Congestive Heart Failure

Abstract

CARDIAC hyperfunction, when sustained, commonly leads to a decline in myocardial contractility. Long standing hemodynamic overloading, whether it is due to systemic or pulmonary hypertension, valvular heart disease or loss of functional myocardial tissue (as in ischemic heart disease), calls into play a number of mechanisms that compensate for the increased demands for mechanical energy. To overcome the hemodynamic overload, the myocardium must increase its expenditure of chemical energy. Yet the energy-generating capacity of the myocardium is limited, so that there is little reserve even when circulatory hemodynamics are normal. For this reason a rebudgeting of the energy-producing and energy-consuming . . .