Patent ductus arteriosus

With patent ductus arteriosus, or PDA, “patent” comes from the Latin word patere, meaning “to lie open”, while ductus arteriosus refers to a blood vessel that normally connects the pulmonary artery to the aorta. During fetal development, the ductus arteriosus allows blood to bypass the lungs, but normally it closes soon after birth. So, in patent ductus arteriosus, this blood vessel fails to close and remains open.

But before we proceed, first, let’s look at how fetal circulation works. During fetal development, the baby’s lungs are filled with fluid and not yet involved in breathing, so the fetus relies entirely on oxygen-rich blood from the mother. This oxygen-rich blood travels from the placenta through the umbilical vein and eventually reaches the right atrium of the heart. From here, most of it takes a shortcut through the opening between the right and left atria, called the foramen ovale. This allows oxygen-rich blood to completely bypass the lungs and enter the left atrium directly. From the left atrium, blood enters the left ventricle, and from there it’s pumped into the aorta and systemic circulation.

However, not all blood follows this path. A small amount still reaches the right ventricle and gets pumped into the pulmonary artery. However, since the fetal lungs are not yet functioning, the pulmonary vessels are squeezed, creating high resistance that makes it difficult for blood to flow into the lungs. As a result, most of the blood follows the path of least resistance and slips from the pulmonary artery through another fetal shunt called the ductus arteriosus into the aorta.

Anatomically, the ductus arteriosus sits right on the aortic arch, just after the arteries that branch off to supply the brain and upper extremities. This setup allows oxygen-rich blood from the left ventricle to reach the brain and upper extremities first, while blood from the right ventricle via the ductus arteriosus supplies the lower body. This arrangement helps prioritize oxygen delivery to the most important organs, like the brain and heart, while the ductus arteriosus sends the remaining oxygenated blood to the rest of the body.

During fetal development, the placenta produces prostaglandin E2, which helps keep the ductus arteriosus open. At birth, everything shifts. The placenta is no longer in play, so prostaglandin E2 levels drop. Next, the lungs take over as the primary source of oxygen, increasing oxygen levels from approximately 60% in the uterus to over 90% after birth. Higher oxygen levels also support the closure. At the same time, lungs begin releasing bradykinin, which is a small peptide that causes smooth muscle cells of the ductus arteriosus to constrict, speeding things up. Together, the drop in prostaglandin E2, the rise in oxygen, and the release of bradykinin all help close the ductus arteriosus, transforming it into a fibrous band called the ligamentum arteriosum. This usually occurs within the first 3 weeks of life.

If the ductus arteriosus fails to close after birth, the baby is left with a patent ductus arteriosus. Like in fetal life, blood flows from the right atrium to the right ventricle and then into the pulmonary artery. But now that the lungs are up and running, pulmonary vessels are wide open, which makes resistance in pulmonary circulation lower than in the aorta. Freshly oxygenated blood then comes over into the left atrium, the left ventricle, and into the aorta. Some of the oxygenated blood in the aorta follows the path of least resistance across the ductus and shunts into the lower-pressure pulmonary artery. This creates a left-to-right shunt. And because no deoxygenated blood enters the systemic circulation, PDA is classified as an acyanotic heart defect, literally meaning “not blue”.

However, this inefficient circuit causes volume overload in both the pulmonary circulation and the left side of the heart, which now must handle significantly more blood returning from the lungs. Over time, this increased workload strains the left ventricle, forcing it to pump up to twice the normal cardiac output. Eventually, this chronic strain can lead to heart failure.

PDA accounts for about 10% of all congenital heart defects, of which about 90% are isolated heart defects, meaning there are no other associated heart problems. PDA is more common in preterm infants, where immature tissues and higher prostaglandin levels delay ductal closure. It is strongly associated with neonatal respiratory distress syndrome, where poor lung expansion and low oxygen tension make the ductus less likely to constrict. Another well-known association is congenital rubella syndrome, where maternal rubella infection during the first trimester interferes with normal vascular development and leads to PDA. Finally, PDA can be seen in genetic conditions, like Down syndrome.