A. Symptoms
The symptoms of cardiac failure have been discussed in part in earlier sections. The most common complaint is shortness of breath, chiefly exertional dyspnea at first and then progressing to orthopnea, paroxysmal nocturnal dyspnea, and rest dyspnea. A more subtle and often overlooked symptom of heart failure is a chronic nonproductive cough, which is often worse in the recumbent position. Nocturia due to excretion of fluid retained during the day and increased renal perfusion in the recumbent position is a common nonspecific symptom of heart failure. Patients with heart failure also complain of fatigue and exercise intolerance.

These symptoms correlate poorly with the degree of cardiac dysfunction and result in part from changes in peripheral blood flow and blood flow to skeletal muscle, which are part of the syndrome of heart failure. Patients with right heart failure may experience right upper quadrant pain due to passive congestion of the liver, loss of appetite and nausea due to edema of the gut or impaired gastrointestinal perfusion, and peripheral edema.

Cardiac failure may present acutely in a previously asymptomatic patient. Causes include myocardial infarction, myocarditis, and acute valvular regurgitation due to endocarditis or other conditions.

These patients usually present with pulmonary edema. The management of acute heart failure has been discussed under myocardial infarction and centers around initial stabilization with diuretics and parenteral vasodilators or inotropic agents.

Patients with episodic symptoms may be having left ventricular dysfunction due to intermittent ischemia. This potentially reversible form of heart failure should be considered, especially in patients with angina pectoris and those with diabetes mellitus. Patients may also present with acute exacerbations of chronic, stable heart failure. Exacerbations are usually caused by alterations in therapy (or patient noncompliance), excessive salt and fluid intake, arrhythmias, excessive activity, pulmonary emboli, intercurrent infection, or progression of the underlying disease.

Patients with heart failure are often categorized by the New York Heart Association classification as class I (asymptomatic), class II (symptomatic with moderate activity), class III (symptomatic with mild activity), or class IV (symptomatic at rest). However, this classification has major limitations in that patient reports are highly subjective and in that symptoms vary from day to day. In any case, the classification is insufficiently sensitive to be useful in predicting outcomes or assessing the results of treatment.

B. Signs
Many patients with heart failure, including some with severe symptoms, appear comfortable at rest. Others will be dyspneic during conversation or minor activity, and those with long-standing severe heart failure may appear cachectic or cyanotic. The vital signs may be normal, but tachycardia, hypotension, and reduced pulse pressure may be present. Patients often show signs of increased sympathetic nervous system activity, including cold extremities and diaphoresis. Important peripheral signs of heart failure can be detected by examination of the neck, the lungs, the abdomen, and the extremities. Right atrial pressure may be estimated through the height of the pulsations in the jugular venous system. In addition to the height of the venous pressure, abnormal pulsations such as regurgitant v waves should be sought. Examination of the carotid pulse may allow estimation of pulse pressure as well as detection of aortic stenosis. The thyroid examination is important, since occult hyperthyroidism and hypothyroidism are readily treatable causes of heart failure. In the lungs, crackles at the lung bases reflect transudation of fluid into the alveoli. Pleural effusions may cause bibasilar dullness to percussion. Expiratory wheezing and rhonchi may be signs of heart failure. Patients with severe right heart failure may have hepatic enlargement - tender or nontender - due to passive congestion. Systolic pulsations may be felt in Tricuspid regurgitation. Sustained moderate pressure on the liver may increase jugular venous pressure (a positive hepatojugular reflux is an increase of > 1 cm). Ascites may also be present. Peripheral pitting edema is a common sign in patients with right heart failure and may extend into the thighs and abdominal wall.

The cardiac examination has been discussed. Cardinal signs in heart failure are a parasternal lift, indicating pulmonary hypertension; an enlarged and sustained left ventricular impulse, indicating left ventricular dilation and hypertrophy; a diminished first heart sound, suggesting impaired contractility; and S₃ gallops originating in the left and sometimes the right ventricle. An S₄ is usually present in diastolic heart failure. Murmurs should be sought to exclude primary valvular disease; secondary mitral regurgitation and Tricuspid regurgitation murmurs are common in patients with dilated ventricles. In chronic heart failure, many of the expected signs of heart failure may be absent despite markedly abnormal cardiac function and hemodynamic measurements.

