As the umbilical vessels are obliterated and the infant starts breathing at birth, the source of oxygen changes from the placenta to the lungs. This major trigger will facilitate the transformation from fetal to postnatal circulation in many ways. First, the ductus venosus was previously kept open by the blood flow from the umbilical vein. The reduced blood flow through the umbilical vein at birth will collapse and close the ductus venosus. Hence, the IVC will only carry deoxygenated blood from the infant's organs and lower extremities. Second, as the infant breathes, the lungs will expand and fill the
alveoli with oxygen. The increased oxygen content will dilate the pulmonary capillaries and also trigger the release of
nitric oxide, which further dilates the blood vessels within the lungs. Together, these forces will decrease the pulmonary vascular resistance. With decreased resistance in the lungs, there will be increased blood flow to the lungs from the right ventricle of the heart through the pulmonary arteries, establishing the newborn's pulmonary circulation. With each of the newborn's breaths, blood perfuses the pulmonary capillary beds and undergoes oxygenation before exiting the lungs via the
pulmonary veins and returning to the heart. Thus, as more blood flows through the pulmonary circulation, there will be a higher volume of blood returning to the left atrium from the lungs. The increased venous return will elevate the pressure of the left atrium until it exceeds the pressure of the right atrium. The difference in pressure between these two chambers of the heart will close the foramen ovale. Lastly, due to the decreased pulmonary vascular resistance, the pressure of the pulmonary artery will fall until it is lower than the pressure of the aorta. Since blood flows from high to low pressure systems, the direction of blood flow across the ductus arteriosus reverses. As the oxygen-rich blood from the aorta flows across the ductus arteriosus to the pulmonary artery, the ductus arteriosus will constrict in response to the high oxygen content of the blood. While oxygen serves as a vasoconstrictor of the ductus arteriosus,
prostaglandins can keep the ductus arteriosus open to maintain blood flow to the lower extremities in cases of
hypoplastic left heart syndrome where the mitral valve is shut. The removal of the placenta, a source of prostaglandin, is another mechanism by which the ductus arteriosus closes at birth. Within the next 2 to 3 weeks, the constriction results in decreased blood flow to the structure which induces the death of the tissue to keep the structure permanently closed. As a result of these changes, postnatal circulation will direct deoxygenated blood from the inferior and superior vena cava to the right heart, from which the blood will flow to the lungs via the pulmonary circulation. Blood will be oxygenated in the lungs and return to the left heart, which will pump oxygen-rich blood out through the aorta to supply the rest of the body via the systemic circulation. In certain cases, the transition from fetal to postnatal circulation may not occur as described above due to complications leading to persistently high pulmonary vascular resistance. Preterm infants are born without fully mature lungs lacking the
surfactant compound that allows alveoli to remain open by overcoming the surface tension of water. The resulting difficulty in lung expansion prevents the necessary reduction in pulmonary vascular resistance for the infant to make the normal cardiopulmonary transition, resulting in
infant respiratory distress syndrome. The presence of meconium within the lungs, known as
meconium aspiration syndrome, can obstruct the airways and also deactivate the newborn's surfactant. The inflammation that also results from the inhalation of meconium also causes airway constriction, resulting in poor ventilation of the alveoli and inadequate oxygenation of the pulmonary capillary beds. With a lack of oxygen entering the lungs, pulmonary vascular resistance will remain high and the newborn's blood will no longer be oxygenated, preventing fetal shunt closure. In both cases of infant respiratory distress syndrome and meconium aspiration syndrome, fetal shunts will remain open due to the high pulmonary vascular resistance until appropriate measures, such as administration of surfactant or mechanical ventilation, are taken to help the infant breathe on its own. If the problem is not corrected, the infant will undergo hypoxia, acidosis, and other serious complications, such as seizures. == Adult remnants ==