Acetaldehyde and cardiac arrhythmias.

Administration of acetaldehyde (i.v.) into cats anesthetized with halothane elicits severe cardiac ventricular arrhythmias which begin in about 10-13 sec with bolus doses of 5-10 mg/kg, and last about 2 min. Systemic blood pressure and heart rate rise concurrently with the arrhythmias. The cardiac effects are attributed to the release of endogenous catecholamines from cardiac tissue because they are prevented by beta-adrenergic blockade and are not dependent on adrenomedullary and splenic stores of catecholamines, since acute surgical removal of these tissues does not prevent the arrhythmias and other cardiovascular changes. This indirect arrhythmogenic action of acetaldehyde has not been previously reported, probably because other investigators have used anesthetics like pentobarbital which exert an antiarrhythmic effect that masks acetaldehyde's arrhythmogenic potential. The use of halothane to sensitize the heart to catecholamines greatly enhanced the arrhythmogenic effect of acetaldehyde. The question is raised whether the concomitant industrial or medical exposure of human subjects to large amounts of exogenous or endogenous acetaldehyde and certain hydrocarbons could provide the substrate for the expression of this arrhythmogenic effect of acetaldehyde.