EFFECT OF THORACIC EPIDURAL-ANESTHESIA ON SPONTANEOUS POSTINFARCTION VENTRICULAR DYSRHYTHMIA IN AWAKE DOGS

Background and Objectives. Sympathetic neural activity contributes to the genesis of ventricular ectopic activity, particularly in the setti ng of myocardial ischemia and infarction, so thoracic epidural anesthe sia should diminish ventricular ectopy by blocking sympathetic innerva tion of the heart. However, the possible antidysrhythmic effect of epi dural anesthesia has been studied only in the presence of general anes thesia. We therefore examined changes in spontaneous postinfarction ve ntricular dysrhythmia during thoracic epidural anesthesia in awake dog s. Methods. A survivable myocardial infarction was created by two-stag e ligation of the left anterior descending coronary artery. The follow ing day, multifocal idioventricular tachycardia was the predominant ca rdiac rhythm. Lidocaine was administered either by thoracic epidural c atheter to achieve block of at least the first five thoracic segments or intravenously as a control for direct effects, without concurrent g eneral anesthesia or sedation. Electrocardiographic recordings were an alyzed for the number of ventricular ectopic and sinoatrial depolariza tions. Results. Epidural and intravenous administration both produced plasma lidocaine concentrations of about 2 mg/mL. There was no change in rhythm following intravenous lidocaine. During epidural anesthesia, total ectopic beats per minute decreased from 167 +/- 8 to 135 +/- 14 (mean +/-SE, P <.05), and the dysrhythmic ratio (ventricular beats/to tal beats) decreased from 0.93 +/- 0.03 to 0.81 +/- 0.08 (P < .05). Ho wever, ventricular tachydysrhythmia remained the predominant rhythm. C onclusions. Epidural block modestly reduces spontaneous ventricular dy srhythmia in a perioperative setting in dogs following a large myocard ial infarction. These findings do not support the choice of thoracic e pidural anesthesia for the purpose of preventing or decreasing severe ventricular dysrhythmia.