Children with left heart hypoplasia refer to poor left ventricular development. The reason for poor development is generally attributed to problems with the inlet mitral valve and outlet aortic valve of the left ventricle, which may be underdevelopment or direct atresia. The left ventricular cavity is small
The chain reaction is that the ascending aorta becomes smaller, changing from a large blood vessel to a small blood vessel.
We know that the left ventricle is very important to the human body. The blood pumped out must support the systemic circulation. The small left ventricle and the small aorta that come out reduce the blood flow pumped to the systemic circulation, causing ischemia and hypoxia in children. In order to maintain
If the blood flow pumped out is sufficient to maintain systemic circulation, the child's heart can only speed up its operation, leading to and aggravating heart failure. As a result, a series of clinical symptoms mentioned above appear.
To sum up, several links of the left heart system all have problems under the influence of each other during the development process, so it is called hypoplastic left heart syndrome.
Why don't this child's current symptoms seem serious?
"He was shunted due to multiple atrial septal defects and patent ductus arteriosus." Xie Wanying added some of her own speculations.
We talked about the situation of the child when it is in the mother's belly in the chapter on interatrial separation. The cardiac and circulatory system during the fetal period is different from that after birth. The same principle applies to this disease. You have to wait until the child is born to breathe on his own.
Only by realizing the serious consequences of this heart abnormality can the symptoms of the disease gradually appear.
From this point of view, the best way to prevent the child from ischemia and hypoxia is to, theoretically speaking, perhaps return the child's cardiac and circulatory system to the condition of the child's fetal stage. The atrial septal defect is large, which is exactly the same.
The wall that is not closed during the fetal period acts as a shunt. At the same time, the ductus arteriosus is not closed during the fetal period, allowing blood from the pulmonary artery to flow to the aorta to support systemic circulation just like it did during the fetal period.
As classmate Xie said, this child’s heart has grown like this, so it’s no wonder that the symptoms are mild.
Can this situation continue?
The answer is impossible. First of all, normally, the ductus arteriosus begins to functionally close hours to days after birth, and anatomically closes after one or two months, which is the same as the closure of the foramen ovale. Even if it does not close,
If this situation lasts for a long time——
"If we don't do the surgery quickly, it's definitely not possible. If we delay it any longer, I'm afraid it will turn into pulmonary hypertension. With pulmonary hypertension, there's no possibility of Fontan surgery," Xie Wanying said.
This means that according to the above principles, whether it is patent ductus arteriosus or atrial septal defect providing shunt support, it only solves the problem of insufficient blood flow in part of the systemic circulation. It cannot prevent the existence of arterial mixed blood, and the mixed blood is pumped out into the systemic circulation.
It also causes hypoxia in the body. Fontan surgery uses a total cavopulmonary anastomosis, which directly connects the upper and lower vena cava to the pulmonary artery. This allows only arterial blood with high oxygen content in the heart cavity and avoids the mixing of arterial blood. The pumped blood
Only arterial blood enters the systemic circulation, which can greatly improve the body's hypoxia.
The prerequisite for fontan surgery is good pulmonary circulation and no pulmonary hypertension. What to do? This comes to the Norwood surgery, which is the preferred first-stage surgery to treat left heart hypoplasia. Simply cut out the entire atrial septal defect to expand the communication between the rooms.
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Then cut the main pulmonary artery at the bifurcation of the left and right pulmonary arteries, connect the side of the main pulmonary artery to the side of the aorta and enlarge the aorta.