HEART FAILURE

Description

 HF is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and
nutrients.
 In the past, HF was often referred to as congestive heart failure (CHF), because many patients
experience pulmonary or peripheral congestion.
 Currently HF is recognized as a clinical syndrome characterized by signs and symptoms of fluid
overload or of inadequate tissue perfusion.
 Fluid overload and decreased tissue perfusion result when the heart cannot generate a CO sufficient to
meet the body’s demands.
 The term HF indicates myocardial disease in which there is a problem with contraction of the heart
(systolic dysfunction) or filling of the heart (diastolic dysfunction) that may or may not cause pulmonary
or systemic congestion.
 Some cases of HF are reversible, depending on the cause. Most often, HF is a progressive, life-long
condition that is managed with lifestyle changes and medications to prevent episodes of acute
decompensated heart failure.
 These episodes are characterized by an increase in symptoms, decreased CO, and low perfusion
(Varughese, 2007). They are associated with increased hospitalizations, increased health care costs,
and decreased quality of life.
CHRONIC HEART FAILURE
Description

 As with coronary artery disease, the incidence of HF increases with age. More than 5 million people in
the United States have HF, and 550,000 new cases are diagnosed each year (American Heart
Association [AHA], 2007).
 Although HF can affect people of all ages, it is most common in people older than 75 years of age; as
the U.S. population ages, HF has become an epidemic that challenges the country’s health care
resources.
 HF is the most common reason for hospitalization of people older than 65 years of age and is the
second most common reason for visits to a physician’s office.
 The increase in the incidence of HF reflects not only the increased number of elderly people but also
improvements in treatment of cardiac diseases such as MI, resulting in increased survival rates.
 Many hospitalizations for HF can be prevented by appropriate outpatient care. Prevention and early
intervention to arrest the progression of HF are major health initiatives in the United States.
 Two major types of HF are identified by assessment of left ventricular functioning, usually by
echocardiogram:
- The more common type is an alteration in ventricular contraction called systolic heart failure,
which is characterized by a weakened heart muscle.
- The less common type is diastolic heart failure, which is characterized by a stiff and noncompliant
heart muscle, making it difficult for the ventricle to fill.
 An assessment of the ejection fraction (EF) is performed to assist in determining the type of HF. EF is
calculated by subtracting the amount of blood present in the left ventricle at the end of systole from the
amount present at the end of diastole and calculating the percentage of blood that is ejected. A normal
EF is 55% to 65% of the ventricular volume; the ventricle does not completely empty between
contractions. The EF is normal in diastolic HF but severely reduced in systolic HF
 Although a low EF is a hallmark of systolic HF, which is the most common type of HF, the severity of
HF is frequently classified according to the patient’s symptoms.
 The New York Heart Association (NYHA) Classification is described in Table 30-1.
Table 30-1 NEW YORK HEART ASSOCIATION
(NYHA) CLASSIFICATION OF HEART FAILURE
Clas Signs and Symptoms Prognosi
sifica s
tion
I Ordinary physical activity does Good
not cause undue fatigue,
dyspnea, palpitations, or chest
pain
No pulmonary congestion or
peripheral hypotension
Patient is considered
asymptomatic
Usually no limitations of activities
of daily living (ADLs)
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 II Slight limitation on ADLs Good
Patient reports no symptoms at
rest but increased physical
activity will cause symptoms
Basilar crackles and S3
murmur may be detected
III Marked limitation on ADL Fair
Patient feels comfortable at
rest but less than ordinary
activity will cause symptoms

IV Symptoms of cardiac Poor

insufficiency at rest

 The American College of Cardiology and the American Heart Association (ACC/AHA) have developed
another a HF classification system (Hunt, Abraham, Chin, et al., 2005). This system, described in Table
30-2, takes into consideration the natural history and progressive nature of HF. Treatment guidelines
have been developed for each stage.

