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  • Left ventricular dysfunction by echocardiography.

  • Dyspnea on exertion and fatigue are common, but paroxysmal nocturnal dyspnea, orthopnea, and peripheral edema are more diagnostic.

  • Unintentional weight loss, intractable volume overload, and signs of inadequate perfusion (eg, hypotension and narrowed pulse pressure) may represent advanced heart failure.

  • Third (S3) heart sound, displaced cardiac apex, jugular venous distension, hepatojugular reflux, rales, murmur.

  • Any electrocardiographic (ECG) abnormality, radiographic evidence of pulmonary venous congestion, cardiomegaly, or pleural effusion.

  • Elevated B-type natriuretic peptide (BNP) or N-terminal pro-BNP levels.


According to the 2016 statistical update from the American Heart Association (AHA) and the Centers for Disease Control and Prevention, approximately 5.7 million adults in the United States are diagnosed with heart failure. This correlates to 1.77% of the overall population, with men having a higher incidence than women, and this incidence increases with age. The age-adjusted incidence of heart failure has declined by only 11% per decade in men and by 17% per decade in women over a 40-year observation period, despite improved treatments for ischemic heart disease, hypertension, and valvular heart disease. These advances in treatment during the four-decade period of observation did not translate into significant improvements in overall survival after onset of heart failure. The delineation of heart failure has changed in recent decades as well, with a lower prevalence of left ventricular systolic dysfunction (LVSD) or heart failure with reduced ejection fraction (HFrEF) and an increased occurrence of heart failure with preserved ejection fraction (HFpEF). In patients with clinical symptoms of heart failure, 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 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.” As cardiac output decreases in response to the stresses placed on the myocardium (Table 21–1), activation of the sympathetic nervous and renin-angiotensin-aldosterone system occurs. These neurohormonal adaptations help increase blood pressure for tissue perfusion and also increase blood volume to enhance preload, stroke volume, and cardiac output. These compensatory mechanisms, which increase afterload, also lead to further myocardial deterioration and worsening myocardial contractility.

Table 21–1.Causes of heart failure.

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