Fundamental Critical Care Support 6e

Fundamental
Critical Care Support

Sixth Edition
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Fundamental Critical Care Support
Sixth Edition
Editors
Keith Killu, MD, FCCM
Henry Ford Hospital
Detroit, Michigan, USA
No disclosures
Babak Sarani, MD, FCCM

George Washington University
Washington, DC, USA
No disclosures
FCCS Sixth Edition Planning Committee

Marie R. Baldisseri, MD, FCCM
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania, USA
No disclosures
Thomas P. Bleck, MD, FCCM

Rush Medical College
Chicago, Illinois, USA
Sage Therapeutics: DSMB chair
Edge Therapeutics: DSMB chair
Zoll Corporation: clinical trial steering committee
Gregory H. Botz, MD, FCCM

University of Texas MD Anderson Cancer Center
Houston, Texas, USA
No disclosures
David J. Dries, MD, MCCM

Regions Hospital
St. Paul, Minnesota, USA
No disclosures
Mark E. Hamill, MD, FCCM

Virginia Tech Carilion School of Medicine
Roanoke, Virginia, USA
No disclosures
Muhammad Jaffar, MD, FCCM

University of Arkansas for Medical Sciences
Little Rock, Arkansas, USA
No disclosures
Edgar Jimenez, MD, FCCM

Scott and White Memorial Hospital
Temple, Texas, USA
No disclosures
Rahul Nanchal, MD
The Medical College of Wisconsin
Milwaukee, Wisconsin, USA
No disclosures
John M. Oropello, MD, FCCM

Mount Sinai School of Medicine
New York, New York, USA
No disclosures
David Porembka, DO, PhD

Avera Medical Group
Sioux Falls, South Dakota, USA
No disclosures
Mary J. Reed, MD, FCCM

Geisinger Medical Center
Danville, Pennsylvania, USA
No disclosures
Sophia Chu Rodgers, ACNP, FNP, FAANP, FCCM

Lovelace Medical Group
Lovelace Health Systems
Albuquerque, New Mexico, USA
No disclosures
Janice L. Zimmerman, MD, MCCM, MACP

Houston Methodist Hospital
Houston, Texas, USA
No disclosures
Contributors
Adebola Adesanya, MB, MPH
Medical City Dallas Hospital
Dallas, Texas, USA
No disclosures
Masooma Aqeel, MD
Medical College of Wisconsin
Milwaukee, Wisconsin, USA
No disclosures
Patricia Beauzile, MD
Carilion Clinic
Roanoke, Virginia, USA
No disclosures
Tessa W. Damm, DO
University of Wisconsin School of Medicine
and Public Health
Madison, Wisconsin, USA
No disclosures
Danielle Davison, MD
George Washington University Medical Center
Washington, DC, USA
No disclosures
Luiz Foernges, MD
No disclosures
Jeremy Fulmer, RCP, RRT-ACCS, NPS

No disclosures
Kristie A. Hertel, ACNP, CCRN, MSN, RN

Vidant Medical Center
Greenville, North Carolina, USA
No disclosures
Richard Iuorio, MD
Mount Sinai Hospital
No disclosures
Martha Kenney, MD
Johns Hopkins University
Baltimore, Maryland, USA
No disclosures
Camila Lyon, MD
Vanderbilt University
Nashville, Tennessee, USA
No disclosures
Nancy Maaty, MD
The George Washington University
Washington, DC, USA
No disclosures
Michael S. Malian, MD
Henry Ford West Bloomfield Hospital
West Bloomfield, Michigan, USA
No disclosures
Richard May, MD
Rutgers New Jersey Medical School
Newark, New Jersey, USA
No disclosures
Patrick C. McKillion, MD, FCCP

No disclosures
Rodrigo Mejia, MD, FCCM

Children’s Cancer Hospital
Houston, Texas, USA
No disclosures
Don C. Postema, PhD

HealthPartners
Minneapolis, Minnesota, USA
No disclosures
Sri-Sujanthy Rajaram, MD, MPH

Hackensack University Medical Center
Hackensack, New Jersey, USA
No disclosures
Peter Rattner, DO
No disclosures
John B. Sampson, MD
Johns Hopkins University
Baltimore, Maryland, USA
No disclosures
Marian E. Von-Maszewski, MD
Houston, Texas, USA
No disclosures
Jennifer Williams, MD
No disclosures
Acknowledgments
The following individuals contributed to the development of Fundamental Critical Care Support, Sixth Edition, by
reviewing the material and offering valuable insight.
Kazuaki Atagi, MD, PhD, FCCM

Nara Prefecture General Medical Center
Nara, Japan
No disclosures
Steven M. Hollenberg, MD, FCCM

Cooper Health System
Camden, New Jersey, USA
No disclosures
Eric G. Honig, MD
Emory University
Atlanta, Georgia, USA
No disclosures
Frank M. O’Connell, MD, FACP, FCCP

AtlantiCare Regional Medical Center
Pomona, New Jersey, USA
No disclosures
Ehizode Udevbulu, MD
Mount Sinai Hospital
No disclosures
Contents
Preface
1. Recognition and Assessment of the Seriously Ill Patient
2. Airway Management
3. Cardiopulmonary/Cerebral Resuscitation
4. Diagnosis and Management of Acute Respiratory Failure
5. Mechanical Ventilation
6. Monitoring Oxygen Balance and Acid-Base Status
7. Diagnosis and Management of Shock
8. Neurologic Support
9. Basic Trauma and Burn Support
10. Acute Coronary Syndromes
11. Life-Threatening Infections: Diagnosis and Antimicrobial Therapy Selection
12. Management of Life-Threatening Electrolyte and Metabolic Disturbances
13. Special Considerations
14. Critical Care in Pregnancy
15. Ethics in Critical Care Medicine
16. Critical Care in Infants and Children: The Basics
Appendix
1. Rapid Response System
2. Airway Adjuncts
3. Endotracheal Intubation
4. Intraosseous Needle Insertion
5. Arterial Blood Gas Analysis and Treatment
6. Brain Death and Organ Donation
PREFACE
Pioneers in critical care medicine drafted the first edition of the Fundamental Critical
Care Support (FCCS) textbook when the concept of FCCS training was first conceived
more than a quarter of a century ago. Over the years, the book has served as a resource
for learners and teachers in critical care. With the sixth edition, we continue the
tradition and build on the efforts and successes of all previous authors.
The purpose of this book is to serve as a resource for teaching the basic concepts in the
recognition of the critically ill patient and provision of the support needed until a
critical care specialist arrives.
The FCCS course focuses on the initial assessment and management of the critically ill
patient. Changes were made throughout the book to reflect new concepts, guidelines,
and practices. All of these changes were made after researching the latest evidence-
based literature available at the time of publication.
The book chapters use both an organ system-based and problem-based format. The
chapters revolve around commonly encountered case scenarios. Many callout boxes are
included, and they are designed to direct the reader’s attention to specific and important
concepts for that chapter. International experts were consulted, and feedback from
learners and educators throughout the world was taken into consideration. In the end, we
tried to produce a textbook that addresses the needs of different populations and various
countries.
The journey to publication of this edition included many Society of Critical Care
Medicine staff members and behind-the-scenes workers who spent countless hours
editing the book and tracking all the logistics, making sure we have an excellent end
product. For all of them, we are thankful. We are also honored and thankful to have such
a distinguished group of experts to help compose and edit the sixth edition chapters.
Many have been practicing and teaching critical care, as well as leading FCCS courses,
for many years. They selflessly offered their time, effort, and expertise in editing this
book.
The sixth edition of the FCCS textbook is a key component of the FCCS program, which
continues to expand and grow to meet the needs of critical care learners and educators
for the present and future generations.
Keith Killu, MD, FCCM
Editor
2016-2018 Chair,
FCCS Program Committee
Babak Sarani, MD, FACS, FCCM
Editor
2016-2018 Vice Chair,
FCCS Program Committee
CHAPTER 1
RECOGNITION AND ASSESSMENT OF THE

SERIOUSLY ILL PATIENT
Objectives
Explain the importance of early identification of patients at risk for life-threatening

illness or injury and the importance of early intervention.
Recognize the early signs and symptoms of critical illness.
Discuss the initial assessment and early stabilization and treatment of the critically
ill or injured patient.
Case Study
A 54-year-old woman with diabetes was admitted with an intra-abdominal abscess

following laparoscopic cholecystectomy. She underwent placement of a drain by the
interventional radiology department. Two hours later, she developed a temperature of
39.4°C (103°F), heart rate of 128 beats/min, and blood pressure of 80/40 mm Hg.
– What do you detect?
– Which aspects of the physical examination would you concentrate on initially?
– Which laboratory and radiographic investigations would you order for this patient?
I. INTRODUCTION
“An ounce of prevention is worth a pound of cure” is a common idiom that often applies
to the care of critically ill patients. Early identification of patients at risk for life-
threatening illness makes it easier to manage them initially and prevents further
deterioration. Many clinical problems, if recognized early, can be managed with simple
measures such as supplemental oxygen, respiratory therapy interventions, intravenous
fluids, or effective analgesia. The early identification of patients in trouble allows
clinicians to identify the main physiological problem, determine its underlying cause,
and begin specific treatments. The longer the interval between the onset of an acute
illness and the appropriate intervention, the more likely it is that the patient’s condition
will deteriorate, even to cardiopulmonary arrest. Several studies have demonstrated that
physiological deterioration precedes many cardiopulmonary arrests by hours, suggesting
that early intervention could prevent the need for resuscitation, admission to the ICU,
and other sentinel events. Many hospitals are using rapid response systems to identify
patients at risk and begin early treatment. (See Appendix 1 for further information on the
organization and implementation of a rapid response systems.) The purpose of this
chapter is to describe the general principles involved in recognizing and assessing
acutely ill patients. This chapter also introduces the key Fundamental Critical Care
Support course learning and management concept of DIRECT: detection, intervention,
reassessment, effective communication, and teamwork (Figure 1-1).
Figure 1-1. DIRECT Methodology
Detection: Using the history, physical exam, and the behavioral, cardiovascular and respiratory system
changes, the critical care team is alerted to the patient’s physiological status. These items then guide the
appropriate laboratory and radiographic evaluations to establish a working/presumptive diagnosis,
differential diagnosis, and worst possible diagnosis.
Intervention: This is the process of treating and correcting the disease or injury while keeping in mind the
critical care maxim to minimize morbidity and prevent mortality.
Reassessment: This ensures the treatment is appropriate for the severity of the disease and/or injury.
Effective Communication: The greatest source of injury and death in healthcare is communication error.
The more complicated the patient, the more important it is for everyone to communicate their perspective to
the team so that multiple and often time-sensitive tasks can be done expertly and promptly.
Teamwork: The patient does best when all members of the healthcare team bring their specialized training
to work together synergistically to care for the needs of the critically ill or injured patient.
Reproduced from Madden MA, ed. Pediatric Fundamental Critical Care Support. 2nd ed. Mount Prospect, IL:
Society of Critical Care Medicine; 2013.
II. RECOGNIZING THE PATIENT AT RISK
Patients seldom deteriorate abruptly,

even though clinicians may recognize
the deterioration suddenly.
Recognizing that a patient is seriously or critically ill is usually not difficult. It may be
more challenging, however, if the patient is in the very early stages of the process.
Young and otherwise healthy patients are usually much slower to exhibit the typical
signs and symptoms of acute illness than elderly patients or those with comorbidities
and/or impaired cardiopulmonary function. Individuals who are immunosuppressed or
debilitated may not demonstrate a vigorous and clinically obvious inflammatory
response. Some conditions, such as cardiac arrhythmias, do not evolve with
progressively worsening and easily detectable changes in physiology but rather present
as an abrupt change of state. In most circumstances, a balance exists between the
patient’s physiologic reserve and the acute disease. Patients with limited reserve are
more likely to be susceptible to severe illness and to experience greater degrees of
organ-system impairment. Therefore, identifying patients at risk for deterioration
requires assessment of their background health, their current disease process, and their
current physiological condition.
A. Assessing Severity
Even normal vital signs may be early
indicators of impending deterioration if
they differ from prior measurements.
“How sick is this patient?” is one of the most important questions a clinician must
answer. Determining the response requires the measurement of vital signs and other
specific physiological variables (Appendix 1). Acute illness typically causes
predictable physiological changes associated with both disease-specific and general
clinical signs. For example, a patient’s physiological response to a bacterial infection
may result in fever, delirium, shaking chills, and tachypnea. The most important step is
to recognize these signs and initiate physiologic monitoring in order to quantify the
severity of disease and take appropriate action. Sick patients may present with
confusion, irritability, impaired consciousness, or a sense of impending doom. They
may appear short of breath and demonstrate signs of a sympathetic response, such as
pallor, sweating, or cool extremities. Symptoms may be nonspecific, such as nausea and
weakness, or they may identify the involvement of a particular organ system (for
example, chest pain). Therefore, a high index of suspicion is required when measuring
vital signs: pulse rate, blood pressure, respiratory rate, oxygenation, temperature, and
urine output. Clinical monitoring helps to quantify the severity of the disease process,
tracks trends and rates of deterioration, and directs attention to those aspects of
physiology that most urgently need treatment. The goals at this stage of assessment are to
recognize that a problem exists and to maintain physiological stability while pursuing
the cause and initiating treatment.
Tachycardia in response to physiological

abnormalities (ie, fever, low cardiac
output) may be increased with pain and
anxiety or suppressed in patients who
have conduction abnormalities or are
receiving ß-blocker medications.
B. Making a Diagnosis
A primary and secondary survey
approach is recommended in the
assessment of a seriously ill patient.
Making an accurate diagnosis in the acutely ill patient often must take second place to
treating life-threatening physiological abnormalities. It is important to ask the question,
“What physiological problem needs to be corrected now to prevent further deterioration
of the patient’s condition?” Correcting the problem may be as simple as providing
oxygen or intravenous fluids. There may not be sufficient time for a lengthy pursuit of a
differential diagnosis initially if the patient is seriously ill and needs to be stabilized.
However, an accurate diagnosis is essential for refining treatment options once
physiological stability is achieved. The general principles of taking an accurate history,
performing a brief, directed clinical examination followed by a secondary survey, and
organizing laboratory and radiographic investigations are fundamentally important.
Good clinical skills and a disciplined approach are required to accomplish these tasks.
III. INITIAL ASSESSMENT OF THE CRITICALLY ILL PATIENT

A framework for assessing the acutely ill patient is provided in Table 1-1 and discussed
below. Further information on specific issues and treatments can be found in later
chapters of this text.
A. History
The patient’s history usually provides the greatest contribution to diagnosis. Often the
current history, past medical history, and medication list must be obtained from family
members, caregivers, friends, neighbors, or other healthcare providers. The risk of
critical illness is increased in patients with the following characteristics:
Emergency admission (limited information)

Advanced age (limited reserve)
Severe coexisting chronic illness (limited reserve, limited options for
management)
Severe physiological abnormalities (limited reserve, refractory to therapy)
Need for, or recent history of, major surgery, especially an emergency procedure
Severe hemorrhage or need for a massive blood transfusion
Deterioration or lack of improvement
Immunodeficiency
Combination of these factors
Table 1-1 Framework for Assessing the Acutely Ill or Injured Patient
PHASE I PHASE II
Initial Contact—First Minutes Subsequent Reviews
(Primary Survey) (Secondary Survey)
What is the main physiological problem? What is the underlying cause?
History Main features of circumstances and More detailed information

environment
Present complaint
Witnesses, healthcare personnel, Past history, chronic
relatives diseases, surgical
Main symptoms: pain, dyspnea, altered procedures
mental status, weakness Hospital course (if
Trauma or no trauma applicable)
Operative or nonoperative Psychosocial and
Medications and/or toxins physical independence
Medications and
allergies
Family history
Ethical or legal issues,
code status
Systems review
Examination Look, listen, feel Structured examination of

organ systems
Airway
Breathing and oxygenation Respiratory system
Circulation Cardiovascular system
Level of consciousness Abdomen and
genitourinary tract
Central nervous and
musculoskeletal
systems
Endocrine and
hematologic systems
Chart Review: Essential physiology, vital signs Case records and note
Documentation keeping
Heart rate, rhythm
Blood pressure Examine medical
Respiratory rate and pulse oximetry records, if available
Level of consciousness Formulate specific
diagnosis or differential
diagnosis
Document current
events
Investigations
Arterial blood gas analysis (can obtain Laboratory blood tests
venous blood gas if arterial access not Radiology
possible) Electrocardiography
Blood glucose Microbiology
Treatment Proceeds in parallel Refine treatment, assess

responses, review trends
Ensure adequate airway and oxygen
Provide intravenous access ± fluids Provide support for
Assess response to immediate specific organ systems
resuscitation as required
CALL FOR ASSISTANCE FROM AN Choose most
EXPERIENCED COLLEAGUE appropriate hospital site
for care
Obtain specialist advice
and assistance
A complete history includes the present complaint, treatment history, hospital course to
the present (if applicable), past illnesses, past operative procedures, current
medications, and any medication allergies. A social history, including alcohol, tobacco,
or illicit drug use, and a family history, including the degree of physical, emotional, and
psychosocial independence, are essential and often overlooked. The history of the
present complaint must include a brief review of systems that should be replicated in the
examination that follows.
Critical illness is often associated with inadequate cardiac output, respiratory
compromise, and a depressed level of consciousness. Specific symptoms will typically
be associated with the underlying condition. Patients may complain of nonspecific
symptoms such as malaise, fever, lethargy, anorexia, or thirst. Organ-specific symptoms
may direct attention to the respiratory, cardiovascular, or gastrointestinal systems.
Distinguishing acute from chronic disease is important at this point, as chronic
conditions may be difficult to reverse and may act as rate-limiting factors during the
recovery phase of critical illness.
B. Examination
Tachypnea may reflect pulmonary,

systemic, or metabolic abnormalities
and should always be fully evaluated.
Look, listen, and feel. The patient must be fully exposed for a complete examination.
The initial examination must be brief, directed, and concentrated on the basic elements
of airway, breathing, circulation, and level of consciousness. As the treatment proceeds,
a more detailed secondary survey should be conducted to refine the preliminary
diagnosis and assess the response to the initial treatment. A full examination must be
performed at some point and will be guided by the history and other findings. Ongoing
deterioration or development of new symptoms warrants repetition of the primary
survey followed by a detailed secondary survey.
Remember the ABCs of resuscitation: airway, breathing, and circulation. The airway
and respiratory system should be assessed first, as summarized in Table 1-2. Observe
the patient’s mouth, chest, and abdomen. There may be obvious signs suggesting airway
obstruction as vomitus, blood, or a foreign body. The patient’s respiratory rate, pattern
of breathing, and use of accessory respiratory muscles will help to confirm and assess
the severity of respiratory distress or airway obstruction (Chapter 2). Tachypnea is the
single most important indicator of critical illness. Therefore, the respiratory rate must
be accurately measured and documented. Although tachypnea may result from pain or
anxiety, it may also indicate pulmonary disease, severe metabolic abnormalities, or
infection. Look for cyanosis, paradoxical breathing, equality and depth of respiration,
use of accessory muscles, and tracheal tug. An increase in the depth of respiration
(Kussmaul breathing) may indicate severe metabolic acidosis. Periodic breathing with
apnea or hypopnea (Cheyne-Stokes respiration) usually indicates severe brainstem
injury or cardiac dysfunction. Ataxic breathing (Biot respiration) indicates severe
neuronal damage, which is associated with poor prognosis. Agitation and confusion may
result from hypoxemia, whereas hypercapnia will usually depress the level of
consciousness. Low oxygen saturation can be detected with pulse oximetry, but this
assessment may be unreliable if the patient is hypovolemic, hypotensive, or
hypothermic. Noisy breathing (eg, grunting, stridor, wheezing, gurgling) may indicate
partial airway obstruction, whereas complete airway obstruction will result in silence.
Table 1-2 Assessment of Airway and Breathing

Airway
Causes of Obstruction Direct trauma, blood, vomitus, foreign body, central nervous system
depression (with soft tissue or tongue blocking airway), infection, inflammation,
laryngospasm
LOOK for Cyanosis, altered respiratory pattern and rate, use of accessory respiratory
muscles, tracheal tug, paradoxical breathing, altered level of consciousness
LISTEN for Noisy breathing (grunting, stridor, wheezing, gurgling); silence indicates
complete obstruction
FEEL for Decreased or absent airflow
Breathing
Causes of Inadequate Breathing or Oxygenation
Depressed respiratory Central nervous system
drive
Decreased respiratory Muscle weakness, nerve/spinal cord damage, chest wall abnormalities, pain
effort
Pulmonary disorders Pneumothorax, hemothorax, aspiration, chronic obstructive pulmonary
disease, asthma, pulmonary embolus, lung contusion, acute lung injury, acute
respiratory distress syndrome, pulmonary edema, rib fracture, flail chest
LOOK for Cyanosis, altered level of consciousness, tracheal tug, use of accessory
respiratory muscles, altered respiratory pattern, altered respiratory rate,
equality and depth of breaths, oxygen saturation
LISTEN for Dyspnea, inability to talk, noisy breathing, dullness to percussion, auscultation
of breath sounds
FEEL for Symmetry and extent of chest movements, position of trachea, crepitus,
abdominal distension
Paradoxical breathing is a sign of

severe respiratory compromise.
Inadequate circulation may result from primary abnormalities of the cardiovascular

system or secondary abnormalities caused by metabolic disturbances, sepsis, hypoxia,
or drugs (Table 1-3). A decrease in the blood pressure may be a late sign of
cardiovascular disturbance signaling failure of the compensatory mechanisms.
Central and peripheral pulses should be assessed for rate, regularity, volume, and
symmetry. Capillary or nail-bed refill exam may aid in detecting hypovolemia if
delayed.
Table 1-3 Assessment of Circulation

Causes of Circulatory Inadequacy
Primary — directly Ischemia, arrhythmias, valvular disorders, cardiomyopathy, pericardial
involving the heart tamponade
Secondary — pathology Drugs, hypoxia, electrolyte disturbances, dehydration, sepsis, acute blood loss,
originating elsewhere anemia
LOOK for Reduced peripheral perfusion (pallor) and delayed capillary refill, hemorrhage
(obvious or concealed), altered level of consciousness, dyspnea, decreased
urine output, jugular venous distension
LISTEN for Additional or altered heart sounds, carotid bruits
FEEL for Precordial cardiac pulsation, central and peripheral pulses (assessing rate,
quality, regularity, symmetry), cool extremities
Patients with hypovolemia or low cardiac output will have weak and thready peripheral
pulses. A bounding pulse suggests hyperdynamic circulation, and an irregular rhythm
usually signifies atrial fibrillation. A ventricular premature beat is often immediately
followed by a compensatory pause, and the subsequent beat often has a larger pulse
volume. Pulsus paradoxus is seen as a greater than 10 mm Hg decrease in the systolic
blood pressure with deep inspiration; it can occur with profound hypovolemia,
constrictive pericarditis, cardiac tamponade, asthma, and chronic obstructive pulmonary
disease. The location and character of the left ventricular impulse may suggest left
ventricular hypertrophy, congestive heart failure, cardiac enlargement, severe mitral
regurgitation, or severe aortic regurgitation. The turbulent flow of blood through a
stenotic heart valve or a septal defect may produce a palpable thrill.
In addition to the ABCs, a quick external examination should look for pallor, cyanosis,
diaphoresis, jaundice, erythema, or flushing. The skin may be moist or dry; appear thin,
edematous, or bruised; or demonstrate a rash (ie, petechiae, hives). Fingernails may be
clubbed or show splinter hemorrhages. The eyes might reveal abnormal pupils or
jaundice. The conjunctiva may be pale, indicating an anemia. The patient may be alert,
agitated, somnolent, asleep, or obtunded.
Palpation of the abdomen is an essential part of the examination of the critically ill
patient. Areas of abdominal tenderness and palpable masses must be identified. The
size of the liver and spleen must be noted as well as any associated tenderness. It is
important to assess the abdomen for rigidity, distension, fluid wave, or rebound
tenderness. Auscultation may reveal a vascular bruit or the absence of bowel sounds.
Intrauterine or ectopic pregnancy must be considered in all women of childbearing age.
The flanks and back should be examined, if possible.
The Glasgow Coma Scale score should be recorded during the initial assessment of
central nervous system function and limb movement (Chapter 8). Pupillary size and
reaction should be documented, and a more detailed assessment of central and
peripheral sensory and motor functions should be undertaken when time permits.
Difficulty in obtaining a pulsatile

waveform by pulse oximetry may be
indicative of a vasoconstricted state.
C. Chart Review and Documentation

Critically ill patients have abnormal physiology that must be documented and tracked.
Physiological monitoring provides parameters that are useful only when they are
accurate and interpreted by trained personnel (Chapter 6). The values and trends of
these data provide key information for the assessment of the patient’s status and
guidance for treatment. Data must be charted frequently and correctly to ensure good
patient care. Particular attention must be paid to the accuracy and reliability of the data.
For example, a true and reproducible central venous pressure measurement depends
upon patient position, equipment calibration, and proper zeroing of the instruments, as
well as on heart rate and valvular function. The source of the data should also be noted.
Is the recorded temperature a rectal measurement or an oral measurement? Was the
blood pressure measured with a manual cuff or with a pressure transducer in an arterial
line? The medication record is an invaluable source of information about prescribed
and administered drugs.
An accurate measure of urine output,

usually with an indwelling catheter, is
essential in critically ill patients.
Routine monitoring and charting should include heart rate, heart rhythm, respiratory rate,
blood pressure, core temperature, fluid balance, and Glasgow Coma Scale score. The
fluid balance should include loss from all tubes and drains. The inspired oxygen
concentration should be recorded for any patient receiving oxygen, and oxygen
saturation should be charted if measured with pulse oximetry. Patients in the ICU setting
may have central venous catheters or continuous cardiac output catheters in place. These
catheters can measure central venous pressure, various cardiac pressures, stroke
volume variations, cardiac output, and mixed venous saturation. These complex
monitoring devices require specific operational expertise. Likewise, the data must be
interpreted by someone with clinical experience and expertise in critical care.
D. Investigations
Additional investigative tests should be based on the patient’s history and physical
examination as well as on previous test results. Standard biochemistry, hematology,
microbiology, and radiology tests should be performed as indicated. The presence of a
metabolic acidosis is one of the most important indicators of critical illness. In the
evaluation of electrolyte results, decreasing total serum carbon dioxide and/or an
increased anion gap are evidence of metabolic acidosis. An arterial blood gas analysis
is one of the most useful tests in an acutely ill patient, providing information about
blood pH, arterial oxygen tension, and arterial carbon dioxide tension. Additional tests,
such as lactate, blood glucose, serum electrolytes, and renal function, can often be
obtained from the same blood sample. The presence of lactic acidosis following
cardiorespiratory resuscitation can be an ominous sign that should be closely monitored.
IV. TRANSLATING INFORMATION INTO EFFECTIVE ACTION

The framework in Table 1-1 lays out a course of action based on first ensuring
physiological stability and then proceeding to treatment of the underlying cause. The
basic principles are summarized as the ABCs of resuscitating the severely ill patient:
airway—ensuring a patent airway; breathing—providing supplemental oxygen and
adequate ventilation; and circulation—restoring circulating volume. These early
interventions should proceed regardless of the situation, while the context of the clinical
presentation (ie, trauma, postoperative situation, presence of chronic illness, advanced
age) directs attention to the differential diagnosis and potential treatments. The clinical
history, physical examination, and laboratory tests should aid in clarifying the diagnosis
and determining the patient’s degree of physiological reserve. Because the typical
features of critical illness may be more effectively disguised in young and previously
healthy patients than in the elderly or chronically ill, an acute deterioration may seem to
occur more abruptly in younger individuals. Thus, it is particularly important to assess
trends in vital signs and physiological parameters as the patient undergoes treatment.
These trends can help determine a patient’s response and clarify the diagnosis.
More experienced help must be obtained if a patient’s condition is deteriorating and
there is uncertainty about the diagnosis or treatment. Transfer to the most appropriate
site for care is influenced by local resources, but transfer to a high-dependency unit or
ICU must be considered.
Key Points
Recognition And Assessment Of The Seriously Ill Patient

Early identification of a patient at risk is essential to prevent or minimize critical
illness.
The clinical manifestations of impending critical illness are often nonspecific.
Tachypnea and metabolic acidosis are two of the most important predictors of risk;
they signal the need for more detailed monitoring and investigation.
Resuscitation and physiological stabilization often precede a definitive diagnosis
and treatment of the underlying cause.
A detailed history is essential for making an accurate diagnosis, determining a
patient’s physiological reserve, and establishing a patient’s treatment preferences.
Frequent clinical and laboratory monitoring of a patient’s response to treatment is
essential.
Suggested Readings
Current and updated resources for this chapter may be accessed by visiting
http://www.sccm.me/fccs6.
1. Cooper DJ, Buist MD. Vitalness of vital signs, and medical emergency teams. Med
J Aust. 2008;188:630-631.
2. Cretikkos MA, Bellomo R, Hillman K, et al. Respiratory rate: the neglected vital
sign. Med J Aust. 2008;188:657-659.
3. Hillman KM, Bristow PJ, Chey T, et al. Duration of life-threatening antecedents
prior to intensive care admission. Intensive Care Med. 2002;28:1629-1634.
4. Harrison GA, Jacques TC, Kilborn G, et al. The prevalence of recordings of the
signs of critical conditions and emergency responses in hospital wards: the
SOCCER study. Resuscitation. 2005;65:149-157.
5. Hodgetts TJ, Kenward G, Vlachonikolis IG, et al. The identification of risk factors
for cardiac arrest and formulation of activation criteria to alert a medical
emergency team. Resuscitation. 2002;54:125-131.
6. O’Grady NP, Barie PS, Bartlett JG, et al. Guidelines for evaluation of new fever in
critically ill adult patients: 2008 update from the American College of Critical
Care Medicine and Infectious Diseases Society of America. Crit Care Med.
2008;36:1330-1349.
7. National Institute for Health and Care Excellence (NICE) Guidelines. Acutely ill
adults in hospital: recognising and responding to deterioration. Published July
2007. https://www.nice.org.uk/guidance/cg50. Accessed April 15, 2016.
Chapter 2
AIRWAY M ANAGEMENT
Objectives
Recognize signs of a threatened airway.

Describe manual techniques for establishing an airway and for mask ventilation.
Explain proper application of airway adjuncts.
Describe preparation for endotracheal intubation, including the recognition of a
potentially difficult intubation.
Describe alternative methods for establishing an airway when endotracheal
intubation cannot be accomplished.
Case Study
A 65-year-old man was admitted from the emergency department for worsening
shortness of breath. He has a history of diabetes, hypertension, and chronic kidney
disease for which he receives hemodialysis three times each week. He has missed his
last two sessions of dialysis due to a gastrointestinal illness. You are called because the
patient’s oxygen saturation is 86% on 100% non-rebreather mask. He is using his
accessory muscles to breathe and has visible nasal flaring. A portable chest radiograph
shows pulmonary edema with small bilateral pleural effusions. An initial point-of-care
arterial blood gas results yield a pH of 7.18, PaCO2 21 mm Hg, and PaO2 54 mm Hg.
Lactic acid measured 5.2 mmol/L and potassium 6.9 mmol/L.
– Should this patient be intubated?
– If so, what drugs would be appropriate to use?
I. INTRODUCTION
This chapter focuses on the effective assessment and management of the airway. The
primary goal is to maintain an open airway in order to facilitate adequate gas exchange,
the A in the ABCs of resuscitation. Secondary goals include the preservation of
cardiovascular stability and the prevention of aspiration of gastric contents during
airway management. Endotracheal intubation will often be required, but establishing
and maintaining a patent airway instead of, or prior to, intubation are equally important
and often more difficult. Healthcare providers must be skilled in the manual support of
an open airway and in providing the essential processes of oxygenation and ventilation.
Securing an artificial airway via orotracheal or nasotracheal intubation, cricothyrotomy,
or tracheostomy is an extension of, not a substitute for, the ability to maintain an open
airway.
II. ASSESSMENT
Assessment of airway patency and spontaneous breathing effort is the crucial first step.
The clinician must look, listen, and feel for diminished or absent air movement.
Observe the patient’s level of consciousness and determine if apnea is present. If

respiratory efforts are absent and an immediate remedy is not available, proceed to
manual support and assisted ventilation while preparing to establish an artificial
airway.
Identify injury to the airway or other conditions (eg, cervical spine injury) that will
affect assessment and manipulation of the airway.
Observe chest expansion. Ventilation may be adequate with minimal thoracic
excursion, but respiratory muscle activity and even vigorous chest movement do
not ensure that tidal volume is adequate.
Observe for suprasternal, supraclavicular, or intercostal retractions; laryngeal
displacement toward the chest during inspiration (a tracheal tug); or nasal flaring.
These often represent respiratory distress with or without airway obstruction.
Auscultate over the neck and chest for breath sounds. Complete airway obstruction
is likely when chest movement is visible but breath sounds are absent. Airway
narrowing due to soft tissue, liquid, or a foreign body in the airway may be
associated with snoring, stridor, gurgling, or noisy breathing.
Absence of chest movement suggests
apnea.
III. MANUAL METHODS TO ESTABLISH AN AIRWAY

Initial interventions to ensure a patent airway in a spontaneously breathing patient with
no possible injury to the cervical spine include the following maneuvers (Figure 2-1):
1. Slight neck extension

2. Elevation of the mandible (jaw thrust maneuver)
3. Opening of the mouth
If a cervical spine injury is suspected, neck extension should not be done. After the
cervical spine is immobilized, manual elevation of the mandible and opening of the
mouth are performed.
Figure 2-1. Establishing an Open Airway
The operator extends the neck and maintains extension with his/her hands on both sides of the mandible.
The mandible is elevated with the fingers of both hands to lift the base of the tongue, and the thumbs or
forefingers are used to open the mouth.
Airway adjuncts such as properly sized oropharyngeal or nasopharyngeal airways may

be useful. The oropharyngeal airway is not used if airway reflexes are intact, as
gagging, laryngospasm, and emesis may be provoked. The diameter of a nasopharyngeal
airway should be the largest that will easily pass through the nostril into the
nasopharynx. Its length should extend to the nasopharynx, but it should not be so long as
to obstruct gas flow through the mouth or touch the epiglottis. A nasopharyngeal airway
is contraindicated in patients with suspected basilar skull fracture or coagulopathy. The
correct length for each airway may be estimated by placing the device against the face
in the correct anatomic position (Figure 2-2).
Figure 2-2. Nasopharyngeal Airway
During manual airway support, supplemental oxygen should be supplied with a device
providing a high concentration of oxygen (100%) at a high flow rate. Such devices
include a face mask or a bag-mask resuscitation unit, possibly with a positive end-
expiratory pressure valve.
The patient’s tongue is the most common

cause of airway obstruction.
IV. MANUAL MASK VENTILATION

Manual assisted ventilation by means of a bag-mask resuscitation unit is indicated:
if the patient is apneic.

if spontaneous tidal volumes are determined to be inadequate based on physical
examination or arterial blood gas analysis.
to reduce the work of breathing by assisting spontaneous inspiration.
if hypoxemia is associated with poor spontaneous ventilation.
Successful manual mask ventilation depends upon: (1) maintaining an open airway, (2)
establishing a seal between the patient’s face and the mask, and (3) delivering an
adequate minute ventilation from the resuscitation bag to distal lung units. The first two
elements are achieved through the correct placement of the mask over the patient’s nose
and mouth (Figure 2-3) and establishment of an open airway, as previously described. It
is useful to have masks of different sizes available in the event that the initial selection
does not achieve a good seal with the face.
Figure 2-3. Application of Face Masks
Single-handed (A) and two-handed (B) techniques for placement of a face mask.
A. When No Cervical Spine Injury is Suspected
1. If needed and tolerated by the patient, an oropharyngeal or nasopharyngeal airway

may be placed to maintain a patent airway. A small pad or folded towel may be
positioned under the occiput.
2. The operator stands above and behind the head of the supine patient. The height of
the bed should be quickly adjusted for the comfort of the operator.
3. The base of the mask is first placed into the skin crease between the lower lip and
the chin, and the mouth is gently opened.
4. The apex of the mask is placed over the nose, using care to avoid pressure on the
eyes.
5. As most operators are right-handed, the mask is stabilized on the face with the left
hand by holding the superior aspect of the mask apex between the thumb and first
finger, adjacent to its connection to the bag. This allows gentle downward pressure
on the mask over the face.
6. The fifth, fourth, and perhaps third fingers of the left hand are then placed along the
left side of the mandible. It is helpful to gently encircle the left side of the mask
with the soft tissues of that cheek to reinforce the seal along that edge. This further
secures the mask to the patient’s face while allowing the mandible to be partially
elevated.
7. The operator gently rotates the left wrist to cause slight neck extension and
contracts the fingers around the mandible to raise it slightly. The composite
motions of the left hand, therefore, produce slight neck extension, mandibular
elevation, and gentle downward pressure on the face mask.
B. When a Cervical Spine Injury is Suspected
1. The operator stands in the same position, and an oropharyngeal or nasopharyngeal

airway is inserted, if possible.
2. Successful manual ventilation occasionally can be accomplished while the neck is
stabilized in a cervical collar (Figure 2-4). Most often, however, an assistant is
required to stand to the side, facing the patient. The anterior portion of the collar is
removed, and the assistant places one hand or arm along each side of the neck to
limit movement of the neck during manipulation of the airway. Linear traction is not
applied.
3. The operator then proceeds with the steps described above, except the left wrist is
not rotated to produce neck extension. Alternatively, the operator may choose the
two-handed method for mask placement, which further assures that no neck
movement occurs. This method is discussed below.
Figure 2-4. Cervical Stabilization
C. Alternative Two-Handed Method to Ensure Airway Patency and Mask Application
The alternative two-handed method is useful if the patient has a large face or a beard,
after neck injury, or in any other situation when a mask seal is difficult to secure.
1. The operator stands at the head of the bed as before, and adjunctive airway
devices are used as previously suggested.
2. The base and apex of the mask are placed in the manner previously described.
3. The operator places the third, fourth, and fifth fingers of both hands along the
mandible on each side of the face while the thumbs rest over the apex of the mask
and first fingers rest over the base of the mask.
4. Soft tissues of the cheek are brought upward along the side edges of the mask and
held in place by each hand to reinforce the mask’s seal.
5. In the absence of possible cervical spine injury, the neck is slightly extended as the
operator gently elevates the mandible from both sides and provides gentle pressure
on the mask over the face.
6. An assistant provides ventilation, as needed, by compressing the resuscitation bag.
D. Compression of the Resuscitation Bag to Provide Assisted Manual

Mask
Ventilation
The goal of manual mask ventilation is to provide adequate minute ventilation, the
product of the tidal volume delivered during each resuscitation bag compression and the
number of compressions per minute. Overzealous resuscitation bag compressions at a
rapid rate may produce dangerous hyperventilation and respiratory alkalemia, as well
as gastric distension.
The total gas volume within most adult

resuscitation bags is 1 to 1.5 liters.
1. If a single-handed method of mask placement is used, the resuscitation bag is

compressed over 1 second by the operator’s right hand.
2. The delivered tidal volume must be estimated from the observed chest expansion
and auscultated breath sounds.
3. During bag compression, the operator should listen carefully for any gas leaks
around the mask. When a good seal is achieved, the feel of the bag during lung
inflation reflects some resistance caused by the normal airway anatomy. If gas is
moving from the bag too easily, a leak is likely to be present.
4. If the patient is apneic but has a pulse, one-handed bag compressions should be
delivered 10 to 12 times per minute. If spontaneous breathing is present, bag
compression should be synchronized with the patient’s inspiratory efforts. If the
patient is breathing easily and inhaling adequate tidal volumes frequently enough to
produce sufficient minute ventilation, the bag need not be compressed at all.
5. Oxygen (100%) is delivered to the resuscitation bag, usually at a flow rate of 15
L/min.
6. If the mask-to-face seal is not adequate and a leak is detected, the operator should
consider the following interventions:
Reposition the mask and hands.
Adjust the inflation of the facial cushion of the face mask, if possible, to
improve the seal or change to a larger or smaller mask.
Apply slightly more downward pressure to the face or displace the mandible
in an upward fashion, provided cervical spine manipulation is not
contraindicated.
Convert to the two-handed technique described earlier.
Reposition any orogastric or nasogastric tube to another part of the mask.
Leaks are common when a tube is present, but rarely will it need to be
removed.
Consider compensating for a small leak by increasing the frequency of bag
compressions or the volume of gas delivered in each compression.
If the resuscitation bag has a pressure-relief (pop-off ) valve designed to
prevent transmission of high pressures to the lungs, adjust the pop-off valve to
ensure adequate tidal volumes in patients with stiff lungs or high airway
resistance.
Manual assisted ventilation should be continued in preparation for intubation or until the
cause of inadequate ventilation is reversed. An assistant should prepare medications
and equipment for intubation while the primary operator maintains ventilation. Pulse
oximetry and cardiac monitoring are valuable adjuncts throughout assisted ventilation.
The patient should be evaluated continuously for evidence of cyanosis, although this is a
late finding in the setting of hypoxemia.
The SOAP ME mnemonic is helpful in preparation for airway management (Table 2-1).
Table 2-1 SOAP ME: Mnemonic for Preparation for Airway Management
1. Suction
a. Use a suction device (Yankauer or catheter) to clear secretions, as needed.
b. Check device and tubing for adequate suction strength.
2. Oxygen
a. Assure oxygen is connected and functioning.
b. Prepare a bag-valve-mask device with a PEEP valve.
c. Continue high flow supplemental oxygen by nasal cannula or face mask.
3. Airways
a. Prepare appropriately sized cuffed endotracheal tube(s) with stylet. Consider size 7-7.5 for
females, and size 7.5-8 for males. Check cuff for leaks.
b. Consider airway adjuncts.
i. Oropharyngeal and/or nasopharyngeal airways
ii. Laryngeal mask airways
iii. Esophageal-tracheal double-lumen airway device
4. Position
a. Adjust the bed height for airway operator’s comfort.
b. Place patient in sniffing position. Align the external auditory canal with the sternal notch.
c. Consider elevating the back and shoulders of obese patients.
5. Monitoring and Medications
a. Continual monitoring of vital signs, including oximetry and end-tidal CO2
b. Consider induction drugs (consider rapid sequence induction) [Table 2.2].
i. Hypnotic
ii. Neuromuscular blocking agent
iii. Postintubation sedation and analgesia
6. Equipment
a. Laryngoscope(s) with curved and/or straight blades (MAC 3,4; Miller 2,3)
b. Optical or video laryngoscope (with appropriate stylets)
c. Bougie and/or airway exchange catheter
d. End-tidal CO2 detector, if continual end-tidal CO2 monitoring not available
e. Endotracheal tube fastener or tape to secure endotracheal tube
Adapted from: SOAP ME Mnemonic. University of Maryland Department of Emergency Medicine

Educational Pearls. https://umem.org/educational_pearls/2577. Accessed September 1, 2015.
Abbreviation: PEEP, positive end-expiratory pressure
E. Cricoid Pressure
Cricoid pressure (Sellick maneuver) is the application of downward (posterior)
pressure on the anterior neck overlying the cricoid cartilage, with an intended effect of
physical occlusion of the esophagus. Cricoid pressure has been recommended for use
during mask ventilation and intubation of patients who lack protective airway reflexes
and during rapid sequence intubation. New guidelines no longer recommend cricoid
pressure, except as a means of positioning the glottis for better visualization during
laryngoscopy. It does not reduce risk of aspiration as previously thought. Proper
application of cricoid pressure may improve vocal cord visualization. Excess pressure
can compress the trachea and hypopharynx, compromise mask ventilation, and increase
the difficulty of endotracheal intubation. Guidelines for managing the difficult airway,
whether identified or unrecognized, are presented in Figure 2-5.
The absence of cyanosis or hypoxemia

does not guarantee adequacy of
ventilation.
Figure 2-5. Management of the Difficult Airway
Abbreviations: LMA, laryngeal mask airway

aAirway adjuncts: LMA; esophageal-tracheal-double-lumen airway
V. AIRWAY ADJUNCTS
In approximately 5% of the general population, manual mask ventilation is difficult or
impossible to achieve. Predictors of difficulty are the presence of a beard, absence of
teeth, history consistent with obstructive sleep apnea, body mass index greater than 26
kg/m2, and age older than 55 years. The presence of two predictors indicates a high
probability of difficulty in manual mask ventilation. Intubation via direct laryngoscopy
is difficult in approximately 5% of the general population and impossible in 0.2% to
0.5%. A crisis situation occurs when manual mask ventilation and intubation are
impossible. The laryngeal mask airway and esophageal-tracheal double-lumen airway
device are useful adjuncts to provide an open airway and permit gas exchange in such
situations. These devices are inserted blindly and their use may offer additional time
after a failed intubation attempt. The choice of device depends on the operator’s
experience, equipment availability, and specific clinical circumstances.
A. Laryngeal Mask Airway

A laryngeal mask airway is a tube attached to a bowl-shaped cuff that fits in the pharynx
behind the tongue. The standard type is reusable, but a single-use device is also
available. A laryngeal mask airway may be used to ventilate the lungs when mask
ventilation is difficult, provided that the patient does not have periglottal abnormalities.
It may also serve as a conduit for intubation when a bronchoscope is used or as a rescue
technique after failure to intubate. Less sedation is required with the laryngeal mask
airway than with direct laryngoscopy because stimulation to the airway (eg, gagging,
laryngospasm, sympathetic stimulation) in passing the device is only moderate. It is
effective in ventilating patients ranging from neonates to adults, but it does not provide
definitive airway protection. (For specific details regarding use of a laryngeal mask
airway, see Appendix 2.)
B. Esophageal-Tracheal Double-Lumen Airway Device

Another tool for providing an emergency airway is a double-lumen device with two
inflatable balloon cuffs. Although this item was designed primarily for blind intubation
during cardiorespiratory arrest, it can provide ventilation if the distal cuffed portion of
the tube device is inserted in the esophagus or trachea. Its use is contraindicated for
patients with central airway obstruction, intact laryngeal or pharyngeal reflexes, known
esophageal pathology, or ingestion of caustic substances. Adequate training is required
to ensure appropriate use. (For information about inserting an esophageal-tracheal
double-lumen airway device, see Appendix 2.)
VI. ENDOTRACHEAL INTUBATION

Direct laryngoscopy with orotracheal intubation is the principal method for tracheal
intubation because of its speed, success rate, and availability of equipment. Blind
nasotracheal intubation may be useful for selected patients. The indications for tracheal
intubation are summarized in Table 2-2, and the techniques for orotracheal and
nasotracheal intubation are discussed and illustrated in Appendix 3.
Table 2-2 Indications for Tracheal Intubation
Airway protection
Relief of obstruction
Provision of mechanical ventilation and oxygen therapy
Respiratory failure
Shock
Hyperventilation for intracranial hypertension
Reduction of the work of breathing
Facilitation of suctioning/pulmonary toilet
In preparation for intubation, important issues include:
Assessment of airway anatomy and function to estimate degree of difficulty for

intubation (discussed later).
Assurance of optimal ventilation and oxygenation. Preoxygenation with 100%
oxygen, using a bag-mask resuscitation device, occurs during periods of apnea and
before intubation attempts.
Decompression of the stomach with an existing orogastric or nasogastric tube.
However, the insertion of such tube to decompress the stomach prior to intubation
is often counterproductive, as it may elicit emesis and promote passive reflux of
gastric contents.
Provision of appropriate analgesia, sedation, amnesia, and neuromuscular
blockade as required for a safe procedure (discussed later).
Although emergent intubation leaves little time for evaluation and optimization of
conditions, elective and urgent intubation allows for assessment of factors that promote
safe airway management. The patient’s clinical situation, intravascular volume status,
hemodynamics, and airway evaluation (degree of difficulty) should be assessed as a
plan for airway management is formulated. Airway evaluation includes assessment of
physical characteristics that together determine if visualization of the vocal cords will
be difficult or impossible. This evaluation will suggest whether alternative techniques
to direct laryngoscopy (eg, video laryngoscopy, awake intubation, flexible fiberoptic
intubation, surgical airway) are likely to be necessary and whether a more experienced
individual should be summoned immediately. Keep in mind that many of these physical
characteristics also cause difficulty with mask ventilation and the ability to perform an
emergent cricothyrotomy. These characteristics are easy to remember if they are
considered in the same order as the steps used in oral intubation — that is, head
position, mouth opening, displacement of the tongue and jaw, visualization, and
insertion of endotracheal tube:
Neck mobility. The presence of possible cervical spine injury, short neck, or
limited neck mobility due to prior surgery or arthritis will restrict the ability to
position adequately. If there is a possibility of cervical spine injury, neck extension
should be avoided and an appropriately sized cervical collar should be placed for
cervical motion restriction (Figure 2-4).
External face. The patient should be examined for evidence of a small mandible or
the presence of surgical scars, facial trauma, small nares, or nasal, oral, or
pharyngeal bleeding.
Mouth. Mouth opening may be limited due to temporomandibular joint disease or
facial scarring. An opening of less than three finger breadths (approximately 6 cm)
is associated with an increased risk of difficult intubation.
Tongue and pharynx. Tongue size relative to the posterior pharynx provides an
estimate of the amount of room in the pharynx to visualize glottic structures.
Jaw. Thyromental distance is the distance in finger breadths between the anterior
prominence of the thyroid cartilage (Adam’s apple) and the tip of the mandible
(chin), and is an estimate of the length of the mandible and the available space
anterior to the larynx. A distance of less than three finger breadths (approximately
6 cm) indicates that the larynx may appear more anterior and be more difficult to
visualize and enter during laryngoscopy. A more acute angulation of the stylet at the
distal end of the endotracheal tube may be helpful (see above).
If one or a combination of these physical characteristics indicates the possibility of

difficult intubation and if time allows, other options for obtaining a secure airway and
summoning someone with additional airway expertise should be considered.
Failed intubation attempts can result in
periglottic edema and create subsequent
difficulty with mask ventilation, leading
to a “can’t intubate and can’t ventilate”
situation.
When difficulty in mask ventilation or intubation is anticipated, care is advised before

suppressing spontaneous ventilation with neuromuscular blocking drugs or sedatives
that cannot be reversed. Video laryngoscopy has shown to be an effective method of
airway management as both a primary intubation technique and in management of the
difficult airway. Options for safe airway management include the following, all of
which preserve spontaneous ventilation:
Awake intubation by direct or video laryngoscopy, or blind nasotracheal intubation

Flexible fiberoptic intubation (expert consultation required)
Awake tracheostomy (expert consultation required)
In the event that visualization of the glottis and mask ventilation are both impossible and
there is no spontaneous ventilation, options include:
Laryngeal mask airway or esophageal-tracheal double-lumen airway device

Needle cricothyrotomy (expert consultation required)
Surgical cricothyrotomy/tracheostomy (expert consultation required)
Percutaneous tracheostomy (expert consultation required)
An algorithm for managing a potential or confirmed difficult airway is shown in Figure

2-5.
After tracheal intubation, significant alterations in hemodynamics should be anticipated.
Hypertension and tachycardia may result from sympathetic stimulation, and some
patients may require therapy with antihypertensive medications or sedatives.
Hypotension is common, and decreased cardiac output, due to reduced venous return
associated with positive pressure ventilation, can precipitate arrhythmias or cardiac
arrest. The effects of sedative agents on the vasculature or myocardium, hypovolemia,
and a possible postintubation pneumothorax may also contribute to hypotension. Other
complications associated with positive pressure ventilation are discussed in Chapter 5.
VII. PHARMACOLOGIC PREPARATION FOR INTUBATION

During the process of airway management, both parasympathetic and sympathetic
responses are common and may require control with proper pharmacologic therapy. The
pharmacologic goal before intubation is to provide the patient with optimal
analgesia/anesthesia, amnesia, and sedation without altering cardiopulmonary stability.
At times, preservation of spontaneous ventilatory drive is necessary. The selection of
particular methods or drugs depends upon the clinical circumstances and the patient’s
status, patient allergies, and the experience and preferences of the operator.
A. Analgesia/Anesthesia
A variety of topical anesthetic sprays are available, or lidocaine may be delivered

via an aerosol. Anatomic areas for special emphasis include the base of the tongue,
directly on the posterior wall of the pharynx, and bilaterally in the tonsillar fossae.
Care should be taken not to exceed 4 mg/kg of lidocaine (maximum dose 300 mg),
as it is easily absorbed from the airway mucosa.
Administration of nerve blocks and transcricoid membrane lidocaine requires
special expertise outside the scope of this course.
Some sedative agents also have analgesic properties; most do not.
Excessive use of benzocaine topical

sprays can produce clinically significant
methemoglobinemia.
B. Sedation/Amnesia
Rapid-acting, short-lived, and potentially reversible agents are preferred for sedation.
No single agent has every desirable feature, and often more than one agent may be
considered to provide a balanced technique. The status of the patient’s intravascular
volume and cardiac function must be carefully considered during the selection of an
agent and its dosage. Most may induce hypotension when heart failure or hypovolemia
is present. Examples of commonly used medications are listed in Table 2-3. Be
prepared to manage hypotension following induction with fluid boluses and/or
vasopressors (Chapters 5 and 7).
Table 2-3 Drugs Used to Facilitate Tracheal Intubationa

Agent Dosing Benefits Cautions
Fentanyl 0.5-2 μg/kg IV bolus Rapid onset of action Chest wall rigidity with rapid
every several minutes Short acting administration
titrated to analgesic Reversible with naloxone Respiratory depression
effect Does not inhibit patient
awareness of procedure
Midazolam 0.1-0.3 mg/kg bolus Provides amnesia Additive respiratory
titrated to sedative Rapid onset of action depression when combined
effect every several Short acting with narcotic
minutes Reversible with flumazenil Does not provide analgesia
Etomidate 0.1-0.3 mg/kg single IV Provides hypnosis May induce myoclonus,
bolus May be preferred in head including mild trismus
injury (consider premedication with
No adverse 50 μg fentanyl)
cardiovascular effects No reversal agent
Transient adrenal suppression
Lidocaine 1-1.5 mg/kg IV bolus Blunts hemodynamic and Should not exceed 4 mg/kg
2-3 minutes before tracheal response to total dose due to neurotoxicity
laryngoscopy intubation (seizures)
May reduce elevations of
intracranial pressure
during laryngoscopy
Ketamine 1-4 mg/kg IV bolus Rapid onset May increase intracranial
No adverse pressure
cardiovascular effects May result in hallucinations
(except in severe upon emergence
congestive heart failure) Consider small dose of
Short acting benzodiazepine (midazolam
0.5-1 mg IV) as an adjunct
Propofol 1-2 mg/kg IV bolus Rapid onset Severe hypotension in
Short acting volume-depleted patients
Provides amnesia Does not provide analgesia
Respiratory depression
aThe medications and doses listed are for induction in intubation in adult patients and are not intended for
ongoing sedation or pain control.
C. Neuromuscular Blockers
Often, intubation can be safely and easily performed after topical anesthesia (ie, an
awake intubation), or with sedation alone. Therefore, neuromuscular blockade is not
always required before endotracheal intubation. Obviously, if the operator cannot
intubate the patient after neuromuscular blockers have been given, effective manual
mask ventilation must be continued while a more experienced person is sought, an
alternative plan to secure the airway is developed, or the agent is metabolized with
return of spontaneous ventilation. Hence, a short-acting agent is advantageous. The
following are examples of neuromuscular blockers:
Succinylcholine, 1 to 1.5 mg/kg intravenous bolus: rapid onset; shortest duration,

which provides an element of safety; may cause muscle fasciculations because this
agent depolarizes skeletal muscle; emesis may occur if abdominal muscle
fasciculations are severe; contraindicated when ocular injury is present; relatively
contraindicated when head injury or hyperkalemia is present (potassium release of
0.5-1 mmol/L will occur routinely, and massive potassium release may occur in
burn and crush injury, upper motor neuron lesions, or primary muscle disease);
may precipitate malignant hyperthermia. Effects are prolonged in patients with
atypical cholinesterase or decreased pseudocholinesterase levels.
Vecuronium, 0.1 to 0.3 mg/kg; rocuronium, 0.6 to 1 mg/kg; or cisatracurium, 0.1 to
0.2 mg/kg intravenous bolus: no fasciculations because these are nondepolarizing
agents; slower onset of muscle paralysis; significantly longer duration of effects
than with succinylcholine.
D. Rapid Sequence Intubation

Rapid sequence intubation is the simultaneous administration of a sedative agent and a
neuromuscular blocker, designed to facilitate intubation and reduce the risk of gastric
aspiration. It is the technique of choice when there is an increased risk of aspiration (eg,
full stomach, pain, gastroesophageal reflux) and examination does not suggest a difficult
intubation. Patients in whom intubation is likely to be difficult should not have rapid
sequence intubation. The emergency methods described earlier will be necessary if the
patient cannot be intubated and is impossible to ventilate, because the ability to
ventilate via mask is not tested before administration of the neuromuscular blocker.
E. Intracranial Pressure
Intracranial pressure may rise during laryngoscopy and intubation, and this may be
harmful in patients with preexisting intracranial hypertension. Intravenous lidocaine (1-
1.5 mg/kg) has been shown to blunt this response and should be administered before
laryngoscopy when intracranial pathology is suspected.
Key Points
Airway Management
Assessment of the patient’s level of consciousness, airway protective reflexes,
respiratory drive, obstruction(s) to gas flow into the airway, and work of breathing
will determine the steps necessary to ensure appropriate respiratory support.
Every primary care provider must be skilled in manual methods to secure and
maintain a patent airway.
Manual assisted ventilation performed with a bag-mask resuscitation unit is a skill
expected of every healthcare provider. The goal is to optimize oxygenation and
CO2 removal before, or in lieu of, intubation of the patient.
Proper application of cricoid pressure may reduce the risk of gastric distension
and passive aspiration.
The laryngeal mask airway and esophageal-tracheal double-lumen airway device
are useful airway adjuncts when expertise in intubation is lacking or intubation is
unsuccessful.
Before intubation, patient evaluation is necessary to assess the degree of difficulty
and determine the appropriateness of analgesia, sedation, amnesia, and possible
neuromuscular blockade.
A plan for managing a potentially difficult intubation includes maintenance of
spontaneous ventilation, video laryngoscopy, alternatives to endotracheal
intubation, and requests for expert assistance. When manual mask ventilation is
impossible after failed intubation, proper use of adjunct devices, cricothyrotomy,
or percutaneous tracheostomy may be lifesaving.
Suggested Readings
1. American Society of Anesthesiologists Task Force on Management of the Difficult

Airway. Practice guidelines for management of the difficult airway: an updated
report by the American Society of Anesthesiologists Task Force on Management of
the Difficult Airway. Anesthesiology. 2013;118(2):251-270.
2. Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the
management of pain, agitation and delirium in adult patients in the intensive care
unit. Crit Care Med. 2013;41(1):263-306.
3. Consilvio C, Kuschner WG, Lighthall GK. The pharmacology of airway
management in critical care. J Intensive Care Med. 2012;27(5):298-305.
4. Danks RR, Danks B. Laryngeal mask airway: review of indications and use. J
Emerg Nurs. 2004;30:30-35.
5. DeJong A, Molinari N, Conseil M, et al. Video laryngoscopy versus direct
laryngoscopy for orotracheal intubation in the intensive care unit: a systematic
review and meta-analysis. Intensive Care Med. 2014;40(5):629-639.
6. El-Orbany M, Woehlck HJ. Difficult mask ventilation. Anesth Analg.
2009;109(6):1870-1880.
7. Ellis DY, Harris T, Zideman D. Cricoid pressure in emergency department rapid
sequence tracheal intubations: a risk-benefit analysis. Ann Emerg Med.
2007;50(6):653-665.
8. Galvagno S, Restrepo R. Airway complications and management [video]. Society
of Critical Care Medicine. Uploaded Oct 18, 2012. www.sccm.org/Education-
Center/Clinical-Resources/Pages/Mechanical-Ventilation.aspx
9. Hurford WE. The video revolution: a new view of laryngoscopy. Respir Care.
2010;55(8): 1036-1045.
10. Mayglothling J, Duane TM, Gibbs M, et al. Emergency tracheal intubation
immediately following traumatic injury: an Eastern Association for the Surgery of
Trauma practice management guideline. J Trauma Acute Care Surg.
2012;73(5):S333-S340.
11. Stollings JL, Diedrich DA, Oyen LJ, et al. Rapid-sequence intubation: a review of
the process and considerations when choosing medications. Ann Pharmacother.
2014;48(1):62-76.
12. Walz JM, Zayaruzny M, Heard SO. Airway management in critical illness. Chest.
2007;131:608-620.
13. Mehta M, Bhagat M, Song YB, et al. Intubation and airway monitoring. In: Rajaram
SS, ed. Critical Care Procedure Book. Hauppauge, NY: Nova Publishers;
2015:89-99.
Suggested Website
1. Society of Critical Care Medicine. http://www.SCCM.org/Guidelines

Chapter 3
CARDIOPULMONARY/CEREBRAL RESUSCITATION
Objectives
Identify patients who are likely to benefit from cardiopulmonary resuscitation.

Propose a process for delegating responsibilities during the resuscitative process.
Discuss important treatment issues in cardiopulmonary arrest.
Emphasize goals and interventions for brain protection and recovery, including use
of therapeutic hypothermia.
Review specific cardiopulmonary events that occur in critically ill, ventilated
patients.
Case Study
A code blue (cardiac arrest) is called on the overhead paging system. You respond to
the indicated room on a general floor to find a 42-year-old woman who is pulseless and
apneic. A nurse is placing oxygen on the patient. Another nurse is attempting to place an
IV line.
– What should be your immediate actions?
– What are the next steps if you are the team leader?
– What tasks are delegated to team members during the resuscitation?
I. INTRODUCTION
The immediate response to an in-hospital cardiac arrest is frequently the responsibility
of primary care providers, hospitalists, nurses, house staff, and other members of the
healthcare team. The Society of Critical Care Medicine and the Fundamental Critical
Care Support program recognize the valuable training provided by the American Heart
Association’s Basic Life Support (BLS), Advanced Cardiovascular Life Support
(ACLS), and Pediatric Advanced Life Support (PALS) curricula. All healthcare
practitioners are encouraged to successfully complete the appropriate courses.
II. ETHICAL ISSUES
A. Who Should Be Resuscitated?

The purpose of cardiopulmonary resuscitation (CPR) and advanced life support is to
reverse sudden, unexpected death resulting from reversible disease processes or
iatrogenic complications. If possible, resuscitation status and any limitations should
always be discussed with the patient, the patient’s family, or the surrogate decision
maker before a cardiac arrest event (Chapter 15). Resuscitation is unlikely to benefit
patients experiencing a cardiac arrest despite maximal medical therapy for progressive
cardiogenic or septic shock. Out-of-hospital arrest can carry a very high mortality rate
in conjunction with prolonged CPR. Several other underlying conditions (eg,
pneumonia, congestive heart failure, renal failure, and sepsis) make survival from
cardiac arrest exceedingly unlikely but not unprecedented. No set of variables is
sensitive enough to accurately predict a poor outcome.
CPR and advanced life support may not

be indicated for all patients based on
the patient’s wishes and expected quality
of life.
B. Level of Therapeutic Support

CPR is instituted based on implied consent, without a physician’s order. However, any
limitation of resuscitation requires a physician’s order. Do-not-attempt-resuscitation
(DNAR/DNR) orders should be documented in the chart with a detailed explanation of
the rationale. Such orders do not and should not indicate that the patient is not to be
treated. Patients and their families should not be abandoned emotionally because of such
orders. “No resuscitation” does not mean “no care and no treatment.” Individual
resuscitative plans suited to a patient’s particular wishes and condition should be
clearly delineated in the chart by the attending physician. Pain and anxiety should be
treated in all cases regardless of a patient’s resuscitation status.
Whenever doubt exists regarding

resuscitation status, the provider should
institute resuscitation until further
information is obtained.
C. Documentation
The intended level of therapeutic support should be documented in the patient’s chart so
that the medical and nursing staff knows exactly how to proceed should a
cardiorespiratory arrest occur unexpectedly. A discussion of potential resuscitative
measures should occur with all patients on admission regardless of the acuity of their
clinical status. The staff should follow valid DNAR/DNR orders. Information about
advance directives, living wills, durable powers of attorney, and related forms also
should be documented and respected.
A do-not-resuscitate order does not

imply that no care or treatment will be
administered. Treatment should be
administered for pain and anxiety as
well as measures other than CPR and
artificial respiration and ventilation.
III. PRIMARY RESPONSE
Responders will usually have resuscitation resources available for cardiorespiratory
arrests that occur within the hospital. Often, however, the most important aspects of a
successful resuscitation relate to the interactions, knowledge, and skills of the
responders and the ability to delegate and accept responsibility for components of the
resuscitation effort.
A well-trained team experienced in

resuscitation offers the best potential for
success.
A. Assessment of the Immediate Situation

Has an appropriate individual assumed the leadership role?
If so, how can you assist? Identify yourself and offer help. Be ready to accept a
delegated role and to focus your efforts upon that role while remaining aware of
other evolving resuscitation activities.
You may be required to assume the leadership role until a more qualified
individual or the designated team member arrives.
B. The Leader’s Role

Proceed with primary assessment and intervention, and delegate appropriate activities
to others.
The presence or absence of a pulse

should be determined in ≤10 seconds.
1. Evaluation and Initial Cardiac Resuscitation
Assess patient responsiveness.

If the patient is unresponsive, assess the respiratory effort and pulses. If these are
absent, activate your emergency response system, obtain an automated external
defibrillator (AED) or monitor/defibrillator, and start chest compressions (CPR)
immediately at a rate of at least 100/min, and at a depth of at least 2 inches (5 cm)
in adults. Push hard, push fast. Healthcare providers should provide 2 breaths
over 1 second each, with a ratio of compression to ventilation of 30:2, during each
2-minute cycle of CPR. The breaths should be of sufficient volume to see the chest
rise and contain the maximum oxygen concentration available. Compressions-only
CPR is acceptable for non-healthcare providers.
Defibrillation should be initiated as soon as possible if monitoring (eg, quick-look
paddles) indicates ventricular fibrillation or pulseless ventricular tachycardia. A
single shock should be delivered at the energy level appropriate for the
defibrillator (360 joules with a monophasic defibrillator or 200 joules with a
biphasic defibrillator). Chest compressions should be resumed immediately after
the shock is delivered without checking the pulse or rhythm. Rhythm analysis
should usually occur after 2 minutes of compressions, but this sequence may be
modified in the hospital setting with continuous electrocardiographic (ECG)
monitoring.
If intubated and connected to a mechanical ventilator, the patient must be
disconnected and changed to manual bag-mask ventilation.
Continue CPR while the defibrillator is

charging.
2. Delegation
Delegate tasks to the most appropriate personnel available whenever possible.

This allows the resuscitation leader to maintain an overall perspective, monitor
cardiac rhythm, direct assessments and interventions, and prescribe medications.
The leader may need to perform some of these tasks or reassign them if the primary
designee is unsuccessful. Obviously, if the number of responders is not sufficient,
team members must establish priorities for performance. Delegated duties should
include the following:
a. Manage the airway (Chapter 2). Establish a patent airway, provide manual
bag-mask ventilation, utilize available airway adjuncts, and/or perform
endotracheal intubation. Ventilations should not exceed the recommended 8 to
10 breaths/min to optimize coronary artery perfusion pressure by decreasing
the percentage of time in positive intrathoracic pressure. Avoid
hyperventilation.
b. Perform chest compressions. The resuscitation leader should designate a
second person for relief and instruct the rescuers to exchange responsibilities
every 2 minutes. Evidence shows that a compression rate of at least 100/min
results in maximal blood flow for the patient. The ratio of compression to
ventilation is 30:2 without an advanced airway in place, and the depth of
compressions for adults is at least 2 inches (5 cm). The chest should recoil
completely between compressions. If the patient has an advanced airway in
place, compressions are continuous, and asynchronous ventilation is provided
at a rate of 8 to 10 breaths/min. The person on relief should monitor the
effectiveness of compressions by checking the carotid or femoral pulse. Chest
compressions are interrupted only for shock delivery and rhythm checks once
the airway is secured. Pulse checks are performed only if an organized rhythm
is noted.
Minimize the interruptions of chest

compressions and maximize the
depth of compressions.
c. Attach ECG monitor/machine.

d. Obtain intravenous or intraosseous access. Peripheral venous access with a
large catheter is preferred because it does not require interruption of chest
compressions. The intraosseous route can be used as a temporary measure
when other vascular sites are not immediately available in children or adults
(Chapter 4).
e. Provide medications as requested (eg, to manage the code cart,
defibrillator/pacer).
f. Maintain record of resuscitation interventions and patient assessments.
g. Obtain medical record and/or provide pertinent patient information.
h. Notify the patient’s personal attending physician of the cardiopulmonary event
and obtain further guidance. Discuss the patient’s status, medical history,
existence of advance directives, and related topics.
i. Remove furniture, unnecessary equipment, and extra personnel from the
resuscitation area.
j. Notify the patient’s family of current events and provide emotional support. If
family members are present at the bedside, allow them to remain and provide
explanation of the procedures and emotional support. (Nurses and/or staff
chaplains often assume this role.)
IV. CONTINUING RESUSCITATION

Once the primary response and assigned tasks have been successfully initiated, each
team member continues an appropriate role as the resuscitation interventions are
implemented.
Critical laboratory data should be obtained to assist with decisions during the
resuscitation and, perhaps, to reveal a cause for the cardiac arrest. Important data
include levels of glucose and measures of arterial blood gases, potassium, ionized
calcium, phosphorus, and magnesium. Suspected abnormalities or those
documented in recent laboratory values may be treated empirically. Laboratory
personnel should be notified of the ongoing resuscitation.
During cardiopulmonary resuscitation events, many institutions use bedside
ultrasound as a diagnostic tool to evaluate the patient’s cardiac tamponade status,
cardiac function, or return of circulation. This is done where bedside ultrasound is
available.
The patient’s chart should be reviewed for history and any possible medication
reaction that could lead to cardiac arrest, arrhythmia, or decreased ventilatory
drive.
It is appropriate to assume that the initial cardiopulmonary arrest would not have
been announced if a DNAR/DNR or similar directive had been ordered by a
physician – but this should be confirmed as other patient information and data are
obtained. Whenever doubt exists about a patient’s resuscitation status, full
resuscitative measures should be initiated and continued until clarified with the
patient’s attending physician and/or family/surrogate.
The point at which family members are notified of the cardiopulmonary arrest will
vary. If family is present, a team member should provide information periodically
during the resuscitation. The presence of family during resuscitation should be
carefully considered and planned for if this practice is accepted by the institution
and the resuscitation team.
Arrangements for patient transfer to an ICU should be considered. A transport cart,
emergency drugs, external pacer, portable monitors, oxygen, and other crucial
supplies should be available to facilitate immediate transfer as the patient
stabilizes. The ICU will need to prepare, so additional patient needs (eg, presence
of arterial or central lines and mechanical ventilation) should be communicated.
V. OTHER CONSIDERATIONS IN
CARDIOPULMONARY/CEREBRAL RESUSCITATION
The method that best produces blood flow to the coronary arteries, brain, and other
organs during a cardiopulmonary arrest has not yet been determined. At present,
closed-chest compressions remain the standard technique for circulatory support.
Interposed abdominal compression CPR and active compression-decompression
CPR (device not available in the United States) may be considered acceptable
alternatives whenever personnel trained in the techniques are available. Use of
mechanical chest compression devices is increasing in CPR. The invasive
alternative of open-chest cardiac massage requires a team with special expertise
and early institution for optimal outcome. Immediate cardiopulmonary bypass may
be effective in improving the success of resuscitation but is not available in most
hospitals.
Early restoration of perfusion to the brain and other organs offers the best chance
for recovery of function. Patients who are mildly hypothermic after cardiac arrest
should not be actively warmed because warming increases oxygen demand and
alters vascular tone. Targeted temperature management (32°C to 36°C [89.6°F to
98.6°F]) for at least 24 hours has been recommended to improve neurologic
outcome and reduce mortality in comatose patients following initial resuscitation
from and arrest (see Section VI). Febrile patients should be treated to reach a
normal temperature as soon as possible. Seizures must be aggressively treated to
avoid further brain injury. Hyper- and hypoglycemia should be avoided because
these conditions have been correlated with a worsened neurologic outcome. Other
strategies to protect the brain during and after no-flow states and in conjunction
with CPR are under investigation.
Quantitative end-tidal CO2 measurement with waveform display is recommended
for the intra- and post-resuscitation management of cardiac arrest. Detection of or a
rapid increase in end-tidal CO2 is often the earliest indication of return of
spontaneous circulation (ROSC). Normocapnia (PCO2 38-42 mm Hg) is the goal.
Closed-chest compressions produce

approximately one-third of normal
cardiac output.
VI. TARGETED TEMPERATURE MANAGEMENT

Targeted temperature management (TTM), or therapeutic hypothermia, is a critical part
of the cardiocerebral resuscitation process. Early restoration of perfusion to the brain
and other organs offers the best chance for functional recovery. Avoidance of
hyperthermia in the post-cardiac arrest period is essential. TTM as low as 32°C to
34°C (89.6°F to 96.8°F) core body temperature is recommended for patients with out-
of-hospital or in-hospital cardiac arrest due to ventricular fibrillation or pulseless
ventricular tachycardia who remain unconscious after ROSC (Figure 3-1). TTM with a
goal of 32°C to 36°C (89.6°F to 96.8°F) core body temperature for at least 24 hours is
recommended for patients who remain unconscious after ROSC (Figure 3-1). TTM is
associated with both reduced mortality rates and improved neurological recovery after
out-of-hospital cardiac arrest due to ventricular fibrillation and pulseless ventricular
tachycardia. Although definitive evidence is lacking, TTM is also strongly
recommended for nonshockable rhythms and for patients following in-hospital arrest
because of the high morbidity and mortality associated with these circumstances. The
options of TTM at lower and higher temperatures allows flexibility to tailor the
treatment to the patient and avoid adverse effects of deeper hypothermia. Select group
of post-cardiac arrest patients who are unconscious may benefit from TTM (Table 3-1).
Figure 3-1. Example of Targeted Temperature Management Algorithm a
Abbreviations: ROSC, return of spontaneous circulation; TTM, targeted temperature management; MAP,
mean arterial pressure; SBP, systolic blood pressure
a Reproduced with permission from Lippincott, Williams & Wilkins. Seder DB, Van der Kloot TE. Methods of
cooling: Practical aspects of therapeutic temperature management. Crit Care Med. 2009; 37:S211–S222.
Table 3-1 Considerations for Targeted Temperature Management

Patients for whom therapeutic hypothermia should be considered:
Adult patients who remain comatose (ie, patients with a Glasgow Coma Scale Score less than 8
and/or patients who do not obey any verbal command after restoration of spontaneous circulation,
but before the initiation of cooling) following successful resuscitation from a witnessed out-of-
hospital cardiac arrest of presumed cardiac cause; in-hospital cardiac arrest survivors (of any initial
rhythm) may also benefit.
Patients with an initial rhythm of ventricular fibrillation or pulseless ventricular tachycardia; patients
with initial rhythms of asystole or pulseless electrical activity may also benefit.
May be used in hemodynamically unstable patients
Patients for whom therapeutic hypothermia should not be considered:
Patients with advanced directives that proscribe aggressive care

Patients with active non-compressible bleeding, but temperature management (<36°C) is
reasonable
No specific time frame has been established for the start of TTM after cardiac arrest.
However, it is generally recommended that the induction phase of cooling begin as soon
as possible if the patient remains comatose. Although the target temperature should be
reached as soon as possible, lifesaving cardiac procedures should not be delayed to
initiate TTM. Active temperature management during rewarming is favored over
passive rewarming. Avoid rebound fever. Warming should be performed slowly over 12
or more hours.
The most significant side effects of TTM are the potential for coagulopathy and
increased risk of infection. The potentials for cardiac arrhythmias and hyperglycemia
are also present.
A. Temperature Management Devices

Invasive and external devices are available for TTM, but no one strategy has proven to
be superior. In the absence of specific temperature management devices, the use of iced
saline and ice packs can be effective, although hypervolemia from excessive
administration of iced saline should be avoided.
B. Potential Organ System Effects of TTM

Adverse effects of hypothermia are less likely if cooling to higher temperatures near
36°C.
Neurologic: shivering
Cardiac: dysrhythmias
Renal: diuresis and potassium shifts
Platelets: coagulopathy
Skin: frostbite
C. Sedation and Pain Protocol

There are no specific pain or sedation protocols for TTM. Drug pharmacokinetics and
pharmacodynamics are altered during therapeutic hypothermia. Aggressive attention to
shivering is important; neuromuscular blockade may be necessary if conventional
management fails.
VII. RESPIRATORY ARREST
Case Study
You are called to the bedside of an intubated ICU patient who has had a sudden onset of
hypoxia and bradycardia. When you arrive, the pulse rate is 30 beats/min and SpO2
values are 62%.
– What are the possible etiologies for the patient’s deterioration?
– What steps should you take to optimize the patient’s respiratory status?
A. Respiratory Arrest in the Nonintubated Patient
1. Immediate Concerns
One of the most common catastrophic events in nonintubated patients is respiratory
arrest. These patients are typically found in asystole or pulseless electrical activity
(PEA) but may be in ventricular fibrillation. The first responders should institute
immediate basic life support, including bag-mask ventilation. Early endotracheal
intubation allows for the most effective ventilation and oxygenation. Manual bag-mask
ventilation with 100% oxygen until a provider experienced in endotracheal intubation
arrives is preferable to prolonged, unsuccessful attempts at intubation.
2. Patient Assessment
In many instances, careful assessment of vital signs (including pulse oximetry), air
movement, and work of breathing will indicate that respiratory impairment is present.
Tachypnea progressing to bradypnea, paradoxical abdominal breathing, and
progressively decreasing alertness may herald imminent respiratory arrest. Noninvasive
respiratory monitoring may identify patients who are decompensating. Normal arterial
blood gas measurements do not rule out the need for mechanical ventilatory support
since decompensation can occur precipitously once respiratory muscle fatigue becomes
manifest. Moreover, certain acute conditions (eg, asthma or pulmonary embolus) cause
tachypnea. A normal PCO2 in these instances portends advanced respiratory failure and
fatigue.
B. Special Management Issues
1. Cardiac Arrest in Patients Receiving Mechanical Ventilation

If a patient suffers cardiac arrest while receiving mechanical ventilation, a complication
related to ventilation must be suspected, especially if the initial cardiac rhythm is
bradycardia or asystole. Etiologic possibilities include tension pneumothorax,
ventilator failure or disconnection, or displacement or obstruction of the endotracheal
tube. Patients should be disconnected from the ventilator immediately, and manual
ventilation with 100% oxygen should be initiated while further assessment is
undertaken. If high resistance to airflow is present, the endotracheal tube should be
unsecured and checked for kinks, and attempts should be made to pass a suction
catheter. Verification of tube placement with expired CO2 monitoring is recommended
as an adjunct to physical assessment. If tube position or patency is in question, the tube
should be removed and the patient reintubated after being adequately oxygenated and
ventilated by means of a bag-mask device. Tension pneumothorax also should be
considered as a cause of high airway resistance. In instances of cardiac arrest, there is
not sufficient time to obtain a chest radiograph to check for this possibility. The chest
should be decompressed urgently with a needle placed at the level of the second
intercostal space in the mid-clavicular position if breath sounds are absent or
subcutaneous crepitus is noted.
2. Tension Pneumothorax
Patients with tension pneumothorax typically have hypotension and/or PEA with narrow
complex tachycardia. Physical assessment may reveal jugular venous distension and
ipsilateral decreased or absent breath sounds. Ipsilateral tympanitic percussion or
subcutaneous emphysema may be noted as well. In mechanically ventilated patients,
airway pressures for normal tidal volume values will be high, and the ventilator high-
pressure alarm limit may be exceeded. Resistance to bag-mask ventilation will increase
as well. For patients with severe hypotension or PEA and findings consistent with
tension pneumothorax, treatment should be instituted at once, without waiting for
radiologic confirmation. Needle thoracostomy can be accomplished on the affected side
by sterile placement of a 16- or 18-gauge catheter (a 23-gauge butterfly needle may be
used in infants) through the anterior chest wall in the second intercostal space, at the
midclavicular line. Successful decompression is associated with a rush of air,
restoration of pulses, and a decrease in airway pressures in response to bag-mask or
mechanical ventilation. All needle thoracostomy procedures should be followed by
standard tube thoracostomy because this procedure can result in: 1) temporary relief of
a tension pneumothorax; 2) creation of a pneumothorax if the presumption of a tension
pneumothorax was wrong; or 3) no change in the patient’s condition if the needle does
not decompress the pleural space. Endotracheal tube obstruction (from a patient biting
the tube or buildup of secretions) can mimic some of the findings described but does not
usually cause severe hypotension or PEA.
VIII. ADVANCED LIFE SUPPORT IN THE CRITICAL CARE UNIT
A. General Issues
To be prepared for critical events such as cardiopulmonary arrest, clinicians should
know the clinical background and status of patients in the critical care unit. They should
review each patient’s record during checkout rounds for signs of potential problems,
such as electrolyte abnormalities. In addition, the clinical history and course may give
clues to the etiology of a potential complication. For instance, a ventilated patient who
is known to have a large emphysematous bulla and who suddenly develops PEA has a
high likelihood of developing a tension pneumothorax secondary to bleb rupture.
Making patient rounds at the beginning of each tour of duty also gives the staff an
opportunity to clarify the resuscitation or code status of each patient.
B. Principal Concerns
Airway management and oxygenation/ventilation are important issues in the initial
approach to acute decompensation of an ICU patient. Adequate oxygenation/ventilation
should be evaluated by physical assessment as well as expired CO2 monitoring (if
intubation is performed). If there is evidence of abrupt cardiac or respiratory
compromise, patients who are mechanically ventilated at the time of the arrest should
be disconnected from the ventilator immediately and should receive 100% oxygen by
bag-mask ventilation. Early endotracheal intubation should be performed for those who
are not intubated already; tube placement should be verified by physical assessment,
chest radiograph, and exhaled CO2 detection. Pulselessness can be verified by
observing the arterial waveform if a functioning arterial line is in place or by carotid or
femoral pulse checks. Chest compressions should be performed and early defibrillation
for ventricular fibrillation should be undertaken as recommended by Advanced
Cardiovascular Life Support guidelines.
Key Points
Cardiopulmonary/Cerebral Resuscitation
The patient’s resuscitation status should be in accordance with documented
directives.
Familiarity with recommendations for cardiopulmonary resuscitation is
encouraged for all members of the resuscitation team.
The person assuming the leadership role during resuscitation must effectively
delegate specific duties and supervise the process of resuscitation.
Resuscitation team members must accept delegation and remain focused upon those
duties.
Chest compressions should be optimized by ensuring a rate of at least 100/min,
changing compressors every 2 minutes, continuing compressions before and after
shock delivery, and minimizing interruptions.
A complication related to mechanical ventilation should be suspected in patients
who sustain an arrest while receiving ventilation, especially if the initial
dysrhythmia is bradycardia or asystole.
In patients with hypotension and/or PEA and findings consistent with tension
pneumothorax, needle thoracostomy should be instituted without waiting for a chest
radiograph to be performed
Critically ill patients, or patients at risk of becoming critically ill, should be
monitored for early signs of physiologic deterioration, and appropriate
intervention should be instituted to avoid cardiopulmonary arrest.
TTM is associated with both reduced mortality rates and improved neurological
recovery after cardiac arrest.
Suggested Readings
1. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary

resuscitation during in-hospital cardiac arrest. JAMA. 2005;293:305-310.
2. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of
hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-
563.
3. Holzer M. Targeted temperature management for comatose survivors of cardiac
arrest. N Engl J Med. 2010;363:1256-1264.
4. Holzer M, Bernard SA, Hachimi-Idrissi S, et al. Hypothermia for neuroprotection
after cardiac arrest: Systematic review and individual patient data meta-analysis.
Crit Care Med. 2005;33:414-418.
5. Kellum MJ, Kennedy KW, Barney R, et al. Cardiocerebral resuscitation improves
neurologically intact survival of patients with out-of-hospital cardiac arrest. Ann
Emerg Med. 2008;52:244-252.
6. Nadkarni VM, Larkin GL, Peberdy MA, et al. First documented rhythm and clinical
outcome from in-hospital cardiac arrest among children and adults. JAMA.
2006;295:50-57.
7. Nolan JP, Soar J, Zideman DA, et al. European Resuscitation Council Guidelines
for Resuscitation 2010 Section 1. Executive summary. Resuscitation.
2010;81:1219-1276.
8. Nunnally ME, Jaeschke R, Belligan GJ, et al. Targeted temperature management in
critical care: A report and recommendations from five professional societies. Crit
Care Med. 2011;39:1113-1125.
9. Seder DB, Van der Kloot TE. Methods of cooling: Practical aspects of therapeutic
temperature management. Crit Care Med. 2009;37:S211–S222.
10. Hazinski MF, Nolan JP, Aickin R, et al. Part 1: Executive Summary: 2015
International Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science with Treatment Recommendations. Circulation.
2015;132:S2-S39.
11. Jabre P, Belpomme V, Azoulay E, et al. Family presence during cardiopulmonary
resuscitation. N Engl J Med. 2013;368:1008-1018.
12. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at
33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369:2197-2206.
Suggested Websites
1. Society of Critical Care Medicine. http://www.SCCM.org.

2. American Heart Association. http://www.americanheart.org.
3. Circulation. http://www.circulationaha.org.
4. European Resuscitation Council. http://www.erc.edu.
Chapter 4
DIAGNOSIS AND M ANAGEMENT OF ACUTE

RESPIRATORY FAILURE
Objectives
Define and classify acute respiratory failure.

