Ventricular septal defect refers to the embryonic underdevelopment of the ventricular septum, which creates abnormal traffic and produces a left-to-right shunt at the level of the ventricles. Ventricular septal defects are the most common form of congenital heart disease and can account for 25%-40% of all congenital heart disease, either alone or in combination with other malformations. The defect is often between 0.1 and 75 px, larger in the membranous part and smaller in the muscular part, the latter also known as Roger’s disease. If the defect is <12.5px, the fractional flow is small and there are no clinical symptoms. The size of the heart can be normal for small defects, while the left ventricle is significantly larger than the right ventricle for large defects. According to the location of the septal defect, it can be divided into four types: 1, perimembranous defect: the most common, accounting for 60%-70%, the defect is mostly extended to the peripheral muscle, and the upper edge of the notch is always the junction of the aortic valve and the central fiber body. 2, subarterial type defect: national people can account for as much as 20-30%, Westerners are rare, this type of ventricular septal defect is prone to aortic valve prolapse, regurgitation and aortic sinus aneurysm rupture. 3, atrioventricular access type defect: located in the posterior lower part of the membrane, behind the tricuspid septal valve, the lower part of the conical papillary muscle, between the mitral valve and tricuspid valve. This type is less common clinically. 4, myocardial defect: Located in the apical part, it is a myocardial trabecular defect. The septal myocardium contracts during systole to make the defect smaller, so the left-to-right shunt flow is small. At the ventricular level, a left-to-right shunt is generated, and the amount of the shunt depends on the size of the defect. In large defects, symptoms appear early and are so pronounced that they affect development. There is shortness of breath, dyspnea, sweating, feeding difficulties, fatigue and recurrent pulmonary infections, and in severe cases, heart failure; the patient is susceptible to infective endocarditis. If the defect is small, it may be asymptomatic. Chest radiograph: if the defect is large resulting in high fractional flow may lead to enlargement of the whole heart, increased pulmonary blood, and thickening of pulmonary vessels. Echocardiography: A confirmatory test to determine the location and size, as well as an accurate description of the ventricular outflow tract, aortic valve and atrioventricular valve. The diagnosis can be made based on the etiology, clinical manifestations and laboratory tests. Treatment can be divided into medical treatment and surgical treatment. 1.Medical treatment mainly prevents and treats infective endocarditis, pulmonary infection and heart failure. 2.Surgical treatment Under direct vision, defect repair is feasible. If the defect is small and the X-ray and electrocardiogram are normal, surgery is not necessary; if there is or is not pulmonary hypertension, left-to-right shunt is the main effect, surgery is best at the age of 4-6 years; if the symptoms appear early or there is heart failure, surgery can also be performed in infancy; if there is significant pulmonary hypertension, bidirectional or right-to-left shunt is the main effect, surgery is not recommended. Surgical method: A median sternotomy is performed under general anesthesia with tracheal intubation to establish extracorporeal circulation. After blocking the cardiac circulation, the anterior wall of the right ventricular outflow tract is incised, which can reveal various types of ventricular septal defects, but there is some damage to the myocardium, affecting the right heart function and damaging the right bundle branch. Currently, a trans-right atriotomy approach is used, which is better for revealing membrane defects. For higher defects, the transpulmonary route is preferred. Smaller defects with fibrous tissue at the edges can be sutured directly, and those with defects smaller than 1 cm can be patched with polyester sutures. This disease is a congenital disease, there is no effective preventive measures, early detection, early diagnosis and early treatment should be achieved. The prognosis is good for those with small septal defects, and their natural life expectancy can even be over 70 years; those with small defects may even close by themselves before the age of 6. For large defects, heart failure can occur at the age of 1 to 2 years, and those with pulmonary hypertension have a poor prognosis. Timely surgical treatment can generally achieve results that are indistinguishable from those of normal people.