THORACIC EPIDURAL-ANESTHESIA ATTENUATES HALOTHANE-INDUCED MYOCARDIAL SENSITIZATION TO DYSRHYTHMOGENIC EFFECT OF EPINEPHRINE IN DOGS

Background: The autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blocka de by thoracic epidural anesthesia has been documented to protect pati ents from various stress responses, the authors speculate that epidura l anesthesia can attenuate the dysrhythmogenic interaction between hal othane and epinephrine. Methods: In adult mongrel dogs anesthetized wi th halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contra ctions within a 15-s period, was determined in the presence of thoraci c epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the D D of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterall y vagotomized dogs. Results: Epidural mepivacaine significantly increa sed the DD of epinephrine compared with epidural saline. However, intr avenous mepivacaine did not affect the DD of epinephrine, even when th e plasma concentration of mepivacaine during the dysrhythmias was twic e that in the epidural mepivacaine group, The beneficial effect of epi dural mepivacaine was not seen in bilaterally vagotomized dogs. Conclu sions: Thoracic epidural anesthesia attenuated the myocardial sensitiz ation by halothane, and vagal activity had an essential role in this a ction.