanced practice provider for significant findings.

6. Teach the patient and significant others the signs and symptoms
of infection of both the incision site and the respiratory tract: cough,
sputum production, fever, dyspnea, chills, headache, myalgia.
Explain that the older adult with an infection may be confused and
disoriented and may run low-grade fevers even though few other
indicators are present.

Infection Control; Cough Enhancement; Exercise Promotion;

Surveillance; Medication Prescribing; Home Maintenance
Assistance

For patients with a pacemaker (temporary or

permanent) or patients with third-generation ICDs with
cardiac pacing

1218
Decreased cardiac output 
related to malfunction of cardiac pacemaker
Goals/Outcomes: Within the 24-hour period preceding hospital
discharge or throughout the duration of temporary cardiac pacing,
the patient has adequate CO as evidenced by systolic BP at least 90
mm Hg, RR 12 to 20 breaths/min, HR less than 100 bpm, urinary
output at least 0.5 mL/kg/h, warm and dry skin, and ECG indicative
of effective capture, sensing, response to sensing, and function of
antitachycardia pacing (if operational).
Circulation Status

Cardiac care: Acute

1. Recognize and document paced rhythms. Events to document

include the following: (1) recognition of pacing spike preceding P
wave and/or QRS complex as appropriate for settings; (2) sensing of
patient’s inherent pacing; (3) response of pacemaker when
triggering and/or inhibiting pacing; (4) response of HR to activity if
pacemaker is programmed “rate responsive”; and (5) initiation of
antitachycardia pacing or electric shock (with ICD) for
dysrhythmias.

2. Promptly detect problems with pacemaker functions. Include

assessment of potential electromagnetic interference (EMI) (Table 5-
18). Ensure that temporary pacemaker battery is still functional or
changed as needed, and that cable connectors for temporary
pacemakers are appropriately connected to the pulse generator
(pacemaker box). For problems with functions of permanent
pacemakers and ICDs, the advanced practice provider should be
notified immediately.

3. Provide electrical safety measures for temporary cardiac pacing

to include proper grounding and protection of exposed catheter tips
and/or heart wires. Caregiver must wear nonconductive gloves
when handling pacing lead wires/catheter so that microshocks are
avoided. Microshocks can induce lethal dysrhythmias.

4. Observe for complications of temporary pacing, which include

dysrhythmias, lead displacement or fracture, and lead perforation

1219
of the heart that could lead to cardiac tamponade, pericarditis,
infection, and bleeding.

5. Perform threshold checks per hospital policy.

Table 5-18
ELECTROMAGNETIC INTERFERENCE AND THE THIRD-
GENERATION ICDs AND SOME PROGRAMMABLE PACEMAKERS

Unsafe Hospital Safe Home

Unsafe Home Equipment: Use Caution
Procedures/Equipment Equipment
MRI (magnetic Large magnets: junkyards, construction sites, Microwave ovens
resonance imaging) other areas that may have large magnets
Nerve stimulator Hand-held wands at airport security Refrigerator
magnets
Electrocautery Bingo wands Electric blankets
Diathermy Certain slot machines Tanning bed
Lithotripsy Large stereo speakers (unsafe to carry) Riding
Cellular telephones lawnmower
High-tension wires Jacuzzi
Industrial transformers CB radio
Robotic jacks HAM radio
Arc welders (except for
Power generators in dams antennas)
Industrial motors Table saw
Large boat motors Gas welder
Electric drill
Weed eater
Small boat motors
ICD, Implantable cardioverter defibrillator.
Magnetic fields are measured in units (Gauss) or 1000th of a gauss, milliGauss
(mG). Ten Gauss will affect an ICD or some programmable pacemakers. Common
household electrical appliances (interferences) are less than 50 mG. Electrical fields
are measured in volts per meter. 750 V is approximately 30 J.

Dysrhythmia Management; Vital Signs Management;

Surveillance; Environmental Management: Safety

For patients with an ICD

Sexual dysfunction (or risk for same) 

related to fear of inducing dysrhythmias during sexual activity.
Goals/Outcomes: Within the 24-hour period before discharge
from the ICU, the patient and significant other verbalize
understanding of interventions during and alternatives for sexual
intercourse.

1220
 Sexual Identity; Role Performance

Sexual counseling

1. Ask patient to describe any symptoms of dysrhythmias during

presurgical sexual experiences.

2. Explain the following interventions or alternatives that can be

made if the patient continues to experience dysrhythmias during
sexual intercourse:

• Patient may need to take a less active role.

• Patient may find that taking a prescribed

vasodilator before engaging in sexual intercourse
will prevent dysrhythmias. Should be advised not
to take a vasodilator with NTG.

• Suggest that during periods when dysrhythmias are

a problem, less stressful forms of sexual activity,
such as caressing and hugging, are positive
alternatives.
3. As appropriate, advise patient that stressful situations, such as
extramarital relations or unfamiliar environment/partner, may
contribute to symptoms during sexual activity.

4. Explain that the device may shock at any time. If the patient’s
partner is in contact with the patient’s body at that time, the shock
may be experienced as a tingling sensation by the partner.

Teaching: Sexuality; Anxiety Reduction; Coping

Enhancement; Support Group

Additional nursing diagnoses

The patient with ICD is at risk for pneumothorax. As indicated, also

1221
see Pneumothorax, Chapter 4, for information related to this
disorder. Also see nursing diagnoses and interventions in
Hemodynamic Monitoring (Chapter 1) and Emotional and Spiritual
Support of the Patient and Significant Others (Chapter 2).

Hypertensive emergencies
Pathophysiology
A hypertensive emergency is present when severely elevated BP
results in end-organ damage. Severe hypertension adversely affects
the CNS, cardiovascular, and renal systems. Both malignant
hypertension and accelerated hypertension are considered
emergencies, and they have similar outcomes and management
strategies. Malignant hypertension is BP elevation with
encephalopathy or nephropathy with papilledema. Progressive
kidney failure and permanent blindness can occur if treatment is
not provided. Accelerated hypertension is defined as a recent
marked increase of BP over normal baseline pressure, associated
with end-organ damage. Vascular damage is seen on funduscopic
examination, including hemorrhages or exudates, but without
papilledema.
Hypertensive urgency is managed differently from hypertensive
emergency. Urgency is present when severely elevated BP is noted
(e.g., systolic BP greater than 220 mm Hg or diastolic BP greater
than 120 mm Hg) without end-organ damage. Signs and symptoms
include severe headache, severe anxiety, and SOB. BP can be
reduced within the subsequent 24 to 48 hours following diagnosis.
IV treatment of BP is not necessary. Oral treatment is satisfactory.
Hypertensive emergencies require immediate management to
reduce the BP. The patient may experience life-threatening signs
and symptoms, such as severe pulmonary edema, cerebral edema,
ischemia or hemorrhage of the brain, aortic dissection, AMI, and
eclampsia (during pregnancy). Immediate vascular necrosis is
possible if the diastolic pressure exceeds 120 mm Hg. Necrosis has
also manifested with MAPs greater than 150 mm Hg. Conversely,
no evidence suggests patients benefit from rapidly reducing BP in

1222
minutes to a few hours during hypertensive urgency. Aggressive
therapy may result in cardiac, renal, or cerebral perfusion deficits
resulting from low BP.
The morbidity and mortality of hypertensive emergencies
depend on the extent of end-organ damage when the patient
presents and subsequent BP control. Following a crisis, those with
BP control and medication compliance have a 10-year survival rate
of nearly 70%.
Hypertension causes more deaths and disease than any other
cardiovascular risk factor worldwide. Hypertension prompts
ventricular remodeling and increases the risk of heart attack, HF,
stroke, and kidney failure. The Eighth Joint National Committee (8)
did not define “hypertension,” but rather prescribed thresholds for
treatment applicable to all hypertensive populations except when
the evidence supported variance in a particular subgroup. The
guideline was submitted for external peer review in January 2013
by the National Heart, Lung, and Blood Institute (NHLBI) to 20
expert reviewers and 16 federal agencies. The guideline review
focused on 3 key questions surrounding management of adults
with hypertension: (1) Does initiating antihypertensive medications
at specific BP thresholds improve outcomes? (2) Do medications
targeted at a specific BP goal improve outcomes? (3) Do various
classes of medications differ in benefits vs harms reflected in the
outcomes? Lifestyle modifications were not revised, but rather,
were supported by endorsing the evidence-based recommendations
of the 2013 Lifestyle Work Group.
Following an exhaustive review of the literature, the following
nine recommendations emerged from JNC-8:

• For those older than 60 years of age, initiate drug therapy for
a systolic BP greater than 150 mm Hg and diastolic BP greater
than 90 mm Hg. Goal: Systolic BP less than 90 mm Hg, diastolic
BP less than 90 mm Hg.

Corollary Recommendation: Those in this age group

currently controlled at a lower BP do not need a
medication adjustment to allow for a higher BP.

1223
• For those younger than 60 years of age, initiate drug therapy for a
diastolic BP above 90 mm Hg. Goal: Diastolic BP less than 90 mm
Hg.

• For those younger than 60 years of age, initiate drug therapy for a
systolic BP above 140 mm Hg. Goal: Systolic BP less than 140 mm
Hg.

• For those older than 18 years of age with chronic kidney disease
(CKD), initiate drug therapy to keep systolic BP below 140 mm
Hg and diastolic BP below 90 mm Hg.

• For those older than 18 years of age with diabetes mellitus,

initiate drug therapy to keep systolic BP below 140 mm Hg and
diastolic BP below 90 mm Hg.

• In the general nonblack population, including those with diabetes

mellitus, initial medications to control BP should include a
thiazide-type diuretic, calcium channel-blocking agent, ACEI, or
ARB.

• In the general black population, including those with diabetes

mellitus, initial medications to control BP should include a
thiazide-type diuretic or calcium channel-blocking agent.

• In those older than 18 years of age with CKD, initial (or added)
medications should include an ACEI or ARB to improve kidney
outcomes. This applies to people of all races, with or without
diabetes mellitus.

• The main objective of hypertension treatment is to attain and

maintain goal BP. If goal BP is not achieved within 30 days, the
dose of the initial medication should be increased, or another
medication from one of the four recommended classes (thiazide
diuretic, CCB, ACEI, or ARB) should be added to the treatment
plan. If the goal BP is not reached using two antihypertensive
medications, a third drug may be added and titrated. If BP goal is
not reached using careful monitoring of BP with three drugs, a
drug from another class outside the four recommended classes

1224
 may be used. Referral to a hypertension specialist may be needed
when the patient’s BP is not controlled with three medications.

The risk of death from ischemic heart disease and stroke

increases in tandem with BP. The risk of heart attack or stroke
increases several times when hypertension exists with obesity,
smoking, high blood cholesterol levels, or diabetes. Patients with
comorbidities such as diabetes or CKD are at higher risk of the
cardiovascular complications of hypertension when systolic BP
exceeds 140 mm Hg or DBP exceeds 90 mm Hg.
Elevation of systolic versus diastolic BP is related to age. Systolic
BP and diastolic BP rise simultaneously until about 60 years of age,
after which systolic BP continues to increase, while diastolic BP
generally decreases. Age also affects the impact of systolic BP and
diastolic BP as risk factors for heart attack and stroke. For persons
younger than 60 years, diastolic BP is the main risk factor, while for
those older than 60 years, systolic BP is more important.

Pathophysiology
The pathophysiology of hypertensive emergencies is not well
understood. Initially, there is a failure of the normal autoregulation
and an abrupt rise in SVR. It is thought that the wall of a stressed
vessel causes the release of humoral vasoconstrictors, which
increases the SVR. The increased pressure within the vessel then
starts a cycle of endothelial damage, local intravascular activation
of the clotting cascade, fibrinoid necrosis of small blood vessels, and
release of more vasoconstrictors. The cycle of vascular injury leads
to tissue ischemia and autoregulatory dysfunction. Single-organ
involvement is found in approximately 83% of patients presenting
with hypertensive emergencies. Two-organ involvement is found in
14% of patients, and multiorgan involvement (more than three
organ systems) is found in approximately 3% of patients presenting
with a hypertensive emergency.
Hypertensive crisis can lead to hypertensive encephalopathy as
cerebral blood vessels dilate resulting from inability to affect
autoregulation. Cerebral autoregulation is the ability of the cerebral
vasculature to maintain a constant pressure or cerebral blood flow
(CBF). When autoregulation is disrupted, increased intercranial

1225
pressure and cerebral edema may result. Hallmark signs of
hypertensive encephalopathy include cerebral edema and
microhemorrhages, altered mental status, and papilledema. Blood
flow is increased, and the excessive pressure drives fluid into the
perivascular tissue, resulting in cerebral edema. The extreme
pressure can cause arteriolar damage, as demonstrated by fibrinoid
necrosis of the intima and media of the vessel wall. Although any
organ is vulnerable, the eyes and the kidneys are most likely to
suffer damage, leading to retinopathy, blindness, and renal failure.
Patients with hypertension who are admitted to the ICU may have
a rebound elevation of the BP if their usual antihypertensive
regimen is interrupted. In addition, a loss of BP control can occur
because of the nature of the primary disorder, trauma, or the stress
of being in the ICU.
Patients also have increased cerebrovascular resistance and are
more prone to ischemia when the BP decreases. Normotension
achieved with BP control may result in decreased CBF. Rapid rises
in BP can cause hyperperfusion with an increased CBF. The
rapidity of the rise in pressure may be more destructive than the
level of BP elevation. The 1-year mortality rate is 79% for patients
with untreated hypertensive emergencies. The 5-year survival rate
among all patients with treated hypertensive crisis is approximately
74%. Progressive stiffness occurs in the arteries, which increases
systolic BP, resulting in a widened pulse pressure, which decreases
coronary perfusion pressures, increases myocardial oxygen
consumption, and causes the left ventricle to enlarge. The
remodeled left ventricle is unable to compensate for an acute rise in
SVR, leading to LV failure, pulmonary edema, and myocardial
ischemia. Small renal arteries exhibit endothelial dysfunction and
impaired vasodilation, which affects renal autoregulation. Once the
renal autoregulatory system is disrupted, the intraglomerular
pressure varies directly with the systemic arterial pressure. The
kidney is no longer protected from fluctuations in perfusion caused
by BP changes, resulting in acute renal ischemia during a
hypertensive crisis.

Assessment

1226
Goal of assessment
The history and physical examination determine the nature,
severity, and management of the hypertensive event. Patients
should be questioned regarding compliance with antihypertensive
drug therapy, intake of over-the-counter preparations and
sympathomimetic agents, and illicit drug use. Identifying the
presence of end-organ dysfunction, particularly renal and
cerebrovascular disease, is of paramount importance. Duration and
severity of preexisting hypertension and the degree of BP control
should be clearly defined by the history.

History and risk factors

The most common hypertensive emergency is a rapid unexplained
rise in BP in a patient with chronic essential hypertension. Most
patients who develop hypertensive emergencies have a history of
inadequate hypertensive treatment or an abrupt discontinuation of
their medications. Other causes include the following (see also Box
5-5):

• Coarctation of the aorta

• Drugs and drug interactions: Amphetamines, antidepressants,

antihistamines, cocaine, clonidine withdrawal, cyclosporine, diet
pills, monoamine oxidase inhibitors with tricyclic
antidepressants, oral contraceptives, phencyclidine, recreational
sympathomimetic drugs, serotonin syndrome, steroid use,
tyramine-containing food

• Endocrine: Cushing syndrome, pheochromocytoma, primary

hyperaldosteronism

• Hypertension of pregnancy: Preeclampsia/eclampsia

• Neurologic disorders: CNS trauma or spinal cord disorders

including Guillain-Barré syndrome

• Postoperative hypertension

• Renal parenchymal and renovascular disease: Chronic

1227
 pyelonephritis, primary glomerulonephritis, tubulointerstitial
nephritis (comprises 80% of all secondary causes),
atherosclerosis, fibromuscular dysplasia, polyarteritis nodosa

• Systemic disorders with renal involvement: Systemic lupus

erythematosus, systemic sclerosis, vasculitis

• Other factors: Hypertension is a familial disease; genetic and

environmental factors contribute to its etiology. Psychologic
stress, a diet high in sodium, and cigarette smoking increase the
risk.

Box 5-5
CAUSES OF SECONDARY HYPERTENSION
Renal disease
• Acute glomerulonephritis

• Chronic pyelonephritis

• Hydronephrosis

• Renal tumors

• Renovascular hypertension

Endocrine disorders
• Cushing syndrome

• Pheochromocytoma

• Primary aldosteronism

• Thyroid/parathyroid disease

Congenital disorders
• Adrenal hyperplasia

1228
• Coarctation of the aorta

Pregnancy-induced disorders
• Pregnancy-induced hypertension

• Preeclampsia

• Eclampsia

Drug-induced disorders
• Cyclosporine

• Oral contraceptives

• Steroids

Other
• Sleep apnea

Observation

Early indicators
Although most patients are free of symptoms, vague discomfort,
fatigue, dizziness, and headache can occur. The heart’s initial
response to systemic hypertension is to develop LV hypertrophy,
which progresses to dilated cardiomyopathy.

Late indicators (nearly always present during a

hypertensive crisis)
Throbbing suboccipital headache, irritability, confusion,
somnolence, stupor, visual loss, focal deficits, and coma. Cardiac
symptoms may include angina, MI, paroxysmal nocturnal dyspnea,
congestive HF, pulmonary edema, and orthostatic hypotension.
Chest pain may also indicate a dissecting aortic aneurysm. Renal

1229
symptoms include hematuria, nocturia, and azotemia. Nausea and
vomiting also may occur.

Eye assessment
A funduscopic examination is performed to determine whether
hemorrhage, fluffy cotton exudates, or arteriovenous nicking of the
vessels has occurred. When these changes occur, visual perception
is decreased. Nurses should assess the patient’s gross visual acuity
by the ability to read and recognize objects and people. Retinal
hemorrhages and exudates as well as papilledema may occur.

Neurologic assessment
Assess level of consciousness, visual fields, and focal neurologic
signs. May reveal evidence of a residual neurologic deficit from a
cerebral infarct or ischemic event, as manifested by a positive
Babinski reflex (upgoing toe), hemiparesis, hemiplegia, ataxia,
confusion, or cognitive alterations. Assessment should include any
onset of headache, nausea, vomiting, lethargy, restlessness, or
agitation. Neurologic presentations during crisis include occipital
headache, stroke (infarction or hemorrhage), and visual
disturbances. Hypertensive encephalopathy (severe hypertension,
headache, vomiting, visual disturbances, altered mental status,
seizures, and retinopathy with papilledema) may be present. A
complete neurologic examination should be done to screen for
localizing signs. Focal neurologic signs might not be attributable to
encephalopathy; focal signs may reflect cerebral hemorrhage,
infarct, or presence of a mass.

Vital signs

Blood pressure measurements

BP must be checked in both arms to screen for aortic dissection
or coarctation of the aorta. Those with suspected coarctation should
have BP measured in the legs. An accurate cuff pressure must be
obtained after 5 minutes of rest, with 2 or more measurements
taken at least 2 minutes apart. Average these readings unless there
is a 5 mm Hg or greater difference. Greater differences warrant
additional readings. A well-calibrated manometer with a properly

1230
fitting cuff or an automatic BP recorder should be selected for use.
The bladder of the cuff must encircle 80% of the arm and cover two
thirds of the length of the upper portion of the arm. BP
measurement in both the supine and standing positions (if able)
may help in assessment for volume depletion. A significant
difference between the arms may be suggestive of an aortic
dissection. Note when the patient last smoked or used any nicotine
product, how much caffeine was consumed during the previous 4
hours, and whether adrenergic stimulants (e.g., over-the-counter
decongestants or bronchodilators) have been used within the past
24 hours, as they elevate BP.

Pheochromocytoma assessment
Paroxysmal elevations of BP associated with palpitations,
tachycardia, headache, diaphoresis, pallor, warmth or flushing,
tremor, excitation, fright, nervousness, feelings of impending doom,
tachypnea, abdominal pain, nausea, and vomiting. Episodes also
are associated with hyperglycemia and hypermetabolism. Postural
hypotension and paradoxic response to antihypertensive
medications may occur.

Renal insufficiency assessment

Oliguria, hyperkalemia, anemia, or any of the typical features of
kidney disease.

Palpation

Evaluate for LV hypertrophy

Results from the need of the heart to pump against the high SVR or
afterload. An LV heave or lift may be palpated with the palm of the
hand at the mitral area (fifth intercostal space at the midclavicular
line [MCL]). If cardiac failure is present or the left ventricle is
enlarged, the apical impulse will be felt nearer to the anterior
axillary line instead of the MCL.

Peripheral pulses
Pulsus alternans, an alteration in pulse pressure with a regular
rhythm, may be palpated at any of the major pulse points. All

1231
peripheral pulses should be palpated bilaterally. With coarctation
of the aorta, the femoral pulses will be bilaterally weak with a slow
upstroke; whereas the radial and brachial pulses will be normal or
bounding

Auscultation

Heart sounds
When dilated cardiomyopathy is developing, an S3 or S4 heart
sound may be auscultated in the mitral area with the bell of the
stethoscope. Murmurs may be audible. In addition, crackles may be
auscultated in the presence of cardiac failure along with jugular
venous distention and peripheral edema.

Vascular sounds
Screen for carotid or renal bruits.

Diagnostic tests
The definitive test for hypertension is BP measurement. Once
hypertension has been documented, many tests may be performed
to determine the amount of end-organ damage or to diagnose the
condition responsible for the development of secondary
hypertension.

Diagnostic Tests for Hypertensive Urgencies and Emergencies

1232
 See diagnostic tests for patients with Acute Coronary Syndrome
(Chapter 5), Aortic Aneurysm/Dissection (Chapter 5), Heart Failure
(Chapter 5), Stroke: Acute Ischemic and Hemorrhagic (Chapter 7),
and Acute Kidney Injury/Acute Renal Failure (Chapter 6).
Additional studies such as a toxicology screen, pregnancy test, and
endocrine testing may be necessary.

Collaborative management

1233
Care priorities
In the treatment of hypertensive emergencies complicated by (or
precipitated by) CNS injury, IV labetalol or nicardipine may be
recommended, since they both are nonsedating and do not cause
significant cerebral vasodilation, which can increase intracranial
pressure (a potential problem with sodium nitroprusside). In
hypertensive emergencies arising from catecholaminergic
mechanisms, such as pheochromocytoma or cocaine use, beta
blockers can worsen the hypertension because of unopposed
peripheral vasoconstriction; phentolamine may be effective.
Labetalol is useful in these patients if the HR must be controlled.

1. Control the BP within minutes to 2 hours during

hypertensive crisis
The initial goal in hypertensive emergencies is to reduce the
pressure by no greater than 25% (within minutes to 1 or 2 hours)
and achieve a level of 160/100 mm Hg within 2 to 6 hours.
Parenteral therapy is indicated in hypertensive emergencies
associated with end-organ damage such as encephalopathy or
aortic dissection. Constant BP monitoring is necessary. Rapid
reductions in pressure may precipitate coronary, cerebral, or renal
ischemia. The use of an antihypertensive that is titratable and
predictable is preferred.

2. Manage patients with acute ischemic stroke

according to the American stroke association (ASA)/AHA
guidelines
With acute ischemic stroke, antihypertensives should only be used
if the BP exceeds 220/120 mm Hg, and BP should be reduced
cautiously by 10% to 15%. If thrombolytics are to be given, the BP
should be maintained at less than 185/110 mm Hg during treatment
and for 24 hours following treatment. In hemorrhagic stroke, the
aim is to minimize bleeding with a target MAP of less than 130 mm
Hg.

3. Manage patients with acute subarachnoid hemorrhage

For patients who will not undergo an intervention, the goal is to

1234
prevent further bleeding while maintaining cerebral perfusion in
the face of cerebral vasospasm.

• Parenteral antihypertensive therapy:

Nitroprusside: A short-acting, rapid arterial and

venous dilator. BP will rise almost immediately if
the drip is stopped. The usual initial dose is 0.3 to
0.5 µg/kg/min. AHA guidelines recommend
beginning with 0.1 µg/kg/min and titrating upward
every 3 to 5 minutes to desired effect. Usual dose is
3 µg/kg/min, rarely is more than 4 µg/kg/min
needed, and maximum dose is 10 µg/kg/min. Direct
arterial pressure monitoring is essential for titration
of this drug, with constant vigilance to prevent
hypotension. Nitroprusside is metabolized to
thiocyanate, a toxin, which can cause fatigue,
nausea, tinnitus, blurred vision, and delirium.
Serum thiocyanate levels should be drawn after 48
hours of use and regularly thereafter, especially
with patients with impaired renal function. Levels
of less than 10 mg/dL are considered safe.
Concomitant administration of parenteral and oral
therapy should be initiated before weaning
nitroprusside. When oral antihypertensives begin to
reduce the BP, weaning is done carefully to prevent
hypotensive episodes.

Fenoldopam: A peripherally acting rapid-acting

vasodilator and a selective dopamine1 receptor
agonist. Initial dose is 0.1 µg/kg/min and it can be
increased by 0.05 µg/kg/min; the maximum

1235
 recommended dose is 1.7 µg/kg/min. The half-life is
9.8 minutes. The patient must still be kept in the
ICU and undergo arterial monitoring with this
drug.

Labetalol: A fast-acting alpha/beta-blocking agent,

which also can be used to treat the patient in
hypertensive crisis. Given slowly by IV push,
beginning with a 20- to 80-mg dose, repeated every
10 minutes, or a continuous infusion of 2 to 8
mg/min can be administered. The usual cumulative
dose is 50 to 200 mg. Do not exceed a total dose of
300 mg. Keep the patient supine during the
injection and until stable. Check BP every 5 minutes
and then every 30 minutes until blood pressure is
stabilized. Monitor for bronchospasm, heart block,
or orthostatic hypotension.

Esmolol: A short/quick-acting beta-blocker with an

onset of action of 1 to 2 minutes and a duration of
10 to 20 minutes. Initial dose is 250 to 500
µg/kg/min for 1 minute and then 50 to 100
µg/kg/min for 4 minutes. May repeat the sequence.
Observe for hypotension, nausea, vomiting, and,
with asthmatics, bronchospasm.

Nicardipine: A potent CCB given at a rate of 5 to 15

mg/h. When desired BP reduction is achieved,
consider reducing to the average maintenance dose
of 3 mg/h. When discontinuing, can lose 50% of
effect within 30 minutes, but gradually decreased

1236
 effects persist for up to 50 hours. It may cause
tachycardia, headache, flushing, and aggravation of
angina. Do not exceed 150 mL/h (15 mg/h).

Enalaprilat: An ACEI that reduces peripheral arterial

resistance. The usual dose is 1.25 to 5 mg by IV
bolus, administered over a 5-minute period. Dose
may be repeated every 6 hours. Patients on
diuretics should receive a lower standard dose.
Initial response may take 15 minutes to 1 hour. Peak
BP reduction occurs in 1 to 4 hours, and effects last
up to 6 hours. Enalaprilat should be used with
caution in patients with renal failure or those with
bilateral renal artery stenosis (because of high renin
states). Avoid in AMI.

Hydralazine: A potent vasodilator administered as a

10 to 20 mg IV bolus or a 10 to 40 mg intramuscular
injection. The onset is 10 to 30 minutes, with a
duration of 2 to 6 hours. Adverse effects include
tachycardia, headache, vomiting, and aggravation
of angina.

Nitroglycerin: A coronary and peripheral vasodilator

supplied in a 50-mg vial, which is added to a 250-
mL glass bottle of D5W. The IV infusion may be
concentrated to prevent fluid overload if higher
doses are needed to control BP. NTG is
administered via an infusion pump starting at 5
µg/min. Onset is rapid, so BP must be monitored
closely during titration. Increase by 5 to 10 µg every

1237
 3 to 5 minutes. Headache is common and controlled
with analgesics.

Phentolamine: An alpha adrenergic-blocking agent

that reduces afterload and has minimal effect in
reducing BP except for secondary hypertension
caused by pheochromocytoma. A dose of 5 to 20 mg
is administered via IV push. The onset is
immediate, and the half-life is approximately 19
minutes. Use with caution in patients with CAD.

HIGH ALERT!
Nifedipine is no longer recommended for the management of
hypertensive emergencies.
Liquid nifedipine had been used for rapid treatment of
hypertension; the capsule was pierced and the contents were
squeezed out under the tongue, with rapid sublingual absorption
the goal. However, the drug was not absorbed sublingually but
rather was swallowed and absorbed in the stomach, producing a
quick onset of action. Effects were varying and dangerous.
Variations in dosage occurred, since the amount removed from the
capsule by squeezing liquid from the small pierced hole was
variable, as was the amount actually swallowed, versus that left
pooled in the mouth. Serious side effects, including stroke, have
been reported.

4. Facilitate adjustment to a routine antihypertensive

regimen
As the patient is adjusted to a routine antihypertensive regimen,
diuretics, ACEIs, CCBs, or ARBs may be used in various

1238
combinations. If ineffective in a combination of three of the four
categories, medications in other categories, including beta blockers
and alpha-adrenergic blockers, may be used. A hypertension
specialist may be needed for optimal medication management for
patients with resistant hypertension. For persons with severe
hypertension, three to five medications are often needed to achieve
normal BP. Resistant hypertension is defined as BP that remains
above goal despite the concurrent use of three antihypertensive
agents of different classes.

5. Provide patient education regarding lifestyle alterations

Behavioral changes are the cornerstone of medical treatment for
early and established hypertension. Normal body weight should be
achieved and maintained. Alcohol consumption should be less than
1 oz ethanol per day. Daily intake of sodium for the average adult
should be modified to 2 to 3 g for the person with hypertension.
Smoking cessation is imperative (1) to halt the injury to the intima
of the coronary and peripheral vessels and (2) to reduce the
workload of the heart. A regular aerobic program has been proven
beneficial in maintaining better control of BP. This should consist of
30 minutes of exercise 3 to 5 times per week at a target HR of 60% to
80% of the anaerobic threshold (determined by an exercise
physiologist). Maintenance of adequate potassium, calcium, and
magnesium intake is important.

6. Educate patients regarding ongoing pharmacotherapy

Maintenance pharmacotherapy for hypertension is now
approached by evaluating on an individual basis the best treatment
option based on the patient’s other disease states or demographic
factors. For persons with severe hypertension, three to five
medications are often needed to achieve normal BP. Patients must
be informed that taking more than one drug is to be expected and
not a sign of failure or worsening of disease. Healthcare providers
must set patient expectations for compliance. This approach is
promoted by the JNC-8 and the AHA. After an adequate trial of the
first drug, a second drug from a different category may be tried.

7. Discuss surgical treatment of appropriate conditions that

1239
prompt hypertension
Although there is no surgical intervention for primary
hypertension, several forms of secondary hypertension respond
well to the surgical correction of the primary problem. A
coarctation of the aorta can be repaired by removing the narrowed
area of the vessel and inserting an aortic graft. Renal artery stenosis
may be corrected by grafting or by renal artery angioplasty. For
patients with pheochromocytoma, surgical removal of the tumor(s)
will return the patient to a normotensive state.

Care plans for hypertensive emergencies

Ineffective tissue perfusion: Cardiopulmonary, cerebral, and
renal 
related to interruption of arterial flow secondary to vasoconstriction that
occurs with interruption of the normal BP control mechanism;
interruption of venous flow secondary to vasodilation or tissue edema that
occurs with loss of autoregulation.
Goals/Outcomes: Tissue perfusion is established within 24 hours
as evidenced by systemic arterial BP 110 to 160/70 to 110 mm Hg (or
within patient’s normal range); MAP 70 to 105 mm Hg; equal and
normoreactive pupils; strength and tone of the extremities
bilaterally equal and normal for patient; orientation to time, place,
and person; urinary output 0.5 mL/kg/h or greater; and stable
weight. Within 48 hours, systolic BP is less than 140 mm Hg and
diastolic BP is less than 90 mm Hg, with MAP 70 to 105 mm Hg.
Circulation Status

Hemodynamic regulation

1. Monitor BP and MAP every 1 to 5 minutes during titration of the

medications. As patient’s condition stabilizes, perform these
assessments every 15 minutes to 1 hour. Be alert to sudden drops or
elevations in BP. As the oral medications begin to affect BP,
gradually wean IV nitroprusside and other potent vasodilators to
prevent hypotensive episodes. Continuous monitoring is
recommended.

1240
• Correlate cuff pressure with pressure from arterial
cannulation.

• Determine ideal range for BP control and maximal

nitroprusside dose with advanced practice
provider. Usually the following guidelines are used:
systolic BP less than 140 to 160 mm Hg; MAP less
than 110 mm Hg; diastolic BP less than 90 mm Hg
(see table 5-19.).

• If hypotension develops, decrease or stop

nitroprusside infusion until the pressure rises.
2. Assess patient for neurologic deficit by performing hourly
neurostatus checks. Be alert to sensorimotor deficit if MAP is
greater than 140 mm Hg. As patient’s condition stabilizes and BP
becomes controlled, perform neurostatus checks at least every 4
hours.

3. Monitor patient for changes in funduscopic examination. Consult

advanced practice provider if hemorrhages or fluffy cotton
exudates are present.

4. Assess patient for evidence of decreasing renal perfusion by

monitoring I&O and weighing patient daily. Consult advanced
practice provider if urinary output is less than 0.5 mL/kg/h for 2
consecutive hours or if weight gain is at least 1 kg (2.2 lb). Be alert
to azotemia (increasing BUN), decreasing creatinine clearance, and
increasing serum creatinine. Optimal laboratory values are BUN 20
mg/dL or less, creatinine clearance 9.5 mL/min or higher, and
serum creatinine 1.5 mg/dL or less.

Table 5-19
MEDICATIONS USED IN THE TREATMENT OF HYPERTENSION

1241
1242
1243
*
Cardioselective.
BP, Blood pressure; ISA, intrinsic sympathomimetic activity; IV, intravenous; PO, by
mouth.
Some drug combinations available in multiple fixed doses. Each drug dose is
reported in milligrams.

Medication Administration; Cardiac Care; Circulatory Care

Acute pain 
related to headache secondary to cerebral edema occurring with high
perfusion pressures.
Goals/Outcomes: Patient’s subjective evaluation of pain
improves within 12 to 24 hours, as documented by a pain scale.
Nonverbal indicators, such as grimacing, are absent or diminished.
Pain Control

Pain management

1. Monitor patient for headache pain at frequent intervals. Devise a

1244
pain scale with patient, rating discomfort from 0 (no pain) to 10
(severe pain).

2. Provide pain medications as prescribed. A variety of analgesics

may be used, ranging from acetaminophen with codeine to
morphine, depending on the severity of the symptoms. Assess
effectiveness of the pain medication, using the pain scale to
determine degree of relief obtained.

3. Use of meperidine should be avoided.

Concurrent use of meperidine and a monoamine oxidase

inhibitor may result in hypertensive crisis, hyperpyrexia,
cardiovascular collapse, and death.

4. Teach the patient relaxation techniques to use in conjunction with

the medications. Guided imagery, meditation, progressive muscle
relaxation, and music therapy often are effective. Maintain a quiet,
low-lit environment that is free of extensive distraction and
stimulation. Limit visits as indicated.

Analgesic Administration; Environmental Management:

Comfort; Progressive Muscle Relaxation

Disturbed sensory perception 

related to decreased visual acuity secondary to retinal damage occurring
with high perfusion pressures; pain secondary to cerebral edema.
Goals/Outcomes: Within 24 to 48 hours of this diagnosis, the
patient reads print, recognizes objects or people, and demonstrates
coordination of movement.
Vision Compensation Behavior

Environmental management: Safety

1. Assess patient for signs of decreased visual acuity by monitoring

1245
patient’s ability to read and recognize objects or people. Evaluate
patient’s movement coordination to determine depth perception.
Perform a funduscopic examination per institutional guidelines, if
appropriate and allowable.

2. If the patient has decreased visual acuity, assist with feeding and
other ADLs and keep patient’s personal effects within his or her
visual field.

3. Reassure patient and significant others that visual problems

usually resolve when the BP is lowered sufficiently.

Surveillance: Safety

Additional nursing diagnoses

For other nursing diagnoses and interventions, see the following as
appropriate: Hemodynamic Monitoring (Chapter 1) and Emotional
and Spiritual Support of the Patient and Significant Others (Chapter
2).

Peripheral vascular disease

Pathophysiology
Peripheral vascular disease includes all vascular disorders of the
blood vessel system outside of the heart. Both chronic disease states
and acute disorders are included. This chapter discusses care of
chronic diseases of the carotid arteries and lower extremity PAD
and the acute development of critical limb ischemia.
Chronic, as well as many acute, vascular diseases develop from
progressive atherosclerotic plaque formation in arterial walls
throughout the body. The presence of PAD may indicate
cardiovascular disease. Atherosclerosis, as defined by the World
Health Organization, is a combination of changes in the intimal and
medial layers of the vessel wall in which lipids, hemorrhage,
fibrous tissue, and calcium deposits occur. The intima is the
innermost layer composed of endothelial cells within a matrix of

1246
collagen and elastin fibers. The media is the thick middle layer of
the vessel composed of varying amounts of smooth muscle,
collagen, and elastic fibers. The adventitia is the outermost layer
composed of collagen and elastin, making it a key element in
providing the strength of the arterial wall.
Atherosclerotic plaque formation occurs in three stages. The early
stage is development of fatty streaks during childhood or young
adult life. The fatty streaks are formed from lipid-laden
macrophages called foam cells. Low-density lipoprotein cholesterol
is the main lipid component of the fatty streaks. The second stage is
the appearance of fibrous plaque later in life from progression of
the fatty streaks from foam cells to a more permanent fibrous
plaque. These plaques are most often found at areas of bifurcation
of the arterial vessels. The last stage occurs as the fibrous plaque
develops into a complicated lesion with necrosis and ulceration of
the plaque surface with exposure, leading to thrombogenesis
through platelet aggregation and thrombus formation. Elasticity of
the arterial wall is lost and there is progressive narrowing of the
vessel lumen. The vessel wall may also degenerate and dilate,
leading to aneurysmal development.
The primary risk factors known to accelerate this process are
smoking, hypertension, hyperlipidemia, and diabetes mellitus. The
presence of CAD and renal artery stenosis has been correlated with
carotid artery disease of 50% stenosis or greater. Exercise and
modification of risk factors can slow the progression and even
promote regression of the fatty streaks.
Symptoms of atherosclerosis emerge over time with the
progressive narrowing and occlusion of the arterial bed until the
vessel that provides the main perfusion of a limb or tissue is
critically narrowed to 50% or more of lumen diameter (noted as a
hemodynamically significant stenosis). Symptoms of chronic
progressive atherosclerosis include subtle changes in skin
appearance, color, and temperature. Other factors, such as length of
stenosis, blood viscosity, peripheral resistance, and acute versus
chronic development, affect blood flow and tissue perfusion. As
plaque progresses along the arterial walls in an uneven pattern, the
laminar flow of blood becomes turbulent and can be heard with a
stethoscope as a bruit. Generally, the progressive and chronic

1247
development of disease allows for the development of collateral
blood flow and perfusion to be maintained at a minimal level for
the person at rest without symptoms present at this time. Pain
occurs when the tissue needs more oxygen, such as with walking or
other exercises.
Autonomic neuropathy, which occurs when blood is shunted
away from peripheral cutaneous capillary beds, may occur with
PAD alone, or in conjunction with diabetes or other comorbidities.
Motor neuropathy causes changes in gait and pressure distribution,
which may lead to ulceration. Skin is less elastic with diminished
capillary perfusion and reparative mechanisms. Loss of protective
sensation and proprioception resulting in increased force with each
step can lead to callus formation at pressure areas, which decreases
elasticity and increases skin ischemia. Bone and joint changes
occurring with comorbidities, such as diabetes, can add additional
abnormal weight-bearing mechanisms to the feet, leading to callus
and ulcer formation. This can become critical in the presence of
PAD and diminished perfusion.
Sudden blockage of an artery presents with an acute onset of
symptoms that are more pronounced. An acute blockage of a lower
extremity artery (acute limb ischemia [ALI]) may present with pain,
pallor, and neurosensory impairment in the lower limb, while an
acute occlusion of a cerebrovascular artery may present as a stroke.

Carotid artery occlusive disease

The pathogenesis of atherosclerosis in the carotid arteries is very
similar to the formation in all coronary and peripheral arterial
vessels. Stenosis in the carotid arteries is not only associated with
stroke or transient ischemic attacks (TIA), which are warnings of
impending stroke, but it is also associated with an increased risk of
MI and PAD. Ischemic stroke compose 87% of all strokes, and of
those, carotid stenosis is associated with 15% to 20%. Additionally,
the risk increases with the progressive increase in stenosis of the
carotid artery, especially with ulcerative plaque. Other sources of
ischemic stroke include thromboemboli from a variety of sources
(see Box 5-6). Without intervention, significant carotid stenosis
(greater than 70%) in a patient who has experienced a TIA or stroke
is associated with an increased risk of a second stroke. Thus, the

1248
goal of treating significant carotid stenosis is to prevent stroke.

Box 5-6
CAUSES OF ACUTE ARTERIAL
OCCLUSION
General pathologic processes
Arterial versus atheroembolization
Thrombosis of a diseased artery (acute-on-chronic disease)
Acute occlusion of a vascular bypass graft
Arterial traumas
Specific sources or processes
Cardiac Causes Noncardiac Causes
Atherosclerotic heart disease (most Aneurysms (most common noncardiac source)
common cardiac source)
Arrhythmias—atrial fibrillation
Myocardial infarction (left ventricular mural Atherosclerotic plaque ulcers (in aorta or
thrombus formation) (second most common common iliac artery; also source of stroke in
source) carotid artery disease)
Cardiomyopathy Prosthetic grafts
Left ventricular aneurysms Iatrogenic sources or arterial trauma (such as
catheter-induced thrombus formation)
Endocarditis (valvular vegetation) Paradoxical sources (secondary to an intracardiac
defect and a patent foramen ovale)
Prosthetic cardiac valves
Rheumatic heart disease

Stenosis of the carotid arteries is generally measured in the

internal carotid arteries and described as a percentage of the artery
measured at defined points. Flow velocities measured per Doppler
ultrasonography at these points are used in defining the percentage
of stenosis.
The internal carotid artery bifurcates at the distal common
carotid (at the level of the thyroid cartilage), providing perfusion to
the intercerebral circulation (the circle of Willis) and middle and
anterior cerebral arteries. Bifurcations are common areas of plaque
formation. Significant stenosis or occlusion of this artery may
present with classic symptoms of TIA or stroke, consisting of
transient monocular blindness (amaurosis fugax) on the side of the
lesion relating to temporary reduction in blood flow to the
ophthalmic artery off the internal carotid artery, contralateral
neurosensory deficits (hemiparesis or hemiparesthesias), or
difficulties with speech and/or swallowing. See Box 5-7 for a

1249
detailed listing of manifestations of TIA or stroke relating to
stenosis of the right or left internal carotid artery. TIA or strokes
may also occur from ischemia or infarction of the vertebrobasilar
system secondary to stenosis of the vertebral arteries. Symptoms
related to vertebral artery stenosis include cranial nerve deficits,
visual field loss, ataxia, dizziness, imbalance, incoordination, and
ataxic gait.

Lower extremity peripheral artery occlusive disease:

Acute
Acute occlusion of a lower extremity artery may occur from chronic
PAD with development of an acute thrombosis, referred to as
“acute-on-chronic” disease. When the chronic development of
peripheral artery occlusive disease in the lower extremity becomes
severe, it is referred to as “critical limb ischemia” (CLI) and usually
is manifested by rest pain and/or ischemic ulcers of the foot. Acute
thrombosis of sites of stenosis in which the blood flow impairment
was hemodynamically significant can occur and present with acute
symptoms. However, most often ALI is caused by an embolic
source. Cardiac disease is one of the most common embolic sources,
with atrial fibrillation being one of the most frequent cardiac
sources. Aneurysmal disease is another common embolic source.
See Box 5-6 for a listing of embolic sources. Diagnostic workup will
include looking for the source of emboli, especially ruling out a
cardiac or aneurysmal source.
The acute occlusion of a limb presents with a sudden onset of
symptoms that are characteristic and essential in determining the
diagnosis of ALI. These prominent symptoms, referred to as the six
“P”s, include pain, pallor, paresthesias, paralysis, pulselessness,
and poikilothermia. The severity of the symptoms depends on a
number of factors, such as the acuteness of development of the
vessel occlusion, presence of chronic disease with collateral
circulation, and duration of the ischemic event. Symptoms of
paresthesias and paralysis indicate advanced ischemia that is
affecting nerve pathways of the extremity. Additionally, the
presentation may include decreased sensation along the dorsum of
the foot and loss of great toe or ankle dorsiflexion. With acute
disease, critical ischemia develops within hours and is associated

1250
with irreversible anoxic injury to skeletal muscle or peripheral
nerves within 4 to 6 hours. Skin and subcutaneous tissue remain
viable for longer periods because of increased tolerance to ischemia.
In less than 8 hours’ duration of acute ischemia, the limb may
appear pale, waxy white with a cadaveric appearance. At 8 to 12
hours, areas of local stasis develop with bluish skin mottling
followed by blebs, superficial skin necrosis, and dry gangrene
mummification of toes.
Evaluation and diagnosis of the cause of ALI are crucial to
prevent tissue injury and necrosis. In general, an onset of symptoms
indicative of ALI presenting within the past 14 days is considered
acute. Early diagnosis would include duplex ultrasound or vascular
noninvasive Doppler studies, angiography, echocardiogram, and
possible magnetic resonance angiography (MRA) or computer
tomography angiography (CTA). Treatment will include a number
of options including anticoagulation, thrombolytic therapy, surgical
thromboembolectomy, endovascular procedures of stent,
angioplasty, or atherectomy, and surgical bypass or amputation of
the limb. Complications include those secondary to the treatment,
as well as complications related to the acute ischemic event and
reperfusion injury. These include catheter-induced vessel injury,
bleeding, reocclusion, compartment syndrome, and reperfusion
injury.
Compartment syndrome and reperfusion injury occur when
ischemia to a limb is absent for an extended period of time.
Compartment syndrome is defined by the swelling of tissues within
closed fascial compartments leading to increased pressure,
compression, and further necrosis and nerve injury. In anticipation
of this, a fasciotomy of the involved limb may be performed at the
time of surgical thromboembolectomy or at a later time.
Reperfusion injury also involves the development of severe
acidosis, hyperkalemia, renal failure secondary to myoglobinuria,
and pulmonary insufficiency (see Compartment Syndrome
Ischemic Myositis, Chapter 3).

Peripheral vascular assessment: Arterial

occlusive disease

1251
Goal of system assessment
• Evaluate for decreased blood flow and tissue perfusion so as to
evaluate for focal diminished perfusion of the cerebrovascular or
lower extremity peripheral arterial systems.

History and risk factors

• Family or personal history of tobacco abuse, hyperlipidemia,
hypertension, diabetes, obesity, stress, sedentary living,
cardiovascular disease, renal insufficiency, clotting disorders,
foot ulcers, or noncompliance with medical management (daily
antiplatelet inhibitors, statins, or other medications to control
above risk factors).

• Age younger than 50 years, with diabetes and one other

atherosclerosis risk factor (smoking, dyslipidemia, hypertension,
or hyperhomocysteinemia)

• Age 50 to 69 years with history of smoking or diabetes

• Age 70 years and older

• Leg symptoms with exertion (suggestive of claudication) or

ischemic rest pain

• Abnormal lower extremity pulse examination

• Known atherosclerotic coronary, carotid, or renal artery disease

Carotid artery occlusive disease

• CAD and renal artery stenosis greater than 60% are associated
with increased risk for carotid disease.

• Retinal ischemic events, especially in the absence of migraine or

cardiac embolic events, warrant evaluation for carotid artery
disease.

• Patients with a bruit and/or two or more risk factors for PAD

1252
 should be evaluated for carotid stenosis.

• Significant stenosis may be present without symptoms.

• Symptomatic carotid stenosis or occlusion may present with TIA

symptoms.

• TIA is defined by symptoms that last less than 24

hours.

• TIA symptoms indicative of stenosis or occlusion of

the internal carotid artery (see Box 5-7).
• Atypical symptoms of dizziness, vertigo, syncope, unsteady gate,
bilateral paresthesias/paresis may be attributed to other causes,
such as cardiac disease, hypovolemia, medication side effects,
vertebrobasilar insufficiency, and others.

Box 5-7
SYMPTOMS OF TIA AND ISCHEMIC
STROKE RELATED TO STENOSIS OF THE
CAROTID ARTERY
Right Internal Carotid Artery (RICA) Left Internal Carotid Artery (LICA)
Right eye monocular blindness (amaurosis Left eye monocular blindness (amaurosis
fugax) fugax)
Right homonymous hemianopsia (visual loss Left homonymous hemianopsia (visual loss
involving right visual field) involving left visual field)
Aphasia in ambidextrous or left-handed Aphasia
persons
Left-sided weakness (hemiparesis) Right-sided weakness (hemiparesis)
Left-sided sensory loss (paresthesia) Right-sided sensory loss (paresthesia)

Peripheral artery occlusive disease with or without

distal limb involvement, chronic
• Associated with the presence of CAD.

• May be chronic or acute-on-chronic disease.

1253
• Intermittent claudication is the most common manifestation of
PAD.

• The calf, thigh, hip, or buttock develops tightening

or cramping pain with exertion, such as walking a
predictable distance, and is relieved with rest.

• The site of claudication is indication of the location

of occlusion, which will be above the presentation
of pain.
• Claudication that is considered to be lifestyle limiting is
significant to the point that it substantially interferes with the
person’s ability to perform ADLs or to work.

• Symptoms may also be described as “fatigue” or “numbness” of

the extremity that occurs with walking.

• Nocturnal rest pain indicates a worsening of the disease. It occurs

at night and is usually relieved by sitting, standing, or dangling
the affected limb, using gravity to increase perfusion.

• Rest pain, which is present all the time without relief, indicates a
critically ischemic limb and is generally present in the distal foot,
forefoot, and toes.

• Most common symptom of rest pain is a burning sensation across

the dorsum of the foot.

• Chronic symptoms may be masked by the presence of other

diseases limiting the ability to walk, such as cardiac or
respiratory disease causing fatigue or dyspnea before lower
extremity symptoms are present or the presence of neuropathy.

Peripheral artery occlusive disease with or without

distal limb involvement, acute

1254
• Acute occlusions are commonly associated with a
thromboembolic source, which needs to be identified.

• Hallmark signs: The six “P”s (pain, pallor, pulselessness,

paresthesia [numbness], poikilothermia [coldness], and
paralysis).

• Paralysis is a late and grave sign; the limb already

has necrotic muscle and will not likely regain
function, resulting in foot drop. It may require
amputation.

• Presence of “blue toe syndrome” is indicated by bluish, mottled

spots scattered over the toes and represents an embolic process.

• Outcome depends on duration of tissue ischemia, site of

obstruction, extent of thrombus propagation, adequacy of
collateral circulation, and hemodynamic state of the patient.

Observation
Symptoms of PAD may vary depending on the vessels involved
and may include intermittent claudication if it involves the limbs or
TIAs if it involves the carotid arteries, which provide perfusion to
the brain. Most patients with intermittent claudication require no
intervention, approximately 20% require surgical reconstruction,
and approximately 5% to 10% progress to require an amputation.
The presence of pain at rest or a nonhealing necrotic ulcer defines
CLI and indicates disease in greater than one artery and impending
loss of the limb without treatment. Evaluate blood flow quality and
tissue perfusion of cerebrovascular and peripheral vascular vessels:

• Cerebrovascular perfusion

• Level of consciousness, alertness, speech,

responsiveness

1255
• Neurologic assessment of cranial nerve function

• Extremity strength, movement

• Lower extremity perfusion

• Look for decreased hair growth, shiny skin, nail

changes, distal joint abnormalities, or skin ulcers.

• Evaluate for change in skin color in neutral,

elevated, and dependent positions (pallor with limb
elevation versus rubor with dependency).

• Neurosensory function of peripheral nerves:

sensation, strength

Carotid artery occlusive disease

• Evaluate for cranial nerve (CN) deficit, presenting with unilateral

paralysis of extremities or facial features, or gait ataxia (see
chapter on stroke for details of CN assessment)

• Evaluate for CN damage status post carotid procedure.

• CN VII: facial movement, symmetry of face (as in

drooping at the corner of the mouth), unable to
smile symmetrically.

• CN IX: taste to posterior third of tongue, gag reflex;

injury may cause mild dysphagia or loss of taste.

• CN X: palatal, pharyngeal, and laryngeal, gag

1256
 movement; injury may affect tongue movement,
dysphagia, or dystonia.

• CN XI: sternocleidomastoid, trapezius muscle

movement; injury may cause an inability to shrug
shoulders or move head side to side against
resistance.

• CN XII: tongue movement; injury may cause an

inability to move the tongue from side to side or
dysarthria.

Peripheral artery occlusive disease

• Presence of pallor in the foot when the extremity is elevated 30 to

45 degrees for several seconds to a minute.

• Presence of dependent rubor (intense deep red color) in the foot

when it is dependent for several minutes.

• Presence of bluish or deep purple, mottled discolorations of the

foot or toes.

• Ulceration, fissures, or gangrene lesions present at the digits,

interdigits, or heel.

• Presence of extremity paralysis, or gait ataxia.

Vital signs
Check temperature, HR, BP, and peripheral pulses to evaluate
blood flow quality and tissue perfusion.

• Temperature: Possible fever if cellulitis or infected wounds are

present.

1257
• HR: Symptomatic bradycardia may develop post carotid
procedure caused by vagal stimulation.

• BP: Unequal BP in arms may indicate carotid or subclavian artery

disease. Arm with the lower pressure indicates a possible
subclavian stenosis. The higher of the two arm pressures should
be considered the accurate pressure.

• BP may increase or decrease with stimulation of baroreceptors in

the carotid bulb during or following carotid procedures.

• Severe hypertension or hypotension is worrisome for impending

stroke or MI and will need immediate attention.

• Obtain an ankle-brachial index (ABI), see Box 5-8. Decreased ABI

can indicate presence of PAD. The ABI is also used to assess
perfusion in the lower extremity and checks for changes in
perfusion to a limb after an endovascular or surgical intervention
to a limb.

• Monitor for changes in BP, HR, and RR after the carotid

procedure to assess for increased intracranial pressure secondary
to hemorrhage, edema, or ischemia.

• May also represent reperfusion injury following carotid

procedures; hemorrhage or headache may occur with increased
blood flow, usually after repair of a high-grade stenosis.

Box 5-8
ANKLE-BRACHIAL INDEX
To obtain an ankle-branchial index (ABI):

• With the patient lying flat, measure blood pressure (BP) of both
arms. If the BP differs between arms, use the higher reading.

• Apply BP cuff over ankles. Take BP reading over dorsalis pedis

(DP) and posterior tibial (PT) arteries of both legs using a
Doppler ultrasound.

1258
• Calculate the ABI by dividing the systolic reading at the DP/PT
level by the systolic reading at the arm (brachial artery).

• Normal ABI ranges from 1.0 —1.4; Pressure is normally higher in

the ankle than the arm.

Palpation
• Check skin temperature and pulse assessment to evaluate for
decreased tissue perfusion.

• Check bilateral pulse quality and regularity (scale of 0 to 4+;

0=absent pulse to 4+=bounding pulse).

• Pulse amplitude may be increased or decreased depending on

disease process. Change in pulse is palpable below the level of
disease.

• Decrease in pulse quality or absent pulse may indicate occluded

or stenotic arteries.

• Bounding pulses may be indicative of aneurysmal development

of the artery.

• Palpate the femoral and popliteal arteries for

presence of an aneurysm affecting distal circulation.

• Aneurysmal arteries have an increased diameter

and may have an easily palpable or bounding
pulse.

• Pseudoaneurysm can occur because of injury of an

artery such as the catheter insertion point for
angiogram or thrombolysis.

1259
• Presence of edema (scale 0 to 4+) of extremities is indicative of
other secondary problems (such as HF, liver or renal disease,
venous insufficiency, or venous thrombosis)

• Edema with erythema may be indicative of

infection.

• Lymphedema may be present after bypass

procedure because of disruption of the lymph
system when making incision or creating vein graft
(not caused by arterial disease).
• Slow capillary refill (greater than 2 seconds) is indicative of
sluggish circulation and arterial occlusions.

• Temperature changes: increased warmth may indicate tissue

inflammation or infection. Coolness may be present distal to the
site of occlusion.

• After repair of an acutely ischemic limb, palpate affected limb for

compartment syndrome. Most common site is the anterior
compartment of the lower leg. Presents with tightness of the skin
and muscle pain to a higher degree than expected.

Auscultation
Listen for presence of bruits, which indicate disturbances in flow
(plaque formation).

• Bilateral carotid arteries

• Abdominal aortic and bilateral femoral

• Bruits in the carotid arteries, the aorta, or the renal arteries may
be indicative of stenosis or dilation of arteries.

• Bruits are high-pitched pulsations (similar to a

murmur) best heard with the bell of the stethoscope

1260
 and correlate with the presence of turbulent flow.

• Carotid bruits are assessed by auscultation of the

carotid artery from the base of the neck to the angle
of the jaw; they are usually loudest in the upper
third of the neck in the area of the carotid
bifurcation.

• Renal and aortic bruits are assessed in the

midabdominal or epigastric area of the abdomen.
• Doppler auscultation of the peripheral pulses for quality of pulse
signal.

• A healthy artery has 3 phases (sounds) heard when

using a Doppler for assessment of pulses. A
repaired or diseased artery may have 1 or 2 phases.

• A change in the Doppler signal from 3 (triphasic) or

2 phases (biphasic) to only 1 (monophasic) may be
indicative of complications.

Screening labwork
Blood studies can help to determine risk of vascular disease or its
complications.

• Chemistries: checking for blood glucose and renal function

(elevated creatinine, BUN, potassium).

• CBC: anemia, high or low platelet level evaluating for increased

clotting/bleeding propensity.

1261
• Coagulation studies: PT/INR or PTT evaluating for increased
clotting/bleeding propensity.

• HgbA1c: evaluating risk factor control (presence of, or

uncontrolled diabetes).

• Lipid profile: evaluating for control of risk factor (presence of, or

uncontrolled hyperlipidemia).

Postprocedural screening labwork

Blood studies can reveal postprocedural or surgical complications
such as bleeding, fluid overload, early infection, renal insufficiency,
or muscle damage associated with reperfusion injury.

• CBC: possible anemia related to surgical blood loss or

postoperative bleeding; increased WBCs indicating possible
infection.

• Electrolytes: fluid shift or volume changes with increased use of

IV fluids;

• Blood glucose: HbAIC indicates long-term effectiveness of blood

glucose control in patients with diabetes, and should be reviewed
along with blood glucose level to anticipate the probability of
complications.

• Creatinine, BUN: possible changes in perfusion of the kidneys.

• Liver enzymes, CPK: possible muscle injury related to reperfusion

or compartment syndromes.

• Coagulation panel: protime, INR, partial thromboplastin time to

evaluate anticoagulation management.

Diagnostic Tests for Arterial Disease

1262
1263
ALI, acute limb ischemia; ASCVD, atherosclerotic cardiovascular disease; AST,
aspartate aminotransferase; CLI, critical limb ischemia; CPK, creatine
phosphokinase; CT, computed tomography; EDV, end-diastolic velocity; HDL-C,
high-density lipoprotein cholesterol; LDH, lactate dehydrogenase; LDL-C, low-density
lipoprotein cholesterol; LE, lower extremity; PAD, peripheral artery disease; PSV,
peak systolic velocity; TBI, toe brachial index; VLDL, very low-density lipoprotein.

Carotid duplex and arteriogram

Carotid duplex ultrasound (DUS) is used to detect the presence of
carotid artery stenosis. At centers where the DUS has been
internally validated in comparison with angiography and a
comparable level of performance has been documented, surgeons
may choose to proceed with surgery based on the DUS without the
extra risks of a carotid angiogram. At centers where the DUS results
are less reliable, it is used as a screening tool for carotid artery

1264
disease. Stenosis greater than 70% may indicate the need for CTA or
angiogram, especially if symptoms are present. A CTA may also be
used if unilateral symptoms are present and there are conflicting
findings on the DUS.

Ankle-brachial index
BP is taken in both arms, with the highest pressure used for
calculating indices (unequal arm pressures may indicate the
presence of carotid or subclavian artery disease and the need for a
carotid/subclavian DUS). Segmental pressures are also taken with a
thigh cuff placed above the knee for a low thigh pressure and above
the ankle to obtain ankle pressures of the dorsalis pedis and
posterior tibial artery. A hand-held Doppler is used to acquire the
dorsalis pedis and posterior tibial pulses. Normally, the pressure in
the leg is equal to or slightly higher than brachial pressure. A
difference of greater than 30 mm Hg between segments indicates
disease of the artery proximal to where the pressure was taken. The
ankle pressure is divided by the brachial pressure to obtain the ABI.
Calcification of the arterial wall provides a falsely high
measurement preventing compression of the vessel to obtain the
pressure; this is referred to as a “noncompressible” vessel. In these
patients, diagnosis must be based on Doppler waveform analysis.

Collaborative management
Care priorities: Peripheral artery occlusive disease
Priorities for the care of a patient with chronic peripheral artery
occlusive disease should focus on early identification of disease and
prevention of disease progression, disability secondary to ischemic
injury, and thrombotic ischemic events. Prevention of disease
progression would include the control of risk factors, prevention of
thrombus formation (i.e., antiplatelet therapy or other
anticoagulants), and management of medications to control risk
factors.
To assist and guide the identification and management of
patients with PAD, many national organizations have collaborated
to produce evidence-based guidelines. Selective recommendations

1265
from the guidelines that are related to acute care settings are
outlined in the following tables.

GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH

PERIPHERAL ARTERY DISEASE

1266
*
2014, JNC-8 Guidelines for Management of Hypertension in Adults
†
2013, ACC/AHA Task Force Cholesterol Management Guidelines
ABI, Ankle-brachial index; ACEI, angiotensin-converting enzyme inhibitor; ASCVD,
atherosclerotic cardiovascular disease; CHF, congestive heart failure; CV,
cardiovascular; DM, diabetes mellitus; HLD, hyperlipidemia; HTN, hypertension;
LDL-C, low-density lipoprotein cholesterol; LE, lower extremity; MI, myocardial
infarction; PAD, peripheral artery disease; PTFE, polytetrafluoroethylene; PVR, pulse
volume recording; TBI, toe-brachial index.

Lower extremity peripheral artery occlusive disease:

Critical limb ischemia
In CLI, rest pain and/or ischemic ulcers are present. For a patient

1267
with ischemic ulcers, specific care priorities would include wound
care, preventing or treating infection, and protecting the limb to
prevent further tissue damage. Additional measures would include
the following.

1. Relief of ischemic pain

In general, relieving ischemic pain requires improving perfusion to
the limb. However, depending on the length of ischemic time and
amount of ischemic nerve injury, administration of a narcotic
analgesic is usually required.

2. Prevention of injury to the ischemic limb

Pressure to an already ischemic limb diminishes perfusion even
further, leading to tissue breakdown. Maintain the heel and other
pressure points of the extremity free from sustained pressure.
In the surgical or endovascular management, care priorities
should focus on promoting perfusion to the extremity, preventing
infection, and promoting wound healing. Promotion of perfusion in
an extremity includes preventing limb edema that could impair
graft perfusion and wound healing, maintaining perfusion of the
stent or graft, and preventing thrombus or occlusion of the stent or
graft. For more information and description of endovascular
techniques and instruments, such as intra-arterial stent placement,
balloon angioplasty, or atherectomy (see Acute Coronary
Syndromes, Chapter 5).

3. Promoting perfusion of the extremity

Activities include keeping the extremity warm to prevent
vasoconstriction, maintaining hydration, preventing hypotension,
and preventing edema to the limb. If a surgical incision has been
made to the limb, the limb will have a propensity for edema to
develop, which not only promotes graft compression, but also
impairs wound healing. Elevation of the extremity will help
prevent or diminish edema.

Maintaining hydration and preventing hypotension in a

1268
patient who has undergone lower extremity bypass or stent
placement are important to prevent graft occlusion. Hypotension
decreases perfusion to the graft and dehydration increases blood
viscosity, leading to thrombosis and graft or stent occlusion.

4. Prevention of peripheral artery clot formation

Antiplatelet therapy is the recommended medication used to
prevent thrombus formation in individuals with PAD and no
history of an event. However, antithrombotics may be required in
those persons with a history of a thrombotic event or
hypercoagulable condition. Antithrombotics include warfarin,
direct factor X inhibitor (such as rivaroxaban or betrixaban), UH,
and LMWH (such as enoxaparin, fondaparinux, or dalteparin). A
direct thrombin inhibitor, such as argatroban, may be used if
allergic to heparin or if there is a history of heparin- induced
thrombocytopenia. Antiplatelet therapy includes the use of the
following:

• Aspirin: Low doses of 75 to 325 mg orally are given on a daily

basis.

• Clopidogrel: The standard dose is 75 mg daily. If a stent has been

placed, clopidogrel is recommended. For patients who have not
been on a regimen of daily clopidogrel and are about to undergo
a carotid or peripheral stent, a loading dose of 300 mg of
clopidogrel before stent placement is required.

• In patients who are unable to take aspirin or clopidogrel, other

antiplatelet drugs will be considered, such as ticlopidine.
Ticlopidine is not used as a first-line drug because of the adverse
effects of life-threatening neutropenia, agranulocytosis, and
thrombotic thrombocytopenia purpura.

• Dipyridamole and aspirin combination may be used for arterial

graft patency but is most often used in stroke prevention. It is
considered to be a third-line treatment option.

1269
• Ticagrelor is a newer antiplatelet medication that is currently
recommended only for coronary patients as there is no data on its
use in PAD patients.

5. Prevent contrast-induced nephropathy (CIN)

secondary to contrast during angiography
Prevention is required for endovascular intervention, especially in
patients with evidence of renal insufficiency (serum creatinine
levels greater than 1.4 mg/dL and/or glomerular filtration rate less
than 60 mL/min/1.73 m2). Additional measures may be taken if
glomerular filtration rate is less than 40 mL/min/1.73 m2.

• Hydration is paramount and is accomplished with IV fluids.

Normal saline is recommended for 12 hours before and after the
contrast study. In addition to IV hydration, administration of the
following medication is generally used:

• N-acetylcysteine: Although previously used as a standard

protocol for CIN in the recent past, it is now fallen out of favor
and its efficacy is controversial in preventing CIN. Currently, it is
suggested for use in patients with baseline serum creatinine
above 2.0 mg/dL. If given, the dosing is 600 mg as an oral
solution or a compounded tablet twice daily for 4 doses, starting
the day before the procedure.

• NaHCO3 infusion: Infusion rate of 3 mL/kg/h for 1 hour before

the procedure, then 1 mL/kg/h for 6 hours after the contrast
procedure.

6. Endovascular or surgical treatment of cli/ali

• A significant arterial stenosis or occlusion is performed using

endovascular techniques of angioplasty, atherectomy, or stent
placement. Surgical treatments include thromboendarterectomy
or bypass around occluded vessels.

• Angioplasty, atherectomy, and/or stent placement (see Acute

Coronary Syndromes, Chapter 5)

1270
• Thromboendarterectomy or endarterectomy: This procedure is
similar to that described above with a carotid endarterectomy
(CEA). An incision is made along the length of the artery where
the stenosis is located. The plaque is removed and the artery is
sewn closed. A vein patch may be placed in the vessel during
closure to provide an adequate size for blood flow. This is
generally performed on the proximal vessels of the distal aorta,
iliac, or femoral arteries. A shunt, as may be used in the CEA to
ensure cerebral perfusion, is not required in the distal limbs.

• Surgical placement of a bypass graft or reconstruction: Through

surgical incisions, a conduit is surgically attached forming an
anastomosis that is end-to-end or end-to side to the artery above
the site of an occlusion or hemodynamically significant lesion to
provide “inflow” of blood to the extremity. The distal graft is
surgically attached below the occlusions to provide “outflow” of
blood to the extremity. Synthetic material, such as Dacron or
polytetrafluoroethylene, is often used as a conduit for bypasses
above the knee, since the patency rate is equal to that of vein.
This preserves the vein for future need. A vein, usually the
greater saphenous vein (GSV), is the conduit of choice for a
bypass extending below the knee. The patient’s vein may be
harvested by excising the GSV and placing it in a reversed
position to allow blood flow to pass valves. The GSV may also be
used in situ, without completely excising, after a valvulotome is
used to destroy the 1-way flow of the valve leaflets. The bypass is
referred to by its anatomic placement. For example, an
aortobifemoral bypass indicates that the proximal graft is
attached at the aorta and bifurcated grafts are inserted bilaterally
into each femoral artery. A femoropopliteal bypass indicates that
the proximal graft is sewn to the femoral artery and the distal end
of the graft is attached at the popliteal artery.

Lower extremity peripheral artery occlusive disease:

Acute limb ischemia
In ALI resulting from acute arterial occlusion, the care priorities are
similar to those of CLI, which would include early identification of
an acutely ischemic limb and early intervention to diminish

1271
ischemic time and restore blood flow to the ischemic limb. In the
limb with an acute arterial occlusion, thrombolysis is the
recommended emergent procedure used to dissolve the arterial clot
and restore limb perfusion. Time is of great concern in an acute
arterial occlusion. Anticoagulation may be initiated with a heparin
bolus and continuous infusion. If the patient is unable to undergo
thrombolytic therapy, a thromboembolectomy may be performed to
treat an acute arterial occlusion to quickly restore perfusion of the
limb.

1. Thrombolysis
See Acute Coronary Syndromes Chapter 5, for a complete
discussion of this procedure and care priorities related to its use.
Care priorities for a patient undergoing thrombolysis for an acute
peripheral artery occlusion are essentially the same as in the patient
with an acute coronary thrombus.

2. Thromboembolectomy
A surgical arteriotomy is performed and an embolectomy balloon
catheter is passed past the thrombus, the balloon is inflated, and the
clot is extracted. Neighboring arteries are checked for clot. Distal
embolization is of great concern with this procedure because of the
manipulation of the catheter around the thrombus.
Care priorities for ALI also include monitoring and early
recognition of compartment syndrome, thromboembolic injury, and
neuromuscular injury. For a full discussion and care priorities of
compartment syndrome, see Compartment Syndrome/Ischemic
Myositis, Chapter 3.
In ALI, care priorities would also include facilitating the
identification of the source of emboli. Given that the heart is a
common source, an echocardiogram will be performed as soon as
perfusion to the limb has been restored. Additional studies that
would be considered include an abdominal/pelvic CTA scan or
angiogram to look for any aneurysmal source. A lower extremity
ultrasound may be performed to look for peripheral aneurysms of
the femoral or popliteal arteries.

1272
 High potential for distal emboli to the foot, referred to as
“trashed foot” or “blue toe syndrome.” The risk for distal
embolism from dislodgment of thrombus or thrombotic plaque is
significant in any procedure in which catheters are manipulated
around or through the clot, causing clot fragmentation, such as
with thrombolysis, thromboendarterectomy, angioplasty, or
stenting. Incorporate monitoring for distal emboli into care
priorities.

Collaborative management
Care priorities: Carotid artery occlusive disease
The focus of care is similar to PAD but includes the early
recognition and intervention of carotid artery stenosis to reduce
progression of disease and to prevent stroke. Multiple large
randomized trials have demonstrated an association between
carotid stenosis and other significant risk factors (ischemic heart
disease, TIA/stroke, PAD, hypertension, dyslipidemia, and
smoking). Many of these same trials have demonstrated a
decreased risk of stroke and MI with medical management. Several
trials have evaluated the risk of stroke in asymptomatic persons
with carotid artery stenosis, finding that persons with 60% to 80%
stenosis had higher stroke rates. Many trials have demonstrated
decrease in stroke and cardiovascular events with management of
the risk factors. Treatment of carotid disease includes medical
management and possibly a surgical approach of CEA or
endovascular placement of a carotid artery stent.

CLINICAL PRACTICE GUIDELINES FOR THE MANAGEMENT OF

ATHEROSCLEROTIC CAROTID ARTERY DISEASE

1273
1274
*
2014, JNC-8 Guidelines for Management of Hypertension in Adults
†
2013, ACC/AHA Task Force Cholesterol Management Guidelines
ASCVD, Atherosclerotic cardiovascular disease; BP, blood pressure; CAD, coronary
artery disease; CAS, carotid artery stent; CEA, carotid endarterectomy; CTA,
computed tomography angiography; CV, cardiovascular; DUS, duplex
ultrasonography; HTN, hypertension; IMT, intramural thickness; LDL-C, low-density
lipoprotein cholesterol; LVEF, left ventricular ejection fraction; MI, myocardial
infarction; MRA, magnetic resonance angiography; TIA, transient ischemic attack.

Provide management of patients to help prevent stroke and to

manage patients following preventive procedures.

1275
1. Facilitate recovery from cea

• Prevent impaired cerebrovascular perfusion secondary to

hypotension, hypertension, or bradycardia.

• Prevent respiratory impairment secondary to bleeding or

hematoma formation at the incision leading to tracheal deviation
and respiratory distress.

• Postoperative complications of a CEA related to the surgical

approach include neurologic deficits, hypertension, bradycardia,
neck hematoma with potential for airway obstruction, and local
nerve injuries of the laryngeal or hypoglossal nerves that require
prompt treatment.

2. Facilitate recovery from an endovascular stenting

• Monitor for potential embolic TIA or stroke, as is done with the

surgical approach.

• Monitor for bradycardia or hypotension relative to vasovagal

stimulation.

• Observe for and prevent limb ischemia related to the access site
for the endovascular procedure.

• For patients with a carotid stent: Continue antiplatelet therapy

(generally with clopidogrel) to prevent stent occlusion.

3. In a patients undergoing cea or carotid artery stent with

100% occlusion of the contralateral carotid artery, prevent
hypotension

• After revascularization in a patient with 100% occlusion of the

contralateral carotid artery, a hyperemia can occur secondary to
increased cerebral perfusion. The hyperemia can lead to
increased intracranial pressure. This may occur immediately
postoperatively, but may also occur days later. Manifestations to
observe for include headache, cloudy thinking, or altered mental
status.

1276
4. Initiate medical management, including antiplatelet
medications

There is a relationship between the presence of

cerebrovascular disease and coronary artery disease (CAD). The
most common cause of mortality following carotid
endarterectomy is myocardial infarction; the highest risk after a
carotid stent placement is for stroke. There is also a relationship
between peripheral arterial disease (PAD) and CAD. The prognosis
of patients with lower extremity PAD is characterized by an
increased risk for cardiovascular ischemic events caused by
concomitant CAD and cerebrovascular disease. Cardiovascular
ischemic events are more frequent than ischemic limb events in any
patient with lower extremity PAD and/or carotid stenosis.

Care plans for generalized peripheral

vascular disease
Activity intolerance 
related to compromised tissue perfusion and pain
Goals/Outcomes: Within the 12- to 24-hour period before
discharge from the ICU, the patient exhibits tolerance to increasing
levels of activity as evidenced by RR less than 24 breaths/min, NSR
on ECG, BP within 20 mm Hg of patient’s normal range, HR less
than 120 bpm (or within 20 bpm of resting HR for patients on beta-
blocker therapy), and generalized pain less than 4 on a 1 to 10 scale.
Endurance; Energy Conservation; Activity Tolerance

Energy management

1. Determine patient’s physical limitations.

2. Determine causes of fatigue and perceived causes of fatigue.

1277
3. Monitor for muscle pain during activity.

4. Reduce all causes of discomfort, including those induced by the

patient’s environment, such as uncomfortable room temperature or
position, thirst/dry mouth, and wrinkled or damp bedding.

5. Provide alternating periods of rest and activity.

6. Assist patient in prioritizing activities to accommodate energy

levels.

Self-care assistance: Instrumental activities of daily living

(IADLS)

1. Determine need for assistance with IADLs including walking,

bathing, dressing, cooking, shopping, housekeeping,
transportation, and money management.

2. Provide for methods of contacting assistance support (such as

home health nursing, lifeline services, emergency response services,
including readily accessible telephone numbers if the patient is not
within 911 access area).

3. Determine financial resources and personal preferences for

modifying the patient’s home to accommodate any disabilities or
assisting with medication costs or other home healthcare costs.

Deficient fluid volume 

related to procedure-related blood loss or inadequate hydration.
Goals/Outcomes: Within the 12-hour period before discharge
from the ICU, the patient exhibits a normal fluid balance as
evidenced by normal laboratory results of Hgb, Hct, potassium,
sodium, creatinine, BUN; good skin turgor; warm, pink skin;
normal level of consciousness (or maintenance of preprocedure
LOC if baseline is impaired); normal vital signs and weight.
Fluid Balance

Fluid/electrolyte management

1. Maintain adequate fluid volume.

1278
2. Assess urine output, condition of skin, wound drainage, and
I&O.

3. Monitor potassium, sodium, creatinine, and BUN; notify

advanced practice provider if abnormal.

4. Monitor vital signs, weight, restlessness, skin temperature, and

decreased LOC.

Hemorrhage control

1. Monitor vital signs, Hgb, and Hct; notify advanced practice

provider if abnormal.

2. Assess for excess drainage from dressing or drains (if present).

3. Assess for restlessness, pallor, skin temperature, decreased

capillary refill, or decreased tissue perfusion.

4. Check operative site for bruising or excessive swelling.

Ineffective tissue perfusion: Peripheral 

related to reduced circulation resulting from vascular disease.
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate tissue perfusion as evidenced by warm, dry skin;
brisk capillary refill; normal color, temperature, and sensory and
motor function; RR less than 24 breaths/min; NSR on ECG; BP
within 20 mm Hg of patient’s normal range; HR less than 120 bpm
(or within 20 bpm of resting HR for patients on beta-blocker
therapy).
Circulation Status; Tissue Perfusion: Peripheral

Circulatory care: Arterial insufficiency

1. Monitor vital signs.

2. Assess skin color, temperature; peripheral pulses as appropriate.

3. Provide warmth; avoid prolonged exposure to cold temperatures.

1279
4. Promote smoking cessation and decreased caffeine intake.

5. Encourage activity as tolerated; passive and active ROM exercises

if confined to bed.

Peripheral sensation management

1. Assess neurologic functions; decreased sensations.

2. Avoid constrictive clothing around operative site.

3. Minimize external pressure points.

Deficient knowledge: Peripheral vascular disease process 

related to lifestyle implications.
Goals/Outcomes: Within the 24-hour period before discharge
from the hospital, the patient verbalizes understanding of his or her
disease, as well as the necessary lifestyle changes that may modify
risk factors.
Knowledge: Diabetes Management; Knowledge: Diet;
Knowledge: Disease Process; Knowledge: Energy Conservation;
Knowledge: Health Behaviors; Knowledge: Medication

Teaching: Peripheral vascular disease process

1. Teach the patient about arterial stenosis or occlusion and its

resultant symptoms such as TIAs, claudication, or rest pain.

2. Discuss the pathophysiologic process underlying the patient’s

arterial stenosis or occlusion, using drawings as indicated.

3. Assist patient in identifying his or her own risk factors (e.g.,

cigarette smoking, high-fat diet, hyperglycemia, high-stress
lifestyle).

4. Teach the patient about risk factor modification:

• Smoking cessation: Teach the patient that smoking

causes arteries to constrict and increases platelet

1280
 viscosity, thus decreasing blood flow to the brain,
muscles, and tissues.

• Hyperglycemia control: Discuss how high blood

sugar levels accelerate the course of atherosclerosis;
cause structural changes in the collagen of skin,
joint capsules, and tendons leading to limitations of
flexion and extension that result in increased foot
pressures and risk of ulcerations; are associated
with developing neuropathy; and accelerate wound
sepsis.

Teaching: Diet and prescribed medications

1. Diet low in cholesterol and saturated fat: Provide sample diet

plan for meals that are low in cholesterol and saturated fat. Teach
the patient about foods that are high in cholesterol and low in
cholesterol and saturated fat. Stress the importance of reading food
labels. (See Tables 5-16 and Table 5-17 for more information.)

2. Blood pressure control: If the patient was found to have

hypertension, he or she should be taught the importance of taking
appropriate medications to control BP and to follow recommended
dietary guidelines to minimize sodium intake. (See Table 5-4 for
more information.) Sodium promotes water retention, which can
increase BP. High BP may accelerate the process of atherosclerosis.

• Teach the patient about the prescribed medications,

including name, purpose, dosage, action, schedule,
precautions, and potential side effects.

1281
Table 5-16
LOW-CHOLESTEROL DIETARY GUIDELINES

Foods to Avoid Foods Allowed

Egg yolks (no more than 3/week) Egg whites; cholesterol-free egg substitutes
Foods made with many egg yolks (e.g., Lean, well-trimmed meats; minimize servings of
sponge cakes) beef, lamb, and pork
Fatty cuts of meat, fat on meats Fish (except shellfish), chicken, and turkey
Skin on chicken and turkey (without the skin)
Luncheon meats and cold cuts Dried peas and beans as meat substitutes
Sausage, frankfurters Nonfat (skim) or low-fat (2%) milk
Shellfish (e.g., lobster, shrimp, crab) Low-fat cheese
Whole milk, cream, whole milk cheese Ice milk, sherbet, low-fat yogurt
Ice cream Monosaturated oils for cooking and food
Commercially prepared foods with preparation: canola, safflower, olive
hydrogenated shortening, which is Margarines that list one of the above oils as their
saturated fat first ingredients
Coconut and palm oils and products Foods prepared “from scratch” with the above
made with them (e.g., cream suggested oils
substitutes) Meats (in acceptable quantity) and vegetables
Butter, lard, hydrogenated shortening prepared by broiling, steaming, or baking (never
Meats and vegetables prepared by frying frying)
Seasonings containing large amounts of Spices, herbs, lemon juice, wine, flavored wine
sugar and saturated fats vinegars
Sauces and gravies
Salad dressings containing cream, cheese,
or mayonnaise

Table 5-17
GUIDELINES FOR A DIET LOW IN SATURATED FAT

Foods to Avoid Foods to Choose

Red meat especially when highly Lean cuts of meat, fresh fish, poultry from which skin
“marbled”; salami, sausages, was removed before cooking; meats that have been
bacon grilled
Whole milk, whipping cream Low-fat or skim milk
Tropical oils (coconut, palm oils; Monosaturated cooking oils, such as olive or canola oil
cocoa butter) Fresh fruit, vegetables
Candy Whole grain breads, cereals
Sweet rolls, donuts Nonfat yogurt, sherbet
Ice cream Vinegar, lemon juice
Salad dressings Unbuttered popcorn
Peanut butter, peanuts, hot dogs, Margarine (safflower oil listed as the first ingredient)
potato chips
Butter

Teaching: Activity/exercise
Discharge Instruction:

1282
1. Increase activity slowly; do not push, pull, or lift anything over
10 lb for 2 to 6 weeks. Do not drive until you talk with your
practitioner.

2. Try to develop a regular exercise and/or walking program. Start

off slowly and build up.

3. Plan for regular rest periods; let your body guide you in
decreasing or increasing activities.

4. Inform your practitioner of any changes in activity tolerance,

such as the development of new symptoms with the same activity.

Teaching: Disease Process; Teaching: Prescribed Diet and

Medications; Teaching: Prescribed Activity/Exercise; Risk
Identification

Care plans for carotid artery occlusive

disease
Ineffective tissue perfusion: Cerebral 
related to cerebral vascular disease.
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate cerebral perfusion as evidenced by RR less than 24
breaths/min, NSR on ECG, BP within 20 mm Hg of patient’s normal
range, HR less than 120 bpm (or within 20 bpm of resting HR for
patients on beta-blocker therapy), and cranial nerves II to XII intact
or equal to baseline.
Circulation Status; Neurological Status; Tissue Perfusion:
Cerebral

Cerebral perfusion promotion

1. Monitor vital signs per unit standards.

2. Assess for increased BP, decreased HR, and Cheyne–Stokes

respiration (may indicate increased intracranial pressure secondary
to hemorrhage).

1283
3. Assess for decreased BP, increased HR, and increased
respirations (may indicate cerebral ischemia).

4. Monitor for symptomatic bradycardia caused by vagal nerve

stimulation.

Neurologic monitoring

1. Monitor neurologic checks per unit standards.

2. Assess for presence of a gag reflex, difficulty swallowing, tongue

deviation to one side, or biting of tongue when eating.

3. Assess for symmetry of lip movements by having the patient

smile or show teeth.

4. Assess speech for hoarseness, and assess uvula for symmetry.

5. Assess shoulder alignment, strength of sternocleidomastoid

muscle by having the patient shrug his or her shoulders and rotate
his or her head to one side then the other while you provide
resistance to the head and shoulder movements.

Deficient fluid volume 

related to surgical blood loss
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate fluid volume with no signs of hematoma or
hemorrhage and normal Hgb and Hct.
Fluid Balance; Electrolyte and Acid-Base Balance

Hemorrhage control

1. Monitor vital signs, Hgb, and Hct.

2. Monitor dressing and drain (if present) for excessive

drainage/output.

3. Assess operative site for bruising or excessive swelling.

4. Monitor airway for any respiratory compromise or tracheal

1284
deviation related to cervical hematoma.

Care plans for peripheral artery occlusive

disease
Ineffective tissue perfusion: Peripheral 
related to decreased circulation resulting from atherosclerotic lower limb
vascular disease.
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
has adequate peripheral perfusion as evidenced by warm, dry skin;
normal or improved pedal pulses; normal color and temperature of
skin; normal or improved sensory and motor function; and brisk
capillary refill.
Sensory Function: Cutaneous; Tissue Integrity: Skin and
Mucous Membranes; Tissue Perfusion: Peripheral

Circulatory care: Arterial insufficiency

1. Palpate and/or auscultate per Doppler peripheral pulses distal to

treatment site (also pulses distal to catheter insertion site for
endovascular procedures). Report any decrease in pulse quality or
strength immediately.

2. Monitor capillary refill and temperature and color of skin.

3. Position extremity to optimize circulation.

4. Encourage passive and active ROM exercises.

5. Provide warmth and avoid prolonged exposure to the cold.

6. Instruct patient to avoid crossing legs.

Neurologic monitoring

1. Assess for decreased sensation of extremities and skin (skin

immediately surrounding incisions may be numb if a skin nerve is
cut during the incision).

1285
2. Ask the patient to wiggle his or her toes and flex and extend foot
and knee to assess motor function.

Skin surveillance

1. Assess skin integrity of both extremities and pressure points;

minimize external pressure points.

2. Change patient’s position as appropriate.

3. Promote proper foot care for operative leg and opposite foot as
opposite foot will be bearing more weight during convalescence.

4. Provide pressure-relieving mattress as appropriate.

Impaired skin integrity 

related to inadequate perfusion to maintain tissue integrity.
Goals/Outcomes: Within 12 to 24 hours of treatment, the patient
will maintain intact skin surfaces with healing wounds as
evidenced by normal skin temperature, color, and sensation (or
baseline); if open wound, minimal drainage present without odor; if
open wound, granulation tissue will be present; normal vital signs
and white blood count.
Tissue Integrity: Skin and Mucous Membranes; Wound
Healing: Primary Intention; Wound Healing: Secondary Intention

Pressure management

1. Assess skin integrity of both extremities and pressure points;

minimize external pressure points.

2. Change patient’s position as appropriate.

3. Provide pressure-relieving mattress as appropriate.

Wound care

1. Assess for decreased perfusion of the wound by assessing pain,

swelling, erythema, and drainage.

1286
2. Avoid further skin injury by not using tape directly on the skin.

3. Monitor for wound infection by assessing patient’s temperature,

WBC count, and exposure of bypass graft (if present).

4. Use aseptic technique for all dressing changes and incisional care.

5. Monitor incisions for drainage, erythema, tenderness, or

separation of suture/staple sites.

6. Monitor nutritional status: assess weight, albumin, and

prealbumin.

Care plans for patients undergoing

endovascular repair of stenosis or occlusion
Ineffective tissue perfusion: Peripheral 
related to presence of a device within the vessel.
Goals/Outcomes: See Goals/Outcomes and plan under Care
Plans for Peripheral Vascular Disease, (Chapter 5).

Deficient knowledge 
related to endovascular procedure and postprocedure care.
Goals/Outcomes: Within the 24-hour period before the
procedure, the patient describes the rationale for the procedure,
how it is performed, and postprocedure care. Patient relates
discharge instructions within the 24-hour period before discharge
from the ICU.
Knowledge: Treatment Procedures; Knowledge: Disease
Process; Knowledge: Medication; Knowledge: Prescribed Activity

Teaching: Carotid/peripheral arterial disease process

1. Discuss location of the patient’s disease using drawings as

possible.

2. Assess patient’s understanding of carotid/PAD and the purpose

of the endovascular procedure. Evaluate patient’s style of coping

1287
and degree of information desired.

Teaching: Procedure/treatment
As appropriate for coping style, discuss the following with patient
and significant others:

1. Use of local anesthesia and sedation during procedure

2. Insertion site of catheter: groin or arm

3. Sensations that may occur: mild pressure and/or a feeling of heat

as the dye is injected

4. Use of fluoroscopy during procedure. Determine patient’s history

of sensitivity to contrast material and use of medications that may
cause complications such as metformin.

5. Ongoing observations made by nurse after procedure: BP, HR,

leg or arm pulses, blood tests, observation of insertion site, neuro
checks as indicated, ABIs as indicated

6. Importance of lying flat in bed for 6 to 12 hours after procedure

unless a vascular closure device is used. Patients are able to get out
of bed sooner when a closure device is used.

7. Necessity for nursing assistance with eating, drinking, and

toileting needs after procedure while lying flat

8. Need for increased fluid intake after procedure to flush dye from
system

9. If the patient and significant others express or exhibit evidence of

anxiety regarding the procedure, try to arrange for them to meet
with another patient who has had a successful angioplasty.

Teaching: Prescribed medications/activity

Discharge Instructions:

1. Importance of taking antiplatelet medications to prevent

restenosis

1288
2. Avoidance of strenuous activity during the first few weeks at
home

3. Follow-up visit with vascular surgeon/primary care provider 1

week after hospital discharge

4. Signs and symptoms to report to physician

• Any pain or bruising at catheter insertion site

• Fever or drainage from insertion site

• Muscular pain or coolness in the extremity used for

the catheter insertion, not experienced before the
procedure

• Any return of symptoms present before procedure

Teaching: Disease Process; Teaching: Prescribed

Activity/Exercise; Anxiety Reduction; Infection Protection;
Decision-Making Support

Additional nursing diagnoses

Also see nursing diagnoses and interventions as appropriate in
Nutritional Support (Chapter 1), Hemodynamic Monitoring
(Chapter 1), Wound and Skin Care (Chapter 1), Pain (Chapter 1),
Prolonged Immobility (Chapter 1), Emotional and Spiritual Support
of the Patient and Significant Others (Chapter 2), Compartment
Syndrome/Ischemic Myositis (Chapter 3), Stroke: Acute Ischemic
and Hemorrhagic (Chapter 7), and Bleeding and Thrombotic
Disorders (Chapter 10).

Valvular heart disease

1289
Pathophysiology
Valves facilitate the unidirectional flow of blood from atrium to
ventricles (AV valves) or ventricles to pulmonary and systemic
circulation (semilunar valves). Disease that alters the valve’s
structure can affect any or all of the cardiac valves, resulting in
either stenosis or insufficiency. Stenosis results from the narrowing
of the valve orifice because of the inability of the valve to open
properly, causing partial obstruction. Insufficiency is the leaking of
blood around the orifice when the valve does not close properly,
resulting in regurgitation or backward flow of blood through the
valve. Both conditions result in higher pressure behind the valve
that reduces forward blood flow and CO. Stenosis and insufficiency
can occur independently or together and affect a single or multiple
valves.

Atrioventricular valves
AV valves are connected by chordae tendineae to papillary
muscles, enabling the valve cusp to point in the direction of blood
flow. Papillary muscle contraction holds the AV valves in place,
preventing them from being forced into the atria by the increased
ventricular pressure during contraction.

• Mitral: Has two leaflets/cusps and is located between the left

atrium and the left ventricle.

• Tricuspid: Has three leaflets/cusps and is located between the

right atrium and right ventricle.

Semilunar valves
Semilunar describes the half-moon shape of the valves. When
intraventricular pressures increase and exceed atrial and
pulmonary pressures, valves open, allowing blood to flow forward
into the pulmonary and systemic vasculature. Closure of the valves,
after ventricular contraction and ejection, prevents blood from
reversing or flowing backwards.

• Pulmonic: The pulmonic valve has three leaflets/cusps and is

1290
 located between the right ventricle and the pulmonary artery.

• Aortic: The aortic valve has three leaflets/cusps and is located

between the left ventricle and the aorta.

Valvular heart disease, whether from stenosis or insufficiency,

results in decreased CO because of the increase in pressure behind
the valve and reduced forward flow through the valve orifice.
Narrowing of the valve opening because of stenosis requires the
heart to pump harder through the smaller opening, thereby
reducing CO and increasing myocardial oxygen demand. A stenotic
aortic or pulmonic valve results in increased intramyocardial wall
tension. Over time, the increased cardiac workload leads to
thickening of the myocardial wall, reduced heart chamber size, and
subsequent reduced volume capacity and CO. This persistent
increase in wall tensions leads to ventricular hypertrophy and
remodeling as the heart compensates for the excess workload.
Atrial and ventricular dilatation caused by prolonged increased
pressure increases the incidence of atrial fibrillation.
Insufficiency from inadequate closing of the valve leaflets causes
reverse flow, which causes blood to accumulate in the pulmonary
and systemic vasculature. Blood is unable to flow forward through
the heart and systemic circulation, resulting in symptoms of fluid
overload including orthopnea with pulmonary and peripheral
edema. Impaired perfusion within the coronary vasculature results
in decreased oxygen-rich blood within the myocardium, which
causes chest pain, dysrhythmias, and dyspnea. When the demand
for increased flow becomes greater than the supply during exertion
or extreme stress, the result is fatigue and dyspnea.

Mitral valve disease

• Mitral stenosis: Mitral stenosis is most commonly caused by the
inflammatory response to rheumatic heart disease resulting in
thickening or stiffening of the valve leaflets, commissures, or
chordae tendineae. The formation of small lesions known as
Aschoff bodies and tiny pin-head size deposits called rheumatic
vegetations embed in the endocardial, myocardial, and valvular
structures and lead to stenosis of valve structures many years

1291
 after the acute phase of rheumatic endocarditis. Diastolic doming
of the anterior leaflet (hockey-stick deformity) and an immobile
posterior leaflet give the valve a fish-mouth appearance and
restrict the valve orifice. Pressure in the left atrium increases
caused by the extra force needed to drive blood through the
narrowed opening. Eventually, left atrial hypertrophy and
stiffening of the left atrial wall change the surrounding structures
and increase pulmonary artery pressure. Additionally, the
structural abnormalities of the atria contribute to changes in atrial
conduction patterns leading to atrial fibrillation in half of
individuals with mitral stenosis.

• Mitral insufficiency/regurgitation (MR): Can be caused by injury

or disruption to any part of the valve including the mitral
annulus, the leaflets (a large anterior [aortic] leaflet and a small
posterior [mural] leaflet), the chordae tendineae, and the
papillary muscles. The most common etiologies of MR include
mitral valve prolapse, rheumatic heart disease, infective
endocarditis, annular calcification, cardiomyopathy, and ischemic
heart disease. Pure MR is most commonly caused (71%) by a
myxomatous (floppy, prolapse) process. Rheumatic heart disease
(postinflammatory disease) accounts for 9% of cases. HF may
occur acutely following rupture of an infarcted papillary muscle
or chronically from papillary muscle fibrosis, hypertrophy, or LV
dilatation.

Tricuspid valve disease

• Tricuspid stenosis: Usually associated with mitral stenosis
resulting from rheumatic heart disease. In the absence of mitral
stenosis, the possibility of right atrial myxoma (tumor) should be
eliminated.

• Tricuspid regurgitation (TR)/insufficiency (TI): TR/TI is more

common than tricuspid stenosis. Two types of patients are noted:
those with normal leaflets and those with abnormal leaflets.
Functional TR results from annular dilatation secondary to
pulmonary hypertension associated with other valvular
disorders. Acquired TR is less common, originating from an

1292
 abnormality of the leaflets because of a variety of disease
processes. Medications used to treat migraine (e.g.,
methysergide), Parkinson disease (e.g., pergolide), and obesity
(e.g., fenfluramine) have been associated with TR.

Aortic valve disease

• Aortic stenosis (AS): A bicuspid (versus tricuspid) aortic valve is
congenital and occurs predominantly in males and in 1% to 2% of
the population. Most develop stenosis as a result of excess
stresses on the valve from asymmetrical flow patterns and
turbulence causing structural thickening, calcification, leaflet
retraction, or aortic regurgitation. In adults, stenosis usually
develops over a period of many years. Left ventricular diastolic
dysfunction, reduced coronary reserve, and myocardial ischemia
from longstanding systolic pressure overload eventually leads to
depressed contractility and LV systolic dysfunction, HF, and
finally sudden death. Often these patients remain symptom free
until the late stage of the disease. The onset of symptoms (i.e.,
angina, syncope, and HF) depicts poor prognosis and mortality
within 2 to 5 years. Mortality rates are worse for those with
moderate to severe AS treated medically, at 25% and 50% at 1
and 2 years, respectively. Approximately 50% of deaths are from
sudden cardiac death.

• Aortic insufficiency (AI)/regurgitation (AR): Acute AR results

from a rapid increase in end-diastolic volume caused by
regurgitant blood flow from endocarditis or aortic dissection. The
left ventricle fills from both the left atrium and by retrograde or
reverse flow from the aorta through the leaky aortic valve. In
acute AR, the left ventricle does not have time to dilate in
response to the volume load, resulting in chest pain and acute
respiratory distress secondary to pulmonary edema. In severe
cases, ventricular dilatation and hypertrophy cannot compensate
for AI and HF develops, deteriorating to CS when CO no longer
meets the systemic demand. Early surgical intervention should be
considered. AR caused from aortic dissection requires immediate
surgical intervention.

1293
• Chronic AR occurs in response to gradual dilatation of the left
ventricle and symptoms are masked by compensatory
mechanisms. Once symptoms become severe, rapid decline
follows.

Pulmonic valve disease

• Pulmonic stenosis: Obstruction of the RV outflow tract may be
acquired or congenital. Pulmonary stenosis accounts for 5% to 8%
of all congenital heart defects. Mild pulmonary stenosis may not
require intervention but is susceptible to infective endocarditis.
Severe pulmonary stenosis (pulmonary atresia) is complete
fusion of commissures with complete obstruction of the
pulmonary artery outflow tract. An increased pressure gradient
across the valve results in RV hypertrophy and right HF.

• Pulmonic insufficiency (PI)/regurgitation (PR): PI/PR causes

include leaky valve after repair, RV conduit to pulmonary artery
obstruction, pulmonary hypertension, congenital defects
including large ducts (Ebstein anomaly), and tetralogy of Fallot
with ventricular septal defect, pulmonary stenosis, RV
hypertrophy, or overriding aorta. Abnormalities in sizes of heart
structures cause variations in directional flow, vessel and heart
chamber pressures, volume, and function, resulting in poor
cardiac and systemic oxygenation and circulation.

Assessment: Valvular heart disease

Goal of system assessment
Evaluate for LV and RV failure, decreased CO, and decreased tissue
perfusion. Many persons with longstanding valvular disease
leading to atrial enlargement develop atrial fibrillation and should
be monitored for the dysrhythmia, HF, and thrombosis. Cardiac
cachexia may be seen in persons with longstanding valvular
dysfunction as inflammatory processes release catecholamines,
endotoxins, and tumor necrosis factors, causing cell breakdown,
weight loss, and weakness. Early recognition of clinical changes
and timely intervention are essential to improved outcomes.

1294
History and risk factors
Causes of valvular heart disease

• Rheumatic heart disease

• Congenital malformations

• Connective tissue disease (Marfan syndrome, systemic lupus

erythematosus)

• Rheumatoid arthritis

• Chronic inflammatory disease (ankylosing spondylitis, giant cell

arteritis)

• Acute myocardial infarction with papillary muscle rupture

• Drug use (intravenous drug abuse, combination weight loss

drugs fenfluramine, dexfenfluramine, and phentermine)

• Advanced age

• Mitral valve prolapse

• Infective endocarditis

• Annular calcification

• Cancer

• Syphilis

• Pulmonary hypertension

• Cardiomyopathy

• Ischemic heart disease

Physical assessment
Murmurs: Auscultation of heart sounds is the most effective

1295
 screening tool for valvular disease. Evaluate changes in quality,
pitch, and intensity to obtain insight into the patient’s clinical
condition, functional capacity, and quality of life. Changes in the
quality and sound of murmurs can provide essential information
regarding the clinical condition of patients with valvular heart
disease.

Classifications of Murmurs: Murmurs are classified as systolic,

diastolic, or continuous (throughout the cardiac cycle) with the
characteristics described as holosystolic/pansystolic,
midsystolic/systolic ejection, early, or late systolic. Diastolic
murmurs are early, middiastolic, or presystolic.

MITRAL VALVE DISEASE

Assessment Mitral Stenosis Mitral Insufficiency

Findings
Observation Dyspnea, pulmonary congestion, Dyspnea, pulmonary congestion,
edema, hemoptysis, slight cyanosis, edema, fatigue, weakness,
fatigue, weakness symptoms related to left-sided heart
failure
Auscultation Increased amplitude of S1; opening snap Holosystolic murmur loudest in the
and mid-diastolic murmur at the mitral mitral area and transmitted to the
area axilla or left sternal edge
Chest Atrial enlargement Left and right ventricular
radiograph enlargement
12-lead ECG Left atrial abnormality; humped or Left ventricular hypertrophy; large S
notched P wave (P “mitrale”); right wave in V1, large R wave in V4, and
ventricular hypertrophy; deep S in minor atrial abnormality; atrial and
leads I and V5, tall R in V1; atrial ventricular arrhythmias
fibrillation
Hemodynamics Elevated pulmonary artery occlusive V waves in the pulmonary artery,
pressure (PAOP), elevated pulmonary increased systolic PAP, decreased
artery pressure (PAP), elevated venous CO. Acute mitral regurgitation (MR)
pressure, decreased cardiac output causes increased preload and
(CO), elevated left atrial pressure decreased afterload with an increase
(LAP). Patients will not experience in end-diastolic volume (EDV) and
valve-related symptoms until the valve decrease in end-systolic volume
area is >2 to 2.5 cm2, when moderate (ESV). The total stroke volume (TSV)
exercise may cause exertional dyspnea. is markedly increased, but forward
Severe mitral stenosis (valve area <1 stroke volume (FSV) is decreased
cm2) results in an increased resting because much of the TSV
diastolic mitral valve gradient and regurgitates, resulting in increased
increased LAP. Pulmonary LAP. In chronic compensated MR,
hypertension may develop. As PAP the left atrium and ventricle dilate to
increases, the right ventricle (RV) accommodate the regurgitant
dilates and tricuspid regurgitation may volume, so LAP may be normal or
develop, resulting in increased jugular minimally elevated. In the chronic
venous pressure, liver congestion, decompensated phase, muscle

1296
 ascites, and pedal edema. LV end- dysfunction decreases both TSV and
diastolic pressure (LVEDP) and CO are FSV, but EF may be normal. ESV
often normal when only the mitral and EDV increase, then LAP and
valve is stenosed. With progressive LVEDP increase, pulmonary edema
stenosis, the CO becomes subnormal at may occur, and if unmanaged,
rest and fails to increase during cardiogenic shock ensues.
exercise.

TRICUSPID VALVE DISEASE

Assessment
Aortic Stenosis Aortic Insufficiency
Findings
Observation Faint slow radial pulse, low blood Dyspnea, pulmonary congestion, edema,
pressure and pulse pressure, symptoms related to left-sided heart
dizziness, fainting, syncope, failure. Aortic regurgitation (AR) is
pallor, dyspnea, fatigue; chest indicated by three findings: Corrigan
pain caused by coronary pulse is a palpated pulse with rapid and
insufficiency, irregular heart forceful distention of the artery followed

1297
 sounds, and left-sided heart by quick collapse. DeMusset sign is
failure forward and backward bobbing of the
head. Quincke sign is visible pulsation
seen with slight compression of nail beds.
Hill sign is popliteal cuff systolic blood
pressure 40 mm Hg higher than brachial
cuff systolic blood pressure.
Auscultation Increased amplitude of S1; Diastolic blowing murmur heard loudest
opening snap and mid-diastolic at the second right intercostal space
murmur at the mitral area beginning with S2. Duroziez sign is a
systolic murmur over the femoral artery
with proximal compression of the artery,
and a diastolic murmur with distal
compression of the artery.
Chest Left ventricular (LV) enlargement LV enlargement
radiograph and dilation of the ascending
aorta
12-lead ECG LV hypertrophy; large S in V2, LV hypertrophy; large S in V2, large R in
large R in V5; strain results in V5; strain results in inverted T and
inverted T and depressed ST depressed ST segments in I and II and Vl,
segments in I and II and Vl, V5, V5, and V6.
and V6, bradydysrhythmias
Hemodynamics Increased LV pressure, increased Increased LV pressure, increased
pulmonary artery end-diastolic peripheral artery disease (PAD) and
pressure and wedge pressure; pulmonary artery occlusive pressure
increased gradient across the (PAOP), decreased cardiac output;
aortic valve on pullback from LV increased systolic blood pressure and
end-diastolic pressure to aortic widened pulse pressure. Peripheral pulses
pressure; narrow pulse pressure, are prominent or bounding. Symptoms
decreased cardiac output. LV may result from the elevated stroke
systolic function is preserved and volume during systole and the
cardiac output is maintained for incompetent aortic valve allowing
many years despite an elevated significantly decreased aortic diastolic
LV systolic pressure. Despite the pressure (often <60 mm Hg), with pulse
cardiac output at rest being pressures often >100 mm Hg. During early
normal, it fails to increase chronic AR, the LV ejection fraction (EF) is
appropriately during exercise, normal or increased. As AR progresses,
causing exercise-induced syncope LV enlargement exceeds preload reserve
or near syncope. With severe and the EF decreases to normal and then
aortic stenosis, atrial contraction subnormal levels. The LV end-systolic
is vital to diastolic filling of the volume increases and reflects progressive
LV so atrial fibrillation can be myocardial dysfunction. The LV gradually
catastrophic to maintaining stroke transforms from an elliptical to a spherical
volume. configuration.

Diagnostic Tests for Evaluation of Valvular Disease

1298
Collaborative management
Care priorities

1. Consider antibiotic prophylaxis for infective endocarditis

and rheumatic fever
Prophylaxis, which was once mandatory for all patients, is now
controversial. Providing prophylactic antibiotics has not been
shown to prevent the development of endocarditis valve disease in
all patient populations. Varying levels of evidence support the
following recommendations from the 2014 ACC/AHA Task Force
Writing Committee.

2014 ACC/AHA GUIDELINES FOR ANTIBIOTIC PROPHYLAXIS

FOR INVASIVE DENTAL PROCEDURES

1299
High-Risk Recommended Not Recommended
•Patients with prosthetic valves • Aggregated lifetime risk of endocarditis
• Prior infective endocarditis • GU and GI procedures (TEE,
• Cardiac transplant patients with esophagogastroduodenoscopy, colonoscopy,
regurgitation caused by abnormal valve cystoscopy) (See Acute Infective Endocarditis,
structure Chapter 5).
• Unrepaired and palliated cyanotic
congenital heart defects (surgically
constructed palliative shunts and conduits)
• Repaired congenital heart defects
(prosthetic material or devices) first 6
months postprocedure
• Congenital heart defects with residual
defects at or adjacent to the prosthetic
patch or device that inhibits
endothelialization

Prevention of endocarditis continues to be important for all

patients with valvular heart disease (VHD). Patient education
including good daily oral hygiene and regular dental visits is
essential. Additionally, aseptic measures during catheter
manipulation or any invasive procedure, to reduce the rate of
healthcare-associated infective endocarditis, have been included in
the recommendations by the European Society of Cardiology (ESC).

2. Manage aortic stenosis

• Monitoring: Frequently for progression of the disease, including

asymptomatic patients; stenosis requires initial and serial visits
for grading severity and evaluation of symptoms.
Echocardiography is indicated annually for severe AS, every 1 to
2 years for moderate AS, and every 3 to 5 years for mild AS.

• Medical management: The overall goal using medical therapy is

to manage and treat related cardiovascular conditions and
comorbidities that exacerbate AS. Patient education including
lifestyle and behavioral modifications, infection prevention, and
nutrition, as well as symptom recognition and self-management
techniques, is essential in optimizing management and reducing
hospital readmissions. Additionally, palliative care and end-of-
life discussions should be included early in the plan of care.

• Hypertension: Use antihypertensive agents cautiously.

1300
• Decision about surgery: Need is based largely on the patient’s
symptoms, rather than exclusively on the transvalvular pressure
gradient. Angina, syncope, and HF can develop suddenly,
sometimes following a lengthy asymptomatic period. Following
onset of symptoms, survival averages 2 to 3 years.

• Aortic valve replacement (AVR): AVR was the first effective

treatment shown to improve symptoms and long-term survival
in patients with severe symptomatic AS, including the very
elderly; it is the only class I recommendation by ACC/AHA and
ESC (2013). Furthermore, patients undergoing coronary bypass
surgery with known moderate AS should have the valve replaced
simultaneously. Valve replacement during coronary bypass
surgery for patients with mild AS is unsupported. According to
the Society of Thoracic Surgeons (STS) registry, the mortality rate
is less than 3% for all patients undergoing AVR. However, risk
stratification is necessary especially in elderly patients with
comorbid conditions. Valve types can be mechanical or
bioprosthetic (tissue). Mechanical valves are preferred in younger
patients because of the longevity of the valve. On the other hand,
in the elderly, tissue valves have been favored over mechanical,
because of improvements in valve durability and reduced need
for anticoagulation.

• Transcatheter aortic valve replacement (TAVI/TAVR): First

performed in 2002, TAVR using the transapical or transfemoral
approach has become one of the most widely used methods to
treat AS, especially in patients with high surgical risk. Procedural
success rates are reported to be greater than 90%. Patients
undergoing TAVR can have their valve repaired or replaced in
the cardiac catheterization lab under moderate sedation.
Currently, most data regarding TAVR are based on the use of
two replacement valves, the Sapien valve from Edwards Life
Sciences, Inc., and the Core Valve from Medtronic, Inc. Data are
limited as TAVR/TAVI is a relatively new procedure. However,
there have been no reports of structural deterioration to date.
Studies are ongoing and according to a multicenter randomized
clinical trial comparing TAVR with standard therapy, benefits

1301
 greatly outweigh risks in inoperable patients with severe
symptomatic AS. Results show significantly improved quality of
life during the first year following TAVR/TAVI.

• Aortic balloon valvotomy: In patients with a high risk for surgery,

balloon aortic valvuloplasty may be a reasonable option of
therapy. However, there is a high rate of recurrence of AS, and
restenosis often recurs within 6 months.

3. Manage aortic insufficiency/regurgitation

• Crisis: Can occur acutely resulting in pulmonary edema

and/or CS. Death from CS, ventricular dysrhythmias, and PEA is
common with acute, severe AR.

• Urgent surgery: Inodilators such as milrinone and inamrinone are

used to help increase CO. Dopamine and dobutamine may be
used to increase contractility and, along with vasodilators such as
nitroprusside, reduce LV afterload for preoperative stabilization.
Immediate surgery is recommended for symptomatic patients
with acute AR resulting from infective endocarditis.

• Balloon counterpulsation: NOT recommended for acute AR; may

be harmful.

• Compensatory tachycardia: Vital for survival in acute AR; beta

blockers must be used with caution, especially when treating
aortic dissection.

• Medications: Vasodilators are used for those with chronic severe

AR who are not surgical candidates. Diuretics, nitrates, and
digoxin are sometimes used to help control symptoms, but there
are insufficient data to justify recommending or discouraging
these therapies.

• Chronic AR: Management is based on LV systolic function. If LV

systolic dysfunction occurs (a reduced EF at rest) and cannot be
controlled with antihypertensive therapy, patients may require
AVR. Initially, the process of ventricular remodeling is reversible

1302
 with management of afterload (BP/SVR) using vasodilators.

4. Manage mitral stenosis

• Monitoring: A progressive, lifelong disease generally resulting

from rheumatic fever. Patients’ symptoms can remain
insignificant for up to 10 years then suddenly develop HF and
decline rapidly. When severe pulmonary hypertension develops,
average survival is 3 years.

• Atrial fibrillation: Up to 40% of patients develop atrial

fibrillation. Anticoagulation, is recommended to avoid clot
formation and thromboembolism. Heart rate can be controlled
using amiodarone, CCBs, beta adrenergic-blocking agents, or
digoxin. Cardioversion may be required if the patients are
uncontrolled with oral medications and become symptomatic.
Ablation may be an option for select patients.

• Percutaneous balloon mitral valvotomy (PBMV): Recommended

for symptomatic patients without severe pulmonary
hypertension. Moderate to severely symptomatic patients with
PA systolic pressure of greater than 60 mm Hg may require a
mitral commissurotomy or mitral valve replacement (MVR).

5. Manage mitral regurgitation

• Crisis: May occur acutely, as in AMI, resulting in CS. Sodium

nitroprusside, NTG, or ACEIs are used in combination with
inotropic agents (e.g., dobutamine or dopamine) to avoid severe
hypotension.

• Balloon counterpulsation therapy: Provides stabilization by

helping to increase forward blood flow, resulting in increased
MAP and reducing the volume of regurgitation and LV preload
(LV end-diastolic pressure).

• MVR: May be necessary for stabilization of severely symptomatic

patients.

1303
• Transcatheter interventions: Increasingly studied for carefully
selected patients with severe MR. Data are limited and there is
FDA approval for only one device to date. ACC, AATS, SCAIF,
and STS recommendations and guidelines are in development.

• Mitral valve repair: Recommended for patients with a lesser

degree of LV dysfunction.

• Chronic MR: Patients may remain in a stable, compensated state

for many years. Incidence of sudden death in asymptomatic
patients varies widely among documented studies. There is no
universally recommended medical therapy.

• LV systolic dysfunction: Patients may benefit from ACEIs or beta

adrenergic–blocking agents (e.g., carvedilol) and biventricular
cardiac pacing to reduce regurgitant volume.

• Acute atrial fibrillation: Managed with CCBs, beta blockers,

digoxin, and sometimes amiodarone to promote control of
tachycardia.

• Chronic atrial fibrillation: May require a Maze procedure

(ablation); may be done simultaneously with mitral valve repair
to help prevent stroke. All patients with chronic atrial fibrillation
require long-term anticoagulation with warfarin.

6. Manage tricuspid valve disease

• Surgery: Tricuspid valve repair, valve replacement, or

annuloplasty for TR often occurs during mitral valve surgery.

• Severe TR: Patients have poor long-term outcomes because of RV

dysfunction with or without systemic venous congestion.

7. Manage pulmonic valve disease

• Pulmonic valve stenosis: Pulmonic stenosis is usually congenital,

not likely because of acquired heart disease, and managed with
percutaneous balloon valvotomy. Most patients undergoing
valvotomy for stenosis also have MR.

1304
• Pulmonic regurgitation: Generally not seen unless other valve
disease is present. It is also likely to be a congenital defect and
typically managed with pulmonic valve replacement if HF is
present.

8. Provide lifelong anticoagulation for patients with

prosthetic heart valves

• Warfarin: Maintain the international normalized ratio (INR) as

follows:

• Aortic valve: INR 2.5 to 3.0

• Mitral valve: INR 3.0

• Low-dose aspirin: 75 to 100 mg daily is recommended in addition
to warfarin therapy for both aortic and mitral valves with or
without risk factors for thromboembolism (e.g., atrial fibrillation,
previous thromboembolism, or a hypercoagulable state, and
older generation mechanical AVR).

9. Provide short-term anticoagulation for patients with

biological heart valves

• Warfarin is recommended for the first 3 months following

surgery, unless at higher risk of thromboembolism, wherein
anticoagulation may be continued long-term.

• At least two-thirds of patients do not require lifelong

anticoagulation.

10. Reverse excessive anticoagulation

• INR greater than 5: Increases the possibility of bleeding

and/or hemorrhage

• Prosthetic heart valve: If the patient with an INR 5 to 10 is not

bleeding, withholding warfarin and giving vitamin K
(phytonadione) 1 to 2.5 mg orally daily until INR normalizes is

1305
 appropriate. In the case of uncontrolled bleeding, fresh-frozen
plasma or prothrombin complex concentrate is recommended
over higher-dose parenteral (IV) vitamin K1, which often results
in a hypercoagulable state. Low-dose IV vitamin K (1 mg) has
been found to be safer, if needed. Aspirin should also be
discontinued.

11. Manage thrombosis of prosthetic valves

• Emergency surgery: Recommended for patients with left-

sided heart valves with NYHA class III to IV HF and a large clot
burden.

• Fibrinolytic therapy: May be appropriate for patients with right-

sided valves with class II to IV HF and large clot burden, or those
with left-sided valves with NYHA class I to II HF and smaller clot
burden.

Surgical interventions
• Valve replacement: Procedure with a mortality rate of about 6%,
performed in patients with moderate to severe calcification,
stenosis with insufficiency, and pure insufficiency. Three types of
replacement valves are available: homografts and heterografts,
which are tissue grafts, and mechanical valves. Homografts are
specially treated human cadaver valves and are seldom used
because of a lack of availability. The more commonly used
heterograft is a specially prepared valve from an animal, usually
a pig or a cow. These valves are readily available and more
advantageous because there is less of a tendency for clot
formation and adherence to the valve structures. Thus, patients
do not require anticoagulation therapy after valve replacement.
The disadvantage is that they function for only 5 to 8 years.
Mechanical valves are made from stainless steel, carbon, plastic,
and other durable materials. Mechanical valves have a 10- to 15-
year life span and require lifelong anticoagulation because of
their susceptibility to clot formation. Postoperative care is similar
to that of the patient who has undergone myocardial
revascularization for CAD (see Acute Coronary Syndromes,

1306
 Chapter 5). Patients undergoing valve surgery are at increased
risk for thrombosis, embolism, and valvular endocarditis
(particularly with mechanical mitral valves and patients with
atrial fibrillation).

• Commissurotomy: A procedure in which the stenotic valve is

opened using a dilating instrument. When performed early in the
course of the disease, chances of success are good, although the
procedure may result in valve regurgitation and recurrent
stenosis.

• Reshaping: A portion of the diseased valve is removed and the

valve is sewn back together to promote more effective closure.

• Decalcification: Calcium deposits are removed to allow the

smooth surface of the valve to close more effectively.

• Patching: Covering damaged portions or “holes” in valves with

tissue to improve valve closure.

• Surgical valvuloplasty: Valvular repair may be possible in select

patients. In addition, insertion of a valvular ring can improve
native valve function.

• Percutaneous balloon valvuloplasty: For dilation of stenotic heart

valves. Candidates for this procedure may (1) be at high risk for
surgery, (2) refuse surgery, (3) be older adults (often older
than 80 years), or (4) be informed of treatment choices and choose
this procedure over others. The procedure parallels the technique
for percutaneous coronary intervention (see Acute Coronary
Syndromes, Chapter 5). The patient undergoes this procedure in
the cardiac cath lab, and a transfemoral approach is used. The
femoral artery and vein are accessed and supravalvular and LV
pressures are obtained. The valve gradient is measured pre- and
postdilatation of the valve. Despite modifications in procedural
techniques peri- and postprocedure complications and restenosis
rates remain high. Complications include thromboembolic stroke,
disruption of the valve ring, acute valve regurgitation, valvular
restenosis, hemorrhage at the catheter insertion site, guidewire

1307
 perforation of the left ventricle, and dysrhythmias.

Care plans for valvular heart disease

For patients undergoing valve replacement

Ineffective protection 
related to risk of bleeding/hemorrhage secondary to
anticoagulation.

Patients undergoing aortic valve replacement are at a higher

risk for postoperative hemorrhage than are those undergoing
coronary artery bypass grafting.

Goals/Outcomes: Throughout hospitalization, the patient is free

of symptoms of bleeding or hemorrhage as evidenced by RAP 4 to 6
mm Hg, PAWP 6 to 12 mm Hg, BP within patient’s normal range,
CO 4 to 7 L/min, CI 2.5 to 4 L/min/m2, urine output 0.5 mL/kg/h or
greater, urine specific gravity 1.010 to 1.030, and chest tube
drainage 100 mL/h or less.
Circulation Status

Circulatory precautions

1. Monitor for hemorrhage and clotting: Monitor vital signs and

measure chest tube drainage hourly. Report chest tube drainage
greater than 100 mL/h. Maintain patency of chest tubes at all times.

2. Monitor clotting studies: Report and manage prolonged PT, PTT,

and ACT and decreased platelet count. Optimal values are as
follows: PT 11 to 15 seconds, PTT 30 to 40 seconds (activated), and
ACT 120 seconds or less. For a patient with prolonged PT, PTT, or
ACT, administer IV protamine sulfate as prescribed if heparin was
the anticoagulant used. After discharge from the hospital, the INR
should be maintained at 2.5.

1308
3. Monitor hemodynamics for hypovolemia: RAP less than 4 mm
Hg, PAWP less than 6 mm Hg, decreased BP, decreased measured
CO/CI, urine output less than 0.5 mL/kg/h, increased urine specific
gravity, and excessive chest tube drainage (more than 100 mL/h). Be
alert to a decreased Hct. Optimal values are Hct greater than 37%
(female) and greater than 40% (male).

4. Assess postoperative chest radiograph for a widened

mediastinum, which may indicate hemorrhage and possible cardiac
tamponade.

5. Manage hemorrhage: Orders may include administration of

platelets, fresh-frozen plasma, or cryoprecipitate to replace clotting
factors and blood volume.

6. Administer packed RBCs as prescribed to replace blood volume

or use chest tube drainage for autotransfusion.

7. Manage hyperfibrinolytic state (increased fibrin degradation

products): Orders may include aminocaproic acid given slowly per
IV bolus (Box 5-9).

Box 5-9
NURSING IMPLICATIONS FOR
ADMINISTRATION OF EPSILON-
AMINOCAPROIC ACID
• Be aware that rapid administration may induce hypotension,
bradycardia, or cardiac dysrhythmias.

• Monitor for and report the following side effects: nausea, cramps,
diarrhea, dizziness, tinnitus, headache, skin rash, malaise, nasal
stuffiness, postural hypotension.

• Be alert to clotting or thrombosis, which can be precipitated by

this medication. Assess for indicators of thrombophlebitis: calf
erythema, warmth, tenderness, or increase in size or positive
reaction for Homan sign. Provide pneumatic compression

1309
 stockings as prescribed.

• Assess for indicators of pulmonary emboli: chest pain, dyspnea,

fever, tachycardia, cyanosis, falling blood pressure, restlessness,
agitation.

• Monitor and report blood levels of epsilon-aminocaproic acid via

use of chromatography, if available in the institution.

• Consult advanced practice provider promptly for significant

findings.

Bleeding Reduction; Autotransfusion; Hemorrhage Control

Decreased cardiac output (or risk for same) 

related to negative inotropic changes secondary to intraoperative
subendocardial ischemia and administration of myocardial depressant
drugs.

After cardiac surgery, some myocardial depression is always

present, usually lasting 48 to 72 hours. Patients with long-
standing aortic stenosis or ventricular failure caused by mitral
valve disease are at an even greater risk for postoperative low
cardiac output.

Goals/Outcomes: Within 48 to 72 hours, the patient has adequate

CO as evidenced by NSR on ECG, measured CO of 4 to 7 L/min, CI
greater than 2.5 L/min/m2, BP within patient’s normal range, PAP
20 to 30/8 to 15 mm Hg, PAWP 6 to 12 mm Hg (or range specified
by physician), SVO2 60% to 80%, SVR 900 to 1200 dynes/sec/cm-5,
peripheral pulses greater than 2+ on a 0 to 4+ scale, warm and dry
skin, and hourly urine output greater than 0.5 mL/kg/h. Patient is
awake, alert, and oriented.
Cardiac Pump Effectiveness

1310
Shock prevention

1. Monitor peripheral pulses and color and temperature of

extremities every 2 hours.

2. Provide oxygen therapy as prescribed.

3. Maintain an adequate preload (i.e., PAWP greater than 10 mm

Hg, RAP 10 mm Hg) via administration of IV fluids.

With aortic stenosis and severe LV hypertrophy, a high

filling pressure (i.e., pulmonary artery wedge pressure greater than
18 mm Hg) may be necessary to ensure an adequate cardiac output.

4. Maintain a normal or reduced afterload (SVR less than 1200

dynes/sec/cm-5) by administering prescribed IV vasodilating drugs
such as nitroprusside and NTG.

5. Maintain NSR by administering antidysrhythmic agents as

prescribed. Atrial fibrillation is common in aortic and mitral valve
disease and may result in a 20% to 50% decrease in CO. If a
junctional rhythm or bradycardia occurs, a pacemaker may be
necessary.

6. Administer inotropic agents as prescribed to maintain CI greater

than 2.5 L/min/m2 and systolic BP greater than 90 mm Hg.
Commonly used agents include dobutamine, dopamine, milrinone,
and amrinone. Monitor for side effects, including
tachydysrhythmias, ventricular ectopy, headache, and angina.

Cardiac Care; Hemodynamic Regulation

Ineffective tissue perfusion (or risk for same): Cerebral 

related to impaired blood flow to the brain secondary to embolization
resulting from cardiac surgery.

1311
An air embolus, particulate emboli from calcified valves, and
thrombotic emboli from prosthetic valves may lodge in the brain,
leading to varying degrees of stroke.

Goals/Outcomes: Throughout hospitalization, the patient has

adequate or baseline brain perfusion as evidenced by orientation to
time, place, and person; equal and normoreactive pupils; and
ability to move all extremities, communicate, and respond to
requests (or comparable to patient’s preoperative baseline).
Neurologic Status

Neurologic monitoring

1. Monitor patient immediately after surgery and hourly for signs of

neurologic impairment: diminished LOC, pupillary response,
ability to move all extremities, and response to verbal stimuli.

2. Assess patient’s orientation and ability to communicate, answer

yes/no questions, point to objects, write responses and requests,
identify family members, and state his or her location. Inform other
healthcare personnel about patient’s LOC and communication
deficits.

3. Assess patient’s PT, PTT, and INR as heparin is tapered off and
warfarin therapy is instituted. Heparin and warfarin may be
initiated simultaneously to reduce the time needed to stabilize the
lab values.

4. If CNS impairment is noted, report findings to the physician and

administer medications for brain resuscitation as prescribed.

5. In the presence of CNS impairment, implement the following

measures:

• Assist patient with turning and moving as needed.

Teach the patient to use unaffected extremities to

1312
 assist with moving.

• Perform ROM to all extremities 4 times daily. Have

patient assist as much as possible.

• Progress patient’s activity level, as tolerated, with

the assistance of a physical therapist.
6. Assess patient’s ability to swallow food and fluids. If the patient’s
voice is hoarse or patient coughs when swallowing, consult
advanced practice provider. Patient may require nothing-by-mouth
status and an enteric tube until the swallowing reflex has improved.

Surveillance; Cerebral Perfusion Promotion

Deficient knowledge 
related to risk of infective endocarditis after valve surgery and preventive
strategies.

All patients who have undergone valve surgery are at risk

for infective endocarditis as a result of bacteria entering the
bloodstream and traveling to the heart, leading to destruction of a
new tissue valve or obstruction of a new artificial valve.

Goals/Outcomes: Within the 24-hour period before discharge

from the CCU, the patient verbalizes knowledge about the risk of IE
after valve surgery and the precautions that must be taken to
prevent it.
Knowledge: Disease Process

Teaching: Disease process

1. Teach the patient about IE (see Acute Infective Endocarditis,

Chapter 5), describing what it is, how it develops, and how it may

1313
affect the repaired valve.

2. Teach the patient to caution dentists and other healthcare

providers so antibiotics can be prescribed to prevent development
of endocarditis after valve surgery. Antibiotics must be taken before
any dental work or examination by instrument, including teeth
cleaning, fillings, extractions, cystoscopy, endoscopy, or
sigmoidoscopy.

3. Instruct patient to cleanse all wounds and apply antibiotic

ointments to help prevent infection.

Teaching: Prescribed Medication; Surveillance

Deficient knowledge 
related to risk of bleeding or clotting caused by excessive or insufficient
anticoagulation therapy.

It can be difficult to find and maintain the dosage of warfarin

needed to maintain target international normalized ratio. Foods,
medications, vitamins, and food supplements can enhance or
inhibit efficacy.

Goals/Outcomes: Within the 24-hour period before discharge

from the hospital, the patient or significant others verbalize
knowledge about the risk of warfarin therapy after valve surgery
and the precautions that must be taken to prevent embolism or
hemorrhage.
Knowledge: Treatment Regimen

Teaching: Prescribed medication

Teach the patient and significant others:

1. How to institute bleeding precautions after discharge. Shave with

an electric razor. Take care when handling sharp objects. Prevent
injury through an annual safety home check. Use a soft-bristle
toothbrush.

1314
2. To call advanced practice provider if bleeding or bruising is
noted.

3. To report all changes in medication to healthcare provider who is

managing warfarin or other anticoagulant therapy.

4. To avoid altering the intake of foods that may be high in vitamin

K. Excessive intake of vitamin K can block warfarin and lower the
INR.

Teaching: Prescribed Diet; Surveillance

For patients undergoing percutaneous balloon

valvuloplasty

Deficient knowledge 
related to procedure for percutaneous balloon valvuloplasty (PBV) and
postprocedural assessment.
Goals/Outcomes: Within the 24-hour period before PBV, the
patient verbalizes rationale for the procedure, the technique, and
postprocedural care.
Knowledge: Treatment Regimen

Teaching: Preoperative

1. Assess patient’s understanding of aortic stenosis and the purpose

of valvuloplasty. Evaluate patient’s style of coping and the degree
of information desired.

2. Discuss with patient and significant others the valvuloplasty

procedure, including the following:

• Location of diseased valve, using heart drawing

• Use of local anesthesia and sedation during

procedure

• Insertion site of catheter: femoral artery and vein

1315
• Use of fluoroscopy during procedure. Evaluate
patient for a history of sensitivity to contrast
material.

• Postprocedural observations made by nurse: BP,

HR, ECG, pulses, and catheter insertion site

• Importance of lying flat for 6 to 12 hours after the

procedure to minimize the risk of bleeding

Teaching: Procedure/Treatment

Decreased cardiac output (or risk for same) 

related to altered preload and negative inotropic changes associated with
valve regurgitation or hemorrhage secondary to PBV; Altered rate,
rhythm, or conduction associated with dysrhythmias secondary to PBV.
Goals/Outcomes: Throughout the postoperative course, the
patient has adequate CO as evidenced by NSR, CO 4 to 7 L/min, CI
greater than 2.5 L/min/m2, HR 60 to 100 bpm, RAP 4 to 6 mm Hg,
PAWP 6 to 12 mm Hg, PAP 20 to 30/8 to 15 mm Hg, BP within
patient’s normal range, urinary output greater than 0.5 mL/kg/h,
peripheral pulses greater than 2+ on a 0 to 4+ scale, orientation to
time, place, and person; and absence of new murmurs, pulsus
paradoxus, or jugular vein distention.
Cardiac Pump Effectiveness

Shock prevention

1. Monitor ECG continuously after procedure. Document any

changes. Consult advanced practice provider for dysrhythmias, and
treat according to hospital protocol.

2. Monitor CO/CI, HR, RAP, PAWP, and PAP hourly or as

prescribed. Report a fall in CO/CI, a change in HR, and an increase
or decrease in RAP, PAWP, or PAP.

1316
3. Monitor Hct and electrolyte values. Observe for a decrease in Hct
or any change in electrolyte levels (particularly potassium) that
could precipitate dysrhythmias. Optimal values are Hct greater
than 37% (female) or greater than 40% (male) and serum potassium
3.5 to 5 mEq/L.

4. Assess heart sounds immediately after procedure and every 4

hours. Report the development of a new murmur.

5. Monitor patient for evidence of cardiac tamponade: hypotension,

tachycardia, pulsus paradoxus, jugular vein distention, elevation
and plateau pressuring of PAWP and RAP, and possibly an
enlarged heart silhouette on chest radiograph study. For more
information, see Acute Cardiac Tamponade, Chapter 5.

Cardiac Care; Hemodynamic Regulation

Ineffective protection 
related to risk of hemorrhage or hematoma formation secondary to
heparinization with PBV.
Goals/Outcomes: Throughout the postoperative course, the
patient has minimal or absent bleeding or hematoma formation at
the catheter insertion site. PTT is within therapeutic anticoagulation
range (as prescribed or according to institutional procedure).
Circulation Status

Bleeding precautions

1. Monitor catheter insertion site for evidence of bleeding. Report

hematoma formation, and outline the bleeding on the dressing for
subsequent comparison.

2. Keep patient’s catheterized leg straight for the prescribed amount

of time.

3. Monitor heparin drip as prescribed. Usually heparin drip is

maintained until 1 to 2 hours before the sheaths are removed.

4. Monitor PTT for therapeutic range, which is usually 1.5 times

1317
that of normal.

5. When IV or invasive lines (arterial or venous sheaths) are

removed, apply firm pressure either manually or with a mechanical
clamp for 30 minutes.

Surveillance; Bleeding Reduction: Wound

Additional nursing diagnoses

Also see Deficient Knowledge in Pulmonary Embolus (Chapter 4).
Also see Altered Tissue Perfusion in Acute Coronary Syndromes
(Chapter 5). See all nursing diagnoses in the discussion of Coronary
Artery Bypass Graft in Acute Coronary Syndromes (Chapter 5).
Also see nursing diagnoses and interventions in Hemodynamic
Monitoring (Chapter 1), Prolonged Immobility (Chapter 1), and
Emotional and Spiritual Support of the Patient and Significant
Others (Chapter 2).

1318
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CHAPTER 6

Kidney injury
Genitourinary assessment: General
Goal of system assessment
Evaluate for decreased renal function and assess the severity of
renal dysfunction.

Detailed health history

• Chronic symptoms of fatigue, weight loss, anorexia, nocturia, and
pruritus.

• Renal-related symptoms including dysuria, edema, frequency,

hematuria, flank pain, pyuria, frothy urine, bloody urine, and
renal colic.

• Presence of comorbidities: hypertension, congestive heart failure,

diabetes, multiple myeloma, chronic infection, and
myeloproliferative disorder.

• Current medications including over-the-counter medications.

• Exposure to chemicals.

• Recent trauma or unaccustomed exertion.

• Recent diagnostic studies requiring dye administration.

• Considerations for the bariatric patient: History of difficult

1341
 urinary catheterization

Observation
Evidence of chronic versus acute process:

• Skin: petechiae, purpura, ecchymosis, livedo reticularis, dryness,

pallor, yellowness, decreased turgor.

• Eyes: uveitis, ocular palsy, findings suggestive of hypertension,

atheroembolic disease.

• Inspection of the flank area in a standing and supine position for

raised masses or unusual pulsations.

• Considerations for the bariatric patient: Large folds of

abdominal skin covering the genitourinary area causing retracted
penis or vagina. Look for bulging areas that could be a hernia.
Adequate urinary output is 0.5/kg/h.

Vital sign assessment

Evaluate for changes indicative of fluid volume excess or depletion
and infection.

• Blood pressure (BP) and pulse both lying and standing.

• Respiratory rate (RR).

• Height and weight.

• Temperature.

Palpation
Abdominal assessment to identify renal pathology:

• Costovertebral angle tenderness, which may occur with

pyelonephritis.

• Enlarged liver, which may occur with congestive heart failure.

1342
• Kidneys are difficult to palpate because of location. If they are
enlarged and palpable, this could represent polycystic kidney
disease or hydronephrosis.

• Ascites may occur with liver failure or acute renal failure.

• Lower extremity or sacral edema.

• Bladder tenderness and distension.

Auscultation
• Cardiac auscultation for the presence of murmurs, pericardial
friction rub, S3 and/or S4 and congestive heart failure.

• Lung auscultation for the presence of pleural rub, rales, decreased

breath sounds, and volume excess states.

Labwork
Renal dysfunction causes marked changes in fluid and electrolyte
balance, acid-base balance, and red cell production, and increased
concentrations of blood urea nitrogen (BUN) and creatinine.

• Complete blood count (CBC) to evaluate anemia.

• Electrolytes including calcium, phosphorus, and magnesium.

• BUN and creatinine.

• Estimated glomerular filtration rate (eGFR) to evaluate clearance.

• 24-hour urine collection for creatinine clearance, protein, and

metanephrines.

• Urinalysis.

• Urine electrolytes.

• Considerations for the bariatric patient: Monitor creatinine

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 levels.

Acute kidney injury

Pathophysiology
Acute kidney injury (AKI) is a complex syndrome characterized by
a rapid decline in GFR that results in disturbances in fluid,
electrolyte, and acid-base balances. The evolution of AKI can occur
over a number of hours to days and is usually accompanied by a
marked decline in urine output and retention of metabolic wastes
including urea and creatinine. The Kidney Disease/Improving
Global Outcomes (KDIGO) clinical practice guidelines define three
stages of AKI that reflect changes in serum creatinine and urine
output (Table 6-1). These stages provide the basis for early
recognition and stage-based management of AKI.

Table 6-1
KIDNEY DISEASE/IMPROVING GLOBAL OUTCOMES (KDIGO)
CRITERIA FOR THE DIAGNOSIS OF ACUTE KIDNEY INJURY

Stage Serum Creatinine Urine Output Criteria

1 1.5 to 1.9 baseline <0.5 mL/kg/h for 6 to 12 hours
OR
≥0.3 mg/dL (≥26.5 µmol/L) increase
2 2.0 to 2.9 times baseline <0.5 mL/kg/h for ≥12 hours
3 3.0 times baseline <0.3 mL/kg/h for ≥24 hours
OR OR
Increase in serum creatinine to ≥4.0 mg/dL Anuria for ≥12 hour
(≥353.6 µmol/L)
OR
Initiation of renal replacement therapy
OR
in patients <18 years, decrease in estimated
glomerular filtration rate to <35 mL/min per 1.73 m2

Formation of urine is a three-step process consisting of (1)

ultrafiltration of delivered blood by the glomeruli (renal cortex), (2)
internal processing of the ultrafiltrate via tubular secretion and
reabsorption (renal parenchyma), and (3) excretion of waste
products from the kidneys through the ureters, bladder, and
urethra. Corresponding to those steps, AKI is categorized as

1344
prerenal, intrarenal, and postrenal (Table 6-2).

Table 6-2
CAUSES OF ACUTE KIDNEY INJURY

Prerenal Intrarenal Postrenal

Decreased Effective Arterial Tubular Injury Bladder Neck
Volume • Ischemia • Prostatic disease
• Hypovolemia • Toxins (drugs, pigments) • Pelvic
• Decreased cardiac contractility • Interstitial malignancies
• Systemic vasodilation (sepsis) • Allergic: beta-lactams, sulfa drugs, • Bladder
NSAIDs carcinoma
Renal Vasoconstriction • Infection: pyelonephritis • Neurogenic
• NSAIDs • Infiltrative: sarcoid, lymphoma, bladder
• ACEIs leukemia
• Angiotensin blockers Ureteral
• Calcineurin inhibitors Glomerular Diseases • Nephrolithiasis
• Hypercalcemia • Poststreptococcal • Urethral strictures
• Hepatorenal syndrome glomerulonephritis • Blood clots
• IgA nephropathy (e.g., Berger’s • Retroperitoneal
Large Vessel-Renal Artery Issues disease) disease
• Renal artery stenosis • Lupus glomerulonephritis Tubular
• Thrombosis • Precipitation of
• Embolism Renal Vessel Disease crystals
• Dissection • Thrombosis
• Vasculitis • Vasculitis
• Atheroembolic
Increased Intraabdominal • Microangiopathy
Pressure
• Intraabdominal compartment
syndrome
ACEIs, Angiotensin-converting enzyme inhibitors; GI, gastrointestinal; IgA,
immunoglobulin A; NSAIDs, nonsteroidal antiinflammatory drugs.

Prerenal AKI, or azotemia, is the result of decreased blood flow

to the kidneys below the limit of autoregulation. Autoregulation is
the process by which the kidneys maintain a relatively constant
level of renal blood flow and GFR. In response to low renal blood
flow, preglomerular arterioles vasodilate whereas postglomerular
arterioles vasoconstrict. The net effect is relatively constant
glomerular capillary hydrostatic pressure. Autoregulation is
effective until the mean arterial pressure (MAP) drops lower than
75 to 80 mm Hg. While autoregulation fails, there is a reduction in
GFR. Drugs that interfere with autoregulation such as angiotensin-
converting enzyme inhibitors (ACEIs) and nonsteroidal
antiinflammatory drugs (NSAIDs) may provoke prerenal AKI
through exacerbating renal hypoperfusion. In response to reduced

1345
perfusion, stretch receptors in the glomerular afferent arterioles
cause vasodilation. Vasodilation is also enhanced by the production
of prostaglandins, kallikrein, kinins, and nitric oxide. NSAIDs
inhibit prostaglandin production, thereby diminishing afferent
arteriole vasodilation prompting low filtration pressure. Efferent
arterioles normally increase vasoconstriction in response to
angiotensin II. Angiotensin II inhibitors and blockers interfere with
the efferent arteriole response to hypoperfusion. Patients receiving
ACEIs with a glomerular filtration critically dependent on the
angiotensin II–regulated efferent arteriole vascular tone (patients
with heart failure or severe volume depletion) can experience low
efferent arteriolar pressure, which contributes to reduced filtration.
Prerenal AKI is reversible if treated promptly. Treatment is directed
at the underlying cause of decreased renal blood flow. Intravascular
volume depletion, reduced cardiac output, systemic vasodilation,
renal vasoconstriction, and increased intraabdominal pressure are
causes of hypoperfusion. A consequence of prolonged
hypoperfusion includes renal tissue ischemia and the subsequent
development of intrarenal AKI.
Intrarenal AKI is caused by direct insults to the glomerular or
tubular structures. The most common form of intrarenal AKI is
acute tubular necrosis (ATN). In addition to renal ischemia, ATN
may be the result of nephrotoxic injury produced by medications,
radiocontrast media, infection, and exposure to toxic substances
such as heavy metals, pesticides, and organic solvents. Conditions
that produce myoglobinuria and hemoglobinuria can also lead to
tubular injury. Contrast material–induced nephropathy (CIN) is a
form of ATN that develops within 12 to 48 hours of contrast
administration. Risk factors for CIN include diabetes mellitus,
chronic kidney disease, hypotension, volume depletion, cirrhosis,
heart failure, and administration of nephrotoxic agents. Although
the development of low-osmolality contrast agents and prevention
protocols have reduced the incidence of CIN, most patients in the
intensive care unit would have one or more risk factors for the
development of CIN. Clinicians weigh the diagnostic benefit of
using contrast material during imaging procedures and the risk of
CIN.

1346
6-1
RESEARCH BRIEF
Purpose: The authors conducted a systematic review and
metaanalysis of controlled studies comparing the incidence of
acute kidney injury (AKI) in patients who received intravenous
(IV) contrast media with patients who underwent an imaging
procedure without contrast media.
Methods: MEDLINE, EMBASE, Scopus, and the Cochrane
Library were searched for studies that compared the incidence of
AKI in patients exposed to IV contrast medium with the incidence
of AKI in unexposed patients. Changes in serum creatinine level or
estimated glomerular filtration rate 48 to 72 hours following
imaging procedures or admission were used for the detection of
AKI. Relative risk was calculated and tested in subgroups of
different patient comorbidities, contrast medium types, and AKI
diagnostic criteria.
Results: Thirteen nonrandomized studies (25,950 patients) met
inclusion criteria. The average rate of AKI was 6.4% in the contrast
medium group and 6.5% in the noncontrast group. The risks of
AKI, dialysis, and death were similar for both groups regardless of
IV contrast medium type, diagnostic criteria for AKI, or whether
patients had diabetes mellitus or renal insufficiency.
Conclusion: Controlled contrast medium–induced nephropathy
studies demonstrate a similar incidence of AKI, dialysis, and death
between the contrast medium group and control group.
ATN is characterized by tubular cell necrosis, cast formation,
and tubular obstruction caused by casts and cellular debris.
Therapy is focused on maintenance of renal perfusion pressure,
administering renal vasodilators to restore blood flow, and
promoting diuresis to “wash out” the intratubular debris. ATN is
sometimes nonoliguric. Oliguria may occur with both toxic ATN
and ischemic ATN. Common nephrotoxic agents are found in
Table 6-3.
From McDonald J, McDonald R, Comin J, et al: Frequency of acute kidney injury following
intravenous contrast medium administration: a systematic review and meta-analysis.
Radiology 267:119-128, 2013.

1347
Table 6-3
COMMON NEPHROTOXINS

Exogenous Endogenous
Antineoplastics Rhabdomyolysis
• Methotrexate Hemolysis
• Cisplatin Tumor Lysis Syndrome

Antimicrobials
• Amphotericin
• Aminoglycosides
• Acyclovir
• Penicillins

Nonsteroidal Antiinflammatory Drugs

• Ibuprofen
• Ketorolac

Chemicals
• Ethylene glycol
• Pesticides
• Organic solvents
• Radiocontrast Medium

Postrenal failure is the least common cause of AKI and may be

either intrarenal (within the kidney) or extrarenal (outside the
kidney in another area of the elimination tract) obstruction.
Intrarenal obstruction is often attributable to crystal deposition
caused by medications (e.g., acyclovir, indinavir, sulfonamides,
methotrexate) or endogenous substances (oxalate, uric acid).
Extrarenal obstruction may be related to bladder outlet problems
(prostate and urethral obstruction) or stones, clots, pus, tumor,
fibrosis, or ligation of or papilla within the ureters.
Fluid, electrolyte, and acid-base disorders that occur with AKI
include hypervolemia, hyperkalemia, hyperphosphatemia,
hypocalcemia, hypermagnesemia, and metabolic acidosis (Table 6-
4). Phosphate levels rise because of impaired excretion of
phosphorus by the renal tubules with continued gastrointestinal
(GI) absorption. Hypocalcemia results from the lack of active
vitamin D, which is activated by the kidney, which would
otherwise stimulate absorption of calcium from the GI tract, or high
phosphate levels, which inhibit absorption of calcium.
Hypocalcemia triggers the parathyroid glands to secrete
parathyroid hormone (PTH), which mobilizes calcium from the
bone into the blood. Hypermagnesemia is generally moderate (2 to

1348
4 mg/dL) and is rarely symptomatic unless the patient receives
magnesium-containing antacids (e.g., Maalox, Milk of Magnesia).

Table 6-4
ALTERED ELECTROLYTE BALANCE IN ACUTE KIDNEY INJURY

Condition/Cause Nursing Implications

Hyperkalemia
Decreased ability to excrete K+; K+ release • Monitor ECG for tall and peaked T waves, loss of
with catabolism P waves, prolonged PR interval, widened QRS
when K+ is greater than 6.5 mEq/L. Cardiac arrest
is more likely seen with K+ greater than 7.5 mEq/L.
• Monitor serum K+ levels for values greater than 5
mEq/L.
• Monitor the patient for indicators such as
paresthesias, muscle weakness or flaccidity, and
HR less than 60 bpm.
• Teach the patient and significant others the
indicators of hyperkalemia and the importance of
notifying the nurse promptly if they occur.
• Provide a list of foods high in potassium and
emphasize the importance of avoiding these
foods.
• Implement the following to help minimize the
cellular release of potassium:
• Ensure the patient consumes only the amount of
protein prescribed by the advanced practice
provider ; enforce sound infection control
techniques to minimize risk of infection; and treat
fevers promptly. Catabolism of protein, which
occurs in these situations, causes potassium to be
released from tissues.
• Ensure the patient consumes the allotted amounts
of carbohydrates, and limit strenuous patient
activity as prescribed, both of which will spare
protein.
• Be aware that hyperkalemia can be a fatal
complication, especially during the oliguric phase
of AKI, because of its adverse effect on cardiac
status. Keep emergency supplies (i.e., manual
resuscitator, crash cart, emergency drug tray)
readily available.
Hypokalemia
Prolonged, inadequate oral intake; use of • Monitor ECG for prolonged PR interval, flattened
potassium-losing diuretics without or inverted.
proper replacement; excessive loss from • T wave, depressed ST segment, presence of U
vomiting, diarrhea, or gastric or wave, and ventricular dysrhythmias; ECG
intestinal suctioning changes are more likely to occur at serum K+ levels
less than 3 mEq/L.
• Be alert to serum K+ less than 3.5 mEq/L.
• Monitor the patient for muscle weakness, soft and
flabby muscles, paresthesias, decreased bowel
sounds, ileus, weak and irregular pulse, and
distant heart sounds.

1349
 • Neuromuscular symptoms are seen at serum
levels of approximately 2.5 mEq/L.
• Teach the patient and significant others the
indicators of hypokalemia and the importance of
notifying the nurse promptly if they occur.
• Provide a list of foods high in potassium and
assist with planning menus that incorporate them.
• Administer potassium-sparing diuretics (e.g.,
spironolactone, triamterene) as prescribed.
• Administer oral or IV potassium supplements as
prescribed; for oral route, administer with at least
4 oz water or juice to minimize gastric irritation.
Hypernatremia
The inability of the kidneys to excrete • Monitor serum sodium levels for serum Na+
excess sodium; decreased water intake; greater than 147 mEq/L.
increased water losses via osmotic • Monitor VS and I&O hourly; weigh the patient
diuresis; excessive parenteral daily.
administration of sodium-containing • Be alert to dry mucous membranes, flushed skin,
solutions (e.g., sodium bicarbonate, 3% firm and rubbery tissue turgor, hyperthermia,
sodium chloride) oliguria, or anuria.
• Assess sensorium for restlessness and agitation;
institute seizure precautions as indicated.
• Administer prescribed IV replacement fluids.
• Administer diuretics as prescribed.
Hyponatremia
Loss through vomiting, diarrhea, profuse • Monitor for serum Na+ less than 137 mEq/L.
diaphoresis; use of potent diuretics; salt- • Monitor input and output hourly; record weight
losing nephropathies; administration of daily for trend.
large amount of sodium-free IV fluids • Assess the patient for abdominal cramps,
(may be associated with fluid volume diarrhea, nausea, dizziness when changing
excess or postobstructive diuresis) position, postural hypotension, cold and clammy
skin, and apprehension.
• Provide parenteral replacement therapy as
prescribed.
• Institute a safe environment for individuals with
altered LOC.
Hypocalcemia
Poor absorption of dietary calcium; • Monitor for serum Ca2+ less than 8.5 mg/dL.
precipitation of calcium out of tissues in • Monitor for numbness and tingling around the
the presence of elevated phosphorus mouth, muscle twitching, facial twitching, and
level; inadequate absorption and use of tonic muscle spasms.
calcium occurring with lack of • Assess for Trousseau sign (carpopedal spasm)
conversion of vitamin D to its usable and Chvostek sign (spasm of lip and cheek).
form • Administer calcium and vitamin D supplements
as prescribed.
• Reinforce the necessity of taking these
medications as prescribed.
• Teach the patient and significant others the
indicators of hypocalcemia.
• Teach the importance of continued medical
follow-up to check serum Ca2+ levels.
Hyperphosphatemia
Abnormal retention of phosphates • Monitor for serum phosphate greater than 4.5
caused by the inability of the kidneys to g/dL.
excrete excess phosphorus • Although most foods contain generous amounts
of phosphate, those especially high in phosphate
include beef, pork, dried beans, dried mature

1350
 peas, and dairy products. Monitor the patient’s
diet accordingly.
• Administer phosphate binders as prescribed.
Assess for constipation, which may result from
use of phosphate binders.
• Teach the patient and significant others the
relationship between calcium and phosphate
levels in the body.
• Emphasize that maintaining good phosphate
control and calcium balance may help control
itching and prevent future problems with bone
disease.
• Reinforce the need for follow-up visits to check
serum phosphate levels.
Hypermagnesemia
Administration of magnesium- • Monitor serum Mg2+ levels greater than 2.5
containing medications to patients with mEq/L.
impaired renal function • Assess for diaphoresis, flushing, hypotension,
drowsiness, weak-to-absent DTRs, bradycardia,
lethargy, and respiratory impairment.
• Teach the indicators listed above to the patient
and significant others.
• Avoid giving medications that contain
magnesium (see Box 1-7). Emphasize to the
patient that such medications should not be taken
without the physician’s approval.
Metabolic Acidosis
The inability of the kidneys to excrete • Monitor for HCO3− less than 22 mEq/L and pH
excess acid produced by normal less than 7.35.
metabolic processes; marked tissue • Monitor input and output, LOC, and VS.
trauma, infection, and diarrhea may • Be alert to Kussmaul’s respirations, SOB,
contribute to a more rapid development anorexia, headache, nausea, vomiting, weakness,
of acidosis (often associated with K+ apathy, fatigue, and coma.
greater than 5 mEq/L) • Institute seizure precautions in the presence of
altered LOC.
• Administer IV fluids and bicarbonate as
prescribed.
• Teach the patient the importance of dietary
restrictions, particularly of protein, and of
maintaining adequate carbohydrate intake to
prevent worsening acidosis.
• Emphasize that the patient should report to the
advanced practice provider increased temperature
and other signs of infection.
• Teach the patient the importance of taking
sodium bicarbonate as prescribed and of
maintaining the dialysis schedule (both
hemodialysis and peritoneal dialysis help correct
acidosis)
Uremia
Failure of the kidneys to excrete urea, • Monitor the patient for chronic fatigue, insomnia,
creatinine, uric acid, and other metabolic anorexia, vomiting, metallic taste in the mouth,
waste products pruritus, increased bleeding tendency, muscular
twitching, involuntary leg movements, decreasing
attention span, anemia, muscle wasting, and
weakness.
• Teach the patient and significant others that the

1351
 indicators of uremia develop gradually and are
very subtle. Explain the importance of notifying
the nurse of sudden worsening of the symptoms
that may be present.
• Monitor and record dietary intake of protein,
potassium, and sodium.
• Use lotions and oils to lubricate the patient’s skin
and relieve drying and cracking.
• Provide oral hygiene at frequent intervals, using a
soft-bristle toothbrush and mouthwash, to help
combat the patient’s thirst and the metallic taste
caused by uremia. Chewing gum and hard candy
may also help alleviate thirst and the unpleasant
taste.
• Encourage isometric exercises and short walks, if
the patient is able, to help maintain the patient’s
muscle strength and tone, especially in the legs.
• Teach significant others that because of the
patient’s decreasing concentration level, they
should communicate with the patient by using
simple and direct statements.
• Teach the patient to maintain good nutrition by
ingesting the allotted amounts of carbohydrates
and high–biological value protein to support cell
rebuilding and decrease waste products from
protein breakdown.
• Explain that profuse bleeding can occur with
uremia and that knives, scissors, and other sharp
instruments should be used with caution.
• Stress that OTC medications such as aspirin and
ibuprofen may enhance bleeding tendency.
• Emphasize the importance of follow-up visits to
evaluate the progression of uremia.
• Stress that the dialysis schedule should be
maintained to decrease the symptoms of uremia
and correct many of the metabolic abnormalities
that occur.

AKI, Acute kidney injury; Ca2+, calcium; DTR, deep tendon reflex; ECG,
electrocardiogram; HCO3−, bicarbonate; HR, heart rate; I&O, intake and output; IV,
intravenous; K+, potassium; LOC, level of consciousness; Mg2+, magnesium; Na+,
sodium; OTC, over-the-counter; SOB, shortness of breath; VS, vital signs.

There are three identifiable stages/phases of AKI:

1. Oliguric phase: A drop in the 24-hour urinary output to less than

400 mL lasting approximately 7 to 14 days. Approximately 30% of
patients have nonoliguric kidney failure.

2. Diuretic phase: A doubling of the urinary output from the

previous 24-hour total. During this phase the patient may produce
as much as 3 to 5 L of urine in 24 hours.

1352
3. Recovery phase: A return to a normal 24-hour volume (1500 to
1800 mL). Usually, kidney function continues to improve and may
take 6 months to 1 year from the initial insult to return to baseline
functional status.

Assessment
Goal of assessment
AKI impacts most of the major organs and the focus of assessment
is to determine how AKI is affecting these organs. Assessment
findings contribute to the development of a treatment plan that
manages fluid, electrolyte, and acid-base imbalances, as well as
prevents or minimizes metabolic encephalopathy, anemia, and
infection.

History and risk factors

The assessment of AKI begins with a comprehensive history of the
patient including the presence of chronic illness (e.g., diabetes
mellitus, hypertension, heart failure, cancer, chronic kidney
disease). Recent changes in urine patterns and weight as well as
recent infections, trauma, procedures, or surgery may establish the
risk as well as a time frame for the onset of AKI. A review of patient
medications including prescriptions, over-the-counter medications,
and herbal/complimentary practices is important in the
development of the treatment plan. Some herbal products such as
mu tong, fangchi, and Aristolochia fangchi contain aristolochic acid,
which can cause acute interstitial nephritis. A. fangchi is listed as the
ingredients “aristolochia,” “bragantia,” or “as arum” on the label.
Aristolochia is sometimes substituted for other botanicals,
including Stephania tetrandra, Clematis armandii, and akebia extract.
Juicing is a popular health practice that has been implicated in
the development of AKI related to oxalate nephropathy. The
practice of “juicing” or “juice cleansing” typically refers to a 3- to
10-day period where the diet consists of fruit and vegetable juice.
Oxalate is a nephrotoxin found in fruits, vegetables, and nuts.
Typically, oxalate absorption and secretion occurs in the GI tract. If
the concentration of oxalates consumed during juicing exceeds the

1353
secretion capacity of the intestine, oxalate enters the circulatory
system with subsequent renal tubular exposure. Recreational drug
use (e.g., cocaine, methamphetamines, and bath salts) has also been
implicated in the development of AKI.

Special populations at risk

Morbid Obesity: According to the World Health Organization,
morbid obesity is defined as a body mass index greater than 40
kg/m2. This measure expresses weight in relation to height and
provides an estimate of fat burden for the human body. The
incidence of AKI among patients who are morbidly obese is
unknown. Detection of AKI is complicated by an unclear
association between weight and urine production. Weight-based
formulas for collecting creatinine clearance have not been validated
for this population. Several factors may contribute to the
development of kidney dysfunction. Creatinine production is
increased as a result of body mass. Structural and functional
nephron changes include glomerular hyperfiltration,
glomerulomegaly, and glomerulosclerosis. Comorbidities
associated with obesity including chronic kidney disease, diabetes
mellitus, sleep-disordered breathing, heart failure, and
hypertension also increase the risk of AKI. The risk of increased
intraabdominal pressure and abdominal compartment syndrome is
greater in individuals who are obese. Orlistat is a GI lipase inhibitor
prescribed for weight loss and has been associated with the
development of acute oxalate nephropathy. Drug prescription
based on actual weight may result in nephrotoxic doses of
lipophilic drugs. The volume distribution of a drug is influenced by
lipophilicity. The use of adjusted body weight (ABW) is
recommended for lipophilic drugs including unfractionated
heparin, aminoglycosides, corticosteroids, and propofol. The
formula for ABW is:

Older Adult: Chronic illnesses, polypharmacy, impaired

1354
thirst sensation, and the structural /functional changes of aging
increase the risk of AKI in older adult patients. There is a natural
decline in kidney size, GFR, and renal blood flow with advancing
age. An impaired ability to concentrate urine increases the risk of
volume depletion and may predispose the older adult patient to
prerenal azotemia. Diagnosis of AKI in older adults can be
challenging. KDIGO guidelines use serum creatinine and urine
production for staging AKI. Serum creatinine levels are influenced
by age, muscle mass, hydration status, and race. AKI may be
obscured by a low or normal serum creatinine level in the older
adult population. Serial changes in creatinine values, urine output,
and weight may be more helpful in the detection of AKI in the older
adult.

Prerenal presentation
• Oliguric or nonoliguric.

• Urinary sodium (Na+) less than 20 mEq/L.

• Urine specific gravity greater than 1.020.

• Urine osmolality greater than 500 mOsm/L.

• Hyaline casts possible.

• Elevated plasma BUN/creatinine ratio (greater than 20:1).

• Fractional excretion of sodium (FENa) less than 1%. FENa is the

ratio between urine sodium excretion and the filtered load of
sodium. It reflects how well the kidney can concentrate urine and
conserve sodium. It can be greater than 1% in prerenal AKI, with
diuretic and bicarbonate use, and with chronic kidney disease.

Intrarenal presentation

• Oliguric or nonoliguric.

• Urinary Na+ greater than 20 mEq/L.

1355
• Urine specific gravity 1.010.

• Urinary osmolality less than 350 mOsm/L.

• Abnormal sediment with red blood cell (RBC) casts and cellular
debris in the urine.

• Decreased plasma BUN/creatinine ratio (10:1).

• Fractional excretion of sodium (FENa) greater than 1% FENa is the

ratio between urine sodium excretion and the filtered load of
sodium. It reflects how well the kidney can concentrate urine and
conserve sodium. The ratio can be less than 1% in ATN
associated with radiocontrast administration and
rhabdomyolysis.

Postrenal presentation
• Likely oliguric but may be nonoliguric.

• Urinary chemical indices are typically normal.

• Normal or mildly abnormal sediment (hematuria, pyuria, and

crystals).

• Often associated with urinary tract or pelvic cancer.

• Often associated with renal/ureteral calculi.

Vital signs
• BP may be elevated in states of fluid volume excess or decreased
in states of fluid volume deficit.

• Heart rate (HR) may be increased or decreased with abnormal

rhythms based on fluid and electrolyte abnormalities.

• Weight may be increased or decreased based on fluid volume

status.

1356
• Temperature: may be hyperthermic or hypothermic with sepsis.

Observation
• Peripheral edema and periorbital edema.

• Jugular venous distention.

• Shortness of breath.

• Kussmaul respirations associated with metabolic acidosis.

• Poor skin turgor, flushed skin, and dry mucous membranes.

• Pallor.

• Purpura.

• Weakness.

• Altered mental status and disorientation.

• Signs of central nervous system depression.

• Neuromuscular dysfunction.

• Dysrhythmias.

Palpation
• Edema (scale 0 to 4+): extremities and sacrum.

• Muscle tenderness.

• Suprapubic tenderness or distention.

• Flank tenderness.

Auscultation
• S3 and S4 gallops indicative of heart failure.

1357
• Pericardial friction rub.

• Tachycardia or dysrhythmias.

• Pulsus paradoxus in the presence of pericardial effusion/cardiac

tamponade.

• Crackles.

• Bruits over the renal arteries indicative of renovascular disease.

Uremic manifestations
• Drowsiness, confusion, irritability, and coma.

• Anemia and bleeding tendencies.

• Pallor, yellow dry skin, pruritus.

• Hypertension.

• Heart failure.

• Pericarditis with cardiac tamponade.

• Pulmonary edema.

• Anorexia, nausea, vomiting.

• Tremors, twitching, seizures.

• Uremic halitosis and stomatitis.

• Increased susceptibility to infection.

Screening laboratory tests

• BUN and creatinine: Elevations indicative of renal impairment.
Elevated BUN is an early indication of hydration and
possible renal issues in the older adult.

1358
• GFR: Most reliable estimation of GFR is the measurement of 24-
hour creatinine clearance.

• Electrolyte levels: Elevated or decreased potassium, phosphorus,

magnesium, and sodium.

• Urinalysis: Presence of sediment including tubular epithelial cells,

debris, casts, protein, RBC casts, or myoglobin.

• Urinary sodium: Prerenal disease results in urinary sodium levels

less than 10 mEq/L.

• Fractional excretion of sodium (FENa): Assesses how well the

kidney can concentrate urine, it is affected by numerous
conditions that affect the renal parenchyma and is not a sensitive
indicator of AKI.

• CBC and coagulation studies (prothrombin time [PT], partial

thromboplastin time [PTT]): Evaluate for hematologic
complications.

• Arterial blood gas (ABG) values: Evaluate for metabolic acidosis

associated with AKI.

Diagnostic Tests for Acute Kidney Injury

Test Purpose Abnormal Findings

Ultrasonography Provides general appearance of Small scarred kidneys
kidney; integrity of collecting Renal mass
system Kidney stones
Hydronephrosis
Computed Evaluates kidney and collection Renal mass
tomography system Ureteral stones
without contrast
Magnetic More specific in detecting renal Tumors or cysts
resonance masses and vessel malformations Vessel malformation
imaging/Magnetic
resonance
angiography
Cystoscopy Diagnoses partial or complete Bladder or ureteral stenosis or
obstruction obstruction.
Renal Evaluates renal vessels Thrombotic, stenotic lesions in the
angiography main renal vessels.
Renal biopsy Determines intrarenal pathology Acute glomerulonephritis, vasculitis,
or interstitial nephritis.

1359
Blood Studies
Complete blood Assesses for anemia, inflammation, Decreased RBCs, Hgb, or Hct reflects
count (CBC) and infection; assists with anemia or recent blood loss.
Hemoglobin differential diagnosis of septic
(Hgb) cause of acute renal failure/acute
Hematocrit (Hct) kidney injury (ARF/AKI)
Red blood cell
(RBC) count
White blood cell
(WBC) count

Coagulation Assesses for the presence of Decreased PT with low INR promotes
profile: bleeding or clotting and clotting; elevation promotes bleeding.
Prothrombin disseminated intravascular
time (PT) with coagulation (DIC)
international
normalized
ratio (INR)
Partial
thromboplastin
time (PTT)
Blood urea Assesses for the severity of renal Elevation indicates renal dysfunction.
nitrogen (BUN) dysfunction Creatinine may be markedly elevated
Creatinine in the presence of massive skeletal
Estimated muscle injury (e.g., multiple trauma,
glomerular crush injuries).
filtration rate BUN is influenced by hydration,
(eGFR) catabolism, gastrointestinal
bleeding, infection fever, and
corticosteroid therapy.
The eGFR in ARF/AKI is usually less
than 50 mL/min. BUN may elevate
before creatinine in the setting of
dehydration or hypovolemia,
particularly in older adults.
Electrolytes: Assesses for abnormalities Increase or decrease in K+ may cause
Potassium (K+) associated with AKI arrhythmias. Elevated Na+ may
Sodium (Na+) indicate dehydration.
Calcium (Ca2+) Decreased Na+ may indicate fluid
Magnesium retention.
(Mg2+) Low Mg2+ or Ca2+ may cause
dysrhythmias.
Arterial blood Assesses for the presence of Low Paco2 and plasma pH values
gases metabolic acidosis reflect metabolic acidosis.
Urinalysis Assesses for the presence of Presence of sediment containing
sediment tubular epithelial cells, cellular
debris, and tubular casts supports
diagnosis of ARF/AKI.
Increased protein and many RBC
casts are common in intrarenal
disease.
Sediment is normal in prerenal
causes.
Large amounts of myoglobin may be
present in severe skeletal muscle
injury or rhabdomyolysis.
Urinary sodium Differentiates prerenal from Urinary Na+ is less than 20 mEq/L

1360
 intrarenal cause; often overlooked (prerenal).
as a significant finding Urinary Na+ is more than 20 mEq/L in
intrarenal causes.

Kidney attack: Early recognition of AKI with urinary

and serum biomarkers
AKI is a global health problem associated with significant
morbidity and mortality. Just as in the case of myocardial infarction
and stroke, early recognition of AKI is crucial to reverse or limit the
progression of injury. Changes in urine output and serum
creatinine levels are evidence-based markers for the identification
of AKI. However, these changes are measured over time and can be
affected by muscle mass, age, sex, medications, and hydration
status. Several urinary and serum proteins are being investigated
for early detection of AKI. Preliminary studies have been
inconclusive. None have yet been approved for clinical use in the
United States. See Box 6-1 for a listing of investigational markers.

Box 6-1
INVESTIGATIONAL BIOMARKERS FOR
ACUTE KIDNEY INJURY
• Interleukin-18

• Neutrophil gelatinase-associated lipocalin

• Kidney injury molecule-1

• Cystatin C

• N-Acetyl-beta-d-glucosaminidase

• Urinary liver-type fatty acid–binding protein

Collaborative management

1361
Care priorities for AKI
The management of AKI focuses on interventions to limit nephron
damage and restore fluid, electrolyte, and acid-base balances.
Supportive therapies are implemented to manage uremia and
associated complications (Table 6-5).

Table 6-5
MANAGEMENT CONSIDERATIONS: ACUTE KIDNEY INJURY

Issue Treatment
Intravascular volume Restriction of salt (1 to 1.5 g/day) and water (1 L/day).
overload Consider diuretic therapy to decrease filtrate reabsorption and
enhance water excretion. Use only after adequate hydration to
increase urine output or in an attempt to prevent onset of oliguria.
If volume overload is present, they are used to prevent pulmonary
edema. Osmotic diuretics such as mannitol may be used to increase
intravascular volume, promote renal blood flow, increase
glomerular filtration rate, and stimulate urinary output.
Ultrafiltration may be considered for extracorporeal fluid removal.
Hemodynamic monitoring of central venous pressure.
Oxygen/high flow, continuous positive airway pressure
Rhabdomyolysis/Tumor Forced alkaline diuresis with isotonic sodium bicarbonate solution at
lysis syndrome 100 mL/h to manage pigmenturia (myoglobinuria, hemoglobinuria)
resulting from rhabdomyolysis or severe crush or skeletal muscle
injury. In addition, aggressive volume replacement to maintain renal
perfusion pressure and reduce cast formation leading to renal tubular
obstruction.
Hyponatremia Restriction of oral and intravenous free water.
Hyperkalemia Restriction of dietary potassium.
Discontinuation of potassium supplements or potassium-sparing
diuretics.
Loop diuretics in diuretic-responsive patients.
Potassium-binding resin.
Glucose (50 mL of 50% with regular insulin 10 units intravenously).
Calcium gluconate (10 mL of 10% solution over 5 minutes).
Sodium bicarbonate (50 mEq intravenously): Sodium bicarbonate is
given in acidosis to promote the shift of potassium back into the
cells.
Albuterol 20 mg nebulized.
Renal replacement therapy.
Metabolic acidosis Careful management of dietary protein.
Renal replacement therapy.
Sodium bicarbonate: Sodium bicarbonate is given to control
metabolic acidosis and promote the shift of potassium back into the
cells.
Management of Restriction of dietary phosphate intake.
hyperphosphatemia Phosphate-binding agents: Phosphate binders (calcium carbonate
antacids, calcium acetate) that bind phosphorus and control
hyperphosphatemia and hypermagnesemia are given with meals.
Hypermagnesemia Discontinuation of magnesium-containing drugs such as antacids.
Prevention of contrast- Aggressive hydration with normal saline or bicarbonate solution 12
induced nephropathy hours before contrast administration. N-Acetylcysteine may be added

1362
 with hydration for patients with glomerular filtration rate of less than
30 undergoing major procedures.
Uremic Renal replacement therapy.
encephalopathy/ Monitor for high risk of bleeding and injury.
Uremic pericarditis

Nutrition therapy Enteral feeding is preferred.

Total energy intake of 20 to 30 kcal/kg/day.
Protein intake of 0.8 to 1.0 g/kg/day for noncatabolic patients with
acute kidney injury.
Protein intake of 1.0 to 1.5 g/kg/day for patients with acute kidney
injury receiving renal replacement therapy. Higher amounts may
be required for hypercatabolic patients.
Hematologic problems Packed red blood cells are given to maintain hematocrit. Anemia
caused by decreased erythropoietin, low-grade gastrointestinal
bleeding from mucosal ulceration, blood drawing, and shortened
life of the red blood cells. Erythropoietin is used for primary
prevention and treatment of anemia.
Prolonged bleeding time is caused by decreased platelet
adhesiveness.
Drug dosage Adjust all dosages for glomerular filtration rate and renal
replacement therapy.
Relief of obstruction Achieved via catheterization with indwelling urinary catheter or
nephrostomy tube, or ureteral stent to relieve obstruction before
surgical intervention or lithotripsy to disintegrate stones.

1. Maintain renal perfusion

a. Administer intravenous (IV) fluids to achieve/maintain central

venous pressure (CVP) of 10 to 12 mm Hg and/or urine output
greater than 0.5 mL/kg/h.

b. After volume repletion, consider vasopressor or inotropic

support to achieve MAP greater than 60 mm Hg.

c. Low-dose dopamine is not recommended to prevent or treat AKI.

d. Treat underlying cause of volume depletion (e.g., hemorrhage,

burns, GI losses, extravasation into extravascular compartments).

e. Correct underlying cause of renal hypoperfusion (e.g., sepsis,

compartment syndrome, cardiogenic shock).

2. Minimize exposure to nephrotoxic agents

a. Review current medications for potential nephrotoxicity (e.g.,

NSAIDS, antibiotics, ACEIs/angiotensin blockers).

1363
b. Aminoglycosides should be avoided unless a therapeutic
alternative is not available.

c. Avoid diuretics unless in the management of fluid overload.

See Table 6-6 Diuretic Use in Acute Kidney Injury.

Table 6-6
DIURETIC USE IN ACUTE KIDNEY INJURY

Potential Fluid
Types Mechanisms of Action and Electrolyte
Abnormalities
Osmotic Diuretics
Mannitol Increase osmotic pressure of the filtrate, which Hyponatremia
Urea attracts water and electrolytes and prevents their Hypokalemia
reabsorption Rebound volume
expansion
Loop Diuretics
Furosemide Inhibit reabsorption of Na+ and Cl− at the ascending Hypokalemia
Ethacrynic acid loop of Henle in the medulla; they produce a Hyperuricemia
Bumetanide vasodilatory effect on the renal vasculature Hypocalcemia
Torsemide Hyperglycemia
and impairment
of glucose
tolerance
Dilutional
hyponatremia
Hypochloremic
alkalosis
Thiazides
Bendroflumethiazide Inhibit Na+ in the ascending loop of Henle at the Hypokalemia
Benzthiazide beginning of the distal loop Dilutional
Chlorothiazide hyponatremia
sodium Hypercalcemia
Hydrochlorothiazide Metabolic
Hydroflumethiazide alkalosis
Polythiazide Hypochloremia
Trichlormethiazide Hyperuricemia
Hyperglycemia
and impaired
glucose
tolerance
Thiazide-like Diuretics
Chlorthalidone Action same as thiazides Same as thiazides
Indapamide
Metolazone
Quinethazone
Potassium-sparing Diuretics*

1364
 Amiloride HCl Inhibit aldosterone effect on the distal tubule, Hyperkalemia
Spironolactone causing Na+ excretion and K+ reabsorption Hyponatremia
Triamterene Dehydration
Acidosis
Transient increase
in BUN
Carbonic Anhydrase Inhibitors

Acetazolamide Block the action of the enzyme carbonic anhydrase, Hyperchloremic

sodium producing excretion of Na+, K+, HCO3–, and water acidosis
Dichlorphenamide Hypokalemia
Methazolamide Hyperuricemia
*
Used with caution in patients with oliguria.
BUN, Blood urea nitrogen; Cl−, chloride; HCO3−, bicarbonate; K+, potassium; Na+,
sodium.
Note: Loop or osmotic diuretics (or a combination of both) are used in patients with
acute kidney injury to prevent hypervolemia and to stimulate urinary output.

d. Consider alkaline diuresis for patients with crush injuries or

rhabdomyolysis.

e. Avoid radiocontrast material when possible. If necessary,

administer isotonic saline at 1 mL/kg/h for 12 hours before and after
contrast administration. An alternative regimen is 3 mL/kg/h for 1
hour before the procedure followed by 1 to 1.5 mL/kg/h for 6 hours
after the procedure. Sodium bicarbonate is another strategy to
prevent contrast induced nephropathy (CIN). A typical protocol is
the addition of 150 mEq of sodium bicarbonate to 1 L of 5%
dextrose administered at 3 mL/kg/h for 1 hour before contrast
administration and continued at 1 mL/kg for 6 hours after contrast
administration. Risks associated with the addition of sodium
bicarbonate are alkalemia, exacerbation of heart failure, and
hypocalcemia. N-Acetylcysteine (NAC) has been used for the
prevention of CIN. However, there is conflicting evidence
regarding efficacy. The usual oral dose of NAC is 600 mg twice
daily before and the day of contrast administration. It can also be
administered IV as a one-time dose immediately before contrast
administration. The most common side effects of NAC are nausea
and vomiting. KDIGO guidelines do not recommend the use of
NAC for postsurgical patients or patients with hypotension.

1365
3. Provide nutrition support

a. Enteral feeding route is preferred.

b. Total energy intake of 20 to 30 kcal/kg/day.

c. Protein intake of 0.8 to 1.0 g/kg/day for noncatabolic patients with

AKI; 1.0 to 1.5 g/kg/day for patients with AKI receiving renal
replacement therapy; hypercatabolic patients may require up to 1.7
g/kg/day. Patients with diabetes mellitus with AKI require vigilant
management to ensure a balance of both carbohydrates and
proteins to meet the needs of both conditions.

4. Avoid hyperglycemia
Provide insulin therapy targeting plasma glucose 110 to 149
mg/day.

5. Continue assessment and monitoring of hemodynamic

and oxygenation measurements
This is to prevent development or worsening of AKI in patients
who are critically ill.

6. Initiate renal replacement therapy

Renal replacement therapies include hemodialysis and continuous
renal replacement therapies.

a. Refractory fluid overload.

b. Hyperkalemia.

c. Metabolic acidosis.

d. Uncontrolled azotemia.

e. Drug overdose.

Care plans for acute kidney injury

Excess fluid volume 

1366
related to inability of kidney to normally excrete urine
Goals/Outcomes: Within 24 to 48 hours of onset, intravascular
volume is stabilized, as evidenced by balanced intake and output
(I&O), urinary output greater than 0.5 mL/kg/h, body weight within
the patient’s normal range, MAP greater than 60 mm Hg and within
the patient’s normal range, CVP 10 to 12 mm Hg, HR 60 to 100
beats/min (bpm), and improvement of edema, crackles, gallop, and
other clinical indicators of fluid overload.
Fluid Overload Severity; Fluid Balance.

Although the patient is retaining sodium, his or her serum

sodium level may be within normal limits or decreased from
baseline because of the dilution effect of the fluid overload.

Fluid management

1. Document input and output hourly. Consult the advanced

practice provider if urinary output falls to less than 0.5 mL/kg/h.

2. Weigh the patient daily; consult the advanced practice provider

regarding significant weight gain (e.g., 0.5 to 1.5 kg/24 h).

3. Assess for and report the presence of new or increased basilar

crackles, jugular vein distention, tachycardia, pericardial friction
rub, gallop, increased BP, increased CVP, or shortness of breath
(SOB), any of which are indicative of fluid volume overload.
Chronic heart failure may require additional support measures to
help resolve AKI.

4. Assess for and report new or increasing peripheral, sacral, or

periorbital edema.

5. Restrict total fluid intake to 1200 to 1500 mL/24 h or as

prescribed. Measure all output accurately, and replace milliliter for
milliliter at intervals of 4 to 8 hours or as prescribed.

1367
6. Provide ice chips, chewing gum, or hard candy to help quench
thirst and moisten mouth.

7. Monitor serum osmolality and serum sodium values. Values are

decreased in the setting of fluid overload resulting from dilution by
excess volume.

8. Patients receiving total parenteral nutrition will receive the

largest fluid intake volume. If total fluid intake is greater than 2000
mL/day, ultrafiltration with hemodialysis or continuous renal
replacement therapy (CRRT) (continuous venovenous
hemofiltration [CVVH], continuous venovenous hemodialysis
[CVVHD], continuous venovenous hemodiafiltration [CVVHDF],
slow continuous ultrafiltration [SCUF], or continuous arteriovenous
hemofiltration) may be required to maintain fluid and electrolyte
balance.

9. If the patient is retaining sodium, restrict sodium-containing

foods, avoid diluting IV medications with saline diluents or
intravenous solutionsand avoid sodium-containing medications
such as sodium penicillin.

Electrolyte Management: Hypokalemia; Electrolyte

Management: Hyponatremia; Fluid/Electrolyte Management; Fluid
Management; Fluid Monitoring. Additional, optional interventions
include Dysrhythmia Management; Hemodialysis Therapy;
Hemodynamic Regulation; Invasive Hemodynamic Monitoring;
Medication Management; Positioning; Skin Surveillance; and
Weight Management.

