Understanding Pulmonary Embolism (PE)

A pulmonary embolism, usually shortened to PE, is one of those conditions that deserves respect.

It may present with collapse, severe breathlessness and hypotension. It may also present with unexplained shortness of breath, mild tachycardia or pain when breathing in.

That unpredictability is what makes recognition so important.

The student nurse’s job is not to diagnose a PE independently. It is to notice that something does not fit, complete an accurate assessment and escalate promptly.

What is a pulmonary embolism?

A pulmonary embolism occurs when material travelling through the circulation blocks part of the pulmonary arterial system.

Most pulmonary emboli are caused by a blood clot that began as a deep vein thrombosis (DVT) in a deep vein of the leg or pelvis.

If part of the clot breaks away, it travels through the venous circulation into the right atrium, through the right ventricle and into the pulmonary artery. It eventually becomes stuck within part of the pulmonary circulation.

Think of it as a clot that went travelling and chose the worst possible destination.

DVT and PE are collectively known as venous thromboembolism (VTE).

What happens inside the body?

The blocked pulmonary artery prevents blood from reaching part of the lung normally.

The affected area may still receive air, but there is not enough blood flow available to collect the oxygen. This creates a ventilation–perfusion mismatch, usually shortened to V/Q mismatch.

In other words:

Air is arriving, but the blood cannot reach it properly.

This may impair oxygenation, although a normal oxygen saturation does not exclude PE.

A significant obstruction also increases pressure within the pulmonary circulation. The right ventricle must suddenly work harder to pump blood past the blockage.

If the right ventricle cannot compensate, it may dilate and begin to fail. Less blood then reaches the left side of the heart, causing cardiac output and blood pressure to fall.

In a severe PE, this can lead to obstructive shock, pulseless electrical activity or cardiac arrest.

Smaller clots near the outer edge of the lung may irritate the pleura or cause pulmonary infarction. This helps explain why some patients experience sharp pain when breathing in or cough up a small amount of blood.

Who is at greater risk?

PE should be considered more readily when symptoms occur in someone with known risk factors.

These include previous DVT or PE, recent surgery, trauma, reduced mobility, active cancer, pregnancy, the postnatal period, oestrogen-containing contraception, hormone replacement therapy, thrombophilia and significant acute illness.

Age, obesity, heart failure and long-distance travel may also contribute to risk, particularly when combined with other factors.

However, not everyone with a PE has an obvious risk factor. A clot occurring without a clear temporary trigger is described as an unprovoked PE.

Do not dismiss PE simply because the person is young or mobile.

What might the patient look like?

There is no single PE presentation.

The person may report sudden or unexplained breathlessness, sharp pleuritic chest pain, cough, dizziness or haemoptysis. Their respiratory rate or heart rate may be raised.

Some patients experience syncope or presyncope. Others present with unilateral leg swelling, tenderness or pain caused by the original DVT.

A larger PE may cause hypoxaemia, cyanosis, hypotension, altered consciousness or collapse.

Breathlessness, pleuritic chest pain and haemoptysis are sometimes described as the “classic triad,” but all three appearing together is uncommon.

A patient can have a PE without haemoptysis, without visible leg swelling and without a marked fall in oxygen saturation.

That is why the whole clinical picture matters.

PE or a panic attack?

PE can look surprisingly similar to anxiety or a panic attack.

Both may cause breathlessness, tachycardia, chest discomfort, dizziness, tingling and an intense feeling that something is wrong.

But anxiety should not become the automatic explanation for unexplained physical symptoms.

Complete the observations, assess how the symptoms began, consider risk factors and escalate concerns. Anxiety can exist alongside a PE,it does not rule one out.

And please, never assume:

“Their oxygen saturation is normal, so it can’t be a PE.”

It can.

How is PE investigated?

There is no single observation or blood test that can diagnose PE on its own.

The clinical team will consider the history, symptoms, risk factors, examination findings and haemodynamic stability. The patient may also have an electrocardiogram, chest X-ray and blood tests to assess their condition and look for alternative causes.

If clinical suspicion is low and another diagnosis is considered feasible, clinicians may use the Pulmonary Embolism Rule-out Criteria (PERC) to determine whether further investigation is needed.

If PE remains suspected, NICE recommends using the two-level PE Wells score.

A score above four means PE likely, while a score of four or fewer means PE unlikely.

The score considers features such as clinical signs of DVT, tachycardia, recent surgery or immobilisation, previous VTE, haemoptysis and malignancy. It also considers whether PE appears more likely than another diagnosis.

This is a clinical decision-making tool, not a casual checklist for students to complete from partial information.

