Treatment of congestive heart failure

Abstract

Congestive heart failure (CHF) can be defined as the inability ofthe heart to provide

cardiac output sufficient to meet tissue demands at normal ventricular filling pressures.

The goals of treatrnent in CHF inelude relief of symptoms and activity limitation,

prevention of progression of the syndrome and prolongation of survival. There are two

basic approaches to treatrnent, to increase of myocardial contractlity and decrease of

preload and/or afterload.

Diuretics are the first line of therapy in most patients with symptomatic CHF. They

produce rapid and consistent relief improvement of symptoms, since more of them are

associated with fluid retention, as manifested by edema and signs of pulmonary congestions.

Digoxin is the only indicated oral agent that increase myocardial contractility in the

failing heart. It inhibits the membrane bound Na/K-ATPase. Recent studies, however,

have also indicated that digoxin restores abnormal baroreceptor function and inhibits

central sympathetic outflow. In contrast, phosphodiesterase inhibitors exacerbated cardiac

arrhythmias, accelerated progression of the underlying disease and increased mortality.

The rationale for vasodilator therapy in CHF is that agents that alter left ventricular

loading conditions can improve the performance ofthe failing heart. Angiotensin converting

enzyme inhibitors interfere with the activated neurohumoral systems that produce

vasoconstriction and fluid retention and reduced survival. When added to digoxin and

diuretics they produced hemodynarnic improvement, reduced symptoms and improved

the survi val.