Mangano D T, Siliciano D, Hollenberg M, Leung J M, Browner W S, Goehner P, Merrick S, Verrier E
Department of Anesthesia, University of California, San Francisco 94121.
Anesthesiology. 1992 Mar;76(3):342-53.
Recent data suggest that postbypass and postoperative myocardial ischemia are related to adverse cardiac outcome following myocardial revascularization. Therapeutic trials to suppress postoperative ischemia are warranted. Because anesthetics can suppress a variety of physiologic responses to stress as well as myocardial ischemia intraoperatively, we examined whether use of intensive analgesia in the stressful postoperative period could decrease postoperative ischemia. In 106 patients undergoing elective myocardial revascularization, we standardized the anesthetic prior to bypass (sufentanil 5-10 micrograms/kg [induction] and 4.2-6.0 micrograms.kg-1.h-1 [infusion] supplemented with up to 0.5 mg/kg of diazepam). During bypass, patients were randomly assigned to receive either morphine sulfate (group M, n = 54, up to 2 mg/kg) or sufentanil (group S, n = 52, 1 microgram/kg and 1 microgram.kg-1.h-1). In the intensive care unit (ICU), group M received low-dose analgesia (morphine sulfate 1-10 mg intravenously every 30 min, average dose = 2.2 +/- 2.1 mg/h), while group S continued to receive intensive analgesia (infusion of sufentanil at 1 microgram.kg-1.h-1). Both groups received supplemental midazolam in the ICU (group M = 1.1 +/- 1.1 mg/h; group S = 0.6 +/- 0.6 mg/h; P = 0.01). All analgesic and sedative-hypnotic medications were discontinued at 18 hours following myocardial revascularization. Using continuous two-channel electrocardiographic (ECG) monitoring (CC5 and CM5), we documented and characterized ECG changes consistent with ischemia during the preoperative, intraoperative (pre- and postbypass), and postoperative (on- and off-treatment) periods. The total ECG monitoring time was 8,486 h, averaging 81 h per patient. During the prebypass (anesthetic control) period, groups M and S had a similar incidence, but group S episodes were more severe: maximum ST-segment change (median), S versus M: -1.8 mm versus -1.4 mm (P = 0.04). During the postbypass period, both groups had a similar incidence of ischemia, but episodes in group S were less severe: maximum ST-segment change, S versus M: -1.8 mm versus -2.7 mm (P = 0.0005). During the ICU-on-therapy period, the incidence of ischemic episodes was less in group S patients, and the severity was less: area-under-the-ST-time curve, S versus M: -21 mm.min versus -161 mm.min (P = 0.05). After discontinuation of the drug regimen in the ICU, the incidence and severity of ischemic episodes was similar. The incidence of hypotension, hypertension, and tachycardia was similar in both groups in both the intraoperative and ICU periods.(ABSTRACT TRUNCATED AT 400 WORDS)
近期数据表明，体外循环后及术后心肌缺血与心肌血运重建术后不良心脏结局相关。开展抑制术后缺血的治疗性试验很有必要。由于麻醉药可抑制术中对应激的多种生理反应以及心肌缺血，我们研究了在应激性术后阶段使用强化镇痛是否能减少术后缺血。在106例行择期心肌血运重建术的患者中，我们在体外循环前对麻醉进行了标准化（舒芬太尼5 - 10微克/千克[诱导]以及4.2 - 6.0微克·千克⁻¹·小时⁻¹[输注]，补充最多0.5毫克/千克的地西泮）。在体外循环期间，患者被随机分配接受硫酸吗啡（M组，n = 54，最多2毫克/千克）或舒芬太尼（S组，n = 52，1微克/千克和1微克·千克⁻¹·小时⁻¹）。在重症监护病房（ICU），M组接受低剂量镇痛（硫酸吗啡静脉注射每30分钟1 - 10毫克，平均剂量 = 2.2 ± 2.1毫克/小时），而S组继续接受强化镇痛（舒芬太尼以1微克·千克⁻¹·小时⁻¹输注）。两组在ICU均接受补充咪达唑仑（M组 = 1.1 ± 1.1毫克/小时；S组 = 0.6 ± 0.6毫克/小时；P = 0.01）。所有镇痛及镇静催眠药物在心肌血运重建术后18小时停用。使用连续双导联心电图（ECG）监测（CC5和CM5），我们记录并描述了术前、术中（体外循环前和后）及术后（治疗中和治疗后）期间与缺血一致的ECG变化。总的ECG监测时间为8486小时，平均每位患者81小时。在体外循环前（麻醉控制）阶段，M组和S组发生率相似，但S组发作更严重：最大ST段变化（中位数），S组对M组：-1.8毫米对-1.4毫米（P = 0.04）。在体外循环后阶段，两组缺血发生率相似，但S组发作程度较轻：最大ST段变化，S组对M组：-1.8毫米对-2.7毫米（P = 0.0005）。在ICU治疗期间，S组患者缺血发作发生率较低，且严重程度较低：ST段时间曲线下面积，S组对M组：-21毫米·分钟对-161毫米·分钟（P = 0.05）。在ICU停用药物方案后，缺血发作的发生率和严重程度相似。术中及ICU期间两组低血压、高血压和心动过速的发生率相似。（摘要截短于400字）
