Morbidity
Atrial septal defect is the most common type of lesion in congenital heart disease. According to the autopsy of 1000 cases of simple congenital heart disease by Abbott, atrial septal defect was the first one, accounting for 37.4%. In 1982, Huang Mingxin et al. counted 4043 cases of congenital heart disease in Shanghai, among which 1054 cases of atrial septal defect, accounting for 26.1%, were the first in congenital heart disease. Among 7745 cases of direct heart surgery in Renji Hospital of Shanghai Second Medical University, there were 693 cases of atrial septal defect, accounting for 8.9%. Jiang Xionggang, Department of Cardiac Surgery, Wuhan Union Medical College Hospital
The incidence of atrial septal defect is more frequent in females, and the ratio of incidence to males is about 2:1. However, in the surgical cases of the author and others, there are more males, and the ratio to females is about 1.7:1.
Classification
There are many ways to classify the disease, and there is no agreement among scholars. Based on embryology and pathological anatomy, the author et al. divided into two major categories, namely primary foramen ovale defects and secondary foramen ovale defects, with the latter being far more common than the former. According to the data from Shanghai Chest Hospital, Fu Wai Hospital of China Medical College, Shanghai Second Medical University and the Affiliated Hospital of the Fourth Military Medical University of the People’s Liberation Army: (including internal data), a total of 2970 cases of atrial septal defects were performed from 1957 to the end of 1989, of which secondary foramen defects accounted for 95.7% (Table 33-0I). Because of the different clinical presentations and treatments, they will be described in separate sections.
Secondary foramen ovale defects
Pathologic anatomy
Secondary foramen defects vary in number, size, shape, and location. The vast majority of defects are solitary. Sometimes there can be two or many small foramina present at the same time. Large defects occupy several of the entire septum, and small ones can only accommodate probes. In general; even in cases that survive to adulthood, the defect is not small and is approximately 2 to 4 cm in diameter. the shape and location of the defect are often related to the type.
Secondary foramen defects can be divided into four types
(a) Foramen ovale type or central foramen ovale defect
is the most common type in clinical practice, with an incidence of more than 75% of the total The vast majority of cases. The defect is solitary, oval in shape, about 2-4 cm long, and located in the posterior superior part of the coronary sinus. It is surrounded by a well-defined rim, which is especially pronounced superiorly (Figure 33-03). The defect is distant from the conduction system, easily sutured and well divided. The defect in individual cases, however, can be sieve-shaped.
(B) Inferior foramen ovale type or low level defect
Far less common than the foramen ovale type, accounting for about 12% or more of the total. The defect is solitary, low lying, oval in shape, with an absent inferior border and no clear demarcation from the entrance to the inferior vena cava (Figure 33-04). It is sometimes accompanied by an inferior vena cava flap, and special attention should be paid during surgery.
(C) Superior vena cava type or high defect
Also known as sinus venosus defect, many cases have been reported abroad, but it is rare in China, accounting for about 3.5% or more of the total. The defect is located above the foramen ovale, immediately above the population of the superior vena cava. The defect is usually small, about 1.5 to 1.75 cm, with a distinct crescent-shaped interatrial septum at its inferior border and an absent superior border, often connected to the superior vena cava, allowing superior vena cava blood flow to the left and right atria (Figure 33-05). These cases are almost always associated with anomalies of the right upper or right middle lobe pulmonary veins, with blood flowing back into the superior vena cava.
(iv) Mixed type or said to have both of these defects
It is less common clinically.
Cases with secondary foramen ovale defects can sometimes be associated with other anomalies, such as pulmonary stenosis, ectopic regurgitation of the right pulmonary vein, mitral stenosis (Lutembacher syndrome), double superior vena cava, and right aortic arch, in about 15% of cases.
Pathophysiology
Normally, the left atrial pressure (8-10 mmHg) is higher than the right atrium (3-5 mmHg) in both systole and diastole. o Therefore, when a septal defect exists, blood is shunted from left to right, and there is no clinical symptom of cyanosis. The amount of shunt flow is proportional to the size of the defect and the pressure step difference between the left and right atria, and inversely proportional to the level of pulmonary vascular resistance. It generally varies from 7 to 20 L per minute (normal right heart flow is about 5 L), exceeding the circumferential circulation volume by 2 to 3 times or even 4 times. The effect on the circumferential circulating volume is usually small, and blood pressure changes are rare.
