Hyperventilation impairs oxygenation after bidirectional superior cavopulmonary connection

• Published in: Circulation (New York, N.Y.) Vol. 98; no. 19 Suppl; pp. II372 - 6; discussion II376-7
• Main Authors: Bradley, S M, Simsic, J M, Mulvihill, D M
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 10.11.1998
• Subjects: Adolescent; Adult; Arteries; Blood Flow Velocity - physiology; Cerebrovascular Circulation - physiology; Child; Child, Preschool; Female; Heart Bypass, Right; Hemodynamics - physiology; Humans; Hyperventilation - blood; Infant; Male; Oxygen - blood; Postoperative Period; Respiration, Artificial
• ISSN: 0009-7322; 1524-4539

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.