Describe the pathophysiology and manifestations of acute respiratory failure.
Review oxygen supplementation strategies in acute respiratory failure.
Case Study
A 75-year-old man with a long history of smoking, chronic lung disease, and treatment
noncompliance is brought to the emergency department by his daughter, who says that he
complained of progressive dyspnea overnight. The patient is awake, alert, and in
moderate respiratory distress, with evident use of accessory muscles during inspiration
and expiration and a respiratory rate of 30 breaths/min. There are audible expiratory
wheezes. You are called to assess the patient and initiate treatment.
– What tests would be useful to evaluate the severity of the patient’s condition?
– Which oxygen supplementation device should be used?
– What pharmacologic treatment should be initiated?
I. INTRODUCTION
Acute respiratory failure (ARF) is one of the leading causes of admission to the ICU. It
is defined as the inability of the respiratory system to meet the oxygenation, ventilation,
or metabolic requirements of the patient. The pulmonary system is involved in two
crucial functions: elimination of carbon dioxide (CO2) and oxygenation of the blood.
There are three types of respiratory failure: hypoxemic, hypercapnic, and mixed.
Hypoxemic respiratory failure is defined by a room air PaO2 of ≤50 to 60 mm Hg (≤6.7-
8 kPa) or an abnormal ratio of PaO2 to fraction of inspired oxygen (PaO2:FIO2, or P:F
ratio; see below). This abnormality of PaO2 should exist in the absence of intracardiac
right-to-left shunting. Hypercapnic respiratory failure is defined by a PaCO2 ≥50 mm Hg
(≥6.7 kPa) that is not due to respiratory compensation for metabolic alkalosis. Mixed
respiratory failure has features of both hypercapnia and hypoxemia and is a common
form of respiratory failure in critically ill patients. Respiratory failure is considered
chronic once the renal system begins to compensate by retaining bicarbonate. This
usually occurs within a few days of persistent hypercapnia and the resulting respiratory
acidosis. Frequently, in patients with chronic lung disease, ARF may be superimposed
on chronic respiratory insufficiency. The acute component in such circumstances is
distinguishable from the chronic component by the degree of respiratory acidosis in
relation to PaCO2 and knowledge of baseline oxygen requirements, PaCO2 levels, and
bicarbonate values.
II. CAUSES OF ACUTE RESPIRATORY FAILURE

Acute respiratory failure develops in a variety of clinical settings. It may result from
primary pulmonary insults or from other systemic nonpulmonary disorders, as
summarized in Table 4-1. Diseases of the central nervous system, neuromuscular
system, upper and lower airways, pulmonary parenchyma, pulmonary vasculature,
thoracoabdominal cavity, and cardiovascular system may all give rise to ARF.
Table 4-1 Causes of Respiratory Failure

DISORDERS ASSOCIATED WITH ABNORMAL OXYGEN ONLOADING
(HYPOXEMIC RESPIRATORY FAILURE)
Lower Airway and Parenchyma
NEOPLASM TRAUMA OTHER
INFECTIONS Pulmonary contusion Bronchospasm
Viral Pulmonary laceration Heart failure
Bacterial Acute respiratory distress syndrome
Fungal Interstitial lung disease
Mycoplasmal Atelectasis
Other Cystic fibrosis
DISORDERS ASSOCIATED WITH INADEQUATE CARBON DIOXIDE OFFLOADING

(HYPERCAPNIC RESPIRATORY FAILURE)
Brain
DRUGS METABOLIC NEOPLASMS INCREASED
Opioids Hyponatremia INFECTIONS INTRACRANIAL
Benzodiazepines Hypocalcemia Meningitis PRESSURE
Propofol Alkalosis Encephalitis OTHER
Barbiturates Myxedema Abscess Central alveolar
General anesthetics Polio hypoventilation
Poisons West Nile myelitis Central sleep apnea
Nerves and Muscles
TRAUMA DRUGS/POISONS METABOLIC NEOPLASM OTHER
Spinal cord injury Neuromuscular Hypokalemia, INFECTIONS Motor neuron
Diaphragmatic blocking agents hyperkalemia Tetanus disease
injury Aminoglycoside Hypophosphatemia West Nile myelitis Myasthenia gravis
antibiotics Hypomagnesemia Multiple sclerosis
Arsenic Muscular dystrophy
Strychnine Guillain-Barré
Botulism syndrome
Botulism
Upper Airway
TISSUE ENLARGEMENT INFECTIONS OTHER
Tonsil and adenoid hyperplasia Epiglottitis Bilateral vocal-cord paralysis
Malignant neoplasm Laryngotracheitis Laryngeal edema
Polyps TRAUMA Tracheomalacia
Goiter Cricoarytenoid arthritis
Obstructive sleep apnea
Chest Bellows
TRAUMA OTHER CONTRIBUTING FACTORS
Rib fractures Kyphoscoliosis Fibrothorax
Flail chest Scleroderma Supine position
Burn eschar Spondylitis Obesity
Pneumothorax Pain
Pleural effusion Ascites
Hypoxemic respiratory failure is often seen in patients with severe pneumonia, acute
lung injury, or acute pulmonary edema, disorders that interfere primarily with adequate
oxygenation of the blood as it circulates through the alveolar capillaries. Hypercapnic
respiratory failure is seen in patients with severe airflow obstruction, central
respiratory failure, or neuromuscular respiratory failure. Hypercapnia most often results
from inadequate alveolar ventilation, which causes ineffective CO2 clearance.
The cause of ARF in adults is often

multifactorial.
The following are common ICU scenarios that lead to ARF:
Exacerbations of chronic obstructive pulmonary disease (COPD), characterized by

thick mucopurulent secretions as well as bronchospasm, are often associated with
both hypoxemic and hypercapnic acute respiratory failure (ie, mixed ARF).
Pneumonia is most commonly associated with hypoxemic respiratory failure,
although it also can be associated with hypercapnic respiratory failure, especially
in the setting of other diseases such as COPD.
Acute respiratory distress syndrome is a manifestation of a systemic inflammatory
response caused by pulmonary or nonpulmonary injury or disease. The
predominantly hypoxemic respiratory failure is caused primarily by an increased
shunt fraction due to alveolar filling.
Traumatic brain injury is associated with predominantly hypercapnic respiratory
failure, although it can be complicated by hypoxemic respiratory failure in the
setting of concurrent aspiration, pulmonary contusions, neurogenic pulmonary
edema, or chronic pulmonary disease.
Overdose with central nervous system-depressing agents, such as benzodiazepines,
opioids, or barbiturates, presents with alveolar hypoventilation and thus acute
hypercapnic respiratory failure.
Decompensated congestive heart failure is associated with predominantly
hypoxemic failure (secondary to alveolar filling and increased shunt); however,
hypercapnic respiratory failure may also occur in severe exacerbations or in the
presence of pulmonary disease.
III. PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILURE
A. Hypoxemia
The most common underlying physiologic abnormality in hypoxemic respiratory failure
is a mismatch of alveolar ventilation V̇ and pulmonary perfusion Q̇ , as illustrated in
Figure 4-1. The mismatch of ventilation and perfusion, where ventilation is decreased
relative to perfusion, is called low V̇/Q̇.
Figure 4-1. Ventilation and Perfusion Matching in the Lung
A, At one end of the pathologic continuum, areas of limited ventilation relative to perfusion produce shunt
effect and hypoxemia. B, Ventilation and perfusion are matched in the normal lung. C, At the opposite end of
the continuum, areas of better ventilation than perfusion produce dead space effect.
V̇ /Q̇ matching is of particular importance to oxygenation of blood as opposed to

elimination of CO2 (discussed in Section IV) because of the kinetics of the hemoglobin
oxygen dissociation curve (Chapter 6, Figure 6-1 for the oxyhemoglobin dissociation
curve). Lung areas with high V̇ /Q̇ ratios, which provide a high PaO2, cannot compensate
for areas with a low V̇ /Q̇ ratio (providing low PaO2) as the hemoglobin molecule is
already about 90% saturated at a PaO2 of about 60 mm Hg. The admixture of poorly
oxygenated blood returning from abnormal alveoli dilutes oxygenated blood from more
normal lung units, resulting in systemic hypoxemia. The hypoxemia caused by V̇ /Q̇
mismatch is usually easily corrected by supplemental oxygen.
Disease processes that cause progressive obstruction of distal airways, alveolar filling,
or atelectasis (eg, pneumonia, aspiration, pulmonary edema) result in a decrease in the
amount of oxygen available in distal airways for uptake through the pulmonary
capillaries. Through hypoxic pulmonary vasoconstriction, blood flow to such abnormal
lung units decreases, but this decline is of lesser magnitude than the decrease in oxygen
availability. This allows for a greater proportion of deoxygenated blood (venous
admixture) to return to the left side of the heart.
One extreme of V̇ /Q̇ mismatch is shunt, as there is perfusion of the unventilated lung. In
diseases that cause diffuse alveolar flooding (eg, acute respiratory distress syndrome),
refractory hypoxemia may be due to shunt physiology. Treatment of hypoxemia due to ̇ V
/Q̇ mismatch should be directed towards treating the underlying cause such as
infections, reversing airway obstruction, reopening (recruiting) atelectatic lung zones,
and preventing closure (de-recruitment) of the affected lung units. Oxygen therapy
and/or mechanical ventilation are cornerstones in providing support until such time that
the cause of V̇ /Q̇ mismatch has been reversed.
Other, less common causes of hypoxemia include:
Decreased diffusion of oxygen across the alveolocapillary membrane complex

because of interstitial edema, inflammation, fibrosis, etc.
Alveolar hypoventilation
High altitude with low inspired partial pressure of oxygen
The P:F ratio can be helpful for

following trends in a patient’s condition
and evaluating ventilation strategies.
Diffusion abnormality is rarely the primary cause for hypoxemia as oxygen transport
across the alveolocapillary membrane is generally perfusion limited and not diffusion
limited; however, in cases such as increased cardiac output and tachycardia, diffusion
may be limited when the transit time across pulmonary capillaries is reduced. Therapy
for diffusion abnormalities, in addition to maintaining adequate circulating volume,
includes treatment of the cause of interstitial pathology (ie, diuretics for cardiogenic
pulmonary edema, corticosteroids for inflammatory disorders). Ensuring adequate
minute ventilation will correct hypoxemia that is solely due to hypoventilation. High
altitude is a rare cause of acute hypoxemia in patients. As a compensatory strategy,
increasing oxygen supplementation (FIO2) while the cause of the hypoxemia is sought and
corrected may improve oxygenation.
Numerous methods for quantifying hypoxemia have been proposed to provide a means
of following the degree of hypoxemia and to communicate this information to other
providers. The P:F ratio (where PaO2 is measured as mm Hg and FIO2 is the fraction of
inspired oxygen) is a commonly used method for quantifying the degree of patient
hypoxemia. It requires accurate assessment of FIO2, which is difficult in the nonintubated
patient. Calculating the P:F ratio is a simple method for assessing the degree of
hypoxemia and following it over time. A normal P:F ratio ranges between 300 and 500
mm Hg, with values below 300 mm Hg indicating abnormal gas exchange and values
below 200 mm Hg indicating severe hypoxemia. However, one must be cognizant of the
fact that PaO2 — hence, the P:F ratio — can be greatly modified by the application of
positive end-expiratory pressure and other recruitment maneuvers. Thus, different P:F
ratios may be obtained for the same amount of FIO2.
B. Hypercapnia
Hypercapnic respiratory failure is caused by either excess CO2 production or decreased
effective alveolar ventilation. Alveolar minute ventilation (VA) is determined by the
tidal volume (VT ), and the respiratory rate frequency (f). VD is dead space.
VA = (VT – VD)f
Hypercapnia, resulting from either decreased VT or the respiratory rate frequency,
occurs with drug ingestion, anesthesia, depression of the medullary center for
respiration, and fatigue, for example. An elevated PaCO2 normally increases ventilatory
drive. Therefore, hypercapnic respiratory failure implies that the patient is unable to
sustain minute ventilation (f × VT ).
Treatment of decreased VT or respiratory rate may require reversal of sedation or other
drugs, intubation/mechanical ventilation to rest fatigued muscles, nutrition, respiratory
stimulants, or treatment of other possible primary causes. Measures of ventilatory
mechanics, such as peak negative inspiratory pressure and forced vital capacity, monitor
a patient’s course and may signal when endotracheal intubation and mechanical
ventilation are warranted, especially in neuromuscular disorders such as myasthenia
gravis and Guillain-Barré syndrome. A single measurement is less useful than
measurements made over time. Negative inspiratory pressures below –20 to 25 cm H2O
or forced vital capacity <10 mL/kg, or both, should raise concern that a patient’s
ventilatory mechanics may be sufficiently impaired to warrant tracheal intubation and
mechanical ventilation.
The more rapidly the negative

inspiratory pressure and forced vital
capacity deteriorate, the lower the
threshold for intubation and mechanical
ventilation.
Increased physiologic dead space (VD) may also produce hypercapnia and is another
type of mismatch illustrated in Figure 4-1. When gas flow to and from airways remains
adequate but blood flow is absolutely or relatively diminished, CO2 does not have the
opportunity to diffuse out of the pulmonary circulation, and CO2-rich blood is returned
to the left atrium. Increased dead space ventilation may occur in respiratory muscle
fatigue from any cause, leading to rapid shallow breathing. Increased VD may also be
seen in hypovolemia, pulmonary embolism, poor cardiac output, or when the regional
airway pressure is relatively higher than the regional perfusion pressure, reducing
pulmonary blood flow in that area.
Strategies to reduce dead space may include reduction in peak or mean airway
pressures, if the patient is receiving mechanical ventilation, augmentation of
intravascular volume and/or cardiac output, or treatment of other causes for limited
pulmonary blood flow. It may be possible to compensate for hypercapnia due to high VD
by modifying parameters to increase minute ventilation during mechanical ventilation
while the cause of hypercapnia is sought and corrected. Because of the high solubility of
CO2, a diffusion barrier rarely ever occurs. Increased CO2 production may contribute to
hypercapnia secondary to either excess carbohydrate nutritional calories or extreme
hypercatabolic conditions (eg, burns, hyperthyroidism, persistent fever).
C. MIXED RESPIRATORY FAILURE

Patients commonly demonstrate characteristics of both pathophysiologic categories of
ARF during the course of illness. An understanding of the underlying pathophysiology of
each, therefore, is necessary for planning therapeutic support. Several related disease
processes often act in concert or synergistically to compound respiratory failure. For
example, the patient with chronic pulmonary disease and a large dead space often has
associated heart failure, which increases V̇ /Q̇ mismatching and worsens hypoxemia.
IV. MANIFESTATIONS OF ACUTE RESPIRATORY FAILURE
A. Clinical Presentation of Respiratory Distress

Clinical manifestations of respiratory distress commonly include signs and symptoms of
hypoxemia, hypercapnia, or both. These include:
Altered mental status ranging from agitation to somnolence

Evidence of increased work of breathing, such as nasal flaring in infants, use of
accessory respiratory muscles, intercostal/suprasternal/supraclavicular muscle
retraction, tachypnea, hyperpnea, or a paradoxical or dysynchronous breathing
pattern (Figure 4-2)
Bradypnea
Cyanosis of mucosal membranes (eg, tongue, mouth) or nail beds
Diaphoresis, tachycardia, hypertension, and other signs of catecholamine release
Figure 4-2. Normal Versus Abnormal Respiration
A, The abdominal wall moves outward as the diaphragm moves downward in normal inspiration. B, With
respiratory muscle fatigue, the diaphragm becomes flaccid and moves upward during inspiration resulting in
inward movement of the abdominal wall.
B. Diagnostic Tests
Pulse oximetry can be used to rapidly evaluate oxygenation in a patient with respiratory
distress by estimating the arterial oxyhemoglobin saturation (Chapter 6). However,
pulse oximetry provides no assessment for hypercapnia. Arterial blood gas analysis is
commonly used in severely ill patients to determine the two primary measures of
respiratory failure, the PaO2 and PaCO2, as well as pH. Additional tests such as
electrolytes, hematocrit, and drug levels may provide clues to the underlying etiology of
ARF. Chest radiography in combination with these laboratory tests is invaluable in
suggesting the underlying pathophysiology of ARF.
V. MANAGEMENT CONSIDERATIONS
A. Oxygen Supplementation
Most patients with ARF require supplemental oxygen. Oxygen transfer from alveolar
gas to capillary blood occurs by diffusion across the alveolar-capillary membrane and
is driven by the oxygen partial-pressure gradient between the partial pressure of
alveolar oxygen (PAO2) and the PO2 of the pulmonary capillary blood. In most cases of
ARF, the PAO2 can be substantially increased by use of supplemental oxygen, thus
increasing the gradient across the membrane and improving the PaO2.
Supplemental oxygen can be provided by a variety of devices (Figure 4-3). The

effectiveness of each is determined by its capacity to deliver sufficient oxygen at a high
enough flow rate to match the patient’s spontaneous inspiratory flow rate. Matching
between the flow capacity of the oxygen device and the patient’s inspiratory flow
demand determines how much room air is entrained by the nonintubated patient
breathing in an open system. Any entrained room air (FIO2 = 0.21) will dilute (decrease)
the FIO2 of the delivered gas in such a way that the tracheal FIO2, and hence PAO2, may be
considerably lower than the FIO2 delivered from the oxygen source. Therefore, oxygen-
supplement systems are usually classified as high oxygen (capable of delivering up to
100% oxygen), controlled oxygen (set oxygen percentage), or low oxygen. Similarly, the
devices are also categorized as either high flow, moderate flow, or low flow, reflecting
the flow-delivery capacity of the gas at the preset FIO2 level.
Supplemental oxygen should be

considered a temporizing intervention
while the primary etiology of hypoxemia
is diagnosed and treated.
For example, a tachypneic and hyperpneic patient will have a high inspiratory flow rate
during each breath. In such cases, hypoxemia is not likely to respond well to oxygen
supplementation by nasal cannula because it is a low-oxygen, low-flow system and
cannot match the patient’s high inspiratory flow rate. Room air will be entrained during
inspiration, and the tracheal FIO2 will be reduced. A high-oxygen, high-flow system
should be selected for this type of patient.
Figure 4-3. Oxygen Delivery Devices
A. Venturi Mask
Delivers humidified oxygen (aerosol adapter can be added)

FIO2 is set by entrainment dial on mask
Low concentrations = 24%, 26%, 28%, 31%
High concentrations = 35%, 40%, 50%
B. High-flow Nasal Cannula

Uses up to 100% oxygen source
Flow rate <60 L/min
C. Non-rebreathing Mask
Delivers non-humidified oxygen
Used for emergency delivery
FIO2 range = 60 - ?100%
Reservoir bag provides 100% FIO2 and minimizes room air dilution
Flap valves minimize entrainment of room air (which will dilute FIO2)
Flow rate is adjusted according to the patient’s ventilator pattern to keep reservoir bag inflated
D. Simple Oxygen Mask

Delivers humidified oxygen
Minimum flow rate = 6 L/min (to clear exhaled CO2 from mask)
Approximate concentrations: 6 L = 40%; 7 L = 50%; 8L = 60%
E. Aerosol Mask
Delivers cool, aerosolized oxygen or air

FIO2 is set by dial on oxygen adapter
Maximum FIO2 = 40%-60%
Minimum flow rate = 8 L/min
F. Tracheostomy Mask
Delivers heated, aerosolized oxygen or air
FIO2 is set by dial on blender
G. Nasal Cannula
Delivers humidified oxygen

Nasal passages must be patent
Blender setup: FIO2 is set by dial; 1-2 L flow can be used as continuous positive airway pressure for
infants
Wall setup: FIO2 is set by flow rate
Approximate FIO2 (if respiratory rate and tidal volume are normal):
Adult
1L = 24% 4L = 36%
2L = 28% 5L = 40%
3L = 32% 6L = 44%
H. Face Tent
Delivers cool, aerosolized oxygen or air

Loose fit under the chin for patient comfort, speaking, etc.
FIO2 is set by dial on oxygen adapter (concentration is unstable)
1. Low-Flow Nasal Cannula

Short prongs of the nasal cannula are inserted into the nares. Oxygen (100%) is
delivered through the cannula, but at a rate between 0.5 and 5 L/min. The resulting FIO2
depends on the patient’s minute ventilation and, therefore, cannot be precisely
controlled, but the maximal tracheal FIO2 is not likely to exceed 0.4 to 0.5 (40% to
50%). Higher flow rates do not result in much higher FIO2 levels and have a drying and
irritating effect on nasal mucosa. The nasal cannula is comfortable and well tolerated by
many patients with ARF in whom precise control of FIO2 is not necessary. It is a low-
flow, low-oxygen device.
2. High-Flow Nasal Cannula

In contrast to the low-flow cannulas, high-flow nasal cannula systems involve delivery
of heated and humidified oxygen via special devices (eg, Vapotherm®, Optiflow™) at
rates up to 60 L/min in adults. These devices may be better tolerated than face masks in
terms of comfort. They also provide higher amounts of FIO2 (0.32-1.0) in patients with
high minute ventilation requirements by matching the patients’ inspiratory demands and
minimizing air dilution. These devices may generate positive end-expiratory pressure
that is difficult to measure and have the potential for causing barotrauma.
3. Air-Entrainment Face Mask

Air-entrainment masks (also called Venturi masks) deliver oxygen through a jet-mixing
device that increases the velocity of oxygen and causes a controlled entrainment. The
FIO2 can be more precisely controlled from 0.24 to 0.5 (24% to 50%) at high-flow rates
simply by selecting the interchangeable jet nozzle and adjusting the oxygen flow rate. It
is a high-flow, controlled-oxygen device.
4. Aerosol Face Mask

The commonly used aerosol face mask combines a variable oxygen setting and moderate
flows. The mask, which has large side holes, is attached by large-bore tubing to a
nebulizer that blends 100% oxygen and room air to deliver gas at a preset FIO2 level.
Flow matching can be evaluated by observing the patient during spontaneous breathing.
If the entire aerosol mist disappears from the mask during inhalation, the patient’s
inspiratory flow demands are probably exceeding the capacity of the nebulizer and
room air is being entrained. The aerosol face mask is a variable oxygen, moderate-flow
device.
A reservoir mask is frequently used for

improving oxygenation in patients with
severe hypoxemia until further
evaluation and treatments are
accomplished.
5. Reservoir Face Mask
The reservoir face mask incorporates a reservoir bag from which the patient breathes.
This bag is filled with 100% oxygen from a supply source. The flow rate is adjusted so
that the bag remains completely or partially distended throughout the respiratory cycle.
When the mask is properly applied, oxygen delivery to the nonintubated patient can be
maximized but rarely exceeds an FIO2 of 0.6 to 0.9. The reservoir face mask is a high-
oxygen, high-flow device.
6. Resuscitation Bag-Mask Unit

Although not commonly considered an oxygen-supplement device, bag-mask units are
usually included with other emergency equipment and, therefore, are readily accessible.
When the mask is held firmly over the patient’s face, room air entrainment is largely
excluded. If the oxygen flow to the bag is kept high (≥15 L/min), a high-oxygen supply is
provided at sufficient flow. The resuscitation bag need not be compressed to supply
oxygen. It is a high-oxygen, high-flow device.
B. Pharmacologic Adjuncts
Many diseases that cause ARF produce similar anatomic and physiologic derangements,
including bronchial inflammation, mucosal edema, smooth muscle contraction, and
increased mucus production and viscosity. Each of these processes may contribute to
obstruction of airway gas flow, increased airway resistance, mismatch, and elevated
VD. Some pharmacologic agents may be helpful in the care of such patients and may
directly alter shunt or dead-space effects.
1. β2-Agonists
Inhaled β2-agonists are important therapy in patients with ARF secondary to many
causes. Stimulation of β2-adrenergic receptors causes bronchial and vascular smooth-
muscle relaxation. These agents are typically administered by metered-dose inhaler or
by intermittent or continuous nebulization (Table 4-2). On rare occasions, in very
critically ill patients with obstructive airway disease, β2-agonists are administered by
both inhalation and subcutaneous injection. Long-acting inhaled agents do not have a
role in the management of patients with acute respiratory deterioration. Racemic
epinephrine aerosol is an established therapy for upper airway obstruction in children
with croup and is also used for laryngeal edema in adults.
Table 4-2 Pharmacologic Agents for Obstructive Airway

Disease
Drug Preparation Route of Dosage
Administration
Albuterol 0.05% solution Inhaled Adult: 2.5–5 mg q 2–4 ha
(aerosol) Pediatric: 0.05–0.15 mg/kg q 4–6 ha
MDI (90 µg/puff) Inhaled Adult: 1–2 puffs q 2–4 ha
Pediatric: 1–2 puffs q 4–6 ha
Levalbuterol 0.31, 0.63, or Inhaled Adult and children ≥12 y: 0.63–1.25 mg q
1.23 mg/unit (aerosol) 6–8 h
dose solution Pediatric (6–11 y): 0.31–0.63 mg q 6–8 h;
more aggressive dosing may be used in
acute exacerbations
MDI (45 µg/puff) Inhaled Adult: 1–2 puffs q 4–6 h
Pediatric (age ≥4 y):1–2 puffs q 4–6 h
Metaproterenol 5% solution Inhaled Adult: 0.3 mL q 2–4 ha
Sulfate (aerosol) Pediatric: 0.25–0.5 mg/kg q 2–4 ha
MDI (0.65 µg/puff) Inhaled Adult: 2–3 puffs q 4–6 ha
Terbutaline MDI (0.2 µg/puff) Inhaled Adult: 1–2 puffs q 4–6 ha
0.1% solution Subcutaneous Adult: 0.2–0.4 mL; repeat in 15–30 min
Pediatric: 0.2 mg/kg; maximum 6 mg
Epinephrine 1 mg/mL (1:1000) Subcutaneous Adult: 0.1–0.5 mg; repeat in 20–30 min
Pediatric: 0.01 mg/kg
Inhaled Epinephrine 1 mg/mL (1:1000) Inhaled Adult: 2.5-5 mL q 3 h
Pediatric: >4 y: 2.5-5 mL q 3 h; <4 y: 2.5
mL q 3 h
Ipratropium 0.025% solution Inhaled Adult: 500 µg q 6–8 h;
(aerosol) Pediatric: Infant and child: 250 µg q 6–8 h:
>12 y: 250–500 µg q 6–8 h
MDI (18 µg/puff) Inhaled Adult: 2–4 puffs q 6 h
Pediatric: 1–2 puffs q 8 h
Abbreviations: q, every; MDI, metered-dose inhaler; NS, normal saline

aIn patients with severe asthma, frequency of administration of inhaled β-agonists should be guided by
response to therapy and risk for side effects. Therapy is routinely initiated with three treatments every 20
minutes. Further therapy adjustments are then based on response. Continuous nebulization may also be
employed. Caution should be exercised when considering use of continuous nebulized β2-agonists,
particularly in older patients and those with underlying cardiac disease.
2. Anticholinergic Agents
Ipratropium bromide competes with acetylcholine at the bronchial receptor site,
resulting in bronchial smooth-muscle relaxation. This agent is delivered by metered-
dose inhaler or nebulization (Table 4-2). Ipratropium has a more delayed onset of
action than β2-agonists and has more consistent bronchodilatory effects in COPD than in
asthma. The addition of ipratropium to albuterol appears to have an additive benefit in
approximately 30% of asthma patients. Tiotropium is a long-acting anticholinergic
bronchodilator that has sustained effects in COPD patients, but its use in acute
exacerbations is not recommended.
3. Corticosteroids
The central role of inflammation in obstructive airway disease is well established, and
the benefit from aggressive corticosteroid use in asthmatic patients with ARF is well
documented. In addition, corticosteroids may decrease β-receptor tachyphylaxis.
Limited consensus exists on dosing schedules in asthma. Doses of methylprednisolone
of 80 mg/24 h have been as effective as >360 mg/24 h. Some clinicians use doses
equivalent to those given for asthma when treating COPD, whereas others begin with
doses equivalent to 1 mg/kg/24 h, adjusting as patient response dictates. The
intravenous and oral routes are equally effective. Careful monitoring of corticosteroid
side effects is warranted. Acute myopathies have been described after moderate to high
dosages of corticosteroids in patients with COPD and/or asthma. After the acute
exacerbation, inhaled corticosteroids are often useful adjuncts to therapy and may allow
reduction in systemic corticosteroid dosage. However, routine use of inhalational agents
is not recommended in the setting of acute severe bronchospasm.
4. Antibiotics
Bacterial infection (bronchitis/pneumonia) frequently precipitates ARF. Antibiotics
should be used when there is clinical suspicion that bacterial pulmonary infection is
present (eg, change in sputum characteristics, pulmonary infiltrates on the chest
radiograph, fever, leukocytosis), and they should be chosen to effectively treat usual
pathogens (Chapter 11). Therapy should be subsequently adjusted when culture and
sensitivity data become available.
Several randomized trials have compared clinical outcomes in patients hospitalized
with acute exacerbation of COPD and have shown antibiotic treatment has been
associated with decreased risk of adverse outcomes. When the decision is made to use
antibiotics, it is important to distinguish a simple from a complicated case of acute
exacerbation of COPD and a 5-day course is usually recommended.
C. Miscellaneous Agents and Treatments

Agents to hydrate or otherwise alter the composition, elasticity, or viscosity of mucus
have been used, although their efficacy has not been demonstrated except in selected
patient groups (eg, patients with cystic fibrosis). Examples of these agents include
mucolytics such as acetylcysteine or propylene glycol, bronchorrheic agents such as
saturated solution of potassium iodide or glyceryl guaiacolate, and alkalinizing agents
such as aerosolized sodium bicarbonate.
Postural drainage, chest physical therapy, nasotracheal suctioning, incentive spirometry,
intermittent positive pressure breathing, and cough/deep-breathing exercises have long
been used. Also available are newer measures such as positive expiratory pressure
therapy, vest devices (high-frequency chest oscillator), and mattress percussion devices.
Many of these modalities may be applied to treat specific symptoms of ARF or the
cause of respiratory failure. The effectiveness and positive impact of the contributions
of the bedside nurse or the respiratory care practitioner and the avoidance of
intubation/mechanical ventilation should not be underestimated.
Key Points
Diagnosis And Management Of Acute Respiratory Failure

Acute respiratory failure is classified as hypoxemic, hypercapnic, or mixed.
Arterial blood gas measurements are the primary assessment tool for determining
this classification.
The most common pathophysiologic mechanism for hypoxemic acute respiratory
failure is ventilation/perfusion mismatch.
Hypercapnic acute respiratory failure is primarily the result of a change in one or
more determinants of the alveolar minute ventilation equation: tidal volume,
respiratory frequency, and physiologic dead space.
Oxygen supplementation is commonly used to treat hypoxemia. The oxygen supply
device that is chosen must be capable of matching the oxygen and respiratory flow
demands of the patient.
Pharmacologic and therapeutic adjuncts should be considered when treating
patients with acute respiratory failure.
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doi:10.1002/14651858. CD001740.
3. Pontoppidan H, Geffin B, Lowenstein E. Acute respiratory failure in the adult: 3. N
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Suggested Website
1. Society of Critical Care Medicine. http://www.SCCM.org/Guidelines

Chapter 5
M ECHANICAL VENTILATION
Objectives
Discuss the indications and techniques for noninvasive positive pressure

ventilation.
Describe the clinical parameters that should be reviewed to decide whether the
patient is failing noninvasive methods and requires invasive mechanical
ventilation.
Describe the characteristics of different types of breaths and modes of mechanical
ventilation.
Outline ventilator settings and monitoring needs for the initiation of mechanical
ventilation.
Describe interactions between ventilatory parameters and modifications needed to
avoid harmful effects of mechanical ventilation.
Review the guidelines for initial ventilator management that apply to specific
clinical situations.
Case Study
A 67-year-old woman with severe chronic obstructive pulmonary disease presents to

the hospital with complaints of an upper respiratory tract illness and increasing
shortness of breath of 2 days’ duration. She has been using her home nebulizers without
relief. Her vital signs are blood pressure 140/90 mm Hg, heart rate 122 beats/min,
respirations 32 breaths/min, and temperature 37.2°C (99.0°F). Physical examination is
remarkable for use of accessory muscles of respiration and diffuse wheezing bilaterally.
She is alert but unable to speak in full sentences. An arterial blood gas analysis
demonstrates pH 7.25, PCO2 62 mm Hg , and PO2 59 mm Hg. Bronchodilator therapy is
started, and the woman is given IV steroids.
– What type of respiratory support should be initiated?
– What settings should be selected for respiratory support?
– What are the goals of respiratory support?
I. INTRODUCTION
When hypoxic or hypercapnic respiratory failure cannot be treated by other means, as
discussed in Chapter 4, advanced support with positive pressure ventilation may be
needed. A ventilator is a device used to assist or replace the work of the respiratory
system. Positive pressure ventilation can be delivered noninvasively via a mask or
helmet or invasively via an endotracheal tube. Generally accepted indications for
initiating positive pressure ventilatory support are summarized in Table 5-1.
Table 5-1 Indications for Positive Pressure Ventilatory Support

Ventilation abnormalities Respiratory muscle dysfunction
Respiratory muscle fatigue
Chest wall abnormalities
Neuromuscular disease
Decreased ventilatory drive

Increased airway resistance and/or obstruction
Oxygenation Refractory hypoxemia

abnormalities
Need for positive end-expiratory pressure
Work of breathing Need for decreased work of breathing

alterations Shock
Respiratory muscle fatigue
Severe acidosis
Need for sedation and/or neuromuscular blockade

Need to decrease systemic or myocardial oxygen consumption
Use of hyperventilation to reduce intracranial pressure
Facilitation of alveolar recruitment and prevention of atelectasis
The choice between noninvasive or invasive positive pressure ventilation is dependent

on patient characteristics, the type and severity of the respiratory and/or systemic
condition, anticipated clinical course, availability of resources, and the experience and
training of the clinician and healthcare team.
II. NONINVASIVE POSITIVE PRESSURE VENTILATION
A. What is Noninvasive Positive Pressure Ventilation?

Noninvasive positive pressure ventilation (NPPV) refers to a form of mechanical
ventilation that provides respiratory assistance without an invasive artificial airway.
The potential beneficial effects of NPPV are similar to those of invasive mechanical
ventilation and include decreased work of breathing, improved oxygenation, and
improved gas exchange. In addition, this type of ventilation avoids many of the
complications associated with intubation and invasive mechanical ventilation. Potential
advantages and disadvantages of NPPV are listed in Table 5-2.
Advantages and Disadvantages of Noninvasive Positive Pressure

Table 5-2
Ventilation
Advantages Disadvantages
Reduced need for sedation Claustrophobia

Preservation of airway-protective reflexes Increased workload for respiratory practitioner
Avoidance of upper airway trauma Facial/nasal pressure lesions
Decreased incidence of nosocomial sinusitis Unprotected airway and pneumonia
Improved patient comfort Inability to suction deep airway
Shorter length of stay in ICU and hospital Gastric distension with use of face mask or
helmet
Improved survival Possible upper-extremity edema, axillary vein
thrombosis, tympanic membrane dysfunction,
and intrahelmet noise with use of helmet
Delay in intubation
B. How Does NPPV Work?

NPPV utilizes two levels of positive airway pressure, combining the modalities of
pressure support ventilation (PSV) and continuous positive airway pressure (CPAP)
(discussed later). By convention, the PSV modality is referred to as IPAP (inspiratory
positive airway pressure), and the CPAP modality is referred to as EPAP (expiratory
positive airway pressure). CPAP alone can also be delivered noninvasively but does
not provide support of ventilation. CPAP allows spontaneous breathing from a gas
source at an elevated baseline system pressure (higher than atmospheric pressure) and
is functionally equivalent to positive end-expiratory pressure (PEEP). The difference
between these two pressure levels (∆P) determines tidal volume generated. NPPV can
be delivered using a standard ICU ventilator or a portable device. The benefits of using
an ICU ventilator include delivery of a more precise and higher concentration of
oxygen, the separation of inspiratory and expiratory tubing to prevent rebreathing CO2,
better monitoring and alarm features, and improved detection of air leaks. Alarm setups
may need to be altered on standard ventilators because the alarms are typically
triggered by exhalation, and noninvasive ventilation inherently has more gas leakage
compared to ventilation via an endotracheal tube. Ventilators specifically designed to
provide patient-triggered noninvasive pressure support or patient-triggered volume-
cycled breaths are optimal.
C. What Types of Interfaces Are Available?

The ventilator connects to a tightly fitted face mask, nasal mask, nasal plugs, or a helmet
(Figure 5-1). Many patients with acute respiratory failure are mouth breathers, so the
face mask is preferred as it is associated with smaller leaks than the nasal plugs and
nasal mask. The nasal passages may offer significant resistance to airflow, limiting the
benefits of NPPV. Some gas leakage is anticipated with both masks and can be
compensated for by increasing pressure settings or increasing the set tidal volume (VT )
level. When a nasal mask is used, the patient’s mouth should be kept closed or chin
straps should be employed to reduce leakage.
Figure 5-1. Devices for Delivery of Noninvasive Positive Pressure Ventilation
Examples of noninvasive positive pressure ventilation delivery devices: A, face mask; B, total face mask; C,
nasal mask with chin strap; and D, helmet.
D. Which Patients Benefit From NPPV?

Before NPPV is initiated, patient characteristics and the potential for successfully
treating the underlying respiratory condition should be evaluated. Table 5-3 lists
conditions leading to respiratory failure that are likely to improve with use of NPPV. Of
these, acute exacerbations of chronic obstructive pulmonary disease and cardiogenic
pulmonary edema are the two conditions best studied and they have accepted
indications for the application of NPPV. An approach to initiating NPPV after
appropriate patient evaluation is outlined in Table 5-4. NPPV is best utilized in the
alert, cooperative patient whose respiratory condition is expected to improve in 48 to
72 hours. Potential candidates should be hemodynamically stable, able to control
airway secretions, and able to synchronize with the ventilator. If a provider skilled in
the application of NPPV is not available, if the patient is too sick for this support, or if
NPPV has failed to benefit the patient, it is critical to move quickly to invasive
mechanical ventilation.
Respiratory Conditions Likely to Respond to Noninvasive Positive

Table 5-3
Pressure Ventilation
Hypoxemic Respiratory Failure
Cardiogenic pulmonary edema without hemodynamic instability

Respiratory failure in patients with mild to moderate Pneumocystis pneumonia
Respiratory failure in immunocompromised patients (especially in hematologic malignancies and
transplant patients)
Hypercapnic Respiratory Failure
Acute exacerbation of chronic obstructive pulmonary disease

Acute exacerbation of asthma
Respiratory failure in patients with cystic fibrosis
Table 5-4 Initiation of Noninvasive Positive Pressure Ventilation
Do not delay intubation if needed and keep in mind the patient’s resuscitation status.
Consider ABG analysis prior to initiation.
Explain the procedure.
Keep head of bed at ≥45°.
Ensure appropriate mask or helmet size.
Assess the patient’s tolerance of the mask by applying it by hand before securing the harness.
Use the following initial ventilator settings:
Mode: Spontaneous
Trigger: Maximum sensitivity
FIO2: 1.00
EPAP: 4-5 cm H2O (higher levels are poorly tolerated initially)
IPAP: 10-15 cm H2O
Backup rate: Start at 6/min
Adjust the difference between EPAP and IPAP to achieve and effective VT and CO2 clearance. Adjust
EPAP for alveolar recruitment in increments of 2 cm H2O per step to improve oxygenation.
Depending on the ventilator, a similar increase in IPAP may be required to maintain the same VT.
If assist-control volume ventilation is used, begin with a VT of 6 to 8 mL/kg (depending on the
underlying pulmonary condition).
Titrate pressures, volume, and FIO2 to achieve appropriate pH, PaO2, and PaCO2 levels. Ventilator
changes can be made every 15 to 30 minutes.
Follow vital signs, pulse oximetry, mental status, clinical appearance, and ABG (if indicated).
Remember that goals of NPPV may include a respiratory rate <30 breaths/min, VT >7 mL/kg of
predicted body weight, improved gas exchange, and patient comfort.
It is also important to be cognizant that IPAP > 20 cm H2O may lead to gastric distension.
Abbreviations: NPPV, noninvasive positive pressure ventilation; ABG, arterial blood gas; EPAP, expiratory
positive airway pressure; IPAP, inspiratory positive airway pressure; VT, tidal volume
E. Which Patients Should Not Receive Noninvasive Mechanical Ventilation?

In general, NPPV should not be initiated in the following circumstances: uncooperative
patients; patients with difficulty clearing secretions, recurrent emesis, or post-cardiac or
respiratory arrest; and patients with hemodynamic instability. A more detailed list of
contraindications for the use of NPPV is presented in Table 5-5.
Contraindications to Use of Noninvasive Positive Pressure

Table 5-5
Ventilation
Cardiac or respiratory arrest

Hemodynamic instability
Myocardial ischemia or arrhythmias
Patient who is unable to cooperate
Inability to protect the airway
High risk for aspiration
Active upper gastrointestinal hemorrhage
Severe hypoxemia
Severe encephalopathy
Facial trauma, recent surgery, and/or burns
Significant agitation
F. How are Patients Monitored on NPPV?

Patients receiving NPPV must be monitored closely in a proper setting, and continuous
pulse oximetry and cardiac monitoring are suggested. Close clinical follow-up
assessments are required, including evaluations of the pH, PaO2, and PaCO2. Consider
transition to invasive ventilation when a clear trend toward improvement has not been
observed over the first 1 or 2 hours, or when the therapeutic goals have not been
achieved within the first 4 to 6 hours. Sedation should be used cautiously and with
adequate monitoring when NPPV is initiated. Additional measures that may be
considered include application of a protective nose patch when using a nasal mask and
gastric decompression if a face mask or helmet is used. Oral intake should be restricted
until the patient has stabilized and intubation is no longer a consideration. An algorithm
for assessing NPPV is presented in Figure 5-2.
Avoid inspiratory pressures greater than

20 cm H2O, as gastric distension can
occur.
Figure 5-2. Assessment of Noninvasive Positive Pressure Ventilation
Abbreviations: NPPV, noninvasive positive pressure ventilation; ARF, acute respiratory failure
Case Study (continued)

Noninvasive positive pressure ventilation is initiated. Two hours after initiation, the
patient exhibits persistent marked accessory muscle use. Vitals signs are heart rate 130
beats/min, blood pressure 160/90 mm Hg, respiratory rate 32 breaths/min, and
temperature 36.6ºC (98°F). Arterial blood gas demonstrates pH 7.27, PCO2 60 mm Hg,
and PO2 90 mm Hg.
– Should this patient be intubated and invasive mechanical ventilation initiated?

– What are the initial setting on invasive mechanical ventilation?
– How should patients on invasive mechanical ventilation be monitored?
III. DECISION TO INTUBATE

The decision to initiate invasive mechanical ventilation is a crucial and time-sensitive
one. Delay in intubation, inability to identify a difficult airway, and inability to
anticipate possible hemodynamic consequences of intubation can reduce the likelihood
of good patient outcomes. In general, consideration of three quick bedside questions can
help facilitate a prompt decision to proceed with invasive mechanical ventilation,
especially when transitioning from noninvasive ventilation.
Is there failure in airway maintenance or protection (eg, inability to handle

secretions)?
Is there failure to achieve desired goals with current respiratory support
(oxygenation, ventilation, or work of breathing)?
Is the illness anticipated to worsen in the next 24 to 48 hours?
IV. INVASIVE MECHANICAL VENTILATION

Mechanical ventilation via an endotracheal tube is commonly used to support critically
ill patients. It is a definitive intervention with the goal of obtaining acceptable
oxygenation and ventilation with a secure airway.
Each mechanical ventilation respiratory cycle can be divided into two phases:
inspiration and expiration (Figure 5-3A).
Figure 5-3. Respiratory Cycle During Mechanical Ventilation and Spontaneous Breathing
(Above left) Triggering (A signals the transition from expiration to inspiration; cycling (C indicates the
transition from inspiration to expiration. Inspiratory pause (BC, total respiratory cycle (ABCD, inspiration
(ABC, and expiration (CD.
(Above Right) Start of inspiration (A, start of expiration (B, inspiration (AB, expiration (BC, and total
respiratory cycle (ABC
The respiratory cycle is the time from the initiation of one breath until the initiation of
the next breath. Triggering (A) signals the transition from expiration to inspiration;
cycling (C) indicates the transition from inspiration to expiration. Other components of
the total respiratory cycle (ABCD) include inspiratory pause (BC), inspiration (ABC),
and expiration (CD). Spontaneous breaths do not include an inspiratory pause. The
spontaneous respiratory cycle (ACD) is demonstrated in Figure 5-3B.
Inspiration is the point at which the exhalation valve closes and fresh gas under
pressure from the ventilator enters the chest. The amount of gas delivered during
inspiration is determined by any of three targets that can be set on the ventilator:
volume, pressure, and/or flow.
Cycling is the changeover from the end of inspiration to the expiratory phase. It occurs
in response to one of three parameters: elapsed time, delivered volume, or a decrease in
flow rate. During expiration, the ventilator gas flow is stopped, and the exhalation
circuit is opened to allow gas to escape passively from the lungs. Expiration continues
until the next inspiration begins.
Triggering is the changeover from expiration to inspiration. Triggering a ventilator-
delivered breath depends on the patient’s interaction with the ventilator:
Assisted breath: The patient initiates a breath, and this inspiratory effort produces
a drop in airway pressures or a diversion of constant gas flow in the ventilator
circuitry. A signal triggers the ventilator to deliver a breath. This is an example of
partial ventilator control.
Unassisted, mandatory, or controlled breath: In the absence of patient interaction
with the ventilator, breaths are delivered based on elapsed time (eg, at a set rate of
10 breaths/min and no detection of patient effort, the ventilator will be triggered
every 6 seconds). This is an example of full ventilator control.
Spontaneous breaths (no ventilator assistance) are also possible in synchronized

intermittent mandatory ventilation (SIMV) and bilevel ventilation. The most common
ventilator breaths are described later. CPAP allows spontaneous breathing at a higher
baseline pressure.
V. TYPES OF TARGETED/CYCLED BREATHS
A. Volume-Cycled Breath
A volume-cycled breath, often called volume assist-control breath, ensures the delivery
of a preset tidal volume (unless the peak pressure limit is exceeded). On most
ventilators, the setting of peak inspiratory flow rate and the choice of inspiratory flow
waveform (square, sine, or decelerating) determine the length of inspiration. Some
ventilators change the peak inspiratory flow rate to maintain constant inspiratory time on
switching between a constant flow (square) and decelerating flow (ramp) waveforms.
With volume-cycled breaths, worsening airway resistance or lung/chest-wall
compliance results in increases in peak inspiratory pressure with continued delivery of
the set tidal volume (unless the peak pressure limit is exceeded).
B. Time-Cycled Breath
A time-cycled breath, often called pressure assist-control breath, applies a constant
pressure for a preset time. The application of pressure throughout inspiration results in a
square (constant) pressure-over-time waveform during inspiration and a decelerating
inspiratory flow waveform as the pressure gradient falls between the ventilator and the
patient (since pressure rises as the lung fills). Flow in this breath format is variable and
this leads to variable tidal volume depending on lung compliance. Flow depends on the
resistance of the lung, the compliance of the lung, and patient effort. With this type of
breath, changes in airway resistance or lung/chest-wall compliance will alter tidal
volume (ie, worsening of airway resistance or lung compliance results in a decrease in
tidal volume).
C. Flow-Cycled Breath
A flow-cycled breath, usually called a pressure support breath, is a spontaneous mode
of ventilation. The patient initiates every breath and the ventilator delivers support with
the preset pressure value. With this support, the patient self-regulates the respiratory
rate and tidal volume. The set inspiratory pressure support level is kept constant with a
decelerating flow. The patient triggers all breaths. A change in the mechanical
properties of the lung/thorax and patient effort affects the delivered tidal volume. The
pressure support level must be regulated to obtain the desired ventilation.
Pressure support breaths are terminated when the flow rate decreases to a
predetermined percentage of the initial peak flow rate (typically 25%). As the patient’s
inspiratory effort decreases, the flow decreases, marking the proximity of the end of
inspiration.
VI. MODES OF MECHANICAL VENTILATION

The mode of ventilation describes how one or more types of ventilator breaths interface
with the patient to provide ventilatory support. When mechanical ventilation is initiated,
the optimum ventilatory support for a given clinical circumstance and the specific needs
of the patient must be determined. Commonly used modes of ventilation include assist-
control (AC) ventilation, SIMV, and PSV. The various modes are achieved by using
some combination of the three types of ventilator breaths and may be combined with the
application of PEEP.
A. Assist-Control Ventilation
AC ventilation can be delivered with either volume-cycled (volume assist-control) or
time-cycled (pressure assist-control) breaths. We will emphasize volume control, since
it is the most commonly used mode.
In volume AC, the preset tidal volume (VT ) is guaranteed at a preset flow rate and with
a set minimum respiratory rate. The patient can initiate breaths and trigger the ventilator,
and the ventilator will assist to achieve the preset VT delivered at the preset flow. Thus,
patients receive the minimum number of ventilator breaths (set rate), but the total
number of breaths is higher if the patient triggers the ventilator with additional
inspiratory efforts.
With proper use of AC, the work of breathing may be significantly decreased. However,
if the ventilator and the patient are not in synchrony or if the ventilator inspiratory flow
rates are not matched to the patient’s demand, this mode may result in an increase in the
patient’s work of breathing.
The total number of breaths during AC ventilation may be higher than the minimum set
rate, based on the patient’s respiratory drive and ability to trigger the ventilator. This
mode has also been called continuous mandatory ventilation (CMV). However, CMV
more accurately represents a situation in which the patient doesn’t trigger additional
breaths (ie, absent respiratory drive, as when the patient is paralyzed) [discussed
below].
B. Pressure Support Ventilation

PSV provides a preset level of inspiratory pressure assist with each ventilator-detected
patient effort. This inspiratory assist is selected to overcome the increased work of
breathing imposed by the disease process, endotracheal tube, inspiratory valves, and
other mechanical aspects of ventilatory support. The set amount of pressure that is
applied augments each patient-triggered breath. All breaths are flow cycled (usually, the
assist will decelerate when flow falls <25% of the initial flow rate generated by the
patient-initiated breath). The patient controls the respiratory rate and exerts a strong
influence on the duration of inspiration, flow rate, and VT . In addition, the delivered VT
is influenced by pulmonary compliance and resistance. Rapid changes in these
parameters potentially alter the VT and work of breathing. PSV may be coupled with
SIMV (see below), primarily as a means to diminish excess work of breathing for
spontaneous breaths occurring between mandatory breaths.
The amount of pressure support is titrated according to the patient’s VT measured by the
ventilator during expiration. Suggested parameters include a setting that achieves one or
more of the following goals:
A VT of 6 to 8 mL/kg, depending on patient needs
A slowing of spontaneous breathing rate to an acceptable range (<30 breaths/min)
The desired minute ventilation
Appropriate apnea alarms and a backup ventilation setting are essential. Potential
benefits of PSV include the comfort and tolerance this ventilatory mode offers some
patients. In addition, PSV may reduce the work of breathing by diminishing patient-
ventilator asynchrony. Typically, as pressure support is increased in patients with lung
disease, the patient’s work of breathing and respiratory rate decrease and VT increases.
With PSV, an endotracheal tube cuff leak may interfere with appropriate cycling because
flow may never drop to the preset threshold for cycling (ie, 25% of the peak flow rate).
C. Synchronized Intermittent Mandatory Ventilation

SIMV delivers either volume-cycled or time-cycled breaths at a preset mandatory rate.
Volume cycling is most commonly used for the mandatory breaths. Breaths may be
triggered by the patient or by the time elapsed. If the patient-initiated breath falls within
a certain period of time before the onset of the mandatory breath, the ventilator
synchronizes its support by delivering the mandatory breath early, thus essentially
converting a controlled breath to an assisted one. The number of breaths that will be
synchronized in this fashion is the preset (mandatory) rate. When no effort is detected,
the ventilator delivers the preset VT at the preset (time-elapsed) rate. When the patient
initiates breaths over the set mandatory rate spontaneously, these breaths are usually
supported by the ventilator (assisted breaths) with the addition of pressure support.
Notice the difference from assist control—volume control ventilation, where each
breath (patient- or ventilator-initiated) had the same guaranteed VT .
PSV augments the patient’s own

respiratory effort and is best adjusted by
observing changes in the patient’s
respiratory rate, VT, and comfort.
In SIMV, the addition of pressure support to these spontaneous patient-initiated breaths

is recommended, using a value that offsets the resistance of the endotracheal tube.
Synchronization allows for enhanced patient-ventilator synchrony by delivering the
preset machine breaths in conjunction with the patient’s inspiratory effort for each
mandatory breath.
It is recommended that PSV be used in

conjunction with SIMV to decrease the
patient’s work of breathing during
spontaneous breaths.
The SIMV mode allows patients to contribute to and determine a portion of their
ventilatory requirement. The negative inspiratory pressure generated by spontaneous
breathing may lead to increased venous return to the right side of the heart, which may
improve cardiac output and cardiovascular function. When no pressure support is
added, potential increases in work of breathing may delay weaning from mechanical
ventilation.
D. Controlled Mechanical Ventilation

CMV delivers unassisted ventilator breaths at a preset rate. All breaths are mandatory
and are either volume cycled or time cycled. No additional spontaneous assisted breaths
are initiated beyond the set number of controlled breaths. Current ventilators do not
allow direct setting of CMV, and this mode can be achieved only in patients who are not
capable of spontaneous respiratory effort, such as those who are heavily sedated or
receiving neuromuscular blockade.
Do not confuse the CMV (assist-control)

setting on modern ventilators for
controlled mechanical ventilations.
E. CPAP And Weaning

CPAP is seldom used as initial support for acute respiratory failure in an intubated
patient and is not considered a mode of mechanical ventilation. Here continuous
positive pressure is applied throughout the respiratory cycle with the patient breathing
spontaneously around the applied pressure. Therefore, respiratory rate and VT depend
entirely on the patient’s inspiratory effort (without help from the ventilator) as the
patient inspires against the resistance of the endotracheal tube. CPAP with low levels of
pressure support (typically 5-7 cm of water) may be used for weaning during the final
stages of invasive ventilation when patients are being assessed for their potential
readiness for extubation.
Airway pressure and flow tracings of spontaneous respiration, CPAP, and the different
modes of mechanical ventilation are illustrated in Figure 5-4.
Figure 5-4. Airway Pressure and Flow Tracings
Figure 5-4. Airway Pressure and Flow Tracings

The advantages and disadvantages of the various modes of invasive mechanical
ventilation are summarized in Table 5-6. In choosing a mode of ventilation, it is
important to consider specific goals, the most important of which are adequacy of
ventilation and oxygenation, reduction in the work of breathing, and the assurance of
patient comfort and synchrony with the ventilator.
Potential Advantages and Disadvantages of Selected Modes of

Table 5-6
Mechanical Ventilation
Mode Advantages Disadvantages
AC ventilation Patient can increase ventilatory support; Excessive inspiratory
reduced work of breathing compared with pressures
spontaneous breathing
AC volume ventilation Guarantees delivery of set VT (unless peak Excessive inspiratory
pressure limit is exceeded) pressures
AC pressure ventilation Limitation of peak inspiratory AC pressure VT decreases or increases with
ventilation pressures; variable flow rates lung resistance/compliance
accommodate to patients’ demands changes
Pressure support Apnea alarm may not trigger backup Patient comfort; improved
ventilation ventilation mode; variable patient tolerance patient-ventilator interaction;
decreased work of breathing
Synchronized Less interference with normal cardiovascular Increased work of breathing
intermittent mandatory function compared with AC
ventilation
Controlled mechanical Rests muscles of respiration completely Requires use of
ventilation sedation/neuromuscular
blockade; adverse
hemodynamic effects
Abbreviations: AC, assist-control; VT, tidal volume
VII. CHOOSING A MODE AND INITIAL VENTILATOR SETTINGS

Choosing a mode of mechanical ventilation depends on the reason it is required and the
underlying disease process. In general, AC is used as the initial mode for a patient
needing invasive mechanical ventilation.
When initiating ventilatory support in adults, a fraction of inspired oxygen (FIO2) of 1.0
is used to ensure maximal amount of available oxygen during the patient’s adjustment to
the ventilator and during the initial attempts to stabilize the patient’s condition. In
addition, the high level of oxygen offers support for complications that may have
occurred before and during intubation. The usual recommended VT level is 6 to 8 mL/kg
of the predicted body weight. Higher VT levels should be avoided to reduce the
possibility of lung injury. An appropriate respiratory rate should be set to achieve the
desired minute ventilation. Normal minute ventilation (VT × respiratory rate) is
approximately 7 to 8 L/min, but certain conditions may require levels that more than
double this baseline. Minute ventilation should be adjusted to produce the PaCO2 level
that allows an acceptable acid-base (pH) status for the patient’s clinical condition. As a
general rule, FIO2, mean airway pressure, and PEEP affect the PaO2, whereas the
respiratory rate, dead space (VD), and VT affect alveolar minute ventilation and PaCO2.
To estimate predicted body weight
Males:
50 + 2.3 (height in inches – 60)
50 + 0.91 (height in cm – 152.4)
Females:
45.5 + 2.3 (height in inches – 60)
45.5 + 0.91 (height in cm – 152.4)
Although a normal or close to normal acid-base (pH) status may allow resumption of
optimal functioning of the cellular metabolism essential to the recovery of a critically ill
patient, in some circumstances (acute respiratory distress syndrome and severe
obstructive lung disease), the goals of mechanical ventilation are not to normalize blood
gases. Hypercapnia and respiratory acidosis are tolerated in such situations to achieve
goals such as minimizing dynamic hyperinflation and avoiding ventilator-associated
lung injury. Hence, individual ventilator settings and their titration contribute to a
dynamic process that must be tailored to the patient’s changing needs. Guidelines for the
initiation of mechanical ventilation are listed in Table 5-7.
Table 5-7 Guidelines for the Initiation of Mechanical Ventilation
1. Choose the ventilator mode with which you are most familiar. The primary goals of ventilatory support
are adequate oxygenation/ventilation, reduced work of breathing, synchrony between patient and
ventilator, and avoidance of high end-inspiration alveolar pressures.
2. The initial FIO2 should be 1.0. The FIO2 thereafter can be titrated downward to maintain the SpO2 at 92%
to 94%. In severe acute respiratory distress syndrome, SpO2 ≥88% may be acceptable to minimize
complications of mechanical ventilation.
3. Initial VT = 8 to 10 mL/kg in patients with relatively normal lung compliance. In patients with poor lung
compliance (eg, ARDS), a target VT of 6 mL/kg by PBW is recommended to avoid overdistension
and maintain an inspiratory plateau pressure ≤30 cm H2O.
4. Choose a respiratory rate and minute ventilation appropriate for the particular clinical requirements.
Target pH, not PaCO2.
5. Use PEEP in diffuse lung injury to maintain an open alveoli at end expiration. If volume is held
constant, PEEP may increase peak inspiratory plateau pressure, a potentially undesirable effect in
ARDS. PEEP levels >15 cm H2O are rarely necessary
6. Set the trigger sensitivity to allow minimal patient effort to initiate inspiration. Beware of auto cycling if
the trigger setting is too sensitive.
7. In patients at risk of obstructive airway disease, avoid choosing ventilator settings that limit expiratory
time and cause or worsen auto-PEEP.
8. Call the critical care consultant or other appropriate consultant for assistance.
Abbreviations: VT, tidal volume; SpO2, oxyhemoglobin saturation as measured by pulse oximetry; ARDS,
acute respiratory distress syndrome; PBW, predicted body weight; PEEP, positive end-expiratory pressure
VIII. CONTINUING CARE DURING MECHANICAL VENTILATION

After mechanical ventilation has been initiated, the following parameters should be
assessed and titrated to achieve the desired goals. Many important interrelationships
exist among ventilator settings, and the consequences of making any change must be
appreciated. This interdependency of parameters may lead to beneficial or harmful
effects in the respiratory and/or cardiovascular systems. Critical care consultation
should be obtained for continuing ventilator management.
A. Inspiratory Pressures
During positive pressure volume assist-control ventilation, airway pressure rises
progressively to a peak inspiratory pressure (Ppeak; Figure 5-5), which is reached at
end inspiration. The Ppeak is the sum of the pressure required to overcome airway
resistance and the pressure required to overcome the elastic properties of the lung and
chest wall. Ppeak, sometimes referred to as peak airway pressure, is affected by many
other variables, such as the flow rate, diameter of the endotracheal tube, secretions, and
diminished bronchial diameter. When an inspiratory hold is applied at the end of
inspiration, gas flow ceases, all dynamic factors are eliminated, and the pressure drops
to a measurement called the inspiratory plateau pressure (Pplat). The Pplat reflects the
pressure required to overcome the elastic recoil within the lung and chest wall and,
contrary to the Ppeak, is a static pressure. The Pplat is the best estimate of peak
alveolar pressure, which is an important indicator of alveolar distension. Accurate
measurement of Pplat requires the absence of any patient effort and an inspiratory hold
for a minimum of 0.5 seconds (usually 1 second).
Potential adverse effects from high inspiratory pressures include barotrauma,
volutrauma, and reduced cardiac output. Barotrauma (pneumothorax,
pneumomediastinum) and volutrauma (lung parenchymal injury due to overinflation),
although linked to high Ppeak, correlate best with Pplat. The relation of Ppeak and Pplat
is illustrated in Figure 5-5. This figure demonstrates airway pressure tracings for
typical volume assist-control ventilation under conditions of normal compliance and
resistance, increased airway resistance, and decreased respiratory system compliance.
Figure 5-5. Relationship of Peak Inspiratory Pressure and Inspiratory Plateau Pressure
As mentioned earlier, an example of the relationship of Ppeak and Pplat to alveolar

distension is demonstrated by the effect of endotracheal tube size on Ppeak and Pplat.
As the internal diameter of an endotracheal tube is decreased in a patient receiving
(fixed volume) ventilation, the same VT will result in higher Ppeak, yet Pplat (obtained
during inspiratory hold) and alveolar distension remain unchanged as the pressure is
dissipated across the resistance of the endotracheal tube. The same VT , regardless of the
type of breath, produces the same alveolar distension at end inspiration. To avoid injury
in patients receiving mechanical ventilation, Pplat should be maintained <30 cm H2O.
When compliance is decreased, both Ppeak and Pplat rise for a fixed VT. As resistance is
unchanged, the difference between peak pressure and plateau pressure is not affected.
Elevated Pplat may be reduced by the following interventions:
Decrease PEEP, which may also decrease oxygenation and worsen alveolar
collapse (if PEEP is used to improve oxygenation and alveolar stability).
Decrease VT , which may lead to hypercapnia due to a reduction in minute
ventilation.
Avoid and decrease auto-PEEP (see below) with interventions that prolong the
expiratory time, understanding that this may lead to hypercapnia.
B. Relation of Inspiratory Time to Expiratory Time and Auto-PEEP

If the expiratory time is too short to allow full exhalation, the previously delivered
breath is not completely expired and the next lung inflation is superimposed upon the
residual gas in the lung. This results in lung hyperinflation and PEEP above the preset
level on the ventilator. This increase in end-expiratory pressure is called auto-PEEP,
or intrinsic, inadvertent, or occult PEEP. Auto-PEEP can be quantified by using
manual methods or through electronic programs within some ventilators during an
expiratory hold maneuver. However, it is most easily diagnosed qualitatively by
viewing the flow-versus-time graphic waveform tracing available on most mechanical
ventilators, as the expiratory flow fails to reach the zero flow level before the initiation
of the next breath (Figure 5-6). The potentially harmful physiologic effects of auto-
PEEP on peak, plateau, and mean airway pressures are the same as those of preset
PEEP. In addition, high levels of PEEP may decrease venous return to the heart,
resulting in hypotension and higher PCO2 due to increased dead space, and adversely
affect oxygenation (especially with asymmetric lung disease).
Figure 5-6. Flow-Time Waveform Demonstrating Auto-PEEP
Auto-PEEP may be reduced by the following interventions:
Decrease respiratory rate by changing the set rate or sedating the patient. These
interventions result in fewer inspirations per minute and thus increase the total
expiratory time available; this is the most effective way of decreasing auto-PEEP.
Decrease VT , which requires less time to deliver a smaller breath and allows more
time for exhalation.
Increase gas flow rate, delivering the VT faster and allowing more time in the cycle
for exhalation. This intervention has little impact unless the initial flow rate was
set at an extremely low level. It will also lead to an increase in the airway
pressure.
Change the inspiratory waveform from decelerating (ramp) to constant (square),
which delivers VT in a shorter time, allowing more time for exhalation.
As discussed earlier, the first two interventions may lead to hypercapnia due to a
reduction in minute ventilation; however, the benefits of a decrease in auto-PEEP
despite the lower minute ventilation may lead to little change in PaCO2. When severe air
trapping occurs, allowing sufficient expiratory time may improve ventilation and CO2
removal. Hypercapnia and a controlled reduction in pH (permissive hypercapnia) may
be acceptable in some clinical conditions but requires expert consultation. This
approach may not be suitable for patients with intracranial hypertension because
hypercapnia causes cerebral vasodilation and further increases in the intracranial
pressure.
C. FIO2
High levels of inspired oxygen may be harmful to lung parenchyma after prolonged
exposure. Although the precise threshold for concern is not known, it is desirable to
reduce the FIO2 ≤0.5 (50% oxygen) within the first 24 hours. However, hypoxemia is
always considered a greater risk to the patient than high FIO2 levels. The primary
determinants of oxygenation during mechanical ventilation are FIO2 and mean airway
pressure. Other minor determinants include VT , inspiratory-expiratory ratio, inspiratory
flow rate, PEEP, auto-PEEP, use of inspiratory pause, and the inspiratory flow
waveform pattern (volume breaths). In the patient with acute respiratory distress
syndrome (ARDS), PEEP becomes a major determinant of mean airway pressure. The
interrelationships of these various parameters, as already demonstrated, often lead to
complex adjustments within the mechanical ventilation plan.
D. Minute Ventilation and Alveolar Minute Ventilation

Minute ventilation, defined as the amount of gas exchanged by an individual in 1 minute,
is calculated as the respiratory rate multiplied by mean VT . The primary determinant of
CO2 exchange during mechanical ventilation is the alveolar minute ventilation,
calculated as:
VA = (VT − VD)f
where VD is dead space and f is the respiratory rate (Chapter 4). The VT , the
respiratory rate, and their interrelationships with other ventilatory parameters have
already been discussed. Physiologic VD represents, in general, lung units that are
relatively well ventilated but under-perfused. The physiologic effect of high amounts of
VD is hypercapnia (impaired CO2 clearance). Dead space may result from the
pathologic process in the lung or from mechanical ventilation complicated by high
airway pressures, low intravascular volume, or low cardiac output.
As previously discussed, adequate ventilation is assessed by consideration of both the
PaCO2 and the pH. Hyperventilation resulting in a low PaCO2 level may be an appropriate
short-term compensatory goal during metabolic acidosis while the primary etiology is
corrected. Similarly, a patient with chronic hypercapnia has an increased baseline PaCO2
and maintains a near-normal pH by renal compensation (increased bicarbonate
retention). Patients with chronic compensated hypercapnia should receive sufficient
minute ventilation during mechanical ventilation to maintain the PaCO2 at their usual
(baseline) level, and utmost attention should be paid to the pH to avoid severe
alkalemia and loss of retained bicarbonate.
E. Humidification
Gases delivered by mechanical ventilators are typically dry, and the upper respiratory
tract is bypassed by artificial airways, resulting in loss of heat and moisture. Heating
and humidification of gases are routinely provided during mechanical ventilation to
prevent mucosal damage and minimize inspissation of secretions. Available systems
include passive humidifiers (artificial nose) or active, microprocessor-controlled heat
and humidifying systems (heated humidifiers). The passive humidifiers are
contraindicated in the presence of copious secretions, minute ventilation >12 L/min, air
leaks >15% of delivered tidal volume, or blood in the airway.
F. Use of Positive End-Expiratory Pressure

Adjustment of PEEP is the cornerstone strategy employed for disease states that cause
alveolar collapse or airway closure (eg, ARDS). It causes alveolar recruitment and
prevents repeated opening and closing of the alveoli (atelectrauma). Titration of PEEP
for hypoxemic respiratory failure secondary to ARDS can be performed according to
the PEEP/FIO2 combinations given in Table 5-8.
Table 5-8 Suggested Combinations of PEEP and FIO2 to Reach Goal PaO2
FIO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7
PEEP (cm H2O) 5-14 5-14 8-16 8-16 10-20 10-20 10-20 12-20 14-20
FIO2 0.8 0.8 0.9 0.9 0.9 1.0 1.0 1.0
PEEP (cm H2O) 14-22 14-22 14-22 16-22 18-22 20-22 22 24
Abbreviations: PEEP, positive end-expiratory pressure; FIO2, fraction of inspired oxygen
In cases of severe obstructive lung disease, applying external PEEP and setting it close
to the auto-PEEP value can help offset the work of breathing to trigger the ventilator.
Seeking expert consultation is prudent if higher levels of PEEP are required to maintain
oxygenation.
G. Prophylactic Therapies
Mechanical intubation is a risk factor for venous thromboembolism, gastric stress
ulceration, and nosocomial pneumonia. Measures to prevent venous thromboembolism
include the prophylactic use of anticoagulation (unless contraindicated) and/or
pneumatic compression devices. Using a proton pump inhibitor or histamine 2-receptor
blocker is warranted for stress ulcer prevention. The risk of ventilator-associated
pneumonia (ventilator bundle) is reduced by elevation of the head of the bed to ≥30°,
oral hygiene, and daily evaluations for liberation from mechanical ventilation.
IX. SEDATION, ANALGESIA, AND NEUROMUSCULAR

BLOCKADE
Endotracheal intubation and mechanical ventilation can be uncomfortable and anxiety
provoking. To improve the patient’s comfort and synchrony with the ventilator,
anxiolytics, sedatives, and analgesics may be administered. Neuromuscular blocking
agents should be used with caution, and expert consultation should be sought before
initiation. Guidelines for the use of these agents are outlined in the Society of Critical
Care Medicine’s Clinical Practice Guidelines for Sustained Neuromuscular Blockade
in the Adult Critically Ill Patient and in Clinical Practice Guidelines for the
Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care
Unit. Caution also should be exercised with use of sedation in nonintubated patients
with acute respiratory insufficiency or impending respiratory failure.
X. VENTILATORY GUIDELINES FOR SPECIFIC CLINICAL

SITUATIONS
Case Study
A 36-year-old previously healthy man presents to the hospital with complaints of a

cough, sputum production, and fever of 2 days’ duration. Admission chest radiograph
reveals a developing infiltrate in the left lower lobe. The man is admitted to the general
ward and started on antibiotics for community-acquired pneumonia. Less than 24 hours
later, the patient continues to deteriorate and requires oxygen, 10 L/min. He is not in
obvious respiratory distress; however, pulse oximetry reveals severe hypoxemia (83%
to 89% on supplemental oxygen, 10 L/min.) Sputum cultures show Streptococcus
pyogenes (group A) colonies, and a new chest radiograph reveals new, diffuse bilateral
alveolar infiltrates. The patient is intubated due to worsening hypoxemia.
– What initial ventilator settings would you use for this patient?
– What steps should be taken to minimize barotrauma during ventilation?
– What parameters should be measured and monitored?
A. Acute Respiratory Distress Syndrome

ARDS causes a decrease in lung compliance, making the lungs stiff and difficult to
inflate, and produces hypoxemic respiratory failure (Chapter 4). Guidelines for
mechanical ventilation in ARDS are outlined in Tables 5-8 and 5-9. High Ppeak and
Pplat complicate mechanical ventilation because of the low lung compliance or high
airway resistance. Lower VT (4-6 mL/kg of predicted body weight) is required, and the
Pplat should be maintained at the desired level of ≤30 cm H2O; permissive hypercapnia
may be required to accomplish that goal. The FIO2 is increased as necessary to prevent
hypoxemia but reduced as soon as other ventilatory interventions are effective. Because
of increased shunt in ARDS, hypoxemia may be severe. PEEP is the most effective way
to improve oxygenation and is typically applied in the range of 8 to 15 cm H2O, based
on the severity of hypoxemia. Higher PEEP levels may be indicated in severe lung
injury. Although patients with ARDS are somewhat less likely to develop auto-PEEP
because expiratory time requirements are reduced due to decreased lung compliance
(stiffness), its presence should be monitored, especially at higher inspiratory-expiratory
ratios. Table 5-9 outlines the recommended strategy for ventilating patients with ARDS.
Table 5-8 outlines the recommended FIO2 and PEEP combinations.
Table 5-9 Mechanical Ventilation in Acute Respiratory Distress Syndrome

Goals
PaO2: 55-80 mm Hg (7.3-10.7 kPa)

Pplat: ≤30 cm H2O
VT: 4-6 mL/kg PBW
pH: >7.15 is acceptable
Start with Assist-Control with VT of 8 mL/kg PBW
Decrease by 1 mL/kg over the next 4 hours until VT of 4-6 mL/kg is reached.
If Pplat is >30 cm H2O, decrease VT by 1 mL/kg until VT is 4 mL/kg or arterial pH reaches 7.15.
If using VT of 4 mL/kg and Pplat is <25 cm H2O, VT can be increased by 1 mL/kg until Pplat is 25 cm
H2O or VT is 6 mL/kg.
If a Pplat of ≤30 cm H2O has been achieved with a VT >6 mL/kg and a lower VT is clinically
problematic (ie, need for increased sedation), it is acceptable to maintain the higher VT.
Initiation of PEEP in Acute Respiratory Distress Syndrome
Initiate PEEP at 5 cm H2O and titrate up in increments of 2-3 cm H2O (Table 5-8).
Full recruitment effect may not be apparent for several hours.
Monitor blood pressure, heart rate, and PaO2 or pulse oximetry during PEEP titration and at intervals
while the patient is receiving PEEP therapy.
Optimal PEEP settings are typically 8-15 cm H2O.
NOTE: These guidelines are summarized to facilitate early intervention in critical patients. The physician
should be familiar with these situations and seek appropriate consultation as soon as possible.
Abbreviations: Pplat, plateau pressure; VT, tidal volume; PBW, predicted body weight; PEEP, positive end-
expiratory pressure
Case Study
A 28-year-old woman with a history of asthma is intubated and admitted to the ICU for
an acute asthma exacerbation. Peak airway pressure on admission was 40 cm H2O, and
Pplat was 25 cm H2O immediately after intubation; however, 6 hours later, peak airway
pressures have arisen to 55 cm H2O while the Pplat has remained the same.
– What is the likely etiology of her high peak airway pressures in the setting of
unchanged plateau pressures?
– What adjunctive therapies, in addition to ventilator support, does this patient need
to reduce the elevated airway pressures?
– Which parameter (ie, peak airway pressure or Pplat) has been associated with a
higher risk of barotrauma in an intubated patient?
B. Obstructive Airway Disease

Mechanical ventilation for patients with asthma and chronic obstructive pulmonary
disease is designed to support oxygenation and assist ventilation until airway
obstruction has improved. After initial intubation, airway secretions and persistent
small airway obstruction may manifest as elevated peak airway pressures and a normal
Pplat. This suggests an airway obstruction (not worsening compliance), and
bronchodilators and steroids should be used aggressively to help alleviate this
obstruction while mechanical ventilation supports the patient. As airflow improves, the
patient will tolerate higher VT levels and longer inspiratory times.
Mechanical ventilation in these patients may also produce hyperinflation, auto-PEEP,
and resultant hypotension. Therefore, careful attention is needed to balance cycle,
inspiratory, and expiratory times. The initial VT should be 6 to 8 mL/kg, and the minute
ventilation should be adjusted to a low normal pH. With volume ventilation, the
inspiratory flow rate should be set to optimize the inspiratory-expiratory ratio and
allow complete exhalation. Such management reduces breath stacking and the potential
for auto-PEEP.
C. Asymmetric Lung Disease

Asymmetric lung disease or injury that occurs after aspiration, contusion, or a localized
pneumonia may cause abnormal distribution of ventilation and gas exchange during
mechanical ventilation. Because the conditioned gas from the ventilator follows the path
of least resistance along the bronchi, the VT is distributed primarily to the less-affected
(more-compliant) lung and may overexpand it. Overdistension of the less-affected lung
and poor expansion of the diseased/injured lung worsen ventilation-perfusion
relationships in both lungs, and hypoxemia and hypercapnia may occur, persist, or
worsen, in addition to causing injury to the normal lung. Standard settings and principles
of ventilator support should be initiated. However, if this is unsuccessful, expert
consultation should be obtained to facilitate further efforts at patient management.
Putting the less-involved lung in the gravitationally dependent (decubitus) position may
be helpful in directing pulmonary blood flow to lung units receiving better ventilation.
Other techniques, such as differential lung ventilation, could be considered, and
immediate expert consultation may be required.
D. Heart Disease
The major goals of ventilatory support in patients with myocardial ischemia are to
decrease the work of breathing and ensure adequate oxygen delivery to the heart.
Decreasing the work of breathing will reduce the consumption of oxygen by respiratory
muscles, thus increasing oxygen availability to the heart. Patients with cardiogenic
pulmonary edema who are mechanically ventilated receive additional benefit from the
decrease in preload as a result of increased intrathoracic pressure. Left ventricular
afterload also decreases through application of positive juxtacardiac pressure during
systole.
E. Neuromuscular Disease
Patients with peripheral neuromuscular disease typically have an intact respiratory
drive and normal lungs. These patients may require a higher VT level to avoid the
sensation of dyspnea. Adjustments are made in other ventilatory parameters to ensure a
normal arterial pH.
XI. MONITORING MECHANICAL VENTILATORY SUPPORT

Patients who receive mechanical ventilatory support require continuous monitoring to
assess the beneficial and potential adverse effects of treatment (Table 5-10). Arterial
blood gas measurements provide valuable information about the adequacy of
oxygenation, ventilation, and acid-base balance. This information is essential during the
initial phases of ventilatory support and during periods of patient instability. If
available, a pulse oximeter (Chapter 6) and end-tidal capnometer (for measuring end-
tidal CO2) can be used to further monitor the patient’s progress.
Table 5-10 Recommendations for Monitoring Mechanical Ventilatory Support
Obtain a chest radiograph after intubation and repeat as indicated to evaluate any deterioration in
status.
Obtain arterial blood gas measurements after initiation of mechanical ventilation and intermittently
based on patient status.
Measure vital signs frequently and observe the patient directly (including patient-ventilator interaction).
Measure inspiratory plateau pressure as clinically appropriate.
Use pulse oximetry to monitor oxygenation.
Use ventilator alarms to monitor key physiologic and ventilator parameters.
Ventilators are equipped with sophisticated alarms and monitors to assist with patient
management and detection of adverse events. When initiating ventilatory support, the
respiratory care practitioner usually establishes alarm parameters for low and high
minute ventilation, high inspiratory pressures, and low exhaled volumes and pressures.
Many ventilators allow for the measurement of auto-PEEP.
The low-pressure alarm is intended to alert the clinician to a leak in the circuit or to
ventilator disconnection. A high-pressure alarm warns that the set maximum peak
airway pressure has been exceeded; this alarm is usually set 10 cm H2O above the
patient’s baseline peak airway pressure. If a patient receiving volume ventilation
develops mucous plugging or a marked change in airway resistance or lung compliance,
the peak pressure will rise acutely. If the peak pressure alarm sounds with volume
ventilation, it implies that the patient is not receiving the set VT , as inspiration ends
when the pressure alarm limit is exceeded. Conversely, in pressure preset modes of
ventilation, changes in airway resistance or lung compliance will trigger the low
exhaled volume alarm.
XII. HYPOTENSION ASSOCIATED WITH INITIATION OF

MECHANICAL VENTILATION
A. Tension Pneumothorax
When hypotension occurs immediately after initiation of mechanical ventilation, tension
pneumothorax should be one of the first considerations. This diagnosis is based on a
physical examination that finds decreased or absent breath sounds and tympany to
percussion on the side of the pneumothorax. Tracheal deviation away from the side of
the pneumothorax may be observed, although it is uncommon after placement of an
endotracheal tube. Treatment includes emergent decompression by inserting a large-
bore catheter or needle into the second or third intercostal space in the midclavicular
line. Treatment should not be delayed awaiting a chest radiograph. The insertion of a
catheter or needle is both diagnostic and therapeutic: it improves blood pressure and
reverses the findings of physical examination. The insertion of the catheter or needle
must be followed by chest tube placement.
B. Conversion from Negative to Positive Intrathoracic Pressure

Normal intrathoracic pressure is slightly negative relative to the atmosphere. When
positive pressure ventilation is initiated, intrathoracic pressure becomes positive. As
intrathoracic pressure rises, right atrial pressure rises and the intravascular pressure
gradient for return of blood from the large extrathoracic veins into the right heart
decreases. As a result, blood return to the heart may be reduced. Left ventricular
preload, stroke volume, cardiac output, and blood pressure then may decrease in
sequence. Underlying intravascular volume depletion exacerbates the deleterious effects
of the increased intrathoracic pressure on cardiac output and blood pressure. Treatment
of this common complication includes volume resuscitation by means of rapidly infused
fluid boluses to raise extrathoracic venous pressure and increase venous return to the
right heart until the blood pressure increases. Oxygen saturation should be monitored to
avoid overly aggressive fluid resuscitation. Use of ventilation techniques associated
with high mean airway pressure may exacerbate the deleterious hemodynamic
consequences of mechanical ventilation.
C. Auto-PEEP
As previously discussed, auto-PEEP occurs when the combination of ventilator settings
and patient physiology results in an inadequate expiratory time. Excessive end-
expiratory pressure may increase intrathoracic pressure and cause hypotension due to
decreased venous return to the heart. Although auto-PEEP may occur in any patient,
those with obstructive airway disease are particularly predisposed to this condition
because of the need for a prolonged expiratory phase.
D. Acute Myocardial Ischemia/Infarction

Stress from the cause of acute respiratory failure, as well as the stress of intubation
itself, may lead to increased myocardial oxygen demand and to acute myocardial
ischemia, infarction, and subsequent hypotension. Patients at high risk should be
evaluated with serial electrocardiograms and myocardial markers of injury.
Key Points
Mechanical Ventilation
The primary goals of noninvasive and invasive positive pressure ventilation are to
support ventilation and oxygenation, and to reduce work of breathing while
ensuring patient comfort.
NPPV is best utilized in the alert, cooperative patient whose respiratory condition
is expected to improve in 48 to 72 hours.
The advantages and disadvantages of the different modes of invasive mechanical
ventilation must be considered when determining the optimal ventilatory support
for the patient’s clinical condition.
Guidelines for initiating mechanical ventilation should be carefully followed, with
adjustments made based on patient assessment and monitoring.
The complex interactions of inspiratory pressures, inspiratory-expiratory ratio,
FIO2, and PEEP must be appreciated to evaluate the potential benefits and harmful
effects in each patient.
The primary determinants of oxygenation are FIO2 and mean airway pressure,
whereas alveolar ventilation primarily affects CO2 exchange.
During mechanical ventilation, a patient must be closely monitored using the

ventilator alarm systems, continuous pulse oximetry, attentive physical assessment,
measurement of inspiratory Pplat (as clinically appropriate), and intermittent
arterial blood gases and chest radiographs as needed.
High inspiratory plateau pressures are associated with a higher incidence of
ventilator-induced lung injury and should be maintained below 30 cm H2O.
Hypotension occurring immediately after initiation of invasive mechanical

ventilation should prompt evaluation for tension pneumothorax, decreased venous
blood return due to intrathoracic pressure, auto-PEEP, or myocardial ischemia.
Suggested Readings
1. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal

volumes as compared with traditional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308.
2. Caples SM, Gay PC. Noninvasive positive pressure ventilation in the intensive
care unit: a concise review. Crit Care Med. 2005;33:2651-2658.
3. Fink M, Abraham E, Vincent J, et al, eds. Chapter 66: Controlled mechanical
ventilation. In: Textbook of Critical Care. 5th ed. Philadelphia, PA: WB Saunders
Co; 2005.
4. Fink M, Abraham E, Vincent J, et al, eds. Chapter 67: Patient-ventilator
interaction. In: Textbook of Critical Care. 5th ed. Philadelphia, PA: WB Saunders
Co; 2005.
5. Hess DR, Kacmarek RM. Essentials of Mechanical Ventilation. 2nd ed. New
York, NY: McGraw-Hill Companies; 2002.
6. Kallet RH, Jasmer RM, Pittet JF, et al. Clinical implementation of the ARDS
Network protocol is associated with reduced hospital mortality compared with
historical controls. Crit Care Med. 2005;33:925-929.
7. Leisching T, Kwok H, Hill NS. Acute applications of noninvasive positive
pressure ventilation. Chest. 2003;124:699-713.
8. MacIntyre N. Ventilatory management of ALI/ARDS. Semin Respir Crit Care Med.
2006;27:396-403.
9. MacIntyre N, Branson RD. Mechanical Ventilation. Philadelphia, PA: WB
Saunders Co; 2000.
10. Marini JJ. Dynamic hyperinflation and auto-PEEP end-expiratory pressure: lessons
learned over 30 years. Am J Respir Crit Care Med. 2011;184:756-762.
11. Marini JJ, Gattinoni L. Ventilatory management of acute respiratory distress
syndrome: a consensus of two. Crit Care Med. 2004;32:250-255.
12. Murray MJ, Cowen J, DeBlock H, et al. Clinical practice guidelines for sustained
neuromuscular blockade in the adult critically ill patient. Crit Care Med. 2002;30:
142-156.
13. Petrucci N, Iacovelli W. Ventilation with smaller tidal volumes: a quantitative
systematic review of randomized controlled trials. Anesth Analg. 2004;99:193-
200.
14. Tobin MJ. Advances in mechanical ventilation. N Engl J Med. 2001;344:1986-
1996.
15. Tobin MJ. Principles and Practice of Mechanical Ventilation. Third Edition.
McGraw Hill Companies; 2013
Suggested Website
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org.
Chapter 6
M ONITORING OXYGEN BALANCE AND ACID-

BASE STATUS
Objectives
Outline the determinants of oxygen balance.

Recognize disorders of oxygen delivery.
Identify the principles and limitations of techniques for monitoring oxygen balance.
Explain the use of acid-base status in monitoring the seriously ill patient.
Case Study
A 67-year-old woman was admitted to the hospital 3 days ago with abdominal pain,
fever, and general malaise. She was found to have acute cholecystitis and underwent a
laparoscopic cholecystectomy 1 day ago. Today she developed shortness of breath and
altered mental status. Her abdominal exam is benign except for mild tenderness at the
trocar sites. The patient’s pulse is 136 beats/min, blood pressure 106/55 mm Hg,
respiratory rate 28 breaths/min and oxygen saturation on pulse oximetry (Spo2) 94%
while breathing room air.
– What monitoring should be immediately implemented?
– What additional parameters should be assessed to determine if the oxygen balance
is adequate?
I. INTRODUCTION
Monitoring is never therapeutic, and information from monitoring tools must be
integrated with patient assessment and clinical judgment to determine optimal care. In
addition, the clinician must be aware of the limitations and risk-benefit ratio of a
monitoring system. Monitoring may be as simple as measuring the pulse or temperature
or as complex as invasive hemodynamic techniques with direct and calculated
measurements. More invasive monitoring strategies that carry a higher risk should be
considered if they provide sufficient new information to guide therapy. As an example,
neuroendocrine responses to physiological stress lead to early effects on heart rate,
respiratory rate, vascular tone, and blood pressure. Abnormalities of these combined
signs may suggest the need for more intensive monitoring to appropriately evaluate and
treat the patient. This chapter will emphasize basic monitoring techniques that can be
accomplished in most care environments.
The goals of monitoring in seriously ill patients are to recognize physiological
abnormalities and to guide interventions to ensure adequate blood flow and oxygen
delivery for maintenance of cellular and organ function. Tissue oxygenation cannot be
directly measured or monitored, but estimates of the adequacy of oxygenation can be
made based on knowledge of the oxygen balance, which is determined by oxygen
delivery and oxygen consumption. An understanding of these principles is required to
appreciate the usefulness and limitations of various monitoring tools.
II. PRINCIPLES OF OXYGEN DELIVERY

Oxygen delivery is the amount of oxygen presented to the tissues, and it is the
component of oxygen balance that can more often be altered by interventions in the
seriously ill patient. Normally, the amount of oxygen delivered to the tissues is three to
four times greater than the tissue needs. In critical illness, physiologic derangements that
result in an absolute decrease in the oxygen delivered or an increase in tissue oxygen
demand may compromise this margin of safety. In addition, sufficient oxygen delivery
does not always guarantee adequate oxygen utilization at the tissue level. Oxygen
delivery is dependent on cardiac output (blood flow) and the oxygen content of arterial
blood. Invasive and/or more complex noninvasive monitoring is required for exact
measurement of cardiac output. However, an understanding of the variables that
determine oxygen content in the blood and cardiac output, along with less invasive
monitoring, may guide appropriate treatment.
A. Oxygen Content of Arterial Blood

Arterial oxygen content (CaO2) is defined as the amount of oxygen bound to hemoglobin
plus the amount of oxygen dissolved in arterial blood. The components of arterial
oxygen content are related by the formula:
CaO2 (mL O2/dL) = [Hemoglobin (g/dL) × 1.34 × SaO2 (%)] + [0.0031 × PaO2 (mm Hg)]
where SaO2 is the arterial oxyhemoglobin saturation and PaO2 is the partial pressure of
oxygen in arterial blood. Each fully saturated gram of hemoglobin transports 1.34 to
1.39 mL of oxygen, depending on the affinity of hemoglobin for oxygen. Hemoglobin is
the major contributor of oxygen for tissue demands and releases bound oxygen based on
cellular uptake of dissolved oxygen as blood flows through the capillaries. The ability
of hemoglobin to release more oxygen when supply is inadequate or cellular demand is
increased is one of the main compensatory mechanisms to sustain cellular function. The
oxyhemoglobin dissociation curve shows the relationship of hemoglobin saturation and
PO2 (Figure 6-1). When the PO2 drops to approximately 40 mm Hg (5.3 kappa) in the
capillaries, the decrease in oxyhemoglobin saturation to 75% reflects the amount of
oxygen released to the tissues. During physiological stress, oxyhemoglobin saturation at
the tissue level may decrease to <20%, reflecting the release of additional oxygen to
tissues. Acidosis and fever will shift this curve to the right, resulting in a lower affinity
of oxygen for hemoglobin and greater delivery of oxygen to the tissues.
The usual arterial oxygen content (CaO2)

is 18-20 mL/dL when hemoglobin
concentration and saturation are
normal.
Figure 6-1. Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation curve relates the PO2 to oxyhemoglobin saturation. Near-maximal
saturation of hemoglobin occurs at a PO2 of 60 mm Hg (8.0 kPa). PO2 values above this point provide only a
modest increase in oxyhemoglobin saturation. Note, however, that a rapid decrease in oxyhemoglobin
saturation occurs when the PO2 drops below 60 mm Hg (8.0 kPa).
Arterial oxygen content can be estimated by using the direct measurement of the
hemoglobin concentration and arterial oxyhemoglobin saturation in intermittent blood
samples, as dissolved oxygen (0.0031 × PaO2) contributes minimally to oxygen content.
Although hemoglobin is not monitored continuously, oxyhemoglobin saturation measured
by pulse oximetry (SpO2) allows continuous assessment of this determinant of arterial
oxygen content.
Calculated CaO2 reflects oxygen that is

available in the arterial circulation and
not necessarily the oxygen that is
delivered to or consumed by specific
tissues.
B. Cardiac Output
If the oxygen content of arterial blood is optimum, then an appropriate cardiac output is
needed to ensure delivery of oxygen to the tissues. Cardiac output (in mL/min or L/min)
is the product of heart rate and stroke volume (Figure 6-2). Stroke volume is the
quantity of blood pumped out of the left heart with each beat and is determined by the
difference between the end-diastolic volume and end-systolic volume of the ventricle.
Variables that determine stroke volume are preload, afterload, and contractile function.
The first compensatory mechanism to increase oxygen delivery is often an increase in
heart rate. Patients who are unable to increase their heart rate (eg, beta-blockade or
fixed pacing) will have a limited ability to compensate.
Figure 6-2. Cardiac Output as the Product of Heart Rate and Stroke Volume
Although the heart rate is easily measured and evaluated, an evaluation of stroke volume
requires special noninvasive, minimally invasive, or invasive methods. The option of
measuring cardiac output by assessing stroke volume depends on the training, expertise,
and resources available. The pulmonary artery catheter is infrequently used as an
invasive method of measuring intermittent or continuous cardiac output but requires
critical care expertise. Minimally invasive hemodynamic methods measure cardiac
output using analysis of the arterial waveform or aortic blood flow. Devices that
analyze the arterial waveform to determine pulse pressure, stroke volume, and cardiac
output require an arterial catheter, and some also require a central venous catheter.
Esophageal Doppler devices estimate cardiac output from measurement of blood flow
in the descending aorta. Noninvasive hemodynamic monitors use principles of
bioimpedance or bioreactance to determine stroke volume and cardiac output. The
clinician must be aware of the limitations that affect measurement accuracy and
interpretation of any chosen technique. If cardiac output is not directly measured, an
indirect assessment of variables involved in determining cardiac output (Table 6-1) and
knowledge of hemodynamic principles can be useful.
Persistent tachycardia should be

considered as a possible compensatory
mechanism to increase oxygen delivery.
Table 6-1 Clinical Assessment of Determinants of Cardiac Output
Variable Method of Assessment

Heart rate and rhythm Finger on pulse
Pulse oximetry
Electrocardiography
Preload
Right heart Neck vein distension, liver enlargement, dependent edema
Central venous pressure
Left heart Presence of dyspnea of exertion, orthopnea
Pulmonary edema, rales on lung examination
Afterload (left heart) Mean arterial blood pressure

Contractility Ejection fraction and stroke volume estimate by echocardiography*
*Requires special training and expertise
1. Contractility
Contractility is the ability of myocardial fibers to shorten during systole. It is highly
dependent on preload and afterload and is difficult to measure as an independent
variable. Additional factors that can affect contractility in the critically ill patient are
endogenous sympathetic activation, acidosis, ischemia, inflammatory mediators, and
vasoactive agents. An increase in contractility would result in a larger stroke volume.
Echocardiographic measurement of the ejection fraction provides some information to
the clinician on contractility.
2. Preload
Preload is a measure or estimate of the ventricular volume at the end of diastole (end-
diastolic volume) and is determined by venous return and ventricular compliance. The
distensibility or stretch (compliance) of the ventricle and the volume load (venous
return) it can accept are the basis for the Frank-Starling curve. In general, a greater end-
diastolic volume leads to increased stretch on the myocardium, resulting in a larger
stroke volume (Figure 6-3). Because it is difficult to measure volume, preload is most
often estimated from the ventricular end-diastolic pressure, which is transmitted and
reflected in the atrial pressure. The atrial pressure is estimated by the measurement of
pressure in a central vein or the pulmonary artery. Thus, the right ventricular preload is
estimated by measurement of the central venous pressure (CVP) and the left ventricular
preload by the measurement of pulmonary artery occlusion pressure. These pressures
indirectly reflect the end-diastolic volume as well as the compliance of the ventricular
wall. Using bedside ultrasonography, assessment of the change in the diameter of the
inferior vena cava with respiration may aid in the assessment of right ventricular
preload.
Figure 6-3. Relationship Between Ventricular Preload and Stroke Volume
When end-diastolic volume of the ventricle (preload increases, stroke volume usually increases
proportionately.
The relationship between the measured pressure and volume in the ventricular chambers
depends upon the compliance or distensibility of the ventricle. During myocardial
ischemia, sepsis, valvular dysfunction, and even tachycardia, the ventricles may become
less compliant and may not fully relax during diastole. This diastolic dysfunction
reduces the ventricular volume at end diastole but may be associated with a higher
filling pressure; therefore, the clinician may misinterpret pressure measurements to
indicate adequate volume loading. Changes in intrathoracic pressures (eg, tension
pneumothorax, positive pressure ventilation) may also affect the filling pressures.
3. Afterload
Afterload is the myocardial wall tension required to overcome the resistance, or
pressure load, that opposes ejection of blood from the ventricle during systole. The
higher the afterload, the more tension the ventricle must develop, the more work is
performed, and the less efficient the contraction may become. Afterload is usually
estimated from the systemic mean arterial pressure (left ventricle) and mean pulmonary
artery pressure (right ventricle) and by calculations of systemic and pulmonary vascular
resistance.
III. ASSESSMENT OF OXYGEN BALANCE

In addition to oxygen delivery, oxygen consumption by the tissues affects oxygen
balance. However, less is known about the factors that determine oxygen utilization at
the cellular and tissue levels, and no direct routine measures of oxygen consumption are
available. Indirect calculated measurement of oxygen consumption requires invasive or
complex techniques. These measures reflect global oxygen utilization and do not
provide information on oxygen utilization by specific tissues or organs.
Measurements of global oxygen balance that may be useful in monitoring the seriously
ill patient include central venous oxyhemoglobin saturation (ScvO2) and lactate
concentrations. ScvO2 can be obtained continuously or intermittently from a catheter
placed in the internal jugular or subclavian vein and correlates with the mixed venous
oxyhemoglobin saturation (SVO2) obtained from a pulmonary artery catheter in the
pulmonary artery. The SVO2 measures the oxyhemoglobin saturation of blood from the
superior vena cava and the inferior vena cava that has been mixed in the right ventricle.
These measures of venous oxyhemoglobin saturation represent the amount of oxygen
still bound to hemoglobin after traversing the tissue capillaries and returning to the right
heart; the decrease from the SaO2 estimates the amount of oxygen utilized (Figure 6-4).
In normal individuals, the SVO2 is >65% and the ScvO2 is 2% to 3% lower. However, in
patients with shock and/or hypoperfusion, the ScvO2 may be 5% to 7% higher than the
SVO2 due to greater desaturation of venous blood from the gastrointestinal tract
contributing to SVO2. Low values of ScvO2 suggest an imbalance in the oxygen supply and
demand. This imbalance may be due to decreases in cardiac output, hemoglobin
concentration, or SaO2, or increases in tissue oxygen consumption. Patients may have
more than one abnormality contributing to oxygen imbalance. A normal ScvO2 may still
be associated with tissue hypoxia in conditions such as severe sepsis and certain
poisonings (eg, cyanide). Further evaluations of lactate concentration and organ function
are needed to assess oxygen balance in the seriously ill patient when the ScvO2 is
normal.
Figure 6-4. Determinants of Oxygen Balance
Abbreviations: Hgb, hemoglobin; SaO2, arterial oxyhemoglobin saturation

Oxygen balance depends on the oxygen delivered to the tissues and the metabolic needs of those tissues.
An estimate of the oxygen utilized by the tissues is provided by the central venous oxyhemoglobin value
(Sc VO2 and mixed venous oxyhemoglobin saturation (SVO2.
Lactate is another indicator of the overall oxygen balance. It is produced during

anaerobic metabolism when cellular hypoxia occurs. The elevation of blood lactate in
shock and hypoperfusion may be due to inadequate oxygen supply to tissue but also may
be affected by altered hepatic metabolism, use of vasoactive drugs, and other factors.
Lactate concentrations do not have high sensitivity or specificity for inadequate tissue
oxygenation, but elevated concentrations often are associated with tissue hypoperfusion.
A decreasing lactate concentration may be a useful indicator of effective interventions.
Elevated lactate concentrations

correlate with worse prognosis in
severely ill patients.
IV. MONITORING DETERMINANTS OF OXYGEN BALANCE

Precise monitoring of oxygen balance is not easily accomplished because techniques
may not be available to assess some variables (contractility, tissue oxygen consumption)
or special expertise and resources are required (stroke volume determination,
echocardiography). However, monitoring of variables such as oxyhemoglobin
saturation, blood pressure, ScvO2, lactate concentration, and fluid responsiveness
combined with other clinical information, may provide guidance in evaluating the
adequacy of oxygen balance in seriously ill patients.
Pulse oximetry measurements will be

affected by inflation of a blood pressure
cuff on the same extremity as the
oximetry sensor due to disappearance of
the pulsatile waveform.
A. Monitoring of Oxyhemoglobin Saturation
1. Principles
The pulse oximeter is a simple, noninvasive device that estimates arterial
oxyhemoglobin saturation. The transmission of red and infrared light through the
capillary bed creates several signals throughout the pulsatile cardiac cycle. These
signals measure the absorption of the transmitted light by the tissue or venous and
arterial blood. Calculations made from the processed signals provide estimates of the
oxygen saturation of hemoglobin, expressed as a percentage. This is not the same as the
PaO2 in the blood, although PaO2 is a primary determinant of the saturation of
hemoglobin. Neither does it reflect adequacy of oxygen delivery or ventilation. The
value measured by the device is commonly called the SpO2 to distinguish it as the
oxyhemoglobin saturation measurement by a pulse oximeter rather than the SaO2, which
is determined directly from an arterial blood sample by co-oximetry. Pulse oximetry is
useful in detecting hypoxemia and titrating the delivered oxygen concentration in
patients receiving supplemental oxygen.
Trends in the values of measured

variables are usually more helpful than
single values.
2. Clinical Issues
Studies have shown that to ensure a PaO2 of 60 mm Hg (8.0 kPa), an SpO2 of 92% should
be maintained in patients with light skin, whereas 94% saturation may be needed in
patients with dark skin. Oximetry sensors can be applied to the finger, toe, earlobe,
bridge of nose, mouth, or any skin surface from which a reliable pulsatile signal can be
obtained. Factors that can affect signal detection or fidelity are listed in Table 6-2.
Pulse oximeters display a digital heart rate derived from the pulsatile signal detected by
the sensor. This rate should equal the patient’s heart rate as measured by another
method, so these two rates should be compared as the first step in the analysis of an
SpO2 measurement. Additional hemodynamic information may be obtained from the
pulse oximeter waveform, which is related to the arterial blood pressure waveform and
stroke volume. Variation in the pulse oximeter waveform (pulse pressure) with positive
pressure ventilation may suggest hypovolemia and responsiveness to fluid
administration (see next section).
Table 6-2 Factors That Affect Accuracy of Pulse Oximetry

