The ductus arteriosus (DA) is a vital component of the fetal circulation, when the placenta is the source of oxygen to the fetus. The DA provides a conduit for blood to bypass the high resistance pulmonary vascular bed and shunt toward the descending aorta and low-resistance placental circulation. At birth, the lungs are inflated and resistance in the pulmonary vascular bed decreases as the lungs become the source of oxygenation, rendering the DA no longer necessary. Over the first few days of life, the DA undergoes active constriction and occlusion; failure of this process results in a patent ductus arteriosus (PDA). In the majority (> 95%) of term infants and those born > 28 weeks of gestation, closure of the ductus occurs within hours. In contrast, PDAs occur in 70% of infants born prior to 28 weeks of gestation, with an incidence that is inversely proportional to gestational age (GA) at birth.
Closure of the DA involves a number of cellular and molecular processes that occur over 2 phases: (1) “functional” closure within hours after birth, characterized by ductal smooth muscle constriction; (2) “anatomic” occlusion over the next several days, characterized by ductal remodeling in response to hypoxia/ischemia of smooth muscle cells, resulting in permanent closure. Premature birth interrupts the normal maturation of ductal contractile mechanisms, increasing the likelihood of a PDA.
Pathophysiology and Functional Closure of the Da
In the fetus, most of the cardiac output from the right ventricle bypasses the lungs and flows from the main pulmonary artery (MPA) into the descending aorta via the DA. A number of factors regulate the magnitude of ductal shunting, including its size (diameter, length), pressure differences between the aorta and pulmonary artery, and systemic and pulmonary vascular resistances (SVR and PVR, respectively). If the diameter of the PDA is small, the diminutive cross-sectional opening offers a high resistance to flow; thus, shunting is minimal despite potentially large pressure differences. On the other hand, with a large ductal diameter, pressures tend to be similar, and the magnitude of the ductal shunting is determined primarily by a balance between SVR and PVR. The right-to-left ductal shunting in utero is due to the high PVR, which in combination with a low SVR, results in a low pulmonary blood flow during fetal life.
At birth, ventilation of the lungs triggers a large decrease in PVR, which coincides with an increase in SVR following removal of the placental circulation by clamping of the umbilical cord. These events result in a marked increase in pulmonary blood flow, and as PVR falls below SVR, there may be left-to-right ductal shunting through the DA from the aorta and into the pulmonary circulation (see also Chapter 45).
At birth, the dramatic, rapid rise in arterial oxygen content upon ventilation of the lungs triggers a cascade of events ...