title: Cardiac electrophysiologic effects of fentanyl and combinations of fentanyl and neuromuscular relaxants in pentobarbital-anesthetized dogs.
abstract: 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.
authors.affiliation: Department of Anesthesia, Wake Forest University Medical Center, Winston-Salem, NC 27103.
authors.forename: R L
authors.initials: RL
authors.lastname: Royster
authors.forename: D K
authors.initials: DK
authors.lastname: Keeler
authors.forename: W K
authors.initials: WK
authors.lastname: Haisty
authors.forename: W E
authors.initials: WE
authors.lastname: Johnston
authors.forename: D S
authors.initials: DS
authors.lastname: Prough
mesh_terms: D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D005283:Fentanyl / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006329:Heart Conduction System / Q000187:drug effects / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology*; D010424:Pentobarbital
chemical_list: D009467:Neuromuscular Depolarizing Agents; D010424:Pentobarbital; D005283:Fentanyl