Low cardiac output in acute
heart failure can result in a functional impairment of organs, when tissue
hypoxia occurs and
cardiogenic shock develops. To restore cardiac output, various forms of
therapy can be considered. Fluid replacement is sometimes beneficial in acute situations where oedema can reduce effective plasma volume.
Vasodilators are often contra-indicated in
shock, when arterial pressure is usually low. Inotropic
therapy consists primarily of the administration of
adrenergic agents.
Dopamine and
noradrenaline can be indicated in severe
hypotension, to maintain coronary perfusion.
Dobutamine is the
catecholamine of choice to increase myocardial contractility. However, decreased responsiveness of the myocardial receptors to
adrenergic stimulation rapidly becomes an important limitation.
Phosphodiesterase inhibitors represent an interesting option to increase contractility, also by increasing
cyclic AMP levels in the myocardium. In this respect, the combination of
phosphodiesterase inhibitors with
adrenergic agents is attractive. The additional vasodilatory properties of these agents can contribute to the increase in cardiac output with limited risk of further reduction in arterial pressure. In 13 patients with
cardiogenic shock persisting despite the use of
adrenergic agents, the addition of
enoximone, 0.5 mg/kg, resulted in significant increases in cardiac index and stroke volume index and a significant decrease in pulmonary artery balloon occlusion pressure without consistent change in mean arterial pressure. In 8 patients, a second infusion of 0.5 g/kg amplified these effects. All but one of these patients survived the episode of
cardiogenic shock, and 5 patients were discharged alive. In some cases, even lower doses of
enoximone resulted in dramatic increases in cardiac output and
oxygen transport in patients already treated with
dobutamine with limited success.