Pulmonary Embolism

Pulmonary embolism (PE) is the obstruction of the pulmonary arterial tree, usually by a thrombus that has embolised from the deep veins of the legs or pelvis. It is the most lethal manifestation of venous thromboembolism (VTE) and a perennial favourite in NEET PG because it blends physiology, ECG, imaging, risk-scoring and emergency management into high-yield clinical vignettes.

Definition & classification

PE is the lodgement of embolic material (thrombus, fat, air, amniotic fluid, tumour, septic vegetation) within the pulmonary arteries. The commonest cause by far is thromboembolism arising from a deep vein thrombosis (DVT) of the lower limb — hence PE and DVT are two ends of the single disease spectrum VTE.

Classification is clinically driven and dictates therapy:

Category	Haemodynamics	RV dysfunction / biomarkers	30-day mortality
Massive (high-risk)	Sustained hypotension (SBP <90 mmHg ≥15 min, or drop ≥40 mmHg), or need for inotropes/arrest	Present	>15%
Submassive (intermediate-risk)	Normotensive	RV strain on echo/CT and/or raised troponin/BNP	3–15%
Low-risk	Normotensive	No RV dysfunction, normal biomarkers	<1%

High-yield: The dividing line between massive and submassive is systemic hypotension, NOT the size of the clot on imaging. A "saddle embolus" that is haemodynamically stable is still classified as submassive, not massive.

Anatomical terms also appear in exams: a saddle embolus straddles the bifurcation of the main pulmonary artery.

Etiology & risk factors — Virchow's triad

All causes of VTE can be mapped onto Virchow's triad, a guaranteed exam favourite:

1. Venous stasis → immobilisation, long-haul flights ("economy-class syndrome"), bed rest, surgery, plaster casts, paralysis.
2. Endothelial injury → trauma, surgery, central venous catheters, prior DVT.
3. Hypercoagulability → inherited and acquired thrombophilias.

Inherited thrombophilia	Key point
Factor V Leiden	Commonest inherited cause; resistance to activated protein C
Prothrombin G20210A	Second commonest
Protein C deficiency	Risk of warfarin-induced skin necrosis
Protein S deficiency	—
Antithrombin III deficiency	Most thrombogenic; heparin resistance

Acquired risk factors: malignancy (Trousseau syndrome — migratory thrombophlebitis, classically pancreatic Ca), antiphospholipid antibody syndrome, pregnancy and puerperium, oestrogen (OCPs, HRT), nephrotic syndrome, obesity, smoking, prior VTE.

High-yield: The single most common identifiable cause of PE is DVT of the proximal lower-limb veins (iliofemoral/popliteal). Distal calf-vein thrombi rarely embolise unless they propagate proximally.

Pathophysiology

Embolic obstruction produces a cascade:

Clot lodges in pulmonary artery → increased pulmonary vascular resistance (PVR) → RV afterload rises → RV dilatation & dysfunction → interventricular septum bows into LV → reduced LV preload → fall in cardiac output → systemic hypotension → coronary hypoperfusion of the already-strained RV → RV ischaemia → cardiogenic shock/death.

Two parallel respiratory consequences:

• Increased dead space (ventilated but not perfused alveoli) → V/Q mismatch.
• Hypoxaemia from V/Q mismatch, right-to-left shunting and low mixed-venous oxygen.
• Reflex hyperventilation → respiratory alkalosis with hypocapnia (the classic ABG: low PaO₂, low PaCO₂, raised A–a gradient).

Pulmonary infarction is actually uncommon (~10%) because the lung has a dual blood supply (pulmonary + bronchial arteries); when it occurs it tends to be peripheral and causes pleuritic pain and haemoptysis.

Clinical features

PE is the "great masquerader". Presentations range from asymptomatic to sudden death.