Table 30-2 AMERICAN COLLEGE OF

CARDIOLOGY AND AMERICAN HEART
ASSOCIATION (ACC/AHA) CLASSIFICATION OF
HEART FAILURE
Classification Criteria
Stage A Patients at high risk for developing
left ventricular dysfunction but
without structural heart disease or
symptoms of heart failure
Stage B Patients with left ventricular
dysfunction or structural heart
disease who have not developed
symptoms of heart failure
Stage C Patients with left ventricular
dysfunction or structural heart
disease with current or prior
symptoms of heart failure
Stage D Patients with refractory end-stage
heart failure requiring specialized
interventions

PATHOPHYSIOLOGY
 HF results from a variety of cardiovascular conditions, including chronic hypertension, coronary artery
disease, and valvular disease. These conditions can result in systolic failure, diastolic failure, or both.
 Significant myocardial dysfunction usually occurs before the patient experiences signs and symptoms
of HF such as shortness of breath, edema, or fatigue.
 As HF develops, the body activates neurohormonal compensatory mechanisms. These
mechanisms represent the body’s attempt to cope with the HF and are responsible for the signs and
symptoms that eventually develop. Understanding these mechanisms is important because the
treatment of HF is aimed at opposing them and relieving symptoms.
 Systolic HF results in decreased blood volume being ejected from the ventricle. The decreased
ventricular stretch is sensed by baroreceptors in the aortic and carotid bodies.
 The sympathetic nervous system is then stimulated to release epinephrine and norepinephrine (Fig. 30-
2). The purpose of this initial response is to increase heart rate and contractility and support the failing
myocardium, but the continued response has multiple negative effects.
 Sympathetic stimulation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys. A
decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the
kidneys.
 Renin promotes the formation of angiotensin I, a benign, inactive substance. Angiotensin-converting
enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to angiotensin II, a
potent vasoconstrictor, which then increases the blood pressure and afterload.
 Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium
and fluid retention by the renal tubules and stimulation of antidiuretic hormone. These mechanisms lead
to the fluid volume overload commonly seen in HF.
 Angiotensin, aldosterone, and other neurohormones (eg, endothelin, prostacyclin) lead to an increase
in preload and afterload, which increases stress on the ventricular wall, causing an increase in the
workload of the heart.
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  A counter regulatory mechanism is attempted through the release of natriuretic peptides. Atrial
natriuretic peptide (ANP) and B-type (ie, brain type) natriuretic peptide (BNP) are released from the
overdistended cardiac chambers. These substances promote vasodilation and diuresis. However, their
effect is usually not strong enough to overcome the negative effects of the other mechanisms.
 As the heart’s workload increases, contractility of the myocardial muscle fibers decreases. Decreased
contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the
myocardial muscle fibers and increasing the size of the ventricle (ventricular dilation). The increased
size of the ventricle further increases the stress on the ventricular wall, adding to the workload of the
heart. One way the heart compensates for the increased workload is to increase the thickness of the
heart muscle (ventricular hypertrophy). However, hypertrophy results in an abnormal proliferation of
myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones
(eg, angiotensin II), large myocardial cells are produced that are dysfunctional and die early, leaving the
other normal myocardial cells to struggle to maintain CO. The compensatory mechanisms of HF have
been called the “vicious cycle of HF” because the heart does not pump sufficient blood to the body,
which causes the body to stimulate the heart to work harder; thus, the heart cannot respond and failure
becomes worse.
 Diastolic HF develops because of continued increased workload on the heart, which responds by
increasing the number and size of myocardial cells (ie, ventricular hypertrophy and altered cellular
functioning). These responses cause resistance to ventricular filling, which increases ventricular filling
pressures despite a normal or reduced blood volume. Less blood in the ventricles causes decreased
CO. The low CO and high ventricular filling pressures can cause the same neurohormonal responses
as described for systolic HF.

