Pulmonary Embolism – PE
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Pulmonary Embolism (also known as pulmonary embolusis most commonly a complication of venous thromboembolism (VTE) from another source – e.g. a clot in the legs or pelvis (a DVT) that becomes dislodged, flows via the bloodstream through the right side of the heart and gets lodged in the pulmonary circulation.

It is not always a clot that causes a pulmonary embolism. Fat, air, amniotic fluid can all also be causes. For fat and amniotic fluid, these will normally resolve themselves with supportive care. Air is often an iatrogenic cause (e.g. accidentally injected intravenously).

Some studies suggest that ‘silent’ pulmonary embolism occurs in up to 40% of DVT patients.
This article discusses Pulmonary Emobilism as caused by Venous Thrombolism.
  • <5% if no haemodynamic instability
  • 30% if shock present
  • 70% with cardiac arrest (in hospital)
Pulmonary Embolism
Image showing the route of a venous thrombolembolism as it travels from a peripheral vein, through the right side of the heart, and then becomes lodges in the pulmonary circulation, resulting in pulmonary embolus. Image by Servier Medical Art by Servier and is licensed under a Creative Commons Attribution 3.0 Unported License

Risk factors

For VTE pulmonary embolism:

  • Age
  • Malignancy
  • Infection
  • Family History
  • Immobility
    • Bed rest >24 hours
    • Immobility >48 hours
    • POP – plaster of Paris over limb
  • Pregnancy (oestrogen) – risk is highest in the 4 weeks after birth
  • Previous DVT / embolism
  • Oestrogen therapy (Pill, HRT) – note only the combined pill, not the progesterone only pill
  • Trauma
  • Surgery – especially pelvic and orthopaedic
  • Recent MI (10% of MI patients will have a DVT)
  • Dehydration
  • Smoking
  • Congestive heart failure
  • Antithrombin deficiency
  • Protein C deficiency
  • Inherited clotting deficiencies – thrombophilia – factor V Leiden
  • Obesity
  • Varicose veins

Clinical features

Symptoms can be wide ranging, from none at all – to sudden death! They are often, but not always, correlated to severity.
Always make sure you ask about a family history of thrombosis!


  • Pyrexia
  • Cyanosis
  • Tachypnoea – 90% of patients have RR >16
  • Tachycardia – 45% of patients
  • Hypotension – 25% of patients
  • Raised JVP
  • Pleural rub
  • Pleural effusion
  • Look for signs that could indicate a cause – e.g. DVT, recent surgery, air travel – only 33% of patients have clinical evidence of DVT
  • Atrial fibrillation (rare)


  • Pleuritic chest pain (pain worse on inspiration) – 75% of patients
  • Breathlessness – 85% of patients
  • Cough – 50% of patients
  • Haemoptysis – as a result of pulmonary infarct – 30% of patients
  • Dizziness / pre-syncope – 15% of patients
  • Syncope (loss of consciousness/fainting) – 15% of patients
  • Non-pleuritic chest pain – 15% of patients

Shortness of breath typically occurs within seconds to minutes of onset, and pain develops later.

Beware of patients with unexplained syncope. In one study, 25% of patients admitted to hospital with unexplained syncope had PE.


Probably the most important question is should I investigate? 

Defining risk of the probability of PE is important. There are two tools to help with this:

PERC Score

PERC stands for Pulmonary Embolism Rule-out Criteria.The PERC score is useful to rule out PE in low risk patients. If the patient’s score = 0, then there is a <2% chance of PE, and in the absence of convincing clinical signs, you can usually safely exclude PE as a differential.

Each factor below gives a score of 1. All factors must be negative for a negative PERC score. Any positive factor results in the need for further work up (move onto the Well’s Score)

  • Age >50
  • HR >100
  • SaO2 on room air <95%
  • Unilateral leg swelling
  • Haemoptysis
  • Recent surgery or trauma
  • Previous PE or DVT
  • Exogenous Oestrogen – oral contraceptives, hormone resplacement or other oestrogen hormones

Well’s score for PE

This can stratify patients as low or high risk. In high risk patients, you should proceed straight to imaging. In low risk patient, you should consider a D-dimer test.

Clinically suspected DVT3
PE is most likely diagnosis3
Tachycardia >100bpm1.5
Immobilisation >3 days OR surgery – in previous 4 weeks1.5
History of DVT or PE in past1.5

Interpretation of Well’s Score

Traditional interpretation

  • Score >6.0 — High (probability 59%)
  • Score 2.0 to 6.0 — Moderate (probability 29%)
  • Score <2.0 — Low (probability 15%)

Alternative interpretation

  • Score > 4 — PE likely. Consider diagnostic imaging.
  • Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.


