CHAPTER 35 Cardiac Disorders

CHAPTER 35 Cardiac Disorders
JUDY L. MALTAS
Objectives
After reading and studying this chapter, you should be able to:
 1. Label the major parts of the heart.

 2. Describe the flow of blood through the heart and coronary vessels.
 3. Name the elements of the heart's conduction system.
 4. State the order in which normal impulses are conducted through the heart.
 5. Explain the nursing considerations for patients having procedures to detect or evaluate
cardiac disorders.
 6. Identify nursing implications for common therapeutic measures, including drug, diet,
or oxygen therapy; pacemakers and cardioverters; cardiac surgery; and cardiopulmonary
resuscitation.
 7. Explain the pathophysiology, risk factors, signs and symptoms, complications, and
treatment for selected cardiac disorders.
 8. List the data to be obtained in assessing the patient with a cardiac disorder.
 9. Assist in developing nursing care plans for patients with cardiac disorders.
Key Terms
afterload
(p. 631)
arteriosclerosis
( , p. 652)
atherosclerosis
( , p. 653)
bradycardia
( , p. 633)
contractility
(p. 631)
diastole
(p. 631)
dysrhythmia
( , p. 655)
hemodynamics
( , p. 661)
murmur
( , p. 633)
myocardial infarction
( , p. 654)
palpitation
( , p. 632)
perfusion
( , p. 648)
preload
(p. 631)
regurgitation
( , p. 670)
syncope
( , p. 632)
systole
(p. 627)
tachycardia
( , p. 633)
thromboembolism
( , p. 655)
The cardiovascular system carries oxygenated blood and nutrients to the cells and transports
carbon dioxide and wastes from the cells. It requires a reservoir for blood coming from the
tissues, pumping action to send blood to the lungs and the body, and an intact vascular system to
transport the blood. A malfunction in any of these components may affect other body systems
and may threaten the life and health of the person.
The heart is a hollow muscular pump located in the mediastinum (Fig. 35-1). The right and left
sides of the heart receive blood from and send blood to different parts of the body. The heart is
covered and protected by the sternum and the ribs anteriorly and flanked by the lungs laterally.
The esophagus, the descending aorta, and the fifth through the eighth thoracic vertebrae are
directly behind the heart. The heart rests on the diaphragm, with two thirds of it to the left of the
sternum. The right side of the heart is located under the sternum. The heart is approximately the
size of the person's fist, weighs 10 to 14 ounces in the adult, and is covered by membranes called
the visceral and parietal pericardium. The space between the pericardial membranes contains
fluid that lubricates the membranes and decreases friction.
ANATOMY AND PHYSIOLOGY OF THE HEART

CHAMBERS
The heart is divided into four chambers: two upper atria (right and left) and two lower ventricles
(right and left). The four chambers are separated by septa (walls) with two chambers on the right
(right atrium and ventricle) and two chambers on the left (left atrium and ventricle). Valves
separate the atria from the ventricles.
The right atrium (RA) is a thin-walled reservoir and conduit for systemic blood. It receives blood
from the inferior and the superior venae cavae and from the coronary sinuses. The right ventricle
(RV) has thicker walls than the RA and receives blood from the RA through the tricuspid valve.
Blood moves rather passively from the RA to the RV. When the RV contracts (systole), blood is
ejected through the pulmonic valve into the pulmonary artery. The pulmonary artery carries the
blood to the lungs, where it releases carbon dioxide as waste and picks up oxygen to be taken to
the tissues. Pulmonary veins carry the blood from the lungs to the left atrium (LA).
FIGURE 35-1 Anatomic location of the heart.

The blood passes from the LA through the mitral valve into the left ventricle (LV), the chamber
with the thickest, strongest muscle. The LV is cone-shaped and contains the apex of the heart
located at the midclavicular line at the fourth or fifth intercostal space. An apical pulse is taken
by auscultating the heartbeat at this location.
When the LV contracts (systole), blood is ejected through the aortic valve into the aorta and the
systemic circulation. The systemic circulation carries oxygen and nutrients to all active cells and
transports wastes to the kidneys, liver, and skin for excretion (Fig. 35-2).
The pressures in the RA and RV are very low compared with the pressures in the LA and LV.
This is because the LV pumps blood out into the systemic circulation. The pressure in the LV is
the highest of all the chambers.
MUSCLE LAYERS
There are three layers of cardiac muscle tissue: the endocardium, the myocardium, and the
epicardium. The endocardium is the inner layer that lines the heart chambers. The middle layer,
the myocardium, is made of muscle fibers. It is responsible for the pumping action of the heart.
The thickness of the myocardium varies with each chamber. The outer layer, the epicardium, is
also the visceral pericardium. The coronary arteries are embedded in the epicardium.
VALVES
There are four valves in the heart: the mitral, the tricuspid, the aortic, and the pulmonic. Their
purpose is to retain blood in one chamber until the next chamber is ready to receive it. The
valves keep blood flowing in one direction. The valves open and close passively in response to
changes in pressure and volume. A valve opens when the pressure behind it is greater than the
pressure ahead of it. A valve closes when the pressure ahead of it is greater than the pressure
behind it.
Atrioventricular Valves
The mitral and tricuspid valves are called atrioventricular (AV) valves because they separate the
atria from the ventricles. The mitral valve is between the LA and the LV. The tricuspid valve
separates the RA from the RV. The cusps, or leaflets, are attached by chordae tendineae to the
papillary muscles that line the floor of the ventricles. These valves are closed during systole and
open in diastole.
Semilunar Valves
The semilunar valves, called aortic and pulmonic, separate the ventricles from the aorta and the
pulmonary artery, respectively. These valves are open during systole and are closed during
diastole. The semilunar valves have three cusps (cup-shaped structures) each.
FIGURE 35-2 Normal circulation through the heart.

Heart Sounds
Closure of the valves produces the heart sounds auscultated over the heart. The first heart sound
(S1), referred to as “lub,” occurs when the ventricles contract during systole and when the mitral
and tricuspid valves close. The second heart sound (S2), called “dub,” occurs during ventricular
relaxation or diastole and is caused by the closing of the aortic and pulmonic valves.
CORONARY BLOOD FLOW
The coronary arteries are the first branches of the systemic circulation. These arteries supply
blood to the myocardium and the conductive tissue of the heart. The two major coronary arteries,
the left coronary artery and the right coronary artery, arise from the aorta just beyond the aortic
valve. Blood flow through the coronary arteries occurs during diastole. The left coronary artery,
which branches into the left anterior descending and circumflex arteries, supplies blood to the
LA, most of the LV, and most of the septum between the two ventricles (interventricular
septum). The right coronary artery branches to supply the sinoatrial (SA) and the atrioventricular
(AV) nodes, the RA and RV, and the inferior part of the LV. Variations in the pattern of arterial
branching are common.
Collateral arteries are connections between two branches of arteries. They are more common in
certain areas of the heart. It is thought that collateral circulation protects the heart and that
coronary collaterals develop over time as a result of gradual coronary occlusion.
In general, the venous system parallels the arterial system: the great cardiac vein follows the left
anterior descending artery; and the small cardiac vein follows the right coronary artery. The
veins meet to form the coronary sinus (the largest coronary vein), which returns deoxygenated
blood from the myocardium to the right atrium (Fig. 35-3).
CONDUCTION SYSTEM
For the heart to pump blood through the chambers, nerves must stimulate muscle contractions in
an orderly fashion. The conduction pattern follows a particular route. The SA node, also called
the pacemaker, initiates the impulse. The impulse is carried throughout the atria to the AV node,
located on the floor of the RA. The impulse is delayed in the AV node and then transmitted to
the ventricles through the bundle of His. The bundle is made up of Purkinje cells and is located
where the atrial and ventricular septa meet. The bundle of His divides into the left and right
bundle branches. The left bundle branch divides into anterior and posterior branches called
fascicles. The terminal ends of the right and left branches are called the Purkinje fibers. When
the impulse reaches the Purkinje fibers, the ventricles contract (Fig. 35-4).
FIGURE 35-3 Coronary arteries and veins.
FIGURE 35-4 The conduction system of the heart.

The impulse produces a change in the movement of electrically charged ions across the
membrane of cardiac cells. Cardiac cells at rest are electrically polarized, with the inside of the
cell negatively charged and the outside of the cell positively charged. When stimulated, cardiac
cells lose their internal negativity by a process called depolarization. Depolarization moves from
cell to cell, producing a wave of electrical activity that is transmitted throughout the heart. Once
depolarization is complete, the resting state (i.e., inside of the cell more negative than the
outside) is restored through a process called repolarization.
The SA node normally generates these impulses at a rate between 60 and 100 beats per minute
(bpm). The SA node is called the pacemaker of the heart. The AV node is also capable of
generating an impulse if the SA node should fail. The AV node rate is 40 to 60 bpm. The
Purkinje network also can generate an impulse, but at less than 40 bpm, which could prevent
cessation of heart function for a short time (Table 35-1).
Cardiac Innervation
The heart is innervated by sympathetic and parasympathetic fibers of the autonomic nervous
system. Sympathetic fibers are distributed throughout the heart. Sympathetic stimulation results
in increased heart rate, increased speed of conduction through the AV node, and more forceful
contractions. Parasympathetic fibers, which are part of the vagus nerve, are found primarily in
the SA and AV nodes and the atrial tissue. Parasympathetic stimulation results in slowing of the
heart rate, slowing of conduction through the AV node, and decreased strength of contraction.
CARDIAC FUNCTION
The primary function of the heart is to pump blood through the pulmonary and systemic
circulations. This is accomplished by a continually repeating pattern of contraction and
relaxation.
Cardiac Cycle
Contraction and relaxation of the heart make up one heartbeat and are called the cardiac cycle.
When the ventricles are at rest (relaxation phase), they are filling up with blood coming from the
atria. This is called diastole. At the end of diastole, the atria contract to eject more blood into the
ventricles (called the atrial kick). Once the ventricles have filled with blood and the electrical
impulse has reached the terminal fibers of the conduction system, the ventricles contract and
eject blood into the pulmonary artery from the RV and into the aorta from the LV. This is called
systole. In a person with a heart rate of 60 bpm, there would be 60 cardiac cycles per minute.
Cardiac Output
The volume of blood ejected by the heart each minute is determined by the stroke volume and
the heart rate. Stroke volume is the amount of blood ejected with each ventricular contraction.
The normal stroke volume is 60 to 100 mL. Cardiac output is the amount of blood (in liters)
ejected by the heart per minute. It is calculated by multiplying the heart rate by the stroke volume
(CO 5 HR 3 SV). The normal cardiac output is 4 to 8 L/min. In the normal heart, cardiac output
responds to the increased demands for oxygen and nutrients that occur with exercise, infection,
or stress.
Table 35-1 Intrinsic Heart Rates

INITIATION OF IMPULSE RATE
Sinoatrial node 60-100 bpm
Atrioventricular node 40-60 bpm
Ventricle 15-40 bpm
Three factors affect stroke volume: preload, contractility, and afterload.
Preload.
Preload is the amount of blood remaining in a ventricle at the end of diastole or the pressure
generated at the end of diastole. Increased preload results in increased stroke volume and,
therefore, increased cardiac output. Factors that increase preload include increased venous return
to the heart and overhydration. Factors that decrease preload include dehydration, hemorrhage,
and venous vasodilation.
Contractility.
Contractility is the ability of cardiac muscle fibers to shorten and produce a muscle contraction.
Inotropy is a term used to refer to the contractile state of the cell. Factors that increase
contractility are said to have a positive inotropic effect, and factors that decrease contractility
create a negative inotropic effect.
Afterload.
Afterload is the amount of pressure the ventricles must overcome to eject the blood volume. It is
determined primarily by the pressure in the arterial system. Afterload is decreased by
vasodilation and increased by vasoconstriction.
Myocardial Oxygen Consumption
Myocardial tissue routinely needs 70% to 75% of the oxygen delivered to it by the coronary
arteries. Skeletal muscles, by contrast, need 35% at rest and up to 75% during exercise. The only
ways to increase oxygen supply to the myocardium are to (1) increase the coronary blood flow
by coronary artery vasodilation or to (2) increase the oxygen in the blood by administering
supplemental oxygen.
AGE-RELATED CHANGES
It is difficult to separate the normal age-related changes in the heart and blood vessels from the
changes caused by disease. In general, age-related changes progress slowly, whereas pathogenic
changes are more likely to be sudden.
HEART
Changes in the heart muscle include increased density of connective tissue and decreased
elasticity. Cardiac contractility may decline, making the heart less able to adapt to changes in
circulating blood volume. The valves may thicken and stiffen. If they do not close properly, the
patient may have a murmur. The valves may also partially block the path of blood flow, causing
incomplete emptying of the chambers.
The number of pacemaker cells in the SA node decreases, as does the number of nerve fibers in
the ventricles. The aging heart takes longer to respond to stress and then responds less
dramatically. It also takes longer to return to normal after exercise or stress. Cardiac
dysrhythmias are more common in older people but should still be evaluated because they can be
dangerous.
Health Promotion Considerations

Long-Term Conditioning
Long-term conditioning with an exercise program may help decrease arterial stiffening and
improve the function of the left ventricle in older individuals. Physical exercise does not have to
be strenuous to be helpful. Activity should become a part of an individual's regular routine.
BLOOD VESSELS
Changes in connective tissue and elastic fibers in arteries cause them to become stiffer. Physical
activity can help reverse or delay this process (see the Health Promotion Considerations box
above). Pulse pressure (the difference between the systolic and diastolic pressures) and systolic
blood pressure generally increase. Experts disagree about what exactly constitutes hypertension
in older adults. The veins stretch and dilate, leading to venous stasis and sometimes impaired
venous return. Thrombophlebitis and varicosities are more common in older people.
The cardiovascular system adapts more slowly to changes in position; therefore postural
hypotension may occur.
NURSING ASSESSMENT OF CARDIAC FUNCTION

HEALTH HISTORY
A complete assessment is important for the cardiac patient. If the patient is having acute
symptoms, however, a detailed assessment must be deferred until the patient is stable.
Chief Complaint and History of Present Illness
Determine the patient's reason for seeking medical care. Common symptoms that may be related
to cardiac disorders include fatigue, edema, palpitations, dyspnea, and pain. Note when
symptoms occur, what aggravates them, and what relieves them.
Medical History
Ask whether the patient has had specific conditions that may be related to cardiac disease. These
include hypertension, kidney disease, pulmonary disease, stroke, rheumatic fever, streptococcal
sore throat, and scarlet fever. Document previous cardiac disorders and hospitalizations. List
recent and current medications and note allergies in appropriate records. It is also important to
ask whether the patient is taking any vitamins, herbs, or homeopathic remedies. It may be easier
to ask something such as “What are you doing to stay healthy or to help you feel better?”
Family History
Because cardiovascular problems are often familial or hereditary, ask whether immediate
relatives have had hypertension, coronary artery disease (CAD), other cardiac disorders, or
diabetes mellitus.
Review of Systems
Inquire whether the patient has experienced the following specific symptoms: weight gain,
fatigue, dyspnea (shortness of breath), cough, orthopnea (difficulty breathing in a supine
position), paroxysmal nocturnal dyspnea (sudden dyspnea during sleep), palpitations, chest pain,
syncope (fainting), concentrated urine, or leg edema.
If the patient has had dyspnea or orthopnea, determine when it occurred and whether the onset
was gradual or sudden. Pain also requires detailed descriptions. The pain of heart problems may
radiate or be referred to other areas. The pain may radiate down either arm, to the jaw, or to just
below the sternum. The severity may range from mild, intermittent discomfort to severe,
crushing chest pain. Ask the patient to rate the severity of the pain on a scale of 1 (mildest) to 10
(worst possible). Chest pain may be different in women and may be described as indigestion, as a
feeling of anxiety, as nausea, or as a feeling of fatigue. Document the exact description, location,
and severity, whether there is radiation, events causing the pain, and what relieves the pain.
Functional Assessment
Determine how this illness has affected the patient's ability to carry out usual activities. Describe
activity and rest patterns and usual diet. It is especially important to record salt and fat intake.
Ask the patient about sources of stress and coping strategies.
PHYSICAL EXAMINATION
Begin the physical examination with measurement of height and weight and recording of vital
signs.
Vital Signs
Blood Pressure.
The correct-size blood pressure cuff must be used. Position the arm at the heart level, and check
the blood pressure in both arms. Note the pulse pressure (difference between the systolic and
diastolic pressures) because it is a noninvasive measure of cardiac output. Next, measure blood
pressures and pulse rates in the lying, sitting, and standing positions. A blood pressure decrease
of 20 mm Hg or more with a position change indicates decreased blood volume or an autonomic
response. As blood pressure decreases, the pulse should increase as a compensatory mechanism.
Pulses.
Palpate the radial pulses for rate, rhythm, quality, and equality. Auscultate the apical pulse for
rate and rhythm. Apical and radial pulses may be taken simultaneously to detect a pulse deficit.
The normal heart rate is 60 to 100 bpm. A rate of less than 60 bpm is considered to be
bradycardia; tachycardia is characterized by a heart rate in excess of 100 bpm. The rhythm is
described as regular, irregular, or regularly irregular. The quality of the pulse is graded on a
four-point scale: 0, absent pulse (not palpable); 1, weak or thready pulse (pulse easily obliterated
by slight finger pressure, returning as pressure is released); 2, normal pulse (easily palpable); and
3, bounding pulse (forceful, not easily obliterated by finger pressure). With a stethoscope, listen
at the fifth intercostal space at the midclavicular line to assess the apical pulse. In addition to the
radial pulse, assess the carotid, brachial, femoral, popliteal, posterior tibial, and dorsalis pedis
pulses at appropriate times in the physical examination.
Respirations.
Observe the patient's respiratory effort and skin color. Count the respiratory rate, and auscultate
the breath sounds for crackles and wheezes. If the patient produces sputum, describe the color,
amount, and appearance.
Skin
Inspect the skin for color, hair distribution, and capillary refill, and palpate the temperature. Skin
color and temperature should be relatively the same over the entire body.
Heart Sounds
The heart sounds are systole (lub) and diastole (dub). To auscultate heart sounds, place the
diaphragm of the stethoscope firmly on the anterior chest. Avoid auscultating heart sounds
through clothing. Figure 35-5 shows where the heart sounds, made by closing of the valves, may
be heard best. With practice, you can learn to distinguish these. The following pattern of
auscultation is recommended:
 1.Listen to the aortic area first and then the pulmonic. As the aortic and the pulmonic
valves close, the dub should be louder than the lub in the aortic and pulmonic areas.
 2.Listen to the tricuspid and mitral valves in the areas indicated. In these areas, the lub
should be louder than the dub.
 3.After listening to each area with the diaphragm, repeat the pattern with the bell of the
stethoscope. Note additional sounds of S3 and S4. The S3 and S4 sounds are heard best
with the bell of the stethoscope placed at the apex when the patient is positioned on the
left side. S3, also called a ventricular gallop, occurs early in diastole. S3 is normal in
children and young adults and may be pathologic after age 30. S4, also called an atrial
gallop, occurs late in diastole. S4 is an abnormal heart sound.
 FIGURE 35-5 Auscultation of the heart. A, Aortic valve at the second intercostal space to
the right of the sternum. B, Pulmonic valve at the second intercostal space to the left of
the sternum. C, Tricuspid valve at the fifth intercostal space to the left of the sternum. D,
Mitral valve at the fifth intercostal space in the midclavicular line.

 Table 35-2 Grading of Heart Murmurs
GRADE DESCRIPTION
I Very faint
II Faint, but recognizable
III Loud, but moderate in intensity
IV Loud and accompanied by a palpable thrill
Very loud, accompanied by a palpable thrill, and audible with the stethoscope partially
V
off the client's chest
VI Extremely loud, may be heard with the stethoscope slightly above the client's chest
From Ignatavicius, D.D., Workman, M.L., & Mishler, M.A. (1999).
Medical-surgical nursing across the health care continuum (3rd ed., p. 735). Philadelphia:
Saunders.
 Heart Murmurs.
 A heart murmur is the sound produced by turbulent blood flow across the valves.
Murmurs are recorded as having high, low, or medium pitch, and they are located using
the anatomic landmarks where they are heard best. The timing of a murmur relates to
when it is heard in the cardiac cycle: systole or diastole. Murmurs are graded according to
intensity or loudness (Table 35-2).
 A rub is heard when the pericardium is inflamed. A scratchy or muffled sound may be
heard best by having the patient sit upright and lean forward. This position brings the
pericardium closer to the chest wall. A pericardial friction rub is best heard along the left
sternal border throughout the cardiac cycle. It may help to ask patients to hold their
breath briefly. If a rub is heard during this brief time, it is a pericardial rub rather than
pleural.
 Box 35-1 ASSESSMENT of Patients with Cardiac Disorders
 Health History
 Present Illness:
 Fatigue, edema, palpitations, pain; aggravating and relieving factors
 Past Medical History:
 Hypertension, kidney disease, pulmonary disease, diabetes mellitus, stroke, rheumatic
fever, streptococcal sore throat, scarlet fever, previous cardiac diseases or conditions,
previous hospitalizations, recent and current medications, allergies
 Family History:
 Hypertension, coronary artery disease or other cardiac conditions, diabetes mellitus
 Review of Systems:
 Weight gain, fatigue, dyspnea, cough, orthopnea, palpitations, chest pain, fainting,
concentrated urine, leg edema
 Functional Assessment:
 Effects of illness on usual activities, activity and rest pattern, lifestyle, diet, sodium and
fat intake, sources of stress, coping strategies
 Physical Examination
 General Survey:
 Apparent distress
 Height and Weight
 Vital Signs:
 Blood pressure in both arms and while supine, sitting, standing; apical heart rate and
rhythm; peripheral pulses: rate, rhythm, quality, equality; respiratory effort and rate
 Skin:
 Color, hair distribution, capillary refill, temperature
 Thorax:
 Heart sounds, heart murmurs, rubs; breath sounds, crackles, wheezes; presence and
appearance of sputum
 Extremities:
 Pulses, color, warmth, edema, hair distribution
 Extremities
 Inspect and palpate the extremities for color, edema, warmth, temperature, pulse quality,
and hair distribution.
 Assessment of the cardiac patient is summarized in Box 35-1.
 DIAGNOSTIC TESTS AND PROCEDURES
 A number of tests or procedures may be employed to assess cardiac structure and
function. More common tests are described here. Patient preparation and postprocedure
care are detailed in the Diagnostic Tests and Procedures table on pp. 635 and 636.
 ELECTROCARDIOGRAM
 The electrocardiogram (ECG) allows study of the electrical activity (conduction system)
through the heart muscle. An electrical impulse causes contractions as it passes through
the heart muscle. Electrodes placed on the surface of the skin pick up the electrical
impulses of the heart. Moving electrodes to various positions permits detection of
conduction disturbances in specific areas of the heart.
The ECG is graphed on standardized paper or viewed on an oscilloscope. Each cardiac cycle is
represented by a series of P, Q, R, S, and T waves. The activity represented by each wave is
explained in the Interpretation of Electrocardiograms section on pp. 673 to 675. The ECG is
interpreted to detect abnormalities in rate, rhythm, or impulse conduction. The normal finding is
called a normal sinus rhythm, which is characterized by the following:
 1.A rate of 60 to 100 bpm

 2.A regular rhythm
 3.A P wave preceding each QRS complex
 4.A PR interval that is within 0.12 to 0.20 second
 5.A QRS complex that is 0.10 second or less
AMBULATORY ECG (HOLTER MONITOR)
An ambulatory ECG uses a portable ECG machine with a memory to provide continuous cardiac
monitoring for 24 to 48 hours. A complete record of the heart rhythm is stored and analyzed
later. This type of monitoring is used to detect dysrhythmias that occur infrequently, to determine
if symptoms correlate with any underlying cardiac disease, to assess the effects of medications,
and for research purposes. The patient records in a diary all activity that occurs during the
monitoring, such as walking, stair climbing, sleeping, and engaging in sexual activity. The
monitor strip is computer scanned and then interpreted by a physician.
Even more sophisticated monitoring is accomplished by transtelephonic means. An audio signal

is sent over telephone lines to a station operated by personnel trained to recognize potentially
dangerous dysrhythmias.
DIAGNOSTIC TESTS and PROCEDURES The Heart

