Pathophysiology of Heart Failure: Changing Perceptions

Abstract

Heart failure occurs when myocardial muscle dysfunction prevents the heart from pumping enough blood at normal cardiac pressures to meet the metabolic needs of the body, especially during exercise, and compensatory hemodynamic and neurohormonal mechanisms are overwhelmed or maladaptive. Pathologic classifications are broadly based on the presence of systolic dysfunction (dilated cardiomyopathy) and diastolic dysfunction (hypertrophic or restrictive cardiomyopathies). Coronary artery disease, idiopathic dilated cardiomyopathy, and hypertension are the most frequent causes, and myocardial function may be impaired by some drugs. When contractility is reduced, stroke volume and cardiac output are decreased, and alterations in the kidneys may induce fluid retention to compensate for the perceived low output and reduced circulating blood volume. Fluid retention, in turn, causes increased preload or filling pressure and symptoms of pulmonary congestion. Depressed contractility also results in a reduction in blood pressure, leading to compensatory neurohormonal activation and vasoconstriction, which significantly elevate afterload, further reduce stroke volume, and lead to deleterious cardiac remodeling. The overall clinical approach includes defining the etiology, identifying precipitant factors, and assessing the severity of myocardial dysfunction and clinical symptoms.