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A systematic search of the medical literature was performed on January 11, 2008. The search, limited to human subjects and English language journals, included National Guideline Clearinghouse, the Cochrane database, PubMed, pier® and UpToDate®. The current American College of Cardiology/ American Heart Association Chronic Heart Failure Guidelines can be found at The European Society of Cardiology Acute Heart Failure and Chronic Heart Failure Guidelines can be found at and the HFSA 2006 Heart Failure Practice Guideline can be found at

Heart failure (HF) is a serious and growing health problem affecting approximately 5 million persons in the United States with an additional 550,000 individuals diagnosed yearly. HF contributes to approximately 300,000 deaths each year. The estimated direct and indirect costs attribute to HF for 2006 is $29.6 billion.1

HF was once described as “a condition in which the heart fails to discharge its contents adequately” (Thomas Lewis 1933); however, the simplistic model of pump failure has evolved into a complex disorder that affects the cardiovascular, musculoskeletal, renal, and neuroendocrine systems.

The cardinal manifestations of HF include dyspnea, fatigue, and fluid retention. The development of symptoms characteristic in HF result from pulmonary and systemic congestion. The presence of signs and symptoms of HF (Table 2-1) may vary considerably over time in a given patient. The mechanism of fatigue in HF is complex and originates from low cardiac output, peripheral hypoperfusion, and skeletal muscle deconditioning. As left ventricular function deteriorates and the ability to accept and eject the increased blood volume is impaired, pulmonary venous and capillary pressures elevate, leading to interstitial and bronchial edema, increased airway resistance, and dyspnea. In early HF, dyspnea may occur only with exertion. As HF progresses, the degree of exertion necessary to induce dyspnea decreases and eventually leads to dyspnea at rest.2 Associated symptoms include orthopnea and paroxysmal nocturnal dyspnea (PND). Orthopnea, that is, dyspnea in the supine position, results from redistribution of fluid from the abdomen and lower extremities into the chest, which increases the pulmonary capillary pressure, combined with elevation of the diaphragm. Orthopnea is relieved by sitting upright and typically is prevented by elevating the head with pillows. PND is a result of severe pulmonary and bronchial congestion and refers to severe shortness of breath and coughing that generally occurs after 2 to 4 hours of sleep; patients awaken with a sense of suffocation.3 The period between the initiation of ventricular dysfunction and the onset of symptoms may occur very quickly after a myocardial infarction (MI) or extend for a long period of time. With more chronic processes, such as hypertension or idiopathic cardiomyopathies, this interval may extend for months to years. There is a discordance between the degree of ventricular dysfunction and the degree of functional impairment in HF; therefore, the severity of symptoms does not directly correlate with the amount of left-ventricular (LV) dysfunction.4

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