ALTERATIONS IN

OXYGENATION
 ALTERATIONS IN
OXYGENATION
 Assessing Clients with Cardiac Disorders
 Anatomy, Physiology and Functions of the
Heart
 Systemic, Pulmonary and Coronary
Circulation
 Gas Transport
 Cardiac Cycle and Cardiac Output
NURSING ASSESSMENT OF THE
CARDIAC PATIENT
 Effective cardiac nursing requires application of
critical thinking to patient care activities. The
challenge to the cardiovascular nurse is to anticipate
precipitous changes in the patient’s condition by
using data derived from physical assessment and
sophisticated bedside hemodynamic monitoring
equipment.
 The nursing process, a systematic problem solving
method, is the recognized framework for patient care.
As in all other areas of nursing, assessment is the
vital first phase of the nursing process.
 Components
 INTERVIEW, to obtain subjective data
 PHYSICAL EXAMINATION, to obtain
objective data
 NURSING HISTORY
 Asking relevant questions about the patient’s current and past
health status and practices can elicit valuable information about
the patient’s prior experiences within the health care system,
his or her attitudes regarding health, and etiologic factors that
may have contributed to the development of cardiovascular
disease.

Chief Complaint

 Determining WHY the person sought medical treatment helps

to establish priorities of care and evaluates the person’s
perception of the illness. Common c/o include CHEST PAIN,
SHORTNESS OF BREATH, FATIGUE, PALPITATION, and
PERIPHERAL SKIN CHANGES. If the patient has more than
one c/o, priority should be assigned according to the amount of
concern they generate in the patient.
 NURSING HISTORY
 Answers to the following questions can
provide information about the perceived
significance of these symptoms:
 How long has the symptoms been experienced?
 What tends to trigger the symptom?
 What interventions or activities alleviate the
symptoms?
 How does the symptom affect the patient’s
lifestyle?
 NURSING HISTORY
 The patient’s perception of the illness may or may not
correlate with the actual physical condition.
Perception of the disease state is dependent upon
three factors:
 The patient’s understanding or knowledge of the illness
 The patient’s immediate concerns. A problem at work or at
home may have a higher priority
 Outcome expected by the patient regarding present illness
and hospitalization. These include the perceived impact on
a coronary event on lifestyle, the symbolic meaning of
heart disorders, fear of impending death, and anxiety
regarding the necessity for and length of a hospital stay.
 Medical History
 Information about childhood diseases, particularly RH fever or
Congenital anomalies, should be obtain. Any history of
previous hospitalization and chronic or major illnesses must
also be determined. Of particular interest are conditions that
influence current cardiovascular performance, such as DM.
HTN. Thyroid disorders, Kidney disease, Stroke, Anemia,
Gout, Thrombophlebitis, or bleeding disorders.
 Because many drugs can affect the overall performance of the
cardiovascular system, it is imperative to assess current use of
prescription or over- the- counter drugs; not only
cardiovascular drugs but also anticoagulants, bronchodilators,
steroids, antidepressants, contraceptives, antihistamines, and
antineoplastic agents.
 Identifying Risks Factors
 Based on the determination of existing risk
factors, a plan can be formulated to assist the
patient in making necessary lifestyle changes
to promote health and lessen the impact of
heart disease.
 NON-MODIFIABLE RISK FACTORS
(Factors that can not be change)

 Age- persons above 40 years of age are at risks to develop

cardiovascular diseases. This is due to degenerative changes in
the heart and blood vessels.
 Gender- males are more prone to cardiovascular disorders
before the age of 65 years. However, females have higher
propensity to cardiovascular disorder after the age of 65 years.
This is due to decrease estrogen levels I menopause. HDL
decreases, LDL increases. Atherosclerosis develops.
 Race- cardiovascular disorders are among the 10 leading
causes of death worldwide.
 Heredity- persons with family history for cardiovascular
disorders are at risk to develop these diseases.
 MODIFIABLE RISK FACTORS
(Factors that can be change)
Lifestyle or behavioral factors can be controlled or completely eliminated

 Cigarette smoking- Nicotine causes vasoconstriction and spasm of the

arteries; increased myocardial oxygen demands; and adhesion of platelets; in
addition cigarette smoking has been associated with decreased levels of HDL
(good cholesterol). Male cigarette smoker has 2-3X the risk of developing
heart disease of the non-smoker; the female who smokes has up to 4X the
risk. For both men and women who stop smoking, the risk of mortality is
reduced by half.
 Second-hand (or environmental) tobacco smoke also increases the risk of
death from CHD, by as much as 30%
 Tobacco smoke promotes CHD is several ways:
 Carbon monoxide damages vascular endothelium, promoting cholesterol
deposition.
 Nicotine also constricts arteries, limiting tissue perfusion (blood flow and oxygen
delivery). Further nicotine reduces HDL levels and increases platelet aggregation,
increasing risk of thrombus formation.
 FACTS: Cigarette smoking is the leading independent risk factor for CHD
and a primary target of risk factor management.
 MODIFIABLE RISK FACTORS
(Factors that can be change)
 Alcohol. Positively correlates with high blood pressure.
 Stress. Sympathetic response stimulation causes increased secretion of
norepinephrine; this results to vasoconstriction and tachycardia. Increased BP and
increased cardiac workload occur.
 Diet. Increased dietary intake of foods high in sodium, fats and cholesterol
predisposes a person to cardiovascular disorder.
 Exercise. Regular pattern of exercise improves circulation to different body parts,
maintains vascular tone and enhances release of chemical activators (tissue-type
plasminogen activators), which prevent platelet aggregation.
 Hypertension. Increased systemic vascular resistance, endothelial damage, increased
platelet adherence, increased permeability of endothelial lining, result from elevated
BP.
 Hyperlipidemia, Hypercholesterolemia. Increased LDL cholesterol (“bad
cholesterol”) damages endothelium and causes accumulation or endothelial lining and
proliferation of smooth muscle cells. Low-density lipoproteins (LDLs) are the
primary carriers of cholesterol; high levels promotes atherosclerosis because LDL
deposits cholesterol on artery walls; (LDLs=less desirable lipoproteins). In contrast,
high-density lipoproteins (HDLs=highly desirable lipoproteins) help clear cholesterol
from the arteries transporting it to the liver for excretion.
 MODIFIABLE RISK FACTORS:
(Factors that can be change)
 Diabetes Mellitus. Glucose from carbohydrates cannot be
transported into the cells due to insulin deficiency or increased
resistance to insulin.
The body then, mobilizes fats (lipolysis), to become a
source of glucose. However, not all of the fats mobilized are
converted into glucose.
 Hyperlipidemia results, which enhances the risk of
atherosclerosis.
 Obesity. This results to increased cardiac workload. May also
be characterized by rise in serum lipid levels.
 Personality type or Behavioral Factors. The type A behavioral
pattern, characterized by competitiveness, impatience,
aggressiveness and time urgency has been correlated to CAD,
although the mechanism is unknown.
 Contraceptive Pills.May precipitate thromboembolism and
HPN.
 SUBJECTIVE FINDINGS
(clinical manifestations)
The common symptoms of cardiac patients
described below are usually caused by one or
all of three physiologic disorders: cardiac
ischemia, pump insufficiency, and rhythm
disturbances.
 CHEST PAIN. Pain (or related discomfort)

caused by an O2 supply inadequate to meet

myocardial oxygen demand is a cardinal
symptom of heart disease.
 SUBJECTIVE FINDINGS
(clinical manifestations)
The following elements of pain are usually assessed to confirmed
ischemic cardiac pain and to differentiate angina from
myocardial infarction.
 Characteristics. Chest pain maybe described as a “strange feeling”,
discomfort, dull heavy pressure, indigestion, crushing, burning,
constricting, acting, stabbing, and tightness.
 Location. Pain maybe substernal, precordial, across the chest, or
around the nipple line. It maybe diffuse or localized.
 Radiation. The pain may also radiate to the jaw, teeth, neck, left
shoulder, left arm or both arms, and the back. In some patients, the
radiated pain rather than the chest pain is the only presenting
discomfort.
 Severity. Using a scale of 1(least severe) to 10(most severe), ask the
patient to indicate the intensity of the pain.
The following elements of pain are usually assessed to confirmed ischemic
cardiac pain and to differentiate angina from myocardial infarction.

 Duration. The exact time period of a continuous pain episode lay last
from minutes to hours. Several intermittent small episodes, however,
are not considered a long pain period.
 Precipitating or Aggravating Factors. Such factors as exertion,
emotional excitement, nervousness, extreme coldness, deep breathing,
position changes, and deep sleep are known to precipitate chest pain.
However, pain may occur spontaneously without apparent precipitating
factors.
 Accompanying Symptoms. Chest pain is often accompanied by
anxiousness, shortness of breath, palpitation, sweating, nauseas, or
vomiting.
 Alleviating Factors. Interventions taken by the patient to relieve chest
pain may include resting, sublingual nitroglycerine, oxygen
administration, and change of position. Pain lasting more than 20
minutes without relief is usually suggestive of MI.
 SUBJECTIVE FINDINGS
(clinical manifestations)
 FATIGUE. Increasing weakness and fatigue are common
complaints of cardiac patients when ventricular function fails
and cannot supply sufficient blood to meet even slight increases
in the metabolic needs of the body cells. It is important to note
what amount of activity is tolerated by the patient (e.g., walking
to the main entrance gate), when changes in activity tolerance
were first noted, and wether fatigue Is relieved by rest.
 SHORTNESS OF BREATH. In cardiac patients, dyspnea is
usually due to pulmonary congestion caused by left ventricular
failure. It may occur at rest or with exertion.
 PALPITATION. This is a sensation of rapid, skipping,
irregular, or pounding heartbeats. It is often caused by a
tachyarrhythmia, premature ectopic beats, or increased force of
myocardial contraction ( as can occur with stress and anxiety or
ingestion of caffeine).
 SUBJECTIVE FINDINGS
(clinical manifestations)
 SYNCOPE . Episodes of dizziness, lightheadedness, or
momentarily loss of consciousness may result from
momentary reduction in blood flow to the brain due to
precipitous drop in cardiac output.
 WEIGHT CHANGES AND EDEMA. Recent weight gain and
ankle swelling may suggest sodium and water retention
associated with CHF and HTN. A weight gain of 3lb or more
in 24 hours is highly suggestive of fluid retention.
 EXTREMITY PAIN. Ischemia from peripheral vascular
disease can cause pain in the extremities, especially in anching
sensation in the legs. If this pain is associated with activity and
is relieved with rest, intermittent claudication (arterial
insufficiency) is indicated. Pain related to dependency of the
extremities indicates venous insufficiency. Thrombophlebitis
is often made evident by eliciting a positive Homan’s
sign(pain in the calf) when the foot is dorsiflexed).
 PHYSICAL EXAMINATION
Objective Findings

 General Appearance. At a glance, the nurse should observe the patient’s

facial expression, affect, level of consciousness, tone of voice, posture,
movements, respiration rate and pattern, skin color and turgor, status in
regard to diaphoresis and cachexia, nutritional state and reactions to
surroundings.
 Inspection of Neck Veins. The distensibility of the neck veins reflects the
pressure and volume changes of the right atrium. Therefore, purposed of
neck vein inspection is to estimate CVP and to evaluate the pressure wave
form.
 Palpation of the Carotid Arteries. Cardiac activity, such as stroke volume
and aortic competency, can be assessed indirectly through palpation of the
carotid arteries. A Bruit (a blowing sound) maybe heard by a stethoscope. A
bruit usually indicates a narrowing of the carotid artery or a radiation of an
aortic valve murmur.
 Inspection and Palpation of the Precordium. This is performed to determined
presence of normal and abnormal pulsations.
Objective Findings

