Patent ductus arteriosus

Definitions & Key takeaways

Patent ductus arteriosus (PDA) is a congenital heart defect in which the ductus arteriosus, a blood vessel that normally closes after birth, remains open. During fetal development, the ductus arteriosus connects and shunts blood from the pulmonary artery to the aorta, because the fetus doesn't use its lungs yet.

Initially, PDA causes a left-to-right shunt, resulting in pulmonary hypertension. Over time, as the pulmonary artery pressure increases, this is converted into a right-to-left shunt. This switch in the shunt is known as Eisenmenger's syndrome. PDA can be treated with the drug indomethacin, or by surgical ligation.

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Introduction0:00–0:58

With patent ductus arteriosis or PDA, patent comes from the Latin word pare, meaning to lie open, while ductus arteriosis refers to a blood vessel that normally connects the pulmonary artery to the aorta.
During fetal development, the ductus arteriosis allows blood to bypass the lungs, but normally it closes soon after birth.
So in patent ductus arteriosis, 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 foramino alley. This allows oxygen-rich blood to completely bypass the lungs and enter the left atrium directly.

Physiology0:58–2:11

From the left atrium, blood enters the left ventricle, and from there it's pumped into the aorta in 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 arteriosis into the aorta.
Anatomically, the ductus arteriosis 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 arteriosis supplies the lower body.

Causes2:11–2:41

This arrangement helps prioritize oxygen delivery to the most important organs, like the brain and heart, while the ductus arteriosis sends the remaining oxygenated blood to the rest of the body.
During fetal development, the placenta produces prostaglandin E2, which helps keep the ductus arteriosis 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.

Pathology2:41–3:44

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 arteriosis 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 arteriosis, transforming it into a fibrous band called the ligamentum arteriosum.
This usually occurs within the 1st 3 weeks of life. If the ductus arteriosis fails to close after birth, the baby is left with a patent ductus arteriosis.
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.

Signs and Symptoms3:44–4:55

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 cyanotic 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.

Treatment4:55–5:20

PDA is more common in preterm infants, where immature tissues and higher prostaglandin levels delay ductal closure. It's strongly associated with neonatal respiratory distress syndrome, where poor lung expansion and low oxygen tension make the ductus less likely to constrict.

Review5:20–9:31

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. Usually PDA is asymptomatic, especially when the amount of blood flowing from the aorta to the pulmonary artery is small.
In fact, many small PDAs are discovered only because they produce a continuous machine-like murmur from the continuous blood flow from the aorta to the pulmonary artery through the whole cardiac cycle.
In contrast, infants with a large PDA may develop signs of heart failure early, such as rapid breathing, poor feeding, and hepatomegaly, because the left heart must pump two or more times the usual cardiac output to handle the extra blood returning from the lungs.
Later in life, from years of increased pulmonary blood volume, the pulmonary arteries thicken and stiffen. These changes increase the pressure in the pulmonary circulation and eventually lead to pulmonary hypertension.
If the pressure in the pulmonary artery rises high enough to exceed the pressure in the aorta, the shunt flips from left to right to right to left.
When this happens, deoxygenated blood from the pulmonary artery bypasses the lungs and flows through the PDA into the aorta and systemic circulation.
Because of the ductus arteriosis's position, deoxygenated blood mainly reaches the lower part of the body. The result is differential cyanosis, where the lower body appears bluish or purple, while the upper body remains pink and well perfused.
This la complication of PDA is called Eisenmanger syndrome. It marks an irreversible stage where pulmonary vessels have undergone permanent remodeling.
So what started as a harmless little duct can turn into a serious condition that deprives tissues of oxygen. PDA is generally suspected upon auscultation of the classic machine-like murmur.
However, the diagnosis primarily relies on Doppler echocardiography, which visualizes flow through the ductus, estimates the size, and detects signs of pulmonary overcirculation or pulmonary hypertension.
Small PDAs may close spontaneously within the first few months and often don't require treatment. For larger or symptomatic PDAs, first-line therapy includes non-steroidal anti-inflammatory medications, or NSAIDs like indomethacin or ibuprofen, which inhibit prostaglandin E2 synthesis to promote closure.
If NSAIDs fail, closure can be done via a minimally invasive trans catheter procedure with an occlusion device or by surgical ligation.
All right, as a quick recap, patent ductus arteriosis is an ascyanonic congenital heart defect caused by the failure of the ductus arteriosis to close after birth, resulting in a persistent communication between the aorta and pulmonary artery.
This creates a left to right shunt, leading to pulmonary overcirculation, volume overload of the left heart, and potentially heart failure.
PDA is more common in preterm infants and classically presents with a continuous machine-like murmur. Small PDAs are often asymptomatic, while larger ones can cause symptoms like tachypnia and poor feeding.
If left untreated, PDA can progress to pulmonary hypertension and even Eisenmacher syndrome, with reversal of the shunt to right to left.