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

George M. Hoffman*, James S. Tweddell, Nancy S. Ghanayem, Kathy A. Mussatto, Eckehard A. Stuth, Robert D.B. Jaquis, Stuart Berger

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

114 Scopus citations


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 (SaO2) as an index of pulmonary/systemic flow balance, attempting to maintain SaO2 within a theoretically optimal critical range of 75% to 80%. This optimal range of SaO2 has not been verified clinically, and strategies targeting SaO2 may be limited by the fact that SaO2 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 SvO2. In this investigation, we tested the hypothesis that intense afterload reduction with phenoxybenzamine would modify the SvO 2-SaO2 relationship by preventing deterioration of systemic oxygen delivery at high SaO2. Methods: Seventy-one consecutive neonates undergoing the Norwood procedure with and without phenoxybenzamine were studied. Perioperative hemodynamic management targeted SvO2 greater than 50%. Hemodynamic data were prospectively acquired for 48 hours postoperatively and analyzed to assess the effect of phenoxybenzamine on the relationship between SaO2 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, SvO2 peaked at an SaO 2 of 77%, with reduced SvO2 at SaO2 > 85% and SaO2 < 70% (P < .01), while arteriovenous oxygen content difference increased with SaO2 greater than 80% (P < .001). In patients receiving phenoxybenzamine, the SvO2 increased linearly with SaO2 greater than 65% (P < .001), and arteriovenous oxygen content difference was constant at all SaO2 (P = ns). The SvO 2 was higher, and the arteriovenous oxygen content difference lower, across the whole SaO2 range with phenoxybenzamine (P < .0001). Conclusions: A critical range of SaO2 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 SaO2. This effect allows higher SaO2 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 SaO2 is low in both groups, emphasizing the importance of SV02 measurement in these patients.

Original languageEnglish (US)
Pages (from-to)738-745
Number of pages8
JournalJournal of Thoracic and Cardiovascular Surgery
Issue number3
StatePublished - Mar 2004

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pulmonary and Respiratory Medicine
  • Surgery


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