Epinephrine-induced arrhythmias and cardiovascular function after verapamil during halothane anesthesia in the dog.

The antiarrhythmic and cardiovascular effects of the slow channel inhibitor, verapamil, were studied during 1.1 MAC halothane anesthesia in the dog. The control epinephrine arrhythmogenic dose to induce ventricular arrhythmias was 2.58 +/- 0.77 microgram . kg-1 . min-1 (mean +/- SEM). Three consecutive doses of 0.2 mg/kg verapamil each elevated the dose of epinephrine required to produce a ventricular arrhythmia to 5.17 +/- 1.27, 8.07 +/- 1.85, and 12.03 +/- 2.76 microgram . kg-1 . min-1, respectively, all of which were significantly elevated above the control value of the preceding values. A second group of dogs, unperturbed by epinephrine, received the same sequence of verapamil doses at similar time intervals for evaluation of effects on cardiovascular function and atrioventricular conduction. Heart rate remained unchanged. Mean arterial pressure decreased maximally by 37 per cent of control, left ventricular dP/dt by 24 per cent, and systemic vascular resistance by 51 per cent. These effects were transient with recovery times up to one hour. Central venous pressure increased by 44 per cent and left ventricular end diastolic pressure by 27 per cent, while PR interval was prolonged by 40 per cent. Thus, verapamil raised the dose of epinephrine required to elicit a ventricular arrhythmia during halothane anesthesia promptly and cumulatively. At the same time verapamil produced transient peripheral vasodilation, direct depression of myocardial contractility, and prolongation of atrioventricular conduction time that was not cumulative at the intervals studied.