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The ductus arteriosus is a central vascular shunt that interconnects the pulmonary artery and aorta during fetal life. A ductus or similar structure is present in mammals and most other vertebrates and is embryologically derived from the distal portion of the left sixth branchial arch.1,2 As a result of the relatively large size of the ductus and the high resistance of the pulmonary vascular circuit in utero, approximately 90% of right ventricular output flows though the ductus and into the systemic circulation, thus bypassing the unaerated fetal lung.

Constriction of the ductus arteriosus is a critical step in postnatal circulatory transition. The normal physiological shift from a placental to a pulmonary respiration pattern is marked by a rapid sequence of events, including loss of umbilical flow and a subsequent fall in right atrial pressures, along with separation from the low-resistance vascular bed of the placenta and an accompanying increase in systemic vascular resistance (SVR)3 (Figure 22-1). The abrupt decrease in pulmonary vascular resistance (PVR) that occurs with the onset of respiration leads to an 8- to 10-fold increase in pulmonary blood flow. As a result, left atrial pressure increases, facilitating closure of the foramen ovale. The combined increase in SVR and arterial blood pressure and decrease in PVR redirects blood flow through the ductus arteriosus in a left-to-right pattern until closure takes place via smooth muscle constriction and obstruction of the lumen. Luminal obstruction is a result of subendothelial thickening, the formation of intimal mounds that protrude into the vessel lumen, and endothelial cell proliferation and crowding with ongoing muscular constriction. The formation of cell-cell adhesions and recruitment of circulating leukocytes or platelets might also contribute to ductus closure.4, 5, 6, and 7


Cardiopulmonary transition at birth. The normal physiological shift from a placental to a pulmonary respiration pattern is marked by a rapid sequence of events illustrated by this block diagram of the transitional circulation. (Adapted from Smith and Nelson.3)

Normal closure of the ductus arteriosus involves well-characterized anatomic changes that result in the remodeling of this structure to become the ligamentum arteriosum. Full-term infants with persistent patency of the ductus arteriosus do not undergo this remodeling. The result is a structural defect that occurs in full-term infants and often is associated with other cardiovascular anomalies.

In contrast to the timely closure of the ductus in full-term infants, premature infants, particularly those with lung disease, do not always undergo ductus closure shortly after birth. Unlike the full-term infant, in whom the patent ductus arteriosus (PDA) is a congenital structural defect, the ductus of a premature infant with symptomatic PDA would have closed normally but for the misfortune of the infant being delivered prematurely.


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