PATIENT POSTPROCEDURE
TEST PURPOSE/PROCEDURE
PREPARATION NURSING CARE
Electrodes are placed on the
Tell the patient what
skin to detect electrical activity
to expect and that the
of the heart.
procedure is painless. Remove gel from skin.
Electrocardiogram
(ECG) Detects abnormalities in
No special No special care needed.
conduction of impulses,
preparation is
including changes caused by
needed.
heart damage.
Tell patient to wear
loose clothing, take
Provides continuous ECG only sponge bath,
monitoring for a 24-to-48–hour avoid magnets and
period. metal detectors, and
Return at scheduled
monitor placement of
time. ECG recording
Holter monitor Detects occasional electrodes.
will be retrieved for
dysrhythmias that may be
inspection.
correlated with specific Emphasize keeping
activities noted in patient's accurate diary of
diary. activities and to push
“event button” if
symptoms occur.
Tell patient/family
Provides ECG monitoring for
member/significant
longer time periods and saves Return at scheduled
other to activate
Implantable loop on a memory loop for analysis. time. ECG recording
recorder when
recorder (ILR) will be retrieved for
symptoms occur and
Detects dysrhythmias causing inspection.
to keep a written
syncopal episodes.
record of events.
Echocardiogram Uses ultrasound to create Tell the patient what Remove gel from skin.
images of the heart. Gel is
placed on the patient's skin and to expect and that the
a transducer moved over the procedure is painless.
area.
No special
No special care needed.
Detects valve abnormalities, preparation is
left ventricular hypertrophy, needed.
hypertrophic cardiomyopathy.
Used when conventional
echocardiogram not diagnostic. Tell patient what to
expect: throat will be
Probe inserted through anesthetized, may Monitor vital signs, gag
Transesophageal
esophagus into stomach have IV. reflex, and, if sedated,
echocardiogram
(behind heart). level of consciousness.
Signed consent
Same purpose as required.
echocardiogram.
Creates images of body
structures without radiation.
The patient lies on a firm pad All metal must be

No special care needed.
that rolls into a circular device. removed. Sedation
Magnetic
“Open MRI” better tolerated by may be ordered if
resonance imaging Safety precautions if
claustrophobic patients because patient is very
(MRI) sedative has been
machine does not surround anxious or unable to
given.
patient. be still.
Clanging sounds are heard as

the machine works.
Tell patient what to
expect.
Radioactive material is injected Nothing by mouth

Multiple-gated intravenously and the heart (NPO) for 2 hr before
acquisition scanned to evaluate function. procedure. No special care needed.
scanning May be done at rest or during
exercise. Start intravenous
infusion as ordered.
Signed consent
required.
Stress test Assess presence and severity of Tell the patient what No special care needed.
(exercise tolerance coronary artery disease by to expect. NPO for 2
test) having the patient exercise hr before test.
during ECG monitoring.
Give beta-blocker if
prescribed.
Blood pressure is monitored.
Have patient wear
The test is stopped if symptoms
loose clothing and
of coronary artery disease
comfortable shoes.
occur.
Signed consent
required.
Same as stress test.
Thallium-201 is given
Tell patient
intravenously and the heart
intravenous injection
Thallium imaging scanned to assess blood flow. No special care needed.
will be given and that
Scanning may be done at rest
radiation dose is
or after exercise.
small and quickly
eliminated.
Imaging technology that expect (lie on table,
provides images used to assess hold very still, may
Ultrafast myocardial perfusion, right and be asked to hold
Computed left ventricular muscle breath for a few No special care needed.
tomography (CT) mass/function, and measure seconds at a time).
calcium deposits in coronary No special
circulation. preparation is
needed.
A catheter is passed through a expect. Assess
vein or artery and dye is allergies to seafood Check puncture site;
injected. or iodine and inform maintain pressure per
radiologist. NPO for protocol if a vascular
Radiographs are taken to specified time before sealing device is not
visualize heart structures and procedure. used.
Cardiac blood vessels.
catheterization Tell patient to expect Monitor vital signs and
The procedure is done in a flushing sensation peripheral pulses on
special room. when dye is injected. affected extremity.
Give sedative if
Blood pressure, pulse, and ordered. Enforce bed rest as
ECG are monitored throughout ordered.
test. Signed consent
required.
Electrophysiology A catheter with multiple Tell the patient what Similar to cardiac
electrodes is passed into the
to expect. NPO for 6
right side of the heart through
hr before procedure.
the femoral vein. The
Premedicate with
electrodes record electrical catheterization
study (EPS) prescribed sedatives.
activity of the conduction (described above).
system and may be used to
Signed consent
stimulate the patient's
required.
dysrhythmia.
Remove air bubbles
from sample. Place
Tell patient about
tube on ice and send for
arterial puncture.
Assesses acid-base balance by immediate analysis.
Arterial blood
measuring pH, PCO2, PO2,
gases Prepare heparinized
HCO3− and base excess. Apply pressure to
syringe and obtain
puncture site for 5 min.
blood sample.
Report results.
Tell patient a blood
sample will be
drawn. No special
Measures creatine
preparation. Check venipuncture
phosphokinase, lactate
site.
dehydrogenase, and aspartate
Cardiac enzymes To detect acute
aminotransferase to detect
myocardial Apply pressure if
elevation associated with heart
infarction, draw oozing.
damage.
specimen before
other invasive
procedures.
Check venipuncture
Measures protein released after site.
sample will be
Troponin myocardial injury. Troponin T
drawn. No special
(cTnT) and Troponin I (cTnI). Apply pressure if
preparation.
oozing.
Check venipuncture
site.
Measures myoglobin levels in sample will be
Myoglobin
the blood. drawn. No special
Apply pressure if
preparation.
oozing.
Counts white and red blood
Check venipuncture
cells, hemoglobin and Tell patient a blood
site.
Complete blood hematocrit, red blood cell sample will be
count (CBC) indices, and sometimes drawn. No special
Apply pressure if
platelets. (See Normal Values preparation.
oozing.
in Table 35-5.)
Tell patient to expect
Measures common serum Check venipuncture
venipuncture. NPO
lipids (cholesterol, site.
for 12 hr before
Lipid profile triglycerides, lipoproteins).
sample drawn. Usual
Used to evaluate risk of Apply pressure if
diet for 2 weeks
coronary artery disease. oozing.
before test.
Measures naturally occurring Tell patient a blood
Check venipuncture
BNP levels. Elevated in HF, sample will be
site.
B-type natriuretic CMP. Helps differentiate drawn.
peptide (BNP) dyspnea related to cardiac
Apply pressure if
problems from non–cardiac No special
oozing.
related dyspnea. preparation.
Check venipuncture
Acute phase protein that is Tell patient a blood
site.
C-reactive protein elevated in system sample will be
(CRP) inflammation. Elevated levels drawn. No special
Apply pressure if
seen with ACS. preparation.
oozing.
ACS, Acute coronary syndrome; CMP, cardiomyopathy; HF, heart failure.
IMPLANTABLE LOOP MONITOR/RECORDER
For longer monitoring time periods, to record a patient's ECG during syncopal episodes, an
implantable loop monitor/recorder (ILR) may be used. This device, implanted just under the
patient's skin in the chest area, continually monitors the ECG activity of the patient in a memory
loop. The patient and/or family member/significant other is taught to activate the recorder when
symptoms are felt. The ECG can then be analyzed and appropriate treatment implemented. The
device can be used for up to 14 months, as needed (Morton, Tucker, & Van Roeden, 2005).
ECHOCARDIOGRAM (HEART SONOGRAM)
The echocardiogram visualizes and records the size, shape, position, and behavior of the heart's
internal structures, especially the valves. Ultrasonic waves are beamed into the heart, and their
echoes are recorded. This painless test may be performed at the bedside or in a laboratory. Gel is
applied to the skin, and a special device called a transducer is moved over the precordium. The
transducer picks up sound waves and converts them to electrical impulses that are recorded as
waveforms on an oscilloscope, a videotape, or a strip chart. Common echocardiogram types
include motion mode (M-mode) and two-dimensional mode (2-D mode). Echocardiograms can
also be enhanced using Doppler technology (Doppler echocardiogram) and color-flow imaging.
TRANSESOPHAGEAL ECHOCARDIOGRAM
At times, the echocardiogram is not diagnostic and a transesophageal echocardiogram (TEE) is

used. A flexible endoscopic probe with an ultrasound transducer is passed down the back of the
throat into the esophagus. A local anesthetic to the throat decreases the gag reflex. Occasionally,
an intravenous sedative is needed to reduce patient anxiety. Images are obtained from behind the
heart as the probe moves down into the stomach. The probe is down for approximately 15 to 20
minutes. The TEE provides information useful in the evaluation of ventricular wall motion and
function and possible heart valve disorders.
MAGNETIC RESONANCE IMAGING
A magnetic resonance imaging (MRI) scan provides high-resolution, three-dimensional images

of body structures. Cardiac tissue is imaged without lung or bone interference. The patient is
enclosed in a chamber for approximately 5 minutes for an MRI scan of the heart. No loose
metallic objects are permitted in the chamber during the procedure. Patients with intracranial
aneurysm clips, intraocular metal foreign bodies, heart valves manufactured before 1964, and
some middle-ear prostheses should not have MRI scans because the devices may be affected by
the magnetic field or may interfere with the MRI. Other implanted devices that contraindicate
MRI include pacemakers, automatic implantable cardioverter-defibrillators (AICDs), and
implanted infusion pumps. For patients who are claustrophobic, an open MRI may be available.
MULTIPLE-GATED ACQUISITION SCAN
In a multiple-gated acquisition scan (MUGA), the patient is injected with technetium 99m, which
concentrates in acutely necrotic myocardial tissue. The heart is then scanned to assess left
ventricular structure and function, to evaluate myocardial wall motion, to detect intracardiac
shunting, to assess valvular disease, and to identify location and size of an acute myocardial
infarction (AMI). Assessment of ventricular function can be done while the patient is resting or
exercising. Sublingual nitroglycerin may be administered to assess its effect on ventricular
function.
STRESS TEST (EXERCISE TOLERANCE TEST)
The stress test is a noninvasive method of assessing the presence and severity of CAD by
recording a person's cardiovascular response to exercise. It is also used to measure functional
capacity for work, sport, or participation in a rehabilitation program. The stress test is not
flawless—false-positive and false-negative results are common. A negative test result does not
absolutely exclude CAD. It is, however, the best noninvasive screening procedure available. The
alternative is the much more invasive cardiac catheterization.
For the stress test, a continuous ECG is monitored while the patient uses a treadmill or a
stationary bicycle. Every 2 to 3 minutes the speed and incline angle of the treadmill are increased
(or pedal resistance is increased with a bicycle) until (1) the patient cannot continue for whatever
reason, (2) the patient's maximum heart rate is achieved (220 2 patient's age 5 maximum heart
rate), (3) symptoms intervene, or (4) significant changes are detected on the ECG. The target
heart rate is 85% of the predicted maximum heart rate for the patient's age and gender.
Significant CAD limits blood flow to the myocardium. The increased demands of exercise may
cause the patient to have symptoms of CAD, which are angina, dizziness, dyspnea,
dysrhythmias, a falling blood pressure, and certain ECG findings. If these symptoms occur, the
test must be stopped immediately.
Contraindications for the test include acute systemic illness, severe aortic stenosis, uncontrolled
congestive heart failure (CHF), severe hypertension, angina at rest, and significant dysrhythmia.
Although the mortality rate for test participants is very low, cardiopulmonary resuscitation
equipment must be available.
PERFUSION IMAGING
Perfusion studies, performed most commonly in conjunction with exercise tolerance testing,
provide information about the presence of coronary artery disease and the location and extent of
ischemic and infarcted myocardium. There are several radioactive tracers approved for perfusion
scanning. Thallium-201 is the most widely used over the years and will be addressed here.
Thallium Imaging
Thallium-201 may be administered to assess myocardial blood flow during stress testing.
Thallium, which is taken up by normal myocardial cells, is used to detect old or new myocardial
ischemia and to evaluate patency of coronary artery bypass grafts. After thallium-201 is injected
intravenously, the heart is scanned to assess the areas of concentration. The scan takes
approximately 1 hour to complete and is repeated in 2 to 4 hours to assess for redistribution.
Thallium does not enter infarcted or scarred areas and, therefore, shows “cold spots” in areas
without blood flow. Exercise-induced ischemia resolves with rest. Scar-induced ischemia, such
as that caused by AMI, does not resolve with rest.
For patients who are physically not able to exercise, the heart can be stressed with medications
such as dipyridamole (Persantine). These medications mimic the effects of exercise by causing
vasodilation of the coronary arteries, which increases blood flow to well-perfused areas, thereby
stealing blood from ischemic areas. These differences in flow will show up on the scan.
ULTRAFAST COMPUTED TOMOGRAPHY
Ultrafast CT (also known as electron-beam CT or EBCT) is a fast form of imaging technology

that allows for high-quality images not affected by the movement of the heart as it contracts and
relaxes. The images obtained are used to assess myocardial perfusion, along with right and left
ventricular muscle mass and function. In addition, Ultrafast CT can measure calcium deposits in
the coronary arteries, and a coronary calcium score can be derived. The greater the amount of
coronary calcium, the higher the score and the higher the risk of coronary occlusive disease. This
procedure is not a substitute for cardiac catheterization (Morton, Tucker, & Van Roeden, 2005).
CARDIAC CATHETERIZATION (CARDIAC ANGIOGRAPHY, CORONARY

ARTERIOGRAPHY)
Cardiac catheterization is a procedure in which a catheter is inserted into a vein or artery and is
threaded into the heart chambers, coronary arteries, or both, under fluoroscopy (Fig. 35-6). A
contrast dye is injected through the catheter, and films are made of the visualized heart
structures. Vital signs and ECG are monitored during the procedure.
In a catheterization of the right side of the heart, the catheter is inserted into a vein and threaded
into the vena cava, RA, RV, and pulmonary artery. Pressures in the RA, RV, and pulmonary
artery may be determined. The function of the pulmonic and tricuspid valves may be assessed.
In a catheterization of the left side of the heart, the catheter is inserted into an artery and threaded
against the flow of blood into the coronary arteries or the LV. The femoral vein and artery are
the preferred insertion sites. The function of the coronary arteries and the aortic and mitral valves
may be assessed. Blood samples may be drawn, and pressures in the various structures are
measured.
Complications of cardiac catheterization include bleeding, hematoma formation, infection, and

embolus or thrombus formation. Nursing care before and after the procedure is very important.
ELECTROPHYSIOLOGY STUDY
The electrophysiology study (EPS) is used to record the heart's electrical activity from within the
heart using catheters with multiple electrodes inserted through the femoral vein into the right side
of the heart. The electrodes record the electrical activity of the heart's conduction system. In
addition, the electrodes can be used to stimulate dysrhythmias that will help locate the source of
the patient's dysrhythmia.
LABORATORY TESTS
Arterial Blood Gases
Arterial blood gases are analyzed to determine the body's ability to maintain the acid-base
balance. Acidity or alkalinity is determined by pH. If the serum pH is less than 7.35, the blood is
acidic; greater than 7.45 indicates alkalinity. Carbonic acid dissociates into carbon dioxide and
water. The lungs regulate carbon dioxide. The partial pressure of carbon dioxide in the blood is
abbreviated Pco2. A Pco2 greater than 45 with an acidic pH is a respiratory acidosis and indicates
that the body is unable to excrete the excess carbon dioxide through the lungs. With a pH in
excess of 7.45 and a Pco2 of less than 35, a respiratory alkalosis is present.
The kidneys regulate bicarbonate (HCO32) through excretion and retention. The HCO32 (or base
excess—a combination of all serum bases) is assessed to determine metabolic causes of
imbalance. If the pH is less than 7.35 and the HCO32 is less than 22, the body is in metabolic
acidosis. With a pH greater than 7.45 and an HCO32 greater than 26, the interpretation is
metabolic alkalosis (Table 35-3).
Pulse Oximetry
Pulse oximetry, though not a laboratory test, noninvasively measures arterial oxygen saturation.
Light is passed through a pulsating artery and interpreted mechanically to determine the oxygen
saturation. The transdermal clip or patch may be applied to a digit (finger or toe), the ear, or the
nose (Fig. 35-7).
FIGURE 35-6 Right-sided (A) and left-sided (B) heart catheterization.

Table 35-3 Interpreting Arterial Blood Gases
CONDITION pH Pco2 HCO3−
Normal range 7.35–7.45 35–45 22–26
Respiratory acidosis ↓ ↑ Normal
Respiratory alkalosis ↑ ↓ Normal
Metabolic acidosis ↓ Normal ↓
Metabolic alkalosis ↑ Normal ↑
↑, Elevated; ↓, decreased. If the arrows are in the same direction, a metabolic problem exists. If
arrows are in opposite directions, a respiratory problem exists.
Cardiac Enzymes
Cardiac enzymes are released when heart cells die as a result of damage. These enzymes are
measured in the serum, and their values rise as indicators of damage to the heart cells. Table 35-4
lists normal cardiac enzyme levels.
Creatine Phosphokinase.
The creatine phosphokinase enzyme is found in high concentration in three tissues: the brain, the
heart, and the skeletal muscle. The type of creatine phosphokinase (CPK) specific to heart tissue
is CPK-MB. Elevation of the CPK-MB level indicates damage to the myocardial cells. The CPK-
MB can be expected to rise 4 to 6 hours after an AMI, peak in 12 to 24 hours at more than 6
times the normal value, and return to normal within 2 to 3 days if no new damage occurs. Serial
trends should be observed. The nurse can plot these trends. Musculo-skeletal injuries (especially
fractures and surgery) and recent excessive athletic activity can also elevate the total CPK level.
FIGURE 35-7 Pulse oximeter. A, Ear probe. B, Clip on finger.

Table 35-4 Cardiac Enzymes and Markers
TEST* NORMAL VALUES
Male: 55–170 U/L
Creatine Phosphokinase (CPK)
Female: 96–140 U/L
MM: 100%
CPK Isoenzymes MB: 0%
BB: 0%
Troponin T (cTnT) <0.1 ng/mL
Troponin I (cTnI) <0.3 ng/mL
Myoglobin Male: <92 ng/mL
Female: <76 ng/mL
Cardiac Protein Markers

Troponin.
Troponin is a protein involved in the contraction of muscles. Two subtypes, troponin T (cTnT)
and troponin I (cTnI) are specific to cardiac muscle and are released into the circulation after an
acute myocardial infarction. Troponin levels, generally not detectable in healthy individuals, will
elevate significantly after an acute myocardial infarction. Levels may elevate slightly as a result
of lesser insults, such as an episode of angina. Troponin levels rise in 3 to 6 hours from onset of
symptoms, peak in 24 hours, and remain in the circulation for up to 2 weeks. This test is done in
the emergency department because the results are available more quickly than the cardiac
enzymes.
Myoglobin.
Myoglobin is another protein found in cardiac and skeletal muscle that is released into the
circulation very quickly after myocardial infarction. Myoglobin levels increase in 1 to 4 hours
after symptoms. Because it is found also in skeletal muscle, myoglobin levels may be elevated
by such things as strenuous exercise, renal failure, and neuromuscular diseases. This makes
interpreting myoglobin levels difficult in some circumstances.
Complete Blood Count
The complete blood count is a basic screening test. Included in this test are the white blood cell
(WBC) count, the red blood cell (RBC) count, the hemoglobin (Hgb) and hematocrit (Hct)
measurements, the RBC indices, and, in some laboratories, the platelet count. Components of the
complete blood count are presented in Table 35-5.
White Blood Cell Count.
The WBC count indicates the body's ability to defend itself against infection and inflammation.
The WBC level usually is elevated with inflammatory processes such as AMI and bacterial
infections, but it may be below normal with viral infections and bone marrow depression.
Red Blood Cell Count.
The RBC count is assessed to determine the ability of the blood to carry oxygen from the lungs
to the tissues and carbon dioxide from the tissues to the lungs. The RBC level may be below
normal with anemias and malignancies and may be elevated in dehydration.
Table 35-5 Complete Blood Count

TEST* NORMAL VALUES
White Blood Cells: 5,000–10,000/mm3
Differential:
Neutrophils 60%–70%
Eosinophils 1%–4%
Basophils 0.5%–1.0%
Lymphocytes 20%–40%
Monocytes 2%–6%
TEST* NORMAL VALUES
Red Blood Cells:
Male 4,200,000–5,400,000/mm3
Female 3,600,000–5,000,000/mm3
Hematocrit:
Male 40%–54%
Female 37%–47%
Hemoglobin:
Male 13.5–17.5 g/dL
Female 12–16 g/dL
Platelets 150,000–350,000/mm3
Hematocrit.
The hematocrit is the percentage of packed RBCs in the total sample of whole blood. With
severe dehydration, the plasma portion of the blood decreases and the Hct is elevated. In anemias
and hemorrhage, the Hct is below normal. In general, the Hct is three times the Hgb
measurement.
Hemoglobin.
Hemoglobin is the main component of the RBCs. Its function is to transport oxygen to the cells.
The Hgb measurement may be below normal in anemias and hemorrhage. It is elevated in
dehydration, chronic obstructive pulmonary disease (COPD), and CHF. An Hgb of less than 5
g/dL leads to heart failure and death if not corrected.
Platelet (Thrombocyte) Count.
The platelets (thrombocytes) are the smallest of the formed elements in the blood. They are
necessary for coagulation. The platelet count is below normal with anemias, bone marrow
depression, and bleeding. The count may be increased in acute infections and some heart
diseases. A count of less than 20,000 may result in spontaneous bleeding.
Lipid Profile
A lipid profile is a battery of tests that measure the most common serum lipids: cholesterol,
triglycerides, and lipoproteins.
Cholesterol is a blood lipid produced by the liver. It is used to form bile salts for the digestion of
fat and for the production of adrenal, ovarian, and testicular hormones. The normal adult serum
cholesterol level is less than 200 mg/dL. Elevated cholesterol levels (hypercholesterolemia) are
associated with increased risk of CAD, hypertension, and AMI. The cholesterol accumulates in
the arterial lumen and in time results in decreased blood flow and occlusion.
Several forms of cholesterol are identified; however, the high-density lipoproteins (HDLs) and
the low-density lipoproteins (LDLs) are the two that most closely correlate with coronary artery
disease. The HDLs are desirable because they promote the excretion of cholesterol; therefore
higher levels of HDLs are encouraged. On the other hand, elevated LDL levels are associated
with a higher risk of CAD; therefore lower LDL levels are encouraged. A good way to remember
the difference is that HDLs are healthy and LDLs are lethal. Currently, the recommendations are
for HDL levels greater than 40 mg/dL and for LDL levels less than 100 mg/dL (American Heart
Association, 2007). See the Health Promotion Considerations box above for advice about
increasing HDL levels.
Triglycerides are a major contributor to CAD. They are produced in the liver. Triglyceride levels
increase when LDL levels increase. The normal triglyceride level is less than 150 mg/dL.