Anatomic or Physiologic Factors
Dark skin
False nails
Nail polish
Hypothermia
Vasoconstriction
Hypotension
Poor regional perfusion
Hematocrit <15%
Hyperlipidemia
Carboxyhemoglobin
Tachycardias
External Factors
Lipid suspensions, propofol (falsely elevate the oxygen saturation)
Bright room lighting
Electrical interference
Poorly adherent probe
Excessive motion of the sensor
B. Blood Pressure Monitoring

Although blood pressure is not a direct determinant of oxygen balance, an appropriate
driving pressure is necessary for oxygen delivery at the tissue level. Blood pressure is
determined by the cardiac output and systemic vascular resistance according to the
following relationship:
Blood Pressure = Cardiac Output × Systemic Vascular Resistance
Blood pressure may be monitored invasively or noninvasively.
1. Automated Noninvasive Devices
a. Principles
Automated blood pressure devices are frequently used to obtain intermittent blood
pressure measurements. These devices use one of several methods to measure systolic
and diastolic pressures, but the most common method is oscillometry. Systolic and
diastolic pressures and the mean arterial pressure are directly measured via
appearance, disappearance, and amplitude of oscillating waves. The arm is the
preferred measurement site in adults, but alternative sites include the calf, forearm, or
thigh, the latter being the least comfortable site for patients. The cuff should not be
placed on an extremity that is being used for intravenous infusion or in an area
susceptible to circulatory compromise. The appropriate cuff size is necessary for
accurate measurements. A cuff that is too large will underestimate the true blood
pressure, and a cuff that is too small yields artificially high measurements.
b. Clinical Issues
An adequate blood pressure measurement does not ensure adequate tissue perfusion.
Automated blood pressure devices are less accurate in clinical situations commonly
encountered with the critically ill patient, such as shock, vasoconstriction, mechanical
ventilation, and arrhythmias. Shivering, muscle contraction, and movement of the
extremity can lead to erroneous measurements. In such circumstances, repeat
measurement is advised when these conditions are not present. Blood pressure
monitoring via an arterial catheter is preferable to the use of an automated blood
pressure device in hemodynamically unstable patients.
2. Arterial Cannulation
a. Principles
An indwelling arterial catheter allows for continuous measurement of blood pressure,
pulse volume or pressure, and mean arterial pressure (Figure 6-5) by transduction of
pressure via a specialized monitoring setup. Pulse pressure is the difference between
the systolic and diastolic pressure measurements. It may also be used for arterial blood
gas measurement. The primary indications for insertion of an arterial cannula are the
need for frequent arterial samples and continuous assessment of arterial blood pressure.
Use of an arterial catheter should be considered for arterial blood sampling if more than
four samples are required in 24 hours. Arterial pressure monitoring may also be used
with minimally invasive hemodynamic monitoring systems to evaluate cardiac output,
stroke volume, or pulse pressure variation.
Figure 6-5. Appearance of Arterial Pressure Wave with Invasive Monitoring
When invasive monitoring is used, the calculation of the mean arterial pressure is based on the area under
the curve.
The most common insertion sites for arterial catheters are (in order of preference for
adults) the radial, femoral, axillary, and dorsalis pedis arteries. Brachial artery
cannulation is usually avoided if possible because it is an end artery and hand ischemia
is a potential complication. Shorter catheters are used for radial and dorsalis pedis
artery insertion and longer catheters for insertion in femoral and axillary sites. Preferred
sites have alternative collateral circulations. The choice of site is based on the presence
of palpable pulses, general hemodynamic state, and other anatomic or physiologic
factors unique to each patient.
The dorsalis pedis artery is less reliable

for pressure monitoring in adults
because of its size and distance from the
heart.
b. Clinical Issues
The arterial catheter is never used for infusion of any medications or fluids and must be
monitored continuously. Concern about the accuracy of the intra-arterial pressure
measurements should lead to a return-to-flow assessment with a manual blood pressure
cuff. Measurements should be made after calibration of the catheter/transducer system at
or near the level of the heart.
Several technical and anatomic factors may affect the accuracy of the pressures obtained
with the catheter system. Distortion of the arterial waveform signal may occur due to
vascular alterations, the hydraulic coupling system of the transducer, the calibration of
the transducer, or the maintenance of the pressurized system tubing. Inspection of the
result may show an overdamped and domed waveform or the high-spiking “overshoot or
ringing” pattern of the underdamped waveform. Both distortions have the greatest effect
on the systolic and diastolic pressures, whereas the mean arterial pressure is less
affected.
Pulse Pressure = Systolic Pressure –

Diastolic Pressure; Normal = 30-40 mm
Hg
As with noninvasive monitoring, intra-arterial blood pressure monitoring may not be a

sensitive indicator of hypoperfusion because of compensatory vasoconstriction.
Additional clinical information regarding volume status can be obtained by visual
inspection of the arterial blood pressure waveform in mechanically ventilated patients
(Figure 6-6). Positive pressure during inspiration may decrease the stroke volume in
patients with inadequate intravascular volume due to decreased venous return. The
decrease in stroke volume leads to a decreased pressure that is visually represented as
a systolic variation of blood pressure and a decrease in the pulse pressure. (See Section
F.)
Hypotension is not always associated

with the presence of shock or tissue
hypoperfusion.
Figure 6-6. Variation of Blood Pressure in a Mechanically Ventilated Patient with Hypovolemia
With positive pressure applied during inspiration, the decrease in systolic pressure is greater than the
decrease in diastolic pressure, resulting in a decrease in pulse pressure.
Possible complications associated with arterial catheter insertion are listed in Table 6-
3. These can be minimized by careful insertion technique, appropriate catheter size for
the artery, proper site care, and a continuous flush system. The arterial waveform must
be continuously monitored and displayed, with alarm settings to prevent inadvertent
blood loss through a catheter that is accidentally opened to the atmosphere. The
extremity with the arterial catheter should be inspected frequently for evidence of
ischemia or infection. Any sign of ischemia distal to the catheter or infection at the site
of insertion requires immediate removal of the catheter. Arterial catheters should be
removed as soon as possible to minimize the risk of infection.
Table 6-3 Possible Complications of Arterial Catheters
Hematoma formation
Blood loss
Arterial thrombosis
Proximal or distal embolization
Arterial pseudoaneurysm
Infection
Accidental administration of fluids or medications
C. Monitoring Right Ventricular Filling Pressures and ScVO2
A central venous catheter in the internal jugular or subclavian vein allows measurement
of CVP and ScvO2. Placement of a central venous catheter may be indicated for other
reasons as well (Table 6-4). Confirmation of catheter placement in the internal jugular
or subclavian vein and the tip in the superior vena cava by chest radiography is
recommended to ensure accurate measurements of CVP and ScvO2 and to detect
complications of the procedure.
Table 6-4
Common Indications for Central Venous Cannulation
Measurement of mean central venous pressure
Measurement of central venous oxygen saturation
Large-bore venous access
Difficult or long-term venous access
Administration of irritating drugs and/or parenteral nutrition
Hemodialysis
Placement of a temporary pacing wire
Placement of a pulmonary artery catheter
CVP, obtained from an appropriately positioned catheter, estimates the right ventricular
filling pressure as a reflection of preload (end-diastolic volume). Normal values for
CVP are 2 to 8 mm Hg, and measurements should be made at the end of expiration.
Significant variation of the CVP waveform may occur during spontaneous breathing and
mechanical ventilation, requiring visual assessment of the waveform to identify the end
of expiration (Figure 6-7). In general, a low CVP indicates a low intravascular volume
associated with a low preload. Normal or high CVP measurements must be evaluated
cautiously, as they may not predict adequate or increased preload volume due to
changes in intrathoracic pressures or ventricular compliance. Additional clinical
assessment, such as fluid responsiveness, is required to estimate adequacy of preload
with normal or elevated CVP measurements. Right ventricular preload estimates do not
necessarily correlate with left ventricular preload.
Figure 6-7. Typical Cyclic Pattern for CVP Waveform
Typical cyclic pattern for continuous venous pressure (CVP waveform that shows inspiration (I and
expiration (E. A, Respiratory variation during spontaneous ventilation: CVP decreases during spontaneous
inspiration as intrapleural pressure decreases. B, Respiratory variation during positive pressure mechanical
ventilation: CVP increases during delivery of the mechanical breath as positive pressure is transmitted from
the airway to the intrapleural space and great vessels. The vertical arrows denote the point of end-expiration
during spontaneous and mechanical ventilation
ScvO2 can be monitored intermittently by withdrawal of blood for analysis or
continuously with a catheter containing an oximeter to evaluate oxygen balance. Clinical
protocols have used ScvO2 measurements along with other parameters to determine
adequacy of resuscitation. Normal ScvO2 values are usually >65%.
D. Measuring Left Ventricular Filling Pressures

Left ventricular filling pressures are usually estimated from measurement of the
pulmonary artery occlusion pressure. A pulmonary artery catheter is necessary to obtain
this information but requires expertise in insertion, data collection, and data
interpretation. The clinician should consult with a critical care practitioner if invasive
monitoring with a pulmonary artery catheter is needed to obtain additional
hemodynamic information. Static single measurements of left ventricular filling pressure
can often be provided by echocardiography.
E. Measuring Cardiac Output

Cardiac output plays a key role in determining oxygen delivery to the tissues.
Measurement methods – such as thermodilution with a pulmonary artery catheter,
esophageal Doppler ultrasonography, and arterial waveform pulse pressure analysis –
require varying degrees of invasiveness as well as special expertise. In the absence of
direct measurement of cardiac output, less-specific indicators of tissue oxygenation,
such as lactate concentration and ScvO2, may guide specific interventions until critical
care expertise is available.
F. Monitoring Fluid Responsiveness

The practical question that clinicians often face in caring for critically ill patients is
whether further fluid administration will improve cardiac output and oxygen delivery.
This dilemma may not be adequately addressed by single measurements of heart rate,
CVP, or blood pressure.
Significant variation (greater than 10% to 15%) in the cardiac output, stroke volume,
systolic blood pressure, or pulse pressure in mechanically ventilated patients with
evidence of impaired oxygen delivery may suggest the need for additional fluids to
optimize cardiac output or the need to reduce intrathoracic pressures by decreasing tidal
volume or positive end-expiratory pressure. With each positive pressure breath from the
ventilator, venous return and right ventricular preload are decreased. If the right
ventricle is dependent on preload, then positive pressure breaths will result in a
decrease in the right ventricular stroke volume, leading to a decrease in left ventricular
preload and left ventricular stroke volume (cardiac output) [Figure 6-6]. A variety of
devices are available that can monitor variation in systolic blood pressure, pulse
pressure, and/or stroke volume. All have limitations in accuracy that must be
considered, such as adequate tidal volume, tachyarrhythmias, and adequate sedation.
Passive leg raising (PLR) is another technique that may be used at the bedside with
less-invasive monitoring techniques to determine if additional fluid is beneficial. This
maneuver is performed by placing the head of the bed flat from the semi-recumbent
position and then raising both legs simultaneously to a 45° angle (Figure 6-8). This
action results in a gravitational transfer of approximately 300 mL of blood from the
lower limbs and splanchnic compartment toward the right heart. No fluid is infused and
the clinical effects are completely reversible. If a significant increase in cardiac output
or stroke volume is noted within 30 to 60 seconds of PLR, the patient is determined to
be fluid responsive. PLR has been noted to be reliable in mechanically ventilated
patients and patients with spontaneous respiratory effort who are not mechanically
ventilated. If monitoring of cardiac output or stroke volume is not possible, a significant
increase in blood pressure after the passive leg raise suggests that cardiac output has
increased. No increase or an insignificant increase in blood pressure is less helpful in
this circumstance. PLR should not be performed in patients with increased intracranial
pressure and may not be reliable when intra-abdominal pressures are increased.
Figure 6-8. Effects of Passive Leg Raising
Fluid boluses may also be used to determine if a patient is fluid responsive. Boluses of
isotonic crystalloid (usually 250-500 mL) are administered over a short period (5-10
minutes) and subsequent cardiac output or stroke volume measurements are noted. If a
significant increase in cardiac output or stroke volume occurs following the bolus, the
patient is fluid responsive. This technique must be used carefully as additional fluid
may be detrimental to the patient’s cardiac or respiratory status.
V. ACID-BASE DISORDERS
Acid-base disorders are common in the critically ill patient, and assessment of acid-
base status may indicate specific diagnoses and/or therapeutic interventions. The
presence of a metabolic acidosis should suggest hypoperfusion and prompt further
assessment of the adequacy of the oxygen balance. An appropriate evaluation of acid-
base status requires accurate interpretation of simultaneous measurements of
electrolytes, albumin, and arterial blood gases, as well as knowledge of compensatory
physiologic responses. Appendix 5 includes acid-base case studies for practice in
analyzing arterial blood gas and electrolyte information and in determining appropriate
interventions.
A. Evaluation of Acid-Base Disorders

Analysis of acid-base disorders in seriously ill patients requires a systematic approach.
Although several methods can be utilized (base excess, strong ion difference), the
approach below relies on traditional analysis using formulas based on hydrogen ion and
bicarbonate (HCO3) concentrations that can be applied at the bedside.
1. Determine the overall acid-base condition by measuring pH. Is acidemia or

alkalemia present?
2. If an abnormality is present, determine if the primary process is metabolic (change
in [HCO3]) or respiratory (change in partial pressure of arterial carbon dioxide
[PaCO2]).
3. If a respiratory disturbance is present, determine if it is an acute or a chronic

process.
4. If a metabolic disturbance is present, determine if respiratory compensation is
adequate.
5. Always calculate the anion gap (AG).
B. Metabolic Acidosis
Metabolic acidosis results from an increase in endogenous acid production that
overwhelms renal excretion (eg, ketoacidosis, lactic acidosis), exogenous acid input
(eg, toxin ingestion), excessive loss of bicarbonate (eg, diarrhea), or decreased renal
excretion of endogenous acids (eg, renal failure). Compensation is achieved primarily
by increasing minute ventilation to eliminate CO2. The adequacy of respiratory
compensation can be estimated by the following formulas:
Appropriate PaCO2 = 1.5 × [HCO3] + 8 ± 2; or ΔPaCO2 = 1.2 × Δ[HCO3]

The lower limit of respiratory compensation is usually a PaCO2 of approximately 10 mm
Hg (1.3 kPa). This means the PaCO2 will not go lower than 10 mm Hg to compensate for
a metabolic acidosis.
Metabolic acidosis is further characterized by a normal or increased anion gap.
Normally, unmeasured anions exceed unmeasured cations, and the difference results in
the AG, which is estimated by the following formula:
AG = [Na] – ([Cl] + [HCO3])
The normal AG value is approximately 10 ± 4 mmol/L but the normal range varies by
laboratory. An increased AG indicates an increase in unmeasured anions and/or a
decrease in unmeasured cations. An increased AG has limitations as the sole indicator
of a metabolic acidosis. In patients with severe hypoalbuminemia, an AG acidosis can
exist even when a normal AG is measured. In such patients, the expected AG may be as
low as 4 to 5 mmol/L. For every albumin decrease of 1 g/dL, a decrease of 2.5 to 3
mmol in AG will occur. The corrected AG can be calculated using the following
formula:
AGcorrected = AGobserved + 2.5 x [normal albumin-measured albumin (in g/dL)]
Another exception can occur when an elevated AG does not reflect an underlying
acidosis. In patients with significant alkalemia (usually pH >7.5), albumin is more
negatively charged, which increases unmeasured anions.
An increased respiratory rate may be a

compensatory mechanism for metabolic
acidosis.
In seriously ill patients, the most common causes of metabolic acidosis with an
increased AG are lactic acidosis, renal failure, and diabetic ketoacidosis. Metabolic
acidosis with a normal AG, often called hyperchloremic acidosis, may result from
gastrointestinal or renal loss of HCO3 or volume resuscitation with normal saline.
C. Metabolic Alkalosis
Metabolic alkaloses are usually characterized as chloride-depleted (hypovolemic,
which is the most common type) and chloride-expanded (hypervolemic). Hypokalemia
is common to both types of metabolic alkalosis. Measurement of urine chloride is
helpful in distinguishing the two categories, with urine chloride <20 mmol/L in
chloride-depleted metabolic alkaloses and urine chloride >20 mmol/L in chloride-
expanded metabolic alkaloses. Diuretic therapy is a common cause of hypovolemic
metabolic alkalosis in hospitalized patients. Normal compensation for metabolic
alkalosis is hypoventilation, which is limited by hypoxemia as PaCO2 increases in
patients breathing spontaneously. PaCO2 may rise 6 to 7 mm Hg (0.8-0.9 kPa) for every
increase of 10 mmol/L in [HCO3]. Treatment includes volume replacement for chloride-
depleted states and assessment of the renal-adrenal axis for chloride-expanded
conditions. Potassium deficiencies should be corrected. Severe alkalemia is associated
with high mortality and requires aggressive treatment.
D. Respiratory Acidosis
Respiratory acidosis is most commonly due to ineffective alveolar ventilation. If the
respiratory acidosis is acute, the pH decreases by 0.08 units for each increase of 10 mm
Hg (1.3 kPa) in PaCO2. A very small increase in plasma [HCO3] can be seen acutely
because of titration of intracellular non-bicarbonate buffers. For each acute increase of
10 mm Hg (1.3 kPa) in PaCO2, the [HCO3] increases by 1 mmol/L to a maximum of 30 to
32 mmol/L. In chronic respiratory acidosis, the pH decreases 0.03 units and the [HCO3]
increases 3.5 mmol/L for each increase of 10 mm Hg (1.3 kPa) in PaCO2. The limit of
normal renal compensation in chronic respiratory acidosis is an [HCO3] of
approximately 45 mmol/L. Higher values suggest an associated metabolic alkalosis.
Treatment of respiratory acidosis involves the rapid identification of the etiology and
implementation of corrective action. In some circumstances, intubation and mechanical
ventilation may be necessary to support alveolar ventilation.
E. Respiratory Alkalosis
Respiratory alkalosis results from primary hyperventilation due to a variety of
etiologies. Acute pulmonary processes or an acidosis should be considered in the
seriously ill patient. Similar to changes noted in respiratory acidosis, pH increases 0.08
for every decrease of 10 mm Hg (1.3 kPa) in PaCO2 in acute respiratory alkalosis, and
pH increases 0.03 for each decrease of 10 mm Hg (1.3 kPa) in PaCO2 in chronic
respiratory alkalosis. The [HCO3] decreases 2 mmol/L in acute respiratory alkalosis
and 5 mmol/L in chronic respiratory alkalosis for each decrease of 10 mm Hg (1.3 kPa)
in PaCO2. Chronic respiratory alkalosis is unique among acid-base disorders in that pH
may return to normal if the condition is prolonged. Therapy is directed to the underlying
cause.
F. Complex Acid-Base Disorders

Simple acid-base disorders result from a single process such as metabolic alkalosis. In
many critically ill patients, multiple acid-base disturbances exist concurrently and result
in complex acid-base disorders. For example, sepsis often presents with respiratory
alkalosis and metabolic acidosis. A systematic approach to acid-base analysis is
needed to identify the ongoing disturbances and determine appropriate diagnoses and
interventions. Formulas that are helpful in evaluating acid-base status are listed in Table
6-5.
Table 6-5 Acid-Base Formulas

Acid-Base Disorder Equation
Respiratory Acidosis
Acute Decrease in pH = 0.08 × (PaCO2 – 40)
10
Increase in [HCO3 = ΔPaCO2 ± 3
10
Chronic Decrease in pH = 0.03 × (PaCO2 – 40)
10
Increase in [HCO3 = 3.5 × ΔPaCO2
10
Respiratory Alkalosis
Acute Increase in pH = 0.08 × (40 – PaCO2)
10
Decrease in [HCO3 = 2 × ΔPaCO2
10
Chronic Increase in pH = 0.03 × (40 – PaCO2)
10
Decrease in [HCO3 = 5 – 7 × ΔPaCO2
10
Metabolic Acidosis Anion Gap = [Na] – ([Cl] + [HCO3)
Expected PaCO2 = 1.5 × [HCO3 + 8 ± 2 or expected ∆PCO2 = 1.2 × ∆[HCO3
Metabolic Alkalosis Increase in PaCO2 = 0.6 – 0.7 × Δ[HCO3
Key Points
Monitoring Oxygen Balance and Acid-Base Status

Oxygen delivery is dependent on cardiac output (blood flow) and the oxygen
content of arterial blood.
Hemoglobin is the major contributor of oxygen for tissue demands.
Normal ventricular filling pressure measurements may not indicate adequate
preload volume.
Measurements of global oxygen balance that may be useful to monitor in the
seriously ill patient include central venous oxyhemoglobin saturation (ScvO2) and
lactate concentrations.
Low ScvO2 values suggest an oxygen imbalance that may be due to decreases in
cardiac output, hemoglobin concentrations, or arterial oxyhemoglobin saturation,
or increases in tissue oxygen consumption.
The pulse oximeter estimates arterial oxyhemoglobin saturation but does not reflect
adequacy of oxygen delivery.
Blood pressure monitoring via an arterial catheter is preferable to the use of an
automated blood pressure device in unstable patients.
Determination of systolic blood pressure, pulse pressure, or stroke volume
variation and fluid responsiveness using special monitoring devices may be helpful
in optimizing cardiac output and oxygen delivery.
Assessment of acid-base status may suggest specific diagnoses and/or therapeutic
interventions.
Suggested Readings
1. Gauthier PM, Szerlip HM. Metabolic acidosis in the intensive care unit. Crit Care
Clin. 2002;18:289-308.
2. Kellum JA. Disorders of acid-base balance. Crit Care Med. 2007;35:2630-2636.
3. Marx G, Reinhart K. Venous oximetry. Curr Opin Crit Care. 2006;12:263-268.
4. Whittier WL, Rutecki GW. Primer on clinical acid-base problem solving. Dis
Mon. 2004;50:122-162.
5. Mohammed I, Phillips C. Techniques for determining cardiac output in the
intensive care unit. Crit Care Clin. 2010;26:355-364.
6. Monnet X, Teboul J-L. Minimally invasive monitoring. Crit Care Clin.
2015;31:25-42.
7. Jubran A. Pulse oximetry. Crit Care. 2015;19:272.
8. Monnet X, Teboul J-L. Assessment of volume responsiveness during mechanical
ventilation: Recent advances. Crit Care. 2013;17:217.
9. Monnet X, Teboul J-L. Passive leg raising. Intensive Care Med. 2008;34:659-663.
10. Hartog C, Bloos F. Venous oxygen saturation. Best Prac Res Clin Anaesthesiol.
2014;28:4194-28.
11. Magder S. Central venous pressure: A useful but not so simple measurement. Crit
Care Med. 2006;34:2224-2227.
12. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med. 2014;371:2309-2319.
Suggested Website
1. Ortega R, Hansen CJ, Elterman K, et al. Videos in clinical medicine: Pulse

oximetry. N Engl J Med. 2011;364:e33. http://www.nejm.org/multimedia/medical-
videos.
Chapter 7
DIAGNOSIS AND M ANAGEMENT OF SHOCK
Objectives
Identify the four main categories of shock.

Discuss the goals of resuscitation in shock.
Summarize the general principles of shock management.
Describe the physiologic effects of vasoactive and inotropic agents.
Discuss the diagnosis and management of oliguria and acute kidney injury.
Case Study
A 54-year-old man was admitted to the floor with an edematous and erythematous right
lower extremity. Purulent drainage is seen. Vital signs include a temperature 39.0°C
(102.2°F), heart rate of 140 beats/min, respiratory rate 26 breaths/min, and blood
pressure of 110/58 mm Hg.
– What information is needed to determine if this patient has shock?
– What initial interventions are needed to stabilize the patient?
I. INTRODUCTION
Shock is a syndrome of impaired tissue oxygenation and perfusion caused by many
different etiologies. Prompt recognition of shock and early, effective intervention are
needed to prevent irreversible injury, organ dysfunction, and death. Inadequate tissue
oxygenation and perfusion may result from one or more of the following mechanisms:
An absolute or relative decrease in systemic oxygen delivery (inadequate cardiac

output, low blood oxygen content)
Ineffective tissue perfusion (maldistribution of blood flow to tissues or inadequate
perfusion pressure)
Impaired utilization of delivered oxygen (cellular or mitochondrial dysfunction)
Shock results when the oxygen balance is disturbed and demand exceeds supply. Shock
is not defined by the presence of hypotension, although hypotension is frequently
associated with shock. In some patients with shock, the blood pressure initially may be
normal even though it has significantly dropped from baseline, or it may be preserved
due to compensatory sympathetic responses. Management of shock should be directed
toward correcting tissue oxygenation and hypoperfusion as the primary end points.
II. CLINICAL ALTERATIONS IN SHOCK

The presentation of patients with shock may be subtle (eg, mild confusion, sinus
tachycardia) or easily identifiable (profound hypotension, anuria). Shock may be the
initial manifestation of an underlying condition, or it may develop as the condition
progresses. A strong index of suspicion and vigilant clinical assessment and monitoring
are needed to identify the early signs and initiate appropriate treatment. The clinical
manifestations of shock result from inadequate tissue oxygenation and perfusion,
compensatory responses, and the specific etiology of shock. Hypoperfusion may cause
hypotension, altered mental status, oliguria/anuria, and other organ dysfunction. In
addition, hypoperfusion is associated with some degree of inflammatory response that
may contribute to organ injury. Direct and indirect effects of hypoperfusion may be
reflected in laboratory findings of abnormal oxygenation, blood urea nitrogen,
creatinine, bilirubin, hepatic transaminases, and coagulation parameters. An anion gap
metabolic acidosis is a common finding of hypoperfusion and is often associated with
an elevated lactate concentration. Although neither sensitive nor specific for the
diagnosis of shock, the lactate concentration is an indicator of global oxygen balance
and hypoperfusion and is a useful monitoring tool for assessment of therapeutic
interventions (See Chapter 6).
Compensatory mechanisms in shock involve complex neuroendocrine responses that
attempt to increase tissue perfusion and oxygenation. In many forms of shock,
sympathetic vasoconstriction redirects blood flow from low-oxygen-requiring organs
(eg, skin) toward oxygen-dependent organs (eg, brain and heart). Compensatory
vasoconstriction can maintain blood pressure early in shock and lead to an increase in
the diastolic pressure and a narrowing of the pulse pressure. Intense vasoconstriction
correlates with cold, clammy extremities and contributes to organ hypoperfusion.
Hypothermia also may be a manifestation of severe vasoconstriction. Patients with
distributive shock (see below) often have vasodilation and warm extremities, but other
signs of hypoperfusion are usually present. Tachycardia, mediated by the sympathetic
response, reflects an attempt to increase cardiac output in shock. Tachypnea may be a
compensatory response to metabolic acidosis, a response to lung injury, or a reaction to
direct stimulation of the respiratory center.
The increased systemic vascular

resistance present in cardiogenic,
hemorrhagic, and obstructive shock is
the body’s attempt to maintain blood
pressure (perfusion pressure).
Additional changes in shock alter oxygenation at the tissue level. As discussed in

Chapter 6, hemoglobin releases more oxygen as it traverses the capillaries in order to
meet tissue demands. A rightward shift of the oxyhemoglobin saturation curve due to
acidosis or increased temperature facilitates release of hemoglobin-bound oxygen. The
greater extraction of oxygen is reflected in lower mixed venous oxyhemoglobin
saturation (SVO2) or central venous oxyhemoglobin saturation (ScvO2) measurements in
many forms of shock (Chapter 6). However, a normal value for either of these
measurements does not imply that tissue oxygenation is adequate, because some forms
of shock (eg, septic shock) may lead to impaired tissue or cellular utilization of oxygen
or result in maldistribution of blood flow.
III. CLASSIFICATION OF SHOCK

There are four main categories of shock based on cardiovascular characteristics:
hypovolemic, distributive, cardiogenic, and obstructive (Table 7-1). A careful history
and a physical examination often provide information that is helpful in determining the
likely cause of shock. However, many patients will have components of more than one
type (mixed shock). Septic shock is a form of distributive shock, but it may have a
hypovolemic component before fluid resuscitation. Likewise, myocardial dysfunction
may be present in septic shock and hypovolemic shock.
Table 7-1 Classification of Shock
Hypovolemic Cardiogenic
Hemorrhagic Myopathic (ie, ischemic)
Nonhemorrhagic Mechanical (ie, valvular)
Arrhythmic
Distributive Obstructive
Septic Massive pulmonary embolism
Adrenal crisis Tension pneumothorax
Neurogenic (upper spinal Cardiac tamponade
cord injury)
Constrictive pericarditis
Anaphylactic
Knowledge of the expected hemodynamic profiles associated with different types of

shock is helpful in determining appropriate therapy, even when specific measurements
are not available. Table 7-2 presents the usual hemodynamic profiles for more common
forms of shock, but variations occur depending on the patient’s specific etiology,
cardiac function, and resuscitation status.
Table 7-2 Hemodynamic Profiles of Shock
Type of Heart Cardiac Ventricular Filling Systemic Vascular Pulse SVO2 or

Shock Rate Output Pressures Resistance Pressure Scv O2
Cardiogenic ↑ ↓ ↑ ↑ ↓ ↓
Hypovolemic ↑ ↓ ↓ ↑ ↓ ↓
Distributive ↑ ↑ or Na ↓ ↓ ↑ ↑ or Na
Obstructive ↑ ↓ ↑ or Nb ↑ ↓ ↓
Abbreviations: SVO2, mixed venous oxyhemoglobin saturation; ScvO2, central venous oxyhemoglobin
saturation; N, normal
aMay be decreased before or early in resuscitation.
bLeft ventricular filling pressures may be normal or low in massive pulmonary embolism.
A. Hypovolemic Shock
Hypovolemic shock occurs when intravascular volume is depleted relative to the
vascular capacity as a result of hemorrhage, gastrointestinal or urinary fluid losses,
dehydration, or third-space fluid losses. Third-space fluid losses resulting from
interstitial fluid redistribution may be prominent in burn injury, trauma, pancreatitis, and
any severe form of shock. The hemodynamic findings in hypovolemic shock are
decreased cardiac output, decreased right and left ventricular filling pressures
(preload), and an increased afterload (systemic vascular resistance [SVR]) due to
compensatory vasoconstriction. The SVO2 or ScvO2 is decreased as a result of decreased
cardiac output with unchanged or increased tissue oxygen demands and potentially
decreased hemoglobin concentration (hemorrhage). In addition to the usual clinical
findings, patients with hypovolemic shock have flat, nondistended jugular veins.
B. Distributive Shock
Distributive shock is characterized by loss of peripheral vascular tone (vasodilation).
However, these patients often have components of hypovolemic shock and cardiogenic
shock. The most common form of distributive shock is septic shock, with neurogenic
shock and anaphylactic shock being much less common. The hemodynamic profile
usually includes a normal or increased cardiac output with a low SVR and low to
normal ventricular filling pressures. A decreased cardiac output may result if
intravascular volume is not optimized. ScvO2 or SVO2 may be normal or increased due to
shunting of blood in the microvasculature or the inability of tissue to utilize oxygen (as
in sepsis). In contrast to other forms of shock, the vasodilation of fluid-resuscitated
distributive shock results in warm extremities, decreased diastolic pressure, and
increased pulse pressure. Neurogenic shock due to cervical or upper thoracic spinal
cord dysfunction or injury may be associated with bradycardia rather than tachycardia.
Fever may be present in septic shock and adrenal crisis.
Anterior myocardial infarctions are

more likely to lead to cardiogenic shock.
C. Cardiogenic Shock
In cardiogenic shock, forward blood flow is inadequate because of cardiac pump
failure due to loss of functional myocardium (ischemia, cardiomyopathy), a mechanical
or structural defect (valvular failure, septal defect), or arrhythmias. Most commonly,
cardiogenic shock results from acute myocardial infarction or a subsequent
complication. Cardiogenic shock is the most severe form of heart failure and is
distinguished from less severe chronic heart failure by the presence of hypoperfusion,
hypotension, and the need for different therapeutic interventions (Chapter 10). The
typical hemodynamic characteristics are decreased cardiac output, elevated ventricular
filling pressures, and increased afterload (SVR). When cardiac output is low, the SVO2
or ScvO2 declines due to decreased oxygen delivery and increased extraction of oxygen
from the hemoglobin at tissue level. Clinical manifestations associated with cardiogenic
shock may include distended jugular veins, pulmonary edema, and S3 gallop.
D. Obstructive Shock
The common features in obstructive shock are obstruction of flow due to impaired
cardiac filling and excessive afterload. Cardiac tamponade impairs diastolic filling of
the right ventricle, while tension pneumothorax limits right ventricular filling by
obstruction of venous return. Massive pulmonary emboli increase right ventricular
afterload. The hemodynamic profile is characterized by decreased cardiac output,
increased afterload, and variable left ventricular filling pressures, depending on the
etiology. In cardiac tamponade, the pressures of the right heart chambers, the pulmonary
artery, and the left heart chambers equilibrate in diastole. A drop of >10 mm Hg in
systolic blood pressure during inspiration (pulsus paradoxus) is an important clinical
finding in patients with suspected cardiac tamponade. Distended jugular veins may be
seen, depending on the time course of development and intravascular volume status.
IV. GENERAL PRINCIPLES OF SHOCK MANAGEMENT
Restoration of hemodynamic stability

should be a priority while efforts to treat
the cause of shock are implemented.
The overall goal of shock management is to improve oxygen delivery or utilization in

order to prevent cellular and organ injury. Effective therapy requires treatment of the
underlying etiology, restoration of adequate perfusion, monitoring, and comprehensive
supportive care. Interventions to restore perfusion center on achieving an adequate
blood pressure, increasing cardiac output, and/or optimizing the oxygen content of
blood. Oxygen demand should also be decreased when possible. These goals are
usually accomplished with a combination of interventions, as summarized in Table 7-3
and Figure 7-1.
Table 7-3 Interventions for Managing Shock
Component Intervention
Blood pressure Fluids, vasopressor or vasodilator agents a
Cardiac Output
Preload Fluids, vasodilator agents a
Contractility Inotropic agents
Afterload Vasopressor or vasodilator agents a
Oxygen Content
Hemoglobin Blood transfusion
Hemoglobin saturation Supplemental oxygen, mechanical ventilation
Oxygen demand Mechanical ventilation, sedation, analgesia, antipyretics
aVasodilator agents are used only when blood pressure is adequate.
Figure 7-1. Approach to the Patient With Shock

Key aspects of initial shock management include a blood pressure goal, with titration of fluids and
vasoactive drugs to assure adequate intravascular volume and mean arterial pressure >65 mm Hg. After
these initial objectives are achieved, oxygen delivery and organ perfusion may be assessed by using such
monitors as lactate levels, central venous oxygen saturation (SCVO2, urine output and evidence of end
organ performance. Fluid responsiveness may be determined by invasive hemodynamic monitoring
systems or simple tests such as straight leg raising.
The first goal in treating hypotensive shock is to achieve a minimum blood pressure
(driving pressure). This is needed to maintain blood flow to the heart and other organs
while optimizing other components of oxygen delivery. A mean arterial pressure (MAP)
≥65 mm Hg is usually recommended as an initial goal. A higher MAP may be needed in
patients with myocardial ischemia or chronic hypertension, but an increase in blood
pressure is beneficial only if it translates into improved perfusion. Otherwise, higher
blood pressures may increase myocardial oxygen demands. Following initial
resuscitation, the MAP goal should be individualized based on further assessment of the
adequacy of systemic and organ perfusion. A blood pressure goal is usually achieved
with fluids and/or vasoactive agents (see below).
Many patients with shock require

intubation.
The next goal in the management of shock is to optimize oxygen delivery. As outlined in
Chapter 6, this can be enhanced by increasing cardiac output, hemoglobin
concentration, or oxyhemoglobin saturation. In the absence of specific measurement of
cardiac output or stroke volume, an assessment of adequacy depends on the etiology of
shock and the presence of hypoperfusion abnormalities (see below). Fluids and/or
vasoactive agents are often needed to optimize cardiac output. The determinants of the
oxygen content of blood (hemoglobin and oxyhemoglobin saturation) can be easily
measured and optimized when indicated. Increasing the hemoglobin concentration by
transfusion may be one of the most efficient ways of improving oxygen delivery in some
patients. For example, increasing the hemoglobin concentration from 7 g/dL to 9 g/dL
increases oxygen delivery by almost 30%, even if cardiac output remains constant. The
oxyhemoglobin saturation can be increased by raising the partial pressure of arterial
oxygen with oxygen supplementation and mechanical ventilation. However, once the
partial pressure of arterial oxygen has been increased to a range of 60 to 70 mm Hg (8-
9.3 kPa), little additional benefit is gained by increasing it further. An oxyhemoglobin
saturation ≥95% is recommended in patients with shock.
A. Monitoring
Patients with shock require monitoring to determine appropriate interventions and
assess response to interventions (Chapter 6). Continuous electrocardiographic
monitoring is needed to assess changes in heart rate and rhythm. Blood pressure is best
monitored with an arterial catheter due to the inaccuracies of noninvasive devices in
patients with shock. Pulse oximetry should be monitored routinely to ensure adequate
oxyhemoglobin saturation. A low central venous pressure in the appropriate clinical
situation may suggest inadequate intravascular volume. Measurement of ScvO2 via a
central venous catheter may be useful as an indicator of oxygen balance, but a normal
ScvO2 value does not rule out hypoperfusion. A urinary catheter should be inserted to
monitor urine output as an indicator of renal perfusion, with a suggested goal of 0.5 to 1
mL/kg/h. Lactate concentrations and acid-base status should be assessed initially and at
appropriate intervals. Normal or decreasing lactate concentrations or improving
acidosis suggest improved oxygen balance. Other laboratory data should be considered
to assess progression or improvement of organ dysfunction.
The trend of measurements over time,

especially in response to interventions,
is often more valuable than a single
measurement.
B. Fluid Therapy
The initial therapy for most forms of shock is expansion of intravascular volume.
Physical examination may provide valuable information about the intravascular volume
status. Diffuse or dependent crackles, as well as distended neck veins, suggest high
ventricular filling pressures, unless acute respiratory distress syndrome or diffuse
pneumonia is present (or other causes of increased pulmonary pressure). Clear lung
fields and flat neck veins suggest inadequate preload in the hypotensive patient. While
orthostatic changes in blood pressure and heart rate may be helpful in determining the
degree of volume depletion, the tachycardic hypotensive patient should not be subjected
to these positional changes. The nature and degree of fluid deficits should be determined
to identify the type and appropriate quantity of fluid replacement. Monitoring of fluid
responsiveness, as described in Chapter 6, may be helpful in determining the
appropriate volume of fluids.
Intravascular volume deficiency in the patient who is not anemic may be replenished
with either crystalloid or colloid solutions. Crystalloids are less expensive than
colloids and typically accomplish the same goals, although a higher total volume is
needed due to their higher volume of distribution. Isotonic rather than hypotonic
crystalloid solutions, such as lactated Ringer solution or normal saline, should be used
for volume resuscitation. Dextrose 5% in water offers little expansion of intravascular
volume since it is quickly distributed throughout body fluid compartments and should
not be used to treat hypovolemic shock. For the same reasons, 0.45% saline is not
appropriate for volume expansion. Colloid solutions include hetastarch, albumin, and
gelatins. Use of albumin is limited by cost in some areas. Hetastarch use has been
associated with an increased risk of renal injury in septic shock. Crystalloid in titrated
boluses of 500 to 1000 mL (10-20 mL/kg) or colloid in titrated boluses of 250 to 500
mL may be given initially to most adult patients and repeated as necessary while
appropriate parameters are closely monitored. Smaller bolus amounts are indicated for
patients with suspected or known cardiogenic shock.
In addition to crystalloid or colloid solutions, packed red blood cells are indicated to
increase oxygen-carrying capacity in the patient with significant bleeding or anemia. In
many critically ill patients, a hemoglobin concentration of 7 to 9 g/dL may be adequate
after stabilization. Fresh frozen plasma should be used only for correction of a
coagulopathy and not for volume replacement. Priorities in the administration of fluids
are resuscitation and then replacement of ongoing losses. As the clinical course
continues, the solution that most closely approximates the patient’s losses should be
used, with serum electrolytes guiding therapy.
The first goal in fluid resuscitation is correction of hypovolemia. Often, this correction
manifests clinically as resolution of tachycardia, hypotension, or oliguria. However,
these end points may remain altered despite euvolemia in states such as septic
(distributive), neurogenic, or obstructive shock. Vasoactive drug support is indicated in
patients who continue to have a low blood pressure or impaired cardiac output after
euvolemia has been established, or who no longer have a beneficial response to fluid
challenge or passive leg raising. The potential deleterious effects of overly aggressive
fluid resuscitation include deterioration of oxygenation due to pulmonary edema, ileus
or bowel edema, and compartment syndromes. Therefore, frequent auscultation of the
chest for the presence of crackles, and monitoring of partial pressure of arterial oxygen
or oxyhemoglobin saturation by pulse oximetry, should be performed during fluid
resuscitation. Intra-abdominal pressure monitoring should be considered in patients
requiring massive fluid resuscitation (Chapter 13). In the absence of advanced
hemodynamic monitoring, volume therapy should be administered carefully in patients
with persistent hypotension and/or hypoperfusion until no further change is noted in the
blood pressure following a fluid bolus. This suggests that additional fluid no longer
improves the patient’s cardiac output and administration of more fluid can lead to the
deleterious effects noted. Further correction of hypotension or other perfusion
abnormalities may require pharmacologic support with vasoactive drugs. This approach
to volume therapy presents minimal risk in patients with adequate oxygenation.
No one vasoactive agent or combination

of agents has been demonstrated to be
superior in managing shock.
C. Vasoactive Agents
Vasoactive agents for the acute management of shock include medications with
vasopressor, inotropic, and vasodilator effects. A vasopressor is a medication that
results in arteriolar constriction, a rise in systemic vascular resistance, and a rise in
arteriolar blood pressure. An inotrope is a medication that augments cardiac
contractility. Many agents have more than one hemodynamic effect, and results may vary
among individual patients and with dosage. The goals of resuscitation are usually more
important than the specific agent chosen. Table 7-4 summarizes each vasoactive drug
and its mechanism of action. An intensivist should be consulted when the decision to use
vasoactive medications is made.
Table 7.4 Vasoactive Agents

DA-R (↑UOP) β1a (↑ HR) β2b (↓BP) α1c (↑ BP)
Dopamine 1-20 1-5 µg/kg/min 6-10 µg/kg/min >10 µg/kg/min

µg/kg/min
Phenylephrine 1-300 +++
µg/min
Norepinephrine 0.01-0.5 + ++++
µg/kg/min
Epinephrine 0.01-0.5 ++++ +++ ++++
µg/kg/min
Dobutamine (1-20 +++ ++
µg/kg/min)
Milrinoned (0.125-0.5 +++ +++
µg/kg/min)
Abbreviations: DA-R, dopamine receptor; UOP, urine output; HR, heart rate; BP, blood pressure
Potency scale is from 1+ to 4+
aβ = adrenergic receptor that increases cardiac contractility and/or heart rate
1
bβ = adrenergic receptor that mediates bronchodilation and arteriole dilation
2
cα = adrenergic receptor that mediates arteriole constriction and increase in peripheral vascular resistance
1
dMilrinone is a phosphodiesterase inhibitor with indirect β and β effects.
1 2
1. Norepinephrine
Norepinephrine is the initial vasoactive drug recommended in the treatment of septic
shock. It is a potent α-adrenergic vasoconstrictor with greater potency than either
dopamine or phenylephrine, and it also has β1-mediated inotropic and chronotropic
effects. In adults, the infusion rate of norepinephrine starts at 0.05 μg/kg/min and is
titrated to desired effects. As with other vasoconstrictors, cardiac output may decrease
as afterload and blood pressure are increased. Norepinephrine usually increases renal
blood flow in patients with adequate volume resuscitation. An increase in heart rate is
uncommon with use of norepinephrine.
2. Dopamine
Dopamine is a less frequently used vasoactive agent with dose-dependent inotropic and
vasopressor effects. It is no longer a drug of choice in the treatment of septic shock.
Although dose response varies greatly among patients, some generalizations about dose
and anticipated effect may be helpful. At low rates of infusion (1-5 µg/kg/min),
dopamine has modest inotropic and chronotropic effects. In this dose range, it acts on
the dopaminergic receptors in the kidney and may increase urine output; however, its
use for renal effects is not recommended because it does not prevent renal dysfunction
or improve outcomes. At intermediate rates of infusion (6-10 μg/kg/min), dopamine has
primarily inotropic effects. At higher infusion rates (≥10 μg/kg/min), it has significant
α-agonist effects that produce dose-related vasoconstriction. At infusion rates ≥20
μg/kg/min, dopamine usually offers no advantage over norepinephrine, which may have
greater vasopressor effect. Potential adverse effects include arrhythmias (particularly
atrial fibrillation) and tachycardia.
3. Epinephrine
Epinephrine has both α-adrenergic and β-adrenergic effects, potent inotropic and
chronotropic effects, and at higher doses, vasopressor effects. Doses start at 0.05
μg/kg/min and can be titrated as desired. The epinephrine-induced increase in
myocardial oxygen consumption may limit the use of this agent in adults, especially in
the presence of coronary artery disease. Epinephrine can also increase aerobic lactate
production rather than hypoperfusion-induced anaerobic lactate production.
4. Phenylephrine
Phenylephrine is a pure α-adrenergic vasoconstrictor. In adults, the infusion rate starts at
25 μg/min and can be titrated to the desired blood pressure. Because its mechanism of
action involves solely arterial constriction, it is most useful in states with arterial
dilation without concomitant cardiac depression, such as neurogenic shock or
hypotension caused by an epidural anesthetic.
5. Vasopressin
Vasopressin is a potent vasopressor that acts through V1 receptors to produce
vasoconstriction. As blood pressure is increased, cardiac output may decrease, similar
to the effect of norepinephrine. The recommended dose in adults is 0.01 to 0.04
units/min. Higher doses may lead to ischemic events. Vasopressin may be considered
for use in hypotensive shock refractory to other agents and fluid resuscitation, but it has
not been found to improve mortality. Further studies are needed to define the role of
vasopressin in the management of shock.
6. Dobutamine
Dobutamine is a non-selective β-adrenergic agonist with inotropic effects. It is used in
doses of 5 to 20 μg/kg/min and is usually associated with an increase in cardiac output,
which is mediated mostly by an increase in stroke volume. Arterial blood pressure may
remain unchanged, decrease, or increase slightly. Dobutamine must be introduced with
care in the hypotensive patient; in the face of inadequate intravascular volume
replacement, blood pressure can drop precipitously, and tachycardia may be
problematic. This agent has variable chronotropic effects.
7. Milrinone
Milrinone is a phosphodiesterase inhibitor that inhibits the breakdown of cyclic
adenosine monophosphate, the second messenger for catecholamines. Therefore,
milrinone is a sympathomimetic agent with mostly β-adrenergic-like effects. It will
increase cardiac output mostly by increasing stroke volume and will decrease afterload
by causing arteriolar dilation. It should be used with caution in hypovolemic patients
because it can cause significant hypotension.
D. End Points of Resuscitation

No one end point can be used to assess resolution of shock and return to normal
homeostasis. Furthermore, fluid and pharmacologic therapy should be titrated based on
the trend for the particular end point rather than its absolute value.
Blood pressure, pulse, and urine output are the most commonly used end points in
resuscitation of shock. All parameters can be easily measured but lack sensitivity and
specificity for either detection of impending shock or its resolution. As such, they may
be normal if the patient is in a state of compensated shock, and they may remain
abnormal despite appropriate therapy (eg, low blood pressure and urine output despite
reaching a euvolemic state). Similarly, urine output may not be a reliable end point in
patients with preexisting or new renal dysfunction.
In addition to the clinical evaluation of vital signs and urine output, monitoring
techniques that assess cardiac output or stroke volume may be helpful in determining
when fluid resuscitation is optimized as an end point (Chapter 6, Monitoring Fluid
Responsiveness). More invasive and complex monitoring techniques and measurements,
such as pulmonary artery catheters, require special expertise to obtain, interpret, and
apply results. ScvO2 and lactate concentrations as measurements of global oxygen
balance may also be useful in monitoring the patient in shock and assessing the impact
of interventions. Neither measurement assesses the need for fluid versus pharmacologic
support of the circulation. Normalization of organ function as assessed by laboratory
values (such as renal or liver chemistries) is another end point to assess, but these
measurements are not usually helpful in the first 24 hours.
V. MANAGEMENT OF SPECIFIC TYPES OF SHOCK
A. Hypovolemic Shock
The treatment goals in hypovolemic shock are restoration of intravascular volume and
prevention of further volume loss. Therapy for hypovolemic shock should be targeted to
reestablish normal blood pressure, pulse, and organ perfusion. For initial resuscitation,
either colloid or crystalloid fluids are effective if given in sufficient volume.
Subsequently, the fluid that is used should replace the fluid that has been lost. For
example, blood products may be needed to replace blood loss (Chapter 9), and
crystalloid should be used for vomiting and dehydration. For hypotension, the
crystalloid of choice is normal saline or lactated Ringer solution because of the
osmolality needed to restore intravascular volume. In large volume resuscitation,
however, normal saline infusion may produce hyperchloremic metabolic acidosis.
Vasoactive medications should be considered only as a temporizing measure while fluid
resuscitation is ongoing or when hypotension persists despite adequate volume
resuscitation. Central venous pressure monitoring may help to guide fluid resuscitation
in patients without significant heart or lung disease.
B. Distributive Shock
The initial approach to the patient with septic shock is restoration and maintenance of
adequate intravascular volume. Obtaining cultures and prompt administration of
appropriate antibiotics are essential, as are other interventions to control the infection
(removal of catheter, surgery, drainage, debridement). Lactate concentration should be
measured and repeated if abnormal as one component of assessing the resuscitation
efforts. Hypotension and lactate ≥4 mmol/L identify more severely ill patients with
greater risk of dying.
Volume expansion can be initiated with isotonic crystalloid solutions. Vasodilation and
diffuse capillary leakage are common in septic shock, and fluid requirements may be
large. Colloid solutions can be considered along with crystalloids initially for patients
with severe hypotension or those who require substantial amounts of crystalloids. If the
patient with septic shock remains hypotensive despite adequate fluid resuscitation,
norepinephrine is recommended as the initial vasoactive drug. Epinephrine can be
considered for patients who fail to respond adequately to norepinephrine, but no agent
has been shown to improve survival. Dobutamine may be considered in those with
adequate blood pressure who have hypoperfusion and evidence of low cardiac output
with adequate preload. Reversible myocardial dysfunction with ventricular dilation and
decrease in ejection fraction frequently occurs in shock, especially septic shock. An
initial MAP <65 mm Hg may require initiation of vasoactive pharmacologic therapy
until fluid resuscitation is optimized. Corticosteroids (hydrocortisone 200 mg in 24
hours administered in divided doses or continuous infusion) may be considered in
patients with septic shock when adequate fluids and vasoactive medications fail to
restore hemodynamic stability. Anaphylactic shock is treated with volume resuscitation
and subcutaneous epinephrine. In circumstances of very low blood pressure and poor
peripheral perfusion, titrated intravenous epinephrine is indicated. Acute adrenal
insufficiency is treated with volume therapy, intravenous corticosteroids, and
vasoactive medications, if needed (Chapter 12). Chapter 8 contains information about
the management of neurogenic shock.
Afterload and preload reduction should

be avoided in cardiac failure when
hypotension is present.
C. Cardiogenic Shock
The primary goal in treating cardiogenic shock is to improve myocardial function.
Arrhythmias should be treated promptly. Reperfusion by percutaneous intervention is the
treatment of choice in cardiogenic shock due to myocardial ischemia (Chapter 10).
Diastolic dysfunction during myocardial ischemia may decrease ventricular compliance
and elevate the left ventricular filling pressures, falsely indicating adequate preload.
Therefore, a cautious trial of fluid administration may be warranted (250-mL bolus
amounts). When blood pressure is decreased in cardiogenic shock, initial therapy with a
single agent that has inotropic and vasopressor effects (eg, norepinephrine or dopamine)
is indicated. Severely hypotensive patients (systolic arterial pressure <70 mm Hg)
should be treated with norepinephrine to rapidly raise the systolic arterial pressure. The
addition of an intravenous inotrope, such as milrinone or dobutamine (or dopexamine,
which is available in some countries), may be considered to augment myocardial
contractility after blood pressure stabilizes, with the goal of decreasing vasopressor
therapy. If moderate hypotension is not responsive to initial therapy, consultation should
be sought for potential interventions such as intra-aortic balloon counterpulsation or
left/right ventricular assist devices.
The elevated afterload (SVR) may also impair cardiac output if it is a primary
hemodynamic alteration, as occurs in chronic congestive heart failure. Often in acute
cardiogenic shock, the SVR is secondarily elevated to maintain vascular perfusion
pressure. Treatment aimed primarily at reducing afterload with a vasodilator should be
initiated very cautiously and only in patients with hypoperfusion accompanied by
adequate blood pressure.
When cardiac failure is characterized by low cardiac output, normal or elevated blood
pressure, and hypoxemia due to high pulmonary capillary pressure, reduction of preload
and afterload is helpful in improving hypoxemia. High pulmonary capillary pressure can
be diagnosed clinically. Preload reduction is accomplished with loop diuretics
(furosemide or bumetanide) and venodilators (nitroglycerin and morphine), whereas
afterload reduction is accomplished with arterial vasodilators (angiotensin-converting
enzyme inhibitors or, occasionally, nitroprusside). If the blood pressure can be
increased to normal levels with inotropes, then the cautious addition of afterload and
preload reduction is feasible in the presence of low cardiac output or high pulmonary
capillary pressure.
D. Obstructive Shock
In the patient with obstructive shock, relief of obstruction is the treatment of choice.
Additionally, maintenance of intravascular volume is vitally important. Fluid
resuscitation may improve the patient’s cardiac output and hypotension temporarily.
Inotropes or vasopressors have a minimal role in the management of obstructive shock,
and these agents provide only temporary improvement, if any. Massive pulmonary
embolus is a common cause of obstructive shock. Treatment is centered on fluid
resuscitation to maintain cardiac output and prompt anticoagulation to prevent clot
propagation (Chapter 13). Thrombolytic therapy or thrombectomy is needed in rare
cases of refractory cardiac collapse. If cardiac tamponade is present, pericardiocentesis
may be lifesaving. Tension pneumothorax must be treated promptly by needle
decompression and subsequent tube thoracostomy.
Diuretics and venodilators should be

avoided in obstructive shock.
VI. OLIGURIA AND ACUTE KIDNEY INJURY

The kidneys are frequently affected by impaired oxygen balance and perfusion in all
forms of shock. Oliguria, defined as urine output <0.5 mL/kg/h in adults, is an important
manifestation of hypoperfusion or decreased glomerular filtration rate. Oliguria may be
an earlier indicator of renal dysfunction than changes in laboratory parameters.
Persistence of oliguria for at least 6 hours is one criterion for acute kidney injury (AKI).
Hypoperfusion may also result in an increase of serum creatinine and blood urea
nitrogen, which are the most common measures of renal function. Acute changes in
serum creatinine and urine output are used to define AKI and classify severity across a
broad range of renal dysfunction. A key point is that small alterations in creatinine (even
a serum creatinine increase of 0.3 mg/dL [26.5 μmol/L] within 48 hours) or urine output
predict an increased risk of renal failure and require further evaluation. Along with
other parameters mentioned previously, resolution of oliguria may be considered a goal
of resuscitation in shock. Oliguria also may be due to inherent renal injury or postrenal
obstruction, in which case urine output cannot be used as a goal of adequate
resuscitation. Causes of oliguria and AKI are categorized as prerenal, renal, and
postrenal, as outlined in Table 7-5.
Table 7-5 Differential Diagnosis of Oliguria and Acute Kidney Injury

Prerenal
Decreased cardiac output (eg, volume depletion, cardiac failure,
tamponade)
Redistribution of blood flow (distributive shock) with peripheral vasodilation
and/or shunting
Renal
Glomerular disease (glomerulonephritis)
Vascular disease (eg, vasculitis)
Interstitial disease (eg, antibiotics)
Renal tubular disease
Ischemia
Nephrotoxic drugs
Postrenal (Obstructive)
Bilateral ureteral obstruction
Urethral stricture
Bladder outlet obstruction
Urinary catheter obstruction
aFractional excretion of sodium = ([urine sodium ÷ serum sodium] ÷ [urine creatinine ÷ serum creatinine]) ×
100.
Additional laboratory tests may help differentiate prerenal causes of oliguria and AKI
from other etiologies. Some laboratory tests of renal function are shown in Table 7-6.
Laboratory Tests to Distinguish Prerenal Conditions from Acute

Table 7-6
Tubular Necrosis
Laboratory Tests Prerenal Acute Tubular Necrosis
Blood urea nitrogen/creatinine ratio >20 10-20
Urine specific gravity >1.020 >1.010
Urine osmolality (mOsm/L) >500 <350
Urinary sodium (mmol/L) >20 >40
Fractional excretion of sodium (%)a <1 >2
Management of oliguria or AKI due to shock or other etiologies in the critically ill
patient should follow an organized approach. The patient should be evaluated promptly
to determine the cause of renal dysfunction. Reversible causes should always be rapidly
identified and corrected. Insertion of a urinary catheter and a renal ultrasound scan will
exclude urinary obstruction in most patients. The urinary catheter is also a useful device
to monitor urine output and should be utilized in patients with shock. More frequent
measurements of blood urea nitrogen, serum creatinine, and urine output are needed.
Volume status should be assessed using clinical examination and the monitoring
techniques outlined in Chapter 6. Intravascular volume should be optimized with
crystalloid and/or colloid solutions to improve renal perfusion. Vasoactive drugs along
with fluids may be needed in patients with shock in order to achieve an adequate blood
pressure. Loop diuretics may be considered (if blood pressure is adequate) in the
setting of volume overload. Although the conversion to a nonoliguric state does not
change outcome, fluid management is usually easier, especially in patients with severe
hypoxemic respiratory failure. No evidence supports the use of low-dose dopamine in
oliguric patients. Once oliguric or anuric AKI is confirmed and persistent, fluids should
be restricted to the replacement of ongoing losses (including insensible losses). In
disease states associated with ongoing loss of intravascular volume, fluid
administration is necessary to maintain adequate left ventricular preload. These losses
may be substantial, as in pancreatitis, severe sepsis, and large open wounds.
Because there is no specific treatment for most cases of AKI, expectant and supportive
care is maintained. Drug dosages need adjustment not only for the severity of AKI but
also for the type of renal replacement therapy that may be utilized. Nephrotoxic drugs
(such as intravenous contrast) should be avoided if possible. Monitoring of drug
concentrations should be utilized to guide therapy when possible. Problems with
extracellular fluid overload, hyperkalemia, and hypermagnesemia should be anticipated
and avoided if possible. Hyperkalemia usually can be managed medically until dialysis
is available (Chapter 12). Nutritional therapy must be adjusted for renal function and
renal replacement therapy.
Renal replacement therapy is necessary when uremic symptoms develop or whenever
extracellular volume excess, hyperkalemia, or metabolic acidosis is refractory to
medical therapy. Various intermittent or continuous therapies are available to
accomplish fluid removal (ultrafiltration) or solute removal (dialysis, hemofiltration,
hemodiafiltration). An appropriate selection depends on the circumstances of the
individual patient (especially hemodynamic status) and the resources available.
Consultation with a nephrologist is advised to assist with determining the most
appropriate treatment.
Key Points
Diagnosis and Management of Shock

Shock is characterized by impaired tissue oxygenation and hypoperfusion.
The four major categories of shock with characteristic hemodynamic patterns are
hypovolemic, distributive, cardiogenic, and obstructive.
The clinical manifestations of shock result from inadequate tissue oxygenation and
perfusion, compensatory responses, and the syndrome’s specific etiology.
Interventions to restore perfusion center on achieving an adequate blood pressure,
increasing cardiac output, optimizing the oxygen content of blood, and/or
decreasing oxygen demand.
The initial therapy for most forms of shock is replacement of intravascular volume
with crystalloid or colloid solutions.
The selection of a vasoactive agent to treat shock should be based on the
hemodynamic effect desired for an individual patient and knowledge of the
pharmacology of available agents.
Reversible causes of acute oliguria or AKI should always be excluded, and
intravascular volume should be optimized with crystalloid and/or colloid
solutions.
Suggested Readings
1. Dabrowski GP, Steinberg SM, Ferrara JJ, et al. A critical assessment of endpoints
of shock resuscitation. Surg Clin North Am. 2000;80:825-844.
2. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign:
International guidelines for management of severe sepsis and septic shock: 2012.
Crit Care Med. 2013;41:580-637.
3. Gutierrez G, Reines HD, Wulf-Gutierrez ME. Clinical review: Hemorrhagic
shock. Crit Care. 2004;8:373-381.
4. Havel C, Arrich J, Losert H, et al. Vasopressors for hypotensive shock. Cochrane
Database Syst Rev. 2011;(5):CD003709. doi:10.1002/14651858.CD003709.pub3.
5. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work
Group. KDIGO: Clinical practice guideline for acute kidney injury. Kidney Int
Suppl. 2012;2:1-138.
6. Tharmaratnam D, Nolan J, Jain A. Management of cardiogenic shock complicating
acute coronary syndromes. Heart. 2013;99:1614-1623.
7. Vincent J-L, De Backer D. Circulatory shock. N Engl J Med. 2013;369:1726-
1734.
8. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and
hemodynamic monitoring. Task Force of the European Society of Intensive Care
Medicine. Intensive Care Med. 2014;40:1795-1815.
9. Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med. 2013;369:1243-
1251.
Suggested Websites
1. Kidney Disease: Improving Global Outcomes. www.kdigo.org.

2. Surviving Sepsis Campaign. www.survivingsepsis.org.
3. Society of Critical Care Medicine. www.SCCM.org.
Chapter 8
NEUROLOGIC SUPPORT
Objectives
Review the principles of primary and secondary brain insult and the common
mechanisms of neuronal injury.
Apply the concepts of intracranial hypertension and brain oxygen delivery and
consumption to the management of the brain-injured patient.
Review the clinical and diagnostic assessment of a brain-injured patient.
List general treatments that are common in brain injury.
Review specific management principles and options for selected pathophysiologic
conditions.
Case Study
A 57-year-old woman is brought to the emergency department 80 min after the

witnessed onset of aphasia and right hemiplegia. She has a history of hypertension and
type 2 diabetes mellitus. Her current medications include aspirin and metformin. On
examination, her blood pressure is 180/100 mm Hg, pulse 90 beats/min and regular,
respiration 19 breaths/min, and temperature 37.2°C (98.9°F). She is alert but unable to
speak or follow commands. Her cranial nerve exam shows a left conjugate gaze
preference, absent movement of the right lower face with sparing of the forehead,
absence of response to noxious stimuli on the right side of her face, and a diminished
gag reflex on the right. She has a right hemiplegia and does not respond to noxious
stimuli applied to the right side of her body. The remainder of her physical examination
is unremarkable. An immediate computed tomography (CT) scan of the head is
unremarkable.
– What type of primary brain injury is likely to be present?
– What are the immediate concerns?
– What interventions and monitoring should be instituted in addition to the CT scan?
I. INTRODUCTION
Primary injuries to the brain include ischemic events, trauma, hemorrhage, and anoxia,
which may occur either in isolation or in combination. Mechanisms for these and other
primary injuries are shown in Table 8-1.
Table 8-1 Common Mechanisms of Primary Brain Injuries
Trauma: concussion, contusion, shear injury, penetrating injury, and diffuse axonal injury
Ischemia: global (eg, cardiac arrest with anoxia) or regional (eg, vasospasm, compression of blood
vessels, stroke)
Inflammation: meningitis, encephalitis
Compression: tumor, cerebral edema, hematoma (eg, epidural, subdural, or intraparenchymal)
Metabolism: encephalopathies (eg, hepatic, electrolyte, drugs, toxins)
Often, little can be done to reverse the immediate and frequently devastating effects of
the primary cerebral insult that produces neuronal injury or death. In some
circumstances, the immediate effects of an injury may be reversed by prompt surgical
intervention. As with the injury seen in myocardial infarction, many types of brain
insults produce a region of maximum injury associated with a surrounding area of tissue,
or penumbra, that may survive and recover if further damage can be prevented. Common
mechanisms of secondary injury are shown in Table 8-2; these can also occur as
primary injuries. The mechanisms of secondary brain injury may evolve over time from
other primary insults. For example, edema after head trauma commonly produces
secondary brain compression, vasospasm after subarachnoid hemorrhage may cause
regional ischemia and stroke, or secondary hemorrhagic conversion after an ischemic
stroke may induce compression and further ischemia.
Table 8-2 Common Mechanisms of Secondary Brain Injuries
Hypoperfusion: global (ie, secondary to high intracranial pressure, systemic arterial hypotension, or
severe anemia) or regional (eg, secondary to high intracranial pressure, local edema, or vasospasm)
Hypoxia: systemic hypoxemia, regional hypoperfusion, or high tissue consumption (ie, seizures,
hyperthermia)
Electrolyte or acid-base changes from systemic or regional ischemia
Reperfusion injury with free radical formation
II. BRAIN INJURY MANAGEMENT PRINCIPLES
The focus of treatment for a neurologically compromised patient is the same as that for
patients with other illnesses and injuries, that is, to ensure adequate oxygen delivery to
meet the needs of both the damaged and the undamaged brain tissue. The primary goal
is prevention of secondary injury. The initial care team must take early and aggressive
action to ensure that secondary brain injury is prevented, minimized, or reversed with
careful monitoring and treatment, particularly the prevention and early treatment of
hypoxia and hypotension. Optimizing oxygen delivery to the brain requires attention to
oxygenation, hemoglobin concentration, cardiac output, and blood pressure. Prevention
and early treatment of fever, seizures, pain, agitation, and anxiety can minimize oxygen
demands.
A. Intracranial Hypertension
Intracranial pressure reflects the balance of volume-control mechanisms within the
noncompliant cranial compartment. Because the brain is enclosed within the rigid skull
and relatively inflexible dura, with tissues and fluids that are incompressible, control of
the different intracranial components is essential to maintain brain homeostasis, regulate
intracranial pressure, and preserve cerebral perfusion. The critical compartment
relationship depends on the volume occupied by each component. An increase in one
component (eg, brain) must be accompanied by a decrease in another component (eg,
blood). When the compensatory mechanisms are overwhelmed, intracranial pressure
(ICP) increases and injury may ensue. In addition to the impaired cerebral perfusion,
which may be a consequence of globally increased ICP, small pressure gradients within
the skull may cause herniation of the brain around dural reflections (the falx and the
tentorium), with shift of the midline structures. These movements within the skull may
compromise function (eg, cause stupor or coma by disrupting the activity of the
brainstem reticular formation) or lead to vascular compression and stroke.
Increased ICP has an important effect

on the regional and global supplies of
oxygen to the brain because it
compresses arteries and decreases
cerebral blood flow.
An intensivist or a neurosurgeon should be consulted if intracranial hypertension is

suspected. The patient may need a catheter inserted into a lateral ventricle for
monitoring and drainage of cerebrospinal fluid, or into the brain parenchyma for
monitoring (Table 8-3). This monitoring includes intracranial pressure, temperature,
and/or brain oxygen. Measurements of cerebral oxygenation require special equipment
and expertise that are not available in most facilities. When direct measures are not
available, the initial care team must treat based on the principles of oxygen supply and
demand.
Conditions Potentially Requiring Invasive Intracranial Pressure

Table 8-3
Monitoring
Traumatic brain injury (Table 8-6)

Acute subarachnoid hemorrhage with hydrocephalus, coma, or clinical deterioration
Intracranial hemorrhage with intraventricular blood
Large ischemic stroke
Fulminant hepatic failure
Global brain ischemia/anoxia with increasing edema
B. Hypoperfusion
Cerebral autoregulation reflects the normal arteriolar dilation or constriction that
controls regional cerebral blood flow (CBF) and links oxygen demand to its delivery;
thus, global CBF normally remains constant over a defined range of mean arterial
pressures (MAP). Loss of autoregulation occurs in many pathologic conditions, and may
lead to regional or global vasodilation and edema formation, which can further increase
ICP. Increases in blood volume also profoundly affect the pressure inside the
noncompliant cranial vault.
Although related, changes in CPP may

not always result in similar changes in
CBF.
CBF is usually evaluated by the cerebral perfusion pressure (CPP), which is the MAP
(the driving pressure) minus the ICP (the pressure impeding blood flow):
CPP = MAP – ICP
The MAP must be measured at the same location as the ICP to be accurate; this is
usually done by zeroing the arterial line transducer at the ear, and keeping it at the same
height as the head when the head is elevated. The normal CPP is between 60 and 100
mm Hg. If the ICP increases without a change in MAP, CPP decreases, and CBF will
also decrease if autoregulation has failed. The decrease in CBF increases the risk of
brain ischemia. Clinicians should pay particular attention to changes in mental status, as
these may indicate inadequate perfusion (among many other possibilities).
C. Recommendations for Therapy

To minimize damage to the brain, therapies are primarily designed to minimize oxygen
demand and increase CBF and oxygen delivery. Table 8-4 summarizes commonly
accepted principles and therapeutic guidelines for treating a variety of brain insults and
avoiding secondary brain injury. Note the focus on factors that minimize oxygen
consumption and maximize oxygen delivery.
Table 8-4 General Principles of Managing Brain Injury

Prevent Abnormal Oxygen Demands
1. Avoid fever. Fever increases metabolic demand, resulting in neuronal injury and elevating intracranial
pressure.
2. Avoid seizures. Prophylactic anticonvulsant administration is indicated after moderate or severe
traumatic brain injury to prevent seizures in the first week, but the available evidence does not
support longer use in head trauma or use in other neurologic injuries.
3. Avoid anxiety, agitation, or pain. Neuronal oxygen consumption may be decreased by an antianxiety
agent, sedation, and analgesia.
4. Avoid shivering.
5. Minimize stimulation, particularly for the first 72 hours.
Promote Oxygen Delivery
1. Ensure systemic oxygen transport with adequate oxygenation, hemoglobin concentration, and
cardiac output.
2. Ensure optimal blood pressure. Many primary insults are associated with hypertension that may be a
physiologic compensation or may be injurious. Elevated blood pressure may be undesirable in
patients with unsecured aneurysms and recent intracranial hemorrhage. However, excessive
lowering of blood pressure may result in secondary ischemia.
3. Avoid prophylactic or routine hyperventilation because an increase in extracellular brain pH constricts
responsive vessels and may reduce cerebral blood flow to ischemic zones. Brief hyperventilation
while instituting other methods to lower elevated intracranial pressure may be lifesaving in the patient
with evidence of herniation.
4. Ensure euvolemia because hypovolemia may result in systemic hypotension and hypoperfusion of
brain tissue.
5. Rapid-sequence intubation should be used for patients with increased intracranial pressure.
Consider administration of intravenous lidocaine or intravenous propofol to blunt the rise in
intracranial pressure associated with intubation.
6. Institute nimodipine immediately in patients with aneurysmal subarachnoid hemorrhage.
III. ASSESSMENT
After appropriate management of airway, breathing, and hemodynamic concerns, the
priority in neurologic assessment is to distinguish among ischemic, structural,
metabolic, and infectious injuries. Suspected ischemic stroke requires an immediate
decision regarding thrombolytic therapy, and emergent neurologic consultation should
be obtained. The presence of an expanding mass lesion accompanied by significant
brain shift may indicate the need for immediate surgical evaluation and possible
intervention. The most common causes of such an event include epidural, subdural, and
intracerebral hematomas. Intracranial hematomas should be suspected in the settings of
head trauma, recent neurosurgery, anticoagulant therapy, alcohol abuse, coagulopathies,
and chronic or acute hypertension. The diagnostic procedure of choice, CT scan of the
brain, characterizes the extent of structural injury. Medical treatment may be a
temporizing option until more definitive therapy is available and implemented.
Early identification of patients with

ischemic stroke or potential surgical
lesions provides the best opportunity to
minimize secondary brain injury.
Serial examinations are necessary to detect the possible sequelae of many brain insults.
Any change in the examination is a sensitive indicator of deterioration and should
prompt an immediate and thorough reevaluation. For example, decreased consciousness
without lateralizing findings may be due to elevated ICP, hydrocephalus, fever, toxic
ingestants, or worsening of an encephalopathy, among others.
When physical examination or CT scan

suggests significant brain compression,
medical therapy to reduce ICP should be
instituted immediately while awaiting
definitive treatment.
The Glasgow Coma Scale score is widely used in the initial and serial assessment of
patients with head trauma, and it may be useful in evaluating patients with other brain
insults. Table 8-5 lists its components.
Table 8-5 Components of Glasgow Coma Scale Score
Clinical Parameters Adults Points

Eye opening Spontaneous 4
Response to speech 3
Response to pain 2
No response 1
Verbal response Oriented and appropriate 5
Disoriented and confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Best motor response Obeys commands 6
Localizes pain 5
Withdraws from pain 4
Flexor response 3
Extensor response 2
No response 1
Total Glasgow Coma Scale score = eye + verbal + motor scores; best possible score = 15, worst
possible
score = 3.
Serial examinations, including evaluation of brainstem and cranial nerve function,

should be performed. Pupillary asymmetry may be an important sign of horizontal shift
of the brain, which commonly precedes downward herniation in patients with
supratentorial masses. Disconjugate eye movements, a change in respiratory pattern, or
deterioration in motor response may suggest an increase in intracranial mass effect and
should be investigated immediately.
When clinical findings suggest herniation, emergent administration of mannitol or
hypertonic saline should be initiated to lower ICP, and emergent neurosurgical
assistance should be obtained. A brief period of hyperventilation may be considered.
Whether repetition of an imaging study or immediate surgical therapy is required
depends upon the nature, location, and progression of the pathologic process.
The Cushing reflex of hypertension

followed by bradycardia, and altered
respiration may indicate brain
herniation.
Neurosurgical consultation is advised for any patient who: (1) is at risk for developing
an expanding intracranial mass lesion; (2) has an open or depressed skull fracture or
acute ventricular obstruction; (3) demonstrates blood in the fourth ventricle, cerebellar
bleeding, or subarachnoid hemorrhage; or (4) has cerebrospinal fluid leakage.
Nontraumatic disease processes, such as spontaneous intracerebral hematoma, large
brain tumors, or brain abscesses, require urgent neurosurgical consultation if clinical
findings or an imaging study indicate significant mass effect (midline deviation,
ventricular obliteration, brainstem or basal cistern compression).
Urgent neurosurgical consultation should be obtained for hemorrhages and infarcts in the
posterior fossa regardless of the level of consciousness. Although such patients may
have few findings on initial clinical examination, progressive swelling around the
lesion may necessitate emergent surgical decompression. Typically, any cerebellar mass
>3 cm in diameter with hydrocephalus or brainstem compression requires evacuation.
IV. SPECIFIC DIAGNOSES AND CONSIDERATIONS
A. Traumatic Brain Injury
Cerebellar hemorrhage with altered

consciousness is a surgical emergency.
Approximately 25% of patients who experience blunt head trauma require urgent
evacuation of a subdural hematoma (Figure 8-1A) or an epidural hematoma (Figure 8-
1B) to relieve compression of the brain. Neurosurgical consultation should be
considered early. Because 20% of patients with severe traumatic brain injury will have
concomitant cervical spinal cord injuries, immobilization of the cervical spine until it
can be appropriately assessed is very important.
(left) Figure 8-1A. Subdural Hematoma
(right) Figure 8-1B. Epidural Hematoma
Penetrating and nonpenetrating head injuries are often associated with the formation of
cerebral edema, brain contusions, or hemorrhage within the parenchyma. Because the
skull cannot expand to accommodate increased intracranial volume and the
compensatory space in the subarachnoid space of the spinal canal is very limited, the
ICP commonly becomes elevated. Monitoring and treatment of increased ICP are
considered important in such patients.
Guidelines for the management of severe traumatic brain injury have been developed by
the Brain Trauma Foundation on the basis of established evidence. These principles are
included in the recommendations in Table 8-6.
Table 8-6 General Principles for Treatment of Traumatic Brain Injury
Ensure the ABCs of resuscitation are performed.

Avoid hypotension and maintain systolic blood pressure >90 mm Hg. It may be valuable to maintain
mean arterial pressure higher than the mean arterial pressure associated with a systolic blood
pressure of 90 mm Hg. Optimal mean arterial pressure is unknown.
Avoid hypoxemia (PaO2 <60 mm Hg [8.0 kPa] or oxygen saturation <90%) while adequate oxygenation
is maintained.
Maintain alignment between head and trunk to avoid jugular compression.
Keep the head of the bed at 30° to 45°elevation unless the patient is hypotensive. Elevation of the
head promotes venous drainage and cerebrospinal fluid displacement to the spinal compartment.
Adjust any devices that may constrict the neck, including cervical collars.
Maintain the PaCO2 at 35 to 40 mm Hg (4.7-5.3 kPa). Prophylactic hyperventilation is not
recommended. Hyperventilation is recommended as a temporizing measure for reduction of elevated
intracranial pressure. Cerebral blood flow is often reduced in the first 24 hours after head trauma,
and hyperventilation should be avoided in this period to prevent further reductions.
Use normal saline as the primary maintenance fluid. Do not use hypotonic fluids.
Actively treat fever to maintain body temperature at normal levels.
Control harmful agitation with sedation if necessary. Use medications with a relatively short half-life to
facilitate reliable and ongoing neurologic assessments.
Maintain the usual electrolyte homeostasis and treat hyperglycemia/hypoglycemia.
Assess and treat coagulation defects.
Provide nutrition to attain full caloric replacements as tolerated.
Prophylactic anticonvulsants are appropriate during the first week after traumatic brain injury.
Give mannitol (0.25-1 g/kg IV push) or hypertonic saline (eg, 5-10 mL/kg of 3% NaCl as rapidly as
possible) for signs of herniation or for neurologic deterioration not attributable to other factors. Expert
consultation should be obtained if this type of hyperosmolar therapy is considered.
Avoid steroid use. These agents are contraindicated in patients with head trauma.
Initiate appropriate intracranial pressure monitoring:
For a patient with a Glasgow Coma Scale score between 3 and 8 after resuscitation or a score
between 9 and 12 with an abnormal computed tomography scan
For a patient who has a normal computed tomography scan but at least two of the following
factors:
1. Age >40 years
2. Systolic blood pressure <90 mm Hg
3. Unilateral or bilateral motor posturing (decerebrate/decorticate)
Maintain the lowest perfusion pressure compatible with adequate cerebral blood flow. The target
cerebral perfusion pressure is in the range of 50 to 70 mm Hg, although patients with intact
autoregulation may tolerate higher values. The ideal is the pressure that provides adequate cerebral
perfusion and oxygenation while intracranial pressure is maintained <20 mm Hg.
B. Intracerebral Hemorrhage
Patients with intracerebral hemorrhage frequently have a history of hypertension. Blood
pressure control is controversial in these cases. Elevated blood pressure may contribute
to rebleeding and edema formation but may also preserve regional CPP. Recent studies
suggest that lowering the systolic blood pressure to 140 mm Hg may improve outcome.
If elevated ICP is suspected, expert consultation is advised for assistance with blood
pressure management. Preferred agents include labetalol and nicardipine. Use of
vasodilators remains controversial, but drugs that cause substantial intracranial
vasodilation (eg, nitroprusside, nitroglycerin) should be avoided.
Expansion of the hematoma occurs commonly, especially in patients taking
anticoagulants or who have liver disease or low platelet counts. Some neurosurgeons
may consider removal of the hematoma, especially in a young, clinically deteriorating
patient with a large lobar hemorrhage or when the hemorrhage is associated with a
surgically treatable lesion, such as an aneurysm, arteriovenous malformation, or
cavernous angioma. Deep basal ganglionic hemorrhages do not yet have a commonly
accepted surgical therapy (Figure 8-2A). Small hemorrhages may not require specific
therapy (Figure 8-2B).
Figure 8-2A. CT Scan Demonstrating Large Right Basal Ganglion Intracerebral Hemorrhage with Midline
Shift and Intraventricular Extension
Figure 8-2B. CT Scan Demonstrating Small Left Parietal Lobar Intracerebral Hemorrhage
C. Subarachnoid Hemorrhage
Characteristics from the patient history (“worst headache of their life”) and CT findings
usually confirm the diagnosis of subarachnoid hemorrhage (Figure 8-3). Classification
systems (eg, the Hunt and Hess scale) have been used to categorize findings and suggest
prognosis but do not alter the care provided by the primary team, as outlined in Table 8-
7. Early aneurysm repeat rupture is frequently fatal, so initial therapy is aimed at
decreasing its risk. Guidelines are available from the American Heart
Association/American Stroke Association (AHA/ASA) and the Neurocritical Care
Society. Prompt consultation with a center experienced in the care of these patients is
essential. Almost all patients, regardless of severity, should be stabilized and evaluated
for rapid transfer to such center for management.
Figure 8-3. CT Scan Demonstrating Subarachnoid Hemorrhage
Table 8-7 Treatment of Subarachnoid Hemorrhage
Ensure the ABCs of resuscitation are performed.

Control blood pressure early, before definitive surgical therapy. Rebleeding is the major early
complication until the aneurysm is clipped or coiled. A variety of intravenous agents have been useful.
Labetalol and nicardipine have been advocated. Nitroprusside should be avoided because of its
tendency to induce cerebral vasodilation. Consider the effects of nimodipine on blood pressure when
using other antihypertensive agents.
Initiate oral nimodipine, 60 mg every 4 hours. (An intravenous preparation is available in some
countries.) Hypotension should be avoided.
Maintain euvolemia. Some advocate gentle intravascular volume expansion. Significant cardiac injury
can occur as a result of catecholamine levels; thus, careful attention to arrhythmias and cardiac
function is necessary.
Avoid hyponatremia, which is commonly encountered. Normal saline should be used as the primary
intravenous fluid. Hyponatremia usually reflects cerebral salt wasting rather than SIADH; cerebral salt
wasting should not be treated with the volume restriction utilized for SIADH. Both groups of patients
will have inappropriately high urine osmolality, so this marker cannot be used to indicate SIADH. If salt
administration is indicated for cerebral salt wasting, small amounts of hypertonic saline may be
necessary. Hyponatremia should be corrected slowly, as central pontine myelinolysis can occur from
rapid and aggressive sodium correction.
Perform rapid evaluation of the aneurysm location for surgical clipping or coiling, which requires
urgent neurosurgical and/or neurointerventional radiology consultation.
Manage patients in centers with the capacity for aneurysm clipping and coiling, and for vasospasm
treatment.
Abbreviation: SIADH, syndrome of inappropriate antidiuretic hormone
D. Ischemic Stroke
Ischemic stroke usually occurs due to the thromboembolic obstruction of arteries.
Administration of intravenous recombinant tissue plasminogen activator during the first
3 to 4.5 hours following the known onset of ischemic stroke substantially improves
outcome in one-third of patients. For patients with larger artery occlusion (Figure 8-4),
intra-arterial treatment with a stent-retriever device within 8 hours results in meaningful
improvement in about 60% of patients.
Figure 8-4. CT Angiogram Demonstrating Occlusion of Left Middle Cerebral Artery (arrow)
Onset of symptoms, or the last time the patient was known to be at baseline, is the time
used to determine whether a patient is a candidate for thrombolytic therapy. After an
initial CT scan rules out the presence of hemorrhage, intravenous recombinant tissue
plasminogen activator should be administered in a dosage of 0.9 mg/kg (10% as a bolus
over 1 minute and 90% in a 1-hour infusion) for patients in whom treatment can be
started within 4.5 hours. Personnel who are not familiar with the use of recombinant
tissue plasminogen activator for the acute treatment of nonhemorrhagic stroke should
seek immediate neurologic consultation before administering therapy. Intra-arterial clot
retrieval is an important option for patients with large artery occlusion, regardless of
whether recombinant tissue plasminogen activator has been administered. Guidelines
are available from the AHA/ASA.
Supportive care includes management of hypertension. Although elevated blood
pressure is often present early, a decrease in pressure usually occurs in the first hours
after stroke without specific medical treatment. No evidence defines a level of blood
pressure that requires emergent intervention. The AHA/ASA have compiled consensus
recommendations for patients who are candidates for thrombolytic therapy (Table 8-8).
For those who are not candidates for thrombolysis, emergency administration of
antihypertensive agents is not indicated unless the diastolic blood pressure is >120 mm
Hg, systolic blood pressure is >220 mm Hg, or there is evidence of end-organ injury
(eg, pulmonary edema). If treatment is indicated, the blood pressure should be lowered
cautiously with a reasonable goal of lowering the pressure approximately 15% in the
first 24 hours after stroke onset.
Determination of when the initial stroke

symptoms appeared is critical.
Blood Pressure Management in Patients Eligible for Recombinant

Table 8-8
Tissue Plasminogen Activator Treatmenta
Blood Pressure Treatment
Pretreatment
SBP >185 mm Hg or DBP Labetalol 10-20 mg IV bolus (1-2 doses)
>110 mm Hg Nicardipine infusion 5 mg/h titrated to goal BP (maximum 15 mg/h); reduce
infusion to 3 mg/h when goal BP attained
Post-treatment
SBP >230 mm Hg or DBP Labetalol 10-20 mg IV bolus; may repeat every 10-20 min, maximum 300
121-140 mm Hg mg
Labetalol 10 mg IV bolus followed by infusion at 2-8 mg/min
Nicardipine 5 mg/h IV infusion and titrate, maximum 15 mg/h
SBP 180-230 mm Hg or Labetalol 10 mg IV bolus; may repeat every 10-20 min to maximum 300
DBP 105-120 mm Hg mg
Labetalol 10 mg IV bolus followed by infusion at 2-8 mg/min
Abbreviations: SBP, systolic blood pressure; DBP, diastolic blood pressure; BP, blood pressure.
aAdapted with permission from Wolters Kluwer Health. Adams HP, del Zoppo G, Alberts MJ, et al.
Guidelines for the early management of adults with ischemic stroke. Stroke. 2007;38:1655-1711.
Urgent anticoagulation with unfractionated or low-molecular-weight heparin is not

indicated in acute stroke. Prophylactic heparin should be administered to immobilized
patients to prevent venous thromboembolism, but the ideal time to start this therapy is
not known. Aspirin administration within 24 to 48 hours of stroke onset is recommended
for most patients after hemorrhage is excluded, but clopidogrel administration is not
recommended. Significant edema formation, typically within the first 72 hours, or
extensive hemorrhage within the ischemic zone may indicate emergent hemicraniectomy.
E. Anoxic Injury
Relative anoxia may be a part of other injuries and may be due to airway loss, systemic
hypoxemia, hypoperfusion, and other causes. Anoxia may also be the primary brain
insult, as occurs during cardiac arrest. Neuronal damage may occur as a direct result of
the primary insult of hypoxemia or hypoperfusion.
The initial team should maintain the usual standards of optimal oxygen delivery. Despite
extensive studies of many agents and therapy options, none has proven selectively
beneficial, nor has the poor prognosis from anoxic brain injury improved over time.
Systemic cooling to 32°C or 36°C (89.6°F or 98.6°F) for 12 to 24 hours improves
neurologic outcome in comatose patients after cardiac arrests. The inability to follow
simple commands constitutes an acceptable threshold to consider cooling. Guidelines
are available from the AHA and the International Liaison Committee on Resuscitation.
F. Metabolic Abnormalities, Infectious Emergencies, And Seizures

In adult patients with depressed consciousness after initial resuscitation, the use of 50%
dextrose (50 mL intravenously) and thiamine (100 mg intravenously) should be
considered for the treatment of potential hypoglycemia and the prevention of Wernicke
encephalopathy if an immediate determination of the blood glucose concentration is not
available. Intravenous naloxone should be administered if narcotic intoxication is a
possibility. Other metabolic abnormalities, such as electrolyte disorders (ie, acute
hyponatremia, hypercalcemia), liver failure, or uremia may also cause coma. Because
headache or altered state of consciousness accompanied by fever, nuchal rigidity, and
leukocytosis suggests meningitis or encephalitis, the cerebrospinal fluid should be
submitted for physical, chemical, and bacteriologic (culture and Gram stain) studies. If
clinical examination suggests a mass lesion or elevated ICP, a CT scan should be
performed before lumbar puncture. If the scan reveals evidence of mass effect or
generalized cerebral edema, a lumbar puncture may precipitate a herniation syndrome
and should be postponed. When infection is part of the differential diagnosis,
appropriate antibacterial and antiviral treatment should be initiated before performing
the imaging study because early therapy for bacterial meningitis or encephalitis may be
lifesaving. Blood cultures should be obtained before antibiotic therapy unless this
would delay treatment. Antibiotics should also be given if lumbar puncture is delayed
for any other reason. Treatment recommendations for adults are outlined in Chapter 11
and those for children are in Chapter 16.
In the absence of papilledema or focal

neurologic signs, a lumbar puncture may
be performed without a prior CT scan
for evaluation of meningitis.
Seizure activity after an acute brain injury increases cerebral oxygen requirements and
typically elevates the ICP. Appropriate therapy should be administered to terminate
seizure activity as soon as possible. The intravenous administration of anticonvulsants,
many of which have a potent sedative effect, may depress respiratory function and
requires appropriate supportive therapy. In addition, hypotension may occur, requiring
additional intravenous fluids and/or vasopressors to preserve MAP and CPP.
Intravenous benzodiazepines are administered at the onset of prolonged or repeated
seizure activity. Status epilepticus requires emergent neurologic consultation, and
lorazepam 0.1 mg/kg should be administered intravenously. Intramuscular midazolam,
0.15 mg/kg, is an alternative if intravenous access is not immediately available.
Anticonvulsants used in refractory status epilepticus include propofol (3 mg/kg loading
dose, then infusion of 1-5 mg/kg/h) or midazolam (0.2 mg/kg loading dose, then infusion
of 1-20 μg/kg/min) with electroencephalography and other ICU monitoring. After
stabilization, loading with phenytoin or fosphenytoin may be appropriate to prevent
recurrent seizures.
If possible, avoid the use of

neuromuscular blocking agents in
patients at risk for seizure because these
agents obscure detection of seizure
activity.
G. Spinal Cord Injury
Cervical spine injury in awake patients is usually apparent from neck pain and
weakness. If awareness is impaired, suspect cervical spinal cord injury in patients with
respiratory weakness, extremity weakness without facial weakness, hypotension with
bradycardia, and difficulty maintaining normothermia. Patients with lesions below C4
may breathe adequately on presentation but could progress to abrupt respiratory failure
and thus must never be left unmonitored.
Thoracolumbar spine injury spares the upper extremities but involves leg weakness;
depending on the level, the patients may have hypotension with tachycardia or unusual
swings in blood pressure.
Initial management includes immobilization (cervical collar, backboard) while
obtaining emergent neurosurgical consultation. However, patients should not be left on
backboards after arrival in the emergency department. Use of methylprednisolone is
controversial and should be discussed with the consultant.
CT scans of the spine can be obtained without removing immobilizing devices.
H. Other Neurologic Causes of Acute Respiratory Failure

Patients with conditions causing global weakness, such as myasthenia gravis and the
Guillain-Barré syndrome, may have problems maintaining upper airway patency and
clearing secretions in addition to respiratory muscle weakness. In such patients,
endotracheal intubation may be needed for airway protection before being mandated by
the falling tidal volume. Measurement of vital capacity and negative inspiratory
pressure is important. Patients with <20 mL/kg vital capacity should be moved to an
ICU and will likely need intubation soon. One should intubate based on tachypnea and
discomfort without waiting for an elevation of PaCO2. Hypoxia due to atelectasis in
patients with adequate airway protection may be treated with continuous positive
airway pressure. A neurologist should be consulted when the diagnosis is suspected, as
treatment with intravenous immunoglobulin or plasma exchange may slow or halt
disease progression and speed recovery.
Autonomic dysfunction is common in the Guillain-Barré syndrome and may lead to large
and rapid swings in blood pressure and heart rate requiring intravenous therapy.
I. Brain-death Criteria and Organ Donation

Despite the best efforts of medical and surgical teams, massive injury, cerebral
infarction, or hemorrhage may result in a loss of all cerebral and brainstem functions.
Evaluation of brain death and the guidelines for organ donation are variable, depending
on the country, state, and facility. For more information about brain death and organ
donation, see Appendix 6.
Key Points
Neurologic Support
Brain injury occurs as a consequence of a primary insult and secondary injury. The
prevention of secondary brain injury is a critical goal for the initial care team.
The most significant mechanisms for secondary injury in brain-injured patients are
hypotension and hypoxia.
Optimizing oxygen delivery while controlling oxygen consumption is a general
treatment principle for all types of brain injury.
Important principles/guidelines for initial treatment apply to all types of primary
brain injury and help prevent harmful secondary sequelae.
Blood pressure management is dependent on the initial brain injury. However,
excessive lowering of blood pressure in any acute brain injury may induce
secondary ischemia.
Avoid prophylactic or routine hyperventilation in patients with brain injuries.
Mannitol should be given and hyperventilation initiated for signs of herniation or if
neurologic deterioration is not attributable to other factors.
Ensure euvolemia using normal saline as the primary maintenance fluid.
Seizure activity after acute brain injury should be terminated with an intravenous
dose of a benzodiazepine, followed by an intravenous loading dose of phenytoin or
fosphenytoin.
Suggested Readings
1. Bleck TP. Bacterial meningitis and other nonviral infections of the nervous system.
Crit Care Clin. 2013;29:975-987.
2. Boland TA, Lee VH, Bleck TP. Stress-induced cardiomyopathy. Crit Care Med.
2015;43:686-693.
3. Brain Trauma Foundation, American Association of Neurological Surgeons,
Congress of Neurological Surgeons, AANS/CNS Joint Section on Neurotrauma
and Critical Care. Guidelines for the management of severe traumatic brain injury.
3rd ed. J Neurotrauma. 2007;24(suppl 1):S1-S106.
4. Brophy GM, Bell R, Claassen J, et al. Guidelines for the evaluation and
management of status epilepticus. Neurocrit Care. 2012;17:3-23.
5. Busl KM, Bleck TP. Neurogenic pulmonary edema. Crit Care Med. 2015;43:1710-
1715.
6. Callaway CW, Donnino MW, Fink EL, et al. Part 8: Post–cardiac arrest care: 2015
American Heart Association guidelines update for cardiopulmonary resuscitation
and emergency cardiovascular care. Circulation. 2015;132(suppl 2):S465–S482.
7. Chesnut RM, Bleck TP, Citerio G, et al. A consensus-based interpretation of the
Benchmark Evidence from South American Trials: Treatment of Intracranial
Pressure Trial. J Neurotrauma. 2015;32:1722-1724.
8. Connolly ES, Rabenstein AA, Carhuapoma JR, et al. Guidelines for the
management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare
professionals from the American Heart Association/American Stroke Association.
Stroke. 2012;43:1711-1737.
9. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of
patients following aneurysmal subarachnoid hemorrhage: recommendations from
the Neurocritical Care Society’s Multidisciplinary Consensus Conference.
Neurocrit Care. 2011;15:211-240.
10. Hemphill JC, Greenberg SM, Anderson CS, et al. Guidelines for the management
of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals
from the American Heart Association/American Stroke Association. Stroke.
2015;46:2032-2060.
11. Kamel H, Navi BB, Nakagawa K, et al. Hypertonic saline versus mannitol for the
treatment of elevated intracranial pressure: a meta-analysis of randomized clinical
trials. Crit Care Med. 2011;39:554-559.
12. Kotloff RM, Blosser S, Fulda GJ, et al. Management of the potential organ donor
in the ICU: Society of Critical Care Medicine/American College of Chest
Physicians/Association of Organ Procurement Organizations Consensus Statement.
Crit Care Med. 2015;43:1291-1325.
13. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of
patients with acute ischemic stroke: a guideline for healthcare professionals from
the American Heart Association/American Stroke Association. Stroke.
2013;44:870-947.
14. Powers WJ, Derdeyn CP, Biller J, et al. 2015 American Heart
Association/American Stroke Association focused update of the 2013 guidelines
for the early management of patients with acute ischemic stroke regarding
endovascular treatment: a guideline for healthcare professionals from the
American Heart Association/American Stroke Association. Stroke. 2015;48:3020-
3035.
15. Rossetti AO, Bleck TP. What’s new in status epilepticus? Intensive Care Med.
2014;40:1359-1362.
16. Shemie SD, Hornby L, Baker A, et al. International guideline development for the
determination of death. Intensive Care Med. 2014;40:788-797.
17. Silbergleit R, Durkalski V, Lowenstein D, et al. Intramuscular versus intravenous
therapy for prehospital status epilepticus. N Engl J Med. 2012;366:591-600.
18. Torbey MT, Bösel J, Rhoney DH, et al. Evidence-based guidelines for the
management of large hemispheric infarction: a statement for health care
professionals from the Neurocritical Care Society and the German Society for
Neurointensive Care and Emergency Medicine. Neurocrit Care. 2015;22:146-164.
19. Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant
infarction of the middle cerebral artery: a pooled analysis of three randomised
controlled trials. Lancet Neurol. 2007;6:215-222.
20. Walters BC, Hadley MN, Hurlbert RJ, et al. Guidelines for the management of
acute cervical spine and spinal cord injuries: 2013 update. Neurosurgery. 2013;60
(Suppl 1):82-91.
Suggested Websites
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org.

