The role of enoximone in the treatment of cardiogenic shock.
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.
Vincent
J L
JL
Department of Intensive Care, Erasmus University Hospital, Free University of Brussels, Belgium.
Léon
M
M
Berré
J
J
D002303:Cardiac Output, Low / Q000188:drug therapy; D000242:Cyclic AMP / Q000378:metabolism; D004359:Drug Therapy, Combination; D017335:Enoximone; D006801:Humans; D007093:Imidazoles / Q000627:therapeutic use*; D009206:Myocardium / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D012770:Shock, Cardiogenic / Q000188:drug therapy*; D013566:Sympathomimetics / Q000627:therapeutic use
D007093:Imidazoles; D010726:Phosphodiesterase Inhibitors; D013566:Sympathomimetics; D017335:Enoximone; D000242:Cyclic AMP