Ventricular septal defect is one or more cavities between two ventricles of the heart and is responsible for about 20% of all precordial diseases, either alone or in combination with other malformations. The defect is between 0.1-3 cm, larger in the membranous part and smaller in the muscular part, which is also known as Roger’s disease. If the defect is <0.5 cm, the flow is small and there are no clinical symptoms. In small defects, the right ventricle is predominantly enlarged, while in large defects, the left ventricle is more enlarged than the right ventricle. According to the location of the defect, it can be divided into five types: a. supraventricular crest defect: located in the right ventricular outflow tract, above the supraventricular crest and under the main and pulmonary valves, and in a few cases combined with the main and pulmonary valves closed insufficiently. The inferior supraventricular crest defect: located in the septal membrane, this type is the most common, accounting for about 60-70%. Posterior septal defect: located in the right ventricular inflow tract, posterior to the tricuspid septal valve, accounting for about 20% of cases. Fourth, the myocardial defect: located in the apical part, for myocardial trabecular defect, systolic time septal myocardial contraction to make the defect smaller, so the left to right shunt flow is small. V. Common ventricle: Both the septal membrane and myocardial parts are undeveloped, or multiple defects, which are less common. Symptoms A left-to-right shunt is produced at the ventricular level, and the amount of shunt flow depends on the size of the defect. In large defects, the blood flow of pulmonary circulation increases significantly, and after flowing into the left atrium and ventricle, it flows back into the right ventricle at the ventricular level through the defective opening and enters the pulmonary circulation, thus increasing the load on the left and right ventricles, enlarging the left and right ventricles, increasing the blood flow of pulmonary circulation leading to an increase in pulmonary artery pressure and an increase in the systolic load of the right ventricle, and finally entering the phase of obstructive pulmonary hypertension, which can occur in both directions or right-to-left shunts. I. Symptoms: The defect is small and may be asymptomatic. In large defects, the symptoms appear early and obvious, so that development is affected. There are palpitations and shortness of breath, weakness and susceptibility to lung infection. In severe cases, heart failure may occur. Cyanosis may occur in cases of significant pulmonary hypertension, and the disease may predispose to infective endocarditis. The typical sign is a rough systolic murmur of grade 4-5 between ribs III-IV at the left edge of the sternum, conducted to the precordial region, accompanied by fine systolic tremor. If the fractional flow is high, there may be a functional diastolic murmur in the apical region. The second pulmonary valve sound is hyperactive and split. In severe pulmonary hypertension, there is a diastolic murmur of relative pulmonary valve insufficiency in the pulmonary valve region, and the systolic murmur of the original septal defect may be diminished or absent. Examination I. X-ray: The heart shadow is mostly unchanged in small defects. When the defect is moderately large, the heart shadow has different degrees of enlargement, mainly in the right ventricle. In large defects, both left and right ventricles are enlarged, the pulmonary artery trunk is protruding, the pulmonary vascular shadow is enhanced, and in severe pulmonary hypertension, the lateral band of the lung field is clear instead. Electrocardiogram: The electrocardiogram is not abnormal in small defects. If the defect is moderately large or above, it shows right ventricular or left and right ventricular hypertrophy. Echocardiography: The left atrium, left and right ventricular internal diameters are enlarged, and there is continuous interruption of septal echo. Doppler ultrasound: maximum turbulence can be deeply measured by tracing from the defective right ventricular surface to the defective foramen and left ventricular surface. Fourth, cardiac catheterization: the oxygen content of blood at the right ventricular level is higher than 0.9% of the volume of the right atrium, and occasionally the catheter can reach the left ventricle through the defect. Depending on the amount of fractional flow, there are varying degrees of increased pulmonary artery or right ventricular pressure. Treatment Timing of treatment: Small ventricular septal defects have the potential to heal on their own, so there is no need to rush to surgery, and treatment can wait until about 3 years of age. However, in large ventricular septal defects, the child is prone to pneumonia or even frequent heart failure and pulmonary hypertension, and should be operated early. Regular checkups should be performed, with cardiac ultrasound every 3 months or so, and if pulmonary hypertension appears, surgery should be done early to avoid losing the time for surgery. Methods: I. Medical treatment: At present, many ventricular septal defects can be cured by minimally invasive interventional therapy, with small surgical risks and few complications, generally until the age of 3 years or above. If the defect is small and the X-ray and electrocardiogram are normal, surgery is not needed. If there is/ or there is no pulmonary hypertension and left-to-right shunt is predominant, the best effect of surgery is preferred before 2-6 years old. The surgery is not recommended for those with significant pulmonary hypertension with bidirectional or right-to-left shunts.