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functioning cardiac myocytes, or, alternatively, disrupts the ability of the myocardium to generate force, thereby preventing the heart from
contracting normally. This index event may have an abrupt onset, as in the case of a myocardial infarction (MI); it may have a gradual or
insidious onset, as in the case of hemodynamic pressure or volume overloading; or it may be hereditary, as in the case of many of the genetic
cardiomyopathies. Regardless of the nature of the inciting event, the feature that is common to each of these index events is that they all in
some manner produce a decline in the pumping capacity of the heart. In most instances, patients remain asymptomatic or minimally
symptomatic after the initial decline in pumping capacity of the heart or develop symptoms only after the dysfunction has been present for some
time.
Although the precise reasons why patients with LV dysfunction may remain asymptomatic is not certain, one potential explanation is that a
number of compensatory mechanisms become activated in the presence of cardiac injury and/or LV dysfunction allowing patients to sustain and
modulate LV function for a period of months to years. The list of compensatory mechanisms that have been described thus far include (1)
activation of the renin-angiotensin-aldosterone (RAA) and adrenergic nervous systems, which are responsible for maintaining cardiac output
through increased retention of salt and water (Fig. 234-2), and (2) increased myocardial contractility. In addition, there is activation of a family
of countervailing vasodilatory molecules, including the atrial and brain natriuretic peptides (ANP and BNP), prostaglandins (PGE2 and PGI2), and
nitric oxide (NO), that offsets the excessive peripheral vascular vasoconstriction. Genetic background, sex, age, or environment may influence
these compensatory mechanisms, which are able to modulate LV function within a physiologic/homeostatic range so that the functional capacity
of the patient is preserved or is depressed only minimally. Thus, patients may remain asymptomatic or minimally symptomatic for a period of
years; however, at some point patients become overtly symptomatic, with a resultant striking increase in morbidity and mortality rates. Although
the exact mechanisms that are responsible for this transition are not known, as will be discussed below, the transition to symptomatic HF is
accompanied by increasing activation of neurohormonal, adrenergic, and cytokine systems that lead to a series of adaptive changes within the
myocardium collectively referred to as LV remodeling.
Figure 234-1
Pathogenesis of heart failure with a depressed ejection fraction. Heart failure begins after an index event produces an initial decline in the heart's
pumping capacity. After this initial decline in pumping capacity, a variety of compensatory mechanisms are activated, including the adrenergic nervous
system, the renin-angiotensin-aldosterone system, and the cytokine system. In the short term, these systems are able to restore cardiovascular function to
a normal homeostatic range with the result that the patient remains asymptomatic. However, with time the sustained activation of these systems can lead
to secondary end-organ damage within the ventricle, with worsening left ventricular remodeling and subsequent cardiac decompensation. (From D Mann:
Circulation 100:999, 1999.)
Figure 234-2
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In contrast to our understanding of the pathogenesis of HF with a depressed EF, our understanding of the mechanisms that contribute to the
development of HF with a preserved EF is still evolving. That is, although diastolic dysfunction (see below) was thought to be the only
Activation of neurohormonal systems in heart failure. The decreased cardiac output in HF patients results in an "unloading" of high-pressure
baroceptors (circles) in the left ventricle, carotid sinus, and aortic arch. This unloading of the peripheral baroreceptors leads to a loss of inhibitory
parasympathetic tone to the central nervous system (CNS), with a resultant generalized increase in efferent sympathetic tone, and non-osmotic release of
arginine vasopressin (AVP) from the pituitary. AVP [or antidiuretic hormone (ADH)] is a powerful vasoconstrictor that increases the permeability of the renal
collecting ducts, leading to the reabsorption of free water. These afferent signals to the CNS also activate efferent sympathetic nervous system pathways
that innervate the heart, kidney, peripheral vasculature, and skeletal muscles.