 Apical Impulse (Point of Maximal Impulse, PMI). A visible pulsation

maybe observed in the area of the midclavicular line in the fifth left inter
costal space. It corresponds with ventricular systole, and is a single faint,
instantaneous “tap” approximately 2 cm in diameter. In the presence of
hypertrophy or dilation and aneurysm, the apical impulse maybe larger in
size and more laterally or inferiorly located.
 Retractions. Marked or actual retraction of a rib just medial to the left
midclavicular line in the 5th inter costal space is abnormal and may result in
pericardial disease.
 Heaves (Lifts). A diffuse lifting impulse observed along the the left sternal
border or at the apex implies an increased contact of right ventricle with
chest wall as found with dilatation-hypertrophy associated with various
disorders such as valvular diseases and hypertension.
 Thrills. The abnormal turbulent blood flow causing an audible murmur of
Grade V and VI intensity also results in palpable thrills. Best felt over the
left precordium. It may occur as a resuly of severe mitral regurgitation or a
ruptured ventricular septum.
Auscultation

 Heart Sounds
 S1 is produced by asynchronous closure of the mitral and tricuspid valves. It
signals the onset of ventricular systole “lubb”.
 S2 is produced by asynchronous closure of the aortic and pulmonic valves. It
signals the onset of ventricular diastole “dub”.
 S3 or ventricular diastolic gallop is a faint, low pitched sound produced by rapid
ventricular filling in early diastole. It is normal in children and young adults. It
indicates CHF in older adults.
 S4 or atrial diastolic gallop is a low frequency sound which is present in CHF.
 Murmurs
 These are audible vibrations of the heart and great vessels that are produced by
turbulent blood flow.
 Pericardial Friction Rub
 It is an extra heart sound originating from the pericardial sac. This maybe a
sign of inflammation, infection or infiltration. It is described as a short, high
pitched, scratchy sound.
ASSESSMENT OF MURMURS
Note the following characteristics:
 Timing and Duration of maximal intensity:
 Systolic: early, mid, or late systole
 Diastolic: early, mid, or late diastole
 Quality: blowing, harsh, rumbling
 Pitch: high, heard best with the diaphragm
 low, heard best with the bell
 Location: where heard the loudest; 3rd or 4th left
inter costal space, apical area, or base of the heart
 Radiation: transmission of sound
 Intensity
(not necessarily equal to degree of disease)

 Grade I Faint, not heard with every beat.

 Grade II Soft, but heard with every beat.
 Grade III Moderately loud without accompanying
thrill
 Grade IV Loud with possible palpable thrill
 Grade V Very loud, heard only with the
stethoscope and accompanied by a thrill.
 Grade VI Very loud, heard without the stethoscope
and accompanied by a thrill.
 AUSCULTATION OF
LUNG SOUNDS
 Is an essential component of cardiovascular
assessment and provides information about
cardiac function, especially left ventricular
performance.
 Types:
 Normal breath sounds
 Adventitious breath sounds
 ASSESSMENT OF THE
ABDOMEN
 On inspection, the abdomen should be symmetrical in
contour and should appear flat or slightly rounded. A
distended abdomen may result from fluid (ascites),
adipose tissue, gas. Feces, or malignancy and
warrants further investigation.
 On Auscultation, bowel sounds should be assessed in
all four abdominal quadrants. Decreased motility
accompanies electrolyte disturbances, peritonitis, or
pneumonia.
ASSESSMENT OF PERIPHERY
 Skin. As the body’s largest organ, the skin
reflects changes in the internal environment.
 Color. Cyanosis, a dusky blue color, is best
detected in areas of least pigmentation---lips, oral
mucosa, nail beds, ear lobes, conjuctiva, palms,
and soles. It results from increased amount of
reduced hemoglobin (deoxygenation) of venous
blood seen in severe pulmonary disease and
cardiovascular incompetence.
 Pallor. Is observed as peripheral blood flow
diminishes or hemoglobin decrease.
ASSESSMENT OF PERIPHERY
 Temperature. Skin temp. reflects blood flow to dermis.
Decreased cardiac output, shock, and stress precipitate an
outpouring of catecholamines. The resulting widespread
vasoconstriction produces cool, moist, clammy skin.
 Clubbing. A chronic decrease in oxygenation may result in
clubbing of the fingers (“drumstick fingers”). Nails become
wide and flattened and lie at an angle of 180 degrees or more
to the nail base.
 Turgor. Skin elasticity is determined by picking up a fold of
skin on the lower abdomen, radial surface of the wrist, or inner
thigh and observed how quickly it returns to its normal shape.
Loss of turgor reflects an extra cellular volume deficit or the
normal changes that occur with aging, excessive weight loss,
and chronic steroid used.
 DIAGNOSTIC TESTS OF
CARDIAC DISORDERS
Laboratory Studies:

 Complete Blood Count

 For evaluation of general health status.
 Elevated RBC”s suggests inadequate tissue oxygenation. Hypoxia
stimulates renal secretion of erythropoietin. This stimulates the bone
marrow to increase rbc production (polycythemia)
 Elevated WBC”s may indicate infectious heart diseases and myocardial
infarction.
 Erythrocyte Sedimentation Rate (ESR)
 It is a measurement of the rate at which RBc’s “settle out” of
anticoagulated blood in an hour.
 It is elevated in infectious heart disorders or MI
 Normal range is as follows:
 Male : 15-20 mm/hr.
 Females : 20-30 mm/hr.
 DIAGNOSTIC TESTS OF
CARDIAC DISORDERS
 Blood Coagulation Tests
 Prothrombin time (PTTTT, Pro-time)

 It measures the time required for clotting to occur after

thromboplastin and calcium are added to decalcified plasma.

 It is valuable in evaluating effectiveness if coumadin. Therapeutic

range is 1.5 to 2 times the normal or control.

 Normal range is 11 to 16 seconds.

 Partial Thromboplastin Time (PTT)

 it measures the time required for clotting to occur after a “partial

thromboplastin reagent” is added to blood plasma

 it is the best single screening test for disorder of coagulation

 it is determined to evaluate the effectiveness of heparin. Therapeutic

range is 2 to 21/2 times the normal or control.

 Normal range is 60 to 70 secs.
 DIAGNOSTIC TESTS OF
CARDIAC DISORDERS
 Activated Partial Thromboplastin Time (APTT)
 It has the same purpose as PTT. It is most specific
 Test to evaluate effectiveness of heparin. Therapeutic range
is 2-2.5 times the normal or control.
 Normal range is 30-45 secs.
 Blood Urea Nitrogen (BUN)
 it is an indicator of renal function.
 decreased cardiac output leads to low renal tissue perfusion
and reduction in glomerular filtration rate (GFR). The BUN
level becomes elevated.
 Normal range is 10-20 mg/dl.
Blood Lipids
 Cholesterol

 the client should be on NPO for 10-12 hours

 normal range is 150-250 mg/dl
 Triglycerides
 fasting for 10-12 hours
 normal range 140-200 mg/dl
 Blood Culture
 to assist in the diagnosis of infectious diseases of
the heart; e.g., pericarditis
Enzyme studies
 Enzymes are proteins that catalyzed chemical reactions found in
every cells of various organs in the body and skeletal muscle as
well as in the plasma (small amount). Cardiac enzymes are
organ-specific enzymes that are present in high concentration in
myocardial tissue.
 Isoenzymes often has slightly different molecular forms. Both
creatinine kinase (CK) and lactic dehydrogenase (LDH) have
isoenzymes specific for the heart.
 Rationale:
 Tissue damage can release enzymes from their intracellular storage
areas. MI cause cellular anoxia w/c alters membrane permeability and
allows leakage of cellular contents. Prolonged anoxia leads to edema
and rupture, with consequent spillage of enzymes into surrounding
tissue. Enzymes are liberated into the blood stream via the coronary
lymphatic drainage system.
Types of Major cardiac enzymes
a. Creatine Phosphokinase (CK-MB)
 it is the most cardiac specific enzyme
 it is an accurate indicator of myocardial damage
 normal range is:
 males : 50-325 mu/ml
 females : 50-250 mu/ml.
 Range with MI:
 Onset : 3-6 hours
 Peaks : 12-18 hrs.
 Returns to normal : 3-4 days
Types of Major cardiac enzymes
b. Lactic Dehydrogenase (LDH)
 among the five LDH isoenzymes, LDH1 is the
most indicator of myocardial damage.
 In MI, LDH is elevated and its level exceeds
LDH2. this makes LDH1/LDH2 ratio
“flipped”
 Normal range is 100-225 mu/ml
 Range with MI
 Onset : 12 hrs.
 Peaks : 48 hrs.
 Returns to normal : 10-14 days
c. Aspartate Aminotransferase (AST)
 formerly, SGOT
 elevated level indicates tissue necrosis
 normal range is 7 to 40 mu/ml.
 range with MI
 Initial elevation : 4-6 hrs.
 Peaks : 24-36 hrs.
 Returns to normal: 4-7 days
d. Hydroxybutyrate Dehydrogenase (HBD)
 elevation of HBD is always accompanied by elevation of
LDH level
 it is valuable in detecting “silent MI” because it remains
elevated for a long period of time,even after the other
enzymes have returned to normal.
 The HBD/LDH ratio maybe increase in MI
 Normal range is 140-350 mu/ml.
 Range with MI
 Onset : 10-12 hrs.
 Peaks : 48-72 hrs.
 Returns to normal : 12-13 days.
Urinalysis
 This test is performed to assess the effects of cardiovascular disease on
renal function and the existence of concurrent renal or systemic disease;
e.g., glumerolunephritis, HTN or DM
 Albuminuria is detected in client with malignant HTN and CHF.
 Myoglobinuria supports diagnosis of MI.

Blood Uric Acid (BUA)

 This test reflects adequacy of renal tissue perfusion thereby glomerular
filtration of metabolites.
 Cardiovascular disorders result to decreased renal tissue perfusion. This
will cause impairment of the ability of the kidneys to clear the plasma of
end products of metabolism like uric acid.
 Normal range is 2.5-8 mg/dl.
Serologic Tests
 VDRL helps indicates presence of syphilis. This

disease involves development of aortic disorder.

