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Publications

Journal Article Epublish

PubMed: 42774534 DOI: 10.1016/j.resplu.2026.101480

Effects of systemic mild hypercapnia on brain function in a refractory cardiac arrest model treated with extracorporeal cardiopulmonary resuscitation.

Resusc Plus 32:101480

Authors: Anthony Moreau, Fuhong Su, Lorenzo Ferlini, Nicolas Gaspard, Francesca Pischiutta, Elisa Zanier, Jacques Creteur, Filippo Annoni, Fabio Silvio Taccone

Affiliations

  • Department of Intensive Care, Hôpital Universitaire de Bruxelles (HUB), Université libre de Bruxelles (ULB), Brussels, Belgium. Laboratoire Expérimental des Soins Intensifs, Université libre de Bruxelles (ULB), Brussels, Belgium.
  • Department of Neurology, Hôpital Universitaire de Bruxelles (HUB), Université libre de Bruxelles (ULB), Brussels, Belgium.
  • Department of Neurology, Hôpital Universitaire de Bruxelles (HUB), Université libre de Bruxelles (ULB), Brussels, Belgium. Neurology Department, School of Medicine, Yale University, New Haven, CT, USA.
  • Laboratory of Traumatic Brain Injury and Neuroprotection, Department of Acute Brain and Cardiovascular Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156 Milan, Italy.
  • Department of Intensive Care, Hôpital Universitaire de Bruxelles (HUB), Université libre de Bruxelles (ULB), Brussels, Belgium.

Abstract

INTRODUCTION

Cardiac arrest (CA) is a major cause of mortality and neurologic disability. Extracorporeal cardiopulmonary resuscitation (ECPR) may be used in refractory CA to potentially reduce hypoxic-ischemic brain injuries. Currently, no recommendation exists regarding optimal carbon dioxide levels in ECPR patients.

METHODS

Twelve pigs were submitted to 5 min of untreated ventricular fibrillation followed by 25 min of CPR; 30 min after CA induction, ECPR was initiated and defibrillations delivered until ROSC. Pigs were randomly assigned to normocapnia (NC; PaCO 2 35-45 mmHg, n = 6) or hypercapnia (HC; PaCO 2 50-55 mmHg, n = 6). Animals underwent continuous multimodal neurological and cardiovascular monitoring. The primary outcome of the study was the change of brain tissue oxygen tension (PbtO 2) over time. Other parameters were secondary outcomes. At 12 h post-ROSC, animals were euthanized and brain tissues were harvested for molecular analyses.

RESULTS

Mean PbtO 2 tended to be higher in the HC group (49.9 vs 36.4 mmHg in the NC group; p = 0.13), while mean intracranial pressure was similar between the two groups (19.9 vs 22.6 mmHg, respectively - p = 0.42). Cerebral glucose concentrations were significantly higher in the HC group (p = 0.01), without differences in lactate/pyruvate ratio, glycerol or glutamate. Caspase-8 gene expression in the parietal lobe was significantly lower in the HC group, with no differences in EEG cortical activity or serum biomarkers of brain injury.

CONCLUSIONS

In this model of ECPR, HC was associated with increased cerebral glucose concentrations and reduced caspase-8 expression, without changes in PbtO 2 levels, intracranial pressure, cortical activity, or neurobiomarkers.

MeSH

Brain Injuries, Resuscitation, Intracranial Pressure, Cardiopulmonary Resuscitation, Brain, Biomarkers, Heart Arrest, Tissues, Hypercapnia