Pulmonary Embolism occurs when material, most commonly a blood clot originating in the venous circulation, travels to and obstructs an artery or smaller branch within the lungs. Most clinically important pulmonary emboli arise from Deep Vein Thrombosis in the deep veins of the legs or pelvis, although embolic material can originate elsewhere. The obstruction interferes with pulmonary blood flow and can create a mismatch between ventilation and perfusion. The physiological consequences range from small emboli producing limited symptoms to extensive obstruction causing acute strain on the right side of the heart, severe oxygenation problems, circulatory collapse or death. Pulmonary Embolism is therefore a potentially life-threatening cardiovascular and respiratory emergency.
The clinical effects of Pulmonary Embolism depend on the size and location of the embolus, the amount of pulmonary vascular obstruction, the patient's underlying cardiopulmonary reserve and whether multiple emboli are present. An embolus can increase resistance within the pulmonary circulation and suddenly increase the workload imposed on the right ventricle. If right-ventricular output falls substantially, left-sided cardiac filling can decrease and systemic blood pressure may collapse. Smaller emboli may produce pleuritic chest pain, shortness of breath or unexplained tachycardia without major haemodynamic instability. Pulmonary infarction can occur when an embolus obstructs smaller vessels, particularly when collateral circulation is insufficient, and may cause localised pain or haemoptysis.
Risk factors for Pulmonary Embolism largely overlap with those for venous thromboembolism. Recent surgery, prolonged immobility, hospitalisation, major trauma, active cancer, previous venous thromboembolism, pregnancy and the postpartum period can increase risk. Certain hormonal exposures and inherited or acquired thrombophilias can also contribute. Risk may be transient, persistent or absent despite careful investigation. Clinicians commonly distinguish provoked events associated with identifiable transient or persistent risk factors from unprovoked events because this affects recurrence assessment and decisions about anticoagulation. A person's overall risk is determined by the combination of circumstances rather than by any one factor considered in isolation.
Symptoms of Pulmonary Embolism commonly include sudden or relatively rapid-onset breathlessness, chest pain that may worsen with breathing, increased heart rate and sometimes coughing or coughing blood. Severe cases can cause dizziness, fainting, low blood pressure, cyanosis or cardiac arrest. Symptoms are not unique to Pulmonary Embolism and overlap with myocardial infarction, pneumonia, asthma, pneumothorax and other conditions. This makes clinical probability assessment important. A normal oxygen saturation does not necessarily exclude Pulmonary Embolism, particularly when the embolus is small or the person's physiological reserve is good. Conversely, low oxygen saturation has numerous possible causes and is not diagnostic by itself.
Diagnosis combines clinical assessment with laboratory and imaging techniques. D-dimer can help exclude Pulmonary Embolism in appropriately selected people with sufficiently low or intermediate clinical probability, but it becomes less useful when the pre-test probability is high or when numerous non-thrombotic conditions can elevate the result. Computed tomography pulmonary angiography is a major diagnostic imaging technique because it can directly demonstrate filling defects in pulmonary arteries. Ventilation-perfusion scanning is an alternative in selected circumstances, particularly when iodinated contrast or radiation exposure considerations affect the choice of imaging. Electrocardiography and cardiac biomarkers can provide information about cardiac strain but do not independently establish or exclude the diagnosis.
Anticoagulation is the foundation of treatment for most Pulmonary Embolism because it prevents further thrombus formation and embolisation. Direct oral anticoagulants are commonly used in appropriate patients, while heparin-based regimens or other strategies may be selected according to clinical circumstances. People with haemodynamic instability caused by severe pulmonary vascular obstruction may require reperfusion treatment, such as systemic thrombolysis, catheter-directed intervention or surgical embolectomy, depending on the situation and available expertise. The treatment objective differs between stabilising the immediate circulatory threat and preventing recurrent venous thromboembolism over the subsequent months or longer.
Long-term management depends on recurrence risk, bleeding risk and the circumstances of the initial event. Anticoagulation may be stopped after a defined treatment period in some people with a transiently provoked event, whereas extended treatment may be considered when recurrence risk remains substantial. Inferior vena cava filters have a limited role and are generally considered when anticoagulation cannot be given or in selected situations despite anticoagulation. Persistent breathlessness after Pulmonary Embolism warrants assessment because recovery varies and other explanations, including chronic thromboembolic pulmonary hypertension, can occur. Most people do not develop chronic severe pulmonary vascular obstruction, but recognition of persistent symptoms is important.
Pulmonary Embolism should not be confused with ordinary pulmonary artery obstruction caused by a tumour, air or other rare embolic material, although those processes can also produce pulmonary vascular obstruction. The term embolism describes material travelling through the circulation, whereas thrombosis describes clot formation within a vessel. Sudden unexplained breathlessness, chest pain, fainting, rapid heart rate or coughing blood can be manifestations of Pulmonary Embolism and require urgent medical assessment, particularly when risk factors for venous thrombosis are present. The condition is not reliably excluded by the absence of leg symptoms because the original Deep Vein Thrombosis may be clinically silent or may have partially embolised before detection.
