Grand Johannes, Hassager Christian, Skrifvars Markus B, Tiainen Marjaana, Grejs Anders M, Jeppesen Anni Nørgaard, Duez Christophe Henri Valdemar, Rasmussen Bodil S, Laitio Timo, Nee Jens, Taccone FabioSilvio, Søreide Eldar, Kirkegaard Hans
Department of Cardiology, Rigshospitalet - Copenhagen University Hospital, Denmark.
Department of Anesthesia and Intensive Care, Helsinki University Hospital and University of Helsinki, Finland.
Eur Heart J Acute Cardiovasc Care. 2021 Apr 8;10(2):132–141. doi: 10.1177/2048872620934305. Epub 2020 Jun 17.
Comatose patients admitted after out-of-hospital cardiac arrest frequently experience haemodynamic instability and anoxic brain injury. Targeted temperature management is used for neuroprotection; however, targeted temperature management also affects patients' haemodynamic status. This study assessed the haemodynamic status of out-of-hospital cardiac arrest survivors during prolonged (48 hours) targeted temperature management at 33°C.
Analysis of haemodynamic and vasopressor data from 311 patients included in a randomised, clinical trial conducted in 10 European hospitals (the TTH48 trial). Patients were randomly allocated to targeted temperature management at 33°C for 24 (TTM24) or 48 (TTM48) hours. Vasopressor and haemodynamic data were reported hourly for 72 hours after admission. Vasopressor load was calculated as norepinephrine (µg/kg/min) plus dopamine(µg/kg/min/100) plus epinephrine (µg/kg/min).
After 24 hours, mean arterial pressure (mean±SD) was 74±9 versus 75±9 mmHg (=0.19), heart rate was 57±16 and 55±14 beats/min (=0.18), vasopressor load was 0.06 (0.03-0.15) versus 0.08 (0.03-0.15) µg/kg/min (=0.22) for the TTM24 and TTM48 groups, respectively. From 24 to 48 hours, there was no difference in mean arterial pressure (=0.32) or lactate (=0.20), while heart rate was significantly lower (average difference 5 (95% confidence interval 2-8) beats/min, <0.0001) and vasopressor load was significantly higher in the TTM48 group (=0.005). In a univariate Cox regression model, high vasopressor load was associated with mortality in univariate analysis (hazard ratio 1.59 (1.05-2.42) =0.03), but not in multivariate analysis (hazard ratio 0.77 (0.46-1.29) =0.33).
In this study, prolonged targeted temperature management at 33°C for 48 hours was associated with higher vasopressor requirement but no sign of any detrimental haemodynamic effects.
院外心脏骤停后入院的昏迷患者常出现血流动力学不稳定和缺氧性脑损伤。目标温度管理用于神经保护；然而，目标温度管理也会影响患者的血流动力学状态。本研究评估了院外心脏骤停幸存者在33°C下进行延长（48小时）目标温度管理期间的血流动力学状态。
对10家欧洲医院进行的一项随机临床试验（TTH48试验）中纳入的311例患者的血流动力学和血管升压药数据进行分析。患者被随机分配到33°C目标温度管理24（TTM24）或48（TTM48）小时。入院后72小时每小时报告血管升压药和血流动力学数据。血管升压药负荷计算为去甲肾上腺素（μg/kg/min）加多巴胺（μg/kg/min/100）加肾上腺素（μg/kg/min）。
24小时后，TTM24组和TTM48组的平均动脉压（均值±标准差）分别为74±9与75±9 mmHg（P = 0.19），心率分别为57±16和55±14次/分钟（P = 0.18），血管升压药负荷分别为0.06（0.03 - 0.15）与0.08（0.03 - 0.15）μg/kg/min（P = 0.22）。从24小时到48小时，平均动脉压（P = 0.32）或乳酸（P = 0.20）无差异，而TTM48组的心率显著更低（平均差异5（95%置信区间2 - 8）次/分钟，P < 0.0001），血管升压药负荷显著更高（P = 0.005）。在单变量Cox回归模型中，高血管升压药负荷在单变量分析中与死亡率相关（风险比1.59（1.05 - 2.42），P = 0.03），但在多变量分析中无关（风险比0.77（0.46 - 1.29），P = 0.33）。
在本研究中，33°C下延长48小时的目标温度管理与更高的血管升压药需求相关，但没有任何有害血流动力学效应的迹象。
