1.Clinical manifestations of ventricular septal defect ① Symptoms: small defects, generally no obvious symptoms. If the defect is large, the child will have poor development, and will be prone to shortness of breath, cough and recurrent pulmonary infections, and in severe cases, congestive heart failure. In larger defects, pulmonary infections and right heart failure are more pronounced, and the disease progresses rapidly. When the resistance of pulmonary circulation gradually increases, the fractional flow gradually decreases, the symptoms of pulmonary infection and heart failure will gradually decrease, and the general condition improves. However, symptoms of shortness of breath and palpitations still exist and even worsen. As the lesion progresses, palpitations, fatigue and weakness will gradually worsen, and when it develops into a “right-to-left shunt”, right heart failure symptoms such as cyanosis, hepatomegaly and limb edema may appear. ②Signs: In typical cases, a grade III-IV systolic murmur can be heard between the third and fourth ribs at the left edge of the sternum, often accompanied by systolic tremor. In late stage patients, there may be no murmur and only a distinct hyperactive and split second heart sound of the pulmonary valve. Pulmonary hypertension may develop, and when Eisenmenger syndrome develops further, central cyanosis may appear, gradually worsening, often accompanied by pestle-like fingers (toes). Examination methods Electrocardiography; X-ray; echocardiography; right heart catheterization; left ventriculography, etc. 2.Septal defect surgical method Indications and contraindications for ventricular septal defect surgery: small defects without clinical symptoms or with mild clinical symptoms and gradually reduced, the defect has signs of self-closing, can temporarily not operate, observation to about 5 years old, and then decide whether to operate. Small and medium-sized defects with symptoms should be operated early. Large defects, which are prone to pulmonary infection and heart failure in infancy, should be operated as soon as possible after active medical treatment to control them and save lives. Patients with pulmonary hypertension should still seek surgical treatment as long as the pulmonary vascular lesion is reversible and Eisenmenger syndrome is not present. Patients of any age who present clinically with cyanosis should be listed as contraindicated for surgery. ①Pulmonary artery annuloplasty: This is a transitional procedure for those who are 6 months to 1 year old, with poor physical fitness, frequent pneumonia or heart failure, with pulmonary hypertension or giant ventricular septal defect that cannot tolerate major surgery. ②Direct vision repair: This is the most ideal procedure for the treatment of ventricular septal defects. Most of them adopt micro-invasive right small-incision open-heart surgery, and the success rate of the surgery is 99.8%. ③Interventional treatment: Because of the lower success rate and more complications than open-chest surgery, most foreign countries prohibit interventional treatment of ventricular septal defect. At present, many doctors in China also do not advocate interventional treatment for ventricular ischemia. Pulmonary arterial hypertension (PAH) is a clinical syndrome characterized by a progressive increase in pulmonary vascular resistance and pulmonary artery pressure due to structural and/or functional changes in the pulmonary vascular bed caused by various reasons, which eventually leads to right ventricular dilatation, heart failure, and even death. Normal systolic (sPAP), diastolic (dPAP) and mean (mPAP) pulmonary artery pressures are approximately 24, 9 and 16 mmHg. sPAP >30 mmHg, dPAP >15 mmHg, mPAP >20 mmHg at rest or mPAP >30 mmHg during exercise can be diagnosed as PAH. mPAP between 21 and 30 mmHg, 31 ～In patients with left-to-right shunt congenital heart disease with PAH, organic PAH mostly occurs after 2 years of age. However, some congenital heart diseases can develop pulmonary vascular lesions early, such as complete transposition of the great arteries with ventricular septal defect, complete atrioventricular access, and double outlet of the right ventricle with PAH. Under normal conditions, the resistance of the pulmonary circulation is higher than that of the body circulation during fetal life. After birth, the lungs expand and gas exchange begins, and the resistance of the pulmonary circulation decreases, while the pressure of the body circulation is significantly higher than that of the pulmonary circulation. Due to the presence of “left-to-right shunt”, the amount of blood returning from the pulmonary veins to the left heart system increases, and the preload of the left ventricle increases, thus causing left ventricular hypertrophy. With prolonged increase in pulmonary blood flow, the pulmonary vasculature may be in spasm, resulting in higher pulmonary vascular resistance and higher pulmonary artery pressure. The endothelium and middle layer of small pulmonary vessels thicken, and progressive organic changes of pulmonary vascular lumen obstruction, pulmonary interstitial fibrosis, etc. occur, and the right ventricular pressure gradually increases. The larger the defect, the more pronounced and the earlier such changes occur.