Hypoventilation improves oxygenation after bidirectional superior cavopulmonary connection

Abstract

Objective Bidirectional superior cavopulmonary connection may be complicated by systemic hypoxemia. Previous work has shown that hyperventilation worsens systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism is that hyperventilation-induced hypocarbia decreases cerebral, superior vena caval, and pulmonary blood flow. The aim of the current study was to determine whether the converse approach, hypoventilation, improves oxygenation after bidirectional superior cavopulmonary connection. Methods This is a prospective, patient-controlled study of 15 patients (median age 8.0 months, range 4.7-15.5) who underwent bidirectional superior cavopulmonary connection. Patients were studied in the intensive care unit, within 8 hours of surgery, while sedated, paralyzed, and mechanically ventilated. To avoid acidosis during hypoventilation, sodium bicarbonate was administered before hypoventilation. Cerebral blood flow velocity was measured by transcranial Doppler sonography of the middle cerebral artery. Results Hypoventilation following administration of sodium bicarbonate (pH-buffered hypoventilation) produced hypercarbia (mean P co 2 = 58 mm Hg versus 42 mm Hg at baseline). During hypoventilation, there were significant increases in both mean arterial P o 2 (from 50 mm Hg at baseline to 61 mm Hg; P < .05) and mean systemic oxygen saturation (from 86% at baseline to 90%; P < .05). These increases occurred despite accompanying, small increases in pulmonary artery pressure and transpulmonary gradient. Hypoventilation also produced an increase in mean cerebral blood flow velocity (from 37 cm/s at baseline to 55 cm/s; P < .05) and a decrease in the arteriovenous oxygen saturation difference across the upper body (from 33% at baseline to 23%; P < .05), consistent with increased cerebral blood flow. Conclusions This study demonstrates that hypoventilation improves systemic oxygenation in patients after bidirectional superior cavopulmonary connection. The likely mechanism for this effect is that hypoventilation-induced hypercarbia decreases cerebral vascular resistance, thus increasing cerebral, superior vena caval, and pulmonary blood flow. Hypoventilation may be a useful clinical strategy in patients who are hypoxemic in the early postoperative period after bidirectional superior cavopulmonary connection.