What Is an Atrial Septal Defect Repair?

Atrial septal defect (ASD) is a clinically common congenital heart malformation. It is the abnormality of the original atrial septum during embryonic development that results in pores left and right atrium. Atrial septal defect can occur alone or coexist with other types of cardiovascular malformations. It is more common in women, and the ratio of male to female is about 1: 3. Due to the shunt at the atrial level, corresponding hemodynamic abnormalities can be caused.

Basic Information

nickname: Pediatric atrial septal defect
English name: atrial septal defect
Visiting department: Cardiovascular Medicine, Cardiovascular Surgery
Common locations: heart

Common causes: Remaining open defect in the atrial septum during embryonic development
Common symptoms: Generally asymptomatic in childhood, shortness of breath, palpitations, fatigue, etc. in youth
Contagious: no

Causes of atrial septal defect

At the 4th week of embryonic development, the atrium is divided into the left and right atria from the original atrial septum that is emitted from the posterior upper wall and grows towards the endocardial pad. As the endocardium grows, it gradually separates from the original atrium Edge contact, fusion, and finally close the remaining gap (primary hole) between the two. Before the primary hole was closed, the upper part of the original atrial septum gradually deteriorated and absorbed, forming a new channel, the secondary hole. After the formation of the secondary hole, a downward growth interval appeared on the right side of the primary septum, that is, the secondary septum. A single flap is formed to cover the secondary hole, but the two do not fuse with each other, forming an oval hole, and blood flow can be shunted from the right atrium to the left atrium through the oval hole. The oval foramen gradually closes after birth, but a small gap may be left in about 20% of adults. Due to the left atrial valve tissue coverage, there is no shunt under normal circumstances. If the lower edge of the original atrial septum cannot contact the endocardial cushion during embryonic development, a gap remains in the lower part of the atrial septum, forming the primary foramen atrial septal defect. However, if the upper part of the original atrial septum is overabsorbed, the secondary foramen is too large, or the growth and development of the secondary septum is impaired, the two cannot be in contact with each other and a secondary foramen septal defect appears.

Atrial septal defect staging

From the etiology of atrial septal defect, it can be divided into two categories: primary atrial septal defect and secondary atrial septal defect. Due to the primary foratrial septal defect, the mitral and tricuspid valves are often deformed. Secondary foratrial septal defects are classified into four types: central type (oval fossa type defect), upper cavity type (sinus type defect), inferior cavity type, and mixed type defect according to the location of the defect.

Clinical manifestations of atrial septal defect

Most children with secondary atrial septal defect can be asymptomatic, and their activities are not restricted, except for susceptible to respiratory infections such as colds. Generally, they have shortness of breath, palpitations, and fatigue in their youth. After the age of 40, the majority of patients' symptoms worsen, and arrhythmia such as atrial fibrillation and atrial flutter often occur, and congestive heart failure is also an important cause of death.

Physical examination revealed that most children were thin and often showed a slight bulge on the left anterior chest wall, increased heart pulsation, and could touch the right ventricle. It is typically manifested as intercostal odors of the second and third intercostal spaces of the left margin of the sternum, and - grade systolic whistle-like murmurs, accompanied by second heart sounds and fixed division. Patients can also experience systolic tremor. Diastolic rumbling murmurs from tricuspid valve stenosis can be heard in the tricuspid area with large shunts. For example, if the right ventricular lift is increased, the systolic murmur in the pulmonary valve area is weakened, but the second heart sound is more hyperactive and divided, indicating the presence of pulmonary hypertension. The advanced stage of the disease will be congestive heart failure, jugular veins flared, and the liver enlarged.

Atrial septal defect inspection

Imaging examination

(1) Chest X-ray mainly shows pulmonary congestion, mild to moderate enlargement of heart shadow, and prominent pulmonary artery segment. The left ventricle and aorta are normal or slightly smaller than normal.

(2) Echocardiography and color Doppler can generally establish a diagnosis, showing that the right atrium and the right ventricle are enlarged, the ventricular septum is moving in the same direction as the left ventricular posterior wall, and the right ventricular overload is manifested. And measure the size of the defect. Color Doppler can determine the direction and speed of blood shunt and estimate the shunt flow. Ultrasound imaging of sinus-type defects may be difficult. Hydrogen peroxide imaging can help find the shunt site, and transesophageal ultrasound can obtain very clear images.

2. Other inspections

ECG examination: manifested as right axis deviation, incomplete right bundle branch block and right ventricular hypertrophy. Adult patients may have arrhythmias, with atrial fibrillation and atrial flutter being the most common.

