Electrophysiologic Interaction between Class I Antiarrhythmic Drugs and Volatile Anesthetics in Depressant Effects on Ventricular Activation in a Canine Myocardial Infarction Model

Abstract

ABSTRACT-Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarryhthmic drugs depress the ven tricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial ac tivation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs mark edly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

Sevoflurane in Paediatric Anaesthesia

“…[5] Sevoflurane does not affect the magnitude of lidocaine serum protein binding [152] but is synergistic with lidocaine and procainamide in prolonging ventricular activation time. [153] It does not interact pharmacodynamically with nicardipine [154,155] or diltiazem. [155] …”

New-Onset Intermittent Deceleration-Dependent Left Bundle Branch Block Following Induction of General Anesthesia in a Healthy Patient: A Case Report

“…Volatile anesthetics have the potential to impact sinoatrial node discharge rates [ 13 ] and alter ion channel functions [ 14 ], which could be particularly relevant in cases of ADA and DDA. For ADA, the goal is to prevent tachycardia by minimizing sympathetic stimulation, particularly during critical phases like laryngoscopy or surgical incision.…”