KINETICS OF CEREBRAL DEOXYGENATION DURING DEEP HYPOTHERMIC CIRCULATORY ARREST IN NEONATES

Brain injury associated with neonatal congenital heart operations performed during deep hypothermia and/or total circulatory arrest is often attributed to cerebral hypoxia. We studied the kinetic changes in cerebrovascular hemoglobin O2 saturation (Hb(O2)%) and total hemoglobin concentration (Hb(total)) in 17 neonates undergoing cardiac surgery as they were cooled to 15-degrees-C, underwent total circulatory arrest, and were rewarmed. Hb(O2)% and Hb(total) in brain vasculature were monitored noninvasively by near-infrared spectroscopy. Neonates were cooled over 12 min and rewarmed over 15 min while being perfused using cardiopulmonary bypass (CPB). Total circulatory arrest lasted from 20 to 70 min. We found that Hb(O2)% in brain vasculature increased during the initial 8 min of CPB as nasopharyngeal temperature decreased, and then remained constant until circulatory arrest. After the onset of circulatory arrest, cerebrovascular Hb(O2)% decreased curvilinearly for 40 min; no further hemoglobin desaturation was observed from 40 to 70 min of arrest. The changes in cerebrovascular Hb(total) were quite different from those in Hb(O2)%, as Hb(total) decreased during the initial minute of CPB and circulatory arrest and then remained constant until recirculation. Brain intravascular Hb(O2)% and Hb(total) increased within 3 min after the onset of recirculation to prearrest levels, and during rewarming, Hb(O2)% decreased to normothermic baseline values. The results demonstrate that cerebral oxygenation increased during CPB cooling; O2 was consumed by the neonatal brain during the initial 40 min of deep hypothermic circulatory arrest; and cerebral oxygenation was restored on recirculation. These observations may be important in identifying the etiologies of brain injury during neonatal congenital heart surgery.