As a result of intracardiac shunting, the blood flow through the right atrium, right ventricle and lungs is much more than that through the left heart, and the right atrium, right ventricle and main pulmonary artery are enlarged as a result, which is a typical type of diastolic overload; the left atrium, left ventricle and aorta are reduced accordingly.
In 1961, Besterman reported that there are two types of pulmonary hypertension: (1) dynamic hypertension, which is the result of increased pulmonary blood circulation and small pulmonary artery resistance, within 5 wood/m2; (2) obstructive hypertension, which is the result of increased pulmonary blood circulation and small pulmonary artery resistance, within 5 wood/m2; and (3) pulmonary hypertension. obstructive hypertension, refers to the small pulmonary arteries have lesions, the result of increased resistance, the resistance of more than 5 wood/m2 West the former is more common, the latter only accounted for 15% to 18%. After the occurrence of pulmonary hypertension, not only can cause pulmonary complications, such as respiratory infections and thrombosis, but also can make the right heart blood output is impaired, resulting in right ventricular and right atrial hypertrophy, finally causing right heart failure. However, because the right heart has the physiological function of bearing high blood volume, the age of failure generally occurs later, mostly above 20 to 30 years old.
When the pressure in the right heart increases to a certain limit, part of the blood in the right atrium may reverse into the left atrium, forming a right-to-left shunt and clinically producing cyanotic symptoms. This indicates that the evolution of the disease process enters an advanced stage.
Clinical manifestations
(1) Symptoms
The symptoms of atrial septal defect are inconsistent and closely related to the size of the defect and the amount of shunt flow. In large defects, symptoms appear earlier; in small defects, they can be asymptomatic for a long time and remain latent until old age. Most cases are asymptomatic in childhood and are often detected during physical examination; generally, symptoms begin to appear in young adulthood, mostly between the ages of 21 and 40.
The main symptoms are shortness of breath after labor, palpitations or respiratory infections and heart failure.
In infant cases, because the resistance of pulmonary circulation is still high after birth, a small amount of blood can be shunted from the right to the left if the defect is huge. However, in the late stage of the disease, when the blood turns to reverse flow (right to left), cyanosis appears to a certain extent and continues to worsen until death.
Pediatric cases are prone to recurrent severe pulmonary infections because of pulmonary congestion, manifesting as multiple coughs, shortness of breath, and even pneumonia symptoms. Due to the decrease in left heart blood flow, patients tend to have a lack of physical strength and are prone to idleness and dyspnea. They are more likely to feel shortness of breath and palpitations after labor. In addition, prolonged diastolic overload of the right heart can lead to pulmonary hypertension and right heart failure. However, its evolution is slow and can be delayed for several years.
(B) Physical signs
Physical development is mostly normal. The right ventricle is enlarged, and with age, the adjacent sternum and left rib cage may show enlargement and fullness. On auscultation, elevated pulsatility may be found. On auscultation, the cardiac border may be enlarged, especially in the second and third intercostal spaces of the left chest due to the dilated pulmonary artery.
On auscultation, the main findings are a systolic murmur in the pulmonary valve area and a hyperactive and split second tone; these are important for diagnosis. The systolic murmur usually appears late and can be heard at 3 to 4 years of age. The loudness of the murmur is mostly grade II-IV, jet-like, with the left side of the 2nd and 3rd intercostal spaces near the sternal border being the loudest, sometimes accompanied by tremors. This systolic murmur is not produced by blood flow through the defect, but is caused by a large amount of blood passing through the normal pulmonary valve and entering the enlarged pulmonary artery. The hyperacusis and splitting of the second pulmonary artery sound is also caused by a large amount of blood entering the pulmonary artery from the right ventricle, causing the pulmonary valve to close forcefully and slightly late. In some cases with large defects, a transient roller-like diastolic murmur of relative tricuspid stenosis can be heard in the precordial region, which is produced when a large amount of blood enters the right ventricle through the tricuspid orifice.j In some cases, an enhanced systolic murmur can be heard between the 4th and 5th ribs at the left border of the sternum or a diastolic murmur can be heard. The former is caused by relative tricuspid insufficiency after right ventricular enlargement, while the latter is caused by relative pulmonary insufficiency. When pulmonary hypertension develops; the systolic murmur in the pulmonary valve area is seen to decrease, but the second tone is more pronounced in hyperacusis, and the division is narrowed or absent.
In advanced cases of right heart failure, there are signs such as jugular vein anger, hepatomegaly and drop edema.
