Effects of altered heart rate on chloroformepinephrine cardiac arrhythmia.

Abstract

In chloroform-anesthetized dogs receiving epinephrine, slowing of the heart rate invariably accompanies conversion of arrhythmia to normal supraventricular rhythm by vagal stimulation, and restoring the faster heart rate reestablishes arrhythmia. Increasing the heart rate during epinephrine infusion can induce arrhythmia or increase the proportion of ventricular ectopic beats. These observations are taken to indicate that the vagal influence on ventricular arrhythmia in these conditions is indirect and mediated through the frequency of excitation entering the ventricle. It is suggested that during chloroform anesthesia an increased heart rate favors the emergence of ventricular arrhythmia when activity propagated after successively shorter intervals encounters delay or local conduction block in the Purkinje system, and re-entry excitation is made possible. It is proposed that in these conditions ventricular tachycardia is a self-sustaining arrhythmia that must maintain a critical frequency, either intrinsically or from external (supraventricular) input. The arrhythmia is susceptible to termination by vagal stimulation when atrial slowing decreases the probability of an atrial impulse entering the ventricle at a critical time.