HYPERVENTILATION IMPAIRS OXYGENATION AFTER BIDIRECTIONAL SUPERIOR CAVOPULMONARY CONNECTION

Background-Bidirectional superior cavopulmonary connection (BSCC) may be complicated by systemic hypoxemia. Hyperventilation, which is stand ard therapy for postoperative hypoxemia, has opposing effects on the p ulmonary and cerebral vascular beds, which are connected after BSCC. I t is unknown which of these effects predominates and, therefore, wheth er hyperventilation improves or impairs systemic oxygenation after BSC C. Methods and Results-Twelve consecutive patients (median age, 6.4 mo nths; age range, 6.0 to 32.0, months) undergoing BSCC were studied pro spectively. Patients were studied in the intensive care unit within 6 hours of surgery and while sedated, paralyzed, and mechanically ventil ated. 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 hyper ventilation, and finally again during normal ventilation. Hyperventila tion resulted in significant decreases in arterial PO2, systemic oxyge n saturation, and transpulmonary gradient. Cerebral blood flow velocit y was measured in 6 patients through transcranial Doppler sonography o f the middle cerebral artery. Mean cerebral flow velocity decreased si gnificantly during hyperventilation. Conclusions-Hyperventilation sign ificantly impairs systemic oxygenation after BSCC. This fall in oxygen ation occurs despite a decrease in transpulmonary gradient. A possible mechanism for this effect is that hyperventilation lowers arterial PC O2, raising cerebral vascular resistance, and lowering cerebral, super ior vena caval, and pulmonary blood flows. Supportive evidence for thi s mechanism is the decrease in cerebral flow velocity that occurs duri ng hyperventilation. After BSCC, normal ventilation rather than hyperv entilation should be used to improve systemic oxygen levels.