Bradley S M, Simsic J M, Mulvihill D M
Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425-1095, USA.
Circulation. 1998 Nov 10;98(19 Suppl):II372-6; discussion II376-7.
Bidirectional superior cavopulmonary connection (BSCC) may be complicated by systemic hypoxemia. Hyperventilation, which is standard therapy for postoperative hypoxemia, has opposing effects on the pulmonary and cerebral vascular beds, which are connected after BSCC. It is unknown which of these effects predominates and, therefore, whether hyperventilation improves or impairs systemic oxygenation after BSCC.
Twelve consecutive patients (median age, 6.4 months; age range, 6.0 to 32.0, months) undergoing BSCC were studied prospectively. Patients were studied in the intensive care unit within 6 hours of surgery and while sedated, paralyzed, and mechanically ventilated. Inotropes were not altered, and no transfusions were given. FIO2 was set at 100%, and peak end-expiratory pressure was set at 0. Each patient was studied first during normal ventilation, then during hyperventilation, and finally again during normal ventilation. Hyperventilation resulted in significant decreases in arterial PO2, systemic oxygen saturation, and transpulmonary gradient. Cerebral blood flow velocity was measured in 6 patients through transcranial Doppler sonography of the middle cerebral artery. Mean cerebral flow velocity decreased significantly during hyperventilation.
Hyperventilation significantly impairs systemic oxygenation after BSCC. This fall in oxygenation occurs despite a decrease in transpulmonary gradient. A possible mechanism for this effect is that hyperventilation lowers arterial PCO2, raising cerebral vascular resistance, and lowering cerebral, superior vena caval, and pulmonary blood flows. Supportive evidence for this mechanism is the decrease in cerebral flow velocity that occurs during hyperventilation. After BSCC, normal ventilation rather than hyperventilation should be used to improve systemic oxygen levels.
双向腔肺连接（BSCC）可能并发全身性低氧血症。高通气作为术后低氧血症的标准治疗方法，对BSCC术后相连的肺和脑血管床具有相反的作用。目前尚不清楚这些作用中哪种占主导，因此也不清楚高通气在BSCC术后是改善还是损害全身氧合。
对连续12例接受BSCC手术的患者（中位年龄6.4个月；年龄范围6.0至32.0个月）进行前瞻性研究。患者在术后6小时内于重症监护病房接受研究，当时处于镇静、麻痹和机械通气状态。未改变血管活性药物，未进行输血。将吸入氧浓度（FIO2）设定为100%，呼气末峰值压力设定为0。每位患者首先在正常通气时进行研究，然后在高通气时进行研究，最后再次在正常通气时进行研究。高通气导致动脉血氧分压（PO2）、全身氧饱和度和跨肺压梯度显著降低。通过经颅多普勒超声对6例患者的大脑中动脉进行检测，测量脑血流速度。高通气期间平均脑血流速度显著降低。
高通气显著损害BSCC术后的全身氧合。尽管跨肺压梯度降低，但仍出现氧合下降。这种效应的一个可能机制是高通气降低动脉血二氧化碳分压（PCO2），增加脑血管阻力，降低脑、上腔静脉和肺血流量。高通气期间脑血流速度降低为这一机制提供了支持性证据。BSCC术后，应采用正常通气而非高通气来改善全身氧水平。
