Most blood clots found in the lung start somewhere else, typically in the deep veins of the legs or pelvis. A piece of the clot breaks free, rides the bloodstream through the right side of the heart, and wedges into one of the lung’s arteries. Three conditions drive the original clot’s formation: blood that pools instead of flowing, damage to the blood vessel lining, and blood that is chemically primed to clot too easily. Those three factors, recognized in medicine for more than a century, interact in different combinations depending on the person and the situation, which is why lung clots strike after surgery, during pregnancy, in cancer patients, and sometimes in seemingly healthy people on a long flight.
How a Clot Travels From a Vein to the Lung
A clot lodged in a lung artery is called a pulmonary embolism. In the vast majority of cases, the clot did not originate in the lung itself. It formed in a deep vein, most often in the thigh or calf, then partly or fully detached. Once loose, the fragment follows the only path available: through progressively larger veins, into the right atrium, through the right ventricle, and out into the pulmonary arteries. Because those arteries branch into smaller and smaller vessels, the traveling clot eventually reaches a channel too narrow to pass through and gets stuck. The blockage cuts off blood flow to the lung tissue beyond it, which impairs gas exchange and forces the right side of the heart to pump against increased resistance.
The framework used to explain why clots form in veins in the first place centers on three overlapping conditions: venous stasis (sluggish or pooled blood), endothelial injury (damage to the vessel wall), and a hypercoagulable state (blood that clots more readily than normal).1Europe PMC / Thieme. Pathophysiology and Management of Pulmonary Embolism In practice, most people who develop a lung clot have at least two of these conditions at the same time. A hospitalized patient recovering from hip surgery, for example, has all three: they are lying still (stasis), the surgical procedure damaged blood vessels (endothelial injury), and the body’s post-surgical inflammatory response has ramped up clotting activity (hypercoagulability).2Vascular & Endovascular Review. Deep Vein Thrombosis and Pulmonary Embolism: A Shared Postoperative Concern in Prolonged Immobilised Patients
Stalled Blood Flow and Immobility
Blood is supposed to keep moving. When it slows down or pools, clotting proteins have more time to interact and form a clot. This is why prolonged immobility is one of the strongest and most common triggers. It does not take a dramatic event. A large population study of older adults found that being immobile at home, even without hospitalization, roughly quintupled the odds of developing a venous clot over a three-month window. Being immobile in a hospital raised the risk even further and accounted for an estimated 27 percent of all clots in the study population.3Journal of Thrombosis and Haemostasis. The contribution of immobility risk factors to the incidence of venous thrombosis in an older population
The situations that create this kind of stasis are familiar: long hospital stays, recovery after a fracture, air travel lasting several hours, and even desk work without regular movement. Fractures were the single strongest risk factor in that same study, with odds roughly twelve times higher than in people without fractures, partly because the fracture itself damages tissue and blood vessels while the cast or bed rest enforces immobility. Surgery carries a similar double hit, combining tissue trauma with a recovery period that keeps the patient still.
Inherited Clotting Tendencies
Some people are born with blood that is simply more prone to clotting. Several inherited mutations affect proteins in the clotting cascade and tilt the balance toward forming clots too readily. The two most studied are Factor V Leiden and the prothrombin gene mutation (G20210A). Factor V Leiden makes a clotting protein resistant to being switched off, so once a clot starts forming, it is harder for the body to rein it in. The prothrombin mutation leads to higher baseline levels of prothrombin, the precursor to the enzyme that actually builds the clot’s fibrin mesh.
