HEART FAILURE

HD Despite aggressive medical and surgical treatment, C ure. may eventually lead to the development of
heart failue

Heart failure is a physiologic state in which the heart can not pump enough blood to meet the metabolic
needs of the body (determined as oxygen consumption). Heart fail.

ure results from changes in systolic or diastolic function of the left ventricle. The heart fails when,
because of intrinsic

disease or structural defects, it cannot handle a normal blood volume or, in the absence of disease,
cannot tolerate a sudden expansion in blood volume (e.g., during exer cise). Heart failure is not a
disease itself; instead, the term refers to a clinical syndrome characterized by manifesta tions of volume
overload, inadequate tissue perfusion, and poor exercise tolerance. Whatever the cause, pump failure
results in hypoperfusion of tissue, followed by pul- monary and systemic venous congestion. Because
heart failure causes vascular congestion, it is often called conges tive hearn failure, although most
cardiac specialists no lon

ger use this term. Other terms used to denote heart failure

failure, cardiac decompensation,

Heart ilure affects bout 5 million people in the year. In contrast to decreases in mortality associated with

cardiac insufficiency, and ventricular failure.

inclu chronic hea

ted States, with 00,000 new cases diagnosed each

other cardiovascular diseases, the incidence of heart fail ure and the mortality associated with it have
increased steadily since 1975. Annually about 300,000 clients die
from direct or indirect consequences of heart failure,

and the number of deaths attributed to heart failure has increased six-fold over the past 40 years. Heart
failure can affect both women and men,

although the mortality is higher among women. There are also racial differences; at all ages death rates
are higher in African Americans than in non-Hispanic whites. Heart failure is primarily a disease of older
adults,

affecting 6% to 10% of those older than 65. It is also the leading cause of hospitalization in older people.

bobho

Heart failure is caused by conditions that weaken or

Etiology and Risk Factors

lamage the myoc cardium. Heart failure can be caused

originating from the heart (i.e., intrinsic dis- ev Ppathology) or from external factors that place

by factors orig

sive demands upon the heart. Etiologies of heart failure are shown in Table 56-1.

Intrinsic Factors The most common cause of heart failure is coronary artery disease. CAD reduces blood
flow through the coronaary arteries and therefore reduces oxygen delivery to the myo-

cardium. Without oxygen, the muscle cells cannot function. Another common cause of heart failure is
myocardial
infarction (MD. During MI, myocardium is starved of blood, and the tissue dies and therefore cannot
contract. The

remaining myocardium must compensate for the loss of tis- Sue. Other intrinsic causes of heart failure
incude valve dis- case, cardiomyopathy, and dysrhythmias.

Certain conditions externally compress the heart, thereby Iimiting ventricular fRlling and myocardial con
tractility, Disorders that greatly restrict cardiac chamber filling and myocardial fiber stretch include
constrictive pericarditis, an inflammatory and fibrotic process of the pericardial sac; and cardiac
tamponade, which involves the accumulation of fluid or blood within the pericardial sac. Because the
pericardium encloses all four heart chambers, compression of the heart both decreases dia- stolic
relaxation, thereby elevating diastolic pressure, and hampers forward blood flow through the heart.

Extrinsic Factors

Factors external to the heart include increased afterload

(e.g, hypertension), increased stroke volume from hypervolemia or increased preload, and increased
body demands (high output failure; e.g., thyrotoxicosis, preg nancy). The weakened myocardium cannot
tolerate the usual changes in the volume of blood entering the left ventricle. These conditions include
abnormal volumes

of blood reaching the left ventricle (called a load), abnormal muscle in the ventricle from scarring after

injury, and problems that reduce the contractility of the heart muscle. They will be examined in more
detail Abnormal loading occurs when either the pressure or the volume of blood in the ventricle
increases. The effect

of increasing volume on the ventricle can be explained by the analogy that the heart muscle is like a
stretched rubber band. When the rubber band is stretched, it con-

