EPINEPHRINE DYSRHYTHMOGENICITY IS NOT ENHANCED BY SUBTOXIC BUPIVACAINE IN DOGS

Since bupivacaine and epinephrine may both precipitate dysrhythmias, c irculating bupivacaine during regional anesthesia could potentiate dys rhythmogenic effects of epinephrine. We therefore examined whether bup ivacaine alters the dysrhythmogenicity of subsequent administration of epinephrine in conscious, healthy dogs and in anesthetized dogs with myocardial infarction. Forty-one conscious dogs received 10 mu g . kg( -1) . min(-1) epinephrine. Seventeen animals responded with ventricula r tachycardia (VT) within 3 min. After 3 h, these responders randomly received 1 or 2 mg/kg bupivacaine or saline over 5 min, followed by 10 mu g . kg(-1) . min(-1) epinephrine. In the bupivacaine groups, epine phrine caused fewer prodysrhythmic effects than without bupivacaine. V T appeared in fewer dogs and at a later time, and there were more sino atrial beats and less ectopies. Epinephrine shortened QT less after bu pivacaine than in control animals. One day after experimental myocardi al infarction, six additional halothane-anesthetized dogs received 4 m u g . kg(-1) . min(-1) epinephrine until VT appeared. After 45 min, 1 mg/kg bupivacaine was injected over 5 min, again followed by 4 mu g . kg(-1) . min(-1) epinephrine. In these dogs, the prodysrhythmic respon se to epinephrine was also mitigated by preceding bupivacaine. Bupivac aine antagonizes epinephrine dysrhythmogenicity in conscious dogs susc eptible to VT and in anesthetized dogs with spontaneous postinfarct dy srhythmias. There is no evidence that systemic subtoxic bupivacaine ad ministration enhances the dysrhythmogenicity of subsequent epinephrine .