Fluid volume deficit 

related to overdiuresis and/or dehydration resulting in AKI
Goals/Outcomes: Within 24 hours of this diagnosis, volume
status is stabilized, as evidenced by balanced I&O, urinary output
greater than 0.5 mL/kg/h, CVP 10 to 12 mm Hg, HR 60 to 100 bpm,
MAP greater than 60 mm Hg, absence of thirst, and other indicators
of hypovolemia. Weight stabilizes within 2 to 3 days.
Hydration; Fluid Balance.

1368
Hypovolemia management

1. Weigh the patient daily. Consult the advanced practice provider

for weight loss of 1 to 1.5 kg/24 h. Weight is often the most reliable
indicator of fluid status in patients with kidney impairment.

2. Assess for and manage dehydration and hypovolemia (e.g., poor

skin turgor, dry and sticky mucous membranes, thirst, hypotension,
tachycardia, decreasing CVP, increasing BUN and creatinine).

3. Promote hydration: Monitor and document I&O hourly. Report if

the patient’s output is less than 0.5 mL/kg/h. With a deficit,
supplemental fluid intake should exceed output by 0.5 to 1 L/day
(depending on severity of dehydration). Encourage oral fluids if
allowed. Ensure that IV fluid rates are maintained as prescribed.

4. Monitor for additional fluid losses: Report increased losses from

vomiting, diarrhea, wound drainage, or sudden onset of diuresis.
Fluid intake may need to be increased.

5. Patients with AKI are at risk for GI bleeding related to uremia,

which may cause platelet dysfunction, acidosis, and the stress of
critical illness. Monitor hemoglobin (Hgb), hematocrit (Hct), and
BUN levels. ABGs are drawn to assess pH, HCO3−, and CO2 levels,
reflective of acid-base balance.

A patient with acute kidney injury may have a hematocrit in

the range of 20% to 30% if prerenal azotemia has occurred over
time. Anemia occurs as a result of prolonged renal insufficiency
leading to failure. Blood urea nitrogen will increase in the presence
of gastrointestinal bleeding without a concomitant rise in serum
creatinine level.

6. Monitor for occult bleeding: Test all stools, emesis, and peritoneal
dialysate drainage for occult blood. Check urine and dialysate

1369
drainage at least every 8 hours.

7. Minimize the risk of bleeding: Implement fall precautions,

minimize invasive procedures, use small-gauge needles for
injections, minimize blood drawing, and promote the use of electric
razors and soft-bristle toothbrushes. If possible, avoid
intramuscular (IM) or subcutaneous injections for 1 hour after
hemodialysis. Apply gentle pressure to injection sites for at least 2
to 3 minutes.

8. Inspect hemodialysis insertion, peritoneal access sites, and other

invasive sites for bleeding when interacting with the patient at least
every 8 hours.

Imbalanced nutrition, less than body requirements 

related to the adverse effects of AKI on digestion and absorption of
nutrients.
Goals/Outcomes: Within 72 hours of this diagnosis, the patient
has adequate nutritional intake, as evidenced by a caloric intake
that ranges from 35 to 45 calories/kg normal body weight, a daily
protein intake consisting of 50% to 75% high–biological value
proteins, and a nitrogen intake of 4 to 6 g greater than nitrogen loss
(calculated from 24-hour urinary urea excretion and protein intake).
Nutritional Status.

Nutrition therapy

1. Augment nutritional intake: Administer nutritional

supplements/enteral feedings as prescribed and record amount of
intake every shift.

2. Reduce incidence of nausea: Present appetizing food in small,

frequent meals. Provide a pleasant atmosphere; eliminate any
noxious odors. Administer prescribed antiemetic 30 minutes before
meals.

3. Control catabolism:

• Manage fever: As prescribed, use cooling blanket or

1370
 antipyretic agents to control fever. Fever increases
tissue catabolism, which in turn increases metabolic
needs. Patients who are critically ill are often
catabolic and require careful nutrition management,
especially when hemodialysis, peritoneal dialysis,
or CRRT is implemented. Protein target is 0.8 to 1.0
g/kg/day to provide essential amino acids for a
noncatabolic patient with AKI. The end products of
protein metabolism that accumulate are reflected by
an increase in BUN level. Ensure intake of protein
with high biological value (e.g., eggs, meat, fowl,
milk, fish), which contains essential amino acids
necessary for cell building.

• Provide adequate calories: Be sure that caloric

intake ranges from 20 to 30 kcal/kg/day for a
critically ill adult patient with AKI. The exact
amount will vary with age, sex, activity, and the
degree of preexisting malnutrition. Foods that may
be used to increase caloric intake include fats and
concentrated carbohydrates.

4. Manage electrolytes:

• Restrict high-potassium foods such as bananas,

citrus fruits, potatoes, fruit juices, nuts, tea, coffee,
legumes, and salt substitute. In acute renal failure
(ARF) or acute kidney injury (AKI), the kidneys are
unable to excrete potassium effectively.

• Assess sodium requirement, because it will vary

1371
 greatly. If oliguria is present, sodium intake may be
restricted in the diet. If diuresis is present, sodium
intake may be increased because of excess sodium
loss in the urine. Intervene accordingly.

• Measure ionized calcium to avoid inappropriate

treatment of malnourished patients whose values
may appear falsely low as a result of serum calcium
being bound to albumin, which is decreased in
patients with renal failure.

• Manage hypocalcemia: Reduced intestinal calcium

absorption coupled with hyperphosphatemia is
managed by replacing calcium orally (e.g., with
dairy products, Tums) or IV. Administer phosphate
binders as prescribed.

• Recognize that catabolism of protein, which occurs

with infection, causes potassium to be released
from the tissues.

Nutrition Management; Nutrition Monitoring; Fluid

Management; Fluid Monitoring. Additional, optional Nursing
Interventions Classification (NIC) interventions include: Bowel
Management; Energy Management; Enteral Tube Feeding; Exercise
Promotion; Gastrointestinal Intubation; Hyperglycemia
Management; Hypoglycemia Management; Intravenous Insertion;
Intravenous Therapy; Medication Management; Mutual Goal
Setting; Phlebotomy: Venous Blood Sample; Positioning; Teaching:
Individual; Teaching: Prescribed Diet; Total Parenteral Nutrition
Administration; and Venous Access Devices Maintenance.

Risk for infection 

1372
related to immunocompromised state associated with renal failure
Goals/Outcomes: At the time of discharge from the intensive care
unit, infection is controlled, as evidenced by normothermia,
negative culture results of dialysate and body secretions, and white
blood cell (WBC) count less than 11,000/mm3.
Immune Status.

After the initial insult, infection is the primary cause of

death in acute kidney injury.

Infection protection

1. Monitor and record the patient’s temperature every 8 hours. If

elevated (i.e., greater than 37° C [98.6° F]), monitor temperature
every 4 hours. AKI may be accompanied by hypothermia. A slight
rise in temperature of 1 to 2 degrees may be significant; especially if
the patient is receiving CRRT (an extracorporeal therapy.)

2. Identify possible sources of infection: Inspect and record the

color, odor, and appearance of all body secretions. Be alert to
cloudy or blood-tinged peritoneal dialysate return, cloudy and foul-
smelling urine, foul-smelling wound exudate, purulent drainage
from any catheter site, foul-smelling and watery stools, foul-
smelling vaginal discharge, or purulent sputum.

3. Vigilantly monitor open wounds: Recognize that uremia retards

wound healing. All wounds (including scratches resulting from
pruritus) should be assessed for infection. Send samples of any
suspicious fluid or drainage for culture and sensitivity tests.

4. Monitor for infection: Monitor WBC count with differential

analysis for elevation.

5. Prevent infection: Use aseptic technique when manipulating

central lines, peripheral IV lines, and indwelling catheters. Avoid
use of indwelling urinary catheter in patients with oliguria and

1373
anuria. The presence of a catheter further increases the risk of
infection.

6. Provide oral hygiene every 2 to 4 hours to help maintain the

integrity of the oral mucous membranes.

7. Reposition the patient every 2 to 4 hours to help maintain the

barrier of an intact integumentary system. Provide skin care at least
every 8 hours.

8. Encourage good pulmonary hygiene: Instruct the patient to

practice deep-breathing exercises (and coughing, if indicated) every
2 to 4 hours. Implement ventilator-associated pneumonia (VAP)
prevention (e.g., VAP Bundle) on patients who are mechanically
ventilated.

Infection Control. Additional, optional interventions include

Airway Management; Exercise Promotion and Therapy; Medication
Management; Respiratory Monitoring; Teaching: Disease Process;
Tube Care: Urinary; and Vital Signs Monitoring.

Knowledge deficit 
related to disease process of AKI
Goals/Outcomes: Within 72 hours of admission, the patient and
significant others verbalize accurate information regarding AKI and
the plan of care.
Knowledge: Disease Process.

Teaching: Disease process

1. Provide education regarding AKI including the signs and

symptoms of the biochemical alterations (hyperkalemia,
hypokalemia, hypernatremia, hyponatremia, hypocalcemia,
hyperphosphatemia, hypermagnesemia, metabolic acidosis, and
uremia) that can occur (see Table 6-4).

2. Provide lists of foods high in potassium, sodium, and magnesium

that the patient should avoid when planning meals. Provide a list of
medications that contain magnesium that should not be taken

1374
without approval of the advanced practice provider.

3. Explain the importance of consuming only the amount of protein

prescribed by the advanced practice provider.

4. Discuss the need to avoid exposure to persons with infection or a

febrile illness to prevent infection. Infection and strenuous activity
promote protein catabolism, which causes potassium to be released
from the tissues.

5. Teach the patient to report to the advanced practice provider an

increase in temperature or other signs of infection.

6. Reinforce the importance of taking vitamin D and calcium

supplements as prescribed.

7. Teach the relationship between calcium and phosphate levels.

Emphasize that maintaining good phosphate control and calcium
balance may help control itching and prevent future problems with
bone disease.

8. Stress the importance of taking phosphate binders (e.g.,

Amphojel, Alternagel, PhosLo) as prescribed and to avoid antacids
containing magnesium (e.g., Maalox, Milk of Magnesia).

9. Teach the patient not to take over-the-counter medications

without first consulting the advanced practice provider. Aspirin, for
example, exacerbates the bleeding tendency caused by uremia.

10. Instruct the patient about the importance of maintaining the

prescribed dialysis schedule, because dialysis will help correct
acidosis, uremia, and many of the metabolic abnormalities that
occur.

11. Teach the patient to use lotions and oils to lubricate the skin and
relieve drying and cracking.

12. Stress the importance of follow-up monitoring of serum

electrolyte levels.

1375
 Teaching: Individual; Teaching: Prescribed Medication.
Additional, optional interventions include Discharge Planning;
Medication Management; and Weight Management.

Acute confusion 
related to altered level of consciousness that results from fluid and
electrolyte imbalance and/or uremia.
Goals/Outcomes: Within 48 to 72 hours of onset, the patient
verbalizes orientation to time, place, and person and maintains his
or her normal mobility.
Neurologic Status.

Neurologic monitoring

1. Monitor the patient for the following mentation and motor

dysfunctions associated with AKI:

• Hyperkalemia (during oliguric phase): muscle

weakness, irritability, paresthesias.

• Hypokalemia (during diuretic phase): lethargy;

muscle weakness, softness, flabbiness; paresthesias.

• Hypernatremia: fatigue, restlessness, agitation.

• Hyponatremia: dizziness when changing position,

apprehension, personality changes, agitation,
confusion.

• Hypocalcemia: neuromuscular irritability, tonic

muscle spasms, paresthesias.

• Hyperphosphatemia: excessive itching, muscle

weakness, hyperreflexia.

1376
• Hypermagnesemia: drowsiness, lethargy, sensation
of heat.

• Metabolic acidosis: confusion, weakness.

• Uremia: confusion, lethargy, itching, metallic taste,

muscle twitching.
2. Explain to significant others that the patient’s decreasing
attention level necessitates simple and direct communication
efforts.

3. To alleviate the unpleasant metallic taste caused by uremia,

provide frequent oral hygiene. Because the patient with uremia is at
increased risk for bleeding, ensure the use of soft-bristle brushes.

4. Implement fall prevention interventions.

5. Promote early mobilization: Encourage isometric exercises and

short walks, if the patient is able, to help maintain muscle strength
and tone, especially in the legs.

6. Assess for delirium: Decrease environmental stimuli, and use

calm, reassuring manner in caring for the patient.

7. Balance rest and activities: Encourage establishment of sleep/rest

patterns by scheduling daytime activities appropriately and
promoting relaxation methods.

8. Monitor for development of neuropathies: Assess for decreased

tactile sensations in the feet and legs, which may occur with
peripheral neuropathy. Be alert to the potential for pressure sores
and friction burns, which may occur with peripheral neuropathy.

9. Use splints and braces to aid in mobility for patients with severe
neuropathic effects.

Nutrition Management; Nutrition Therapy; Nutrition

1377
Counseling; Pressure Management; Pressure Ulcer Prevention; and
Teaching: Individual.

Constipation 
related to fluid and electrolyte imbalance and reduced activity level.
Goals/Outcomes: Within 48 hours of onset, the patient has bowel
movements of soft consistency.
Bowel Elimination.

Constipation/impaction management

1. Monitor and record the number and quality of the patient’s

bowel movements.

2. Administer prescribed stool softeners and bulking agents, such as

psyllium husks.

3. Additional measures: Administer oil retention or tap water

enemas as prescribed. Because excess fluid can be absorbed from
the gut, avoid using large-volume water enemas.

4. Encourage moderate exercise on a routine basis.

5. Establish a regular schedule for fluid intake within the patient’s

prescribed limits.

6. Administer metoclopramide as prescribed to increase motility in

the presence of autonomic neuropathy. Treatment with
metoclopramide for more than 12 weeks is not recommended,
given the risk of developing tardive dyskinesia.

Exercise Promotion; Medication Administration: Oral;

Medication Management; Pain Management; and Skin Surveillance.

Impaired skin integrity 

related to uremia
Goals/Outcomes: The patient’s skin remains intact.
Tissue Integrity: Skin and Mucous Membranes.

1378
Pruritus management

1. Monitor the patient for presence of pruritus with resulting

frequent and intense scratching. Pruritus decreases with reduced
BUN level and control of hyperphosphatemia. Monitor laboratory
values of BUN and phosphorus, and report levels outside the
optimal range (BUN greater than 20 mg/dL and phosphorus greater
than 4.5 mg/dL or less than 2.6 mEq/L). Pruritus increases in the
presence of secondary hyperparathyroidism. Monitor serum
calcium and PTH levels, and report elevations (Ca2+ greater than
10.5 mg/dL and PTH greater than 30% above the upper limit of the
test used).

2. Administer phosphate binders (e.g., Alternagel) as prescribed,

and, if possible, reduce the patient’s dietary intake of phosphorus
(see Box 1-6).

3. Ensure that the patient’s fingernails are cut short and that the nail
tips are smooth.

4. Because of reduced oil gland activity associated with uremia, the

patient’s skin may be very dry. Use skin emollients liberally, and
avoid harsh soaps and excessive bathing.

5. Advise the patient of the potential for bruising because of clotting

abnormality and capillary fragility.

6. Administer oral antihistamine, such as diphenhydramine, to

relieve itching as prescribed.

Skin Surveillance; Pressure Ulcer Prevention. Additional,

optional interventions include Bathing; Bleeding Reduction;
Cutaneous Stimulation; Exercise Promotion and Therapy (all
listed); Electrolyte Monitoring; Exercise Promotion: Stretching;
Fluid/Electrolyte Management; Infection Control; Infection
Protection; Medication Management; Nail Care; Nutrition
Management; Perineal Care; Surveillance; and Vital Signs
Monitoring.

1379
Additional nursing diagnoses
For patients undergoing dialytic therapy (conventional
hemodialysis), see nursing diagnoses and interventions in
Continuous Renal Replacement Therapies, as follows.

Continuous renal replacement

therapies
The patient with ARF or AKI may progress to a physiologic
disequilibrium requiring support with renal replacement therapy to
prevent metabolic complications. CRRT has gained acceptance
throughout Europe and the United States for the treatment of
hemodynamically unstable patients who may not tolerate or have
not tolerated hemodialysis, or have not responded to conservative
management and pharmacologic interventions. The initiation of this
therapy is variable throughout institutions and physician practices.
Patient characteristics that are considered include age, severity of
illness, and existing comorbidities.
The goals of CRRT include:

1. Prevention of uremic complications.

2. Acid-base balance.

3. Electrolyte and fluid volume homeostasis.

4. Maintenance of cardiopulmonary function and hemodynamics.

5. Maintenance of adequate nutrition support.

The most common indications for CRRT include:

1. Hyperkalemia and other electrolyte disturbances refractory to

medical management.

2. Metabolic acidosis unresponsive to medical therapy.

3. Intravascular volume excess refractory to diuretics.

1380
4. Uremic intoxication.

• Neurologic (encephalopathy).

• Hematologic (bleeding caused by platelet

dysfunction).

• Gastrointestinal (anorexia, nausea, vomiting).

• Cardiovascular (pericarditis).
5. Need for removal of dialyzable substances (metabolites, drugs,
toxins).

Other indications for CRRT include:

1. Massive fluid overload: congestive heart failure, overaggressive

fluid resuscitation in multiple trauma.

2. Fluid overload in the presence of hemodynamic instability.

3. Cardiogenic shock with pulmonary edema.

4. Oliguria unresponsive to diuretics.

5. Severe hypovolemia with anuria: helps stabilize fluid balance in

patients with multiple organ dysfunction syndrome requiring
aggressive volume resuscitation to stabilize hemodynamics.

Indications for early initiation of CRRT include:

1. Predicted impending electrolyte or acid-base disturbances.

2. Presence of oliguria and the need for infusion of large volumes of

fluid.

3. Presence of ARF/AKI with a poor prognosis for immediate

recovery.

1381
4. ARF/AKI in the presence of sepsis or systemic inflammatory
response syndrome.

Pathophysiology
Historically, CRRT has evolved from an arteriovenous to a
venovenous extracorporeal process to achieve solute and fluid
removal in the patient who is critically ill. For this reason,
arteriovenous therapy will not be included in this chapter. Venous
access has proven to be safer, and the evolving technology has
improved the efficacy of treatment. CRRT has been traditionally
limited to the intensive care unit setting based on the requirement
for close hourly monitoring and fluid adjustments. The multiple
acronyms and description of therapies are available in Table 6-7.

Table 6-7
COMPARISON OF MODES OF CONTINUOUS RENAL
REPLACEMENT THERAPY

SCUF Slow continuous ultrafiltration: Indicated primarily to remove fluids. A filter with a
large surface area, high sieving coefficient, and low resistance facilitates continuous
fluid removal and minimal solute removal.
CVVH Continuous venovenous hemofiltration: Ultrafiltration is used to remove fluid.
Convective clearance is used to remove solutes. Replacement solution is infused via
prefilter, postfilter, or both prefilter and postfilter to create a solute drag effect (a
large volume of fluid is infused into the patient’s bloodstream, which facilitates
solutes to be returned or “dragged” to the filter. CVVH does not use dialysate
solution.
CVVHD Continuous venovenous hemodialysis: Ultrafiltration is used to remove fluid.
Diffusive clearance is used to remove solutes. Dialysate solution is infused into the
filter countercurrent to the blood flow. Solutes diffuse from the blood (high solute
concentration) to the dialysate solution (low solute concentration). Replacement
solution is not used.
CVVHDF Continuous venovenous hemodiafiltration: Ultrafiltration is used to remove fluid.
Both convective and diffusive clearance is used to remove solute so that both
replacement and dialysis fluids are used.
SLED Sustained low-efficiency dialysis: Hybrid form of continuous renal replacement
therapy using a reduced blood flow and rate of dialysate infusion to remove both
solute through diffusive clearance and fluid by ultrafiltration. Therapy is usually
sustained 4 to 12 hours per day.

The principles of solute and water removal during CRRT are

similar to other methods of renal replacement therapy (e.g.,
hemodialysis) and include diffusion, ultrafiltration, and convection.
These therapies provide solute clearance and fluid removal slowly
and continuously. Conventional hemodialysis is more aggressive

1382
and may not be tolerated in unstable patients.

Diffusion: Movement of solutes, including high concentrations of

waste products and excess electrolytes, from an area of greater
concentration to an area of lesser concentration. Diffusion
requires a concentration gradient. During CRRT, high
concentrations of these excess particles diffuse into the
dialysate/effluent, which contains much lower concentrations of
these solutes.

Ultrafiltration: Removal of water from the blood compartment of

the hemofilter by generating a lower pressure in the effluent
compartment. In hemodialysis, lower or negative pressure in the
dialysate facilitates more rapid removal of excess water from the
blood compartment in which positive or higher pressure exists.

Convection: Removal of a solute along with fluid through a filter

with a semipermeable membrane over time. This occurs in
response to the pressure gradient across the filter. Small
molecules freely pass into the ultrafiltrate. Large molecule
removal is dependent on the pore size of the filter. Larger
molecules tend to move through membranes in the filter more
easily by using convection rather than diffusion. Various
elements in plasma fluid (e.g., urea) are conveyed across the filter
as a result of the differences in hydrostatic pressure. The removal
of large amounts of plasma fluid results in the removal of large
amounts of filterable solutes.

Improved and enhanced technology for CRRT has not resulted in

standardization of when therapy should be initiated, dosage, choice
of modality, or the intensity and duration of therapy. The use of a
highly permeable filter, the infusion of various types of replacement
solution, and the continuous nature of each of the techniques make
them highly effective and versatile in managing the control of
fluids. CRRT techniques can serve as a regulatory system for fluids
without compromising the metabolic balance. More recent
literature suggests that the use of daily hemodialysis may provide
equally effective therapy in patients with AKI or for those with
more complex disease processes who are unable to receive

1383
consistent therapy as a result of machine problems, such as clotting
of the filter. Frequent machine alarms indicate that therapy has
ceased or will cease shortly, which undermines the efficacy of
CRRT. Continuous replacement requires a fully operational system
that provides uninterrupted therapy. If the system is frequently
alarming, diffusion, ultrafiltration, and convection are interrupted
with the sounding of each alarm.

Assessment: Pre-CRRT
Goal of assessment
Evaluate fluid, electrolyte, and acid-base balances to prevent the
development of metabolic complications attributable to AKI.

History and risk factors

Chronic illness (e.g., hypertension, diabetes, cardiomyopathy,
peripheral vascular disease), recent infections or sepsis (e.g.,
streptococcal), recent episodes of hypotension (e.g., major bleeding,
septic shock, major surgery), exposure to nephrotoxins (e.g., carbon
tetrachloride, diuretics, aminoglycoside antibiotics, contrast media),
recent blood transfusion, urinary tract disorders, toxemia of
pregnancy or abortion, recent severe muscle damage (e.g.,
rhabdomyolysis with myoglobinuria), crush injury, and burn
trauma.

Vital signs
• BP may be elevated in states of fluid volume excess or decreased
in states of fluid volume deficit.

• HR may be increased or decreased with abnormal rhythms based

on fluid and electrolyte abnormalities.

• Baseline electrocardiogram (ECG) and rhythm.

• Hemodynamic measurements of cardiac output, cardiac index,

ejection fraction, CVP, and pulmonary artery occlusion pressure.

1384
• Weight may be increased or decreased based on fluid volume
status.

• Temperature may be hyperthermic or hypothermic if the patient

is septic.

• Pulse oximetry.

Observation
• Peripheral edema and periorbital edema.

• Jugular venous distention.

• Dyspnea.

• Kussmaul respirations.

• Poor skin turgor, flushed skin, and dry mucous membranes.

• Pallor.

• Purpura.

• Weakness.

• Altered mental status and disorientation.

• Signs of central nervous system depression.

• Neuromuscular dysfunction.

• Asterixis.

• Mechanical ventilation measurements.

• Presence of any assist devices such as extracorporeal membrane

oxygenator.

Palpation

1385
• Edema (scale 0 to 4+): extremities and sacrum.

• Muscle tenderness.

• Suprapubic tenderness or distention.

• Flank tenderness.

Auscultation
• S3 and S4 gallops indicative of heart failure.

• Pericardial friction rub.

• Tachycardia or dysrhythmias.

• Pulsus paradoxus in the presence of fluid volume excess.

• Crackles.

• Bruits over the renal arteries indicative of renovascular disease.

Uremic manifestations
• Accumulation of urea, creatinine, and uric acid.

• Anemia and bleeding tendencies.

• Fatigue and pallor.

• Increased BP.

• Congestive heart failure.

• Pericarditis with tamponade.

• Pulmonary edema.

• Anorexia, nausea, vomiting, and diarrhea.

• Behavioral changes.

1386
• Decreased wound-healing ability.

• Increased susceptibility to infection.

Screening labwork
Blood and urine tests will determine the level of renal dysfunction
and can provide clues to the cause of ARF/AKI.

• BUN and creatinine: Elevations indicative of renal impairment.

• GFR: Most reliable estimation of renal function using 24-hour

creatinine clearance or laboratory estimation, which is part of the
renal panel in most laboratories.

• Electrolyte levels: Elevated or decreased potassium, phosphorus,

magnesium, and sodium.

• Urinalysis: Presence of sediment including tubular epithelial cells,

debris, casts, protein, RBC casts, or myoglobin.

• Urinary sodium: Prerenal disease results in urinary sodium less

than 20 mEq/L.

• CBC and coagulation studies: Evaluate for hematologic

complications.

• ABG values: Evaluate for metabolic acidosis associated with

ARF/AKI.

Diagnostic Tests Used In Association With Continuous Renal

Replacement Therapy Blood Studies

Test Purpose Abnormal Findings

Complete blood Assesses for anemia, inflammation, and Decreased RBCs, Hgb, or Hct
count (CBC) infection. Assists with differential reflects anemia or recent blood
Hemoglobin diagnosis of septic cause of acute renal loss. Increased WBCs may be
(Hgb) failure/acute kidney injury (ARF/AKI). indicative of infection/sepsis.
Hematocrit (Hct)
Red blood cell
(RBC) count
White blood cell
(WBC) count

1387
 Coagulation Assesses for the presence of bleeding or Decreased PT, aPTT with low
profile: clotting and disseminated intravascular INR promotes clotting.
Prothrombin coagulation (DIC). Elevation promotes bleeding.
time (PT) with
international
normalized
ratio (INR)
Activated partial
thromboplastin
time (aPTT)
Blood urea Assesses for the severity of renal Elevation indicates renal
nitrogen dysfunction. dysfunction.
(BUN) Creatinine may be markedly
Creatinine elevated in the presence of
Estimated massive skeletal muscle injury
glomerular (e.g., multiple trauma, crush
filtration rate injuries).
(eGFR) BUN is influenced by hydration,
catabolism, gastrointestinal
bleeding, infection, fever, and
corticosteroid therapy.
The eGFR in ARF/AKI is usually
less than 50 mL/min.
Electrolytes: Assesses for abnormalities associated Increase or decrease in K+ may
Potassium (K+) with ARF/AKI. cause dysrhythmias. Elevated
Sodium (Na+) Na+ may indicate dehydration.
Calcium (Ca2+) Decreased Na+ may indicate
Magnesium fluid retention.
(Mg2+) Low Mg2+ or Ca2+ may cause
dysrhythmias.
Arterial blood Assesses for the presence of metabolic Low Paco2 and plasma pH values
gases acidosis. reflect metabolic acidosis.
Urinalysis Assesses for the presence of sediment. Presence of sediment containing
tubular epithelial cells, cellular
debris, and tubular casts
supports diagnosis of
ARF/AKI.
Increased protein and many RBC
casts are common in intrarenal
disease.
Sediment is normal in prerenal
causes.
Large amounts of myoglobin
may be present in severe
skeletal muscle injury or
rhabdomyolysis.
Urinary sodium Differentiates prerenal from intrarenal Urinary Na+ <20 mEq/L indicates
etiology. prerenal etiology.
Urinary Na+ >20 mEq/L indicates
intrarenal etiology.

Determining type and modality of CRRT used

The availability of CRRT in the institution and the therapeutic

1388
options available on existing equipment are part of the
considerations used to determine the modality of CRRT used.
Treatment goals for removal of water and potentially toxic solutes
are considered. Therapeutic options may target removal of water
plus solutes, water only, or solutes only to be removed. All
modalities use a highly permeable, hollow-fiber filter. The type of
filter used is a crucial element contributing to efficacy of treatment
when removing solutes, coupled with the functionality of the
venous access device. Dysfunctional vascular access can undermine
the best of technology and filters, given that the blood flow through
the extracorporeal system must be adequate to achieve treatment
goals. Solutes removed are generally unbound substances,
including urea, calcium, sodium, potassium, chloride, vitamins, and
unbound drugs with a molecular weight between 500 and 10,000
Da. Types/modalities of CRRT include:

• Slow continuous ultrafiltration (SCUF).

• Continuous venovenous hemofiltration (CVVH).

• Continuous venovenous hemodialysis (CVVHD).

• Continuous venovenous hemodiafiltration (CVVHDF).

• Sustained low-efficiency daily dialysis (SLEDD).

Indications, advantages, disadvantages, and complications of

CRRT modes of therapies are found in Table 6-8. Approaches to
troubleshooting major problems of CRRT are found in Table 6-9.

Table 6-8
INDICATIONS, ADVANTAGES, AND
DISADVANTAGES/COMPLICATIONS OF MODES OF CONTINUOUS
RENAL REPLACEMENT THERAPY

1389
CVVH, Continuous venovenous hemofiltration; CVVHD, continuous venovenous
hemodialysis; CVVHDF, continuous venovenous hemodiafiltration; SCUF, slow
continuous ultrafiltration.

Table 6-9
TROUBLESHOOTING MAJOR PROBLEMS IN CONTINUOUS
RENAL REPLACEMENT THERAPY

Problem Cause Intervention

Hypotension Cardiac dysfunction Cardiotonic and vasopressor support
Excessive intravascular Fluid replacement
volume removal Reduce ultrafiltration rate
Poor High hematocrit Predilution fluid replacement
ultrafiltration Clotted filter Flush filter; replace if necessary
Clotted filter Inadequate Consult the licensed independent practitioner to
anticoagulation assess effectiveness of anticoagulation
Poor blood flow rates Check tubing hourly to guard against kinks
Kinks in blood tubing Change filter and restart therapy

SCUF, CVVH, CVVHD, and CVVHDF are types of continuous

renal replacement therapies used to manage fluid and solute
overload in patients who are critically ill. Their advantage over
conventional hemodialysis is that ultrafiltration occurs more
gradually, thus avoiding large volume changes and rapid fluid
shifts. A hybrid form of CRRT, SLEDD, is a modification to
intermittent hemodialysis. The dialysis duration is 6 to 12 hours per
day. CRRT duration will depend on the total amount of fluid
and/or solute to be removed. The type best suited for each situation
is chosen based on clinical status, including the ability to safely
provide anticoagulation therapy to the patient and the type of
vascular access. Catabolism, for example, causes rapid rises in BUN,
creatinine, and potassium values, thus requiring rapid removal of
these metabolic wastes. For this reason, patients may require
hemodialysis with supplemental CRRT (see Table 6-7).

1390
Principles applied to specific therapies
Ultrafiltration: For ultrafiltration to occur, there must be a pressure
gradient across the filter compartments; the pressure in the blood
compartment must exceed the pressure in the filtrate compartment.
This pressure gradient is called transmembrane pressure (TMP). Its
major determinants are hydrostatic pressure and oncotic pressure.
The rate of ultrafiltration depends on the type of filter, the
hydrostatic pressure of the blood, and blood flow. The hydrostatic
pressure forces small and middle size molecules such as creatinine,
urea, glucose, and cytokines from the blood across the filter. The
longer it takes for blood to exit the filter, the longer the blood is in
contact with the porous filter surface, the dialysate (if used), and the
filtration pressure. Longer exposure increases the likelihood that
the molecules of solute will be filtered from the patient’s blood.
Hydrostatic pressure from the dialysis system is opposed by
oncotic pressure, which is maintained by plasma proteins that do
not pass through the filter because of their larger size. When
hydrostatic pressure exceeds oncotic pressure, filtration of water
and solutes occurs.
Ultrafiltration Prescription: To achieve optimal fluid
management, the right amount of ultrafiltration must be prescribed
and delivered. The net ultrafiltrate (fluid loss) is the difference
between the amount of urine output and plasma water removed
and the amount of fluid administered to the patient. Fluid balance
is normally calculated hourly and is adjusted in response to
hemodynamic changes.
Calculation of the ultrafiltration prescription can be found in Box
6-2.

CRRT Dose Prescription: The CRRT dose prescription includes the

flow rate of dialysate and replacement fluids, the rate of
ultrafiltration, and the blood flow rate. Depending on the
patient’s condition, the licensed independent practitioner (LIP)
may prescribe a higher intensity therapy (40 mL/kg/h) versus a
lower intensity therapy (25 mL/kg/h) based on ideal body weight.

Sieving Coefficient (SC): Clearance of medication during CRRT is

impacted by the SC of the drug while it passes through the

1391
 membrane. The SC is equal to the ultrafiltrate concentration of
the drug divided by the plasma concentration. Drugs that are
more protein-bound have a lower clearance during CRRT.
However, as a result of the long duration of CRRT, more of these
drugs may be removed.

Box 6-2
ULTRAFILTRATION PRESCRIPTION
Example 1: Calculate ultrafiltrate based on anticipated
fluid balance
• Anticipated fluid intake is 4 L/24 h

• Desired net fluid loss equals 2 L/24 h

• Ultrafiltration rate equals 6 L + 2 L/24 h

• 6 L/24 h = 250 mL/h

• Set ultrafiltration pump to remove 250 mL/h

Example 2: Calculate precise ultrafiltration balance

• Calculate hourly intake from previous hour = 200 mL

• Calculate hourly urine output from previous hour = 50 mL

• Subtract output from intake to obtain net volume = 150 mL

• Add desired hourly fluid loss = 100 mL to net volume = 250 mL

• Set ultrafiltration pump to remove 250 mL/h

Procedure
The filter and lines are primed with normal saline to remove all air
bubbles before the treatment is initiated. A large, double-lumen

1392
catheter is placed in the internal jugular, subclavian, or femoral
vein. The catheter must have radiographic confirmation of
placement before beginning therapy. Although the system is driven
by venous access, dialysis terminology states that blood flows from
the patient into the “arterial” or proximal port of the vascular access
through the filter and returns to the patient through the “venous”
or distal port of the access. If the “arterial” or proximal lumen of the
catheter becomes occluded by being pulled up against the vessel
wall, the proximal and distal lumens may be interchanged so that
the blood is being removed from the patient via the “venous” or
distal lumen of the catheter and returned via the “arterial” or
proximal lumen. This phenomenon is sometimes signaled by the
presence of increased air in the system, or low-flow alarms, which
indicate that lower blood volume is being filtered.
For most patients, a continuous method of anticoagulation is
necessary to prevent clotting in the lines and filter, heparin or
citrate is most commonly used. A pump is used to drive the blood
flow. While the blood flows through the filter, water, electrolytes,
and most drugs not bound to plasma protein diffuse across the
filter and thus become part of the filtrate, referred to as effluent.
If the objective is the removal of large amounts of fluid and solute
(e.g., urea, potassium, creatinine) through convective clearance, it is
necessary to infuse large volumes of replacement fluid to maintain
fluid and electrolyte balance. Nursing responsibilities include
initiating treatment, monitoring the patient and the system, and
discontinuing treatment. Tables 6-9 and 6-10 list the advantages,
disadvantages, and complications of the various therapeutic CRRT
modes. Table 6-9 evaluates troubleshooting major problems with
CRRT.

Table 6-10
APPROACHES TO CONTINUOUS RENAL REPLACEMENT
THERAPY FILTRATION FLUID REPLACEMENT

Predilution: Replacement Fluid Infused Proximal to the Filter Postdilution: Replacement

Fluid Infused Distal to the
Filter
Patient population: Those with elevated BUN and Hct levels Patient population: All types
Replacement fluid infused into access line Replacement fluid infused
into return line

1393
 Used to enhance urea clearance to ≥18%; decreases oncotic Used to maintain fluid and
pressure, increasing net TMP; moves urea from erythrocytes electrolyte balance
into plasma
Increases net fluid removal Less replacement fluid
required
Potentially increases filter life Simplified clearance
determination
*Urea clearance 12.5 mL/min Urea clearance 10.6 mL/min
*
If increased urea clearance is desired, predilution mode of fluid replacement is used.
BUN, Blood urea nitrogen; Hct, hematocrit; TMP, transmembrane pressure.

The current preference of most practitioners is pump-assisted

venovenous CRRT. The advancements in technology have provided
several alternatives for automated devices that monitor system
pressures, ultrafiltration rates, dialysate solution rates, and various
alarm systems.

Anticoagulation
Patients who are critically ill may have an increased tendency for
coagulation and/or bleeding. All CRRT modalities require the
patient’s blood to be in contact with artificial tubing and
membranes, which stimulates the coagulation cascade. The
complement cascade may also be stimulated if a biocompatible
filter is not used. The goal of anticoagulation is to prevent clotting
in the CRRT circuit, preserve filter performance, and optimize
survival of the circuit. Care providers strive to achieve a balance
between preventing blood loss within the circuit as a result of
clotting and preventing excessive anticoagulation leading to
bleeding. Clotted blood remaining in the circuit is “lost” from the
patient. The patient who is critically ill is at increased risk for
bleeding as a result of coagulopathy and endothelial disruption.
AKI/ARF may be associated with a procoagulant state because of
downregulation of natural anticoagulants and inhibition of
fibrinolysis. If AKI has evolved slowly resulting from an underlying
disease, platelets may also be dysfunctional.

Factors related to coagulation

Patient factors

1394
• Decrease in natural anticoagulants.

• Platelet count and function.

• Transfusions.

• Fibrinolysis inhibition.

Vascular access factors

• Catheter characteristic (e.g., diameter and length).

• Kinking or malposition.

• Patient position change.

Treatment variations

• Intermittent blood flow reductions.

• Predilution or postdilution fluid replacement.

• Reaction time to alarms.

• Blood–air contact in the system.

The choice of anticoagulation generally depends on patient

condition, physician preference, and nursing staff experience with
specific regimens. Collaboration between providers promotes
patient safety and efficacy of treatment. Evidence supports three
considerations in maintaining a clot-free system: type of renal
replacement therapy, the anticoagulant, and the desired blood flow
rate.

Heparin
Heparin is the most common and least expensive of the choices. It
can be administered either systemically or regionally.

Systemic heparinization: Heparin can be infused in a separate IV

line for systemic heparinization or into the “arterial” line of the

1395
 CRRT device. In addition to the complication of bleeding,
heparin-induced thrombocytopenia can occur. Potential for
thrombocytopenia has limited the use of systemic heparin in
recent years.

Regional heparinization: A relatively uncommon procedure that

produces anticoagulation in the circuit but not systemically to the
patient. There is little research available on regional
heparinization. When done, it requires two infusion devices: one
to infuse heparin prefilter (before the hollow-fiber filter) and
another for protamine, a heparin antagonist that is run postfilter
into the return line to neutralize the heparin. This process
requires determining the activated PTT systemically from the
patient and postfilter preprotamine infusion. The goal is to
heparinize the circuit without systemically heparinizing the
patient. This process is labor-intensive and requires meticulous
monitoring and frequent dose adjustment of both the heparin
and protamine. Use of protamine in this manner is rather
uncommon, thus few centers engage in this method of
anticoagulation.

Direct thrombin inhibitors

These agents are used for anticoagulation in patients with heparin-
induced thrombocytopenia. The most common agents are
Argatroban, Bivalirudin (e.g., Angiomax), and Lepirudin (e.g.,
Refludan). Argatroban is eliminated by the liver and is more
suitable for most patients on CRRT. Lepirudin is excreted renally
and therefore not the choice for patients with AKI/ARF. Bivalirudin
is not widely used in this setting, but is under investigation. These
agents are considerably more expensive than heparin, are generally
administered systemically, and tend to exert prolonged
anticoagulation in patients with renal impairment. Careful
monitoring and dosage adjustments are required. Reversal of the
effects of direct thrombin inhibitors cannot be achieved
immediately, because there is no reversal agent available.

Citrate
Citrate is a common alternative to heparin for regional

1396
anticoagulation. Citrate is infused into the arterial line to chelate or
bind with calcium and magnesium, thus inhibiting the coagulation
cascade in the extracorporeal circulation. The deficit in ionized
calcium is present only outside the body in the extracorporeal
circuit, because before reinfusion of the filtered blood, calcium is
substituted into the venous line to target normal ionized calcium.
The goal is to maintain ionized calcium less than 0.35 mmol/L in the
extracorporeal circuit to prevent clotting within the filter. It is
important to infuse calcium systemically to maintain normal levels
of ionized calcium in the patient’s circulation. If dialysate and
predilution replacement fluids are used, they should be calcium-
free to prevent reversal of the citrate effect in the circuit. The
amount of citrate infused into the preblood pump is determined by
systemic ionized calcium levels, which are sampled every 6 hours.
During regional citrate anticoagulation, a minimum amount of
citrate enters the systemic circulation; however, a systemic calcium
infusion is used to assure that normal levels of ionized calcium are
maintained in the patient’s circulation.
Monitoring all laboratory values, including ionized calcium,
sodium, and acid-base balance, is essential.

Isotonic sodium chloride solution

If the patient’s condition prohibits anticoagulation, this presents a
challenge in maintaining circuit patency. The system may need to
be flushed with small boluses of isotonic sodium chloride to reduce
stagnation of blood in the system. Specific unit protocol may
require flushing with 50 to 100 mL every hour to maintain patency
and decrease the potential for clotting.
The use of predilution replacement fluid hemodilutes the blood,
which decreases the chance for clotting. Predilution also helps
separate all solute particles, making it easier for solutes to pass into
the filter. The fluid provides continuous flushing of the circuit. Use
of sodium chloride must be done judiciously, with monitoring of
acid-base balance and electrolytes.
Chloride can accumulate, prompting acidosis.

Replacement fluid

1397
Electrolyte imbalances that may occur with CRRT include
hypokalemia, hypocalcemia, hypophosphatemia, and
hypoglycemia. Free water can be depleted. Use of large amounts of
normal saline replacement fluid can prompt hyperchloremic
acidosis. The replacement fluid may be infused prefilter or
postfilter and is tailored to the specific needs of individual patients.
Three types of solutions are available: citrate-based, lactate-based,
and bicarbonate-based. Lactate solutions can prompt the
development of acidosis, and are not used in patients with liver
abnormalities or in patients with lactic acidosis. Citrate is generally
not used in patients with liver dysfunction.

Assessment: During continuous renal

replacement therapy
Goal of system assessment
Evaluate hemodynamic stability and maintain homeostasis.

History and risk factors

• Events leading to the development of ARF/AKI.

• Underlying chronic kidney disease.

• Presence of cardiovascular disease.

• Presence of pulmonary compromise.

• Nutritional state.

• Neurologic status.

Vital signs
• BP may increase or decrease based on fluid volume status.

• HR may increase or decrease in response to fluid and electrolyte

changes.

1398
• A change in baseline temperature in the presence of sepsis.

• Hypothermia, a common complication of CRRT, increases energy

demands.

• Cardiac dysrhythmias may occur with hypothermia.

• Pulmonary artery occlusion pressure and CVP will fluctuate in

tandem with changing volume status.

• Oxygen saturation to assess respiratory status.

• Body weight to assess fluid balance.

• Urine output and other fluid losses (blood loss drainage fluid).

Observation

Hourly monitoring of the CRRT circuit

• Blood flow rate.

• Venous (return) pressure.

• Arterial (access) pressure.

• Filter pressures.

• Balance pressures.

• Effluent pressures.

• Color of the blood in the circuit.

• Presence of air in the system.

• Dialysate flow rate (if applicable).

• Replacement flow rate (if applicable).

• Transmembrane pressure.

1399
• Ultrafiltration rate.

• Calculate fluid balance.

• Filter patency.

• Anticoagulation.

Hourly monitoring of the vascular access

• Catheter patency.

• Access pressure.

• Return pressure.

• Access site for signs of bleeding or infection.

Palpation
• Pulse quality and regularity bilaterally (scale 0 to 4+).

• Vascular access site for tenderness or expression of exudate.

• Edema extremities and sacrum (scale 0 to 4+).

Auscultation
• Heart sounds to evaluate for contributors to decreased cardiac
output.

• Friction rub indicative of pericarditis.

• S3 and S4 indicative of heart failure.

• Pleural rub indicative of pulmonary pathology.

• Bowel sounds to evaluate gastric motility.

Screening labwork

1400
• Electrolytes, BUN, and creatinine to determine renal function and
effectiveness of CRRT.

• CBC to assess for the presence of anemia.

• Ionized calcium if using citrate anticoagulation to assess for

hypocalcemia.

• Coagulation profile to monitor effects of other anticoagulants.

Collaborative management
Goals for patients undergoing CRRT: The goal is the removal of
excess fluid and solutes, while maintaining electrolyte balance and
adequate fluid intake for homeostasis. In the adult patient who is
critically ill, catabolic rate is two to three times that of normal.
Key Considerations Goals
Enteral nutrition Maintain nutritional requirements
Predilution fluid Used if increased solute removal is required
replacement
Replacement fluid Used for convective clearance and to maintain fluid and electrolyte
balance
Anticoagulation Used to prevent clotting in the circuit
Vasopressors Used to maintain adequate blood pressure
Vascular access Double-lumen catheter, preferably in the subclavian or internal
jugular vein

Care priorities
Prevention of hemodynamic instability and maintenance of
homeostasis are the goals of CRRT. This includes fluid removal and
electrolyte replacement. Continuous monitoring and frequent
prescription changes based on patient condition and needs are
required to meet the goal of therapy. Fluid removal, electrolyte
balance, and maintaining nutrition in these catabolic patients who
are critically ill present a major care challenge for the treatment
team.

1. Maintain hemodynamic stability

Evaluate the volume status based on weight, pulmonary artery
occlusion pressure, cardiac output, CVP, and the clinical signs of

1401
hypervolemia or hypovolemia. Determine electrolyte balance with
particular attention to sodium, potassium, and calcium. Determine
the state of catabolism based on BUN and creatinine levels, along
with the presence of metabolic acidosis.

2. Provide adequate nutrition to promote healing

Assess the nutrition requirements based on the rate of catabolism,
serum albumin, and loss of protein. Most patients will require
enteral or parenteral nourishment to meet nutrition requirements.
All forms of fluid intake (e.g., IV and enteral fluids) must be
accounted for when calculating the desired fluid loss.

3. Replacement fluids
Use physiologic solutions (more chemically similar to normal body
chemistry) to replace the majority of the filtrate removed hourly,
maintain volume stability, and replace electrolyte losses. The use of
plain normal saline may not be appropriate for patients with high-
volume replacement fluid, because electrolyte imbalances or
hyperchloremic acidosis may ensue. Determine hourly fluid
balance to maintain hemodynamic stability. Frequent changes in
the CRRT prescription (orders) may be necessary based on intake
changes. If the patient is receiving citrate-based anticoagulation,
systemic calcium must be measured by ionized calcium levels, and
replaced by a calcium infusion to prevent hypocalcemia.

4. Vascular access adequacy

Maintain adequate flow rates. Inappropriate positioning may cause
blood flow interruption from the patient into the device or from the
CRRT circuit into the patient as a result of catheter movement
against the vessel wall or kinking of the access device. Changing the
patient’s position may increase the ability of the device to maintain
more adequate blood flow. Assess for alignment and signs of
infection. Sterile technique is required when performing access care.

5. Maintain patency of the CRRT machine circuit

Monitor coagulation measurements every 6 hours or as prescribed
in the presence of anticoagulant infusions. Check the circuit for any
signs of blood stasis in lines or filter. Flush with normal saline if

1402
there is evidence of clotting. If using regional anticoagulation of the
circuit, adjust the rate of the anticoagulant infusion as necessary to
maintain blood flow within the circuit without causing systemic
anticoagulation of the patient.

Care plans for continuous renal replacement

therapy
Decreased cardiac output 
related to fluid overload creating heart failure
Goals/Outcomes: The patient’s cardiac output is adequate, as
evidenced by stabilization of vital signs and heart rhythm to the
patient’s normal range. Classic measurements include systolic BP
100 mm Hg or greater, HR 60 to 100 bpm, RR 12 to 20 breaths/min,
peripheral pulses greater than 2+ on a 0-to-4+ scale, brisk capillary
refill (less than 2 seconds), and normal sinus rhythm.
Circulation Status.

Hemodynamic regulation

1. Promote hemodynamic stabilization: Before, during, and after

CRRT, assess and document BP, HR, and RR every 15 minutes
during periods of instability; and then hourly once stabilized.
Indicators of fluid volume overload and deficit include decreased
systolic BP to less than 100 mm Hg, tachycardia, and tachypnea.

2. Monitor perfusion: Assess for decreased amplitude of peripheral

pulses, coolness, pallor, and delayed capillary refill in the
extremities indicative of decreased perfusion every 4 hours.

3. Fluid removal: Measure and record I&O hourly. Consult the

advanced practice provider for a loss of greater than 200 mL/h over
desired fluid removal volume.

4. Dysrhythmia management: Monitor cardiac rhythm

continuously; notify the advanced practice provider of a decrease in
BP greater than 20 mm Hg from baseline resulting from a HR or
rhythm change, including tachycardia, bradycardia, and depressed

1403
T waves and ST segments, associated with intravascular fluid
volume or electrolyte changes.

5. Collaborate with all members of the healthcare team to ensure

that the prescription of CRRT is achieving the desired results
during the appropriate time frame.

6. Monitor for abnormalities and changes in serum electrolyte

values (potassium, calcium, phosphorus, and bicarbonate). Normal
ranges: potassium 3.5 to 5 mEq/L, calcium 8.5 to 10.5 mg/dL,
phosphorus 2.5 to 4.5 mg/dL, and bicarbonate 22 to 26 mEq/L (see
the sections on Fluid and Electrolyte Disturbances, and Acid-Base
Imbalances, Chapter 1).

Risk for deficient fluid volume 

related to ultrafiltration during CRRT
Goals/Outcomes: The patient achieves normovolemia without
further destabilization, as evidenced by a gradual weight loss (less
than 2.5 kg/day) and recovery of a urinary output greater than 0.5
mL/kg/h in nonanuric patients. Ultrafiltration fluid removal rate
remains within 50 mL of the desired hourly rate.
Fluid Balance.

Fluid monitoring

1. Measure and record I&O hourly. Ensure that it is within desired

limits.

2. Weigh the patient daily. Be alert to a daily loss of greater than 2.5
kg.

3. Record ultrafiltrate hourly.

4. Check replacement fluid infusion hourly to ensure that it is

within prescribed limits.

5. Check dialysate fluid infusion rate hourly to ensure that it is

within prescribed limits.

6. Consult the LIP for unanticipated fluid loss from vomiting,

1404
diarrhea, fever, and wound drainage.

Electrolyte Management: Hyperkalemia; Electrolyte

Management: Hypermagnesemia; Electrolyte Management:
Hypernatremia; Electrolyte Management: Hyperphosphatemia;
Fluid Management; Fluid Monitoring; Hypovolemia Management;
Intravenous Therapy. Additional, optional interventions include
Dysrhythmia Management; Feeding; Fever Treatment;
Gastrointestinal Intubation; Hemodynamic Regulation; Invasive
Hemodynamic Monitoring; Medication Management; Nutrition
Management; Weight Management; and Phlebotomy: Arterial
Blood Sample and Venous Blood Sample.

Excess fluid volume 

related to renal insufficiency
Goals/Outcomes: The patient experiences a gradual fluid loss
and stabilization of intravascular volume, as evidenced by vital
signs achieving baseline range, CRRT system functioning
effectively, CVP 4 to 8 mm Hg, improvement of edema, crackles,
and other physical indicators of hypervolemia.
Fluid Overload Severity.

Fluid/electrolyte management

1. Check tubes for kinks hourly.

2. Maintain anticoagulation therapy within prescribed goals. The

system must be functional for the patient to get the full benefit of
CRRT.

3. Inspect vascular access, filter, and lines for patency hourly. If

clotting or clogging with protein is suspected, flush the system with
50 mL normal saline to check patency.

4. If clots are present, consult the advanced practice provider,

change the filter as needed.

5. On an hourly basis, assess for and document the presence of

physical indicators of hypervolemia: CVP greater than 10 mm Hg,

1405
BP elevated greater than 20 mm Hg over baseline, tachycardia,
jugular venous distention, basilar crackles, increasing edema
(peripheral, sacral, periorbital), and tachypnea.

Electrolyte Management: Hypokalemia; Electrolyte

Management: Hyponatremia; Fluid/Electrolyte Management; Fluid
Management; Fluid Monitoring. Additional, optional interventions
include Dysrhythmia Management; Feeding; Gastrointestinal
Intubation; Hemodialysis Therapy; Hemodynamic Regulation;
Invasive Hemodynamic Monitoring; Medication Management;
Phlebotomy: Arterial and Venous Blood Samples; Positioning; Skin
Surveillance; and Weight Management.

Deficient knowledge 
related to CRRT procedure/treatment
Goals/Outcomes: The patient or significant other verbalizes
accurate information about the CRRT procedure within 24 to 48
hours of instruction.
Knowledge: Treatment/Procedure.

Teaching: Procedure/treatment

1. Assess the patient’s knowledge of CRRT, explain necessity of

vascular access and what can be expected during vascular access
insertion. Typical access sites are the internal jugular or the
subclavian vein. Occasionally femoral access is required.

2. Explain the importance of and rationale for limited movement of

the area of catheter insertion following catheter placement.

3. Describe the equipment used for the procedure (e.g., CRRT

machine, filter, lines). Explain that their blood will be visible in the
filter and lines throughout therapy.

4. Discuss that vital signs will be assessed and blood tests will be
performed at frequent intervals to monitor for stability throughout
therapy. Reinforce that staff members are close at all times to
provide support and additional information as needed.

1406
5. Explain that the use of CRRT may require 24 hours or longer to
attain fluid balance.

Teaching: Disease Process; Teaching: Individual; Teaching:

Prescribed Medication. Additional, optional interventions include
Discharge Planning; Medication Management; and Weight
Management.

Impaired physical mobility 

related to weakness ensuing with critical illness
Goals/Outcomes: The patient exhibits ability to move about in
bed with assistance without evidence of disruption of
hemofiltration equipment. The patient’s skin remains intact, no
evidence of muscle atrophy or contracture formation caused by
imposed immobility.
Mobility.

Positioning

1. Secure the access device and tape to ensure safe movement

without disruption of the catheter.

2. Explain to patient the need for care and assistance when moving.

3. Try to avoid use of physical restraint to restrict movement. If the

access site is near or within a limb and movement prompts device
occlusion, initiate a limb immobilizer.

4. Turn and reposition the patient at least every 2 hours,

maintaining good body alignment.

5. Advance mobility as tolerated by the patient and position of

catheter.

6. Massage bony prominences during every position change to

promote comfort and circulation.

7. Support involved extremities with pillows.

8. Teach patient-assisted range-of-motion exercises on uninvolved

1407
extremities. Encourage isometric, isotonic, and quadriceps setting
exercises on uninvolved extremities.

Exercise Therapy: Ambulation; Exercise Therapy: Joint

Mobility. Additional, optional interventions include Activity
Therapy; Body Mechanics Promotion; Circulatory Care; Circulatory
Precautions; Fall Prevention; Pain Management; Progressive Muscle
Relaxation; Skin Surveillance; and Weight Management.

Risk for injury 

related to CRRT equipment
Goals/Outcomes: The patient’s CRRT filter and line connections
remain intact, and ultrafiltrate test results are negative for blood.
Fluid Balance.

Fluid monitoring

1. Secure all connections within the system and check hourly.

2. Avoid concealing lines, filter, or connections with linen.

3. Inspect ultrafiltrate hourly for blood. If unsure whether

ultrafiltrate contains blood, check the solution for occult blood.

4. If the test result is positive for blood, clamp the ultrafiltrate port
and consult the advanced practice provider for further
interventions.

Electrolyte Management: Hyperkalemia; Electrolyte

Management: Hypermagnesemia; Electrolyte Management:
Hypernatremia; Electrolyte Management: Hyperphosphatemia;
Fluid Management; Fluid Monitoring; Hypovolemia Management;
Intravenous Therapy. Additional, optional interventions include
Dysrhythmia Management; Feeding; Fever Treatment;
Gastrointestinal Intubation; Hemodynamic Regulation; Invasive
Hemodynamic Monitoring; Medication Management; Nutrition
Management; Weight Management; and Phlebotomy: Arterial
Blood Sample and Venous Blood Sample.

1408
Additional nursing diagnoses
For more information about fluid and electrolytes, see sections on
Fluid and Electrolyte Disturbances, and Prolonged Immobility,
Chapter 1.

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51. Waikar S, Liu K, Chertow G. Diagnosis, epidemiology and
outcomes of acute kidney injury. Clin J Am Soc Nephrol.
2008;13:844-861.
52. Wang X, Yuan WJ. Timing of initiation of renal
replacement therapy in acute kidney injury: a systematic
review and meta-analysis. Ren Fail. 2012;34:396-402.
53. Zhang JD, Hongying M. Efficacy and safety of regional
citrate anticoagulation in critically ill patients undergoing
continuous renal replacement therapy. Intensive Care Med.
2012;38:20-28.

1413
CHAPTER 7

Neurologic disorders
General neurologic assessment
Level of consciousness
• Assess for orientation, drowsiness, inappropriate use of words,
slurred speech, arousability, confusion, and amnesia.

• Close monitoring of level of consciousness (LOC) is essential to

assess for determining deterioration, and even a slight change
may indicate that emergent intervention is needed.

• For specifics of how to assess using levels of stimulation, refer to

Appendix 2, Glasgow Coma Scale (GCS).

• Considerations for the bariatric patient: The increased ratio of

adipose to lean body mass changes the volume of distribution of
lipophilic drugs. Propofol and benzodiazepines used for sedation
and control of anxiety are lipophilic. Increased adipose tissue
prompts an accumulation of these and all lipophilic drugs.
Increased dose is required to achieve the desired effects, and the
elimination half-life is prolonged. The dose of many lipophilic
medications in the bariatric population is considered more
effective using the actual body weight rather than ideal body
weight. If doses of propofol and benzodiazepines (e.g.,
lorazepam, diazepam, midazolam) are prescribed using actual
body weight, the patient may remain agitated. Patients may also
experience prolonged sedation, particularly with

1414
 benzodiazepines, when the drugs are weaned. Underlying mood
changes and memory loss may be present, because these
conditions are associated with obesity.

Vital signs
Refer to specific sections for key vital sign changes specific for the
type of neurologic disorder.

Key cranial nerve assessment

It is not always necessary to assess all 12 cranial nerves (see
Appendix 3). Specific neurologic disorders will address cranial
nerve impairments.

• Assess the nerves responsible for vision (optic), pupillary

response (oculomotor), and eye movements (oculomotor,
trochlear, abducens).

• Assess facial/corneal sensation and chewing (trigeminal) and

facial muscle movement and taste (facial).

• All functions are evaluated bilaterally (e.g., both eyes, both sides
of face, etc.).

• A full examination includes all 12 nerves.

• Considerations for the geriatric patient: Obesity accelerates

aging, including changes seen in cranial nerve assessment in
older adults. Diabetic neuropathy may manifest in patients
who are insulin-resistant, with persistent hyperglycemia.

Assess motor and cerebellar function

Evaluate bilaterally (both sides of body, both arms and legs) for
muscle size, strength, tone, and coordination. Note muscle atrophy
or hypertrophy.

• If the patient can walk, assess gait.

• Ask the patient to walk heel to toe to check for balance and

1415
 coordination.

• Perform Romberg test: Ask the patient to close eyes and stand
with feet close together while you stand nearby in case the
patient sways/falls (abnormal response indicative of cerebellar
dysfunction).

• Ask the patient to squeeze your hands and push feet against your
hands, to assess if strength is equal on both sides.

• Note any involuntary movements (tremors, jerking,

fasciculations) and general posture.

• Move the patient’s joints through passive range-of-motion (ROM)

exercises, noting any tenderness of involved muscle groups.

• To further evaluate muscle strength, have the patient perform

active ROM exercises while you apply resistance against the
movements. Use the following rating scale for muscle strength:

MUSCLE STRENGTH RATING

Score Description of Strength

5/5 Patient moves joint with full ROM against normal resistance and gravity
4/5 Patient moves joint with full ROM against mild resistance and gravity
3/5 Patient moves joint with full ROM against gravity only
2/5 Patient moves joint with full ROM but not against gravity
1/5 Patient’s muscle contracts in an attempt to move joint; joint does not move
0/5 Patient does not visibly attempt to move; no muscle contraction; paralysis
ROM, Range of motion.

• Assess for abnormal motor movements unilaterally and

bilaterally:

• Decorticate posturing (abnormal flexion).

• Decerebrate posturing (abnormal extension).

• Flaccidity.

1416
 Motor deficits (weakness or paralysis) are caused by injury or
edema to the primary motor cortex and corticospinal (pyramidal)
tracts.

• Perform specific testing for abnormalities as appropriate:

• Grasp: Place two fingers within the patient’s palm

and ask the patient to squeeze your fingers. Ask the
patient to let go. Abnormal grasp: The patient
cannot let go once grasp is in progress. May reflect
frontal lobe disease; observed occasionally with
occipital lobe disease, Alzheimer disease, or
bilateral thalamic disease.

• Babinski sign: Upward or dorsiflexion of the big toe

when stroking the outer sole and ball of the foot can
indicate a lesion of the pyramidal tract.

• Kernig sign: Painful resistance to full extension of

the leg at the knee when the hip is flexed; used in
the diagnosis of meningitis resulting from
meningeal irritation.

• Brudzinski sign: Flexion of the hip and knee

involuntarily with neck flexion and used in the
diagnosis of meningitis resulting from meningeal
irritation.

• Considerations for the bariatric patient: Assess exercise

history, noting weakness in extremities. The spine and joints are
burdened by the additional weight, and are at risk for
deterioration and instability. Pain assessment may reveal the

1417
 reasons for limited mobility, in addition to reduced level of
endurance. Posture analysis is done to help classify the body
type, which helps to anticipate risk factors. Functional ability,
mobility, and disabilities should be noted, including simple
findings such as the ability to transfer from bed to chair.

Sensory assessment
Sensory deficits occur when the primary sensory cortex, the sensory
association areas of the parietal lobe, or the spinothalamic tracts are
injured or edematous. Sensory deficits include inability to
distinguish objects according to characteristics (e.g., size, shape,
weight) and inability to distinguish overall changes in temperature,
touch, pressure, and position.

• Assess perception of touch, proprioception, pain, temperature,

and vibration (if possible). Ask the patient to close eyes while you
apply stimuli. The patient should not be given the opportunity to
anticipate your moves. Compare the same stimulus on the right
side of the body to the identical location on the left side of the
body. Note if the patient perceives stimuli symmetrically and
appropriately (sharp versus dull using a needle versus a cotton
swab, or hot versus cold). Compare proximal and distal parts of
arms and legs when testing pain and touch.

• Superficial and deep reflexes are tested on symmetrical sides of

the body and compared noting the strength of contraction.

• Test vibratory sense (with vibrating tuning fork) distally (on the
tip of big toe or finger) and ask when the patient feels the
vibration stop.

• For position sense, move distal joints about using very light touch
and ask about the position the patient perceives of the joint.

• Two-point discrimination can be done using a bent paper clip.

Note the smallest distance between the two points at which the
patient senses two points are pressing on the skin. Document
using a dermatome map.

1418
 Improvement in both motor and sensory perception may be seen
while cerebral edema subsides.

Fundoscopic assessment
Generally done by the advanced practice provider and may
reveal retinal hemorrhage(s) at the side of the optic disc.
Hemorrhage is caused by blood from the subarachnoid space (SAS)
being forced along the optic nerve sheath under high pressure. The
patient may complain of blurred vision or blind spots (scotomata).
Terson hemorrhage associated with vitreous and/or subhyaloid
hemorrhage has been seen as a subarachnoid complication and its
presence has been noted with increased mortality and morbidity
rates.

Dysphagia screening
Should be performed early, particularly when stroke has
occurred, to prevent complications of aspiration and to initiate
appropriate nutrition therapy. People with neurologic dysfunction
are poor judges of their own ability to swallow, thus a thorough
evaluation and intervention by a speech pathologist may be
required, following routine screening procedures recommended by
institutional protocol.

Diagnostic Tests for Neurologic Disorders

Test Purpose Abnormal Findings

Cerebral angiography Digital subtraction Areas of reduced cerebral blood
angiography visualizes blood flow, aneurysms, arteriovenous
flow. malformations (AVMs), vascular
Involves use of intravascular abnormalities.
catheter. Used with interventional
The gold standard for neuroradiologic procedures such
evaluating cerebral as coiling, AVM embolization
vasculature. (gluing).
Invasive procedure with Provides specific information on the
minimal risk used to cause of stroke by identifying the
visualize the cerebral blood blood vessel involved
vessels.
Computed tomography Performed emergently, is the Shift of structures caused by
(CT) of brain gold standard of enlarged mass, edema, exudate,
differentiating ischemic from abscesses, fresh hemorrhage,
hemorrhagic stroke; may be hematomas, infarction, and
done at intervals to monitor hydrocephalus.

1419
 progress. Can visualize facial skeleton and
Assesses details of structures soft tissue structures for
of bone, tissue, and fluid- abnormalities (e.g., tumors, brain
filled space. injury).
Detects exudate, abscesses, Within the first few hours after an
and intracranial pathology acute ischemic stroke, the scan
(e.g., tumors, brain injury). may appear normal. Intracranial
Assesses for hydrocephalus. hemorrhage is easily diagnosed
on CT—blood appears as a bright
white signal.
Continuous Evaluates cardiovascular Phenytoin and other antiepileptic
electrocardiographic status, especially during drugs can cause dysrhythmias and
monitoring medication administration. hypotension.
CT angiography Less invasive than cerebral Visualizes intraarterial clot, small
angiography; involves use of intracranial aneurysm, and AVM.
contrast media injection into
peripheral vein and use of CT
scanner.
CT perfusion or CT- Provides information related Compromised blood flow; a limited
xenon scan to cerebral blood flow (CBF) test; cannot detect infarcted tissue.
and volume.
Used to guide clinical
decision-making regarding
the use of thrombolysis or
interventional procedures.
Electroencephalography Evaluates electrical activity of Diagnosis of seizures and
the brain for ongoing seizures, localization of structural
even if there are no clinical abnormalities.
signs of seizures. Also used as element of criteria for
brain death.
Electromyography Assesses NCV deficit as a result EMG and NCV demonstrate
(EMG) or nerve of the demyelination of profound slowing of motor
conduction velocity peripheral nerves. conduction velocities and
(NCV) conduction blocks several weeks
into the illness.
Lumbar puncture (LP) Measures CSF pressures and Elevated protein, low glucose,
with cerebrospinal fluid obtains CSF specimen when elevated white blood cell count.
(CSF) specimen for infection, such as meningitis
analysis or neurosyphilis, is
suspected.
May be performed when
subarachnoid hemorrhage is
suspected and CT is normal.
Magnetic resonance Minute oscillations of Infarcts, areas at risk or ischemic
imaging (MRI) and hydrogen atoms in the brain areas, vascular defects, stenosis,
arteriography (MRA) of create graphic image of bone, occlusion.
brain fluid, and soft tissue.
Provides a more detailed
image.
MRI is most useful for patients
with ischemia in identifying
the cause and area involved.
Provides detailed information
regarding the area of injury
or its vascular supply
(magnetic resonance
arteriogram or MRA).

1420
 Diffusion-weighted imaging is
a measurement of edema,
whereas perfusion-weighted
imaging is a measurement of
global CBF.
Positron emission To evaluate brain metabolism Demonstrates abnormal function of
tomography (PET) and and blood flow using three- the brain by revealing abnormal
single-photon emission dimensional imaging produced structures, metabolism, and
computed tomography using a radioactive tracer. perfusion.
Locates areas of brain causing
seizures, head injury, and some
disorders (e.g., Alzheimer
disease).
Radioisotope brain scan Examines areas of blood flow Increased or decreased blood flow
through concentration of intraoperatively or assesses for
isotope uptake in the brain. postoperative cerebral infarction.
Lack of uptake may indicate
cerebral brain death.
Transcranial Doppler Noninvasive and can be done Arterial narrowing, vasospasm,
serially at the bedside. cerebral circulatory arrest, emboli
Evaluates the intracranial as a result of vasospasm.
vessels and assesses the Can also be used to confirm absent
velocity of blood flow in the blood flow in brain death.
anterior and posterior
cerebral circulation.
Also used to evaluate
vasospasm, to determine
brain death via detection of
cerebral circulatory arrest,
for intraoperative
monitoring, and to locate
emboli.

Brain death
Pathophysiology
Brain death is defined as irreversible loss of function of the brain,
including the brainstem and respiratory centers. Cardiac death is
the cessation of mechanical action/pumping of the heart, resulting
in absence of pulse, heart sounds, blood pressure (BP), and
respirations. Brain death is most frequently the result of increased
intracranial pressure (ICP) caused by severe traumatic head injury
or hemorrhagic stroke caused by ruptured cerebral aneurysm with
subarachnoid hemorrhage (SAH) or intracranial hemorrhage (ICH).
A significant number of patients with large acute ischemic strokes
(AIS) experience cerebral edema and herniation. Hypoxic-ischemic

1421
encephalopathy with massive brain swelling after prolonged
cardiopulmonary resuscitation or asphyxia and encephalopathy
with cerebral edema resulting from fulminant hepatic failure may
also result in increased ICP, herniation, and brain death.
If brain death occurs quickly, cardiac death may occur
immediately. If brain death occurs more slowly, with time to
initiate mechanical ventilation before cardiac death, the heart can
continue to beat/pump because the cardiac pacing cells operate
independently from brain regulation. Mechanical ventilation
provides the oxygen necessary to maintain viable cardiac pacing
cells and conduction pathways if the patient is circulating adequate
amounts of blood cells carrying oxyhemoglobin, acidosis is
controlled, and electrolytes are managed. Over time, without a
functional hypothalamus and pituitary gland, patients experience
further instability of BP caused by loss of regulation of the thyroid
and adrenal glands. Massive diuresis is common when the
posterior pituitary gland ceases to function.
If the patient is an organ donor, the organs must be sustained
before removal, requiring management of all sequelae of brain
death. Guidelines for managing brain dead organ donors have
common elements internationally, with most controversy stemming
from the need to provide additional hormones to help control
endocrine-related crises associated with loss of function of the
pituitary and hypothalamus and use of prophylactic antibiotics to
prevent infection.
The President’s Commission report regarding “guidelines for the
determination of death” drafted a proposal for a legal definition of
death resulting in the Uniform Determination of Death Act
(UDDA). The document states: “An individual who has sustained
either (1) irreversible cessation of circulatory and respiratory
functions, or (2) irreversible cessation of all functions of the entire
brain, including the brainstem, is dead. A determination of death
must be made with accepted medical standards.” In the United
States, the majority of state laws reflect the UDDA. Amendments
including physician qualifications, confirmation by a second
physician, or religious exemption have also been included by
legislators in several states.
The UDDA does not define “accepted medical standards.” The

1422
American Academy of Neurology (AAN) brain death practice
guidelines were initially written in 1995 to define medical standards
for determination of brain death. The guidelines highlighted that
three key clinical findings must be present to confirm irreversible
cessation of brain functions, including the brainstem: coma (with a
known cause), absence of brainstem reflexes, and apnea. Despite
the AAN guidelines, patients are inconsistently managed in U.S.
hospitals and worldwide. Differences in prerequisites, the number
of required physician assessments, the lowest “living person” core
temperature, and other measurements varied. Medical record
documentation of those diagnosed with brain death consistently
reveals deficiencies in documentation.
In 2010, the AAN incorporated the majority of available evidence
into updated guidelines. Five questions emerged, and were
answered following a thorough review of the literature, to address
variations in brain death determination and to facilitate more
consistency in diagnosis:

• Question: Are there patients who fulfill the clinical criteria of

brain death who recover brain function? Answer: In adults,
recovery of neurologic function has not been reported after the
clinical diagnosis of brain death has been established using the
criteria given in the 1995 AAN practice parameter.

• Question: What is an adequate observation period to ensure that

cessation of neurologic function is permanent? Answer: There is
insufficient evidence to determine the minimally acceptable
observation period to ensure that neurologic functions have
ceased irreversibly.

• Question: Are complex motor movements that falsely suggest

retained brain function sometimes observed in brain death?
Answer: For some patients diagnosed as brain dead, complex,
non–brain-mediated spontaneous movements can falsely suggest
retained brain function. Ventilator autocycling may falsely
suggest patient-initiated breathing.

• Question: What is the comparative safety of techniques for

determining apnea? Answer: Apneic oxygenation diffusion to

1423
 determine apnea is safe, but there is insufficient evidence to
determine the comparative safety of techniques used for apnea
testing.

• Question: Are there new ancillary tests that accurately identify

patients with brain death? Answer: Because of a high risk of bias
and inadequate statistical precision, there is insufficient evidence
to determine if any new ancillary tests accurately identify brain
death.

Only one study has prospectively developed criteria for the

determination of brain death. Despite the lack of evidence, the
principles used for the development of “accepted medical
standards” for declaration of brain death are easily understood, and
derived from the definition of brain death within the UDDA. To
determine “cessation of all functions of the entire brain, including
the brainstem,” physicians must diagnose unresponsive coma,
absence of brainstem reflexes, and absence of respiratory drive after
an apnea test/CO2 challenge. To ensure cessation of brain function
is “irreversible,” physicians must diagnose the cause of coma,
exclude other medical conditions, and evaluate the patient over
time to exclude the possibility of recovery.
Despite having reasonably clear guidelines for evaluation, the
lack of evidence prompts clinicians to exercise considerable
judgment when using the criteria on each unique patient.
Adherence to the AAN guidelines varies among the large medical
centers in the United States. Diabetes insipidus, myxedema coma,
and adrenal crisis may result from loss of the
hypothalamic/pituitary regulatory axis as part of brain death. Large
amounts of dextrose-containing intravenous (IV) fluids and insulin
resistance may prompt hyperglycemia. Neurologists,
neurosurgeons, and intensivists may diagnose brain death
approximately two to three times monthly in large referral centers.
Herniation, or displacement of a portion of the brain through
openings in the intracranial cavity, results from increased ICP.
Herniation occurs when there is a difference between the cranial
compartment pressures above (supratentorial) and below
(infratentorial) the tentorium, the rigid membrane that divides the

1424
skull. If additional blood or cerebrospinal fluid (CSF), edematous
tissue, or tumor occupies space inside the skull, there is little ability
to expand to “make room” for anything not normally present.
These “mass lesions” or “space-occupying lesions” cause
“crowding” within their cavity, which increases the pressure.
When pressure in one of the two compartments (supratentorial or
infratentorial) is markedly elevated, the brain structures and blood
vessels within the cavity are compressed, resulting in ischemia,
hypoxia, and, if uncontrolled, cerebral anoxia. When blood flow is
minimal to absent, the hypoxic/anoxic brain tissues become more
edematous. Eventually, no space remains for further expansion.
The skull cannot expand and the tentorium expands minimally,
thus the brain is forced through the available openings. The
movement or displacement through an opening causes further
compression of blood vessels, with possible laceration and
destruction, which leads to necrosis of brain tissues and brain death
(see Traumatic Brain Injury, Neurologic Herniation Syndromes,
Chapter 3).

Neurologic assessment: Brain death

Goal of system assessment
The assessment validates absence of function of the brain and
brainstem. If mechanical ventilation is terminated, natural death
results. Severity of brain injury should be determined following two
expert clinical assessments and diagnostic testing.

History and risk factors

• Severe traumatic head injury (motor vehicle accident,
gunshot/other assault, recreational/industrial accidents).

• Ruptured cerebral aneurysm with SAH.

• ICH resulting in intracerebral hematoma.

• Large AIS resulting in massive cerebral edema and/or brain

herniation.

1425
• Prolonged cardiopulmonary resuscitation.

• Asphyxia (asthmatic cardiac arrest, drug overdose, hanging,

carbon monoxide poisoning, drowning, meningitis).

• Fulminant hepatic failure.

Apnea test (CO2 challenge)

• Determines absence of respirations when mechanically induced

ventilations cease. Testing must be done carefully to avoid
cardiac death during the test. If the patient begins to deteriorate
while off the ventilator, the patient should be placed back on the
ventilator.

Vital signs
• Mild hypothermia: Core temperature greater than 32° C (90° F),
but less than 36.5° C (97° F).

• Hypotension: With mechanical ventilation in place, BP is greater

than 90 mm Hg. Without mechanical ventilation, the heart rate
(HR) will decrease, resulting in hypotension and eventually
asystole.

• Apnea: No spontaneous respirations when mechanical ventilation

is suspended. A formal apnea test is required to confirm the
absence of respirations.

Observation/inspection/palpation
• Coma: The patient does not respond to verbal stimuli, touch, or
deep pain induced by pressure exerted on nail beds, the
supraorbital area of the skull, or the temporomandibular joint or
rubbing the sternum. The cause of coma is most often determined
by history and physical examination, coupled with
neuroradiologic imaging and laboratory testing. If the patient has
received central nervous system (CNS) depressing medications,
neuromuscular blocking agents, has consumed alcohol, has

1426
 severe electrolyte, acid-base, or endocrine disease, diagnosis of
brain death cannot be made until residual effects of the drugs or
other conditions are fully resolved. Core temperature must be
raised and maintained at ≥36° C. Two neurologic examinations
should be done. Any physician is legally allowed to perform the
examination in most U.S. states, but neurologists, neurosurgeons,
and intensivists may have a great level of comfort and expertise
in determining a brain death diagnosis.

• Brainstem reflexes/cranial nerve function: Absent

• Pupils: Unresponsive to bright light.

• Ocular movement: No oculocephalic reflex (“doll’s

eyes” negative). No oculovestibular reflex: No
deviation of eyes toward irrigation of ear canal with
50 mL ice-cold water within 1 minute following
irrigation. Irrigation of each ear canal should be
done several minutes apart (cold caloric test).

• Facial sensory and motor responses: No corneal

reflex to touch with a cotton swab, no jaw reflex, no
grimacing to deep pain, no facial muscle movement
to noxious stimuli.

• Pharyngeal and tracheal reflexes: No coughing or

gagging when posterior pharynx is stimulated by a
tongue blade; no cough response to bronchial
suctioning. (See Appendix 5 Major Superficial
Reflexes and Appendix 3 Cranial Nerves”.)
• Apnea test/CO2 challenge: No spontaneous respirations (absence
of a respiratory drive). Paco2 levels elevated above normal must
be documented. Structured testing is required for diagnosis.

1427
 Prerequisites for testing include normotension, normothermia,
euvolemia, normal Paco2 level, absence of hypoxia and no
previous history of CO2 retention (chronic obstructive pulmonary
disease, severe obesity). All prerequisite conditions must be
normalized before testing.

Screening labwork
• Toxicology screen: Evaluates for presence of toxic doses of
recreational drugs, medications, or poisons (see Drug Overdose,
Chapter 11).

• Basic metabolic panel/blood chemistry: Identifies electrolyte

imbalance, including hypoglycemia, hyperglycemia, and acidosis
(using bicarbonate/CO2). May also reflect the patient’s volume
status, including dehydration and hypovolemia (see Fluid and
Electrolyte Disturbances, Chapter 1).

• Arterial blood gas (ABG) analysis: Evaluates for hypoxia,

acidosis, and hypercapnia (see Acid-Base Balance, Chapter 1).

Diagnostic Tests for Brain Death

1428
Collaborative management
ORGAN DONOR MANAGEMENT FOLLOWING BRAIN DEATH

1429
Care priorities

1. Confirm a clinical diagnosis of brain death

Unresponsiveness or coma, absence of brainstem reflexes, and
apnea. Complete additional diagnostics as needed.

2. Allay doubts about the diagnosis

When the patient manifests the three cardinal findings of brain
death recognized by the AAN, the healthcare team should educate
the patient’s family members about signs and symptoms that may
be present. The following findings commonly cause doubt about
the diagnosis of brain death in both care providers and the patient’s
family:

• Spontaneous movement of limbs: spinal reflex movements may

occur.

• Respiratory-like movements of the chest and abdomen: shoulder

elevation and adduction, back arching, intercostal expansion,
which do not produce effective tidal volume.

• Sweating, blushing, and tachycardia: residual autonomic

1430
 responses.

• Normal BP without vasopressors or sudden increases in BP:

residual autonomic responses.

• Absence of diabetes insipidus: does not occur in some patients.

• Reflexes are present: deep tendon, superficial abdominal, triple

flexion, Babinski sign.

3. Discuss organ donation only after the clinical diagnosis

of brain death has been made and the family understands
the patient is dead
Contact with the organ procurement organization should be done
in a timely manner when death is imminent. Collaborate with the
organ procurement organization to enhance the experience of the
donation process. Do not broach the subject of donation or hint
about donation before the time the patient has been pronounced
dead, unless the patient had resolved the issue of organ donation
with the family before death. The subject of organ donation is
generally better discussed after the patient has been pronounced
dead and the family understands that despite the patient having a
beating heart, without mechanical ventilation, cardiac death will
ensue. Choose a quiet, private, comfortable place to discuss organ
donation, ideally leaving the lead role to a professional from the
organ procurement agency. The family requires privacy, so they
can express their grief regarding the death and can be left alone to
discuss donation, if needed. Ensure all members of the team
participating in the discussion are introduced to family members.
All family members/significant others should be introduced to the
team by name, and their role in the family/life of the deceased
should be explained. Only those whom the next of kin requests to
be present should participate in the discussion. Adequate time
should be given asking/answering questions. The words used
during the discussion are very important:

• Words to avoid: harvest, cadaver, remains, breathing, respirator,

corpse, or any complex medical terminology.

1431
• Phrases to avoid: artificial life support, will live on in others,
deeply comatose.

• Words to include: the deceased patient’s name, ventilator,

procurement, retrieval, donation, dead.

• Phrases to include: time of death, wishes regarding organ

donation, reasons for declining the opportunity, religious beliefs
on organ donation.

4. Maintain organs for donation if the family/significant

others agree
If the family agrees to donation, the next of kin/others chosen by
next of kin are interviewed by the organ procurement team
regarding the patient’s medical and social history. Reassure the
family that the patient’s body will be handled with utmost
care/respect to maintain dignity and will not be visibly disfigured.
Offer the opportunity to view the patient’s body following
donation. Major immediate threats to organ donation are
development of pulmonary edema, hypotension, polyuria leading
to dehydration from diabetes insipidus, and infection. Initiate
measures discussed in the table on Diagnostic Tests for Brain Death
in this chapter.

5. Discontinue life support after the family has had time to

visit the patient, if the family declines the opportunity to
donate the patient’s organs
Weaning of mechanical ventilation and vasoactive drugs is
unnecessary because the patient is dead. Reasons for declining
donation generally relate to the wishes of the patient, religious
convictions, fear of disfigurement/mutilation of the patient’s body,
and mistrust of the motives or anger with the procurement team
members. Mistrust and anger often ensue if the family is
improperly approached regarding organ donation. Involving the
experienced healthcare professionals from the organ procurement
team has been shown to yield a higher success rate with donation.

Care plans for brain death

1432
Decreased intracranial adaptive capacity 
related to increased ICP resulting from imminent brain death. When brain
death is imminent, mechanisms that normally compensate for increases in
ICP are failing. When failed, brain herniation occurs.
Goals/Outcomes: The patient is maximally supported for
reduction of ICP until efforts are proved futile, when brain
herniation ensues, resulting in brain death. Following brain death,
hemodynamic status is supported until decisions are made
regarding organ donation and/or discontinuation of life support.
Tissue Perfusion: Cerebral; Neurologic Status: Consciousness.

Cerebral perfusion promotion

1. Consult with the advanced practice provider to determine

hemodynamic measurements.

2. Maintain hemodynamics within set measurements.

3. Administer osmotic diuretics/rheologic agents (e.g., mannitol,

dextran) as ordered.

4. Administer vasopressin as ordered if diabetes insipidus ensues.

5. Keep blood glucose level within ordered range, avoiding

hyperglycemia unless using medications that induce osmotic
diuresis.

6. Avoid neck flexion or extreme hip/knee flexion.

7. Consult with the advanced practice practitioner regarding

optimal elevation of the head of the bed (HOB).

Cerebral edema management

1. Monitor neurologic status closely and compare with baseline.

2. Monitor respiratory status: rate, rhythm, depth of respirations,

PaO2, Pco2, pH, and bicarbonate.

3. Monitor ICP and cerebral perfusion pressure (CPP) at rest and in

1433
response to patient care activities. Minimize activities that result in
further increases in ICP.

Neurologic monitoring

1. Monitor pupillary size, shape, symmetry, and reactivity.

2. Assess LOC, orientation, and trend of GCS score.

3. Monitor vital signs: temperature, BP, pulse, and respirations.

4. Monitor for corneal reflex, and cough and gag reflexes.

5. Monitor extraocular movements and gaze characteristics.

6. Monitor Babinski response.

7. Monitor for the Cushing response; a late indicator of increased

ICP.

Decisional conflict 
related to the uncertainty regarding the proper course of action related to
the discontinuation of life support and possible organ donation following
brain death.
Goals/Outcomes: Family/support system is maximally supported
in making judgments, and choosing between immediate
discontinuation of life support, organ donation, or possibly
continuing life support until information about brain death can be
processed and accepted.
Decision-Making; Information Processing; Dignified Life
Closure; Acceptance: Health Status.

Dying care

1. If cerebral perfusion promotion measures fail and brain death

ensues, provide care appropriate for the dying.

2. Encourage family to share feelings about death.

3. Monitor deterioration of the patient’s physical (and mental)

1434
capabilities.

4. Facilitate obtaining spiritual support for the family/significant

others.

5. Facilitate discussion of funeral arrangements.

Coping enhancement

1. Assess the impact of the patient’s life situation on roles and

relationships within family/support system.

2. Use a calm, reassuring approach.

3. Provide factual information concerning diagnosis, treatment, and

prognosis.

4. Seek to understand the family’s perception of the stressful

situation.

5. Acknowledge the patient and significant others’ religious,

spiritual, and cultural beliefs surrounding death, dying, and organ
donation.

6. Encourage gradual mastery of the situation if resistance or denial

is impacting the family’s ability to accept the diagnosis of brain
death.

7. Ensure that the family understands that brain dead patients are
dead. Patients are no longer able to breathe without mechanical
ventilation, will experience cardiac death when removed from
mechanical ventilation, will never regain consciousness, will never
interact with others, and have no ability to experience joy related to
human life.

8. Explain the difference among brain death, persistent vegetative

state, and cardiac death. The family and significant others may have
difficulty understanding why brain dead patients are different than
those in a coma who can recover from their insult/injury and those
in a vegetative state who can recover brainstem function to begin

1435
breathing spontaneously. Families may not be able to comprehend
why when the brain is dead, the heart still functions unless
mechanical ventilation is removed. Guilt may be associated with
removal of mechanical ventilation because the patient appears
“alive” with mechanical ventilation in place.

Emotional Support; Environmental Management;

Fluid/Electrolyte Management; Fluid Monitoring; Hypovolemia
Management; Infection Control; Intravenous Therapy; Mechanical
Ventilation; Positioning; Surveillance; Respiratory Monitoring;
Spiritual Support; Vital Signs Monitoring.

Additional nursing diagnoses

As appropriate, see nursing diagnoses and interventions in
Nutrition Support (Chapter 1), Acute Respiratory Failure (Chapter
4), Mechanical Ventilation (Chapter 1), Prolonged Immobility
(Chapter 1), and Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2).

Cerebral aneurysm and subarachnoid

hemorrhage
Pathophysiology
A cerebral aneurysm is an abnormal, localized dilation of an artery
within the cranial vault caused by weakness in the vessel wall.
Ninety percent of cerebral aneurysms are saccular (berry)
aneurysms, whereas the other 10% are fusiform, traumatic, septic,
dissecting, and Charcot-Bouchard aneurysms. Recent research
suggests that cerebral aneurysms result from degenerative vascular
diseases complicated by hypertension and atherosclerosis. Cerebral
aneurysms most often occur at the bifurcation and branches of the
blood vessels of the circle of Willis, with 85% in the anterior
cerebral circulation and 15% in the posterior cerebral circulation.
Approximately 25% of patients have multiple aneurysms.
The critical care nurse may provide care patients with an

1436
unruptured aneurysm or those postrupture with a diagnosis of
SAH. Unruptured aneurysms may be asymptomatic, but nearly half
of the affected population experiences some warning sign or
symptom before rupture as a result of expansion of the lesion and
compression of cerebral tissue. When an aneurysm ruptures, a
hemorrhage occurs in the SAS and basal cisterns. If the patient
survives the initial compromise of cerebral circulation from the
force of the arterial hemorrhage resulting in sharply increased ICP,
the next challenges are surviving possible rebleeding and cerebral
arterial vasospasms. The greatest incidence of rebleeding following
SAH is between 3 and 11 days following the rupture, with the peak
at day 7. Mortality is approximately 70% from SAH. Theories
regarding the cause(s) of rebleeding propose a problem with the
normal process of clot dissolution coupled with “spikes” in arterial
pressure.
The major complication postrupture is the occurrence of
delayed cerebral ischemia from cerebral arterial vasospasm. This
occurs as a result of the constriction of the arterial smooth muscle
layer of the major cerebral arteries and causes a dramatic decrease
in cerebral blood flow that leads to cerebral ischemia and
progressive neurologic deficit. Vasospasm occurs in as many as
60% of patients from 4 to 21 days following SAH, with incidence
peaking between 7 and 10 days. The pathogenesis of the
vasospasms is poorly understood, but ongoing research indicates a
direct relationship to the amount of blood in the SAS and basal
cisterns. The greater the volume of blood, the greater is the risk of
vasospasm. While clots in the basal cisterns begin to hemolyze,
substances may be released that prompt vasospasms. A current
prophylactic treatment includes careful fluid balance and “triple H”
(hypervolemia-hemodilution-hypertension) therapy. Recent
evidence has suggested that intravascular volume management
should target euvolemia and avoid prophylactic hypervolemic
therapy. Aggressive administration of fluid aimed at achieving
hypervolemia has been shown to be harmful by several studies.
Other treatments include the use of calcium antagonists to relieve
vasospasms, balloon or chemical angioplasty to normalize the
vessel lumen, and possibly cisternal fibrinolytic drugs to alter the
natural process of clot breakdown for those with a larger cisternal

1437
blood accumulation. The patient with a ruptured cerebral aneurysm
and SAH is also at risk for communicating or obstructive
hydrocephalus, hypothalamic dysfunction, and hyponatremia.
Some patients present with an obstructive hydrocephalus from
intraventricular blood. However, communicating hydrocephalus
develops in approximately 20% of patients with SAH as a result of
the presence of blood in the SAS and ventricular system.
Hydrocephalus may be acute (occurs within less than 24 hours),
subacute (occurs within less than 4 hours to 1 week), or delayed
(beginning 10 or more days after SAH). Blood in the SAS and
ventricles obstructs the flow of CSF, interferes with circulation and
resorption of CSF, and causes increased ICP, with concomitant
worsening of neurologic status. Hydrocephalus sometimes
produces minimal symptoms and resolves without medical
intervention, whereas some patients may require temporary or
permanent diversion of CSF circulation to achieve symptom relief.
Hypothalamic dysfunction, seen in approximately one third of
patients with hydrocephalus after SAH, may result from
mechanical pressure on the hypothalamus from a dilated third
ventricle. The increased pressure causes an increase in the releasing
hormones from the hypothalamus, which activates the
hypothalamic-pituitary axis of the anterior pituitary, as well as
stimulating the production of antidiuretic hormone (ADH) by the
posterior pituitary gland. The response to the increased
adrenocorticotropic hormone from the anterior pituitary gland
mimics an exaggerated stress response, which includes a marked
increase in serum catecholamines leading to overstimulation of the
sympathetic nervous system. The vasoconstrictive response is
severe enough in a subset of patients to cause “stunned
myocardium,” similar to what is seen with an acute myocardial
infarction (MI).
The surge of ADH from the posterior pituitary results in
syndrome of inappropriate antidiuretic hormone (SIADH), which
may include hyponatremia caused by cerebral salt-wasting (CSW)
syndrome, or a combination of factors influencing sodium and
water metabolism (Table 7-1). Recent studies emphasize that the
diagnosis of CSW requires the presence of hypovolemia versus
SIADH, which usually results in euvolemia or moderate

1438
hypovolemia. Patients with an SAH may have CSW and SIADH
occurring simultaneously, manifested by excessive urine output
coupled with excessive free water retention. Fluid management
strategies in this patient population may be difficult (see Syndrome
of Inappropriate Antidiuretic Hormone, p. 734). Hyponatremia
occurs in 30% to 50% of patients with SAH. Untreated
hyponatremia may lead to intracranial hypertension, cerebral
ischemia, seizures, coma, and death.

Table 7-1
CLINICAL PRESENTATION WITH CEREBRAL SALT-WASTING
SYNDROME VERSUS SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE

Syndrome of Inappropriate Antidiuretic

Cerebral Salt-Wasting Syndrome
Hormone
Hypotension Normotension
Postural hypotension Normotension
Tachycardia Normal pulse rate or bradycardia
Elevated hematocrit Normal or low hematocrit
Decreased glomerular filtration rate Increased glomerular filtration rate
Normal or elevated blood urea nitrogen and Normal or decreased blood urea nitrogen and
creatinine creatinine
Normal or low urine output Normal or low urine output
Hypovolemia Normovolemia or hypervolemia
Dehydration Normal hydration
True hyponatremia Dilutional hyponatremia
Hypoosmolality Hypoosmolality
Decreased body weight Increased body weight

Note: Both hypothalamic dysfunction and hyponatremia are

seen more frequently in patients with extensive SAH and are
positively correlated with the subsequent development of cerebral
vasospasm.

Neurologic assessment: Cerebral

aneurysm(s) and subarachnoid hemorrhage
Goal of system assessment
Evaluate for key nursing diagnoses requiring emergent
intervention: Alteration in cerebral tissue perfusion resulting from
vasospasm of cerebral vessels, increased ICP as a result of

1439
decreased intracranial adaptive capacity, risk for seizure activity
with potential impairment of cerebral tissue perfusion, impaired
gas exchange or ineffective airway clearance attributable to altered
LOC, potential need for management of hyperglycemia, and fluid
volume imbalance and potential for aspiration.

History and risk factors

Evidence reveals that outcomes for patients with ruptured
aneurysms and SAH are affected by factors such as patient’s age,
having the worst clinical grade on the Fisher Scale, or other
predictive scales including the World Federation of Neurosurgeons
Scale (WFNS), the Claassen Scale, the Ogilvy and Carter Scale, or
the commonly used Hunt and Hess Scale (see later). The Fisher
Scale is predictive of the possibility of vasospasm, which is
indicative of the amount of blood in the SAS. The Claassen Grading
System quantifies the risk of delayed cerebral ischemia from
vasospasm associated with SAH. Unlike the Fisher Scale, the
Claassen Scale considers the additional risk of SAH and
intraventricular hemorrhage. The Claassen Scale has not yet been
prospectively validated. The WFNS Grading System is widely used
and includes objective terminology to determine grades. Similar to
the Hunt and Hess Scale, the predictive power of the WFNS Grades
are inconsistent. The Ogilvy and Carter Scale includes several
features that may affect the outcome, including age, Hunt and Hess
Grade, initial presentation, Fisher Grade (SAH volume and
vasospasm risk), and computed tomography (CT) scan findings. A
noncontrast CT scan confirms the diagnosis of SAH by establishing
the presence, amount, and location of blood in the SAS, the
presence and degree of hydrocephalus, and the presence or absence
of intraventricular hemorrhage or intraparenchymal hemorrhage.
The Ogilvy and Carter Scale is more complicated to administer than
the Hunt and Hess Scale, and has been tested only on patients who
have undergone aneurysm surgery. Patient outcomes are also
affected by aneurysm size, occurrence of fever following the SAH,
and new-onset hyperglycemia on admission with SAH.

Hunt and hess classification system

Permits objective evaluation of progression of the patient’s initial

1440
symptoms and is used to predict clinical outcomes and for choosing
treatments. Critical care nurses can benefit from using this grading
system. Grading is first determined by the initial symptoms and
LOC upon presentation, and is used as a basis of comparison over
time.

Grade I: Asymptomatic, alert, and oriented, minor headache,

moderate nuchal rigidity.

Grade II: Alert, oriented, headache, and stiff neck.

Grade III: Lethargic or confused; minor focal deficit such as

hemiparesis.

Grade IV: Stuporous, moderate to severe focal deficits, hemiplegia,

possible early decerebrate rigidity, and vegetative disturbances.

Grade V: Deep coma, decerebrate rigidity, moribund appearance.

The critical care nurse must carefully review the patient’s history
and diagnostic findings to understand the potential risk for
complications. Patients with unruptured aneurysms are at risk for
rupture, depending on the location and size of the aneurysm.
Unruptured aneurysms may be found during diagnostic testing for
headaches or other neurologic symptoms and may produce
symptoms of cerebral ischemia. A patient with new onset of
oculomotor nerve palsy, visual field loss, or lower cranial nerve
deficits should be evaluated for a potential aneurysm. Patients with
unruptured aneurysms are typically encountered in the critical care
setting after elective aneurysm securement (treatment). The two
main options for aneurysm treatment are craniotomy with
aneurysm neck clipping, wrapping or ligation; and the more
recently developed option of a neurovascular interventionalist
performing endovascular coiling or embolization (“chemical
gluing”). Patients admitted for management of a ruptured cerebral
aneurysm may have additional unruptured aneurysms, which will
be secured at a later date.
The distinguishing characteristic of a ruptured aneurysm is often
a patient who complains of the “worst headache of my life.” This is

1441
usually accompanied by severe nausea and vomiting, nuchal
rigidity, visual disturbances, and photophobia. There is a 2% to 4%
risk for rebleeding within the first 24 hours. “Sentinel” or warning
headaches are associated with an aneurysm that begins leaking
days to weeks before rupturing. Very few patients report having a
sentinel headache before aneurysm rupture.
Rupture results in hemorrhage producing seizures, neurologic
deficits, deterioration in LOC, and a mortality rate of 20% to 50% if
the aneurysm rebleeds. Vasospasms may ensue, which increases the
probability for a negative outcome.

Vital signs
BP, HR, and respiratory rate (RR)/pattern may change
secondary to altered cerebral tissue perfusion. BP control is an
essential strategy to prevent rebleeding of an aneurysm.
Continuous intraarterial monitoring is essential for prompt
detection of subtle changes/trends. Many patients are hypertensive
following hemorrhage. BP and headache may fluctuate in tandem;
higher BP increases the severity of the headache. Treatment
involving intravascular volume expansion can increase BP, and is
generally withheld until after the aneurysm has been surgically
clipped or managed with endovascular coils or chemical
embolization. Conversely, hypotension can decrease cerebral blood
flow and perfusion. Hypertension must be managed with great care
to avoid creating hypotension. Temperature should be monitored
closely to avoid worsening outcomes post-SAH. Fever increases
cerebral metabolic rate, which can worsen cerebral ischemia, with
resultant negative outcomes.

Intracranial pressure
Blood in the SAS can produce acute hydrocephalus within the
first 24 hours, which may result in increased ICP. Subacute, or
chronic, hydrocephalus occurs in approximately 10% to 15% of
patients, usually 10 or more days following the SAH. It is caused by
a clot within the ventricular system that blocks the pathways for the
resorption of CSF leading to ventricular enlargement and nonfocal
neurologic deterioration. Intraventricular extension (distension of
the ventricles) at the time of aneurysm rupture can result in acute

1442
hydrocephalus and requires temporary external ventricular
drainage for management of ICP. Nuchal rigidity may be present.
Indicators of increased ICP are listed in Box 7-1.

Box 7-1
INDICATORS OF INCREASED
INTRACRANIAL PRESSURE*
• Alterations in consciousness: increasing restlessness, confusion,
irritability, disorientation, increasing drowsiness, and lethargy.

• Bradycardia.

• Increasing systolic blood pressure with a widening pulse

pressure.

• Irregular respiratory patterns (e.g., Cheyne-Stokes respiration,

ataxic, apneustic, central neurogenic, hyperventilation).

• Hemisensory changes and hemiparesis or hemiplegia: caused by

involvement of hemispheric sensory and motor pathways.

• Worsening headache.

• Papillary changes.

• Dysconjugate gaze and inability to move one eye beyond

midposition: caused by involvement of cranial nerves III, IV, and
VI.

• Seizures.

• Involvement of other cranial nerves: depends on the severity of

neurologic insult.

*If these indicators of increased intracranial pressure are left

untreated, the patient will undergo irreversible brain damage or
death. If these indicators occur suddenly, there will be
displacement of brain substance (herniation), which will progress

1443
rapidly to permanent brain damage or death. For additional
information about herniation syndromes, see Traumatic Brain
Injury (Chapter 3).

Indicators of hydrocephalus
• Acute: Persistent or sudden onset of coma with loss of
pupillary reflexes within 24 hours of SAH.

• Subacute: Gradual onset of confusion, drowsiness, lethargy, or

stupor within 1 to 7 days of SAH.

• Delayed or chronic: Gradual onset of confusion, incontinence, or

impaired balance, mobility, and gait; intellectual impairment
(slowness, mutism); lack of affect; and presence of the grasp and
sucking frontal lobe reflexes (abnormal in adults), at about 10
days following SAH.

Observation and functional assessment

Diminished level of consciousness

Acute deterioration in a patient’s neurologic function may
signal rerupture in a patient with a ruptured, unsecured aneurysm
or herald the onset of vasospasm. At the onset of significant
hemorrhage, unconsciousness may occur with only reflexive or
pathologic motor responses seen. Morbidity and mortality are high
in those with massive hemorrhage. Approximately 10% to 30% of
patients with an acute SAH will die before obtaining medical
treatment. Of those who survive the initial hemorrhage, up to 30%
to 60% will die from the initial hemorrhage or sequelae.

Pupillary changes
Depending on location of the aneurysm, visual changes may vary;
assess for visual field loss, oculomotor palsy, diplopia, immobile
eye, retroorbital pain, or hemianopsia.

1444
Motor/sensory assessment
Fluctuating hemiparesis or aphasia with increasing confusion can
be clinical symptoms of vasospasm. Hydrocephalus is generally not
associated with focal neurologic deficits. Anxiety, confusion,
agitation, disorientation, lethargy, stupor, and coma may indicate
hydrocephalus, vasospasm, or early hyponatremia. Anorexia,
nausea, vomiting, abdominal pain, cold and clammy skin,
generalized weakness, and lower extremity muscle cramps are late
signs of untreated hyponatremia. Flushing, diaphoresis, pupillary
dilation, decreased gastric motility, increased serum glucose, fever,
hypertension, tachycardia, cardiac dysrhythmias, ischemia, and
infarction can be attributable to increased circulating
catecholamines.

Fundoscopic assessment
See Chapter 7 “General Neurologic Assessment.”

Screening labwork
• CSF analysis may be performed to confirm the presence of blood
in the CSF in patients with symptoms suggestive of SAH but with
no clear abnormalities detected on the CT scan. The presence of
xanthochromia (yellow-tinged) CSF is caused by the breakdown
of hemoglobin and signals possible hemorrhage. CSF pressure,
normally 0 to 15 mm Hg (75 to 180 mm H2O), may be elevated.
The pressure is proportionate to the amount of bleeding. Protein
may increase to 80 to 130 mg/dL (normal is 15 to 50 mg/dL).
Note: Performance of lumbar puncture in the patient with SAH
and increased ICP carries substantial risk of herniation and
rebleeding; thus, it is not a routine study in this patient
population. In patients with SAH and an external ventricular
drain for the management of hydrocephalus, CSF may be
sampled as part of a workup of infectious causes of sustained
fever.

• Electrolytes and glucose levels should be monitored at least daily

to detect hyponatremia and hyperglycemia. Fluid management in
SAH after an aneurysm is secured can be associated with

1445
 hypokalemia, hypomagnesemia, and hypophosphatemia, thus
these electrolytes should also be monitored on at least a daily
basis.

• ABG analysis: To detect hypoxemia and hypercapnia and to

determine appropriate respiratory therapy.

Diagnostic testing
Refer to Neurologic Diagnostic Testing, Chapter 7.

Collaborative management
Care priorities

1. Pharmacotherapy

• Calcium channel blocker: Nimodipine (Nimotop) inhibits calcium

influx across the cell membrane of vascular smooth muscles. The
resulting decrease in peripheral vascular resistance and
vasodilation is believed to increase perfusion in cerebral vessels.
Although nimodipine does not prevent vasospasm, its use has
been shown to be associated with improved long-term outcomes
in patients who experience vasospasm. Nimodipine is given
within 96 hours after hemorrhage as 60 mg enterally every 4
hours for 21 days (the recommended course of therapy). Some
patients experience significant decreases in BP with nimodipine
and may require a dosage schedule of 30 mg every 2 hours. IV
administration of calcium antagonists is not recommended at this
time.

• Antihypertensives: Antihypertensive therapy is used cautiously

in this patient population because allowing hypertension is a
significant element of standard therapeutic management in
aneurysmal SAH. Hydralazine hydrochloride (Apresoline),
labetalol (Normodyne), or nicardipine (Cardene) may be
administered to control BP both before definitive securing of the
ruptured aneurysm and after clipping or coiling to maintain BP

1446
 in desired measurements. Maintaining BP at less than 200 mm
Hg has been recommended.

• Osmotic diuretics: Mannitol (Osmitrol), urea (Ureaphil), and

glycerin (Glycerol) may be used to reduce ICP and treat cerebral
edema via diuresis to remove fluid from the brain. Patients
should be monitored for electrolyte imbalances, other systemic
side effects, and adverse reactions related to fluid shifting.

HIGH ALERT!
With the rapid movement of extracellular fluid from brain
tissue to plasma with associated decrease in brain volume,
potential for rebleeding may be increased after giving mannitol.
Mannitol may cause a rebound increase in intracranial pressure 8
to 12 hours after administration, while fluid shifts from cells into
the vascular compartment. Furosemide (Lasix) is often used to
decrease the rebound effect of mannitol.

• Loop diuretics: Furosemide (Lasix) is often used as a sole agent to

decrease cerebral edema without causing the rise in intracranial
blood volume that occurs with mannitol.

• Corticosteroids: Dexamethasone (Decadron) is a controversial

medication used to relieve cerebral edema and decrease ICP. Use
of dexamethasone is most likely to be seen in the immediate
postoperative management of the patient who has undergone
surgical intervention to secure the aneurysm. The patient should
be monitored carefully for side effects, including gastrointestinal
(GI) tract irritation. Medications such as H2-blockers or proton
pump inhibitors may be used to reduce the risk of gastritis and
ulceration.

• Antipyretics: Acetaminophen is used to control fever, which

increases cerebral metabolism. Aspirin is usually avoided,
because its platelet action impairs clotting and promotes

1447
 bleeding. In patients requiring multiple interventions to manage
increased ICP, sustained fever can compromise outcome and
aggressive measures may be required to control the fever.
Clinical trials have been conducted to evaluate conventional
treatment (use of acetaminophen and cooling blankets) compared
with addition of an intravascular catheter–based heat exchange
system for patients with temperatures higher than 38° C and
have shown the effect to decrease fever.

• Anticonvulsants: Patients with aneurysmal SAH are at high risk

for seizures, thus antiepileptic drugs such as phenytoin (Dilantin)
or levetiracetam (Keppra) may be used to control or prevent
seizures. If phenytoin is used, monitoring of drug levels is
required to ensure the optimal dose and avoid toxicity.

• Analgesics: Blood in the SAS is very irritating and the headache

associated with SAH can be difficult to control. Acetaminophen is
commonly used along with a combination of IV and oral narcotic
analgesics as necessary. Pain medications should not routinely be
withheld solely out of concern for the ability to detect future
neurologic deficits. Pain should always be treated. Stress
management techniques can be a helpful adjuvant therapy.
Photophobia may persist for several days after SAH and
contribute to patient discomfort. Maintaining a low light
environment even after the aneurysm is secured can be helpful
with this issue.

• Stool softeners: Restrictions in activity related to hospitalization

and narcotic analgesic use can predispose the patient to
constipation. Docusate sodium (Colace) is the drug of choice for
preventing straining, which can increase ICP.

• Insulin: Glucose control particularly intraoperatively. More

research is needed to determine specific critical timing of stricter
glucose controls for patients with aneurysmal SAH.

• Statins: The use of statins is a newer therapy supported by

metaanalysis, which has indicated that the initiation of statins
after SAH reduces the incidence of vasospasm, delays ischemic

1448
 deficits, and affects mortality. Liver function tests and creatine
kinase should be assessed before initiation of statin therapy and
then monitored on a weekly basis during acute management of
aneurysmal SAH. Patients who do not otherwise require statin
therapy will require it only during hospitalization.

• Triple H therapy: Each of the following therapies may be used

singly or in combination.

Although hypervolemic-hypertensive therapy with

hemodilution (triple H therapy) represents standard management
in subarachnoid hemorrhage for vasospasm, it carries great risks.
The patient’s cardiovascular status requires close monitoring,
because patients with existing cardiovascular disease may be
unable to tolerate the hypervolemia. Additionally, the patient
should be very closely monitored to establish whether their
neurologic function varies with changes in blood pressure or fluid
status. If used before the aneurysm is secured (rare), this modality
may precipitate intracranial pressure with rerupture of and
rebleeding from the aneurysm. When used after definitive
intervention, the patient may experience cerebral edema with
cerebral ischemia and subsequent neurologic deficit.

• Hypervolemia (saline, whole blood, packed cells, plasma protein

fraction, albumin, or hetastarch): Increases circulating volume to
prevent ischemia caused by vasospasm. The patient’s neurologic
status is often used to gauge the effectiveness of hypervolemic
therapy. If concern exists about the patient’s ability to tolerate
hypervolemia, noninvasive methods of monitoring cardiac
output and index can be employed. Use of central venous
catheters and central venous pressure (CVP) monitoring is
restricted to patients with clinical symptoms of vasospasm. Very
rarely, invasive hemodynamic monitoring with a pulmonary
artery catheter may be required.

1449
• Hemodilution (albumin and crystalloid fluids): Decreases blood
viscosity. CVP greater than 8 mm Hg is usually sufficient to
maintain hypervolemia and dilute the hematocrit to less than
35%.

• Hypertension: By increasing BP, CPP increases and may help

prevent ischemia and infarction. Once the ruptured aneurysm is
definitively secured, hypertension is allowed up to systolic BPs
(SBPs) of 200 to 220 mm Hg. If a patient develops clinical
symptoms of vasospasm, continuous IV vasopressors such as
phenylephrine or norepinephrine may be used to assess for
clinical improvement with elevation of BP to a maximum systolic
pressure of 240 mm Hg. Ideally, BP is maintained 60 mm Hg
above baseline.

2. Surgical/endovascular intervention
Initial management involves stabilizing the patient and minimizing
the risk of rerupture of the aneurysm. The National Institute of
Neurological Disorders and Stroke (NINDS), a division of the
National Institutes of Health (NIH), is recognized as the leader in
research on the brain and nervous system in the United States. The
NINDS sponsored the International Study of Unruptured
Intracranial Aneurysms, including more than 4000 patients at 61
sites in the United States, Canada, and Europe. Results revealed
that the risk of rupture for aneurysms less than 7 mm in size is low.
The findings provide a comprehensive evaluation of these vascular
defects, offering guidance to both patients and healthcare
professionals facing the difficult decision about the best treatment
for a cerebral aneurysm.
Advances in imaging, use of microscopes intraoperatively,
dedicated neurologic intensive care units, endovascular treatment
methods, and aggressive cerebral vasospasm prevention and
management have reduced morbidity and mortality. Treatment
options depend on assessment of preoperative risk factors,
predictive indicators, and location and size of the aneurysm.
Successful treatments include endovascular embolization
(“gluing”), surgical clipping, and endovascular detachable coiling.
Recent studies confirm improved patient outcomes when the

1450
ruptured aneurysm is secured within the first 24 to 72 hours for
patients with grade I or II symptoms (Hunt and Hess Scale). Early
intervention may prevent rebleeding, an often fatal complication,
and allows for the management of vasospasm without risk of
rebleeding. Securing of the aneurysm during the time period
associated with the highest risk of development of cerebral arterial
vasospasm has been shown to be associated with increased
morbidity and mortality. If the aneurysm is not secured within 24
to 72 hours of rupture, repair should be delayed until the peak time
for vasospasm (7 to 10 days after SAH) has passed. Patients with
grades III to V symptoms are generally considered poor
interventional risks, especially in the period immediately after
SAH. If these patients are clinically unstable, they may be treated
medically until they improve or stabilize enough for endovascular
or surgical intervention. Surgery is considered for a patient with a
large intracranial clot causing life-threatening, intracranial brain
shifting. Intervention is delayed for a patient with cerebral
vasospasm until the vasospasm subsides.
Although surgical clipping of aneurysms had previously been the
only method of intervention available, neurovascular
interventionalists can now use an alternative to surgery using
Guglielmi detachable coils (GDC coils). The overall size and
location of the aneurysm and the aneurysmal neck size are
evaluated to decide if this option is feasible. GDC coils are
microcoils composed of a soft platinum alloy that are placed with
use of a microcatheter through the femoral artery. The catheter is
advanced into the cerebral circulation using radiographic imaging.
Low-voltage current is applied to the guide wire to detach the
coil(s) placed into the sac of the aneurysm. Placement of one or
more coils fills the sac, reduces the pressure inside, and isolates the
aneurysm from normal circulation. When this is performed for the
management of unruptured aneurysm, the patient’s hospital stay is
very brief (24 to 48 hours) unless the aneurysm ruptures or another
complication of angiography occurs. Endovascular treatment
complications differ from those associated with surgical clipping
and can include arterial dissection, arterial perforation, distal
embolization, and groin hematomas. Aneurysmal recurrence has
been seen in a small number of cases. However, endovascular

1451
methods have become an acceptable alternative to microsurgical
clipping in appropriate cases.
Neurovascular interventionalists can also perform cerebral
angioplasty for arterial vasospasm to decrease vascular narrowing
and reverse ischemia in patients with new-onset vasospasm within
6 to 12 hours of onset. Patient selection for this is limited to those
whose vasospasm involves accessible major cerebral vessels; distal
cerebral arterial vasospasm is not amenable to angioplasty.

3. Management of hydrocephalus

• External ventricular drainage: Hydrocephalus develops in 20% to

25% of patients with SAH from a ruptured cerebral aneurysm.
Patients with symptomatic hydrocephalus generally require
placement of an external ventricular drainage system for
management of their hydrocephalus. For those with massive
hydrocephalus, coma and Hunt and Hess classification of III or
IV, placement of an external ventriculostomy drain can
decompress the ventricles enough to produce significant
improvements in the patient’s neurologic function and make the
patient a candidate for intervention to secure the ruptured
aneurysm.

• Ventricular shunt: Most patients do not develop chronic

hydrocephalus following SAH. For those who do develop a
chronic problem, the percentage of those who initially require
extraventricular drainage who progress to needing a shunt is not
clearly reflected in the literature. When a shunt is necessary, one
end of a small catheter is positioned into a ventricle, with the
other end draining into a body cavity or space (e.g., SAS, cistern,
peritoneum, vena cava, pleura). Major complications include
infection and malfunction. If the shunt has a valve for the
purpose of controlling drainage or preventing reflux of CSF, the
surgeon may request that the valve be pumped periodically to
ensure proper functioning. For nursing interventions after shunt
placement, see Box 7-2.

Box 7-2

1452
NURSING INTERVENTIONS AFTER
SHUNT PLACEMENT
• After the shunting, assess the patient for indicators of increased
ICP (see Box 7-1) caused by either the disease itself or shunt
malfunction.

• Position the patient on side opposite the insertion site, either flat
or with head elevated slightly (as prescribed) to prevent pressure
on shunt mechanism.

• Assess vital signs; LOC (orientation to time, place, and person);

papillary light reflex; and motor function.

• Monitor I&O, and limit fluids as prescribed.

• Avoid severe head and neck rotation, flexion, or hyperextension

to prevent kinking, compression, or twisting of the shunt
catheter, which would impede CSF flow.

• If the shunt has a valve for controlling drainage or preventing

reflux of CSF, pump the valve to ensure proper functioning,
according to the surgeon’s directive. Usually the valve is located
behind or above the ear and is the approximate diameter of a
fingertip. Pumping involves gentle, serial compressions of the
tissue over the shunt. If the valve is working properly, the
emptying and refilling of the valve will be felt with palpation.

• Assess for indicators of meningitis including peritonitis and

sepsis, caused by presence of shunt mechanism. (See Peritonitis,
Chapter 9, and Systematic Inflammatory Response Syndrome,
Sepsis, Septic Shock, and Multiple Organ Dysfunction Syndrome,
Chapter 11.)

CSF, Cerebrospinal fluid; ICP, intracranial pressure; I&O, intake

and output; LOC, level of consciousness.

1453
Care plans for cerebral aneurysm and
subarachnoid hemorrhage
Risk for ineffective cerebral tissue perfusion 
related to vasospasm of cerebral vessels and/or decreased intracranial
adaptive capacity related to increased ICP.
Goals/Outcomes: Maintain normal ICP and/or minimize clinical
effects on cerebral adaptability through preventive measures,
aggressive volume management, regulation of cerebral blood flow,
and close hemodynamic monitoring.
Circulation Status.

Cerebral perfusion promotion

1. Bed rest, with aneurysm precautions and prevention of ICP.

2. Subarachnoid precautions are instituted while the patient is

awaiting definitive management of a ruptured cerebral aneurysm.
Try to keep the patient quiet and calm in a soothing environment,
with lowered lights and noise level.

3. Active ROM and isometric exercises are restricted during acute

and preoperative stages to prevent increased ICP.

4. Passive ROM is prescribed to prevent formation of thrombi, with

subsequent pulmonary emboli.

5. Bowel management program is essential to prevent straining at

stool. Instruct the patient to avoid activities using isometric muscle
contractions (e.g., pulling or pushing side rails, pushing against the
foot board), which raise SBP, with resultant increased ICP.

Instruct the patient to avoid coughing because increased

intrathoracic pressure increases ICP.

Intracranial pressure monitoring

1. Increased ICP is common after SAH, but its manifestations range

from minimal (e.g., persistent headache or drowsiness) to severe

1454
(e.g., coma or death). Elevated ICP that does not respond to
treatment has been associated with poor patient outcomes.

2. Cerebral perfusion pressure: In patients who require invasive

devices to manage their ICP, the critical care nurse strives to
maintain normal ICP (0 to 10 mm Hg with an upper limit of 15 mm
Hg) and CPP of 60 to 80 mm Hg. Calculate CPP by the formula:
CPP − MAP (mean arterial BP) = ICP. CPP of less than 30 mm Hg
causes cerebral anoxia.

3. Head-of-the-bed elevation: A 30- to 45-degree angle facilitates

venous outflow from the intracranial cavity and lowers ICP. The
head should be kept in straight alignment to prevent increased ICP
secondary to obstruction of jugular venous outflow. Values of 180
to 220 mm Hg as prescribed end points of management of SBP.

Impaired gas exchange or ineffective airway clearance 

related to altered LOC
Goals/Outcomes: Effective airway clearance and gas exchange
and maintain appropriate Paco2 level, which can affect ICP.
Respiratory Status: Gas Exchange.

Ventilation assistance

1. Supplemental oxygen, maintenance of patent airway, possible

intubation, and ventilation if needed. Serial ABG tests are
performed to identify hypoxemia (PaO2 less than 80 mm Hg) and
hypercapnia (Paco2 greater than 45 mm Hg). Carbon dioxide is a
potent cerebral vasodilator that can increase ICP in patients who
are already at risk. Note : Mechanical ventilation may be
implemented to manage potential hypoxemia and to control the
level of carbon dioxide effectively, without prompting hypocapnia.
Hypocapnia has been used in the management of acute brain injury
and is life-saving in some situations, but can produce neuronal
ischemia, injury, and potentially worsen the outcome. Use should
be limited exclusively to emergency management of life-threatening
intracranial hypertension while awaiting additional treatment
measures. Carbon dioxide level should be normalized as soon as

1455
possible when hyperventilation has been used. Improper use of
hypocapnia may result in more harm than benefit.

Oxygen therapy

1. Suctioning: Avoid vigorous, prolonged suctioning, which

precipitates hypoxemia and hypercapnia.

• Preoxygenation using 100% oxygen helps prevent

cerebral vasodilation associated with hypercapnia.
Adjusting the FIO2 to 1.0 (100% oxygen) on the
ventilator is preferred to bag-valve-tube manual
preoxygenation.

Risk for injury 

related to the potential impact of hyperglycemia
Goals/Outcomes: Glucose levels are controlled within
normalized measurements throughout all phases of treatment.
Risk Control.

Risk identification

1. Hyperglycemia: Studies have shown that admission

hyperglycemia or perioperative hyperglycemia is associated with
poor outcome after aneurysmal SAH. Daily glucose monitoring is
encouraged. More frequent monitoring and intervention are
required in patients with persistent hyperglycemia.

2. Further research is underway to determine the critical timing for

strict glucose control, effect on neurologic outcome, and how serum
glucose levels impact brain glucose concentrations.

Risk for imbalanced fluid volume  

related to initiation of measures to maintain hypervolemia
Goals/Outcomes: Adequately managed intake and output with

1456
control of fluid volumes affecting systemic and cerebral blood flow
and electrolyte levels.
Fluid Balance.

Fluid/electrolyte management

1. Fluid balance is maintained based on CVP, weight, and

monitoring of intake/output (I&O) balance.

2. Electrolytes should be replaced on the basis of the patient’s

laboratory values.

3. Hyponatremia is often seen in this patient population. Standard

fluid management can make it difficult to determine whether the
underlying cause is CSW or SIADH. Regardless of the underlying
cause, hyponatremia is treated with salt repletion because the fluid
restriction commonly used in other patient populations to manage
SIADH is contraindicated in patients with SAH who are still at high
risk for vasospasm and cerebral ischemia. In mild hyponatremia,
initial repletion is oral (e.g., salt tablets with meals). If
hyponatremia does not respond to oral replacement, IV use of
hypertonic saline (1.8% or 3%) is initiated. Hyponatremia requires
frequent monitoring of laboratory values to assess effectiveness of
therapy. Once the patient’s sodium normalizes, therapy is slowly
tapered to assess the patient’s ability to maintain a normal serum
sodium level.

4. Triple H therapy may lead to fluid volume overload and

must be closely monitored. Multiple electrolyte abnormalities are
often seen with triple H therapy, and serum magnesium and
phosphorus levels should be monitored regularly along with
standard blood chemistries.

5. Maintain adequate nutrition intake using enteral feedings, oral

intake, parenteral nutrition, or lipid emulsions as indicated by the
patient’s neurologic status. Initially patients may have severe
nausea and vomiting following aneurysmal rupture, but this
generally resolves in the first 24 hours.

1457
Additional nursing diagnoses
As appropriate, see nursing diagnoses and interventions in
Nutrition Support (Chapter 1), Mechanical Ventilation (Chapter 1),
Alterations in Consciousness (Chapter 1), Prolonged Immobility
(Chapter 1), Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2), Diabetes Insipidus (Chapter 8), and
Syndrome of Inappropriate Antidiuretic Hormone (Chapter 8).

Care of the patient after intracranial

surgery
Cranial surgery can be performed to remove a space-occupying
lesion such as a tumor, to evacuate a hematoma or abscess, or
remove a foreign object. A patient may have a surgical repair of a
vascular abnormality, such as an aneurysm or arteriovenous
malformation (AVM), or to correct skull fractures. The
neurosurgeon may elect to perform a procedure as a treatment
modality, such as to drain CSF from the ventricular system or to
divert CSF to promote dural repair, control seizures or tremors, and
reduce pain. Minimally invasive intracranial procedures using
stereotactic techniques are used for some biopsies and for
implantation of deep brain stimulators for control of essential
tremors. Endoscopic and stereotactic aspiration is being performed
for noncomatose patients with basal ganglia hemorrhages. The type
of surgical approach the neurosurgeon takes depends primarily on
the location of the pathologic condition. The supratentorial
approach is used to remove or correct problems in the frontal,
temporal, or occipital lobes, as well as in the diencephalic area (i.e.,
pituitary, hypothalamus). Lesions of the cerebellum and brainstem
usually require an infratentorial (i.e., suboccipital) approach. The
transsphenoidal approach gains access to the pituitary gland to
remove a tumor, control bone pain associated with metastatic
cancer, or attempt to arrest the progression of diabetic retinopathy
in a patient with diabetes mellitus.

Neurologic assessment: Postoperative care

1458
Goal of system assessment
Evaluate for several key nursing diagnoses requiring emergent
intervention:

• Alteration in cerebral tissue perfusion caused by increased ICP or

cerebral vasospasm.

• Impaired gas exchange and/or ineffective airway clearance

resulting from altered LOC.

• Risk of infection at site or as a result of CSF leak.

• Fluid volume deficit or excess.

• Impaired mobility.

• Altered sensory perception involving trunk, extremities, or

cranial nerves.

• Alteration in cardiac output from dysrhythmias.

• Pain.

History and risk factors

The critical care nurse caring for a postoperative neurosurgical
patient must have a thorough understanding of the patient’s
preoperative history and condition requiring surgical intervention
and, most importantly, knowledge of the patient’s baseline or
immediate preoperative neurologic assessment findings. It is
essential to note any changes in assessment to evaluate for new
postoperative neurologic changes resulting from the surgical
intervention. Neurologic assessment data must be closely
monitored for new focal changes, noting a trend in assessment data
and correlated to the pathophysiologic process to identify
appropriate nursing interventions. Three key causes of acute
deterioration in a patient’s neurologic status in the immediate
postoperative period are cerebral edema, hemorrhage into or
around the surgical site, and new onset of seizure activity.

1459
Vital signs
• BP, HR, and RR changes: May further alter cerebral tissue
perfusion. Uncontrolled high BP can lead to intracranial
hemorrhage (ICH); therefore, close monitoring is important to
keep the SBP less than 160 to 200 mm Hg to prevent bleeding.
Hypotension reduces cerebral perfusion and may cause cerebral
ischemia. Monitor rate, rhythm, and depth of respirations for
changes or abnormal breathing patterns.

• Hyperthermia: May be associated with injury or irritation of the

hypothalamic temperature-regulating centers, presence of blood
in the cerebral spinal fluid (CSF), or infection. Elevated
temperature increases the metabolic needs of the brain,
potentially leading to increased blood flow to the area, with
concomitant cerebral hyperemia.

• Intracranial pressure: If intracranial pressure (ICP) monitoring is

used, the critical care nurse must understand the dynamics of
cerebral perfusion pressure (CPP). A postoperative increase in
the volume of brain tissue (e.g., edema), CSF, or blood or the
addition of a hematoma can cause intracranial hypertension. The
normal ICP is generally 0 to 10 mm Hg (up to 15 mm Hg). CPP is
inversely related to ICP and in pressures less than 50 to 60 mm
Hg can lead to cerebral ischemia or infarction: CPP = MAP − ICP.

Observation
• Level of consciousness: The improvement in the degree of LOC
depends on preoperative damage to cerebral tissue.
Consciousness often improves while anesthesia wears off, or
while cerebral edema subsides, and while ICP approaches
normal.

• Pupillary changes: Pupillary abnormalities can indicate unilateral

or bilateral brain dysfunction, interruption of sympathetic or
parasympathetic pathways, damage in the brainstem, cranial
nerve damage, and herniation.

1460
• Communicative and cognitive deficits: The ability to
communicate and understand spoken or written words after
surgery depends on the level of preoperative dysfunction, the site
of the lesion, extent of the procedure, and the degree of
postoperative cerebral edema.

• Broca (expressive, motor, nonfluent) aphasia: Inability to

communicate verbally or in writing. Can understand situations,
follow commands.

• Wernicke (receptive, sensory, fluent) aphasia: The patient does

not understand the situation and cannot follow commands
appropriately.

• Cerebrospinal fluid (CSF) leakage: Assess for CSF leakage from

the ear (otorrhea), from the nose (rhinorrhea), which is seen
particularly with transsphenoidal surgery, and also from the
surgical site. The leakage of CSF indicates an open pathway to
the subarachnoid space (SAS), which carries a serious risk of
infection. Causes specific to craniotomy include the use of an
external ventricular drainage device (used as a treatment
modality), which can be a source of entrance of organisms, a
remote site infection, and if additional surgery is required.
Treatment of a CSF leak depends upon severity, site, and the risk
for infection. It may include the use of an external drainage
system (e.g., lumbar subarachnoid drain) to divert CSF flow and
thus reduce pressure. Keeping the patient flat (if not
contraindicated) will allow time for the dural tear to heal.
Surgical intervention may be done to seal the dural leak at the
site of origin.

Observation and functional assessment

1. Assess motor function and sensory responses

Improvement in both motor and sensory perception may occur
while cerebral edema subsides.

• Motor: Motor deficits (weakness or paralysis) are caused by

injury or edema to the primary motor cortex and corticospinal

1461
 (pyramidal) tracts.

• Sensory: Sensory deficits occur when the primary sensory cortex,

the sensory association areas of the parietal lobe, or the
spinothalamic tracts are injured or edematous. Sensory deficits
include inability to distinguish objects according to characteristics
(e.g., size, shape, weight) and inability to distinguish overall
changes in temperature, touch, pressure, and position.

2. Assess for cranial nerve impairment

The degree of cranial nerve deficit(s) depends on site of the lesion,
preoperative deficit, degree of postoperative cerebral edema, and
surgical approach. Infratentorial surgery for lesions in the posterior
fossa (brainstem and cerebellum) involves significant cranial nerve
manipulation with high risk of injury to cranial nerves IX, X, and
XII, which innervate the pharynx and tongue. Risk of airway
obstruction is high. Removal of tumors (i.e., acoustic neuromas)
may injure the cranial nerve VII and result in facial paralysis and
loss of corneal reflex. The loss of corneal reflex may be caused by
surgical trauma to frontal lobe motor pathways or brainstem cranial
nerve nuclei. Corneal abrasion, ulceration, and blindness may occur
if not recognized and treated promptly. Always prevent corneal
abrasion and irritation. Keep cornea moist with prescribed
ophthalmic solution and use an eye shield if indicated.
Cranial nerve deficit(s) may improve while cerebral edema
resolves or may be permanent. Nursing assessment of cranial nerve
dysfunction is important. For more information about the function
of all the cranial nerves, see Appendix 3.

Screening labwork
• Sodium levels and osmolality: Important for management of
SIADH and diabetes insipidus (DI). Close monitoring during
hyperosmolar therapy is important. Hypernatremia may indicate
dehydration if associated with DI. Hyponatremia may be
associated with SIADH. If sodium level is not managed
appropriately, cerebral edema may result.

1462
• Cerebrospinal fluid (CSF) analysis: Evaluates the color, white
blood cell (WBC) count, differential, glucose content, and protein
level, which are important whenever a CSF leak develops.

• Complete blood count (CBC), electrolytes, and coagulation

studies: Evaluates for anemia, hypoglycemia or hyperglycemia;
hyponatremia or hypernatremia; potential for hemorrhage or
infection.

• Anticonvulsant medication levels: If the patient is receiving

anticonvulsant therapy, monitor for subtherapeutic and
supratherapeutic levels.

Diagnostic testing
Refer to Neurologic Diagnostic Testing, Chapter 5.

Collaborative management after intracranial

surgery
Care priorities

1. Respiratory support
Supplemental oxygen, intubation, and mechanical ventilation as
needed. In patients requiring mechanical ventilation who have
potential or actual increased ICP, use of hyperventilation needs
careful monitoring to avoid cerebral vasoconstriction. The Brain
Trauma Foundation standard emphasizes that in the absence of
increased ICP, prophylactic hyperventilation (Paco2 less than 25 mm
Hg) is not recommended. Paco2 is maintained within normal limits
unless acute elevation in ICP is present with the possibility of
imminent cerebral herniation. A brief period of hyperventilation
may be instituted in the setting of imminent herniation. Use of
prophylactic hyperventilation (Paco2 less than 35 mm Hg) should be
avoided during the first 24 hours or used only if increased ICP does
not respond to other measures such as CSF drainage, sedation, or
use of neuromuscular blocking agents.

1463
2. Positioning
The HOB is most often elevated 30 degrees to promote venous
drainage, which reduces ICP. The head should be kept in straight
alignment with the trunk to prevent increased ICP and to facilitate
venous return.

• In posterior fossa surgery (infratentorial approach), the

supporting muscles of the neck are altered. Patients should be
turned with the neck in alignment with the head and with the
head, neck, and shoulders supported.

• After hemicraniectomy, to avoid injury, patients may not be

turned to the side from which hemicraniectomy has been
removed unless appropriate support is provided to keep the head
and neck aligned with the shoulders to keep the weight of the
head from directly laying on the flap. Label head dressing, chart,
and bed with location of missing bone. A head protective device
such as a specially sized helmet should be worn.

• After procedures in which a large intracranial space is left after

extensive surgery, to avoid a sudden shift in intracranial
contents, with subsequent hemorrhage or herniation, the patient
should not be positioned on operative side immediately after
surgery.

3. Manage pain

• Analgesics: Clinical trials have shown that the addition of

tramadol or nalbuphine to acetaminophen controls pain more
adequately in patients who have undergone craniotomy. Patients
may also require opiate medications including fentanyl,
morphine, hydromorphone, and remifentanil for pain relief.

Note: The effect of morphine and tramadol patient-controlled

analgesia (PCA) on arterial carbon dioxide tension is still unknown
for patients who have undergone craniotomy.

4. Reduce cerebral edema:

1464
• Corticosteroids (e.g., dexamethasone): To decrease cerebral
edema.

Note: Not indicated for patients with traumatic brain injury (TBI).
Research is ongoing to determine whether steroids are effective in
the treatment of cerebral edema. They are prescribed for the
treatment of vasogenic cerebral edema and edema caused by
cerebral tumor.

Steroids can cause a hyperosmolar state and dehydration.

Monitor serum osmolality and electrolytes and assess fluid status
before and after administration.

• Osmotic diuretics (e.g., mannitol): To control cerebral edema

causing increased ICP. Dose is usually 0.25 to 1 g/kg of 20%
solution administered over 20 to 30 minutes, and ICP levels
should be measured before, during, and after administration of
mannitol. When the ICP reaches a desired fixed reduced level
(usually within 15 minutes), the dose of mannitol needs to be
gradually reduced.

• Fluid and electrolyte management: Hypertonic saline may be

used to prevent or treat increasing cerebral edema. Serum
sodium levels should be maintained at less than 155 mEq/L.
Patients with serum sodium levels greater than 160 mEq/L are at
higher risk for treatment-related renal failure, pulmonary edema,
and heart failure. If serum sodium levels are elevated greater
than 160 mEq/L for more than 48 hours, the risk for
complications, including seizures, increases.

5. Perioperative and postoperative deep venous thrombosis

(DVT) prevention

1465
 A systematic review of literature done for the Agency for
Healthcare Research and Quality (AHRQ) showed that the risk of
neurosurgical patients for deep venous thrombosis (DVT) is 28%.
The 5 Million Lives Campaign, National Hospital Quality
Measure of The Joint Commission, National Hospital Quality
Measure by the Centers for Medicare and Medicaid Services, and
the National Quality Forum all endorse aspects of DVT
prophylaxis. Craniotomy patients without contraindications for
anticoagulation should receive DVT prophylaxis using either a
low–molecular-weight heparin or low-dose unfractionated heparin
given as an alternative. Pharmacologic agents can be used as an
adjunct to mechanical prophylaxis using intermittent pneumatic
compression, elastic stockings, or both. Venous imaging techniques
such as ultrasonography can be used before discharge to detect
thrombosis.

6. Control seizures
Antiepileptic agents: Phenytoin, fosphenytoin, and levetiracetam
should be considered for prophylaxis of provoked or early seizures
occurring within 7 days of surgery. Use of other agents such as
carbamazepine, phenobarbital, and valproate remains controversial
and in some studies has not shown to reduce postoperative
seizures.

7. Prevent infection
Antibiotics: Prevent postoperative surgical site infection or
respiratory or urinary tract infection. Randomized controlled trials
have shown that in patients undergoing craniotomy, the use of
prophylactic antibiotics reduces the frequency of postoperative
meningitis.
The American Society of Health System Pharmacists and the
Centers for Disease Control and Prevention have recommended
that antibiotic administration be via the intravenous route at
induction of anesthesia and/or that the bactericidal concentration of
the drug be established in the tissues and serum when the incision

1466
is made.

8. Nutrition support
The method and type of nutrition support are determined by the
patient’s condition and may include any of the following: oral
feedings, enteral feedings, supplements, or parenteral nutrition (i.e.,
total parenteral nutrition, fat emulsion therapy). See Nutrition
Support (p. 117).

9. Reduce fever
Antipyretics: Treat elevated temperature, which can increase use of
oxygen and glucose supplies.

10. Prevent gastric ulcers

Histamine H2-receptor antagonists/proton pump inhibitors: To
inhibit gastric secretions and thus prevent or facilitate healing of
gastric ulcers and prevent bleeding.

11. Facilitate mobility and return of functions needed for

activities of daily living
Physical medicine consultation: To evaluate the patient and plan for
rehabilitation: physical and occupational therapies for planning
return of function.
Speech therapy may be important for dysphagia screening,
monitoring for meeting communication needs.

12. Implement therapeutic hypothermia

The effects of cooling of the injured brain continues to be studied to
evaluate the effects of mild to moderate hypothermia on protection
against ischemic and nonischemic brain hypoxia, traumatic brain
injury, and anoxic injury with cardiac arrest. Prophylactically
induced hypothermia has yet to be shown as having beneficial
effects on outcomes of traumatic brain injury.

Care plans: Complications after intracranial

1467
surgery
Decreased intracranial adaptive capacity 
related to possible changes in intracranial fluid or brain tissue volume
following surgery.
Goals/Outcomes: Maintain normal ICP (0 to 10 mm Hg with
upper limit of 15 mm Hg) through regulation of cerebral flow and
cerebral spinal circulation.
Neurologic Status: Consciousness.

Cerebral perfusion promotion

1. Monitor for increased ICP with potential for herniation: Cerebral

edema, hemorrhage, infection, and surgical trauma can all lead to
increased ICP with herniation (see Box 7-1). Some cerebral edema is
expected after intracranial surgery, and usually peaks
approximately 72 hours after surgery (see Traumatic Brain Injury,
Chapter 3). Postoperative uncontrolled nausea and vomiting can
cause high intraabdominal and also increased intrathoracic
pressure (e.g., high positive-end expiratory pressure [PEEP]
ventilator settings) leading to high ICP.

2. Monitor for intracranial bleeding: Postoperative bleeding can be

related to the surgical site and may be intracerebral, intracerebellar,
subarachnoid, subdural, epidural, or intraventricular. Coagulation
profiles and platelet counts should be monitored closely. Bleeding
may be caused by the lengthy and extensive surgical procedure,
high BP, prolonged anesthesia, preexisting medical problems, or
medications. Contusions can develop after evacuation of epidural
or subdural hematomas and may create a mass effect.

3. Control seizures: Generalized or partial seizures can occur as a

result of surgical trauma, irritation of cerebral tissue by the
presence of blood, cerebral edema, cerebral hypoxia, hypoglycemia,
preexisting seizure disorder, or inadequate anticonvulsant levels.
The use of anticonvulsants prophylactically remains controversial.

4. Monitor for hydrocephalus: May appear before surgery or occur

after surgery as an acute or chronic complication. Usually it is

1468
caused by a slowing or complete stoppage of the flow of CSF
through the ventricular system secondary to edema, bleeding,
scarring, or obstruction. For further discussion, see Cerebral
Aneurysm and Subarachnoid Hemorrhage (p. 629).

5. Assess for tension pneumocephalus: Uncommon but can occur as

a result of air entering the subdural, extradural, subarachnoid,
intracerebral, or intraventricular spaces and is an emergent
situation. May be a complication of infratentorial/posterior fossa
craniotomy, burr holes for removal of chronic subdural hematoma,
and transsphenoidal hypophysectomy. Rapid decompression is
usually required.

Ineffective breathing pattern 

related to altered level of consciousness (LOC) and inability to maintain
adequate airway and respiratory rate (RR)
Goals/Outcomes: Maintain adequate airway, provide
supplemental oxygenation, ventilate the lungs as necessary to
maintain Paco2 to 35 mm Hg. Increase in Paco2, hypercapnia, can
lead to cerebral vasodilation with a subsequent increase in
intracranial volume, and thus increased ICP. A severe drop in Paco2
can lead to cerebral vasoconstriction and cerebral ischemia.
Respiratory Status: Gas Exchange.

Ventilation assistance

1. Monitor for partial or complete airway obstruction caused by

accumulation of secretions, improper positioning, or change in
LOC.

2. Assess for increased crackles caused by neurogenic pulmonary

edema resulting from a sudden increase in ICP.

3. Assess for changes in LOC caused by cerebral edema that causes

compression of brainstem respiratory centers.

4. Discourage vigorous coughing, because it increases ICP.

5. Encourage deep breathing to help prevent atelectasis and

1469
pneumonia.

6. Follow institutional protocol for venous thromboembolism

(VTE)/DVT prophylaxis to help prevent pulmonary embolism.

Risk for infection 

related to presence of invasive devices within the cranium.
Goals/Outcomes: Prevent infection at site or secondary
infections, such as meningitis, encephalitis, or ventriculitis, or as a
result of invasive procedures.
Risk Control.

Infection control

1. Monitor for a central nervous system (CNS) infection: Can be

caused by a preoperative event such as organisms introduced at the
time of injury (e.g., gunshot wound) or a break in sterile technique
or as a result of the nature of the surgical procedure involving
opening of the dura. (See Meningitis, Chapter 7.)

2. Monitor for a ventriculostomy-related infection: A

ventriculostomy may be performed with the introduction of an
intraventricular catheter to monitor and manage postoperative ICP
or to provide external ventricular drainage for CSF diversion
secondary to dural leaks. Extended duration of catheterization has
been correlated with increasing risk of CSF infections. Antibiotic
coated intraventricular catheters are also available for use.

Deficient fluid volume or excess fluid volume 

related to hormonal or electrolyte imbalances
Goals/Outcomes: Adequately managed I&O, control of fluid
imbalances resulting from hormonal or electrolyte disturbances,
and prevention of fluid loss.
Fluid Balance.

Fluid management

1. Monitor for sodium imbalance secondary to diabetes insipidus

and SIADH: Results from disturbance of the hypothalamus or

1470
posterior lobe of the pituitary gland. ADH is produced in the
hypothalamus and stored in the posterior pituitary.

• Diabetes insipidus results from decreased ADH

production, which leads to excessive urinary
output, with potentially serious fluid and
electrolyte problems (see Diabetes Insipidus,
Chapter 8). Diabetes insipidus may result from
cerebral edema, gland manipulation, or partial or
total removal of the gland.

• SIADH, a less common problem, results from an

increase in the release of ADH, which leads to
resorption of large amounts of water via the renal
tubules with concurrent loss of large amounts of
sodium. Similar to diabetes insipidus, SIADH can
cause serious fluid and electrolyte problems (see
Syndrome of Inappropriate Antidiuretic Hormone,
Chapter 8).
2. Assess for hypovolemic shock: May occur as a result of general
fluid loss associated with treatment using osmotic diuretics;
therefore, close monitoring is essential. Close observation for the
development of diabetes insipidus postoperatively is required
because severe dehydration and hypovolemic shock may occur.

3. Monitor for gastrointestinal bleeding: GI bleeding associated with

cerebral trauma and the postoperative period after neurosurgery
can cause fluid volume deficit. Although the cause is unclear, stress
from the trauma or the surgery can produce continuous vagal
stimulation leading to a hyperacidic state resulting in gastric
erosion, ulceration, and ultimately hemorrhage. These conditions
also result from medications, especially corticosteroids (see Acute
Gastrointestinal Bleeding, Chapter 9). Other GI conditions may

1471
occur, such as constipation, after neurologic surgery. Decreased or
absent peristalsis results from prolonged anesthesia, immobility,
trauma, electrolyte deficiencies, and mechanical bowel obstruction
(e.g., obstipation).

Impaired physical mobility 

related to prolonged bed rest or motor dysfunction
Goals/Outcomes: Prevent vascular complications through
appropriate pharmacotherapy and mechanical prophylaxis, and
prevent atrophy and/or joint contractures through passive
exercises, early mobilization, and activity progression.
Mobility.

Exercise promotion

1. Thrombophlebitis, DVT, and pulmonary embolism: May result

from prolonged bed rest and immobility after intracranial surgery.
Other factors such as a prolonged surgical procedure, preexisting
hypercoagulable states, and other blood dyscrasias may influence
the postoperative complications. VTE is the most frequent
complication following craniotomy for removal of brain tumors.
Prophylactic management standards have been developed for the
prevention of DVT.

Decreased cardiac output 

related to unstable BP or cardiac dysrhythmias
Goals/Outcomes: Stabilize BP and HR within normal limits to
maintain adequate cardiac output, thereby promoting appropriate
cerebral blood flow.
Circulation Status.

Cardiac precautions

1. Monitor for cardiac dysrhythmias: May occur as a result of

cerebral hypoxia or ischemia, manipulation of the brainstem, or the
irritating effects of blood in the CSF (see Dysrhythmias and
Conduction Disturbances, Chapter 5).

Pain 

1472
related to headache or discomfort secondary to surgical intervention
Goals/Outcomes: Pain and discomfort are controlled based on
the patient’s self-reported pain score (if verbal) or appropriate
nonverbal pain scale, stable vital signs, and lack of skeletal muscle
tension and behavioral signs. Pain and autonomic system
stimulation and physical agitation can increase ICP, produce sleep
deprivation, and mask neurologic changes and thereby lead to
further complications.
Pain Control.

Pain management

1. Medicate and intervene appropriately to keep the patient’s pain

controlled and maintain comfort level. Use of an evidence-based
pain scale measurement such as a numerical rating scale (1 to 10) or
a behavioral pain scale may be appropriate for patients with
impaired communication ability.

2. Assess level of sedation appropriately. Overmedication with

analgesics or sedatives in postoperative patients with altered LOC
can produce impaired gas exchange and compromised airway.

Additional nursing diagnoses

See also nursing diagnoses and interventions in Traumatic Brain
Injury (Chapter 3), Sedation and Neuromuscular Blockade (Chapter
1), Cerebral Aneurysm and Subarachnoid Hemorrhage (Chapter 7),
Status Epilepticus Chapter 7, Meningitis (Chapter 7), Diabetes
Insipidus (Chapter 8), Syndrome of Inappropriate Antidiuretic
Hormone (Chapter 8), Nutrition Support (Chapter 1), Prolonged
Immobility (Chapter 1), and Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2).

Meningitis
Pathophysiology
Meningitis is an inflammation of the brain and spinal cord, the

1473
CNS, affecting the meninges (i.e., dura, arachnoid, pia), brain
surface, and cranial nerves. Meningeal infection comes about
through environmental exposure or as a result of direct
contamination through invasive procedures or surgeries.
Meningitis is a reportable disease in all states. There are several
types of meningitis, broadly classified as bacterial (pyogenic), viral,
aseptic, tuberculous, fungal, and eosinophilic (parasitic). The
causative agent travels in the bloodstream from various sources
before entering the cerebral spinal fluid (CSF. The CSF is unable to
mount an antimicrobial response because it lacks immunoglobulins
and complement. Therefore, when contamination of the CSF takes
place, phagocytosis and opsonization of the microbes do not occur.
Bacterial meningitis, a consequence of bacterial invasion, progresses
through four interconnected phases: (1) invasion of host leading to
central nervous system (CNS) infection, (2) inflammation of the
subarachnoid and ventricular space while bacteria multiply, (3)
pathophysiologic changes consistent with progression of
inflammation, and (4) neuronal damage.

Bacterial meningitis
The most common type of meningitis is bacteria, which can be
community-acquired or hospital-acquired. Transmission of
bacterial meningitis can occur through environmental exposure or
because of an invasive procedure (placement of external ventricular
device or craniotomy), injury (e.g., open/penetrating wounds),
facial or basilar skull fractures, shunt occlusion/malfunction, otitis
media, sinusitis, or bacteremia (e.g., endocarditis, pneumonia).
Bacterial types usually appear within 3 to 7 days after exposure.
The most common agents associated with bacterial meningitis are
discussed as follows.
Streptococcus pneumoniae, a gram-positive cocci, has been the
leading cause of adult meningitis in the United States.
Pneumococcal meningitis occurs in crowded conditions and is
spread seasonally (fall and winter). S. pneumoniae is not as prevalent
a cause of meningitis since the development of Pneumovax and
Prevnar vaccines. Pneumococcal meningitis may occur following an
upper respiratory tract infection or nasopharyngeal colonization
with a pneumococcal strain, is a complication of conditions

1474
associated with CSF leaks, is associated with asplenia, and is more
prevalent in immunocompromised persons and in older adults.
Neisseria meningitidis, a gram-negative cocci, is the second
leading cause of meningitis in the United States. N. meningitidis is
endemic in the United States, can cause community epidemics, and
has resulted in death in previously healthy young adults. Infection
is more likely to occur in young children, persons with immune
deficiencies (human immunodeficiency virus [HIV]), or
complement component deficiencies (e.g., congenital, associated
with nephrotic syndrome, hepatic failure, systemic lupus
erythematosus, or multiple myeloma). Other risk factors include
nasopharyngeal carrier states and high-risk sexual behaviors.
Vaccinations have reduced the number of cases since 2005.
Haemophilus influenzae, a gram-negative bacilli, had been the most
common cause of meningitis in children before 1990. Since 1990, the
H. influenzae vaccine type B (Hib vaccine) has reduced the incidence
of bacterial meningitis substantially in infants and children, making
it a disease predominantly of adults. Before 1990, H. influenzae type
B serotype was the leading cause of bacterial meningitis in all age
groups. Other serotypes continue to affect children and adults.
Predisposing factors include upper respiratory tract infections,
diabetes mellitus, hypogammaglobulinemia, alcoholism, and head
trauma.
Listeria monocytogenes, a gram-positive bacilli, is being seen more
frequently as a cause of meningitis, especially in patients who are
immunocompromised and those of extreme ages (very young
and very old). Outbreaks have been linked to consumption of
contaminated dairy products, undercooked chicken, fish, and
meats.
Gram-negative species (Escherichia coli, Klebsiella pneumoniae,
Proteus mirabilis, and Pseudomonas aeruginosa) are increasing in
prevalence as a hospital-acquired cause secondary to trauma or
neurosurgical procedures. Spontaneous gram-negative
meningitis is found in older adults, the immunocompromised, or
persons with underlying conditions such as cirrhosis, diabetes
mellitus, malignancy, or splenectomy. The urinary tract is the usual
portal of entry of bacteria. Other surgical procedures complicated
by gram-negative infections are ventriculoperitoneal shunts,

1475
craniofacial repair, ventriculostomy, hypophysectomy, reservoir
insertion, and myelography.

Other microbes
Also associated with meningitis are Mycobacterium pneumoniae,
Borrelia burgdorferi, and Treponema pallidum.

Tuberculous meningitis
Mycobacterium tuberculosis as a CNS disease and manifested as
meningitis is documented in children and adults where
tuberculosis has a regional prevalence. In more developed regions,
M. tuberculosis meningitis is related more to reactivation of the
disease. Other risk factors for development of M. tuberculosis are
older age, alcoholism, malnutrition, and immunocompromised
states including HIV and patients with malignancies. Older adults
and children living among people with tuberculosis have increased
risk.

Fungal meningitis
Cryptococcus neoformans, an opportunistic organism seen with
acquired immune deficiency syndrome (AIDS), is the leading cause
of CNS fungal infection. Other fungi-associated meningitis include
Candida albicans, and histoplasmosis meningitis is also seen in
immunocompromised patients and evolving from progressive
disseminated histoplasmosis.

Viral meningitis
Enteroviruses are the most common cause of viral meningitis that
occurs in the spring and fall seasons. The condition generally lasts 7
to 10 days and, although serious, is rarely fatal in people with
normal immune systems. Herpes viruses, including herpes simplex
viruses (the cause of chickenpox, Epstein-Barr virus, and shingles),
measles, and influenza may lead to viral meningitis. Mosquitoes
and other insects spread arboviruses, which cause infections that
lead to viral meningitis.

Eosinophilic meningitis

1476
Infestation by Angiostrongylus cantonensis, a parasitic nematode,
results in severe gastrointestinal (GI) or CNS disease in humans,
depending on the species. A. cantonensis, also known as the rat
lungworm, causes eosinophilic meningitis. Prevalent in Southeast
Asia and Tropical Pacific Islands, the nematode resides in rodents
and transmission is through larvae found in rat feces. Slugs or
mollusks ingest the larvae. Humans are incidental hosts as a result
of eating infected slugs, raw vegetables, or vegetable juices
contaminated with the slugs or their slime.

Aseptic meningitis syndrome

In aseptic meningitis, the clinical and laboratory evaluations
provide evidence for inflammation, but bacterial culture results are
negative. It may be drug-induced, related to infection, or unrelated
to infection. Aseptic meningitis has been linked to adverse drug
reactions with nonsteroidal antiinflammatory drugs, antimicrobials
such as trimethoprim-sulfamethoxazole, antiepileptics, and
immunoglobulin. The syndrome is also associated with oncologic
diagnoses (hematologic malignancies, lymphomas, leukemias,
breast, lung, melanomas, and GI), systemic lupus erythematosus,
and brain surgery or brain trauma.

Noninfectious causes
Sarcoidosis, leptomeningeal carcinomatosis, systemic lupus
erythematosus, Wegener granulomatosis, and Behçet disease.

Acute meningitis may manifest as a community-acquired

illness with a negative Gram stain. The pathogen causing the
disease may never be determined. Syphilis, bacteremia, and
Borrelia burgdorferi (Lyme disease) have been identified in
some cases. Variables affecting diagnosis of meningitis include
presentation in winter months, age older than 60 years, and
comorbid disease, especially immunodeficiency.

1477
Neurologic assessment: Meningitis
Goal of system assessment
A complete neurologic examination should be performed to
establish the patient’s baseline neurologic function. Examination of
associated systems (head, eye, ear, nose, and throat [HEENT] and
respiratory) provides additional data. When diagnosed one or more
signs of meningitis are positive (Table 7-2).

Table 7-2
POSITIVE MENINGEAL SIGNS

Test/Description Positive Findings

Stiff neck sign (nuchal rigidity): Raise the patient’s head by Pain and resistance to neck
flexing the neck and attempting to make the patient’s chin motion.
touch the sternum.
Brudzinski sign: Assess for nuchal rigidity. Flexion of the hips and knees
when the examiner flexes the
patient’s neck.
Kernig sign: Flex the patient’s leg at the knee and hip when Pain in the lower back and
the patient is supine, and then attempt to straighten the leg. resistance to straightening the
leg.

Bacterial meningitis presents with classic symptoms of fever,

altered mental status, headache, photophobia, nuchal rigidity, and
nausea and vomiting. Immediate diagnosis and isolation of the
organisms are paramount in this life-threatening disease. Delay in
obtaining the necessary information needed to diagnosis and treat
the underlying organism will increase morbidity and mortality.

History and risk factors

• Age

• Community setting

• College dormitories, military barracks

• Exposure to insects or rodents

1478
• Recent surgery or medical problems

• Cochlear implants, brain surgery, or traumatic brain

injury

• Antibiotic use

• Tuberculosis risk

• Work exposure (healthcare workers)

• Lifestyle

• Recent travel

• High-risk sexual activity

• IV drug use

• Immunocompromised

• Splenectomy

• HIV

• Hepatitis

• Chemotherapy

• History of present illness

• Time course for symptom development

• Recent infection (respiratory/ear)

1479
• Recent trauma to the head

• Exposure to meningitis

• Use of antibiotics

• Petechial or ecchymotic rash

• Ear or nose drainage

• Medical/social history

• Drug allergies

• Past medical history

• Recent surgical procedure

• Immunocompromising condition

• IV drug use

• HIV status or risk behavior

• Travel to endemic meningococcal area

• Critical History

• Exposure

• Drug allergies

1480
Vital signs
• BP, HR, and RR changes: May further alter cerebral tissue
perfusion. Monitor rate, rhythm, and depth of respirations for
changes or abnormal breathing patterns. Use of pulse oximetry
and electrocardiographic (ECG) monitoring is recommended.

• Hyperthermia: May be associated with injury or irritation of the

hypothalamic temperature-regulating centers, presence of blood
in the CSF, or infection. Elevated temperature increases the
metabolic needs of the brain, potentially leading to increased
blood flow to the area, with concomitant cerebral hyperemia and
ischemia.

Observation
A constellation of early symptoms is associated with most types of
meningitis and includes headache, fever, neck stiffness, and altered
mental status. At least one of these symptoms is found in most
types of meningitis. Other symptoms such as papilledema, seizures,
focal deficits (cranial nerve palsies), and coma may be seen early or
late in the development of meningitis. Meningitis is associated with
cerebral infarction and arthritis in some cases. The clinical features
of specific types of meningitis are described as follows. Common
meningeal signs demonstrated in meningitis are found in Table 7-2.

Level of consciousness
When assessing LOC it is important not to use subjective terms
such as “stupor or lethargy” but rather to assess and communicate
clearly the description of the patient’s spontaneous activity,
response to verbal stimuli and reaction to painful stimuli, and how
this differs from previous assessment. Assess for an acute change in
mental status or fluctuation in mental status; various scales can be
used that include LOC and other key indicators. Examples are the
Richmond Agitation and Sedation Score (RASS) and Glascow Coma
Scale (GCS).

Pupillary changes
Examine pupils for size (in mm), shape, symmetry, reactivity to

1481
light, constriction, consensual response, and accommodation.
Pupillary abnormalities can indicate unilateral or bilateral brain
dysfunction, interruption of sympathetic or parasympathetic
pathways, damage in the brainstem, cranial nerve damage, and
herniation.

Clinical presentation

• S. pneumoniae: The classic presentation of pneumococcal

meningitis is fever, headache, meningismus (meningeal
irritation), and altered mental status that progresses quickly to
coma. Nuchal rigidity and Kernig or Brudzinski sign are present.
Nausea, vomiting, profuse sweats, weakness, myalgia, seizures,
and cranial nerve palsies may also be present.

• N. meningitidis: Patients may quickly deteriorate, beginning with

fever and early macular erythematous rash that progresses
rapidly to petechial and purpuric states, conjunctival petechiae,
and aggressive behavior. Dysfunctions of cranial nerves VI, VII,
and VIII (see Appendix 4) and aphasia, ventriculitis, subdural
empyema, cerebral venous thrombosis, arthritis with positive
joint cultures, and disseminated intravascular coagulation may
occur. Age-phasic patterns are noted with increases in patients
younger than 1 year old, increasing in ages 18 to 24 years old, and
increasing again in those older than 65 years old .

• H. influenzae: The most distinguishing sign is early development

of deafness, which can occur within 24 to 36 hours after onset. A
morbilliform or petechial rash may be present.

• L. monocytogenes: Seizures may occur and rhombencephalitis may

be present. Rhombencephalitis seen early in the course of
infection is characterized by focal deficits such as ataxia, cranial
nerve palsies, and nystagmus. Conclusive diagnosis may require
serology testing.

• Gram-negative species: In older adults, fever may be absent

or low grade and headache may not be reported. Meningeal signs
may be subtle, but confusion, severe mental status changes, and

1482
 pneumonia are commonly reported. Nuchal rigidity in older
adults must be differentiated from degenerative changes of the
cervical spine.

• B. burgdorferi: The symptoms of meningitis may be preceded by

symptoms of Lyme disease, which occur in three stages. The first
stage is a “bull’s eye” rash within a few days of the tick bite
followed by headache, stiff neck, lethargy, irritability, and
changes in mental status, especially memory loss. Stage two,
weeks to months after the tick bite, causes persistent headache,
nausea, vomiting, malaise, irritability, cranial nerve deficits,
mental status changes, peripheral neuropathies, and myalgias. In
the last or third stage, arthritic types of symptoms and brain
parenchymal changes are apparent.

• A. cantonensis or Angiostrongylus costaricensis: Presence of these

parasites is difficult to detect because there is no specific blood
test or method to identify the larvae. Symptoms include severe
headache, stiff neck, paresthesias, and facial nerve palsy.
Symptoms of meningitis may be preceded by GI impairment. A
high blood or CSF eosinophil level indicates the presence of
parasites. History of ingesting raw vegetables, undercooked
snails, slugs or other transport hosts may provide clues to the
diagnoses.

• M. tuberculosis: A slow-onset process that causes neurologic

damage before treatment is sought. Three stages are identified:
(1) prodromal occurs over 2 to 3 weeks associated with general
malaise, headache, and low-grade fever; (2) meningitis phase
with common signs and symptoms; and (3) paralytic phase with
coma, seizures, and hemiparalysis. Common symptoms include
headache, lethargy, confusion, nuchal rigidity, cranial nerve
abnormalities, SIADH, weight loss, and night sweats. Kernig and
Brudzinski sign are present. The chest radiographic results may
be clear, and purified protein derivative may be nonreactive.
Maintain a high index of suspicion in tuberculosis-prevalent
regions, persons with history of tuberculosis (reactivation
infection in adults), and those with active tuberculosis in other
systems.

1483
• C. neoformans: Because the infection is subacute, fever and
headache may have a subtle pattern lasting for weeks while other
symptoms of meningitis occur, including positive meningeal
signs (Table 7-2), alterations in mental status (e.g., hyperactivity,
bizarre behavior, emotional labiality, poor judgment),
photophobia, focal cranial nerve deficits, nausea, vomiting, and
(rarely) seizures.

• C. albicans: Same clinical manifestations as bacterial meningitis. In

patients with neutropenia only fever may be present.

• Aseptic meningitis syndrome: Fever, headache, stiff neck, fatigue,

anorexia, and altered LOC are seen several hours after ingestion
of causative drug. Severity varies with amount of drug taken and
previous exposures. CSF glucose may be slightly elevated.

• Acute meningitis with negative Gram stain: Fever and neck

stiffness are the most frequent findings. The Gram stain for
bacteria is negative, but CSF WBC count is elevated. Symptoms
are similar to those for other types of meningitis.

• Other associated clinical signs: Asymmetrical facial weakness,

oropharyngeal thrush, cervical lymphadenopathy,
maculopapular rash, parotitis, and vesicular/ulcerated genitals
may be present with viral or bacterial causes of meningitis.

Functional assessment

1. Assess motor function and sensory responses

• Motor: Assess bilateral muscle strength, symmetry of movement,

and coordination. Assess for abnormal motor movements
unilaterally and bilaterally, such as decorticate posturing
(abnormal flexion), decerebrate posturing (abnormal extension),
or flaccidity. Motor deficits (weakness or paralysis) are caused by
injury or edema to the primary motor cortex in the precentral
gyrus and corticospinal (pyramidal) tracts.

• Babinski sign, Kernig sign, and Brudzinski sign: See

1484
 Chapter 7 General Neurologic Assessment.
• Sensory: Assess perception of touch, proprioception, pain,
temperature, and vibration (if possible). Superficial and deep
reflexes are tested on symmetrical sides of the body and
compared noting the strength of contraction. Sensory deficits
occur when the primary sensory cortex, the sensory association
areas of the parietal lobe, or the spinothalamic tracts are injured
or edematous. Sensory deficits include the inability to distinguish
objects according to characteristics (e.g., size, shape, weight) and
inability to distinguish overall changes in temperature, touch,
pressure, and position. Improvement in both motor and sensory
perception may be seen while cerebral edema subsides.

2. Assess for cranial nerve impairment

Cranial nerve deficit(s) may improve while cerebral edema resolves
or may be permanent. Nursing assessment of cranial nerve
dysfunction is important. For more information about the function
and testing of all the cranial nerves, see Appendix 3.

Screening labwork
• CSF analysis: Evaluates the color, WBC count, differential,
glucose content, and protein level.

• CBC including differential, electrolytes, blood cultures, and

coagulation studies: Evaluate for anemia, hypoglycemia, or
hyperglycemia; potential for hemorrhage or infection.

• Specimen analysis: Nasopharyngeal and rectal swaps, and stool

cultures to identify causative agents.

• Viral assays, cultures, and serology testing: Venereal Disease

Research Laboratory test (VDRL), HIV, lymphocytic
choriomeningitis virus, polymerase chain reaction, Lyme
serology, and other viral testing including mumps and measles.

Diagnostic tests

1485
 Bacterial meningitis presents with classic symptoms of fever,
altered mental status, headache, and nuchal rigidity. Immediate
diagnosis and isolation of the organisms are paramount in this life-
threatening disease. Delay in obtaining the necessary information
needed to diagnosis and treat the underlying organism will increase
morbidity and mortality.

Diagnostic Tests for Meningitis

Table 7-3
MENINGITIS: TYPICAL CEREBROSPINAL FLUID FINDINGS

Collaborative management
Care priorities

1. Control infection

• Antibiotic therapy: There are three major caveats to treating

bacterial meningitis. First, the bactericidal agent must be effective
against the organism; second, the agent must achieve a
bactericidal effect within the CSF, only IV antibiotics should be
used, except for rifampin that is useful as a synergistic agent; and
third, the drug has optimal pharmacodynamics.

• Rapid sterilization of CSF via appropriate pharmacologic therapy

1486
 (Table 7-4): Prophylaxis, using appropriate antimicrobials for
people exposed to N. meningitidis (rifampin or spiramycin) or H.
influenzae meningitis, is recommended.

Table 7-4
COMMON DRUG THERAPY FOR THE MANAGEMENT OF
MENINGITIS*

Causative Agent Characteristic Age/Therapy

Bacterial Meningitis
Streptococcus pneumoniae Gram- 2 to 50 years: Vancomycin with
positive cocci third-generation cephalosporin
(cefotaxime or ceftriaxone)
Older than 50 years: Vancomycin
with third-generation
cephalosporin (cefotaxime or
ceftriaxone) plus ampicillin
Consider rifampin if
dexamethasone is given
Haemophilus influenzae Gram- Cefotaxime or ceftriaxone, add
negative rifampin if pharyngeal colonization
bacilli
Neisseria meningitidis Gram- 2 to 50 years: Vancomycin with
negative cocci third-generation cephalosporin
(cefotaxime or ceftriaxone)
Older than 50 years: Vancomycin
with third-generation
cephalosporin (cefotaxime or
ceftriaxone) plus ampicillin
Consider rifampin if
dexamethasone is given
Listeria monocytogenes Gram- Vancomycin with third-generation
positive cephalosporin (cefotaxime or
bacilli ceftriaxone) plus ampicillin
or
Ampicillin or penicillin G
(Infectious Diseases Society of
America)
Mycobacterium tuberculosis Acid-fast Isoniazid, rifampin, ethambutol,
bacteria pyrazinamide
Borrelia burgdorferi Spirochete Ceftriaxone or penicillin G
Fungal
Cryptococcus neoformans Fungus Amphotericin B, flucytosine,
fluconazole, or itraconazole
Bacilli
Gram- Older than 50 years: Vancomycin
negative, with third-generation
aerobic cephalosporin plus ampicillin
Pseudomonas aeruginosa, Klebsiella Gram- High doses of third-generation
pneumonia, Escherichia coli, Citrobacter, negative cephalosporins, aminoglycosides
Acinetobacter, Enterobacter, Serratia
marcescens

1487
*
These therapies are subject to change based on the Centers for Disease Control
and Prevention recommendations and new studies.
Adapted from Tunkel A: Initial therapy and prognosis of bacterial meningitis in adults.
In Calderwood S, editor: UpToDate, Waltham, 2014, Wolters Kluwer. Retrieved from
www.uptodate.com/contents/initial-therapy-and-prognosis-of-bacterial-meningitis-in-
adults; Friedman N, Sexton D: Gram-negative bacillary meningitis: epidemiology,
clinical features, and diagnosis. In Sexton D, editor: UpToDate, Waltham, 2014,
Wolters Kluwer. Retrieved from www.uptodate.com/contents/gram-negative-
bacillary-meningitis-epidemiology-clinical-features-and-diagnosis?source=see_link;
Tunkel A, Hartman B, Kaplan S, et al: Practice guidelines for the management of
bacterial meningitis. Clin Infect Dis 39:1267-1284, 2004.

If mechanical ventilation is already in place, ventilator

settings will vary, depending on the patient’s size and arterial
blood gas results. Check ventilator settings at set intervals.
Consult with an intensivist, pulmonologist, associated advanced
practice provider, and/or respiratory therapy staff members
regarding setting changes as the patient’s needs change.

2. Reduce inflammation with adjunctive pharmacologic

therapies
Dexamethasone may decrease inflammation by reducing cytokines
produced by bacterial products. In recent studies, improvement in
outcome, decrease in neurologic sequelae, and reduction in
mortality with the use of dexamethasone have been reported.
Recommended dosage is 0.15 mg/kg every 6 hours for 4 days. Start
dose with or just before first antibiotic dose. Given if suspected
bacterial meningitis occurs in a developed country; NOT
recommended for bacterial meningitis in undeveloped countries.

3. Monitor
It is important to monitor neurologic status, vital signs, and
respiratory status. The patient may need to be intubated and placed
on a ventilator. Watch for signs of increased ICP or hydrocephalus.

4. Maintain fluid and electrolyte balance

Overhydration and underhydration can lead to adverse effects.
Research supports the use of IV maintenance fluids over fluid

1488
restriction during the first 48 hours of treatment of bacterial
meningitis. Electrolyte imbalances should be corrected. Monitor
urine output and serum osmolality and watch for signs and
symptoms of SIADH.

5. Provide adequate nutrition

Oral feeding should be encouraged when possible. Enteral or
parenteral feeding may be initiated. Parenteral nutrition is used if
enteral feeding is not tolerated. Hydration should be maintained.

6. Control seizures with antiepileptic therapy

Used prophylactically or if seizures occur as a result of neuronal
irritability. Seizures increase metabolic rate and cerebral blood flow,
which may cause deterioration in patients with cerebral edema and
intracranial hypertension. Use seizure precautions and protect from
injury if seizures occur.

7. Maintain normothermia/control fever

Keep normothermic to decrease oxygen demand. Normothermia
helps to prevent intracranial hypertension associated with
increased metabolic rate. Fever should be controlled by antipyretics
such as acetaminophen or use of other noninvasive or invasive
cooling measures.

8. Prevent infection
Vaccines are currently available for meningitis prophylaxis. These
include the following: (1) influenza type B (Hib), given as a
childhood immunization; (2) bacillus Calmette-Guérin (BCG), used
for tuberculosis, also prevents tuberculosis meningitis; (3)
pneumococcal vaccine recommended for those who are chronically
ill and adults older than 65 years of age; and (4) N. meningitides
vaccines for specific or combined prophylaxis for five
investigational subgroups. The Centers for Disease Control and
Prevention (CDC) guidelines recommend that “Transmission-Based
Precautions” be implemented until effectiveness of antimicrobial
treatment is established.

9. Facilitate mobility

1489
Physical therapy, occupational therapy, and speech therapy should
be initiated as soon as the patient is stable, to minimize physical
(contractures and muscle atrophy) and cognitive complications.
Prevent pressure ulcers, pneumonia, or DVTs related to immobility.
Initiate DVT prophylaxis including sequential stockings and
prophylactic anticoagulants as indicated.

10. Evaluate the need for support services

Evaluate the need for home healthcare, support groups, and social
services.

Care plans: Meningitis

Decreased intracranial adaptive capacity 
related to altered fluid dynamics secondary to brain and spinal cord
inflammation.
Goals/Outcomes: Within 72 hours of initiation of antimicrobial
therapy, the patient’s ICP returns to normal range (less than 15 mm
Hg), as evidenced by improved neurologic status that may include
orientation to time, place, and person; bilaterally equal and
normoreactive pupils; bilaterally equal strength and tone of
extremities; absence of cranial nerve palsies; RR 12 to 20
breaths/min with normal depth and pattern; cardiopulmonary
improvement: HR 60 to 100 beats/min (bpm), and BP within the
patient’s normal range; and abatement of clinical signs and
symptoms of increased ICP: absence of headache, vomiting,
papilledema, and other clinical indicators of increased ICP. After
instruction, the patient verbalizes knowledge of the importance of
avoiding Valsalva-like activities.
Neurologic Status.

Neurologic monitoring

1. Assess neurologic status at least hourly. Monitor pupils, LOC,

and motor activity; perform cranial nerve assessments (see
Appendix 3). Early indicators of increased ICP and possible
herniation include decreased LOC, changes in pupillary size and
reaction, a decreased motor function (weakness, posturing), and

1490
cranial nerve palsies.

2. Monitor the patient and report physical indicators of increased

ICP (see Box 7-2) to the advanced practice provider. If no ICP
monitor is inserted, then monitor neurologic status as discussed in
point 1.

3. Monitor vital signs at least every 15 minutes if the patient has

signs of increased ICP. Be alert to changes in respiratory pattern,
fluctuations in BP and pulse, widening pulse pressure, and slow
HR.

4. Optimize cerebral oxygenation. Keep the patient’s head in

neutral alignment, maintain a patent airway, and provide
supplemental oxygen as prescribed. Ensure that the patient’s neck
is not constricted by the endotracheal (ET) tube securement device,
tracheotomy ties, and oxygen tubing.

5. Avoid overhydration, which increases cerebral edema. Ensure

precise delivery of IV fluids and timely delivery of medications
prescribed for the prevention of sudden increases or decreases in
ICP, BP, HR, or RR. Do not use IV fluids that contain dextrose.

6. Teach the patient to avoid activities that increase ICP: coughing,

straining, and bending over.

7. If the patient shows evidence of increased ICP, implement

measures to decrease ICP.

Cerebral Edema Management; Cerebral Perfusion Promotion;

Intracranial Pressure Monitoring: Neurologic Monitoring.

Acute pain 
related to headache, photophobia, and fever secondary to meningeal
irritation
Goals/Outcomes: Within 2 hours of initiating interventions to
relieve pain, the patient reports pain relief, as documented by a
pain scale.
Comfort Level.

1491
Pain management

1. Monitor the patient for pain and discomfort. Devise a pain rating
scale with the patient. Administer analgesics as prescribed. (See
Pain, Chapter 1.)

2. Monitor temperature every 2 hours and as needed. Implement

external or internal cooling or warming methods and prescribed
antipyretics/antibiotics to keep temperature within prescribed
limits.

3. Maintain an environment of comfort for each individual patient.

4. Provide care and visiting hours to allow for uninterrupted

periods (at least 90 minutes) of rest. If ICP is elevated, clustering
care is contraindicated.

5. Darken the patient’s room or provide blindfold to minimize the

discomfort of photophobia.

Risk for infection 

related to possible cross-contamination secondary to communicable
bacterial and aseptic meningitis
Goals/Outcomes: Other patients, staff members, and patient’s
significant others do not exhibit evidence of having acquired
meningitis: diminished LOC, confusion, fever, headache, nuchal
rigidity, and other signs (see previous sections for Meningitis on
Neurologic Assessment, Chapter 7, and Diagnostic Tests for
Meningitis, Chapter 7).
Infection Severity.
For patients with bacterial meningitis

Infection control

1. Some forms of bacterial meningitis are transmitted via droplet

contact. Provide the patient with a private room.

2. Initiate “Transmission-Based Precautions”: Droplet, on

admission, and maintain them for at least 24 hours after start of

1492
antimicrobial therapy.

• Standard precautions should be instituted to

provide safety and protection regardless if infection
is bacterial, fungal, or viral. Be alert for airborne
pathogens and those in stool or oral secretions.

• Contact (fecal and oral) precautions should be

initiated for enteroviral causes of meningitis.

Additional nursing diagnoses

See Risk for Trauma (Oral and Musculoskeletal) in Status
Epilepticus (Chapter 7). Because these patients are at risk for
SIADH, see Syndrome of Inappropriate Antidiuretic Hormone
(Chapter 8). See SIRS, Sepsis, and MODS (Chapter 11), because
these patients are at risk for septic shock; Nutrition Support
(Chapter 1), Prolonged Immobility (Chapter 1), and Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2).

Neurodegenerative and
neuromuscular disorders
Pathophysiology
Neurodegenerative diseases are conditions wherein the neurons, or
the myelin sheath of the neurons of the brain and spinal cord, are
destroyed. Cells of the brain and spinal cord do not effectively
regenerate in large numbers, thus profound destruction is
sometimes devastating. Over time, the progressive destruction
leads to dysfunction and disabilities. The disorders are divided into
two groups: conditions affecting movements (e.g., ataxia) and
conditions affecting memory (e.g., dementia), which are not

1493
mutually exclusive. Alzheimer, Pick, Parkinson, Huntington, and
Lou Gehrig (amyotrophic lateral sclerosis[ALS]) diseases, prion
diseases (Creutzfeldt-Jakob[CJD]), and multiple sclerosis are a few
of the more commonly recognized conditions. Some of the diseases
are genetic, whereas alcoholism, cancer, and vascular disease are
associated with other conditions. Environmental toxins, chemicals,
or viruses may cause other disorders. Neurodegeneration often
begins long before the patient manifests symptoms. Treatments
vary with each disorder.
Neuromuscular disorders include the neurodegenerative
diseases, which affect voluntary movements. Communication
between the nervous system and muscles is not possible when
nerves are destroyed. Muscles weaken and atrophy as a result of
disuse. Weakness may also be associated with muscle twitching,
cramps, and pain, along with joint and movement deficits. These
disorders may affect the heart and respiratory muscles. Many
neuromuscular disorders are genetic, whereas others are immune-
mediated (associated with an immunologic disorder). Myasthenia
gravis (MG), Guillain-Barré syndrome (GBS), and muscular
dystrophy are several of the more commonly recognized
conditions. Most of the diseases are incurable. The goal of treatment
is to improve symptoms, increase mobility, and lengthen life.
Patients with MG may experience difficulties with medication
management resulting in a crisis, which is rather easily corrected
with the proper medication adjustment. Patients with other
neuromuscular disorders may require more elaborate treatments
including high-dose corticosteroids, plasmapheresis, and more
prolonged hospitalization.
Diagnosis of neuromuscular diseases depends on the
identification of a specific defect of neuromuscular function. The
functional defect can sometimes be inferred by a physical
examination done by a physician or advanced practice provider
coupled with laboratory testing of blood and possibly CSF. A more
extensive diagnostic process evaluates the function of nerves,
muscles, and the connections between them by using two
complementary techniques—nerve conduction velocity (NCV)
testing and electromyography (EMG).
Care of patients who are critically ill may involve managing

1494
patients with respiratory failure and cardiovascular instability
related to exacerbations of neuromuscular disorders. Patients at this
stage of instability may be terminally ill. Patients with either MG or
GBS may be treated and fully recover. This chapter will focus on
MG and GBS; however, the nursing diagnoses, interventions, and
outcomes are common to most neurodegenerative and
neuromuscular disorders.

Myasthenia gravis
Pathophysiology
Myasthenia gravis (MG) is a chronic, progressive autoimmune
disorder causing weakness and abnormal fatigability of the
voluntary striated skeletal muscles. MG usually affects women
between 20 and 40 years of age and men after age 40 years; the peak
incidence for women is during the second and third decades and
for men during the sixth decade. The overall ratio of affected
women to men is 3:2. Of patients with MG, 85% to 90% have an
anti–acetylcholine receptor (anti-AChR) antibody
(immunoglobulin). MG is associated with other autoimmune
disorders. The thymus gland undergoes pathologic changes in 80%
of patients with MG and may produce anti-AChR antibodies when
exposed to inflammation. The course of the disease depends on the
muscle groups involved and the degree of their involvement.
MG causes changes in the structural integrity of the postsynaptic
membrane at the neuromuscular junction by markedly reducing the
number of AChRs. Acetylcholine (ACh), a neurotransmitter, is
synthesized and stored in the terminal expansion of motor nerve
axons. ACh is released into the synaptic cleft. The attachment of
ACh to AChR on the postsynaptic membrane activates muscle
action potential, resulting in muscle contraction. Contraction
terminates when ACh is deactivated by acetylcholinesterase in the
neuromuscular junction.
Patients may experience remissions and exacerbations. Many
medications can increase the weakness associated with MG,
including several commonly administered antibiotics
(erythromycin, aminoglycosides, and azithromycin) and cardiac

1495
medications such as magnesium or antidysrhythmic agents
including procainamide, beta-adrenergic–blocking agents, and
quinidine. Paradoxical weakness may occur when a patient receives
an excessive dose of anticholinesterase medications (cholinesterase
inhibitors such as physostigmine or neostigmine), which are used to
treat MG. Distinguishing worsening MG from side effects from
prescribed medication effects can be difficult. Exacerbations can be
profound, and thus are called crises.
A myasthenic or cholinergic crisis may occur rapidly or
incipiently. Myasthenic crisis can occur as part of the natural course
of MG or may result from other factors, including infection,
tapering of immunosuppressive medications, administration of
various other medications, pregnancy, childbirth, or following a
surgical procedure, ultimately resulting in respiratory failure from
weakness of the respiratory muscles. Severe weakness of the
oropharyngeal muscles (bulbar signs) is often associated with
respiratory muscle weakness, resulting in dysphagia and
aspiration. Endotracheal (ET) intubation with mechanical
ventilation may be needed. A cholinergic crisis results from excessive
doses of anticholinesterase medications and rarely occurs if the
dose of medications remains within the normally prescribed range.
The patient is acutely aware of all sensations. Crisis is dramatic and
frightening.