Sympathetic stimulation of the kidney leads to the release of renin, with a resultant increase in the circulating levels of angiotensin II and aldosterone. The
activation of the renin-angiotensin-aldosterone system promotes salt and water retention and leads to vasoconstriction of the peripheral vasculature,
myocyte hypertrophy, myocyte cell death, and myocardial fibrosis. Although these neurohormonal mechanisms facilitate short-term adaptation by
maintaining blood pressure, and hence perfusion to vital organs, the same neurohormonal mechanisms are believed to contribute to end-organ changes in
the heart and the circulation and to the excessive salt and water retention in advanced HF. [Modified from A Nohria et al: Neurohormonal, renal and
vascular adjustments, in Atlas of Heart Failure: Cardiac Function and Dysfunction, 4th ed, WS Colucci (ed). Philadelphia, Current Medicine Group 2002, p.
104.]
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Patients with HF also may present with gastrointestinal symptoms. Anorexia, nausea, and early satiety associated with abdominal pain and
fullness are common complaints and may be related to edema of the bowel wall and/or a congested liver. Congestion of the liver and stretching
of its capsule may lead to right-upper-quadrant pain. Cerebral symptoms such as confusion, disorientation, and sleep and mood disturbances
may be observed in patients with severe HF, particularly elderly patients with cerebral arteriosclerosis and reduced cerebral perfusion. Nocturia is
common in HF and may contribute to insomnia.
Physical Examination
A careful physical examination is always warranted in the evaluation of patients with HF. The purpose of the examination is to help determine the
cause of HF as well as to assess the severity of the syndrome. Obtaining additional information about the hemodynamic profile and the response
to therapy and determining the prognosis are important additional goals of the physical examination.
GENERAL APPEARANCE AND VITAL SIGNS
In mild or moderately severe HF, the patient appears to be in no distress at rest except for feeling uncomfortable when lying flat for more than a
few minutes. In more severe HF, the patient must sit upright, may have labored breathing, and may not be able to finish a sentence because of
shortness of breath. Systolic blood pressure may be normal or high in early HF, but it generally is reduced in advanced HF because of severe LV
dysfunction. The pulse pressure may be diminished, reflecting a reduction in stroke volume. Sinus tachycardia is a nonspecific sign caused by
increased adrenergic activity. Peripheral vasoconstriction leading to cool peripheral extremities and cyanosis of the lips and nail beds is also
caused by excessive adrenergic activity.
JUGULAR VEINS
(See also Chap. 227) Examination of the jugular veins provides an estimation of right atrial pressure. The jugular venous pressure is best
appreciated with the patient lying recumbent, with the head tilted at 45°. The jugular venous pressure should be quantified in centimeters of
water (normal 8 cm) by estimating the height of the venous column of blood above the sternal angle in centimeters and then adding 5 cm. In the early stages of HF, the venous pressure may be normal at rest but may become abnormally elevated with sustained ( 1 min) pressure on
the abdomen (positive abdominojugular reflux). Giant v waves indicate the presence of tricuspid regurgitation.
PULMONARY EXAMINATION
Pulmonary crackles (rales or crepitations) result from the transudation of fluid from the intravascular space into the alveoli. In patients with
pulmonary edema, rales may be heard widely over both lung fields and may be accompanied by expiratory wheezing (cardiac asthma). When
present in patients without concomitant lung disease, rales are specific for HF. Importantly, rales are frequently absent in patients with chronic
HF, even when LV filling pressures are elevated, because of increased lymphatic drainage of alveolar fluid. Pleural effusions result from the
elevation of pleural capillary pressure and the resulting transudation of fluid into the pleural cavities. Since the pleural veins drain into both the
systemic and the pulmonary veins, pleural effusions occur most commonly with biventricular failure. Although pleural effusions are often bilateral
in HF, when they are unilateral, they occur more frequently in the right pleural space.
CARDIAC EXAMINATION
Examination of the heart, although essential, frequently does not provide useful information about the severity of HF. If cardiomegaly is present,
the point of maximal impulse (PMI) usually is displaced below the fifth intercostal space and/or lateral to the midclavicular line, and the impulse
is palpable over two interspaces. Severe LV hypertrophy leads to a sustained PMI. In some patients, a third heart sound (S3) is audible and
palpable at the apex. Patients with enlarged or hypertrophied right ventricles may have a sustained and prolonged left parasternal impulse
extending throughout systole. An S3 (or protodiastolic gallop) is most commonly present in patients with volume overload who have tachycardia
and tachypnea, and it often signifies severe hemodynamic compromise. A fourth heart sound (S4) is not a specific indicator of HF but is usually
present in patients with diastolic dysfunction. The murmurs of mitral and tricuspid regurgitation are frequently present in patients with advanced
HF.