Having one of these mutations roughly triples the odds of developing a deep vein clot that can travel to the lung. Having both at the same time dramatically compounds the risk, with one study reporting odds more than 80 times higher for the combination than for people carrying neither mutation.4PubMed. Inherited thrombophilic risk factors and venous thromboembolism: distinct role in peripheral deep venous thrombosis and pulmonary embolism These mutations are not rare. Factor V Leiden is carried by roughly 5 percent of people of European descent. A study examining patients who had experienced clots found that carrying multiple genetic mutations was actually more common than carrying just one: about 44 percent of patients had two mutations, and about 30 percent had three.5PubMed. Combined genetic mutations have remarkable effect on deep venous thrombosis and/or pulmonary embolism occurence The risk of a lung clot also climbs with age for both men and women, likely because older individuals accumulate more of these risk factors over time.6PubMed Central. Inherited trombophilic states and pulmonary embolism
Cancer and Blood Clots
Cancer and clotting are deeply intertwined. Many tumors actively promote clot formation through several mechanisms. Tumor cells can express tissue factor, a protein that kicks off the clotting cascade, essentially behaving as though the body has suffered a wound even though no vessel is torn. Tumors also make nearby blood vessels leaky, allowing clotting proteins to seep into surrounding tissue and form fibrin deposits.7PubMed. Thrombosis and cancer On top of that, cancer patients often undergo surgery, spend long stretches in bed, and may have central venous catheters, all of which independently raise clot risk. A blood clot in the lung is sometimes the first sign that a cancer exists, particularly with pancreatic, lung, and ovarian tumors that are potent activators of the clotting system.
Hormones, Pregnancy, and Birth Control
Estrogen has a direct effect on the clotting system. It increases the production of several clotting factors while reducing some of the body’s natural anticoagulants, shifting the balance toward easier clot formation. This matters in two common contexts: pregnancy and estrogen-containing medications like combined oral contraceptives or hormone replacement therapy.
During pregnancy, the shift toward easier clotting begins almost immediately. Researchers have found that markers of a hypercoagulable state appear in the first trimester and correlate with rising levels of estradiol and progesterone.8PubMed. Changes in laboratory markers of thrombotic risk early in the first trimester of pregnancy may be linked to an increase in estradiol and progesterone The overall risk of a venous clot during pregnancy is four to five times higher than in non-pregnant women of the same age, and it jumps to roughly twenty times higher in the weeks after delivery.9Translational Research. Hormones and thrombosis: risk across the reproductive years and beyond Other estimates put the increase during pregnancy as high as six to tenfold.10PubMed. Hormones and pregnancy: thromboembolic risks for women The postpartum spike reflects the combined effects of hormonal changes, blood loss triggering clotting activity, and reduced mobility during recovery.
Estrogen-containing contraceptives and hormone replacement therapy carry a similar, smaller increase in risk. The estrogen in these medications alters the same clotting balance, which is why prescribers weigh a patient’s other risk factors, such as smoking, obesity, or a family history of clots, before starting these medications.11PubMed Central. Oral Contraceptives and HRT Risk of Thrombosis
Infection and Inflammation
Severe infections can trigger clotting through a process where the immune system and the clotting system activate each other in a feedback loop. COVID-19 made this mechanism impossible to ignore. Early in the pandemic, clinicians noticed an unusually high rate of lung clots in hospitalized COVID patients, even in people who were not immobile for long periods. The virus damages the cells lining blood vessels, which activates both immune cells and clotting pathways simultaneously.12PubMed Central. Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19
One specific mechanism involves neutrophils, a type of white blood cell. When activated, neutrophils can expel webs of DNA and antimicrobial proteins meant to trap bacteria. These webs also trap platelets and clotting factors, creating a scaffold for clot formation inside blood vessels. In COVID-19 and other severe infections, this process can become widespread enough to form clots in the lung’s small vessels even without a traditional deep vein clot sending material upstream.13PubMed Central. COVID-19: Lung-Centric Immunothrombosis The same kind of inflammation-driven clotting can occur with other severe infections, sepsis, and autoimmune conditions, though COVID made it especially visible because of the sheer number of cases.
Surgery and Physical Trauma
Surgery is one of the most well-established triggers, and orthopedic procedures like hip and knee replacements carry particularly high risk. The reason involves all three elements of the framework discussed earlier. Cutting through tissue and bone releases clotting activators directly into the bloodstream. Researchers measuring coagulation markers during hip replacement found that clotting activation spiked during the bone preparation phase of surgery.14Thrombosis Research. Sequential intrapulmonary and systemic activation of coagulation and fibrinolysis during and after total hip replacement surgery Even before the operation begins, orthopedic patients can show elevated levels of clotting factor VII, suggesting that the underlying condition requiring surgery has already begun tipping the clotting balance.15Blood Coagulation & Fibrinolysis. Altered regulation of in-vivo coagulation in orthopedic patients prior to knee or hip replacement surgery
Major trauma works through similar pathways. Broken bones release fat and marrow into the bloodstream, damaged vessels expose the tissue beneath their lining, and injured patients are often immobilized for days or weeks afterward. This is why blood-thinning medications are now standard after major surgery and serious injuries, a practice that has significantly reduced but not eliminated the risk.
