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. We have previously reported higher venous saturation (SvO(2)), lower arteriovenous oxygen content difference, lower systemic vascular resistance, lower pulmonary/systemic flow ratio, and improved survival with the perioperative use of phenoxybenzamine and continuous monitoring of SvO(2). In this investigation, we tested the hypothesis that intense afterload reduction with phenoxybenzamine would modify the SvO(2)-SaO(2) relationship by preventing deterioration of systemic oxygen delivery at high SaO(2).
METHODS: Seventy-one consecutive neonates undergoing the Norwood procedure with and without phenoxybenzamine were studied. Perioperative hemodynamic management targeted SvO(2) greater than 50%. Hemodynamic data were prospectively acquired for 48 hours postoperatively and analyzed to assess the effect of phenoxybenzamine on the relationship between SaO(2) and SvO(2) and other hemodynamic indices. Sixty-two patients received phenoxybenzamine 0.25 mg/kg on cardiopulmonary bypass; 9 who did not served as controls.
RESULTS: In control patients, SvO(2) peaked at an SaO(2) of 77%, with reduced SvO(2) at SaO(2) > 85% and SaO(2) < 70% (P <.01), while arteriovenous oxygen content difference increased with SaO(2) greater than 80% (P <.001). In patients receiving phenoxybenzamine, the SvO(2) increased linearly with SaO(2) greater than 65% (P <.001), and arteriovenous oxygen content difference was constant at all SaO(2) (P = ns). The SvO(2) was higher, and the arteriovenous oxygen content difference lower, across the whole SaO(2) range with phenoxybenzamine (P <.0001).
CONCLUSIONS: A critical range of SaO(2) for optimizing systemic oxygen delivery was confirmed in control patients, and was effectively eliminated by phenoxybenzamine, specifically by eliminating the systemic hypoperfusion associated with high SaO(2). This effect allows higher SaO(2) to be included in a rational hemodynamic strategy to improve systemic oxygen delivery in the early postoperative management of patients receiving intense afterload reduction with phenoxybenzamine. The predictability of SvO(2) from SaO(2) is low in both groups, emphasizing the importance of SvO(2) measurement in these patients.