Low HDL Levels
Low HDL levels can be raised by being physically active at least 30 minutes every day, by not
smoking, and by losing weight (or maintaining a healthy weight).
B-type Natriuretic Peptide
B-type natriuretic peptide (BNP) is a cardiac hormone released when there is ventricular dilation
and stretch (such as occurs in heart failure). Less than 100 pg/mL is considered a normal BNP
level, and elevated levels relate closely to the severity of heart failure (e.g., the higher the levels,
the more severe the failure). In addition, BNP levels can be monitored to assess the effectiveness
of treatment.
C-reactive Protein
C-reactive protein (CRP) is an acute-phase protein and a marker for systemic inflammation.
Elevated levels of CRP are present in patients with acute coronary syndromes. CRP is being
studied to determine its usefulness in predicting recurrent and new cardiovascular events.
COMMON THERAPEUTIC MEASURES

DRUG THERAPY
Commonly used cardiac drugs are cardiac glycosides, antianginals, antidysrhythmics, and
miscellaneous and emergency drugs. Examples of these drugs, their actions and adverse effects,
and associated nursing considerations are provided in the Drug Therapy table on pp. 642 to 646.
Cardiac Glycosides
The cardiac glycosides are also called cardiotonics or digitalis glycosides. Examples are digoxin
(Lanoxin) and digitoxin. These drugs have several important pharmacologic actions on the heart.
They slow the heart rate (negative chronotropic effect) and increase the force of myocardial
contraction (positive inotropic effect), causing increased stroke volume and cardiac output.
Cardiac glycosides are widely used in the treatment of heart failure (HF). They are also used to
treat some cardiac dysrhythmias.
When rapid effects are needed, a patient can be given a loading dose (called a digitalizing dose)
of cardiac glycosides. Once therapeutic blood levels are obtained, a maintenance dose is
prescribed to maintain the therapeutic effects. These drugs have high potential for toxicity and
require close monitoring. Common practice is to count the apical pulse before giving each dose.
If the rate is below 60 bpm in adults, withhold the dose and contact the physician. Because
patients are often on cardiac glycosides for long-term therapy, they must be taught to monitor
their own pulse and to report symptoms of toxicity (anorexia, nausea, visual disturbances). Other
specific nursing considerations are presented in the Drug Therapy table on p. 642.
Antianginals
Drugs used to treat angina (chest pain related to myocardial ischemia) include nitrates, beta-
adrenergic blockers, and calcium channel blockers. Nitrates are used to treat actual anginal
episodes and to prevent angina. Beta-adrenergic blockers and calcium channel blockers are used
in the long-term management of angina. Examples of each classification and nursing
considerations are presented in the Drug Therapy table on pp. 642 and 643.
Antidysrhythmics
Drugs used to treat abnormal cardiac rhythms are called antidysrhythmics or antiarrhythmics.
There are four main classes of antidysrhythmics, each with various actions. In general, they work
by slowing the rate of impulse conduction, depressing automaticity, or increasing resistance to
premature stimulation. All antidysrhythmics have the potential to cause additional dysrhythmias.
Specific drugs and nursing considerations are presented in the Drug Therapy table on pp. 644
and 645.
Angiotensin-Converting Enzyme Inhibitors
Angiotensin-converting enzyme (ACE) inhibitors (ACEI) work against the renin-angiotensin-

aldosterone system to dilate arteries and decrease the resistance to blood flow in the arteries
(reduced afterload). In addition, less fluid is retained because aldosterone release is blocked.
ACE inhibitors are prescribed for patients with heart failure, some cases of hypertension, and in
some cases after myocardial infarction Examples of these medications are captopril (Capoten),
enalapril (Vasotec), and quinapril (Accupril). Information about these medications is presented
in the Drug Therapy table on p. 721.
DRUG THERAPY Cardiovascular Drugs

DRUG USE/ACTION NURSING INTERVENTIONS
CARDIAC GLYCOSIDES
Digoxin (Lanoxin) Delays impulse conduction through Obtain baseline vital signs, ECG, and
AV node to slow heart rate (negative electrolytes before administering first
chronotropic effect). Increases dose. Assess apical pulse for 1 min;
strength or force of myocardial hold and notify physician if <60.
Cannot be administered
intramuscularly. Monitor K+ levels;
administer K+ supplements as ordered.
Decreased renal function may delay
excretion and lead to toxicity. Toxic
effects may be indicated by
dysrhythmias, pulse <60, anorexia,
contraction (positive inotropic
nausea, syncope, visual disturbances,
effect). Increases stroke volume and
and abdominal pain.
CO. Used for HF, atrial fibrillation
and flutter, and paroxysmal atrial
Therapeutic level: 0.8–2.0 ng/mL.
tachycardia.
Toxic level: >2.0 ng/mL.
Teach the patient:
• Take radial pulse for 1 min at the

same time each day.
ANTIANGINALS
Nitroglycerin Vasodilator (arteries and veins). Assess BP and pulse before
Relaxes all smooth muscles, administration. Apply ointment in
Available as especially vascular smooth muscle. uniform layer on paper provided;
sublingual tablets, Decreases preload, afterload, BP, apply to nonhairy skin (chest, back,
ointment, CO, and systemic vascular upper arm); do not touch (causes
transdermal patch, resistance. Used to prevent and treat headache); rotate sites.
buccal tablets, mist, angina.
and sustained-release IV drug is delivered in glass
oral tablets containers with special tubing; use an
infusion pump; monitor closely.
Teach the patient:
• Sit or lie down at onset of chest

pain.
• Place tablet under tongue; tablet

causes tingling sensation if effective
(older adults may not detect this).
• Repeat q 5 min for total of three

doses; if chest pains not relieved,
have someone else drive to
emergency department.
• Keep tablets in containers in which

supplied; drug decomposes on

exposure to light and air.
• Headache decreases with tolerance.
• Drug may be taken before activities

likely to cause angina (exercise, sex).
Assess vital signs before
administration. Teach the patient:
• Take 1-2 hr before meals and at

bedtime.
• Sit when taking the sublingual or

Vasodilator that works by relaxing chewable medications.
smooth muscles. Decreases preload,
afterload, left ventricular end- • Change positions slowly to avoid
Isosorbide dinitrate
diastolic pressure, and myocardial orthostatic hypotension.
(Isordil)
oxygen consumption. Used for acute
angina and maintenance of chronic • Avoid hot showers, tubs, saunas.
angina.
• Headache decreases over time.
• Alcohol potentiates hypotension.
• If three sublingual or chewable

doses do not relieve angina, go to the
emergency department.
Beta-adrenergic blocker. Decreases Assess BP and apical pulse before
Nadolol (Corgard)
HR and CO at rest and with exercise. administration.
Monitor weight (fluid retention with
HF). Teach the patient:
• Take radial pulse for 1 min.

Dosage increased Decreases conduction velocity
gradually until through the AV node. Used in • Hold medication and notify
optimal response is hypertension and prophylactically physician if HR
achieved for chronic stable angina.
• Weigh daily; report a gain of 3-4 lb.
• Do not discontinue this drug

abruptly; taper off over 1-2 weeks.
Propranolol (Inderal) Nonselective beta-adrenergic Monitor vital signs. May be
administered with diuretic to decrease
Na+ and water retention. May cause
bronchial constriction. Use with
caution in all patients with obstructive
lung disease. Auscultate lungs for
crackles and heart for S3 and S4.
Monitor weight daily; check for
peripheral edema. Monitor blood
glucose with diabetes.
blocker. Decreases HR, myocardial Teach the patient:

irritability, and contractibility.
Decreases BP in hypertension. • Do not discontinue this drug
Decreases CO. Used in dysrhythmia, abruptly; taper over 2 weeks.
myocardial infarction, hypertension,
migraines, and chronic stable angina. • Take at the same time(s) each day.
• While on this drug, use alcohol only

in moderation; no smoking; decrease
sodium intake.
• There is not the normal increase in

heart rate with exercise and stress;
increase activity slowly.
• Weigh daily; check for edema.

Monitor vital signs. Continuous ECG
monitoring with IV administration.
Take apical pulse before each dose.
Teach the patient:

Cardioselective beta-adrenergic
blockers used to treat angina and • Take with or after meals.
Atenolol (Tenormin) hypertension.
and metoprolol • Do not discontinue abruptly.
tartrate (Lopressor) Reduce heart rate, BP, cardiac
output, and myocardial oxygen • Take pulse and report to physician if
consumption. below 60
• Avoid alcohol and smoking.
• Avoid over-the-counter cold

remedies.
Diltiazem Calcium channel blocker. Dilates Dosage may need to be reduced in
hydrochloride coronary arteries; increases
older adult patients.
availability of oxygen to the Teach the patient:

myocardium. Decreases total PVR,
afterload, and systolic blood • Take radial pulse for 1 min.
pressure. Slightly decreases
(Cardizem)
myocardial contractility. Prolongs • Limit caffeine intake.
AV node refractory period. Used in
chronic stable angina, coronary • Change positions with caution to
artery spasm, and hypertension. prevent postural hypotension.
• Take before meals and at bedtime.

Monitor BP during titration (during
dosage adjustment).
Calcium channel blocker. Decreases
Teach the patient:
myocardial oxygen consumption.
Dilates coronary arteries. Decreases
Nifedipine • Smoking is contraindicated (nicotine
PVR. Increases CO. Used for
(Procardia) constricts coronary arteries).
angina, mild to moderate
hypertension, vascular headaches,
• Do not discontinue this drug
coronary artery spasms.
abruptly.
• Limit caffeine intake.

Assess baseline vital signs, hepatic
and renal function. Assess for signs of
CHF (pulmonary or peripheral
edema). Monitor pulse and BP before
each dose. Administer IV bolus more
slowly to older adults.
Calcium channel blocker. Slows AV
Teach the patient:
conduction. Dilates peripheral and
coronary arteries. Increases oxygen
Verapamil • Take radial pulse for 1 min; report
supply to myocardium. Used to treat
hydrochloride irregular or slow pulse.
supraventricular tachycardias, atrial
(Calan, Isoptin)
fibrillation and flutter, angina,
• No caffeine (opposes calcium
hypertension, and vascular
channel–blocking effect).
headaches.
• Change position slowly until
tolerance develops.
• Exercise with caution; drug's effects

may give false impression of
tolerance.
ANTIDYSRHYTHMICS
Continuously monitor ECG for a
decrease in dysrhythmia. Observe for
thyroid dysfunction (each 200-mg
tablet contains 75 mg of iodine) and
neurologic effects (tremors, ataxia,
headache, insomnia).
Antidysrhythmic. Increases action
potential duration and effective
Teach the patient:
Amiodarone refractory period. Increases CO.
hydrochloride Decreases PVR, coronary artery
• Take radial pulse daily.
(Cordarone) resistance, and HR. Used for severe
tachycardia and supraventricular
• Photosensitivity and photophobia
tachycardias.
may occur.
• Pharmacologic action may have a

delayed onset of 5 days to 3 mo.
• Skin discolorations fade with time.

Adrenergic blocker. Suppresses
Monitor vital signs, ECG.
ventricular fibrillation and
ventricular tachycardia. Used for
Have resuscitation equipment
Bretylium tosylate short-time treatment of life-
available.
(Bretylol) threatening ventricular tachycardias
in patients who do not respond to
If nausea and vomiting occur,
conventional therapy, ventricular
decrease the rate of infusion.
fibrillation, and cardioversion.
Disopyramide Reduces the rate of spontaneous Assess apical pulse before
phosphate (Norpace) diastolic depolarization in administration; hold if <60 or >120
pacemaker cells. and notify physician. Monitor BP.
Monitor intake and output. Urinary
Increases SVR. Decreases retention and constipation may occur.
myocardial conductivity. Suppresses
ectopic focal activity. Used to Teach the patient:
suppress and prevent recurrent PVCs
and ventricular tachycardia. • Take radial pulse daily.
• Weigh daily; observe for edema.
• Change position slowly.
• No alcohol (severely decreases BP).
• Relieve dry mouth with sugarless

gum or dry candy.
• Avoid sunlight (photosensitivity).

Antidysrhythmic. Decreases
conduction velocity. Increases
Flecainide acetate ventricular refractory period. Used
Monitor ECG.
(Tambocor) to treat PVCs, atrial tachycardia, and
other dysrhythmias not responsive to
other antidysrhythmics.
Increases the electrical stimulation Administer with an infusion pump.
threshold of the ventricular
conduction system. Used for rapid Monitor BP and ECG. May
Lidocaine
control of ventricular dysrhythmias precipitate malignant hyperthermia
(Xylocaine)
during myocardial infarction, cardiac (tachycardia, tachypnea, elevated
surgery, cardiac catheterization, and temperature). Assess breath sounds
digitalis intoxication. for crackles.
Administer with food or antacids.
Antidysrhythmic structurally similar
Mexiletine
to lidocaine. Used to suppress Monitor ECG.
hydrochloride
symptomatic ventricular
(Mexitil)
dysrhythmias. Mix IV solution immediately before
administration.
May need lower dosage in older
adults.
Administer only in normal saline

Used to treat paroxysmal atrial (drug crystallizes in dextrose). Do not
Phenytoin sodium
tachycardia and ventricular exceed 50 mg/min IV.
(Dilantin)
dysrhythmias.
Teach the patient:
• Alcohol potentiates the action and

therefore may precipitate toxicity.
Propranolol (Inderal) See description under Antianginals.
Antidysrhythmic. Depresses If administered with digoxin, may
myocardial excitability, contractility, produce toxicity or unpredictable
automaticity, and conduction dysrhythmias. Administer with meals
velocity. Anticholinergic effects to decrease gastric distress. Severe
Quinidine
increase the ventricular rate. hypotension may occur with large
doses. Monitor electrolytes;
Relaxes muscles. Used for atrial and continuing diarrhea may indicate
ventricular dysrhythmias. electrolyte imbalance.
Tocainide Antidysrhythmic. Primary analogue Monitor ECG. Administer with food
of lidocaine. Used for life- or antacids to decrease gastro-
hydrochloride threatening ventricular dysrhythmias intestinal side effects. Monitor CBC
(Tonocard) associated with prolonged QT for blood dyscrasias (agranulocytosis,
interval. leukocytosis, neutropenia).
Verapamil (Calan,
See description under Antianginals.
Isoptin)
ANTIPLATELET AGENTS
Monitor bleeding time, CBC with
differential, platelet count. Avoid
OTC medications with aspirin or
NSAIDs unless prescribed by
Decreases platelet aggregation.
physician.
Prolongs bleeding time. Used to
Clopidogrel (Plavix)
prevent thromboembolic disorders
Teach the patient:
such as stroke and MI.
• Report bleeding.
• Keep appointments for blood work.

Monitor liver function studies, CBC,
prothrombin time.
Teach the patient:

Ticlopidine (Ticlid) Same as Plavix.
• Report bleeding.
• Take with food.
• Keep appointments for blood work.

Used only in the hospital. Monitor
vital signs, ECG, and level of
Inhibits platelet aggregation.
consciousness. Assess hemoglobin,
hematocrit, platelet count, and
Abciximab (ReoPro) Given IV to reduce ischemic
clotting factors frequently.
complications with angioplasty or
arthrectomy.
Watch for bleeding. Protect from
trauma.
LIPID-LOWERING AGENTS
Cholestyramine Prescribed when diet, exercise, and Interferes with absorption of some
(Questran) weight loss fail to bring cholesterol other drugs, so check drug-drug
levels under control. Lowers LDL interactions before giving.
cholesterol. Increases HDL
cholesterol. To get the best effect, teach patients:
• Continue diet and exercise.
• Increase fluid intake to counter

constipating effects.
For best effect, teach patient:
Decreases synthesis and secretion of
Gemfibrozil (Lopid) VLDL by liver. Decreases • Continue diet and exercise.
triglyceride levels.
• Take with meals.
Decreases synthesis/secretion of
Nicotinic acid • Continue diet and exercise.
VLDL and LDL by liver. Increases
(niacin)
HDL.
• Take with meals to decrease GI side
effects.
Monitor liver function tests.
Pravastatin
(Pravachol)
Increases rate of removal of LDL • Continue diet and exercise.
Simvastatin (Zocor)
from plasma. Decreases synthesis of
LDL. • Report muscle tenderness.
Lovastatin (Mevacor)
• Take as single dose in the evening.
Atorvastatin (Lipitor)
• Have routine eye examinations.
MISCELLANEOUS AND EMERGENCY DRUGS
Inotropic agent. Vasodilator.
Increases myocardial contractions
Administer with an infusion pump.
without increasing HR. Increases
Titrate to target BP. Monitor intake
Amrinone lactate blood flow through collateral
and output. Avoid extravasation.
(Inocor) coronary vessels. Increases stroke
Discard solution 24 hr after
volume and CO. Decreases preload
preparation.
and afterload. Used to treat HF
refractory to other medications.
Vagal blocker. Increases HR and CO
in heart blocks and severe
Atropine sulfate Assess HR and rhythm and BP.
bradycardia. Used in symptomatic
bradycardia and bradydysrhythmias.
Calcium chloride Necessary for cardiac rhythm, tone, Monitor ECG, BP, and arterial blood
and contraction. Increases muscle gases. Avoid extravasation; causes
tone and force of contraction. Used necrosis. Alkalosis decreases the
in cardiac resuscitation and in absorption of calcium. Acidosis
cardiac irregularities associated with
increases the absorption of calcium.
hyperkalemia.
Continuous monitoring of ECG,
cardiac parameters, and urinary
output; titrate to HR and BP. Urinary
output should increase with improved
Synthetic catecholamine. Beta-
CO and renal function. Often used
adrenergic agonist. Increases CO
with nitroprusside or dopamine for
with less increase in HR and BP than
Dobutamine additive effects. Causes less increase
other catecholamines. Used in CHF
(Dobutrex) in HR, PVR, and dysrhythmias than
and after cardiac surgery to increase
dopamine. At a rate <7 mcg/kg/min,
myocardial contractility, stroke
expect increased myocardial
volume, and CO.
contraction, CO, and renal blood
flow. At a rate of >7 mcg/kg/min,
expect peripheral vasoconstriction
and increased MAP.
Avoid extravasation; causes necrosis.
Neurotransmitter, precursor to
Monitor vital signs, ECG, urine
norepinephrine. Increases CO and
Dopamine output, and extremity color. Titrate to
BP. Improves renal blood flow and
hydrochloride target BP; use an infusion pump.
therefore urine output with lower
(Intropin) Peripheral vasoconstriction is noted
doses. Used for hemodynamic
with cold upper and lower
support in shock.
extremities.
Monitor vital signs and ECG
continuously. Avoid extravasation;
Catecholamine. Strengthens causes sloughing. Titrate to cardiac
myocardial contraction; increases response. Caution: available in
Epinephrine
BP, HR, and CO. Dilates bronchial several concentrations (1:100, 1:1000,
hydrochloride
tree. Used in anaphylactic shock and 1:10,000); be sure to check for
(Adrenalin chloride)
to restore cardiac rhythm in cardiac prescribed solution. May be
arrest. administered by endotracheal tube
because drug is rapidly absorbed from
the lungs.
Isoproterenol Cardiac stimulant (positive inotropic Continuously monitor ECG. Monitor
hydrochloride and chronotropic effects). vital signs, urine output, and
(Isuprel) Bronchodilator. Peripheral peripheral blood flow. Titrate to
vasodilator. Increases HR and desired HR, BP, and urine output.
contractility. Decreases PVR and Avoid extravasation.
diastolic BP, resulting in increased
CO and systolic BP, decreased
MAP, and increased myocardial
oxygen consumption. Used as a
cardiac stimulant in cardiac arrest,
cardiogenic shock, ventricular
dysrhythmias, and heart block.
Light-sensitive preparation; wrap in
aluminum foil. Administer with an
infusion pump. Titrate to maintain
Vasodilator. Decreases preload and
Sodium nitroprusside CO. Continuously monitor BP.
afterload. Used in hypertensive
(Nipride) Discard solution 4 hr after
crises.
preparation. Assess thiocyanate levels
daily for patients on long-term
therapy.
Mix only with dextrose in water or
Catecholamine. Vasoconstrictor.
dextrose in saline. Administer with an
Cardiac stimulant: increased BP,
infusion pump. Report decreased
Norepinephrine myocardial oxygen, and coronary
urine output immediately.
(Levophed) artery blood flow. Used in acute
Continuously monitor and titrate to
hypertensive states, myocardial
desired BP. Monitor peripheral blood
infarction, and cardiac arrest.
flow. Avoid extravasation.
Do not infuse with calcium. Monitor
Systemic alkalinizer. Used to correct
Sodium bicarbonate arterial blood gases. Avoid extra-
metabolic acidosis in cardiac arrest.
vasation; causes severe tissue damage.
Inotropic agent. Increases
Monitor vital signs, intake and output,
myocardial contractility and cardiac
and daily weight during therapy.
output.
Milrinone (Primacor)
Monitor ECG continuously. Give
Vasodilation decreases preload and
potassium as ordered for
afterload. Used to treat CHF that
hypokalemia.
does not respond to usual therapy.
AV, Atrioventricular; BP, blood pressure; CBC, complete blood count; CHF, congestive heart
failure; CO, cardiac output; ECG, electrocardiogram; HDL, high-density lipoprotein; HF, heart
failure; HR, heart rate; IV, intravenous; LDL, low-density lipoprotein; MAP, mean arterial
pressure; NSAID, nonsteroidal anti-inflammatory drug; OTC, over-the-counter; PVC, premature
ventricular contraction, PVR, peripheral vascular resistance; SVR, systemic vascular resistance;
VLDL, very-low-density lipoprotein.
Diuretics
Diuretics are often prescribed for cardiac conditions. Many patients with heart problems have
fluid retention that is treated with diuretics. The most frequently used diuretics are the loop
diuretics such as furosemide (Lasix), the thiazide diuretics such as hydrochlorothiazide (Esidrix,
HCTZ) and the potassium-sparing diuretics such as spironolactone (Aldactone). Information
about these and other diuretics is presented in the Drug Therapy table on p. 850.
Anticoagulants
Anticoagulants are used to prevent clot formation. Heparin, low-molecular-weight heparin

(LMWH), and warfarin are the most commonly used preventive anticoagulants.
Heparin
Heparin interferes with factor III in the clotting process. It is administered by continuous
intravenous drip or subcutaneously. When a patient has a clotting episode, a heparin bolus is
administered and a continuous infusion is started. The infusion rate is set to deliver a prescribed
number of heparin units per hour. The physician adjusts the heparin dosage based on the
activated partial thromboplastin time (aPTT). When the aPTT has stabilized (generally at 1.5 to
2.0 times the control level), the drug can be changed to the subcutaneous route. Because heparin
cannot be administered orally, the patient must remain hospitalized during its administration.
Heparin is recommended for use with acute coronary syndrome (ACS), during percutaneous
coronary interventions (PCI) and surgical revascularization, and in conjunction with fibrinolytic
therapy (Ante, 2004; Deglin & Vallerand, 2005).
Low-Molecular-Weight Heparin.
Low-molecular-weight heparins (LMWHs), such as enoxaparin (Lovenox), are fragments

derived from heparin that work by blocking the formation of thrombin and preventing the
development of a clot. The advantages of using LMWHs are that the anticoagulant effect is more
predictable, they are administered subcutaneously once or twice a day, and they do not require
such close monitoring of aPTT. LMWHs are recommended for patients with deep vein
thrombosis, with unstable angina, and in some cases of acute myocardial infarction (before a
thrombus occludes the coronary vessel) (Ante, 2004; Deglin & Vallerand, 2005).
Warfarin
The anticoagulant that may be administered orally, warfarin (Coumadin), is started as soon as
possible. The warfarin dosage is regulated by the prothrombin time and international normalized
ratio (INR). The prothrombin time is kept in a therapeutic range of 1.5 to 2.0 times the normal
level. The INR may be kept at 2.0 to 4.5. Patients who have had artificial valve replacements
must remain on anticoagulant therapy for life.
All patients on anticoagulants must be monitored closely for any signs of bleeding. Also, patients
should be taught how to reduce the risk of bleeding, such as to use an electric razor and a soft-
bristle toothbrush.
Pharmacology Capsule
Heparin dosage is adjusted based on the patient's activated partial thromboplastin time (aPTT).
Warfarin dosage is adjusted based on the patient's prothrombin time (PT) and international
normalized ratio (INR).
Antiplatelet Agents
Antiplatelet therapy is often used after an AMI to prevent additional myocardial infarction and
strokes. The dosage of aspirin as an antiplatelet agent in stroke prevention is under investigation.
Some studies have shown that one baby aspirin (81 mg) a day is sufficient, and other studies
indicate that an even smaller dosage may produce a therapeutic effect. Dipyridamole
(Persantine), ticlopidine (Ticlid), and clopidogrel (Plavix) also exhibit antiplatelet effects and
may be prescribed for patients who are unable to tolerate aspirin.
Glycoprotein (GP) IIb/IIIa inhibitors block the platelet receptor sites that bind with fibrinogen
and lead to platelet aggregation. GP IIb/IIIa inhibitors such as abciximab (ReoPro) and
eptifibatide (Integrilin) are used in combination with heparin and aspirin as part of the medical
treatment for unstable angina and acute myocardial infarction. They are also being used in
conjunction with fibrinolytic therapy and/or percutaneous coronary interventions after acute
myocardial infarction.
Anticoagulants and antiplatelet agents prevent formation of new clots, but fibrinolytic agents
destroy clots that have already formed.
Fibrinolytic Agents
Whereas anticoagulants and antiplatelet agents prevent the continued formation of clots, the
fibrinolytic agents (also called thrombolytics) act to destroy clots that have already formed.
Streptokinase, Reteplase, and tissue plasminogen activator are examples of thrombolytics. They
are best used as soon as there is evidence of clot formation. They are administered intravenously
when certain criteria have been met. Administration is continued until there is evidence of
reperfusion or until the maximum dosage has been given.
Information about anticoagulant, antiplatelet, and fibrinolytic agents is presented in the Drug
Therapy tables on pp. 464 and 465 and pp. 697 and 698. Selected antiplatelet agents are also
listed in the Drug Therapy table on p. 645.
Lipid-Lowering Agents
Lipid-lowering medications are frequently part of the overall treatment plan, along with diet and
exercise, for many patients with heart disease. The goal of therapy is for the patient to have
decreased serum triglyceride and LDL levels and an improved HDL level. Patients on this group
of medications need to be encouraged to adhere to diet restrictions, exercise, and quit smoking.
Serial laboratory tests (lipid profile and liver function) will be closely monitored. Selected lipid-
lowering medications are included in the Drug Therapy table on p. 645.
Analgesics
The patient who has an AMI experiences severe chest pain. The first medication administered to
a patient with chest pain is nitroglycerin, which is a vasodilator. When this drug does not relieve
the pain, morphine is the preferred analgesic. Morphine relieves pain, reduces anxiety, and
reduces the workload of the heart by trapping some of the venous blood in the periphery of the
body. An alternative to morphine is meperidine hydrochloride (Demerol). Meperidine is less
effective in relieving anxiety and cardiac workload than morphine. Morphine and meperidine are
most effective when administered intravenously.
DIET THERAPY
Reduction of body weight lessens the workload on the heart. A low-fat, high-fiber diet usually is
recommended for cardiac patients. Patients would be encouraged to eat a well-balanced diet that
includes an emphasis on fruits, vegetables, grains, and proteins low in fat (fish, legumes, poultry
and lean meats). Cholesterol intake should be limited to 200 mg/day for individuals with heart
disease or at high risk for heart disease. It is also recommended that foods with trans fatty acids
be limited (American Heart Association, 2007). An exercise program may help the patient
achieve optimal weight.
Sodium
If fluid retention accompanies the cardiac problem, the physician may order sodium restriction.
A diet containing sodium 2 g/day is most often prescribed. Restrictions greater than this are
difficult to achieve, and studies have shown that patients quickly become noncompliant with the
dietary regimen. Salt substitutes are available.
Potassium
Patients taking potassium-wasting diuretics (e.g., furosemide, hydrochlorothiazide) need to

include adequate potassium in the diet to counteract the depletion. Patients taking large doses of
potassium-wasting diuretics need to have potassium supplements prescribed.
Potassium-wasting diuretics such as furosemide and hydrochlorothiazide may cause

hypokalemia, which can lead to dangerous dysrhythmias.
Consider the Alternative
Some people use garlic to reduce plasma lipids and lower blood pressure. The best garlic
preparation is an enteric-coated dried preparation that contains adequate allicin and allinase—the
“active ingredients” in the preparation. Most of the allicin and allinase are destroyed when fresh
garlic is cooked or eaten raw. Garlic irritates the GI tract and increases the effects of
anticoagulants and insulin.
OXYGEN THERAPY
The myocardium needs an adequate blood supply to function properly. Any patient complaining
of chest pain unrelieved by nitroglycerin should have supplemental oxygen administered. A
nasal cannula or facemask should be applied and set to deliver the prescribed liter flow, and the
patient's response to this therapy should be monitored.
PACEMAKERS
Pacemakers were first introduced in 1958. Their purpose is to restore regular rhythm and to
improve cardiac output and tissue perfusion. Pacemakers may be temporary or permanent.
Methods for temporary pacing are transcutaneous, transvenous, or epicardial. Transcutaneous
pacemakers deliver impulses through the skin from externally placed electrode pads. A
transvenous pacemaker has a pacing electrode that is threaded through a vein into the right side
of the heart. Epicardial pacing wires are placed into the epicardial wall of the heart during
cardiac surgery and the wires are brought through the chest wall. Temporary pacemakers all
require an external pulse generator to provide the electrical energy needed to stimulate
depolarization. A permanent pacemaker is surgically place subcutaneously in the wall of the
chest, with the electrical lead placed into the heart through a vein. Impulses are conducted from
the power source (external pulse generator or implanted pacemaker) to the heart to stimulate
contraction of the myocardium.
Pacemakers can be used to stimulate the atrium or ventricle (called single-chamber pacing), or
they can be used to stimulate both chambers (called dual-chamber pacing). Dual-chamber pacing
produces conduction and contraction that is near normal.
Table 35-6 Revised NASPE/BPEG Generic Code for Antibradycardia Pacing*