Catheters and Upper-Body Clots
Not all clots that reach the lung start in the legs. Central venous catheters, the lines placed in large veins of the chest, neck, or arm for chemotherapy, antibiotics, or nutrition, can irritate the vessel wall and serve as a surface where clots form. In one study, catheter-related clots in the upper extremities led to a pulmonary embolism about 17 percent of the time.16PubMed. Pulmonary embolism in deep venous thrombosis of the upper extremity: more often in catheter-related thrombosis This is a meaningful risk in cancer patients and others who need long-term intravenous access. Whether to remove the catheter promptly or continue anticoagulation while leaving it in place remains a judgment call that depends on the patient’s situation.17PubMed Central. Risk of pulmonary emboli after removal of an upper extremity central catheter associated with a deep vein thrombosis
When Clots Form Directly in the Lung
The standard story of a lung clot is that it travels from somewhere else. But growing evidence suggests that clots can also form right inside the pulmonary arteries themselves, without any deep vein clot as a source. This phenomenon, known as in situ pulmonary arterial thrombosis, challenges the assumption that every filling defect on a CT scan of the lung represents an embolism that came from elsewhere.18PubMed Central. In situ Pulmonary Artery Thrombosis: A Previously Overlooked Disease
The proposed mechanism involves sluggish blood flow within the lung itself. When areas of the lung are poorly ventilated due to underlying lung disease, blood flow through those regions slows, creating conditions for local clot formation. A recent case series found that all instances of in situ thrombosis occurred in areas of significant lung tissue damage where ventilation and blood flow were reduced, and none of the patients had evidence of a clot elsewhere in the body.19PubMed Central. In Situ Pulmonary Artery Thrombosis and Low Flow Stasis Artifact in Parenchymal Lung Disease: An Under-Recognized Phenomenon People with chronic lung conditions like severe emphysema or pulmonary fibrosis may be especially susceptible. This is an area where the science is still catching up, and clinicians are increasingly recognizing that not every clot seen on a lung CT scan needs to be treated as a classic embolism.20PubMed. In Situ Pulmonary Arterial Thrombosis: Literature Review and Clinical Significance of a Distinct Entity
Blockages That Are Not Blood Clots at All
Blood clots account for the vast majority of pulmonary emboli, but they are not the only material that can block a lung artery. Fat released from broken bones, air introduced through an IV line or during surgery, amniotic fluid during childbirth, tumor fragments, and even parasites can all travel to the lung and cause obstruction.21PubMed Central. Non-thrombotic pulmonary emboli: imaging findings and differential diagnoses These non-thrombotic pulmonary emboli are rare but can be just as dangerous. A forensic study spanning 30 years found that about 10 percent of fatal pulmonary emboli were non-thrombotic. Bone marrow embolism was the most common type, followed by septic, fat, and amniotic fluid emboli.22PubMed. Forensic evidence from a 30-year study of non-thrombotic pulmonary embolism
These are typically associated with specific clinical scenarios. Fat embolism follows long-bone fractures. Amniotic fluid embolism, though exceedingly rare, is one of the most feared obstetric emergencies. Air embolism is almost always an iatrogenic event, meaning it happens during medical procedures. Because the treatment and prognosis differ from standard blood-clot emboli, recognizing that not every lung blockage is a clot matters for getting the right care.23PubMed Central. Nontrombotic Pulmonary Embolism: Different Etiology, Same Significant Consequences
What Happens Inside the Lung When a Clot Lodges
Once a clot blocks a pulmonary artery, blood that would have flowed through that vessel gets rerouted to the remaining open vessels. This overloads those areas, creating a mismatch between the air flowing into the lung’s small sacs and the blood flowing past them. The result is that oxygen exchange becomes inefficient: some areas have too much blood and not enough ventilation, while others have air but no blood flow at all.24PubMed Central. Blood flow redistribution and ventilation-perfusion mismatch during embolic pulmonary arterial occlusion Research in animal models has confirmed that the low oxygen levels seen after a clot are mostly explained by this mechanical rerouting of blood rather than by the lung tissue shutting down entirely.25PubMed. Spatial pattern of ventilation-perfusion mismatch following acute pulmonary thromboembolism in pigs