Serum Electrolytes
 Electrolytes affect cardiac contractility, specifically

Na, K, Ca.
 Normal range is as follows:
 Na : 135 – 145 mEq/L
 K : 3.5 – 5.0 mEq/L
 Ca : 4.5 – 5.5 mEq/L
 HEMODYNAMIC MONITORING WITH
NON-INVASIVE PROCEDURES
ELECTROCARDIOGRAPHY AND CARDIAC MONITORING
Definitions:

 Polarized State
 The cell is at rest in a polarized state. Although, the inside of the cell is
negative with respect to the outside its membrane remains electrically
intact. The membrane resting potential (MRP) is -90 mv.
 Depolarization
 It is the propagation of an electrical impulse due to an abrupt change
in the permeability of the cell membrane, allowing the inside of the cell
to become increasingly positive with respect to outside (Na+ and Ca++
enters the cell and K+ leaves).
 Repolarization
 The cell returns to its resting state (Na+ leaves the cell and K+ enters).
 HEMODYNAMIC MONITORING WITH
NON-INVASIVE PROCEDURES
 Electrocardiogram (EKG,ECG)
 An electrocardiogram is a recorded graph of waves that represent
variations in the time sequence of the electrical potentials produced by
depolarization and repolarization of the myocardium.
 Electrocardiography
 Is the science of taking and interpreting electrocardiograms in order to
diagnose cardiac disease by consistent correlation of characteristic
patterns.
 Rationale
The movement of ions that produces the depolarization and
repolarization of the myocardium can be detected on the body
surface. Electrodes placed upon the surface of the body will
pick up various components of this ionic movement. By
connecting this electrodes to an ECG machine, the electrical
potentials of the heart are recorded depicted as wave forms.
 HEMODYNAMIC MONITORING WITH
NON-INVASIVE PROCEDURES
 An upright deflection represents a positive electrical potential and occurs
when the current travels towards the recording electrode.
 A downward deflection represents a negative electrical potential and occurs
when the current travels away from the recording electrode.
 Indications:
 Arrhythmia pericarditis
 Chest Pain effect of drugs (cardiac)
 MI electrolyte disturbances (K+)
 Determination of heart rate effect of certain systemic
 Chamber dilation or hypertrophy diseases on the heart
 Pacemaker function
 Limitation:
 The ECG should always be correlated with the patient’s clinical assessment. A
patient with a normal heart may show non-specific ECG changes, whereas a
patient with a diseased heart may have a normal ECG.
 HEMODYNAMIC MONITORING WITH
NON-INVASIVE PROCEDURES
 ECG Grid
 Voltage
 1mm = 0.1mv
 5mm = 0.5mv
 Time
 1 mm = .04 second
 5 mm = .20 second
 Is a graph that allows for measurement of electrical activity
during the cardiac cycle. The horizontal axis represents time,
whereas the vertical axis represents voltage. All fine
horizontal and vertical lines are present at 1-mm intervals,
with a heavier line present every 5mm.
 Routine recording speed is 25mm per second.
 COMPONENTS OF ECG
P wave
 represents atrial depolarization
 contour
 in leads I,II, and AVF, it is upright, usually rounded, although it maybe slightly
pointed or slightly notched.
 In V1 it maybe diphasic or negative
 Normal range lead II
 Height is 0.3 to 2.0 mm
 Duration is 0.05 second to 0.12 second

P-R Interval
 Represents atrioventricular conduction time, including the normal delay in the AV
junction.
 Measured from the beginning of the P wave to the beginning of the QRS complex.
 Normal range is 0.12 second to 0.20 second
 The portion of this interval from the end of the P wave to the beginning of the QRS
complex (P-R segment) is normally isoelectric.
 COMPONENTS OF ECG
QRS Complex
 Represents ventricular depolarization.

 Measured from the beginning of the Q wave (or R

wave if no Q is present) to the end of the S wave
 Normal range is up to .11 second in duration.

Q-T Interval
 Represents the duration of ventricular systole.

 Measured from the beginning of Q wave to the end of

the T wave
 normal range should be a corrected figure (QT), as it
varies with heart rate.
 COMPONENTS OF ECG
J Point
 This is the point marking the end of the QRS complex and the beginning of
the ST segment.

S-T Segment
 represents the time during which the ventricle remain in the depolarized
state until the time ventricular repolarization begins
 measured from the end of the S wave (J point) to the beginning of the T
wave.
 normal range
 Usually isoelectric
 In precoridal leads may vary from (-0.5mm) to + 2.0mm from the baseline
 In standard leads may vary from ( -0.5mm) to + 1.0mm to the baseline.
 COMPONENTS OF ECG
T wave
 Represents ventricular depolarization.
 Contour.
 normally upright in leads I,II, and V3-6
 slightly rounded and slightly asymmetrical
 Normal range
 Standard limb leads, 1.0 to 5.0 mm in height.
 Precordial leads, n o greater than 10mm in height.

U Wave
 Significance is not known, however, it maybe noted in association with
low serum potassium levels, high serum calcium levels, bradycardia, left
ventricular hypertrophy, and subarachnoid hemorrhage
 Immediately follows the T wave and precedes the next P wave
 Same polarity as the T wave
 Normal range in height is not more than 1 mm
 COMPONENTS OF ECG
T-P Interval
 Represents the electrical resting potential of the heart
 Measured from the end of the T wave to the beginning of the P wave
 Contour is isoelectric and represents the baseline; i.e., elevation or
depression of other ECG components are determined by comparison to the
isoelectric line.
 Normal range varies with the heart rate; i.e., the T-P interval shortens with
tachycardia and lengthens with bradycardias.

P-P Interval
 Represents atrial rate
 Measured as the distance between two successive P waves.

R-R Interval
 Represents ventricular rate
 Measured as the distance between two successive R waves
 If rhythm is regular, R-R interval maybe used to compute heart rate.
 Leads of the Electrocardiogram
Definition
 A lead is defined as the connection of a positive and a negative electrode
through an ECG machine (galvanometer) for continuous recording the
potential differences (voltages) between the two electrodes during the
cardiac cycle.

Types
 Standard 12 Leads:
 Standard Limb Leads. Leads I,II, and III are the standard limb leads. These are
bipolar leads used to compare the electrical potential of a positive and negative
electrode, representing two limbs ( except right leg)
 Augmented Limb Leads. AVR,AVL, and AVF are unipolar leads used to
compare the electrical potential of an exploring electrodes (positive) placed on
one limb and a central terminal (negative), which represents an average potential
( close to zero) of two other limbs.
 Precordial (Chest) Leads. Leads V1,V2,V3,V4,V5, and V6 are also unipolar
leads used to compare the electrical potential of a positive exploring electrode
(in various location on the chest) and a central terminal (negative), which
represents an average potential of right arm, left arm, and left leg.
 CALCULATION OF
HEART RATE
 If the rhythm is irregular, heart rate should be determined by
counting the number of heartbeats (QRS) in a full-minute ECG
strip.
 If the rhythm is regular, any of the following methods can be
used.
 Count the number of small squares in the ECG paper within
one R-r interval and divide this number into 1500 (1-minute
length of ECG paper consist of 1500 small squares)
 Count the numbers of big squares within one R-R interval and
divide this number into 300 (1-minute length of ECG paper
consist of 300 big squares). This method can be simplified by
using the following formulas.
 CALCULATION OF
HEART RATE
If the number of big

Squares between R-R is Heart Rate should be

1 300
2 150
3 100
4 75
5 60
6 50
7 43
8 37
9 33
10 30

Count the number of QRS complexes within a 6-second time period on the ECG
strip and multiply by 10
ANALYSIS OF ECG RHYTHM
 A systematic approach to analysis is recommended to ensure
accuracy and inclusiveness. The following items are suggested
content. Analysis may begin with any of these steps. However
it should begin with the most striking feature noted
1. Regularity of the rhythm (R-R interval).
2. Ventricular rate
3. Width of the QRS complex
4. Presence of P wave.
5. P-QRS relationship
6. Regularity of P-P interval
7. Atrial rate
8. P-R interval and its consistency
9. Consistency of the shapes and contours of the waves and
complexes.
NORMAL SINUS RHYTHM (NSR)
ECG Criteria
 Rate and Rhythm. Rate is 60 to 100 beats per minute, and rhythm is regular
 QRS Complex. This is usually normal, 0.08 to 0.11 second.
 P wave. This is upright in lead I and II and is negative in AVR. Normal contour.
 P-QRS Relationship. There is one P wave per one QRS complex; P precedes QRS
with a P-R interval of normal and constant duration, 0.12 to 0.20 second.
 Origin. NSR originates in the sinus node
 Significance. NSR indicates that electrical conductions normal.

Holter Monitoring
 It is continuous (24hr.) ECG monitoring.
 The portable monitoring system is called telemetry unit.
 This attempts to assess the activities which precipitate dysrhythmias, and the time of
the day when the client experiences dysrhythmias.
 The nurse should log/record the activities of the client, and any unusual sensations
experienced.
 INVASIVE HEMODYNAMIC
MONITORING
Central Venous Pressure

 Monitors the pressures within the right antrium.

 Monitors blood volume, adequacy of venous return to the heart, pump function
of the right side the the heart.
 The O level of the manometer be placed at the right, mid-axillary, 4th ICS, the
approximate level of right atrium when in supine position.
 Place the client in supine position or in the same position as during the initial
reading.
 Practice strict asepsis. Cleanse catheter insertion site and change sterile
dressings daily.
 Normal readings:
 Superior vena cava: 0-12cm. H20
 Right atrium: 5-12cm. H20
 Use other parameters to validate CVP reading-BP, urine output, pulse.
 INVASIVE HEMODYNAMIC
MONITORING
Pulmonary Artery Pressure &
Pulmonary Capillary Wedge Pressure
 Swan- Ganz catheter is inserted via antecubital vein into the right side of
the heart and is floated into the pulmonary artery. It reflects pressures in
the left heart.
 Swan- Ganz catheter is a flow- directed, balloon- tipped, 4- lumen
catheter.
 The catheter allows continuous monitoring of the following:
 Right and left ventricular function.
 Pulmonary artery pressures (PAP, PCWP).
 Cardiac output.
 Arterial – venous oxygen difference.
 Normal range:
 PAP : 4-12 mmHg
 PCWP : 4-12 mmHg
 PCWP reading above 25 mmHg suggests impending pulmonary edema.
 INVASIVE HEMODYNAMIC
MONITORING
Nursing Interventions:
 Inflate balloon only for PCWP readings;

deflate betweens readings.

 Observe catheter insertion site; culture site

every 48 hrs.
 Assess extremity for color, temperature,

capillary fillings and sensation.

 SONIC STUDIES
Echocardiography.
 Uses ultra sound to assess cardiac structure and mobility.

 NO special preparation is required.

 It is painless and takes approximately 30 to 60 minutes to

complete.
 The client has to remain still, in supine position slightly turned

to the left side, with HOB elevated 15 to 20 degrees.

Transesophageal Echocardiography (TEE)

 Allows ultrasonic imaging of the cardiac structures and great

vessels via esophagus.

 SONIC STUDIES
Nursing Intervention Before TEE.
 Ascertain history of esophageal surgery, malignancy, or
allergy to anesthetic or sedatives.
 NPO for 4 to 6 hrs. before the procedure.

 Encourage to void before the procedure.

 Remove dentures and the other oral prosthetics.

 Administer sedatives as ordered.

 Keep suction and resuscitation equipment readily available.

 Cardiac monitoring is done during the entire procedure.

 Topical spray anesthetic is administered to depress gag reflex.

 Place the patient in chin – to – chest position to facilitate

passage of endoscope.
 SONIC STUDIES
Nursing Interventions after TEE
 After the procedure: NPO until gag reflex returns.

 Place in latheral or semi – Fowler’s position.

 Encourage to cough.

 Throat lozengers or rinses may be used to relieve

throat soreness.
 Observe for signs and symptoms of complication, e.g.

pharyngeal bleeding, cardiac dysrhytmias, vasovagal

reaction, and transient hypoxemia.
 SONIC STUDIES
Phonocardiography
 Involves the use of electrically recorded

amplified cardiac sounds

 It is helpful in assessing the exact timing and

characteristic of murmurs and extra heart

sounds.
 Preparation of client is similar to

echocardiogram
 STRESS TESTING OR
EXERCISE TESTING
 ECG is monitored during exercise on a
treadmill or a bicycle – like device.
 The purpose of stress test are as follows:
 Identify ischemic heart disease
 Evaluate patients with chest pain
 Evaluate effectiveness of therapy
 Develop individual firmness program
 STRESS TESTING OR
EXERCISE TESTING
NURSING INTERVENTIONS: Treadmill Test
 Get adequate sleep the night before the test.

 Avoid tea, coffee and alcohol on the day of the test.

 Avoid smoking and taking nitroglycerine, 2 hours before the

test
 Wear comfortable, loose – fitting clothes

 Eat a light breakfast / lunch at least 2 hours before the test.

 Wear low – heeled, rubber – soled pair of shoes.

 Inform the physician if any unusual sensations develop during

the test.
 Rest after the test.
 RADIOLIGIC TESTS
Chest Roentgenograms ( X – Rays)
 To determine overall size and configuration of the heart and size of the
cardiac chambers.

Cardiac Fluoroscopy
 Facilitates observation of the heart fro varying views while is is in motion.

