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PubMed1989

[Coronary artery spasm under thoracic epidural anesthesia].

Three paroxysmal episodes of ST-segment elevation in lead II of ECG were observed during bullectomy and chest closing under epidural anesthesia supplemented with enflurane in compressed air in a patient who had history of variant angina with 50% obstruction of right coronary artery. The first and the third episodes were followed by ventricular tachycardia, complete A-V block and hypotension. These attacks were preceded by decreases in heart rate and blood pressure. It was suspected that coronary artery spasm developed with increased vagal tone under thoracic epidural block. The first and the second attacks were successfully treated with intravenous injection of nitroglycerin and lidocaine. The third attack needed additional treatments which included intravenous administrations of atropine, epinephrine, isoproterenol and phenylephrine and direct heart massage through the thoracic incision. Postoperative serial examinations of ECG showed inverted T in lead V1-V4, and serum enzymes (GOT, GPT, LDH, CPK, CPK-MB) were elevated. However ratio of CPK-MB to total CPK was only 1.5%. The patient was discharged two weeks after the operation with normal ECG and serum enzymes. It is speculated that coronary artery spasm was induced by hypotension and vagal stimulation under epidural anesthesia which blocks cardiac sympathetic nerves.

Aged↗
PubMed1986

Comparison of resuscitation of sheep and dogs after bupivacaine-induced cardiovascular collapse.

This study evaluated interspecies sensitivity and ability to resuscitate pentobarbital anesthetized sheep and dogs after cardiovascular toxic doses of bupivacaine. Every minute, 3 mg/kg of bupivacaine was injected into the right atrium over the course of 10 sec until cardiovascular collapse occurred. While the bupivacaine was given, the animals were made apneic for 90 sec and then ventilated with 100% oxygen. After the bupivacaine administration, cardiovascular collapse occurred in the form of electromechanical dissociation progressing to asystole in dogs, whereas in sheep the predominant rhythm was ventricular fibrillation leading to asystole. Resuscitation was performed using open chest heart massage, bretylium for treatment of ventricular tachycardia and fibrillation, and epinephrine with atropine for treatment of electromechanical dissociation or asystole. The initial dose of bupivacaine used to cause cardiovascular collapse was 3.5 +/- 1.2 mg/kg in sheep and 24.6 +/- 8.5 mg/kg in dogs (P less than 0.01). All sheep and dogs were resuscitated from the first cardiovascular collapse. The resuscitation time was 2.1 +/- 1.0 min in dogs and 36.9 +/- 15.4 min in sheep (P less than 0.01). All dogs could be resuscitated after two additional cardiovascular collapses induced by bupivacaine, but no sheep could be resuscitated after a second cardiovascular collapse. Concentrations of bupivacaine in cardiac tissue and serum levels of bupivacaine after the last resuscitation attempt were significantly greater in the dogs than in the sheep. We conclude that sheep are more sensitive to bupivacaine than dogs, but that even sheep can be resuscitated after cardiovascular collapse produced by bupivacaine.

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