Assessment
Goal of assessment
The assessment differentiates between acute and chronic neurologic
assessment findings. Signs of myasthenic and cholinergic crises
may be subtle. Increasing anxiety, apprehension, or insomnia may
indicate the onset of crisis.

History and risk factors

History of rheumatoid arthritis, systemic lupus erythematosus,
thyrotoxicosis, Sjögren syndrome, polymyositis, ulcerative colitis,
Hashimoto thyroiditis, and pernicious anemia. Recent infection,
trauma, surgery, temperature extremes, stress, endocrine

1496
imbalance, or intake of medications with neuromuscular-blocking
properties, such as sedatives, tranquilizers, opiates, or antibiotics
(e.g., neomycin, kanamycin, gentamicin, streptomycin, tetracycline),
may prompt crisis.

Vital signs
• Findings vary significantly, depending on whether the patient is
experiencing a crisis.

• RR may be normal or slightly tachypneic.

• Tachycardia may be present with impending respiratory failure.

Observation
• Patients may be asymptomatic or have mild symptoms if crisis
develops slowly.

• Weakness and abnormal fatigability of skeletal muscles, which

worsens with sustained efforts.

Symptom progression

Ocular muscle group

First muscle group to be affected in 65% of patients. During course
of disease, 90% will have ocular involvement. Eye signs include
ptosis (drooping of one or both eyelids), diplopia (double vision),
and inability to maintain upward gaze.

Muscles of face, neck, and oropharynx with bulbar signs

Second area of involvement. Bulbar signs are present, with
increased risk of aspiration as a result of difficulty chewing,
dysphagia, dysarthria, inability to close mouth, nasal regurgitation
of fluids, mushy and nasal tone to voice, neck-muscle weakness
with head bob, inability to raise chin off chest, and loss of facial
expression.

Muscles of limbs and trunk

1497
Weakness is greater in proximal muscles than distal. Strength is
decreased in all extremities, with inability to maintain position
without support. Diaphragmatic and intercostal weakness,
dyspnea, ineffective cough, and accumulation of secretions are
present, which increases the risk for respiratory arrest.

Myasthenic and cholinergic crises

Increasing anxiety, apprehension, or insomnia may indicate the
onset. ABG values may be normal. Note subtle decreases in chest
expansion and air movement and increased dysphagia, dysarthria,
and dysphonia. Accumulation of oropharyngeal secretions
increases the risk of aspiration.

• Myasthenic crisis: Occurs when the patient needs increased

medication as a result of drug tolerance or an exacerbation of the
disease. Signs and symptoms: Increasing muscle weakness
despite normal or increased drug dose, increasing anxiety and
apprehension, severe ocular and bulbar weakness, with rapid
onset of respiratory muscle weakness, which can lead to
respiratory arrest.

• Cholinergic crisis: Results from an overdose of

anticholinesterase medication, causing a depolarizing
neuromuscular blockade. Signs and symptoms: Increasing
muscle weakness, increasing anxiety and apprehension,
fasciculations (twitching) around the eyes and mouth, diarrhea
and cramping, sweating, pupillary constriction, sialorrhea
(excessive salivation), and difficulty breathing and swallowing.

Auscultation
• Breath sounds may reflect reduced movement of air or shallow
breaths.

Diagnosis of Myasthenic or Cholinergic Crisis

1498
Collaborative management
Care priorities for patients with myasthenia gravis

1. Manage respiratory failure

ET intubation with mechanical ventilation may be necessary,
depending on the degree of involvement of the respiratory muscles.
(See Mechanical Ventilation, Chapter 1.) Bilevel positive-pressure
ventilation (BiPAP) may also be used effectively in a subset of
patients, if able to breathe somewhat effectively.

2. Provide emergency interventions for myasthenic or

cholinergic crisis
Once the patient is stabilized in the intensive care unit (ICU), the
type of crisis is identified, and specific treatment is begun.
Anticholinesterase medications may be withheld or reduced
temporarily. A “drug holiday” will improve subsequent patient
responsiveness to medication. With the resumption of
anticholinesterase medications, dose, timing, and combinations of
medications will need readjustment. In severe MG, plasmapheresis
(see later) may hasten improvement of signs and symptoms.

3. Initiate nutrition support

If the patient has dysphagia, enteral or parenteral feedings may be
needed. (See Nutrition Support, Chapter 1.)

1499
4. Manage pharmacotherapy during noncrisis periods
Medications must be given on time to maintain therapeutic effects.
Drug combinations are patient-specific.

• Cholinesterase inhibitors: Pyridostigmine bromide (Mestinon),

neostigmine bromide (Prostigmin), and ambenonium chloride
(Mytelase) are used to inhibit the hydrolysis of ACh by
acetylcholinesterase at the neuromuscular junction.
Pyridostigmine is often used, because it has fewer side effects
and is longer acting. The patient is given a dose every 3 hours
during the day, and the dose is adjusted based on effects.
Sustained-release preparations usually are given at bedtime to
maintain the patient’s strength throughout the night and early
morning hours.

• Immunosuppression: Glucocorticosteroids (e.g.,

adrenocorticotropic hormone and prednisone) and other
immunosuppressive agents: Glucocorticosteroids are used alone
or in conjunction with anticholinesterase drugs. They provide
clinical improvement for 70% to 100% of patients with MG who
refuse thymectomy and have weakness uncontrolled by
anticholinesterase drugs. Although the mechanism of action of
steroids is uncertain, studies indicate that they directly influence
neuromuscular transmission, suppress the action of the immune
system by decreasing the size of the thymus gland and lymphatic
tissue, decrease circulating lymphocytes, and decrease
antireceptor reactivity of peripheral lymphocytes. Treatment is
continued indefinitely. Glucocorticosteroids produce favorable
results in all patients with muscle involvement, from ocular to
severe respiratory impairment. Azathioprine (Imuran) may be
used alone or in combination with other therapies in situations in
which response to steroids is poor. Side effects of azathioprine
include toxic hepatitis, thrombocytopenia, leukopenia, leukemia,
lymphoma, infections, vomiting, and teratogenic effects.

• Immune globulin: Routine use of human immunoglobulin (IG) is

not recommended, but administration of IV immunoglobulin
(IVIG) may be considered in patients with severe MG for whom

1500
 other treatments have been unsuccessful or are contraindicated.

5. Consider plasmapheresis
A complete exchange of plasma with removal of abnormal
circulating antibodies that interfere with AChRs. Box 7-3 describes
potential complications, nursing assessments, and interventions.
(For additional information, see Fluid and Electrolyte Disturbances,
Chapter 1.)

6. Carefully consider thymectomy

Removal of the thymus gland may prompt clinical improvement in
70% of patients, particularly newly diagnosed females with
hyperplasia of thymic tissue. A suprasternal approach, a
transsternal approach with sternal splitting, or the minimally
invasive technique called video-assisted thoracic surgery may be
used. Plasmapheresis is sometimes used before surgery to increase
strength and allow for a decrease in medication dose.

Care plans for myasthenia gravis

Impaired gas exchange 
related to altered oxygen supply associated with decreases in chest
expansion and air movement secondary to weakness and abnormal
fatigability of pharyngeal, diaphragmatic, intercostal, and accessory
muscles of respiration.
Goals/Outcomes: Within 12 to 24 hours of initiation of treatment,
the patient has adequate gas exchange, as evidenced by orientation
to time, place, and person; RR less than 20 breaths/min with normal
depth and pattern (eupnea); PaO2 greater than 80 mm Hg; Paco2 less
than 45 mm Hg; and oxygen saturation greater than 95%.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation; Mechanical Ventilation Response: Adult.

Respiratory monitoring

1. Assess the patient for indicators of impending respiratory failure

or hypoxia: diminished or adventitious breath sounds; changes in

1501
rate, rhythm, or depth of respirations; pallor; nasal flaring; use of
accessory muscles; and restlessness, irritability, confusion, or
somnolence.

2. Monitor ventilatory capability via pulmonary function tests. Vital

capacity less than 75% of predicted value, tidal volume less than
1000 mL (or the patient’s normal/baseline volume), and RR greater
than 34 breaths/min are signals of need for assisted ventilation.

3. Monitor ABG and pulse oximetry results. Falling PaO2 (less than
60 mm Hg), rising Paco2 (greater than 50 mm Hg), and falling
oxygen saturation, coupled with changes in vital capacity, tidal
volume, and increasing RR, indicate the need for additional
respiratory support.

4. Provide pulmonary toilet every 2 hours when the patient is

awake and as needed. In addition, turn the patient after each
physiotherapy session to facilitate lung expansion, decrease risk of
atelectasis, and prevent consolidation of secretions.

To prevent aspiration of secretions, always suction

secretions from the trachea and mouth before deflating
endotracheal or tracheostomy cuff. Consider use of endotracheal
tube with continuous supraglottic suction, if available. This is
especially important because of the increase in saliva.

Airway Management; Coping Enhancement; Acid-Base

Monitoring; Oxygen Therapy; Mechanical Ventilation Response:
Adult.

Ineffective airway clearance 

related to ineffective cough; decreased energy; abnormal fatigability of
diaphragmatic, intercostal, pharyngeal, and accessory muscles of
respiration.
Goals/Outcomes: Within 24 to 48 hours of

1502
intervention/treatment, the patient’s airway is clear, as evidenced
by absence of adventitious breath sounds.
Aspiration Prevention; Respiratory Status: Airway Patency.

Airway management

1. Assess breath sounds, effectiveness of the patient’s cough, and

the quality, amount, and color of sputum. Consult the physician or
advanced practice provider for significant findings, including the
patient’s inability to raise secretions; for secretions that are
tenacious, thick, or voluminous.

2. Suction secretions as indicated, using hyperoxygenation before

and after procedure.

Range of motion is done gently during the acute phase.

Overly aggressive exercise may exacerbate weakness and
accelerate the demyelinating process.

3. Place the patient in semi-Fowler to high Fowler position to

facilitate chest excursion and decrease risk of aspiration. Fully
elevate HOB during feedings.

4. Assess vital signs for indicators of atelectasis and upper

respiratory tract infection (see Risk for Infection, which follows).
Report significant findings to the advanced practice provider.

5. Increase activity as tolerated to minimize stasis of secretions and

to facilitate lung expansion.

6. Administer or assist with noninvasive BiPAP as needed.

7. Keep a tracheostomy tube and obturator at the bedside in the

event of inadvertent extubation.

1503
 Artificial Airway Management; Cough Enhancement:
Oxygen Therapy; Ventilation Assistance.

Risk for infection 

related to inadequate primary defenses (stasis of secretions); inadequate
secondary defenses (suppressed inflammatory response); invasive
procedures (e.g., insertion of ET tube); chronic disease.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia; HR 60 to 100 bpm; pulmonary secretions that are
clear, thin in consistency, and odorless; and WBC count less than
11,000/mm3.
Immune Status.

Health screening

1. Monitor for temperature greater than 37.7° C (100° F),

tachycardia, and diaphoresis.

2. Assess color, consistency, amount, and odor of secretions. Report

changes in sputum color to the provider. Obtain sputum specimens
for culture as indicated.

3. Monitor CBC results for elevation of WBC count (greater than

11,000/mm3).

4. Administer antibiotics as prescribed.

5. Protect the patient from persons with infection, particularly

upper respiratory tract infection.

6. Turn and reposition the patient at least every 2 hours to prevent

stasis of secretions.

Impaired swallowing 
related to decreased or absent gag reflex; decreased strength or excursion of
muscles involved in mastication; facial paralysis; mechanical obstruction
(tracheostomy tube).
Goals/Outcomes: Before oral foods and fluids are given or
reintroduced, the patient demonstrates capability for safe and

1504
effective swallowing, as evidenced by the presence of gag reflex
and adequate strength and excursion of muscles involved in
mastication.
Aspiration Prevention; Swallowing Status.

Aspiration precautions

1. Assess the patient for the presence of the gag reflex, ability to
swallow, and strength and excursion of muscles involved in
mastication. As indicated, consult with a speech therapist to
determine the patient’s ability to swallow.

2. If the patient cannot swallow, confer with the provider regarding

alternate method of nutrition support, such as enteral or parenteral
nutrition (see Nutrition Support, Chapter 1).

3. After the patient’s gag reflex and ability to swallow return, begin
oral feedings cautiously.

• When reinstating oral intake, offer a few ice chips to

help stimulate the swallowing reflex, progress to
semisolid foods (e.g., textured food, applesauce)
and then to solid foods. Confer with the
speech/swallowing therapist regarding a dysphagia
diet and teaching swallowing techniques.

• Elevate the HOB greater than 70 degrees to facilitate

gravity flow through the pylorus and to minimize
regurgitation and aspiration.

• Provide small feedings at frequent intervals (e.g.,

every 4 hours while the patient is awake).

• Avoid cold foods and beverages, which cause

bloating and upward pressure on the diaphragm.

1505
• Keep suction equipment at the bedside; suction
excess secretions as necessary after each feeding.
Inspect the mouth for residual food after meals.
Provide for oral hygiene after every meal.

4. If the patient begins oral feedings with a tracheostomy tube in

place, elevate the HOB greater than 70 degrees. Inflate
tracheostomy tube cuff for 30 minutes before and after feeding to
prevent aspiration. Progress the diet slowly, as described in the
previous intervention.

5. If the patient is unable to communicate verbally, be alert to signs

of severe aspiration: dyspnea, tachypnea, restlessness, agitation,
pallor, and presence of adventitious breath sounds. If these signs
occur, discontinue feeding immediately; elevate the HOB; and
provide oxygen. If a tracheostomy tube is in place, suction to
remove food or secretions obstructing the airway.

Swallowing Therapy; Positioning; Nutrition Management.

Disturbed sensory perception (visual) 

related to altered sensory perception associated with diplopia or ptosis.
Goals/Outcomes: Within 48 to 72 hours of this diagnosis, the
patient relates that vision is adequate to perform activities of daily
living (ADLs).
Neurologic Status: Cranial/Sensory/Motor Function.

Environmental management: Safety

1. Assess for and document signs of weakness of the ocular muscles

(i.e., diplopia, ptosis, incomplete closure of the eye).

2. Provide an eye patch or frosted lens for the patient with diplopia;
alternate the patch or lens to the opposite eye every 2 to 3 hours
during the patient’s waking hours.

3. Provide eyelid crutches for the patient with ptosis, or loosely tape
eyelids open but only when providing direct care.

1506
4. Administer artificial tears in each eye at least every 4 to 6 hours to
lubricate and protect corneal tissue.

5. As indicated, provide assistance with ADLs and ambulation to

protect the patient from injury.

6. Keep the patient’s environment consistent to facilitate location of

desired objects.

Communication Enhancement: Visual Deficit; Environmental

Management; Fall Prevention; Surveillance: Safety.

Deficient knowledge 
related to thymectomy procedure, including preoperative and postoperative
care.
Goals/Outcomes: Before surgery, the patient verbalizes
understanding of the surgical procedure, including preoperative
and postoperative care.
Knowledge: Treatment Procedure(s).

Teaching: Procedure/treatment

1. Explain thymectomy and its relationship to MG.

2. Provide information about preoperative routine. Discuss

medications, application of antiembolic hose, the potential for
postoperative discomfort, and the availability of analgesic agents.
Advise the patient that medications may change after surgery,
because the patient may improve. With a thoracotomy approach,
explain postoperative chest tubes. With a transcervical approach, a
wound drainage system (e.g., Hemovac) is used.

3. Teach coughing and deep-breathing techniques used after

surgery.

4. Explain that plasmapheresis may be performed preoperatively to

improve the patient’s clinical state. (See Deficient Knowledge:
Purpose and Procedure for Plasmapheresis, which follows.)

5. Explain that pulmonary function and ABG tests will be

1507
performed preoperatively and postoperatively to assist in
determining the patient’s respiratory status.

6. Explain the possibility of tracheostomy with assisted ventilation

to prevent respiratory problems that can occur from stresses of
surgery or myasthenic or cholinergic crisis.

7. Explain that results of a thymectomy vary and may not be

apparent for several months to years.

Deficient knowledge 
related to purpose and procedure for plasmapheresis
Goals/Outcomes: Before the first plasma exchange, the patient
verbalizes knowledge of the purpose and procedure for
plasmapheresis.
Knowledge: Treatment Procedure(s).

Teaching: Procedure/treatment

1. Assess the patient’s previous experience with and knowledge of

plasmapheresis.

2. As appropriate, teach the patient the following about

plasmapheresis: (1) blood is withdrawn via an arterial catheter,
anticoagulated, and then passed through a cell separator; (2) the
plasma portion of the blood that contains the AChR antibodies is
removed; (3) red blood cells (RBCs), WBCs, and platelets are mixed
with saline, potassium, and plasma protein fraction and then are
returned to the body.

3. Advise the patient that plasmapheresis is generally performed to

control severe symptoms until other modalities (i.e., medications,
thymectomy) take effect, when other treatments have failed, or to
increase the patient’s strength and improve general status before
surgery.

4. Explain that the nurse will make assessments before, during, and
after plasmapheresis (see Box 7-3).

1508
5. Advise the patient that the procedure takes several hours and
may be performed daily.

6. Explain that the degree of weakness may increase during and

after the procedure because of the removal of plasma-bound
medications (corticosteroids, anticholinesterase agents). Reassure
the patient that he or she will be monitored closely during the
procedure and will receive appropriate medication after
plasmapheresis.

Deficient knowledge 
related to signs and symptoms of myasthenic and cholinergic crises.
Goals/Outcomes: Within 24 hours of stabilization of respiratory
status, the patient and significant others verbalize the signs and
symptoms of impending myasthenic and cholinergic crises.
Knowledge: Disease Process.

Teaching: Disease process

1. Assess the patient’s/family’s knowledge of myasthenic and

cholinergic crises.

2. Explain the differences between myasthenic crisis: an

exacerbation of the myasthenic symptoms, frequently triggered by
an infection; and cholinergic crisis: an episode triggered by toxic
levels of anticholinesterase medication. The crisis, regardless of
type, may manifest similar symptoms, including abdominal
cramping, diarrhea, generalized weakness, increased pulmonary
secretions, and impaired respiratory function.

3. Advise the patient/family to immediately report signs and

symptoms of crisis.

4. Prepare the patient for potential discharge when stabilized and

consider the use of home health services for follow-up after
discharge.

5. Teach the patient and significant others how to use emergency

respiratory support equipment (manual resuscitator bag and

1509
suction apparatus) and facilitate it being available in the home if the
patient has a history of crisis events.

6. Advise the patient to carry an identification card with diagnosis,

medications, medication contraindications, advanced practice
provider and/or physician’s name and phone number.

7. Provide contact information for Myasthenia Gravis Foundation of

America, Inc., 355 Lexington Avenue, 15th Fl., New York, NY
10017; Tel: 800-541-5454; fax: 212-370-9047; website: www.
myasthenia.org.

Additional nursing diagnoses

See also Nutrition Support (Chapter 1), Mechanical Ventilation
(Chapter 1), and Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2).

Guillain-barré syndrome
Pathophysiology
Guillain-Barré syndrome (GBS) is a disorder wherein the immune
system mistakenly attacks the peripheral nervous system, causing
weakness and paresthesias of the lower extremities. Symptoms can
intensify and ascend toward the head, resulting in loss of ability to
use all muscles. When severe, the patient is totally paralyzed and
the disorder is life threatening, with impending respiratory muscle
paralysis and cardiovascular instability. GBS is not considered a
classic neuromuscular or neurodegenerative disorder, because the
onset is sudden, with rapid progression, and once peaked, patients
have the potential for a complete recovery.
This disorder is an acute inflammatory, immune-mediated,
demyelinating polyneuropathy of the peripheral nervous system,
affecting 1.5 to 2 individuals per 100,000 population.
GBS affects mainly the Schwann cell, which synthesizes and
maintains the peripheral nerve myelin sheath. Studies suggest that
macrophages penetrate the basement membrane and strip
apparently normal myelin from intact peripheral nerve axons,

1510
causing the characteristic signs and symptoms of GBS. The ventral
(motor) root axons of the anterior horn cells, which innervate
voluntary skeletal muscles, are primarily involved. Dorsal (sensory)
root axons of the posterior horn are not as affected. Recovery of
neurologic function depends on proliferation of Schwann cells and
remyelination of axons. Recovery can be expected in 80% to 90% of
cases, with minor residual deficits in less than half of the patients,
and 2% to 5% experiencing recurrence after complete recovery.

Assessment: Guillain-barré syndrome

Goal of assessment
Identify the extent of current neurologic deficits, compared with the
baseline, and intervene in profound deterioration. There are several
clinical variations of signs and symptoms: ascending, descending,
the Miller Fisher variant, or pure motor. The disease generally has
three phases: (1) acute phase of 1 to 3 weeks after onset of the first
symptom; (2) plateau phase beginning with no further clinical
deterioration and lasting several days to weeks; and (3) recovery
phase, which can last 4 months up to 2 years and correlates with the
remyelination and axonal regrowth process.

History and risk factors

Respiratory or GI illness 10 to 14 days before onset of the neurologic
symptoms, in which (1) a viral agent such as parainfluenza 2 virus,
measles, mumps, rubella, varicella, or herpes zoster is present (50%
of cases); (2) recent vaccination (15% of cases), such as for influenza;
and (3) recent surgical procedure (5% of cases). Miller Fisher
syndrome, an acute axonal variant of GBS, has been shown to
follow infection with Campylobacter jejuni.

Vital signs
• Autonomic nervous system involvement (a type of autonomic
dysreflexia): Occurs in most patients with GBS: sinus tachycardia,
bradycardia, orthostatic hypotension, hypertension, excessive
diaphoresis, bowel and bladder dysfunction, loss of sphincter

1511
 control, increased pulmonary secretions, SIADH, and cardiac
dysrhythmias (a common cause of death).

Observation
• Ascending flaccid motor paralysis is the most common presenting
sign and is associated with the early loss of deep tendon reflexes.

• Symmetric motor weakness, decreased or absent deep tendon

reflexes, hypotonia or flaccidity of affected muscles, presence of
respiratory abnormalities (e.g., nasal flaring, hypoventilation),
facial paralysis.

• Weakness, usually preceding the paralysis, is symmetrical, begins

in distal muscle groups, and ascends to involve more proximal
muscles.

• Muscles of respiration (intercostals and diaphragm) are

frequently involved. Approximately half of all patients will
require mechanical ventilation.

• Complaints of distal paresthesias are common. In more serious or

prolonged cases, proprioceptive and vibratory dysfunctions are
present. Sensory complaints usually appear first, with muscle
weakness developing rapidly over 24 to 72 hours. Approximately
90% of patients reach the peak of dysfunction within 2 weeks.

• Loss of pain and temperature sensations in a glove-and-stocking

distribution has been reported.

• Cranial nerve involvement: All cranial nerves except I and II may

be involved. See Appendix 3.

Diagnosis of Guillain-Barré Syndrome

1512
Collaborative management
Care priorities

1. Provide respiratory support

ET intubation with assisted mechanical ventilation, as necessary.

2. Perform plasmapheresis
Involves a complete exchange of plasma with the removal of
abnormal circulating antibodies that affect the peripheral nerve
myelin sheath. Removal of these autoantibodies may lessen the
duration and severity of GBS. For nursing interventions for
complications of plasmapheresis, see Box 7-3.

3. Administer ivig (IV immunoglobulin g or ivig)

IVIG given at 0.4 mg/kg/body weight/day for 5 days has been
recommended as an alternative to plasma exchange in children and
adults with GBS.

4. Support cardiovascular function and carefully monitor for

dysrhythmias
Continuous cardiac monitoring may be initiated to assess for
dysrhythmias, which are a common cause of death; arterial
pressure monitoring may be used to evaluate hypertension or
hypotension; and antihypertensive agents or vasopressors may be

1513
administered to maintain BP within normal levels.

5. Manage bowel and bladder dysfunction

Some patients may experience a paralytic ileus. Nasogastric suction
and parenteral infusion may be started; stool softeners and
laxatives may be given for constipation. A urinary catheter may be
inserted in patients with urinary retention.

6. Provide nutrition support

Parenteral feedings are given until return of peristalsis. Tube
feedings or gastrostomy feedings are used for patients with severe
dysphagia. With recovery of gag reflex and swallowing ability, the
diet will progress to semisolid and solid foods, which are more
readily swallowed than are liquids.

7. Rehabilitation
Active and passive ROM exercises are performed at frequent
intervals during all phases of GBS. Activity must be balanced with
caloric intake to prevent muscle wasting. When the patient’s
condition stabilizes, a physiatrist consultation to plan rehabilitation
with physical and occupational therapy should be done while the
patient is in critical care. The primary goal is to pace recovery to
obtain maximum mobility, promote self-care, and adapt to changes
in body image. Rehabilitation does not improve nerve regeneration.

Because of the risk of fatal cardiac dysrhythmias in

Guillain-Barré syndrome, continuous cardiac monitoring is
recommended for the first 10 to 14 days of hospitalization.

Care plans for guillain-barré syndrome

Impaired gas exchange 
related to altered oxygen supply associated with decreased lung expansion

1514
secondary to weakness or paralysis of intercostal and diaphragmatic
muscles.
Goals/Outcomes: Within 12 to 24 hours of this diagnosis, the
patient has adequate gas exchange, as evidenced by orientation to
time, place, and person; RR 12 to 20 breaths/min with normal
pattern and depth; HR less than 100 bpm; BP within the patient’s
normal range; PaO2 greater than 80 mm Hg; Paco2 less than 45 mm
Hg; and oxygen saturation greater than 94%.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation; Mechanical Ventilation Response: Adult.

Respiratory monitoring

1. Monitor for respiratory distress. Report adventitious breath

sounds (crackles, rhonchi); decreased or absent breath sounds;
temperature greater than 37.7° C (100° F); increased HR and BP;
tidal volume or vital capacity decreased from baseline; decreased
PaO2 or Paco2 increased by greater than 10 to 15 mm Hg from
baseline; abnormal RR or rhythm; increasing restlessness, anxiety,
or confusion.

2. Assess for weakness hourly, or as often as needed. Ascending

motor and sensory dysfunctions usually occur rapidly (over 24 to
72 hours) and can lead to respiratory arrest.

3. Prepare to assist with intubation for respiratory failure.

4. Maintain mechanical ventilation as indicated. (See Mechanical

Ventilation, Chapter 1.)

5. Monitor ABG results and pulse oximetry. Consult the advanced

practice provider for continued abnormalities.

Airway Management; Acid-Base Monitoring; Oxygen

Therapy; Mechanical Ventilation, Respiratory Status: Ventilation.

Ineffective airway clearance 

related to ineffective cough; decreased energy; increasing paralysis of
respiratory, pharyngeal, and facial muscles; absence of the gag reflex.

1515
 Goals/Outcomes: Within 12 to 24 hours of this diagnosis, the
patient’s airway is clear, as evidenced by absence of adventitious
breath sounds; HR 60 to 100 bpm; BP within the patient’s baseline
range; RR 12 to 20 breaths/min with normal depth and pattern; tidal
volume within baseline measurements; PaO2 greater than 80 mm
Hg; Paco2 less than 45 mm Hg.
Aspiration Prevention; Respiratory Status: Airway Patency.

Airway management

1. Monitor for crackles, rhonchi, and decreased or absent breath

sounds; increased HR and BP; tidal volume or vital capacity
decreased from baseline; abnormal RR or rhythm; decrease in PaO2
or increase in Paco2; and increasing restlessness or anxiety.

2. Suction the airway as needed is determined by auscultation

findings. When the paresis or paralysis subsides (usually after 2 to 4
weeks) cranial nerve function will begin to return (i.e., gag reflex,
swallowing, coughing). Evaluate the patient’s ability to cough,
whether or not he or she has been placed on mechanical ventilation.
Assess for the presence of adventitious sounds to determine
effectiveness of the patient’s cough.

3. Deliver oxygen and humidification as prescribed.

4. Maintain mechanical ventilation as prescribed. (See Mechanical

Ventilation, Chapter 1.)

5. Maintain adequate hydration to minimize thickening of

pulmonary secretions.

6. Turn and reposition the patient at least every 2 hours to prevent

stasis of secretions.

Positioning; Airway Suctioning; Respiratory Monitoring;

Cough Enhancement; Aspiration Precautions: Positioning.

Risk for disuse syndrome 

related to ascending flaccid paralysis and paresthesias

1516
 Goals/Outcomes: The patient maintains baseline/optimal ROM of
all joints and baseline muscle size and strength; no evidence of
DVT.
Endurance.

Energy management

1. Assess neurologic function hourly or as often as indicated.

Ascending motor and sensory dysfunction usually occurs rapidly
(over 24 to 72 hours). When neurologic dysfunction is progressing
in GBS crisis, assess motor and sensory deficits by starting with the
lower extremities and working upward.

• Assess muscle symmetry by using a side-to-side

comparison.

• Assess for DVT. Monitor for fever and calf

tenderness. Apply antiembolic stockings as
prescribed to help promote tissue perfusion.

• Assess muscle strength. For lower extremities: Have

the patient pull heel of foot toward the buttocks as
you provide resistance by holding onto the foot. For
upper extremities: Have the patient extend and flex
the wrists and arms against your resistance.

• Assess deep tendon reflexes of the Achilles, patellae,

biceps, triceps, and brachioradialis. Normal
response is +2; report decreased (+1) or absent (0)
response.

• Assess for paresthesia, including the location,

degree, and whether it is ascending.

1517
• Assess position sense by moving the patient’s big
toe or thumb up and down while patient’s eyes are
closed. Note vibratory sense by placing a vibrating
tuning fork over bony prominences.

• Assess response to light touch or pinprick by

starting at the feet and working upward to
determine the level of dysfunction. Note: Sensory
symptoms are usually milder than motor
complaints, with vibration and position sensations
affected most often. However, approximately 25%
of affected patients will experience pain, requiring
analgesia. When light touch, pinprick, and
temperature sensations are affected, they most often
are found in a glove-and-stocking distribution.
Patients frequently experience muscle tenderness
and sensitivity to pressure.

• Assess for cranial nerve dysfunction (see Appendix

3).
2. Turn and record and report sensorimotor deficit, including
degree of involvement.

3. Reposition the patient in correct anatomic alignment every 2

hours or more often if requested by the patient. Support the
patient’s position with pillows and other positioning aids.

Activity therapy

1. To maintain the patient’s muscle function and prevent

contractures, ensure that active or passive ROM exercises are
performed every 2 hours during all phases of GBS. Involve
significant others in exercises, if appropriate.

1518
2. Obtain a physical therapy referral, and begin rehabilitation
planning process during the early stages of the disorder.

3. As indicated, apply splints to hands-arms and feet-legs to help

prevent contracture; alternate splints so that they are on for 2 hours
and off for 2 hours.

4. Specialty beds may be used to manage the respiratory,

integumentary, autonomic, and musculoskeletal problems.

Neurologic Monitoring; Exercise Therapy (All); Exercise

Promotion; Positioning.

Autonomic dysreflexia (AD) (or risk for same)

related to excessive or inadequate activity of the sympathetic or
parasympathetic nervous system.
Goals/Outcomes: The patient has no symptoms of AD, as
evidenced by normal T wave configuration on ECG, HR 60 to 100
bpm, BP within the patient’s normal range, cool and dry skin,
patient’s normal strength, and absence of headache and chest and
abdominal tightness.
Neurologic Status: Autonomic; Symptom Severity; Vital
Signs.

Dysreflexia management

1519
1. Assess for signs of AD: cardiac dysrhythmias; HR less than 60
bpm or greater than 100 bpm; elevated and sustained BP (greater
than 250 to 300/150 mm Hg); facial flushing; increased sweating,
possibly caused by loss of thermal regulation; extreme generalized
warmth; profound weakness; and complaints of severe headache or
tightening in the chest and abdomen.

2. Place the patient on cardiac monitor as prescribed.

Care must be taken to avoid stimulation of autonomic

dysreflexia by using generous amounts of anesthetic ointment and
ensuring gentle insertion when giving suppository or enema.

3. Monitor the patient carefully during activities that are known to

precipitate AD: position changes, vigorous coughing, and
suctioning. The patient should be taught to avoid straining with
bowel movements.

4. Be aware of and implement measures to prevent and intervene

immediately to remove causes that may precipitate AD such as the
following:

• Bladder stimuli: urinary tract infection, cystoscopy,

urinary catheter insertion, clogged urinary catheter,
urinary calculi.

• Bowel stimuli: fecal impaction, rectal examination,

enemas, suppositories. Ensure that the patient is
well hydrated and has stool softeners and laxatives
prescribed to reduce the chance of constipation.

1520
• Sensory stimuli: pressure caused by tight clothing,
dressings, bed covers, thigh straps on urinary
drainage bags; prolonged pressure on skin surface
or over bony prominences; temperature changes,
such as exposure to a cool breeze or draft.

5. If indicators of AD are present, implement the following:

a. Elevate the HOB or place the patient in a sitting position to

promote decrease in BP.

b. Monitor BP and HR every 3 to 5 minutes until the patient’s

condition stabilizes.

c. Determine and remove offending stimulus:

• For example, if the patient’s bladder is distended,

catheterize cautiously, using sufficient lubricant.

• If the patient has an indwelling urinary catheter,

check for obstruction such as granulation in
catheter or kinking of tubing. As indicated, irrigate
catheter, using no greater than 30 mL normal saline.
If infection is suspected, obtain a urine specimen for
culture and sensitivity testing once crisis stage has
passed.

• Carefully check for fecal impaction. Perform the

rectal examination gently, using an ointment that
contains a local anesthetic (e.g., Nupercainal).

• Check for sensory stimuli, loosen clothing, bed

covers, or other constricting fabric as indicated.

1521
6. Consult the advanced practice provider if symptoms do not abate
within 15 to 30 minutes, especially elevated BP. This may lead to
seizures, subarachnoid (SAH) or intracerebral hemorrhage (ICH),
or other stroke.

7. As prescribed, administer antihypertensive agents and monitor

effectiveness.

Neurologic Monitoring; Vital Signs Monitoring; Urinary

Elimination Management.

Decreased cardiac output (or risk for same) 

related to decreased afterload secondary to reduced peripheral vascular
tone. Normovolemic patients may have a decreased cardiac output as a
result of vasodilation. This is similar to the vascular response seen in
distributive (e.g., anaphylactic, septic) shock.
Goals/Outcomes: The patient has adequate cardiac output, as
evidenced by BP within the patient’s normal range; HR 60 to 100
bpm; urinary output greater than 0.5 mL/kg/h; peripheral pulses
greater than 2+ on a 0-to-4+ scale; orientation to time, place, and
person; CVP 4 to 6 mm Hg, pulmonary artery wedge pressure 6 to
12 mm Hg; systemic vascular resistance 900 to 1200 dynes/s/cm–5;
cardiac output 4 to 7 L/min; and normal sinus rhythm.
Tissue Perfusion: Peripheral; Tissue Perfusion: Cerebral.

Hemodynamic regulation

1. Monitor the patient for indicators of decreased cardiac output:

drop in SBP greater than 20 mm Hg from baseline, SBP less than 80
mm Hg, or a continuing drop in SBP of 5 to 10 mm Hg with every
assessment; HR greater than 100 bpm; irregular HR; restlessness,
confusion, and dizziness; warm and flushed skin; edema; and
decreased urinary output less than 0.5 mL/kg/h for 2 consecutive
hours. Monitor hemodynamic pressures, particularly pulmonary
artery wedge pressure, cardiac output, and systemic vascular
resistance.

2. Assess and report changes in cardiac rate and rhythm.

1522
3. Implement measures to prevent decreased cardiac output caused
by orthostatic hypotension:

• Change the patient’s position slowly.

• Perform ROM exercises every 2 hours to prevent

venous pooling.

• Apply elastic antiembolic stockings as prescribed to

promote venous return.

• Keep the patient’s legs straight. Do not use pillows

or “gatch” the knees on the bed.

• Collaborate with the physical therapist to use a tilt

table to help stand the patient.
4. As prescribed, administer fluids to treat hypotension.

5. Administer a vasopressor (e.g., norepinephrine) to counteract

peripheral vasodilation.

Cardiac Care: Acute; Circulatory Precautions; Resuscitation;

Shock Prevention.

Sensory/perceptual alterations (or risk for same) 

related to altered sensory transmission secondary to cranial nerve
involvement with GBS.
Goals/Outcomes: The patient reports normal vision and exhibits
normal pupillary and gag reflexes, intact corneas, ability to
masticate, and full ROM of head and shoulders.
Neurologic Status: Cranial/Sensory/Motor Function.

Environmental management: Safety

1. Assess cranial nerve function (see Appendix 3).

1523
• If the patient experiences a deficit, place objects
where the patient can see them and assist with
ADLs.

• Cover one eye with a patch or frosted lens if the

patient has diplopia; alternate patch or lens every 2
to 3 hours during patient’s waking hours.

• Use eyelid crutches for patients with ptosis.

• Assess the patient for corneal irritation or abrasion.

Apply artificial tear drops or ointments as
prescribed. Secure the eyelid in a closed position if
corneal reflex is diminished or absent.

• Suction during oral hygiene. Do not feed the patient

an oral diet until the gag reflex returns.

• Position the patient’s head in a position of comfort

and proper anatomic alignment.

Neurologic Monitoring; Peripheral Sensation Management;

Surveillance: Safety.

Constipation 
related to hypoperistalsis or paralytic ileus associated with neuromuscular
impairment.
Goals/Outcomes: Within 3 to 5 days of this diagnosis, the patient
has a bowel movement.
Bowel Elimination; Hydration.

Bowel management

1524
1. Assess the patient’s GI status: bowel sounds, abdominal
distension, nausea, vomiting, and abdominal discomfort. In the
presence of hypoperistalsis or paralytic ileus, the patient will
exhibit (1) high-pitched, tinkling sounds that will be heard early in
obstruction or ileus or (2) a decrease or absence of sounds occurring
with complete obstruction or paralytic ileus.

2. If the patient is having bowel movements, determine the amount,

consistency, and frequency. Question the patient about his or her
usual pattern of bowel elimination.

3. Provide 2 to 3 L/day of fluid to prevent dehydration and

constipation. This may be contraindicated for the patient with
impaired renal or cardiac status.

4. Begin bowel training program based on the patient’s needs and

status of dietary intake:

• Provide a high-fiber diet if the patient is able to

chew and swallow without difficulty.

• If the patient is bedbound, bulk-forming laxatives

should be avoided.

• Give the patient prune juice every evening.

• Establish a regular time for elimination and have a

bedpan readily available.

• Facilitate the patient’s normal bowel habits; ensure

privacy.

• Administer stool softeners (e.g., docusate sodium).

• Carefully administer prescribed medicated

1525
 suppositories.

High doses of phenytoin can cause seizure activity; therefore,

greater than 30 mg/kg is not recommended. If seizures persist after
20 mg/kg dose, an additional 5 to 10 mg/kg may be given, up to a
maximum total dose of 30 mg/kg.

5. See Risk for Disuse Syndrome (p. 664), for neuroassessment

measurements. Also see Box 7-3 for the following complications:
hypovolemia, clotting abnormalities, hypokalemia, and
hypocalcemia.

Box 7-3
NURSING INTERVENTIONS FOR
COMPLICATIONS OF PLASMAPHERESIS
Hypovolemia
Can result from rapid removal of up to 3 L of body fluid during
plasmapheresis with volume replacement that is too slow during
the procedure.

• Perform a baseline assessment of the patient’s weight, skin turgor,

and VS before the procedure is begun. During plasmapheresis,
monitor the patient for thirst, poor skin turgor, dizziness,
confusion, nausea, and flattened neck veins. Assess VS
continuously for evidence of hypovolemia, including decreased
BP and increased HR. Monitor Hct for elevation, which occurs
with hypovolemia. Weigh the patient after procedure. Remember
that liter of fluid equals 1 kg; thus, hypovolemia can be reflected
readily in weight changes.

• Provide fluids during plasmapheresis as prescribed, via oral,

enteral, or IV access.

1526
• Monitor and record I&O throughout the procedure. Be alert to
oliguria (urinary output less than 30 mL/h for 2 consecutive
hours).

• Protect patients who are dizzy or confused by keeping side rails

up and the bed in its lowest position.

Clotting abnormalities
Can result from removal of clotting factors during plasmapheresis.

• Assess PT, PTT, and platelet count before and after procedure. Be
alert to PT and PTT greater than those of control values and to
increased platelet count. Normal ranges are as follows: PT 11 to
15 seconds, PTT 30 to 40 seconds, and platelet count 150,000 to
400,000/mm3.

• Be alert to signs of impaired clotting, such as oozing from arterial

puncture, venous access, or IV sites. Monitor the patient for
epistaxis or other signs of hemorrhage, such as elevated pulse
rate, decreased BP, or changes in the patient’s mental status.

• Apply firm, continuous (e.g., for 10 minutes) pressure to the

arterial puncture site once the catheter or needle is removed. A
pressure dressing is recommended.

• Check gastric aspirate and stools for occult blood.

• Instruct the patient to alert staff to the presence of bleeding from

puncture and other sites.

Hypokalemia*
Can result from removal of potassium during the plasma exchange.

• Assess serum potassium before, during, and after plasma

exchange. Be alert to decreasing levels (less than 3.5 mEq/L).

• Monitor for physical signs of hypokalemia, including

bradycardia, fatigue, leg cramps, nausea, and paresthesias.

1527
• Observe cardiac monitor for signs of cardiac dysrhythmias: ST
segment depression, flattened T wave, presence of U wave, and
ventricular dysrhythmias. Report abnormal cardiac rhythms to
the physician.

• During reinfusion of blood, administer potassium as prescribed to

prevent hypokalemia and dangerous dysrhythmias. If prescribed,
administer antidysrhythmic agents.

Hypocalcemia
Can result from binding of calcium to ACD, the anticoagulant used
during plasmapheresis.

• Assess serum calcium levels before, during, and after

plasmapheresis. Be alert to decreasing levels (less than 8.5
mg/dL).

• Monitor the patient for signs of hypocalcemia, such as numbness

with tingling of fingers and circumoral area, hyperactive reflexes,
muscle cramps, tetany, paresthesia, Chvostek sign, diffuse
irritability, emotional instability, impaired memory, and
confusion.

• Observe cardiac monitor for evidence of hypocalcemia: prolonged

QT interval caused by elongation of ST segment.

• Encourage the patient to drink milk before and during the plasma
exchange.

• As prescribed, administer calcium gluconate during

plasmapheresis if indicators of hypocalcemia occur.

Myasthenic crisis
Can result from removal of circulating anticholinesterase drugs
during plasmapheresis.
Cholinergic crisis
Can result from removal of antibodies and decreased need for
anticholinesterase drugs after plasmapheresis.

1528
• In the event of either crisis, have the following available: IV
infusion apparatus, medications (edrophonium chloride
[Tensilon], neostigmine bromide, atropine, and pralidoxime
chloride [Protopam Chloride]), manual resuscitator bag,
automatic external defibrillator (antiepileptic drug), oxygen,
suction equipment, and intubation tray if intubation is not
already in place.

• Monitor the patient for evidence of crisis, such as decreased vital

capacity (less than 1 L), inability to swallow, ptosis, diplopia,
dysarthria, dysphonia, dyspnea, muscle weakness, and nasal
flaring. Stay with the patient if these signs appear and notify the
physician promptly.

*Caution: Patients on prednisone or digitalis therapy are at

increased risk for hypokalemia and should be monitored closely
for its occurrence.
ACD, Acid-citrate-dextrose; BP, blood pressure; Hct, hematocrit;
HR, heart rate; I&O, intake and output; IV, intravenous; PT,
prothrombin time; PTT, partial thromboplastin time; VS, vital
signs.

Constipation/Impaction Management; Fluid Monitoring;

Nutrition Management.

Resources for education

GBS/CIDP Foundation International

Address: The Holly Building 104 1/2 Forrest Ave, Narberth, PA

19072

E-mail: info@gbs-cidp.com

Website: www.gbs-cidp.org

Tel: 610-667-0131; 866-224-3301

Fax: 610-667-7036

1529
 For more information on neurologic disorders or research
programs funded by the National Institute of Neurological
Disorders and Stroke, contact the Institute’s Brain Resources and
Information Network (BRAIN) at:

Brain Resources and Information Network (BRAIN)

P.O. Box 5801

Bethesda, MD 20824

Tel: 800-352-9424

Fax: 301-402-2186

Email: braininfo@ninds.nih.gov

http://www.ninds.nih.gov

Additional nursing diagnoses

See also Urinary Retention in Acute Spinal Cord Injury (Chapter 3).
See Deficient Knowledge: Related to Postorgan Transplant Care
(Chapter 11). For other nursing diagnoses and interventions, see the
following as appropriate: Nutrition Support (Chapter 1),
Mechanical Ventilation (Chapter 1), Prolonged Immobility (Chapter
1), and Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2).

Status epilepticus
Pathophysiology
Status epilepticus (SE) is a state of recurring or continuous seizures
of at least 30 minutes’ duration, in which the patient does not return
to full consciousness from the postictal state before another seizure
occurs. A practical definition of SE may be revised to include
seizures of only 5 minutes’ duration, because of a high likelihood
that they will continue. If possible, treatment should be initiated

1530
immediately to prevent neuronal injury, which may begin within 20
to 30 minutes of the onset of SE. The mortality rate for SE is
estimated to be from 12% to 25%.
There are two major types of SE: convulsive and nonconvulsive.
Another classification is based on Gastaut and used by Engel in
which generalized SE includes convulsive SE (generalized tonic-
clonic seizures) and partial SE. Convulsive SE is more common and
is considered a life-threatening medical emergency, because the
hypoxia and metabolic exhaustion of neuronal tissue may cause
neuronal death. Partial SE includes simple partial SE (focal motor or
epilepsia partialis continua) and complex partial SE (temporal or
nontemporal seizures). The term “nonconvulsive status” may also
be used to describe absence, complex partial SE, and simple partial
SE. Clinical diagnosis of the type of nonconvulsive seizure activity
is difficult, and thus requires continuous video-
electroencephalographic (video-EEG) monitoring to validate that
the condition is present.
Refractory SE is present when the seizures, either convulsive or
nonconvulsive, continue despite treatment with a therapeutic dose
of a benzodiazepine and an initial loading dose of an
anticonvulsant.
SE in persons with epilepsy is often as a result of nonadherence
with medications or a drop in anticonvulsant serum levels caused
by alcohol abuse or infection. Other causes for individuals with and
without preexisting epilepsy include acute metabolic disturbances
(e.g., hypoglycemia, hyponatremia, hypocalcemia), stroke, CNS
infection (e.g., meningitis, encephalitis), CNS trauma or tumors,
sepsis, hypoxia, and alcohol or drug abuse. Prompt treatment may
prevent complications including cardiac dysrhythmias,
hyperthermia, aspiration, hypertension or hypotension, anoxia,
hyperglycemia or hypoglycemia, dehydration, rhabdomyolysis,
myoglobinuria, and oral and/or musculoskeletal injuries. The
prognosis of SE is thought to be related to the etiology and how fast
treatment is initiated.

Assessment
Goal of system assessment

1531
Evaluate for cessation of seizures, return to baseline neurologic
function, injury, and to determine cause of seizures.

History and risk factors

Epilepsy, drug or alcohol abuse, recent head injury, stroke or brain
tumor, CNS infection, headaches; if patient is in critical care or
hospital: sepsis and metabolic disturbance. If the patient is taking
anticonvulsant medications, note the following: drug name, dosage,
time last taken, length of time drug has been taken, and any recent
medication changes. Determine if the patient is taking any other
medications, including name, dosage, and time last taken. Some
medications may lower the seizure threshold.

Vital signs
Changes resulting from the massive sympathetic nervous system
response to continuous, generalized seizures include hypertension,
tachycardia, dysrhythmias, tachypnea, and hyperthermia.

Observation and seizure assessment

Evaluate for ongoing seizures.

• Changes or fluctuations in mental status such as confusion,

dreamy state, stupor, or changes in behavior.

• Automatisms.

• Lip smacking, chewing, swallowing.

• Speech difficulty.

• Twitching of the face, hand, arm, leg (focal motor seizures).

• Mild clonic movements (e.g., fluttering of the eyelids).

• Eye deviation or nystagmus.

• Tonic-clonic activity of all extremities.

Screening labwork

1532
Blood tests can reveal causes of seizures.

• Blood chemistries: Electrolyte imbalance or metabolic

disturbance.

• CBC: Elevated WBCs may indicate infection as cause.

• Anticonvulsant blood levels: Decreased or low levels may be

cause of return of seizures.

• Serum drug screen: Rule out drug or alcohol intoxication.

• ABGs: Obtain baseline levels and state of oxygenation.

Electroencephalography
Continuous EEG monitoring is used to determine whether the
patient is still in SE even though there are no clinical signs or very
subtle clinical signs and for those patients who are placed in a
medication-induced coma for refractory SE.

Diagnostic Tests for Status Epilepticus

Test Purpose Abnormal Findings

Electrolytes Assesses for possible causes of Hyponatremia, hypocalcemia,
Sodium status epilepticus (SE) hypoglycemia
Calcium
Magnesium
Glucose
Complete blood count Assesses for infection Infection may be a precipitant for
SE
Serum drug screen Assesses for drug and/or alcohol May be a precipitant for SE
intoxication
Antiepileptic drug Determines amount of drugs in Low levels may be cause of SE
levels the system
Arterial blood gases Obtains baseline levels and Acidosis: Respiratory and lactic;
determines oxygen saturation decreased oxygen saturation
attributable to convulsive SE and
medication administration
Continuous Evaluates cardiovascular status, Phenytoin and other antiepileptic
electrocardiographic especially during medication drugs can cause dysrhythmias and
monitoring administration hypotension
Continuous Evaluates electrical activity of Epileptiform discharges and
electroencephalographic the brain for ongoing seizures seizure activity
monitoring even if there are no clinical signs
of seizures
Computed tomography Evaluates for any brain Space-occupying lesions

1533
 brain scan abnormalities responsible for See meningitis section
Lumbar puncture SE
Assesses for abnormalities in the
central nervous system that
may indicate infection as a
reason for refractory status

Collaborative management
Care priorities

1. Support of ventilation and perfusion

Cardiopulmonary function and vital signs are closely monitored.
Measures should be initiated to maintain a patent airway, including
intubation, as well as ventilatory and cardiovascular support. The
metabolic rate and oxygen demands are high during constant
seizures, which prompt tachycardia to try to meet the demand. The
patient may need support to try to augment cardiac output if the
response is insufficient to meet the demand. Cardiac dysrhythmias,
hypertension or hypotension, and dehydration are common
complications of SE. More extensive evaluation for muscle damage
should be done if lengthy tonic-clonic seizures continue or occur
frequently. Patients can develop rhabdomyolysis, which may lead
to acute kidney injury if not appropriately managed.

2. Establish IV access
For medication administration, fluid resuscitation, and to draw
blood for needed labwork.

3. Pharmacotherapy
Prevention of Wernicke-Korsakoff syndrome: 100 mg IV thiamine
and 50 mL of 50% glucose are administered if chronic alcohol
ingestion or hypoglycemia is suspected.
First-line or emergent therapies
Administration of fast-acting anticonvulsant: Given to quickly
achieve high serum and brain concentrations. Not used as long-
acting anticonvulsant. First-line agents are benzodiazepines.
Treatment is most effective when started promptly.

1534
• Lorazepam (Ativan)

• Preferred by most epileptologists because

therapeutic effect is longer lasting.

• 0.1 mg/kg, up to 4 mg per dose, given IV, may

repeat in 5 to 10 minutes. Do not infuse faster than 2
mg/min.

• Monitor respiratory and cardiovascular status

continuously.
OR

• Diazepam (Valium)

• 0.15 mg/kg, up to 10 mg per dose, given IV, may

repeat in 5 minutes.

• Do not infuse faster than 5 mg/min to avoid

respiratory depression and hypotension, which
may occur with faster infusion rate.

OR

• Midazolam (Versed)

• 0.2 mg/kg intramuscularly up to maximum of 10

mg.

• Short duration of action, usually used in the field

before hospitalization or when IV access is not
available.

1535
• Monitor respiratory and cardiovascular status.

Second-line or urgent therapy

It is recommended to immediately start a second antiepileptic
drug after benzodiazepines. The drug of choice depends on several
factors, including etiology, comorbidities, and side effects. Several
trials have suggested that IV valproate may be as effective as
phenytoin. Phenobarbital is not used as frequently because of its
side effects and long half-life.
Administration of a long-acting anticonvulsant:

• Fosphenytoin (Cerebyx)

• Usual IV loading dose is 20 mg/kg PE (phenytoin

equivalents). Infusion rate is 100 to 150 mg PE/min.
Most IV solutions are compatible with
fosphenytoin, including dextrose solutions.
Phlebitis and soft tissue damage at IV site are not
seen as frequently with fosphenytoin.

• Monitor vital signs closely. Hypotension and

cardiac dysrhythmias may develop.

• If SE persists after 20 mg/kg, an additional 5 mg/kg

may be given 10 minutes after loading infusion.

OR (if fosphenytoin is not used)

• Phenytoin (Dilantin)

• Usual loading dose is 20 mg/kg given IV. Do not

infuse faster than 50 mg/min to avoid serious

1536
 dysrhythmias, including asystole.

• Phlebitis and soft tissue damage at IV site may

occur.

• Flush line with normal saline only.

Microcrystallization, which occurs when phenytoin
is used with dextrose, may also occur when it is
used in saline as a continuous drip.

• Monitor closely for hypotension and dysrhythmias,

and purple glove syndrome.

If given simultaneously with or after lorazepam or

diazepam, respiratory depression and hypotension can occur,
possibly necessitating ventilatory support.

Administration of IV valproate (Depacon)

• Usual dose is 20 to 40 mg/kg IV, an additional 20 mg/kg may be

given 10 minutes after initial dose.

• Infuse at 3 to 6 mg/kg/min.

• Monitor for hyperammonemia, pancreatitis, thrombocytopenia,

hepatotoxicity.

Administration of IV levetiracetam (Keppra)

• Usual dose is 1000 to 3000 mg IV.

• Infused at 2 to 5 mg/kg/min IV.

1537
 Administration of IV phenobarbital: Used if the patient is allergic
to phenytoin.

• Usual dose is 20 mg/kg. Do not infuse faster than 50 to 100

mg/min. May give additional 5 to 10 mg/kg, 10 minutes after
loading dose.

Neuromuscular blockade stops only movements (not brain

electrical activity) and should be administered only when
continuous electroencephalographic monitoring is available.

4. Treatment of refractory status

Aggressive treatment is required for refractory SE that continues
despite administration of benzodiazepines, phenytoin or
fosphenytoin, valproate, levetiracetam, and phenobarbital.
Consider deep sedation/general anesthesia using propofol,
midazolam, or pentobarbital.

• Consider use of additional IV boluses of antiepileptic drugs, IV

lacosamide, or topiramate by nasogastric tube.

• Continuous EEG monitoring is required for patients in refractory

SE to determine effectiveness of treatment.

• There are no current studies comparing these agents to help

determine which is the most effective in the treatment of
refractory SE.

Pentobarbital coma

• Loading dose is 5 to 15 mg/kg, may give additional

5 to 10 mg/kg; administer at an infusion rate less
than 50 mg/min. Maintenance dosage is 0.5 to 5

1538
 mg/kg/h to stop seizures.

• Monitor respiratory and cardiovascular activity

continuously.

• Mechanical ventilation required; vasopressors are

usually required.

• Periodic tapering of pentobarbital is done to see if

seizures have remitted.

• The patient may be in a coma for days to weeks.

Propofol

• Start at 20 µg/kg/min, with a loading dose of 1 to 2

mg/kg given IV. Initial maintenance dosage of 30 to
200 µg/kg/min to stop seizure activity. Adjust dose
according to EEG findings.

• Monitor respiratory and cardiovascular activity

continuously.

• Mechanical ventilation required; vasopressors are

usually required.

• Periodic tapering of propofol is done to see if

seizures have remitted.

Midazolam

• Loading dose is 0.2 mg/kg given by IV, administer

at an infusion rate of 2 mg/min. Maintenance

1539
 dosage of 0.05 to 2 µg/kg/h to stop seizure activity.

• Monitor respiratory and cardiovascular activity

continuously.

• Mechanical ventilation required; vasopressors are

usually required.

• Periodic tapering of midazolam is done to see if

seizures have remitted.

Other pharmacologic agents being used and studied in the

treatment of refractory status include ketamine, corticosteroids,
inhaled anesthetics, and IVIG and plasmapheresis.
Nonpharmacologic treatments that are being studied are vagus
nerve stimulation, ketogenic diet, hypothermia, electroconvulsive
therapy, transcranial magnetic stimulation, and emergency surgical
management. These are typically being done in patients in whom
all of the therapies discussed in this section have been ineffective in
controlling the status.
There is much to be gained in more research studies looking at
the best treatment for status that are based on better evidence than
is in the current literature.

Use of Sedation

A thorough neurologic evaluation to rule out organic causes of

agitation is indicated. Sedation may be used as adjunctive therapy
for patients with increased intracranial pressure (ICP) to reduce the
risk of extending the stroke, which in the worst case scenario may
result in permanent loss of ability to interact with the environment
or death. Benzodiazepines, fentanyl (Sublimaze), or morphine
sulfate are effective. Propofol (Diprivan) is a short-acting,

1540
intravenous hypnotic agent that is also cautiously used for sedation.
Pentobarbital coma is occasionally used for patients who experience
high ICP that does not respond to other forms of therapy. (See
Sedation and Neuromuscular Blockade, Chapter 1.)

5. Nutrition support
Enteral or parenteral nutrition may be necessary, depending on the
duration of the SE and the patient’s underlying nutritional state.

Care plans for status epilepticus

Impaired gas exchange 
related to altered oxygen supply associated with hypoventilation and
bradypnea secondary to depressant effect of seizures and medications on
respiratory center.
Goals/Outcomes: Within 1 hour of treatment/intervention, the
patient has adequate gas exchange, as evidenced by PaO2 greater
than 80 mm Hg, Paco2 35 to 45 mm Hg, pH 7.35 to 7.45, and RR 12 to
20 breaths/min with normal depth and pattern.
Respiratory Status: Ventilation.

Respiratory monitoring

1. Monitor for respiratory distress. Note RR, depth, and rhythm and
skin color. Report use of accessory muscles, rapid or labored
respirations, and cyanosis.

2. Monitor ABG values to assess oxygenation. Be alert to hypoxemia

(PaO2 less than 80 mm Hg) and respiratory acidosis (Paco2 greater
than 45 mm Hg; pH less than 7.35).

3. Keep intubation equipment ready for airway and ventilation

assistance.

4. Position an oral airway to help maintain open airway. Suction as

necessary.

5. Keep the patient turned to the side to allow secretions to drain.

1541
6. Administer oxygen as prescribed.

7. Administer antiepileptic medications within prescribed criteria to

avoid further depression of respiratory center.

Airway Management; Oxygen Therapy; Aspiration

Precautions.

Altered tissue perfusion: Cerebral and cardiopulmonary 

related to altered blood flow during continuous seizure activity or
vasodilatory effects of specific antiepileptic medications. Note: metabolic
demands of the brain and heart are increased greatly during seizure
activity; adequate cerebral perfusion is essential to maintain brain
function.
Goals/Outcomes: Within 1 hour of treatment/intervention, the
patient has adequate cerebral and cardiopulmonary perfusion, as
evidenced by orientation to time, place, and person; normal sinus
rhythm on ECG; BP within the patient’s normal range; RR 12 to 20
breaths/min with normal depth and pattern (eupnea); and absence
of headache, papilledema, and other clinical indicators of increased
ICP.
Tissue Perfusion: Cerebral; Tissue Perfusion: Cardiac.

Cerebral perfusion promotion

1. Support ventilation and perfusion for maximal delivery of

oxygen to the brain. Monitor vital signs every 2 to 5 minutes.
Respiratory depression, decreased BP, and dysrhythmias can occur
with rapid infusion of diazepam and phenytoin. BP must be
maintained within normal limits for optimal brain perfusion.

2. Monitor for dysrhythmias, especially during medication

administration.

3. Ensure safe administration of antiepileptic drugs: diazepam at 5

mg/min; lorazepam at 2 mg/min; phenobarbital at 50 to 100
mg/min; or phenytoin at 50 mg/min.

4. Perform baseline and serial neurologic assessments to determine

1542
the presence of focal findings that suggest an expanding lesion.

Cerebral Perfusion Promotion; Neurologic Monitoring;

Seizure Management; Cardiac Care: Acute.

Risk for trauma (oral and musculoskeletal) 

related to seizure activity
Goals/Outcomes: The patient’s mouth and extremities are not
injured during the seizure.
Tissue Integrity: Skin and Mucous Membranes.

Environmental management: Safety

1. Keep side rails padded and up at all times, with bed in the lowest
position.

2. Perform protective measures during the seizures:

• Put a soft object such as a flat pillow under the

patient’s head.

• Move sharp or potentially dangerous objects away

from the patient.

• Loosen any tight clothing.

• Avoid restraining the patient. The force of tonic-

clonic movements may cause strains and fractures
of extremities if thrashing occurs with restraints in
place.

• Avoid forcing airway into the patient’s mouth when

jaws are clenched. Force could break teeth, and the
patient could swallow or aspirate them.

1543
• Avoid use of tongue blade, which could splinter
and cut the mouth.

• Stay with the patient; assess and record seizure type

and duration. Record any automatic behavior (e.g.,
lip smacking, chewing movements), motor activity,
incontinence, tongue biting, and postictal state.

3. After seizure, reorient and reassure the patient.

Environmental Management: Safety; Positioning; Seizure

Precautions; Seizure Management.

Noncompliance with prescribed medication regimen 

related to misunderstanding of healthcare recommendations, not
understanding importance of following medication schedule, running out
of medication, stopping medication intentionally.
Goals/Outcomes: Within the 24-hour period before discharge
from the critical care unit, the patient verbalizes understanding of
the rationale and importance of taking the medication as
prescribed, as well as the consequence of noncompliance.
Compliance Behavior.

Mutual goal setting

1. Once a diagnosis of noncompliance with the medication regimen

has been established, determine the patient’s reason for
noncompliance.

2. Assess patient’s understanding of epilepsy and its treatment.

3. Ensure that the patient is aware that stopping the antiepileptic

medication can result in serious problems, including SE. If the
patient plans to stop the medication for any reason, he or she
should consult with the physician.

4. Evaluate the effect epilepsy has on the patient’s lifestyle.

1544
5. Once the cause of noncompliance is identified, work to find a
solution. If the patient has side effects from the medication, such as
gastric upset, suggest that the patient try taking the medication
after meals. If the gastric upset is a result of increasing the
medication, advise the patient to increase the dose more slowly.

6. Refer the patient to regional epilepsy support groups and the

Epilepsy Foundation of America (EFA), including regional affiliate
and national headquarters.

7. As appropriate, refer the patient to a nurse specialist or social

worker at a regional center for individual counseling.

Teaching: Prescribed Medication; Decision-Making Support;

Coping Enhancement; Values Clarification.

Deficient knowledge 
related to disease process, treatment, and lifestyle changes that epilepsy
necessitates.
Goals/Outcomes: Within the 24-hour period before discharge
from the critical care unit, the patient verbalizes understanding of
epilepsy, including its etiology and pathophysiology and seizure
classification, as well as its treatment and the lifestyle changes it
necessitates.
Knowledge: Disease Process.

Teaching: Disease process

1. Assess knowledge level and provide necessary information about

epilepsy.

2. Ask the patient to describe seizure(s) in detail, including warning

signals (aura) at the beginning of seizures. Explain that the aura or
warning signals onset of seizures and that the patient should lie
down or get into a safe position to prevent injury.

3. Assess the patient’s knowledge of antiepileptic medications,

including name(s), purpose, schedule, dosage, precautions, and
side effects. Reinforce importance of maintaining a constant blood

1545
level of medication by taking it as prescribed. Reinforce importance
of keeping appointments for labwork. Explain if the medication is
missed or taken erratically, he or she cannot attain the blood level
needed to prevent seizure breakthrough. If a dosage of medication
is missed, instruct the patient to notify the physician and/or
advanced practice provider.

4. Emphasize to the patient that a normal life is possible.

5. Ensure that the patient knows that sleep deprivation can

precipitate SE. Every patient must know his or her own limits.
Having epilepsy does not mean it is necessary to get more sleep
than do persons who do not have epilepsy.

6. Teach the patient/significant others the importance of safety

measures used during a seizure. Emphasize how to ease the patient
to the floor and turn him or her to a side-lying position.

7. Inform the patient of local driving regulations/laws for persons

with epilepsy.

8. Teach the patient the importance of avoiding dangerous

machinery and heights if his or her seizures are not being controlled
adequately by medications.

Teaching: Individual; Support Group.

Ineffective coping 
related to frustration related to unpredictable nature of the disease.
Goals/Outcomes: Within 24 to 48 hours of this diagnosis, the
patient verbalizes feelings, identifies strengths and ineffective
coping behaviors, and understands responsibility for self-care.
Coping.

Coping enhancement

1. Assess the patient’s knowledge of the disease and its treatment.

2. Encourage the patient to express feelings so that areas of major

concern are known.

1546
3. Involve the patient in decisions regarding care so that he or she
has more sense of control over life (e.g., encourage the patient to
participate in the decision for scheduling the medications). Problem
solve for major concerns.

4. Help the patient set realistic goals for employment and living
arrangements. Refer the patient to regional or local EFA as
appropriate.

5. Encourage the patient to educate others in what to do should a

seizure occur.

6. Encourage involvement in support groups; coping strategies can

be learned from other persons with seizures.

Coping Enhancement; Crisis Intervention; Emotional

Support; Support System Enhancement.

Additional nursing diagnoses

For other nursing diagnoses and interventions, see the following as
appropriate: Mechanical Ventilation (Chapter 1) and Emotional and
Spiritual Support of the Patient and Significant Others (Chapter 2).

Stroke: Acute ischemic and

hemorrhagic
Pathophysiology
The term stroke refers to a neurologic deficit caused by an acute
focal injury of the central nervous system (CNS) of vascular cause,
including cerebral infarction, intracerebral hemorrhage (ICH), and
subarachnoid hemorrhage. Stroke, previously termed
cerebrovascular accident (CVA), is the fourth-leading cause of
death in the United States. The American Heart Association (AHA)
estimates that approximately 795,000 people will have a new or
recurrent stroke annually of which 610,000 will be first-time strokes
and 185,000 will be recurrent strokes. Stroke was the underlying

1547
cause of death in 129,476 cases in 2010. Stroke is the leading cause
of long-term disability in the United States. Cost to treat stroke may
increase from $71.55 billion in 2010 to $183.13 billion in 2030 per
year, according to the American Heart Association/American Stroke
Association (AHA/ASA). One third of patients with stroke do not
survive, one third suffer with long-term disability, and one third
with no or minimal disability. Although men have a higher
incidence of stroke at younger ages, the incidence is reversed
and higher for women by age 75 years and older. Women
experience 55,000 more strokes each year than do men. In addition,
the risk of stroke varies with ethnicity and age. Blacks and
Hispanics are at increased risk compared with whites. The risk of
stroke increases with age; however, in 2009 34% of hospitalized
patients with stroke were younger than 65 years of age.
The classification of stroke depends on the preceding
pathophysiologic event. Eighty-seven percent are ischemic strokes,
10% are ICHs, and the remaining 3% are SAHs. Subcategories are
shown in Figure 7-1. Acute ischemic stroke (AIS) and ICH are
discussed here. Subarachnoid hemorrhage (SAH) from cerebral
aneurysmal rupture was discussed in an earlier section of this
chapter (see Cerebral Aneurysm and Subarachnoid Hemorrhage,
Chapter 7). A transient ischemic attack (TIA) is a temporary episode
of neurologic dysfunction, caused by focal brain, spinal cord, or
retinal ischemia, without acute infarction. Although not considered
a stroke, TIAs presage 15% of all strokes, and 12% of patients with a
TIA will die within 1 year. A TIA may precede an AIS by hours to
years. Studies of patients in Northern California showed that 5%
had strokes within 2 days, 11% within 3 months, and 33% within 1
year of having a TIA. Atherosclerosis of the arteries supplying the
brain is the most common cause of TIA. TIAs generally last less
than 24 hours, with most episodes persisting less than 1 hour.

1548
 FIGURE 7-1 Types of Stroke.

Before the introduction of thrombolytic therapy, a stroke was not

always considered a medical emergency, because there was little to
offer patients to stop the process. While therapies evolved, an AIS
became an emergency because treatment with thrombolytics must
be provided within 3 to 4.5 hours after symptom onset (also known
as “Time Last Known Well [TLKW]” or “Last Known Normal
[LKN]”) to be effective. The U.S. Food and Drug Administration
(FDA) has approved thrombolytic therapy within the first 3 hours
of TLKW. However, in one randomized clinical trial, IV
thrombolytics were shown to be beneficial when administered 3 to
4.5 hours after TLKW. Although not FDA-approved for use after 3
hours, the AHA/ASA guidelines do recommend initiation for
patients who meet the criteria. Exclusion criteria for thrombolytic
therapy 3 to 4.5 hours after TLKW include further criteria in
addition to those included in the 3-hour time window: persons
older than 80 year of age, a history of previous stroke and diabetes,

1549
any anticoagulant use before admission (even if international
normalized ratio [INR] is less than 1.7), NIH Stroke Scale greater
than 25, and CT findings involving more than one third of the
middle cerebral artery (MCA) territory (as evidenced by
hypodensity, sulcal effacement, or mass effect estimated by visual
inspection or use of the ABC/2 formula (ellipsoid) revealing a mass
of greater than 100 mL). Ideally, thrombolytics should be
administered within the first hour of arrival in a hospital/stroke
center. In many states, emergency medical services (EMS) have
been instructed to bypass noncertified primary stroke centers, and
take patients with stroke to advanced primary stroke centers or
comprehensive stroke centers for evidence-based care and best
possible outcomes. Patieents with hemorrhagic strokes may require
immediate treatment intervention to reduce intracranial pressure
(ICP), such as inserting a ventriculostomy to drain cerebral spinal
fluid (CSF). Regardless of the type of stroke, early assessment and
intervention is crucial in minimizing complications.
AIS most commonly results from atherosclerosis of blood vessels
perfusing the brain. Approximately 20% of AIS results from large
artery atherosclerotic disease (extracranial or intracranial), most
often associated with thrombus formation related to an unstable
plaque. A thrombus is a clot formed in the artery, usually in
branches with low flow resulting from plaque. Thrombotic strokes
are usually caused by local atherosclerosis of cerebral arteries.
Characteristic deficits are produced depending on the artery
involved (Table 7-5). Another 25% of AIS results from thrombosis of
small perforating intracranial arteries that result in lacunar or
subcortical strokes. An additional 20% of AIS results from low to
absent cerebral perfusion caused by cardiogenic emboli, most often
resulting from atrial fibrillation. Cerebral emboli may be formed in
the heart, in the carotid, or other cerebral arteries, and migrate to
occlude an artery in the brain. The remaining 30% are cryptogenic
and can include critically ill patients in shock experiencing systemic
hypoperfusion.

Table 7-5
CEREBRAL PERFUSION NEUROANATOMY RELATED TO
NEUROLOGIC DEFICIT

1550
Vessel Area Supplied Deficit
Internal Right or left hemisphere Contralateral motor or sensory deficit, aphasia with
carotid dominant hemisphere, neglect with nondominant
artery hemisphere, contralateral visual field deficit
(hemianopia), contralateral eye deviation
Middle Right or left convex surface of Contralateral hemiplegia (arm and face and leg),
cerebral the brain, most of the basal sensory involvement, aphasia of dominant
artery ganglia, internal capsule, hemisphere, neglect of nondominant hemisphere
putamen, and globus pallidus (denial of weakness), homonymous hemianopsia
Anterior Right or left frontal lobe, Weakness or sensory loss of contralateral leg and
cerebral corpus callosum, caudate proximal arm; behavior disturbance: abulia,
artery nucleus, internal capsule confusion, memory loss, urinary incontinence
Posterior Midbrain thalamus, choroid Contralateral visual field deficit, color blindness,
cerebral plexus, occipital lobe, and impaired depth perception, occasional sparing of
artery medial temporal lobe central vision, memory loss, sensory loss,
nystagmus, pupillary abnormalities, ataxia
Vertebral Medulla and/or cerebellum Face, nose, or eye ipsilateral numbness with
artery contralateral body numbness, facial weakness,
vertigo, ataxia, nystagmus, dysphagia, dysarthria
Basilar Pons, midbrain, and/or Quadriplegia or hemiplegia/paresis, dysarthria,
artery locked-in syndrome (pons) dysphagia, ataxia, nystagmus, vertigo, coma
cerebellum

Cerebral ischemia disrupts the sodium/potassium (Na+/K+) pump,

leading to neuronal depolarization and neurotransmitter release,
followed by a massive flux of ions and water resulting in brain cell
edema, extracellular K1, and intracellular calcium (Ca2+) increase.
Brain cells deprived of oxygen begin anaerobic metabolism, and the
resulting lactic acidosis and high concentration of intracellular Ca2+
lead to cellular death. Lactic acidosis prompts the CNS ischemic
response: The vasomotor center is stimulated, which causes
vasoconstriction with marked elevation in BP. Systolic BPs (SBPs)
less than 220 mm Hg and diastolic BPs (DBPs) less than 120 mm Hg
are not treated, because this is a natural response to perfuse the
ischemic brain. EMS is encouraged not to treat hypertension in the
field so as to maintain perfusion to the penumbra. If thrombolytic
therapy is to be initiated, the BP is lowered to less than 185/110 mm
Hg. This CNS ischemic response is seen during the acute phase of
stroke.
ICH can occur anywhere in the brain (Table 7-6 ). Although
various pathophysiologic events can result in ICH, the most
common cause is hypertension, usually resulting in the rupture of a
small penetrating artery in the subcortical region. Other causes
include bleeding disorders from anticoagulants, abnormal
vasculature, alcohol abuse, and liver disease. Damage occurs
because accumulated blood destroys and displaces the brain tissue.

1551
Disrupted tissue and the ruptured vessel reduce normal blood flow
to the area that surrounds the already injured brain tissue, resulting
in some ischemic injury. Intracerebral blood may rupture into the
ventricles, creating risk for communicating hydrocephalus. Lobar
hemorrhages are less common and most often occur in older adults
with cerebral amyloid angiopathy. Other common causes of
hemorrhage include vascular anomalies such as arterial venous
malformations (AVMs), arterial venous fistulas (AVFs), vasculitis,
neoplasms, hematologic disorders, and stimulant abuse (e.g.,
cocaine, amphetamines). Tighter BP control in the setting of acute
ICH to less than 160/90 mm Hg can limit the increase in ICH size
during the acute period.

Table 7-6
HEMORRHAGIC LOCATIONS AND SYNDROMES

Area Syndrome
Putamen Contralateral hemiplegia, hemisensory loss, hemianopsia, slurred speech
Thalamic Contralateral hemiplegia; hemisensory loss; small, poorly reactive pupils; decreased
level of consciousness
Pontine Locked-in syndrome (awake, aware, unable to verbally communicate,
quadriplegia), coma
Cerebellar Occipital headache, ataxia, dizziness, headache, nausea, vomiting
Lobar Mimics cerebral infarct (e.g., contralateral motor and sensory signs)

Assessment of stroke: Acute ischemic

stroke and intracranial hemorrhage
Goal of system assessment
During the hyperacute phase, determine stroke type, cause,
location, and eligibility for thrombolytic therapy. Then, evaluate for
risk factors of stroke extension or secondary neurologic injury.

History and risk factors

Evaluation can provide valuable clues that help facilitate the
diagnosis of stroke. Important aspects of a patient’s history include
the time a patient was last witnessed to be in their normal state
(TLKW or LKN), current anticoagulant use, history of previous

1552
stroke with residual disability, and history of recent surgeries,
bleeding, or any previous history of ICH.

• Risk factors commonly associated with AIS include the following:

Hypertension, smoking, diabetes mellitus, hypercholesterolemia,
atrial fibrillation, hormone replacement therapy, oral
contraceptives, dilated cardiomyopathy, ventricular thrombus
after acute MI, valvular disease, sedentary lifestyle, aging,
obesity, previous history of TIA or stroke, ethnicity including
Native American, Alaska Native, African American, or Hispanic
origin, previous MI, or family history of stroke or TIA. Risk
factors specific to women include pregnancy-associated
hypertension and preeclampsia. Additionally, the metabolic
syndrome, a combination of insulin resistance, abdominal
adiposity, hypercholesterolemia, and hypertension, contributes to
significantly more strokes in women than men.

• Risk factors commonly associated with ICH include hypertension,

smoking, African-American ethnicity, aging, excessive alcohol
consumption, bleeding disorders, and liver dysfunction, in
addition to known underlying vascular anomalies.

Vital sign assessment

• Measure BP according to stroke classification, and guidelines
pretherapy and posttherapy.

• Document mean arterial pressure (MAP) and track trends; titrate

medications to maintain measurements.

• Respiratory status: Rate, rhythm quality, and breath sounds;

proper positioning and turning to maintain adequate
oxygenation.

• Maintain PaO2 greater than 94% for adequate

oxygenation to the brain.

• A Glasgow Coma Scale (GCS) score of 8 or less,

1553
 rapidly decreasing GCS scores, or compromised
ventilation require emergent airway control via
rapid sequence intubation.

• Implement continuous cardiac monitoring: Observe

for dysrhythmias including QT prolongation, ST
segment depression, T wave inversion, U waves,
and ventricular ectopy.

• Dysrhythmias after stroke may be caused by the

release of catecholamines, resulting in
hypertension, cardiac irritability, and/or muscle
damage.

• ECG monitoring for the first 24 to 72 hours is

recommended. Individuals with new ECG changes
have a less favorable prognosis.

• Monitor for hyperthermia and hypothermia:

Maintain normal thermal temperature.
• Monitor blood glucose throughout hospitalization. Typically, it is
measured four times a day before meals and at bedtime, although
it varies depending on the level.

• Severe hyperglycemia is associated with decreased

reperfusion after thrombolytic therapy, expansion
of the infarcted area, and a poor prognosis.
Therefore, it must be measured before
administration of tissue plasminogen activator (tPA)
therapy.

1554
• Blood glucose should be maintained with a goal of
normoglycemia (less than 180 mg/dL).
Normoglycemic patients should not be given IV
fluids with excessive glucose, to avoid exacerbation
of ischemic injury resulting from hyperglycemia.

Neurologic evaluation: Observation

General presentation: Acute ischemic stroke and

intracranial hemorrhage
Signs and symptoms of stroke include sudden onset of weakness or
numbness of the face, arm, and/or leg, one-sided facial droop,
blurred or loss of vision in one eye, inability to produce or
understand speech, fixed gaze to the right or left side, change in
level of consciousness (LOC), neglect or ignoring of one side, ataxia,
and possible headache.

• Use a recognized Stroke Assessment Scale to identify deficits and

the time of onset: Several stroke assessment scales are available,
including the FAST (Face, Arm, Speech, Time), the Cincinnati
Prehospital Stroke Scale (CPSS), the Los Angeles Prehospital
Stroke Scale (LAPSS), Miami Emergency Neurologic Deficit
(MEND) examination, the Recognition of Stroke in the
Emergency Room Scale (ROSIER), and the Melbourne
Ambulance Stroke Scale (MASS). EMS is encouraged to do a
MEND assessment in the field, which is a combination of the
CPSS and NIH Stroke Scale (NIHSS). The MEND examination is
reproducible in the hospital setting.

• Rate stroke severity: Use the NIHSS, the shortened prehospital

version (sNIHSS), the Los Angeles Motor Scale, the European
Stroke Scale, or the Canadian Neurological Scale.

• Perform a complete neurologic assessment to establish baseline

status (see Neurological Assessment, Chapter 7).

1555
• Obtain information regarding baseline neurologic function (e.g.,
dementia, previous stroke, and neuropathy) and identify risk
factors associated with stroke.

Clinical presentation: Acute ischemic stroke (table 7-5)

• Sudden or acute onset of symptoms. Although both thrombotic

and embolic strokes can begin abruptly, the former are more
likely to evolve over several hours and may fluctuate over several
hours or days.

• Those with AIS do not usually experience pain other than a

headache, nor do they have altered LOC unless the stroke causes
mass effects as a result of swelling or involves the brainstem or
thalamic regions bilaterally.

• Women more often report stroke symptoms such as face and limb
pain, hiccups, nausea, general weakness, chest pain, palpitations,
fainting, shortness of breath, and seizures. Further research is
being conducted to better understand the gender differences
related to stroke.

• Embolic stroke: The deficit caused is usually maximal at onset

and often occurs during activity.

• Ischemic stroke caused by MCA occlusion: In the dominant

hemisphere, patients are usually awake with hemiparesis,
aphasia, visual field cut, and sensory loss. In the nondominant
hemisphere, patients are usually awake with hemiparesis, neglect
including denial of their own weakness and denial of their own
contralateral limbs, visual field cut, and sensory loss.

• Acute hemispheric infarction: People have elevated arterial BP

and often appear drowsy even in the absence of swelling.

Clinical presentation: Intracranial hemorrhage (table 7-6)

• Severe headache, altered LOC, vomiting, very high BP, and

increased ICP.

1556
• Symptoms of ICH depend on the size and location of the
hematoma. A relatively small hemorrhage into the brainstem
may produce quadriplegia and coma, whereas a hematoma of
similar size in the basal ganglia may produce hemiparesis
without altered LOC. A larger hematoma (as measured by CT
brain scan) may indicate a poorer prognosis.

• The neurologic deficit may evolve over minutes to a few hours.

Screening neurologic imaging

CT imaging of the head without contrast is diagnostic for ICH
and guides decision-making for treatment.

• Prepare to transfer the patient to radiology for immediate acute

imaging of the brain.

• Continue aggressive monitoring of vital signs and neurologic

status while maintaining safety of the patient during transport.

Screening labwork
• Biochemical profile: Evaluates for abnormal glucose and
electrolyte imbalances.

• On admission, screening for hypoglycemia is the

only mandatory laboratory test, although other tests
may be performed.
• Coagulation profile: To determine risk for bleeding and/or
clotting.

• Complete blood count: Evaluates for abnormal platelets, sepsis,

and anemia.

• Cardiac biomarkers: Troponin may be used to evaluate for

cardiac ischemia.

• Toxicology: May be used to determine if intoxication is related to

1557
 neurologic changes.

Diagnosis of Acute Ischemic Stroke versus Hemorrhagic Stroke

1558
Collaborative management
AMERICAN HEART ASSOCIATION/AMERICAN STROKE
ASSOCIATION GUIDELINES FOR ACUTE ISCHEMIC STROKE AND
HEMORRHAGIC STROKE MANAGEMENT ARE THE MOST
REFERENCED PUBLICATIONS FOR SETTING THE STANDARDS
OF PRACTICE

*
Indicators for both acute ischemic stroke and intracranial hemorrhage.

For certification by The Joint Commission, stroke centers

must meet specific standards. Guidelines indicate that tPA must be
administered within 60 minutes of arrival. To maintain certification,
stroke centers must meet these time requirements in at least 50% of
patients with stroke.

1. Door to physician time (less than 10 minutes).

2. Door to laboratory time (less than 10 minutes).

3. Door to CT (less than 25 minutes).

4. Door to laboratory results (less than 45 minutes).

5. Door to needle time (less than 60 minutes).

Care priorities

1559
Goals of management are to prevent secondary neurologic damage,
secondary complications, and to promote optimal functional
outcome. Early detection via accurate neurologic examination and
immediate medical or surgical intervention help prevent stroke
extension, increased brain edema, and hydrocephalus. Physical
examination findings guide medical and nursing interventions. The
Joint Commission requires the following list of interventions for
certified stroke centers: initiation of DVT prophylaxis, discharge on
antithrombotic medications, anticoagulation therapy for patients
with atrial fibrillation/flutter, administration of thrombolytic
therapy, initiation of antithrombotic therapy by the end of the
second hospital day, stroke education, and assessment for
rehabilitation.

1. Rapidly evaluate patients for type of stroke and

minimize brain damage
Medical Therapies:

• Oxygen therapy: Maintain oxygen saturation of at least 94% using

2 to 3 L nasal cannula oxygen. Maximizing oxygenation is of
paramount importance for all patients with stroke.

• Hydration: IV fluids (initially without dextrose) help maintain

adequate circulating blood volume.

• For intracranial hemorrhage: Replace platelets or coagulation

factors if needed. If INR is elevated, hold warfarin and treat with
prothrombin complex concentrate, fresh-frozen plasma, and/or
vitamin K.

Acute Ischemic Stroke:

• Thrombolysis: Clots are “dissolved” using IV recombinant tissue

plasminogen activator (rtPA). The window of treatment for
ischemic stroke has been extended from 3 hours to 4.5 hours after
onset of symptoms. Stroke centers strive to provide rtPA within 1
hour of arrival. Vital signs and neurologic assessments should be
performed every 15 minutes after rtPA initiation for a total of 2
hours. Following these 2 hours, monitor vital signs and perform

1560
 neurologic examinations every 30 minutes for 6 hours and then
every hour for 16 hours. Heparin, aspirin, clopidogrel,
dipyridamole, or warfarin should NOT be given for the initial 24
hours, after which these antithrombotic agents should be started
as prescribed. During and following infusion, monitor for major
and minor bleeding complications. Continuous cardiac
monitoring should remain in place for at least 72 hours.

HIGH ALERT!
If the patient experiences profound deterioration in neurologic
status during recombinant tissue plasminogen activator (rtPA)
infusion, a hemorrhagic complication may have ensued. If
suspected, the rtPA infusion should be discontinued immediately.
Subsequent measurements include vital signs and neurologic
assessments every 15 minutes, and consideration of
hyperventilation, mannitol infusion, administration of blood
products (cryoprecipitate, fresh-frozen plasma, platelets, factor
VIIa, and packed red blood cells), possible initiation of
hemodynamic monitoring, and further neurodiagnostic testing and
laboratory tests to evaluate the potential for further bleeding.
Antithrombotic Therapy: Antithrombotics should be ordered
within the first 24 hours of admission for those who are ineligible
for thrombolysis. Continuous cardiac monitoring should be
provided for up to 48 hours for patients ineligible for thrombolysis.

• Antiplatelet therapy: Used to reduce risk of ischemic stroke and

decrease frequency of TIAs. Aspirin (50 to 325 mg/day dosage
range) is the most common agent, usually given once daily.
Aspirin/extended-release dipyridamole 25/200 mg (Aggrenox) is
given twice daily, but more than 30% of patients who take it have
headaches. However, the dose may be titrated to reduce this side
effect. Clopidogrel (Plavix) 300 mg may be given as a loading
dose followed by 75 mg daily.

• Anticoagulation: If long-term anticoagulation is planned, the

1561
 patient is converted to oral warfarin (Coumadin) therapy or
newer anticoagulants, including direct thrombin inhibitors.

Interventional approaches for acute ischemic stroke

• Intraarterial thrombolysis using rtPA has a 6-hour window in

which to implement the therapy directly into the cerebral
vasculature. This approach is much more successful with strokes
secondary to large vessel occlusion.

• Mechanical disruption of the clot using stent retrievers have been

shown to be most effective as revascularization tools and consist
of deploying a stent into the clot and subsequently pulling the
stent and associated clot out. The Penumbra Stroke System is a
suction device that breaks down and sucks the clot back through
the catheter. Both devices may dislodge the clot and cause it to
migrate distally.

• Carotid stenting: Stents may be used for carotid stenosis. Patients

who meet criteria include those who are not surgical candidates
and are symptomatic from their carotid stenosis.

Endovascular surgery: Interventional approaches for

intracranial hemorrhage

• Patients may have an AVM or AVF as an underlying cause for

hemorrhage. These lesions are embolized using a single therapy
or an adjunctive therapy before surgical removal of the vascular
anomaly or use of radiosurgery. Embolization may be achieved
using either a polymer or “glue,” or GDC coils, which are placed
to occlude the malformation (see Cerebral Aneurysm and
Subarachnoid Hemorrhage, Chapter 7).

2. Manage hypertension and stabilize vital signs

Antihypertensives are frequently used in the stroke population to
control hypertension. If IV thrombolysis is administered, SBP must
remain less than 185 mm Hg and DBP less than 110 mm Hg during
and following therapy, to reduce risk of symptomatic ICH. For
long-term management, antihypertensive agents are selected based

1562
on the individual’s medical history. Long-term therapy may be
prescribed based on the Eighth Joint National Committee (JNC 8)
guidelines (Table 7-7). SBP is often elevated in the acute phase and
requires vasoactive IV medications such as nicardipine (Cardene
IV) or labetalol (Normodyne). Hypotension is a concern, especially
in the patient with ICH, because MAP is decreased. If MAP is
decreased in the presence of normal or elevated ICP, a decrease in
CPP results, further compromising neurologic status. Vasopressors
and/or inotropes may be titrated to keep MAP high enough to
maintain CPP greater than 60 mm Hg.
Acute Ischemic Stroke:

• Patients eligible for a reperfusion strategy (including tPA) with

SBP of greater than 185 mm Hg or DBP greater than 110 mm Hg
should have BP reduced to less than 185 mm Hg and DBP to less
than 110 mm Hg before beginning the reperfusion strategy. tPA
is contraindicated if BP cannot be reduced to these
measurements. For at least 24 hours after reperfusion, SBP for
those who were initially hypertensive should be maintained at
less than 180 mm Hg with DBP less than 105 mm Hg. The
advanced practice provider should be notified of an SBP greater
than 180 mm Hg or less than 110 mm Hg, DBP greater than 105
mm Hg or less than 60 mm Hg, HR less than 50 bpm or greater
than 110 bpm, RR greater than 24 breaths/min, temperature
greater than 37.5° C (99.6° F), or a deterioration in neurologic
status.

• Patients who have concomitant medical problems that require

management of hypertension should be provided with
aggressive BP reduction.

• Patients who are not eligible for thrombolytic therapy should

have BP reduced to less than 220 mm Hg, with DBP reduced to
less than 120 mm Hg. The advanced practice provider should be
called if the SBP is greater than 220 mm Hg or less than 110 mm
Hg, the DBP is greater than 120 mm Hg or less than 60 mm Hg,
HR is less than 50 bpm or greater than 110 bpm, RR is greater
than 24 breaths/min, temperature is greater than 37.5° C (99.6° F),
or if there is a deterioration in neurologic status.

1563
 Intracranial Hemorrhage:
The AHA/ASA guidelines recommend the following for
management of BP in patients with ICH/acute cerebral hemorrhage:

• If SBP is greater than 200 mm Hg or MAP is greater than 150 mm

Hg, aggressive BP reduction should be considered with
continuous IV infusion; BP should be monitored every 5 minutes.

• If SBP is greater than 180 mm Hg or MAP is greater than 130 mm

Hg with possibly elevated ICP, reduction of BP with concurrent
ICP monitoring should be considered to assist in keeping CPP at
60 to 80 mm Hg.

• If SBP is greater than 180 mm Hg or MAP is greater than 130 mm

Hg and there is no indication of increased ICP, reduction of MAP
to less than 110 mm Hg or 160/90 mm Hg (a moderate reduction)
should be considered.

• Patients with hypotension should be evaluated and treated using

standard therapy with aggressive fluid resuscitation, and
determination of the etiology of low BP, including hypovolemia
and dysrhythmias. Vasopressors may be used if absolutely
necessary to raise BP to improve cerebral blood flow.

3. Monitor icp and manage cpp

CPP − MAP = ICP (keep CPP greater than 60 mm Hg). Invasive
monitoring may be necessary for patients with increased infarct
size, increased edema, and hydrocephalus. Patients with increased
ICP may receive mannitol or hypertonic saline, which lowers ICP
by reducing water within brain cells. Careful monitoring of ICP for
rebound effect is necessary after mannitol infusion. Patients should
remain on bed rest until stabilized. Serum osmolality should be
assessed to prevent excessive dehydration. Patients with
hydrocephalus often require a ventriculostomy. For more
information about ICP monitoring and CPP management, see
Traumatic Brain Injury, Chapter 3.

• Invasive monitoring: Assessment and maintenance of neurologic

monitors is an essential part of the neurologic assessment.

1564
• ICP monitoring: Ensure an adequate wave form, zero balance
equipment, and patency of tubing (if applicable), and maintain
sterility of system. Increased ICP is attributable to extension of
the infarct or hematoma and its associated edema. May cause
midline shift and herniation; increased ICP is associated with
hydrocephalus after ICH; seizures generally occur within the first
24 hours but may present at any time.

• Extraventricular drainage: Maintain sterility of system and proper

positioning for drainage. Maintain patency. Observe/document
color, consistency, and amount of CSF.

4. Prevent stroke extension

The opportunity to prevent further stroke depends on adequate
perfusion of the penumbra, which is the ischemic brain tissue
surrounding the initial infarct that is at immediate risk of infarction.
Perfusing the penumbra decreases the potential infarct size and
optimizes patient outcome. A “normal” BP may be too low, causing
further ischemia and infarct by decreasing cerebral perfusion.
Arterial BP should not be lowered abruptly in patients with AIS. At
times, maintenance of a somewhat elevated BP may be warranted,
depending on the underlying vascular and brain pathology. In
contrast, with ICH many practitioners believe that an elevated BP
should be reduced aggressively. The best approach is unclear, and
therefore the treatment of increased BP in ICH requires individual
consideration (Table 7-7).

Table 7-7
CLASSIFICATION AND MANAGEMENT OF BLOOD PRESSURE
FOR ADULTS

*
ACEIs and ARBs should not be used in combination. Beta-blockers, aldosterone

1565
antagonists, or other antihypertensives may be added if initial therapy combination is
ineffective.
†
Initial combined therapy should be used cautiously in those at risk for orthostatic
hypotension.
From Dennison-Himmelfarb C, Handler J, Lackland DT, et al: 2014 evidence-based
guideline for the management of high blood pressure in adults report from the panel
members appointed to the Eighth Joint National Committee (JNC 8). JAMA 311:507-
520, 2014.
ACEI, Angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker;
BP, blood pressure; CCB, calcium channel blocker.

Choose evidence-based tools for monitoring neurologic changes:

• NIH Stroke Scale (NIHSS) (Table 7-8): Provides a better

measurement of deficits and is easy to use. It also guides the
examiner in evaluating cognitive, language, and motor deficits
that are unique to stroke. A comprehensive neurologic
assessment assists the critical care nurse in detecting changes in
neurologic status and the response to interventions.

• Glasgow Coma Scale (GCS) (see Appendix 2): Used to measure

changes in LOC in those who cannot participate in NIHSS.

5. Prevention of recurrent stroke

• Target BP should be individualized to each patient. Patients with

moderate hypertension may benefit from a drop of 10 mm Hg
SBP and 5 mm Hg DBP.

• Lifestyle changes should be part of all stroke prevention

programs.

• The JNC 8 report should be used to guide the choice of

antihypertensive medications. Ideal choices remain uncertain. A
diuretic coupled with an angiotensin-converting enzyme
inhibitor (ACEI) is acceptable. For some patients, the choice of a
specific class of antihypertensive medication is clearer (see Table
7-7).

6. Manage agitation

1566
 Antibiotics are given immediately after lumbar puncture or
CT and after blood cultures.

7. Optimize regulatory functions

To prevent secondary complications, see Table 7-9. In general,
patients with stroke need adequate cerebral blood flow and
perfusion with adequate glucose and oxygenation. Nursing
interventions help facilitate optimal cerebral perfusion.

Table 7-9
MAINTENANCE OF NORMAL REGULATORY FUNCTIONS IN
STROKE

Function Goal/Rationale Intervention(s)

Optimal body Facilitate cerebral blood flow: Keep HOB elevated 25 to 30 degrees.
position An ideal position has not been Lower HOB to flat to increase cerebral
determined. Patient response perfusion. HOB should be elevated to
determines the best position. decrease ICP in patients with
Arterial perfusion improves with hemorrhagic strokes. Keep neck neutral;
head down, whereas venous avoid bending at the waist.
drainage improves with head
elevated.
Temperature Maintain normothermia: Temperature greater than 38° C (100.4°
Decreases metabolic demands and F) should be treated with
ICP. acetaminophen.
Breathing and Maximize oxygenation: Administer O2, individualize
patent airway Optimizes O2 delivery to the brain, positioning, pulmonary toilet;
prevents atelectasis and Suctioning: No longer than 10 seconds
pneumonia; reducing in duration; preoxygenate with 100% for
intrathoracic and intraabdominal full 2 minutes between each attempt; his
pressures helps to prevent or her do not provide overly aggressive
increased ICP; the patient may be manual ventilation when suctioning.
unable to protect his or her
airway, resulting in aspiration of
secretions.
Circulation Control dysrhythmias and Monitor dysrhythmias for at least 24
promote electrolyte balance: hours; cardiac monitoring should be
Normal sinus rhythm optimizes continued for 72 hours if thrombolytics
CO to promote perfusion to the were used. Manage fluid and electrolyte
brain; hemorrhagic strokes are imbalances. Administer IV fluids at 75
more likely to cause mL/h during the first 1 to 3 days,
dysrhythmias. depending on the patient’s initial
Promote hydration: Helps hydration status.

1567
 maintain normal circulating
blood volume.
Digestion and Prevent aspiration pneumonia: NPO until ability to swallow has been
bowel Swallowing dysfunction may be evaluated within the 24 hours of
elimination present. Reduce incidence of stress hospitalization. Bedside swallow may
ulcers and constipation: Straining precede modified barium swallow.
with bowel movements increases Initiate proton pump inhibitors or H2-
ICP. blockers and a bowel program. H2-
blockers may cause delirium.

Cellular glucose Maintain a normal blood glucose Aggressively manage blood glucose to
supply level: Optimizes brain cell function control hyperglycemia and prevent/treat
by ensuring adequate intracellular hypoglycemia; avoid glucose-containing
supply of glucose. IV solutions in the emergency
department.
Nourishment Maintain an anabolic state; prevent Initiate nutrition as soon as possible;
catabolism: Promote optimal enteral feeding, then long-term diet to
healing opportunity and prevent meet caloric needs; low-Na+, low-fat,
recurrent stroke by controlling weight reduction if needed.
CVD/ASHD risk factors.
Urinary Prevent urinary tract infection and Prevent unnecessary use of urinary
continence skin breakdown: Removal of Foley Foley catheter; remove within 48 hours
catheter may prompt skin if possible; bladder training as soon as
breakdown if the patient is possible.
incontinent.
Mobility and Promote proper body alignment Perform ROM exercises, regular
endurance and muscle strengthening: repositioning; increase activity as
Prevents contractures, DVT, and tolerated; use mobility beds if needed.
complications of immobility. Initiate DVT prophylaxis.
Skin integrity Prevent skin breakdown and Keep skin clean and dry; use pressure
dependent edema relief surfaces.
Communication Develop appropriate Provide pictorial board so that the
communication techniques; patient can point at needs, ask yes and
promotes sense of well-being and no questions that do not require long
facilitates more timely response to answers, provide pencil and paper for
patient needs when requests are those who can write; ensure glasses and
understood. hearing aides are in place for those who
use them.
CO, Cardiac output; CVD/ASHD, cardiovascular disease/atherosclerotic heart
disease; DVT, deep venous thrombosis; HOB, head of the bed; ICP, intracranial
pressure; IV, intravenous; Na1, sodium; NPO, nothing by mouth; O2, oxygen; ROM,
range of motion.

8. Provide rehabilitation
Should begin immediately once stabilized. Consults to a physiatrist,
physical therapist, occupational therapist, and speech therapist
should be made within the first 24 hours. Death within the first
month after stroke is commonly caused by acute MI, pneumonia,
and sepsis, which can result from inactivity. Pulmonary embolism,
DVT, skin breakdown, and depression are also common.

1568
9. Manage seizures
Anticonvulsant therapy is used for seizures in the acute phase.
Generally, the patient is given a loading dose of phenytoin
(Dilantin) or fosphenytoin (Cerebyx), followed by a maintenance
dosage. Benzodiazepines (e.g., Ativan) may be used initially.
Patients with ICH are given seizure prophylaxis, whereas patients
with AIS are managed only when active seizures are present.
Temperature greater than 38° C (100.4° F) should be treated with
acetaminophen.

10. Surgical management

• Carotid endarterectomy: Surgical removal of plaque in the

obstructed carotid artery to promote blood supply to the brain
should be performed within 2 weeks following a minor,
nondisabling stroke. Carotid endarterectomy is the treatment of
choice for patients with greater than 70% symptomatic carotid
stenosis.

• Craniotomy: Often young patients with AIS need to be watched

carefully for signs of increased ICP and pending herniation as a
result of the lack of space in the cranium. A hemicraniectomy
may be considered as a preventative measure for patients
younger than 60 years of age with large MCA infarcts who have
limited comorbidities. Hematoma evacuation may be performed
by aspiration through a burr hole or clot evacuation by
craniotomy for patients who have expanding clot, uncontrolled
ICP, edema, or mass effect.

Nursing care plans: Acute ischemic stroke

and intracranial hemorrhage
Decreased intracranial adaptive capacity 
related to interrupted blood flow secondary to thrombus or embolus.
Goals/Outcomes: Within 72 hours of diagnosis, the patient has
adequate cerebral tissue perfusion, as evidenced by no decrease in
LOC; no deterioration in motor function on affected side; and no

1569
new or further deterioration of language, cognition, or visual field
per NIHSS (see Table 7-8).

Table 7-8
NATIONAL INSTITUTES OF HEALTH STROKE SCALE (NIHSS)

Patient Identification __ __.__ __ __.__ __ __

Pt. Date of Birth __ __/__ __/__ __
Hospital ______(__ __.__ __)
Date of Exam __ __/__ __/__ __
Interval: [ ] Baseline   [ ] 2 hours post treatment   [ ] 24 hours post onset of symptoms ±20
minutes [ ] 7-10 days   [ ] 3 months   [ ] Other ______(___ ___)
Time: ___ ___:___ ___ [ ]am [ ]pm
Person Administering Scale _______________________________________________
Administer stroke scale items in the order listed. Record performance in each category after
each subscale exam. Do not go back and change scores. Follow directions provided for each
exam technique. Scores should reflect what the patient does, not what the clinician thinks the
patient can do. The clinician should record answers while administering the exam and work
quickly. Except where indicated, the patient should not be coached (i.e., repeated requests to
patient to make a special effort).
Instructions Scale Definition Score
1a. Level of Consciousness (LOC): The investigator must 0 Alert; keenly responsive. ______
choose a response if a full evaluation is prevented by 1 Not alert; but arousable
such obstacles as an endotracheal tube, language barrier, by minor stimulation to
orotracheal trauma/bandages. A 3 is scored only if the obey, answer, or
patient makes no movement (other than reflexive respond.
posturing) in response to noxious stimulation. 2 Not alert; requires
repeated stimulation to
attend, or is obtunded
and requires strong or
painful stimulation to
make movements (not
stereotyped).
3 Responds only with
reflex motor or
autonomic effects or
totally unresponsive,
flaccid, and flexic.
1b. LOC Questions: The patient is asked the month and 0 Answers both questions ______
his/her age. The answer must be correct; there is no correctly.
partial credit for being close. Aphasic and stuporous 1 Answers one question
patients who do not comprehend the questions will correctly.
score 2. Patients unable to speak because of endotracheal 2 Answers neither
intubation, orotracheal trauma, severe dysarthria from question correctly.
any cause, language barrier, or any other problem not
secondary to aphasia are given a 1. It is important that
only the initial answer be graded and that the examiner
not “help” the patient with verbal or nonverbal cues.
1c. LOC Commands: The patient is asked to open and 0 Performs both tasks ______
close the eyes and then to grip and release the correctly.
nonparetic hand. Substitute another one-step command 1 Performs one task
if the hands cannot be used. Credit is given if an correctly.
unequivocal attempt is made but not completed as a 2 Performs neither task
result of weakness. If the patient does not respond to correctly.

1570
 command, the task should be demonstrated to him or
her (pantomime), and the result scored (i.e., follows
none, one, or two commands). Patients with trauma,
amputation, or other physical impediments should be
given suitable one-step commands. Only the first
attempt is scored.
2. Best Gaze: Only horizontal eye movements will be 0 Normal. ______
tested. Voluntary or reflexive (oculocephalic) eye 1 Partial gaze palsy; gaze
movements will be scored, but caloric testing is not is abnormal in one or
done. If the patient has a conjugate deviation of the eyes both eyes, but forced
that can be overcome by voluntary or reflexive activity, deviation or total gaze
the score will be 1. If a patient has an isolated peripheral paresis is not present.
nerve paresis (cranial nerves III, IV, or VI), score a 1. 2 Forced deviation, or
Gaze is testable in all aphasic patients. Patients with total gaze paresis not
ocular trauma, bandages, preexisting blindness, or other overcome by the
disorder of visual acuity or fields should be tested with oculocephalic maneuver.
reflexive movements, and a choice made by the
investigator. Establishing eye contact and then moving
about the patient from side to side will occasionally
clarify the presence of a partial gaze palsy.
3. Visual: Visual fields (upper and lower quadrants) are 0 No visual loss.
tested by confrontation, using finger counting or visual 1 Partial hemianopia.
threat, as appropriate. Patients may be encouraged, but 2 Complete hemianopia.
if they look at the side of the moving fingers 3 Bilateral hemianopia (blind
appropriately, this can be scored as normal. If there is including cortical blindness).
unilateral blindness or enucleation, visual fields in the
remaining eye are scored. Score 1 only if a clear-cut
asymmetry, including quadrantanopia, is found. If the
patient is blind from any cause, score 3. Double
simultaneous stimulation is performed at this point. If
there is extinction, the patient receives a 1, and the
results are used to respond to item 11.
4. Facial Palsy: Ask or use pantomime to encourage the 0 Normal symmetrical
patient to show teeth or raise eyebrows and close eyes. movements.
Score symmetry of grimace in response to noxious 1 Minor paralysis (flattened
stimuli in the poorly responsive or noncomprehending nasolabial fold, asymmetry on
patient. If facial trauma/bandages, orotracheal tube, smiling).
tape, or other physical barriers obscure the face, these 2 Partial paralysis (total or near-
should be removed to the extent possible. total paralysis of lower face).
3 Complete paralysis of one or
both sides (absence of facial
movement in the upper and
lower face).
5. Motor Arm: The limb is placed in the appropriate 0 No drift; limb holds 90 (or 45)
position: extend the arms (palms down) 90 degrees (if degrees for full 10 seconds.
sitting) or 45 degrees (if supine). Drift is scored if the 1 Drift; limb holds 90 (or 45)
arm falls before 10 seconds. The aphasic patient is degrees, but drifts down before
encouraged using urgency in the voice and pantomime, full 10 seconds; does not hit bed
but not noxious stimulation. Each limb is tested in turn, or other support.
beginning with the nonparetic arm. Only in the case of 2 Some effort against gravity; limb
amputation or joint fusion at the shoulder, the examiner cannot get to or maintain (if
should record the score as untestable (UN), and clearly cued) 90 (or 45) degrees, drifts
write the explanation for this choice. down to bed, but has some effort
against gravity.
3 No effort against gravity; limb
falls.
4 No movement.

1571
 UN Amputation or joint fusion,
explain: _______
5a. Left Arm
5b. Right Arm
6. Motor Leg: The limb is placed in the appropriate 0 No drift; leg holds 30-degree
position: hold the leg at 30 degrees (always tested position for full 5 seconds.
supine). Drift is scored if the leg falls before 5 seconds. 1 Drift; leg falls by the end of the
The aphasic patient is encouraged using urgency in the 5-second period but does not hit
voice and pantomime, but not noxious stimulation. Each bed.
limb is tested in turn, beginning with the nonparetic leg. 2 Some effort against gravity; leg
Only in the case of amputation or joint fusion at the hip, falls to bed by 5 seconds, but has
the examiner should record the score as untestable (UN), some effort against gravity.
and clearly write the explanation for this choice. 3 No effort against gravity; leg
falls to bed immediately.
4 No movement.
UN Amputation or joint fusion,
explain: _______
6a. Left Leg
6b. Right Leg
7. Limb Ataxia: This item is aimed at finding evidence of a 0 Absent.
unilateral cerebellar lesion. Test with eyes open. In case 1 Present in one limb.
of visual defect, ensure testing is done in intact visual 2 Present in two limbs.
field. The finger-nose-finger and heel-shin tests are UN Amputation or joint fusion,
performed on both sides, and ataxia is scored only if explain: _______
present out of proportion to weakness. Ataxia is absent
in the patient who cannot understand or is paralyzed.
Only in the case of amputation or joint fusion, the
examiner should record the score as untestable (UN),
and clearly write the explanation for this choice. In case
of blindness, test by having the patient touch nose from
extended arm position.
8. Sensory: Sensation or grimace to pinprick when tested, 0 Normal; no sensory loss.
or withdrawal from noxious stimulus in the obtunded or 1 Mild-to-moderate sensory loss;
aphasic patient. Only sensory loss attributed to stroke is the patient feels pinprick is less
scored as abnormal, and the examiner should test as sharp or is dull on the affected
many body areas (arms [not hands], legs, trunk, face) as side; or there is a loss of
needed to accurately check for hemisensory loss. A score superficial pain with pinprick,
of 2, “severe or total sensory loss,” should only be given but the patient is aware of being
when a severe or total loss of sensation can be clearly touched.
demonstrated. Stuporous and aphasic patients will, 2 Severe-to-total sensory loss; the
therefore, probably score 1 or 0. The patient with patient is not aware of being
brainstem stroke who has bilateral loss of sensation is touched in the face, arm, and
scored 2. If the patient does not respond and is leg.
quadriplegic, score 2. Patients in a coma (item 1a = 3) are
automatically given a 2 on this item.
9. Best Language: A great deal of information about 0 No aphasia; normal.
comprehension will be obtained during the preceding 1 Mild-to-moderate aphasia; some
sections of the examination. For this scale item, the obvious loss of fluency or facility
patient is asked to describe what is happening in the of comprehension, without
attached picture, to name the items on the attached significant limitation on ideas
naming sheet, and to read from the attached list of expressed or form of expression.
sentences. Comprehension is judged from responses Reduction of speech and/or
here, as well as to all of the commands in the preceding comprehension, however, makes
general neurologic exam. If visual loss interferes with conversation about provided
the tests, ask the patient to identify objects placed in the materials difficult or impossible.
hand, repeat, and produce speech. The intubated patient For example, in conversation
should be asked to write. The patient in a coma (item 1a about provided materials, the

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 = 3) will automatically score 3 on this item. The examiner can identify picture or
examiner must choose a score for the patient with stupor naming card content from the
or limited cooperation, but a score of 3 should be used patient’s response.
only if the patient is mute and follows no one-step 2 Severe aphasia; all
commands. communication is through
fragmentary expression; great
need for inference, questioning,
and guessing by the listener.
Range of information that can be
exchanged is limited; listener
carries burden of
communication. The examiner
cannot identify materials
provided from the patient
response.
3 Mute, global aphasia; no usable
speech or auditory
comprehension.
10. Dysarthria: If the patient is thought to be normal, an 0 Normal.
adequate sample of speech must be obtained by asking 1 Mild-to-moderate dysarthria;
the patient to read or repeat words from the attached the patient slurs at least some
list. If the patient has severe aphasia, the clarity of words and, at worst, can be
articulation of spontaneous speech can be rated. Only if understood with some difficulty.
the patient is intubated or has other physical barriers to 2 Severe dysarthria; the patient’s
producing speech, the examiner should record the score speech is so slurred as to be
as untestable (UN), and clearly write an explanation for unintelligible in the absence of
this choice. Do not tell the patient why he or she is being or out of proportion to any
tested. dysphasia, or is mute/anarthric.
Intubated or other physical
barrier, explain:
11. Extinction and Inattention (formerly Neglect): 0 No abnormality.
Sufficient information to identify neglect may be 1 Visual, tactile, auditory, spatial,
obtained during the previous test. If the patient has a or personal inattention or
severe visual loss preventing visual double extinction to bilateral
simultaneous stimulation, and the cutaneous stimuli are simultaneous stimulation in one
normal, the score is normal. If the patient has aphasia of the sensory modalities.
but does appear to attend to both sides, the score is 2 Profound hemiinattention or
normal. The presence of visual spatial neglect or extinction to more than one
anosognosia may also be taken as evidence of modality; does not recognize
abnormality. Because the abnormality is scored only if own hand or orients to only one
present, the item is never untestable. side of space.
______

Neurologic Status.

Neurologic monitoring

1. Assess for neurologic changes hourly in the acute phase. Use

NIHSS to record and monitor neurologic changes after stroke.

2. Maintain ICP less than 15 mm Hg and CPP greater than 60 mm

Hg: CPP − MAP = ICP.

1573
3. Position the patient to maintain adequate cerebral perfusion.
Keep the HOB at 25 to 30 degrees or less as tolerated for patients
with ischemic stroke. Keep the HOB raised at 30 degrees as
tolerated for patients with hemorrhagic stroke. Avoid extreme hip
flexion. When positioning, monitor tolerance to position change.

4. Maintain SpO2 of at least 94%. Consider ICP effects of respiratory

care. Suction only if needed. Assess breath sounds frequently.
Avoid activities that can increase ICP (e.g., excessive coughing).
Avoid hypercapnia and hypoxia.

5. Maintain adequate SBP. Higher pressures (140 to 180 mm Hg)

may be necessary to perfuse an area of brain at risk of infarction if
ischemia is present. For patients with hemorrhagic stroke, maintain
adequate BP. Use vasodilators or vasopressors as necessary to
optimize BP and maintain CPP at greater than 60 mm Hg for all
patients with stroke. For patients with AIS, lower the HOB to flat to
promote cerebral perfusion.

6. Notify the advanced practice provider of deterioration in

neurologic status or the vital sign changes as described in
Collaborative Management.

7. Use sedation as prescribed and monitor response: Effects of

sedation and changes in ICP.

Cerebral Perfusion Promotion; Positioning: Neurologic;

Neurologic Monitoring.

Impaired physical mobility 

related to decreased motor function of upper and/or lower extremities and
trunk after stroke.
Goals/Outcomes: At time of discharge from ICU, the patient has
no complications of immobility such as skin breakdown,
contracture formation, pneumonia, or constipation.
Mobility Level.

Exercise promotion: Strength training

1574
1. Turn and position frequently as tolerated. Transfer toward
unaffected side.

2. Teach methods for turning and moving using stronger extremity

to move weaker extremity.

3. Position weaker extremities to avoid contracture formation,

frozen shoulder, or foot drop.

4. Begin passive ROM within 24 hours of admission. Modify

exercises if BP or ICP increases.

5. Obtain physical therapy and occupational therapy referrals as

soon as possible to establish appropriate therapy.

6. Have the patient cough and breathe deeply as tolerated at

scheduled intervals.

Positioning; Exercise Therapy: Joint Mobility; Self-Care

Assistance.

Impaired verbal communication 

related to aphasia secondary to cerebrovascular insult.
Goals/Outcomes: At a minimum of 24 hours before discharge
from ICU, the patient demonstrates improved self-expression and
relates decrease in frustration with communication.
Communication Ability.

Communication enhancement: Speech deficit

1. Evaluate for aphasia: Partial or complete inability to use or

comprehend language and symbols. Assess nature and severity of
aphasia: Ability to point to and name specific objects, follow simple
directions, understand “yes/no” and complex questions, repeat
simple and complex words and sentences, relate purpose or action
of the objects, fulfill written request, write request, and read. May
occur with dominant (typically left) hemisphere damage.

• Receptive aphasia (e.g., Wernicke, sensory):

1575
 Inability to comprehend spoken words. The patient
may respond to nonverbal cues.

• Expressive aphasia (e.g., Broca, motor): Difficulty

expressing words or naming objects. Gesture,
groans, swearing, or nonsense words may be used.
Use of a picture or word board may be helpful.

2. Assess for dysarthria, which signals risk for aspiration resulting

from ineffective swallowing and gag reflexes. Consult with the
speech therapist to assess ways to promote independence and
facilitate swallowing.

3. Decrease environmental distractions, such as television or others’

conversations. Fatigue affects ability to communicate; plan
adequate sleep/rest.

4. Communicate frequently as follows: Face the patient, establish

eye contact, speak slowly and clearly, give the patient time to
process information and give answer, keep messages short and
simple, stay with one clearly defined subject, avoid questions with
multiple choices, and instead phrase questions that can be
answered “yes” or “no,” and use the same words each time when
repeating a statement or question. If the patient does not
understand after repetition, try different words. Use gesture, facial
expressions, and pantomime to supplement and reinforce message.

5. Help patients regain use of symbolic language: Start with nouns

and progress to more complex statements. Keep a record at the
bedside of words to be used (e.g., “pill” rather than “medication”).
Treat the patient as an adult. Do not speak louder unless the patient
is hard of hearing. Be respectful.

6. Facilitate verbal expression and naming objects: Encourage the

patient to repeat words after you say them to practice verbal
expression. Expect labile emotions, because patients are frustrated
and emotional about impaired speech. Patients who cannot monitor

1576
their speech may not speak sensible language but may think they
are making sense.

7. Avoid labeling the patient “belligerent” or “confused” when the

problem is aphasia and frustration. Patients with nondominant
(right) hemisphere damage may speak well, but may give overly
detailed information, or go off on tangents. Redirect by saying,
“Let’s go back to what we were talking about.”

8. Ensure that call light is available and the patient knows how to
use it. If the patient is unable to use call light, check frequently and
anticipate needs to ensure safety and trust.

Communication Enhancement: Speech, Visual, Hearing

Deficits; Active Listening: Anxiety Reduction; Touch.

Additional nursing diagnoses

See care of the patient after Intracranial Surgery (Chapter 7),
Cerebral Aneurysm and Subarachnoid Hemorrhage (Chapter 7),
Risk for Trauma (Oral and Musculoskeletal) in Status Epilepticus
(Chapter 7), Traumatic Brain Injury (Chapter 3), and Prolonged
Immobility (Chapter 1).

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in adultsreport of the Quality Standards Subcommittee of
the American Academy of Neurology. Neurology.
2010;74:1911-1918.
95. Working Group on Status Epilepticus. Treatment of
convulsive status epilepticus: recommendations of the
Working Group on Status Epilepticus. JAMA. 1993;270:854-
859.

1586
CHAPTER 8

Endocrinologic
disorders
Endocrine assessment
Assessment of the endocrine system is complex when assessing the
system as a whole because it regulates all body functions in
conjunction with the nervous system. Focusing on assessment
appropriate to critically ill patients, the following principles should
be considered:

1. Critical illness initiates the stress response.

2. The stress response increases the metabolic rate.

3. The hypothalamic-pituitary axis (Figure 8-1) regulates the

metabolic rate. The thyroid and adrenal glands are extremely
stressed by the stimulus of critical illness to maintain the increased
metabolic rate, along with meeting the energy demands at the
cellular level. Hypofunction of the thyroid and adrenal glands
requires assessment of not only those (the primary) glands but also
the hypothalamus (produces releasing factors) and anterior
pituitary (produces stimulating hormones.) The hypothalamic-
pituitary-target organ feedback loop must be fully intact to
maintain normal metabolism.

1587
 FIGURE 8-1 Endocrine system: hypothalamic-pituitary
axis feedback loop.

4. The stress response markedly increases endogenous

glucocorticoids, which increase blood glucose. The pancreas may
not be able to produce sufficient insulin to manage the glucose
level, resulting in hyperglycemia. Insulin may be required to
manage hyperglycemia until the stress of illness resolves. People
with diabetes mellitus are always challenged with hyperglycemia
and, with additional illness, can experience the crisis states of
diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic
syndrome (HHS).

5. Under prolonged extreme stress, both the adrenal glands and

thyroid may be unable to sustain hormone production to support
the stress level. Supplemental glucocorticoids (corticosteroids) and
thyroid hormones may be needed.

6. The assessment of the patient who is critically ill should focus on

the signs of failure of the endocrine system to support the stress
response. Signs of hypofunction are explained the sections on

1588
hyperglycemia, adrenal crisis, and myxedema coma. Patients with
adequate function of the pancreas, thyroid, and adrenal glands
under normal conditions may not be able to maintain balance when
exposed to the stress of critical illness. Those with underlying
hypofunction are more likely to experience crises.

7. Hyperthermia and cardiac symptoms can make diagnosis of

thyroid storm difficult, as the crisis mimics other cardiac crises and
infection. Thyroid storm results from underlying Graves
disease/hyperthyroidism rather than being a complication of critical
illness. Some patients with Graves disease are undiagnosed when
critical illness manifests from any cause.

8. Assessment of the causes of unusual fluid and electrolyte

imbalances should include evaluation of posterior pituitary
function in addition to screening for renal dysfunction. Posterior
pituitary dysfunction may result in abnormal levels of antidiuretic
hormone (ADH) and may be a complication of critical illness or
may result from hypothalamic or pituitary disease. Posterior
pituitary hypofunction results in diabetes insipidus (DI), which
produces dehydration. Posterior pituitary hyperfunction results in
syndrome of inappropriate antidiuretic hormone (SIADH), which
results in hyponatremia that can reach critical states if not properly
addressed. Nephrogenic DI results from failure of the kidneys to
respond to ADH. The elderly are at higher risk of complications
with DI as a result of age-related changes to the thirst mechanism
and renal function.

9. Medication noncompliance for management of existing

endocrine disease must be assessed. People with lower income are
at higher risk of crisis because of an inability to purchase
medications, and teenagers may not practice meticulous
management, particularly those with diabetes mellitus. Elders may
not take medications appropriately because of a lack of
understanding or misdosing caused by deteriorating short-term
memory. Poor historians or those with undiagnosed endocrine
disease must be carefully assessed to discover underlying glandular
dysfunction. Occasionally, patients referred to as “failure to thrive”

1589
are found to have underlying endocrine dysfunction.

Considerations for the bariatric patient: Postoperative

bariatric (weight loss) surgery patients require frequent blood
glucose monitoring to avoid hypoglycemia. Response to the
surgery is individual. Conversely, if the patient is hyperglycemic,
insulin resistance is often the cause. All patients should have a
baseline glycated hemoglobin (HbA1c) test to determine glucose
control preoperatively, given that Type 2 diabetes is extremely
common in the overweight population. Manage all patients
according to serial laboratory results and assessment.

Acute adrenal insufficiency (adrenal

crisis)
Pathophysiology
Acute adrenocortical insufficiency, also known as adrenal crisis
and Addisonian crisis, is a life-threatening condition that manifests
as shock with profound, refractory hypotension and may be
induced by hypothalamic-pituitary axis dysfunction. The function
of the adrenal cortex is dependent on the hypothalamic-pituitary
axis, consisting of a cascade of events beginning with the
hypothalamus secreting releasing factors, which:

1. Stimulate the pituitary to secrete stimulating hormones

(adrenocorticotropic hormone [corticotropin, or ACTH]), which

2. Stimulates the cortex of the adrenal glands to secrete

glucocorticoids (cortisol), mineralocorticoids (aldosterone), and
androgens, which

3. Facilitates cellular functions throughout the body (metabolism),

which

4. Creates signals back to the hypothalamus from the cells to

increase or decrease releasing hormones (see Figure 8-1).

1590
 The most common disease process associated with adrenal
insufficiency is severe sepsis with pituitary suppression.
Inappropriately rapid withdrawal of pharmacologic steroids can
also result in a crisis during critical illness or may cause critical
illness. Adrenal crisis is also associated with acute exacerbation of
chronic adrenocortical insufficiency in patients who become
stressed by sepsis, surgery, adrenal hemorrhage (septicemia-
induced Waterhouse-Friderichsen syndrome from
meningococcemia), and anticoagulation complications. There are
approximately 50 total hormones produced by the adrenal glands,
with cortisol and aldosterone being by far the most abundant.
If primary adrenal insufficiency is the cause of the crisis, the
adrenal glands are the root cause of the problem. Addison disease
manifests when the entire adrenal cortex is destroyed, which stops
the production of glucocorticoids (cortisol) and mineralocorticoids
(aldosterone). Glucocorticoids are essential hormones produced by
the adrenal cortex that help maintain vascular tone and cardiac
contractility, facilitate wound healing, and support immunity.
Cortisol deficiency intensifies the clinical effects of hypovolemia by
promoting a decrease in vascular tone, which is partially related to
unopposed endothelial production of nitric oxide, and a decreased
vascular response to the catecholamine hormones epinephrine and
norepinephrine. Relative hypoglycemia may be present, as the
breakdown of stored glycogen is not possible without cortisol.
Mineralocorticoid hormones are primary regulators of fluid and
electrolyte balance, and, when unavailable, patients experience
hyponatremia, hypovolemia, hyperkalemia, and metabolic acidosis.
Large amounts of sodium and water are excreted in the urine.
Severe hypotension, shock, and eventually death may occur
without intravenous (IV) adrenocortical hormone and fluid
replacement. In patients with chronic primary adrenocortical
insufficiency or Addison disease, physical stress or trauma may
exacerbate a crisis. Acute crises may be prevented by tripling
hormone replacement doses during periods of stress.
Primary adrenal insufficiency is relatively rare, can be acute or
chronic, and is most often caused by autoimmune-mediated,
idiopathic atrophy. Other causes include tuberculosis, fungal
infection, hemorrhage, congenital adrenal hyperplasia, enzyme

1591
inhibitors (e.g., metyrapone), cytotoxic agents (e.g., mitotane), and
other diseases infiltrating the adrenal glands.
Secondary adrenal insufficiency results from any process that
involves the hypothalamus and/or pituitary gland which reduces
corticotropin secretion. Inflammatory mediators or trauma may
suppress or damage the hypothalamus or pituitary. Pituitary or
other tumors may impair pituitary function or, in rarer cases,
produce glucocorticoids, which suppress the hypothalamic-
pituitary axis.
Exogenous or pharmacologic glucocorticoids (e.g.,
hydrocortisone) elevate the circulating level of the hormones, which
results in hypothalamic-pituitary-adrenal axis dysfunction. With
higher levels of circulating glucocorticoids, the adrenal glands do
not receive signals to produce endogenous cortisol. When
glucocorticoid therapy is abruptly discontinued or weaned too
quickly, the adrenal gland cannot immediately respond, given the
axis has been “turned off” during pharmacologic therapy and the
patient experiences adrenal crisis.

Critical illness induced adrenal insufficiency

Adrenal insufficiency is common in patients who are critically ill
and is increasingly reported in sepsis, severe pneumonia, adult
respiratory stress syndrome, trauma, HIV infection, or after
treatment with etomidate (anesthetic agent used for rapid sequence
endotracheal intubation). A large body of evidence demonstrates
significant neuroendocrine dysfunction in the anterior and
posterior hypothalamic-pituitary-adrenal axis in adults who are
critically ill, including abnormalities in adrenal gland modulation,
vasopressin release, and thyroid hormone metabolism. During
critical illnesses such as sepsis, adrenal hypofunction can result
from overwhelming destruction of adrenal glands themselves
(bleeding/ischemic necrosis or Waterhouse-Friderichsen syndrome).
The neuroendocrine response to critical illness is varied and
complex. Stress-induced increase in the output of cortisol results in
marked changes in substrate mobilization, resulting in a ready
supply of energy sources for use by vital organs. A surge in ADH
results in water retention to maintain operating ranges of volume
and osmolality. Glucose mobilization and synthesis provide energy

1592
and result in osmotic changes that temporarily recruit volume from
the intracellular fluid. Catecholamines not only augment vascular
tone but also liberate free fatty acids to fuel the heart and skeletal
muscles and hepatic gluconeogenesis and to serve as substrates for
hepatic ketone body production. If sustained, however, these
profound responses come with substantial costs. Substrate
mobilization via proteolysis results in unsustainable losses of
structural and muscle proteins that manifest as atrophy and
wasting. Unbalanced stress metabolism leads to hyperglycemia
with far-reaching effects on immune competence and neurologic
morbidities. Often the presenting signs are hemodynamic
instability and persistent hypotension, as well as a
petechial/purpuric rash. This syndrome is complicated by
hypoglycemia, hyponatremia, and hyperkalemia. It is a medical
emergency and needs to be treated urgently with antibiotics and
hydrocortisone. Critical illness-induced adrenal insufficiency is not
readily identified by all practitioners. Patients with pituitary
dysfunction generally do not require mineralocorticoid
replacement, because the release of aldosterone is dependent on
release of angiotensin II rather than ACTH from the pituitary.

8-1
RESEARCH BRIEF
Sprung and colleagues published a multicenter, double-blind,
randomized clinical trial in 2008. Fifty-two ICUs enrolled 500
patients who were older than 18 years of age with onset of septic
shock within the previous 72 hours (SBP less than 90 mm Hg
systolic despite fluids or need for vasopressors for longer than 1
hour). An ACTH 250 µg stimulation test was performed on all
patients meeting criteria. Nonresponders were those patients
whose serum cortisol level rose less than 9 µg/dL after stimulation.
All of these patients then received hydrocortisone dosing or
placebo. Hydrocortisone was administered in the following pattern
of deceleration:

1. 50 mg IV every 6 hours for 5 days

1593
2. 50 mg IV every 12 hours on Days 6 to 8

3. 50 mg IV every 24 hours on Days 9 to 11 and then stopped

The results were dismal in terms of mortality reduction because

there was little difference from placebo. Of note, however, was that
the group receiving hydrocortisone spent less time in shock by the
prior mentioned definition.
From Sprung CL, Annane D, Keh D, et al: Hydrocortisone therapy for patients in septic
shock. N Engl J Med 358:111–124, 2008.

Endocrine assessment adrenal glands

Goal of system assessment
The goal of system assessment is to evaluate for severe
hypotension refractory to volume and vasopressor administration.

History and risk factors

• Hypotension, refractory to volume and vasopressors.
Glucocorticoids (steroids) have been abruptly withdrawn and
patients are not given sufficient steroids to manage additional
stress

• Adrenalectomy, hypophysectomy, sepsis, HIV

• Other medications: β-adrenergic blockers, diuretics, angiotensin-

converting enzyme (ACE) inhibitors, angiotensin release blockers
(ARBs), nitrates, aspirin, and other platelet inhibitors

Observation and vital signs: Primary (first-degree) and

secondary (second-degree) insufficiency
• Severe hypotension resulting from vascular collapse

• Acute abdomen assessment findings: abdominal pain, distention,

tachypnea

1594
Observation and vital signs: Primary (first-degree)
insufficiency only
• Prominent nausea and vomiting, weight loss

• Bronze hue to the skin secondary to excess production of ACTH

Screening lab work

For suspected acute adrenal crisis

The gold standard for assessing adrenal insufficiency is the use of
the insulin tolerance test, which involves the IV injection of insulin.
Insulin injections are intended to cause extreme hypoglycemia (<2.2
mmol/L [40 mg/dL]). Normally, ACTH and growth hormone (GH)
are released during the stress response. ACTH elevation causes the
adrenal cortex to release cortisol. Cortisol and GH serve as
counterregulatory hormones, counteracting the action of insulin,
which should abate hypoglycemia. Plasma glucose and cortisol
(and sometimes ACTH) are measured before injection and again at
15, 30, 45, 60, 75, and 90 minutes. If the stress response is abnormal,
the patient will become hypoglycemic. This test is not typically
performed in patients who are critically ill, because it is considered
unsafe in unstable or unconscious patients and contraindicated in
patients with coronary heart disease or seizures.

• Random plasma cortisol level: Drawn before initiating

hydrocortisone replacement, but must be interpreted with
caution in critically ill patients because greater than 90% of
circulating cortisol is protein-bound. When patients are
hypoproteinemic, with serum albumin less than 2.5 g/dL, low
values may be gleaned from all cortisol testing in patients who
have normal adrenal function. A random plasma cortisol level of
greater than 25 µg/dL excludes both primary and secondary
adrenal insufficiency.

• Free cortisol level: Done in the setting of hypoproteinemia to

better determine the cortisol level. An abnormal test may require
a complete endocrinology assessment when the patient stabilizes.

1595
 At this time, free cortisol is the most reliable test.

For noncritical adrenocortical insufficiency

• Corticotropin (ACTH) stimulation test: The goal is to differentiate

primary from secondary adrenocortical insufficiency or to assess
if the adrenal cortex is capable of producing cortisol. Testing of
the hypothalamic-pituitary-adrenal axis using this test can
differentiate primary from secondary insufficiency. Baseline
plasma cortisol level is drawn immediately before ACTH
administration.

1. A dose of 250 µg of synthetic ACTH is given by IM or IV

injection.

• Low-dose protocol: Doses as low as 1 µg/kg of ACTH have been

used to more closely mimic the amount of normal physiologic
ACTH released.

2. Within 15 to 30 minutes of receiving ACTH, the normal adrenal

cortex releases two to five times the baseline or basal plasma
cortisol level.

3. Thirty or 60 minutes following the ACTH injection, another

cortisol level is measured. If the low-dose protocol was used, only
the 30-minute cortisol level is accurate.

4. If evaluating for primary adrenal insufficiency, aldosterone levels

are drawn with the cortisol levels. The 30-minute aldosterone level
is more accurate than the 60-minute level.

• Cortisol level: Does not increase at least a total of 9 mg/dL at 30 or

60 minutes following ACTH administration. Typically will rise to
above 20–30 mg/dL.

• Aldosterone level (if testing specifically for primary

insufficiency): An initial value of less than 5 ng/100 mL that fails
to double or increase by at least 4 ng/100 mL at 30 minutes
following ACTH administration.

1596
 The 2012 Surviving Sepsis Campaign Guidelines recommend
an evidence-based protocol approach to possible adrenal
insufficiency in severe sepsis:

1. IV hydrocortisone should not be used to treat adult septic shock

patients if adequate fluid resuscitation and vasopressor therapy are
able to restore hemodynamic stability, as defined by capillary refill
of ≤2 seconds, normal blood pressure (BP) for age, normal pulses
with no differential between peripheral and central pulses, warm
extremities, and urine output more than 1 mL/kg/h; and are able to
hemodynamic stability, as defined by achievable, dose
hydrocortisone alone at 200 mg/d (evidence grade 2C).

2. When hydrocortisone is given, a continuous infusion should be

used rather than repetitive bolus injections (evidence grade 2D).

3. The ACTH stimulation test should not be used to identify which

adults with septic shock should receive hydrocortisone (evidence
grade 2B).

4. Corticosteroids should not be administered for the treatment of

sepsis in the absence of shock (evidence grade 1D).

5. Clinicians should taper the treated patient from steroid therapy

when vasopressors are no longer required (evidence grade 2D).

Diagnostic Tests for Acute Adrenal Insufficiency

1597
Collaborative management
DIAGNOSIS AND MANAGEMENT OF CORTICOSTEROID
INSUFFICIENCY IN CRITICALLY ILL PATIENTS

From Marik PE, Pastores SM, Annane D, et al: Crit Care Med 36:1937–1949, 2008.

1598
Care priorities

1. Correct hypovolemia
Initiate replacement of intravascular fluid volume. Rapid volume
replacement is essential, using normal saline crystalloid IV solution.
Administer 1 L over the first hour, followed by an additional 1 to 2
L over the next 6 to 8 hours. If hypovolemia persists,
colloid/volume-expanding IV solutions may be necessary.

2. Manage hypotension
Use vasopressors if intravascular volume replacement fails to
effectively increase BP (see Appendix 6). Response to catecholamine
infusions (epinephrine, norepinephrine, dopamine) is reduced in
adrenal insufficiency; higher-than-normal doses may be needed to
manage refractory hypotension.

3. Replace cortisol
During stressful situations, the normal adrenal gland output of
cortisol is approximately 250 to 300 mg over 24 hours. IV
hydrocortisone should be given only to adult patients with septic
shock after it has been confirmed their BP is poorly responsive to
fluid resuscitation and vasopressor therapy.

• Hydrocortisone 100 mg in 100 mL of normal saline solution by

continuous IV infusion at a rate of 12 mL/h. Infusion may be
initiated with 100 mg of hydrocortisone as an IV bolus.

• The infusion method maintains plasma cortisol levels more

adequately at steady stress levels, especially in the small
percentage of patients who are rapid metabolizers and who may
have low plasma cortisol levels between the IV boluses. Rapid
metabolizers have a greater likelihood of having low plasma
cortisol levels between IV boluses.

• As the patient improves and as the clinical situation allows, the

hydrocortisone infusion can be gradually tapered over the next 4
to 5 days to daily replacement doses of approximately 3 mg/h (72

1599
 to 75 mg over 24 h) and eventually to daily oral replacement
doses when oral intake is possible.

• An alternative method of hydrocortisone administration is 50 to

75 mg IV every 4 to 6 hours for 5 days.

• After 2 to 3 days, the stress hydrocortisone dose should be

reduced to 100 to 150 mg, administered over a 24-hour period,
regardless of the patient’s clinical status. In addition to helping
with adrenal recovery, lower doses may help abate
gastrointestinal (GI) bleeding.

• If the patient receives at least 100 mg of hydrocortisone in 24

hours, no mineralocorticoid replacement is necessary, because the
mineralocorticoid activity of hydrocortisone in this dosage is
sufficient.

• As the hydrocortisone dose continues to be weaned,

mineralocorticoid replacement should begin in doses equivalent
to the daily adrenal gland aldosterone output of 0.05 to 0.1 mg
daily or every other day.

4. Maintain normal blood glucose level

If the patient is initially hypoglycemic, 50% dextrose may be needed
to correct hypoglycemia. When hydrocortisone or other cortisol
replacement is initiated, hyperglycemia may result. An insulin
infusion may be needed to control the blood glucose (see
Hyperglycemia, Chapter 8).

The need for aggressive insulin titration is reduced if the

patient is managed using a continuous (24-hour) infusion of
cortisol replacement rather than bolus doses every 6 hours.

Care plans for adrenal insufficiency

1600
 Deficient fluid volume 
related to failure of regulatory mechanisms secondary to impaired
secretion of aldosterone, causing increased sodium excretion with resultant
diuresis.
Goals/Outcomes: Within 12 hours of initiating treatment, the
patient is moving toward normovolemia as evidenced by BP
approaching normal range; heart rate (HR) 60 to 100 beats/min
(bpm); respiratory rate (RR) 12 to 20 breaths/min with normal
pattern and depth, or, if on the ventilator, weaning from the
ventilator; central venous pressure (CVP) 2 to 6 mm Hg; if
hemodynamic monitoring is in place, pulmonary artery wedge
pressure (PAWP) approaching 6 to 12 mm Hg; normal sinus
rhythm on electrocardiogram (ECG); and improvement in level of
consciousness (LOC).
Fluid Balance

Fluid and electrolyte management

1. Monitor vital signs and hemodynamic measurements every 15

minutes until stabilized for 1 hour. Consult advanced practice
provider promptly for deterioration in vital signs or
hemodynamics.

2. Administer IV fluids to replace fluid volume. Initially, rapid fluid

replacement is essential.

3. Maintain accurate input and output (I&O) record. Weigh the

patient daily.

4. Monitor for electrolyte imbalance. Imbalances associated with

adrenal insufficiency include the following:

• Hyponatremia: Headache, malaise, muscle

weakness, abdominal cramps

• Hyperkalemia: Lethargy, nausea, hyperactive bowel

sounds with diarrhea, numbness or tingling in

1601
 extremities, muscle weakness. Be aware that
hyperkalemia will worsen in the presence of
metabolic acidosis.
5. Monitor ECG continuously; observe for potassium-related
changes. Increased ventricular irritability may signal hypokalemia.
(See Fluid and Electrolyte Disturbances, Hypokalemia, Chapter 1.)

6. Monitor laboratory results. With appropriate treatment, serum

sodium levels should rise to normal and serum potassium levels
should fall to normal. Prevent rapid correction or overcorrection of
hyponatremia. Serum sodium levels should not be allowed to
increase by more than 12 mEq/L during the first 24 hours of
treatment because of the risk of neurologic damage. (See Fluid and
Electrolyte Disturbances, Hyponatremia, Chapter 1, or Syndrome of
Inappropriate ADH, Chapter 8.)

7. Assess mental and respiratory status at frequent intervals.

Institute safety measures as indicated. Reorient and reassure the
patient as needed.

8. Encourage oral fluid intake as the patient’s condition stabilizes.

Add sodium-rich foods (see Box 8-1) as tolerated. Begin oral
glucocorticoid replacement therapy as prescribed.

9. Consult advanced practice provider if signs and symptoms of

fluid and/or electrolyte imbalance persist or worsen.

Box 8-1
PATIENT AND FAMILY EDUCATION
CONCERNING GLUCOCORTICOID AND
MINERALOCORTICOID REPLACEMENT
Glucocorticoids (e.g., cortisone acetate, prednisone)
Glucocorticoids (e.g., Cortisone Acetate, Prednisone) and
mineralocorticoids: two-thirds of dose in the morning and one-

1602
 third of dose in the afternoon).

Glucocorticoids (e.g., cortisone acetate, prednisone): Be alert for

indicators of infection (e.g., fever, nausea, diarrhea, malaise).

Glucocorticoids: Take with food to decrease gastric irritation.

Glucocorticoid overreplacement: Weight gain (moon face, truncal

obesity); edema, thin, fragile skin (striae, easy bruising); slow
wound healing; chronic fatigue; emotional lability

Glucocorticoid underreplacement: Weight loss, hyperpigmentation,

skin creases, anorexia, nausea, abdominal discomfort, chronic
fatigue, depression, irritability

Mineralocorticoids (e.g., Fludrocortisone, Desoxycorticosterone

Acetate)

• Weigh self regularly, and report to provider: Sudden gains or

losses >2 lb/wk, chronic fatigue, depression, and irritability.

• Mineralocorticoid overreplacement: Edema, muscle weakness,

hypertension

• Mineralocorticoid under-replacement: Excessive urination,

weight loss, decreased skin turgor

Fluid Monitoring; Neurologic Monitoring; Hypovolemia

Management; Electrolyte Management: Hyponatremia; Electrolyte
Management: Hyperkalemia

Risk for injury 

related to potential for acute regulatory dysfunction (cortisol and
aldosterone deficiency) secondary to increased psychological, emotional, or
physical stressors with increased hormonal demand and inadequate
adrenal reserves.
Goals/Outcomes: The patient does not manifest symptoms of
sepsis; is able to verbalize orientation to time, place, and person, has

1603
stable weight, urine output less than 80 to 125 mL/h, HR 60 to 100
bpm, BP within the patient’s normal range, and normothermia.
Immune Status; Infection Status; Energy Conservation

Energy management

1. Monitor and report signs of increasing crisis: urinary output

increased from usual amount, changes in LOC, orthostatic
hypotension, nausea, vomiting, and tachycardia.

2. Provide a quiet, nonstressful environment. Adjust lighting to

meet needs of individual activities, avoiding direct light in the eyes.
Control noise when possible. Prevent unnecessary interruptions,
and allow for rest periods. Limit the number of visitors and the
length of time they spend with patient. Speak softly and
reassuringly to patient.

3. Monitor for and manage hyperthermia using tepid baths,

antipyretics, and cooling blankets.

4. Maintain a cool environmental temperature. Maintain strict

environmental asepsis, and monitor the patient carefully for signs
of infection. Avoid exposing the patient to staff members or visitors
who have colds or infections.

Fluid Monitoring; Environmental Management; Infection

Protection

Deficient knowledge: Illness care 

related to prevention of adrenal crisis in patients with chronic adrenal
insufficiency or those undergoing steroid therapy.
Goals/Outcomes: Before discharge from the intensive care unit
(ICU), the patient understands factors that increase the risk of
adrenal crisis, how to avoid adrenal crisis, precautions that must be
taken, and when to notify advanced practice provider.
Knowledge: Disease Process; Knowledge: Energy
Conservation; Knowledge: Medication

Teaching: Disease process

1604
1. Teach the patient about prescribed medications, including
purpose, dosage, route of administration, and potential side effects
(Box 8-1). Medication administration should mimic normal diurnal
pattern of plasma cortisol levels (e.g., two-thirds in the morning
and one-third in late afternoon).

2. Provide dietary instruction: dietary sodium and potassium may

need to be adjusted on the basis of the patient’s clinical condition
and drug therapy (see discussions of sodium and potassium in
Fluid and Electrolyte Disturbances, Chapter 1).

3. Explain the importance of controlling stress, both emotional and

physiologic, which increases adrenal demand. Teach the patient to
seek medical intervention during times of increased stress (e.g.,
fever, infection). Medication dosages may need to be increased.

4. Teach indicators of overreplacement and underreplacement of

steroids, which require prompt medical attention (see Box 8-1).

5. Stress the importance of never abruptly discontinuing use of any

steroid preparation. Use must be tapered to avoid precipitation of
crisis.

6. Remind the patient of the importance of continued medical

follow-up.

7. Explain the procedure for obtaining a medical alert bracelet or

card.

Teaching: Prescribed Medication; Emotional Support

Diabetes insipidus
Pathophysiology
Diabetes insipidus (DI) is a metabolic disorder that affects total
body free water regulation, resulting in an abnormally high output
of extremely dilute urine, increased fluid intake, and constant thirst.
The volume of hypotonic urine excreted is 3 to 20 L per day.

1605
Vasopressin (antidiuretic hormone [ADH]) is a key component in
the regulation of fluid and electrolyte balance through direct effects
on renal water regulation. Vasopressin is produced in the
hypothalamus, is stored in the posterior pituitary gland, and exerts
action in the kidneys for water regulation. Three subtypes of
receptors respond to the effects of vasopressin (Table 8-1).

Table 8-1
LOCATIONS AND ACTIONS OF VASOPRESSIN RECEPTORS

When any aspect of water regulation fails, if free water is lost, the
extracellular fluid volume rapidly decreases, causing plasma
osmolality and serum sodium to rise. Plasma osmolality is the main
determinant of vasopressin secretion from the posterior pituitary.
The osmoregulatory systems for thirst and vasopressin secretion,
and the actions of ADH on renal water excretion, maintain plasma
osmolality between 284 and 295 mOsmol/kg. Thirst and drinking
are key processes in the maintenance of fluid and electrolyte
balance. Thirst perception and the regulation of water ingestion
involve complex neural and neurohormonal pathways. Thirst
occurs when plasma osmolality rises above 281 mOsmol/kg, similar
to the threshold for ADH release. The osmoreceptors regulating
thirst are located in the hypothalamus.
Situations that alter the balance between plasma osmolality and
vasopressin concentration include:

• Rapid changes of plasma osmolality: Rapid increases in plasma

osmolality result in an abnormal increase in ADH/vasopressin
release.

1606
• Drinking fluids: Oral fluid consumption rapidly suppresses the
release of ADH, through afferent pathways originating in the
oropharynx.

• Pregnancy: The osmotic threshold for ADH release is lowered in

pregnancy.

• Aging: Plasma vasopressin concentrations increase with age,

together with enhanced ADH responses to osmotic stimulation.
Age-related changes in ADH production can result in blunting of
the thirst response, decreased fluid intake, impaired ability to
excrete a free water load, and reduced ability of the kidneys to
concentrate urine. These changes predispose the elderly to both
hypernatremia and hyponatremia.

There are four major subtypes of DI, based on which mechanism

involved with concentrating urine has failed (Table 8-2):

• Central, hypothalamic, or pituitary DI (neurogenic DI) is the most

common type and is caused by lack of vasopressin (ADH)
production by a diseased or destroyed posterior pituitary gland.
The lack of ADH results in massive diuresis because ADH
normally prompts the kidney to concentrate the urine.
Approximately 50% of central DI is idiopathic, as diagnostic
testing does not reveal a cause. Central DI is usually permanent,
but the signs and symptoms (i.e., thirst, drinking fluids, and
urination) are controlled by daily use of synthetic vasopressin.

• Nephrogenic DI (NDI) is caused by inability of the kidneys to

respond to normal amounts of ADH, resulting from a variety of
drugs or kidney diseases, including genetic predisposition. The
collecting tubules have decreased permeability to water caused
by decreased response to vasopressin by the nephrons. NDI does
not improve with synthetic vasopressin and may not improve
when probable causes are managed. Familial NDI requires
lifelong management. Treatments partially relieve the signs and
symptoms. Medications, including lithium, amphotericin B, and
demeclocycline can induce NDI. Hypercalcemia can sometimes
prompt NDI.

1607
• Gestational or gestogenic DI results from a lack of vasopressin
that develops during the third trimester of pregnancy if the
pregnant woman’s thirst center is abnormal, causing a blunted
thirst response, and/or the placenta destroys vasopressin too
rapidly. The placenta may increase the action of vasopressinase,
the enzyme that breaks down vasopressin. The condition is
controlled using synthetic vasopressin until the DI resolves.
Vasopressin can generally be discontinued 4 to 6 weeks after
delivery. Signs and symptoms of DI will recur with subsequent
pregnancies.

• Dipsogenic DI or primary polydipsia results from vasopressin

suppression caused by excessive fluid intake. Primary polydipsia
is most often caused by an abnormality in the thirst center of the
brain. Unquenchable thirst results in water intoxication.
Dipsogenic DI is differentiated from central (pituitary) DI using
the water deprivation test. There is no cure for dipsogenic DI at
present, but symptoms can be safely relieved. Psychogenic
polydipsia is another subtype; it is because of psychosomatic
causes and has no treatment that is recognized as consistently
effective.

Table 8-2
FOUR MAJOR SUBTYPES OF DIABETES INSIPIDUS

Subtypes of
Pathophysiology Common Etiology
DI
Central Lack of ADH production by the Head injury, pituitary tumor and
posterior pituitary gland postpituitary tumor resection, cerebral
ischemia, intracerebral hemorrhage, CNS
infection, brain death, idiopathic
Nephrogenic Inability of the kidneys to respond Medications, ethanol abuse, chronic
to normal amounts of ADH hypercalcemia, hypokalemia osmotic
diuresis, congenital disorder, polycystic
kidney disease, pyelonephritis, Sjögren
syndrome, sickle cell anemia
Gestational Blunted thirst response related to Last trimester of pregnancy in women who
pregnancy, and placenta increases have oligohydramnios, preeclampsia, and/or
the action of vasopressinase, hepatic dysfunction
which results in decreased
circulating ADH
Dipsogenic ADH suppression Unquenchable thirst, massive water intake;
Caused by increased fluid intake psychogenic causes may be associated with
mental illness

1608
 The most common presentation of DI is following head trauma or
intracranial surgery. When a person cannot adequately respond to
stimulation of the thirst center by drinking fluids, extracellular and
intracellular dehydration may result. Electrolyte imbalance,
primarily hypernatremia, may produce neurologic symptoms
ranging from confusion, restlessness, and irritability to seizures and
coma. DI sometimes occurs in brain-dead organ donors and must
be managed to effectively preserve organs.
In normal individuals, a more concentrated circulating volume
stimulates ADH release through activation of osmoreceptors that
monitor serum osmolality. ADH is also released as part of the
renin-angiotensin-aldosterone mechanism as a result of
hypotension sensed by the juxtomedullary apparatus located
outside the glomerulus of the kidney. A 5% to 10% decrease in
arterial BP is necessary to increase circulating vasopressin
concentrations. Progressive hypotension in individuals who are
healthy results in an exponential increase in plasma ADH via
baroreceptor stimulation, whereas osmoregulated ADH release in
response to dehydration is more linear. If the hypothalamus is
damaged, production of ADH may not be possible and both the
ability to regulate circulating volume and vascular tone may be
affected. Baroregulated (pressure response) release of vasopressin is
a key physiologic mediator in an integrated hemodynamic response
to volume depletion.

Endocrine assessment: Diabetes insipidus

Goal of assessment
The clinical presentation of DI is dependent on the overall health of
the patient and the primary cause. Evaluate for degree of
dehydration and its effects on overall hemodynamics, heart
rate/rhythm, and mental status. Generally, DI is recognized and
managed before resulting in serious complications. Practitioners
working with brain-dead organ donors must be particularly alert to
the occurrence of DI. Severe, unmanaged, or undermanaged
dehydration in cases of DI may cause hemoconcentration, which
may predispose the patient to thrombosis. Dehydration and

1609
electrolyte imbalance must be prevented or managed immediately
to avoid possible organ damage.

History and risk factors

Central/hypothalamic/pituitary diabetes insipidus

Brain tumors, especially in the hypothalamus or pituitary region;
neoplasms such as leukemia or breast cancer; surgery in the area of
the pituitary gland; intracranial hemorrhage; brain death; head
injury, especially to the base of the brain; meningitis or encephalitis;
any disorder that causes increased intracranial pressure; cerebral
hypoxia; and various inheritable defects. Those with genetic defects
have the onset in early childhood. Genetic predisposition is
revealed by family history.

Nephrogenic diabetes insipidus

From medications (e.g., lithium, demeclocycline, glyburide,
phenytoin), insufficient dose prescribed of ADH, ethanol abuse,
chronic hypercalcemia, hypokalemia, osmotic diuresis, congenital
disorder of defective expression of renal vasopressin 2 (V2)
receptors, or patients with polycystic kidney disease,
pyelonephritis, renal amyloidosis, myeloma, Sjögren syndrome, or
sickle cell anemia.

Gestational diabetes insipidus

Seen in patients during the last trimester of pregnancy who have
oligohydramnios, preeclampsia, and/or hepatic dysfunction. In
addition to the blunted thirst response associated with pregnancy,
these patients break down only endogenous vasopressin (ADH)
and can be managed with synthetic vasopressin (desmopressin).

Dipsogenic diabetes insipidus

Unquenchable thirst with massive water intake; psychogenic causes
may be associated with patients with a history of mental illness.
Water intoxication from massive fluid intake presents with
headache, loss of appetite, lethargy, and nausea and signs such as
an abnormally large decrease in the plasma sodium concentration

1610
(hyponatremia).

Vital signs
• Tachycardia and tachypnea are present with dehydration.

• Diuresis alone may have no effect on vital signs if the patient is

able to drink enough fluids.

• Orthostatic hypotension if dehydration is present.

Observation
• Polyuria with dilute urine; 3 to 20 Ld of urine may be excreted,
with specific gravity of 1.000 to 1.005.

• History may include nocturia (getting up frequently at night to

urinate) and/or enuresis (bed-wetting).

• Extreme thirst

• Dehydration: Poor skin turgor, dry mucous membranes, sunken

eyes, slow capillary refill

1. Electrolyte imbalance: Generalized weakness,

possible exhaustion, nausea and vomiting,
impaired vision and leg cramps may be present;
patients may become unable to get out of bed.

2. Urine output: More than 200 mL/h for 2

consecutive hours or greater than 500 mL/h,
especially if risk factors are present.

3. Hemodynamics: CVP less than 2 mm Hg; PAWP

less than 6 mm Hg. It is not routine practice to
use hemodynamic monitoring solely to manage

1611
 DI, but if DI develops in a critically ill patient,
readings typically reflect hypovolemia.
• Altered mental status: Serum hyperosmolality and hypernatremia
affect consciousness and behavior. Changes may also be related
to the underlying disease.

1. Cranial nerve examination may be abnormal,

with nerve palsies present.

2. Altered level of consciousness (confusion,

disorientation, agitation) is more common with
older adults; in extreme unmanaged cases, coma
and seizures are possible.

Auscultation
• In rare cases, bowel sounds may be lessened if hypovolemic
shock has reduced abdominal vessel perfusion.

Screening lab work

• Point-of-care (POC) capillary blood glucose to rule out
hyperglycemia as the cause of diuresis

• Fluid and electrolyte imbalance screening:

a. Electrolyte panel: To assess for hypernatremia

and concentrations of other electrolytes
associated with hemoconcentration

b. Urinalysis/specific gravity: Assesses for dilute,

poorly concentrated urine

1612
 c. Urinary and serum osmolality: Values may
become similar. When kidneys properly
concentrate urine, urine osmolality is generally
four times the value of serum osmolality.

Diagnostic Testing for Diabetes Insipidus

Collaborative management
Care priorities

1. Rehydrate if dehydration and/or hypovolemia are present

1613
• Place at least two large-bore IV lines, or have a central line
inserted.

• Administer hypotonic IV fluids (5% dextrose solution, 0.45%

saline). Hyperglycemia and volume overload should be avoided.

• In the geriatric population, be aware of individual

comorbidities such as diabetes and congestive heart failure
during rehydration.

• Avoid overly aggressive correction of hypernatremia. Do not

decrease sodium level by more than 5mEq/L/h or more than 12
mEq/L within 24 hours.

• The patient may be allowed to drink fluids, with the volume

accurately recorded.

• Monitor urine output every 1 to 2 hours. Fluid can be replaced

milliliter for milliliter. Total water deficit may be estimated by
assuming body water composes approximately 60% of total body
weight in kilograms.

• Formula for calculating body water deficit: (0.6 [weight in

kilograms]) × (serum sodium − 140)/140 = body water deficit (in
liters)

• Monitor continuous ECG for tachycardia and dysrhythmias.

• Evaluate basic ABCs (airway, breathing, and circulation) if the

patient becomes hypotensive.

• Monitor daily weights.

2. Administer exogenous ADH (vasopressin) (for central DI

and gestational DI)

• Use of desmopressin acetate (DDAVP) is popular because it

produces fewer side effects (Table 8-3).

• Several preparations are available, and dosage is adjusted to the

1614
 patient’s response to DI management. Vasopressin’s potential
vasoconstrictive effects occur rarely with appropriate dosing for
management of DI. Excessive dosing of ADH may cause
hypertension and cardiac symptoms; other side effects include
abdominal cramping and increased peristalsis.

Table 8-3
VASOPRESSIN PREPARATIONS

CDI, Central diabetes insipidus; NDI, nephrogenic diabetes insipidus.

3. Manage electrolyte imbalances, focusing on

hypernatremia

• Before rehydration, patients are hypernatremic. Hypernatremia

should resolve with aggressive hydration.

• Serum osmolality, electrolyte levels (sodium and potassium)

should be measured at least daily. They should be monitored
more frequently if the patient has hemodynamic instability.

4. Identify and manage the precipitating cause

• As dehydration is managed, efforts should be underway to

identify the cause of DI, if not initially known, using the water

1615
 deprivation test and ADH test. A thorough history and physical
examination may help identify possible causes. Consider NDI in
the elderly patients using polypharmacy. Consider NDI in
patients with a history of mental illness. NDI can occur in
patients with a remote history of lithium use.

• Subsequent diagnostics may be needed to identify additional

disease processes that may have resulted in DI.

5. Manage NDI (ADH-insensitive) with pharmacotherapy

• Thiazide diuretics (e.g., hydrochlorothiazide [HCTZ]) in

combination with a low-sodium diet are the major form of
therapy for NDI to reduce the loss of free water in the urine.

• Chlorpropamide stimulates the release of ADH and facilitates the

renal response to ADH.

• Amiloride hydrochloride (a potassium-sparing diuretic) is the

medication of choice for the treatment of lithium-induced NDI.

• Nonsteroidal antiinflammatory drugs (NSAIDs) such as

indomethacin have been used as adjunctive therapy in NDI.

Care plans for diabetes insipidus

Deficient fluid volume 
related to diuresis secondary to ADH deficiency or altered ADH action.
Goals/Outcomes: Within 12 hours of initiating treatment, the
patient is euvolemic, reflected by BP 90/60 mm Hg or greater (or
within patient’s normal range), mean arterial pressure (MAP) 70
mm Hg or greater, HR 60 to 100 bpm, CVP 2 to 6 mm Hg, urinary
output 0.5 to 1.5 mL/kg/h, intake equal to output plus insensible
losses, firm skin turgor, pink and moist mucous membranes, and
stable weight. ECG exhibits normal sinus rhythm. Electrolyte
values are serum sodium 137 to 147 mEq/L, serum osmolality 275 to
300 mOsmol/kg, urine osmolality 300 to 900 mOsmol/24 h, and
urine specific gravity 1.010–1.030.

1616
 Fluid Balance, Electrolyte and Acid-Base Balance, Hydration

Hypovolemia management

1. Monitor vital signs every 15 minutes until the patient is stable for
1 hour. Monitor CVP, MAP, and, if hemodynamic monitoring was
in place, pulmonary artery pressure (PAP), and pulmonary
capillary wedge pressure (PCWP), if ordered. Consult advanced
practice provider for the following: HR greater than 140 bpm or BP
less than 90/60 mm Hg or decreased more than 20 mm Hg from
baseline, or MAP decreased more than 10 mm Hg from baseline,
CVP less than 2 mm Hg, and PAWP less than 6 mm Hg. Manage
judiciously in all patients, including organ donors who are brain-
dead.

2. Monitor hydration status: mucous membranes, pulse rate and

quality, and BP. Excessive water intake may result in fluid
overload, particularly in elders and children.

3. Administer hypotonic solutions (e.g., D5W, D50.25, or 0.45 NaCl)

for intracellular rehydration. Usually, fluids are administered as
follows: 1 mL IV fluid for each 1 mL of urine output. In patients
with brain injury, moderate diuresis may be permitted to avoid the
need for administering osmotic diuretics. Hypernatremia, if
present, must be corrected slowly (at a rate no greater than 0.5
mEq/L/h or 12 mEq/L/d) to prevent cerebral edema, seizures,
permanent neurologic damage, or death.

4. Administer exogenous ADH as ordered. Observe for a reduction

in urine output. Monitor for side effects: hypertension, cardiac
ischemia, and hyponatremia.

5. Weigh the patient daily, at the same time and using the same
scale and while the patient is wearing the same garments to prevent
error. Consult an advanced practice provider for weight loss greater
than 1 kg/d.

6. Observe for indications of dehydration (e.g., poor skin turgor,

delayed capillary refill, weak/thready pulse, dry mucous

1617
membranes, hypotension).

7. Monitor for fluid overload, which can occur as a result of rapid

infusion of fluid or excessive fluid intake in patients with heart
failure: jugular vein distention, dyspnea, crackles (rales), and CVP
greater than 12 mm Hg.

8. If urinary catheter has been removed, observe for resolution of

nocturia (waking up at night to urinate) and enuresis (bed-wetting)
as treatment progresses.

Fluid/electrolyte management

1. Monitor laboratory studies, observing for an appropriate

response to treatment, including a decrease in serum sodium,
increase in serum and urine osmolality, and increase in urine
specific gravity.

2. Monitor urine specific gravity hourly to evaluate response to

therapy. Patients may be allowed to develop hypotonic polyuria
between doses of vasopressin to demonstrate persistence of DI
when transient DI is suspected.

3. Report lack of improvement or deterioration to the advanced

practice provider. Urine output greater than 200 mL/h for 2
consecutive hours, or 500 mL/h in the presence of risk factors,
should be reported.

4. Instruct patients with permanent DI to wear a medical alert

bracelet labeled with DI. Immediate family members should be
familiar with the patient’s current treatment plan in case they are
contacted in an emergency.

Fluid Monitoring; Intravenous (IV) Therapy; Invasive

Hemodynamic Monitoring; Electrolyte Management:
Hypernatremia

Disturbed sensory perception (visual and auditory) 

related to hyperosmolality, dehydration, or hypernatremia.

1618
 Goals/Outcomes: The patient verbalizes orientation to time,
place, and person; the patient is protected from unnecessary
complications and bodily injury.
Cognitive Orientation

Surveillance

1. Monitor neurologic status frequently. Notify advanced practice

provider of deterioration.

2. Keep bed in lowest position with side rails raised if the patient is
confused.

3. Consider nasogastric tube with suction for comatose or brain-

dead organ donor patients to decrease likelihood of aspiration.

4. Elevate head of the bed (HOB) to 30 degrees to minimize the risk

of aspiration.

Neurologic Monitoring

Risk for infection 

related to inadequate primary defenses secondary to incisional opening
into sella turcica for patients who have undergone transphenoidal
hypophysectomy.
Goals/Outcomes: The patient is free of infection as evidenced by
normothermia; verbalization of orientation to time, place, and
person; and absence of cerebrospinal fluid (CSF) leakage or nuchal
rigidity. HR 100 bpm or less, BP within patient’s normal range,
white blood cell (WBC) count 11,000/mm3 or less, and negative
culture results.
Infection Severity, Immune Status

Infection protection

1. For patients who have undergone transphenoidal

hypophysectomy, inspect nasal packing often for frank bleeding or
evidence of CSF leak. If glucose is detected in clear nasal drainage
(tested using a glucose reagent stick), CSF is leaking, which

1619
indicates a flaw in cranial bone integrity. (See Care of the Patient
After Intracranial Surgery, Chapter 7.)

2. Elevate the HOB to minimize the chance of bacterial migration

into the brain if CSF leak is suspected. Consult advanced practice
provider promptly.

3. Monitor for infection, including elevated temperature, nuchal

rigidity, and altered LOC.

4. Monitor for increased WBC count, which initially may reflect

dehydration or the stress response.

5. Because the patient is at higher risk for bacterial infection,

invasive lines should be managed carefully to avoid bloodstream
infection (BSI). Central lines should be removed as soon as possible.

6. To prevent injury and contamination of operative site, patients

should not brush their teeth until instructed to do so by the
physician. Provide sponge-tipped applicators for oral hygiene.

Incision Site Care; Infection Protection; Neurologic

Monitoring

Deficient knowledge: Illness care

related to the need to manage transient to permanent DI and possible
management of additional hormonal imbalance if anterior pituitary was
damaged or removed; care after transphenoidal hypophysectomy.
Goals/Outcomes: Before discharge from ICU, the patient
verbalizes understanding of the basics of DI management and care
after transphenoidal hypophysectomy, if appropriate.
Knowledge: Illness Care; Knowledge: Medication;
Knowledge: Treatment Regimen

Teaching: Procedure/treatment

1. Teach the patient appropriate administration of exogenous

vasopressin and its side effects.

2. Explain exogenous hormone replacement if the anterior pituitary

1620
gland was damaged or removed during surgery. If the patient is
also experiencing anterior pituitary dysfunction
(panhypopituitarism), teach the indicators of hormone replacement
excess or deficiency.

• Adrenal hormone excess: weight gain, moon face,

easy bruising, fatigue, polyuria, polydipsia

• Adrenal hormone deficiency: weight loss, easy

fatigability, abdominal pain, excess pigmentation

• Thyroid hormone excess: heat intolerance,

irritability, tachycardia, weight loss, diaphoresis

• Thyroid hormone deficiency: bradycardia, cold

intolerance, weight gain, slowed mentation

• Androgen replacement deficiency: some degree of

sexual dysfunction, ranging from menstrual
irregularities to infertility and impotence
3. Demonstrate the method for accurate measurement of urine
specific gravity and the importance of keeping accurate records of
test results.

4. Teach when to seek medical attention, including signs of

dehydration (hypernatremia) and water intoxication
(hyponatremia).

5. Explain the importance of obtaining a medical alert bracelet and

identification (ID) card.

6. Stress the importance of continued medical follow-up.

7. For patients with permanent need for hormone replacement,

explain the method for obtaining a medical alert bracelet and ID

1621
card outlining diagnosis and appropriate treatment in the event of
an emergency.

Teaching: Disease Process; Teaching: Prescribed Medication;

Emotional Support

Additional nursing diagnoses

If the patient has developed DI following a transphenoidal
hypophysectomy, see Decreased intracranial adaptive capacity,
Ineffective breathing pattern, Risk for infection, and Pain in Care of
the Patient after Intracranial Surgery, Chapter 7; also see
Hypernatremia and Hyponatremia in Fluid and Electrolyte
Disturbances, Chapter 1.

Hyperglycemia
Pathophysiology
Over the last several decades, the incidence of diabetes mellitus has
risen. According to the 2014 National Diabetes Statistics Report,
29.1 million Americans, or 9.3% of the U.S. population, have
diabetes. Of these, 8.1 million people are undiagnosed. The disease
is associated with serious complications, including heart disease,
stroke, kidney disease, various eye diseases, and nerve damage,
which contribute to increased medical costs. Direct costs of care are
about $176 billion dollars; 2.3 times higher than for people without
diabetes.
Type 1 and type 2 diabetes result from separate causes. People
with type 1 diabetes are genetically predisposed to a trigger, often a
viral illness, which results in destruction of the insulin-producing
beta cells in the pancreas, leading to an abrupt, permanent loss of
insulin production. Insulin is the hormone that attaches cells,
allowing passage of glucose from the bloodstream into the cell.
People with type 1 diabetes require daily insulin injections to
support their basal metabolic needs and to manage hyperglycemia
resulting from food ingestion.
People with type 2 diabetes are initially insulin-resistant and

1622
subsequently have a gradual decline in insulin production and
secretion over years of time. T-defective cellular insulin receptors
do not allow transport of glucose into the cell by insulin. The lack of
receptor insulin sensitivity is associated with increased hepatic
glucose production, given cells “signal” that the intracellular
environment lacks glucose needed to produce sufficient energy for
effective cellular function of all organs and body systems.
Additional hepatic glucose production further increases blood
glucose levels. Type 2 diabetes is initially treated with oral agents
and is likely to require insulin as the disease progresses.
The importance of managing hyperglycemia in hospitalized
patients came to the forefront in 2001 with a landmark study by
Van den Berghe and colleagues. The study revealed dramatic
improvement in outcomes of postoperative cardiovascular surgical
intensive care patients when glucose was maintained at 80 to 110
mg/dL using IV insulin as opposed to a conventional treatment goal
of 180 to 200 mg/dL. With this goal for “tight control,” patients with
no previous history of diabetes often required treatment as well
because, postoperatively, the stress response elevated blood
glucose. After 12 months of study, intensive insulin therapy
reduced ICU mortality to 4.6% from 8.0% with conventional
therapy (P < 0.04 with adjustment for sequential analyses). For
patients who remained in the unit longer than 5 days, mortality
using intensive insulin therapy was reduced to 10.6% from 20.2%
using conventional therapy. Total in-hospital mortality was
reduced 34%, BSIs by 46%, acute renal failure requiring dialysis or
hemofiltration by 41%, the median number of red blood cell
transfusions by 50%, and critical illness polyneuropathy by 44%.
The greatest reduction in mortality involved deaths caused by
multiple organ failure with a proven sepsis focus. Many hospitals
found this target unachievable, given that the risk of hypoglycemia
was too high, unless there was a knowledgeable champion to
oversee safe, effective, and efficient methods of insulin
administration.
The Van den Berghe study raised awareness of the importance of
glycemic control. In early 2009, the NICE SUGAR study improved
practice by providing a more realistic, safer, and achievable target
glucose range. The trial highlighted the unacceptably high

1623
incidence of hypoglycemia seen with tight control and
recommended hypoglycemia could be avoided while maintaining
glucose control using a less stringent target. On the basis of this
study, the American Diabetes Association (ADA) and American
Association of Clinical Endocrinologists (AACE) now recommend
patients who are critically ill be controlled to glucose values of 140
to 180 mg/dL. For more stable hospitalized patients who are eating
meals, the recommendation is for premeal blood glucose values be
less than 140 mg/dL. There are patients who may benefit from a
lower target, but, given the nature of critical illness, the target
glucose range should not be lower than 110 mg/dL for patients who
are critically ill. The Society of Thoracic Surgeons recognizes use of
IV insulin for cardiac surgery patients to maintain a target of 110 to
140 mg/dL as a class I treatment recommendation.
No “best” method for dosing and delivery of IV insulin has
been established. Evidence revealed insulin binds to IV tubing, and
therefore 20 to 50 ml must be flushed through the tubing into an
external receptacle before initiating the insulin infusion. Binding
sites within the wall of the tubing are “saturated” with insulin by
this procedure, allowing for all insulin within the infusion to be
delivered to the patient. There are no guidelines for standardization
of a “loading dose” or initial IV bolus, at what rate to begin the
infusion, or titration to the patient’s response. Thus, glucose
management targets have been set without a “road map” for how
to safely achieve them. Institutions are best served to have an
interprofessional committee decide the type of dosing and
monitoring regimen that is both safe and feasible. The patient
population, available infusion pumps, nurse and physician
expertise with evidence-based hyperglycemia management
practices, nurse staffing, and physician support must be considered
to both control blood glucose and protect patients from
hypoglycemia. Many published protocols require hourly glucose
monitoring and dosage adjustment. Given the workload associated
with hourly monitoring, several computerized insulin-dosing
systems are available to assist nurses with ongoing infusion
management.
Despite quality organizations and insurers’ familiarity with the
challenges of glycemic control, in October 2009, occurrences of

1624
hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic
hyperosmolar syndrome (HHS) were deemed “never events” for
hospitalized patients. If patients can be harmed by the occurrence of
a problem acquired in the hospital, insurers are not required to pay
for care associated with a selection of those events considered
preventable. If patients are admitted with a history of the selected
condition, hospitals are paid if the problem reoccurs during
hospitalization. Careful admission screening of all patients related
to past experience with both hyperglycemia and hypoglycemia is of
paramount importance to realize payment for treatment of the
patients.

Diabetic ketoacidosis
Pathophysiology
DKA is a life-threatening complication of diabetes mellitus
characterized by hyperglycemic crisis, ketosis, acidosis,
hypovolemic shock caused by dehydration, and electrolyte
imbalance involving potassium. Progressive hyperglycemia occurs
because of inadequate circulating insulin, preventing cellular
uptake of glucose and resulting in a state of starvation at the
cellular level. Without glucose available inside the cells, the cells are
unable to perform their work effectively. Starvation prompts
glucagon secretion from the pancreas and release of other stress
hormones, including catecholamines, cortisol, and GH, which
facilitate glycogenolysis and gluconeogenesis, further raising
plasma glucose. Intracellular hypoglycemia continues to prompt a
series of responses in an effort to produce glucose to “feed” the
“starving cell.” Proteolysis and lipolysis ensue, forming free fatty
acids, which are converted to ketoacids (acetoacetate, β-
hydroxybutyrate, and acetone), caused by lack of intracellular
glucose required for normal metabolic conversion of the acids.
Accumulation of ketones creates a metabolic acidosis. The
excessive glucose and ketones in the blood cause severe osmotic
diuresis as intracellular fluids move into the vascular compartment
to dilute the blood; however, the excess fluid is eliminated by the
kidneys, which also lose the ability to effectively eliminate excess

1625
glucose. A vicious cycle of progressive metabolic disruption begins
and will continue until hydration, insulin, and additional
management of acidosis/fluid and electrolyte imbalance are
provided. Osmotic diuresis causes loss of sodium, potassium,
phosphorus, magnesium, and body water, which leads to
dehydration and, possibly, hypovolemic shock. Increased blood
viscosity and platelet aggregation can result in thromboembolism.
Despite significant loss of potassium in the urine, the patient may
initially manifest normal or elevated plasma potassium because of
the dramatic shift of potassium out of the cells secondary to insulin
deficiency, acidosis, and tissue catabolism. Dehydration lowers BP
and decreases tissue perfusion. Because of a lack of oxygen
delivery, cells begin anaerobic metabolism. The resulting lactic acid
waste products worsen acidosis. Low pH stimulates the respiratory
center, producing deep, rapid Kussmaul respirations. Abundant
plasma ketones cause fruity or acetone breath. If not managed,
elevated serum osmolality, acidosis, and dehydration depress
consciousness to a coma state. Death can result.
The cause of death in patients with DKA and the other
hyperglycemic emergency, HHS, is rarely caused by the metabolic
complications of hyperglycemia or metabolic acidosis. Death is
related to the underlying medical illness that caused the metabolic
decompensation. Successful treatment depends on a prompt and
careful evaluation for the precipitating cause(s). The clinical
symptoms of DKA generally appear within 24 hours of failure to
manage hyperglycemia.

Hyperglycemic hyperosmolar syndrome

Pathophysiology
Hyperglycemic hyperosmolar syndrome (HHS) is a life-
threatening emergency created by a relative insulin deficiency and
significant insulin resistance, resulting in severe hyperglycemia
with profound osmotic diuresis, leading to life-threatening
dehydration and hyperosmolality. HHS is also known as
hyperosmolar hyperglycemic state, hyperosmolar nonketotic
syndrome (HONK), hyperosmolar nonketotic state (HNS),

1626
hyperglycemia hyperosmolar nonketotic syndrome (HHNS), and,
traditionally, hyperosmolar hyperglycemic nonketotic coma
(HHNK). HHNK, HHNS, HNS, and HONK are somewhat incorrect
titles for the syndrome, as recent evidence reveals a mild degree of
ketosis is often present with HHS, and true coma is uncommon. The
mortality rate of HHS ranges from 10% to 50%, higher than that for
DKA (1.2% to 9%). Mortality data are difficult to interpret because
of the high incidence of coexisting diseases or comorbidities.
Historically, HHS and DKA were described as distinct
syndromes, but one-third of patients exhibit findings of both
conditions. HHS and DKA may be at opposite ends of a range of
decompensated diabetes, differing in time of onset, degree of
dehydration, and severity of ketosis. HHS occurs most commonly
in older people with type 2 diabetes, but with the recent obesity
epidemic, occasionally obese children and teenagers with both
diagnosed and undiagnosed type 2 diabetes manifest HHS. The
cascade of events in HHS begins with osmotic diuresis. Glycosuria
impairs the ability of the kidney to concentrate urine, which
exacerbates the water loss. Normally, the kidneys eliminate glucose
above a certain threshold and prevent a subsequent rise in blood
glucose level. In HHS, the decreased intravascular volume or
possible underlying renal disease decreases the glomerular
filtration rate, causing the glucose level to increase. More water is
lost than sodium, resulting in hyperosmolarity. Insulin is present,
but not in adequate amounts to decrease blood glucose levels, and
with type 2 diabetes, significant insulin resistance is present. DKA
and HHS are compared in Table 8-4.

Table 8-4
COMPARISON OF DIABETIC KETOACIDOSIS (DKA) AND
HYPERGLYCEMIC HYPEROSMOLAR SYNDROME (HHS)

Criterion DKA HHS

Diabetes Type 1 Type 2; rarely, Type 1
type
Typical More common in young children and 57 to 69 years with average age 60 years
age group adolescents than adults
Signs and Polyuria, polydipsia, polyphagia, Same as DKA, but slower onset Also, very
symptoms weakness, orthostatic hypotension, commonly, neurologic symptoms
lethargy, changes in LOC, fatigue, predominate
nausea, vomiting, abdominal pain

1627
 Physical Dry and flushed skin, poor skin Same as DKA, but no Kussmaul
assessment turgor, dry mucous membranes, respirations or fruity odor to the breath;
decreased BP, tachycardia, altered instead, occurrence of tachypnea with
LOC (irritability, lethargy, coma), shallow respirations
Kussmaul respirations, fruity odor to
the breath
History Recent stressors such as surgery, Undiagnosed type 2 diabetes mellitus;
and risk trauma, infection, MI; insufficient recent stressors such as surgery, trauma,
factors exogenous insulin; undiagnosed type 1 pancreatitis, MI, infection; high-calorie
diabetes mellitus enteral or parenteral feedings in a
compromised patient; use of diabetogenic
drugs (e.g., phenytoin, thiazide diuretics,
thyroid preparations, mannitol,
corticosteroids, sympathomimetics)
Monitoring ECG: Dysrhythmias associated with ECG evidence of hypokalemia as listed
parameters hyperkalemia: peaked T waves, with DKA Hemodynamic measurements:
widened QRS complex, prolonged PR CVP <3 mm Hg below patient’s baseline;
interval, flattened or absent P wave. PADP and PAWP <4 mm Hg below
Hypokalemia (K+ <3 mEq/L), which patient’s baseline
may produce depressed ST segments,
flat or inverted T waves, or increased
ventricular dysrhythmias
Diagnostic Serum glucose: >250 mg/dL >600 mg/dL
tests
Serum ketones: Large presence Usually absent to mild presence because
of dehydration
Urine glucose: Positive Positive
Urine acetone: “Large” Usually negative
Serum osmolality: >290 mOsmol/L >320 mOsmol/L
Bicarbonate: <15 mEq/L >15 mEq/L
Serum pH: <7.2 Normal or mildly acidotic (pH ≤7.4)
Anion Gap: Elevated >13 Normal
Serum potassium: normal or elevated Normal or >3.5 mEq/L
>5.0 mEq/L initially and then
decreased
Serum sodium: elevated, normal, or Elevated, normal, or low
low
Serum Hct: elevated because of Elevated because of hemoconcentration
osmotic diuresis with
hemoconcentration
BUN: elevated >20 mg/dL Elevated
Serum creatinine: >1.5 mg/dL Elevated
Serum phosphorus, magnesium, Elevated
chloride: decreased
WBC: elevated, even in the absence of Normal unless infection present
infection
Onset A few days Days to weeks
Mortality 1 to 10% 14 to 58% because of age group and
complications such as stroke, thrombosis,
renal failure
BP, Blood pressure; BUN, blood urea nitrogen; CVP, central venous pressure; DKA,
diabetic ketoacidosis; ECG, electrocardiogram; Hct, hematocrit; HHS, hyperglycemic
hyperosmolar syndrome; LOC, level of consciousness; MI, myocardial infarction;
PADP, pulmonary artery diastolic pressure; PAWP, pulmonary artery wedge
pressure; WBC, white blood cell count.