Cardiac Catheterization
 The purpose of the test are as follows:
 Assess: oxygen levels, pulmonary blood flow, cardiac ouput, heart structures.
 Coronary artery visualization.
 Right – sided heart catherization is done by passing a catheter via a
cutdown into a large vein, e.g. medial cubital or brachial vein.
 Left – sided heart catherization is done by passing a catheter into the aorta
via the brachial or femoral artery.
 RADIOLIGIC TESTS
NURSING INTERVENTIONS: Cardiac Catheterization
Before the Procedure:
 Provide psychosocial support.
 Asses for allergy to iodine/seafood
 Obtain baseline VS
 Withhold meals before the procedure
 Have client void
 Administer sedative as ordered
 Mark distal pulses
 Do cardiac monitoring
 Done under local anesthesia
 May experience warm or flushing sensation as the contrast medium is
injected.
 “fluttering” sensation is felt, as the catheter enters the chambers of the
heart.
 RADIOLIGIC TESTS
NURSING INTERVENTIONS: Cardiac Catheterization
After the Procedure
 Bed rest: if the catheter insertion site is an upper extremity,
until VS are stable; while if it is a lower extremity , for 24 hrs.
 Monitor VS, especially peripheral pulses

 Monitor ECG, note for dysrhythmias

 Apply pressure dressing and a small sand bag or ice ovet the
puncture site to prevent bleeding
 Immobilize affected extremity in extension to promote
adequate circulation
 Do not elevate HOB more than 30 degrees if femoral site was
used
 Monitor extremities for color, temperature and tingling.
 ANGIOGRAPHY/
ARTERIOGRAPHY
 Involves introduction of contrast medium into
the vascular system to outline the heart and
blood vessels
 It may be done during cardiac catheterization
 Nursing interventions are similar to that of
cardiac catheterization
 Observe the hypotension after the procedure
because the contrast medium may cause
profound diuretic effect
 MAGNETIC RESONANCE
IMAGING (MRI)
 Strong magnetic field and radiowaves are used to
detect and define difference between healthy and
diseased tissues
 MRI can actually show the heart beating and the
blood flowing in any directions, it can image over
three spatial dimensions and over time.
 It is used for examination of the aorta, detection of
tumors, cardiomyopathies and pericardiac disease.
 MAGNETIC RESONANCE
IMAGING (MRI)
NURSING INTERVENTION: MRI
 Secure written consent.

 Inform the client that the procedure lasts 45 to 60 minutes.

 Asses for claustrophobia. The client will be placed in a tunnel

– like device.
 Remove all metal items, e.g. watch, eyeglasses and jewelry.

 Instruct the client to remain still during the procedure.

 Inform the client that MRI unit makes a loud, knocking noise.

CAUTION: client with pacemakers, prosthetic valves or recently

implanted clips or wires are not eligible for MRI scans.
 MYOCARDIAL SCINTIGRAPHY
 The procedure involves intravenous injection of a
radioactive isotope via a catheter.
 Myocardial function, motion and perfusion are
studied through the use of an external gamma camera.
 Techniques used are as follow:
 Thallium 201 scintigraphy
 Dipyridamole – thallium – 201 test
 Technetium 99m ventriculography
 First – pass cardiac study
 MYOCARDIAL SCINTIGRAPHY
NURSING INTERVENTIONS: Myocardial Scintigraphy
 Inform client that ECG or treadmill test may be done during

the procedure
 Asses for pregnancy because the test involves radiation

exposure.
 Instruct the client a light meal, to prevent nausea and stomach

cramping during exercise and for better uptake of the

radioisotope
 Omit the usual dose of prescribed beta – blockers, calcium –

channel blockers and xanthenes before the procedure

 Instruct the client to report any chest pain experienced during

procedure
 NON–INVASIVE HEMODYNAMIC MONITORING:
INTRA–ARTERIAL PRESSURE MONITORING

 This provides continuous detection of arterial BP via an

indwelling intra – arterial catheter
 It is valuable in monitoring the BP of the clients with low
cardiac output, fluctuating hemodynamic status and excessive
peripheral vasoconstriction and in whom cuff BP measurements
are undetectable.
 Intra – arterial readings are at least 10 mmHg higher than cuff
BP readings.
 The intra – arterial BP line can be used for obtaining blood
samples for ABG and blood studies.
 Heparinize the catheter to maintain patency
 Check catheter insertion site for hemorrhage, hematoma,
redness or signs of infection.
 Do neurovascular check distal to catheter insertion site – color,
temperature, capillary filling and sensation.
 CORONARY
ARTERY DISEASE (CAD)/
CORONARY
ATHEROSCLEROTIC
HEART DISEASE (CABD)
 SELF MANAGEMENT EDUCATION GUIDE:
DECREASING RISK FOR CORONARY ARTERY DISEASE

 Daily management of hypertension. Take medication at regular

basis. Do not stop.
 Stop smoking as soon as possible. Smoking reduces available
oxygen to the heart and can precipitate angina. Smoking
increases heart rate and blood pressure.
 Avoid passive smoke. Two hours of passive smoke decreases
oxygen to the heart, decreases exercise time and increases heart
rate and blood pressure.
 Plan a regular exercise under medical supervision.
 If overweight, lose weight. Seek help from professionals.
 Follow a healthy heart diet. Reduce cholesterol and increase
fiber.
 Reduce stress.
 Allow adequate time for rest and relaxation.
 These are life – long life – style changes.
HEART VALVES
 CORONARY ARTERY DISEASE (CAD)
CORONARY ATHEROSCLEROTIC HEART DISEASE (CAHD)

Pathophysiology: ATHEROGENESIS

RISK FACTORS

Nonmodifiable Modifiable
Age Stress
Gender Diet
Race Sedentary Living
Heredity Smoking
Alcohol
Hypertension
Diabetes Mellitus
Obesity
Hyperlipidemia / Hypercholesterolema
Behavioral Factors
Contraceptive Pills

A. Nonspecific injury to Arterial Wall (Endothelial Injury)

Desquamation of Endothelial Lining

Increased Permeability / Adhesion Molecules

B. Lipids (LDL, VLDL) and Platelets Assimilate into the Area

 C. Oxydized LDL attracts Monocytes And Macrophages to the Site

D. Plaques Begin to Form from cells Which Imbed into the Endothelium

E. Lipids are Engulfed by the Cells (foam cells) and Smooth Muscle Cells
Develop

Coronary Atherosclerotic Heart Disease

Decreased Coronary Tissue Perfusion

Coronary Ischemia

Decreased Myocardial Oxygenation

 Causes
 Coronary Atherosclerotic heart Disease
 Coronary Thrombosis / Embolism
 Decreased Blood Flow with Shock and / or Hemorrhage
 Direct Trauma

Myocardial Ischemia Myocardial Oxygen Cellular

Supply Hypoxia

Cardiac Output Myocardial Altered Cell

Contractility Membrane Int.

Arterial Stimulation of Stimulation of

Pressure Baroreceptors Sympathetic Receptors

Peripheral Afterload
Vasoconstriction

Decreased
Myocardial Heart Diastolic Myocardial
Contractility Rate Filling tissue per.

Myocardial
Oxygen Demand
 CLINICAL MANIFESTATIONS
OF ANGINA PECTORIS
 Pain
Transient, paroxysmal subternal or precoridal pain
Described as heaviness or tightness of the chest, “indigestion”, crushing
Radiates down one or both arms, left shoulder, jaw, neck and back
Precipitated by activity/exertion
Relieved by rest and nitroglycerine
 Pallor
 Diaphoresis
 Dyspnea
 Palpitations
 Dizziness
 Digestive disturbances (due to vagal stimulation)
 TYPES OF ANGINA PECTORIS
 Stable Angina
Chest pain lasts for less than 15 minutes
Recurrence is less frequent
 Unstable Angina (Preinfarction Angina, Crescendo Angina, Intermittent Coronary Syndrome)
Chest pain last for more than 15 minutes but less than 30 minutes
Recurrence is more frequent, may occur at night
Intensity of pain increases
 Variant Angina (Prinzmetal’s Angina)
Chest pain is of longer duration and may occur at rest
The attacks tend to occur in the early hours of the day
May result from coronary artery spasm
 Nocturnal Angina
Occurs only during the night and is possibly associated with rapid eye movement (REM)
sleep
 Angina Decubitus
Paroxysmal chest pain that occurs when the client sits or stands up
 Intractable Angina
Chronic, incapacitating angina unresponsive to intervention
 Postinfarction Angina
Occurs after MI, when residual ischemia may cause episodes of angina
 PRECIPITATING EVENTS OF
ANGINA PECTORIS
 Exertion. Vigorous exercise done very
sporadically
 Emotions. Excitement, sexual activity.
 Eating Heavy meal.
 Environment. Exposure to cold
 These events increase myocardial oxygen
demands. Further disequilibrium between
oxygen supply and oxygen demand occurs.
 COLLABORATIVE MANAGEMENT
OF ANGINA PECTORIS
Medications

 Vasodilators: Nitroglycerine, Amyl Nitrate,

Isosorbide
Effects:
Direct relaxing effect on vascular smooth muscle, resulting in
generalized vasodilation
Decrease peripheral resistance, decrease systolic pressure,
produce venouspooling, and decrease preload
Coronary vasodilation redistributes myocardial blood flow
more efficiently
 COLLABORATIVE MANAGEMENT
OF ANGINA PECTORIS
 Beta – adrenergic blocking agents
Propranolol (Inderal)
Metoprolol (Lopressor)
Nadolol (Corgard)
Atenolol (Tenormin)
Pindolol (Visken)
Esmolol (Brevibloc)
Effects:
Decrease myocardial oxygen demand by decreasing heart rate,
blood pressure, myocardial contractility and calcium output
 COLLABORATIVE MANAGEMENT
OF ANGINA PECTORIS
 Calcium – channel blockers
Verapamil (Isoptin, Calan)
Nifedipine (Procardia, Adalat, Calcibloc)
Diltiazen (Cardizem)
Effects:
Inhibit calcium ion transportation into myocardial cells to
depress inotropic and chronotropic activity, decreasing
cardiac workload
It has vasodilation effect
It reduces coronary vasospasm
 COLLABORATIVE MANAGEMENT
OF ANGINA PECTORIS
Other Medications

 Platelet Aggregation Inhibitors

ASA
Dipyridamole (Persantin)
Ticlopidine (Ticlid)
Effect: inhibit platelet aggregation, thereby prevent thrombus
formation

 Anticoagulants
Heparin Sodium
Effect: inactivates thrombin and other clotting factors inhibiting
conversion of fibrinogen to fibrin, fibrin clot formation is prevented.
Warfarin Sodium (Coumadin)
Dicumarol
Effect: Inhibit hepatic synthesis of Vitamin K
Nitroglycerine Therapy

 Assume sitting or supine position when taking the drug. To prevent orthostatic
hypotension.
 Take maximum of three doses at five-minute interval.
 Gradual change of position to prevent orthostatic hypotension.
 If taken sublingual, the medication causes burning or stinging sensation under
the tongue.
 Sublingual route produces onset of action within 1 to 2 minutes, duration of
action is 30 minutes.
 Offer sips of water before giving sublingual nitrates; dryness of mouth may
inhibit drug absorption.
 Instruct client to avoid drinking alcohol, to avoid hypotension, weakness and
faintness.
 Advise client to always carry three tablets in his pocket.
 NURSING INTERVENTIONS IN
DRUG THERAPY
 Store nitroglycerine in cool, dry place; use dark/amber –
colored, air-tight container, may be destroyed by heat, light or
moisture.
 Change stock of nitroglycerine every 6 months.
 Observe for side effects: headache, flushed face, dizziness,
faintness, tachycardia; these are common during first few
doses of the medication. Do not discontinue the drug.
 Transderm – Nitropatch is applied once a day, usually in the
morning.
 Rotation of skin sites is necessary, usually on the chest wall.
 Evaluate effectiveness relief of chest pain.
 NURSING INTERVENTIONS IN
DRUG THERAPY
Beta–adrenergic Blockers
 Assess pulse rate before administration of the drug, withhold if

bradycardia is present.
 Administer with food to prevent GI upset.

