Key Facts

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by material (usually thrombus) that has travelled from elsewhere in the body. It exists on a spectrum from small subsegmental PEs to massive saddle embolism causing cardiac arrest.

Epidemiology

• Annual incidence: ~60-70 per 100,000 population
• ~25,000 deaths per year in the UK attributed to VTE
• Leading cause of preventable hospital death
• Accounts for ~10% of in-hospital deaths
• Third most common cardiovascular cause of death after MI and stroke

Aetiology

Virchow's triad:

• Stasis: immobility (surgery, long-haul travel, bed rest), pregnancy
• Endothelial injury: surgery, trauma, central venous catheters
• Hypercoagulability: malignancy, thrombophilia (Factor V Leiden, prothrombin gene mutation, antiphospholipid syndrome), OCP/HRT, pregnancy, nephrotic syndrome

Pathophysiology

• Thrombus (usually from ileofemoral DVT) embolises to pulmonary arteries
• Obstruction increases pulmonary vascular resistance → right ventricular pressure overload
• RV dilation → interventricular septum shift → impaired LV filling → reduced cardiac output
• V/Q mismatch → hypoxaemia
• Massive PE: acute RV failure → cardiogenic shock → cardiac arrest
• Release of vasoactive mediators (serotonin, thromboxane) causes additional vasoconstriction

Typical Presentation

• Acute onset breathlessness (most common symptom)
• Pleuritic chest pain
• Haemoptysis
• Tachycardia, tachypnoea
• Often with identifiable risk factor

Massive PE

• Cardiovascular collapse: hypotension (SBP <90 mmHg), syncope
• Signs of acute RV failure: raised JVP, RV heave, loud P2
• Cyanosis
• Cardiac arrest (PEA most common rhythm)

Submassive PE

• Haemodynamically stable but with RV dysfunction on echo/CT
• Elevated troponin and/or BNP

Small/Subsegmental PE

• May be asymptomatic or mild dyspnoea only
• Incidental finding on CT

Red Flags

• Haemodynamic instability (massive PE)
• Syncope
• New-onset AF
• Signs of RV strain
• Cardiac arrest in context of VTE risk factors
• Pregnancy (PE is leading cause of direct maternal death)

Bedside

• Two-level Wells score: calculate before investigation
  • PE likely (>4): proceed to CTPA
  • PE unlikely (≤4): check D-dimer first
• ECG: sinus tachycardia (most common), S1Q3T3 (classic but uncommon), right axis deviation, RBBB, T-wave inversion V1-V4, AF
• ABG: hypoxaemia, hypocapnia (type 1 respiratory failure), raised A-a gradient
• Pulse oximetry: hypoxia

Bloods

• D-dimer: if Wells ≤4; negative D-dimer effectively excludes PE (high sensitivity, low specificity)
• Troponin: elevated in submassive/massive PE (RV strain)
• BNP/NT-proBNP: RV dysfunction marker, prognostic
• FBC, U&Es, coagulation screen: baseline
• Thrombophilia screen: if unprovoked PE (defer until 3 months after anticoagulation)

Imaging

• CTPA: gold standard; sensitivity >95%, specificity >95%
• V/Q scan: if CTPA contraindicated (contrast allergy, severe renal impairment, pregnancy — lower radiation dose to breast tissue)
• Echocardiography: RV dilation, McConnell sign (RV free wall hypokinesis with apical sparing), interventricular septum bowing
• Compression duplex USS legs: if DVT suspected concurrently
• CXR: often normal; may show Westermark sign (oligaemia), Hampton hump (wedge-shaped opacity), effusion, atelectasis

Special Tests

• RV/LV ratio on CT: >0.9 indicates RV strain
• CT lower limb venography: can be combined with CTPA
• Pulmonary angiography: rarely needed; historical gold standard

Non-pharmacological

• Haemodynamic support: IV fluids (cautious — avoid RV overload), vasopressors (noradrenaline) if needed
• Supplemental oxygen (target SpO₂ 94-98%)
• Early mobilisation (for stable PE)

Pharmacological

Anticoagulation (NICE NG158):

• Start treatment-dose anticoagulation immediately if clinical suspicion is high (don't wait for CTPA)

First-line (non-massive):

• Apixaban: 10mg BD for 7 days, then 5mg BD
• Or rivaroxaban: 15mg BD for 21 days, then 20mg OD
• Alternative: LMWH (e.g. enoxaparin 1.5mg/kg OD or 1mg/kg BD) for ≥5 days → warfarin (target INR 2-3)

Duration:

• Provoked PE (identifiable transient risk factor): 3 months
• Unprovoked PE: 6 months minimum, consider lifelong if low bleeding risk
• Recurrent VTE or strong thrombophilia: lifelong
• Cancer-associated: DOAC or LMWH; duration dependent on ongoing cancer treatment

Massive PE (haemodynamically unstable):

• Thrombolysis: alteplase 50mg IV bolus (cardiac arrest) or 100mg IV over 2 hours
• Followed by IV unfractionated heparin infusion
• Consider thrombolysis in cardiac arrest with suspected PE

Submassive PE (stable but RV dysfunction):

• Standard anticoagulation
• Close monitoring; some guidelines suggest considering thrombolysis if deteriorating

Surgical/Interventional

• Catheter-directed thrombolysis: massive PE where systemic thrombolysis contraindicated
• Surgical embolectomy: last resort for massive PE with failed thrombolysis
• IVC filter: if anticoagulation absolutely contraindicated (temporary, retrieve when possible)

Referral Criteria

• Massive PE: immediate ICU/critical care
• Ambulatory PE management: consider for low-risk PE (PESI class I-II) with appropriate follow-up
• Haematology: unprovoked PE for thrombophilia screening
• Oncology screening: consider occult malignancy in unprovoked PE

• Untreated PE mortality: ~30%
• Treated PE mortality: ~2-8% (depending on severity)
• Massive PE mortality: ~15-25% (even with treatment); ~65% if cardiac arrest
• Submassive PE: ~3-5% mortality
• VTE recurrence: ~5% per year while anticoagulated; ~10% per year after stopping
• Chronic thromboembolic pulmonary hypertension (CTEPH) develops in 2-4% of PE survivors
• Post-PE syndrome: persistent dyspnoea and exercise limitation in ~50%
• Early anticoagulation dramatically improves survival

Two-Level Wells Score for PE

PESI Score (Prognostic)

Classic ECG Findings in PE