Résumé
BACKGROUND: Bupivacaine is a amide type local anesthetic agent, widely used for its excellent quality of analgesia and long duration of action. But unintended intravenous injection causes severe complication such as convulsion and cardiovascular collapse, which is known for its difficulty in resuscitation. With all the study, the exact mechanism is still unclear and there are much debate on the method of resuscitation. METHOD: We studied the effect of clonidine pretreatment on bupivacaine-induced cardiac toxicity and resuscitation in anesthetized dog. Twelve dogs were divided into two groups. : saline pretreatment group (control, N=6) and clonidine pretreatment group (clonidine group, N=6). The dogs were anesthetized with N2O-O2-enflurane and vecuronium. Thoracotomy was done in 4th or 5th intercostal space for open cardiac massage. After confirming stability of vital signs, we administered clonidine (10 mcg/kg) or saline, and then administered bupivacaine with the rate of 2 mg/kg/min. When the electeocardiogram showed asystole, 20 mcg/kg of epinephrine was administered via central venous line and open cardiac massage with the rate of 120 beat/min. was performed. We observed electrocardiogram (lead II), arterial blood pressure, heart rate, dose of infused bupivacaine to be required for QRS widening and arrest, required time and administered dose of epinephrine for resuscitation. RESULTS: Clonidine group showed significant decrease of heart rate after pretreatment (p<0.05). There was no significant difference in required dose for QRS widening between two groups. The dose administered for inducing arrest was less in clonidine group than control group (p<0.05). The time required for resuscitation was shorter in clonidine group than control group (p<0.05). The total dose of epinephrine required for resuscitation was less in clonidine group than control group (p<0.05). The blood concentration of catecholamine did not showed significant difference during the whole course of experiment. CONCLUSIONS: Above results demonstrated that clonidine, a central nervous system-mediated sympatholytic agent, facilitated cardiac arrest when bupivacaine was infused intravenously and cardiac rescucitation.