Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model
Loading...
Official URL
Full text at PDC
Publication date
2009
Advisors (or tutors)
Editors
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier
Citation
Zaballos M, Jimeno C, Almendral J, Atienza F, Patiño D, Valdes E, Navia J, Anadón MJ. Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model. Br J Anaesth. 2009 Aug;103(2):191-8. doi: 10.1093/bja/aep131
Abstract
Background. Remifentanil has been implicated as causing intraoperative bradyarrhythmias, but little information is available regarding its cardiac electrophysiological effects. Thus, we evaluated the cardiac electrophysiological properties before and after remifentanil in a closed- chest porcine model.
Methods. Eighteen Landrace–Large pigs were premedicated with ketamine and anaesthetized with propofol (4.5 mg kg21 bolus followed by 13 mg kg21 h21). After instrumentation, an elec- trophysiological evaluation was performed under propofol and repeated after remifentanil (bolus of 1 mg kg21, followed by an infusion of 0.5 mg kg21 min21). We evaluated sinus node function [sinus node recovery time (SNRT) and sinoatrial conduction time (SACT)], atrioven- tricular (AV) nodal function [AH intervals during sinus rhythm (SR) and atrial pacing, Wenckebach cycle length (WCL), and effective refractory periods (ERP)], atrial, His-Purkinje, and ventricular conduction and refractoriness. Significant changes between ‘propofol protocol’ and ‘propofolþremifentanil protocol’ were evaluated.
Results. Remifentanil caused a significant increase in sinus cycle length (21%, P1⁄40.001) and a significant prolongation of SNRT (43%, P1⁄40.001), corrected SNRT (136%, P1⁄40.003), SACT (40%, P1⁄40.005), AH interval during SR (17%, P1⁄40.02), AH interval during atrial pacing (25%, P1⁄40.01), and ventricular ERP (12%, P1⁄40.004). There was a tendency towards a prolongation of WCL and AV nodal refractoriness. Similar significant changes were observed in a reference group of seven animals in which sevoflurane was used instead of propofol. No significant changes were observed in atrial parameters, His-Purkinje function, parameters of intraventricu- lar conduction, and QT intervals.
Conclusions. Remifentanil depresses sinus node function and most parameters of AV nodal function. This contributes to an explanation for clinical observations of remifentanil-related severe bradyarrhythmias.