tracts with more force. The heart muscle does the same.
Venous return stretches the heart and improves contrac- tility. When the rubber band is overstretched,
however, it becomes limp and cannot contract. Likewise, when the heart is overloaded with blo0d,
excessive stretch and decreased Contraction occur. Overload develops because blood does not leave the
ventricles during con- traction. Therefore the workload on the heart increases in an effort to move
blood. Loading, called preload and afterload, can occur in normal or abnormal conditions. Preload can
be defined as the initial stretching of the cardiac muscle fiber length before contraction. Changes in
ventricular preload dramatically affect ventricular stroke volume by what is called the Frank-Starling
mechanism. Increased preload increases stroke volume, whereas decreased preload decreases stroke
volume by altering the force of contraction of the cardiac muscle. Preload, therefore, is related to the
sarcomere length, but since sar Comere length cannot be determined in the intact heart, other indices
of preload are used such as ventricular end- diastolic volume or pressure. For example, when venous
return is increased, the end-diastolic pressure and volume of the ventricle are increased, which
stretches the sarco- meres increases their preload). As another example, hypovolemia resulting from a
loss of blood by hemorrhage leads to less ventricular filling and therefore shorter sarco mere lengths
(reduced preload). Increased pressure load in the ventricde is related to afterload, the amount of ten-
sion the heart must generate to overcome systemic pres- sure and to allow adequate ventricular
emptying. Thus afterload indicates how hard the heart must pump to force blood into circulation. The
tone of systemic arterioles, the elasticity of the aorta and large arteries, the size and thick- ness of the
ventricle, the presence of aortic stenosis, and the viscosity of the blood all determine afterload. High
peripheral vascular resistance and high blood pressure force the ventricde to work harder to eject
blood. Subjected to prolonged high pressures, the ventricle eventually fails.

Pathophysiology The healthy heart can meet the demands for oxygen deliv ery through the use of
cardiac reserve, Cardiac reserve is the heart's ability to increase output in response to stress. The normal
heart can increase its Output up to five times the resting level. The failing heart, even at rest, however,
is pumping near its capacity and thus has lost much of its reserve. The compromised heart has a limited
ability to respond to the body's needs for increased output in situa-

tions of stress. When cardiac output is not sufficient to meet the meta- bolic needs of the body,
compensatory mechanisms, including neurohormonal responses, become activated. These mechanisms
initially help to improve contraction and maintain integrity of the circulation, but if continued lead to
abnormal cardiac muscle growth and reconfigura-

tion (remodeling) of the heart. The compensatory res- ponses to a decrease in cardiac output are
ventricular dilation, increased sympathetic nervous system stimula- tion, and activation of the renin-
angiotensin system. Fig- ure 56-5 depicts the pathophysiology of heart failure in an algorithm.

Ventricular Dilation Ventricular dilation reters to lengthening of the muscle fibers that increases the
Volume in the heart chambers
Dilation causes an increase in preload, and thus card rdiac output, because a stretched muscle contracts
more forc fully (Starling's law); however, dilation has limits as a compensatory mechanism. Muscle
fibers, if stretched beyond a certain point, become inetfective. Second, a dilated heart requires more
oxygen. Thus the dilated heart with a normal coronary blood flow can suffer from a lack of oxygen.
Hypoxia of the heart further decreases the muscle's ability to contract.

ob

odounsrbn

Increased Sympathetic Nervous System Stimulation Sympathetic adrenergic stimulation produces

arteriolar Constriction, tachycardia, and increased myocardial con tractility, all of which work to increase
cardiac output and

improve delivery of oxygen and nutrients to tissues. Arte

rial baroreceptors are important components of this response. This compensatory effect occurs at the
cost o f ad) and

increasing peripheral vascular resistance (afterload) and pathetic

myocardial workload, however. n addition, sympathe

stimulation reduces renal blood flo and stimulates the

renin-angiotensin system. Stimulation of the Renin-Angiotensin System

When blood flow through the renal artery is lecreased,

the baroreceptor reflex is stimulated and enin is released

into the bloodstream. Renin interacts with angiotens gen to produce angiotensin I. When angiotensin Ic
tacts ACE, it is converted to angiotensin II, a potent vasoconstrictor. Angiotensin II increases arterial
vasoe striction, promotes the release of norepinephrine from sympathetic nerve endings, and stimulates
the adrenal medulla to secrete aldosterone, which enhances sodium and water absorption. Stimulation
of the renin-angioten sin system causes plasma volume to expand and preload

to increase.

bs

Cardiac compensation exists when the initial compen- satory mechanisms of ventricular dilation,
sympathetic ner vous system stimulation, and renin-angiotensin system stimulation succeed in
maintaining an adequate cardiac output and oxygen delivery to the tissues in the presence of pathologic
changes. Once cardiac output is restored,

the body produces counter-regulatory substances that

restore cardiovascular homeostasis. If underlying patno logic changes are not corrected, prolonged
activation o

the Compensatory mechanisms eventually leads to

changes in the function of the myocardial cell and ex cess

production of the neurohormones. These proces responsible for the transition from compensated to uc
pensated heart failure. At this point manifestations Ot failure develop because the heart cannot
maintaina

are
quate circulation.

