EFFECTS OF VOLATILE ANESTHETICS ON ATRIAL AND AV NODAL ELECTROPHYSIOLOGICAL PROPERTIES IN GUINEA-PIG ISOLATED-PERFUSED HEART

Background Knowledge of the anesthetic effects on atrial and atriovent ricular (AV) nodal electrophysiologic properties is fundamental to und erstand the modulatory pole of anesthetics on the pathogenesis of supr aventricular tachycardias, and to individualize the perioperative mana gement of patients with supraventricular tachycardias or AV nodal cond uction disturbances. Therefore the authors studied the effects of thre e commonly used volatile anesthetics on the electrophysiologic propert ies of the atrium and AV node. Methods: The concentration-dependent el ectrophysiologic effects of halothane, isoflurane, and desflurane (0-2 minimum alveolar concentration [MAC]) were studied in guinea pig Lang endorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action pot ential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulati on protocol. The concentrations of anesthetics in the gas phase were m onitored by an infrared gas analyzer. Results: Volatile anesthetics ca used markedly different concentration-dependent effects on atrial cond uction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conductio n the most, whereas desflurane caused the greatest shortening of atria l monophasic action potential duration. Halothane had no significant e ffect on atrial refractoriness, whereas at 2 MAC desflurane significan tly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1 +/- 13.5% and 13.2 +/- 14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics t o prolong AV nodal conduction time and AV nodal ERP was halothane > de sflurane > isoflurane. Conclusion: The different electrophysiologic ef fects of vola tile anesthetics in the atrium and AV node suggest that these agents may modulate atrial dysrhythmogenesis in distinctly diffe rent ways.