Ventricular septal defect is a common congenital heart disease, the vast majority of which is due to congenital dysplasia, and a few are due to septal perforation after trauma or myocardial infarction. At the end of the fourth embryonic week, the primitive heart chambers begin to separate. At the same time as the septum forms, the muscle at the bottom of the primitive ventricle grows upward and fuses with the endocardial cushion, dividing the primitive ventricle into two parts, with a hole temporarily left above it, called the interventricular foramen, forming the myocardial part of the septum. At about the end of the seventh week, the membranous septum of the cardiosphere grows from above downward, while the endocardial cushions also extend downward, closing the interventricular foramen and forming the membranous part of the septum. Therefore, during embryonic development, poor development of the myocardial part of the septum may result in a low septal defect, and if the membranous part is poorly fused, a high septal defect, i.e., a membranous defect, may be formed. Ventricular septal defects are mainly due to the presence of abnormal blood traffic between the right and left ventricles. If the defect is small and the left-to-right flow is small, the patient may not show any discomfort for a long time or may have only mild symptoms, which usually do not affect normal development. If the defect is large and the left-to-right shunt is large, the patient may have recurrent respiratory infections in infancy and childhood, palpitations and shortness of breath after exertion, and cyanosis during crying if there is pulmonary stenosis. The patient is less developed in appearance and has weaker physical strength than normal peers. On examination, the doctor may find an elevated precordial area, systolic tremor between the third and fourth ribs at the left edge of the sternum, and a rough all-systolic murmur. If there is pulmonary stenosis, the second sound in the pulmonary artery may not be hyperactive or split. If untreated, the pulmonary artery pressure increases due to increased blood flow and pulmonary hypertension develops, which worsens the symptoms of discomfort. If the pressure in the pulmonary artery continues to rise and exceeds the aortic pressure, the resistance of the small vessels in the lung rises, resulting in a right-to-left shunt, and blood with low oxygen content in the right ventricle passes through the defect into the left ventricle. The natural course of ventricular septal defects has three possibilities: self-closing, progressive worsening or early deterioration, and early death. In general, it is possible for a ventricular septal defect to close on its own. Small defects have a high rate of closure, large defects have a low rate of closure, and the rate of closure is high up to 5 years of age and less likely over 5 years of age. Indications for surgery: Ventricular septal defects larger than 5 mm, recurrent heart failure, pulmonary hypertension, or small defects older than 6 years of age that have not closed should be considered for surgical treatment. Large defects with high left-to-right flow should be operated as early as possible in infancy to avoid pulmonary hypertension or heart failure. Defects less than 5 mm in size may heal on their own during infancy without surgery because of the small left-to-right shunt flow, which does not affect growth and development, and can be treated with observation. If the defect does not close by the age of 6 years, we should not wait any longer because the child is at risk of frequent infections and even endocarditis, which can be life-threatening. If the defect is large and Eisenmenger’s syndrome is present, the child is lost to surgery and a heart-lung transplant is considered. Surgery: The defect is repaired by a cardiac surgeon using an artificial heart-lung machine under extracorporeal circulation with direct cardiac vision. The safety of the procedure is now very high and the operative mortality rate has been reduced to 0.5-1% or less. In recent years, catheter interventions have also been investigated to repair defects, with better results for some small defects. After surgery, children with ventricular septal defects can generally grow and develop normally and lead a completely normal life without leaving any sequelae, and generally do not inherit to the next generation. Therefore, people should have a correct understanding of congenital heart disease so that patients can get timely treatment early. The relationship between congenital heart disease and the presence of certain infections, such as colds, during the mother’s pregnancy is not fully understood. Of course, it is better for pregnant women to avoid exposure to some harmful factors such as radiation, harmful gases and harmful drugs during pregnancy, especially in the early stages of pregnancy when the fetus is more susceptible to abnormal development due to harmful factors. Nowadays, tests such as echocardiography can help to diagnose congenital heart disease such as ventricular septal defect at an early stage, and abroad it is already possible to diagnose whether the fetus is developing normally in the later stages of pregnancy, so that congenital heart disease can be diagnosed and treated in the fetus if it is found to have congenital heart disease, if necessary.