PE should be regarded as a complication of underlying venous thrombosis. In the normal situation, tiny microthrombi are continually formed and lysed in equal measure within the venous circulatory system i.e. there is a balance between the thrombotic and fibrinolytic systems. In some pathological situations, microthrombi escape the fibrinolytic system and are allowed to propagate into larger thrombi.
The predisposing factors that may underlie this change can be broadly described under the three headings of Virchows Triad:
All known clinical risk factors for venous-thromboembolism have their basis in one of these three factors.
Most pulmonary emboli occur when fragments of a thrombus break free from the deep venous system, typically in the pelvis and lower limb, travel up the vena cava, through the right atrium and into the pulmonary vasculature. 79% of patients with proven pulmonary emboli also have thrombus detectable in the leg or thigh6. Although clots can also form in the upper arm veins they rarely embolise, and when they do they tend to cause smaller, less significant pulmonary emboli.
The lungs act as a filter for all blood returning to the heart so all but the smallest clots will get stuck there rather than travelling to the arterial circulation. The lungs have a dual blood supply from both the pulmonary artery and bronchial arteries which helps them recover function after small pulmonary emboli.
Provoked pulmonary embolism is a pulmonary embolism associated with a transient risk factor such as significant immobility, surgery, trauma, and pregnancy or puerperium.
Unprovoked pulmonary embolism is a pulmonary embolism occurring in the absence of a transient risk factor. The person may have no identifiable risk factor or a risk factor that is persistent and not easily correctable ( NICE CKS PE).
In massive PE (i.e. more than 50% obstruction of the pulmonary vascular bed) the most immediate problem is usually circulatory collapse due to a fall in cardiac output as the right heart fails to pump an adequate volume of blood through the reduced pulmonary vasculature to the left side of the heart.
In younger patients with normal cardiopulmonary function, oxygen saturations may be correctable with high flow oxygen as all of the blood getting to the left heart is still passing through good quality lung tissue giving good oxygenation. However, in patients with underlying lung pathology such as COPD a non-massive PE may present major problems with maintaining oxygenation despite the absence of haemodynamic compromise, as the function of the lung unaffected by the PE is already impaired.