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|Title: ||Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients|
|Authors: ||Meex, Ingrid|
De Deyne, Cathy
|Issue Date: ||2013|
|Citation: ||RESUSCITATION, 84(6), p. 788-793|
|Abstract: ||Aim of the study:
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 (SctO2) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO2 (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, SctO2 was 68% (65–72) and PaCO2 was 47.2mmHg (36.9–51.4). SctO2 and PaCO2 significantly decreased to 59% (57–64; p=0.006) and 36.6mmHg (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 PaCO2 was similar in both groups. During TH maintenance, SctO2 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 (32–38mmHg) throughout the hypothermic period. During rewarming, SctO2 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 SctO2 was less pronounced in patients surviving to hospital discharge.|
|ISI #: ||000320996800028|
|Type: ||Journal Contribution|
|Validation: ||ecoom, 2014|
|Appears in Collections: ||Research publications|
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