 Do not administer propranolol to clients with asthma. It causes

bronchoconstriction.
 Do not administer propranolol to clients with DM. It causes

hypoglycernia.
 Give with extreme caution in clients with heart failure.

 Observe for side-effects which are as follows: nausea,

vomiting, mental depression, mild diarrhea, fatigue, and

impotence.
 NURSING INTERVENTIONS IN
DRUG THERAPY
Calcium-channel Blockers
 Assess heart rate and BP

 Monitor hepatic and renal function

 Administer 1 hour before or 2 hours meals. Food delays

absorption and decreases plasma levels of the drug.

Platelet Aggregation Inhibitors

 Assess for signs and symptoms of bleeding

 Avoid straining at stool

 Do not give ASA with coumadin

 ASA should be given with food

 Observe for ASA toxicity – tinnitus

 NURSING INTERVENTIONS IN
DRUG THERAPY
Heparin Sodium
 Assess for signs and symptoms of bleeding

 Keep protamine sulfate available. It is the antidote of heparin Na

 If administered s.c., do not aspirate, do not massage, to prevent

hematoma formation
 Monitor PTT or APTT levels

 Used for a maximum of 2 weeks

Coumadin
 Assess for signs and symptoms of bleeding

 Keep vitamin K readily available. It is the antidote of coumadin.

 Monitor Prothrombin Time.

 Minimize green leafy vegetables in the diet. These contain vitamin

K.
 TREATMENT
Percutaneous Transluminal Coronary Angioplasty
(PTCA)

 Mechanical dilatation of the coronary vessel wall by

compressing the atheromatous plaque.
 It is recommended for clients with single – vessel
coronary artery disease.
 A specially designed balloon – tipped catheter is
inserted under fluoroscopic guidance and advanced
to the site of the coronary obstruction.
 TREATMENT
Intravascular Stenting

 Biologic stent is produced through coagulation of

collagen, elastin and other tissues in the vessel wall
by laser, photocoagulation or radio frequency-
induced heat.
 Prosthetic intravascular cylindric stents maintain
good luminal geometry after balloon deflation and
withdrawal
 Intravascular stenting is done to prevent restenosis
after PTCA[
 TREATMENT
Laser Therapy

 Laser light produces necrosis, hemostatis,

coagulation, evaporation of tissue.
 NURSING INTERVENTIONS
Diet
 Low Na, low fat and low cholesterol, high fiber diet

 Avoid saturated fats (animals fats)

 White meat, e.g. chicken without skin, fish are low in

cholesterol.
 Read labels

Activity
 No restrictions are placed on activity within the
patient’s limitations
 SURGICAL MANAGEMENT OF
ANGINA PECTORIS
Coronary Artery Bypass Graft (CABG)
 Reduces angina and improves activity

tolerance
 It is recommended if severe narrowing of one

or more branches of the coronary arteries exist.

 The main purpose of CABG is myocardial

revascularization
 The commonly used grafts are the saphenous

vein and internal mammary artery

 NURSING MANAGEMENT IN
CABG
Promoting comfort
 Relieve pain

 Nitroglycerine is the drug of choice for relief of pain

from acute ischemic attacks

Promoting tissue perfusion

 Instruct the client to avoid over-fatigue

 Stop activity immediately in the presence of chest

pain, dyspnea, lightheadedness or faintness which

indicate low tissue perfusion
 NURSING MANAGEMENT IN
CABG
Promoting activity and rest
 Encourage slower activity or shorter periods of activity with more rest
periods. Avoid overexertions.
 Plan for regular activity program
 Take nitroglycerine before exercise
 Increase extent of exercise gradually

Facilitating learning
 Promote a positive attitude and active participation of the client and the
family to encourage compliance

Promoting relief of anxiety and feeling of well-being

 Facilitate reduction in the client’s present level of anxiety
 Advise the client to minimize emotional outbursts, worry and tension.
 Encourage to maintain an optimistic outlook to help relieve the work of the
heart
MYOCARDIAL INFARCTION
 The formation of localized necrotic areas
within the myocardium. MI usually follows
sudden coronary and the abrupt cessation of
blood and oxygen flow to the heart muscle.
 Prolonged ischemia lasting more than 35 to 45
minutes produces irreversible cellular damage
and necrosis of the myocardium
 Causes
 Coronary Atherosclerotic heart Disease
 Coronary Thrombosis / Embolism
 Decreased Blood Flow with Shock and / or Hemorrhage
 Direct Trauma

Myocardial Ischemia Myocardial Oxygen Cellular

Supply Hypoxia

Cardiac Output Myocardial Altered Cell

Contractility Membrane Int.

Arterial Stimulation of Stimulation of

Pressure Baroreceptors Sympathetic Receptors

Peripheral Afterload
Vasoconstriction

Decreased
Myocardial Heart Diastolic Myocardial
Contractility Rate Filling tissue per.

Myocardial
Oxygen Demand
 PATHOPHYSIOLOGY OF
MYOCARDIAL INFARCTION
 Ischemic injury evolves over several hours toward complete
necrosis and infarction.
 Ischemia almost immediately alters the integrity and permeability
of the cell membrane to vital electrolytes, thereby decreased
myocardial contractility.
 The autonomic nervous system attempts to compensate for the
depressed cardiac performance. This results to further imbalance
between myocardial oxygen supply and demand.
 MI almost always occurs in the left ventricle and often
significantly depresses left ventricular function. This is due to
occlusion of the LADA ((left anterior descending artery). This is
referred to as anterior wall infarction.
 Alterations in function depend on the size and location of an
infarct.
 Contractile function in the necrotic area ceases permanently.
 PATHOPHYSIOLOGY OF
MYOCARDIAL INFARCTION
 The three areas which develop MI are as follows:
 Zone of infarction which records pathologic Q wave in the ECG
 Zone of injury which gives rise to elevated ST segment
 Zone of ischemia which produces inversion of T wave
 MI may be classified as follows:
 Transmural infarct, which extends from endocardium to epicardium.
 Subendocardial infarct, which affects the endocardial muscles and
 Intramural infarct, which is seen in patchy areas of the myocardium
and is usually associated with longstanding angina pectoris.
 Healing requires formation of scar tissues that replace the
necrotic myocardial muscle; scar tissue inhibits contractility.
 CLINICAL MANIFESTATIONS
OF MYOCARDIAL INFARCTION
 Pain
 Crushing severe, prolonged, unrelieved by rest or nitroglycerine; often
radiating to one or both arms, the neck and the back.
 Characterized by “Levine’s sign”

 Pathophysiologic Basis
 Cessation of blood supply to myocardium caused by thrombotic
occlusion causes accumulation of metabolites within ischemic part of
myocardium, this affects nerve endings.

 Anxiety and apprehension

 Feeling of “doom”, restlessness
 Pathophysiologic Basis
 Severe pain of a heart attack is terrifying; most clients are aware of the
significance of a heart attack; restlessness from shock and pain.
 PATHOPHYSIOLOGY OF
MYOCARDIAL INFARCTION
 Shock
 Systolic pressure below 80mmHg, gray, facial color, lethargy,

cold diaphoresis, peripheral cyanosis, tachycardia/bradycardia,

weak pulse
 Pathophysiologic Basis

This may be due to severe pain, severe reduction in cardiac output

and inadequate tissue perfusion, thereby tissue hypoxia.

 Oliguria
 Urine flow of less than 30 ml/hr

 Pathophysiologic Basis

This indicates renal hypoxia due to inadequate renal tissue

perfusion
 PATHOPHYSIOLOGY OF
MYOCARDIAL INFARCTION
 Fever
 Slight elevation of temperature occurs within 24 hrs and extends 3 to 7 days
accompanied by leukocytosis and elevated ESR
 Pathophysiologic Basis
Fever and leukocytosis result from destruction of myocardial
tissue and ensuing inflammatory process

 Indigestion
 Gas pains around the heart, nausea and vomiting
 Pathophysiologic Basis
Client may prefer to believe that pain is caused by “gas” or
“indigestion” rather than by heart disease; nausea and vomiting
may result from severe pain or from vasovagal reflexes conducted
from an area of damaged myocardium to gastrointestinal tract.
 PATHOPHYSIOLOGY OF
MYOCARDIAL INFARCTION
 Acute pulmonary edema
 Sense of suffocation, dyspnea, orthopea, gurgling/bubbling respiration
 Pathophysiologic Basis
Left ventricle becomes severely weakened in pumping action owing to infarction; severe
pulmonary congestion results

 ECG changes
 MI causes elevation of ST segment, inversion of T wave and enlargement of Q wave
 Pathophysiologic Basis
Pathologic Q wave develops from the area of infarction; elevated ST segment results from the area
of injury; and inverted T wave originated from the zone of ischemia
Elevation of ST segment heralds a pattern of injury and usually occurs as an initial change in acute
MI

 Elevated Ck-MB, elevated LDH, elevated AST

 Pathophysiologic Basis
These cardiac enzymes are produced in abnormally large amounts because of cellular
damage and death.
Elevation of Ck-MB is the most definitive finding in MI, especially in the presence of
increased levels of LDH
 COLLABORATIVE MANAGEMENT
OF MYOCARDIAL INFARCTION
Medications

 Analgesic
 For relief of pain. This is priority. Pain may cause shock.
 Morphine sulfate, lidocaine or nitroglycerine administered intravenously.

 Thrombolytic therapy.
 To disintegrate blood clot by activating the fibrinolytic processes
 Streptokinase, urokinase and tissue plasminogen activator (TPA) are currently used.
 Detect for occult bleeding during and after thrombolytic therapy
 Assess neurologic status changes which may indicate G.I. bleeding or cardiac
tamponade.

 Anticoagulant and antiplatelet medications are administered after thrombolytic

therapy to maintain arterial patency.

 Other medications: Beta-adrenergic blocking agents; diazepam (valium)

 TREATMENT
 Goals
 Prevention of further tissue injury and limitation of infarct size
 Maximize myocardial tissue perfusion and reduce myocardial tissue
demands
 Supplemental oxygen by nasal cannula. This increases
myocardial oxygen supply and relieves pain
 Cardiac monitoring to detect occurrence of dysrhythmias
 Percutaneous transluminal coronary angioplasty may be done
to reopen an occluded artery.
 Diet: low-cholesterol, low-salt diet is prescribed.
 Activity: Bed rest is usually prescribed for 24 to 48 hours to
decrease oxygen demand. Progressive ambulation is
implemented as soon as possible, unless complications
occurred.
 NURSING MANAGEMENT
 Promoting oxygenation and tissue perfusion
 Instruct the patient to avoid overfatigue, stop activity immediately in the
presence of chest pain, dyspnea, lightheadedness or faintness.
 Oxygen therapy by cannula for the first 24 to 48 hours or longer if pain,
hypotension, dyspnea or dysrhythmias persist. Monitor VS changes,
indicative of complications.
 Position the client in semi-Fowler’s to allow greater diaphragm expansion
thereby lung expansion and better carbon dioxide-oxygen exchange.
 Promoting adequate cardiac output
 Monitor the following parameters:
 Dysrhythmias on ECG tracings
 VS
 Effects of daily activities on cardiac status
 Rate and rhythm of pulse
 Administer pharmacotherapy as prescribed
 Promote rest and minimize unnecessary disturbances
 NURSING MANAGEMENT
 Promoting comfort
 Relieve pain. Administer morphine sulfate as ordered. This is to decrease
sympathetic stimulation, which increase myocardial oxygen demand. In addition,
this will prevent shock which may result from severe pain.