• Dyspnoea (most common symptom) — typically acute in onset.
• Pleuritic chest pain — suggests peripheral/infarction.
• Tachypnoea (most common sign) and tachycardia.
• Haemoptysis, syncope (suggests large/central PE), apprehension.
• Signs of DVT: unilateral calf swelling, tenderness, Homans sign (low sensitivity/specificity).
• Massive PE: hypotension, raised JVP, loud P2, RV heave, gallop, cyanosis, cardiac arrest (often pulseless electrical activity).

High-yield: Tachypnoea is the commonest physical sign; dyspnoea is the commonest symptom; syncope and hypotension indicate a large central (often haemodynamically significant) embolus.

Diagnosis — risk stratify first

The diagnostic pathway hinges on pre-test probability, assessed with a validated score. The Wells score is the most examined.

Wells score for PE

Criterion	Points
Clinical signs/symptoms of DVT	3.0
PE is the most likely diagnosis	3.0
Heart rate >100/min	1.5
Immobilisation ≥3 days or surgery in last 4 weeks	1.5
Previous DVT/PE	1.5
Haemoptysis	1.0
Malignancy (treated within 6 months)	1.0

Three-tier: ≤1 low, 2–6 moderate, >6 high. Two-tier (dichotomised): ≤4 = "PE unlikely"; >4 = "PE likely".

High-yield: Mnemonic for Wells — think "the patient who is THrombosed". The two 3-point items (clinical DVT, PE most likely) carry the most weight.

D-dimer

• A degradation product of cross-linked fibrin; highly sensitive, poorly specific.
• Use: in low/moderate pre-test probability, a normal D-dimer reliably rules out PE (high negative predictive value).
• A raised D-dimer is non-specific (sepsis, malignancy, pregnancy, post-op, age) and never confirms PE.
• Do NOT order D-dimer in high pre-test probability — proceed straight to imaging.
• Age-adjusted cut-off (for patients >50 yr) = age × 10 µg/L improves specificity.

Investigation of choice / gold standard

Test	Role
CT pulmonary angiography (CTPA)	Investigation of choice & practical gold standard; shows filling defects, allows alternative diagnosis
V/Q (ventilation–perfusion) scan	Preferred when contrast/radiation contraindicated — pregnancy, renal failure, contrast allergy; shows mismatched defects
Conventional pulmonary angiography	Historic gold standard; now rarely used (invasive)
Compression USG lower limbs	Detects the source DVT; useful when CT contraindicated
Echocardiography	Bedside in unstable patient — RV dilatation, McConnell sign, septal flattening

High-yield: CTPA = investigation of choice. In pregnancy with a positive leg Doppler, treat without irradiating; if imaging needed, V/Q (or perfusion-only) scan is preferred over CTPA to reduce breast radiation. CTPA is contraindicated in significant renal impairment / contrast allergy.

Supportive (non-diagnostic) investigations

• ECG — most common finding is sinus tachycardia. The classic but uncommon pattern is S1Q3T3 (S wave in lead I, Q wave and inverted T in lead III) signifying acute RV strain. Other clues: T-wave inversion in V1–V4, new RBBB, right-axis deviation, P pulmonale, atrial fibrillation.
• CXR — usually normal; useful to exclude mimics. Named signs (rare): Hampton hump (peripheral wedge-shaped pleural-based opacity from infarction), Westermark sign (regional oligaemia/avascularity), Fleischner sign (enlarged pulmonary artery), Palla sign.
• ABG — hypoxaemia, hypocapnia, respiratory alkalosis, raised A–a gradient (a normal ABG does not exclude PE).
• Troponin & BNP/NT-proBNP — elevated values mark RV strain and reclassify a normotensive patient into the intermediate-risk group; prognostic, not diagnostic.

High-yield: Remember the three eponymous CXR signs — Hampton hump = infarction, Westermark = oligaemia, Fleischner = enlarged PA. And McConnell sign on echo = RV free-wall akinesia with apical sparing (relatively specific for acute PE).

