A pulmonary embolism, abbreviated PE, occurs when a blood vessel supplying the lungs becomes blocked, most commonly by a blood clot that has travelled from a deep vein elsewhere in the body. The blockage is usually within a pulmonary artery or one of its branches. Because pulmonary arteries carry deoxygenated blood from the right side of the heart towards the lungs, an embolus can prevent blood from reaching functioning lung tissue.
The result is impaired matching between ventilation and blood flow and, in larger emboli, increased pressure against which the right ventricle must pump. A pulmonary embolism can range from a small event causing limited symptoms to a massive obstruction causing severe cardiovascular compromise and potentially death.
Most pulmonary emboli arise from venous thromboembolism, particularly a DVT in the deep veins of the leg or pelvis. A portion of the thrombus can detach and become an embolus, travelling through the venous circulation to the right atrium, right ventricle and then pulmonary arteries. The pulmonary vascular network acts as a filter, trapping the embolus before it can enter the arterial circulation beyond the lungs. The size and location of the embolus determine the physiological consequences.
Multiple smaller emboli can occur, and the number seen on imaging does not necessarily correspond directly to clinical severity. A PE can occasionally arise from a clot that formed in another venous location, and not every patient has an identifiable DVT at the time of diagnosis.
A PE affects circulation and gas exchange simultaneously. Obstruction of pulmonary vessels reduces perfusion to portions of the lung while ventilation may continue, producing ventilation-perfusion mismatch and impaired oxygenation. A significant embolus also increases pulmonary vascular resistance, forcing the right ventricle to pump against a higher pressure. If the right ventricle cannot compensate, it can dilate and fail, reducing the amount of blood reaching the left side of the heart and lowering systemic blood pressure. Severe PE can therefore cause obstructive shock. Smaller emboli may produce mainly respiratory symptoms and pleuritic pain without severe haemodynamic instability. The physiological response depends on clot burden, location, pre-existing cardiopulmonary function and the body's ability to compensate.
Typical symptoms include sudden breathlessness, chest pain that may be worse when breathing in, rapid heartbeat and sometimes coughing up blood. Some patients experience dizziness, faintness or collapse, particularly when pulmonary obstruction is severe. Chest pain can arise from irritation of the pleura adjacent to affected lung tissue and is often described as pleuritic when it increases with deep inspiration. Not every patient has all of these symptoms. A PE can resemble pneumonia, heart disease, asthma, anxiety or other respiratory disorders, so clinicians use clinical probability assessment and appropriate investigations rather than relying on a single symptom.
A pulmonary embolism is considered potentially life-threatening because a large obstruction can abruptly impair the circulation through the lungs. Severe PE may produce marked breathlessness, chest or upper-back pain, very rapid heartbeat, low blood pressure, fainting or cardiac arrest. NHS guidance advises calling 999 or attending A&E for severe difficulty breathing, significant chest or upper-back pain, very rapid heartbeat or loss of consciousness. These symptoms can also result from other emergencies, but PE must be considered because rapid treatment can be lifesaving. A suspected PE is therefore not equivalent to ordinary shortness of breath and requires appropriate urgency.
Diagnosis commonly involves clinical assessment followed by tests selected according to the estimated probability of PE. D-dimer testing can help exclude PE in selected patients when the pre-test probability is low or intermediate, while CT pulmonary angiography can directly visualise filling defects in pulmonary arteries. A ventilation-perfusion scan can be used in circumstances where CT pulmonary angiography is unsuitable or where an alternative diagnostic approach is appropriate. ECG, blood tests, chest imaging and oxygen measurements can provide supporting information but generally cannot establish PE by themselves. Ultrasound of the legs may identify a DVT and support the diagnosis, particularly when pulmonary imaging is unsuitable.
Treatment usually involves anticoagulation to prevent existing clot from enlarging and to reduce the risk of additional emboli. NHS guidance states that suspected PE is generally treated promptly with anticoagulant medication while diagnostic testing is undertaken, and confirmed PE usually requires anticoagulation for at least several months. The precise treatment and duration depend on severity, provoking factors, recurrence risk and bleeding risk. In severe PE with haemodynamic instability, stronger reperfusion strategies may be considered, including thrombolysis or catheter-based or surgical interventions in selected cases. Anticoagulation is not the same as clot-busting treatment: anticoagulants mainly prevent further clot formation, whereas thrombolytic therapy actively accelerates clot breakdown.
PE belongs to the spectrum of venous thromboembolism and is closely connected to DVT. The term "embolism" describes obstruction caused by material that has travelled from another location, whereas "thrombosis" describes clot formation within a vessel. A DVT that embolises to the lungs therefore produces a pulmonary embolism.
Other forms of embolic material can theoretically enter the pulmonary circulation, including fat droplets after major bone trauma, air and rarely other substances, but thromboembolic PE is by far the usual clinical entity referred to by the term pulmonary embolism. The distinction is useful because not every pulmonary artery obstruction has the same cause, even though the typical PE in everyday clinical practice is a venous blood clot.
