Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial.

Abstract

We assessed the effects of targeting low-normal or high-normal arterial carbon dioxide tension (PaCO₂) and normoxia or moderate hyperoxia after out-of-hospital cardiac arrest (OHCA) on markers of cerebral and cardiac injury. Using a 2³ factorial design, we randomly assigned 123 patients resuscitated from OHCA to low-normal (4.5-4.7 kPa) or high-normal (5.8-6.0 kPa) PaCO₂ and to normoxia (arterial oxygen tension [PaO₂] 10-15 kPa) or moderate hyperoxia (PaO₂ 20-25 kPa) and to low-normal or high-normal mean arterial pressure during the first 36 h in the intensive care unit. Here we report the results of the low-normal vs. high-normal PaCO₂ and normoxia vs. moderate hyperoxia comparisons. The primary endpoint was the serum concentration of neuron-specific enolase (NSE) 48 h after cardiac arrest. Secondary endpoints included S100B protein and cardiac troponin concentrations, continuous electroencephalography (EEG) and near-infrared spectroscopy (NIRS) results and neurologic outcome at 6 months. In total 120 patients were included in the analyses. There was a clear separation in PaCO₂ (p < 0.001) and PaO₂ (p < 0.001) between the groups. The median (interquartile range) NSE concentration at 48 h was 18.8 µg/l (13.9-28.3 µg/l) in the low-normal PaCO₂ group and 22.5 µg/l (14.2-34.9 µg/l) in the high-normal PaCO₂ group, p = 0.400; and 22.3 µg/l (14.8-27.8 µg/l) in the normoxia group and 20.6 µg/l (14.2-34.9 µg/l) in the moderate hyperoxia group, p = 0.594). High-normal PaCO₂ and moderate hyperoxia increased NIRS values. There were no differences in other secondary outcomes. Both high-normal PaCO₂ and moderate hyperoxia increased NIRS values, but the NSE concentration was unaffected. ClinicalTrials.gov, NCT02698917. Registered on January 26, 2016.