Atrioventricular Conduction Times and Atrioventricular Nodal Conductivity during Enflurane Anesthesia in Dogs

Abstract

Because alterations in conduction may be important as a cause of arrhythmias during anesthesia, the authors used His-bundle electrocardiography to evaluate the effects of enflurane on atrioventricular (AV) nodal, His–Purkinje, and ventricular conduction times in dogs. Evaluations were made in hearts beating spontaneously and during atrial pacing at rates between 120 and 200 beats/min. To test the effects of enflurane on the atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity, atrial extrastimuli (test beats) were delivered at various cycle lengths (500 msec or less) after the last of a series of paced beats at 120 or 200 beats/min. AV nodal conductivity was evaluated by measurements of minimum conduction time, fatigue (the relation of minimum conduction time to change in heart rate), and interval-related conductivity (the prolongation of AV nodal conduction time beyond minimum conduction time related to prematurity of test response). Increasing concentrations of enflurane from 1.0 to 2.0 MAC prolonged AV nodal, but not His–Purkinje or ventricular, conduction times. AV nodal conduction time increased as heart rate was increased, and this rate-dependency was enhanced by enflurane. His–Purkinje and ventricular conduction times were not affected by rate or enflurane. The atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity were depressed by enflurane. For the His–Purkinje and ventricular conduction system, the present results are in contrast to those previously reported for halothane. Conduction changes are necessary for ventricular arrhythmias caused by re-entry of excitation. These findings may in part explain the clinical impression that ventricular arrhythmias appear less likely to occur with enflurane than with halothane.