Brain tissue oxygen monitoring identifies cortical hypoxia and thalamic hyperoxia after experimental pediatric cardiac arrest

BACKGROUND: Optimization of cerebral oxygenation after pediatric cardiac arrest (CA) may reduce neurological damage associated with the post-CA syndrome. We hypothesized that important alterations in regional partial pressure of brain tissue oxygen (PbO(2)) occur after resuscitation from CA and that clinically relevant interventions such as hyperoxia and blood pressure augmentation would influence PbO(2). METHODS: Cortical and thalamic PbO(2) were monitored in immature rats subjected to asphyxial CA (9 or 12 min asphyxia) and sham-operated rats using oxygen sensors. RESULTS: Thalamus and cortex showed similar baseline PbO(2). Post-resuscitation there was early and sustained cortical hypoxia in an insult-duration fashion. In contrast, thalamic PbO(2) initially increased four-fold, and afterwards returned to baseline values. PbO(2) was FiO(2)-dependent, and the response to oxygen was more pronounced after a 9 min vs. 12 min CA. After a 12 min CA, PbO(2) was modestly affected by blood pressure augmentation using epinephrine in the thalamus but not cortex. CONCLUSION: After asphyxial pediatric CA, there is marked regional variability of cerebral oxygenation. Cortical hypoxia is pronounced and appears early, while thalamic hyperoxia is followed by normoxia. Compromised PbO(2) in the cortex may represent a relevant and clinically measurable therapeutic target aimed at improving neurological outcome after pediatric CA.