Anesthetics, Catecholamines, and Ouabain on Automaticity of Primary and Secondary Pacemakers

Abstract

Publisher Summary The elucidation of mechanisms for arrhythmias during anesthesia has been the focus of investigation for a long period of time. Cardiac arrhythmias are usually seen as disturbances of impulse generation, propagation, or both. The potent inhalation anesthetic agents, by direct or indirect effects, can alter automaticity of the sinoatrial (SA) node and latent pacemakers in a manner conducive to the formation of ectopic atrial or atrioventricular (AV) junctional rhythm disturbances. However, volatile anesthetics would oppose a possible effect of digitalis to enhance automaticity of subsidiary or ectopic atrial pacemakers to explain paroxysmal atrial tachycardia (PAT) with toxic digitalis. These hypotheses have been tested in both in vitro and in vivo canine models. Variable depression of the inhalation anesthetics must be considered for anesthetic effects on automaticity of primary and secondary pacemakers. Although halothane (HAL), enflurane (ENF), and isoflurane (ISO) produce equivalent depression of SA node automat city, ENF (not HAL or ISO) enhances automaticity of Purkinje fibers exposed to epinephrine (EPI) compared to HAL or ISO. The relative contribution of baroreflex-mediated suppression varies among inhalation anesthetics, depending on their ability to depress the baroreflex arc. Finally, rate responses to ouabain or catecholamines make it unlikely that enhanced automaticity of subsidiary atrial pacemakers (SAP) can explain paroxysmal atrial tachycardia. The findings to date can have relevance to the management of patients with SA node dysfunction, susceptibility to atrial tachyarrhythmias, or advanced AV heart block, or those receiving digitalis.