Atrial septal defect (ASD) is a common congenital heart disease in pediatrics and is the most common congenital heart disease in adulthood. The incidence of this disease is about 1/1500 of live births and accounts for 5-10% of the total incidence of congenital heart disease. About 30% to 50% of children with other types of congenital heart disease also have atrial septal defect. The atrial septal defect can be divided into the following three types: 1. Secondary foramen type atrial septal defect, also known as second foramen type atrial septal defect, is the most common, accounting for about 50% to 70%. The defect is located in the central fossa of the atrial septum, also known as the central defect. About 10% of them are combined with partial pulmonary vein ectopic drainage. 2, primary foramen type atrial septal defect, also known as the first foramen type atrial septal defect, accounting for about 15%, the defect is located at the intersection of the endocardial cushion and the atrial septum. It is often combined with anterior mitral valve cleft or tricuspid septal cleft, which is called partial endocardial cushion defect. 3, venous sinus type atrial septal defect about 10%, divided into superior and inferior ventricular type. Most of the defects are often located at the entrance of the superior vena cava, and the right superior pulmonary vein often drains ectopically into the right atrium through this defect. A small number of defects are located at the entrance of the inferior vena cava and often combine with ectopic drainage of the right inferior pulmonary vein into the right atrium, which is commonly seen in scimitar syndrome. Pathophysiology After birth, the left atrial pressure is higher than the right atrium, and if there is atrial defect, left-to-right shunt occurs. The flow depends on the size of the defect, the pressure difference between the two atria, the compliance of the two ventricles and the relative resistance of the body and pulmonary circulation. In neonates and early infants, the shunt flow through the atrial septal defect is small because the left and right ventricular filling pressures are similar; with age, the pulmonary vascular resistance and right ventricular pressure decrease, the pressure of the body circulation increases, and the shunt flow increases. The right atrium and right ventricle are enlarged due to increased right heart blood flow and increased diastolic load. In a few patients, increased blood volume and pressure in the pulmonary circulation can lead to thickening of the myocardium and intima of the small pulmonary arteries and narrowing of the lumen in the late stage, and pulmonary hypertension in adulthood. Clinical manifestations Most of the infants are asymptomatic. In childhood, there may be weakness, shortness of breath after activity, and susceptibility to respiratory tract infection. In children with larger defects, the fractional flow is larger, resulting in insufficient blood flow in the body circulation and affecting growth and development, manifested as long and thin body shape, pale face, weakness, excessive sweating and shortness of breath after activity. Due to the increased blood flow in the pulmonary circulation, the child is prone to recurrent respiratory infections, and in severe cases, heart failure occurs early. When crying, pneumonia or heart failure, the pressure in the right atrium may exceed that in the left atrium, and temporary cyanosis may occur due to right-to-left shunt. Physical examination: The precordial region is fuller, the right heart beat is increased, and the turbinate is enlarged. Increased blood flow through the pulmonary valve causes relative stenosis of the pulmonary valve, and a grade 2 to 3 jet systolic murmur can be heard between the second ribs at the left sternal border. Delayed closure of the pulmonary valve produces a fixed splitting of the second heart sound in the pulmonary valve area. In the case of large left-to-right shunts, increased blood flow through the tricuspid valve results in relative stenosis of the tricuspid valve, and an early to mid-diastolic rumbling murmur can be heard at the lower left sternal border. In patients with significant pulmonary artery dilatation or pulmonary hypertension, a hyperactive second heart sound and early systolic karate may be heard in the pulmonary valve area. If mitral valve prolapse is combined, a full systolic murmur can be heard in the apical region and is conducted to the axilla. 1.Electrocardiogram: right-sided electrical axis, mean frontal electrical axis between +90°~+180°, mild right ventricular hypertrophy, incomplete right bundle branch block, typical pattern of rsR’ in V1 leads, P-R interval may be prolonged. 2.X-ray: mild to moderate enlargement of heart shape, cardiothoracic ratio greater than 0.5, enlarged right atrium and right ventricle. The pulmonary veins are prominent, the lung fields are obviously congested, and the aortic shadow is reduced. Under fluoroscopy, the general trunk and branches of the pulmonary artery are seen to be pulsating together with the heart, and the heart shadow is slightly pear-shaped. 3.Echocardiography: It has diagnostic value. Due to the overload of the right ventricle in diastole, M-mode echocardiography can show the enlarged right atrium and right ventricle and dilated pulmonary artery. Two-dimensional echocardiography can show the location and size of the atrial septal defect, and the combination of color Doppler ultrasound can improve the diagnostic reliability and determine the direction of the shunt, and the application of Doppler ultrasound can estimate the size of the shunt, and color Doppler flow imaging can detect the left-to-right shunt beam. In older obese patients with poor transthoracic ultrasound transmission, transesophageal echocardiography can be used for diagnosis. 4.Magnetic resonance: In older patients, the subxiphoid echocardiographic window is limited and the image is not clear enough. Magnetic resonance can clearly show the location and size of the defect and its pulmonary venous return to establish the diagnosis. 5.Cardiac catheterization: Generally, cardiac catheterization is not needed, but it is feasible when combined with pulmonary hypertension. During right heart catheterization, the catheter can easily pass through the defect from the right atrium into the left atrium, and the oxygen content of the right atrial blood is higher than that of the upper and lower vena cava blood. V. Prognosis and complications About 40% of children can close spontaneously within 4 years of age, and atrial septal defects smaller than 3 mm mostly close spontaneously within 3 months and 100% within 1.5 years of age, while atrial defects larger than 8 mm usually do not close spontaneously. Treatment: Atrial septal defects with large flow rates such as pulmonary circulation and body circulation blood flow (QP/Qs) greater than 1 and 5 require surgical treatment, and can generally be closed by direct vision under extracorporeal circulation at the age of 2 to 5 years. Those with recurrent respiratory infections, heart failure or combined pulmonary hypertension should be treated surgically as early as possible. The operative mortality rate is less than 1%. At present, interventional treatment is preferred for secondary foramen ovale septal defect, i.e., the application of double-sided mushroom umbrella (Amplatzer device) to close the defect, which is safe and effective, with short hospitalization days, rapid recovery, and no chest surgical scars. The indications are: 1, secondary foramen ovale septal defect; 2, diameter is 3~35mm; 3, the distance between the edge of atrial defect and pulmonary vein, vena cava, mitral valve orifice and coronary sinus orifice is more than 5mm; 4, the extension diameter of atrial septum should be more than 14mm in diameter of atrial defect.