When compensatory mechanisms fail, the amount

of

blood remaining in the left ventricle at the end of d

liastole increases. This increase in residual blood in turn de the ventricle's capacity to receive blood from
the lete a

he left atrium.

The left atrium, having to work harder to eject blood, dilates and hypertrophies. It is unable to receive
the full amount of incoming blood from the pulmonary veins, and left atrial pressure increases; this
leads to pulmonaryy edema (Figure 56-6). Left ventricular failure LVF) results. The right ventricle,
because of the increased pressure in the pulmonary vascular system, must now dilate and hypertrophy
to meet its increased workload. It too eventu- ally fails. Engorgement of the venous system then extends
backward to produce congestion in the gastrointestinal tract, liver, viscera, kidneys, legs, and sacrum;
edema is the main manifestation. Right ventricular failure (RVE) results. RVF usually follows LVF,
although occasionally it may develop independently.

Decompensated Heart Failure

Remodeling Several structural changes, known as remodeling, occur in the ventricle during
decompensated heart failure. Remodeling is thought to result from hypertrophy of the myocardial cells
and sustained activation of the neuro hormonal compensatory systems. Recall that one of the initial
compensatory responses to a decrease in cardiac output is dilation of the ventricle. This dilation
increases cardiac output but also increases wall stress in he ventri- cle. To reduce wall stress, the
myocardial cells hypertro- phy, resulting in a thickening of the ventricular wall. According to Laplace's
law, an increase in wall thickness reduces wall stress.

ry responses When used over time, these compensatory resn.

gene produce changes in the structure, function, and

expression of the myocardial cell. Changes in the my

myocar dial cells eventually increase failure by reducing mvo

stress, and dial contractility, increasing ventricular wall strese

increasing oxygen demand. In addition to increasing m

cardial dysfunction, the genetically abnormal myocytes di

ess prematurely and at an accelerated rate through the pror

of apoptosis (programmed cell death). Apoptosis affects cells scattered throughout the myocardium and
causes a

further reduction in cardiac function.

Sustained Neurohormonal Activation

Remodeling changes continue to increase wall stress and further stimulate neurohormonal activity.
Long-term sympathetic activation exerts a direct toxic effect on the heart that promotes myocyte
hypertrophy and apoptosis Prolonged activation of the renin-angiotensin system also stimulates
myocyte hypertrophy and myocardial fibrosis. This creates a self-perpetuating cycle of cell

death and further hypertrophy.

In addition, if renal artery pressure falls, a lowered glo merular filtration rate (GFR) increases retention
of sodn and water. In response to a continued reduction in blood flow, the renin-angiotensin-
aldosterone mechau

ism
is activated. Aldosterone, released from the adrenal co rtex

promotes further retention of sodium and water by the

renal tubule. This results in an expansion in bloOun volume in

of up to 30% and edema. As the sodium concentr in

the extracellular fluid increases, so does the osmotic pr he Sure of the plasma. The hypothalamus respon
one

the

higher osmotic pressure by releasing antidiuretc oles

hormone

CADH) from the posterior pituitary. This in turt eve promotes

renal tubular reabsorption of water. Aldosterone, dem ever

15 more important than ADH in the production O

edema

because it promotes sodium retention. Clinical Manifestations The manifestations of heart failure
depend on the specifi ventricle involved, the precipitating causes of failure, the degree of impairment,
the rate of progression, the dura tion of the failure, and the client's underlying condition Conditions that
precipitate heart failure are listed in Box 56-3. Manifestations of pulmonary congestion and edema
dominate the clinical picture of LVE; RVF is asso- ciated with manifestations of abdominal organ
distention and peripheral edema. Heart failure has been classifed into several stages based on a client's
functional ability and clinical manifestations (Table 56-2).

Types of Heart Failure

Heart failure may be categorized as (1) LVF versus R

2) backward versus forward, and (3) high output versus low output.

Left Ventricular Versus Right Ventricular Failure The theory of LVF versus RVF is based on the fact that

fluid accumulates behind the chamber that fails first. Because the circulatory system is a closed circuit,
how-

ever, impairments of one ventricle commonly progress to failure of the other. This is referred to as
ventricular

interdependence. Figure 56-7 depicts clinical manifesta- tions that differentiate LVF from RVE.

