The effects of dobutamine and phenylephrine on atrioventricular conduction during combined use of halothane and thoracic epidural lidocaine

The purpose of this study was to measure cardiac sympathetic nerve activity (CSNA) and atrioventricular (AV) conduction and to test the effects of dobutamine (DOB) and phenylephrine (PHE) on AV conduction during combined use of halothane and thoracic epidural lidocaine. Cats were anesthetized with 1% halothane and an epidural catheter was inserted through T-9 laminectomy. His bundle and atrial electrocardiograms were obtained and atrial electric stimulation was performed using quadripolar catheter electrodes. Cats underwent left thoracotomy, and CSNA was recorded directly from the left ventrolateral or ventromedial nerve. In addition to sinus cycle length (SCL) measurement during spontaneous beating, the functional refractory period (FRP) of the atrioventricular node (AV node), effective refractory period (ERP) of the atrium, atrium-His (A-H) intervals were determined just before and 10, 20, and 30 min after epidural administration of 1% lidocaine (0.2 mL/kg) in Group C. DOB 5 μg.kg -1 .min -1 (Group DOB) and PHE 0.5-1.0 μg.kg -1 .min -1 (Group PHE) were intravenously administered from 12 to 22 min after epidural lidocaine. CSNA and mean arterial pressure (MAP) were markedly decreased and SCL, FRP of AV node, ERP of atrium and A-H interval were significantly prolonged after epidural lidocaine. MAP increased to baseline level during DOB or PHE infusion. Worsening of cardiac electrophysiological variables was improved with DOB infusion, but did not change with PHE infusion. We conclude that thoracic epidural lidocaine during halothane anesthesia almost eliminates CSNA, and thereby attenuates sinus node automaticity and AV node function. DOB restored normal cardiac electrophysiological variables, and therefore is preferable to phenylephrine as a pressor drug.