Mokriski B K, Nagle S E, Papuchis G C, Cohen S M, Waxman G J
Department of Anesthesiology, University of Maryland School of Medicine, Baltimore 21201.
J Clin Anesth. 1992 May-Jun;4(3):208-12. doi: 10.1016/0952-8180(92)90067-b.
To determine the frequency of electroconvulsive therapy (ECT)-induced arrhythmias under methohexital, thiamylal, or thiopental sodium anesthesia with and without atropine premedication.
A randomized, double-blind study, placebo-controlled for atropine.
The inpatient psychiatric unit at a university medical center.
Forty-nine patients scheduled for ECT.
Atropine 0.6 mg intravenously (IV) or an equal volume of normal saline IV was given before IV induction of anesthesia with methohexital 0.5 to 1.0 mg/kg, thiamylal 1.5 to 2.5 mg/kg, or thiopental sodium 1.5 to 2.5 mg/kg.
Single-lead electrocardiogram (ECG) recordings were made for 1 minute before induction, during induction of anesthesia, and for 5 minutes after the ECT stimulus. Each ECG was evaluated for arrhythmias and evidence of ischemia in a blinded fashion. Blood pressure and ECG evidence of ischemia did not differ among the groups. Seizure duration was significantly (p less than 0.05) prolonged by a mean of 5 seconds during methohexital anesthesia compared with thiopental sodium and thiamylal (47.6 +/- 18.6 seconds, 42.7 +/- 13.2 seconds, and 42.7 +/- 15.2 seconds, respectively). The frequency of sinus bradycardia was decreased (p less than 0.05) with methohexital (8%) compared with thiopental sodium (20%) and thiamylal (20%). The frequency of premature atrial contractions was decreased (p less than 0.05) with methohexital (43%) compared with thiamylal (61%) but not with thiopental sodium (57%). The frequency of premature ventricular contractions was decreased (p less than 0.05) with methohexital (27%) compared with thiopental sodium (44%) but not with thiamylal (40%). Atropine decreased the frequency of bradycardia (9% vs. 24%) and premature atrial contractions (47% vs. 61%) and increased the frequency of sinus tachycardia (88% vs. 75%).
These data suggest that anesthesia for ECT therapy should be induced with methohexital to minimize the possibility of potentially life-threatening cardiac arrhythmias. Atropine premedication may further decrease the frequency of premature atrial contractions and bradycardia, while increasing the frequency of tachycardia.
确定在使用美索比妥、硫喷妥钠或硫喷妥麻醉且有或无阿托品预处理的情况下,电休克治疗(ECT)诱发心律失常的频率。
一项随机、双盲研究,对阿托品使用安慰剂对照。
一所大学医学中心的住院精神科病房。
49例计划接受ECT治疗的患者。
在静脉注射0.5至1.0mg/kg美索比妥、1.5至2.5mg/kg硫喷妥钠或1.5至2.5mg/kg硫喷妥钠进行麻醉诱导前,静脉注射0.6mg阿托品或等量生理盐水。
在诱导前、麻醉诱导期间以及ECT刺激后5分钟进行单导联心电图(ECG)记录1分钟。以盲法评估每份心电图的心律失常情况和缺血证据。各组间血压和心电图缺血证据无差异。与硫喷妥钠和硫喷妥相比,美索比妥麻醉期间癫痫发作持续时间显著延长(p<0.05),平均延长5秒(分别为47.6±18.6秒、42.7±13.2秒和42.7±15.2秒)。与硫喷妥钠(20%)和硫喷妥(20%)相比,美索比妥组窦性心动过缓的频率降低(p<0.05)(8%)。与硫喷妥(61%)相比,美索比妥组房性早搏的频率降低(p<0.05)(43%),但与硫喷妥钠(57%)相比无差异。与硫喷妥钠(44%)相比,美索比妥组室性早搏的频率降低(p<0.05)(27%),但与硫喷妥(40%)相比无差异。阿托品降低了心动过缓(9%对24%)和房性早搏(47%对61%)的频率,并增加了窦性心动过速的频率(88%对75%)。
这些数据表明,ECT治疗的麻醉应采用美索比妥诱导,以尽量减少潜在危及生命的心律失常的可能性。阿托品预处理可能进一步降低房性早搏和心动过缓的频率,同时增加心动过速的频率。