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  • Left ventricular failure.
  • Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, fatigue, and peripheral edema.
  • Third or fourth heart sound, increased jugular venous pressure, hepatojugular reflux, displaced cardiac apex, rales, wheezing, murmur, or peripheral edema.
  • Any electrocardiographic (ECG) abnormality, radiographic evidence of pulmonary venous congestion, cardiomegaly, or pleural effusion; elevated B-type natriuretic peptide; echocardiographic evidence of left ventricular dysfunction.
  • Right ventricular failure: increased jugular venous pressure, hepatomegaly, peripheral edema.

General Considerations

Increased survivorship after acute myocardial infarction (MI) and improved treatment of hypertension, valvular heart disease, and coronary artery disease (CAD) have led to a significant increase in the prevalence of heart failure in the United States. Overall prevalence of any congestive heart failure (CHF) diagnosis is estimated at 2.6% (2.7% in men; 1.7% in women). In addition, 10% of the population may have isolated moderate to severe diastolic dysfunction, with age greater than 65 years and female gender being consistent predictors of preserved left ventricular systolic function. Diastolic dysfunction is rarely associated with acute MI. Based on this apparent bias, the possibility of biological changes associated with increasing age and female gender have been proposed as underlying reasons for the increased likelihood of diastolic heart failure in these populations.

The prevalence of any type of heart failure increases with age. Asymptomatic left ventricular systolic dysfunction (LVSD) has been found to be as prevalent as symptomatic LVSD: 1.4% and 1.5%, respectively. Moderate or severe isolated diastolic dysfunction appears to be as common as systolic dysfunction, and systolic dysfunction appears to increase with the severity of diastolic dysfunction.


As defined by the American Heart Association (AHA) and the American College of Cardiology (ACC), heart failure is "a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood."

Heart failure results from a complex interplay of compensatory mechanisms used by the body to adjust for decreased cardiac output in response to stresses placed on the myocardium (Table 20-1). These compensatory mechanisms are rooted in the activation of the sodium-retaining renin-angiotensin-aldosterone and sympathetic nervous systems (neurohormonal adaptations). The purpose is to maintain blood pressure and tissue perfusion. However, these compensatory mechanisms, which increase afterload, lead to myocardial deterioration and worsening myocardial contractility. The heart then enters into a vicious cycle of increasing release of neurohormones (norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines) that further increases afterload, allowing the heart to spiral into failure in a progressive fashion through cardiac remodeling. These neurohormones act both in an indirect and in a directly toxic fashion to affect hemodynamic stressors and myocardial cell performance and phenotype.

Table 20-1. Possible Causes of Heart Failure.

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