The effects of etomidate on the contractility of failing and nonfailing human heart muscle

We measured the effects of etomidate on contractility of human cardiac musc le. Muscles were obtained from the left ventricle and right atrium of 12 pa tients undergoing cardiac transplantation, and from the right atrium of 12 patients undergoing coronary artery bypass surgery. Muscles were studied at 37 degrees C and 1.0 Hz. Variables of isometric contraction were recorded before and after etomidate (0.04-80 mu M) or its solvent, propylene glycol. The ability of beta-adrenergic stimulation to cause an inotropic effect af ter etomidate was also assessed. Etomidate caused a dose-dependent decrease in developed tension, which was statistically significant only at concentr ations exceeding clinical doses (greater than or equal to 20 mu M; P < 0.05 ). Decreases in maximum rates of contraction and relaxation paralleled chan ges in developed tension. beta-Adrenergic stimulation reversed the etomidat e-induced decreases in developed tension and rates of contraction and relax ation to baseline (P > 0.05 compared with baseline). Thus, in human myocard ium, etomidate exerts a dose-dependent negative inotropic effect, which is reversible with beta-adrenergic stimulation. Concentrations required to pro duce these negative inotropic effects are, however, in excess of those reac hed during clinical use. Therefore, etomidate-induced negative inotropy is unlikely to be a problem clinically, even in patients with cardiac dysfunct ion.