ABDOMEN AND EXTREMITIES
Hepatomegaly is an important sign in patients with HF. When it is present, the enlarged liver is frequently tender and may pulsate during systole
if tricuspid regurgitation is present. Ascites, a late sign, occurs as a consequence of increased pressure in the hepatic veins and the veins
draining the peritoneum. Jaundice, also a late finding in HF, results from impairment of hepatic function secondary to hepatic congestion and
hepatocellular hypoxemia and is associated with elevations of both direct and indirect bilirubin.
Peripheral edema is a cardinal manifestation of HF, but it is nonspecific and usually is absent in patients who have been treated adequately with
diuretics. Peripheral edema is usually symmetric and dependent in HF and occurs predominantly in the ankles and the pretibial region in
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depressed EF by stabilizing and/or reversing cardiac remodeling. In this regard, ACE inhibitors and beta blockers have emerged as the
cornerstones of modern therapy for HF with a depressed EF.
ACE Inhibitors
There is overwhelming evidence that ACE inhibitors should be used in symptomatic and asymptomatic patients (Figs. 234-3 and 234-4) with a
depressed EF (<40%). ACE inhibitors interfere with the renin-angiotensin system by inhibiting the enzyme that is responsible for the conversion
of angiotensin I to angiotensin II. However, because ACE inhibitors also inhibit kininase II, they may lead to the upregulation of bradykinin,
which may further enhance the beneficial effects of angiotensin suppression. ACE inhibitors stabilize LV remodeling, improve symptoms, reduce
hospitalization, and prolong life. Because fluid retention can attenuate the effects of ACE inhibitors, it is preferable to optimize the dose of
diuretic before starting the ACE inhibitor. However, it may be necessary to reduce the dose of diuretic during the initiation of ACE inhibition to
prevent symptomatic hypotension. ACE inhibitors should be initiated in low doses, followed by gradual increments if the lower doses have been
well tolerated. The doses of ACE inhibitors should be increased until they are similar to those which have been shown to be effective in clinical
trials (Table 234-5). Higher doses are more effective than lower doses in preventing hospitalization.
Figure 234-3
Meta-analysis of angiotensin-converting enzyme (ACE) inhibitors in heart failure patients with a depressed ejection fraction.
A. The Kaplan-Meier curves for mortality for 5966 HF patients with a depressed EF treated with an ACE inhibitor after acute myocardial infarction (three
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The majority of adverse effects are related to suppression of the renin-angiotensin system. The decreases in blood pressure and mild azotemia
that may occur during the initiation of therapy generally are well tolerated and do not require a decrease in the dose of the ACE inhibitor.
However, if hypotension is accompanied by dizziness or if the renal dysfunction becomes severe, it may be necessary to reduce the dose of the
inhibitor. Potassium retention may also become problematic if the patient is receiving potassium supplements or a potassium-sparing diuretic.
Potassium retention that is not responsive to these measures may require a reduction in the dose of ACE inhibitor.
The side effects of ACE inhibitors related to kinin potentiation include a nonproductive cough (10–15% of patients) and angioedema (1% of
patients). In patients who cannot tolerate ACE inhibitors because of cough or angioedema, angiotensin receptor blockers (ARBs) are the
recommended first line of therapy (see below). Patients intolerant of ACE inhibitors because of hyperkalemia or renal insufficiency are likely to
experience the same side effects with ARBs. In these cases, the combination of hydralazine and an oral nitrate should be considered (Table 234-
5).
Angiotensin Receptor Blockers
These drugs are well tolerated in patients who are intolerant of ACE inhibitors because of cough, skin rash, and angioedema. ARBs should be
used in symptomatic and asymptomatic patients with an EF <40% who are ACE-intolerant for reasons other than hyperkalemia or renal
insufficiency (Table 234-5). Although ACE inhibitors and ARBs inhibit the renin-angiotensin system, they do so by different mechanisms. Whereas
ACE inhibitors block the enzyme responsible for converting angiotensin I to angiotensin II, ARBs block the effects of angiotensin II on the
angiotensin type 1 receptor. Some clinical trials have demonstrated a therapeutic benefit from the addition of an ARB to an ACE inhibitor in
trials).