Left Ventricular Failure. Left ventricular failure causes

either pulmonary congestion or a disturbance in the respi ratory control mechanisms. These problems in
turn precip- 1tate respiratory distress. The degree of distress varies with the client's position, activity,
and level of stress. Dyspnea (difficult breathing) is a subjective problem, and it does not always correlate
with the extent of heart lailure. Because breathing is usually effortless at rest, the

feeling of breathlessness can mean anythin8 from an may be more aware of dyspnea than a client with

awareness of breathing to extreme distress. An appre- failure

ensive client with only moderate ventricular failure with

hensive

client

uvanced disease. To some degree, exertional dyspnea occurs in all clients. Therefore elicit from the
client a description of the degree of exertion that results in the sensation of breathlessness. The
mechanism of dyspnea may be related to the decrease in the lung's air volume (vital capacity) as air is
displaced by blood or interstitial fluid. Pulmonary congestion can eventually reduce the vital capacity of
the lungs to 1500 ml or less. Othopnea is a more advanced stage of dyspnea. The client often assumes a
"three-point position," sitting up with both hands on the knees and leaning forward. Orthopnea
develops because the supine position increases the amount of blood returning from the lower
extremities to the heart and lungs (preload). The client learns to avoid respiratory distress at night by
supporting the head and thorax on pillows. In severe heart failure, the client may resort to sleeping
upright in a chair. Paroxysmal nocturnal dyspnea (PND) resembles the frightening sensation of
suffocation. The client suddenly awakens with the feeling of severe suffocation and seeks relief by sitting
upright or opening a window for a breath of fresh air." Respirations may be labored and wheezing
(cardiac asthma). PND represents an acute exacerbation of pulmonary congestion. It stems from a
combination of increased venous return to the lungs during recumbency and suppression of the
respiratory center to sensory input from the lungs during sleep. Once the client is upright, relief from
the attack of PND may not OCCur for 30 minutes or longer Cheyne-Stokes respirations sometimes occur
in cli- ents with severe forms of heart failure. Cheyne-Stokes respirations probably result from the
prolonged circula- tion time between the pulmonary circulation and the central nervous system (CNS).
Cough is a common manifestation of LVE. The cough, often hacking, may produce large amounts of
frothy, blood-tinged sputum. The client coughs because a large amount of fluid is trapped in the
pulmonary tree,

irritating the lung mucosa. On auscultation bilateral crackles may be heard. Cardiovascular
manifestations also denote LVF

Inspecting and palpating the precordium may reveal anenlarged or left laterally displaced apical pulse.
This occurs because the left ventricle dilates in an effort to

supplement ventricular contraction and emptying. Heart gallop (S, or S4) sounds may be an early finding
in heart

failure as the lef ventricle becomes less compliant and

ee Walls vibrate in response to filling during diastole The aDpearance of pulsus alternans (alternating
strong nd weak heartbeats) may also herald the onset of LVF Cerebral hypoxia may occur as a result of a
decrease in cardiac output, causing inadequate brain perfusion. Depressed cerebral function can cause
anxiety, irritabil-

ity, restlessness, confusion, impaired memory, bad

dreams, and insomnia. Impaired ventilation with resul- tant hypercapnia may also be a precipitant.
Fatigue and muscular weakness are often associated with LVF. Inadequate cardiac output leads to
hypoxic tis- sue and slowed removal of metabolic wastes, which in turn cause the client to tire easily.
Disturbances in sleep

and rest patterns may worsen fatiguue. Renal changes can occur in both RVF and LVF but are more
striking in LVF. Nocturia occurs early in heart fail- ure. During the day the client is upright, blood flow is
away from the kidneys, and the formation of urine is reduced. At night urine formation increases as
blood flow to the kidneys improves. Nocturia may interfere with effective sleep patterns, which may
contribute to fatigue. As cardiac output declines, decreased renal blood flow may result in oliguria, a
late manifestation of heart failure.

Complications of Left Ventricular Failure. Acute pulmo- nary edema, a medical emergency, usually
results from LVE In clients with severe cardiac decompensation, the

capillary pressure within the lungs becomes so elevated that fluid is pushed from the circulating blood
into the interstitium and then into the alveoli, bronchioles, and bronchi. The resulting pulmonary
edema, if untreated, may cause death from suffocation. Clients with pulmo nary edema literally drown
in their own fluids. The dra- matic manifestations of acute pulmonary edema, listed in the Critical
Monitoring feature above, right, terrify the Client and the client's significant others.