C. Laboratory Findings
A blood count may reveal anemia, a cause of high-output failure and an exacerbating factor in other forms of cardiac dysfunction. Biochemical studies may show renal insufficiency as a possible compounding factor. Renal function tests also determine whether cardiac failure is associated with prerenal azotemia. Serum electrolytes may disclose hypokalemia, which increases the risk of arrhythmias; hyperkalemia, which may limit the use of inhibitors of the renin-angiotensin system; or hyponatremia, an indicator of marked activation of the renin-angiotensin system and a poor prognostic sign. Thyroid function should be assessed in older patients to detect occult thyrotoxicosis or myxedema. In unexplained cases, appropriate biopsies may lead to a diagnosis of amyloidosis, and additional assessment should include iron studies to exclude hemochromatosis. Myocardial biopsy may exclude specific causes of dilated cardiomyopathy but rarely reveals specific reversible diagnoses.

Assays of serum “B-type” natriuretic peptide (BNP) or amino terminal pro-BNP can be a useful adjunct to the clinical history and physical examination in the diagnosis of heart failure. BNP is expressed primarily in the ventricles and is elevated when ventricular filling pressures are high. It is quite sensitive in patients with symptomatic heart failure - whether due to systolic or to diastolic dysfunction - but less specific in older patients, women, and patients with COPD. The roles of these assays in screening asymptomatic individuals or as a guide to management have not been established.

D. Electrocardiography and Chest X-Ray
Electrocardiography may indicate an underlying or secondary arrhythmia, myocardial infarction, or nonspecific changes that often include low voltage, intraventricular conduction defects, left ventricular hypertrophy, and nonspecific repolarization changes. Chest radiographs provide information about the size and shape of the cardiac silhouette. Cardiomegaly is an important finding. Evidence of pulmonary venous hypertension includes relative dilation of the upper lobe veins, perivascular edema (haziness of vessel outlines), interstitial edema, and alveolar fluid. In acute heart failure, these findings correlate moderately well with pulmonary venous pressure. However, patients with chronic heart failure may show relatively normal pulmonary vasculature despite markedly elevated pressures. Pleural effusions are common and tend to be bilateral or right-sided.

E. Additional Studies
Many studies have indicated that the clinical diagnosis of systolic myocardial dysfunction is often inaccurate. The primary confounding conditions are diastolic dysfunction of the heart with decreased relaxation and filling of the left ventricle (particularly in hypertension and in hypertrophic states) and pulmonary disease. Because patients with heart failure usually have significant resting electrocardiographic abnormalities, stress imaging procedures such as perfusion scintigraphy or dobutamine echocardiography are often indicated.

The most useful test is the echocardiogram. This will reveal the size and function of both ventricles and of the atria. It will also allow detection of pericardial effusion, valvular abnormalities, intracardiac shunts, and segmental wall motion abnormalities suggestive of old myocardial infarction as opposed to more generalized forms of dilated cardiomyopathy.

Radionuclide angiography measures left ventricular ejection fraction and permits analysis of regional wall motion. This test is especially useful when echocardiography is technically suboptimal, such as in patients with severe pulmonary disease. When myocardial ischemia is suspected as a cause of left ventricular dysfunction, stress testing should be performed.

F. Cardiac Catheterization
In most patients with heart failure, clinical examination and noninvasive tests can determine left ventricular size and function well enough to confirm the diagnosis. Left heart catheterization is necessary when significant valvular disease must be excluded and when the presence and extent of coronary artery disease must be determined. The latter is particularly important when left ventricular dysfunction may be partially reversible by revascularization. The combination of angina or noninvasive evidence of significant myocardial ischemia with symptomatic heart failure is often an indication for coronary angiography if the patient is a potential candidate for revascularization. Right heart catheterization may be useful to select and monitor therapy in patients refractory to standard therapy.

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Drazner MH et al: Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med 2001;345:574.

Maisel AS et al: Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161.