Cardiac electrophysiologic effects of fentanyl and combinations of fentanyl and neuromuscular relaxants in pentobarbital-anesthetized dogs.

The effects of fentanyl, both alone and in combination with pancuronium bromide or succinylcholine, on atrioventricular (AV) node and ventricular conduction times and refractory periods were studied. Twenty-four pentobarbital-anesthetized dogs were instrumented both with an intraaortic catheter to measure cardiac conduction times and, through a thoracotomy, with atrial and ventricular epicardial pacing electrodes to provide premature stimulation that would allow measurement of atrial and ventricular refractoriness. Fentanyl prolonged the RR interval in both low- (100 micrograms/kg) and high-dose (400 micrograms/kg) groups by 26 and 45%, respectively, and prolonged AV node conduction time by 28 and 25%, respectively. During atrial pacing at a rate sufficient to capture the atria, AV node conduction time lengthened in the low- and high-dose groups by 27 and 25%, respectively. Fentanyl also significantly lengthened AV node effective and functional refractory periods and ventricular effective refractory periods in both groups. Pancuronium (0.1 mg/kg) administered after fentanyl shortened RR intervals in the low- and high-dose groups by 14 and 22%, respectively, and shortened AV conduction times by 18 and 20%, respectively, but did not restore all values to baseline. Pancuronium significantly shortened AV node refractory periods in the low-dose but not the high-dose group. When administered after fentanyl, succinylcholine (2 mg/kg) significantly shortened the RR interval in the low- and high-dose groups by 14 and 12%, respectively. Succinylcholine shortened AV node conduction slightly but without significance and had no effect on cardiac refractoriness. His-Purkinje conduction remained unaffected by any drug intervention. These data demonstrate that fentanyl depresses cardiac conduction; subsequent administration of pancuronium and succinylcholine partially reverses this effect.