Right ntricular Failure ing decreases, peripheral

lar Failure. When right ventricle function-

hen right ventricle function- edema and venous congestion

ing

and abdominal pain occur as the liver becomes congested galy)

of the organs devel Liver enlargement (hepatomegaly)

ith venous blood. If this oCcurs rapidly, stretching of the

caDsule surrounding the liver causes severe discomfot. The client may notice either a constant aching or
a sharp pain in the right upper quadrant. In chronic heart failure, abdominal tenderness generally
disappears. In severe RVF, the lobules of the liver may become so congested with venous blood that
they become anoxic. Anoxia leads to necrosis of the lobules. In long-standing heart tailure, these
necrotic areas may become fibroe

Sclerotic. As a result, a condition called cardiac TDOSIS develops, manifested by ascites and jaunaie

Chronic heart failure. the increased workload increase o abolic demands of the body. Anorexia, nausea,
and

heart and the extreme work of breathing increase the bloating develop secondary to venous congestion
of the gastrointestinal tract. The combination of increased meta- bolic needs and decreased caloric
intake results in a

marked wasting of tissue mass, called cardiac cachexia. Anorexia and nausea may also result from
digitalis toxicity. Dependent edema is one of the early manifestations of RVE. Venous congestion in the
peripheral vascular beds causes increased hydrostatic capillary pressure. Capillary hydrostatic pressure
overwhelms the opposing pressure of plasma proteins, and fluid shifts out of the capillary beds and into
the interstitial spaces, with resultant pitting edema. Edema is usually symmetrical and occurs in the
dependent parts of the body, where venous pressure is highest. In ambulatory clients edema begins in
the feet and ankles and moves up the lower legs. It is most notice- able at the end of the day and often
subsides after a night's rest. In the recumbent client, pitting edema may develop in the presacral area
and, as it worsens, progress to the genital region and medial thighs. Concurrent jugular vein disten- tion
differentiates the edema of heart failure from that of
lymphatic obstruction, cirrhosis, and hypoproteinemia. Anasarca, a late manifestation in heart failure, is
sub- stantial and generalized edema. It can involve the upper extremities, genital area, and thoracic and
abdominal walls. Cyanosis of the nail beds appears as venous con- gestion reduces peripheral blood
flow. Clients with heart failure often feel anxious, frightened, and depressed. Almost all clients realize
that the heart is a vital organ and that when the heart begins to fail, health also fails. As the course of
the disease progresses and man- ifestations worsen, the client may have an overwhelming fear of
permanent disability and death. Clients express their fears in varying ways: nightmares, insomnia, acute
anxiety, depression, or withdrawal from reality, Backward Versus Forward Failure

The clinical presentation of heart failure arises from inad equate cardiac output, the pooling of blood
behind the failing chamber, or both. Backward failure focuses on the ventricle's inability to eject
completely, which increases ventricular filling pressures, causing venous and pulmonary congestion.
Forward failure is a problem of inadequate perfusion. It results when reduced contrac- tility produces a
decrease in stroke volume and cardiac output. As cardiac output falls, blood flow to vital organs and
peripheral tissues diminishes. This causes mental Confusion, muscular weakness, and renal retention of
sodium and water. Each of these types of failure is usually present to some degree in the client with
heart failure.

High-Output Versus Low-Output Failure Higb-output failure occurs when the heart, despite nor- mal-
output to high-output levels, is simply not able to meet the accelerated needs of the body. Causes
include sepsis, Paget's disease, beriberi, anemia, thyrotoxicosis, arteriovenous fistula, and pregnancy.
Low-output failure occurs in most forms of heart dis- ease, resulting in hypoperfusion of tissue cells. The
underlying disorder is related not to increased metabolic needs of the tissues but to poor ventricular
pumping action and a low cardiac output.

The

Decompensated Versus Chronic Heart Failure The onset of heart failure may be acute, decompensation,
or stable, called chronic heart failure

leading to Decompensated Versus Chronic Heart Failure The onset of heart failure may be acute, leading
to

decompensation, or stable, called chronic heart failure.

Diagnostic Findings The diagnosis of heart failure rests primarily on present- ing manifestations and
pertinent data from the client's health history. Diagnostic studies assist in determining the underlying
cause and the degree of heart failure. B-type natriuretic peptide (BNP) is a protein secreted from the
ventricles in response to overload, such as occurs in heart failure. As the degree of heart failure wor-
sens, the level of BNP secreted into the blood increases. Liver enzymes may reflect the degree of liver
failure. Ele- vated blood urea nitrogen (BUN) and creatinine levels reflect decreased renal perfusion.
Additional studies include an echocardiogram, chest x- ray, and ECG. A two-dimensional (2-D)
echocardiogram, coupled with Doppler flow studies, provides information about cardiac chamber size
and ventricular function. These tests aid in assessing myocardial, valvular, congen- ital, endocardial, and
pericardial heart disease, allowing the clinician to determine whether the dysfunction is sys- tolic or
diastolic. In LVF, chest x-ray often depicts an enlarged cardiac silhouette, pulmonary and venous con-
gestion, and interstitial edema. On x-ray interstitial edema produces images called Kerley's B lines.
Pleural effusione may develop and generally reflect biventricular failure An ECG may give clues to the
cause of LVF. Abnormalities in the ECG arise from the underlying cardiac disorder and from therapeutic
agents. It may demonstrate evidence of a prior MI, dysrhythmias, or left ventricular dysfunction. Arterial
blood gas analysis may be performed. Early heart failure with pulmonary edema may lead to respira tory
alkalosis that is due to hyperventilation. As the dis order progressesand Oxygenation becomes more
impaired, acidosis develops. Pulse oximetry values show decreased oxygen levels. Medical Management

