Persistent pulmonary hypertension of the newborn

Persistent pulmonary hypertension of the newborn is a very significant issue for babies that experience it. During the life of a fetus the blood flow to the lungs is much less than what it would be for a child already born or for an adult. Slightly less than 10% of the cardiac output is actually directed toward the lungs. During the life of a fetus pulmonary vascular resistance is maintained generally by hypoxia. Once a baby is born the pulmonary vascular resistance reduces and the blood flow to the lungs increases greatly because they begin to assume the function of exchanging air. There are two things that stimulate this. These are the increase in the alveolar oxygen tension and the rhythmic ventilation of the lung itself. Each one of these stimuli will work by itself to help decrease the pulmonary vascular resistance and when they occur together the largest effects are seen. However, some newborns do not have this normal decrease in the pulmonary vascular tone and when this does not occur persistent pulmonary hypertension of the newborn is present. Generally, most of these infants are otherwise healthy but having PPHN results in substantial mortality and morbidity for these infants despite their otherwise healthy birth (www.emedicine.com,2004).

Persistent pulmonary hypertension of the newborn is generally a failure of the transition that would normally take place in the circulatory system at birth. It is characterized by pulmonary hypertension that causes hypoxemia and can also cause a right to left extrapulmonary shunting of the blood. When this occurs neonates often develop respiratory distress, refractory hypoxemia, and acidosis. The hypoxemia and respiratory failure in newborns that are carried to term can result from a group of disorders and the approach that is taken therapeutically often strongly depends on any underlying disease that may be present. PPHN can often result when pulmonary vessels that are structurally normal constrict in response to alveolar hypoxia. This can be due to parenchymal disorders such as meconium aspiration syndrome or hyaline membrane disease, or hypoventilation. PPHN, however, sometimes also occurs in the absence of any underlying disease. When this takes place the cause is believed to be a vasculature that is abnormally remodeled and that develops incorrectly in utero, generally in response to pulmonary hypertension, hypoxia, or prolonged fetal stress. In these cases peripheral and excessive muscularization of many of the pulmonary arterioles is often seen. PPHN has also been commonly associated with hypoplasia of the lungs, which is seen generally in congenital diaphragmatic hernias. The underlying causes of this are quite different structurally and generally functional differences are also seen. These differences are generally witnessed in response to the inhalation of nitric oxide or other vasodilators. Learning more about the biological alterations that take place with PPHN is very important in expanding the options that are available to newborns therapeutically (neonatal.peds.washington.edu, 2000).