Chapter: Medicine and surgery: Respiratory system

Pulmonary embolism

Thrombus within the pulmonary arteries causing lack of lung perfusion. Thrombus within the systemic veins or uncommonly from the heart embolises to the lungs. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Pulmonary embolism



Thrombus within the pulmonary arteries causing lack of lung perfusion. Thrombus within the systemic veins or uncommonly from the heart embolises to the lungs.






The causes of thrombosis can be considered according to Virkhow’s triad:


·        Disruption in blood flow particularly stasis: Prolonged bed rest, air travel, pelvic and lower limb fractures, pelvic or abdominal surgery, pregnancy and childbirth. Right sided cardiac thrombosis may occur in atrial fibrillation, septal or right ventricular infarcts.


·        Abnormalities of the vessel wall: Following direct trauma to the vein in leg trauma.


·        Abnormalities in the blood such as hypercoagulable states – antithrombin III, protein C and S deficiencies and Factor V Leiden (a single point mutation in the Factor V gene, which causes resistance to activated protein C), oral contraceptives, malignant disease and smoking.



Following a pulmonary embolus there is a reduction in the perfusion of the lung supplied by the blocked vessel. Ventilation perfusion mismatch occurs, leading to hypoxaemia. Production of surfactant also stops if perfusion is interrupted for a number of hours after which the alveoli collapse. Infarct is rare (only occurring in around 10% of cases) as the lung is also supplied by the bronchial circulation, but there is an increase in pulmonary arterial pressure.


Clinical features


The result of a pulmonary embolism depends on the size and number of the emboli.


·        Small emboli may be silent or present with symptoms such as dyspnoea on exertion, haemoptysis, pleuritic pain or rarely cardiac arrhythmias.


·        Mediumsized emboli typically present with sudden onset pleuritic pain and dyspnoea. There may be a dry cough or haemoptysis.


·        A large embolus may present with syncope, sudden onset of severe central chest pain, shock, loss of consciousness or sudden death. Signs include hypotension, a loud pulmonary component of the second heart sound, tachycardia with third and fourth heart sounds heard as a gallop rhythm. There is a right ventricular (parasternal) heave due to increased stroke work, a raised JVP with a prominent ‘a’ wave due to increased right atrial pressure.


·        There may be chest signs resulting from alveolar atelectasis or complicating pneumonia. Pleural inflammation results in a pleural friction rub and a lowgrade pyrexia.


·        Clinical signs of a deep vein thrombosis may also be present.




Blood enters the pulmonary vasculature and thus there is congestion proximal to the blockage. Affected areas appear haemorrhagic and are frequently wedge shaped. Repair results in the formation of a white scar.




Typical features include haemorrhage (due to extravasation of blood), loss of cell architecture, cellular infiltration and occasionally necrosis.




Cardiopulmonary arrest and death in the acute stages. Atrial fibrillation and other arrhythmias. Recurrent thromboembolic disease may cause pulmonary hyper-tension.




The chest X-ray may be normal. Atelectasis and areas of hypoperfusion may be seen, and large emboli may cause an elevated hemidiaphragm and enlarged proximal pulmonary arteries. Blood D-dimers (breakdown products of fibrin) are of reasonable sensitivity but high specificity and are therefore useful for exclusion in cases of low clinical suspicion. A ventilation perfusion (V/Q) scan is usually diagnostic, but is less helpful if the chest X-ray is abnormal. Spiral CT pulmonary angiogram normally demonstrates the clot(s) within the pulmonary vasculature. The ECG may be normal or (particularly in larger emboli) reveal:


·        Tachycardia.

·        A characteristic S1 Q3 T3 pattern. This refers to an S wave in lead I, and Q and inverted T wave in lead III.

·        Right ventricular ‘strain’ pattern – T wave inversion in leads V1–V4.

·        Tall peaked P waves in lead II (p pulmonale).

·        Right bundle branch block: RSR’ in lead V1 (may be transient).




1.     In massive pulmonary embolism, there is haemodynamic compromise which may require resuscitative therapy. With large emboli, thrombolysis or surgical thrombectomy with cardiac bypass may be life-saving.


2.     Prevention of propagation and recurrence: Unfractionated intravenous heparin is started immediately titrated according to the APTT. For small or moderate emboli subcutaneous low molecular weight heparin is as effective and does not require monitoring of APTT. Therapy is converted to warfarin after 48 hours (for 3 months minimum – usually 6 months). Lifelong warfarin may be indicated depending on the underlying cause, or in recurrent embolism.


3.     If anti-coagulants are unsuccessful or contraindicated a filter may be inserted into the inferior vena cava to prevent further pulmonary embolism.


4.     Standard prophylaxis pre- and postoperatively, and for bed bound patients or those at risk – subcutaneous low molecular weight heparin, graduated compression stockings and early mobilisation if possible.




Ten per cent of symptomatic emboli are fatal.

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