2. Brain Trauma Foundation. http://www.braintrauma.org.
3. Brain Attack Coalition. http://www.stroke-site.org.
4. Neurocritical Care Society. http://www.neurocriticalcare.org.
Chapter 9
Basic Trauma and Burn Support
Objectives
Prioritize and initiate a timely assessment of the traumatized patient.

Initiate treatment of life-threatening traumatic injury.
Utilize radiography in identifying significant traumatic injury.
Identify and respond to significant changes in the patient’s status after traumatic
injury.
Initiate early burn management.
Review indications for initiating surgical consultation and/or transferring the
patient to a higher level of care.
Case Study
A middle-aged man has been brought to the emergency department after his car collided
with a large truck. He was not wearing a seat belt and was ejected. He is making
incoherent sounds and is unable to clear his oral secretions. He has an open femur
fracture with hemorrhage, and contusions are present over the left chest wall and upper
quadrant of the abdomen. Vital signs include a blood pressure of 90/60 mm Hg, pulse
rate of 125 beats/min, and respiratory rate of 35 breaths/min.
The patient is lethargic but moves all extremities voluntarily. His skin is cool and
clammy.
– What does the primary survey indicate?
– What are the most urgent initial interventions?
I. INTRODUCTION
It is not the intention of the FCCS program to replace the Advanced Trauma Life
Support (ATLS) course provided by the American College of Surgeons. The material
presented here is intended to highlight evaluation and treatment issues for the provider
confronted with a deteriorating patient in the setting of injury. Care providers who
regularly encounter patients with traumatic injuries are encouraged to enroll in an ATLS
course or obtain other similar training.
A. Death Following Injury

In the United States, traumatic injuries remain the leading cause of death in individuals
aged 1 to 44 years. Death due to injury occurs in one of three periods. The first period
is within seconds to minutes of injury, when deaths generally result from severe brain or
high spinal cord injury, loss of the airway, or rupture of the heart, aorta, or other large
blood vessels. Few of these patients can be salvaged because of the severity of injury,
and prevention is the only way to reduce such trauma-related deaths. The second period
occurs within minutes to hours following injury; these deaths are usually due to subdural
and epidural hematomas, hemopneumothorax, solid organ rupture (spleen or liver),
pelvic fractures, or other injuries associated with blood loss. The “golden hour” after
trauma is characterized by the need for rapid assessment and resolution of these
injuries. The third period occurs days to weeks after the initial injury and is most often
due to sepsis with associated multiple organ failure.
Three principles guide the approach to injury. The most important is that the greatest
threat to life must be treated first. The second premise is that it is not necessary to
establish a definitive diagnosis before beginning lifesaving treatment. The third is that a
detailed history is not essential to begin care in the setting of acute injury.
II. Trauma Management

Early management of the seriously injured patient requires simultaneous evaluation and
treatment. The first goal is to ensure adequate oxygen delivery to vital organs by
following an established sequence of priorities that allows identification and treatment
of injuries causing immediate threats to life (primary assessment). Patient management
should begin with the rapid primary evaluation and simultaneous resuscitation of vital
functions, followed by a more detailed secondary assessment (head-to-toe examination),
and finally, the initiation of definitive care. This process begins with the ABCDE of
trauma care, which guides the identification of life-threatening conditions through the
initial assessment sequence of airway, breathing, circulation, disability, and exposure
(Table 9-1).
Table 9-1 Initial Assessment of Trauma
Airway: maintenance with cervical spine precautions

Breathing: ventilation and oxygenation
Circulation: hemorrhage control
Disability: brief neurologic examination
Exposure/environment: clothing removed, avoiding hypothermia
A surgeon skilled in trauma management should be consulted early in the course of all
serious trauma cases. Routing trauma patients to a center with trauma surgeons is crucial
in the survival of the victims. When a surgeon is not immediately available or when the
patient is awaiting transfer, evaluation (tertiary assessment) and intervention should
continue.
A. Primary Assessment: Initial Evaluation and Resuscitation
1. Airway and Breathing

If the patient is able to communicate verbally, the airway is unlikely to be in immediate
jeopardy; however, repeated assessment of airway patency is essential. Patients with
severe head injury (Glasgow Coma Scale [GCS] score of 8 or less) usually require
placement of a definitive, protective airway. Nonpurposeful motor responses support
the need for immediate airway management.
Airway patency should be reassessed

frequently, particularly in patients with
head injury, shock, and facial fractures.
The airway should first be assessed for patency. Assessment for signs of airway
obstruction includes inspection for foreign bodies and facial, mandibular, or
tracheal/laryngeal fractures that may result in airway obstruction. Patients can develop
signs of airway obstruction after benign initial presentation. Profuse bleeding from an
oropharyngeal injury may warrant a definitive airway placement.
After blunt trauma, airway control should proceed on the assumption that an unstable
fracture or ligamentous injury of the cervical spine (C-spine) exists. Airway patency
must be established, supplemental oxygen provided, and adequacy of ventilation
ensured, as discussed in Chapter 2. If active airway intervention is needed before
evaluation for possible C-spine fracture, the technique chosen for airway control
(intubation, adjunctive device, or surgical airway) should take into account the expertise
of available personnel, type of equipment available, patient factors, and injuries. If the
patient is apneic or deteriorating rapidly, effective bag-mask ventilation can be
lifesaving. Standard orotracheal intubation should be attempted with the use of in-line
manual stabilization of the head and neck. Proper in-line stabilization may be
accomplished from the front or the side of the patient. One care provider supports the
occiput and mandible with both hands to maintain neck alignment without applying
traction or distraction. With secure stabilization, the anterior portion of the cervical
collar may be removed to allow airway interventions. In-line stabilization is continued
until the cervical collar is replaced and the endotracheal tube or other airway device is
secured. If an airway cannot otherwise be secured, a laryngeal mask airway,
esophageal-tracheal double lumen airway device, or surgical cricothyrotomy is
indicated.
If the patient is combative and needs an

airway, a rapid-sequence intubation
should be performed.
a. Key Issues in Airway Control

Facial fractures are not an immediate priority unless heavy bleeding or uncontrollable
secretions are present. Similarly, facial fractures usually do not require that the patient
be intubated. Mandibular fractures, however, are more likely to be associated with soft-
tissue injury that may compromise the airway. Care should be taken to avoid
nasotracheal intubation in patients with suspected midface and basal skull fractures.
A cricothyrotomy should be avoided
when tracheal/laryngeal disruption is
suspected.
Further details regarding advanced airway management can be found in Chapter 2.
b. Key Injuries
While many injuries can eventually effect the ability to ventilate and oxygenate, several
important injuries need to be urgently identified and managed.
Pneumothorax is frequently associated with rib fractures and can require chest tube
placement. Any patient who has a pneumothorax on plain chest films and is receiving
general anesthesia should have a chest tube in place. Tension pneumothorax should be
evaluated and treated (Chapter 5). Open pneumothorax is generally associated with
soft-tissue loss requiring dressing closure and chest-tube placement. Massive
hemothorax is suggested by physical examination and chest radiograph. Immediate
evacuation of more than 1500 mL of blood after placement of a chest tube or ongoing
blood loss of >200 mL per hour for 2 to 4 hours is an indication for thoracotomy.
Rib fractures are often missed on a chest radiograph; however, a fracture may be
suspected and documented when tenderness over the fracture is identified during
physical examination. Pain control may be required to ensure adequate spontaneous
ventilation. Flail chest resulting from segmental rib fractures is manifested by
paradoxical movement of the involved portion of the chest wall (ie, inward movement
of the segment during inhalation). Flail chest is also associated with contusion of the
underlying lung, pain, and hypoxemia.
2. Circulation
Case Study
A young man arrives in the emergency department with an epigastric stab wound, but the
character of the weapon is unknown. Presenting systolic blood pressure is 90 mm Hg
and the patient is tachycardic. His systolic blood pressure improves (>100 mm Hg) with
administration of intravenous fluids but deteriorates when bolus fluids are stopped.
Extremities are cool and the patient is anxious.
– Is this patient in shock?
– What is the primary concern?
– What therapy is recommended?
If the initial fluid bolus produces only

transient improvement or no response,
immediate surgical consultation is
required.
The leading cause of shock in a trauma patient is hemorrhage. Initial empiric treatment
in adults consists of isotonic crystalloid infusion (2 L of warmed lactated Ringer or
normal saline solution) via two large-bore peripheral intravenous catheters and control
of external hemorrhage by means of manual compression. Targets for empiric fluid
therapy are normalization of blood pressure, reversal of tachycardia, and maintenance
of adequate organ perfusion (Chapter 7). Patients with no traumatic brain injury, but
extensive hemorrhage that may require operative intervention, are better managed by
resuscitation with permissive hypotension to a systolic blood pressure of 90 to 100 mm
Hg until operative control of the hemorrhage can be accomplished. This supports
control of vessels that may have thrombosed and are not presently bleeding, but that may
re-bleed if the blood pressure is normalized. When hypoperfusion and vascular
compensation limit peripheral access, cannulation of a central vein (ideally with a 7F,
8.5F, or 9F introducer) is an alternative, as is intraosseous access. Concomitant
diagnostic studies for the source of bleeding can include chest radiographs
(hemothorax), pelvic radiograph (pelvic fracture, open-book or vertical pelvic shear
injury), focused assessment sonography in trauma (FAST), or diagnostic peritoneal
lavage (DPL) [intraperitoneal hemorrhage]. If the patient is hemodynamically stable, a
computed tomography (CT) scan of the abdomen and pelvis may be performed to better
delineate the injuries unless a definitive indication to operate is present. A
hemodynamically unstable patient should not be moved for CT scanning. Immediate
control of external hemorrhage should proceed simultaneously with rapid resuscitation.
In trauma to an extremity, direct pressure is recommended. Blind clamping at bleeding
vessels is discouraged to avoid potential injury to adjacent structures.
It is critical not to equate the absence of
hypotension with the absence of shock.
Patients may have significant blood loss
(Class I or II shock) without a change in
blood pressure.
As shown in Table 9-2, a patient’s systolic blood pressure, heart rate, respiratory rate,
and mental status can be used to assess blood loss. The American College of Surgeons
also validates a decrease in pulse pressure as a sign of occult hypoperfusion.
Circulating blood volume corresponds to 7% of normal body weight (70 mL/kg) in an
adult and 8% to 9% of normal body weight (80-90 mL/kg) in children. Blood loss up to
1,200 mL may occur in a normotensive adult (70 kg) with minimal tachycardia. Class II
hemorrhage is uncomplicated shock, but crystalloid resuscitation may be sufficient.
Class III hemorrhage requires crystalloid resuscitation and often blood replacement.
Class IV hemorrhage can be considered preterminal and requires aggressive measures
to restore intravascular volume and red blood cell mass and to control bleeding.
Treatment should be directed by the initial response to therapy rather than by a
classification scheme. Patients will respond to fluid resuscitation in one of three ways.
One group of patients will regain normal vital signs with small volumes of fluid. A
second group of patients will initially respond to the fluid resuscitation, but then
demonstrate signs of hemodynamic deterioration with time or a decrease in the fluid
resuscitation; they will require additional fluids and focused evaluation of the etiology
and treatment of the injuries. This transient response is suggestive of ongoing
hemorrhage. The third group of patients will not show signs of physiologic improvement
despite volume resuscitation; these patients often need immediate operative
intervention. They likely have ongoing major hemorrhage. Without rapid and aggressive
intervention, their mortality will be high.
Table 9-2 Hemorrhage Classificationa
Shock Class
I II III IV
Blood loss (mL)b Up to 750 750-1500 1500-2000 >2000

Blood loss (% blood volume) Up to 15% 15%-30% 30%-40% >40%
Pulse (beats/min) <100 100-120 120-140 >140
Systolic blood pressure (mm Normal Normal Decreased Decreased
Hg)
Pulse pressure Normal or Decreased Decreased Decreased
increased
Respiratory rate 14-20 20-30 30-40 >35
(breaths/min)
Urine output (mL/h) >30 20-30 5-15 Negligible
Mental status Slightly anxious Mildly Anxious, confused Confused, lethargic
anxious
Resuscitation fluid Oral or crystalloid Crystalloid Crystalloid and Blood and
blood crystalloids
aAdapted with permission from the American College of Surgeons. American College of Surgeons
Committee on Trauma. Advanced Trauma Life Support for Doctors (ATLS): Student Course Manual. 9th
ed. Chicago, IL: American College of Surgeons; 2012.
bFor 70-kg man.
When beginning resuscitation for patients in shock, isotonic crystalloid can be used.
However, the volume should be controlled and minimized to no more than 1 or 2 L. If
there is an inadequate physiologic response, this should be followed by the early
administration of packed red blood cells (PRBCs). Fully crossmatched blood is rarely
available for emergency trauma resuscitation. Uncrossmatched type-specific blood can
be safely administered and is available in many hospitals within 15 to 20 minutes after a
request is received. If type-specific blood is not available and the patient is unstable,
O-negative PRBCs should be used. In most trauma centers, uncrossmatched blood is
almost immediately available in the trauma resuscitation area for use in the unstable
trauma patient.
Citrate in PRBCs may chelate calcium,

promoting a coagulation defect in
patients receiving massive transfusion.
Ionized calcium levels should be
monitored and calcium administered as
needed.
In situations where massive transfusion is anticipated or probably likely, the early use
of a balanced resuscitation using a combination of PRBCs, fresh frozen plasma,
platelets, and cryoprecipitate should be strongly considered. In these situations, the most
urgent priority is control of ongoing hemorrhage. Typically this involves operative
intervention; however, with certain injuries−especially severe pelvic fractures with
active bleeding into a pelvic hematoma−other interventions, such as angiography with
embolization, can be lifesaving. Many trauma centers have a massive transfusion
protocol in place to allow the rapid procurement of blood products for administration in
the critically injured, unstable, massively bleeding patient. Developing evidence
suggests that the administration of crystalloid solutions should be minimized, especially
in this population. There is also increasing evidence that the use of ratio-based blood
product resuscitation (PRBCs, fresh frozen plasma, and platelets close to a 1:1:1 ratio)
improves outcomes and may decrease the physiologic insult to these critically ill
patients. Ratio-based resuscitation likely provides some of the same benefits as the use
of fresh whole blood and may be helpful in minimizing the coagulopathy that can
develop in the massively injured.
Patients with massive blood loss require

an early and aggressive balanced
resuscitation with PRBC, fresh frozen
plasma, and platelets, along with
aggressive hemorrhage control.
3. Disability/Exposure
Rapid neurologic evaluation is performed in the emergency department and includes
determination of level of consciousness, pupillary size and reaction, lateralizing signs,
and level of spinal cord injury. The GCS score is a quick, simple method for
determining the level of consciousness and is predictive of outcome (particularly the
best motor response). A decrease in the level of consciousness may reflect decreased
cerebral perfusion or may be due to direct brain injury. Hypoglycemia, ethanol,
narcotics, and other drugs may also be involved. An altered level of consciousness
indicates the need for immediate reevaluation of oxygenation, ventilation, and tissue
perfusion. Changes in consciousness should be assumed to be due to intracerebral
conditions until proven otherwise. If the patient’s condition permits, a good exam prior
to sedation and intubation is essential to determine the presence of any localizing
intracranial or spinal cord injury.
Throughout the initial resuscitation period, efforts should be made to control and
prevent hypothermia. Patients are often hypothermic after environmental exposure, and
the body temperature may fall further after administration of room temperature
resuscitation fluids and cold blood, removal of clothing for examination purposes, loss
of normal temperature-regulating reflexes in shock, or the use of some medications.
Hypothermia contributes to coagulation abnormalities, cardiovascular collapse, and
poor outcome, and so should be avoided and treated. Warm intravenous fluids, heated
respiratory gases in mechanical ventilation, warm rooms, insulating covers, and heat
lamps can be used.
4. Monitoring
Improvements in parameters such as heart rate, blood pressure, pulse pressure,
respiratory rate, acid-base status, body temperature, and urinary output are the best
guides to adequacy of resuscitation. Evaluation begins during the initial survey and
should be repeated frequently. Pulse oximetry is a valuable adjunct for monitoring
hemoglobin saturation with oxygen in injured patients, but it is not useful for evaluating
the adequacy of ventilation. Blood pressure, as the sole marker of resuscitation, may be
a poor measure of actual tissue perfusion. Additional metabolic markers, such as serum
lactate, base deficit, and pH, will assist in the determination of the adequacy of
resuscitation. Perfusion of extremities may be evaluated by examining capillary refill
and hematoma formation, as well as the presence of the peripheral pulses.
A urinary catheter should be inserted as soon as is practical to monitor urine output as a
gauge of renal perfusion, although it must be used with caution in male patients when
urethral injury is suspected (eg, blood at the urethral meatus, scrotal hematoma, or
abnormal prostate on rectal exam). In these cases, a retrograde urethrogram can be used
to rapidly evaluate for urethral injury.
5. Hemorrhagic Shock
As resuscitation proceeds, it is crucial to identify potential causes of hypotension. A
search for occult blood loss should be undertaken after any external hemorrhage is
controlled. The most frequent sites for such blood loss are the chest, abdomen, pelvis,
and the soft tissues adjacent to long bone fractures.
a. Hemothorax
A chest radiograph (ideally with the patient in upright or reverse Trendelenburg position
if hemodynamically stable) is a reliable screen for intrathoracic bleeding.
Ultrasonography of the chest also may reliably detect hemothorax or pericardial fluid.
Hemothorax should be drained promptly by chest tube placement, with a subsequent
radiograph to verify the location of the chest tube, blood evacuation, and lung
expansion. As noted earlier, rapid loss of 1500 mL of blood upon chest tube insertion or
continued losses of >200 mL/h for 2 to 4 hours may necessitate thoracotomy. If
available, autotransfusion devices should be attached to any chest tube drainage canister
placed for massive hemothorax.
b. Intra-abdominal Hemorrhage
Abdominal examination is often misleading in the detection of acute bleeding,
especially in patients with lower chest trauma, rib fractures, spinal cord injury,
intoxication, or altered level of consciousness. Any patient who has sustained
significant blunt torso injury from a direct blow or deceleration, or a penetrating torso
injury must be considered to have an abdominal visceral or vascular injury. Focused
ultrasound for trauma and DPL are the most expedient and reliable methods of
identifying significant intraperitoneal hemorrhage, although the FAST exam has largely
replaced the use of DPL in most institutions. When readily available and used by trained
individuals, FAST has the sensitivity, specificity, and accuracy of DPL in detecting
hemoperitoneum, an injury that requires immediate surgical evaluation to determine the
need for an operative intervention. In stable cases with a positive FAST result,
abdominal CT scan may be appropriate to identify the source of bleeding and determine
the need for any further intervention. Abdominal hemorrhage frequently comes from
splenic or liver laceration, other visceral injury, or retroperitoneal hematoma. Patients
with unstable or abnormal vital signs are usually not candidates for CT scanning and
require surgery to control bleeding.
c. Pelvic Hemorrhage
Assessment of bony stability by means of physical examination and plain radiographs of
the pelvis is crucial for early identification of major pelvic fractures. Patients with
pelvic fractures (open-book or vertical shear) are at high risk for major bleeding, which
is usually venous. Initial management includes vigorous blood volume replacement and,
possibly, mechanical tamponade with a pelvic binder or bedsheet wrapped tightly
around the pelvis to produce circumferential compression. External skeletal fixation
may be helpful if the fracture anatomy is appropriate, and an orthopedic surgeon should
be consulted early in the course of treatment. In patients with arterial bleeding
associated with pelvic injury, CT scanning will reveal a blush of contrast. Pelvic
angiography for embolization should be considered in the persistently hypotensive
patient due to an increased likelihood for arterial bleeding. Angiography may be
required in approximately 10% of patients with pelvic fractures. Recently, angiography
has become the treatment of choice for control of bleeding from pelvic fractures and
hematomas, even in the unstable patient.
d. Long Bone Fractures

Patients with long bone fractures will likely have associated hemorrhage in the
surrounding injured tissue. Humerus and femur fractures may result in 1 to 3 units of
blood loss, which can be problematic in the patient with multiple long bone fractures.
Repeated physical examination for soft tissue swelling and changes in the diameter of
the extremity will assist in the management of these patients.
e. External Hemorrhage
External hemorrhage can be very dramatic, as with a lacerated major arterial or venous
blood vessel where direct pressure will decrease blood loss. Other cases, such as scalp
lacerations, may go unrecognized as a possible source of significant blood loss. Rapid
application of direct pressure, temporizing suture repair, or application of a tourniquet
to a bleeding extremity may be lifesaving. One technique employs a blood pressure cuff
inflated to a pressure higher than the patient’s systolic blood pressure. Tourniquet use
should be followed by surgical consultation as the tourniquet places the extremity in
jeopardy of ischemic injury. In some situations, including military conflict and
intentional mass casualty events, the early control of hemorrhage along with the liberal
use of tourniquets can be lifesaving and may take priority in the initial evaluation and
management.
6. Nonhemorrhagic Shock
The differential diagnosis of nonhemorrhagic shock in the trauma patient includes
obstructive shock (tension pneumothorax, cardiac tamponade), blunt cardiac injury, air
embolism, and neurogenic shock with acute spinal cord injury. Head injury is a rare
cause of hypotension, but when it occurs, it is usually a preterminal event.
a. Tension Pneumothorax
Tension pneumothorax causes hemodynamic compromise and pulmonary dysfunction
due to acute compression of the lung parenchyma and a shift of the mediastinum away
from the hemithorax with the increased pressure. Do not wait for a chest radiograph to
make this diagnosis. Breath sounds will be diminished, lung expansion will be
asynchronous, and patients may develop respiratory distress, acute desaturation,
bradycardia, and occasionally, distended neck veins. Classic venous distension may be
absent in the setting of pneumothorax complicated by hypovolemia. All but gross
changes in breath sounds may be difficult to detect in the resuscitation room. Tracheal
shift is a late sign and may not be a presenting finding. In adults, needle chest
decompression is performed via the midclavicular line in the second intercostal space;
this is a lifesaving intervention that is followed by placement of a chest tube.
If tension pneumothorax is suspected in
an intubated patient, disconnect the
patient from the ventilator and manually
ventilate to evaluate for increasing
resistance.
b. Cardiac Tamponade
The classic signs of cardiac tamponade — hypotension, distant heart sounds, jugular
venous distension, and pulsus paradoxus — may be obscured due to noise and
hypovolemia (decreasing jugular distention). Ultrasound (FAST) is a sensitive test for
fluid in the pericardial sac. Pericardiocentesis via a surgical pericardial window
should be considered for the patient with refractory shock, persistent central venous
hypertension, and a high-risk penetrating wound (between the nipples, above the costal
margin, below the clavicles). When surgical expertise is not available, a
needle/catheter pericardiocentesis may be performed as a temporizing measure.
Occasionally, major blunt chest trauma ruptures the cardiac surface. Most cases involve
atrial tears and can be repaired if diagnosed early.
c. Blunt Cardiac Injury

The diagnosis of blunt cardiac injury should be suspected in a patient involved in a
high-speed, frontal impact accident who has unexplained hypotension or arrhythmia or,
less commonly, cardiogenic shock. Changes in the electrocardiograms (ECGs) are
usually nonspecific and can include premature ventricular contractions, bundle branch
block, atrial fibrillation, unexplained sinus tachycardia, and ST-segment changes. If
blunt cardiac injury is a possibility, a screening ECG should be obtained in the
emergency department. Abnormalities other than tachycardia warrant 24 hours of
monitoring for arrhythmias. Hemodynamically stable individuals with no ECG
abnormalities need no further cardiac evaluation or observation. Echocardiography may
be indicated in hypotensive patients to evaluate cardiac function. Use of cardiac
troponins in diagnosing blunt cardiac injury is sometimes helpful. Treatment includes
correction of acidosis, hypoxia, and electrolyte abnormalities; judicious administration
of fluid; and pharmacologic treatment of life-threatening arrhythmias.
Inotropes may be indicated to support hemodynamic function. It is important to ensure
that refractory hypotension is not due to ongoing blood loss. Patients may present with
acute myocardial infarction secondary to cardiac injury, or an acute myocardial
infarction may have led to trauma (ie, fall, motor vehicle crash).
d. Neurogenic Shock
Neurogenic shock occurs when a cervical or high thoracic spinal cord injury (above T6
level) causes sympathectomy. It is characterized by hypotension, frequently associated
with relative or absolute bradycardia. Flaccid paralysis, loss of extremity reflexes, and
priapism may be associated neurologic findings. Treatment for hypotension includes
volume resuscitation and vasopressors (phenylephrine or norepinephrine) if volume
loading does not reverse the hypotension. Atropine or dopamine may be considered in
the presence of bradycardia associated with hemodynamic instability.
The right ventricle is most frequently

involved in blunt cardiac injury, and
volume challenge is the initial therapy
for hypotension in the absence of
pulmonary edema.
B. Secondary Assessment: Diagnosis and Treatment of Other Injuries

Most patients with acute injuries can be resuscitated to a hemodynamically stable state.
The primary survey should immediately identify acute life-threatening injuries. The next
goal is to complete a secondary assessment to identify and treat other injuries. This
assessment is crucial to allow proper triage to the operating room, radiology suite, or
ICU.
1. History
Essential components of a patient’s history include details of the mechanism of injury,
previous medical illness, current medications, allergies, and tetanus immunization.
2. Physical Examination
The patient should be examined from head to toe. The skull is carefully inspected to
identify occult injuries. Signs of basilar skull fracture include hemotympanum,
rhinorrhea, or otorrhea; Battle sign (ecchymosis of the skin over the mastoid); and
raccoon eyes. Facial bones, mandible, and neck are palpated for tenderness and
crepitus. The GCS score and limited neurologic examination from the initial assessment
are used to evaluate for head trauma (Chapter 8). Extraocular eye movements are
checked to exclude muscle or nerve entrapment. The neck is inspected for distended
neck veins, the position of the trachea, or subcutaneous emphysema. Neck pain or
tenderness over the cervical spine warrants additional radiographs (see later section),
CT, or magnetic resonance imaging. The chest is auscultated and palpated for tenderness
and crepitus. The patient is log-rolled so that the thoracic and lumbar spine can be
palpated for tenderness and other injuries can be detected. In penetrating trauma,
exclude occult entrance or exit wounds in the axillary, cervical, or inguinal regions. The
abdomen is likewise inspected, auscultated, and palpated. The pelvic bones are
assessed for stability with lateral compression, anterior-posterior compression, and a
gentle rocking motion; lack of pain with these motions in an awake patient without
competing pain issues is usually sufficient to rule out significant pelvic bone fractures.
The rectum is evaluated for tone and the presence or absence of blood and to ensure that
the prostate gland is not displaced or difficult to palpate. The presence of
perineal/scrotal hematoma and blood at the urethral meatus implies potential urogenital
injury, which is a risk for urinary catheter insertion. The extremities are inspected,
palpated, and evaluated for range of motion and neurovascular integrity.
3. Laboratory Studies
Minimal testing includes complete blood count, electrolyte measurements, blood
glucose level, blood alcohol level, and toxicology screening. In any patient with
evidence of hypovolemia, blood-group typing and a coagulation profile should be
performed. Arterial blood gas measurements should be analyzed in selected patients to
confirm adequate ventilation and perfusion (presence of acidosis). An elevated serum
amylase level may be an indicator of pancreatic or bowel injury in the patient with blunt
abdominal trauma. Creatinine phosphokinase should be checked if rhabdomyolysis is
suspected. The hematocrit may not reflect the patient’s acute volume status; without
ongoing resuscitation equilibration by transcapillary fluid shifts can take hours to be
reflected as a decrease in hematocrit. In general, a fall of 3% in the hematocrit is
equivalent to 1 unit of blood loss. Serum lactate level measurements and follow-up to
monitor clearance can help management and prognosis.
Reevaluate laboratory results after

initial resuscitation.
4. Radiologic Evaluation
a. General
In the evaluation of blunt multiple-system trauma, a supine chest radiograph and supine
view of the pelvis are obtained as the primary survey is performed. This allows for
interpretation of completed radiographs as the secondary survey begins. Plain films of
the pelvis are crucial for early identification of major fractures and may allow for early
placement of a pelvic binder to help reduce ongoing blood loss.
b. Head
CT scanning is essential for initial evaluation of a head-injured patient or in any patient
with a decreased or altered level of consciousness. Many centers will also obtain a CT
scan of the cervical spine when the head scan is obtained.
c. Spine
The initial lateral C-spine radiograph has been largely abandoned for the diagnosis of
cervical spine injury. Given the common issues in obtaining adequate cervical spine
images, including inadequate visualization of the spine between C7 and T1 and poor
definition of the occiput, most centers now obtain a CT evaluation of any areas that
cannot be clinically cleared or have concerning results on physical exam. In the patient
with increased risk of C-spine injury, cervical immobilization is crucial until these
studies are reviewed and correlated with a reliable physical examination for evidence
of tenderness. However, patients should be removed from a rigid spine board
expeditiously due to the risk of skin pressure injury with extended immobilization.
Magnetic resonance imaging is helpful for disc, spinal cord, and ligament injuries. If a
C-spine fracture is found, radiographic screening of the entire spine is indicated
because ~10% of these patients will have a second, noncontiguous vertebral column
fracture. CT scans of chest and abdomen often can be reformatted to provide
information on spine injury without the need for additional plain radiographs or
additional radiation exposure.
Neurologic examination alone does not exclude a C-spine injury. The following
considerations apply to patients at risk for C-spine injury:
Patients who are alert, awake, and have no changes in neurologic status or neck
pain may be considered to have a stable C-spine and need no radiologic studies.
Beware of injuries that could distract the patient with C-spine injury.
Early CT scans may facilitate evaluation of the C-spine in any head-injured or
intubated patient. Adding CT evaluation of the C-spine to the initial CT scan of the
head is an appropriate strategy after injury.
The presence of paraplegia or quadriplegia is presumptive evidence of spinal
instability.
Patients with neurologic deficits potentially due to a C-spine injury require spine
surgery consultation.
Exclusion of any bony injury does not eliminate the possibility of ligamentous
disruption. Magnetic resonance imaging can facilitate clearance of ligamentous
injury if the examination is not reliable.
d. Chest
Once the spine is cleared for fractures, an upright (or reverse Trendelenburg) chest
radiograph is indicated to better define or identify pneumothorax, hemothorax,
mediastinal widening or irregularity (concern for aortic transection), or fractures, as
well as to confirm the position of various tubes. Chest radiographs are inadequate to
rule out aortic injury when a significant lateral impact or deceleration injury exists.
Suspect this lethal injury where the mediastinum is widened on chest radiographs and an
appropriate mechanism is involved. CT angiography provides an excellent method to
screen for aortic injury and define other thoracic injuries. Its use has largely replaced
traditional angiography in the initial diagnosis of thoracic aortic injuries.
Persistent pneumothorax despite a

functioning chest tube or persistent air
loss through the chest tube system may
indicate a tracheobronchial injury.
e. Abdomen
Plain abdominal radiographs are not usually helpful. In the hemodynamically stable
patient, a CT scan of the abdomen and pelvis and the FAST examination are the
mainstays of abdominal evaluation in a trauma patient. FAST can be followed up with a
CT scan of the abdomen if free peritoneal fluid is identified in the stable patient. DPL
may still be used in certain circumstances, but has generally been replaced by the CT
imaging and the FAST exam.
f. Genitourinary Tract
Hematuria may be evaluated with a CT scan or other contrast studies. It provides
anatomic detail about abdominal and retroperitoneal structures and any direct injury to
the kidney(s). If physical examination suggests that a urethral injury is present, a
urethrogram should be obtained before urinary catheterization. A cystogram may be
indicated if bladder injury is suspected. Intravenous pyelograms are not commonly
performed.
g. Skeletal Fractures
Films of the extremities (anterior posterior and lateral views) should be obtained on the
basis of physical examination or patient complaint. Films should include the joint above
and below the site of injury.
5. Other Issues
Remember to consult specialty services

early so that they can offer input into
treatment decisions.
A nasogastric tube serves to decompress the stomach and may reduce the risk of
pulmonary aspiration; however, it should be placed orally in patients with midfacial
fractures or possible basilar skull fractures. Blood in the gastric aspirate may be the
only sign of an otherwise occult injury to the stomach or duodenum, and further
investigation may be indicated. Tetanus prophylaxis is routine (Table 9-3). Systemic
antibiotics should usually be withheld until a specific indication is determined, but they
are employed in three situations: (1) patients undergoing intracranial pressure
monitoring or chest tube placement frequently receive gram-positive coverage when the
device is inserted; (2) patients with penetrating abdominal trauma may be given
coverage for gram-negative aerobic and anaerobic organisms for the first 24 hours after
injury; and (3) patients with open fractures are given gram-positive coverage for 24
hours as orthopedic evaluation is arranged.
Table 9-3 Guide to Tetanus Prophylaxis in Routine Wound Managementa
History of Absorbed Clean Minor Wounds All Other Wounds b

Tetanus Toxoid (Not prone to tetanus b) (Tetanus-prone c)
Tdap or Tdb TIGd Tdap or Tdb TIGd

Unknown or <3 doses Yes No Yes Yes
≥3 doses e Nof No Nog No
Abbreviations: Tdap, tetanus toxoid, reduced diphtheria toxoid, acellular pertussis vaccine; Td, tetanus
toxoid and reduced diphtheria toxoid — for adult use (dose = 0.5 mL; TIG, tetanus immune globulin —
human (dose = 250 IU.
aPatients who have completed a three-dose primary tetanus vaccination series and have received a tetanus
toxoid-containing vaccine <5 years before the injury do not require a tetanus toxoid-containing vaccine for
wound management.
bChildren <7 years = Tdap is recommended; if pertussis vaccine is contraindicated, Td is given. Children 7-
9 years or adults >65 years = Td is recommended. Children and adults 10-64 years = Tdap is preferred to
Td if the patient has never received Tdap and has no contraindication to pertussis vaccine. For patients >7
years of age, if Tdap is not available or not indicated because of age, Td is preferred to tetanus toxoid.
cSuch 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.
dEquine tetanus antitoxin should be used when TIG is not available.
eIf only three doses of fluid toxoid have been received, a fourth dose – preferably an adsorbed toxoid –
should be given. Although licensed, fluid tetanus toxoid is rarely used.
fYes, if ≥10 years since the last tetanus toxoid-containing dose.
gYes, if ≥5 years since the last tetanus toxoid-containing dose; more frequent boosters are not needed and
can accentuate side effects.
Female patients of childbearing age should be questioned about the possibility of

pregnancy or be checked with a β-human chorionic gonadotropin test before extensive
radiographic evaluation is performed unless significant hemodynamic instability is
present. The priority with the unstable pregnant patient always has to be maternal
resuscitation and stabilization. Anyone in her second or third trimester should be
positioned with a wedge under her back to elevate the right side, avoiding compression
of the vena cava. This is done only after examination of the spine and pelvis does not
reveal any pain or tenderness, which may indicate a fracture. Remember that the optimal
care of the mother yields optimal care for the fetus. Obstetrical consultation should be
considered (Chapter 14).
Another important issue is the need for adequate tetanus prophylaxis in patients with
open wounds. The patient’s current vaccination status must be verified and updated if
needed. In those who have an unclear immunization status or with especially
contaminated tetanus-prone wounds, the use of tetanus immune globulin should be
considered (Table 9-3).
C. Tertiary Assessment: Ongoing Evaluation
Case Study
A middle-aged man sustained multiple liver lacerations in a motor vehicle crash. He

also had mesenteric lacerations and bowel resection was performed. The ends of the
bowel were stapled, and the abdomen was filled with packs to control venous bleeding
from the liver. He continues to require fluid resuscitation and administration of blood
products due to coagulopathy. Several hours after admission to the ICU, increased
airway pressures and falling urine output are noted.
– What are possible causes of increased airway pressures?
– Why has the urine output fallen?
After life- and limb-threatening injuries have been addressed and metabolic
derangements have been corrected, periodic systematic assessment is performed to
identify occult injuries not evident at presentation.
1. Head Injury
Evaluation of the head-injured patient is an ongoing process requiring early
neurosurgical consultation. Serial assessment of the GCS scores, pupil size and
response, and presence or absence of lateralizing neurologic signs is crucial. Any
changes in examination results are noted and acted upon as they are discovered.
Serial CT scans of the head may offer clinically useful information, but the key to
patient management is detection of changes in physical examination. Continued
resuscitation is imperative to avoid secondary brain injury, which typically occurs when
a patient becomes hypoxic or hypotensive during acute care. These secondary insults
increase the likelihood of poor outcome (Chapter 8).
The administration of atropine or

dopamine, as well as mydriatic agents,
may dilate the pupils and lead to a false
diagnosis of a more severe head injury.
2. Pulmonary Injury
Trauma patients often have a full stomach at the time of injury and experience
aspiration. Aspiration of the acidic gastric contents may cause a chemical pneumonitis
initially and predispose patients to an infective pneumonitis or acute respiratory distress
syndrome later. Antibiotics are not indicated in initial management. Bronchoscopy may
be needed for removal of large particulate matter.
Delayed onset of pneumothorax or hemothorax may follow chest trauma. Additionally,
pulmonary contusions and resulting acute respiratory distress syndrome may not become
obvious until later (12-48 hours). Continued assessment includes physical examination,
oximetry and/or arterial blood gas measurements, chest radiographs, and ventilatory
mechanics.
3. Cardiac Injury
Continuous ECG monitoring and frequent measurements of blood pressure are
mandatory in the emergency department and ICU. Continuous arterial blood pressure
monitoring may be indicated (Chapter 6). Electrolyte disturbances may lead to cardiac
contractile dysfunction or arrhythmias in the aggressively resuscitated trauma patient.
Common electrolyte disturbances include hyperchloremia, hypokalemia and
hyperkalemia, hypomagnesemia, and hypocalcemia.
4. Abdominal Injury
Substance abuse or neurologic injury may not allow reliable initial abdominal
examination. Perforation of a hollow viscus in blunt trauma is sometimes difficult to
diagnose. Free air under the diaphragm on an upright chest radiograph, over the liver on
a left lateral decubitus radiograph, or on an abdominal CT indicates the need for
operative exploration. CT scanning also provides information about the
retroperitoneum. In the head-injured patient who is undergoing a head CT scan and has a
nonoperative neurologic injury, abdominal scanning should be considered, as physical
examination may be unreliable. However, caution must be used in the clinical
interpretation of CT imaging for hollow viscus injury - a negative scan does not
absolutely rule out the possibility of an occult injury.
A frequently missed condition is abdominal compartment syndrome. This condition
occurs when intra-abdominal pressure increases due to intraperitoneal or
retroperitoneal hemorrhage, ascitic fluid accumulation, edema secondary to massive
fluid resuscitation, or intraoperative surgical closure of the abdomen under tension.
Increased intra-abdominal pressure decreases cardiac output and compresses the
vascular bed and kidneys. The diaphragm is displaced upward by increased intra-
abdominal pressure, which results in decreased thoracic volume and compliance.
Decreased volume within the pleural cavity predisposes to atelectasis, and ventilated
patients with intra-abdominal hypertension require increased airway pressure to deliver
a fixed tidal volume. Vascular compression can decrease blood flow to the liver and
kidneys with resultant dysfunction. Finally, intra-abdominal hypertension significantly
increases intracranial pressure (Chapter 13).
5. Musculoskeletal Injury
The neurologic and vascular evaluation of the extremities is an ongoing process. A
swollen and tense extremity should be watched closely for the development of a
compartment syndrome, particularly in patients with decreased responsiveness. In alert
patients, serial physical examination is the best monitoring method. Classical signs
include pain, pallor, pulselessness, paresthesia, and/or paralysis. Loss of pulse is a very
late finding. The most helpful early signs are complaints of pain out of proportion to
physical findings and severe pain on passive stretch of the involved muscle groups. In
the unconscious patient or when the examination is unreliable, compartment pressure
may be monitored using a needle with a standard gauge. Pressures >30 mm Hg warrant
consideration of fasciotomy.
Urgent fasciotomy is required for

compartment syndrome.
Musculoskeletal examination should be repeated, either as patients recover from other

injuries or as their mental status clears, to identify new pain or tenderness. Plain
radiographs should then be obtained to identify occult fractures. Commonly missed
orthopedic injuries include fractures of the scapula, thoracic and lumbar spine, pelvis,
ankle, and wrist.
Crush syndrome should be considered when patients have been trapped, injury to large
muscle mass is involved, prolonged compression has occurred with protracted
immobilization, or vascular compromise is present (such as tourniquet use or
compartment syndrome). Crush syndrome develops when damaged myocytes lyse,
releasing myoglobin, potassium, phosphorus, and calcium. Manifestations of this
syndrome include cardiac dysrhythmias, renal failure, metabolic acidosis, and
hypovolemia. Preemptive hydration before reperfusion of crushed muscle mass usually
is accomplished before arrival at the hospital. Revascularization of ischemic
extremities, fasciotomy for compartment syndrome, or release of tourniquets can mimic
this situation. Before reperfusion, normal saline should be administered (1- to 2-L bolus
or 10-15 mL/kg/h). Careful monitoring for cardiac signs of hyperkalemia should be
instituted. After reperfusion, aggressive hydration to maintain urine output above 3 to 4
mL/kg/h helps prevent heme pigment-associated renal injury. Adjuvants such as
bicarbonate and mannitol may be used.
6. Other Considerations
Resuscitation is an ongoing process. Traditional end points such as normalization of
blood pressure, heart rate, and urine output may not always reflect complete correction
of the shock state. The attainment of normal vital signs can occur even in the setting of
tissue hypoperfusion resulting in a compensated state of shock. Lactate concentration
and resolution of metabolic acidosis may provide more definitive end points for
adequacy of resuscitation. Because the time to normalization of these parameters is
predictive of survival, additional resuscitation in the form of volume replacement, red
cell transfusion, or support with vasoactive agents may be indicated within the first 24
hours following injury despite normal or near-normal vital signs. Persistence of a
metabolic acidosis or elevated lactate concentration may be an early indicator of
complications, including ongoing hemorrhage or abdominal compartment syndrome.
Damage control surgery (initially limited to control of bleeding and decontamination of
hollow organ ruptures with spillage) may be needed in the first 24 to 48 hours, before
definitive surgery is performed. Many trauma patients benefit from delayed definitive
surgery, particularly the repair of fractures, during this period of ongoing stabilization.
Decisions to proceed with surgery should be made after appropriate consultation with
the primary surgical service, a critical care physician, and other consultants as
indicated.
Some patients will benefit by undergoing

stabilizing procedures such as washout,
debridement, and placement of external
fixation for open fractures followed by
delayed definitive repair.
In the immediate resuscitation period, periodic reassessments are important. Once a
patient is stabilized, all intravenous access sites should be reassessed. Because full
sterile precautions to prevent line-related infections may not be feasible during
emergency vascular access, many lines will need to be replaced. If central venous
access is no longer indicated, it should be discontinued.
III. BURN INJURY: INITIAL EVALUATION AND STABILIZATION
Case Study
A young man is brought in after a gasoline can exploded as he was burning brush. The
patient sustained a full-thickness burn injury to both forearms and showed signs of flash-
burn injury to his face. He is in no respiratory distress and has received no fluids since
his injury. Although he has no abdominal burns, he complains of abdominal pain. Family
members recall that the patient was thrown into a tree stump by the explosion. You are
asked to see the patient in the emergency department to assist during his initial wound
care.
– What are the initial evaluation priorities?
– What is the greatest risk to this patient?
A. General
Burn injuries represent a significant cause of morbidity and mortality. Deaths from burn
injury occur with greatest frequency as a result of residential fires with smoke
inhalation. Like other forms of injury, burns tend to be frequent in the young and the
elderly. Scalds are the most common form of childhood injury, whereas electrical and
chemical injuries affect adults in the workplace. Factors that affect burn mortality
include size of cutaneous injury, patient age, and presence or absence of inhalation
injury. Burn injuries should not distract providers from seeking other potential traumatic
injuries. The initial evaluation and treatment of a serious burn injury follows the same
pathway as trauma, including the primary and secondary surveys.
B. Airway/Breathing
The initial evaluation of the airway is directed, in part, by the history of the injury.
Patients who are at the greatest risk of smoke inhalation injury typically have a history
of being in a closed space with flame and smoke. With increased exposure time, the
likelihood of injury increases. Smoke inhalation injury can be described by three
mechanisms. These include particulate injury, toxic byproducts of combustion injury,
and direct thermal injury. Particulates found in the soot and smoke of the fire are
responsible for a reactive airway injury that may result in bronchospasm. Toxic
exposure may have direct cytotoxic effect on alveolar tissue or affect energy-generating
pathways, or bind hemoglobin and reduce the availability of oxygen for intracellular
use. Direct thermal injury can result in oral, nasal, and upper respiratory injury with
airway swelling.
Inhalation injury is generally diagnosed by a combination of clinical signs and
symptoms confirmed by bronchoscopy. Clinical findings include facial burns, parched
oral mucosa, nasal singeing, soot in the oral and nasal passages, and symptoms of
reactive airway exacerbation. Bronchoscopic findings include mucosal edema,
ulceration, sloughing, and mucous plugging. Chest radiographs are frequently normal at
admission, and hypoxemia often is not appreciated.
At room air, the half-life of carbon

monoxide in association with
hemoglobin is 4 hours; at 100% oxygen,
the half-life is only 30 minutes.
Three stages of inhalation injury have been identified:
1. Acute hypoxia with asphyxia typically occurs at the scene of the fire.
2. Upper airway and pulmonary edema may evolve during the first hours to days after
injury.
3. Infectious complications that stem from exposure to heat and chemical irritants may
appear later (eg, pneumonia).
Treatment of inhalation injury is largely supportive. If exposure to carbon monoxide is

suspected, 100% oxygen should be provided. Early intubation is advocated, especially
if the patient will be transferred, because pulmonary and laryngeal injury may quickly
evolve even though the initial airway assessment is satisfactory. Caution should be
exercised in the use of succinylcholine due to the possibility of clinically significant
hyperkalemia. Intravascular resuscitation should not be delayed or withheld because
inhalation injury increases resuscitation fluid requirements. Humidification of inhaled
gases helps in secretion control and reduces desiccation injury to the airway.
C. Circulation
Patients sustaining small burns (<20% total body surface area [TBSA]) typically will
have normal vital signs. Those with larger burns (>20% TBSA) may develop burn
shock. This is due to a diffuse capillary leak syndrome resulting from the release of
cytokines, interleukins, and vasoactive amines and causing third spacing of fluid. The
combined loss of fluid from the burned surface area and the interstitial edema may result
in the loss of circulating volume. Systemic hypotension may ensue. Resuscitation
following the American Burn Association recommendations (discussed later) should be
followed as it permits large volumes of fluid to be administered over an extended
period. Large-bore peripheral intravenous catheters should be placed (through the burn,
if necessary). The preferred resuscitation fluid is lactated Ringer solution.
D. Assessment of Injury
The approach to the initial assessment is the same as in trauma. An initial primary
survey (ABCDE) is performed, followed by a head-to-toe examination. All clothes must
be removed to determine burn size, and the patient must be covered with blankets
because heat is lost quickly. Depending upon the history, the patient may have other
injuries and should be assessed for trauma in accordance with the guidelines outlined.
1. Depth of Burns
There are three burn depths:
1. First-degree (superficial): erythematous, painful

2. Second-degree (partial thickness): red, swollen, blistered, weeping, very painful
3. Third-degree (full thickness): white, leathery, painless
Third-degree or full-thickness injuries involve all layers of the epidermis and dermis
and require surgical reconstruction. Burns that involve deep structures, such as tendon,
muscle, and bone, have been called fourth-degree burns.
2. Burn Area (Rule of Nines)

The rule of nines is commonly used to estimate the surface area that has been burned
(Figure 9-1). The head and upper extremities each represent 9% of the TBSA. The
anterior and posterior trunk and the lower extremities each represent 18%, and the
perineum represents 1% of the TBSA. In children, the head is proportionally larger,
leading to a relative decrease in the area of other body segments. Alternatively, the
patient’s hand, which equals roughly 1% of TBSA, may be used to estimate the size of a
small or irregular burn. An often used tool to estimate the total body surface area in
children younger than 15 years is the Lund-Browder Chart (Figure 9-2).
Figure 9-1. Rule of Nines
Most appropriate for adults and children over 15 years of age.
Figure 9-2. Lund-Browder Chart

LUND-BROWDER CHART
Relative Percentage of Body Surface Area Affected by Growth
Age in years 0 1 5 10 15 Adult
A-head (back or front) 9½ 8½ 6½ 5½ 4½ 3½
B-1 thigh (back or front) 2¾ 3¼ 4 4¼ 4½ 4¾
C-1 leg (back or front) 2½ 2½ 2¾ 3 3¼ 3½
The Lund-Browder chart is the most accurate method for estimating burn extent and must be used in the
evaluation of pediatric patients under 15 years of age.
E. Resuscitation
Burn shock presents with profound hypovolemia, which has both interstitial and
intracellular components. Increased capillary permeability is one of the key components
of the burn shock response. In small burns, maximal edema is seen 8 to 12 hours after
injury; larger burns at 12 to 24 hours. Plasma volume loss coincides with edema
formation and increased extracellular fluid. Edema is affected by fluid administration
during resuscitation. Fluid and electrolytes should be replaced as dictated by organ
perfusion indicators and electrolyte imbalance. Because fluid and electrolyte losses in
burns are primarily insensible, fluid lost cannot be quantified adequately. Venous access
should be obtained and a urinary catheter placed. The American Burn Association
recommends the consensus formula of 2 to 4 mL/kg/% TBSA as an estimation of the
fluid requirements in the initial 24 hours after serious burn injuries. Beginning at the
low end of this range may reduce edema and extravascular complications such as
abdominal compartment syndrome. The TBSA is calculated only for second- or third-
degree burns. Resuscitation is carried out with Ringer lactate solution. Half of the
crystalloid resuscitation should be administered in the first 8 hours, the remaining over
the next 16 hours. Surrogate markers of adequate resuscitation include normalization of
blood pressure, heart rate, and urine output. Appropriate urine output in adults is 0.5 to
1 mL/kg/h and 1 to 1.5 mL/kg/h in children. An arterial blood gas measurement to
monitor the pH and base deficit and serum lactate levels are also good markers of
adequate resuscitation. While appropriate resuscitation is critical to maintain
physiology, care must be taken to avoid over-resuscitation as this can lead to significant
increases in edema and result in progression of the burn injury.
While volume resuscitation formulas

give a good estimate of the initial
volume requirements for resuscitation in
the critically burned patient, the most
important indicator of appropriate
resuscitation is adequate urine output.
A circumferential burn to an extremity may develop significant edema that the

underlying tissue cannot accommodate due to the constrictive nature of the burn wound.
Impaired limb and tissue perfusion may ensue that can only be managed by performing
an escharotomy to the extremity and/or digits. In larger burns of the abdomen and chest
wall, a compartment syndrome may develop whereby cardiovascular and respiratory
compromise may mandate torso escharotomies or abdominal decompression. Surgical
consultation should be sought immediately for any of these problems.
F. Carbon Monoxide Exposure

A fire in an enclosed space mandates consideration of carbon monoxide poisoning in
addition to the worry for inhalation injury. The typical oxygen saturation monitor will
not detect carbon monoxide and can give artificially elevated oxygen saturation levels;
therefore, if carbon monoxide poisoning is suspected, an arterial blood gas with a
carboxyhemoglobin level will clarify the clinical picture. High-flow 100% oxygen will
reduce the half-life of carbon monoxide in the plasma and is the primary treatment.
Early use of hyperbaric oxygen for patients with high carboxyhemoglobin levels
(>25%) or evidence of significant neurologic or cardiovascular toxicity has been
recommended, but data supporting this recommendation are limited.
G. Burn Wound
Local wound care begins with serial debridement of nonviable tissue and blisters by
appropriate surgical consultants. Little care is required for the burn wound before
transfer to the burn center or surgical consultation. If gross contamination is present, a
gentle washing and coverage with clean linen may be appropriate. If the patient cannot
be rapidly transferred to a burn center, it may be necessary to apply silver sulfadiazine
(or appropriate antibiotic ointment) and occlusive dressings to help prevent evaporative
heat loss.
H. Other Considerations
Placement of a nasogastric tube is indicated if the patient vomits, requires intubation, or
has a burn >20% of TBSA. This may also prove beneficial to provide nutritional
support for large burns, given the high nutritional requirements. Intravenous opiates
should be given for pain. Rings and bracelets should be removed as they may cause
constriction early in resuscitation. Burns are tetanus-prone injuries, and tetanus
prophylaxis should be reviewed (Table 9-3).
I. Special Considerations
1. Chemical Burns
Chemical burns may be caused by acid (eg, cleaning products, industrial applications),
alkali (eg, hydrides of sodium, potassium, and sodas of ammonia), or organic
compounds (eg, petroleum products). Severity of injury relates to the agent involved, its
concentration, and the duration of contact. Initial care requires removing the patient
from the source of chemical injury immediately. In general, removal of clothing is
essential. Dry substances should be brushed off and the area irrigated copiously with
water. Do not use neutralizing agents as they may increase the severity of burn.
Contact with petroleum products (such as spilled gasoline at the scene of a motor
vehicle crash) is associated with rapid skin penetration and late multiple-organ failure.
Again, rapid removal of the patient from the source and vigorous irrigation of exposed
surfaces are warranted. Advice regarding chemical burns is available from regional
burn centers.
2. Electrical Injury
Electrical injury is a syndrome with a variety of presentations. Exposure to an electrical
source <1,000 volts produces a low voltage injury similar to other cutaneous burns.
When exposure exceeds 1,000 volts, a greater potential for deep as well as cutaneous
injury exists.
Three types of skin injury can occur with electrocution:
1. Entrance and exit wounds, typically circumscribed, deep lesions, occur at points of
contact with the electrical source or ground (usually hands and feet).
2. Cutaneous burns may be caused by arc injury from the primary site to the patient, a
flash injury, or an actual flame injury if clothing catches fire.
3. Deep soft tissue injuries involve muscle, nerve, or the vascular bed as current
passes through the tissue.
Beware of pneumothorax, airway compromise, cardiac arrest, and blunt injury

secondary to falls and violent muscle contraction. Muscle compartment pressures may
increase, necessitating fasciotomy, not just escharotomy. If myoglobin is present in the
urine or creatine kinase concentrations are elevated, provide adequate intravascular
fluid to increase the urine output to 3 to 4 mL/kg/h until resolution of the
rhabdomyolysis. Patients may develop ileus after electrocution. The ECG should be
reviewed in electrical injury.
The initial priority in the management of electrocution is removal of necrotic tissue and
decompression of compromised deep tissue compartments, particularly muscle.
Resuscitation is begun at 4 mL/kg/% TBSA cutaneous injury and titrated to maintain
urine output of 0.5 to 1 mL/kg/h unless rhabdomyolysis is present and higher urine
output is desirable. Aggressive fluid resuscitation potentiates filtering of pigment and
dilution of iron (nephrotoxic). Alkalinization of the urine may be considered to decrease
the nephrotoxic potential despite lack of supportive evidence. If large areas of soft-
tissue injury are present, surgical consultation should be requested. As with other burns,
infection is the chief risk, but other potential problems are myocardial and vascular
injury, encephalopathy, cataracts, and gut perforation.
Lightning injury may be thought of as massive exposure to direct current. Most injury is
topical because exposure times are extremely brief. Mortality rates associated with
lightning relate to early cardiac and respiratory arrest. Aggressive basic and advanced
life support may be lifesaving for these patients.
IV. REFERRAL AND TRANSFER CONSIDERATIONS

Early involvement of surgical expertise is important in the care of the injured patient. A
surgeon should be summoned as soon as it is known that a seriously injured patient is
arriving. Early neurosurgical consultation is advised for patients with head injury.
General guidelines for field triage and interfacility transfer have used physiologic,
anatomic, and high-risk mechanistic criteria to suggest triggers for triage and transfer.
One may extrapolate that these parameters can be used to initiate involvement of a
trauma surgeon as well. Some triggers are suggested in Table 9-4 and Table 9-5.
American Burn Association Criteria for Patient Transfer to a Burn

Table 9-4
Centera
Partial-thickness burns greater than 10% of total body surface area

Third-degree burns in any age group
Burns involving the face, hands, feet, genitalia, perineum, or major joints
Patients at the extremes of age or those with significant comorbid disease
Electric burns and chemical burns
Smoke inhalation injury
Patients with combined trauma and significant burn injury
Children at hospitals with no expertise in caring for pediatric burn patients
Burns suspected to be due to child or elder abuse
Burn patients with a delayed presentation or evidence of burn wound infection
aAdapted with permission from the American College of Surgeons. American College of Surgeons
Committee on Trauma. Guidelines for the operation of burn centers. In: Resources for Optimal Care of the
Injured Patient. Chicago, IL: American College of Surgeons; 2006:79-86.
Table 9-5 Indications for Field Triage and Interfacility Transfera
Physiologic Criteria
Glasgow Coma Scale score of <13
Systolic blood pressure <90 mm Hg
Respiratory rate <10 breaths/min or >29 breaths/min (<20 breaths/min in infant <1 year)
Anatomic/Injury Triggers
Penetrating injuries to head, neck, torso, and extremities proximal elbow or knee
Chest wall instability or deformity
Amputation proximal to the wrist or ankle
Two or more proximal long bone fractures
Crushed, degloved, mangled, or pulseless extremity
Pelvic fracture
Open or depressed skull fracture
Paralysis
Mechanism of Injury Triggers
Adult: falls >20 feet

Children: falls >10 feet
High-risk automobile crash
Intrusion: >12 inches occupant side; >18 inches any side (including roof)
Ejection (partial or complete) from automobile
Death in same passenger compartment
Vehicle telemetry data consistent with high risk of injury
Auto vs. pedestrian/bicyclist: thrown, run over, or with significant ( >20 mph) impact
Motorcycle crash >20 mph
Patient Triggers
Age >55 years

Systolic blood pressure <110 mm Hg in persons aged >65 years
Falls in older adults (including ground level falls)
Pediatric trauma transport
Anticoagulant use or bleeding disorders
Burns
Pregnancy >20 weeks
Judgment of emergency medical services provider
aAdapted
from Centers for Disease Control and Prevention. Guidelines for field triage of injured patients:
Recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012;61(1:1-
21.
If appropriate surgical services are unavailable, early transfer to the closest trauma or
burn center should be initiated. This should not be delayed for additional radiologic
studies if surgical resources are unavailable, unless those studies are requested by the
accepting physician. The trauma center should be contacted for advice and to discuss
potential problems or concerns with transport personnel.
Common pitfalls in the transfer of seriously ill patients include failure to intubate before
transfer, failure to recognize the need for transfer to a higher level of care, and a general
failure to stabilize the patient adequately before transport. Unrecognized ongoing
hemorrhage, delayed onset of tension pneumothorax, and reversible/preventable causes
of secondary brain injury must be considered.
Key Points
Basic Trauma and Burn Support

The first goal in trauma management is to identify and treat immediately life-
threatening injuries by following the ABCDE sequence of priorities.
After blunt trauma, airway control should proceed on the assumption that an
unstable cervical spine injury exists.
A diagnosis of tension pneumothorax should be based on clinical criteria and not
on a chest radiograph.
Hemorrhage is the most likely cause of shock after injury, and initial empiric
treatment consists of crystalloid infusion to normalize blood pressure, reverse
tachycardia, and maintain adequate organ perfusion.
In general, blood should be added to resuscitation early if the response is
inadequate or if continued ongoing hemorrhage is suspected. Uncrossmatched,
type-specific blood can be administered safely.
A secondary assessment includes a head-to-toe examination to identify and treat
potentially life-threatening injuries.
Computed tomographic scanning is essential for the initial evaluation of head-
injured patients with a depressed level of consciousness.
Burn resuscitation is proportional to the area sustaining second- and third-degree
burns and is titrated to signs of perfusion. Adequate urine output is one of the key
indicators of adequate resuscitation.
Closed-space smoke inhalation injury places the patient at high risk for upper
airway and inhalation injury that may not be obvious at the initial presentation.
Surgical expertise should be secured early and transfer considered for those
patients who require a higher level of care.
Transfer to a specialized care setting should not be delayed for additional
radiologic studies unless the accepting physician requests the studies.
Suggested Readings
1. American College of Surgeons Committee on Trauma. Advanced Trauma Life

Support for Doctors (ATLS): Student Course Manual. 9th ed. Chicago, IL:
American College of Surgeons; 2012.
2. American College of Surgeons Committee on Trauma. Guidelines for the operation
of burn centers. In: Resources for Optimal Care of the Injured Patient. Chicago,
IL: American College of Surgeons; 2006:79-86.
3. Bagley LJ. Imaging of spinal trauma. Radiol Clin North Am. 2006;44:1-12.
4. Brain Trauma Foundation. Management and prognosis of severe traumatic brain
injury. J Neurotrauma. 2007;24(Suppl 1):i-S106.
5. Chan O, Wilson A, Walsh M. Major trauma. BMJ. 2005;330:1136-1138.
6. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal
Compartment Syndrome, II: Recommendations. Intensive Care Med. 2007;33:951-
962.
7. Elliott DC. An evaluation of the end points of resuscitation. J Am Coll Surg.
1998;187:536-547.
8. Herndon DN, ed. Total Burn Care. 3rd ed. Philadelphia, PA: Saunders-Elsevier
Inc; 2007.
9. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in damage control for
exsanguinating penetrating abdominal injury. J Trauma. 2001;51:261-271.
10. Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: Directly
addressing the early coagulopathy of trauma. J Trauma. 2007;62:307-310.
11. Mattox KL, Moore EE, Feliciano DV, eds. Trauma. 7th ed. New York, NY:
McGraw-Hill; 2012.
12. Morrison CA, Carrick MM, Norman MA, et al. Hypotensive resuscitation strategy
reduces transfusion requirements and severe postoperative coagulopathy in trauma
patients with hemorrhagic shock: Preliminary results of a randomized controlled
trial. J Trauma. 2011;70:652-663.
13. Pryor JP, Braslow B, Reilly PM, et al. The evolving role of interventional
radiology in trauma care. J Trauma. 2005;59:102-104.
14. Rhee P, Nunley MK, Demetriades D, et al. Tetanus and trauma: A review and
recommendations. J Trauma. 2005;58:1082-1088.
15. Rossaint R, Bouillon B, Cerny V, et al. Management of bleeding following major
trauma: An updated European guideline. Crit Care. 2010;14(2):R52.
16. Sarrafzadeh AS, Peltonen EE, Kaisers U, et al. Secondary insults in severe head
injury: Do multiply injured patients do worse? Crit Care Med. 2001;29:1116-
1123.
17. Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care Med
2009; 37:2819–26.
18. Society of Critical Care Medicine. Fundamental Disaster Management. 3rd ed.
Mount Prospect, IL: Society of Critical Care Medicine; 2009.
19. Stengel D, Bauwens K, Sehouli J, et al. Emergency ultrasound-based algorithms
for diagnosing blunt abdominal trauma. Cochrane Database of Syst Rev. 2005;
(2):CD004446. doi: 10.1002/14651858.CD004446.pub2.
20. Sasser SM, Hunt RC, Faul M, et al; Centers for Disease Control and Prevention.
Guidelines for field triage of injured patients: Recommendations of the National
Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012;61(1):1-21.
21. American College of Surgeons. Hartford Consensus Compendium. Bulletin of the
American College of Surgeons. 2015;100(1S):1-88
Suggested Websites
1. Society of Critical Care Medicine. www.sccm.org

2. American Burn Association. www.ameriburn.org
3. Burn Surgery. www.burnsurgery.org. Brain Trauma Foundation
www.braintrauma.org
4. American Association for the Surgery of Trauma. www.aast.org
5. Centers for Disease Control and Prevention – Data & Statistics. www.cdc.gov
6. Eastern Association for the Surgery of Trauma. www.east.org
7. Trauma.org. www.trauma.org
8. World Society of the Abdominal Compartment Syndrome. www.wsacs.org
9. American College of Surgeons. www.facs.org
Chapter 10
ACUTE CORONARY SYNDROMES
Objectives
Identify patients who have acute coronary syndromes with various

electrocardiographic and clinical presentations.
Outline diagnostic procedures and the acute management of non–ST-elevation acute
coronary syndrome (NSTE-ACS), and ST-elevation myocardial infarction
(STEMI).
Identify appropriate reperfusion interventions for patients with STEMI and high-
risk patients with NSTE-ACS.
Recognize the complications of myocardial infarction and outline the appropriate
management.
Case Study
A 68-year-old man with a long-standing smoking history, type 2 diabetes, and

hypertension develops sudden-onset severe chest pain associated with difficulty
breathing and diaphoresis. His vital signs on arrival in the emergency department are as
follows: blood pressure 158/94 mm Hg, heart rate 98 beats/min, respiratory rate 28
breaths/min, and oxygen saturation measured by pulse oximetry 97% on room air. His
physical examination is remarkable only for a fourth heart sound (S4) and mild
diaphoresis.
– What information is needed to determine if this patient has an acute coronary
syndrome?
– What immediate interventions should be performed?
I. INTRODUCTION
Acute coronary syndrome (ACS) refers to a group of symptoms indicative of acute
myocardial ischemia covering the spectrum of clinical conditions ranging from unstable
angina, non–ST-elevation myocardial infarction (NSTEMI) and ST-elevation
myocardial infarction (STEMI) [Figure 10-1]. An important distinction is made
clinically between patients with ACS who have ST elevation on an electrocardiogram
(ECG) and those who do not. Patients with ST elevation should be considered for
immediate reperfusion.
Figure 10-1. Overlapping Spectrum of Acute Coronary Syndromes
Abbreviations: ECG, electrocardiogram; NSTE-ACS, non-ST-elevation acute coronary syndrome; MI,

myocardial infarction Acute coronary syndromes are distinguished by initial ECG findings and cardiac
markers.
Unstable angina and NSTEMI are grouped together as non–ST-elevation acute coronary
syndrome (NSTE-ACS). They differ in the severity of ischemia and myocardial damage.
Damage resulting in elevation of biochemical markers of myocardial injury establishes
the diagnosis of NSTEMI. Although unstable angina and NSTEMI are managed initially
with pharmacologic interventions, high-risk patients may also require an invasive
strategy with urgent reperfusion. Unstable angina and NSTEMI are characterized
pathologically by various degrees of coronary artery occlusion that result in decreased
myocardial oxygen supply relative to myocardial oxygen demand. Rupture or erosion of
atherosclerotic plaques leads to a complex process of inflammation, platelet activation
and aggregation, thrombus formation, and microembolization to the distal vasculature.
The patient’s specific syndrome depends on the severity and duration of occlusion.
Myocardial ischemia less commonly results from severe anemia or hypoxemia that
limits myocardial oxygen delivery.
Be aware of changes in the management

of ACS as new evidence becomes
available.
Hospitals should establish multiprofessional teams (including primary care physicians,

emergency medicine physicians, cardiologists, nurses, and others) to develop evidence-
based protocols for triaging and managing patients with symptoms suggestive of ACS.
These protocols must be updated periodically based on the best current evidence.
The consequences of ACS are often so

severe that therapy is indicated even
when the diagnosis is presumptive.
Identification of patients at risk for ACS is based on an assessment of risk factors for
coronary artery disease (Table 10-1) and detection of previous myocardial ischemia.
Table 10-1 Risk Factors for Coronary Artery Disease
Family history of myocardial infarction Obesity

Hypertension Diabetes mellitus
Smoking history Other vascular disease
Hyperlipidemia Sedentary lifestyle
Increasing age Cocaine/amphetamine use
Postmenopausal state
Patients with other critical illness or injury have an increased risk for ACS and
frequently have atypical presentations. Definitive diagnosis of ACS often is not possible
on initial evaluation and requires continuous observation, electrocardiographic (ECG)
monitoring, and/or laboratory evaluations. The initial physical examination should
include vital signs and general observation, assessment of jugular venous distension,
auscultation of the lungs and heart, evaluation of the peripheral pulses, detection of
neurologic deficits, and assessment for evidence of systemic hypoperfusion.
II. NON–ST-ELEVATION ACUTE CORONARY SYNDROME

At presentation, patients with ischemic-type chest pain and an ECG with no ST-segment
elevation are presumed to have NSTE-ACS. Other causes of prolonged chest pain
(Table 10-2) should also be considered. Based on serial ECGs and levels of
biochemical markers of cardiac injury, patients are subsequently diagnosed with an
NSTEMI or unstable angina.
Table 10-2 Differential Diagnosis of Prolonged Chest Pain
Acute myocardial ischemia

Aortic dissection/aortic aneurysm
Myocarditis
Pericarditis
Pain associated with hypertrophic cardiomyopathy or esophageal and gastrointestinal disorders
Pulmonary diseases such as pneumothorax, pulmonary embolism, and pleuritis
Hyperventilation syndrome
Aortic stenosis
Musculoskeletal or chest wall diseases, costochondral pain
Psychogenic pain
Adapted with permission from the Agency for Healthcare Research and Quality. Braunwald E, Mark DB,
Jones RH, et al. Unstable angina: diagnosis and management. AHCPR Publication 94-0602. Rockville, MD:
Agency for Health Care Policy and Research and National Heart, Lung, and Blood Institute; 1994.
A. Diagnosis
New-onset shortness of breath and/or

new left bundle branch block should be
considered possible evidence of ACS,
particularly in women and diabetic
patients, who may have atypical
presentations.
The most important factors that suggest the likelihood of myocardial ischemia are the
character of the pain, prior history of coronary artery disease, age, and number of risk
factors. Results of the physical examination may be normal, although a fourth heart
sound (S4) may be heard during episodes of pain. A 12-lead ECG should be obtained
and interpreted as soon as possible by prehospital personnel to facilitate diagnosis,
triage, and treatment. If this ECG was not obtained earlier, it should be done and
interpreted within 10 minutes of the patient’s arrival at the hospital. The ECG is most
helpful if it shows transient ST-segment depression (Figure 10-2) during anginal
episodes—but it may be normal, or it may reveal nondiagnostic T-wave inversions or
peaked T waves. The history, findings from physical examination, ECG interpretation,
and cardiac biomarkers should be used in the diagnosis of NSTE-ACS and in assessing
the patient’s short-term risk of an adverse outcome, such as death or nonfatal myocardial
ischemia (Table 10-3).
Figure 10-2. Electrocardiogram of a Patient With NSTE-ACSa
The ST-segment depression in lead V6 is characteristic of non-ST-elevation acute coronary syndrome.

a Reproduced with permission of Shih-Chung Lin, MD.
Table 10-3 Risk Factors for Death or Nonfatal Myocardial Ischemiaa
High Risk Intermediate Risk Low Risk

(1 or more of the following) (No high risk factors (no high or intermediate
and 1 of the following) risk factors and
1 of the following)
Ongoing pain at rest (>20 min) Prolonged rest pain (>20 Increasing frequency,
min) now resolved severity, or duration of pain
Pulmonary edema, S3, or rales Rest pain <20 min or Lower threshold for pain
relieved with
nitroglycerin
Hypotension Age >70 y Normal or unchanged
electrocardiogram during
pain
Bradycardia, tachycardia T-wave inversions >0.2 Normal troponin
mV
Age >75 y Pathologic Q waves
Rest angina with dynamic ST- Slightly elevated troponin
segment changes >0.05 mV (<0.1 ng/mL)
Elevated troponin (>0.1 ng/mL)
aAdapted with permission from the Agency for Healthcare Research and Quality. Braunwald E, Mark DB,
Jones RH, et al. Unstable Angina: Diagnosis and Management. Rockville, MD: Agency for Health Care
Policy and Research and National Heart, Lung, and Blood Institute. US Public Health Service, US
Department of Health and Human Services; 1994. AHCPR Publication 94-0602.
Several risk stratification scores have been developed and validated to assist in
predicting the risk of death and ischemic events in NSTE-ACS. The GRACE 2.0
(Global Registry for Acute Cardiac Events) score
(http://www.gracescore.org/WebSite/default.aspx?ReturnUrl=%2f) requires an app or a
web-based calculator, whereas the TIMI (Thrombolysis in Myocardial Infarction) risk
score can be easily determined at the bedside (Table 10-4). High-risk patients are
considered to have a greater than 6% risk of dying within 6 months, and intermediate-
risk patients have a 6-month mortality rate of 3% to 6%. This risk assessment has
implications for the location of care, selection of medical therapy, and use of
reperfusion interventions. B-type natriuretic peptide may provide additional prognostic
information. Additional tests, such as hemoglobin/hematocrit, electrolytes, thyroid
function, and arterial oxygen saturation, may be helpful in identifying a precipitating
factor as conditions such as anemia, metabolic derangements, endocrine abnormalities,
fever, infection, and inflammation may precipitate ischemic cardiac events.
Table 10-4 TIMI Risk Score for Adverse Cardiac Events
1 point for each:
Age ≥65 y
Known coronary artery disease (coronary stenosis ≥50%)
ST-segment deviation of at least 0.5 mm
At least 2 angina events in prior 24 hours
Use of aspirin in prior 7 days
At least 3 risk factors for coronary artery disease (family history of premature coronary artery
disease, hypertension, hyperlipidemia, diabetes, smoking)
Elevated serum cardiac markers
Risk Level Score Risk of Adverse Cardiac Event

Low 0-2 5% to 8%
Intermediate 3-4 13% to 20%
High 5-7 26% to 41%
Abbreviation: TIMI, Thrombolysis in Myocardial Infarction
If equipment and expertise are available, the use of transthoracic echocardiography

allows bedside assessment of wall motion abnormalities as a marker for current or past
ischemia and the detection and follow-up of new abnormalities. It also provides an
estimate of left ventricular function and identification of valvular dysfunction and/or
pericardial fluid.
B. Management
Management of the patient with chest pain includes increasing myocardial oxygen
delivery by improving perfusion and decreasing myocardial oxygen demand. Reversing
myocardial ischemia and confirming the diagnosis of NSTE-ACS are the initial
priorities. Patients with NSTE-ACS should be admitted to a unit with cardiac
monitoring (eg, telemetry unit, chest pain or observation unit) and placed on bed or
chair rest (see treatment algorithm in Figure 10-3). Oxygen (2-4 L/min by nasal
cannula) should be administered to patients with dyspnea, hypoxemia (oxygen saturation
measured by pulse oximetry <90% on room air), or evidence of heart failure or shock.
Emerging data suggest that routine use of supplemental oxygen in cardiac patients with
normal oxygenation may have untoward effects, including increased coronary vascular
resistance, reduced coronary blood flow, and an increased risk of death. If precipitating,
reversible causes — such as fever, anemia, hypoxemia, infection, hypertension, anxiety,
hyperthyroidism, arrhythmias, or sympathomimetic drug ingestion (eg, cocaine,
amphetamines) — can be identified, they should be treated aggressively. Further
management includes relief of pain and anti-ischemic therapy, therapy for platelet
aggregation/thrombosis, ongoing risk stratification, and consideration of invasive
reperfusion procedures.
Figure 10-3. Treatment Algorithm for Non−ST-Elevation Acute Coronary Syndrome
Abbreviations: NSTEMI, non-ST-elevation myocardial infarction; NSTE-ACS, non-ST-elevation acute
coronary syndrome; ECG, electrocardiogram; MI, myocardial infarction; LMWH, low-molecular-weight
heparin; PCI, percutaneous coronary intervention
1. Pain relief and analgesia

Pain relief is an important element in the early management of the patient with NSTE-
ACS. Management should be directed toward acute relief of symptoms of ongoing
myocardial ischemia and general relief of anxiety and apprehension. Immediate control
of ischemic pain is typically accomplished with a combination of nitrates and opiate
agents. Antianginal medications that are effective in stabilizing patients with unstable
angina are listed in Table 10-5. The goal is to reduce ischemia without causing
hypotension or reflex tachycardia. Patients with ongoing ischemic discomfort should
receive up to three doses of sublingual or spray nitroglycerin. Nitrates should not be
administered if the systolic blood pressure measures <90 mm Hg or ≥30 mm Hg below
the patient’s baseline blood pressure. Additional contraindications to nitrate
administration are heart rate <50 beats/min, tachycardia >100 beats/min in the absence
of heart failure symptoms and in suspected right ventricular infarction or severe aortic
stenosis. If sublingual or spray nitroglycerin does not relieve pain, an assessment should
be made about the need for IV nitroglycerin for persistent ischemia. Excessive
decreases in blood pressure with nitroglycerin are predominantly due to increased
venous capacitance and can often be treated with careful IV crystalloid infusion. If the
mean arterial pressure decreases by more than 25% when hypertension is present or if
the systolic pressure falls below 110 mm Hg in normotensive patients, the nitroglycerin
dose should not be increased. Instead, a second antianginal agent should be
administered. Tolerance to the hemodynamic effects of nitroglycerin becomes important
after 24 hours of continuous infusion, and efforts should be made to switch to other
dosing regimens. The dose of IV nitrates should be tapered and discontinued when
ischemic manifestations have resolved for 12 to 24 hours. Nitrates are contraindicated
in patients who have received a phosphodiesterase inhibitor for erectile dysfunction in
the previous 24 hours (48 hours for tadalafil). Morphine sulfate is a reasonable
analgesic for management of pain refractory to initial antianginal therapy. Nonsteroidal
anti-inflammatory drugs, other than aspirin, and COX-2 inhibitors should not be
initiated and should be discontinued during hospitalization because of the potentially
increased risk for major adverse cardiac events, especially with long-term use.
Table 10-5 Anti-ischemic Therapy
Agent Oral Dose Spray Dose Intravenous Dose

Nitroglycerin 0.3- to 0.4-mg tablet 0.4 mg every 5 min to Initial infusion rate 10 μg/min; increases
sublingually to a a maximum of 3 of 10 μg/min every 3-5 min as needed to
maximum of 3 doses; doses; control pain; discontinue rate increases
contraindicated when contraindicated when for significant drops in blood pressure or
systolic blood pressure systolic blood maximum of 200 μg/min
<90 mm Hg pressure <90 mm Hg
Morphine 1-5 mg every 5-30 min as needed for
sulfate pain
β-blockers
Propranolol 20-80 mg every 6-8 h 0.5-1 mg as a single dose
Metoprolol 50-100 mg every 12 h 5 mg every 5 min to a total dose of 15
mg
Atenolol 50-200 mg every 24 h 5 mg every 10 min to a total dose of 10
mg
Carvedilol 6.25 mg every 12 h
titrated to maximum 25
mg every 12 h
Diltiazem 30-60 mg every 6-8 h
Oral β-blockers should be initiated within the first 24 hours in patients with no
contraindications to their use (Table 10-6). Routine use of IV β-blockers in the initial
management of patients with suspected NSTE-ACS is not supported by current
evidence, but may be considered in patients with ongoing chest pain, especially with
concomitant hypertension or tachycardia; IV dosing should be followed by oral
administration. Caution is advised with the use of IV β-blockers in patients with risk
factors for shock (age >70 years, heart rate >110 beats/min, systolic blood pressure
<120 mm Hg, or late presentation).
Table 10-6 Contraindications to β-Blocker Use in Acute Coronary Syndromes
Heart rate <50 beats/min

Moderate to severe left ventricular dysfunction (uncompensated)
Shock or increased risk for cardiogenic shock
Marked first-degree atrioventricular block (with PR interval >0.24 s)
Second-degree or third-degree heart block (without a cardiac pacemaker)
Systolic blood pressure <90 mm Hg
Peripheral hypoperfusion
Active bronchospastic disease (asthma or chronic obstructive pulmonary disease)
Non-dihydropyridine calcium channel blockers (eg, diltiazem, verapamil) do not reduce

the risk of myocardial infarction (MI). In the absence of contraindications (such as
significant left ventricular dysfunction), they may be considered only if patients cannot
tolerate a β-blocker or symptoms are not controlled with nitroglycerin and β-blockers
together.
Aspirin improves survival and reduces

the incidence of MI.
2. Antiplatelet therapy
The use of antiplatelet and anticoagulant agents (Table 10-7) is important in patients
with NSTE-ACS because of the contributions of platelet activation/aggregation and the
coagulation system to platelet-rich thrombus formation. Three classes of antiplatelet
drugs may be of benefit in acute myocardial ischemia: aspirin, adenosine diphosphate
inhibitors (eg, clopidogrel, prasugrel, and ticagrelor), and glycoprotein (GP) IIb/IIIa
inhibitors. The intensity of therapy with these agents is often tailored to the patient’s risk
assessment and to plans for early invasive procedures. Non−enteric-coated aspirin at a
dose of 162 to 325 mg should be administered (and chewed) as soon as possible to all
patients with NSTE-ACS (including those in the prehospital setting) if no aspirin
allergy is suspected. Aspirin should be administered indefinitely. Clopidogrel or
ticagrelor should be considered as an alternative antiplatelet agent if aspirin is
contraindicated. If an early invasive strategy or noninterventional conservative
approach is planned, clopidogrel or ticagrelor should be added to aspirin to decrease
the risk of cardiovascular death, MI, and stroke. Clopidogrel, prasugrel, or ticagrelor
should be administered in patients undergoing percutaneous coronary interventions
(PCIs), but prasugrel is contraindicated in those with a prior history of stroke or
transient ischemic attack and is associated with an increased risk of bleeding. The
choice of a specific adenosine diphosphate inhibitor should be discussed with the
cardiologist when possible. Therapy with an adenosine diphosphate inhibitor is
recommended for at least 12 months.
Table 10-7 Antiplatelet Drugs Used in Acute Coronary Syndromes
Antiplatelet Agents
Aspirin 162-325 mg chewed and swallowed initially, then 81-325 mg as a minimum oral dose daily
Adenosine diphosphate inhibitors (thienopyridines)
Clopidogrel Loading dose of 300 mg orally can be used with a noninvasive approach or fibrinolysis;
loading dose of 300 to 600 mg orally with PCI; maintenance dose of 75 mg orally daily
Prasugrel Loading dose of 60 mg orally may substitute for clopidogrel in patients with STEMI
managed with early PCI who are not at high risk of bleeding; maintenance dose of 10 mg
daily (consider 5 mg daily if weight <60 kg); not studied for STEMI treated with fibrinolysis
Ticagrelor Loading dose of 180 mg orally may be an option instead of clopidogrel in NSTE-ACS or
STEMI managed with early PCI; maintenance dose of 90 mg twice daily; not studied for
STEMI treated with fibrinolysis
Abbreviations: PCI, percutaneous coronary intervention; STEMI, ST-elevation myocardial infarction; NSTE-
ACS, non−ST-elevation acute coronary syndrome
Selected high-risk patients (those with continuing ischemia, elevated troponin levels)
may be candidates for additional antiplatelet therapy with GP IIb/IIIa inhibitors when an
early invasive strategy is chosen. However, the benefit of GP IIb/IIIa inhibitors may be
limited when dual antiplatelet therapy (aspirin and an adenosine diphosphate inhibitor)
and anticoagulation are instituted. A cardiologist should be consulted regarding
selection and initiation of a GP IIb/IIIa inhibitor. Baseline coagulation and platelet
studies should be completed before the administration these agents.
3. Anticoagulant therapy
The combination of aspirin and an anticoagulant agent is more beneficial than aspirin
alone in NSTE-ACS. The selection of a specific agent should take into account the risks
of ischemia and bleeding complications, as well as the presence of renal dysfunction. In
ACS patients treated with a conservative ischemia-guided approach, low-molecular-
weight heparin, unfractionated heparin, bivalirudin, or fondaparinux should
administered as soon as possible unless there are significant contraindications. Patients
managed with fondaparinux require an additional anticoagulant to prevent catheter
thrombosis if a PCI is subsequently performed. Unfractionated heparin is continued at
least 48 hours, and enoxaparin or fondaparinux for the duration of the hospital stay (up
to 8 days), in patients managed with medical therapy or until PCI is performed. If an
early invasive strategy is planned, unfractionated heparin, enoxaparin, or bivalirudin
should be initiated as soon as possible. Serial platelet counts are required to monitor
for heparin-induced thrombocytopenia. Argatroban is an alternative anticoagulant in
patients with known heparin-induced thrombocytopenia. Patients who are adequately
anticoagulated with warfarin still require antiplatelet therapy, but anticoagulation with
heparin or alternative agents is generally not needed unless the international normalized
ratio is less than 2.0.
4. Reperfusion interventions
Fibrinolytic agents have no proven efficacy in NSTE-ACS. Most patients with NSTE-
ACS can be medically stabilized, and consultation can then be obtained for further risk
stratification and/or invasive strategies (cardiac catheterization). Patients who have
NSTE-ACS but no serious comorbidities and who have refractory angina, hemodynamic
or electrical instability, or other high-risk indicators (Table 10-8) are candidates for an
immediate or early invasive strategy. An immediate cardiology consultation should be
obtained for patients who cannot be medically stabilized or who have serious
comorbidity. Patients with NSTE-ACS and shock benefit from early reperfusion with
PCI or coronary artery bypass graft and should be triaged to the catheterization
laboratory as soon as possible.
High-Risk Indicators for an Early Invasive Strategy in Non–ST-

Table 10-8 Elevation Acute Coronary Syndrome
Refractory angina
Recurrent angina at rest or with minimal exertion despite therapy
Hemodynamic instability
Signs or symptoms of heart failure
Signs or symptoms of new or worsening mitral regurgitation
Sustained ventricular tachycardia or ventricular fibrillation
Very high prognostic risk (high TIMI or GRACE score)
Temporal change in troponin level
New ST-segment depression
Abbreviations: TIMI, Thrombolysis in Myocardial Infarction; GRACE, Global Registry for Acute Cardiac
Events
5. Other interventions
An angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker
should be administered in the first 24 hours to patients with NSTE-ACS and evidence of
pulmonary congestion or left ventricular ejection fraction <40% unless
contraindications are present. In addition, a statin should be initiated or continued after
consideration of contraindications. Aldosterone blockade is an option in patients
receiving an ACE inhibitor and β-blocker who have an ejection fraction <40%, diabetes
or heart failure, and no contraindications. Risk-factor modification, including weight
reduction and information about smoking cessation, is recommended in all cases of
ACS.
III. ST- ELEVATION MYOCARDIAL INFARCTION

Patients with STEMI have a high likelihood that a thrombus occludes a coronary artery,
resulting in a wave front of myocardial necrosis that begins at the endocardial surface
within 15 minutes. The infarction progresses outward to the epicardium over
approximately 6 hours unless collateral flow, spontaneous reperfusion, or reperfusion
via an intervention is established. This progression may be modulated by the extent of
collateral flow and determinants of myocardial oxygen consumption, which affords an
opportunity for myocardial salvage. As with the patient with NSTE-ACS, prompt
diagnosis and early treatment of the patient with STEMI have great influence on
morbidity and mortality rates.
A. Diagnosis
Patients with STEMI typically present with prolonged chest pain and associated
symptoms, but some patients have MIs that are painless (silent infarction/ischemia) or
have other related symptoms, such as dyspnea and fatigue. In the critically ill patient
population, STEMIs may not be associated with classic symptoms and are often
suspected when complications occur, new arrhythmias develop, or ECG changes are
noted. The physical examination findings are nonspecific.
The most common finding in patients with normal sinus rhythm is the S4 heart sound,
indicating decreased left ventricular compliance at the end of ventricular filling.
Bibasilar crackles due to pulmonary edema may be present and are helpful in assessing
the hemodynamic status. A brief, focused physical examination aids in the diagnosis and
assessment of possible complications of STEMI. A limited neurological examination for
evidence of prior stroke or cognitive deficits also should be conducted.
When possible, a prehospital 12-lead ECG should be obtained and interpreted to
facilitate diagnosis, triage, and treatment on arrival at the medical facility. Otherwise, a
patient with chest discomfort or symptoms suggestive of ACS should have this ECG
performed and read within 10 minutes of arrival or detection of symptoms. The ECG is
diagnostic of STEMI in the absence of QRS confounders (ie, bundle branch block,
pacing, left ventricular hypertrophy, Wolff-Parkinson-White syndrome) if it shows ≥2
mm of ST-segment elevation in 2 or more contiguous leads in men or ≥1.5 mm of ST-
segment elevation in women in leads V2-V3 and/or ≥1 mm in other contiguous leads
(Figure 10-4).
Figure 10-4. ECG Indicating an Anterolateral STEMI
This electrocardiogram (ECG shows classic findings of ST-elevation in the anterior (V2 through V4 and
lateral (I, aVL, V5, V6) leads, indicating an anterolateral ST-elevation myocardial infarction (STEMI).
Reproduced with permission from Barbara McLean.
A right-sided ECG is indicated in patients with an inferior STEMI to determine if ST-

segment elevation suggesting right ventricular infarction is present. Patients with ECG
findings of new or undiagnosed left bundle branch block and chest pain compatible with
myocardial ischemia are treated similarly to those with ST-segment elevation. If the
initial ECG is not diagnostic but the patient remains symptomatic with a high clinical
suspicion for ischemia, serial ECGs at 5- to 10-minute intervals or continuous 12-lead
ST-segment monitoring (if available) may be performed to detect the development of
ST-segment elevation.
If the diagnosis is in doubt, echocardiography may add helpful information by showing
focal wall motion abnormalities The diagnosis is confirmed by elevated serum levels of
cardiac-specific troponins. The delay in elevation of these markers, however, prevents
their use in determining reperfusion therapy.
B. General Management
Once STEMI is suspected or diagnosed, the immediate concerns are to ensure the
patient’s hemodynamic stability and to limit infarct size by restoring blood flow to the
affected artery as soon as possible (Figure 10-5). Cardiology expertise should be
sought promptly. Treatment of STEMI in the patient with other critical illness requires
careful individualization. Absolute and relative contraindications to therapies must be
considered and relative risk assessed. Choices may be limited by the availability of
specialized procedures, the need to transport the patient to another facility, significant
comorbidities, bleeding risk, or the unavailability of the oral route for administering
medication.
Figure 10-5. Treatment Algorithm for Myocardial Infarction With ST-Elevation
Abbreviations: ECG, electrocardiogram; PCI, percutaneous coronary
intervention.
1. Early Therapy
Early therapy in STEMI is similar to the management of NSTE-ACS. Immediate 12-lead
ECG, cardiac-specific troponin measurement, and related laboratory tests should be
completed. Immediate therapy includes the administration of supplemental oxygen in the
presence of dyspnea, hypoxemia, heart failure, or shock; the control of pain; and
consideration of reperfusion therapy. Aspirin should be administered immediately. The
addition of a loading dose and subsequent maintenance doses of clopidogrel or
ticagrelor as part of dual antiplatelet therapy decreases the rates of mortality and major
vascular events. An anticoagulant agent, unfractionated heparin or bivalirudin, should
also be administered to patients undergoing PCI. Intravenous nitroglycerin may be
useful in patients with STEMI and ongoing chest pain, hypertension, or heart failure,
unless the systolic blood pressure is below 90 mm Hg. Intravenous β-blockers are not
routinely administered but may be considered at presentation if hypertension or ongoing
ischemia is present and there are no contraindications.
2. Acute Reperfusion Therapy

