Neonatal and Infant Congenital Cardiac Surgery
Think in terms of ductal dependency and transitional circulation
A neonate with congenital heart disease is a physiology problem before it is a surgical one. Two questions organize everything: is the ductus supplying pulmonary blood flow (pulmonary atresia, critical pulmonary stenosis, tetralogy with pulmonary atresia) or systemic perfusion (hypoplastic left heart, interrupted aortic arch, critical coarctation, critical aortic stenosis)? Prostaglandin E1 at 0.01–0.05 mcg/kg/min keeps the duct open while transfer is arranged; expect apnea in roughly one in ten infants and be ready to intubate. In mixing lesions such as transposition, arterial switch is ideally performed in the first two weeks, before the left ventricle loses mass and pressure-generating capacity; beyond about 4–8 weeks a two-stage strategy with pulmonary artery banding may be required. Obstructed total anomalous pulmonary venous connection is a surgical emergency and is not rescued by prostaglandin.
Traps
Do not chase a normal saturation in a single-ventricle or mixing lesion: supplemental oxygen lowers pulmonary vascular resistance, increases pulmonary runoff, and can precipitate systemic hypoperfusion and acidosis. A reassuring murmur does not exclude critical disease; an asymptomatic-looking infant with coarctation may present in shock at ductal closure. Prematurity and low birth weight shift the risk-benefit calculus toward staged palliation, as does a genetic syndrome with airway or feeding concerns. Necrotizing enterocolitis risk demands careful feeding and avoidance of excessive systemic vasoconstriction.
Rule of thumb
Target saturations of 75–85% after stage I palliation; a saturation above 90% with a narrow pulse pressure and rising lactate suggests pulmonary overcirculation, not success.