Halothane concentration does not alter the threshold for epinephrine-induced arrhythmias in dogs.

Halothane lessens the dose of epinephrine necessary to induce ventricular arrhythmias. However, results of a previous study in dogs anesthetized at two halothane concentrations suggested, but did not confirm, that at the higher concentration (1.7%) myocardial sensitization to epinephrine was less pronounced. This study was designed to determine the myocardial sensitizing effect of halothane at four concentrations: 0.5, 1.0, 1.5, and 2%. To define the appropriate time interval between repeated epinephrine infusions, plasma epinephrine decay curves were assessed. These data indicated that at 7 min the contribution of the residual epinephrine level to the peak level was negligible. Therefore, 7 min was selected as the interval between epinephrine infusions. The arrhythmogenic dose of epinephrine (ADE) was measured at four concentrations of halothane, 0.5, 1.0, 1.5, and 2.0%. To determine the ADE at the subanesthetic concentration of halothane (0.5%), anesthesia was supplemented with etomidate. In a preliminary study, the authors confirmed that this intravenous hypnotic agent did not affect the halothane-epinephrine arrhythmogenic interaction. By analysis of variance, halothane concentration was shown to have no significant influence on the ADE (P greater than 0.05). The authors' data indicate that, over a clinically appropriate range, halothane concentration does not alter the threshold for the development of epinephrine-induced ventricular arrhythmias.