Cardiac arrhythmias continue to be an important cause of anesthetic morbidity and mortality. Of particulat concern are supraventricular arrhythmias, which because of A-V dyssynchrony or tachycardia, may lead to circulatory impairment or reduced myocardial oxygenation. Either could result in more life-threatening ventricular arrhythmias. Also of concern are catecholamine-mediated ventricular arrhythmias, which could be the result of stress or the exogenous administration of epinephrine. Utilizing a chronically instrumented dog model, the effects of commonly used inhalation anesthetics - enflurane, halothane and isoflurane - on supraventricular conduction, refractory periods and electrically provoked atrial arrhythmias will be compared to awake. Data from these experiments will be related to the propensity of these anesthetics to cause or contribute to reentrant supraventricular tachyarrhythmias and A-V junctional or ventricular escape rhythms. Additionally, in separate experiments, the dose and corresponding plasma levsel of epinephrine for ventricular arrhythmias will be compared with each of these anesthetics in dogs. Since each dog will serve as his own control, the propensity for enflurane, halothane and isoflurane to facilitate or protect against epinephrine-induced ventricular arrhythmias will be directly compared for the first time. Results of these investigations will further our understanding of mechanisms for cardiac arrhythmias during anesthesia and surgery. Familiarity with mechanisms for arrhythmias, and how anesthetics and other drugs may affect these, is critical to effective arrhythmia prevention and management,