What does the D-dimer tell us?

For someone assessed as PE unlikely, a D-dimer blood test may help determine whether further imaging is required.

A negative result can help exclude PE when used in the correct pathway.

A positive result does not confirm a clot.

D-dimer can also rise because of infection, inflammation, trauma, recent surgery, pregnancy, cancer and increasing age.

For people aged over 50, NICE advises considering an age-adjusted D-dimer threshold.

The easiest way to remember it is:

A negative D-dimer may help rule PE out. A positive D-dimer does not rule PE in.

CTPA and V/Q scans

For someone assessed as PE likely, NICE recommends an immediate computed tomography pulmonary angiogram (CTPA) where appropriate.

CTPA uses intravenous contrast and computed tomography imaging to visualise the pulmonary arteries. It is the usual first-line imaging investigation, but it should not simply be called the universal “gold standard.”

Renal function, contrast allergy, pregnancy, radiation exposure, image quality and clinical stability can all influence the choice of test.

A ventilation–perfusion scan, or V/Q scan, compares the distribution of air and blood flow within the lungs. It may be considered when CTPA is unsuitable, such as in severe renal impairment, significant contrast allergy or situations where radiation exposure requires particular consideration.

Pregnancy and the postnatal period require pregnancy-specific assessment and imaging pathways.

What about the ECG, chest X-ray and blood gas?

Sinus tachycardia is one of the more common electrocardiogram findings in PE. Other changes may suggest right-heart strain, but they are not diagnostic.

The famous S1Q3T3 pattern can occur, but it is neither common nor specific enough to confirm PE.

A normal electrocardiogram does not exclude it.

The chest X-ray may also be normal. Its value is often in identifying other causes of breathlessness or helping clinicians choose the most appropriate imaging test.

A blood gas may show hypoxaemia and a low carbon dioxide level, but results vary. A normal blood gas cannot safely rule out PE.

How is PE treated?

Treatment depends on the patient’s haemodynamic stability, bleeding risk, renal function, comorbidities, active cancer, pregnancy and other medicines.

The immediate priorities are assessment, escalation, appropriate monitoring and treatment of hypoxaemia.

Oxygen

Oxygen is used to treat hypoxaemia and should be prescribed to a target range.

For most acutely unwell adults who are not at risk of hypercapnic respiratory failure, the usual target is 94–98%.

For patients at risk of hypercapnic respiratory failure, the usual initial target is 88–92%, pending clinical assessment and blood-gas results.

Not every person with chronic obstructive pulmonary disease automatically requires the lower range. Follow the patient’s prescribed target and local oxygen policy.

Anticoagulation

Anticoagulants help prevent the clot from growing and reduce the formation of new clots while the body gradually breaks down the embolus.

For many adults with confirmed PE, NICE recommends apixaban or rivaroxaban as treatment options. However, they are not suitable for everyone.

Other patients may receive low-molecular-weight heparin, unfractionated heparin, edoxaban, dabigatran or a vitamin K antagonist.

The prescriber chooses the appropriate medicine and dose according to the individual clinical situation.

If imaging or test results are delayed, the medical team may prescribe interim therapeutic anticoagulation while investigations continue, provided it is safe to do so.

What is a high-risk PE?

You may still hear the phrase “massive PE,” but high-risk PE with haemodynamic instability is more clinically useful.

This describes a PE causing persistent hypotension, obstructive shock or cardiac arrest.

Management requires immediate senior and specialist input. Treatment may involve unfractionated heparin, thrombolysis, catheter-based treatment or surgical embolectomy.

Thrombolysis can dissolve clot rapidly, but it carries a significant bleeding risk. It is not routinely offered to haemodynamically stable patients simply because imaging shows right-heart strain.

Fluid administration must also be carefully guided. Large or poorly judged fluid volumes can worsen right-ventricular strain, so this is not a “just hang some fluids” situation.

What if the patient arrests?

PE is one of the potentially reversible causes considered during cardiac arrest.

Pulseless electrical activity can occur, although it is not specific to PE.

If a patient arrests, call for immediate help, begin high-quality cardiopulmonary resuscitation and follow the current Resuscitation Council UK algorithm.

The 2025 guidance advises considering immediate thrombolytic treatment when PE is the suspected or confirmed cause of cardiac arrest. In selected patients, prolonged resuscitation may be considered after thrombolysis.

These are decisions for the resuscitation team,not for a student nurse to make independently.

How long does anticoagulation continue?

NICE recommends anticoagulation for at least three months after a confirmed PE.

Treatment is then reviewed.