B. The Kaplan-Meier curves for mortality for 12,763 HF patients with a depressed EF treated with an ACE inhibitor in five clinical trials, including
postinfarction trials. The benefits of ACE inhibitors were observed early and persisted long-term. (Modified from MD Flather et al: Lancet 355:1575, 2000.)
Figure 234-4
Treatment algorithm for chronic heart failure patients with a depressed ejection fraction. After the clinical diagnosis of HF is made, it is important
to treat the patient's fluid retention before starting an ACE inhibitor (or an ARB if the patient is ACE-intolerant). Beta blockers should be started after the
fluid retention has been treated and/or the ACE inhibitor has been uptitrated. If the patient remains symptomatic, an ARB, an aldosterone antagonist, or
digoxin can be added as "triple therapy." The fixed-dose combination of hydralazine/isosorbide dinitrate should be added to an ACE inhibitor and a beta
blocker in African-American patients with NYHA class II–IV HF. Device therapy should be considered in addition to pharmacologic therapy in appropriate
patients. HF, heart failure; ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; NYHA, New York Heart Association; CRT, cardiac
Analogous to the use of ACE inhibitors, beta blockers should be initiated in low doses (Table 234-5), followed by gradual increments in the dose
if lower doses have been well tolerated. The dose of beta blocker should be increased until the doses used are similar to those which have been
reported to be effective in clinical trials (Table 234-5). However, unlike ACE inhibitors, which may be titrated upward relatively rapidly, the
titration of beta blockers should proceed no more rapidly than at 2-week intervals, because the initiation and/or increased dosing of these agents
may lead to worsening fluid retention consequent to the withdrawal of adrenergic support to the heart and the circulation. Thus, it is important to
optimize the dose of diuretic before starting therapy with beta blockers. If worsening fluid retention does occur, it is likely to do so within 3–5
days of the initiation of therapy, and it will be manifest as an increase in body weight and/or symptoms of worsening HF. The increased fluid
retention usually can be managed by increasing the dose of diuretics. In some patients the dose of the beta blocker may have to be reduced.
Contrary to early reports, the aggregate results of clinical trials suggest that beta-blocker therapy is well tolerated by the great majority ( 85%)
of HF patients, including patients with comorbid conditions such as diabetes mellitus, chronic obstructive lung disease, and peripheral vascular
disease. Nonetheless, there is a subset of patients (10–15%) who remain intolerant to beta blockers because of worsening fluid retention or
symptomatic hypotension or bradycardia.
Adverse Effects
The adverse effects of beta-blocker use generally are related to the predictable complications that arise from interfering with the adrenergic
nervous system. These reactions generally occur within several days of the initiation of therapy and generally are responsive to adjustments of
concomitant medications, as described above. Therapy with beta blockers can lead to bradycardia and/or exacerbate heart block. Accordingly,
the dose of beta blocker should be reduced if the heart rate decreases to <50 beats/min and/or second- or third-degree heart block or
symptomatic hypotension develops. Beta blockers are not recommended for patients who have asthma with active bronchospasm. Beta blockers
that also block the 1 receptor can lead to vasodilatory side effects.
Aldosterone Antagonists
Although classified as potassium-sparing diuretics, drugs that block the effects of aldosterone (spironolactone or eplerenone) have beneficial
effects that are independent of the effects of these agents on sodium balance. Although ACE inhibition may transiently decrease aldosterone
secretion, with chronic therapy there is a rapid return of aldosterone to levels similar to those before ACE inhibition. Accordingly, the
administration of an aldosterone antagonist is recommended for patients with NYHA class IV or class III (previously class IV) HF who have a
depressed EF (<35%) and are receiving standard therapy, including diuretics, ACE inhibitors, and beta blockers. The dose of aldosterone
Meta-analysis of beta blockers on mortality rates in HF patients with a depressed EF. Effect of beta blockers vs. placebo in patients who were not
(A) or who were (B) receiving an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) at baseline in six clinical trials.