1628
 Primary causes of HHS include infections, noncompliance with a
diabetes management regimen, undiagnosed diabetes, medications,
substance abuse, and coexisting diseases. Infections are the leading
cause (57% of patients); pneumonia (often Gram-negative) is the
most common, followed by urinary tract infection (UTI) and sepsis.
Lack of compliance with diabetic medications or other aspects of
diabetes management may be a frequent cause (21%). Undiagnosed
diabetes prompts a failure to recognize early symptoms of the
complications of unmanaged hyperglycemia. Acute coronary
syndrome (myocardial infarction [MI]), stroke, pulmonary embolus,
and mesenteric thrombosis have caused HHS. At least one study
revealed that, in urban populations, the three leading causes are
lack of compliance with medications, drinking alcohol, and using
cocaine. Chronic use of steroids and gastroenteritis are commonly
associated with HHS in children.
The blood glucose level is higher with HHS than with DKA. A
global electrolyte loss is present. Sodium and potassium levels vary
at diagnosis, but deficiencies of both are present. Magnesium,
calcium, phosphate, and chloride deficiencies evolve. Patients may
lose from 15% to 25% of total body water, or approximately 100 to
200 mL/kg. Fluids are drawn from cells to dilute the concentrated
bloodstream, resulting in significant intracellular dehydration.
Neurologic deficits occur in response to severe dehydration and
hyperosmolality. The blood is highly viscous and flow slows,
increasing risk for the formation of thromboemboli. Increased
cardiac workload and decreased renal and cerebral blood flow may
result in MI, renal failure, and stroke.
Unlike DKA, wherein acidosis produces severe symptoms,
HHS develops slowly, and frequently symptoms are nonspecific.
Polyuria and polydipsia occur but may be ignored. Neurologic
deficits may be mistaken for dementia. Similarity of symptoms to
other disease processes in older adults may delay diagnosis and
treatment, allowing the process to progress.

Metabolic assessment: Hyperglycemia

Goal of metabolic assessment

1629
Evaluate for degree of hyperglycemia and its effects on overall
hemodynamics, respiratory rate/pattern, and mental status.
Hyperglycemia may be asymptomatic or, with DKA, result in
hypotension causing decreased perfusion, increased work of
breathing with Kussmaul respirations, ineffective breathing
patterns, abdominal pain, and neurologic deficits, including coma
and/or stroke-like symptoms. HHS findings are similar but are
more likely to result in neurologic changes, cause abdominal pain
less often, and almost never cause compensatory Kussmaul
respirations, because acidosis is mild, if present at all. Dehydration,
hyperglycemia, and acidosis must be managed immediately.
Associated electrolyte imbalances may be managed as the patient’s
glucose level normalizes and hydration is provided.

History and risk factors

Hyperglycemia manifests more commonly in hospitalized patients
with diabetes mellitus or impaired glucose tolerance than in
hospitalized patients without diabetes who experience an
exaggerated response to stress. Patients who are obese are more
likely to have insulin resistance associated with metabolic
syndrome, impaired tolerance for glucose, or undiagnosed type 2
diabetes mellitus. Type 2 diabetic patients generally manifest HHS
when hyperglycemia is ineffectively managed. Rarely, a patient
with type 2 diabetes will manifest DKA. The majority of patients
with DKA have type 1 diabetes mellitus. The patient with type 1
diabetes will die without adequate insulin administration.

Recent stressors that prompt DKA in patients with diabetes

mellitus infection (20% to 55%)
This may be overestimated because DKA may prompt leukocytosis
and vasodilation, which mimic sepsis.

Inadequate insulin/noncompliance (15% to 40%)

Teenagers may be at higher risk for noncompliance; all illnesses
increase stress, which increases the need for insulin. Patients with
type 1 diabetes are totally reliant on administration of exogenous
insulin to control hyperglycemia, because without functional beta

1630
islet cells in the pancreas, they have no ability to produce insulin.

Undiagnosed diabetes (10% to 25%)

Onset of type 1 diabetes is generally preceded by a significant
illness; often a viral infection or childhood disease.

Other medical illness (10% to 15%)

Pneumonia, UTI, ischemic bowel, pregnancy, hypothyroidism,
pancreatitis, pulmonary embolism, surgery, and new medications
(notably corticosteroids, sympathomimetics, alpha- and beta-
blockers, fluoroquinolone antibiotics [Levaquin; Janssen
Pharmaceuticals, Titusville, NJ], and diuretics)

Cardiovascular disease (3% to 10%)

Significant cardiovascular disease may be the result of diabetes
mellitus, and thus unstable patients may experience variable stress
levels, making control of hyperglycemia difficult. Vascular events
such as MI, cerebrovascular accident (CVA), or ischemic bowel may
precipitate or worsen DKA.

Cause unknown (5% to 35%)

Any physiologically stressing illness or event has the potential to
cause the condition. Certain women are more likely to go into DKA
at the time of menstruation. Severe emotional stress is associated
with onset of DKA.

Recent stressors that prompt HHS in patients with diabetes

mellitus
Diabetes: First symptomatic presentation of undiagnosed
hyperglycemia; poor control of hyperglycemia (noncompliance,
inadequate resources, abuse or neglect of the patient by caregivers
or self-inflicted, accidental omission of medication, or ingestion of
excessive carbohydrates)

Associated medical conditions

1. Infection: Urinary tract, pneumonia, cellulitis, sepsis, dental

infection/abscess

1631
2. Cardiovascular disease: MI or other acute coronary syndromes

3. Cerebral vascular disease: Stroke or intracranial hemorrhage

4. Temperature alteration: Hyperthermia or hypothermia

5. Mesenteric ischemia: Intestinal/bowel ischemia or bowel

infarction

6. Pancreatitis

7. Pulmonary embolism

8. Acute abdomen

9. Acute renal failure or decompensated chronic renal failure

(“acute on chronic”)

10. Burns

11. Hyperthyroidism

12. GI bleeding

13. Cushing syndrome or other ACTH-secreting tumor

Medication-related

1. Beta-blockers: Metoprolol, atenolol, propranolol

2. Carbonic anhydrase inhibitors: Diazoxide

3. Calcium channel blockers: Diltiazem, verapamil

4. Antipsychotics: Chlorpromazine, olanzepine

5. Loop and thiazide diuretics: Furosemide, bumetanide, HCTZ

6. Glucose-containing fluids: Total parenteral nutrition, tube

feedings, dialysis solutions

1632
7. Glucocorticoids/steroids: Cortisone, hydrocortisone, prednisone,
methylprednisolone

8. H2-receptor antagonists: Ranitidine, cimetidine, famotidine

9. Anticonvulsants: Phenytoin

10. Substance abuse: Alcohol, amphetamines, cocaine, 3,4-

methylenedioxy-methamphetamine, popularly known as “ecstasy”)

Vital signs
• Findings vary significantly, depending on patient’s situation.
Mild to moderate hyperglycemia generally has no effect on vital
signs.

• Tachycardia and tachypnea are present if a hyperglycemic crisis

(DKA, HHS) is present or if hypoglycemia is present.
Hypovolemia alone may prompt tachycardia and possibly
associated tachypnea.

• Hypotension is present with DKA and HHS or if hypoglycemia is

present.

Observation
• Mild to moderate hyperglycemia alone may not cause overt
physical assessment changes.

• Skin should be examined for lesions, rashes, cellulitis, and other

signs of possible infection.

• If the patient presents to the emergency department, observe for

signs of recent alcohol consumption.

• DKA: Kussmaul respirations (rapid, deep) are present to exhale

CO2 as a compensatory response to relieve metabolic acidosis;
may appear fatigued, with or without diaphoresis from
Kussmaul breathing.

1633
• DKA and HHS:

1. Significant abdominal pain: Present in at least 40% of patients;

paralytic ileus or gastroparesis may be present but will resolve
when hyperglycemia and dehydration are managed.

2. Hypoperfusion: Ashen, pale, or grayish blue facial color, lip

color, or nail beds caused by severe hypotension and decreased
blood volume because of dehydration

3. Dehydration: Poor skin turgor, dry mouth and/or lips, sunken

eyes, slow capillary refill

4. Malaise: Generalized weakness, possible exhaustion, nausea and

vomiting, impaired vision, and leg cramps may be present; patients
may become unable to get out of bed.

5. Cranial nerve dysfunction: Examination may be abnormal with

nerve palsies present.

6. Altered mental status: Confusion, disorientation and

agitation are more common with older adults. Stroke-like
symptoms may be present. Coma is present in about 10% of
patients presenting with HHS. Seizures are present in 25% of HHS
patients.

7. Severe shock: If severe shock has ensued, agitation is more

commonly associated with hypoxemia; somnolence is associated
with hypercarbia (elevated CO2 level) and acidosis.

8. Associated findings: Heart failure, pneumonia, and other risk

factors if hyperglycemic crisis is present.

Auscultation
• Hyperglycemia does not change baseline physical assessment,
unless it has progressed to crisis level (DKA, HHS).

• Clear breath sounds with DKA and HHS because dehydration is

1634
 present.

• Bowel sounds may be absent if paralytic ileus and gastroparesis

are present with DKA and HHS.

• Heart sounds may reflect heart failure with DKA and HHS.

Palpation
• DKA: Abdomen may be palpated if abdominal pain is present.

Percussion
• DKA and HHS: Lung percussion may reveal presence of
consolidation or fluid (dullness) indicative of a pulmonary
infection.

Screening lab work

• POC capillary blood glucose: Bedside glucose monitoring using a
glucose meter for immediate evaluation of capillary glucose level.

• If POC glucose is elevated, a plasma glucose sample

should be drawn.

• In addition, if DKA or HHS is suspected:

• Arterial blood gas (ABG) analysis: Done promptly to evaluate for

acidosis, hypoxemia, and hypercapnia

• Complete blood count (CBC): Evaluate for elevated WBCs

indicative of infection

• Sputum and urine culture and sensitivity: Identifies infecting

organism

• Blood culture and sensitivity: If positive, indicates organism has

migrated into the bloodstream to cause a systemic infection

1635
Diagnostic Tests for Hyperglycemia and Hyperglycemic
Emergencies

Test Purpose Abnormal Findings

Hemoglobin Assesses for control of blood HbA1C target: <6.5–7 for most people.
A1c (HbA1c) glucose for the 6 to 8 weeks A less stringent target of 7 to 8%
or preceding the test. Recommended may be appropriate for patients with
glycosylated screening for a ll hospitalized limited life expectancy, advanced
hemoglobin: patients so poorly controlled blood complications, sever hypoglycemic
Performing this glucose readings can be addressed unawareness or extensive
test more immediately to avoid development comorbidities. An abnormal HbA1C
frequently of DKA (diabetic ketoacidosis) or result may be used to help
than every 6 to HHS (hyperglycemia hyperosmolar determine if a change in the
8 weeks does syndrome) previous home plan is required.
not yield If a patient without diabetes has an
useful elevated value, the patient should
information undergo a full evaluation for
about blood presence of undiagnosed diabetes.
glucose
control
Fasting blood Evaluates the effectiveness of basal ≤40 mg/dL: Severe hypoglycemia
glucose (FBG): insulin dosage by assessing for 41 to 69 mg/dL: Hypoglycemia
Test is presence of hyperglycemia or 70 to 110 mg/dL: Normoglycemia
performed in hypoglycemia; used for daily 111 to 125 mg/dL: Borderline
the morning screening of blood glucose control hyperglycemia
after fasting all during hospitalization 126 to 180 mg/dL: Hyperglycemia
night and 181 to 220 mg/dL: Significant
before hyperglycemia
consuming >220 mg/dL: Possible impending DKA
breakfast. or HHNS if glucose is not managed
Mealtime blood Assesses blood glucose control with Premeal glucose: < 110 mg/dL. If <140
glucose: existing hyperglycemia mg/dL, no change in premeal dose of
Generally, a management program short-acting insulin is required. Once
point-of-care >140 mg/dL a supplemental dose of
(POC) reading short-acting insulin may be necessary.
is done either
15 to 30
minutes before
a meal or as
the meal
begins.
Postprandial Evaluates ability of glucose to 180 mg/dL: If glucose is >180 mg//dL
blood glucose: normalize following a meal. at 1 hour following a meal, the
May be done 1 Readings may be done 1–2 hours patient is unable to produce enough
to 2 hours following the meal. insulin, or has not received enough
following mealtime insulin, or may be insulin-
meals using resistant, or may require initiation of
serum glucose mealtime insulin.
or point of 140 mg/dL: If glucose is >140 mg/dL at
care capillary 2 hours following a meal, the patient
glucose is unable to produce enough insulin
readings or may be insulin-resistant.
Oral glucose Used to test for diabetes, insulin FBG 126 mg/dL with 2-hour reading
tolerance test: resistance, and reactive 200 mg/dL: Confirms diagnosis of
Following at hypoglycemia. Fasting blood diabetes mellitus (DM)

1636
 least 8 hours glucose (FBG) is used at the FBG 111 to 125 mg/dL with 2-hour
of fasting, oral beginning of the test. Additional reading >140 mg/dL: Patient has
glucose is readings are done 2 hours later. impaired glucose tolerance (IGT)
consumed by Fasting readings are compared to 2 FBG 111< to 125 mg/dL with 2-hour
the patient to hours after glucose ingestion to reading >140 mg/dL: Patient has
determine determine extent of glucose impaired fasting glucose (IFT)
how quickly it intolerance.
is cleared from
the blood.
Arterial blood Assess for abnormal gas exchange pH changes: With DKA, may be 6.8 to
gas analysis or compensation for metabolic 7.2; acidosis results from ketosis or
(ABG): derangements in patients in lactic acidosis
Done promptly, hyperglycemic crisis; profound Carbon dioxide: With DKA, decreased
following acidosis can indicate DKA is CO2 reflects tachypnea and
confirmation present, since HHS typically Kussmaul respirations
of presents with minimal to mild Hypoxemia: With DKA or HHS, Pao2
hyperglycemia acidosis unless prolonged, severe <80 mm Hg may indicate
to assess for hypovolemic shock is present. pneumonia precipitated the crisis
DKA and Oxygen saturation: If pneumonia or
HHS. heart failure is present, Sao2 may be
<92%
Bicarbonate:
HHS: HCO32 15 to 22 mEq/L;
DKA: HCO32 may be <15 mEq/L
Base deficit: HHS at or above −2;
DKA, above −10
Complete blood Evaluates for presence of infection Increased WBC count: >11,000/mm3 is
count (CBC) seen with bacterial pneumonias,
urinary tract infections and other
infections.
Sputum Gram Screens for pneumonia, a common Gram stain-positive: Indicates
stain, culture, underlying cause of hyperglycemic organism is present
and sensitivity crisis; identifies infecting organism Culture: Identifies organism
Sensitivity: Reflects effectiveness of
drugs on identified organism
Blood culture Screens for sepsis, a common Secondary bacteremia: A frequent
and sensitivity underlying cause of finding; patients with bacteremia are at
hyperglycemic crisis higher risk for developing respiratory
Identifies whether an organism has failure.
become systemic
Blood chemistry Screens for electrolyte imbalances; DKA and HHS: Hypernatremia is
potassium imbalances may create present: BUN, creatinine, and K1
potentially dangerous dysrhythmias may be elevated, normal, or low.
Anion gap DKA: >13
Anion gap HHS: 10 to 12
Plasma Screens for elevated osmolality Osmolality is increased more with
osmolality associated with severe HHS than with DKA.
hyperglycemia DKA: 290 to 320 mmol/L
HHS: >320 mmol/L
Urine ketones Screens for the presence of ketones DKA: Ketones strongly positive
to confirm diagnosis of DKA; HHS: Ketones negative, or mildly
HHS does not cause ketonuria. positive
12-Lead ECG Used to rule out myocardial Hyperkalemia: Tall, peaked T waves if
infarction as the cause of HHS or increased K+ is present before
DKA management of hyperglycemia,
hypovolemia and acidosis;

1637
 PVCs/ventricular irritability is seen
with decreased K+ seen as insulin
normalizes glucose.
Chest Screens for pneumonia and acute “Fluffy whiteness” may not initially be
radiograph respiratory distress syndrome, present caused by dehydration, but
which may prompt DKA and HHS may appear as patient is rehydrated if
patient has underlying pneumonia or
ARDS

Computed Screens for ischemic and Generally not done until patient has
tomography hemorrhagic stroke, which may had at least 1 hour of rehydration and
(CT) brain scan prompt DKA and HHS insulin therapy to see if symptoms
to altered mental resolve spontaneously.
status or “stroke-
like” symptoms

Collaborative management
When managing hyperglycemia in hospitalized patients, the
following key elements should be considered in evaluating current
management blood glucose control strategies:

1. Oral hypoglycemic agents are not recommended for use in

acutely ill or unstable hospitalized patients, because the response to
therapy is unpredictable

2. Guidelines should be evidence-based and parallel the

recommendations of the recognized expert organizations (ADA and
AACE).

3. Protocols and/or order sets must be “user-friendly” and clearly

written with minimal abbreviations and strive to keep
mathematical calculations to a minimum.

4. A system should be in place to identify patients who need insulin

or adjustment in an existing insulin regimen.

5. Variations in nutritional requirements and/or nutritional support

should be identified, recognized, and included in the planning of
any insulin-dosing regimen for patients with varying levels of
stability as they move through the hospital.

6. Requirements for safe insulin administration, including

availability of POC testing, IV pumps that can deliver volumes less

1638
than 1 mL accurately, and staffing with competent nurses must be
considered before implementation of a glycemic control program.

7. Expert nurse consultants and/or certified diabetes educators who

can provide education should be available to both patients and staff
nurses.

8. An interdisciplinary team should be formed to address the

following questions about the hospital’s hyperglycemia
management practices:

A. Does the current insulin dosing regimen:

1. Assume all patients can be placed into one of a

few subgroups for dosage adjustment?

2. Take into consideration the patient’s insulin

sensitivity and/or insulin resistance when
titrating toward the target level?

3. Provide small, incremental dosage changes to

keep the patient safely within the target range
without causing extreme fluctuations in glucose
(hypoglycemia, when treated, resulting in
hyperglycemia)?

4. Have equipment/infusion reconstitution available

for insulin dosage adjustments of 0.1 U/h, which
several best practice dosing regimens require?

B. Has the total hyperglycemia management approach been proved

to be effective and safe and meet current evidence-based
guidelines? Have data been gathered on the patients to measure

1639
both glucose control and incidence of hypoglycemia?

C. Can nurses throughout the hospital safely implement the insulin-

dosing regimen? During IV insulin infusions and when patients are
transitioned from IV to subcutaneous insulin, nurses must be
appropriately educated and have sufficient staffing to safely
manage the patients.

Care priorities

1. Resuscitate patients with severe dehydration in

hypovolemic shock

• Evaluate basic ABCs: airway, breathing, and circulation.

• Intubate and ventilate patients with hypoxemia/decreasing

oxygen saturation.

• Place at least two large-bore IV lines or have a central line

inserted.

• Monitor continuous ECG, pulse oximetry, and frequent, if not

constant, BP.

• Apply oxygen, or set oxygen appropriately if mechanical

ventilation is used.

• Monitor urine output judiciously.

• Consider inserting a nasogastric tube if high risk for aspiration.

2. Provide aggressive rehydration to replace fluid loss

from polyuria

HHS:

• Large amounts of isotonic IV fluids (normal saline, sometimes

greater than 9 L) may be required to rehydrate the patient. Half-
normal saline is sometimes used. Osmotic diuresis causes a 100 to
200 mL/kg fluid loss. At least 1 L of saline should be

1640
 administered during the first hour of therapy. The remaining 8 L
should ideally be infused within the next 24 hours.

• Once the blood sugar falls below 300 mg/dL, change the IV fluid
to 5% dextrose with 45% NaCl at 150 to 250 ml/h.

• Hemodynamic or CVP monitoring may be needed to provide

aggressive rehydration, as large amounts of fluids may not be
well tolerated in older adults. Highly viscous blood is prone to
thrombosis. Patients, particularly elders, are at risk of developing
thrombotic complications before, during, and after a severe
hyperglycemic crisis.

DKA:

• Large amounts of nondextrose, isotonic IV fluids are needed.

Half-normal saline is sometimes used. From 1 to 2 L may be
needed over the first 60 to 90 minutes. Approximately 4 L should
be infused over the first 5 hours, and then the patient should be
reevaluated for need for further hydration.

• Once the blood sugar falls below 300 mg/dL, change the IV fluid
to 5% dextrose with 45% NaCl at 150–250 ml/h.

• Older patients or those with comorbidities that complicate

therapy may require hemodynamic or CVP monitoring to guide
fluid replacement. Rehydration improves perfusion, which
improves oxygen delivery and thus helps to reestablish aerobic
metabolism.

• As cellular metabolism normalizes, lactic and ketotic acidosis

resolve.

3. Support hemodynamics/perfusion
Hemodynamic monitoring may be useful in guiding fluid
replacement tolerance and efficacy and may help recognize the
patient’s response to the effects of other comorbidities. Although
hypovolemic shock is the primary problem associated with
hyperglycemia, cardiogenic shock may ensue if the patient has had

1641
an MI, or septic shock is possible if severe infection is present. Use
of catecholamine infusions and steroids should be avoided, if
possible, until hyperglycemia is resolved.

4. Control hyperglycemia
Continuous IV insulin infusion via infusion pump is the preferred
method for delivering insulin. An initial IV insulin bolus may be
administered at 0.1 U/kg. Many institutions use a concentration of 1
U of insulin in 1 mL of IV fluid to simplify rate and dosage
calculations. The IV insulin infusion dose may be initiated at up to
0.1 U/kg/h during crisis states. It is imperative to perform hourly
glucose monitoring for drip titration to ensure effectiveness of the
dosage regimen. If the blood glucose does not decreased by 10%, or
50 mg/dL in the first hour, the infusion dose may need to be
increased by 0.05–0.1 U/kg/h. Titrate the infusion to achieve a
gradual blood glucose decrease of 50–70 mg/dL/h. Once the blood
glucose is below 200 mg/dL for DKA and 300 mg/dL for HHS,
decrease the insulin infusion rate by 50% to very gradually decrease
blood glucose to achieve a target range of 140 to 180 mg/dL. For
blood sugar less than 80 mg/dL, the insulin infusion can be held
(paused) for 1 hour, then restarted at a lower rate. Achievement of
target range or overshooting target range does not mean the insulin
infusion can be permanently discontinued. The rationale is similar
to the use of BP control medications. Achievement of the target is
only the first step to sustained control. The transition from the
insulin drip to a subcutaneous basal/bolus insulin regimen can
occur when the patient can tolerate eating, the blood glucose falls is
200 mg/dL, HCO32 is above 18 mEq/L, pH is higher than 7.3, and
anion gap is normal.

5. Manage electrolyte imbalances, focusing on

potassium imbalances
Before rehydration, patients are hypernatremic and may be
hyperkalemic. Those with DKA are more likely to be hyperkalemic
because of the presence of metabolic acidosis, during which
hydrogen ions force K1 (potassium ions) out of the cells into the
bloodstream. As hydration progresses, perfusion improves, acidosis
resolves, and potassium moves back into the cells, with a high

1642
probability of creating hypokalemia. Electrolytes should be
measured every 2 hours. Begin adding 20 to 30 mEq/L potassium to
the IV solution when the level falls below 5.2 mEq/L, with the aim
of keeping the potassium level between 4–5 mEq/L. Should the
potassium level fall below 3.3 mEq/L during the process of
controlling the hyperglycemic crisis, immediately hold (pause) the
IV insulin to slow movement of potassium out of the blood stream
and into the cell, to avoid life-threatening dysrhythmias.
Replacement of calcium, magnesium, and phosphates may be done
as needed. Chlorides are replaced by the normal saline IV solutions.
Use of bicarbonate for management of acidosis is not
recommended, unless the acidosis does not respond to hydration
and insulin or when essential medications needed for support of
hemodynamics fail to work in the acidotic environment (e.g., if
catecholamines are needed to support BP).

6. Identify and manage the precipitating cause

As hyperglycemia is managed, further efforts should be underway
to identify the cause of the hyperglycemic crisis. A robust listing of
risk factors and probable causes was included in the beginning of
the hyperglycemia section with infections and cardiac and vascular
occlusive events as the most likely precipitating events for the
hyperglycemic crisis. If the pH and anion gap fail to improve with
hydration and insulin, other causes of shock and acidosis should be
evaluated and managed accordingly.

Care plans for hyperglycemia

Glucose, risk for unstable blood 
related to hyperglycemia resulting from the stress response associated with
critical illness, and in those who have or may be at risk for diabetes
mellitus.
Goals/Outcomes: The patient is free of hyperglycemia reflected
by normoglycemia and normovolemia; pH and serum osmolality
are within normal limits.
Blood Glucose Level, Hydration

Hyperglycemia management

1643
1. Monitor blood glucose levels as ordered or according to protocol.

2. Facilitate the patient having HbA1c measured to assess for

glycemic control before hospitalization. If the patient has received
transfusions, HbA1c is no longer a reliable measure of blood
glucose control, because the patient is circulating blood that
includes another person’s glycohemoglobin.

3. Assess for signs and symptoms of hyperglycemia, including

polyuria, polyphagia, blurred vision, headache, change in LOC,
weakness, and lethargy.

4. Monitor for urine ketones if the patient has type 1 diabetes, is

prone to ketosis because of type 2 diabetes, or manifests severe
hyperglycemia.

5. Monitor ABGs in severely hyperglycemic patients to assess if

acidosis is present.

6. Identify possible causes of hyperglycemia and work with

physicians to construct an individualized management plan.

7. Evaluate hydration status if the patient has been hyperglycemic

with polyuria caused by osmotic diuresis.

8. Encourage oral noncaloric fluid/water intake.

9. Monitor for potassium imbalance, with awareness that

hyperglycemic patients can experience wide variation in potassium
when IV insulin therapy is used to control hyperglycemia. As
glucose normalizes, hypokalemia may be present and should be
managed with careful potassium replacement.

10. Instruct the patient and significant others on how to prevent,

recognize, and manage hyperglycemia.

11. Encourage the patient to participate in POC testing to assist in

refining testing techniques if needed.

12. Discuss the need to count and control ingested carbohydrates to

1644
provide the best opportunity for glycemic control. Explain the
difference in simple (bad) and complex (good) carbohydrates and
how they are metabolized.

13. Ensure the patient understands the need for adherence to the
prescribed diet and exercise regimen.

14. Assess whether or not the patient has the financial means to
procure the proper food and medications to control hyperglycemia
following discharge from the hospital.

Hypoglycemia management

1. Identify patients at increased risk for hypoglycemia.

2. Monitor blood glucose levels carefully as ordered, especially if

insulin is used to manage hyperglycemia.

3. Assess for signs and symptoms of hypoglycemia, including

changes in personality, irritability, shakiness or tremors, sweating,
nervousness, palpitations, tachycardia, nausea, headache, dizziness,
weakness, faintness, blurred vision, difficulty concentrating,
confusion, coma, or seizures.

4. Maintain IV access for more precise management of

hypoglycemia using IV 50% dextrose rather than glucagon for
instances of severe hypoglycemia that render the patient unable to
take glucose tablets, juice, or milk.

5. Ensure the patient is given IV fluids containing 5% dextrose

when glucose approaches 250 mg/dL if receiving an IV insulin
infusion for management of severe hyperglycemia.

6. Keep the patient off oral food and fluids or on a no-calorie liquid
diet while receiving an insulin infusion. If patients receive meals
while insulin is infusing, additional mealtime subcutaneous insulin
should be given, rather than adjusting IV insulin to cover glucose
increases resulting from meals. If the IV insulin infusion is titrated
upward throughout the day for meals, the probability of
hypoglycemia is high when the patient stops eating meals at night.

1645
7. Instruct the patient and significant others regarding the signs,
symptoms, and management of hypoglycemia.

8. Collaborate with the patient and care team members to make

changes in the insulin regimen if hypoglycemic episodes occur
more than occasionally.

Fluid volume, deficient 

related to hyperglycemia-induced dehydration and osmotic diuresis.
Goals/Outcomes: Within 12 hours of initiating treatment, the
patient is euvolemic as evidenced by BP 90/60 mm Hg or greater (or
within patient’s normal range), MAP 70 mm Hg or greater, HR 60
to 100 bpm, CVP 2 to 6 mm Hg, balanced I&O, urinary output 0.5
mL/kg/h or greater, firm skin turgor, and pink and moist mucous
membranes. ECG exhibits normal sinus rhythm.
Fluid Balance, Electrolyte and Acid–Base Balance, Hydration

Hypovolemia management

1. Monitor vital signs every 15 minutes until the patient is stable for
1 hour. Monitor CVP, MAP, and possibly PAP and PCWP, if
ordered. Consult advanced practice provider for the following: HR
greater than 140 bpm or BP less than 90/60 or decreased 20 mm Hg
or greater, or MAP decreased 10 mm Hg or greater from baseline,
CVP less than 4 mm Hg, and PAWP less than 6 mm Hg.

2. Monitor hydration status: mucous membranes, pulse rate and

quality, and BP.

3. Monitor I&O. Decreased urine output may indicate inadequate

fluid volume or impending renal failure. Consult physician for
urine output less than 0.5 mL/kg/h for 2 consecutive hours.

4. Replace volume with IV fluids. Monitor for fluid overload, which

can occur as a result of rapid infusion of fluids: jugular vein
distention, dyspnea, crackles (rales), and CVP greater than 6 mm
Hg.

Fluid/electrolyte management

1646
1. Monitor for abnormal electrolyte levels as ordered.

2. Note an increase in anion gap (greater than 14 mEq/L), signaling

increased production or decreased excretion of acids. Anion gap
should decrease steadily with successful treatment of DKA.

3. Monitor for symptomatic cardiac dysrhythmias. (See Fluid and

Electrolyte Disturbances, Chapter 1.)

4. Observe for clinical signs of electrolyte imbalance associated with

DKA and its treatment:

• Hypokalemia: Ventricular dysrhythmias, muscle

weakness, anorexia, and hypoactive bowel sounds

• Hypophosphatemia: Muscle weakness, malaise,

confusion, respiratory failure, decreased oxygen
delivery, and decreased cardiac function

• Hypomagnesemia: Anorexia, nausea, vomiting,

lethargy, weakness, personality changes, tetany,
tremor or muscle fasciculations, seizures, confusion,
and difficulty managing hypokalemia
5. Weigh the patient daily, and monitor trends.

Fluid Monitoring; Invasive Hemodynamic Monitoring; Acid-

Base Management: Metabolic Acidosis; Electrolyte Management:
Hypokalemia

Risk for infection 

related to inadequate secondary defenses (suppressed inflammatory
response) caused by protein depletion and hyperglycemia.
Goals/Outcomes: The patient is free of infection as evidenced by
normothermia; HR 100 bpm or less, BP within patient’s normal
range, WBC count 11,000/mm3 or less, and negative culture results.

1647
 Infection Severity, Immune Status

Infection protection

1. Monitor for signs of infection. Fever may be suppressed

secondary to acidosis. Monitor for increased WBC count, which
initially may reflect dehydration or the stress response.

2. Because the patient is at higher risk for bacterial infection,

invasive lines should be managed carefully to avoid BSI. Central
lines should be removed as soon as possible.

3. Manage urinary catheters meticulously to prevent UTI.

4. Maintain skin integrity. Assess for areas of decreased sensation.

Skin Surveillance

Confusion, acute 
related to hyperosmolality, dehydration, or hypoglycemia
Goals/Outcomes: The patient verbalizes orientation to time,
place, and person; the patient is protected from unnecessary
complications and bodily injury.
Cognitive orientation

Neurologic monitoring

1. Monitor neurologic status frequently. Notify advanced practice

provider of deterioration.

2. Keep bed in lowest position with side rails raised, if the patient is
confused.

3. Consider nasogastric tube with suction for comatose patients to

decrease likelihood of aspiration.

4. Elevate HOB to 30 degrees to minimize the risk of aspiration.

5. Monitor blood glucose hourly while the patient is receiving

insulin infusion. Consult advanced practice provider if blood

1648
glucose drops faster than 100 mg/dL/h or if it drops to less than 250
mg/dL. Obtain prescription for glucose-containing IV solution to
prevent hypoglycemia and allow the continued administration of
insulin necessary to correct acidosis.

Hyperglycemia Management; Hypoglycemia Management

Deficient knowledge 
related to new-onset diabetes or misunderstanding of the causes and
prevention of DKA or HHS.
Goals/Outcomes: By discharge from the hospital, the patient will
be able to explain causes, symptoms, and prevention of DKA or
hyperglycemic crisis.
Hyperglycemia management, hypoglycemia management

Teaching, disease process

1. Consider referral to a diabetes educator for new onset of diabetes

or new to insulin, poor understanding of sick day management,
poor control as evidenced by elevated HbA1C.

2. Explain relationship of illness and stress to DKA or HHS.

3. Review symptoms of hyperglycemia, such as polyuria,

polydipsia, blurred vision, lethargy, weakness, and headache. GI
symptoms such as nausea, vomiting, and abdominal pain are more
common with DKA, whereas confusion, change in mentation, and
neurologic symptoms similar to stroke are more common with
HHS.

4. Review diabetes sick day management guidelines:

• Patients should continue their insulin or other

medication. During illness, sometimes additional
insulin is required.

• Monitoring of blood sugar should be done more

frequently. If not eating, the patient should monitor

1649
 it every 2 to 4 hours or more.

• People with type 1 diabetes should monitor for

ketones every 4 hours. Notify the advanced practice
provider if moderate to large amounts of ketones
are present.

• The patient should drink large amounts of clear

liquids not containing caffeine. If unable to eat solid
food, the patient should increase intake of
nutritious caloric liquids as tolerated

• Patients must understand the need to contact the

advanced practice provider or seek care in a
hospital emergency room if symptoms of
hyperglycemia worsen, vomiting persists, unable to
tolerate liquids, urine testing reveals moderate to
large amount of ketones, or unable to control blood
sugar.

5. Ensure the patient has follow-up physician and/or advanced

practice provider appointment before discharge.

6. Provide community resources for outpatient education. The

American Diabetes Association (ADA) website is another option for
patients who have limited access to community resources.

7. Provide the address and websites for the ADA: American

Diabetes Association, 18 East 48th Street, New York, NY 10017;
www.ada.org and www.diabetes.org

Teaching: Prescribed Diet; Teaching: Prescribed Medication;

Teaching: Prescribed Activity/Exercise; Emotional Support

1650
Additional nursing diagnoses
See also nursing diagnoses and interventions in Hyperkalemia,
Hypokalemia, and Hypovolemia in Fluid and Electrolyte
Disturbances, Chapter 1; Alterations in Consciousness, Chapter 1;
Prolonged Immobility, Chapter 1; and Emotional and Spiritual
Support of the Patient and Significant Others, Chapter 2.

Myxedema coma
Pathophysiology
Myxedema coma is a life-threatening condition that occurs
when hypothyroidism is untreated or when a stressor such as
infection affects an individual with known or unknown
hypothyroidism. The clinical picture of myxedema coma includes
exaggerated hypothyroidism, with decreased mental status or
coma, hypoventilation, hypothermia, hypotension, seizures, and
shock. Myxedema coma usually develops slowly, has a greater than
50% mortality rate, and requires prompt, aggressive treatment.
Even with early diagnosis and treatment, mortality is nearly 45%.
Hypothyroidism is a common endocrine disorder reflecting
inadequacy of production or uptake of the thyroid hormone.
Localized disease of the thyroid gland that results in decreased
thyroid hormone production is the most common cause of
hypothyroidism. Normally, the thyroid gland releases 100 to 125
nmol of thyroxine (T4) daily and only small amounts of
triiodothyronine (T3). T4 is a prohormone that functions as a
reservoir for the more metabolically active form of the thyroid
hormone, T3. Primary conversion occurs in the peripheral tissues
via 5’-deiodination. Decreased production of T4 and failure of
deiodinization to T3 causes an increase in the secretion of thyroid-
stimulating hormone (TSH) by the functional pituitary gland. TSH
stimulates hypertrophy and hyperplasia of the thyroid gland and
an increase in thyroid T4–5’-deiodinase activity. Early in the disease
process, compensatory mechanisms maintain T3 levels; however,
this compensatory mechanism may be short-lived.

1651
 Individuals who are acutely or critically ill may have an extreme
disruption of the normal hypothalamic–anterior pituitary–thyroid
axis, particularly related to the nocturnal surge that is normally
seen with thyrotropin. These patients will have a low T3 level even
after the TSH is restored to normal, and they are commonly
referred to as presenting with low T3 syndrome. Patients with poor
heart function or more intense inflammatory reaction show more
pronounced downregulation of the thyroid system. During sepsis,
the pituitary gland is activated via blood-borne proinflammatory
cytokines and through a complex interaction between the
autonomic nervous system and the immune cells. Sepsis elicits a
pattern of pituitary hormone dysfunction that may cause a
significant decrease in the secretion of TSH.
Hypothyroidism results in inadequate amount of circulating
thyroid hormone, causing a decrease in metabolic rate that affects
all body systems.
Primary hypothyroidism, the most common presenting form of
thyroidal disorders, is caused by thyroid suppression for any direct
reason (i.e., cancer, radiation, autoimmune dysfunction).

1. Autoimmune: The most frequent cause of acquired

hypothyroidism is autoimmune thyroiditis (Hashimoto thyroiditis).
The body recognizes the thyroid antigens as foreign, and a chronic
immune reaction ensues, resulting in lymphocytic infiltration of the
gland and progressive destruction of functional thyroid tissue.
Most affected individuals have circulating antibodies to thyroid
tissue.

2. Postpartum thyroiditis: Ten percent of postpartum women

develop lymphocytic thyroiditis 2 to 10 months after delivery. The
frequency may be 5% in women with type 1 diabetes mellitus. The
condition may only last 2 to 4 months but usually requires
treatment with levothyroxine; however, postpartum patients with
lymphocytic thyroiditis are at increased risk of permanent
hypothyroidism. The hypothyroid state may be preceded by a short
thyrotoxic state.

3. Subacute granulomatous thyroiditis: Inflammatory conditions or

1652
viral syndromes may be associated with transient hyperthyroidism
followed by transient hypothyroidism. This presentation is linked
to fever, malaise, and a painful and tender gland.

Secondary hypothyroidism results from inadequate secretion of

TSH from the anterior pituitary gland. The cause of the deficiency is
not always clear, but it is often associated with surgery, trauma, or
radiation therapy. If TSH level is inadequate, the thyroid lacks the
proper stimulus to produce T4.
Tertiary hypothyroidism is related to hypothalamic dysfunction
and is diagnosed by the release of thyrotropin-releasing hormone
(TRH). Other causes are listed in Box 8-2.

Box 8-2
COMMON CAUSES OF ACUTE
HYPOTHYROIDISM
Primary hypothyroidism
• Hashimoto thyroiditis (autoimmune)

• Surgical removal of thyroid gland

• Ablation with radioactive iodine

• External irradiation

• Defective iodine organification

• Thyroid tumor

• Drug related

• Lithium

• Interferon

• Amiodarone

1653
Secondary hypothyroidism
• Pituitary or hypothalamic disease

Because all metabolically active cells require thyroid hormone,

the effects of hormone deficiency vary. Systemic effects are caused
by either derangements in metabolic processes or direct effects by
myxedematous infiltration in the tissues. The patient’s presentation
may vary from asymptomatic to, rarely, coma with multisystem
organ failure (myxedema coma). The incidence of hypothyroidism
is 0.1–2% in the general population and is eight times more likely to
occur in women than in men. It frequently presents in the later
years of life. Older women are the most likely candidates to
present with myxedema.

Euthyroid sick syndrome (ESS) may manifest as a low

T3, low T4, low TSH, or all three. ESS results from inactivation of
5’-deiodinase, resulting in conversion of FT4 to rT3 (a reverse form
of T3 that is not metabolically active). ESS may occur in critically
ill patients without any known cause but may also present in
patients who have diabetes mellitus, malnutrition, or iodine loads
or as the result of medications (amiodarone, PTU, glucocorticoids).

Euthyroid sick syndrome (ESS) should be considered when TSH

and/or T4 are normal, T3 is low, and the patient presents with
symptoms that suggest hypothyroidism.

Endocrine assessment: Myxedema coma

Goal of system assessment
Evaluate for end-organ effects of hypothyroidism, including altered
mental status, hypothermia, hypoglycemia, hypotension,
bradycardia, and hypoventilation. Not all patients have noticeable

1654
myxedema (polysaccharide accumulation).

History and risk factors

Signs and symptoms may be life-threatening in a patient with
history of hypothyroidism who has experienced a recent stressful
event. Undiagnosed patients may report early fatigue, weight
gain, anorexia, lethargy, cold intolerance, menstrual irregularities,
constipation, depression, and muscle cramps. Family may report
depression, psychosis, cognitive dysfunction, or poor memory.

A change in mental status may be the most compelling

sign to assist in making the diagnosis.

Vital signs
Cardinal signs and symptoms of myxedema coma include
hypothermia (may be less than 26.6° C, 80° F), hypoventilation,
hypotension, and bradycardia, as well as hyponatremia and
hypoglycemia. The presentation of any three of these signs and
symptoms together should be considered in differential diagnosis
as signs of acute hypothyroidism until proven otherwise.

The presence of a normal temperature in a patient who

appears to present with acute hypothyroid dysfunction is
abnormal and should be considered an indicator of infection.

Observation
Cardiac: Nonspecific ECG changes, prolonged conduction times,
prolonged QT syndrome. Cardiac enlargement, possible effusion,
or low cardiac output. If hypotensive, may be refractory to

1655
 volume and vasopressors until thyroid hormone given.

Respiratory: Respiratory depression from reduced hypoxic drive

and decreased ventilatory response and increasing CO2. The
increase in CO2 is a major factor in the induction of coma. May
also have edema of the conducting airways.

Gastrointestinal: Anorexia, nausea, abdominal pain, and

constipation. Quiet abdomen, ileus, and megacolon are not
uncommon.

Hypothyroidism
• Possible presence of obesity and/or weight gain from fluid
retention

• The skin may be dry, cool, and coarse, and the hair may be
thin, coarse, and brittle. The tongue may be enlarged
(macroglossia), and the reflexes may be slowed. Periorbital
edema may be noted.

• There may be a surgical scar or a goiter when evaluating the neck.

Nodules may be palpated.

• The patient may have muscle weakness, memory and mental

impairment, and constipation.

• Polysaccharide substances may be deposited beneath the skin

(myxedema), which may prompt hypovolemia.

A change in mental status may be the most important

sign. It is commonly noted first to be lethargy, then stupor, and
ultimately coma.

1656
Screening lab work
Blood studies may reveal the presence of thyroid dysfunction.
Expected abnormalities include (see also Figure 8-2):

• TSH increased or normal (chronic thyroiditis)

• T4 decreased

• Hypercholesterolemia

• Elevated serum lactate

• Hypoglycemia

• Hyponatremia

• Hypoxemia

• Hypercapnia

1657
 FIGURE 8-2 Diagnosing hypothyroidism.

Common Diagnostic Tests for Hypothyroid Crisis: Myxedema

Coma

1658
Collaborative management
Care priorities

1. Stabilize the patient

• Perform emergent endotracheal intubation and provide

mechanical ventilation support: Required to relieve or prevent
profound hypoxemia and CO2 narcosis detected by Spo2 and
ETCO2 monitoring. ABG monitoring is done periodically to
validate Spo2 and ETCO2 and to monitor pH.

• Treat hypothermia: Although the hypothermia will be addressed

1659
 ultimately by the institution of thyroid hormone, it may take
several days. Extreme caution must be taken when rewarming
(only passive techniques should be used) to avoid
uncompensated vasodilation and profound hypotension.

• Treat hypotension: Before institution of even passive rewarming,

careful volume resuscitation should occur. Administer of IV
isotonic fluids (normal saline and lactated Ringer’s solution).
Hypotonic solutions, such as 5% dextrose in water (D5W), are
contraindicated because they decrease serum Na1 levels further.
These patients respond poorly to vasopressors because of
alteration in sympathetic response. Consider IV vasopressin or IV
corticosteroids.

2. Administer IV thyroid hormone as soon as possible:

Patients may die without prompt treatment
The best dose or approach to rapidly returning the circulating and
active hormones to normal is uncertain, and therefore
recommendations tend to be empiric at best. Practitioners often
initially administer T4 (levothyronine ). An effective approach is to
use IV LT4 at a dose of 4 µg/kg of lean body weight, or
approximately 200–250 µg as a bolus in a single or divided dose,
depending on the patient’s risk of cardiac disease (if at risk, give
one-half the dose), followed by 100 µg 24 hours later for
stabilization, then 50 µg IV or by mouth (PO) daily, given with IV
or PO glucocorticoids.
The best dose or approach to rapidly returning the circulating and
active hormones to normal is uncertain, and therefore
recommendations tend to be empiric at best. Practitioners often
initially administer T4 (levothyronine ). An effective approach is to
use IV LT4 at a dose of 4 µg/kg of lean body weight, or
approximately 200–250 µg as a bolus in a single or divided dose,
depending on the patient’s risk of cardiac disease (if at risk, give
one-half the dose), followed by 100 µg 24 hours later for
stabilization, then 50 µg IV or by mouth (PO) daily, given with IV
or PO glucocorticoids.

Thyroid hormone supplementation 

1660
Use of IV triiodothyronine (LT3): Controversial therapy because it
has a higher frequency of adverse cardiac events and is generally
reserved for patients who are not improving clinically on LT4. Oral
thyroid hormone (i.e., levothyroxine): This is not the avenue of
choice in myxedema coma. It is given early in treatment for primary
hypothyroidism. To prevent hyperthyroidism caused by too much
exogenous hormone, patients are started on low doses that are
increased gradually based on serial laboratory tests (TSH and T4)
and adjusted until the TSH is in a normal range. This therapy is
continued for the patient’s lifetime. For patients with secondary
hypothyroidism, thyroid supplements can promote acute
symptoms and therefore are contraindicated.

Rapid IV administration of thyroid hormone should be done

with careful monitoring, as this may cause hyperadrenalism.
Concomitant administration of IV hydrocortisone helps prevent
adrenal problems but may cause hypoadrenalism if not carefully
monitored.

3. Manage hyponatremia
If serum Na1 is greater than 120 mEq/L, fluids are restricted. If
serum Na1 is less than 120 mEq/L, consider administration
hypertonic (3%) saline followed by water diuresis.

4. Manage hypoglycemia
IV solutions containing glucose or 50% dextrose (D50).

5. Manage associated illnesses such as infections

6. Administer stool softeners

To minimize constipation caused by decreased gastric secretions
and peristalsis.

7. Avoid barbiturates

1661
Because of alterations in metabolism, patients with hypothyroidism
do not tolerate barbiturates and sedatives, and therefore central
nervous system (CNS) depressants are contraindicated.

Care plans for myxedema coma

Ineffective protection (myxedema coma) 
related to inadequate response to treatment of hypothyroidism or stressors
such as infection.
Goals/Outcomes: The patient is free of symptoms of myxedema
coma as evidenced by HR greater than 60 bpm, BP greater than
90/60 mm Hg (or within patient’s normal range), RR greater than 12
breaths/min with normal depth and pattern, and orientation to
person, place, and time.
Risk Control

Risk identification

1. Monitor vital signs frequently and note bradycardia,

hypotension, or decrease in RR. Report systolic BP greater than 90
mm Hg, HR less than 60 bpm, or RR less than 12 breaths/min.

2. Monitor the patient for hypoxia. Report significant findings to

advanced practice provider.

3. Monitor serum electrolytes and glucose levels. Note decreasing

Na1 (less than 137 mEq/L) and glucose (less than 60 mg/dL).

• Restrict fluids or administer hypertonic saline as

prescribed to correct hyponatremia. Do not correct
too rapidly, to avoid central pontine myelinolysis.

• In chronic, severe symptomatic hyponatremia, the

rate of correction should not exceed 0.5–1 mEq/L/h,
with a total increase not to exceed 12 mEq/L/d. It is
necessary to correct the hyponatremia to a safe

1662
 range (usually to no greater than 120 mEq/L) rather
than to a normal value.
4. Administer IV thyroid replacement hormones with IV
hydrocortisone and IV glucose to treat hypoglycemia.

5. Monitor for heart failure: jugular vein distention, crackles (rales),

shortness of breath (SOB), peripheral edema, weakening peripheral
pulses, and hypotension. Notify advanced practice provider of any
significant findings.

6. Keep an oral airway and manual resuscitator at the bedside in the

event of seizure, coma, or the need for ventilatory assistance.

Vital Signs Monitoring; Respiratory Monitoring; Shock

Prevention; Cardiac Care: Acute

Ineffective breathing pattern 

related to enlarged thyroid gland and/or decreased ventilatory drive caused
by greatly decreased metabolism.
Goals/Outcomes: The patient maintains effective breathing
pattern as evidenced by RR 12 to 20 breaths/min with normal depth
and pattern, normal skin color, oxygen saturation greater than 95%,
and absence of adventitious breath sounds. If ineffective breathing
pattern occurs, it is reported and treated promptly.
Respiratory Status: Ventilation; Vital Signs

Respiratory monitoring

1. Assess rate, depth, and quality of breath sounds. Monitor for

inadequate ventilation: changes in respiratory rate or pattern,
falling Spo2, pallor, or cyanosis. Report findings to advanced
practice provider promptly, including presence of adventitious
sounds (e.g., from developing pleural effusion) or decreasing or
crowing sounds (e.g., from swollen tongue or glottis).

2. Measure ecto2 and Spo2 intermittently or continuously in patients

with decreased ventilatory drive.

1663
3. Teach the patient coughing, deep breathing, and use of incentive
spirometer. For respiratory distress, assist provider with intubation
or tracheostomy and maintenance of mechanical ventilatory
assistance. Suction upper airway as needed.

Airway Management

Excess fluid volume 

related to compromised regulatory mechanisms occurring with associated
adrenal insufficiency.
Goals/Outcomes: By a minimum of 24 hours before hospital
discharge, the patient is normovolemic as evidenced by urinary
output greater than 0.5 mL/kg/h, stable weight, nondistended
jugular veins, presence of eupnea, and peripheral pulse amplitude
≥2+ on a 0 to 4+ scale.
Fluid Balance

Hypervolemia management

1. Monitor I&O hourly for evidence of decreasing output.

2. Weigh the patient at the same time every day, using the same
scale. Monitor for the following indicators of heart failure: jugular
vein distention, crackles (rales), SOB, dependent edema of
extremities, and decreased pulse amplitude. Report significant
findings to provider.

3. Restrict fluid and Na1 intake as prescribed.

Fluid Management; Electrolyte Monitoring

Activity intolerance 
related to weakness and fatigue secondary to slowed metabolism and
decreased cardiac output caused by pericardial effusions, atherosclerosis,
and decreased adrenergic stimulation.
Goals/Outcomes: During activity patient rates perceived exertion
at 3 or less on a 0 to 10 scale and exhibits cardiac tolerance to
activity as evidenced by HR 20 bpm or less over resting HR, systolic
BP 20 mm Hg or less over or under resting systolic BP, warm and

1664
dry skin, and absence of crackles (rales), murmurs, chest pain, and
new dysrhythmias.
Activity Tolerance; Endurance; Energy Conservation

Energy management

1. Monitor vital signs frequently for hypotension, slow pulse,

dysrhythmias, complaints of chest pain or discomfort, decreasing
urine output, and changes in mentation. Promptly report significant
changes to provider

2. Balance activity with adequate rest to decrease workload of the

heart.

3. Administer IV isotonic solutions such as normal saline to help

prevent hypotension.

Activity Therapy; Exercise Promotion: Strength Training

Risk for infection 

related to compromised immunologic status secondary to alterations in
adrenal function.
Goals/Outcome: The patient is free of infection as evidenced by
normothermia, absence of adventitious breath sounds, normal
urinary pattern and characteristics, and well-healing wounds.
Status; Infection Severity

Infection protection

1. Monitor for infection: fever, erythema, swelling, or discharge

from wounds or IV sites; urinary frequency, urgency, or dysuria;
cloudy or malodorous urine; presence of adventitious sounds on
auscultation of lung fields; and changes in color, consistency, and
amount of sputum. Minimize risk of UTI by providing care of
catheters.

2. Provide care to maintain skin integrity and prevent pressure

ulcers.

3. Advise visitors who have contracted or been exposed to a

1665
communicable disease not to enter patient’s room without
appropriate infection control precautions.

Identification; Infection Protection

Risk for imbalanced nutrition: More than body

requirements 
related to slowed metabolism
Goals/Outcomes: The patient does not gain weight. Within the
24-hour period before hospital discharge, the patient verbalizes
understanding of the rationale and measures for the dietary
regimen.
Status: Food and Fluid Intake; Weight Control

Nutritional management

1. Provide a diet that is high in protein and low in calories and

sodium.

2. Encourage foods that are high in fiber content (e.g., fruits with
skins, vegetables, whole-grain breads and cereals, nuts) to improve
gastric motility and elimination.

3. Administer vitamin supplements as prescribed.

Counseling; Weight Management

Constipation 
related to inadequate dietary intake of roughage and fluids, bed rest, and/or
decreased peristalsis secondary to slowed metabolism.
Goals/Outcomes: Within 48 to 72 hours of admission, the patient
resumes normal pattern of bowel elimination.
Elimination

Bowel management

1. Monitor bowel function; report problems to the physician. Note

decreasing bowel sounds, distention, and increased abdominal
girth (may indicate ileus or an obstruction).

1666
2. Encourage the patient to maintain a diet with adequate roughage
and fluids. Ensure that fluid intake in persons without underlying
cardiac or renal disease is at least 2 to 3 L/d.

3. Administer stool softeners and laxatives as prescribed.

Suppositories may be contraindicated because of the risk

of stimulating the vagus nerve (decreases HR and BP).

Constipation/Impaction Management; Fluid Management

Deficient knowledge: Illness care 

related to management of hypothyroidism.
Goals/Outcomes: Within the 24-hour period before hospital
discharge, the patient verbalizes knowledge of potential side effects
of prescribed medications, dietary guidelines, signs and symptoms
that require medical attention, and importance of following the
prescribed medical regimen.
Knowledge: Disease Process

Teaching: Disease process

1. Provide teaching about medications, including drug name,

purpose, dosage, schedule, precautions, drug–drug and food–drug
interactions, and potential side effects. Remind the patient that
thioamides, iodides, and lithium are contraindicated because they
decrease thyroid activity. Be sure the patient is aware that thyroid
replacement medications are to be taken for life.

2. Review dietary requirements and restrictions, which may change

as hormone replacement therapy takes effect.

3. Explain expected changes with hormone replacement therapy:

increased energy level, weight loss, and decreased peripheral
edema. Neuromuscular problems should improve.

1667
4. Stress the importance of continued, frequent medical follow-up.

5. Discuss the importance of avoiding physical and emotional

stress, and ways for the patient to maximize coping mechanisms for
dealing with stress.

6. Review signs and symptoms that require medical attention: fever

or other symptoms of upper respiratory, urinary, or oral infections
and signs and symptoms of hyperthyroidism, which may result
from excessive hormone replacement.

7. Women trying to become pregnant, who have subclinical

hypothyroid, may require an increase in levothyroxine to increase
the chance of conception.

Management; Exercise Promotion; Teaching: Prescribed Diet;

Teaching: Disease Process; Anxiety Reduction

Syndrome of inappropriate
antidiuretic hormone
Syndrome of inappropriate antidiuretic hormone (SIADH), also
known as syndrome of inappropriate antidiuresis (SIAD), is a
potentially lethal condition that involves an alteration in sodium
and water balance. It is associated with water retention caused by a
failure to suppress ADH secretion. SIADH is one of the most
common etiologies of hyponatremia in hospitalized patients,
including those in the ICU. The syndrome occurs in the absence of
renal dysfunction or recognized stimuli that would typically induce
release of ADH. Patients with SIADH have hypoosmolality and
hyponatremia, but are euvolemic. The sodium level is normal, but
there is an increase in total body water in the intravascular space.
SIADH is considered a paraneoplastic syndrome as it can be
caused by an alteration in the immune system caused by the
presence of tumor cells. Several other etiologies, including those
that are pulmonary, neurologic, or hormonal in nature, as well as
several medications, have been implicated in its development.
Prompt and accurate diagnosis and initiation of therapies to correct

1668
serum sodium levels are essential. Management depends on the
degree of hyponatremia, associated manifestations, and how
rapidly it occurred. Meticulous critical care nursing care is pivotal
to avoid life-threatening sequelae in the acute phase of this
condition.

Pathophysiology
ADH (the type in humans is termed arginine vasopressin [AVP]) is
a hormone composed of nine amino acids. It is therefore considered
a peptide hormone (as opposed to a steroid hormone). Its two main
functions are to control levels of body water and BP. For the
purposes of this chapter, the focus is on ADH’s role in control of
body water.
ADH is synthesized by the supraoptic nucleus (a collection of
nerve cell bodies) in the hypothalamus and is secreted from the
posterior pituitary gland (neurohypophysis). When triggered, the
nerve cells release ADH. Production of ADH triggers absorption of
free water in the distal convoluted tubules and collecting duct of
the kidneys. This occurs because of binding of ADH to the V2
receptor.
The primary trigger of the supraoptic nucleus to release ADH is
an elevated serum osmolality. Other significant triggers include a
decrease in circulating blood volume, hypotension, and angiotensin
II (part of the renin-angiotensin-aldosterone system). Pain, other
sources of stress, nausea, pregnancy, hypoglycemia, nicotine, and
some drugs (e.g., morphine sulfate) are also implicated as stimuli
affecting ADH release. Cancer cells may also secrete ADH; this is
especially true of small cell lung cancer. Conversely, the two main
inhibitors of ADH secretion are hypoosmolality and hypervolemia.
Normally, ADH is secreted by the posterior pituitary when
triggered by an increase in serum osmolality; changes in serum
osmolality are detected by osmoreceptors in the hypothalamus.
ADH secretion is also stimulated by decreased circulating blood
volume or BP. These pressure changes are sensed by baroreceptors
located in the aortic arch, carotid sinus, and right atrium. ADH then
stimulates V2 receptors in the collecting duct cells of the kidney,
causing reabsorption of water, which lowers serum osmolality.

1669
 Secretion of ADH results in urine concentration and decreased
urine output. There is a direct relationship between serum ADH
levels and concentration of urine, meaning that as serum ADH
levels increase, the concentration of urine increases.
In SIADH, the amount of ADH release is higher than expected,
given the patient’s serum osmolality. AVP secretion remains
increased despite a serum osmolality that normalizes. Further, in
patients with SIADH, increasing water intake does not decrease
ADH secretion and concentrated urine persists. When the body
produces excess ADH, the kidneys are unable to eliminate the
excess water. This results in an increase in total body water, despite
the absence of renal dysfunction. As fluid accumulates, sodium
levels are diluted; this results in hypotonic hyponatremia.
Four types of SIADH have been identified based on the
impairment in patterns of AVP secretion. These are delineated in
Table 8-5.

Table 8-5
TYPES OF SIADH

8-2
RESEARCH BRIEF
The incidence of SIADH-induced hyponatremia is up to 15% in
patients with small cell lung cancer (SCLC). This condition has
high morbidity and mortality rates and frequently delays initiation
of antineoplastic therapies. This prospective case series describes
management of hyponatremia with tolvaptan in 10 patients with

1670
SCLC. Treatment with tolvaptan led to an improved performance
status on all patients, allowing them to begin chemotherapy in
time. Rapid and effective correction of symptoms and serum
sodium levels were achieved. There were no prolonged
hospitalizations associated with the patient’s condition or
therapies.
From: Petereit C, Zaba O, Teber I, et al: A rapid and efficient way to manage hyponatremia
in patients with SIADH and small cell lung cancer: treatment with tolvaptan. BMC Pulm
Med 13:55, 2013.

Assessment
History and risk factors
A number of etiologic factors for the development of SIADH have
been identified. These factors can cause release of ADH but are not
directly related to serum osmolality or fluid volume status. These
factors are listed in Table 8-6.

Table 8-6
ETIOLOGIC FACTORS OF SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE AND HYPONATREMIA

Pulmonary-related Medication-related
Abscess Amantadine
Acute respiratory failure Amiodarone
Asthma Amitriptyline
Atelectasis Angiotensin-converting enzyme inhibitors
Pneumonia (e.g., Legionella, Bromocriptine
Mycoplasma) Carbamazepine
Pneumothorax Carboplatin
Tuberculosis Chlorpropamide
Vasculitis Ciprofloxacin
Cisplatin
Cyclophosphamide (high-dose)
Haloperidol
Ifosfamide
Imatinib (high-dose)
Interferon-α
Interferon-γ
Lamotrigine
Levetiracetam
Lorcainide

1671
 Melphalan
Methotrexate
Monoamine oxidase inhibitors
Moxifloxacin
Nonsteroidal anti-inflammatory drugs
Opiates
Oxcarbazepine
Phenothiazines
Prostaglandins
Quinolones
Serotonin and norepinephrine reuptake inhibitors (e.g.,
venlafaxine)
Selective serotonin reuptake inhibitors
Sodium valproate
Tacrolimus
Thioridazine
Thiothixene
Tolbutamide
Tolterodine
Tricyclic antidepressants
Vinblastine
Vincristine
Vinorelbine
Neurology-related Hormone-related
Brain trauma Hypopituitarism
CNS infection (e.g., meningitis, Hypothyroidism
meningoencephalitis) Exogenous hormone administration (e.g., vasopressin,
Guillain-Barré syndrome desmopressin, oxytocin)
Intracranial
bleeding/hemorrhage (e.g.,
subdural or subarachnoid
hemorrhage)
Lambert-Eaton myasthenic
syndrome
Multiple sclerosis
Psychosis
Stroke
Cancer-related Other
Adrenal tumors Chemotherapy-induced nausea
Brain tumors “Ecstasy” (3,4-methylenedioxymethamphetamine)
Breast cancer Exercise (prolonged, strenuous)
Endometrial cancer Genetic abnormalities (i.e., gene for renal vasopressin-2 (V2)
Extrapulmonary small cell receptor, gene affecting hypothalamic osmolality sensing)
carcinomas Graft-versus-host disease (acute)
Gastric cancer HIV infection (symptomatic) or AIDS
Genitourinary tract malignancy Idiopathic
(e.g., bladder, ureteral) Interventional procedures (e.g., cardiac catheterization)
Head and neck cancer (e.g., Porphyria (acute intermittent)
oropharyngeal, Positive pressure ventilation
nasopharyngeal) Stem cell transplant
Lymphoma Surgical procedures (e.g., transphenoidal pituitary, surgery
Mesothelioma on bones and joints, carotid endarterectomy, cardiac, open
Multiple myeloma and laparoscopic abdominal)
Olfactory neuroblastoma Vasculitis
Pancreatic cancer
Prostate (poorly differentiated
acinar adenocarcinoma)

1672
 Sarcoma (Ewing)
Small cell lung cancer
Thymoma

Vital signs
In the absence of comorbidities (e.g., heart failure, hypokalemia), as
patients with SIADH are euvolemic, they will not have orthostatic
BP changes. HR and CVP values will be within the expected range
for the patient.

Observation
The manifestations of SIADH depend on the degree of
hyponatremia and how rapidly it developed. Patients are more
likely to be symptomatic if sodium levels decline rapidly and may
be asymptomatic if serum sodium levels are 130 mEq/L or above.
Manifestations based on degree of hyponatremia appear in Table 8-
7.

Table 8-7
MANIFESTATIONS OF SIADH BASED ON DEGREE OF
HYPONATREMIA

Degree of Hyponatremia Associated Symptoms

Mild: sodium 130 to 134 mEq/L Weakness
Headache
Memory difficulties
Malaise
Gait disturbances
Falls
Apathy
Fatigue
Myalgia
Irritability
Restlessness
Moderate: sodium 125 to 129 mEq/L Headache
Trouble thinking clearly
Nausea
Vomiting
Confusion
Seizures
Hyporeflexia
Muscle weakness, spasms, or cramps
Hypotension
Oliguria
Lethargy
Anorexia

1673
 Abdominal pain
Severe: sodium <125 mEq/L Altered mental status (e.g., lethargy, delirium)
Seizures
Decreased deep tendon reflexes
Agitation
Hallucinations
Incontinence
Pseudobulbar palsy
Coma
Respiratory collapse
Death

Patients with SIADH are euvolemic. As such, there will be

absence of edema.

Lab work
Blood and urine test results are evaluated concomitantly with
assessment of extracellular fluid volume status. Evaluation of
volume status is essential for accurate interpretation of laboratory
results. Results of blood and urine tests in SIADH are as follows:

• Serum sodium level decreased: Less than 134 mEq/L

• Serum osmolality decreased: Less than 280 mOsmol/kg

• Urine sodium level increased: Greater than 40 mmol/L with

normal dietary intake of sodium and water (no fluid restriction in
progress) (spot or 24-hour urine sample)

• Urine osmolality: Greater than 100 mOsmol/kg (spot or 24-hour

urine sample)

• Serum uric acid level low or within range: Less than 4 mg/dL

• Blood urea nitrogen decreased: Less than 10 mg/dL

• Plasma vasopressin level: Inappropriately elevated in relation to

plasma osmolality

• Serum potassium: Within appropriate range for patient

• Absence of acid–base imbalance

1674
• Serum glucose level: Within appropriate range for the patient (to
validate that hyperglycemia is not causing a false hyponatremia)

Differential diagnosis
When attempting to diagnose a patient with SIADH, the following
conditions associated with hyponatremia and euvolemic
hyponatremia should be ruled out:

• Hypothyroidism

• Hypocortisolism

• Adrenal insufficiency

• Glucocorticoid deficiency (especially in patients with

neurosurgical disorders)

• “Reset osmostat” (may be seen in pregnancy, chronic

malnutrition, epilepsy, and paraplegia)

• Illnesses causing diarrhea

• Inappropriate volume repletion following exercise

• Extreme intake of water

• Very low protein intake

• Primary polydipsia

Collaborative management
The management of patients with SIADH varies, depending on the
patient symptomatology and associated degree of hyponatremia. It
is essential for patients with severe hyponatremia that developed
within the past 48 hours to be treated to avoid life-threatening
neurologic complications. Mainstays of treatment for all patients
include eliminating the underlying cause of SIADH and correction
of serum sodium levels. The latter may be accomplished in a
number of different ways, including fluid restriction,

1675
administration of sodium, vasopressin receptor antagonist
administration, or combinations of these therapies. Each of these
treatment modalities has associated drawbacks. Hyponatremia is
the primary complication associated with SIADH. The suggested
treatment goal for patients with SIADH is serum sodium of at least
130 mEq/L. This will help mitigate neurologic symptoms associated
with lower sodium levels.

Care priorities

1. Correct acute, symptomatic hyponatremia

• Hypertonic saline

Patients with severe symptomatic hyponatremia

(presence of seizures or intracranial conditions)
may receive hypertonic (3%) saline. Infusion via a
central venous catheter is recommended. The
suggested bolus dose is 100 mL. This may be
repeated once or twice more in 10-minute intervals
if the patient’s neurologic symptoms worsen or do
not improve. Administration of hypertonic saline is
the most effective way to correct severe
hyponatremia and improve associated neurologic
function. It is essential that serum sodium levels be
corrected by no more than 0.5 to 1 mEq/L/h to avoid
central pontine myelinolysis.

Patients with a serum sodium less than 120 mEq/L

that developed over more than 48 hours who have
less severe neurologic symptoms should receive
hypertonic saline to raise serum sodium levels by 1
mEq/L for 3 to 4 hours. Subsequent infusion rates
should be titrated so that serum sodium levels

1676
 correct less than 10 mEq/L in 24 hours and no more
than 18 mEq/L in 48 hours.
• Fluid restriction

Fluid restriction is indicated for patients who have

mild symptoms associated with hyponatremia (e.g.,
gait disturbances, forgetfulness). The purpose of
fluid restriction is to attain a negative water
balance. Fluid restriction entails limiting total intake
to no more than 1000 mL/d. In some cases, if the
patient does not respond adequately, total intake
may be limited to no more than 500 mL/d. It may
take several days before appreciable increases in
serum sodium levels are realized. Fluid restriction
is indicated primarily for chronic hyponatremia
associated with SIADH. Difficulties with the patient
compliance with prolonged fluid restriction are
reported. Fluid restriction is contraindicated in
patients who recently had a subarachnoid
hemorrhage; in these patients, fluid restriction may
cause cerebral vasospasm, which may be fatal.
• Isotonic saline infusions with diuretics

Serum sodium levels may also be corrected with

infusions of isotonic saline (0.9%) with
administration of IV loop diuretics (e.g.,
furosemide). Isotonic saline may be administered to
patients with SIADH who are hyponatremic but
asymptomatic. It is not recommended in patients
who are symptomatic. Loop diuretic administration

1677
 results in an increase in free water excretion. Loop
diuretics are typically indicated for patients with a
urine osmolality two times greater than serum
osmolality. Administration results in decreased
concentration of urine and increased water
excretion. Loop diuretics are reported not to be
useful in long-term therapy. Monitoring for
hypokalemia and hypovolemia is essential with
loop diuretic therapy as the diuretic effect is more
significant in patients with SIADH and normal
renal function.

It is possible for serum osmolality and serum sodium

levels to decrease further when patients receive
isotonic saline. This is caused by the osmolality of
isotonic sodium being lower than urine osmolality.
In this case, the isotonic saline serves as a source of
free water. This usually occurs in patients with a
urine osmolality greater than 530 mOsmol/kg. Salt
tablets administered orally may also be used to
correct hyponatremia in patients with mild
symptoms associated with hyponatremia.

2. Vasopressin-receptor antagonist therapy

Of the three vasopressin receptors in the body, the V2 receptors
have implications for the treatment of SIADH. The V2 receptors are
responsible for regulating the antidiuretic response. The other two
receptors, V1a and V1b, produce vasoconstriction and release of
ACTH, respectively.
As their name connotes, vasopressin receptor antagonists block

1678
AVP from binding to receptors in the collecting ducts, thereby
inhibiting the actions of vasopressin. Administration of a
vasopressin receptor antagonist results in an increase of free water
excretion by the kidneys (aquaresis); sodium and potassium
excretion are not affected. This results in an increased sodium level
and decreased urine osmolality. Mental status improvement has
also been reported in patients with SIADH who have a serum
sodium level less than 130 mEq/L. Vasopressin receptor antagonists
are not indicated in patients who are hyponatremic but
asymptomatic.
Vasopressin receptor antagonists are available in oral and IV
formulations. As it may be challenging to predict the rate of sodium
correction with vasopressin receptor antagonists, their use is
generally reserved for when fluid restriction has not been
successful.
Tolvaptan is the oral agent and conivaptan is an IV formulation
of this class of drugs that are approved by the Food and Drug
Administration (FDA). Dosing of tolvaptan starts at 15 mg/d; up to
60 mg/d may be given. It is FDA-approved for patients with
hypervolemic or euvolemic hyponatremia (serum sodium 125
mEq/L or less.). Patients with less severe hyponatremia who have
not been successfully treated with fluid restriction may also be
given tolvaptan. Side effects of tolvaptan include liver toxicity, dry
mouth, constipation, and excess thirst. Because of the risk of
hepatotoxicity, administration of tolvaptan is typically limited to no
more than 30 days and is contraindicated in patients with liver
dysfunction, as an increase in liver enzymes was reported in clinical
trials. Tolvaptan is also contraindicated in patients with
hypovolemic hyponatremia or anuria and in those with inability to
recognize and respond to thirst.
Conivaptan, because it is an IV formulation, requires hospital
admission. However, its administration will increase sodium levels
more quickly than fluid restriction and salt tablets (for patients with
mild to moderate levels of hyponatremia and who have few or no
related symptoms). Patients with more severe levels of
hyponatremia or with mild or moderate symptoms may receive
conivaptan with or without hypertonic saline. The initial dose of
conivaptan is 20 mg over 30 minutes; this is followed by another

1679
infusion of 20 mg over 24 hours. Side effects include nausea,
vomiting, diarrhea, and infusion site reactions.

3. Manage chronic hyponatremia

Patients with chronic hyponatremia may be treated in the
ambulatory setting. These patients may receive demeclocycline, a
derivative of tetracycline (Declomycin®; Wyeth Ayerst
Pharmaceuticals, Collegeville, PA) administered at 600 to 1200
mg/d in divided doses. Demeclocycline causes a decrease in ADH
response by the distal convoluted tubules; this results in an increase
in free water excretion. Concomitant fluid restriction is not
required. Typically, patients with malignancy are treated with
demeclocycline. It takes 2 to 3 days for treatment to start to become
effective; response rates as long as weeks in duration have also been
reported. Notable side effects include skin photosensitivity,
nephrotoxicity (mainly in patients with actual or potential renal
dysfunction), nausea, diarrhea, and anorexia. Patients with baseline
renal dysfunction may also develop renal toxicity from
demeclocycline. Patients receiving demeclocycline should be
monitored for polyuria. They should have their sodium levels
monitored while on therapy, as hypernatremia may develop in the
face on ongoing fluid restriction.
Lithium has been used in the past in the management of chronic
SIADH. Some preclinical studies have suggested that lithium may
increase the efficacy of aquaretic agents. Like demeclocycline,
lithium causes a decrease in ADH response by the distal convoluted
tubules. Administration results in polyuria and polydipsia by
causing nephrogenic DI. It takes 4 days for the drug to take effect.
Because of the potential to cause nephrotoxicity and
neuropsychiatric side effects, use of lithium has mostly ended.
Other side effects are GI and hypothyroidism. Lithium also is
effective in fewer patients than demeclocycline is.
Oral urea administration causes an osmotic diuresis. It increases
excretion of water and fosters promotes sodium retention. Because
of its associated bitter taste, its use is not widely accepted. Side
effects include hypersensitivity, azotemia, and liver failure. Some
data suggest that urea may have some favorable results in the long-
term setting. Data on patients in the ICU suggest that urea may be

1680
useful in patients in the ICU with hyponatremia associated with
SIADH. Its use seems limited to patients who have a moderate
increase in urine osmolality. Urea administration is rarely used in
the United States because of its lack of availability in pharmacies.
Correction of chronic hyponatremia should not exceed 10 mEq/L
over 24 hours and 18 mEq/L over 48 hours. Monitoring of serum
sodium should be conducted initially every 2 to 3 hours and then
every 3 to 4 hours until the patient’s condition stabilizes.

4. Identify and manage underlying cause

A number of the underlying causes of SIADH can be managed
successfully. These include discontinuation of medications that may
be causing the syndrome, treatment of the underlying infection, or
managing any hormone-related etiologies. Other causes, such as
small cell lung cancer and other malignancies, may pose challenges
in treating SIADH.

5. Monitor for complications

Nursing care during therapy for SIADH includes monitoring for
complications, monitoring serum electrolyte results daily, obtaining
daily weights, and monitoring intake and output.
While serum sodium levels are being addressed, it is pivotal to
ensure that these levels do not correct too rapidly. Some patients in
clinical trials with vasopressin receptor antagonist therapy had too
rapid a correction of sodium. Sodium correction in the acute setting
should not exceed 0.5 to 1mEq/L/h. Such can result in severe
neurologic complications such as central pontine myelinolysis,
which is shrinkage of brainstem cells causing quadriparesis,
pseudobulbar palsy, coma, and death. Meticulous monitoring of
sodium levels is required.
Patients receiving demeclocycline or lithium should have renal
function monitoring because of the potential for nephrotoxicity
associated with these agents. Patients receiving tolvaptan therapy
must be monitored for liver dysfunction. Symptoms that should be
reported include jaundice, fatigue, anorexia, discomfort in the area
of the right upper quadrant of the abdomen, and dark urine.
Patients with hyponatremia are at risk for the development of
seizures. Monitoring and implementation of seizure precautions are

1681
recommended to protect the patient from harm.
Patients with severe SIADH and chronic hyponatremia are at risk
for the development of alterations in bone metabolism that can lead
to osteoporosis. Bone protection therapy and monitoring of bone
density is recommended in these patients.

Care plans for syndrome of inappropriate

antidiuretic hormone
Impaired neurologic functioning 
related to hyponatremia
Goals/Outcomes: Patient’s neurologic function will improve as serum
sodium level normalizes. The patient will not develop complications
related to too rapid a correction of serum sodium level. Vital signs will
remain within range appropriate for the patient.
Neurological Status: Consciousness; Fluid Balance

Electrolyte management: Hyponatremia

1. Minimize stimuli that can increase ADH release (e.g., pain,

stress).

2. Ensure medications prescribed for other comorbid conditions do

not trigger ADH release

3. Monitor for changes in neurologic status, vital signs, intake and

output, and daily weight.

4. Monitor for symptoms associated with hyponatremia.

5. Monitor trends in laboratory values (serum sodium, serum

osmolality, urine sodium).

6. Administer hypertonic saline to initiate correction of acute

hyponatremia. Carefully titrate infusion to avoid central pontine
myelinolysis.

7. Administer pharmacotherapy to increase sodium levels, as

1682
prescribed. Note and document efficacy.

8. Monitor for signs and symptoms of fluid overload (e.g., elevated

CVP, tachycardia, edema, SOB when lying flat, crackles, jugular
vein distention).

9. Implement seizure precautions (e.g., functioning suction

equipment, appropriately sized oropharyngeal airway, avoiding
restraint use, side rails raised and appropriately padded.)

See Fluid and Electrolyte Imbalances, Hyponatremia. Chapter

1

Thyrotoxicosis crisis (thyroid storm)

Pathophysiology
Thyroid storm is a medical emergency caused by uncontrolled
hyperthyroidism. Patients occasionally present with cardiovascular
collapse and shock. Hyperthyroidism or thyrotoxicosis is a
condition of increased circulating thyroid hormone. The crisis
results from a surge of thyroid hormones into the bloodstream,
which results in profound stimulation of the sympathetic nervous
system (SNS), with marked increases in body metabolism. The
hypothalamus, anterior pituitary, and thyroid normally work
together to balance the level of circulating thyroid hormone.
Hyperthyroidism may be caused by an increased synthesis and
secretion of thyroid hormones (thyroxine and triiodothyronine )
from the thyroid or from increased secretion of TSH from the
anterior pituitary, possibly by an increase in TRH from the
hypothalamus or by autonomous thyroid hyperfunction.
Symptoms of hyperthyroidism can also result from excessive
release of thyroid hormone from the thyroid without increased
synthesis. Such release is commonly caused by the destructive
changes of various types of thyroiditis. Thyrotoxicosis crisis may
also follow subtotal thyroidectomy because of manipulation of the
gland during surgery. Various clinical syndromes also produce
hyperthyroidism, but thyroid storm is most often associated with

1683
Graves disease, also known as diffuse toxic goiter. Causes of acute
hyperthyroid states are listed in Box 8-3. Not all conditions listed
are associated with thyroid storm.

Treatment with amiodarone (a common K+ antagonist

used for dysrhythmia management) may cause either
hyperthyroidism OR hypothyroidism and must be considered
when evaluating either condition.

Box 8-3
COMMON CAUSES OF ACUTE
HYPERTHYROID STATES
• Graves disease

• Toxic multinodular goiter

• Solitary hyperfunctioning nodules

• Autoimmune and subacute postpartum thyroiditis

• Thyrotropin-secreting tumors

• Iodine-induced hyperthyroidism

• Excessive pituitary thyroid-stimulating hormone or trophoblastic

disease

• Excessive ingestion of thyroid hormone

Low TSH may also indicate euthyroid sick syndrome

1684
(ESS). When serum thyrotropin is decreased or suppressed by
severe or critical illness or by medications, particularly high doses
of glucocorticoids and dopamine, this abnormality may be the
diagnosis.

Life-threatening illness in patients with preexisting

thyroid disorders may be precipitated by extremes of the primary
disorder. These conditions present with exaggerated nonspecific
signs and symptoms of the underlying thyroid dysfunction.

Exacerbated hyperthyroidism occurs in 1 in 500

pregnancies and is second in frequency only to diabetes as an
endocrine disorder of pregnancy. During pregnancy, thyroid storm
is seen most often in patients with undertreated or undiagnosed
hyperthyroidism. As many as 20% to 30% of cases may result in
maternal and fetal mortality.

Abnormal laboratory analysis of thyroid function provides a

relatively definitive diagnosis. Initial serum measurements should
include free T4 and TSH, but concerns regarding thyroid
dysfunction should be referred to an endocrinology specialist for a
more thorough and evaluative diagnostic panel. Calcium regulation
may also be affected by thyroid disease if there is a problem with
the level of thyrocalcitonin, a third thyroid hormone that is
stimulated by increased calcium levels to help lower the calcium
level. Recent diagnostic tests have isolated a long-acting thyroid
stimulator, suggesting the disease is an autoimmune response. An
acute decrease in thyroxine-binding globulin (inactivating or
binding thyroid hormone) facilitates high levels of free and

1685
metabolically active hormone. The increased circulating levels of
active thyroid hormone increase the response of β-adrenergic
receptors (sympathetic stimulation increase) and also increase the
system responsiveness to catecholamines.

Endocrine assessment: Hyperthyroidism

Goal of system assessment
Evaluate for end-organ effects of hyperthyroidism. Thyroid
hormones work with adrenal glucocorticoid hormones to facilitate
carbohydrate, fat, and protein metabolism; work with insulin and
GH to promote growth; increase HR and the force of contraction;
help to regulate respiratory drive; help increase production of red
blood cells; and increase metabolism.

History and risk factors

A patient with a history of hyperthyroidism resulting from Graves
disease, thyroid nodules, or toxic goiter who has undergone a
recent stressful experience, including severe infection, trauma,
major surgery, thromboembolism, DKA, or preeclampsia,
pregnancy, labor, and/or delivery. Complaints include night
sweats, unexplained weight loss, rapid gastric turnover with
increased bowel movements or diarrhea, feelings of impending
doom, rapid HR, and sleep disturbances. (See SIRS, Sepsis, and
MODS, Chapter 11, Hyperglycemia, Chapter 8, High-Risk
Obstetrics, Chapter 11.)

Vital signs
• May have hyperpyrexia (fever)

• Acute exacerbation of tachycardia, palpitations, or new-onset

atrial fibrillation with chest discomfort in a patient with
enlargement of the thyroid gland

• Both hypertension and widened pulse pressure are common.

1686
Observation
• Confused, possibly psychotic, disoriented person with CNS
irritability

• Hyperreflexia and fine tremor may be present.

• Coma, heart failure, and generalized muscle weakness may be

present.

• Possible recent weight loss

• Patients with Graves disease (only in this form of thyrotoxicosis)

have significant immune system components that may express as
soft tissue swelling around the eye orbit, causing the protrusion
of the eyes (exophthalmos), stare, and/or lid lag.

• Males often have gynecomastia. Many patients have fine hair and
thin skin.

• Dependent lower-extremity edema, alteration in appetite, change

in vision, and fertility or menstrual dysfunctions are possible.

Palpation
• The thyroid gland in Graves disease will usually be enlarged, soft,
and symmetrical, although occasionally it may be firm and
irregular.

• Older patients may not have enlarged thyroid glands, which may
lead to dismissal of the diagnosis.

• Palpation is not the definitive method to evaluate thyroid

dysfunction.

Screening lab work

• TSH level: Any type or cause of hyperthyroid disease (except
when the cause is secondary excessive TSH production) will
create a suppression of TSH. The development of TSH-sensitive

1687
 testing has made the diagnosis of thyroid dysfunction much
simpler.

• T4 level: Unstable patients who have been diagnosed previously

and/or are treated for thyroid disorders require a serum
thyroxine (T4) assessment, which will be significantly more
valuable in diagnosis. See Figure 8-1 for diagnostic principles.

Common Diagnostic Tests for Thyrotoxic Crisis

Collaborative management
Care priorities

1. Stabilize the patient

1688
• Reduce the stress response with β-adrenergic–blocking agents
(e.g., esmolol, metoprolol, propranolol): Control tachycardia,
manage atrial fibrillation if present, anxiety, heat intolerance, and
tremor. Does not decrease the metabolic rate and has a mild effect
on global oxygen consumption. Do not assume improvement in
the thyroid disorder itself, only its symptoms. Calcium channel
blockers may be used if β-blockers are contraindicated.

• Oxygen: Used per nasal cannula or mask as needed to maintain

Spo2 greater than 95%.

• Control fever: Antipyretic medications (i.e., acetaminophen) or

hypothermia blanket is used. Aspirin is contraindicated, as it
worsens thyroid crisis.

• Rehydrate using IV fluids: Fever and rapid metabolism can lead

to dehydration.

• Correct electrolyte imbalance: Various imbalances may occur.

Replace electrolytes as appropriate.

• Glucocorticoids: Administered to help inhibit conversion of

thyroxine (T4) to T3 and prevent adrenal insufficiency.

• Minimize anxiety with mild tranquilizers: Also promote rest.

2. Treat the thyroid with antithyroid agents (thioamides)

Noninvasive, relatively cost-effective therapy with low risk of
permanent hypothyroidism and a low cure rate.

1689
• Propylthiouracil (PTU) has been the first line of treatment and is
more effective in thyroid storm than methimazole. Can be used in
pregnant patients. If the patient is unable to swallow, the
medication is given using a nasogastric tube. Iodides (potassium
iodide or Lugol solution) are given several hours after PTU to
avoid a buildup of hormones stored in the thyroid gland.

• Methimazole may also be used. Both thioamides may cause

leukopenia, rash, urticaria, fever, arthralgias, and, rarely,
agranulocytosis. Methimazole may have a lower rate of these
effects. Agranulocytosis (complete lack of granulocytes) causes
fever and sore throat. If agranulocytosis is confirmed by CBC, the
thioamide should be stopped.

• Iodides (SSKI): Sodium or potassium iodide drops may be given

to help inhibit the release of thyroid hormone or to help abate
accumulation of hormones stored in the thyroid. May stain the
teeth.

3. Cure the thyroid with radioactive iodine

It is the most cost-effective and commonly used agent. Use usually
results in hypothyroidism, requiring replacement therapy. Cannot
be used for the pregnant patient, as the thyroid gland of the fetus
may also be destroyed. Usually reserved for the following
indications:

• Failure to respond to antithyroid drugs

• Relapse after 1 to 2 years of therapy

• Toxic multinodular goiter

• Solitary toxic nodules

• Noncompliant patients

4. Perform a subtotal thyroidectomy to provide a rapid,

effective, curative therapy

1690
Most invasive and expensive therapy; hypothyroidism is inevitable.
Surgical removal of part of the gland often is the best treatment for
patients with extremely enlarged glands or multinodular goiter.
Surgery is avoided in the pregnant patient because of risk of
miscarriage or preterm delivery. The patient is prepared with
antithyroid agents until normal thyroid function is achieved
(usually 6 to 8 weeks). The most frequent postoperative
complication is hemorrhage at the operative site. The following
complications are rare but can be extremely serious:
hypoparathyroidism, laryngeal nerve injury, and tetany from
damage to the parathyroid glands.

Care plans for thyroid storm

Ineffective protection 
related to potential for thyrotoxic crisis (thyroid storm) secondary to
emotional stress, trauma, infection, pregnancy (especially labor and
delivery), or surgical manipulation of the gland.
Goals/Outcomes: The patient is free of symptoms of thyroid
storm as evidenced by normothermia, BP 90/60 mm Hg or greater
(or within patient’s baseline range), HR 100 bpm or less, and
orientation to person, place, and time. If thyroid storm occurs, it is
noted promptly and reported immediately.
Immune Hypersensitivity Response

Risk identification

1. Measure and report rectal or core temperature greater than 38.3°

C (101° F): often the first sign of impending thyroid storm.

2. Monitor vital signs hourly for evidence of hypotension and

increasing tachycardia and fever.

3. Monitor the patient for signs of congestive heart failure, which

occurs as an effect of thyroid storm: jugular vein distention, crackles
(rales), decreased amplitude of peripheral pulses, peripheral
edema, and hypotension. Immediately report any significant
findings to physician, and prepare to transfer the patient to ICU if

1691
they are noted. Maternal and fetal monitoring is initiated on
pregnant patients.

4. Provide a cool, calm, protected environment to minimize

emotional stress if possible. Reassure patient, and explain all
procedures. Limit the number of visitors.

5. Ensure good handwashing and meticulous aseptic technique for

dressing changes and all procedures. Advise visitors who have
contracted or been exposed to a communicable disease either not to
enter patient’s room or to use appropriate infection control
precautions.

6. Administer acetaminophen to decrease temperature.

Aspirin is contraindicated because it releases thyroxine

from protein-binding sites and increases free thyroxine levels.

7. Provide cool sponge baths or apply ice packs to patient’s axilla

and groin areas to decrease fever. If high temperature continues,
obtain a prescription for a hypothermia blanket.

8. Administer PTU as prescribed to prevent further synthesis and

release of thyroid hormones.

9. Administer β-blockers as prescribed to block SNS effects.

10. Administer IV fluids as prescribed to provide adequate

hydration and prevent vascular collapse. Fluid volume deficit may
occur because of increased fluid excretion by the kidneys or
excessive diaphoresis. Carefully monitor I&O hourly to prevent
fluid overload or inadequate fluid replacement. Decreasing output
with normal specific gravity may indicate decreased cardiac output,
whereas decreasing output with increased specific gravity can
signal dehydration.

1692
11. Administer iodides as prescribed, 1 hour after administering
PTU.

If given before PTU, iodides can exacerbate symptoms

in susceptible persons.

12. Administer small doses of insulin as prescribed to control

hyperglycemia. Hyperglycemia can occur as an effect of thyroid
storm because of the hypermetabolic state.

13. Administer prescribed supplemental oxygen to support

increased metabolism. Monitor with pulse oximetry to maintain
oxygen saturation of 95% or more.

Cardiac Care: Acute; Surveillance: Late Pregnancy;

Fluid/Electrolyte Management; Hyperglycemia Management;
Energy Management; Nutritional Monitoring; Vital Signs
Monitoring

Impaired swallowing (or risk for same) 

related to edema or laryngeal nerve damage resulting from surgical
procedure.
Goals/Outcomes: The patient reports swallowing with minimal
difficulty, has minimal or absent hoarseness, and is free of
symptoms of respiratory dysfunction as evidenced by RR 12 to 20
breaths/min with normal depth and pattern and absence of
inspiratory stridor. Laryngeal nerve damage, if it occurs, is detected
promptly and reported immediately.
Aspiration Prevention, Swallowing Status

Aspiration precautions

1. Monitor respiratory status for signs of edema (i.e., dyspnea,

choking, inspiratory stridor, inability to swallow). Assess patient’s
voice. Slight hoarseness is normal after surgery. Persistent

1693
hoarseness indicates laryngeal nerve damage. If bilateral nerve
damage is present, upper airway obstruction can occur. Report
findings to advanced practice provider promptly.

2. Elevate HOB 30 to 45 degrees to minimize edema and incisional

stress. Support patient’s head with flat or cervical pillows so that it
is in a neutral position.

3. Keep tracheostomy set and oxygen equipment at the bedside at

all times. Suction upper airway as needed, using gentle suction to
avoid stimulating laryngospasm.

4. To minimize pain and anxiety and enhance patient’s ability to

swallow, administer analgesics promptly and as prescribed.

Management; Nutrition Therapy; Respiratory Monitoring;

Swallowing Therapy

Anxiety 
related to SNS stimulation
Goals/Outcomes: Within 24 hours of hospital admission, the
patient is free of harmful anxiety as evidenced by a HR 100 bpm or
less, RR 12–20 breaths/min with normal depth and pattern, and
absence of or decreases in irritability and restlessness. The patient
and significant others verbalize knowledge about the causes of the
patient’s behavior.
Anxiety Level, Anxiety Self-control

Anxiety reduction

1. Assess for anxiety; administer short-acting sedatives (e.g.,

lorazepam) as prescribed.

2. Provide a quiet, stress-free environment away from loud noises

or excessive activity.

3. Limit number of visitors and the amount of time they spend with
patient. Advise significant others to avoid discussing stressful
topics and to refrain from arguing with the patient.

1694
4. Administer β-blockers as prescribed to reduce anxiety,
tachycardia, and heat intolerance.

5. Reassure the patient that anxiety is related to the disease and that
treatment decreases severity.

6. Inform significant others that the patient’s agitated behavior

should not be taken personally.

Coping Enhancement; High-Risk Pregnancy Care

Imbalanced nutrition: Less than body requirements 

related to hypermetabolic state and/or inadequate nutrient absorption.
Goals/Outcomes: By a minimum of 24 hours before hospital
discharge, the patient has adequate nutrition as evidenced by stable
weight and a positive nitrogen balance.
Nutritional Status

Nutrition therapy

1. Provide foods high in calories, protein, carbohydrates, and

vitamins.

2. Administer vitamin supplements as prescribed, and explain their

importance to patient.

3. Administer prescribed antidiarrheal medications, which increase

absorption of nutrients from the GI tract.

4. Weigh the patient daily, and report significant losses to advanced

practice provider.

Weight Management; Weight Gain Assistance; Nutritional

Counseling

Disturbed sleep pattern 

related to accelerated metabolism
Goals/Outcomes: Within 48 hours of hospital admission, the
patient relates the attainment of sufficient rest and sleep.

1695
Sleep enhancement

1. Adjust care activities to patient’s tolerance.

2. Provide frequent rest periods of at least 90-minute duration. If

possible, arrange for the patient to have bed rest in a quiet, cool
room.

3. Administer short-acting sedatives (e.g., lorazepam) as prescribed

to promote rest.

Anxiety Reduction; Meditation Facilitation

Impaired tissue integrity of the cornea 

related to dryness that can occur with exophthalmos in persons with
Graves disease.
Goals/Outcomes: Within 24 hours of admission, patient’s corneas
are moist and intact.
Tissue Integrity: Skin and Mucous Membranes

Eye care

1. Teach the patient to wear dark glasses in the sun or for highly lit
areas to protect the cornea.

2. Administer lubricating eye drops as prescribed to supplement

lubrication and decrease SNS stimulation, which can cause lid
retraction.

3. If appropriate, apply eye shields or tape the eyes shut at bedtime.

4. Administer thioamides as prescribed to maintain normal

metabolic state and halt progression of exophthalmos.

Skin Care: Topical Treatments

Deficient knowledge: Medications 

related to the potential for side effects from iodides and thioamides or
stopping thioamides abruptly.
Goals/Outcomes: Within the 24-hour period before hospital

1696
discharge, the patient verbalizes knowledge about potential side
effects of prescribed medications, signs and symptoms of
hypothyroidism and hyperthyroidism, and the importance of
following the prescribed medical regimen. The patient understands
that he or she must be seen within 4 months for endocrine follow-
up.
Knowledge: Medications; Knowledge: Illness Care

Teaching: Individual

1. Explain importance of taking antithyroid medications daily, as

prescribed.

2. Teach indicators of hypothyroidism (e.g., early fatigue, weight

gain, anorexia, constipation, menstrual irregularities, muscle
cramps, lethargy, inability to concentrate, hair loss, cold intolerance,
and hoarseness), which may occur from excessive antithyroid
medication, and the signs and symptoms that necessitate medical
attention, including cold intolerance, fatigue, lethargy, and
peripheral or periorbital edema.

3. Teach side effects of thioamides and symptoms that require

medical attention: appearance of a rash, fever, or pharyngitis, which
can occur in the presence of agranulocytosis and require prompt
medical intervention.

4. Discuss signs of worsening hyperthyroidism, including high

body temperature, palpitations, rapid HR, irritability, anxiety, and
feelings of restlessness or panic.

5. Explain importance of continued and frequent medical follow-up.

6. Indicators that require medical attention: fever, rash, or sore

throat (side effects of thioamides), and symptoms of
hypothyroidism or worsening hyperthyroidism.

7. For patients receiving radioactive iodine, explain the importance

of not holding children to the chest for 72 hours following therapy,
because children are more susceptible to the effects of radiation.
Explain that there is negligible risk for adults.

1697
8. Stress the importance of avoiding physical and emotional stress
early in the recuperative stage and maximizing coping mechanisms
for dealing with stress.

9. For patients at risk for heart failure with or without

hypothyroidism or hyperthyroidism may have an exacerbation of
heart failure symptoms.

Learning Facilitation; Health Education; Teaching: Disease

Process; Teaching: Prescribed Medication; Teaching:
Activity/Exercise

Additional nursing diagnoses

See Compromised Family Coping, in Oncologic Emergencies,
Chapter 11; Nutritional Support, Chapter 1; Alterations in
Consciousness, Chapter 1; Emotional and Spiritual Support of the
Patient and Significant Others, Chapter 2; Dysrhythmias and
Conduction Disturbances, Chapter 5; Heart Failure, Chapter 5.

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Med J. 2011;70:139-143.
84. Torgersen C, Luckner G, Schröder DC. Concomitant
arginine vasopressin and hydrocortisone therapy in severe
septic shock: association with mortality. Intensive Care Med.
2011;37:1432-1437.
85. Venkatesh B, Cohen J. Adrenocortical (dys)function in
septic shock—a sick euadrenal state. Best Pract Res Clin
Endocrinol Metab. 2011;25:719-733.
86. Wartofsky L. Myxedema coma. Endocrinol Metab Clin North
Am. 2006;35:687-698.
87. Webster Marketon JI, Sternberg EM. The glucocorticoid
receptor: a revisited target for toxins. Toxins (Basel).
2010;2:1359-1380.
88. Wei J, Xiao Y, Yu X. Early onset of syndrome of
inappropriate antidiuretic hormone secretion (SIADH) after
allogeneic haematopoietic stem cell transplantation: case
report and review of the literature. J Int Med Res.
2010;38:705-710.
89. Wesche D, Deen PMT, Knoers NVAM. Congenital
nephrogenic diabetes insipidus: the current state of affairs.
Pediatr Nephrol. 2012;27:2183-2204.
90. Yam FK, Eraly SA. Syndrome of inappropriate antidiuretic
hormone associated with moxifloxacin. Am J Health Syst
Pharm. 2012;69:217-220.
91. Zietse R, van der Lubbe N, Hoorn EJ. Current and future
treatment options in SIADH. NDT Plus. 2009;2(Suppl
3):iii12-iii19.

1706
CHAPTER 9

Gastrointestinal
disorders
Gastrointestinal assessment: General
Goal of system assessment
Evaluate for dysfunctional ingestion and digestion of food and
elimination of waste products. When assessing the surgical
bariatric patient (person of size), assess the type of gastric bypass
performed, the number of days that have elapsed since surgery,
and the amount of weight lost as a result of the surgical procedure.

Vital sign assessment

• Heart rate (HR), blood pressure (BP), and peripheral pulses to
identify volume status, because significant fluid losses can occur
with gastrointestinal (GI) bleeding or diarrhea.

• Note temperature, because infections of the GI tract are common.

• Considerations for the surgical bariatric patient: HR greater

than 110 beats/min (bpm), BP decrease of greater than 10% from
baseline, and temperature elevated greater than 38.6° C
(101.5° F) are signs of anastomotic leak and is a surgical/medical
emergency that can lead to death.

1707
Observation
Observe the abdomen for distension and skin color changes, which
may be signs of other system disorders.

• Cullen sign (bluish umbilicus) may indicate intraabdominal

hemorrhage.

• Turner sign (bruising on the flanks) may indicate retroperitoneal

hemorrhage.

• Visible, torturous, dilated abdominal veins may indicate inferior

vena cava obstruction.

• Cutaneous abdominal angiomas may indicate liver disease.

• Considerations for the bariatric patient: Assess for abdominal

hernias around the umbilicus or anywhere along the abdominal
wall resulting from the pressure the excess abdominal fat exerts
on the musculature during movement.

• Assess urine output to help determine hydration status.

Auscultation
Evaluate bowel sounds in each of the quadrants in a systemic
manner.

• Hyperactive bowel sounds may indicate diarrhea or early

intestinal obstruction.

• Hypoactive to absent bowel sounds may indicate paralytic ileus

or peritonitis.

• High-pitched rushing sounds may indicate intestinal obstruction.

• Considerations for the bariatric patient: Query the patient and

assess for what is the normal bowel pattern.

• Assess for constipation and diarrhea.

1708
 Evaluate for systolic bruits (humming, swishing, or blowing
sounds) over:

• Abdominal aorta: partial arterial obstruction.

• Renal artery: renal artery stenosis.

• Iliac artery: hepatomegaly.

Palpation
The normal abdomen should be soft and nontender to palpation.
Palpate for liver enlargement and tenderness. The spleen is not
normally palpable. If found palpable, the spleen is enlarged.
Further palpation must be discontinued, because it may cause
splenic rupture.

If the abdomen is rigid, do not palpate; it is a sign of

peritoneal inflammation. Palpation could cause rupture of the
inflamed organ.

Nutrition assessment
Evaluate for risk factors and indications of malnutrition for which
patients who are critically ill are at risk. Malnutrition may occur
resulting from negative caloric intake with concomitant GI
obstruction, malabsorption syndromes, infectious diseases, certain
medications, and surgical treatment. Additionally, caloric needs are
greatly increased in the critically ill as a result of hypermetabolic
states produced by trauma, fever, sepsis, and wound healing.

• Evaluate for general signs of malnutrition (Table 9-1).

• Considerations for the surgical bariatric patient: Never insert

a nasogastric (NG) or any type of feeding tube, because the

1709
 gastric bypass  surgery has altered the anatomy of the stomach.

• Considerations for the surgical bariatric patient: Pills must be

crushed. Find alternative medications for extended or sustained
release, because they will not be absorbed.

• Considerations for the bariatric patient (person of size):

Malnutrition is common in the person of size. When critically ill,
the person of size will need the appropriate calories to support
metabolic demands resulting from the state of illness. A critical
illness is not the appropriate time to place a person of size on a
diet.

• Evaluate weight for increases and decreases.

• Laboratory identification of malnutrition:

• Serum albumin less than 3 g/dL.

• Serum transferrin less than 200 mg/dL.

• Serum prealbumin less than 16.0 mg/dL.

• Total lymphocyte count between 15% and 40% of

the WBC with an absolute lymphocyte count of
1000-3500/cm3

• Triglycerides less than 150mg/dL.

Table 9-1
GENERAL SIGNS OF MALNUTRITION

Body System Signs Deficiency

Skin, nails Dry skin Vitamin deficiency

1710
 Brittle nails; spooned-shaped nails Iron deficiency
Considerations for the surgical bariatric patient:
Will have vitamin deficiencies if not on
multivitamins

Mouth Cracks; beefy, red tongue Vitamin deficiency

Stomach Decreased gastric acidity Protein deficiency

Delayed gastric emptying
Intestines Decreased motility and absorption Protein deficiency
Diarrhea Altered normal flora
Considerations for the surgical bariatric patient:
Will have protein deficiency unless on high
protein diet
Liver/biliary Hepatomegaly Decreased absorption
Ascites of fat-soluble
vitamins
Protein deficiency
Cardiovascular Edema Protein deficiency
Tachycardia; hypotension Fluid volume
deficiency
Musculoskeletal Decreased muscle mass Protein,
Subcutaneous tissue loss carbohydrate, and
fat deficiency

Screening labwork
• Serum electrolyte levels.

• Complete blood count (CBC).

• Serum amylase.

• Serum lipase.

• Liver function tests (LFTs).

Acute gastrointestinal bleeding

Pathophysiology
Bleeding can occur at any point along the upper (esophagus,
stomach, and duodenum) and lower (small intestine, large
intestine/colon, rectum) portions of the alimentary tract, but is more
prevalent in the upper segment. Both upper and lower GI bleeding
account for significant morbidity, with a mortality rate of 3% to

1711
14%. Mortality may reach 40% in the presence of hemodynamic
instability. The occurrence of acute GI bleeding is decreasing in the
United States resulting from a reduced incidence of Helicobacter
pylori infection and advances in ulcer-prevention strategies
including consistent use of prophylactic medications in
nonsteroidal antiinflammatory drug (NSAID) users. The following
overview presents common GI bleeding sites and occurrences.

Upper gastrointestinal bleeding

Esophagus
Esophageal varices (EVs) are the most common cause of massive
and persistent esophageal hemorrhage. EVs are caused by
significant portal hypertension causing bleeding to occur under
high pressure. Acute variceal bleeding is severe, difficult to control,
and rarely resolves spontaneously. Less frequent causes of EV
bleeding include esophagitis, esophageal ulcers, and tumors.
Maneuvers that increase intraabdominal pressure (IAP) (e.g.,
retching, vomiting, straining, coughing, blunt abdominal trauma)
can lead to a Mallory-Weiss (MW) tear (a laceration at the
esophagogastric junction), which can result in massive bleeding.
MW tears are commonly found in patients with hiatal hernia.

Stomach and duodenum

The most common cause of upper GI bleeding (UGIB) is peptic
ulcer disease (PUD), accounting for greater than 50% of UGIB
disorders. Peptic ulcers are chronic lesions that are most prevalent
in the stomach and duodenum. These lesions extend from the
protective mucosa of the GI tract into the submucosa, exposing
tissue to gastric acids with eventual autodigestion. Bleeding occurs
when the ulcer erodes into a blood vessel. H. pylori and NSAID use
account for the majority of PUD cases. H. pylori infection is more
strongly associated with the pathogenesis of peptic ulceration than
gastric hyperacidity. The toxins and enzymes released by the H.
pylori organism are believed to cause mucosal injury through
proinflammatory processes and by decreasing duodenal mucosal
bicarbonate production resulting in ulceration.
Stress ulceration is a common and potentially life-threatening

1712
phenomenon that occurs in patients who are critically ill, with
higher incidence in those who are mechanically ventilated. Stress
ulcers comprise multiple lesions, generally confined to the gastric
fundus. Ulcers primarily result from stress-related hyperacidity of
critical illness and gastric mucosal ischemia secondary to diversion
of blood away from the GI tract during the stress response. Curling
ulcers occur in the proximal duodenum and are seen in patients
with major burn injuries or major trauma. Ischemia and necrosis of
the mucosa results from decreased plasma volume. Cushing ulcers
are a related condition associated with high gastric acid output and
prone to perforation that occurs in patients with increased
intracranial pressure. These patients have sustained a serious head
injury or are experiencing a critical central nervous system (CNS)
disorder. PUD resulting from a hypersecretory state is observed in
Zöllinger-Ellison syndrome (ZES). In ZES, ulcerations occur in the
stomach, duodenum, and jejunum resulting from excessive gastrin
secretion by a tumor, resulting in hyperacidity with mucosal
erosion. Benign or malignant GI neoplasms may initiate severe
bleeding episodes, especially tumors located in the vascular system
that supplies the GI tract.
Ulcer bleeding from the upper GI (UGI) tract is usually self-
limiting, most often ceasing spontaneously with the exception of
EVs. Recurrent bleeding arises in a substantial proportion of
patients and is associated with a poor prognosis. The need for
accurate diagnosis and effective therapy is crucial.

Lower gastrointestinal bleeding

Small intestine
The structures distal to the ligament of Treitz (a thin muscular band
that wraps around the small intestine where the duodenum and
jejunum meet) are affected by conditions including arteriovenous
malformation, intussusception of the small bowel, acute superior
mesenteric artery occlusion, and Crohn disease.

Large intestine
The most common cause of significant lower GI bleeding (LGIB) is
colonic diverticulosis, accounting for up to 50% of all cases.

1713
Arteriovenous malformation of the ascending colon and the cecum
is also a usual cause of massive colonic bleeding. Inflammatory
bowel diseases such as ulcerative colitis and Crohn disease result in
friable intestinal mucosa, which can lead to massive hemorrhage
and other serious complications, including bowel obstruction and
perforation. Other causes include colonic polyps, benign or
malignant neoplasms and congenital malformation such as
hemangioma or telangiectasia.

Rectum
Hemorrhoids and neoplasms frequently cause LGIB but are usually
hemodynamically insignificant.

Neighboring organs

Pancreas and vascular grafts

Acute pancreatitis (discussed later in this chapter) and pancreatic
pseudocyst are disorders associated with hemorrhage. Patients with
intraabdominal vascular grafts are at risk for the development of
aortoenteric fistulas with massive GI hemorrhage.

Systemic organ diseases

Hypoperfusion associated with decreased cardiac output (CO) or
volume depletion can lead to GI ischemia, resulting in necrosis and
hemorrhage. A high incidence of GI bleeding is associated with
uremia in patients with kidney failure because of platelet
dysfunction from abnormal adhesiveness, resulting in prolonged
bleeding time. Collagen vascular diseases such as systemic lupus
erythematosus can result in thrombosis of small vessels in the small
intestine, eventually leading to ulceration. Coagulopathic
conditions (e.g., disseminated intravascular coagulation [DIC],
thrombocytopenia) are associated with hematemesis and melena
caused by decreased clotting ability.

Medications
Long-standing use of aspirin, corticosteroids, or anticoagulants is
associated with serious GI bleeding. Ethanol may cause or

1714
potentiate ulcer bleeding because it induces gastric mucosal injury.
NSAIDs cause increased risk of serious GI bleeding, ulceration, and
perforation of the stomach and intestines. Traditional NSAIDs are
nonselective inhibitors of both cyclooxygenase-1 (COX-1) and
cyclooxygenase-2 (COX-2) enzymes. COX-1 enzymes regulate
gastroduodenal mucosal protective mechanisms. COX-2 enzymes
are involved in inflammatory and pain responses. The newer COX-
2 selective inhibitors were believed to block pain and inflammation
while leaving protective mucosal mechanisms intact, thereby
significantly lowering the incidence of GI ulceration and bleeding
compared with traditional NSAIDs. However, the COX-2 inhibitors
were shown to increase the risk of cardiovascular disease,
especially in older adults, resulting in the removal of two of three
COX-2 agents from the market. Currently, celecoxib (celebrex)
is the only COX-2 selective inhibitor available in the United States.
This COX-2 inhibitor is still associated with an increased risk for GI
bleeding, while to a lesser degree than traditional NSAIDS;
additionally, it does not appear to pose any greater risk for
cardiovascular disease than traditional NSAIDs.

Other
Obscure GI bleeding is bleeding from an unknown site despite
endoscopic and colonoscopy evaluation. These patients are believed
to have a source in the small intestine that cannot be pinpointed.
These patients may present with visible or occult bleeding (iron
deficiency anemia and/or positive for fecal occult blood). Bleeding
as a result of minor trauma: In addition to major abdominal trauma
(Chapter 3), foreign bodies such as razors, screws, or nails may
lacerate gastric or intestinal mucosa, causing bleeding.

Gastrointestinal assessment: Acute

gastrointestinal bleeding
Goal of assessment
Evaluate patients for severity of active bleeding, shock states, or
risk of rebleeding.

1715
History and risk factors
History and risk factors include critical illness, especially that
caused by major injury, surgery, CNS disorder, or burns; prolonged
shock or hypoperfusion; organ failure; EVs, excessive alcohol,
NSAIDs, or corticosteroid ingestion; inflammatory bowel disease;
foreign body ingestion; hiatal hernia; hepatic, pancreatic, or biliary
tract disease; blood dyscrasias; penetrating or blunt trauma; familial
cancer; recent abdominal surgery; and the presence of H. pylori.
Identification of those at risk for recurrent bleeding is essential to
guide therapy and prevent recurrence. Risk factors associated with
rebleeding are listed in Box 9-1.

Box 9-1
RISK FACTORS TO PREDICT RECURRENT
BLEEDING
• Large-volume blood loss on admission with transfusion of greater
than 6 units

• Shock

• Age greater than 60 years

• Hematemesis as the initial sign of hemorrhage

• Stigmata of ulcer bleeding as identified endoscopically (see Box 9-

2)

• Bleeding that occurs while hospitalized for another problem

Vital sign assessment

• Systolic BP less than 90 to 100 mm Hg with an HR greater than
100 bpm in a previously normotensive individual signals a 20%
or greater reduction in blood volume.

1716
• Orthostatic hypotension signs will be positive revealing a
decrease in systolic BP greater than 10 mm Hg with an increase in
HR of 10 bpm. Orthostatic hypotension is indicative of recent
blood loss of 500 to 1000 mL in the adult.

• Respiratory rate (RR) will be mildly elevated as a response to the

diminished oxygen-carrying capacity of the blood. If abdominal
pain is present, ventilatory excursion may be limited.

• Urine output will be decreased as a result of volume depletion.

Blood loss
• The amount of blood lost and rate of bleeding will have varying
effects on cardiovascular and other body systems.

• Blood loss of 1000 mL within 15 minutes usually produces

tachycardia, hypotension, nausea, weakness, and diaphoresis.
Adults can lose up to 500 mL of blood in 15 minutes and remain
free of associated symptoms.

• Massive hemorrhage, which is generally defined as loss of greater

than 50% of total blood volume within 3 hours.

• Syncope associated with hypotension may also occur.

• Sequestration of fluid into the peritoneum and interstitium

further depletes intravascular volume.

• Severe hypovolemic shock and decreased CO can lead to

ischemia of various organs, especially the brain and kidneys.

Abdominal pain
• Mild to severe epigastric pain is often associated with
gastroduodenal ulcerative or erosive disease. The pain is
described as dull or gnawing.

• Pain may diminish when blood covers and protects the eroded
tissue.

1717
• Blood can irritate the bowels, thereby increasing transit time in
the lower GI tract, causing diarrhea.

Observation
• Extremities are cool and diaphoretic.

• Pallor or cyanosis may be present.

• Alterations in level of consciousness (LOC) with restlessness and

confusion.

• Emesis or gastric aspirate contains obvious whole blood or old

blood that resembles coffee grounds.

• Hematemesis usually occurs with UGIB from above the ligament

of Treitz. Bleeding originating below the level of the duodenum
is not usually associated with hematemesis. Emesis of bright red
blood is suggestive of recent or ongoing bleeding, and dark,
coffee-ground emesis suggests that the bleeding stopped some
time ago.

• Abnormal stool:

• Melena (black, tarry, shiny, stools containing blood,

with a distinctive fetid odor) is usually present with
UGIB. May also be present with bleeding from the
small intestine or proximal large intestine.

• Hematochezia refers to bright red blood per rectum

that is usually caused by a colonic or anorectal
source. If the patient is acutely hypotensive
however, hematochezia would indicate a severe,
brisk UGI bleed with rapid transport through the
GI tract.

1718
• Massive LGIB is associated with dark red “currant
jelly” stools or passing fresh blood with clots.
• Jaundice, vascular spiders, ascites, and hepatosplenomegaly are
suggestive of liver disease.

Auscultation
• Abdominal auscultation may reveal hyperactive bowel sounds
caused by mucosal irritation by blood.

• A silent abdomen suggests serious complications such as ileus,

perforation, or vascular occlusion.

Palpation
• Palpation may reveal epigastric tenderness, which is expected in
peptic ulceration.

• An epigastric mass or enlarged lymph nodes may indicate gastric

malignancy.

• Decreased peripheral pulses, delayed capillary refill (greater than

2 seconds).

Nutrition assessment
• Evidence of malnutrition will be noted in the presence of chronic
liver disease or active, excessive alcohol use.

Screening labwork
• CBC: May identify decreased hemoglobin (Hgb) and decreased
hematocrit (Hct).

• LFTs: May be elevated if advanced liver disease is present.

• Serum chemistry: May identify increased blood urea nitrogen

(BUN).

1719
Hemodynamic measurements
• Decreased central venous pressure (CVP).

• Decreased mean arterial pressure (MAP).

• Increased stroke volume variation (SVV).

Diagnostic Tests for Acute Gastrointestinal Bleeding

Blood urea nitrogen–to–creatinine ratio

1720
Elevated BUN:creatinine ratio up to 36:1 mg/dL reflects a
disproportionate increase in BUN compared with a mild increase in
serum creatinine with UGIB resulting from red blood cells (RBCs)
that have bled and pooled in the UGI tract being consumed and
digested by duodenal/proximal small intestinal bacteria. The
resulting urea is absorbed. BUN increases without a corresponding
increase in creatinine. BUN increases are NOT seen with bleeding
from the colon or the lower portion of the small intestine.
Dehydration contributes to the increased BUN and total protein
levels. Mild reduction in glomerular filtration rate from volume
depletion causes a mild creatinine elevation.

Esophagogastroduodenoscopy
Esophagogastroduodenoscopy is the most accurate means of
determining the source of UGI ulcer bleeding. Visualization of the
esophagus, stomach, and duodenum using a fiber optic endoscope
passed through the mouth is usually performed within the first 12
hours after admission of the patient to identify the exact source of
bleeding and characteristics of ulcers, if present. Endoscopic ulcer
findings are referred to as endoscopic stigmata. Stigmata indicative
of bleeding ulcers, bleeding EVs, or ulcers at risk for rebleeding are
identified in Box 9-2, Stigmata of Active or Recent Hemorrhage
(SARH). SARH findings are helpful in determining the course of
direct therapy as well as providing prognostic information.
Antacids and sucralfate should be withheld until after the
procedure, because they can alter the appearance of lesions. Gastric
biopsy is usually obtained with endoscopy for H. pylori diagnosis as
well as to exclude gastric malignancy.

Box 9-2
STIGMATA OF ACTIVE OR RECENT
HEMORRHAGE
Endoscopic Ulcer Findings From Active or Recent Upper
Gastrointestinal Hemorrhage:
Diagnostic Endoscopic Findings Rebleeding Rate Without Rebleeding Rate With
(Prevalence) Treatment (%) Treatment (%)
• Active arterial spurting (12%) 90 15-30

1721
 • Nonbleeding visible vessel (22%) 50 15-30
• Active oozing of blood (14%) 10
• Adherent or overlying clot without 33 5
oozing (10%)
• Flat, pigmented slough or spot on 7
the ulcer base (10%)
• Clean ulcer base (32%) 3

Endoscopic findings in descending order are indicative of high

risk for continued bleeding or rebleeding, requiring more
aggressive therapy. For patients who do not exhibit these findings,
the risk of rebleeding is significantly lower.
(Adapted from Wilkins T, Khan N, Nabh A, et al: Diagnosis and management of upper
gastrointestinal bleeding. Am Fam Phys 85:469-476, 2012.)

Electrocoagulation, injection therapy (epinephrine), laser,

hemoclips, and other therapeutic techniques such as scleral therapy
and variceal ligation (banding) may be used during this procedure
to stop current bleeding or prevent further bleeding.

Colonoscopy
Colonoscopy is diagnostic for patients with LGIB for identification
of bleeding through visualization. Colonoscopy is usually
performed within 12 to 24 hours of presentation. If a visible vessel
or adherent clot is noted, direct therapy can be provided. Direct
therapy includes laser therapy, heater probes, electrocoagulation,
injection, and argon plasma coagulation. Bleeding from colonic
diverticula is usually from multiple sites and intermittent,
therefore, direct intervention is frequently limited.

Collaborative management
Acute GI bleeding can occur from various lesions or sites in the GI
tract. The amount of blood loss can vary from minor to massive
(Table 9-2) depending on the cause, resulting in hypovolemic shock
with significant associated mortality. The patients requiring
intensive care management are those with severe bleeding,
advanced age, and significant comorbidities such as end-stage renal
disease, hepatic disease, or cardiovascular disease. Severe
gastrointestinal bleeding is defined as GI bleeding:

1722
• Identified by documented hematemesis, melena, hematochezia,
or positive NG lavage;

• Accompanied by shock or orthostatic hypotension;

• Causing a decrease in the hematocrit value by at least 6% (or a

decrease in the hemoglobin level of at least 2 g/dL), or requiring
transfusion of at least 2 units of packed RBCs (pRBCs).

Table 9-2
SEVERITY OF BLOOD LOSS

Severity of Percent of Intravascular Blood Pressure (BP, bpm) and Heart Rate (HR,
Bleed Blood Loss mm Hg) Findings
Massive 20% to 25% Systolic BP < 90 mm Hg HR >100 bpm
Moderate 10% to 20% Orthostatic hypotension HR ≥100 bpm
Minor <10% Normal BP HR ≤100 bpm
Adapted from Rockey DC: Gastrointestinal bleeding. In Sleisenger MH, Feldman M,
Fordtran JS, et al, editors: Sleisenger & Fordtran’s gastrointestinal and liver disease:
pathophysiology, diagnosis, management, ed 8, Philadelphia, 2006, Saunders.

Collaborative management focuses on cessation of active

bleeding, identification and treatment of the underlying
pathophysiology, and the prevention of rebleeding. Some patients
develop GI bleeding during hospitalization for another reason as in
the case of stress ulceration. Stress ulcer prophylaxis has been
included in the management of patients who are critically ill and
mechanically ventilated.

Care priorities
Assessing the bleeding severity and restoration of
hemodynamic stability of the patient are immediate priorities in the
acute phase of GI bleeding. Intensive care unit monitoring is
necessary to reduce morbidity and mortality. Once stabilized, care
priorities will shift to the identification and management of the
bleeding source.

1. Fluid and electrolyte management

Volume replacement in acute GI bleeding must be a priority. Large-
bore intravenous (IV) lines should be placed and rapid fluid

1723
resuscitation initiated. Volume replacement should include a
combination of crystalloid and blood products. Unstable patients
with poor tissue perfusion may require blood products. Packed
cells and fresh-frozen plasma should be balanced to provide for
both the replacement of cells and clotting components. Large
transfusions will cause Ca2+ to bind with the citrate (the
preservative in stored blood) and deplete free Ca2+ levels. In
addition, large-volume blood transfusions can lead to coagulation
disorders. Vasopressors and inotropic agents should be used only if
tissue perfusion remains compromised despite adequate
intravascular volume replacement. Hemodynamic monitoring is
essential for continuous evaluation of the patient’s volume status,
especially in patients older than 50 years or those with chronic
illnesses such as cardiovascular, pulmonary, renal, or hepatic
disease. Overaggressive volume resuscitation may result in fluid
volume excess with complications of cardiac failure and pulmonary
edema. Electrolyte levels should be closely monitored, especially in
patients with renal or hepatic disease.

2. Respiratory support
Provide oxygen therapy by nasal cannula or face mask.
Supplemental oxygen is necessary as a result of blood loss, which
reduces the number of RBCs available for oxygen-carrying capacity.
Continuous or frequent pulse oximetry monitoring is
recommended in patients who are actively bleeding to monitor
oxygen saturation, but arterial blood gas (ABG) analysis may be
needed to check SaO2 if the patient is markedly anemic. More
aggressive ventilatory support may be required for patients with
persistent hypoxemia, evidence of early respiratory failure, or
impending acute respiratory distress syndrome (ARDS), as well as
for patients who were aggressively volume resuscitated.

3. Nutrition support
As soon as the hemodynamic status of the patient stabilizes,
nutrition support must be considered. Patients with active bleeding,
visible vessels, or clots may receive clear liquids following
successful endoscopic hemostasis. Patients with clean-based ulcers
may receive a regular diet following endoscopy.

1724
4. Gastric intubation
Gastric intubation may be performed but is not required for
patients with UGIB for diagnosis, prognosis, visualization, or
therapeutic effect. Gastric lavage is performed using room
temperature normal saline or water to clear blood and clots from
the stomach and to allow for estimation of ongoing blood loss. A
lavage free of blood suggests a lower GI source of bleeding. There is
no evidence that lavage stops the bleeding. Gastric intubation is
avoided if EVs are the suspected bleeding source. Balloon
tamponade may be necessary for the patient with variceal bleeding
refractory to medical and endoscopic therapy.

5. Endoscopic therapies
Coagulopathy and thrombocytopenia should be corrected before
endoscopy. In cases of respiratory insufficiency, altered mental
status, with ongoing bleeding, endotracheal intubation is indicated
before endoscopy to stabilize the patient and protect the airway.
Early endoscopy, within the first 24 hours of admission increases
diagnostic accuracy, reduces the risk of rebleeding, and decreases
the length of hospitalization. Endoscopy should be performed
within 12 hours of admission for the patient with suspected varices.
Endoscopic modalities for the achievement of hemostasis include:
thermal therapy (electrocoagulation or heater probe and injection of
sclerosant), epinephrine injection therapy (should be used in
conjunction with second modality), and the application of
hemoclips (clips that serve to apply mechanical pressure to the
bleeding site) are generally effective in stopping bleeding for both
UGIB and LGIB. Complications of endoscopy include perforation
and MW tears.

6. Pharmacotherapy
Pharmacotherapy including vasopressin and nitroglycerin is only
available for the management of UGIB. No pharmacologic therapies
for LGIB are currently available. In the upper GI tract, increased
gastric acidity is believed to impede blood clotting, although gastric
alkalinization may facilitate platelet aggregation, thus promoting
acid-lowering pharmacotherapies. Pharmacologic agents involved
in ulcer treatment include antacids, H2-receptor antagonists,

1725
proton-pump inhibitors (PPIs), prostaglandin analogues,
somatostatin, and octreotide.
Antacids (aluminum hydroxide, calcium carbonate,
citrocarbonate, magaldrate, magnesium hydroxide, simethicone):
Oral antacids raise gastric pH levels and decrease the corrosiveness
of gastric acid. They may relieve dyspepsia but have no effect on
bleeding ulcers.
Histamine H2-receptor antagonists (e.g., famotidine, ranitidine,
cimetidine, nizatidine): Inhibit gastric acid and pepsin secretion,
and are useful in the treatment of ulcerative disease and for stress
ulcer prophylaxis. The usefulness in an active bleeding ulcer is
unsupported. They provide inferior acid inhibition to PPIs.
Cimetidine is avoided in patients who are critically ill because it
inhibits certain liver enzymes, resulting in potential drug
interactions.
Proton-pump inhibitors (e.g., esomeprazole, lansoprazole,
omeprazole, pantoprazole, rabeprazole): PPIs deactivate the
enzyme system that pumps hydrogen ions from parietal cells,
thereby inhibiting gastric acid secretion. PPIs have become the
preferred agent for erosive ulcer disease with bleeding. Acid-
inhibitory effects of PPIs are significantly stronger than H2-receptor
antagonists. IV PPIs or high-dose oral PPIs following a bleeding
episode are effective in reducing the incidence of rebleeding, the
number of transfusions, and the need for further endoscopic
therapy. Preendoscopic IV PPIs may reduce high-risk stigmata in
patients with UGIB and is recommended. IV PPIs are additionally
recommended in patients for whom endoscopy must be delayed or
cannot be tolerated.
Prostaglandin analogues (e.g., misoprostol [Cytotec]): Synthetic
prostaglandin E1 enhances the body’s normal mucosal protective
mechanisms by stimulating mucosal blood flow and bicarbonate
secretion, and reducing mucosal cell turnover. They are useful in
reducing the incidence of ulcer development in patients taking
NSAIDs.
Vasoconstrictors: Vasopressin may help slow variceal bleeding.
Octreotide, a somatostatin analogue: Causes splanchnic
vasoconstriction and reduced portal pressure. In combination with
endoscopic therapies, it has been shown to control variceal bleeding

1726
and reduce the risk of recurrence. No improvement in mortality has
been shown with its use in this population.
Sucralfate (Carafate): Oral sucralfate may be prescribed for
patients with gastric erosions. Sucralfate combines with gastric acid
and forms an adhesive-protective coating over damaged mucosa
and does not alter gastric pH. Sucralfate frequently causes
constipation and should be avoided in patients with chronic renal
insufficiency.
Pharmacotherapy for H. pylori: Eradication of H. pylori is
effective with combination therapies, monotherapy is useless.
“Triple therapy” includes two antibiotics (clarithromycin and
amoxicillin or metronidazole) and a PPI. “Quadruple therapy”
includes bismuth salicylate, metronidazole, tetracycline, and a PPI
or H2-blocker. There are several triple therapy combination
preparations available to allow the patient to receive the
combination in one pill.

7. Surgical management
Many surgical techniques are used for both acute UGIB and LGIB,
depending on the location and severity of the lesion. EVs are best
managed with endoscopic ligation (banding) or sclerotherapy. Band
ligation involves wrapping elastic bands over the varices in the
distal esophagus; sclerotherapy involves the injection of a
sclerosing agent. Ulcerative disease requires surgery if the lesion
continues to bleed despite aggressive medical and endoscopic
therapy or if complications such as perforation or obstruction
develop. Oversewing of the bleeding vessel is usually followed by
an acid-reducing procedure such as antrectomy, which removes
acid-secreting cells, or vagotomy, which denervates the acid-
producing fundic mucosa. Pyloroplasty is performed if there is
impairment of gastric emptying. In the patient whose condition is
unstable, both vagotomy and pyloroplasty are performed.
Antrectomy and vagotomy may be performed in patients whose
condition is more stable with anastomosis of the stomach to the
duodenum (Billroth I procedure). Also common is the Billroth II
procedure for duodenal ulcers involving antrectomy with
gastrojejunostomy. Massive LGIB is difficult to control and may
require aggressive surgical procedures such as a colectomy with the

1727
creation of a permanent ileostomy or internal ileal pouch.

Care plans for acute gastrointestinal

bleeding
Deficient fluid volume 
related to active loss secondary to hemorrhage from the GI tract.
Goals/Outcomes: Within 8 hours of diagnosis, the patient will be
normovolemic, as evidenced by systolic BP greater than 100 mm
Hg, HR less than 100 bpm, CVP 2 to 6 mm Hg, urinary output
greater than 0.5 mL/kg/h, Hct greater than 24%, platelet count
greater than 50,000/mm3, and prothrombin time (PT) less than 15
seconds.
Electrolyte and Acid-Base Balance; Fluid Balance.

Fluid management

1. Monitor BP continuously with an arterial catheter for the patient

with severe GI bleeding. Be alert to MAP decreases of greater than
10 mm Hg.

2. Monitor postural vital signs for the patient with mild to moderate
GI bleeding on admission, every 4 to 8 hours, and more frequently
if recurrence of active bleeding is suspected: measure BP and HR
with the patient in a supine position, followed immediately by
measurement of BP and HR with the patient in a sitting position (as
tolerated). A decrease in systolic BP greater than 10 mm Hg or an
increase in HR of 10 bpm with the patient in a sitting position
suggests a significant intravascular volume deficit, with
approximately 15% to 20% loss of volume.

3. Monitor HR, electrocardiogram (ECG), and cardiovascular status

hourly, or more frequently in the presence of active bleeding or
unstable vital signs. Be alert to a sudden increase in HR, which
suggests hypovolemia.

4. Continuously monitor SVV and stroke index (SI) in patients who

are mechanically ventilated whose volume status is unstable when

1728
available. Assist-control mode is recommended for patients
undergoing SVV monitoring. Be alert to low or decreasing CVP.
CVP less than 2 mm Hg, SI less than 33, and SVV greater than 13%
to 15% are suggestive of hypovolemia and the need for volume
restoration.

5. Measure urinary output hourly. Be alert to output less than 0.5

mL/kg/h for 2 consecutive hours. Increase fluid intake or consider
fluid bolus if decreased output is caused by hypovolemia and
hypoperfusion.

Fluid resuscitation

1. Obtain two large-bore IV lines (16- or 18-gauge) and/or central

venous access.

2. Initiate crystalloid replacement therapy with a combination of

normal saline and Lactated Ringer (LR) solution. Fluid may be
warmed to prevent hypothermia.

3. Administer pRBCs for persistently low Hct of less than 21% to

24%. Anticipate that Hct will increase by 3% following 1 unit of
pRBCs.

4. Fresh-frozen plasma may be administered after 3 units of pRBCs

are transfused.

5. Monitor PT and activated partial thromboplastin time (aPTT);

administer fresh-frozen plasma if PT is greater than 1.5 times
normal or aPTT is greater than 2 times normal.

6. Monitor ionized calcium levels closely because of the tendency of

calcium to bind with citrate. Administer calcium gluconate for
ionized calcium based on institutional protocol.

7. Prepare for platelet transfusion before endoscopy if platelets fall

below 50,000/dL with normal function or 100,000/dL if dysfunction
is suspected.

Shock management

1729
1. Initiate fluid replacement (see Fluid and Electrolyte Disturbances,
Chapter 1).

2. Collaborate with the physician or nurse practitioner to administer

vasoactive medication if shock persists with volume resuscitation.

3. Monitor for cerebral ischemia or indications of insufficient

cerebral blood flow.

4. Monitor renal function (BUN and creatinine levels for elevations),

because intravascular volume depletion can lead to prerenal acute
kidney injury.

5. Monitor tissue oxygenation using ABG, central venous oxygen

saturation (ScVO2), and serum lactate measurements as ordered.

6. Monitor ECG for ST segment depression and T wave inversion,

which may be seen as a result of the shock state.

Bleeding reduction: Gastrointestinal

1. Administer PPIs IV as ordered before endoscopy. Vasopressin

(Pitressin) may help slow variceal bleeding.

2. Measure and record all GI blood losses from hematemesis,

hematochezia, and melena.

3. Check all stools and gastric contents for occult blood.

4. Ensure proper function and patency of NG tubes. Do not occlude

the air vent because this may result in vacuum occlusion. Confirm
placement of gastric tube by x-ray, capnography or colorimetric
capnometry, and reposition as necessary.

5. Balloon tamponade may be necessary as a temporizing measure

for the patient with bleeding EVs. Balloons should be inflated for no
more than 12 hours.

6. Teach the patient signs and symptoms of actual or impending GI

hemorrhage: pain, nausea, vomiting of blood, dark stools,

1730
lightheadedness, and passage of frank blood in stools. Reinforce the
importance of seeking medical attention promptly if signs of
bleeding occur.

7. Teach the patient the importance of avoiding medications/agents

with the potential for gastric irritation: aspirin, NSAIDs, and
ethanol.

Blood Products Administration; Hemodynamic Regulation;

Gastrointestinal Intubation; Bleeding Precautions; Teaching:
Individual; Surgical Preparation.

Decreased cardiac output 

related to decreased preload secondary to acute blood loss.
Goals/Outcomes: Within 8 hours of diagnosis, CO approaches
normal limits with adequate tissue perfusion, as evidenced by
cardiac index (CI) greater than 2.5 L/min/m2, MAP greater than 65
mm Hg, CVP 2 to 6 mm Hg, urinary output greater than 0.5
mL/kg/h, normal sinus rhythm on ECG, distal pulses greater than
2+ on a 0-to-4+ scale, and brisk capillary refill (less than 2 seconds).
Blood Loss Severity.

Hemodynamic regulation

1. Administer vasopressors and inotropic agents as prescribed if

tissue perfusion remains inadequate following intravascular
volume replacement.

2. Monitor ECG for evidence of myocardial ischemia (i.e., ST

segment depression, T wave inversion, and ventricular
dysrhythmias).

3. Monitor for physical indicators of diminished CO, including

pallor, cool extremities, capillary refill greater than 2 to 3 seconds,
and decreased or absent amplitude of distal pulses.

4. Monitor vital signs and CO, and replace volume as indicated (see
Fluid and Electrolyte Disturbances, Chapter 1).

1731
5. Monitor for oliguria hourly; report urine output less than 0.5
mL/kg/h for 2 consecutive hours.

Respiratory monitoring

1. Administer oxygen via nasal cannula or facemask to facilitate

maximal oxygen delivery.

2. Monitor pulse oximetry and ABG values for hypoxemia. Report

arterial PaO2 less than 80 mm Hg and oxygen saturation below 92%,
demonstrates altered mental status with severe bleeding.

3. Prepare for endotracheal intubation and mechanical ventilation if

the patient is distressed with oxygen saturation less than 90% with
supplemental oxygen.

4. Monitor for respiratory crackles, which can result from

overaggressive fluid resuscitation.

Cardiac Care: Acute; Oxygen Therapy; Invasive

Hemodynamic Monitoring; Dysrhythmia Management.

Acute pain 
related to chemical or physical injury of GI mucosal surfaces caused by
digestive juices and enzymes or tissue trauma.
Goals/Outcomes: Within 2 hours of diagnosis, the patient’s
subjective evaluation of discomfort improves, as demonstrated by a
decreased reported pain level. Nonverbal indicators of discomfort,
such as grimacing, are absent.
Comfort Level; Pain Control.

Pain management

1. Monitor and document presence of abdominal pain or

discomfort. Utilize appropriate pain scale. Pain may disappear
during a bleeding episode because blood covers and protects
eroded tissue.

2. Administer opiate analgesics with caution to patients who are

1732
hypovolemic to avoid hypotension and respiratory depression.

3. Supplement analgesics with nonpharmacologic maneuvers to aid

in pain reduction. Head of bed (HOB) elevation may be useful in
reducing the discomfort of gastric reflux, as long as it does not
compromise hemodynamic status. Reflux may prompt variceal
bleeding.

Analgesic Administration; Distraction; Environmental

Management; Vital Signs Monitoring.

Diarrhea 
related to irritation and increased motility secondary to the presence of
blood in the GI tract.
Goals/Outcomes: By hospital discharge, the patient’s stools are
normal in consistency and frequency, and results are negative for
occult blood.
Fluid Balance; Bowel Elimination; Electrolyte and Acid-Base
Balance.

Diarrhea management

1. Monitor and record the amount, frequency, and characteristics of

the patient’s stools.

2. Provide bedpan or bedside commode (only for patients who are

hemodynamically stable). Consider use of a contained bowel
management system device such as Flexiseal or Actiflo. Use with
caution in patients who may be anticoagulated.

3. Minimize embarrassing odor by removing stool promptly and

using room deodorizers.

4. Use matter-of-fact approach when assisting the patient with

frequent bowel elimination. Reassure the patient that frequent
elimination is a common problem for most patients with GI
bleeding.

5. Evaluate bowel sounds every 4 hours. Anticipate normal to

1733
hyperdynamic bowel sounds. Absence of bowel sounds (especially
in association with severe pain or abdominal distension) may signal
serious complications such as ileus or perforation.

6. Report abnormal serum sodium, potassium, and calcium levels to

the physician or nurse practitioner.

Electrolyte Monitoring; Fluid/Electrolyte Management.

Imbalanced nutrition: Less than body requirements 

related to inability to ingest or digest food secondary to vomiting, mucosal
ulceration, ileus, or active GI bleeding.
Goals/Outcomes: Within 7 days of diagnosis (or by hospital
discharge), the patient has adequate nutrition, as evidenced by
stable weight, prealbumin 20 to 30 mg/dL, and a state of nitrogen
balance on nitrogen studies.
Nutrition Status.

Nutrition management

1. Collaborate with intraprofessional team to estimate the patient’s

individual metabolic needs on the basis of activity level, underlying
disease process, and nutrition status before hospitalization.

2. Provide clear liquid diet (for high-risk stigmata) or regular diet

(for patients with a clean ulcer base) following endoscopic
hemostasis as prescribed.

3. Monitor prealbumin and report decreasing levels.

4. Weigh the patient daily at the same time of day, using the same
scale. Weight can be a practical indicator of nutrition status if the
patient’s weight changes are interpreted on the basis of the
following factors: fluid shifts (edema, diuresis, third spacing),
surgical resection, and weight of dressings and equipment.

Nutrition Monitoring; Aspiration Precautions.

For additional information, see Nutrition Support, Chapter 1.

1734
Additional nursing diagnoses
See other nursing diagnoses and interventions as appropriate:
Hemodynamic Monitoring (Chapter 1), Prolonged Immobility
(Chapter 1), and Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2).

Acute pancreatitis
Pathophysiology
Acute pancreatitis (AP) is an autodigestive process of the pancreas
and surrounding tissue by pancreatic enzymes, resulting in the
most common cause of GI disease–related hospitalizations in the
United States. Normally, pancreatic acinar cells produce and secrete
inactive proteolytic enzymes. These proenzymes travel through the
pancreatic duct safely until reaching the duodenum, where they are
activated by other enzymes found in the intestinal brush border. In
AP, the proenzyme trypsinogen is prematurely activated to the
proteolytic enzyme trypsin within the acinar cells of the pancreas.
Once secreted into the pancreatic duct, trypsin activates other
proenzymes, resulting in enzymatic autodigestion of the pancreas.
The exact mechanisms prompting trypsin to be prematurely
activated remains unanswered. AP is created by a series of events.
Initially, the activated digestive enzymes within the pancreas digest
pancreatic tissue, leading to inflammation and capillary leakage.
Eventually, these enzymes may also digest elastin in blood vessel
walls, causing vascular injury that sometimes leads to hemorrhage.
The spread of inflammatory mediators (kinins, complement,
coagulation factors) released at the site of tissue and vessel injury
cause further edema, inflammation, thrombosis, and result in
systemic inflammatory response syndrome (SIRS). Significant
pancreatic edema leads to rupture of the pancreatic ducts and
spillage of pancreatic enzymes into the peripancreatic tissue,
resulting in injury. Pancreatic necrosis develops when the
pancreatic blood supply is significantly disrupted. Pancreatic
necrosis along with organ failure are defining features of severe
disease. Shock, distant organ dysfunction, and/or multiple organ

1735
dysfunction syndrome (MODS) can ensue.
AP is clinically classified as mild or severe. In cases of mild AP,
there is local inflammation, interstitial edema identified by imaging,
and the absence of pancreatic necrosis and/or organ failure. The
pancreatic blood supply is preserved. Patients usually improve in
48 to 72 hours with supportive management. Mild AP accounts for
the majority of cases with a mortality rate of less than 1%. The
incidence of progression from mild to severe AP may be increasing.
Approximately, 15% to 20% of patients with mild AP will develop
severe disease. Severe acute pancreatitis (SAP) is a life-threatening
condition currently described in two distinct phases: early (within
the first week) and late (after the first week). Early disease is
characterized by persistent organ failure and/or SIRS lasting longer
than 48 hours. Organ failure may be identified by two or more of
the following: shock (systolic BP less than 90 mm Hg), pulmonary
insufficiency (PaO2 ≤60 mm Hg), kidney failure (serum creatinine
greater than 2 mg/dL), or GI bleeding (greater than 500 mL/24 h).
Late SAP involves the development of one or more local
complications that include sterile or infected
pancreatic/peripancreatic necrosis, acute pseudocyst, acute
peripancreatic fluid collection, and walled-off pancreatic necrosis
(WOPN) (see Complications).
Alcoholism and gallstones account for 80% of all AP cases.
Alcohol sometimes has a direct toxic effect on the pancreatic acinar
cells or may cause inflammation of the sphincter of Oddi, resulting
in the retention of enzymes in the pancreatic duct. In patients with
gallstones, AP may be caused by obstruction of the pancreatic duct
by gallstones lodged at the shared outlet of the pancreatic duct and
common bile duct into the duodenum. When the outlet is blocked,
bile can reflux into the pancreatic duct. Once AP ensues,
hypercalcemia, hyperlipidemia, and hypertriglyceridemia are often
found to be present and may cause AP. AP is often associated with
a recent endoscopic retrograde cholangiopancreatography (ERCP)
procedure: the most common iatrogenic cause. Other causative
factors include blunt or penetrating trauma, metabolic factors,
infectious agents, and certain drugs (Box 9-3). Despite the capacity
for thorough investigation, the cause of AP is idiopathic in
approximately 15% to 20% of cases.

1736
Box 9-3
PRECIPITATING FACTORS FOR ACUTE
PANCREATITIS
Mechanical blockage of pancreatic ducts
• Biliary tract disease (e.g., gallstones)

• Structural abnormalities (e.g., pancreas divisum)

• Post-ERCP

• Tumors

Toxic/metabolic factors
• Ethyl alcohol

• Hyperlipidemia

• Hypertriglyceridemia (may cause up to 5% of cases)

• Hypercalcemia

• Pregnancy

Infection
• Viral (e.g., mumps, Coxsackie virus B, hepatitis B, HIV, CMV)

• Bacterial (e.g., Mycoplasma pneumoniae, Salmonella typhi)

Trauma
• External

• Surgical

1737
Ischemia
• Prolonged/severe shock

• Vasculitis

Drugs
• Corticosteroids

• Estrogens

• NSAIDs

• Sulfonamides

• Thiazides

• Tetracycline

CMV, Cytomegalovirus; ERCP, endoscopic retrograde

cholangiopancreatography; HIV, human immunodeficiency virus;
NSAIDs, nonsteroidal antiinflammatory drugs.

Risk stratification
Timely identification of patients at risk for developing SAP is
crucial to planning appropriate care to achieve the best outcomes.
Predicting severity early is crucial in preventing complications and
mortality. It is difficult to distinguish mild from severe disease in
the early stages. Several classification systems have been developed
to determine severity. Ranson’s criteria for non–gallstone AP
provide a scale of severity for AP based on age, blood gas,
hematologic, and biochemical changes. Pancreatitis is classified as
severe when three or more of Ranson’s 11 criteria are met during
the first 48 hours following presentation (Box 9-4). The Acute
Physiology and Chronic Health Evaluation (APACHE) II scoring
system (Table 9-3) is another tool to determine severity. An
APACHE II score of less than 8 points within the first 48 hours is
directly related to better survival. Higher scores during this time

1738
interval are associated with increased morbidity and mortality
rates. Scoring systems are often cumbersome and should be used in
conjunction with ongoing clinical findings and other laboratory
data. The less cumbersome Bedside Index of Severity in Acute
Pancreatitis (BISAP) was recently developed for risk stratification
during the first 12 hours of admission. The index includes five
commonly available clinical variables that are each assigned 1
point. A simple score of 3 points or greater is associated with
increased risk of complications and mortality (Box 9-5).

Table 9-3
THE ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION
(APACHE) II SCORING SYSTEM

*
Use if Fio2 <50%.
†
Use if percentage of inspired oxygen (Fio2) >50%.
‡
Use only if no arterial blood gas measurements are available.
§
APACHE II score ≥ 8 identifies severe acute pancreatitis and the need for intensive
care.
From Knaus WA, Draper EA, Wagner DP, Zimmerman JE: APACHE II: a severity of
disease classification system. Crit Care Med 13:818-829, 1985.

1739
A-aPo2, alveolar-arterial oxygen pressure; Pao2, partial pressure of oxygen in arterial
blood.

Box 9-4
RANSON CRITERIA FOR CLASSIFYING
THE SEVERITY OF PANCREATITIS
At presentation
• Age ≥55 years

• WBCs ≥16,000/mm3

• Glucose ≥200 mg/dL

• AST ≥250 units/L

• LDH ≥350 units/L

After initial 48 hours

• Base deficit ≥4 mEq/L

• BUN increased ≥5 mg/dL

• Fluid sequestration ≥6 L

• Serum Ca2+ >8 mg/dL

• Hematocrit decrease >10%

• Po2 (from ABG) >60 mm Hg

Ranson criteria scoring mechanism

Score 0 to 2—minimal mortality rate

Score 3 to 5—10% to 20% mortality rate

Score >5—50% mortality rate

1740
 ABG, Arterial blood gas; AST, aspartate aminotransferase; BUN,
blood urea nitrogen; Ca2+, calcium; LDH, lactate dehydrogenase;
PO2, partial pressure of oxygen; WBCs, white blood cells.

Box 9-5
BEDSIDE INDEX OF SEVERITY IN ACUTE
PANCREATITIS (BISAP) SCORE
Clinical Variables Point Allocation
BUN (blood urea nitrogen) >25 mg/dL 1
Impaired mental status 1
SIRS (systemic inflammatory response syndrome) 1
2 or more of the following:
• Temperature <36° C or >38° C
• Pulse >90bpm
• Respiratory rate >20 breaths/min or Pao2 <32 mm Hg
• White blood cell count <4000 or >12,000 or 10% bands
Age >60 years 1
Pleural effusion 1

A score of 3 is associated with 5% to 8% mortality; 4 is associated with 13% to 19%

mortality; 5 is associated with 22% to 27% mortality.

Complications
The inflammation associated with AP is nonbacterial. Pancreatic
necrosis is usually sterile but can become infected. In SAP, the
inflammatory process results in extensive pancreatic and
peripancreatic necrosis of mesenteric and retroperitoneal fat tissue
that prompts late-phase local complications, which increase
mortality and significantly lengthen the clinical course of disease.
Infected pancreatic necrosis should be suspected when worsening
of pain, fever, and leukocytosis manifest between 7 and 10 days
after admission. Infective necrosis often leads to sepsis and MODS
as a result of translocation of bacteria from the poorly functioning
gut. Pancreatic pseudocysts can form, comprising encapsulated
fluid collections with high enzyme concentration and variable
amounts of tissue debris. Although the majority of pseudocysts are
sterile, some become infected resulting in hemorrhage or rupture,
which prompts pancreatic ascites. Pseudocysts usually form within
or adjacent to the pancreas but can migrate into the chest or other

1741
locations. Other unencapsulated acute peripancreatic fluid
collections form in the peripancreatic area in approximately 30% of
AP cases. WOPN defines a collection of pancreatic and
peripancreatic debris and liquefied dead tissue encased in a fibrous
tissue wall. WOPN develops over a 4-week period in patients with
necrotizing pancreatitis.
A major initial complication of SAP is hypovolemia resulting
from plasma volume fluid sequestration into the interstitium,
retroperitoneum, and the gut. Massive, life-threatening hemorrhage
from rupture of necrotic tissue results in severe anemia and
hypotension. SIRS ensues, wherein inflammatory mediators trigger
vasodilation and increased capillary permeability, which further
contributes to severe hypovolemia and hypotension.
Hypoalbuminemia is frequently present, which prompts
intravascular fluids to move through the permeable capillaries
more rapidly, because oncotic pressure is reduced. Severe
hypotension may persist despite volume repletion given there is too
little protein to hold the volume within the blood vessels. If
hypovolemia is not adequately corrected promptly, acute kidney
injury and MODS may develop (see Systemic Inflammatory
Response Syndrome, Sepsis, Septic Shock, and Multiple Organ
Dysfunction Syndrome, Chapter 11).
Mild to severe respiratory failure with hypoxemia is common in
AP patients with SIRS. Respiratory complications are related to
right-to-left vascular shunting within the lung and alveolar-
capillary leakage caused by the circulating inflammatory mediators
resulting in ARDS (see Acute Lung Injury and Acute Respiratory
Distress Syndrome, Chapter 4). In addition, elevation of the
diaphragm, atelectasis, and pleural effusion caused by
subdiaphragmatic inflammation of the pancreas and surrounding
tissues, and/or pancreatic ascites, can compromise ventilation
further. Inflammatory mediators and vascular injury may lead to
intravascular coagulopathy or DIC, resulting in life-threatening
complications such as major thrombus formation and pulmonary
emboli. The circulatory and respiratory failures that ensue are often
the cause of death in these patients.

Assessment

1742
Goal of system assessment: Acute pancreatitis
Evaluate for organ and systemic involvement of dysfunctional
pancreatic secretions.

History and risk factors

• Excessive alcohol ingestion; biliary tract disease; recent ERCP;
hypertriglyceridemia greater than 1000 mg/dL; use of drugs such
as steroids, furosemide, thiazides, and certain NSAIDs; viral
infections (human immunodeficiency virus [HIV]); penetrating
and blunt injuries to the pancreas; pregnancy; primary
hyperparathyroidism; uremia.

Vital sign assessment

• Tachycardia and hypotension result from massive intravascular
losses.

• Increased temperature greater than 38.5° C (101.3 F) and

tachycardia are associated with an inflammatory response.

Abdominal pain
• Sudden onset of epigastric pain (often after excessive food or
alcohol ingestion) lasting 12 to 48 hours, described as mild
discomfort to severe distress, and located from the
midepigastrium to the right upper quadrant (RUQ). Occasionally
pain is reported in the left upper quadrant.

• Pain is typically described as boring and deep.

• Pain may radiate to the back.

• Nausea, vomiting, hematemesis, and restlessness typically

accompany the pain; diarrhea and melena may also be present.

Observation
• Mild to moderate ascites may be present.

1743
• Dyspnea and cyanosis may be observed if ARDS is present (see
Acute Lung Injury and Acute Respiratory Distress Syndrome,
Chapter 4).

• Jaundice may be present with biliary tract disease.

• Grey Turner sign (flank ecchymosis) and Cullen sign (umbilical

ecchymosis) occur in approximately 1% of cases and are
associated with a poor prognosis.

• Severe hypocalcemia may elicit Chvostek sign (facial twitching

after a facial tap) or Trousseau sign (hand spasms when BP cuff
inflates). Hypocalcemia causes numbness or tingling in the
extremities that progresses to tetany if calcium is severely
depleted.

• Abdominal distension is often present in SAP resulting from

gastric, small bowel, or colonic ileus.

Auscultation
• Diminished, sluggish, or absent bowel sounds reflective of GI
dysfunction and paralytic ileus.

• Breath sounds may be decreased or absent, suggesting focal

atelectasis or pleural effusion. Effusions are usually left-sided but
can be bilateral. Auscultation of crackles reflects hypoventilation
caused by pain, early ARDS, or microemboli.

Palpation
• Abdominal tenderness is common.

• Abdominal palpation will reveal localized tenderness in the RUQ

or diffuse discomfort over the upper portion of the abdomen
without rigidity or rebound.

• An upper abdominal mass may be palpated as a result of the

inflamed pancreas or a pseudocyst.

1744
• In the presence of hemorrhage or severe hypovolemia, the hands
are cool and sweaty to touch.

• Peripheral pulses will be diminished and capillary refill delayed

with hemorrhage or severe hypovolemia.

Nutrition assessment
• Malnutrition may be present, especially if there is a history of
alcoholism (see Table 9-1).

Screening labwork
• Serum electrolyte levels: Hypercalcemia.

• CBC: Leukocytosis.

• Serum amylase: ↑↑↑.

• Serum lipase: ↑↑↑.

• LFTs: Elevated with alcoholic or biliary involvement.

• Serum triglycerides: Elevated to greater than 1000 mg/dL

(hypertriglyceridemia may cause up to 5% of cases of AP).

Hemodynamic measurements for complications of

SAP
• Hypovolemic shock: Decreased CVP and CO from hemorrhage or
dehydration.

• SIRS: CO may be elevated and systemic vascular resistance (SVR)

decreased initially. Urine output decreases while the body
attempts to conserve intravascular volume.

• ARDS or pulmonary emboli: Increase in pulmonary vascular

resistance.

Diagnostic Tests for Acute Pancreatitis

1745
The diagnosis of acute pancreatitis (AP) is based on the presence
of two of the following three criteria:

(1) Abdominal pain characteristic of AP;

(2) Characteristic radiographic evidence of AP on imaging

(abdominal ultrasonography);

(3) Elevation of amylase and/or lipase ≥ three times upper limit of

normal.

The following tests are used to support the diagnosis and trend
the progression of the disease.

1746
Serum lipase and amylase
Serum lipase has become a primary diagnostic marker for AP.
Serum amylase is not sensitive diagnostically in cases of delayed
clinical presentation; pancreatitis caused by hypertriglyceridemia;
and in patients with chronic pancreatitis experiencing an acute
attack. Prolonged clamp time with coronary artery bypass grafting
or valve replacement can lead to AP in which only amylase is
elevated.

Collaborative management
Management includes risk stratification, monitored supportive care,
efforts to prevent, limit and treat complications, and recurrences.
The American College of Gastroenterology (ACG) guidelines
“Management of Acute Pancreatitis” frame the management
priorities. Because AP is a disease of significant variability, there is
a paucity of large randomized controlled trials. The ACG practice
guidelines (Box 9-6) present recommendations based on: scientific
studies and best evidence of new understandings and
developments in the diagnosis, etiology, and management of AP.

Box 9-6
AMERICAN GASTROENTEROLOGY
ASSOCIATION RECOMMENDATIONS FOR
ACUTE PANCREATITIS
Diagnosis
• Established by the presence of two out of three of the following
criteria: abdominal pain consistent with the disease, serum
amylase and/or lipase greater than three times the upper normal
limit, and/or characteristic findings from abdominal imaging.

• Contrast-enhanced computed tomography and/or magnetic

resonance imaging should be reserved for patients in whom the
diagnosis is unclear or who fail to improve in the first 48 to 72
hours.

1747
Determination of etiology
• Transabdominal ultrasound should be performed on all patients.

• In the absence of gallstones and significant history of alcohol use,

serum triglycerides should be obtained and considered the
etiology if greater than 1000 mg/dL.

• A pancreatic tumor should be considered in patients older than 40

years.

• Patients with idiopathic pancreatitis should be referred to centers

of expertise.

Assessment of severity
• Assess hemodynamic status on presentation and begin
resuscitative measures.

• Risk assessment should be performed for appropriate triage.

• Patients with organ failure should be admitted to an intensive

care unit.

Management
• Aggressive fluid resuscitation is most beneficial in the first 12 to
24 hours.

• Fluid requirements should be reassessed at frequent intervals for

the next 24 to 48 hours.

• Endoscopic retrograde cholangiopancreatography should be

performed within 24 hours of admission in patients with acute
pancreatitis and concurrent acute cholangitis.

• Antibiotics should be administered for extrapancreatic infections.

• Routine use of prophylactic antibiotics in patients with severe

acute pancreatitis is NOT recommended.

1748
• The use of antibiotics in patients with sterile necrosis to prevent
the development of infected necrosis is not recommended.

Data from the American College of Gastroenterology Guideline: Management of acute

pancreatitis. Am J Gastroenterol 108:1400-1415, 2013.

Care priorities for severe acute pancreatitis

A team approach is necessary to optimize the management of the
patient with SAP. Care priorities reflect adequate fluid
resuscitation, the correction of electrolyte and metabolic
abnormalities, effective pain control, provision of nutrition, and the
prevention of complications and recurrences.

1. Aggressive fluid resuscitation

The inflammatory process results in fluid sequestration and
extensive intravascular volume loss into the pancreas and abdomen
leading to hypovolemia and hemoconcentration. Vomiting, gastric
suctioning, and hemorrhage contribute to the hypovolemic state.
The hypovolemia and hemoconcentration lead to shock wherein the
capillary beds are poorly perfused. Colloids and crystalloids are
administered to replace volume losses and minimize interstitial
edema. Crystalloids reduce hemoconcentration and improve
perfusion. LR solution is recommended for initial fluid
resuscitation. LR appears to be more beneficial as the initial IV
solution resulting in fewer patients developing SIRS as compared
with patients receiving normal saline. Albumin may be considered
for serum albumin less than 2 g/dL, but the proteins may leak from
capillaries and increase interstitial edema. pRBCs may be
transfused for Hct less than 24%. Fresh-frozen plasma may be
needed for evidence of coagulopathy. Peritoneal and interstitial
fluid sequestration continues throughout the acute phase. Volume
replacement is essential. CVP monitoring may assist fluid
management. Pulmonary artery pressure, CI, stroke volume index,
and ScVO2 monitoring and vasopressors may be needed. Fluid
overload is a concern, especially in patients with cardiovascular
dysfunction and/or ARDS.

2. Support ventilation and oxygenation

1749
In SAP-related pulmonary congestion, pleural effusion and
atelectasis result in respiratory insufficiency or failure. Abdominal
distension and retroperitoneal fluid sequestration cause
diaphragmatic elevation and ventilatory restriction. Oxygen
administration is initiated if hypoxemia is present. Early respiratory
failure is detected by a decrease in PaO2 with increase in Paco2. If
severe pulmonary insufficiency develops, intubation and positive-
pressure ventilation is required. Mechanical ventilation is
frequently necessary for the patient with SAP. ARDS is a
complication found in 20% of patients with SAP. IV fluids are given
cautiously to prevent fluid overload resulting in cardiopulmonary
compromise.

3. Correct electrolyte and metabolic abnormalities

Hypocalcemia commonly occurs in patients with SAP and is a
marker of poor prognosis. Ionized levels should be monitored,
because with low albumin levels the amount of measured protein-
bound calcium is falsely low. If levels are low or if the patient
develops signs of neuromuscular instability, replace with calcium
chloride. Because hypercalcemia is a cause of AP, calcium
replacement is prescribed cautiously. Ensure magnesium and
albumin levels are adequate. Magnesium can be lost caused by
vomiting, urinary loss, or resulting from deposition in areas of fat
necrosis.
Hyperglycemia is also included as a poor prognostic marker.
Hyperglycemia and glycosuria are consequences of glucagon
release in the patient with SAP as a response to stress.
Hyperglycemia is also related to the decreased release of insulin by
impaired pancreatic islet cells. Hyperglycemia can worsen
neutrophil function, increasing the risk of pancreatic infection.
Insulin should be administered IV and titrated to keep glucose less
than 180 mg/dL. Meticulous serum glucose control management
facilitates control of serum triglycerides.

4. Provide effective pain control

Acute abdominal pain is caused by peritoneal irritation from the
inflamed pancreas. Opioid analgesics are administered for relief of
severe pain. Continuous or intermittent IV therapy is used,

1750
depending on the severity of the pain. Patient-controlled analgesia
(PCA) is a helpful mode of delivery. Morphine has been implicated
in the past as causing spasm of the sphincter of Oddi, thus
worsening the pancreatitis. However, no evidence has been found
to demonstrate this in humans. Its use in AP has not been shown to
adversely affect outcomes. Meperidine was the analgesic of choice
but has an active neurotoxic metabolite that accumulates with long-
term use, causing agitation, seizures, and muscle fibrosis. Because
of these side effects, many hospitals have limited the availability of
IV meperidine. Hydromorphone or sublimaze are alternatives.

Although short-term meperidine can be used safely, use of

longer than a few days, at doses exceeding 100 mg every 3 hours,
must be avoided.

5. Initiate nutrition support

Nutrition supplementation should be considered early to promote
tissue repair in patients with SAP, because they are unable to
tolerate eating for several days. Enteral feedings should be the
primary therapy in patients with or predicted SAP and should be
started within the first 48 hours of admission. Enteral nutrition has
been shown to assist in maintaining the mucosal barrier of the gut,
and preventing the translocation of gut bacteria that seed pancreatic
necrosis. Although the nasojejunal (NJ) route has been preferred to
avoid stimulation of gastric secretions, NG enteral nutrition also
appears to be safe. Either elemental or polymeric enteral nutrition
formulations can be used. Weighted NJ tubes should be positioned
beyond the ligament of Treitz. The ligament of Treitz is a
musculofibrous band that extends from the ascending part of the
duodenum and jejunum to the right crus of the diaphragm and
tissue around the celiac artery. NG enteral nutrition requires the
patient to be placed on aspiration precautions. Enteral nutrition can
therefore be administered either by the NJ or NG route. Enteral
feedings are tolerated in most patients with meticulous attention to

1751
feeding tolerance and consulting with dieticians and nutrition
support pharmacists regarding elemental or polymeric feedings
(see Nutrition Support, Chapter 1). If enteral feedings are not
tolerated, total parenteral nutrition (TPN) can be administered as
second-line therapy, necessitating insertion of a central IV catheter.
TPN continues to be associated with significant complications from
the catheter, ranging from catheter-related sepsis, local abscess,
localized hematomas, pneumothorax, venous thrombosis, venous
air embolism, and metabolic complications such as hyperglycemia
and electrolyte imbalance. Low-fat oral feedings are begun after the
initial episode subsides and bowel function returns.

6. Suppress pancreatic secretions

The assumption that the inflamed pancreas requires rest by fasting
until complete resolution of AP no longer appears to be supported
by laboratory and clinical observations. Bowel rest is associated
with intestinal mucosal atrophy and increased infectious
complications. Enteral tube feeding should be primary therapy for
patients with SAP either by the NJ or NG route and should be
started within 48 hours of hospitalization.
Aspiration of gastric secretions via NG suction demonstrated no
benefit in patients with mild to moderate AP and is therefore not
recommended in these cases. NG suction is only useful for cases of
SAP with unremitting vomiting, abdominal distension, or pain not
relieved by analgesia. Reducing gastric acidity by administering
histamine H2-receptor antagonists or PPIs may help to prevent
stress ulceration. Agents that suppress pancreatic secretions such as
somatostatin and octreotide have generally produced disappointing
results in human studies and are no longer recommended.
Peritoneal lavage has been used in the past to remove toxic necrotic
compounds present in peritoneal exudates. This procedure has not
been shown to reduce mortality or morbidity in patients with SAP
and is no longer recommended.

7. Manage medically versus surgically

In patients with gallstone AP, cholecystectomy should be
performed upon recovery to prevent recurrence. SAP is generally
managed medically. Surgical intervention is no longer indicated for

1752
patients with asymptomatic pseudocysts and sterile necrosis
regardless of size or location. Minimally invasive necrosectomy by
laparoscopic, radiologic, or endoscopic approach is indicated for
stable patients with infected necrosis or pseudocysts, but should be
delayed for more than 4 weeks after initial presentation to allow
liquefaction of the contents and for the development of a fibrous
wall. Any type of invasive intervention before the 4-week period is
associated with increased mortality.

8. Prevent infection; the role of antibiotics

The routine use of prophylactic antibiotics to prevent the
development of infected pancreatic necrosis in patients with SAP is
no longer recommended. Patients with suspected or proven
infected necrosis should receive antibiotics. Choice of antibiotic
should be determined by initial computed tomography (CT)-guided
fine needle aspiration (FNA) for Gram stain and culture. If FNA is
unattainable, empirical antibiotics should be used. Antibiotic choice
must provide adequate penetration of necrotic tissue, such as
carbapenems, quinolones, and metronidazole. These have been
shown to delay or sometimes totally avoid the need for surgical
intervention.

9. Intraabdominal pressure monitoring

The measurement of IAP for intraabdominal hypertension (IAH)
should be considered in patients with SAP who are mechanically
ventilated when signs of deterioration are present (2012
International Association of Pancreatology/American Pancreatic
Association [IAP/APA] guidelines). Patients with AP who have not
yet developed SAP may benefit from IAP monitoring before
mechanical ventilation has been initiated. IAH is defined by a
repeated pathologic increase in IAP greater than 12 mm Hg and is
reported to occur in 60% to 80% of patients with SAP. A subset of
these patients will develop abdominal compartment syndrome,
which is defined as a sustained IAP greater than 20 mm Hg that is
associated with new-onset organ failure. Medical treatment should
target hollow viscera volume reduction, intravascular/extravascular
fluid correction, and abdominal wall expansion. Invasive
management should only be considered in patients with sustained

1753
IAP greater than 25 mm Hg refractory to medical therapy (see
Abdominal Hypertension and Abdominal Compartment
Syndrome, Chapter 11).

10. Prevent recurrence

Patients with alcohol-related pancreatitis should be referred for
substance abuse counseling services despite alcohol cessation not
always preventing further attacks. Patients with gallbladder-related
pancreatitis should undergo cholecystectomy and endoscopic
sphincterotomy if medically cleared for these procedures to prevent
recurrence. Avoid the use of ERCP as an initial diagnostic tool for
unexplained abdominal pain to reduce the risk of post-ERCP
pancreatitis, given that pancreatitis is the most common
complication of ERCP.

Care plans for acute pancreatitis

Deficient fluid volume 
related to decreased intake, vomiting, NG suction, fluid loss into the
pancreas and abdomen or with SAP, massive fluid sequestration within
the peritoneum and retroperitoneal space; hemorrhage associated with
tissue necrosis; and systemic vasodilation and increased capillary
permeability from inflammatory mediators.
Goals/Outcomes: Within 24 hours of diagnosis, the patient
becomes normovolemic, as evidenced by MAP 65 to 85 mm Hg, HR
less than 120 bpm, sinus rhythm on ECG, CVP 2 to 6 mm Hg, CO 4
to 6 L/min, brisk capillary refill (less than 2 seconds), peripheral
pulses at least 2+ on a 0-to-4+ scale; urinary output greater than 0.5
to 1 mL/kg/h; Hct 35% to 44%.
Electrolyte and Acid-Base Balance; Fluid Balance.

Fluid resuscitation

1. Obtain and maintain large-bore IV, central venous access, and

CVP monitoring.

2. Administer IV fluids; LR is recommended for initial fluid

resuscitation; 5 to 10 mL/kg/h initially until goals are met.

1754
3. Aggressive IV hydration with volumes of 250 to 500 mL/h may be
necessary in patients with no cardiac or renal comorbidities and is
of most benefit the first 12 to 24 hours.

4. Consider administering pRBCs for Hct less than 30%. Anticipate

an increase in Hct of 3% following 1 unit of pRBCs.

5. Consider administering albumin for serum albumin less than 2

g/dL, but observe for worsening of edema if capillary leak is severe.

6. Monitor coagulation studies and CBC.

7. Administer fresh-frozen plasma for coagulopathy and to replace

lost circulating proteins.

8. Monitor BUN for appropriate reductions.

9. Assess for signs of overaggressive fluid resuscitation (see Fluid

Volume Excess).

Fluid management

1. Administer crystalloids, colloids, or a combination of both as

prescribed.

2. Monitor BP every 1 to 2 hours if losses are caused by fluid

sequestration, inadequate intake, or slow bleeding. Monitor BP
continuously with arterial line, or hourly and increase to every 15
minutes if the patient has active blood loss or massive fluid
sequestration.

3. Monitor cardiovascular status at least every 1 to 2 hours, and

more often with SAP.

4. Measure urinary output hourly. Report output less than 0.5

mL/kg/h for 2 consecutive hours. Evaluate intravascular volume
and cardiovascular function, and increase fluid intake promptly if
decreased urinary output is caused by hypovolemia and
hypoperfusion.

1755
5. Monitor for indicators of hypovolemia, including cool
extremities, delayed capillary refill (greater than 2 seconds), and
decreased amplitude of or absent distal pulses.

6. Estimate ongoing fluid losses. Measure all drainage from tubes,

catheters, and drains. Note the frequency of dressing changes
because of saturation with fluid or blood. Compare 24-hour urine
output with 24-hour fluid intake, and record the difference.

7. Administer room temperature IV fluids.

8. Continuously monitor HR and ECG. Be alert to increases in HR,

which suggest hypovolemia.

9. Monitor cardiovascular status hourly including CVP.

10. Measure hemodynamic measurements every 1 to 4 hours: CVP,

CI, stroke volume index or continuously using an arterial-based
system, SVV when appropriately available. Be alert to low or
decreasing values in patients with borderline cardiac function or
respiratory function. An elevated HR, decreased CVP, decreased CI
less than 2.5 L/min/m2, stroke volume index less than 33
mL/m2/beat, and SVV greater than 15% (on assist-control mode
mechanical ventilation) are suggestive of hypovolemia.

11. Consider fluid bolus for urine output less than 0.5 mL/kg/h for 2
consecutive hours. If SAP is present, initiate fluid resuscitation and
shock management.

12. Weigh the patient daily, using the same scales and method.
Weight may increase as a result of significant capillary leak and
anasarca with intravascular volume depletion.

13. Evaluate characteristics of all fluids lost. Note color and odor. Be
alert to the presence of particulate matter, fibrin, and clots. Test GI
aspirate, drainage, and excretions (including stool) for the presence
of occult blood.

Shock management

1756
1. Monitor fluid status (see Fluid Management, Fluid Resuscitation).

2. Collaborate with the physician or advanced practice provider to

administer vasoactive medication if shock persists with volume
resuscitation.

3. Monitor for cerebral ischemia or indications of insufficient

cerebral blood flow.

4. Monitor renal function (BUN and creatinine levels for elevations),

because intravascular volume depletion can lead to prerenal
azotemia.

5. Monitor tissue oxygenation using ABG, SVO2 or ScVO2

monitoring, and serum lactate measurements.

6. Monitor ECG for ST segment depression and T wave inversion,

which may be seen as a result of the shock state.

Electrolyte management

1. Monitor for manifestations of electrolyte imbalance. Calcium,

sodium, magnesium, and potassium are lost with fluid
sequestration and vomiting.

2. Maintain IV solutions containing electrolytes at a constant rate.

3. Continuously monitor ECG for alterations related to electrolyte

imbalances.

4. Monitor ionized calcium. Widening of the QT interval is

suggestive of severe hypocalcemia. Hypocalcemia may produce
numbness or tingling in the extremities that can progress to tetany.

5. Administer calcium gluconate or calcium chloride for low

ionized calcium. Calcium chloride will provide a higher level of
calcium replacement given the strength and chemical composition.

6. Monitor T wave as a sign of alterations in serum potassium

levels.

1757
 Fluid/Electrolyte Management; Fluid Monitoring;
Hemodynamic Regulation; Hypovolemia Management; Invasive
Hemodynamic Monitoring; Shock Prevention; Bleeding
Precautions; Bleeding Reduction; Hypervolemia Management.

Decreased cardiac output 

related to myocardial depression secondary to circulating vasoactive
amines or hypocalcemia with SAP; decreased preload secondary to
hypovolemia.
Goals/Outcomes: Within 12 hours of diagnosis, CO becomes
adequate, as evidenced by CI greater than 2.5 L/min/m2, brisk
capillary refill (less than 2 seconds), peripheral pulses greater than
2+ on a 0-to-4+ scale, urinary output greater than 0.5 mL/kg/h, and
warm skin.
Circulation Status.

Hemodynamic regulation

1. Restore acceptable preload by correcting hypovolemia (see

preceding nursing diagnosis, Fluid Volume Deficit).

2. Administer inotropic agents. Consider dobutamine for

myocardial contractile support. Monitor hemodynamic
measurements carefully to observe for vasodilation if dose of
dobutamine is low.

3. Space out procedures and treatments to allow long periods (at

least 90 minutes) of uninterrupted rest.

4. Minimize anxiety-producing situations and assist the patient

with reducing anxiety.

Care: Acute; Shock Management; Cardiac: Dysrhythmia

Management; Anxiety Reduction; Energy Management.

Acute pain 
related to chemical injury to the pancreas and peripancreatic tissue
secondary to release of pancreatic enzymes.
Goals/Outcomes: Within 2 to 4 hours of diagnosis, the patient’s

1758
subjective evaluation of discomfort improves, as documented by a
pain scale. Ventilation and hemodynamic status are
uncompromised, as evidenced by MAP greater than 70 mm Hg, HR
60 to 100 bpm, and RR 12 to 20 breaths/min with normal depth and
pattern (eupnea).
Pain Control; Pain Level; Comfort Level.

Analgesia administration

1. As prescribed, administer IV opiate analgesic before pain

becomes severe.

2. Meperidine may be used initially for up to 3 days, but should not

be administered long-term because of metabolite accumulation,
which can cause neurologic adverse effects. Meperidine is avoided
in patients with SAP, because analgesia is needed for more than 3
days. Hydromorphone may be a better alternative.

3. Monitor HR and BP at least every 1 to 2 hours in patients with

SAP. Opiates cause vasodilation and can add to the serious
hypotension of the patient who has SAP with volume depletion.
Monitor every 15 minutes if severe pain is uncontrolled. Consult
with the physician or advanced practice provider for changes in
analgesic medications and dosages.

4. Evaluate effectiveness of medication and consult the physician or

advanced practice provider for dose and drug manipulation.

5. Consider continuous infusion or PCA for more effective pain

control.

6. Consider epidural route if IV route is ineffective.

7. If medications are not effective, prepare the patient for splanchnic

block or other pain-relieving procedure.

8. Assess for anxiety and consider sedatives in conjunction with

analgesia.

1759
 Opioid analgesics decrease intestinal motility and delay
return to normal bowel function.

9. Monitor respiratory pattern and LOC closely because both may

be depressed by the large amounts of opiate analgesics usually
required to control pain.

Pain management

1. Pancreatitis can be very painful. Prepare significant others for

personality changes and behavioral alterations associated with
extreme pain and opiate analgesia. Family members sometimes
misinterpret the patient’s lethargy or unpleasant disposition and
may even blame themselves. Reassure them that these are normal
responses.

2. Supplement analgesics with nonpharmacologic maneuvers to aid

in pain reduction. Modify the patient’s body position to optimize
comfort. Many patients with abdominal pain find a dorsal
recumbent or lateral decubitus bent-knee position most
comfortable.

3. Consider cultural influences on pain response.

4. Anxiety reduction contributes to pain relief, ensure consistency

and promptness in delivering analgesic.

5. Provide continual reassurance to both patients and their families

that all possible measures are being implemented to relieve pain.

Patient-Controlled Analgesia (PCA) Assistance;

Environmental Management: Comfort; Coping Enhancement;
Teaching: Prescribed Medication; Simple Guided Imagery;
Respiratory Monitoring.

Impaired gas exchange 

1760
related to atelectasis and ARDS; elevation of the diaphragm and pleural
effusion caused by subdiaphragmatic inflammation of the pancreas, and
with SAP, alveolar-capillary membrane changes secondary to
microatelectasis, inflammatory mediators, and pulmonary fluid
accumulation.
Goals/Outcomes: Within 4 hours of diagnosis, the patient has
adequate gas exchange, as evidenced by SaO2 greater than 92%;
PaO2 greater than 80 mm Hg; Paco2 35 to 45 mm Hg; RR 12 to 20
breaths/min with normal depth and pattern; orientation to time,
place, and person; and clear and audible breath sounds.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation.

Airway management

1. Administer oxygen via nasal cannula to maintain oxygen

saturation greater than 92%. Check oxygen delivery system at
frequent intervals to ensure proper delivery.

2. Monitor and document RR every 1 to 2 hours as indicated. Note

pattern, degree of excursion, and whether the patient uses
accessory muscles of respiration. Consult the physician for
significant deviations from baseline.

3. Auscultate both lung fields every 4 hours. Note presence of

abnormal sounds (crackles, rhonchi, wheezes) or diminished
sounds.

4. Be alert to early signs of hypoxia, such as restlessness, agitation,

and alterations in mentation.

5. Monitor SpO2 via continuous pulse oximetry or frequent SaO2 by

ABG values during the first 48 hours. Many patients with
pancreatitis do not have obvious clinical symptoms of respiratory
failure, and a decreased arterial oxygen tension may be the first
sign of ARDS or failure. Consult the physician or advanced practice
provider if PaO2 is less than 60 to 70 mm Hg or if oxygen saturation
falls below 92%.

1761
6. Maintain a body position that optimizes ventilation and
oxygenation. Elevate HOB 30 degrees or higher, depending on the
patient’s comfort. If pleural effusion or other defect is present on
one side, position the patient with the unaffected lung dependent to
maximize the ventilation-perfusion relationship.

7. If the patient fails to stabilize, prepare for endotracheal intubation

and mechanical ventilation.

8. Hypoxemia in the absence of preexisting pulmonary disease may

be an early sign of ARDS.

9. Monitor pulmonary artery pressures, because pulmonary

hypertension is anticipated in patients with ARDS.

10. Avoid overaggressive fluid resuscitation (see Excess Fluid

Volume in the following section).

Acid-Base Management; Airway Management; Oxygen

Therapy; Respiratory Monitoring; Positioning; Fluid Monitoring;
Hypervolemia Management.
See Acute Lung Injury and Acute Respiratory Distress Syndrome,
Chapter 4, for additional information.

Excess fluid volume 

related to excessive intake secondary to overaggressive fluid
resuscitation.
Goals/Outcomes: Within 24 hours of diagnosis, the patient will
be normovolemic, as evidenced by MAP 65 to 85 mm Hg, HR 60 to
100 bpm, RR 12 to 20 breaths/min with normal pattern and depth,
and absence of adventitious breath sounds and S3 gallop.
Fluid Overload Severity; Fluid Balance; Electrolyte and Acid-
Base Balance.

Hypervolemia management

1. Evaluate the patient every 1 to 2 hours for clinical indicators of

fluid volume excess: dyspnea, orthopnea, increased RR and effort,
S3 gallop, or crackles. Document new findings and report changes.

1762
2. Consider administering furosemide (Lasix) or other diuretic as
prescribed to promote diuresis, after volume status has been
evaluated. Patients may be intravascularly hypovolemic despite
significant weight gain resulting from third spacing of fluids.
Diuresis may not prove to be beneficial. Document response to
diuretic therapy.

Fluid/Electrolyte Management; Fluid Monitoring;

Hemodynamic Regulation.

Risk for infection 

related to tissue destruction and loss of protective barriers.
Goals/Outcomes: The patient remains free of infection, as
evidenced by core or rectal temperature less than 38° C (100.4° F),
negative culture results, HR 60 to 100 bpm, RR 12 to 20 breaths/min,
BP within the patient’s normal range, CVP 2 to 6 mm Hg, and
orientation to time, place, and person. See Chapter 11 for additional
information on Sepsis.
Infection Severity; Immune Status.

