Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model.
Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model.
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DOI：
10.1093/bja/aep131
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发表时间：
2009-08
影响因子：
9.8
通讯作者：
Matilde Zaballos;C. Jimeno;J. Almendral;Felipe Atienza;D. Patiño;E. Valdes;J. Navia;M. Anadon
中科院分区：
文献类型：
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作者：
Matilde Zaballos;C. Jimeno;J. Almendral;Felipe Atienza;D. Patiño;E. Valdes;J. Navia;M. Anadon
背景技术瑞芬太尼被认为会引起术中缓慢心律失常，但关于其心脏电生理效应的信息很少。因此，我们在闭胸猪模型中评估了瑞芬太尼前后的心脏电生理特性。方法 18头长白猪预先注射氯胺酮并用异丙酚麻醉（4.5 mg·kg(-1)推注，随后13 mg·kg(-1)·h(-1)）。仪器安装后，在异丙酚下进行电生理学评估，并在瑞芬太尼后重复进行电生理学评估（推注1微克·千克（-1），然后输注0.5微克·千克（-1）·分钟（-1））。我们评估了窦房结功能[窦房结恢复时间（SNRT）和窦房传导时间（SACT）]、房室（AV）结功能[窦性心律（SR）和心房起搏期间的AH间隔、温克巴赫周期长度（WCL）和有效不应期（ERP）]、心房、希氏-浦肯野以及心室传导和不应期。评估了“异丙酚方案”和“异丙酚+瑞芬太尼方案”之间的显着变化。结果 瑞芬太尼导致窦性周期长度显着增加（21%，P=0.001），SNRT 显着延长（43%，P=0.001），校正 SNRT（136%，P=0.003），SACT（40%，P=0.005），SR 期间的 AH 间隔（17%，P=0.02），心房起搏期间的 AH 间隔（25%，P=0.01）和心室 ERP（12%，P=0.004）。 WCL 和 AV 结不应期有延长的趋势。在七只动物的参考组中观察到类似的显着变化，其中使用七氟烷代替丙泊酚。心房参数、His-Purkinje 功能、心室内传导参数和 QT 间期未观察到显着变化。结论 瑞芬太尼会抑制窦房结功能和房室结功能的大部分参数。这有助于解释瑞芬太尼相关的严重缓慢性心律失常的临床观察结果。
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 kg(-1) bolus followed by 13 mg kg(-1) h(-1)). After instrumentation, an electrophysiological evaluation was performed under propofol and repeated after remifentanil (bolus of 1 microg kg(-1), followed by an infusion of 0.5 microg kg(-1) min(-1)). We evaluated sinus node function [sinus node recovery time (SNRT) and sinoatrial conduction time (SACT)], atrioventricular (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 'propofol+remifentanil protocol' were evaluated. RESULTS Remifentanil caused a significant increase in sinus cycle length (21%, P=0.001) and a significant prolongation of SNRT (43%, P=0.001), corrected SNRT (136%, P=0.003), SACT (40%, P=0.005), AH interval during SR (17%, P=0.02), AH interval during atrial pacing (25%, P=0.01), and ventricular ERP (12%, P=0.004). 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 intraventricular 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.