Stepwise diagnostic approach

1. Assess pre-test probability with Wells.
2. Unstable patient → bedside echo (RV strain) → if positive and CTPA not feasible, treat as PE / consider thrombolysis. If stable enough → CTPA.
3. Stable, PE unlikely (Wells ≤4) → D-dimer → normal: PE excluded; raised: → CTPA.
4. Stable, PE likely (Wells >4) → CTPA directly (skip D-dimer).
5. Contrast/radiation contraindicated → V/Q scan ± leg Doppler.

The PERC rule (Pulmonary Embolism Rule-out Criteria) can exclude PE without even a D-dimer in very-low-probability patients if all 8 criteria are negative (age <50, HR <100, SpO₂ ≥95%, no haemoptysis, no oestrogen, no prior VTE, no recent surgery/trauma, no unilateral leg swelling).

Management

General / supportive

Oxygen, analgesia, IV fluids cautiously (over-filling worsens RV dysfunction — small boluses ~500 mL), vasopressors (noradrenaline preferred) for shock.

Anticoagulation — the backbone for all confirmed PE

Drug class	Examples	Notes
LMWH	Enoxaparin, dalteparin	First-line parenteral; drug of choice in cancer-associated VTE and pregnancy
Fondaparinux	—	Used in heparin-induced thrombocytopenia (HIT)
UFH	Unfractionated heparin	Preferred when thrombolysis likely, severe renal failure, or haemodynamic instability (short half-life, reversible)
DOACs	Rivaroxaban, apixaban (no lead-in), dabigatran, edoxaban (need heparin lead-in)	First-line oral in most haemodynamically stable patients
Warfarin (VKA)	Target INR 2–3	Overlap with heparin ≥5 days until INR therapeutic for 2 days

High-yield: In stable PE, start anticoagulation immediately — DOACs (rivaroxaban/apixaban) are first-line. In cancer-associated VTE, LMWH or edoxaban/rivaroxaban; in pregnancy, LMWH (warfarin and DOACs are teratogenic/contraindicated). UFH is preferred when you anticipate thrombolysis or in renal failure.

Duration: provoked PE (transient risk factor) → 3 months; unprovoked or recurrent or ongoing risk (cancer, thrombophilia) → extended/indefinite.

Reperfusion — thrombolysis

High-yield: Thrombolysis is indicated in MASSIVE (high-risk) PE — i.e. PE with haemodynamic instability/hypotension, provided no contraindication. The agent of choice is alteplase (tPA) 100 mg IV over 2 hours.

• In submassive PE, thrombolysis is not routine; consider only if there is haemodynamic deterioration ("rescue thrombolysis") — weigh against bleeding risk.
• Absolute contraindications: prior intracranial haemorrhage, known intracranial neoplasm/AVM, ischaemic stroke <3 months, active bleeding, recent significant closed head/spinal trauma or surgery.
• Catheter-directed thrombolysis delivers lower-dose lytic locally — useful when systemic lysis is risky.
• Surgical embolectomy — for massive PE with contraindication to or failure of thrombolysis.

IVC filter

High-yield: IVC filter is indicated when anticoagulation is contraindicated (e.g. active bleeding) or fails despite adequate therapy (recurrent PE on full anticoagulation). It prevents propagation of leg clot to lungs but does NOT treat existing PE and does not replace anticoagulation once safe.

Risk-adapted summary flow

Confirm PE → assess haemodynamics → Stable + low-risk: anticoagulate (DOAC), consider outpatient (PESI/sPESI low) → Stable + intermediate: admit, anticoagulate, monitor, rescue thrombolysis if deteriorates → Unstable (massive): thrombolysis (alteplase) → embolectomy if lysis contraindicated/fails.

The PESI / simplified PESI (sPESI) score predicts 30-day mortality and identifies low-risk patients suitable for early discharge/outpatient management.