Early reperfusion of the infarct-related coronary artery is associated with improved
survival in patients with STEMI. Prompt restoration of flow can be achieved by
primary PCI, fibrinolysis, or surgical intervention. The percutaneous procedure is
clearly preferred if it can be done in a timely fashion. A plan for early reperfusion in
patients with STEMI should be developed based on the resources available in the
facility and community.
a. Percutaneous Coronary Interventions

PCIs include angioplasty, usually with deployment of an intracoronary bare-metal or
drug-eluting stent, along with pharmacologic measures to prevent thrombosis. Primary
PCI results in higher patency rates of the infarct-related coronary artery and lower rates
of recurrent ischemia, reinfarction, and death. Primary PCI is the preferred reperfusion
technique if the procedure can be performed by experienced personnel within 12 hours
of symptom onset. It is also preferred with clinical or electrocardiographic evidence of
ongoing ischemia, even if more than 12 hours have elapsed since symptom onset. A goal
of 90 minutes or less from hospital presentation to balloon inflation is optimal.
Time to open the infarct-related

coronary artery is the most important
determining factor when choosing
options for reperfusion.
Primary PCI is particularly preferred over fibrinolysis for patients with

contraindications to fibrinolysis or at a high risk of bleeding, for patients with STEMI
and severe heart failure or cardiogenic shock, and for patients in whom the diagnosis of
MI is in doubt. If primary PCI is not available, transfer to a facility with invasive
reperfusion capability should be initiated as soon as possible (preferably within 30
minutes).
In general, the higher the patient’s mortality risk (as with large infarctions, heart failure
or hemodynamic instability, previous infarctions, or acute left bundle branch block), the
more primary PCI is preferred. Similarly, the higher the risk of fibrinolysis, the more
primary PCI is preferred. Conversely, the longer the time required for performance of
PCI or transfer to another facility, the more fibrinolysis may be preferred. Patients
presenting within 3 hours of the onset of symptoms who have a low risk of bleeding
appear to derive particular benefit from prompt reperfusion with fibrinolytic therapy.
Transfer for PCI is preferred over fibrinolysis in patients who present 3 to 12 hours
after onset of symptoms if transfer can be accomplished in a timely manner. For patients
who fail to reperfuse after fibrinolytic therapy, PCI is recommended, even if it requires
transfer to another institution.
Pre-procedure management should include all of the strategies for ACS outlined
previously. The use of an adenosine diphosphate inhibitor and an IV anticoagulant agent
(unfractionated heparin or bivalirudin) before PCI is recommended. A loading dose of
clopidogrel, prasugrel, or ticagrelor should be administered as soon as possible before
PCI. Additional boluses of unfractionated heparin may be needed during the procedure.
Bivalirudin may be used with or without prior unfractionated heparin administration.
The addition of a GP IIb/IIIa inhibitor may be considered by the cardiologist in selected
patients. Potential complications of an invasive strategy for treating STEMI include
problems with the arterial access site; adverse reactions to volume loading, the contrast
medium, and antithrombotic medications; technical complications; and reperfusion
events.
PCI is not contraindicated by the

presence of coma or a need for targeted
temperature management after cardiac
arrest.
Regardless of the reperfusion strategy chosen, timely implementation by experienced

personnel is optimal. Routine use of PCI in the first 2 to 3 hours after fibrinolytic
therapy is not recommended. In the event of cardiac arrest from ACS, local protocols
for treatment of acute MI and coronary reperfusion, including targeted temperature
management (TTM), should be activated. Even in the absence of ST-elevation, medical
or interventional treatments may be considered for the treatment of ACS.
b. Fibrinolysis
Ideally, thrombolytic therapy should be

initiated within 30 minutes of the
patient’s arrival to the hospital.
If PCI is not available or cannot be performed within 120 minutes of arrival,

fibrinolytic therapy should be considered. Limitation of infarct size is optimized when
fibrinolytics are administered within 6 hours of symptom onset, but they may have some
benefit as long as 12 hours after symptom onset. The physician must weigh the potential
risks against the benefits of fibrinolysis for each patient. If the decision to proceed is
made and no absolute contraindications exist (Table 10-9), fibrinolytic therapy should
be administered expeditiously. Several agents are available, and all are effective (Table
10-10). Findings that suggest reperfusion include relief of symptoms, maintenance or
restoration of hemodynamic and/or electrical stability, and reduction of at least 50% of
the initial ST-segment elevation injury pattern on a follow-up ECG performed 60 to 90
minutes after the initiation of therapy. STEMI patients who develop cardiogenic shock
or severe heart failure, or who have evidence of reperfusion failure or reocclusion after
fibrinolytic therapy, should be transferred to PCI-capable facilities as soon as possible.
Patients with STEMI who are hemodynamically stable and achieve successful
reperfusion also should be considered for transfer to a PCI-capable facility. Antiplatelet
and anticoagulant therapy is continued after fibrinolysis and before transfer.
Table 10-9 Contraindications for Fibrinolytic Therapy

Absolute Contraindications
Prior intracranial hemorrhage
Known cerebral vascular lesion
Ischemic stroke within past 3 months
Allergy to the agent
Significant head or facial trauma within past 3 months
Known intracranial neoplasm
Suspected aortic dissection
Active internal bleeding or bleeding diathesis (except menstruation)
Intracranial or intraspinal surgery within past 2 months
Severe uncontrolled hypertension (unresponsive to urgent therapy)
Relative Contraindications
Severe uncontrolled hypertension on presentation (blood pressure >180/110 mm Hg)
History of chronic, severe, poorly controlled hypertension
Ischemic stroke >3 months ago or intracerebral pathology
Current use of oral anticoagulants
Traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Major surgery within past 3 weeks
Previous use of streptokinase/anistreplase: allergy or prior exposure (>5 days ago)
Active peptic ulcer disease
Recent internal bleeding (within past 2-4 weeks)
Noncompressible arterial or central venous puncture
Pregnancy
Table 10-10 Fibrinolytic Agents Used in ST-Elevation Myocardial Infarction
Streptokinase 1.5 million units intravenously over 30-60 min

Alteplase 15 mg intravenous bolus, then 0.75 mg/kg (maximum 50 mg) intravenously over 30 min,
then 0.50 mg/kg (maximum 35 mg) intravenously over 60 min
Reteplase 10 units intravenously over 2 min followed in 30 min by 10 units intravenously over 2 min
Tenecteplase Intravenous bolus adjusted for weight (30 mg if <60 kg; 35 mg if 60-70 kg; 40 mg if 70-80
kg; 45 mg if 80-90 kg; 50 mg if >90 kg)
3. Continuing Therapy
Patients who undergo PCI with angioplasty, with or without stent placement, should be
treated with aspirin, an adenosine diphosphate inhibitor (clopidogrel, prasugrel, or
ticagrelor), and an anticoagulant agent. Administration of clopidogrel or an alternative
agent should be discussed with the cardiologist because the optimum duration may vary
with the type of stent used. Anticoagulation with heparin is continued. Bivalirudin, a
direct thrombin inhibitor, may be considered as an alternative to heparin. After
fibrinolysis with a plasminogen activator, heparin should be used to maintain vessel
patency for at least 48 hours. Enoxaparin is preferred over unfractionated heparin
following fibrinolysis. Infusion rates of unfractionated heparin should be adjusted to
keep the partial thromboplastin time at 1.5 to 2 times the control value. Heparin
anticoagulation after use of streptokinase is not necessary; fondaparinux, a factor Xa
inhibitor, can be considered in these situations. Heparin should be used in patients with
large anterior infarctions who do not receive fibrinolysis or PCI and in those who have
intramural thrombus detected or suspected on echocardiography. Aspirin (81-325
mg/day) should be continued. Clopidogrel is the antiplatelet agent of choice in patients
treated with fibrinolytics who undergo delayed invasive reperfusion interventions.
Intravenous nitroglycerin may be useful in STEMI patients with hypertension or heart
failure. In the absence of recurrent ischemia, heart failure, or arrhythmias, bed rest
should not be continued beyond 12 to 24 hours.
Oral β-blockers should be initiated in the first 24 hours after the patient with STEMI has
stabilized. Long-term use of these agents is helpful in all patients who are at risk for
recurrent cardiovascular events and who have no contraindications to their use (Table
10-6).
Use of ACE inhibitors decreases the risk of death in all patients with STEMI. The
greatest benefit is seen in those with left ventricular dysfunction (ejection fraction
<40%), anterior infarction, or pulmonary congestion. ACE inhibition should be started
within the first 24 hours of the infarction with low doses of oral agents unless
hypotension (systolic blood pressure <100 mm Hg) or other contraindications are
present. An angiotensin receptor blocker may be administered if the patient cannot
tolerate an ACE inhibitor. High-dose statin therapy should be initiated early after
hospital admission.
Long-acting calcium channel blockers may be a useful secondary therapy for recurrent
myocardial ischemia but are not appropriate for first-line treatment. Immediate-release
nifedipine is contraindicated in treatment of an acute MI. Diltiazem and verapamil are
contraindicated in patients with STEMI and left ventricular dysfunction and heart
failure.
Expert consultation should be obtained, and transfer to facility providing a higher level
of care is indicated for patients who have persistent ischemic symptoms after MI, who
develop cardiogenic shock, who have heart failure despite aggressive therapy, or who
have recurrent ventricular fibrillation or tachycardia despite aggressive antiarrhythmic
therapy.
C. Complications
Common early complications of MI are heart failure and cardiogenic shock, recurrent
ischemia and/or infarction, and arrhythmias. Urgent cardiology consultation should be
obtained as soon as possible to assist with management and decisions regarding
advanced interventions
1. Heart Failure and Cardiogenic Shock

Bedside evaluation allows accurate determination of a patient’s hemodynamic status
(Table 10-11) and the need for hemodynamic monitoring and intervention. Patients with
Killip classes I and II heart failure can be managed without advanced hemodynamic
monitoring but class III patients should be considered for this monitoring if they do not
respond promptly to medical therapy. Class IV patients generally require advanced
hemodynamic monitoring. Expert consultation should be sought and/or transfer arranged
for patients with class III or IV findings. Advanced hemodynamic monitoring may also
be warranted for those with suspected mechanical complications resulting in shock,
such as papillary muscle rupture or dysfunction, ventricular septal defect, or cardiac
tamponade.
Table 10-11 Killip-Kimball Hemodynamic Subsets
Class Description
I No dyspnea; physical examination results are normal
II No dyspnea; bibasilar crackles or S3 on examination
III Dyspnea present; bibasilar crackles or S3 on examination, no hypertension
IV Cardiogenic shock
Pharmacologic treatment of heart failure should be tailored to the patient’s clinical and
hemodynamic state. Patients with systolic arterial pressure >100 mm Hg and low
cardiac output should be treated initially with a vasodilator, either IV nitroglycerin or
IV nitroprusside (doses of 0.3 to 1 μg/kg/min, titrated up in increments of 0.5 μg/kg/min
every 10 minutes). If arterial pressure decreases or cardiac output remains inadequate,
inotropic support with dobutamine should be initiated (1 to 2 μg/kg/min) and titrated to
≤15 μg/kg/min. Milrinone is an alternative inotropic agent with less arrhythmogenic
effect than dobutamine, though it is often associated with hypotension. In countries
where it is available, levosimendan has shown favorable hemodynamic benefits in
cardiogenic shock. Loop diuretics, such as furosemide (20-40 mg intravenously or
orally every 2-4 hours), should be used to reduce pulmonary congestion. Diuretics
should be used with caution in hypotensive patients.
Patients with systolic arterial pressure <90 mm Hg and low cardiac output have
cardiogenic shock. This hypotension should be treated with norepinephrine to raise the
pressure. Once it has stabilized to at least 90 mm Hg, dobutamine can be added to
further increase cardiac output and reduce the dosage of vasopressor.
Interventional therapy with assistive devices may be indicated in patients with pump
failure who do not respond promptly to medical therapy. These devices can stabilize the
hemodynamic status sufficiently to allow PCI or coronary bypass surgery. Expert
consultation is needed to determine if the patient is a candidate for this type of
intervention.
Cardiogenic shock in the setting of acute

MI is an indication for emergent
revascularization (either percutaneous
intervention or coronary artery bypass
grafting).
Evidence suggests that patients with STEMI who develop shock within 36 hours benefit
from early invasive reperfusion regardless of the time delay from the onset of MI. In
patients with 1- or 2-vessel disease, PCI is preferred. Patients who remain symptomatic
and have 3-vessel disease or significant left main coronary artery disease should
undergo urgent consultation for coronary bypass surgery. PCI should also be performed
in STEMI patients with severe heart failure and/or pulmonary edema and onset of
symptoms within 12 hours
a. Right Ventricular Infarction/Ischemia
Some patients have heart failure from ischemia of the right ventricle, which results in
elevation of right atrial and right ventricular filling pressures and low cardiac output.
These hemodynamic abnormalities result in characteristic clinical findings of
hypotension, clear lung fields, and distended internal jugular veins. The ECG usually
reveals an inferior infarction, and the ST segment in lead V1 may be elevated in the
absence of elevation in any other standard precordial lead. An ECG tracing of the right
precordial leads should be obtained and may reveal characteristic ST-segment
elevation, especially in V4R. Initial therapy includes maintenance of right ventricular
preload with volume expansion until the blood pressure is stabilized. Associated
bradycardia or high-degree heart block may require chemical or electrical intervention.
Agents that reduce preload should be avoided, such as morphine, nitrates, ACE
inhibitors/angiotensin receptor blockers, and diuretics. If volume expansion is
inadequate to stabilize the patient, inotropic support with dobutamine should be
considered. Cardiology consultation should be obtained for assistance in managing
patients with refractory hypotension.
b. Mechanical Complications
Serious mechanical complications following MI include ventricular free wall rupture,
ventricular septal rupture, and acute mitral regurgitation, all of which typically occur
during the first week after infarction. Urgent cardiology and/or surgical consultation is
needed for these conditions. Although the incidence is low (<1%), ventricular free wall
rupture is a serious, often lethal complication. Risk factors include an absence of
collateral flow, anterior location of the infarct, use of corticosteroids or nonsteroidal
anti-inflammatory agents, age >70 years, and female sex. Clinical presentation ranges
from chest pain, nausea, and restlessness to sudden death. Echocardiography reveals
pericardial effusion, and salvage is only possible following prompt recognition and
thoracotomy for repair. Ventricular septal rupture presents as hypotension, severe
biventricular heart failure, and cardiogenic shock with physical findings of a
pansystolic murmur and parasternal thrill. Ischemic mitral regurgitation may be seen
following an inferior MI due to compromised blood flow to the posterior papillary
muscle. The typical presentation is that of acute-onset pulmonary edema and
cardiogenic shock.
2. Recurrent Ischemia or Infarction

Recurrent ischemia or infarction occurs in up to 20% of patients treated with
fibrinolytic therapy for MI, whereas patients receiving primary PCI have a lower
incidence of recurrent ischemia. Ischemia after MI can be caused by residual stenosis in
the infarct-related artery, by disease in another coronary artery, or by occlusion of a
new stent. An ECG recorded during recurrent pain should be compared with those from
the index MI event. Reinfarction may present special diagnostic difficulties because
cardiac troponin levels can be elevated for 5 to 14 days. If the first blood sample
reveals an elevated troponin value when recurrent ischemia is suspected, then serial
levels of a cardiac marker with a shorter time course, such as creatine kinase MB, could
be analyzed to clarify the possibility of recurrent infarction. No cardiac marker is
reliable for the diagnosis of reinfarction in the first 18 hours after the onset of STEMI.
However, if there is high suspicion for reinfarction, PCI should be considered
regardless of cardiac biomarker values. Nonischemic etiologies, such as pericarditis
and pulmonary embolism, should also be considered as potential causes of recurrent
chest pain.
Detection of reinfarction is clinically
important because it carries incremental
risk for the patient.
Medical treatment of post-MI ischemia is similar to management of the initial MI but

also includes cardiac catheterization and reperfusion, if possible. Acute reperfusion
with PCI or coronary artery bypass graft may be required for stabilization.
3. Arrhythmias
Arrhythmias associated with ACS and reperfusion include atrial bradycardias, atrial
tachycardias, atrioventricular (AV) blocks, ventricular tachyarrhythmias, and asystole.
Hemodynamically significant atrial bradycardia or AV block can be treated initially
with IV atropine in a dose of 0.5 mg every 3-5 minutes to a total dose of 3 mg while
preparing for transcutaneous pacing. Atropine rarely corrects complete heart block or
type II second-degree AV block. Temporary transvenous pacing is indicated for
complete heart block, bilateral bundle branch block, new or indeterminate-age
bifascicular block with first-degree AV block, type II second-degree AV block, and
symptomatic sinus bradycardia that is unresponsive to atropine. Transcutaneous pacing
should be initiated for patients who have indications for emergent temporary pacing
until transvenous pacing can be instituted.
Atrial tachycardias, such as atrial fibrillation, may cause hemodynamic instability and
precipitate myocardial ischemia, or they may be clinically insignificant and transient.
Immediate cardioversion is indicated in unstable patients. Depending upon the specific
arrhythmia, IV adenosine, β-blockers, diltiazem, digoxin, or amiodarone may be
effective. Careful attention must be given to contraindications for any of these agents.
Ventricular tachycardia and ventricular fibrillation should be treated according to
current advanced cardiac life support guidelines. After defibrillation and if indicated,
amiodarone is the drug of choice in patients with an acute MI. Antiarrhythmic drugs are
not recommended as prophylaxis for ventricular arrhythmias in the setting of acute MI.
To aid in the prevention of post-infarction arrhythmias, prompt recognition and
correction of systemic precipitants (including hypoxemia, acid-base abnormalities, and
electrolyte disturbances) is recommended.
D. Special Considerations
1. Perioperative MI
Perioperative MI can occur before surgery, intraoperatively, and during the
postoperative period. The latter is the most common, with the peak incidence on the
third postoperative day. Perioperative MI is often associated with atypical presentations
and is frequently painless; these patients rarely experience classic symptoms and signs
of acute coronary syndromes. New-onset or increased atrial or ventricular arrhythmia is
often the presenting finding, as is postoperative pulmonary edema. Other possible
presentations may include hemodynamic instability and respiratory distress The
diagnosis can be confirmed with serial ECG and cardiac marker determinations.
Treatment is similar to standard treatment, except that fibrinolytic therapy may be
contraindicated, depending on the type of surgery. Primary PCI should be considered for
these patients.
2. Effects of Coexisting Diseases

Many, if not most, critically ill patients suffer from more than one medical condition that
may require significant alterations in the standard therapeutic approach. Some have
relative or absolute contraindications to standard medications or procedures. Patients
with stress ulceration or gastritis may not be candidates for aspirin therapy.
Postoperative patients or those with a bleeding diathesis may not be candidates for
clopidogrel, heparin, fibrinolytic therapy, or aspirin. β-blockers should be avoided in
patients with significant bronchospasm or decompensated heart failure. Certain drugs
will need dose adjustments for renal or hepatic dysfunction. Critical illness of a non-
cardiac origin may result in decreased oxygen delivery to the myocardium and
subsequent myocardial dysfunction. Recommended management of multiple organ
failure in critical illness focuses on supportive care and treatment of the underlying
disease.
3. Targeted Temperature Management After Cardiac Arrest

Neurological injury is the most common cause of death in patients with out-of-hospital
cardiac arrest. Patients who do not follow commands or have purposeful movements
should receive TTM. Lowering the core body temperature to between 32°C and 36°C
(89.6°F and 96.8°F) for 24 hours after cardiac arrest with appropriate supportive care
can improve neurological outcome. TTM is associated with an increased risk of
coagulopathy and infection.
Key Points
Acute Coronary Syndromes
The preliminary diagnosis of NSTE-ACS is based on the clinical symptoms,
assessment of risk factors for coronary artery disease, and ECG interpretation.
A 12-lead ECG should be obtained and interpreted within 10 minutes in patients
with possible MI.
For patients with suspected NSTE-ACS, perform risk stratification, select an
initial management strategy, complete the diagnostic evaluation, and use medical
therapy and revascularization as appropriate.
Non–enteric-coated aspirin at a dose of 162 to 325 mg should be administered
(and chewed) as soon as possible in all patients with suspected or diagnosed ACS.
Antiplatelet and anticoagulant agents are important interventions in all patients
with ACS.
High-risk patients (continuing ischemia, elevated troponin levels) with NSTE-ACS
may be candidates for additional therapy with an early invasive strategy.
Oral β-blockers should be initiated in the first 24 hours for all patients with ACS
unless there are strong contraindications present.
A plan for early reperfusion of patients with STEMI should be developed based on
resources available in the facility and community.
Primary PCI is the preferred reperfusion technique if it can be performed by
experienced personnel within 12 hours of symptom onset. Fibrinolytic therapy for
reperfusion in STEMI ideally should be initiated within 30 minutes of the patient’s
arrival to the hospital if PCI cannot be performed.
All patients with acute MI, whether or not they undergo reperfusion therapy, should
be treated with aspirin and another antiplatelet agent, such as clopidogrel,
prasugrel, or ticagrelor.
Use of ACE inhibitors decreases the mortality rate in all patients with STEMI.
PCI is not contraindicated in patients with coma or a need for targeted temperature
management after cardiac arrest.
Patients with cardiogenic shock in the setting of acute MI should undergo emergent
revascularization.
Suggested Readings
1. Amsterdam EA, Wenger NA, Brindis RG, et al. 2014 ACC/AHA guideline for the
management of patients with non-ST-elevation acute coronary syndromes: a report
of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. Circulation. 2014;130:e344-e426.
2. Anderson JL, Adams CD, Antman EM, et al. 2012 ACCF/AHA focused update
incorporated into the ACCF/AHA 2007 guidelines for the management of patients
with unstable angina/non-ST-elevation myocardial infarction: a report of the
American College of Cardiology Foundation/American Heart Association Task
Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(23):e179-347.
3. Braunwald E, Mark DB, Jones RH, et al. Unstable Angina: Diagnosis and
Management. Rockville, MD: Agency for Health Care Policy and Research and
National Heart, Lung, and Blood Institute. US Public Health Service, US
Department of Health and Human Services; 1994. AHCPR publication 94-0602.
4. Hollenberg SM. Myocardial ischemia. In: Hall J, Schmidt G, Kress J. Principles
of Critical Care. 4th ed. New York, NY: McGraw-Hill Education; 2015:1108-
1151.
5. Nikolaou NI, Welsford M, Beygui F, et al. Part 5: Acute coronary syndromes: 2015
International Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science with Treatment Recommendations. Resuscitation.
2015;95:e121-e146.
6. Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction
in patients presenting with persistent ST-segment elevation: the Task Force on the
Management of ST-segment Elevation Acute Myocardial Infarction of the European
Society of Cardiology. Eur Heart J. 2008;29:2909-2945.
7. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the
management of ST-elevation myocardial infarction: a report of the American
College of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines. Circulation 2013;127:e362-e425.
8. Roffi M, Patrono C, Collet JP, et al. 2015 ESC guidelines for the management of
acute coronary syndromes in patients presenting without persistent ST-segment
elevation. Task Force for the Management of Acute Coronary Syndromes in
Patients Presenting without Persistent ST-Segment Elevation of the European
Society of Cardiology (ESC). Eur Heart J. 2016;37:267-315.
9. Steg PG, James SK, Atar D, et al. ESC guidelines for the management of acute
myocardial infarction in patients presenting with ST-segment elevation. Eur Heart
J. 2012;33:2569-2619.
Suggested Websites
1. American College of Cardiology. http://www.acc.org.

2. American Heart Association. http://www.americanheart.org.
3. European Society of Cardiology. http://www.escardio.org.
4. Global Registry of Acute Cardiac Events (GRACE). http://www.outcomes-
umassmed.org/GRACE/default.aspx.
5. National Institute for Health and Clinical Excellence. http://www.nice.org.uk.
6. Thrombolysis Myocardial Infarction (TIMI) Study Group. http://www.timi.org.
Chapter 11
LIFE-THREATENING INFECTIONS: DIAGNOSIS

AND ANTIMICROBIAL THERAPY SELECTION
Objectives
Understand and apply the terminology specific to life-threatening infections.

List the risk factors for the development of infection.
Identify systemic and site-specific clinical manifestations of life-threatening
infections, and understand the diagnostic use of clinical laboratory testing.
Describe the different clinical and epidemiologic variables used to guide the
selection of antimicrobial therapy.
Outline antimicrobial empiric therapy and treatment of specific infections.
Case Study
A 75-year-old nursing home patient was transferred to the emergency department

because of change in mental status and abdominal pain. The nursing home staff reported
that the patient has been having abdominal pain and loose stools for the last 24 hours.
This morning he was found to have a change in mental status, where he was more
lethargic. His vital signs at the emergency department showed a blood pressure of 90/60
mm Hg, heart rate of 120 beat/min, temperature 39°C (102.2°F), and respiratory rate 24
breaths/min with pulse oximetry 90% on 2-L nasal cannula. You are the responsible
caregiver for the patient, and you are admitting the patient to the hospital.
– Does this patient have sepsis?
– What level of care is needed for this patient?
– What initial immediate interventions should be instituted?
I. INTRODUCTION
Life-threatening infections are both a cause and a consequence of critical illness. The
incidence of life-threatening infections or sepsis is increasing as a reflection of the
growing population of patients at risk: the elderly, immunocompromised patients, and
those with malignancy, chronic illness, or multiple trauma. Septic shock, the most
severe form of systemic response to infection, is a common cause of death in critically
ill adults and children. Early recognition and appropriate management of infections and
their sequelae can decrease the mortality rate.
Definitions of sepsis may be difficult to

apply to an individual patient.
Sepsis is defined as life-threatening organ dysfunction caused by host response to

infection. Abnormalities that suggest organ dysfunction may include, but are not limited
to, lactic acidosis, oliguria, coagulation disorders, and an acute alteration in mental
status. These abnormalities are not specific for sepsis and may be present in other
conditions. Septic shock is identified in the clinical setting of sepsis with hypotension
requiring vasoactive drugs to maintain mean arterial pressure >65 mm Hg and having a
serum lactate level >2 mmol/L despite adequate fluid administration. Patients with
suspected infection who are likely to have a prolonged ICU stay or die in the hospital
can be identified at the bedside by alteration in mental status, systolic blood pressure
<100 mm Hg, or a respiratory rate of >22 breaths/min.
Initial considerations in resuscitation and infection management are described in
Chapters 6 and 7.
II. DIAGNOSIS OF INFECTION

The diagnosis of serious or life-threatening infection is based on a careful and complete
assessment of the patient’s history, including risk factors, and the presence of
characteristic clinical manifestations. Atypical presentations that may occur,
particularly in the elderly and in the immunocompromised patient, must also be
considered. Laboratory, microbiologic, and imaging results also support the diagnosis
of documented or suspected infection.
A. Evaluation of New Fever in Critically Ill Adult Patients

In some ICUs, the measurement of a newly elevated temperature triggers an automatic
order set that includes tests that are sometimes unnecessarily time consuming, costly,
and disruptive to the patient and staff. Moreover, the patient may experience discomfort,
be exposed to unneeded radiation, require transport outside the controlled environment
of the ICU, or lose considerable blood to this testing, which is often repeated several
times within 24 hours and daily thereafter. In an era when utilization of hospital and
patient resources is under intensive scrutiny, such fevers should be evaluated in a
prudent and cost-effective manner. A new fever in a patient in the ICU should trigger a
careful clinical assessment rather than automatic orders for laboratory and radiologic
tests. The goal of such an approach is to determine, in a directed manner, whether
infection is present so that additional testing can be avoided and therapeutic decisions
can be made.
Some literature defines fever as a temperature >38°C, whereas other sources define it
as two consecutive measurements of >38.3°C. It is often difficult to determine whether
an abnormal temperature is a reflection of a physiological process, a drug, or an
environmental influence. When evaluating a new fever, an attempt should be made to
rule out causes other than infection before subjecting the patient to a barrage of
investigations. Additionally, not all infected patients are febrile. Evaluation should
include a review the patient’s chart, a thorough examination and review of all
environmental factors as well as drugs that the patient has received recently, and
consideration of physiological fever that can occur in patients in the ICU, such as
postoperative fever. A new onset of temperature >38.3°C (≥100.9°F) or ≤36°C
(≤96.8°F) in the absence of a known cause of hypothermia (eg, hypothyroidism, cooling
blanket) is a reasonable trigger for a clinical assessment but not necessarily a
laboratory or radiologic evaluation for infection. All of the patient’s new medications
and blood products should be considered. Ideally, the new drug should be stopped or a
similar agent substituted. Fever induced by drugs may take several days to resolve.
If infection is suspected, the temperature in the ICU is most accurately measured by an
intravascular, esophageal, or bladder thermistor, followed by rectal, oral, and tympanic
membrane measurements. Axillary measurements, temporal artery estimates, and
chemical dot thermometers should not be used in the ICU. Rectal thermometers should
be avoided in neutropenic patients.
The diagnosis of drug-induced fever is usually established by the temporal relationship
of the fever to starting and stopping the drug. Patients can be rechallenged with the drug
to confirm the diagnosis, but this is rarely done unless the drug in question is essential
and alternatives are not available. Patients developing anaphylaxis or toxic epidermal
necrolysis as a result of drug exposure should not be rechallenged.
Fever is a common phenomenon during the initial 48 hours after surgery. Fever in this
early postoperative period is usually non-infectious in origin, presuming that unusual
breaks in sterile technique or pulmonary aspiration did not occur. Considerable money
can be wasted in overzealous evaluation of early postoperative fever. However, 96
hours after surgery, fever is more likely to represent infection.
Surgical site infections alone account for approximately 25% of overall costs related to
treatment of nosocomial infections. The rate of surgical site infection is approximately
3%. This varies based on the degree of contamination of the incision, the patient’s
medical comorbidities (eg, diabetes mellitus and obesity increase risk), whether surgery
is prolonged or an emergency, and whether any antimicrobial prophylaxis is
administered correctly (eg, appropriate narrow spectrum of activity, administration just
before incision, and discontinuation within 24 hours [48 hours for cardiac surgery]).
B. EPIDEMIOLOGIC FACTORS
Serious or life-threatening infections may occur in patients from the community, long-
term care facilities (ie, nursing homes), or hospital settings. Serious or life-threatening
community-acquired infections include bacterial pneumonia, central nervous system
(CNS) infections or meningitis, urosepsis, intra-abdominal sepsis due to a ruptured or
obstructed viscus, or sporadic uncommon infections, such as necrotizing fasciitis.
Patients from long-term care facilities share this spectrum but often have infections with
more resistant pathogens, and they may develop device-related infections. Finally,
hospitalized patients are exposed to antimicrobial-resistant flora and numerous invasive
devices, and they have more comorbidities and greater severity of illness than the other
populations.
Healthcare-associated infections are acquired while the patient is receiving treatment
for other conditions within a healthcare setting. It is estimated that these infections are
associated with almost 100,000 deaths annually in the United States. Infection could
occur during the current hospitalization or an admission in the last 60 days, residence in
a nursing home or extended-care facility, home intravenous antibiotic therapy or
chemotherapy, and chronic dialysis or home wound care.
C. PREDISPOSING CONDITIONS
The presence of predisposing conditions should alert the care team to patients at higher
risk of developing infections (Table 11-1). Permanent prosthetic implants, such as heart
valves, intravascular grafts, or orthopedic devices, may become infected in either the
early or late postoperative period. Invasive procedures (eg, surgery, vascular
catheterization, placement of urinary catheters, and endotracheal intubation) breech the
normal mucosal defense barriers and predispose patients to infection. The lack of
predisposing conditions does not eliminate the possibility that a serious infection is
present, particularly in patients admitted directly to the ICU from the community.
Table 11-1 Conditions Predisposing to Infection
Extremes of age Diabetes

Transplant recipients Hepatic failure
Multiple trauma Malnutrition
Alcoholism Malignancy
HIV Corticosteroid use
Chemotherapy/radiotherapy Burns
Absence of spleen Prosthetic implants
Invasive procedures
D. CLINICAL MANIFESTATIONS
The clinical manifestations of life-threatening infections are diverse, and they may be
subtle or overt and localized or systemic. An awareness of the signs and symptoms
associated with specific infections allows early recognition and prompt institution of
appropriate empiric antimicrobial and supportive management. However, most of the
clinical manifestations are not specific.
Hypothermia predicts poor outcome in

serious infections.
1. Systemic Signs and Symptoms

Fever is the most frequent systemic manifestation of infection, but patients with serious
infection may be normothermic or even hypothermic, particularly if they are elderly or if
antipyretic medications, alcoholism, or renal or hepatic failure are involved.
Temperature probes on a urinary catheter, when available, are the most reliable methods
to measure the core temperature. Temperature measurement is most practically obtained
via the oral or rectal routes, although the limitations of each method should be
considered. Axillary temperatures are unreliable, and tympanic measurements have not
been validated in the critically ill.
Other systemic manifestations include chills, rigors, hypotension, tachypnea, dyspnea,
tachycardia, and nausea and vomiting. Tachycardia is almost always present but may be
absent in the presence of cardiac conduction disturbances, autonomic dysfunction, β-
blockers or calcium channel blockers, and drug fever. Hypotension may be due to
dehydration and hypovolemia but may also indicate septic shock, particularly if the
blood pressure does not respond to volume resuscitation. Hypoperfusion of the kidneys
may result in oliguria or anuria. Encephalopathy is a common clinical manifestation and
ranges from lethargy/irritability to delirium and coma. Petechiae and/or ecchymosis may
be present, particularly on distal extremities.
2. Site-Specific Signs and Symptoms

Some signs and symptoms of infection could be associated with the specific source of
infection:
Infections of the CNS may be associated with headache, seizures, meningismus, or

focal neurologic findings. Altered mental status is often present but not specific for
CNS infections.
Diffuse or localized respiratory tract infections may be associated with dyspnea,
tachypnea, cough, sputum production, or (rarely) hemoptysis. Chest auscultation
findings, such as crackles, rhonchi, or tubular breath sounds, indicate whether the
process is localized or diffuse. Diminished breath sounds and dullness on
percussion are suggestive of a pleural effusion.
Intra-abdominal infections may cause abdominal pain, abdominal distension,
nausea and/or vomiting, diarrhea, and anorexia. Diaphragmatic irritation can be
perceived as pain in the side of the neck and proximal shoulder area or may cause
hiccups. Findings on examination may include diffuse or local tenderness, rebound
tenderness, ileus, or guaiac-positive stool. A wound infection with evidence of
fascial disruption may signal an intra-abdominal infection below the fascia.
Urinary tract infections may produce flank pain or abdominal pain, tenderness,
dysuria, hematuria, and oliguria. Typically, a urinary catheter–associated infection
does not produce localized symptoms.
Cutaneous manifestations may result from a primary infection of the skin or skin
structures (eg, pain, erythema, and induration due to cellulitis; wound margin
erythema; tenderness or purulent discharge; vesicular lesions due to herpes
infection) or be a consequence of disseminated systemic infection (eg,
erythematous indurated papules or nodules of ecthyma gangrenosum due to
bacteremia, septic emboli due to infective endocarditis, diffuse macular erythema
due to toxic shock syndrome, distal symmetric purpura fulminans due to
meningococcemia).
E. Laboratory Manifestations
Routine laboratory tests are not specific in the diagnosis of life-threatening infections
but may be suggestive and allow assessment of organ function. The white blood cell
count is usually elevated with a shift to more immature forms (called a left shift).
Leukocytosis is commonly observed in noninfectious processes such as the early
postoperative period, corticosteroid therapy, massive transfusions, and polytrauma.
Conversely, a normal leukocyte count may be observed despite active infection in the
elderly and in patients with hypersplenism or chronic myelosuppressive disorders.
Neutropenia may result from overwhelming infection (especially in neonates and AIDS
patients), severe viral infection, typhoid fever, brucellosis, and other infections. Toxic
granulation within neutrophils may also be noted.
The most common coagulation abnormality in sepsis is isolated thrombocytopenia. A
decline in platelet count may be a subtle, early clue to the presence of infection.
Disseminated intravascular coagulation is a less common finding but is a poor
prognostic sign. It is characterized by elevations in prothrombin time, partial
thromboplastin time, fibrin split products, and/or D-dimer, and decreased fibrinogen.
Sepsis causes relative insulin resistance, usually resulting in hyperglycemia, whereas
hypoglycemia is less frequent and often reflects low hepatic glycogen stores. Arterial
blood gas measurements usually reflect metabolic acidosis, a low PaCO2 due to
respiratory compensation and often hypoxemia. An elevated serum lactate level is a
significant sign of compromised peripheral perfusion and oxygen balance due to severe
sepsis or septic shock. Hepatic dysfunction is usually not severe but presents as a
cholestatic picture with elevated bilirubin and mild elevation of transaminases. Renal
insufficiency often occurs due to multiple factors, such as hypotension and hypovolemia.
Other possible nonspecific markers of inflammation/infection include procalcitonin and
C-reactive protein.
F. Microbiologic Studies
Microbiologic studies are divided into those with immediately available results
(minutes to a few hours) and those requiring a period for incubation or laboratory
determination. Among the studies with quickly available results is Gram stain of body
fluids. Special stains (such as fungal and acid-fast stains), immunoassays (such as urine
Legionella antigen and Clostridium difficile toxins), and counterimmunoelectrophoresis
panels require time to process.
Empiric antimicrobial therapy for the

patient with a presumptive life-
threatening infection should be initiated
based on clinical and epidemiologic
clues.
Ideally, all cultures should be obtained before initiation or modification of

antimicrobial therapy, but this may not be possible in the rapidly deteriorating patient.
The selection of culture site(s) should be guided by clinical manifestations.
Indiscriminate sampling from many sites not only may yield misleading results due to
culture contamination or site colonization, but is also not cost-effective and may pose
additional risks to the patient. Repeat cultures may be appropriate to assess for changes
in the type of organism or resistance patterns.
At least two sets of peripheral blood cultures (aerobic and anaerobic bottles) should be
obtained either from different anatomic sites or from the same site. A blood volume of
10 to 15 mL per culture set is optimal in adults. Obtaining blood cultures from
indwelling peripheral or central intravascular catheters may yield false-positive results
because of microbial contamination of the catheter hub. Isolator blood cultures may
improve the diagnostic yield for some organisms (eg, Candida, Mycobacterium) or in
patients already receiving antimicrobial therapy.
Respiratory tract cultures require expectorated sputum from the nonintubated patient and
tracheal suction or bronchoscopic specimens from an intubated patient. Many
microbiology laboratories will screen the specimen for the number of epithelial cells
and neutrophils to determine adequacy for culture. Quantitative cultures of lower
respiratory tract secretions may discriminate between colonizing and pathogenic
bacteria.
In the absence of catheterization, urine cultures should be clean-catch voided
specimens; in catheterized patients, specimens should be aspirated from the urinary
catheter tubing. If the catheter has been in place for few days, replacement is
recommended and the culture obtained from the new catheter. Semiquantitative culture
is needed; however thresholds for significance differ for clean-catch urine (>105
organisms/mL) and catheter-obtained urine (103 organisms/mL). Urinalysis for the
detection of pyuria will help to discriminate bacteriuria from cystitis or upper tract
infection.
Intravascular catheters should be removed (by applying chlorhexidine to the surrounding
skin and external part of the catheter adjacent to the skin exit), and the catheter tip
segment should be sent for semiquantitative culture. However, clinical correlation
between the catheter culture result, blood culture(s), and appearance of the catheter exit
site is required to discriminate between catheter-related bacteremia, local catheter-
related infection, and simple colonization of the catheter itself. The best method for
diagnosis of intravascular catheter-related bloodstream infections is the testing of
paired cultures from peripheral and catheter blood samples.
III. ANTIMICROBIAL THERAPY
Case Study
A 70-year-old woman, status post laparoscopic cholecystectomy day 4, was scheduled

to be discharged from the hospital the next morning. She was found sitting in bed,
slightly confused, agitated, coughing, with evidence of vomitus around the mouth and on
her clothing. The nurse evaluating the patient found that she was tachycardic and febrile,
and her oxygen saturation was 88% on room air where previously it was 99%. The
white blood cell count was elevated, and a chest radiograph confirmed new-onset
pneumonia. You are asked to evaluate her.
– What is the likely source of this patient’s infection?
– What factors would influence your choice of antimicrobial agent?
The first priority in managing a hemodynamically unstable patient with a severe or life-
threatening infection is resuscitation (Chapters 6 and 7). After evaluation of the
patient’s history, physical examination, and auxiliary test results (laboratory and
imaging studies), antimicrobial agents should be instituted promptly.
Early source control (suspected source of infection) is paramount to favorable outcomes
and is an essential adjunct to adequate antimicrobial therapy. Examples of source
control include wound debridement, percutaneous or surgical drainage of a closed-
space infection, foreign body removal, and surgery. The antimicrobial therapy
recommendations found in this chapter are general guidelines only. For each clinical
scenario, antimicrobial choices must be individualized to match the clinical
manifestations and the available epidemiologic and microbiologic information,
including the patterns of microbial prevalence and resistance in the institution or local
community.
Early use of appropriate empiric

antimicrobial therapy reduces infection-
associated mortality.
The selection of appropriate antimicrobial therapy depends on the following factors:
1. The suspected microbial pathogen(s) and site of infection: The most common sites
for life-threatening infections in adult patients involve the lower respiratory tract,
the intra-abdominal cavity, and the bloodstream. Rapidly progressive soft tissue
infections and CNS infections should also be considered and are often clinically
obvious. Antimicrobial penetration to the site of infection should also be
considered. The CNS and lungs are two sites that allow limited penetration of
certain antimicrobials; therefore, the pharmacokinetic characteristics of the
selected agents must be understood to ensure maximal antimicrobial activity at
those sites.
2. Gram stain results of available specimens from the suspected site: The description
of early stain results directs the clinician to the broad categories of organism(s)
that should be covered. Examples include gram-positive cocci in clusters
(staphylococci) or pairs and chains (enterococci, streptococci), lancet-shaped
diplococci (pneumococcus), gram-positive bacilli (Corynebacterium, Nocardia),
gram-negative bacilli (Escherichia coli, Klebsiella, Pseudomonas), small
pleomorphic gram-negative bacilli (Bacteroides spp), gram-negative coccobacilli
(Haemophilus spp, Moraxella, Acinetobacter), and yeast (Candida). However,
the clinician should wait for final culture results to make changes to the initial
antimicrobial therapy.
If the source of infection is not

obvious on initial examination,
reconsider the possibility of the lungs
or abdomen as the source.
3. Assessment for antimicrobial resistance: Factors predicting that a particular

bacterial pathogen may be resistant to a wider range of antimicrobials include the
following:
– Prior isolation of resistant strains from the same patient
– Prior antimicrobial therapy (broad-spectrum antimicrobial therapy such as
antipseudomonal penicillin/β-lactamase inhibitor combinations, third- and
fourth-generation cephalosporins, fluoroquinolones, carbapenems,
vancomycin)
– Extended hospital or ICU stay
– High endemic rate of multidrug-resistant bacteria in the institution or ICU (eg,
methicillin-resistant Staphylococcus aureus, vancomycin-resistant
Enterococcus, multidrug-resistant Pseudomonas, Stenotrophomonas)
– Ongoing epidemic outbreak in the hospital or ICU
– Long-term dialysis
– Residence in a nursing home or extended-care facility
– Immunosuppressive diseases or therapy
Certain common organisms have become increasingly resistant to formerly

effective antimicrobials. This category includes Streptococcus pneumoniae with
intermediate- and high-level resistance to penicillin and ceftriaxone, Enterococcus
faecium strains resistant to ampicillin and vancomycin, S aureus resistant to
oxacillin/methicillin (methicillin-resistant S aureus [MRSA]), gram-negative
bacilli (E coli, Klebsiella pneumoniae) with extended-spectrum β-lactamase or
chromosomal-mediated β-lactamase production observed in strains of
Pseudomonas aeruginosa, or other mechanisms of multiple resistance to broad-
spectrum antimicrobial therapy. It is vital to know and update the resistance pattern
of the different bacterial pathogens in each institution and each ICU.
4. Comorbid conditions: Less nephrotoxic antimicrobials may be preferable in
patients with diminished renal function or patients at risk for renal failure unless
the benefit of use outweighs the risk of renal dysfunction. Other comorbidities to
consider include bone marrow suppression, chronic or acute liver failure, prior
hearing deficits, pregnancy, and a history of major hypersensitivity or other strong
adverse reactions to a specific antimicrobial.
IV. RECOMMENDED ANTIMICROBIAL THERAPY

The use of the antimicrobial therapies recommended here is based on the suspected site
of infection in the absence of culture results. The clinician should always consider the
dose, dose adjustments, possible interactions, and side effects of selected agents.
Antimicrobial therapy should be given in maximum appropriate therapeutic doses. In
critically ill patients, intravenous administration is preferred to intramuscular or oral
routes. Oral dosing of antimicrobials with similar bioequivalence (eg, quinolones) and
adequate gastrointestinal absorption may be substituted after the patient stabilizes.
Dosage adjustments must be made for the elderly, neonates, children, and patients with
renal or hepatic dysfunction. Antimicrobial de-escalation should be implemented in
appropriate clinical situations once cultures are negative. In the treatment of infection,
antimicrobial agents must be used appropriately and responsibly. A list of selected site
infections with empiric antibiotic therapy is found in Table 11-2.
Table 11-2 Site Infections and Empiric Antibiotic Therapies
Suspected Site of Possible Organism Initial Empiric Dose

Infection Antibiotics
Severe intra-abdominal Pseudomonas, extended Imipenem-cilastatin, Imipenem-cilastatin, 500
infection (non-biliary) spectrum β- lactamase- meropenem, or mg IV q6h
producing piperacillin-tazobactam Meropenem, 1 g IV q8h
Enterobacteriaceae, or combination of Piperacillin-tazobactam,
Acinetobacter, multidrug- cefepime and 4.5 g IV q6h
resistant GNB, metronidazole Cefepime, 2 g IV q12h
Bacteroides spp Metronidazole, 500 mg IV
q8h
Urinary infection Escherichia coli, Ceftriaxone or Ceftriaxone, 1 g IV daily

Pseudomonas piperacillin-tazobactam Piperacillin-tazobactam,
aeruginosa, and other 4.5 g IV q6h
GNB
Lower respiratory P aeruginosa, E coli, Cefepime or Cefepime, 2 g IV q12h
infection Klebsiella pneumoniae, carbapenem; Meropenem, 1 g IV q8h
Acinetobacter and other vancomycin added Vancomycin, 1 g IV q12h
GNB spp, GPC like whenever MRSA is
MRSA considered
Necrotizing soft tissue Usually multi-microbial, Vancomycin plus Cefepime, 2 g IV q12h
infection GPC, GNB, and cefepime or Meropenem, 1 g IV q8h
anaerobes carbapenem, and Clindamycin, 600 mg IV
clindamycin q8h
Vancomycin, 1 g IV q12h
Gastrointestinal tract Clostridium difficile Metronidazole PO or IV, Metronidazole, 500 mg
and vancomycin PO or PO or IV q8h
rectally (if ileus) Vancomycin, 125 mg PO
q6h
Meninges, bacterial Streptococcus Ceftriaxone for S Ceftriaxone, 1 g IV daily
infection pneumoniae, Neisseria pneumoniae, ampicillin Ampicillin, 2 g IV q4h
meningitidis, Listeria, for Listeria, cefepime and Cefepime, 2 g IV q8h
Staphylococcus aureus, vancomycin for others Vancomycin, 1 g IV q12h
and GNB following
procedures (eg, shunt
placement)
GNB, gram-negative bacilli; GPC, gram-positive cocci; MRSA, methicillin-resistant S aureus.
A. Central Nervous System
1. Meningitis
Bacterial meningitis causes one of the crucial emergencies. When it is suspected
clinically, antimicrobial therapy should be instituted immediately, without waiting for
the results of lumbar puncture. Community-acquired acute bacterial meningitis in adults
is most commonly caused by S pneumoniae or Neisseria meningitidis, and initial
empiric therapy with a third-generation cephalosporin (ceftriaxone or cefotaxime)
provides adequate empiric coverage, with vancomycin added if penicillin-resistant S
pneumoniae is suspected or confirmed. If S pneumoniae is isolated, a third-generation
cephalosporin should be continued until penicillin sensitivity is confirmed, at which
point the patient should be switched to high-dose penicillin G. N meningitidis in
cerebrospinal fluid (CSF) or blood culture should be treated with high-dose parenteral
penicillin G. If N meningitidis is isolated, healthcare workers with significant exposure
require antimicrobial prophylaxis. In addition to antimicrobial therapy, adjunctive
dexamethasone (0.15 mg/kg intravenously every 6 hours for 2-4 days) is also
recommended to decrease the risk of morbidity and mortality, particularly in
pneumococcal meningitis.
Prudent antimicrobial therapy involves

early initiation as well as suitable de-
escalation.
Special circumstances require different empiric antimicrobial coverage. Listeria

monocytogenes may be a cause of bacterial meningitis in extremes of age (neonates,
infants, and the elderly) and in patients with T-lymphocyte defects, usually due to
diabetes, corticosteroid use, and immunosuppressive therapy (eg, organ recipients and
patients with autoimmune disease). Patients with suspected Listeria meningitis should
receive ampicillin (trimethoprim-sulfamethoxazole in the penicillin-allergic patient).
Those who have undergone recent neurosurgical procedures or placement of CSF shunts
are at increased risk for S aureus, coagulase-negative staphylococci, and gram-negative
bacilli (Pseudomonas, Klebsiella). Therefore, such patients require initial empiric
antimicrobial coverage with high-dose vancomycin and a third- or fourth-generation
cephalosporin. If methicillin-susceptible S aureus is confirmed, nafcillin is the drug of
choice.
Meningitis presenting in a subacute fashion over several weeks or longer, with
predominance of CSF lymphocytes, is more likely to occur in immunocompromised
patients. Pathogens such as Mycobacterium tuberculosis, Toxoplasma gondii, and
Cryptococcus neoformans should be considered in this setting.
2. Encephalitis or Meningoencephalitis
Many viral agents can cause encephalitis or meningoencephalitis, but only herpes
simplex (HSV) and cytomegalovirus (CMV) encephalitis are amenable to therapy.
Herpes simplex encephalitis usually occurs in immunocompetent individuals presenting
from the community. This is considered an emergency. Fever, lethargy, confusion, and
seizures are the most common presenting complaints. Hemorrhagic CSF and temporal
lobe involvement on imaging studies (computed tomography or magnetic resonance
imaging) or electroencephalography are suggestive of HSV encephalitis. Polymerase
chain reaction testing of CSF is sensitive for diagnosis of this infection. If HSV
encephalitis is suspected or confirmed, a 14- to 21-day course of parenteral acyclovir
should be initiated promptly, pending further studies. CMV encephalitis usually occurs
in patients with suppressed immune status (HIV and transplant patients) and could have
the same clinical manifestations as HSV encephalitis. Polymerase chain reaction testing
of CSF for CMV is also highly sensitive, and therapy should include ganciclovir or
foscarnet.
3. Brain Abscess
Brain abscess is an uncommon infection but should be suspected in patients with
chronic infections of parameningeal structures, left-sided endocarditis, or congenital
cyanotic heart disease. Brain abscesses also have been associated with
immunosuppression, as in patients with AIDS, intravenous drug abusers, or transplant
recipients. Infections are often polymicrobial, and etiologic organisms include aerobic
and anaerobic streptococci, staphylococci, gram-negative bacteria, and anaerobes.
Initial antimicrobial therapy should include vancomycin, high-dose metronidazole, and a
third-generation cephalosporin (ceftriaxone). In patients at high risk for toxoplasmosis
(eg, those with AIDS, cardiac transplant recipients), pyrimethamine/sulfadiazine should
be part of the initial antimicrobial regimen. Less common causes of brain abscess
include tuberculosis, nocardiosis, syphilis, amoeba, and other parasites. The diagnostic
yield of CSF cultures for brain abscess is extremely low, and brain biopsy may be
needed in patients who fail to respond to empiric therapy.
B. Respiratory Tract
1. Severe Community-Acquired Pneumonia (Immunocompetent Host

The most common organism resulting in hospitalization for community-acquired
pneumonia is S pneumoniae, but other causative organisms include Legionella,
Mycoplasma, and Chlamydia. Haemophilus influenzae is an uncommon pathogen in the
United States because of the introduction of the vaccine against H influenzae type B in
children. A β-lactam (ceftriaxone, cefotaxime, ampicillin-sulbactam) plus either a
macrolide (azithromycin) or a respiratory fluoroquinolone are recommended in patients
admitted to the ICU. If the patient is allergic to penicillin, a respiratory fluoroquinolone
and aztreonam are recommended. If aspiration pneumonia is suspected (alcoholic
patients, presence of poor dentition), the addition of clindamycin is warranted unless a
β-lactam/β-lactamase inhibitor combination is utilized. If Pseudomonas is a
consideration, an antipseudomonal β-lactam (piperacillin-tazobactam, cefepime,
imipenem, or meropenem) should be used. Vancomycin or linezolid may be added if
community-acquired MRSA is suspected.
2. Community-Acquired Pneumonia (Immunocompromised Host)

Immunocompromised patients with pneumonia may have the same pathogens as an
immunocompetent host but with more severe infection. Radiographic evidence of
interstitial pneumonia or a normal chest radiograph in a patient with prominent
respiratory symptoms who has T-cell deficiency (AIDS, chronic steroid use) should
prompt the addition of trimethoprim-sulfamethoxazole in appropriate doses for possible
Pneumocystis jirovecii infection (The nomenclature for Pneumocystis species that
infects humans has been changed from Pneumocystis carinii to Pneumocystis jirovecii).
Consider the addition of steroids in P jiroveci pneumonia associated with significant
hypoxemia. Focal lesions (eg, abscess, nodules) are suggestive of fungal infections, M
tuberculosis, or Nocardia; empiric coverage with antifungal agents, antimycobacterial
agents, and trimethoprim-sulfamethoxazole may be warranted in these circumstances.
Patients with suspected M tuberculosis infection also require respiratory isolation.
CMV or other viral infection also should be considered in the differential of an
interstitial pneumonitis.
3. Nosocomial and Ventilator-Associated Pneumonia

Gram-negative organisms and S aureus are frequent causes of pneumonia in
hospitalized patients or those who require mechanical ventilation. Nosocomial
organisms tend to be more resistant and are more likely to be present in patients with
extended hospital stays, prior antimicrobial therapy, and comorbidities. If possible,
attempts should be made to obtain lower respiratory tract samples for quantitative
microbiologic evaluation in mechanically ventilated patients. Adequate antimicrobial
coverage can usually be provided with a third- or fourth-generation cephalosporin, β-
lactam/β-lactamase inhibitor combinations, or a carbapenem, plus a fluoroquinolone or
an aminoglycoside. If Pseudomonas is a consideration, an antipseudomonal β-lactam
(piperacillin-tazobactam, cefepime, imipenem, or meropenem) should be used. Therapy
with trimethoprim-sulfamethoxazole should be included if the possibility of
Stenotrophomonas maltophilia is suspected or confirmed. Vancomycin should be
considered if methicillin-resistant S aureus is a possible pathogen. Pneumonia due to
methicillin-sensitive strains of S aureus should be treated with an antistaphylococcal
penicillin as these agents are superior to vancomycin. Patients with methicillin-resistant
S aureus who are vancomycin-intolerant or are not responding to vancomycin may be
treated with linezolid. If vancomycin is utilized, serum trough levels should be
maintained no lower than 15 to 20 μg/mL as lung penetration of this agent is limited.
Shorter courses (8 days) of therapy may be appropriate as long as non-lactose-
fermenting organisms are not isolated. Consideration may be given to stop the antibiotic
therapy if the lower respiratory tract cultures are negative.
Utilize short courses of antimicrobial
therapy when appropriate.
C. Heart
Infections of the heart are usually severe and life-threatening and require coordinated
medical care with a cardiologist and sometimes with a cardiovascular surgeon.
Microbiologic studies and echocardiography (transthoracic or transesophageal) are the
cornerstones for the diagnosis and management of any infection in the heart.
Infective endocarditis, or infection of the endocardial surface of the heart, most
frequently involves the heart valves. Intravenous drug abuse, prosthetic valves,
sclerosing of natural valves due to aging, hospital-acquired infections, and newly
identified pathogens (Bartonella spp, Coxiella burnetii, Tropheryma whipplei, fungi)
are the main risk factors for this condition. Demonstration of bloodstream infection and
positive echocardiographic evidence of valvular vegetations are key to making the
diagnosis, although peripheral embolic phenomena and other findings are strongly
suggestive. Gram-positive cocci, mainly Staphylococcus and Streptococcus, but also
Enterococcus, are the most common microorganisms isolated in infective endocarditis
in the general population and in specific risk groups (intravenous drug users and
prosthetic valve endocarditis), but gram-negative, polymicrobial, fungal, and culture-
negative cases of endocarditis are becoming more common. Bactericidal antimicrobial
therapy (eg, penicillins/third-generation cephalosporins, daptomycin with or without an
aminoglycoside, glycopeptides, linezolid), high drug concentrations, the resistance
pattern of the microorganism, and long-term therapy are the cornerstones of treatment.
D. Intravascular Catheters
In patients with confirmed or suspected intravascular catheter infection associated with
organ dysfunction, systemic emboli, or cardiovascular instability, the intravascular
catheter should be removed promptly. In addition, local changes at the catheter site
(purulence, erythema) mandate catheter removal. In the absence of local changes or
sepsis, an option is to insert a new catheter in the existing site over a guidewire;
however, this approach needs to be supported with negative blood cultures as well as
negative culture of the intradermal portion of the removed catheter. Coagulase-negative
Staphylococcus and S aureus are the most common pathogens in catheter-related
bloodstream infections. In the immunocompetent patient who has a coagulase-negative
staphylococcal line infection but no systemic symptoms, the removal of the infected
catheter line may be sufficient. Vancomycin is recommended in immunocompromised
patients with coagulase-negative staphylococcal line infections, patients with systemic
manifestations, or those with prosthetic devices at risk for becoming secondarily
infected. If S aureus is the infecting organism, nafcillin is recommended; however, if
there is a high rate of MRSA in the hospital or MRSA is confirmed, vancomycin should
be used. Daptomycin can also be used; linezolid is less likely to be helpful. A third- or
fourth-generation cephalosporin or fluoroquinolone should be added if a nosocomial
gram-negative organism is suspected.
Because of the increasing incidence of

vancomycin-resistant organisms, attempt
to limit the indiscriminant use of
vancomycin.
Candida is occasionally isolated from catheter tips and should increase the suspicion
that occult candidemia may have been recently present. The treatment of choice is
fluconazole; if there is a possibility of Candida, such as Candida glabrata or Candida
krusei, caspofungin should be used. When a fungal microorganism is identified in an
intravascular catheter-related bloodstream infection, a non-tunneled catheter always
should be removed, whereas the removal of a tunneled catheter should be based on the
likelihood of catheter-related candidemia rather than candidemia from another source.
Antimicrobial-impregnated catheters appear to have a lower rate of bloodstream
infection, but the maximum longevity of such catheters is still under investigation.
E. Abdomen
When an intra-abdominal infection is suspected, a surgeon must be involved in the
evaluation of the patient. Both the infecting flora and the antimicrobial therapy are
related to whether the infection was acquired in the community or healthcare setting. For
community-acquired infections, location of a possible perforation determines the
probable organism, with gram-positive, facultative, and aerobic gram-negative bacteria
beyond the proximal small bowel and anaerobes beyond the proximal ileum.
Recommended therapies include β-lactam/β-lactamase inhibitor combinations and
carbapenems as monotherapy or cephalosporins/fluoroquinolones with metronidazole.
Antimicrobial therapy should be continued until clinical resolution, which typically
occurs in 5 to 7 days. Further diagnostic workup should be pursued in patients with
persistent or recurrent symptoms. Flora isolated from healthcare-associated intra-
abdominal infections resembles that of other nosocomial infections. Antimicrobial
therapy should be based on knowledge of the flora and antimicrobial susceptibilities of
the institution. Anti-enterococcal therapy is indicated only when enterococci are
isolated from patients with healthcare-associated infections. Antifungal therapy is
indicated only in those who have isolated fungi and comorbid conditions – like recent
immunosuppressive therapy for neoplasms, transplantation, and inflammatory disease –
or who have postoperative or recurrent infections.
F. Urinary Tract
The most common pathogens in urinary tract infections are gram-negative enteric
bacteria.Hospitalized patients with urinary catheters in place commonly have
bacteriuria yet exhibit no pyuria or localized symptoms. Such patients (in the absence of
urologic obstruction) rarely develop sepsis or bacteremia arising from the urinary tract,
and removal of the catheter may allow resolution of the bacteriuria. Patients who
develop upper urinary tract infection always merit antimicrobial therapy. More serious
complications may be seen in diabetic patients or other immunocompromised
individuals, including those with emphysematous pyelonephritis, papillary necrosis, or
perinephric abscess, which may require surgical intervention. Empiric antimicrobial
options for gram-negative urinary tract infections are dictated by susceptibility testing
and include the following:
Third-generation cephalosporins
Aminoglycosides
Piperacillin-tazobactam
Trimethoprim-sulfamethoxazole
Enterococcal infection in the urinary system should be suspected in patients who have
had urinary catheters in place for long periods or who have had recent manipulation of
the urinary tract. Therapy should include ampicillin, piperacillin, or vancomycin.
Candiduria is not uncommon and usually occurs in patients who have long periods of
urinary catheterization and are receiving broad-spectrum antimicrobial therapy or
patients with glycosuria. Therapeutic options include a short course of fluconazole (not
effective against C glabrata or C krusei) or continuous amphotericin bladder irrigation;
however, relapse rates are significant with either treatment. If candiduria is treated in a
patient with an indwelling catheter, the catheter should be changed or removed during
the treatment course.
G. Cutaneous Infection
S aureus or group A β-hemolytic streptococci are the most likely etiologic organisms in
cellulitis or cutaneous abscess. H influenzae must also be considered in facial or
orbital cellulitis. Onset of postoperative wound infections usually occurs 5 to 7 days
after surgery. However, rapidly progressive wound infections occurring within 24 to 48
hours after surgery should prompt the consideration of Clostridium perfringens or
group A β-hemolytic streptococci (Streptococcus pyogenes). This type of infection
warrants surgical debridement and prompt antimicrobial therapy directed by Gram stain
and culture results. Antimicrobial choices include the following:
Cefazolin or nafcillin if methicillin-resistant S aureus is unlikely

Vancomycin or linezolid if there is a possibility of methicillin-resistant S aureus
Penicillin G with or without clindamycin for wound infections developing within
48 hours to cover C perfringens and β-hemolytic streptococci
Daptomycin because of its bactericidal properties
Wound toxic shock syndrome is a rare condition that can occur within 48 hours of a
wound or surgical incision. The causes are toxin-producing S aureus or β-hemolytic
streptococci, but often the wound does not appear infected. Presenting symptoms
include fever, diarrhea, vomiting, hypotension, and uremia. Erythroderma and
subsequent desquamation are characteristic but may be delayed for several days.
Treatment involves opening the wound and prompt use of specific antimicrobial therapy.
H. Necrotizing Soft Tissue Infection

Infection of the subcutaneous tissue, fascia, and muscle can occur in any patient but may
be more common in immunocompromised patients, particularly individuals with
diabetes. If gas is present in the tissue, cutaneous gangrene or bullae are noted, or
infection progresses rapidly, a necrotizing soft tissue infection must be considered. This
condition requires prompt surgical debridement in addition to broad-spectrum
antimicrobial therapy. These infections are usually polymicrobial, involving aerobic
and anaerobic gram-positive and gram-negative organisms.
Antibiotics are adjuvant therapy to early
and repeated debridement in necrotizing
soft tissue infection.
Adequate empiric therapy should include vancomycin and a β-lactam/β-lactamase

inhibitor, a carbapenem and fluoroquinolone, or an aminoglycoside and clindamycin
(the latter to reduce the amount of toxins).
I. Immunocompromised or neutropenic patients

In the absence of a specific source, pending culture results, broad-spectrum
antimicrobial therapy is indicated in the immunocompromised or neutropenic patient
with fever. Monotherapy can be effective, but combination therapy is indicated initially
for more severely ill patients. To reduce the emergence of resistance, a third-generation
cephalosporin as monotherapy should be avoided if Pseudomonas spp, Acinetobacter
spp, Enterobacter spp, Citrobacter spp, or Serratia spp are prevalent.
Suggested antimicrobial regimens include the following:
Third- or fourth-generation cephalosporin (ceftazidime or cefepime for P

aeruginosa coverage) with an aminoglycoside or fluoroquinolones
Carbapenems
Piperacillin-tazobactam
Addition of vancomycin if gram-positive organisms are likely
The use of white cell growth factors (ie, granulocyte colony-stimulating factor,
granulocyte-macrophage colony-stimulating factor) may improve outcome by shortening
the duration of neutropenia. These progenitor cell stimulants should be targeted for
patients with an anticipated duration of neutropenia of 5 to 7 days and a high risk for
serious infection.
J. Clostridium Difficile Infection

Antibiotic-associated diarrhea and colitis resulting from C difficile infection can
complicate the course of treatment for many patients. The antimicrobials most
commonly involved include clindamycin, penicillins, cephalosporins, and quinolones,
although C difficile has been described in association with almost all antimicrobials.
Patients do not need to receive antimicrobial therapy to develop this condition.
C difficile is also recognized as an important nosocomial pathogen capable of cross
transmission to patients in adjacent areas. Diagnosis is usually based on identification
of C difficile toxins and detection of cytotoxin activity in tissue culture. Toxin testing is
hampered by lack of sensitivity, and the polymerase chain reaction testing appears to be
rapid, sensitive and specific, and ultimately addresses testing errors.
Treatment begins with discontinuation of the implicated antimicrobial therapy (if
possible) and initiation of specific antimicrobial therapy against C difficile if symptoms
are moderate, severe, or persistent. The preferred regimen is oral metronidazole, 500
mg three times daily for 10 to 14 days. Oral vancomycin, 125 mg four times daily for 10
to 14 days, is also effective, and is the preferred therapy for severe infections. For
patients who are unable to take oral medications, intraluminal vancomycin with or
without intravenous metronidazole is recommended. Fidaxomicin is a first-in-class,
narrow-spectrum macrocyclic antibiotic that acts by eradicating C difficile with
minimal disruption of the normal intestinal flora. It is used when the vancomycin option
fails. Fulminant colitis unresponsive to these measures or progressing to toxic
megacolon may require total colectomy.
Proper infection control is important in

the management of C difficile infections.
K. Fungal diseases
Life-threatening infections caused by fungi may be extremely difficult to diagnose by
routine physical examination or routine cultures. Candida albicans is the most common
etiologic organism in critically ill patients. Non-albicans species of Candida and other
fungi have increased significantly in recent years. Fungal infection should be considered
in certain geographic regions and in the presence of predisposing factors, such as HIV,
malignancy, neutropenia, long-term use of steroids, broad-spectrum antimicrobial
therapy, parenteral nutrition, severe burns or organ transplantation, or central venous
vascular catheters.
The polyenes (amphotericin B and lipid preparations of amphotericin B) have been the
most commonly utilized antifungal agents for serious infections. Newer agents
(caspofungin, voriconazole) have shown comparable or superior clinical outcomes
compared with the polyenes and have much less toxicity than usually associated with
amphotericin B. All lipid formulations have less nephrotoxicity, and their efficacy
against Candida is equivalent to conventional amphotericin B. Fluconazole is still
active against most Candida species and Cryptococcus, and itraconazole may be used
for some of the mold infections. Both agents have an important role in primary or
secondary prophylaxis. The newer agents, such as voriconazole, posaconazole, and
caspofungin, have activity against resistant Candida strains and some of the mold
infections resistant to other regimens. Voriconazole is the drug of choice for Aspergillus
infection.
L. Other therapy
In addition to antimicrobial therapy, surgical intervention must be considered in patients
with life-threatening infections. Any abscess must be drained, and injured or ischemic
organs must be repaired or removed. Vascular catheters that may be a source of
infection should be removed.
Early surgical consultation should be sought when the abdomen may be a source of
infection in the critically ill patient. Guidelines for tetanus prophylaxis are found in
Chapter 9. Further management of the patient with septic shock is discussed in Chapter
7.
M. Healthcare-associated infection control

Patients can acquire healthcare-associated infections (HAIs) during the course of
receiving treatment for other conditions within a healthcare setting. For example,
pneumonia would meet the healthcare-associated criteria if the patient was hospitalized
for at least 2 of the preceding 90 days, was a resident in a nursing home or extended-
care facility, received home intravenous (antibiotics or chemotherapy) therapy, or
received chronic dialysis or home wound care (or both) during the preceding 30 days.
Recent data estimate that one of every 25 hospitalized patients experience a HAI each
year. Pneumonia and surgical site infection from any inpatient surgery were the most
common HAIs. Many studies show that HAI increases hospital length of stay and
morbidity and mortality rates. Strategies have been proposed to prevent HAI. More
details are available in the Web sites listed at the conclusion of this chapter. Guidelines
cannot always account for variations among patients and are not intended to supplant
physician judgment with respect to individual patients or special clinical situations.
Key Points
Life-Threatening Infections
Fever is the most frequent systemic manifestation that raises the suspicion of
infection.
Ideally, appropriate cultures should be obtained before initiation of antibiotics in
patients with suspected infection.
Selection of appropriate empiric antimicrobial therapy depends on the suspected
pathogen(s) and site of infection, Gram stain results of available specimens from
the suspected site, assessment for antimicrobial resistance, and comorbid
conditions.
When bacterial meningitis is suspected clinically, antimicrobial therapy should be
instituted immediately, without waiting for the results of lumbar puncture.
The most common organism resulting in community-acquired, life-threatening
pneumonia is Streptococcus pneumoniae.
Resistant gram-negative organisms and Staphylococcus aureus are frequent causes
of pneumonia in hospitalized patients or in those who require mechanical
ventilation.
Bactericidal antimicrobial therapy, high concentrations of the antimicrobial agent,
the resistance pattern of the microorganism, and long-term therapy are the
cornerstones of therapy for infective endocarditis.
Suspicion of intra-abdominal infection requires the prompt involvement of a
surgeon.
Necrotizing soft tissue infection requires prompt surgical debridement in addition
to broad-spectrum antimicrobial therapy.
In the absence of a specific source and pending culture results, broad-spectrum
antimicrobial therapy is indicated in the immunocompromised or neutropenic
patient with fever.
Fungal infection should be considered in the presence of predisposing factors, such
as malignancy, neutropenia, broad-spectrum antimicrobial therapy, parenteral
nutrition, severe burns, or organ transplantation, or if central venous vascular
catheters are in place.
Suggested Readings
1. O’Grady NP, Barie PS, Bartlett JG, et al. 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.
2. American Thoracic Society, Infectious Diseases Society of America. Guidelines
for the management of hospital-acquired, ventilator-associated, and healthcare-
associated pneumonia. Am J Respir Crit Care Med. 2005;171:388-416.11
3. Avecillas JF, Mazzone P, Arroliga AC. A rational approach to the evaluation and
treatment of the infected patient in the intensive care unit. Clin Chest Med.
2003;24:645-669.
4. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus
Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315:801-910.
5. Shankar-Hari M, Phillips GS, Levy ML, et al. Developing a new definition and
assessing new clinical criteria for septic shock: For the Third International
Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA.
2016;315:775-787.
6. Seymour CW, Liu VX, Iwashyna TJ, et al. Assessment of clinical criteria for
sepsis: For the Third International Consensus Definitions for Sepsis and Septic
Shock (Sepsis-3). JAMA. 2016;315:762-774.
7. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign:
International guidelines for management of severe sepsis and septic shock: 2012.
Crit Care Med. 2013; 41:580-637.
8. Leone M, Bourgoin A, Cambon S, et al. Empirical antimicrobial therapy of septic
shock patients: Adequacy and impact on the outcomes. Crit Care Med.
2003;31:462-467.
9. Ferrer R, Martin-Lochese I, Phillips G, et al. Empiric antibiotic treatment reduces
mortality in severe sepsis and septic shock for the first hour: Results from a
guideline based performance improvement program. Crit Care Med.
2014;42:1749-1755.
10. Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of
America/American Thoracic Society consensus guidelines on the management of
community-acquired pneumonia in adults. Clin Infect Dis. 2007;44:S27-S72.
11. Mermel LA, Allon M, Bouza E, et al. Clinical practice guidelines for the diagnosis
and management of intravascular catheter-related infection: 2009 update by the
Infectious Diseases Society of America. Clin Infect Dis. 2009;49:1-45.
12. Pappas PG, Kaufman C, Andes D, et al. Clinical practice guidelines for the
management of candidiasis: 2009 update by the Infectious Diseases Society of
America. Clin Infect Dis. 2009;48:503-535.
13. Solomkin JS, Mazuski JE, Bradley J, et al. Diagnosis and management of 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.
14. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management
of bacterial meningitis. Clin Infect Dis. 2004;39:1267-1284.
15. Yokoe DS, Anderson DJ, Berenholtz SM, et al. A compendium of strategies to
prevent healthcare-associated infections in acute care hospitals: 2014 update.
Infect Control Hosp Epidemiol. 2014;35:455-459.
Suggested Websites
1. Society of Critical Care Medicine. http://sccm.org.

2. Centers for Disease Control. http://www.cdc.gov.
3. Infectious Diseases Society of America. http://www.idsociety.org.
Chapter 12
M ANAGEMENT OF LIFE-THREATENING
ELECTROLYTE AND M ETABOLIC DISTURBANCES
Objectives
Review the emergent management of severe electrolyte disturbances.

Recognize manifestations of acute adrenal insufficiency and initiate appropriate
treatment.
Describe the management of severe hyperglycemic syndromes.
Case Study
A 78-year-old woman with diabetes mellitus, heart failure, and chronic renal
insufficiency is admitted to the hospital with altered mental status. She has continued to
take her home medications, including furosemide and metformin. According to her
family, she has had a decreased appetite over the past week and increasing lethargy. Her
vital signs are as follows: blood pressure 98/52 mm Hg, heart rate 110 beats/min,
respiratory rate 18 breaths/min, and temperature 36.4°C (97.6°F). The
electrocardiography monitor shows frequent premature ventricular contractions.
– What risk factors does this patient have for electrolyte disturbances?
– Which electrolyte abnormalities might contribute to her presentation?
– How would you initiate the evaluation and treatment of this patient?
I. INTRODUCTION
Electrolyte and metabolic disturbances are common in critically ill and injured patients.
These abnormalities alter physiologic function and contribute to morbidity and
mortality. The most common life-threatening electrolyte and metabolic disorders in
critically ill patients are disturbances in potassium, sodium, calcium, magnesium,
phosphate, and glucose levels. With early recognition and treatment of these
abnormalities, potentially life-threatening complications may be avoided and outcomes
improved.
II. ELECTROLYTE DISTURBANCES

Electrolyte disturbances result from an underlying disease process. It is important to
seek the cause of the abnormality, as well as to treat the electrolyte change itself. Many
clinical manifestations are not specific to a particular electrolyte change and may be due
to multiple abnormalities. The urgency of treatment depends on the clinical
circumstances rather than the absolute electrolyte concentration. All severe electrolyte
abnormalities require frequent reassessment during correction.
A. Potassium
Potassium is primarily an intracellular ion that is essential for maintenance of the
electrical membrane potential. Approximately 2% of total body potassium is present in
the extracellular compartment. Alterations in this ion primarily affect the
cardiovascular, neuromuscular, and gastrointestinal systems.
1. Hypokalemia
Hypokalemia (potassium <3.5 mmol/L) results from renal or extrarenal losses,
transcellular shifts, and decreased intake (Table 12-1). Life-threatening clinical
manifestations of hypokalemia primarily involve the cardiac and neuromuscular
systems. Dysrhythmias (ventricular and supraventricular, conduction delays, sinus
bradycardia), electrocardiogram (ECG) abnormalities (U waves, QT-interval
prolongation, flat or inverted T waves), muscle weakness or paralysis, paresthesias,
ileus, abdominal cramps, nausea, and vomiting are common manifestations.
Table 12-1 Causes of Hypokalemia
Transcellular Shifts Renal Losses Extrarenal Losses Decreased Intake

Acute alkalosis Diuresis Diarrhea Malnutrition
Hyperventilation Metabolic alkalosis Profuse sweating Alcoholism
Insulin Renal tubular defects Nasogastric suction Anorexia nervosa
β-Adrenergic agonists Diabetic ketoacidosis
Drugs (diuretics,
aminoglycosides,
amphotericin B)
Hypomagnesemia
Vomiting
Hyperaldosteronism
Cushing syndrome
Treatment of hypokalemia is aimed at correcting the underlying cause and administering

potassium (Figure 12-1). Discontinue offending drugs (if possible), correct
hypomagnesemia and other electrolyte disturbances, and correct alkalosis. Because
potassium is primarily an intracellular ion, an estimated deficit cannot be calculated
from serum values. Therefore, administration must be titrated against periodic
reassessment of the serum levels. Infusion of 20 mmol potassium in 100 mL fluid over 1
hour, with additional doses administered sequentially, is recommended to avoid
potential complications with more concentrated solutions. This concentration must be
administered through a central line, although more dilute solutions can be administered
peripherally. The infusion rate can be slowed after life-threatening symptoms resolve.
Serum potassium levels must be monitored at frequent intervals during repletion (ie,
every 3-4 hours during initial replacement). If acidemia is present, correct the
potassium level before correcting the pH, since potassium shifts intracellularly as the
pH increases.
Always consider the possibility of

hypomagnesemia when significant
hypokalemia exists.
Figure 12-1. Treatment of Hypokalemia

2. Hyperkalemia
Hyperkalemia (potassium >5.5 mmol/L) in critically ill patients most often results from
renal dysfunction. Other causes are listed in Table 12-2. Pseudohyperkalemia may
result from a white blood cell count >100,000/mm3 or platelet count >600,000/mm3.
Hemolysis secondary to phlebotomy technique must also be considered.
Table 12-2 Causes of Hyperkalemia
Renal dysfunction Cell death

Rhabdomyolysis
Acidemia Tumor lysis
Hypoaldosteronism Burns
Hemolysis
Drugs (eg, potassium-sparing diuretics,
angiotensin-converting enzyme inhibitors, Excessive intake
succinylcholine, nonsteroidal anti-inflammatory
drugs, trimethoprim-sulfamethoxazole)
Clinical manifestations of hyperkalemia relate primarily to the heart and muscle (Figure
12-2). Arrhythmias, heart block, bradycardia, diminished conduction and contraction,
ECG abnormalities (eg, diffuse peaked T waves, PR interval prolongation, QRS
widening, diminished P waves, sine waves), muscle weakness, paralysis, paresthesias,
and hypoactive reflexes are common manifestations.
Figure 12-2. Electrocardiographic Effects of Hyperkalemia
Two rhythm strips showing the electrocardiographic effects of hyperkalemia. A, peaked T waves and
widened QRS complex. B, sine wave pattern.
Treatment of hyperkalemia involves the recognition and treatment of underlying

diseases, the removal of offending drugs, the limitation of potassium intake, and the
correction of acidemia or electrolyte abnormalities. Any serum potassium level >6
mmol/L should be addressed, but the urgency of treatment depends on the clinical
manifestations and ECG findings. Options for treating hyperkalemia are summarized in
Table 12-3. Serum potassium levels, continuous cardiac monitoring, and serial ECG
tracings should be obtained during evaluation and treatment.
Hyperkalemia with significant ECG

changes, such as widened QRS and sine
wave, mandates immediate therapy.
Table 12-3 Options for Treating Hyperkalemia
If Significant Electrocardiographic Abnormalities Are Present

Administer calcium chloride, 5-10 mL of a 10% solution, intravenously over 5-10 minutes to stabilize the
myocardial cell membrane and decrease the potential for arrhythmias. If calcium gluconate is used, 10-20
mL of a 10% solution is needed for treatment because of the lower elemental calcium content. The effect
lasts only 30-60 minutes and should be followed by additional treatment.
For Redistribution of Potassium
1. Administer insulin and glucose (10 units of regular insulin with 50 g of 50% dextrose over 5-10
minutes intravenously). Glucose monitoring is necessary to avoid hypoglycemia.
2. Administer sodium bicarbonate (1 mmol/kg intravenously over 5-10 minutes). Be aware of the
potential for sodium overload. Sodium bicarbonate is less effective than glucose and insulin for
decreasing the potassium level in patients with end-stage renal failure.
3. Administer inhaled β2-agonists in high doses (albuterol [salbutamol], 10-20 mg), which can
decrease serum potassium by approximately 0.5 mmol/L.
For Removal of Potassium From the Body
1. Increase urine output with a loop diuretic (furosemide, 1-2 mg/kg) and isotonic fluids.
2. Increase gastrointestinal potassium loss with sodium polystyrene, 25-50 g in sorbitol, enterally or by
enema. (Be aware of potential for sodium overload. This may not be a good option in critical illness.)
3. Initiate dialysis.
B. Sodium
Sodium functions as the primary determinant of blood osmolality and is involved in the
regulation of extracellular volume. Abnormalities in circulating sodium primarily affect
neuronal and neuromuscular function.
1. Hyponatremia
Understanding the cause of hyponatremia starts by assessing the patient’s intravascular
volume status. The most common cause of hyponatremia (sodium <135 mmol/L)
associated with a low serum osmolality (hypo-osmolar hyponatremia) is excess
secretion of antidiuretic hormone (ADH) (ie, euvolemic hyponatremia). Hypo-osmolar
hyponatremia or dilutional hyponatremia can also be associated with hypovolemic or
hypervolemic conditions. A common defect is impaired ability to excrete free water
through the kidneys. Less frequently, hyponatremia can result from the presence of a
nonsodium solute, such as glucose and mannitol. These causes are characterized by a
normal or elevated serum osmolality. Pseudohyponatremia, a spurious form of iso-
osmolar hyponatremia, may occur in the presence of severe hyperlipidemia,
hyperproteinemia, or hyperglycemia when the sodium concentration is measured by
flame photometry. Figure 12-3 outlines a diagnostic approach to determining the
etiology of hyponatremia.
Figure 12-3. Diagnostic Approach to the Etiology of Hyponatremia
Abbreviations: FE Na, fractional excretion of sodium; SIADH, syndrome of inappropriate antidiuretic
hormone
Clinical manifestations of hyponatremia involve the central nervous system (CNS) and
muscular system and include disorientation, decreased mentation, irritability, seizures,
lethargy, coma, nausea/vomiting, weakness, and respiratory arrest. Treatment requires
identifying the type of hyponatremia, treating the underlying disease, removing offending
drugs, and improving the circulating sodium level. Hypovolemic hyponatremia usually
responds to intravascular volume repletion (ie, with normal saline). As volume is
replaced, the release of ADH is appropriately suppressed and the kidneys begin to
excrete free water. Hypervolemic hyponatremia is usually not severe and improves with
successful treatment of the underlying condition.
Adrenal insufficiency should be ruled

out in patients with euvolemic and
hypovolemic hyponatremia.
Euvolemic hyponatremia is almost always secondary to elevated levels of ADH.

Diagnosis is facilitated by determining urine osmolality before treatment (especially
with diuretics) to compare with a calculated serum osmolality [(2 × serum sodium) +
glucose/18 + blood urea nitrogen/2.8]. The urine osmolality is inappropriately higher
than serum osmolality (usually >300 mOsm) in the syndrome of inappropriate ADH
(SIADH). If the hyponatremia is acute or the patient is symptomatic, the serum sodium
level should be increased by restricting free-water intake, increasing free-water
clearance with loop diuretics, and replacing intravascular volume with normal saline
(154 mmol/L) or hypertonic 3% saline (513 mmol/L). Hypertonic saline is indicated for
treatment in the presence of severe symptoms, such as seizures, coma, or impending
respiratory arrest. The goal of therapy in this situation is to remove free water and not
sodium. The increase in serum sodium should be controlled, and although the precise
rate of increase is controversial, the serum sodium increase should be limited to
approximately 6 to 8 mmol/L in the first 24 hours. One option is to accelerate the rate of
serum sodium elevation early in the treatment course in the presence of life-threatening
symptoms, such as seizures, and then slow the rate of increase after resolution of the
symptoms. When hypertonic saline is used in symptomatic patients, 1 mmol/kg sodium
chloride should be infused initially (3% saline contains ~0.5 mmol/mL). The same
amount can be administered in incremental doses to a maximum of 3 to 5 mmol/kg or
until symptoms resolve. Alternatively, the change in serum sodium expected after
administering 1 liter of fluid can be estimated by using the following formulas:
Change in Serum Sodium = Infusate Sodium – Serum Sodium
Total Body Water + 1
Change in Serum Sodium = (Infusate Sodium + Infusate Potassium) – Serum Sodium

Total Body Water = 0.6 × Weight (kg) for men; 0.5 × Weight (kg) for women
The sodium concentrations of various infusates are listed in Table 12-4. The formulas
presented above do not take into account other fluid gains and losses (ie, urine output),
and therefore, should serve only as guides to intervention. Serum sodium levels should
be monitored at frequent intervals during therapy for hyponatremia. When serum sodium
is greater than 125 to 130 mmol/L, restriction of free water alone allows for slower
return of the sodium level to normal. Correction of the serum sodium level that is too
rapid may result in CNS injury (ie, osmotic demyelinating syndrome), particularly in the
setting of chronic hyponatremia. Osmotic demyelinating syndrome rarely occurs in
patients whose serum sodium is greater than 120 mmol/L. Symptoms of demyelination
are typically seen after initial improvement in mentation. In 1 to 7 days following a
hasty reversal of chronic hyponatremia, patients may develop focal motor deficits,
respiratory insufficiency, and progressive loss of consciousness. Patients at greatest risk
for osmotic demyelinating syndromes are those with malnutrition or hypokalemia,
alcohol abusers, elderly women, and burn patients. If hyponatremia is chronic and the
patient is asymptomatic, regardless of the magnitude of hyponatremia, free-water
restriction alone may be sufficient to allow for slow return of serum sodium to normal.
Table 12-4 Sodium Characteristics of Selected Infusates
Infusate Sodium Concentration (mmol/L)

5% sodium chloride 855
3% sodium chloride 513
0.9% sodium chloride 154
Ringer lactate solution 130
0.45% sodium chloride 77
5% dextrose in water 0
Although controversial, vasopressin receptor antagonists, such as conivaptan and

tolvaptan, are available for use in the management of hyponatremia. These agents should
not be used in the management of acute hyponatremia and expert consultation should be
sought before their use. They inhibit resorption of water via their action on the V2
receptor of the kidney and result in a slow rise in the serum sodium level. Alternative
therapy, such as hypertonic saline, should be given to patients with severe hyponatremia
complicated by neurologic symptoms due to the need to initially rapidly correct the
sodium level. Vasopressin receptor antagonists can cause hypotension and volume
depletion and therefore should be avoided in patients with hypovolemia. After a
vasopressin receptor antagonist is administered, serum sodium levels should be
monitored frequently (every 4 hours) due to concerns for rapid sodium correction and
neurological sequelae (specifically, demyelination). To prevent over-correction, avoid
using vasopressin antagonists in combination with hypertonic saline. Once an increase
of 6 to 8 mmol/L is achieved, consider replacing free water (orally or intravenously) to
match urine output and prevent an excessive rise in sodium levels.
Do not use vasopressin antagonists in

patients with severe neurologic
symptoms and do not co-administer with
hypertonic saline.
2. Hypernatremia
Hypernatremia (sodium >145 mmol/L) indicates intracellular volume depletion with a
loss of free water that exceeds sodium loss. Causes of hypernatremia are listed in Table
12-5.
Table 12-5 Causes of Hypernatremia
Water Loss Reduced Water Intake Excessive Sodium Intake

Diarrhea Altered thirst Salt tablets
Vomiting Impaired access Hypertonic saline
Excessive sweating Sodium bicarbonate
Diuresis
Diabetes insipidus
The clinical manifestations of hypernatremia relate to CNS and muscle function.

