Current therapy of acute heart failure.

Abstract

Acute heart failure involves various pathophysiological mechanisms among which primary reduction of myocardial contractility due to acute myocardial infarction, cardiomyopathy, and after open heart surgery are the most common. Therapy should be as causally related as possible. In patients with mechanical defects such as rupture of the interventricular reptum or acute mitral regurgitation due to papillary muscle rupture, surgical correction is mandatory. Systemic hemodynamics can often be temporarily stabilized by mechanical circulatory assist devices until spontaneous recovery has occurred or definitive treatment is possible. The objectives of medical therapy are to relieve pulmonary congestion and to provide adequate systemic tissue perfusion. This is achieved by carefully balancing and monitoring a selection of pharmacological approaches according to each patient's hemodynamic profile. Ventricular filling pressure may be reduced by potent loop diuretics and venous dilating drugs with preservation of an optimal pressure range of 15-18 mmHg; cardiac output can be increased by afterload reduction and/or positive inotropic drugs; preservation of systemic perfusion pressure may necessitate use of arteriolar constrictor therapy. Most of these hemodynamic objectives are met by agents with combined vasodilatory and inotropic effects, e.g., dobutamine and amrinone. Whilst both agents are equally effective at improving pump performance, amrinone, unlike dobutamine, has the advantage of doing so without increaseing myocardial oxygen consumption and without tolerance development or significant arrhythmogenicity.