Complications

• Acute: cardiogenic shock, RV failure, sudden death (often PEA arrest), pulmonary infarction, arrhythmias.
• Recurrent VTE.
• Chronic thromboembolic pulmonary hypertension (CTEPH) — develops in ~2–4% of survivors; persistent dyspnoea months after PE; diagnosed by V/Q scan (screening test of choice) and confirmed by pulmonary angiography; treated definitively by pulmonary thromboendarterectomy (± riociguat).
• Bleeding from anticoagulation/thrombolysis; HIT from heparin.

High-yield: Persistent breathlessness and pulmonary hypertension months after a PE = CTEPH; screen with V/Q scan (more sensitive than CTPA here), treat with pulmonary endarterectomy.

Key differentials

• Acute coronary syndrome / MI — overlapping chest pain, troponin rise; ECG and CTPA differentiate.
• Aortic dissection — tearing pain, BP differential, widened mediastinum.
• Pneumonia / pleurisy — fever, consolidation, productive cough.
• Pneumothorax — sudden dyspnoea, absent breath sounds, hyper-resonance.
• Pericardial tamponade — Beck triad, pulsus paradoxus.
• Heart failure exacerbation, anxiety/hyperventilation, costochondritis, musculoskeletal pain.

Special situations

• Pregnancy: leading cause of maternal mortality in the developed world; LMWH for treatment; V/Q (perfusion) scan preferred imaging.
• Fat embolism: 24–72 h after long-bone fracture; triad of dyspnoea, petechiae (axilla/conjunctiva) and altered mentation; treatment supportive.
• Amniotic fluid embolism: peripartum cardiovascular collapse, DIC.
• Air embolism: central line manipulation; treat in left lateral Durant position, head down.
• Septic embolism: IV drug use, right-sided endocarditis (tricuspid, S. aureus).

Recently asked / exam angle

NEET PG and INI-CET vignettes cluster around predictable hooks:

• A post-operative or post-partum patient with sudden dyspnoea + tachycardia + hypoxia → "next best investigation?" Answer pathways: D-dimer if low probability, CTPA if high.
• ECG showing S1Q3T3 → diagnosis = acute PE / RV strain (but remember sinus tachycardia is commonest).
• CXR sign matching — Hampton hump (infarct), Westermark (oligaemia), Fleischner (enlarged PA).
• Investigation of choice = CTPA; gold standard (historic) = conventional pulmonary angiography; best in pregnancy/renal failure = V/Q scan.
• Thrombolysis indication = massive (hypotensive) PE; drug = alteplase.
• Cancer-associated VTE drug of choice = LMWH (or specific DOACs).
• IVC filter indication = anticoagulation contraindicated or failed.
• Virchow triad components and Factor V Leiden as commonest inherited thrombophilia.
• McConnell sign on echo as a relatively specific finding.
• ABG pattern: hypoxaemia + hypocapnia + respiratory alkalosis + raised A–a gradient.

Rapid revision

1. Virchow triad = stasis + endothelial injury + hypercoagulability; commonest source = proximal lower-limb DVT.
2. Commonest symptom = dyspnoea; commonest sign = tachypnoea; commonest ECG = sinus tachycardia.
3. Classic ECG pattern = S1Q3T3; also T-inversion V1–V4 and new RBBB.
4. Wells >4 → straight to CTPA; Wells ≤4 → D-dimer first.
5. D-dimer = sensitive, non-specific; only used to rule out in low/moderate probability.
6. CTPA = investigation of choice; V/Q scan preferred in pregnancy/renal failure/contrast allergy.
7. CXR eponyms: Hampton hump (infarct), Westermark (oligaemia), Fleischner (enlarged PA).
8. Massive PE = hypotension → thrombolysis with alteplase (if no contraindication).
9. Stable PE → anticoagulate; DOACs (rivaroxaban/apixaban) first-line.
10. Cancer VTE → LMWH; pregnancy → LMWH (warfarin/DOAC contraindicated).
11. IVC filter when anticoagulation is contraindicated or has failed.
12. Long-term sequela = CTEPH → screen with V/Q scan → treat with pulmonary endarterectomy; Factor V Leiden is the commonest inherited thrombophilia.