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麻醉期间血压逐步升高时的动态大脑自动调节:一项非随机干预试验

2023-08-04 14:44

在全身麻醉期间,动态CA依赖于自动调节范围内的MAP。这种现象在丙泊酚麻醉期间比七氟醚麻醉期间更明显。

以下文章来源于罂粟花 ,作者anesthGH

本文由“罂粟花”授权转载

麻醉期间血压逐步升高的动态大脑自动调节一项非随机干预试验

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贵州医科大学  麻醉与心脏电生理课题

翻译:  宋雨婷

编辑:  严旭

审校: 曹莹

背景

大脑自动调节(CA)通过脑血管张力的改变使脑血流量(CBF)保持恒定,以适应平均动脉压(MAP)在60至150 mmHg之间的波动。然而,这不是CA的开关机制;先前的研究表明,血管舒缩张力与CA功能成比例相关。在丙泊酚麻醉期间,存在脑血管收缩,静态CA保持完整。在七氟烷的麻醉诱导期间,脑血管舒张,并呈剂量依赖性减弱CA。目前尚不清楚这如何转化为自动调节范围内血压相关的动态CA。

目的

本研究的目的是量化在丙泊酚和七氟烷麻醉期间,使用去氧肾上腺素在60至100mmHg之间逐步增加的MAP对动态CA的影响。

设计

一项非随机干预试验。

试验设置:

本试验为一项单中心试验,于2019年1月11日进行,并于2019年9月23日结束。

病人

在全身麻醉下接受非心胸外科、非神经外科和非腹腔镜手术且美国麻醉医师协会健康状态分级为(ASA)I/II的患者。

干预措施:

在接受丙泊酚或七氟烷麻醉的患者中,通过使用去氧肾上腺素逐步增加自动调节血压范围内的MAP来调节脑血管张力。在用丙泊酚(n = 26)或七氟烷(n = 28)麻醉且ASA I/II的患者中,维持MAP在60-100mmHg,MAP每增加10mmHg,测量MAP和平均大脑中动脉血流速度(MCAVmean)。通过绘制2分钟MCAVmean—MAP曲线来确定静态CA。使用传递函数确定动态CA,并表示为MAP和MCAVmean振荡之间的相位超前(°),通过正压通气产生,频率为 6 min−1。

主要结局指标

本研究的主要结局指标是在丙泊酚和七氟烷麻醉期间MAP逐步增加时动态CA的变化。

结果

两个麻醉方案之间每一增量达到的MAP水平相当(丙泊酚和七氟醚分别为63±3、72±2、80±2、90±2、100±3mmHg和61±4、71±2、80±2、89±2、98±4mmHg)。与丙泊酚麻醉相比,随着MAP逐步增加,七氟烷麻醉期间MCAVmean增加更多(P ≤0.001)。丙泊酚麻醉期间动态CA得以改善(0.73° mmHg−1,95%CI 0.51-0.95;P ≤0.001)),并且在七氟烷麻醉期间不太明显(0.21° mmHg−1(95% CI 0.01-0.42,P = 0.04)。

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结论

在全身麻醉期间,动态CA依赖于自动调节范围内的MAP。这种现象在丙泊酚麻醉期间比七氟醚麻醉期间更明显。

原始文献来源

van den Dool, Rokus E.C.; Sperna Weiland, Nicolaas H.; Schenk, Jimmy; Kho, Eline; Veelo, Denise P.; van der Ster, Björn J.P.; Immink, Rogier V.. Dynamic cerebral autoregulation during step-wise increases in blood pressure during anaesthesia: A nonrandomised interventional trial. European Journal of Anaesthesiology 40(6):p 407-417, June 2023.

英文原文:

Dynamic cerebral autoregulation during step-wise increases in blood pressure during anaesthesia: A nonrandomised interventional trial

BACKGROUND: Classically, cerebral autoregulation (CA) entails cerebral blood flow (CBF) remaining constant by cerebrovascular tone adapting to fluctuations in mean arterial pressure (MAP) between ∼60 and ∼150 mmHg. However, this is not an on–off mechanism; previous work has suggested that vasomotor tone is proportionally related to CA function. During propofol-based anaesthesia, there is cerebrovascular vasoconstriction, and static CA remains intact. Sevoflurane-based anaesthesia induces cerebral vasodilation and attenuates CA dose-dependently. It is unclear how this translates to dynamic CA across a range of blood pressures in the autoregulatory range.

OBJECTIVE: The aim of this study was to quantify the effect of step-wise increases in MAP between 60 and 100 mmHg, using phenylephrine, on dynamic CA during propofol- and sevoflurane-based anaesthesia.

DESIGN: A nonrandomised interventional trial.

SETTING: Single centre enrolment started on 11 January 2019 and ended on 23 September 2019.

PATIENTS: We studied American Society of Anesthesiologists (ASA) I/II patients undergoing noncardiothoracic, nonneurosurgical and nonlaparoscopic surgery under general anaesthesia.

INTERVENTION: In this study, cerebrovascular tone was manipulated in the autoregulatory range by increasing MAP step-wise using phenylephrine in patients receiving either propofol- or sevoflurane-based anaesthesia. MAP and mean middle cerebral artery blood velocity (MCAVmean) were measured in ASA I and II patients, anaesthetised with either propofol (n = 26) or sevoflurane (n = 28), during 10 mmHg step-wise increments of MAP between 60 and 100 mmHg. Static CA was determined by plotting 2-min averaged MCAVmean versus MAP. Dynamic CA was determined using transfer function analysis and expressed as the phase lead (°) between MAP and MCAVmean oscillations, created with positive pressure ventilation with a frequency of 6 min−1.

MAIN OUTCOMES: The primary outcome of this study was the response of dynamic CA during step-wise increases in MAP during propofol- and sevoflurane-based anaesthesia.

RESULTS: MAP levels achieved per step-wise increments were comparable between anaesthesia regiment (63 ± 3, 72 ± 2, 80 ± 2, 90 ± 2, 100 ± 3 mmHg, and 61 ± 4, 71 ± 2, 80 ± 2, 89 ± 2, 98 ± 4 mmHg for propofol and sevoflurane, respectively). MCAVmean increased more during step-wise MAP increments for sevoflurane compared to propofol (P≤0.001). Dynamic CA improved during propofol (0.73° mmHg−1, 95% CI 0.51 to 0.95; P ≤ 0.001)) and less pronounced during sevoflurane-based anaesthesia (0.21° mmHg−1 (95% CI 0.01 to 0.42, P = 0.04).

CONCLUSIONS: During general anaesthesia, dynamic CA is dependent on MAP, also within the autoregulatory range. This phenomenon was more pronounced during propofol anaesthesia than during sevoflurane.

免责声明:

本公众平台所刊载原创或转载内容不代表米勒之声的观点或立场。文中所涉及药物使用、疾病诊疗等内容仅供医学专业人士参考。

END

编辑:Michel.米萱

校对:MiLu.米鹭

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