Ventricular septal defects, especially those of high and atrioventricular canal type, are prone to complications during repair: atrioventricular block; aortic valve or tricuspid valve injury; air embolism, etc. 1, atrioventricular block in the early stage of ventricular septal defect repair, the incidence of permanent atrioventricular block is 1%-12%. With the improvement of surgical techniques, such as the use of beyond sutures, gentle operation and avoidance of excessive pulling or clamping, this complication of AV block has been greatly reduced. In the author’s 210 cases of direct visual suturing and repair of ventricular septal defects, no permanent AV block occurred in 1 case. In cases of complete AV block immediately after resuscitation, cardiopulmonary diversion should be performed again, the cardiac incision should be opened, 1-2 sutures should be removed at the posterior inferior corner of the defect, and 1 or 2 additional sutures should be placed slightly distant from the posterior inferior edge of the defect. If the ventricular rhythm is slow and the blood pressure is low, isoprenaline 0.5 mg should be administered intravenously to maintain the heart rate above 80 beats/min. Before closing the chest, place pacing electrodes on the myocardial surface and connect the pacemaker to set the heart rate at 90-100 beats/min for pacing. The effect of complete or incomplete right bundle branch block on the patient is not significant and does not require special treatment. 2, aortic valve closure incomplete large defects, aortic valve annulus without septal tissue under the suture, such as suture pulling too tight, can make the aortic valve annulus deformation, easy to cause closure incomplete. If the sutures are placed too deep and too high; they can injure the aortic valve and also lead to incomplete closure. Therefore, for large defect repair, plastic fabric should be used and the aortic valve site should be identified and the sutures should be placed at the aortic valve annulus. Once incomplete closure is detected during surgery, it should be promptly removed and re-sutured. 3, tricuspid valve closure or narrow suture septal posterior defect, it is easy to injure the valve or its tendons, resulting in incomplete closure. The author had a case of severe clinical closure insufficiency after defect repair and died 21 months after surgery. Autopsy revealed that the defect was not adequately repaired and re-teared, and a suture was passed through the septal tendon at the posterior inferior border of the defect and fixed to the inferior border of the defect, creating an incomplete closure and turning the septal defect into a simultaneous shunt from the left ventricle to the right one and the right atrium, with serious consequences. Another possibility for tricuspid valve insufficiency is that the tendon cords were cut without suturing or repositioning when the defect was exposed. Therefore, after repairing a large defect, if the anterior valve is not retracted, the posterior edge of the defect may be sewn together with the root of the septal valve and the root or annulus of the anterior valve, resulting in narrowing or stenosis of the tricuspid valve. 4, defect repair imperfection defect repair still has a large residual shunt after the repair, about 6%. It often occurs in large defect repair, mostly at the posterior inferior angle. The reasons may be that the suture distance is too large, leaving a gap; the suture is too shallow and easily dislodged; the transfer suture does not close the angle between the lower part of the septum and the edge of the defect, etc. Therefore, attention should be paid to these points when the defect is repaired. After the repair is completed, the defect repair should be tested for perfection, and the gap between the sutures at the edge of the defect should be probed with a curved blunt-tipped probe; or an expansion lung test should be performed, and isotonic saline should be injected under pressure in the left ventricle to observe whether there is blood and fluid leakage around the patch. 5, air or other emboli embolism in the process of septal defect repair, especially in those who use left atrial drainage, air can enter the left ventricle through the defect and lead to coronary artery air embolism after suturing the heart incision, causing serious consequences. Routinely, the operating table is swung to a low head height and the left ventricular apical drainage tube is used to remove gas from the left ventricle. The right hand is placed behind the heart and gently shaken, while the apical end is elevated and the air that may remain in the heart chambers, pulmonary artery and ascending aorta is withdrawn by puncturing the apical end with a syringe, then a deflating slotted needle is inserted in the root of the ascending aorta, while the ascending aorta is loosened and clamped shut to resuscitate the heart. If coronary artery air embolism is found, the flow is immediately increased, the perfusion pressure is raised, and the coronary artery is squeezed in the distal direction with the fingers to expel the air embolism. If embolism occurs in the brain, high concentration of oxygen or pure oxygen should be used for mechanical respiration after surgery to promote the absorption of micro-air embolism; in those with coma and convulsions, hypothermia should be adopted within 5 days after surgery to maintain the pharyngeal temperature at 32-34℃ and to adopt measures to prevent and control cerebral edema. In addition, when applying artificial fabric to repair the defect, the fabric piece should be cleaned and the edges should be flattened by electrocautery so that the threads will not fall off and form emboli; in extracorporeal circulation perfusion system, microporous filters are used in many places to make effective measures to prevent microemboli embolism. 6, to prevent heart expansion and ventricular fibrillation large defects combined with pulmonary hypertension, especially in patients with high resistance – low reserve type, the left and right ventricles are often hypertrophic, even strain, poor tolerance to hypoxia; pulmonary artery pressure and resistance generally fall unsatisfactorily after surgery; this requires not only maintaining a good left ventricular function, but also maintaining a good right ventricular function. Therefore, during direct intracardiac surgery, myocardial protection should be enhanced to minimize the ischemic time of the heart. Resuscitation should never inflate the heart, damage the myocardial fibers and obstruct the subendocardial blood supply, and the heart must be kept in the evacuated state. If ventricular fibrillation occurs, it must be defibrillated as early as possible with low-power electroshock, otherwise the subendocardial blood supply will also be reduced and the oxygen consumption of the fibrillating myocardium will increase compared to that of the empty-beaters. Both conditions are detrimental to the recovery of myocardial contractility, weakening the power of the heart, especially the right ventricle, to expel blood through higher pulmonary vascular resistance and increasing the likelihood of low cardiac output signs and even heart failure after surgery.