Immediately after delivery, the infant begins to breathe and cry, leading to lung expansion. It is for this reason mucous/fluid is suctioned from the oral cavity at birth, in order to prevent aspiration.
As the lungs expand with inhaled air, pulmonary vascular pressure decreases. This allows more blood flow to the lungs to promote gas exchange.
As pulmonary vascular pressure decreases, the right heart is no longer pumping against a high pressure system. Thus, right heart pressure is decreased compared to the left heart.
As right heart pressure decreases, a disparity in right vs. left heart pressure is created. Comparatively, the left atrial pressure is now of higher pressure than the right atrium. Because of this, there is no longer a gradient for blood to pass into the left heart through the foramen ovale as it used to in the fetus.
A disparity in atrial pressure leads to increased pressure in the left atrium vs. the right, halting the right-to-left atrial shunting which occured in the fetus. This forces the septum primum against the septum secundum, functionally closing the foramen ovale. In time the septa eventually fuse, leaving a remnant of the foramen ovale, the fossa ovalis.
Inhalation leads to increased oxygen content in left sided cardiac vessels. As the infant is now capable of creating its own oxygen supply, flow from the ductus arteriosus is no longer paramount for supplying the aorta with oxygenated blood. Furthermore, vasoconstriction is induced as higher arterial oxygen content releases endothelin, a local vasoconstrictor.
The placenta produces prostaglandins, which maintain prenatal patency of the ductus and, in early gestation, inhibit the ability of the ductus to contract in response to oxygen. The ductus arteriosus itself also produces prostaglandins and nitric oxide-like vasodilators. Postnatally, removal of placental prostaglandin and a decrease in the number of prostaglandin E2 receptors in the ductal wall occurs.
During the postnatal period, final closure of the ductus arteriosus results from increased production of local vasoconstrictors (like endothelin) in response to higher arterial oxygen and decreased prostaglandins.
As prostaglandins are used for maintaining the ductus arteriosus, these are often used in patients with congenital heart defects. In severe congenital defects, the ductus arteriosus is the only way for the fetus to oxygenate tissues postnatally.
Indomethacin is an inhibitor of prostaglandin synthesis and is used to close a clinically significant PDA.
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