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心脏骤停后,存活与较高的平均动脉血压相关,而非缺氧缺血性脑病的严重程度:一项回顾性队列研究。

Survival, but not the severity of hypoxic-ischemic encephalopathy, is associated with higher mean arterial blood pressure after cardiac arrest: a retrospective cohort study.

作者信息

Preuß Sandra, Multmeier Jan, Stenzel Werner, Major Sebastian, Ploner Christoph J, Storm Christian, Nee Jens, Leithner Christoph, Endisch Christian

机构信息

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Department of Cardiology and Angiology, Charité Campus Mitte, Charité Universitätsmedizin Berlin, Berlin, Germany.

出版信息

Front Cardiovasc Med. 2024 May 7;11:1337344. doi: 10.3389/fcvm.2024.1337344. eCollection 2024.

DOI:10.3389/fcvm.2024.1337344
PMID:38774664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11106407/
Abstract

BACKGROUND

This study investigates the association between the mean arterial blood pressure (MAP), vasopressor requirement, and severity of hypoxic-ischemic encephalopathy (HIE) after cardiac arrest (CA).

METHODS

Between 2008 and 2017, we retrospectively analyzed the MAP 200 h after CA and quantified the vasopressor requirements using the cumulative vasopressor index (CVI). Through a postmortem brain autopsy in non-survivors, the severity of the HIE was histopathologically dichotomized into no/mild and severe HIE. In survivors, we dichotomized the severity of HIE into no/mild cerebral performance category (CPC) 1 and severe HIE (CPC 4). We investigated the regain of consciousness, causes of death, and 5-day survival as hemodynamic confounders.

RESULTS

Among the 350 non-survivors, 117 had histopathologically severe HIE while 233 had no/mild HIE, without differences observed in the MAP (73.1 vs. 72.0 mmHg, = 0.639). Compared to the non-survivors, 211 patients with CPC 1 and 57 patients with CPC 4 had higher MAP values that showed significant, but clinically non-relevant, MAP differences (81.2 vs. 82.3 mmHg, < 0.001). The no/mild HIE non-survivors ( = 54), who regained consciousness before death, had higher MAP values compared to those with no/mild HIE ( = 179), who remained persistently comatose (74.7 vs. 69.3 mmHg, < 0.001). The no/mild HIE non-survivors, who regained consciousness, required fewer vasopressors (CVI 2.1 vs. 3.6, < 0.001). Independent of the severity of HIE, the survivors were weaned faster from vasopressors (CVI 1.0).

CONCLUSIONS

Although a higher MAP was associated with survival in CA patients treated with a vasopressor-supported MAP target above 65 mmHg, the severity of HIE was not. Awakening from coma was associated with less vasopressor requirements. Our results provide no evidence for a MAP target above the current guideline recommendations that can decrease the severity of HIE.

摘要

背景

本研究调查心脏骤停(CA)后平均动脉血压(MAP)、血管升压药需求与缺氧缺血性脑病(HIE)严重程度之间的关联。

方法

2008年至2017年期间,我们回顾性分析了CA后200小时的MAP,并使用累积血管升压药指数(CVI)对血管升压药需求进行量化。通过对非幸存者进行尸体脑解剖,HIE的严重程度在组织病理学上被分为无/轻度和重度HIE。在幸存者中,我们将HIE的严重程度分为无/轻度脑功能分类(CPC)1和重度HIE(CPC 4)。我们调查了意识恢复情况、死亡原因以及作为血流动力学混杂因素的5天生存率。

结果

在350名非幸存者中,117例组织病理学诊断为重度HIE,233例为无/轻度HIE,MAP无差异(73.1对72.0 mmHg,P = 0.639)。与非幸存者相比,211例CPC 1患者和57例CPC 4患者的MAP值更高,显示出显著但临床上无相关性的MAP差异(81.2对82.3 mmHg,P < 0.001)。在死亡前恢复意识的无/轻度HIE非幸存者(n = 54)与持续昏迷的无/轻度HIE非幸存者(n = 179)相比,MAP值更高(74.7对69.3 mmHg,P < 0.001)。恢复意识的无/轻度HIE非幸存者所需血管升压药较少(CVI 2.1对3.6,P < 0.001)。与HIE严重程度无关,幸存者从血管升压药撤药更快(CVI 1.0)。

结论

尽管较高的MAP与接受血管升压药支持且MAP目标高于65 mmHg治疗的CA患者的生存相关,但与HIE的严重程度无关。从昏迷中苏醒与较少的血管升压药需求相关。我们的结果没有为高于当前指南建议的MAP目标可降低HIE严重程度提供证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/b07b94363213/fcvm-11-1337344-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/d4d9975aeca3/fcvm-11-1337344-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/c09a986fc236/fcvm-11-1337344-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/2d4f62406b85/fcvm-11-1337344-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/b07b94363213/fcvm-11-1337344-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/d4d9975aeca3/fcvm-11-1337344-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/c09a986fc236/fcvm-11-1337344-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/2d4f62406b85/fcvm-11-1337344-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b287/11106407/b07b94363213/fcvm-11-1337344-g004.jpg

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