 Providing test
 The client is usually placed on bed rest with commode privileges for 24 to 48 hours
 Administer diazepam (valium) as ordered
 Explain that the purpose of CCU is for continuous monitoring and safety during the
early recovery period.
 Provide psychosocial support to the client and his family. Calmness and
competency are extremely reassuring.

 Promoting activity
 Gradual increase in activity is encouraged after the first 24 to 48 hours. May be
allowed to sit on a chair for increasing periods of time and begins ambulation on the
4th and 5th day.
 Monitor for signs of dysrhythmias, chest pain, and changes in VS during the
activity.
 NURSING MANAGEMENT
 Promoting nutrition and elimination
 Provide small, frequent feedings
 Provide low-calorie, low cholesterol, low-sodium diet
 Avoid stimulants
 Avoid taking very hot or very cold beverages and gas-forming foods. Vasovagal
stimulation may occur, thereby bradycardia and cardiac arrest.
 Use of bedpan and straining at stool should be avoided. Valsalva maneuver causes
changes in blood pressure and heart rate, which may trigger ischemia,
dysrhythmias, pulmonary embolism or cardiac arrest.
 Use bedside commode
 Administer stool softener as ordered, e.g. sodium decussate (colace).
 Promoting relief of anxiety and feeling of well-being
 Provide an opportunity for the client and family to explore their concerns and to
identify alternative methods of coping as necessary
 Facilitating learning
 Teaching is started once the client is free of pain and excessive anxiety
 Promote a positive attitude and active participation of the client and the family.
CARDIAC REHABILITATION
 Is a process by which a person is restored to
health and maintains optimal physiologic,
psychosocial, vocational and recreational
functions.
 It begins the moment a client is admitted to the
hospital for emergency care, it continues for
months and even years after the client is
discharged from the health care facility.
GOALS OF REHABILITATION
 To live as full, vital and productive a life as possible
 Remain within the limits of the heart’s ability to respond to activity and stress

Progressive activity
 Activity progression is based on the metabolic equivalent of the task (MET),
the energy expenditure for various activities
 In the hospital, exercise may be gradually implemented as follows:
Lying or sitting exercises (arms, legs and trunk), then exercises progress to
standing and slow walking in the hall. (VS and heart rhythmns are constantly
monitored)
An exercise session is terminated if any one of the following occurs:
 Cyanosis, cold sweats, faintness, extreme fatigue, severe dyspnea, pallor, chest pain,
PR more than 100 beats/min, dysrhythmias, BP greater than 160/95 mmHg.
Exercise must be done twice a day for about 20 minutes
Exercise provides the clients a positive sign of progress and recovery, a sense
of control over their bodies, and tends to decrease anxiety and depression
during the recovery period.
Home exercise program includes 2 to 12 weeks structured walking program.
 TEACHING AND COUNSELLING
SELF-MANAGEMENT EDUCATION GUIDE:
DISCHARGE AFTER MI.

 Discontinue smoking
 Control hypertension with continued medical supervision
 Eat a diet low in calories, saturated fats and cholesterol; decrease in salt intake.
 Participate in weight reduction program
 Progressive exercise based on the discharge MET level under medical
supervision
 Take prescribed medications at regular basis
 Resumption of sexual activity after 4 to 6 weeks from discharge, if appropriate.
Or when the client with uncomplicated MI (no dysrhythmias, shock of CHF) is
capable of walking two flights of stair without difficulty.
 Stress management techniques
 Return to usual home activities, relationships and to work at earliest
opportunity would be beneficial.
TEACHING GUIDE ON RESUMPTION ON
SEXUAL ACTIVITY
 Assume less fatiguing position
 The non-MI partner takes the active role
 Perform sexual activity in a cool, familiar
environment
 Take nitroglycerine before sexual activity
 Refrain from sexual activity during a fatiguing day,
after eating a large meal or after drinking alcohol
 If dyspnea, chest pain, dizziness, or palpitations
occur, moderation should observed; if symptoms
persist, stop sexual activity
 Develop other means of sexual expression
 COMPLICATIONS OF MI
 Dysrhythmias
 Cardiogenic shock
 Thromboembolism
 Pericarditis
 Rupture of the myocardium
 Ventricular aneurysm
 Congestive heart failure
 DYSRHYTHMIAS
 Abnormal cardiac rhythms which are due to the following factors:
 Tissue ischemia
 Hypoxemia
 SNS and PNS influences
 Lactic acidosis
 Hemodynamic abnormalities
 Drug toxicity
 Electrolyte imbalances
 These are due to abnormal automaticity, abnormal conduction or
both.
 The most common complications and most major cause of death
among clients with MI
 The most common dysrhythmias in MI is premature ventricular
contractions (PVCs)
 PVCs of 6 or more per minute is life-threatening
 COMMON DYSRHYTHMIAS
AFTER MI
 Sinus
 Sinus tachycardia
 Sinus bradycardia
 Sinus dysrhythmias
 Sick sinus syndrome
 Atrial
 Premature atrial contraction
 Paroxysmal atrial tachycardia
 Atrial flutter
 Atrial fibrillation
 Ventricular
 Premature ventricular contractions
 Ventricular bigeminy
 Ventricular fibrillation
 Ventricular tachycardia
 Conduction defects
 First degree AV block
 Second degree AV block
 Third degree AV block
 SINUS DYSRHYTHMIAS
 Sinus tachycardia is a dysrhythmias that is normal, except that the
rate exceeds 100 beats per minute.
 Etiology:
 The sympathetic fibers are stimulated thereby, speed up excitation of the SA
node
 Treatment:
 Digitalis administration
 Treat underlying cause (fever, shock, electrolyte disturbances, etc)
 Sinus bradycardia is a dysrhythmias that is normal, except that the
rate falls below 60 beats per minute.
 Etiology:
 The parasympathetic fibers (vagal tone) are stimulated and cause the sinus node
to slow.
 Treatment:
 Atropine 0.5 to 1.0 mg/IV push to block vagal stimulations
 Isoproterenol 1 mg/500 ml D5W to stimulate sympathetic response
 Pacemaker
 SINUS DYSRHYTHMIAS
 Sinus arrhythmia is a regular irregularity in rhythm
which is related to respiratory exchange. No
treatment.
 Sick sinus syndrome is a dysrhythmias that is caused
by a diseased sinus node. The sinus node conducts at
a slow rate or may fail to conduct at all, producing
sinus block or pauses. There is related tachycardia,
thus it is also “brady-tachycardia syndrome”.
 Treatment:
 Treatment of ischemia due to arteriosclerotic heart disease, MI.
 Pacemaker
 ATRIAL DYSRYTHMIAS
 Premature atrial contraction (PAC) is an ectopic beat that
originates in the atria and is discharged at a rate faster that that
of the sinus node.
 Treatment:
 Generally does not require treatment
 Quinidine or calcium-channel blocker if it increases in frequency.
 Paroxysmal atria tachycardia (PAT) is a suddent onset of an
atrial tachycardia which rates that vary between 140 and 250
beats per minute.
 Treatment:
 Valsalva maneuver to reduce the heart rate through vagal stimulation.
 Digitalis
 Beta adrenergic blockers (propranolol)
 Calcium-channel blockers (verapamil)
 Cardioversion
 Morphine sulfate, diazepam
 Avoid excess use of alcohol, cigarettes, caffeine.
PATHOPHYSIOLOGY OF PREMATURE VEN TRICULAR CONTRACTIONS

Premature Ventricular Contractions

Ventricular Fibrillations

Cardiac Standstill / Arrest

Dysrhythemias

Cardiac Output

Cardiac Irritability

Myocardial Perfusion
 ATRIAL DYSRYTHMIAS
 Atrial flutter is a dysrhythmias in which an ectopic atrial focus
captures the heart rhythm and discharges impulses at a rate of
between 200 and 400 times per minute.
 Treatment:
 Digitalis preparation
 Quinidine
 Calcium-channel blockers
 Beta-adrenergic blockers
 Cardioversion
 Atrial fibrillation is a dysrhythmia that is caused by the rapid and
chaotic firing of atrial impulses by a multitude of foci.
 Treatment:
 Digitalis, if uncontrolled fibrillation (rate is above 100 beats per minute)
 Quinidine
 Beta adrenergic blockers
 VENTRICULAR
DYSRHYTHMIAS
 Premature ventricular contraction (PVC) is a dysrhythmia that is
produced by an ectopic beat originating in a ventricle and being
discharged at a rate faster than that of the next normally occurring
beat. PVC’s of 6/minute or more is life threatening.
 Treatment:
 Lidocaine/IV push, drip
 Initial bolus dose: 75-100 mg then 50-100 mg within 10-15 minutes as needed
 Continuous IV drip in D5W 4:1 concentration
 Procainamide IV push, drip bolus dos: 300 mg
 Bretylium/continuous infusion if lidocaine and procainamide are ineffective.

 Ventricular bigeminy is a PVC where every other beat is a

ventricular complex.
 Treatment:
 Refer to PVC
 VENTRICULAR
DYSRHYTHMIAS
 Ventricular tachycardia is a life threatening dysrhythmia that
originates from an irritable focus within the ventricle. It is an
ineffective rhythm for maintaining cardiac output. It is an
emergency.
 Treatment:
 Lidocaine, bolus dose; followed by a continuous IV drip from 1-4 mg/min
 Defibrillation, if loss of consciousness occurs
 Cardioversion if conscious
 Ventricular fibrillation is a dysrhythmia that is characterized by
the random chaotic discharging of impulses within the ventricle
at rates that exceed 300 beats per minute. It produces clinical
death and must be reversed immediately. It is an emergency.
 Treatment:
 Immediate defibrillation; use 200-400 watt/sec (joules)
 Na bicarbonate to relieve lactic acidosis, which causes unsuccessful
defibrillation
 Epinephrine
TREATMENT OF AV BLOCKS
 First degree AV block requires no treatment
 Second degree AV block requires treatment if
the ventricular rate falls too low to maintain
effective cardiac output.
 Third degree AV block requires treatment if
C.O. is compromised.
 Treatment of choice: Ventricular pacemaker
CONDUCTION DEFECTS/HEART
BLOCKS/AV BLOCKS
Conduction is altered at the level of the AV node
 First degree AV block – the impulse is transmitted

normally, but it is delayed longer at the level of the

AV node.
 Second degree AV block – some, but not all of the

impulses are transmitted. The AV node becomes

selective about which impulses are conducted to the
ventricles.
 Third degree AV block – no impulse from the SA

node is transmitted by the AV node.

