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Increasing mean arterial pressure or cardiac output in comatose out-of-hospital cardiac arrest patients undergoing targeted temperature management: effects on cerebral tissue oxygenation and systemic hemodynamics
Resuscitation ( IF 6.5 ) Pub Date : 2021-08-27 , DOI: 10.1016/j.resuscitation.2021.08.037
Johannes Grand 1 , Sebastian Wiberg 1 , Jesper Kjaergaard 1 , Michael Wanscher 2 , Christian Hassager 1
Affiliation  

Introduction

Few data exist on the effects of increasing norepinephrine doses or increasing arterial CO2 (PaCO2) on hemodynamics and cerebral oxygenation in comatose out-of-hospital cardiac arrest (OHCA) patients.

Methods

We prospectively studied 10 resuscitated OHCA-patients undergoing targeted temperature management (36C°). The trial consisted of 5 phases with 20 minutes steady state in-between: Phase 1-4 were increasing doses of norepinephrine to reach targets of mean arterial pressure (MAP). First 65, second 75, third 85, fourth 65 mmHg again. In the fifth phase, MAP was constant while PaCO2 was increased to 6.5-7.3 kPa to increase cardiac output. Primary outcome was cerebral near-infrared spectroscopy (NIRS). Secondary outcomes were hemodynamic variables from Swan-Ganz catheters and blood samples from the radial artery and jugular bulb.

Results

To reach a MAP at 85 mmHg, norepinephrine was increased from 0.11±0.02 to 0.18±0.02 µg/kg/min (P < 0.001). Norepinephrine uptitration significantly increased systemic vascular resistance (SVR) and pulmonary vascular resistance, without affecting cardiac output, heart rate or cerebral oxygenation.

Increasing PaCO2, resulted in a significant increase in cardiac output and cerebral NIRS, but arterial-venous cerebral oxygen-uptake decreased. Norepinephrine demand to keep MAP at 65 mmHg was unaffected by increasing PaCO2.

Conclusions

A short-term increase in MAP with norepinephrine in resuscitated comatose cardiac arrest-patients is associated with increased SVR and pulmonary vascular resistance without affecting cardiac output or cerebral NIRS. Increased cardiac output caused by an increase in PaCO2 increased cerebral NIRS, but not cerebral oxygen uptake.



中文翻译:

在接受目标温度管理的昏迷院外心脏骤停患者中增加平均动脉压或心输出量:对脑组织氧合和全身血流动力学的影响

介绍

关于增加去甲肾上腺素剂量或增加动脉 CO2 (PaCO2) 对昏迷的院外心脏骤停 (OHCA) 患者血流动力学和脑氧合的影响的数据很少。

方法

我们前瞻性地研究了 10 名接受目标温度管理 (36C°) 的复苏 OHCA 患者。该试验包括 5 个阶段,中间有 20 分钟的稳定状态:第 1-4 阶段是增加去甲肾上腺素的剂量以达到平均动脉压 (MAP) 的目标。第一次 65,第二次 75,第三次 85,第四次 65 mmHg。在第五阶段,MAP 保持不变,而 PaCO2 增加到 6.5-7.3 kPa 以增加心输出量。主要结果是大脑近红外光谱(NIRS)。次要结果是来自 Swan-Ganz 导管的血流动力学变量以及来自桡动脉和颈静脉球的血液样本。

结果

为了达到 85 mmHg 的 MAP,去甲肾上腺素从 0.11±0.02 增加到 0.18±0.02 µg/kg/min (P < 0.001)。去甲肾上腺素增加显着增加全身血管阻力 (SVR) 和肺血管阻力,而不影响心输出量、心率或脑氧合。

增加PaCO2,导致心输出量和脑近红外光谱显着增加,但动静脉脑氧摄取减少。将 MAP 保持在 65 mmHg 的去甲肾上腺素需求不受增加 PaCO2 的影响。

结论

在复苏的昏迷心脏骤停患者中,MAP 和去甲肾上腺素的短期增加与 SVR 和肺血管阻力增加有关,而不会影响心输出量或脑近红外光谱。由 PaCO2 增加引起的心输出量增加会增加脑 NIRS,但不会增加脑氧摄取。

更新日期:2021-08-27
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