The management of heart failure is divided into two sih

situa

tions: the treatment of decompensated heart failure ana

d the treatment of stable chronic heart failure. Diuretiel

tics, nitrates, analgesics, and inotropic agents are indicated fo the treatment of decompensated heart
failure and puln nary edema. The goals of the management are to reduce myocardial workload, improve
ventricular pump perfor mance, perfuse essential organs, and prevent further hean failure by affecting
the process of cardiac remodeling

Reduce Myocardial Workload Diuretics are an important aspect of treatment because of the central role
of the kidney as the target organ of many of the neurohormonal changes in response to the failing
heart. First-line therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium
chloride reabsorption in the ascending loop of Henle. Diuretics reduce circulating blood volume,
diminish preload, and lessen systemic and pulmonary congestion. Loop diuretics can also produce mild
to severe electrolyte imbalance. Hypokalemia, a particularly dangerous side effect, can cause myocardial
weakness and cardiac dysrhythmias Hypokalemia also potentiates digitalis toxicity. Moreover, vigorous
diuresis may produce hypovolemia and hypo tension, jeopardizing cardiac output. Vasodilators also
reduce myocardial workload by redue ing both preload and afterload. Nitroglycerin reduces cardial
oxygen demand by lowering preload and afterlo lt is often given intravenously. Morphine IV is often ue
1or clients with acute heart failure. In addition to beung an anxiolytic and an analgesic, its most
important ettect i venodilation, which reduces preload. Morphine causes arterial dilation, which reduces
systemic va resistance (SVR) and increases cardiac outpu Medicatio the can be direct vasodilators acting
through nitric Ox also vessel walls. Nesiritide is a newer medication an Works by dilating arteries and
veins.

oth

also

also Reta-adrenergic antagonISts (beta-blockers) are used inhibit the effects of the sympathetic nervous
system and reduce the oxygen needs of the myocardium. They

increase clinical improvement and decrease mortality.

These findings are apparent when clients are concurrently receiving ACE inhibitory therapy, suggesting
that the combination of two agents that have inhíbitory effects on two neurohormonal systems may
have an additive effect. Beta-blockers, possibly by restoring beta-receptor activity or via prevention of
catecholamine activity, appear to be cardioprotective in clients with depressed left ventricular function.
g.uipi

prroabrod

cinoes Elevate the Client's Head

aichsd lo ase

The client is placed in a high Fowler position or chair to

uuce pulmonary venous congestion and to relieve the uyspnea, The legs are maintained in a dependent
posi-
tion as much as possible. Even though the legs are

cuematous, they should not be elevated. Elevating the egs rapidly increases venous return. Controlling
sodium and water retention improves cardiac Prom the use of some loop diuretics, potassium is lost
Cardium to digitalis and erefore predisposes the client

duce Fluid Retention Sodium restrictions are placed on the diet

formance. So

sodium are usually prescribed (Table 56-3). kidneys, which can lead to dysrhythmias and

nt, control, or eliminate edema. Diets with 2 to

to preve

and

awolvte imbalances. Hypokalemia sensitizes the myo-

to digitalis toxicity. Potassium supplements and ade-

ate dietary potassium are important. t is usually not necessary to restrict fluid intake in cli.

ents with mild or moderate heart failure. In more

advanced cases, however, it is beneficial to limit water to 1000 ml/day (1 L/day). The reason is that
excessive water intake tends to dilute the amount of sodium in
body fluids and may produce a low-salt syndrome Cbyponatremia). Hyponatremia is characterized by
leth- angy and weakness; it results more often from the combi- nation of a restricted sodium diet,
increased sodium loss during diuresis, and excessive water intake.

lmprove Ventricular Pump Performance

ions. gotensin-converting enzyme (ACE) inhibilOtS hemodynamics, and are discussed below.

