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急性呼吸窘迫综合征患者的脑血管自动调节与动脉二氧化碳:一项前瞻性观察队列研究

Cerebrovascular autoregulation and arterial carbon dioxide in patients with acute respiratory distress syndrome: a prospective observational cohort study.

作者信息

Kahl Ursula, Yu Yuanyuan, Nierhaus Axel, Frings Daniel, Sensen Barbara, Daubmann Anne, Kluge Stefan, Fischer Marlene

机构信息

Department of Anesthesiology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.

Department of Intensive Care Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

出版信息

Ann Intensive Care. 2021 Mar 16;11(1):47. doi: 10.1186/s13613-021-00831-7.

DOI:10.1186/s13613-021-00831-7
PMID:33725209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7962086/
Abstract

BACKGROUND

Early hypercapnia is common in patients with acute respiratory distress syndrome (ARDS) and is associated with increased mortality. Fluctuations of carbon dioxide have been associated with adverse neurological outcome in patients with severe respiratory failure requiring extracorporeal organ support. The aim of this study was to investigate whether early hypercapnia is associated with impaired cerebrovascular autoregulation during the acute phase of ARDS.

METHODS

Between December 2018 and November 2019, patients who fulfilled the Berlin criteria for ARDS, were enrolled. Patients with a history of central nervous system disorders, cerebrovascular disease, chronic hypercapnia, or a life expectancy of less than 24 h were excluded from study participation. During the acute phase of ARDS, cerebrovascular autoregulation was measured over two time periods for at least 60 min. Based on the values of mean arterial blood pressure and near-infrared spectroscopy, a cerebral autoregulation index (COx) was calculated. The time with impaired cerebral autoregulation was calculated for each measurement and was compared between patients with and without early hypercapnia [defined as an arterial partial pressure of carbon dioxide (PaCO) ≥ 50 mmHg with a corresponding arterial pH < 7.35 within the first 24 h of ARDS diagnosis].

RESULTS

Of 66 patients included, 117 monitoring episodes were available. The mean age of the study population was 58.5 ± 16 years. 10 patients (15.2%) had mild, 28 (42.4%) moderate, and 28 (42.4%) severe ARDS. Nineteen patients (28.8%) required extracorporeal membrane oxygenation. Early hypercapnia was present in 39 patients (59.1%). Multivariable analysis did not show a significant association between early hypercapnia and impaired cerebrovascular autoregulation (B = 0.023 [95% CI - 0.054; 0.100], p = 0.556). Hypocapnia during the monitoring period was significantly associated with impaired cerebrovascular autoregulation [B = 0.155 (95% CI 0.014; 0.296), p = 0.032].

CONCLUSION

Our results suggest that moderate permissive hypercapnia during the acute phase of ARDS has no adverse effect on cerebrovascular autoregulation and may be tolerated to a certain extent to achieve low tidal volumes. In contrast, episodes of hypocapnia may compromise cerebral blood flow regulation. Trial registration ClinicalTrials.gov; registration number: NCT03949738; date of registration: May 14, 2019.

摘要

背景

早期高碳酸血症在急性呼吸窘迫综合征(ARDS)患者中很常见,且与死亡率增加相关。二氧化碳波动与需要体外器官支持的严重呼吸衰竭患者的不良神经学结局有关。本研究的目的是调查早期高碳酸血症是否与ARDS急性期脑血管自动调节功能受损有关。

方法

2018年12月至2019年11月期间,纳入符合ARDS柏林标准的患者。有中枢神经系统疾病、脑血管疾病、慢性高碳酸血症病史或预期寿命小于24小时的患者被排除在研究之外。在ARDS急性期,在两个时间段内至少60分钟测量脑血管自动调节功能。根据平均动脉血压和近红外光谱值,计算脑自动调节指数(COx)。计算每次测量时脑血管自动调节功能受损的时间,并在有和没有早期高碳酸血症的患者之间进行比较[定义为ARDS诊断后24小时内动脉血二氧化碳分压(PaCO)≥50 mmHg且相应动脉血pH<7.35]。

结果

纳入的66例患者中,有117次监测记录。研究人群的平均年龄为58.5±16岁。10例患者(15.2%)为轻度ARDS,28例(42.4%)为中度ARDS,28例(42.4%)为重度ARDS。19例患者(28.8%)需要体外膜肺氧合。39例患者(59.1%)存在早期高碳酸血症。多变量分析未显示早期高碳酸血症与脑血管自动调节功能受损之间存在显著关联(B=0.023[95%CI -0.054;0.100],p=0.556)。监测期间的低碳酸血症与脑血管自动调节功能受损显著相关[B=0.155(95%CI 0.014;0.296),p=0.032]。

结论

我们的结果表明,ARDS急性期适度允许性高碳酸血症对脑血管自动调节功能没有不良影响,并且在一定程度上可以耐受以实现低潮气量。相比之下,低碳酸血症发作可能会损害脑血流调节。试验注册ClinicalTrials.gov;注册号:NCT03949738;注册日期:2019年5月14日。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/eb36a97497e6/13613_2021_831_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/0349229034d2/13613_2021_831_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/f02fb29f6585/13613_2021_831_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/eb36a97497e6/13613_2021_831_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/0349229034d2/13613_2021_831_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/f02fb29f6585/13613_2021_831_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8930/7966654/eb36a97497e6/13613_2021_831_Fig3_HTML.jpg

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