I II III IV V
Chamber(s) Response to Multisite
Chamber(s) Paced Rate Modulation
Sensed Sensing Pacing
O = None O = None O = None O = None O = None
R = Rate
A = Atrium A = Atrium T = Triggered A = Atrium
modulation
V = Ventricle V = Ventricle I = Inhibited V = Ventricle
D = Dual
D = Dual (A+V) D = Dual (A+V) D = Dual
(A+V)
S = Single (A or V)† S = Single (A or V)† (T+I)
From Bernstein, A.D., Daubert, J.C., Fletcher, R.D., Hayes, D.L., Luderitz, B., Reynolds, D.W.,
Schoenfeld, M.H., & Sutton R. (2002). The revised NASPE/BPEG generic code for
antibradycardia, adaptive-rate, and multisite pacing. Pacing and Clinical Electrophysiology, 25
(2), 261.
Table 35-7 Pertinent Definitions Related to Pacemakers

Ability of the pacemaker to detect intrinsic myocardial electrical activity
Sensing The pacemaker either is inhibited from delivering a stimulus or initiates an
electrical impulse, based on the programmed response
Occurs when the pacemaker produces a programmed current for a set duration
Pulse This energy travels through the transvenous lead wires to the myocardium—this
generation is known as pacemaker firing and usually produces a line or spike on the ECG
recording
Capture Refers to the successful stimulation of the myocardium by the pacemaker
impulse that results in depolarization
Evidenced on the ECG by a pacemaker spike/stimulus followed by either an
atrial or ventricular complex, depending on the chambers being paced
Pacemaker does not discharge a pacing stimulus at its programmed time to the
Failure of pulse
myocardium
generation
Evidenced by the absence of a pacemaker spike on the ECG where expected
Pacemaker has either detected extraneous signals that mimic intrinsic cardiac
activity (oversensing) or did not accurately identify intrinsic activity
(undersensing)
Oversensing is recognized on the ECG by pauses where paced beats were
Sensing failure
expected and prolongation of the interval between paced beats
Undersensing is recognized on the ECG by inappropriate pacemaker spikes
relative to the intrinsic electrical activity (pacemaker spikes occurring within the
P wave, QRS complex, or T wave) and shortened distances between paced beats)
Pacemaker has delivered a pacing stimulus that was unable to initiate
Failure to depolarization of the myocardium and subsequent myocardial contraction
capture Evidenced on the ECG by pacemaker spikes that are not followed by a P wave
for atrial pacing or spikes not followed by a QRS complex for ventricular pacing
ECG, Electrocardiogram.
Pacemakers have multiple settings related to pacing and sensing. A coding system was
developed in the 1970s and has undergone a number of revisions. The most recent revision is
found in Table 35-6. A set of pertinent definitions related to pacemakers is found in Table 35-7.
Temporary Pacemakers
Temporary pacemakers can be used electively or for emergency situations. Elective uses include
gaining control of very rapid supraventricular tachycardic rhythms, assessing the need for
permanent pacing in patients with bradycardias, and following cardiac surgery.
Permanent Pacemakers
Permanent pacemakers are indicated in a number of patient situations in which conduction

defects or dysrhythmias compromise the normal function of the heart. Several clinical conditions
indicate the need for permanent pacing. A few of these conditions are the following: acquired
atrioventricular (AV) block, sinus node dysfunction, chronic bifascicular or trifascicular block,
symptomatic tachycardias, and carotid sinus syndrome. A permanent implantable pacemaker is
inserted under local anesthesia. The batteries, usually lithium, have an 8- to 10-year expected
life. Permanent pacemakers are inserted in the operating room, catheterization laboratory, or
special procedures area. The pacing lead is positioned (through the subclavian or cephalic vein)
in the right atrium, right ventricle, left ventricle, or a combination of these (depending on the
patient's problem). The generator is placed in a subcutaneous pocket, usually under the clavicle
or in the abdomen.

Sensing Ability of the pacemaker to detect intrinsic myocardial electrical activity
The pacemaker either is inhibited from delivering a stimulus or initiates an
recording
Refers to the successful stimulation of the myocardium by the pacemaker
Capture
Failure of pulse
myocardium
generation
(undersensing)
Sensing failure

or in the abdomen.

Ability of the pacemaker to detect intrinsic myocardial electrical activity
Sensing The pacemaker either is inhibited from delivering a stimulus or initiates an
recording
Refers to the successful stimulation of the myocardium by the pacemaker
Capture
Failure of pulse myocardium
generation
(undersensing)
Sensing failure

or in the abdomen.
NURSING CARE of the Patient with a Pacemaker
Patients with inserted pacemakers recover in the postanesthesia care unit and then go to a unit
with telemetry capability. Monitor the patient for proper pacemaker functioning. Examine the
ECG for rhythm, pacemaker spike, and dysrhythmias (premature ventricular contractions and
ventricular tachycardia are seen most often). The pacemaker spike is a mark observed on the
ECG tracing that represents the impulse generated by the pacemaker. Assess vital signs and
inspect the incision frequently. Patients rest for 24 hours after the insertion of a permanent
pacemaker. Following that, patients are ambulated and are encouraged to resume normal
activities.
After insertion of a temporary pacemaker, microshock precautions should be followed. Monitor

the ECG and transport the patient with a portable cardiac monitor and a nurse in attendance.
Assess the pacemaker for misfiring. Plan a gradual increase in activities.
There are three major problems that can occur with pacing. The first problem, failure to pace,
means that the pacemaker did not initiate the electrical stimulus when it was due to fire.
Frequently caused by battery failure or lead wire displacement, it is recognized by the lack of a
pacer spike on the ECG tracing. The second problem, failure to capture, means that the electrical
stimulus from the pacemaker is not followed by electrical activity in the patient's heart. Caused
by dislodgement of the lead or the pacemaker output setting set too low, failure to capture is
recognized by noting the presence of a pacer spike without ECG activity following the spike.
The third problem, failure to sense, means that the pacemaker does not sense the patient's cardiac
rhythm and initiates an electrical impulse when it is not needed. Failure to sense is most often
caused by displacement of the electrode and can be recognized by pacer spikes that fall too close
to the patient's rhythm.
When a permanent pacemaker has been inserted, teach the patient how to count the pulse for 1
full minute daily. Explain wound care and the healing process. Advise the patient to notify the
physician of symptoms of decreased cardiac output: dyspnea, dizziness, syncope, weakness,
fatigue, and chest pain. Also instruct the patient to carry an identification card describing the
type of pacemaker implanted.
CARDIOVERSION
Cardioversion is the delivery of a synchronized shock to terminate atrial or ventricular

tachydysrhythmias (rapid abnormal heart rhythms). It may be done as an emergency or elective
procedure. The shock is synchronized with the R wave to avoid shocking during the vulnerable
period of the T wave. A shock delivered during ventricular relaxation can initiate ventricular
fibrillation.
If the patient is receiving digoxin, the drug is withheld for 24 hours before the procedure.
Emergency drugs are made available, and the patient has a patent intravenous line in place before
the procedure. Explain the procedure, and obtain informed consent. A short-acting sedative is
usually given. The cardioverter is set to the synchronized mode, and two electrodes are placed on
the chest. One electrode is placed to the right of the sternum just below the clavicle and the other
is placed at the apex of the heart. The initial impulse varies from 25 to 100 joules depending on
the type of dysrhythmia. If the initial impulse does not convert the dysrhythmia to normal sinus
rhythm, the impulse energy is increased and the procedure is repeated.
After cardioversion, the patient usually recovers very quickly from the sedation and does not
remember the event. Inspect the skin under the electrodes for irritation. Monitor the patient's
heart rate and rhythm, vital signs, and neurologic status. Transient dysrhythmias and a drop in
blood pressure are common. Be especially alert for atrial fibrillation, which can contribute to the
formation of atrial wall thrombus and emboli.
CARDIOPULMONARY RESUSCITATION
Cardiopulmonary resuscitation is the restoration of heart and lung function after cardiac arrest.
The procedure is used in basic cardiac life support and advanced cardiac life support. The reader
is referred to materials prepared by the American Heart Association for current, in-depth
coverage of the procedure. See Chapter 16 for an overview.
CARDIAC SURGERY
The most common surgical procedures involving the heart are pacemaker insertion, heart surgery
to repair or replace valves or septa or remove tumors, and coronary artery bypass surgery.
Pacemaker insertion is described earlier in this section. Coronary artery bypass surgery is
described as a surgical treatment for AMI on pp. 657 and 658.
With some of the surgical procedures on the heart, the heart muscle must be at rest during the
procedure. This requires placing the patient on a machine to direct the blood away from the heart
and lungs and to maintain appropriate oxygen and carbon dioxide levels. The heart's rhythm is
interrupted by an electrolyte solution and may be restarted after the surgery by electrical
stimulation. During this type of surgery, the patient's core temperature usually is reduced to
decrease the oxygen needs of the entire body, especially the brain.
PREOPERATIVE NURSING CARE of the Cardiac Surgery Patient

Assessment
Nursing assessment of the patient with cardiac disorders is summarized in Box 35-1. When a
patient is facing cardiac surgery, also assess the patient's fears and anxiety. Patients are usually
upset and very concerned when heart surgery is recommended. Determine what patients know
about the surgery and what more they would like to know.
Nursing Diagnoses, Goals, and Outcome Criteria: Preoperative Cardiac Surgery

Nursing Diagnoses Goals and Outcome Criteria
Fear related to perceived threat of death or Reduced fear: patient states is less fearful,
unfamiliarity with setting and procedures demonstrates relaxed manner
Anxiety related to threat to health status or Reduced anxiety: patient states is less
uncertain outcome anxious, is calmer
Interventions
Fear and Anxiety
Encourage the patient to identify feelings and then explore the basis of those feelings. Do not
assume you know how the patient feels. Accept the patient's feelings and do not give trite
reassurance (“Don't worry; everything will be fine.”). Accurate information about what to expect
helps reduce fear of the unknown. Physical comfort measures such as a massage or back rub may
also be soothing. If the patient's anxiety level remains high, notify the physician.
Good patient teaching is essential to address fear and anxiety. The physician reviews necessary
diagnostic tests, the surgical procedure itself, and what to expect after surgery. Nevertheless, the
nurse must be able to clarify and further explain what the patient will experience. If the surgery
is to be done as an emergency, little time is available to do preoperative teaching. Planned
cardiac surgery allows time for the patient to accept the need for surgery and to explore why the
procedure is necessary. Include the family in the preoperative teaching to decrease their anxiety
and allow them to participate in the patient's recovery. The patient teaching plan must be
individualized for the type of surgical procedure.
Patient Teaching Plan

Cardiac Surgery, Preoperative
The specifics of the teaching plan depend on the exact procedure and agency/surgeon
procedures. General content of the teaching plan incudes the following:
 •Preoperative routines: NPO, monitoring, diagnostic tests, any special preparation

 •Where the patient will be after surgery: in intensive care unit after extensive procedures;
to regular units after pacemaker insertion
 •The postoperative care setting: the room and the equipment
 •Postoperative routines: how to turn, cough, deep breathe, and exercise the leg muscles;
monitoring; procedures
 •Postoperative pain: amount of pain to expect, relief measures such as splinting,
positioning, medication
 •Communication: because most patients are intubated for 4 to 8 hours after surgery,
establish a means of communication before surgery
 Put on Your Thinking Cap!
 A patient is scheduled for extensive cardiac surgery and will be on a ventilator for up to 8
hours postoperatively. What means of communication can you establish in advance?
What if the patient is illiterate? What if the patient is deaf?
 POSTOPERATIVE NURSING CARE of the Cardiac Surgery Patient
 Nursing care needs vary considerably depending on the type of surgical procedure. Care
specific to certain conditions is discussed with those conditions. In addition, see Chapter
17 for thorough coverage of care of the surgical patient. This section addresses needs
common to many patients having cardiac surgery.
 Assessment
 Assessment of the cardiac patient is summarized in Box 35-1. After surgery, be
especially alert to changes in vital signs, breath sounds, urine output, mental alertness,
and color. In the intensive care unit, monitor cardiac rhythm, arterial blood gases, and
hemodynamic pressures. Assess chest tube function. Frequently inspect all dressings for
type and amount of drainage. Examine the surgical wound and insertion sites of tubes and
cannulas for increasing redness, swelling, and purulent drainage. Assess urine amount,
appearance, and odor.
 Nursing Diagnoses, Goals, and Outcome Criteria: Postoperative Cardiac Surgery
Ineffective Breathing Pattern related to mechanical
Adequate oxygenation: arterial blood
ventilation, general anesthesia, pain, or restrictive
gases within normal limits
surgical dressings
Pain relief: patient states pain reduced
Acute Pain related to tissue trauma
or relieved, relaxed manner
Ineffective Thermoregulation related to cooling during Normal body temperature: temperature
surgery of at least 36.7° C (98° F) orally
Decreased Cardiac Output related to fluid loss or Normal cardiac output: fluid intake
decreased fluid intake equal to output
Absence of infection: no fever;
Risk for Infection related to altered skin integrity decreasing drainage, redness, and
swelling of wound
Anxiety related to unfamiliar routines and stressful Reduced anxiety: patient states anxiety
experience is reduced
Interventions
Ineffective Breathing Pattern
Patients with open heart or bypass surgery are unresponsive on arrival in the intensive care unit.
Ventilatory assistance is of prime importance. Reassess breath sounds and arterial blood gases
frequently. Connect chest tubes to underwater seal drainage. (See Chapter 30 for the care of
chest tubes.) Reposition the patient often to promote removal of pulmonary secretions and
improve respiratory excursion.
When the patient is extubated, provide an oxygen mask or nasal cannula as ordered to provide
supplemental oxygen. Assist the patient to cough and deep breathe frequently. A pillow or a
blanket in a pillowcase can be used as an incisional splint during coughing. An incentive
spirometer is usually ordered. Monitor its use, and remind the patient to use it. Assist with early
ambulation, as ordered, to reduce the risk of pulmonary complications.
Acute Pain
Effective pain relief makes it easier for the patient to turn, cough, and deep breathe. Assess the
patient's pain: location, severity, aggravating factors, and relieving factors. Administer analgesics
as ordered. Intravenous morphine in small doses is most frequently prescribed for analgesia. You
may also use independent measures, including position changes, back rubs, relaxation
techniques, and imagery. Assess the effectiveness of the interventions in managing pain. Provide
for periods of rest and sleep after pain relief efforts.
Ineffective Thermoregulation
Warmed blankets, heating blankets, and warming lights may be used to assist rewarming.
Monitor body temperature continuously until the patient is stable.
Decreased Cardiac Output
Monitor cardiac pressures continuously in the intensive care unit until they stabilize. Prescribed
medications are adjusted based on vital signs, hemodynamic pressures, and cardiac rhythms.
Pacing wires are connected to a temporary pacemaker. Monitor fluid and blood administration,
and assess urinary and other drainage outputs. Volume expanders (albumin, dextran, hetastarch)
and vasoactive drugs may be necessary to maintain blood pressure. Oral fluids are ordered
shortly after extubation.
Risk for Infection
The patient is at risk for incisional, respiratory tract, and urinary tract infections. In addition, the
presence of multiple tubes and cannulas provides additional sites for potential nosocomial
infection. To reduce the risk of infection, practice good hand-washing technique and use aseptic
technique when handling dressings and invasive equipment. Provide wound care as ordered or
per agency policy. Administer antibiotics as ordered. Before discharge, begin teaching the
patient how to care for the surgical wound. Emphasize signs or symptoms that should be reported
to the physician: fever, increasing or purulent wound drainage, increasing redness or swelling,
and separation of wound margins.
Anxiety
Inform the patient and the family what is being done and how the patient is responding.
Remember to talk to the patient and offer reassurance. When the patient is on a ventilator, use
the previously established nonverbal means of communication. It is often necessary to repeat
instructions because of the effects of pain, medications, and anxiety. As the patient improves,
explain the importance of follow-up care and rehabilitation.
Consider the Alternative
For pain relief, many complementary therapies are used with analgesics. Some examples are
massage, relaxation techniques, and imagery.
CARDIAC DISORDERS
CORONARY ARTERY DISEASE
Coronary artery disease (CAD) occurs when the major coronary arteries supplying the
myocardium are partially or completely blocked. Blockage of the arteries is caused by coronary
artery spasm, arteriosclerosis, or atherosclerosis and may result in ischemia or infarction of
myocardial tissue. In 1998, there were 208 deaths per 100,000 population. A Healthy People
2010 objective is to reduce that number by 20 percent (Centers for Disease Control and
Prevention/National Institutes of Health, 2005). See the Health Promotion Considerations box on
p. 653 for a review of cardiac risk factor modification.
Arteriosclerosis
Arteriosclerosis is an abnormal thickening, hardening, and loss of elasticity of arterial walls.

Smooth muscle cells and collagen migrate into the tunica intima (innermost layer of the artery)
and cause the arterial wall to stiffen and thicken and the lumen to decrease in diameter. Lipids,
cholesterol, calcium, and thrombi adhere to the damaged arterial wall. This process limits the
elasticity of the wall and decreases the flow of oxygen-carrying blood to tissues. Some effects of
arteriosclerosis are hypertension, impaired tissue perfusion, and aneurysms.

Risk Factor Modification
Risk factor modification will help reduce an individual's risk for developing CAD, angina, and
acute coronary syndromes. Controlling HTN, reducing serum cholesterol and LDLs, smoking
cessation, participating in regular, moderate exercise, obtaining/maintaining ideal body weight,
and learning to handle stress are recommended lifestyle changes that can help decrease risk.
Signs and Symptoms
Coronary artery disease usually is asymptomatic until the tissue's blood supply is reduced by at
least 50%. Then, the clinical manifestations of CAD include angina pectoris, acute coronary
syndrome (unstable angina and acute myocardial infarction), and sudden cardiac death. Acute
myocardial infarction has been further categorized into non–ST-segment elevation myocardial
infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI).
ANGINA PECTORIS
Angina pectoris (shortened to angina), or chest pain, the most common symptom of CAD, results
when the demand for oxygen by the myocardial cells exceeds the supply of oxygen delivered.
There are different types of angina: stable, unstable, and variant. Stable angina (also called
chronic angina or exertional angina) occurs most often with exercise or activity and usually
subsides with rest. Other precipitating factors are smoking, physical exertion, emotional stress,
and heavy meals. The pain is usually substernal and described by the patient as viselike, burning,
squeezing, or smothering. The pain may radiate to either arm, the shoulder, the jaw, the neck, or
the epigastrium. Accompanying symptoms are diaphoresis, dyspnea, nausea, and vomiting.
Stable angina occurs intermittently and is often predictable. Usually, stable angina lasts only a
few minutes and is relieved by rest or with nitroglycerine (NTG).
Unstable angina (categorized and treated as an acute coronary syndrome) is also called
crescendo angina or preinfarction angina. The pain of unstable angina is more severe, occurs at
rest or with minimal exertion, is often not relieved by NTG or requires more frequent NTG
administration, and is not predictable. Unstable angina may occur in a patient with a history of
stable angina. The patient may describe a change in the pain pattern or in the severity of the pain.
Or, unstable angina may be the first clinical manifestation of CAD that a patient experiences. In
either case, unstable angina is considered more serious than stable angina and will be treated
differently. Patients with unstable angina are at higher risk for acute myocardial infarction (AMI)
and are often hospitalized for diagnostic workup and treatment.
Variant angina (also known as Prinzmetal's angina) is caused by coronary artery spasm and may
not be associated with CAD. This type of angina is unpredictable and often occurs at rest. When
the coronary spasm occurs, the patient experiences angina and, if the patient is being monitored,
transient ST elevation may be seen. When the spasm subsides, the pain goes away and the ST
segment returns to normal. The treatment for variant angina is usually administration of calcium
channel blockers to prevent the spasms from occurring.
Medical Treatment
Treatment of CAD includes diet therapy, drug therapy, and reduction of modifiable risk factors
(e.g., smoking, obesity, hypertension). Recommendations for medical therapy have been
developed for both stable and unstable angina. Initial therapy for patients with angina should
follow the mnemonic below (Braunwald, et al., 2002; Gibbons, et al., 2002):
A Aspirin and antianginal therapy

