Persistent Pulmonary Hypertension in the Newborn: Causes and Therapeutic Horizons

Abstract

In order to understand the concept of persistent pulmonary hypertension, it is necessary to review briefly the transition of the pulmonary and cardiovascular circuit that occurs when the infant passes from the fetal state to the newborn state. In utero there is a relatively high pulmonary vascular resistance and relatively low systemic vascular resistance. In addition, the ductus arteriosus and the foramen ovale are wide-open shunts. The result is that 90% of the blood flow that returns from the superior vena cava and is pumped by the right ventricle and out the pulmonary artery, shunts through the ductus thereby bypassing the lungs. About 10 percent of the blood flow is used for the growth and development of the lung, while 90% is shunted through the ductus and down the descending aorta. The alveoli at this time are fluid-filled and relatively collapsed. At the time of birth, with the expansion of the lungs, there is a decrease in pulmonary vascular resistance and an increase in systemic vascular resistance. In addition, the increasing amounts of oxygen cause the ductus arteriosus to constrict. The result is an increase in pulmonary blood flow. In addition, as the pressure on the left side of the heart increases compared to the right, there is a functional closing of the foramen ovale.