The potentiation of the response to blunt cardiac trauma by ethanol in dogs.

Acute changes in mechanical performance and electrical activity were followed after blunt cardiac trauma, ethanol infusion, and ethanol infusion and blunt cardiac trauma in 21 anesthetized dogs. Impact was delivered to most of the pericardium with an impact velocity of 10 m/sec and a contact compression of 5 cm. Impact alone caused transient arrhythmias and significant reductions in all hemodynamic parameters with ultimate recovery of rhythm and cardiac performance within 60 minutes after impact. Intravenous infusion of ethanol (average blood alcohol concentration, 65 +/- 1 mg %), resulted in no significant alterations in either mechanical performance or electrical activity but, when combined with trauma, caused a mortality rate of 67%. All animals died from excitation-contraction decoupling; a dissociation of electrical from mechanical activity such that an electrical event does not elicit a mechanical event strong enough to sustain life. It is concluded that even low blood alcohol concentrations can significantly reduce cardiac performance in the presence of otherwise nonfatal cardiac injury.