The mechanism of sensitization of the ventricle to epinephrine by halothane

Abstract

Epinephrine-induced ventricular arrhythmias were studied in dogs anesthetized with pentobarbital during inhalation of oxygen with or without halothane. Bigeminy or multifocal ventricular tachycardia was produced by intravenous injection of epinephrine when its positive chronotropic effect was at its maximum. These arrhythmias were readily induced under halothane which slowed the sinus rate. The severity and the duration of these arrhythmias were dependent on the supraventricular input which was conducted from the atrium and controlled by an electronic stimunator. Atrial driving at a sufficiently high rate could override these arrhythmias. This rate was almost the same as the maximal sinus rate which was attained by the same dose of epinephrine without halothane. Decrease of supraventricular input by destroying the sinus node also facilitated the induction of ventricular arrhythmia and the threshold dose of epinephrine was the same either in the presence or in the absence of halothane. It is concluded that the mechanism of sensitization to epinephrine by halothane to produce minor ventricular arrhythmia is mainly due to the slowing of the sinus rate by halothane and its direct effect on the ventricular myocardium is a cubsidiary factor.