Sharpe M D, Dobkowski W B, Murkin J M, Klein G, Yee R
Department of Anaesthesia, University Hospital, University of Western Ontario, London, Canada.
Anesthesiology. 1995 Apr;82(4):888-95. doi: 10.1097/00000542-199504000-00011.
Propofol has been implicated as causing intraoperative bradyarrhythmias. Furthermore, the effects of propofol on the electrophysiologic properties of the sinoatrial (SA) node and on normal atrioventricular (AV) and accessory pathways in patients with Wolff-Parkinson-White syndrome are unknown. Therefore, this study examined the effects of propofol on the cardiac electrophysiologic properties in humans to determine whether propofol promotes bradyarrhythmias and its suitability as an anesthetic agent in patients undergoing ablative procedures.
Twelve patients with Wolff-Parkinson-White syndrome undergoing radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (50 micrograms/kg), midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (2 micrograms.kg-1.min-1) and midazolam (1-2 mg, every 15 min, as needed). A electrophysiologic study was performed consisting of measurement of the effective refractory period of the right atrium, AV node, and accessory pathway and the shortest cycle length of the AV node and accessory pathway during antegrade stimulation plus the effective refractory period of the right ventricle and accessory pathway and the shortest cycle length of the accessory pathway during retrograde stimulation. Determinants of SA node function including sinus node recovery time, corrected sinus node recovery time, and SA conduction time; intraatrial conduction time and atrial-His interval also were measured. Reciprocating tachycardia was induced by rapid right atrial or ventricular pacing, and the cycle length and atrial-His, His-ventricular, and ventriculoatrial intervals were measured. Alfentanil/midazolam was then discontinued. Propofol was administered (bolus 2 mg/kg + 120 micrograms.kg-1.min-1), and the electrophysiologic measurements were repeated.
Propofol caused a statistically significant but clinically unimportant prolongation of the right atrial refractory period. The effective refractory periods of the AV node, right ventricle, and accessory pathway, as well as the shortest cycle length, were not affected. Parameters of SA node function and intraatrial conduction also were not affected. Sustained reciprocating tachycardia was inducible in 8 of 12 patients, and propofol had no effect on its electrophysiologic properties. All accessory pathways were successfully identified and ablated.
Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduction system. In addition, propofol has no direct effect on SA node activity or intraatrial conduction; therefore, it does not directly induce bradyarrhythmias. It is thus a suitable agent for use in patients undergoing ablative procedures who require either a neuroleptic or general anesthetic.
丙泊酚被认为可导致术中缓慢性心律失常。此外，丙泊酚对窦性（SA）结电生理特性以及对预激综合征患者正常房室（AV）和附加通路的影响尚不清楚。因此，本研究检测了丙泊酚对人体心脏电生理特性的影响，以确定丙泊酚是否会促发缓慢性心律失常及其作为接受消融手术患者麻醉剂的适用性。
对12例接受射频导管消融的预激综合征患者进行研究。用阿芬太尼（50微克/千克）、咪达唑仑（0.15毫克/千克）和维库溴铵（20毫克）诱导麻醉，并用阿芬太尼（2微克·千克⁻¹·分钟⁻¹）和咪达唑仑（根据需要每15分钟1 - 2毫克）维持麻醉。进行电生理研究，包括测量右心房、房室结和附加通路的有效不应期以及顺向刺激时房室结和附加通路的最短周期长度，加上右心室和附加通路的有效不应期以及逆向刺激时附加通路的最短周期长度。测量SA结功能的决定因素，包括窦房结恢复时间、校正窦房结恢复时间和SA传导时间；还测量了心房内传导时间和心房 - 希氏束间期。通过快速右心房或心室起搏诱发折返性心动过速，并测量周期长度以及心房 - 希氏束、希氏束 - 心室和心室 - 心房间期。然后停用阿芬太尼/咪达唑仑。给予丙泊酚（静脉推注2毫克/千克 + 120微克·千克⁻¹·分钟⁻¹），并重复电生理测量。
丙泊酚使右心房不应期出现统计学上显著但临床上无重要意义的延长。房室结、右心室和附加通路的有效不应期以及最短周期长度未受影响。SA结功能参数和心房内传导也未受影响。12例患者中有8例可诱发出持续性折返性心动过速，丙泊酚对其电生理特性无影响。所有附加通路均成功识别并消融。
丙泊酚对附加通路的电生理表现和正常房室传导系统的不应期无临床显著影响。此外，丙泊酚对窦房结活动或心房内传导无直接影响；因此，它不会直接诱发缓慢性心律失常。所以，它是适用于需要使用安定药或全身麻醉的接受消融手术患者的药物。