B Beta blocker and blood pressure
C Cigarette smoking and cholesterol
D Diet and diabetes
E Education and exercise
Low-dose aspirin is administered to interfere with platelet aggregation and it can reduce the risk
of myocardial infarction. If the patient cannot tolerate aspirin, another antiplatelet medication
(e.g., Ticlid, Plavix) will be prescribed. Antianginal therapy includes nitrates, beta-adrenergic
blockers, and calcium channel blockers. Nitrates such as NTG are used to treat actual episodes of
angina and to prevent the occurrence of angina. Various forms of nitroglycerin are prescribed for
treatment of acute angina. These are administered sublingually or buccally at the onset of pain.
They are quickly absorbed and usually effective. Oral, topical, and transdermal nitrates may be
ordered to prevent angina attacks. Beta-adrenergic blockers and calcium channel blockers are
prescribed in the long-term management of angina.
After the initial relief and control of the anginal pain, the focus of therapy will turn to risk
reduction to include optimizing blood pressure, smoking cessation, lipid control (diet alone or
diet plus lipid-lowering medications), healthy diet and tight glucose control for diabetic patients,
exercise training, and patient education (i.e., medication therapy, risk reduction, and what to do if
symptoms of an AMI occur).
ACE inhibitors may also be prescribed to patients with stable angina to reduce the risk of AMI.
In addition, some patients may be recommended for further treatment with percutaneous
coronary interventions (PCI), such as angioplasty, stent placement, or atherectomy (Gibbons, et
al., 2002).
Additional information about various drug therapies is presented in the Drug Therapy table on p.
646.
Unstable angina may be treated conservatively or more aggressively, depending on the situation.
Because unstable angina may be a “warning” of more serious events, it has been classified as an
acute coronary syndrome. In current recommendations, unstable angina and NSTEMI are
addressed together because they are so closely related. Patients with unstable angina should
receive the A-B-C-D-E's discussed in the previous section. However, in addition to antiplatelet
therapy, anticoagulation therapy with LMWH may be administered. For patients who will be
undergoing cardiac catheterization and PCI, a platelet GP IIb/IIIa antagonist will also be
administered (Braunwald, et al., 2002).
Surgical Intervention
Surgical procedures to treat CAD are discussed on pp. 656 and 657.
What Does Culture Have to Do with Heart Disease?
American Indians and African Americans develop CAD at an earlier age than other Americans.
The incidence of CAD is highest among middle-aged Caucasian males. Latinos have lower death
rates from CAD than non-Latinos. Nurses can educate high-risk patients about risk factors that
can be modified: obesity, hypertension, and stress. Role models from the target population are
especially influential.
ACUTE MYOCARDIAL INFARCTION
An AMI is the death of myocardial tissue as a result of prolonged lack of blood and oxygen
supply. Approximately 700,000 Americans have a new myocardial infarction every year and
500,000 Americans have recurrent attacks annually. Approximately 225,000 individuals in the
United States will die each year from myocardial infarction. The average age for men having a
first heart attack is 65 to 66 years, and the average age in women for a first heart attack is 70
years (American Heart Association, 2007).
Risk Factors
Risk factors for AMI include obesity, smoking, a high-fat diet, hypertension, family history,
male gender, diabetes mellitus, sedentary lifestyle, and excessive stress. Smoking, a high-fat diet,
hypertension, sedentary lifestyle, and stress are considered modifiable risk factors. This means
that risk can be reduced by cessation of smoking, diet modification, management of
hypertension, regular exercise, and stress reduction.
Pathophysiology
An AMI begins with the occlusion of a coronary artery. Over a period of 4 to 6 hours, a process
of ischemia, injury, and infarction develops. Ischemia results from a lack of blood and oxygen to
a portion of the heart muscle. If ischemia is not reversed, injury occurs. Deprived of blood and
oxygen, the affected tissue becomes soft and loses its normal color. With continued ischemia, an
infarction, or death of myocardial tissue, occurs. Ischemia lasting 20 minutes or more is
sufficient to produce irreversible tissue damage.
Within 24 hours after an infarction, the healing process begins. By the third day, necrotic tissue
has been broken down by enzymes and removed by macrophages. Collateral circulation develops
to supply the injured area, and scar tissue begins to form. About 10 to 14 days after the AMI, the
myocardium is especially vulnerable to stress because of the weakness of the healing tissue.
Complete healing takes about 6 weeks.
An AMI is considered an acute coronary syndrome, along with unstable angina as mentioned
earlier. Health care providers divide AMI into two types: non–ST-elevation MI (NSTEMI) and
ST-elevation MI (STEMI) for purposes of diagnosis and treatment. The ST segment of an ECG
is usually flat or isoelectric (see the Interpretation of Electrocardiograms section on p. 673).
Because the ST segment can be displaced when there is partial or complete lack of oxygen flow
to the myocardial cells, the appearance of a patient's ST segment is an important component of
the assessment of an AMI. Patients with NSTEMI usually have transient or partial occlusion of a
coronary artery, whereas patients with STEMI have total occlusion of a coronary artery from
coronary thrombosis.
Complications
The major complications of AMI are dysrhythmias, heart failure, cardiogenic shock,
thromboembolism, and ventricular aneurysm/rupture.
Dysrhythmias.
Dysrhythmias are disturbances in heart rhythm, including excessively rapid, slow, or irregular
heartbeats. They occur in approximately 80% of all patients with AMI. Because some
dysrhythmias are life-threatening, continuous cardiac monitoring is usually ordered for patients
with AMI. This permits early detection and prompt treatment of dysrhythmias. Recognition and
treatment of specific dysrhythmias are addressed on pp. 673 to 682.
Heart Failure.
The AMI may cause the heart to fail as a pump if the injured LV is unable to meet the body's
circulatory demands. The ventricle fails to empty efficiently. Increased preload leads to systemic
and pulmonary edema. Cardiac output and blood pressure fall. Untreated cardiac failure
progresses to cardiogenic shock and death. Early symptoms of congestive failure are dyspnea,
restlessness, and increasing heart rate.
Cardiogenic Shock.
Cardiogenic shock is the most frequent cause of death after an AMI. It is usually related to
extensive injury to the LV and is more common when the patient has had a previous infarction.
Cardiogenic shock is marked by hypotension; cool, moist skin; oliguria; and decreasing
alertness.
Thromboembolism.
After an AMI, thrombi may form in the injured heart chambers or in the veins of the legs. The
thrombi may break loose, travel through the circulation, and lodge in the lung. Pallor, cyanosis,
and heart failure may be caused by pulmonary emboli. Massive pulmonary embolism is
characterized by sudden, severe dyspnea. It is usually fatal. Pulmonary emboli are discussed in
detail in Chapter 30.
Ventricular Aneurysm/Rupture.
Weakened areas of the ventricular wall may bulge during contractions. If scar tissue is
inadequate to strengthen the wall, an aneurysm may develop and rupture. Ventricular rupture is
fatal.
Signs and Symptoms
Pain is the classic symptom of AMI. It is typically a heavy or constrictive pain located below or
behind the sternum, as described with angina. It may radiate to the arms, back, neck, or jaw. The
pain may begin with or without exertion. If not relieved by rest and nitroglycerin, it progresses.
The patient becomes diaphoretic and lightheaded and may experience nausea, vomiting, and
dyspnea. The skin is frequently cold and clammy. The patient experiences great anxiety and
often a feeling of impending doom. Not all patients experience the more classic signs and
symptoms. Women, older adults, and diabetic patients often have atypical symptoms. Women
may complain of fatigue, shortness of breath, and atypical chest pain. Older adults and diabetic
patients may not experience chest pain but will complain of other symptoms such as shortness of
breath, dizziness, and nausea.
Medical Diagnosis
The diagnosis of an AMI is based primarily on the patient's history and the physical signs and
symptoms. The AMI can be confirmed by laboratory evidence and ECG changes.
Cardiac Markers
Troponin.
Troponin T (cTnT) and troponin I (cTnI) are proteins released from cardiac muscle when the
muscle is damaged. Troponin levels elevate in 3 hours after myocardial injury, peak in 24 hours,
and remain in the circulation for up to 2 weeks (cTnI remains elevated for 5 to 7 days; cTnT for
10 to 14 days). Troponin levels may be drawn in the emergency room, helping to establish an
early diagnosis.
Myoglobin.
Myoglobin is released within 1 hour after an acute myocardial infarction, and levels rise before
CK-MB levels; therefore myoglobin levels can be helpful in the early diagnosis of AMI.
Myoglobin levels will also be increased after strenuous exercise or renal failure and in the
presence of neuromuscular disease.
Cardiac Enzymes.
A blood sample is drawn from anyone with prolonged chest pain to measure cardiac enzymes.
With sustained ischemia, the cell membrane is impaired and enzymes are released from their
intracellular location into the interstitial fluid. These enzymes can be measured in the serum and
are assessed at regular intervals to confirm an AMI. CPK and its isoenzyme CPK-MB
(myocardial) elevate rapidly with infarction. Beginning 4 to 6 hours after infarction, the CPK
rises to 5 or more times the normal level within 12 to 24 hours and returns to normal in 2 to 3
days.
Electrocardiogram.
Changes in the normal waveform and dysrhythmias can be seen on an ECG. With ischemia, the
ST segment is often depressed and the T wave is inverted. If there has been total occlusion of a
coronary artery, the ECG will show ST elevation (STEMI). This is the more common
occurrence. If there has been transient or partial occlusion of the artery, the ECG may not show
ST elevation (NSTEMI). After infarction, another change often seen on the ECG waveforms is a
significant Q wave (Fig. 35-8). A significant Q wave is one that is greater than one-third the
height of the R wave. The most frequently observed dysrhythmias are premature ventricular
contractions, ventricular tachycardia, and ventricular fibrillation.
Medical Treatment
The goals of medical therapy after an AMI are to limit the amount of cardiac muscle injury, to
relieve symptoms, and to prevent or minimize complications.
Drug Therapy.
Sublingual or intravenous nitroglycerin is administered to dilate coronary arteries and increase

blood flow to the damaged area. If the nitroglycerin relieves the pain, the infarction may not
extend. Morphine sulfate is also used for chest pain. It has many effects in addition to analgesia.
Morphine causes peripheral pooling of blood, which decreases the blood returning to the heart
and lungs. It also diminishes anxiety, decreases tachypnea, and relaxes bronchial smooth
muscles, thereby improving gas exchange. If the patient cannot tolerate morphine, meperidine
(Demerol) may be ordered, but it does not have all the other beneficial properties of morphine
and may increase the heart rate.
Oxygen is administered at 4 to 6 L/min to assist in oxygenating myocardial tissue to support

pumping activity and to repair damaged tissue.
Fibrinolytic therapy is recommended for patients with STEMI (patients with total occlusion)
(Ante, et al., 2004). Streptokinase and tissue plasminogen activator are administered
intravenously or into the coronary arteries (during cardiac catheterization) to dissolve the
thrombus. This treatment is most effective when initiated early but may be administered up to 12
hours from the onset of chest pain. The patient must meet strict criteria (no recent surgery or
active bleeding; no history of a stroke; no bleeding disorders) and provide informed consent
before the administration of fibrinolytics. After administration of the fibrinolytics, heparin is
administered to prevent further clot formation.
FIGURE 35-8 Electrocardiographic changes with myocardial infarction.

Aspirin and beta-adrenergic blockers should be administered as soon as the patient can tolerate
them and if not contraindicated. Beta-adrenergic blockers improve survival rates by decreasing
the heart rate, reducing the work of the heart, and lessening the oxygen demand of the
myocardium. ACE inhibitors may be prescribed for some patients to minimize the abnormal
shaping or remodeling that can occur in the damaged ventricular muscle. Unstable patients may
require dopamine or dobutamine, or both, as inotropic agents (Ante, et al., 2004). As the
myocardium receives blood and oxygen, reperfusion dysrhythmias that require treatment may be
noted.
Percutaneous Coronary Intervention.
Emergency percutaneous coronary intervention (PCI) is an option for treatment after AMI, either
instead of fibrinolytic therapy or after fibrinolytic therapy (Ante, et al., 2004). There are several
PCI procedures that can be performed in the cardiac catheterization laboratory: percutaneous
transluminal coronary angioplasty (PTCA), intracoronary stent placement, atherectomy, laser
angioplasty, and radiation therapy. PTCA involves passage of a catheter through a peripheral
artery (usually the femoral artery) into the occluded coronary artery. The tip of the catheter
contains a balloon that is inflated to compress the atherosclerotic plaque and dilate the artery.
PTCA is often utilized when there is single-vessel disease, non-calcified lesions, or lesions that
are not at bifurcations. PTCA is not recommended for lesions of the left main coronary artery.
When appropriate, this procedure is preferred over coronary artery bypass surgery because it can
be done under local anesthetic, it is less invasive, and the recovery time is faster. The procedure
is safer than bypass surgery but is not without risks. Complications of PTCA include coronary
artery dissection, dysrhythmias, coronary spasm, hematoma at the catheter site, restenosis, and
death. In approximately 30% of patients, the vessel narrows again within 6 months.
Intracoronary stents are devices that are positioned within the blockage through a balloon-tipped
catheter, expanded into place, and left to support the arterial wall. Over time, endothelial cells
will completely line the inner wall of the stent to produce a smooth inner lining (Fig. 35-9). After
an intracoronary stent is placed, the patient will be on antiplatelet or anticoagulant agents to
decrease the chance of occlusion in the stent. Complications of stents are injury to the vessel wall
and bleeding.
The coronary atherectomy is a procedure that widens the coronary artery by removing the
atherosclerotic plaque using a device that shaves the plaque off the vessel walls.
FIGURE 35-9 Intracoronary stent.
A newer procedure is laser angioplasty. It uses a catheter with a laser on the tip. The laser is used
to widen the lumen of the artery by destroying atherosclerotic plaque.
Radiation therapy is used primarily to treat restenosis of intracoronary stents. Radiation is

delivered to the area of stenosis for several minutes. The patient requires no special precautions
after the procedure related to the radiation.
Coronary Artery Bypass Graft Surgery.
Coronary artery bypass graft surgery may be performed to improve the blood supply to the
myocardium. Arterial bypass surgery uses the patient's own vasculature as replacement for
occluded coronary arteries. From one to six vessels may be bypassed. The saphenous veins and
the internal mammary artery are most commonly used. The saphenous veins are removed from
one or both legs, inspected for patency, and reversed so that the valves do not inhibit blood flow.
The replacement vessels are attached above and below the occlusions in the coronary arteries and
serve as new conduits for oxygenated blood to the myocardium (Fig. 35-10). This is major
surgery requiring the heart beat to be stopped and the patient to be placed on a cardiopulmonary
bypass (CPB) machine during the surgery. The survival rate is higher in patients who are in
stable condition.
Another approach to surgical revascularization is being used on patients requiring surgery on the
arteries of the anterior heart. This procedure is called minimally invasive direct coronary artery
bypass grafting and is performed through a small anterior thoracotomy incision. The patient's
internal mammary artery is used to bypass the stenosed vessel, and the bypass is accomplished
on a beating heart. The patient does not have to be placed on CPB. Postoperative care is similar
to that of other cardiac surgery, although patients do not require as lengthy ventilatory support
and total length of hospital stay is shorter.
A third option, off-pump coronary artery bypass (OPCAB), usually uses a full sternotomy
incision (as with the traditional CABG) to provide the surgeon access to all coronary vessels
(anterior and posterior). The OPCAB surgery is then accomplished on a beating heart without the
use of CPB. Specially developed vacuum-assisted stabilizers are used by the surgeon to stabilize
the graft site.
A new approach to CABG is done endoscopically. Called totally endoscopic CAB (TECAB),
three tiny incisions are made on the patient's chest between ribs, and a small camera and two
robotic arms are inserted. The surgeon sits at a console to view the surgical area and manipulates
the robotic arms with his or her hands/wrists. The surgery is done on a beating heart, is less
traumatic to the patient due to the small incisions, and is easier to recover from.
Another method of revascularization, used for patients with diffuse coronary vessel disease, is
transmyocardial laser revascularization. Tiny holes are drilled in the myocardium using a laser,
which helps provide collateral circulation to the ischemic myocardial muscle (Fig. 35-11).
FIGURE 35-10 Coronary artery bypass graft surgery.
NURSING CARE of the Patient with Acute Myocardial Infarction

Assessment
General assessment of the cardiac patient is summarized in Box 35-1. When a patient has AMI,
be especially concerned with assessment of pain. When chest pain is present, early evaluation
and treatment are paramount. Ask the patient to describe the pain, including type, location,
duration, and severity. It is recommended that chest pain be assessed using the mnemonic
PQRST.
P Precipitating factors, palliative: What was the patient doing when the pain began? Did
anything make the pain better? Worse?
Q Quality: Have the patient describe what the pain feels like (in his or her own words).
R Region, radiation: Where is the pain located? Does it hurt anywhere else?
S Severity, symptoms: Have the patient rate the pain. Use the pain scale 0-10. Note other
symptoms (e.g., nausea, diaphoresis).
T Time: When did the pain start? How long did it last?
Record what the patient was doing when the pain started, what action was taken, and the effects
of any actions or treatments. Inspect the patient's skin for color and palpate for temperature and
moisture. Frequently assess vital signs. Document the mental status and level of anxiety. When
cardiac monitoring is initiated, evaluate the rate and rhythm.
Nursing Diagnoses, Goals, and Outcome Criteria: Acute Myocardial Infarction

Anxiety related to feeling of impending doom, Reduced anxiety: patient statement of lessened
lack of understanding of routines anxiety, calm manner and self-care
Acute Pain related to lack of oxygen to the Pain relief: patient statement of relieved pain,
myocardium relaxed manner
Decreased Cardiac Output related to Normal cardiac output: normal pulse, blood
dysrhythmia and abnormal heart rate pressure, and cardiac rhythm
Interventions
Acute Pain
Administer analgesics as ordered, and monitor for relief of pain. Morphine is usually
administered in small amounts (2 to 4 mg) intravenously every few minutes until pain relief is
evident. Provide supplemental oxygen as ordered through nasal cannula at 2 to 4 L/min to
provide adequate oxygen to the heart muscle. The head of the bed is usually elevated at least 30
degrees. Inform the physician if the patient has an increasing respiratory rate or dyspnea.
Monitor vital signs hourly or more frequently until stable. Monitor the ECG for changes in
normal waveform (inverted T wave, ST elevation, and Q wave) and for dysrhythmias. Notify the
physician of changes in the rhythm. In an intensive care unit, standing orders prescribe drug
therapy for specific dysrhythmias. An intravenous line is usually established so that emergency
drugs can be administered quickly and directly. Prompt treatment of dysrhythmias may prevent
fatal alterations in rhythm. Monitor the patient for fluid volume excess (crackles, cough, jugular
vein distention), and report any such evidence to the physician.
FIGURE 35-11 Transmyocardial laser revascularization.
Interventions to decrease demands on the heart include assisting the patient to rest, spacing
activities and providing rest periods, providing adequate ventilation and oxygenation, relieving
pain, and maintaining a calm, quiet environment.
Anxiety
Provide as calm an environment as possible. Explain procedures and equipment to the patient
and family, using simple terms. Keep family members informed of the patient's progress. They
can be helpful in calming the patient during the acute episode.
During the acute phase of AMI, provide simple explanations of the procedures and routines.
Reinforce information given by the physician about the diagnosis and treatment. Patient teaching
is especially important in the rehabilitation phase.
Cardiac Rehabilitation
As soon as the patient is stable, begin rehabilitation by teaching the patient and family about
exercise, medications, and diet. If surgical intervention has been proposed, you may also teach
the patient about that procedure.
The purpose of rehabilitation is to minimize the risk of repetition of adverse cardiac events. The
goal of rehabilitation is to enable patients to attain the highest level of wellness and work ability.
The program is individualized to the patient for maximal success. The four phases of cardiac
rehabilitation are (1) inpatient management; (2) immediately after discharge, using telemetry
monitoring during exercise; (3) later rehabilitation, which is unmonitored; and (4) maintenance.
A team of medical professionals (e.g., nurse, physician, physical therapist, nutritionist, social
worker) plans the individual program. Education during the rehabilitation process should include
normal anatomy and physiology of the heart; pathophysiology of coronary artery disease, angina,
and AMI; risk factor modification; activity and exercise; medications; diet; and when to seek
medical advice. See the Nutrition Concepts box below for a discussion of dietary considerations
for patients with heart disease.

Acute Myocardial Infarction
After AMI, the following are some key points in the discharge teaching plan:
 •It is very important to take your medications as prescribed and to contact the physician if
you have any problems. (Provide written information about drug names, dosages,
purpose, interactions with other medications and foods, and adverse effects that should be
reported.)
 •Your physician may prescribe a low-fat, low-sodium diet to decrease weight and to
reduce the workload on your heart.
 •Participation in cardiac rehabilitation will help you become active again in a safe
manner.
 •Stop smoking. Smoking stimulates the heart rate and causes blood vessels to constrict,
which makes the heart work harder.
 •Maintain normal weight (or lose weight if obese) to decrease the work of the heart.
 •The local chapter of the American Heart Association is a helpful resource for
information and guidance on diet, smoking cessation, and exercise.
Put on Your Thinking Cap!
A new patient is being seen in the physician's office. Basic information and health history data
include the following: 58-year-old white male, height 599°, weight 190 lbs; vital signs: T, 98° F;
P, 82; R, 14; BP, 152/84.
SOCIAL HISTORY
Real estate salesman (describes himself as “pretty successful” and able to maintain a good
quality of life). Plays tennis 3 times a week; walks 2 miles, 4 times a week. Divorced father of
three adult children; one son who recently was admitted to rehabilitation for substance abuse has
no insurance. Patient has conflict with ex-wife related to son's situation. Enjoys a “few beers” in
the evening. Has eggs, bacon, biscuits, coffee for breakfast, has lunch (sandwich, fries) at fast-
food restaurant, and cooks dinner (usually “meat and potatoes”). Sleeps 7 to 8 hrs; usually rested
on arising. Some recent trouble sleeping because of son's problems. No current significant other.
HEALTH HISTORY
Hypertension for 5 years treated with daily antihypertensive drug; chronic sinusitis; arthritis in
left knee related to sports injury.
FAMILY HISTORY
Mother, age 78, living and in moderately good health. Had mild stroke last year without
permanent effects. Has diabetes. Father died suddenly at age 66 of acute myocardial infarction.
Two living brothers, ages 52 and 49. Both are hypertensive.
ANALYSIS
 1. Based on the data available, identify modifiable and unmodifiable risk factors for
coronary artery disease.
 2. Identify one strategy to address each modifiable factor.
 3. Identify current factors that reduce his risk of coronary artery disease.
HEART FAILURE
Heart failure is the inability of the heart to meet the metabolic demands of the body. The
pumping ability of the heart is ineffective.
Etiology and Risk Factors
Heart failure (HF) is the preferred term used to describe the clinical picture of failure. Congestive
heart failure (CHF) is a commonly used term for heart failure; it describes the symptoms seen
when the heart fails to pump effectively and blood “backs up” into the vasculature of the lungs,
producing congestion. The two terms (HF and CHF) are often used interchangeably in the
clinical setting. Causes of heart failure are primarily of two types: disorders that increase the
workload of the heart and disorders that interfere with the pumping ability of the heart. Therefore
patients at risk for HF include those with CAD, AMI, cardiomyopathy, hypertension, COPD,
pulmonary hypertension, anemia, disease of the heart valves, and fluid volume overload. Other
conditions that increase metabolic needs, such as fever and pregnancy, may also precipitate heart
failure. Approximately 4.9 million Americans have heart failure and over half a million new
cases of heart failure are diagnoses every year. After age 65, 10 of every 1000 individuals have
heart failure, and 75% of heart failure patients have a history of hypertension (American Heart
Association, 2007).
Nutrition Concepts
 1. A major part of treatment for people with heart disease is reduction of fat and
cholesterol in the diet.
 2. When fats are used in cooking or eating, unsaturated fats (vegetable oil such as corn
oil, canola oil, or olive oil) should be substituted for saturated fats (animal fat such as
butter or lard).
 3. Fats and oils used in cooking or eating should be limited to five to eight servings daily
in normal adults.
 4. Saturated fat can be limited by eating only 5 to 7 ounces of meat daily.
 5. Foods that contain omega-3 fatty acids (certain fish, walnuts, and soybeans) lower
serum triglycerides and decrease the number of deaths resulting from heart disease.
Pathophysiology
The LV, RV, or both fail as pumps. Usually the left side of the heart fails first. In time, the right
side fails as a result of the left-sided failure. Heart failure can be classified as systolic HF
resulting from ineffective pumping of the ventricles or as diastolic HF resulting from impaired
filling of the ventricles. With either classification, cardiac output is decreased. Heart failure can
occur acutely, with onset over several hours or days, or it can be chronic, with onset over months
to years.
Compensation.
Compensation is a term used to describe the cardiac and circulatory adjustments that maintain or
restore cardiac output to normal or near normal. Compensation occurs through three
mechanisms: sympathetic nervous system stimulation, regulation of blood volume by the
kidneys, and enlargement of the ventricular myocardium.
Sympathetic Compensation.
The sympathetic nervous system responds to decreased cardiac output and blood pressure.
Catecholamines are released that increase heart rate, stroke volume, cardiac output, and venous
tone. Increased venous tone increases systemic vascular resistance, venous return, and
ventricular filling.
Renal Compensation.
The second mechanism that responds to decreased cardiac output is renal compensation. When
cardiac output falls, so does renal perfusion. This initiates the renin-angiotensin-aldosterone
(RAA) mechanism. Renin, secreted by the kidneys, activates angiotensinogen to convert to
angiotensin I. Angiotensin I is converted to angiotensin II, which causes vasoconstriction and
triggers release of aldosterone. Vasoconstriction raises the blood pressure by increasing
peripheral resistance to blood flow. Aldosterone causes the kidneys to retain sodium and water,
which increases blood volume.
Natriuretic Peptides.
Natriuretic peptides are neurohormonal substances released with heart failure. Atrial natriuretic
peptide (ANP) is released in response to increased volume and stretch in the cardiac atria. B-type
natriuretic peptide (BNP) is released when the cardiac ventricles stretch, usually from increased
blood volume. The natriuretic peptides are thought to counter the vasoconstrictive and volume-
increasing effects of the SNS and RAA systems. BNP levels can be measured in the blood and
can be used as a diagnostic tool for HF (Saul & Shatzer, 2003).
Ventricular Hypertrophy.
The final mechanism is enlargement of the ventricular myocardium, called ventricular

