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When the baby is born, the lungs are needed for oxygen transfer and need high blood flow which is encouraged by low PVR. The failure of the circulatory system of the newborn to adapt to these changes by lowering PVR leads to persistent fetal circulation. [2] The newborn is therefore born with elevated PVR, which leads to pulmonary hypertension.
A 1973 World Health Organization meeting was the first attempt to classify pulmonary hypertension by its cause, and a distinction was made between primary PH (resulting from a disease of the pulmonary arteries) and secondary PH (resulting secondary to other, non-vascular causes).
A pulmonary artery wedge pressure being less than 15 mmHg (also measured by right heart catheterization) excludes post-capillary bed (in the veins distal to the capillary bed) pulmonary hypertension. Pulmonary arterial hypertension is a subgroup of pulmonary hypertension and is categorized as World Health Organization as group 1. [3]
If an echocardiogram is performed, marked thickening of the right ventricle will be seen, resulting from highly elevated pulmonary blood pressure. ACD is generally resistant to treatment. Babies who have persistent symptoms that are poorly relieved by standard therapies for neonatal pulmonary hypertension is commonly observed in ACD. [1]
This chronic hypoxia also places IUGR infants at elevated risk of persistent pulmonary hypertension of the newborn, which can impair an infant's blood oxygenation and transition to postnatal circulation. [17] If the cause of IUGR is intrinsic to the fetus, growth is
Transient tachypnea of the newborn occurs in approximately 1 in 100 preterm infants and 3.6–5.7 per 1000 term infants. It is most common in infants born by caesarian section without a trial of labor after 35 weeks of gestation. Male infants and infants with an umbilical cord prolapse or perinatal asphyxia are at higher risk.
Pulmonary haemorrhage, recurrent infections and pulmonary hypertension may hinder the possibility of long-term survival. [12] Survival is probable until patients reach their sixties. [13] Common causes of death include right heart failure, respiratory failure, massive pulmonary hemorrhage and high-altitude pulmonary edema. [6]
Common causes include pulmonary hypertension, which can be the primary defect leading to RAE, or pulmonary hypertension secondary to tricuspid stenosis; pulmonary stenosis or Tetralogy of Fallot i.e. congenital diseases; chronic lung disease, such as cor pulmonale.