At birth, the transition from fetal to neonatal circulation involves closure of three key shunts: ductus venosus (liver bypass), foramen ovale (atrial communication), and ductus arteriosus (pulmonary artery to aorta). In congenital heart defects (CHDs), structural abnormalities disrupt this transition. Acyanotic defects (left-to-right shunts like VSD, ASD, PDA) cause increased pulmonary blood flow, leading to heart failure from volume overload. Cyanotic defects (right-to-left shunts like Tetralogy of Fallot, transposition of great arteries) cause deoxygenated blood to enter systemic circulation, producing cyanosis. Some ductal-dependent lesions require prostaglandin E1 to maintain ductus arteriosus patency until surgical repair.