ETIOLOGY
 Myocardial dysfunction is most often caused by coronary artery disease, cardiomyopathy,
hypertension, or valvular disorders.
 Patients with diabetes mellitus are also at high risk for HF. Atherosclerosis of the coronary arteries is
the primary cause of HF, and coronary artery disease is found in more than 60% of the patients with HF
(Zipes, Libby & Bonow, 2005).
 Ischemia causes myocardial dysfunction because it deprives heart cells of oxygen and leads to
acidosis from the accumulation of lactic acid. MI causes focal heart muscle necrosis, the death of
myocardial cells, and a loss of contractility; the extent of the infarction correlates with the severity of HF.
 Revascularization of the coronary artery by a percutaneous coronary intervention (PCI) or by coronary
artery bypass surgery (CABG) may improve myocardial oxygenation and ventricular function.
 Cardiomyopathy is a disease of the myocardium. There are three types: dilated, hypertrophic, and
restrictive (see Chapter 29). Dilated cardiomyopathy, the most common type of cardiomyopathy,
causes diffuse cellular necrosis and fibrosis, leading to decreased contractility (systolic failure). Dilated
cardiomyopathy can be idiopathic (unknown cause) or it can result from an inflammatory process, such
as myocarditis, or from a cytotoxic agent, such as alcohol or doxorubicin (Adriamycin). Hypertrophic
cardiomyopathy and restrictive cardiomyopathy lead to decreased distensibility and ventricular
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 filling (diastolic failure). Usually, HF due to cardiomyopathy becomes chronic and progressive.
However, cardiomyopathy and HF may resolve following removal of the causative agent, such as with
the cessation of alcohol ingestion.
 Systemic or pulmonary hypertension increases afterload (resistance to ejection), which increases the
workload of the heart and leads to hypertrophy of myocardial muscle fibers. This can be considered a
compensatory mechanism because it increases contractility. However, the hypertrophy may impair the
heart’s ability to fill properly during diastole, and the hypertrophied ventricle may eventually dilate and
fail.
 Valvular heart disease is also a cause of HF. The valves ensure that blood flows in one direction. With
valvular dysfunction, blood has increasing difficulty moving forward, increasing pressure within the
heart and increasing cardiac workload, leading to HF. Chapter 29 discusses the effects of valvular heart
disease.
 Several systemic conditions, including progressive renal failure and uncontrolled hypertension,
contribute to the development and severity of HF (Varughese, 2007). Acute illness such as pneumonia
with fever and hypoxia increase the metabolic rate and may precipitate HF. All of these conditions
require an increase in CO to satisfy the systemic oxygen demand, and they stress the compromised
myocardium. Cardiac dysrhythmias may cause HF or may be a result of HF; either way, the altered
electrical stimulation impairs myocardial contraction and decreases the overall efficiency of myocardial
function. Other factors, such as acidosis (respiratory or metabolic), electrolyte abnormalities, and
antiarrhythmic medications, can worsen myocardial function.
CLINICAL MANIFESTATIONS
 The clinical manifestations produced by the different types of HF (systolic, diastolic, or both) are similar
(Chart 30-1) and therefore do not assist in differentiating the types of HF. The signs and symptoms of
HF can be related to which ventricle is affected. Left-sided heart failure (left ventricular failure) causes
different manifestations than right-sided heart failure (right ventricular failure). In chronic HF, patients
may have signs and symptoms of both left and right ventricular failure.
CHART 30-1 ASSESSING FOR HEART FAILURE
Be alert for the following signs and symptoms:
General
 Fatigue
 Decreased activity tolerance
 Dependent edema
 Weight gain
Cardiovascular
 Third heart sound (S3)
 Apical impulse enlarged with left lateral
displacement
 Pallor and cyanosis
 Jugular venous distention (JVD)
Respiratory
 Dyspnea on exertion
 Pulmonary crackles that do not clear with
cough
 Orthopnea
 Paroxysmal nocturnal dyspnea (PND)
 Cough on exertion or when supine
Cerebrovascular
 Unexplained confusion or altered mental
status
 Lightheadedness
Renal
 Oliguria and decreased frequency during the
day
 Nocturia
Gastrointestinal
 Anorexia and nausea
 Enlarged liver
 Ascites
 Hepatojugular reflux

Left-Sided Heart Failure

 Pulmonary congestion occurs when the left ventricle cannot effectively pump blood out of the
ventricle into the aorta and the systemic circulation.
 The increased left ventricular end-diastolic blood volume increases the left ventricular end-diastolic
pressure, which decreases blood flow from the left atrium into the left ventricle during diastole.