Infection protection

1. Check temperature every 4 hours. Be aware that hypothermia

may precede hyperthermia in some patients.

2. Temperature may be slightly elevated resulting from the

inflammatory process. If temperature remains elevated for longer
than 1 week, suspect that the patient may have developed bacterial
(infected) pancreatic necrosis.

3. If temperature suddenly rises, obtain specimens for culture of

blood, sputum, urine, and other sites as prescribed. Monitor culture
reports and report positive findings promptly.

4. Evaluate orientation and LOC every 2 to 4 hours. Report

significant deviations from baseline.

5. Monitor BP, HR, RR, CO/CI, and CVP every 1 to 4 hours. An

elevated CO/CI and decreased CVP may suggest systemic

1763
inflammatory response or sepsis. Be alert to increases in HR and RR
associated with temperature elevations.

6. Monitor white blood cell (WBC) count and anticipate a mild

leukocytosis of 11,000 to 20,000/mm3 as a result of the inflammatory
response of SAP. If WBC count is greater than 20,000/mm3, suspect
infected pancreatitis. If total WBC count is elevated, monitor WBC
differential for an elevation of bands (immature neutrophils).

7. Prophylactic antibiotics are NOT recommended for sterile

pancreatitis unless the pancreas is greater than 30% necrosed, as
evidenced by CT scan.

8. If prescribed, administer parenteral antibiotics in a timely

manner. Reschedule antibiotics if a dose is delayed for greater than
1 hour. Recognize that failure to administer antibiotics on schedule
can result in inadequate blood levels and treatment failure.

9. Do not administer prophylactic antibiotics for SAP.

10. Patients with infected pancreatitis evidenced by FNA-positive

result for bacteria on Gram stain or culture require antibiotic
therapy and may require laparoscopic, endoscopic, or radiologic
intervention.

Medication Management; Vital Signs Monitoring;

Temperature Regulation; Intravenous (IV) Therapy.

Imbalanced nutrition: Less than body requirements 

related to decreased oral intake secondary to nausea, vomiting, and
nothing-by-mouth (NPO) status; increased need secondary to tissue
destruction.
Goals/Outcomes: The patient maintains baseline body weight
and demonstrates a positive nitrogen balance.
Nutrition Status; Nutrition Status: Food and Fluid Intake.

Nutrition management

1. Collaborate with the advanced practice provider, dietitian, and

1764
pharmacist to estimate the patient’s individual metabolic needs,
based on activity level, presence of infection or other stressor, and
nutrition status before hospitalization. Overuse of calcium
supplements can cause AP; this mechanism should be added as
noted earlier. Develop a plan of care accordingly.

2. Determine preexisting malnutrition with a nutrition assessment.

3. If the patient’s condition improves after 48 hours of resting the

bowel, oral intake of clear liquids can be slowly started. Mild to
moderate increases in serum amylase and lipase may be noted.
Feedings should continue unless these elevations are threefold
above normal range.

4. If the patient’s condition does not improve after 48 hours of

bowel rest, administer elemental enteral feedings via NJ feeding
tube or jejunostomy as prescribed. Pancreatic secretions are not
stimulated with the delivery of enteral elemental nutrition into the
mid- or distal jejunum. Ensure tube placement beyond the ligament
of Treitz.

5. Monitor bowel sounds every 4 hours. Document and report

deviations from baseline. Withhold jejunal feedings if bowel sounds
are absent unless elemental feedings are used.

6. Monitor blood glucose levels every 4 to 8 hours or as prescribed.

Treat blood glucose levels greater than 180 mg/dL with exogenous
insulin.

7. If enteral feedings are not tolerated, begin TPN as prescribed.

Monitor closely for evidence of hyperglycemia (e.g., Kussmaul’s
respirations; rapid respirations; fruity, acetone breath odor; flushed,
dry skin; deteriorating LOC), which is commonly associated with
pancreatitis. Administer insulin as prescribed.

8. Begin low-fat oral feedings when acute episode has subsided and
bowel function has returned. This may take several weeks in some
patients.

Enteral Tube Feeding; Aspiration Precautions; Total

1765
Parenteral Nutrition (TPN) Administration; Venous Access Device
(VAD) Maintenance; Hyperglycemia Management; Hypoglycemia
Management.
For additional details, see Nutrition Support, Chapter 1.

Deficient knowledge 
related to lack of exposure to healthcare information
Goals/Outcomes: Before hospital discharge, the patient
verbalizes knowledge regarding availability of alcohol
rehabilitation programs, prescribed medications, importance of a
low-fat diet, indicators of actual or impending GI hemorrhage,
indicators of infection, and the importance of seeking medical
attention promptly if signs of recurring pancreatitis appear.
Knowledge: Disease Process; Knowledge Treatment:
Regimen.

Teaching: Disease process

1. Inform patients whose pancreatitis is caused by excessive alcohol

intake about the availability of alcohol rehabilitation programs.

2. Teach the patient about prescribed medications including drug

name, dosage, purpose, schedule, precautions, and side effects.

3. Advise the patient about the importance of adhering to a low-fat

diet if prescribed.

4. Instruct the patient about the indicators of actual or impending

GI hemorrhage: nausea, vomiting blood, dark stools,
lightheadedness, and passing frank blood in stools.

5. Teach the indicators of infection: fever, unusual drainage from

surgical incisions or peritoneal lavage site, warmth or erythema
surrounding surgical sites, and abdominal pain. Have the patient
demonstrate oral temperature-taking technique using the type of
thermometer that will be used at home.

6. Stress the importance of seeking medical attention promptly if

signs of recurrent pancreatitis (i.e., pain, change in bowel habits,

1766
passing blood in the stools, or vomiting blood) or infection (see Risk
for Infection) appear.

Prescribed Activity Exercise; Prescribed Diet; Prescribed

Procedure/Treatment; Prescribed Medication; Behavior
Modification.

Additional nursing diagnoses

As appropriate, see nursing diagnoses and interventions in the
following: Acute Respiratory Distress Syndrome (Chapter 4), Acute
Renal Failure (Chapter 6), and Systemic Inflammatory Response
Syndrome, Sepsis, Septic Shock, and Multiple Organ Dysfunction
Syndrome (Chapter 11). Also see Prolonged Immobility (Chapter 1)
and Emotional and Spiritual Support of the Patient and Significant
Others (Chapter 2).

Enterocutaneous fistula
Pathophysiology
Enterocutaneous fistulas (ECFs) are formed when trauma, surgery,
infection, neoplastic disease, or other pathologic condition results in
a GI-cutaneous communication. Classifications include
spontaneous (15% to 25%) or postoperative (75% to 85%) (.
Spontaneous fistulas occur in patients with inflammatory bowel
disease (IBD) (Crohn disease > indeterminate colitis > ulcerative
colitis), cancer, diverticular disease, appendicitis, perforated bowel
disease, radiation enteritis, or ischemic bowel. Postoperative fistulas
account for the majority of ECFs and are observed following
abdominal surgery for IBD, intestinal malignancy, recurrent
explorations, or after extensive lysis of adhesions for conditions
such as small bowel obstruction. For patients with severe
abdominal trauma, severe intraabdominal sepsis, or complex
surgical pathologies, open abdominal (OA) management has
become a recurrent treatment option. In OA management, the
peritoneal cavity is left open and abdominal contents are protected
with a temporary dressing until bowel edema reduces or washouts

1767
are no longer required and the peritoneum can be closed. A new
type of ECF has emerged as a complication of OA management
called enteroatmospheric fistula (EAF). EAFs develop from
edematous loops of bowel within the wound bed of an open
abdomen that became injured.
Fistulas can be classified as high output (greater than 500 mL/d),
moderate output (200 to 500 mL/d), and low output (less than 200
mL/d). High-output proximal small bowel fistulas are the most
difficult to manage with losses as high as 2 L in 24 hours. Drainage
from proximal fistulas is hypertonic; rich in enzymes, electrolytes,
and proteins; thin in consistency and tends to be copious. Extensive
skin and tissue breakdown often occur because of the presence of
activated pancreatic enzymes in fistula drainage. Electrolyte and
protein loss is great with high-output proximal fistulas. Drainage
from distal sites, such as the ileum and colon, is thick and of less
volume than is proximal fistula drainage.
Three factors are associated with mortality in patients with ECFs:
(1) fluid and electrolyte imbalance, (2) malnutrition, and (3) sepsis.
Fluid, potassium, sodium, proteins, and bicarbonate may be lost in
great quantities. Replacement by enteral nutrition or parenteral
nutrition (TPN) is complex, and proper balance is often difficult to
achieve. Sepsis is frequently associated with bowel fistulization
caused by anastomotic breakdown, local wound contamination, or
inadequate drainage. Hypercatabolism and malnutrition are
associated with both sepsis and fistulization, creating a great
demand for calories and protein. Aggressive nutrition support and
meticulous local wound management are crucial to patient survival.
Mortality rates for ECF have declined overall because of advances
in nutrition, wound care, and surgical technique to 5% to 15%.

Gastrointestinal assessment:
Enterocutaneous fistula
Goal of assessment: Enterocutaneous fistula
Evaluate the functional integrity of the intestinal tract.

History and risk factors

1768
• Direct trauma to the GI system, especially the bowel.

• Infection of surgical wound, drainage tract, or peritoneum.

• Prolonged catabolic state in association with bowel injury, GI

neoplasm, GI abscess, or severe inflammatory bowel disease.

• Complex GI surgical procedures, such as extensive lysis of

adhesions for intestinal obstruction or complicated intestinal
anastomosis.

• Trauma surgery with missed injuries; emergency surgery with

inadequate bowel preparation; damage control operations, where
the abdomen is left open as a result of packing, or edematous
bowel unable to be closed.

• History of IBD, especially Crohn disease. ECFs affect

approximately 30% of people with Crohn disease.

Vital sign assessment

• Increased temperature and tachycardia resulting from infection or
dehydration.

• Irregular HR as a result of fluid loss and hypokalemia.

• Decreased urinary output with increased specific gravity caused

by excessive fluid loss.

Abdominal pain
• Tenderness, erythema, and possibly pain at the incision/fistula
site caused by irritation from fistula output or infection.

• Muscle weakness from hypokalemia.

Abdominal drainage
• Discharge of bile, enteric contents, or gas through a surgical
incision.

1769
• Sudden increase in the amount of drainage from a surgical
incision or drainage catheter.

• Change in the nature of drainage from serous or serosanguineous

to yellow, green, brown, or foul-smelling.

• Change in pancreatic drainage to milky white suggests a

pancreatic fistula.

Observation
• Mental confusion is often present as a result of electrolyte
imbalance, dehydration, or early sepsis.

• Sunken eyes, poor skin turgor, and dry oral mucosa are
associated with dehydration.

• Peripheral edema and muscle wasting related to protein loss.

• Erythema, maceration, and edema may be present on the

abdomen because of irritating fistula drainage.

Auscultation
• Diminished or absent bowel sounds if peritonitis or ileus is
present.

Palpation
• Discomfort and guarding on abdominal palpation over an
abdominal mass (abscess) or near a drain site or surgical incision.

Nutrition assessment
• Weight loss and loss of muscle mass resulting from protein losses
and hypercatabolism.

• Decreased serum albumin and transferrin both indicate

malnutrition.

1770
Screening labwork
• Serum electrolyte levels: Depleted as a result of external losses
through the fistula.

• Fistula fluid can be analyzed for electrolyte determination.

Electrolyte replacement can be formulated on the basis of the
results.

• CBC: Anemia may be present reducing oxygen-carrying capacity.

Hemodynamic measurements
• Decreased BP, MAP, and CVP if severe dehydration is present.

• If early sepsis is present, expect elevated CO and decreased SVR.

• Oxygen demand is increased and may exceed supply. SVO2, ScVO2

will fall without aggressive pulmonary and cardiovascular
support.

• The patient will exhibit general hemodynamic instability until

fluid balance, inflammation, and infection are controlled.

Diagnostic Tests for Enterocutaneous Fistula

Test Purpose Abnormal Findings

Blood Studies
Complete blood Assesses for Leukocytosis with WBC count >12,000/mm3.
count (CBC): inflammation, Leukopenia with WBC count <4000/mm3. Normal
White blood cell infection, and WBC with >10% bands.
(WBC) count sepsis.
Red blood cell Reflective of blood Hct and Hgb levels will be elevated as a result of the
(RBC) count: volume status and presence of significant dehydration. Anemia will
Hemoglobin oxygen-carrying develop as a result of the prolonged period of illness.
(Hgb) capacity.
Hematocrit (Hct)
Electrolytes: Determines Hypokalemia
(Serum) accurate electrolyte Hypocalcemia
potassium levels to dictate Hypomagnesemia
Magnesium appropriate Metabolic acidosis
Calcium replacement,
Bicarbonate because large
quantities may be
lost through fistula

1771
 drainage.
Nutrition profile: Evaluates nutrition These laboratory tests will vary in individual patients.
Serum albumin, status and initiates Serum transferrin levels >140 mg/dL have been
transferrin, aggressive shown to correlate with the spontaneous closure of
prealbumin nutrition support enterocutaneous fistulas, thereby reducing mortality
early. among these patients. Levels <140 is a poor
prognostic finding. Serum albumin 3 g/dL or less at
the time of fistula presentation is a poor prognostic
indicator.
Prealbumin levels will rise with effective nutrition
therapy.

Noninvasive
Cardiology
Electrocardiogram Assesses and Hypokalemia may result in flattening of T wave or U
monitors for wave development. Hypocalcemia, hypokalemia, and
cardiac rhythm hypomagnesemia can result in widening of the QT
disturbances interval.
related to
hypokalemia,
hypocalcemia, and
hypomagnesemia.
Radiology
Fistulogram: To identify the Radiographs will confirm anatomic site of origin and
Water-soluble anatomy and fistula tract.
contrast characteristics of
medium the fistula tract.
injected into the
suspected
fistula
Computed CT may be used to Confirmation of intraperitoneal abscess is made.
tomography (CT) identify abscesses Percutaneous drainage may be performed.
scan associated with
fistulization.
Upper An upper GI series Upper GI series may reveal esophageal, gastric, or
gastrointestinal may be indicated if duodenal fistulas.
(GI) series the suspected
fistula is proximal
to the intestines.

Nonradiographic evaluation
Bedside maneuver: An external fistula can be simply confirmed
without radiology by the oral administration of charcoal. The
visible presence of dye in the drainage confirms the presence of a
fistula.
Biopsy: In patients with neoplastic disease, a biopsy specimen of
the fistula tract may be obtained to determine the presence of
malignancy within the tract.
Culture: Fistula effluent from the stomach, duodenum, biliary
tree, and pancreas may be cultured for evidence of infection. Small

1772
and large bowel fistulas are generally not cultured because of the
expected presence of bacteria.

Collaborative management
Early management of ECF presents a considerable challenge
requiring advanced support of a multidisciplinary team in a
surgical intensive care unit setting. The patient with ECF is
typically malnourished with a recent history of malignancy,
inflammatory or infectious disease, postoperative or traumatic
bowel injury, dehiscence, or inadvertent enterotomy. Their
physiologic and nutrition reserves are significantly compromised.
Treatment is usually complicated by sepsis and the metabolic and
fluid derangements caused by the fistula. Early fistula identification
is imperative to implement appropriate management strategies,
including patient stabilization, investigation of the fistula,
evaluation of surgical need, and the promotion of healing.

Care priorities
Once the fistula is diagnosed, immediate management should focus
on fluid restoration and the correction of electrolyte abnormalities.
The control of sepsis and septic complications, nutrition support,
and fistula management are key components to positive outcomes
and should be addressed concurrently.

1. Fluid and electrolyte replacement

Crystalloid resuscitation with normal saline or LR solution. Often,
the amount to be delivered is prescribed in direct relation to fistula
output, especially when the output is widely variable. Effluent from
each fistula is measured separately for accurate estimation of
specific electrolyte and fluid losses. In general, fistulas more
proximal result in greater fluid, electrolyte, and protein losses.

2. Control of sepsis
Sepsis is often seen in the patient with postoperative ECF following
a bowel procedure where bowel contents escape into the
peritoneum. All team members should participate in the evaluation
of a septic foci. Blood, wound, fistula drainage, sputum, and venous

1773
catheter tips should be cultured. Empirical antibiotic therapy is
indicated with diagnosis of sepsis followed by specific therapy.
Intraperitoneal abscesses should be drained cautiously, because
manipulation of the septic foci may lead to its spread. If no
evidence of sepsis is observed, antibiotic therapy should be
withheld in the postoperative period. In patients with ECF,
indiscriminate antibiotic use will lead to the emergence of highly
resistant bacteria. (See Sepsis, Chapter 11.)

3. Nutrition support
Patients with a fistula are typically malnourished because of their
postoperative NPO status, the hypercatabolism of sepsis, and the
protein- and mineral-rich intestinal fluid loss from the fistula. Both
TPN and enteral nutrition can be used to manage patients with ECF
based on a thorough nutrition assessment.
Enteral nutrition is currently advocated over TPN, because
enteral nutrition enhances mucosal proliferation, promotes villus
growth, improves hepatic protein synthesis, and stimulates the
enterocyte, whereas TPN has been shown to cause intestinal
mucosal atrophy. However, TPN remains a valuable therapeutic
modality for patients who cannot tolerate enteral nutrition and in
combination with enteral nutrition for patients who are unable to
absorb sufficient calories from enteral feedings alone. Enteral
feedings can be initiated by a weighted nasoduodenal intestinal
feeding tube if there is sufficient (approximately 4 feet) functioning
small bowel length between the ligament of Treitz (a thin muscle
that wraps around the small intestine where the duodenum and
jejunum meet) and the fistula. Enteral feedings can be optimized in
patients with a feeding jejunostomy (placed at the time of their
surgery) distal to the fistula, as is the case of many postoperative
ECFs. In some cases, enteral feedings may be infused into the fistula
itself. The volume and concentration of enteral feedings are started
low and increased incrementally; supplementation with TPN is
necessary to meet caloric and protein requirements during this
time. For some patients, TPN supplementation is needed
throughout the duration of care. Enteral feedings are slowed or
discontinued if fistula output increases after initiation of feedings.
Patients with proximal small bowel fistulas, prolonged ileus, or

1774
extensive intraabdominal sepsis usually require TPN. Optimizing
nutrition status will enhance the immune system, preserve lean cell
mass, and promote wound healing. Improved nutrition status
correlates with spontaneous fistula closure.

4. Fistula management
Ideally, drainage from each fistula is collected separately to assess
individual fistula activity and healing. Individualized systems of
gravity or gentle suction drainage and barrier skin protection are
devised for each patient. Good local management reduces the
incidence of wound-related bacteremias and increases the rate of
wound healing. EAFs are managed with negative pressure wound
management therapy (NPWT) devices previously referred to as
vacuum-assisted closure (VAC) systems. The system consists of a
porous foam pad that connects to subatmospheric suction under an
occlusive dressing. NPWT devices divert fistula drainage away
from the wound by providing continuous negative pressure suction
to the wound surface. NPWTs protect the skin and reduce patient
discomfort from multiple dressing changes, because they require
changes only once every 2 to 3 days. This system effectively
promotes wound healing by increasing the rate of tissue
granulation and augmenting wound contracture.
Somatostatin analogues: Somatostatin analogues such as
octreotide have been shown to inhibit gastric secretions and should
decrease fistula output. However, studies showed no significant
improvement in fistula closure rate or improvement in mortality
rates. Somatostatin is associated with a frequent incidence of
hyperglycemia and can cause increased nausea. Therefore,
somatostatin analogs are not indicated for routine use in patients
with ECF. Octreotide has been shown to provide improved healing
time in patients with high-output fistulas, perhaps by decreasing a
high-output fistula to a low-output fistula. The role of octreotide is
currently limited for use with high-output fistulas.
Surgery: Spontaneous fistula closure occurs in approximately
30% of patients with ECF with adequate nutrition support and
successful treatment of sepsis. If spontaneous closure does not
occur after 4 to 6 weeks of management, surgical resection is
considered. Surgery is indicated in the following instances: (1) to

1775
close fistulas that continue to drain significant amounts despite
absence of infection and appropriate nutrition support; (2) to
explore and drain fistula tracts that could not be identified or
drained by less invasive techniques; and (3) if overwhelming sepsis
fails to respond to antibiotics and supportive therapy. Persistently
draining fistulas are surgically closed with a procedure involving
resection with end-to-end anastomosis. Postoperatively, parenteral
nutrition and antibiotic coverage are continued. A gastrostomy is
usually created to allow for prolonged intestinal decompression
and drainage. The patient may remain NPO for greater than 1 to 2
weeks after surgery, depending on the rate of healing and the
return of bowel function. An alternate feeding strategy is initiated
during this time.

Care plans for enterocutaneous fistula

Deficient fluid volume 
related to the active loss of intestinal fluids rich in electrolytes, minerals,
and protein through fistula output.
Goals/Outcomes: Within 8 hours of diagnosis, the patient’s
volume status is stabilized, as evidenced by balanced daily input
and output, urinary output ≥0.5 mL/kg/h, HR less than 100 bpm,
CVP 2 to 8 mm Hg, and MAP ≥ 60 mm Hg; moist mucous
membranes, good skin turgor, warm extremities, peripheral pulses
greater than 2+ on a 0-to-4+ scale, brisk capillary refill (less than 2
seconds); orientation to time, place, and person; and stable weight.
The goals of improvement for patients who are extremely ill are
adjusted according to the predicted best values the patient can
achieve with their level of organ impairment.
Fluid Balance.

Fluid/electrolyte management

1. Evaluate the fluid balance by calculating and comparing daily

intake and output. In patients with high-output fistulas, evaluate
total intake and output every 8 hours. Record all sources of output,
including drainage from each fistula.

1776
2. Administer IV crystalloids to replace fistula output. Generally,
fistula output is isosmotic with high potassium content. Thus,
normal saline with a potassium supplement should be
administered.

3. Measure and evaluate vital signs, every 1 to 2 hours, depending

on hemodynamic stability. Be alert to increasing HR, decreasing
CVP, and decreasing MAP, which indicate inadequate intravascular
volume.

4. Monitor fluid responsiveness measurements such as systolic

pressure variation (SPV), pulse pressure variation (PPV), and SVV
when available. If SPV greater than 5 mm Hg, PPV greater than
13% to 15%, and SVV greater than 13% to 15%, the patient is
deemed fluid responsive.

5. Consider administering pRBCs for Hct less than 21%.

Transfusion should be based on the symptoms of the patient.
Transfusion of pRBCs will improve oxygen-carrying capacity.
Anticipate an Hct increase of 3% following 1 unit of pRBCs.

6. Measure urine output every 1 to 2 hours. Consult the advanced

practice provider if urine output is less than 0.5 mL/kg/h or if
specific gravity increases and urine volume decreases.

7. Assess and document condition of mucous membranes and skin

turgor. Dry membranes and inelastic skin indicate inadequate fluid
volume and the need for increase in fluid intake (per os [PO] or IV
route).

8. Control sources of insensible fluid loss by humidifying oxygen,

maintaining comfortable environment, and controlling fever (if
present) with antipyretics such as acetaminophen.

9. Monitor for manifestations of electrolyte imbalance, most

commonly hypokalemia, hypocalcemia, and hypomagnesemia that
are lost through fistula output.

10. Monitor ECG for T wave flattening or the presence of a U wave,

indicative of hypokalemia.

1777
11. Monitor ECG for prolongation of the QT interval, a result of
hypokalemia, hypocalcemia, and hypomagnesemia.

Fluid Monitoring; Hemodynamic Regulation; Hypovolemia

Management; Invasive Hemodynamic Monitoring; Shock
Prevention.

Infection, risk for and actual 

related to inadequate primary defenses (altered integumentary system,
disruption in continuity of GI system), hypercatabolic state, presence of
invasive lines, protein loss/malnutrition, and gut contamination of bowel
contents.
Goals/Outcomes: The patient remains free of infection, as
evidenced by core or rectal temperature less than 37.8° C (100° F),
negative culture results, HR 60 to 100 bpm, RR 12 to 20 breaths/min,
BP within the patient’s normal range, and orientation to time, place,
and person.
Wound Healing: Secondary Intention.

Infection control

1. Use standard precautions if contact with drainage is possible.

Effective handwashing is essential.

2. Check rectal or core temperature every 4 hours for increases or

decreases. If temperature suddenly rises, assess the patient for
potential sources, noting presence of purulent secretions; erythema
around wound, drain, or fistula site; and pain, tenderness, or
masses with abdominal palpation. Consult the advanced practice
provider for temperature elevation and assessment findings. Obtain
specimens for culture of likely sites for infection as prescribed by
the physician or unit protocol.

3. Evaluate mental status every 1 to 2 hours. Document and report

significant deviations from baseline values.

4. Monitor BP, HR, RR every 1 to 2 hours. Be alert to increases in

HR and RR associated with temperature elevations.

1778
5. Administer IV antibiotics in a timely manner. Reschedule
antibiotics if a dose is delayed for greater than 1 hour. Recognize
that failure to administer antibiotics on schedule can result in
inadequate blood levels and treatment failure.

6. Optimize gravity drainage of fistula by prone or upright

positioning as tolerated by the patient.

See Systemic Inflammatory Response Syndrome, Sepsis, Septic

Shock, and Multiple Organ Dysfunction Syndrome care plans,
Chapter 11.
Medication Management; Hemodynamic Regulation; Vital
Signs Monitoring; Temperature Regulation; Intravenous (IV)
Therapy; Wound Care.

Imbalanced nutrition: Less than body requirements 

related to decreased intake, protein loss via fistula output, disruption of GI
tract continuity, and the hypercatabolism of sepsis.
Goals/Outcomes: By the time of hospital discharge, the patient
has adequate nutrition, as evidenced by food intake that increases
to his or her recommended daily allowance, and body weight that
returns to baseline or within 10% of the patient’s ideal weight.
Nutrition Status: Nutrient Intake.

Nutrition management

1. Collaborate with the physician or advanced practice provider,

dietitian, and pharmacist to estimate the patient’s metabolic needs
on the basis of activity level, estimated metabolic rate, and baseline
nutrition status.

2. Determine preexisting malnutrition status.

3. Monitor nutrition laboratories. Serum albumin and transferrin

are good prognostic indicators for mortality, morbidity, and
spontaneous fistula closure.

4. Monitor for the presence of bowel sounds every 2 hours. If bowel

sounds are absent, consider duodenal or jejunal elemental feedings.

1779
5. If fistula output increases in response to enteral feedings, slow
the rate of infusion or reduce the strength of the feeding. If the
patient tolerates oral feedings but they increase fistula output,
increase the frequency of the feedings and decrease the amount
consumed at each feeding.

6. Elemental feeding formulas may be more readily absorbed when

the entire intestine is not available for normal absorption.

7. Prepare the patient for parenteral feedings if enteral feedings are

inadequate for the patient’s requirements.

8. Apply NG suction only in the presence of obstruction or

prolonged ileus. In their absence, NG drainage shows little benefit.
They may inappropriately contribute to complications such as
patient discomfort, sinusitis, pulmonary aspiration, and
gastroesophageal reflux.

Nutrition Monitoring; Fluid/Electrolyte Management; Total

Parenteral Nutrition (TPN) Administration; Enteral Tube Feeding.
For additional information, see Nutrition Support, Chapter 1.

Impaired tissue integrity 

related to chemical trauma, infection, and malnutrition
Goals/Outcomes: Within 72 hours of diagnosis, the patient’s
tissue adjacent to the fistula is free of erythema, excoriation, and
edema.
Wound Healing: Secondary Intention; Tissue Integrity: Skin
and Mucous Membranes.

Wound care

1. Assess the extent of the local problem (Box 9-7). Consult the
physician for signs of extensive damage to the tissue adjacent to the
fistula (i.e., severe local erythema, excoriation, edema, maceration).

2. Establish drainage and collection system for each fistula (Box 9-

8). Consult the advanced practice provider regarding use of
device(s).

1780
3. Note characteristic, color, odor, and volume of output from each
fistula. Consult the advanced practice provider for significant
changes in these indicators.

4. If increased fistula output results from oral or enteral feedings,

eliminate or modify the feedings as prescribed.

5. Consult the wound ostomy continence nursing (WOCN) services

for recommendations in pouching complex or multiple fistulas.

6. Consider wound management with an NPWT device; currently

used to effectively divert intestinal output from the wound and
increase blood flow to the area.

7. NPWT dressing is changed approximately every 3 to 7 days by a

WOCN. With this frequency of dressing change, the surrounding
skin is protected and patient discomfort is reduced.

Box 9-7
NURSING ASSESSMENT OF
ENTEROCUTANEOUS FISTULA
• Evaluate size, shape, and location of the fistula. Reposition or lift
skin folds as necessary.

• Identify any potential leakage tracks created by skin folds or body

hollows.

• Examine the condition of adjacent skin and tissue. Note the

presence and spread of both erythema and excoriation, which
suggest leakage tracks.

• Note the consistency and characteristic of fistula output.

• Assess each fistula separately.

Document all findings and compare them with baseline

assessment made at the time of initial evaluation.

1781
Box 9-8
RECOMMENDATIONS FOR CONTAINING
FISTULA DRAINAGE
• Clean the intact skin surrounding the fistula with a nonirritating
antibacterial cleanser.

• Clip body hair (if present) around the fistula.

• Remove pooled drainage from the wound and surrounding area

by using sterile absorbent pads or gentle suction. The help of an
assistant may be necessary to maintain a dry field during
application of the collection device.

• Apply a barrier powder (e.g., karaya or Orahesive) to excoriated

skin. A flexible transparent dressing (e.g., Op-Site) can be used to
protect intact skin.

• Use a skin paste (e.g., Stomahesive or karaya) to fill in any

grooves surrounding recessed fistulas.

• Apply a sized barrier sheet (e.g., Stomahesive, HolliHesive) to the

surrounding skin, being careful not to overlap the fistula.

• Attach a collecting bag to the barrier sheet base. For high-output

fistulas, a urostomy bag and collecting system may be necessary.
Transparent appliances enable observation of drainage. Devices
that have a drainage opening permit emptying and measurement
of output.

Reposition the patient frequently to optimize gravity of fistula

output.

Ostomy Care; Tube Care; Fluid/Electrolyte Management.

Disturbed body image 

1782
related to biophysical change secondary to presence of external fistula.
Goals/Outcomes: By hospital discharge, the patient
acknowledges body changes, as evidenced by viewing fistula and
not exhibiting preoccupation with or depersonalization of fistula.
Body Image.

Body image enhancement

1. Evaluate the patient’s reaction to the fistula by observing and

noting evidence of body image disturbance.

2. Anticipate feelings of shock and repulsion initially. Be aware that

the development of an external fistula is usually an unanticipated
complication and patients are not emotionally prepared for the
disfigurement.

3. Anticipate and acknowledge normalcy of feelings of rejection,

isolation, and uncleanliness (because of odor and possible presence
of feces).

4. Offer the patient an opportunity to view fistula/wound as

desired. Use mirrors if necessary.

5. Encourage the patient and significant others to verbalize feelings

regarding fistula/wound.

6. If possible, offer the patient an opportunity to participate in

wound care. The patient may be able to perform simple tasks, such
as holding the bag into which you will deposit the soiled dressing
or applying the pouch that collects drainage.

7. Convey an accepting attitude toward the patient. Many fistulas

that require critical care involve open and infected wounds. If the
attending nurse is inexperienced in dressing these complex
wounds, another, more experienced nurse should be present during
the initial dressing change.

8. Reassure the patient that the fistula is not permanent.

Acknowledge that a scar will be visible but the fistula will close
with appropriate care.

1783
 Coping Enhancement; Self-Care Assistance; Support System
Enhancement.

Impaired oral mucous membrane 

related to prolonged NPO status
Goals/Outcomes: Within 24 hours of diagnosis, the patient’s oral
mucosa is intact, moist, and free of pain and oral lesions.
Oral Hygiene; Tissue Integrity: Skin and Mucous
Membranes.

Oral health maintenance

1. Inspect the patient’s oral cavity, noting the degree of moisture,

inflammation, bleeding, or lesions. Consult the physician for open
lesions and bleeding.

2. Assist the patient with brushing teeth with a soft-bristle

toothbrush. Provide mouth care every 4 hours.

3. For patients with altered LOC, massage gums and teeth with
saline-moistened, sponge-tipped applicator and brush teeth gently
if there is no evidence of bleeding. Carefully suction the solution
from the oral cavity throughout the procedure with a tonsil suction
device.

4. Keep the lips moist with emollients such as lanolin. Take care to
apply emollient to external tissue only. Oil-containing emollients
are harmful if aspirated or otherwise introduced into the
respiratory tract.

Oral Health Promotion.

Additional nursing diagnoses

See Nutrition Support (Chapter 1) for additional information about
the patient with extra nutrition needs. See Emotional and Spiritual
Support of the Patient and Significant Others (Chapter 2) for
psychosocial nursing diagnoses and interventions. Also see nursing
diagnoses and interventions related to sepsis under Systemic

1784
Inflammatory Response Syndrome, Sepsis, Septic Shock, and
Multiple Organ Dysfunction Syndrome (Chapter 11).

Hepatic failure
Pathophysiology
There are various manifestations of acute and chronic liver failure.
Fluid retention, edema, and ascites are common to acute and
chronic hepatic failure and are attributed to: (1) intrahepatic
vascular obstruction with transudation of fluid into the peritoneum;
(2) defective albumin synthesis, resulting in decreased colloid
osmotic pressure with failure to retain intravascular fluid; and (3)
disturbances of various hormones, including renin, aldosterone,
and renal prostaglandins, resulting in sodium and water retention.
Massive ascites is usually the result of cirrhosis.
Hepatic encephalopathy occurs in both acute and chronic liver
failure. A state of decreased mentation, neuromuscular function,
and consciousness are the hallmarks of hepatic encephalopathy.
Patients with stage one (mild) hepatic encephalopathy have
problems concentrating, difficulty writing, memory loss, subtle
personality changes, mood swings, and sleep alteration that may
result in loss of awareness of time of day or night; often switching
daytime activities into night activities. Patients with stage two
(moderate) hepatic encephalopathy have less energy, have slurred
speech, behave strangely, forget more frequently, and have
problems with basic math. Patients with stage three (severe) hepatic
encephalopathy are somnolent, may have syncopal episodes, and
exhibit extreme changes in behavior. Monitoring patients for
seizures and dementia is crucial. These patients are often poorly
functional at home and are reported to be jumpy, fearful, and have
absolutely no basic math skills. Patients in stage four (hepatic coma)
are admitted directly to the ICU, usually arriving unconscious or
semiconscious. Patients with stage one and two are usually
ambulatory and receive outpatient treatment for hepatic
encephalopathy with oral medications. Patients with stage three are
often bordering on critical illness, whereas patients with stage four

1785
generally require mechanical ventilation and sedation in the ICU.
Complications of hepatic encephalopathy include brain swelling
with herniation, coma, and death.
Both acute and chronic hepatic failure affect the physiologic
status of all organs. Key differences between the two include
progression rate of liver failure, previous history of liver disease,
type of treatments required, and prognosis.

Acute liver failure

Acute liver failure (ALF) is defined as a severe, sudden loss of
hepatocytes resulting in failure of hepatic function, accompanied by
encephalopathy and coagulation disorder. ALF occurs without a
previous history of liver disease. Although there are approximately
2000 cases per year in the United States, ALF is more common in
less developed countries with 50% mortality. In the United States,
acetaminophen overdose is the leading etiology, whether
intentional overingestion (suicide) or through inappropriate self-
medication or “therapeutic misadventure.” Other common causes
of ALF in the United States include misuse of medications and
herbal supplements (prescription, over-the-counter, and
complementary/alternative), viral hepatitis, autoimmune liver
disease, shock, mushroom poisoning (commonly Amanita
phalloides), hypoperfusion of the liver (i.e., Budd-Chiari syndrome),
Wilson disease, acute fatty liver of pregnancy, herpes viruses, and
malignant infiltration. Outcomes have improved considerably in
the past decade, resulting from more timely admission of patients
to specialty ICUs of liver transplant centers. Transplant centers are
familiar with appropriate crisis management, including palliative,
non–disease-specific treatments (i.e., N-acetylcysteine [NAC]). The
outcomes of the Acute Liver Failure Study Group revealed that
patients with slowly evolving etiologies have a poorer prognosis
than when ALF developed hyperacutely (within less than 1 week).
For those who fail to show signs of spontaneous recovery, liver
transplantation using a whole cadaver graft is considered standard
of care. Survival rates for the first year of transplant in patients with
ALF are lower than those patients transplanted for chronic liver
failure (CLF). After the first year, survival rates are essentially the
same.

1786
 Heart failure may occur in worsening ALF. While the condition
progresses, dysrhythmias result from reduced beta-adrenergic
receptor signal transduction, defective cardiac excitation-
contraction coupling, and conduction abnormalities. Right
ventricular failure ensues and causes venous engorgement resulting
in hepatic congestion. The decreased forward flow of blood from
the failing right-to-left heart circulation results in reduced CO.
Decreased hepatic blood flow, with congestion of the vena cava
from blood “backing up” from the failing right side of the heart,
impedes the emptying of the portal vein into the vena cava.
Heart failure progressively damages the hepatocytes attributable
to hypoxia resulting from circulatory impairment. The portal vein
supplies up to 83% of the blood flow to the liver, with the hepatic
artery supplying up to 34% (varies from person to person by
approximately ±17%). In the final stages of ALF, profound
peripheral vasodilation results in severe vascular congestion and
third spacing of intravascular fluids including ascites, which causes
hemodynamic collapse. Hypotension, tachycardia, heart murmur,
warm extremities, an exaggerated precordial impulse, palmar
erythema, and/or spider angiomas are present.

Chronic liver failure

Loss of hepatocytes, abnormal microcirculation, and impaired
hepatic function of 6 months or longer duration are hallmarks of
chronic liver failure (CLF), eventually requiring transplant resulting
from end-stage liver disease (ESLD). Chronic liver disease is
associated with slowly progressing, widespread tissue necrosis,
fibrosis, liver nodule formation, and cirrhosis, ultimately resulting
in hepatic failure. The usual causes are long-term alcohol ingestion,
chronic viral hepatitis, prolonged cholestasis, long-term use of
certain medications, alpha1-antitrypsin deficiency, diabetes,
hemochromatosis, malnutrition, glycogen storage disease, and
cystic fibrosis. CLF is a leading cause of morbidity and mortality in
the United States with alcohol consumption and chronic viral
hepatitis being responsible for the majority of ESLD cases
necessitating liver transplantation. Most patients with cirrhosis
remain asymptomatic for years until hepatic decompensation
ensues. Approximately 40% of liver transplants performed in the

1787
United States are attributable to ESLD secondary to hepatitis C. The
U.S. Food and Drug Administration (FDA) has recently approved
direct-acting antivirals for hepatitis C that will profoundly change
the face of ESLD and liver transplantation in the future.
Nonalcoholic fatty liver disease attributable to risk factors such as
lipidemia (hypertriglyceridemia), obesity, and diabetes is quickly
becoming a more prevalent liver disease and in the near future will
be responsible for more cases of ESLD. In the great majority of
cases, CLF takes decades to manifest itself with symptoms
requiring treatment and eventual referral to a liver transplant
center.
In patients with cirrhosis, portal hypertension creates
hyperdynamic circulation, reflected by decreased SVR,
hypotension, increased CO, tachycardia, and bounding pulses.
Progression to advanced liver disease correlates with worsening
hyperdynamic circulation.
Patients with chronic liver disease may have hepatopulmonary
syndrome (HPS) that results from intrapulmonary microvascular
dilation that may or may not be coupled with portal hypertension.
There may be diffuse or localized dilated pulmonary capillaries.
Less common are the presence of pleural and pulmonary
arteriovenous communications. Arterial hypoxemia, commonly
present in chronic liver disease, is attributable to multiple
coexisting causes such as ascites, hepatic hydrothorax, and/or
chronic obstructive pulmonary disease. Dyspnea (shortness of
breath) may be present at rest or during exertion and is the main
symptom, particularly after long-standing liver disease. Upon
examination, spider angioma, digital clubbing, cyanosis, and
platypnea (shortness of breath relieved when lying down) are
common findings. Liver transplantation can reverse HPS if the
patient survives longer than 6 months posttransplant and can
improve to the point that supplemental oxygen may no longer be
needed.
As defined by the National Institutes of Health Patient Registry
for the Characterization of Primary Pulmonary Hypertension, a
patient has portopulmonary hypertension (POPH) in the presence
of portal hypertension with a mean pulmonary artery pressure ≥25
mm Hg and pulmonary capillary wedge pressure less than 15 mm

1788
Hg. Symptoms include fatigue, dyspnea, peripheral edema,
syncope, chest pain, and a systolic murmur. ECG in 90% of patients
reflects right bundle branch block, right-axis deviation, or a right
ventricular hypertrophy. According to the American Association
for the Study of Liver Diseases (AASLD) practice guidelines, POPH
can potentially improve with liver transplantation and has
acceptable short-term outcomes. In some patients, vasodilator
therapy can even be discontinued posttransplant. Transjugular
intrahepatic portosystemic shunting (TIPS) is useful for treating
portal hypertension associated with refractory ascites and
esophageal varices in the patient with cirrhosis who has ESLD. In
over 90% of patients, TIPS procedures decompress the portal vein.
Studies have shown that the rate of new or worsening hepatic
encephalopathy after TIPS is 20% to 31%.
Spontaneous bacterial peritonitis is a spontaneous infection that
affects up to one third of patients with ESLD. The most common
organism found in the peritoneal fluid of patients with spontaneous
bacterial peritonitis is Escherichia coli, believed to be attributable to
translocation of the bacteria from the intestinal lumen. Prevention
of spontaneous bacterial peritonitis is key with the use of oral
antibiotics.
Hepatorenal syndrome (HRS) is defined by the International
Club of Ascites as renal impairment or failure that occurs in
patients with advanced chronic liver disease, liver failure, and
portal hypertension. Patients have marked abnormalities in the
arterial circulation and activity of the endogenous vasoactive
systems. There are two types of HRS defined by the International
Club of Ascites: type 1 is rapidly progressive, with baseline
creatinine level doubling in less than 2 weeks to a value greater
than 2.5 mg/dL. Type 2 is a slower disease that consists of moderate
renal failure and is commonly associated with refractory ascites.
The vast majority of patients have no intrinsic renal disease.
Significant renal vasoconstriction results in low glomerular
filtration rate, whereas arterial vasodilation in the extrarenal
circulation results in reduction of SVR and hypotension. Factors
that reduce renal perfusion in patients with chronic liver disease are
dehydration, lactulose therapy, use of NSAIDs, hemorrhage, and
paracentesis. For patients with cirrhosis who develop renal

1789
dysfunction, the risk of death increases sevenfold and 50% of
patients die within a month of onset.

Benefits of care in a transplant center

Regardless if liver failure is acute or chronic, expert
interdisciplinary collaboration provides rapid evaluation for
etiology and timely access to appropriate treatment. Severity of
liver damage is accurately assessed for possible listing as a liver
transplantation candidate. Failure of other organs is often linked to
liver dysfunction. Highly specialized evaluation is needed to
identify and vigilantly manage these complex patients.

Hepatic assessment
Goal of system assessment
A thorough physical assessment along with an accurate history
should produce a correct liver disease diagnosis in the majority of
cases. Evaluate for cause of and subsequent hepatic and
multisystem effects of ALF, because severe liver damage has
already occurred upon presentation for care.

History and risk factors

Evaluate for family/personal history of liver disease, exposure to
toxins, exposure to complementary and alternative medications,
street or prescription drug use, acetaminophen use and abuse,
alcohol use and abuse, exposure to Bacillus cereus toxin (through
food ingestion), and Amanita phalloides mushroom poisoning.

• Enquire about adherence with taking antibiotics for spontaneous

bacterial peritonitis prophylaxis, diuretics, beta-blockers (for
control of portal hypertension), lactulose (to keep ammonia level
from rising, thereby preventing hepatic encephalopathy), and
any nonprescribed or non–physician-recommended over-the-
counter medications.

• Enquire about depression, recent travel abroad, and prescription,

over-the-counter, and street drug use.

1790
Vital sign assessment
• Neurologic assessment, including Glasgow Coma Scale score, in
some cases an intracranial pressure (ICP) monitor, and an arterial
line may be needed for patients who are severely ill.

• HR (preferably apical), heart rhythm, and BP to evaluate if liver

disease is affecting CO and perfusion; risk of hemorrhage is also
a complication.

• Normal to bounding pulses, low to normal BP, elevated CO

associated with decreased peripheral vascular resistance and
expanded total blood volume.

• Take BP while the patient is lying down, sitting up, and standing
(if able)—this also helps to observe for platypnea.

• Take temperature; if elevated may be attributable to an acute

bacterial, viral, or fungal process that may be affecting the liver.

• If the temperature is low, hypothermia may herald the onset of

hepatic encephalopathy.

Observation
• Evaluate for pallor, jaundice, and scleral icterus and signs of
coagulopathies.

• Note spider angioma, skin excoriation (from scratching as a result

of increased bilirubin), ecchymosis, petechiae, prominent
abdominal collateral veins, palmar erythema, gynecomastia,
testicular atrophy, jugular vein distension, needle marks, loss of
body hair, loss of muscle mass, peripheral edema, obvious
ascites, eye signs mimicking hyperthyroidism, exertional
dyspnea, digital clubbing, cyanosis of the nail beds, and umbilical
hernias.

• Note muscle weakness and tenderness; a common finding in

ESLD from alcohol (EtOH). Measure abdominal girth.

1791
• Note if asterixis (brief periods of “flapping” or irregular flexion of
the hands at the wrist) is present.

• Observe for signs of respiratory distress, impaired renal function,

and bacterial, viral, and fungal infections.

• Note if questions are answered appropriately and if the patient is

awake, alert, and oriented; disoriented or confused.

• Fetor hepaticus may be present (pungent breath odor in some

patients with cirrhosis).

• In the presence of tense ascites (which increases intraabdominal

pressure), impaired right ventricular filling with decreased stroke
volume and decreased CO may be evident.

• If the patient has had a massive variceal hemorrhage or is in

septic shock, pulses will be diminished and BP will be low,
reflecting circulatory collapse.

Palpation
Liver palpation can aid in the diagnosis of liver disease etiology
and confirm cirrhosis.

• Examine the abdomen; palpate all nine sections of the abdomen,

palpate the liver and spleen, and assess for abdominal masses.

• Palpate the liver and other abdominal organs (i.e., spleen). Note
liver firmness, size, edges, and possible pain with palpation.
Hepatomegaly may be evident. Many times in liver disease,
splenomegaly is also appreciated. Gallbladder (if not previously
removed) may be palpated (and if palpable and/or painful may
be attributable to stones or infection); also assess for the presence
of any abdominal masses.

• Note pulse quality and regularity bilaterally (scale 0 to 4+),

because bilateral lower extremity edema is common in ESLD and
can obscure pulses.

1792
• Ascites can be diagnosed if not obvious with palpation and
observation of an abdominal fluid wave upon palpation.

• Assess for lymphadenopathy.

Auscultation
• Listen to the heart, carotid artery, lungs, and abdomen.

• Listen to abdominal sounds in all nine sections of the abdomen.

• Bruits and/or rubs may be present (liver disease–related

abdominal bruits can be caused by hepatocellular carcinoma,
portosystemic shunt, hepatic artery aneurysm, or alcoholic
hepatitis).

• Abdominal friction rub, although rare, is reflective of peritoneal

inflammation and may be diagnostic for infection (liver abscess),
infarction of the liver, or tumor (hepatocellular carcinoma/liver
metastasis).

• Listen for inspiratory crackles in the lungs, particularly at the

bases, and end-expiratory wheezing and egophony (if effusions
are present). Egophony is tested by asking the patient to say “e”
repeatedly as all lung fields are auscultated. The “e” sounds the
same over all healthy tissue. Over consolidated areas the “e”
sounds like “ay”.

• Note if second heart sound and right ventricular heave are

present together.

Screening labwork
Blood testing may differentiate between ALF and chronic liver
disease, as well as aid in diagnosing the severity of liver injury and
degree of liver function/dysfunction.

• Elevated liver function tests: alanine aminotransferase (ALT),

aspartate aminotransferase (AST), gamma-glutamyl
transpeptidase (GGT), bilirubin, alkaline phosphatase, with

1793
 decreased albumin to check for hepatocyte injury, or a cholestatic
cause for liver disease (see chart).

• Viral hepatitis studies, drug panel to check for drug-induced liver

injury, EtOH level to screen for alcoholic liver disease.

• Coagulation studies: elevated international normalized ratio

(INR), prothrombin time (PT), and partial thromboplastin time
(PTT) herald a failing liver (see chart).

• Alpha-fetoprotein (AFP): nonspecific cancer marker to screen for

hepatocellular carcinoma as a potential cause of liver disease (see
chart).

• Electrolytes to monitor for hyponatremia and hypokalemia (see

chart).

• Chemistry profile to monitor glucose (because it is often seen)

and creatinine/BUN (renal function tests [see chart]).

• Street and therapeutic drug levels.

• Acetaminophen levels and adducts of the main metabolite of

acetaminophen (the adducts are detectable even when the
acetaminophen is not).

• Arterial ammonia levels.

Liver biopsy
Once thought of as a diagnostic tool, liver biopsy now serves three
important roles according to the AASLD liver biopsy position
paper: (1) for diagnosis, (2) for assessment of prognosis (disease
staging), and/or (3) to assist in making therapeutic management
decisions. Liver biopsy is invaluable in patients that present with
atypical clinical features, coexisting disorders, and “overlap”
syndrome of two liver diseases (such as primary biliary cirrhosis
and autoimmune hepatitis).

Other studies

1794
Chest radiography, Doppler echocardiography, and ABGs are
useful in the diagnoses of HPS and POPH.

Diagnostic Tests for Acute and Chronic Hepatic Failure

Test Purpose Abnormal Findings

Noninvasive Testing
Electrocardiogram (ECG): To assess for cardiac Hypokalemia, acidosis, or
12-Lead ECG: Must be dysrhythmias related to hypoxia may cause cardiac
obtained upon admission to end-stage liver disease. dysrhythmias. Abnormal rate,
the intensive care unit rhythm may be part of
hepatopulmonary syndrome, or
portopulmonary hypertension.
Electroencephalogram (EEG) For the diagnosis and Often abnormal if hepatic
quantification of hepatic encephalopathy is present. Some
encephalopathy. correlation with ammonia levels
and stage of encephalopathy has
been reported.
Neuropsychological testing To establish a baseline at A battery of six tests, called the
admission (if the patient is psychometric hepatic
not in a hepatic coma). encephalopathy score (PHES). A
normal score is 0.5 ± 1.83. Those
scoring >4 are considered
abnormal.
Blood Studies
Liver function tests Assesses for enzyme Elevated enzymes reflect liver
changes indicative of damage.
hepatic damage.
Alanine aminotransferase ALT is useful in Values >300 units/L are present
(ALT) determining whether with acute liver failure. Found
Aspartate jaundice is caused by liver primarily in the liver, ALT is the
disease or has a hemolytic primary marker of hepatic
cause. damage.
Aminotransferase (AST) AST: Present in organs with high
metabolic activity. Damage to the
hepatocytes will cause a rise in
AST 12 hours after injury and
levels will remain elevated for 4
to 6 days. Levels 10 to 100 times
normal are not unusual in liver
disease.
Alkaline phosphatase (Alk Alk Phos: Found in almost all
Phos) tissue, but most elevations can be
localized to the liver or bone. Alk
Phos is elevated to varying
degrees in various liver diseases.
Bilirubin (TBili or Bili) To assess the ability of the Bilirubin: Total bilirubin is a
liver to process bilirubin, byproduct of hemolysis.
which helps with Elevations occur with excessive
differential diagnosis, and to red blood cell destruction or
predict the prognosis. when the liver is unable to
process normal amounts of
bilirubin. Elevations commonly

1795
 occur in viral hepatitis and
cirrhosis. Consistently elevated
levels are a poor prognostic sign.
Gamma-glutamyl To assist with diagnosing Present in numerous tissues, but
transpeptidase (GGT) that liver disease is present. highest in liver disorders. This
test can be used to confirm that
Alk Phos is elevated resulting
from a hepatic-related condition.
Usually elevated in cholestatic
liver disease, cirrhosis, alcoholic
liver disease, and metastasis to
the liver.

Albumin To assess the ability of the Synthesized in the liver,

liver to synthesize albumin, maintains blood oncotic pressure,
which helps predict the and coagulation proteins needed
prognosis. to form a fibrin clot. Low levels
are found in altered synthetic
liver function. Decreased levels
are seen with ascites and severe
liver function, and persistently
low levels suggest a poor
prognosis.
Glucose To assess possible cause for Impaired gluconeogenesis and
altered mentation and glycogen depletion in the
lethargy. cirrhotic liver cause
hypoglycemia, which is usually
present in severe or terminal liver
dysfunction, causing altered
mentation and/or lethargy.
Blood urea nitrogen (BUN) To assess kidney In liver failure, BUN is decreased.
and serum creatinine (Cr) function/presence of However, if the patient has
hepatorenal syndrome. bleeding or has renal
insufficiency (impending or
actual hepatorenal syndrome),
BUN:Cr is elevated.
Arterial ammonia To rule out hepatic Increased as a result of the
encephalopathy or other inability of the failing liver to
causes of altered mentation. clear nitrogenous and other
waste products.
Gastrointestinal (GI) bleeding
or an increase in intestinal
protein from dietary intake can
increase ammonia levels.
Elevated levels may herald the
development of intracranial
hemorrhage.
Electrolytes
Sodium (Na+) To differentiate between Decrease in sodium seen in
potential diagnoses. patients with cirrhosis, tense
ascites, hepatorenal syndrome.
Potassium (K+) Decreased potassium observed in
those with liver disease
accompanied by ascites and in
those with alcoholic liver disease.
In hepatorenal syndrome,
hyperkalemia is observed.

1796
Hematologic Tests
Hemoglobin (Hgb) To assess if anemia is GI bleeding may be present with
Hematocrit (Hct) present. decreased Hgb/Hct. Anemia seen
in hepatic failure is termed
macrocytic (attributable to
increase in mean corpuscular
volume) and normochromic
(normal Hgb).

Platelets To evaluate for the Low as a result of platelet

possibility of bleeding. destruction and malfunctioning
hepatic synthesis of platelets.
White blood count (WBC) To evaluate for possible Elevated if sepsis is present.
infection and inflammation.
Coagulation Profile
Prothrombin time (PT) with Useful prognostic indicators A prolonged PT/INR/PTT is an
international normalized in liver disease. ominous sign in patients with
ratio (INR) liver failure, particularly in
Partial thromboplastin time acetaminophen overdose, or
(PTT) unknown causes of liver failure.
King’s College Hospital criteria
(Box 9-9) is a useful prognostic
tool for predicting survival of
patients with acute liver failure
(ALF).
Other
Urinalysis Monitors for development Decreased urine sodium
of hepatorenal syndrome excretion, with normal urinary
(HRS). sediment is a sign of HRS. In the
presence of ascites, the 24-hour
urine volume will be decreased
and the 23-hour sodium value
will be reduced sometimes to <5
mEq/d in severe cases.
Alpha-fetoprotein (AFP) A major plasma protein that Normal levels are < 20 ng/mL.
is a nonspecific marker in
hepatocellular carcinoma
monitoring and treatment.
Also elevated in patients
with chronic hepatitis C
virus and in patients with
cirrhosis.
Acetaminophen level Useful in patients with ALF Time from ingestion to peak
upon presentation to rule levels approximately 4 hours.
out other causes of ALF. Therapeutic levels 10 to 25
µg/mL.
Acetaminophen adducts When acetaminophen Levels ≥1.0 mmol/L is a positive
overdose is suspected and result. However, a serum
no longer detectable, the bilirubin >10 mg/dL may cause a
adducts are specific false-positive result.
biomarkers of drug-related
toxicity.
Polymorphonuclear Useful to quickly diagnose if PMN ≥250 cells/mm3.
leukocyte count (PMN) spontaneous bacterial
Note: A dipstick specifically peritonitis is present. Can
designed for ascitic fluid is initiate empirical antibiotic
available to give bedside treatment for spontaneous

1797
 results in 2 to 3 minutes bacterial peritonitis if PMN
count is ≥250 cells/mm3
while awaiting culture and
sensitivity results.
Radiology
Chest x-ray Assesses for any pathology Tumors, lymph nodes, atelectasis,
in the lungs and chest cardiomegaly, infiltrates,
cavity, confirms diagnosis of tortuous cardiac vessels, and
portopulmonary diaphragm elevation (bilateral or
hypertension and unilateral).
hepatopulmonary
syndrome.
Magnetic resonance imagingAssesses liver size, Enlarged liver, cirrhosis, tumors,
(MRI): morphology, function, cysts, hemangiomas, steatosis,
Hepatic MRI presence of cirrhosis, macronodular lesions,
steatosis, and lesions. Used hemochromatosis (if large iron
to characterize known stores are present), sarcoid
lesions and status of hepatic nodules, biliary cystadenomas,
circulation. Can produce a adenomas, focal nodular
sharp contrast between hyperplastic nodules,
tissues and water and/or fat. cholangiocarcinoma, abscesses,
Can image in transverse, thromboses, and hepatic
longitudinal, coronal, or congestion.
oblique planes.
Computed tomography (CT): Assesses liver size, Enlarged liver, cirrhosis, tumors,
Hepatic CT scan presence of cirrhosis, cysts, hemangiomas, steatosis,
looks for the presence of macronodular lesions,
lesions to characterize hemochromatosis (if large iron
known lesions and status stores are present), sarcoid
of hepatic circulation. nodules, biliary cystadenomas,
Oral or intravenous adenomas, focal nodular
contrast can be hyperplastic nodules,
administered to help cholangiocarcinoma, abscesses,
distinguish the bowel thromboses, and hepatic
lumen and blood vessels congestion.
and tissue, respectively.
Ultrasound: Assesses for fluid-filled Main anatomic features of the
Hepatic ultrasound lesions and vascular liver can be identified, as well as
abnormalities. Also used cysts, infections, abscesses,
to “mark the spot” before steatosis, hemangiomas,
liver biopsy. malignant neoplasms, adenomas,
Note: Ultrasound is best hyperplastic lesions, lymphomas,
suited to thinner patients. increased echogenicity, hydatid
cysts, amebiasis (caused by
Entamoeba histolytica that can
spread to the liver causing liver
abscesses), and fungal disease.
Cerebral CT Used for diagnosis when a Cortical and subcortical atrophy;
subdural hematoma or benign, neoplastic, and metastatic
doubt about etiology of lesions; hemorrhaging;
altered consciousness in the aneurysms; and hematomas.
patient with end-stage liver
disease is in question.
Brain flow studies: To confirm brain death Brain death, as evidenced by lack
Technetium scan of the brain when the patient is in a of blood flow into the brain.
hepatic coma when EEG is
not confirmatory.

1798
 Radioisotope liver scan To determine the presence Hepatocellular carcinoma,
Injection with radioactive of three-dimensional lesions melanoma, Hodgkin and non–
compound and scanned in the liver. Hodgkin lymphoma.
with a scintillation camera
or radiography
Invasive Testing
Liver biopsy (can be Used as a diagnostic and Inflammation, fibrosis, cirrhosis,
percutaneous at the bedside prognostic tool. Can grade hepatocellular carcinoma,
or transvenous in and stage liver disease. Can regenerative changes, apoptosis,
interventional radiology) differentiate between necrosis, iron, complex
Note: Even when platelets are various liver diseases. Can carbohydrates, steatosis, copper,
low, this test can still be be used to follow the granulomas, hepatitis B surface
performed in interventional progression of liver antigen, Mallory bodies, talc
radiology transjugularly after diseases. crystals, inflammatory cells,
platelet infusions, microabscesses, Cowdry type A
desmopressin (DDAVP), or inclusions, etc.
recombinant factor VIIa,
according to local practice.

Liver function tests

LFTs are nonspecific for diagnosing types of liver disease or
measuring efficacy of liver function but rather identify hepatocyte
damage or biliary abnormalities (e.g., cholestasis). Once liver
dysfunction is established, tests monitor the progression,
stabilization, or improvement of liver damage. In treatable liver
diseases, such as hepatitis, the tests monitor effectiveness of
treatment. Testing is often done serially to increase specificity and
sensitivity.

Box 9-9
KING’S COLLEGE HOSPITAL CRITERIA
ALF from acetaminophen
• pH <7.30 (24 hours after ingestion and after adequate fluid
resuscitation)—irrespective of coma grade

• PT* >100 seconds or INR >6.5 with

• Serum creatinine >3.4 mg/dL in grade 3 or 4 encephalopathy

ALF from other causes

1799
• PT >100 seconds (INR >6.5)—regardless of coma grade or any
three of the following regardless of encephalopathy grade:

1. Age <10 years

2. Age >40 years

3. Drug toxicity, indeterminate cause of ALF

4. Duration of jaundice before onset of coma of >7

days

5. PT >50 seconds (INR ≥3.5)

• Serum bilirubin >17.5 mg/dL

*PT is the most sensitive prognostic marker.

ALF, Acute liver failure; INR, international normalized ratio; PT,
prothrombin time.

Alanine aminotransferase (ALT) and aspartate

aminotransferas (AST)
These enzymes are the most frequently measured indicators of liver
dysfunction, because values are elevated in all liver disorders.
Although the enzymes are also present in the brain, kidneys,
skeletal and cardiac muscles, the concentration is highest in the
liver. Values elevate most markedly in acute hepatitis and liver
injury from exposure to hepatotoxins. ALT seems to be the more
sensitive enzyme specific to hepatocyte damage.

Serum bilirubin (bili)

Bilirubin in the urine is usually diagnostic for biliary liver disease.
Up to 80% of bilirubin comes from the breakdown of hemoglobin,
whereas the other 20% comes from prematurely destroyed cells
found in bone marrow and from hemoproteins throughout the
body. Bilirubin alone is not diagnostic for determining the cause of

1800
jaundice in a patient. Usually, bilirubin levels are higher in a
neoplastic process in the liver than in other causes of liver disease.

Alkaline phosphatase
Similar to the other “liver function” tests, alkaline phosphatase is
found in many parts of the body. The liver and bone appear to be
the main sources of this enzyme. Elevation of this enzyme is usually
seen in hepatobiliary diseases.

Serum albumin
Albumin levels tend to be normal regardless of the cause of liver
disease. Hypoalbuminemia is usually found in patients with ESLD
and/or cirrhosis where decreased albumin synthesis, ascites, and
severe liver damage are present.

Prothrombin time (PT)

The liver synthesizes at least seven blood coagulation proteins.
Although a prolonged PT is not specific in diagnosing diseases of
the liver, it is prognostic in outcomes in acetaminophen overdose
and in patients with alcoholic steatonecrosis, fulminant hepatic
necrosis, and acute hepatocellular disease.

Liver biopsy
Liver biopsy is the “gold standard” of testing used to diagnose the
type of liver disease, screen for familial disease, monitor and stage
the disease, evaluate the degree of hepatocellular injury, evaluate
effectiveness of treatment, and confirm rejection episodes in the
transplanted liver.

HIGH ALERT!
Risk of death from a liver biopsy complication is estimated to be 1
in 10,000. The patient MUST be adequately prepared for the liver
biopsy procedure and the aftercare to minimize potential
complications and prevent mortality. The patient and their vital
signs must be monitored very closely for signs and symptoms of
complications from a biopsy if they are in a hepatic coma or
induced coma. If platelets are less than 60,000, the biopsy can still

1801
be performed transjugularly in interventional radiology after
administration of a platelet transfusion, desmopressin (DDAVP),
or administration of recombinant factor VIIa.

Before biopsy

• Explain the procedure to the patient and significant others. The

patient must be able to demonstrate they can exhale and hold
their breath during needle insertion, if biopsy is to be performed
percutaneously at the bedside.

• The patient should sign informed consent for the procedure

before sedation is administered.

• PT, INR, and platelet count values should be done immediately

before the biopsy in patients with ALF. If the patient has CLF and
is not in decompensation, values should be less than 30 days old.

• Ensure that the patient has not had salicylates (e.g., aspirin or
bismuth) or NSAIDs (e.g., ibuprofen, naproxen) for 7 days before
the biopsy.

• All anticoagulants must be stopped 72 hours before the biopsy,

unless the biopsy is being done emergently for ALF.

• The patient should not have eaten for 4 to 8 hours before the
procedure.

During biopsy

• Assist the patient with proper positioning and with remaining

motionless during the procedure.

• Coach the alert patient to exhale and hold their breath during the
procedure (or manually ventilate the intubated patient to prevent
lung inflation during puncture) to avoid movement of the lung
and possible resulting pneumothorax.

1802
After biopsy

• Apply direct pressure to the biopsy site for 15 minutes followed

by a pressure dressing.

• Auscultate breath sounds immediately after the procedure and at

1- to 2-hour intervals to detect pneumothorax or hemothorax
(unlikely but serious complications). Diminished sounds on the
right side and tachypnea suggest one of these conditions.

• Position the patient on the right side for a minimum of 2 hours

after the biopsy to tamponade the puncture site to minimize the
risk of hemorrhage.

• Monitor hemoglobin and hematocrit to screen for intraperitoneal

bleeding.

• Assess for signs/symptoms of peritonitis and intraperitoneal

bleeding: severe abdominal pain, abdominal distension and
rigidity, rebound tenderness, nausea, vomiting, tachycardia,
tachypnea, pallor, decreased BP, and rising temperature.

• If bleeding is suspected, contact the advanced practice provider to

obtain an abdominal/liver ultrasound study.

• Remind the patient that mild shoulder pain may persist for 24 to
48 hours after the biopsy.

Collaborative management

1803
HEPATIC FAILURE MANAGEMENT GUIDELINES

*
All guidelines and position papers are available on the AASLD website:
www.aasld.org. AASLD, American Association for the Study of Liver Diseases.

Care priorities
Hepatic failure may develop suddenly in a patient with
compensated liver disease. Sustained hypoxia or hypotension from
any cause can aggravate hepatocellular failure and must be
corrected promptly. EtOH, hepatotoxic drugs, and hepatotoxic
alternative therapies are eliminated. Minimize use of sedatives and
tranquilizers because they may contribute to hepatic
encephalopathy.

1. Manage fluid and electrolyte imbalance

1804
When the patient first presents for care, a central line should be
inserted. This will assist with restoration of intravascular volume
thereby ensuring systemic perfusion, which can help to keep other
organs from failing. Maintaining hemodynamics is particularly
important if intracranial hemorrhage (ICH) is present or renal
function is compromised. The AASLD guidelines recommend that
hypotensive patients with ALF be resuscitated with normal saline
first. After initial resuscitation, if the patient is acidotic, half-normal
saline containing 75 mEq/L sodium bicarbonate should be given.
Inotropic or pressors may be needed to maintain an MAP of at least
75 mm Hg or a cerebral perfusion pressure of 60 to 80 mm Hg.
Norepinephrine may be used to assist peripheral organ perfusion
and preserve splanchnic (hepatic) blood flow. CVP monitoring may
be initiated to ensure adequate tissue perfusion without fluid
overload. Hypoglycemia is common and a continuous glucose
infusion should be used. In addition, potassium, magnesium, and
phosphorus move from the intravascular space to the intracellular
space, thereby necessitating the need to monitor these electrolytes
closely and supplement as needed.

HIGH ALERT
Accurate measurements and careful interpretation of
hemodynamic measurements are essential because fluid balance is
delicate in critically ill patients with hepatic failure. Hemodynamic
measurements can be difficult to interpret because circulation is
hyperdynamic. SVO2 or ScVO2 monitoring is helpful in evaluating
the adequacy of tissue oxygenation.

2. Provide nutrition therapy

The catabolic rate in ALF increases four times over normal and is
associated with negative nitrogen balance. Patients with CLF are
usually malnourished and dehydrated upon presentation, because
they have increased fat oxidation and gluconeogenesis with protein
catabolism. It is imperative that metabolic homeostasis be
maintained. AASLD guidelines recommend that enteral or

1805
parenteral feedings be initiated early. Restriction of protein should
be avoided. It is recommended that 60 g/d be given initially.
Sodium is moderately restricted (up to 2000 mg/d) unless
significant ascites and peripheral edema are present, wherein a less
than 500-mg sodium diet is prescribed. Total caloric intake should
be 2500 to 3000 per day.

3. Provide pharmacotherapy that will minimize or avoid

further liver dysfunction because all drugs have hepatotoxic
potential in a patient with compromised liver function
Some commonly used drugs are hepatotoxic and Box 9-10 lists
medications that patients with ALF/their families reported to
researchers that were taken before going into ALF. There are
numerous medications/classes of medications necessary for the
management of liver failure:

• Sedatives: May be needed to sedate and paralyze a patient with

grade 3 or grade 4 encephalopathy. A nonpolarizing
neuromuscular blocking agent, such as cisatracurium, because it
does not cause an increase in ICH. After the patient is on a
ventilator, propofol can be used because it has a long half-life and
therefore smaller doses can be used in the case of inadequate
liver function.

• Histamine H2-receptor antagonists: Prophylactic H2-receptor

antagonists are prescribed to block acid secretion and prevent
gastric erosions, which are common in patients with chronic or
severe hepatic failure. Famotidine, ranitidine hydrochloride,
cimetidine, and nizatidine are competitive blockers of histamine
and thereby inhibit all phases of gastric acid secretion.

• Sucralfate (Carafate): Binds to gastric erosions, aiding in healing

established ulcers, and coats the gastric/duodenal mucosa,
thereby preventing stress ulcers.

• Dextrose: Moderate to severe hypoglycemia can occur because of

impaired gluconeogenesis and impaired insulin degradation.
Check blood glucose levels every 1 to 2 hours initially upon

1806
 admission and then every 2 to 4 hours once stabilized.
Hypoglycemia should be corrected expeditiously with a bolus of
50% dextrose (D50) or continual infusion of a 10% dextrose
solution (D10).

• N-Acetylcysteine: Administering NAC protects the liver against

free radical injury and is useful in acetaminophen overdose and
carbon tetrachloride or trichloroethylene exposure. NAC helps
replace glutathione stores in the liver, protecting hepatocytes. It
can be administered orally at 140 mg/kg or parenterally 140
mg/kg in 5% dextrose with subsequent doses at 70 mg/kg.
Careful observation is necessary during IV administration,
because an anaphylaxis-like reaction has been observed.

• Penicillin/silibinin: Used commonly as an antidote in Europe for

Amanita phalloides poisoning; penicillin 300,000 to 1,000,000
units/kg/d and silibinin 20 to 50 mg/kg/d given IV is alleged to be
hepatocyte-protective if treatment is started within 24 hours of
ingestion. This combination protects as-yet unaffected
hepatocytes, thereby preventing further hepatocyte necrosis.

• Zinc: In individuals who are malnourished, it is useful not only as

a mineral replacement therapy but also to reduce the chance for,
or severity of, encephalopathy because it increases hepatic urea
synthesis. In other countries, the use of ornithine-aspartate is
advocated to improve hepatic and muscular ammonia
elimination.

4. Prevent spontaneous bacterial peritonitis

Norfloxacin (400 mg twice a day) is commonly prescribed
prophylactically by transplant centers. Other strategies to prevent
spontaneous bacterial peritonitis include a single oral dosage of
ciprofloxacin (750 mg) weekly or five dosages of double-strength
trimethoprim/sulfamethoxazole per week to prevent infection.
Critics argue that not giving a dosage to patients daily may select
for resistant bacteria species. Patients with ascites that present to
the hospital should have a paracentesis with cultures and
sensitivities. Until cultures are available, broad-spectrum third-
generation IV cephalosporins (i.e., cefotaxime) that cover up to 95%

1807
of flora can be given. PPIs have been associated with the rate of
spontaneous bacterial peritonitis in patients with cirrhosis. The
majority of patients may have no documented indication for their
use.

5. Manage accumulation of ascites

Ascites is the most common complication of cirrhosis. Fluid intake
and physical activity are restricted. Dietary restrictions, therapeutic
paracentesis, and diuretics are commonly used, while TIPS is
usually placed for refractory ascites.

• Sodium: If ascites causes discomfort or dyspnea, sodium is

limited to less than 2000 mg/d and diet education is important so
that the patient learns to avoid “hidden sodium” in processed
and canned foods.

• Diuretics: If more conservative measures are ineffective in

controlling ascites, spironolactone (Aldactone), an aldosterone
antagonist with weak diuretic action and potassium
conservation, or amiloride, another potassium-sparing diuretic,
may be used. AASLD guidelines state that if potassium-sparing
diuretics alone are ineffective, more potent diuretics such as
furosemide (Lasix) or thiazides are added with concurrent use of
potassium supplement. For severe ascites, a TIPS may be
indicated.

• Paracentesis: Patients with severe ascites are managed with

diuretics and large-volume (greater than 5 L) therapeutic
paracentesis with or without infusion of albumin or another
plasma volume expander (based on local practice). Repeated
removal of 4 to 8 L/week of ascitic fluid may be attempted as a
temporary measure to relieve refractory ascites. An increase in
CO is noted immediately after the procedure. Once discharged
from the ICU, if patients cannot make frequent trips to the
hospital, a TIPS is indicated, and in some rare instances a
peritoneovenous shunt.

• Transjugular intrahepatic portosystemic shunt (TIPS): A

nonsurgical, invasive radiology procedure performed that uses a

1808
 stent to decompress the portal vein and create a new circulatory
pathway for blood to flow around the liver back to the heart to
help relieve portal hypertension. AASLD guidelines recommend
that a polytetrafluoroethylene-covered stent is preferable for TIPS
procedures versus bare stents, with studies showing less stent
dysfunction, and perhaps improved patient outcomes. In
addition, a TIPS can prevent rebleeding from varices and reduce
or stop ascites. See Box 9-11 and Fluid Volume Excess, Chapter 9,
for nursing implications.

• Peritoneovenous shunt: First introduced in 1974, a

peritoneovenous shunt (e.g., LeVeen or Denver shunt) is a long,
perforated catheter connected to a pressure-sensitive valve that
drains into the superior vena cava. Fluid can flow in only one
direction, from the peritoneum into the bloodstream. Because of
frequent obstruction, these shunts have fallen out of favor and
are usually restricted for patients who (1) live far from a
physician or transplant center that can perform paracentesis; (2)
the patient is deemed not a candidate for a TIPS; (3) for patients
who, as a result of multiple abdominal
surgeries/scarring/adhesions, are not candidates for paracentesis;
and (4) are used in diuretic-resistant patients who are not
transplant candidates. These shunts no longer need to be inserted
surgically and can be placed in interventional radiology. See Box
9-11 and Fluid Volume Excess, Chapter 9, for nursing implications.

6. Eliminate or correct the precipitating factors of

encephalopathy
Up to 80% of patients with cirrhosis and liver failure have cerebral
dysfunction or encephalopathy. The causes and precipitating
factors include changes in the permeability of the blood-brain
barrier, an increase in endogenous benzodiazepines, impairment of
neuronal membrane sodium-potassium adenosine triphosphatase
(ATPase), abnormal neurotransmitter balance, GI bleed, increased
dietary protein, and electrolyte disturbance.

• Restrict physical activity: Permits less stress on all the organs of

the body. Less activity reduces the number of metabolites that

1809
 must be processed by the liver.

• Manage bleeding complications: Factor VIIa, fresh-frozen plasma,

and platelets may be given to correct abnormal clotting factors
and thrombocytopenia. Vitamin K helps correct bleeding
tendencies. Serious coagulopathies require specialized
component therapy (see Bleeding and Thrombotic Disorders:
Disseminated Intravascular Coagulation, Chapter 10).

• Administer antibiotics: Bacterial translocation is problematic in

the patient with chronic hepatic failure as a result of preexisting
cirrhosis. Patients who develop infections have a higher mortality
rate. A 5- to 7-day course of prophylactic, broad-spectrum
antibiotics (i.e., third-generation cephalosporins) is
recommended.

• Administer lactulose: A synthetic disaccharide that contains both

galactose and lactose decreases the pH of the colon by its
conversion into lactic, acetic, and formic acids. The
unmetabolized lactulose left in the colon causes osmotic diarrhea
and migration of ammonia from the blood to the colon.

Lactulose use can cause gaseous distension, which may pose

technical difficulties for the surgeon should the patient go to
transplant.

• Intracranial pressure monitoring: ICP monitoring is controversial

in this patient population with approximately half of 20 U.S.
transplant centers polled putting ICP monitoring into practice.
ICP monitors are used to monitor for early signs of ICH, which
causes fatal uncal herniation. Brain damage may occur quickly
and without obvious symptoms when ICP exceeds 20 mm Hg.
ICP monitoring may be needed for the most critically ill patients
awaiting orthotopic liver transplant to detect cerebral edema and

1810
 guide pharmacologic management (e.g., mannitol, furosemide)
and other therapeutic measures. See discussion in Traumatic
Brain Injury, Chapter 3.

• Manage respiratory failure: Intubation or mechanical ventilation

may be indicated when gag reflex is impaired by advanced
encephalopathy, ventilation is impaired by ascites, or if gastric
contents are aspirated. Frequent assessments and continuous
pulse oximetry are used to monitor those at high risk for
respiratory failure. Adequate tissue oxygenation is crucial
because hepatic hypoxia significantly contributes to hepatic
failure. Hyperventilation to a Paco2 of 25 to 30 mm Hg restores
cerebrovascular autoregulation causing vasoconstriction and
reduced ICP.

• Hypertonic saline administration: AASLD guidelines report that

prophylactic induction of hypertonic saline in patients with
severe encephalopathy (stage four) causes hypernatremia (serum
sodium range of 145 to 155 mEq/L), which lowers the incidence of
ICH, compared with patients with ALF under normonatremic
conditions.

7. Infection control
Whether in acute or chronic liver failure, patients are susceptible to
infections. These patients have decreased phagocyte function,
decreased complement, and their need for invasive procedures
makes them more exposed to various bacteria, viruses, and fungi.

• Monitor laboratory results daily: Daily CBCs with differential

should be drawn and monitored for upward trends of WBCs.

• Monitor vitals: Temperature trends, downward trends in BP,

rapid RR (if not intubated) can be signs of infection.

• Reverse isolation: Protecting the patient with a reduced ability to

fight infection is important. All healthcare providers and visitors
should put on a gown, gloves, and wear a mask. Those healthcare
providers that have a respiratory infection should not care for
this patient.

1811
• Monitor ascitic fluid: Bedside dipsticks are available that will
provide a result within 2 to 3 minutes to inform healthcare
providers if an infection is present in ascites. This can easily be
done at the bedside during a paracentesis. These results can
correlate with an upward trend of WBCs.

• Monitor for respiratory infection: Patients that are

encephalopathic may not be able to cough, deep breath, or use an
incentive spirometer, therefore they should be watched for
problems breathing, coughing, shortness of breath, and upward
trends in WBCs and temperature. Those patients on a ventilator
will also need to be monitored for respiratory infection (i.e.,
change in color of sputum). Lungs should be auscultated on each
shift.

8. Prevent skin breakdown

Patients who are immobile are prone to skin breakdown over bony
prominences. Patients with liver failure (particularly those with
CLF) are usually malnourished, vitamin-depleted, and dehydrated.
In addition, patients with liver failure are not able to fight infections
as easily and any damage to skin integrity can cause larger
problems such as localized infections, tissue necrosis, bacteremia,
and sepsis from bacteria, viruses, and/or fungi entering the
compromised skin.

• Assess and manage skin breakdown: Every shift should do a

thorough assessment of the patient’s skin from head to toe, back
and front. Appropriate treatment should be initiated if
breakdown is apparent (i.e., pressure-relieving mattress, air
mattress, egg crate mattress, etc.). Appropriate dressing to be
applied, consult with a wound care nurse if available, and
increase frequency of turning and repositioning.

• Worsening edema: While peripheral edema

worsens, the chance for “weeping skin” causing a
breach in skin integrity can occur. The amount of
interstitial fluid exceeds the capillary and the ability

1812
 of the skin to retain it causing it to weep. The limb
may feel cold and wet, blistering may be evident.
This can lead to erysipelas and cellulitis. More
frequent sheet changes to keep the rest of the skin
dry, dressing changes of the area with foam, or a
hydrofiber composite dressing material and a
compression dressing may help. Severe weeping
may call for hourly dressing changes.

9. Pain management
Patients with ascites and edema are uncomfortable as a result of
excess fluid compressing internal organs and the skin stretching. In
severe cases, skin splitting prompts more significant pain, similar to
a burn or ruptured blister. Pain assessments should be done at least
every 2 hours and medication for pain administered as needed.
Any changes in vital signs must be thoroughly evaluated to discern
if fluctuations are attributable to worsening pain or worsening of
condition. Nonpharmacologic pain-relief strategies including a
change of position, imagery, relaxation exercises, biofeedback, hot
or cold compresses, or distraction techniques may be helpful.
Spiritual support during a time of suffering may be meaningful,
such as having a chaplain or other appropriate religious figure visit
the patient. All measures that are effective in relieving pain should
be reported to team members and documented in the healthcare
record.

• Manage worsening or unrelieved pain: Assess pain level at least

hourly; more often if pain is becoming intolerable. Dosage and
types of medications should be revised if not effective. Covering
open areas of split skin can relieve dermal pain. Ascites pain may
be relieved by paracentesis or increased dose of diuretics. Pain
associated with worsening edema is sometimes relieved by
additional doses of diuretics.

1813
• Monitor for change in location of pain: A change in location of
pain can herald disease progression.

10. Hepatic transplantation

The orthotopic liver transplant 1-year survival rate is greater than
90% in patients with CLF and is approximately 65% for patients
with ALF. The orthotopic procedure entails a donor organ being
placed in the same location as the patient’s diseased liver following
removal of the native liver. In cases of chronic progressive or acute
hepatocyte damage, it is the only treatment available. Because
organs are in such limited supply, adult-living donor liver
transplantation is being used in recipients whose diagnosis
necessitates a liver, but whose “model for end-stage liver disease”
(MELD) scores are not high enough to place them at the top of the
Organ Procurement Transplant Network/United Network for
Organ Sharing transplanted organ waiting list. Hospitalized,
critically ill patients are generally eligible to receive a whole liver
cadaver graft because their MELD scores place them in the top
three on the list. New methods are being sought to extend the life of
the native liver until a donor liver becomes available. Auxiliary
liver transplantation allows the native liver to remain in the
recipient, which will allow it to regenerate. This procedure is only
used in potentially reversible conditions. Hepatocyte
transplantation, bioartificial liver support, extracorporeal whole-
organ perfusion, and other methods such as stem cell
transplantation and xenotransplantation are being explored as tools
to bridge and increase waiting time to transplantation.

Care plans for hepatic failure

Deficient fluid volume 
related to intravascular volume depletion resulting from third-spaced
fluids.
Goals/Outcomes: Within 24 hours of this diagnosis, the volume
status is improved, as evidenced by MAP greater than 60 mm Hg,
HR 60 to 100 bpm, brisk capillary refill, distal pulses greater than 2+
on a 0-to-4+ scale, CVP 2-6 mm Hg, pulmonary artery wedge

1814
pressure (PAWP) 6 to 12 mm Hg, CI greater than 5 L/min/m2, SVR
900 to 1200 dynes/s/cm-5, urinary output greater than 0.5 mL/kg/h,
and orientation to person, place, time, and situation. The goals of
improvement for patients who are extremely ill are adjusted
according to the predicted best values the patient can achieve with
their level of organ impairment.
Risk Control: Fluid Volume Deficit, Fluid Balance, Fluid
Status, Electrolyte, and Acid-Base Balance.

Fluid management

1. Vital signs and hemodynamics: Assess vital signs and central

pressures from hemodynamic monitoring at least hourly. Persistent
tachycardia may signal hypovolemia, fever, or decompensation.
Fever may be related to infection or cerebral edema.

2. Dysrhythmias: Result from electrolyte imbalances secondary to

diarrhea, gastric suctioning, diuretic therapy, or long-standing
malnutrition (primarily seen in patients with CLF).

3. Altered vascular responsiveness: Support hyperdynamic

circulation, remembering hemodynamic values are deceiving. SVR
may not be increased in patients with hypovolemic hepatic failure.
A “normal” CO value may actually be too low. Monitor SVO2 as
possible to evaluate the adequacy of tissue oxygenation.

4. Maintain hydration: Be alert to urine output less than 0.5

mL/kg/h for 2 consecutive hours and body weight changes. Weigh
daily at the same time, in the same clothing, using the same scale
and method. Weight loss should not exceed 0.5 kg/d. If the patient
is on a ventilator and/or unable to get out of bed to be weighed, a
bed scale should be used. Measure or estimate other sources of fluid
loss. Consider cautious increases in fluid intake (e.g., 50 to 100
mL/h). Reevaluate volume status frequently, using extreme caution
if administering potent diuretics, which may precipitate
encephalopathy or renal insufficiency from rapid fluid and
electrolyte changes.

5. Decreasing oncotic pressure: Consult the advanced practice

1815
provider if serum albumin and total protein are trending
downward.

Cerebral Edema Management; Electrolyte Management;

Fluid Management; Electrolyte Management: Hypokalemia;
Electrolyte Management: Hyponatremia.

Excess fluid volume 

related to significant third-spaced fluids resulting in total body weight
gain.
Goals/Outcomes: Within 48 hours of this diagnosis, the patient
becomes normovolemic, as evidenced by CVP 2 to 6 mm Hg,
PAWP 6 to 12 mm Hg, HR 60 to 100 bpm, RR 12 to 20 breaths/min
with normal depth and pattern, decreasing or stable abdominal
girth, and absence of crackles, edema, uncomfortable ascites, and
other clinical indicators of fluid volume excess. The goals of
improvement for patients who are extremely ill are adjusted
according to the predicted best values the patient can achieve with
their level of organ impairment.
Risk Control: Fluid Volume Deficit, Fluid Balance, Fluid
Status, Electrolyte, and Acid-Base Balance.

Hemodynamic regulation

1. Vital sign and hemodynamics considerations: Monitor and record

vital signs and central pressures from hemodynamic monitoring at
least hourly. Measure more frequently if the patient is undergoing
ultrafiltration or other continuous renal replacement therapy and
immediately after ventriculoperitoneal shunt surgery. Consult the
advanced practice provider for CVP greater than 8 mm Hg and
PAWP greater than 12 mm Hg.

2. Peripheral edema: Note severity and location because this may

indicate fluid overload. Jugular vein distension (at a 45-degree HOB
elevation) and a CVP greater than 8 mm Hg may indicate fluid
overload or decreased CO.

Fluid management

1816
1. Fluid overload: Consult the advanced practice provider for fluid
overload: weight gain, presence of dyspnea, tachypnea, rhonchi,
orthopnea, basilar crackles that do not clear with coughing, labored
and/or shallow breathing, elevated BP, or S3 heart sound.

2. Restrict fluids: Use minimal amounts of fluids necessary to

administer IV medications and maintain IV catheter patency. When
fluids are restricted, offer mouth care and/or ice chips (included as
part of oral fluid intake measurement).

3. Intraabdominal hypertension: Carefully measure and record

abdominal girth daily. Abdominal girth measurements are subject
to error. Measure at the widest point with the patient in a tolerable
position, and mark this level for subsequent measurements with a
permanent marker. Consider using an IAP monitor, via a Foley
bladder catheter. Abdominal hypertension is a measurement
greater than 12 mm Hg and abdominal compartment syndrome is a
measurement greater than 20 mm Hg. Measure IAP hourly. Once a
trend is established, measurements can be every 4 hours. If the
patient complains of abdominal pain, measurements should revert
back to hourly. Measure the patient in the same position each time.

Electrolyte management: Hypernatremia

1. Hypernatremia and hypokalemia: Consult the advanced practice

provider for significantly abnormal serum electrolyte levels,
especially sodium and potassium.

2. Malfunctioning TIPS: Ensure proper functioning of TIPS in

patients after placement (see Box 9-11).

Box 9-11
NURSING CARE AFTER TRANSJUGULAR
INTRAHEPATIC PORTOSYSTEMIC SHUNT
OR PERITONEAL VENOUS SHUNT
PROCEDURE
Measure urinary output hourly and CVP every 1 to 2 hours.

1817
• Anticipate rapid fluid mobilization, as evidenced by increased
CVP and increased urinary output.

• Notify the advanced practice provider of abnormal CVP or lack of

diuresis. Failure to mobilize ascitic fluid may signal shunt
occlusion or failure.

• Consider use of IAP monitoring to assist with monitoring for IAP

increases or intraabdominal hypertension, which can signal a
blocked shunt.

• Report lessening of urinary output, because renal function may

diminish after this procedure.

Administer IV diuretics as prescribed; monitor K+ levels; and

administer K+ supplements as prescribed.

• Anticipate prescribed K+ supplements during the first 24 hours

after surgery.

• Be aware that furosemide (Lasix), which is frequently prescribed,

may cause K+ depletion. Likewise, the anticipated diuresis
depletes K+.

• Instruct and coach the patient in the use of an incentive

spirometer or similar hyperinflation device.

• Devices that create inspiratory resistance and encourage deep

inspiration promote negative inspiratory pressure and facilitate
flow of ascitic fluid.

• Encourage the patient to cough hourly.

• Apply elastic abdominal binder.

• This intervention facilitates the flow of ascitic fluid by increasing

the pressure gradient externally.

Monitor for evidence of variceal bleeding; report evidence of

bleeding to the advanced practice provider.

1818
• Expanded blood volume may increase variceal pressure, resulting
in bleeding. Bleeding is evidenced by a sudden decrease in
hematocrit (a mild dilutional decrease is anticipated in the
immediate postprocedural period), unexplained nausea,
lightheadedness, dark stools, or hematemesis.

Monitor for evidence of peritonitis, endocarditis, or other

infection.

• Infection occurs frequently. Anticipate antibiotic coverage during

the immediate postprocedural period.

Monitor for evidence of postshunt coagulopathy.

• See Ineffective Protection Care Plan in Hepatic Failure, Chapter 9,

for details.

• Monitor for other postshunt complications.

Assess for lower extremity edema. After some shunting

procedures, none of the venous blood passes through the liver and
protein end products are not completely detoxified.

• Monitor for development of hepatic encephalopathy or

worsening encephalopathy, because this is the number one side
effect from TIPS procedures.

CVP, Central venous pressure; IAP, intraabdominal pressure; IV,

intravenous; K+, potassium; PAP, pulmonary artery pressure; TIPS,
transjugular intrahepatic portosystemic shunt.

Imbalanced nutrition: Less than body requirements 

related to inability to digest food secondary to anorexia, nausea, and
medically prescribed dietary restrictions; decreased absorption of nutrients
secondary to decreased intestinal motility, altered portal blood flow,
decreased intestinal absorption of vitamins and minerals, altered protein
metabolism; and the inability of the diseased liver to use nutrients.

1819
 Goals/Outcomes: The patient has adequate nutrition, as
evidenced by a state of nitrogen balance as shown by daily fecal
excretion of 2 to 3 g of nitrogen and 4 to 20 g of urinary nitrogen,
thyroxine-binding prealbumin 200 to 300 µg/mL, and retinol-
binding protein 40 to 50 µg/mL. During protein catabolism
(proteolysis), nitrogen is excreted in the feces, urine, and blood. If
nitrogen balance is negative, the patient is using muscle for protein.
At least 5 g of feces needs to be collected with for the test. Urine
should be collected for 24 hours. Thyroxine-binding prealbumin
(measures protein-calorie malnutrition) and retinol-binding protein
(measures visceral protein mass) are serum tests. Blood glucose
levels remain within an acceptable range of 100 to 160 mg/dL.
Nutrition Status; Biochemical Measures.

Nutrition monitoring

1. Comprehensive nutrition assessment: Confer with the advanced

practice provider, dietitian, and pharmacist (if parenteral feedings
are necessary) to estimate the patient’s current nutrition and
metabolic needs, based on anthropometric data, creatinine
excretion, albumin, and transferrin, as well as presence of
encephalopathy, chronic hepatic disease, infection, and nutrition
status before hospitalization. For general information, see Nutrition
Support, Chapter 1.

2. Appropriate feeding modality: Consult the advanced practice

provider regarding administration of parenteral or enteral
nutrients. If insertion of a feeding tube becomes necessary, use
caution to minimize the risk of rupturing gastroesophageal varices.
If parenteral feedings are being administered, monitor IV site for
infection and other complications.

3. Food intake: Note, monitor, and record food/fluid ingested and

daily caloric intake.

4. Additional vitamins: Administer prescribed vitamin

supplements, particularly fat-soluble.

5. Favorite foods: Encourage food to be brought from home if

1820
desired by the patient and ensure it meets prescribed dietary
restrictions.

Energy management

1. Balance rest and activity: Encourage bed rest to reduce metabolic

demands on the liver and to promote hepatic regeneration. Increase
the patient’s activity levels gradually while the condition improves.

Hypoglycemia management

1. Blood glucose management: Monitor blood glucose levels every 1

to 2 hours initially, every 2 to 4 hours when stabilized or as
prescribed. Assess for clinical indicators of hypoglycemia: altered
mentation, irritability, diaphoresis, anxiety, weakness, and
tachycardia. Clinical signs of hypoglycemia can be confused with
hepatic encephalopathy. Validate clinical signs with blood glucose
levels. Administer D10 or D50 as prescribed for hypoglycemia.
Changes in blood glucose are anticipated with chronic liver disease
from changes in gluconeogenesis. Administer hypoglycemic agents
as prescribed for blood glucose levels greater than 180 mg/dL.

Impaired gas exchange 

related to altered oxygen supply secondary to arteriovenous shunting,
ventilation-perfusion mismatch, and diaphragmatic limitation associated
with ascites, hydrothorax, or central respiratory depression occurring with
encephalopathy.
Goals/Outcomes: Within 4 hours of this diagnosis, the patient has
adequate gas exchange, as evidenced by PaO2 greater than 80 mm
Hg, Paco2 less than 45 mm Hg, RR 12 to 20 breaths/min with normal
depth and pattern, oxygen saturation greater than 95% with or
without oxygen supplementation or mechanical ventilation, and
orientation to person, place, and time. The goals of improvement
for patients who are extremely ill are adjusted according to the
predicted best values the patient can achieve with their level of
organ impairment.
Respiratory Status: Gas Exchange; Respiratory Status:
Ventilation.

1821
 Level of consciousness is difficult to evaluate in the presence
of moderate to severe hepatic encephalopathy, and obtaining a
baseline level of consciousness is imperative.

Oxygen therapy

1. Respiratory management: Monitor and document RR at least

hourly. Note pattern, excursion, depth, and effort. Administer
supplemental oxygen as prescribed to enhance cerebral and hepatic
oxygenation. Continuous pulse oximetry should be in use. Monitor
ABGs and electrolytes to assess acid-base balance as needed.

2. Avoid lying flat: Maintain body positions that optimize

ventilation, given the abdomen is enlarged and impairing normal
movement of the diaphragm. Elevate HOB 30 degrees or higher,
depending on patient comfort and hemodynamic status.

3. Respiratory insufficiency: Consult the advanced practice provider

for abnormal PaO2, Paco2, and oxygen saturation.

Aspiration precautions

1. Possible aspiration: Assess the patient every 4 hours for

atelectasis, hydrothorax (e.g., diminished breath sounds, dullness to
percussion), and pulmonary infection. Consult the advanced
practice provider if findings suggest respiratory complications.

2. Prevent aspiration: Evaluate the obtunded patient for presence of

gag reflex. Consult the speech pathologist for swallowing
evaluation. Keep NPO with HOB elevated until the patient’s risk
for aspiration is fully evaluated. If severe, consult the advanced
practice provider regarding the need for endotracheal intubation.
Suction secretions from the mouth frequently; offer/assist with
frequent mouth care.

1822
Disturbed sensory perception 
related to endogenous chemical alteration (accumulation of ammonia or
other CNS toxins occurring with hepatic dysfunction), therapeutically
restricted environment, sleep deprivation, hypoxia, sensory overload
(noise, personnel) in ICU, and medication (side effects, toxic levels from
the inability of the liver to detoxify appropriately).
Goals/Outcomes: By the time of hospital discharge, the patient
exhibits stable personality patterns, age-appropriate behavior,
intact intellect appropriate for level of education, distinct speech,
and coordinated gross and fine motor movements. Handwriting is
legible, and psychometric test scores are improved from baseline
range.
Distorted Thought Self-Control; Information Processing;
Neurologic Status: Consciousness.

Fluid and electrolyte management

1. Prevent encephalopathy: Avoid or minimize precipitating factors

for hepatic encephalopathy (Box 9-12).

a. Support circadian rhythms: Modify the

environment to help keep circadian rhythms in
sync (e.g., keep lighting in room appropriate for
the time of day, correlate activities of daily living
to the correct time of day). Minimize unnecessary
noise, lights, and other environmental stimuli.

b. GI bleeding: Check gastric secretions, vomitus,

and stools for occult blood. Evaluate Hct and Hgb
for evidence of bleeding. Consult the advanced
practice provider for low values that deviate from
baseline. Anticipate mild to moderate anemia.

c. Ammonia: Evaluate serum ammonia levels

(normal levels are 40 to 110 mg/dL). Report

1823
 significant elevations from baseline. Ammonia
values and their measurement vary greatly and
do not always correlate directly with
encephalopathy.

d. Manage sources of mental confusion:

(1) Stressing the liver: Avoid use of conventional

and alternative drugs that are hepatotoxic (see
Box 9-10).

(2) Correct hypoxemia: Administer supplemental

oxygen as necessary (see Impaired Gas Exchange,
Chapter 9).

(3) Electrolyte imbalance: Manage potential sources

of electrolyte imbalance (e.g., diarrhea, vomiting,
occult bleeding).

e. Mental status changes: Evaluate patient for CNS

effects such as personality changes, childish
behavior, intellectual impairment, slurred speech,
ataxia, and asterixis.

f. Testing: Administer daily handwriting or

psychometric tests (if appropriate for patient’s
LOC) to evaluate mild or subclinical
encephalopathy. Report significant deterioration
in handwriting or in test scores.

g. Neomycin: Administer neomycin as prescribed to

reduce intestinal bacteria, which contribute to the

1824
 production of cerebral intoxicants. Monitor the
patient for evidence of ototoxic effects (i.e.,
decreased hearing) and nephrotoxic effects (e.g.,
urinary output less than 0.5 mL/kg/h, increased
creatinine levels) of neomycin use. Avoid
neomycin administration for patients with renal
insufficiency.

h. Injury protection: Protect the patient who is

confused or unconscious from injury.

a. Tube removal: If the patient is pulling out tubes,

discuss with family or significant other to see if
someone can stay around the clock, or if a sitter
can be provided. As a last resort, apply mittens
rather than wrist restraints.

b. Call light: Have call light within the patient’s

reach at all times.

c. Secure tubes: Tape all catheters and tubes

securely to prevent dislodgment.

2. Manage complications of encephalopathy: Consider the

possibility of seizures; have airway management equipment readily
available.

3. Intracranial pressure management: If ICP monitor is in place,

monitor ICP and cerebral perfusion pressure. For patients with
increased intracranial pressure (IICP), position carefully (HOB less
than 30 degrees) and avoid fluid overload, hypercarbia, and
hypoxemia. Administer mannitol and furosemide (Lasix) as

1825
prescribed. Sedation or coma induction may be indicated if cerebral
edema does not respond to the measures just mentioned.

4. Inform family/significant other(s): Keep family/significant other

abreast of all changes, and the possibility of complications and
deterioration.

Box 9-12
FACTORS THAT CONTRIBUTE TO
HEPATIC ENCEPHALOPATHY
Chronic factors
• Portal-systemic shunting (entry of portal blood into systemic
veins without being metabolized by the liver): May occur via
damaged liver, collateral vessels, or surgically created portacaval
anastomosis

• Dietary protein intake

• Intestinal bacteria

• Acid-base imbalance

• Progressive hepatic insufficiency

Precipitating factors
• Dehydration/electrolyte imbalance: May occur with overdiuresis,
diarrhea, vomiting, or other factors

• Excessive paracentesis

• Surgery in a patient with cirrhosis

• Excessive alcohol ingestion

• Sedatives/hypnotics

• Infection

1826
• Constipation

• Extrahepatic bile duct obstruction

• Acute hepatocellular damage

• Viral hepatitis

• Alcoholic hepatitis

• Drug/chemical reactions (see Box 9-10)

• Drug overdose (see Box 9-10)

Box 9-10
DRUGS AND SUBSTANCES WITH
HEPATOTOXIC POTENTIAL
• Acetaminophen

• Allopurinol

• Amiodarone

• Amoxicillin-clavulanate

• Amphetamines

• Ampicillin

• Antidepressants

• Carbamazepine

• Carbenicillin

• Carbon tetrachloride

• Chloramphenicol

1827
• Chlorpromazine

• Clindamycin

• Cocaine

• Dantrolene

• Dapsone

• Didanosine

• Diclofenac

• Disulfiram

• Efavirenz

• Ethanol

• Etoposide

• 5-Fluorouracil deoxyribonucleoside (FUDR-[intraarterial])

• Flutamide

• Gemtuzumab

• Halothane

• Hydrochlorothiazide

• Imipramine

• Isoflurane

• Isoniazid

• Ketoconazole

• Labetalol

1828
• Lisinopril

• Metformin

• Methotrexate

• Methyldopa

• Monoamine oxidase inhibitors

• Nefazodone

• Nicotinic acid

• Nonsteroidal antiinflammatory drugs

• Ofloxacin

• Oral contraceptives

• Penicillin

• Phenytoin

• Propylthiouracil

• Pyrazinamide

• Quetiapine

• Rifampin

• Rifampin-isoniazid

• Salicylates

• Statins

• Sulfonamides

• Tetracyclines (especially parenteral)

1829
• Tolcapone

• Trimethoprim-sulfamethoxazole

• Troglitazone

• Valproic acid

• Yellow phosphorus

• Numerous complementary and alternative medications

Environmental Management; Delirium Management;

Intracranial Pressure Monitoring.

Risk for infection 

related to inadequate secondary defenses (impaired reticuloendothelial
system phagocytic activity and portal-systemic shunting), multiple
invasive procedures, and chronic malnutrition in the patient with
cirrhosis.
Goals/Outcomes: The patient is free of infection, as evidenced by
normothermia, HR less than 100 bpm, RR less than 20 breaths/min,
negative culture results, WBC count less than 11,000/mm3, clear
urine, and clear, thin sputum. The goals of improvement for
patients who are extremely ill are adjusted according to the
predicted best values the patient can achieve with their level of
organ impairment.
Immune Status.

Infection protection

1. Vital signs: Monitor vital signs for evidence of infection (e.g.,

increases in temperature, heart, and RRs). Avoid measuring
temperatures rectally in the patient with rectal varices.

2. Signs of infection: If temperature or WBC elevation is sudden,

obtain specimens for blood, sputum, and urine cultures or from
other sites as prescribed. Consult the advanced practice provider

1830
for positive culture results.

• Underlying leukopenia: Normal or mildly elevated

leukocyte count may signify infection in patients
with hepatic failure because patients with chronic
liver disease often have leukopenia (WBC counts
less than 3000/mm3).

• Secretions: Evaluate secretions and drainage for

evidence of infection (e.g., sputum changes, cloudy
urine).

• Invasive sites: Evaluate IV, central line, and

paracentesis site(s) for evidence of infection
(erythema, warmth, unusual drainage). It is normal
for a paracentesis puncture site to have a small
amount of drainage immediately after the
procedure. Prolonged or foul-smelling drainage can
indicate infection. Use ascitic fluid dipsticks at the
bedside to test for infection.
3. Teaching: Teach significant others and visitors proper
handwashing technique, use reverse isolation personal protective
equipment (gown, mask, and gloves). Restrict visitors with
evidence of communicable disease.

Ineffective protection 
related to clotting anomaly, thrombocytopenia, itching, and disorientation.
Goals/Outcomes: The patient’s bleeding, if it occurs, is not
prolonged. The patient’s skin is not damaged from scratching. The
patient’s confusion (if present) and LOC will not lead to injury (see
Alterations in Consciousness, Chapter 1).
Blood Coagulation.

1831
Bleeding precautions

1. Intramuscular injections: Avoid giving intramuscular injections.

If they are necessary, use small-gauge needles and maintain firm
pressure over injection sites for several minutes. Avoid massaging
intramuscular injection sites.

2. Hold pressure: Maintain pressure for several minutes over

venipuncture sites. Inform laboratory personnel of the patient’s
bleeding tendencies.

3. Avoid arterial punctures: If it is necessary to obtain ABG values,

consult the advanced practice provider regarding use of an
indwelling arterial line. If this is not possible, be certain to maintain
pressure over the arterial puncture site and elevation for at least 10
minutes.

4. Blood clotting: Monitor PT/INR levels and platelet counts daily.

Consult the physician for significant prolongation of the PT or for
significant reduction in the platelet count.

5. Bleeding: Report bleeding to the advanced practice provider.

Note oral and nasal mucosal bleeding and ecchymotic areas, and
test stools, emesis, urine, and gastric drainage for occult blood.

6. Avoid trauma: Use electric rather than safety razor for patient
shaving. Provide soft-bristle toothbrush or sponge-tipped
applicator and mouthwash for oral hygiene. Avoid indwelling,
large-bore gastric drainage tubes if possible, because they may
irritate gastric mucosa or varices, causing bleeding to occur.

7. Manage bleeding: Administer fresh-frozen plasma and platelets

as prescribed. Monitor carefully for fluid volume overload (see
Excess Fluid Volume, Chapter 9). Administer vitamin K as
prescribed.

8. Postshunt coagulopathy: A postshunt coagulopathy may develop

in some patients after peritoneal-venous shunt surgery.

9. Disseminated intravascular coagulation: If fibrin degradation

1832
products are present in the blood and thrombocytopenia is
significant, the patient may have DIC (see Bleeding and Thrombotic
Disorders: Disseminated Intravascular Coagulation, Chapter 10).

Ineffective tissue perfusion: Renal 

related to risk of diminished arterial flow secondary to increased
preglomerular vascular resistance.
Goals/Outcomes: The patient has adequate renal perfusion, as
evidenced by urinary output greater than 0.5 mL/kg/h.
Circulatory Status.

Fluid/electrolyte management

1. Hyponatremia: Consult the advanced practice provider for serum

sodium less than 120 mEq/L and urine sodium less than 10 mEq/L,
associated with the development of HRS.

2. Renal insufficiency: Consult the advanced practice provider for

significant increases in creatinine and potassium values. BUN level
is not an accurate indicator of renal function, especially in the
patient with hepatic failure, because alterations in hepatic function
can cause decreased BUN values, and GI bleeding results in
increased BUN values.

3. Sodium management: Minimize infusion of sodium-containing

fluids because they contribute to ascites and peripheral edema and
may potentiate functional renal failure.

4. Phosphates: Report hypophosphatemia (mental confusion,

metabolic acidosis, anorexia, cardiac dysrhythmias, hemolytic
anemia, lethargy, and bone pain) to the advanced practice provider.

5. Magnesium: Report hypomagnesemia (muscle weakness, nausea,

vomiting, tremors, tetany, and lethargy) to the advanced practice
provider.

6. For additional information, see nursing diagnoses and

interventions in Acute Renal Failure, Chapter 6, and Fluid and
Electrolyte Disturbances, Chapter 1.

1833
Impaired tissue integrity 
related to chemical irritants (bile salts), impaired mobility, and fluid excess
(tissue edema).
Goals/Outcomes: The patient’s tissue remains intact; pruritus is
relieved or reduced within 12 hours of this diagnosis.
Comfort.

Skin surveillance

1. Keep skin smooth: Bathe the patient with a non–soap cleanser.

Apply an unscented, non–alcohol-containing lotion while skin is
still moist.

2. Prevent scratching: If the patient is confused or obtunded, place

the hands in soft gloves or mitts to minimize damage from
scratching, and keep nails short.

3. Reduce itching: Administer cholestyramine (e.g., Questran,

LoCholest, Colestid) as prescribed to reduce bile acids in the serum
and skin, and thereby relieve itching. Avoid administration of other
oral medications within 2 hours of cholestyramine administration
because they may bind with it in the intestine and reduce its
absorption.

4. Initiate pressure ulcer prevention:

• Use a low-pressure, pressure-reduction, or pressure-

redistribution (low air lost) mattress to minimize
pressure on fragile tissues.

• When moving the patient, avoid applying shearing

forces to skin. Avoid wrinkled sheets, clothing, and
pads under the patient. Keep sheets, clothing, and
pads from bunching against the patient’s skin.
Score the patient’s pressure ulcer risk and monitor
skin integrity.

1834
5. Prevent skin damage:

• Dry skin well after morning care. Provide adequate

lotion to skin, avoid massaging it in deeply, and rub
gently.

• Use appropriate tape or dressings (i.e., SorbaView,

Tegaderm) for skin condition. If possible, use gauze
to secure a dressing or IV line, and tape over the
gauze to prevent it from unwrapping.

Deficient knowledge 
related to lack of exposure to healthcare information; cognitive limitation
secondary to hepatic encephalopathy.
Goals/Outcomes: The patient/family/significant other states signs
and symptoms of early hepatic encephalopathy, importance of
medical follow-up, understanding of disease state, and how to keep
it stabilized (i.e., alcohol/drug treatment programs, proper diet,
proper infection control methods, taking prescribed medications).
Knowledge: Disease Process; Knowledge: Diet; Knowledge:
Medication; Knowledge: Substance Use Control, Risk Control Drug
Use, Risk Control Alcohol Use.

Teaching: Disease process

1. Emphasize the basics: Stress the importance of sufficient rest and

adherence to prescribed diet.

2. If hepatic failure is related to hepatitis B virus (HBV) infection:

a. HBV prophylaxis: Should be considered for

sexual partners and household members with
possible exposure to HBV (e.g., those who

1835
 unknowingly shared a toothbrush or razor).

b. Prevent transmission: Teach the patient and

exposure contacts practices that reduce the risk of
exposure (e.g., condom use, having own personal
grooming items). Prescreening for the presence of
hepatitis B (HB) antibodies is encouraged if it
does not delay treatment for greater than 14 days
after last exposure.

c. Hepatitis B immune globulin (HBIG): A dose of

HBIG is recommended immediately for sexual
contacts and household contacts with possible
blood and body fluid exposure. A second
administration of HBIG vaccine should follow 1
month later.

d. HB vaccination: The HB vaccine series should be

initiated for sexual and household contacts at
risk. The first and second vaccines can be given at
the same time the two HBIG vaccines are given.
Make sure both vaccines are given in separate
areas. The HB vaccines are to be given via
intramuscular injection in the deltoid muscle
only. Stress the importance of not sharing
intimate items (e.g., razors, toothbrush, nail
clippers).

3. If hepatic failure is related to hepatitis C virus (HCV): No

prophylaxis is available to exposed persons. Therefore, baseline
hepatitis C (HC) antibodies should be measured, and 1 month later
a second sample should be drawn and tested. Based on results, an

1836
infectious disease consult may be indicated, along with possible
treatment. It is important to note, however, that those with sexual
exposure have less than a 5% chance of seroconversion. Those with
exposure to blood, particularly through hollow-bore needles, have
the greatest chance of seroconversion.

• HC evolving evidence: The face of HCV treatment is

changing. Approximately 40% of transplants in the
United States are attributable to ESLD secondary to
HCV. The U.S. Centers for Disease Control and
Prevention has recommended that all persons born
between 1945 and 1965 be tested for HCV given
that this group contains the highest number of
persons infected. Having medications with minimal
side effects, shorter treatment courses make getting
more people treated appealing before they reach a
point of cirrhosis and declining liver function
leading to ESLD, and eventual liver transplantation.
HCV is an RNA flavivirus of the Hepacivirus genus.
There are six confirmed genotypes (1 through 6),
with genotype 1 the most difficult to treat and the
most prevalent in the United States. In 2011, the
FDA approved the first direct-acting HCV antivirals
to be used in combination with pegylated interferon
(PEG) and ribavirin (RBV). These first-generation
direct-acting antivirals (boceprevir and telaprevir)
increased treatment response rates when using PEG
plus RBV alone from 50% for genotype 1 HCV
infection to 75% when boceprevir or telaprevir were
added to the PEG plus RBV combination. In 2013,
the second generation of direct-acting antivirals was
approved by the FDA. Sofosbuvir (SOF) inhibits the

1837
 HCV NS5B RNA-dependent RNA polymerase. The
combination of SOF plus RBV has been shown to be
effective against multiple genotypes without PEG
use and thereby decreases numerous side effects,
including severe effects. Response rates are nearly
100% in patients with genotypes 2 and 3 HCV using
an oral regimen, and greater than 90% in patients
with genotype 1 HCV. Simeprevir, a second-
generation protease inhibitor developed to treat
patients with genotype 1, binds to its target
differently than boceprevir or telaprevir. Response
rates are in the 75% to 80% range in combination
with PEG plus RBV. Other treatments are in various
stages of development including NS3 protease
inhibitors, NS4B inhibitors, NS5A inhibitors, NS5B
nucleoside inhibitors, and NS5B nonnucleoside
inhibitors. Drugs being developed to attack other
host targets include cyclophilin A inhibitors,
MiR122 inhibitors, and entry inhibitors.

4. Substance abuse: Inform the patient about the availability of

alcohol treatment and drug treatment programs if alcohol- and
drug-related hepatic failure has occurred. Explain the availability of
support groups (i.e., Alcoholics Anonymous, Al-Anon) for patients
and family members when hepatic failure is related to chronic
alcohol ingestion.

5. Over-the-counter medications: Caution about the importance of

avoiding over-the-counter medications without first consulting a
physician. Advise the patient to confer with a physician regarding
use of NSAIDs, aspirin, and other medications that contain
salicylates for minor aches and pains after hospital discharge.

6. Signs and symptoms of infection: fever; unusual drainage from

1838
paracentesis or other invasive procedure sites; warmth and
erythema surrounding the invasive sites; or abdominal pain. Have
the patient demonstrate the technique for measuring oral
temperature with type of thermometer used at home.

7. Signs and symptoms of unusual bleeding: Prolonged mucosal

bleeding, very large or painful bruises, and dark stools. Caution
that if possible, major dental procedures should be postponed until
bleeding times normalize.

8. Sodium and ascites: Inform the patient about sodium restriction if

ascites developed during the course of the illness.

9. Protein and encephalopathy: Advise protein restriction if the

patient has residual or chronic encephalopathy. Instruct the patient
to avoid constipation by increasing bulk in the diet or by using
agents prescribed by the physician or advanced practice provider.

10. Alcohol use: Caution about the necessity of alcohol cessation for
at least several months after complete recovery from the acute
episode. After full recovery, one or two glasses of beer or wine a
week are usually allowed if hepatic failure was not related to
alcoholism or alcohol ingestion.

11. Weight monitoring: Instruct the patient to weigh himself or

herself daily and to report weight loss or gain of greater than 5 lb.

Substance Use Treatment: Drug Withdrawal; Substance Use

Treatment: Overdose; Substance Use Treatment: Alcohol
Withdrawal, Medication Management, Nutrition Management.

Risk for injury 

related to invasive procedures
Goals/Outcomes: The patient does not sustain an injury related
to liver biopsy, ICP monitoring, or other invasive procedures.
Knowledge Health Promotion; Risk Control: Infection.

Teaching individual

1839
1. Liver biopsy: Fully prepare the patient emotionally and
physically for the procedure.

2. Possible bleeding: Monitor the patient closely after the procedure;

observe changes in vital signs that correlate with observations of
patient.

• Monitor dressing over puncture wounds for

bleeding. Document amount, frequency of dressing
changes, what types of dressings are applied, what
the drainage looks like/smells like (if applicable),
and what the wound looks like.
3. Infection: Monitor for fever.

4. Encephalopathic patients: Ensure the airway is clear, and

reassure the patient someone will accompany and remain with
them before, during, and after the procedure.

Additional nursing diagnoses

As appropriate, see the following topics for additional nursing
diagnoses and interventions in Chapters 1 and 2: Nutrition Support,
Mechanical Ventilation, Prolonged Immobility, and Emotional and
Spiritual Support for the Patient and Significant Others.

Peritonitis
Pathophysiology
Peritonitis is an inflammation of the peritoneum and can be
classified as primary, secondary, or tertiary. Secondary peritonitis,
the most common form of peritonitis, is an inflammation of all or
part of the peritoneal cavity caused by diffuse microbial
proliferation or chemical irritation from leakage of corrosive gastric
or intestinal contents into the peritoneum. Ruptured appendix,
leaky anastomoses from weight loss surgery (e.g., Roux-en-Y,

1840
gastric bypass), perforated peptic ulcer, bowel rupture related to
ulcerative colitis or Crohn disease, pancreatitis, abdominal trauma,
and ruptured abdominal abscesses are among the many etiologic
factors associated with secondary peritonitis. Indwelling tubes and
catheters, such as those used for postoperative drainage and
peritoneal dialysis, are foreign bodies that compromise peritoneal
integrity and permit the entry of infective organisms that can
trigger peritonitis. Peritonitis is a leading cause of morbidity in
patients with kidney failure who are treated with continuous
ambulatory peritoneal dialysis (CAPD). CAPD-associated
peritonitis is caused by bacteria (Staphylococcus epidermidis and other
skin flora) most often, entering the abdominal cavity by the dialysis
catheter site.
Primary peritonitis is a bacterial infection of the serous
membrane lining the abdominal cavity that occurs spontaneously
without any apparent source of contamination, such as bowel
perforation. The most common etiology of primary peritonitis is
spontaneous bacterial peritonitis, which occurs most commonly in
patients with cirrhosis of the liver with ascites. Bacterial seeding of
ascitic fluid is believed to result from the translocation of enteric
bacteria across the gut wall or mesenteric lymphatic vessels and is
associated with a high mortality rate. Tertiary peritonitis represents
persistent or recurrent infection following an apparently
successfully treated episode of primary spontaneous bacterial
peritonitis or secondary peritonitis. Tuberculosis-related peritonitis
is rare in the United States with the exception of patients with
acquired immunodeficiency syndrome (AIDS), who are frequently
infected with multidrug-resistant strains of the bacillus.
Regardless of the initiating factor, the inflammatory process is
similar. Initial manifestations are triggered by histamine release and
include hyperemia, edema, and vascular congestion. Fluid shifts
from intravascular to interstitial spaces creating hypovolemia as a
result of increased vascular permeability caused by inflammatory
mediators. The circulating blood volume is depleted and
hypovolemic shock may ensue. The transudated fluid within the
interstitium contains high levels of fibrinogen and thromboplastin.
The fibrinogen is converted to fibrin by the thromboplastin. Under
normal conditions, the healthy peritoneum is naturally fibrinolytic,

1841
and can block fibrin formation. When the peritoneum is weakened
or injured, fibrinolysis is hampered and fibrin adheres to the
damaged area and forms a barrier that harbors and protects
bacteria from the normal immune responses, resulting in pockets of
infection and abscess formation. In most cases, the fibrin deposits
dissolve. The continued presence of fibrin can lead to adhesions
and potentially bowel obstruction. With severe inflammation,
intraabdominal sepsis may develop.

Gastrointestinal assessment: Peritonitis

Goal of system assessment
Identify early findings of peritoneal irritation.

History and risk factors

Inflammatory processes such as diverticulitis, appendicitis, or
Crohn’s disease; obstructive events in the small bowel and colon;
vascular events such as ischemic colitis, mesenteric thrombosis, or
embolic phenomena; blunt or penetrating trauma, especially to
hollow viscera; severe hepatobiliary disease; and CAPD. General
risk factors include those related to poor tissue healing and
infection (e.g., advanced age, diabetes, and vascular disease,
advanced liver disease, malignancy, malnutrition, and debilitation).
Some patients with severe peritonitis may present in overt septic
shock.

Vital sign assessment

• Fever of greater than 38° C (100° F to 101° F) is present in most
cases.

• Tachypnea and tachycardia result from increased metabolic

demands.

• Hypotension may be present resulting from dehydration from

vomiting, fever, and third-space losses.

• Hypothermia may be present if the peritonitis advances to severe

1842
 sepsis.

Abdominal pain
• Abdominal pain is the hallmark of peritonitis and may be severe,
causing the patient to maintain a fetal position and resist any
movement that aggravates the pain. The onset can be sudden or
insidious, with the location varying according to the underlying
pathology.

• Nausea, vomiting, anorexia, diarrhea, and other changes in bowel

habits may also be present and are reflective of GI dysfunction.

• Anorexia and nausea may precede the development of abdominal

pain.

• Abdominal pain can be reduced or even absent in older adults

resulting in missed diagnosis.

Observation
• Occasionally, mild to moderate ascites is observed, depending on
the cause of the peritonitis.

• RR is rapid and the patient usually has a shallow ventilatory

pattern to minimize abdominal movement and pain.

• Restlessness and confusion occur because of impaired cerebral

perfusion.

Auscultation
• Auscultation of all four quadrants usually reveals diminished or
absent bowel sounds. The complete absence of bowel sounds
suggests an ileus—a frequent complication of peritonitis.

• Breath sounds are diminished as a result of shallow respiratory

pattern.

1843
Palpation
• Palpation of the abdomen elicits tympany and tenderness that can
be generalized or localized, depending on the nature and extent
of infection.

• Rebound tenderness, guarding, and involuntary rigidity may also

be present.

• The abdomen may feel firm and boardlike. Occasionally, the

abdominal examination reveals an inflammatory mass.

• The abdomen is often distended, a finding that reflects a

generalized ileus and may not be present if the infection is well
localized.

Nutrition assessment
• Evidence of malnutrition will be noted in the presence of chronic
liver or renal disease.

Screening labwork
• Abdominal paracentesis: Ascitic fluid for cell count, Gram stain,
and culture.

• CBC: May reveal anemia and leukocytosis.

• LFTs: Elevated.

• Serum chemistry may indicate kidney dysfunction and electrolyte

imbalances.

• Radiologic tests: Abdominal radiograph may reveal free air,

abdominal CT of the abdomen.

Hemodynamic measurements
• Hypovolemia with marked tachycardia, hypotension, decreased
MAP, and decreased urine output may occur as a result of

1844
 massive fluid shifts from the intravascular space into the
abdominal interstitium and peritoneum and from vasodilation
caused by inflammatory mediators.

• Endotoxemic vasodilation is manifested as hypotension with a

widened pulse pressure and low CVP, with an initial increase in
HR.

• Persistent hypovolemia may result in a dangerously low MAP,

thus impairing renal, cardiac, and cerebral perfusion.

Diagnostic Tests for Peritonitis

Test Purpose Abnormal Findings

Blood Studies
Complete blood Assesses for bacterial infection Leukocytosis (≥11,000 cells/mm3) with a shift
count with and anemia. to the left or elevation of immature
differential: neutrophils (bands).
Hemoglobin
Hematocrit
Red blood cell
count
White blood cell
(WBC) count
Serum Assesses for electrolyte Elevated amylase and lipase with pancreatic
chemistry: imbalances and organ involvement (acute pancreatitis).
Blood urea involvement. Elevated BUN and creatinine with renal
nitrogen dysfunction.
(BUN) Elevated bilirubin with gallbladder disease.
Creatinine Elevated CO2 with low Cl– reflects metabolic
CO2 alkalosis. Electrolyte losses, especially
Glucose potassium with vomiting and diarrhea.
Serum chloride C-Reactive protein elevation indicates
Serum inflammation.
potassium Elevated lactate level may indicate
Serum sodium sepsis/systemic inflammatory response
Total bilirubin syndrome.
Serum amylase
C-Reactive
protein
Lactic
acid/lactate
Diagnostic
Paracentesis
Peritoneal Fluid
Analysis
Peritoneal This analysis is useful in WBC count ≥250 cells/mm3 with >50%
neutrophil count confirming the diagnosis of polymorphonuclear leukocytes is an
bacterial peritonitis and assists indication to begin antibiotic therapy.
in driving therapy.

1845
Peritoneal total Useful in confirming the Total protein >1 g/dL; ascetic low-density
protein and diagnosis of bacterial lipoprotein greater than serum low-density
lactate peritonitis. lipoprotein.
dehydrogenase
levels
Peritoneal Useful in confirming the Decreased peritoneal fluid glucose level (<50
glucose level diagnosis of bacterial mg/dL).
peritonitis.

Gram stain and Identifies causative Spontaneous bacterial peritonitis:

culture organism(s) to begin proper Monomicrobial infection; Escherichia coli,
empirical or specific antibiotic Klebsiella pneumoniae, and Streptococcus
therapy. pneumoniae are most common.
Secondary peritonitis: Multiple organisms
will be present in peritoneal fluid Gram
stain and culture.
Radiologic
Procedures
Abdominal Identifies the presence of Free air is present in most cases of
radiograph dilated bowel and free air. perforation.
Plain films
Abdominal Assesses for an Abscess or mass may be identified.
computed intraabdominal source of
tomography infection.
(CT) scan
Ultrasonography Useful in locating small Loculated fluid, abscess, bile duct dilation,
amounts of fluid, as well as in and pancreatitis may be identified.
differentiating fluid collections
in the abdomen.

Hematologic tests
Leukocytosis will be present. A low total WBC count may indicate
an exhausted bone marrow, with a poor prognosis. Initially, the
Hgb and Hct values may be increased because of
hemoconcentration, but they will decrease to baseline levels when
normal intravascular volume is restored.

Blood chemistry tests

Depending on the severity of the patient’s condition, blood
electrolyte levels may be abnormal. If vomiting is present,
metabolic alkalosis is expected. Serum albumin levels are often
decreased as a result of increased capillary permeability and
leakage. The underlying disease process affects chemistry tests (e.g.,
patients with pancreatitis, gallbladder disorders, and renal failure).
Renal failure is a common complication of peritonitis and a major
cause of death.

1846
Radiologic procedures
The abdominal radiograph test usually reveals dilation of the large
and small bowel, with edema of the small bowel wall. Free air in
the abdomen suggests visceral perforation. With abdominal CT,
abscesses can be visualized and sometimes drained during the
procedure, thus avoiding surgery. Free fluid in the abdomen on
ultrasound suggests hemorrhage or ascites.

Nuclear medicine scans

(Gallium, Indium, Technetium) are useful for persistent fever
despite adequate antibiotic coverage and negative CT findings.

Diagnostic paracentesis
Abdominal paracentesis involves the insertion of a catheter or
trocar into the abdomen to obtain a specimen. Sterile saline is
infused through the catheter, and the return fluid is analyzed for
RBC, WBC, and bacteria content. If ascites is present, it may not be
necessary to infuse saline because fluid can be removed directly for
analysis. Paracentesis may be repeated 48 hours after the initiation
of treatment to assess patient response. Multiple organisms on
peritoneal or ascitic fluid Gram stain or culture are diagnostic of
secondary peritonitis, whereas spontaneous bacterial peritonitis is
caused by monomicrobial infection.

Collaborative management
Management should be geared toward controlling the infectious
source, eliminating bacteria and toxins, modulating the
inflammatory process, and preventing organ system failure.
Patients should be cared for in an intensive care setting, even if they
do not appear critically ill initially.

Care priorities
Care priorities begin with volume resuscitation, electrolyte
replacement, and empirical antibiotic coverage. Medical, nursing,
interventional, and surgical therapies should be complementary
involving hemodynamic management, pulmonary support, and

1847
renal replacement therapy, and nutrition and metabolic support.

1. Correct fluid and electrolyte imbalances

Significant intravascular volume depletion may occur with
peritonitis. In patients who are severely ill, fluid replacement
should be guided by invasive hemodynamic monitoring. In most
cases, crystalloids are used initially. If there is evidence of
decreased intravascular proteins, colloids such as albumin are
indicated. The use of IV albumin has also been shown to reduce the
incidence of renal failure. If peritonitis is complicated by
hemorrhage, pRBCs may be given. Electrolyte replacement,
typically potassium, is implemented according to laboratory
findings. (See Systemic Inflammatory Response Syndrome, Sepsis,
Septic Shock, and Multiple Organ Dysfunction Syndrome, Chapter
11, for additional information.)

2. Control peritoneal infection with antimicrobial therapy

Initiate empirical broad-spectrum parenteral antibiotic therapy
early for all suspected cases of peritonitis. Antibiotic therapy should
be started as soon as the diagnosis is suspected. Suspicion is
identified by clinical findings more so than culture results because a
large percentage of patients will exhibit negative culture results.
Patients with culture-negative results must also receive antibiotic
therapy because without it, severe sepsis and death may follow.

• Third-generation cephalosporins are recommended in cases of

spontaneous bacterial peritonitis initially, then, tailor therapy in
conformity with cultures. For secondary and tertiary bacterial
peritonitis, broad-spectrum gram-negative and anaerobic
coverage should be initiated, followed by definitive therapy
based on culture sensitivities.

• In severe hospital-acquired cases, imipenem, piperacillin-

tazobactam, and a combination of aminoglycoside and
metronidazole may be effective. Quinolones are also considered
effective therapy.

• The duration of antibiotic therapy must be individualized

1848
 according to the infectious source, infection severity, underlying
disease, and the patient’s response to therapy. Therapy for 5 to 10
days is sufficient for most patients.

• The administration of intraperitoneal antibiotics should be

considered over parenteral administration for patients with
peritoneal dialysis–associated peritonitis. Aminoglycoside
therapy should be avoided in patients with chronic liver disease
because of an increased risk of nephrotoxicity.

• Antimicrobial prophylaxis should be considered for

gastroduodenal procedures involving patients at high risk for
postoperative infections including risk factors such as
gastroduodenal perforation, decreased gastric motility, gastric
outlet obstruction, morbid obesity, and patients receiving acid-
suppression therapy. A single dose of cefazolin is recommended.

3. Control peritoneal infection with surgical procedure(s)

Surgical laparotomy is an important therapy in all cases of
peritonitis to remove the source of infection and prevent
reinfection. Surgical débridement allows for the removal of all
intraabdominal foreign material and nonviable tissue. Leaky
anastomoses are identified and repaired. If present, bowel
perforations and obstructions are corrected and abscesses are
drained.

• Laparoscopy: Laparoscopy is currently used for diagnosis and

determination of etiology. Laparoscopic procedures have become
common for some forms of peritonitis such as for the treatment of
peritonitis caused by uncomplicated appendicitis.

• Open wound management of the abdomen with scheduled

reoperations is often advocated for severe disease. Open-
abdomen technique may reduce the risk of abdominal
compartment syndrome, and allow for better management of
bowel edema and subsequent inflammatory changes in the
postoperative period. Disadvantages of open-technique include
alteration in respiratory mechanics and risk of abdominal
contamination with nosocomial pathogens.

1849
• Interventional therapies include percutaneous drainage of
abscesses and percutaneous and endoscopic stent placements.
Ultrasound- and CT-guided percutaneous drainage has been
shown to be efficacious and safe and preferred in some cases,
allowing for a delay in surgery until the acute process and sepsis
can be resolved.

4. Control pain resulting from peritoneal inflammation

The degree of discomfort caused by peritonitis varies greatly.
Opiate analgesics are used parenterally to ensure patient comfort
but are given cautiously to avoid compromise of abdominal and
respiratory function. These analgesics usually require frequent
administration, with the dose titrated for each individual.

5. Provide nutrition support

Nutrition support is crucial for healing and survival. GI function is
compromised and motility minimal or absent as a result of
inflammatory processes.

• A large-bore NG tube is inserted to reduce or prevent distension

caused by obstruction or ileus to reduce IAP. Placement of a
small-bore enteric tube (nasoduodenal or NJ tube) is done to
provide enteral (tube) feedings and administer medications.
Radiographic confirmation of correct placement should be done
for all enteric tubes before enteral or medication infusion. Oral
intake may be restricted until GI function is regained.

• Jejunal feeding should be initiated as soon as tolerated. Elemental

feedings can be administered with or without bowel sounds
present. More recent enteral feeding guidelines have challenged
the validity of older guidelines for feeding intolerance. Gastric
residual volumes exceeding 450 mL and absence of bowel sounds
are no longer absolute contraindications for feeding. Newer
feeding methods, such as “trickle feedings,” may be better
tolerated. If enteral feeding is not possible, TPN should be
initiated. (See Nutrition Support, Chapter 1.)

• When resumption of bowel sounds or passage of flatus signals

1850
 the return of GI motility, enteral nutrition with nonelemental
(conventional) tube feedings can begin.

6. Intraabdominal pressure monitoring

Peritonitis is a risk factor for IAH. IAH is defined as a pathologic
increase in IAP greater than 12 mm Hg and may result in
abdominal compartment syndrome. Abdominal compartment
syndrome is defined as a sustained IAP greater than 20 mm Hg. If
IAH is present, patient management should follow the medical
management algorithm of the World Society of the Abdominal
Compartment Syndrome (www.wsacs.org). (See Abdominal
Hypertension and Abdominal Compartment Syndrome, Chapter
11.)

Care plans for peritonitis

Deficient fluid volume 
related to active loss secondary to fluid sequestration within the
peritoneum.
Goals/Outcomes: Within 6 hours of diagnosis, the patient
becomes normovolemic, as evidenced by the following
measurements: MAP ≥65 mm Hg; HR 60 to 100 bpm; normal sinus
rhythm on ECG; CVP 2-6 mm Hg: superior vena cava oxygenation
(ScVO2) or mixed venous oxygen saturation (SVO2) 70% or 65%,
respectively; urinary output ≥0.5 mL/kg/h; warm extremities,
peripheral pulses greater than 2+ on a 0-to-4+ scale, brisk capillary
refill (less than 2 seconds); normalization of serum lactate;
orientation to time, place, and person; and stable weight.
Fluid Balance.

Fluid/electrolyte management

1. Monitor BP continuously with an arterial catheter. Be alert to

MAP decreases of greater than 10 mm Hg, which is indicative of
possible sepsis.

2. Monitor HR and ECG every 1 to 2 hours or more often if vital

signs are unstable. Be alert to increases in HR, which suggest

1851
hypovolemia. Usually, the ECG will show sinus tachycardia. In the
presence of hypokalemia caused by prolonged vomiting or gastric
suction, ECG may show ventricular ectopy, prominent U wave, and
depression of the ST segment.

Heart rate increases may be caused by fever, hypovolemia,

and vasodilation related to sepsis.

3. Maintain crystalloid therapy guided by hemodynamic and fluid

responsiveness measurements. Vasopressor therapy should target
an MAP of 65 mm Hg.

4. Echocardiography may be used to evaluate CO and ejection

fraction. Inotropic therapy may be added to assist CO in
conjunction with fluid replacement modalities.

5. Monitor BUN, creatinine, total protein, and albumin levels.

6. Albumin administration at 1 to 1.5 g/kg may be needed to replace

losses resulting from capillary leak.

7. Measure urinary output hourly. Be alert to output less than 0.5

mL/kg/h for 2 consecutive hours, which may signal intravascular
volume depletion. Consult the advanced practice provider and
increase fluid intake promptly if decreased urinary output is caused
by hypovolemia and hypoperfusion.

8. Monitor the patient for physical indicators of hypovolemia,

including cool extremities, capillary refill greater than 2 seconds,
decreased amplitude of peripheral pulses, and neurologic changes
such as restlessness and confusion.

9. Estimate ongoing fluid losses. Measure all drainage from tubes,

catheters, and drains. Note the frequency of dressing changes as a
result of saturation with fluid or blood. Weigh the patient daily,

1852
using the same scales and method. Compare 24-hour body fluid
output with 24-hour fluid intake, and record the difference.

10. Assess for signs of pulmonary edema resulting from aggressive

fluid replacement and increased capillary permeability caused by
inflammatory mediators.

Fluid Monitoring; Hemodynamic Regulation; Hypovolemia

Management; Invasive Hemodynamic Monitoring; Shock
Prevention; Dysrhythmia Management.

Risk for infection 

related to inadequate primary defenses (traumatized tissue, altered
perfusion), tissue destruction, and environmental exposure to pathogens.
Goals/Outcomes: Severe sepsis does not develop, as evidenced
by HR 60 to 100 bpm, RR 12 to 20 breaths/min; CVP 2-6 mm Hg:
ScVO2 ≥70% or SVO2 ≥65%; serum lactate less than 3 mmol/L; urinary
output ≥0.5 mL/kg/h; normothermia, negative culture results, and
orientation to time, place, and person. (See Sepsis, Chapter 11.)
Infection Severity.

Medication management

1. Administer empirical broad-spectrum parenteral (IV) antibiotics

within 1 hour of recognition of severe sepsis with or without septic
shock as recommended by the 2012 Surviving Sepsis Campaign.
Reschedule antibiotics if a dose is delayed for greater than 1 hour.
Recognize that failure to administer antibiotics on schedule may
result in inadequate drug blood levels and treatment failure.

a. Combination empirical antimicrobial therapy should be

administered as ordered.

b. Intraperitoneal antibiotics should be considered for patients with

peritoneal dialysis-associated peritonitis because the peritoneal
dialysis catheter provides immediate access to the peritoneum.

2. Administer norepinephrine as the first choice vasopressor to

maintain MAP ≥65 mm Hg. Norepinephrine preserves splanchnic

1853
blood flow. Vasopressin or epinephrine may be added as ordered.
Dopamine is not recommended except in highly selective patients
such as those with low risk for tachydysrhythmias or with absolute
or relative bradycardia according to the 2012 Surviving Sepsis
Campaign guidelines.

3. A trail of antibiotic cessation could be considered for the patient

with no defined infectious focus. Continued broad-spectrum
antibiotics in these patients may allow resistant organisms to
emerge.

Vital signs monitoring

1. Monitor for signs of tissue hypoperfusion: CVP less than 8 mm

Hg: ScVO2 less than 70% or SVO2 less than 65%; serum lactate ≥4
mmol/L; MAP less than 65 mmHg; urinary output ≥0.5 mL/kg/h.

2. Monitor fluid responsiveness measurements such as SPV, PPV,

and SVV when available. If SPV is greater than 5 mm Hg, PPV
greater than 13% to 15%, SVV greater than 13% to 15%, the patient
is deemed fluid responsive.

3. Monitor vital signs for evidence of severe sepsis: Increases in HR,

RR, and rectal or core temperature every 1 to 2 hours for increases.
Be aware that hypothermia may precede hyperthermia in some
patients. Hypothermia with leukopenia is a poor prognostic
marker.

4. Also note that older adults and those who are

immunocompromised may not demonstrate a fever, even with
severe sepsis.

5. If the patient has a sudden temperature elevation, obtain culture

specimens of blood, sputum, urine, and other sites as prescribed.
Monitor culture reports and report positive findings promptly.

Wound care

1. To minimize microbial growth, facilitate drainage of pus, GI

secretions, old blood, necrotic tissue, foreign material such as feces,

1854
and other body fluids from wounds.

2. Evaluate wounds for evidence of infection (e.g., erythema,

warmth, swelling, unusual drainage). Culture any unusual
drainage.

3. Evaluate the patient’s orientation to time, place, and person and

LOC every 2 to 4 hours. Document and report significant deviations
from baseline.

Hemodynamic Regulation; Temperature Regulation;

Intravenous (IV) Therapy.
See Systemic Inflammatory Response Syndrome, Sepsis, Septic
Shock, and Multiple Organ Dysfunction Syndrome, Chapter 11, for
additional information.

Hyperthermia 
related to infectious process, increased metabolic rate, and dehydration
secondary to peritonitis.
Goals/Outcomes: The patient’s temperature remains within
acceptable limits (36° C to 38.9° C [97° F to 102° F]) or returns to
acceptable limits within 4 to 6 hours of diagnosis. An open airway
is secured in the event of hyperthermic seizures.
Thermoregulation.

Temperature regulation

1. Monitor rectal or core temperature every 1 to 2 hours.

2. If a hypothermia blanket is required, perform the following

interventions for the patient:

a. Protect skin in contact with the blanket by

placing a sheet between the blanket and patient.

b. Inspect the skin every 2 hours for evidence of

tissue damage caused by local vasoconstriction
and massage to promote circulation and

1855
 minimize tissue damage.

c. Check body temperature at frequent intervals to

ensure that shivering does not occur, which
increases metabolic demand.
3. If high fever (i.e., greater than 38.9° C [102° F]) ensues, tepid
baths may be helpful in reducing the fever.

4. Administer antipyretics as prescribed.

5. An appropriate-size oral airway and suction equipment is kept in

the patient’s room for use in the event of seizure activity.

Fever Treatment; Vital Signs Monitoring.

Impaired tissue integrity 

related to tissue destruction; surgical intervention with exposure to
environmental pathogens.
Goals/Outcomes: By hospital discharge, the patient exhibits no
further GI tissue destruction, as evidenced by reduction in pain,
return of bowel sounds and bowel function, and wound healing.
Tissue Integrity: Skin and Mucous Membranes.

Infection control

1. See Medication Management for Risk of Infection.

2. Adjust antibiotic therapy specific to culture sensitivity reports.

3. Monitor renal function for signs of nephrotoxicity secondary to

antibiotic therapy.

4. Discuss repeat of paracentesis 48 to 72 hours following the

initiation of antibiotic therapy to evaluate effectiveness of therapy.

Wound care

1. Monitor for surgical site infection (warmth, tenderness, and

1856
purulent drainage).

2. If surgical wound is open:

a. Consider a negative pressure wound device,

which applies localized negative pressure
directly to the wound. This removes fluid that
causes swelling, increases blood flow, and
accelerates granulation tissue formation.

b. Maintain dressing membrane, ensure adequacy

of drainage, and monitor for granulation tissue
formation.

c. Avoid wet-to-dry dressings because they create a

lack of a physical barrier to bacterial entry;
prompt tissue cooling in wounds, which heal best
when kept normothermic; disrupt angiogenesis;
and prolong inflammation.

3. Record volume and characteristics of drainage and obtain

specimens as needed.

4. Assess for overall improvement within 24 to 72 hours. Failure to

progress indicates recurrent, persistent, or new infectious focus.

Acute pain 
related to biological or chemical agents causing injury to the peritoneum
and intraperitoneal organs.
Goals/Outcomes: Within 2 hours of diagnosis, the patient’s
subjective evaluation of discomfort improves, as documented by a
pain scale. Nonverbal indicators of discomfort, such as grimacing,
are absent.
Pain Control.

1857
Analgesic administration

1. Monitor the patient for the presence of discomfort. Use a pain

scale to rate discomfort.

2. Administer parenteral analgesics promptly and consistently,

before pain becomes severe, to help decrease anxiety, which
contributes to the severity of pain. Rate the degree of pain relief
using the pain scale.

3. Position the patient to optimize comfort. Many patients with

severe abdominal pain find a dorsal recumbent or lateral decubitus
bent-knee position more comfortable than other positions.

4. Monitor for diminished RR and depth and decreased LOC hourly

if large amounts of opiates are required to control the pain. Many
opiates also cause vasodilation and can result in serious
hypotension, especially in patients with volume depletion. Opiate
analgesics also decrease GI motility and may delay the return of
normal bowel function.

5. Monitor HR and BP every 1 to 2 hours or more frequently in

patients whose condition is unstable. Consult the advanced practice
provider for significant deviations.

6. Evaluate effectiveness of the medication on an ongoing basis. On

the basis of the patient’s clinical response, discuss dose and drug
manipulation with the physician.

7. Avoid administering analgesics to newly admitted patients

before they have been fully evaluated by a surgeon, because
analgesics can mask important diagnostic clues.

Pain Management; Environmental Management: Comfort;

Coping Enhancement; Simple Guided Imagery; Respiratory
Monitoring.

Imbalanced nutrition, less than body requirements 

related to decreased intake secondary to impaired GI function.

1858
 Goals/Outcomes: The patient maintains baseline body weight,
and nitrogen tests show a state of nitrogen balance within 5 to 7
days of this diagnosis.
Nutrition Status: Food and Fluid Intake.

Nutrition management

1. Monitor bowel sounds every 1 to 4 h; report significant changes

(i.e., sudden absence or return).

2. Maintain NPO status during the acute phase of peritonitis with

stomach decompression via an NG tube.

3. Initiate postpyloric (jejunal) elemental feedings within the first 24

to 48 hours. Gradually increase enteral intake when gastric motility
returns.

4. Consider TPN if jejunal feedings are contraindicated or not

tolerated.

5. If abdominal distension is noted, initiate IAP monitoring.

Distention can signal complications such as ileus, ascites, or IAH.

6. Administer histamine H2-receptor antagonists as prescribed to

reduce corrosiveness of gastric acid and prevent complications such
as stress ulcers.

7. Administer prescribed antiemetic medications as indicated.

8. Ensure that NG and enteral tubes are functioning properly.

Evaluate characteristics of the drainage. Irrigate or reposition tubes
as necessary.

Nutrition Monitoring; Gastrointestinal Intubation; Total

Parenteral Nutrition (TPN) Administration; Enteral Tube Feeding;
Aspiration Precautions; Tube Care: Gastrointestinal.
For additional information, see Nutrition Support, Chapter 1.

Risk for intraabdominal hypertension 

related to intraabdominal inflammation

1859
 Goals/Outcomes: The patient displays no signs of increased IAPs
through discharge.
(See Abdominal Hypertension and Abdominal Compartment
Syndrome, Chapter 11.)

Additional nursing diagnoses

For other nursing diagnoses and interventions, see the following as
appropriate: Hemodynamic Monitoring (Chapter 1), Prolonged
Immobility (Chapter 1), Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2), and Systemic
Inflammatory Response Syndrome, Sepsis, Septic Shock, and
Multiple Organ Dysfunction Syndrome, (Chapter 11).

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Sleisenger and Fordtran’s gastrointestinal and liver disease
pathophysiology, diagnosis, management ed 9
Gastrointestinal bleeding. Philadelphia: Saunders Elsevier.
2010.
53. Schmidt R. Regulation of hepatic blood flow: the hepatic
arterial buffer response revisited. World J Gastroenterol.
2010;16:6046-6057.
54. Schmidt LE, Larsen FS. MELD score as a predictor of liver
failure and death in patients with acetaminophen-induced
liver injury. Hepatology. 2007;45:789.
55. Shirtliff MD. Necrotizing pancreatitis: halting a harmful
progression. Adv NPs PAs. 2011;2:23 -44.
56. Slade DA, Carlson GL. Takedown of enterocutaneous
fistula and complex abdominal wall reconstruction. Surg
Clin North Am. 2013;93:1163-1183.

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57. Solomkin JS, Mazuski JE, Bradley JS. Diagnosis and
management of complicated intra-abdominal infection in
adults and children: guidelines by the Surgical Infection
Society and the Infectious Diseases Society of America. Clin
Infect Dis. 2010;50:133-164.
58. Stevenson K, Carter CR. Acute pancreatitis. Surgery.
2013;31:295-303.
59. Tenner S, Baillie J, Dewitt J, Vege SS. American College of
Gastroenterology Guideline: management of acute
pancreatitis. Am J Gastroenterol. 2013;108:1400-1415.
60. Tenner S, Steinberg WM. Feldman M Friedman LS Brant LJ
Sleisenger and Fordtran’s gastrointestinal and liver disease
pathophysiology, diagnosis, management ed 9 Acute
pancreatitis. Philadelphia: Saunders Elsevier. 2010.
61. Trevino CM, Verhaalen A, Bruce ML. Conversion of an
enterocutaneous fistula associated with an open abdominal
wound into a drain-controlled enterocutaneous fistula.
Wounds. 2014;26:43-46.
62. Triadafilopoulos G. Management of lower gastrointestinal
bleeding in older adults. Drugs Aging. 2012;29:707-715.
63. Wilkins T, Khan N, Nabh A. Diagnosis and management of
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Diabetes, obesity and hypertension increase mortality in
HCV patients. Oral presentation at the 44th Annual
Meeting of the European Association for the Study of the
Liver, Copenhagen, Denmark. April 22, 2009.

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CHAPTER 10

Hematologic/immunologi
disorders
General hematology assessment
Goal of assessment
The goal of a basic hematology assessment is to identify assessment
and historical factors that correlate with findings on the complete
blood count (CBC) to assist in diagnosing a hematologic disorder.
Correlation of findings helps with diagnosis and treatment of
anemias, allergies, bleeding and clotting disorders, infections, and
cancer (especially in patients requiring chemotherapy). The use of
many medications and chemotherapy may have a negative effect on
the bone marrow, resulting in reduced production of cells reflected
on the CBC.

Observation
Changes in various blood components place patients at higher risk
for infection, fatigue, weakness, lethargy, bleeding, and clotting.
Patients may report:

• General: Chills, night sweats, altered mental status, confusion,

restlessness, vertigo, visual changes.

• Pain: Painful lymph nodes, painful joints, sore throat, sinusitis,

headaches, abdominal pain.

1866
• Respiratory: Shortness of breath (SOB), exertional or chronic
dyspnea, cough, hemoptysis, orthopnea.

• Cardiovascular: Activity intolerance, dizziness, palpitations, chest

discomfort, painful legs, swollen legs.

• Skin: Unusual bruising, itching, paleness, jaundice, grayness,

ulcers, difficulty stopping bleeding from small cuts.

• Musculoskeletal: Swollen and/or tender joints, sore muscles,

weakness.

• Gastrointestinal: Decreased appetite, feeling of fullness,

hematemesis, melena, black stools, “coffee grounds” stomach
secretions, weight loss, diarrhea, constipation.

• Genitourinary: Cystitis, hematuria, heavy menstrual periods,

enlarged groin lymph nodes.

Considerations for the bariatric patient: Polycythemia may be

present as a result of obstructive sleep apnea–associated
polycythemia. Hypercoagulability increases the risk for venous
thromboembolism. Observing for swelling and tenderness in the
lower limbs, and throughout the body if the obese person is not
getting out of bed, are of paramount importance. Focusing on early
ambulation is a key preventive strategy.

History
Patients at risk of hematologic or immunologic problems may
report having the following disorders:

• Infections: Recent or recurrent; previous blood transfusion.

• Allergies: Foods, beverages, medications, plants, animals, birds,

fish, detergents, household cleaners, fragrances, seasonal patterns
of respiratory symptoms.

• Immunologic compromise: Cancer, human immunodeficiency

virus (HIV), liver or renal disorders; previous splenectomy,

1867
 diabetes mellitus, rheumatoid arthritis, systemic lupus
erythematosus, Sjögren syndrome, Hashimoto thyroiditis.

• Healing: Prolonged bleeding or delayed healing with previous

surgeries, including dental procedures.

• Presence of foreign bodies: Prosthetic heart valves, inferior vena

cava filter, implantable defibrillators or other cardiac devices,
vascular access devices.

• Social history: Multiple sexual partners, excessive alcohol

consumption, exposure to chemicals or radiation.

• Medications, including over-the-counter medications: Aspirin,

aspirin-containing drugs, nonsteroidal antiinflammatory drugs
(NSAIDs); glucocorticoids/steroids, anticoagulants, platelet
inhibitors (e.g., clopidogrel), chemotherapy, hormone therapy,
oral contraceptives.

Considerations for the bariatric patient: Inflammation and

hypercoagulability are present. Adipose tissue produces tumor
necrosis factor and interleukin-6. Neutrophils have impaired
chemotaxis and activation. Concentrations of fibrinogen and
plasminogen activator inhibitor-1 are increased, whereas
concentration of antithrombin III (AT-III) and decreased fibrinolysis
are decreased in patients who are obese.

COMMONLY REVIEWED COMPONENTS OF THE COMPLETE

BLOOD COUNT*

Components Significance Normal Values

Hemoglobin Protein in red blood cells containing iron that carries oxygen 14 to 18 g/dL
(Hgb) to tissues. (male)
12 to 16 g/dL
(female)
Hematocrit The percentage of red blood cells in the bloodstream. When 42% to 52%
(Hct) Hct is too low, those with anemia may experience fatigue. (male)
37% to 47%
(female)
White blood Cells of the immune system that protect the body from 5000 to
cells (WBCs) bacterial, fungal, and viral infections. Incidence of infection 10,000/mm3
increases when WBCs are decreased.

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 Absolute The number of neutrophils (mature white cells) in the blood. 2000/mm3 and
neutrophil Neutrophils are a type of WBC that help fight infection. greater
count (ANC) When ANC decreases, the patient is neutropenic and more
prone to infection. Risk of infection increases when the ANC
falls below 2000 and the greatest risk is below 500; a “right
shift” on the WBC differential.

WBC Measures the percentage of each type of WBC in the total Neutrophils:
differential WBC count; a “left shift.” Indicates that a large percentage 50% to 62%
of WBCs are neutrophils; indicates that the bone marrow Bands: 3% to
has been stimulated by a severe infection to produce 6%
neutrophils to fight the infection. Bands are immature Monocytes: 3%
neutrophils. to 7%
“Right shift”: Indicates that a small percentage of WBCs are Basophils: 0%
neutrophils, putting the patient at higher risk for an to 1%
infection; neutropenia. Eosinophils:
Eosinophilia: Increased eosinophils indicate that an allergic 0% to 3%
reaction is present. Lymphocytes:
Monocytes and lymphocytes: Act as “backup” to the 25% to 40%
neutrophils. Percentages increase during infection when
oncology patients begin bone marrow recovery. If levels
do not rise and then fall in a normal pattern, this can be an
indication that the patient has a poor prognosis for
recovery.
Platelets Cells that form the matrix on which blood clots are formed. 150,000 to
(thrombocytes) 400,000/mm3
*
Information specific to hematologic and/or immunologic findings for each section is
presented in disease-specific sections. The basic assessment can be a part of every
patient’s assessment to determine the risk of development or presence of a
hematologic or immunologic disorder.

Anaphylactic shock
Pathophysiology
Anaphylaxis (anaphylactic shock) is a potentially life-
threatening condition resulting from an exaggerated or
hypersensitive response to an antigen or allergen. The typical
presentation occurs in a sensitized person (i.e., someone who has
been exposed previously to the same antigen) and is within 1 to 30
minutes of exposure to the antigenic substance, although symptoms
may not develop for several hours. The most common triggers
include drugs, foods, insect stings or bites, antisera, and blood
products. Recent studies have found that exercise may induce
anaphylaxis. This syndrome may or may not occur independently
of food-allergen ingestion. The hypersensitive response results in

1869
airway inflammation that causes obstruction and respiratory
distress, which can lead to respiratory arrest. In addition, there is a
relative hypovolemia caused by massive vasodilation. Fluids shift
from the vasculature into interstitial spaces, creating a false
hypovolemia or vasogenic (vasodilated) shock, which progresses to
end-organ dysfunction secondary to tissue hypoxia from poor
perfusion.
The hypersensitivity response occurs primarily on the surface of
the mast cells of the lungs, small blood vessels, and connective
tissue. The antigen combines with sensitized antibodies from
previous exposure (usually immunoglobulin E [IgE] type) and
attaches to basophils circulating in the blood. Inflammatory
mediators, including histamine, serotonin, kinins, and eosinophil
and neutrophil chemotactic factors, are then released from the
granules within the cells. Histamine is the primary mediator of an
anaphylactic response. Activation of histamine receptors causes
increased capillary permeability, increased pulmonary secretions,
bronchoconstriction, and systemic vasodilation.
The antigen-antibody complexes activate production of
prostaglandins and leukotrienes, which are termed slow-reacting
substances of anaphylaxis. These chemical mediators produce
systemic effects with potentially deadly results, including profound
shock. The leukotrienes produce severe bronchoconstriction and
cause venule dilation and increased vascular permeability. The
prostaglandins exaggerate bronchoconstriction and potentiate the
effects of histamine on vascular permeability and pulmonary
secretions. Kinins contribute to bronchoconstriction, vasodilation,
and increased vascular permeability. Eosinophilic chemotactic
factor of anaphylaxis is then released to attract eosinophils, which
work to neutralize mediators such as histamine. However, the
amount of neutralization is ineffective in reversing the anaphylaxis.
(See Figure 10-1 for a depiction of the pathophysiologic process of
anaphylaxis.)

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 FIGURE 10-1 Pathophysiologic process of
anaphylaxis. Source: (Major chemical mediators are in boldface.) SRS-
A, Slow-reacting substance of anaphylaxis.

Researchers have made a distinction between “true anaphylaxis”

and “pseudoanaphylaxis” or an “anaphylactoid reaction.” The

1871
symptoms, treatment, and mortality risk are identical, but “true”
anaphylaxis results directly from degranulation of mast cells or
basophils mediated by IgE. Pseudoanaphylaxis results from other
causes not directly mediated by antibodies. Differential diagnosis is
based on studying the allergic reaction.

10-1
RESEARCH BRIEF
Exercise-induced anaphylaxis (EIA) is a rare and unpredictable
form of anaphylaxis that is poorly understood. Between 5% and
10% of anaphylactic episodes are associated with or caused by
exercise. EIA may be food-dependent or occur independent of
food.
Although the pathophysiology behind EIA is not fully
understood, researchers believe that possible causes may include
alterations in plasma osmolality and/or pH during exercise, tissue
transglutaminase activity, redistribution of blood flow, and
changes in gut permeability. Additional research is needed to
better understand EIA. Based on current knowledge, if food is
contributing to EIA, dietary management is required, and the
specific food should be avoided 3 hours before exercise and 1 hour
after exercise.
From Robson-Ansley P, Du Toit G: Pathophysiology, diagnosis and management of
exercise-induced anaphylaxis. Curr Opin Allergy Clin Immunol 10:312-317, 2010.

Assessment: Anaphylactic shock

Goal of system assessment
Identify ineffective breathing patterns, altered tissue perfusion,
and impaired gas exchange. The clinical presentation will vary in
degree, depending on the magnitude of the sensitivity response.
History of asthma, previous allergen exposures, and other
respiratory diseases should be queried to help optimize the
treatment.

• Assess the symptoms: Assess for airway obstruction, ineffective

1872
 breathing patterns, and impaired gas exchange, along with
altered tissue perfusion related to vasodilation and third-spaced
intravascular fluids. Symptoms vary with means of antigen entry.

• Classify severity of reaction: Evaluate the severity of the reaction

following the initial assessment. Treatment must begin
immediately, before diagnostic test results are available.
Shock may progress rapidly to circulatory collapse and
cardiopulmonary arrest if improperly managed. The severity of
the reaction varies with the means of antigen entry, the amount
of antigen absorbed, rate of antigen absorption, and the degree of
hypersensitivity. Dramatic symptoms usually develop within
minutes and progress rapidly. A more rapid onset correlates with
more severe symptoms.

• Evaluate effectiveness of previous treatments: Determine the

patient’s previous treatment regime if asthmatic, and classify
which “step” of treatment has been needed to control symptoms.
The patient may need to move to the next step of treatment to
maintain control (see Acute Asthma Exacerbation, Chapter 4).

History and risk factors

Recent exposure to:

• Pharmacologic agents: Penicillin, anesthetics, vaccines, contrast

media.

• Allergenic foods: Seafood, shellfish, nuts, grains, dairy products.

• Insect bites or stings: Wasps, hornets, bees, fire ants.

• Latex.

• Recent blood transfusion.

Vital signs
• Severity of all findings varies with the level of sensitivity to the
antigen. Patients who are highly sensitive are at risk for

1873
 impending death if the condition is inappropriately managed.

• Pulse oximetry: Oxygen saturation is decreased from the patient’s

baseline value.

• Heart rate: Tachycardia (heart rate [HR] greater than 140

beats/min [bpm]).

• Respiratory rate: Tachypnea (respiratory rate [RR] greater than 40

breaths/min).

• Blood pressure: Hypotension may be present. It is exacerbated by

underlying vasodilation coupled with increased capillary
permeability prompting third spacing of intravascular fluids.

Observation (see table 10-1)

• Red to purple discoloration of face and body; “extreme flushing”
with swelling of lips, eyelids, and face caused by angioedema.

• Tears coming from eyes with strained facial expression.

• Severe reactions render patients unable to speak resulting from

breathlessness.

• Use of accessory muscles; fatigued, with or without diaphoresis.

• Chest expansion may be decreased or restricted.

• Altered level of consciousness (LOC) (confusion, disorientation,

agitation).

• Agitation is more commonly associated with hypoxemia, whereas

somnolence is associated with hypercarbia (elevated carbon
dioxide level).

• General early indicators (occurring within seconds to minutes)

include uneasiness, lightheadedness, tingling feeling, flushing,
and pruritus.

1874
• General late indicators (occurring within minutes to hours)
include rapid progression of urticaria involving large areas of
skin; angioedema (tissue swelling; more commonly the eyes, lips,
tongue, hands, feet, and genitalia); cough, hoarseness, dyspnea,
and respiratory distress; lightheadedness or syncope; and
abdominal cramps, diarrhea, and vomiting.

• Ingestion of antigen: Cramping, diarrhea, nausea, and vomiting

may precede systemic shock symptoms.

• Inhalation of antigen: Cough, hoarseness, wheezing, dyspnea.

• Allergic reaction: Edema, urticaria, itching at the site of a bee

sting or drug injection.

Table 10-1
SYSTEMIC EFFECTS OF ANAPHYLAXIS

System Effects Cause

Neurologic Apprehension; headache; confusion; decreased Vasodilation;
LOC progressing to coma hypoperfusion; cerebral
hypoxia or cerebral
edema occurring with
interstitial fluid shifts
Respiratory Dyspnea progressing to air hunger and complete Laryngeal edema;
respiratory obstruction; hoarseness; noisy bronchoconstriction;
breathing; high-pitched, “barking” cough; increased pulmonary
wheezes; crackles; rhonchi; decreasing breath secretions
sounds; pulmonary edema (some patients)
Cardiovascular Decreased BP leading to profound hypotension; Increased vascular
increased HR; decreased amplitude of peripheral permeability; systemic
pulses; palpitations and dysrhythmias (atrial vasodilation; decreased
tachycardias, premature atrial beats, atrial cardiac output with
fibrillation, premature ventricular beats decreased circulating
progressing to ventricular tachycardia, or volume; reflex increase
ventricular fibrillation); lymphadenopathy in HR; vasogenic shock
Renal Increased or decreased urine output; incontinence Decreased renal
perfusion; smooth
muscle contraction of
urinary tract
Gastrointestinal Nausea, vomiting, diarrhea, abdominal cramping Smooth muscle
contraction of GI tract;
increased mucus
secretion
Cutaneous Urticaria; angioedema (hands, lips, face, feet, Histamine-induced
genitalia); itching; erythema; flushing; cyanosis disruption of cutaneous
vasculature;
vasodilation, increased

1875
 capillary permeability;
decreased oxygen
saturation
BP, Blood pressure; HR, heart rate; GI, gastrointestinal; LOC, level of
consciousness.

Auscultation
• Wheezing bronchial breath sounds.

• Chest may be nearly silent if airflow is severely obstructed.

Palpation
• Palpate to assess for chest expansion; chest may be hyperinflated
if the patient is asthmatic.

• Decreased tactile fremitus may be present if the patient is

asthmatic.

Percussion
• May reveal hyperresonance (pneumothorax), a complication of
asthma (if present).

Diagnostic Tests for Anaphylaxis

1876
Collaborative management (see figure 10-2)
Care priorities

Prevention
The goal of management of patients with severe allergies is to
quickly identify the offending stimulant and control the allergic
response using a stepwise approach to therapies and to prevent
exposure to the antigen. Ideally, patients should be educated
regarding avoidance of the allergen, but for those with severe
allergies, avoidance may not be possible for all substances, such as
various substances in the air. For patients with asthma, ideal control
is attained when patients are free of daytime symptoms, do not
awaken breathless or coughing at night, and have few or no
limitations on activities. For those with allergies to insects,
immunotherapy with hymenoptera venoms is used worldwide as
an effective treatment for most patients hypersensitive to stings
from bees, wasps, hornets, yellow jackets, or white-faced hornets or
bites from fire ants. Food allergy research, including sublingual
preparations and vaccines to prevent anaphylaxis from peanuts and
other common foods, is underway in leading research centers,
including the Johns Hopkins Children’s Center. A recent report
from the Centers for Disease Control and Prevention revealed that
incidence of all food allergies is increasing. Up to 6 million children

1877
in the United States, including almost 8% of young children, have at
least one food allergy.

FIGURE 10-2 Algorithm for the treatment of acute

anaphylaxis. Source: (From Nicklas RA, Bernstein I, Li J, et al; Joint
Task Force on Practice Parameters for Allergy and Immunology: The
diagnosis and management of anaphylaxis. J Allergy Clin Immunol 101(6 Pt

1878
 2):S465-S528, 1998.)

When prevention fails, the potential for life-threatening

respiratory failure is high during exacerbations unresponsive to
treatment within the first hour. Management is directed toward
decreasing bronchospasm and increasing ventilation. Other
interventions are directed toward treatment of complications. Close
monitoring of the patient is necessary after treatment. Biphasic
anaphylaxis in which symptoms recur within 1 to 72 hours (usually
within 8 to 10 hours) may occur and should be treated as needed.

1. Position the patient and maintain a patent airway

Patients in anaphylactic shock should be placed in supine position
with their lower extremities elevated. Early, rapid endotracheal
(ET) intubation should be done to manage rapidly progressing
laryngeal edema. Severe laryngeal edema may cause complete
airway obstruction in minutes. A tracheostomy or an emergency
cricothyroidotomy is necessary if ET intubation is not possible.

2. Provide supplemental oxygen

Administered to support ventilation and aerobic metabolism.
Amount and method of oxygen administration are guided by
arterial blood gas (ABG) results. Supplemental oxygen should be
initiated at 6 to 8 L/min via face mask.

3. Manage vasodilation and increased capillary permeability

a. Epinephrine: Epinephrine reverses anaphylaxis by increasing

myocardial contractility, dilating bronchioles, constricting blood
vessels, inhibiting histamine release, and counteracting histamine.
Epinephrine is a first-line medication in anaphylaxis and should be
a priority.

Individuals taking beta-adrenergic–blocking agents such

as propranolol may not respond as rapidly as expected to

1879
epinephrine and may require higher or additional doses. Glucagon
may help to counteract the effects of beta-blocking drugs.

• Standard adult dose: 0.01 mg/kg (typically 0.2 to 0.5

mg) of a 1:1000 (1 mg/mL) solution, to a maximum
of 0.5 mg given intramuscularly (IM) in the mid-
anterolateral thigh.

• Repeat dose: May be repeated every 5 to 15 minutes

as needed.

• Intravenous (IV) dose: Preferred if the patient is in

shock and/or has severe airway obstruction: initial
dose of 0.1 to 0.25 mg (1.0 to 2.5 mL of 1:10,000
solution) over 5 to 10 minutes. The dose may be
increased to 0.3 to 0.5 mg. Repeat every 5 to 15
minutes as needed.

• IV infusion: After initial dose, an IV drip of

epinephrine 1.0 mg in 250 mL 5% dextrose in water
(D5W) may be infused at 1 µg/min and increased to
4 µg/min (or more) as needed to achieve desired
response.
b. Fluid resuscitation: IV crystalloids (e.g., lactated Ringer, 0.9%
normal saline) and/or colloids (e.g., albumin and plasma protein
fraction) to increase intravascular volume. Colloids increase colloid
osmotic pressure to help retain fluid in the blood vessels. May
require rapid infusion of 2 to 3 L of fluids.

c. Vasopressors: Used if fluid replacement does not increase blood

pressure (BP). Drugs are titrated for the desired response (see

1880
Appendix 6). Usual doses are as follows:

• Dopamine hydrochloride: Effects are dose-

dependent. Increases cardiac contractility at 5 to 10
µg/kg/min and systemic vascular resistance at 10 to
20 µg/kg/min. Consider switching to
norepinephrine if dose exceeds 20 µg/kg/min.

• Norepinephrine: Initial dose is 2 to 8 µg/min and

can be increased to achieve the necessary BP.

• Phenylephrine: Usual dose is 40 to 60 µg/min. Doses

exceeding 200 µg/min have been used.
d. Antihistamines: Diphenhydramine: Usual dose is 20 to 50 mg,
but 50 to 100 mg may be given IV or IM to relieve urticaria and
abdominal cramping. IV H2-antagonists (e.g., cimetidine, ranitidine)
are also used.

e. Corticosteroids: Used to help decrease release of chemical

mediators that increase capillary permeability. Hydrocortisone
sodium succinate: loading dose is 100 to 1000 mg IV; or
methylprednisolone sodium succinate: loading dose is 125 to 250
mg IV, followed by IV or oral (per os [PO]) corticosteroids for
several days.

f. Inhaled bronchodilators (e.g., albuterol): May be given for

continued bronchospasm (see Acute Asthma Exacerbation, Chapter
4).

g. Glucagon IV bolus: Use is controversial for counteracting effects

of beta-blocking drugs or for other patients who have limited
response to treatment. Relaxes smooth muscle and increases HR
and force of contraction.

4. Electrocardiogram (ECG) monitoring

1881
To detect dysrhythmias.

Care plans for anaphylaxis and anaphylactic

shock
Ineffective airway clearance 
related to airway obstruction secondary to bronchoconstriction, increased
secretions from the histamine response, and presence of leukotrienes and
prostaglandins.
Goals/Outcomes: Within 20 minutes of treatment/intervention,
the patient has adequate spontaneous tidal and expiratory volumes,
as evidenced by easier breathing; audible breath sounds in expected
range, and no adventitious breath sounds.
Respiratory Status: Ventilation; Vital Signs Status;
Respiratory Status: Airway Patency; Symptom Control Behavior;
Comfort Level; Endurance.

Airway management

1. Assess continuously for obstructed airway and increased

respiratory effort: Note increased pulmonary secretions, cough,
expiratory wheezing, SOB, and dyspnea. Suction secretions as
needed. Caution: An oral airway provides airway support only as
far as the posterior pharynx. If laryngeal edema is present, the oral
airway cannot relieve symptoms because the obstruction is below
the oral airway. If ET intubation is attempted and is not possible as
a result of laryngeal edema, prepare for tracheostomy or
cricothyroidotomy.

2. Monitor for decreased breath sounds or changes in wheezing at

frequent intervals: Absent breath sounds in the patient who is
distressed may indicate impending respiratory arrest. Identify the
patient requiring actual/potential airway insertion. Consult the
physician and prepare for ET intubation if lingual edema is present
and/or respiratory distress continues.

3. Position the patient for comfort and to promote optimal gas

exchange: High Fowler position, with the patient leaning forward

1882
and elbows propped on the over-the-bed table to promote maximal
chest excursion, may reduce use of accessory muscles and
diaphoresis resulting from work of breathing. May not be possible
with severe hypotension, as further decrease in BP may result.

Ventilation assistance

1. Monitor for signs of increasing hypoxia at frequent intervals:

Restlessness, agitation, and change in mental status are indicative of
severe reaction. Cyanosis of the lips (central) and nail beds
(peripheral) are late indicators of hypoxia, but may be difficult to
see with severe angioedema.

2. Monitor for signs of hypercapnia at frequent intervals:

Confusion, listlessness, and somnolence are indicative of
respiratory failure.

3. Provide medications to abate allergic response: Administer

epinephrine and IV and inhaled bronchodilators as appropriate to
attain control of deterioration.

Airway Insertion and Stabilization; Airway Management;

Anaphylaxis Management; Medication Administration, Medication
Management, Respiratory Monitoring.

Impaired gas exchange 

related to alveolar-capillary membrane changes secondary to increased
capillary permeability associated with histamine response.
Goals/Outcomes: Within 20 minutes of initiation of
treatment/intervention, the patient has adequate alveolar exchange
of CO2 or O2, as evidenced by easier breathing, PaO2 80 mm Hg or
greater, and SpO2 90% or greater.
Respiratory Status: Ventilation.

Anaphylaxis management

1. Monitor Fio2 to ensure that oxygen is within prescribed

concentrations. If the patient does not retain carbon dioxide, a 100%
nonrebreather mask may be used to provide maximal oxygen

1883
support. If the patient retains CO2 and is unrelieved by positioning,
lower-dose oxygen, bronchodilators and steroids, intubation, and
mechanical ventilation may be necessary sooner than in patients
who are able to receive higher doses of oxygen by mask.

2. Monitor ABGs when continuous pulse oximetry values or patient

assessment reflects progressive hypoxemia or development of
hypercapnia. Monitor and report ABG values with increasing Paco2
(greater than 50 mm Hg) or decreasing PaO2 (less than 60 mm Hg)
indicative of impending respiratory failure.

3. Administer antihistamines as prescribed.

4. Administer glucocorticoids as prescribed.

5. Position the patient to alleviate dyspnea (assist the patient to

sitting position if BP is stable).

6. Stay with the patient to promote safety and reduce fear. Use
calm, reassuring approach.

Respiratory Monitoring; Emotional Support; Medication

Administration, Medication Management.

Decreased cardiac output 

related to decreased preload and afterload secondary to vasodilation and
increased capillary permeability.
Goals/Outcomes: Within 4 hours of initiation of treatment, the
patient has adequate cardiac output (CO), as evidenced by BP 90/60
mm Hg or greater, strong peripheral pulses, CO 4 L/min or greater,
cardiac index (CI) 2.5 L/min/m2 or greater, systemic vascular
resistance (SVR) 900 dynes/s/cm−5 or greater, urinary output 0.5
mL/kg/h or greater, and normal sinus rhythm on ECG.
Circulation Status; Tissue Perfusion: Cardiac; Vital Signs.

Hemodynamic regulation

1. Assess for physical and hemodynamic indicators of decreased

CO:

1884
• Palpate peripheral pulses for decreasing amplitude,
assess the patient for mottling, decreased urine
output, or altered mental status.

• Assess arterial BP or mean arterial pressure (MAP)

for any decrease, an indicator of failed
compensatory mechanisms.

• Monitor SVR. A decrease (less than 800 dynes/s/cm

−5) is associated with decreased afterload
(vasodilation) and may precipitate decreased CO.

• Monitor CO, ScVO2, and CI if available. A CI of less

than 2.0 L/min/m2 and ScVO2 less than 80% are
usually associated with hypoperfusion.

• Hemodynamic measurements: While vasogenic

shock evolves, decreased arterial BP, MAP, CO (less
than 4 L/min), CI (less than 2.5 L/min), SVR (less
than 800 dynes/s/cm−5), and pulmonary artery
wedge pressure (less than 5 mm Hg) are present
from worsening vasodilation, progressive shifting
of intravascular fluid to interstitial spaces, and
decreasing venous return.

2. Monitor for dysrhythmias, such as atrial tachycardias, premature

ventricular contractions, ventricular tachycardia, and ventricular
fibrillation, which may signal hypoxemia or occur as side effects of
drugs such as aminophylline or epinephrine.

3. Monitor for increasing edema.

1885
 Continued swelling, despite treatment, may indicate
ineffective treatment, overaggressive fluid therapy, or heart or
kidney failure.

4. Administer epinephrine as prescribed. Observe for therapeutic

effects, as evidenced by increased arterial BP and MAP, increased
SVR, increased CO/CI, increased ScVO2, stronger peripheral pulses,
warming of extremities, and increased urine output.

5. Administer fluid replacement therapy as prescribed, using a

large-bore IV catheter. Colloids and crystalloids may be given
together.

During fluid resuscitation, assess the patient for

indicators of fluid volume excess, including crackles with chest
auscultation, presence of S3 heart sounds, and jugular venous
distention. If hemodynamic monitoring lines are present, be alert
to increasing pulmonary artery pressure, pulmonary artery wedge
pressure, and right atrial pressure.

6. Prepare for possible vasopressor infusion if hypotension persists

after fluid resuscitation and epinephrine administration.

Anaphylaxis Management; Hypovolemia Management;

Medication Administration, Medication Management; Cardiac
Care: Acute.

Altered tissue perfusion: Peripheral, renal, and cerebral 

related to hypovolemia secondary to fluid shift from the vascular space to
the interstitial space.
Goals/Outcomes: Within 4 hours of initiation of treatment, the

1886
patient has adequate perfusion, as evidenced by strong proximal
peripheral pulses, brisk capillary refill, warm extremities
temperature, urinary output 0.5 mL/kg/h or greater,
uncompromised neurologic status, and no restlessness, listlessness,
and unexplained anxiety.
Tissue Perfusion: Abdominal Organs; Tissue Perfusion:
Peripheral; Tissue Perfusion: Cerebral.

Hypovolemia management

1. Assess peripheral pulses. Report decreased amplitude of pulses.

2. Assess capillary refill. Delayed capillary refill (greater than 2

seconds) is likely with edema and decreased vascular volume.

3. Assess degree of peripheral edema.

4. Assess color and warmth of extremities. Report presence of

coolness and pallor.

5. Monitor BP at frequent intervals. Be alert for indicators of

hypotension such as BP readings greater than 20 mm Hg below the
patient’s normal pressure, dizziness, restlessness, altered
mentation, and decreased urinary output.

6. Monitor urine output hourly. Continuous CO monitoring using a

noninvasive system or a pulmonary artery catheter may be needed
to guide fluid resuscitation.

7. Observe for indicators of decreased cerebral perfusion such as

anxiety, restlessness, confusion, and decreased LOC.

HIGH ALERT!
Changes in level of consciousness may signal either decreased
cerebral perfusion (tissue hypoxia) or increasing intracranial
pressure caused by interstitial swelling from capillary
permeability. This may be a late sign.

1887
8. Administer fluid and pharmacologic agents as prescribed (see
previous nursing diagnosis).

Hemodynamic Regulation; Anaphylaxis Management;

Medication Administration, Medication Management.

Impaired skin integrity 

related to urticaria and angioedema secondary to allergic response.
Goals/Outcomes: Within 4 hours of initiation of treatment, the
patient states that urticaria is controlled. Skin remains intact.
Tissue Integrity: Skin and Mucous Membranes.

Pruritus management

1. Assess the patient for urticaria (hives) and itching of hands, feet,
neck, and genitalia.

2. Administer antihistamines as prescribed to relieve itching.

3. Discourage the patient from scratching the skin. If unavoidable,

teach the patient to use pads of fingertips rather than nails.

4. Apply cool washcloths or covered ice as a soothing measure to

irritated and edematous areas.

Environmental Management: Comfort; Medication

Administration.

Deficient knowledge illness care: Severe

hypersensitivity reaction, its causes, and its symptoms 
italic>Related to no previous exposure or incomplete understanding.
Goals/Outcomes: By the time of discharge from the critical care
unit, the patient demonstrates increased knowledge of severe
hypersensitivity reactions, as evidenced by verbalization of
potential causative factors, symptoms of allergic reaction, need to
inform healthcare providers of allergies, importance of wearing
medical-alert identification, prescribed treatment modalities when

1888
in contact with allergen, and the necessity of informing the primary
healthcare provider immediately of any allergic symptoms.
Knowledge: Treatment Regimen; Knowledge: Illness Care;
Knowledge: Health Behavior; Knowledge: Disease Process.

Teaching: Disease process

1. Provide information about the antigenic agent that caused the

anaphylaxis, including ways to avoid it in the future.

2. Explain the need for wearing a medical-alert identification tag or

bracelet to identify the allergy.

3. Give information about anaphylaxis emergency treatment kits.

Teach the patient self-administration technique and the importance
of prompt treatment.

4. Stress the importance of seeking treatment immediately if

symptoms of allergy occur, including flushing, warmth, itching,
anxiety, and hives.

5. Explain the importance of identifying and checking all over-the-

counter (OTC) medications for the presence of potential allergens.

Health Education; Risk Identification; Teaching: Prescribed

Medication.

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Hemodynamic
Monitoring (Chapter 1), Emotional and Spiritual Support of the
Patient and Significant Others (Chapter 2), and Mechanical
Ventilation (Chapter 1).

Profound anemia and hemolytic crisis

Pathophysiology

1889
Anemia
Anemia reflects a reduction in total body hemoglobin (Hgb)
concentration and is common in patients who are critically ill. By
the third day in an intensive care unit, 95% of patients have reduced
Hgb concentrations. While Hgb decreases, the oxygen-carrying
capacity of the blood is reduced, resulting in tissue hypoxia unless
compensatory mechanisms are adequate to assist the body with
oxygen delivery. Anemia may be classified under one of three
functional classes after initial evaluation of the CBC and
reticulocyte index. (See Table 10-2 for functional classification.)

