Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients

Abstract

Aim of the studyThis 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. MethodsWe 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. ResultsAt 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). ConclusionsInduction 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.