Manifestations of hypernatremia include altered mentation, lethargy, seizures, coma, and
muscle weakness. Polyuria suggests the presence of diabetes insipidus or excess salt
and water intake.
Treatment focuses on correcting the underlying cause of hypernatremia. Nearly all
patients with hypernatremia require free-water repletion. The water deficit can be
estimated by using the following equation:
Water Deficit (L) = 0.6 (0.5 for women) × weight (kg) [(measured Na/normal Na) – 1]
Example: Water deficit of a 70-kg man with sodium measurement of 160 mmol/L
0.6 × 70 [(160/140) – 1]
42 [1.14 – 1]
42 × 0.14 = 5.88 L water deficit
A portion of free water should be replaced initially at a speed commensurate with the
severity of symptoms, and the patient should be reevaluated for subsequent replacement.
Regardless of the serum sodium level, if the patient shows signs of hypovolemic shock
(eg, hypotensive, orthostatic, or significantly tachycardic), administer normal saline
until the intravascular volume is corrected. When the patient is hemodynamically stable,
replete the remaining water deficit with 5% dextrose in water, 0.45% NaCl, or 0.2%
NaCl with 5% dextrose. To estimate the change in serum sodium expected after
administering 1 liter of fluid, use the same formulas as for hyponatremia:
Change in Serum Sodium = Infusate Sodium – Serum Sodium
Change in Serum Sodium = (Infusate Sodium + Infusate Potassium) – Serum Sodium

In stable patients, water may be replaced via the enteral route (ie, nasogastric tube). In
the rare patient with extreme sodium overload, sodium may be removed with loop
diuretics or dialysis (provided intravascular volume is adequate). Administration of
aqueous vasopressin or desmopressin should be considered for patients with central
diabetes insipidus.
Rapid correction of serum sodium can

result in cerebral edema and neurologic
injury.
Sodium concentrations should be measured frequently during treatment, and therapy
should be adjusted for optimal correction of the sodium level. If hypernatremia
developed over a period of hours, reducing the serum sodium by 1 mmol/L/h is
appropriate. In hypernatremia of longer or unknown duration, a slower rate of
correction (0.5 mmol/L/h) is recommended. Increasing free-water intake in maintenance
fluids allows for a slow return to normal sodium levels.
C. OTHER ELECTROLYTE ABNORMALITIES
1. Calcium
Calcium is required for muscle contraction, nerve impulse transmission, hormone
secretion, blood clotting, cell division, cell motility, and wound healing. Effective
calcium levels in a seriously ill patient are best assessed by using ionized calcium
measurements, if available. If treatment decisions are based on total serum calcium, the
albumin concentration must be considered as 40% of circulating calcium is protein
bound, mainly to albumin. In general, for each increase or decrease in serum albumin of
1 g/dL, the serum calcium increases or decreases by 0.8 mg/dL (0.2 mmol/L). However,
the relationship between albumin and serum calcium is less reliable in critically ill
patients.
a. Hypocalcemia
Hypocalcemia (total calcium <8.5 mg/dL [<2.12 mmol/L], ionized calcium <1 mmol/L)
is common in critically ill patients and results from impairment of the parathyroid
and/or vitamin D systems (Table 12-6). Cardiovascular abnormalities, the most
common clinical manifestations of hypocalcemia in critically ill patients, include
hypotension, bradycardia, arrhythmias, heart failure, cardiac arrest, digitalis
insensitivity, and QT-interval and ST-segment prolongation. Neuromuscular
manifestations include weakness, muscle spasm, laryngospasm, hyperreflexia, seizures,
tetany, and paresthesias.
Table 12-6 Causes of Hypocalcemia
Hypoparathyroidism Pancreatitis Calcium chelators

Sepsis Malabsorption Hypomagnesemia
Burns Liver disease Massive transfusion
Rhabdomyolysis Renal disease
Treatment is aimed at correcting the underlying disease process and any concomitant
electrolyte abnormalities, and administering calcium. Mild hypocalcemia is well
tolerated, and aggressive treatment may result in tissue injury (especially during
ischemic and septic states). If the hypocalcemia is severe or if the patient is
symptomatic, administer 100 mg calcium intravenously over 5 to 10 minutes (3-4 mL of
10% calcium chloride or 10 mL of 10% calcium gluconate), followed by calcium in the
amount of 0.3 to 2 mg/kg/h. Calcium preparations vary in their content of elemental
calcium: 1 g of 10% calcium chloride contained in 10 mL has 272 mg of calcium; 1 g of
10% calcium gluconate contained in 10 mL has 90 mg of calcium. When the circulating
calcium concentration is stable, calcium may be replaced via the enteral route (ie, 500-
1,000 mg every 6 hours).
Monitor ionized or total calcium levels frequently during treatment, and adjust repletion
to maintain calcium in the lower normal range so as not to suppress parathyroid gland
function. If calcium replacement alone fails to maintain the circulating calcium level,
consider administration of vitamin D and confirm normal magnesium levels. Adverse
effects of calcium administration include hypercalcemia, bradycardia, nausea/vomiting,
flushing, and tissue calcium precipitation.
b. Hypercalcemia
The most common causes of hypercalcemia (total calcium >11 mg/dL [>2.75 mmol/L],
ionized calcium >1.3 mmol/L) are the result of calcium release from bone (Table 12-7).
The clinical manifestations of hypercalcemia relate primarily to the cardiovascular and
neuromuscular systems and include hypertension, cardiac ischemia, arrhythmias,
bradycardia, conduction abnormalities, digitalis toxicity, dehydration, hypotension,
weakness, depressed mentation, coma, seizures, and sudden death. Gastrointestinal
manifestations include nausea/vomiting, anorexia, abdominal pain, constipation,
pancreatitis, and ulcer disease. Nephrogenic diabetes insipidus with polyuria may occur
and contribute to volume depletion. Renal stones, nephrocalcinosis, and renal failure
may also be encountered.
Table 12-7 Causes of Hypercalcemia
Hyperparathyroidism Excess intake of vitamin A or vitamin D

Malignancy Thyrotoxicosis
Immobilization Granulomatous disease
Treatment of hypercalcemia is aimed at controlling the underlying disease, rehydrating

the patient, and lowering the calcium level. The circulating calcium level frequently
needs to be lowered while the primary disease is being evaluated and treated.
Intravascular volume should be restored with normal saline to ensure adequate tissue
perfusion and renal blood flow (urine output 2-3 mL/kg/h). Saline also decreases renal
tubular calcium reabsorption. Once adequate volume status is secured, diuresis with a
loop diuretic further increases calcium excretion. Serum potassium and magnesium
levels should be monitored and low levels corrected. In patients with renal failure,
pulmonary edema, or life-threatening hypercalcemia, calcium levels may be lowered
with dialysis. After initial stabilization, therapy with calcitonin and bisphosphonates
can be considered.
2. Phosphorus
Phosphate is important in cellular energy metabolism. Hypophosphatemia (phosphate
<2.5 mg/dL [0.81 mmol/L]) results from transcellular shifts, renal loss, gastrointestinal
loss, or inadequate intake (Table 12-8). Phosphate depletion primarily affects the
neuromuscular and central nervous systems. Clinical manifestations include muscle
weakness, respiratory failure, rhabdomyolysis, paresthesias, lethargy, disorientation,
obtundation, coma, and seizures. Other possible complications include impaired renal
tubular function, impaired pressor response, hepatic dysfunction, immune dysfunction,
impaired protein synthesis, hemolysis, impaired platelet function, and impaired oxygen
off-loading from hemoglobin.
Table 12-8 Causes of Hypophosphatemia
Transcellular Shift Renal Loss Gastrointestinal Loss Decreased Intake

Acute alkalosis Hyperparathyroidism Malabsorption Malnutrition
Carbohydrate administration Diuretic use Diarrhea Parenteral nutrition
Drugs (insulin, epinephrine) Hypokalemia Intestinal fistulas
Hypomagnesemia Antacids
Steroids
Treatment of hypophosphatemia consists of controlling the underlying disease, removing

offending drugs, correcting electrolyte abnormalities, and replacing phosphate.
Phosphate levels <1 mg/dL (<0.32 mmol/L) associated with symptoms are considered
life-threatening and require immediate treatment. For emergency treatment, administer
phosphate at 0.6 to 0.9 mg/kg daily intravenously. When circulating levels are stable,
maintenance replacement of phosphate is 1,000 mg/day intravenously plus excess
estimated losses (ie, in urine or stool). Phosphate may be administered as potassium
phosphate (93 mg/mL phosphate, 1.1 mmol/mL potassium) or sodium phosphate (93
mg/mL). Enteral administration of phosphate is preferred in patients with serum
phosphate levels >1.0 to 1.5 mg/dL (>0.32-0.48 mmol/L).
Serum phosphate should be monitored during repletion and therapy adjusted to achieve
a circulating level of 3 to 4 mg/dL (0.97-1.29 mmol/L). Adverse effects of phosphate
administration include hyperphosphatemia, hypocalcemia, tissue calcium precipitation,
renal injury, and diarrhea (enteral phosphate).
Hyperphosphatemia is uncommon in critical illness except with renal failure. Increased
bone metabolism secondary to tumors or increased gut absorption also may cause
hyperphosphatemia. Symptoms are similar to those of hypocalcemia: ventricular
arrhythmias, prolonged QT interval, seizures, paresthesias, and muscle cramps.
Hyperphosphatemia is treated with intravenous calcium and enteral phosphorus binders.
Dialysis may be initiated with renal failure.
3. Magnesium
Magnesium is important to the body for energy transfer and electrical stability. Causes
of hypomagnesemia (magnesium <1.8 mg/dL or 1.5 mEq/dL [<0.75 mmol/L]) are listed
in Table 12-9.
Table 12-9 Causes of Hypomagnesemia
Renal Loss Gastrointestinal Transcellular Decreased

Loss Shift Intake
Renal tubular dysfunction Malabsorption Refeeding Malnutrition
Diuresis Diarrhea Recovery from Alcoholism
Hypokalemia Nasogastric suction hypothermia Parenteral
nutrition
Drugs (eg, aminoglycosides,
amphotericin)
Clinical manifestations of hypomagnesemia overlap those of hypokalemia and

hypocalcemia, including cardiovascular abnormalities (ie, QT-interval prolongation,
arrhythmias, vasospasm, myocardial ischemia), neuromuscular abnormalities (eg,
weakness, tremor, seizures, tetany, obtundation, coma), and electrolyte abnormalities
(eg, hypokalemia, hypocalcemia).
Treatment of hypomagnesemia consists of addressing the underlying disease,
discontinuing problematic drugs, correcting concomitant electrolyte abnormalities, and
replenishing magnesium. For emergency treatment (ie, arrhythmias), administer 1 to 2 g
magnesium sulfate intravenously over 5 to 10 minutes. The agent can be administered
over a longer interval (10-60 minutes) in less-urgent situations. Depending on the
clinical situation, subsequent intravenous replacement ranges from 1 to 2 g magnesium
sulfate every 4 to 6 hours. Once serum levels stabilize, intravenous maintenance doses
are 0.1 to 0.2 mmol/kg daily (1 g magnesium sulfate = 8 mmol). Maintenance
magnesium may be administered enterally. The dose should be reduced if renal failure
is present. Magnesium levels should be monitored during repletion. Deep tendon
reflexes can be used to assess for hypermagnesemia during replacement (ie, decreased
at serum level 4-5 mg/dL [1.65-2.06 mmol/L]).
Hypermagnesemia is uncommon in critical illness but may be seen with renal failure or
shifts in magnesium from intracellular fluid due to soft tissue injury as with crush, burn
trauma, and rhabdomyolysis. Hyporeflexia, lethargy, and apnea may result. Treatment
consists of administration of intravenous calcium, diuretic administration, and dialysis
in severe cases.
III. METABOLIC DISTURBANCES
Case Study
A 21-year-old man presented to the emergency department with nonspecific complaints

of a flu-like syndrome. He has a history of HIV but has not been taking his medications.
His vital signs include respiratory rate 24 breaths/min, heart rate 132 beats/min, blood
pressure 86/45 mm Hg, and temperature 39°C (102.2°F). His laboratory results are
remarkable for a white blood cell count 3,400/mm3. Blood cultures are obtained, and
patient received broad-spectrum antibiotics as well as a 30 mL/kg intravenous fluid
bolus. Due to persistent hypotension, he is started on 10 μg/min of norepinephrine, yet
remains hypotensive.
– What metabolic disorders may contribute to the refractory hypotension?
– What testing is needed?
– What interventions should be considered?
A. Acute Adrenal Insufficiency

Acute adrenal insufficiency in the critically ill patient may result from preexisting or
previously undiagnosed chronic disease of the adrenal glands or hypothalamic-pituitary
axis, or acute conditions affecting these endocrine organs (Table 12-10). Patients with
chronic disease may develop acute adrenal insufficiency precipitated by infection or
other stressors. In addition, functional impairment during serious illness may result from
relative or absolute insufficiency of glucocorticoid production, which usually reverses
with recovery from the illness. Relative adrenal insufficiency occurs when cortisol
response is normal or high, but is reduced relative to the severity of illness.
Table 12-10 Etiologies of Adrenal Insufficiency
Chronic Conditions
Adrenal glands
Autoimmune destruction
Granulomatous disease (tuberculosis)
HIV infection
Other infection (cytomegalovirus, fungal)
Primary or metastatic malignancy
Drug effects (ie, ketoconazole)
Hypothalamic/pituitary axis
Withdrawal from exogenous glucocorticoid therapy
Hypopituitarism (tumors, infarction, radiation)
Sarcoidosis, histiocytosis
Head trauma
Acute Conditions
Critical illness (affects adrenal glands and hypothalamic-pituitary axis)
Hypoperfusion
Cytokine effects (altered cortisol metabolism, receptor affinity)
Acute adrenal hemorrhage
Meningococcemia
Disseminated intravascular coagulation
Anticoagulation (eg, warfarin, heparin)
Drug effects
Increased cortisol metabolism (phenytoin, phenobarbital, rifampin)
Interference with glucocorticoid synthesis (ketoconazole, etomidate)
Lack of specific signs and symptoms of acute adrenal insufficiency makes for a
challenging early diagnosis in the critically ill population. Clinical manifestations
consistent with acute adrenal insufficiency include weakness, nausea and vomiting,
abdominal pain, tachycardia, and orthostatic hypotension. A diagnostic clue is
hypotension refractory to volume resuscitation. Suggestive laboratory findings may
include eosinophilia, hyponatremia, hyperkalemia, acidosis, and hypoglycemia. Acute
adrenal hemorrhage may cause abdominal, flank, or back pain. Clinical and laboratory
manifestations overlap significantly with manifestations of other common critical
illnesses, such as sepsis.
Electrolyte abnormalities are less likely
with acute adrenal insufficiency
compared to chronic adrenal
insufficiency.
Important clues for possible adrenal insufficiency in seriously ill patients are
vasopressor-dependent states and/or failure to respond to appropriate fluid
administration, fever without apparent source, and a discrepancy between the expected
disease severity and the patient’s condition.
The value of standard tests for hypothalamic-pituitary-adrenal axis function using
baseline cortisol levels and/or the short adrenocorticotropic hormone (ACTH)
stimulation test is limited in the critically ill patient due to variation in testing
methodology and lack of consensus criteria for absolute or relative adrenal
insufficiency. Cortisol levels generally reflect total cortisol rather than metabolically
active free cortisol. Thus, the decision to provide steroid therapy is made on clinical
grounds. Current recommendations call for administration of 200 mg of hydrocortisone
per day, in a continuous infusion or divided boluses for vasopressor-resistant septic
shock. Improvement in hemodynamic status after administration of hydrocortisone may
be an important physiologic indicator. Emergent treatment is indicated in critically ill
patients, even if the diagnosis is not firmly established. Note that high-dose steroid
therapy, previously employed in trials of shock management, has been deemphasized.
Hydrocortisone also provides some

mineralo-corticoid effects.
If a clinical response to glucocorticoid (hydrocortisone) administration is observed and

relative adrenal insufficiency is suspected, treatment should be continued until
resolution of the critical illness. Steroids should be tapered when vasopressors are no
longer required. Patients with evidence of persistent adrenal insufficiency (chronic or
newly diagnosed) should be converted to oral steroid therapy. There is a limited role, if
any, for steroid therapy in shock states other than anaphylaxis.
B. Hyperglycemic Syndromes
1. Diabetic Emergencies
Serious metabolic complications of diabetes result from a relative or absolute lack of
insulin coupled with increased production of counter-regulatory hormones such as
glucagon, catecholamines, cortisol, epinephrine, and others. Life-threatening
hyperglycemic syndromes include diabetic ketoacidosis (DKA) and hyperglycemic
hyperosmolar state (HHS). These syndromes differ in the severity of dehydration and
degree of acidosis (ketosis) but share many clinical manifestations and therapeutic
interventions. In addition, patients may manifest components of both syndromes. Table
12-11 lists characteristics that may distinguish the syndromes, but considerable
variability is possible. Although DKA and HHS may be the initial presentation of
diabetes, the most common precipitating factors are infection and medication
noncompliance. Other precipitants include corticosteroid use, myocardial infarction,
stroke, alcohol abuse, pancreatitis, trauma, and pregnancy.
HHS develops over days to weeks and

results in greater dehydration than does
DKA, which usually evolves in <24
hours.
Table 12-11 Characteristics of Hyperglycemic Syndromes
Diabetic Ketoacidosis Hyperglycemic Hyperosmolar State

Glucose >250 mg/dL >600 mg/dL
Arterial/venous pH <7.3 >7.3
Anion gap Increased Variable
Serum/urine ketones Positive Negative or small
Serum osmolality Normal Increased
Clinical manifestations result from hyperglycemia in both syndromes and from excess
ketone production in DKA. Hyperglycemia causes hyperosmolality, osmotic diuresis,
fluid and electrolyte loss, dehydration, and volume depletion. Ketones, specifically
beta-hydroxybutyrate and acetate, are responsible for the metabolic acidosis and can be
measured indirectly by the anion gap. Clinical features of both hyperglycemic
syndromes may include weakness, dehydration, polyuria, polydipsia, tachycardia,
hypotension, anorexia, nausea/vomiting, and ileus. Abdominal pain, hyperpnea
(Kussmaul respirations), and fruity odor to the breath are more characteristic of DKA,
whereas altered mental status (ranging from lethargy to coma) and dysrhythmias are
more common in HHS. Laboratory investigation may reveal hyperglycemia,
hyperosmolality (more common in HHS), glucosuria, anion gap metabolic acidosis
(DKA), hyperkalemia (when acidemia is present) or hypokalemia and
hypophosphatemia (after insulin therapy is initiated), lactic acidosis, leukocytosis, and
azotemia. Serum sodium concentrations may be low due to translocation of water to the
extracellular space. An elevated serum sodium concentration suggests severe
dehydration.
The corrected serum sodium

concentration [measured sodium + (1.6
× x glucose/100)] should be used to
assess the severity of dehydration.
An initial rapid evaluation of the patient with a possible hyperglycemic condition

should include assessment of mental status, degree of dehydration (vital signs,
orthostatic changes, urine output), and presence of infection. Laboratory studies should
include complete blood count, electrolytes, renal function, glucose (plasma or
fingerstick), urine or serum ketones, and arterial blood gas (venous pH can be used as a
substitute). An electrocardiogram should be obtained to evaluate for ischemia and
changes due to electrolyte abnormalities. If infection is suspected, appropriate cultures
are indicated.
The goals for treatment of hyperglycemic syndromes are to restore the fluid and
electrolyte balance, provide insulin, and identify precipitating factors. The initial
management of DKA and HHS is outlined in Table 12-12. Volume deficits correlate
with the severity of hyperglycemia and are usually greater in HHS. Urine output should
be maintained at 1 to 3 mL/kg/h to ensure adequate tissue perfusion and clearance of
glucose.
Table 12-12 Initial Management of Hyperglycemic Syndromes

Fluids
1. Assess severity of dehydration.

2. Institute crystalloid resuscitation, initially with normal saline at approximately 15-20 mL/kg/h in the
first hour in the absence of cardiac dysfunction to restore hemodynamic stability and renal
perfusion. Subsequent fluid infusion rates should be guided by assessment of hydration and urine
output, and 250-500 mL/h is often adequate.
3. After stabilization of the hemodynamic status, fluids with less chloride (eg, 0.45% saline) should be
considered to avoid or minimize the development of hyperchloremic metabolic acidosis. The
corrected serum sodium should also be used to guide fluid selection.
4. Add glucose to fluids when glucose is 250-300 mg/dL (13.9-16.7 mmol/L) in DKA. Administer 10%
dextrose if necessary to maintain glucose >150 mg/dL (>8.3 mmol/L). In HHS, add glucose to fluids
when glucose is 300 mg/dL (16.7 mmol/L) to maintain the glucose concentration between 250-300
mg/dL (13.9-16.7 mmol/L).
Insulin
1. Administer a regular insulin loading dose as an intravenous bolus (0.1-0.15 units/kg), followed by an
infusion at 0.1 units/kg/h. If potassium concentration is <3.3 mmol/L, hold insulin until potassium is
replaced.
2. If the glucose concentration does not fall by 50 mg/dL (2.8 mmol/L) in the first hour, consider
increasing the insulin infusion rate or administering additional insulin boluses (10 units regular
insulin hourly). Lack of response may also be due to inadequate volume resuscitation or serious
infection.
3. In DKA, continue insulin infusion or decrease by 50% when the glucose reaches 250 mg/dL (13.9
mmol/L). Maintain the glucose concentration between 150 and 200 mg/dL (8.3 and 11.1 mmol/L)
until acidosis and ketosis are resolved.
4. In HHS, decrease insulin infusion when the glucose concentration reaches 300 mg/dL (16.7
mmol/L) to maintain the glucose at 250-300 mg/dL (13.9-16.7 mmol/L) until the plasma osmolality is
≤315 mOsm/kg and the patient is alert.
Electrolytes
1. If serum potassium is <3.3 mmol/L, hold insulin and administer potassium, 40 mmol/h as
potassium chloride or potassium phosphate (or combination), until potassium is >3.3 mmol/L to
avoid arrhythmias or severe weakness.
2. If serum potassium is >3.3 mmol/L but <5 mmol/L and urine output is adequate, administer
potassium, 20-30 mmol, in each liter of fluids to maintain the potassium at 4-5 mmol/L.
3. If serum potassium is >5 mmol/L, do not administer potassium in fluids until <5 mmol/L.
4. Consider phosphate replacement with potassium phosphate if serum levels are low (<1 mg/dL,
0.32 mmol/L) or severe symptoms are present.
Abbreviations: DKA, diabetic ketoacidosis; HHS, hyperglycemic hyperosmolar state
The intravenous route for insulin administration is the most reliable and easiest to
titrate. Because of the short half-life of intravenous insulin, a continuous infusion is
necessary with serial monitoring of the glucose and electrolyte concentrations. Smaller
doses of insulin may be adequate in HHS. In the case of DKA, insulin infusion should
be continued until the removal of beta-hydroxybutyrate and acetone, as measured by
normalization of the anion gap. Normalization of the anion gap usually occurs many
hours after normalization of the serum glucose levels.
Glucose concentrations should be

monitored every 1-2 hours.
Glucose-containing fluids may be started earlier than recommended if blood glucose

cannot be monitored frequently. When glucose and/or serum osmolality are controlled,
acidosis has cleared, and the patient is stable, subcutaneous insulin may be
administered; an insulin sliding scale of regular and longer-acting preparations can be
started and should overlap for 1 to 2 hours with discontinuation of the insulin infusion.
Be aware that bicarbonate therapy in

addition to insulin will lower the serum
potassium concentration.
Insulin and correction of acidosis shifts potassium intracellularly and may lead to
precipitous drops in serum potassium levels. Oral potassium replacement can be
considered if nausea and vomiting are not present. Potassium and other electrolyte
levels should be monitored frequently (especially in the first 6 hours) until levels
stabilize and acidosis is resolved.
Acidosis is well tolerated by patients with DKA, and bicarbonate therapy is
controversial. No benefit has been found when bicarbonate is administered to DKA
patients with pH of 6.9 to 7.1, and fluid and insulin therapy results in rapid
improvement in pH. Bicarbonate administration may be considered if the arterial pH is
<6.9 (give 100 mmol bicarbonate over 1 hour to increase pH >7). Do not attempt to
normalize blood pH with bicarbonate, because acidosis resolves as ketones are
metabolized.
2. Hyperglycemia in Critical Illness

Hyperglycemia is common in diabetic and nondiabetic patients with critical illness and
may be due to stress hormones, inflammatory mediators, glucocorticoid therapy,
excessive nutritional calories, decreased activity, and other mechanisms. Significant
hyperglycemia is associated with poor wound healing, impaired immune function,
increased inflammation, endothelial dysfunction, and other adverse effects leading to
increased illness and death. Early studies of tight glucose control (80-110 mg/dL, 4.4-
6.1 mmol/L) suggested benefit in a surgical population, but this target has been difficult
to achieve in subsequent studies without increasing the risk for severe hypoglycemia. In
addition, in multiple subsequent trials, no consistent reduction in mortality was
observed with intensive control of glucose levels. Some recent studies of tight glycemic
control have actually demonstrated increased mortality associated with higher rates of
hypoglycemia.
In critically ill patients, insulin therapy should be initiated for persistent hyperglycemia.
Once it has been initiated, a glucose of less than 180 mg/dL (7.8-10 mmol/L) with the
avoidance of hypoglycemia is recommended. Intravenous insulin infusions are the
preferred method to achieve and maintain control. During intravenous insulin therapy,
frequent monitoring of blood glucose is essential to minimize the risk of hypoglycemia
and achieve optimal control.
The ability to provide adequate nursing support and monitoring may affect the blood
glucose goals chosen. Different types of blood sampling and glucose measurement
methods may also yield different results. The institution’s protocol for blood sampling,
insulin infusion, and glucose management targets should be followed to achieve
consistency and minimize the risk of hypoglycemia.
Patients with renal dysfunction require

lower rates of insulin infusions.
Key Points
Management of Life-Threatening Electrolyte and Metabolic

Disturbances
In the presence of life-threatening dysrhythmias or paralysis associated with
hypokalemia, give potassium chloride, 20 mmol/h, through a central venous
catheter.
If hyperkalemia-associated ECG abnormalities are present, administer calcium
chloride or calcium gluconate intravenously over 5 to 10 minutes, then consider
shifting potassium intracellularly with 50% dextrose and regular insulin
intravenously, inhaled β-agonists, and/or sodium bicarbonate.
In symptomatic euvolemic hyponatremia, limit the increase in serum sodium to 6 to
8 mmol/L in the first 24 hours. Too-rapid correction of serum sodium may result in
CNS injury.
Patients with hypernatremia and hemodynamic instability should have normal
saline administered until intravascular volume is corrected. Subsequently, replace
water with 5% dextrose in water, 0.45% NaCl, or 0.2% NaCl with 5% dextrose.
Enteral replacement with water is an effective strategy in stable patients.
Emergent treatment with a glucocorticoid is indicated in critically ill patients with
vasopressor-resistant shock, even if the diagnosis is not established.
The goals of treatment in hyperglycemic syndromes are to restore the fluid and
electrolyte balance, provide insulin, and identify precipitating factors.
In diabetic ketoacidosis, insulin infusion should be continued until the ketosis and
acidosis have resolved. Glucose-containing fluids should be administered to
prevent hypoglycemia during insulin infusion.
Maintain the glucose between 250 and 300 mg/dL (13.9-16.7 mmol/L) in
hyperglycemic hyperosmolar syndrome until the plasma osmolality is <315
mOsm/kg and the patient is alert.
Potassium should be added to the fluid therapy for hyperglycemic syndromes as
soon as serum potassium is recognized to be <5 mmol/L and urine output is
adequate.
A protocol of blood sampling, insulin infusion, and target glucose levels should be
followed to avoid hyperglycemia and minimize hypoglycemia in critically ill
patients.
Suggested Readings
1. Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342:1493-1499.

2. Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342:1581-1599.
3. Berl T. Vasopressin antagonists. N Engl J Med. 2015;372:2207-2216.
4. Brown GR, Greenwood JK. Drug- and nutrition-induced hypophosphatemia:
mechanisms and relevance in the critically ill. Ann Pharmacother. 1994;28:626-
632.
5. Charron T, Bernard F, Skrobik Y, et al. Intravenous phosphate in the intensive care
unit: more aggressive repletion regimens for moderate and severe
hypophosphatemia. Intensive Care Med. 2003;29:1273-1278.
6. Gennari FJ. Disorders of potassium homeostasis: hypokalemia and hyperkalemia.
Crit Care Clin. 2002;18:273-288.
7. Kamel KS, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol
Dial Transplant. 2003;18:2215-2218.
8. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes.
Diabetes Care. 2004;27(suppl 1):S94-S102.
9. Marik PE. Critical illness-related corticosteroid insufficiency. Chest.
2009;135:181-193.
10. Marik PE, Pastores SM, Annane D, et al. Recommendations for the diagnosis and
management of corticosteroid insufficiency in critically ill adult patients.
Consensus statements from an international task force by the American College of
Critical Care Medicine. Crit Care Med. 2008;36:1937-1949.
11. Moghissi ES, Korytkowski MT, DiNardo M, et al. American Association of
Clinical Endocrinologists and American Diabetes Association consensus statement
on inpatient glycemic control. Diabetes Care. 2009;32:1119-1131.
12. Noronha JL, Matuschak GM. Magnesium in critical illness: metabolism,
assessment, and treatment. Intensive Care Med. 2002;28:667-679.
13. Tzamaloukas AH, Malhotra D, Rosen BH, et al. Principles of management of
severe hyponatremia. J Am Heart Assoc. 2013 23;2(1):e005199. Available at:
http://jaha.ahajournals.org/content/2/1/e005199.long. Accessed October 5, 2015.
14. Verbalis JG, Goldsmith SR, Greenberg A, et al. Hyponatremia treatment guidelines
2007: Expert panel recommendations. Am J Med. 2007;120:S1-S21.
Suggested Website
1. Society Critical Care Medicine. http://www.SCCM.org/Guidelines

Chapter 13
SPECIAL CONSIDERATIONS
Objectives
Outline the diagnosis and management of pulmonary embolism.

Describe appropriate prophylactic therapy for venous thromboembolism.
List general management principles of severe gastrointestinal hemorrhage.
Describe appropriate prophylactic therapy for the prevention of stress-related
gastritis.
Summarize the principles of poisoning management.
Review the management of hypertensive crises.
Outline the diagnosis and management of intra-abdominal hypertension and
abdominal compartment syndrome.
Case Study
An obese woman (body mass index of 40) with chronic tobacco abuse and congestive
heart failure arrives at the emergency department complaining of shortness of breath and
right pleuritic chest pain for the past 2 days. She has a heart rate of 110 beats/min with
clear lung fields and mild bilateral pretibial edema. When she arrived, her oxygen
saturation on pulse oximetry (SpO2) with room air was 89%; that has increased to 94%
on oxygen, 3 L/min by nasal cannula. A chest radiograph did not show any infiltrates.
You are called for assistance in her management.
– What is the differential diagnosis based on the patient’s risk factors and clinical
findings?
– What tests are indicated?
I. INTRODUCTION
In addition to the medical conditions discussed in previous chapters, the clinician may
be called on to care for patients with other severe and/or life-threatening problems. The
management and prevention of some of these commonly encountered conditions are
reviewed in this chapter.
II. PULMONARY EMBOLISM
A. Diagnosis
A patient’s history and clinical findings may be unreliable for diagnosis of a pulmonary
embolism (PE). Risk factors for PE and other venous thromboembolic diseases (Table
13-1) often contribute to a high index of suspicion. Predisposing factors include any
condition that may cause venous stasis, injury to the vascular endothelium, or
hypercoagulability (Virchow triad).
Table 13-1 Risk Factors for Pulmonary Embolism/Venous Thromboebolism
Family history Central venous catheterization

Advanced age Recent surgery
Obesity (body mass index >30) Immobility, paralysis
Prior history of deep vein thrombosis/pulmonary embolism Stroke with partial or full paralysis
Venous insufficiency Trauma
Venous injury or repair Malignancy (past or current)
Inherited hypercoagulable disorders Cancer therapy
(protein C or S deficiency, lupus anticoagulant, etc) Selective estrogen receptor modulators
Acute medical illness, ICU admission Pregnancy and postpartum period
Heart or respiratory failure Estrogen therapy
Nephrotic syndrome Smoking
The classic combination of dyspnea, pleuritic chest pain, and hemoptysis occurs in a
minority of patients with PE. Routine blood studies are not diagnostic. Chest
radiographs are frequently unremarkable but may show nonspecific findings of
atelectasis, pleural effusion, elevated hemidiaphragm, and/or infiltrates. Chest
radiographs may be useful in ruling out other life-threatening problems, such as
pneumothorax. The electrocardiogram (ECG) may show nonspecific ST-T wave
changes, QR pattern in lead V1, an S1Q3T3 pattern, or right bundle-branch block, but a
pattern of acute cor pulmonale is generally not present.
An arterial blood gas measurement may

be considered if the oxyhemoglobin
saturation measurement is unreliable or
an assessment of ventilation is needed.
Sinus tachycardia and premature atrial contractions are the most frequently encountered
dysrhythmias. Often the most relevant information provided by the ECG is the exclusion
of other potential sources of chest pain, such as acute ischemia or pericarditis.
Hypoxemia, a nonspecific finding in cardiopulmonary disease, is commonly present, but
a normal PaO2 value or normal alveolar-arterial oxygen partial pressure difference [P(A
– a)O2] does not rule out PE. Signs and symptoms of PE are shown in Table 13-2.
Table 13-2 Clinical Manifestations of Pulmonary Embolism
Dyspnea Fever (usually low-grade)

Chest pain Hypoxemia
Cough Cyanosis
Tachypnea Apprehension
Tachycardia Syncope
Diaphoresis Previously noted leg swelling
Hemoptysis
A correct diagnosis of PE is essential because early initiation of appropriate therapy

decreases mortality. The current diagnostic strategy recommends that the clinician
formulate a clinical likelihood of low, moderate, or high clinical suspicion of PE
(Figure 13-1). One scoring system used to determine pretest probability is presented in
Table 13-3. D-dimer assays with high sensitivity and high negative predictive value are
frequently used as an initial step in algorithms for the diagnosis of PE in outpatients. A
negative D-dimer result in a patient with low clinical probability of PE may reliably
exclude the diagnosis. Patients with a positive D-dimer result or with a moderate or
high clinical probability assessment require further diagnostic evaluation. D-dimer
measurements have limited utility for the evaluation of PE in hospitalized, critically ill,
injured, and postoperative patients because of the high proportion of positive results.
Figure 13-1. A Diagnostic Approach to Pulmonary Embolism
aConsider pulmonary angiogram if clinical suspicion is high; negative predictive value is increased by a
negative lower extremity study
Abbreviations: PE, pulmonary embolism; CT, computed tomography; V̇/Q̇, ventilation/perfusion
Table 13-3 Clinical Probability Assessment for Pulmonary Embolism

Clinical signs and symptoms of DVT (objective new onset, leg swelling with palpation) 3
PE as likely, or more likely, than an alternative diagnosis 3
Immobilization (bed rest, except to access bathroom, for ≥3 consecutive days or surgery in the 1.5
previous 4 weeks)
Previous objective diagnosis of DVT or PE 1.5
Heart rate >100 beats/min 1.5
Hemoptysis 1
Active cancer (treatment ongoing or within previous 6 months or palliative treatment) 1
0-1: Low probability
2-6: Moderate probability
≥7: High probability
Abbreviations: PE, pulmonary embolism; DVT, deep venous thrombosis
Multidetector computed tomography angiography demonstrating thrombus up to the

segmental-level pulmonary arteries is diagnostic for PE, whereas a negative scan can be
safely used to exclude it. In patients with an allergy to contrast, venous lower limbs
Doppler scanning can be used to aid in the diagnosis of thromboembolism, and further
diagnostic testing is not needed as therapy is similar to that for PE. A negative Doppler
exam does not rule out deep venous thrombosis (DVT) since the majority of PEs
originate from the iliac veins. A ventilation/perfusion (V̇ /Q̇) scan can be used to aid in
the diagnosis in patients who can’t receive intravenous contrast. A normal V̇ /Q̇ scan
can exclude PE. Similarly, a high probability V̇ /Q̇ scan establishes the diagnosis of PE.
In all other combinations of V̇ /Q̇ scan and clinical suspicion, further tests are
performed. Bedside echocardiography can be used to infer the diagnosis but is only
diagnostic if it shows new-onset right ventricular dilatation or strain. A normal
echocardiogram does not rule out PE.
B. Therapy
The treatment of PE can usually be limited to anticoagulation, starting with initial
administration of a parenteral agent (low-molecular-weight heparin [LMWH],
unfractionated heparin, fondaparinux). LMWH and fondaparinux can be effective in
treating PE and are preferred over unfractionated heparin due to convenient dosing,
absence of need for laboratory monitoring, and low incidence of heparin-induced
thrombocytopenia. Both agents are dosed based on weight and require dosage
adjustment with renal impairment. Unfractionated heparin is preferred in patients with
severe renal dysfunction, those at high risk of bleeding, and when thrombolytic therapy
is being considered. In patients with suspected PE and no contraindications to
anticoagulation, baseline-activated partial thromboplastin time, prothrombin time, and
complete blood cell count should be obtained, and heparin or fondaparinux therapy
should be initiated while waiting for test results unless there is a high risk of bleeding.
Contraindications to heparin therapy include recent major trauma with hemorrhage,
recent central nervous system hemorrhage or infarction, active gastrointestinal (GI)
bleeding, and heparin-induced thrombocytopenia. When unfractionated heparin is used,
the activated partial thromboplastin time should be monitored to achieve a value 1.5 to
2.5 times the mean normal value.
Oral warfarin therapy is started on day 1 and adjusted to achieve an international
normalized ratio of 2 to 3. Heparin or fondaparinux therapy can be discontinued after 5
days if the international normalized ratio is 2 or above for at least 24 hours with
warfarin. Oral anticoagulation should continue for at least 3 months, but some patients
(those with unprovoked first PE/DVT or recurrent unprovoked PE/DVT) may have
indications for longer therapy unless there is a high risk of bleeding. For patients with
underlying malignancy, extended therapy with LMWH is suggested over warfarin, but
the choice of agent may be influenced by costs, tolerance of injections, and need for
monitoring. In patients who receive long-term anticoagulant treatment, the risk/benefit
ratio of continuing such treatment should be reassessed at regular intervals.
In the last decade, new options for anticoagulation have become available in the form of
direct oral anticoagulation (DOAC), providing a greater number of agents for the
prevention and treatment of thromboembolic disease. These anticoagulants can directly
target the enzymatic activity of thrombin and factor Xa. The direct thrombin inhibitors
prevent thrombin from breaking the fibrinogen into fibrin; they bind directly to thrombin.
Examples are bilavirudin, argatroban, and dabigatran (oral agent). The direct factor Xa
inhibitors prevent factor Xa from breaking prothrombin into thrombin; they bind directly
to factor Xa. Examples are rivaroxaban and apixaban
The overall mortality from DOAC appears to be lower than that from warfarin,
primarily because of a decrease in intracranial bleeding. DOAC is generally used
without a requirement for monitoring of drug levels or coagulation (clotting) times. This
can be an advantage for patients for whom frequent monitoring is required. Whether
laboratory monitoring of any of the DOAC agents can further improve their efficacy or
safety remains to be seen. The reversal of the anticoagulation effect of DOAC is more
difficult than with heparin and warfarin.
Systemic thrombolysis for PE may improve pulmonary arterial hemodynamics, lung
perfusion, and right ventricular function, but the quality of evidence suggesting
improved mortality is low. The use of thrombolytic agents in the treatment of PE should
take into account the patient’s hemodynamic status, right ventricular function, and risk of
bleeding. Systemic thrombolytic therapy is currently suggested for patients with acute
PE with hypotension who are at low risk of bleeding. Thrombolysis is not
recommended for most hemodynamically stable patients with PE. Although
thrombolysis is suggested for a subgroup of patients with a high risk of developing
hypotension, there are no validated clinical findings that can be used to identify such
patients. Multiple clinical signs such as tachycardia, decrease in blood pressure,
hypoxemia, evidence of hypoperfusion, and right ventricular dysfunction can be
considered in decision making. Tissue plasminogen activator is preferred at a dose of
100 mg infused over a 2-hour period. Streptokinase has also been used with a loading
dose of 250,000 international units, followed by 100,000 international units each hour
for 24 hours. Short administration times are preferred over prolonged infusion times.
Recently, interest has been renewed in pulmonary artery, catheter-directed instillation of
thrombolytic agents. Surgical embolectomy or extraction/fragmentation of the embolus
via transvenous catheters requires specialized expertise not commonly available, but it
can be considered when shock is likely to cause death before thrombolytics can affect
clot dissolution or systemic administration of thrombolytic agents is risk-prohibitive.
Inferior vena cava filters increase the

risk of developing deep venous
thromboses.
An inferior vena cava filter should be considered in patients with PE when:
Anticoagulation is strongly contraindicated

Emboli recur during anticoagulation
Bleeding occurs during anticoagulation
Physiologic reserve is insufficient to withstand a recurrent PE
Retrievable filters may be an option in some centers. If possible, anticoagulation for

treatment of the embolus should be resumed as soon as possible after insertion of a
filter.
C. Prevention of Venous Thromboembolism

Case Study
A middle-aged man presents with an acute ischemic stroke and right hemiparesis. He
received tissue plasminogen activator and experienced improvement in the neurologic
deficits.
– Should this patient receive prophylaxis for venous thromboembolism?
– What type of venous thromboembolism prophylaxis would be appropriate if the
decision were made to treat?
Many critically ill or injured patients are at risk of developing venous
thromboembolism, either PE or DVT. The development of thrombosis can lead to longer
hospital stays, increased resource utilization, venous insufficiency, and death.
Thromboprophylaxis is cost-effective and highly efficacious in preventing venous
thromboembolism. Both pharmacologic (heparins, direct thrombin inhibitors such as
fondaparinux and dabigatran [not approved for this indication in United States], factor
Xa inhibitors such as rivaroxaban and apixaban, and warfarin) and mechanical
interventions (intermittent pneumatic compression device, graduated compression
stockings) may be used for prophylaxis in hospitalized patients. Mechanical methods for
prophylaxis are generally less effective but are acceptable options for patients at high
risk of bleeding and when combined with anticoagulants.
Recommendations are based on specific patient groups (nonsurgical, nonorthopedic
surgical, orthopedic surgical), level of risk for venous thromboembolism, and risk of
bleeding. Clinicians should follow manufacturers’ instructions for dosing of LMWH,
especially in the setting of renal failure and obesity. Caution must be used when
instituting anticoagulant therapy in patients with recent or ongoing hemorrhage, renal
failure, or concomitant use of antiplatelet therapy.
A formal hospital strategy for

thromboprophylaxis is recommended.
III. SEVERE GASTROINTESTINAL HEMORRHAGE

Case Study
A 64-year-old man with arthritic pain had been taking ibuprofen four times daily for
months without significant relief. He starts to complain of fatigue and progressive
weakness. Today he developed nausea and started vomiting bright red blood. He called
an ambulance and was brought to the emergency department. He is pale, tachycardic,
and dizzy with a blood pressure of 95/60 mm Hg and hematocrit of 28%.
– What additional clinical and laboratory assessments are indicated?
– How would you prioritize interventions?
A. General Management Principles

Medications for ulcer prophylaxis and treatment have reduced the incidence of stress
gastritis and severe upper GI bleeding. However, when present, such bleeding can be
life-threatening and requires early gastroenterologic and surgical consultation as well as
rapid assessment, diagnosis, and intervention. The distinction between upper and lower
GI sources of hemorrhage is important in determining the appropriate
diagnostic/therapeutic approach. The ligament of Treitz is the anatomic marker that
separates the upper GI tract from the lower GI tract when discussing hemorrhage.
Typically, patients with life-threatening GI hemorrhage are older and have other chronic
organ system disease(s). Therefore, the critical consequences of hemorrhage,
hypotension, and anemia may be poorly tolerated and may lead to other systemic
manifestations of poor oxygen delivery, such as myocardial ischemia and renal failure.
Prompt assessment, resuscitation, early diagnosis (even during resuscitation), and
intervention are needed to prevent these secondary consequences.
An ECG should be obtained in patients

with GI bleeding and heart disease or
advanced age to assess for myocardial
ischemia.
A general approach to managing GI bleeding is outlined in Table 13-4. Obtain blood for
typing and cross matching as soon as possible. An appropriate hemoglobin level should
be maintained based on patient condition and coexisting disease. Two large-bore
peripheral catheters or a large-bore central venous catheter should be maintained at all
times. Gastroenterology and surgery consultations (in case of severe bleeding) should
be requested. If a reserve of blood products (eg, four units packed red cells) is not
immediately available, early patient transfer should be planned.
Table 13-4 Management of Gastrointestinal Bleeding
Assessment Airway
Protective reflexes
Level of consciousness
Volume status
Vital signs, orthostatic changes
Central venous pressure
Urine output
Severity of condition
Visible blood loss
Hemoglobin, hematocrit, platelet count
Coagulation status (APTT, PT)
Hypoperfusion abnormalities (ie, cardiac ischemia)
Nasogastric or orogastric tube
Confirm or rule out upper GI source
Lavage stomach for upper endoscopy
Resuscitation Consider intubation

Altered mental status
Inability to protect airway
Copious hematemesis
Need for sedation/endoscopy
IV access
Large-bore (≥16 gauge) peripheral catheter(s) or
large central venous catheter (9F-12F)
Fluid administration
Normal saline or lactated Ringer solution
Transfusion of red blood cells
Diagnostic/Therapeutic Endoscopy with directed therapy

Interventions Radiolabeled red blood cell scan, CT angiogram, or conventional angiography
to localize the site of lower GI bleeding
Surgical assessment/intervention
Correct coagulopathy
Administer plasma, prothrombin complex concentrate, or other appropriate
reversal agent
Platelet transfusion if <50,000/mm 3
Pharmacologic therapy for variceal bleeding
IV proton pump inhibitors
Transfer to facility with diagnostic and/or therapeutic capability
Continuing Care Monitored environment
Adequate blood bank resources
Frequent assessment
Volume status
Hypoperfusion abnormalities
Laboratory parameters
Abbreviations: APTT, activated partial thromboplastin time; PT, prothrombin time; GI, gastrointestinal; CT,
computed tomography
B. Severe Upper Gastrointestinal Hemorrhage

Severe upper GI hemorrhage is diagnosed by hematemesis or the presence of blood in
the gastric aspirate, although 10% to 15% of patients with duodenal ulcer may have
little or no blood in the gastric aspirate due to bleeding below the level of the pylorus.
When obtaining a patient’s history and physical examination, it is important to note
previous upper GI bleeding, the presence of ulcer disease, alcohol consumption,
stigmata of cirrhosis, coagulation disorders, and use of aspirin and other antiplatelet
medications, nonsteroidal anti-inflammatory agents, or anticoagulants. Upper GI
hemorrhage is categorized as variceal (VUGIH) and nonvariceal hemorrhage
(NVUGIH) because of differing prognoses and managements. Common causes of
NVUGIH include duodenal and gastric ulcers, Mallory-Weiss tear, malignancy, and
gastritis.
Endoscopy is needed to establish the diagnosis and control hemorrhage. If this
procedure is not quickly available, consider transfer to a facility with endoscopic
capabilities. In patients taking anticoagulants, correction of coagulopathy is
recommended but should not delay early endoscopy.
When uncontrolled variceal bleeding is suspected before endoscopic diagnosis, the
following splanchnic vasoconstrictors may be considered:
Somatostatin, 250-μg bolus, followed by 250 μg/h

Octreotide, 25- to 100-μg bolus, followed by 25 to 50 μg/h
Vasopressin, 20 units over 20 minutes, followed by 0.1 to 0.4 units/min
Terlipressin, 1 to 2 mg every 4 hours (not available in the United States)
Somatostatin or a somatostatin analogue, such as octreotide, is the agent of choice

because of the favorable side-effect profile. Nausea and abdominal pain are sometimes
associated with bolus doses, but significant adverse effects are uncommon. Maintenance
infusions are usually continued for 3 to 5 days and may be effective in stopping acute
variceal bleeding and preventing early rebleeding from varices. High-dose vasopressin
is an alternative but may cause coronary artery vasospasm, angina, or hypertension.
Concomitant nitroglycerin may prevent the deleterious effects of vasopressin on the
coronary circulation. Terlipressin is a synthetic vasopressin analogue with fewer side
effects and a longer half-life. None of the above agents are recommended in the routine
management of NVUGIH. Antibiotics – usually a second or third-generation
cephalosporin – should be administered in cirrhotic patients with VUGIH to protect
against spontaneous bacterial peritonitis. If variceal hemorrhage cannot be controlled,
balloon tamponade can be considered as a temporizing measure (maximum 24 hours) if
expertise in placement is available until more definitive therapy, such as a porto-venous
shunt, can be instituted. This often necessitates urgent transfer to a regional center.
Following endoscopy, an IV bolus of a proton pump inhibitor, followed by continuous
infusion for 72 hours, is effective in decreasing NVUGIH repeat bleeding and mortality
due to peptic ulcer disease. Pre-endoscopic administration of a proton pump inhibitor
may reduce the need for endoscopic therapeutic interventions, particularly if endoscopy
is delayed. If endoscopy is unsuccessful in controlling the bleeding, surgical
intervention or angiographic embolization may be needed for control.
C. Severe Lower Gastrointestinal Hemorrhage

Frequent causes of lower GI hemorrhage are diverticular disease, angiodysplasia, large
hemorrhoids, colonic polyps, inflammatory bowel disease, rectal ulcer/tear, upper GI
source, and malignancy. Evaluation should include special attention to a history of
diverticular disease, inflammatory bowel disease, previous abdominal aortic aneurysm
repair (may suggest life-threatening aortoenteric fistula), or the presence of a
coagulation disorder. Physical examination must include inspection and a careful rectal
examination to identify hemorrhoids or rectal/anal carcinoma.
Upper GI hemorrhage may mimic lower

GI hemorrhage when associated with
rapid bowel transit of blood.
Gastric aspiration should be performed to eliminate an upper GI source of hemorrhage.

A nasogastric aspirate that is negative for occult blood and contains bile makes an upper
GI bleeding source unlikely. Upper GI endoscopy may be considered based on
assessment of the most likely bleeding source. Lower GI endoscopy is important for
diagnosis and assessment of potential for rebleeding in addition to planning other
diagnostic interventions or surgery. Although lower GI endoscopy may offer a
therapeutic means to arrest hemorrhage, its role as a therapeutic intervention decreases
as the rate of bleeding increases. Besides lower endoscopy, the use of CT angiography,
radionuclide imaging scan, and angiography with embolization therapy should be
considered for unstable patients or those who are poor surgical risks.
D. Prevention Of Stress-related Gastritis

Identification and treatment of patients at risk for stress-related gastritis will reduce
complications, length of stay, and costs. To minimize the potential complications of
pharmacologic prophylaxis for stress ulceration (ie, nosocomial pneumonia), routine
use of such therapy should be limited to patients with known risk factors for stress
gastritis. The risk of stress ulceration and GI bleeding depends on a patient’s underlying
illness, its severity, and related comorbidities. Significant risk factors include
mechanical ventilation for longer than 48 hours, coagulopathy, severe infection,
hypotension, severe head trauma (Glasgow Coma Scale score <10), severe burns or
trauma, renal or hepatic failure, major surgery, and prolonged ICU stay. Appropriate
therapeutic agents include histamine receptor-blocking agents (H2-receptor antagonists)
and proton pump inhibitors.
IV. POISONING AND DRUG TOXICITY
Case Study
A young woman was found on the bathroom floor by her parents the morning after a
party. She was difficult to arouse and, when she was stimulated, she became agitated
and violent. Her parents transported her to the emergency department.
– What are the immediate priorities and interventions in caring for this patient?
– What are the likely toxins, based on the patient’s history and clinical presentation?
Patients who have ingested prescription, over-the-counter, or recreational drugs present
with a variety of clinical manifestations. General categories of patient presentation and
possible responsible agents are listed in Table 13-5. Reliable information about the
substance(s), amount(s) ingested, and time of ingestion is often not available. Similarly,
although qualitative urine toxicology screens and quantitative blood tests may be
available, they cannot identify all agents that could have been ingested. Quantitative
drug levels should be obtained if the patient’s medication or medical history suggests
ingestion of a specific drug, or if the signs and symptoms are compatible with toxicity
from that drug. Acetaminophen levels should be checked in all cases. The anion gap
should be calculated in cases of unknown toxins.
Table 13-5 Clinical Characteristics That Aid in Diagnosis of Poisoning/Overdose
Clinical Examination Possible Agents

Agitation, confusion, Cocaine, amphetamines, antidepressants, phencyclidine, hallucinogens, SSRIs
bizarre behavior
Bradycardia/hypotension β-Blockers, barbiturates, calcium-channel blockers, clonidine, digoxin,
sedatives/hypnotics
Coma, lethargy Alcohols, antidepressants, barbiturates, benzodiazepines, gamma-
hydroxybutyrate, lithium, opiates, salicylates, SSRIs
Hyperadrenergic, Amphetamines, anticholinergics, cocaine, theophylline
hyperthermia
Hypotension Antidepressants, anticholinergics, opiates, organophosphates/carbamates,
sedatives, hypnotics
Hypothermia Ethanol, hypoglycemic agents, opiates, sedatives/hypnotics
Miosis Cholinergic drugs, opiates, organophosphates, phencyclidine
Mydriasis Antihistamines, atropine, tricyclic antidepressants, ethanol, sympathomimetic
drugs
Nausea/vomiting Acetaminophen, alcohols, iron, salicylates, theophylline
Nystagmus Alcohols, carbamazepine, phenytoin, phencyclidine, sedative/hypnotics
Seizures Amphetamines, antidepressants, cocaine, cyanide, isoniazid, lithium,
organophosphates/carbamates, salicylates, SSRIs, theophylline
Tachyarrhythmias Amphetamines, antidepressants, caffeine, cocaine, digoxin, theophylline
Ventilatory compromise Opiates, alcohols, antidepressants, barbiturates, benzodiazepines, gamma-
(respiratory acidosis) hydroxybutyrate
Laboratory Tests Possible Agents
Increased osmolar gap Ethanol, methanol, ethylene glycol, acetone, isopropyl alcohol, propylene glycol
Increased oxygen Methemoglobinemia, carbon monoxide
saturation gap
Metabolic acidosis Acetaminophen, salicylates, methanol/ethylene glycol, iron-isoniazid, carbon
monoxide, cyanide, propylene glycol, propofol
Abbreviation: SSRI, selective serotonin reuptake inhibitor
These patients often require a symptom-based initial evaluation and treatment. Specific
antidotes, treatments, and/or precautions based upon historical or laboratory evidence
of particular ingestants can be utilized when applicable. In some countries, specialized
resource centers are available to assist in the treatment of poisoning. The overall
mortality from acute poisoning is low, but the treating clinician must quickly evaluate
critical issues and attempt to identify patients at highest risk.
A. General Management
1. Initiate airway support as required. Assessing the patient to ensure adequate

ventilation, oxygenation, and protective airway reflexes is critical.
2. Initiate management of cardiovascular compromise as indicated. Obtain adequate
venous access and establish monitoring (eg, pulse oximeter, ECG, automated blood
pressure device). Address initial concerns in monitored variables (eg, isotonic
fluid administration, supplemental oxygen, seizure control, cooling or warming the
patient, vasopressors, or inotropes).
Respiratory failure is a common cause

of death in overdose and poisoning.
3. Consider the following interventions for a patient with altered mental status:
a. 50% dextrose (50 g), 50 mL intravenously, preferably after a blood glucose
test.
b. Naloxone, 0.2 to 2 mg, intravenously, intramuscularly, or via an endotracheal
tube. Larger doses (6 to 10 mg), repeat dosing, or an infusion may be
required, especially when synthetic and long-acting opiates are involved.
c. Thiamine, 100 mg, slow intravenous administration. Administer before
concentrated dextrose solutions to reduce the risk of Wernicke
encephalopathy.
4. Little evidence exists for use of gastric-emptying procedures. Ipecac is not used in
poisoned patients, and gastric lavage may be considered only in life-threatening
overdoses within 1 hour of ingestion. Contraindications include an unprotected
airway and ingestion of substances with high potential for aspiration injury,
including hydrocarbons and acid or alkali ingestions.
5. In patients with significant toxic ingestions, administer activated charcoal within 1
to 2 hours of ingestion at an initial dose of 1 g/kg. The effectiveness of activated
charcoal decreases with time from ingestion, so early administration is indicated.
Caution is required with decreased level of consciousness and an unprotected
airway.
6. Be aware that although cathartics have been used in overdoses, there is no
evidence of efficacy. Caution is warranted in the very young and elderly (because
of potential fluid losses) and those with the potential for obstruction.
7. Recognize that hemodialysis, rather than continuous renal replacement therapy, is
the preferred intervention in patients with life-threatening overdoses of dialyzable
substances. Common dialyzable drugs include carbamazepine, valproic acid,
lithium, toxic alcohols, salicylates, and metformin.
B. Specific Management
After the patient is stabilized, more specific therapy may be warranted. Specific
antidotes and/or interventions that may be considered are listed in Table 13-6. The use
of more advanced interventions, such as hemodialysis or hemoperfusion, should be
individualized to each patient and may require consultation or transfer.
Do not overlook the possibility of

acetaminophen ingestion in patients
with drug overdoses.
Table 13-6 Antidotes and Interventions for Specific Toxins
Toxin Antidote or Intervention

Acetaminophen N-acetylcysteine
Alcohols (methanol, Ethanol, fomepizole, hemodialysis, thiamine and pyridoxine (vitamin B6) for
ethylene glycol) ethylene glycol, folic acid for methanol
Amphetamines Benzodiazepines
Benzodiazepines Flumazenila
β-Blockers Glucagon, calcium chloride, pacing, catecholamines, insulin and dextrose
Calcium-channel Calcium chloride, glucagon, insulin and dextrose, pacing, catecholamines
blockers
Carbon monoxide 100% oxygen, hyperbaric oxygen
Cocaine Benzodiazepines
Cyanide Nitrites and thiosulfate, hydroxocobalamin
Cyclic antidepressants Benzodiazepines (for seizures), blood alkalinization/sodium loading (pH 7.5-
7.55), hypertonic saline, magnesium, α-agonist for hypotension (norepinephrine)
Digoxin Digoxin-specific Fab fragments, atropine, lidocaine, pacing
Heparin Protamine sulfate
Hypoglycemic agents 50% dextrose, somatostatin or octreotide
Iron Deferoxamine
Isoniazid Pyridoxine (vitamin B6)
Lithium Hemodialysis
Nitrites Methylene blue
Opiates Naloxone, intubation/ventilation
Organophosphates, Atropine, pralidoxime or obidoxime
carbamates, nerve
gases
Salicylates Urine alkalinization, hemodialysis
Theophylline Multiple-dose charcoal, hemoperfusion
Warfarins Vitamin K1
aFlumazenil should not be administered to patients who chronically ingest benzodiazepines or have
overdosed on cyclic antidepressants.
V. HYPERTENSIVE CRISES
A. Clinical Presentation
Acute hypertension or severe elevation in blood pressure may occur as a primary or
secondary condition in seriously ill patients. Frequently, patients have an underlying
diagnosis of chronic hypertension. New or progressive end-organ injury secondary to
elevation in BP constitutes a hypertensive emergency, while severely elevated BP
without evidence of organ injury is defined as hypertensive urgency. Although the BP is
often >180/120 mm Hg, no specific BP defines a hypertensive emergency. The rate of
blood pressure increase may be more important than the absolute value. The organs
most severely affected by elevations of BP are the brain, heart, and kidney, and injury
can manifest as encephalopathy, stroke, intracranial hemorrhage, unstable angina or
myocardial infarction, acute left ventricular dysfunction (with pulmonary edema), acute
aortic dissection, and deteriorating renal function. Hypertensive disorders associated
with pregnancy are discussed elsewhere (see Chapter 14).
Symptoms related to an elevated BP at presentation reflect the organ affected and
consequent injury but may be nonspecific. The patient’s history of use of monoamine
oxidase inhibitors, recreational drugs (including cocaine and amphetamines), over-the-
counter medications, and antihypertensive agents as well as medication compliance
should be ascertained. Physical examination and laboratory investigation should be
directed to determine the presence of end-organ injury. Initial workup usually includes
complete blood count, renal function, urinalysis with microscopy, ECG to assess for
cardiac ischemia, and chest radiography to evaluate for pulmonary edema or widened
mediastinum. Patients with altered mental status or focal neurological deficits warrant
imaging of the brain.
A complication of uncontrolled hypertension is acute aortic dissection. Symptoms are
often severe and can include unrelenting chest pain, frequently associated with back or
epigastric pain, and neurological deficits such as altered mental status, focal deficits,
hemiplegia, and paraplegia. A patient with severe hypertension, severe chest pain
radiating to the back, and a wide mediastinum on chest radiograph should be evaluated
for possible aortic dissection. Aortic dissection is frequently misdiagnosed as acute
myocardial infarction, PE, stroke, esophagitis, pancreatitis, peptic ulcer disease, biliary
colic, and ureteral colic. Physical examination should include careful auscultation for a
new murmur of aortic insufficiency, assessment for asymmetric blood pressure or pulses
in upper extremities, and careful palpation of pulses in all extremities for significant
asymmetry. The diagnostic standard has been contrast angiography, but computed
tomography angiography is more commonly used. Magnetic resonance imaging and
transesophageal echocardiography may also be useful for diagnosis.
Acute hypertension secondary to increased sympathetic drive and catecholamine surge
is also a frequent manifestation of common disease processes in seriously ill patients,
such as respiratory failure, acute pain, alcohol or drug withdrawal syndromes, agitated
delirium, and increased intracranial pressure (Cushing reflex). Initial therapy in such
circumstances should be targeted to treating the underlying problem and not lowering of
elevated BP.
B. Therapy
Hypertensive urgency can be managed with oral or intravenous agents, and gradual
blood pressure control over 24 to 48 hours. The goal is to reduce the pressure over
hours to days to a safer, but not necessarily normal, level of BP. Hypertensive
emergencies require continuous monitoring of BP, neurological status, urine output, and
other parameters in a monitored environment. Parenteral and titratable antihypertensive
agents should be administered to lower the BP within minutes to hours. The initial goal
of therapy should be to reduce mean arterial pressure by no more than 20% to 25% in
first few hours. If the BP is lowered too rapidly, it may result in hypoperfusion of major
arterial beds, resulting in cerebral infarction, myocardial infarction, and blindness
secondary to changes in autoregulation of organ blood flow.
Rapid-acting antihypertensives are preferred, including labetalol, esmolol,
nitroprusside, nicardipine, nitroglycerin, and clevidipine. Agents that can be considered
in some specific situations are given in Table 13-7. Oral antihypertensives appropriate
for the patient can usually be initiated within 6 to 12 hours of presentation and
parenteral agents weaned.
Parenteral Antihypertensive Agents Used in the Management of

Table 13-7
Hypertensive Emergencies
Primary Condition Therapy Primary Condition Therapy
Acute aortic dissection Labetalol Diastolic dysfunction with pulmonary Nicardipine
Esmolol edema Labetalol
Nicardipine Fenoldopam
Nitroglycerin
Nitroprusside
Hypertensive encephalopathy Labetalol Acute ischemic stroke/ intracerebral bleed Nicardipine
Nicardipine Labetalol
Clevidipine Fenoldopam
Fenoldopam Clevidipine
Nitroprusside
Acute myocardial ischemia Nitroglycerin Acute renal failure Nicardipine
Labetalol Labetalol
Fenoldopam Fenoldopam
Systolic heart failure Nicardipine Perioperative hypertension Nicardipine
Nitroglycerin Nitroglycerin
Loop diuretic Clevidipine
Labetalol
Esmolol
Eclampsia/severe Hydralazine
preeclampsia Labetalol
Nicardipine
Pheochromocytoma Phentolamine
Labetalol
Specific Situations:
1. In patients with acute aortic dissection, a rapid reduction of systolic BP to 100 to

120 mm Hg with a heart rate 60 to 80 beats/min should be achieved within 5 to 10
minutes. A beta-blocker or an agent with combined alpha- and beta-blockade, such
as labetalol, is preferentially used in this condition to decrease the shear forces on
the aorta and try to limit the extent of dissection. Additionally, opiate analgesics
may be needed for pain control.
2. In patients with normal renal function and signs of volume depletion (due to
pressure natriuresis), gentle volume expansion with normal saline will help
suppress renin secretion and prevent significant hypotension from vasodilating
medications.
VI. INTRA-ABDOMINAL HYPERTENSION AND ABDOMINAL

COMPARTMENT SYNDROME
Increased intra-abdominal pressure (IAP), the pressure within the abdominal cavity
typically measured as bladder pressure, has been increasingly recognized as both the
cause and consequence of many complications in critically ill patients. The perfusion
pressure to the abdomen, termed abdominal perfusion pressure (APP), is the mean
arterial pressure minus the IAP. Similar to cerebral perfusion pressure, APP is the
critical determinant of perfusion to the abdominal visceral organs.
Intra-abdominal hypertension (IAH) is defined as a sustained increase of IAP to >12
mm Hg, while abdominal compartment syndrome is defined as IAP >25 mm Hg with
new onset of organ failure at a lower IAP.
While normal IAP is in the range of 3 to 7 mm Hg, it can reach 9 to 14 mm Hg in obese
individuals. Hence, the physiologic state must be taken into account when interpreting
IAP measurements. Increases can come from increased abdominal volume, decreased
abdominal wall compliance, or more commonly a combination of the two. Some
conditions leading to IAH/abdominal compartment syndrome are listed in Table 13-8.
Abdominal compartment syndrome is classified as primary, secondary, or recurrent.
Primary abdominal compartment syndrome is a condition associated with injury or
disease in the abdominopelvic region that frequently requires early surgical or
radiological intervention, whereas secondary abdominal compartment syndrome
develops from conditions that do not originate primarily from that region (eg, sepsis,
capillary leak, burns). Abdominal compartment syndrome can progress and recur even
after initial therapy is successful.
IAH has deleterious effects on both intra- and extra-abdominal organ systems. Most of
these effects are either from decreased abdominal perfusion causing ischemia of
abdominal organs or from reduced thoracoabdominal compliance leading to reduced
cardiac output and respiratory compromise. Specifically:
1. Decreases in APP can cause acute kidney injury, splanchnic hypoperfusion, and gut
ischemia. These effects may occur in the absence of decreased cardiac output.
2. Intrathoracic pressure increases secondary to reduced thoracoabdominal
compliance and cephalad displacement of the diaphragm (20% to 80%
transmission of abdominal pressure). This has negative effects on the
cardiovascular, respiratory, and central nervous systems:
a. Cardiovascular
i. Decreased venous return leading to diminished preload and end-
diastolic volume
ii. Increased systemic afterload
b. Respiratory
i. Decreased total compliance
ii. Increased inspiratory pressures or decreased tidal volumes, depending
on the mode of mechanical ventilation
c. Intracranial
i. Increased intracranial pressures secondary to elevated thoracic
pressures and diminished cerebral venous return
Significant IAH will lead to increased measured filling pressures, such as central
venous pressure, secondary to reduced chest wall compliance; however, venous return
is significantly reduced, and the transmural pressures are actually low. Thus, these
values will have different interpretations with IAH, and higher physiological targets
may be appropriate for resuscitation.
IAP measurements are made at end-expiration with the patient in the supine position,
after ensuring that abdominal muscle contractions are absent and with the transducer
zeroed at the level of the mid-axillary line. The reference standard for intermittent IAP
measurement is via the bladder with a maximal instillation volume of 25 mL of sterile
saline.
A. Management
The cornerstones of management of IAH/abdominal compartment syndrome are early
recognition by serial monitoring of IAP (every 4 to 6 hours), maintenance of abdominal
(APP >60 mm Hg) and systemic perfusion, prompt institution of medical therapies to
reduce IAP and prevent adverse consequences on organ function, and early surgical
decompression for refractory IAH. Patients with the risk factors for developing IAH
(Table 13-8) should have their bladder pressure measured routinely. Physical exam
alone is not sufficiently sensitive to be useful in the early detection of IAH.
Conditions Associated with Intra-abdominal Hypertension/Abdominal

Table 13-8
Compartment Syndromea
Increased Intra- Decreased Abdominal Wall Compliance Combination
abdominal Volume
Gastrointestinal tract Abdominal surgery, especially with tight Obesity
dilation abdominal closures Sepsis, severe sepsis, and
septic shock
Ileus Abdominal wall bleeding or rectus sheath
Volvulus hematomas Severe acute pancreatitis
Colonic pseudo-
obstruction Surgical correction of large abdominal hernias, Massive fluid resuscitation
Intra-abdominal or gastroschisis, or omphalocele
Major burns (with or without
retroperitoneal masses abdominal eschars)
Abdominal tumor Complicated intra-abdominal

infection
Ascites or
hemoperitoneum
Retroperitoneal
edema/hemorrhage
Pneumoperitoneum (eg,
during laparoscopy)
aClassified partly using Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I.
Definitions. Intensive Care Med. 2006;32:1722-1732.
Medical Therapies
1. Evacuate intraluminal contents by nasogastric or colonic decompression.

2. Evacuate intra-abdominal space-occupying lesions (eg, drainage of large volume
ascites).
3. Optimize fluid administration and avoid both hypo- and hypervolemia. Consider
diuretics and renal replacement therapy in cases of hypervolemia.
4. Improve thoracoabdominal compliance by ensuring adequate sedation and
analgesia, and drainage of pleural effusions and ascites. Avoid constrictive
bandages, and consider neuromuscular blockade.
5. Ensure abdominal and systemic perfusion by keeping APP >60 mm Hg.
Surgical Therapy
1. Decompressive laparotomy is the “gold standard” and most definitive therapy for
IAH. However, patients can develop recurrent IAH, even with an “open abdomen”
if the temporary abdominal closure device used to protect the viscera is too tight.
Key Points
Special Considerations
A negative result with a high-sensitivity D-dimer assay in outpatients with low
clinical probability of PE can exclude the diagnosis, whereas those with moderate
or high clinical probability and hospitalized patients require further diagnostic
testing.
In patients with suspected PE and no contraindications to anticoagulation,
unfractionated or low-molecular-weight heparin or fondaparinux therapy should be
initiated while diagnostic tests are being obtained.
Patients at risk for venous thromboembolism should receive appropriate
pharmacologic and/or mechanical prophylaxis.
In facilities with limited blood bank capabilities, consideration should be given to
transferring patients with serious GI bleeding to a facility with a higher level of
care.
Endoscopy is needed to establish the etiology of upper GI hemorrhage and to
institute potentially definitive therapy.
Lower GI endoscopy is important for diagnosing, possibly treating, and planning
interventions for patients with severe lower GI hemorrhage.
Patients at risk for stress-related gastritis should be started on an H2-receptor
antagonist or proton pump inhibitor.
In the treatment of patients with known or suspected poisoning/overdose,
maintaining airway patency and circulatory stabilization are the initial priorities.
Control of blood pressure and heart rate is critical in the management of patients
with aortic dissection.
Intra-abdominal pressure should be monitored frequently in patients at risk for
developing intra-abdominal hypertension and abdominal compartment syndrome.
Therapy for control of intra-abdominal pressure and maintenance of abdominal and
systemic perfusion should be initiated promptly.
Suggested Readings
1. Alapat PM, Zimmerman JL. Toxicology in the critical care unit. Chest.
2008;133:1006-1013.
2. Anderson FA Jr., Spencer FA. Risk factors for venous thromboembolism.
Circulation. 2003(suppl);107:I-9–I-16.
3. Barkun AN, Bardou M, Kuipers EJ, et al. International consensus
recommendations on the management of patients with nonvariceal upper
gastrointestinal bleeding. Ann Intern Med. 2010;152:101-113.
4. Braverman AC. Aortic dissection: prompt diagnosis and emergency treatment are
critical. Cleve Clin J Med. 2011;10:685-696.
5. Cheatham ML. Abdominal compartment syndrome. Curr Opin Crit Care.
2009;15:154-162.
6. Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of
elevated intra-abdominal pressure. Chest. 2011;140:1428-1435.
7. Falck-Ytter Y, Francis CW, Johanson NA, et al. Prevention of VTE in orthopedic
surgery patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed:
American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines. Chest. 2012;141:e278S-e325S.
8. Garcia-Tsao G, Sanyal AJ, Grace ND, et al. Prevention and management of gastro-
esophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46:
922-938.
9. Gould MK, Garcia DA, Wren SM, et al. Prevention of VTE in nonorthopedic
surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed:
American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines. Chest. 2012;141:e227S-e277S.
10. Kahn IA, Nair CK. Clinical, diagnostic, and management perspectives of aortic
dissection. Chest. 2002;122:311-328.
11. Kahn SR, Lim W, Dunn AS, et al. Prevention of VTE in nonsurgical patients:
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of
Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest.
2012;141:e195S-e226S.
12. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease:
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of
Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest.
2012;141:e419S-e494S.
13. Konstantinides S. Clinical practice. Acute pulmonary embolism. N Engl J Med.
2008;359:2804-2813.
14. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International
Conference of Experts on Intra-abdominal Hypertension and Abdominal
Compartment Syndrome. I. Definitions. Intensive Care Med. 2006;32:1722-1732.
15. Marik PE, Varon J. Hypertensive crises: challenges and management. Chest.
2007;131:1949-1962.
16. Papadopoulos DP, Mourouzis I, Thomopoulos C, et al. Hypertension crisis. Blood
Press. 2010;19:328-336.
17. Torbicki A, Perrier A, Konstantinides S, et al. Guidelines on the diagnosis and
management of acute pulmonary embolism: the Task Force for the Diagnosis and
Management of Acute Pulmonary Embolism of the European Society of Cardiology
(ESC). Eur Heart J. 2008;29:2276-2315.
18. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the
bedside without diagnostic imaging: management of patients with suspected
pulmonary embolism presenting to the emergency department by using a simple
clinical model and D-dimer. Ann Intern Med. 2001;135:98-107.
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Suggested Websites
1. Society of Critical Care Medicine/Guidelines. www.sccm.org

2. Institute for Clinical Systems Improvement. http://www.icsi.org.
3. World Society of Abdominal Compartment Syndrome. http://www.wsacs.org
Chapter 14
CRITICAL CARE IN PREGNANCY
Objectives
Describe the physiologic and metabolic alterations unique to pregnancy.

Discuss the diagnosis and management of hypertensive disorders of pregnancy.
Identify clinical manifestations and treatment of HELLP syndrome.
Outline the approaches to managing peripartum cardiomyopathy, thromboembolic
disease, and other conditions in pregnancy.
List priorities for managing the traumatized pregnant patient.
Case Study
A 28-year-old primigravid woman presents at 34 weeks’ gestation in labor. She has an

elevated blood pressure (BP) of 190/110 mm Hg, heart rate 125 beats/min, and oxygen
saturation 86% while on room air. She is in severe respiratory distress, and her chest
radiograph shows diffuse bilateral lung infiltrates. You are called to evaluate and
manage her deterioration.
– What are the possible diagnoses?
– What immediate interventions are needed?
– What additional diagnostic tests are indicated?
I. INTRODUCTION
A pregnant woman may present for critical care support either with a disease state that
is unique to pregnancy or with a critical illness that is not unique to pregnancy. Diseases
specific to pregnancy include preeclampsia, eclampsia, HELLP syndrome (hemolysis,
elevated liver enzymes, and low platelet count), and amniotic fluid embolism syndrome,
all of which usually require immediate therapy that may be lifesaving. Some critical
illnesses not unique to pregnancy—such as preexisting maternal hypertension,
thromboembolic disease, cardiac and respiratory diseases, and trauma—can be
unmasked, precipitated, or aggravated by pregnancy. The normal physiologic,
metabolic, and hormonal changes of pregnancy may alter the presentation of disease
processes and add a level of complexity to diagnosis and treatment. Understanding the
normal physiologic changes during pregnancy, delivery, and the postpartum period is the
key to managing critically ill obstetric patients with underlying medical diseases and
pregnancy-related complications. The most common critical illnesses in obstetric
patients are hypertensive disorders and hemorrhage.
II. PHYSIOLOGIC ALTERATIONS
A. Cardiovascular Alterations
Alterations in blood volume and cardiovascular status are among the most dramatic
changes that occur in pregnancy. These are adaptive mechanisms that accommodate the
increased metabolic needs of both the mother and the fetus during pregnancy, labor, and
delivery. Blood volume increases in each trimester, reaching 40% to 50% above normal
values by the end of gestation. Cardiac output also increases up to 50% above pre-
pregnancy values by the 24th week of gestation and remains elevated until the
immediate postpartum period. This is primarily a result of increased stroke volume
during the first and second trimesters and increases in heart rate (15 to 20 beats/min)
during the third trimester until term. Improved myocardial contractility may account in
part for the increase in cardiac output. A significant decrease of 25% to 30% in this
output may occur if the patient is placed in the supine position; this causes the gravid
uterus to compress the aorta and inferior vena cava, increasing afterload and restricting
venous return to the heart. The left lateral decubitus position is the preferred position
for pregnant women with serious illness, particularly as gestation progresses and the
gravid uterus increases in size. The decrease in cardiac output in the supine position is
exaggerated in women with poorly developed venous collaterals who exhibit significant
hypotension and bradycardia; this is known as the supine hypotensive syndrome of
pregnancy. Filling pressures, such as the central venous and pulmonary artery pressures,
typically do not change during pregnancy. A decrease in BP is seen in the second
trimester as a result of diminished systemic vascular resistance secondary to the
vasodilating effects of progesterone. Peak reduction in BP occurs between 24 and 26
weeks when systolic pressures are reduced by 5 to 10 mm Hg and diastolic pressures
by 10 to 15 mm Hg. By term, the BP returns to pre-pregnancy values. Venous flow in the
legs is delayed in pregnancy, and this slower velocity of blood return can contribute to
occlusion of the pelvic veins and inferior vena cava by the enlarged uterus. This venous
stasis also contributes to the common finding of dependent edema and development of
varicose veins in the legs and vulva, as well as hemorrhoids. This venous stasis can put
patients at risk for deep-vein thrombosis.
It is abnormal for BP during pregnancy

to exceed nonpregnant values.
Another normal cardiovascular change of pregnancy that may cause or exacerbate

illness is remodeling of the heart with enlargement of all four chambers. In particular,
left atrial enlargement may precipitate supraventricular and atrial arrhythmias. Systolic
ejection murmurs and a third heart sound are commonly detected during pregnancy, but
diastolic, pansystolic, and late systolic murmurs suggest a more serious underlying
cardiac disorder.
In addition to chamber enlargement, the heart is rotated upward and to the left as the
uterus enlarges and the diaphragm is pushed superiorly. This displacement can be seen
as cardiomegaly and increased vascular markings on the chest radiograph, although the
changes have no clinical significance if the patient has no other evidence of cardiac
disease.
Healthy pregnant women tolerate the cardiovascular and hemodynamic effects
associated with pregnancy, as do patients with mild to moderate cardiac disease;
however, the incidence of heart failure and arrhythmias is higher in pregnant patients
with cardiac disease. Concurrent hemodynamic and fetal monitoring is often necessary
for pregnant patients with New York Heart Association (NYHA) functional class III or
class IV heart disease.
B. Pulmonary Alterations
The pregnant woman is considered to have a “difficult airway” complicated by edema
of the upper respiratory tract as a result of increased blood volume and hormone-
induced mucosal edema and hypervascularity. Pulmonary changes in pregnancy include
an increase in tidal volume of approximately 40%, a decrease in functional residual
capacity of 20% to 30% or 400 to 700 mL
during pregnancy, and an increase in oxygen consumption by 20% as a result of the
rising metabolic needs of the mother and the fetus. Total lung capacity remains
unchanged or decreases by less than 5% at term. During pregnancy, metabolic demands
can be elevated up to 32% above nonpregnant values by term. The increases in
metabolic demands are due to the expanding uterine mass and the size of the fetus, but
only 4% is attributed to maternal metabolic demands. The combination of decreased
functional residual capacity and increased oxygen consumption during pregnancy
diminishes maternal oxygen reserves and subsequently increases the hypoxic risk to
both the mother and the fetus in the event of maternal hypoventilation or apnea.
Oxygen requirements rise by approximately 30 to 40 mL/min (15% to 20%) in
pregnancy and are met by an increase in minute ventilation, primarily as a result of an
expanded tidal volume. The increase in minute ventilation results in a mild compensated
respiratory alkalosis with a change in the PaCO2 to 26 to 34 mm Hg (3.5 to 4.5 kPa). The
pH does not change due to renal compensation, which results in a decrease in serum
bicarbonate concentration. Pregnant women who present with a “normal” PaCO2 level of
35 to 40 mm Hg (4.7 to 5.3 kPa) should prompt the clinician to look for a cause of
impending ventilatory failure.
The reduction in functional residual

capacity predisposes the patient to
atelectasis if critical illness develops.
C. Gastrointestinal Alterations
Hormonal and anatomic changes in pregnancy affect the gastrointestinal tract. Starting at
the end of the first trimester, a reduction in lower esophageal sphincter tone caused by
high progesterone levels contributes to an increased risk for aspiration.
Gastroesophageal reflux and decreased gastric emptying are also present during
pregnancy. Alterations in gastric motor function may cause nausea, vomiting, and
dyspepsia.
D. Hematologic Alterations
The 40% to 60% increase in plasma volume that occurs by the third trimester is
associated with a gain in red cell mass of only 25% at term. The disproportionate rise
in plasma volume results in dilutional anemia (physiologic anemia of pregnancy).
Hemoglobin concentration is ~11 g/dL (110 g/L) at 24 weeks, when it stabilizes;
however, it may increase slightly later in the pregnancy, when there is less discrepancy
between the increases in blood volume and red cell mass. The white blood cell count
climbs to 10,000 cells/μL (10.0 x 109/L) at term, with a slight reduction in platelet
count. Plasma concentrations of all clotting factors except XI, XIII, and antithrombin III
increase in pregnancy. Fibrinogen levels may be as high as 600 mg/dL (6.0 g/L) at term.
Fibrinogen levels <150 mg/dL (<1.5 g/L) are considered abnormal. Although
coagulation test results and bleeding times do not change, these compositional changes
result in a hypercoagulable state that, in association with venous stasis and vessel wall
trauma, raises the risk for thromboembolic disease. Increased coagulation factors, fibrin
generation, inhibited fibrinolysis, and venous stasis contribute to the hypercoagulable
state of pregnancy.
E. Metabolic Alterations
Creatinine levels are lower in pregnancy as a result of a rise in the glomerular filtration
rate due to increased blood flow to the kidneys. Corticotropin and cortisol levels are
increased during pregnancy, with an enlargement of the pituitary gland resulting in a
greater risk of postpartum infarction (Sheehan syndrome) if significant blood loss
occurs. Occult adrenal insufficiency can result in adrenal crisis from the stress of labor
and delivery.
III. HYPERTENSIVE DISORDERS

Hypertensive disorders complicate between 5% and 10% of all pregnancies. Of these
disorders, preeclampsia, either alone or superimposed on chronic hypertension, is the
most life-threatening condition. Women with a preexisting history of diabetes mellitus,
renal disease, or vascular disease, or with a family history of hypertension are more
predisposed to developing hypertension during pregnancy.
Hypertension is defined as either a systolic BP of 140 mm Hg or greater, a diastolic of
90 mm Hg or greater, or both. Hypertension is considered mild until blood pressures
reach or exceed a systolic BP of 160 mm Hg or a diastolic of 110 mm Hg.
A. Diagnosis of Hypertensive Disorders
1. Gestational Hypertension
Gestational hypertension is defined as hypertension without the presence of proteinuria.
It usually manifests as diastolic hypertension that resolves by 12 weeks postpartum,
although many women will later develop chronic hypertension. A relatively high rate of
recurrence of diastolic hypertension occurs with subsequent pregnancies.
2. Chronic Hypertension with Superimposed Preeclampsia

Chronic hypertension is defined as hypertension before conception or detected before
20 weeks’ gestation. When preeclampsia complicates a known hypertensive patient, it is
considered chronic hypertension with superimposed preeclampsia. When preeclampsia
complicates chronic hypertension, the maternal and fetal prognoses are worse than
either condition alone.
Echocardiography can reveal left ventricular hypertrophy, which suggests chronic
disease. Other causes of hypertension that are not related to pregnancy, such as renal
artery stenosis, pheochromocytoma, and Cushing syndrome, may need to be considered.
3. Preeclampsia-Eclampsia
Preeclampsia is a multisystem disease that usually occurs after 20 weeks, most often
near term. It is the most common form of hypertension that complicates pregnancy. It is
classically defined as new onset hypertension plus new onset proteinuria; however,
some women may present with new onset hypertension with other multiorgan
involvement, without proteinuria. Severe symptoms concerning for multisystem
involvement include thrombocytopenia (platelet count <100,000/µL), impaired liver
function, new onset renal failure (creatinine >1.1 mg/dL or doubling of previous value),
pulmonary edema, or new onset cerebral or visual disturbances.
A creatinine level of 0.5-0.9 mg/dL (40-

80 μmol/L) is normal in a pregnant
woman.
Proteinuria is defined as the excretion of >300 mg of protein in a 24-hour urine

collection or protein/creatinine ratio of at least 0.3. A urine dipstick reading of 1+ can
also be used only if no other quantitative methods are available.
Eclampsia is the convulsive phase of preeclampsia, with generalized tonic-clonic
seizures. It is the more severe manifestation of the disease. Although seizures are its
most dramatic manifestation, other intracranial catastrophes, such as hemorrhage,
stroke, or intracranial hypertension, are more likely to cause death.
4. Postpartum Hypertension
Preeclampsia with and without severe features can manifest in the postpartum period.
Blood pressures can remain elevated and labile from 2 weeks to 6 months postpartum.
B. Management of Hypertensive Disorders
1. General Guidelines
Patients with eclampsia or severe preeclampsia require hospital admission.
Administration of magnesium sulfate for the prevention of seizures, judicious control of
BP, and maternal and fetal monitoring should be initiated early. Issues such as ICU
admission, management, and delivery of the fetus should be discussed with an
obstetrician and the critical care physician as soon as possible. Preventing maternal
injury, ensuring maternal and fetal oxygenation, and initiating seizure prophylaxis are the
most important aspects of therapy. The treatment of choice in severe preeclampsia is
delivery, but fetal maturity must be considered. In most cases of severe preeclampsia
that occur after 32 weeks’ gestation, delivery is indicated. Consultation with a maternal-
fetal medicine specialist is recommended.
2. Seizure Prophylaxis
Intravenous magnesium sulfate is used prophylactically to prevent seizures in
preeclampsia with severe features. Magnesium sulfate therapy should be initiated in
patients with severe features or symptoms considered premonitory to seizures, such as
headache, altered mental status, blurred vision, scotomata, clonus, and right upper
quadrant abdominal pain. Magnesium sulfate therapy should also be initiated with the
appearance of any signs of progression from mild preeclampsia to severe disease.
The intravenous route must be used for

prophylactic or therapeutic
administration of magnesium sulfate for
preeclampsia or eclampsia.
Women treated with magnesium sulfate to prevent or treat eclamptic seizures should
receive an intravenous loading dose of 4 to 6 g, followed by a maintenance dose of 1 to
2 g/h continued for at least 24 hours.
Magnesium levels are checked 2 to 4 hours later and should be in the range of 2.0 to 3.5
mmol/L (4-7 mEq/L). Maternal respiratory rate, deep tendon reflexes, level of
consciousness, and urine output are monitored regularly and correlate well with serum
magnesium levels. Respiratory depression, somnolence, or loss of patellar reflexes
suggests magnesium levels in excess of the therapeutic range (>3.5 mmol/L or 7 mEq/L).
Because magnesium is excreted renally, the infusion rate should be decreased if urine
output drops. The maintenance infusion should also be decreased or withheld on the
basis of the serum creatinine level. The antidote for magnesium toxicity is 1 g of
calcium chloride (10 mL of 10% solution) given intravenously over several minutes.
3. Blood Pressure Control

The goal of antihypertensive therapy is prevention of maternal complications such as
stroke, intracranial hemorrhage, acute myocardial infarction, or acute heart failure.
There are no convincing data to determine the optimal blood pressure at which
antihypertensive medications should be initiated, but sustained systolic BP of at least
160 mm Hg or diastolic BP of at least 110 mm Hg should be treated. Admission to the
hospital for acute antihypertensive therapy is recommended for marked elevations in BP
or if the patient has end-organ involvement. Intravenous therapy is the standard method
of delivering antihypertensive agents for life-threatening conditions.
Angiotensin-converting enzyme
inhibitors are contraindicated in
pregnancy because of associated fetal
and neonatal complications.
Hydralazine, labetalol, or oral nifedipine can be used to treat acute severe hypertension
in pregnancy. The drug choice and route of administration should be based on the
provider’s comfort and experience.
Parenteral hydralazine (5 mg administered as a slow intravenous push every 15-20

minutes)
Labetalol (20 mg intravenously initially, and titrated every 10-15 minutes). If the
initial 20-mg dose of labetalol is not effective, 40 mg should be given. If the 40-mg
dose does not lower the BP to the desired level, it should be followed by an 80-mg
dose up to a maximum dose of 300 mg.
Precipitous drops in BP can occur with aggressive antihypertensive therapy,
particularly in the volume-depleted preeclamptic patient. Diuretics should be
avoided because most preeclamptic patients have a significantly decreased plasma
volume.
4. Supportive Measures
Cardiogenic and non-cardiogenic pulmonary edema often occur during severe
preeclampsia. Treatment includes supplemental oxygen to maintain maternal PaO2 >70
mm Hg (>9.3 kPa) or oxygen saturation ≥94% to prevent fetal hypoxia. The indications
for tracheal intubation and mechanical ventilation are the same as those for the
nonpregnant patient. Because of increased maternal oxygen consumption and a decrease
in the functional lung surface area, the mother is at greater risk for hypoventilation and
apnea. Intubation should be approached cautiously in the pregnant woman due to the
potential for hypoxemia during induction, the increased risk of aspiration, and the
possibility of oropharyngeal edema. Usually, small endotracheal tubes (6.5 or 7.0 mm)
are necessary. A pregnant woman who requires intubation should be approached as a
full-stomach intubation. Ventilation with a bag-mask device and intubation should
proceed with cricoid pressure throughout the procedure to mitigate the increased risk of
aspiration. Because preeclamptic and eclamptic patients frequently have intravascular
volume depletion, invasive hemodynamic monitoring may be required to optimize
management of pulmonary edema. Central venous pressure values have not been shown
to correlate with pulmonary artery filling pressures during pregnancy but may guide
volume resuscitation. Noninvasive techniques such as echocardiography may be used to
assess cardiac output, volume status, and ejection fraction. Vasoconstriction of the renal
vasculature in severe preeclampsia frequently leads to oliguria. Intravenous fluid
challenges should be instituted cautiously. The empiric use of diuretics without invasive
hemodynamic monitoring of intravascular volume is discouraged. Most preeclamptic
women with oliguria will respond to 1 to 2 L of crystalloid without the need for
invasive monitoring. The patient’s failure to respond to repeated fluid challenges, or the
presence of cardiac or respiratory failure, should prompt consideration of hemodynamic
monitoring and critical care consultation. Vasodilator therapy may be beneficial if
intravascular volume is adequate.
5. Monitoring
All patients should have their blood pressure monitored regularly, and those who are
hypertensive require more frequent assessment. When magnesium sulfate is used,
monitoring should include checking patellar reflexes, respiratory rate, and periodic
magnesium levels. Invasive hemodynamic monitoring is not usually required in
preeclamptic patients, although it is recommended for those with significant cardiac,
respiratory, or renal abnormalities.
IV. HELLP SYNDROME

HELLP syndrome is a life-threatening condition that can occur during pregnancy or in
the immediate postpartum period. Seen in 4% to 12% of preeclamptic patients, the
syndrome is characterized by the following:
Hemolysis: hemolytic microangiopathic anemia with an abnormal result on

peripheral smear, a total bilirubin level >1.2 mg/dL (21 μmol/L), or serum lactate
dehydrogenase level >600 U/L
Elevated liver enzymes: aspartate aminotransferase value >70 U/L or lactate
dehydrogenase level >600 U/L
Low platelet count: <150,000/μL
Variations of the syndrome do not necessarily include all of these manifestations.