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  The blood volume and pressure in the left atrium increases, which decreases blood flow from the
pulmonary vessels.
 Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary capillaries
into the pulmonary tissues and alveoli, causing pulmonary interstitial edema and impaired gas
exchange.
 The clinical manifestations of pulmonary congestion include dyspnea, cough, pulmonary crackles,
and low oxygen saturation levels. An extra heart sound, the S3, or “ventricular gallop,” may be
detected on auscultation. It is caused by a large volume of fluid entering the ventricle at the beginning
of diastole
 Dyspnea, or shortness of breath, may be precipitated by minimal to moderate activity (dyspnea on
exertion [DOE]); dyspnea also can occur at rest.
 The patient may report orthopnea, difficulty breathing when lying flat. Patients with orthopnea usually
prefer not to lie flat. They may need pillows to prop themselves up in bed, or they may sit in a chair and
even sleep sitting up.
 Some patients have sudden attacks of dyspnea at night, a condition known as paroxysmal nocturnal
dyspnea (PND).
 Fluid that accumulates in the dependent extremities during the day may be reabsorbed into the
circulating blood volume when the patient lies down. Because the impaired left ventricle cannot eject
the increased circulating blood volume, the pressure in the pulmonary circulation increases, shifting
fluid into the alveoli. The fluid-filled alveoli cannot exchange oxygen and carbon dioxide. Without
sufficient oxygen, the patient experiences dyspnea and has difficulty sleeping.
 The cough associated with left ventricular failure is initially dry and nonproductive. Most often,
patients complain of a dry hacking cough that may be mislabeled as asthma or chronic obstructive
pulmonary disease (COPD). The cough may become moist over time. Large quantities of frothy
sputum, which is sometimes pink (blood-tinged), may be produced, usually indicating severe pulmonary
congestion (pulmonary edema).
 Adventitious breath sounds may be heard in various areas of the lungs. Usually, bibasilar crackles that
do not clear with coughing are detected in the early phase of left ventricular failure. As the failure
worsens and pulmonary congestion increases, crackles may be auscultated throughout all lung fields.
At this point, oxygen saturation may decrease.
 In addition to increased pulmonary pressures that cause decreased oxygenation, the amount of blood
ejected from the left ventricle decreases. The dominant feature in HF is inadequate tissue perfusion.
The diminished CO has widespread manifestations because not enough blood reaches all the tissues
and organs (low perfusion) to provide the necessary oxygen. The decrease in SV can also lead to
stimulation of the sympathetic nervous system, which further impedes perfusion to many organs.
 A reduction in CO decreases blood flow to the kidneys, reducing urine output (oliguria). Renal perfusion
pressure falls, which results in the release of renin from the kidney. Release of renin leads to
aldosterone secretion and increased intravascular volume. However, when the patient is sleeping, the
cardiac workload is decreased, improving renal perfusion, which in some patients leads to frequent
urination at night (nocturia).
 As HF progresses, decreased CO may cause other symptoms. Decreased gastrointestinal perfusion
causes altered digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion,
restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety increases, so does
dyspnea, increasing anxiety and creating a vicious cycle. Stimulation of the sympathetic system also
causes the peripheral blood vessels to constrict, so the skin appears pale or ashen and feels cool and
clammy.
 A decrease in SV causes the sympathetic nervous system to increase the HR (tachycardia), often
causing the patient to complain of palpitations. The pulses become weak and thready. Without
adequate CO, the body cannot respond to increased energy demands, and the patient becomes easily
atigued and has decreased activity tolerance. Fatigue also results from the increased energy expended
in breathing and the insomnia that results from respiratory distress, coughing, and nocturia.