Right ventricular catheter examination: The right atrial blood oxygen content exceeds the vena cava mean blood oxygen content by more than 1.9%. The right ventricular catheter can also pass through the defect and enter the left atrium. Right heart catheterization can calculate pulmonary and systemic blood flow, determine intracardiac shunt conditions, and measure pulmonary arterial pressure.

Differential diagnosis of atrial septal defect

According to the above typical signs, combined with ECG, chest X-ray and cardiac ultrasound, diagnosis of atrial septal defect is generally not difficult. Cardiac catheterization can help in atypical patients or those with other comorbidities. The conditions to be distinguished from atrial septal defect are simple pulmonary valve stenosis and primary pulmonary artery dilatation.

1. Pulmonary valvular systolic murmurs with simple pulmonary valve stenosis are rough and loud, and often tremble, and the second heart sound in the pulmonary valve region weakens or even disappears. The chest X-ray showed a prominent pulmonary artery segment, but the pulmonary blood was less than normal or in the normal range, and cardiac ultrasound could confirm the diagnosis. Right heart catheterization showed no significant difference in blood oxygen content between right atrium and vena cava, and pressure difference between right ventricle and pulmonary artery was more than 20mmHg.

2. Grade II systolic murmur can also be heard in the pulmonary valve area with primary pulmonary artery dilatation. Chest radiographs may have prominent pulmonary artery segments, but the pulmonary blood is normal. There is no echo interruption and shunt in the atrial septum during cardiac ultrasound examination. Check the right atrium and right ventricle for no changes in blood oxygen content, no pressure step between the right ventricle and the pulmonary artery.

Atrial septal defect treatment

Secondary spontaneous atrial septal defects over 1 year old rarely have spontaneous closure. For asymptomatic children, if the defect is less than 5mm, it can be observed. If the right atrium and right ventricle are enlarged, surgical repair is generally recommended before school age. About 5% of infants develop congestive heart failure within 1 year after birth. Surgery can also be performed for patients with poor medical treatment. Adults with a defect less than 5 mm and no right ventricle enlargement can be clinically observed without surgery. Adult diseases such as right atrial ventricular enlargement can be treated surgically, and those with atrial fibrillation can also be operated at the same time, but those with pulmonary vascular resistance greater than 12 units, right to left shunt and cyanosis are contraindicated.

Some of the secondary foratrial septal defects can be treated with minimally invasive transcatheter catheterization if the location is appropriate. The femoral vein was intubated, and the nickel-titanium occluder was clamped to the atrial septal defect, and the atrial septal defect was closed to achieve the purpose of treatment. No thoracotomy.

Secondary foratrial septal defect is often repaired directly under the CPB through the sternal approach. The right anterior lateral incision can also provide good surgical exposure, but it must be ruled out that other types of cardiac malformations are combined. Small secondary foramen atrial septal defects can be directly sutured. If the defect is large, it needs to be repaired with a pericardial sheet or polyester patch. It is important to fill the left atrium with water before the repair to prevent air embolism after the heart beats.

Sinus-atrial septal defect repair is more complicated. Generally, the drainage tube is directly inserted through the superior vena cava to increase the exposure of the defect. During the repair, the right upper pulmonary vein opening must be identified and the sinoatrial node must be avoided. On the wall to ensure that the pulmonary veins flow into the left atrium, and if necessary, a patch is needed to widen the superior vena cava entrance to prevent venous return from being blocked.

Older patients with atrial septal defect have a higher incidence of sinus bradycardia after surgery. Isoproterenol or atropine can be used to increase the heart rate. Temporary pacing electrodes during the operation are effective measures.

Atrial septal defect prognosis

The natural course of patients with non-surgical atrial septal defect is related to the type of defect, the amount of shunt, and whether it is combined with other types of cardiac malformations. Most of them can grow to adulthood, but their life span is shortened, and patients die of congestive heart failure. The mortality rate for simple secondary atrial septal defect surgery is less than 1%. Due to the improvement of hemodynamics after surgery, the symptoms of patients were significantly reduced or disappeared, and their long-term survival rate was not significantly different from that of normal people. Adult patients, especially those with cardiac insufficiency, arrhythmia, or pulmonary hypertension, have relatively high surgical mortality. Sometimes despite successful surgical repair, existing pulmonary hypertension and right ventricular hypertrophy still exist, but the patient's cardiac function can be improved. Its long-term survival rate is also significantly higher than that of non-surgical cases.