hypertrophy, which results from strain. The increased blood volume raises the pressure in the
ventricles, which can also cause the ventricles to dilate. The ventricle changes in size and shape,
which impairs pumping effectiveness. This process is called ventricular remodeling.
After a period, the compensatory mechanisms may no longer be able to meet the increased
demands. Contractility decreases; the heart muscle can stretch just so far before becoming
inefficient. The force of contraction of the LV decreases. Stroke volume and cardiac output
decrease as pumping action fails. Afterload increases with left-sided heart failure. Blood backs
up in the LA and then the pulmonary veins. Because of the high pressure in the pulmonary veins
(pulmonary hypertension), fluid leaks from the capillaries, causing pulmonary edema.
Pulmonary hypertension eventually causes the right side of the heart to fail as well. Then, blood
returning to the heart from the body meets resistance, which causes systemic pressure to rise.
This results in peripheral edema and enlargement of the liver and spleen. If heart failure is not
corrected, death eventually ensues.
With left-sided HF, there is increased left ventricular end-diastolic pressure, increased left atrial
pressure, increased pulmonary pressure, and resulting pulmonary edema as the excess fluid leaks
into the lung tissues. In right-sided HF, right ventricular pressure increases, right atrial pressure
increases, and fluid accumulates in the systemic vasculature.
Put on Your Thinking Cap!
 1. Explain why a patient with heart failure might (1) feel anxious, and (2) gain weight.
 2. A patient with heart failure is advised to try to lose 30 pounds. What nursing strategies
would help her achieve this goal?
 3. You suspect that a patient with HF and hypertension is not taking her blood pressure
medication regularly as prescribed. What strategies might improve her compliance?
Signs and Symptoms
The patient with left-sided heart failure is typically very anxious, pale, and tachycardic.
Consecutive blood pressure readings may show a downward trend. Auscultation of the lung
fields may reveal crackles, wheezes, dyspnea, and cough. When assessing heart sounds, S3 and S4
may be heard as a result of the backup of fluid and the heart's inability to handle the excess
fluids.
With right-sided heart failure, there is increased central venous pressure, jugular venous
distention, abdominal engorgement, and dependent edema. Anorexia, nausea, and vomiting may
result from the abdominal engorgement. Fatigue, weight gain, and decreased urinary output are
common complaints.
Medical Diagnosis
The diagnosis of HF is made on the basis of the history, physical examination, radiographs, and
laboratory test results. A chest radiograph may reveal hazy lung fields, distended vasculature,
and cardiomegaly. An echocardiogram may reveal heart enlargement and ineffective ventricular
contraction. Laboratory tests indicative of HF are decreased serum sodium and Hct from
hemodilution and decreased saturated arterial oxygenation from poor pulmonary perfusion. The
blood urea nitrogen (BUN) and creatinine are elevated with decreased renal function. BNP levels
are elevated in HF, and the higher the levels, the more severe the failure. Liver function test
results are elevated with hepatomegaly (liver enlargement). The patient who is critically ill with
HF may require more intensive monitoring of hemodynamics parameters.
Medical Treatment
Medical treatment includes management of the underlying cause, drug therapy to improve
cardiac output and eliminate excess fluid, and conservative measures to decrease demands on the
heart. Sodium restriction is prescribed for most HF patients.
Treatment of the underlying problem may involve such interventions as correction of

dysrhythmias, management of hypertension, and valve replacement or repair.
Drug Therapy.
A number of drugs are used to treat heart failure. Current recommendations include ACE
inhibitors, diuretics, beta-adrenergic blockers, inotropic agents, cardiac glycosides, and nitrates.
In addition, certain patients will benefit from B-type natriuretic peptide. ACE inhibitors decrease
preload and afterload by blocking the RAA system, resulting in vasodilation, decreased blood
volume, and lower blood pressure. In addition, ACE inhibitors are thought to limit the
progression of ventricular remodeling. Diuretics are prescribed to decrease circulating fluid
volume and decrease preload. Loop diuretics such as furosemide (Lasix) are usually used in HF.
Spironolactone, a weak potassium-sparing diuretic, may be prescribed for some patients because
it acts by blocking aldosterone and may slow the process of remodeling. Beta-adrenergic
blockers improve survival rates by decreasing the heart rate, reducing the work of the heart, and
lessening the oxygen demand of the myocardium. Inotropic agents such as dopamine,
dobutamine, and amrinone are prescribed to improve cardiac contractility, improve renal
perfusion and decrease fluid retention. Digoxin, a cardiac glycoside with inotropic effects, is
prescribed to improve pump function by increasing contractility and decreasing heart rate.
Nesiritide (Natrecor) is a recombinant human B-type natriuretic peptide that is often prescribed
in patients with decompensated HF. Nesiritide counteracts the vasoconstriction and fluid
retention of the RAA system and relieves the severe dyspnea seen in these patients. Nitrates,
such as NTG, are venodilators and reduce preload for patients with HF. This helps reduce the
workload on the heart. Morphine may be used to decrease anxiety, dilate the vasculature, and
reduce myocardial oxygen consumption in the acute stage. The Drug Therapy table on pp. 642 to
646 provides additional information about drugs used to treat HF.
Other Therapy.
Other therapies are available for decreasing cardiac workload and increasing myocardial
oxygenation. The intra-aortic balloon pump (IABP), ventricular assist devices (VADs), and
biventricular pacing may be utilized. The intra-aortic balloon pump is a temporary device used in
the intensive care unit to increase cardiac output and coronary artery perfusion. VADs can
partially or completely support a patient's failing heart. Currently considered a temporary
intervention, VADs are used as a “bridge” to transplantation. Biventricular pacing is useful in
approximately 30% of HF patients who have conduction delays in the right or left bundle branch.
These conduction delays result in the ventricles being depolarized and contracting out of
synchrony. This reduces cardiac output and can contribute to the worsening of HF. In
biventricular pacing, leads are placed in both ventricles and they are stimulated at the same time.
Cardiac contraction occurs in both ventricles at the same time and cardiac output is improved
(Lagrotteria, 2003).
Surgery.
Coronary artery bypass grafting is recommended in HF patients who experience angina. Valve
repair or replacement is recommended when valve dysfunction contributes to the HF. Partial left
ventriculectomy may be useful in some patients. Cardiac transplantation is often the last option
for patients with end-stage HF whose symptoms are not responding to conventional therapy.
Complications
Dysrhythmias, pulmonary edema, and cardiogenic shock are possible complications.
NURSING CARE of the Patient with Heart Failure

Assessment
Complete assessment of the cardiac patient is outlined in Box 35-1 (see also Nursing Care Plan:
The Patient with Heart Failure on p. 663). It is especially important to assess heart sounds, rate,
and rhythm. The point of maximum impulse is noted. Assess the apical and radial pulses
frequently. Inspect for jugular vein distention. A baseline respiratory assessment of rate, rhythm,
and breath sounds is vital. Measure weight and blood pressure accurately. Inspect the skin and
palpate for turgor and edema. Intake and output records and daily weights may be done to
evaluate fluid retention or loss. If ordered, take central venous pressure and hemodynamic
readings as well. If cardiac monitoring is done, observe for dysrhythmias. Nurses who work in
intensive care units routinely interpret ECGs. Interpretation is discussed on pp. 673 to 675.
Nursing Diagnoses, Goals, and Outcome Criteria: Heart Failure

Fluid Volume Excess related to Normal fluid volume: no edema or dyspnea, blood
ineffective cardiac pumping pressure consistent with patient norms
Impaired Gas Exchange related to Adequate oxygenation: clear breath sounds,
decreased pulmonary perfusion respiratory rate 12 to 20/min without dyspnea
Anxiety related to edema and difficulty Reduced anxiety: patient statement of reduced anxiety,
breathing calm manner
Decreased Cardiac Output related to Improved cardiac output: normal heart rate and
mechanical failure rhythm, fluid intake and output equal
Activity Intolerance related to inability Increase activity tolerance: performance of activities
to meet oxygen demands of daily living without fatigue
Interventions
Give medications as ordered, and monitor the patient for therapeutic and adverse effects. Older
adult patients are more susceptible to adverse drug effects because they may metabolize and
excrete drugs more slowly. This is especially true when the older patient is taking digitalis.
Advise the patient to report early signs of digitalis toxicity: anorexia, nausea, and visual
disturbances. Bed rest and stress reduction decrease the cardiac workload. When the patient is
acutely ill, eliminate unnecessary activity. Give partial baths rather than complete bed baths.
Assist the patient to change positions at least every 2 hours so that the skin can be inspected for
signs of pressure. Visitors may be permitted, but advise them to sit quietly with the patient for
short periods.
NURSING CARE PLAN

The Patient with Heart Failure
ASSESSMENT
Health History: A 73-year-old Chinese-American woman is admitted through the Emergency

Department. She is a retired business owner who lives alone and has no immediate family in the
area. She began having dyspnea and orthopnea that has become progressively worse over the
past 3 days. Her past medical history includes a myocardial infarction 1 year ago and a 10-year
history of hypertension treated with diet and verapamil 240 mg daily. In addition to the
verapamil, she takes only an occasional laxative. She complains of fatigue, restlessness,
nervousness, irritability, insomnia, anorexia, and a productive cough with pink sputum.
Physical Examination: Vital signs: temperature 98° F orally; pulse 104, slightly irregular;
respirations 24; blood pressure 168/96. Height 5′2′; weight 152 lbs (a 7-lb increase in 1 week).
She is alert but appears anxious. Her skin is pale and diaphoretic. An S3 is present. Jugular vein
distention is noted. Auscultation of the lungs reveals crackles in the lower lobes of both lungs.
The abdomen is distended. Bowel sounds are present in all four quadrants. There is 3+ pitting
edema in both feet and ankles.
She is being admitted to the telemetry unit for treatment, where she will have continuous
electrocardiography and be placed on oxygen.
Goals and Outcome

Nursing Diagnosis Interventions
Criteria
The patient's cardiac output
Monitor vital signs, heart and lung sounds,
will improve, as evidenced
level of consciousness, electrocardiography.
by normal heart rate and
Enforce bed rest with head of bed elevated.
rhythm, normal blood
Decreased Cardiac Schedule activities to allow rest. Request
pressure, normal
small, frequent meals. Administer
hemodynamic measure, and
cardiotonics, vasodilators, and ACE
breath sounds clear to
inhibitors as ordered.
auscultation.
Output related to
decreased myocardial
contractility
Fluid Volume Excess Monitor for jugular venous distention and
The patient will have normal
related to decreased peripheral edema. Auscultate heart and lung
fluid balance as evidenced
glomerular filtration sounds q 4 hr. Measure weight daily and
by weight of 145 lbs,
rate, increased intake and output accurately. Maintain
absence of edema, absence
aldosterone, sodium intravenous lines and correct fluid infusion
of crackles and wheezes in
and water retention, rate. Administer diuretics as ordered. Teach
lungs, and ability to
and increased about sodium restriction and rationale.
participate in activities of
antidiuretic hormone Protect edematous extremities from
daily living without dyspnea.
release pressure or injury.
Assess lung sounds and respiratory status q
The patient's gas exchange
4 hr. Monitor O2 saturation. Elevate head of
Impaired Gas Exchange will be evidenced by pulse
bed. Administer oxygen as ordered. Assist
related to pulmonary oximetry >95%, normal skin
to cough and deep breathe q 2 hr.
congestion color, absence of dyspnea,
Administer diuretics and morphine sulfate
and clear lung sounds.
as ordered.
Activity Intolerance The patient's activity Assess response to activity when permitted.
related to imbalance tolerance will improve, as Monitor for dyspnea, changes in vital signs.
between oxygen supply evidenced by performance of Limit fatiguing activities. Gradually
and demand activities of daily living increase activity as tolerance improves.
without excessive fatigue or
Goals and Outcome
Nursing Diagnosis Interventions
Criteria
dyspnea.
Explain procedures and equipment. Tell
The patient's anxiety will be
patient about congestive heart failure and
Anxiety related to reduced, as evidenced by
how it is being treated. Point out signs of
hypoxia, life- calm demeanor and
improvement. Visit often, and respond to
threatening situation statement that she feels less
call bell promptly. Offer spiritual counselor
anxious.
if desired.
Provide simple explanation of congestive
heart failure, its effects, and its treatment.
The patient will verbalize As discharge nears, discuss diet, exercise,
Deficient Knowledge information about her and drug therapy. Explain signs and
of condition, treatment, condition, treatment, self- symptoms that should be reported to
self-care, and resources care measures, and physician. Advise of services of American
resources. Heart Association for information. Explore
sources of support and need for visiting
nurse or home health services.
CRITICAL THINKING QUESTIONS
 ▪ What is the rationale behind sodium restriction in patients with heart failure?
 ▪ Describe three signs of improvement in a patient with heart failure.
Before each dose of digitalis, the apical pulse is counted for 1 full minute. If the heart rate is less
than 60 bpm, the drug is withheld and the physician is notified.
The most common adverse effects of diuretic therapy are fluid and electrolyte imbalances.
Impaired Gas Exchange
Hypoxia is a common finding with left-sided heart failure because of pulmonary edema. It is
common with right-sided heart failure because of decreased blood flow to the lungs. The patient
with HF usually breathes more easily in a semi- or high-Fowler's position. Elevation of the upper
body facilitates breathing by reducing pressure of the abdominal organs on the diaphragm.
Supplemental oxygen is usually prescribed at 4 to 6 L/min per nasal cannula. The flow rate is
reduced to 2 L/min for patients with chronic hypoxia. Assess respiratory status and blood gases
frequently.
Prescribed bed rest can lead to other pulmonary complications related to immobility: hypostatic
pneumonia and pulmonary emboli. Teach the patient to cough and deep breathe at least every 2
hours to promote respiratory excursion and to mobilize secretions. Other interventions to prevent
complications of immobility are detailed in Chapter 21.
On discharge, the physician may order portable oxygen for use at home. The nurse or a
respiratory therapist instructs the patient in the use of the equipment and the safety precautions to
take when using oxygen (see Chapter 30).
Fluid Volume Excess
Fluid retention is a response to HF, an attempt to maintain normal cardiac output. Unfortunately,
it compounds the problem by increasing the workload on the heart. Therefore measures are taken
to reduce the fluid volume to normal while improving the function of the heart. Administer
diuretics as ordered, and monitor the patient for adverse effects. The most common adverse
effects of diuretic therapy are fluid and electrolyte disturbances. Signs and symptoms that may
indicate fluid or electrolyte disturbances include cardiac dysrhythmias, muscle weakness or
twitching, cramps, changes in mental status, and abdominal distention. Frequent serum
electrolyte measurements are usually ordered. Note the results and notify the physician of
abnormal findings. If hourly urine output is being measured, report an output of less than 30
mL/hr to the physician as well. The patient should be weighed daily.
An intravenous catheter is usually placed to provide a line for drug administration. If intravenous
fluids are administered, monitor the rate of administration very carefully. If fluid retention is not
relieved by other means, fluid restriction may be instituted. All staff should know the exact
amount of fluid allowed and must record all intake. Fluid restriction can be very uncomfortable
for the patient. Even with fluid volume excess, the patient may feel thirsty because of electrolyte
imbalances. Present oral fluids in small containers, and offer them at reasonable intervals.
Frequently provide mouth care. The patient and family must understand why fluids are restricted
so that the patient does not exceed the prescribed intake.
The most common therapeutic dietary measure for CHF is sodium restriction. The patient may
be limited to 2 g of sodium/day. In severe cases, a limitation of 500 to 1000 mg/day may be
prescribed. Reduced sodium intake decreases fluid retention, thereby reducing the cardiac
workload. For a 2-g sodium diet, advise the patient to avoid foods high in sodium (a list should
be provided), not to add salt before or after cooking, and to use no more than 2 cups of milk
products daily. Patients often have difficulty changing their use of seasonings. Acknowledge the
difficulty, and explain how sodium limitation contributes to improvement of cardiac function.
It is best to identify the type of diet to be prescribed on discharge as early as possible. This
allows time for a dietary consultation to be arranged, which should be followed by reinforcement
by the nurse. The person who prepares the patient's meals at home must be included in the
teaching sessions.
Activity Intolerance
Frequent rest periods, pacing of activities, and relaxation techniques help the patient conserve
energy. As the fluid volume is decreased and the cardiac output is increased, the patient can
expect to be less fatigued.
The patient may be referred to a rehabilitation facility for exercise training. In general, the
patient is advised to plan rest periods before and after tiring activities. Activity should be
increased gradually, with rest periods taken when fatigue or dyspnea occurs. The physician may
prescribe vasodilators for patients who experience chest pain with some activities. If monitoring
is indicated after discharge, request a referral to a home nursing agency.
Instruct the patient to notify the physician if the following problems develop: increasing dyspnea
or edema, excessive fatigue, or pain that is not relieved by rest or prescribed medications. Early
recognition of signs and symptoms that the patient's condition is deteriorating is crucial to
avoiding rehospitalization (see the Health Promotion Considerations box above). In addition,
advise the patient to avoid smoking and smoky environments and to refrain from wearing
constricting clothing on the lower extremities.

Heart Failure: Discharge Instructions
A major goal for heart failure patients is to prevent rehospitalization. A critical factor in reaching
this goal is for the patient or family member to recognize early signs and symptoms of worsening
failure and to contact their provider. Examples of what to call about are the following: difficulty
breathing (especially with activity); dry, hacking cough; weakness, increased fatigue; foot/ankle
swelling; dizziness; and weight gain of 3-5 lbs in a week or less.
Anxiety
Factors that may cause the patient to become anxious are dyspnea, unfamiliar setting and
routines, and uncertainty about what is happening. Acknowledge the patient's anxiety and
attempt to identify the basis. While taking immediate measures to relieve dyspnea, calmly
explain what is being done. It may be helpful to tell the patient how specific measures help
relieve symptoms. The presence of family members may have a calming effect if the relatives
understand that they, too, must remain calm.

Chronic Heart Failure
 • Reducing sodium in your diet will help control swelling and reduce the workload on
your heart.
 • Excess weight makes your heart work harder. Your physician may prescribe a weight-
loss diet for you.
 • Take your medications as prescribed to improve your heart function. (Provide written
information about drug names, actions, dosage, schedule, side and adverse effects, special
aspects of administration, and interactions with other medications and food.)
 • Gradually increase your activity. Avoid activity that causes shortness of breath or
severe fatigue.
 • Weigh yourself each morning, before breakfast, on the same scale and with the same
amount of clothing.
 • Contact your physician if you gain 2 or more pounds in a week, develop a persistent
cough, or have shortness of breath or chest pain.
 • Resources: The American Heart Association provides information about diet and
exercise. The Visiting Nurses Association or a home health agency can monitor your
home.
Older adults are more susceptible to adverse drug effects because they metabolize and excrete
drugs more slowly.
INFLAMMATORY DISORDERS
Inflammation of the heart most often results from systemic infections. The endocardium,
myocardium, and pericardium may be affected.
Infective Endocarditis
Microbial infections of the endocardium affect primarily the valves. Organisms present in the
blood easily colonize valves damaged by rheumatic heart disease or congenital defects or a
mitral valve that is prolapsed.
Although the incidence of infective endocarditis (IE) has decreased with the use of antibiotics,
there has been a resurgence of the problem in intravenous drug abusers. The more frequent use
of invasive intravascular catheters for severely compromised patients has also contributed to the
frequency with which IE occurs.
Patients with known valvular disease are also at risk for IE. They should be treated with
prophylactic antibiotics before dental or invasive procedures. Immunosuppression or any source
of bacterial contamination (lacerations, pneumonia, invasive procedures, intravenous drug use
with contaminated needles) places patients at risk.
Pathophysiology
Pathogens, usually bacteria, enter the bloodstream by any of the previously mentioned means.
The pathogen accumulates on the heart valves and/or the endocardium and forms vegetations.
The mitral valve is the most common site for these vegetations. The turbulence of the blood flow
through the heart weakens the vegetations and causes pieces to break off. These emboli can then
obstruct circulation and impair tissue perfusion in the lungs, brain, kidneys, and heart.
Complications
Complications of IE include HF and embolization. HF is the most frequent cause of death with
IE.
Signs and Symptoms
Patients usually present with fever, chills, malaise, fatigue, and weight loss. The fever may be
low grade (37.2° to 38.9° C [99° to 102° F]) or higher (38.9° to 40.6° C [102° to 105° F]). The
fever is accompanied by chills and night sweats. Chest or abdominal pain may be reported,
possibly indicating embolization. Vegetative fragments and microembolizations can produce
petechiae inside the mouth and on the ankles, feet, and antecubital areas. Pea-size, tender, red-to-
purple lesions known as Osler's nodes may be on the patient's fingertips or toes.
Medical Diagnosis
The diagnosis of IE is based on the history, physical examination, and results of laboratory
studies. A history of recent dental or surgical procedures may precede IE. Auscultation may
reveal a heart murmur. Echocardiography helps visualize lesions and valvular regurgitation.
Right-sided or left-sided heart failure may be evident. Serial blood cultures may give clues to the
causative organism or organisms. The WBC count may be elevated.
Medical Treatment
Antimicrobials, rest, and limitation of activities are the primary therapeutic measures for IE.
Antimicrobials are given intravenously for 2 to 6 weeks, depending on the organism. The patient
is usually hospitalized for at least 1 week and then receives home intravenous therapy if that is
available. Prophylactic anticoagulants may be necessary. Surgery may be necessary to replace an
infected valve.
NURSING CARE of the Patient with Infective Endocarditis

Assessment
Complete assessment of the cardiac patient is summarized in Box 35-1. With IE, review the
patient's history for risk factors, recent invasive procedures, known pathologic cardiac
conditions, and onset of symptoms. Assess for temperature elevation, heart murmur, evidence of
HF (cough, peripheral edema), and embolization.
Nursing Diagnoses, Goals, and Outcome Criteria: Infective Endocarditis

Decreased Cardiac Output related to Normal cardiac output: normal pulse and blood
impaired valve function pressure
Impaired Physical Mobility related to Resumption of usual physical activities without
fatigue and prolonged intravenous symptoms: performance of activities of daily living
therapy without fatigue
Ineffective Tissue Perfusion related to Normal tissue perfusion: absence of dyspnea or signs
embolization of circulatory obstruction
Interventions
Administer prescribed antibiotics. Throughout the course of the illness, continue to assess
cardiac output and monitor for complications. Teach the patient about the medications prescribed
and any restrictions imposed. Encourage adequate rest, which is necessary during the healing
process. Range-of-motion exercises may be necessary during the acute stage and until the patient
is ambulatory.
Pericarditis
Pericarditis is an inflammation of the pericardium. It may be a primary disease or associated with

another inflammatory process. The disease may be acute or chronic. Acute pericarditis is caused
by viruses, bacteria, fungi, chemotherapy, or AMI (Dressler's syndrome). Chronic pericarditis is
caused by tuberculosis, radiation, or metastases.
Pathophysiology
In acute pericarditis, the inflammatory process causes an increase in the amount of pericardial
fluid and inflammation of the pericardial membranes. In chronic pericarditis (also called
constrictive pericarditis), scarring of the pericardium fuses the visceral and parietal pericardia
together. Loss of elasticity results from the scarring. This constrictive process prevents adequate
ventricular filling.
Complications
The major complication of pericarditis is pericardial effusion or accumulation of fluid in the

pericardial space. This may lead to cardiac tamponade when sufficient fluid accumulation
decreases ventricular filling. The resulting drop in cardiac output is an emergency. It is treated
with pericardiocentesis to remove the accumulated fluid.
Signs and Symptoms
Chest pain is the hallmark symptom of pericarditis. The pain is most severe on inspiration. It is
most often sharp and stabbing but may be described as dull or burning. It is relieved by sitting up
and leaning forward. Dyspnea, chills, and fever accompany pericarditis. ST segment elevation
may be noted on the ECG. A pericardial rub may be present. Slowly progressing pericardial
effusion does not result in hemodynamic compromise until 400 to 500 mL of fluid has
accumulated. Rapidly accumulating fluid may precipitate sudden symptoms with only 250 mL of
fluid.
Medical Diagnosis
The diagnostic challenge is to differentiate pericarditis from AMI. Serial ECGs show that the ST
segment elevation resolves in several weeks. QRS voltage may decrease because of the
accumulated fluid in the pericardial space. An echocardiogram may show pericardial thickening
and effusion. Atrial fibrillation may occur because of the irritation. The CPK-MB may be
elevated. Blood cultures may identify the causative organism or organisms. One differentiating
feature to consider is that ischemic chest pain or angina is not relieved by position change and
the chest pain that accompanies pericarditis often is relieved by change in position.
Medical Treatment
The patient is treated with analgesics, antipyretics, anti-inflammatory agents, and antibiotics.
With constrictive pericarditis, the patient would be treated as for HF. Surgical creation of a
pericardial window (removal of a segment of parietal pericardium to allow continuous drainage
of pericardial fluid) may be necessary for treating chronic pericarditis with effusion.
NURSING CARE of the Patient with Pericarditis

Assessment
General nursing assessment of the cardiac patient is summarized in Box 35-1. With pericarditis,
assessment of heart sounds is especially important.
Nursing Diagnoses, Goals, and Outcome Criteria: Pericarditis

Acute Pain related to pericardial Pain relief: patient statement that pain is reduced,
inflammation relaxed manner
Decreased Cardiac Output related to Improved cardiac output: normal pulse and blood
pericardial constriction pressure
Decreased anxiety: patient statement that anxiety is
Anxiety related to illness
reduced, calm manner
Interventions
Rest and reduction of activity decrease the workload of the heart. Administer medications and
teach the patient about the medications. Emotional support from the nursing staff and significant
others is vital. The patient can be instructed in relaxation techniques. Monitor vital signs and
auscultate for a pericardial friction rub. The rub is heard during inspiration with the diaphragm of
the stethoscope placed between the second and the fourth intercostal spaces at the left sternal
border. It is heard when there is no fluid accumulation. Distant heart sounds may be heard when
there is fluid accumulation. Note pain characteristics and response to analgesics and anti-
inflammatory agents. Monitor the ECG for dysrhythmias.
What Does Culture Have to Do with Cardiomyopathy?
African-American males are at increased risk for dilated cardiomyopathy. Be alert to complaints
of decreasing exercise tolerance and dyspnea in this population.
FIGURE 35-12 Cardiomyopathy. A, Dilated cardiomyopathy. B, Hypertrophic cardiomyopathy.

