Abstract
Prolonged cerebral hypoperfusion after the return of spontaneous circulation (ROSC) from cardiac arrest (CA) may lead to poor neurological recovery. In a 7-min asphyxia-induced CA rat model, four combinations of inhaled oxygen (iO2) and carbon dioxide (iCO2) were administered for 150 min post-ROSC and compared in a randomized animal trial. At the end of administration, the partial pressure of brain tissue oxygenation (PbtO2) monitored in the hippocampal CA1 region returned to the baseline for the 88% iO2 [ΔPbtO2, median: -0.39 (interquartile range: 5.6) mmHg] and 50% iO2 [ΔpbtO2, -2.25 (10.9) mmHg] groups; in contrast, PbtO2 increased substantially in the 88% iO2+12% iCO2 [ΔpbtO2, 35.05 (16.0) mmHg] and 50% iO2+12% iCO2 [ΔpbtO2, 42.03 (31.7) mmHg] groups. Pairwise comparisons (post hoc Dunn's test) indicated the significant role of 12% iCO2 in augmenting PbtO2 during the intervention and improving neurological recovery at 24 h post-ROSC. Facilitating brain reoxygenation may improve post-CA neurological outcomes.