O'Hare B, Bissonnette B, Bohn D, Cox P, Williams W
Department of Anaesthesia, Hospital for Sick Children, Toronto, Ontario, Canada.
Can J Anaesth. 1995 Nov;42(11):964-71. doi: 10.1007/BF03011066.
Acute neurological morbidity following repair of congenital heart disease (CHD) in infancy is well recognized, particularly with the modalities of hypothermic cardiopulmonary bypass (CPB) and profound hypothermic circulatory arrest (PHCA). Reduced O2 delivery (perfusion defect) during rewarming following PHCA has been shown in the operating room. This reduction in cerebral blood flow coincides with disordered cerebral metabolism and oxygen utilisation after PHCA. The objective of this study was to extend the period of investigation of cerebral blood flow velocity (CBFV) behaviour in infants following PHCA to determine if hypoperfusion persisted in the paediatric intensive care unit (PICU). Ten patients undergoing CHD surgery were divided, based on the pump modality employed, into either mild hypothermic CPB or profound hypothermic CPB with circulatory arrest. Following admission to the PICU, sequential recordings of the mean CBFV in the middle cerebral artery, anterior fontanelle pressure, haemodynamic variables, tympanic membrane temperature, haematocrit and PaCO2 were performed. The PHCA group had a consistently reduced CBFV compared with the control group (P < 0.05). The CBFV values at one, two and four hours were 60 +/- 11, 51.8 +/- 11.4 and 52.6 +/- 11.9 respectively in the mild hypothermic CPB group. The CBFV values at one, two and four hours were 26.6 +/- 6.8, 32.6 +/- 10 and 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. This study demonstrates a sustained reduction in the CBFV pattern following PHCA into the postoperative period despite adequate cerebral perfusion pressures. This abnormality correlates with electroencephalographic aberrations documented after PHCA. It supports the concept of a prolonged unreactive cerebrovascular bed which could potentially contribute to the acute neurological morbidity following PHCA in neonates.
婴儿期先天性心脏病（CHD）修复术后的急性神经功能障碍已得到充分认识，尤其是在低温心肺转流（CPB）和深度低温循环停搏（PHCA）的手术方式下。在手术室中已显示，PHCA复温期间氧输送减少（灌注缺陷）。这种脑血流量的减少与PHCA后脑代谢和氧利用紊乱同时出现。本研究的目的是延长对PHCA后婴儿脑血流速度（CBFV）行为的研究时间，以确定在儿科重症监护病房（PICU）是否持续存在灌注不足。10例接受CHD手术的患者根据所采用的泵模式，分为轻度低温CPB组或伴有循环停搏的深度低温CPB组。进入PICU后，对大脑中动脉平均CBFV、前囟压力、血流动力学变量、鼓膜温度、血细胞比容和PaCO2进行连续记录。与对照组相比，PHCA组的CBFV持续降低（P<0.05）。轻度低温CPB组在1小时、2小时和4小时的CBFV值分别为60±11、51.8±11.4和52.6±11.9。PHCA组在1小时、2小时和4小时的CBFV值分别为26.6±6.8、32.6±10和34±8。两组之间的脑灌注压没有差异。鼓膜温度、血细胞比容和PaCO2在任何时间段内组间均无变化。本研究表明，尽管脑灌注压充足，但PHCA后至术后期间CBFV模式持续降低。这种异常与PHCA后记录的脑电图异常相关。它支持了脑血管床长时间无反应的概念，这可能是新生儿PHCA后急性神经功能障碍的潜在原因。
