CEREBRAL OXYGEN-SUPPLY AND UTILIZATION DURING INFANT CARDIAC-SURGERY

The survival of infants with congenital heart disease has improved dra matically. However, the incidence of neurological injury in infants su rviving cardiac surgery remains considerable. These neurological seque lae are attributable at least in part to hypoxia-ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypotherm ia, cardiopulmonary bypass, and circulatory arrest. To begin to identi fy mechanisms of brain injury during infant cardiac surgery, we used n ear-infrared spectroscopy to study the relationship between cerebral i ntravascular (hemoglobin) and mitochondrial (cytochrome aa(3)) oxygena tion in 63 infants (aged 1 day to 9 months) undergoing deep hypothermi c repair of congenital heart defects, throughout the intraoperative pe riod. Moreover, we assessed the effect of postnatal age on these chang es. The cerebral concentration of oxidized cytochrome aa(3) decreased from the onset of deep hypothermic cardiopulmonary bypass, despite app arent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this i nterval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa(3) than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa(3) remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cyt ochrome aa(3) was belayed, despite a rapid recovery of intravascular o xygenation (HbO(2)). After rewarming and 60 minutes of reperfusion, on ly 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa(3). These findings demonstrate a paradoxical dissociati on of changes in intravascular and mitochondrial oxygenation during hy pothermic cardiopulmonary bypass; a pronounced decrease of mitochondri al oxygenation is established during induction of hypothermia and a de lay in recovery of mitochondrial oxygenation occurs following circulat ory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterio us impairments of intrinsic mitochondrial function or of delivery of i ntravascular oxygen to the mitochondrion or both, effects previously u ndetected and apparently influenced by cerebral maturation.