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

Abstract

Abstract Background 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. Methods 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. Results 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. Conclusions 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.