Cardiovascular Disorders of the Newborn
Ductal dependence and shock drive urgency
Congenital heart disease may present with cyanosis, heart failure, or shock as the ductus closes. Cyanotic lesions include transposition, tetralogy of Fallot, tricuspid atresia, and total anomalous pulmonary venous return; acyanotic lesions include ventricular septal defect, coarctation, and hypoplastic left heart. Prostaglandin E1 maintains ductal patency in ductal-dependent lesions, but causes apnea and hypotension, so airway support must be ready. Pulse-oximetry screening detects critical congenital heart disease, though false positives occur. In preterm infants, a hemodynamically significant PDA causes pulmonary overcirculation and systemic hypoperfusion; treatment options include indomethacin, ibuprofen, acetaminophen, or conservative management.
Traps: interpreting a normal oxygen saturation as excluding heart disease; missing coarctation because upper-extremity pressures are normal; and giving prostaglandin without anticipating apnea. Differential cyanosis suggests persistent pulmonary hypertension or coarctation, not transposition.
Worked example: a 3-day-old infant presents with poor feeding, mottling, and absent femoral pulses. Four-limb blood pressures show a gradient, and echocardiography confirms coarctation. Prostaglandin is started and the infant is transferred for surgery.
Rule of thumb: “Cyanosis without respiratory distress is cardiac until proven otherwise; start prostaglandin and prepare for apnea.”