The effects of induced apneic episodes on cerebral cortical oxygenation in newborn piglets

The effect of different inspiratory oxygen levels (FiO₂) on cortical oxygenation (pO₂) during and after recovery from apnea, was investigated in 18 anesthetized, paralyzed, and mechanically ventilated newborn piglets. Heart rate (HR) and mean arterial blood pressure (MABP) were continuously monitored as the piglets were subjected to repeated episodes of apnea initiated by disconnecting the ventilator and terminated when HR decreased to less than 80 beats/min by reconnecting the ventilator. A closed cranial window was placed over the parietal cortex of the animals and cortical pO₂ was measured optically by phosphorescence quenching. Apneic episodes induced in animals ventilated with 15%, 22% and 40% oxygen had mean duration's of apnea (time before HR decreased to less than 80 beats/min) of 80, 128 and 134 s, respectively. By the end of the apnea the MABP decreased to 82%, 64%, and 54% of control, respectively. The cortical pO₂ decreased from control values of 24.1, 32.3 and 38.3 Torr at 15%, 22% and 40% oxygen, respectively, to 1.7 to 3.2 Torr at the end of the apneic episode. The duration of apnea necessary for the cortical pO₂ to drop below 20.3 Torr was 18, 44 and 81 s at 15%, 22% and 40% oxygen, respectively. There was an inverse correlation between the rate of decline of cortical pO₂ and baseline FiO₂ levels. With reventilation, the cortical pO₂ reached maximal values of 42.8, 51.9 and 57.2 Torr at 15%, 22%, and 40% oxygen, respectively, before returning to the pre-apnea values. The present results show that apnea of less than 30 s duration at an FiO₂ of 22% do not result in significant cortical hypoxia in hemodynamically stable piglets. Increasing the FiO₂ to above 22% may possibly increase the rate of recovery of tissue oxygenation but it also may facilitate post-hypoxic cortical hyperoxia, a factor that may predispose the immature brain to free radical injury.