PERSISTENT LOW CEREBRAL BLOOD-FLOW VELOCITY FOLLOWING PROFOUND HYPOTHERMIC CIRCULATORY ARREST IN INFANTS

Acute neurological morbidity following repair of congenital heart dise ase (CHD) in infancy is well recognized particularly with the modaliti es of hypothermic cardiopulmonary bypass (CPB) and profound hypothermi c circulatory arrest (PHCA). Reduced O-2 delivery (perfusion defect) d uring rewarming following PHCA has been shown in the operating room. T his reduction in cerebral blood flow coincides with disordered cerebra l metabolism and oxygen utilisation after PHCA. The objective of this study was to extend the period of investigation of cerebral bloodflow velocity (CBFV) behaviour in infants following PHCA to determine if hy poperfusion persisted in the paediatric intensive care unit (PICU). Te n patients undergoing CHD surgery were divided based on the pump modal ity employed into either mild hypothermic CPB or profound hypothermic CPB with circulatory arrest. Following admission to the PICU sequentia l recordings of the mean CBFV in the middle cerebral artery, anterior fontanelle pressure, haemodynamic variables, tympanic membrane tempera ture, haematocrit and PaCO2 were performed. The PHCA group had a consi stently reduced CBFV compared with the control group (P < 0.05). The C BFV values at one, two and four hours were 60 +/- 11, 51.8 +/- 11.4 an d 52.6 +/- 11.9 respectively in the mild hypothermic CPB group. The CB FV values at one, two and four hours were 26.6 +/- 6.8, 32.6 +/- 10 an d 34 +/- 8 respectively in the PHCA group. There was no difference in cerebral perfusion pressure between both groups. Tympanic temperature, haematocrit and PaCO2 did not vary between groups at any interval. Th is study demonstrates a sustained reduction in the CBFV pattern follow ing PHCA into the postoperative period despite adequate cerebral perfu sion pressures. This abnormality correlates with electroencephalograph ic aberrations documented after PHCA. It supports the concept of a pro longed unreactive cerebrovascular bed which could potentially contribu te to the acute neurological morbidity following PHCA in neonates.