 SUMMARY OF THERAPEUTIC
MODALITIES FOR DYSRHYTHMIAS

 Antidysrhythmic drugs
 Artificial cardiac pacemaker
 Cardioversion/defribillation
 Cardiopulmonary resuscitation
ANTIDYSRHYTHMIC DRUGS
 Class I
 Fast (Sodium) channel blockers I
 Disopyramide (norpace)
 Procainamide (pronestyl)
 Quinidine sulfate (cardioquin)
 Fast (Sodium) channel blockers II
 Lidocaine (xylocaine)
 Mexilitine Hcl (mexitil)
 Fast (Sodium) channel blockers III
 Flecainide (tambocor)
 Propafenone (rhythmol)
 Tocainide (tonocard)
 ANTIDYSRHYTHMIC DRUGS
 Class II
 Beta – adrenergic blockers
 Acebutolo (sectral)
 Propranolol (inderal)
 Class III
 Prolong repolarization
 Adenosine (adenocard)
 Amiodarone (cardarone)
 Bretylium tosylate (bretylol)
 Class IV
 Calcium channel blockers
 Verapamil HCl (calan)
 Diltiazem (cardizem)
 Others
 Phenytoin (dilantin)
 Digoxin (lanoxin)
 PACEMAKERS
 A cardiac pacemaker is an electronic device
that delivers direct stimulation to the heart,
causing electrical depolarization and cardiac
contraction.
 The pacemaker initiates and maintains the
heart rate when the natural pacemakers of the
heart are unable to do so.
 CLINICAL INDICATIONS
 Symptomatic bradyarrhythmias
 Sinoatrial bradyarrhythmias
 Sinoatrial arrest
 Sick sinus syndrome
 Heart block
 Second degree heart block
 Complete heart block
 Prophylaxis
 Following acute MI; arrhythmias and conduction defects
 Before or following cardiac surgery
 During coronary arteriography
 Before permanent pacing
 Tachyarrhythmias
 Supraventricular
 Ventricular
 PACING MODES
 Demand (synchronous, non-competitive)
atrial/ventricular.
 It triggers electrical firings only when the heart rate goes
slow.
 It does not compete with the heart’s basic rhythm.
 If the client’s heart rate falls below a predetermined escape
interval (programmed into pulse generator), an electrical
stimulus is delivered to the heart
 Fixed rate (asynchronous, competitive)
atrial/ventricular
 It delivers an electrical stimulus at a preset constant rate
that is independent of the patient’s own rhythm.
 Does not allow atrial contribution to the cardiac output.
May be valuable in complete heart block.
 PACING MODES
 Synchronous atrial/ventricular
 A demand form of pacing which is able to increase
heart rate to accompany the physiological demands
of the body
 An actual electrode senses the patient’s atrial
depolarization, waits for a preset interval (simulated
PR interval) and triggers firing of ventricular pacer.
 If rapid atrial rhythm occurs, the ventricular
pacemaker stimulates the ventricle at a fixed rate
independent of atrial activity.
TEMPORARY PACEMAKERS
Temporary pacing of the heart is usually done as
an emergency procedure that allows
observation of the effects of pacing on heart
function before a permanent pacemaker is
implanted.
 Transvenous approach to position the electrode in
the apex of right ventricle is done.
 The external pulse generator is attached to the
patient.
 PERMANENT PACEMAKERS
 Permanent pacing of the heart may be implanted through the
following techniques:
 Transvenous (endocardial)
 The electrode is threaded through cephalic or external jugular vein into the
right ventricle. This is done under local anesthesia.
 The peripheral end of the electrode is connected to the pulse generator
which is implanted underneath the skin below the right or left pectoral
region.
 Treansthoracic (epicardial)
 Anterior chest is opened and electrodes are sutured to the surface of the
right or left ventricle atrium, then threaded subcutaneously to the
abdominal wall either above or below the waist.
Note:
Paced beats are characterized by sharp spikes that precede each
ECG complex.
 NURSING INTERVENTIONS FOR CLEINTS
WITH ARTIFICIAL CARDIAC PACEMAKERS

 Monitor ECG following implantation of pacemaker, including VS

 Observe for indications of pacemaker malfunction as dizziness,
faintness, lightheadedness, chest pain, shortness of breath.
 Make sure all equipment in the client’s unit is grounded, to
prevent ventricular fibrillation
 Practice sterile technique for dressing changes to prevent wound
infection.
 Provide psychosocial support:
 Explore concerns of the client
 Encourage to utilize coping mechanisms
 Ensure client comfort
 Maintain a positive body image
 NURSING INTERVENTIONS FOR CLEINTS
WITH ARTIFICIAL CARDIAC PACEMAKERS
 Provide client education which includes the following:
 Take daily pulse for one full minute
 Report any sudden slowing of pulse greater than 4 to 5 beats per minutes or any
increase in pulse rate.
 The best time to take the daily pulse is in the morning upon awakening
Report signs and symptoms of dizziness, fainting, palpitation,
prolonged hiccups
and chest pain to the physician (indicative of pacemaker failure)
May use electrical devices with caution
 If dizziness occurs, stop using the device
 Sources of electromagnetic inference (EMI) that may effect some pulse
generators are as follows:
 High-energy radar
 Tv and radio transmitters
 Electrocautery machines
 Airport screening devices
 Antitheft devices
 Move 5 to 10 feet away from the source of EMI if dizziness occurs
 NURSING INTERVENTIONS FOR CLEINTS
WITH ARTIFICIAL CARDIAC PACEMAKERS

 Avoid going near or using microwave oven

 Move 3 feet away from the device
 Wear loose-fitting clothing around the near of
the pacemaker
 Observe for signs and symptoms of infection
around generator and leads – fever, heat, pain,
skin impairment at the implant site.
 Avoid contact sports.
 Electrode may be displaced.
 CARDIOVERSON AND
DEFIBRILLATION
 Cardioversion is the synchronous application of an
electrical shock of short duration to the heart through
the use of chest paddles.
 It is done to convert cardiac dysrhythmia (other than
ventricular fibrillation) into a more hemodynamically
stable, sinus rhythm
 Electric shock is applied during the R wave; never on the
T wave
 Defribillation is unsynchronized passing of an electric
shock of short duration through the heart to terminate
ventricular fibrillation or ventricular tachycardia
without pulse.
 NURSING INTERVENTIONS DURING
CARDIOVERSION AND FIBRILLATION
 Place the client in a flat, firm surface
 Apply interface material (gel, paste, saline pads) to the paddles
 This is for better contact with the skin and to prevent burns
 Grasp the paddles only by the insulated handles. To prevent
electrocution.
 Give command for personnel to STAND CLEAR of the client
and the bed
 Apply the chest paddles as follows: one at the right of the
sternum, third ICS; and the other one on the left midaxillary,
fifth ICS.
 Push the discharge buttons in both paddles simultaneously
 For defribillation, release 200 to 360 watts/sec (joules); for
cardioversion, power energy is required
 Defibrillation is done before initiating CPR
 CARDIOPULMONARY
RESUSCITATION (CPR)
 Indication
 Cardiopulmonary arrest/clinical death (breathlessness,
pulselessnesls)
 Crucial time
 CPR is instituted within 4 to 6 minutes after the arrest, to
prevent brain death
 Two types of CPR
 Basic life support (BLS)
 Involves the use of the hands, mouth and the sincere desire to give
the person a second chance for life
 Advanced cardiac life support (ACLS)
 Involves BLS and the use of equipment, emergency drugs and
fluids to monitor the client and stabilize his condition
 CPR involves the ABCD
of life support
A – open airway
B – restore breathing
C – restore circulation
D – provide definitive treatment (ACLS)
 TECHNIQUES OF BASIC LIFE
SUPPORT
 Step I. Assess level of consciousness
 Shake the victim’s shoulders and ask “Are you okey?”
 If no response, place the client in supine position on a firm surface.
 Step II. Open the airway.
 The tongue is the most common cause of airway obstruction in the unconscious
person.
 Use the head tilt – chin lift and the jaw thrust methods for opening and maintaining
airway.
 Jaw thrust is recommended for clients with suspected neck injury
 Take 3 to 5 seconds to look, listen and feel for spontaneous breathing
 Step III. Initiate artificial ventilation
 Mouth-to-mouth ventilation
 Mouth-to-nose ventilation
 Mouth-to-stoma ventilation
 Mouth-to-barrier ventilation
Note:
Give 2 initial breaths lasting for 1 ½ to 2 seconds. If no rise and fall of the chest is
observed, consider airway obstruction.
 TECHNIQUES OF BASIC LIFE
SUPPORT
 Step IV. Assess Circulation
 Check carotid pulse (adult) for 5 to 10 seconds; brachial pulse for infant and child
 No pulse, cardiac compressions are initiated
 Step V. Initiate External Cardiac Compression/External Cardiac Massage
 Place the heel of the hand of the area of 2 fingerbreadths from the xiphoid process
(adult); midsternum for infant
 Depress the sternum with heels of both hands, one on top of the other 1 ½ to 2
inches (adult); heel of one hand 1 to 1 ½ inches (child); 2 fingers ½ to 1 inch
(infant)
 If 2 – man rescue: 80-100 cardiac compressions per minute; with ratio of 5:1
(compression to ventilation)
 If 1 – man rescue: 80-100 cardiac compressions per minute; with ratio of 15:2
(compression to ventilation)
 Reassess the client after 4 cycles; if pulse is absent, continue CPR
 Recheck pulse every 3 to 4 minutes thereafter
 Most common complication of CPR is fracture of ribs. Most commonly punctured
internal organ during CPR is the liver
 TECHNIQUES OF BASIC LIFE
SUPPORT
 Step IV. Assess Circulation
 Check carotid pulse (adult) for 5 to 10 seconds; brachial pulse for infant and child
 No pulse, cardiac compressions are initiated
 Step V. Initiate External Cardiac Compression/External Cardiac Massage
 Place the heel of the hand of the area of 2 fingerbreadths from the xiphoid process
(adult); midsternum for infant
 Depress the sternum with heels of both hands, one on top of the other 1 ½ to 2
inches (adult); heel of one hand 1 to 1 ½ inches (child); 2 fingers ½ to 1 inch
(infant)
 If 2 – man rescue: 80-100 cardiac compressions per minute; with ratio of 5:1
(compression to ventilation)
 If 1 – man rescue: 80-100 cardiac compressions per minute; with ratio of 15:2
(compression to ventilation)
 Reassess the client after 4 cycles; if pulse is absent, continue CPR
 Recheck pulse every 3 to 4 minutes thereafter
 Most common complication of CPR is fracture of ribs. Most commonly
punctured internal organ during CPR is the liver
 TECHNIQUES OF BASIC LIFE
SUPPORT
 When to stop CPR?
 When the client is revived
 When the EMS has been activated
 When the rescuer is exhausted
 When the client is dead
 CARDIOGENIC SHOCK
(POWER/PUMP FAILURE)
 Is a shock state which results from profound
left ventricular failure usually from massive
MI
 It results to low cardiac output, thereby
systemic hypoperfusion
 It has a high mortality rate
 Pathophysiology
 NURSING INTERVENTIONS
 Perform hemodynamic monitoring PAP, PCWP
measurements, Intra-arterial BP.
 Administer oxygen therapy
 Correct hypovolemia. Administer IV fluids as ordered
 Pharmacotherapy:
 Vasodilators: nitroprusside, phentolamine, nitroglycerine
 Isotropic agents: digitalis, dopamine, dobutamine
 Diuretics: furosemide.
 Na bicarbonate to relieve lactic acidosis
 Monitor hourly urine output, LOC, arrhythmias
 Provide psychosocial support
 NURSING INTERVENTIONS
 Decrease pulmonary edema
 Ausculate lung fields for crackles and wheezes
 Note for dyspnea, cough, hemoptysis, orthopnea
 Monitor ABG for hypoxia and metabolic acidosis
 Place in Fowler’s position to reduce venous return
 Administer during therapy as ordered:
 Morphine sulfate to reduce venous return

 Aminophylline to reduce bronchospasm caused by severe

congestion
 Vasodilators to reduce venous return (nitroprusside,

nitroglycerine)
 Diuretics to decrease circulating volume
 NURSING INTERVENTIONS
 Utilize counterpulsation to decrease ventricular work of the client with
severe shock.
 Counterpulsation (mechanical cardiac assistance/diastolic

augmentation) involves introduction of the intra-aortic balloon catheter

via the femoral artery.
 The intra-aortic balloon pump (IABP) augments diastole, resulting in

increased perfusion of the coronary arteries and the myocardium and a

decrease in left ventricular workload.
 The balloon is inflated during diastole; it is deflated during systole.