Right-Sided Heart Failure

 When the right ventricle fails, congestion in the peripheral tissues and the viscera predominates. This
occurs because the right side of the heart cannot eject blood and cannot accommodate all the blood
that normally returns to it from the venous circulation. Increased venous pressure leads to JVD and
increased capillary hydrostatic pressure throughout the venous system
 The systemic clinical manifestations include edema of the lower extremities (dependent edema),
hepatomegaly (enlargement of the liver), ascites (accumulation of fluid in the peritoneal cavity),
anorexia and nausea, and weakness and weight gain due to retention of fluid
 Edema usually affects the feet and ankles and worsens when the patient stands or sits for a long
period. The edema decreases when the patient elevates the legs. The edema can gradually progress

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 up the legs and thighs and eventually into the external genitalia and lower trunk. Edema in the
abdomen, as evidenced by increased abdominal girth, may be the only edema present. Sacral edema
is common in patients who are on bed rest, because the sacral area is dependent. Pitting edema, in
which indentations in the skin remain after even slight compression with the fingertips (Fig. 30-3), is
obvious only after retention of at least 4.5 kg (10 lb) of fluid (4.5 L).
 Hepatomegaly and tenderness in the right upper quadrant of the abdomen result from venous
engorgement of the liver. The increased pressure may interfere with the liver’s ability to function
(secondary liver dysfunction). As hepatic dysfunction progresses, increased pressure within the portal
vessels may force fluid into the abdominal cavity, causing ascites. Ascites may increase pressure on
the stomach and intestines and cause gastrointestinal distress. Hepatomegaly may also increase
pressure on the diaphragm, causing respiratory distress.
 Anorexia (loss of appetite) and nausea or abdominal pain result from the venous engorgement and
venous stasis within the abdominal organs. The weakness that accompanies right-sided HF results
from reduced CO, impaired circulation, and inadequate removal of catabolic waste products from the
tissues.

ASSESSMENT AND DIAGNOSTIC FINDINGS

 HF may go undetected until the patient presents with signs and symptoms of pulmonary and peripheral
edema. However, the physical signs that suggest HF may also occur with other diseases, such as renal
failure and COPD.
 Assessment of ventricular function is an essential part of the initial diagnostic workup.
 An echocardiogram is usually performed to confirm the diagnosis of HF, identify the underlying cause,
and determine the EF, which helps identify the type and severity of HF.
 This information may also be obtained noninvasively by radionuclide ventriculography or invasively
by ventriculography as part of a cardiac catheterization procedure.
 A chest x-ray and an electrocardiogram (ECG) are obtained to assist in the diagnosis.
 Laboratory studies usually performed during the initial workup include serum electrolytes, blood urea
nitrogen (BUN), creatinine, thyroid-stimulating hormone, complete blood cell count, BNP, and
routine urinalysis.
 The BNP level is a key diagnostic indicator of HF; high levels are a sign of high cardiac filling
pressure and can aid in the diagnosis of HF (Heart Failure Society of America [HFSA], 2006). The
results of these laboratory studies assist in determining the underlying cause and can also be used to
establish a baseline to assess effects of treatment.
 Cardiac stress testing or cardiac catheterization may be performed to determine whether coronary
artery disease and cardiac ischemia are causing the HF.
MEDICAL MANAGEMENT
 The overall goals of management of HF are to relieve patient symptoms, to improve functional status
and quality of life, and to extend survival. Medical management is based on the type, severity, and
cause of HF. Specific objectives of medical management include the following:
- Eliminate or reduce any etiologic contributory factors, such as uncontrolled hypertension or atrial
fibrillation with a rapid ventricular response
- Optimize pharmacologic and other therapeutic regimens
- Reduce the workload on the heart by reducing preload and afterload
- Promote a lifestyle conducive to cardiac health
- Prevent episodes of acute decompensated HF
 Treatment options vary according to the severity of the patient’s condition and may include oral and IV
medications, major lifestyle changes, supplemental oxygen, implantation of assistive devices, and
surgical approaches, including cardiac transplantation.
 Managing the patient with HF includes providing comprehensive education and counseling to the
patient and family. It is important that the patient and family understand the nature of HF and the
importance of their participation in the treatment regimen.
 Lifestyle recommendations include restriction of dietary sodium; avoidance of excessive fluid intake,
alcohol, and smoking; weight reduction when indicated; and regular exercise. The patient must know
how to recognize signs and symptoms that need to be reported to a health care professional.

