About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Suspect PE in any patient with acute dyspnoea, pleuritic chest pain, or haemoptysis — especially with VTE risk factors
- Two-level Wells score: ≤4 = unlikely → D-dimer; >4 = likely → CTPA
- D-dimer: highly sensitive but poorly specific — useful to rule OUT PE when clinical probability is low
- CTPA is the gold-standard imaging investigation for PE
- Treatment: DOAC (apixaban or rivaroxaban) first-line; LMWH bridging to warfarin as alternative
- Massive PE with haemodynamic instability → IV thrombolysis (alteplase) or surgical embolectomy
Overview
Pulmonary embolism occurs when a thrombus — usually originating from the deep veins of the lower limbs or pelvis — embolises to the pulmonary vasculature. The resulting obstruction increases pulmonary vascular resistance, leading to right ventricular strain and impaired gas exchange. PE exists on a clinical spectrum: small subsegmental emboli may be asymptomatic, while massive PE obstructing >50% of the pulmonary vasculature can cause cardiovascular collapse and cardiac arrest. PE and DVT together constitute venous thromboembolism (VTE).
Epidemiology
VTE affects approximately 1 in 1,000 adults per year in the UK, with PE accounting for roughly one-third of presentations. PE is the third most common cardiovascular cause of death after MI and stroke, responsible for an estimated 25,000–30,000 deaths annually in the UK. Virchow triad: stasis (immobilisation, long-haul travel), endothelial injury (surgery, trauma), and hypercoagulability (malignancy, combined oral contraceptive, pregnancy, thrombophilia). The case fatality rate for untreated PE approaches 30% but falls to <5% with appropriate anticoagulation.
Clinical Features
Symptoms
Acute-onset dyspnoea — the commonest symptom
Pleuritic chest pain
Haemoptysis (usually small volume)
Cough
Syncope or presyncope (suggests massive PE)
Leg swelling/pain (concurrent DVT in ~70%)
Signs
Tachycardia — often the earliest and most consistent sign
Tachypnoea
Hypoxia (may have normal SpO₂ in small PE)
Low-grade fever
Signs of DVT: unilateral leg swelling, warmth, pitting oedema
Hypotension (systolic <90 mmHg) — massive PE
Raised JVP, RV heave — acute right heart strain
Cardiovascular collapse / PEA cardiac arrest
Investigations
First-line
Two-level Wells scoreClinical probability assessment: ≤4 = PE unlikely → request D-dimer; >4 = PE likely → proceed to CTPA
D-dimerOnly if Wells ≤4. Negative D-dimer effectively rules out PE (high sensitivity, ~95% NPV). Raised in infection, malignancy, pregnancy, post-op
ABGHypoxia, hypocapnia (hyperventilation), raised A-a gradient. May be normal in small PE
Second-line
CTPAGold standard investigation — directly visualises thrombus in pulmonary arteries. Sensitivity and specificity >95%
ECGSinus tachycardia (commonest), S1Q3T3 (classic but uncommon), right axis deviation, RBBB, T-wave inversion in V1–V4 (RV strain)
CXROften normal. May show wedge-shaped opacity (Hampton hump), oligaemia (Westermark sign), or small pleural effusion
BloodsFBC, U&Es, coagulation screen, troponin and BNP (risk stratification)
Specialist
V/Q scanAlternative to CTPA if contrast allergy, severe renal impairment, or pregnancy (lower radiation dose to breast tissue)
EchocardiogramRV dilatation, McConnell sign (RV free wall akinesia with apical sparing), raised PASP — useful in massive PE at bedside
Lower limb Doppler USSConfirms DVT source — may guide management if CTPA unavailable
1
Immediate (if PE likely, Wells >4)
- Start anticoagulation immediately while awaiting CTPA — do not delay treatment for imaging
- Apixaban or rivaroxaban (DOACs) are first-line — can be started immediately without LMWH bridge
- Alternative: LMWH (e.g. dalteparin/enoxaparin) as bridge to warfarin if DOAC contraindicated
- Oxygen to maintain SpO₂ ≥94%
2
Submassive PE (RV dysfunction without hypotension)
- Anticoagulation as above
- Risk stratify with troponin, BNP, and echocardiogram
- Close monitoring — may deteriorate to massive PE
- Consider thrombolysis only if clinical deterioration
3
Massive PE (haemodynamic instability)
- IV unfractionated heparin bolus
- Systemic thrombolysis: alteplase 50 mg IV bolus (or 100 mg over 2 h)
- If thrombolysis contraindicated or failed: surgical embolectomy or catheter-directed therapy
- IV fluids (cautious — RV is preload-dependent but overloading worsens RV distension)
- Cardiac arrest with suspected PE: give alteplase 50 mg bolus and continue CPR for ≥60 min
4
Duration of anticoagulation
- Provoked PE (clear transient risk factor e.g. surgery, immobilisation): 3 months
- Unprovoked PE: ≥3 months, then assess bleeding risk — consider indefinite anticoagulation
- Recurrent VTE: indefinite anticoagulation
- Cancer-associated PE: DOAC (apixaban/edoxaban) or LMWH for ≥6 months; continue while cancer active
Complications
- Cardiovascular collapse: Massive PE — obstructive shock from acute RV failure
- Death: Untreated PE mortality ~30%; treated <5%
- Chronic thromboembolic pulmonary hypertension (CTEPH): 2–4% develop persistent pulmonary hypertension post-PE — presents with progressive dyspnoea months later
- Recurrent VTE: ~10% recurrence at 1 year if unprovoked and anticoagulation stopped
- Post-PE syndrome: Persistent exercise intolerance and dyspnoea despite clot resolution
- Pulmonary infarction: Haemorrhagic infarction → pleuritic pain, haemoptysis, pleural effusion
UKMLA Exam Tips
- 1Wells ≤4 → D-dimer → if negative, PE ruled out. Wells >4 → straight to CTPA. Know this algorithm
- 2S1Q3T3 on ECG is classic but uncommon — sinus tachycardia is the most common ECG finding in PE
- 3DOACs (apixaban, rivaroxaban) are first-line — they do NOT need LMWH bridging. Warfarin does
- 4Massive PE with arrest: give alteplase 50 mg bolus and continue CPR for at least 60 minutes
- 5In pregnancy: LMWH is the anticoagulant of choice (DOACs and warfarin are contraindicated)
- 6If the question mentions a young woman on COCP with acute dyspnoea and pleuritic chest pain → think PE first, not pneumonia
- 7CTEPH: suspect if persistent dyspnoea 3–6 months post-PE despite anticoagulation → refer for V/Q scan and specialist assessment
practicetest your knowledge on pulmonary embolismApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — respiratory and beyond.
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