The pulmonary artery carries oxygen-poor blood from your heart to your lungs, where it picks up fresh oxygen and drops off carbon dioxide. It is the only artery in the body that transports deoxygenated blood, which makes it a common source of confusion for people learning how the cardiovascular system works.
How Blood Moves Through the Pulmonary Artery
After your body’s tissues have used up the oxygen in your blood, that oxygen-depleted blood returns to the right side of your heart. The right ventricle, your heart’s lower-right chamber, pumps it through the pulmonary valve into the main pulmonary artery, also called the pulmonary trunk. This trunk quickly splits into a right and left branch, each directing blood toward the corresponding lung.
The pulmonary artery and the aorta are the two “great vessels” that carry blood out of the heart. The key difference: the aorta sends oxygen-rich blood out to the body, while the pulmonary artery sends oxygen-poor blood to the lungs. Blood in the pulmonary artery typically has an oxygen saturation around 58 to 59%, compared with roughly 95 to 100% in blood leaving the lungs.
Why the Pulmonary Artery Is Built Differently
If you compared a pulmonary artery to a similarly sized artery elsewhere in the body, you’d notice it has much thinner walls. The muscular layer of a pulmonary artery is only about 5% of the vessel’s outer diameter, versus 15 to 20% in a systemic artery. That’s because the pulmonary circulation operates at far lower pressures. Normal mean pressure in the pulmonary artery sits between about 9 and 18 mmHg, a fraction of the pressure in the aorta.
As the pulmonary arteries branch deeper into the lungs, they get progressively thinner. Vessels smaller than about 100 micrometers have only a partial spiral of muscle. Below 30 micrometers, the tiniest precapillary vessels have no muscle at all, just thin elastic tissue perfectly suited for gas exchange.
Gas Exchange in the Lungs
The pulmonary artery’s real purpose becomes clear at its endpoint: the capillaries surrounding tiny air sacs called alveoli. This is where blood trades carbon dioxide for oxygen. The barrier between air and blood at this point is extraordinarily thin, as little as 0.3 micrometers in many places, and the total surface area available for exchange is between 50 and 100 square meters, roughly half a tennis court.
Oxygen moves from the air in the alveoli into the blood, and carbon dioxide moves the other direction. Both gases cross by simple diffusion, flowing from where their concentration is higher to where it’s lower. The process is remarkably fast. Blood entering the capillaries has an oxygen pressure of about 40 mmHg, while the air in the alveoli sits at about 100 mmHg. That large gap drives oxygen across the barrier so quickly that the blood reaches near-alveolar oxygen levels within about a quarter of a second. Carbon dioxide crosses even faster, roughly 20 times more efficiently than oxygen, because it dissolves more easily in tissue.
Once this exchange is complete, the now oxygen-rich blood flows through the pulmonary veins back to the left side of the heart, which pumps it out to the rest of the body through the aorta.
The Pulmonary Artery Before Birth
In a fetus, the lungs aren’t yet inflated with air, so the pulmonary artery plays a very different role. Only about 5 to 10% of the right ventricle’s output actually flows through the fetal lungs. The rest is rerouted through a short vessel called the ductus arteriosus, which connects the pulmonary artery directly to the aorta. This bypass is essential for normal fetal development because the fetus gets its oxygen from the placenta, not from breathing. Shortly after birth, as the baby takes its first breaths and the lungs expand, the ductus arteriosus closes and the pulmonary artery begins its lifelong job of routing blood to the lungs for gas exchange.
What Happens When the Pulmonary Artery Is Blocked
A pulmonary embolism occurs when a blood clot, usually originating in a leg vein, lodges in a pulmonary artery branch and blocks blood flow. The consequences depend on how much of the vessel is obstructed.
Pulmonary artery pressure typically starts to rise once more than 30% of the vascular bed is blocked. In severe cases, mean pressure can jump from its normal range to above 40 mmHg. The right ventricle, which isn’t built to pump against high resistance, can dilate and begin to fail under that strain. A large clot in the main or lobar branches can obstruct over 40% of the pulmonary vasculature, dropping blood oxygen levels by 10 to 20 mmHg and sometimes pushing them below 60 mmHg.
The body tries to compensate. Breathing rate may increase by 20 to 30%. But the blocked areas create “dead space,” regions of the lung that are being ventilated with air but aren’t receiving blood flow, so the extra breathing effort can’t fully make up for the lost gas exchange. Normally, dead space accounts for about 25% of each breath. With a significant embolism, that can climb above 50%. The lungs also become stiffer, requiring 40 to 60% more effort to inflate, which leads to the severe breathlessness that is a hallmark symptom of pulmonary embolism.
Pulmonary Hypertension
When pressure in the pulmonary artery stays chronically elevated, the condition is called pulmonary hypertension. As of the 2022 guidelines from the European Society of Cardiology and European Respiratory Society, the diagnostic threshold is a mean pulmonary artery pressure above 20 mmHg, measured by catheter. This was lowered from the previous cutoff of 25 mmHg to catch the condition earlier, before the right ventricle sustains significant damage.
Pulmonary hypertension can develop from a variety of causes: chronic lung disease, blood clots that never fully dissolve, left-sided heart failure, or conditions that directly affect the pulmonary artery walls. Regardless of the trigger, the progression follows a similar pattern. The right ventricle has to work harder against the elevated resistance, its walls thicken and eventually weaken, and cardiac output drops. Early symptoms are often subtle, usually just shortness of breath during physical activity, which is why the condition frequently goes undiagnosed for years.