Table 10-2
FUNCTIONAL CLASSES OF ANEMIA WITH EXAMPLES

Decreased Red Blood Maturation

Blood Loss/Hemolysis
Cell Production Disorders
Autoimmune diseases: Thrombotic Damaged bone Abnormal red blood
thrombocytopenia purpura, Goodpasture’s marrow: malignancy, cell cytoplasm
syndrome, systemic lupus erythematosus, lead poisoning, Phenylketonuria,
Wegener granulomatosis aplastic/hypoplastic glucose-6-phosphate
anemia, chemotherapy, dehydrogenase
viruses
Abnormal hemoglobin: Sickle cell disease, Iron deficiency: Abnormal red blood
hemoglobin S, C, D, E malignancy, cell nucleus
autoimmune disorders
Abnormal red blood cell membranes: Erythropoietin Iron deficiency:
Spherocytosis, hemolytic uremic syndrome, deficiency: renal failure, dietary, chronic
paroxysmal nocturnal hematuria malaria, thalassemias alcoholism
Bleeding/hemorrhage: Physical trauma to blood Inflammation/infection:
(bypass, balloon, valves), antibodies (drug- chronic inflammatory
induced antibodies), endotoxins (malaria, disease; critical illness
clostridia), gastrointestinal bleed, trauma,
rupture, excess menstruation
Excessive phlebotomies: laboratory sampling Metabolic disturbance:
pernicious anemia,
hypothyroidism,
megaloblastic anemia

Hemolytic crisis
Hemolytic crisis is an acute disorder that frequently accompanies
hemolytic anemias. It is characterized by premature pathologic
destruction (hemolysis) of red blood cells (RBCs). While RBC
destruction accelerates, the oxygen-carrying capacity of the blood
decreases, which results in a reduction in the amount of oxygen

1890
delivered to the tissues. This hypoxic state produces tissue ischemia
and can progress to tissue infarction. Hemolytic episodes can be
triggered by both emotional and physiologic states, including
stress, trauma, surgery, acute infectious processes, and abnormal
immune responses.

Assessment
Goal of system assessment
Evaluate for decreased oxygen-carrying capacity with subsequent
organ dysfunction as a result of decreased production or increased
destruction or loss of RBCs.

Anemia

Risk factors
Advanced age; environmental exposure to certain chemicals,
liver dysfunction, autoimmune or other immunologic disorders,
malignancy (and its treatment), drug use (such as aspirin, NSAIDs,
warfarin); diets low in protein and iron, iron or folic acid deficiency,
B12 deficiency, chronic alcoholism, autoimmune disorders.

Clinical presentation (chronic indicators)

• Pallor, melena, hematochezia, fatigue, weight loss, dyspnea on

exertion, uremia, sensitivity to cold, intermittent dizziness,
excessive menstruation, paresthesias.

• Chronic hemolytic anemia: Jaundice, renal failure, hematuria,

arthritis, increased incidence of gallstones, skin ulcers.

Clinical presentation (acute indicators)

• Fever, chest pain, acute heart failure, confusion, irritability,

tachycardia, orthostatic hypotension, dyspnea, tachypnea, frank
bleeding, critical illness for longer than 3 days.

Vital signs

1891
• Tachypnea, orthopnea, tachycardia, fever.

Observation

• Altered mental status, unusual fatigue or weakness.

• Spider angiomas, unusual bleeding (i.e., stool, urine, emesis).

• ECG changes.

• Monoarticular or polyarticular arthritis.

• Smooth tongue, skin ulcers.

Palpation
• Bone tenderness (especially rib and sternal areas), joint
tenderness.

• Enlargement of the liver and/or spleen.

Auscultation
• Crackles associated with heart failure.

Hemolytic crisis

Risk factors
Individuals with mild or chronic hemolytic anemia may be
asymptomatic until they are exposed to a severe stressor, such as an
acute infectious process, profound emotional upset, critical illness,
surgery, or trauma. With added stress, hemolysis can accelerate to a
crisis state in which patients experience organ congestion from
massive amounts of hemolyzed blood cells, precipitating multiple
organ dysfunction syndrome (MODS), and shock.

Clinical presentation (acute)

Fever; abdominal, chest, joint, and back pain; jaundice; headache;
dizziness; palpitations; SOB; hemoglobinuria; lymphadenopathy;

1892
splenomegaly; and signs of peripheral nerve damage including
paresthesias, paralysis, chills, and vomiting.

Clinical presentation (chronic)

Anemia; pallor; fatigue; dyspnea on exertion; mentation changes;
icterus; bone infarctions; monoarticular and polyarticular arthritis;
hematuria; renal failure; increased gallstone formation; skin ulcers
and itching.

Vital signs

• Tachypnea, tachycardia, hypertension.

Observation

• Impaired growth and development, depending on severity and

duration of anemia.

• Jaundice; retinal detachment and associated vitreous hemorrhage.

• SOB, with dyspnea on exertion.

• Monoarticular or polyarticular arthritis.

• Hemiplegia, paresthesias.

Palpation

• Splenomegaly, hepatomegaly, lymphadenopathy, or abdominal

guarding.

• Chronic skin ulcers, particularly in the ankle area.

Auscultation

• Crackles associated with heart failure.

• Murmurs related to valvular damage.

Diagnostic Tests for Anemias and Hemolytic Crisis

1893
Test Purpose Abnormal Findings
Red blood cell Enumeration of red cells found in Reduced; in hemolytic crisis, an
(RBC) count each cubic millimeter of blood increased number of premature RBCs
(nucleated RBCs) will be present

Hemoglobin Hgb content of RBCs Decreased

(Hgb)
Hematocrit (Hct) Percentage of RBCs in relation to Decreased
total blood volume
Reticulocyte RBC precursors; measures how fast Elevated: Because of increased bone
count, RBCs are produced in the bone marrow production of RBCs resulting
reticulocyte marrow from blood loss or RBC destruction;
index, corrected also a sign of marrow recovery after
reticulocyte chemotherapy
Mean Morphologic classification of RBCs: Low in microcytic anemia; high in
corpuscular Average size of individual RBCs. macrocytic anemia
volume Obtained by dividing Hct by total
(MCV) RBC count
(subcategory
of red cell
indices):
Macrocytic:
MCV >100 µg3
Microcytic:
MCV <80 µg3
Normocytic:
MCV 80-100
µg3
Sickle cell test Indicative of sickle cell anemia Presence of Hgb S
(trait, disease)
Hgb Screens for abnormal Hgbs often Hgbs A1, A2, and F: Normal Hgb
electrophoresis present in hemolytic anemias. Hgb C: Generally benign; may cause
Many hemoglobinopathies are joint pain, splenomegaly, and
interrelated. gallstones; may protect against
Disease expression is based on the malaria
degree of genetic abnormalities. Hgbs D and E: Rarely occur “singly”;
Various combinations of abnormal sometimes present with sickle cell
Hgbs are possible disease or thalassemias
Hgb H: Causes premature destruction
of RBCs and abnormal binding of O2
to RBCs; causes alpha thalassemia
Hgb S: Most common abnormal Hgb,
occurring in 10% of the African-
American population; causes sickle
cell disease or sickle cell trait
Erythrocyte Rate at which RBCs precipitate in a Elevated in hemolytic anemia;
sedimentation period of 1 hour: Nonspecific decreased in sickle cell anemia,
rate, measure of inflammation polycythemia and congestive heart
sedimentation failure
rate or
Biernacki’s
reaction
C3 proactivator Proactivator of complement 3 in the Increased in hemolytic anemia
alternate pathway of complement
activation

1894
Total iron- Measures the capacity of the blood Normal or reduced, depending on the
binding capacity to bind iron with transferrin; also type of anemia
(TIBC) indirect test of liver function
(although rarely used).
TIBC is typically measured along
with serum iron to evaluate
people suspected of having either
iron deficiency or iron overload
Ferritin Iron stores: With damage to organs Reduced with iron deficiency anemia;
that contain ferritin (especially the normal or elevated with anemia of
liver, spleen, and bone marrow), critical illness; elevated with
ferritin levels can become elevated hemochromatosis
even though the total amount of
iron in the body is normal
Transferrin Used to determine the cause of Reduced with anemia of chronic
anemia, to examine iron metabolism inflammation, anemia of critical illness
(e.g., in iron deficiency anemia), and
to determine the iron-carrying
capacity of the blood
Transferrin The iron concentration divided by Reduced with anemia of chronic
saturation TIBC; a more useful indicator of inflammation, anemia of critical illness
iron status than iron or TIBC alone
Folate; folic acid Measures folic acid in the blood Reduced with nutrition deficiency
leading to megaloblastic anemia
Erythropoietin Measures the amount of a hormone Reduced with renal disease and
(EPO) called erythropoietin (EPO) in the normal in those who are critically ill
blood; acts on stem cells in the bone who should have an elevated level if
marrow to increase the production anemia of any cause is present.
of RBCs; made by cells in the Reticulocyte response to EPO has been
kidney, which release the hormone shown to be reduced in many critically
when oxygen levels are low ill patients with elevated EPO levels.
Vitamin B12 Measures the amount of vitamin B12 Reduced with pernicious or
in the blood; used with folic acid megaloblastic anemia
test, because a lack of either can
cause megaloblastic anemia
Unconjugated Measures bilirubin that has not been Elevated in hemolytic anemia as a
bilirubin: Free conjugated in the liver. It gives an result of the inability of the liver to
bilirubin, indirect reaction to the Van Den process increasing bilirubin released
indirect bilirubin Bergh test during hemolysis
Serum lactic General indicator of the existence Elevated in hemolytic anemia because
dehydrogenase and severity of acute or chronic of their release when an RBC is
isoenzymes tissue damage and, sometimes, as a destroyed
(LDH1 and monitor of progressive conditions;
LDH2) monitor damage caused by muscle
trauma or injury and to help
identify hemolytic anemia
Haptoglobin Used to detect and evaluate Decreased in hemolytic anemia as a
level hemolytic anemia; not to diagnose result of increased binding of
cause of the hemolysis. Haptoglobin haptoglobin, which facilitates removal
levels should be drawn before of increased Hgb from blood
transfusion
Peripheral blood Microscopic examination of cells May reveal abnormally shaped RBCs,
smear from a drop of blood; investigates such as spherocytes. RBC hyperplasia
hematologic problems or parasites (abnormal number) is present in nearly
such as malaria and filarial all cases of chronic hemolysis with
intact bone marrow

1895
Bone marrow Evaluates bone marrow status; May reveal abnormal size, shape, or
aspiration diagnoses blood disorders and amounts of RBCs, WBCs, or platelets
determines if cancer or infection has
spread to the bone marrow
Coombs test: Detects antibodies that may bind to Positive in antibody-mediated
Direct RBCs and cause premature RBC immunologic hemolysis
antiglobulin test; destruction
indirect
antiglobulin test
Immunoglobulin Measures the level of Elevated: Autoimmune disorders,
levels immunoglobulins, also known as sickle cell; lower in
antibodies, in the blood. immunocompromised states
Glucose-6- Measures G6PD—enzyme levels are Decreased in G6PD deficiency,
phosphate normal in newly produced cells but hemolysis Elevated: myocardial
dehydrogenase fall as RBCs age and only deficient infarction, liver failure, chronic blood
(G6PD) levels cells are destroyed loss, hyperthyroidism
Radiologic x-rays and bone scans Liver/spleen Decreased density, aseptic necrosis of
examinations scans bones Hepatomegaly, splenomegaly,
lesions

Collaborative management: Anemias

Care priorities

1. Oxygen therapy: Administered to relieve SOB or dyspnea

Methods of oxygen delivery range from nasal cannulas, to various
face masks, to mechanical ventilation in severe cases.

2. Transfusions/blood component replacement

Packed RBCs may be necessary in the management of profound
anemia to help increase the oxygen-carrying capacity of the blood.
For patients who refuse blood transfusions, aggressive strategies to
augment RBC production such as IV iron therapy and
subcutaneous administration of erythropoietin may be
implemented. These therapies may take up to 7 days or longer to
promote significant improvement in reticulocyte count and Hgb
and hematocrit (Hct) levels. The oxygen-carrying capacity of
banked blood is best when used within 14 days of collection. Blood
transfused more than 21 days after collection has been linked to
increased mortality rates in the critically ill, especially patients who
are HIV-positive. Benefits must be weighed against risks,
particularly in patients who are immunosuppressed.

1896
10-2
RESEARCH BRIEF
Marik and colleagues conducted a systematic review of 45 cohort
studies to determine the correlation between red blood cell
transfusion and negative outcome. Outcome measures included
mortality, infection, multiorgan dysfunction, and acute respiratory
distress syndrome. Forty-two of the 45 studies revealed that risks
of transfusion outweighed benefit in treating anemia. Transfusion-
related acute lung injury and transfusion-related circulatory
overload are some of the most common adverse events. Risks of
transfusion must be weighed individually against the risks of
anemia, and other treatments such as iron or erythropoiesis-
stimulating agents.
From Marik PE, Corwin HL: Efficacy of red blood cell transfusion in the critically ill: a
systematic review of the literature. Crit Care Med 36:2667-2674, 2008.

3. Volume replacement
If the patient is hypovolemic, aggressive fluid and/or blood
replacement is mandatory to prevent profound hypotension and
shock. Fluid challenges/boluses also assist in prevention of
deposition of hemolyzed RBCs in the microvasculature.

4. Elimination of causative factor

Certain drugs and chemicals, cold temperatures, and stress can
worsen many anemias, but most profoundly affected are hemolytic
and aplastic anemias. Identifying and removing the causative agent
can prevent life-threatening crisis. If the patient is bleeding, the
cause of the bleeding must be addressed and the bleeding
controlled.

5. Folic acid supplement

Necessary for RBC production. Supplements of 1 mg/day are used
to treat megaloblastic anemia and, theoretically, to prevent
hemolytic crisis in patients with hemolytic anemia. It is not effective
in all patients with hemolytic anemia.

1897
6. Iron supplements
Administered for iron-deficiency states to help increase production
of normal-size RBCs. May be given IV or enterally. Iron levels must
be normal to facilitate the action of erythropoietin injections.

7. Epoetin alfa/erythropoietin, recombinant

(epogen/procrit)
Stimulates production of RBCs in patients with bone marrow
hypofunction/lack of production of RBCs, particularly when related
to renal failure. Has been used as an alternative strategy in patients
who refuse blood transfusions (in conjunction with IV iron, if
needed) and in anemia associated with critical illness. Patients who
are critically ill may or may not respond to erythropoietin.

8. Vitamin B12
Administered by injections or IV infusion for management of
pernicious anemia, a type of megaloblastic anemia caused by failure
of the gastric mucosa to absorb vitamin B12.

9. Bone marrow transplantation

Recommended for some patients with bone marrow malignancies,
sickle cell disease, or aplastic anemia to provide a mechanism for
regenerating normal RBC production.

Care plans for anemias

Impaired gas exchange 
related to lack of RBCs; hemoglobin abnormalities
Goals/Outcomes: Within 3 to 24 hours of onset of treatment, the
patient has adequate gas exchange, as evidenced by HR and RR
within 10% of the patient’s baseline (or HR 60 to 100 bpm and RR
12 to 20 breaths/min), Hgb and Hct returned to the patient’s
baseline (or Hgb greater than 12 mg/dL and Hct greater than 37%),
oxygen saturation greater than 95%, and BP returned to the
patient’s baseline (or greater than 90 mm Hg systolic within 24
hours of initiation of treatment).
Respiratory Status: Gas Exchange; Tissue Perfusion:

1898
Pulmonary.

Respiratory monitoring

1. Administer supplemental oxygen, using appropriate device (i.e.,

nasal cannula, face mask/shield, or mechanical ventilation as
necessary). Monitor oxygen liter flow. Provide for oxygen when the
patient is transported.

2. Monitor rate, rhythm, and depth of respirations.

3. Monitor for increased restlessness, anxiety, and air hunger.

4. Monitor oxygen saturation using pulse oximetry continuously.

Consult the advanced practice provider for persistent values less
than 92% or, if oxygen saturation is chronically decreased, a
sustained drop of greater than 10% of baseline.

5. Note changes in SaO2, SVO2, ScVO2, Sto2 (if available) and changes
in ABG values, as appropriate.

6. Maintain large-bore (18-gauge) IV catheter(s) in case transfusion

or rapid volume expansion is necessary. Administer IV fluids to
maintain hydration.

7. Transfuse with packed cells (RBCs) (Table 10-3) as prescribed to

facilitate oxygen delivery and assist in volume expansion, and/or
implement aggressive strategy to augment RBC production.

8. Describe the purpose of blood product transfusion therapy to the

patient and significant others.

9. Carefully evaluate dyspnea and chest pain in patients with sickle

cell disease because of the possibility of pulmonary infarction.

Table 10-3
BLOOD AND BLOOD PRODUCTS*

1899
*
Use correct filter with each blood product; most filters can be used to administer 2 to
4 units; either piggyback or flush products with normal saline solution only.

Airway Management; Oxygen Therapy; Circulatory

Precautions; Cardiac Precautions.

Activity intolerance 
related to anemia/lack of oxygen-carrying capacity of the blood
Goals/Outcomes: Within 24 hours of onset of treatment, the
patient’s activity tolerance improves, as evidenced by HR and RR
returning to within 10% of baseline (or HR 60 to 100 bpm and RR 12
to 20 breaths/min) and BP returning to within 10% of the patient’s
baseline (or systolic BP greater than 90% mm Hg). Within 24 hours
of initiation of treatment, the patient is able to assist minimally with
self-care activities.
Endurance; Activity Tolerance.

Energy management

1900
1. Alternate periods of rest and activity to avoid stress that increases
oxygen demand.

2. Collaborate with occupational therapy, physical therapy, and/or

recreational therapy personnel in planning and monitoring an
activity program as appropriate.

3. Determine the patient’s physical limitations. Focus on what the

patient can do rather than on deficits.

4. Reposition the patient slowly while monitoring effects on

myocardial and cerebral perfusion.

5. Reduce fear, pain, and anxiety to decrease oxygen demand.

6. Determine causes of fatigue (e.g., treatments, pain, medications).

7. Monitor nutrition intake to ensure adequate energy resources.

8. Teach the patient to avoid stressful situations, which can

exacerbate symptoms of anemia and precipitate hemolytic crisis in
patients with hemolytic anemia.

9. Teach signs of hypoxemia: altered mental status, activity

intolerance, SOB, chest pain, and weakness.

10. Teach the patient and significant others about the specific
anemia affecting the patient.

11. See this diagnosis in Prolonged Immobility, Chapter 1.

Activity Therapy; Teaching: Prescribed Activity/Exercise.

Risk for impaired skin integrity 

related to impaired oxygen transport secondary to chronic anemia.
Goals/Outcomes: The patient’s skin remains intact during
hospitalization.
Tissue Integrity: Skin and Mucous Membranes.

Pressure management

1901
1. Keep extremities warm to promote circulation and help prevent
tissue hypoxia.

2. Perform a comprehensive appraisal of peripheral circulation (e.g.,

check peripheral pulses, edema, capillary refill, color, and
temperature of extremity).

3. Monitor for sources of pressure and friction.

4. Monitor for infection, especially of edematous areas.

5. Use a bed cradle to reduce pressure of covers on extremities.

6. Monitor skin and mucous membranes for areas of discoloration

and bruising.

7. Monitor skin for rashes, abrasions, excessive dryness, and

moisture.

8. Provide adequate nutrition and nutrition supplements as

appropriate. Negative nitrogen state or low serum protein or
albumin increases the risk for skin breakdown.

9. Teach the patient the signs of skin breakdown, because it can

occur at any time with chronic anemia.

10. Instruct the patient on the importance of preventing venous

stasis.

11. Teach the patient about appropriate nutrition, as discussed in

Nutrition Support, Chapter 1.

12. Apply appropriate skin-saving dressing (e.g., DuoDerm) or

initiate aggressive skin care regimen to areas of breakdown.

13. For additional interventions, see Wound and Skin Care, Chapter
1.

Pressure Ulcer Prevention; Skin Surveillance; Nutrition

Management; Circulatory Precautions.

1902
Collaborative management: Hemolytic crisis
Care priorities

1. Oxygen therapy
Administered to relieve SOB or dyspnea. Methods of oxygen
delivery range from nasal cannulas, to various face masks, to
mechanical ventilation in severe cases.

2. Pain management
Aspirin, acetaminophen, NSAIDs, narcotics, and sedatives may be
necessary for relief of pain and anxiety associated with hemolytic
anemia, particularly during hemolytic crisis.

3. Volume replacement
If the patient is hypovolemic, aggressive fluid and/or blood
replacement is mandatory to prevent profound hypotension and
shock. Fluid challenges/boluses also assist in the prevention of
deposition of hemolyzed RBCs in the microvasculature.

4. Transfusions/blood component replacement

Packed RBCs may be necessary in the management of profound
anemia to help increase the oxygen-carrying capacity of the blood.
For patients who refuse blood transfusions, aggressive strategies to
augment RBC production such as IV iron therapy and
subcutaneous administration of erythropoietin may be
implemented. These therapies may take up to 7 days or longer to
promote significant improvement in reticulocyte count and Hgb
and Hct levels. The oxygen-carrying capacity of banked blood is
best when used within 14 days of collection. Blood transfused more
than 21 days after collection has been linked to increased mortality
rates in the critically ill, especially patients who are HIV-positive.
Benefits must be weighed against risks, particularly in patients who
are immunosuppressed.

5. Red cell exchange therapy for sickle cell crisis

Cytapheresis procedure used to replace sickled RBCs with normal

1903
RBCs for patients who are unresponsive to other treatments for
sickle cell disease.

6. Thrombocytapheresis
Cytapheresis procedure for patients experiencing symptoms of
excessive thrombosis, to attempt rapid platelet reduction to
decrease clotting before onset of MODS (see Multiple Organ
Dysfunction Syndrome in Systemic Inflammatory Response
Syndrome, Sepsis, and Multiple Organ Dysfunction Syndrome,
Chapter 11).

7. Therapeutic phlebotomy
Removal of 200 to 500 mL of whole blood from the patient when
iron overload exists.

8. Corticosteroids
Therapy used with limited success in the management of hemolytic
anemia.

9. Splenectomy
Removal of the spleen is sometimes recommended for patients
suspected of having splenic sequestration crisis related to hemolytic
anemia.

Care plans for hemolytic crisis

Ineffective tissue perfusion: Peripheral, cardiopulmonary,
gastrointestinal, renal, and cerebral 
related to interruption of arterial or venous blood flow secondary to
formation of microthrombi.
Goals/Outcomes: Within 24 hours of institution of treatment, the
patient has adequate perfusion, as evidenced by warm extremities,
pink nail beds; peripheral pulses at least 2+ on a 0-to-4+ scale or the
patient’s baseline, capillary refill less than 2 seconds, BP within 10%
of the patient’s normal range (or systolic BP greater than 90 mm
Hg), HR and RR within 10% of the patient’s baseline (or HR 60 to
100 bpm, RR 12 to 20 breaths/min with a normal depth and

1904
pattern), oxygen saturation greater than 95%, urinary output 0.5
mL/kg/h or greater, and orientation to time, place, and person.
Circulation Status.

Circulatory care: Arterial insufficiency

1. Initiate aggressive IV fluid volume replacement as prescribed to

prevent deposition of hemolyzed RBCs in the microvasculature.

2. Assess extremities for inadequate peripheral perfusion:

amplitude of peripheral pulses, coolness, pallor, and prolonged
capillary refill. Use Doppler if unable to palpate pulses.

3. Evaluate chest pain. Note cardiac dysrhythmias and symptoms of

decreased CO. Monitor respiratory status for symptoms of heart
failure.

4. Monitor vital signs frequently for signs of impending shock:

increased HR and RR, increased restlessness and anxiety, and cool
and clammy skin, followed by a decrease in BP.

5. Monitor abdomen for signs of decreased perfusion.

6. Keep lower extremities elevated slightly to promote venous

blood flow.

7. Monitor ventilation and perfusion: assess ABG values for acidosis

(i.e., pH less than 7.35, hypercarbia/CO2 retention [Paco2 greater
than 45 mmHg]), indicating hypoperfusion, and respiratory
insufficiency. Assess for hypoxemia using continuous pulse
oximetry and ScVO2 or SVO2 monitoring to detect decreased oxygen
saturation. Consult the advanced practice provider for sustained
deterioration in status.

8. Monitor urinary output for decrease, which can signal decreased

renal perfusion. Consult the advanced practice provider for urine
output less than 0.5 mL/kg/h for 2 consecutive hours.

9. Monitor neurologic status every 2 to 4 hours, using the Glasgow

Coma Scale (see Appendix 2).

1905
10. Teach the patient and significant others about hemolytic anemia,
including the signs of impending hemolytic crisis, rendering
information on the following:

• Indicators of impending hemolytic crisis: Fever,

abnormal pain, headache, blurred vision, dizziness,
change in mentation, unsteady gait, palpitations,
paresthesias, and paralysis.

• Support groups: Names, telephone numbers, and

addresses of other persons/groups that can assist
with support of people with hemolytic anemias.

• Smoking cessation: Support groups and programs

that assist in stopping cigarette smoking to decrease
vasoconstriction associated with nicotine intake.

• Medications: Drug name, dosage, frequency, and

possible side effects, especially related to steroids:
increased appetite, weight gain, “moon face,”
“buffalo hump,” increased possibility of infection,
headaches, and increased BP. Explain possible
steroid-induced diabetes mellitus.

• Prevention of infection: Important if the patient is

on long-term steroid therapy or had a splenectomy.
The patient should obtain an annual flu vaccine;
practice good personal hygiene; obtain regular
dental checkups; and get adequate rest, sleep, and
relaxation. For splenectomy, patients should have a
pneumococcal vaccine and wear a medical-alert
identification bracelet.

1906
 Cardiac Care: Acute; Circulatory Care: Venous Insufficiency;
Respiratory Monitoring; Shock Management: Cardiac; Cerebral
Perfusion Promotion; Neurologic Monitoring; Peripheral Sensation
Management; Fluid/Electrolyte Management; Fluid Management;
Vital Signs Monitoring.

Acute pain 
Related to tissue ischemia secondary to vessel occlusion;
inflammation/injury secondary to blood within the joints.
Goals/Outcomes: Within 1 to 2 hours of initiating treatment, the
patient’s subjective evaluation of discomfort improves, as
documented by a pain scale; nonverbal indicators of discomfort are
reduced or absent.
Pain Control; Pain Level.

Pain management

1. Monitor the patient for signs of discomfort, including increases in

HR, BP, and RR. Devise a pain scale with the patient, rating
discomfort from 0 (no pain) to 10.

2. Perform a comprehensive assessment of pain to include location,

characteristics, onset/duration, frequency, quality, intensity or
severity of pain, and precipitating factors.

3. Medicate for pain as prescribed. Assess effectiveness of

medication using the pain scale. Confer with the advanced practice
provider if pain relief is ineffective; devise an alternate plan for
analgesia.

4. Recognize that components of chronic and acute pain are present

and tolerance may be higher than expected for age and size. During
a crisis, exacerbation of pain may be unpredictable as a result of
intermittent vessel occlusion, thus both baseline and breakthrough
medications will be required to achieve pain relief.

5. If pain medication injections are frequent, consider an IV rather

than an IM route, when possible.

1907
6. Administer adjuvant analgesics and/or medications when needed
to potentiate analgesia.

7. Consider continuous infusion (alone or with bolus opioids) to

maintain serum levels.

8. Collaborate with the advanced practice provider if drug, dose,

route of administration, or interval changes are indicated, making
specific recommendations based on equianalgesic principles.

9. Consider complementary method of pain control such as

relaxation techniques: guided imagery, controlled breathing,
meditation, and listening to soft, soothing music. Use
therapeutic/healing touch to relieve pain if the practitioner is
trained and the patient agrees to participate. Alternatively, consult
the trained practitioner.

10. Control environmental factors that may add to discomfort (e.g.,

room temperature, light, noise).

11. Apply warm compresses to joints to increase circulation and

thereby improve tissue oxygenation.

12. Apply elastic stockings to promote venous return and enhance

circulation.

13. Teach the patient to perform isometric or range-of-motion

exercises to promote circulation.

14. Help allay fears by reassuring the patient that pain will decrease
when the crisis subsides.

15. Provide emotional support to the patient during the crisis

episode. Reassure the patient that the crisis is time-limited, and
enable significant others to be with the patient, if possible, during
the crisis.

16. Teach the patient to assess extremities daily for evidence of

tissue breakdown or blood sequestration (i.e., swelling, erythema,
tenderness) so that early interventions can be implemented in an

1908
attempt to prevent severe pain.

Analgesic Administration; Medication Administration;

Medication Administration: Intravenous (IV); Heat/Cold
Application; Anxiety Reduction; Therapeutic Touch; Music
Therapy; Meditation Facilitation.

Risk for deficient fluid volume 

related to failure of renal regulatory mechanisms of fluid and electrolyte
balance secondary to microthrombi occluding the nephrons.
Goals/Outcomes: The patient’s volume status returns to
normal/baseline, as evidenced by urinary output greater than 0.5
mL/kg/h, stable weight, BP within the patient’s normal range, HR
60 to 100 bpm, RR 12 to 20 breaths/min, good skin turgor, moist
mucous membranes, urine specific gravity 1.005 to 1.025, and
central venous pressure (CVP) 4 to 6 mm Hg.
Fluid Balance; Electrolyte and Acid-Base Balance.

Fluid/electrolyte management

1. Monitor intake and output (I&O) hourly. Consult the advanced

practice provider for a urinary output less than 0.5 mL/kg/h for 4
consecutive hours. Insert urinary catheter if patient is unable to
void.

2. Monitor and document HR, rhythm, pulses, and BP.

3. Evaluate efficacy of volume expansion by closely monitoring

CVP. Overzealous volume expansion can lead to heart failure and
pulmonary edema, with CVP greater than 20% to 25% of normal
values.

4. Administer diuretics as prescribed in the well-hydrated patient

with urine output less than 0.5 mL/kg/h.

5. Assess the patient for volume depletion, including poor skin

turgor, dry mucous membranes, hypotension, tachycardia, and
decreasing urine output and CVP.

1909
6. Monitor electrolytes and serum osmolality. A universal increase
in electrolytes and osmolality is indicative of dehydration. A
universal decrease signals fluid overload.

7. Assess pH (normal range is 7.35 to 7.45) before replacing

electrolytes. Acidosis and alkalosis alter electrolyte values. Replace
potassium if the pH is outside the normal range.

Electrolyte Monitoring; Fluid Management; Fluid

Monitoring; Intravenous (IV) Therapy; Hypervolemia Management;
Shock Management: Volume.

Additional nursing diagnoses

Uncontrolled pain, bleeding, and complications of hemolysis
can be terrifying to the patient and significant others, who may fear
that the patient will die. Chronic illness with episodic acute
exacerbations may require more individualized intervention when
handling long-term illness and its sequelae. See Emotional Support
of Patient and Significant Others, Chapter 2.

Bleeding and thrombotic disorders

Pathophysiology
Bleeding can result from qualitative (dysfunctional) or quantitative
(lack of) abnormalities of platelets and/or coagulation factors,
including proteins, in the plasma. Thrombocytopenia is common in
the critically ill and, like anemia, necessitates differential diagnosis.
The cause of thrombocytopenia, rather than simply the decreased
numbers of platelets, poses the greatest threat to the patient who is
critically ill. The four main causes of thrombocytopenia are as
follows:

1. Hemodilution: Related to administration of large amounts of

retained fluids, IV fluids, multiple medications given in 50- to 100-
mL “piggybacks,” or blood/blood products.

1910
2. Increased platelet destruction or consumption: Includes heparin-
induced thrombocytopenia (HIT); antiphospholipid antibody
syndrome or lupus anticoagulant syndrome; idiopathic
thrombocytopenic purpura (ITP); thrombotic thrombocytopenic
purpura (TTP); hemolytic-uremic syndrome; febrile reactions;
severe sepsis; and hemolysis, elevated liver enzymes, and low
platelet count (HELLP) syndrome. Disseminated intravascular
coagulation (DIC) presents with a combined coagulopathy and
platelet consumption.

3. Platelet sequestration: Related to hypersplenism and

hypothermia.

4. Decreased production of platelets: Caused by alcohol (EtOH)

abuse, bone marrow irradiation, bone marrow/stem cell disease,
graft-versus-host disease, aplastic anemia, vitamin B12 or folate
deficiencies, metastatic carcinoma, some renal diseases, leukemia,
and myeloproliferative disorders.

Platelet destruction may be mediated by congenital autoimmune

or alloimmune disorders, or by acquired immunologic or
nonimmunologic mechanisms. Causative or related factors include
septicemia, systemic inflammatory response syndrome (SIRS),
pulmonary hypertension, extracorporeal circulation, thrombotic
disorders, acute transplant rejection, severe allergic reactions,
rheumatic disorders, intravascular catheters and prosthetics, fat
emboli, acute respiratory distress syndrome, and HIV infection. The
most significant diagnostic finding associated with severe
thrombocytopenia is the presence of petechiae in dependent areas
(i.e., back, ankles, posterior thighs of patients who are bedridden).
Larger purpura such as ecchymoses and hematomas may also be
present but are nonspecific for diagnosis of platelet disorders.
Patients must be assessed for risk of bleeding with
thrombocytopenia, considering the severity and cause as well as
comorbid factors.
Coagulopathies leading to bleeding (with/without associated
thrombi) may be caused by liver disease, vitamin K deficiency,
pregnancy-induced hypertension associated with HELLP
syndrome, or other defects of blood coagulation factors, such as

1911
hemophilia, Von Willebrand disease, and DIC.
Patients prone to thromboembolic conditions include those with
platelet abnormalities, including thrombocytosis, diabetes mellitus,
hyperlipidemia, heparin-induced thrombocytopenia, systemic
lupus erythematosus; blood vessel defects, including venous
disease/stasis, roughened surface of vascular endothelium (seen
with arteriosclerosis, trauma, severe sepsis, SIRS, or infection), atrial
fibrillation, grafts or other devices in place, hyperviscosity, TTP,
hemolytic uremic syndrome, vasculitis; and those with systemic
illness and conditions, including long bone fractures, orthopedic
surgery, abdominal surgery, malignancy, pregnancy or postpartum
(risk of venous thromboembolism is five times higher than for
nonpregnant women), oral contraceptives, nephrotic syndrome,
inflammatory bowel disease, slow/stagnant blood flow through the
vessels (e.g., shock states, severe peripheral vascular disease),
infusion of prothrombin complex, and sickle cell disease.
When patients are evaluated for a bleeding disorder, the process
should include evaluation of platelets, deficiency of a single
coagulation factor (factors VII, VIII, IX, X, or XI) or multiple
coagulation factors, for endogenous or exogenous antibiotics in the
circulation, and consumptive coagulopathy (e.g., ITP, TTP,
vasculitis, hemolytic uremic syndrome, paroxysmal nocturnal
hematuria, obstetric complication, trauma, liver disease). Adequate
levels of calcium and vitamin K are also needed for adequate
function of the clotting cascade.
Those suspected of having thromboembolic disease may require
evaluation of coagulation factors, circulating antibodies, abnormal
proteins (deficient protein C or S), and other endogenous chemicals.
Normal blood coagulation is activated most often as a result of
injury to blood vessels, causing the following series of events:

1. Reflex vasoconstriction: Vascular spasm that decreases blood

flow to the site of injury.

2. Platelet aggregation: Accumulation of platelets that leads to

formation of a platelet plug to help support the repair of the injury.
If the damage to the vessel is small, the plug is sufficient to seal the
injury. If the hole is large, a blood clot is necessary to stop the
bleeding.

1912
3. Activation of plasma clotting factors: Stimulation of factors that
leads to the formation of a fibrin clot. The pathways that initiate
clotting factors (Figure 10-3) include the following:

a. Intrinsic system: Initiated by “contact activation”

subsequent to an endothelial injury. The problem
is “intrinsic” to the circulation, or begins with an
injury to the blood or circulatory system.

b. Extrinsic system: Initiated by tissue

thromboplastin released from injured tissue. The
problem is “extrinsic” to the circulation, or begins
with an injury to tissue rather than within the
blood system.

c. Common pathway: The final part of the

coagulation system, which completes the clot
formation process begun by either the intrinsic or
extrinsic pathway.

d. Clot retraction: Several minutes after its

formation, the clot contracts for 30 to 60 minutes
to express most of the fluid from within the clot.
The expressed fluid is called serum, because most
of the clotting factors have been used or removed
via the clot formation process. Serum is unable to
clot. The absence of clotting factors differentiates
serum from plasma.
4. Growth of fibrous tissue: Rubbery tissue that completes the clot
within approximately 7 to 10 days after injury. This process results
in permanent closure of the vessel injury. Both the intrinsic and
extrinsic pathways are activated after rupture of a blood vessel.

1913
Tissue thromboplastin from the vessel initiates the extrinsic
pathway, whereas contact of factor XII and platelets with the
injured vessel wall traumatizes the blood and initiates the intrinsic
pathway. The extrinsic pathway is able to form clots in as little as 15
seconds with severe trauma, whereas the intrinsic pathway requires
2 to 6 minutes for clot formation. Both are necessary to maintain
clot.

FIGURE 10-3 Coagulation pathway. Source: (From Janz TG,

Hamilton GC: Disorders of hemostasis. In Marx J, Hockberger R, Walls R,
editors: Rosen’s emergency medicine: concepts and clinical practice, ed 7,
St Louis, 2009, Mosby.)

Heparin-induced thrombocytopenia
Pathophysiology
Heparin is the most widely used IV anticoagulant and one of the
most frequently prescribed drugs in the United States. Heparin
prevents the conversion of fibrinogen to fibrin. HIT, also called
heparin-induced thrombocytopenic thrombosis (HITT), white clot
syndrome, or heparin-associated thrombocytopenia (HAT), types I
and II, occurs when heparin therapy causes either a mild to

1914
moderate (i.e., HAT type I) or severe (i.e., HAT type II) decrease in
the number of freely circulating platelets. Platelets in affected
patients exhibit unusual aggregation and can result in heparin
resistance, arterial and venous thrombosis, and subsequent emboli
in extreme cases (Figure 10-4). Depending on the source of the
heparin received, HIT is reported in approximately 5% of all
patients receiving heparin. Bovine (beef-based) heparin has been
associated with HIT more frequently than other heparins. It is
estimated that as many as 50% of patients on heparin may be
asymptomatic but generate antibodies to heparin-platelet factor 4
(H-PF4), which increases the risk of HIT on their next exposure to
heparin. HIT is not related to the heparin dose and has been seen in
patients receiving low-dose subcutaneous heparin, as well as in
patients receiving simple heparin “flushes” to maintain patency of
IV lines.

1915
 FIGURE 10-4 Heparin-induced thrombocytopenia. IgG,
Immunoglobulin G.

Two types of HIT have been described:

• Mild to moderate, low morbidity: Generally occurs 1 to 2 days

after initiation of heparin. It may resolve within 5 days after
symptoms begin. Platelets may decrease to levels as low as
100,000/mm3 or may remain in the low-normal range. No
treatment is required, and heparin therapy may be continued if
the patient is asymptomatic.

1916
• High morbidity (immune-mediated): Generally begins 5 to 7 days
after initiation of heparin. Symptoms persist until heparin is
discontinued. Platelets decrease to less than 100,000/mm3.
Thrombosis with subsequent embolization and bleeding is
apparent. Complications may include pulmonary emboli,
myocardial infarction, cerebral infarction, and circulatory
impairment resulting in limb amputations. Mortality rate is 29%.
Overall, 0.6% of all patients receiving heparin therapy develop
thromboembolization.

Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.

Risk factors
Previous drug-induced or immunologic thrombocytopenia.

Vital signs
Tachypnea, tachycardia, hypertension.

Observation
Patients may present with high or low acuity states. Those without
clinical symptoms with a slight decrease in platelets are much
easier to manage than patients with severe, high morbidity.
Extreme cases manifest arterial thrombosis of the distal aorta and
proximal lower limb arteries. High morbidity patients present with:

• Petechiae, purpura, ecchymosis, gingival bleeding, hemoptysis,

epistaxis, bruising from mucosal surfaces or wounds.

• Signs of arterial occlusion: cold, pulseless extremities.

• Paresthesias; paralysis.

1917
• Severe chest pain and SOB, indicative of myocardial ischemia.

• Diminished LOC, indicative of cerebral ischemia.

Palpation
• Bone tenderness (especially rib and sternal areas).

• Enlargement of the liver and/or spleen.

• Joint tenderness.

• Enlargement of the liver and/or spleen.

• Abdominal tenderness.

Diagnostic Tests for Heparin-induced Thrombocytopenia

Test Purpose Abnormal Findings

Platelet count Used to diagnose bleeding Mild to moderate: 100,000 to
disorders or bone marrow disease 150,000/mm3; severe: <100,000/mm3
caused by severe clumping or
aggregation of platelets
Bleeding time Measures how quickly blood clots, Prolonged if platelets are
using platelets, coagulation <100,000/mm3
factors, and small vessel
vasospasm
Platelet antibody Identifies antibodies against Positive findings because of the
screen platelets presence of immunoglobulin G
platelet antibodies
Coagulation screening PT: extrinsic pathway (Coumadin) Normal, because the clotting
(prothrombin time PTT: intrinsic pathway (Heparin) factors that govern these test
[PT]; partial results are normal
thromboplastin time
[PTT], thromboplastin
time)
Fibrinogen Measures clot formation ability: May be low-normal or low as a
May be ordered as a follow-up to result of increased consumption.
an abnormal PT or PTT and/or an Normal is 200 to 400 mg/dL
episode of prolonged or
unexplained bleeding
Fibrin degradation Measures fibrin degradation Elevated to ≥40 µg/mL as a result
products (FDPs), products (which result from clots of fibrinolysis of platelet-fibrin
fibrin split products dissolving) in blood thrombi
(FSP), fibrin Normal is <10 µg/mL
breakdown products
Platelet aggregation Measures the rate and degree to Results will be >100% (or high
which platelets form a clump value of specific laboratory)

1918
 because of release of platelet
membrane antibody leading to
“clumping”
Heparin-induced Adds patient platelet-poor plasma Reflects abnormal aggregation
platelet aggregation (as a source of immunoglobulin) curve with a decrease in the optical
to normal platelet-rich plasma in density in the aggregometer
the presence of heparin to induce
platelet aggregation
Serotonin release Detects the presence of antibodies Helps in the differential diagnosis
testing and ELISA to PF4/heparin/TSP-1 complexes of heparin-induced
heparin PF4 thrombocytopenia
Bone marrow Evaluates bone marrow status; Normal or increased number of
aspiration diagnoses blood disorders and megakaryocytes (platelet
determines if cancer or infection precursors), indicative of normal
has spread to the bone marrow production of platelets or
increased response to need for
platelets

Collaborative management
Care priorities

1. Screen preheparin platelet count, and monitor

platelets and amount of heparin needed
A preheparin platelet count is made to establish baseline values.
Daily platelet counts should be done for at least the first 4 days of
heparin therapy. Subsequent counts are made every 2 days. If
increasing amounts of heparin are needed to maintain therapeutic
levels (i.e., partial thromboplastin time [PTT] 40 to 60 seconds),
heparin resistance should be suspected, which sometimes precedes
HIT (see Figure 10-4).

• Consider stopping heparin therapy: If the platelet count is greater

than 100,000/mm3 and the patient is symptom-free, heparin is
sometimes continued, but an alternate thrombin inhibitor may be
recommended. Oral anticoagulation should begin immediately, if
possible. If the platelet count is less than 100,000/mm3 and the
patient develops bleeding or thrombosis, heparin must be
discontinued immediately (including heparin flushes), alternate
anticoagulant initiated, and subsequent complications managed
when they occur. Use of low–molecular-weight heparins is
contraindicated.

1919
2. Administer defibrinogenating agents if high morbidity
symptoms are present
Ancrod (Arvin) may be given to reduce the possibility of
thrombosis.

3. Prevent pulmonary emboli with a vena cava filter

If the patient experiences thrombosis with a decrease or loss of
perfusion to an extremity, the physician or midlevel practitioner
may consider surgical insertion of a vena cava filter to reduce the
risk of pulmonary emboli caused by clot migration from an
extremity. See Pulmonary Embolus, Chapter 4.

• Warfarin, thrombolytics, and platelet inhibitors: Streptokinase,

urokinase, and alteplase (recombinant tissue plasminogen
activator [rtPA]) have been used successfully to manage
pulmonary emboli in HIT.

4. Maintain anticoagulation, if needed, with a direct

thrombin inhibitor
Argatroban and hirudin, direct thrombin inhibitors, block thrombin
generation needed for fibrin formation. They may be used alone or
in combination with warfarin, as an alternate anticoagulation
strategy for patients with HIT. Ximelagatran is the first orally
available thrombin inhibitor. Bivalirudin is not licensed for use with
HIT but can be used in patients undergoing percutaneous coronary
interventions. If the patient needs further anticoagulation, warfarin
sodium (Coumadin) should be considered. Platelet inhibitors are
contraindicated as a result of current platelet dysfunction.

5. Consider use of newer anticoagulation agents in those

who are difficult to manage
New medications using recombinant DNA technology focus on
each step of the coagulation process; many are under development.
These agents are grouped into three stages of coagulation:
initiation, propagation, and fibrin formation. Tissue factor pathway
inhibitor, nematode anticoagulant peptide, and factor VIIa target
initiation of coagulation. Soluble thrombomodulin, drotrecogin alfa
(activated protein C), protein C concentrate, fondaparinux, and

1920
idraparinux inhibit clot propagation. Direct thrombin inhibitors
(antithrombins) block fibrin formation for clot completion.

6. Provide platelet transfusions for high morbidity patients

who continue to bleed
May be initiated after heparin therapy is discontinued if bleeding
fails to subside.

7. Provide plasma exchange for high morbidity patients who

fail to respond to other therapies
In severe cases, 2 to 3 L of plasma is removed and replaced with
albumin, crystalloids, or fresh-frozen plasma to assist in decreasing
bleeding by removing bound heparin from the body.

Care plans: Heparin-induced

thrombocytopenia
Ineffective protection 
related to decreased platelet count with risk of bleeding and
thromboembolization.
Goals/Outcomes: Within 24 hours of discontinuing heparin
therapy, the patient exhibits no signs of new bleeding, bruising, or
thrombosis, as evidenced by HR 60 to 100 bpm or within 10% of the
patient’s baseline, RR 12 to 20 breaths/min with normal depth and
pattern, systolic BP at least 90 mm Hg, and all peripheral pulses at
the patient’s baseline or greater than 2+ on a 0-to-4+ scale.
Blood Coagulation.

Bleeding precautions

1. Assess the patient at least every 2 hours for signs of bleeding,

including hemoptysis, ecchymosis, petechiae on dependent areas,
gastrointestinal (GI) bleeding, hematuria, and bleeding from
invasive procedure sites or mucous membranes. Monitor the
patient closely for hemorrhage. Note Hgb and Hct levels before and
after blood loss, and at least daily as indicated.

1921
2. Assess for signs of internal bleeding including tachycardia and
dysrhythmias, tachypnea and hypotension. Sustained increase in
HR and RR or ECG changes, such as ST segment depression or
elevation, may precede hypotension.

3. Protect the patient from trauma that may cause bleeding. Do not
use rectal temperatures to monitor for fever. Avoid IM injections
and venous and arterial punctures as possible until bleeding time
normalizes.

4. Perform a comprehensive assessment of peripheral circulation

(e.g., check peripheral pulses, edema, capillary refill, and color and
temperature of extremities) at least every 2 hours and assess the
patient for signs of thrombosis, including decreased peripheral
pulses, altered sensation in extremities (i.e., paresthesias,
numbness), pallor, coolness, cyanosis, or capillary refill time more
than 2 seconds. Monitor extremities for areas of heat, pain, redness,
or swelling.

5. Maintain adequate hydration to prevent increased blood

viscosity and to help prevent constipation.

6. Administer stool softeners to help reduce straining with bowel

movements, which may prompt rectal bleeding.

7. Monitor platelet count daily for significant changes. Consult the

advanced practice provider for values that remain less than
150,000/mm3 or below the patient’s baseline.

8. Monitor heparin dosage carefully. If increasing doses are

required to maintain a therapeutic level (PTT 40 to 60 seconds or 2
to 2.5 times the patient’s baseline), consult the advanced practice
provider regarding possible heparin resistance, an early indicator of
HIT. If heparin has been discontinued and new anticoagulants
initiated, monitor appropriate values. If a direct thrombin inhibitor
(e.g., Argatroban) is used alone, or in combination with warfarin,
monitor prothrombin time (PT) and international normalized ratio
(INR).

1922
9. Assess the patient’s neurologic status hourly if platelet count
decreases to less than 30,000.

10. Monitor for signs of MODS secondary to thrombosis or

prolonged hypotension, if the patient has hemorrhaged. (See
Systemic Inflammatory Response Syndrome, Sepsis, and Multiple
Organ Dysfunction Syndrome, SIRS, Chapter 11.)

11. Teach the patient and significant others about the basic
pathophysiology of HIT, and instruct them to report this problem
to all subsequent healthcare providers. Teach the patient to wear a
medical-alert bracelet to alert healthcare providers if the patient
becomes unable to speak.

Surveillance: Safety; Vital Signs Monitoring.

Deficient fluid volume (or risk for same) 

related to active blood loss
Goals/Outcomes: The patient becomes normovolemic within 24
hours of onset of treatment, as evidenced by HR within the
patient’s normal range or 60 to 100 bpm, RR 12 to 20 breaths/min
with normal depth and pattern and urinary output at least 0.5
mL/kg/h, and absence of abdominal discomfort, back pain, or pain
from invasive procedure sites.
Fluid Balance.

Hypovolemia management

1. Monitor the patient for signs of hypovolemia, including increased

HR and RR, decreased BP, increased restlessness or fatigue, and
decreased urine output.

2. Administer supplemental oxygen if the patient is actively

bleeding.

3. Maintain accurate I&O record. Weigh daily and monitor trends.

4. Assess for intraabdominal bleeding: Note any abdominal pain,

tenderness, guarding, or back pain.

1923
5. Check excretions for occult blood, and observe for blood in
emesis, sputum, feces, urine, nasogastric drainage, and wound
drainage as appropriate.

6. Instruct the patient and/or family on the need for blood

replacement as appropriate.

7. Replace lost volume with plasma expanders (e.g., albumin,

hetastarch) or blood products as indicated. See Table 10-3 for more
information.

Electrolyte Management; Fluid Management; Fluid

Monitoring; Intravenous (IV) Therapy; Bleeding Reduction:
Gastrointestinal; Shock Management: Volume; Blood Products
Administration.

Additional nursing diagnoses

Uncontrolled bleeding or thrombotic complications can be
terrifying for the patient and significant others, who may fear that
the patient will die. See nursing diagnoses and interventions in
Emotional and Spiritual Support of the Patient and Significant
Others, Chapter 2.

Immune thrombocytopenia purpura

Pathophysiology
Immune (often idiopathic) thrombocytopenia purpura (ITP) is a
disorder characterized by premature platelet destruction as well as
impaired platelet production, resulting in a decrease in the platelet
count to below 100,000/mm3. Normal platelet life span averages 1 to
3 weeks, whereas in ITP the platelet life span averages 1 to 3 days
because of the presence of antiplatelet IgG and IgM antibodies,
which destroy platelets in the reticuloendothelial system of the
spleen. The coagulopathy is believed to be an autoimmune
response and manifests as both an acute and a chronic problem.
Acute ITP is primarily a childhood disease, characterized by an
abrupt onset of severe thrombocytopenia with evident purpura.

1924
Usually it occurs within 21 days following a viral infection. At the
onset, platelets decrease to less than 20,000/mm3. The chronic form
is typically a disease of adults aged 20 to 50 years, but it has
occurred in a small percentage of children and older adults. The
chronic disease rarely resolves spontaneously, sometimes responds
to treatment of the underlying disorder, and usually is not
associated with infection but can be related to autoimmune
disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis)
and neoplastic disorders (e.g., chronic lymphocytic leukemia,
lymphoma). Women are affected three times more often than men.
Petechiae and purpura are commonly seen on the distal upper and
lower extremities. Patients may feel symptom-free until actual
bleeding begins. Intracranial hemorrhage is a potential
complication. Platelet counts decrease to as low as 5000/mm3 in
some patients, but may be as high as 75,000/mm3 in others.

Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.

Risk factors
• Acute ITP: History of antecedent viral infection occurring
approximately 3 weeks before the hemorrhagic episode.

• Chronic ITP: Insidious and sometimes associated with

autoimmune hemolytic anemia, HIV disease, hemophilia,
lymphoma, chronic lymphocytic leukemia, systemic lupus
erythematosus, sarcoidosis, high-titer anticardiolipin antibodies,
pregnancy, malabsorption, and thyrotoxicosis. The cause is often
unknown.

Vital signs
• Tachypnea, tachycardia, hypotension, fever.

1925
 Observation
• Petechiae, purpura, bruising on skin and mucous membranes,
prolonged bleeding; intracranial hemorrhage occurs in less than
1% of patients if the thrombocytopenia is severe.

• Diminished LOC, indicative of intracranial hemorrhage.

• Epistaxis, gingival bleeding, GI, genitourinary (GU), gynecologic

(GYN) bleeding such as increased menstrual flow.

• Retinal disturbances.

Palpation
• Enlargement of the liver and/or spleen.

• Lymphadenopathy, hepatomegaly, splenomegaly.

• Joint tenderness.

Diagnostic Tests for Immune Thrombocytopenia Purpura

Test Purpose Abnormal Findings

Platelet count Used to diagnose bleeding disorders or bone Decreased to 5000 to
marrow disease 75,000/mm3 (or lower)
because of premature
destruction
Normal range is 150,000 to
400,000/mm3
Bleeding time Measures how quickly blood clots, using Prolonged if platelets are less
platelets, coagulation factors, and small than 100,000/mm3
vessel vasospasm
Platelet Identifies antibodies against platelets Positive findings because of the
antibody screen presence of immunoglobulins
G and M antiplatelet antibodies
Coagulation PT: extrinsic pathway (Coumadin) PTT: Normal, because these tests
screening intrinsic pathway (Heparin) measure nonplatelet
(prothrombin components of the coagulation
time [PT]; pathway
partial
thromboplastin
time [PTT];
thromboplastin
time)
Complete blood Measures red blood cells, white blood cells Decreased hemoglobin and

1926
count with (WBCs), platelets, and the WBC differential hematocrit resulting from
differential insidious blood loss or
simultaneous hemolytic
anemia (Evans syndrome)
Normal WBC count: Unless
idiopathic thrombocytopenic
purpura is associated with
another disease impacting
differential leukocyte count
Capillary- Method to determine a patient’s Will show >1+, which signals
fragility test: hemorrhagic tendency: Assesses fragility of that more than 11 petechiae
Rumpel-Leede capillary walls: Used to identify were present in a 2.5-cm radial
capillary- thrombocytopenia. Seldom used in current area on the skin after prolonged
fragility test practice, but may be used to discern from application of a blood pressure
damage as a result of prolonged cuff cuff Normal is 1+ or <10
inflation in patients with blood dyscrasias petechiae
Bone marrow Evaluates bone marrow status; diagnoses Biopsy will reveal
aspiration blood disorders and determines if cancer or megakaryocytes (platelet
infection has spread to the bone marrow precursors) in normal or
increased numbers with a
“nonbudding” appearance,
possibly indicating defective
maturation or failure of platelet
production

Collaborative management: Immune

thrombocytopenic purpura
Care priorities

1. Suppress immune response to reduce platelet

destruction

• Corticosteroid therapy: Adrenocorticosteroids (e.g., prednisone 1

to 2 mg/kg/day) are effective in increasing the platelet count in 1
to 3 weeks after initiation of treatment. Effectiveness is attributed
to suppression of phagocytic activity of the macrophage system
(particularly the spleen), which increases the life span of the
antibody-coated platelets. If improvement does not occur within
2 to 3 weeks, excessive doses of steroids are required, or if patient
cannot tolerate tapering of steroids, splenectomy should be
considered. “Normal” responders are able to have steroid dosage
tapered over several weeks until platelets reach a sustained value
of 50,000/mm3. Relapse during or after tapering prednisone is a
common occurrence.

1927
• IV immunoglobulin (IVIG): Given at 400 mg/kg/day for 2 to 5
consecutive days, resulting in increased platelet count in 60% to
70% of patients. Serum sickness (fever, chills, rash) is not
uncommon between 9 and 14 days. It is less effective in patients
with long-standing chronic ITP. The platelet level at initiation of
treatment and incidence of serum sickness is not necessarily
correlated to individual response. Duration of response may be
longest in individuals who achieve the highest initial platelet
increases.

• Danazol: 400 to 800 mg/day has resulted in complete remission or

partial improvement in 60% to 70% of patients in several studies.
Use is controversial because other researchers have reported poor
results and many untoward side effects.

• Splenectomy: Treatment of choice in cases refractory to

corticosteroid therapy. The condition stabilizes in 60% to 70% of
patients who undergo splenectomy. The positive results are
attributed to the removal of the site of destruction of the
antibody-sensitized platelets. Prospective splenectomy
candidates should have pneumococcal, meningococcal, and
Haemophilus influenzae type B vaccinations before a planned
splenectomy, to reduce the risk of postoperative infection with
these organisms.

• Immunosuppression: Various immunosuppressive drugs,

including azathioprine, cyclophosphamide, methotrexate,
vincristine, and cyclosporine, given alone or in combination with
prednisone, have been used successfully in limited situations. A
trial of immunosuppression therapy may be indicated in patients
who fail to respond to splenectomy or in those who are too
unstable to be surgical candidates.

• Anti-Rh immunoglobulin: Low dose (200 to 1000 µg) given IV for

1 to 5 days has been effective in limited studies. Success of
treatment is attributed to sensitization of recipient RBCs, which
results in low-grade hemolysis and blockade of the platelet
destruction by the reticuloendothelial system.

1928
• Colchicine: A small percentage of patients refractory to other
treatments may improve with 1.2 mg colchicine daily for 2 weeks
or longer. The drug has been used successfully in limited studies.

• Plasmapheresis: Several days of machine-assisted plasma

exchange to remove approximately 1 to 1.5 times the total plasma
volume per procedure and replace it with a suitable solution
(e.g., colloids, crystalloids, plasma). Therapy is reserved for
patients with life-threatening hemorrhage unresponsive to other
measures. It is costly and of marginal benefit.

2. Increase platelet count

• Romiplostim: A treatment approved for use in patients with

chronic ITP who are refractory to corticosteroids,
immunoglobulins, or splenectomy. A thrombopoietin receptor
agonist that stimulates bone marrow megakaryocytes to increase
platelet production; 1 µg/kg is given as a subcutaneous injection
once weekly, titrated to a maximum dose of 10 µg/kg to achieve a
platelet count of greater than 50,000. Rare side effects include
bone marrow fibrosis and reticulin formation.

• Platelet transfusions: Platelets are given only in cases of life-

threatening hemorrhage. The shortened platelet life span renders
prophylactic transfusions ineffective.

• Vinca “alkaloid-loaded” platelets: Transfusions of platelets

“loaded” with vinblastine may reduce the phagocytic destruction
of platelets in patients who fail to respond to other treatments.

• Rituximab: Primary monoclonal antibody used to treat

lymphoma, now showing promise in treatment of ITP.

Care plans for immune thrombocytopenic

purpura
Ineffective protection 
related to decreased platelet count, resulting in increased risk of bleeding.

1929
 Goals/Outcomes: Within 72 hours of onset of treatment, the
patient exhibits no clinical signs of new bleeding or bruising
episodes. Secretions and excretions are negative for blood, and vital
signs are within 10% of the patient’s normal range. Within the 24-
hour period before discharge from intensive care, the patient and
significant others verbalize understanding of the indicators of
potential or actual bleeding.
Blood Coagulation.

Bleeding precautions

1. Monitor the patient for bleeding and hemorrhage, including

elevated HR and RR, decreasing BP, oozing from invasive
procedure sites, bleeding mucous membranes, hematuria, and GU,
GYN, and GI bleeding. Note Hgb and Hct levels before and after
blood loss, as indicated.

2. Protect the patient from trauma that may cause bleeding. Avoid
taking rectal temperatures.

3. Maintain fluid intake to prevent constipation and administer

stool softeners to minimize straining.

4. Monitor skin or mucous membranes for pallor, discoloration,

bruising, breakdown, and erythema.

5. Monitor coagulation studies, including PT, PTT, fibrinogen, fibrin

degradation products (FDPs), fibrin split products (FSPs), and
platelet counts as appropriate.

6. Consult the advanced practice provider for sustained low platelet

values (less than 100,000/mm3 or as appropriate for the individual).

7. Avoid administering NSAIDs (e.g., aspirin, ibuprofen). Teach the

patient to avoid all medications that potentially decrease platelet
aggregation, especially aspirin or aspirin-containing products.

8. For severe menorrhagia, confer with the advanced practice

provider regarding the need for progestational hormones for
suppression of menses. Assess blood loss by weighing perineal

1930
pads or tampons.

9. During the acute (bleeding) phase of ITP, teach the patient to

perform oral hygiene using sponge-tipped applicators soaked in
water or dilute mouthwash to help prevent gum bleeding. Avoid
hydrogen peroxide or lemon-coated swabs.

10. Teach the patient that it is always safer to use an electric razor
for shaving.

11. Instruct family member/caregiver about signs of skin

breakdown, as appropriate.

12. Teach the patient and significant others to recognize the signs of
impending hemorrhage: more rapid pulse and breathing, easy
bruising, painful joints, and blood in sputum, urine, or stool.

Skin Surveillance.

Decreased intracranial adaptive capacity: (or risk for

same 
related to potential for intracranial hemorrhage (less than 1% of patients)
secondary to decreased platelet level.
Goals/Outcomes: Throughout the hospitalization, the patient
remains free of symptoms of intracranial hemorrhage, as evidenced
by orientation to time, place, and person; normoreactive pupils and
reflexes; the patient’s normal visual acuity, motor strength, and
coordination; and absence of headache and other clinical indicators
of increased intracranial pressure.
Neurologic Status.

Neurologic monitoring

1. Assess the patient for initial signs of increased intracranial

pressure, including diminished LOC, headaches, pupillary
responses (e.g., unequal, sluggish/absent response to light), visual
disturbances, weakness and paralysis, slow HR, and change in
respiratory rate and pattern.

1931
2. Monitor trend of Glasgow Coma Scale (Appendix 2), intracranial
pressure, and cerebral perfusion pressure.

3. Increase frequency of neurologic monitoring as appropriate.

4. Avoid activities that increase intracranial pressure (i.e., Valsalva

maneuver, hyperthermia, pain, etc.). Administer stool softeners and
cough suppressants as prescribed.

5. If initial signs of increased intracranial pressure are noted,

consult the physician immediately. Severe intracranial bleeding can
lead to herniation. Intracranial pressure can increase rapidly with
severe bleeding, sometimes causing death within 1 hour of onset.
Signs of impending herniation include unconsciousness, failure to
respond to deeply painful stimuli, decorticate or decerebrate
posturing, Cushing’s triad (i.e., bradycardia, increased systolic BP,
widening pulse pressure), nonreactive/fixed pupils, unequal pupils,
or fixed and dilated pupils. See Traumatic Brain Injury, Chapter 3
for more information about herniation.

6. Consult with the advanced practice provider regarding

management of increased intracranial pressure (see Traumatic
Brain Injury, Chapter 3, for collaborative interventions for increased
intracranial pressure). For additional interventions for increased
intracranial pressure, see Box 3-7.

7. Teach the patient to avoid Valsalva maneuver (e.g., straining at

stool or when lifting; forceful and sustained coughing or nose
blowing), which could cause intracranial bleeding.

8. Teach the importance of avoiding tobacco products (particularly

cigarettes) and excessive caffeine, which may cause
vasoconstriction. Constricted vessels may prevent platelets from
circulating through portions of the capillary network.

Cerebral Edema Management; Cerebral Perfusion Promotion;

Intracranial Pressure Monitoring; Neurologic Monitoring.

Risk for deficient fluid volume 

1932
related to active loss secondary to intraabdominal bleeding or
postsplenectomy intraabdominal bleeding.
Goals/Outcomes: The patient remains normovolemic, as
evidenced by HR, RR, and BP within 10% of the patient’s normal
range (or HR 60 to 100 bpm, RR 12 to 20 breaths/min with normal
depth and pattern, systolic BP ≥90 mm Hg); urinary output at least
0.5 mL/kg/h; and absence of abdominal pain or tenderness, back
pain, and frank bleeding from the splenectomy incision.
Fluid Balance.

Fluid management

1. Monitor fluid status, including I&O, and signs of hypovolemia,

including increases in HR and RR and decreases in BP, and urinary
output, restlessness, fatigue, and orthostatic vital signs.

2. Inspect for bleeding from mucous membranes, bruising after

minimal trauma, oozing from puncture sites, and presence of
petechiae. Maintain patent IV access.

3. Administer supplemental oxygen as necessary for postoperative

status or active bleeding.

4. Replace lost volume with plasma expanders (e.g., albumin,

hetastarch) and/or blood products as indicated. See Table 10-3 for
information about blood products.

5. Inform the patient of the importance of wearing a medical-alert

bracelet and obtaining a pneumococcal vaccination if a splenectomy
has been performed.

Bleeding Precautions; Electrolyte Management; Fluid

Monitoring; Hypovolemia Management; Intravenous (IV) Therapy;
Shock Management: Volume; Blood Products Administration.

Acute pain 
Related to joint inflammation and injury secondary to bleeding into the
synovial cavity of the joint(s); postsplenectomy pain.
Goals/Outcomes: Within 4 hours of initiating treatment, the

1933
patient’s subjective evaluation of discomfort improves, as
documented by a pain scale, nonverbal indicators of discomfort are
absent or decreased, and HR, RR, and BP are within 10% of the
patient’s baseline.
Pain Control.

Pain management

1. Devise a pain scale with the patient, rating discomfort from 0 (no
pain) to 10. Perform a comprehensive assessment of pain to include
location, characteristics, onset/duration, frequency, quality,
intensity or severity, and precipitating factors.

2. Ensure the patient receives appropriate analgesic care. Consult

with the advanced practice provider regularly until the patient’s
pain is controlled. Avoid use of meperidine for pain relief in older
adults or individuals with renal compromise; adverse effects are
common.

3. Teach the patient causes of the pain, how long it may last, and
about discomforts from procedures.

4. Elevate the patient’s legs to decrease joint pain in the lower

extremities. Avoid knee flexion. Support extremities with pillows,
making sure the bed is not “gatched” at the knee.

5. Teach the patient to splint the abdomen when coughing after

splenectomy.

6. Evaluate the patient’s anxiety level, and provide emotional

support to control fear and anxiety. If the patient becomes agitated,
evaluate potential causes including hypoxemia, poor pain or
anxiety control, fluid and electrolyte imbalance, and alcohol or drug
withdrawal, and intervene appropriately.

7. See Pain, Chapter 1, for additional pain interventions. Also see

Prolonged Immobility, Chapter 1, for patients who are unable to
move or who have limited movement.

Analgesic Administration; Pain Management; Coping

1934
Enhancement; Anxiety Reduction.

Additional nursing diagnoses

Uncontrolled bleeding can be terrifying for the patient and
significant others, who may fear that the patient will die. Refer to
nursing diagnoses in Emotional and Spiritual Support of the Patient
and Significant Others, Chapter 2, for appropriate interventions.

Disseminated intravascular coagulation

Pathophysiology
Disseminated intravascular coagulation (DIC) is a syndrome
characterized by overstimulation of the normal coagulation
cascade, often related to severe sepsis or shock. DIC is a
coagulopathy with potential to cause both profuse bleeding and
widespread thrombosis leading to MODS. Inherent bodily control
of bleeding requires a balance between procoagulants and
thrombus formation, along with anticoagulants, inhibitors, and
thrombolysis (see Figure 10-3; Table 10-4). The delicate balance may
be upset by disease processes (Table 10-5), resulting in a cascade of
uncontrolled coagulation and fibrinolysis. The abnormal clotting
cascade that develops during DIC is as follows:

• Platelets and coagulation factors are activated by a disease

stimulus and are rapidly consumed, particularly factors V and
XIII and fibrinogen.

• Thrombin is formed very rapidly, and inherent inhibitors cannot

stop the formation of the vast amounts of thrombin generated.
Thrombin directly activates fibrinogen.

• Fibrin is deposited throughout the capillary beds of organs and

tissues.

• The fibrinolytic system lyses fibrin and impairs thrombin

formation.

1935
• FDPs (or FSPs) result from fibrinolysis, which changes platelet
aggregation and inhibits fibrin polymerization. See Figure 10-3
for the normal coagulation pathway.

Table 10-4
CLOTTING FACTORS: PRIMARY ACTIONS

Table 10-5
DISSEMINATED INTRAVASCULAR COAGULATION:
PREDISPOSING CONDITIONS

1936
 A predisposing event that damages the vascular endothelium
initiates the clotting cascade. Studies reflect that both the intrinsic
and extrinsic pathways are activated initially, resulting in an
abnormal acceleration of the clotting process. Thrombocytopenia
occurs because of thrombin production and microvascular
thrombus formation.

Assessment
Goal of system assessment
Evaluate for increased risk of inappropriate bleeding or clotting as a
result of qualitative or quantitative dysfunction of platelets and
clotting factors.

Risk factors
Any clinical state or pharmacologic therapy (e.g., chemotherapy)
that inhibits the removal of activated clotting factors, FDPs, and
thromboplastin by the reticuloendothelial system. Any patient is at
high risk following severe trauma or with SIRS, a severe infection,
sepsis, severe sepsis, septic shock, or invasive procedures.
Obstetrics patients with abruptio placentae, amniotic fluid
embolism, or eclampsia release procoagulation factors, placing
them at risk. DIC can occur as a paraneoplastic syndrome or
oncologic emergency related to certain malignancies such as acute
promyelocytic leukemia (APL), multiple myeloma, and some solid
tumors. DIC may manifest as a profound bleeding/clotting disorder
in the acute phase or as a less symptomatic chronic disorder.

1937
 In chronic (compensated) DIC, activation of coagulation and
fibrinolysis does not occur rapidly enough to exceed the rate of
production of clotting factors or inhibitors. The course of DIC
depends on the intensity of the stimulus, coupled with the status of
the liver, bone marrow, and vascular endothelium. Whether DIC
leads to bleeding or to thrombosis is profoundly affected by the
underlying disease process.

Vital signs
• Tachypnea, tachycardia, hypotension.

Observation
• Bleeding with abrupt onset: From invasive procedure sites and
mucosal surfaces (e.g., oral, nasal, tracheal, gastric, urethral,
vaginal, rectal); may include hematuria, petechiae, stools or
gastric aspirate positive for occult blood, pallor, tachycardia,
tachypnea, vertigo, hypotension, ecchymoses (e.g., on palate,
gums, skin, conjunctivae), lethargy, irritability, or feeling of
impending doom, and possible back pain and abdominal
tenderness.

• Anxiety, restlessness.

• Petechiae, purpura, ecchymoses, oozing blood, mottling.

• Conjunctival hemorrhage and periorbital petechiae.

• Acrocyanosis.

• Joint pain, weakness.

• SOB, ST segment elevation/depression, T wave inversion.

• Grey Turner sign (flank ecchymoses).

• Hemoptysis, tarry stools, melena.

• Decreased responsiveness, confusion, altered mentation,

1938
 headaches.

• Abnormal thrombosis may manifest with extremity pain,

diminished pulses, oliguria or anuria, diminished or absent
bowel sounds, severe chest pain with SOB (indicative of either
myocardial infarction or pulmonary embolism), or paresis or
paralysis (indicative of cerebral thrombus).

Palpation
• Hepatosplenomegaly.

• Abdominal tenderness.

Auscultation
• Diminished or absent bowel sounds.

• Weakened or absent peripheral pulses.

Diagnostic Tests for Disseminated Intravascular Coagulation

Test Purpose Abnormal Findings

Fibrin Measures fibrin degradation products Increased (>10 µg/mL) as a result
degradation (which result from clots dissolving) in of widespread fibrinolysis, which
products blood produces FDPs as the end
(FDPs), fibrin product of clot lysis Critical
split products value: >40 ng/mL
(FSP), fibrin
breakdown
products
d-Dimer assay Measures cleavage products of fibrin Increased to >500 as a result of
increased thrombin and plasmin
generation. This is a rapid
measurement technique, less
sensitive than FDPs, and not
recommended as a substitute for
FDPs and fibrinogen
determinations
Fibrinogen Measures clot formation ability: May be May remain normal or decrease
ordered as a follow-up to an abnormal in the early acute phase. As the
prothrombin time (PT) or partial process continues, fibrinogen
thromboplastin time (PTT), and/or an levels will decrease. Normal
episode of prolonged or unexplained range is 150 to 400 mg/dL
bleeding
PTT or Measure of the integrity of the intrinsic and Prolonged (>40 seconds) because

1939
activated common pathways of the coagulation of activation of the intrinsic
partial cascade. The aPTT is the time, in seconds, pathway, causing consumption
thromboplastin for patient plasma to clot after the additionof coagulation factors. Critical
time (aPTT) of an intrinsic pathway activator, value: >70 seconds. In chronic
phospholipid, and calcium disseminated intravascular
coagulation (DIC), the value may
be normal (25 to 35 seconds) or
less than normal
PT, Measure of the integrity of the extrinsic Prolonged (>15 seconds) because
international pathway of the coagulation cascade of activation of the extrinsic
normalized pathway, causing consumption
ratio (INR) of the extrinsic clotting factors.
Critical value: >40 seconds
Thrombin Test of the time it takes for a clot to form, Prolonged (>1.5 times the control
time, thrombin measuring the conversion of fibrinogen to value or >2 seconds in excess of a
clotting time fibrin 9- to 13-second control value)
because of rapid conversion of
fibrinogen into fibrin
Antithrombin Evaluates whether the total amount of Decreased (<50% of control value
III (AT-III), functional antithrombin is normal. Activity using a plasma sample, or <80%
functional will be decreased with both type 1 and type using functional values) because
antithrombin 2 antithrombin deficiencies, thus this test of rapid consumption of this
III, can be used as an initial screen for both. If thrombin inhibitor. The action of
antithrombin, the antithrombin activity is low, then the AT-III is catalyzed by heparin
activity, and antithrombin antigen test is performed to
antigen determine the quantity of antithrombin
present
Euglobulin clot Measures overall fibrinolysis; measures Decreased time is seen with DIC.
lysis time fibrinogen activity via measurement of Normal: Lysis in 2 to 4 hours.
plasminogen and plasminogen activator, Critical value: 100% lysis in 1
which assist in prevention of fibrin clot hour
formations
Platelet count Used to diagnose bleeding disorders or Decreased (<140,000/mm3)
bone marrow disease because of rapid rate of platelet
aggregation to form clots during
DIC. Aggregation decreases the
freely circulating platelets
Alpha2- Measures alpha2-antiplasmin, which is an Decreased because of rapid
antiplasmin inhibitor that regulates the fibrinolytic consumption resulting from large
system primarily by blocking the enzymatic amounts of plasmin generated.
activity of plasmin When all alpha2-antiplasmin is
depleted, excessive
hyperfibrinolysis (massive, rapid
clot lysis) occurs
Protamine Associated with the formation of excessive Results are positive (normal:
sulfate test amounts of thrombin and secondary negative), indicative of presence
fibrinolysis of fibrin strands
Peripheral Microscopic examination of cells from a For visualization during
blood smear drop of blood; investigates hematologic microscopic examination of
problems or parasites such as malaria and schistocytes and burr cells, which
filarial indicate the deposition of fibrin
in the small blood vessels

Collaborative management: Disseminated

1940
intravascular coagulation
Care priorities

1. Treat the primary cause of the disease

Aggressively treat the underlying cause. A primary disease
promotes the development of DIC. If treatment of the disease fails,
the mortality rate of DIC is high. When DIC occurs without
apparent cause, the possibility of undiagnosed malignancy (e.g.,
prostate cancer or APL), a large abdominal aortic aneurysm, a
progressive gram-negative bacterial infection, or hepatic cirrhosis
should be explored. If the diagnosis is by laboratory tests alone,
conservative management is appropriate. Other conditions and
medication side effects should be considered (see Table 10-5).

2. Manage abnormal clotting with continuous IV heparin

therapy
There are three conditions associated with DIC in which
heparin may be effective:

• Underlying malignancy/carcinoma.

• Acute promyelocytic leukemia (APL): A leukemia most often seen

in young adults with acute myelocytic anemia, which may also
be linked to patients who received radiotherapy for prostate
cancer.

• Purpura fulminans/extreme purpura, often seen with severe

sepsis.

If used, the patient should have clinically obvious thrombosis.

Low-dose therapy (5 to 10 units/kg/h) is considered. Heparin binds
to antithrombin, resulting in a strong anticoagulant effect. Use of
higher-dose heparin in DIC is associated with a high risk of
bleeding, and greater efficacy has not been documented. Heparin
may be considered for serious bleeding or clotting when the
condition underlying the DIC is not rapidly reversible and the
patient’s vascular system is surgically intact.

1941
 Patients who have acute promyelocytic leukemia with
disseminated intravascular coagulation often experience
accelerated symptoms of fibrinolysis (declotting) when receiving
chemotherapy. If these individuals receive heparin, an
antifibrinolytic agent such as epsilon- (ε-)aminocaproic acid
(Amicar) may be added to decrease bleeding.

3. Manage abnormal bleeding resulting from fibrinolysis

with antifibrinolytics
ε-Aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron)
are used to inhibit fibrinolysis in patients who are bleeding as a
result of a variety of causes. In patients with DIC, these agents
should be used with extreme caution because they may convert a
bleeding disorder into a thrombotic problem. When used in DIC,
these agents are used in combination with heparin to minimize the
potential for thrombosis. Failure rates with use are high.

4. Consider use of thrombolytic agents for abnormal

clotting
Use of streptokinase, urokinase, and rtPA is not indicated for
patients with thrombosis because these agents may facilitate
excessive bleeding.

5. Provide replacement of necessary blood components

Clotting factors and inhibitors are replaced in the form of fresh-
frozen plasma. The PT/INR may be the most accurate
measurement(s) for guiding plasma replacement. Patients with
markedly decreased fibrinogen levels may be given cryoprecipitate,
which contains 5 to 10 times more fibrinogen than plasma contains.
Thrombocytopenia in DIC may not be severe. The platelet count is
usually greater than 50,000/mm3. General replacement therapy
guidelines indicate that approximately 10 units of cryoprecipitate
should be given for every 2 to 3 units of plasma. Platelet

1942
transfusions are used if the patient has impaired platelet production
and profuse bleeding. Antithrombin III (AT-III) concentrate has
been used on a limited basis (see Table 10-3). More recently, DIC is
being managed with antithrombin concentrate, activated protein C
(drotrecogin alfa), tissue factor pathway inhibitor, and synthetic
serine protease inhibitors (e.g., aprotinin).

• RBC replacement: Packed RBCs may be administered to increase

oxygen-carrying capacity to maintain a Hgb value 7 to 9 mg/dL
or greater than 20% below the patient’s baseline if the patient is
chronically anemic and symptomatic.

6. Supplement vitamin K1 (phytonadione) and folate

Patients with DIC are at high risk for deficiency of these substances,
and administration of both vitamins is recommended for most
patients.

7. Prevent viral infections resulting from

immunosuppression with protease inhibitors
Gabexate, nafamostat, and trasylol have been used.

8. Manage hypotension related to heart failure, as

appropriate
If the patient becomes severely hypotensive resulting from heart
failure, the following drugs may be considered: milrinone,
dobutamine, dopamine, epinephrine, and nitroprusside (see
Appendix 6).

Care plans: Disseminated intravascular

coagulation
Ineffective protection
related to bleeding resulting from overstimulation of the clotting cascade
and rapid consumption of clotting factors.
Goals/Outcomes: Within 48 to 72 hours of initiation of treatment,
the patient is free of symptoms of bleeding, as evidenced by
absence of frank bleeding from invasive procedure sites and

1943
mucosal surfaces; secretions and excretions that are negative for
blood; absence of large or increasing ecchymoses; decreasing
purpura; and HR, RR, and BP within 10% of the patient’s baseline
(or HR 60 to 100 bpm, RR 12 to 20 breaths/min, systolic BP greater
than 90 mm Hg).
Blood Coagulation.

Bleeding precautions

1. Discuss bleeding history with the patient or significant others.

Assess previous incidences of bleeding from gums, skin, or urine;
tarry/bloody stools; bleeding from muscles or into joints;
hemoptysis, vomiting of blood, epistaxis, or prolonged bleeding
from small wounds or after tooth extraction; or unusual bruising or
tendency to bruise easily. Provide soft tooth brush.

2. Question patients about current medications, including over-the-

counter preparations, because many medications promote bleeding
(Table 10-6).

3. Monitor coagulation tests daily. Consult the advanced practice

provider for abnormal values (Table 10-7).

4. Monitor closely for increased bleeding, bruising, petechiae, and

purpura. Assess for internal bleeding by testing suspicious
secretions (i.e., sputum, urine, stool, emesis, gastric drainage) for
the presence of blood. Monitor for hemorrhage.

5. Monitor neurologic status (see Glasgow Coma Scale, Appendix 2)

every 2 hours by assessing LOC, orientation, pupillary reaction, and
movement and strength of extremities. Changes in status can
indicate intracranial bleeding.

6. Use alcohol-free mouthwash and swabs for oral care to minimize

gingival/gum injury. Use normal saline solution (NSS) or solution
of NSS and sodium bicarbonate (500 mL NSS with 15 mL
bicarbonate) to irrigate the oral cavity if irritated. Massage gums
gently with a sponge-tipped applicator to help remove debris. Do
not attempt to remove large clots from the mouth, to avoid profuse

1944
bleeding.

7. Use electric rather than safety razor for shaving the patient.

8. Refrain from inserting objects into a bleeding orifice. Avoid

taking rectal temperatures.

9. Protect the patient from trauma. Avoid unnecessary

venipunctures and IM injections.

10. If the patient undergoes an invasive procedure, manually hold

pressure over the insertion site for 3 to 5 minutes for IV catheters
and 10 to 15 minutes for arterial catheters or until bleeding
subsides.

11. Instruct the patient and/or family on signs of bleeding and

appropriate actions.

12. Teach the patient the importance of avoiding vitamin K–

inhibiting and platelet aggregation–inhibiting medications or
vitamin and dietary supplements (see Table 10-6), which promote
bleeding.

Table 10-6
MEDICATIONS THAT MAY PROMOTE BLEEDING

Medications that Inhibit Platelets or Cause Thrombocytopenia

Analgesics: Diuretic Agents: Other:
Nonsteroidal antiinflammatory Sulfonamide derivatives Antihistamines
agents Acetazolamide Ethanol
Aspirin (acetylsalicylic acid) Chlorpropamide Heparin
Acetaminophen Chlorothiazide Beta-adrenergic–blocking
Antipyrine Chlorthalidone agents
Ibuprofen Clopamide General anesthetics
Indomethacin Diazoxide Local anesthetics
Fenoprofen Furosemide Chemotherapeutic agents
Sodium salicylate Bumetanide Vitamin E
Antirheumatic agents Hydrochlorothiazide Estrogens
Oxyphenbutazone Tolbutamide Digitoxin
Phenylbutazone Spironolactone Cimetidine
Hydroxychloroquine Mercurial diuretics Levodopa
Gold salts Glycoprotein IIb/IIIa Propylthiouracil
Antimicrobials inhibitors
Ampicillin Abciximab
Cephalothin Eptifibatide
Methicillin Tirofiban

1945
 Penicillin Phenothiazines
Pentamidine Chlorpromazine
Streptomycin Promethazine
Sulfonamides (antibiotics) Trifluoperazine
Chloramphenicol Phosphodiesterase
Isoniazid inhibitors
Nitrofurantoin Caffeine
Rifampin Dipyridamole
Trimethoprim Theophyllines
Anticoagulants Antiplatelet drugs
Heparin Aspirin (acetylsalicylic
Enoxaparin acid)
Dalteparin Ticlopidine
Thrombolytics Clopidogrel
Alteplase Prostaglandin I2
Reteplase Prostaglandin D2
Streptokinase Prostaglandin E
Urokinase Sedative-hypnotics
Anisoylated plasminogen Benzodiazepines
streptokinase Clonazepam
Tenecteplase Diazepam
Vasodilators
Nitroglycerin
Nitroprusside

Medications that Inhibit Vitamin K

Salicylates: Broad-Spectrum Vitamins:
Aspirin and aspirin-combination Antibiotics: A
drugs Sulfonamides E
Other salicylates Triple sulfa
Coumarins Sulfamethoxazole
Anisindione Sulfasalazine
Dicumarol Sulfisoxazole
Warfarin Sulfamethoxazole-
trimethoprim
Clindamycin
Gentamicin
Neomycin
Tobramycin
Vancomycin
Imipenem
Cefamandole
Cefoxitin

Table 10-7
DISSEMINATED INTRAVASCULAR COAGULATION:
LABORATORY VALUES

1946
DIC, Disseminated intravascular coagulation

Infection Control; Infection Protection; Surveillance: Safety.

Risk for deficient fluid volume 

related to bleeding/hemorrhage
Goals/Outcomes: The patient remains normovolemic, as
evidenced by HR and RR within 10% of the patient’s baseline (or
HR 60 to 100 bpm) and RR 12 to 20 breaths/min with normal depth
and pattern; BP within the patient’s baseline (or systolic BP greater
than 90 mm Hg), warm extremities, distal pulses at least 2+ on a 0-
to-4+ scale, urinary output greater than 0.5 mL/kg/h, and capillary
refill less than 2 seconds. Within 24 hours of initiating treatment,
the patient verbalizes orientation to time, place, person, and self.
Fluid Balance.

Fluid monitoring

1. Monitor every 2 hours for increases in HR and RR, decreased BP,

and decreasing pulse pressure.

2. Measure urinary output every 2 to 4 hours. Consult the advanced

practice provider for output less than 0.5 mL/kg/h.

3. Maintain accurate I&O record. Weigh daily and monitor trends.

4. Increase measurement of vital signs and urine output to at least

every 30 minutes for active bleeding. For profuse bleeding, check
vital signs at least every 15 minutes. Inspect invasive procedure
sites and dressings for bleeding.

5. Monitor CBC daily for significant alterations in Hct, Hgb, and

platelets (Table 10-8).

1947
6. Ensure that the patient has typed and cross-matched blood
available for transfusion.

7. Monitor coagulation studies (PT, PTT, fibrinogen, FDP/FSP,

platelet counts), as appropriate.

8. Assess for signs of impending shock if the following signs are

noted: increased HR and RR; decreased BP; or pallor, diaphoresis,
cool extremities, delayed capillary refill, decreased pulse amplitude,
restlessness, or disorientation.

9. Maintain at least one 18-gauge or larger IV catheter for use

during shock management, at which time rapid infusion of blood
products or IV fluids may be necessary.

10. Evaluate the effects of fluid therapy.

Table 10-8
COMPLETE BLOOD COUNT VALUES

Complete Blood Count Values Common Measurement Value Population

Red blood cells (RBCs) 4 to 5.5 million/mm3 Adult females
4.5 to 6.2 million/mm3 Adult males
Hemoglobin (Hgb) 12 to 16 g/dL Adult females
14 to 18 g/dL Adult males
Hematocrit (Hct) 37% to 47% Adult females
Mean corpuscular volume (MCV) 83 to 93 µg3 Adults
Mean cell hemoglobin (MCH) 26 to 34 pg Adults
Mean cell hemoglobin concentration (MCHC) 31% to 38% Adults
White blood cells (WBCs) 4500 to 11,000/mm3 Adults
Differential White Blood Cells (Granulocytes)
Segmented neutrophils (Segs) 54% to 62% Adults
Band neutrophils (Bands) 3% to 5% Adults
Eosinophils (Eos) 1% to 3% Adults
Basophils (Basos) 0% to 0.75% Adults
Monocytes (Monos) 3% to 7% Adults
Lymphocytes (Lymphs) 25% to 33% Adults
Platelets 150,000 to 400,000/mm3 Adults

Electrolyte Management; Fluid Management; Hypovolemia

Management; Intravenous (IV) Therapy; Shock Management:
Volume.

Ineffective tissue perfusion (or risk for same)

1948
Peripheral, cardiopulmonary, cerebral, gastrointestinal, and
renal 
related to blood loss or presence of microthrombi.
Goals/Outcomes: The patient has adequate perfusion, as
evidenced by peripheral pulses greater than 2+ on a scale of 0-to-4+,
brisk capillary refill (less than 2 seconds), BP within the patient’s
normal range, CVP 2 to 6 mm Hg, and HR regular and less than 100
bpm. The patient is oriented to time, place, person, and self and has
urinary output at least 30 mL/h (0.5 mL/kg/h) and oxygen
saturation greater than 96%.
Circulation Status.

Shock prevention

1. Assess and document peripheral perfusion every 2 hours,

including temperature, sensation, pulses, and movement in
extremities. Perform a comprehensive assessment of peripheral
circulation (i.e., check peripheral pulses, edema, capillary refill, and
color and temperature of extremities).

2. Monitor vital signs frequently. Evaluate chest pain. Document

cardiac dysrhythmias.

3. Monitor BP and assess for early signs of perfusion deficit at least

every 2 hours, including dizziness, confusion, and decreased
urinary output.

4. Monitor for decreased myocardial or pulmonary perfusion, as

evidenced by chest pain, ST segment depression or elevation, T
wave inversion, SOB, dyspnea, and decreased oxygen saturation
using continuous pulse oximetry.

5. Monitor CVP, observing for both high and low readings.

Decreased pressures are indicative of hypovolemia/hemorrhage.
Anticipate vasoconstriction with hypovolemia: CO may increase or
decrease from normal range of 4 to 7 L/min, depending on cardiac
contractility.

6. Monitor GI status by observing tolerance to diet or tube feedings,

1949
bowel habits (e.g., constipation, diarrhea), characteristic of stool
(e.g., tarry, bloody), and presence or absence of bowel sounds.

Cardiac Care: Acute; Circulatory Care: Arterial Insufficiency;

Circulatory Care: Venous Insufficiency; Respiratory Monitoring;
Shock Management: Cardiac; Cerebral Perfusion Promotion;
Neurologic Monitoring; Peripheral Sensation Management;
Fluid/Electrolyte Management; Fluid Management; Vital Signs
Monitoring.

Impaired gas exchange (or risk for same) 

related to loss of oxygen-carrying capacity through hemorrhage or
pulmonary microembolus formation.
Goals/Outcomes: The patient’s gas exchange is adequate, as
evidenced by PaO2 at least 80 mm Hg, Paco2 35 to 45 mm Hg, pH
7.35 to 7.45, RR 12 to 20 breaths/min with normal depth and
pattern, oxygen saturation at least 95%, HR 60 to 100 bpm, SVO2 at
least 60%, and orientation to time, place, and person.
Respiratory Status: Gas Exchange.

Respiratory monitoring

1. Assess respiratory status every 2 hours, noting rate, rhythm,

depth, and regularity of respirations. Provide supplemental oxygen
as appropriate.

2. Monitor for signs of respiratory failure: restlessness, anxiety, and

air hunger indicative of hypoxemia; ABG values for increased Paco2
and decreased pH indicative of hypoventilation; or oxygen
saturation less than 95% via pulse oximetry indicative of decreased
ventilation. Consult the advanced practice provider if signs of
respiratory insufficiency are present.

3. Monitor ScVO2 or SVO2: steady increase or decrease from the

patient’s normal level may indicate deterioration.

4. Assess lungs for bibasilar crackles (rales), indicative of

pulmonary edema.

1950
5. Monitor the patient’s respiratory secretions. Institute respiratory
therapy treatments as needed.

6. Monitor for pulmonary embolus, including sharp, stabbing chest

pain, dyspnea, pallor, cyanosis, pupillary dilation, rapid or
irregular pulse, profuse diaphoresis, and anxiety. Assess the need
for supplemental oxygen and consult the physician immediately.
Patients with severe pulmonary emboli may require mechanical
ventilation. See Pulmonary Embolus, Chapter 4.

7. Assess the patient for changes in sensorium (i.e., confusion,

lethargy, somnolence), indicative of inadequate cerebral
oxygenation or CO2 retention (respiratory insufficiency).

Airway Management; Oxygen Therapy; Respiratory

Monitoring.

Risk for injury 

related to blood product administration
Goals/Outcomes: Throughout the transfusion and up to 8 hours
after transfusion, the patient does not exhibit signs of a blood
transfusion reaction, as evidenced by stable mentation, absence of
fever and chills, normal appearance of skin (i.e., no flushing, rash,
lesions), and baseline RR, BP, and HR.
Risk Control.

Surveillance: Safety

1. Check blood to be transfused with another professional to ensure

that the patient receives the correct blood. Verify the following:
patient’s name, patient’s birthday and hospital number, blood unit
number, blood expiration date, blood group, and blood type.

2. Discuss signs and symptoms of potential reaction with the

patient and family. Premedicate if there is a history of reaction or
antibodies are present.

3. When blood products are being infused, check vital signs every
15 minutes for the first hour. Check the patient frequently

1951
throughout the first 15 minutes of the transfusion to observe for
signs of an acute hemolytic transfusion reaction, including fever,
chills, dyspnea, hypotension, flushing, tachycardia, back pain,
hematuria, mentation changes, and shock.

4. Observe for transfusion reactions throughout the transfusion and

during the 8-hour period afterward. If a transfusion reaction (Table
10-9) occurs, implement the following:

• If the transfusion is in progress, stop the infusion

immediately.

• Maintain IV access with NSS.

• Maintain BP with a combination of volume infusion

and vasoactive drugs, if indicated.

• Monitor HR and ECG for changes. Treat

symptomatic dysrhythmias as prescribed by the
physician or midlevel practitioner.

• Administer ordered diuretics and fluids to promote

diuresis (urine output approximately 100 mL/h).

• Obtain blood and urine for a transfusion workup

according to institution blood bank protocol.

• Perform blood cultures if the patient exhibits signs

of sepsis.

5. If an intravascular hemolytic reaction is confirmed, implement

the following:

• Monitor coagulation studies, including PT, PTT, and

1952
 fibrinogen levels (see Table 10-7).

• Monitor renal status by measuring the following:

blood urea nitrogen, creatinine, potassium, and
phosphate levels.

• Monitor laboratory values for hemolysis: increased

lactate dehydrogenase, bilirubin, and haptoglobin.

6. With massive transfusion for severe bleeding, manage

hypocalcemia caused by citrated blood, hyperkalemia of uncertain
etiology, hypothermia from refrigerated blood, acute respiratory
distress syndrome, coagulopathy, and hemochromatosis (iron
overload).

Table 10-9
ACUTE TRANSFUSION REACTIONS

Type Symptoms Time Frame

Acute Fever, chills, dyspnea, tachycardia, hypotension, After start of transfusion
intravascular back pain, flushing, hematuria, shock within 5 to 30 minutes
hemolytic
Acute Fever, elevated bilirubin, unusually low Usually within 8 hours
extravascular posttransfusion hematocrit and hemoglobin Delayed: 7 to 10 days
hemolytic
Allergic (mild) Rash, hives, pruritus Within 1 hour
Anaphylactic Dyspnea, shortness of breath, bronchospasms, Within 30 minutes to 1
tachycardia, flushing, hypotension, shock hour
Febrile Fever, chills Within 4 hours
Hypervolemic Dyspnea, tachycardia, bibasilar crackles, jugular Within 1 to 2 hours
venous distention, possible hypertension, headache
Septic Fever, chills, tachycardia, hypotension, vomiting, Within 5 minutes to 4
shock, muscle pain, cardiac arrest hours

Bleeding Precautions; Bleeding Reduction; Blood Products

Administration.

Additional nursing diagnoses

The uncontrolled bleeding related to DIC can be terrifying to
the patient and significant others, who may fear that the patient will
die. Refer to nursing diagnoses in Emotional and Spiritual Support

1953
of the Patient and Significant Others, Chapter 2. For patients who
manifest activity intolerance, see nursing diagnosis in Prolonged
Immobility, Chapter 1. For patients with sepsis or septic shock, see
Systemic Inflammatory Response Syndrome, Sepsis, and Multiple
Organ Dysfunction Syndrome, Chapter 11.

Selected references
1. Abraham J. Romiplostim for treating thrombocytopenia in
chronic idiopathic thrombocytopenic purpura. Commun
Oncol. 2008;5:651-656.
2. American Association of Blood Banks.
http://www.aabb.org/tm/coi/Documents/coi1113.pdf
Circular of information for the use of human blood and blood
components. Bethesda: American Association of Blood
Banks. 2013.
3. American Society of Anesthesiologists. Practice guidelines
for perioperative blood transfusion and adjuvant therapies.
Anesthesiology. 2006;105:198-208.
4. American Society of Anesthesiologists Committee on
Standards and Practice Parameters. Practice guidelines for
perioperative blood management. An updated report by the
American Society of Anesthesiologists Task Force on
Perioperative Blood Management. Anesthesiology.
2015;122:1A.
5. American Society of Hematology. Red blood cell
transfusions: a clinical practice guideline from AABB. Ann
Intern Med. 2012;157:49-58.
6. Bickley L. Bates guide to physical examination and history
taking ed 11. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins. 2013.
7. Gentry CA, Gross KB, Sud B, Drevets DA. Adverse
outcomes associated with the use of drotrecogin alfa
(activated) in patients with severe sepsis and baseline
bleeding precautions. Crit Care Med. 2009;37:19-25.
8. Ghanima W, Godeau B, Cines DB, Bussel JB. How I treat
immune thrombocytopenia: the choice between
splenectomy or a medical therapy as a second-line

1954
 treatment. Blood. 2012;120:960-969.
9. Gould S, Cimino M, Gerber D. Packed red cell transfusion
in the intensive care unit: limitations and consequences. Am
J Crit Care. 2007;16:39-49.
10. Harmon S. http://www.scientificamerican.com/article/food-
allergy-therapies/ Bring on the peanuts: food allergy
therapies move closer to approval. Scientific American. June
30, 2011.
11. Hebert P, Tinmouth A, Corwin H. Controversies in RBC
transfusion in the critically ill. Chest. 2007;131:1583-1590.
12. Horvath KA, Acker MA, Chang H. Blood transfusion and
infection after cardiac surgery. Ann Thorac Surg.
2013;95:2194-2201.
13. Keating GM. Romiplostin: a review of its use in immune
thrombocytopenia. Drugs. 2012;72:415-435.
14. Kelton J, Warkentin T. Heparin induced thrombocytopenia:
a historical perspective. Blood. 2008;112:2607-2616.
15. Klein H, Spahn D, Carson J. Red blood cell transfusion in
clinical practice. Lancet. 2007;370:415-426.
16. Lee A, Peterson E. Treatment of cancer-associated
thrombosis. Blood. 2013;122:2310-2317.
17. Lelubre C, Vincent J. Red blood cell transfusion in the
critically ill patient. Ann Intensive Care. 2011;1:43.
18. Marik P, Corwin H. Efficacy of red blood cell transfusion in
the critically ill: a systematic review of the literature. Crit
Care Med. 2008;36:2667-2674.
19. McEvoy M, Shandra A. Anemia, bleeding, and blood
transfusion in the intensive care unit: causes, risks, costs,
and new strategies. Am J Crit Care. 2013;22:eS1-eS13.
20. McMahon B. Malignancy-associated thrombosis. Oncol
Issues. 2009;24:20-23.
21. Pieracci FM, Barle PS, Pomp A. Critical care of the bariatric
patient. Crit Care Med. 2006;34:1796-1804.
22. Robson-Ansley P, Du Toit G. Pathophysiology, diagnosis
and management of exercise-induced anaphylaxis. Curr
Opin Allergy Clin Immunol. 2010;10:312-317.
23. Rome S, Doss D, Miller K, Westphal J. IMF Nurse
Leadership Board: Thromboembolic events associated with

1955
 novel therapies in patients with multiple
myelomaconsensus statement of the IMF nurse leadership
board. Clin J Oncol Nurs. 2008;12(Suppl 3):21-28.
24. Sampson HA, Muñoz-Furlong A, Campbell RL. Second
symposium on the definition and management of
anaphylaxis: summary report—Second National Institute of
Allergy and Infectious Disease/Food Allergy and
Anaphylaxis Network symposium. J Allergy Clin Immunol.
2006;117:391-397.
25. Simons FE. Anaphylaxis. J Allergy Clin Immunol.
2008;121(Suppl 2):S402-S407.
26. Simons FE. Anaphylaxis: recent advances in assessment
and treatment. J Allergy Clin Immunol. 2009;124:625-636.
27. Simons FE, Ardusso LR, Bilo MB. World allergy
organization guidelines for the assessment and
management of anaphylaxis. World Allergy Organ J.
2011;4:13-37.
28. Weldon B, Yu S, Neale-May T. The safety of peanut oral
immunotherapy in peanut allergic subjects in a single
center trial. J Allergy Clin Immunol. 2011;127:AB25.
29. Yap C, Lau L, Krishnaswamy M. Age of transfused red
cells and early outcomes after cardiac surgery. Ann Thorac
Surg. 2008;86:554-559.

1956
C H A P T E R 11

Complex special
situations
Abdominal hypertension and
abdominal compartment syndrome
“ . . . the end result of a progressive, unchecked increase in intra-abdominal
pressure from a myriad of disorders that eventually leads to multiple organ
dysfunction.”

John Hunt, MD

Pathophysiology
Intraabdominal hypertension (IAH) occurs when the amount of
intraabdominal contents (through edematous bowel or fluid
accumulating in the cavity) exceeds the distendable capability of
the fascia. The result is an intraabdominal hypertensive state, which
can lead to abdominal compartment syndrome (ACS). As the fluid
accumulates (because of bleeding, ascites, volume overload, and
other causes), the resulting increase in pressure (change in
compliance/change in volume) initially affects regional blood flow
and results in impaired tissue perfusion, which is then associated
with a systemic inflammatory response. The resulting ischemia and
inflammatory response further cause capillary leakage and

1957
compression of the intraabdominal viscera. If untreated, the
continually elevated free fluid and measured pressure begin to
compress blood vessels, causing organ dysfunction both inside and
outside the abdomen, and lead to ACS. The inflammatory response
promotes the release of cytokines, causing vasodilation and cell
membrane dysfunction. The cell membrane loses integrity, which
causes further inflammation, profound edema, and ultimately cell
death. The elevated pressure in the abdominal cavity generated by
the severe increase in extravascular fluid load increases the
intraabdominal contents (free water) and further impairs intestinal
tissue perfusion as compression of the arteries and veins continues.
This process underlies the multiorgan effects of rising
intraabdominal pressure (IAP). When the IAP rises above critical
level, blood flow to the abdominal viscera and organs decreases
and ACS is imminent. Although initially described in surgical
patients, IAH and ACS also occur in medical patients without
abdominal conditions. IAP can be measured easily and reliably in
patients through the bladder using simple tools.

Risk factors
Diminished abdominal wall compliance

• Major trauma and burns; acute respiratory failure;

abdominal surgery.
Increased intraluminal contents

• Gastroparesis; ileus; pseudoobstruction.

Increased abdominal contents

• Ascites/liver dysfunction;
hemoperitoneum/pneumoperitoneum.
Capillary leak/fluid resuscitation

1958
• Acidosis (pH less than 7.2); hypotension;
hypothermia (below 33°C [91.4° F]); massive fluid
resuscitation; poly transfusion; coagulopathy;
sepsis, major trauma and burns.

Definitions
Bladder pressure reflects the IAP and is measured using the
indwelling urinary catheter. The pressure is expressed in mm Hg.

Intraabdominal pressure is the pressure within the abdominal

cavity. Normal IAP is ∼5 to 7 mm Hg, with baseline levels in
morbidly obese individuals often ranging from 9 to 14 mm Hg.
IAP is considered to be significant when consistently above 12
mm Hg, although a higher pressure often appears to be tolerated
in obese individuals. The pressure within the cavity reflects the
presence of extravascular fluids, which compress the blood
vessels and organs in the abdominal cavity as well as displacing
the diaphragm into the thoracic cage, which limits lung
expansion. Elevated intrabladder pressure indirectly reflects high
pressure within the abdominal cavity.

Intraabdominal hypertension (IAH) is defined by the World

Society of Abdominal Compartment Syndrome (WSACS) as a
measured IAP of 12 mm Hg or greater, recorded 3 times using
standardized measurement methods 4 to 6 hours apart and/or an
abdominal perfusion pressure (APP) of less than 60 mm Hg
(mean arterial pressure [MAP] − intraabdominal bladder
pressure), recorded using 2 standardized measurements 1 to 6
hours apart). These measurements should be evaluated in the
context of clinical symptomatology. Increased IAP may reflect a
critical finding in patients with multiorgan dysfunction
syndrome (MODS) or multisystem failure, which contributes to
global hypoperfusion, aggravating the effects of increased IAP
(Table 11-1).

1959
Abdominal compartment syndrome is defined as an IAP greater
than 15 mm Hg and the onset of new organ failure. ACS is
defined as “intraabdominal hypertension with a gradual and
consistent increase in the IAP value of [equal to or greater than]
20 mm Hg,” recorded by at least 3 standardized measurements
taken 1 to 6 hours apart and in conjunction with at least one new-
onset organ dysfunction. ACS can be fatal and often complicates
or results in a clinical condition refractory to treatment. The
astute clinician suspects IAH and ACS when MODS is evolving
and/or the patient presents with persistent lactic acidosis.

Abdominal perfusion pressure is APP 5 MAP 2 IAP. In adults,

keeping this greater than 50 to 60 mm Hg significantly improves
morbidity and mortality.

Table 11-1
PRESSURE AND SYMPTOM GRADE FOR INTRAABDOMINAL
HYPERTENSION

Pressure
Graded
Measurement and Physiologic Events and Clinical Signs
Measurement
Relevance
Pressure 12 to 15 mm Hg Cytokine release and capillary leak
grade I Significant in the Third spacing of resuscitative fluid
presence of organ Decreasing venous return and preload
dysfunction Early effects on ICP and CPP
Abdominal wall perfusion decreases 42%
Marked reduction in intestinal and intraabdominal
organ blood flow leading to regional acidosis and free
radical formation
Pressure 16 to 20 mm Hg Markedly decreased venous return, CO, and splanchnic
grade II Significant in most perfusion
patients Increased SVR, CVP, PAWP
Decreased blood pressure, particularly systolic blood
pressure, and pulse pressure
Decreased TLC, FRC, RV
Increased vent pressures, hypercapnia, hypoxia
Reduction to 61% of baseline mucosal blood flow and
increasing gut acidosis
Oliguria, anuria
Increasing ICP and decreasing CPP
Pressure 21 to 25 mm Hg Hemodynamic collapse, worsening acidosis, hypoxia,
grade III Significant in all hypercapnia, anuria
patients Inability to oxygenate, ventilate, or resuscitate
Pressure >25 mm Hg Hemodynamic collapse, worsening acidosis, hypoxia,
grade IV Significant in all hypercapnia, anuria
patients Inability to oxygenate, ventilate, or resuscitate

1960
If both pressure and clinical symptoms are met for grade III and/or grade IV, patient
has abdominal compartment syndrome. CPP: Cerebral Perfusion Pressure. CVP:
Central Venous Pressure; FRC: Functional Residual Capacity; ICP: Intracranial
Pressure; PAWP: Pulmonary Artery Wedge Pressure; RV: Residual Volume; SVR:
Systemic Vascular Resistance; TLC: Total Lung Capacity.

Selected definitions from the WSACS:

• Definition 1: IAP is the steady-state pressure within the

abdominal cavity.

• Definition 7: IAH is defined by a sustained or repeated pathologic

increase in IAP ≥ 12 mm Hg.

• Definition 9: ACS is defined as a sustained IAP greater than 20

mm Hg (with or without APP less than 60 mm Hg) that is
associated with new organ dysfunction/failure.

Historically, most critical care providers believed that IAH and

its more serious evolution, ACS, were solely related to traumatic
injury of the abdomen, including surgery. Within the last decade,
the understanding of the pathophysiology of IAH and ACS has
been enhanced by studies revealing the prevalence in all critical
patients: medical as well as surgical and trauma. The progressive
conditions have been divided into primary and secondary
abdominal hypertension disorders. The causes may differ, but
outcomes are similar if either condition remains untreated.
Primary ACS is a condition associated with injury or disease in
the abdominopelvic region that frequently requires early surgical or
angioradiologic intervention. Any abnormal event that raises
abdominal pressure can induce acute IAH, including blunt or
penetrating abdominal trauma, abdominal aortic aneurysm,
hemorrhagic pancreatitis, gastrointestinal (GI) obstruction,
abdominal surgery resulting in retroperitoneal bleeding or
secondary peritonitis, and tight closure of abdominal incisions.
Primary ACS also includes patients with abdominal solid organ
injuries who were initially managed medically and then developed
ACS. The condition has been relatively well understood by
surgeons and their colleagues but is frequently misdiagnosed
and/or untreated until surgical intervention is required.
Secondary ACS includes conditions that do not originate from

1961
abdominal injury that creates IAH, including sepsis or any
condition prompting capillary leak (e.g., major burns, conditions
requiring massive fluid resuscitation). A large multicenter study by
Malbrain and colleagues in 2005 found the prevalence of IAH was
54% among medical intensive care unit (ICU) patients and 65% in
surgical ICU patients. This was remarkable, as most medical
patients are not evaluated for or even considered to have IAH and
ACS.
ACS treatments are the same regardless of the cause; however,
the caregiver must be very careful in managing secondary ACS. The
opportunity for early intervention may be lost because of the subtle
development of signs and symptoms of IAH and ACS. The lack of
definitive signs often leads to delayed diagnosis and delayed
recognition, and an urgent medical condition becomes an
emergency surgical situation. Increased organ failure, increased
mortality, increased resource use, and longer ICU lengths of stay
may result. Similar to sepsis and severe sepsis, the greatest
challenge is early recognition and diagnosis. Monitoring all high-
risk patients would enable clinicians to trend the IAP, facilitating
early, appropriate interventions when the syndrome is more likely
to be responsive to medical therapy. The best management strategy
is to prevent ACS via early monitoring, early medical interventions,
and early surgical decompression if needed.

Assessment
Goal of system assessment
To rapidly evaluate for significant primary and secondary IAH and
correlating reduction of blood flow to other organs

History and risk factors

Patients with a history of abdominal trauma, abdominal surgery,
intraabdominal infection, damage control laparotomy with
intraabdominal packing, severe infection, sepsis, peritonitis,
bleeding pelvic fractures, postoperative bleeding, massive
retroperitoneal hematoma, liver transplantation, ruptured
abdominal aortic aneurysm, visceral tissue edema,

1962
pneumoperitoneum, hypovolemic or vasogenic shock or any
patient with aggressive fluid resuscitation, acute ascites, and/or
pancreatitis.

Vital signs and other values

The following values may be increased

Hemodynamic values: Central venous pressure (CVP), pulmonary

artery occlusive pressure (PAOP), systemic vascular resistance
(SVR), inferior vena cava (IVC) pressure.

Respiratory: Pleural pressure, peak inspiratory pressure.

Screening lab values: Paco2, serum creatinine, serum blood urea

nitrogen (BUN).

The following may be decreased

Respiratory: Tidal volume, PaO2.

Cardiovascular: Cardiac output (CO), systolic blood pressure (BP),

cerebral perfusion pressure.

Renal: Glomerular filtration rate, serum creatinine, serum BUN.

Observation
Observe for upward trends in respiratory and heart rates (RR and
HR, respectively) and decrease in urine output. Signs and
symptoms are nonspecific and subtle and may be attributed to
other clinical conditions (Table 11-1). Elevated IAP affects the
cardiovascular, pulmonary, renal, and neurologic systems.

Cardiovascular: Hypotension may result from decreased CO, which

results from IAH-induced vasoconstriction. Signs of shock,
including pallor, tachycardia, and cool and clammy skin, may be
present. Venous return is diminished caused by compression of
the IVC, resulting in loss of compliance (increased IVC pressure)
and decreased preload (volume), which further reduces CO.

1963
 Increased IAP compresses the aorta, resulting in elevated SVR
(increased afterload), which reduces CO. The compensatory
vasoconstriction affects blood flow to the hepatic and renal veins,
leading to renal compromise, oliguria, and hepatic
hypoperfusion; if untreated, kidney and liver failure can result.

Pulmonary: Respiratory distress results from the elevated

abdominal pressure impeding diaphragmatic movement by
forcing the diaphragm upward, which decreases functional
residual capacity, promotes atelectasis, and decreases lung
surface area. Tachypnea and increased work of breathing may be
present. The worsening hypoxemia promotes elevated peak
inspiratory pressures, with refractory hypoxemia and a poor P/F
ratio, similar to acute respiratory distress syndrome (ARDS).
Alternative ventilatory support is often required to maintain
oxygenation and ventilation.

Neurologic: Altered mental status results from obstruction of

cerebral venous outflow, leading to vascular congestion and
increased intracranial pressure. Increased IAP increases
intrathoracic pressure, which compresses the veins within the
thoracic cavity, making it difficult for cerebral veins to drain
properly. The combination of decreased CO and increased
intracranial pressure can lead to decreased CPP, which prompts
further deterioration in level of consciousness.

Renal: Renal dysfunction results as the increasing abdominal

pressure compresses the bladder and urethra as well as the renal
arteries and veins. Urine output decreases and serum creatinine
and BUN increase, although they may not do so in proportion to
each other (BUN/creatinine ratio).

11-1
RESEARCH BRIEF
The findings of this study revealed the mean IAP within 24 hours
of ICU admission is an independent predictor of mortality. IAP
measurements assist with the identification of patients at increased

1964
risk of death in the first 24 hours of admission. This is a time when
therapy could save the patient’s life. Although no definitive risk
factor profile is identified, serial IAP measurements are an
excellent indicator when patients have significant evidence of lactic
acidosis.
Reintam Blaser A, Sarapuu S, Tamme K, et al: Expanded measurements of intra-
abdominal pressure do not increase the detection rate of intra-abdominal hypertension: a
single-center observational study. Crit Care Med 42:378-386, 2014.

Diagnostic tests
Methods of intraabdominal pressure measurement
The best method for measurement of IAP is controversial. The most
common method is measuring the response of intrabladder
compliance to an instillation of 25 mL of sterile fluid by measuring
the resulting pressure.

Direct intraperitoneal measurement

The most accurate method requires an intraperitoneal catheter
inserted into the abdomen with a fluid manometer or pressure
transducer attached to measure the pressure. This method requires
expert catheter placement and is highly linked to infection.

Indirect methods
Bladder pressure is commonly used, while other methods are
infrequently used. Indirect methods include gastric pressure
measurement through gastrostomy or a nasogastric tube, intrarectal
pressure measurement using an esophageal stethoscope catheter, or
bladder pressure measurement through a urinary catheter.
Bladder pressure measurement: As physical examination is
notoriously inaccurate in detecting the presence of IAH, bedside
IAP monitoring is essential to both recognizing IAH and avoiding
IAP-induced organ failure. An indwelling urinary catheter is
connected to either a pressure transducer or a fluid manometer to
measure the pressure. Readings are reliable and easier to perform
than direct intraperitoneal measurement. More information
regarding the different methods to measure IAP, including the pros

1965
and cons of each technique, can be found on the WSACS website
(www.wsacs.org).
The urinary bladder normally has a compliant wall. Many studies
reveal compliance decreases when there is a high presence of
intraabdominal fluids, which increases the pressure in the
abdominal cavity and compresses the bladder, increasing
resistance. When fluid is injected into the bladder pressure system,
any decrease in bladder compliance is reflected by increased
intrabladder pressure. The procedure is generally easier and safer if
a prepackaged closed bladder pressure system is used. If
assembling the system without a prepackaged tool, use the
urinary/Foley catheter with an aspiration or infusion port:

1. The nurse will connect a fluid-filled pressure system to a

transducer, then connect a needle to the distal end of the tubing
(farthest from the transducer and after a stopcock).

2. The cable connecting the system to the monitor should allow for
visualization of a small pressure (scale either at auto or 30 mm Hg).

3. The connected system will be inserted into the catheter infusion

port.

4. After zeroing the system (transducer at the symphysis pubis and

the stopcock will be turned off to the patient), the nurse will clamp
the catheter drainage system just below the infusion port.

5. Using the stopcock, the system will be turned off to the monitor
and 25 mL of sterile fluid (an intravenous [IV] fluid is fine) will be
injected rapidly into the infusion port on the urinary catheter. The
stopcock will be then turned off to the injecting port, leaving a
connected pressure system from patient to monitor.

6. Bladder pressure must be read during end expiration and the

patient must be as flat as tolerated to facilitate accuracy. There is no
dynamic waveform associated with bladder pressure. One should
just observe the level of pressure in the first 10 to 20 seconds after
fluid is instilled.

1966
7. A normal value is generally considered between 0 and 5 mm Hg,
although levels as high as 15 mm Hg are not unusual in the first 24
hours after abdominal surgery (see Table 11-1). If the pressures are
elevated, document and repeat in the next hour using the same
techniques. Inform the physician or midlevel practitioner if both
measures are elevated.

8. Occlusion is then released and fluid is drained into the urine

collection bag. Subtract the amount of fluid from the hourly output.

The measurement of IAP is key to IAH and ACS. The process

must be standardized, and definitions are crucial. IAP is measured
(in mm Hg) at end expiration; the patient should be supine and
refrain (or be controlled) from spontaneous muscle contractions.
The midaxillary line is used as the zero reference level for IAP
measurement. Methods for continuous IAP measurement also are
available. It is advised that IAP monitoring be based on a protocol,
known risk factors, monitoring equipment available, and nursing
staff experience and should be linked directly to a treatment
protocol. Patients with any of the conditions associated with IAH
should be monitored using a transvesicular technique at least every
4 hours until IAP decreases to less than 12 mm Hg and the decrease
is sustained for at least 24 hours.

11-2
RESEARCH BRIEF
In this retrospective, nonexperimental, observational analysis
performed in a large urban trauma center, many risk factors
appeared for IAH and ACS. As expected, there was a very strong
relationship between polytransfusion and death in patients with
ACS. However, what was most significant was that, in the setting
where ACS is highly probable, developing and adhering to a
protocol for assessing ACS and monitoring IAP were considered
essential. Serial measures were not performed, much to the
authors’ dismay, and the suggestion is that, were they performed
according to a protocol, mortality may be decreased.
Harrell BR, Melander S: Identifying the association among risk

1967
factors and mortality in trauma patients with intra-abdominal
hypertension and abdominal compartment syndrome. J Trauma
Nurs 19:182–189, 2012.

Collaborative management
Care priorities

1. Prevent abdominal compartment syndrome

Patients who have a high index of suspicion should have bladder
pressure monitoring initiated to identify IAH earlier and possibly
avoid decompressive laparotomy, which is the only documented
evidence-based therapy for ACS (Box 11-1). Many approaches may
be used to reduce IAH; all are directed at reducing increased
abdominal cavity volume or decreasing compliance.

Box 11-1
MANAGEMENT OF ABDOMINAL
COMPARTMENT SYNDROME
1. Improvement of abdominal wall compliance

Sedation

Pain relief (not fentanyl!)

Neuromuscular blockade

Body positioning

Negative fluid balance

1968
Percutaneous abdominal wall component separation

2. Evacuation of intraluminal contents

Nasogastric suction

Rectal tube/enemas

Gastro/colonic prokinetic agents

Paracentesis

Percutaneous drainage of abscess/hematomas

3. Evacuation of periintestinal and abdominal fluids

Ascites evacuation in cirrhosis

CT- or ultrasound-guided aspiration of abscess

CT- or ultrasound-guided aspiration of hematoma

Percutaneous drainage of (blood) collections

Ascites evacuation in cirrhosis

4. Correction of capillary leak and positive fluid balance

Diuretics/colloids/hypertonic fluids

Hemodialysis/ultrafiltration

Dobutamine (not dopamine!)

1969
Ascorbic acid in burn patients

Modified from Ivatury R, Cheatham M, Malbrain M et al: In Vincent JL, editor: Yearbook of
intensive care and emergency medicine. Berlin, 2008, Springer, Chapter 5.

Therapies include:

• Draining free intraperitoneal fluid: Paracentesis is performed by

the advanced practitioner. Some centers may place a peritoneal
drainage catheter and leave it in place if abdominal fluid
accumulation is persistent and severe.

• Volume replacement with small volumes of higher osmotic

gradient intravenous fluids: More highly concentrated IV
solutions (e.g., hypertonic [3%] saline, plasma, Hextend, blood
products) can sometimes facilitate fluid stabilization within the
vasculature for longer periods of time than isotonic solutions.

• Continuous renal replacement therapy: Enables minute-to-minute

control of intravascular fluid removal and replacement and more
exact fluid management. This technique was thought to benefit
the patient by removal of cytokines, but more recent evidence
indicates that it may not be of benefit (see Continuous Renal
Replacement Therapies, Chapter 6).

• Other options: Include sedation and analgesic management of

patients and ultimately the consideration of neuromuscular
blockade or chemical paralysis.

2. Perform a decompressive laparotomy to relieve

abdominal compartment syndrome
Sudden release of the abdominal pressure may lead to further
complications including ischemia-reperfusion injury, acute
vasodilation, cardiac dysfunction, and arrest. Arteries and veins
within the abdomen are suddenly able to expand to normal size
and “refill” with normal blood volume. If the patient has
insufficient volume to accommodate the renewed space within the

1970
vasculature, hypotension ensues. Patients should be hydrated with
at least 2 L of IV fluid, which may include a “cellular protection
cocktail,” such as 25 g of mannitol 12.5% given along with 2
ampules of bicarbonate/L. IV fluids and vasopressors should be
immediately available in case severe hypotension occurs as the
abdomen is decompressed.
After opening the abdomen, temporary closure will be applied.
The goal is to permanently close the abdomen as soon as possible.
For most patients who require emergent opening of the abdomen
for ACS, a vacuum-assisted closure device (abdominal wound
VAC) attached to a negative pressure device is commonly applied.
An open abdomen may precipitate loss of liters of volume. The
modified negative pressure wound VAC facilitates open wound
fluid management and supports tissue granulation, as well as local
perfusion, which facilitate eventual closure of the open wound.

Care plans for abdominal compartment

syndrome and intraabdominal hypertension
Deficient fluid volume 
related to either active intravascular fluid loss secondary to physical injury
or a condition resulting in capillary leak syndrome with third spacing of
fluids.
Goals/Outcomes: Within 12 hours of this diagnosis, the patient is
becoming normovolemic, as evidenced by MAP at least 70 mm Hg,
HR 60 to 100 beats per minute (bpm), normal sinus rhythm on
electrocardiogram (ECG), central venous pressure (CVP) 2-6 mm
Hg, cardiac index (CI) at least 2.5 L/min/m2, bladder pressure
measurements of less than 15 mm Hg, APP at least 60 mm Hg,
stroke volume variation (SVV) less than 15%, urinary output at least
0.5 mL/kg/h, warm extremities, brisk capillary refill (less than 2
seconds), distal pulses at least 2+, bladder pressure measurements
of less than 15 mm Hg, and APP at least 60 mm Hg. Stroke volume
resuscitation, serum lactate, and base deficit are required to
evaluate cellular perfusion.
Fluid Balance; Electrolyte and Acid-Base Balance

1971
Fluid/electrolyte management

1. Monitor BP at least hourly or more frequently in the presence of

unstable vital signs. Be alert to changes in MAP of more than 10
mm Hg. Even a small but sudden decrease in BP signals the need to
consult the physician or midlevel practitioner, especially with the
trauma patient in whom the extent of injury is unknown.

2. Once stable, monitor BP at least hourly, or more frequently in the

presence of any unstable vital signs. Be alert to changes in MAP of
more than 10 mm Hg.

3. If massive fluid resuscitation was necessary for either the trauma

patient or a patient with third-spaced fluid, the patient is at higher
risk for IAH and should be observed closely for signs of decreased
perfusion, respiratory distress, and deterioration in mental status.

4. In the patient with evidence of volume depletion or active blood

loss, administer pressurized fluids rapidly through several large-
caliber (16-gauge or larger) catheters. Use short, large-bore IV
tubing (trauma tubing) to maximize flow rate. Avoid use of
stopcocks, because they slow the infusion rate. Fluids should be
warmed to prevent hypothermia.

5. Measure central pressures and CO continuously if possible, or at

least every 2 hours if blood loss is ongoing. Be alert to low or
decreasing CVP and PAWP. Be aware that profound tachycardia
may be indicative of hypovolemia. Measure central pressures and
CO continuously if possible, or at least every 2 hours if blood loss is
ongoing. Calculate SVR and pulmonary vascular resistance (PVR) if
data is available at least every 8 hours—more often in unstable
patients with concurrent thoracic injury, such as pulmonary
contusion, smoke inhalation, or early ARDS. ARDS is a concern in
patients who have sustained major abdominal injury, inasmuch as
there are many potential sources of infection and sepsis that make
the development of ARDS more likely (see Acute Lung Injury and
Acute Respiratory Distress Syndrome, Chapter 4).

6. Measure urinary output at least every 2 hours. Urine output less

1972
than 0.5 mL/kg/h usually reflects inadequate intravascular volume
in the patient with abdominal trauma. Decreasing urine output may
also signify compression of the renal arteries in ACS.

7. Monitor for physical indicators of arterial hypovolemia, which

may include cool extremities, capillary refill greater than 2 seconds,
absent or decreased amplitude of distal pulses, elevated serum
lactate, and base deficit.

8. Estimate ongoing blood loss. Measure all bloody drainage from

tubes or catheters, noting drainage color (e.g., coffee grounds,
burgundy, bright red). Note the frequency of dressing changes as a
result of saturation with blood to estimate amount of blood loss by
way of the wound site.

Electrolyte Management; Fluid Management; Fluid

Monitoring; Hypovolemia Management

Ineffective tissue perfusion: Gastrointestinal 

related to interruption of arterial or venous blood flow or hypovolemia
secondary to physical injury or any condition resulting in third-spaced
fluid or development of ascites.
Goals/Outcomes: Within 12 hours of this diagnosis, the patient is
becoming normovolemic, as evidenced by MAP at least 70 mm Hg,
HR 60 to 100 bpm, normal sinus rhythm on ECG, CVP 2-6 mm Hg,
bladder pressure measurements of less than 15 mm Hg, APP at
least 60 mm Hg, CI at least 2.5 L/min/m2, SVV less than 15%,
urinary output at least 0.5 mL/kg/h, warm extremities, brisk
capillary refill (less than 2 seconds), distal pulses at least 2+, SVV
less than 15%, urinary output at least 0.5 mL/kg/h, and warm
extremities. By the time of hospital discharge, the patient has
adequate abdominal tissue perfusion as evidenced by normoactive
bowel sounds; soft, nondistended abdomen; and return of bowel
elimination.
Tissue Perfusion: Abdominal Organs

Circulatory care: Arterial insufficiency

1. Identify patients who are at high risk for IAH.

1973
2. Monitor BP at least hourly or more frequently in the presence of
unstable vital signs.

3. Monitor HR, ECG, and cardiovascular status every 15 minutes

until vital signs are stable.

4. Auscultate for bowel sounds hourly during the acute phase of

abdominal trauma and every 4 to 8 hours during the recovery
phase. Report prolonged or sudden absence of bowel sounds
during the postoperative period, because these signs may signal
bowel ischemia or mesenteric infarction, which requires immediate
surgical intervention.

5. Evaluate the patient for peritoneal signs (see Box 3-3, Chapter 3),
which may occur initially as a result of injury or may not develop
until days or weeks later, if complications caused by slow bleeding
or other mechanisms occur.

6. Ensure adequate intravascular volume.

7. Evaluate labwork for evidence of bleeding (e.g., serial hematocrit

[Hct]) or organ ischemia (e.g., aspartate aminotransferase [AST],
alanine aminotransferase [ALT], lactate dehydrogenase [LDH]).
Desired values are Hct greater than 28% to 30%, AST 5 to 40 IU/L,
ALT 5 to 35 IU/L, and LDH 90 to 200 U/L.

8. Measure bladder pressure manually: See Diagnostic Tests,

Bladder Pressure Measurement, Chapter 11.

9. Prepackaged closed-system bladder pressure monitoring:

Complete bladder pressure monitoring systems became available
approximately 10 years ago. They remain completely closed
throughout injection of fluid into the bladder, making them more
useful in preventing catheter-associated urinary tract infections.

10. Assess for changes in level of consciousness, possibly resulting

from increased IAP, which may inadvertently affect draining of the
cerebral veins.

Risk for infection 

1974
related to inadequate primary defenses secondary to physical trauma,
surgery, underlying infection, temporary closure of abdomen, or insertion
of urinary catheter for measurement of IAP; inadequate secondary defenses
caused by debilitated condition, decreased hemoglobin, or inadequate
immune response; tissue destruction and environmental exposure
(especially to intestinal contents); multiple invasive procedures.
Goals/Outcomes: The patient is free of infection as evidenced by
core or rectal temperature less than 37.7°C (100°F); normal white
blood cell count and no bandemia; HR less than 100 bpm;
orientation to time, place, and person; and absence of unusual
redness, warmth, or drainage at surgical incisions and drain sites.
Immune Status; Infection Severity

Infection protection

1. Note color, character, and odor of all drainage. Report the

presence of foul-smelling or abnormal drainage. See Table 3-2 for a
description of the usual character of GI drainage.

2. As prescribed, administer pneumococcal vaccine to patients with

total splenectomy to minimize the risk of postsplenectomy sepsis.

3. If evisceration occurs initially or develops later, do not

reinsert tissue or organs. Place a saline-soaked gauze over the
evisceration, and cover with a sterile towel until it can be evaluated
by a surgeon.

4. For more interventions, see this diagnosis in Abdominal Trauma

(Chapter 3).

Table 11-2
COMMON BARBITURATES

Generic Name Common Trade Name Half-life (Hours)

Amobarbital Amytal 8 to 42
Secobarbital Seconal 19 to 34
Pentobarbital Nembutal 15 to 48
Phenobarbital Luminal and others 24 to 140
Butabarbital Butisol 34 to 42
Secobarbital/amobarbital Tuinal 8 to 42
Note: Withdrawal symptoms can be correlated with the half-life of the drug that was

1975
taken. Withdrawal from drugs with shorter half-lives produces more intense
symptoms that last for shorter periods; whereas, withdrawal from drugs with longer
half-lives produces less intense symptoms that can be prolonged. Moreover, the
severity of the withdrawal is directly related to the drug’s dosage.

Infection Control

Additional nursing diagnoses

Also see Major Trauma, Chapter 3. For additional information, see
nursing diagnoses and interventions in the following sections:
Hemodynamic Monitoring (Chapter 1), Prolonged Immobility
(Chapter 1), Emotional and Spiritual Support of the Patient and
Significant Others (Chapter 2), Peritonitis (Chapter 9),
Enterocutaneous Fistula (Chapter 9), SIRS, Sepsis and MODS
(Chapter 11), and Acid-Base Imbalances (Chapter 1).

Drug overdose
Overview/epidemiology
Over 2.3 million human toxic exposure cases are reported annually
to American poison control centers. Most cases are unintentional,
involve a single agent, and can be handled on site with help from a
poison control center. Although the overall mortality of these cases
is low, over a quarter of them require an emergency department
visit and 7.1% result in inpatient admissions.
The type, amount, and route of the agent determine the
signs/symptoms, physical presentation, prognosis, management,
and outcome of a toxic exposure. Every drug has a threshold for
occurrence of serious toxic effects. Drugs of abuse are more
dangerous than prescription drugs, as they are uncontrolled and
unregulated, with a haphazard nature of administration. The
patient’s history is often unavailable or of poor quality. Time is
critical to successful treatment. A thoughtful and stepwise approach
to laboratory testing, medical and nursing interventions,
pharmacologic support, and general supportive measures is
essential. No organ or body system is protected from the
detrimental effects of drug overdose.

1976
Ingestion of unknown substances
Many patients with drug overdose present with altered mental
status and without a useful or reliable history. Identification of the
ingested substance is difficult. Labwork is done for common drugs
of abuse, including amphetamines, barbiturates, benzodiazepines,
cocaine, opioids, phencyclidine, and cannabinoids. Specific drug
levels are available for salicylates, acetaminophen, digoxin,
theophylline, iron, and lithium. When one of these drugs is not the
offending agent, a number of signs and symptoms should be noted
and tests done to determine the list of potential offending agents.

Assessment
It is beyond the scope of this chapter to include all the drugs and
toxins leading to common presenting symptoms, but important
clues to the poison may be gleaned from answering the following
questions:

• HR and rhythm: Is the patient bradycardic or tachycardic? Is a

dysrhythmia present?

• Mental status: Is the patient overall depressed or agitated? Is

delirium present?

• Temperature: Is hypothermia or hyperthermia present? Is the

patient diaphoretic?

• Seizures: Is the patient having seizures?

• Eyes: Are pupils showing miosis or mydriasis? Is nystagmus

present?

• Muscle tone: Is the patient flaccid or rigid? Are dyskinesias

present?

• Lungs: If respiratory failure is occurring, is it related to

depression, aspiration, edema, hemorrhage, bronchospasm, or
cardiac failure? What is the pulse oximetry?

1977
• Arterial blood gas (ABG): Is the pH acidotic or alkalotic?

• Anion gap: If abnormal, is it increased or decreased?

• Blood glucose: Is the patient hyperglycemic or hypoglycemic?

• Psychosocial: Does the patient have a history of psychiatric

disorders, drug abuse, or depression? Is the patient on any drugs
with narrow therapeutic windows, and is a list of current
medications (including over-the-counter drugs) available?

General treatment options: Gastric

decontamination
Gastric decontamination is a general term referring to interventions
used to reduce the total bioavailability of a toxin, usually through
decreased absorption. Timely administration is essential for
success. Best results are obtained if done within an hour of
ingestion. If the ingested substance is nontoxic, not amenable to
decontamination, or already absorbed, gastric decontamination is
contraindicated.

Activated charcoal
Activated charcoal (AC) is a fine, insoluble, nonabsorbable powder
that binds with many toxic drugs to enhance their elimination. A
review of the literature yields mixed results on the efficacy of AC.
The dose is 25 to 100 g initially. Repeat dosing of half that amount
every 4 hours is recommended by the American Academy of
Clinical Toxicology if the poisoning involves life-threatening
overdoses of carbamazepine, dapsone, phenobarbital, quinine, or
theophylline. A combination product of AC and sorbitol is
available; the latter component increases the tolerability of charcoal
and may help reduce constipation. Contraindications to AC are
bowel obstruction or perforation, depressed mental status (unless
the airway is protected), delayed presentation, and need for
endoscopy. AC does not bind with inorganic ions such as lithium,
potassium, and magnesium; with alcohols such as ethanol,
methanol, propylene glycol, and isopropyl alcohol; with heavy

1978
metals such as iron, lead, mercury, and arsenic; with acidic or
alkaline corrosives; or with hydrocarbons.

Gastric lavage
Commonly known as “pumping the stomach,” gastric lavage is the
insertion of an orogastric tube followed by repeatedly instilling and
aspirating small quantities of fluid. It is no longer recommended as
routine management by American and European toxicology
associations. In the rare case that it is used, it must be done as soon
as possible, within 60 minutes of the ingestion. When using lavage,
the airway must be protected and lavage should continue until the
fluid is clear of fragments (it usually requires about 5 L of fluid).
Gastric lavage should not be attempted if it delays or interferes with
AC administration in appropriate patients.
Large, life-threatening amounts of recently ingested toxin (which
may be poorly bound to AC used before lavage) may justify use.
Contraindications include the risk or presence of esophageal
hemorrhage or perforation, unprotected airways, and caustic or
hydrocarbon ingestions.

Whole bowel irrigation

The administration of a polyethylene glycol-balanced electrolyte
solution to rapidly cleanse the bowel may be useful in cases where
AC is ineffective, such as with ingestions of iron, lithium, illicit
drug packets, and sustained-released tablets. It may diminish the
effectiveness of AC, but one study showed that the combination led
to decreased absorption of extended-release venlafaxine. Whole
bowel irrigation is contraindicated when ileus, GI bleeding, severe
vomiting, hemodynamic instability, bowel obstruction, or bowel
perforation is present.

General treatment options: Extracorporeal

removal of toxins
Techniques include all types of dialysis, continuous renal
replacement therapy, and plasmapheresis. These methods are most
often used to remove methanol, ethylene glycol, lithium,

1979
theophylline, salicylates, sotalol, and phenobarbital. Extracorporeal
therapies may be used in extreme cases when other management
strategies are ineffective for drugs that are not highly protein
bound, have a reasonable molecular size, are water soluble (rather
than lipid soluble), have a limited volume of distribution, and are
not highly charged or ionized. Hemofilters used for continuous
renal replacement therapy are often able to accommodate larger-
sized molecules than conventional hemodialysis therapy.

Illicit and prescription drugs commonly seen

in overdose situations
Acetaminophen
Acetaminophen is one of the most commonly ingested drugs in
overdose, and historically it has accounted for the most deaths.
Most patients admit taking this drug. Unintentional overdose may
occur because of polypharmacy, wherein acetaminophen is
contained in one or more other medications being used.
Unintentional overdose is more common in children. Signs and
symptoms of toxicity vary significantly depending on the dose,
time elapsed since ingestion, and whether overdose resulted from
acute or chronic ingestion. Toxicity from acute ingestion may be
asymptomatic for up to 12 hours. Any person who has ingested
greater than 10 g (adult) or 200 mg/kg (child) (or unknown
quantity) should be referred to an emergency department.

Routes of administration
Oral (most common); rectal per suppository.

Effects on body systems

Cardiovascular: Hepatic damage may prompt cardiac

complications including dysrhythmias, ischemia, and injury
(chest pain/pressure, nausea, shortness of breath, T-wave
inversion, and ST-segment elevation on ECG).

Respiratory: Bronchospasm (wheezing and difficulty breathing)

1980
 and tachypnea have been reported as a hypersensitivity reaction
or as a side effect of N-acetylcysteine. See the Collaborative
Management section that follows.

Neurologic: Coma and seizures.

Hepatic: Acute ingestion will cause hepatic necrosis, which can lead
to liver failure. Hypoglycemia, right-sided abdominal pain, and
nausea with vomiting may be noted, usually 1 to 2 days after
ingestion.

Renal: Acute tubular necrosis with renal failure is seen in some

cases but often resolves.

Associated findings: Hypophosphatemia, metabolic acidosis,

hypothermia, thrombocytopenia, and hemorrhagic pancreatitis.

Collaborative management

Care priorities

1. Support of cardiovascular and respiratory systems: Supplemental

oxygen should be given if ABG values indicate a trend toward
respiratory failure. If the patient has an ineffective or absent
breathing effort, mechanical ventilation is provided. Serial ECGs
monitor for dysrhythmias. Symptomatic ventricular dysrhythmias
and bradyarrhythmias are treated per Advanced Cardiac Life
Support (ACLS) guidelines.

2. Removing acetaminophen from the patient: N-acetylcysteine

(Mucomyst), either orally or intravenously administered, is the
drug of choice for acetaminophen overdose. If ingestion occurred
within the previous 1 to 2 hours, AC should be administered. It can
be given with N-acetylcysteine, either orally or via a gastric tube. N-
acetylcysteine prevents systemic toxicity, especially if given 8 to 10
hours after ingestion. Lavage may be used only if less than 1 hour
has elapsed since ingestion, but administration of AC and N-
acetylcysteine should not be delayed to perform lavage.
Acetaminophen levels and liver function tests should be followed

1981
closely

3. Treatment of nausea and vomiting: Fluid replacement therapy

with lactated Ringer solution or D5NS (dextrose 5% in 0.9% normal
saline solution); antiemetics, such as promethazine hydrochloride
(Phenergan) or ondansetron (Zofran).

4. Rewarming: Warming therapies (such as warm IV solutions,

warm blankets, or water-filled heating blankets) may be used if the
patient has significant hypothermia.

5. Treatment of hypoglycemia: Usually done with a bolus of

dextrose 50% solution (D50) and continuous infusion of dextrose 5%
solution (D5W), based on serum glucose results. Hypoglycemia
occurs because of the potent hepatotoxic effects of acetaminophen.

Alcohols
Ethanol

Route of administration
Oral.

Effects on body systems

Cardiovascular: Tachycardia, atrial fibrillation, cardiac arrest.

Respiratory: Hypoventilation with acute intoxication, respiratory

failure, aspiration.

Neurologic: Confusion, aggressive behavior, irritability, tremors,

hallucinations (especially auditory), memory loss, stupor, coma,
seizures, loss of deep tendon reflexes.

Renal: May have a large urine output initially; will demonstrate

dehydration with low urine output with acute intoxication.

Associated findings: Dry oral mucosa, odor of alcohol on breath,

1982
 hypoglycemia, hypothermia, lactic acidosis, hypokalemia.

Collaborative management

Care priorities

1. Support of cardiovascular and respiratory systems to prevent

collapse: Oxygen supplementation; treatment of ventricular
dysrhythmias and bradyarrhythmias according to ACLS guidelines.

2. Fluid/potassium replacement: Manage hypovolemia with IV fluid

infusion. Include IV multivitamins in fluid replacement, and
provide thiamine to prevent Wernicke encephalopathy. Potassium,
calcium, phosphorus, and magnesium should be monitored and
supplemented as necessary.

3. Removing alcohol from the patient: As alcohol is metabolized,

the blood alcohol level decreases 15 mg/dL/h, according to recent
literature (legal limit for driving is less than 100 mg/dL). Coma may
occur if the level is greater than 300 mg/dL, but this is influenced by
each individual’s metabolic process and tolerance. When extreme
amounts of alcohol have been absorbed into the system, the liver
and kidneys may not be able to break down and excrete the alcohol.
Hemodialysis may be used for a life-threatening intoxication.

4. Prevention of emesis: Antiemetics are given, and a gastric tube is

inserted and maintained at low continuous suction.

5. Anticipation and treatment of withdrawal: Benzodiazepines are

the drugs of choice for treating alcohol withdrawal. Lorazepam,
which can be given IV, intramuscularly (IM), orally (PO), or
sublingually (SL), is the preferred agent in most alcohol withdrawal
protocols. Longer-acting agents such as diazepam are also used,
because of the decreased risk of recurrent withdrawal and/or
seizures. Oxazepam and lorazepam have a mechanism of
metabolism that is less liver dependent and are useful in cases
involving cirrhosis. Medications are given as needed for
withdrawal symptoms. In patients at high risk for severe
withdrawal symptoms or if withdrawal would be dangerous,

1983
benzodiazepines may be given on a schedule. If withdrawal is
severe and benzodiazepine doses become excessive, barbiturates
may be added. Agents that have glutamate-blocking properties,
such as lamotrigine, memantine, and topiramate, are showing
promise in alcohol detoxification.

6. Treatment of hypoglycemia: A bolus of D50 and continuous

infusion of D5W, based on serum glucose. Thiamine should be
given with glucose to avoid sudden onset of heart failure and
worsening neurologic impairment.

7. Treatment of delirium tremens (DTs): The most severe

manifestation of withdrawal, which can result in death. Symptoms
develop 48 to 96 hours after cessation of alcohol ingestion and
include confusion, disorientation, delirium, agitation, severe
diaphoresis, tachycardia, fever, and hypotension. Intubation may
be required to protect the airway. Delirium tremens generally
resolve within 3 to 5 days. Patients are sedated with
benzodiazepines, allowed to rest and sleep, and oriented frequently
to reality.

8. Treatment/prevention of seizures: Alcohol withdrawal seizures

may occur in a range from the first 6 to 48 hours to late onset at 10
days after abstinence. Benzodiazepines are given to raise the
seizure threshold during the withdrawal period. Additional seizure
management should reflect institution protocol. If the patient has a
history of a primary seizure disorder, an anticonvulsant agent may
also be indicated.

9. Prevention of Wernicke-Korsakoff syndrome: Caused by

thiamine deficiency and manifested by diplopia (the first real
diagnostic clue), confusion, excitation, peripheral neuropathy,
severe recent memory loss, impaired thought processes, and
confabulation. Prophylactic administration of thiamine is
recommended: IM thiamine on admission; supplemental oral
thiamine; and multivitamins and multiminerals high in C, B
complex, zinc, and magnesium. Multivitamins and minerals are
given to prevent malnutrition related to inadequate food intake and
malabsorption caused by alcohol’s irritating effect on the GI tract.

1984
Ingestion of carbohydrates, either orally or parenterally, increases
the body’s demand for thiamine. Traditionally thiamine has been
recommended to be administered before glucose, but evidence
supporting a benefit of this practice is lacking. One reason for this
may be that thiamine is taken up into the cells more slowly than
dextrose, so the order of administration is consequently relatively
minor. Thiamine repletion is very important, however, and 100
mg should be administered promptly, via a parenteral route for the
first dose in severe cases.

Methanol and ethylene glycol

Route of administration
Oral; found in household cleaning and automotive products,
especially antifreeze. Methanol poisoning can be associated with
illicit distillation of alcohol (“moonshine”) or intentional
substitution for ethanol.

Effects on body systems

The parent compounds have effects that are similar to ethanol. The
metabolites, however, can be extremely toxic.
Formate, a metabolite of methanol, causes retinal injury and
edema. Untreated, it can lead to permanent blindness.
Ethylene glycol metabolites target the kidney and lead to
reversible acute kidney injury. This compounds the situation by
slowing elimination of the ethylene glycol. Hypocalcemia is also a
serious sequela of ethylene glycol ingestion.
With both ingestions, a profound anion gap metabolic
acidosis develops, which can complicate and accelerate damage
from the metabolites ultimately leading to hypoxia and coma or
death.

Collaborative management
Similar to ethanol for hypoglycemia/seizures. Administer
bicarbonate if the pH is less than 7.3 and provide thiamine, folate,
and multivitamins in all patients. Fomepizole is a specific antidote,
followed by hemodialysis if the patient does not respond. In severe
cases (pH less than 7.25, high plasma levels of alcohol, kidney

1985
injury, or severe electrolyte disturbances), hemodialysis should be
done immediately. Ethanol has also traditionally been used as an
antidote for methanol and ethylene glycol but, while cheaper, has a
worse side effect profile. The preferred IV dosage form has also
been removed from the market.

Aspirin and other salicylates

Common Agents: Include Acetylsalicylic acid (aspirin, ASA), Ben
Gay topical ointment, methyl salicylate, magnesium salicylate,
salicylic acid, bismuth subsalicylate. Ingestion of topical products
containing salicylates, including Ben-Gay, salicylic acid
(keratolytic), and methyl salicylate (oil of wintergreen), can result in
severe salicylate toxicity. One teaspoon (5 mL) of 98% methyl
salicylate contains 7000 mg of salicylate (the same as 90 baby
aspirins), which is greater than 4 times the toxic dose for a 10-kg
child. Salicylate toxicity can occur with use of salicylate-containing
teething gels in infants. Use of alternative medicines, herbs, and
traditional medicines is increasing, and many of these substances
may contain salicylate. Salicylate poisoning should be considered
when herbal medicines, including topical oils, have been used.

Routes of administration
Oral, rectal (suppository), topical.

Effects on body systems

Early symptoms/blood levels: Tinnitus, nausea, vomiting, diarrhea,
hyperpnea, and vertigo. Signs of toxicity can be seen at therapeutic
levels (10 to 30 mg/dL) but are more common at 40 to 50 mg/dL.
Adult patients with toxicity usually present with a mixed
respiratory alkalosis and metabolic acidosis. Respiratory alkalosis
may be transient in children and metabolic acidosis may manifest
earlier. Occasionally, patients with mixed acid-base disturbances
have normal anion gap metabolic acidosis. Normal anion gap
acidosis does not rule out salicylate toxicity. Chronic ingestion of
salicylates may result in anxiety with tachypnea, difficulty con
centrating, diaphoresis, and hallucinations with agitated delirium.
Elderly patients may report a deterioration in functional status or

1986
symptoms of pneumonia, caused by the presence of tachypnea and
fever.
Later signs and symptoms include the following:

Metabolic: Increased cellular metabolic activity may result in

clinical signs and symptoms of hypoglycemia with blood glucose
levels that are sometimes normal, caused by a discrepancy
between blood and cerebrospinal fluid glucose levels.
Intracellular glucose is depleted before blood glucose reflects the
change.

Respiratory: Hyperventilation, tachypnea, hyperpnea,

noncardiogenic pulmonary edema. Acute lung injury may be
seen in pediatric patients and in elderly patients with chronic
salicylate toxicity.

Cardiac: Tachycardia and, later, ventricular dysrhythmias (cardiac

effects secondary to other factors such as hypovolemia, agitation,
and electrolyte disturbances).

Neurologic: Salicylates are neurotoxic. The first manifestation is

tinnitus. Later, coma, seizures, and cerebral edema with
increased intracranial pressure may be present (see Box 7-1 ).
Hearing loss may occur at serum levels greater than 30 to 45
mg/dL. Central nervous system (CNS) toxicity depends on the
amount of drug bound to CNS tissue and is more common with
chronic poisoning than with acute ingestions.

Renal: Renal failure secondary to rhabdomyolysis, resulting from

muscle breakdown caused by abnormal glucose metabolism. All
patients with poisoning are at least 5% to 10% dehydrated.
Clearance of salicylate by the kidneys is decreased by
dehydration. Hypokalemia and hypocalcemia are prompted by
the respiratory alkalosis created by tachypnea and hyperpnea.

Hepatic: Liver dysfunction, hepatitis. Hepatitis manifests in

children who ingest doses ≥ 30.9
mg/dL.javascript:showrefcontent(‘refrenceslayer’); Reye
syndrome is a form of pediatric salicylate-induced hepatic

1987
 disease characterized by nausea, vomiting, hypoglycemia,
elevated levels of liver enzymes and ammonia, fatty infiltration of
the liver, increased intracranial pressure, and coma.

Hematolgic findings: Hypoprothrombinemia and platelet

dysfunction are common. Bleeding may result from inhibition of
vitamin K-dependent enzymes or from platelet dysfunction.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse: Electrical

rhythm is monitored. Ventricular dysrhythmias and
tachydysrhythmias are treated per ACLS guidelines. When all
compensatory mechanisms fail, bradydysrhythmias may occur
before cardiac arrest.

2. Removal of salicylates: AC is administered orally or via gastric

tube to bind with the substance in the stomach; several doses of AC
may be necessary to achieve a 10:1 ratio of charcoal to salicylate.
Hemodialysis may be necessary if the substance has been more
extensively absorbed. Charcoal hemoperfusion may clear salicylates
somewhat but cannot correct acid-base, electrolyte, and fluid
problems associated with severe poisoning. Hemodialysis may be
necessary if cerebral edema, severe fluid overload, clinical
deterioration, or salicylate levels greater than 100 mg/dL occur.

3. Fluid replacement: Replace fluids with lactated Ringer solution or

normal saline (NS; 0.9% saline) 20 mL/kg over 1 to 2 hours. Sodium
bicarbonate may be added to promote forced alkaline diuresis, even
if the pH is normal or mildly elevated. Acetazolamide should not
be used.

4. Potassium replacement: See Fluid and Electrolyte Imbalances:

Hypokalemia, Chapter 1.

5. Treatment of hyperthermia: A cooling blanket, cool saline

infusion, intravascular cooling, or applications of ice may be used.

1988
6. Glucose administration/treatment of hypoglycemia: Blood
glucoses should be maintained in the upper normal range (110 to
140 mg/dL). There is a risk of cerebral hypoglycemia even with
normal blood glucoses so glucose should be administered to
patients with altered mental status even if normoglycemic.

7. Treatment of cerebral edema: Hyperventilation (via mechanical

ventilation) or mannitol is used.

8. Respiratory support: Intubation and mechanical ventilation

should be avoided if at all possible, but if necessary, high tidal
volumes and rates are important to maintain an adequate pH.

9. Treatment of pulmonary edema: Nitrates, morphine, diuretics,

potassium replacement, and noninvasive positive pressure
mechanical ventilation (NPPV) are possible. Prevention of
aspiration: A gastric tube is inserted, and then connected to low
suction.

10. Replacement of blood loss: Through delivery of blood and blood

products

Barbiturates

Common agents: See table 11-2.

Street names
Barbs, downers, ludes, rainbows, red dolls, reds, sleepers,
stumblers, tootsies, yellow jackets.

Routes of administration
Oral, IV, IM.

Effects on body systems

Cardiovascular: Hypotension, bradycardia, cardiac arrest.

Respiratory: Hypoventilation leading to respiratory failure and

respiratory arrest.

1989
Neurologic: Symptoms may include headache, vertigo, dizziness,
lethargy, ataxia, stupor, flaccidity, seizures, absent dolls-eye
reflex, coma, loss of deep tendon reflexes, and nystagmus.

Renal: Acute renal failure is possible.

Associated findings: Hypothermia, nausea, vomiting. Patient may

experience euphoria and excitability before the normal sedative
effects occur. Withdrawal symptoms (tremors and convulsions)
may occur.

Collaborative management

Care priorities

1. Removing barbiturates: If less than 1 hour has passed since

ingestion, gastric lavage may be initiated (provided there is no
delay in the administration of AC). AC is administered orally or via
gastric tube to bind with the substance in the stomach, and repeat
doses are recommended. Hemodialysis may be considered in
severe cases, especially if coma is present, usually correlating with
serum levels of 65 to 100 µg/mL. Similar to ASA, sodium
bicarbonate can be given to alkalinize the urine and promote
elimination.

2. Support of cardiovascular and respiratory systems to prevent

collapse: Electrical rhythm is monitored; bradyarrhythmias are
treated according to ACLS guidelines. After fluids are replaced,
vasopressor therapy (see Appendix 6), including dopamine and
norepinephrine bitartrate (Levophed), may be initiated for
hypotension. Mechanical ventilation may be required, depending
on the degree of hypoxia and CO2 retention.

3. Prevention/treatment of seizures: Phenytoin or diazepam may be

given.

4. Sedation for withdrawal symptoms: Typically the barbiturate

that was ingested is tapered gradually to zero.

1990
5. Prevention of aspiration: A gastric tube is inserted, which is then
connected to low suction.

6. Treatment of nausea and vomiting: Antiemetics may be

administered.

7. Treatment of hypothermia: A warming blanket is used.

Benzodiazepines

Common agents
See Table 11-3.

Table 11-3
COMMON BENZODIAZEPINES

Generic Name Common Trade Name Half-life (Hours)

Chlordiazepoxide Librium and others 7 to 28
Diazepam Valium and others 20 to 90
Lorazepam Ativan 10 to 20
Oxazepam Serax 3 to 21
Prazepam Centrax 24 to 200*
Flurazepam Dalmane 24 to 100*
Chlorazepate Tranxene 30 to 100
Temazepam Restoril 9.5 to 12.4
Clonazepam Klonopin 18.5 to 50
Alprazolam Xanax 12 to 15
Halazepam Paxipam 14
*
Includes half-life of major metabolites.
Note: Withdrawal symptoms can be correlated with the half-life of the drug that was
taken. Withdrawal from drugs with shorter half-lives produces more intense
symptoms that last for shorter periods; whereas, withdrawal from drugs with longer
half-lives produces less intense symptoms that can be prolonged. Moreover, the
severity of the withdrawal is directly related to the drug’s dosage.

Street names
Benzos, BZDs, downers, heavenly blues, qual, robital, stupes, tranx,
Valley girl.

Routes of administration
Oral, IM, IV.

1991
Effects on body systems

Cardiovascular: Hypotension, tachycardia.

Respiratory: Respiratory arrest.

Neurologic: Drowsiness, ataxia, slurred speech, coma. Withdrawal

may be manifested by seizures.

Renal: Renal failure because of rhabdomyolysis.

Associated findings: Hypothermia.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse: Electrical

rhythm is monitored. Atrial fibrillation or flutter may be treated
with digoxin or amiodarone, with initial rate control using
diltiazem or beta blockers. Severe supraventricular
tachyarrhythmias may be treated with adenosine. Hypotension is
treated with fluid replacement, followed by dopamine or
norepinephrine.

2. Support of respiratory system: Apnea monitoring and mechanical

ventilation may be indicated. Flumazenil administration may be
considered if hypoventilation ensues. Naloxone may be added if
mixed ingestion, including opiates, is suspected.

3. Removing benzodiazepines from the patient: Gastric lavage is

initiated if less than 60 minutes after ingestion; AC charcoal is used
to bind with the substance in the stomach.

4. Prevention of seizures: Phenytoin is administered.

5. Prevention of aspiration: Gastric tube is inserted, which is then

connected to low intermittent suction.

6. Rhabdomyolysis: Seizure activity and breakdown of muscle

1992
cause protein to precipitate in the kidneys, leading to renal failure.
Creatine kinase levels of five times the upper limit of normal, with
possible increases in BUN, creatinine, and urine protein, are noted
when rhabdomyolysis is present. Prevention of seizures and
aggressive fluid administration are the best means of preventing
rhabdomyolysis; fluids are also the main treatment modality.
Patients should be monitored closely for hyperkalemia if
rhabdomyolysis develops.

7. Treatment of hypothermia: A warming blanket is used if

indicated.

8. Flumazenil administration: Sedative and respiratory depressant

effects may be reversed by flumazenil. Repeat doses may be
necessary, since the duration of action of many benzodiazepines
exceeds that of flumazenil. Use with caution, especially in patients
with possible multidrug overdose. Flumazenil may precipitate
seizures in benzodiazepine-dependent patients and causes
arrhythmias in patients who also have high levels of cyclic
antidepressants.

Beta blockers

Common agents
Metoprolol, propranolol, nadolol, atenolol, bisoprolol, carvedilol,
sotalol, acebutolol, and nebivolol.

Routes of administration
Oral (for chronic use).

Effects on body systems

Cardiovascular: Bradycardia, hypotension, widened QRS,

ventricular arrhythmias.

Respiratory: Depression.

Neurologic: Depressed level of consciousness, seizures.

1993
Other: Hypoglycemia, hyperkalemia, rhabdomyolysis, renal failure,
mesenteric ischemia.

Collaborative management
Decontamination strategies can be used if 1 to 2 hours since
ingestion. ACLS measures, including fluids for hypotension and
atropine for severe bradycardia or heart block, may be necessary. IV
calcium and glucagon are given to address negative inotropy and
chronotropy. Glucose and insulin may be needed for blood sugar
and electrolyte imbalances. Beta agonists (vasopressors) such as
norepinephrine or epinephrine and sometimes inotropes such as
dobutamine or milrinone are often needed to maintain
hemodynamics in severe overdose.

Calcium channel blockers

Common agents
Verapamil, diltiazem, nifedipine, amlodipine, felodipine,
isradipine, nisoldipine, and nicardipine.

Routes of administration
Oral (for chronic use).

Effects on body systems

Cardiovascular: Bradycardia, hypotension, widened PR interval,

jugular venous distension if heart failure present.

Respiratory: Crackles and edema if heart failure present.

Other: Hyperglycemia (a potential means of differentiating from

beta-blocker overdose).

Collaborative management
Decontamination strategies can be used if 1 to 2 hours since
ingestion. ACLS measures should be initiated, including fluids for
hypotension, atropine for severe bradycardia or heart block, and
airway and hemodynamic stabilization as necessary. IV calcium is

1994
given at high doses in an attempt to displace the overdosed drug
and reopen calcium channels, though it is often ineffective. In
animal models high-dose insulin has been effective in severe
overdose, with or without dextrose depending on blood glucose
levels. Other modalities that may be used include glucagon and
vasopressors. Electrolytes should be closely monitored and treated
accordingly.

Cannabinoids
Marijuana

Street names
Ashes, ashitshi, Aunt Mary, baby bhang, blanket, blunt, bobo,
bomber, boom, broccoli, cheeba, chronic, cripple, dinky dow, Dona
Juana, dope, flower tops, gange, giggle smoke, grass, hash, herb, jay
joints, jolly green, joy smoke, Maryjane, pot, reefer, roach, skunk,
weed.
Sometimes marijuana is combined with other drugs (narcotics,
heroin, PCP, LSD, crack, cocaine, alcohol) to achieve a certain high.

Routes of administration
Smoked or ingested most commonly. Less common but presenting
as more severely symptomatic is IV use of hashish oil.
Cannabinoids contain tetrahydrocannabinol (THC).

Effects on body systems

Cardiovascular: Tachycardia, postural hypotension, atrial

fibrillation, and angina.

Respiratory: Minimal effects unless mixed with other drugs.

Neurologic/psychiatric: Euphoria, poor concentration, confusion,

somnolence, ataxia, memory impairments, perceptual alterations,
mood fluctuations, panic disorders.

Renal: Urinary retention.

1995
Collaborative management
Supportive care, benzodiazepines, gastric decontamination
measures if ingested recently, IV fluids.

Synthetic cannabinoids

Street names
Aroma, barely legal, bliss, K2, krypto buds, spice, spicestar fire.

Routes of administration
Like bath salts these are relatively recent drugs of abuse (use
beginning around 2008), which are composed of a plant/herbal
component, such as bay beans, dwarf skullcap, lousewart, red
clover, rose, or vanilla, mixed with synthetic cannabinoid
derivatives to mimic the effects of marijuana. They are marketed as
incense or potpourri (as with bath salts labeled “not for human
consumption”), sold via the internet, convenience stores, liquor
stores, and head shops, and usually smoked. These synthetic agents
bind as full agonists to the CB1 cannabinoid receptor, which is the
target receptor, as opposed to THC, which is only a partial agonist,
so the effects are more potent and the potential for
overdose/toxicity is greater.

Effects on body systems

Similar to marijuana (THC), but more severe. May additionally
cause nausea and vomiting, seizures, psychosis, and
supraventricular tachycardia.

Collaborative management
Supportive care. No antidote is available similar to THC. Some of
the synthetic cannabinoids have a longer duration (CP-47, 497) and
some shorter (JWH018 and JWH-073). Benzodiazepines for
agitation and seizures, antipsychotics for severe or prolonged
psychotic symptoms or a comorbid history of psychotic disorder,
and IV fluids as needed are given.

Cocaine

1996
Street names
Badrock, base, ball, bazooka, beam, beat, berni, big C, big flake,
biscuits, blast, blizzard, blow, bones, boost, bouncing powder,
boulders, boy, brick, bump, bunk, C, Cabello, cakes, caine, candy,
casper, caviar, chalk, Charlie, chicken scratch, coca, cocaine blues,
cocktail, coconut, coke, cola, Colombian, cooking up, cookies, crack,
crumbs, cubes, do a line, Damablanca, devil drug, dust, esnortiar,
everclear, fatbags, flake, flame cooking, flame throwers, flash, flex,
Florida snow, foo, freebase, freeze, G rock, girl, goofball, gravel,
happy dust, happy powder, happy trails, hardball, heaven, hell,
kibbles ‘n bits, king, kryptonite, lady, lady caine, late night, line,
love, mama coca, marching dust, marching powder, mojo, monster,
moonrocks, mujer and nieve (Spanish words), nose, nose candy,
nuggets, onion, P dogs, pebbles, Peruvian, piedras (Spanish word),
peace, pimp, powder, press, prime time, ready rock, Roca, rock,
rock star, Roxanne, rush, Scott, Scottie, Scrabble, shootin’ caine,
sleigh ride, smoke houses, smoking gun, sniff, snow, snort, soda,
speedball, sporting, stardust, stone, sugar, sweet stuff, teeth, toke,
toot, tornado, trails, white horse, white lady, white powder,
working bags, Yeyo (Spanish), zip.

Routes of administration
Nasal or IV (cocaine, snow); smoked (crack, rock); cooked;
freebased (flame cooking, flame throwers).

Effects on body systems

Cardiovascular: Hypertension; sinus tachycardia and less

commonly sinus bradycardia; ventricular dysrhythmias such as
premature ventricular contractions, ventricular tachycardia and
ventricular fibrillation; myocardial infarction; heart failure;
cardiomyopathy; acute endocarditis; and aortic dissection.
Intraventricular thrombus, as well as other thrombotic events,
have been reported since cocaine enhances thrombus formation.
Acute intoxication may result in profound hypotension and
shock.

Respiratory: Sharp pleuritic pain, hemoptysis, pneumothorax,

1997
 bronchospasm, pulmonary edema, and respiratory failure. Both
lactic acidosis and metabolic acidosis have been seen.

Gastrointestinal: Vomiting and other GI symptoms are common; if

the patient has had a rupture of a cocaine packet in the GI tract,
damage can be severe and include GI ulceration and bleeding, as
well as ischemia and necrosis.

Neurologic: The degree of CNS stimulation depends on the route

and amount of drug taken. Headache, hyperexcitation, paranoia,
delirium, hallucinations, tremors, hyperreflexia, and aggression
may be seen. Mentation may vary from stimulated, euphoric, and
excited states to delirium, stupor, and coma. Seizures are
common, usually tonic-clonic, and may last for hours. Initially
patients may seem well coordinated, but later may show tremors
and fasciculations as their condition deteriorates. CNS ischemia
and infarction, intracranial hemorrhage, and strokes have been
reported with cocaine intoxication.

Renal: Renal failure can occur and has been related to profound
hypotension and rhabdomyolysis. Renal infarction has been
reported.

Associated findings: Hyperthermia is common, and rectal

temperatures may be elevated to as high as 43°C (109.4°F).
Perforated nasal septum, track marks related to IV use, and
mydriasis (dilated pupils) occur. “Track marks” on arms and
scarring on arms and in hidden locations of the body, including
between the toes and in the vessels underneath the tongue.

Indicators of withdrawal: Poor concentration, anergia, anhedonia,

bradykinesis, sleep disturbance, decreased libido, intense cocaine
craving, depression, and suicidal tendencies.

Indicators of cocaine psychosis: Tactile and visual hallucination and

paranoia.

Peak action

1998
• Intranasal: 20 to 60 minutes.

• Oral: 60 to 90 minutes.

• IV: 5 minutes.

• Smoked: less than 5 minutes.

Cutting agents
Cutting agents are substances mixed with pure cocaine to increase
bulk. Cutting agents are often unknown but may include procaine,
caffeine, ephedrine, APAP, theophylline, phencyclidine,
amphetamine, quinine, talc, and strychnine, and the clinical effects
of a mixed intoxication may vary accordingly. Agents used in the
preparation of crack include powdered cocaine, water, baking soda,
and lidocaine. Cutting agents can become emboli that shower into
cerebral and pulmonary circulation, with subsequent effects.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse. Electrical

rhythm is monitored. Supraventricular tachycardia and ventricular
dysrhythmias are managed according to ACLS guidelines. Monitor
ECG for ischemic changes or infarction pattern (T-wave inversion
or ST-segment elevation or depression).

2. Support of respiratory system: Comatose patients are placed on

mechanical ventilation.

3. Identification of route of administration and removing cocaine

following oral ingestion: A radiograph of the GI tract may reveal a
cocaine-filled condom. Surgery may be performed to remove it.
Activated charcoal may be administered to bind with cocaine in the
stomach, or a laxative or suppository may be given to facilitate
rectal excretion. Flushing cocaine from the circulation using IV
ammonium chloride is being investigated.

1999
4. Treatment of hypotension or hypertension: Antihypertensives or
vasopressors are administered as indicated.

5. Treatment of volume deficiency: IV fluid replacement is done,

such as with lactated Ringer solution or D5NS.

6. Prevention/treatment of seizures: Diazepam, phenytoin, or

phenobarbital is administered.

7. Treatment of hyperthermia: A cooling blanket, ice, and/or

acetaminophen is used. Core temperature is the most accurate
measurement.

8. Prevention of aspiration: A gastric tube is inserted, then

connected to low continuous suction.

9. Rhabdomyolysis: see discussion in Benzodiazepines section.

Cyclic antidepressants
Examples include amitriptyline hydrochloride (Elavil), doxepin
hydrochloride (Sinequan), imipramine hydrochloride (Presamine,
Tofranil), trimipramine maleate (Surmontil), nortriptyline (Pamelor,
Aventyl), and desipramine (Norpramin).

Route of administration
Oral. Overdose has become less common with the much more
widespread use of the safer antidepressant class of serotonin
reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine,
citalopram, escitalopram, and sertraline. Rarely, an SSRI can cause
dangerously high levels of serotonin resulting in serotonin
syndrome. The condition is often accidental, resulting from when
two medications that raise serotonin levels are combined.
Offending agents include other antidepressants, pain or headache
medications, and St. John’s Wort (herbal supplement). Signs and
symptoms include restlessness, agitation, confusion, diaphoresis,
anxiety, tremors, lack of coordination, and tachycardia.

Effects on body systems

2000
Cardiovascular: Hypotension, sinus tachycardia, supraventricular
tachycardia, ventricular dysrhythmias, conduction defects,
myocardial infarction, cardiopulmonary arrest. Hypertension has
been noted. Monitor ECG for widening QRS complex.
Progressive QRS widening signals worsening toxicity.

Respiratory: Respiratory arrest, pulmonary edema, ARDS.

Hyperventilation also has been noted.

Neurologic: CNS depression, coma, seizures, delirium,

hallucinations.

Renal: Acute tubular necrosis; renal failure secondary to

rhabdomyolysis.

Pancreatic: Pancreatitis.

Associated findings: Hyperthermia or hypothermia.

Collaborative management

Care priorities

1. If the patient is symptom free, monitor for a minimum of 6 to 8

hours, noting vital signs and width of QRS complex.

2. Support of cardiovascular system to prevent collapse: Electrical

rhythm is monitored for at least 6 hours to enable assessment for a
widening QRS complex, which is a signal of worsening toxicity.
Manage supraventricular and ventricular dysrhythmias using
ACLS guidelines.

3. Removing cyclic antidepressants: Activated charcoal is

administered via gastric tube to bind with the ingested substance in
the stomach.

4. Reversal of the effects of the drugs: IV sodium bicarbonate is

used. An alternative approach is to promote a state of respiratory
alkalosis by increasing respiratory rate via mechanical ventilation.

2001
5. Prevention/treatment of seizures: Phenytoin and diazepam are
administered.

6. Respiratory support: Mechanical ventilation is used. Pulmonary

edema is treated with nitrates, morphine, diuretics, potassium
replacement, and intermittent positive pressure breathing IPPB
treatments.

7. Treatment of hypotension: Fluid replacement is carried out,

followed by administration of dopamine and norepinephrine as
indicated.

8. Treatment of hyperthermia or hypothermia: A cooling or a

warming blanket is used as indicated.

9. Prevention of aspiration: A gastric tube is inserted and then

connected to low intermittent suction.

Digoxin

Routes of administration
Oral/IV.
Digitalis glycosides like digoxin are very serious and potentially
life threatening in the event of an overdose; these drugs can
accumulate quickly if renal dysfunction develops or worsens. Like
tricyclic antidepressants, reports of toxicities are decreasing in
frequency as evidence-based use of the drug in heart failure and
arrhythmias is decreasing.

Effects on body systems

Cardiovascular: Bradycardia/atrioventricular block with atrial or

ventricular ectopy and tachycardia at high levels.

Gastrointestinal: Nausea vomiting abdominal pain.

Neurologic: Lethargy, malaise, weakness, confusion.

Other findings: Hyperkalemia is a marker for severe overdose, and

2002
 serum digoxin levels are readily available to evaluate.

Collaborative management
AC if recent ingestion. Digoxin immune fab is a specific binding
antidote that will quickly reverse toxicity. Since it is expensive and
whole digoxin levels are unusable after administration, it should be
reserved for cases where arrhythmias or other serious signs and
symptoms are present and not used to treat moderately elevated,
asymptomatic digoxin levels.

Hallucinogens

Street names
Acid, battery acid, blotter, boomers, California sunshine, cids,
doses, dots, golden dragon, heavenly blue, hippie, looney tunes,
LSD, Lucy in the sky with diamonds, mesc, microdot, pane, purple
heart, superman, tab, window pane, yellow sunshine, Zen.

Common agents
Lysergic acid diethylamide (LSD), mescaline (peyote cactus),
ketamine (special K, K, ket, kitkat, super K), morning glory seeds,
nutmeg, psilocybin (mushrooms, magic mushrooms, shrooms,
magics, blue meanies, liberty caps, golden tops, mushies),
phencylclidine (PCP, angel dust, peace pill).

Routes of administration
Oral, IV, nasal, smoked.

Effects on body systems

Effects will depend on the amount and type of drug ingested.

Respiratory: Apnea, respiratory arrest.

Neurologic: Hallucinations and paranoid behavior patterns,

tremors, seizures, coma.

LSD: Patient may describe tasting or hearing colors or exhibit

mental dissociation.

2003
Mescaline: Sense of being followed by moving geometric shapes.

Associated findings: “Track marks” on arms and scarring on arms

and in hidden locations of the body, including between the toes
and in the vessels underneath the tongue. Hyperthermia and
diaphoresis. In addition, visual hallucinations may occur. Taking
large doses of PCP and ketamine can result in coma, seizures,
respiratory arrest, and death. LSD, mescaline, and magic
mushrooms have not been reported to directly cause death. Rare
fatalities have been a result of accidents, behavior caused by the
drug, or plant poisoning.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse. Manage BP

and HR/rhythm according to ACLS guidelines.

2. Removing hallucinogens from patient: If oral ingestion was

within 1 hour, gastric lavage may be attempted, as long as AC
therapy is not delayed. AC is administered orally or via gastric tube
to bind with the substance in the stomach.

3. Prevention of seizures: Anticonvulsants such as phenytoin or

diazepam are administered.

Opioids

Common agents
Codeine, fentanyl, heroin, hydrocodone, hydromorphone
(Dilaudid), levorphanol (Levo-Dromoran), pethidine or meperidine
(Demerol), methadone (Dolophine), morphine, opium, oxycodone
hydrochloride (Percocet-5, Tylox, Oxycontin), buprenorphine
(Subutex), and oxymorphone (Numorphan). Heroin is the most
abused opioid. There has been a steady increase in abuse of
prescription opioids such as morphine.

Street names

2004
China white, Chinese H, dope, dragon, Harry cone, junk, OC, oxy,
painkillers, white, white dynamite.

Routes of administration
Oral, IV, IM, smoked.

Effects on body systems

Cardiovascular: Profound hypotension, bradycardia,

cardiovascular collapse, sudden death.

Respiratory: Atelectasis, acute pulmonary edema, infiltrates related

to aspiration complications, respiratory depression, apnea,
hypoventilation, and bronchospasm.

Neurologic: Range from decreased mental alertness to stupor and

coma; pinpoint pupils; seizures.

Renal: Renal failure has been associated with profound hypotension

and rhabdomyolysis.

Associated findings: “Track marks” and scarring on arms and in

hidden locations of the body, including between the toes and in
the vessels underneath the tongue.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse: Electrical

rhythm is monitored; bradyarrhythmias are treated per ACLS
guidelines. Vasopressor therapy is initiated for hypotension after
fluids have been replaced.

2. Removal of orally ingested opioids from patient: AC is

administered orally or via gastric tube to bind with the substance in
the stomach.

3. Reversal of opioid effects: Administration of naloxone

2005
hydrochloride (Narcan) to manage respiratory depression. After the
initial dose of naloxone, the patient’s respiratory status must be
monitored closely, since additional doses may be required.
Respiratory depression and coma may occur when the effects of
naloxone wear off and the opiate effects predominate. The half-life
of naloxone is 60 to 90 minutes, and effects last 2 to 3 hours. If the
narcotic effects last longer than the effects of the naloxone, the
patient may slip into coma once the naloxone wears off. If persistent
respiratory depression is present, a continuous naloxone infusion
may be considered.

4. Treatment of drug withdrawal symptoms: Hallucinations are

treated with haloperidol (Haldol).

5. Support of respiratory system: Pulmonary edema is treated with

diuretics and restriction of IV fluid intake. An individual whose
respiratory system is deteriorating is placed on apnea monitoring or
mechanical ventilation.

6. Prevention of aspiration: A gastric tube is inserted and then

connected to low continuous suction.

7. Prevention/treatment of seizure activity: Anticonvulsant therapy

is done, such as phenytoin administration.

8. Rhabdomyolysis: See discussion in Benzodiazepines section.

Phencyclidine

Street names
Angel dust, mist, PCP, peep, hog, crystal.

Routes of administration
Oral, nasal, smoked.

Effects on body systems

Cardiovascular: Hypertension, hypertensive crisis, tachycardia.

2006
Respiratory: Respiratory depression, respiratory arrest, laryngeal
stridor, bronchospasm.

Neurologic: Rage and “superhuman strength” are hallmark signs.

Ranges from hyperexcitability, hyperreflexia, muscle rigidity,
and paranoid and psychotic behavior to stupor, seizures, and
coma. Coma: eyes may be open in a blank stare, nystagmus, and
pinpoint pupils.

Renal: Renal failure precipitated by rhabdomyolysis and

myoglobinuria.

Associated findings: Hypothermia or hyperthermia, hypoglycemia.

Collaborative management

Care priorities

1. Support of cardiovascular system to prevent collapse: Electrical

rhythm is monitored and tachydysrhythmias are treated as
previously discussed. Nitroprusside or labetalol may be used for
antihypertensive therapy. Nitroglycerin may be given to treat
ischemia.

2. Removal of phencyclidine from the patient: No specific antidote

is available, although multiple administrations of charcoal to bind
with the ingested substance in the stomach are standard practice.
Charcoal is ineffective if phencyclidine was smoked, rather than
swallowed. The first dose of AC may be accompanied with sorbitol.
After ruling out the possibility of rhabdomyolysis, acidification of
the urine with ammonium chloride or ascorbic acid to a pH around
5.5 is done.

3. Prevention/treatment of seizure activity: Phenytoin and

diazepam are given. Diazepam is administered IV at an initial dose
of 2 to 5 mg. May be repeated every 30 minutes until sedation is
achieved. Haloperidol may be given 5 to 10 mg IV to control
psychosis. Its effects usually occur within 5 to 10 minutes of
administration.

2007
4. Respiratory support: Pulmonary edema is treated with diuretics
and restriction of IV fluid intake. Persons with hypoxia and
respiratory distress require monitoring of pulse oximetry and may
require mechanical ventilation.

5. Prevention of aspiration: A gastric tube is inserted and then

connected to intermittent low suction.

6. Rhabdomyolysis: See discussion in Benzodiazepines section.

7. Treatment of hypothermia or hyperthermia: A warming or

cooling blanket is used as appropriate.

Stimulants
Amphetamines
Street names
Crank, crystal meth, ecstasy, ice, methamphetamine, speed, white
crosses.

Routes of administration
Oral, IV, IM, intranasal, smoked.

Effects on body systems

Cardiovascular: Tachycardia, atrial and ventricular dysrhythmias,
hypertension, myocardial ischemia and infarction, cardiovascular
collapse.

Respiratory: Hyperventilation and respiratory failure related to

cardiovascular collapse.

Neurologic: Confusion, aggressive behavior, hyperactivity,

convulsions, delusions, irritability, tremors, hallucinations,
memory loss, stupor, stroke, coma.

2008
Renal: Renal failure related to dehydration and rhabdomyolysis.

Associated findings: Mydriasis, fasciculations, hyperthermia,

thrombocytopenic purpura.

Collaborative management
1. Support of cardiovascular and respiratory systems to prevent
collapse: Antidysrhythmic agents are given per ACLS guidelines to
manage tachycardias. Ischemia is treated with nitrates; myocardial
infarction is treated per ACLS guidelines for acute coronary
syndromes.

2. Removing amphetamines from the patient: For oral ingestion, AC

is administered orally or via gastric tube. Acidification of the urine
with ammonium chloride helps clear amphetamine.

3. Treatment of hypertension: Antihypertensives such as

nitroprusside or labetalol may be needed to decrease BP.

4. Prevention/treatment of seizures: IV diazepam 0.1 to 0.2 mg/kg is

administered slowly and repeated every 5 minutes until sedation is
achieved. Lorazepam is an alternative benzodiazepine.

5. Psychosis: Haloperidol 5 mg is given IM or IV. Repeat dose may

be required to control behavior.

6. Treatment of hyperthermia: A cooling blanket, antipyretics, and

iced IV fluids are used.

7. Treatment of dehydration: Done by fluid replacement, such as

lactated Ringer solution and NS continuous IV infusions

8. Anticipation and treatment of rhabdomyolysis: Usually treated

with sodium bicarbonate infusion, mannitol, or furosemide (Lasix)

Cathinones (bath salts)

Street names

2009
Bloom, blue silk, cloud nine, ivory snow, ivory wave, lunar wave,
white rush, scarface, sextacy, stardust, vanilla sky, white lightning,
and zoom. The energizing and agitating effects mimic other drugs
such as amphetamines and cocaine, which raise the level of
dopamine, a neurotransmitter, in the brain areas that regulate
reward and movement. The surge in dopamine prompts feelings of
euphoria and increased energy.

Routes of administration
Oral or nasally insufflated. Less commonly used rectally IV, IM,
gingivally, or via inhalation. A recently emerging drug of abuse,
bath salts are popular because they are generally cheap, easy to
acquire through the internet or at gas stations, convenience stores,
liquor stores, or head shops, and have only recently (September
2011) been placed under Schedule 1 as a drug with no medical
value and high abuse potential. An easily manipulated chemical
structure has been exploited to weaken such control; this chemical
family in part led to the Drug Abuse Prevention Act of 2012, which
broadened the spectrum and gave a general definition to Schedule 1
substances.

