ABSTRACT
Heart failure covers a spectrum of conditions ranging from asymptomatic reduced left ventricular function to symptomatic ventricular failure at rest. The changes which occur in heart failure can be considered in terms of three major determinants - contractility, pre-load and after-load. Impaired contractility is due not only to loss of functioning muscle but also to abnormal responses in surviving muscle, probably induced by neurohormonal activation. Loop diuretics are the preferred agents since they have steep dose-response relationships, produce acute venodilation and increase renal blood flow independent of their diuretic effects. The rationale for using vasodilator drugs in the treatment of heart failure came initially from observations with sodium nitroprusside in acute heart failure, when cardiac output increased markedly with reductions in pre-load and after-load. The adverse effects of digoxin are well documented and can be divided into three groups, namely gastrointestinal effects, cardiac dysrhythmias and neurological effects.
