Atrioventricular Conduction Times and Atrioventricular Nodal Conductivity during Enflurane Anesthesia in Dogs
Atrioventricular Conduction Times and Atrioventricular Nodal Conductivity during Enflurane Anesthesia in Dogs
复制标题
犬安氟烷麻醉期间的房室传导时间和房室结电导率
作者：
J. L. Atlee;B. Rusy
由于传导改变可能是麻醉期间心律失常的重要原因，因此作者使用希氏束心电图评价了安氟醚对犬房室（AV）结、希氏-浦肯野和心室传导时间的影响。在自发跳动的心脏和心房起搏期间以120和200次/分钟之间的速率进行评估。为了测试安氟醚对心房有效不应期、AV结功能不应期和AV结传导率的影响，心房期外刺激（测试搏动）以不同的周期长度输送（500 msec或更少）。通过测量最小传导时间，疲劳（最小传导时间与心率变化的关系）和间期相关传导率（AV结传导时间延长超过与测试反应过早相关的最小传导时间）。增加安氟醚浓度从1.0到2.0 MAC延长AV结，但不是希氏浦肯野或心室，传导时间。房室结传导时间随心率增加而增加，安氟醚可增强这种心率依赖性。希氏-浦肯野和心室传导时间不受心率或安氟醚的影响。心房有效不应期、房室结功能性不应期和房室结传导率被安氟醚抑制。对于希氏浦肯野和心室传导系统，目前的结果是在对比以前报道的氟烷。传导改变对于由兴奋重入引起的室性心律失常是必要的。这些发现可能部分解释了临床印象，即与氟烷相比，恩氟烷发生室性心律失常的可能性较小。
Because alterations in conduction may be important as a cause of arrhythmias during anesthesia, the authors used His-bundle electrocardiography to evaluate the effects of enflurane on atrioventricular (AV) nodal, His–Purkinje, and ventricular conduction times in dogs. Evaluations were made in hearts beating spontaneously and during atrial pacing at rates between 120 and 200 beats/min. To test the effects of enflurane on the atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity, atrial extrastimuli (test beats) were delivered at various cycle lengths (500 msec or less) after the last of a series of paced beats at 120 or 200 beats/min. AV nodal conductivity was evaluated by measurements of minimum conduction time, fatigue (the relation of minimum conduction time to change in heart rate), and interval-related conductivity (the prolongation of AV nodal conduction time beyond minimum conduction time related to prematurity of test response). Increasing concentrations of enflurane from 1.0 to 2.0 MAC prolonged AV nodal, but not His–Purkinje or ventricular, conduction times. AV nodal conduction time increased as heart rate was increased, and this rate-dependency was enhanced by enflurane. His–Purkinje and ventricular conduction times were not affected by rate or enflurane. The atrial effective refractory period, functional refractory period of the AV node, and AV nodal conductivity were depressed by enflurane. For the His–Purkinje and ventricular conduction system, the present results are in contrast to those previously reported for halothane. Conduction changes are necessary for ventricular arrhythmias caused by re-entry of excitation. These findings may in part explain the clinical impression that ventricular arrhythmias appear less likely to occur with enflurane than with halothane.