【罂粟摘要】确定右美托咪定预防老年患者全麻大手术后出现躁动的中位有效剂量：一项前瞻性、双盲、剂量反应试验
确定右美托咪定预防老年患者全麻大手术后出现躁动的中位有效剂量：一项前瞻性、双盲、剂量反应试验
贵州医科大学 麻醉与电生理课题组
翻译：任文鑫 编辑：佟睿 审校：曹莹
右美托咪定可有效降低成年患者出现躁动（EA）的发生率，但随着右美托咪定剂量增加会产生严重的副作用。本研究的目的是确定右旋美托咪定预防老年患者全身麻醉下大手术后出现EA的中位有效剂量。本研究共纳入50例老年患者。第一名患者以0.5μg.kg-1h-1持续静脉输注右美托咪定。根据狄克逊上下法，根据前一个病人的反应，下一个剂量增加或减少0.05。“有效”或 “无效”的反应是根据Riker镇静-激动评分（RSAS）确定的，我们将 "有效 "定义为RSAS<5，而 "无效 "定义为RSAS≥5。右美托咪定预防EA的ED50为0.30μg.kg-1h-1（95%CI，0.27-0.33），预测的ED95为0.42μg.kg-1h-1（95%CI，0.38-0.51）。无EA组与有EA组相比，心动过缓的发生率明显增加（57.1% vs 13.6%，P = 0.002）。预防EA的右美托咪定的ED50为0.30μg.kg-1h-1（95%CI，0.27-0.33），预测的ED95为0.42μg.kg-1h-1（95%CI，0.38-0.51）。心动过缓是主要的并发症。
WeiBing Wang, Hui Zhou, AiJiao Sun, et al.Determination of the Median Effective Dose of Dexmedetomidine for the Prevention of Emergence Agitation in Geriatric Patients Undergoing Major Open Surgery With General Anesthesia: A Prospective,Double-Blinded, Dose-Response Trial.Dose Response 2021 Jul-Sep;19(3).
Determination of the Median Effective Dose of Dexmedetomidine for the Prevention of Emergence Agitation in Geriatric Patients Undergoing Major Open Surgery With General Anesthesia: A Prospective,Double-Blinded, Dose-Response Trial
Abstract
Dexmedetomidine can effectively decrease the incidences of emergence agitation (EA) in adult patients, but there are major side effects related to increased dose of dexmedetomidine. The purpose of this study was to determine the median effective dose of dexmedetomidine in the prevention of EA among geriatric patients undergoing major open surgery with general anesthesia. A total of 50 geriatric patients were enrolled in this study. Dexmedetomidine 0.5 μgkg1h1 continuous intravenous infusion was administered to the first patient. The next dose was increased or decreased by .05 depending on the response of the previous patient, according to the Dixon up-and-down method. An “effective” or “ineffective” response was determined based on the Riker sedation-agitation score (RSAS), we defined “effective” as RSAS<5, and “ineffective” as RSAS≥5. The ED50 of dexmedetomidine in prevention of EA was .30 μgkg1h1 (95% CI, .27–.33) and the predicted ED95 was .42 μgkg1h1 (95%CI, .38–.51). The incidence of bradycardia was significantly increased in the group without EA compared to the group with EA
(57.1% vs 13.6%, P = .002). The ED50 of dexmedetomidine in prevention of EA was .30 μgkg1h1 (95% CI, .27–.33) and the predicted ED95 was .42 μgkg1h1 (95% CI, .38–.51). Bradycardia was the main complication.
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