Changes in cerebral and somatic oxygenation during stage 1 palliation of hypoplastic left heart syndrome using continuous regional cerebral perfusion

Abstract

Objectives Stage 1 palliation of hypoplastic left heart syndrome requires the interruption of whole-body perfusion. Delayed reflow in the cerebral circulation secondary to prolonged elevation in vascular resistance occurs in neonates after deep hypothermic circulatory arrest. We examined relative changes in cerebral and somatic oxygenation with near-infrared spectroscopy while using a modified perfusion strategy that allowed continuous cerebral perfusion. Methods Nine neonates undergoing stage 1 palliation for hypoplastic left heart syndrome had regional tissue oxygenation continuously measured by frontal cerebral and thoraco-lumbar (T10-L2) somatic (renal) reflectance oximetry probes (rSO 2, INVOS; Somanetics, Troy, Mich). Surgery was accomplished using cardiopulmonary bypass with whole-body cooling (18°C-20°C) and regional cerebral perfusion through the innominate artery at flow rates guided by estimated minimum flow requirements and measured rSO 2 during reconstruction of the aortic arch. Data were logged at 1-minute intervals and analyzed using repeated measures analysis of variance. Results A total of 3176 minutes of data were analyzed. Prebypass cerebral rSO 2 was 65.4 ± 8.9, and somatic rSO 2 was 58.9 ± 12.4 ( P < .001, cerebral vs somatic). During regional cerebral perfusion, cerebral rSO 2 was 80.7 ± 8.6, and somatic rSO 2 was 41.4 ± 7.1 ( P < .001). Postbypass cerebral rSO 2 was 53.2 ± 14.9, and somatic rSO 2 was 76.4 ± 7.7 ( P < .001). The risk of cerebral desaturation was significantly increased after cardiopulmonary bypass. Conclusions Cerebral oxygenation was maintained during regional cerebral perfusion at prebypass levels with deep hypothermia. However, after rewarming and separation from cardiopulmonary bypass, cerebral oxygenation was lower compared with prebypass or somatic values. These results indicate that cerebrovascular resistance is increased after deep hypothermic cardiopulmonary bypass, even with continuous perfusion techniques, placing the cerebral circulation at risk postoperatively.