Mild hypercapnia improves brain tissue oxygen tension but not diffusion limitation in asphyxial cardiac arrest: an...

We sought to evaluate the effect of mild hypercapnia on brain tissue oxygen tension (Pbto₂) and diffusion limitation (impaired ability of oxygen extraction) in a porcine post asphyxial cardiac arrest model.

In 16 Bama pigs, asphyxial cardiac arrest was induced by endotracheal tube clamping and remained untreated for another 4 min. After return of spontaneous circulation (ROSC), animals were randomly assigned to mild hypercapnia (end-tidal carbon dioxide (EtCO₂): 45 ~ 50 mmHg) and normocapnia (EtCO₂: 35 ~ 40 mmHg) groups for 12 h. Intracranial pressure (ICP), Pbto₂, and brain tissue temperature were invasively measured by multimodality monitors. Blood gas analysis, neuron specific enolase (NSE), and S100β were tested at baseline, ROSC 1 h, 6 h, and 12 h. Generalized mixed model with a compound symmetry covariance matrix was used to compare the time-variables of the two groups.

Twelve (75%) pigs had ROSC and 11 pigs survived for the study period, with 6 pigs in mild hypercapnia group and 5 in the normocapnia group. The mean EtCO₂ in the mild hypercapnia was significantly higher than normocapnia group (48 vs 38 mmHg, p <  0.001). Compared with normocapnia, mild hypercapnia group had higher Pbto₂ (p <  0.001), slightly higher mean arterial pressure (p = 0.012) and ICP (p = 0.009). There were no differences in cerebral perfusion pressure (p = 0.106), gradient of partial pressure of jugular venous bulb oxygen (Pjvo₂) and Pbto₂ (p = 0.262), difference of partial pressure of jugular venous CO₂ and arterial CO₂ (p = 0.546), cardiac output (p = 0.712), NSE (p = 0.822), and S100β (p = 0.759) between the two groups.

Short term mild hypercapnia post-resuscitation could improve Pbto₂. However, no corresponding improvements in the gradient of Pjvo₂ to Pbto₂ and biomarkers of neurological recovery were observed in the porcine asphyxial cardiac arrest model.