At or Shortly after Birth, Umbilical Vessels Rupture, PulmonaryVascuIar Resistance Decreases, and the Foramen Ovale and Ductus Arteriosus Close
At term, the fetus is dependent on the placenta and the mother for exchange with the environment, but the lung and other organs must be ready to assume their postnatal functions.
During a normal birth, the newborn emerges from the birth canal at about the time the placenta is detaching from the uterine wall. Placental gas exchange probably continues well into third-stage labor. If labor is prolonged, the placenta may detach before the newborn is delivered. This is a medical emergency.Normally, the newborn takes the first breath immediately after delivery. The stimuli for this include (I) hypoxia and hypercarbia, which result from the loss of the placental gas exchanger; (2) cooling of the fetus as the fetal fluids evaporate from the skin; and (3) a generalized increase in sensory input to the fetus as it is licked and nuzzled by its dam. To expand the lungs initially, the respiratory muscles must create an intra- thoracic pressure that is 60 cm H2O less than atmospheric pressure. This is vastly lower than the 5 cm H2O generated by adults breathing tidal volume. The large effort during the first breath is necessary to move viscous fluids down the airways before air can enter the alveoli and to open the fluid-filled alveoli. Not all alveoli may inflate during the first breath, but subsequent inhalations inflate the entire lung and distribute surfactant over the alveolar surface. This surfactant makes the alveoli stable and prevents their collapse so that a stable end- expiratory lung volume, known as functional residual capacity, can be established. After the first few breaths, arterial oxygen tension (Pao2) is much higher than it was before birth, yet breathing continues. It therefore appears that breathing is inhibited in utero, and the chemoreceptors are insensitive to hypoxia. This inhibition is removed after birth.
Inflation and oxygenation of the lung reduce the pulmonary vascular resistance, which leads to a decreased pressure in the pulmonary artery, right ventricle, and right atrium.
At about the same time, the umbilical vessels rupture because the animal struggles to stand or the umbilical cord is torn by the mother. Umbilical blood flow is arrested by local vasoconstriction in the umbilical vessels. The loss of the low- resistance placental circulation increases systemic vascular resistance, which results in an increased pressure in the aorta, left ventricle, and left atrium. As a result of these changes, aortic pressure exceeds pulmonary arterial pressure, and left atrial pressure exceeds right atrial pressure. Therefore, blood flow through the ductus arteriosus and foramen ovale reverses. Flow reversal in the foramen ovale causes a flap valve to close and occlude the foramen. Over succeeding days to weeks, this valve becomes adherent to the wall of the atrium, thus permanently closing the foramen.Reversal of flow in the ductus arteriosus exposes the ductus wall to well-oxygenated blood. This causes constriction of smooth muscle in the wall of the ductus, thus arresting blood flow. Ductus closure involves a decrease in the concentration of vasodilator prostaglandins. Administration of drugs, such as indomethacin, that inhibit prostaglandin synthesis constricts the ductus in fetal sheep, and administration of prostaglandin E2 dilates it. Once the ductus has constricted and flow has been arrested, the ductus is gradually converted into a fibrous band of scar tissue.
The changes just described convert the fetal circulation into the adult circulation, which is able to support the gasexchange function of the lung. Remarkably, these changes occur routinely and without medical assistance in almost all animal births.