PHARMACOLOGIC THERAPY
Angiotensin-Converting Enzyme Inhibitors
 Found to relieve the signs and symptoms of HF and significantly decrease mortality and morbidity.
 Slows the progression of HF, improve exercise tolerance, and decrease the number of hospitalizations
for HF.

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  ACE inhibitors promote vasodilation and diuresis by decreasing afterload and preload. By doing so,
they decrease the workload of the heart.
 Vasodilation reduces resistance to left ventricular ejection of blood, diminishing the heart’s workload
and improving ventricular emptying.
 In promoting diuresis, ACE inhibitors decrease the secretion of aldosterone, a hormone that causes
the kidneys to retain sodium and water. ACE inhibitors stimulate the kidneys to excrete sodium and
fluid (while retaining potassium), thereby reducing left ventricular filling pressure and decreasing
pulmonary congestion.
 Recommended for prevention of heart failure in patients who are at risk.
 Patients receiving ACE inhibitors are monitored for hypotension, hypovolemia, hyperkalemia, and
alterations in renal function, especially if they are also receiving diuretics.
 Hypotension is most likely to develop from ACE inhibitor therapy in patients older than 75 years of age
and in those with a systolic blood pressure of 100 mm Hg or less, a serum sodium level of lower than
135 mEq/L, or severe HF.
 Because ACE inhibitors cause the kidneys to retain potassium, the patient who is also receiving a
diuretic may not need to take oral potassium supplements. However, patients receiving potassium-
sparing diuretics must be carefully monitored for hyperkalemia, an increased level of potassium in the
blood.
 Before the initiation of the ACE inhibitor, hyperkalemic and hypovolemic states must be corrected. ACE
inhibitors may be discontinued if the potassium level remains greater than 5.5 mEq/L or if the serum
creatinine rises.
 Other side effects of ACE inhibitors include a dry, persistent cough that may not respond to cough
suppressants.

Angiotensin II Receptor Blocker

 ARBs and ACE inhibitors have similar hemodynamics: decreased blood pressure, decreased
systemic vascular resistance, and improved cardiac output.
 ACE inhibitors and ARBs also have similar side effects: hyperkalemia, hypotension, and renal
dysfunction.
 Alternative to ACE inhibitors, especially when patients cannot tolerate ACE inhibitors because of cough

Hydralazine and Isosorbide Dinitrate

 A combination of hydralazine and isosorbide dinitrate may be another alternative for patients who
cannot take ACE inhibitors.
 Nitrates cause venous dilation, which reduces the amount of blood return to the heart and lowers
preload.
 Hydralazine lowers systemic vascular resistance and left ventricular afterload.

Beta-Blockers
 Beta-blockers have been found to reduce mortality and morbidity in patients with HF by reducing the
adverse effects from the constant stimulation of the sympathetic nervous system.
 The most frequent side effects are dizziness, hypotension, and bradycardia.

Diuretics
 Diuretics are prescribed to remove excess extracellular fluid by increasing the rate of urine produced in
patients with signs and symptoms of fluid overload.
 Loop diuretics, such as furosemide (Lasix), inhibit sodium and chloride reabsorption mainly in the
ascending loop of Henle.
 Thiazide diuretics, such as metolazone (Zaroxolyn), inhibit sodium and chloride reabsorption in the
early distal tubules.
 Diuretics may be most effective if the patient assumes a supine position for 1 or 2 hours after taking
them.
 Spironolactone (Aldactone) is a potassium-sparing diuretic that blocks the effects of aldosterone in the
late distal tubule and collecting duct. Serum creatinine and potassium levels are monitored frequently.

