Clinical meaning
Septal defects are the most common congenital heart defects, with ventricular septal defects (VSDs) accounting for 25-30% of all CHD and atrial septal defects (ASDs) accounting for 10-15%. These are acyanotic left-to-right shunt lesions. In VSD, an opening in the interventricular septum allows oxygenated blood from the higher-pressure left ventricle to shunt into the lower-pressure right ventricle during systole. The magnitude of shunting depends on defect size and the pressure gradient between ventricles. Small restrictive VSDs generate high-velocity jets and loud murmurs but have minimal hemodynamic impact; large nonrestrictive VSDs allow pressure equalization, causing significant volume overload of the pulmonary circuit. In ASD, the defect in the interatrial septum allows left-to-right shunting during diastole, as left atrial pressure is slightly higher than right atrial pressure. ASD shunting is lower velocity and more gradual, often remaining asymptomatic until adulthood. Both defects cause pulmonary overcirculation: increased pulmonary blood flow leads to pulmonary vascular remodeling, elevated pulmonary artery pressure, and eventually pulmonary hypertension. If uncorrected, chronic volume overload leads to Eisenmenger syndrome — irreversible pulmonary hypertension with shunt reversal (right-to-left), producing cyanosis and contraindicating surgical repair. The pathologic sequence is: left-to-right shunt → pulmonary overcirculation → pulmonary vascular remodeling → pulmonary hypertension → shunt reversal → Eisenmenger syndrome.