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危重症患者终末期心血管衰竭相关的动脉血压:一项回顾性队列研究。

The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients: a retrospective cohort study.

作者信息

Brunauer Andreas, Koköfer Andreas, Bataar Otgon, Gradwohl-Matis Ilse, Dankl Daniel, Dünser Martin W

机构信息

Department of Anesthesiology, Perioperative Care and Intensive Care Medicine, University Hospital Salzburg and Paracelsus Private Medical University, Müllner Hauptstrasse 48, 5020, Salzburg, Austria.

Department of Emergency and Critical Care Medicine, Central State University Hospital, Marx Street, Ulaanbaatar, Mongolia.

出版信息

Crit Care. 2014 Dec 19;18(6):719. doi: 10.1186/s13054-014-0719-2.

DOI:10.1186/s13054-014-0719-2
PMID:25524592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4299308/
Abstract

INTRODUCTION

Liberal and overaggressive use of vasopressors during the initial period of shock resuscitation may compromise organ perfusion and worsen outcome. When transiently applying the concept of permissive hypotension, it would be helpful to know at which arterial blood pressure terminal cardiovascular collapse occurs.

METHODS

In this retrospective cohort study, we aimed to identify the arterial blood pressure associated with terminal cardiovascular collapse in 140 patients who died in the intensive care unit while being invasively monitored. Demographic data, co-morbid conditions and clinical data at admission and during the 24 hours before and at the time of terminal cardiovascular collapse were collected. The systolic, mean and diastolic arterial blood pressures immediately before terminal cardiovascular collapse were documented. Terminal cardiovascular collapse was defined as an abrupt (<5 minutes) and exponential decrease in heart rate (> 50% compared to preceding values) followed by cardiac arrest.

RESULTS

The mean ± standard deviation (SD) values of the systolic, mean and diastolic arterial blood pressures associated with terminal cardiovascular collapse were 47 ± 12 mmHg, 35 ± 11 mmHg and 29 ± 9 mmHg, respectively. Patients with congestive heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.04), left main stem stenosis (39 ± 11 mmHg versus 34 ± 11 mmHg; P = 0.03) or acute right heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.03) had higher arterial blood pressures than patients without these risk factors. Patients with severe valvular aortic stenosis had the highest arterial blood pressures associated with terminal cardiovascular collapse (systolic, 60 ± 20 mmHg; mean, 46 ± 12 mmHg; diastolic, 36 ± 10 mmHg), but this difference was not significant. Patients with sepsis and patients exposed to sedatives or opioids during the terminal phase exhibited lower arterial blood pressures than patients without sepsis or administration of such drugs.

CONCLUSIONS

The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients was very low and varied with individual co-morbid conditions (for example, congestive heart failure, left main stem stenosis, severe valvular aortic stenosis, acute right heart failure), drug exposure (for example, sedatives or opioids) and the type of acute illness (for example, sepsis).

摘要

引言

在休克复苏初期,过度随意且激进地使用血管升压药可能会损害器官灌注并使预后恶化。在短暂应用允许性低血压概念时,了解终末期心血管功能衰竭发生时的动脉血压会有所帮助。

方法

在这项回顾性队列研究中,我们旨在确定140例在重症监护病房死亡且接受有创监测的患者中与终末期心血管功能衰竭相关的动脉血压。收集了人口统计学数据、合并症以及入院时、终末期心血管功能衰竭前24小时及发生时的临床数据。记录终末期心血管功能衰竭前即刻的收缩压、平均动脉压和舒张压。终末期心血管功能衰竭定义为心率突然(<5分钟)且呈指数下降(相较于先前值下降>50%),随后发生心脏骤停。

结果

与终末期心血管功能衰竭相关的收缩压、平均动脉压和舒张压的均值±标准差分别为47±12 mmHg、35±11 mmHg和29±9 mmHg。患有充血性心力衰竭(39±13 mmHg对34±10 mmHg;P = 0.04)、左主干狭窄(39±11 mmHg对34±11 mmHg;P = 0.03)或急性右心衰竭(39±13 mmHg对34±10 mmHg;P = 0.03)的患者的动脉血压高于无这些危险因素的患者。患有严重瓣膜性主动脉狭窄的患者与终末期心血管功能衰竭相关的动脉血压最高(收缩压,60±20 mmHg;平均动脉压,46±12 mmHg;舒张压,36±10 mmHg),但差异不显著。与无脓毒症或未使用此类药物的患者相比,脓毒症患者以及终末期接受镇静剂或阿片类药物治疗的患者的动脉血压较低。

结论

危重症患者终末期心血管功能衰竭相关的动脉血压非常低,且因个体合并症(如充血性心力衰竭、左主干狭窄、严重瓣膜性主动脉狭窄、急性右心衰竭)、药物暴露(如镇静剂或阿片类药物)以及急性疾病类型(如脓毒症)而异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f8/4299308/6d07c4c9385c/13054_2014_719_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f8/4299308/d6df0ddf525b/13054_2014_719_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f8/4299308/6d07c4c9385c/13054_2014_719_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f8/4299308/d6df0ddf525b/13054_2014_719_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0f8/4299308/6d07c4c9385c/13054_2014_719_Fig2_HTML.jpg

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