Clinical meaning
Congenital heart disease (CHD) encompasses structural heart defects present at birth, affecting approximately 1% of live births. Understanding CHD requires knowledge of fetal circulation and the transition to postnatal life. In utero, three shunts bypass the non-functioning lungs: the ductus venosus (bypasses liver), foramen ovale (right-to-left atrial shunt), and ductus arteriosus (connects pulmonary artery to aorta). At birth, the first breath decreases pulmonary vascular resistance (PVR), increasing pulmonary blood flow. Increased left atrial pressure functionally closes the foramen ovale. Rising PaO2 triggers ductal constriction, and the ductus arteriosus closes within 24-72 hours (functionally) and 2-3 weeks (anatomically). CHD is classified as acyanotic (left-to-right shunts) or cyanotic (right-to-left shunts). In left-to-right shunts (VSD, ASD, PDA), oxygenated blood recirculates through the lungs, causing pulmonary overcirculation and volume overload. In right-to-left shunts (Tetralogy of Fallot, transposition of great arteries), deoxygenated blood enters systemic circulation, producing cyanosis. Chronic left-to-right shunting can lead to Eisenmenger syndrome, where pulmonary hypertension reverses the shunt direction (becomes right-to-left), producing irreversible cyanosis. Ductal-dependent lesions require prostaglandin E1 (PGE1) to maintain ductal patency until surgical intervention.