(iii) Radiological examination
The radiographic signs are: (1) enlargement of the heart, especially the right atrium and right ventricle, which is most obvious in the right anterior oblique photograph. This is clearer in the right anterior oblique photograph; (ii) protrusion of the pulmonary artery segment; deepening of the hilar shadow, congestion of the pulmonary field, and sometimes hilar dancing can be seen under fluoroscopy, and calcification may be formed in advanced cases; (iii) narrowing of the aortic arch (Figure 33-06). In addition, there is no left ventricular enlargement in general cases, which can be distinguished from ventricular septal defect or patent ductus arteriosus.
(iv) Electrocardiographic examination
A typical atrial septal defect often shows an increased P wave and a rightward deviation of the electrical axis, often between +60 and +180 degrees. Most cases may have incomplete or complete right bundle branch block and right ventricular hypertrophy, and those with pulmonary hypertension may have right ventricular strain. The frontal cardiac vectorogram shows that the QRS ring is transposed in a cis-clockwise direction, and the main body of the ring is located below the X axis.
(E) Cardiac catheterization
Cardiac catheterization is a valid diagnostic method for atrial septal defect. At present, it is generally agreed by scholars. In suspicious or severe cases, the cardiac catheter should be inserted from the saphenous vein route of the lower extremity, which can easily pass through the defect and enter the left atrium with a passage rate of up to 85%. However, in cases of superior ventricular type defects, it is more convenient to take the route of upper extremity vein insertion.
The size of the defect can be estimated by noting the range of movement of the cardiac catheter within the defect. Only then can the correct diagnosis be made.
In general, in cases of atrial septal defect, the oxygen level in the right atrium is often 2 volume percent higher than in the superior vena cava.
As mentioned above, 20% to 25% of normal subjects generally have an unclosed foramen ovale. In this case, the cardiac catheter can be inserted into the left atrium without abnormal shunts, and the pressure and oxygen content of the right atrium are not altered, so it can be distinguished from an atrial septal defect. In early surgical cases such as the author’s, there was a case where the procedure was mistakenly performed because this was not noted. Similarly, if only the increased oxygen level in the right atrium is emphasized and the passage of the cardiac catheter is ignored, it may also lead to a wrong diagnosis. Simple ectopic reflux of the right pulmonary vein, for example, can cause this phenomenon. In conclusion, the diagnosis can be confirmed only if the cardiac catheter is inserted into the left atrium and the right atrial oxygen level simultaneously exceeds 2 volume percent of the superior vena cava.
If the foramen ovale defect is large,. The right edge is close to the lateral wall of the atrium, the cardiac catheter can easily pass through the defect and enter the right pulmonary vein, which can be easily misdiagnosed as right pulmonary vein ectopic return. However, if the cardiac catheter is estimated to have passed through the defect at the time of intubation, this error can be avoided by trying to push it in with its curved tip toward the left rather than to the right. When the cardiac catheter has been inserted into the right pulmonary vein, the direction of transfer of the tip of the cardiac catheter should be noted at the time of extubation, which can help in the differential diagnosis. In right pulmonary vein ectopic regurgitation, the tip of the catheter is always oriented to the right as it returns to the atrium, whereas in the normal position of the pulmonary vein, the tip of the catheter may shift somewhat to the posterior or left as it returns to the atrium.
In patients with atrial septal defects; saphenous vein cannulation is often used. Compared with the upper extremity insertion route, this insertion method is certainly not easy to insert into the pulmonary artery, so that sometimes the pulmonary artery pressure cannot be measured, but it has been proved from practice that in cases of secondary pulmonary hypertension, the right ventricular systolic pressure is almost equal to the pulmonary artery pressure (but the mean pressure is slightly lower than the pulmonary artery). Therefore, according to the right ventricular pressure and fractional flow, the author and others can classify the disease into five groups of three levels.
Class I: those with right ventricular systolic pressure less than 60 mmHg or mean pressure less than 25 mmHg, in which the left-to-right fractional flow is less than 20% of pulmonary blood flow, classified as group A; greater than 20%, classified as group B.
Class II: Those with right ventricular systolic pressure between 60 and 90 mmHg or mean pressure between 25 and 35 mmHg, both with higher fractional flow.
Grade III: Those with right ventricular systolic pressure greater than 90 mmHg or mean pressure greater than 35 mmHg, in which the fractional flow was predominantly left-to-right, were classified as group A; those with predominantly right-to-left, were classified as group B.
This graded grouping of hemodynamic changes is basically related to clinical symptoms and signs, and can be used as a reference for surgical selection.