Pathophysiology of congestive heart failure.
Over the past several years, additional information has been accumulated on the pathophysiology of congestive heart failure. The primary cardiac defect is a decrease in intrinsic contractility of the myocardium, usually brought on by prolonged pressure or volume overload. Several associated biochemical changes have been described, although no precise cause-and-effect relation has been determined. A number of neurohumoral changes occur, which increase systemic vascular resistance. This increased resistance contributes further to a decrease in cardiac output. In fact, many such "compensatory mechanisms" that are initially beneficial may overshoot and produce deleterious hemodynamic effects. Therapeutic interventions such as diuretics, inotropic drugs and vasodilators are frequently helpful by correcting compensatory mechanisms that overshoot.
D001145:Arrhythmias, Cardiac / Q000150:complications / Q000503:physiopathology; D002302:Cardiac Output; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology; D004039:Diet, Sodium-Restricted; D006321:Heart / Q000503:physiopathology*; D006330:Heart Defects, Congenital / Q000150:complications / Q000503:physiopathology; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D009200:Myocardial Contraction; D012965:Sodium Chloride / Q000009:adverse effects; D014655:Vascular Resistance
D012965:Sodium Chloride