OS powerful way to increase contractility of the Lo use adrenergic agonist, or inotropic medica The 1

also commonly yield pronounced improvement in

Opes.Principal inotropic agents include dobuta-

mine, milrinone,

dopexamine, and digoxin. In the hypo- Client with heart failure, dopamine

tensive client

and dobutamine are agents usually used. These medications facilitate myocardial Contractility and
enhance stroke volume. They also can lead to dysrhythmias. Dobutamine is a very useful medication for
heart fail- ure because it produces strong beta-stimulatory effects within the myocardium; it increases
heart rate, atrioven- tricular (AV) conduction, and myocardial contractility. Dobutamine is capable of
increasing cardiac output without increasing myocardial oxygen demands or

reducing coronary blood flow. Dopamine is a naturally occurring catecholamine with alpha-adrenergic,
beta-adrenergic, and dopa- minergic activity. Dopamine, given in small doses (<4 mcg/kg/min), opens
the kidney's vascular beds. Vasodilation in the kidney is especially advantageous, leading to improved
GFR, urine output, and excretion of sodium. When dopamine is given in higher doses it produces
tachycardia and dysrhythmias; therefore it is not commonly used in decompensated heart failure.
Milrinone is another inotropic medication and also dilates the pulmonary vascular beds. Amrinone, the
first of the phosphodiesterase inhibitors, is seldom used because it leads to thrombocytopenia.
Dopexamine has been used in some clients, and is still being investi- gated. Digoxin is used less and less
in the emergency management of heart failure. Digoxin is discussed with chronic heart failure; it has
little to no role in the treat- ment of decompensated heart failure.

Supplement Oxygen High concentrations of oxygen by mask or cannula are

provided to relieve hypoxia and dyspnea and to

improve oxygen-carbon dioxide exchange. For hypox- emia, partial rebreather masks with a flow rate of
8 to 10 L/min can be used to deliver oxygen concentrations of 40% to 70%. A non-rebreathing mask can
achieve even higher oxygen concentrations. If these methods do not raise the arterial Oxygen tension
(Pao2) above 60 mm Hg, the client may need intubation and ventila- tory management. Intubation also
provides a route for removing secretions from the bronchi. If severe bron- chospasm or
bronchoconstriction Occurs, bronchodila- tors are given. The heart rhythm is monitored because some
bronchodilators may lead to dysrhythmias. Control Dysrhythmias Atrial fibrillation with a rapid
ventricular response is the most common dysrhythmia seen in heart failure clients. Atrial fibrillation can
lead to embolic stroke, so clients

are given anticoagulants. The rhythm is often controlled with medications such as amiodarone.

Reduce Myocardial Remodeling

Angiotensin-converting enzyme inhibitors are now con- sidered first-choice treatment and are the
cornerstone of

heart failure drug therapy. ACE inhibitors have proved to slow the progression of heart failure by
reducing remo deling changes in the heart. ACE inhibitors reduce after load by blocking the production
of angiotensin, a potent vasoconstrictor. They also increase renal blood flow and decrease renal vascular
resistance, which enhances diure- sis. Side effects include orthostatic hypotension, persistent hacky
cough and kidney problems, skin rashes, an altered sense of taste, and hyperkalemia. Potassium levels
should be monitored, especially if diuretics or potassium supple-

ments are being used.

Reduce Stress and Risk of Injury In addition to improving ventricular pump performane and reducing
myocardial workload, the client also eeds to reduce physical and emotional stress. Sometimes clin. icians
overlook rest as an intervention to diminish the workload of the heart. The proper use of rest as the ini
tial step in management offers many benetits. Rest can

promote diuresis, slow the heart rate, and relieve

relieve

dyspnea, all of which allow more conservative use of pharmacologic agents (e.g., ACE inhibitors,
diuretics, beta-blockers).

d or

Whether the physician prescribes complete, modified bed rest depends on the seriousness of the
client's con- dition. The physician may prescribe a mild sedative or small doses of barbiturates and
tranquilizers to promote rest and overcome problems of restlessness, insomnia, and anxiety.

