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

Pekka Jakkula, Matti Reinikainen, Johanna Hästbacka, Pekka Loisa, Marjaana Tiainen, Ville Pettilä, Jussi Toppila, Marika Lähde, Minna Bäcklund, Marjatta Okkonen, Stepani Bendel, Thomas Birkelund, Anni Pulkkinen, Jonna Heinonen, Tuukka Tikka, Markus B Skrifvars, COMACARE study group, Pekka Jakkula, Matti Reinikainen, Johanna Hästbacka, Pekka Loisa, Marjaana Tiainen, Ville Pettilä, Jussi Toppila, Marika Lähde, Minna Bäcklund, Marjatta Okkonen, Stepani Bendel, Thomas Birkelund, Anni Pulkkinen, Jonna Heinonen, Tuukka Tikka, Markus B Skrifvars, COMACARE study group

Abstract

Purpose: 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.

Methods: 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.

Results: 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.

Conclusions: Both high-normal PaCO2 and moderate hyperoxia increased NIRS values, but the NSE concentration was unaffected.

Registration: ClinicalTrials.gov, NCT02698917. Registered on January 26, 2016.

Keywords: Carbon dioxide; Cardiac arrest; Hypoxic ischemic encephalopathy; Intensive care; Mechanical ventilation; Neuron-specific enolase (NSE); Oxygen.

Figures

Fig. 1
Fig. 1
Median (interquartile range) a PaCO2 during the intervention in the low-normal and high-normal PaCO2 groups. b PaO2 during the intervention in the normoxia and moderate hyperoxia groups
Fig. 2
Fig. 2
Baseline, 24 h, 48 h and 72 h median (interquartile range) serum neuron-specific enolase (NSE) concentrations for patients allocated to targeting a low-normal and high-normal PaCO2, b normoxia and moderate hyperoxia
Fig. 3
Fig. 3
Baseline, 24 h, 48 h and 72 h median (interquartile range) serum S100B concentrations for patients allocated to targeting a low-normal and high-normal PaCO2, b normoxia and moderate hyperoxia
Fig. 4
Fig. 4
Baseline, 24 h, 48 h and 72 h median (interquartile range) plasma cardiac troponin (TnT) concentrations for patients allocated to targeting a low-normal and high-normal PaCO2, b normoxia and moderate hyperoxia
Fig. 5
Fig. 5
Median (interquartile range) regional cerebral oxygen saturation (rSO2) during the intervention in the a low-normal and high-normal PaCO2 groups. b normoxia and moderate hyperoxia groups

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Source: PubMed

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