Effects on body systems

Body systems effects are similar to amphetamines but less potent.
Gastritis, liver toxicity, esophagitis, anorexia, and psychosis have
also been associated with ingesting the natural alkaloid in the khat
plant. Synthetic cathininones include methylenedioxypyrovalerone
(MDPV), methylone, and mephedrone (“drone, meph, meow-
meow”), which, in addition to the sympathomimetic toxidrome,
have also less commonly been associated with severe hyponatremia
and myocarditis.

Collaborative management
Primarily supportive; similar to amphetamines.

Specific antidotes for common drug

overdoses/toxicities

2010
Table 11-4 gives specific drug treatments for a few of the more
common and critical drug overdoses not discussed in the preceding
section.

Table 11-4
MANAGEMENT OF DRUG OVERDOSE/TOXICITIES

Target (toxic) Drug or Class Treatment or Antidote

Acetaminophen N-Acetylcysteine
Anticholinergics Physostigmine
Arsenic, lead, mercury, or other Dimercaprol injection
heavy metals
Benzodiazepines Flumezanil
Beta blockers Glucagon, beta agonists
Calcium channel blockers Calcium intravenous, glucagons
Copper Trientene
Cyanide Sodium thiosulfate, sodium nitrite, amyl nitrite,
hydroxocobalamin
Cyclic antidepressants Sodium bicarbonate
Digitalis glycosides Digoxin immune Fab
Heparin Protamine
Insulin Glucagon, dextrose, octreotide
Iron Deferoxamine
Lead Succimer, edetate calcium disodium (EDTA)
Methanol/Ethylene glycol Fomepizole, ethanol
Nitrites Methylene blue
Opiates Nalmefene, naltrexone, naloxone
Organophosphate insecticides Atropine, pralidoxime
Warfarin Vitamin K (oral or intravenous)

Care plans for all drug overdoses

Ineffective airway clearance 
related to presence of tracheobronchial secretions or obstruction; decreased
sensorium.
Goals/Outcomes: Chest radiograph normalizes. Within 2 to 24
hours of intervention/treatment, the patient has a patent airway and
is free of congestion as evidenced by clear breath sounds over the
upper airways and lung fields, RR 12 to 20 breaths/min with normal
depth and pattern, PaO2 at least 90 mm Hg, Paco2 35 to 45 mm Hg,
pH 7.35 to 7.45, and SpO2 at least 95%.
Respiratory Status: Airway Patency; Aspiration Prevention;
Respiratory Status: Ventilation

2011
Respiratory monitoring

1. Assess for respiratory distress hourly and as needed. Note

secretions; stridor; gurgling; shallow, irregular, or labored
respirations; use of accessory muscles of respiration; restlessness
and confusion; and cyanosis (a late sign of respiratory distress).

2. Suction oropharynx or use suction via endotracheal tube as

needed.

3. Administer bronchodilators as appropriate.

4. Monitor ABG values for evidence of hypoxia (PaO2 less than 90

mm Hg) and respiratory acidosis (Paco2 greater than 45 mm Hg, pH
less than 7.35).

5. Monitor respiratory patterns; provide continuous apnea

monitoring if available.

6. If the patient has been placed on mechanical ventilation, monitor

for indicators of airway obstruction (see Mechanical Ventilation,
Chapter 1).

7. Monitor oxygen saturation continuously. Be alert to values less

than 95% with response depending on patient’s baseline and
clinical presentation.

8. Monitor for nausea and vomiting. Evaluate effects of antiemetics.

Airway Management, Aspiration Precautions

Hyperthermia 
related to overdose of cocaine, hallucinogens, phencyclidine, salicylates, or
cyclic antidepressants.
Goals/Outcomes: Optimally, within 24 to 72 hours of
intervention, the patient becomes normothermic.
Thermoregulation

With massive overdose, temperature regulation may never

2012
be achieved.

Temperature regulation

1. Monitor for hyperthermia: temperature greater than 38.3° C

(greater than 101° F), pallor, absence of perspiration, and torso that
is warm to the touch. If means are available, provide continuous
monitoring of temperature. Otherwise, measure rectal or core
temperature hourly, and as needed.

2. Monitor effects of cooling blanket, cooling baths, and ice packs to

the axillae and groin.

3. Maintain fluid replacement as prescribed. Monitor hydration

status and trend of input and output (I&O).

4. Monitor neurologic status hourly and as needed until stabilized.

5. Monitor vital signs continuously or hourly and as needed until

stabilized.

6. Administer and evaluate effects of antipyretic medications.

Fever Treatment; Vital Signs Monitoring; Medication

Prescribing

Deficient fluid volume 

related to low intake or losses secondary to vomiting or diaphoresis and
shock conditions.
Goals/Outcomes: Patient remains normovolemic as evidenced by
urine output greater than 0.5 mL/kg/h, moist mucous membranes;
balanced I&O, BP within patient’s normal range, HR less than 100
bpm, stable weight, CVP 8 to 12 mm Hg, and PAWP 6 to 12 mm
Hg.
Hydration; Fluid Balance

Fluid management

2013
1. Monitor hydration status. Note signs of continuing dehydration:
poor skin turgor, dry mucous membranes, thirst, weight loss
greater than 0.5 kg/day, urine specific gravity greater than 1.020,
weak pulse with tachycardia, and postural hypotension.

2. If the patient has a pulmonary artery catheter:

• Monitor SVR and PVR as appropriate.

• Monitor CO as appropriate.

• Monitor PCWP/PAWP and central venous/right

atrial pressures.

• Administer positive inotropic/contractility

medications.
3. Evaluate the effects of fluid therapy.

4. Assess for indicators of electrolyte imbalance, especially the

presence of hypokalemia. Be alert to irregular pulse, cardiac
dysrhythmias, and serum potassium level less than 3.5 mEq/L.

5. Monitor I&O hourly; assess for output elevated

disproportionately to intake, bearing in mind the insensible losses.

6. Monitor laboratory values, including serum electrolyte levels and

serum and urine osmolality. Note BUN values elevated
disproportionately to the serum creatinine (indicator of
dehydration rather than renal disease), high urine specific gravity,
low urine sodium, and rising Hct and serum protein concentration.
Optimal values are the following: serum osmolality 275 to 300
mOsm/kg, urine osmolality 300 to 1090 mOsm/kg, BUN 10 to 20
mg/dL, serum creatinine 0.7 to 1.5 mg/dL, urine sodium 40 to 180
mEq/24 hr (diet dependent), Hct 37% to 47% (female) or 40% to 54%
(male), and serum protein 6 to 8.3 g/dL.

2014
7. Maintain fluid intake as prescribed; administer prescribed
electrolyte supplements.

Fluid/Electrolyte Management; Surveillance; Hypovolemia

Management

Disturbed sensory/perceptual perception: Visual, tactile,

auditory, kinesthetic 
related to chemical alterations secondary to ingestion of mind-altering
drugs.
Goals/Outcomes: Within 48 hours of intervention, the patient
verbalizes orientation to time, place, and person and is free of
abnormal sensory and perceptual experiences.
Cognitive Orientation; Distorted Thought Self-Control

Reality orientation

1. Establish and maintain a calm, quiet environment to minimize

the patient’s sensory overload.

2. Assess patient’s orientation to time, place, and person. Reorient

as necessary.

3. Explain procedures before performing them. Include significant

others in orientation process.

4. Do not leave the patient alone if agitated or confused.

5. Administer antianxiety agents as prescribed.

6. If the patient is hallucinating, intervene in the following ways:

• Be reassuring. Explain that hallucinations may be

very real to the patient but they are not real. They
are caused by the substance that the patient
consumed, and they will go away eventually.

• Try to involve family and significant others, because

2015
 the patient may have more trust in them.

• Explain that restraints are necessary to prevent

harm to the patient and others. Reassure the patient
that restraints will be used only as long as they are
needed.

• Tell the patient that you will check on him or her at

frequent intervals (e.g., every 5 to 10 minutes) or
that you will stay at patient’s side.

Delusion Management; Environmental Management; Fall

Prevention; Surveillance: Safety

Risk for violence: Self-directed and/or other-directed 

related to mind-altering drugs or depressed state.
Goals/Outcomes: Patient, staff, and patient’s significant others
are free of injury.
Impulse Self-Control

Behavior management

1. If patient’s condition is stable, provide a sitter or auxiliary staff

member, such as an orderly or nursing assistant, to observe the
patient when he or she is awake.

2. Speak with the patient in a quiet and calm voice, using short
sentences.

3. Establish a therapeutic relationship with patient.

4. Encourage the patient to take control over his or her own

behavior.

5. Facilitate support by significant others.

2016
6. Limit the number of interventions as much as possible to avoid
frequently disturbing the patient.

7. Administer and evaluate effectiveness of sedation to calm

patient.

8. Keep all sharp instruments out of patient’s room. Follow agency

protocol accordingly.

9. Develop appropriate behavior expectations and consequences,

given the patient’s level of cognitive functioning and capacity for
self-control.

Behavior Management: Self-Harm; Substance Use Treatment:

Alcohol Withdrawal; Substance Use Treatment: Overdose, Suicide
Prevention

Additional .nursing diagnoses

See nursing diagnoses and interventions in the following as
appropriate: Nutritional Support (Chapter 1), Mechanical
Ventilation (Chapter 1), Hemodynamic Monitoring (Chapter 1),
Prolonged Immobility (Chapter 1), Emotional and Spiritual Support
of the Patient and Significant Others (Chapter 2), Acute Lung Injury
and Acute Respiratory Distress Syndrome (Chapter 4), Acute
Respiratory Failure (Chapter 4), Acute Coronary Syndromes
(Chapter 5), Heart Failure (Chapter 5), Cardiomyopathy (Chapter
5), Dysrhythmias and Conduction Disturbances (Chapter 5), Aortic
Aneurysm/Dissection (Chapter 5), Acute Renal Failure (Chapter 6),
Status Epilepticus (Chapter 7), Hepatic Failure (Chapter 9), Acute
Pancreatitis (Chapter 9), Fluid and Electrolyte Disturbances
(Chapter 1), and Acid-Base Imbalances (Chapter 1). In addition, see
Traumatic Brain Injury for Impaired Corneal Tissue Integrity
(Chapter 3).

High-risk obstetrics: Hypertension in

pregnancy

2017
Most pregnant women are healthy and rarely in need of critical
care. The high-risk obstetric patient presents the unique challenge
of caring for the mother and the fetus simultaneously. In most
cases, the survival of the mother will take precedence over fetal
survival, but the optimal outcome is survival of both. Two basic
principles should underlie the care of the pregnant patient. First,
maternal anatomic and physiologic changes occur during
pregnancy to facilitate adequate blood flow to the fetus and protect
the mother after delivery (Box 11-2). The pregnant patient may
require hemodynamic monitoring, and the critical care nurse
should be familiar with the different hemodynamic changes and
pressure values in pregnancy and labor as outlined in Table 11-5.
Second, the fetus is totally dependent on the mother for all of his or
her oxygenation and growth needs, so any intervention performed
on the mother will most likely affect the fetus. Despite the unique
challenges presented by the critically ill obstetric patient, transfer of
the patient to a critical care unit should not be delayed.

Table 11-5
EXPECTED HEMODYNAMIC CHANGES DURING PREGNANCY,
LABOR, DELIVERY, AND POSTPARTUM

2018
Box 11-2
PHYSIOLOGIC ANATOMICAL CHANGES
IN PREGNANCY
Body position
Supine hypotension: After 20 weeks, supine positioning
significantly reduces CO and uterine blood flow by compressing
the inferior vena cava.

Lateral positioning or hip wedge under right or left hip is

recommended to displace the gravid uterus to avoid supine
hypotension.

Cardiovascular
Heart rate: 10 to 15 bpm increase from prepregnancy rate by 32
weeks

Blood pressure: 10 to 15 mm Hg decrease from prepregnancy value

between 14 and 24 weeks returning to prepregnancy value by 37
to 40 weeks’ gestation

Blood volume: 40% to 50% increase by 24 weeks

Stroke volume: 30% increase by 32 weeks

CO: 30% to 50% increase by 24 weeks

Fetal circulation
More than 10% of maternal CO is diverted into the uterine
circulation. Maternal CO increases by at least 25% during
pregnancy. Fetal oxygenation is dependent on maintenance of
sufficient maternal CO.

Gastrointestinal
Gastric motility: decreased

2019
Gastric emptying time: decreased

IAP: increased

These changes can cause increased risk of aspiration with general

anesthesia.

Neck/throat
Larynx: displaced anteriorly, prompting increased incidence of
airway edema and bleeding, leading to failed intubation.

Pulmonary and acid-base balance

Oxygen consumption: increases

Functional residual capacity and volume: decreased by elevated

maternal diaphragm, resulting in increased risk of rapid
development of hypoxemia and apnea compared with the
nonpregnant patient

Acid-base imbalance: respiratory alkalosis

Renal
Glomerular filtration rate: increased by 50% at term

Obstetric complications account for less than 1% of intensive care

unit (ICU) admissions and less than 0.5% of all deliveries. Despite
this relatively low incidence, the acuity of obstetric critical care
patients is high because of the unique pathophysiology and the
associated clinical disorders. Maternal mortality rates range from
5% to 20% when pregnant women require critical care. Obstetric
patients may be admitted into critical care because of complications
of obstetric conditions, such as eclampsia, or complications of an
underlying medical condition, such as heart disease. Those with
obstetric conditions are admitted more frequently and generally
have better outcomes than those admitted with underlying medical

2020
conditions. The most prevalent indication for obstetric ICU
admissions is hypertension in pregnancy. This chapter will focus on
the hypertensive complications of pregnancy that may result in
admission to a critical care unit.

Hypertension in pregnancy
Classification
Hypertensive disease occurs in up to 22% of pregnancies. The study
of hypertension in pregnancy has been hindered by a lack of
agreement on a set of definitions to define subsets of the disease.
This chapter uses terms recommended by the American Congress
of Obstetricians and Gynecologists and endorsed by the National
Institutes of Health Working Group on High Blood Pressure to
define hypertensive disease in pregnancy (refer to Box 11-3). Of
these hypertensive disorders, preeclampsia, eclampsia, and HELLP
(hemolysis, elevated liver enzymes and low platelet count)
syndrome were responsible for 30% of obstetric ICU admissions.
These conditions, their management, and care will be discussed.

Box 11-3
CLASSIFICATION OF HYPERTENSIVE
STATES OF PREGNANCY
• Chronic hypertension: Hypertension that is present before
pregnancy or develops before 20 weeks’ gestation.

• Preeclampsia and eclampsia: A systemic syndrome of

hypertensive disease, with proteinuria diagnosed after 20 weeks’
gestation. Eclampsia indicates the additional presence of
convulsions.

• Preeclampsia superimposed on chronic hypertension:

Preeclampsia and/or eclampsia diagnosed in a patient with
chronic hypertension.

• Gestational hypertension: Hypertension diagnosed after 20 weeks

2021
 of pregnancy without proteinuria.

Preeclampsia and eclampsia

Preeclampsia is the most common hypertensive disorder of
pregnancy, occurring in 6% to 8% of all pregnancies. Preeclampsia
is a syndrome that affects both mother and fetus. It is clinically
defined as an increase in blood pressure or hypertension of greater
than140/90 mm Hg on two occasions at least 4 hours apart or
160/110 mm Hg on two occasions after 20 weeks gestation
accompanied by proteinuria in a previously normotensive woman.
In the absence of proteinuria, presence of any of the following also
confirms a preeclamptic diagnosis: platelet count below 100,000
mm3, creatinine above 1.1 mg/dL, elevated liver transaminases,
pulmonary edema, or cerebral or visual symptoms. Preeclampsia is
also known as toxemia, pregnancy-induced hypertension, and
preeclamptic toxemia.
Eclampsia is defined as the occurrence of seizures in a woman
with preeclampsia who has no known cause for seizure. The
seizures of eclampsia are almost always tonic-clonic in nature and
are typically self-limited. Eclampsia complicates only 1% to 2% of
preeclamptic pregnancies. Eclampsia may develop antepartum
(38% to 53%), intrapartum (18% to 36%), or postpartum (11% to
44%) Overall, preeclampsia and eclampsia are responsible for 15%
of maternal deaths, mostly from complications resulting from
eclampsia.

Pathophysiology
Preeclampsia has been called the “disease of theories” because true
mechanisms behind the pathogenesis remain unclear. Many women
with preeclampsia have smaller than normal blood vessels feeding
the placenta. However, why this happens to some women and not
others is not completely understood. Preeclampsia is characterized
by widespread arteriolar vasospasm resulting in increased
peripheral vascular resistance. Areas of vasospasm cause breaks or
roughened areas in the endothelial layer. These roughened areas

2022
trigger fibrin deposition and leakage of intravascular fluid into the
extravascular space. Decreased colloid oncotic pressure, a normal
physiologic change during pregnancy, also contributes to fluid
leakage and proteinuria. These widespread arteriolar vasospasms
result in decreased perfusion to virtually all organs, including the
placenta, a decrease in plasma volume, activation of coagulation
cascade, and alteration in glomerular capillary endothelium. The
physiologic process of vasospasm manifests in the development of
classic symptoms associated with preeclampsia resulting in
decreased blood flow to the major maternal organs such as the
kidney, brain, and liver, as well as the placenta. These generalized
cyclic vasospasms lead to tissue ischemia and eventually end-organ
dysfunction. One of the more common problems related to
preeclampsia is pulmonary edema caused by increased capillary
permeability. Thrombocytopenia complicates severe preeclampsia
in about 7% to 11% percent of women. Abruptio placentae and the
release of procoagulants, such as thromboplastin, can result in acute
disseminated intravascular coagulation (DIC).

Signs and symptoms

Most women with preeclampsia do not experience signs other than
mild high blood pressure and a small amount of excess protein in
the urine. The changes are asymptomatic. Thus, prenatal visits to
assess for hypertension and measure urinary protein are scheduled
frequently in the last half of pregnancy.
In some cases, preeclampsia can worsen and develop features of
severe disease; however, the symptoms may be subtle. Patients
should not hesitate to mention concerns about symptoms of
preeclampsia to their provider: The increase in severity generally
occurs over several days to weeks but may occur more quickly.
Features of severe preeclampsia consist of one or more of the
following signs or symptoms:

• Blood pressure is greater than 160/110 mm Hg. Women with

blood pressures in this range have an increased risk of stroke.

• Abnormal kidney tests (e.g., serum creatinine above 1.1 mg/dL).

2023
• Low platelet count (may be rapidly falling).

• Liver abnormalities (detected by blood tests).

• Pulmonary edema (fluid in the lungs).

• Persistent severe headache.

• Cerebral or visual disturbances (blurred vision, spots or flashes of

light, loss of vision, CNS irritability).

• New shortness of breath (caused by fluid in the lungs).

• Pain in the mid- or right-epigastrium (similar to heartburn).

• Oliguria (decreased urine output).

• Intrauterine abnormalities (fetal growth restriction and/or

oligohydramnios- decreased amniotic fluid).

Refer to Table 11-6 for more specific changes in physiology.

Table 11-6
HEMODYNAMIC PROFILES IN OLIGURIC PATIENTS WITH
PREECLAMPSIA

Risk factors for preeclampsia and eclampsia

Demographics: African American and Hispanic women, maternal
age over 35 years, and nonsmokers.

Comorbidities: Chronic hypertension, renal disease, obesity,

2024
 diabetes, vascular disease, connective tissue disease, and
maternal infections.

Pregnancy-fetus: Multiple pregnancy (twin, triplet), molar

pregnancy, personal history (previous preeclampsia), and family
history (mother or sister).

Maternal immunity: History of condom use, fertilization with

donor sperm, new sexual partner.

HELLP syndrome
HELLP syndrome is an acronym for a unique pregnancy condition
representing increased severity of a variant of severe preeclampsia
or eclampsia. HELLP syndrome affects 2% to 20% of patients with
severe preeclampsia or eclampsia. Maternal mortality ranges from
3.5% to 24%, with perinatal mortality ranging from 10% to 60%. The
etiology of HELLP is uncertain. Approximately 10% to 15% of
pregnant patients with HELLP syndrome do not have elevated
proteinuria of hypertensive disease. The clinical manifestations of
HELLP syndrome, which include nausea, vomiting, malaise, flulike
symptoms, and epigastric pain, may suggest a multitude of other
clinical diagnoses. Misdiagnosis is common and may result in a
delay of correct treatment. Any pregnant woman demonstrating
clinical manifestations and hemolysis, elevated liver enzymes, and
low platelets must be diagnosed with HELLP syndrome.
Worsening of systemic arteriolar vasospasm produces such
complications as liver damage, subcapsular hematoma, pulmonary
edema, liver rupture, abruption placentae, DIC, and acute renal
failure. The HELLP patient should be closely monitored for right
upper quadrant pain or shoulder pain because these complaints
may be indicative of liver hematoma or liver rupture. The only
known treatment for HELLP syndrome is to empty the uterus of the
fetus and the placenta.

Diagnostic Tests for Hypertensive Obstetric Disorders

Test Findings
Complete blood Hemoglobin and hematocrit (Hct) may be elevated (>35 Hct) and steadily

2025
count rising with severe preeclampsia-eclampsia.
Peripheral blood Schistocytes or burr cells are present with HELLP syndrome.
smear
Urinalysis Positive for protein spillage
24-hour urine Mild/moderate: 0.3 to 5 g protein with normal urine output. Severe
collection preeclampsia-eclampsia: >5 g protein with low urine output.

Serum albumin Decreases as urine protein spillage increases; severe: <2.5 mg/dL.
Liver enzymes Aspartate transaminase, alanine amino transferase, and lactate
dehydrogenase are elevated with severe preeclampsia-eclampsia and
HELLP syndrome. Bilirubin may be elevated with HELLP.
Renal serum Mild-moderate: BUN, creatinine, and uric acid levels may be elevated.
chemistry Severe preeclampsia-eclampsia: BUN, creatinine, and uric acid will be
elevated.
Platelet count Mild-moderate: <100,000/mm3. Severe preeclampsia-eclampsia and
HELLP syndrome: <100,000/mm3
Bleeding time Prolonged when platelet count is <100,000/mm3.
Fibrinogen Decreased (<300 mg/dL)
Screening Normal unless the patient develops HELLP syndrome that progresses to
coagulation tests DIC, wherein all values are elevated.
(PT, PTT, thrombin
time)

Caring for the hypertensive patient

Collaborative care
Collaboration between the critical care and obstetrics nurses is
necessary in providing safe and comprehensive obstetric critical
care for the hypertensive patient. Nurses from each specialty bring
unique and complementary knowledge and skills for patient
management. Obstetric nurses have experience with fetal heart
monitoring and interpretation, and critical care nurses have
experience with managing patients requiring invasive monitoring,
ventilatory support, and specific critical care procedures. A written
protocol should be established to facilitate maternal transfer from
the obstetric unit to the ICU or to an institution that can provide the
appropriate level of care for both mother and fetus before and after
delivery. The protocol should also include planning and support for
both obstetric and critical care nurses to work collaboratively to
care for the patient. If the baby has been delivered, families may
desire unrestricted visitation, or the mother may desire to have the
baby remain in her ICU room. The collaborative team should
develop a plan of care to address the physiologic, psychosocial, and
family needs of the patient. The following guidelines are given to

2026
aid the critical care nurse, but optimally, there would be an
obstetric nurse as part of the care team for any obstetric patient
admitted to the ICU for severe hypertensive conditions.

Provide fetal surveillance

1. Electronic fetal monitoring: All undelivered obstetric patients
admitted to the ICU should be placed on electronic fetal monitoring
once the infant is viable. An electronic fetal monitor has two
external devices, which are strapped to the maternal abdomen. It
includes a transducer that records fetal heart rate (FHR) and a
tocodynamometer, or “toco,” that records uterine activity.

The use of an electronic fetal monitor requires an obstetrics

registered nurse with appropriate training and competency in fetal
heart rate interpretation. This can be achieved by having both a
critical care and an obstetrics nurse at the patient’s bedside.
Having a labor nurse “on call” if the critical care nurse notices an
abnormal fetal heart rate or the onset of labor is not sufficient and
could compromise patient safety.

2. On admission: Ultrasound, Doppler flow studies, biophysical

profile, nonstress test (NST), and amniotic fluid volume studies are
ordered to evaluate fetal well-being

3. Fetal nonstress testing: An NST is a frequently ordered

noninvasive test to monitor fetal status. NSTs are performed by the
obstetric nurse who is trained in the procedure and interpretation
of results. This test is used to determine fetal well-being and is
reflective of fetal oxygenation and placental function. A reactive
NST indicates adequate fetal well-being. A nonreactive NST may
indicate a problem with placental functioning or fetal oxygenation
and should be followed up with additional testing.

2027
4. Biophysical profile: The biophysical profile uses a combination of
NST and fetal parameters observed via ultrasound to measure fetal
well-being. The fetus is scored as 0, 1, or 2 for each of 5 parameters:
fetal breathing movement, gross fetal movement, fetal tone,
amniotic fluid volume, and NST test results.

5. Amniocentesis: Withdrawal of amniotic fluid under direct

ultrasonography is called amniocentesis. Examination of amniotic
fluid can be used to determine fetal maturity in pregnancies less
than 34 weeks. An LS (lecithin:sphingomyelin) ratio above 2:1
represents fetal maturity.

Positioning of the pregnant patient

The supine position should be not be used with pregnant women
after 20 weeks’ estimated gestational age. At that time, the maternal
vena cava is compressed by the growing maternal abdomen when
the mother lies in a supine position. This effect is called “supine
hypotension” and, if left unchecked, will lead to decreased blood
return to the heart, decreased maternal BP and CO, and
subsequently to decreased blood flow to the uterus, placenta, and
fetus. The appropriate position for the pregnant patient is lateral
positioning, which avoids the risk of supine hypotension and
maximizes blood flow to the uterus, placenta, and fetus. Turning
some pregnant women on the left side may improve CO more than
the right side. Semi-Fowler positioning with a hip roll tilting the
maternal abdomen off of the vena cava is another acceptable
position for the pregnant woman in the latter half of pregnancy. If
supine positioning is required, manual displacement of the gravid
uterus can also alleviate venacaval compression.

Monitoring for preterm labor

Obstetrical hypertensive conditions can increase the risk of preterm
labor, which is defined as labor that occurs before 37 weeks’
estimated gestational age. Signs and symptoms of preterm labor
may be subtle and are likely to go unnoticed by nurses unfamiliar
with labor assessment.

1. Routinely screen or observe for the following signs and

2028
symptoms of preterm labor:

• Increase or change in vaginal discharge.

• Bloody vaginal discharge.

• Leakage of amniotic fluid.

• Signs and symptoms of urinary tract infection.

• Dull backache.

• Uterine cramping (menstrual-like cramps,

intermittent or constant).

• Pelvic pressure or pain (feeling that the baby is

“pushing down”).

• Abdominal cramping with or without diarrhea.

• If the patient is unconscious, observe for restlessness

or nonverbal indications of intermittent pain.

2. If the patient has any signs or symptoms of labor, notify the

physician or midlevel practitioner and

• Position mother in the lateral position (turn to the

left or right side).

• Encourage bladder emptying every 2 hours.

• Report all new onsets of contractions or any change

in contraction pattern immediately to the

2029
 obstetrician or midlevel practitioner, because
cervical examination is the most accurate method
for diagnosing preterm labor.
3. Monitor uterine contractions (preterm labor) and fetal status:

• Preterm labor contractions may be infrequent,

irregular, and painless or frequent, regular, and
painful. Preterm labor, left undetected and
untreated, can progress into an emergency delivery
of a neonate in the critical care unit.

• Tocolytics are used to stop preterm labor, but they

must be started early in the labor process to be
effective.

If frequent, strong, painful uterine contractions continue,

notify the obstetrician immediately as placental abruption may be
occurring. Placental abruption refers to the detachment of the
placenta from the wall of the uterus, which will result in life-
threatening maternal hemorrhage and fetal hypoxia. The only
definitive treatment of a complete placental abruption is delivery
of the fetus by Caesarean section within minutes.

Management of preeclampsia and eclampsia

Collaborative management for patients with severe preeclampsia,
eclampsia, or HELLP syndrome is basic to stabilize the mother and
fetus. Continuous assessment and hemodynamic monitoring of the
cardiovascular, renal, central nervous, and pulmonary systems
provide early indications of worsening maternal condition. Fetal
surveillance may include continuous fetal monitoring, biophysical
profile, and fetal lung maturity testing. Delivery of the fetus may be

2030
indicated because of the maternal condition or fetal compromise.
The goal of the healthcare team is to accurately monitor ongoing
organ system dysfunction and prevent further damage leading to
end-organ failure and maternal-fetal mortality.

Prevention of eclampsia/seizure management

The treatment goals of severe preeclampsia are to prevent seizures,
decrease arterial spasms, and effect prompt delivery of the fetus.
Magnesium sulfate is the most effective anticonvulsant for
preeclampsia, eclampsia, and HELLP syndrome, reflected by
results of the Magpie Trial International Study Collaborative.

Magnesium sulfate is listed as a high-risk medication by The

Joint Commission (formerly the Joint Commission on
Accreditation of Healthcare Organizations). Obstetric nurses
should be familiar with safety recommendations related to the
administration of magnesium sulfate to pregnant or delivered
patients.

Mode of administration: 
Magnesium is given iv as a loading (bolus) dose followed by a
continuous drip.

Action: Magnesium works by decreasing the maternal seizure

threshold, and it relaxes the uterine smooth musculature by
decreasing or stopping uterine contractions.

Complications: The patient receiving magnesium is at higher risk

for postpartum hemorrhage caused by uterine atony (failure of
the uterus to contract after delivery).

Excretion: Magnesium is metabolized by the kidneys so a decrease

in urine output will cause a subsequent rise in magnesium levels.

Administration of magnesium sulfate

2031
• Administer using an infusion pump. Two nurses should verify
the infusion pump settings when magnesium is initiated or
dosage changed.

• Magnesium solutions should be premixed and labeled in

standard solutions.

• An initial loading dose of 4 to 6 g is given over 15 to 30 minutes

followed by a maintenance dose of 2 to 3 g/h.

• Magnesium therapy is continued after delivery for 12 to 24 hours.

Side effects of magnesium include flushing, nausea, muscle
weakness, headache, and toxicity.

• Serum magnesium levels are drawn 2 hours following the loading

dose, then every 6 hours. Serum magnesium levels of 4 to 7
mEq/L are considered therapeutic for prevention of seizure
activity.

• Magnesium levels greater than 8 mg/dL are associated with signs

of toxicity; refer to Table 11-7.

• If toxicity is suspected, discontinue infusion, administer oxygen,

obtain stat magnesium level, and notify physician.

• The antidote for magnesium toxicity is calcium gluconate 10 mg

of 10% calcium gluconate solution IV push IVP or direct IV
injection over 10 minutes and should be readily available.

• Control of eclamptic seizures: Accomplished through

administration of 4 to 6 g of IV MgSO4 over 5 to 10 minutes. This
bolus is followed by a continuous infusion of 2 to 3 g/h. If a
patient has a recurrent seizure, another bolus of 2 to 4 g can be
given over 3 to 5 minutes. Sodium amobarbitol I (for injection),
benzodiazepines, or phenytoin can be used for seizures that are
not responsive to magnesium sulfate. Avoid the use of multiple
agents to decrease eclamptic seizures, unless necessary. The
patient must be closely monitored during magnesium
administration. It is recommended that the obstetric nurse be

2032
 present at the bedside with the critical care nurse to monitor fetal
and uterine response during magnesium infusion.

Table 11-7
CLINICAL EFFECTS OF MAGNESIUM

Serum Magnesium Level Signs/Symptoms to Watch for

1.7 to 2.4 mg/dL Normal
5 to 8 mg/dL Therapeutic
8 to 12 mg/dL Loss of pateller reflexes
10 to 12 mg/dL Somnolence
12 to 16 mg/dL Respiratory difficulty and depression
15 to 17 mg/dL Muscle paralysis
<18 mg/dL Altered cardiac conduction
30 to 35 mg/dL Cardiac arrest

Blood pressure control and management

Severe hypertension must be addressed after magnesium infusions.
Antihypertensive agents need to be used to keep diastolic BP
between 90 and 100 mm Hg. Sudden or extreme drops in maternal
BP should be avoided as they may precipitate maternal stroke
and/or decreased blood flow to the fetus. Venodilators are often
used to lower BP. A drug’s effect on the fetus must be considered.
Diuretics are used only in the setting of pulmonary edema.
Antihypertensive agents used in pregnancy are chosen because of
their ability to avoid vasodilation of placental vessels.
The most commonly used antihypertensives are:

• Hydralazine 5 to 10 mg may be given every 10 to 15 minutes.

Maximum dosage: 30 mg.

• Labetalol 20 to 40 mg may be given every 10 to 15 minutes.

Maximum dosage: 220 mg.

• Labetalol should be used cautiously in patients with

asthma and cardiac failure.
• Nifedipine 10 to 20 mg may be given every 30 minutes. Maximum
dosage: 50 mg.

2033
Fluid management
Severely preeclamptic patients are easily overloaded with IV fluid,
predisposing them to pulmonary edema. Strict observation of I&O
is warranted. Total fluid intake is typically maintained at 125 to 150
mL/h. Hemodynamic monitoring may be indicated if pulmonary
edema develops. Urine output of less than 0.5 mL/kg/h should be
reported to the physician or midlevel practitioner.
A nonglucose solution should always be available as part of a
fetal resuscitation protocol, and a bolus of 500 to 1000 mL of
lactated Ringer or normal saline is usually given to improve
maternal circulating volume and subsequently improve uterine
perfusion and fetal oxygenation.

Pain management
Medications used in pregnancy are generally limited to classes A
and B, to decrease potential negative effects on the fetus. The
benefits of medications in classes C, D, and E should be carefully
weighed against the risk to the fetus. Butorphanol (Stadol),
nalbuphine (Nubain), and fentanyl (Sublimaze) may all be given IM
or as an IV bolus/IV push and are commonly given for pain relief
during labor.

Meperidine (Demerol) and morphine are not often used

because of their long half-lives and potential to cause neonatal
neurobehavioral depression, which may last several days.

Neuraxial analgesia techniques (spinal, epidural, or combined

spinal-epidural) are commonly used because they are more
effective at relieving pain and do not cause respiratory depression
in the mother or fetus. Medications used are generally a
combination of local anesthetics and opioids, which produce
greater pain relief with less motor block than local anesthetics
alone. Lumbar epidurals may be given continuously or as a patient-
controlled analgesia. Contraindications to neuraxial analgesia
include allergy to local anesthetics, administration of low-

2034
molecular-weight heparin within 12 hours, coagulation disorders,
maternal shock, or infection at the insertion site. Common side
effects of neuraxial analgesia include maternal hypotension and
itching. Hypotension is generally treated with IV fluid boluses
and/or IV ephedrine. Ephedrine is the preferred vasopressor
because it causes peripheral vasoconstriction without affecting the
umbilical vessels. Loratadine (Claritin) or cetirizine (Zyrtec) may be
given to alleviate itching.

Delivery of the fetus

Preeclampsia arising at 34 weeks’ (or more) gestation is generally
managed by delivery. Fetal viability, or the gestational age at which
the fetus can survive outside the womb, is generally thought to be
24 to 25 weeks’ gestation. After 34 weeks’ gestation, the majority of
infants will avoid major complications from prematurity. Before 34
weeks, patients with severe preeclampsia-eclampsia require
delivery unless the gestational age is less than 26 weeks, wherein
attempts to prolong the pregnancy may be initiated. If the mother
exhibits signs of HELLP syndrome, such as thrombocytopenia or
epigastric or right upper quadrant pain, or has visual disturbances,
delivery should be strongly considered regardless of fetal age, since
the mother is at risk of life-threatening illness if delivery is delayed.
Management of the severely preeclamptic patient will depend on
three conditions: maternal status, fetal status, and gestational age. If
the pregnancy is at least 34 weeks, delivery is planned as there is
little benefit in prolonging gestation. If the pregnancy is 33 to 34
weeks, glucocorticoids are given to the mother to accelerate the
development of fetal lung maturity. The glucocorticoids are given
intramuscularly in 2 doses 12 hours apart with maximum effect
achieved 24 hours after the second dose. Both the maternal and fetal
status must be closely monitored. If either deteriorates, definitive
steps must be taken regarding plans for delivery. The medical team
carefully and constantly weighs the benefits of delivery for the
mother versus the risks of preterm delivery for the fetus. The
decision to proceed to delivery in a preterm pregnancy should be
made in consultation with the obstetrician, pediatrician, critical care
physician, and neonatologist (if available).
The following factors should be considered in choosing the best

2035
clinical placement for the patient based on availability of
equipment, skills, and trained personnel:

• Is continuous electronic fetal monitoring available?

• Are there resources for the administration and monitoring of

medications for labor induction or augmentation, anesthesia, and
analgesia?

• Are care providers appropriately trained to provide fetal

resuscitation?

• Is timely access to operating rooms for an emergency caesarean

section feasible?

• Are care providers able to provide maternal

hemodynamic/cardiac/respiratory monitoring and treatment?

• Are there resources available for neonatal support should

complications arise?

Preparation for delivery

Labor and delivery of the critically ill obstetric patient may occur
either in the labor and delivery unit or the critical care unit,
depending on several factors. A multidisciplinary discussion by
medical specialists and nursing regarding the pros and cons of
critical care versus the delivery room or operating room setting will
determine the best placement of the patient for optimal maternal
and fetal care during labor and delivery.
Vaginal delivery is the safest method of delivery for the
preeclamptic/eclamptic patient with a cervix that is favorable for
induction of labor. Caesarean section should be reserved for
obstetric indications. The goal of delivery method is to minimize
the incidence of complications. If operative delivery is the selected
method of delivery, 5 to 10 U of platelets may be ordered
preoperatively for a platelet count of less than 50,000 mm3. The
patient should be typed and cross-matched for blood and blood
products to be used if hemorrhage and/or DIC develops
intraoperatively or postoperatively. General anesthesia is typically

2036
selected, since regional anesthesia (entering the spine) is generally
contraindicated with thrombocytopenia. Because of the potential
for difficult intubation caused by airway edema and hyperemia,
fiberoptic intubation may be used. The patient will require close
observation postoperatively for the first 24 to 48 hours.

Emergency delivery in the critical care unit

To improve communication and facilitate timely emergency
response, the names, specialties, and pager/cell phone numbers of
the medical and nursing care team members should be compiled on
one sheet of paper or written on one specific white board in all of
the units possibly involved in the care of the pregnant critical care
patient. The teams would minimally include medical and nursing
personnel from critical care, labor and delivery, anesthesiology,
neonatology, and possibly nursery and respiratory therapists. Other
medical specialists should be added as appropriate for the patient’s
condition. It is helpful to have core team members communicate
every shift to discuss emergency plans, update the plan of care, and
discuss any possibility of emergent interventions.

Care plans for the high-risk obstetric patient

in critical care
Ineffective protection 
related to hemodynamic, hematologic, and neurologic changes associated
with preeclampsia/eclampsia/HELLP.
Goals/Outcomes: Within 1 hour of development of severe
preeclampsia, eclampsia, or severe HELLP syndrome, the pregnant
patient (mother and child) is monitored intensively and prepared
for delivery, to avoid life-threatening complications of pregnancy-
induced hypertension.
Blood Coagulation; Fetal Status: Intrapartum

Intrapartum

1. Verify HRs of mother and fetus before initiating electronic

monitoring.

2037
2. Monitor BP of mother at least every 5 minutes if severe
hypertension or seizures have occurred. Monitor FHR for slowing,
indicative of fetal distress.

3. Initiate fetal resuscitation measures to treat abnormal fetal heart

rhythms, as appropriate. Note response to all supportive
interventions.

4. Instruct woman and support person(s) about the need for

monitoring and data to be obtained.

5. Keep advanced practice provider informed of significant changes

in FHR, interventions for abnormal patterns, fetal response, labor
progress, and maternal response to interventions.

6. Administer anticonvulsive medications as ordered to control

seizures.

7. Monitor magnesium levels and be alert to hypermagnesemia,

decreased respiratory rate and depth, loss of deep tendon reflexes.

8. Assist with application of forceps or vacuum extractor, as

needed, during delivery.

9. Monitor the patient closely for hemorrhage if HELLP syndrome

is present.

10. Note hemoglobin and Hct levels before and after blood loss, as
indicated.

11. Monitor coagulation studies, including prothrombin time (PT),

activated partial thromboplastin time (aPTT), fibrinogen, fibrin
degradation products (FDPs), fibrin split products (FSPs), and
platelet counts as appropriate.

Ineffective protection 
related to potential for seizures and neurologic complications secondary to
eclampsia or HELLP syndrome.
Goals/Outcomes: Throughout the hospitalization, the patient
remains free of seizures and neurologic complications as evidenced

2038
by orientation to time, place, and person; normoreactive pupils and
reflexes; her normal visual acuity, motor strength, and
coordination; and absence of headache and other clinical indicators
of increased intracranial pressure.
Risk control

Seizure precautions

1. Monitor for and document seizures. Protect the patient from

injury by initiating seizure precautions. When the patient is seizing,
turn her to the side to promote placental perfusion and prevent
aspiration.

2. Assess the patient for initial signs of increased intracranial

pressure, including diminished length of consciousness, headaches,
abnormal pupillary responses (i.e., unequal; sluggish/absent
response to light), visual disturbances, weakness and paralysis,
slow HR, and change in RR and pattern. Patient may be
experiencing problems related to seizure management, or may
experience intracranial bleeding if platelets are extremely low.

3. Monitor trend of Glasgow Coma Scale if the patient has difficulty

awakening after seizures. If the patient exhibits signs of magnesium
toxicity, consult physician and consider calcium gluconate
administration.

4. Increase frequency of neurologic monitoring as appropriate.

5. Assess the epidural site (as appropriate), if the patient received

epidural analgesia during labor and delivery. Patients with
coagulopathy may develop an epidural hematoma, manifested by
sensory or motor deficits, bowel or bladder dysfunction, or back
pain. Report problems to the physician immediately. The epidural
catheter should remain in place until coagulation studies normalize.

6. Avoid activities that increase intracranial pressure.

7. If initial signs of increased intracranial pressure are noted,

consult physician immediately. Signs of impending herniation
include unconsciousness, failure to respond to deeply painful

2039
stimuli, decorticate or decerebrate posturing, Cushing triad (i.e.,
bradycardia, increased systolic BP, widening pulse pressure),
nonreactive/fixed pupils, unequal pupils, or fixed and dilated
pupils. See Traumatic Brain Injury, Chapter 3, for more information
about herniation. For additional interventions for increased
intracranial pressure, see Box 3-7.

Environmental Management: Comfort; Medication

Administration

Risk for deficient fluid volume 

related to active loss secondary to antepartum, postpartum,
intraabdominal, or other bleeding.
Goals/Outcomes: The patient remains normovolemic as
evidenced by HR, RR, and BP within 10% of expected normal
range; urinary output 0.5 mL/kg/h or greater and absence of
epigastric or abdominal pain or tenderness, and frank bleeding
resulting from HELLP syndrome.
Fluid and Electrolyte Balance;

Fluid monitoring

1. Monitor fluid status, including I&O, signs of hypovolemia,

including increases in HR and RR, decreases in BP and urinary
output, restlessness, and vital signs.

2. Initiate hemodynamic monitoring if necessary to assess shock

state and/or manage hemodynamics.

3. Optimize venous return through lateral positioning and/or

manual uterine displacement once the patient has a gravid uterus.

4. Monitor hemoglobin and Hct as ordered. Postpartum, the uterus

contracts and blood is released into the central circulation as it
decreases in size. Despite a normal 500-mL vaginal delivery blood
loss, hemoglobin and Hct often increase.

5. Inspect for bleeding from mucous membranes, bruising after

minimal trauma, oozing from puncture sites, and presence of

2040
petechiae. Maintain patent IV access.

6. Administer supplemental oxygen as necessary for active

bleeding.

7. Perform fundus checks and initiate gentle fundal massage to help

the uterus remain firm and promote hemostasis.

8. Initiate bleeding control therapy as ordered. Methylergonovine,

ergonovine, and carboprost may be used to manage prolonged
bleeding or hemorrhage.

9. Replace lost volume with plasma expanders (e.g., albumin,

Hetastarch) and/or blood products as indicated. See Table 10-3 for
information about blood products.

Shock Management: Cardiac; Cerebral Perfusion Promotion;

Fluid/Electrolyte Management

Risk for infection 

related to inadequate secondary defenses (HELLP syndrome causes liver
dysfunction, which may impair the reticuloendothelial system phagocytic
activity and portal-systemic shunting); multiple invasive procedures;
stress and risks associated with pregnancy, labor, and delivery.
Goals/Outcomes: The patient is free of infection as evidenced by
normothermia, HR less than 100 bpm, RR less than 20 breaths/min,
negative culture results, WBC count less than 11,000/mm3, clear
urine, and clear, thin sputum.
Infection Severity

Infection protection

1. Monitor vital signs for evidence of infection (e.g., increases in HR

and RR). Check rectal or core temperature every 4 hours for
increases.

2. If temperature elevation is sudden, obtain specimens for blood,

sputum, and urine cultures or from other sites as prescribed.
Consult advanced practice provider for positive culture results.

2041
3. Monitor CBC, and consult advanced practice provider for
significant increases in WBCs. Be aware that a normal or mildly
elevated leukocyte count may signify infection in patients with liver
dysfunction.

4. Evaluate secretions and drainage for evidence of infection (e.g.,

sputum changes, cloudy urine).

5. Evaluate IV, central line, and other site(s) for evidence of

infection (i.e., erythema, warmth, unusual drainage).

6. Provide routine episiotomy care by spraying the area with warm

water at least every 4 hours. Sitz baths are usually not possible with
critically ill patients. Ice packs and topical anesthetics may be used
to enhance comfort.

7. Provide daily breast care by cleansing the breasts with mild soap
and water. Breast engorgement should be managed per physician’s
orders to help prevent infection and control pain. If left unrelieved,
breast engorgement can result in stoppage of lactation. If breast-
feeding is planned, breasts can be massaged and milk manually
expressed or pumped.

8. Prevent transmission of infectious agents by washing hands well

before and after caring for the patient and by wearing gloves when
contact with blood or other body substances is possible. Dispose of
all needles and other sharp instruments in puncture-resistant, rigid
containers. Keep containers in each patient room and in other
convenient locations. Avoid recapping and manipulating needles
before disposal. Teach significant others and visitors proper hand-
washing technique. Restrict visitors with evidence of communicable
disease.

9. Administer antibiotics as prescribed. Use caution and reduced

dosage when administering antibiotics (especially aminoglycosides)
to patients with low urinary output or renal insufficiency.

Medication management;

2042
Compromised family coping 
related to abnormal circumstances surrounding labor, delivery, and
postpartum; creating need for mother to be separated from infant and other
family members.
Goals/Outcomes: The patient and family demonstrate adequate
coping behaviors and are facilitated in being together as soon as
possible in the postpartal hospitalization.
Surveillance: Safety; Anxiety: Self-Control, Concentration,
Coping.

Coping enhancement

1. Provide regular updates to family members about the condition

of both mother and infant.

2. Invite family members to participate in care of the mother as

possible.

3. Promote infant-mother bonding by allowing baby visitations in

the ICU as soon as mother and infant stabilize. Allow mother to
feed baby if possible. Maintain infant safety if mother’s condition is
marginally stable.

4. Discuss feelings about labor, delivery, and complications with the

patient and family members. Relay information about the condition
of the infant as often as possible, if mother is unable to visit with the
baby.

5. If the infant or mother expires, provide all possible support

measures, including pastoral care and referrals to community
support groups or professional counseling.

Family Involvement Promotion; Family Process Maintenance;

Normalization Promotion

Oncologic emergencies
An oncologic emergency is defined as a life-threatening situation
occurring as a manifestation of a malignancy or the result of

2043
antineoplastic treatment or tumor progression. Such emergencies
most commonly arise from the ability of cancer to (1) spread by
direct infringement on adjacent structures or metastasize to distant
sites leading to thrombosis or hemorrhage; (2) produce abnormal
amounts of hormones or cellular products leading to fluid and
electrolyte imbalances and organ failure; (3) infiltrate serous
membranes with effusion; (4) obstruct vessels, ducts, or hollow
viscera; or (5) replace normal organ parenchyma. As more
aggressive therapies are used in the treatment of these cancers, side
effects are more intense and the use of critical care to manage such
side effects will only increase.
Early recognition and intervention are essential to enhance
positive outcomes. Once an oncologic emergency is recognized, the
aggressiveness of management is influenced by the reversibility of
the immediate situation, the probability of long-term survival, and
the ability to provide effective supportive care.
Oncologic emergencies can be classified as hematologic,
structural, metabolic, or side effects from treatment such as
chemotherapy, radiation therapy, biologic therapy, surgery, or bone
marrow transplantation. Neutropenic sepsis, tumor lysis syndrome
(TLS), and superior vena cava syndrome (SVCS) will be discussed
in this chapter as examples of oncologic emergencies seen in the
critical care arena. When recognized early and managed
appropriately, these acutely ill individuals have a high likelihood of
recovery. An overview of additional oncologic emergencies,
associated causes, and signs and symptoms is given in Table 11-8.

Table 11-8
ONCOLOGIC EMERGENCIES DEFINED

2044
2045
Sources: Recommendations for end-of-life care in the intensive care unit: a
consensus statement by the American College of Critical Care Medicine. Crit Care
Med 36:1394-1396, 2008; Guidelines for evaluation of new fever in critically ill adult
patients: 2008 update from the American College of Critical Care Medicine and the
Infectious Diseases Society of America. Crit Care Med 2008 36:1330-1349, 2008;
Clinical practice guideline: red blood cell transfusion in adult trauma and critical care.
Crit Care Med 37:3124-3157, 2009; Dellinger RP, Levy MM, Carlet JM, et al:
Surviving Sepsis Campaign: international guidelines for management of severe
sepsis and septic shock: 2008 [correction appears in Crit Care Med 41(2):580-637,
2013; Crit Care Med 2008;36:296-327; National Comprehensive Cancer Network
Clinical Practice Guidelines in Oncology, retrieved from www.nccn.org; American
Society of Clinical Oncology Practice Guidelines, retrieved from http://www.asco.org;
Oncology Nursing Society Practice Guidelines and Resources, retrieved from
www.ons.org/ClinicalResources/

Cancer patients may require intensive care for several reasons: (1)
overwhelming infection and sepsis; (2) structural complications of
cancer or cancer treatment; or (3) metabolic complications of cancer
or cancer treatment. Intensivists sometimes refuse admission to
cancer patients needing critical care, which may result in denial of
effective care for some deserving patients. A cancer patient may
need admission to an intensive care unit for a variety of reasons.
The outcomes of patients with hematologic malignancies,
previously dismal, have improved over the last 10 years. The
previously known indicators of poor outcome are no longer valid in
view of recent advances in intensive care. A select group of patients
with hematologic malignancies may be offered aggressive therapy
for a limited duration and then prognosis can be reassessed. Cancer
chemotherapy can produce toxicities affecting all major organ
systems. Such patients may be admitted with acute organ
dysfunction or years afterward for incidental illnesses. Knowledge
of these toxicities is essential for early diagnosis, management, and
prognostication in such patients. The postsurgical cancer patient
has unique problems; care can range from monitoring alone after
major surgery to fully aggressive intensive care for postsurgical
anastomotic dehiscence, mediastinitis, septic shock, and multiorgan
dysfunction. The metabolic and mechanical complications
commonly seen in nonsurgical cancer patients are also reasons for
admission. Intensive care should be offered to all patients who have
a reasonable chance of cure or supportive care of their disease. The
intensivist must be able to recognize the potentially reversible
critical illnesses among the various groups of cancer patients and

2046
discourage admission to terminally ill cancer patients. He or she
must also be aware that alleviation of suffering in the last hours of
life for a terminal cancer patient is one of the functions of an ICU,
once a decision to discontinue aggressive therapy has been made, if
there isn’t time for transfer to a hospice.

Neutropenic sepsis
Pathophysiology
Neutropenia is defined as an abnormally low level of neutrophils in
the blood. The normal level of neutrophils in human blood varies
slightly by age and race. Infants have lower counts than older
children and adults, and African Americans have lower counts than
whites or Asians. The average adult level is 1500 cells/mm3 of
blood. Neutrophil counts (in cells/mm3) are interpreted as follows:

• Greater than 1000: Normal protection against infection.

• 500 to 1000: Some increased risk of infection.

• 200 to 500: Great risk of severe infection.

• Lower than 200: Risk of overwhelming infection; requires hospital

treatment with antibiotics.

Untreated bacteremia in patients with neutropenia is fatal: septic

shock is associated with a 50% to 70% mortality rate. Mortality is
associated with causative organism, site of infection, and level and
duration of neutropenia. The faster the rate of neutrophil count
decline and the longer the duration of neutropenia, especially if it
lasts longer than 10 days, the greater the risk of infection. Infections
in neutropenic patients typically take 2 to 7 days to respond to
antimicrobial therapy. Fever (or any inflammatory response related
to white cells or cytokines) may not be present in some infected
neutropenic patients who are dehydrated or taking steroids or
NSAIDs, and the possibility of infection must be considered in any
neutropenic patient who is unwell.

2047
Asssessment: Neutropenic sepsis
History and risk factors
Granulocytopenia, immunosuppression, recent cancer treatment,
diabetes, organ-related disease, age older than 65 years, indwelling
catheters, long hospital stays, loss of skin or mucosal integrity,
malnutrition, hypothermia, intubation/mechanical ventilation,
aspiration, alcoholism, renal failure, hepatic failure, chronic illness.
The risk of death is twice as great for sepsis patients with cancer as
for those without and is comparable to the risk observed in sepsis
patients who are HIV positive.

The four stages of sepsis

The progression of sepsis is subtle, rapid, and often deadly. It is
usually broken down into four stages.

Stage 1
Systemic inflammatory response syndrome (SIRS) describes a
systemic inflammation without a defined source of infection
resulting from any major insult to the body, such as trauma, burns,
or myocardial infarction, in which two or more of the following are
present:

• HR at least 90 bpm.

• Body temperature less than 36°C (96.8°F) or greater than 38° C

(100.4° F).

• Tachypnea greater than 20 breaths/min or, on blood gas, a Paco2

less than 32 mm Hg.

• WBC less than 4000 cells/mm3 or greater than 12,000 cells/mm3 or

the presence of greater than 10% immature neutrophils.

Patients with SIRS can be routinely cared for on the medical-

surgical floor but should be closely monitored for signs and
symptoms of sepsis.

2048
Stage 2
Sepsis is identified by the presence of two of the SIRS criteria in
response to pathogenic microorganisms and associated endotoxins
in the blood. However, in many cases of sepsis, the actual cause of
infection is never identified. The delay in waiting for confirmation
of infection can slow the treatment of sepsis; the most effective
course of action once SIRS is identified and infection is suspected is
to treat the infection and monitor the patient for signs and
symptoms of organ failure, which will indicate that the condition
has progressed to severe sepsis.

Stage 3
Severe sepsis occurs when a patient who meets the sepsis criteria
shows one of the signs and symptoms of organ failure. Once severe
sepsis is suspected, the patient requires aggressive treatment in a
critical care area.

Stage 4
Septic shock is defined as severe sepsis plus hypotension (a systolic
BP less than 90 mm Hg) that does not respond to fluid resuscitation.
Septic shock is associated with a high mortality rate. The patient’s
chances of recovery are significantly reduced if, by this stage of
sepsis, she or he has not already been transferred to the ICU.

Observation: Rapid progression if untreated

Signs and symptoms of infection may be absent because of
decreased WBCs.

• General: Fever, hypothermia, chills, pain.

• Neurologic: Confusion, anxiety, restlessness, decreased level of

consciousness, coma.

• Pulmonary: Tachypnea, rales, rhonchi, wheezes, dry cough,

cyanosis, hypoxia, ARDS.

• Cardiovascular: Tachycardia, hypotension, fluctuating pulse

pressure, thready pulse.

2049
• Digestive: Nausea, vomiting, anorexia, decreased GI motility, GI
bleed.

• Renal: Decreased urine output, anuria, renal failure.

• Integument: Warm, flushed changing to damp, cool, clammy.

Diagnostic Tests for Neutropenic Sepsis

Test Purpose Abnormal Findings

Blood cultures (at baseline Check for bacteria Gram-positive cocci: coagulase-negative
and every 24 hours if signs or other staphylococci, Viridans streptococci, and
and symptoms of sepsis microorganisms in Staphylococcus aureus
persist) a blood sample. Gram-negative pathogens: Escherichia coli,
Klebsiella spp., and Pseudomonas aeruginosa.
Fungal: Candida spp., Aspergillus spp.
Viral: herpes simplex, respiratory syncytial
virus
Cultures (throat, stool, Determine source As above
urine, CV catheter, other of infection.
sites of exudates) before
antibiotics to determine
pathogen
Chest radiographic Evaluates lung Pulmonary infiltrates, pulmonary edema
examination status.
Complete blood count Evaluates Increased WBC with infection, decreased
composition and WBC with sepsis, chemotherapy, radiation,
concentration of leukemias
cellular
components of
blood.
Chemistries: electrolytes, Evaluate blood Increased BUN, creatinine reveal
liver function tests chemistries and dehydration. Increase to decrease in glucose
liver function. caused by shock. Increased transaminase,
bilirubin, and serum lactate in sepsis caused
by shock
Coagulation profile Examines the Prolonged PT, PTT
factors most often
associated with a
bleeding problem.
Pulse oximetry, ABGs Measures Respiratory alkalosis followed by metabolic
oxygenation, acid- acidosis
base balance.
Electrocardiogram Records the Tachycardia, arrhythmias
electrical activity
of the heart.

Collaborative management
Fever (even low grade) is often the only reliable sign of infection in

2050
the neutropenic patient. No specific patterns of fever or clinical
features can positively distinguish between fever because of
infection and one of noninfectious cause. Therefore, all febrile
neutropenic patients should be considered for the administration of
empirical broad-spectrum antibiotics within 1 hour of presentation.
Many patients are outpatients during their cancer treatments, and it
is vital to their survival that they and their significant others be
educated about early recognition (and timing during treatment) of
neutropenia to minimize the risk of sepsis. All healthcare providers
should be educated about this potential life-threatening situation
and be aware of strategies to minimize risk to patients by
systematically and regularly evaluating response to treatment and
progress toward desired outcomes.
Because sepsis-related mortality is unacceptably high, the Society
of Critical Care Medicine (SCCM) set a quality improvement goal to
reduce mortality caused by severe sepsis and septic shock by 25%.
Clearer definitions of sepsis, severe sepsis, and septic shock will
help in achieving this goal, as will recently updated evidence-based
management guidelines for severe sepsis and septic shock. To be
effective, these definitions and guidelines need to be applied to the
early identification and aggressive treatment of patients who have
severe sepsis or septic shock. Early goal-directed therapy to achieve
hemodynamic stabilization has been demonstrated to decrease
mortality in patients who have septic shock. See SIRS, Sepsis, and
MODS, Chapter 11.

Care priorities

1. Manage hypovolemia
Once severe sepsis or septic shock has been identified, the highest
management priorities are to establish vascular access and initiate
fluid resuscitation to improve tissue perfusion. Failure to manage
global hypoxia can lead to MODS. Fluid resuscitation guidelines are
defined by the SCCM and are a part of early goal-directed therapy
(see Sepsis, SIRS, and MODS, Chapter 11).

2. Restore tissue oxygenation

Measurements commonly used are SVO2 ScVO2, and lactate. Low

2051
values indicate several possible causes of poor oxygenation,
including inadequate oxygen delivery, high oxygen demand, or
inability of tissues to extract oxygen from hemoglobin (see Sepsis,
SIRS, and MODS, Chapter 11).

3. Identify and manage the underlying infection

Selection of an appropriate antimicrobial agent, often in the absence
of microbiologic confirmation, requires consideration of patient-
related characteristics such as drug intolerances, recently used
antibiotics, previous infections, underlying disease, and clinical
syndrome. Awareness of the prevalence of infections caused by
specific organisms can provide clinicians with insight into
appropriate empiric antimicrobial therapy. Pathogen resistance
patterns in the hospital and community, along with hospital
protocols to limit antibiotic resistance, should also be considered.

Care plans for neutropenia

Ineffective protection: Potential for life-threatening
infections 
related to reduced numbers and activity of WBCs.
Goals/Outcomes: No fever, no clinical signs or symptoms of
sepsis, no growth in blood, excrement, or skin surface cultures
Immune Status

Infection control

1. Assess for signs and symptoms of infection, sepsis, septic shock.

• Monitor temperature every 2 to 4 hours.

• Monitor vital signs frequently for signs of

impending shock: increased HR and RR, increased
restlessness and anxiety, and cool and clammy skin,
followed by a decrease in BP.

2052
• Monitor WBC and differential for evidence of
infection and response to interventions.

• Auscultate breath sounds for adventitious sounds

or diminished breath sounds.

• Observe all dressing sites daily for signs and

symptoms of infection.

• Observe all orifices daily for evidence of localized

infection.

• Assess areas of localized pain for erythema,

swelling, exudate, or rebound tenderness.
2. Control environmental risks of infection.

• Strict handwashing.

• Universal precautions.

• Do not assign neutropenic patients with those

known to be infected.

• Monitor visitors for recent history of communicable

disease and institute precautions as needed.

• Clean all multipurpose equipment between patient

use.

• Live flowers cannot be kept in standing water.

3. Implement patient care routines to minimize infection.

2053
• Assist with daily bathing, oral, and perineal
hygiene; change linens daily.

• Ensure sleep and nutritional needs are met to

promote immune system recovery.

• Sterile technique for insertion and care of IV

catheters.

• Encourage incentive spirometry or deep breathing

and coughing.

• Encourage ambulation if patient is able or turn

every 2 to 4 hours to minimize skin breakdown or
atelectasis.

Cardiac Care: Acute; Circulatory Care: Arterial Insufficiency;

Respiratory Monitoring; Shock Management: Cardiac; Cerebral
Perfusion Promotion; Neurologic Monitoring; Fluid/Electrolyte
Management; Vital Signs Monitoring

Decreased cardiac output 

related to infection or sepsis-induced myocardial infarction
Goals/Outcomes: The patient will have normal BP and will
exhibit signs of adequate tissue perfusion as evidenced by adequate
urinary output and normal mental status.
Circulation Status

Hypovolemia management

1. Monitor I&O hourly. Consult physician for a urinary output less

than 0.5 mL/kg/h for 4 consecutive hours. Insert urinary catheter if
appropriate.

2054
2. Monitor and document HR, rhythm, pulses, and BP.

3. Evaluate efficacy of volume expansion by closely comparing

CVP, PAWP, and CO. Overzealous volume expansion can lead to
heart failure and pulmonary edema.

4. Administer diuretics as prescribed in the well-hydrated patient

with urine output less than 0.5 mL/kg/h.

5. Assess the patient for volume depletion, including poor skin

turgor; dry mucous membranes; hypotension; tachycardia; and
decreasing urine output, CVP, and CO.

6. Monitor electrolytes and serum osmolality. A universal increase

in electrolytes and osmolality is indicative of dehydration. A
universal decrease signals fluid overload.

7. Assess pH (normal range is 7.35 to 7.45) before replacing

electrolytes. Acidosis and alkalosis alter electrolyte values. Replace
potassium if the pH is outside the normal range.

Electrolyte Monitoring; Fluid Management; Fluid

Monitoring; Intravenous (IV) Therapy; Hypervolemia Management;
Shock Management: Volume

Acute pain 
related to fever, chills, headaches, myalgias, and arthralgias associated
with neutropenia and infection.
Goals/Outcomes: The patient will not experience chills and will
be able to perform activities of daily living without discomfort;
temperature will stay below 38° C (100.4° F).
Comfort Level

Pain management

1. Administer acetaminophen as ordered for fever or mild

discomfort.

2. Encourage restful environment.

2055
3. Apply warmth to muscles or joints or cool compress to head as
needed.

4. Administer meperidine 12.5 to 25 mg IV or other opiate or

benzodiazepine as ordered for chills.

5. Monitor temperature 30 minutes after chill subsides.

6. Bathe the patient and change linens after fever subsides.

7. Monitor platelet count as it may decrease with hypermetabolism

of hyperthermia.

8. Monitor and document HR, rhythm, pulses, and BP.

Analgesic Administration; Medication Administration;

Medication Administration: Intravenous (IV); Heat/Cold
Application; Anxiety Reduction; Therapeutic Touch; Music
Therapy; Meditation Facilitation

Additional nursing diagnoses

Refer to nursing diagnoses in Emotional and Spiritual Support of
the Patient and Significant Others (Chapter 2). For patients who
manifest activity intolerance, see that nursing diagnosis in
Prolonged Immobility (Chapter 1). For patients with sepsis or septic
shock, see Sepsis, SIRS, and MODS (Chapter 11).

Superior vena cava syndrome

Pathophysiology
The superior vena cava (SVC) is a low-pressure vessel between two
immovable bone structures: clavicle and scapula. When mediastinal
structures become edematous or mass-occupying lesions are
introduced, there is insufficient room and the soft-walled SVC
becomes occluded and surrounding lymph nodes become enlarged.
SVCS is a disorder defined by internal or external obstruction of the
SVC leading to reduced blood return to the right side of the heart.
Venous congestion and low CO result.

2056
 Complications include laryngeal edema, cerebral edema,
decreased CO with hypotension, and pulmonary embolism (when
an associated thrombus is present). Potential issues include:

• Failure to establish the correct diagnosis and the underlying

etiology.

• Failure to initiate immediate treatment.

• Failure to recognize a thrombus in the SVC.

• Failure to consult a medical oncologist and radiation therapist.

• Failure to expeditiously diagnose and appropriately manage

heparin-related complications.

Assessment
Goal of assessment
Minimize life-threatening complications of cancer and its treatment
through early recognition and effective management.

History and risk factors

Malignancy
Primary intrathoracic malignancies are the cause of SVCS in
approximately 87% to 97% of cases. The most frequent malignancy
associated with the syndrome is lung cancer, followed by
lymphomas and solid tumors that metastasize to the mediastinum.
SVCS develops in approximately 3% to 15% of patients with
bronchogenic carcinoma, and it is 4 times more likely to occur in
patients with right- rather than left-sided lesions. Breast and
testicular cancers are the most common metastatic malignancies
causing SVCS, accounting for more than 7% of cases. Metastatic
disease to the thorax is responsible for SVCS in about 3% to 20% of
patients.

Nonmalignant causes

2057
The most common nonmalignant cause of SVCS in cancer patients
is thrombosis secondary to venous access devices. Other
nonmalignant causes include cystic hygroma, substernal thyroid
goiter, benign teratoma, dermoid cyst, thymoma, tuberculosis,
histoplasmosis, actinomycosis, syphilis, pyogenic infections,
radiation therapy, silicosis, and sarcoidosis. Some cases are
idiopathic.

Observation

Classic symptoms
Patients with SVCS most often present with complaints of facial
edema or erythema, dyspnea, cough, orthopnea, or arm and neck
edema. These classic symptoms are seen most commonly in
patients with complete obstruction, as opposed to those with mildly
obstructive disease.

Other associated symptoms

Other associated symptoms may include hoarseness, dysphagia,
headaches, dizziness, syncope, lethargy, and chest pain. The
symptoms may be worsened by positional changes, particularly
bending forward, stooping, or lying down.

Common physical findings

The most common physical findings include edema of the face,
neck, or arms; dilatation of the veins of the upper body; and
plethora or cyanosis of the face. Periorbital edema may be
prominent.

Other physical findings

Other physical findings include laryngeal or glossal edema, mental
status changes, and pleural effusion (more commonly on the right
side).

Diagnostic Tests for Superior Vena Cava Syndrome

Test Purpose Abnormal Findings

Chest Evaluates lung status at Identify hilar, mediastinal masses, right middle

2058
radiograph baseline and every 24 hours lobe congestion, masses, or nodes between clavicle
(CXR) if signs and symptoms of and scapula.
sepsis persist.

Spiral chest Further evaluates lung status Precisely identify location and size of masses
CT scan to help clarify findings from around SVC, clarify growth versus compression.
with CXR.
contrast
Magnetic Provides further data Precisely identifies location and size of masses
resonance regarding the area of the around SVC.
imaging of superior vena cava.
the chest
Doppler Noninvasively assesses the Presence of thrombus or ineffective thrombolysis
ultrasound entire vascular tree to when therapies are rendered.
of the identify thrombosis or
vasculature effects of thrombolysis.
Contrast Invasively assesses the entire Presence of thrombus or ineffective thrombolysis
and vascular tree to identify when therapies are rendered.
radionuclide thrombolysis; may be used
venography to validate Doppler
ultrasound findings.
Complete Evaluates the composition Declining platelet count may signal the presence of
blood count: and concentration of the heparin-induced thrombocytopenia or “white clot
platelet cellular components of syndrome.” If unmanaged, may lead to extremity
count blood, particularly platelets. gangrene and life-threatening venous
thromboembolism.

Collaborative management
Care priorities

1. Provide anticoagulation and thrombolysis

Anticoagulation for SVCS has become increasingly important
because of thrombosis related to intravascular devices. In certain
situations, the device remains in place. Both streptokinase and
urokinase have been used for thrombolysis, although urokinase has
been more effective in lysing clots in this setting. Urokinase is given
as a 4400 U/kg bolus followed by 4400 U/kg/h; whereas
streptokinase is administered as a 250,000 U bolus followed by
100,000 U/h. The use of thrombolytic therapy is controversial for
catheter-related thrombosis.

2. Monitor for heparin-induced thrombocytopenia

In particular, one must monitor platelet count and be vigilant
should a rapid decline in platelets occur. This suggests the

2059
possibility of platelet-induced thrombocytopenia syndrome (white
clot syndrome). This rare syndrome may lead to extremity
gangrene and life-threatening venous thromboembolism.
Management requires urgent discontinuation of heparin and urgent
evaluation by a hematologist for appropriate pharmacotherapy.
Vascular surgical evaluation may also be indicated.

3. Provide surgical intervention/stenting

Placement of an expandable wire stent across the stenotic portion of
the vena cava is an appropriate therapy for supportive care of SVCS
symptoms when other therapeutic modalities cannot be used or are
ineffective. Use of stents is limited when intraluminal thrombosis is
present.

4. Provide radiotherapy and/or chemotherapy

Both radiotherapy and chemotherapy are treatment options for
SVCS, depending on the tumor type. The specific drugs and doses
used are those active against the underlying malignancy. Radiation
therapy is the standard treatment of non–small-cell lung cancer
with SVCS. Recent studies suggest that chemotherapy may be as
effective as radiotherapy in rapidly shrinking small-cell lung cancer
(SCLC). Combination chemoradiation therapy may result in
improved ultimate local control over chemotherapy alone in SCLC
and non-Hodgkin lymphoma. Retrospective reviews of patients
with SCLC have reported equivalent survival in patients with or
without SVCS treated definitively with chemoradiation therapy.

Life-threatening symptoms, such as respiratory distress, are

indications for urgent radiotherapy. A preliminary determination
of the treatment goal (potentially curative or supportive only) is
necessary before initiation of treatment, even in the emergent
setting.

5. Provide additional interventions to assist with

2060
maintaining patency of the superior vena cava
Balloon angioplasty is rare but may be considered in patients with
SVCS, significant clinical symptoms, and critical SVC obstruction
demonstrated by angiography.

Care plans for superior vena cava syndrome

Decreased cardiac output 
related to reduced venous blood return to the heart.
Goals/Outcomes: The patient will show evidence of normal
tissue perfusion and will not experience upper extremity edema.
Circulatory Status; Tissue Perfusion: Cardiac; Tissue
Perfusion: Peripheral; Tissue Perfusion: Pulmonary

Circulatory care: Venous insufficiency

1. Monitor I&O hourly. Consult advanced practice provider if

urinary output is less than 0.5 mL/kg/h for 4 consecutive hours.
Insert urinary catheter if appropriate.

2. Monitor and document HR, rhythm, pulses, and BP.

3. Evaluate efficacy of volume expansion by monitoring CVP and

CO. Overzealous volume expansion can lead to heart failure and
pulmonary edema, with CVP greater than 20% of normal values
and CO less than 5 L/min.

4. Administer diuretics as prescribed in the well-hydrated patient

with urine output less than 0.5 mL/kg/h.

5. Assess the patient for volume depletion, including poor skin

turgor, dry mucous membranes, hypotension, tachycardia, CVP
less than 2 mm Hg, and decreasing urine output.

6. Monitor electrolytes and serum osmolality. A universal increase

in electrolytes and osmolality is indicative of dehydration. A
universal decrease signals fluid overload.

7. Assess skin and mucous membranes for cyanosis and pallor and

2061
skin temperature for signs of change in perfusion.

8. Assist in care of patients receiving therapy to treat SVCS.

Electrolyte Monitoring; Fluid Management; Fluid

Monitoring; Intravenous (IV) Therapy; Hypervolemia Management;
Shock Management: Volume

Impaired gas exchange (or risk for same) 

related to decreased blood flow to the lungs.
Goals/Outcomes: The patient’s gas exchange is adequate as
evidenced by PaO2 at least 90 mm Hg, Paco2 35 to 45 mm Hg, pH
7.35 to 7.45, RR 12 to 20 breaths/min with normal depth and
pattern, oxygen saturation at least 95%, HR 60 to 100 bpm, and
orientation to time, place, and person.
Respiratory Status: Gas Exchange; Vital Signs Monitoring

Respiratory monitoring

1. Assess respiratory status every 2 hours, noting rate, rhythm,

depth, and regularity of respirations.

2. Monitor for signs of respiratory failure: restlessness, anxiety, and

air hunger indicative of hypoxemia; ABG values for increased Paco2
and decreased pH indicative of hypoventilation; or oxygen
saturation less than 90% via pulse oximetry indicative of decreased
ventilation. Consult advanced practice provider if signs of
respiratory insufficiency are present.

3. Monitor SVO2: steady increase or decrease from patient’s normal

level may indicate deterioration.

4. Assess lungs for bibasilar crackles (rales), indicative of

pulmonary edema.

5. Monitor patient’s respiratory secretions. Institute respiratory

therapy treatments as needed.

6. Monitor for pulmonary embolus, including sharp, stabbing chest

2062
pain, dyspnea, pallor, cyanosis, pupillary dilation, rapid or
irregular pulse, profuse diaphoresis, and anxiety. Assess need for
supplemental oxygen, and consult advanced practice provider
immediately. Patients with severe pulmonary emboli may require
mechanical ventilation. See Pulmonary Embolus, Chapter 4.

7. Assess the patient for changes in sensorium (i.e., confusion,

lethargy, somnolence), indicative of inadequate cerebral
oxygenation or CO2 retention (respiratory insufficiency).

Airway Management; Oxygen Therapy; Acid-Base

Monitoring

Tumor lysis syndrome

Pathophysiology
Tumor lysis syndrome (TLS) is most commonly seen in individuals
with rapidly growing tumors that are acutely responsive to
chemotherapy because of the rapid release of intracellular contents
into the bloodstream, leading to life-threatening concentrations of
intracellular electrolytes. If the resulting metabolic
abnormalities remain uncorrected, patients may develop acute
renal failure and sudden death resulting from a lethal dysrhythmia
secondary to hyperkalemia.
The syndrome is caused by rapid lysis of malignant cells
resulting in hyperuricemia, hyperkalemia, hyperphosphatemia,
hypocalcemia, and an increase in BUN. These abnormalities can
occur as early as 6 hours following chemotherapy and in the last 5
to 7 days after treatment. The hyperuricemia is caused by the
massive release of intracellular nucleic acids and their metabolism
by xanthine oxidase into uric acid. Urate crystals can form in the
renal collecting ducts and result in acute renal failure. Similarly,
potassium and phosphate are released from the tumor cells, and
their excretion is hampered by the hyperuricemia. The best
approach to management is to prevent its occurrence by proper
hydration. Patients with the diagnosis of rapidly growing
lymphoma, uric acid levels of greater than 10 mg/dL, a high blast
count in leukemia and a high lactate dehydrogenase level before

2063
treatment are at greatest risk of developing TLS.
TLS is also seen in small-cell lung cancer and metastatic breast
cancer. Because of clinicians’ increased awareness of TLS during the
past decade and the use of adequate prophylaxis before initiation of
chemotherapy, the number of cases has decreased. Occasionally,
TLS occurs following treatment with radiation, glucocorticoids,
tamoxifen, or interferon.

Assessment
History and risk factors
The typical patient at risk for TLS tends to be young (under 25 years
of age) and male with an advanced, highly proliferative, high-grade
disease (lymphoma, leukemia, etc.), and a markedly elevated lactate
dehydrogenase level. Abdominal disease is often present.
Comorbid conditions include renal insufficiency and diabetes.
Volume depletion, concentrated acidic urine pH, and excessive
urinary uric acid excretion rates may also increase the risk.
TLS most commonly develops during the rapid growth phase of
high-grade lymphomas and leukemia in patients with high
leukocyte counts; it is less common in patients with solid tumors.
The syndrome is often iatrogenic, caused by cytotoxic
chemotherapy.

Observation
Signs and symptoms reflect electrolyte imbalance, coupled with
those of acute renal failure. The syndrome is characterized by
hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia,
and oliguric renal failure (see Fluid and Electrolyte Disturbances,
Chapter 1, and Acute Renal Failure, Chapter 6). The diagnosis of
TLS is based on the development of increased levels of serum uric
acid, phosphorus, and potassium; decreased levels of serum
calcium; and renal dysfunction following chemotherapy.

Collaborative care
Care priorities

2064
1. Identify patients at risk and initiate prophylactic
measures
Patients at risk for TLS should be identified before the initiation of
chemotherapy and should be adequately hydrated and given
agents to alkalinize the urine. Treatment with allopurinol (IV or
PO) may be instituted to minimize hyperuricemia. The
recommended dosage of IV allopurinol ranges from 200 to 400
mg/m2/day. This regimen should be started 24 to 48 hours before
initiation of cytotoxic treatment. The dose may be equally divided
into 6-, 8-, or 12-hour increments, but the final concentration should
not exceed 6 mg/mL.

2. Monitor electrolytes
Serum electrolytes, uric acid, phosphorus, calcium, and creatinine
levels should be checked repeatedly for 3 to 4 days after
chemotherapy is initiated, with the frequency of monitoring
dependent on the patient’s clinical condition and risk profile.

3. Provide aggressive, immediate treatment of electrolyte

imbalances and acute renal failure
Once tumor lysis is established, treatment is directed at vigorous
correction of electrolyte abnormalities, hydration, and hemodialysis
(see Fluid and Electrolyte Disturbances, Chapter 1 and Acute Renal
Failure, Chapter 6).

Care plans for tumor lysis syndrome

Fluid volume excess 
related to acute renal failure resulting from hyperuricemia with formation
of uric acid crystals lodging in the kidneys.
Goals/Outcomes: Patient’s volume status returns to
normal/baseline as evidenced by urinary output at least 0.5
mL/kg/h, stable weight, BP within patient’s normal range, HR 60 to
100 bpm, RR 12 to 20 breaths/min, good skin turgor, moist mucous
membranes, urine specific gravity 1.005 to 1.025, and CVP 2 to 6
mm Hg. Serum potassium, phosphorus, calcium, uric acid, BUN,

2065
and creatinine levels will be within normal limits.
Electrolyte and Acid-Base Balance

Fluid/electrolyte management

1. Monitor I&O hourly. Consult advanced practice provider if

urinary output is less than 0.5 mL/kg/h for 4 consecutive hours.
Insert urinary catheter if appropriate.

2. Monitor electrolytes every 6 to 12 hours during high-risk period.

3. Monitor and document HR, rhythm, pulses, and BP.

4. Administer IV fluids before and after cancer treatment.

5. Administer allopurinol as prescribed to manage hyperuricemia.

6. Administer aluminum hydroxide as prescribed to manage

hyperphosphatemia.

7. Administer cation-exchange resins as prescribed to manage

hyperkalemia.

8. Assist with renal replacement therapies.

9. Administer diuretics as prescribed in the well-hydrated patient

with urine output less than 0.5 mL/kg/h.

10. Monitor electrolytes and serum osmolality. A universal increase

in electrolytes and osmolality is indicative of dehydration. A
universal decrease signals fluid overload.

11. Assess pH (normal range is 7.35 to 7.45) before replacing

electrolytes. Acidosis and alkalosis alter electrolyte values. Replace
potassium if the pH is outside the normal range.

12. Teach patients to restrict foods high in potassium and

phosphorus and to increase fluid intake.

Electrolyte Monitoring; Fluid Management; Fluid

Monitoring; Intravenous (IV) Therapy; Hypervolemia Management;

2066
Shock Management: Volume

Additional nursing diagnoses

Refer to nursing diagnoses in Emotional and Spiritual Support of
the Patient and Significant Others (Chapter 2). For patients who
manifest activity intolerance, see that nursing diagnosis in
Prolonged Immobility (Chapter 1).

Organ transplantation
Solid organ transplantation remains a viable option for end-stage
organ failure. As of May 2014, there were nearly 122,900 people on
the United Network for Organ Sharing (UNOS) organ transplant
waiting list. The major constraint to meeting the demand for
transplants is the availability of donated (cadaver) organs. Dialysis
remains the main lifeline for kidney disease and mechanical devices
for heart failure are becoming increasingly available throughout the
United States. A small number of patients are living at home on
mechanical ventilation. In general, those with end stage liver end-
stage, pancreatic, and lung disease remain dependent on organ
transplantation to sustain life.
Several steps have been taken to alleviate the organ shortage.
National laws mandate that families of every appropriate potential
donor be offered the option to donate organs and tissues. In
addition, the ongoing efforts of the National Organ Donation
Collaborative and laws requiring all deaths to be reported to organ
procurement agencies have prompted an increase in organ
donations. Ongoing efforts of organ recovery coordinators and
others to improve public awareness of organ donation will help
reduce the shortage, as will use of extended donors.
Nationally, major improvements are being made to optimize
organ distribution, improve procurement, and ensure good
matches. Inclusion criteria for the waiting list are being
standardized using listing criteria for all degrees of sickness (see
Box 11-4 for allocation of cardiac organs). UNOS maintains a
computerized registry of all patients awaiting organs for
transplantations. Organs procured within a region are shared first

2067
within that region. If a recipient cannot be found there, UNOS
directs the organ to the recipient in another region with the greatest
need. Organ recovery coordinators are available 24 hours a day, 7
days a week to arrange serologic testing and organ removal from
donors, preserve organs pretransplant, and distribute organs to
appropriate recipients.

Assessment and diagnostic testing

General evaluation for transplantation
All solid organ recipients require multiple tests to evaluate
readiness and appropriateness for transplantation. Health status,
including comorbidities, pretransplantation disease processes, and
donor matching are evaluated as follows:

Labwork
• General laboratory assessment profiles including biochemical,
hematologic, lipid, hepatic, renal, and thyroid studies, and
urinalysis. If findings indicate several organs are impaired, the
patient may be inappropriate for transplant, since
immunosuppressive drugs can cause renal failure, those with
heart disease may have a myocardial infarction in the
postoperative period, those with lung disease may be unable to
wean from mechanical ventilation, and those with liver disease
may be immunocompromised and at higher risk for sepsis and
metabolic complications.

• ABO blood typing: Requires duplicate testing for accuracy and

safety. Testing includes panel reactive antibody (PRA) and
human leukocyte antigen (HLA) testing.

• Virology screening: HIV, hepatitis B and C, herpes,

cytomegalovirus (CMV), Epstein-Barr virus (EBV).

• Other infectious diseases: Syphilis, toxoplasmosis, tuberculosis,

resistant bacterial infections including Burkholderia cepacia.

2068
• Cancer screening: May include pap smears, prostate examination,
prostate-specific antigen, mammogram, colonoscopy, and chest
radiography

Diagnostic testing
• Pulmonary evaluation: Oxygenation assessment using pulmonary
function testing and chest radiograph.

• Cardiovascular evaluation: Exercise stress test and Doppler

imaging for patients with a history of diabetes, coronary artery
disease, claudication, cerebrovascular accident.

• Nutritional evaluation: Body mass index (BMI) less than 16

(cachexia) and BMI greater than 30 are associated with poorer
outcomes.

2069
• Osteoporosis screening: Osteoporosis may place a patient at
higher risk for complications following transplantation, as
maintenance medication may increase the severity, which
increases the probability of bone fractures.

• Dental examination: Poor oral hygiene may be a source of

infection.

• Ultrasound of gallbladder: Presence of gallstones increases the

probability of need for cholecystectomy following
transplantation.

• Psychosocial evaluation: The patient must be ready to comply

with and have an adequate support system to participate in
posttransplant medical care and life maintenance activities,
including medication management, diet, exercise, and abstinence
from substance use and abuse.

• Financial evaluation: The financial burden associated with organ

transplantation is significant. The patient must have appropriate
resources in place to cover the costs.

Organ-specific evaluation
• Cardiac: Cardiac catheterization (right and left heart),
cardiopulmonary exercise testing, cardiac magnetic resonance
imaging or positron emission tomography scan, and MVo2
testing.

• Lung: Computed tomography scan to define the anatomy,

ventilation-perfusion scan, 6-minute walk test, ABG, continuous
pH testing, smoking cessation readiness, and ability to remain
“smoke free.”

• Liver: Alpha-fetoprotein, CA 19-9 tumor markers for

hepatocellular carcinoma and cholangiocarcinoma. Liver biopsy
may be performed to determine staging or presence of disease.
Abdominal imaging and GI testing assess portal vein system and

2070
 hepatic vasculature. A GI evaluation is done to assess for bowel
diseases.

• Alcohol consumption screening: To assess for usage

patterns and readiness to stop drinking alcohol. If
use persists in a person whose need for liver
transplant is directly related to alcohol, he or she is
unable to qualify for organ transplantation. A
complete battery of tests is performed to determine
the cause and acuity of liver failure.
• Kidney: Specific urine testing for preoperative baseline,
hypercoagulopathy screen, abdominal imaging for anatomic and
renal vessel assessment

• Pancreas: Complete testing referred to in the cardiac section, as

well as full assessment of diabetes status. Initial screening
includes a hemoglobin A1C test to assess for average blood
glucose level over the past 8 weeks.

Organ-specific criteria for transplantation

Cardiac
Table 11-9 summarizes the selection criteria that patients must meet
before they can be considered for cardiac transplantation. Box 11-4
reflects the various statuses of cardiac transplantation patients.

Table 11-9
SELECTION CRITERIA FOR CARDIAC TRANSPLANTATION

Inclusion Criteria Exclusion Criteria

• End-stage heart failure Relative
• Refractory and intolerable symptoms; • Active substance abuse
New York Heart Association classes III • Active infection associated with ventricular
and IV assist device
• Failure of maximal medical treatment • Psychological/social issues related to support
(e.g., digoxin, diuretics, vasodilators, ACE or finances
inhibitors, beta blockers) • Age >65 to 70 years

2071
 • 1-year survival expectancy <50% and poor • History of cancer in remission
short-term prognosis or poor functional • Absolute
capacity • Complicated IDDM with end-organ damage
• Age <60 to 65 years • Poor compliance
• Left ventricular ejection fraction 20% to • Severe obesity
35% • Pulmonary hypertension: PVR >6 Wood units
• Chronic, unstable angina • Comorbid diseases
• Peak O2 consumption 14 mL/kg/min • Active infection (until resolved) and infection
• Onset of atrial fibrillation with highly resistant organisms that are nearly
• Decreasing cardiac output impossible to eradicate
• Refractory ventricular dysrhythmias • Irreversible liver and kidney dysfunction
• Otherwise good health • Active peptic ulcer disease
• Coexisting cancer
• Symptomatic peripheral and cerebral vascular
disease
• Severe osteoporosis
• Amyloidosis
ACE: Angiotensin Converting Enzyme; BMI: Body Mass Index; IDDM: Insulin
Dependent Diabetes Mellitus; PVR: Pulmonary Vascular Resistance;

Box 11-4
ALLOCATION OF CARDIAC ORGANS
Status 1A
A patient is admitted to the transplant center and has at least one
of the following:

A. Mechanical circulatory support for acute hemodynamic

decompensation that includes at least one of the following:

• Left or right ventricular assist device implanted

within past 30 days

• Total artificial heart

• Intraaortic balloon pump

• Extracorporeal membrane oxygenator

B. Mechanical circulatory support for >30 days with significant
device-related complications such as thromboembolism, device
infection, mechanical failure, or life-threatening ventricular

2072
 arrhythmias

C. Mechanical ventilation

D. Continuous infusion of a high-dose inotrope or multiple

inotropes with hemodynamic monitoring

E. Patient does not meet the above criteria but has a life expectancy
without a heart transplant of less than 7 days.

Status 1B
A patient listed as status 1B has at least one of the following
devices or therapies in place:

A. Left and/or right ventricular assist device implanted for >30 days

B. Continuous infusion of inotropes

Status 2
A patient who does not meet the criteria for status 1A or 1B is
listed as a status 2.
Status 7
A patient listed as status 7 is considered temporarily unsuitable to
receive a thoracic organ transplant.
From the United Network for Organ Sharing (UNOS) for allocation of thoracic organs. For
complete, detailed criteria, see actual policy at www.UNOS.org.

Lung
Lung transplant candidates generally have a life expectancy of less
than 18 months, are dependent on supplemental oxygen, have
severe exercise intolerance, are under 65 years of age, and report
poor quality of life.

Indications
In adults, irreversible, progressively disabling, end-stage
pulmonary disease encompassing a wide variety of etiologies. The
majority of lung transplants are performed for chronic obstructive

2073
pulmonary disease, followed by idiopathic pulmonary fibrosis,
pulmonary hypertension, and cystic fibrosis (CF). Four groupings
of lung diseases that may result in transplantation are:

1. Nonbronchiectatic: Obstructive lung conditions or changes in the

upper and lower airways NOT resulting from an infectious process,
including emphysema, chronic bronchitis, alpha1-antitrypsin
disease, and bronchiolitis obliterans syndrome (BOS), a disease
associated with chronic transplant rejection. BOS and chronic
bronchitis can evolve into bronchiectasis. Most recently, the BODE
index was introduced (BMI, Obstruction of airflow severity,
Dyspnea severity as measured by the modified Medical Research
Council dyspnea scale, Exercise capacity). Patients scoring greater
than 5 on the BODE index should be referred for transplant.

2. Bronchiectatic: Obstructive lung conditions resulting from

abnormal dilation and thickening of the walls in the bronchi and
bronchioles, which result from recurrent inflammation, leading to
mucus retention. Diseases include CF and severe chronic bronchitis,
which result in chronic bacterial pneumonia.

3. Interstitial: Restrictive lung disease resulting from chronic

inflammation of the lower airways, including idiopathic pulmonary
fibrosis, diseases related to occupational exposure to toxins
(asbestos, coal, or organic dust, crystalline silica), histiocytosis X,
and sarcoidosis. Patients who have been irradiated and/or have
undergone chemotherapy for a nonpulmonary condition and who
then develop lung disease are considered on an individual basis.
Not all centers accept patients with pulmonary fibrosis associated
with connective tissue disease.

4. Pulmonary vascular: Pulmonary hypertension resulting from

vascular disease that severely increases pulmonary vascular
resistance, which leads to right-sided heart failure and chronic
hypoxia. Pulmonary hypertension may be primary (idiopathic
pulmonary vascular disease) or secondary to a shunt associated
with heart disease, thromboembolism, connective tissue disease, or
parenchymal disease.

2074
Contraindications
Relative

• Advanced age: Historically, patients older than 65 years of

age have a higher mortality rate, but centers vary with candidate
acceptance. Generally, the age limit for heart-lung transplantation
is 50 years, for bilateral sequential lung transplantation is 60
years, and for single lung transplantation is 65 years.

• Ventilator dependence: A potential contraindication based on

length of time on the ventilator because of the potential of
developing complications that are absolute contraindications.
Patients requiring prolonged mechanical ventilation are at higher
risk of infection, development of MODS, muscle atrophy, and
other concerns surrounding deconditioning, which impacts
success of attaining a functional lifestyle following
transplantation.

• Corticosteroid therapy: Low dose is now acceptable, while high

dose may be viewed as an absolute contraindication.

• Infection: CF patients may be excluded if infected with the highly

resistant organism B. cepacia because of inability to eradicate the
organism with antibiotics; those with active tuberculosis are
generally not candidates, as well as CF patients with Aspergillus
fumigatus. Infection with nontuberculous Mycobacteria is not a
contraindication.

• Body weight: Patients with BMI less than 16 likely have a poor
nutritional status, which impairs healing. Those with BMI greater
than 30 are at higher risk of developing postoperative atelectasis
and pneumonia.

• Associated organ dysfunction: Patients with left ventricular

systolic or diastolic dysfunction may not be a candidate if disease
is severe, as are those with bilirubin of greater than 2 mg/dL and
those with connective tissue diseases.

Absolute

2075
• Malignancy within the past 2 years (except cutaneous squamous
and basal cell tumors).

• Noncurable, chronic, extrapulmonary infection (e.g., chronic

hepatitis B or C, HIV).

• Untreatable advanced organ dysfunction of another body system.

• Current cigarette smoking (must be smoke free for at least 6

months).

• Poor rehabilitation potential (based on evaluation of issues

mentioned in relative contraindications).

• Significant psychosocial problems, substance abuse, or history of

nonadherence to past medical therapies or disease management
programs.

Liver

Indications
Patients with chronic or acute liver disease who cannot sustain a
normal quality of life or have life-threatening complications are
probable candidates for liver transplant. Complications that
warrant liver transplantation generally include recurrent variceal
hemorrhage, intractable ascites, spontaneous bacterial peritonitis,
refractory encephalopathy, severe jaundice, and sudden
deterioration in status. Reduced-size, split, and living-related liver
transplantation continue to expand the number of donors, and yet
these efforts still fail to meet the demand for organs.

• Chronic end-stage liver disease: Hepatitis C, hepatitis B, alcoholic

cirrhosis, primary biliary cirrhosis, primary sclerosing
cholangitis, hepatocellular carcinoma, autoimmune hepatitis,
metabolic disease (e.g., Wilson disease, inborn errors of
metabolism), and other liver diseases.

• Fulminant hepatic failure (FHF): Severe impairment of hepatic

function in the absence of preexisting liver disease. Those who

2076
 are exposed to or ingest toxins or toxic doses of illicit drugs or
medications (e.g., acetaminophen toxicity) are included in this
group. Hepatotoxic drugs include acetaminophen (paracetamol),
salicylates (aspirin, Pepto-Bismol), methanol (wood alcohol),
isoniazid, IV tetracycline, chlorinated hydrocarbons, and sodium
valproate. The most commonly involved drug is acetaminophen,
and, in some locations, it is the most common cause of FHF.
Other diseases that may cause FHF include heart failure,
cardiomyopathy, sepsis, shock, cyanotic heart disease,
obstructive lesions of the aorta, vascular occlusions, myocarditis,
Hodgkin disease, and severe asphyxia.

Contraindications
Relative

• Chronic renal failure (may require a combined liver/kidney

transplant).

• Advanced cachexia.

• Large hepatocellular cancers/tumors: More advanced than stage

II, as described by the UNOS-modified American Joint
Committee on Cancer (AJCC) classification.

• Medication-resistant hepatitis B viral cirrhosis.

• Portal and mesenteric vein thrombosis.

• History of prior cancer not meeting full AJCC cure criteria.

• Active infections.

• MODS.

• Age: Physiologic age, rather than chronologic age, is used.

Absolute

• Spontaneous bacterial peritonitis (or other active infection).

2077
• Active alcohol or other substance abuse.

• Extrahepatic malignancy that does not meet “cure” criteria.

• Severely advanced cardiac or pulmonary disease.

• Extreme psych/social situations that prohibit adherence to

immunosuppressive therapies.

• Severe portopulmonary hypertension (moderate and mild

pulmonary hypertension are acceptable and sometimes included
in the indication criteria).

• Hepatocellular carcinoma lesion(s) greater than 5 cm or more

than 3 lesions present.

Kidney

Indications

• Chronic end-stage kidney disease.

• Dependency on dialysis or imminent dependence on dialysis.

• Provider and patient to consider transplantation before chronic

kidney disease progresses rather than waiting until the advanced
stage and an often lengthy wait for a donor.

Relative

• Contraindications are transplant site (facility) dependent.

Absolute

• Active or current malignancy.

• Goodpasture disease or systemic lupus erythematosus (can

damage the transplanted kidney).

• Active infection.

2078
• Obesity.

• Significant peripheral vascular disease.

• End-stage diseases of other organs.

• Active systemic vascular disease.

• Noncompliance.

• Active substance abuse.

• Untreated psychiatric illness or mental incapacity.

• Active peptic ulcer disease.

• Limited life expectancy.

Pancreas
Preexisting advanced renal disease is observed in significant
numbers of pancreas transplantation candidates. Many pancreas
transplantation candidates may benefit from a combined
pancreas/kidney transplant.

• Islet cell: A novel less invasive harvesting of pancreatic cells for

transplantation is in limited use. The islet cells are the islets of
Langerhans (alpha, beta, and delta). Islet cells are isolated from a
donor pancreas or from the patient’s own pancreas after the
pancreatectomy. The sample is specially processed and then
infused into the patient via the portal vein. A neovascularization
process takes place. The islet cells begin to produce insulin
shortly after transplantation.

Indications

• Type 1 diabetes with chronic poor metabolic control.

• Patients requiring a total pancreatectomy.

• Mean duration of diabetes 23 to 27 years.

2079
• C-reactive peptide less than 0.8 ng/mL.

• Frequent or severe metabolic complications, e.g.,

hypoglycemia/hyperglycemia and ketoacidosis.

• End-organ failure with numbness of extremities, lethargy, nausea,

dizziness, and blurred or poor vision.

Contraindications
Relative

• Evidence of significant secondary complications of type 1

diabetes, including peripheral neuropathy, retinopathy,
gastroparesis, nephropathy, and coronary artery disease, which
may impede the success of the transplant.

• Persons with type 2 diabetes are seldom evaluated.

Absolute

• Active cancer or history of cancer.

• Severe cardiac, vascular, or pulmonary insufficiency.

• Active/chronic hepatitis B.

• Severe psychiatric or substance abuse issues.

• Although HIV has historically been a contraindication for both

candidates and donors, the HIV Organ Procurement Equity Act
(HOPE Act) requires the US Department of Health and Human
Services to develop criteria for conducting research related to
HIV-positive donors donating to HIV-positive candidates.
Currently over 20 HIV-positive persons have received an HIV-
negative donor organ.

Organ donors
The mainstay of organ supply is the deceased donor or cadaveric
donation. Nationwide, approximately 30% to 40% of all deceased

2080
organ donors are trauma patients. Evaluation of the trauma patient
as a potential organ donor is critical to maximizing the availability
of deceased donor organs for transplantation. Regional transplant
centers vary in absolute and relative criteria for excluding potential
organ donors. Early criteria limited evaluation to ideal donors aged
10 to 50 years without comorbid conditions. In response to the
increasing demand for organs, restrictions have loosened
considerably and the donor pool has expanded. Organs are
now often procured from patients younger than 10 years and older
than 50 years of age. Factors such as hepatitis C or active bacterial
infection are no longer absolute contraindications. “Nonideal”
donors are often used for specific recipients.
There are relatively few absolute contraindications, and most
potential donors are reviewed on an individual or a case-by-case
basis. Additional absolute and relative contraindications are
assessed for donation of specific organs. Some organs must be
transplanted within a very short time following brain death, while
other organs can be preserved for much longer periods of time. The
following are types of organ donors:

Donation after brain death

The patient has sustained an irreversible brain injury causing
cessation of brain function, including the brain stem. The patient is
brain dead but is kept “alive” with respiratory and cardiac support
until organ recovery occurs. Brain death is diagnosed by an absence
of neurologic function, apnea, irreversibility, and physiologic
confirmatory tests.

Donation after cardiac death

Death is declared on the basis of cardiopulmonary criteria
(irreversible cessation of circulatory and respiratory function). The
patient may have sustained catastrophic brain injury that is not
anticipated to progress to brain death (stroke or trauma). If the
family members decide to remove the patient from the ventilator to
allow for natural death, they may be offered the opportunity for
organ donation. Natural death would need to occur within 1 hour
of removal from the ventilator. The organs are procured once the

2081
patient is pronounced dead. The donation should not hasten the
death, and the transplant procurement team enters the operating
room after the patient is pronounced dead and is not part of the
end-of-life care. All normal care, including palliative measures,
occurs until the patient is pronounced. Donation may also be
considered if there is an unplanned cardiac arrest.

Living donors
Living donors are considered for kidney and liver transplants. The
evaluation process is critical for living donors. Postoperative care
for the donor and donor family must also be clearly defined.
Considerations to be assessed include:

1. Risk/Benefit: Is there maximum benefit to the recipient and

minimum risk to the donor? It is important NOT to underestimate
the risk to the donor.

• What is the physical and psychosocial health of the

donor?
2. Freedom of Choice: Is the potential donor making the decision
without pressure or coercion from the recipient or others?

• The donor should be seen separately in the absence

of the prospective recipient.

• Informed consent is complete, neutral, and not

coerced.

• The donor does not overestimate the benefits of

donating.

• Do the healthcare providers understand donor

motivation?

2082
3. Understanding the Costs: Does the donor understand the
potential financial costs he or she will incur and the amount of time
that will be lost from work?

4. Well-Being: What is the overall state of the donor and family’s

emotional well-being?

• Are the donor and family prepared to cope with

feelings of anxiety and remorse associated with
postoperative pain, postoperative complications,
and postoperative depression?

• Are donors concerned about the recipient?

Paired and chain donations

Paired donation is an opportunity for a live donation when a direct
related donation is not possible. Transplant centers strategically
manage a group of potential recipients and potential live donors so
that a donor can give to an unrelated person, while the unrelated
person’s donor can give to their related person. A complex chain of
exchanges (“swaps”), if worked out, potentially benefits a larger
number of individuals.

Laboratory and diagnostic tests

• Laboratory and diagnostic testing varies from center to center, but
general standards are presented below.

General screening for organ donors

• Basic laboratory values (e.g., CBC, electrolytes, glucose, ABG).

• ABO blood typing.

2083
• HLA typing.

• Blood cultures.

• Sputum Gram stain, culture, and sensitivities.

• Urinalysis, culture, and sensitivities.

• HIV, EBV, CMV, human T-cell leukemia virus type 1, and

hepatitis B and C virus serologies.

• Venereal Disease Research Laboratory test or rapid plasma

reagent test.

• Inguinal lymph nodes tested for evaluation of recipient

sensitivity.

Heart donor
• ECG.

• Chest radiograph.

• Echocardiogram.

• Cardiac catheterization (male older than 40 years or female older

than 45 years, or younger if other cardiovascular risk factors
present).

• Creatine kinase (CK), CK-MB, and troponin levels.

Lung donor
• ABG on 100% Fio2; then, serial ABGs.

• Chest radiograph.

• Bronchoscopy.

Pancreas donor

2084
• Serial blood glucose determinations.

• Amylase and lipase levels.

Liver donor
• Liver function tests.

• Liver biopsy for patients with BMI greater than 32, age older
than 70 years (older than 60 years if diabetic), past medical
history suggestive of liver disease, significant history of alcohol
abuse, radiographic studies suggestive of fatty liver infiltration,
or positive hepatitis serology.

• PT/INR.

• aPTT.

Kidney donor
• Electrolytes.

• BUN.

• Creatinine.

Priority/waiting lists/medical urgency

determination
Heart
Demographics including age, ethnicity, gender, and location, with
ABO type, height, weight, diagnosis, and medical urgency, are
matched with the donor information (weight, age, distance to
transplant center, and need for prospective cross-match). Median
time to transplant has been gradually increasing since 2006-2007
when the wait time was at its lowest point for all medical urgency
categories. Median time to transplant is longest for status 2
candidates, at almost 20 months. Median time to transplant for

2085
status 1A and status 1B candidates was 2.4 months and 6.9 months,
respectively, in 2012. The median waiting time for status 1A
candidates has not changed appreciably during the last decade,
although it has increased for status 1B and status 2 candidates. The
median time to transplant among candidates with ventricular assist
devices (when listed) was 3 months in 2006-2007 and has since
increased to 8.7 months in 2012, the same as for candidates without
them.

Lungs
The Lung Allocation Score (LAS) is a numerical scale (0 to 100)
computed from a list of criteria and updated every 6 months.
People who are most likely to die before transplantation and have a
chance of greater survival after transplantation are the candidates
given the highest scores on the list. Along with the LAS, blood type,
age, and distance from the donor are used to determine priority for
the organ. Also under consideration is the bilirubin level and
changes in this level while on the waiting list. A current bilirubin of
at least 1.0 mg/dL or an increase by at least 50% during a 6-month
time period increases the candidate’s risk of dying while on the list.
Pediatric and adolescent patients have priority over adults. LAS
testing is updated every 6 months.
Since implementation of the LAS, transplant rates have increased
for all candidates and are most profound in candidates aged 65
years or older and those in diagnosis group D. Overall median
waiting time for candidates listed for lung transplant in 2012 was 4
months and 3.1 months for group D patients. Median months to
transplant for group B patients listed in 2011 was 9.7 months.
Although 65.3% of lung transplant candidates underwent
transplant within 1 year of listing, the percentage of candidates
undergoing lung transplant was highly variable based on donation
service area (DSA). The variation was from 37.5% to 93.5% for those
with at least 10 listings.

Kidneys
Living donor allocation/timing is dependent on availability and
matching. The waiting time may be less than for a deceased donor.

2086
Waiting times can vary from 2 to 5 years for a deceased donor.
Recipients must have a glomerular filtration rate of no more than 20
mL/min to be considered. Recipient status is either active or
inactive. There is no urgent status. Extended criteria donors are on
the rise. Considerations include ABO type, HLA antibodies, cross-
match, and PRAs. PRAs can be tested as frequently as monthly. A
new algorithm—Life Years from Transplantation—will attempt to
determine the donor and recipient combination that will achieve
the greatest survival benefit relative to dialysis.

Liver
Transplant-appropriate patients are generally determined using the
model for end-stage liver disease (MELD) score. Those patients in
the ICU with life expectancy of less than 7 days with acute liver
failure, hepatic artery thrombosis, primary graft nonfunction, or
acute decompensated Wilson disease are considered status 1 and
are excluded from other requirements of the MELD score. The
overall transplant rate has been gradually declining since 2006. The
greatest decline is in candidates with hepatocellular cancer and
those aged 18 to 34 years. The decrease in transplant rates reflects
the gradually worsening donor shortage. Despite a decline in wait-
list registration, the median pretransplant waiting time among
active wait-listed adult patients increased from 12.9 months in 2009
to 17.6 months in 2010 and to 18.5 months in 2011. Pretransplant
mortality rates decreased in 2012, for the first time in several years.
MELD Score: This score ranges from 6 (less ill) to 40 (gravely ill)
and is used to prioritize liver transplant candidates at least 12 years
of age. It is predictive of risk of 3-month mortality from liver
disease. The number is calculated using a formula that considers
three blood studies: bilirubin, which measures liver excretion of
bile; INR (international normalized ratio), which measures the
ability of the liver to manufacture clotting factors; and creatinine,
which measures kidney function. Bile excretion and the ability to
synthesize clotting factors are impaired by chronic liver disease.
Renal impairment is often associated with liver disease. A
numerical scale is used for liver allocation for chronic liver disease
only. Status 7 patients are considered inactive.

2087
Pancreas
Waiting lists and allocation of organs vary by institution and are
generally based on time waiting and PRA level. Frequent
evaluation is necessary, that is, every 6 months or per program
standard. There are four main types of pancreas transplantation:

• Pancreas transplant alone (PTA): Involves patients with type 1

diabetes who generally have severe, frequent hypoglycemia but
adequate kidney function.

• Simultaneous pancreas-kidney transplant (SPK): The pancreas

and kidney are transplanted simultaneously from the same
deceased donor.

• Pancreas-after-kidney transplant (PAK): A cadaveric, or deceased,

donor pancreas transplant is performed after a previously
performed living or deceased donor kidney transplant.

• Simultaneous deceased donor pancreas and live donor kidney

(SPLK): Has a lower rate of delayed graft function than SPK and
significantly reduced waiting times, resulting in improved
outcome.

Median time to transplant for active candidates listed in 2010-

2011 was 19.1 months for PTA and 16.2 months for SPK. The most
recent estimate available for PAKs was 36.9 months, for candidates
listed in 2008-2009. Waiting times for SPK, PAK, and PTA vary by
DSA. In six DSAs, no transplant program performed pancreas
transplants in 2011-2012. Organ Procurement and Transplant
Network (OPTN) policy allows for local organ procurement
organizations to use their discretion in prioritizing SPK or solitary
pancreas (PTA or PAK) offers. Lack of national policy likely
contributes to the overall geographic variation. The combined
pancreas waiting list will treat SPK, PAK, and PTA candidates
equally, which may eliminate geographic variations in allocation
policy.

Pharmacotherapy

2088
Posttransplant immunosuppression
Goals of therapy include:

1. Prevent rejection.

2. Improve graft survival.

3. Improve patient survival.

4. Maintain quality of life.

Immunosuppression therapy prevents rejection and is required

indefinitely posttransplant. Immunosuppression agents have their
own risks: infection, malignancy, and toxicity. Patient compliance
to therapy and program compliance also affect rejection. Finding
the balance between saving the graft and preventing complications
is a lifelong challenge.

Levels of immunosuppression therapy

Induction
Immunosuppression, usually in high doses, in the initial period of
organ transplantation wipes out T cells completely. Commonly
used drugs typically consist of corticosteroids and monoclonal and
polyclonal antibodies: Orthoclone OKT3, antithymocyte globulin
(ATG), basiliximab, daclizumab, alemtuzumab.

Maintenance
A maintenance dose of immunosuppression for transplant patients
in stable condition serves to maintain a gradual process of healing
and to prevent rejection. The potential for weaning patients off
some of their medication therapies is a high priority. Commonly
used drugs are corticosteroids, calcineurin inhibitors (CNIs),
antiproliferative agents, and mammalian target of rapamycin
(mTOR) inhibitors.

Rejection
Immunosuppression, usually in high doses for a patient whose

2089
organs are acutely rejecting. Commonly used drugs are
corticosteroids and polyclonal and monoclonal antibodies:
Orthoclone OKT3, ATG, basiliximab, daclizumab, and
alemtuzumab.

Desensitization
Therapies to reduce newly formed or preexisting alloantibodies.
Commonly used drugs are IVIG, rituximab, and
cyclophosphamide. Plasmapheresis mechanically removes
antibodies but does not treat the underlying problem.

Categories of drugs

Interleukin 1 inhibitors
Corticosteroids are used to treat and prevent organ rejection and to
suppress production of cytotoxic T-lymphocytes from noncytotoxic
precursor cells. They can be used for maintenance to prevent
rejection or as part of an acute rejection protocol. Evidence indicates
that steroids may prevent release of interleukin (IL)-1 and IL-2. IL-1
is released by the macrophages and promotes differentiation of
helper T cells. The release of IL-2 promotes differentiation of
cytotoxic cells and helps to reduce or prevent edema, to promote
normal capillary permeability, and to prevent vasodilation. Side
effects are numerous, including mood changes, sodium retention,
blurred vision, fragile skin, bleeding, glucose intolerance, increase
in appetite and subsequent weight gain, osteoporosis, and “moon
face” appearance from an accumulation of fatty tissue on cheeks
and upper back.

• Methylprednisolone (Solu-Medrol): A corticosteroid used as an

induction agent in doses ranging from 250 to 1000 mg IV at the
time of transplantation. Generally, three additional daily doses
are administered. The dose is then reduced to 35 mg by mouth
(PO) every 12 hours, until the first biopsy is completed or per
program protocol. Dosage is reduced by 5 mg per dose until the
drug is stopped, or a maintenance daily dose of 10 mg or less is
achieved. Methylprednisolone 125 mg IV every 12 hours for three
doses is also used before poly/monoclonal antibody therapy for

2090
 cytokine release syndrome. The drug is tapered to as low a dose
as tolerated.

Calcineurin inhibitors
Calcineurin is a protein phosphatase (also known as protein
phosphatase 3, and calcium-dependent serine-threonine
phosphatase), which activates the T cells of the immune system.
CNIs are used to block T-cell activation.

• Cyclosporine (CSA, Sandimmune, Neoral, Gengraf): A CNI used

to block the response of cytotoxic T lymphocytes to IL-2, which
inhibits the production and release of lymphokines, and stops the
generation of cytotoxic and plasma cells. Cyclosporine is
metabolized by the cytochrome P-450 enzyme system in the liver,
prompting the need for careful monitoring of cyclosporine drug
levels. Drug levels may vary when the dosage of cyclosporine or
other medications metabolized by the cytochrome P-450 enzyme
pathway is modified. Dosage is dependent on the type of
transplant, formulation (modified or nonmodified), experience of
the practitioner, patient status, and biopsy results.

• Tacrolimus (Prograf): A CNI used to block T-cell activation genes

via a similar mechanism to cyclosporine but more potent than
CSA. It is also metabolized by the cytochrome P-450 enzyme
system in the liver. It is used as a first-line drug or replaces
cyclosporine if there are multiple rejections while on
cyclosporine. The continuous infusion is dosed based on the type
of transplant and peak and trough levels, and then converted to
an oral dose administered twice daily when GI function returns
following surgery. Trough levels are initially 8 to 15 ng/mL and
are maintained at 5 to 15 ng/mL.

Selective T-cell costimulation blocker

Belatacept: A newer immunosuppression drug for the kidney
transplant patient that inhibits T-lymphocyte proliferation and
production of the cytokines IL-2, interferon γ, IL-4, and TNF α.
Belatacept is used as alternative to the CNI drugs and given as an
IV infusion of 10 mg/kg before implant on the day of surgery.

2091
Another dose is given at 96 hours and then at weeks 2, 4, 8, and 12.
Starting at week 16, a maintenance dose of 5 mg/kg is given every 4
weeks.

Antiproliferative agents
Antiproliferative agents are used in maintenance
immunosuppression and treatment of rejection to block the
proliferative phase of activated T- and B-lymphocyte generation.
They are an integral part of most immunosuppression regimens.

• Mycophenolic acid: Mycophenolate mofetile (MMF, Cellcept):

Used as a first-line immunosuppressant to inhibit the
proliferation of T and B lymphocytes, the production of
antibodies, and the generation of cytotoxic T cells. Dosed at 1.0 to
1.5 g every 12 hours IV/PO, no blood level monitoring is
required.

• Mycophenolic acid (Myfortic): A delayed-release form of

mycophenolic acid with the same indications, efficacy, and
adverse effects profile as MMF. Dosing is 720 mg PO every 12
hours.

• Azathioprine (Imuran): Immunosuppressive agent that interferes

with gene transcription and used in combination with other
drugs to prevent rejection. WBC counts are monitored, and
dosage is adjusted accordingly. Maintenance dosage is 1 to 3
mg/kg/day to a maximum of 150 to 175 mg/day. Dosage is
decreased or held if WBC count is less than 5/mm3.

Mammalian target of rapamycin inhibitors

Mammalian target of rapamycin (mTOR), a key regulatory kinase
in the process of cell division, is inhibited by these drugs. The
mTOR inhibitors improve kidney function when used as a
replacement for CNIs associated with higher incidence of renal
insufficiency.

• Sirolimus (Rapamune): An mTOR used to inhibit T- and B-

lymphocyte activation and proliferation, with added
antineoplastic effects. The oral loading dose is 6 mg/day followed

2092
 by a maintenance dose of 2 mg/day regulated by blood level
assessment, divided into 2 doses given every 12 hours.
Therapeutic trough blood levels are seen between 8 and 15
ng/mL. The drug is associated with impaired wound healing, so
it is not used during induction in the posttransplantation period.

• Everolimus (Certican): Very similar to sirolimus in mechanism of

action and side effect profile. Dosage is 0.5 mg to 1.5 mg orally
twice daily. The therapeutic drug level range is 3 to 8 ng/mL.

Monoclonal antibodies
Monoclonal antibodies are monospecific antibodies made by fusing
the spleen cells from a mouse immunized with a target antigen with
myeloma cells. These highly specialized antibodies can detect and
bind to the target antigen to purify the substance. Rabbit B cells
have been used more recently in the production of monoclonal
antibodies.

• OKT3 (Orthoclone): An immunosuppressive monoclonal

antibody used to treat organ rejection. OKT3 is a murine (mouse)
monoclonal antibody that recognizes and binds the CD3 receptor
present on all mature T cells. Anti-CD3 is a homologous antibody
that reacts with and blocks the function of the chemical (T3)
complex on the surface of the T lymphocytes. The T3 complex is
responsible for the T-lymphocyte’s identification of a
transplanted organ as foreign and the attempts to reject it. OKT3
binds to the T3 antigen on the surface of the T cells, enhancing
phagocytosis and entrapment of the cells in the spleen and liver.
The T lymphocytes are removed from the circulation by this
process in approximately 10 to 15 minutes. Patients are
premedicated with acetaminophen, an H2 receptor antagonist,
hydrocortisone, and diphenhydramine to avoid cytokine release
syndrome (fever, chills, tremors, pulmonary edema) during the
first 2 days of therapy. The dosage is 5 mg given via IV push over
1 minute every day for 10 to 14 days. It is associated with higher
infection (especially CMV) and malignancy rates. CD3 levels are
measured to maintain adequate levels of OKT3.

2093
• Basiliximab (Simulect): A chimeric (murine/human) monoclonal
antibody produced by recombinant DNA technology that is used
as an immunosuppressive agent during induction to inhibit IL-2
activation of T lymphocytes. It is not used to treat rejection, but
rather to prevent it. The dosage is 20 mg within 2 hours of
transplantation surgery and repeated 4 days after transplant. Side
effects are rare.

• Daclizumab (Zenapax): Acts similarly to basiliximab. The dosage

is 1 mg/kg/dose for 5 doses, the first dose within 24 hours of
transplant, followed by 4 doses at intervals of 14 days.

• Rituximab (Rituxan): A monoclonal antibody targeted at the

CD20 antigen on B lymphocytes used to prevent and treat
humoral rejection. The dosage is 1 dose of 375 mg/m2 to manage
humoral rejection or 375 mg/m2 every week for 4 doses for
posttransplant lymphoproliferative disorder. Patients are
premedicated with acetaminophen and diphenhydramine. The
drug is started at 50 mg/h and titrated up as tolerated.

• Alemtuzumab (Campath, MabCampath, Campath-1H): A

monoclonal antibody used in a very small population of organ
transplant patients as induction therapy and to treat rejection.
Effective September 4, 2012, Campath is no longer available
commercially, but is provided through the Campath Distribution
Program free of charge. To receive Campath, the healthcare
provider is required to provide written documentation that the
patient’s condition warrants the treatment. Alemtuzumab has
been associated with infusion-related events including
hypotension, rigors, fever, shortness of breath, bronchospasm,
chills, and rash. Other serious infusion-related events were
syncope, pulmonary infiltrates, ARDS, respiratory arrest, cardiac
arrhythmias, myocardial infarction, and cardiac arrest.

Polyclonal antibodies
Polyclonal antibodies are antibodies secreted by various lineages of
B cells within the body. In contrast, monoclonal antibodies originate
from a single cell type. This collection of immunoglobulin
molecules has the capacity to identify and purify many different

2094
antigens. Each type of molecule targets a specific antigen.

• Antilymphocyte sera (antilymphocytic globulin [ALG] or

antithymocyte gamma-globulin [ATGAM or thymoglobulin]):
Polyclonal antibody used for induction of immunosuppression
and management of rejection. The antilymphocyte antibodies in
the sera are useful in the treatment of steroid-resistant rejection
and are potent suppressors of cell-mediated immunity. They are
directed against many different antigens on the surface of human
lymphocytes and affect immunity via reduction of T
lymphocytes. When receiving ATGAM or thymoglobulin,
patients are premedicated with acetaminophen, an H2-receptor
antagonist, hydrocortisone, and diphenhydramine to help avoid
cytokine release syndrome, which may occur during the first 2
days of therapy.

Intravenous immune globulin

Used for desensitization and treatment of humoral rejection. The
dosage is 1 to 2 g/kg, started at a low rate (0.05 to 0.06 mg/kg/h) and
titrated up as tolerated. Patients are premedicated with
acetaminophen and diphenhydramine. Side effects include back
pain, headache, chills, fevers, bronchospasms, and hypotension.

Prevention of opportunistic infections

Antibiotics: Antibiotics are used in accordance with Surgical Care

Improvement Project (SCIP) guidelines.

Antivirals:

• Valganciclovir (Valcyte): Used for prophylaxis and

treatment of CMV, which remains the major cause
of morbidity and mortality for cardiac
transplantation patients. The dosage for induction
is 900 mg every 12 hours for 21 days. For
maintenance and prevention, it is given orally at
450 to 900 mg daily for 3 to 6 months following the

2095
 transplant.

• Acyclovir: Used for prophylaxis against and

treatment of herpes virus. The dosage is 5 to 10
mg/kg IV every 8 hours for 7 to 10 days or 200 to
800 mg PO, given as 2 to 5 doses each day,
depending on whether managing an active
infection or using for suppressive therapy.
Antifungals (Mycostatin, Nystan, Fluconazole): For potential
secondary Candida infections related to immunosuppression. The
dosage is 5 mL for an oral “swish and swallow” or Mycelex as an
oral troche 3 times daily following extubation.

Prevention of pneumocystic pneumonia: (Bactrim, TMP/SMX,

pentamidine, dapsone)

Management of Side Effects: Antiulcer medications, aspirin,

antihypertensive medications, stool softeners, insulin for
hyperglycemia, cholesterol-lowering agents, bone-strengthening
nutrients (calcium, phosphorus, magnesium), and osteoporosis
medications

Pain management
Opiates: Fentanyl is commonly used because it is short acting and,
unlike morphine, does not cause histamine-mediated hypotension.

Pretransplant and posttransplant sensitization

Plasmapheresis may decrease sensitization and reduce PRA levels.
Positive PRA levels detect circulating HLA and reflect level of
sensitization. Elevated PRA levels increase the difficulty of finding
an HLA-compatible donor organ. HLA compatibility will enhance
graft survival and reduce infection and malignancies related to
aggressive immunosuppression. Pregnancy, blood transfusion,
ventricular assist devices, or previous transplants can trigger
sensitization. Poor outcomes, such as CAD, posttransplant

2096
lymphoproliferative disorder, and an increased incidence of
rejection, have been associated with pretransplant sensitization.

Collaborative management
Care priorities

1. Prevent infection
Infection control is paramount because of immunosuppression
therapy. Immunosuppressed patients are vulnerable to bacterial
(Staphylococcus, Streptococcus, Klebsiella, Pseudomonas), viral (CMV,
EBV, herpes simplex, varicella zoster,) and fungal (Aspergillus,
Candida, Cryptococcus, histoplasmosis, Coccidioides, pneumocystis,
and Toxoplasma gondii) infections. Prophylactic antibiotics,
antivirals, and antifungals are used.
Steps to reduce infection postoperatively and beyond:

1. Isolation. Keep door closed and limit visitors; no employees or

visitors with active infection are allowed; avoid taking care of other
patients with infections.

2. Carefully monitor for signs and symptoms of infection.

2. Prevent organ rejection

Graft or organ rejection is the leading concern with transplantation.
A transplanted organ originates from a donor who is genetically
different from the recipient (the exception is a kidney/liver from an
identical twin). The organ contains foreign antigens that trigger an
immune response in the recipient, which leads the organ to reject
that foreign object. Historically, rejection has been classified as
hyperacute, accelerated acute, acute, or chronic (Table 11-10). An
untreated rejection response results in complete destruction of the
organ. Table 11-11 describes the clinical presentation for various
types of acute organ rejection.

Table 11-10
CHARACTERISTICS OF ORGAN REJECTION BY CATEGORY

2097
Type of
Characteristics Outcome
Rejection
Hyperacute Occurs immediately Usually irreversible and untreatable
Antibody-mediated Preventable with crossmatching
Result of preformed circulatory
antibodies
Accelerated Occurs 3–5 days after transplant Irreversible and untreatable
acute Antibody-mediated Preventable with crossmatching
Rapid loss of function
Fever and oliguria
Acute Primarily T cell-mediated Treatable and reversible Multiple
Possible presence of humoral episodes affect long-term graft survival
component
Occurs weeks, months, or years after
transplant
Chronic Develops slowly over months to years Untreatable, eventually leads to graft loss
Probably a combination of cellular-
and humoral-mediated processes

Table 11-11
CLINICAL PRESENTATION WITH ACUTE ORGAN REJECTION

Organ Clinical Presentation

Heart 10 to 14 days after transplantation. Indicators include fever, anxiety, lethargy, low
back pain, atrial or ventricular dysrhythmias, gallop, pericardial friction rub, jugular
venous distention, hypotension, and decreased CO late in rejection.
Lung Expected during the first 21 days after surgery, with increased frequency and
severity 6 to 8 weeks after transplantation
Classic rejection: decreased lung ventilation and perfusion alveolar exudate
containing desquamated pneumocytes and inflammatory cells
Atypical rejection: decreased ventilation without blood flow reduction, ventilation-
perfusion imbalances, and respiratory insufficiency with shunting
Vascular rejection: increased vascular resistance, decreased blood flow to graft
Liver 4 to 10 days after transplantation. Indicators include malaise; fever; abdominal
discomfort; swollen, hard, tender graft; tachycardia; RUQ or flank pain; cessation of
bile flow; change in bile fluid from golden to colorless; jaundice; elevated PT,
bilirubin, transaminase, and alkaline phosphatase.
Kidney Occurs in the immediate postoperative period with fever, pain over graft, decreased
urine output, and edema with increase in creatinine. Renal scan or Doppler is used
for a quick look at blood flow to the kidneys. Patients may even need dialysis for a
short time until the kidney functions.
Pancreas Time of rejection varies. Patient may have hyperglycemia, pancreatitis, or pain over
graft. Open biopsy may be necessary to diagnose rejection.

When the body detects the presence of a foreign substance, the

immune system mounts a defense with nonspecific inflammation
and phagocytosis. Antibody-mediated (humoral) and cell-mediated
immune responses work together to defend after exposure to an
antigen. Antibody-mediated immune response stimulates B-
lymphocyte activity. When an antigen is encountered, the B-

2098
lymphocyte enlarges, divides, and differentiates into a plasma cell
that produces and secretes antigen-specific immunoglobulins, or
antibodies. The formation of this antigen-antibody complex triggers
events that augment the nonspecific responses of inflammation and
phagocytosis. Cell-mediated immune response involves T-
lymphocytes that recognize a foreign antigen on the surface of the
macrophage, bind to the antigen, enlarge, and produce a sensitized
clone, which migrates through the body to the site of the antigen.
When the sensitized T cell combines with the antigen, chemicals are
released that kill foreign cells directly and facilitate phagocytosis
and the inflammatory response.

1. Graft-versus-host disease: Applicable to bone marrow transplant,

rather than solid organ transplant. A rejection process whereby
there is a transplant of functioning allogeneic T cells into an
immunocompromised host, such as in a bone marrow transplant.

2. Vasculopathy: A chronic rejection phenomenon seen in the

allograft vessels as diffuse disease affecting the full wall thickness
of the arteries, rather than solely the intralumen. Atherosclerotic
heart disease affects solely the intralumen of the arteries.

Diagnosis and assessment of rejection

Rejection is assessed using various diagnostics and procedures,
with transplanted organ biopsy being the most invasive direct
assessment. Biopsy provides the means of diagnosing rejection, its
severity, and the possibility of response to antirejection therapy.
Tiny pieces of tissue are removed for pathologic examination to
assess for tissue rejection.

Heart
Biopsy is performed in a cardiac catheterization lab/biopsy lab or
surgery. The cannulation site is generally the right internal jugular
or sometimes the femoral vein. Biopsy samples are graded
according to one of several grading systems. Biopsies are generally
performed at 7 and 14 days after surgery and at specified intervals
thereafter, and the Biopsy Rejection Scale is used:

2099
Biopsy Rejection Scale

Grade Description
0R No evidence of acute cellular rejection
1R Interstitial and/or perivascular infiltrate with up to 1 focus of myocyte damage
2R Two or more foci of infiltrate with associated myocyte damage
3R Diffuse infiltrate with multifocal myocyte damage +/− edema, +/− hemorrhage, +/−
vasculitis

The following assist in assessing the transplanted heart for

rejection:

• Vital signs and heart sounds: May reveal decreased stroke

volume, CO, cardiac tones, and BP and presence of S3 and S4
sounds, pericardial friction rub, extrasystole, and crackles.

• Echocardiogram: Used to assess chamber size, wall thickness,

ejection fraction, thrombus formation, valve function, and systolic
and diastolic function.

• Chest radiograph: Will reveal increased dimensions of the heart

late in rejection.

• ECG: Will show presence of atrial and ventricular dysrhythmias

and decreased QRS voltage.

• CBC: Will show increased total lymphocyte count.

• Intravascular ultrasound: Used to evaluate vasculopathy of the

coronary arteries.

• Blood analysis of rejection: Currently only used to assess cardiac

rejection, AlloMap detects the absence of acute cellular rejection
in clinically stable heart transplant patients. The test uses a
peripheral blood sample <and has replaced biopsies in many
institutions. Studies are currently ongoing for lung transplant
patients, with studies of other transplant types planned for the
future.

Lung

2100
• Transbronchial biopsy: Not particularly helpful in detecting
rejection; the morbidity risk increases with open biopsy.

• Biopsy grading:

• Grade 0: No acute cellular rejection.

• Grade 1: Minimal acute cellular rejection.

• Grade 2: Mild acute cellular rejection.

• Grade 3: Moderate acute cellular rejection.

• Grade 4: Severe acute cellular rejection.

The following assist with assessment of the transplanted lung:

• Symptoms: Cough (although it goes away in the initial stages),

dyspnea, fatigue, fever, flulike symptoms.

• Chest radiograph: Changes indicative of rejection are noted.

• Leukocyte and absolute T-lymphocyte counts: Rise during

rejection.

• Vital signs and hemodynamics: Can change suddenly with

increases in PVR, HR, BP, SVR, and CO.

• ABG values: Decrease in PaO2 and increase in Paco2 occur with

rejection. Decrease in pulmonary function tests, change in forced
expiratory volume.

Kidney
• Renal biopsy: Determines presence, type, and severity of
rejection.

2101
• Kidney biopsy grading: (Table 11-12).

Table 11-12
BANFF DIAGNOSTIC CATEGORIES FOR RENAL ALLOGRAFT
BIOPSIES

Acute Active Rejection

1. Normal
2. Antibody-mediated rejection: immediate (hyperacute), delayed (accelerated acute)
3. Borderline changes: No intimal arteritis is present, but there are foci of mild tubulitis.
4. Acute/active rejection
Type Histopathologic findings
Grade
IA Significant interstitial infiltration (>25% parenchyma affected) and foci of moderate
tubulitis (>4 mononuclear cells/tubular cross-section or group of 10 tubular cells)
IB Significant interstitial infiltration (>25% parenchyma affected) and foci of moderate
tubulitis (>10 mononuclear cells/tubular cross-section or group of 10 tubular cells)
IIA Cases with mild to moderate intimal arteritis
IIB Cases with severe intimal arteritis comprising >25% of the luminal area
III Cases with transmural arteritis and/or arterial fibrinoid change and necrosis of
medical smooth muscle cells
5. Chronic/sclerosing allograft nephropathy
Grade Histopathologic findings
I: Mild Mild interstitial fibrosis and tubular atrophy without Grade 1A or 1B findings or
with (specific changes suggesting chronic rejection
II: Moderate interstitial fibrosis and tubular atrophy withGrade 1A or 1B findings
Moderate
III: Severe interstitial fibrosis and tubular atrophy and tubular loss with Grade 1A or 1B
Severe findings
Other Changes not considered to be because of rejection

The following signs assist in assessment for rejection of the

transplanted kidney:

• Symptoms: Fever, pain over graft, edema.

• BUN and creatinine values: Will increase from previous 24-hour

levels and continue to rise until rejection is reversed.

• 24-Hour urine collection: Will exhibit a change in components

(e.g., decreases in creatinine clearance, total amount of creatinine
excreted, and urinary sodium excretion; increase in protein
excretion).

• Renal scan: Will exhibit decreased blood flow.

• Kidney assessment: May reveal a firm, large kidney that may be

2102
 tender on palpation.

• Renal scan: Evaluates blood flow to the kidney and rate of

excretion of substances into the bladder.

Liver
Several methods are used to obtain liver samples, including
laparoscopic liver biopsy, percutaneous image-guided liver biopsy,
and open surgical liver biopsy.

Laparoscopic liver biopsy

With the use of trocars (shafts with 3-sided points), small incisions
are made in the abdomen to enable insertion of the laparoscope.
Using the monitor to facilitate viewing, the physician uses
instruments within the laparoscope to remove tissue samples from
one or more parts of the liver. This type of biopsy is used when
samples from specific parts of the liver are required.

Percutaneous liver biopsy

A local anesthetic is first administered to numb the area on the
body’s right side. Through a small incision near the rib cage, a
special biopsy needle is inserted to retrieve liver tissue. In some
cases, ultrasound or computed tomography may be used to help
guide the needle to a specific spot. This biopsy method is often used
when the disease process is localized to discrete spots in the liver.

Open surgical liver biopsy

Open liver biopsies are done by a surgeon using a biopsy needle or
through surgical excision of a small piece of liver tissue. This is
generally used during another surgical procedure, because less
invasive techniques are available.
The following signs assist in diagnosis of rejection of the
transplanted liver (Table 11-13):

• Symptoms: Light-colored stools, dark-colored urine, jaundice of

the sclera or skin, fever, right upper quadrant pain, fatigue,
malaise, and pruritus.

2103
• Serum bilirubin level: Total bilirubin will rise in relation to
baseline postoperative level.

• Transaminase level: Will increase from baseline; may be markedly

elevated early in rejection.

• Alkaline phosphatase level: Will increase from baseline.

• Prothrombin time: Will be prolonged.

• CBC: May reveal decreased platelet count and increased total

lymphocyte count.

Table 11-13
LIVER TRANSPLANT DATABASE (LTD GRADING SCHEME)

Grade Criteria
AO No rejection
A Rejection without bile duct loss
1 Rejection infiltrate in some, but not all, of the triads confined within the portal spaces.
2 Rejection infiltrate involving all of the triads, with or without spillover into the lobule.
No evidence of centrilobular hepatocyte necrosis, ballooning, or dropout
3 Infiltrate in some or all of the triads, with or without spillover into the lobule, with or
without inflammatory cell linkage of the triads, associated with centrilobular
hepatocyte ballooning or necrosis and dropout

Pancreas
Open biopsy is the only means by which a definitive diagnosis can
be made.
The following signs also assist in the diagnosis of rejection of the
transplanted pancreas:

• Symptoms: Pain over pancreas graft; malaise, fever, and

hyperglycemia.

• Fasting and 2-hour postprandial plasma glucose: Levels will be

increased above normal ranges.

• Serum amylase: Levels may be elevated, indicating presence of

pancreatitis, an inconsistent marker of rejection.

2104
• Serum creatinine: Elevated.

• C-reactive peptide (serum and urine): Levels may be decreased.

• Pancreas radioisotope flow scan: Determines organ viability;

decreased flow may indicate rejection.

Care plans for organ transplantation

Risk for injury 
related to organ rejection related to inadequate immunosuppressant drug
levels.
Goals/Outcomes: Within 48 hours after the transplant, the patient
verbalizes accurate information about the signs and symptoms of
rejection. Within 72 hours after initiation of medications, the patient
and significant others verbalize accurate information regarding the
prescribed immunosuppressive agents, the side effects that can
occur, and precautions that should be taken.
Immune Status

Environmental risk protection

1. Assess patient’s knowledge of drug therapy.

2. Provide the patient with verbal and written information for the
type of immunosuppressive agent that has been prescribed. Discuss
the generic name, trade name, purpose, usual dosage, route, side
effects, and precautions.

3. Monitor blood levels as appropriate for drug.

4. Instruct the patient to take medication at designated time(s) each

day. Never withhold immunosuppressant without consulting with
physician or midlevel practitioner.

5. Monitor for signs of rejection, as appropriate for each specific

organ.

6. Reinforce the necessity of regularly scheduled appointments with

2105
transplant coordinator. Encourage the patient to bring a significant
other to the visit.

Teaching: Disease Process; Teaching: Individual; Teaching:

Prescribed Medication, Discharge Planning; Medication
Management; Weight Management.

Risk for infection (lungs and heart most common) 

related to immunosuppression.
Goals/Outcomes: The patient is free of infection as evidenced by
normothermia; absence of erythema, swelling, and drainage of
catheter and wound sites; absence of adventitious breath sounds or
cloudy and foul-smelling urine; negative results of urine, wound
drainage, and blood cultures; WBC count 4500 to 11,000/mm3.
Immune Status

Infection protection

1. Patient is to wear a mask when outside his or her immediate

living area, in public areas, near construction, or during “cleaning”
of environment.

2. Notify the physician or transplant coordinator immediately for a

temperature greater than 99.5° F, WBC count increasing, patient
complaints of malaise, or any obvious infection. Review bloodwork
and radiographs.

3. Perform a thorough physical assessment. Auscultate lung fields

every 8 hours, noting presence of rhonchi, crackles, and decreased
breath sounds. Inspect graft wound for erythema, swelling, and
drainage. Consult physician or advanced practice provider for
significant findings.

4. Avoid placement of indwelling catheters; if necessary, remove as

soon as possible.

5. Assess and document condition of indwelling IV sites and other

catheter sites every 8 hours. Be alert to swelling, erythema,
tenderness, and drainage. Consult the physician or advanced

2106
practice provider for any of these findings.

6. As prescribed, obtain blood, urine, and wound cultures when

infection is suspected.

7. Be alert to WBC count greater than 11,000/mm3 or less than

4500/mm3. A below-normal WBC count with increased band
neutrophils on differential (shift to the left) may signal acute
infection.

8. Record volume, appearance, color, and odor of urine. Be alert to

foul-smelling or cloudy urine, frequency and urgency of urination,
and patient complaints of flank or labial pain, all of which are signs
of renal-urinary infection.

9. Use meticulous aseptic technique when dressing and caring for

wounds and catheter sites.

10. Obtain specimens for urine cultures once a week during

patient’s hospitalization and once a month after hospital discharge.

11. Provide care measures to prevent infection

• Perform sterile wound dressing changes.

• Discontinue invasive lines and tubes as soon as

possible.

• Facilitate early extubation.

• Provide early optimal nutrition.

• Use a leukocyte filter for blood administration or

use leukocyte-reduced blood.

Infection Control; Airway Management; Exercise Promotion

2107
and Therapy Medication Management; Respiratory Monitoring;
Teaching: Disease Process; Tube Care: Urinary; Vital Signs
Monitoring.

Impaired oral mucous membranes 

related to treatment with immunosuppressive medication.
Goals/Outcomes: The patient’s oral mucosa, tongue, and lips are
pink, intact, and free of exudate and lesions. Patient states that he or
she can swallow without difficulty within 24 hours after treatment
for altered oral mucous membrane.
Oral Hygiene; Tissue Integrity: Skin and Mucous Membranes

Oral health restoration

1. Inspect the mouth daily for signs of exudate and lesions and
report abnormal findings to the physician. Teach the patient to
perform self-inspection of mouth.

2. Teach the patient to brush with a soft-bristle toothbrush and

nonabrasive toothpaste after meals and snacks.

3. To help prevent monilial infection, provide the patient with

mycostatin prophylactic mouthwash for swish and swallow after
meals and at bedtime.

Oral Health Maintenance; Oral Health Promotion

Impaired skin integrity (or risk for same) herpetic lesions,

skin fungal rashes, pruritus, and capillary fragility 
related to treatment with immunosuppressive medications.
Goals/Outcomes: Patient’s skin is intact and free of open lesions
or abrasions.
Tissue Integrity: Skin and Mucous Membranes

Skin surveillance

1. Assess for and document daily the presence of erythema,

excoriation, rashes, or bruises on patient’s skin.

2108
2. Assess for and document the presence of rashes or lesions in the
perineal area. Herpetic lesions are common in the
immunosuppressed patient.

3. Inspect the trunk area daily for the presence of flat, itchy rashes.
Skin fungal rashes are common in the immunosuppressed patient.

4. Teach the patient the importance of daily skin care with water,
nondrying soap, and lubricating lotion.

5. Use nonallergenic tape when anchoring IV tubing, catheters, and

dressings.

6. Assist the patient with changing position at least every 2 hours;

massage areas that are susceptible to breakdown, particularly areas
over bony prominences.

Pressure Ulcer Prevention. Additional, optional interventions

include Bathing; Bleeding Precautions; Cutaneous Stimulation;
Exercise Promotion and Therapy Electrolyte Monitoring; Exercise
Promotion: Stretching; Fluid/Electrolyte Management; Infection
Control; Infection Prevention; Medication Management; Nail Care;
Nutrition Management; Perineal Care; Surveillance; and Vital Signs
Monitoring.

Sepsis, septic shock, systemic

inflammatory response syndrome,
and multiple organ dysfunction
syndrome
Pathophysiology
Sepsis
Sepsis is the most frequent cause of death in hospitalized patients.
Although sepsis arises through activation of an innate immune

2109
response to a stimulus that represents a danger to the host, it has
also been directly related to current treatments rendered to
critically ill patients who previously would have died. It accounts
for 1,000,000 cases and 200,000 deaths annually in the US alone, but
unlike other major epidemic illnesses, treatment for sepsis is
nonspecific, limited primarily to support of organ function and
administration of IV fluids, antibiotics, and oxygen. There are no
approved drugs that specifically target and treat sepsis. Current
evidence supports that acute infections worsen preexisting chronic
diseases or result in new chronic diseases, which lead to poorer
outcomes and increased morbidity in survivors.
Sepsis represents a syndrome, not a disease, and it is difficult to
identify because the signs and symptoms are often subtle and
evolving and generally mirror the signs and symptoms of other
conditions. This clinical diagnostic term used to describe patients
who have a continuum of abnormalities in organ function evolved
from a 1991 Consensus Conference that defined “sepsis” as
documented or suspected infection combined with two or more
abnormalities in body temperature, HR, RR, or WBC count. Those
individuals with sepsis and evidence of organ dysfunction
(cardiovascular, renal, hepatic, or neurologic) were further
classified as having “severe sepsis,” and those with cardiovascular
dysfunction not responsive to fluid were said to have “septic
shock.” Ten years later the diagnosis of septic shock was expanded
to include evidence of inadequate tissue perfusion (low SVO2, lactic
acidosis, wide anion gap). Recently, evidence shows that patients
with sepsis or septic shock go on to develop “persistent critical
illness” with overt organ dysfunction that may last for weeks or
months. These survivors may be disabled by cognitive dysfunction,
neuropathies, and other complications.

Systemic inflammatory response syndrome

Frequently the first signs of impending sepsis are identified as SIRS,
a state of generalized, uncontrolled inflammation. Inflammation is a
complex response initiated by mechanical, ischemic, chemical, or
microbial sources. Signs of systemic inflammation such as fever and
leukocytosis characterize SIRS. A patient with sepsis presents with
at least two of the SIRS criteria: an abnormal body temperature,

2110
elevated HR and RR, and an altered WBC count as well as a
suspected or proven source of infection. Sepsis is a syndrome
consisting of the combination of a systemic inflammatory response
and the presence of infection. Risk factors for poor outcome in
sepsis include hypothermia, leukopenia, low arterial pH, shock,
multiorgan dysfunction, age greater than 40 years, and medical
comorbidities. The issues associated with identification are related
to this generalized presentation. Almost all acutely ill patients meet
SIRS criteria and often have infection, which is not necessarily
sepsis. Sepsis with one or more organ dysfunctions is considered
severe sepsis.

11-3
RESEARCH BRIEF
The latest definition is that sepsis is a life-threatening condition
when the body’s response to an infection injures its own tissues
and organs. Using this criteria, sepsis cannot be identified until
there is organ dysfunction in the primary easily evaluable
sixsystems: renal, neurological, hepatic, cardiovascular,
respiratory, and coagulation. Other systems may be more difficult
to assess; however, any acute dysfunction in this situation must be
considered a sign of sepsis.
Czura CJ: Merinoff symposium 2010: sepsis—speaking with one
voice. Mol Med 17:2-3, 2011.

In some cases, regulatory mechanisms fail and uncontrolled

systemic inflammation overwhelms the body’s normal protective
response. This leads to systemic vasodilation, arterial hypotension,
generalized increase in vascular permeability, extravascular fluid
sequestration, and increased hematologic cellular aggregation with
microvascular obstruction, which greatly accelerates consumption
of coagulation products.

Severe sepsis
Severe sepsis is the compounding of sepsis by comorbid conditions,
wherein the inflammatory response to a nidus of infection or
inflammation is fulminating and out of control. Severe sepsis has

2111
more recently been viewed as endothelial dysfunction resulting
from overwhelming inflammatory mediation, in conjunction with
profound, unopposed coagulation. The capillary vasculature
sustains a significant injury by a cascade of events that ends in
capillary occlusion. The more massive the occlusion, the greater the
potential for organ failure, as cellular level circulation requires a
functional capillary network for delivery of oxygen and nutrients
and removal of cellular metabolic waste products. When infection
or other injury prompts an initially widespread inflammatory
response, or SIRS, the normally smooth surface of microvascular
(capillary) endothelium is roughened or damaged by the response.
Release of inflammatory mediators prompts vasodilation with
increased capillary permeability. Microscopically, the endothelium
resembles a road riddled with tiny “potholes.” Systemic mediators
are released to facilitate healing of the endothelium, which is aimed
at “filling the tiny potholes.”
The four main factors associated with severe sepsis that may
evolve to septic shock are hyperinflammation, hypercoagulation,
microvascular obstruction, and increased endothelial permeability.
Because endothelial damage is generalized, the extensive or
hyperinflammatory response leads to accelerated formation of
microclots on the non–smooth capillary endothelium, consuming
platelets and inhibiting clot lysis (fibrinolysis). This progresses to
uncontrolled alterations in the vascular tone with vasodilation in
the large vessels (where BP is measured). Both vasodilation and
constriction occur in capillaries, where oxygen delivery takes place.
Stimulated by products of antigen ingestion, activated
neutrophils and other humoral mediators combine, activate, and
potentiate an ongoing vascular endothelial injury with a
concomitant proinflammatory, procoagulating, antifibrinolytic
response. Among other mediators, an increased presence of tissue
factor persistently stimulates thrombin, which ultimately increases
fibrinogen conversion to fibrin and promotes platelet aggregation.
Coupled with microvascular clotting, the process limits oxygen
delivery and may lead to organ ischemia. Unopposed, this process
may lead to a profound consumptive coagulopathy (DIC),
diminished distal blood flow, and cell death by activated cellular
suicide (apoptosis). The blood flow necessary to maintain tissue

2112
oxygenation and aerobic metabolism, nutrient transfer, and
metabolic waste removal is profoundly threatened.
Excessive thrombin production and a secondary decrease in
endothelial production of plasminogen activator, thrombomodulin,
protein C, and other prothrombin and antithrombin mediators,
ultimately, activated protein C, illustrate the overwhelming
response that separates simple infection from severe sepsis. The
endothelial regulation of appropriate blood flow requires a balance
of vasodilators (i.e., nitric oxide) and vasoconstrictors (e.g.,
endothelin). In severe sepsis, when the balance cannot be
maintained, the corresponding maldistribution of blood flow and
loss of vascular tone at the macro- and microvascular levels result
in both ischemia and hyperemia in the cells supplied by the same
capillary beds. In addition, myocardial depressant factor is released
and may contribute to the loss of the compensatory CO, which is
required to keep blood moving through the vascular beds.

Septic shock and multiorgan dysfunction syndrome

Severe sepsis accompanied by hypotension that does not respond to
volume infusion is called septic shock. Impaired perfusion may
cause lactic acidosis, oliguria, or acute alterations in mental status.
Genetic predisposition and other factors compound severe sepsis,
leading to MODS as well as multiple organ failure and may be fatal.
MODS is diagnosed when two or more vital organ systems become
dysfunctional.
Septic shock is severe sepsis with cardiovascular dysfunction
(primary loss of vascular tone) that does not respond to fluid
resuscitation and requires vasopressor therapy to maintain MAP
above 65 mm Hg. Patients with septic shock often have fluid
deficits of 6 to 10 L and need aggressive fluid resuscitation. The
cornerstones of therapy for sepsis are volume resuscitation, early
antibiotic therapy, hemodynamic support with vasopressors as
necessary, and glycemic control.
Over the past 30 years, understanding the malignant, destructive,
uncontrolled inflammatory, and coagulation process has become
the primary focus in the management of patients exhibiting signs
and symptoms of severe sepsis that can ultimately result in MODS.
The process leading from SIRS to MODS to organ failure is a

2113
continuum that often begins with the same event (Table 11-14).
SIRS initiates a process of relative hypovolemia. To the
unsuspecting practitioner, the early signs of arterial hypoperfusion
may be masked by the patient’s near normal appearance resulting
from compensatory vasoconstriction and increased CO, which
maintains a normal BP. If SIRS and/or sepsis is managed
aggressively in the early stages, the incidence of MODS is
decreased. The American College of Chest Physicians
(ACCP)/SCCM Consensus Conference first initiated a suggested
approach to the identification of profound and uncontrolled
inflammatory response in 1992. These guidelines have been
modified and updated several times, with the most recent revisions
reflected in the 2012 Surviving Sepsis Campaign International
Guidelines (Table 11-15). Some of the more specific recognized
signs and laboratory profiles are listed in Table 11-16.

Table 11-14
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

If two or more of the following are present, the patient meets criteria for SIRS:
1 Temperature >38° C or 100.4°F or <36° C or 96.8°F.
2 Heart rate >90 bpm
3 Respiratory rate >20 breaths/min or Paco2 <32 mm Hg
4 White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature (band) forms
Adapted from Levy MM, Fink MP, Marshall JC, et al: 2001
SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care
Med 31:1250-1256, 2003.

Table 11-15
ASSESSMENT FINDINGS FOR THE PATIENT WITH SEPSIS IN THE
EARLY HYPERDYNAMIC STAGE

Clinical Indicator Cause

Cardiovascular
Increased HR (>100 Sympathetic/autonomic nervous system (SANS) stimulation
bpm)
Decreased BP (<90 mm Vasodilation
Hg systolic, MAP <65
mm Hg)
CO >7 L/min, CI >4 Hyperdynamic state secondary to SANS stimulation
L/min/m2, CVP <8 mm
Hg

2114
 Svo2 >80% Decreased use of oxygen by cells
PAWP usually <6 mm Venous dilation, decreased preload
Hg
SVR <900 Vasodilation
dynes/sec/cm-5

Strong, bounding Hyperdynamic cardiovascular system (keeping in mind that patients

peripheral pulses with preexisting cardiomyopathy will have minimal elevation in
cardiac CO and drop in SVR)
Respiratory
Tachypnea (>20 Metabolic acidosis that leads to decreases in cerebrospinal fluid pH
breaths/min) and that stimulate the central respiratory center
hyperventilation
Crackles Interstitial edema occurring with increased vascular permeability
Paco2 <35 mm Hg Tachypnea and hyperventilation
Dyspnea Increased respiratory muscle work
Renal
Decreased urine output Decreased renal perfusion
(<0.5 mL/kg/h)
Increased specific Decreased glomerular filtration rate
gravity (1.025–1.035)
Cutaneous
Flushed and warm skin Vasodilation
Metabolic
Increasing body Increased metabolic activity, release of pyrogens secondary to
temperature (usually invading microorganisms, release of interleukin-I by macrophages
<38.3°C [100.9°F])
pH <7.35 Metabolic acidosis occurring with accumulation of lactic acid
Lactic acid >2.5
Hyperglycemia or at Release of glucagon, insulin resistance
times profound
hypoglycemia
Neurologic
Changes in LOC Decreased cerebral perfusion and brain hypoxia
Fluid
↑ Fluid retention ↑ ADH, ↑ aldosterone
ADH, Antidiuretic hormone; bpm, beats per min; BP, blood pressure; CI, cardiac
index; CO, cardiac output; HR, heart rate; LOC, level of consciousness; MAP, mean
arterial pressure; PAWP, pulmonary artery wedge pressure; SVR, systemic vascular
resistance.

The purpose of the inflammatory response is to protect the body

from further injury and promote rapid healing. Vasodilation with
increased microvascular permeability, neutrophil activation and
adhesion, and enhanced coagulation initially occur in a balanced
framework. The vascular response is initiated at the cellular level
by histamine, prostaglandins, bradykinin, and numerous other
mediators. The term sepsis implies, to many practitioners, an
infectious process that has facilitated SIRS. Sepsis is typically not
associated with a simple infection requiring antibiotic management

2115
to resolve without hospitalization.
In addition to infection, sepsis is associated with multiple injuries
in trauma patients and other patients with significant inflammation
such as pancreatitis. Critically ill patients with sepsis resulting from
infection are often not easily managed, with microorganisms that
require considerable skill to control. Microorganisms commonly
seen in the critically ill include gram-negative enteric pathogens
(e.g., Escherichia coli, Klebsiella spp., Enterobacter spp., Pseudomonas
aeruginosa), Staphylococcus aureus, coagulase-negative staphylococci,
Enterococcus spp., and Candida spp. Antibiotic-resistant bacteria
(e.g., methicillin-resistant S. aureus [MRSA]) are commonly seen.
The American College of Chest Physicians (ACCP)/SCCM
Consensus Conference first initiated one suggested approach to the
identification of profound and uncontrolled inflammatory response
in 1992. The Surviving Sepsis Guidelines for Management of Severe
Sepsis and Septic Shock were first published in 2004, revised in
2008, and recently revised again and published in 2013. The
evidence-based update supports components of the overall
campaign, but there are other directives that have come under
increasing scrutiny. Early identification, antibiotics, and source
control as well as initial volume resuscitation remain as the
foundation of sepsis management, although the endpoints may not
be as clear as they first appeared to be.

Key points
• Shock is a clinical diagnosis defined by inadequate end-organ
perfusion in the setting of hemodynamic instability.

• Definitive treatment is directed at reversing the underlying insult.

Goals of supportive therapy include the maintenance of end-
organ perfusion.

• For refractory hypotension, consider the following possibilities:

overwhelming systemic inflammatory state, adrenal
insufficiency, mixed physiologic condition (e.g., sepsis and
congestive heart failure), and neurogenic shock.

2116
Assessment: Systemic inflammatory
response syndrome, sepsis, severe sepsis,
septic shock and multiorgan dysfunction
syndrome
Goal of system assessment
Evaluate for hypermetabolism, progressive tissue hypoxia, and
prevention of organ dysfunction.

History and risk factors

• Multiple presentations to emergency department or physician’s
office for the same complaint

• Infection, sequential infections, any indwelling catheters,

malnutrition, immunosuppression, bone marrow suppression,
advanced age (older than 65 years of age), infants

• Recent traumatic injuries or surgical or invasive procedures;

presence of intravascular devices or artificial joints

• Chronic health problems (e.g., liver or renal disease, diabetes

mellitus, rheumatic heart disease)

• Underlying diseases or conditions such as splenectomy, IV

substance abuse

Vital signs
• Patients may present with tachycardia, tachypnea, hyper- or
hypothermia, and hyper- or hypoglycemia. Hypoglycemia is
being increasingly recognized and is thought to be related to
depletion of glycogen stores, increased cellular glucose use,
and/or impaired gluconeogenesis. Criteria for diagnosis of sepsis
are evolving.

• SIRS: The 2013 guidelines state that an inflammatory response is

2117
 associated with sepsis, which is now defined as infection
accompanied by two or more of the following signs of systemic
inflammation: hypo- or hyperthermia, tachycardia, tachypnea, or
elevated or depressed leukocyte count. Decreased Paco2, positive
culture, tissue stain, polymerase chain reaction testing, clinical
examination, radiologic imaging, or other laboratory findings
may support the diagnosis of infection. Older adults may
manifest normal or slightly decreased temperature.

• Sepsis: In 2013, the SCCM supported the following definition of

sepsis—A documented or suspected infection with some of the
following: fever, hypothermia, HR greater than 90 bpm or more
than 2 standard deviations (SDs) above the normal for age,
tachypnea, altered mental status, hyperglycemia greater than 120
mg/dL in absence of diabetes, leukocytosis, leukopenia, normal
WBC count with greater than 10% immature forms (bands),
plasma C-reactive protein level more than 2 SDs above normal,
and decreased protein C level (see Tables 11-15 and 11-16).

1. Hemodynamic measurements: The hemodynamic presentation

varies with fluid balance and cardiac function of the patient. There
is no high-level evidence supporting the most effective MAP for
resuscitation of patients with septic shock. When patients
experience hypotension, they may decrease their cerebral blood
flow (below 50 mm Hg) and different organs are more significantly
impacted when BP drops and oxygen delivery is affected The
traditional CVP and PAOP are considered static hemodynamic
measurements as they are obtained under a single ventricular
loading condition and are significantly affected by chamber
compliance as well as volume load. The Surviving Sepsis Campaign
(SSC) guidelines recommend a CVP range of 8 to 12 mm Hg
(spontaneous breather) or 12 to 15 mm Hg (positive pressure
breather). There is contradictory evidence regarding use of CVP as
a predictor of fluid responsiveness and significant discussion
regarding the value of these as stand-alone endpoints. The
measurement of CO and in particular stroke volume (SV) is
considered currently to influence fluid resuscitation. The reference
range for SV is 50 to 100 mL/beat, although a more evidence-based

2118
indicator of the SV response to therapy is to note whether it
increases by 10% to 15% after a specific therapy. Dynamic methods
used to evaluate volume levels and volume responsiveness
measure heart-lung interactions during inspiration. Spontaneous
breathers (negative pressure breathing) may be evaluated using
pulse pressure variation or systolic pressure variation. Pulse
pressure variation, estimated from the arterial waveform, and
stroke volume variations, from pulse contour analysis, pulse
oximeter plethysmographic waveform, or thoracic bioreactance,
have been found to be reliable predictors of fluid responsiveness
when patients receive a challenge test, such as passive leg raise. If
patients are mechanically ventilated, using the pulse contour
analysis, pulse oximeter plethysmographic waveform, or thoracic
bioreactance has been found to be reliable in predicting fluid
responsiveness when patients receive a challenge test, such as
passive leg raise.

2. Monitoring tissue perfusion using a central line with oximeter-

based technology.

3. ScVO2: The ScVO2 (reflecting tissue use of oxygen) in early stages

may be low to normal. The sample is obtained by measuring a
blood sample in the right atrium. The values are generally about 5%
to 13% higher than SO2 levels. Serum lactate levels in conjunction
should measure adequacy of tissue oxygenation with methods of
monitoring central or local hemoglobin saturation to determine the
degree of anaerobic metabolism present and the effects of
resuscitation.

• Tissue metabolic dysfunction: Placement of a

central catheter to measure both pressures on
ventricular filling, as well as the saturation of
hemoglobin after blood has passed the capillaries,
may be an important component of monitoring
for these patients. Uses of SVO2 and ScVO2 include:

2119
• Threats to tissue oxygenation occur, such as a
decrease in blood flow from hypovolemia or low
CO (relative to tissue demand). The compensatory
mechanism is to release more oxygen from
hemoglobin (shift to right), which reflects a lower
than normal measured ScVO2.

• In early sepsis, the lower the ScVO2, the more the

tissue viability may be at risk. As sepsis progresses,
elevated ScVO2 may reflect inability of tissues to
utilize oxygen. As sepsis evolves to severe sepsis
and septic shock, ScVO2 levels do not fall, but rather
increase. Return of ScVO2 to normal may indicate
improvement of blood flow, but in late sepsis it
may also indicate that shunting is worsening
because of vasopressors, microvascular occlusion,
obstruction, and other issues interfering with
oxygen utilization. The pathologic increase in
measured ScVO2 occurs frequently in septic shock.
Differentiation from improving status is vital.

• Declines in ScVO2 (ScVO2) predict the onset of

inadequate myocardial compensation and may
precede cardiogenic shock, capillary blood flow
failure, or arrhythmias, even though vital signs in
many patients remain relatively normal. In early
compensatory sepsis, the oxyhemoglobin curve
shifts to the right often with an ScVO2 as low as 30%
to 40%; later, decompensated sepsis frequently
presents with cardiac shock features and an SVO2

2120
 that is normal to high, in the presence of significant
lactic acidosis.
4. Lactate level: Should be reviewed to assess progress, as increases
in ScVO2 are not always indicative of improvement. Although
lactate provides a valuable reflection of tissue hypoxia, it cannot be
continuously monitored and it changes over time. Lactate is
produced excessively when poor circulation and oxygenation
prompt cells to initiate anaerobic metabolism. Blood lactate
concentrations reflect the balance between lactate production and
clearance. The normal blood lactate concentration in physiologically
unstressed patients is 0.5 to 1 mmol/L. In critical illness, lactate
concentrations of less than 2 mmol/L are considered acceptable.
Hyperlactatemia is defined as a mild to moderate persistent
increase in blood lactate concentration (2 to 4 mmol/L) without
metabolic acidosis. Depending on the hospital or clinical laboratory
protocol, lactic acidosis is diagnosed when increased blood lactate
levels rise above 3 mmol/L. When patients are at risk of cellular
hypoxia, a blood sample to measure the lactate level should be
drawn. This may apply to a patient with suspected sepsis, but also
to those with sustained tachycardia, tachypnea, hyperventilation,
and persistent hypotension.

Table 11-16
ASSESSMENT FINDINGS FOR THE PATIENT WITH SEPSIS IN THE
LATE STAGE

Clinical Indicator Cause

Cardiovascular
Extreme tachycardia with S3 sound, sinus arrhythmia, Compensatory attempt by sympathetic
and atrial fibrillation with rapid ventricular response nervous system to maintain CO
Profound hypotension Decreased stroke volume. Diastolic BP
may remain high because of
vasoconstriction
CO <4 L/min, CI <2.5 L/min/m2 Failure of compensatory mechanisms
PAWP usually >12 mm Hg Increased left ventricular end-diastolic
pressure because of increased residual
volume from decreased stroke volume
SVR >1200 dynes/sec/cm-5 Vasoconstriction
Weak or absent peripheral pulses Decreased peripheral perfusion because
of decreased CO
Svo2 <60% Decreased oxygen binding to

2121
 hemoglobin because of acidosis
Respiratory
Increased >30 breaths/min (even at late stage) or Metabolic acidosis and acute lung
decreased respiratory rate <12 breaths/min injury lead to tachypnea; whereas,
central respiratory center depression
can cause hypopnea

Decreased respiratory rate (< 12 breaths/min) and Central respiratory center depression
depth
Crackles, rhonchi, wheezes Accumulation of lung secretions
Increased Fio2 required to maintain Pao2 (possible Ventilation/perfusion mismatch and
ARDS) decreased lung compliance
Renal
Decreased urine output progressing to anuria Decreased renal perfusion and tubular
ischemia
Low urinary excretion of sodium, with possibly Activation of the aldosterone
decreased fractional excretion of sodium; if patient mechanism and release of ADH, which
develops acute tubular necrosis, sodium excretion stimulate sodium and water retention
typically increases.
Cutaneous
Cool, pale skin or cyanosis Sustained vasoconstriction
Neurologic
Decreased LOC, coma Severe hypoxia and metabolic
derangements leading to reversible
encephalopathy
Hematologic
Oozing from previous venipuncture sites Development of DIC caused by
stimulation of coagulation process, and
fibrinolysis
Acid-Base Status
pH <7.35; Mixed acid-base disorder: respiratory
Paco2 >45 mm Hg, HCO3 <22 mEq/L (or less than acidosis and metabolic acidosis
expected)
ARDS, Acute respiratory distress syndrome; ADH, antidiuretic hormone; BP, blood
pressure; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; DIC,
disseminated intravascular coagulation; LOC, level of consciousness; PAWP,
pulmonary artery wedge pressure; SVR, systemic vascular resistance.

Observation and other assessment findings

• Early signs reflective of systemic inflammatory response
syndrome and sepsis: Anxiety, continuous agitation, discomfort
in excess of condition. Vasodilation may create a “healthy”
flushed appearance of the skin, which may be warm or hot to
touch.

• Signs of severe sepsis, septic shock, and multiorgan dysfunction

syndrome: Flushed skin that changes to pallor; edema of face,
neck, torso, sacrum, and extremities; deteriorating length of

2122
 consciousness with possible obtundation or unresponsiveness as
cerebral perfusion is failing; rales caused by heart failure;
respiratory failure requiring endotracheal intubation and
mechanical ventilation; oliguria; diminished bowel sounds; and
diminished peripheral pulses. Vasodilation may maintain warm-
to-hot skin until the patient totally decompensates with cool-to-
cold, clammy skin.

Diagnostic Tests for SIRS, Sepsis, Severe Sepsis, Septic Shock

and MODS

2123
Collaborative management
Care priorities
Early recognition and therapy are still the cornerstones of acute care
of the septic patient. The advent of new technologies and
biomolecular testing should improve survival rates and give rise to
more accurate incidence statistics. The treatment of severe sepsis
and septic shock is an evolving process, and the guidelines continue
to be updated. Reduction of septic inflammation may involve
several pharmacologic therapies and adjunct therapies.
Management of sepsis and septic shock includes respiratory
support, aggressive fluid resuscitation, inotropic support,
vasopressor therapy, and early antibiotic therapy. In the future less
invasive methods of optimizing a patient’s fluid status and
hemodynamics, along with monitoring the microcirculatory
dysfunction common in sepsis, may become more routine.
There are several models available to simplify the identification
process. The use of standardized order sets for the management of
sepsis should be recommended strongly for better performance in
treatment. Standard order sets use serum lactate values because of
their relationship to organ dysfunction in sepsis. To reduce
mortality rates, sepsis must be identified and treated as early as
possible.
Summary of immediate steps: Identify the patient and engage in
collaborative practices to begin treatment. Delays in patient
identification are often directly related to the nurse’s ability to have
the appropriate conversation with colleagues on the factors present
that are indicative of sepsis. Nurses are crucial to successful patient
identification. Broad-spectrum antibiotics are initiated immediately;
ideally, after blood cultures are drawn to provide therapy within 1
hour in the setting of severe sepsis, with or without septic shock.
Imaging should be done as soon as possible; ideally during the first
hour to try to identify and/or confirm the source of infection so
necessary steps can be initiated as soon as possible to manage the
source. It is crucial to provide aggressive resuscitation within the
first 6 hours of diagnosis. As noted, blood cultures should be
obtained within 1 hour of recognition, before initiating antibiotics if
possible, but delaying antibiotics in lieu of cultures is unacceptable.

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Large-bore IV access should be secured in preparation for large
volume fluid resuscitation, which should be initiated as soon as
possible within the first hour of patient identification. Vasopressor
therapy with norepinephrine is used to stabilize the patient.

1. Manage the infection immediately, regardless of the

ability to obtain blood cultures within 1 hour
Getting broad-spectrum antibiotics on board promptly has been
shown to be as important a priority as fluid resuscitation. Delaying
therapy could mean the difference between a good and a poor
outcome. Once under way, an institution’s antibiotic steward, i.e., a
knowledgeable physician or clinical pharmacist (PharmD), should
be consulted to manage ongoing therapy. Initial antibiotic therapy
should not be continued indefinitely. Antibiotics should be
administered within 1 hour of the patient presenting with severe
sepsis or septic shock and reevaluated daily for appropriateness
and need to continue.

2. Manage hypovolemia with intravenous isotonic fluids

IV volume expansion is implemented to maintain adequate
ventricular filling pressures and volume, which are compromised
by increased capillary permeability and vasodilation. Fluid
resuscitation with crystalloids is the preferred fluid replacement
strategy. Colloids, such as albumin, may be initiated in patients
requiring a large volume of crystalloid to maintain an acceptable
MAP., Adding albumin has not been demonstrated to sustain the
MAP, but rather provides a temporary enhancement in certain
patients. Hetastarch solutions should be avoided. Current
guidelines recommend use of packed red blood cell transfusion and
dobutamine drip if SVO2 remains 70% after initial fluid
resuscitation. The initial fluid challenge should be at least 30 mL/kg
of crystalloids. Patients with suspected severe hypovolemia
resulting in hypoperfusion may require more rapid administration
and a larger volume of fluids. The fluid challenge may be continued
as long as required to improve hemodynamics. Crystalloid solution
such as lactated Ringer or normal saline can be used. Colloids may
include albumin and fresh-frozen plasma.

2125
3. Use early goal-directed therapy to prevent or slow patient
progression to multiorgan dysfunction syndrome and
multiple organ failure
According to current ACCP/SCCM guidelines, the following are
points of early goal-directed therapy:

• Immediate fluid resuscitation should be performed if not

already done. The goal is to infuse no less than 1 L, or 20 mL/kg,
via fluid bolus if tolerated. The rate of fluid infusion should be
reduced if filling pressures rise without improvement in overall
circulation

• Determining the optimal preload level in sepsis is challenging. A

patient who is not considered fluid responsive may be potentially
harmed by aggressive fluid resuscitation. In fact, in patients who
are not fluid responsive, the volume may exacerbate ARDS, acute
kidney injury, and IAH. Traditionally, CVP and/or PAP
monitoring were the methods upon which volume resuscitation
was based. Recent evidence, however, negates the value of the
CVP (and the PAP) end point, with results indicating that fluid
management utilizing CVP-targeted resuscitation significantly
contributes to morbidity and mortality. Newer methods to
evaluate fluid responsiveness, including systolic pressure
variation, stroke volume variation, and passive leg raise
techniques, are becoming more widely utilized.

• All blood for labwork for the sepsis profile (serum lactate, blood
culture, biomedical profile, CBC with differential, coagulation
profile, and biomarkers such as presence of TNF, IL-6, or
procalcitonin if available) should be drawn and then repeated
every 2 to 4 hours initially to assess for progress.

• Vasopressors are administered for MAP less than 65 mm Hg

during fluid resuscitation and after adequate fluid resuscitation.
Vasopressors of choice are norepinephrine, epinephrine, and
vasopressin. They may be given to augment cardiac contractility
and CO. In the late stages of sepsis, positive inotropic drugs may
be given with vasodilators such as nitroprusside and
nitroglycerin, which decrease preload and afterload by dilating

2126
 veins and arteries, to assist in the management of terminal heart
failure. Given that both vasodilation and vasoconstriction are
present throughout the circulation, it is difficult to predict the
most effective strategy for support of circulation. Some
institutions may use noncatecholamine inodilator medications
such as milrinone to provide inotropic support as well as to
decrease resistance to ventricular ejection.

11-4
RESEARCH BRIEF
An increased circulating NT-pro-B-type natriuretic peptide plasma
level is an independent marker of greater systolic cardiac
dysfunction and a better predictor of fluid nonresponsiveness in
septic versus nonseptic critically ill patients.
Turner KL, Moore LJ, Todd SR, et al: Identification of cardiac dysfunction in sepsis with B-
type natriuretic peptide. J Am Coll Surg 213:139-146, 2011.

4. If early resuscitation fails, or the patient presents in

septic shock or multiorgan dysfunction syndrome, the
second group of therapies is instituted in conjunction with
or immediately following early goal-directed therapy

• Support ventilation and oxygenation if patient develops acute

respiratory distress syndrome. Mechanical ventilation: Intubate
and place on low tidal volume, pressure-controlled ventilation if
high-flow oxygen or noninvasive positive pressure ventilation
fails to stabilize ventilation. If on volume control ventilation,
plateau pressure should be on average less than 30 cm H2O for
ventilated patients. Lung-protective ventilation with low tidal
volume (6 to 8 mL/kg of ideal body weight) is recommended.
Assist control volume- or pressure-controlled ventilation may be
initiated (see Mechanical Ventilation, Chapter 1).

• Maintain the Blood Pressure. Vasopressors (e.g., norepinephrine,

vasopressin, phenylephrine, epinephrine): May be administered
in cases when optimal left ventricular preload fails to restore

2127
 adequate tissue perfusion (i.e., the initial MAP is very low or
MAP is persistently less than 60 mm Hg). If norepinephrine is
ineffective, phenylephrine, vasopressin, and high-dose
epinephrine may be used. The goal of therapy is to optimize
cardiac index by providing a balance among promoting venous
return, augmenting cardiac contractility, and creating the ideal
level of resistance to ventricular ejection.

• Consider corticosteroids. In stress situations, the normal adrenal

gland output of cortisol is approximately 250 to 300 mg over 24
hours. Use of corticosteroids remains controversial. IV
hydrocortisone should be given only to adult septic shock
patients after it has been confirmed that their BP is poorly
responsive to fluid resuscitation and vasopressor therapy and
cortisol levels are low. Most important, all patients on chronic
steroid re placement, such as those with rheumatoid arthritis
taking daily prednisone, have to receive high doses of IV steroids
while in shock. Corticosteroids also help to control inflammation
(see Acute Adrenal Insufficiency (Adrenal Crisis), Chapter 8).
Their use, however, remains controversial.

• Administer 100 mg of hydrocortisone in an IV

bolus, regardless of cortisol level, if the patient’s BP
is not responding to fluid volume resuscitation and
vasopressor therapy, followed by a continuous
infusion of 300 mg in 100 to 250 mL of isotonic
sodium chloride solution by continuous IV infusion
over 24 hours. Information regarding efficacy of
steroids in the setting of sepsis is almost equally
divided (pro and con) in the literature. A trial of
hydrocortisone is warranted if all other measures
have failed.

• An alternative method of hydrocortisone

administration is 50 mg as an IV bolus every 6

2128
 hours.

• The infusion method maintains plasma cortisol

levels more adequately at steady stress levels,
especially in the small percentage of patients who
are rapid metabolizers and who may have low
plasma cortisol levels between the IV boluses.

Treat the problems

• Provide antibiotics to control infection: Broad-spectrum antibiotic

coverage for sepsis (often directed at gram-negative sepsis)
should be initiated before identifying a specific microorganism if
patients exhibit physiologic changes and positive signs and
symptoms. Samples for culturing should be obtained before
initiating antibiotics, unless doing so would considerably delay
treatment. Obtain at least two blood samples for cultures, one
percutaneously and another through invasive IV lines that have
been in place more than 48 hours before antibiotic administration.
Timely administration of appropriate antibiotics is critical to
patient outcome. Choice of antimicrobial depends on the organ
and organisms involved. Physicians and midlevel practitioners
will prescribe ceftriaxone, zithromycin, or levofloxacin for severe
community-acquired pneumonia; whereas hospital-acquired
pneumonia may need to be treated with broader-spectrum
antibiotics that cover drug-resistant pathogens. Such antibiotics
may include ceftazidime, meropenem, vancomycin, and
aminoglycosides. The effectiveness of the antibiotics should be
reevaluated daily and use should be anticipated for 7 to 10 days.
Use of the fewest possible antibiotics reduces the possibility of
development of a superinfection with an opportunistic organism
including fungus (Candida), infection with a resistant organism
(MRSA, VRE), or Clostridium difficile-Associated Diarrhea.
Treatment of infection helps control the inflammatory response.

2129
• Control the source of the infection: Other methods for controlling
the source of infection should be weighed carefully for risks and
benefits. Identifying the source of infection is critical. Localizing
and draining an abscess, removing new pleural fluid collections,
and discontinuing infected indwelling catheters are keys to better
outcomes.

• Other pharmaceutical agents: For many years, researchers and

clinicians have been looking for a miracle medication that will
stop the vicious cycle of events that occurs in severe sepsis and
leads to MODS. Unfortunately, many of the medications, such as
the anti-TNF medications, only affected one of many major
cascades involved. Recombinant human activated protein C
(Xigris), which had been shown to reduce mortality in patients
with an APACHE II score greater than 25 or at high risk of dying
from sepsis, was subsequently disproven as an effective agent for
widespread use. It is no longer available. Absolute
contraindications have always been related to the high risk of
bleeding.

• Control blood glucose: Use IV insulin therapy to keep blood

glucose below 180 mg/dL, with a target of 150 mg/dL. Use of
intensive insulin therapy to lower blood glucose to 80 to 110
mg/dL is no longer recommended, as septic shock patients often
become hypoglycemic. (See Hyperglycemia, Chapter 8).

• Provide nutrition support: Current SCCM recommendations for

enteral feedings/nutrition support in the critically ill include
short- and medium-chain fatty acids and branched-chain amino
acids administered to stop protein catabolism. The short- and
medium-chain fatty acids are absorbed more readily and
metabolized more easily than long-chain fatty acids. They may be
given orally (e.g., MCT Oil, which is a proprietary name for
triglycerides of medium-chain fatty acids), as part of enteral
feeding, or via the IV route (e.g., intralipid solutions). Branched-
chain amino acid solutions are used in sepsis, as they are
metabolized by muscle rather than the liver and can therefore be
used in the presence of organ failure. (See Nutrition Support,
Chapter 1).

2130
Care plans for systemic inflammatory
response syndrome, sepsis, and multiorgan
dysfunction syndrome
Deficient fluid volume 
related to active loss from vascular compartment secondary to increased
capillary permeability and shift of intravascular volume into interstitial
spaces and relative hypovolemia resulting from vasodilation.
Goals/Outcomes: Within 4 hours of initiation of therapy, the
patient is normovolemic as evidenced by peripheral pulses greater
than 2+ on a 0 to 4+ scale, stable body weight, urine output 0.5
mL/kg/h or greater, mean BP 60 mm Hg or greater (or within
patient’s normal range), sustained systolic BP 90 mm Hg or greater
(or within patient’s normal range), and absence of edema and
adventitious lung sounds. SVI is 30 to 40 mL/min /m3, SVV is less
than 15%, and ScVO2 or SVO2 is 60% to 80%.
Fluid Balance; Electrolyte and Acid-Base Balance

Hemodynamic regulation

1. Monitor hemodynamic pressures, using noninvasive or invasive

methods to assess CO, SVI, and SVV if available. If a pulmonary
artery catheter is used, PAWP, CO, and SVR are measured. During
the early stage of sepsis, filling pressures (PAWP and CVP) may be
normal to low, but as biventricular dysfunction occurs, these
pressures may increase. If the patient manifests a compensatory
increase in CO, the calculated SVR may initially be low, but the
calculated value may rise as the CO drops.

2. Initiate early goal-directed therapy to support the CO and BP as

prescribed, including IV fluids and positive inotropic agents.
Vasopressors are used if inotropic agents and fluid resuscitation fail
to stabilize BP (see Collaborative Management, Chapter 11). Fluid
replacement therapy is given to maintain a CVP of 2-12 mm Hg or
PAWP of 6 to 12 mm Hg. Assess CVP and/or PAWP and lung
sounds at frequent intervals during fluid replacement to detect
evidence of fluid overload: crackles, wheezing, and increasing CVP

2131
and/or PAWP. Current literature does not support the routine
use of pulmonary artery pressures in lieu of SVO2 and ScVO2 when
managing septic patients, given challenges associated with cellular
oxygenation, which are not reflected unless technology reflective of
oxygen delivery, demand, and consumption is used.

3. Assess fluid volume by monitoring BP, peripheral pulses, and

urine output hourly. Report failure of early goal-directed therapy to
stabilize mean BP to greater than 60 mm Hg or sustained systolic
BP to 90 mm Hg or greater or within patient’s normal range. Weigh
the patient daily; monitor I&O every shift, noting 24-hour trends.
Report urine output less than 0.5 mL/kg/h. The patient’s weight
may actually increase with fluid volume deficit because of a shift of
intravascular volume into interstitial spaces.

4. Assess for interstitial edema as evidenced by pretibial, sacral,

ankle, and hand edema, as well as crackles on auscultation of lung
fields.

5. Position the patient supine with the legs elevated to increase

venous return and preload.

Fluid/Electrolyte Management; Hypovolemia Management;

Fluid Management; Shock Management: Volume

Decreased cardiac output 

related to negative inotropic changes in the heart (late stage) secondary to
effects of tissue hypoxia, worsening during late septic shock.
Goals/Outcomes: Within 8 hours of initiation of therapy, the
patient has improved CO as evidenced by peripheral pulses greater
than 2+on a 0 to 4+ scale, stable body weight, urine output 0.5
mL/kg/h or greater, mean BP 60 mm Hg or greater (or within
patient’s normal range), sustained systolic BP 90 mm Hg or greater
(or within patient’s normal range), and absence of edema and
adventitious lung sounds. CVP is 2-12 mm Hg (add 3 mm Hg to
normal if the patient is on positive pressure ventilation), PAWP is 6
to 12 mm Hg, CO is 4 to 7 L/min, CI is greater than 2.5 L/min/m2,
and calculated SVR is 900 to 1200 dynes/sec/cm–5. SVI is 30 to 40

2132
mL/min/m3, SVV is less than 15%, and ScVO2 or SVO2 is 60% to 80%.
Cardiac Pump Effectiveness; Circulation Status

Cardiac care: Acute

1. Assess the patient for signs of decreased CO: decreasing BP,

increasing HR, decreasing amplitude of peripheral pulses,
restlessness, decreasing urinary output, and increasing PAWP.