C, Restrictive cardiomyopathy.
CARDIOMYOPATHY
Cardiomyopathy (CMP) is disease of the heart muscle. The cause of CMP is often unknown or
CMP may be secondary to another disease process. The disease usually leads to heart failure.
Three types of cardiomyopathy are recognized: dilated, hypertrophic, and restrictive (Fig. 35-
12). Dilated cardiomyopathy is the most common type, accounting for 87% of cases (American
Heart Association, 2007). There are three risk factors associated with dilated CMP: excessive use
of alcohol, pregnancy, and infections. A relatively poor prognosis exists for dilated
cardiomyopathy, with a 50% mortality in 5 years. Hypertrophic CMP often results from valvular
heart disease or HTN. There also appears to be a genetic autosomal dominant link. Hypertrophic
CMP is more common in younger individuals; approximately 36% of young athletes who died
suddenly were found to have hypertrophic CMP. Restrictive cardiomyopathy is the least
common type of CMP. Amyloidosis, sarcoidosis, and other immunosuppressive disorders may
predispose individuals to restrictive cardiomyopathy.
Pathophysiology
With dilated cardiomyopathy, there is dilation of the ventricle and severely impaired systolic
function. This causes decreased contractility, decreased ejection fraction and stroke volume, and
increased left ventricular end-diastolic pressure. Pressure backup results in dilation of all four
chambers and is most pronounced in the ventricles. Left ventricular failure and resulting HF are
seen as the result of excessive back pressure (see Fig. 35-12, A).
In hypertrophic cardiomyopathy, the LV hypertrophies and there is thickening of the ventricular

septum. The left ventricular capacity decreases, and the outflow track of the left ventricle is
decreased in size. The size of the LA increases as a result of the back pressure. The exterior heart
size may appear to be normal. Ventricular dysrhythmias are common (see Fig. 35-12, B).
In restrictive cardiomyopathy, the myocardium becomes rigid and noncompliant. This reduces
ventricular filling and cardiac output. Pulmonary and systemic congestion result (see Fig. 35-12,
C).
Signs and Symptoms
Dilated cardiomyopathy is a progressive, chronic disease. The onset is gradual, with dyspnea,
fatigue, left-sided heart failure, and moderate-to-severe cardiomegaly. Mitral valve regurgitation
and S3 and S4 sounds are evident.
With hypertrophic cardiomyopathy, the progression of symptoms is slow. Dyspnea, orthopnea,

angina, fatigue, syncope, palpitations, ankle edema, and S4 sounds are found.
With restrictive cardiomyopathy, the primary symptom is exercise intolerance. Dyspnea, fatigue,
right-sided HF, S3 and S4 sounds, and mitral valve regurgitation are also noted.
Medical Diagnosis
Diagnosis of dilated cardiomyopathy is made primarily on the basis of echocardiography results.

Cardiac enlargement may be noted on chest radiography. The echocardiogram and chest
radiograph are also used to diagnose hypertrophic cardiomyopathy. Other findings include a
systolic murmur and atrial and ventricular dysrhythmias. An enlarged LV may be accompanied
by left atrial enlargement. The diagnosis of restrictive cardiomyopathy is demonstrated by
decreased cardiac output and HF. It must be differentiated from pericarditis. An echocardiogram
may show thickened ventricular walls and small ventricular cavities.
Medical Treatment
Supportive measures are used for dilated cardiomyopathy. Positive inotropic drugs to improve
cardiac output, diuretics to decrease preload, and ACE inhibitors and vasodilators to decrease
afterload provide this type of therapy. Anticoagulants may be used to prevent thrombi. If all
other measures fail, the patient needs a heart transplant. Medical treatment for hypertrophic
cardiomyopathy includes antidysrhythmics, antibiotics, anticoagulants, calcium channel
blockers, and beta-blockers. Surgical incision of the hypertrophied septal muscle and resection of
some of the hypertrophied muscle may be considered for hypertrophic cardiomyopathy An
alternative for select patients, nonsurgical reduction of the hypertrophied septum with alcohol
ablation, may be done percutaneously in the cardiac catheterization laboratory. Some patients
with hypertrophic CMP may benefit from an implantable cardioverter-defibrillator placed to
prevent sudden cardiac death. Treatment of restrictive cardiomyopathy is similar to that of HF
therapy. Heart transplantation may be considered. Complications observed with all types of
cardiomyopathy are dysrhythmias, HF, and death. There is a poor prognosis with
cardiomyopathy. Mortality from CMP is highest in older adults, men, and blacks.
NURSING CARE of the Patient with Cardiomyopathy

Assessment
These patients are primarily assessed for heart failure. Be alert for dyspnea, cough, edema,
dysrhythmias, and decreased cardiac output.
Nursing Diagnoses, Goals, and Outcome Criteria: Cardiomyopathy

Decreased Cardiac Output related to
Improved cardiac output: normal pulse and blood pressure
ventricular failure
Activity Intolerance related to poor Increased activity intolerance: performance of daily
tissue perfusion activities without excessive fatigue
Hopelessness related to poor More positive outlook: patient's expression of feelings
prognosis about condition and hopeful statements
Interventions
The care of these patients is similar to that of patients with HF. In addition, a hopeful atmosphere
and a careful explanation of care requirements are necessary. Encourage the family to support
the patient. The teaching plan guides the patient to make lifestyle changes. Encourage the patient
to make decisions and choices.
CARDIAC TRANSPLANTATION
The first heart transplantation was performed in 1967 in South Africa by Dr. Christiaan Barnard.
Today, heart transplantations in the United States, approximately 2500 per year, are done for
end-stage heart disease. Most of the cases of end-stage heart disease that require transplantation
are caused by cardiomyopathy. Psychological makeup is carefully assessed before
transplantation. Patients with a history of depression, noncompliance, and inability to cope with
stress are poor candidates. In the United States, there are federal regulations that prohibit the sale
of human organs.
The donor must meet the criteria for brain death, have no malignancies outside the central
nervous system, be free of infection, and not have experienced severe chest trauma. Prolonged
advanced life support measures are avoided. The donor and recipient organs must be carefully
matched. The donor heart size must be sufficient to meet the needs of the recipient. The donor
heart may be preserved for 4 to 6 hours before transplantation.
FIGURE 35-13 Heart transplantation. A, After the recipient is placed on cardiopulmonary

bypass, the heart is removed. B, The posterior walls of the recipient's left and right atria are left
intact. C, The left atrium of the donor heart is anastomosed to the recipient's residual posterior
atrial walls, and the other atrial walls, the atrial septum, and the great vessels are joined. D,
Postoperative result.
The recipient must be free of infection at the time of transplantation. The patient is prepared for
surgery as with any open-heart procedure. Cardiopulmonary bypass is initiated and the
recipient's heart is removed except for the posterior portions of the atria (Fig. 35-13). The donor
heart is trimmed and anastomosed to the remaining native heart. The patient is removed from
bypass, the heart is restarted, and the chest is closed.
Aftercare of the patient with a heart transplant is similar to that of the patient after coronary
artery bypass surgery. Hemodynamic monitoring, ventilation, cardiac assessment, care of chest
tubes, and accurate intake and output measurements are vital. Immediately after surgery, the
patient is placed in a private room in the intensive care unit. Modified protective isolation is
used. The use of gowns, masks, and careful hand washing has been found to be superior to strict
isolation techniques. Invasive lines/tubes (e.g., endotracheal tube, pulmonary artery catheter,
Foley catheter, chest tubes) are removed as rapidly as possible to decrease the chance of
infection. The prevention of postoperative infection is a major goal. Pulmonary infections are
most frequently found after heart transplantations. Moving the patient from the intensive care
unit to a private room and to home as soon as possible decreases the incidence of nosocomial
infections. Patients and families are taught the signs and symptoms of infection and to avoid
crowds and others with infections.
In addition, the patient with a transplant receives immunosuppressive medications. Lifelong

immunosuppression is administered to prevent the body from rejecting the donated heart, which
it recognizes as foreign tissue. Initially, large doses of corticosteroids are administered, and the
dose is decreased over time. At the first indication of rejection (increased temperature, infection,
dyspnea, malaise, fatigue, dysrhythmia), the steroid dose usually is increased. Other drugs used
to prevent and treat rejection are azathioprine (Imuran) and cyclosporine (Sandimmune).
Protocols using several immunosuppressive agents are considered most effective. Reduced
dosages of each drug provide for a lower incidence of toxicity.
Rejection is monitored through endomyocardial biopsies. These are performed frequently in the
immediate period after transplantation and less frequently over time. Patients are taught to
monitor their own progress and to report problems promptly. Patients are followed closely by the
transplant team and are observed for infection, rejection, quality of life, and complications.
Common complications noted after heart transplantation are hypertension, elevated cholesterol,
obesity, and malignancies.
SUDDEN CARDIAC DEATH
Sudden cardiac death occurs when heart activity and respirations cease abruptly. The most
common underlying reason for sudden cardiac death is coronary heart disease.
Patients taking immunosuppressive drugs to prevent rejection of transplanted tissue have reduced
resistance to infection.
The sudden cardiac death event usually occurs during ordinary activity. It is often preceded by
ventricular tachycardia or ventricular fibrillation and occasionally by severe bradydysrhythmias
(slow, abnormal cardiac rhythms). An episode of sudden cardiac death may be the first indication
of CAD. Other causes include left ventricular dysfunction, cardiomyopathy, hypokalemia,
antidysrhythmics, liquid protein diets, and high alcohol consumption.
Those who survive an episode of sudden cardiac death need to have extensive testing done to
determine the nature and cause of the sudden cardiac death. Many of these people will need
treatment of CAD (medical therapy, PTCA, or coronary artery bypass grafting). Most of these
patients have a lethal dysrhythmia that requires intervention. Diagnostic tests include 24-hour
Holter monitoring and/or ILR, stress testing, and electrophysiology study. During the
electrophysiology study, pacing electrodes are placed in the heart and electrical stimuli are used
to elicit the dysrhythmia. This helps the physician determine appropriate medical therapy. In
some patients, the dysrhythmia may be treated during the electrophysiology study with catheter
ablation. The ablation (removal or “burning”) of abnormal conduction pathways or irritable sites
in the heart can prevent the dysrhythmia from recurring. Still other patients are treated
effectively with antidysrhythmics such as amiodarone (Cordarone). If these therapies are
ineffective, the patient may be considered a candidate for an implantable
cardioverter/defibrillator (ICD).
Implantable Cardioverter/Defibrillator
The implantable cardioverter/defibrillator (ICD) is used to treat patients with life-threatening

recurrent ventricular fibrillation who are unresponsive to medications or pacemakers. Its use has
greatly decreased the mortality from sudden cardiac death. The device senses heart rate,
diagnoses rhythm changes, and treats ventricular dysrhythmias. The ICD generator is implanted
in the subcutaneous tissue over the pectoral muscle. The lead system is placed via a subclavian
vein into the endocardium. The cardioverter recognizes ventricular fibrillation and ventricular
tachycardia and uses the shocks to convert the dysrhythmia to normal sinus rhythm. When the
ICD senses these lethal dysrhythmias, it delivers a shock of up to 35 joules to defibrillate. If the
heart rhythm does not return to normal, the device can continue to deliver shocks. The patient is
instructed to sit or lie down when experiencing a shock and to keep a record of the number of
shocks delivered. Patients report that the shocks feel like a blow to the chest. In addition to
defibrillation, the newer generation of ICDs are also able to function as antitachycardia and
antibradycardia pacemakers, have event memory/retrieval, and are capable of programmed self-
testing.
Complications.
Complications associated with the ICD are inappropriate shocks, broken or displaced leads, and
failure to deliver shocks as a result of battery failure or failure to recognize a dysrhythmia.
NURSING CARE of the Patient with an Implantable Cardioverter/Defibrillator
Nurses can promote psychosocial adaptation in patients with ICDs. The patient may be
concerned with body image change and a fear of shocks. It is important to decrease anxiety about
being shocked. Some patients become very dependent on the machine. These patients and
families need much teaching and support. People who touch the patient during a shock will feel a
tingling sensation, which is not harmful. An established support group for the patient and family
is very helpful. The family must be instructed in cardiopulmonary resuscitation. An identification
bracelet and a card with instructions about the ICD setting are carried at all times. Advise
patients to avoid strong magnetic fields (metal detectors, power plants, MRI). The device and
batteries should be checked every 2 months. Batteries should last 4 to 7 years.
VALVULAR DISEASE
The purpose of the heart valves is to maintain blood flow in one direction. If the valves are
damaged through a congenital defect or acquired disease, their function is compromised.
Stenosis and regurgitation are the two major valve problems. Stenosis is narrowing of the
valvular opening. A stenotic valve limits the amount of blood ejected from one chamber to the
next. Regurgitation, the inability of the valve to close completely, allows the blood to flow
backward when a valve does not close efficiently. The left side of the heart is affected most
often, and the mitral valve is the most frequently affected of all the valves. The pulmonic valve
in the right side of the heart is infrequently affected. Only left-sided valvular disease is discussed
here.
Antibiotics have decreased the incidence of valvular disease from rheumatic fever, but the
incidence of nonrheumatic valvular disease has increased. Longer life span and intravenous drug
abuse are the primary causes of the increasing incidence of nonrheumatic valvular disease.
Mitral Stenosis
Mitral stenosis is a narrowing of the opening in the mitral valve that impedes blood flow from
the LA into the LV. The mitral valve leaflets become thickened and fibrotic. Rheumatic heart
disease is the leading cause of mitral stenosis. Congenital malformations of the mitral valve
occur but are not common. Other causes are calcium accumulation on valve leaflets and atrial
myxomas (tumors).
Pathophysiology
The thickening of the valve structures reduces the outflow of blood from the LA to the LV. The
LA dilates to accommodate the amount of blood not ejected, and left atrial pressure increases. As
left atrial pressure increases, the blood volume backs up into the pulmonary system, increasing
pulmonary pressures. This increases the workload on the right side of the heart, leading to right
ventricular hypertrophy. Eventually, the RV fails, and cardiac output decreases because less
blood is delivered to the LV.
Signs and Symptoms
Symptoms may begin soon after the disease process or may be delayed for many years. Dyspnea,
fatigue, cough, chest pain, and activity intolerance are the most frequent symptoms. Exertional
dyspnea and pulmonary edema occur as blood backs up in the pulmonary system and serous
fluid leaks into the pulmonary tissues. Because stenosis causes turbulent blood flow through the
valve, a murmur is present during diastole (best heard at the apex of the heart).
Medical Diagnosis
Diagnosis is made on the basis of the patient history, physical examination, and results of
diagnostic procedures. The chest radiograph shows left atrial, right ventricular, and pulmonary
vascular enlargement. Echocardiography, often transesophageal echocardiography, is used to
visualize the mitral valve. Cardiac catheterization is used to confirm the diagnosis and determine
the extent of the disease process.
Medical Treatment
When symptomatic, the patient with mitral stenosis is treated as for CHF with drug therapy,
sodium and fluid restrictions, and activity restriction. Digoxin, diuretics, beta-blockers, and
antidysrhythmics may be prescribed. If the patient has atrial fibrillation, anticoagulants also may
be prescribed. Prophylactic antibiotics are prescribed before any invasive procedure for patients
with mitral stenosis because bacteria tend to cluster on the damaged valves.
Surgical Treatment
Surgical treatment includes commissurotomy, mitral valve replacement, and balloon

valvuloplasty. Commissurotomy is excision of parts of the leaflets to enlarge the opening. The
mitral valve may be replaced with a biologic or synthetic valve (Fig. 35-14). Both
commissurotomy and mitral valve replacement require major surgery with cardiopulmonary
bypass.
Balloon valvuloplasty, a procedure done in the cardiac catheterization laboratory, has been very
successful in dilating stenosed heart valves. It is less invasive than valve replacement or
commissurotomy. To dilate the mitral valve, a balloon catheter (like the one used for PTCA) is
threaded from the femoral artery to the mitral valve. The balloon is positioned in the valve and
inflated until the valve opens sufficiently. After the procedure, the patient is observed closely in
an intensive care unit for dysrhythmias and complications. Complications include valve
regurgitation, restenosis, perforation of the myocardium, and, rarely, systemic embolization.
FIGURE 35-14 Types of prosthetic and tissue valves. A, Bileaflet mechanical valve. B, Porcine
heterograft. C, Carpentier-Edwards aortic pericardial valve.
NURSING CARE of the Patient with Mitral Stenosis

Assessment
It is most important to obtain a complete history as summarized in Box 35-1 and a record of
signs and symptoms being experienced. Take the vital signs, and auscultate for heart murmurs.
The murmur of mitral stenosis is described as rumbling and low pitched. It is heard best at the
apex of the heart. The ECG may show a notched P wave, indicating left atrial enlargement.
Atrial fibrillation is frequently seen. Tachycardia and tachypnea are common signs. The pulse
pressure may be decreasing, indicating low cardiac output. Jugular venous distention and
crackles are found with pulmonary congestion.
Nursing Diagnoses, Goals, and Outcome Criteria: Mitral Stenosis
The nursing diagnoses and goals for mitral stenosis are the same as those for CHF and for all
valvular diseases:

Decreased Cardiac Output related to narrowing or Increased cardiac output: normal pulse
insufficiency of valvular competence and blood pressure
Improved gas exchange: clear breath
Impaired Gas Exchange related to pulmonary congestion
sounds, normal arterial blood gases
Improved activity tolerance:
Activity Intolerance related to imbalance between
performance of daily activities without
oxygen supply and demand
excessive fatigue
Fluid Volume Excess related to decreased glomerular Normal fluid balance: no edema, clear
filtration rate, increased aldosterone, sodium and water breath sounds, fluid output equal to or
retention, and increased antidiuretic hormone release exceeds fluid intake
Interventions
See the Nursing Care of the Patient with Heart Failure section on pp. 662 to 665 for the
remainder of the nursing process.
Mitral Regurgitation
Mitral regurgitation (insufficiency) allows blood to flow back into the LA during diastole. The
valve does not close completely because one or both of the valve leaflets becomes rigid and
shortens.
The LA and LV hypertrophy as a result of the backflow of blood against the incompetent valve.
Left ventricular hypertrophy is compensatory in an attempt to maintain cardiac output.
Eventually, the left side of the heart fails, and symptoms are then the same as those with mitral
stenosis.
The murmur of mitral regurgitation is high pitched and blowing and occurs during systole. It is
best heard at the apex and may radiate to the axilla. With severe disease, S3 and S4 sounds may
be auscultated. Atrial fibrillation occurs as the LA enlarges.
Mitral regurgitation is treated with vasodilators to decrease the afterload and therefore the
regurgitation. Other medical treatment includes activity restriction, dietary sodium limitation,
diuretics, and digitalis. Surgical treatment includes annuloplasty and mitral valve replacement.
Annuloplasty is reconstruction of the leaflets and the annulus.
Mitral Valve Prolapse
The mitral valve prolapses when one or both leaflets enlarge and protrude into the LA during
systole. It has a tendency to run in families and may be caused by heart infections, rheumatic
fever, or a wide variety of congenital anomalies. The disease is usually benign but may progress
to mitral insufficiency. Mitral valve prolapse occurs in approximately 3% of the population
(American Heart Association, 2007). Most victims are women 20 to 55 years of age.
In most patients, symptoms do not occur or may occur with stress. Symptoms include chest pain,
palpitations, dizziness, and syncope. Some patients exhibit dysrhythmias. The ECG usually
shows normal findings. Evidence of mitral valve prolapse may be found on echocardiography.
The problem is often controlled with stress-reduction techniques. Beta-blockers may be
prescribed to decrease syncope, palpitations, and severe chest pain. Therapeutic management is
matched to the degree of symptoms.
Aortic Stenosis
Stenosis of the aortic valve occurs when the valve cusps become fibrotic and calcify. It may be
caused by a congenital malformation or result from rheumatic fever, syphilis, or the aging
process (atherosclerosis and calcification). When seen in younger patients, it is most often
caused by a congenital malformation. The aortic valve is most commonly diseased in the aging
population.
Pathophysiology
The valve opening decreases to one-third normal size before symptoms occur. As flow is
impeded through the narrowed valve, the LV hypertrophies to compensate for the extra pressure
needed to eject blood. The LA also compensates by delivering a strong atrial kick. These
compensatory mechanisms allow normal function until atrial fibrillation disrupts the atrial kick
or until the LV hypertrophies to the point of dysfunction, with decreased cardiac output and
myocardial ischemia. With left ventricular dysfunction, blood backs up into the LA and the
pulmonary system. If uncorrected, eventually the right side of the heart fails.
Signs and Symptoms
The patient complains of dyspnea on exertion, angina, and syncope. Fatigue, orthopnea, and
paroxysmal nocturnal dyspnea are late symptoms and indicate heart failure. A systolic murmur
may occur.
Medical Diagnosis
The chest radiograph shows atrial and ventricular enlargement, which are late signs. The murmur
of aortic stenosis is heard best in the aortic area, the second intercostal space to the right of the
sternum. The echocardiogram shows left ventricular wall thickening. An exercise tolerance test
may be ordered to evaluate heart function.
Medical Treatment
Prophylactic antibiotics are prescribed to prevent IE with dental and invasive procedures. Heart
failure is treated with digoxin, diuretics, a low-sodium diet, and activity restriction. Surgical
treatment includes balloon valvuloplasty and aortic valve replacement.
NURSING CARE of the Patient with Aortic Stenosis
Monitor for a bounding arterial pulse and widened pulse pressure. The nursing process is the
same as for HF (see Nursing Care Plan: The Patient with Heart Failure on p. 663).
Aortic Regurgitation
Fibrosis and thickening of the aortic cusps progress until the valve no longer maintains
unidirectional blood flow. Aortic regurgitation (insufficiency) is caused primarily by rheumatic
fever. Other causes include IE, blunt chest trauma, calcification of the valve, and chronic
hypertension.
Regurgitation of blood into the LV during diastole increases the amount of blood in the LV. The
LV dilates and hypertrophies. Myocardial ischemia and left ventricular failure occur. Blood
backs up into the pulmonary system and eventually right ventricular failure occurs.
The murmur of aortic regurgitation is high pitched and blowing and occurs in diastole. It is
auscultated best at the aortic area. The point of maximal impulse may be shifted to the left and
down. Tachycardia and palpitations are compensatory mechanisms. Later signs of HF such as
fatigue, dyspnea, and ascites develop. A widened pulse pressure (increased difference between
systolic and diastolic pressures) results from a low diastolic pressure. S3 and S4 sounds are often
auscultated.
Left atrial and ventricular dilation are noted on chest radiography. The echocardiogram shows
left ventricular dilation. Cardiac catheterization is used to determine the extent of incompetence.
As with other patients with valve disease, these patients have prophylactic antibiotics prescribed
before invasive procedures. Digoxin and diuretics are prescribed for left ventricular hypertrophy.
Aortic valve replacement provides long-term correction.
ELECTROCARDIOGRAM MONITORING
Nurses working in critical care areas are responsible for monitoring and interpreting ECGs.
Patients usually are monitored continuously at the bedside and have intermittent monitoring
through a 12-lead ECG.
12-LEAD ELECTROCARDIOGRAM
A 12-lead ECG looks at the heart from 12 directions or perspectives. This permits more precise
evaluation of the heart's electrical activity. Three leads are placed on the limbs (leads I, II, and
III), three leads are augmented (aVR, aVL, and aVF), and there are six chest, or precordial, leads
(V1 to V6). Electricity flows from the negative to the positive lead. If the depolarization wave
flows toward the positive pole (electrode), the deflection is upright. If the wave flows away from
the positive pole, the deflection is negative.
CONTINUOUS MONITORING
For continuous ECG monitoring, only one or two single leads are used. Most units that perform
continuous monitoring use the five-lead system with four limb electrodes and a chest electrode
(which is placed at one of the V lead sites). The electrodes are held in place by adhesive pads.
Thoroughly clean the electrode sites before applying the pads. Change the pads according to
agency policy. Monitor the skin for irritation or breakdown. The lead monitored depends on the
purpose of the monitoring (e.g., detect dysrhythmias, detect ischemia).
INTERPRETATION OF ELECTROCARDIOGRAMS
To interpret an ECG strip, the reader is referred to Figure 35-15. The graph paper consists of
horizontal and vertical small and large squares. The horizontal axis measures time; the vertical
axis measures voltage. Each small square represents 0.04 second on the horizontal axis and 1
mm on the vertical axis. Each large square, bounded by heavy lines, is made up of five small
squares and represents 0.20 second and 5 mm. The electrical activity of the heart is represented
by deflections, positive and negative, from the baseline. A deflection is an upward or downward
movement from the baseline. The baseline is called the isoelectric line. The first positive
deflection (upward movement) is the small, rounded P wave that represents atrial depolarization.
The second positive deflection is the peaked QRS complex that represents ventricular
depolarization. The Q is the first negative deflection, meaning the line moves below the
isoelectric line. The R wave corresponds to the patient's pulse. Atrial repolarization occurs
during ventricular depolarization and is obscured by the QRS complex. The third deflection is
the rounded T wave, which represents ventricular repolarization. The fourth deflection, if
present, is the U wave. It is small, rounded, and usually indicates electrolyte imbalance
(hypokalemia).
The PR interval represents the time it takes the impulse to travel from the atria through the AV
node to the ventricles. The PR interval is measured from the beginning of the P wave to the Q
wave. The normal PR interval is from 0.12 to 0.20 second. The QRS complex is measured from
the point at which the Q leaves the isoelectric line to the point at which the S returns to the
isoelectric line. The normal QRS complex is 0.06 to 0.10 second. The ST segment represents the
time from ventricular depolarization to ventricular repolarization. The ST segment should be
along the isoelectric line. The QT segment represents ventricular refractory time. It is measured
from the beginning of the QRS complex to the end of the T wave. The normal QT segment time
range varies with heart rate; therefore it is necessary to compare the QT obtained with a table
(QT tables are available in most textbooks dealing with dysrhythmias). The QT segment is
affected by age, gender, and heart rate.
FIGURE 35-15 Relationship between the cardiac cycle and the heart sounds.
Criteria for Interpreting Electrocardiograms
Criteria have been established for interpreting an ECG strip. The ECG is evaluated for rate,
regularity, P waves, PR interval, and QRS complexes (Table 35-8).
Rate Calculation.
Most ECG strips have tic marks indicating 3-second time periods. There are several ways to
calculate heart rate from the ECG strip. The quickest but least accurate method is to count the
number of P waves (for atrial rate) or R waves (for ventricular rate) in a 6-second strip (between
3 tic marks or 30 large squares) and multiply by 10 for the estimate of the number of beats per
minute. For example, if there are six R waves in a 6-second strip, the heart rate is 60 bpm.
The more accurate method uses the number of small squares between two P waves (atria) or two
R waves (ventricles). Divide 1500 by the number of small squares. For example, if there are 25
small squares between two R waves, the rate is 60 bpm (1500 divided by 25). The atrial rate is
determined by the number of P waves and the ventricular rate by the number of QRS complexes.
The normal rate is from 60 to 100 bpm.
Rhythm.
The consecutive P-P intervals for the atria and the consecutive R-R intervals for ventricles are
measured for consistency. Using calipers or a blank piece of paper, note the distance between R
waves. If the distances do not vary more than one small square, the rhythm is considered regular.
If the distances are greater than one small square, the rhythm is irregular.
Table 35-8 Criteria for Electrocardiogram Interpretation