Patients can present with a variety of nonspecific clinical signs and symptoms, including
epigastric or right upper quadrant pain, bleeding gums or nose, petechiae, malaise,
nausea, and vomiting. Most HELLP syndrome cases occur at the gestational age of 27 to
36 weeks. Postpartum presentations occur in 20% of cases, usually within 1 to 2 days
after delivery. One-third of patients with HELLP syndrome have no evidence of
preeclampsia, showing neither proteinuria or hypertension during the pregnancy.
If possible, management of patients with

HELLP syndrome should occur in a
tertiary care facility.
HELLP syndrome can be confused with acute fatty liver of pregnancy, thrombotic
thrombocytopenic purpura, or adult hemolytic-uremic syndrome, and it may mimic or
mask severe sepsis. Laboratory tests that are helpful in differentiating acute fatty liver
and HELLP syndrome are listed in Table 14-1. HELLP syndrome almost always
indicates a need for urgent delivery because of significantly increased fetal and
maternal morbidity and mortality rates.
Laboratory Findings in Acute Fatty Liver, HELLP Syndrome, and

Table 14-1
Eclampsia/Preeclampsia
Test Acute Fatty Liver HELLP Eclampsia/Preeclampsia
Fibrinogen ↓ Normal or ↑ Normal or ↑
Glucose ↓ Normal Normal
Ammonia ↑ Normal Normal
ALT (usual range) 300 U/L 150 U/L 60 U/L
Bilirubin ↑ Normal, mild ↑ Normal, mild ↑
DIC 75% 20%-40% Rare
Abbreviations: HELLP syndrome, hemolysis, elevated liver enzymes, and low platelet count ALT, alanine
aminotransferase; DIC, disseminated intravascular coagulation
Treatment of HELLP syndrome includes supportive care, intravenous magnesium

sulfate, and antihypertensive therapy (see section, Hypertensive Disorders). Patients
complaining of persistent, severe, or worsening epigastric or right upper quadrant pain
should be carefully examined for spontaneous fracture or rupture of the liver. Computed
tomography or magnetic resonance imaging can be useful in diagnosing intrahepatic
bleeding. Other complications of HELLP syndrome may include intracerebral
hemorrhage, acute renal failure, and fulminant hepatic failure.
V. POSTPARTUM HEMORRHAGE
While there is no single suitable definition for postpartum hemorrhage, it is classically
defined as an estimated blood loss in excess of 500 mL following a vaginal birth or a
loss of greater than 1,000 mL following cesarean delivery. Postpartum hemorrhage
generally is classified as primary or secondary, with primary hemorrhage occurring
within the first 24 hours of delivery and secondary hemorrhage occurring between 24
hours and 6 to 12 weeks postpartum. Primary postpartum hemorrhage is caused by
uterine atony in the majority of cases. Etiologies for primary and secondary postpartum
hemorrhage include overdistension of the uterus, retained placental products,
coagulation defects, and uterine inversion.
Since uterine atony is the most common cause of postpartum hemorrhage, the diagnosis
is made clinically by palpation of a large and boggy uterus. The second most frequent
cause of primary postpartum hemorrhage is lacerations of the lower genital tract that
occur spontaneously or as a result of traumatic labor. Hematomas resulting from these
lacerations can also lead to significant blood loss at the time of delivery, specifically if
the hematoma is progressively enlarging.
Ongoing blood loss from uterine atony requires the administration of additional
uterotonics as the first-line treatment for hemorrhage (Table 14-2).
Table 14-2 Medical Management of Postpartum Hemorrhagea
Drug* Dose/Route Frequency Comment

Oxytocin IV: 10-40 units in 1 L Continuous Avoid undiluted rapid IV infusion, which causes
normal saline or hypotension.
lactated Ringer
solution
IM: 10 units
Methylergonovine IM: 0.2 mg Every 2-4 h Avoid if patient is hypertensive.
15-methyl IM: 0.25 mg Every 15-90 Avoid in asthmatic patients; relative
prostaglandin F2α min, 8 contraindication if hepatic, renal, and cardiac
doses disease present. Diarrhea, fever, tachycardia can
maximum occur.
Dinoprostone Suppository: vaginal Every 2 h Avoid if patient is hypotensive. Fever is common.
or rectal, 20 mg Stored frozen, it must be thawed to room
temperature.
Misoprostol 800–1,000 µg rectally
(prostaglandin
E1)
Abbreviations: IV, intravenously; IM, intramuscularly

*All agents can cause nausea and vomiting.
aModified from Dildy GA, Clark SL. Postpartum hemorrhage. Contemp Ob/Gyn. 1993;38(8):21-29.
General treatment measures include aggressive and early fluid resuscitation and
attempts to locate the source of the bleeding. Maternal mortality rates increase when
treatment is delayed and blood loss is underestimated. Patients with ongoing blood loss
resulting in hemodynamic instability require packed red blood cell transfusions in
addition to fluid administration. Depending upon the amount of blood loss and the
presence of coagulopathy, additional blood products including fresh frozen plasma,
platelets, and cryoprecipitate may be needed. Angiographic embolization and surgical
interventions, including hysterectomy, may be required for severe uterine hemorrhage
unresponsive to uterotonic drug therapy.
VI. THROMBOEMBOLIC DISEASE

The incidence of thromboembolic disease in pregnant women during the immediate
postpartum period is five times that in nonpregnant women. Risk increases with rising
parity, cesarean delivery, operative vaginal delivery, previous deep venous thrombosis,
and increased maternal age.
Patients receiving heparin are at risk for

heparin-induced thrombocytopenia and
osteoporosis.
Although manifestations of pulmonary embolism in pregnant women are similar to those

in nonpregnant women (Chapter 13), the physiologic changes of pregnancy complicate
evaluation. Lower-extremity edema, leg pain, and dyspnea are common in pregnancy
and create a diagnostic dilemma for the clinician. If a chest radiograph is obtained to
rule out other pulmonary problems, such as pneumonia, the fetus must be shielded. After
16 weeks’ gestation, D-dimer values are elevated above the usual normal range and are
of little diagnostic utility. Doppler scanning of the lower extremities (compression
ultrasound), when available, is usually the first diagnostic test for deep vein thrombosis
in pregnancy, but it is less accurate for calf and isolated iliac vein thrombosis. For
diagnosing pulmonary embolism, ventilation/perfusion scanning is reliable in a pregnant
woman, and it may be beneficial to perform perfusion scanning alone initially. If there
are no perfusion defects, the scan can be considered negative. Computed tomography
angiography (CTA) is an alternative method which is more sensitive for emboli in the
central arteries and less sensitive for subsegmental emboli. The teratogenic and
oncogenic risks to the fetus from these diagnostic tests are not significant, and the
potential for maternal death from undiagnosed thromboembolic disease outweighs the
risk of radiation exposure. An appropriate diagnostic evaluation should always be
performed when indicated. Heparin therapy should be initiated immediately when the
diagnosis of pulmonary embolism is suspected and should be continued if the diagnosis
is confirmed.
The treatment of stable pulmonary embolism in the pregnant patient parallels that in the
nonpregnant patient, except that warfarin is relatively contraindicated in pregnancy and
absolutely contraindicated during the first trimester, when the risk of teratogenicity is
greatest. Instead, unfractionated heparin can be administered intravenously using a
weight-adjusted dose regimen to achieve an activated partial thromboplastin time of 1.5
to 2.5 times control. Treatment is then converted to subcutaneous administration, starting
at 5,000 IU of unfractionated heparin every 12 hours and aiming for the same activated
partial thromboplastin time measured 6 hours after administration. Low-molecular-
weight heparin or dalteparin/tinzaparin is safe for the fetus and can be used for the
treatment of thromboembolic disease. The use of low-molecular-weight heparins may
be preferred given the potential for fewer adverse events, more predictable therapeutic
response, and easier dosing schedules. After delivery, warfarin can be substituted for 3
to 6 months of total therapy, depending upon risk factors.
When considering regional anesthesia for labor pain, intrapartum management requires
that therapeutically dosed unfractionated heparin be discontinued at least 6 hours before
epidural or spinal anesthesia and prophylactically dosed low-molecular-weight heparin
be discontinued 12 hours prior to regional anesthesia. Therapeutically dosed low-
molecular-weight heparin should be held 24 hours before regional anesthesia.
Postpartum therapeutic and prophylactic heparin usually can be resumed at least 1 hour
after the epidural catheter is removed or spinal needle is placed. Prophylactic low-
molecular-weight heparin can be resumed after 4 hours, and therapeutic low-molecular-
weight heparin can be started after 24 hours. The risks with intrapartum use include a
significantly increased likelihood of hemorrhage with cesarean delivery, bleeding and
hematoma formation if a regional or epidural anesthetic is used, and increased bleeding
if an episiotomy or operative vaginal delivery is performed. Patients with massive
pulmonary embolism and/or hemodynamic instability should be managed much like
nonpregnant patients, with careful consideration of risks (Chapter 13).
VII. PERIPARTUM CARDIOMYOPATHY
A. Clinical Manifestations
Peripartum cardiomyopathy is defined as left ventricular systolic dysfunction that occurs
during the last month of pregnancy or within 5 months postpartum, in the absence of
identifiable cause for the cardiac failure and absence of prior heart disease. Clinical
symptoms include severe progressive dyspnea, progressive orthopnea, paroxysmal
nocturnal dyspnea, and syncope with exertion. Signs include evidence of right and left
heart failure, generalized or chamber-specific cardiomegaly seen on a chest radiograph,
evidence of pulmonary hypertension, murmurs, prominent jugular vein distension,
cyanosis, clubbing, or dysrhythmias. Most patients present with dramatic symptoms
soon after delivery. Peripartum cardiomyopathy is associated with maternal age >30
years, first pregnancy, twin pregnancies, preeclampsia, and pregnant women who
receive tocolytic agents. The course tends to be more severe in older patients of higher
parity with later onset of symptoms after delivery. Approximately 50% of women
suffering from peripartum cardiomyopathy recover baseline ventricular function within
6 months of delivery, but in those with persistent cardiac failure, the mortality rate
approaches 85% over 5 years.
B. Management
Initial evaluation of the patient with possible peripartum cardiomyopathy includes a
chest radiograph, electrocardiogram, and echocardiogram. Initial therapy includes bed
rest, sodium restriction, diuretics, and possibly vasodilators. Patients who present with
pulmonary edema and cardiac decompensation often require invasive hemodynamic
monitoring for careful and judicious fluid management, intravenous inotropic support,
and afterload reduction. Useful drugs include digoxin, dobutamine, and milrinone as
inotropic agents and angiotensin-converting enzyme inhibitors for afterload reduction,
although the latter are contraindicated before delivery. Loop diuretics can help with
symptomatic relief of systemic and pulmonary congestion, but should be used cautiously
in the last month of gestation due to their effect on uteroplacental perfusion. If symptoms
develop in the antepartum period, consultation with the obstetrician, critical care
physician, and anesthesiologist can guide decisions regarding early delivery. Early
delivery is not usually recommended because many patients experience worsening of
symptoms postpartum. Urgent delivery may be considered in pregnant women with
advanced heart failure or hemodynamic instability. Critically ill patients who require
inotropic and mechanical support should undergo cesarean delivery. Anticoagulation
should be considered in peripartum cardiomyopathy, enlarged cardiac chambers,
ejection fraction <35%, and atrial fibrillation as systemic and pulmonary emboli are
significantly more common than in other cardiomyopathies. Right and left ventricular-
assist devices can serve as a bridge for patients who may eventually recover or who
require cardiac transplantation as the definitive treatment because of failure of
pharmacologic therapy. Subsequent pregnancies are discouraged in women who have no
resolution of the signs and symptoms of heart failure 6 months after delivery.
VIII. SEVERE ASTHMA

Patients with severe asthma who require intubation and mechanical ventilation should
have the minute ventilation adjusted to avoid hyperventilation and respiratory alkalosis.
An alkalotic pH may lead to reduction of uteroplacental blood flow, impairing fetal
oxygenation. Occasionally, life-threatening asthma can be refractory despite mechanical
ventilation and intensive medical therapy; in such cases, cesarean delivery should be
considered.
IX. AMNIOTIC FLUID EMBOLISM

Amniotic fluid embolism, a catastrophic event with significant morbidity and mortality
rates, may be associated with miscarriages, abortions, and amniocentesis. It occurs most
often during labor and delivery or immediately postpartum. The presentation includes
typical findings of hypoxia, shock, altered mental status, and disseminated intravascular
coagulation; seizure activity, agitation, fetal distress, fever, chills, nausea, and vomiting
may also be present. The diagnosis of amniotic fluid embolism is clinical and a
diagnosis of exclusion. It should be considered in pregnant or postpartum women who
abruptly and dramatically present with profound shock and cardiovascular collapse
associated with severe respiratory distress. Occasionally, disseminated intravascular
coagulation is the first presenting sign. Other life-threatening conditions, such as
pulmonary embolism, sepsis, air embolism, eclampsia, and myocardial infarction,
should be excluded. Radiographic evidence of pulmonary edema with bilateral
interstitial and alveolar infiltrates is possible. Management is supportive and focuses on
rapid maternal cardiopulmonary stabilization and prevention of subsequent end-organ
damage.
X. TRAUMA IN PREGNANCY
Treatment priorities for the pregnant patient with traumatic injury are the same as those
for nonpregnant patients (Chapter 9). There are, however, unique changes that should
be taken into account during clinical assessment. The gravid uterus complicates the
initial abdominal assessment. The height of the uterus is roughly at the symphysis pubis
at 12 weeks and the umbilicus at 20 weeks; thereafter, the height increases by 1 cm each
week up to 36 to 40 weeks, when the uterus encompasses almost the entire abdomen.
Late in pregnancy, a widened symphysis pubis and widened sacroiliac joints are
possible. All pregnant patients with major traumatic injuries should be admitted to a
facility with surgical obstetric capabilities. When evaluating the patient’s mental status,
clinicians should be aware that neurologic symptoms of eclampsia may mimic head
injury. Aortocaval compression in the supine position can contribute to hypotension by
restricting blood return to the heart. Whenever possible, the patient should be placed in
the left lateral decubitus position; at a minimum, the right hip can be raised by 4 to 8 cm
to displace the uterus away from the inferior vena cava. If any question of spinal injury
exists, spinal alignment should be maintained and the patient logrolled.
The pregnant patient can lose up to 35% of blood volume before significant tachycardia,
hypotension, and other signs of hypovolemia are seen. Therefore, the fetus may actually
be in a state of hypoperfusion while the mother’s condition seems stable. An assessment
of the fetal heart rate is an essential part of the initial survey and can be accomplished
easily with a fetoscope or a Doppler fetoscope. A conventional stethoscope can be used
to auscultate the fetal heart rate in the third trimester, although it may be difficult to
differentiate between maternal and fetal heart tones if the mother is tachycardic. If
available, ultrasonography is effective for documenting fetal cardiac activity and
function. Late or persistent decelerations of the fetal heart rate are an ominous sign. If
the fetus cannot be examined adequately at the facility, the patient should be stabilized
and transported as soon as possible to another facility with the capability for fetal
examination and monitoring. A minimum of 4 hours of fetal monitoring is necessary after
trauma.
Secondary assessment should evaluate uterine irritability or contractions, fetal heart
rate, and fetal movement. A pelvic examination should be performed if necessary. If
there is any question of vaginal bleeding, a sterile speculum examination should be
performed by a qualified, experienced caregiver, preferably following a sonographic
examination to exclude placenta previa. A manual vaginal examination is
contraindicated if placenta previa is being considered.
Normal fetal heart rates are between 110

and 160 beats/min.
Definitive care of the pregnant trauma patient includes adequate hemodynamic and
respiratory resuscitation, stabilization of the mother, continued fetal monitoring, and
radiographic studies as necessary, in addition to obstetric care, critical care, and
surgical consultation. If the mother is Rh-negative, Rho(D) immune globulin should be
given within 72 hours of injury, even when trauma is minimal. An assessment of the
amount of fetal red blood cells in the maternal circulation by means of a Kleihauer-
Betke stain is advised. Obstetrical consultation for the appropriate dosage of Rho(D)
immune globulin is recommended.
XI. SEPTIC PELVIC THROMBOPHLEBITIS

Septic pelvic thrombophlebitis, characterized by infected clot(s) in the pelvic veins, can
occur in the antepartum period, after vaginal and cesarean deliveries, as well as after
both spontaneous and therapeutic abortions. Physical findings are nonspecific. Fever
that fails to respond to empiric antibiotics in a postpartum patient should prompt
consideration of septic pelvic thrombophlebitis. Evidence of systemic septic emboli
from sepsis, metastatic abscesses, and septic pulmonary emboli may be present.
Ultrasonography or computed tomography studies are not diagnostic but occasionally
may show evidence of a clot. Because this is a diagnosis of exclusion, patients are
typically treated on the basis of clinical suspicion. Women with septic thrombophlebitis
usually have symptomatic improvement with antimicrobial treatment, and studies have
shown that the addition of anticoagulation to antimicrobial therapy has not proven to be
beneficial.
XII. MECHANICAL VENTILATION DURING PREGNANCY

The indications for intubation and mechanical ventilation in pregnant patients are the
same as those for nonpregnant patients. The maternal oxygen reserve is decreased and
significant arterial desaturation occurs if the patient is hypoventilating or apneic for
even a short time. Such episodes increase the hypoxic risk to the fetus as well.
Mechanical ventilator parameters should be adjusted to maintain the PaCO2 in the range
of 30 to 32 mm Hg (4.0-4.3 kPa). Data about permissive hypercapnic ventilation in the
pregnant patient are limited, although chronic elevations of maternal PCO2 up to 60 mm
Hg (8.0 kPa) in those with congenital heart diseases have not been shown to be
detrimental to the fetus. Caution should be used when considering noninvasive
ventilation due to the increased risk of aspiration during pregnancy.
Expeditious delivery in the patient requiring mechanical ventilation during pregnancy is
indicated only with evidence of placental disruption, disseminated intravascular
coagulation, chorioamnionitis, or severe preeclampsia. It may also be indicated for
patients with stiff, noncompliant lungs requiring high peak airway pressures or pressure
control ventilation. Delivery while the mother is receiving mechanical ventilation may
improve diaphragmatic excursion and decrease elevated airway pressures. Successful
spontaneous delivery is possible during mechanical ventilation.
XIII. ADVANCED LIFE SUPPORT IN PREGNANCY

When cardiac arrest occurs in a pregnant woman, standard advanced life support
resuscitative methods can and should be undertaken. With advanced gestation or a large
uterus, a wedge should be placed under the right flank to displace the uterine contents to
the left, improving venous return to the heart. Alternatively, the uterus can be displaced
manually to the left. Chest compressions are performed slightly above the center of the
sternum to account for elevation of the diaphragm. If initial attempts with standard
advanced cardiac life support resuscitative measures are unsuccessful and the
gestational age and size are estimated to be ≥24 weeks, then a decision to perform a
perimortem cesarean delivery should be made rapidly so that it is accomplished within
4 to 5 minutes of arrest. This option is applicable only when the uterus is deemed large
enough to impede life support efforts by significant aortocaval compression, which
further worsens maternal hemodynamics. The principal reason for performing a
perimortem delivery is to improve cardiac output by augmenting venous return to the
heart with effective cardiac compressions. Standard medications for cardiopulmonary
resuscitation should be used. Obstetric and neonatology assistance should be sought if
possible.
XIV. PHARMACOTHERAPY
Choice of medications for the pregnant woman must take into account the potential for
adverse effects on the fetus (Table 14-3 and Table 14-4). Certain medications, such as
warfarin, angiotensin-converting enzyme inhibitors, diazepam, and phenytoin, have
known or potential adverse effects and should be avoided when acceptable alternatives
are available. In general, the selection of any new medication for a critically ill or
injured pregnant patient should include a review of its indications and pharmacology as
well as alternative approaches to management. A clinical pharmacist should be
consulted to obtain information about fetal risk associated with drug therapy.
Table 14-3 U.S. Food and Drug Administration Categories of Fetal Drug Toxicities
Category Description
A Controlled studies in pregnant women have not demonstrated any risk to the fetus in the first
trimester. These drugs are considered to be relatively safe for use during pregnancy.
B No known specific risks are associated with the use of the drug in pregnancy, but controlled
human studies are lacking. If adverse effects were shown in animal reproduction studies, they
were not confirmed in controlled human trials.
C Studies in women and animals are not available or studies in animals have revealed adverse
effects on the fetus. Most new drugs fall into this category. These drugs should be given only if
the potential benefit justifies the potential fetal risk.
D These drugs have shown a definite fetal risk in controlled human trials. However, their use may
be necessary during pregnancy, and a risk-benefit assessment needs to be performed before
they are used.
X These drugs have shown a definite risk to the fetus, and their use is contraindicated because
the risks outweigh the potential benefits.
Table 14-4 Toxicity Categories for Selected Drugs During Pregnancy a
Antiarrhythmics Anticonvulsants Diuretics

Amiodarone D Carbamazepine D Furosemide C
Lidocaine B Magnesium sulfate B Spironolactone C
Procainamide C Phenobarbital D
Phenytoin D Neuromuscular Blockers
Antibiotics Cisatracurium B
Acyclovir B Antihypertensives Rocuronium C
Aminoglycosides ACE inhibitors Succinylcholine C
Ophthalmic C First trimester C Vecuronium C
gentamicin Second, third
Injectable D trimesters D Sedatives/Analgesics/
gentamicin β-Blockers Anxiolytics
Ophthalmic B Metoprolol C Benzodiazepines D
tobramycin Atenolol D Codeine C
Injectable D Carvedilol C Haloperidol C
tobramycin Labetalol C Morphine C
Amikacin D Clonidine C Propofol B
Azithromycin B Hydralazine C
Cefotetan (avoid) B Steroids
Ceftriaxone (avoid) B Cardiovascular Medications Dexamethasone C
Cephalosporins B Amrinone/milrinone C Hydrocortisone C
Clindamycin B Aspirin D Prednisolone C
Metronidazole Bb Atropine C
Penicillins B Digoxin B Other
Quinolones C Dobutamine C Aminophylline C
Sulfonamides B Dopamine C H2 blockers B
Trimethoprim C Epinephrine C Heparin C
Vancomycin Nitroglycerin C Insulin B
PO B Nitroprusside C Mannitol C
IV C Norepinephrine C Warfarins X
Thrombolytics C
Vasopressin C
Verapamil C
Abbreviations: ACE, angiotensin-converting enzyme; PO, by mouth

aData from Lexi-Comp’s Drug Information Handbook, 2011-2012. Hudson, OH: Lexicomp, Inc.; 2011.
bContraindicated in first trimester
Key Points
Critical Care in Pregnancy

A significant decrease in cardiac output may occur with advanced gestation or a
large uterus when the patient is placed in the supine position because the gravid
uterus restricts venous return and aortic blood flow.
The diagnosis of preeclampsia is based on the development of new onset
hypertension with proteinuria after 20 weeks’ gestation or severe features
indicating multisystem involvement.
Eclampsia is defined as preeclampsia with generalized tonic-clonic seizures.
Magnesium sulfate (20% solution), used as seizure prophylaxis in preeclampsia
and as treatment for eclamptic seizures, requires close monitoring.
Anticoagulation with heparin (unfractionated or low-molecular-weight) is used to
treat pulmonary embolism in pregnancy. Warfarin is contraindicated, particularly in
the first trimester.
Treatment of underlying cause, along with early and aggressive treatment with fluid
and blood products, is necessary in primary postpartum hemorrhage.
Priorities for the resuscitation of the pregnant trauma patient are the same as those
for nonpregnant patients.
The pregnant woman can lose up to 35% of her blood volume before tachycardia,
hypotension, and other signs of hypovolemia are seen. This can mask significant
fetal compromise as well as ongoing maternal blood loss.
If the mother is Rh-negative, Rho(D) immune globulin should be given, even after
minimal truncal trauma.
Indications for intubation and ventilation are the same for pregnant patients as for
nonpregnant patients. Adjust mechanical ventilator settings to maintain the PCO2
level in the range of 30 to 32 mm Hg (4.0-4.3 kPa).
If initial resuscitative measures are ineffective, a perimortem cesarean delivery
should be considered within 4 or 5 minutes of cardiac arrest to improve maternal
hemodynamics.
When choosing medications for the pregnant woman, it is important to take into
account their potential adverse effects on the fetus.
Suggested Readings
1. ACOG Committee on Obstetric Practice. ACOG practice bulletin no. 33.

Diagnosis and management of preeclampsia and eclampsia. Obstet Gynecol.
2002;99:159-167.
2. Ahonen J, Stefanovic V, Lassila R. Management of post-partum haemorrhage. Acta
Anaesthesiol Scand. 2010;54:1164-1178.
3. Guntupalli SR, Steingrub J. Hepatic disease in pregnancy: an overview of
diagnosis and management. Crit Care Med. 2005;33(suppl):S332-S339.
4. Hardy-Fairbanks AJ, Baker ER. Asthma in pregnancy: pathophysiology, diagnosis
and management. Obstet Gynecol Clin North Am. 2010;37:159-172.
5. Leung AN, Bull TM, Jaeschke R, et al. An official American Thoracic
Society/Society of Thoracic Radiology Clinical Practice Guideline: Evaluation of
suspected pulmonary embolism in pregnancy. Am J Respir Crit Care Med.
2011;184:1200-1208.
6. Mallampalli A, Guy E. Cardiac arrest in pregnancy and somatic support after brain
death. Crit Care Med. 2005;33(suppl):S325-S331.
7. Miller MA, Chalhoub M, Bourjeily G. Peripartum pulmonary embolism. Clin
Chest Med. 2011;32:147-164.
8. Oxford CM, Ludmir J. Trauma in pregnancy. Clin Obstet Gynecol. 2009;52:611-
629.
9. Pearson GD, Veille JC, Rahimtoola S, et al. Peripartum cardiomyopathy: National
Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of
Health) workshop recommendations and review. JAMA. 2000;283:1183-1188.
10. Tan M, Huisman MV. The diagnostic management of acute venous
thromboembolism during pregnancy: recent advancements and unresolved issues.
Thromb Res. 2011;127(Suppl 3):S13-S16.
11. Whitty JE. Maternal cardiac arrest during pregnancy. Clin Obstet Gynecol.
2002;45:377-392.
12. Yeomans ER, Gilstrap LC 3rd. Physiologic changes in pregnancy and their impact
on critical care. Crit Care Med. 2005;33(suppl):S256-S258.
13. Cunningham F. Williams Obstetrics. New York: McGraw-Hill Medical; 2014.
14. ACOG Task Force on Hypertension in Pregnancy. Hypertension in Pregnancy.
Washington, DC: American College of Obstetricians and Gynecologists; 2013.
15. ACOG Committee on Practice Bulletins-Obstetrics. ACOG practice bulletin no.
123. Thromboembolism in pregnancy. Obstet Gynecol. 2011;118:718-729.
Suggested Websites
1. American Congress of Obstetricians and Gynecologists. www.acog.org

Chapter 15
ETHICS IN CRITICAL CARE M EDICINE
Objectives
Review the ethical principles guiding decision-making in critical care.

Explore ethical dilemmas that involve withdrawal of life support in critically ill
patients, do-not-attempt-resuscitation orders, nonbeneficial and medically futile
therapy, and triage.
Define and recognize the different types of advance directives used to guide care
for patients lacking medical decision-making capacity.
Outline the decision-making process used in medical ethics in the critical care
setting.
Case Study
Mrs. Clark, a hospitalized 72-year-old woman who had abdominal wall hernia repair
10 days ago, sustained a cardiac arrest after massive aspiration. Cardiopulmonary
resuscitation was initiated. She was found in asystole, but responded to intubation,
defibrillation, and epinephrine after some difficulty. She was transferred to the ICU but
developed severe acute respiratory distress syndrome. She now is unresponsive to
painful stimuli, her pupils are dilated and fixed, and corneal reflexes are absent. She is
hemodynamically stabilized with improving respiratory function. She remains in a deep
coma.
– Who should make decisions regarding the patient’s medical care, and on what
basis?
– What are the goals of care for this patient?
– Should further therapy be limited or withdrawn?
– What process should be utilized to address these issues?
– What potential dilemmas might arise in discussions with the patient’s family?
I. INTRODUCTION
Ethics is one of the foundations of laws, statutes, and regulations that govern the
practice of medicine in many countries. Application of ethical principles may vary in
different regions and nations. Ethics is not identical to existing laws; often it is in
critical tension with laws, leading to statutory change. Ethics is closely related to
morality, culturally accepted norms regarding right and wrong, but it is not reducible to
prevailing or conventional values. At its best, ethics may lead to substantive moral
reform.
Ethics is the branch of philosophy that deals with the concepts of what is right or wrong
conduct and what is good and bad. The basis of medical ethics is rooted in ancient
Greek theories of morality. Modern medical ethics has been influenced by the moral
theories formulated by Immanuel Kant, Jeremy Bentham, and John Stuart Mill.
Ethics is the critical, reflective consideration of moral practices in light of basic
principles of conduct and value. Medical ethics involves critical reflection on practices
such as clinical research, resource allocation criteria, relationships between patients
and their healthcare providers, and healthcare policy formulation. It is at the heart of the
patient-clinician relationship, which is grounded in trust. Healthcare professionals have
an obligation to act in their patients’ best interests, recognizing an inequality of
knowledge, information, and experience. Clinicians possess medical expertise but are
limited in their knowledge of patients’ goals and values. Shared decision-making is one
way of productively engaging these differences to produce what is in the best interest of
the patient while preserving the clinician’s professional integrity.
In the critical care context, three sets of circumstances typically bring patients at risk of
dying in the hospital to the emergency department: (1) an acute event in an otherwise
healthy person (such as trauma, stroke, myocardial infarction, or pneumonia); (2) a
recurrent or relapsing decompensation in a patient with a chronic and progressive
disease (such as respiratory failure in chronic lung disease, pneumonia complicating
dementia, heart failure in cardiomyopathy); or (3) the patient’s arrival at a critical point
in a progressive, unrelenting decline (such as cancer or dementia). Many of these at-risk
patients may be admitted to an ICU. Such patients may be unable to participate in
decisions about their medical care and depend upon advance directives or surrogate
decision-makers to guide the healthcare team regarding treatment.
The critical care team is involved in end-of-life care decision-making in three key
situations: (1) limitation of therapy and/or resuscitation attempts, (2) withdrawal of life
support, and (3) triage. Therefore, the critical care team must be able to effectively
communicate with patients and their families about prognosis and futility, reasonable
goals of therapy, healthcare advance directives, and options for limitation of
resuscitation efforts or removal of life support. Without formal discussions, patients’
preferences are difficult to predict; assumptions based upon quality of life, age, or
functional status may be inaccurate; and physicians’ choices may reflect their own
preferences rather than those of their patients.
Healthcare providers must be both cognitively and emotionally prepared to
communicate among themselves and with patients and families regarding: (1) realistic
goals, (2) expectations for treatments and alternatives, (3) patients’ expressed and
implied desires regarding medical interventions and the implications of those desires,
and (4) acceptable therapeutic options. Meaningful discussions of these issues are
grounded in a thorough understanding of medical ethics, individual and collective
cultural values, and pertinent legal principles. The competency of providers as
communicators correlates directly with patients’ and families’ satisfaction with the
medical care provided and also enhances the professional integrity of the providers.
II. THE GUIDING ETHICAL PRINCIPLES OF HEALTHCARE

In healthcare, ethical principles protect patient interests and inform professional
integrity. The guiding ethical principles of healthcare are a conceptual framework for
providing patient-centered care (care that is appropriately respectful of patients), and
for grounding the professional standards of healthcare practice that define excellence.
These principles are also helpful in identifying, analyzing, and contributing to the
resolution of ethical problems that occur in the practice of medicine. The four
commonly accepted ethical principles of healthcare are:
Autonomy: Respect the right of an individual to be self-directing and to make

decisions freely and independently; this recognizes the patient’s sovereignty over
his or her own body.
Beneficence: Act in the best interest of patients and promote their well-being.
Different value systems can lead to different concepts of what is best for an
individual patient.
Nonmaleficence: Primum non nocere, the Latin tenet which translates as “above
all else, do no harm.” Harm can be defined as the intentional or careless infliction
of physical, psychological, or emotional distress through either actions or
omissions.
Justice: Treat all persons fairly and equitably; treat similar cases in the same
manner and different cases differently.
III. ETHICAL DILEMMAS IN CRITICAL CARE

Many, if not all, ethical dilemmas can be handled professionally with utmost respect for
patient needs and professional integrity when decisions involve consideration of the
treatment situation, truthful exchange of information, thorough discussion of the patient’s
wishes and expectations, understanding of pertinent ethical principles, and coordination
among members of the healthcare team. Uncertainty and ambiguity on the part of the
physician, critical care team, patient, or family make meaningful discussion and
decisions difficult. The team leaders are responsible for ensuring that the healthcare
environment is characterized by open communication, caring, and support. In rare
situations where some members of the team have conflicting deeply held beliefs, serious
emotional conflicts, or conflicts of interest that preclude open and objective
communication and decision-making, they may request to be excused and transfer patient
care responsibilities to a colleague. Patients and families can sense uncertainty and
ambiguity, and are likely to react with suspicion and confusion. A consensus on the
goals of care and treatment plan also facilitates consistent communication and
documentation and minimizes liability risks. In institutions where ethics consultation
teams are available, their involvement has been regarded favorably by most
participants.
Consensus recommendations from the

healthcare team facilitate resolution of
ethical dilemmas.
A. Advance Directives
To make binding decisions such as refusal of recommended medical care or limitation
of resuscitation, a person must be legally able to do so. Incompetency is determined by
a court and is a judgment that a person lacks the abilities required to give or withhold
informed consent. While competent patients are legally empowered to make decisions,
unemancipated minors or mentally impaired individuals may not be competent for
decision-making purposes. Distinct from legal competence, the capacity to make
decisions refers to the ability to make informed, voluntary decisions in a specific
circumstance; because of medications, injuries, or metabolic derangements that impair
judgment, a patient may lack capacity. Patients must have both competence and capacity
to consent, to refuse, or to limit medical care, as well as to establish advance directives
regarding medical care. Their agreement must be obtained without fraud, duress, or
coercion after full, reasonable disclosure. The basis, process, and outcome of all
discussions leading to such decisions should be carefully documented to supplement any
required forms and clinician orders. Unlike consent to treatment, limitation or refusal of
treatment is never implied.
An advance directive is an instructional statement that takes effect at some time in the
future when specific conditions are met. A capable, competent person can often leave
verbal or written instructions directly for healthcare professionals and/or select a
surrogate to guide medical decisions. If patients have left unambiguous and detailed
instructions regarding their preferences for life-sustaining therapy in the event they
become incapacitated, such instructions are usually binding and carried out. However,
most patients’ instructions are neither sufficiently detailed nor unambiguous for the
circumstances of their future illness. The role of the surrogate decision-maker is to
inform the healthcare team of what the patient’s wishes and values would be under the
circumstances; the wishes and values, therefore, are not those of the surrogate but of the
patient. The surrogate makes a substituted judgment based on explicit instructions or
direct and indirect communication of the patient’s preferences and expectations. The
following tools may be used to convey a patient’s preferences:
Advance healthcare directive: This document contains specific, substantive

statements of the patient’s values and wishes regarding medical care. It may also
specify procedures that the patient wants to receive or forgo in specific
circumstances. In most cases, this document also enables the patient to name a
healthcare agent who will make decisions for the patient when incapacitated.
Durable power of attorney for healthcare: A durable power of attorney is a
proxy directive that assigns one person authority to perform specified actions on
behalf of the signer. The power is “durable” because, unlike the usual power of
attorney, it continues to be in effect if the signer becomes incompetent.
Healthcare proxy: A proxy is a person appointed by the patient specifically for
the purpose of making healthcare decisions on the patient’s behalf.
Next of kin: Under some circumstances, in some countries or states, the next of kin
are authorized by law to speak on behalf of an incapacitated patient. Surrogacy
hierarchies that must be considered in healthcare decision-making are often
defined by law. Ethically, the person who knows the patient best is the appropriate
surrogate decision-maker. This person may not be the legally identified next of kin.
The healthcare provider should be certain that the conditions for invoking an
advance directive as intended by the patient have occurred before acting upon the
directive. Similarly, acquiescing to requests made by surrogates occurs only after
consideration of proper medical and ethical decision-making principles. If an
incapacitated patient’s specific wishes and values are unknown, a surrogate is
usually expected to act in the best interests of the patient.
B. End-of-life Care and Termination of Life Support

The goal of end-of-life care is to allow patients to die with dignity and respect and to
exercise an element of control over their death. It is paramount that in all
communications it is made clear that care is not being withdrawn; rather, it is life
support or unwanted medical interventions that are withdrawn after the goals of
treatment have changed. In many cases, the intensity of care may actually escalate
following termination of life support as comfort needs are addressed. “Do not attempt
resuscitation” never means “do not treat.” Before the removal of life support, a proper
do-not-attempt-resuscitation (DNAR) order should be in effect based on local and
institutional regulations. A plan for comfort measures should be developed by the
healthcare team and must address anxiety and analgesia. Though they may have this
effect, comfort care interventions are not intended to directly hasten death; this
distinguishes comfort care from euthanasia and physician-assisted suicide.
C. Do-not-attempt-resuscitation Orders
DNAR orders, also known as do-not-resuscitate (DNR) orders, are explicit physician
orders restricting specific medical interventions in the event of a cardiopulmonary
arrest. Because resuscitation efforts are not always successful, it is more accurate to
refer to these as limitations on attempts to resuscitate. Such orders are usually based on
a patient’s expressed or written wishes or on such wishes as they are known to a proxy
or surrogate decision-maker. DNAR orders may include categorical specifications that
limit blood transfusions, intubation and mechanical ventilation, defibrillation,
cardiopulmonary resuscitation in an already mechanically ventilated patient, or an
escalation of existing ICU treatment. If such orders are agreed upon, it is usually
advisable to review all other treatment modalities to determine if they continue to be
compatible with the changed goals of care (e.g., dialysis, medically provided fluids and
nutrition, antibiotics). Factors that suggest a discriminatory intent must never form the
basis for initiating DNAR discussions; these factors include gender, age, race, and
economic or social status. Suicidal ideation and treatable depression must be excluded
as reasons for a patient’s wishes to limit resuscitation or terminate life support.
DNAR orders do not necessarily

preclude ICU admission or care; they
only limit resuscitation attempts.
D. Medical Futility/nonbeneficial Medical Treatment

Medical futility is a nebulous concept, which is why some prefer the concept of
nonbeneficial medical treatment. Both concepts generally refer to medical interventions
that are highly unlikely to contribute to a beneficial outcome for the patient. The key
problem associated with medical futility or nonbeneficial medical treatment is that it is
based on situational value judgments. Interventions perceived as medically futile or
nonbeneficial in one institution by some providers at a certain time may not be
perceived as such by others at a different time. These concepts are also based on the
anticipated outcome in terms of probability of survival, values regarding minimally
acceptable quality of life, and prognosis or time frame for possible recovery. Thus, a
determination of nonbeneficial or medically futile treatment should take into account the
predicted outcome, available medical evidence or experience, and patient expectations
and wishes. There is considerable ethical debate about whose views should prevail in
decisions regarding discontinuation or limitation of medical interventions when
providers and families disagree about the benefit. Depending on the circumstances, a
determination of nonbeneficial or medically futile treatment may be made by a team of
clinicians, an ethics team, or a legal process. Local conditions and policies will
prescribe the course to follow to implement a judgment that a medical intervention is
not beneficial.
Differences regarding nonbeneficial and

medically futile treatments are best
resolved through a fair, transparent
process.
E. Palliative Care
A relatively recent phenomenon in many hospitals and care delivery systems is the
development of palliative care services, interdisciplinary teams focused on maintaining
a patient’s comfort and quality of life. These teams are composed of medical, nursing,
spiritual, psychological, and complementary therapies integrated around comfort as the
goal of a patient’s treatment. Prolonging life is sometimes a secondary outcome of
palliative care, but it is not its primary intent. How well a patient lives, no matter how
long the patient has to live, is the basic concern for palliative care, which provides
treatments that will enhance a patient’s quality of life. Palliative care teams should be
enlisted when an interdisciplinary approach would help with a patient’s pain, suffering,
and distress. Palliative care can be an important adjuvant to the care of critically ill
patients even before decisions to limit life-sustaining treatments have been made.
Palliative care professionals can assist in end-of-life discussions with patients and
families as the goals of care shift from cure to comfort.
It is important to distinguish palliative care from hospice. Hospice is a modality of care
that focuses on the dying patient and aims to provide the optimal conditions for the end
of life, forgoing a range of medical interventions that are primarily curative or life
prolonging in nature. Palliative care may transition to hospice care, but is appropriate
whenever a patient experiences pain or distress that is medical as well as existential. A
terminal diagnosis may prompt a palliative care consultation.
F. Triage
The ICU is characterized by resource-intensive medical care. Because ICU technology,
physician presence, and staffing are costly and limited, triage decisions regarding the
allocation of these resources are frequently necessary. Triage is most often necessary
when demand for critical care beds exceeds supply. Thus, patients may be denied
admission based on resource constraints; be transferred from the ICU to another level of
care based on severity of illness, prognosis, or wishes; or be transferred to another
institution. The minimum severity of illness required to meet ICU admission criteria is
likely to fluctuate within an institution (such as during influenza season or disaster
situations). Increasingly, however, patients who do not meet some minimum objective
criteria for ICU admission are cared for on the wards regardless of the preference of
patients, attending physicians, or staff. Critically ill patients who are not admitted to
ICUs may have significantly greater morbidity and mortality rates. Therefore, triage
choices represent life-and-death decisions that must be based upon criteria that are as
objective as possible and applied uniformly. The ethical principle of beneficence is
applied at the group or social level in such cases (maximize the benefit to the most) and
is restrained by the principle of justice (treat all similar cases the same and different
cases differently).
G. Organ Donation
After discussions regarding the extent of medical treatments have been completed and a
decision to withdraw life support has been made, organ-procurement representatives
should be allowed to evaluate the patient and conduct discussions with the patient’s
family or surrogate decision-maker about the potential for organ donation. Options
include both conventional organ recovery after declaration of neurological death and
potential organ donation after cardiac death. See Appendix 6 for more information on
brain death and organ donation.
IV. ETHICS AT THE BEDSIDE

When faced with an ethical dilemma, clinicians should incorporate one or more of the
guiding ethical principles of healthcare into a framework for resolution. As each
principle is systematically addressed, specific components of conflict can be identified
and their analysis can often be simplified. The clinician should always start with the
medical facts of the patient’s case and then proceed to related topics. Specific issues
may include:
Who should be involved in the discussion

Whether time constraints apply
Whether the chronology of events or decisions is important
What additional medical, legal, or social information is needed to facilitate
decision- making
What communication pathways will work best to resolve possible conflict
What values or rules are important to the patient, the family, and the institution
What areas of consensus already exist among the participants
Any unsettled matters often can be organized into a series of steps within the process of
resolution. Depending on the nature of the dilemma, other experts may be called upon
for specific input. An ethics consultant is often able to clarify the issues involved and to
work toward a successful resolution of any differences. Some issues may need repeated
examination to determine how to provide the highest level of medical and moral good
for the patient. Some important elements of ethical decision-making are summarized in
Table 15-1.
Table 15-1 Key Elements of Ethical Decision-Making
Whenever possible, initiate discussions with patients regarding their preferences for life support
before a medical crisis occurs and they lose capacity to make informed decisions.
Utilize hospital and/or unit end-of-life care protocols. If protocols are not in place, healthcare
providers should work with appropriate legal and ethical advisers to develop them.
Direct discussions with patients and families to set appropriate goals of care based on patient
values, wishes, and preferences, taking into account the best diagnostic and prognostic judgments.
Ensure that all decisions related to consent, refusal to consent, limitation of resuscitation attempts,
or termination of life support are clearly determined and documented according to policy and
regulation.
Make certain that all end-of-life care decisions are made with full disclosure of alternatives,
implications, and potential conflicts of interest; are free of duress and coercion; and are made by
persons who are competent and have decision-making capacity.
Ensure adherence to ethical principles and professional and legal standards of medical conduct.
Communicate clearly and document extensively.
Develop consensus and a plan with the care team and, when indicated, involve support services
such clergy, ethics committee or consultant, social services, palliative care services, or hospital
council.
Each patient’s situation is unique and requires continual, caring communication and
reassessment of needs and goals. Clinical judgment, practical wisdom, common sense,
compassion, and empathy are the key attributes required by clinicians involved in any
ethically complex problem.
V. CASE STUDIES
A. Case 1: Advance Directives and Treatment Limitations

Mrs. Clark, a hospitalized 72-year-old woman who had abdominal wall hernia repair
10 days ago, sustained a cardiac arrest after massive aspiration. Cardiopulmonary
resuscitation was initiated. She was found in asystole, but responded to intubation,
defibrillation, and epinephrine after some difficulty. She was transferred to the ICU but
developed severe acute respiratory distress syndrome. She now is unresponsive to
painful stimuli, pupils are dilated and fixed, and corneal reflexes are absent. She is
hemodynamically stable with improving respiratory function. She remains in a deep
coma.
Analysis
This is a frequent scenario and often involves issues of limitation or withdrawal of
treatments. The principles of autonomy, beneficence, nonmaleficence, and justice are
presumed to apply in all clinical situations, though the role of each in a specific case
may vary in importance. Whenever possible, the members of the healthcare team should
reach a consensus regarding their prognosis and recommendations before family
discussions are initiated. However, early in the course of ICU care, it must be
determined whether the patient’s preferences were specified in advance and/or who is
authorized to make decisions on the patient’s behalf. The patient’s preferences and
attitudes regarding an acceptable minimum quality of life are essential here. The ICU
team should work closely with the patient’s primary care physician, with whom the
family is likely to have rapport. A palliative care consultation may be helpful. The
palliative care team may facilitate discussions with the family, especially if the goals of
care may transition to a focus on quality of life and comfort. The early involvement of
clergy and members of the ethics team may be beneficial in establishing the values and
goals of care that the patient would find acceptable.
The care team must convey a realistic attitude, using evidence-based data, accepted
prognosis models, case studies, and anecdotal experience whenever possible, while
acknowledging that all prognostication has a subjective component. Communication of
medical information is important, especially regarding reflexes and responses that may
appear to be signs for eventual recovery. Further diagnostic information should be
considered if it may guide the surrogate decision-maker. A computed tomographic scan
may strengthen the prognostic stance. The help of a neurologist may be indicated to
underscore estimates of recovery from anoxic brain injury.
The patient’s values, wishes, and directives, together with the diagnostic and prognostic
information, should lead to establishing the appropriate goals of continued medical
care. In light of these goals, the issues of tracheostomy, medical provision of fluids and
nutrition, and further resuscitation attempts in the event of another cardiac arrest must be
explored. It is appropriate to discuss both possible ramifications of discontinuing life
support and long-term care issues. Documentation is important, and the elements of each
conversation and the bases for prognosis should be clear.
Finally, if the patient has left no advance directives and the surrogate cannot decide on
the goals of care or the appropriateness of specific medical treatments, providers cannot
coerce a decision based on their personal values, the guilt of the surrogate, or resource
constraints. Continued support and guidance are always warranted; a decision may be
forthcoming at a later date. However, when the patient is no longer critically ill and
unstable, transfer to another unit is acceptable.
B. Case 2: Triage
Mrs. Williams, a 93-year-old patient with a history of dementia and medical problems
including hypertension, diabetes, and end-stage renal failure, presents with sudden-
onset seizures and waxing and waning mental status. She was recently discharged with a
recommendation for hospice, which her family declined. She has a lactic acid
measurement of 12 mmol/L, and the hospitalist is uncomfortable managing her on the
medical floor and requests that she be transferred to the ICU. The ICU is full, and the
best candidate for transfer is Mr. Aaron, a 45-year-old man with intracranial
hemorrhage who was admitted 12 hours ago, is hemodynamically stable, and is not
being ventilated. He is in danger of developing intracranial hypertension and worsening
cerebral edema and may require intubation for airway protection.
Analysis
This is a triage/resource-allocation dilemma. The demand for ICU beds at the institution
exceeds the supply, which requires a caring application of distributive justice. If
defined hospital and ICU policies and protocols exist, they must be followed. The
attending intensivist, as the leader of the critical care team, is responsible for
determining how resources will be allocated. Mr. Aaron, the patient with the
intracranial hemorrhage, is at high risk for acute decompensation outside the monitored
setting of the ICU, and his long-term prognosis may not be better than that of Mrs.
Williams; however, his clinical course is indeterminate at this time. Mrs. Williams has
had a progressive decline in function, and medical therapy is becoming less beneficial.
Aggressive care has not changed her course in the past, yet her family continues to hope
for recovery and has chosen not to limit medical treatments or resuscitation attempts. It
is appropriate to revisit the topic of limiting resuscitation attempts, calmly and
dispassionately; however, to avoid coercing the surrogate into a decision based on
feelings of guilt, the triage considerations should not be a focus of the discussion. The
triage decision is made on the basis of criteria that take into account the good of all
patients, not just that of Mrs. Williams. This is a medical staff decision, not an
individual patient care decision. There are three feasible alternatives: transfer Mrs.
Williams to the ICU in place of Mr. Aaron, transfer Mrs. Williams to an institution with
available ICU beds, or deny Mrs. Williams ICU admission at the present time.
Based on the immediate clinical situation, denial of ICU admission may be the most
reasonable option. Though patient autonomy must be respected, it is not the preeminent
ethical principle in situations of triage. Promoting the well-being of the patient with
intracranial hemorrhage (beneficence) must be weighed against possible harm to the
older patient with seizures and dementia (nonmaleficence). If justice requires
maximizing the good to be produced by the allocation of scarce resources, and this is
achieved by refusing to admit Mrs. Williams to the ICU, it is the ethically correct
decision. Supportive measures for Mrs. Williams should continue to the extent possible
on the ward. The family should be notified that she has taken a turn for the worse and
that best available care is being provided. If she continues to deteriorate without a
response to therapy and an ICU bed remains unavailable, discussions with Mrs.
Williams’ family regarding the value of aggressive therapy may be appropriate. Careful
documentation must accompany all treatment decisions and discussions. Clergy and the
ethics committee may be notified if appropriate. Administrative notifications or advice
of hospital counsel may also be needed.
C. Case 3: Nonbeneficial or Medically Futile Treatments and End-of-Life Care

Ms. Crocker is a 40-year-old divorced woman with paralysis from a rare metastatic
spinal cord tumor. She was discharged to hospice from another facility and then
consulted a radiation oncologist with hopes of achieving palliation and more time with
her three young children. The radiation oncologist reluctantly offered to try a single
massive dose of radiation. She was admitted, but before the radiation therapy, she
developed severe respiratory distress. She now is intubated and ventilated, is
hemodynamically unstable, and has progressive neurological deterioration. Her parents
and family indicate that she would like “everything done” to possibly prolong her life
and to complete the planned radiation therapy.
Analysis
This is an unfortunate scenario repeated often in similarly tragic circumstances. Next of
kin often say their loved one would want everything done, even under circumstances that
indicate likely futility. The term medical futility is a value-laden concept and may not
have the same meaning for providers and patients or their families. The term
nonbeneficial medical treatment better reflects a medical judgment as to the possible
effects of a treatment. In this case, progressive neurologic deterioration prohibits any
further consideration of radiation for Ms. Crocker. The family still has hope of recovery
in spite of her grim prognosis. While patient autonomy should be respected, there are
many barriers and limits to exercising autonomy in the ICU. The patient’s loss of
decision-making capacity often leads to disagreements among surrogates and family
members. There may be uncertainty in interpreting the patient’s advance directives.
Determining which values would now be most important to the patient is frequently a
source of discord. In this case, Ms. Crocker’s family must be made aware that in
addition to respecting her wishes, they must consider what would be in the best interests
of their loved one. A reasoned clinical assessment would be that prolonging her life
under these circumstances will result in harm to Ms. Crocker without compensating
benefit. Continuing aggressive medical treatments would not be beneficial.
Recommending compassionate extubation and comfort as the goals of care is ethically
appropriate. Sensitive presentation of this alternative to Ms. Crocker’s family, along
with the grounds for the clinical judgment, may eventually lead the family to agree that
focusing on her comfort is in her best interest. Ethics consultation, clergy counselling,
and palliative care services may assist in this discussion and facilitate this transition in
the goals of her care.
Key Points
Ethics in Critical Care Medicine

Healthcare professionals have an obligation to act in a patient’s best interests
based upon the ethical principles of autonomy, beneficence, nonmaleficence, and
justice.
When faced with an ethical dilemma, consensus from the healthcare team on the
diagnosis, prognosis, and recommended treatment plan facilitates consistent
communication and documentation and minimizes liability risks.
Specific components of conflict within an ethical dilemma can be identified and
the analysis simplified when each ethical principle is addressed systematically.
Life support may be withdrawn at the end of life, but care is never withdrawn.
Suggested Readings
1. Beauchamp TL, Childress JF. Principles of Biomedical Ethics. 4th ed. New York,
NY: Oxford University Press; 2008.
2. Cassell J, Buchman TG, Streat S, et al. Surgeons, intensivists, and the covenant of
care: Administrative models and values affecting care at the end of life. Crit Care Med.
2003;31:1263-1270.
3. Consensus statement of the Society of Critical Care Medicine’s Ethics Committee
regarding futile and other possibly inadvisable treatments. Crit Care Med.
1997;25:887-891.
4. Davidson JE, Powers K, Hedayat KM, et al. Clinical practice guidelines for
support of the family in the patient-centered intensive care unit: American College of
Critical Care Medicine Task Force 2004-2005. Crit Care Med. 2007;35:605-622.
5. Dumanovsky T, Augustin R, Rogers M, et al. The growth of palliative care in US
hospitals – A status report. J Palliat Med 2016;19:8-15.
6. Giacomini M, Cook D, DeJean D, et al. Decision tools for life support: A review
and policy analysis. Crit Care Med. 2006;34:864-870.
7. Kelley A, Morrison R. Palliative care for the seriously ill. N Engl J Med
2015;373:747-755.
8. Kummer HB, Thompson DR, eds. Critical Care Ethics: A Practice Guide. 2nd ed.
9. Luce JM, White DB. A History of ethics and law in the intensive care unit. Crit
Care Clin. 2009;25:221-237.
10. Luce JM. A history of resolving conflicts over end-of-life care in intensive care
units in the United States. Crit Care Med. 2010;38:1623-1629.
11. Prendergast TJ, Puntillo KA. Withdrawal of life support: Intensive caring at the
end of life. JAMA. 2002;288:2732-2740.
12. Siegel MD. Alone at life’s end: Trying to protect the autonomy of patients without
surrogates or decision-making capacity. Crit Care Med. 2006;34:2238-2239.
13. Sur MD, Angelos P. Ethical issues in surgical critical care: The complexity of
interpersonal relations in the surgical critical care unit. J Intensive Care Med.
2016;31(7):442-450.
14. Szalados JE. Do-not-resuscitate and end-of-life care issues: Clinical, ethical, and
legal principles. Curr Rev Clin Anesth. 2003;24:47.
15. Thompson DR, Kaufman D. Critical Care Ethics: A Practical Guide. 3rd ed.
16. Truog RD, Cist AF, Brackett SE, et al. Recommendations for end-of-life care in the
intensive care unit: the Ethics Committee of the Society of Critical Care Medicine.
Crit Care Med. 2001;29:2332-2348.
17. West Yorkshire Adult Critical Care Operational Delivery Network. End of Life
Care Bundle. http://www.wyccn.nhs.uk/Pages/Care%20Bundles.aspx. Accessed
April 28, 2016.
18. White DB, Curtis JR, Lo B, et al. Decisions to limit life-sustaining treatment for
critically ill patients who lack both decision-making capacity and surrogate
decision-makers. Crit Care Med. 2006;34:2053-2059.
19. Wueste DE. A philosophical yet user-friendly framework for ethical decision
making in critical care nursing. Dimens Crit Care Nurs. 2005;24:70-79.
Suggested Website
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org

Chapter 16
CRITICAL CARE IN INFANTS AND CHILDREN: THE

BASICS
Objectives
Review pediatric physiology and pathology.

Understand differences in adult and pediatric critical care.
Describe modifications to adult therapies in order to support children
appropriately.
Case Study
A 6-month-old female infant, who was born at 30 weeks’ gestation, presented with
fever, tachypnea, rhinitis, and coughing for 4 days. On arrival at the pediatric emergency
department, she had a heart rate of 150 beats/min, respiratory rate 60 breaths/min,
oxygen saturation of 90%, and temperature of 38.5°C (101.3°F). She had subcostal and
upper sternal retractions, was tachypneic and agitated, and had copious upper airways
secretions. Auscultation revealed diffuse rhonchi. She was given 100% oxygen and
albuterol via a nebulizer, with minimal improvement.
– What is the most important initial intervention?
– What are the most immediate treatment strategies?
I. INTRODUCTION
The preceding chapters have emphasized principles of critical care and management of
a variety of conditions in adult patients. This chapter focuses on the basic management
of certain pediatric conditions. An in-depth review of this subject can be found in the
Pediatric Fundamental Critical Care Support (PFCCS) program. This chapter will
introduce a key PFCCS learning and management concept that can be summarized with
the acronym, DIRECT: Detection, Intervention, Reassessment, Effective
Communication, and Teamwork. Each section is preceded by a case study that will
illustrate this concept.
Infants and children have different body habitus and immature physiology and anatomy.
Therefore, manifestations of critical illness differ from those in adults, and interventions
must be modified.
Common early signs of distress are

tachypnea and tachycardia.
II. GENERAL EXAMINATION

Because young children are unable to verbalize specific complaints, medical evaluation
depends heavily upon physical examination and information obtained from a parent or
guardian. Although early signs of distress may be subtle, early recognition may increase
the likelihood that interventions will be successful and prevent more serious
progression. When early signs of illness are missed, healthcare providers may assume
that a child’s condition has suddenly deteriorated; in fact, the seemingly abrupt change
reflects an advanced point along a continuum of physiologic compromise. Table 16-1
lists important factors to be considered in the general examination of pediatric patients.
Tables 16-2 and 16-3 provide age-appropriate normal values for vital signs and blood
volume.
Table 16-1 Important Aspects of the Physical Examination
Skin perfusion: Check for loss of normal pink mucosa and nail beds, mottling that has replaced the
usually uniform skin color over the trunk and extremities, skin that has lost its warmth, and the slowing of
capillary refill. Capillary refill should be less than 2 seconds and determined with the extremity above the
level of the patient’s heart.
Degree of hydration: A dehydrated infant may have a sunken fontanelle in addition to signs that may be
seen in older children, such as absent tears, sunken eyes, skin tenting, and dry mucous membranes. A
severely dehydrated child may look toxic and lethargic.
Level of spontaneous reactivity and responsiveness: Ill children may have increased irritability
initially, often followed by decreased responsiveness and increasing flaccidity. In most infants, alertness
can be evaluated by observing their ability to fixate on objects, particularly a parent’s face. Infants should
turn toward sound and should follow an object horizontally and, within 1 month of age, vertically. Older
children should exhibit stranger anxiety and show clear recognition of parents.
Position spontaneously assumed for comfort: Illness may be marked by the inability to find a position
of comfort or to find more than a single position of comfort. Patients should not be forced to assume
another position, as this could potentially compromise a tenuous airway.
Tachypnea: Rapid breathing is an important sign of illness in infants and young children. Etiologies
include respiratory disease, hypovolemia, hyperviscosity syndromes, hyperglycemia, heart failure,
adverse drug effect, metabolic acidosis, fever, pain, and anxiety.
Bradypnea: This ominous sign may be due to hypothermia, central nervous system injury, drug-induced
depression, neuromuscular disease, severe shock, metabolic disorders, and respiratory exhaustion.
Grunting during exhalation: This ominous sign may occur as part of respiratory distress, pain, or intra-
abdominal disorders.
Nasal pathway: The nose is the primary route for normal breathing in an infant. Total airway resistance
and the potential for compromised breathing are increased significantly in infants with nasal congestion or
increased secretions, or by the presence of a nasogastric tube. Nasal flaring is a sensitive indicator of
respiratory distress in the infant.
Early hypovolemic shock: The most reliable indicators of early compensated hypovolemic shock in
children are persistent tachycardia, cutaneous vasoconstriction, and decrease in pulse pressure. Signs of
decreased tissue perfusion include skin mottling, prolonged capillary refill, and cool extremities. Systemic
arterial blood pressure is frequently normal because of a compensatory increase in systemic vascular
resistance. The neurologic status is normal or only minimally impaired. It remains important to measure
blood pressure, as a low value suggests a decompensated state and requires immediate intervention.
Seizures: Seizures may be characterized by decreased alertness (the infant does not regard parents or
track an object across the visual field), staring, autonomic changes (tachycardia, elevated blood pressure,
and dilated pupils), apnea, and subcortical muscle activity (bicycling movements of the legs, swimming
movements of the arms, sucking, or tongue-thrusting movements). Tonic-clonic muscle motion may not
occur in infants due to an immature nervous system.
Infection: Fever should always suggest the possibility of infectious disease. In the neonate, infection
usually involves bacteremia. Respiratory distress, temperature instability (including hypothermia), and
gastrointestinal signs are common clinical findings of sepsis.
Table 16-2 Vital Signs in Childrena
Age Group Heart Beat (beats/min) Respiratory Rate (breaths/min) Blood Pressure (mm Hg)
Premature 120-170 40-70 55-75/35-45
Newbornb 110-160 30-60 65-85/45-55
Infant 90-150 25-45 70-100/50-65
1-3 years 80-125 20-30 90-105/55-70
3-6 years 70-115 20-25 95-110/60-75
6-12 years 60-100 14-22 100-120/60-75
>12 years 60-100 12-18 100-120/70-80
aIn children, MAP can be estimated by 55 + (age x 1.5).
bIn neonates, MAP can be estimated by gestational age.
Table 16-3 Blood Volume in Children
Age Group Weighta (kg) Blood Volume (mL/kg)
Premature 0.5-1.5 100

Neonate 3.5 90
6 months 6.5 80
1 year 10 75
Adolescent >40 65-70
aWeight can be estimated by 2 x (age + 4)
III. EVALUATION BY ORGAN SYSTEM

Healthcare providers attending to critically ill pediatric patients must be able to
promptly recognize respiratory, cardiovascular, metabolic, immunologic, and
neurologic problems in children. Important differences between children and adults and
basic treatment strategies are summarized below.
A. Respiratory System/airway
Pediatric airway management is challenging due to the anatomic differences that exist
between small children and adults as well as among children of different ages.
Recognition and interruption of the progression from respiratory compromise to
respiratory failure is fundamental to pediatric airway management. The ability to
recognize airway compromise and to establish and maintain a patent airway is essential.
1. Anatomic and Physiologic Considerations

In the airway of a child, changes will evolve gradually from birth until approximately 8
years of age, when the airway becomes anatomically similar to that of an adult. In
addition to airway disorders related to small size and normal anatomic development,
congenital abnormalities can affect the pediatric airway. After children reach age 8,
their upper airway problems become similar to those found in adults.
Children have important thoracic and pulmonary differences from adults. The thorax is
more cartilaginous in infants and young children and therefore more compliant.
Increased intrathoracic pressure during respiratory distress is less efficient at
augmenting tidal volume because the chest retracts inward, reducing tidal ventilation
and indirectly increasing the work of breathing. Soft-tissue retractions similarly reduce
thoracic volume during vigorous respiratory efforts. The infant’s ribs are aligned in a
more horizontal plane and decrease the inspiratory displacement of the thorax in the
anteroposterior plane, further decreasing the efficiency of the bellows effect. The points
of muscular insertion of the diaphragm on the thorax also are more horizontal in the
infant, similar to the thorax of an adult with obstructive lung disease and a flattened
diaphragm. Therefore, the lower thorax may be drawn inward during inspiration,
causing reduced inspiratory volume. Immature intercostal muscles cannot assist active
ventilation for several years after birth; thus, more dependency is placed upon
diaphragmatic function and excursion. Compromise of diaphragmatic excursion by
gastric distention, abdominal distension, and surgery may quickly compromise
respiratory function.
Alveolar size and number, as well as lung compliance, increase substantially during
childhood. Tidal volume remains fairly constant through childhood at 6 or 7 mL/kg.
Smaller anatomic conducting airways may produce high resistance if further narrowed
by inflammation, edema, mucus, bronchospasm, and bronchiolitis. High peripheral
airway resistance may also alter exhalation, induce dynamic closure of the airways, and
cause auto-positive end-expiratory pressure (auto-PEEP).
2. Airway Management
The first consideration in airway management is head position. An obtunded child or
one otherwise unable to maintain a position of comfort should be placed in the sniffing
position to minimize upper airway obstruction from soft tissues. The sniffing position is
accomplished by placing the child on a hard surface and rotating the head back so that
the child’s face is directed upward. The head is extended while the neck is flexed. A
roll beneath the shoulders can help maintain the infant’s head position due to the
relatively high head circumference. In the child older than 2 years, the sniffing position
may be accomplished by placing a folded towel or sheet under the child’s occiput. If
able, children should be allowed to choose a position of comfort. Gentle in-line
stabilization in the neutral position is used in children with suspected cervical spine
injury, and further manipulation is restricted to the jaw-thrust maneuver. Insertion of an
oropharyngeal or endotracheal airway must be done with minimal cervical movement.
Assistance from video laryngoscopes may be helpful in this setting.
Simply suctioning the nasal passages
can be an important intervention in
establishing airway patency.
An infant’s oxygen consumption is two to three times that of an adult. Residual oxygen
reserves in the lung are rapidly depleted if oxygen availability is compromised, leading
quickly to hypoxemia. Children have lower hemoglobin levels than adults. Because
cyanosis occurs only when a critical level of unsaturated hemoglobin is present, blood
oxygen content will be lower than adults before cyanosis is evident. Therefore, 100%
oxygen should be administered to all dyspneic children in whom respiratory
compromise is suspected. Pulse oximetry is accurate and should be used to titrate the
fraction of inspired oxygen. The mask used for oxygen supplementation may cause
agitation in children, and several devices should be available for trial. Supplemental
oxygen should be warmed and humidified if possible to avoid heat and evaporative
water losses from the airway or secretion thickening. The nasopharynx in infants is
large compared to the tidal volume and inspiratory flow achieved, so a nasal cannula
will provide a higher inspired oxygen concentration than in an adult. Issues relating to
intubation are summarized in Table 16-4.
100% oxygen should be promptly

administered to children in distress.
Table 16-4 Endotracheal Intubation in Children
Positive pressure created during bag-mask ventilation may quickly cause gastric distension; a
nasogastric tube may be needed. Gastric distension not only promotes vomiting and aspiration but
also interferes with ventilation and leads to acceleration of hypoxemia during mask ventilation.
Because the infant has a large occiput, the head flexes forward onto the chest when the infant is
supine and the head is midline. In the absence of neck injury, the child’s head should be placed in the
sniffing position with the assistance of a shoulder roll. However, extreme neck extension can obstruct
the airway.
The tongue in infants and children up to approximately 2 years of age occupies a relatively large
portion of the oral cavity and may cause obstruction to spontaneous or assisted ventilation and
intubation.
The anterior and cephalad position of the larynx makes blind nasal intubation difficult. In addition, the
adenoidal tissue may be enlarged. Blind passage of a relatively rigid tube through this area can
cause uncontrollable bleeding. The nasal route is discouraged.
The epiglottis is floppy and often obscures the glottic opening because of its angle of attachment to
the larynx and its relative lack of cartilage.
Cricoid pressure may improve exposure of the glottis. The maneuver is accomplished by applying
gentle pressure toward the spine at the level of the cricoid cartilage without displacing the larynx in
the cephalad direction. Lateral displacement may also be helpful for tracheal visualization.
An oversized endotracheal tube may cause inflammation, edema, and permanent injury to the
trachea. In general, a properly sized tube is about the diameter of the child’s small finger. In children
older than 2 years, the following formula is used to determine the appropriate uncuffed endotracheal
tube size: age/4 + 4, with 0.5 subtracted for cuffed tubes. The use of cuffed endotracheal tubes is
safe for infants and children. Cuffed endotracheal tubes may be especially useful in certain clinical
conditions, such as poor lung compliance, large air leak, or high airway resistance. The cuff inflation
pressure should be monitored and ideally <20 cm H2O and not >30 cm H2O.
The trachea is short enough that special care must be taken to avoid bronchial placement of the
endotracheal tube. A formula to estimate depth is the endotracheal tube inner diameter x 3.
3. Respiratory Failure
The anatomical and developmental factors described result in low respiratory reserve
in the pediatric patient. Therefore, the etiology of cardiopulmonary arrest in pediatric
patients is most commonly the result of a respiratory disorder. The majority of deaths in
children (especially those younger than 1 year) involve respiratory disorders resulting
from infection, poisonings, trauma, submersion or suffocation, and sudden infant death
syndrome. Airway obstruction, aspiration, and apnea are also among the most common
hazards to respiratory function. Thus, assuring a patent airway is the most important first
step in care of the child with respiratory compromise. Neonates and young infants use
the nasal airways as their primary route of respiration and so nasal airway obstruction
may lead to dyspnea. In young children, common causes of respiratory failure include
airway obstruction, congenital disorders, infections (viral croup, bacterial tracheitis, or
less commonly, epiglottitis), or ingestion or aspiration of a foreign body (Table 16-5).
Clinical examination helps to identify the site of obstruction and treatment options.
Table 16-5 Causes of Respiratory Failure
Premature Apnea of prematurity

neonates
Infant respiratory distress syndrome (surfactant deficiency and ineffective chest
bellows)
Term neonates Bacterial pneumonia

Meconium aspiration
Congenital airway abnormalities
Infants, toddlers Pneumonia
Bronchiolitis
Asthma
Foreign-body aspiration
Upper airway obstruction due to infection
Airway obstruction above the thoracic inlet tends to cause stridor (inspiratory noise),
whereas intrathoracic obstruction tends to cause wheezing (expiratory noise).
Upper airway infection (viral croup) and other conditions (e.g., laryngeal edema) may
be relieved by racemic epinephrine nebulization (0.05 mg/kg, maximum of 0.5 mg in 3
mL normal saline) and intravenous steroids (dexamethasone 0.3 mg/kg every 6 hours).
Lower airway infections of viral origin (respiratory syncytial virus) are frequent in
small children and can produce significant wheezing that may respond to
bronchodilators.
Children with asthma or acute bronchospasm should receive supplemental oxygen,
inhaled β-agonist, and corticosteroids (methylprednisolone). β-Agonists may be
administered intermittently or as continuous nebulization therapy. The dose will depend
on the patient’s age. Children younger than 1 year may receive 0.63 mg/3 mL normal
saline; those between 1 and 5 years get 1.25 to 2.5 mg/3 mL normal saline. For children
between 5 and 12 years, the dose is 2.5 mg, and those older than 12 years receive 2.5 to
5 mg every 4 to 6 hours. The suggested initial dosage for methylprednisolone is 1 mg/kg
intravenously every 6 hours. Anticholinergic therapy with ipratropium bromide (500
µg/2.5 mL normal saline) may be beneficial. In acute bronchospasm, intravenous
terbutaline: loading dose of 2 to 10 µg/kg infused for 10 minutes, followed by a
continuous infusion of 0.1 to 10 µg/kg/min may also be given.
Primary respiratory disorders are the

most common cause for
cardiopulmonary arrest in children.
Patients with upper or lower conditions, including bronchiolitis or asthma requiring low
oxygen concentrations, may benefit from an oxygen-helium mixture (30% oxygen, 70%
helium).
4. Mechanical Ventilation
The principal concepts of mechanical ventilation are similar in pediatric patients, but
specific settings and adjustments may vary. The suggested initial mechanical ventilation
settings for infants who weigh <5 kg are presented in Table 16-6.
Table 16-6 Initial Mechanical Ventilator Settings: Infants Weighing <5 kg
Mode Time-cycle, pressure- or volume-limited ventilation

Peak inspiratory Start at 18-20 cm H2O and titrate to a pressure that provides adequate chest
pressure movement and tidal volumes
Tidal volume 6-8 mL/kg (avoid >10 mL/kg)
Respiratory rate 30-40 breaths/min, adjust to maintain acceptable PaCO2 levels
Positive end-expiratory 5 cm H2O
pressure
Remember that tidal volumes measured by the ventilator also incorporate breathing
circuit expansion and gas compression volumes, which can constitute a substantial
portion of the total volume. Loss of ventilation can occur because the ventilator tubing is
distended lengthwise and circumferentially by increases in peak airway pressure that
create a backpressure. The amount of gas from the tidal inhalation that is trapped in the
ventilator tubing is a function of the airway pressure and the distensibility (compliance)
of the tubing. Soft plastic used in ventilator tubing distends more than hard plastic,
increasing the compliance volume. As much as 3 to 4 mL of gas per centimeter H2O
airway pressure may be trapped in the adult ventilator tubing at end inspiration. This
gas remains in the tubing at peak inhalation without entering the lung and then exits the
circuit through the exhalation valve as exhalation begins. This loss of alveolar
ventilation is of less consequence in an adult with a tidal volume of 500 mL than it is in
a child with a tidal volume of 150 mL. Specialized pediatric and neonatal circle
systems are recommended, as they are less compliant.
Increased airway pressure is most often

due to increased lung resistance or
decreased compliance or ventilator
tubing/ETT compression.
Suggested initial ventilator settings for pediatric patients >5 kg are summarized in Table
16-7. If volume-controlled ventilation is used, attention to the peak inflation pressure
prevents barotrauma (keep <30 cm H2O). If pressure-controlled ventilation is used,
attention to tidal volume (<8 mL/kg) is necessary to prevent hypoventilation or
volutrauma, and tidal volume may fluctuate with changing lung compliance. Always
observe the chest rise at initiation of mechanical ventilation and when tidal volume is
adjusted. Sedation may be useful with increased respiratory rates and/or increased tidal
volume.
Table 16-7 Initial Mechanical Ventilator Settings: Infants Weighing >5 kg
Mode Time-cycled, (volume- or pressure-limited)

Tidal volume 6-8 mL/kg for normal lungs or 6 mL/kg for acute lung injury/acute
respiratory distress syndrome (do not exceed 10 mL/kg)
Peak inspiratory pressure Start at 18-20 cm H2O and titrate to a pressure that provides adequate
(pressure-limited SIMV) chest movement and tidal volume not to exceed 10 mL/kg
Inspiratory time Babies: 0.5-0.6 sec
Toddlers: 0.6-0.8 sec
School-aged children/teens: 0.8-1.2 sec
Respiratory rate Rates vary according to age:
– Toddlers, 25-35/min
– Preschool, 20-30/min
– School age, 15-25/min
– Teens, 10-20/min
Adjust to maintain acceptable PaCO2 levels
Pressure support 5-10 cm H2O above PEEP to overcome resistance of endotracheal tube
Positive end-expiratory 5 cm H2O; higher levels in acute lung injury for alveolar recruitment
pressure
Abbreviation: SIMV, synchronized intermittent mandatory ventilation; PEEP, positive end-expiratory pressure
B. Cardiovascular System
1. Anatomic and Physiologic Considerations

The circulating blood volume is higher per kilogram in children than in adults, but the
absolute volume remains low because of the small body size. Therefore, small amounts
of blood loss are less tolerated by children. Blood replacement is indicated when 5% to
10% of the circulating volume has been lost. Allowable blood loss can be calculated
using the formula:
Allowable Blood Loss = [EBV*(Hi-Hf)]/Hi
where Hi is initial hemoglobin, Hf is allowed hemoglobin, and EBV is estimated blood
volume in mL/kg.
Cardiac output is high per kilogram of weight at birth, but the absolute amount is small
(~ 600 mL/min) and largely depends on a rapid heart rate because the small
uncompliant heart results in low stroke volume. In children, cardiac output remains
dependent upon changes in heart rate. Therefore, bradycardia may greatly limit systemic
perfusion and is most often an ominous sign of significant hypoxemia or acidosis. In
children younger than 6 years, a heart rate <60 beats/min with decreased perfusion (low
blood pressure, poor pulses) is an indication for chest compressions. Other arrhythmias
usually do not produce significant changes in cardiac output, except when
tachyarrhythmias occur, including sustained supraventricular tachycardia. Ventricular
arrhythmias are uncommon but, when present, may signify congenital heart disease,
myocarditis, cardiomyopathy, electrolyte abnormalities, or asphyxia.
Myocardial maturation influences the heart’s response to volume challenges intended to
increase preload. Before the age of 8 weeks, infants may not respond to a fluid bolus by
increasing cardiac output, but thereafter the response is similar to that of adults. Central
venous pressure does not necessarily reflect circulatory blood volume or left
ventricular efficiency.
Pulmonary vascular resistance falls quickly after birth, reaching normal adult levels by
8 weeks of age. However, the pulmonary vasculature may remain highly reactive to
hypoxia, hypercapnia, hypothermia, or acidosis, thereby increasing afterload to the right
ventricle. Myocardial anatomy changes in such a way that after birth, the larger right
ventricle decreases its mass and the left ventricle increases in size and mass. Similarly,
the neonatal response to catecholamines is limited until sympathetic nervous system
innervations and β1-receptors increase over several weeks. Therefore, the physiologic
effects of exogenous catecholamine administration may be variable, and careful titration
to the individual child’s response is essential.
Maintaining an optimal hemoglobin

concentration for the patient’s age is
desirable for patients in shock (minimum
10 g/dL) in order to maximize delivery
of oxygen.
2. Shock
Case Study
A 2-week-old full-term neonate presents with 3 days of nonbilious projectile vomiting

and agitation, worsened by feeding attempts. The mother reports that he has had
regurgitation of feedings since birth, with worsening in the last 3 days. His last wet
diaper was 1 day ago. Upon examination, the infant is awake and moving his
extremities, but appears weak. Fontanelles are sunken, mucous membranes are dry, and
the infant appears jaundiced. His heart rate is 190 beats/min, respiratory rate 50
breaths/min, blood pressure 44/25 mm Hg, and temperature 37°C (98.6°F).
– What is the differential diagnosis and the most likely etiology?
– What initial intervention is indicated?
– What diagnostic modalities are indicated?
Children are particularly susceptible to shock states. Shock in pediatric patients is

defined and categorized as in adults (Chapter 7), but the etiologies may differ. Timely
recognition of the shock state and aggressive intervention are essential to obtaining an
optimal outcome (Table 16-8). As soon as the diagnosis of shock is considered, early
cardiopulmonary monitoring, vascular access, and treatment must be implemented. Fluid
resuscitation is the initial therapy for most forms of shock. Rapid restitution of
circulating intravascular volume is critical to restore tissue oxygenation and perfusion
and avoid end-organ damage. Initial volume expansion with isotonic crystalloid
solutions (normal saline or Ringer lactate solution) at 20 mL/kg is recommended,
repeated up to a total of 60 mL/kg in the first 15 minutes. If possible, minimize the total
amount of normal saline, preferring Ringer lactate solution or PlasmaLyte, as normal
saline can independently cause acidosis by changing strong ion balance. Smaller
volumes of 5 to 10 mL/kg should be used in patients with suspected myocardial
dysfunction. Although hepatomegaly can be a sign of fluid overload in the pediatric
patient, it must be viewed with caution. Disease processes common to children (e.g.,
asthma, respiratory syncytial virus, pneumonitis) can cause lung hyperinflation and
downward displacement of the liver. Other signs of volume overload also should be
considered in the evaluation of these patients. If a child with an enlarged liver fails to
respond to the initial fluid administration, radiologic examination of the chest may help
to evaluate heart size. In children, crackles may occur late in the process of developing
heart failure, and a gallop may be difficult to discern in infants with tachycardia.
Table 16-8 Management of Pediatric Shock
Detection Evaluate and perform assessment of general appearance, airway, breathing,

circulation, pertinent history, and physical exam
Attach appropriate monitors
Recognize the type of shock and categorize the severity
Intervention Provide 100% oxygen (except if suspecting cyanotic heart disease in a neonate)
Obtain appropriate intravenous/intraosseous access (preferred)
Administer appropriate intravenous fluids
– 20 mL/kg bolus isotonic crystalloids
– Repeat fluid bolus with reassessment
Place urinary catheter
Reassessment Re-evaluate airway, breathing, circulation, and mental status after each intervention
Repeat fluid at 20 mL/kg
Monitor ongoing losses
Check the therapeutic end points in resuscitation
– End-organ function
– Heart rate, blood pressure, signs of perfusion
– Mental status
– Urinary output
Obtain serum electrolyte measurements, monitor hypo/hypernatremia, acidosis, blood
urea nitrogen/creatinine, glucose
Effective Define team member roles and responsibilities

communication Communicate effectively with other caregivers
Promote collegial interaction and knowledge sharing
a. Hypovolemic Shock
The most common cause of shock in the pediatric patient is acute hypovolemia resulting
from increased fluid and electrolyte losses (gastrointestinal disorders) or blood loss
resulting from trauma. Hypovolemia also can be caused by capillary leak due to
intestinal ischemia from volvulus, intussusception, or necrotizing enterocolitis. A
detailed medical history should be obtained from the patient’s caregiver and/or
referring institution. A history of increased fluid losses (vomiting and diarrhea),
lethargy, and decreased urine output is usually found in infants with hypovolemic shock.
Blood pressure is maintained longer in hypovolemic children than in adults. Capillary
refill and extremity temperature are much more reliable indicators of hypovolemia
because they may become abnormal much earlier than blood pressure in the child with
shock. Children with hypovolemic shock may require 40 to 60 mL/kg of isotonic fluids
(Ringer lactate solution preferred, or normal saline). Hypotonic or dextrose-containing
fluids are not indicated during the initial treatment phase. Transfusion of packed red
blood cells (15 mL/kg) should be considered in patients with hemorrhagic shock when
signs of shock persist despite adequate isotonic fluid resuscitation.
Inotrope/vasopressor support should be considered for patients who do not respond to
isotonic fluids. Those with concurrent adrenocortical problems can be refractory to
fluids and inotropes and will respond only to glucocorticoid replacement
(hydrocortisone 1-2 mg/kg/day).
b. Distributive Shock
As in adults, the most common cause of distributive shock in pediatric patients is sepsis.
Other etiologies are similar to those in adults with the addition of congenital adrenal
hyperplasia. Septic shock is characterized by changes in mental status, fever or
hypothermia, and perfusion abnormalities such as vasodilation (warm shock) or
vasoconstriction (cold shock). The therapeutic goal in septic shock is to restore and
maintain optimal organ perfusion and oxygenation. Acceptable goals include restoration
of the patient’s mental status and urine output (1 mL/kg/h). Children in septic shock are
usually severely hypovolemic and will respond to aggressive fluid resuscitation. Initial
rapid fluid resuscitation with isotonic fluids (20 mL/kg) is suggested. Typical fluid
requirements range from 40 to 200 mL/kg during the initial phase of resuscitation. Fluid
choices are crystalloids and colloids (5% albumin, dextran, gelatin). Vasopressor
support with central norepinephrine (0.05-0.3 μg/kg/min) is recommended as the first
choice in patients with fluid-refractory vasodilated shock. Vasopressin (0.001
U/kg/min) or epinephrine (0.05-0.3 μg/kg/min) may be considered in patients
unresponsive to norepinephrine. Dopamine (5-10 μg/kg/min) is recommended as the
first choice in patients with fluid-refractory cold shock. Epinephrine (0.05-0.3
μg/kg/min) may be considered in patients unresponsive to dopamine. Milrinone (0.5-1
μg/kg/min) or dobutamine (5-10 μg/kg/min) may be administered with caution to
patients with low cardiac output and elevated systemic vascular resistance states
(vasoconstricted) after fluid resuscitation. Use of corticosteroids is indicated in those
with vasopressor resistant shock, purpura fulminans, or suspected adrenocortical
problems (chronic steroid use in immunodeficiency, malignant disease, collagen
vascular disorders). The initial recommended dose of hydrocortisone is 1-2 mg/kg/day.
Early transfer to a pediatric ICU for inotropic support and invasive cardiopulmonary
monitoring is indicated in patients not responding to fluid resuscitation. Infants with
sepsis are often profoundly hypoglycemic on presentation and glucose determinations
should be performed in suspected sepsis.
c. Cardiogenic Shock
Congestive heart failure is the most common presentation of congenital heart anomalies
in children and often precedes cardiogenic shock. Congestive heart failure can often be
the result of acute or chronic changes in the heart’s preload, afterload, contractility, or
heart rate and rhythm. Signs and symptoms vary depending on the type of lesion.
Newborn (0-28 days) infants with ductal-dependent lesions (eg, coarctation of the aorta,
transposition of the great vessels, tricuspid atresia) will typically present in profound
shock with a history of poor feeding, tachypnea, lethargy, cyanosis, thready or absent
femoral pulses, and poor or absent urine output (obstructive shock). These patients will
require prompt initiation of prostaglandin E1 (PGE1) and inotropes in addition to
isotonic fluids. Patients with non-ductal-dependent lesions can present beyond the
newborn period with a history of tachycardia, gallop rhythm, heart murmur, tachypnea,
hepatomegaly, and failure to thrive. These patients will often respond to diuresis with a
loop diuretic (furosemide 0.5-1 mg/kg) rather than fluid resuscitation and to inotropic
support (milrinone 0.5-1 μg/kg/min or dobutamine 5-10 μg/kg/min) and/or afterload
reduction. Fluid resuscitation must be titrated cautiously. Early transfer to a pediatric
ICU for further monitoring, inotropic support, and a complete evaluation by a pediatric
cardiologist is recommended. Other common etiologies of cardiogenic shock include
hypoxic-ischemic episodes after acute life-threatening events, near drowning, or
strangulation.
d. Obstructive Shock
Congenital lesions that interfere with outflow from the left ventricle, such as coarctation
of the aorta or interrupted aortic arch, commonly cause obstructive shock in infants.
They develop signs of shock when the ductus arteriosus closes, thus interfering with
blood delivery to the distal aorta. A history of poor feeding, lethargy, decreased or
absent urine output, decreased or absent femoral pulses, and metabolic acidosis is
frequent. When treating hypotension in a child with non-hypovolemic shock, initial
titrated boluses of 10 to 20 mL/kg crystalloid, up to 40 mL/kg, may not be effective.
Inotropic support with dobutamine (5-10 μg/kg/min) and a PGE1 infusion should be
initiated rapidly to reopen the ductus arteriosus and restore perfusion to the distal aorta
in infants and children with suspected left heart lesions. The usual dose is PGE1 0.05 to
0.1 μg/kg/min as a continuous infusion. The side effects of PGE1 infusion include
periodic breathing, apnea, and peripheral vasodilatation, so the clinician must be
prepared to support the patient’s airway, provide ventilation, and administer additional
fluids. Once the ductus arteriosus has reopened, hyperventilation and hyperoxia must be
avoided, because both of these conditions will lead to preferential pulmonary blood
flow through the ductus and will worsen systemic shock and distal perfusion.
Administer PGE1 (0.05-0.1 μg/kg/min)

for newborns in shock until a ductal-
dependent lesion can be ruled out.
C. Metabolism/temperature
Case Study
A 2-year-old male child is brought to the emergency department with a history of

vomiting and diarrhea for 1 week. His heart rate is 150 beats/min, respiratory rate 20
breaths/min, blood pressure 70/50 mm Hg, and temperature 37.5°C (99.5°F). The child
appears lethargic, has dry mucous membranes, and poor skin turgor. During your
examination, he has a tonic-clonic seizure broken with rectal diazepam.
– What is the most likely etiology of the seizures?
– What is your initial management strategy?
– What diagnostic modalities are indicated?
Pediatric patients are particularly susceptible to water and electrolyte abnormalities
and experience temperature regulation problems frequently. The more common issues
that can result in critical illness are examined.
1. Water/Temperature
Insensible water loss is higher in children than in adults because children have a higher
ratio of surface area to body mass. This higher evaporative fluid loss, combined with a
higher metabolic rate, emphasizes that dehydration may occur quickly. Therefore,
children require a greater amount of fluid per kilogram than adults do, but this volume is
still a low absolute amount because of a child’s small size. Titration of these small
volumes usually requires infusion pumps for precise administration and frequent
adjustment of fluids to assure adequate replacement of deficits lost from all sites.
Several approaches to fluid (Table 16-9 and 16-10) and electrolyte replacement help
the clinician estimate the actual requirements. Remember that infusion rates may be so
low (<1 mL/h) that drips may require a carrier fluid, and this should be accounted for in
fluid calculations.
Pediatric Management of Water and Electrolyte Abnormalities

Table 16-9
Detection Evaluate and perform assessment of general appearance, airway, breathing,
circulation, pertinent history, and physical exam
Attach appropriate monitoring devices
Recognize the respiratory physiology disorder and type of dehydration (hyponatremic),
and categorize the severity
Intervention Provide 100% oxygen

Obtain appropriate intravenous/intraosseous access (preferred)
– Administer appropriate intravenous fluids
– 20 mL/kg bolus of isotonic crystalloids
– Repeat fluid boluses with reassessment
Place urinary catheter
Obtain serum electrolyte measurements; monitor hypo/hypernatremia, calcium, and
glucose
Reassessment Reevaluate airway, breathing, circulation, and mental status after each intervention
Repeat fluid at 20 mL/kg if needed
– Correct confirmed symptomatic severe hyponatremia with 3 mL/kg of 3% saline
over 15 min
– Administer lorazepam 0.05 mg/kg if patient actively having a seizure
Monitor ongoing losses
Check therapeutic end points in resuscitation
– End-organ function
– Heart rate, blood pressure, signs of perfusion
– Mental status
– Urinary output
Monitor serum electrolytes, hypo/hypernatremia, acidosis, blood urea
nitrogen/creatinine, glucose at least every 4-6 h
Effective Define team member roles and responsibilities

Communication Communicate effectively with other team members and pediatric ICU
Promote collegial interaction and knowledge sharing
Table 16-10 Estimating Fluid Requirements
Body Weight Fluid

<10 kg 100 mL/kg/day
11-20 kg 1000 mL + 50 mL/kg for each kg above 10 kg
>20 kg 1500 mL + 20 mL/kg for each kg above 20 kg
The method most widely used is the Holliday-Segar method, which relates caloric
expenditure to body weight for a resting healthy patient. For every 100 calories
expended, 100 mL of water is lost (65% urine + 35% insensible water) along with 2 to
4 mEq of sodium and potassium. Thus, a child weighing 25 kg would receive 1,600 mL
water daily (1,500 mL + 100 mL), 50 to 100 mmol of sodium each day, and 25 to 50
mmol of potassium daily. Unfortunately, this method underestimates electrolyte
requirements in sick patients. Pediatric patients have been shown to develop
hyponatremia when given hypotonic fluids in the hospital setting. The amount of
dextrose required will depend on the patient’s age and metabolic needs. Children who
weigh <10 kg should receive a solution of 10% dextrose or higher. Those who weigh
>10 kg typically require a 5% dextrose-containing solution. Dextrose solutions should
be withheld in hyper-glycemic patients (glucose >180 mg/dL [9.9 mmol/ L]). The
recommended solution for the patient weighing 25 kg would be 5% dextrose in normal
saline with 20 mmol potassium chloride in each 1,000 mL (D5 0.9% sodium chloride +
20 mmol potassium chloride/L) or 5% Ringer lactate solution administered at 66 mL/h
(1,600 mL/24 h).
Under normal conditions, maintenance fluid needs are derived from normal urine, stool,
and insensible water losses. Stool water losses are usually negligible in patients
without gastrointestinal abnormalities. Minimally acceptable urine output is ~2 mL/kg/h
for a well-hydrated infant and 1 mL/kg/h for a child.
The use of isotonic fluids (5% dextrose

in normal saline, 5% Ringer lactate
solution) in hospitalized patients is
advocated to prevent the development of
hyponatremia.
The higher ratio of surface area to body mass and the decreased subcutaneous fat
reserves in infants and young children allow greater heat loss through evaporation and
radiation. Maintenance of body temperature is also limited in infants because they have
immature thermoregulatory control, cannot modify behavior (such as get a blanket), have
large heads, have thin skin with lack of keratin, and have ineffective shivering due to
immature muscles. The compensatory process of metabolizing brown adipose tissue to
generate heat can be harmful because it results in metabolic acidosis. Hypothermia can
also increase morbidity by impairing wound healing, increasing the risk of infection and
apnea, and delaying metabolism. It is important, therefore, to maintain an appropriate,
thermal-neutral environmental temperature to assure a rectal temperature of 37°C
(98.6°F) in the neonate.
2. Glucose
Low glycogen stores and an increased metabolic rate make hypoglycemia common in
infants during stress. A continuous infusion of glucose (5 mg/kg/min) is often necessary.
If glucose-containing fluids are withheld, blood glucose should be monitored frequently
(at least every 1-2 hours) to avoid hypoglycemia (glucose <65 mg/dL [3.6 mmol/L]).
Boluses of 10% glucose (0.5-1 g/kg [5-10 mL/kg]) in neonates and 25% glucose (2-4
mL/kg) in children will generally correct hypoglycemia.
3. Sodium
Hyponatremia (sodium <135 mmol/L) is the most common metabolic abnormality found
in the pediatric hospitalized patient. It occurs when hypotonic oral or intravenous
solutions are given to children with increased losses secondary to diarrhea or diuretic
use. Children with cystic fibrosis, adrenal insufficiency, syndrome of inappropriate
antidiuretic hormone (SIADH), and obstructive uropathy are also at risk for
hyponatremia. With severe hyponatremia (sodium <125 mmol/L), children exhibit signs
of irritability, poor feeding, nausea and vomiting, lethargy, seizures, and eventually
coma and death if left untreated. In those with hyponatremia-induced neurologic
symptoms, 3% hypertonic saline can be titrated until seizures resolve, followed by a
slow correction over 24 hours with an isotonic solution. The usual 3% sodium chloride
(0.513 mmol/mL) dose is 3 mL/kg (2.5 mmol/kg). In patients with less severe acute
hyponatremia (sodium 125-130 mmol/L), a slow correction over 12 to 24 hours to
levels of about 130 mmol/L is recommended. The patient’s hydration status must be
considered when treating hyponatremia. Hypovolemic patients must be hydrated with
normal saline. In euvolemic or hypervolemic patients with mild hyponatremia, fluid
restriction and loop diuretics, in addition to the hyponatremia correction, might be
indicated. Early consultation with a pediatric intensivist and transfer to a pediatric ICU
for further monitoring are indicated in symptomatic patients.
Hypernatremia (sodium >145 mmol/L) results from excessive free-water losses in
gastroenteritis, inadequate amounts of free-water intake, withholding of water, or
nephrogenic or central diabetes insipidus. Infants are more susceptible to
hypernatremia. Hypernatremic dehydration can be detected with signs such as
irritability, high-pitched cry, mental status changes, hypertonia, and seizures. Isotonic
fluids (normal saline) are recommended during the initial resuscitation phase to correct
hypovolemia or shock. In children, the free-water deficit can be calculated as 4 mL/kg
for every 1 mmol/L of sodium >145 mmol/L. The serum sodium should be lowered no
faster than 0.5 mmol/L/h over 48 to 72 hours. Five percent dextrose half-strength normal
saline (D5 0.45% sodium chloride) can be used in patients whose serum sodium is
<165 mmol/L, allowing the sodium to drop no faster than 1 mmol/L/h. A more
conservative approach should be considered in patients with serum sodium >165 mmol/
L; in these situations, the solution of choice may be dextrose 5% normal saline (D5
0.9% sodium chloride), provided an adequate hydration state was achieved. Central
diabetes insipidus should be suspected in patients with brisk urine output after severe
head injury or recent intracranial surgery. Early consultation with a pediatric
neurosurgeon or pediatric intensivist is advised.
4. Potassium
Hypokalemia (potassium ≤3.5 mmol/L) is usually the consequence of renal losses
(diuretic therapy), renal tubular disorder resulting from chemotherapy, gastrointestinal
losses (vomiting, fistulas), or decreased intake. In children with life-threatening
hypokalemia (arrhythmia, paralysis), potassium chloride can be administered
intravenously at a rate of <1 mmol/kg/h (maximum 20 mmol/h) with continuous
electrocardiographic monitoring. The usual replacement rate of potassium is 0.2 to 0.3
mmol/kg/h. Serum potassium levels must be monitored at frequent intervals during the
replacement phase. Hyperkalemia (potassium >5.5 mmol/L) is most often the result of
decreased losses, increased intake, or kidney dysfunction. Recommended treatment for
hyperkalemia in children is outlined in Table 16-11.
Table 16-11 Treatment of Hyperkalemia
If significant electrocardiographic abnormalities are presented (peaked T waves, QRS widening, PR-
interval prolongation:
Administer calcium gluconate (10%) 50 mg/kg intravenously OR

Administer calcium chloride (10%) 10 mg/kg intravenously via central line
For redistribution of potassium:
Administer sodium bicarbonate 1 mmol/kg intravenously AND/OR

Administer 25% dextrose 2-3 mL/kg (0.5-1 g/kg) + regular insulin 0.1 U/kg intravenously (1U for
each 5 g dextrose)
Administer inhaled β2-agonist (albuterol 2.5-5 mg per dose has been used successfully)
To remove potassium:
Administer loop diuretic: furosemide 0.5-1 mg/kg

Administer sodium polystyrene sulfonate 1g/kg per dose orally/rectally every 6 h
Perform dialysis
5. Calcium
Critically ill newborns are susceptible to hypocalcemia (total calcium <8.5 mg/dL [2.2
mmol/L], ionized calcium <1 mmol/L) because they experience a sudden withdrawal
from the high rate of calcium intake associated with normal maternal-to-fetal transfer of
calcium during gestation. In neonates with congenital heart disease, hypocalcemia may
be the presenting sign for DiGeorge syndrome (22q11 microdeletion). Children with
hypocalcemia may present with tetany, carpopedal spasm, laryngeal stridor, apnea,
convulsions, hypotension, and congestive heart failure.
To correct life-threatening hypocalcemia in children, calcium gluconate (100 mg/kg per
dose) should be injected through a small needle into a large vein at a rate of
approximately 1.5 mL/min if central venous access is not available. Calcium chloride
(20 mg/kg per dose) may be administered instead of calcium gluconate only if central
venous access is available. Maintenance doses of calcium gluconate or calcium
chloride may be delivered every 6 hours intravenously or by mouth (calcium gluconate
200-500 mg/kg/day) in cases of persistent hypocalcemia.
Hypercalcemia (total calcium >11 mg/dL [>2.75 mmol/L], ionized calcium >1.3
mmol/L) is rare in the pediatric population but suspicious for an underlying malignancy.
Treatment is similar to that for adults: normal saline infusion of 10 to 20 mL/kg
followed by furosemide administered 1 to 2 mg/kg every 6 to 12 hours.
6. Magnesium
Hypomagnesemia (magnesium <1.8 mg/dL or 1.5 mEq/dL [0.75 mmol/L]) is commonly
associated with malnutrition or malabsorption syndromes in children with poor gut
function and in critically ill infants receiving prolonged intravenous fluid
administration. It can be seen in patients with a renal tubular disorder resulting from
chemotherapy for the treatment of bone tumors. Clinical manifestations of
hypomagnesemia overlap those of hypokalemia and hypocalcemia. Life-threatening
hypomagnesemia may be treated with magnesium sulfate, giving 25 to 50 mg/kg
intravenously over 5 to 15 minutes.
7. Phosphorus
Hypophosphatemia (phosphate <2.5 mg/dL [0.81 mmol/L]) is relatively uncommon in
children and is usually associated with malnutrition, malabsorption syndromes, or renal
tubular defects. Life-threatening hypophosphatemia, which may be signaled by muscle
weakness, respiratory failure, coma, and seizures, can be treated with sodium phosphate
or potassium phosphate as 0.4 mmol/kg infused over 6 hours (maximum 21 mmol).
D. Immune System
The following factors increase the risk of infection in neonates:
Decreased polymorphonuclear white cell function and storage reservoir