D-Dimer is a fibrin degradation product – and as such, levels are raised by the presence of a blood clot in the circulation. A D-Dimer blood test can be useful to rule out PE or DVT as a differential. A negative D-Dimer PLUS a low Well’s score means that PE or DVT is extremely unlikely. Conversely, many factors can cause a positive D-Dimer – so having a raised D-Dimer does not necessarily mean there is a clot.

  • D-Dimer should only be used as a ‘rule-out’ test in low probably cases – based on the Well’s score
  • A positive D-Dimer in a low probably case indicates the need for further investigation (e.g. CTPA or VTE)
  • In high probably cases, you should skip the D-Dimer and go straight to imaging

In reality it can be a tricky test to use. Even just a recent common cold can result in a raised D-Dimer! Almost any factor that causes inflammation will also result in a raised D-Dimer. Do be selective when requesting a D-DImer for your patients. Even if your patient has a low risk Well’s score, doing a D-Dimer might not always be the best option – for example if they have recently had cellulitis or some other infection.

“Should I do a D-Dimer?” is often a difficult questions which should involve consultation with your senior clinicians. Common pitfalls include:

  • Delaying of imaging in cases with a high probably – D-Dimer not necessary
  • Clinical confusion in cases which could have been ruled out clinically (e.g. PERC rule), which subsequently report a positive D-Dimer (most likely caused by another factor unrealted to any potential VTE). In these cases patient’s often undergo unnecessary imaging to “exclude” a PE.

D-Dimer also rises with age. Some centres now report an age specific reference range for D-Dimer.

  • Traditional reference range for D-Dimer – normal <0.50
  • Example of age adjusted:
    • Age <50 – normal <0.50
    • Age >50 – normal range is <0.50 PLUS 0.1 for every decade of life over the age of 50, e.g.:
      • Age 60 – normal <0.60
      • Age 70 – normal <0.70

Other factors that caused an increased D-Dimer include liver disease, high rheumatoid factor, malignancy, trauma, pregnancy and recent surgery.



Will often be normal. The main reason CXR is performed is to exclude other causes.

The CXR may show pulmonary oedema signs such as raised hemidiaphragm. May also show atelectasis – this is little areas of collapsed lung. This occurs because there is loss of blood to some areas of the lung, which results in collapse of these areas – as a conservative mechanism.
Look for atelectasis in both lungs!
If the CXR is normal, but the patient is breathless, this raises the suspicion of a pulmonary embolism. If the CXR has bilateral changes, but the patient only has unilateral pain, this also raises the suspicion of pulmonary embolism. 


Changes here are common but often non-specific (e.g. T wave changes, new onset AF, RBBB right axis deviation). Such changes are seen in about 80% of patients. The most common findings are T wave inversion and sinus tachycardia. Larger emboli can cause right heart strain, which will result in the ‘classical’ S1Q3T3 pattern of ECG changes in PE, although this classic sign is actually quite rare (<20% of cases). the S1Q3T3 pattern is:
  • S waves present in lead I
  • Q waves present in lead III
  • T wave inversion in lead III
ECG showing classical S1Q3T3 pattern in PE
ECG showing classical S1Q3T3 pattern in PE. Note that this is not very common – the example above is one of the only times I have seen it in my career!


CT-pulmonary angiogram – a CT with contrast, assessing the pulmonary blood vessels. This is a test that use a CT scanner and radioactive dye to look at the pulmonary circulation. Its main use is in the diagnosis of PE. It is much more sensitive and specific than VQ scan.
CTPA is typically the diagnostic scan in PE, but does require a high dose of radiation, and as such, VQ may still be considered as an alternative in young females, or pregnancy females.
CTPA showing saddle PE
CTPA showing saddle PE. Note the lack of contrast in the pulmonary vessels, as demonstrated by the red arrows which is indicative of thrombus.This file is taken from wikimedia commons and is licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license.