 Indications:

 Cardiogenic shock

 AMI (acute myocardial infarction)

 Unstable angina pectoris

 Open heart surgery

 THROMBOEMBOLISM
 It results when platelets aggregate at the area of
necrosis, an attempt of the body to repair the
tissue injury.
 Emboli occur because clots formed in the
healing area of the myocardium break loose
and escape into the circulation
 Pulmonary embolism may develop and proves
to be fatal
 NURSING INTERVENTIONS
 Administer pharmacotherapy as ordered:
 Anticoagulants
 Thrombolytics
 Observed for signs and symptoms indicative of pulmonary
embolism
 Dyspnea
 Chest pain
 Coughing
 Hemoptysis
 Rapid, weak pulse
 Pallor
 Early ambulation is encouraged to prevent venous
stasis. Venous stasis enhances thromboembolism.
 PERICARDITIS/DRESSLER’S
SYNDROME
 Is an inflammation of the pericardium which occurs
approximately 1 to 6 weeks after acute MI
 In MI, pericarditis results as an antigen – antibody response.
The necrotic tissues play the role of an antigen, which trigger
antibody formation. Inflammatory process follows.
 Pericardial effusion/cardiac tamponade is outpouring of fluid
into the ventricular sac. Compression of the heart occurs,
followed by decrease in ventricular emptying. This further,
may lead to cardiac failure, shock and death. This may follow
pericarditis.
 Constrictive pericarditis is a condition in which a chronic
inflammatory thickening of the pericardium compresses the
heart so that it is unable to fill normally during diastole.
 PERICARDITIS/DRESSLER’S
SYNDROME
 Clinical manifestations of pericarditis include the
following:
 Pain in the anterior chest, aggravated by coughing,
yawning, swallowing, twisting and turning the torso;
relieved by upright, leaning forward position.
 Pericardial friction rub – scratchy, grating or creaking
sound
 Dyspnea
 Fever, sweating, chills
 Joint pains
 Arrhythmias
 NURSING INTERVENTIONS
 Elevate head of bed, place pillow on the
overbed table so that the patient can lean on it.
 Bed rest.
 Administer prescribed pharmacotherapy:
 ASA to suppress inflammatory process
 Conticosteroids for more severe symptoms
 Assist in pericardiocentesis if cardiac
tamponade is present
 Pericardiocentesis is aspiration of blood/fluid
from pericardial sac
 RUPTURE OF THE
MYOCARDIUM
 It is common in transmural MI
 It causes immediate cardiac tamponade and
death
 VENTRICULAR ANUERYSM
 It involves thinning, ballooning and hypokinesis of
the left ventricular wall after a transmural MI
 The dysfunctional area often becomes filled with
necrotic debris and clot and sometimes is rimmed by
the calcium ring.
 The debris or clot may fragment and travel into the
systemic arterial circulation thereby embolization.
 The aneurysm may rupture causing cardiac tamponade
and death.
 CONGESTIVE HEART FAILURE
 It is a state of circulatory congestion produced by
myocardial dysfunction
 MI compromises myocardial function by reducing
contractility and producing abnormal wall motion
 The ability of the ventricle to empty lessens, the
stroke volume falls, residual volume increases
 Heart failure is the inability of the heart to pump the
amount of oxygenated blood necessary to effect
venous return and to meet the metabolic requirements
of the body
 CAUSES OF CONGESTIVE
HEART FAILURE
 Direct change to the heart, e.g. mintral myocarditis,
ventricular aneurysm.
 Ventricular overload
 Increased preload, e.g. mitral aortic regurgitation, atrial or
ventricular septal defects, or rapid infusion of large
volumes of IV fluids
 Increased afterload, e.g. aortic or pulmonary valve
stenosis, systemic hypertension, pulmonary hypertension
 Constriction of the ventricles,e.g. cardiac tamponade,
pericarditis, restrictive cardiomyhopathies
 CLASSIFICATION OF
HEART FAILURE
 Backward heart failure results from damming
up of blood in the vessels proximal to the heart
 Forward heart failure results from inability of
the heart to maintain cardiac output
 COLLABORATIVE
MANAGEMENT
Medications
 Digitalis therapy
 It is the major therapy for CHF
 It has positive inotropic (strengthens force of cardiac contractility) as
negative chronotropic effects (decreases heart rate)
 Assess heart rate before administration of digitalis, if the heart rate is below
60 bpm or above 120 bpm, withhold the drug. Bradycardia rebound
tachycardia may occur.
 Monitor secrum postassium (K) level; hypokalemia enhances digitalis
toxicity because it potentiates the effect of the drug.
 Commonly used digitalis/cardiac glycosides.
 Lanoxin (digoxin)
 Cyrstodigin (digitoxin)
 Lanatoside C (cedilanid C)
 Deslanoside (cedilanid D)
 COLLABORATIVE
MANAGEMENT
 Assess for signs and symptoms of digitalis toxicity:
Bradycardia
G.I. manifestations
 Anorexia
 Nauseas and vomiting
 Diarrhea
 Dysrhythmias (most dangerous)
 Altered visual perceptions (yellow or green vision;
halos around the light among elderly)
 In males:
 Gynecomastia
 Decreased libido
 Impotence
 COLLABORATIVE
MANAGEMENT
 Diuretic therapy
 The purpose is to decrease cardiac workload by reducing
circulating volume and thereby reduce preload
 Assess for signs and symptoms for hypokalemia when
administering Thiazides and loop diuretics
 Give potassium supplement and potassium-rich foods
 Diuretics are best administered early morning and/or early
afternoon to prevent sleep pattern disturbance related to
nocturia
 If Thiazides are ineffective, an oral aldosterone antagonist
(potassium sparing diuretic) may be given Thiazide
 COLLABORATIVE
MANAGEMENT
 The diuretics used in the treatment of CHF are as
follows:
 Thiazides
 Chlorothiazide (Diuril)
 Hydrochlorothiazide (Esidrix, Hydrodiuril)
 Loop Diuretics
 Furosemide (Lasix)
 Bumetazmide (Bumex)
 Potassium-sparing
 Spironolactone (Aldactone)
 Triamterene (Dyrenium)
 COLLABORATIVE
MANAGEMENT
 Vasodilators
 To decrease afterload by decreasing resistance to
ventricular emptying.
 The most commonly used drugs are as follows:
 Nitroprusside (Nipride)
 Hyralazine (Apresoline)
 Nifedipine (a calcium-channel blocker with vasodilator
effect)
 Captopril (Capoten) – also has a vasodilator effect
 Other drugs:
 Sympathomimetics
 Dopamine

 Dobutamine
 TREATMENT

 Diet-sodium – restricted diet to prevent fluid

excess
 Acitivity-balanced program of activity and rest
 Oxygen therapy – to increase oxygen supply
 NURSING MANAGEMENT
 Providing oxygenation
 Administer oxygen therapy per nasal cannula at 2 to 6 L/min as ordered
 Evaluate arterial blood gas analysis results
 Maintain semi-Fowler’s or high Fowler’s position to maximize oxygenation by
promoting greater lung expansion
 Promoting rest and activity
 Bed rest or limited activity may be necessary during the acute phase.
 Provide an overbed table close to the patient to allow resting the head and arms
 The arms may be supported on pillows to reduce the pull on the shoulder muscles
when in high-Fowler’s position, which is most comfortable for the patient
 Administer diazepam (valium) 2 to 10 mg 3 to 4 times a day as ordered allay
apprehension
 Gradual ambulation is encouraged to prevent risk of venous thrombosis and
embolism due to prolonged immobility
 Activities should progress through dangling, sitting up in a chair and then walking
in increased distances under close supervision
 Assess for signs of activity intolerance such as dyspnea, fatigue and increased pulse
rate that does not stabilize readily
 NURSING MANAGEMENT
 Decreasing anxiety
 Identifying feelings and the concerns related to those feelings
 Identify strengths that can be used for coping
 Learn what can be done to decrease anxiety
Note:
Anxiety causes increased breathlessness which may be perceived
by the client as an increase in the severity of the heart failure
and this is turn increases the anxiety
 Facilitating fluid balance
 Control of sodium intake
 Administer diuretics and digitalis as prescribed
 Monitor 1 and 0, weight and VS
 Dry phlebotomy (rotating tourniquet)
 NURSING MANAGEMENT
 Providing skin care
 Edematous skin is poorly nourished and susceptible to
pressure sores
 Change position at frequent intervals
 Assess the sacral area regularly
 Use protective devices to prevent pressure sores
 Promoting nutrition
 Provide bland, low-calorie low-residue with vitamin
supplement during the acute phase
 Frequent small feedings minimize exertion and reduce
gastrointestinal blood requirements
 There may be no need to severely restrict sodium intake of
the client who receives diuretic. However, “no added salt”
diet is prescribed. Salty foods must be omitted.
 NURSING MANAGEMENT
 Promoting elimination
 Advise to avoid straining at defecation which involves Valsalva’s
maneuver. Valsalva maneuver increases cardiac workload
 Administer laxative as ordered e.g. colace
 Encourage use of bedside commode
 Facilitating learning
 Teach the client and his family about the disorder and self-care
 Monitor signs and symptoms of recurring CHF, e.g. weight gain, loss of
appetite, dyspnea, orthopnea, edema of the legs, persistent cough and report
these to the physician
 Avoid fatigue, balance rest with activity
 Observe prescribed sodium restrictions
 Eat small, frequent meals rather than 3 large meals a day
 Take prescribed medications at regular basis, e.g. digitalis, diuretics,
vasodilators
 Observe regular follow-up care as directed
 NURSING MANAGEMENT
If acute pulmonary edema occurs in the client with CHF,
the following are the appropriate management:
 Place in high-Fowler’s position
 Morphine sulfate 10 to 15 mg/IV as ordered to ally anxiety,
reduced preload and afterload
 Oxygen therapy ast 40% to 70% by nasal cannula or face mask
 Aminophylline/IV to relieve bronchospasm, increase urinary
output and increase cardiac output
 Rapid digitalization
 Diuretic therapy
 Vasodilators
 Dopamine or dobutamine
 Monitor serum potassium. Diuresis may result to hypokalemia
 PHLEBOTOMY
 Dry phlebotomy or rotating tourniquets intends to allow pooling of blood in the
lower extremities, thereby reducing preload
 Three extremities are occluded at a time
 Rotate the tourniquets clockwise every 15 minutes
 Each extremity is occluded for a maximum of 45 minutes
 If BP compression cuff is used as tourniquet, inflate up to slightly above
diastolic pressure (10 to 40 mmHg). This allows occlusion of venous return but,
arterial flow remains patent
 Perform neurovascular check distal to the tourniquet application:
 Skin color
 Skin temperature
 Presence of pulse
 Presence of numbness or tingling
 If tourniquet application is too tight, tissue ischemia may occur
 Asses for signs and symptoms of thrombosis and embolism
 Remove tourniquet one at a time every 15 minutes
CLASSIFICATION OF CLIENTS
WITH DISEASES OF THE HEART
Functional Capacity
Class I.
Patients with cardiac disease but without resulting limitations of physical activity.
Ordinarily, physical activity does not cause undue fatigue, palpitation, dyspnea or
anginal pain.

Class II.
Patients with cardiac disease resulting in slight limitation of physical activity. They are
comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea or
anginal pain.

Class III.
Patients with cardiac disease resulting in marked limitation of physical activity. They are
comfortable at rest. Less than ordinary physical activity causes in fatigue, palpitation,
dyspnea or anginal pain.

Class IV.
Patients with cardiac disease resulting inability to carry on any physical activity without
discomfor. Symptoms of cardiac insufficiency or of the anginal syndrome are present
even at rest. If any physical activity is undertaken discomfort increased.
 Therapeutic Classification
Class A.
Patients with cardiac disease whose ordinary physical activity need not be restricted.

Class B.
Patients with cardiac disease whose ordinary physical activity need not be restricted but who
should be advised against severe or competitive physical efforts.

Class C.
Patients with cardiac disease whose ordinary physical activity should be moderately
restricted and whose more strenuous efforts should be discontinued.

Class D.
Patients with cardiac disease whose ordinary physical activity should be marked restricted.

Class E.
Patients with cardiac disease who should be at complete rest, confined to bed or chair.