Halothane-Epinephrine-induced Cardiac Arrhythmias and the Role of Heart Rate

The authors previously showed that cyclopropane-epinephrine-induced bigeminal arrhythmias can best be explained by a re-entrant mechanism. They have now obtained evidence for reentry in bigeminal arrhythmias during infusions of epinephrine (.5-3 mug/kg/min) in dogs anesthetized with .8 per cent halothane. Both a critical level of blood pressure and a critical increase in heart rate were necessary for arrhythmias to be induced in any given animal. Artificial elevation of the blood pressure during infusion of a subthreshold dose of epinephrine could induce bigeminy, and the arrhythmia could be aborted by a sudden reduction of blood pressure. The heart rate accelerated approximately 40 beats/min prior to the onset of bigeminy, and atrial pacing at similarly increased rates during subthreshold infusion of epinephrine could induce bigeminy. Stimulation of the peripheral end of the cut right cervical vagus reduced heart rate and converted bigeminy to sinus rhythm. Bradycardia was not the sole mechanism of the vagal effect since conversion to sinus rhythm could also be achieved with more rapid stimulation of the vagus when the heart rate was maintained constant by atrial pacing. Under these conditions further acceleration of the heart rate could reinstate a bigeminal arrhythmia that was again sensitive to further increases in the frequency of vagal stimulation, and it is concluded that the vagus acts on the spread of the re-entrant impulse. This is best shown with cyclopropane anesthesia, because AV-nodal block occurs more easily with halothane. In addition, very brief periods of increased heart rate caused prolonged periods of bigeminy, which indicates that changes in heart rate may alter the electrophysiology of the halothane-sensitized myocardium to promote bigeminal arrhythmias by a re-entry mechanism.