导语：
近日，一项在瑞士伯尔尼大学医院进行的前瞻性随机对照试验研究发现，在颈动脉内膜切除术中，联合使用右美托咪定和全静脉麻醉，可以显著降低丙泊酚的需求，同时提高患者的血流动力学稳定性。这一成果为临床麻醉提供了新的思路。
一、研究背景
颈动脉内膜切除术是一种治疗颈动脉狭窄的手术。在全静脉麻醉下进行手术时，通常需要使用丙泊酚来实现脑电爆发抑制，降低脑代谢需求。然而，高浓度的丙泊酚可能会延迟患者苏醒，并干扰术中神经生理学监测。
二、研究目的
本研究旨在验证右美托咪定是否能降低颈动脉内膜切除术中实现脑电爆发抑制所需的丙泊酚效应浓度。
三、研究设计
本研究为一项前瞻性随机对照试验，共纳入45名患者，分为对照组（23人）和右美托咪定组（22人）。两组患者均接受全凭静脉麻醉，右美托咪定组患者在诱导前静脉注射右美托咪定（0.4μg/kg，10分钟内），随后持续静脉输注（0.4μg/kg/h）。
四、研究结果
1. 右美托咪定组实现脑电爆发抑制所需的丙泊酚效应浓度为4.0μg/ml，显著低于对照组的6.0μg/ml（P<0.001）。
2. 右美托咪定组所需去甲肾上腺素总量为454μg，低于对照组的1000μg（P=0.015）。
3. 右美托咪定对术中神经生理学监测无影响。
五、研究结论
联合使用右美托咪定和全凭静脉麻醉进行颈动脉内膜切除术，可以降低丙泊酚需求，提高血流动力学稳定性。右美托咪定的丙泊酚节约效应和外周α-激动作用，可能是减少血管活性药物需求的原因。
六、临床试验注册
本研究已在Clinicaltrials.gov注册，注册号为NCT04662177。
总结：
这项研究为颈动脉内膜切除术的麻醉提供了新的优化方案，有望在临床推广应用，为广大患者带来福音。同时，也为其他手术类型的麻醉提供了借鉴意义。
原文摘要
Co-administration of dexmedetomidine with total intravenous anaesthesia in carotid endarterectomy reduces requirements for propofol and improves haemodynamic stability: A single-centre, prospective, randomised controlled trial
Background: Total intravenous anaesthesia guided by electroencephalography and neurophysiological monitoring may be used for carotid endarterectomy. Reduction of brain metabolic demand during cross-clamping of the internal carotid artery with propofol titrated to burst suppression requires effect-site concentrations that may delay emergence and interfere with intraoperative neurophysiological monitoring.
Objective: To test the hypothesis that dexmedetomidine decreases the effect-site concentration of propofol required for burst-suppression in patients undergoing carotid endarterectomy.
Design: Randomised controlled trial.
Participants: Patients undergoing carotid endarterectomy.
Setting: University Hospital of Berne, Switzerland, from October 2018 to September 2024.
Interventions: Patients were randomised into a control (n = 23) and a dexmedetomidine groups (n = 22). Total intravenous anaesthesia was administered to both groups. Patients in the dexmedetomidine group received an intravenous bolus of dexmedetomidine (0.4 μg kg-1 over 10 min) before induction, followed by a continuous intravenous infusion (0.4 μg kg-1 h-1). The effect-site concentrations of propofol were titrated against frontal electroencephalography parameters. Burst suppression was induced with propofol during cross-clamping of the internal carotid artery.
Outcome measures: The primary outcome was the effect-site concentration of propofol required for burst-suppression. The secondary outcomes were the requirement for vasoactive substances, neurophysiological monitoring parameters, and postoperative delirium.
Results: The effect-site concentration of propofol required for burst suppression was 4.0 μg ml-1 [3.50 to 4.90] (median [interquartile range]) in the dexmedetomidine group compared with 6.0 μg ml-1 [5.5 to 7.3] in the control group (P < 0.001). Less norepinephrine was required in the dexmedetomidine group (total 454 μg [246 to 818] compared with 1000 μg [444 to 1326] (P = 0.015) in the control group). Dexmedetomidine did not affect intraoperative neurophysiological monitoring.
Conclusion: Co-administration of dexmedetomidine to total intravenous anaesthesia for carotid endarterectomy decreased the effect-site concentrations of propofol required for burst suppression by 33%. The propofol-sparing effect and peripheral alpha-agonism of dexmedetomidine may explain the reduced requirement for vasopressors.
Trial registration: Clinicaltrials.gov identifier: NCT04662177.
注意：
上述内容仅供参考，如有错误欢迎批评指正，以实际临床医疗为准！
