Pathophysiology of tachycardia- and bradycardia-dependent block in the canine proximal his-purkinje system after acute myocardial ischemia

Abstract

An experimental model for the study of conduction disturbances in the proximal His-Purkinje system after acute myocardial ischemia was produced in 24 dogs by ligation of the anterior septal artery. Eighteen of the 19 dogs that survived the initial vulnerable arrhythmic period showed different degrees of conduction disturbance in the bundle of His, right and left bundles or any combination thereof usually within 1 to 2 1 2 hours after ligation. In 14 experiments normal conduction was restored within 8 hours. In all cases with bundle branch block, the block was initially demonstrated on increasing or slowing the heart rate, with a range of intermediate rates at which conduction was normal. Within 45 minutes the block became constant at all heart rates, but within 2 to 6 hours was again replaced by normal conduction at Intermediate rates and, finally, consistent normal conduction. In 12 experiments showing intra-His bundle block (always demonstrated by splitting of the His potential into two deflections, Hb 1 and Hb 2) increasing the rate resulted in second or third degree block with the blocked impulse localized between the two deflections. In 5 of 12 experiments, slowing the rate gave rise to first degree intra-His bundle block (lengthening of the Hb 1-Hb 2 interval). Our in vitro observations suggested that the initial phase of tachycardia- and bradycardia-dependent block in the proximal His-Purkinje system can be explained by characteristic changes in the electrophysiologic properties of two groups of Purkinje fibers which may be due to differential localization of metabolites released in the ischemic zone. Tachycardia-dependent block was based on a time-dependent response of Purkinje fibers partially depolarized by an increase in extracellular concentration of potassium ion. Bradycardia-dependent block was explained by a slight to moderate decrease of resting potential, a normal slope of phase-4 depolarization and reduced membrane responsiveness associated with shift of the threshold potential toward zero. Contrary to previous data, our findings indicate no relation between enhanced automatlcity of pacemaker cells and bradycardia-dependent conduction disturbances.