Pulmonary Embolism

1. Pathophysiology
2. Presentation
3. Investigations
4. Management
5. Quiz

• A pulmonary embolism (PE) is most commonly a thromboembolism that began as a deep vein thrombosis, has travelled through the right side of the heart, and has become lodged in an area of pulmonary vasculature.
• Risk factors for a PE include pregnancy, prolonged immobilisation, the combined oral contraceptive pill, and obesity.
• PE can cause right ventricular strain and pulmonary vasoconstriction. Hypoxaemia and type 1 respiratory failure may occur, but physiological effects vary with clot burden and cardiopulmonary reserve.
• Symptoms of a PE include dyspnoea, pleuritic chest pain, and a cough, whilst signs include dyspnoea, tachycardia, low BP, and a raised jugular venous pressure.
• Investigations for PE include arterial blood gas, chest x-ray, d-dimers, and an ECG.
• Anticoagulation is used to treat PE; longer-term treatment requires reassessment of recurrence risk, bleeding risk and the patient's preferences.

Pathophysiology

An embolus is material carried in the bloodstream from its site of origin to another site, where it may obstruct a vessel. A thrombus is a clot formed at its original site; a detached fragment travelling through the circulation is a thromboembolus.

A pulmonary embolism (PE) is therefore material that has moved from one part of the vasculature, through the right side of the heart, and lodges in the pulmonary arteries.

An embolus is usually made from a blood clot (thromboembolism), but can also be formed from tumour, air, fat, or amniotic fluid - note that the rest of this article will be focussing on thromboemboli. Pulmonary emboli are the third most common cause of vascular death, after myocardial infarction and stroke, and are the most common cause of preventable death in hospital patients.

Most pulmonary thromboemboli arise from a deep vein thrombosis (DVT) in the legs or pelvis. A detached clot travels through the right heart before lodging in the pulmonary arteries. The main factors that contribute to thrombus formation are stasis of blood flow, hypercoagulability of blood, and endothelial injury, also known as Virchow’s Triad. This means that the risk factors for a DVT (and therefore PE) are factors that will contribute to the causation of part of this triad:

• Pregnancy
• Prolonged immobilisation (e.g. post-operatively or on a long-haul flight)
• Previous venous thromboembolism
• Combined oral contraceptive pill
• Cancer
• Obesity
• Hormone replacement therapy 

Diagram - Virchow's Triad: the relationship between endothelial injury, hypercoagulability, and venous stasis 

Creative commons source by Dr.Vijaya chandar, MBBS [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

The above risk factors can be divided into those that are;

• Temporary; for example, pregnancy, the pill, and immobilisation.
• Persistent while present; for example, active cancer. Risk factors can change over time and should be reassessed.

It is thought that 50% of patients with a PE have a temporary risk factor and that 25% have a permanent, but that 25% don’t have any risk factors at all. It is important to realise that prevention of a PE, for example through the use of compression stockings on a long haul flight, is extremely important, and more easily implemented than treatment.

Pulmonary emboli cause mechanical obstruction of pulmonary arteries. Obstruction and mediator-driven pulmonary vasoconstriction, including effects of serotonin and thromboxane, increase pulmonary vascular resistance and right ventricular afterload. The right ventricle may dilate and fail, reducing blood flow through the lungs and filling of the left ventricle. Cardiac output and systemic blood pressure can then fall. Acute right ventricular failure is the principal lethal mechanism in severe PE.

Ventilated lung supplied by an obstructed artery becomes poorly perfused, increasing alveolar dead space. Redistribution of blood to other lung regions can produce low ventilation-perfusion ratios, contributing to hypoxaemia. Reduced cardiac output and atelectasis can also contribute. Hyperventilation commonly lowers arterial CO₂, so PE may cause type 1 respiratory failure: low arterial O₂ with normal or low CO₂. Normal oxygen saturation does not exclude PE.

The part of the lung that is poorly perfused may undergo infarction, however, this is rare as the bronchial arteries will normally supply the tissue with adequate oxygen. If this does happen then the patient may present with haemoptysis and pleuritic chest pain.  

In a patient with a patent foramen ovale, PE-related elevation of right atrial pressure can permit right-to-left shunting. A venous embolus may then cross into the arterial circulation, causing a paradoxical embolism, including stroke. The risk depends on the presence of a shunt; PE does not make every patent foramen ovale shunt right to left.

Presentation

Symptoms of a PE include:

• Shortness of breath
• Pleuritic chest pain
• Cough
• Substernal chest pain
• Fever
• Haemoptysis
• Syncope
• Unilateral leg pain (DVT)  

Signs of a PE include:

• Dyspnoea
• Tachycardia
• Low BP
• Raised jugular venous pressure
• Pleural rub in cases of pulmonary infarction
• Evidence of DVT, e.g. erythema, increased temperature and tenderness on palpation of the leg

The main differential diagnoses for a pulmonary embolism are pneumothorax, pneumonia, musculoskeletal chest pain, and myocardial infarction.

Preview the Pulmonary Embolism quiz