Fallot’s tetralogy of Fallot is a common type of cyanotic congenital heart disease, accounting for about 10% of congenital heart disease, and the first among cyanotic heart diseases, accounting for 50%-90%. 1888 Fallot first described the pathological anatomy and clinical manifestations of this disease in detail, so it is called the tetralogy of Fallot (TOF), which includes four lesions: 1, ventricular septal defect; 2, pulmonary artery stenosis; 3, aortic riding; 4, right ventricular hypertrophy. Aortic span; 4. Right ventricular hypertrophy. In fact, tetralogy of Fallot can be considered to be caused by a single anatomical abnormality: the forward extension of the funnel septum. In Farrow’s tetralogy of Fallot, because of the large septal defect and the aorta riding over the septal defect, the pressure in both ventricles is equal during systole and the aorta receives blood from both the left and right ventricles. The more the aorta is shifted to the right, the more the aorta receives blood from the right ventricle, and the more cyanosis there is. On the other hand, the severity of cyanosis also depends on the severity of right ventricular outflow tract obstruction and the development of the pulmonary artery. In patients with small pulmonary flow obstruction, their physiology resembles that of a ventricular septal defect with a left-to-right shunt. These patients will present with increased blood volume in the pulmonary circulation, increased pulmonary to body circulation ratio, and symptoms of congestive heart failure. These patients have no or only a small right-to-left shunt. When pulmonary artery flow obstruction is severe, a significant right-to-left shunt may be present at the ventricular level. These patients will present with symptoms of hypoxia, with oxygen saturation at 70% to 80% or less. Despite the symptoms of hypoxia, growth and development in these patients is essentially normal. In between these two groups of patients are mainly those with pulmonary artery stenosis just offsetting pulmonary congestion and pulmonary hypertension. These patients may have only mild hypoxia (oxygen saturation ≈ 90%) and no other symptoms. The more rightward aortic shift rides across, the narrower the right ventricular outflow tract, and the heavier the right ventricular load. In severe right ventricular hypertrophy, the left ventricle is often poorly developed, and both the right and left ventricles are prone to postoperative failure. The clinical symptoms of tetralogy of Fallot are mainly cyanosis: the degree of cyanosis and its early appearance are related to the degree of right ventricular outflow tract stenosis and the degree of aortic span. Most children develop cyanosis after the first 6 months of life, and some patients develop cyanosis in childhood or adulthood. Cyanosis worsens with crying and exercise and decreases with calm rest, and tends to increase with age. ‘Dyspnea and weakness: Due to hypoxia, the child is mostly weak, not noisy and inactive. When episodes of hypoxia occur, dyspnea, cyanosis worsens, lethargy, or even coma, convulsions, and death. ƒ Squatting: It is the characteristic posture of tetralogy of Fallot. Cyanosis and dyspnea are reduced when squatting, and squatting is more frequent in those with heavy cyanosis. In infants who do not walk, they exhibit a flexed back and retracted legs state. The mechanism may be related to the increased resistance of body circulation during squatting, which reduces right-to-left shunt. Pestle-like fingers (toes) are a common sign of tetralogy of Fallot. The more severe the hypoxia, the more pronounced the pestle fingers (toes). There is a systolic murmur between the 2nd, 3rd and 4th ribs at the left margin of the rib cage, and the second sound of the pulmonary valve is diminished or even absent. In patients with tetralogy of Fallot with better pulmonary artery development, the second sound of the pulmonary valve is normal or slightly lower. The diagnosis of tetralogy of Fallot is usually clear based on clinical manifestations, physical examination, electrocardiogram, chest X-ray and echocardiogram. If the right ventricular outflow tract stenosis is severe and the pulmonary vessels are poorly developed, cardiac catheterization should be performed. The pressure curve between the pulmonary artery and the right ventricle can determine the site of right ventricular outflow tract obstruction and the presence of pulmonary valve stenosis, and selective right ventriculography can show the morphology of the right ventricular outflow tract, the degree of aortic riding across, and the location and size of the ventricular septal defect. Currently, 64-row CT and MRI are gradually replacing cardiac catheterization because of their non-invasive, low cost and clear visualization. The indications for corrective surgery for tetralogy of Fallot are not age-restricted, and satisfactory results can be obtained from newborns to adults. Twenty-five percent of those who do not undergo surgery die within 1 year of age, 40% die within 3 years of age, and 70% die within 10 years of age. If corrective surgery is performed within 2 years of age, not only is there less collateral circulation, the surgery is easier to perform, but there are fewer secondary changes in the myocardium and better recovery of cardiac function. Palliative surgery was used more often in the early years, and with the development of cardiac surgery, the majority of patients with tetralogy of Fallot can be treated with radical surgery. TOF is a type of cyanotic congenital cardiac structural anomaly that cannot heal on its own. Once diagnosed, it is indicated for surgery. At present, in addition to conventional cardiac ultrasonography, non-invasive CT or MR is generally used to examine the cardiac vessels and trachea, to clarify the right ventricular outflow tract, the location and degree of pulmonary artery stenosis, the development of pulmonary vessels and left ventricle, whether the coronary artery is malformed, whether there are body-pulmonary collateral branches, whether combined with tracheal stenosis or aortic arch malformation, etc. Invasive cardiac catheterization is gradually being replaced and is particularly unsuitable for small infants. The key to surgery is the complete repair of poorly aligned ventricular septal defects. In the early years, repairing ventricular defects via the right ventricular outflow tract incision had an impact on postoperative right heart function, and in the late 1990s we adopted the right atrial pathway to repair ventricular defects, which is of great benefit to protect right heart function. As for the method of continuous or intermittent repair according to the habits of each attending surgeon, the key is not to have residual leakage, and to closely examine the edges of the defect after the end of the repair, and to strengthen the sutures if there are small gaps. Secondly, the size of the patch should be suitable; too small will cause left ventricular outflow tract obstruction. If 3rd degree atrioventricular block occurs it must be removed and re-sutured. The aortic valve and tricuspid valve must not be damaged during the repair process. Another major factor for successful surgery is precise enlargement of the right ventricular outflow tract and pulmonary artery stenosis. In small infants with TOF, secondary hypertrophy of the right ventricle is mild and does not require excessive resection of the abnormal muscle bundles and protection of the papillary muscles and regulating bundles. If both right and left pulmonary arteries are stenosed, multiple patches can be used to enlarge them separately. If the pulmonary valve annulus is not large enough, expansion with a transvalvular patch is required, with the distal end of the patch exceeding the opening of the right pulmonary artery, and attention should be paid to the size of the distal patch to prevent secondary stenosis. It is better to have a mild to moderate pressure gradient at the pulmonary annulus than to over-expand it and produce massive pulmonary regurgitation.