【罂粟摘要】控制性血压升高对蛛网膜下腔出血患者脑血流速度和氧合的影响

控制性血压升高对蛛网膜下腔出血患者脑血流速度和氧合的影响

贵州医科大学麻醉与心脏电生理课题组

翻译：马艳燕

编辑：宋雨婷

审校：曹莹

背景

动脉瘤性蛛网膜下腔出血(SAH)患者可能出现脑自身调节功能受损，即随着脑灌注压(CPP)的升高，脑血流量及氧输送被动增加。本研究旨在探讨SAH后早期，即出现任何迟发性脑缺血(DCI)症状前控制性升压对脑血流动力学影响。

方法

该研究在发病后5天内进行。在基础状态和输注去甲肾上腺素将平均动脉压(MAP)最多增加30mmHg，血压不超过130mmHg，20分钟后记录数据。主要指标是经颅多普勒超声（TCD）测量的大脑中动脉血流速度（MCAv）的差异，而颅内压（ICP）、脑组织氧分压(PbtO2)，脑氧化代谢和细胞损伤的微透析标志物的差异为次要指标。对使用Benjamini-Hochberg进行多重校正的次要结果，使用Wilcoxon秩检验分析数据。

结果

36名受试者在发病后4天(中位数，IQR:3-4.75)接受了干预。MAP从82（IQR:76-85）增加到95mmHg(IQR：88-98)(P＜0.001)。MCAv保持稳定（基础值，中位数：46,IQR：46-70 cm/s;控制性血压升高，中位数：55，IQR：48-71cm/s;P＝0.054），而 PbtO2显著升高（基础值，中位数：24，95%CI：19-31mmHg;控制性血压升高，中位数：27，95%CI：24-33 mmHg;P＜0.001）。其余的次要指标无改变。

结论

在这项针对SAH患者的研究中，短暂的控制性血压升高对MCAv没有显著影响，但是PbtO2增加。这表明在这些患者中，自身调节可能没有受损，或者可能是其他机制调节使脑氧合增加。或者确实发生了CBF升高，进而增加了脑氧合，但未被TCD检测到。

原始文献来源：

Olsen MH, Capion T, Riberholt CG, Bache S, Ebdrup SR, Rasmussen R, Mathiesen T, Berg RMG, Møller K. Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage. Acta Anaesthesiol Scand. 2023 May 16.

英文原文

Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage

Background: Patients with aneurysmal subarachnoid haemorrhage (SAH) might have impaired cerebral autoregulation, that is, CBF - and thereby oxygen delivery - passively increase with an increase in CPP. This physiological study aimed to investigate the cerebral haemodynamic effects of controlled blood pressure increase in the early phase after SAH before any signs of delayed cerebral ischaemia (DCI) occurred.

Methods: The study was carried out within 5 days after ictus. Data were recorded at baseline and after 20 min of noradrenaline infusion to increase mean arterial blood pressure (MAP) by a maximum of 30 mmHg and to an absolute level of no more than 130 mmHg. The primary outcome was the difference in middle cerebral artery blood flow velocity (MCAv) measured by transcranial Doppler (TCD), while differences in intracranial pressure (ICP), brain tissue oxygen tension (PbtO2 ), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction.

Results: Thirty-six participants underwent the intervention 4 (median, IQR: 3-4.75) days after ictus. MAP was increased from 82 (IQR: 76-85) to 95 (IQR: 88-98) mmHg (p-value: <.001). MCAv remained stable (baseline, median 57, IQR: 46-70 cm/s; controlled blood pressure increase, median: 55, IQR: 48-71 cm/s; p-value: .054), whereas PbtO2 increased significantly (baseline, median: 24, 95%CI: 19-31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24-33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged.

Conclusions: In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO2 increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD.

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