Alteration of the critical arteriovenous oxygen saturation relationship by sustained afterload reduction after the Norwood procedure.

Objectives: Hemodynamic vulnerability after the Norwood procedure for hypoplastic left heart syndrome results from impaired myocardial function, and critical inefficiency of parallel circulation. Traditional management strategies have attempted to optimize circulatory efficiency by using arterial oxygen saturation (SaO(2)) as an index of pulmonary/systemic flow balance, attempting to maintain SaO(2) within a theoretically optimal critical range of 75% to 80%. This optimal range of SaO(2) has not been verified clinically, and strategies targeting SaO(2) may be limited by the fact that SaO(2) is a poor predictor of systemic oxygen delivery.