The client may also be at risk for injury because of immobility. The client should be confined to bed only

long enough to regain cardiac reserve but not so long

as to promote complications of immobility. Give the client confined to bed rest specific guidelines to pre
vent the harmful effects of immobility. Clients shou perform passive leg exercises several times daily t
prevent venous stasis, which may lead to the fora

ma-

tion of venous thrombi and pulmonary emboli. Anti coagulant therapy prevents these potentially deadly

complications. Surgical Management for Heart Failure

Ventricular Assist Devices

Advances continue to be made in perfecting methods of mechanical ventricular support. The goal of
mechanical circulatory support is to decompress the hypokinetic ventricle, decrease myocardial
workload, reduce Oxygen demands, and maintain adequate systemic perfusion to sustain end-organ
function. In the client with heart tail ure, the two most common options are ventricular assist devices
(VADS) as a bridge to transplantation and as per manent support. VADS have the capability to support

circulation, either partially or totally, until the heart

recovers or is replaced. Devices may be right ventricular, left ventricular, or biventricular VADs.
Complications of any VAD include bleeding, hemolysis, thromboembolism, infection, and multiorgan
failure. Intra-aortic balloon pumping as a treatment for VAD is discussed in the Bridge to Critical Care
feature on p. 1423. Traditionally nonpulsatile pumps have been used as VADS. Difficulties with these
devices include end-

organ dysfunction, thromboembolic complications, and the need for full anticoagulation. Their use in cli-
ents with heart failure is diminishing because better technology has become available. These pumps can
be used for a relatively short period of about 10 days. Total artificial hearts provide complete control of
the cardiovascular system and allow total mobility. Their

use is limited in smaller people because the device

ay not fit the client's small body. Complications clude infection, thromboembolism, and the possibility

may

mechanical failure. Initially, total artificial hearts were uted to people awaiting transplantation.
Currently, limited to pe these devices are being used when there are contraindi- cations to
transplantation, such as advanced age. Extracorporeal membrane oxygenation (ECMO) sys- tems are
widely used for short-term hemodynamic stabilization. These devices remove blood from the infe- rior
vena cava to a centrifugal pump that pumps the blood to an oxygenator. The Oxygenated blood is
returned to the client via the femoral artery. Long-term use (<48 hours) does not promote recovery. In
addition, bleeding is a concern because anticoagulation therapy is

needed.
Heart Transplantation When the heart is irreversibly damaged and no longer functions adequately and
when the client is at risk of dying, cardiac transplantation and the use of an artificial heart to assist or
replace the failing heart are measures of last resort. With the development of cyclosporine, and more
recently FK-506 and mycophenolate mofetil, and with improvements in the procurement and
preservation of donor hearts, cardiac transplantation has become an accepted therapeutic procedure.
One-year survival rates after transplantation are greater than 85%. Although

transplantation may not be appropriate for all clients, it may be the only option available to some. Heart
trans- plantation is discussed in Chapter 55.

Cardiomyoplasty For clients with low cardiac output who are not cand- dates for cardiac transplantation,
a procedure called cardiomyoplasty may support the failing heart. This prob cedure involves wrapping
the latissimus dorsi muscle around the heart and electrostimulating it in synchrony with ventricular
systole. Immediate postoperative care is similar to that of any cardiac surgery client. Continuous cardiac
and hemody- namic monitoring is initiated. Inotropic and vasopressor agents are administered to
maintain cardiac output until the pulse generator is activated (within 2 to 3 weeks). Because the muscle
flap obliterates the left upper lobe of the lung and can reduce vital capacity by as much as 20%,
aggressive pulmonary hygiene and judicious pain management are essential to prevent atelectasis or
pneumonia. In addition an upper-extremity exercise reg- imen is prescribed. Modifications for Older
Clients

Heart faiure is becoming increasingly a disorder of the very old. Decompensated heat failure can be
triggered by seemingly minor illnesses and dietary indiscretions. Medications commonly used by older
people may have an impact on heart performance even though they pose little risk of interaction with
cardiovascular medications. Nonsteroidal anti-inflammatory drugs (NSAIDS) tend to worsen heart
disease because they promote sodium retention; tricyclic antidepressants (TCAs) and neurolep- tic
agents lead to orthostatic hypotension. Conversely, cardiac performance can affect the medication's
action. The development of RVF can markedly increase the pro- thrombin time and thereby increase the
action of anti- coagulants. See the Case Management feature on Heart Failure on the website.
Continuous monitoring of home- bound clients with heart failure can be facilitated by Computer-
assisted programs. Nurse researchers are studying the effect of daily interaction via the computer with
heart failure clients.

cONCLUSIONS

Disorders of cardiac function are the leading causes of death in the industrialized world. It is imperative
that you fully understand the care of clients with heart dis- ease to improve the outcomes and quality of
life and to reduce morbidity and mortality, CHD is the precursor to several problems. Your role is to
educate the client about risk reduction. Heart failure is a frequent end- point of cardiac disease. It is
important to maximize

cardiac output and reduce system demands on the heart.