A pulmonary embolism is usually caused by a blood clot that forms in a deep vein and then breaks away, travels through the venous circulation and lodges in a pulmonary artery. This sequence is known as venous thromboembolism: the initial event is thrombosis, most often DVT, and the subsequent migration produces embolism. The clot typically originates in the deep veins of the leg or pelvis.
Once detached, it travels through the vena cava into the right atrium, passes into the right ventricle and is propelled into the pulmonary arterial circulation. The pulmonary vessels become progressively smaller, so the travelling clot eventually becomes lodged at a point where it cannot pass further. This mechanism accounts for most clinically recognised pulmonary emboli.
The formation of the underlying venous clot is commonly explained using Virchow's triad: venous stasis, vessel-wall or endothelial activation and hypercoagulability. Venous stasis occurs when blood flow slows, particularly during prolonged immobility. Endothelial activation or injury can result from surgery, trauma, inflammation or other physiological disturbances. Hypercoagulability means that the coagulation system is more active than normal or natural anticoagulant mechanisms are reduced. These three mechanisms can interact. A postoperative patient, for example, may have tissue injury, inflammation and prolonged immobility simultaneously. The resulting DVT can then become the source of a PE.
Prolonged immobility is a major circumstance associated with PE because it increases the risk of the DVT that usually precedes it. Hospitalisation, prolonged bed rest, recovery from surgery and long journeys can reduce the normal calf-muscle pump that returns venous blood to the heart. Blood pooling in deep veins increases the opportunity for coagulation to occur. NHS guidance identifies journeys lasting more than four hours as a circumstance associated with increased DVT risk, although the risk varies greatly according to individual factors. Sitting for a short period does not ordinarily cause PE by itself. The clinically important issue is prolonged or repeated immobility combined with the person's baseline thrombotic susceptibility.
Surgery and trauma increase PE risk because they can initiate clot formation through several pathways. Surgical injury activates tissue-factor-dependent coagulation and inflammatory responses, while anaesthesia and postoperative recovery often reduce mobility. Major trauma can produce direct vascular injury, inflammation and changes in coagulation, while fractures of large bones can also be associated with fat embolisation. Cancer surgery adds the pro-thrombotic effects of malignancy itself. For this reason, patients undergoing hospital treatment are routinely assessed for venous thromboembolism risk. Depending on the situation, prevention may involve early mobilisation, hydration, mechanical methods such as compression devices and anticoagulant prophylaxis when the expected reduction in clotting risk outweighs bleeding risk.
Cancer can substantially increase the risk of DVT and PE. Tumours can activate coagulation pathways, stimulate platelets and produce inflammatory signals that favour thrombosis. Some cancers also compress veins, reduce mobility or cause systemic illness that increases venous stasis. Certain cancer treatments can further increase thrombotic risk. The relationship varies considerably by cancer type, stage, treatment and individual circumstances. A PE can therefore sometimes be the event that leads to discovery of an underlying malignancy, although most people with PE do not necessarily have cancer. Clinical decisions about cancer-related thrombosis require balancing the risk of recurrent clotting against the risk of bleeding from anticoagulant therapy.
Pregnancy and the postpartum period increase the likelihood of venous thrombosis and consequently PE. Pregnancy produces physiological changes that make clotting more readily activated, while the enlarging uterus can impede venous return from the legs and pelvis. After childbirth, the coagulation system remains altered for a period and mobility may be reduced, particularly following complicated delivery or surgery. Oestrogen-containing contraception and HRT can also increase venous thrombosis risk. Other risk factors include previous DVT or PE, inherited thrombophilia, obesity, smoking, increasing age and certain chronic diseases. These factors do not directly block the pulmonary artery; rather, they increase the probability that a venous thrombus will form and subsequently embolise.
A previous DVT or PE is a significant risk factor for recurrence because some individuals retain persistent biological or anatomical susceptibility to thrombosis. Thrombophilia, active cancer, chronic inflammatory disease and ongoing immobility can similarly maintain an increased risk after the original event. Some pulmonary emboli are described as unprovoked because no major transient trigger can be identified.
This terminology does not mean that the event occurred without any cause in a biological sense; it means that no recognised provoking factor was found. Family history can suggest inherited predisposition, although many clots occur without a known genetic disorder. Clinical assessment therefore distinguishes temporary provoking factors from persistent risk factors and from apparently unprovoked events.
Not every pulmonary embolism is caused by a conventional venous blood clot. Rare forms of pulmonary embolism or pulmonary vascular obstruction can involve fat, air, amniotic fluid or other material, generally in specific clinical circumstances such as major trauma, medical procedures or childbirth. These entities are distinct from the usual thrombotic PE and have different mechanisms and treatments. A thrombotic PE remains the principal condition meant when clinicians refer simply to "pulmonary embolism". The distinction matters because prevention with anticoagulation is directed at thrombosis and does not prevent every possible form of pulmonary vascular embolisation. In suspected PE, the clinical context therefore helps determine which mechanism is plausible and which diagnostic and treatment pathway is appropriate.
