Ventricular septal defect (VSD) is due to dysplasia or dysgenesis of the components of the ventricular septum. Since the pressure in the left ventricle is significantly higher than in the right ventricle, the shunt direction is left to right, resulting in increased blood flow in the pulmonary circulation. Defects smaller than 12.5 px have a small left-to-right shunt and can be free of functional disturbances. Moderate size (0.5-25px) has significant left-to-right shunt, pulmonary circulation flow is more than 2-3 times normal, and pulmonary artery pressure is normal or mildly elevated. Large ventricular defects (greater than 25px) with an area exceeding 1/2 the inner diameter of the aorta and pulmonary circulation flow that can be 3-5 times that of the body circulation are associated with a large shunt. As the disease progresses and the volume of pulmonary circulation continues to increase, very high pressure rushes to the pulmonary circulation, causing the small pulmonary arteries to spasm and producing dynamic pulmonary hypertension (caused by more blood), and later, gradually causing secondary intimal thickening and sclerosis of the small pulmonary arteries, forming resistance pulmonary hypertension (pulmonary vascular lesions have occurred). At this point, the left-to-right shunt gradually decreases, followed by a bidirectional shunt or even a reactive shunt, with clinical cyanosis and the development of Eisenmenger’s syndrome (inoperable again). Symptoms: The clinical presentation depends on the size of the ventricular defect, pulmonary artery blood flow, and pulmonary artery pressure. Symptoms of medium and large ventricular defects can appear in the late neonatal period (at full term) and in infancy (up to 1 year of age): feeding difficulties, shortness of breath during feeding, pallor, excessive sweating, failure to gain weight, recurrent respiratory infections, and often congestive heart failure within 6 months of birth. Prognosis and complications Small ventricular septal defects have the possibility of healing (small chance). For large ventricular defects that do not heal complications include pulmonary hypertension, congestive heart failure, endocarditis, and recurrent respiratory infections. Treatment: Early surgery should be performed for large defects of any age where medical treatment is ineffective, pulmonary hypertension in infancy with a pulmonary:body circulation of greater than 2:1, and supratentorial ventricular septal defects. Small ventricular septal defects should also be surgically repaired before school age because of the risk factors for endocarditis infection.