Aortic atresia is associated with an inferior systemic, cerebral, and splanchnic oxygen-transport status in neonates after the Norwood procedure☆

Abstract

Aortic atresia (AA) is a risk factor for mortality after the Norwood procedure. The mechanisms remain unknown. We compared the profiles of systemic, cerebral, and splanchnic oxygen transport in neonates with hypoplastic left-heart syndrome with AA or aortic stenosis (AS) after the Norwood procedure. Systemic oxygen consumption (VO(2)) was measured using respiratory mass spectrometry for 72 h in 17 neonates (nine in the AA group, eight in the AS group). Cardiac output (CO), systemic vascular resistance (SVR), oxygen delivery (DO(2)), and oxygen extraction ratio (ERO(2)) were calculated combining with blood gases and pressures at 2-4-h intervals. Cerebral (ScO(2)) and splanchnic (SsO(2)) oxygen saturations were measured by near-infrared spectroscopy. The doses of dopamine, milrinone, phenoxybenzamine, and vasopressin were recorded. Preoperative echocardiographic left-ventricular morphology and ejection fraction ratio were measured. Compared with the AS group, the AA group had lower CO (p = 0.03), higher SVR (p = 0.002), lower DO(2) (p = 0.07), VO(2) (p = 0.003), and ScO(2) (p = 0.07) during the first 40 h. SsO(2) was insignificantly lower. Despite a similar ERO(2), the AA group had higher lactate (p = 0.01). The AA group received higher doses of milrinone (p < 0.0001), vasopressin (p = 0.005), and phenoxybenzamine (p = 0.02), and lower higher doses of dopamine (p = 0.07). Vasopressin adversely correlated with systemic oxygen-transport variables and SsO(2) (p < 0.05). The AA group had thicker left-ventricular posterior wall (p = 0.05) that was negatively correlated with CO (p = 0.02). AA is associated with an inferior status of systemic, cerebral, and splanchnic oxygen transport after the Norwood procedure. Aggressive use of vasopressin may worsen systemic oxygen transport and decrease splanchnic perfusion.