2. Administer positive inotropic agents (e.g., dobutamine) as

prescribed to augment cardiac contractility.

3. If continuous or intermittent CO monitoring is not in place,

assess CVP at least every 4 hours. Observe for development of
premature ventricular complexes, which may occur with hypoxia,
and extreme tachycardia. Dysrhythmias and hypoxia may further
reduce CO.

4. Monitor ScVO2 or SVO2 continuously; report values outside

normal range.

Hemodynamic Regulation; Invasive Hemodynamic

Monitoring; Fluid/Electrolyte Management

Ineffective tissue perfusion: Cerebral, renal, and

gastrointestinal 
related to hypovolemia secondary to mixed vasodilation and constriction
interruption of arterial and venous blood flow secondary to
vasoconstriction and thrombus obstruction.
Goals/Outcomes: Within 24 hours of initiating therapy, the
patient has improved perfusion as evidenced by orientation to time,
place, and person; peripheral pulses greater than 2+on a 0 to 4+
scale, stable body weight, urine output 0.5 mL/kg/h or greater,
mean BP 60 mm Hg or greater (or within patient’s normal range),
sustained systolic BP 90 mm Hg or greater (or within patient’s
normal range), and absence of edema and adventitious lung
sounds. CVP is 2-12 mm Hg (add 3 mm Hg to normal if the patient
is on positive pressure ventilation), PAWP is 6 to 12 mm Hg, CO is
4 to 7 L/min, CI greater than 2.5 L/min/m2, and calculated SVR is

2133
900 to 1200 dynes/sec/cm–5. SVI is 30 to 40 mL/min/m3, SVV is less
than 15%, and ScVO2 or SVO2 is 60% to 80%.
Circulation Status

Circulatory precautions

1. Assess for changes in length of consciousness as an indicator of

decreasing cerebral perfusion.

2. Assess for the following signs of decreasing renal perfusion:

urine output less than 0.5 mL/kg/h and increased BUN, serum
creatinine, and serum potassium levels.

• Monitor arterial BP continuously for signs of

deteriorating circulatory status related to cardiac
failure or hypovolemia. Systolic BP will be
decreased because of decreased CO, and the
diastolic BP may be low secondary to vasodilation
or normal to high secondary to compensatory
vasoconstriction.

• Assess peripheral pulses, temperature, color of skin,

and capillary refill. With hypoperfusion, pulse
amplitude decreases, extremities are cool because of
vasoconstriction, skin color is pale or mottled
because of decreased perfusion, and capillary refill
is delayed.

3. Monitor cellular oxygen consumption (V.O2) as an indicator of

tissue perfusion. With sepsis, cellular oxygen delivery is decreased
(precapillary vasoconstriction), and thus cellular oxygen use is
decreased. Mixed venous blood oxygen saturation (SVO2) is
elevated.

4. Administer vasoactive drugs as prescribed. CVP monitoring

2134
using a centrally placed central line or peripherally inserted line is a
good alternative. The goal range is CVP of 2 to 6 mm Hg (add 3 mm
Hg when positive pressure ventilation is used). Pulmonary artery
catheters are associated with high risk and are not used as often for
management of septic patients. When in place, SVR and CO can be
assessed to determine drug effects. Optimally, SVR will increase to
at least 900 dynes/sec/cm-5, CO will be 4 to 7 L/min, and CI will be
2.5 to 4 L/min/m2. Fluid boluses are administered rapidly to obtain
the goal.

5. Assess for evidence of decreasing splanchnic (visceral)

circulation, including decreased or absent bowel sounds, elevated
serum amylase level, and decreased platelet count.

Cerebral Perfusion Promotion; Circulatory Care;

Fluid/Electrolyte Management; Oxygen Therapy; Hemodynamic
Regulation; Shock Management; Nutrition Management;
Hemodialysis Therapy

Impaired gas exchange 

related to alveolar-capillary membrane changes secondary to interstitial
edema, alveolar destruction, and endotoxin release with activation of
histamine and kinins.
Goals/Outcomes: Within 4 hours of initiation of therapy, the
patient’s PaO2 is greater than 80 mm Hg, Paco2 is less than 45 mm
Hg, pH is 7.35 to 7.45, and lungs are clear.
Respiratory Status: Gas Exchange; Electrolyte and Acid-Base
Balance

Ventilation assistance

1. Assess for and maintain a patent airway by assisting patient with

coughing or by suctioning the trachea as necessary.

2. Assess all ABG values. Be alert to decreasing PaO2, increasing

Paco2, and acidosis (decreasing pH). Monitor the patient for the
presence of dyspnea, hypopnea, and restlessness.

3. Listen to breath sounds hourly and with each change in the

2135
patient’s condition. The presence of crackles may indicate fluid
accumulation.

4. If the patient exhibits evidence of inadequate gas exchange (e.g.,

PaO2 less than 60 mm Hg while the patient is on 100% oxygen via
nonrebreather mask) but mental status remains stable, attempt
NPPV. If NPPV fails, prepare for the probability of endotracheal
intubation.

5. If the patient has been placed on mechanical ventilation, monitor

inspiratory peak and plateau pressures for increasing trends, which
may signal decreasing compliance and development of ARDS. As
ARDS develops, an increasing Fio2 (at least 0.50) and increasing
levels of PEEP are required to maintain adequate PaO2 (at least 60
mm Hg) (see Acute Respiratory Distress Syndrome, Chapter 4, and
Mechanical Ventilation, Chapter 1).

6. Monitor end-tidal CO2 trends for changes indicative of

development of ARDS, hypoperfusion, and misplacement of the
endotracheal tube.

7. Turn the patient every 2 hours to maintain optimal ventilation-

perfusion ratios and to prevent atelectasis.

Acid-Base Management: Metabolic Acidosis; Oxygen

Therapy; Respiratory Monitoring; Artificial Airway Management;
Invasive Hemodynamic Regulation

Ineffective breathing pattern 

related to decreased lung expansion secondary to central respiratory
depression occurring in late shock.
Goals/Outcomes: Within 2 hours of initiating respiratory
support, the patient has an effective breathing pattern as evidenced
by normal limits of inspiratory:expiratory ratio (1:1 to 1:2); tidal
volume (at least 6 mL/kg); and maximal inspiratory pressures (less
than 20 cm H2O).
Respiratory Status: Ventilation

2136
Respiratory monitoring

1. Monitor for decreasing respiratory rate, depth, and air

movement. Ensure the patient demonstrates adequate air
movement by noting presence of breath sounds over all lung fields.

2. Assist the patient into a comfortable position to facilitate

respirations. Depending on patient’s hemodynamic stability, the
optimal position may be a 15 to 30 degrees head of the bed
elevation.

3. Assess/measure tidal volume and inspiratory force. Be alert to

tidal volume less than 4 mL/kg and inspiratory force less than 20
cm H2O as indicators of an ineffective breathing pattern.

4. If the patient exhibits respiratory depression/ineffective breathing

pattern, prepare for the probability of endotracheal intubation. (See
Acute Respiratory Failure, Chapter 4.)

Oxygen Therapy; Mechanical Ventilation

Ineffective thermoregulation 
related to illness with concomitant endotoxin effect on hypothalamic
temperature-regulating center.
Goals/Outcomes: Within 24 hours of initiation of treatment, the
patient becomes normothermic.
Thermoregulation

Temperature regulation

1. Monitor patient’s temperature continuously or at frequent

intervals. Use temperature probe (rectal, bladder, or esophageal) for
continuous monitoring of core temperature. Body temperature can
range from 38.3° to 40.6° C (101° to 105° F) in the early stage of
sepsis and can be less than 35.6° C (96° F) in the late stage. Patients
with immunodeficient states on chronic or high-dose steroid
therapy may have a normal or low temperature. Be alert to shaking
chills early in sepsis as temperature increases and to profuse chills
as temperature decreases late in sepsis. Temperatures up to 103°F

2137
may be allowed in the septic patient, as increased temperature may
help control bacteremia. The following are weighed for each patient
to determine the extent of treatment that should be used to decrease
fever (e.g., acetaminophen administration):

• Useful effects of a fever: decreased viral and

bacterial replication

• Harmful effects of a fever: increased cardiac

workload and increased oxygen consumption
2. Administer antimicrobials as prescribed. Discuss appropriate
antibiotic therapy. Observe for untoward effects, including renal
toxicity, ototoxicity, allergic reactions, anaphylaxis,
pseudomembranous colitis (C. difficile-associated diarrhea),
overgrowth of normal flora, and superimposed infectious processes
of the skin, urinary tract, or respiratory tract. Large doses of
antibiotics may cause the release of endotoxins from dying bacteria,
which may potentiate the progression of septic shock.

3. Administer antipyretic agents as prescribed.

4. For patients with hyperthermia, use tepid baths, which decrease

body temperature by releasing internal heat. Cooled IV fluids also
may decrease core temperature. In addition, a cooling blanket may
be prescribed to reduce the metabolic rate, thereby decreasing
myocardial oxygen demand. Avoid “chilling,” which will cause
shivering and thus increase myocardial oxygen demand and
cardiac workload.

5. In the presence of hypothermia, use warm blankets to increase

body temperature. Heating devices can damage ischemic cells in
peripheral tissues and usually are avoided.

Fever Treatment; Temperature Regulation; Environmental

Management

Imbalanced nutrition: Less than body requirements 

2138
related to increased need secondary to increased metabolic rate.
Goals/Outcomes: Within 48 hours of initiation of treatment, the
patient has adequate nutrition as evidenced by stable weight, serum
albumin 3.5 g/dL, prealbumin 20 to 30 mg/dL, retinol-binding
protein 4 to 5 mg/dL, urine urea nitrogen 10 to 20 mg/dL, and a
state of nitrogen balance as determined by nitrogen studies.
Nutritional Status

Nutrition management

1. Monitor laboratory findings for serum albumin, prealbumin,

retinol-binding protein, and nitrogen studies.

2. Administer nutritional supplements as prescribed.

3. Assess and record weight and nutritional intake daily. Consult

with nutritional services for calorie count.

4. Observe for and document areas of tissue breakdown, which may

indicate a negative nitrogen state.

5. If the patient is receiving oral feedings, assess for the presence of

bowel sounds at least every 8 hours. Paralytic ileus can occur
secondary to an ischemic bowel.

6. If the patient is receiving continuous gastric tube feedings, assess

for residual feeding at least every 4 hours. (See Nutrition Support,
Chapter 1.)

• Enteral feedings are recommended whenever

possible, and the choice of feeding formula is
determined based on the individual patient.
However, formulas with supplemental omega-3
fatty acids such as gamma-linoleic acid and
eicosapentaenoic acid are recommended. Total
parenteral nutrition is administered to patients
unable to tolerate enteral feedings. Standard total

2139
 parenteral nutrition solutions are not metabolized
well in the septic state. Branched-chain amino acid
solutions and short-to medium-chain fatty acid
solutions may be used (e.g., MCT Oil or FreAmine
HBC).

TPN Administration; Enteral Tube Feeding

Additional nursing diagnoses

Also see nursing diagnoses and interventions in Hemodynamic
Monitoring Chapter 1), Acute Lung Injury and Acute Respiratory
Distress Syndrome (Chapter 4), Emotional and Spiritual Support of
the Patient and Significant Others (Chapter 2), and Bleeding and
Thrombotic Disorders: Disseminated Intravascular Coagulation
(Chapter 10).

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APPENDIX 1. Heart and breath sounds
ASSESSING HEART SOUNDS

A, Aortic; ICS, intercostal space; LSB, left sternal border; M, mitral; MI, myocardial
infarction; P, pulmonic; RSB, right sternal border; T, tricuspid.

COMMONLY OCCURRING HEART MURMURS

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ICS, Intercostal space; LSB, left sternal border; MCL, midclavicular line; RSB, right
sternal border.

ASSESSING NORMAL BREATH SOUNDS

I, Inspiration; E, expiration.

ASSESSING ADVENTITIOUS BREATH SOUNDS

COPD, Chronic obstructive pulmonary disease.

ASSESSING RESPIRATORY PATTERNS

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CNS, Central nervous system; DKA, diabetic ketoacidosis; IICP, increased
intracranial pressure; MODS, multiple organ dysfunction syndrome; SIRS, systemic
inflammatory response syndrome.

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APPENDIX 2. Glasgow coma scale

2156
APPENDIX 3. Cranial nerves: Assessment
and dysfunctions

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APPENDIX 4. Major deep tendon (muscle-
stretch) reflexes

GRADING OF DEEP TENDON REFLEXES

Scale (0 to
Interpretation
4+)
4+ Very brisk, hyperactive, repetitive, rhythmic flexion and extension (clonus);
indicative of disease
3+ Brisker than average; may be normal for certain individuals or may indicate
disease.
2+ Average/normal
1+ Diminished response or low normal
0 No response

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APPENDIX 5. Major superficial
(cutaneous) reflexes

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APPENDIX 6. Inotropic and vasoactive
medication infusions

—, No effect; ↑or ↓ minimal effect; ↑↑or ↓↓, moderate effect; ↑↑↑ or ↓↓↓, major effect;
CO, cardiac output; HR, heart rate; IV, intravenous; PAOP, pulmonary artery
occlusive pressure; SVR, systemic vascular resistance.

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APPENDIX 7. Sample relaxation technique

Give the patient the following instructions:

1. Sit quietly in a comfortable position. Close your eyes.

2. Relax all your muscles, starting at your feet and progressing to

your facial muscles. Focus your attention on one body area at a time
while you relax the muscles in that area.

3. Breathe through your nose. As you breathe out, say the word
“one” silently to yourself. Become aware of your breathing.
Continue this process for about 20 minutes.

4. Do not worry whether or not you are achieving deep relaxation.

Maintain a passive attitude and permit relaxation to occur at its
own pace. If distractions interfere, see your thoughts floating away
like clouds. Continue breathing and repeating the word “one.”

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APPENDIX 8. Abbreviations used in this
manual

A—aortic valve

AACN—American Association of Critical Care Nurses

AAL—anterior axillary line

ABA—American Burn Association

ABG—arterial blood gas

ACC—American College of Cardiology

ACCP—American College of Chest Physicians

ACE—angiotensin-converting enzyme

ACh—acetylcholine

AChR—acetylcholine receptor

ACLS—advanced cardiac life support

ACS—abdominal compartment syndrome

ACT—activated clotting time

AD—autonomic dysreflexia

ADA—American Diabetes Association

ADH—antidiuretic hormone

ADL—activity of daily living

AED—automatic external defibrillator

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AEG—atrial electrogram

AF—atrial fibrillation

AHA—American Heart Association

AIDS—acquired immunodeficiency syndrome

AIS—acute ischemic stroke

ALI—acute lung injury

ALP—alkaline phosphatase

ALT—alanine aminotransferase

AM—akinetic mutism

AMA—American Medical Association

AMI—acute myocardial infarction

ANA—American Nurses Association

ANP—atrial natriuretic peptide

APAS—antiphospholipid antibody syndrome

APSAC—anisoylated plasminogen streptokinase activator complex

aPTT—activated partial thromboplastin time

ARDS—acute respiratory distress syndrome

ARF—acute respiratory failure; acute renal failure

ARS—adjective rating scale

ASA—acetylsalicylic acid (aspirin)

ASO—antistreptolysin O

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AST—aspartate aminotransferase

AT—antithrombin

AT1—receptor antagonist

ATGAM—antithymocyte gamma globulin

atm—atmosphere (standard)

ATN—acute tubular necrosis

ATP—adenosine triphosphate

AV—atrioventricular; arteriovenous

AVM—arteriovenous malformation

AVNRT—atrial-ventricular nonreciprocating tachycardia

AVRT—atrial-ventricular reciprocating tachycardia

BAL—bronchoalveolar lavage

BEE—basal energy expenditure

BG—blood glucose

BIS—bispectral index

BMI—body mass index

BP—blood pressure

bpm—beats per minute

BS—bowel sounds

BSA—body surface area

BUN—blood urea nitrogen

2164
C—centigrade; Celsius

Ca2+—calcium

CABG—coronary artery bypass grafting

CAD—coronary artery disease

CAPD—continuous ambulatory peritoneal dialysis

CASHD—coronary atherosclerotic heart disease

CAVH—continuous arteriovenous hemofiltration

CBC—complete blood cell count

CBF—cerebral blood flow

CD—Cotrel-Dubousset

CDC—Centers for Disease Control and Prevention

CDI—central diabetes insipidus

CHF—congestive heart failure

CI—cardiac index

CIE—counterimmunoelectrophoresis

CJD—Creutzfeldt-Jakob disease

CK—creatine kinase

Cl—chloride

CK-MB—creatine kinase–myocardial band

CM—cardiomyopathy

CMV—cytomegalovirus; controlled mechanical ventilation

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CNS—central nervous system

CO—cardiac output; carbon monoxide

CO2—carbon dioxide

COPD—chronic obstructive pulmonary disease

CPAP—continuous positive airway pressure

CPK—creatine phosphokinase

CPP—cerebral perfusion pressure; coronary perfusion pressure

CRRT—continuous renal replacement therapy

CRT—cardiac resynchronization therapy

C&S—culture and sensitivities

CSF—cerebrospinal fluid

CT—computed tomography

cTnI—cardiac troponin I

CVA—cerebrovascular accident; costovertebral angle

CVC—central venous catheter

CVP—central venous pressure

CVVH—continuous venovenous hemofiltration

CVVHD—continuous venovenous hemofiltration with dialysis

CVVHDF—continuous venovenous hemodiafiltration

CXR—chest radiograph

CyA—cyclosporine

2166
DAI—diffuse axonal injury

DCM—dilated cardiomyopathy

DFI—diffusion-weighted imaging (or DWI)

DI—diabetes insipidus

DIC—disseminated intravascular coagulation

DKA—diabetic ketoacidosis

DM—diabetes mellitus

DNR—do not resuscitate

Do2—oxygen delivery

DOE—dyspnea on exertion

DPAHC—durable power of attorney for health care

DPL—diagnostic peritoneal lavage

DTR—deep tendon reflex

DVT—deep vein thrombosis

EACA—epsilon-(e)aminocaproic acid

EBV—Epstein-Barr virus

ECG—electrocardiogram

ECHO—electrocardiography

EEG—electroencephalogram

EFA—Epilepsy Foundation of America

ELISA—enzyme-linked immunosorbent assay

2167
EMI—electromagnetic interference

EPS—electrophysiologic studies

ESR—erythrocyte sedimentation rate

ET—endotracheal

ETCO2—end-tidal carbon dioxide

ETOH—alcohol

ETT—endotracheal tube

F—Fahrenheit

FAST—focused assessment with sonography for trauma

FDP—fibrin degradation product

FEF—forced expiratory flow

FEV—forced expiratory volume

FHF—fulminant hepatic failure

Fio2—fraction of inspired oxygen

Fr—French

FRC—functional residual capacity

FSP—fibrin split product

FVC—forced vital capacity

GABA—gamma-(γ) aminobutyric acid

GBS—Guillain-Barré syndrome

GCS—Glasgow Coma Scale

2168
GERD—gastroesophageal reflux disease

GI—gastrointestinal

GKI—glucose-potassium-insulin

G6PD—glucose-6-phosphate dehydrogenase

GU—genitourinary

H2O—water

HAT—heparin-associated thrombocytopenia

HCM—hypertrophic cardiomyopathy

HCO32—bicarbonate

Hct—hematocrit

HDL—high-density lipoprotein

HELLP—hemolysis, elevated liver enzymes, low platelet count

Hgb—hemoglobin

HHS—hyperglycemic hyperosmolar syndrome

HITT—heparin-induced thrombocytopenia thrombosis

HIV—human immunodeficiency virus

HOB—head of bed

HPO4—phosphate

HR—heart rate

HRS—hepatorenal syndrome

HSV—herpes simplex virus

2169
HUS—hemolytic-uremic syndrome

HVPG—hepatic venous pressure gradient

HVWP—hepatic vein wedge pressure

IABP—intraaortic balloon pump

IAP—intraabdominal pressure

ICA—internal cerebral artery

ICD—implantable cardioverter-defibrillator

ICH—intracerebral hematoma

ICP—intracranial pressure

ICS—intercostal space

ICU—intensive care unit

IDDM—insulin dependent diabetes mellitus

IE—infective endocarditis

I/E—inspiration/expiration

IER—in expected range

IgG—immunoglobulin G

IHSS—idiopathic hypertrophic subaortic stenosis

IICP—increased intracranial pressure

IM—intramuscular

INR—international normalized ratio

I&O—intake and output

2170
IPD—intermittent peritoneal dialysis; intracranial pressure
dynamics

IPPB—intermittent positive-pressure breathing

IRV—inverse ratio ventilation

ITP—idiopathic thrombocytopenic purpura

IV—intravenous

IVP—intravenous pyelogram

JNC VII—Joint National Committee VII

JNC 8—Joint National Committee 8

JT—junctional tachycardia

JVD—jugular vein distention

K+—potassium

kcal—kilocalorie

KCl—potassium (K) chloride (Cl2)

kg—kilogram

KUB—kidney, ureter, bladder

L—liter; lumbar

LAD—left anterior descending (coronary artery)

LAP—left atrial pressure

LDH—lactate dehydrogenase; also abbreviated LD

LDL—low-density lipoprotein

LIS—locked-in-syndrome

2171
LMW—low molecular weight

LOC—level of consciousness

LOS—length of stay

LP—lumbar puncture

LR—lactated Ringer

LUQ—left upper quadrant

LUT—lower urinary tract

LV—left ventricular

LVEDP—left ventricular end-diastolic pressure

LVH—left ventricular hypertrophy

m—meter

M—mitral valve

MAP—mean arterial pressure

MCA—middle cerebral artery

MCL—modified chest lead; midclavicular line

MCS—minimally conscious state

MCT—medium-chain triglycerides

MCV—mean corpuscular volume

Mg2+—magnesium

MG—myasthenia gravis

mg—milligram

2172
MI—myocardial infarction

MODS—multiple organ dysfunction syndrome

mOsm—milliosmole

MPAP—mean pulmonary artery pressure; also abbreviated PAM

MRA—magnetic resonance arteriogram

MRI—magnetic resonance imaging

MS—multiple sclerosis

MSO4—morphine sulfate

MUGA scan—multiple-gated acquisition scan

Na/Na+—sodium

NaCl—sodium chloride/saline

NCV—nerve conduction velocity

NDI—nephrogenic diabetes insipidus

NIDDM—non-insulin dependent diabetes mellitus

NG—nasogastric

NHO—National Hospice Organization

nl—normal

NMBA—neuromuscular blocking agent(s)

NPO—nothing by mouth

NRS—numeric rating scale

NSAID—nonsteroidal antiinflammatory drug

2173
NSTEMI—non–ST-segment elevation myocardial infarction

NTG—nitroglycerin

nvCJD—new variant Creutzfeldt-Jakob disease

OT—occupational therapist

OTC—over-the-counter

P—pulmonic valve

PA—pulmonary artery

PAC—premature atrial complexes

Paco2—carbon dioxide (arterial pressure)

PAD—pulmonary artery diastolic

Pao2—oxygen (arterial pressure)

PAOP—pulmonary artery occlusive pressure

PAP—pulmonary artery pressure/positive airway pressure

PASG—pneumatic antishock garment

PAT—paroxysmal atrial tachycardia

PAW—pulmonary artery wedge

PAWP—pulmonary artery wedge pressure

PBV—percutaneous balloon valvuloplasty

PCA—patient-controlled analgesia

PE—pulmonary embolus

PEEP—positive end-expiratory pressure

2174
PEG—percutaneous endoscopic gastrostomy

PEJ—percutaneous endoscopic jejunostomy

PET—positron emission tomography

P/F—PaO2/FiO2 oxygen (arterial pressure) to fraction of inspired

oxygen ratio

PIH—pregnancy-induced hypertension

PJC—premature junctional complexes

PK—pyruvate kinase

PMI—point of maximal impulse

PN—parenteral nutrition

PND—paroxysmal nocturnal dyspnea

PO—by mouth

PO4—phosphates

PPF—plasma protein fraction

Pplat—plateau pressure

PRA—panel-reactive antibody

PRBCs—packed red blood cells

PSB—protected specimen brush

PSV—pressure support ventilation

PSVT—paroxysmal supraventricular tachycardia

PT—physical therapy; physical therapist; prothrombin time

2175
PTCA—percutaneous transluminal coronary angioplasty

PTH—parathyroid hormone

PTT—partial thromboplastin time

PVC—premature ventricular complex; peripheral venous catheter

PVR—pulmonary vascular resistance

PWI—perfusion-weighted imaging

RAP—right atrial pressure

RBC—red blood cell

RCM—restrictive cardiomyopathy

RDA—Recommended Daily Allowance; Recommended Dietary

Allowance

rHuEPO—recombinant human erythropoietin

RLA—Rancho Los Amigos

ROM—range of motion

RPE—rate perceived exertion

RR—respiratory rate

RRT—renal replacement therapy; registered respiratory therapist

rtPA—recombinant tissue plasminogen activator

RV—right ventricle; residual volume

RVP—right ventricular pressure

SA—status asthmaticus

SAH—subarachnoid hemorrhage

2176
SAS—subarachnoid space

SBP—systolic blood pressure

SCCM—Society of Critical Care Medicine

SCI—spinal cord injury

Scvo2—central venous oxygen saturation

SGOT—serum glutamic oxaloacetic acid transaminase

SGPT—serum glutamic pyruvic transaminase

SIADH—syndrome of inappropriate antidiuretic hormone

SIMV—synchronized intermittent mandatory ventilation

SIRS—systemic inflammatory response syndrome

Sjo2—jugular venous oxygen saturation

SOB—shortness of breath

Spo2—pulse oximetry oxygen saturation

SQ—subcutaneous; also abbreviated SC

SS—sensory stimulation

STEMI—ST-segment elevation myocardial infarction

Sto2—tissue oxygen saturation

STSG—split-thickness skin graft

SV—stroke volume

Svo2—mixed venous oxygen saturation

SVR—systemic vascular resistance

2177
T—tricuspid valve

TBSA—total body surface area

TCD—transcranial Doppler

TdP—torsades des pointe

TE—thrombotic emboli

TEA—tranexamic acid

TEC—transluminal extraction catheterization

TEE—total energy expenditure; transesophageal echocardiography

TENS—transcutaneous electrical nerve stimulation

TIA—transient ischemic attack

TIBC—total iron-binding capacity

TIPS/TIPSS—transjugular intrahepatic portal-systemic shunt

TMP—transmembrane pressure

TNA—total nutrient admixtures

TNF—tumor necrosis factor

TOF—train-of-four

TPA—tissue plasminogen activator

TPN—total parenteral nutrition

TSF—triceps skinfold thickness

UF—ultrafiltration

URI—upper respiratory infection

2178
UTI—urinary tract infection

VAD—venous access device; ventricular assist device

VAS—visual analog scale

VC—vital capacity

VCJD—variant (new) Creutzfeld-Jakob disease

VEDP—ventricular end-diastolic pressure

VF—ventricular fibrillation

VLDL—very-low-density lipoprotein

VMA—vanillylmandelic acid

Vo2—oxygen consumption

VS—vital signs/vegetative state

VSD—ventricular septal defect

VT—ventricular tachycardia

Vt—tidal volume

WBC—white blood cell

WNL—within normal limits

WPW—Wolff-Parkinson-White syndrome

2179
Index
Page numbers followed by “b” indicate boxes; “f, ” figures; “t, ”
tables.

A
A/C., See Assist-control ventilation (A/C, ACV).
Abdomen,

intrathoracic, 271–272
pelvic, 272
retroperitoneal, 272
trauma to, 271-284. See also Abdominal trauma.
true, 272
Abdominal compartment syndrome (ACS), 937–945

assessment of, 939–940

care plans for, 943–945
care priorities for, 942–943
collaborative management of, 942–943, 942b
definition of, 938–939

2180
diagnostic tests for, 941–942
with fluid volume deficit, care plan for, 943–944
history and risk factors for, 939
with ineffective tissue perfusion, care plan for, 944
with infection risk, care plan for, 945
observation in, 940
pathophysiology of, 937–939
prevention of, 942–943
risk factors for, 937
vital signs in, 940
Abdominal hypertension, 937–945

assessment of, 939–940

care plans for, 943–945
care priorities for, 942–943
collaborative management of, 942–943
diagnostic tests for, 941–942
with fluid volume deficit, care plan for, 943–944
history and risk factors for, 939
with ineffective tissue perfusion, care plan for, 944
with infection risk, care plan for, 945
observation in, 940
pathophysiology of, 937–939

2181
risk factors for, 937
vital signs in, 940
Abdominal trauma, 271–284

with acute pain, care plan for, 281

assessment of, 273–277
auscultation in, 275
blunt, 271
care plans for, 280–283
care priorities for, 277–280
collaborative management of, 277–280
with deficient fluid volume, care plan for, 280–281
diagnostic evaluation of, 276–277t
with disturbed body image, care plan for, 283
history and risk factors for, 273, 273b
with imbalanced nutrition, care plan for, 283
with impaired skin integrity, care plan for, 277–280
with ineffective tissue perfusion, care plan for, 282
inspection of, 274–275
observation in, 274
palpation in, 275
pathophysiology of, 271–272
penetrating,

2182
mechanisms of action of, 271–272
surgery for, 278–279
percussion in, 275–277
with risk for infection, care plan for, 281–282
subjective/objective symptoms in, 274
vital signs in, 273–274
ABG., See Arterial blood gas (ABG).
ABI., See Ankle-brachial index (ABI).
Abilify., See Aripiprazole (Abilify).
Accelerated junctional rhythm, 552f
Acetaminophen,

overdose of, 947

in pain management, 156–157
safety alert for, 160b
Acid-base imbalances, 1–25

arterial blood gas and, 4-8. See also Arterial blood gas
(ABG).
pathophysiology of, 1–3
pH regulation and, 2–3
Acid-base regulation, principles of, 1–3
Acid producers and regulators, 184t
Acidosis, 1, 7

cellular, 1
compensation for, 2

2183
metabolic, 15-16. See also Metabolic acidosis.
renal, 2
respiratory, 1, 8-10. See also Respiratory acidosis.
ACS., See Abdominal compartment syndrome (ACS); See Coronary
syndrome, acute (ACS).
Acute limb ischemia (ALI), 590–592

care priorities for, 603–604

management guidelines for, 599–601t
Acute respiratory distress syndrome (ARDS), 404-414. See
also Respiratory distress syndrome, acute (ARDS).
ACV., See Assist-control ventilation (A/C, ACV).
Acyclovir, 1001
Addison disease, 758
Addisonian crisis, 757. See also Adrenal crisis.
ADH., See Antidiuretic hormone (ADH).
Adrenal crisis, 757–765

assessment of, 759–761

care plans for, 763–765
care priorities for, 762–763
collaborative management of, 761–763
critical illness-induced, 758–759
with deficient knowledge, care plan for, 764–765
diagnostic tests for, 761t
with fluid volume deficiency, care plan for, 763

2184
history and risk factors for, 759
with injury risk, care plan for, 763–764
observation and vital signs in, 759
pathophysiology of, 757–759
primary adrenal insufficiency and, 758
screening labwork in, 760–761
secondary adrenal insufficiency and, 758
Adrenal glands, endocrine assessment of, 759–761
Adrenal insufficiency, acute, 757-765. See also Adrenal crisis.
Adrenocortical insufficiency, noncritical, screening labwork for,
760–761
Advance directives, 243
Afterload, 82
Agitation, pathologic conditions contributing to, 173b
AI., See Aortic insufficiency (AI)/regurgitation (AR).
Airway,

in burn assessment, 313

patent, securing,
in major trauma, 265
in thoracic trauma, 365
Airway pressure-release ventilation (APRV, BiVent), 112–113
Akinetic mutism (AM), 28
Albumin, serum, 126
Albuterol, for acute asthma exacerbation, 399t
Alcohol ablation, for cardiomyopathy, 535

2185
Alcohol overdose, 948–954
Alcoholism, acute pancreatitis and, 828–829
Aldosterone, 42
Aldosterone antagonists, for cardiomyopathy, 534
Alemtuzumab (Campath, MabCampth, Campath-1H), 1000
ALI., See Acute limb ischemia (ALI).
Alkalosis, 2, 7–8

metabolic, 22-23. See also Metabolic alkalosis.

renal, 2
respiratory, 2, 13. See also Respiratory alkalosis.
Alteplase, 489, 490t
Altered mental status, 25-40. See also Consciousness, alterations in.
Alveolar recruitment, modes of mechanical ventilation to promote,
112–113
Amniotic fluid embolism, 438
Amphetamine overdose, 959–960
Analgesics, for cerebral aneurysm/subarachnoid hemorrhage, 690
Anaphylactic shock, 892–902

with altered tissue perfusion, care plan for, 901

assessment in, 893–896
auscultation in, 896
care plans for, 899–902
care priorities for, 897–899
collaborative management of, 897–899, 897f
with decreased cardiac output, care plan for, 900–901

2186
with deficient knowledge, care plan for, 902
diagnostic tests for, 896t
history and risk factors for, 895
with impaired gas exchange, care plan for, 899–900
with impaired skin integrity, care plan for, 901
with ineffective airway clearance, care plan for, 899
observation in, 895–896, 895t
palpation in, 896
pathophysiology of, 892–893, 894f
percussion in, 896
systemic effects of, 895t
vital signs in, 895
Anaphylaxis., See also Anaphylactic shock.

exercise-induced, 893
Anectine., See Succinylcholine (Anectine).
Anemia,

functional classes of, 903t

profound, 902–913
with activity intolerance, care plan for, 908
assessment of, 903
care plans for, 908–910
care priorities for, 906–907

2187
collaborative management of, 906–907
diagnostic tests for, 904–906t
with impaired gas exchange, care plan for, 908
with impaired skin integrity risk, care plan for, 908–
910
pathophysiology of, 902
in trauma patient, management of, 277–278
Aneurysm,

aortic, 512-518. See also Aortic aneurysm/dissection.

cerebral, 692. See also Cerebral aneurysm.
Angina pectoris, in acute coronary syndrome, 479, 480

care plan for, 496–497

Angiotensin-converting enzyme inhibitors (ACEIs), for
hypertension, 586–588t
Anistreplase, 489, 490t
Ankle-brachial index (ABI), 594b, 598
ANP., See Atrial natriuretic peptide (ANP).
Antacids, for acute GI bleeding, 824
Anterior cord syndrome, 295
Anthrax, 201

assessment for, 201

care plans for, 202–203
care priorities for, 201–202
collaborative management of, 201–202

2188
cutaneous, 201
diagnostic tests for, 201
gastrointestinal, 201
with impaired gas exchange, care plan for, 202–203
inhalation, 201
pathophysiology of, 201
transmission of, 201
Anthropometric data, in nutrition assessment, 125
Antiarrhythmic agents, for cardiomyopathy, 534
Antibiotics,

for anthrax, 201–202

for burn wound infections, 326
for meningitis, 708
for peritonitis, 883
for plague, 206
for transplant patients, 1001
in trauma management, 267, 279
for tularemia, 209
Anticholinergics, for acute asthma exacerbation, 399t, 400
Anticoagulation,

for cardiomyopathy, 534

in continuous renal replacement therapies, 663–665
for heparin-induced thrombocytopenia, 918

2189
for prosthetic heart valves, 621
for superior vena cava syndrome, 985
Anticonvulsants,

for cerebral aneurysm/subarachnoid hemorrhage, 690

in pain management, 157
for status epilepticus, 729–730
in traumatic brain injury management, 378
Antidepressants,

cyclic, overdose of, 956

in pain management, 157
Antidiuretic hormone (ADH), 42

inappropriate, syndrome of, 795-803. See

also Syndrome of inappropriate antidiuretic
hormone (SIADH).
Antidysrhythmic drugs, 564b

for acute myocardial infarction, 487–488, 488b

for cardiomyopathy, 534
Antifibrinolytics, for abnormal bleeding in DIC, 929
Antifungals, for transplant patients, 1001
Antihistamines, for anaphylactic shock, 899
Antihypertensives,

for cerebral aneurysm/subarachnoid hemorrhage, 689

in stroke, 742–744
Antilymphocyte sera, 1001

2190
Antiplatelet therapy, in stroke, 713
Antiproliferative agents, in posttransplant immunosuppression, 999
Antipsychotics,

in agitation/anxiety management, 179

atypical, in agitation/anxiety management, 179
Antipyretics, for cerebral aneurysm/subarachnoid hemorrhage, 690
Antithrombotic therapy, 742
Antithyroid agents, for thyrotoxicosis crisis, 806
Antivirals, for transplant patients, 1001
Anxiety,

in major trauma, management of, 267

in mechanical ventilation, 116
care plans for, 122–123
reduction of, in acute respiratory distress syndrome,
412
in spinal cord injured patient, management of, 301
Aortic aneurysm/dissection, 512–518

with acute pain, care plan for, 517–518

assessment of, 513–514
auscultation in, 514
care plans for, 517–518
care priorities for, 516–517
collaborative management of, 515–517
diagnostic tests for, 514–515, 514–515t, 514b

2191
guidelines for, 515–516t
history and risk factors for, 513
with ineffective tissue profusion, care plan for, 517
observation in, 513
palpation in, 513–514
vital signs in, 513
Aortic insufficiency (AI)/regurgitation (AR), 613

management of, 620

Aortic stenosis, 613

management of, 619–620

Aortic trauma, in thoracic trauma, 363–365
Aortic valve, 612

disease of, 613, 616–617t

APACHE II scoring system, for acute pancreatitis severity, 831t
APCO., See Arterial pressure-based cardiac output measurement
(APCO).
Apnea test, 679
APRV (airway pressure-release ventilation), 112–113
AR., See Aortic insufficiency (AI)/regurgitation (AR).
ARDS., See Respiratory distress syndrome, acute (ARDS).
Aripiprazole (Abilify), in agitation/anxiety management, 179
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
(ARVC/D), 528
Arterial blood gas (ABG), 4–8

analysis of, 7–8

2192
values for, 4–7
Arterial occlusive disease., See also Peripheral vascular disease
(PVD).

assessment of, 592–598

carotid, 590, 591b. See also Carotid artery occlusive
disease.
diagnostic tests for, 596–598t
peripheral, 589, 590-592. See also Peripheral artery
occlusive disease.
Arterial oxygen saturation, 85
Arterial pressure-based cardiac output measurement (APCO), 85
Arterial pressure monitoring, 90–91, 91f

mean, 93
right, 94, 94f
Arteriogram, carotid, 598
Aseptic meningitis syndrome, 702
Aspiration, prevention of, in spinal cord injured patient, 300
Aspirin overdose, 949–950
Assist-control ventilation (A/C, ACV), 108–109
Assisted suicide, 244–245
Asthma exacerbation, acute, 393–404

assessment of, 393–397

auscultation in, 395
care plans for, 400–404
care priorities for, 397–400

2193
collaborative management of, 397–400
diagnostic tests for, 396–397t
history and risk factors for, 393–394
with impaired gas exchange, care plan for, 400–401
with ineffective airway clearance, care plan for, 401–
404
observation in, 394–395
palpation in, 395
pathophysiology of, 393
peak expiratory flow in, 394
percussion in, 395
pulmonary function test for, 398t
screening labwork in, 395–397
spirometry in, 394
stepped medication management for, 402–403t
vital signs in, 394
Asystole, 556f
Atherosclerosis, 589. See also Peripheral vascular disease (PVD).

acute ischemic stroke from, 735

Atherosclerotic carotid artery disease., See Carotid artery occlusive
disease.
Ativan., See Lorazepam (Ativan).
Atrial fibrillation, 551f

2194
catheter ablation for, 568
Atrial flutter, 550f
Atrial hypertrophy, ECG changes found with, 503t
Atrial natriuretic peptide (ANP), 42
Atrial pacemaker, wandering, 549f
Atrial tachycardia, 550f
Atrioventricular (AV) block,

first-degree, 556f
second-degree,
type I (Wenckebach), 557f
type II, 557f
third-degree (complete), 558f
Atrioventricular junctional rhythm, 552f
Autoflow, 113
Automaticity, 539

disturbances of, causes of, 539

Autonomic dysreflexia, in spinal cord injury, 293–294

care plan for, 303–304

Avian influenza (“bird flu”), 224–225

assessment of, 225

care priorities for, 226
collaborative management of, 226
diagnostic tests for, 225–226t, 225–226
history and risk factors for, 225

2195
pathophysiology of, 224–225
signs and symptoms of, 225
transmission of, 225
Axonal injury, diffuse, in traumatic brain injury, 372
Azathioprine (Imuran), 999
Azotemia, 637–638

B
Bacterial meningitis, 701–702
Balloon counterpulsation therapy/IABP, for failing heart, 521–522
Barbiturate coma, in traumatic brain injury management, 378
Barbiturate overdose, 951, 951t
Bariatric patient,

acute renal failure risk in, 644

respiratory assessment in, 390–391
Barotrauma, in mechanical ventilation, 114
Basiliximab (Simulect), 1000
Bath salts overdose, 960
Bed rest,

complications of, 162b

prolonged, 162-172. See also Immobility, prolonged.
Behavior,

abnormal, 27
violent, safety precautions in event of, 232b
Behavioral pain scales, 153

2196
Belatacept, 999
Benzodiazepines,

in agitation/anxiety management, 178

common, 952t
overdose of, 952
Beta2-adrenergic agonist, inhaled, short-acting, for acute asthma
exacerbation, 399t, 400
Beta-agonist therapy, nonselective, for acute asthma exacerbation,
399t
Beta-blockers,

for aortic aneurysm/dissection, 516

for cardiac dysrhythmias, 564
for cardiomyopathy, 534
for heart failure, 472–473
for hypertension, 586–588t
for myocardial workload reduction, 487
overdose of, 953
BiLevel ventilation, 113
Biomarkers, for acute kidney injury, 647–648, 648b
Biopsy(ies), liver,

in hepatic failure assessment, 858, 863–864, 863b

in transplant assessment, 1005
Bioterrorism, 199–209

anthrax in, 201. See also Anthrax.

2197
assessment of, 199–201
botulism in, 203
containment of, 200
hemorrhagic fever viruses in, 204–205
key signs of, 199–200
labwork on, 201
monitoring for, 200
plague in, 206
reporting on, 200
smallpox in, 207
surveillance for, 199–201
tularemia in, 209
BioWatch, 199
“Bird flu”, 224-225. See also Avian influenza (“bird flu”).
BiVent (airway pressure-release ventilation), 112–113
Bladder program, in spinal cord injury, 301–302
Bleeding,

gastrointestinal, acute, 816-828. See

also Gastrointestinal bleeding, acute.
medications promoting, 931t
Bleeding disorders, 913–935

pathophysiology of, 913–915

Blood,

2198
blood products and, 909t
coagulation of., See Coagulation.
Blood count, complete,

components of, commonly reviewed, 892t

values for, 932t
Blood pressure (BP),

afterload and, 82
in burn assessment, 314
classification and management of, for adults, 743t
contractility and, 82–83
control and management of, in pregnancy, 971
determinants of, 80–83
diastolic, hemodynamic measurements and, 93
heart rate and, 11–12
measurements of, in hypertensive emergencies, 580
preload and, 80–82
systolic, hemodynamic measurements and, 93
Blood transfusions,

for anemia, 906–907, 907b

for hemolytic crisis, 910
for pelvic fracture patients, 351
reactions to, acute, 934t

2199
Blood urea nitrogen-to-creatinine ratio, in acute gastrointestinal
bleeding, 821
Blood vessel injuries, in traumatic brain injury, 370
Body fluid disturbances, 42–45, 46–47, 48. See also Fluid and
electrolyte disturbances.
Body image disturbance, indicators of, 237b
Bone marrow transplantation, for anemia, 907
Botulism, 203
Bowel irrigation, for drug overdose, 946
Bowel management, in spinal cord injury, 302
BP., See Blood pressure (BP).
Bradycardia, sinus, 547f
Brain,

damage to, minimizing, in stroke, 741–742

injury to, traumatic, 368-385. See also Traumatic brain
injury (TBI).
Brain death, 677–684

apnea test in, 679

care plans for, 683–684
care priorities in, 682–683
collaborative management of, 681–683
with decisional conflict, care plan for, 684
with decreased intracranial adaptive capacity, care
plan for, 683
definition of, 677

2200
diagnostic tests for, 680–681t
history and risk factors for, 678–679
inspection in, 679
neurologic assessment for, 678–681
observation in, 679
organ donation after, 995
organ donation management after, 681–682t
palpation in, 679
pathophysiology of, 677–678
screening labwork in, 679–681
vital signs and, 679
Brain tissue oxygenation monitoring, in traumatic brain injury, 377
Breathing,

in burn assessment, 313

frequency of, 104
Breathing pattern, ineffective, in mechanical ventilation, care plan
for, 120–122
Bronchodilators,

for acute asthma exacerbation, 400

inhaled, for anaphylactic shock, 899
Brown-Séquard syndrome, 296
Burns, 310–333

ABA Burn Center Referral Guidelines for, 262

2201
with acute pain, care plan for, 330
airway/breathing in, 313
assessment of, 312–321
auscultation in, 316
cardiac output and perfusion in, 314
cardiovascular system in, 317
care plans for, 326–333
care priorities for, 322–326
classification of, 311
collaborative management of, 322–326
with deficient knowledge, care plan for, 333
description and characteristics of, 310–311, 312t
diagnostic tests for, 319–321t, 321–322
with disturbed body image, care plan for, 333
with disturbed sensory perception, care plan for, 332
with disuse syndrome risk, care plan for, 332–333
with fear, care plan for, 332
with fluid volume deficit, care plan for, 327–328
gastrointestinal system in, 317
heart rate and rhythm in, 314
history and risk factors for, 312–313
with hypothermia, care plan for, 329

2202
with impaired gas exchange, care plan for, 327
with impaired tissue integrity, care plan for, 330–331
with ineffective airway clearance, care plan for, 326–
327
with ineffective tissue perfusion, care plan for, 328–
329, 331
with infection risk, care plan for, 329–330
integumentary system in, 318
Lund-Browder chart for extent of, 314, 315f
with nutritional imbalance, care plan for, 331–332
palpation in, 315
pathophysiology of, 310–311
renal system in, 317–318
respiratory system in, 316–317, 316t
rule of nines for, 314, 314f
septic shock in, 318–321
systemic inflammatory response syndrome in, 318–
321
wound extent in, 314–315
wound infection in, 318

C
Calcineurin inhibitors, in posttransplant immunosuppression, 999

2203
Calcium,

deficiency of, 61. See also Hypocalcemia.

excess of, 64. See also Hypercalcemia.
imbalances of, 60–61
Calcium channel blockers (CCBs),

for cardiomyopathy, 535

for cerebral aneurysm/subarachnoid hemorrhage, 689
for hypertension, 586–588t
for myocardial workload reduction, 487
overdose of, 953–954
Calorimetry, indirect, in nutrition requirements estimation, 127
CAM-ICU., See Confusion Assessment Method for ICU (CAM-
ICU).
Campath (alemtuzumab), 1000
Campath-1H (alemtuzumab), 1000
Cancer-related emergencies, 975-989. See also Oncologic
emergencies.
Cannabinoid overdose, 954–959
Carafate., See Sucralfate (Carafate).
Carbapenem-resistant Enterobacteriaceae (CRE), 211
Carbohydrates,

in enteral formulas, 133

requirements for, 128
in TPN, 140
Carbon monoxide poisoning, signs and symptoms of, 316, 316t

2204
Carbonic acid, 2, 3
Cardiac cycle, 538–539
Cardiac death, organ donation after, 995
Cardiac dysrhythmias, 537–576

accelerated junctional rhythm, 552f

assessment of, 544–561
asystole, 556f
atrial fibrillation, 551f
atrial flutter, 550f
atrial tachycardia, 550f
atrioventricular junctional rhythm, 552f
auscultation in, 546
care plans for, 572–576
care priorities for, 563–571
collaborative management of, 563–571
with decreased cardiac output, care plan for, 572
with deficient knowledge, care plan for, 572–573
diagnostic tests for, 559–561t
dietary guidelines for, 571, 571t
dual-chambered pacemaker, 559f
electrocardiographic measurements in, 544–546
first-degree AV block, 556f

2205
hemodynamic measurements in, 544–546
history and risk factors for, 544
idioventricular rhythm, 556f
with ineffective health maintenance, care plan for, 573
junctional escape rhythm, 552f
junctional tachycardia, 553f
normal sinus rhythm, 546f
with sinus arrest, 548f
observation in, 544
palpation in, 546–561
pathophysiology of, 537–544
pharmacologic management of, 563, 564b
premature junctional complexes, 553f
with risk for activity intolerance, care plan for, 572
second-degree AV block,
type I (Wenckebach), 557f
type II, 557f
sinus bradycardia, 547f
sinus dysrhythmia, 548f
sinus tachycardia, 547f
with premature atrial complexes, 549f
third-degree (complete) AV block, 558f

2206
torsade de pointes, 554f
in traumatic brain injury, management of, 381
ventricular demand (VVI) pacemaker, 558f
with failure to capture, 559f
with failure to sense, 559f
ventricular fibrillation, 555f
ventricular tachycardia, 554f
vital signs in, 544
Cardiac index (CI), hemodynamic measurements and, 96
Cardiac injury, blunt, in thoracic trauma, 363
Cardiac output (CO),

afterload and, 82
in burn assessment, 314
contractility and, 82–83
decreased,
acute cardiac tamponade with, care plan for, 290–291
acute coronary syndrome with, care plan for, 492–494
acute GI bleeding with, care plan for, 826–827
acute infective endocarditis with, care plan for, 504–
505
acute pancreatitis with, care plan for, 842
acute spinal cord injury with, care plan for, 304
after intracranial surgery, care plan for, 700

2207
anaphylactic shock with, care plan for, 900–901
cardiogenic shock with, care plan for, 522–524, 525–
526
cardiomyopathy with, care plan for, 536–537
cardiovascular disorders with, care plan for, 463–464
continuous renal replacement therapies with, care
plan for, 667–668
Guillain-Barré syndrome with, care plan for, 725
heart failure with, care plan for, 477
from hyperkalemia, care plan for, 60
from hypocalcemia, care plan for, 63
from hypokalemia, care plan for, 57–58
from hypomagnesemia, care plan for, 76
hypotension with, from mechanical ventilation, 115
neutropenic sepsis with, care plan for, 983
patients undergoing percutaneous balloon
valvuloplasty with, care plan for, 626
pelvic fracture with, care plan for, 351
septic patients with, care plan for, 1020
superior vena cava syndrome with, care plan for, 986
thoracic trauma with, care plan for, 367–368
valve replacement with, care plan for, 623–624
determinants of, 80–83

2208
heart rate and, 11–12
hemodynamic measurements and, 96
preload and, 80–82
Cardiac pacing., See Pacemakers.
Cardiac Resynchronization Therapy (CRT), for cardiomyopathy,
535
Cardiac tamponade, acute, 284–291

assessment of, 285–288

auscultation in, 285–286
care plans for, 290–291
care priorities for, 289–290
collaborative management of, 289–290, 289t
with decreased cardiac output, care plan for, 290–291
hemodynamic monitoring in, 286
with ineffective tissue perfusion, care plan for, 291
observation in, 285
pathophysiology of, 284–285
percussion in, 286
screening diagnostic tests in, 286–288, 287–288t
vital signs in, 285
Cardiac transplantation., See Heart transplantation.
Cardiogenic shock (CS), 518–526

assessment of, 518–519

2209
auscultation in, 519
care plans for, 522–526
care priorities for, 520
collaborative management of, 520–522
with decreased cardiac output, care plan for, 522–524,
525–526
diagnostic criteria for, 519
hemodynamic measurements in, 519
with imbalanced nutrition, care plan for, 526
with impaired gas exchange, care plan for, 523
with impaired tissue integrity, care plan for, 524–525
with ineffective breathing pattern, care plan for, 525
with ineffective protection, care plan for, 525
with ineffective tissue perfusion, care plan for, 523,
524
with infection risk, care plan for, 526
observation in, 519
pathophysiology of, 518
with risk for complications from immobility, care plan
for, 525
vital signs in, 519
Cardiography, impedance, in cardiac output measurement, 85–86
Cardiomyopathy, 526–537

2210
with activity intolerance, care plan for, 537
arrhythmogenic right ventricular, 528
assessment of, 529–532
care plans for, 536–537
care priorities for, 533–536
collaborative management of, 533–536
with decreased cardiac output, care plan for, 536–537
diagnostic tests for, 529–532t
dilated, 528
functional classifications of, 528–529
hypertrophic, 528
observation of, 529–532
pathophysiology of, 526–529
restrictive, 528
types and causes of, 527t
Cardiovascular disorders,

acute coronary syndrome as, 479-498. See

also Coronary syndrome, acute.
acute infective endocarditis as, 498-507. See
also Endocarditis, acute infective.
acute pericarditis as, 507-512. See also Pericarditis,
acute.
aortic aneurysm/dissection as, 512-518. See also Aortic

2211
 aneurysm/dissection.
assessment of, 462–465
auscultation in, 463
cardiogenic shock as, 518-526. See also Cardiogenic
shock (CS).
dysrhythmias and conduction disturbances as, 537-
576. See also Cardiac dysrhythmias; See
also Conduction, disturbances of.
electrocardiogram in., See Electrocardiogram (ECG).
generalized,
with activity intolerance, care plan for, 463
care plans for, 463–465
with decreased cardiac output, care plan for, 463–464
with impaired gas exchange, care plan for, 464–465
heart failure as, 466-479. See also Heart failure.
hypertensive emergencies as, 576–589
labwork in, 463
observation in, 462
palpation in, 462
peripheral vascular disease as, 589-612. See
also Peripheral vascular disease (PVD).
valvular heart disease as, 612-627. See also Valvular
heart disease.

2212
Cardiovascular system, in burn assessment, 317
Cardioversion., See Defibrillation/cardioversion.
Carotid artery occlusive disease, 590, 591b

assessment of, 592

care plans for, 609–610
care priorities for, 604–607
clinical practice management guidelines for, 605–606t
with deficient fluid volume, care plan for, 610
with ineffective tissue perfusion, care plan for, 609–
610
observation in, 593–594
Carotid duplex ultrasound, 598
Carotid endarterectomy, for stroke, 750
Catheter(s),

pulmonary artery, optimal use of, 7–8

Catheter ablation, for cardiac dysrhythmias, 567
Cathinone overdose, 960
Cauda equina syndrome, 297
Cellcept (mycophenolate mofetile), 999
Cellular acidosis, 1
Central cord syndrome, 295–296
Central herniation, 370

assessment of, 371t

Central venous pressure (CVP), 85

hemodynamic measurements and, 93–94, 94f

2213
Cerebellar function, in neurologic assessment, 673–674
Cerebral aneurysm, 684–694

care plans for, 692–694

care priorities for, 689–692
collaborative management of, 689–692
with fluid volume imbalance risk, care plan for, 694
functional assessment in, 688–689
history and risk factors for, 686–687
Hunt and Hess classification system for, 687
with impaired gas exchange, care plan for, 693
with ineffective airway clearance, care plan for, 693
with ineffective cerebral tissue perfusion, care plan
for, 692–693
with injury risk, care plan for, 693
intracranial pressure in, 687–688
neurologic assessment of, 686–689
observation in, 688–689
pathophysiology of, 684–686
screening labwork in, 689
syndrome of inappropriate antidiuretic hormone and,
685
vital signs in, 687
Cerebral edema reduction, after intracranial surgery, 697

2214
Cerebral perfusion pressure (CPP) maintenance, in traumatic brain
injury, 377
Cerebral salt-wasting syndrome, clinical presentation of syndrome
of inappropriate antidiuretic hormone versus, 686t
Cerebrospinal fluid findings, in meningitis, 707t
Cerebyx., See Fosphenytoin (Cerebyx).
Certican (everolimus), 1000
Cervical spine injury, care priorities for, 298–299
Chain donations, 995
Charcoal, activated, for drug overdose, 946
Chemotherapy, for superior vena cava syndrome, 986
Chest pain., See Angina.
Chest physiotherapy, for acute asthma exacerbation, 400
Cholesterol, diet low in, guidelines for, 571t
Cholinergic crisis, 713

complicating plasmapheresis, 717

diagnosis of, 713–714t
emergency interventions for, 714
CI., See Cardiac index (CI).
Cingulate herniation, 370
Cisatracurium (Nimbex), in agitation/anxiety management, 180
Citrate, in continuous renal replacement therapies, 664–665
CJD., See Creutzfeldt-Jakob disease (CJD).
CLI., See Critical limb ischemia (CLI).
Clotting abnormalities, complicating plasmapheresis, 716
Clotting factors, actions of, 925t
CO., See Cardiac output (CO).

2215
Coagulation,

disseminated intravascular, 924-925. See

also Disseminated intravascular coagulation (DIC).
pathway of, 914–915, 914f
Coagulopathies, in traumatic brain injury, management of, 374–375
Cocaine overdose, 955–956
Cognitive-behavioral techniques, in pain management, 159
Cold application, in pain management, 158–159
Collapsed lung, in pneumothorax, reexpansion of, 432–433
Colonoscopy, in acute gastrointestinal bleeding, 822
Coma, 27–29

barbiturate, in traumatic brain injury management,

378
brain death differentiated from, 679
care priorities for, 36
differential diagnosis of, 27–29
myxedema, 787-795. See also Myxedema coma.
Coma Recovery Scale, 31
Comfort care, 245
Commissurotomy, 622
Communication,

in culture of safety, 250–252, 251t, 253b

structured, SBAR recommendations for, 251, 252t
verbal, impaired, care plan for, 241
Compartment syndrome, 334–341, 592

2216
abdominal, 937-945. See also Abdominal compartment
syndrome (ACS).
with acute pain, care plan for, 340
assessment of, 335–338
with body image disturbance, care plan for, 341
care plans for, 339–341
care priorities for, 338–339
causes of, 334t
collaborative management of, 338–339
compartmental pressure monitoring in, 338
diagnostic tests for, 336t
history and risk factors for, 335–336
for ineffective tissue perfusion, care plan for, 339–340
with infection risk, care plan for, 340–341
observation and subjective symptoms of, 336
palpation in, 336–338
pathophysiology of, 334–335
vital signs in, 336
Compensation,

for acidosis, 2
for alkalosis, 2
Complete blood count, components of, commonly reviewed, 892t
Concussion, 372

2217
Conduction,

atrioventricular, anomalous, 545f

disturbances of,
care plans for, 572–576
causes of, 539–544
ECG tracings and, 539
Confidentiality, 243
Confusion,

acute,
acute renal failure with, care plan for, 654–655
hypernatremia-related, care plan for, 54
hyponatremia-related, care plan for, 52–53
nondrug treatment strategies for, 174b
Confusion Assessment Method for ICU (CAM-ICU), 175b
Confusion Assessment Method for ICU (CAM-ICU) Worksheet, 31,
34b
Consciousness, 25

alterations in, 84
assessment of, 29–31
care plans for, 39–40
care priorities for, 33–38
in cerebral aneurysm/subarachnoid hemorrhage, 688
collaborative management of, 33–38

2218
coma as., See Coma.
delirium as., See Delirium.
diagnostic tests for, 31–33
history and risk factors for, 29–30
with impaired physical mobility, care plan for, 40
with impaired verbal communication, care plan for,
39
laboratory studies in, 33
neurologic evaluation in, 31
neuropsychological testing in, 33
observation in, 30–31
pathophysiology of, 25–29
screening labwork in, 31
vegetative state as., See also Vegetative state (VS).
vital signs in, 30
level of,
in meningitis, 704
in neurologic assessment, 673
Consent, informed, 241–242

elements of, 242b

Constipation, from prolonged immobility, care plan for, 170–171
Continuous cardiac output measurement, 85
Contractility, myocardial, 82–83

2219
Contusion,

pulmonary, in thoracic trauma, 363

in traumatic brain injury, 372
Conus medullaris syndrome, 296
Coronary syndrome, acute (ACS), 479–498

with activity intolerance, care plan for, 491–492

with acute chest pain, care plan for, 496–497
with altered protection, care plan for, 495–496
assessment of, 480–485
auscultation in, 481
care plans for, 491–497
care priorities for, 486–488
collaborative management of, 486–491
with decreased cardiac output, care plan for, 492–494
with deficient knowledge, care plan for, 494
diagnostic tests for, 481–484t
ECG changes in, 484–485
ECG monitoring in, 484
electrocardiogram in, 480
history and risk factors for, 480
with injury risk, care plan for, 493
labwork in, 481–484

2220
observation in, 481
palpation in, 481
pathophysiology of, 479
with risk for deficient fluid volume, care plan for, 492
vital signs in, 480–481
Corticol replacement, in adrenal crisis, 762–763
Corticosteroids,

for acute asthma exacerbation, 399t, 400

for anaphylactic shock, 899
for cerebral aneurysm/subarachnoid hemorrhage, 690
for hemolytic crisis, 911
for immune thrombocytopenic purpura, 921
insufficiency of, in critically ill patients, diagnosis and
management of, 761–762t
for septic patients, 1018–1019
CPP., See Cerebral perfusion pressure (CPP).
Cranial nerves,

assessment of, 673

impairment of, assessment for,
in intracranial surgery, 696
in meningitis, 706
Cranial surgery, 694-701. See also Intracranial surgery.
Craniotomy, for stroke, 750

2221
CRE (carbapenem-resistant Enterobacteriaceae), 211
Creutzfeldt-Jakob disease (CJD), 220

assessment of, 220–221

care priorities for, 222
collaborative management of, 222
diagnostic tests for, 221, 221t
familial, 220, 221
iatrogenic, 220
new variant, 220, 221
pathophysiology of, 220
risk factors and history of, 220–221
sporadic, 220–221
transmission of, 220
Critical care, high-risk obstetric patient in, care plans for, 973–975
Critical limb ischemia (CLI), 590–591

care priorities for, 602–603

management guidelines for, 599–601t
CRRT., See Renal replacement therapies, continuous (CRRT).
CSA (cyclosporine), 999
CVP., See Central venous pressure (CVP).
Cyclic antidepressant overdose, 956
Cyclosporine (CSA, Sandimmune, Neoral, Gengraf), 999

2222
Daclizumab (Zenapax), 1000
Death, brain, 677-684. See also Brain death.
Decision-making capacity, 243
Decompressive laparotomy, for abdominal compartment
syndrome, 943
Deconditioning, 162-172. See also Immobility, prolonged.
Deep venous thrombosis (DVT) prevention,

during and after intracranial surgery, 697, 697b

in burn patient, 326
in spinal cord injured patient, 301
in traumatic brain injury patient, 380
Defibrillation/cardioversion,

AED technique of, 565–566, 566b

implantable device for, 566–567, 566t. See
also Implantable cardioverter-defibrillator (ICD).
life vest “wearable” device for, 566
for rapid heart rates, 565–568
Delirium, 27

agitation management and, 174

care priorities for, 33–36
evaluation of, in ICU, 175b
monitoring of, sedation and, 28f
nondrug treatment strategies for, 174b
Demerol., See Meperidine (Demerol).

2223
Dexmedetomidine (Precedex),

in agitation/anxiety management, 177

in pain management, 157
Dextrose, in hepatic failure, 867
DI., See Diabetes insipidus (DI).
Diabetes insipidus (DI), 765–773

auscultation in, 768

care plans for, 771–773
central, 766, 766t, 767
collaborative management of, 769–771
with deficient fluid volume, care plan for, 771–772
with deficient knowledge, care plan for, 772–773
diagnostic testing for, 768–769t
dipsogenic, 766, 766t, 767
with disturbed sensory perception, care plan for, 772
endocrine assessment in, 767–769
gestational, 766, 766t, 767
history and risk factors for, 767
with infection risk, care plan for, 772
nephrogenic, 766, 766t, 767
neurogenic, 766, 766t, 767
observation in, 767–768

2224
pathophysiology of, 765–767, 765t
screening labwork for, 768–769
subtypes of, 766t
vital signs in, 767
Diabetes mellitus,

enteral formulas for, 134–135

hyperglycemia and, 773. See also Hyperglycemia.
Diabetic ketoacidosis (DKA), 774–775

hyperglycemic hyperosmolar syndrome compared

with, 776–777t
pathophysiology of, 774–775
Diastolic blood pressure, hemodynamic measurements and, 93
Diazepam (Valium),

in agitation/anxiety management, 178

for status epilepticus, 729
DIC., See Disseminated intravascular coagulation (DIC).
Dietary guidelines,

low-cholesterol, 571t
low saturated fat, 464
Dietary support., See Nutrition support.
Diffuse axonal injury, in traumatic brain injury, 372
Digoxin,

for cardiomyopathy, 534

overdose of, 957

2225
Dilantin., See Phenytoin (Dilantin).
Dilated cardiomyopathy (DCM), 528
Dilaudid., See Hydromorphone (Dilaudid).
Diprivan., See Propofol (Diprivan).
Direct renin inhibitors, for hypertension, 586–588t
Direct thrombin inhibitors,

in continuous renal replacement therapies, 664

in heparin-induced thrombocytopenia, 918
Dissection, aortic, 512-518. See also Aortic aneurysm/dissection.
Disseminated intravascular coagulation (DIC), 924–925

assessment of, 925–927

auscultation in, 927
care plans for, 930–935
care priorities for, 929–930
collaborative management of, 929–930
conditions predisposing to, 926t
diagnostic tests for, 927–928t
with fluid volume deficit risk, care plan for, 930–933
with impaired gas exchange, care plan for, 933–934
with ineffective protection, care plan for, 930
with ineffective tissue perfusion, care plan for, 933–
935
with injury risk, care plan for, 934–935

2226
laboratory values in, 932t
observation in, 927
palpation in, 927
pathophysiology of, 924–925
risk factors for, 927
vital signs in, 927
Diuretics,

for acute kidney injury, 650t

for ascites in hepatic failure, 868
for cardiomyopathy, 534
for cerebral aneurysm/subarachnoid hemorrhage, 689
for hypertension, 586–588t
DKA., See Diabetic ketoacidosis (DKA).
Dobutamine,

for cardiomyopathy, 534

for failing heart, 520, 521t
Dopamine,

for anaphylactic shock, 898

for failing heart, 520, 521t
Drowning, 341–347

assessment of, 342–344

auscultation in, 343–344
care plans for, 345–346

2227
collaborative management of, 344–345
diagnostic tests for, 343–344t
freshwater versus saltwater, 342
history and risk factors for, 342
with hypothermia, care plan for, 346
with impaired gas exchange, care plan for, 345–346
incidence of, 341
with infection risk, care plan for, 346
observation in, 343
palpation in, 343
pathophysiology of, 341–342
vital signs in, 342–343
wet versus dry, 342
Drug-nutrient interactions, in enteral nutrition, 138

acetaminophen, 947
alcohols, 948–954
amphetamine, 959–960
aspirin, 949–950
assessment in, 946
barbiturate, 951, 951t
benzodiazepine, 952, 952t
beta-blocker, 953

2228
calcium channel blocker, 953–954
cannabinoids, 954–959
care plans for, 961–963
cathinone, 960
cocaine, 955–956
cyclic antidepressant, 956
digoxin, 957
with disturbed sensory/perceptual perception, care
plan for, 963
epidemiology of, 945
ethanol, 948
ethylene glycol, 949
with fluid volume deficit, care plan for, 962–963
gastric decontamination for, 946
hallucinogen, 957–958
with hyperthermia, care plan for, 962
with ineffective airway clearance, care plan for, 961–
962
management of, 961t
methanol, 949
opioid, 958
phencyclidine, 959

2229
salicylates, 949–950
stimulant, 959–964
treatment options for, 946, 947
unknown substance ingestion and, 945
with violence risk, care plan for, 963
Dual-Chamber Pacemaker, for cardiomyopathy, 535
Duodenal bleeding, 816
Durable power of attorney for health care (DPAHC), 243
DVT., See Deep venous thrombosis (DVT).
Dynamic response test, 87–88, 88f
Dysphagia screening, in neurologic assessment, 675–676
Dysreflexia, autonomic,

in Guillain-Barré syndrome, care plan for, 724–725

in spinal cord injury, 293–294
care plan for, 303–304
Dysrhythmia, sinus, 548f
Dysrhythmias, 537-576. See also Cardiac dysrhythmias.

E
Ebola virus disease (EVD), 211–212

case definitions for, 212

control of, 212–213
diagnosis of, 213
prevention of, 212–213

2230
signs and symptoms of, 212
transmission of, 212
treatment of, 213
ECF., See Enterocutaneous fistula (ECF).
Echocardiogram,

transesophageal, in cardiac output calculation, 86

transthoracic, in cardiac output calculation, 86
Eclampsia, 966

management of, 970

risk factors for, 967
seizure prevention in, 970–971
ECMO., See Extracorporeal membrane oxygenation (ECMO).
Elderly., See Older adults.
Electrocardiogram (ECG),

abnormal tracings on, 539

accelerated junctional rhythm, 552f
in acute coronary syndrome, 480
in acute infective endocarditis, 499–501, 503t
in acute pericarditis, 509–510, 509t
in anaphylactic shock, 899
asystole, 556f
atrial fibrillation, 551f
atrial flutter, 550f

2231
atrial tachycardia, 550f
atrioventricular junctional rhythm, 552f
in cardiac dysrhythmias, 544–546
in cardiovascular assessment, 462
chest lead placement for,
left and right leads, 562f
posterior leads, 562f
components of, 543f
dual-chambered pacemaker, 559f
electrical basis of, 541f
first-degree AV block, 556f
idioventricular rhythm, 556f
junctional escape rhythm, 552f
junctional tachycardia, 553f
for myocardial infarction, 485t
normal sinus rhythm, 546f
with sinus arrest, 548f
P wave on, 538
PR interval on, 538
premature junctional complexes, 553f
Q waves in, 485
QRS complex on, 538–539

2232
QT interval on, 539
second-degree AV block,
type I (Wenckebach), 557f
type II, 557f
sinus bradycardia, 547f
sinus dysrhythmia, 548f
sinus tachycardia, 547f
with premature atrial complexes, 549f
ST segment on, 539
changes in, 484–485
T wave on, 539
changes in, 485
third-degree (complete) AV block, 558f
torsade de pointes, 554f
TP segment on, 539
U wave on, 539
ventricular demand (VVI) pacemaker, 558f
with failure to capture, 559f
with failure to sense, 559f
ventricular fibrillation, 555f
ventricular tachycardia, 554f
Electroencephalography (EEG), in status epilepticus, 728

2233
Electrolyte imbalances, in enteral and parenteral nutrition, 143
Electrolytes, 41

disturbances of., See Fluid and electrolyte

disturbances.
Embolism., See also Thromboembolism.

pulmonary, 437-450. See also Pulmonary embolism

(PE).
Emergency(ies),

hypertensive, 576-589. Hypertensive emergencies.

oncologic, 975-989. See also Oncologic emergencies.
Emergency interventions, for cholinergic and myasthenic crisis,
972–973
Emerging infections, 209-226. See also Infection(s), emerging.
Emotional/spiritual support, 226–242

anxiety reduction and, care plan for, 230

body image disturbance and, care plan for, 236–238
care plans for, 230–242
complicated grieving and, care plan for, 238
compromised family coping and, care plan for, 231
deficient knowledge and, care plan for, 240
disabled family coping and, care plan for, 234–235
enhanced family coping and, care plan for, 239–240
fear and, care plan for, 232
grieving and, care plan for, 233

2234
history and risk factors, 229
Howden Spiritual Assessment Scale and, 229b
ineffective denial and, care plan for, 234
ineffective individual coping, care plan for, 234
need for, assessment of, 229
powerlessness and, care plan for, 235–236
sensory perception disturbance and, care plan for,
241–242
sleep pattern disturbance and, care plan for, 236
social isolation and, care plan for, 231
spiritual distress and, care plan for, 233–234
verbal communication impairment and, care plan for,
241
violence prevention and, care plan for, 239
Enalaprilat, for hypertensive emergency, 583
Encephalitis, WNV, 223
Encephalopathy, hepatic, 854

factors contributing to, 875b

precipitating factors for, eliminating or correcting,
868–870
Endarterectomy, carotid, for stroke, 750
Endocarditis, acute infective, 498–507

assessment of, 498–501

auscultation in, 499

2235
care plans for, 504–507
care priorities for, 502–504
collaborative management of, 502–504
with decreased cardiac output, care plan for, 504–505
diagnostic tests for, 500–501t
electrocardiogram in, 499–501
hemodynamic measurements in, 499
history and risk factors for, 499
with impaired gas exchange, care plan for, 505
with ineffective tissue perfusion, care plan for, 506–
507
with infection risk, care plan for, 506
observation in, 499
pathophysiology of, 498
prophylaxis for, 618–619, 619t
screening labwork in, 499
vital signs in, 499
Endocrine assessment, 756–757
Endocrinologic disorders, 756–813

acute adrenal insufficiency as, 757-765. See

also Adrenal crisis.
diabetes insipidus as, 765-773. See also Diabetes
insipidus (DI).

2236
myxedema coma as, 787-795. See also Myxedema
coma.
thyrotoxicosis crisis as, 803-810. See
also Thyrotoxicosis crisis.
Endoscopic therapies, in acute gastrointestinal bleeding, 824
Endovascular interventions,

for cerebral aneurysm/subarachnoid hemorrhage, 691

for critical limb ischemia, 603
for intracranial hemorrhage, 742
patients undergoing, care plans for, 611
Energy needs, in nutrition requirements estimation, 127
Enteral formulas/nutrition, 131-138. See also Nutrition support.

access for, 135–136

administration methods for, 136
in critically ill patients, 131b
drug-nutrient interactions in, 138
nutritional composition of, 133–134
specialized for organ-specific pathology, 134–135
tolerance of, monitoring of, 136
Enterobacteriaceae, carbapenem-resistant, 211
Enterococcus, vancomycin-resistant, 211
Enterocutaneous fistula (ECF), 845–854

abdominal drainage in, 846–847

abdominal pain in, 846

2237
auscultation in, 847
with body image disturbance, care plan for, 853
care plans for, 850–853
care priorities for, 849–850
collaborative management of, 848–850
diagnostic tests for, 847–848t
drainage from, containing, recommendations for, 852b
with fluid volume deficit, care plan for, 850–851
gastrointestinal assessment of, 846–848
hemodynamic measurements in, 847–848
history and risk factors for, 846
with impaired oral mucous membrane, care plan for,
853
with impaired tissue integrity, care plan for, 852–853
with infection risk, care plan for, 851
nonradiographic evaluation of, 848
nursing assessment of, 852b
nutrition assessment in, 847
with nutritional imbalance, care plan for, 851–852
observation in, 847
palpation in, 847
pathophysiology of, 845–846

2238
screening labwork in, 847
vital sign assessment in, 846
Enterostomy tube placement, complications of, 135–136
Eosinophilic meningitis, 702
Epidural hematoma, 372
Epinephrine,

for acute asthma exacerbation, 399t

for anaphylactic shock, 898
for failing heart, 520, 521t
Epoetin alfa/erythropoietin, recombinant (Epogen/Procrit), for
anemia, 907
Epsilon-aminocaproic acid, administration of, nursing implications
for, 623b
Escharotomy, for circumferential burns, 327
Esmolol, for hypertensive emergency, 583
Esophageal bleeding, 816
Esophagogastroduodenoscopy, in acute gastrointestinal bleeding,
821–822
Ethanol overdose, 948
Ethical considerations, 242–247

advance directives as, 243

assisted suicide as, 244–245
care plans for, 246–247
comfort care as, 245
confidentiality as, 243

2239
decision-making capacity as, 243
with deficient knowledge, care plans for, 246
ethical reasoning as, 245
euthanasia as, 244–245
on grieving, care plan for, 246–247
informed consent as, 242
preventive ethics as, 245–246
quality of life as, 244
truth telling as, 244
withholding and withdrawing treatment as, 244
Ethical reasoning, 245
Ethics, preventive, 245–246
Ethylene glycol overdose, 949
Euthanasia, 244–245
Euthyroid sick syndrome, 803b
EVD., See Ebola virus disease (EVD).
Everolimus (Certican), 1000
Exercise-induced anaphylaxis, 893
Extracellular fluid (ECF) compartment, 41
Extracorporeal membrane oxygenation, for cardiogenic shock, 522
Extracorporeal membrane oxygenation (ECMO), for nonfatal
drowning patient, 345
Extracorporeal removal of toxins, for drug overdose, 947
Extracranial herniation, 370

2240
F
Faces Scales for pain, 153, 154f
Family, in patient safety, 254–255, 254b, 255–256t
Family coping,

enhanced, care plan for, 239–240

with high-risk obstetric patient, care plan for, 975
Fast flush test, 87–88, 88f
Fat embolism, 438, 440

auscultation in, 440

care priorities for, 447
diagnostic tests for, 443
history and risk factors for, 440
observation/inspection in, 440
vital signs in, 440
Fats,

in enteral formulas, 134

requirements for, 128
saturated, diet low in, guidelines for, 464
in TPN, 140–141
Fear, care plan for, 232
Feeding tubes,

medication administration via, 136–138

Fenoldopam, for hypertensive emergency, 583
Fentanyl (Sublimaze),

2241
in anxiety management, 176
in pain management, 155, 156b
Fetus,

delivery of, in preeclampsia, 972–973

surveillance of, for hypertensive pregnant patient,
968–969
Fever control,

after intracranial surgery, 698

in meningitis, 708
Fiber, in enteral formulas, 133–134
Fibrillation,

atrial, 551f
catheter ablation for, 568
ventricular, 555f
Fick oxygen consumption method, of cardiac output calculation, 85
Fio2., See Fraction of inspired oxygen (Fio2).
Fistula, enterocutaneous, 845-854. See also Enterocutaneous fistula
(ECF).
Flail chest, in thoracic trauma, 363
Flow rate (V), 106
Flu,

“bird”, 224-225. See also Avian influenza (“bird flu”).

pandemic, 224
Fluconazole, 1001
Fluid and electrolyte disturbances, 40–79

2242
hormonal influence on, 42
hypercalcemia as, 64–65
hyperkalemia as, 58–60
hypernatremia as, 53–54
hyperphosphatemia as, 71–72
hypervolemia as, 46–47, 48
hypocalcemia as, 61–62
hypokalemia as, 55–57
hypomagnesemia as, 73–75
hyponatremia as, 50–52
hypophosphatemia as, 67–68
hypovolemia as, 42–45
osmolality and, 41
Fluid and electrolyte management,

in acute gastrointestinal bleeding, 823

in enterocutaneous fistula, 849
in hepatic failure, 866
in nonfatal drowning patient, 345
in pancreatitis patient, 837, 838–839
Fluid imbalance, from mechanical ventilation, 115
Fluid management, in hypertensive obstetric disorders, 971
Fluid replacement, for acute asthma exacerbation, 400
Fluid requirements, 130

2243
Fluid resuscitation,

for acute pancreatitis, 837

for anaphylactic shock, 898
for burn patient, 324
Fluid therapy, in acute respiratory distress syndrome, 412, 412b
Flutter, atrial, 550f
Folic acid supplement, for anemia, 907
Foods., See also Nutrition support.

high and low cholesterol, 571t

high and low saturated fat, 571t
high in magnesium, 75b
high in phosphorus, 68b
high in potassium, 57b
high in sodium, 48b
Foreign bodies, intravascular., See Intravascular foreign bodies.
Fosphenytoin (Cerebyx), for status epilepticus, 729
Fraction of inspired oxygen (Fio2), 105
Fracture(s),

pelvic, 347-352. See also Pelvic fractures.

skull, associated with traumatic brain injury, 369, 372
vertebral, 292
Frank Starling’s law, 80
Fundoscopic assessment, in neurologic disorders, 675
Fungal meningitis, 702

2244
G
Gallstones, acute pancreatitis and, 828–829
Gas exchange, impaired, in mechanical ventilation, care plans for,
118–120, 122
Gastric bleeding, 816
Gastric decompression, in major trauma management, 267
Gastric decontamination, for drug overdose, 946
Gastric intubation, in acute gastrointestinal bleeding, 824
Gastric lavage, for drug overdose, 946
Gastric ulcer prevention,

in acute spinal cord injury, 300

after intracranial surgery, 698
Gastrointestinal assessment, 814–816

in acute gastrointestinal bleeding, 818–822

auscultation in, 814
nutrition assessment in, 815, 815t
observation in, 814
palpation in, 814–815
screening labwork in, 816
vital sign assessment in, 814
Gastrointestinal bleeding, acute, 816–828

abdominal pain in, 819

with acute pain, care plan for, 827
auscultation in, 819

2245
blood loss in, 818, 823t
blood urea nitrogen-to-creatinine ratio in, 821
care plans for, 825–828
care priorities for, 823–825
collaborative management of, 822–825
colonoscopy in, 822
with decreased cardiac output, care plan for, 826–827
diagnostic tests for, 820–821t
with diarrhea, care plan for, 827
esophagogastroduodenoscopy in, 821–822
with fluid volume deficit, care plan for, 825–826
gastrointestinal assessment in, 818–822
hemodynamic measurements in, 819–821
history and risk factors for, 818
lower, 817
nutrition assessment in, 819
with nutritional imbalance, care plan for, 827–828
observation in, 819
palpation in, 819
pathophysiology of, 816–818
recurrent, risk factors to predict, 818b
screening labwork in, 819

2246
stigmata of, 822b
upper, 816
vital sign assessment in, 818
Gastrointestinal disorders, 814–890

acute gastrointestinal bleeding as, 816-828. See

also Gastrointestinal bleeding, acute.
acute pancreatitis as, 828-845. See also Pancreatitis,
acute.
enterocutaneous fistula as, 845-854. See
also Enterocutaneous fistula (ECF).
hepatic failure as, 854-879. See also Hepatic failure.
from mechanical ventilation, 115
peritonitis as, 879-888. See also Peritonitis.
Gastrointestinal drainage, characteristics of, 281t
Gastrointestinal system,

assessment of, 814-816. See also Gastrointestinal

assessment.
in burn assessment, 317
disorders of, 814-890. See also Gastrointestinal
disorders.
GBS., See Guillain-Barré syndrome (GBS).
Gengraf (cyclosporine), 999
Genitourinary assessment, 636–637

auscultation in, 637

2247
detailed health history in, 636
labwork in, 637
observation in, 636
palpation in, 636
vital sign assessment in, 636
Genitourinary tract trauma, 352–361

AAST Organ Injury Severity Score for, 360t

with acute pain, care plan for, 361
assessment of, 354–358
care plans for, 360–361
care priorities for, 358–359
collaborative assessment of, 358–359
diagnostic tests for, 356–358t
history and risk factors for, 354–355
with impaired urinary elimination, care plan for, 360
with infection risk, care plan for, 361
inspection in, 355–358
observation in, 355
palpation in, 355
pathophysiology of, 352–354, 353–354t
subjective symptoms of, 355
vital signs of, 355

2248
Geodon., See Ziprasidon (Geodon).
Glasgow Coma Scale, 31
Global Health Security Agenda (2014), 200
Glucagon IV bolus, for anaphylactic shock, 899
Glucocorticoids,

replacement of, 764b

in traumatic brain injury management, 381
Glucose management, in traumatic brain injury, 381
Graft-versus-host disease, 1002
Grieving,

care plan for, 233, 246–247

complicated, care plan for, 238
stages of, 233t
Guided imagery, in pain management, 159
Guillain-Barré syndrome (GBS), 720

assessment of, 720–721

with autonomic dysreflexia, care plan for, 724–725
care plans for, 722–726
care priorities for, 722
collaborative management of, 722
with constipation, care plan for, 726
with decreased cardiac output, care plan for, 725
diagnosis of, 721t
with disuse syndrome risk, care plan for, 723–724

2249
history and risk factors for, 720
with impaired gas exchange, care plan for, 722–723
with ineffective airway clearance, care plan for, 723
observation in, 721
pathophysiology of, 720
with sensory/perceptual alterations, care plan for,
725–726
vital signs in, 721

H
Hallucinogens, overdose of, 957–958
Haloperidol lactate (Haldol), in agitation/anxiety management, 179
H2CO3, 2, 3
Healing., See Wound closure/healing.
Health Insurance Portability and Accountability Act of 1996
(HIPAA), 243
Heart,

blunt injury to, in thoracic trauma, 363

dysrhythmias of, 537-576. See also Cardiac
dysrhythmias.
electrical conduction system of, 537, 538f
electrophysiology of, 538–539
valves of,
atrioventricular, 612

2250
disease of, 612-627. See also Valvular heart disease.
prosthetic,
anticoagulation for, 621
thrombosis of, management of, 621
replacement of., See Valve replacement, patients
undergoing.
semilunar, 612
Heart disease, valvular, 612-627. See also Valvular heart disease.
Heart failure (HF), 466–479

with activity intolerance, care plan for, 477–478

assessment of, 467–468t, 467–468
care plans for, 476–478
care priorities for, 472–476
classes of, 468t
collaborative management of, 472–476
with decreased cardiac output, care plan for, 477
with deficient knowledge, care plan for, 478
diagnostic tests for, 469–471t
diuretic dosing in, 472t
with fluid volume excess, care plan for, 476
history and risk factors for, 468–471
with impaired gas exchange, care plan for, 477

2251
left- versus right-sided, 466
pathophysiology of, 466
progression of, 466
systolic and diastolic dysfunction in, 466
Heart rate, 11–12

in burn assessment, 314

Heart rhythm(s),

abnormal, causes of, 539–544

in burn assessment, 314
Heart transplantation,

for cardiomyopathy, 536

donor screening for, 996
for heart failure, 476
priority/waiting lists/medical urgency determination
for, 996–997
rejection in, 1003, 1003t
selection criteria for, 991–994, 991t
Heliox therapy, for acute asthma exacerbation, 398
HELLP syndrome, 967–968
Hematologic disorders, 891-936. See also Hematologic/immunologic
disorders.
Hematologic/immunologic disorders, 891–936

anaphylactic shock., See also Anaphylactic shock.

anaphylactic shock as, 892–902

2252
bleeding disorders as, 913–935. See also specific disorder.
hemolytic crisis as, 902-913. See also Hemolytic crisis.
profound anemia as, 902-913. See also Anemia,
profound.
thrombotic disorders as, 913–935. See also specific
disorder.
Hematology assessment, 891–892

general, 891–892
history in, 891–892
observation in, 891
Hematoma,

epidural, 372
intracranial, 373–374
subdural, 373
Hemodilution, for cerebral aneurysm/subarachnoid hemorrhage,
691
Hemodynamic monitoring, 79–104

in acute cardiac tamponade, 286

in acute gastrointestinal bleeding, 819–821
in acute infective endocarditis, 499
arterial oxygen saturation in, 85
arterial pressure monitoring, 90–91, 91f, 93
blood pressure and, 93

2253
in cardiac dysrhythmias, 544–546
cardiac index and, 96
cardiac output in, 85–86, 96
in cardiogenic shock, 519
for cardiomyopathy, 535
care plans for, 101–104
care priorities for, 100–101
central venous pressure in, 85, 93–94
in collaborative management, 99–101
for complications of acute pancreatitis, 834–837
considerations during setup, line insertion and
placement, 90–93
with deficient knowledge, care plan for, 101–104
diagnostic tests in, 92–93t, 93–98
in enterocutaneous fistula, 847–848
equipment setup for, 86–88
for ineffective peripheral tissue perfusion, care plan
for, 103
with ineffective protection, care plan for, 102–104
left atrial pressure and, 97
pathophysiology and, 80–83
in peritonitis, 881–882

2254
pulmonary artery occlusive pressure and, 96
pulmonary artery pressure monitoring, 91–93
pulmonary artery pressures in, 85, 95–96
right atrial pressure, 85, 94, 94f
right ventricular pressure and, 94–95
with risk for ineffective cardiac tissue perfusion, care
plan for, 102
systemic arterial pressure in, 83–85
tissue oxygenation in, 86
Hemodynamic stability maintenance, in spinal cord injured patient,
299–300
Hemodynamic values,

accurate, promoting, equipment setup for, 86–88

derived, 97–98
normal, 536t
Hemolytic crisis, 902–913

with acute pain, care plan for, 912

assessment of, 904
care plans for, 911–913
care priorities for, 910–911
collaborative management of, 910–911
diagnostic tests for, 904–906t
with fluid volume deficit, care plan for, 912–913

2255
with ineffective tissue perfusion, care plan for, 911–
912
pathophysiology of, 902
Hemorrhage,

gastrointestinal, acute, 816-828. See

also Gastrointestinal bleeding, acute.
intracranial, 734, 735–736
in major trauma, management of, 266
subarachnoid, 373, 692. See also Subarachnoid
hemorrhage.
hypertensive emergency and, management of, 583–
584
Hemorrhagic fever, Ebola, 211-212. See also Ebola virus disease
(EVD).
Hemorrhagic fever viruses (HFVs), 204–205
Hemorrhagic stroke, 734-752. See also Stroke.
Hemothorax, in thoracic trauma, 363
Heparin,

thrombocytopenia induced by, 915. See also Heparin-

induced thrombocytopenia (HIT).
unfractionated, IV infusion dosage titration for, 445,
445t
Heparin-induced thrombocytopenia (HIT), 915

assessment of, 915–917

care plans for, 918–919

2256
care priorities for, 917–918
collaborative management of, 917t
with fluid volume deficit, care plan for, 919
with ineffective protection, care plan for, 918–919
observation in, 915–916
palpation in, 916–917
pathophysiology of, 915, 916f
risk factors for, 915
in superior vena cava syndrome, monitoring for, 985–
986
vital signs in, 915
Heparin therapy,

for abnormal clotting in DIC, 929

in continuous renal replacement therapies, 664
Hepatic encephalopathy, 854

factors contributing to, 875b

precipitating factors for, eliminating or correcting,
868–870
Hepatic failure,

acute, 854–855
ascites in, management of, 868
assessment of, 856–864
auscultation in, 857

2257
care for, in transplant center, benefits of, 856
care plans for, 871–879
care priorities for, 866–871
chronic, 855–856
collaborative management of, 864–871
with deficient knowledge, care plan for, 877–878
diagnostic tests for, 858–862t
with disturbed sensory perception, care plan for, 874–
875
enteral formulas for, 134
with fluid volume deficit, care plan for, 871–872
with fluid volume excess, care plan for, 872
history and risk factors for, 856
with imbalanced nutrition, care plan for, 873
with impaired gas exchange, care plan for, 873–874
with impaired tissue integrity, care plan for, 877
with ineffective protection, care plan for, 876
with ineffective tissue perfusion, care plan for, 876–
877
with infection risk, care plan for, 875–876
with injury risk, care plan for, 879
King’s College Hospital criteria for, 863b

2258
liver biopsy in, 858, 863–864, 863b
liver function tests in, 862–863
management guidelines for, 864–865t
observation in, 857
palpation in, 857
screening labwork in, 857–858
spontaneous bacterial peritonitis in, prevention of,
867–868
vital sign assessment in, 856–857
Hepatic transplantation., See Liver transplantation.
Hepatopulmonary syndrome (HPS), 855
Hepatorenal syndrome (HRS), 856
Herniation syndromes, in traumatic brain injury, 370, 371t
HF., See Heart failure (HF).
HFOV (high-frequency oscillatory ventilation), 113
HFVs (hemorrhagic fever viruses), 204–205
HHS., See Hyperglycemic hyperosmolar syndrome (HHS).
High-frequency oscillatory ventilation (HFOV), 113
High-reliability organizations (HROs), 255–257, 256t
Histamine H2-receptor antagonists,

for acute GI bleeding, 824

in hepatic failure, 866
HIT., See Heparin-induced thrombocytopenia (HIT).
Hormones, in fluid volume regulation, 42
Horowitz classification of pericardial effusions, 284b

2259
Howde Spiritual Assessment Scale (SAS), 229b
HROs (high-reliability organizations), 255–257, 256t
Hunt and Hess classification system, 687
Hydralazine,

for cardiomyopathy, 534

for hypertensive emergency, 583
Hydrocephalus,

in cerebral aneurysm/subarachnoid hemorrhage,

management of, 692, 692b
indicators of, 688
Hydromorphone (Dilaudid),

in anxiety management, 176

in pain management, 155
Hyperbaric oxygen therapy, for venous air embolism, 447
Hypercalcemia, 64

care plans for, 65–66

care priorities for, 65
collaborative management of, 65
diagnostic tests for, 65t
history and risk factors for, 64
with impaired urinary elimination, 66
with ineffective protection, care plan for, 65–66
observation in, 64

2260
pathophysiology of, 64
12-lead ECG in, 64–65
vital signs in, 64
Hypercapnia, permissive, in mechanical ventilation, 111–113
Hyperglycemia, 773–787

with acute confusion, care plan for, 786

auscultation in, 779
care plans for, 784–787
care priorities for, 782–784
collaborative management of, 782–784
with deficient knowledge, care plan for, 786–787
diagnostic tests for, 780–782t
with fluid volume deficit, care plan for, 785
history and risk factors for, 777–779
with infection risk, care plan for, 785–786
metabolic assessment in, 777–782
observation in, 779
palpation in, 779
in pancreatitis patient, correction of, 838–839
pathogenesis of, 773–774
percussion in, 780
with risk for unstable blood glucose, care plan for,

2261
 784–785
screening labwork for, 780–782
vital signs in, 779
Hyperglycemic hyperosmolar syndrome (HHS), 775–777

diabetic ketoacidosis compared with, 776–777t

pathophysiology of, 775–777
Hyperkalemia, 58

in acute kidney injury, 640–643t

assessment of, 58–59
care plans for, 60
care priorities for, 59–60
collaborative management of, 59–60
with decreased cardiac output, care plan for, 60
diagnostic tests for, 59t
observation in, 59
pathophysiology of, 58
screening for, 59–60
vital signs in, 59
Hypermagnesemia, 77

in acute kidney injury, 640–643t

assessment of, 77–78
care plans for, 78–79

2262
collaborative management of, 78
with deficient knowledge, care plan for, 79
diagnostic tests for, 78t
history and risk factors for, 77
with ineffective protection, care plan for, 78–79
observation in, 77
palpation in, 77
pathophysiology of, 77
screening for, 78
vital signs in, 77
Hypernatremia, 53

with acute confusion, care plan for, 54

in acute kidney injury, 640–643t
assessment of, 53–54
care plans for, 54
care priorities for, 54
collaborative management of, 54
diagnostic tests for, 54t
history and risk factors for, 53
observation in, 53
pathophysiology of, 53
vital signs in, 53–54

2263
Hyperosmolar therapy,

for traumatic brain injury, 377

in traumatic brain injury, 377
Hyperphosphatemia, 71

in acute kidney injury, 640–643t

assessment of, 71–72
care plans for, 72–73
care priorities for, 72
collaborative management of, 72
with deficient knowledge, care plan for, 72–73
diagnostic tests for, 72t
history and risk factors for, 71
with ineffective protection, care plan for, 73
observation in, 71
pathophysiology of, 71
percussion in, 71–72
screening for, 72
vital signs in, 71
Hypertension,

abdominal, 937-945. See also Abdominal

hypertension.
for cerebral aneurysm/subarachnoid hemorrhage, 691

2264
medications for, 586–588t
in pregnancy, 964-975. See also Pregnancy,
hypertension in.
pulmonary, 450-457. See also Pulmonary
hypertension.
secondary, causes of, 579b
in stroke, management of, 742–744
Hypertensive emergencies, 578

with acute pain, care plan for, 585

assessment of, 578–581
auscultation in, 580–581
care plans for, 584–589
care priorities for, 582–584
collaborative management of, 582–584
diagnostic tests for, 581–582t, 581–582
with disturbed sensory perception, care plan for, 585–
589
history and risk factors for, 578–579
with ineffective tissue perfusion, care plan for, 584–
585, 586–588t
observation in, 579–580
palpation in, 580
pathophysiology of, 576–578

2265
vital signs in, 580
Hyperthyroidism, uncontrolled, 803-810. See also Thyrotoxicosis
crisis.
Hypertrophic cardiomyopathy (HCM), 528
Hyperventilation,

in acute respiratory failure, correction of, 427

in compensation for acidosis, 2
in compensation for alkalosis, 2
in traumatic brain injury management, 375–376, 375b
Hypervolemia, 46

assessment of, 46–47

auscultation in, 47
care plans for, 48–49
care priorities for, 48
for cerebral aneurysm/subarachnoid hemorrhage, 690,
690b
collaborative management of, 48
diagnostic tests for, 47t
with fluid volume excess, care plan for, 48–49
history and risk factors for, 46
with impaired gas exchange, care plan for, 49
with impaired skin integrity, care plan for, 49
observation in, 47

2266
palpation in, 47
pathophysiology of, 46
radiology in, 47
screening labwork in, 47
vital signs in, 47
Hypocalcemia, 61

in acute kidney injury, 640–643t

assessment of, 58–59
care plans for, 62–64
care priorities for, 62
collaborative management of, 62
complicating plasmapheresis, 716
with decreased cardiac output, care plan for, 63
diagnostic tests for, 62t
history and risk factors for, 61
with ineffective breathing pattern, care plan for, 64
with ineffective protection, care plan for, 62–63
observation in, 61
in pancreatitis patient, correction of, 838
pathophysiology of, 61
vital signs in, 61
Hypokalemia, 55

2267
in acute kidney injury, 640–643t
assessment of, 55–56
auscultation in, 56
care plans for, 57–58
care priorities for, 56–57
collaborative management of, 56–57
complicating plasmapheresis, 716
with decreased cardiac output, care plan for, 57–58
diagnostic tests for, 56t
history and risk factors for, 55–56
with ineffective breathing pattern, care plan for, 58
palpation in, 56
pathophysiology of, 55
screening for, 56
vital signs in, 56
Hypomagnesemia, 73–74

assessment of, 74–75

care plans for, 75–77
care priorities for, 75
collaborative management of, 75
with decreased cardiac output, care plan for, 76
diagnostic tests for, 75t

2268
history and risk factors for, 74
with ineffective protection, care plan for, 75–76
with nutritional imbalance, care plan for, 76–77
observation in, 74
pathophysiology of, 73–74
percussion in, 74
screening for, 74–75
vital signs in, 74
Hyponatremia, 50

with acute confusion, care plan for, 52–53

in acute kidney injury, 640–643t
assessment of, 50–51
care plans for, 52–53
care priorities for, 51–52
chronic, management of, 801–802
collaborative management of, 51–52
diagnostic tests for, 51t
history and risk factors for, 50
observation in, 50
palpation in, 50
pathophysiology of, 50
with readiness for enhanced fluid volume, care plan

2269
 for, 52
screening labwork for, 51
SIADH-induced, 796b
vital sign assessment in, 50
Hypophosphatemia, 67

assessment of, 67–68

care plans for, 69–71
care priorities for, 68
collaborative management of, 68
with compromised immunity, care plan for, 70–71
with decreased cardiac output, care plan for, 70
diagnostic tests for, 68t
history and risk factors for, 67
with impaired gas exchange, care plan for, 69–70
observation in, 67
pathophysiology of, 67
vital signs in, 68
Hypotension,

in adrenal crisis, correction of, 762

with decreased cardiac output, from mechanical
ventilation, 115
Hypothalamic-pituitary axis, 756, 757f
Hypothermia,

2270
therapeutic, after intracranial surgery, 698
in trauma patient, management of, 267, 270, 277
Hypothyroidism,

acute, common causes of, 788b

diagnosing, 791f
myxedema coma and, 787–788, 789. See
also Myxedema coma.
Hypoventilation, in acute respiratory failure, 423

correction of, 427

Hypovolemia, 42

in adrenal crisis, correction of, 762

assessment of, 42–44
care plans for, 45–46
care priorities for, 44–45
collaborative management of, 44–45
complicating plasmapheresis, 716
with fluid volume deficit, care plan for, 45
history and risk factors for, 42–43
with ineffective peripheral tissue perfusion, care plan
for, 46
management of, 44–45t
observation in, 43
palpation in, 43

2271
pathophysiology of, 42
screening labwork for, 43–44
in trauma patient, management of, 266, 277–278
vasodilation-induced, management of, in spinal cord
injured patient, 300
vital signs in, 43
Hypovolemic shock, 42, 43–44b
Hypoxemic hypoxia, in acute respiratory distress syndrome, 407

I
ICG., See Impedance cardiography (ICG).
ICH., See Intracranial hemorrhage (ICH).
ICP., See Intracranial pressure (ICP).
Idioventricular rhythm, 556f
Imagery, guided, in pain management, 159
Immobility, prolonged, 162–172

with activity intolerance, care plan for, 164–165

with altered cerebral tissue perfusion, care plan for,
169–170
care plans for, 164–172
with constipation, care plan for, 170–171
with deficient diversional activity, care plan for, 171–
172
with impaired skin integrity, care plan for, 167
with ineffective peripheral tissue perfusion, care plan

2272
 for, 168–169
with injury risk, care plan for, 172
physiologic effects and complications of, 162b
with risk for disuse syndrome, care plan for, 166–167
with self-care deficit, care plan for, 167–168
Immune globulin, intravenous, in posttransplant
immunosuppression, 1001
Immune thrombocytopenic purpura (ITP), 920

with acute pain, care plan for, 924

assessment of, 920–921
care priorities for, 921–922
collaborative management of, 921–922
with decreased intracranial adaptive capacity, care
plan for, 923
diagnostic tests for, 921t
with fluid volume deficit risk, care plan for, 923–924
with ineffective protection, care plan for, 922–923
observation in, 920
palpation in, 920–921
pathophysiology of, 920
risk factors for, 920
vital signs in, 920
Immunoglobulin, IV, for immune thrombocytopenic purpura, 921

2273
Immunologic disorders, 891-936. See
also Hematologic/immunologic disorders.
Immunosuppression therapy,

drug categories for, 998–1001

levels of, 998
posttransplant, 998
Impedance cardiography (ICG), in cardiac output measurement,
85–86
Impella recover 2.5, for cardiogenic shock, 522
Implantable cardioverter-defibrillator (ICD), 566–567, 566t

patients with,
care plans for, 573–574
with sexual dysfunction, care plan for, 576
third-generation,
electromagnetic interference and, 575t
patients with, care plans for, 575
Imuran (azathioprine), 999
Indirect calorimetry, in nutrition requirements estimation,

2274
127
Infection(s),

emerging, 209–226
avian influenza as, 224-225. See also Avian influenza
(“bird flu”).
Creutzfeldt-Jakob disease as, 220. See also Creutzfeldt-
Jakob disease (CJD).
Ebola virus disease as, 211-212. See also Ebola virus
disease (EVD).
Middle Eastern respiratory syndrome as, 217. See
also Middle Eastern respiratory syndrome (MERS-
CoV).
multidrug-resistant organisms as, 210–211
pandemic flu as, 224
prevention and control of, 209–210
severe acute respiratory syndrome as, 214. See
also Severe acute respiratory syndrome (SARS).
West Nile virus as, 222. See also West Nile virus.
opportunistic, in organ transplantation, prevention of,
1001
prevention/control of,
after intracranial surgery, 698
in genitourinary tract trauma, 358
in hepatic failure, 870

2275
in meningitis, 708–709
in nonfatal drowning patient, 345
in septic patients, 1017, 1019
in spinal cord injury, 302
in transplant patients, 1001–1002
wound, in burn assessment, 318
Infective endocarditis, acute, 498-507. See also Endocarditis, acute
infective.
Influenza, avian, 224-225. See also Avian influenza (“bird flu”).
Informed consent, 241–242

elements of, 242b

Inotropic therapy, for cardiomyopathy, 534
Insulin, for cerebral aneurysm/subarachnoid hemorrhage, 690
Integumentary system, in burn assessment, 318
Intensive Care Delirium Screening Checklist (ICDSC), 31
Interleukin 1 inhibitors, in posttransplant immunosuppression,
998–999
Intestinal bleeding, 817
Intestinal edema, massive, 276b
Intraabdominal hypertension, 937-945. See also Abdominal
hypertension.

definition of, 938

pressure and symptom grade for, 938t
Intraabdominal pressure, definition of, 938
Intraabdominal pressure monitoring,

methods of, 941–942

2276
in pancreatitis patient, 840
in peritonitis, 884
Intraaortic balloon pump (IABP), for cardiomyopathy, 535
Intracellular fluid compartment (ICF), 41
Intracranial hematoma, 373–374
Intracranial hemorrhage (ICH), 734, 735–736

clinical presentation of, 738

Intracranial pressure (ICP),

in cerebral aneurysm, 687–688

dynamics of, changes in, in traumatic brain injury, 368
management of, 375, 375b, 376t
increased,
indicators of, 688b
from mechanical ventilation, 115
nursing interventions for, 384b
nursing care activities raising, modifying, 379–380,
379b, 380b
in subarachnoid hemorrhage, 687–688
Intracranial surgery, 694–701

care priorities after, 696–698

collaborative management after, 696–698
complications after, care plans for, 698–701
with decreased cardiac output, care plan for, 700

2277
with decreased intracranial adaptive capacity, care
plan for, 698–699
with fluid volume deficit or excess, care plan for, 699–
700
functional assessment in, 696
history and risk factors for, 695
with impaired physical mobility, care plan for, 700
with ineffective breathing pattern, care plan for, 699
with infection risk, care plan for, 699
neurologic assessment for, 694–696
observation in, 695
with pain, care plan for, 700–701
screening labwork for, 696
vital signs in, 695
Intravascular foreign bodies,

care priorities for, 448

diagnostic tests for, 443
history and risk factors for, 441–442
pulmonary embolism from, 438
Intubation, reasons to consider, 108b
Invasive mechanical ventilation, 107–108
Inverse ratio ventilation (IRV), 112
Iodides, for thyrotoxicosis crisis, 806

2278
Ipratropium bromide, for acute asthma exacerbation, 399t
Iron, supplemental, for anemia, 907
IRV (inverse ratio ventilation), 112
Ischemic myositis, 334-341. See also Compartment syndrome.
Ischemic stroke, acute, 734-752. See also Stroke.
Isoproterenol, for failing heart, 520
Isotonic sodium chloride solution, in continuous renal replacement
therapies, 665
ITP., See Immune thrombocytopenic purpura (ITP).

J
Joint Commission National Patient Safety Goals (2014), 249–250,
250b
Jugular venous oxygen saturation monitoring, in traumatic brain
injury, 376
Junctional complexes, premature, 553f
Junctional escape rhythm, 552f
Junctional rhythm,

accelerated, 552f
atrioventricular, 463–465
Junctional tachycardia, 553f
“Just Culture”, 252–254, 254b

K
Ketamine, in pain management, 157
Ketorolac (Toradol), in pain management, 157
Kidney(s),

2279
AAST Organ Injury Severity Score for, 360t
failure of, 636-672. See also Renal failure, acute.
injury to, acute., See Renal failure, acute.
protection of, in compartment syndrome, 339
transplantation of, selection criteria for, 993–994
trauma to, 352-361. See also Genitourinary tract
trauma.
Kidney transplantation,

donor screening for, 996

priority/waiting lists/medical urgency determination
for, 997
rejection in, 1004–1005, 1004t

L
Labetalol, for hypertensive emergency, 583
Labor and delivery,

hemodynamic changes during, 965t

in preeclampsia, 972
emergency, in critical care unit, 973
preparation for, 972–973
preterm, monitoring for, in hypertensive patient, 969–
970
Lactic acidosis, metabolic, 17–18
LAP., See Left atrial pressure (LAP).

2280
Laparotomy, decompressive, for abdominal compartment
syndrome, 943
Large intestine, bleeding in, 817
Lateral cord syndrome, 296
Left atrial pressure (LAP), hemodynamic measurements and, 97
Left ventricular noncompaction (LVNC), 528–529
Levalbuterol, for acute asthma exacerbation, 399t
Levosimendan, for failing heart, 520, 521, 521t
Lifestyle alterations, for hypertensive patients, education on, 584
Liver,

biopsy of, in hepatic failure assessment, 858, 863–864,

863b
failure of, 854-879. See also Hepatic failure.
Liver transplantation,

donor screening for, 996

for hepatic failure, 871
priority/waiting lists/medical urgency determination
for, 997
rejection in, 1005, 1005t
selection criteria for, 993
Living organ donation, 995
Living will, 243
Locked-in syndrome (LIS), 28–29

care priorities for, 37

Lorazepam (Ativan),

2281
in agitation/anxiety management, 178
for status epilepticus, 729
Lower extremity peripheral artery occlusive disease, 590–592

care priorities for, 602–604

management guidelines for, 599–601t
Lund-Browder chart in burn estimation, 314, 315f
Lung(s),

acute injury of, 404-405. See also Respiratory distress

syndrome, acute (ARDS).
physical impairment after, risk factors for, 413b
collapsed, in pneumothorax, reexpansion of, 432–433
Lung transplantation,

donor screening for, 996

priority/waiting lists/medical urgency determination
for, 997
rejection in, 1004
selection criteria for, 992–993

M
MabCampth (alemtuzumab), 1000
Macronutrient requirements, 128
“Mad cow” disease, 220
Magnesium,

deficiency of, 73. See also Hypomagnesemia.

2282
excess of, 77. See also Hypermagnesemia.
foods high in, 75b
imbalances of, 73
Magnesium sulfate,

for acute asthma exacerbation, 427

for hypertensive obstetric disorders, 970–971, 970b,
971t
Malignancy-related emergencies, 975-989. See also Oncologic
emergencies.
Malnutrition, 123. See also Nutrition support.

risk factors for, 124–125

signs of, 815t
Mammalian target of rapamycin inhibitors, in posttransplant
immunosuppression, 1000
Mandatory minute ventilation, 113
MAP., See Mean arterial pressure (MAP).
Massage, in pain management, 158
MDROs., See Multidrug-resistant organisms (MDROs).
Mean airway pressure, 106
Mean arterial pressure (MAP), hemodynamic measurements and,
93
Mechanical ventilation, 104–123

for acute asthma exacerbation, 398

for acute pancreatitis, 837–838
for acute pneumonia patient, 419

2283
for acute respiratory distress syndrome, 419
adjuncts to, 110–114
airway pressure-release, 112–113
alveolar mechanics in, 110–111
for anthrax, 202
with anxiety, care plans for, 122–123
anxiety from, 116
appropriate, diagnostic evaluation of, 113–114t
assist-control, 108–109
autoflow in, 113
barotrauma in, 114
bilevel, 113
breath limit, 110
for burns patient, 323
care plans for, 118–123
complications related to, 114–116
fluid imbalance from, 115
gastrointestinal complications of, 115
high-frequency oscillatory, 113
hypotension with decreased cardiac output from, 115
with impaired gas exchange, care plans for, 118–120,
122

2284
with ineffective airway clearance, care plan for, 120
with ineffective breathing pattern, 120–122
with ineffective protection, care plan for, 121–122
intracranial pressure increase from, 115
invasive, 107–108
inverse ratio, 112
low-tidal volume, 111–113
in meningitis, 708b
basic, 108–110
to promote alveolar recruitment, 112–113
negative pressure, 107
for nonfatal drowning patient, 344
noninvasive positive-pressure, 107
permissive hypercapnia, 111–113
for pneumothorax, 432
pneumothorax in, 114
positive end-expiratory pressure in, 110–111
positive-pressure, 107
pressure support, 109
protective lung ventilation, 111–113
restlessness in, management of, 120–122b
for septic patients, 1018

2285
for spinal cord injured patient, 300
spontaneous breathing trials during, 118
synchronized intermittent mandatory, 109
tension pneumothorax in, 114–115
in thoracic trauma, 366
for traumatic brain injury patient, 375–376
troubleshooting ventilator problems in, 118, 119b
ventilator-associated events from, 115–116, 415
volutrauma in, 114
weaning from, 116–118
failure of, 118
traditional methods of, 116–118
Medications., See also Pharmacotherapy.

GI bleeding from, 817

Meningitis, 701–711

with acute pain, care plan for, 710

aseptic, 702
bacterial, 701–702
care plans for, 710–711
care priorities for, 708–710
cerebrospinal fluid findings in, 707t
clinical presentation of, 704–705

2286
collaborative management of, 708–710
with decreased intracranial adaptive capacity, care
plan for, 710
diagnostic tests for, 706–707t, 706–707
eosinophilic, 702
functional assessment of, 705–706
fungal, 702
history and risk factors for, 703–704
with infection risk, care plan for, 711
neurologic assessment in, 703–706
noninfectious causes of, 702–703
observation in, 704–705
pathophysiology of, 701–703
positive signs of, 703t
screening labwork in, 706
tuberculous, 702
viral, 702
vital signs in, 704
WNV, 223
Mental status,

altered, 25-40. See also Consciousness, alterations in.

assessment of, 29–31

2287
Mental status testing, 31, 32b
Meperidine (Demerol),

in anxiety management, 176

in pain management, 155
MERS-CoV., See Middle Eastern respiratory syndrome (MERS-
CoV).
Metabolic acidosis, 15–16

acute, 18–21
in acute kidney injury, 640–643t
chronic, 21–22
lactic acidosis, 17–18
pathophysiology of, 15–16
Metabolic alkalosis, 22–23

acute, 23–24
chronic, 24–25
pathophysiology of, 22–23
Metabolic demand, reduction of, in traumatic brain injury
management, 377–379, 378t
Methanol overdose, 949
Methicillin-resistant Staphylococcus aureus (MRSA), 211
Methimazole, for thyrotoxicosis crisis, 806
Methylprednisolone, for acute asthma exacerbation, 399t
Methylprednisolone (Solu-Medrol), 999
MG., See Myasthenia gravis (MG).
MI., See Mitral insufficiency (MI)/regurgitation (MR).

2288
Midazolam (Versed),

in agitation/anxiety management, 178

for status epilepticus, 729, 730
Middle Eastern respiratory syndrome (MERS-CoV), 217

assessment of, 218–219

care priorities for, 219
diagnostic tests for, 218–219t
history and risk factors for, 218
pathophysiology of, 217
signs and symptoms of, 218–219
transmission of, 217–218
Mifflin St. Jeor formula, for nutrition requirements, 128
Milrinone,

for cardiomyopathy, 534

for failing heart, 520, 521t
Mineralocorticoids, replacement of, 764b
Minerals, trace,

requirements for, 128–129

Mini-Mental Status Examination (MMSE), 31, 32b
Minimally conscious state (MCS), 28
Minimum minute ventilation, 113
Minute ventilation (VE, VTE), of MV), 105
Mitral insufficiency (MI)/regurgitation (MR), 613

management of, 620–621

2289
Mitral stenosis, 612–613

management of, 620

Mitral valve, 612

disease of, 612–613, 615t

Mixed venous oxygen saturation, in hemodynamic values
adjustment, 98
MMF (mycophenolate mofetile), 999
Mobilization, early, for acute respiratory distress syndrome patient,
411b
Modified Penn State Formula, for nutrition requirements, 128
Monoclonal antibodies, in posttransplant immunosuppression, 1000
Morphine,

in anxiety management, 176

in pain management, 155
Motor function, in neurologic assessment, 673–674
MR., See Mitral insufficiency (MI)/regurgitation (MR).
MRSA (methicillin-resistant Staphylococcus aureus), 211
Multidrug-resistant organisms (MDROs), 210–211
Multiorgan dysfunction syndrome (MODS), 261, 1008–1023

assessment of, 1013–1016

with cardiac output decrease, care plan for, 1020
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
diagnostic tests for, 1015–1016t

2290
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
observation and assessment findings in, 1015–1016
pathophysiology of, 1009–1010
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
Multivitamins, in TPN, 141
Murmurs, in valvular heart disease, 614
Muscle strength rating, 674t
Mutism, akinetic, 28
Myasthenia gravis (MG), 712

assessment of, 712–714

auscultation in, 713–714
care plans for, 715–720
collaborative management of, 714–715
with deficient knowledge, care plans for, 719–720
history and risk factors for, 712

2291
with impaired gas exchange, care plan for, 715
with impaired swallowing, care plan for, 718
with ineffective airway clearance, care plan for, 717
with infection risk, care plan for, 717–718
observation in, 713
pathophysiology of, 712
symptom progression in, 713
with visual perception disturbance, care plan for, 718–
719
vital signs in, 713
Myasthenic crisis, 713

complicating plasmapheresis, 717

diagnosis of, 713–714t
emergency interventions for, 714
Mycophenolate mofetile (MMF, Cellcept), 999
Mycophenolic acid (Myfortic), 999
Mycostatin, 1001
Myfortic (mycophenolic acid), 999
Myocardial contractility, ECG tracings and, 539
Myocardial infarction (MI),

acute, hospital quality alliance indicators of, 486t

in acute coronary syndrome, 479, 480
Myocardial oxygen consumption, reduction of, 487
Myocardial workload, reduction of, 487

2292
Myositis, ischemic, 334-341. See also Compartment syndrome.
Myxedema coma, 787–795

with activity intolerance, care plan for, 793–794

care plans for, 792–795
care priorities for, 791–792
collaborative management of, 791–792
with constipation, care plan for, 794–795
with deficient knowledge, care plan for, 795
diagnostic tests for, 790t
endocrine assessment in, 788–790
with fluid volume excess, care plan for, 793
history and risk factors for, 788–789
hypothyroidism and, 787–788, 789
with ineffective breathing pattern, care plan for, 793
with ineffective protection, care plan for, 792–793
with infection risk, care plan for, 794
with nutritional imbalance risk, care plan for, 794
observation in, 789
pathophysiology of, 787–788
screening labwork in, 789–790
vital signs in, 789, 789b

2293
N
N-Acetylcysteine, in hepatic failure, 867
Naloxone, in pain management, 158b
Nasoenteric feeding tube placement, complications of, 135
Nasogastric intubation, for burn patient, 324
Negative pressure ventilation, 107
Neoral (cyclosporine), 999
Nephrotoxins, common, 640t
Neurodegenerative disorders, 711-727. See
also Neurodegenerative/neuromuscular disorders.
Neurodegenerative/neuromuscular disorders, 711–727

Guillain-Barré syndrome as, 720. See also Guillain-

Barré syndrome (GBS).
myasthenia gravis as, 712. See also Myasthenia gravis
(MG).
pathophysiology of, 711–712
Neurogenic shock, in spinal cord injury, 292–293
Neurologic assessment, 673–676

for brain death, 678–681

dysphagia screening in, 675–676
fundoscopic, 675
in hypertensive emergencies, 579–580
for intracranial surgery, 694–696
key cranial nerve assessment in, 673
level of consciousness in, 673

2294
in meningitis, 703–706
motor and cerebellar function in, 673–674
sensory assessment in, 674–675
vital signs in, 673
Neurologic complications, of traumatic brain injury, 370
Neurologic deficit, cerebral perfusion neuroanatomy related to, 736t
Neurologic disorders, 673–755

assessment of, 673–676

brain death as, 677-684. See also Brain death.
cerebral aneurysm as, 684-694. See also Cerebral
aneurysm.
diagnostic tests for, 675–676t
intracranial surgery for, 694-701. See also Intracranial
surgery.
meningitis as, 701-711. See also Meningitis.
neurodegenerative, 711-727. See
also Neurodegenerative/neuromuscular disorders.
neuromuscular, 711-727. See
also Neurodegenerative/neuromuscular disorders.
status epilepticus as, 727-733. See also Status
epilepticus (SE).
stroke as, 734-752. See also Stroke.
subarachnoid hemorrhage as, 692. See
also Subarachnoid hemorrhage.

2295
Neurologic evaluation,

in mental status/consciousness assessment, 31, 32b,

33b, 34b
in stroke, 737–738
Neuromuscular blockade, 173–183

for anxiety reduction, care plan for, 181

care plans for, 181–182
care priorities for, 176–180
collaborative management of, 176–180
with deficient knowledge, care plan for, 182
drugs and physiologic conditions affecting, 181b
with injury risk, care plan for, 182
monitoring, 175–176
Neuromuscular blocking agents (NMBAs),

in agitation/anxiety management, 179–180

Neuromuscular disorders, 711-727. See
also Neurodegenerative/neuromuscular disorders.
Neuroprotective strategies, in traumatic brain injury management,
382
Neutropenic sepsis,

with acute pain, care plan for, 983–984

assessment of, 980–981
care plans for, 982–984
care priorities for, 982

2296
collaborative management of, 982
with decreased cardiac output, care plan for, 983
diagnostic tests for, 981t
history and risk factors for, 980
with ineffective protection, care plan for, 982–983
observation of, 981
pathophysiology of, 980
stages of, 980
Nicardipine, for hypertensive emergency, 583
Nimbex., See Cisatracurium (Nimbex).
Nimodipine (Nimotop), for cerebral aneurysm/subarachnoid
hemorrhage, 689
Nimotop., See Nimodipine (Nimotop).
NiPPV (noninvasive positive-pressure ventilation), 107
Nipride., See Nitroprusside (Nipride).
Nitrates, for cardiomyopathy, 534
Nitrogen balance, in nutrition assessment, 127
Nitroglycerin, for hypertensive emergency, 583
Nitroprusside (Nipride), for hypertensive emergency, 583
NMBAs., See Neuromuscular blocking agents (NMBAs).
Noninvasive positive-pressure ventilation (NiPPV, NPPV), 107

for respiratory acidosis in acute respiratory failure,

427
Nonopioids, in pain management, 156
Nonsteroidal antiinflammatory drugs (NSAIDs),

2297
GI bleeding from, 817
in pain management, 157
Norepinephrine,

for anaphylactic shock, 898

for failing heart, 520, 521t
“Nothing About Me, Without Me”, 254–255
NPPV (noninvasive positive-pressure ventilation).,
See Noninvasive positive pressure ventilation (NiPPV, NPPV).
Numeric Rating Scale for pain, 153, 154f
Nutrition assessment,

in acute gastrointestinal bleeding, 819

in acute pancreatitis, 834
anthropometric data in, 125
diagnostic tests in, 125–127
in enterocutaneous fistula, 847
in gastrointestinal disorders, 815
malnutrition risk factors in, 124–125
malnutrition signs in, 815t
medical/diet history in, 124
nitrogen balance in, 127
in peritonitis, 880
physical assessment in, 125
visceral protein status in, 125–127

2298
Nutrition requirements,

carbohydrates in, 128

estimating, 127–130
fats in, 128
fluids in, 130
proteins in, 128
trace minerals in, 128–129
vitamins in, 128–129
Nutrition support, 123-150. See also Foods.

in acute gastrointestinal bleeding, 823

in acute pneumonia, 420
in acute renal failure, 651
in acute respiratory distress syndrome, 412–413
in acute respiratory failure, 427–428
after intracranial surgery, 698
assessment for, 124-125. See also Nutrition assessment.
in burn, 325
care plans for, 144–150
definition of, 123
with diarrhea, care plan for, 147
enteral nutrition in, 131-138. See also Enteral
formulas/nutrition.

2299
in enterocutaneous fistula, 849
with fluid volume imbalance risk, care plan for, 150
in hepatic failure, 866
with impaired tissue integrity, care plan for, 148
with ineffective protection from aspiration, care plan
for, 147
with infection risk, care plan for, 149
with injury risk, care plan for, 149
in meningitis, 708
modalities for, 131–143
with nutritional imbalance, care plan for, 144–150
for pancreatitis patient, 839
parenteral nutrition in, 138-143. See also Parenteral
(IV) nutrition.
for peritonitis, 884
for septic patients, 1019
in spinal cord injury, 301
transitional feeding in, 143
in trauma management, 268, 279
for traumatic brain injury patient, 380
Nystan, 1001

2300
Obese patient., See Bariatric patient.
Obstetrics., See also Pregnancy.

HELLP syndrome in, 967–968

high-risk, 964–975
in critical care, care plans for, 973–975
Octreotide, for acute GI bleeding, 824
OKT3 (Orthoclone), 1000
Olanzapine (Zyprexa), in agitation/anxiety management, 179
Older adults,

acute renal failure risk in, 644

pain management in, 157–158
Oncologic emergencies, 975–989

classification of, 976

definition of, 975, 976–979t
neutropenic sepsis as, 980. See also Neutropenic
sepsis.
superior vena cava syndrome as, 984. See
also Superior vena cava syndrome (SVCS).
tumor lysis syndrome as, 987
Opioids,

overdose of, 958

in pain management, 155
Opportunistic infections, in organ transplantation, prevention of,
1001
Organ donation/donors, 994–995

2301
after brain death, 995
management of, 681–682t
after cardiac death, 995
living, 995
paired an chain, 995
Organ transplant rejection,

assessment of, 1002–1006

biopsy rejection scale for, 1003t
characteristics of, 1002t
clinical presentation with, 1003t
diagnosis of, 1002–1006
graft-versus-host disease in, 1002
prevention of, 1002
vasculopathy in, 1002
Organ transplantation, 989–1007. See also specific organ, e.g. Heart
transplantation.
allocation of cardiac organs for, 990b
care plans for, 1006–1007
care priorities for, 1001–1002
collaborative management of, 1001–1002
diagnostic testing for, 990
evaluation for, 989
immunosuppression therapy for, 998–1001
with impaired oral mucous membranes, care plan for, 1007

2302
with impaired skin integrity, care plan for, 1007
infection control/prevention in, 1001–1002
with infection risk, care plan for, 1006–1007
with injury risk, care plan for, 1006
laboratory and diagnostic tests for, 996
labwork for, 989–990
pharmacotherapy for, 998–1001
priority/waiting lists/medical urgency determination for, 996–998
rejection in., See Organ transplant rejection.
selection criteria for, organ-specific, 991–994

heart, 991, 991t

kidney, 993–994
liver, 993
lung, 992–993
pancreas, 994
Orthoclone (OKT3), 1000
Orthostatic hypotension, from prolonged immobility, care plan for,
169–170
Osmolality, 41
Osmotic demyelination syndrome, 52b
Oximetry, pulse, 5
Oxygen therapy,

for acute asthma exacerbation, 397–398

for acute gastrointestinal bleeding, 823
for acute pneumonia patient, 418–419

2303
for acute respiratory distress syndrome, 410
for anemia, 906
for burn patient, 322–323
for heart failure, 472
for hemolytic crisis, 910
for nonfatal drowning patient, 344
for pneumothorax, 432
for trauma patient, 277
Oxyhemoglobin dissociation curve, 19f

P
P wave, 538
PA pressures., See Pulmonary artery (PA) pressures.
Pacemaker(s),

atrial, wandering, 549f

atrial overdrive, 570
codes for, NBG, 569t
dual-chamber, for cardiomyopathy, 535
permanent, 568–569
patients with, care plans for, 573–574, 575
temporary cardiac, 569
patients with, care plans for, 575
temporary epicardial, 569–570

2304
transcutaneous, transthoracic cardiac, 570
ventricular demand (VVI), 558f
with failure to capture, 559f
with failure to sense, 559f
wandering atrial, 549f
PACs., See Premature atrial complexes (PACs).
Pain, 150–162

abdominal,
in acute gastrointestinal bleeding assessment, 819
in acute pancreatitis, 833
in enterocutaneous fistula, 846
in peritonitis, 880
assessment of, 151–159
definition of, 151
history and risk factors for, 152–153
management of, 153-158. See also Pain management.
pathophysiology of, 151
types of, 151
undertreated, in ICU, origins for, 152–153
Pain management, 153–158

in acute pericarditis, 510–511

in acute pneumonia patient, 420

2305
after intracranial surgery, 697
for burn patient, 326
care plans for, 159–162
cognitive-behavioral techniques in, 159
ethical obligation for, 153–154
in genitourinary tract trauma, 358
for hemolytic crisis, 910
in hepatic failure, 871
in hypertensive obstetric disorders, 971–972
with impaired skin integrity, care plan for, 162
with ineffective breathing pattern, care plan for, 161
nonpharmacologic interventions in, 158–159
in older adults, 157–158
for organ transplantation, 1001
in pancreatitis patient, 839
pharmacologic therapies in, 155–157
physical techniques in, 158–159
in pneumothorax, 433–434
in spinal cord injured patient, 301
in trauma patient, 267, 269–270, 279–280
with urinary retention, care plan for, 161
Paired organ donation, 995

2306
Pancreas, bleeding in, 817
Pancreas transplantation,

donor screening for, 996

priority/waiting lists/medical urgency determination
for, 997–998
rejection in, 1005–1006
selection criteria for, 994
Pancreatitis, acute, 828–845

abdominal pain in, 833

with acute pain, care plan for, 842–843
AGA recommendations for, 838b
assessment of, 830–837
auscultation in, 833
care plans for, 840–845
care priorities for, 837–840
collaborative management of, 837–840
complications of, 829–830
with decreased cardiac output, care plan for, 842
with deficient knowledge, care plan for, 845
diagnostic tests for, 834–837t
factors precipitating, 829b
with fluid volume deficit, care plan for, 840–842

2307
with fluid volume excess, care plan for, 843–844
hemodynamic measurements for complications of,
834–837
history and risk factors for, 830
with imbalanced nutrition, care plan for, 844–845
with impaired gas exchange, care plan for, 843
with infection risk, care plan for, 844
nutrition assessment in, 834
observation in, 833
palpation in, 834
risk stratification for, 829, 830b, 831t, 833b
screening labwork in, 834
serum lipase and amylase in, 837
severity of,
Acute Physiology and Chronic Health Evaluation
(APACHE) II scoring system for, 831t
Bedside Index of, 833b
Ransons criteria for classifying, 830b
vital sign assessment in, 833
Pancuronium (Pavulon), in agitation/anxiety management, 180
Pandemic flu, 224
PAOP., See Pulmonary artery occlusive pressure (PAOP).
PAPs., See Pulmonary artery pressures (PAPs).

2308
Paracentesis, for ascites in hepatic failure, 868
Paradoxical pulse, measuring, 274b
Parenteral (IV) nutrition, 138-143. See also Nutrition support.

catheter insertion site selection for, 141–143

complications in, 143
electrolyte imbalances from, 143
indications for, 143
solutions for, components of, 140–141
Patient(s), handling of, safe, 163–164
Patient safety, 247–257

AACN standards for health work environments and,

251t
communication and, 250–252
culture of, 250–254, 251b, 251t, 253b, 254b
family involvement in, 254–255, 254b, 255–256t
high-reliability organizations and, 255–257, 256t
Joint Commission National Patient Safety Goals of
(2014), 249–250, 250b
“Just Culture” and, 252–254, 254b
national goals for, 249–250
“never events” in, 250, 250b
organizations for, 250
patient involvement in, 254–255, 254b, 255–256t

2309
resources on, 248t
sentinel events policy and, 248–249, 249b
standards for, 247–250
TeamSTEPPS and, 252, 253t
PAV., Proportional-assist ventilation (PAV).
Pavulon., See Pancuronium (Pavulon).
PCIs., See Percutaneous coronary interventions (PCIs).
PE., See Pulmonary embolism (PE).
Peak expiratory flow (PEF), in acute asthma exacerbation, 394
Peak inspiratory pressure (PIP), 105–106
PEEP., See Positive end-expiratory pressure (PEEP).
PEF., See Peak expiratory flow (PEF).
Pelvic fractures, 347–352

assessment of, 347–350

care plans for, 351–352
care priorities for, 350–351
classification of, 348t
collaborative management of, 350–351
with decreased cardiac output, care plan for, 351
diagnostic tests for, 349–350t
history and risk factors for, 347–350
with impaired physical mobility, care plan for, 352
with infection risk, care plan for, 352

2310
observation in, 349
palpation in, 349–350
pathophysiology of, 347
vital signs in, 348
Pelvis, structures of, 347
Penicillin/silibinin, in hepatic failure, 867
Pentobarbital coma, for status epilepticus, 730
Peptic ulcer disease (PUD), bleeding in, 816
Peptic ulcers, in mechanical ventilation, 115
Percutaneous balloon valvuloplasty, 622

patients undergoing,
care plans for, 625–626
with decreased cardiac output, care plan for, 626
with deficient knowledge, care plan for, 625–626
with ineffective protection, care plan for, 626
Percutaneous coronary interventions (PCIs),

for acute myocardial infarction, 488

patients undergoing, care plans for, 497–498
Percutaneous left ventricular assist devices, for cardiogenic shock,
522
Pericardial effusions, Horowitz classification of, 284b
Pericardiocentesis, 289, 289b
Pericarditis, acute, 507–512

with activity intolerance, care plan for, 511–512

2311
assessment of, 507–510
auscultation in, 508
care plans for, 511–512
care priorities for, 510–511
causes of, 507b
collaborative management of, 510–511
diagnostic tests for, 509t
ECG changes in, 509–510, 509t
hemodynamic measurements in, 508
history and risk factors for, 508
with ineffective breathing pattern, care plan for, 511
observation of, 508
pathophysiology of, 507
screening labwork in, 508
vital sign assessment in, 508
Peripheral artery occlusive disease,

care plans for, 610–611

care priorities for, 598–601
with impaired skin integrity, care plan for, 610–611
with ineffective tissue perfusion, care plan for, 610
management guidelines for, 599–601t
observation in, 594

2312
Peripheral vascular disease (PVD), 589–612

assessment of, 592–598

auscultation in, 595
care priorities for, 598–601
carotid artery occlusive disease and, 590
collaborative management of, 598–607
generalized,
with activity intolerance, care plan for, 607–608
care plans for, 607–609
with deficient knowledge, care plan for, 608–609
with fluid volume deficit, care plan for, 608
with ineffective tissue perfusion, care plan for, 608
history and risk factors for, 592
lower extremity, 590–592
observation in, 593–594
palpation in, 594–595
pathophysiology of, 589–592
screening labwork in, 595
postprocedural, 595–598
vital signs in, 594
Peritoneal irritation, signs and symptoms of, 275b
Peritonitis, 879–888

2313
abdominal pain in, 880
with acute pain, care plan for, 887
auscultation in, 880
blood chemistry tests for, 882
care plans for, 884–888
care priorities for, 883–884
collaborative management of, 883–884
diagnostic procedures for, 882
with fluid volume deficits, care plan for, 884–885
gastrointestinal assessment in, 880–882
hematologic tests for, 882
hemodynamic measurements in, 881–882
history and risk factors for, 880
with hyperthermia, care plan for, 886
with impaired tissue integrity, care plan for, 886–887
with infection risk, care plan for, 885–886
nuclear medicine scans for, 882
nutrition assessment in, 880
with nutritional imbalance, care plan for, 887
observation in, 880
palpation in, 880
pathophysiology of, 879–880

2314
radiologic procedures for, 882
with risk for intraabdominal hypertension, care plan
for, 888
screening labwork for, 881
vital sign assessment in, 880
pH regulation, 2–3
Pharmacotherapy,

for acute asthma exacerbation, 398–400, 399t

for acute gastrointestinal bleeding, 824–825
for acute infective endocarditis, 503–504
for burn patient, 326
for cardiogenic shock, 520–521
for cardiomyopathy, 534–535
for cerebral aneurysm/subarachnoid hemorrhage,
689–691
for diabetes insipidus, 771
for hepatic failure, 866–867
for hypertensive patients, education on, 584
for meningitis, 709t
for myasthenia gravis, 714–715
for organ transplantation, 998–1001
for pelvic fracture patient, 351
for status epilepticus, 729–730

2315
Phencyclidine overdose, 959
Phentolamine, for hypertensive emergency, 583
Phenylephrine, in cardiogenic shock, 521t
Phenytoin (Dilantin), for status epilepticus, 729–730
Pheochromocytoma, assessment of, in hypertensive emergencies,
580
Phlebotomy, therapeutic, for hemolytic crisis, 911
Phosphorus,

deficiency of, 67. See also Hypophosphatemia.

excess of, 71. See also Hyperphosphatemia.
foods high in, 68b
imbalances in, 66–67
PIP., See Peak inspiratory pressure (PIP).
Plague, 206
Plasmapheresis,

complications of, nursing interventions for, 716–717b

for myasthenia gravis, 715
for transplant patients, 1001
Platelet transfusion, for heparin-induced thrombocytopenia, 918
Pneumonia, acute, 414–423

aspiration, 415
assessment of, 416–421
auscultation in, 416
care plans for, 421–422

2316
care priorities for, 418–421
chest radiograph in, 416
collaborative management of, 418–421
community-acquired, 414
congestion relief in, 420–421
cough control in, 419–420
cough in, 416
diagnostic tests for, 417–418t
fever reduction in, 420
with fluid volume deficit, care plan for, 422
history and risk factors for, 416
hydration in, 420
infection control in, 419
with injury risk, care plan for, 421–422
nosocomial, 414–415
nutritional support in, 420
observation in, 416
pain relief in, 420
palpation in, 417
pathophysiology of, 414–415
percussion in, 418–421
screening labwork in, 417–418

2317
severity of, determining, 418–421
ventilator-associated, 415
Institute for Healthcare Improvement bundle for, 420–
421t
pressure ulcers and, 190b
ventilator-associated events and, 415
vital signs in, 416
Pneumothorax, 429–436

with acute pain, care plan for, 436

assessment of, 430–432, 436b
auscultation in, 431–432
care plans for, 434–436
care priorities for, 431
chest radiograph in, 430
collaborative management of, 432–434
diagnostic tests for, 431–432t
history and risk factors for, 430
with impaired gas exchange, care plan for, 434–436
with impaired spontaneous ventilation, care plan for,
434–436
in mechanical ventilation, 114
observation/inspection in, 430–431

2318
palpation in, 431
pathophysiology of, 429–430
percussion in, 431
spontaneous, 429, 430, 431
tension, 429–430
in mechanical ventilation, 114–115
in thoracic trauma, 363
traumatic, 429, 430, 431
vital signs in, 430
Poisoning, carbon monoxide, signs and symptoms of, 316, 316t
Poliomyelitis, WNV, 223
Polyclonal antibodies, in posttransplant immunosuppression, 1000–
1001
Positioning, patient, in acute respiratory distress syndrome, 419
Positive end-expiratory pressure (PEEP), 110–111

for acute respiratory distress syndrome, 411b

for nonfatal drowning patient, 344
Positive-pressure ventilation, 107
Postpartum period, hemodynamic changes during, 965t
Posttrauma syndrome, care plan for, 270–271
Potassium,

deficiency of, 55. See also Hypokalemia.

excess of, 58. See also Hyperkalemia.
foods high in, 57b

2319
imbalances of, 55
supplemental, for cardiomyopathy, 534
PR interval, 538
Prealbumin, 126
Prebiotics, in enteral formulas, 133
Precedex., See Dexmedetomidine.
Prednisolone, for acute asthma exacerbation, 399t
Prednisone, for acute asthma exacerbation, 399t
Preeclampsia, 966

management of, 970

oliguric patients with, hemodynamic profiles in, 967t
pathophysiology of, 966
risk factors for, 967
signs and symptoms of, 966–967
Pregnancy,

HELLP syndrome in, 967–968

hemodynamic changes during, 965t
hypertension in, 964-975. See also Eclampsia; See
also Preeclampsia.
care for, 968–973
classification of, 965–966, 966b
collaborative care of, 968
diagnostic tests for, 968t
HELLP syndrome and, 967–968

2320
monitoring for preterm labor in, 969–970
pathophysiology of, 966–967
patient positioning for, 969
risk factors for, 967
signs and symptoms of, 966–967
hyperthyroidism in, 803b
physiologic anatomical changes in, 964b
venous thromboembolism prophylaxis during, 447
Preload, 80–82
Premature atrial complexes (PACs), sinus tachycardia with, 549f
Premature junctional complexes, 553f
Pressure controlled ventilation, 110
Pressure measured during inspiratory hold (PPlateau, PPlat), 106
Pressure support ventilation (PSV), 109
Pressure ulcers, 183

assessment of, 188–189

care plans for, 190
with impaired tissue integrity, care plan for, 190
prevention of, 190
staging of, 188–189
ventilator-acquired pneumonia and, 190b
Prion disease, 220
PRIS (propofol-related infusion syndrome), 177
Prograf (tacrolimus), 999

2321
Propofol (Diprivan),

for agitation/anxiety management, 177

for status epilepticus, 730
Propofol-related infusion syndrome (PRIS), 177
Propylthiouracil (PTU), for thyrotoxicosis crisis, 806
Prostaglandin analogues, for acute GI bleeding, 824
Proteins,

in enteral formulas, 134

requirements for, 128
in TPN, 140
Proton-pump inhibitors, for acute GI bleeding, 824
PSV (pressure support ventilation), 109
PTU., See Propylthiouracil (PTU).
PUD., See Peptic ulcer disease (PUD).
Pulmonary artery, rupture and occlusion of, 101b
Pulmonary artery catheters, optimal use of, 81b
Pulmonary artery occlusive pressure (PAOP), hemodynamic
measurements and, 96, 97f
Pulmonary artery pressures (PAPs), 85

hemodynamic measurements and, 95–96, 96f

monitoring of, 91–93
Pulmonary contusion, in thoracic trauma, 363
Pulmonary embolism (PE),

amniotic fluid embolism and, 438

assessment of, 438–443

2322
auscultation in, 440
care plans for, 448–450
care priorities for, 443–447
collaborative management of, 443–448
fat embolism and, 438. See also Fat embolism.
history and risk factors for, 438–439
with ineffective cardiopulmonary tissue perfusion,
care plan for, 448–450
intravascular foreign bodies and, 438. See
also Intravascular foreign bodies.
observation/inspection in, 440
palpation in, 440
percussion in, 440
saddle, 440b
saddle, thrombolytic drugs for, 446
venous air embolism and, 438. See also Venous air
embolism.
venous thrombotic, diagnostic tests for, 441–442t
vital signs in, 439–440
Pulmonary hypertension, 450–457

assessment of, 452–454

auscultation in, 453
care plans for, 455–457

2323
care priorities for, 454–455
classifications of, WHO, 451t, 452b
clinical presentation of, 452
collaborative management of, 454–455
with deficient knowledge, care plan for, 456–457
history and risk factors for, 452
with impaired gas exchange, care plan for, 456
observation/inspection in, 453
palpation in, 453
pathophysiology of, 450–452
with risk for ineffective cardiopulmonary tissue
perfusion, care plan for, 455–456
screening diagnostic tests for, 453–454t, 453–454
vital signs in, 452
Pulmonary transplantation., See Lung transplantation.
Pulmonary vascular resistance (PVR), in hemodynamic values
adjustment, 98
Pulmonic insufficiency/regurgitation, 614
Pulmonic stenosis, 614
Pulmonic valve, 612
Pulmonic valve disease, 614, 615–616t

management of, 621

Pulse, paradoxical, measuring, 274b
Pulse oximetry, 5

2324
continuous, in respiratory assessment, 390
in heart failure management, 472, 472b
Pupillary changes,

in cerebral aneurysm/subarachnoid hemorrhage, 688

in meningitis, 704
Purpura, immune thrombocytopenic, 920. See also Immune
thrombocytopenic purpura (ITP).
PVD., See Peripheral vascular disease (PVD).
PVR., See Pulmonary vascular resistance (PVR).

Q
QRS complex, 538–539
QT interval, 539
Quality of life, as ethical consideration, 244
Quetiapine (Seroquel), in agitation/anxiety management, 179
Quick Confusion Scale, 31, 32b

R
Radioactive iodine, for thyrotoxicosis crisis, 806–807
Radiotherapy, for superior vena cava syndrome, 986
Rancho Los Amigos (RLA) Cognitive Functioning Scale, 31
RAP., See Right atrial pressure (RAP).
Rapamune (sirolimus), 1000
Rectal bleeding, 817
Red cell exchange therapy, for sickle cell crisis, 910
Reginol-binding protein, 126
Rehabilitation,

2325
for stroke, 748
for traumatic brain injury, 381–382
Rejection, organ., See Organ transplant rejection.
Relaxation, in pain management, 159
Renal acidosis, 2
Renal alkalosis, 2
Renal disease, enteral formulas for, 134
Renal failure, acute, 636–672

with acute confusion, care plan for, 654–655

assessment of, 643–648
auscultation in, 645
care plans for, 651–656
care priorities for, 648–651
causes of, 638t
collaborative management of, 648–649t, 648–651
with constipation, care plan for, 655
diagnosis of, criteria for, 637t
diagnostic tests for, 646–647t
diuretic use in, 650t
early recognition of, with urinary and serum
biomarkers, 647–648, 648b
electrolyte balance alterations in, 640–643t
with fluid volume deficit, care plan for, 652

2326
with fluid volume excess, care plan for, 651–652
history and risk factors for, 644
with imbalanced nutrition, care plan for, 652–653
with impaired skin integrity, care plan for, 655–656
with infection risk, care plan for, 653–654
intrarenal presentation of, 638–639, 638t, 645
with knowledge deficit, care plan for, 654
observation in, 645
palpation in, 645
pathophysiology of, 637–643
postrenal presentation of, 638t, 639, 645
prerenal presentation of, 637–638, 638t, 644–645
renal replacement therapies for, 656-670. See
also Renal replacement therapies.
screening laboratory tests in, 646–647
special populations at risk for, 644
uremic manifestations in, 646
vital signs in, 645
Renal replacement therapies,

continuous, 656–670
continuous (CRRT), 656–670
anticoagulation in, 663–665

2327
approaches to, 663t
assessment for,
before, 658–660
during, 665–666
auscultation before, 659
care plans for, 667–670
care priorities for, 667
collaborative management of, 666–667
with decreased cardiac output, care plan for, 667–668
with deficient knowledge, care plan for, 669
determining types and modality of, 660–663
diagnostic tests used in association with, 659–660t
with fluid volume deficit risk, care plan for, 668
with fluid volume excess, care plan for, 668
heparin therapy in, 664
with impaired physical mobility, care plan for, 669
with injury risk, care plan for, 669–670
modes of,
comparison of, 657t
indications, advantages, and
disadvantages/complications of, 661t
pathophysiology of, 657–658

2328
principles applied to, 662
procedure for, 662–663
replacement fluid in, 665
troubleshooting major problems in, 661t
uremic manifestations before, 659
initiation of, 651
Renal system, in burn assessment, 317–318
Renal transplantation., See Kidney transplantation.
Renal trauma, 352-361. See also Genitourinary tract trauma.
Renin inhibitors, direct, for hypertension, 586–588t
Reperfusion injury, 592
Respiratory acidosis, 1, 8–10

acute, collaborative management of, 10–11

in acute respiratory failure, correction of, 427
care plan for, 12–13
chronic, 11–12
compensation for, 11
pathophysiology of, 8–10
Respiratory alkalosis, 2, 13

acute, 14
care plan for, 15
chronic, 14–15
pathophysiology of, 13

2329
Respiratory disorders, 390–461

acute pneumonia as, 414-423. See also Pneumonia,

acute.
acute respiratory distress syndrome as, 404-414. See
also Respiratory distress syndrome, acute (ARDS).
acute respiratory failure as, 423-429. See
also Respiratory failure, acute.
assessment of, 390–392
asthma exacerbation as, 393-404. See also Asthma
exacerbation, acute.
auscultation in, 391
care plans for, 391–392
continuous pulse oximetry in, 390
enteral formulas for, 134
with impaired spontaneous ventilation, care plan for,
391–392
observation in, 390–391
pneumothorax as, 429-436. See also Pneumothorax.
pulmonary embolism as, 437-450. See also Pulmonary
embolism (PE).
screening labwork in, 391
vital sign assessment in, 390
Respiratory distress syndrome, acute (ARDS), 404–414

A-a gradient in, 408

2330
assessment of, 406–408
auscultation in, 408
care plans for, 413–414
care priorities for, 410–413
collaborative management of, 410–413
diagnostic tests for, 409–410t, 409–410
history and risk factors for, 406–407, 407t
with impaired gas exchange, care plan for, 413
mild, hypoxemic hypoxia in, 407
moderate to severe, hypoxemic hypoxia in, 407
observation in, 407
palpation in, 408
pathophysiology of, 404–406
percussion in, 408
with risk for injury, care plan for, 413–414
screening labwork in, 408
staging of, based on Berlin definitions, 405t
vital signs in, 407
Respiratory failure, acute, 423–429

A-a gradient in, 425

assessment of, 424–426
auscultation in, 425

2331
care plans for, 428–429
care priorities for, 426–428
collaborative management of, 426–428
diagnostic tests for, 426t
disease processes leading to, 405b
history and risk factors for, 424
with impaired gas exchange, care plan for, 428–429
observation in, 425
palpation in, 425
pathophysiology of, 423–424
percussion in, 425
screening labwork in, 425–426
ventilation-perfusion matching in, 423–424
vital signs in, 424
Respiratory rate (RR), 104
Respiratory support, after intracranial surgery, 696
Respiratory system,

in burn assessment, 316–317

disorders of, 390-461. See also Respiratory disorders.
Restlessness, in mechanical ventilation, management of, 120–122b
Restrictive cardiomyopathy (RCM), 528
Reteplase, 489, 490t
Rewarming, for nonfatal drowning patient, 344

2332
Rheumatic fever, prophylaxis for, 618–619
Richmond Agitation-Sedation Scale (RASS), 31, 37
Right atrial pressure (RAP), 85

hemodynamic measurements and, 94, 94f

Right ventricular pressure (RVP), hemodynamic measurements
and, 94–95, 95f
Riker Sedation-Agitation Scale (SAS), 175b
Risperdal (risperidone), in agitation/anxiety management, 179
Risperidone (Risperdal), in agitation/anxiety management, 179
Rituxan (rituximab), 1000
Rituximab (Rituxan), 1000
Rocuronium (Zemuron), in agitation/anxiety management, 180
RR., See Respiratory rate (RR).
Rule of nines, 314, 314f
RVP., See Right ventricular pressure (RVP).

S
Saddle pulmonary embolism, 440b
Safe patient handling, 163–164
Safety,

establishing culture of, 163–164

patient, 247-257. See also Patient safety.
Salicylates, overdose of, 949–950
Sandimmune (cyclosporine), 999
SARS., See Severe acute respiratory syndrome (SARS).
SE., See Status epilepticus (SE).
Sedation, 173–183

2333
administering, 174–175
for anxiety reduction, care plan for, 181
care plans for, 181–182
care priorities for, 176–180
collaborative management of, 176–180
with deficient knowledge, care plan for, 182
delirium monitoring and, 28f
in hepatic failure, 866
with risk for injury, care plan for, 182
in traumatic brain injury management, 377, 378t
Seizures,

control of,
after intracranial surgery, 698
in meningitis, 708
in traumatic brain injury management, 377–378
prevention of, in eclampsia, 970–971
Selective T-cell costimulation blocker, in posttransplant
immunosuppression, 999
Sensory function, in neurologic assessment, 674–675
Sensory stimulation programs, for critically ill, 38f
Sepsis, 1008–1023

assessment of, 1013–1016

in early hyperdynamic stage, 1011t

2334
in late stage, 1012t
with cardiac output decrease, care plan for, 1020
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
definition of, 1008–1009b
diagnostic tests for, 1015–1016t
in enterocutaneous fistula, control of, 849
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
neutropenic, 980. See also Neutropenic sepsis.
observation and assessment findings in, 1014
pathophysiology of, 1008
severe,
assessment of, 1013–1016
diagnostic tests for, 1015–1016t
observation and assessment findings in, 1015–1016

2335
pathophysiology of, 1009
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
vital signs in, 1013
Septic shock, 1008–1023

assessment of, 1013–1016

in burn assessment, 318–321
with cardiac output decrease, care plan for, 1020
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
diagnostic tests for, 1015–1016t
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
observation and assessment findings in, 1015–1016
pathophysiology of, 1009–1010

2336
in spinal cord injury, 293
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
Seroquel., See Quetiapine (Seroquel).
Serum albumin, 126
Severe acute respiratory syndrome (SARS), 214

assessment of, 214–216

care priorities for, 217, 219
collaborative management of, 216–217
diagnostic tests for, 215–216t
history and risk factors for, 214–215
pathophysiology of, 214
screening labwork for, 215–216
signs and symptoms of, 215
transmission of, 214
Shock,

anaphylactic, 892-902. See also Anaphylactic shock.

cardiogenic, 465. See also Cardiogenic shock (CS).
hypovolemic., See Hypovolemic shock.
in major trauma, 260
neurogenic, in spinal cord injury, 292–293
septic, 1008-1023. See also Septic shock.

2337
spinal, 292, 293
Shunts,

peritoneovenous, for ascites in hepatic failure, 869b

transjugular intrahepatic portosystemic, for ascites in
hepatic failure, 868, 869b
ventricular, for hydrocephalus, 692
nursing interventions after placement of, 692b
SIADH., See Syndrome of inappropriate antidiuretic hormone
(SIADH).
Sickle cell crisis, red cell exchange therapy for, 910
Simulect (basiliximab), 1000
SIMV (synchronized intermittent mandatory ventilation), 109
Sinus arrest, normal sinus rhythm with, 548f
Sinus bradycardia, 547f
Sinus dysrhythmia, 548f
Sinus rhythm, normal, 546f

with sinus arrest, 548f

Sinus tachycardia, 547f

with premature atrial complexes, 549f

Sirolimus (Rapamune), 1000
SIRS., See Systemic inflammatory response syndrome (SIRS).
Six-Item Screen, 31, 33b
Skin care, in spinal cord injury, 301
Skull fractures,

associated with traumatic brain injury, 369

2338
basilar, 372
compound depressed, 372
linear, 372
Sleep promotion, nonpharmacologic measures in, 237t
Small intestine, bleeding in, 817
Smallpox (variola), 207
Sodium,

for ascites in hepatic failure, 868

deficiency of, 50. See also Hyponatremia.
dietary, reducing, 475t
excess of, 53. See also Hypernatremia.
foods high in, 48b, 475t
Sodium chloride solution, isotonic, in continuous renal replacement
therapies, 665
Solu-Medrol (methylprednisolone), 999
Speak up campaign, 254, 255b
Spinal cord injury,

acute, 291–310
assessment of, acute phase, 294–297
with autonomic dysreflexia, care plan for, 303–304
care plans for, 302–310
care priorities for, 298–302
collaborative management of, 298–302
with constipation, care plan for, 308–309

2339
cord syndromes in, 295–297
with decreased cardiac output, care plan for, 304
diagnostic tests for, 297–298
with disturbed visual perception, care plan for, 310
with gastric injury risk, care plan for, 305
with impaired gas exchange, care plan for, 302–303
with impaired skin integrity, care plan for, 306
with ineffective thermoregulation, care plan for, 308
with ineffective tissue perfusion, care plan for, 305–
306
with infection risk, care plan for, 309
levels of, 296t
neurogenic shock in, 292–293
with nutritional imbalance, care plan for, 306–307
pathophysiology of, 291–294
with reflex urinary incontinence, care plan for, 307–
308
with sexual dysfunction, care plan for, 310
spinal shock in, 292
with urinary retention, care plan for, 307–308
vertebral fractures in, 292
classifications and terminology of, 293t

2340
Spinal cord syndromes,

anterior cord syndrome as, 295

cauda equina syndrome as, 297
central cord syndrome as, 295–296
conus medullaris syndrome as, 296
lateral cord syndrome as, 296
Spinal shock, 292, 293
Spiritual distress, care plan for, 233–234
Spiritual support., See Emotional/spiritual support.
Spirometry, in acute asthma exacerbation, 394
Splenectomy, for hemolytic crisis, 911
Square wave testing, 87–88, 88f
ST segment, 539
Standard precautions, in infection prevention, 210
Staphylococcus aureus, methicillin-resistant, 211
Statins, for cerebral aneurysm/subarachnoid hemorrhage, 690
Status epilepticus (SE), 727–733

with altered tissue perfusion, care plan for, 731–732

assessment of, 727–728
care plans for, 731–733
care priorities for, 729–731
collaborative management of, 729–731
with deficient knowledge, care plan for, 733
diagnostic tests for, 728t

2341
electroencephalography in, 728
history and risk factors for, 727
with impaired gas exchange, care plan for, 731
with ineffective coping, care plan for, 733
with noncompliance with prescribed medication
regimen, care plan for, 732
observation in, 728
pathophysiology of, 727
refractory, treatment of, 730–731
screening labwork in, 728
seizure assessment in, 728
with trauma risk, care plan for, 732
vital signs in, 727
Stimulant overdose, 959–964
Stomach, bleeding in, 816
Stool softeners, for cerebral aneurysm/subarachnoid hemorrhage,
690
Streptokinase, 489, 490t
Stress ulceration, bleeding in, 816
Stroke,

AHA/ASA management guidelines for, 741t

assessment of, 737–740
care plans for, 750–752
care priorities for, 741–750

2342
collaborative management of, 741–750
with decreased intracranial adaptive capacity, care
plan for, 750–751
diagnosis of, 739–740t
extension of, preventing, 744
hemorrhagic locations and syndromes in, 736t
history and risk factors for, 737
with impaired physical mobility, care plan for, 751
with impaired verbal communication, care plan for,
751–752
ischemic,
with carotid artery stenosis, symptoms of, 591b
hypertensive emergency and, management of, 582
neurologic evaluation in, 737–738
NIH scale for, 745–748t
pathophysiology of, 734–736
recurrent, preventing, 744
regulatory functions in, maintaining, 748, 749–750t
screening labwork in, 738–740
screening neurologic imaging in, 738
types of, 734f
vital sign assessment in, 737

2343
Stroke volume variability (SVV), in hemodynamic values
adjustment, 98
Stupor, 27
Subarachnoid hemorrhage, 373

care plans for, 692–694

care priorities for, 689–692
collaborative management of, 689–692
functional assessment in, 688–689
history and risk factors for, 686–687
hypertensive emergency and, management of, 583–
584
with imbalanced fluid volume risk, care plan for, 694
with impaired gas exchange, care plan for, 693
with ineffective airway clearance, care plan for, 693
with ineffective cerebral tissue perfusion, care plan
for, 692–693
with injury risk, care plan for, 693
intracranial pressure in, 687–688
neurologic assessment of, 686–689
observation in, 688–689
pathophysiology of, 684–686
screening labwork in, 689
syndrome of inappropriate antidiuretic hormone and,

2344
 685
vital signs in, 687
Subdural hematoma, 373
Sublimaze., See Fentanyl (Sublimaze).
Succinylcholine (Anectine), in agitation/anxiety management, 179–
180
Sucralfate (Carafate),

for acute GI bleeding, 824

in hepatic failure, 866
Suicide, assisted, 244–245
Superior vena cava syndrome (SVCS), 984

assessment of, 984–985

care plans for, 986–987
care priorities of, 985–986
collaborative management of, 985–986
with decreased cardiac output, care plan for, 986
diagnostic tests for, 985t
history and risk factors for, 984
with impaired gas exchange, care plan for, 987
observation in, 984–985
pathophysiology of, 984
Surgical interventions,

for acute GI bleeding, 825

2345
for acute infective endocarditis, 504
for acute ischemic stroke, 742
for acute myocardial infarction, 489
for aortic aneurysm/dissection, 516
for cardiac tamponade, 290
for cardiomyopathy, 535–536
for cerebral aneurysm/subarachnoid hemorrhage, 691
for compartment syndrome, 338–339
for critical limb ischemia, 603
for dysrhythmias, 570
for genitourinary tract trauma, 359, 359t
for intracranial hemorrhage, 742
for major trauma, 268
for pelvic fractures, 350–351
for peritonitis, 883–884
for recurrent pneumothorax, 434
for superior vena cava syndrome, 986
for traumatic brain injury, 374
for valvular heart disease, 621–622
SVCS., See Superior vena cava syndrome (SVCS).
SVR., See Systemic vascular resistance (SVR).
SVV., See Stroke volume variability (SVV).

2346
Synchronized intermittent mandatory ventilation (SIMV), 109
Syndrome of inappropriate antidiuretic hormone (SIADH), 795–803

assessment of, 796–800

care plans for, 802–803
care priorities for, 800–802
collaborative management of, 800–802
differential diagnosis of, 800
history and risk factors for, 796
hyponatremia and, etiologic factors of, 797–798t
with impaired neurologic functioning, care plan for,
802–803
labwork in, 799–800
manifestations of, based on degree of hyponatremia,
799t
observation in, 798–799
pathophysiology of, 796
from subarachnoid hemorrhage, 685
types of, 797t
vital signs in, 798
Systemic inflammatory response syndrome (SIRS), 1008–1023

assessment of, 1013–1016

in burn assessment, 318–321
with cardiac output decrease, care plan for, 1020

2347
care plans for, 1019–1023
care priorities for, 1016–1019
collaborative management of, 1016–1019
diagnostic tests for, 1015–1016t
with fluid volume deficit, care plan for, 1019–1020
history and risk factors for, 1013
with imbalanced nutrition, care plan for, 1023
with impaired gas exchange, care plan for, 1021–1022
with ineffective breathing pattern, care plan for, 1022
with ineffective tissue perfusion, care plan for, 1021
infection control in, 1017, 1019
observation and assessment findings in, 1014
pathophysiology of, 1008–1009, 1010t
with thermoregulation ineffectiveness, care plan for,
1022–1023
ventilation assistance in, 1018
vital signs in, 1013
Systemic vascular resistance (SVR), in hemodynamic values
adjustment, 97–98
Systolic blood pressure, hemodynamic measurements and, 93

T
T wave, 539
Tachycardia,

2348
atrial, 550f
junctional, 553f
persistent, in abdominal trauma, 273b
sinus, 547f
ventricular, 554f
catheter ablation for, 567–568
Tacrolimus (Prograf), 999
Talc embolism, 438
TandemHeart, for cardiogenic shock, 522
TBI., See Traumatic brain injury (TBI).
TeamSTEPPS, 252, 253t
Teamwork, successful, components of, 251b
TEE., See Transesophageal echocardiogram (TEE).
Temperature regulation,

for burn patient, 324

in traumatic brain injury management, 379, 379b
Tenecteplase, 489, 490t
Tension pneumothorax,

auscultation in, 431–432

in mechanical ventilation, 114–115
observation/inspection of, 430–431
palpation in, 431
pathophysiology of, 429–430
percussion in, 431

2349
in thoracic trauma, 363
Terbutaline, for acute asthma exacerbation, 399t
Tetanus prophylaxis,

for burn patient, 326

in wound management, 267, 267t
Therapeutic hypothermia, after intracranial surgery, 698
Thermodilution (TD) method, of cardiac output calculation, 85
Thioamides, for thyrotoxicosis crisis, 806
Thoracic trauma, 361–368

assessment of, 362–365

auscultation in, 363
care priorities for, 365–367
collaborative management of, 365–367
with decreased cardiac output, care plan for, 367–368
diagnostic tests for, 364–365t
history and risk factors for, 362
with ineffective breathing pattern, care plan for, 367
observation in, 362
palpation in, 363
pathophysiology of, 361–362
percussion in, 363
vital signs in, 362
Thrombin inhibitors, direct, in continuous renal replacement

2350
 therapies, 664
Thrombocytopenia,

heparin-induced, 915. See also Heparin-induced

thrombocytopenia (HIT).
pathophysiology of, 913–915
Thrombocytopenic purpura, immune, 920. See also Immune
thrombocytopenic purpura (ITP).
Thrombocytopheresis, for hemolytic crisis, 910–911
Thromboembolectomy, for acute limb ischemia, 604
Thromboembolism,

prevention of, in spinal cord injured patient, 301

venous, 437. See also Venous thromboembolism
(VTE).
Thrombolysis,

for acute ischemic stroke, 742

for acute limb ischemia, 604
for superior vena cava syndrome, 985
Thrombolytic agents,

for abnormal clotting in DIC, 929

for acute myocardial infarction, 489–491, 489b, 490t,
491b
for massive or saddle embolus, 446
Thymectomy, for myasthenia gravis, 715
Thyroid storm, 803-810. See also Thyrotoxicosis crisis.
Thyroidectomy, subtotal, for thyrotoxicosis crisis, 807

2351
Thyrotoxicosis crisis, 803–810

with anxiety, care plan for, 808

care plans for, 807–810
care priorities for, 806–807
collaborative management of, 806–807
with deficient knowledge, care plan for, 809–810
diagnostic tests for, 805–806t
endocrine assessment in, 804–806
history and risk factors for, 804
with imbalanced nutrition, care plan for, 808–809
with impaired swallowing, care plan for, 808
with impaired tissue integrity of cornea, care plan for,
809
with ineffective protection, care plan for, 807–808
observation in, 804
palpation in, 805
pathophysiology of, 803–804
screening labwork in, 805–806
with sleep pattern disturbance, care plan for, 809
vital signs in, 804
TIAs., See Transient ischemic attacks (TIAs).
Tidal volume (VT), 105

2352
low, in mechanical ventilation, 111–113
Time limited ventilation, 110
Tiotropium, in asthma control, 395b
TIPS., See Transjugular intrahepatic portosystemic shunt (TIPS).
TLS (tumor lysis syndrome), 987
Toradol., See Ketorolac (Toradol).
Torsade de pointes, 554f
Total body surface area (TBSA) burn calculation, 314–315, 314f, 315f
Total parenteral nutrition (TPN), components of, 140–141
Touch, types of, 230b
Toxins, extracorporeal removal of, for drug overdose, 947
TP segment, 539
TPN (total parenteral nutrition), components of, 140–141
Trace minerals,

requirements for, 128–129

in TPN, 141
Transcranial herniation, 370
Transesophageal echocardiogram (TEE), in cardiac output
calculation, 86
Transferrin, 126
Transfusion(s),

for anemia, 906–907, 907b

for hemolytic crisis, 910
for pelvic fracture patient, 351
reactions to, acute, 934t
Transient ischemic attacks (TIAs), 590, 734–735

2353
symptoms of, 591b
Transjugular intrahepatic portosystemic shunt (TIPS), for ascites in
hepatic failure, 868, 869b
Transplantation, organ, 989-1007. See also Organ transplantation.
Transtentorial herniation, 370
Transthoracic echocardiogram (TTE), in cardiac output calculation,
86
Trauma, 260–391

abdominal, 271-284. See also Abdominal trauma.

genitourinary tract, 352-361. See also Genitourinary
tract trauma.
major, 260-271. See also Trauma, major.
with acute pain, care plan for, 269–270
airway assessment in, 261–262
assessment of,
primary, 261–262
secondary, 262–265
breathing assessment in, 262
care plans for, 268–271
care priorities for, 265–268
circulatory assessment in, 262
collaborative management of, 265–268
diagnostic tests for, 263–265t
disability assessment in, 262

2354
exposure in, 262
head-to-toe assessment in, 263
history in, 262
with hypothermia, care plan for, 270
with impaired gas exchange, care plan for, 269
with ineffective tissue perfusion, care plan for, 268
laboratory work in, 263–265
pathophysiology of, 260–261
with posttrauma syndrome, care plan for, 270–271
psychological response to, 261
vital signs in, 262
thoracic, 361-368. See also Thoracic trauma.
Traumatic brain injury (TBI), 368–385

assessment of, 370–374

care plans for, 382–385
care priorities for, 374–382
collaborative management of, 374–382
with decreased intracranial adaptive capacity, care
plan for, 383
diagnostic tests for, 373–374t
with disuse syndrome risk, care plan for, 384
herniation syndromes in, 370, 371t

2355
with impaired gas exchange, care plan for, 382
with impaired tissue integrity, care plan for, 385
with ineffective thermoregulation, care plan for, 383–
384
with infection risk, care plan for, 382–383
management of, 381t
neurological complications of, 370
pathophysiology of, 368–370
primary, 368–369
secondary, 369
skull fractures associated with, 369
vascular injuries in, 370
Tricuspid regurgitation/insufficiency, 613
Tricuspid stenosis, 613
Tricuspid valve, 612
Tricuspid valve disease, 613, 616t

management of, 621

Truth telling, as ethical consideration, 244
TTE., See Transthoracic echocardiogram (TTE).
Tube feedings, 131-138. See also Enteral formulas/nutrition; See
also Feeding tubes.
Tuberculous meningitis, 702
Tularemia, 209
Tumor embolism, 438
Tumor lysis syndrome (TLS), 987

2356
U
U wave, 539
Ulcers,

gastric, prevention of,

in acute spinal cord injury, 300
after intracranial surgery, 698
peptic, in mechanical ventilation, 115
pressure, 188. See also Pressure ulcers.
Ultrafiltration,

for cardiomyopathy, 535

in continuous renal replacement therapies,
prescription for, 662b
principles of, 662
Uncal herniation, 370

assessment of, 371t

Uremia, in acute kidney injury, 640–643t
Urinary tract trauma, 352-361. See also Genitourinary tract trauma.

V
Vaccination,

for anthrax, 202

for hemorrhagic fever viruses, 205
VAEs., See Ventilator-associated events (VAEs).
VAI., See Vertebral artery injury (VAI).

2357
Valcyte (valganciclovir), 1001
Valganciclovir (Valcyte), 1001
Valium., See Diazepam (Valium).
Valve replacement, patients undergoing,

with decreased cardiac output, care plan for, 623–624

with deficient knowledge, care plans for, 625
with ineffective protection, care plan for, 622–623
with ineffective tissue perfusion, care plan for, 624
Valvular heart disease, 612–627

aortic valve disease as, 613, 616–617t

assessment of, 614–618
care plans for, 622–626
care priorities for, 618–621
collaborative management of, 618–622
diagnostic tests for, 617–618t
history and risk factors for, 614
mitral valve disease as, 612–613, 615t
pathophysiology of, 612–614
percutaneous balloon valvuloplasty for, care plans
for, 625-626. See also Percutaneous balloon
valvuloplasty.
physical assessment in, 614–618
pulmonic valve disease as, 614, 615–616t

2358
surgical interventions for, 621–622
tricuspid valve disease as, 613, 616t
valve replacement for, care plans for, 622-625. See
also Valve replacement, patients undergoing.
Valvuloplasty, 622
Vancomycin-resistant Enterococcus (VRE), 211
Variola (smallpox), 207
Vascular grafts, intraabdominal, bleeding from, 817
Vascular injuries, in traumatic brain injury, 370
Vasculopathy, in organ rejection, 1002
Vasoconstrictors, for acute GI bleeding, 824
Vasodilators, for cardiomyopathy, 534
Vasopressin, 42

for diabetes insipidus, 769, 770t

for failing heart, 521, 521t
Vasopressin-receptor antagonist therapy, 801
Vasopressin receptors, locations and actions of, 765t
Vasopressors,

for anaphylactic shock, 898–899

for septic patients, 1018
VE (minute ventilation), 105
Vecuronium (Norcuron), in agitation/anxiety management, 180
Vegetative state (VS),

care priorities for, 37–38, 38f

sensory stimulation programs for, 28, 38f

2359
Vena cava filter, in heparin-induced thrombocytopenia, 918
Venous air embolism,

auscultation in, 441

care priorities for, 447
clinical presentation of, 441
diagnostic tests for, 443
history and risk factors for, 441
observation/inspection in, 441
vital signs in, 441
Venous oxygen saturation,

jugular, monitoring of, in traumatic brain injury, 376

mixed, in hemodynamic values adjustment, 98
Venous thromboembolism (VTE),
history of, 438–439
incidence of, in hospitalized patients, 437t
pathophysiology of, 437
prophylaxis for,

based on risk level, 444t

contraindications/complications of, 444t
long-term, 446–447
risk factors for, 438–439, 439t
probability based on, 439
Ventilation,
flow rate in, 106

2360
fraction of inspired oxygen in, 105
inspiratory flow begins in, 106
inspiratory flow end in, 106–107
mean airway pressure in, 106
mechanical, 104-123. See also Mechanical ventilation.
minute ventilation in, 105
peak inspiratory pressure in, 105–106
respiratory rate in, 104
spontaneous, factors affecting, 104b
support of, in major trauma, 265–266
terminology for, 104–107
tidal volume in, 105
Ventilation assistance., See also Mechanical ventilation.
Ventilator-acquired pneumonia, pressure ulcers and, 190b
Ventilator-associated events (VAEs), 115–116, 415
Ventricular demand (VVI) pacemaker, 558f

with failure to capture, 559f

with failure to sense, 559f
Ventricular fibrillation, 555f
Ventricular hypertrophy, ECG changes found with, 503t
Ventricular septal myotomy-myectomy, for cardiomyopathy, 536
Ventricular tachycardia, 554f

catheter ablation for, 567–568

Verbal communication, impaired, care plan for, 241
Verbal Descriptor Scale of pain, 153, 154f
Versed., See Midazolam (Versed).

2361
Vertebral artery injury (VAI), 297b
Vertebral fractures, 292
Vigilance A Test, 31, 33b
Violence, risk for, care plan for, 239
Violent behavior, safety precautions in event of, 232b
Viral meningitis, 702
Virus(es),

Ebola, 211-212. See also Ebola virus disease (EVD).

hemorrhagic fever, 204–205
smallpox, 207
West Nile, 222
Visceral protein status, in nutrition assessment, 125–127
Visual Analog Pain Scale, 153, 154f
Vital signs,

in abdominal hypertension and abdominal

compartment syndrome, 940
in abdominal trauma, 273–274
in acute asthma exacerbation, 394
in acute cardiac tamponade, 285
in acute coronary syndrome, 480–481
in acute gastrointestinal bleeding, 818
in acute infective endocarditis, 499
in acute pancreatitis, 833
in acute pneumonia, 416

2362
in acute renal failure, 645
in acute respiratory failure, 425
in adrenal crisis, 759
in anaphylactic shock, 895
in aortic aneurysm/dissection, 513
in brain death, 679
in cardiac dysrhythmias, 544
in cardiogenic shock, 519
in cerebral aneurysm, 687
in continuous renal replacement therapies,
before, 658
during, 665
in diabetes insipidus, 767
in disseminated intravascular coagulation, 927
in drowning, 342–343
in enterocutaneous fistula, 846
in fat embolism, 440
in gastrointestinal assessment, 814
in Guillain-Barré syndrome, 721
in heparin-induced thrombocytopenia, 915
in hepatic failure, 856–857
in hypercalcemia, 64

2363
in hyperglycemia, 779
in hypermagnesemia, 77
in hypernatremia, 53–54
in hyperphosphatemia, 71
in hypertensive emergencies, 580
in hypervolemia, 47
in hypocalcemia, 61
in hypomagnesemia, 74
in hyponatremia, 50
in hypophosphatemia, 68
in hypovolemia, 43
in immune thrombocytopenic purpura, 920
in intracranial surgery, 695
in major trauma, 262
in meningitis, 673
in mental status/consciousness assessment, 30
in myasthenia gravis, 713
in myxedema coma, 789, 789b
in neurologic assessment, 673
in pain assessment, 153
in pelvic fractures, 348
in peripheral vascular disease, 594

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in peritonitis, 880
in pneumothorax, 430
in pulmonary embolism, 439–440
in pulmonary hypertension, 452
in respiratory disorders, assessment of, 390
in status epilepticus, 727
in stroke, assessment of, 737
in subarachnoid hemorrhage, 687
in syndrome of inappropriate antidiuretic hormone,
798
in thyrotoxicosis crisis, 804
Vitamin B12, for anemia, 907
Vitamins,

requirements for, 128–129

in TPN, 141
Volume controlled ventilation, 110
Volutrauma, in mechanical ventilation, 114
VRE (vancomycin-resistant Enterococcus), 211
VS., See Vegetative state (VS).
VT., See Tidal volume (VT).
VTE., See Venous thromboembolism (VTE).
VTE (minute ventilation), 105
VVI pacemaker., See Ventricular demand (VVI) pacemaker.

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W
Wandering atrial pacemaker, 549f
Water, body, compartments of, primary constituents of, 41
Weaning, from mechanical ventilation, 116–118
Weight, nutrition requirement calculations based on, 127
West Nile virus (WNV), 222

assessment of, 222–224

care priorities for, 224
clinical features of, 223
collaborative management of, 224
diagnostic tests for, 223–224t
history and risk factors for, 222
incubation period for, 222
labwork in, 223–224
mild, 222
pathophysiology of, 222
severe/WNV meningitis, WNV encephalitis, and
WNV poliomyelitis, 223
transmission of, 222
Withholding and/or withdrawing treatment, 244
WNV., See West Nile virus (WNV).
Wound closure/healing,

of burn injuries, 325

by primary intention, 183

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assessment of, 183–184
care plans for, 185
care priorities for, 184–185
collaborative management of, 184–185
diagnostic tests during, 184t
with impaired tissue integrity, care plan for, 185
by secondary intention, 185
assessment of, 185–186

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care plans for, 187
care priorities for, 186–187
collaborative management of, 186–187
diagnostic tests for, 186t
with impaired tissue integrity, care plan for, 187
Wounds, burn,

care of, 325

infection of, in burn assessment, 318
pressure ulcers as, 188. See also Pressure ulcers.

Z
Zemuron (rocuronium), in agitation/anxiety management, 180
Zenapax (daclizumab), 1000
Zinc, in hepatic failure, 867
Ziprasidone (Geodon), in agitation/anxiety management, 179
Zyprexa., See Olanzapine (Zyprexa).

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Ibc

2369
Table of Contents
Title page 2
Table of Contents 4
Copyright 10
Contributors 13
Preface 23
1. General concepts in caring for the critically ill 27
Acid-base imbalances 27
Altered mental status 83
Fluid and electrolyte disturbances 113
Hemodynamic monitoring 199
Mechanical ventilation 246
Nutrition support 289
Pain 341
Prolonged immobility 367
Sedation and neuromuscular blockade 400
Wound and skin care 425
Selected references 442
2. Managing the critical care environment 462
Bioterrorism 462
Emerging infections 486
Emotional and spiritual support of the patient and significant
517
others
Ethical considerations in critical care 554
Patient safety 564
Selected references 584
3. Trauma 592
Major trauma 592
Abdominal trauma 615
Acute cardiac tamponade 642
Acute spinal cord injury 655
Burns 700

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 Compartment syndrome/ischemic myositis 748
Drowning 763
Pelvic fractures 775
Renal and lower urinary tract trauma 786
Thoracic trauma 798
Traumatic brain injury 810
Selected references 846
4. Respiratory disorders 858
Respiratory assessment: General 858
Acute asthma exacerbation 865
Acute respiratory distress syndrome 885
Acute pneumonia 905
Acute respiratory failure 922
Pneumothorax 936
Pulmonary embolism 953
Pulmonary hypertension 983
Selected references 998
5. Cardiac and vascular disorders 1009
Cardiovascular assessment: General 1009
Heart failure 1020
Acute coronary syndrome 1044
Acute infective endocarditis 1082
Acute pericarditis 1100
Aortic aneurysm/dissection 1111
Cardiogenic shock 1121
Cardiomyopathy 1142
Dysrhythmias and conduction disturbances 1158
Hypertensive emergencies 1222
Peripheral vascular disease 1246
Valvular heart disease 1289
Selected references 1319
6. Kidney injury 1341
Genitourinary assessment: General 1341

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 Acute kidney injury 1344
Continuous renal replacement therapies 1380
Selected references 1408
7. Neurologic disorders 1414
General neurologic assessment 1414
Brain death 1421
Cerebral aneurysm and subarachnoid hemorrhage 1436
Care of the patient after intracranial surgery 1458
Meningitis 1473
Neurodegenerative and neuromuscular disorders 1493
Status epilepticus 1530
Stroke: Acute ischemic and hemorrhagic 1547
Selected references 1577
8. Endocrinologic disorders 1587
Endocrine assessment 1587
Acute adrenal insufficiency (adrenal crisis) 1590
Diabetes insipidus 1605
Hyperglycemia 1622
Myxedema coma 1651
Syndrome of inappropriate antidiuretic hormone 1668
Thyrotoxicosis crisis (thyroid storm) 1683
Selected references 1698
9. Gastrointestinal disorders 1707
Gastrointestinal assessment: General 1707
Acute gastrointestinal bleeding 1711
Acute pancreatitis 1735
Enterocutaneous fistula 1767
Hepatic failure 1785
Peritonitis 1840
Selected references 1860
10. Hematologic/immunologic disorders 1866
General hematology assessment 1866
Anaphylactic shock 1869

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 Profound anemia and hemolytic crisis 1889
Bleeding and thrombotic disorders 1910
Selected references 1954
11. Complex special situations 1957
Abdominal hypertension and abdominal compartment syndrome 1957
Drug overdose 1976
Stimulants 2008
High-risk obstetrics: Hypertension in pregnancy 2017
Oncologic emergencies 2043
Organ transplantation 2067
Sepsis, septic shock, systemic inflammatory response syndrome,
2109
and multiple organ dysfunction syndrome
Selected references 2140
Heart and breath sounds 2153
Glasgow coma scale 2156
Cranial nerves Assessment and dysfunctions 2157
Major deep tendon muscle stretch reflexes 2158
Major superficial cutaneous reflexes 2159
Inotropic and vasoactive medication infusions 2160
Sample relaxation technique 2161
Abbreviations used in this manual 2162
Index 2180
Ibc 2369

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