Fa Hasselt University, Agoralaan Gebouw D, 3590 Diepenbeek, Belgium.
Resuscitation. 2013 Jun;84(6):788-93. doi: 10.1016/j.resuscitation.2013.01.003. Epub 2013 Jan 8.
This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest.
We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO(2)) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO(2) (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming.
At the start of mechanically induced TH, SctO(2) was 68% (65-72) and PaCO(2) was 47.2 mmHg (36.9-51.4). SctO(2) and PaCO(2) significantly decreased to 59% (57-64; p=0.006) and 36.6 mmHg (33.9-44.7; p=0.002), respectively, within the first 3h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n=10) compared with survivors (n=18) at 3h after induction of hypothermia (p=0.02) while the decrease in PaCO(2) was similar in both groups. During TH maintenance, SctO(2) gradually returned to baseline values (69% (63-72)) at 24h, with no differences between survivors and non-survivors (p=0.65). Carbon dioxide remained within the range of mild hypocapnia (32-38 mmHg) throughout the hypothermic period. During rewarming, SctO(2) further increased to 71% (67-78).
Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO(2) was less pronounced in patients surviving to hospital discharge.
本观察性研究旨在评估院外心脏骤停后昏迷患者接受治疗性低温治疗（TH）期间和之后的脑组织氧饱和度（SctO2）。
我们对 2011 年 3 月至 2012 年 4 月期间接受 TH 治疗的心脏骤停后患者的 SctO2（通过近红外光谱测量）进行了前瞻性观察性研究。在低温和主动复温期间，28 例心脏骤停后患者连续进行 SctO2 （无创）测量。
在机械诱导 TH 开始时，SctO2 为 68%（65-72），PaCO2 为 47.2mmHg（36.9-51.4）。SctO2 和 PaCO2 在机械诱导 TH 的前 3 小时内分别显著下降至 59%（57-64；p=0.006）和 36.6mmHg（33.9-44.7；p=0.002）。在低温诱导后 3 小时，非幸存者（n=10）的 SctO2 明显低于幸存者（n=18）（p=0.02），而两组之间 PaCO2 的下降相似。在 TH 维持期间，SctO2 在 24 小时时逐渐恢复至基线值（69%（63-72）），幸存者和非幸存者之间无差异（p=0.65）。在整个低温期，二氧化碳仍处于轻度低碳酸血症（32-38mmHg）范围内。在复温期间，SctO2 进一步增加至 71%（67-78）。
在昏迷的心脏骤停后患者中诱导 TH 会改变氧输送和供应之间的平衡。存活至出院的患者 SctO2 下降不明显。
