Dorman B H, Zucker J R, Verrier E D, Gartman D M, Slachman F N
University of Washington School of Medicine, Seattle.
J Cardiothorac Vasc Anesth. 1993 Aug;7(4):386-95. doi: 10.1016/1053-0770(93)90157-g.
The purpose of this study was to determine if clonidine reduces myocardial ischemia or alters anesthetic requirement and perioperative hemodynamic parameters during coronary artery bypass grafting (CABG) surgery. Forty-three patients were randomized in a prospective, double-blind fashion to receive either clonidine (5 micrograms/kg) or placebo. Anesthetic induction and maintenance was accomplished with intravenous sufentanil-midazolam (S-M) in a 1:20 ratio; up to 1.0% enflurane was added during surgery when repeated boluses of S-M failed to maintain the blood pressure within 20% of preinduction values. Continuous ST segment analysis of leads II and V5 was performed throughout surgery with maximal ST segment deflection from baseline recorded every 5 minutes. Catecholamine levels were measured intermittently throughout the perioperative period and myocardial lactate use or excretion was determined just prior to cardiopulmonary bypass (CPB) and at 1, 5, 10, 30, and 60 minutes after release of the aortic cross-clamp. Patients who received clonidine required significantly less sufentanil for their surgical procedure (11.82 +/- 0.66 micrograms/kg v 14.55 +/- 0.90 micrograms/kg, P < 0.05) and also needed less enflurane for blood pressure control, particularly during CPB (P < 0.05). Baseline hemodynamic parameters were similar for both groups prior to induction. In the period between anesthetic induction and the initiation of CPB, patients treated with clonidine had a significantly slower heart rate (HR) (P < 0.01), a lower cardiac output (CO) (P < 0.05), and transiently higher systemic vascular resistance (SVR) (P < 0.05) than placebo-treated patients. Immediately after CPB, patients receiving clonidine continued to have a significantly lower CO (P < 0.01) and a higher SVR (P < 0.01) than placebo-treated patients. Clonidine treatment significantly increased the percentage of patients who required pacing after CPB (P < 0.05). In the intensive care unit, clonidine-treated patients displayed a persistently increased requirement for pacing (P < 0.01), decreased systolic blood pressures, and reduced sodium nitroprusside requirements relative to patients treated with placebo. Epinephrine and norepinephrine levels were lower in clonidine-treated patients throughout the perioperative procedure with significant differences noted immediately following sternotomy and release of the aortic cross-clamp (P < 0.05). Critical ST segment depression was significantly less in clonidine-treated patients for the period from sternotomy until application of the aortic cross-clamp (P < 0.01). Following CPB, absolute deviation of ST segments from isoelectric baseline was significantly less in the clonidine-treated group (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
本研究的目的是确定可乐定是否能减轻冠状动脉搭桥术(CABG)期间的心肌缺血,或改变麻醉需求及围手术期血流动力学参数。43例患者以前瞻性、双盲方式随机分组,分别接受可乐定(5微克/千克)或安慰剂。采用静脉注射舒芬太尼-咪达唑仑(S-M)以1:20的比例进行麻醉诱导和维持;当重复推注S-M未能使血压维持在诱导前值的20%以内时,术中添加高达1.0%的恩氟烷。在整个手术过程中对导联II和V5进行连续ST段分析,每5分钟记录一次ST段相对于基线的最大偏移。在围手术期间歇性测量儿茶酚胺水平,并在体外循环(CPB)前以及主动脉阻断钳松开后1、5、10、30和60分钟测定心肌乳酸利用或排泄情况。接受可乐定治疗的患者手术过程中所需的舒芬太尼显著较少(11.82±0.66微克/千克对14.55±0.90微克/千克,P<0.05),且控制血压所需的恩氟烷也较少,尤其是在CPB期间(P<0.05)。诱导前两组的基线血流动力学参数相似。在麻醉诱导至CPB开始期间,与接受安慰剂治疗的患者相比,接受可乐定治疗的患者心率(HR)显著较慢(P<0.01),心输出量(CO)较低(P<0.05),全身血管阻力(SVR)短暂升高(P<0.05)。CPB后即刻,接受可乐定治疗的患者CO仍显著低于接受安慰剂治疗的患者(P<0.01),SVR较高(P<0.01)。可乐定治疗显著增加了CPB后需要起搏的患者百分比(P<0.05)。在重症监护病房,与接受安慰剂治疗的患者相比,接受可乐定治疗的患者起搏需求持续增加(P<0.01),收缩压降低,硝普钠需求量减少。在整个围手术期,接受可乐定治疗的患者肾上腺素和去甲肾上腺素水平较低,在胸骨切开和主动脉阻断钳松开后即刻有显著差异(P<0.05)。从胸骨切开至主动脉阻断钳应用期间,接受可乐定治疗的患者严重ST段压低显著较少(P<0.01)。CPB后,可乐定治疗组ST段相对于等电位基线的绝对偏移显著较小(P<0.05)。(摘要截短至400字)