There was a similar impact of beta-blocker therapy on the endpoints of all-cause mortality as well as death and heart failure hospitalization in both the
presence and the absence of ACE inhibitor or ARB at baseline. BEST, Beta-Blocker Evaluation of Survival Trial (bucindolol); CIBIS, Cardiac Insufficiency
Patients who present with Profile L ("cold and dry") should be carefully evaluated by right-heart catheterization for the presence of an occult
elevation of LV filling pressures. If LV filling pressures are low [pulmonary capillary wedge pressure (PCWP) <12 mmHg], a cautious trial of fluid
repletion may be considered. The goals of further therapy depend on the clinical situation. Therapy to reach the aforementioned goals may not
Hemodynamic profiles in patients with acute heart failure. Most patients can be categorized into one of the four hemodynamic profiles by performing
a brief bedside examination that includes examination of the neck veins, lungs, and peripheral extremities. More definitive hemodynamic information may
be obtained by performing invasive hemodynamic monitoring, particularly if the patient is gravely ill or if the clinical presentation is unclear. This
hemodynamic classification provides a useful guide for selecting the initial optimal therapies for the management of acute HF. LV, left ventricular; CO,
cardiac output; SVR, systemic vascular resistance. (Modified from Grady et al: Circulation 102:2443, 2000.)
Table 234-6 Drugs for the Treatment for Acute Heart Failure
Initiating Dose Maximal Dose
Vasodilators
Nitroglycerin 20 g/min 40–400 g/min
Nitroprusside 10 g/min 30–350 g/min
Nesiritide Bolus 2 g/kg 0.01–0.03 g/kg per mina
Inotropes
Dobutamine 1–2 g/kg per min 2–10 g/kg per minb
Milrinone Bolus 50 g/kg 0.1–0.75 g/kg per minb
Dopamine 1–2 g/kg per min 2–4 g/kg per minb
Levosimendan Bolus 12 g/kg 0.1–0.2 g/kg per minc
Vasoconstrictors
Dopamine for hypotension 5 g/kg per min 5–15 g/kg per min
Epinephrine 0.5 g/kg per min 50 g/kg per min
Phenylephrine 0.3 g/kg per min 3 g/kg per min
Vasopressin 0.05 units/min 0.1–0.4 units/min
Notes: a Usually <4 g/kg/min.
b Inotropes will also have vasodilatory properties.
c Approved outside the United States for management of acute heart failure.
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be possible in some patients, particularly if they have disproportionate RV dysfunction or if they develop cardiorenal syndrome, in which renal
function deteriorates during aggressive diuresis. Worsening renal dysfunction occurs in approximately 25% of patients hospitalized with HF and is
associated with prolonged hospital stays and higher mortality rates after discharge.
Pharmacologic Management of Acute HF
(Table 234-6)
Vasodilators
After diuretics, intravenous vasodilators are the most useful medications for the management of acute HF. By stimulating guanylyl cyclase within
smooth-muscle cells, nitroglycerin, nitroprusside, and nesiritide exert dilating effects on arterial resistance and venous capacitance vessels,
which results in a lowering of LV filling pressure, a reduction in mitral regurgitation, and improved forward cardiac output without increasing
heart rate or causing arrhythmias. Hypotension is the most common side effect of all vasodilating agents.
Intravenous nitroglycerin generally is begun at 20 g/min and is increased in 20- g increments until patient symptoms are improved or PCWP is
decreased to 16 mmHg without reducing systolic blood pressure below 80 mmHg. The most common side effect of IV or oral nitrates is
headache, which, if mild, can be treated with analgesics and often resolves during continued therapy. Nitroprusside generally is initiated at 10
g/min and increased by 10–20 g every 10–20 min as tolerated, with the same hemodynamic goals as described above. The rapidity of onset
and offset, with a half-life of approximately 2 min, facilitates early establishment of an individual patient's optimal level of vasodilation in the
ICU. The major limitation of nitroprusside is side effects from cyanide toxicity, which manifests predominantly as gastrointestinal and central
nervous system manifestations and is most likely to occur in patients receiving >250 g/min for over 48 h.
