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J Thorac Cardiovasc Surg 2004;127:738-745
© 2004 The American Association for Thoracic Surgery

Surgery for congenital heart disease

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

^a Department of Anesthesiology, Milwaukee, Wis USA
^b Pediatric Critical Care Medicine, Milwaukee, Wis USA
^c Cardiothoracic Surgery, Milwaukee, Wis USA
^d Pediatric Cardiology, Milwaukee, Wis USA
^e Children's Hospital of Wisconsin, Milwaukee, WI, USA
^f Medical College of Wisconsin, Milwaukee, Wis, USA

Presented in part at the annual meeting of the American Society of Anesthesiologists, New Orleans, La, October 2001.

Received for publication March 18, 2003; revisions received April 22, 2003; revisions received May 19, 2003; accepted for publication June 18, 2003.

^* Address for reprints: George Hoffman, MD, Pediatric Anesthesiology and Critical Care Medicine, Children's Hospital of Wisconsin, #735, 9000 West Wisconsin Ave, Milwaukee, WI 53226, USA
ghoffman{at}mcw.edu

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 (SvO₂), 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 SvO₂-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 SvO₂ 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 SaO₂ 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 SvO₂ 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 SvO₂ from SaO₂ is low in both groups, emphasizing the importance of SvO₂ measurement in these patients.

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