The ductus arteriosus is a small blood vessel that connects a baby’s pulmonary artery (the vessel leading to the lungs) to the aorta (the body’s main artery) during fetal development. It exists for one purpose: to reroute blood away from the lungs, which don’t function yet in the womb. Once a baby is born and takes its first breaths, this vessel normally closes on its own within hours. When it doesn’t close, the condition is called patent ductus arteriosus, one of the most common congenital heart defects.
Why the Ductus Arteriosus Exists
Before birth, a baby gets all its oxygen from the placenta, not its lungs. The lungs are filled with fluid and collapsed. Sending large volumes of blood through them would be a waste of energy, so the fetal circulatory system includes several shortcuts that divert blood away from the lungs. The ductus arteriosus is one of the most important.
This vessel forms early in embryonic development, connecting the first portion of the pulmonary artery to a section of the aorta called the isthmus. Oxygen-rich blood returning from the placenta can flow through the ductus arteriosus directly into the aorta, skipping the lungs entirely and reaching the brain, organs, and the rest of the body. Several chemical signals keep the ductus open throughout pregnancy: low oxygen levels in fetal blood, high levels of a hormone-like substance called prostaglandin E2 (produced largely by the placenta), and small amounts of nitric oxide and carbon monoxide.
How It Closes After Birth
The moment a newborn takes its first breath, a cascade of changes begins. Oxygen floods the lungs, and the oxygen pressure in the blood rises sharply, from roughly 18 to 28 mmHg in the womb to 80 to 100 mmHg after birth. This spike in oxygen triggers the muscular wall of the ductus to constrict. That constriction starts within about five minutes of the oxygen rise.
At the same time, clamping the umbilical cord cuts off the placenta, which had been the main source of prostaglandin E2. Without the placenta producing it, and with the now-functioning lungs actively breaking it down, prostaglandin levels drop fast. Since prostaglandins were one of the key signals keeping the ductus relaxed and open, their disappearance removes the brake on closure.
In a healthy full-term baby, functional closure (the vessel squeezing shut so blood can no longer flow through it) typically happens by about 15 hours of life. Permanent, anatomical closure follows over the next few weeks as the tissue remodels and the vessel turns into a small ligament. Blood now flows from the right side of the heart directly into the lungs, picks up oxygen, returns to the left side of the heart, and is pumped out through the aorta, completing the adult circulation pattern.
When It Stays Open: Patent Ductus Arteriosus
Patent ductus arteriosus (PDA) occurs when the vessel fails to close after birth. In full-term infants, PDA is relatively uncommon, affecting about 1 in 2,000 births. It accounts for 5% to 10% of all congenital heart disease. The story is very different for premature babies. PDA occurs in 20% to 60% of preterm infants depending on how early they’re born, and the smaller the baby, the higher the risk. Among infants weighing less than 1,200 grams (about 2.6 pounds) at birth, PDA is present in roughly 80%.
The reason prematurity matters is straightforward: the ductus in a very premature infant hasn’t developed the thick muscular wall needed to constrict tightly, and the chemical signaling systems that trigger closure are less mature. The vessel simply isn’t ready to close on its own.
Symptoms of PDA
A small PDA may cause no symptoms at all, and some people don’t learn they have one until adulthood. A larger PDA, however, allows a significant amount of blood to leak from the aorta back into the pulmonary artery, flooding the lungs with excess blood flow and forcing the heart to work harder. In infants, this can show up as fast breathing, poor feeding, slow weight gain, sweating during crying or eating, easy tiring, and a rapid heart rate.
Doctors often detect PDA by hearing a characteristic continuous “machinery” murmur just below the collarbone, sometimes radiating to the back. Other signs include bounding pulses, a widened pulse pressure (the gap between the upper and lower blood pressure numbers exceeding 30 mmHg), and an overactive heartbeat you can feel on the chest wall. An echocardiogram (heart ultrasound) confirms the diagnosis and shows whether the opening is large enough to be straining the heart.
How PDA Is Treated
Because prostaglandins help keep the ductus open, the first-line treatment is medication that blocks prostaglandin production. Two anti-inflammatory drugs are used for this purpose, and studies comparing them have found they’re equally effective at prompting the ductus to close. These medications work best in the first days of life, when the ductus tissue is still responsive.
When medication fails, or when the baby is too sick or too small to tolerate it, the next step is closing the ductus physically. This can be done through a minimally invasive catheter-based procedure or through surgical ligation, where a surgeon ties off the vessel. Surgery becomes more likely when the opening is large relative to the baby’s size, when the heart chambers are showing signs of enlargement from the extra workload, or when the infant is in shock. In those high-risk scenarios, the probability of needing surgical closure can exceed 60% to 78%.
Risks of Leaving a Large PDA Untreated
A small PDA that causes no symptoms may need only monitoring. A large, untreated PDA is a different situation. The constant overflow of blood into the lungs can lead to pulmonary hypertension, where the blood pressure in the lung arteries rises to dangerous levels. Over time, the heart can weaken from the extra workload, potentially leading to heart failure. In premature infants, a hemodynamically significant PDA is also associated with complications like pulmonary edema, where fluid builds up in the lungs and worsens breathing difficulties.
The good news is that PDA is one of the most treatable congenital heart defects. With medication, catheter procedures, or surgery, the vast majority of affected infants recover fully, and once the ductus is closed, the circulatory system functions normally.