Nesiritide, the newest vasodilator, is a recombinant form of brain-type natriuretic peptide, which is an endogenous peptide secreted primarily
from the LV in response to an increase in wall stress. Nesiritide is given as a bolus (2 g/kg) followed by a fixed-dose infusion (0.01–0.03 g/kg
per min). Nesiritide effectively lowers LV filling pressures and improves symptoms during the treatment of acute HF. Headache is less common
with nesiritide than with nitroglycerin. Although termed a natriuretic peptide, nesiritide has not been associated with major diuresis when used
alone in clinical trials. It does, however, appear to potentiate the effect of concomitant diuretics such that the total required diuretic dose may be
slightly lower. There have, however, been recent concerns about the adverse effects of neseritide on renal function in acute decompensated HF
which may be related to the initial bolus.
Inotropic Agents
Positive inotropic agents produce direct hemodynamic benefits by stimulating cardiac contractility as well as by producing peripheral vasodilation.
Collectively, these hemodynamic effects result in an improvement in cardiac output and a fall in LV filling pressures.
Dobutamine, which is the most commonly used inotropic agent for the treatment of acute HF, exerts its effects by stimulating 1 and
2
receptors, with little effect on 1 receptors. Dobutamine is given as a continuous infusion at an initial infusion rate of 1–2 g/kg per min. Higher
doses (>5 g/kg per min) are frequently necessary for severe hypoperfusion; however, there is little added benefit to increasing the dose above 10 g/kg per min. Patients maintained on chronic infusions for >72 h generally develop tachyphylaxis and require increasing doses.
Milrinone is a phosphodiesterase III inhibitor that leads to increased cyclic AMP by inhibiting its breakdown. Milrinone may act synergistically with
-adrenergic agonists to achieve a greater increase in cardiac output than is achieved with either agent alone, and it may also be more effective than dobutamine in increasing cardiac output in the presence of beta blockers. Milrinone may be administered as a bolus dose of 50 g/kg per min, followed by a continuous infusion rate of 0.1–0.75 g/kg per min. If the patient has a low blood pressure, many clinicians will omit the
bolus dose. Because milrinone is a more effective vasodilator than dobutamine, it produces a greater reduction in LV filling pressures, albeit with
a greater risk of hypotension.
Although short-term use of inotropes provides hemodynamic benefits, these agents are more prone to cause tachyarrhythmias and ischemic
events than vasodilators are. Therefore, inotropes are most appropriately used in clinical settings in which vasodilators and diuretics are not
helpful, such as in patients with poor systemic perfusion and/or cardiogenic shock, patients requiring short-term hemodynamic support after an
MI or surgery, and patients awaiting cardiac transplantation, or as palliative care in patients with advanced HF. If patients require sustained use
of intravenous inotropes, strong consideration should be given to the use of an ICD to safeguard against the proarrhythmic effects of these
agents.
Vasoconstrictors
Vasoconstrictors are used to support systemic blood pressure in patients with HF. Of the three agents that are commonly used (Table 234-6),
dopamine is generally the first choice for therapy in situations in which modest inotropy and pressor support are required. Dopamine is an
endogenous catecholamine that stimulates 1 and 1 receptors and dopaminergic receptors (DA1 and DA2) in the heart and circulation. The
effects of dopamine are dose-dependent. Low doses of dopamine (<2 g/kg per min) stimulate the DA1 and DA2 receptors and cause
vasodilation of the splanchnic and renal vasculature. Moderate doses (2–4 g/kg per min) stimulate the 1 receptors and cause an increase in
cardiac output with little or no change in heart rate or SVR. At higher doses ( 5 g/kg per min) the effects of dopamine on the 1 receptors
overwhelm the dopaminergic receptors, and vasoconstriction ensues, leading to an increase in SVR, LV filling pressures, and heart rate.
Significant additional inotropic and blood pressure support can be provided by epinephrine, phenylephrine, and vasopressin (Table 234-6);
however, prolonged use of these agents can lead to renal and hepatic failure and can cause gangrene of the limbs. Therefore, these agents
should not be administered except in true emergency situations.
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