Are the atrial and ventricular rates the same as measured by the P-P and R-R
Rate
intervals?
Is the rate regular or irregular? If irregular, is there a pattern? Are these ectopic
Rhythm
beats? Where do they occur?
Is there a P wave before every QRS complex? Does each P wave have the same
P waves
size and shape?
PR interval Are all the PRIs the same length? If not, is there a pattern to the irregularity? Are
(PRI) the PRIs within normal range?
QRS Do all the QRS complexes look alike? Are all the QRS complexes within the
complexes normal range (0.06-0.10 sec)?
ST segment Is the ST segment isoelectric, depressed, or elevated?
T waves Do all the T waves look alike? Are the T waves upright or inverted?
FIGURE 35-16 Normal sinus rhythm. Each segment between the dark lines (above the monitor
strip) represents 3 seconds, when the monitor is set at a speed of 25 mm/sec. Characteristics:
Rate—60 to 100 bpm; Regularity—essentially regular (P-to-P and R-to-R intervals are regular
with only minor variation); P wave, PR interval—there is a P before every QRS; each P wave is
the same size and shape; PR interval is between 0.12 and 0.20 sec; QRS—falls between 0.06 and
0.10 sec; T wave—rounded, all the same shape. Interpretation: Normal sinus rhythm.
P Waves.
The next evaluation is of P waves. Is there a P wave before each QRS complex? If so, the rhythm
originates in the SA node. Do all the P waves appear the same size and shape? If so, the impulse
originates in the SA node.
PR Interval.
Does the PR interval fall within the normal range of 0.12 to 0.20 second? If so, there is no
interference in conduction from the SA to the AV node.
QRS Complex.
Does the QRS complex fall within the 0.06- to 0.10-second range? If the QRS is prolonged (0.12
second or greater), there is a delay in conduction through the ventricles.
ST Segment.
Examine the ST segment. Is it isoelectric? Or is it depressed or elevated?
T Waves.
Are the T waves rounded and the same size and shape? Do the T waves follow the QRS
complexes?
QT Interval.
Measuring the QT interval is not always part of dysrhythmia interpretation. The QT interval, if
measured, should be compared with the QT interval table. The QT interval may be affected by
electrolyte imbalances and drugs.
Normal Sinus Rhythm
The most common cardiac rhythm is sinus in origin because the impulse originates in the SA
node, is conducted normally, and meets all of the criteria established earlier. Normal sinus
rhythm is displayed in Figure 35-16.
Common Dysrhythmias
A dysrhythmia is a disturbance of the rhythm of the heart caused by a problem in the conduction
system. Dysrhythmias are categorized according to the site of the origin of the impulse
formation. Dysrhythmias originating in the atria are called atrial dysrhythmias. Dysrhythmias
originating in the AV node are called junctional or escape rhythms. Dysrhythmias originating
below the AV node are called ventricular. Blocks are interruptions in impulse conduction.
Dysrhythmias and blocks have characteristics that are noted on the ECG. See Figures 35-17
through 35-30 for examples. Antidysrhythmic drugs are used to treat dysrhythmias and restore
normal sinus rhythm.
HEMODYNAMIC MONITORING
In addition to noninvasive cardiac assessment and ECG monitoring, more sophisticated measures
may be needed to determine what is going on within the heart or vascular system. Nurses who
work in intensive care areas frequently work with patients who have central venous catheters,
pulmonary artery catheters, or arterial lines.
FIGURE 35-17 Sinus bradycardia. Characteristics: Rate—less than 60 bpm; Regularity—

normal; P wave, PR interval—normal; QRS—normal; T wave—normal. Interpretation: All
characteristics are within normal ranges except for the rate, which is slow. Causes: Drugs,
including digitalis and beta-blockers, vagal stimulation (Valsalva maneuver), severe pain,
hyperkalemia, infection, and myocardial infarction. Frequently seen in athletes as a result of
conditioning. Symptoms: Dizziness, syncope, chest pain, hypotension, sweating, nausea,
dyspnea, and disorientation; sometimes no symptoms. Treatment: Not treated unless the patient
is symptomatic. The underlying cause is treated. Atropine may be given to increase the heart
rate. Isoproterenol is used with extreme caution. A pacemaker may be needed.
FIGURE 35-18 Sinus tachycardia. Characteristics: Rate—greater than 100; usually less than 150
bpm; Regularity—regular; P wave, PR interval—P waves may be buried in T wave of preceding
beat with very rapid rates, more than 140 bpm; QRS—normal; T wave—normal. Interpretation:
All characteristics are within normal range except for the rate, which is excessive. Causes: Fever,
dehydration, hypovolemia, increased sympathetic nervous system stimulation, stress, exercise,
and acute myocardial infarction. Symptoms: Palpitations most common. Angina and decreased
cardiac output from the decreased ventricular filling time may also occur. Treatment: Correction
of underlying cause. Elimination of caffeine, nicotine, and alcohol. Vagal stimulation may
decrease the rate but does not treat the cause. Treatment: Beta-blockers.
CENTRAL VENOUS CATHETER
The central venous catheter is placed through the skin, into a venous access (brachial, femoral,
subclavian, or jugular sites), and threaded into the RA. The catheter may have one to three
lumens. With this catheter, the pressure in the RA (called right atrial pressure [RAP] or central
venous pressure [CVP]) can be measured. This measurement is used as an indication of fluid
volume. The normal CVP or RAP is 2 to 6 mm Hg. Measurements below normal indicate
hypovolemia, and measurements above normal indicate hypervolemia. This catheter may also be
used to infuse fluids, blood and blood products, and medications as well as to withdraw blood for
analysis.
PULMONARY ARTERY CATHETER
The pulmonary artery (PA) catheter, frequently called a Swan-Ganz catheter, is longer than the
central venous catheter. It is inserted like the central venous catheter and is threaded through the
RA, the tricuspid valve, the RV, the pulmonic valve, and into the pulmonary artery. The catheter
is balloon tipped and flows with the blood. Different waveforms are seen on an oscilloscope as
the catheter moves through the different areas of the heart. Pulmonary artery catheters have
multiple lumens and are approximately 110 cm (44 inches) long. Various lumens are used to
measure the pulmonary capillary wedge pressure, inflate the balloon, measure RAP, determine
cardiac output, and administer fluids and drugs. Newer catheters incorporate fiberoptics for
continuous monitoring of saturated venous oxygenation (SvO2), a measure of tissue perfusion or
continuous cardiac output.
FIGURE 35-19 Sinus dysrhythmia. Characteristics: Rate—normal; Regularity—slightly

irregular, varies with respirations; P wave, PR interval—P-to-P intervals vary, the difference
between the shortest and longest P-to-P interval is greater than 0.12 sec; the PR interval is
normal; QRS—normal; T wave—normal. Interpretation: The rate varies with respirations.
Considered normal when the rhythm varies in relation to the respiratory cycle: The R-to-R
interval is shorter during inspiration; therefore the rate is increased; the R-to-R interval is longer
during expiration; therefore the rate is decreased. Causes: When unrelated to respirations, is
often the result of digoxin toxicity, increased intracranial pressure, or inferior wall myocardial
infarction. In older adults, marked variation may indicate a condition known as sick sinus
syndrome. Symptoms: Usually none. Treatment: If treatment is necessary, atropine is used and
the underlying problem is treated.
FIGURE 35-20 First-degree atrioventricular (AV) block. Characteristics: Rate—normal;

Regularity—regular; P wave, PR interval—all P waves are conducted to the ventricles, but AV
conduction is prolonged through the AV node; PR interval is greater than 0.20 sec and constant;
QRS—normal; T wave—normal. Interpretation: The PR interval is prolonged. Causes: Increased
vagal tone, coronary artery disease, digoxin toxicity, heart infections, and quinidine. Symptoms:
Usually none, may be bradycardic. Treatment: Correction of underlying cause.
The purpose of a pulmonary artery catheter is to measure right-sided heart pressures and
pulmonary artery pressures and to assess left-sided heart function. The proximal port is used to
measure the RAP or CVP (normal value, 2-6 mm Hg). The distal port measures the pulmonary
artery pressure (normal value, 20-30/0-10). The lungs are low-pressure organs unless the patient
has COPD.
The pulmonary capillary wedge pressure is used to assess the function of the left side of the
heart. To determine the pulmonary capillary wedge pressure, the balloon is inflated with up to
1.5 mL of air. This allows the tip of the catheter to float into a pulmonary capillary until it
occludes the capillary. This measures the pressure ahead of the catheter, therefore the left
ventricular heart function. The normal pulmonary capillary wedge pressure is 4 to 12 mm Hg.
Once the pressure is recorded, the balloon is deflated. This pressure is lower when fluid is
restricted, when diuretics are being administered, and when patients are receiving vasodilators
such as nitroglycerin or morphine. The pressure is elevated with excess fluid, when fluid volume
expanders such as albumin, dextran, or hetastarch are being administered, or in left heart
dysfunction.
FIGURE 35-21 Second-degree atrioventricular block: type I (Mobitz I; Wenckebach).

Characteristics: Rate—atrial rate is greater than ventricular rate; Regularity—atrial rate is
regular; ventricular rate is irregular; P wave, PR interval—there are more P waves than QRS
complexes; the PR interval increases until a P wave is not followed by a QRS; QRS—some are
absent; T wave—absent when the QRS is dropped. Interpretation: Progressively lengthening PR
interval and a dropped beat. Causes: Myocardial ischemia with progressive increase in
conduction time through the sinoatrial node, inferior wall myocardial infarction, digoxin toxicity,
and electrolyte imbalance. Symptoms: Decreased blood pressure and syncope, if any. Treatment:
Atropine, pacemaker.
Cardiac Output
With a pulmonary artery catheter in place, cardiac output can be measured continuously or by the
thermodilution method. The normal cardiac output is 4 to 8 L/min. Stress increases the cardiac
output. Cardiac output may decrease with AMI, HF, bradycardia, tachycardia, and some drugs. It
is important for the nurse to use consistent technique in measuring cardiac output.
Mixed Venous Oxygen Saturation
PA catheters may have sensors in place that allow for measurement of mixed venous oxygen
saturation (SvO2) or, if the sensor is not part of the catheter, a blood sample can be obtained from
the distal port (which opens in the pulmonary artery). Blood in the pulmonary artery is the blood
returned from all of the organs and tissues in the body and mixed in the PA. When the oxygen
saturation of this mixed venous blood is measured (in a laboratory or through fiberoptics), the
results reflect the degree of oxygen use by the body tissues. SvO2can be decreased when oxygen
delivery is decreased or the body has increased the use of oxygen (fever, pain, stress). SvO2can
be increased when oxygen delivery is increased or when oxygen utilization is decreased
(hypothermia, general anesthesia). Normal SvO2is 60% to 75%.
FIGURE 35-23 Third-degree atrioventricular (AV) block. Characteristics: Rate—atrial rate is

faster than ventricular rate; ventricular rate is generally less than 45 bpm; Regularity—irregular;
P wave, PR interval—no relationship exists between the P waves and the QRS complexes; QRS
—atria and ventricles are beating independently; the QRS is ventricular in origin; T wave—
normal. Interpretation: Impulses originating in the sinoatrial node are blocked at the AV node.
The ventricles respond to a secondary pacemaker. Causes: Digoxin toxicity, conduction damage
during mitral valve replacement, hypoxia, and rheumatic fever. Symptoms: Hypotension,
syncope, decreased cardiac output. The underlying cause is treated. Treatment: Atropine,
pacemaker, isoproterenol with extreme caution. Do not administer lidocaine, which could
suppress ventricular response.
ARTERIAL LINE
An arterial line may be inserted (most often in the radial artery) to provide a direct measurement
of systolic and diastolic blood pressures. Once the line is inserted, it is connected to a pressurized
solution to keep the catheter patent and to a transducer to assess pressure. The mean arterial
pressure is an indication of tissue perfusion. This pressure is elevated with sympathetic
stimulation and increased heart rate.
Key Points
 • The primary function of the heart is to pump blood through the pulmonary and systemic
circulation.
 • The heartbeat has two phases: systole (contraction) and diastole (relaxation).
 • Cardiac output is the amount of blood ejected per minute by each ventricle; stroke
volume is the amount of blood ejected by a ventricle in a single contraction. The factors
that affect stroke volume are preload, contractility, and afterload.
 • The heart sounds are “lub,” heard during systole, and “dub,” heard during diastole.
 • The most common cardiac surgical procedures are pacemaker insertion, valve repair or
replacement, and coronary artery bypass surgery.
 • Nursing concerns after cardiac surgery include Ineffective Breathing Pattern, Acute
Pain, Ineffective Thermoregulation, Decreased Cardiac Output, Risk for Infection, and
Anxiety.
 • Pacemakers are electronic devices that deliver impulses to stimulate contraction of the
myocardium.
 • Coronary artery disease is treated with drug therapy, diet modifications, lifestyle
modifications, surgical intervention, or a combination of these.
 • Risk factors for atherosclerosis are age, gender, race, heredity, diabetes mellitus with
elevated blood glucose, increased serum lipids, nicotine, hypertension, obesity, sedentary
lifestyle.
 • Angina pectoris is the pain that results from myocardial ischemia. It is treated with
vasodilators and rest.
 • Procedures used to improve myocardial blood flow include percutaneous coronary
balloon angioplasty, laser angioplasty, atherectomy, stent placement, coronary artery
bypass grafts, and transmyocardial laser revascularization.
 • Acute myocardial infarction, caused by partial or complete occlusion of a coronary
artery, can lead to dysrhythmias, heart failure, cardiogenic shock, thromboembolism, and
ventricular aneurysm/rupture.
 • Nursing care of the patient with myocardial infarction addresses Anxiety, Acute Pain,
and Decreased Cardiac Output.
 • Patients with acute cardiac conditions often have continuous cardiac monitoring to
detect potentially fatal dysrhythmias for prompt treatment.
 • Cardiac rehabilitation begins with a cardiac incident, lasts throughout life, and includes
the patient and family in teaching about exercise, diet, and medications.
 • Heart failure, the inability of the heart to meet the metabolic demands of the body, may
be caused by disorders that increase the heart's workload or interfere with its pumping
action.
 • Treatment of heart failure may include correction of underlying causes, drug therapy to
improve cardiac function and eliminate excess fluid, and measures to decrease demands
on the heart.
 • Complications of heart failure are dysrhythmias, pulmonary edema, and cardiogenic
shock.
 • Nursing care of the patient with heart failure focuses on Fluid Volume Excess, Impaired
Gas Exchange, Anxiety, Decreased Cardiac Output, and Activity Intolerance.
 • Cardiac inflammatory conditions (endocarditis and pericarditis) are treated with drug
therapy and rest.
 • Cardiomyopathy is a disease of the heart muscle that is treated with supportive
measures but may lead to heart failure that eventually requires cardiac transplantation.
 • Patients who have received heart transplants require immunosuppressive drugs for the
remainder of their lives to prevent rejection of the foreign tissue.
 • Signs and symptoms of cardiac transplant rejection are fever, dyspnea, fatigue, and
dysrhythmias.
 • An implantable cardioverter/defibrillator is an im-planted device that monitors cardiac
activity, detects life-threatening dysrhythmias, and delivers a shock to convert the rhythm
to a normal one.
 • The primary disorders of the heart valves are stenosis, which interferes with blood
movement from one chamber to the next, and regurgitation, which allows blood to flow
backward.
 • Valve disease may be treated with drug therapy to improve cardiac function, with
balloon valvuloplasty to dilate stenosed valves, with commissurotomy to enlarge the
opening, and with valve replacement using a biologic or synthetic valve.
 • General measures to maintain perfusion of vital organs are modified Trendelenburg's
position, oxygen, intravenous fluids, and drugs to maintain or restore blood pressure.
 • A dysrhythmia (also called an arrhythmia) is a disturbance of the heart rhythm caused
by a problem in the conduction system.
REVIEW QUESTIONS Choose the best answer
 1. Normally, the impulse that stimulates a myocardial contraction begins in the:

o 1.AV node
o 2.Bundle of His
o 3.Purkinje cells
o 4.SA node
 2. Which statement correctly describes one of the three factors that affect stroke volume?
o 1.Contractility is the ability of cardiac muscle fibers to shorten and produce a
muscle contraction.
o 2.Preload is the amount of blood remaining in the atria at the end of diastole.
o 3.Cardiac output is the amount of blood ejected by the heart with each ventricular
contraction.
o 4.Afterload is the amount of blood remaining in the ventricles at the end of
systole.
 3. Which of the following age-related changes in the circulatory system can cause heart
murmurs?
o 1.Decreased elasticity of connective tissue in the heart muscle
o 2.Arterial stiffening caused by changes in connective tissue and elastic fibers
o 3.Heart valves that are stiff and do not close properly
o 4.Stretching and dilation of veins resulting in impaired venous return
 4. Before administering digoxin, you count a patient's apical heart rate and find that it is
62 bpm. The patient's usual rate ranges from 65 to 75 bpm. What should you do?
o 1. Withhold the digoxin and notify the physician.
o 2. Administer the digoxin and document the heart rate.
o 3. Hold the drug and recheck the heart rate in an hour.
o 4. Give half of the prescribed dose of digoxin.
 5. An adverse effect common to all antidysrhythmic drugs is:
o 1.Fluid and electrolyte imbalance
o 2.Drowsiness
o 3.Diarrhea
o 4.Additional dysrhythmias
 6. The usual dietary recommendations for cardiac patients include the following:
o 1.No more than 10% saturated fats
o 2.Low fiber and carbohydrates
o 3.Sodium restricted to 1 g/day
o 4.20% or less of total fat intake
 7. Risk factors for atherosclerosis that can be modified include the following:
o 1. Gender
o 3. Heredity
o 2. Race
o 4. Sedentary lifestyle
 8. Characteristics of angina pectoris include that it:
o 1.Most often occurs at rest
o 2.Is accompanied by drop in blood pressure
o 3.Is usually substernal but may radiate
o 4.Is commonly treated with digitalis
 9. Which of the following drugs may be administered after acute myocardial infarction to
dissolve thrombi?
o 1.Heparin
o 2.Tissue plasminogen activator
o 3.Aspirin
o 4.Lidocaine
 10. When cardiac output falls, compensatory mechanisms include the following:
o 1. Elimination of excess fluid by the kidneys
o 2. Dilation of blood vessels in the extremities
o 3. Stimulation of the parasympathetic nervous system
o 4. Enlargement of the ventricular myocardium
 11. Discharge teaching for a patient with heart failure should include instructions to:
o 1.Immediately begin a vigorous program of exercise
o 2.Inform the physician if you gain more than 2 pounds in a week
o 3.Weigh yourself before going to bed each night
o 4.Expect to continue having shortness of breath, chest pain, and cough
 12. Before invasive procedures including dental work, patients with valvular heart
disease usually are prescribed antibiotics to prevent:
o 1.Pericarditis
o 2.Abscess formation
o 3.Infective endocarditis
o 4.Cardiomyopathy
 13. A patient who has had heart transplantation comes into the physician's office
complaining of fever, fatigue, shortness of breath, and an irregular heart beat. You should
suspect:
o 1. Infection in the surgical wound

o 2. Congestive heart failure
o 3. Rejection of the transplanted heart
o 4. Postoperative anxiety and depression
 14. Which of the following findings would you expect in a patient with mitral stenosis?
o 1.Increased left atrial pressure
o 2.Decreased pulmonary pressure
o 3.Increased cardiac output
o 4.Decreased right ventricular pressure

CHAPTER 35 Cardiac Disorders

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CHAPTER 35 Cardiac Disorders

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CHAPTER 35 Cardiac Disorders

 1. Label the major parts of the heart.

ANATOMY AND PHYSIOLOGY OF THE HEART

FIGURE 35-1 Anatomic location of the heart.

FIGURE 35-2 Normal circulation through the heart.

CORONARY BLOOD FLOW

FIGURE 35-3 Coronary arteries and veins.

FIGURE 35-4 The conduction system of the heart.

Table 35-1 Intrinsic Heart Rates

Three factors affect stroke volume: preload, contractility, and afterload.

Myocardial Oxygen Consumption

Health Promotion Considerations

NURSING ASSESSMENT OF CARDIAC FUNCTION

Chief Complaint and History of Present Illness

 1.A rate of 60 to 100 bpm

Even more sophisticated monitoring is accomplished by transtelephonic means. An audio signal

DIAGNOSTIC TESTS and PROCEDURES The Heart

The patient lies on a firm pad All metal must be

Clanging sounds are heard as

Radioactive material is injected Nothing by mouth

ECHOCARDIOGRAM (HEART SONOGRAM)

At times, the echocardiogram is not diagnostic and a transesophageal echocardiogram (TEE) is

MAGNETIC RESONANCE IMAGING

A magnetic resonance imaging (MRI) scan provides high-resolution, three-dimensional images

MULTIPLE-GATED ACQUISITION SCAN

STRESS TEST (EXERCISE TOLERANCE TEST)

ULTRAFAST COMPUTED TOMOGRAPHY

Ultrafast CT (also known as electron-beam CT or EBCT) is a fast form of imaging technology

CARDIAC CATHETERIZATION (CARDIAC ANGIOGRAPHY, CORONARY

Complications of cardiac catheterization include bleeding, hematoma formation, infection, and

FIGURE 35-6 Right-sided (A) and left-sided (B) heart catheterization.

FIGURE 35-7 Pulse oximeter. A, Ear probe. B, Clip on finger.

Cardiac Protein Markers

Complete Blood Count

White Blood Cell Count.

Red Blood Cell Count.

Table 35-5 Complete Blood Count

Platelet (Thrombocyte) Count.

Health Promotion Considerations

B-type Natriuretic Peptide

COMMON THERAPEUTIC MEASURES

Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors (ACEI) work against the renin-angiotensin-

DRUG THERAPY Cardiovascular Drugs

Teach the patient:

• Take radial pulse for 1 min at the

Teach the patient:

• Sit or lie down at onset of chest

• Place tablet under tongue; tablet

• Repeat q 5 min for total of three

• Keep tablets in containers in which

supplied; drug decomposes on

• Headache decreases with tolerance.

• Drug may be taken before activities

• Take 1-2 hr before meals and at

• Sit when taking the sublingual or

• Alcohol potentiates hypotension.

• If three sublingual or chewable

• Take radial pulse for 1 min.

• Do not discontinue this drug

blocker. Decreases HR, myocardial Teach the patient:

• While on this drug, use alcohol only

• There is not the normal increase in