A child with hypoplastic left heart refers to the poor development of the left ventricle. The cause of hypoplasia is generally attributed to problems with the inlet mitral valve and the outlet aortic valve of the left ventricle, which may be hypoplastic or outright atresia. The left ventricular cavity is smaller, and the chain reaction is that the ascending aorta becomes smaller, from a large blood vessel to a small blood vessel.
We know that the left ventricle is very important to the human body, and the blood pumped out must support the systemic circulation. The left ventricle is small and the aorta coming out is small, which reduces the blood flow pumped out to the systemic circulation, causing ischemia and hypoxia in children. In order to maintain the pumped blood flow enough to maintain the systemic circulation, the child's heart can only speed up, causing and aggravating heart failure. Then a series of clinical symptoms mentioned above appeared.
In summary, several links of the left heart system have all gone wrong under the influence of each other during the development process, so it is called left heart dysplasia syndrome.
Why doesn't this child's current symptoms seem serious?
"Because of multiple atrial septal defects, he was shunted, and the ductus arteriosus was patented." Xie Wanying added some of her own speculations.
The situation of the child in the mother's womb, as we discussed in the chapter on the interatrial septum, the cardiac circulatory system in the fetal period is different from that after birth. The same is true for this disease. It is necessary to wait until the child is born to breathe on his own, and finally can realize the serious consequences of this abnormal heart, before the symptoms of the disease can gradually appear.
It seems that the best state to keep the child from ischemia and hypoxia is that, theoretically speaking, it may be best to return the part of the child's cardiac circulatory system to the child's fetal period. The atrial septal defect is large, which is exactly the same as the shunt of the wall that is not closed during the fetal period. At the same time, the ductus arteriosus in the fetal period is not closed, allowing the blood of the pulmonary artery to flow to the aorta to support the systemic circulation as in the fetal period.
As Xie said, this child's heart is just like this, no wonder the symptoms are mild.
Can this continue?
The answer is impossible. First of all, the ductus arteriosus is normally closed in a few hours to a few days after birth, and it is anatomically closed after one or two months, which is the same as the closure of the foramen ovale. Even if it doesn't close, if this situation lasts for a long time——
"It's definitely not possible to do the surgery without hurrying. If it is delayed, it will become pulmonary hypertension. There is no possibility of Fontan surgery for pulmonary hypertension." Xie Wanying said.
This means that according to the above principle, whether it is the shunt support of the patent ductus arteriosus and the atrial septal defect, it only solves the problem of insufficient blood flow in part of the systemic circulation, but the existence of mixed arterial blood cannot be prevented, and the mixed blood is pumped into the systemic circulation. cause hypoxia in the body. The Fontan procedure is a total cavopulmonary anastomosis, which connects the superior and inferior vena cava directly to the pulmonary artery. This allows only arterial blood with high oxygen content in the heart chamber to avoid mixing of arterial blood. The blood pumped out into the systemic circulation is only arterial blood, which can greatly improve the hypoxia of the body.
The premise of Fontan surgery is good pulmonary circulation and no pulmonary hypertension. What to do, this is to say the first-stage operation for the treatment of left heart dysplasia, Norwood surgery, simply cut the entire atrial septal defect to expand the traffic of the room.
The main pulmonary artery is then cut at the bifurcation of the left and right pulmonary arteries, and the side of the main pulmonary artery is connected to the side of the aorta and the aorta is enlarged.
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