Digitalis
 Digoxin increases the force of myocardial contraction and slows conduction through the atrioventricular
node. It improves contractility, increasing left ventricular output, which also enhances diuresis.
 The patient is observed for indications that digitalis therapy is effective: lessening dyspnea and
orthopnea, decrease in pulmonary crackles on auscultation, relief of peripheral edema, weight loss, and
increase in activity tolerance.
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Calcium Channel Blockers
 Blocks calcium entrance to the heart muscles
 They work to reduce cardiac contractility and output to reduce BP, and relaxes blood vessels and
arteries.

Intravenous Infusions
 Nesiritide causes rapid improvement in the symptoms of HF. It is a BNP that is produced by the faiing
myocardium to mount a compensatory response in the presence of the myocardial demands.
Specificallyy, BNP binds to vascular smooth muscle and endothelial cells, causing dilation of arteries
and veins. It also suppresses the neurohormones responsible for fluid retention, thus promoting
diuresis. The result is reduced preload and afterload and increased SV.
 Milrinone is a phosphodiesterase inhibitor that delays the release of calcium from intracellular
reservoirs and prevents the uptake of extracellular calcium by the cells. This promotes vasodilation,
resulting in decreased preload and afterload and reduced cardiac workload.
 Dobutamine is an IV medication administered to patients with significant left ventricular dysfunction
and hypoperfusion. A catecholamine, dobutamine stimulates the beta-1–adrenergic receptors. Its major
action is to increase cardiac contractility.

NUTRITIONAL THERAPY
 A low-sodium (2 to 3 g/day) diet and avoidance of drinking excessive amounts of fluid are usually
recommended.
 Dietary restriction of sodium reduces fluid retention and the symptoms of peripheral and pulmonary
congestion.
 The purpose of sodium restriction is to decrease the amount of circulating blood volume, which
decreases myocardial work.

ADDITIONAL THERAPY
Supplemental Oxygen
 The need is based on the degree of pulmonary congestion and resulting hypoxia. Some patients
require supplemental oxygen only during periods of activity.

Other interventions
 If the patient has underlying coronary artery disease, coronary artery revascularization with
percutaneous coronary intervention or coronary artery bypass surgery may be considered. Ventricular
function may improve in some patients when coronary flow is increased.
 In patients with severe left ventricular dysfunction and the possibility of life-threatening dysrhythmias,
placement of an implantable cardioverter defibrillator (ICD) can prevent sudden cardiac death and
extend survival.
 In the patient with HF who does not improve with standard therapy, cardiac resynchronization
therapy (CRT) is another treatment that may be beneficial. CRT involves the use of a biventricular
pacemaker to treat electrical conduction defects. Left bundle branch block, a type of delayed
conduction that is frequently seen in patients with HF, results in dyssynchronous conduction and
contraction of the right and left ventricles, which can further decrease ejection fraction (EF). This
intervention has been shown to improve cardiac output, optimize myocardial energy consumption,
reduce mitral regurgitation, and slow the ventricular remodeling process.
 Ultrafiltration is an alternative intervention for patients with severe fluid overload. A dual-lumen central
IV catheter is used, which could be a peripherally inserted central catheter or a midline or central
catheter, and the patient’s blood is circulated through a small bedside machine. Liters of excess fluid
and plasma are removed slowly from the patient’s intravascular circulating volume over a number of
hours. This fluid is then discarded, and the filtered blood products are returned to the patient

GERONTOLOGICAL CONSIDERATIONS
 Several normal age-related changes increase the frequency of HF: increased systolic blood pressure,
increased ventricular wall thickness, and increased myocardial fibrosis.
 Elderly people may present with atypical signs and symptoms: fatigue, weakness, and somnolence.
Decreased renal function makes the elderly patient resistant to diuretics and more sensitive to changes
in volume.

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