For a provoked PE, anticoagulation may be stopped after three months if the provoking factor has resolved, the clinical course has been uncomplicated and the balance of risk supports stopping.

After an unprovoked PE, treatment may continue for longer. The decision considers recurrence risk, bleeding risk, comorbidities and the patient’s preferences.

People with active cancer follow cancer-specific recommendations and are generally reviewed after three to six months.

Does every patient need cancer and thrombophilia testing?

No.

After an unprovoked PE, the clinical team should review the person’s history, complete a physical examination and consider baseline blood tests.

Further cancer investigations are not routinely recommended unless symptoms, signs or initial results suggest an underlying malignancy.

Thrombophilia testing is also selective. It is not routinely offered after a provoked PE or when the person will continue anticoagulation.

Specialist testing may be considered in particular unprovoked cases, especially when stopping anticoagulation is being considered or there is a relevant family history.

What should student nurses monitor?

Begin with the patient, not the diagnosis.

Use a structured ABCDE assessment and pay particular attention to respiratory rate, work of breathing, oxygen saturation, heart rate, blood pressure, perfusion, consciousness and pain.

Look for unilateral leg swelling or tenderness and ask about recent surgery, immobility, previous VTE, cancer and hormone treatment.

NEWS2 can help identify deterioration, but it cannot diagnose or exclude PE. A patient may have a significant PE without an extremely high score.

If anticoagulation has been prescribed, ensure it is administered at the correct time and monitor for bleeding. Depending on the medicine and clinical situation, this may include checking relevant blood results and following any required independent-check process.

Possible bleeding signs include haematuria, melaena, haematemesis, unexplained bruising, prolonged bleeding, hypotension, tachycardia or an unexplained fall in haemoglobin.

Haemoptysis may be caused by the PE itself, so report and assess it rather than automatically assuming anticoagulation is responsible.

What about mobilisation?

Routine prolonged bed rest is not required for every patient with PE.

Once the patient is stable and an anticoagulation plan is established, mobilisation may be encouraged according to the multidisciplinary plan.

Do not decide this independently. Consider symptoms, haemodynamic stability, falls risk and the agreed clinical plan.

Red flags: escalate immediately

Call for urgent help if the patient develops:

• sudden collapse or syncope;
• severe or rapidly worsening breathlessness;
• persistent hypotension or signs of shock;
• rapidly increasing oxygen requirements;
• severe hypoxaemia or cyanosis;
• reduced consciousness;
• signs of major bleeding; or
• cardiac arrest.

Do not wait for the next scheduled observation round when the patient looks seriously unwell.

Helpful truths to remember

A normal oxygen saturation does not exclude PE.

A normal chest X-ray does not exclude PE.

S1Q3T3 is not required for the diagnosis.

A raised D-dimer does not confirm PE.

Anxiety should not be used to explain sudden breathlessness until serious physical causes have been considered.

The absence of leg symptoms does not exclude a clot.

And most importantly:

You do not have to prove it is a pulmonary embolism before asking for help.

Bleepbook memory line

The original “Pain + Puffed + Pale” line is memorable, but pallor is not a reliable defining sign and some patients have no chest pain.

A more accurate version is:

New unexplained breathlessness, pleuritic pain, a fast pulse or sudden collapse, pause and consider the clot.

And the line worth remembering on placement:

Normal sats do not automatically mean normal circulation.

What to remember

Pulmonary embolism does not always arrive with flashing lights.

Sometimes the patient collapses.

Sometimes they simply say:

“I don’t know why, but I suddenly can’t catch my breath.”

You are not expected to diagnose the clot independently. Your role is to recognise the change, assess accurately and escalate promptly.

If something feels wrong, do not talk yourself out of raising it.

References

British Thoracic Society (2017) Guideline for oxygen use in adults in healthcare and emergency settings. Available at: https://www.brit-thoracic.org.uk/clinical-resources/guidelines/emergency-oxygen/

National Institute for Health and Care Excellence (2020, updated 2023) Venous thromboembolic diseases: diagnosis, management and thrombophilia testing (NG158). Available at: https://www.nice.org.uk/guidance/ng158

National Institute for Health and Care Excellence (2026) Clinical Knowledge Summary: Pulmonary embolism. Available at: https://cks.nice.org.uk/topics/pulmonary-embolism/

Resuscitation Council UK (2025) Adult advanced life support guidelines. Available at: https://www.resus.org.uk/professional-library/2025-resuscitation-guidelines/adult-advanced-life-support-guidelines

Resuscitation Council UK (2025) Special circumstances guidelines. Available at: https://www.resus.org.uk/professional-library/2025-resuscitation-guidelines/special-circumstances-guidelines