The other major consequence is strain on the right side of the heart. The right ventricle is built to pump blood through a low-pressure system. When a clot obstructs part of that system, pulmonary pressure spikes within minutes, and the right ventricle has to work much harder. If the obstruction is severe, the ventricle can stretch and weaken, reducing the amount of blood it pushes out with each beat. This right ventricular dysfunction is what makes a large pulmonary embolism life-threatening: the heart simply cannot maintain enough output to keep the rest of the body supplied.26PubMed Central. Pulmonary Embolism and Right Ventricular Dysfunction: Mechanism and Management The injury to the heart muscle is driven by a combination of physical stretching, altered blood flow to the heart’s own tissue, and an inflammatory response that amplifies the damage.27Journal of Cardiac Failure. Pathophysiology of Right Ventricular Dysfunction in Pulmonary Embolism and Chronic Pulmonary Hypertension
Seasonal Patterns and Who Gets Lung Clots
Lung clots are not evenly distributed across the calendar. Multiple studies have found that cases peak during colder months and dip during warmer ones. A large Korean epidemiological study found the highest rates in January and February and the lowest in August and September, with the seasonal swing being most pronounced in people over 60.28PubMed Central. Prominent seasonal variation in pulmonary embolism than deep vein thrombosis incidence: a Korean venous thrombosis epidemiology study A European registry-based study also found seasonal patterns, though it identified a main peak in autumn rather than midwinter.29PubMed. Seasonal variation in the occurrence of venous thromboembolism: data from the MASTER Registry The exact reasons are debated, but cold weather may contribute through dehydration, reduced physical activity, respiratory infections, and changes in blood viscosity.
Age is one of the strongest risk factors overall. The rate of lung clots rises steeply after middle age, reflecting the accumulation of genetic predispositions, chronic illness, reduced mobility, and vascular changes. In children, lung clots are far less common and look quite different: the triggers tend to be central venous catheters, congenital heart disease, infections, and cancer rather than the immobility and aging-related factors that dominate in adults.30The Lancet Respiratory Medicine. Acute pulmonary embolism in children and adolescents in the USA (2016 and 2019): a nationwide retrospective cohort study The age-specific risk factors differ enough that pediatric lung clots are essentially a separate clinical problem from the adult version.31Pediatric Clinics. Pulmonary Embolism and in Situ Pulmonary Artery Thrombosis in Pediatrics
An Evolutionary Trade-Off Written Into Human Blood
It is worth stepping back and asking why human blood clots so aggressively in the first place. The answer involves a trade-off that played out over tens of thousands of years. Factor V Leiden, the most common inherited clotting mutation in people of European descent, appeared roughly 22,000 years ago. Today it raises the risk of dangerous clots, but it persisted in the population because it offered survival advantages: less bleeding during childbirth, better iron retention, improved fertility, and higher rates of embryo implantation.32PubMed. Human Evolution: Between Hemorrhage and Thrombosis For most of human history, lethal hemorrhage during injury or childbirth was a far more immediate threat than a blood clot forming in a leg vein. The coagulation system evolved under pressure to err on the side of clotting too much rather than too little. Modern life, with its long periods of sitting, surgical interventions, hormonal medications, and longer lifespans, exposes the downside of that evolutionary bet.
The vessel lining itself plays a role in this balance. Healthy endothelial cells actively prevent clotting by releasing substances that keep platelets from sticking and clotting factors from activating. When that lining is damaged by inflammation, high blood pressure, diabetes, or infection, it loses its protective function and can actively promote clot formation. This endothelial dysfunction is now recognized as a factor that links venous and arterial clotting, which were long treated as completely separate problems.33PubMed Central. The Link Between Venous and Arterial Thrombosis: Is There a Role for Endothelial Dysfunction? The picture that emerges is not one of a single cause but of a system balanced on a knife’s edge, where any combination of slowed blood flow, vessel wall damage, and a blood chemistry tilted toward clotting can push a person over the threshold.