VQ scan

VQ scans use much less radiation than a CTPA. As such, VQ scans are used to assess for PE in patients who are at risk from higher radiation doses – such as pregnant women, and younger female patients.
However, VQ scans are also much less accurate at diagnosing PE. They need to be interpreted carefully by a radiologist. A negative VQ scan has a very high negative predictive value, but positive scans are less useful.
The result of a VQ scan is usually given as a risk probability – high risk, intermediate risk or low risk.
Only 15-20% of scans will show obvious pulmonary embolic disease
20% will obviously have no PE
The rest (60%) you just cannot tell!
  • VQ scans should not be performed in patients with CXR abnormalities –  the abnormalities on the x-ray are likely to cause abnormalities on VQ, irrespective of the presence of PE. VQ is only suitable for patients who have been previously well, and not for those with chronic disease.
VQ scan in PE
On the left – we have the results of the inhaled radioactive element (usually Xenon gas) – showing normal perfusion throughout the bronchial tree. On the right we have the image following injection of technetium. We can see the patchy update in different regions of the lungs, m indicated multiple areas of reduced blood flow – likely due to PE. This file is taken from wikimedia commons and is licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license.


  • O2 may often be low
  • CO2 may often be normal or low
The patient will probably be hyperventilating (hence the low CO2).
Metabolic acidosis is commonly seen in those with a massive PE and cardiovascular collapse.
You cannot exclude a PE with an arterial blood gas.


Troponin is raised in 20-40% of patients with PE as a result of the extras stress and stretch placed on the right ventricle in PE patients (due to increased pulmonary arterial pressure).

Higher troponin has been associated with a worse prognosis.


Is used to look for right ventricle strain and dilatation in patients with suspected massive PE. The degree of RV dysfunction can be used as a predictor of death. 


PE with signs of right heart strain in the haemodynamically unstable patient (raised troponin, heart motion abnormalities on echo – often done at the bedside in ED) should be considered for thrombolysis – e.g. 50mg alteplase (be wary of a long list of contraindications!).

This type of PE is sometimes termed “massive PE”. This scenario is typically caused by a “saddle” PE – sitting at the major bifrucation of the pulmonary veins.

Typically this is a decision made by the treating consulting in hospital (usually ED physician) perhaps in conjunction with respiratory and or haematology specialists. These patient will also require ongoing anticoagulation as below.

The vast majority of patients do not require thrombolysis and do not have massive or saddle PE.

The other main treatment is anticoagulation. This can be done either with warfarin, or a NOAC – such as rivaroxaban. In most circumstances a NOAC is favorable as it does not required monitoring, and it does not require the use of a heparin at the start of the treatment period.

Example of warfarin treatment

  • Anticoagulate with LMWH – e.g. dalteparin 200u/Kg/24hrs. The max dose is 18,000.
  • At the same time start oral warfarin 10mg
  • Stop the heparin when the INR is >2, and continue warfarin for a minimum of 3 months, aiming for an INR of 2-3.

In patients with recurrent thrombus despite anticoagulation a vena cava filter may be considered – but remember that implanting a filter without adequate anticoagulation will increase the risk of thrombus.

Continuation of anticoagulant therapy

This decision made be made in conjunction with a haematologist.

  • At the very minimum – 6 weeks. Usually in cases of obvious ‘provoked’ PE (e.g. after surgery)
  • Those with an identifiable and reversible risk factor – 3 months
  • Those with idiopathic disease – 6 months
  • Those with recurrent clots – often longer than 6 months – sometimes lifelong
  • There is also evidence that low-intensity warfarin (INR 1.5-2.0) not only reduces the risk of thromboembolism, but also has a lower risk of bleeding.
Paradoxical Embolism
This is an embolism that goes through a defect in the heart, and goes on to cause a stroke. The clot passes from a vein to an artery, through some sort of ‘fistula’ – usually a cardiac defect
For example, a DVT could embolise, and travel to the heart. This might in a normal individual, cause a PE. But in the case of a paradoxical embolism it will travel through a defect in the heart from the right side to the left side, and thus miss out the pulmonary circulation. It is then free to travel through the arterial circulation, until it reaches an artery that is so small it cannot travel down it, and thus causes an ischaemic blockage.
  • They will often travel to the brain, and cause a stroke.
These account for about 2% of arterial emboli


Like any chest pain presentation, differentiating PE can be difficult. Typically, larger PE’s (and sicker patients) are easier to differentiate. Using the Chest Pain Differentializer might be useful.

Differentials include:


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

This Post Has 4 Comments

  1. luther

    what are the complications and differential diagnosis. it will be nice if it is added

    1. Dr Tom Leach

      Hi Luther, I’ve added some differentials, but there are often many and the presentations can be quite variable. Its worthwhile having a look at the chest pain differentials page (link in the differentials section of the article). As for complications- there aren’t many – but death is an important one! UpToDate suggests the mortality rate for untreated PE is as high as 30% – and is usually due to shock.

  2. Anon


  3. Dr Tom Leach

    Thanks Anon – the treatment section of this article was quite out of date. I have cleared things up a little now.

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