%0 Journal Article
%A Zaballos García, Matilde
%A Jimeno, Concepcion
%A Almendral Garrote, Jesús
%A Atienza Fernández, Felipe
%A Patiño, Daniel
%A Valdés, Esther
%A Navia Roque, Juan
%A Anadón Baselga, María José
%T Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model
%D 2009
%@ 0007-0912
%U https://hdl.handle.net/20.500.14352/117130
%X 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.
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