Reduced delivery of phagocytes to inflammatory sites
Decreased antibody synthesis
Passive maternal immunity that is depleted by 2 to 5 months after birth;
immunoglobulin levels comparable to adult levels to adult levels are not reached
until 4 to 7 years of age
Because of their incompletely developed immune systems, children are treated with
empiric antibiotic therapy more frequently than are adults. For the same reason,
antibiotics are considered an emergency drug, particularly for febrile infants younger
than 2 months. Before the age of 3 years, the risk of occult bacteremia is increased if the
temperature is >40°C (>104°F) or white blood cell count is <500 cells/mm3 or >15,000
cells/mm3. Absolute neutrophil count <1,000 cells/mm3 or significant bands of 25% to
30% are also markers of severe bacterial infection in children. In such situations, a full
workup is recommended and should include blood culture, urine culture, and lumbar
puncture, if clinically indicated. The stages of physiologic compromise due to infection
in pediatric patients are similar to adult stages of sepsis, with some modifications. The
systemic manifestations of sepsis are age-adjusted for heart rate, blood pressure, and
leukocyte count. Criteria for severe sepsis include cardiovascular dysfunction or acute
respiratory distress syndrome or two or more other organ dysfunctions. Septic shock is
defined by the presence of cardiovascular dysfunction.
In neonates, group B streptococci, Escherichia coli, Listeria, and Enterococcus often
cause life-threatening bacterial infections. Organisms that should be considered in
children ages 2 months to 2 years include Streptococcus pneumoniae, Haemophilus
influenzae, Neisseria meningitidis, and Salmonella. The organisms associated with
serious infections in children and the suggested treatments are summarized in Table 16-
12.
Table 16-12 Most Common Serious Infections in Infants and Children
Site Organism Treatmenta

Neonates
Bacterial meningitis Group B streptococci, Escherichia Cefotaxime 50 mg/kg/dose
coli (and other enteric gram-
negative organisms)
Listeria and Enterococcus Ampicillin 50 mg/kg/dose
Viral meningitis Neonatal HSV and HSV encephalitis Acyclovir 15 mg/kg/dose
Children
Bacterial meningitis Haemophilus influenzae, Cefotaxime 50 mg/kg OR
Streptococcus pneumoniae, ceftriaxone 50 mg/kg;
Neisseria meningitidis, dexamethasone 0.15 mg/kg
Salmonella for H influenzae and S pneumoniae
Viral meningitis HSV encephalitis Acyclovir 15 mg/kg
Epiglottitis H influenzae Cefotaxime 50 mg/kg OR
ceftriaxone 50 mg/kg
Bacterial tracheitis Staphylococcus, Nafcillin 50 mg/kg/dose OR
Streptococcus clindamycin 10 mg/kg/dose and
Moraxella catarrhalis cefotaxime 50 mg/kg/dose
Retropharyngeal abscess Staphylococcus aureus, group A Nafcillin 50 mg/kg OR clindamycin
streptococci (may be mixed 10 mg/kg and gentamicin 2.5 mg/kg
infection), gram-negative enteric OR ampicillin/sulbactam 50-100
organisms, anaerobes mg/kg (based on application) and
gentamicin 2.5 mg/kg
Croup Parainfluenza Supportive care
Influenza
Peritonitis Gram-negative organisms: E coli, Cefotaxime 50 mg/kg,
Klebsiella clindamycin 10 mg/kg, and
Gram-positive organisms: ampicillin 50 mg/kg OR ampicillin
pneumococcus, Staphylococcus, 50 mg/kg,
α-hemolytic Streptococcus, gentamicin 2.5 mg/kg,
Enterococcus and clindamycin or
Anaerobes: Bacteroides metronidazole 7.5 mg/kg
Immunocompromised patients Gram-positive organisms: Vancomycin 10-15 mg/kg
coagulase-negative
Staphylococcus, α-hemolytic
Streptococcus, Enterococcus,
coryneform bacteria
Gram-negative organisms: Cefepime 50 mg/kg OR
Klebsiella, Bacillus, Pseudomonas, ceftazidime 50 mg/kg
E coli
Fungi: Candida, Aspergillus Fluconazole: loading dose 10
mg/kg; maximum loading dose 400
mg
Amphotericin B: 0.25-1 mg/kg/day
OR caspofungin 50 mg/m 2/dose
q24h; maximum dose 50 mg
Abbreviation: HSV, herpes simplex virus

aThese recommendations are general guidelines only. Specific antibiotic choices should be individualized,
taking into consideration clinical circumstances (renal function, liver function), patient age, immunization
status, and local microbial virulence, sensitivities, and patterns of resistance. The antibiotic closing interval
and frequency should be discussed with a pediatric intensivist or pediatric infectious disease expert.
E. Nervous System
The Glasgow Coma Scale is difficult to apply in children, even when it is adapted for
age, as shown in Table 16-13. (See Chapter 8 for its application to adults.) When
assessing the need for further intervention, careful attention should be paid to the
pupillary responses, the patient’s ability to maintain the airway, the motor score, and the
fontanelle fullness in infants. Any young child with a depressed level of consciousness,
seizures, and/or coma should be evaluated for the possibility of occult trauma (eg, child
abuse, especially shaken baby syndrome), even if there are no outward signs of injury.
Infectious, metabolic, or toxic etiologies also should be considered. Boluses of 10%
glucose in neonates and 25% glucose in children will generally correct hypoglycemia-
induced coma and/or seizures (see earlier section). Hyponatremia, hypoglycemia, and
hypocalcemia should be considered in small children with seizures. Diazepam may be
administered rectally to children with ongoing seizure activity and no intravenous
access (0.5 mg/kg per dose; use injectable or gel preparation). Lorazepam, midazolam,
or diazepam can be used in the initial treatment of seizures at a dose of 0.05 to 0.1
mg/kg given intravenously. Subsequently, a full intravenous loading dose of phenytoin or
fosphenytoin (15-20 mg/kg) should be administered if a second dose of benzodiazepine
is ineffective. If the patient is already on phenytoin or the loading dose was ineffective,
phenobarbital (15-20 mg/kg per dose) should be considered. Caregivers should be
aware of the cumulative respiratory depression potential of these medications and the
resulting need for early airway support. Endotracheal intubation and general anesthesia
should be considered in the event that seizures persist despite adequate treatment.
Neuromuscular blocking agents are used only to facilitate endotracheal intubation. Early
consultation with a pediatric neurologist and pediatric intensivist is recommended.
Early airway intervention and close

neurologic monitoring are recommended
in children with seizures.
The unique features in the care of infants and children highlight the very small margin
for error in treating critically ill or injured pediatric patients. Specialty consultation
should be requested early.
Table 16-13 Glasgow Coma Scale Modified for Infants and Children
Clinical Parameter Infants (ages 0-12 months) Children (ages 1-5 years) Pointsa
Eye Opening Spontaneous Spontaneous 4
Response to speech Response to speech 3
Response to pain Response to pain 2
No response No response 1
Verbal Response Coos/babbles Appropriate words 5
Irritable cries Inappropriate words 4
Cries Persistent cry 3
Moans Grunts 2
Best Motor Response Normal Spontaneous 6
Withdraws to touch Localized pain 5
Withdraws from pain Withdraws from pain 4
Flexor response Flexor response 3
Extensor response Extensor response 2
aTotalGlasgow Coma Scale score = eye + verbal + motor points; best possible score = 15; worst possible
score = 3
Key Points
Critical Care in Infants and Children: The Basics

Irritability is an early sign of changes in mental status in the young child.
In children, early signs of respiratory distress include tachypnea, grunting, and
nasal flaring.
Ensuring a patent airway is the most important initial step in treating a child with
respiratory compromise.
Important airway anatomic differences between a child and an adult must be
considered when intubating an infant or child.
Suggested initial ventilator settings for children are tidal volume, 6 to 10 mL/kg in
normal lungs, 6 mL/kg in acute lung injury or acute respiratory distress syndrome.
Respiratory rates in children may need to be higher than those in adults to maintain
acceptable PaCO2 levels.
The perfusion status in children is best assessed initially by capillary refill and
extremity temperature. Hypotension is a late finding in children with shock. Those
with hypovolemic shock may require 40 to 60 mL/kg of isotonic fluids (normal
saline, Ringer lactate solution).
Vasopressor support with norepinephrine is indicated in patients with fluid-
refractory vasodilated shock. Dopamine is indicated for low cardiac output
(vasoconstricted shock) after adequate fluid resuscitation is delivered.
Obstructive shock in infants is commonly caused by congenital lesions that
interfere with outflow from the left ventricle, such as coarctation of the aorta or
interrupted aortic arch.
Intracranial hemorrhage in the young infant can cause hemodynamically significant
blood loss.
Hypoglycemia is common in infants during stress and must be corrected promptly.
Infants do not maintain body temperature well, and care must be taken to avoid
hypothermia.
Young infants are at increased risk of infection due to their immature immune
systems.
Empiric antibiotics are considered an emergency drug for febrile infants younger
than 2 months.
Diazepam may be administered rectally to children with ongoing seizure activity
who have no intravenous access.
Suggested Readings
1. Brierley J, Carcillo JA, Choong K, et al. Clinical practice parameters for

hemodynamic support of pediatric and neonatal septic shock: 2007 update from the
American College of Critical Care Medicine. Crit Care Med. 2009;37:666– 688.
2. Goldstein B, Giroir B, Randolph A, and International Consensus Conference on
Pediatric Sepsis. International pediatric sepsis consensus conference: definitions
for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6:2-8.
3. Mejia R, Greenwald B, Fields A, et al, eds. Pediatric Fundamental Critical Care
Support. 1st ed. Mount Prospect, IL: Society of Critical Care Medicine; 2008.
4. Smith L, Hernan L. Shock states. In: Fuhrman BP, Zimmerman JJ, eds. Pediatric
Critical Care. 3rd ed. St. Louis, MO: Mosby; 2006:394.
5. Thompson AE. Pediatric airway management. In: Fuhrman BP, Zimmerman JJ, eds.
Pediatric Critical Care. 3rd ed. St. Louis, MO: Mosby; 2006:485.
6. Wood EG, Lynch RE. Electrolyte management in pediatric critical illness. In:
Fuhrman BP, Zimmerman JJ, eds. Pediatric Critical Care. 3rd ed. St. Louis, MO:
Mosby; 2006:939.
Suggested Website

APPENDIX 1
RAPID RESPONSE SYSTEM
I. INTRODUCTION
Rapid response systems (RRS) have emerged as important resources that focus on the
hospitalized patient with unexpected, sudden deterioration in a condition from any
cause. Historically, crisis teams were activated only after a significant event, such as
cardiac arrest; there was no organized approach to preventing an untoward event in an
at-risk hospitalized patient. Most patients who have a cardiac arrest while in the
hospital demonstrate identifiable signs of deterioration in the previous 8 hours. Early
recognition of deterioration and timely intervention can reduce the incidence of in-
hospital cardiac arrest or need for intensive care. Rapid response systems have been
shown to reduce in-hospital mortality and cardiopulmonary arrest, although the presence
of a physician is not significantly associated with a mortality reduction.
Unfortunately, the early indicators of clinical deterioration can be difficult to identify.
Assessing a patient’s physiologic reserve is challenging. Rapid response systems bring
additional experienced providers with advanced monitoring tools to the patient’s
bedside. If needed, more advanced monitoring and therapy can be initiated immediately,
and a decision can be made about the most appropriate care level. The most important
action in the process is the call for help.
The RRS model can be divided into four components, each of which plays an integral
role in the success of the system (Figure A1-1). The administrative arm oversees
appropriate staffing, provides resources, drafts protocols and guidelines, and ensures
staff education regarding the presence and utility of the service. The afferent arm is
concerned with detecting impending deterioration, while the efferent arm is focused on
rendering therapy and mobilizing additional resources quickly. Lastly, the performance
improvement arm seeks to identify recurrent patterns of deterioration and assess
improvement in quality measures following system-wide interventions.
Figure A1-1. Rapid Response System Structure
Abbreviations: RRT, rapid response team; MET, medical emergency team; RN, nurse; MD, physician;
VIPPS, ventilation, infusion of volume, pressors/pump, pharmacy, and specific interventions; AMI, acute
myocardial infarction; LOS, length of stay
aAdapted from Sebat F, ed. Designing, Implementing, and Enhancing a Rapid Response System. Mount
Prospect, IL: Society of Critical Care Medicine; 2009:41.
II. BUILDING A MEDICAL EMERGENCY OR RAPID RESPONSE

TEAM
Rapid response teams represent an intuitively simple concept: When a patient
demonstrates signs of imminent clinical deterioration, a team of providers is summoned
to the bedside to immediately assess and treat the patient with the goal of preventing
transfer to the ICU, cardiac arrest, or death. A rapid response team (RRT) is the
intervention limb of the RRS. By consensus, a medical emergency team (MET) is led by
a prescribing clinician (physician or advanced practice provider), whereas an RRT is a
led by a nurse and/or respiratory therapist (nonprescribing clinician). However, most
recently, these two terms have been used interchangeably.
A. Response Team Composition

Although there is no single perfect team composition, the most successful METs and
RRTs have been developed by leveraging existing hospital resources and targeting
particular at-risk patient populations. Multidisciplinary, physician-led teams (METs)
are prevalent in academic centers with training programs. Nurse-led or nurse–
respiratory therapist teams (RRTs) with physician backup (or medical control similar to
the emergency medical services model) are more often found in community hospitals
without training programs. Regardless of the team composition, effective teamwork
skills are essential to the success of the program. The implementation of standardized
protocols or standing orders allows the team to use evidence-based best practices to
address commonly identified clinical issues. The RRS administrative leadership should
develop these protocols and standing orders in accordance with institutional policies
and procedures. Possible members of an MET or RRT are identified in Table A1-1.
Table A1-1 Possible Members of Medical Emergency or Rapid Response Team
Physicians Intensivist, hospitalist, emergency medicine physician, anesthesiologist,

(attending, fellow, pulmonologist, surgeon, internist
resident)
Advanced practice Nurse practitioner, physician assistant
providers
Nurses ICU nurse, postanesthesia care unit nurse, emergency department nurse,
telemetry unit nurse, certified registered nurse anesthetist, nursing supervisor
Other providers Respiratory therapist, electrocardiography technician, emergency medical
technician/paramedic
At an academic hospital, the composition of the responding team may include the
following combinations of caregivers:
ICU attending and/or fellow, ICU nurse, respiratory therapist, pharmacist

Hospitalist, medicine resident or advanced practice provider, ICU nurse,
respiratory therapist
ICU nurse, respiratory therapist, physician (backup)
At a non-teaching hospital, the team may consist of one of the following combinations:
Emergency department physician or advanced practice provider, hospitalist, ICU

nurse, respiratory therapist
Emergency department nurse, ICU nurse, respiratory therapist
Postanesthesia care unit nurse, respiratory therapist, physician (backup)
Typically, physician members are trained (or are training) in critical care, emergency
medicine, anesthesia, or internal medicine. They bring their knowledge of critical
illness and their skills in the management of life-threatening problems to the patient’s
bedside. Nurse members usually have many years of bedside experience and most often
have extensive critical care training. Team members from other disciplines add value to
the MET or RRT with their knowledge of such factors as airway and respiratory
management, drug therapies, traumatic injury management, and critical care transport.
Team members usually are expected to maintain current provider status in basic and
advanced cardiac life support, pediatric advanced life support (where applicable), and
fundamental critical care. Periodic teamwork exercises in mock events or medical
simulation centers can hone members’ evaluation and management skills. Treatment
protocols and standing orders should be reviewed and amended based on feedback from
MET or RRT calls and quality improvement data.
B. Response Team Equipment

The use of advanced physiologic monitors and equipment by appropriately trained MET
members can provide crucial support to the at-risk patient. This can greatly enhance the
team’s ability to evaluate and manage signs and symptoms of clinical deterioration.
Clearly, the earlier clinical abnormalities are identified and addressed, the greater the
potential for a positive outcome and, often, the simpler the needed intervention. The
MET or RRT should first evaluate the resources that are readily available in the areas it
will support and then create a list of additional needed equipment (Table A1-2). The
response team must have access to cardiac, respiratory, and simple hemodynamic
monitors. Other equipment and medications should be selected based on the patient
populations served, the team composition, and local regulations and policies. Since the
MET or RRT is expected to respond quickly, any additional necessary equipment and
supplies should be organized in appropriate bags or carts that can be readily transported
to the patient.
Table A1-2 Response Team Equipment Lista
Physiologic Monitors Cardiovascular Equipment

Monitor/defibrillator with external pacing capability Manual blood pressure device
Noninvasive blood pressure device IV administration kits
Pulse oximetry IV catheters
Portable capnography (if available)
Miscellaneous
Respiratory Equipment Personal protective equipment
Portable oxygen tank Sterile gloves
Portable suction device Dressings and bandages
High-flow oxygen reservoir face mask Antiseptics
Bag-mask device Drug Bag (as appropriate for scope of practice)
Ventimask®, nasal cannula, and simple face mask Vasopressors
Nebulizer mask Inotropes

Oropharyngeal/nasopharyngeal airways Vasodilators
Laryngeal mask airways Sedatives and analgesics
Laryngoscopes and blades Bronchodilators
Endotracheal tubes with stylets Crystalloid and colloid IV fluid
Cricothyrotomy catheter kit Aspirin
Stethoscope
Consider portable ultrasound machine where available
aNecessary equipment and supplies should be available on the patient unit or carried by the team.
III. ACTIVATING THE MEDICAL EMERGENCY OR RAPID

RESPONSE TEAM
A. Activation Criteria and Triggers

The most important activation criterion is the concern of the bedside physician, nursing
staff, or family that something is wrong, even if other indicators are within acceptable
limits. This intuition is often quite sensitive and warrants additional assessment. The
fact that an intuition or a gut feeling is not very specific should not discourage activation
of the MET or RRT.
The distribution of a predefined set of MET or RRT activation criteria may help to
focus attention on important early indicators and empower the bedside staff to call for
help early. These criteria may be based on the detection of acute changes in physiology,
organ system–specific signs and symptoms, and event triggers (Table A1-3). Acute
changes in physiology may include changes in vital signs that exceed predefined limits,
like tachycardia, tachypnea, hypotension, and oliguria. The detection of one or more
indicators of organ system dysfunction may trigger activation of the response team. Such
pattern recognition may be more effective in detecting clinical deterioration when there
is a gradual change in physiologic variables.
Table A1-3 Models of Activation Criteria
Acute Physiologic Criteria

Acute Physiologic Criteria
Acute change in heart rate to <40 or >130 beats/min
Acute change in systolic blood pressure to <90 mm Hg
Acute change in urine output to <50 mL in 4 hours
Acute change in respiratory rate <8 or >30 breaths/min
Acute change in pulse oximetry to <90% despite oxygen administration
Acute change in consciousness
Qualitative deterioration in clinical status
Organ System-Specific Criteria

Airway
Respiratory distress
Threatened airway
Breathing
Respiratory rate >30 breaths/min
Respiratory rate <6 breaths/min
SpO2 <90% on oxygen
Difficulty speaking
Circulation
Blood pressure <90 mm Hg despite treatment
Pulse rate >130 beats/min
Neurology
Any unexplained decrease in consciousness
New agitation or delirium
Repeated or prolonged seizures
Other
Concern about the patient
Uncontrolled pain
Failure to respond to treatment
Inability to obtain prompt assistance
Event Trigger
Unscheduled naloxone dose administered
Increase in oxygen requirement
Any change to a 100% reservoir face mask
Any change in FIO2 delivery by ≥20%
After 3 unanswered pages to medical/surgical team for any patient in a shift
Response time to medical/surgical team page >30 min
Family concern about patient status
Any falls or traumatic injuries
Pain score ≥4 of 10 more than 30 min after highest ordered dose of analgesic
Persistent nausea/vomiting more than 30 min after highest dose of antiemetic
Any newly noted abnormal pulse
Abbreviations: SpO2, oxygen saturation on pulse oximetry; FIO2, fraction of inspired oxygen.
Event triggers help emphasize that some patient incidents or interventions warrant
further evaluation. The event may be a sign or a result of a larger issue that could be an
ongoing threat to the patient’s safety. For example, any administration of naloxone is an
indicator that one or more undesirable side effects of opiates may be present. Although
naloxone may temporarily reverse these side effects, they can recur as the antagonist
effects wane. A focused evaluation by the MET or RRT may avoid the undesirable
consequences of these events.
B. Response Team Scoring Systems

The use of a scoring system in evaluating the at-risk patient can provide a graded
assessment of clinical status and help to determine the level of response needed. An
overall score is calculated based on the aggregate of points assigned to various
symptoms, vital signs, and laboratory studies. Additional points are assigned to results
that vary greatly from normal. Several patented early warning scoring systems are
available, although not all are validated. The Modified Early Warning Score, which
evaluates a patient’s vital signs and mental status, has been validated in hospitalized
medical patients. A score of 5 or greater has been associated with an increased
mortality rate and increased incidence of ICU admission.
Individual MET or RRT programs may choose to define absolute value or trend
thresholds that trigger a move to a higher level of care or mobilization of additional
clinical resources. Collection and analysis of aggregate scores in patients receiving
MET or RRT services can be used for quality improvement efforts, such as evaluation
of standing orders, event cluster identification, and resource utilization.
IV. TEAM RESPONSE
A. Response Team Interventions

Interventions should be aimed at rapidly stabilizing the patient and preventing further
deterioration or full arrest. Studies have shown that the three most common reasons
for activating an MET or RRT are hypoxemia, hypotension, and altered mental
status. Teams should identify the primary activating events in their institutions and build
protocols to address each rapidly.
Respiratory distress is the leading physiologic cause of MET or RRT activation. The
reasons for acute changes can be related to fluid status, medications (eg, narcotics),
progression of underlying disease, or patient noncompliance with physician-ordered
oxygen therapies. Initial treatment is stabilization of the airway and application of high-
flow oxygen to relieve the patient’s distress and improve oxygen saturation. Following
improvement in patient status, the team can evaluate for potential reversible causes.
Hypotension can be related to volume status (both overall volume and blood volume);
medications, including narcotics and antihypertensives; and the potential for sepsis.
Initial treatment is administration of fluids to raise systolic pressure and/or the
immediate reversal of a known cause, such as narcotics. Consideration should be given
to empiric antibiotic therapy in cases of suspected severe sepsis or septic shock.
Altered mental status is most often associated with hypoxemia, hypotension, or
hypoglycemia. These should be evaluated and treated first. Altered mental status
unrelated to those issues should be evaluated for either neurologic or medication
causes. Treatment, including evaluation with computed tomography scanning, should be
guided accordingly.
The responding team should make every effort to involve the patient’s primary physician
and rounding team in decisions regarding disposition and care. The role of a MET or
RRT is not to take the place of the primary team but to act for – and with – them at the
bedside in an emergency.
B. Response Team Communications

In the complex hospital environment, the use of a structured communication tool and a
common critical language fosters the open communication among caregivers that is
essential to the prompt evaluation and management of the at-risk patient. Incorporating
the Situation, Background, Assessment, and Recommendation (SBAR) Tool into MET
or RRT documentation can facilitate effective communication by gathering all pertinent
data in one place for any discussions to follow. This tool has proven to be most
valuable in the effective communication of critical information (Table A1-4).
Table A1-4 SBAR Communication Tool
Situation: What is happening with the patient?

Background: What is the clinical background or context?
Assessment: What do I think is the problem?
Recommendation/interventions: What would I do to evaluate or correct it?
C. Response Team Education

One of the primary goals of METs and RRTs is education. The detection limb of the
RRS model relies heavily on the early recognition of signs and symptoms of clinical
deterioration. Regularly scheduled staff in-services and mock-event drills are effective
in maintaining competencies in identifying the at-risk patient. Public posting and
discussion of activation criteria can further enhance the use of MET or RRT services
and reduce patient clinical crises. Review of aggregate quality improvement data from
response team activity also can reinforce education. Post hoc review of a patient event
with the entire unit staff after an MET or RRT call serves to raise the entire group’s
collective knowledge and skill. This may reduce the likelihood of subsequent problems
and increase the likelihood that signs and symptoms of clinical deterioration will be
detected at the earliest indication in future patients. Topic-of-the-week presentations,
MET or RRT case reviews, and SBAR practice sessions are examples of targeted
educational activities.
V. STRATEGIES FOR SUCCESS

Hospitals that use an RRS report various factors that lead to successful team
implementation. Some common themes in their success include:
1. Training/Education – The MET or RRT members and the bedside nursing staff
must understand when and how to activate the team and the scope of team
capabilities. The response team members will need ongoing training in
management of common indicators in at-risk patients and effective intervention and
communication strategies. The mentoring of the bedside nursing staff in critical
assessment skills and effective communication skills is a primary team education
objective. High-fidelity simulation in a simulation center is helpful, but low-
fidelity simulations with mock medical emergency scenarios or table-top exercises
are effective as well. Scenario-based case presentations using a chalkboard or
paper can be offered in any clinical setting.
2. Equipment/Supplies – The equipment and supplies carried by the response team
should be tailored to the needs of the patient population served, but then
standardized to assure that the appropriate resources reach the bedside with each
call. If multiple RRT bags are used, the items should be organized within each bag
to facilitate rapid access at the bedside. It is impractical to carry every item
available in the ICU. Equipment use should be reviewed as part of the quality
improvement program. Seldom-used items should be removed unless they serve an
important role in the management of infrequent, but high-risk events. The response
team should strive to carry only the necessary equipment and supplies.
3. Culture of Empowerment – Staff nurses should be trained to recognize signs of
clinical deterioration before a crisis and to trust their experience and skills. They
should be empowered, and supported by leadership, to activate the MET or RRT
according to established criteria. There should be no penalty for activating the
MET or RRT, especially if the findings do not point to an impending clinical crisis.
Such events can identify areas for targeted education in the detection of signs of
clinical deterioration or focused review of the risks inherent to that patient
population.
4. Evaluation – Data collection should be embedded into the clinical workflow to
facilitate monitoring of clinical and service outcomes. Regular reporting,
monitoring, and evaluation of response team activities and outcomes guide rapid
cycle improvement of team processes. Patient and family satisfaction data help
prioritize program development and resource allocation. Constant dialogue among
the stakeholders to identify improvement opportunities is essential.
VI. SUMMARY
Hospitalized patients can be at risk for clinical deterioration in part due to the complex
nature of healthcare delivery systems. The goal of the RRS model is to identify and
manage signs and symptoms of clinical deterioration in at-risk patients through detection
strategies at the bedside and mobilization of appropriate resources. Important factors in
the successful implementation of an RRS include: (1) appropriate team composition; (2)
activation criteria based on bedside staff concern, acute changes in physiology, or the
use of scoring systems to identify at-risk patients; (3) interventions aimed at rapidly
stabilizing the patient; (4) effective communication strategies like SBAR; (5) ongoing
education to enhance detection and management of potential clinical crises; (6)
availability of appropriate advanced clinical monitors, equipment, and medications to
conduct MET or RRT activities; and (7) evaluation and correction of processes and
causes of patient risk.
Suggested Readings
1. Bellomo R, Goldsmith D, Uchino S, et al. A prospective before-and-after trial of a

medical emergency team. Med J Aust. 2003;179:283-287.
2. Buist MD, Moore GE, Bernard SA, et al. Effects of a medical emergency team on
reduction of incidence of and mortality from unexpected cardiac arrests in
hospital: preliminary study. BMJ. 2002;324:387-390.
3. DeVita MA, Bellomo R, Hillman K, et al. Findings of the first consensus
conference on medical emergency teams. Crit Care Med. 2006;9:2463-2478.
4. DeVita MA, Hillman K, Bellomo R, eds. Medical Emergency Teams:
Implementation and Outcome Measurement. New York, NY: Springer Science +
Business Media Inc; 2006.
5. Halvorsen L, Garolis S, Wallace-Scroggs A, Stenstrom J, Maunder R. Building a
rapid response team. AACN Adv Crit Care. 2007;18:129-140.
6. Leonard M, Graham S, Bonacum D. The human factor: the critical importance of
effective teamwork and communication in providing safe care. Qual Saf Health
Care. 2004;13(suppl 1):i85-i90.
7. Maharaj J, Raffaele I, Wendon J. Rapid response systems: a systematic review and
meta-analysis. Crit Care. 2015;19:254-268.
8. Murray T, Kleinpell R. Implementing a rapid response team: factors influencing
success. Crit Care Nurse Clin North Am. 2006;18:493-501.
9. Sebat F, ed. Designing, Implementing, and Enhancing a Rapid Response System.
10. Sebat F, Musthafa AA, Johnson D, et al. Effect of a rapid response system for
patients in shock on time to treatment and mortality during 5 years. Crit Care Med.
2007;35:2568-2575.
11. Subbe CP, Kruger M, Rutherford P, Gemmel L. Validation of a modified Early
Warning Score in medical admissions. QJM. 2001;94:521-526.
12. Thomas K, VanOyen Force M, Rasmussen D, Dodd D, Whildin S. Rapid response
team: challenges, solutions, benefits. Crit Care Nurse. 2007;27:20-27.
Suggested Website
1. American College of Cardiology. http://www.acc.org.

APPENDIX 2
AIRWAY ADJUNCTS
I. LARYNGEAL MASK AIRWAY

A. Indications
1. Provide an airway and ventilation when bag-mask ventilation is difficult

2. Provide a temporizing airway when endotracheal intubation is unsuccessful
B. Equipment
1. Bag-mask resuscitation unit with high-flow oxygen source

2. Pulse oximeter
3. Electrocardiographic monitor
4. Blood pressure monitoring
5. Gloves, mask, eye protection
6. Laryngeal mask airway (LMA) of appropriate size (Table A2-1)
7. Syringe for cuff inflation
8. Water-soluble lubricant
9. Qualitative CO2 detector or CO2 monitor
10. Resuscitation cart
Table A2-1 Laryngeal Mask Airway Size and Cuff Inflation
LMA Size Patient Size Maximum Cuff Volume Largest ETT ID (mm)a
1 Neonate/infant to 5 kg Up to 4 mL 3.5
1.5 5-10 kg Up to 7 mL 4.0
2 10-20 kg Up to 10 mL 4.5
2.5 20-30 kg Up to 14 mL 5.0
3 >30 kg/small adult Up to 20 mL 6.0 cuffed
4 Average adult Up to 30 mL 6.0 cuffed
5 Large adult Up to 40 mL 7.0 cuffed
aLargest endotracheal tube size (ETT ID) that will fit through laryngeal mask airway (LMA) tube lumen.
C. Preparation for insertion
1. Don gloves, mask, and eye protection.

2. Assure patent airway and optimal oxygenation and ventilation.
3. Assure intravenous access.
4. Apply pulse oximeter, electrocardiographic and blood pressure monitors.
5. Select appropriate size LMA.
6. Check cuff integrity by inflating and fully deflating.
7. Lubricate only the posterior aspect of the deflated mask with a water-based
lubricant.
8. Preoxygenate with 100% oxygen for 2 to 3 minutes if time permits.
D. Technique (Figure A2-1)
1. The cuff is deflated completely so that it forms a spoon shape and there are no
folds in the mask.
2. The operator stands behind the head of the bed, and the bed is raised to a position
of comfort for the operator.
3. The patient is placed in the sniffing position (ie, head extended, neck flexed),
unless potential or definite cervical spine injury prevents neck extension.
4. Cricoid pressure is not recommended during placement of the LMA because it may
interfere with correct placement.
5. The mask is positioned with the bowl facing anteriorly. Hold the device like a
pencil, with the index finger of the dominant hand at the junction of the bowl and
tube, pressing against the palate and pharyngeal wall with the index finger.
6. The cuff is inserted into the hypopharynx until definite resistance is felt.
7. Without the operator holding the device, the cuff is inflated with enough air to
obtain a seal around the laryngeal inlet. This results in an outward movement of the
tube.
8. The cuff is inflated with enough air to obtain a seal (intracuff pressure of
approximately 60 cm H2O). Maximum volumes are listed in Table A2-1, but lesser
volume may provide an adequate seal.
9. A manual ventilation device is attached, and chest movement and breath sounds are
verified in both lung fields. Correct position should be confirmed with a
qualitative or quantitative end-tidal CO2 detector.
10. If chest movement is inadequate, or if a large air leak is present, the device should
be removed and reinserted.
11. When the LMA is positioned appropriately, the tube is secured with tape.
Figure A2-1. Insertion Technique for Laryngeal Mask Airway

(A) Insert lubricated and deflated mask into the open mouth with the bowl facing anteriorly. (B) Hold the
device like a pencil, pressing against the palate and pharyngeal wall with the index finger. (C) Continue
inserting the cuff behind the tongue into the hypopharynx until definite resistance is felt. (D) Without holding
the device, inflate cuff with enough air to obtain a seal. Attach manual ventilation device and ensure chest
movement.
II. ESOPHAGEAL-TRACHEAL DOUBLE-LUMEN AIRWAY DEVICE

A. Indications
1. Cardiorespiratory arrest and inability to provide an airway by other means
B. Equipment

2. Pulse oximeter
6. Esophageal-tracheal double-lumen device

5. Select appropriate size device. The available sizes for the device are 41 and 37
French. Use the 41 French for patients taller than 5 feet (152 cm) and the 37 French
for patients less than that height.
6. Check integrity of both cuffs by inflating and fully deflating.
1. The cuffs should be deflated completely.

3. The patient is placed in a neutral or sniffing position (ie, head extended, neck
flexed), unless potential or definite cervical spine injury prevents neck extension.
4. The patient’s tongue and jaw are grasped between the thumb and index finger, and
the device is inserted blindly. It is advanced until the placement ring markers on
the tube are positioned as indicated by the manufacturer. Do not force the tube if
resistance is met. A laryngoscope can be used to assist with placement.
Figure A2-2. Esophageal-Tracheal Double-Lumen Airway Device
Some tubes have two pilot balloons to allow for independent inflation of the pharyngeal and
esophageal cuffs, whereas other tubes have a single pilot port and simultaneously inflate both cuffs.
Detection of end-tidal CO2 in the proximal lumen suggests that the tube is in the esophagus. In the
rare instance that the tube enters the trachea, ventilation is only possible via the distal lumen and end-
tidal CO2 will not be detected from the proximal lumen.
5. The pharyngeal cuff is inflated first to seal the posterior pharynx.

6. The distal cuff is then inflated.
7. Ventilation should be attempted first through the pharyngeal lumen, and the chest
should be auscultated for breath sounds and observed for movement. The tube
enters the esophagus approximately 95% of the time.
8. If breath sounds are absent, ventilation should be attempted through the tracheal
lumen while auscultating for breath sounds.
9. Use of the correct lumen for ventilation should be confirmed with a
qualitative/quantitative end-tidal CO2 or esophageal detector device.
10. When the device is positioned appropriately, the tube is secured with tape.
III. VIDEO LARYNGOSCOPE

A. Indications
1. Endotracheal intubation in known or presumed difficult airway

2. Known or suspected cervical spine injury
B. Equipment

2. Pulse oximeter
6. Video laryngoscope with appropriate blade
7. Endotracheal tube (ETT) of appropriate size for patient

5. Prepare ETT with stylet and check cuff.
6. Turn on video laryngoscope power and check light/camera.
7. Assure proper cable and blade attachment.
8. Position video screen for optimal viewing during laryngoscopy.
3. Consider lubricating the tongue side of the laryngoscope blade prior to insertion.
Insert the laryngoscope blade into the oropharynx, and advance into the
hypopharynx while watching the video screen for anatomical landmarks.
4. Once positioned in the hypopharynx, lift up and away, then adjust the position until
the glottis and vocal cords are seen.
5. Insert and advance the ETT into the hypopharynx until the tip is seen near the end
of the laryngoscope blade.
6. Advance the ETT through the glottis opening until the cuff passes the vocal cords.
Make small adjustments in laryngoscope and ETT positioning as necessary to
intubate the trachea.
7. Gently remove the laryngoscope blade while holding the ETT in place. Be careful
not to kink or pinch the camera cable.
8. Inflate the ETT cuff and remove the stylet. Attach the bag-valve device and
provide manual ventilation. Confirm bilateral breath sounds and end-tidal carbon
dioxide.
9. When the ETT is positioned appropriately, the tube is secured with tape.
Figure A2-3. Video Laryngoscopea
IV. OPTICAL LARYNGOSCOPE

A. Indications
1. Endotracheal intubation in known or presumed difficult airway

2. Known or suspected cervical spine injury
B. Equipment

2. Pulse oximeter
6. Appropriately sized optical laryngoscope – color coded
7. ETT of appropriate size for patient
1. Don gloves, mask, eye protection.

5. Prepare ETT, check cuff, and lubricate.
6. Choose appropriately sized optical laryngoscope.
7. Turn on laryngoscope light at least 30 seconds prior to use.
8. Load ETT into optical laryngoscope side channel.
9. Assure ETT tip is seen through eyepiece but is not obstructing view.
Figure A2-4. Optical Laryngoscope
The optical laryngoscope allows the operator to look through the device, whereas the video
laryngoscope in Figure A2-3 is the device with the video camera and screen.
3. Consider lubricating the tongue side of the laryngoscope blade prior to insertion.
Insert the laryngoscope blade in the midline over the tongue into the oropharynx
and advance into the hypopharynx by rotating the laryngoscope along the tongue
until it is perpendicular. Use caution to not displace the tongue posteriorly.
4. Once positioned in the hypopharynx, look through the eyepiece and lift up gently.
Adjust the position until the glottis and vocal cords are seen. If glottis structures
are not seen, gently pull back until seen. DO NOT tilt back or leverage against
upper teeth or gums.
5. Advance the ETT through the glottis opening until the cuff passes the vocal cords.
Make small adjustments in laryngoscope positioning as necessary to intubate the
trachea.
6. Inflate the ETT cuff and separate from the laryngoscope with a gentle spreading or
peeling motion. Be careful to not displace the ETT.
7. Gently remove the laryngoscope blade while holding the ETT in place. Rotate in
opposite direction from insertion.
8. Attach the bag-valve device and provide manual ventilation. Confirm bilateral
breath sounds and end-tidal carbon dioxide.
9. When the ETT is positioned appropriately, the tube is secured with tape.
Suggested Readings
1. Brain AIJ. The Intavent Laryngeal Mask Instruction Manual. Berkshire, UK:
Brain Medical; 1992.
2. Danks RR, Danks B. Laryngeal mask airway: review of indications and use. J
Emerg Nurs. 2004;30:30-35.
3. Krafft P, Schebesta K. Alternative management techniques for the difficult airway:
esophageal-tracheal Combitube. Curr Opin Anaesthesiol. 2005;17:499-504.
4. Lu Y, Jiang H, Zhu YS. Airtraq laryngoscope versus conventional Macintosh
laryngoscope: a systematic review and meta-analysis. Anaesthesia. 2011;66:1160-
1167.
5. Mace SE. The laryngeal mask airway: guidelines for appropriate usage. Resid
Staff Physician. 2001;47:30.
6. Niforopoulou P, Pantazopoulos I, Demestiha T, et al. Video-laryngoscopes in the
adult airway management: a topical review of the literature. Acta Anaesthesiol
Scand. 2010;54:1050-1061.
APPENDIX 3
ENDOTRACHEAL INTUBATION
I. INDICATIONS, PATIENT EVALUATION, MANUAL MASK

VENTILATION, PATIENT PREPARATION
See Chapter 2.
II. EQUIPMENT
A. Bag-mask resuscitation unit with oxygen supplementation (with positive end-
expiratory pressure valve if indicated)
B. Topical anesthetic spray
C. Medications as selected for analgesia/anesthesia, amnesia, and neuromuscular
blockade
D. Towel roll or pad for occipital elevation
E. Pulse oximeter
F. Electrocardiography monitor
G. Automatic blood pressure device or manual blood pressure monitoring device
H. Gloves, mask, eye protection
I. Laryngoscope handle and blade(s): usually sizes #3 and #4 curved, #2 and #3
straight
J. Endotracheal tubes: usually 7.0- or 7.5-mm for adult women and 8.0-mm for adult
men
K. Malleable stylet
L. Yankauer and tracheal suction catheters, suction device
M. Magill forceps
N. 10-mL syringe to inflate cuff
O. Water-soluble lubricant
P. Qualitative CO2 detector, CO2 monitor, or esophageal detector device
Q. Tape or tracheal tube stabilization device

R. Resuscitation cart
III. ROUTE OF INTUBATION

A. Orotracheal intubation via direct laryngoscopy
This route is generally favored in most circumstances, including when cervical

spine injury is suspected.
B. Blind nasotracheal intubation
The nasotracheal route using a blind approach can only be attempted in a

spontaneously breathing patient and may be favored by experienced operators in
select patients and situations. This technique has the advantage of allowing
continued spontaneous ventilation and generally requires less sedation than direct
laryngoscopy. It is more time-consuming than direct laryngoscopy and therefore is
less useful in emergent intubation. Endotracheal tubes used for nasotracheal
intubation have smaller diameters than those used for orotracheal intubation.
Nasotracheal intubation should be avoided if basilar skull fracture is suspected
and in the presence of coagulopathy. Nasotracheal intubation is discouraged in
infants and small children due to anatomic differences compared with adults.
IV. OROTRACHEAL INTUBATION

A. Preparation
1. Don gloves, mask, and eye protection for universal precautions.

2. Explain the procedure, if patient is conscious.
3. Assure patent airway and optimal oxygenation and ventilation (Chapter 2).
5. Apply pulse oximeter, electrocardiography, and blood pressure devices.
6. Assemble all equipment and ensure proper working order.
7. Prepare the endotracheal tube.
a. Check cuff integrity by inflating and fully deflating.
b. Insert stylet into endotracheal tube, bend to predicted configuration to assist
glottic entry. Ensure the distal tip of the stylet does not protrude past the end
of the endotracheal tube.
c. Apply water-soluble lubricant to the cuff end of the tube.
8. Connect laryngoscope blade to handle.
a. Select blade type (operator's choice).
1. Straight blade — used to elevate the epiglottis anteriorly
2. Curved blade — inserted into the vallecula
b. Select blade length — #3 blade is proper unless patient’s neck is very long.
c. Assure that light is sufficiently bright.
9. Place pad or towel under occiput if cervical spine injury is not suspected.
10. Use topical anesthetic on the patient’s oropharynx.
12. As necessary, proceed with sedation and neuromuscular blockade (Chapter 2).
B. Technique
1. The operator stands at the head of the bed, and the bed is raised to a position of
comfort for the operator. The head of the bed may be flat or raised slightly per
operator preference.
2. When no cervical injury is suspected, a small pad is placed under the occiput (the
“sniffing” position) and the neck is gently extended (Figure A3-1). When cervical
spine injury is possible, these steps are omitted, the neck is stabilized by an
assistant (as described in Chapter 2), and the anterior portion of the cervical
collar is removed.
Figure A3-1. Positioning for Orotracheal Intubation
The axial planes of the neck are not lined up with the head in a neutral position (A). Slight extension
and forward movement of the neck will line up the pharyngeal-laryngeal axis and place the oral axis
perpendicular to this line, thereby allowing visualization of the vocal cords (B). Note that this
positioning is contraindicated in patients with possible cervical spine injury.
3. Regardless of the operator’s dominant hand in other contexts, the laryngoscope is

always held in the left hand.
4. Mouth opening in the sedated/relaxed patient may be assisted by a cross-finger
technique wherein the thumb of the right hand is placed on the front lower teeth of
the mandible and the first finger on the front upper teeth (maxilla). The mouth is
gently opened by a “reverse scissor” movement of the fingers, and the
laryngoscope is introduced into the mouth.
5. The tip of laryngoscope blade is inserted into the right side of the patient’s mouth
(Figure A3-2); the blade is advanced to the base of the tongue.
6. The tongue should be swept to the left; proper tongue control is key to laryngeal
visualization.
7. The blade is gently advanced further to its proper position. A straight blade is
placed beneath the epiglottis; a curved blade is placed into the vallecula above the
epiglottis.
8. Caution! Traction should be applied only along the long axis of the laryngoscope
handle as the laryngoscope lifts the tongue upward away from the larynx, revealing
the glottic opening. A rocking or rotating motion of the blade and handle may
damage teeth, gingiva, or lips. The base of the laryngoscope blade should never
contact the upper teeth!
9. The vocal cords and glottic opening should be visualized.
Figure A3-2. Insertion of Laryngoscope
(A) The blade of the laryngoscope is inserted into the patient’s mouth and pushes the tongue to the
left. (B) The curved blade follows the base of the tongue and is inserted into the vallecula and (C) the
straight blade is inserted beneath the epiglottis.
10. If the vocal cords and glottis cannot be visualized, it may be helpful for an assistant
to grasp the thyroid cartilage between the thumb and index finger and exert
pressure in the following sequence: Pressure is applied backward against the
cervical vertebrae and then in an upward direction to shift the larynx superiorly.
Additional pressure is applied to shift the thyroid cartilage no more than 2 cm to
the right side of the patient’s neck. This procedure can be remembered by the
acronym BURP (backward, upward, and rightward pressure on the thyroid
cartilage).
11. The endotracheal tube is inserted gently through the vocal cords (Figure A3-3),
holding the tube/stylet with the right hand. The stylet, if angled, may interfere with
passage of the tube into the trachea. If resistance is encountered as the tube is
advanced, consider having an assistant remove the stylet while the operator holds
the endotracheal tube firmly in the glottic opening.
12. The stylet and laryngoscope should be removed carefully (Figure A3-3). The
operator must continue to hold the endotracheal tube firmly and position it such that
the external centimeter length markers on the tube show 21 cm (female) or 23 cm
(male) adjacent to the front teeth.
13. The cuff is inflated.
Figure A3-3. Placement of Endotracheal Tube
(A) The endotracheal tube is inserted through the vocal cords until the distal end rests approximately
2 to 3 cm above the carina. (B) Once the endotracheal tube is in the proper position, the
laryngoscope and stylet are removed and the cuff is inflated.
14. To ensure proper position of the tube:

a. Auscultate the epigastrium; inspect and auscultate chest to assure equal
bilateral gas entry.
b. Use qualitative CO2 detector or monitor or esophageal detector device. Lack
of color change with a qualitative CO2 detector or low exhaled CO2
measurement may occur with a correctly placed tracheal tube in the patient
with poor pulmonary perfusion, such as during cardiac arrest or profound
hypotension.
c. Observe for condensation in the endotracheal tube during exhalation.
d. Listen for breath sounds through the endotracheal tube as the patient is
breathing spontaneously.
e. Obtain chest radiograph (tube tip 2 to 3 cm above carina).
15. Secure endotracheal tube with tape or endotracheal tube stabilization device.
V. BLIND NASOTRACHEAL INTUBATION

A. Preparation
1. See Section IV-A, for preparation for orotracheal intubation, steps 1-6.
2. Position the patient’s head on a small towel with the neck in a slightly extended
position.
4. Use topical anesthetic on the nasal passages and pharynx and lubricate the nasal
passages.
B. Technique
1. The operator stands at the head of the bed, and the bed is raised to a position of
comfort for the operator. The head of the bed may be flat or raised slightly per
operator preference. The patient should have spontaneous ventilation and an
adequate tidal volume.
2. The larger naris should be used if there is significant deviation of the nasal septum.
3. A well-lubricated endotracheal tube without a stylet is inserted gently through the
nasal passage into the posterior oropharynx.
4. Oxygen may be administered by face mask/blowby or by intermittently connecting
the oxygen source to the endotracheal tube.
5. The oropharynx should be inspected to assure that the endotracheal tube is in the
midline.
6. The amount of air movement at the endotracheal tube connector is assessed by
either listening to air movement through the tube, using a specially designed
“whistle,” or using an exhaled CO2 monitor.
7. The endotracheal tube is advanced slowly while feeling and listening for air
movement at the connector end of the endotracheal tube. Advancement continues if
air movement increases through the tube. If air movement decreases, the
endotracheal tube should be withdrawn until air movement resumes, re-advancing
after repositioning the head.
8. Advancing the tube through the glottis is usually easier during inspiration.
9. The operator must continue to hold the endotracheal tube firmly and position it
such that the external centimeter length markers on the tube show approximately 24
cm (female) or 26 cm (male) adjacent to the naris.
10. The cuff is inflated.
11. To ensure proper position of the tube:
a. Auscultate epigastrium; inspect and auscultate chest to assure equal bilateral
gas entry.
b. Use qualitative CO2 detector or monitor or esophageal detector device. Lack
of color change with a qualitative CO2 detector or low exhaled CO2
measurement may occur with a correctly placed endotracheal tube in the
patient with poor pulmonary perfusion.
c. Observe for condensation in the endotracheal tube during exhalation.
d. Listen for breath sounds through the endotracheal tube as the patient is
breathing spontaneously.
e. Obtain chest radiograph (tube tip 2 to 3 cm above carina).
12. The endotracheal tube is secured with tape or endotracheal tube stabilization
device.
VI. PEDIATRIC CONSIDERATIONS

A. Anatomic differences between adults and children:
1. The larynx is more cephalad in infants than in adults, making it appear more
anterior and resulting in a more difficult visualization during laryngoscopy.
2. In young children, the narrowest part of the airway is at the level of the cricoid
cartilage, not at the larynx, making an anatomic “cuff” below the vocal cords.
3. In general, the diameter of the small finger approximates the properly sized
endotracheal tube. A full-term neonate can accept a tube with a 3.5-mm internal
diameter.
4. Cuffed tubes therefore are usually limited to use in children >8 years old
(endotracheal tube size >6.0-mm internal diameter); uncuffed tubes are generally
used in younger children.
B. Technique differences between adults and children:
1. Head position: a towel roll under the head is often needed in adults to achieve the
sniffing position; a shoulder roll is usually needed to achieve this position in
infants.
2. Laryngoscope blade selection: operator may choose a straight or curved blade;
however, most clinicians do not use curved blades in infants. A common mistake in
intubating a child is choosing a blade that is too small. The blade must be long
enough to reach the epiglottis.
3. Proper depth of insertion (in centimeters) can be estimated by multiplying the
internal diameter of the endotracheal tube by 3 (eg, internal diameter = 4.0; depth
of insertion = 4.0 × 3 = 12.0 cm).
4. Appropriately sized equipment (eg, face mask, laryngoscope, endotracheal tube,
suction catheter) should be used.
VII. PRECAUTIONS/COMPLICATIONS
A. Hypoxia, hypercapnia during procedure
B. Cardiovascular compromise during and immediately after procedure
C. Damaged teeth, lips, gingiva
D. Malpositioned tube (esophagus, right main-stem bronchus)
E. Pharyngeal, laryngeal, tracheal damage
F. Gastric distension and aspiration of gastric contents
G. Bronchospasm
H. Pneumothorax
Suggested Readings
1. Balk RA. The technique of orotracheal intubation. J Crit Illness. 1997;12:316-

323.
2. Knill RL. Difficult laryngoscopy made easy with a “BURP.” Can J Anaesth.
1993;40:279-282.
3. Lavery GG, Jamison CA. Airway management in the critically ill adult. In: Parrillo
JE, Dellinger RP, eds. Critical Care Medicine: Principles of Diagnosis and
Management in the Adult. 3rd ed. Philadelphia, PA: Mosby Elsevier; 2008:17.
4. Wheeler DS, Spaeth JP, Mehta R, et al. Assessment and management of the
pediatric airway. In: Wheeler DS, Wong HR, Shanley TP, eds. Pediatric Critical
Care Medicine: Basic Science and Clinical Evidence. London, England:
Springer-Verlag; 2007:223.
APPENDIX 4
INTRAOSSEOUS NEEDLE INSERTION
I. INTRODUCTION
A. Intraosseous (IO) vascular access was first introduced by Drinker in 1922 and first
reported in humans in 1934 by Josefson.
B. IO access can be easily achieved by users with little training.
C. IO access is recommended as the immediate alternative when IV access cannot be
rapidly achieved.
D. IO access provides a noncollapsible venous plexus for rapid fluid administration.
E. All fluids, blood products, and medications can be given by the IO route.
F. IO access can be used to obtain blood samples for laboratory evaluations.
II. CONTRAINDICATIONS
A. Ipsilateral fracture
B. Compartment syndrome
C. Infection at site of insertion
D. Osteogenesis imperfecta
E. Previous attempts at the same site
F. Previous orthopedic procedures near insertion site
G. Inability to locate landmarks or excessive tissue
III. DEVICES
A. Bone Injection Gun (BIG) [WaisMed Inc., New York, NY], spring-loaded device
B. Arrow EZ-IO Intraosseous Vascular Access System (Teleflex, Morrisville, NC),
battery-powered device
C. FAST1 Intraosseous Infusion System (Pyng Medical Corp., Richmond, BC,
Canada), to apply in the manubrium
D. Jamshidi Intraosseous Needle (Baxter Healthcare Corp., McGaw Park, IL), manual
device
E. Near Needle Holder (Near Manufacturing Ltd., Camrose, AB, Canada), needle
holder device
F. Sussmane-Raszynski Intraosseous Infusion Needle (Cook Medical Inc.,
Bloomington, IN), manual device
IV. EQUIPMENT
A. IO needle or trocar options, depending on the site of insertion and patient age
B. Gloves
C. Antiseptic solution
D. Syringes for infiltration of local anesthetic, blood sampling, and flushes
E. Hypodermic needle
F. Lidocaine 1%
G. Connecting tubing
H. Tape and gauze
V. SITE SELECTION
A. Neonates
1. Proximal anterior tibia, just below the growth plate, distal to the tibial
tuberosity
B. Infants up to 1 year of age
1. Proximal anterior tibia, 1 cm distal to the tibial tuberosity
C. Children older than 1 year
1. Proximal anterior tibia, 1 fingerbreadth distal to the tibial tuberosity
D. Adults
A. Proximal anterior tibia
B. Proximal metaphysis of the humerus
C. Sternum
D. Distal tibia, proximal to the medial malleolus
E. Distal radius and distal ulna
F. Distal femur, above the femur plateau
G. Anterior-superior iliac spine
H. Calcaneus
VI. TECHNIQUE FOR PROXIMAL TIBIAL INSERTION

A. Apply universal precautions.
B. Palpate the tibial tuberosity and locate the insertion site 2 fingerbreadths distal to
the tuberosity.
C. Create a sterile field (if clinical situation permits).
D. Infiltrate a local anesthetic in a conscious patient.
E. Place the patient in the supine position with knee flexed; stabilize the knee with a
hand under the popliteal fossa.
F. Insert the needle 90° through the skin until it touches the bone. Apply downward
pressure for powered devices, and add clockwise and counterclockwise rotation
for manual devices.
G. Advance the needle until the loss of resistance (needle has passed through the bone
cortex); the needle should stand freely and upright without support.
H. Remove the trocar and aspirate marrow into the syringe, discarding the first few
milliliters of blood (thick fibrin mesh).
I. For needles without a trocar (Near Needle Holder), flush the needle with saline
first (needle may be plugged with bone debris).
J. Secure the needle by taping flanges to the skin or stabilize with bulky gauze
dressing.
K. Draw blood for laboratory analysis.
L. Start infusions, observing the surrounding tissues for possible extravasation.
M. Remember to flush the needle with 5 mL of saline solution after administration of
every medication.
Figure A4-1. Intraosseous Needle Insertiona
Approach to puncture of the proximal anterior tibia. aFrom: Fiser DH. Intraosseous infusion. N Engl J Med.
1990;322(22):1579-1581. Copyright © 1990 Massachusetts Medical Society. Reprinted with permission
from Massachusetts Medical Society.
VII. IO REMOVAL
A. Discontinue IO once peripheral or central venous access is established.
B. Stabilize the extremity and withdraw the trocar/needle, maintaining the axial
alignment of the needle. Use an upward clockwise and counterclockwise rotation
until the needle exits the bone cortex.
C. Apply pressure to the puncture site for approximately 5 minutes.
D. Apply a sterile dressing.
VIII. COMPLICATIONS
A. Inability to place the needle, bending or breaking the needle
B. Subcutaneous extravasation
C. Bone fracture
D. Through-and-through penetration
E. Compartment syndrome
F. Clogged needle
G. Local infection (cellulitis, subcutaneous abscess, osteomyelitis)
H. Pneumothorax, mediastinal hematoma, mediastinitis (in sternal IO access)
I. Pulmonary fat embolus
J. Pain
Suggested Readings
1. Leidel BA, Kirchhoff C, Bogner V, Braunstein V, Biberthaler P, Kanz KG.

Comparison of intraosseous versus central venous vascular access in adults under
resuscitation in the emergency department with inaccessible peripheral veins.
Resuscitation. 2012;83(1):40-45.
2. Hansen M, Meckler G, Spiro D, Newgard C. Intraosseous line use, complications,
and outcomes among a population-based cohort of children presenting to
California hospitals. Pediatr Emerg Care. 2011;27(10):928-932.
3. 2005 American Heart Association (AHA) guidelines for cardiopulmonary
resuscitation (CPR) and emergency cardiovascular care (ECC) of pediatric and
neonatal patients: pediatric advanced life support. Pediatrics. 2006;117(5):e1005-
e1028.
4. Brenner T, Bernhard M, Helm M, et al. Comparison of two intraosseous infusion
systems for adult emergency medical use. Resuscitation. 2008;78(3):314-319.
5. Horton MA, Beamer C. Powered intraosseous insertion provides safe and
effective vascular access for pediatric emergency patients. Pediatr Emerg Care.
2008;24(6):347-350.
6. Schwartz D, Amir L, Dichter R, Figenberg Z. The use of a powered device for
intraosseous drug and fluid administration in a national EMS: a 4-year experience.
J Trauma. 2008;64:654-655.
7. Wampler D, Schwartz D, Shumaker J, Bolleter S, Beckett R, Manifold C.
Paramedics successfully perform humeral EZ-IO intraosseous access in adult out-
of-hospital cardiac arrest patients. Am J Emerg Med. 2012;30(7):1095-1099.
8. Lewis P, Wright C. Saving the critically injured trauma patient: a retrospective
analysis of 1000 uses of intraosseous access. Emerg Med J. 2015;32(6):463-467.
9. Helm M, Haunstein B, Schlechtriemen T, Ruppert M, Lampl L, Gäßler M. EZ-
IO(®) intraosseous device implementation in German Helicopter Emergency
Medical Service. Resuscitation. 2015;88:43-47.
10. Pasley J, Miller CH, DuBose JJ, et al. Intraosseous infusion rates under high
pressure: a cadaveric comparison of anatomic sites. J Trauma Acute Care Surg.
2015;78(2):295-299.
APPENDIX 5
ARTERIAL BLOOD GAS ANALYSIS AND

TREATMENT
These acid-base problems are provided for practice in analyzing arterial blood gas and
electrolyte information and determining appropriate interventions.
For complicated acid-base disorders, it may be helpful to understand the utility of the
delta gap (Δgap). In an uncomplicated anion gap (AG) metabolic acidosis, every AG
increase of 1 mmol/L beyond the normal value should result in a concomitant decrease
of approximately 1 mmol/L in [HCO3]. Deviation from this relationship suggests a
mixed acid-base disorder. The difference between the change in the AG and the change
in [HCO3] from the normal values is the Δgap, which can be expressed as:
Δgap = (deviation of AG from normal) – (deviation of [HCO3] from normal)
The normal value for Δgap should be 0. However, variance in measurements can result
in a Δgap of 0 ± 6. If the Δgap is positive, then a simultaneous metabolic alkalosis
exists. If the decrease in [HCO3] is greater than the increase in AG, which results in a
negative Δgap, then a concomitant normal AG acidosis (hyperchloremic) may exist.
Small deviations of the Δgap may not indicate mixed acid-base disorders, and clinical
information must always be considered.
For purposes of analyzing the following cases, assume that a normal HCO3 is 24
mmol/L and a normal AG is 12 mmol/L using the formula:
[Na] – ([Cl] + [HCO3])
Case 1
A 78-year-old woman with hypertension and hyperlipidemia is admitted to the
intermediate care unit for ongoing evaluation and management of a community-acquired
pneumonia. She was admitted 12 hours ago from the emergency department. She
remains tachypneic with increased work of breathing. Vital signs are: heart rate 105
beats/min, blood pressure 110/68 mm Hg, respiratory rate 22 breaths/min, and
temperature 38.4°C (101.2°F). Physical examination reveals bilateral rhonchi and
normal mental status. She is receiving supplemental oxygen at 3 L/min via nasal
cannula, and oxygen saturation on pulse oximetry is 88%. An arterial blood gas
measurement is made as part of her ongoing workup, with the following results:
pH 7.47
PaCO2 31 mm Hg (4.13 kPa)
PaO2 55 mm Hg (7.33 kPa)
HCO3 (calculated) 22 mmol/L
1a. Which one of the following best describes the acid-base disorder?
A. Metabolic acidosis
B. Respiratory alkalosis
C. Respiratory alkalosis and metabolic acidosis
D. Respiratory alkalosis and metabolic alkalosis
1b. Which one of the following is the most appropriate intervention?
A. Intubation and mechanical ventilation

B. Noninvasive ventilation
C. Increase in supplemental oxygen concentration
D. No new intervention
Case 2
A 26-year-old man arrives at the emergency department with multisystem trauma
following a motorcycle collision. He is somnolent with a Glasgow Coma Scale score of
13. The primary survey reveals an open airway with equal breath sounds bilaterally.
Vital signs are: temperature 36.2°C (97.2°F), heart rate 116 beats/min, respiratory rate
20 breaths/min, blood pressure 100/50 mm Hg, and oxygen saturation on pulse oximetry
99% with a non-rebreather mask in place. The patient undergoes diagnostic radiological
evaluations that reveal left rib fractures without hemothorax or pneumothorax. As part
of his initial workup, he has blood sent for laboratory analysis. The results are as
follows:
pH 7.31
PaO2 163 mm Hg (21.73 kPa)
Na 140 mmol/L
Cl 105 mmol/L
HCO3 15 mmol/L
2a. Which acid-base disorder is present?
A. Non-anion gap metabolic acidosis

B. Respiratory acidosis
C. Anion gap metabolic acidosis
D. Metabolic acidosis with respiratory alkalosis
2b. What is the suspected cause of the acid-base disorder?
A. Diabetic ketoacidosis
B. Lactic acidosis
C. Uremia
D. Hyperventilation
2c. Which of the following is the most appropriate intervention?
A. Administration of intravenous bicarbonate

B. Fluid and blood product administration
C. No intervention required at this time
D. Intubation
Case 3
A 21-year-old female college student did not wake up the morning after attending a
fraternity party where alcohol and drugs were available. Emergency services was
called, the patient was placed on supplemental oxygen via non-rebreather mask,
peripheral intravenous access was obtained, and fluids were started. Initial vital signs
in the emergency department are: heart rate 102 beats/min, respiratory rate 10
breaths/min, blood pressure 92/60 mm Hg, and oxygen saturation on pulse oximetry
94%. The patient only moans when exposed to noxious stimuli but does localize. Blood
is drawn for laboratory evaluation, including an arterial blood gas. The result are as
follows:
pH 7.23
Na 141 mmol/L
K 4.0 mmol/L
Cl 110 mmol/L
HCO3 26 mmol/L
A. Non-anion gap metabolic acidosis

B. Respiratory acidosis
C. Respiratory acidosis and non-anion gap metabolic acidosis
D. Respiratory acidosis and metabolic alkalosis
3b. Which of the following should be the initial intervention?
A. Intubation and intravenous administration of naloxone

B. Administration of activated charcoal
C. Noninvasive positive pressure ventilation
D. No additional intervention
Case 4
A 55-year-old man is admitted to the surgical ICU after elective laparoscopic
cholecystectomy. An iatrogenic injury to the hepatic artery required conversion to an
open cholecystectomy and fluid resuscitation with normal saline and blood products.
Vital signs are: heart rate 115 beats/min, respiratory rate 12 breaths/min (ventilator
rate), blood pressure 105/68 mm Hg, and oxygen saturation on pulse oximetry 99% at
fraction of inspired oxygen of 50%. Laboratory values are as follows:
pH 7.32
Na 146 mmol/L
K 3.8 mmol/L
Cl 117 mmol/L
HCO3 18 mmol/L
A. Anion gap metabolic acidosis

B. Anion gap metabolic acidosis and respiratory acidosis
C. Anion gap metabolic acidosis and non-anion gap metabolic acidosis
D. Non-anion gap metabolic acidosis
4b. Which of the following is the most likely cause of the acid-base disorder in this
patient?
A. Cardiogenic shock
B. Hemorrhagic shock
C. Normal saline administration
D. Hypoventilation
Case 5
An 81-year-old man was admitted to the medical floor for an exacerbation of congestive
heart failure. He received high-dose intravenous furosemide over the last 48 hours,
which allowed him to be weaned off noninvasive positive pressure ventilation. He is
currently on supplemental oxygen via nasal cannula. Vital signs are: heart rate 88
beats/min, respiratory rate 18 breaths/min, blood pressure 120/72 mm Hg, and oxygen
saturation on pulse oximetry 97% on supplemental oxygen at 6 L/min. Laboratory values
are as follows:
pH 7.50
Na 136 mmol/L
Cl 96 mmol/L
HCO3 33 mmol/L
A. Metabolic alkalosis and respiratory acidosis

B. Metabolic alkalosis
C. Metabolic alkalosis and non-anion gap acidosis
D. Respiratory acidosis
5b. Which of the following is the most likely cause of the acid-base disorder?
A. Hypercapnic respiratory failure

B. Volume overload related to congestive heart failure
C. Hypercortisolism
D. Diuretic administration
5c. Which of the following is an appropriate treatment option?
A. Restart noninvasive positive pressure ventilation

B. Administer acetazolamide
C. Continue diuresis with furosemide
D. Decrease administration of furosemide and consider administration of fluids
Case 6
A 58-year-old woman with hypertension and chronic kidney disease is admitted to the
hospital with alcohol intoxication. She is somnolent and arouses to painful stimuli. Vital
signs are: heart rate 110 beats/min, blood pressure 142/88 mm Hg, respiratory rate 10
breaths/min, temperature 37°C (98.6°F), and oxygen saturation on pulse oximetry 94%.
Laboratory results are as follows:
pH 7.23
Na 134 mmol/L
K 6.1 mmol/L
Cl 100 mmol/L
HCO3 15 mmol/L
Blood urea nitrogen 62 mg/dL
Creatinine 3.7 mg/dL
Glucose 125 mg/dL
6. Which one of the following best describes the acid-base disorder?

B. Anion gap metabolic acidosis and metabolic alkalosis
C. Anion gap metabolic acidosis and respiratory acidosis
D. Anion gap metabolic acidosis and non-anion gap metabolic acidosis
Case 7
An 80-year-old man with hypertension, diabetes, and malnutrition is admitted to the
hospital with cough, fever, and hypotension. Chest radiograph shows a right lower lobe
pneumonia. Vital signs are: heart rate 115 beats/min, blood pressure 90/52 mm Hg,
respiratory rate 20 breaths/min, temperature 38.3°C (101°F), and oxygen saturation on
pulse oximetry 95% on oxygen supplemented at 8 L/min via nasal cannula. Laboratory
results are as follows:
pH 7.35
Na 132 mmol/L
K 4.0 mmol/L
Cl 103 mmol/L
HCO3 17 mmol/L
Blood urea nitrogen 20 mg/dL
Creatinine 1.4 mg/dL
Albumin 1.5 g/dL

B. Non-anion gap metabolic acidosis
C. Non-anion gap metabolic acidosis and respiratory alkalosis
Case 8
A 60-year-old man with arterial vascular disease and hypertension presented to the
emergency department with complaints of shortness of breath and abdominal pain. Vital
signs are: heart rate 90 beats/min, blood pressure 168/96 mm Hg, respiratory rate 25
breaths/min, temperature 37.2°C (99°F), and oxygen saturation on pulse oximetry 98%
while receiving oxygen at 2 L/min via nasal cannula. Laboratory results are as follows:
pH 7.55
Na 135 mmol/L
K 3.8 mmol/L
Cl 101 mmol/L
HCO3 13 mmol/L
8a. Which one of the following best describes the acid-base disorder?
A. Acute respiratory alkalosis

B. Chronic respiratory alkalosis
C. Acute respiratory alkalosis and metabolic alkalosis
D. Acute respiratory alkalosis and metabolic acidosis
8b. Which one of the following is a potential etiology of the acid-base disorder?
A. Pulmonary embolism
B. Sepsis
C. Diuretics
D. D. Chronic obstructive lung disease and renal failure
Case 9
A 70-year-old woman is admitted to the ICU with syncope after several days of
vomiting. Vital signs are: heart rate 140 beats/min, blood pressure 80/50 mm Hg,
respiratory rate 24 breaths/min, and temperature 37.0°C (98.6°F). Laboratory results
are as follows:
pH 7.30
Na 138 mmol/L
K 3.0 mmol/L
Cl 93 mmol/L
HCO3 20 mmol/L
Glucose 90 mg/dL

B. Anion gap metabolic acidosis and metabolic alkalosis
C. Anion gap metabolic acidosis and respiratory acidosis
Case 10
A 55-year-old diabetic, hypertensive man presents with nausea, vomiting, and
abdominal pain. Vital signs are: heart rate 124 beats/min, blood pressure 102/50 mm
Hg, respiratory rate 22 breaths/min, and temperature 36.4°C (97.6°F). Laboratory
results are as follows:
pH 7.45
Na 134 mmol/L
K 3.2 mmol/L
Cl 85 mmol/L
HCO3 23 mmol/L
Glucose 420 mg/dL
A. Respiratory acidosis and metabolic acidosis

B. Respiratory acidosis, metabolic acidosis, and metabolic alkalosis
C. Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis
D. Respiratory alkalosis and metabolic acidosis
Case Study Answers and Rationales
Case 1
1a. The correct answer is B, Respiratory alkalosis.
The pH is alkalemic. The low PaCO2 suggests a respiratory process rather than a
metabolic process. The formula to determine if the respiratory process is acute is:
Increase in pH = 0.08 ×(40 – PaCO2)
10
Using the information from the case, the expected increase in pH would be 0.072,
resulting in an expected pH 7.47. This finding suggests a pure respiratory process. You
can further analyze it by considering whether there is appropriate buffering of HCO3
using the following formula:
Decrease in [HCO3] = 2 ×∆PaCO2
10
Data from the blood gas measurements suggest a decrease of [HCO3] of 1.8 mmol/L,
which is close to the decrease of 2 mmol/L of the calculated [HCO3].
Although the patient is at risk for a metabolic acidosis, the appropriate decrease of
[HCO3] in relation to the respiratory alkalosis makes that a less likely condition.
Clinically, you would always review the electrolytes along with the arterial blood gas
and calculate the anion gap. There is no suggestion of a metabolic alkalosis with the
near normal [HCO3].
1b. The correct answer is C, Increase in supplemental oxygen concentration.

The patient is significantly hypoxic but based solely on the information presented, she
may not need any more support than an increase in oxygen concentration and continued
monitoring. Any worsening of her respiratory rate or mental status may necessitate
positive pressure support.
Case 2
2a. The correct answer is C, Anion gap metabolic acidosis.
The pH is acidemic. The low bicarbonate concentration is consistent with a metabolic
process. The next step is to determine if appropriate respiratory compensation is
present.
Appropriate PaCO2 compensation = 1.5 x [HCO3] + 8 ± 2
In this case, the appropriate compensation would yield PaCO2 30.5 ± 2 mm Hg. Thus,
respiratory compensation is appropriate. The next step is to calculate the anion gap.
AG = [Na] – ([Cl] + [HCO3])
AG for this case = [140] – [(105+15)] = 20 mmol/L

This patient has an elevated anion gap metabolic acidosis. With an anion gap acidosis,
the Δgap should be calculated to determine if additional metabolic processes are
present.
Δgap = (deviation of AG from normal) – (deviation of [HCO3] from normal)
= (20-12) – (24-15)
= -1 mmol/L
This is within the normal range of 0 + 6, indicating that no additional metabolic process
is present.
2b. The correct answer is B, Lactic acidosis.
The causes of elevated anion gap metabolic acidosis can be remembered with the
following mnemonic MUDPILES, which stands for methanol, uremia, diabetic
ketoacidosis, paracetamol/acetaminophen, isoniazid, lactic acidosis, ethylene glycol or
methanol, and salicylates.
This case depicts a trauma patient in shock with hypoperfusion, resulting in lactic
acidosis.
2c. The correct answer is B, Fluid and blood product administration.
The goal is restore perfusion to the tissues. This patient is experiencing hypovolemic
hemorrhagic shock. The treatment is fluid and blood product administration and control
of the hemorrhage.
Case 3
3a. The correct answer is B, Respiratory acidosis.
The pH is acidemic. The increase in PaCO2 indicates a respiratory process. Next,
determine if this is an acute or chronic respiratory process.
For an acute respiratory acidosis,
the decrease in pH = 0.08 x ∆PaCO2
10
Thus, the decrease in pH = 0.08 x 20/10 = 0.16, which is close to the observed value of
60 mm Hg (8.0 kPa). This is an acute respiratory process.
If metabolic compensation is present, the bicarbonate concentration will increase 1
mmol/L for every 10 mm Hg (1.33 kPa) increase in PaCO2. For this case, there is a 20
mm Hg change in PaCO2 that should translate into a 2 mmol/L increase in bicarbonate.
The HCO3 concentration is 26 mmol/L, which is 2 mmol/L above the normal value of 24
mmol/L and consistent with appropriate metabolic compensation.
3b. The correct answer is A, Intubation and intravenous administration of naloxone
This patient has hypoventilation related to drug and alcohol intoxication. Activated
charcoal will not reverse the respiratory depression. The patient also was not found
until the following morning, making it too late for use of activated charcoal. The
severely depressed mental status prohibits the use of noninvasive positive pressure
ventilation; a patient must be conscious with the ability to protect the airway for
noninvasive positive pressure ventilation to be used. This patient should be intubated to
control her respiratory failure, and naloxone can be administered simultaneously.
Case 4
4a. The correct answer is D, Non-anion gap metabolic acidosis.
The correct answer is D, Non-anion gap metabolic acidosis.
The pH is academic and the change in HCO3 concentration would indicate a metabolic
process. The next step is to evaluate whether the respiratory compensation is
appropriate.
Respiratory compensation: 1.5 x [HCO3] + 8 ± 2
Respiratory compensation: 1.5 x [18] + 8 ± 2 = 35 ± 2

In this case the patient has appropriate respiratory compensation. The next step is to
determine if the anion gap is elevated.
AG =[Na] – ([Cl] + [HCO3])
146 – (117 + 18) = 11 mmol/L
There is no elevation in the anion gap, so this patient has a non-anion gap metabolic
acidosis.
4b. The correct answer is C, Normal saline administration.
Metabolic acidosis with a normal anion gap, which is a hyperchloremic acidosis, may
result from gastrointestinal or renal loss of HCO3 or volume resuscitation with normal
saline. In this case, the patient received excess fluid resuscitation due to hemorrhage in
surgery. This patient has metabolic acidosis as a result of hyperchloremia from normal
saline resuscitation.
Cardiogenic shock and hemorrhagic shock would result in metabolic acidosis with an
elevated anion gap. Hypoventilation would be associated with a respiratory acidosis.
The appropriate intervention is to change to an intravenous fluid with lower chloride
content, such as Ringer lactate.
Case 5
5a. The correct answer is B, Metabolic alkalosis.
The pH is alkalemic. The increase in [HCO3] indicates a metabolic process.
Respiratory compensation in metabolic alkalosis is determined by the following
formula:
Increase in PaCO2 = 0.6-0.7 x Δ[HCO3] = 0.6-0.7 x 9 = 5.4-6.3 mm Hg (0.72-0.84 kPa)
Thus, the increase in PaCO2 is appropriate respiratory compensation. Calculation of the
anion gap yields a normal result of 7 mmol/L.
5b. The correct answer is D, Diuretic administration.
Metabolic alkaloses are usually characterized as chloride-depleted (hypovolemic) or
chloride-expanded (hypervolemic). In this patient, diuretic use is the most likely cause
of the alkalosis.
5c. The correct answer is D, Decrease administration of furosemide and consider
administration of fluids.
Chloride-depleted metabolic alkalosis is corrected by administration of an intravenous
normal saline infusion. Discontinuation of the furosemide should occur to prevent
further depletion of chloride and further exacerbation of metabolic alkalosis. Careful
monitoring of the fluid status is indicated in a patient with history of heart failure, and
expert consultation is required.
Case 6
6. The correct answer is C, Anion gap metabolic acidosis and respiratory acidosis.
The pH is acidemic and the low [HCO3] indicates a metabolic process. The formula for
determining the expected respiratory compensation is:
PaCO2 = 1.5 x [HCO3] + 8 ± 2
The expected PaCO2 would be approximately 30 mm Hg (4.0 kPa). Thus, the finding of a
higher PaCO2 than expected indicates another acid-base process of respiratory acidosis.
The respiratory acidosis is most likely secondary to depressed respiratory drive from
intoxication. This patient has ventilatory insufficiency and must be monitored closely for
worsening and the potential need for more aggressive ventilatory support. The anion gap
is calculated as an increased value of 19 mmol/L, which is likely secondary to chronic
kidney disease, but other unmeasured anions (such as lactate) may be contributing.
The Δgap can be calculated for this case. The deviation of the anion gap from normal is
7 mmol/L, and the deviation of the [HCO33] from normal is 9 mmol/L. The difference of
-2 mmol/L is not likely to represent a third acid-base process.
Case 7
7. The correct answer is A, Anion gap metabolic acidosis.
The pH is acidemic and the low [HCO3] indicates a metabolic process. The formula for
PaCO2 = 1.5 x [HCO3] + 8 ± 2
Thus, the expected PaCO2 would be approximately 33 mm Hg (4.4 kPa). The anion gap is
calculated as 12 mmol/L, which appears normal. However, the albumin concentration
must be taken into account. A limitation of the traditional approach to acid-base analysis
is the effect of hypoalbuminemia on the anion gap. The expected anion gap decreases by
2.5 to 3 mmol/L for every 1 g/dL. In this patient, an albumin of 1.5 g/dL (assuming a
normal albumin of 4 g/dL) would decrease the expected anion gap to 5 to 6 mmol/L.
Thus, the calculated anion gap of 12 mmol/L is increased by 6 mmol/L. It is important to
recognize the presence of the anion gap metabolic acidosis in assessing the severity of
illness of this patient. The clinical scenario is consistent with severe sepsis, and a lactic
measurement is indicated.
Case 8
8a. The correct answer is D, Acute respiratory alkalosis and metabolic acidosis.
The pH is alkalemic and the low PaCO2 indicates a respiratory process. The next step is
to determine if this is an acute or chronic respiratory alkalosis. The formula for acute
respiratory alkalosis is:
Increase in pH = 0.08 × (40 – PaCO2)/10
Using the data from this case, the expected increase in pH would be 0.2 or pH 7.6,
which is higher than 7.55. The formula for chronic respiratory alkalosis is:
Increase in pH = 0.03 × (40 – PaCO2)/10,
Applying it yields a pH increase of 0.075 or pH 7.475. These calculations suggest that
there is likely to be a second acid-base disorder present. Calculation of the anion gap as
21 mmol/L identifies the second process of anion gap metabolic acidosis. The Δgap can
be also be calculated for this case. The deviation of the anion gap from normal is 9
mmol/L, and the deviation of the [HCO3] from normal is 11 mmol/L. The difference of
-2 is not likely to represent a third acid-base process.
8b. The correct answer is B, Sepsis.
The acid-base pattern can be helpful in suggesting an etiology of a patient’s condition. In
this case, respiratory alkalosis with anion gap metabolic acidosis is the typical acid-
base disorder of sepsis. Salicylate intoxication would also be associated with this acid-
base pattern. Pulmonary embolism would typically result in a respiratory alkalosis, with
acidosis being unlikely in a hemodynamically stable patient. Diuretic use would
primarily result in metabolic alkalosis rather than acidosis. Chronic obstructive lung
disease and renal failure would most likely result in a respiratory acidosis and
metabolic acidosis.
Case 9
9. The correct answer is B, Anion gap metabolic acidosis and metabolic alkalosis.
The pH is acidemic and the lower HCO3 indicates a metabolic process. The formula for
PaCO2 = 1.5 x [HCO3] + 8 ± 2
Using this, the expected PaCO2 would be approximately 38 mm Hg (5.07 kPa), which is
close to the PaCO2 of 36 mm Hg (4.8 kPa). The anion gap is calculated as 25 mmol/L,
which identifies the presence of an anion gap metabolic acidosis. The Δgap should also
be calculated for this case. The deviation of the anion gap from normal is 13 mmol/L,
and the deviation of the [HCO3] from normal is 4 mmol/L. The difference of 9 mmol/L
suggests the presence of a metabolic alkalosis. The [HCO3] did not decrease as much as
expected for the degree of acidosis. The clinical scenario is also suggestive of volume
depletion from vomiting, resulting in the metabolic alkalosis. An anion gap metabolic
acidosis (lactic acidosis) was the result of hypotension.
Case 10
10. The correct answer is C, Respiratory alkalosis, metabolic acidosis, and metabolic
alkalosis.
The pH in this very ill patient is nearly normal, which should immediately raise the
suspicion for complex acid-base disorders. The history is suggestive of possible
diabetic ketoacidosis, so the first calculation could be the anion gap, which is increased
at 26 mmol/L. Using the formula for determining the expected respiratory compensation
for a metabolic acidosis—PaCO2 = 1.5 x [HCO3] + 8 ± 2—the expected PaCO2 would be
approximately 42 mm Hg (5.60 kPa). Since the patient’s PaCO2 is lower at 34 mm Hg
(4.53 kPa), a respiratory alkalosis is present. The Δgap should definitely be calculated
for this case. The deviation of the anion gap from normal is 14 mmol/L, and the
deviation of the [HCO3] from normal is 1 mmol/L. The difference of 13 mmol/L
suggests the presence of a metabolic alkalosis. The [HCO3] did not decrease as much as
expected for the degree of acidosis. The clinical scenario is consistent with diabetic
ketoacidosis with volume depletion from vomiting and a respiratory alkalosis, possibly
secondary to pain.
You could also approach the problem by identifying the pH as alkalemic. The lower
PaCO2 would prompt assessment of whether it is an acute or chronic respiratory process.
Acute is more likely, so the formula for acute respiratory alkalosis would be used:
Increase in pH = 0.08 × (40 – PaCO2)/10. Based on the data from this case, the expected
increase in pH would be 0.048 or pH 7.45, which is similar to the patient’s value. The
other acid-base processes would still be identified because the anion gap is always
calculated.
APPENDIX 6
BRAIN DEATH AND ORGAN DONATION
I. BRAIN DEATH (DEATH BY NEUROLOGIC CRITERIA)

Brain death is usually a clinical diagnosis based on total and irreversible cessation of
all brain function, including that of the brainstem. To diagnose brain death, physicians
must verify the presence of unresponsive coma, the absence of brainstem reflexes, and
the absence of respiratory drive after a CO2 challenge. To assure that cessation of brain
function is irreversible, physicians must determine the cause of the coma, exclude
medical conditions that could mimic coma, and observe the patient for a period of time
to exclude the possibility of recovery. Diagnostic criteria and methods in brain death
may be established by national, state, or hospital policies and vary among institutions
and political jurisdictions. Common requirements are summarized in Table A6-1. A
physician experienced in brain death certification, hospital policy, and relevant laws
should always participate in this process.
Local, regional, and national regulations play a significant role in the organ donation
process. Clinicians determining the propriety of organ donation must do this with
consideration of applicable standards.
Most hospitals have the capability to perform and interpret an electroencephalogram,
nuclear medicine scan, or cerebral angiogram. These may be considered the preferred
tests in confirming physical findings consistent with brain death. In some jurisdictions,
ancillary tests are utilized when uncertainty exists about the reliability of components of
the neurologic examination or when the apnea test cannot be performed.
Special interpretation is required for each of these ancillary tests. In adults, ancillary
tests are not needed for the clinical diagnosis of brain death and cannot replace a
neurologic examination.
Table A6-1 Clinical Criteria for Brain-Death Certification
Prerequisites (all must be present):

1. Coma, irreversible and cause known
2. Neuroimaging explains coma
3. Central nervous system depressant drug effect absent (if indicated, toxicology screen; if
barbiturates given, serum level <10 μg/mL)
4. No evidence of residual paralytics (electrical stimulation if paralytics used)
5. Absence of severe acid-base, electrolyte, endocrine abnormality
6. Normothermia or mild hypothermia (core temperature >36°C [96.8°F])
7. Systolic blood pressure ≥100 mm Hg
8. No spontaneous respirations
Examination (all must be present):

1. Pupils nonreactive to bright light
2. Corneal reflex absent
3. Oculocephalic reflex absent (tested only if cervical spine integrity ensured)
4. Oculovestibular reflex absent
5. No facial movement to noxious stimuli at supraorbital nerve, temporomandibular joint
6. Gag reflex absent
7. Cough reflex absent to tracheal suctioning
8. Absence of motor response to noxious stimuli in all four limbs (spinally mediated reflexes are
permissible)
Apnea test (all must be present):

1. Patient is hemodynamically stable
2. Ventilator adjusted to provide normocarbia (PCO2 35-45 mm Hg)
3. Patient preoxygenated with 100% FIO2 for >10 minutes to PaO2 >200 mm Hg
4. Patient well-oxygenated with positive end-expiratory pressure of 5 cm H2O
5. Oxygen provided via a suction catheter to the level of the carina at 6 L/min or attach T-piece with
continuous positive airway pressure at 10 cm H2O
6. Ventilator disconnected
7. Spontaneous respiration absent
8. Arterial blood gas drawn at 8-10 minutes, patient reconnected to the ventilator
9. PCO2 >60 mm Hg or 20 mm Hg rise from normal baseline value
Ancillary testing (only one needs to be performed) to be ordered only if clinical examination
cannot be completed due to patient factors, or if apnea testing inconclusive or aborted:
1. Cerebral angiography
2. Hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography
3. Electroencephalography
4. Transcranial Doppler ultrasonography
Information taken from Wijdicks EFM, Varelas PN, Gronseth GS, Greer DM; American Academy of
Neurology.Evidence-based guideline update: determining brain death in adults: Report of the Quality
Standards Subcommittee of the American Academy of Neurology. Neurology. 2010;74(23):1911-1918.
II. ORGAN DONATION
A. BRAIN DEATH
Organs and tissues obtained from donors who fulfill brain-death criteria can be used in
transplantation. This is facilitated by a local organ procurement organization
representative, the procurement transplant coordinator, who can provide information
about eligibility criteria for specific organs or tissues. The coordinator can assist in or
conduct the process of requesting donation from the family.
Immediate goals for stabilizing the brain-dead organ donor include establishing baseline
organ function and stabilizing physiology. In general, a central venous catheter and
arterial catheter are required. Cultures are obtained with baseline chemistries to rule
out immediate infectious and metabolic complications. Chest radiography,
echocardiography, bronchoscopy, and coronary angiography may be indicated. Blood
type and crossmatch are performed.
Initial fluid management includes crystalloid administration guided by central venous
pressure. Vasoactive drugs are often required to maintain perfusion pressure. Table A6-
2 lists standard physiologic goals for initial resuscitation. Other aspects of donor
management are more controversial. Donors frequently suffer from panhypopituitarism
secondary to ischemia. Vasopressin levels may be extremely low. Dysfunction of the
anterior pituitary also may be seen with hormone administration to counteract the loss of
corticotropin and thyroid-stimulating hormone. Thyroid hormone and insulin are
sometimes given. Insulin therapy is titrated to a blood glucose level of between 120 and
180 mg/dL.
Suggested Parameters for Optimal Donor Organ Function Before

Table A6-2
Procurement
Systolic blood pressure >90 mm Hg

Mean arterial pressure >60 to 65 mm Hg
Central venous pressure 4 to 10 mm Hg
Urine output 100 to 200 mL/h, or 1 to 4 mL/kg/h
Arterial oxygen saturation >95 % or PaO2 >100 mm Hg (13.3 kPa)
Hematocrit >30%
Temperature 97.7°F to 99.5°F (36.5°C to 37.5°C)
Normal electrolyte levels
Serum glucose 120 to 180 mg/dL (6.6 to 9.9 mmol/L)
Eyelids taped shut/eye drops
B. CARDIAC DEATH
Organs may be procured from donors after cardiac death. Once the decision to remove
life-sustaining care has been made, families and appropriate patients may be
approached regarding the possibility of organ donation after cardiac death. This process
is also facilitated by the local organ procurement organization.
Organ procurement takes place in the operating room, where support is withdrawn and a
period of asystole typically ensues. The duration of asystole required is directed by
local policy; typically, a 2- to 10-minute asystolic interval (pulselessness, apnea,
unresponsiveness) is observed. Up to 10% of potential donors maintain cardiac activity
for 60 minutes after discontinuation of life support. Normally, these individuals are not
organ donors and receive ongoing end-of-life care.
Two common contingencies may be encountered in donation after cardiac death:
unexpected cardiac arrest while awaiting withdrawal of care, and failure to progress to
cardiac arrest after withdrawal of support. Management of these episodes is based on
patient and family wishes regarding resuscitation and end-of-life care.
Suggested Readings
1. Shemie SD, Doig C, Dickens B, et al. Severe brain injury to neurological

determination of death: Canada forum recommendations. CMAJ. 2006;174:S1-13.
2. Shemie SD, Ross H, Pagliarello J, et al. Organ donor management in Canada:
recommendations of the Forum on Medical Management to Optimize Donor Organ
Potential. CMAJ. 2006;174:S13-32.
3. Wijdicks EF. Brain death worldwide: accepted fact but no global consensus in
diagnostic criteria. Neurology. 2002;58:20-25.
4. Wijdicks EF. The diagnosis of brain death. N Engl J Med. 2001;344:1215-1221.
5. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM; American Academy of
Neurology. Evidence-based guideline update: determining brain death in adults.
Report of the Quality Standards Subcommittee of the American Academy of
Neurology. Neurology. 2010;74:1911-1918.
6. Wood KE, Becker BN, McCartney JG, D'Alessandro AM, Coursin DB. Care of the
potential organ donor. N Engl J Med. 2004;351:2730-2739.
Suggested Websites
1. Society of Critical Care Medicine/Guidelines. www.SCCM.org/guidelines.
2. United Network for Organ Sharing. http://www.unos.org.
3. Westphal GA, Caldeira Filho M, Vieira KD, et al. Guidelines for potential
multiple organ donors (adult). Part I. Overview and hemodynamic support. Rev
Bras Ter Intensiva. 2011;23(3):255-268.
http://www.scielo.br/pdf/rbti/v23n3/en_v23n3a03.pdf
4. Westphal GA, Caldeira Filho M, Vieira KD, et al Guidelines for potential multiple
organ donors (adult). Part II. Mechanical ventilation, endocrine metabolic
management, hematological and infectious aspects. Rev Bras Ter Intensiva.
2011;23(3):269-282. http://www.scielo.br/pdf/rbti/v23n3/en_v23n3a04.pdf

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Fundamental Critical Care Support 6e

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Fundamental

Critical Care Support

Managing Editor: Janet Thron

Printed in the United States of America

International Standard Book Number: 978-1-620750-55-1

Babak Sarani, MD, FCCM

FCCS Sixth Edition Planning Committee

Thomas P. Bleck, MD, FCCM

Gregory H. Botz, MD, FCCM

David J. Dries, MD, MCCM

Mark E. Hamill, MD, FCCM

Muhammad Jaffar, MD, FCCM

Edgar Jimenez, MD, FCCM

John M. Oropello, MD, FCCM

David Porembka, DO, PhD

Mary J. Reed, MD, FCCM

Sophia Chu Rodgers, ACNP, FNP, FAANP, FCCM

Janice L. Zimmerman, MD, MCCM, MACP

Jeremy Fulmer, RCP, RRT-ACCS, NPS

Kristie A. Hertel, ACNP, CCRN, MSN, RN

Patrick C. McKillion, MD, FCCP

Rodrigo Mejia, MD, FCCM

Don C. Postema, PhD

Sri-Sujanthy Rajaram, MD, MPH

Kazuaki Atagi, MD, PhD, FCCM

Steven M. Hollenberg, MD, FCCM

Frank M. O’Connell, MD, FACP, FCCP

RECOGNITION AND ASSESSMENT OF THE

Explain the importance of early identification of patients at risk for life-threatening

A 54-year-old woman with diabetes was admitted with an intra-abdominal abscess

II. RECOGNIZING THE PATIENT AT RISK

Patients seldom deteriorate abruptly,

Tachycardia in response to physiological

III. INITIAL ASSESSMENT OF THE CRITICALLY ILL PATIENT

Emergency admission (limited information)

History Main features of circumstances and More detailed information

Examination Look, listen, feel Structured examination of

Treatment Proceeds in parallel Refine treatment, assess

Tachypnea may reflect pulmonary,

Table 1-2 Assessment of Airway and Breathing

Paradoxical breathing is a sign of

Inadequate circulation may result from primary abnormalities of the cardiovascular

Table 1-3 Assessment of Circulation

Difficulty in obtaining a pulsatile

C. Chart Review and Documentation

An accurate measure of urine output,

IV. TRANSLATING INFORMATION INTO EFFECTIVE ACTION

Recognition And Assessment Of The Seriously Ill Patient

Recognize signs of a threatened airway.

Observe the patient’s level of consciousness and determine if apnea is present. If

III. MANUAL METHODS TO ESTABLISH AN AIRWAY

1. Slight neck extension

Airway adjuncts such as properly sized oropharyngeal or nasopharyngeal airways may

The patient’s tongue is the most common

IV. MANUAL MASK VENTILATION

if the patient is apneic.

A. When No Cervical Spine Injury is Suspected

1. If needed and tolerated by the patient, an oropharyngeal or nasopharyngeal airway