Pulmonary embolism is among the highest-yield acute presentations in UK exams because it tests a structured diagnostic pathway — probability scoring, D-dimer and imaging — and a clear treatment hierarchy. This guide covers the essentials to the current NICE standard (NG158). Follow current guidance and local protocols in practice; this reflects NICE guidance as of mid-2026.
What PE is
A pulmonary embolism is occlusion of the pulmonary arterial circulation, usually by a thrombus embolising from a deep vein thrombosis in the legs or pelvis — the two are a single condition, venous thromboembolism. The consequences range from a small, almost silent embolus to a massive PE causing right ventricular strain, obstructive shock and sudden death. The clinical spectrum is graded by haemodynamic effect: a low-risk PE with a normal blood pressure and no right heart strain, an intermediate-risk PE with right ventricular dysfunction or raised cardiac biomarkers but a stable blood pressure, and a high-risk (massive) PE with hypotension or shock — a distinction that directly determines whether thrombolysis is considered.
Presentation
Examiners reward awareness that PE is a great mimic. Typical features are pleuritic chest pain, breathlessness, tachycardia and tachypnoea, sometimes with haemoptysis, signs of a deep vein thrombosis, or syncope. A massive PE presents with hypotension and signs of right heart strain. The ECG most often shows sinus tachycardia; the classic S1Q3T3 pattern is uncommon, and its absence means nothing. Risk factors — recent surgery or immobility, malignancy, pregnancy and the postpartum period, oestrogen-containing contraception, long-haul travel and previous venous thromboembolism — are heavily tested. A useful framing is Virchow's triad — venous stasis, endothelial injury and hypercoagulability — which underlies almost every risk factor and is itself a common exam question.
The diagnostic pathway
This is the crux of PE questions, and NICE structures it clearly. Start with the two-level Wells score for PE.
- If PE is "likely" (Wells above 4 points): arrange an immediate CT pulmonary angiogram (CTPA), giving interim anticoagulation if there will be a delay.
- If PE is "unlikely" (Wells 4 points or fewer): measure a D-dimer, and proceed to CTPA only if it is positive; a negative D-dimer effectively excludes PE in this group.
Two refinements are examinable: an age-adjusted D-dimer threshold improves specificity in patients aged 50 and over, reducing unnecessary scans; and the Pulmonary Embolism Rule-out Criteria (PERC) can support ruling out PE in younger, low-probability patients. CTPA is the gold-standard confirmatory test; a ventilation–perfusion (V/Q) scan is the alternative where CTPA is unsuitable, such as significant renal impairment, contrast allergy, or pregnancy. In pregnancy the pathway differs: D-dimer is unreliable, so imaging is used — a chest X-ray first, then a V/Q scan or CTPA depending on the findings and local protocol — and this is a recognised exam scenario.
Management to the NICE standard
Anticoagulation is the foundation. A direct-acting oral anticoagulant — apixaban or rivaroxaban — is first-line for most patients, including as interim treatment while awaiting confirmation. Dabigatran and edoxaban are options after initial low-molecular-weight heparin. Treatment continues for at least three months, with the duration beyond that depending on whether the PE was provoked or unprovoked and on the bleeding risk. A provoked PE with a transient risk factor is typically treated for three months, while an unprovoked PE often warrants longer or indefinite anticoagulation after weighing the bleeding risk.
The key escalation is the unstable patient: systemic thrombolysis is considered for PE with haemodynamic instability (a massive PE). Conversely, NICE specifically advises against systemic thrombolysis in haemodynamically stable PE, even where there is right ventricular dysfunction. Selected low-risk patients can be managed as outpatients using a validated risk tool, and an inferior vena cava filter is reserved for those in whom anticoagulation is contraindicated. In specific groups the choice of anticoagulant changes: people with antiphospholipid syndrome are usually treated with warfarin rather than a DOAC, those with active cancer with a DOAC or low-molecular-weight heparin, and pregnant women with low-molecular-weight heparin, since DOACs are avoided in pregnancy.
High-yield exam points and traps
- The pathway hinges on the Wells score: "likely" goes straight to CTPA; "unlikely" gets a D-dimer first.
- A negative D-dimer only helps in the low-probability group — never use it to exclude PE in a "likely" patient.
- Use an age-adjusted D-dimer in those over 50 to avoid unnecessary scans.
- Thrombolysis is for haemodynamically unstable (massive) PE only — not for stable PE with right heart strain.
- DOACs (apixaban or rivaroxaban) are first-line; warfarin and low-molecular-weight heparin are reserved for specific situations such as antiphospholipid syndrome or pregnancy.
- A normal ECG or absent S1Q3T3 does not exclude PE; sinus tachycardia is the commonest finding.
- Other ECG signs such as right axis deviation or right bundle branch block reflect right heart strain but are neither sensitive nor specific.
A few common questions
How is PE diagnosed? Using the two-level Wells score: if PE is likely, proceed to CTPA; if unlikely, check a D-dimer and image only if positive. CTPA is the gold-standard test.
Which anticoagulant is first-line for PE? A direct-acting oral anticoagulant — apixaban or rivaroxaban — for most patients, including as interim treatment while awaiting confirmation.
When is thrombolysis used in PE? For PE with haemodynamic instability (massive PE); it is not recommended for haemodynamically stable PE, even with right ventricular dysfunction — that intermediate-risk group is anticoagulated and monitored closely instead.
What is an age-adjusted D-dimer? A higher D-dimer threshold for patients aged 50 and over, which reduces unnecessary CTPA scans while remaining safe; it is calculated as the age multiplied by ten micrograms per litre.
Does a normal ECG rule out PE? No — the commonest ECG finding is sinus tachycardia, and the classic S1Q3T3 pattern is uncommon, so a normal or non-specific ECG does not exclude PE. Clinical probability, not the ECG, drives the diagnostic pathway.
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