Cerebral perfusion and metabolism with mild hypercapnia vs. normocapnia in a porcine post cardiac arrest model with and without targeted temperature management

Hilde Karlsen; Runar J Strand-Amundsen; Christiane Skåre; Morten Eriksen; Vidar M Skulberg; Kjetil Sunde; Tor Inge Tønnessen; Theresa M Olasveengen

doi:10.1016/j.resplu.2024.100604

Cerebral perfusion and metabolism with mild hypercapnia vs. normocapnia in a porcine post cardiac arrest model with and without targeted temperature management

Resusc Plus. 2024 Mar 12:18:100604. doi: 10.1016/j.resplu.2024.100604. eCollection 2024 Jun.

Authors

Hilde Karlsen^{1

2}, Runar J Strand-Amundsen³, Christiane Skåre^{4

5}, Morten Eriksen⁶, Vidar M Skulberg⁶, Kjetil Sunde^{4

2}, Tor Inge Tønnessen^{4

2}, Theresa M Olasveengen^{4

2}

Affiliations

¹ Department of Research and Development and Institute for Experimental Medical Research, Oslo University Hospital, Norway.
² Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
³ Department of Clinical and Biomedical Engineering, Oslo University Hospital, Oslo, Norway.
⁴ Department of Anesthesia and Intensive Care Medicine, Oslo University Hospital, Oslo, Norway.
⁵ University of Oslo, Oslo, Norway.
⁶ Institute for Experimental Medical Research, Oslo University Hospital, Oslo, Norway.

Abstract

Aim: To determine whether targeting mild hypercapnia (PaCO₂ 7 kPa) would yield improved cerebral blood flow and metabolism compared to normocapnia (PaCO₂ 5 kPa) with and without targeted temperature management to 33 °C (TTM33) in a porcine post-cardiac arrest model.

Methods: 39 pigs were resuscitated after 10 minutes of cardiac arrest using cardiopulmonary bypass and randomised to TTM33 or no-TTM, and hypercapnia or normocapnia. TTM33 was managed with intravasal cooling. Animals were stabilized for 30 minutes followed by a two-hour intervention period. Hemodynamic parameters were measured continuously, and neuromonitoring included intracranial pressure (ICP), pressure reactivity index, cerebral blood flow, brain-tissue pCO₂ and microdialysis. Measurements are reported as proportion of baseline, and areas under the curve during the 120 min intervention period were compared.

Results: Hypercapnia increased cerebral flow in both TTM33 and no-TTM groups, but also increased ICP (199% vs. 183% of baseline, p = 0.018) and reduced cerebral perfusion pressure (70% vs. 84% of baseline, p < 0.001) in no-TTM animals. Cerebral lactate (196% vs. 297% of baseline, p < 0.001), pyruvate (118% vs. 152% of baseline, p < 0.001), glycerol and lactate/pyruvate ratios were lower with hypercapnia in the TTM33 group, but only pyruvate (133% vs. 150% of baseline, p = 0.002) was lower with hypercapnia among no-TTM animals.

Conclusion: In this porcine post-arrest model, hypercapnia led to increased cerebral flow both with and without hypothermia, but also increased ICP and reduced cerebral perfusion pressure in no-TTM animals. The effects of hypercapnia were different with and without TTM.(Institutional protocol number: FOTS, id 14931).

Keywords: Cardiac arrest; Cerebral perfusion pressure; Experimental study; Haemodynamic; Hypercapnia; Hypothermia; Microdialysis; Post-cardiac arrest care; Resuscitation; TTM; Target temperature management; Ventilation; post-ROSC.