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Acute right ventricular failure in children
Last reviewed: 07.07.2025
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After heart surgery, the occurrence of acute right ventricular failure is associated with the development of residual pulmonary hypertension (systolic form) or with a decrease in the contractility of the right ventricle (diastolic form).
In young children with "pale" congenital heart defects accompanied by reversible pulmonary hypertension, the main reason for unsatisfactory results of surgical treatment is considered to be the formation of pulmonary hypertensive crises. Pulmonary hypertensive crises are a sharp paroxysmal increase in the resistance of the pulmonary arterioles, which prevents blood flow into 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 CO, coronary hypoperfusion and, ultimately, to the death of the patient. For the implementation of pulmonary hypertensive crises, along with a volume overload of the pulmonary circulation, the presence of a hypertrophied muscular membrane (tunica media) of the pulmonary arterioles is necessary.
The pulmonary vascular bed of newborns and young children (up to two years) with reversible pulmonary hypertension is characterized by pronounced reactivity. This is explained by chronic damage to the endothelium of the pulmonary vessels by increased pressure and increased blood flow in them, leading to the loss of the endothelial relaxation factor. In addition, after removing the clamp from the aorta during extracorporeal circulation, the concentration of the potential vasoconstrictor endothelin-1 in the blood plasma increases sharply. The peak increase is recorded within 3-6 hours after surgery. 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 the pulmonary vessels persists for several days after surgery and then decreases significantly. Risk factors for the development of pulmonary hypertensive crises after correction of the ventricular septal defect include young children (under 2.1 years), body weight less than 9.85 kg, and a high ratio of PAP to BP (more than 0.73 and more than 0.43 before surgery and after correction, respectively). An important feature of pulmonary hypertension after correction of congenital heart defects is its paroxysmal nature. Pulmonary hypertensive crises can occur even in children with normal total pulmonary vascular resistance (before surgery).
The trigger factors for the development of pulmonary hypertensive crises are considered to be hypoxia, hypercapnia, acidosis, as well as pain and agitation.
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