Canadian Journal of Anesthesia, Vol 26, 263-268, Copyright © 1979 by Canadian Anesthesiologists' Society

Epinephrine-Induced Dysrhythmias: Comparison During Anaesthesia With Narcotics and With Halogenated Inhalation Agents in Dogs

¹ Department of Anesthesiology, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah 84132, U.S.A.

Reprint requests to K.C. Wong, M.D.

The effects of epinephrine-induced dysrhythmias were evaluated in sixteen 15-20 kg mongrel dogs anaesthetized with halogenated inhalation agents, nitrous oxide and pancuronium and with narcotics, nitrous oxide and pancuronium. Group 1 consisted of eight animals which received 1.2 MAC halothane, enflurane or methoxyflurane in nitrous oxide and oxygen (2.5/2.5 litres) and Group 2 of eight animals which received morphine (1 and 2 mg·kg^-1). fentanyl (0.01 and 0.02 mg·kg^-1) and meperidine (10 and 20 mg·kg^-1) with nitrous oxide and oxygen (2.5/2.5 litres). Pancuronium (0.2 mg·kg^-1) was administered to both groups. Each animal in Group 1 or 2 was studied three times but only once a week and one anaesthetic regimen per study. The order of administration of the anaesthetic regimen was randomized for both groups.

Lead II of the electrocardiogram, oesophageal temperature and arterial pressure were monitored continuously. Arterial blood gases and serum sodium and potassium were determined during control, during the peak pressure response from epinephrine infusion and every 30 minutes for the rest of the study. Epinephrine (5 µg/ml) was infused at a rate of 1 µg.kg^-1·min^-1 up to ten minutes. The persistence of three or more consecutive dysrhythmic beats was used as the endpoint of the epinephrine arrhythmogenic dose. Arterial blood gases showed minimal changes in both groups during the course of the experiment with Pa_OO2 24 ± 2.13 kPa (180 ± 16 torr), Pa_COCO2 4.8 ± 0.4 kPa (36 ± 3 torr) and cH⁺ 43.65 ± 0.14 nmol/l (pH 7.36 ± 0.07). Serum sodium did not change significantly during the experiment, but serum potassium increased to a peak concentration of 6.5 ± 0.4 mmol/1 during the epinephrine infusion. The ventricular dysrhythmic dose of epinephrine was generally higher than the corresponding supraventricular dysrhythmic dose for each anaesthetic regimen for both groups. The arrhythmogenic doses for the halogenated-nitrous oxide anaesthesia groups were significantly higher than for the narcotic-nitrous oxide groups; however, The incidence of ventricular arrhythmias was greater in the halogenated-nitrous oxide groups (20 of 24 vs 20 of 48). The incidence of ventricular arrhythmias was less in the methoxyflurane-nitrous oxide group (4/8) than in the halothane-nitrous oxide (8/8) or enflurane-nitrous oxide (8/8) groups. Ventricular tachycardia and ventricular fibrillation occurred in five of eight in the halothane group, three of eight in the enflurane group and in none of the eight in the methoxyflurane group, compared with an occurrence of one out of 48 epinephrine challenges in the narcotic-nitrous oxide groups. These results suggest that anaesthesia with narcotics or methoxyflurane with nitrous oxide and relaxants may stabilize the heart against serious epinephrine-induced ventricular dysrhythmias better than anaesthesia with halogenated inhalation agents, nitrous oxide and relaxant.