Physiologic limitation of omega exists in patients after the Norwood palliation and is underestimated by the arterial venous oxygen saturation difference.

Background: Survival after the Norwood palliation (NW) is dependent on maximizing systemic oxygen delivery. Omega (Omega) is used to express the excess of oxygen delivery to oxygen consumption. We hypothesized that an intrinsic deficiency in the ability to maximize the relationship between oxygen delivery (DO(2)) and oxygen consumption (VO(2)) is present in infants after NW and is underestimated by arterial venous oxygen saturation difference (a-vO(2)).

Methods: Simultaneous arterial and systemic venous blood gas data were prospectively collected for the first 24 hours after surgery in 10 neonates after NW and 32 infants after biventricular repair (BV). Blood gas data were compared between groups. These data were compared with a group of 11 infants with hypoplastic left heart syndrome (HLHS) status post NW who were undergoing routine hemodynamic evaluation in the cardiac catheterization lab prior to a bidirectional Glenn operation (pre-Glenn).

Results: The mean systemic arterial oxygen saturation was 77% for NW, 83% for pre-Glenn, and 97% for biventricular repair. NW group had a mean systemic venous oxygenation saturation (SvO(2)) of 47% (range 12-67%) vs. 67% (range 29-84%) in the BV group (P = .001). Pre-Glenn patients had a SvO(2) of 46 (not significant [NS] vs. NW, P = .001 vs. BV). In NW, a-vO(2) mean was 32 (range 15-63) compared with mean 32 (range 16-71) in BV group (NS). Pre-Glenn a-vO(2) mean was 33.6 (NS vs. NW or BV). Omega for NW group was 2.6 (range 1.1-4.2) and 3.4 (1.4-6.25) in BV group (P = .001). Omega for pre-Glenn was 2.5 (range 1.7-3.8) (NS vs. NW, P = .001 vs. BV).

Conclusion: Omega is lower for patients in the immediate postoperative period after NW and prior to their bidirectional Glenn operation than in patients after biventricular repair. This places NW patients closer to the critical point of DO(2) and therefore at greater risk for hemodynamic compromise than BV patients. The a-vO(2) difference underestimates this risk.