Acute right ventricular failure in children

After heart surgery, the emergence of acute right ventricular failure is associated with the development of residual pulmonary hypertension (systolic form) or with a decrease in contractility of the right ventricle (diastolic form).

In young children with "pale" congenital heart defects accompanied by reversible pulmonary hypertension, the main cause of unsatisfactory results of surgical treatment is the formation of pulmonary hypertensive crises. Pulmonary hypertensive crises present a sharp paroxysmal increase in the resistance of pulmonary arterioles, which prevents blood flow to the left heart and is accompanied by a sharp increase in CVP. A significant decrease in pulmonary blood flow in combination with a decrease in LV preload leads to the development of hypoxemia, a decrease in CB, coronary hypoperfusion and, ultimately, the death of the patient. For the implementation of pulmonary hypertensive crises, along with volume overload of the small circle of blood circulation, a hypertrophic muscular membrane (tunica media) of pulmonary arterioles is necessary.

The pulmonary vascular bed of newborns and young children (up to two years) with a reversible character of pulmonary hypertension is markedly reactive. This is explained by chronic damage to the endothelium of the vessels of the lung by increased pressure and increased blood flow in them, leading to loss of the endothelium relaxation factor. In addition, after removal of the clamp from the aorta during extracorporeal circulation in blood plasma, the concentration of the potential vasoconstrictor endothelin-1 sharply increases. The peak of ascending is recorded within 3-6 hours after the operation. In children of the first three months of life, a higher concentration of endothelin-1 in the blood plasma is determined than in older children.

Hyperreactivity of pulmonary vessels persists for several days after the operation, and then significantly decreases. The risk factors for the development of pulmonary hypertensive crises after correction of the interventricular septal defect include younger children (up to 2.1 years), body weight less than 9.85 kg, high ratio of DL and BP (more than 0.73 and more than 0.43 before surgery and after correction of the defect, respectively). An important feature of pulmonary hypertension after correction of congenital heart disease is its paroxysmal nature. Pulmonary hypertensive crises can occur even in children with normal pulmonary vascular resistance (before surgery).

Starting factors of the development of pulmonary hypertensive crises are hypoxia, hypercapnia, acidosis, as well as pain and agitation.

[1], [2], [3], [4], [5], [6], [7], [8]