Aorto-pulmonary septal defect
Introduction
Introduction to primary-pulmonary septal defect The main-pulmonary septal defect is rare. During the embryonic development, the main trunk of the artery is incompletely separated, and a septal defect is formed in the aorta and pulmonary artery root. The defect is 0.5 cm to 1.5 cm from the aortic valve. The size is generally between 1.5cm and 2.5cm. Mori divides the disease into three types: type I is a proximal pulmonary artery septal defect, type II is a distal septal defect, and type III is a complete septal defect. The main-pulmonary septal defect leads to a cyclical physiological abnormality. In the early stage, due to the large amount of blood flow, the autonomic artery was shunted to the pulmonary artery, and the blood volume of the pulmonary venous return to the left heart chamber increased, which aggravated the left ventricular burden, thus causing left ventricular hypertrophy and strain, while the systemic blood flow was relatively insufficient, resulting in dysplasia or retardation. . Due to congestion of the lungs, it is easy to cause respiratory infections. In the later stage, secondary lesions such as thickening of the wall and small lumen of the pulmonary arterioles increased pulmonary resistance, increased pressure, and excessive load on the right ventricle, causing hypertrophy of the left and right ventricles. When the pulmonary artery pressure is higher than the aorta, a reverse (right to left) shunt is formed, and systemic purpura appears. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: heart failure
Cause
Main-pulmonary septal defect
The main-pulmonary septal defect leads to a cyclical physiological abnormality. In the early stage, due to the large amount of blood flow, the autonomic artery was shunted to the pulmonary artery, and the blood volume of the pulmonary venous return to the left heart chamber increased, which aggravated the left ventricular burden, thus causing left ventricular hypertrophy and strain, while the systemic blood flow was relatively insufficient, resulting in dysplasia or retardation. . Due to congestion of the lungs, it is easy to cause respiratory infections. In the later stage, secondary lesions such as thickening of the wall and small lumen of the pulmonary arterioles increased pulmonary resistance, increased pressure, and excessive load on the right ventricle, causing hypertrophy of the left and right ventricles. When the pulmonary artery pressure is higher than the aorta, a reverse (right to left) shunt is formed, and systemic purpura appears.
Prevention
Primary-pulmonary septal defect prevention
The occurrence of congenital heart disease is a comprehensive result of various factors. In order to prevent the occurrence of congenital heart disease, publicity and education of popular science knowledge should be carried out, and key populations should be monitored to give full play to the role of medical staff and pregnant women and their families.
1. Get rid of bad habits, including pregnant women and their spouses, such as smoking, alcohol and so on.
2. Actively treat diseases affecting fetal development before pregnancy, such as diabetes, lupus erythematosus, anemia, etc.
3. Actively do prenatal checkups to prevent colds. Try to avoid using drugs that have been proven to have teratogenic effects and avoid contact with toxic and harmful substances.
4. For elderly women, family history of congenital heart disease, and serious illness or defects in couples, it should be monitored.
Complication
Main-pulmonary septal defect complications Complications heart failure
Many patients die of congestive heart failure in infants or early childhood. Survivors are prone to respiratory tract infections and dysplasia. When the advanced pulmonary hypertension is severely reversed, systemic purpura occurs. The disease also often combined with other congenital heart malformations, such as atrial septal defect.
Symptom
Symptoms of main-pulmonary septal defect common symptoms cyanotic palpitations with fatigue, pale systolic tremors, rushing water, fatigue, shortness of breath
Symptom
Similar to patent ductus arteriosus, but blood is passed from the ascending aorta to the pulmonary trunk. So the symptoms appear early and serious. Have palpitations, shortness of breath, fatigue and weakness, and can develop cyanosis in the late stage.
2. Physical examination
Systolic murmurs can be heard in the third intercostal space on the left sternal border. A few patients may have continuous murmurs, the same site may have systolic tremor, and the second sound of the pulmonary artery may be hyperthyroidism or division. There is water and pulse, and the pulse pressure is large.
Examine
Primary-pulmonary septal defect examination
Electrocardiogram
Show left ventricular hypertrophy or double-chamber hypertrophy, if there is right-to-left shunt, right ventricular hypertrophy can occur.
2. X-ray inspection
There are many blood in both lungs, the heart is obviously enlarged, the aortic node is not big, the pulmonary artery segment is prominent, and the lung door shadow is widened.
3. Echocardiography
The aortic-pulmonary wall scan echo was interrupted.
4. Right heart catheter and cardiovascular angiography
Pulmonary arterial pressure and increased oxygen levels can be shown. If the catheter enters the ascending aorta and the aortic arch directly from the pulmonary artery, the diagnosis can be confirmed. Aortic retrograde angiography can show the size and location of the defect and the anatomical relationship with the surrounding tissue.
Diagnosis
Diagnosis and diagnosis of main-pulmonary septal defect
Diagnosis can be performed based on clinical manifestations and examinations. Similar to patent ductus arteriosus, but blood is passed from the ascending aorta to the pulmonary trunk. So the symptoms appear early and serious. Have palpitations, shortness of breath, fatigue and weakness, and can develop cyanosis in the late stage.
