Ventricular septal defect is the most common type of congenital heart disease, accounting for almost half of all congenital heart diseases in children in China. Ventricular septal defect can exist alone or coexist with pulmonary stenosis, atrial septal defect, arterial catheterization, aortic misalignment or incomplete closure of the aortic office. Depending on the location of the defect, it can be divided into the following four types: (1) ventricular septal membrane defect, which is the most common; (2) sub-stem type; (3) muscular ventricular defect, which can have several defects at the same time; and (4) mal-alignment type. 1, clinical manifestations of ventricular septal defect: clinical manifestations are determined by the size of the defect and interventricular pressure difference, small defects can be asymptomatic, generally activity is not limited, growth and development are not affected. On physical examination, only a loud all-systolic murmur is heard between the third and fourth ribs at the left edge of the sternum, often accompanied by tremor, and the second pulmonary artery sound is normal or slightly enhanced. When the defect is large, the flow of left-to-right fraction is reduced, and the child is more likely to have delayed childbirth, no weight gain, wasting, feeding difficulties, weakness after activity, shortness of breath, excessive sweating, susceptibility to anti-inflammatory respiratory tract infections, and congestive heart failure. Sometimes the dilated pulmonary artery compresses the recurrent laryngeal nerve and causes hoarseness. On physical examination, the heart borders are enlarged and pulsating, and a rough III-IV all-systolic murmur can be heard between the third and fourth ribs at the left edge of the sternum, with extensive conduction in all directions, and systolic tremor can be felt. The softer flesh and mid-diastolic murmur of the relatively narrow mitral valve can be heard in the apical region at high fractional flow. In large defects with significant pulmonary hypertension (mostly in childhood or adolescence), the right ventricular pressure rises significantly, reversing to a right-to-left shunt, with cyanosis and progressive worsening, when the heart murmur is lighter and the second pulmonary artery sound is significantly hyperactive. The second pulmonary artery sound is reduced in the presence of funicular hypertrophy. The septal defect is likely to be complicated by bronchitis, congestive heart failure, pulmonary edema, and infective endocarditis. 20%-50% of the terminal and myocardial trabecular defects have the potential to close spontaneously. It usually occurs under 5 years of age, especially within 1 year of age. The septal defect under the pulmonary artery or under the double artery rarely closes and is prone to aortic prolapse resulting in incomplete aortic valve closure when a high-pitched diastolic murmur is heard in the second aortic valve area. 2, the septal defect diagnostic examination: X-ray examination: small ventricular defect cardiopulmonary X-ray examination without obvious changes, or prolongation or slight protrusion of the pulmonary artery segment, the lung field is mildly congested. Medium-sized defects have mild to moderate enlargement of the heart shadow, right and left ventricle enlargement, with left ventricle enlargement predominant, smaller aortic arch shadow, dilated pulmonary artery segment, and congested lung field. In large defects, the heart shadow is moderately enlarged and mitral valve type, the right and left ventricles are enlarged, mostly the right ventricle is enlarged, the pulmonary artery segment is obviously prominent, and the pulmonary field is obviously congested. When pulmonary hypertension turns into bidirectional or right-to-left shunt, Eisenmenger syndrome appears, which is mainly characterized by thickening of the main branches of the pulmonary artery and few peripheral pulmonary vascular shadows, like a withered bald branch, and the heart shadow can be basically normal or mildly enlarged. The ECG of small defects can be normal or show mild left ventricular hypertrophy; medium-sized defects mainly show increased diastolic load of the right ventricle, elevated RV5 and V6 with deep Q waves, upright T waves with high apical symmetry, and mainly left ventricular hypertrophy, while large defects show biventricular hypertrophy or left ventricular hypertrophy. The symptoms are severe and may be accompanied by myocardial strain in the presence of heart failure. Echocardiography: allows for anatomic localization and size measurement. Two-dimensional ultrasound can show direct signs of defect-echo interruptions in multiple views-site, temporal phase, number and size, etc. Color Doppler ultrasound can show the origin, site, number, size and direction of shunt bundles, usually left-to-right shunt bundles for color mosaic during systole. Spectral Doppler ultrasound can measure the shunt velocity, calculate the trans-septal pressure difference and right ventricular systolic pressure, estimate the pulmonary artery pressure, and also calculate the pulmonary circulation blood flow (Qp) by measuring the pulmonary valve orifice and mitral valve orifice blood flow, and measure the aortic valve orifice and tricuspid valve orifice blood flow to calculate the body signal turbulent blood flow (Qs), Qp/Qs≈1 in normal time, and an increase of this value ≥1.5 indicates a moderate amount of left-to-right shunt, ≥2.0 indicates a large amount of left-to-right shunt. A large left-to-right shunt is indicated. Cardiac catheterization: To further confirm the diagnosis and perform hemodynamic examinations, evaluate the degree of pulmonary hypertension, calculate pulmonary vascular resistance and body-pulmonary shunt flow, etc. A left ventricular oxygen level higher than the right atrium by 1 volume % suggests the presence of a left-to-right shunt at the ventricular level. Small defects increase right ventricular and pulmonary artery pressures insignificantly, while large defects tend to increase. In the presence of a right-to-left shunt, aortic oxygen saturation is reduced and pulmonary artery resistance may be significantly higher than normal. The angiogram can show the morphology and size of the cardiac chambers and the origin, location, timing, number and size of the shunt bundles at the ventricular level, except for other concomitant malformations. Treatment of ventricular septal defect: ventricular septal defect may close naturally, small and medium-sized defects can be followed up in the outpatient clinic until preschool age, with clinical symptoms such as recurrent respiratory infections and congestive heart failure, anti-infective, cardiotonic, diuretic, vasodilator and other medical treatment. If a large or medium-sized defect with uncontrollable congestive heart failure has a sustained increase in pulmonary artery pressure exceeding 1/2 of the body circulation pressure or the ratio of pulmonary circulation/body circulation volume is greater than 2:1, it should be treated promptly. Treatment of ventricular septal defects used to rely only on direct visual repair under surgical extracorporeal circulation. Currently, with the development of interventional medicine, certain types of ventricular septum can be blocked by cardiac catheter without open-heart surgery, but the interventional treatment of perimembranous and sub-stem ventricular defects is still quite difficult, but the long-term efficacy and safety are to be confirmed by further clinical practice and research.