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Pulmonary Embolism (PE)

Clinical Subject Page

Pulmonary Embolism (PE)

ICD-10

I26.99

Specialty

Cardiology

Onset

Acute

Reviewed

June 2026

On This Page

Overview

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries, usually by a thrombus originating from a deep vein thrombosis (DVT), leading to impaired pulmonary blood flow and impaired gas exchange.

Etiology & Risk Factors

  • Etiology of Pulmonary Embolism (PE)

    • Deep vein thrombosis (most common)
    • Surgery (especially orthopedic)
    • Trauma
    • Malignancy
    • Pregnancy/postpartum
    • Prolonged immobilization
    • Inherited thrombophilia
    • Estrogen therapy (OCP/HRT)
    • Previous VTE

    Risk Factors for Pulmonary Embolism (PE)

    • Previous DVT/PE
    • Active cancer
    • Recent surgery
    • Hospitalization
    • Long-distance travel
    • Obesity
    • Smoking
    • Heart failure
    • Pregnancy
    • Increasing age

Pathophysiology

      1. A blood clot forms in a deep vein of the leg or pelvis (DVT).
      2. The clot breaks off and travels through the inferior vena cava (IVC) to the pulmonary arteries.
      3. The clot blocks blood flow to part of the lung.
      4. This causes:
        • Less oxygen enters the blood (hypoxemia) because blood cannot reach ventilated alveoli (V/Q mismatch).
        • Chest pain and hemoptysis if lung tissue becomes infarcted.
      5. The blockage also increases pressure in the pulmonary arteries, making the right ventricle work harder.
      6. In a large (massive) PE, the right ventricle can fail, causing:
        • Low blood pressure
        • Shock
        • Collapse

      Flow Chart

      DVT → Clot travels to lungs → Pulmonary artery blockage → V/Q mismatch → Hypoxemia + Increased right heart workload → Right ventricular failure (if severe) → Shock

Clinical Presentation

  1. Symptoms

    • Sudden dyspnea
    • Pleuritic chest pain
    • Cough
    • Hemoptysis
    • Syncope
    • Palpitations
    • Anxiety

    Signs

    • Tachypnea
    • Tachycardia
    • Hypoxemia
    • Fever (low-grade)
    • Elevated JVP (massive PE)
    • Hypotension (massive PE)
    • Signs of DVT

History Taking

  • Key Questions

    • Sudden onset of shortness of breath?
    • Chest pain (pleuritic)?
    • Hemoptysis?
    • Leg swelling or pain?
    • Recent surgery or hospitalization?
    • Long travel or immobilization?
    • Previous DVT or PE?
    • Cancer history?
    • Pregnancy or OCP use?

    Red Flags for Pulmonary Embolism (PE)

    • Hypotension
    • Syncope
    • Severe hypoxemia
    • Cardiac arrest
    • Massive hemoptysis

Classification

Pulmonary Embolism · Classification

PE IS CLASSIFIED BY ANATOMICAL LOCATION, TIMING, AND HAEMODYNAMIC RISK Risk classification (ESC) is the most clinically relevant system — it directly determines management (thrombolysis vs anticoagulation alone vs outpatient treatment) and is based on haemodynamic stability, RV dysfunction, and biomarkers, not clot burden alone.
ESC Risk Classification
High
High-Risk (Massive)
Haemodynamic instability — sustained hypotension (SBP <90 mmHg or drop ≥40 mmHg), cardiogenic shock, or cardiac arrest. Mortality >15%.
Immediate threat to life
Int
Intermediate-Risk (Submassive)
Haemodynamically stable but with RV dysfunction (echo/CT) and/or elevated biomarkers (troponin, BNP). Subdivided into intermediate-high and intermediate-low.
Mortality 3–15%
Low
Low-Risk
Stable, no RV dysfunction, normal biomarkers, low PESI/sPESI score. Often suitable for outpatient anticoagulation.
Mortality <1%
Classification Basis Categories
By Haemodynamic Risk (ESC) High-risk (massive) Intermediate-risk (submassive) Low-risk
By Timing of Presentation Acute (symptoms develop immediately) vs Chronic (CTEPH — persistent perfusion defects ≥3 months post-PE)
By Anatomical Location Saddle embolus (straddles main PA bifurcation) — Lobar — Segmental — Subsegmental
By Source/Provoking Factor Provoked (surgery, immobilisation, malignancy, hormones) vs Unprovoked (no identifiable transient risk factor — longer anticoagulation typically considered)
By Recurrence First episode vs Recurrent PE — influences duration/intensity of anticoagulation
Management by Risk Category
High-risk — systemic thrombolysis (alteplase) or catheter-directed therapy; surgical embolectomy if thrombolysis contraindicated
Intermediate-high risk — anticoagulation + close monitoring; consider rescue thrombolysis if deteriorating
Intermediate-low risk — standard anticoagulation, inpatient monitoring
Low-risk — standard anticoagulation; many suitable for early discharge/outpatient management
PESI / sPESI Risk Scoring
PESI — Pulmonary Embolism Severity Index; estimates 30-day mortality using age, sex, comorbidities, vitals, mental status, SpO2
sPESI — simplified version; 1 point each for age >80, cancer, chronic cardiopulmonary disease, HR ≥110, SBP <100, SpO2 <90%
sPESI = 0 — low risk, may be suitable for outpatient management
sPESI ≥1 — higher risk, generally admit for monitoring

Investigations Approach

Pulmonary Embolism · Investigations by Haemodynamic Status

THE FIRST QUESTION IS ALWAYS: IS THE PATIENT HAEMODYNAMICALLY STABLE? This single branch point determines the entire diagnostic pathway. Unstable patients bypass scoring systems and D-dimer entirely — the priority is rapid confirmation and treatment, not stepwise risk stratification.
Suspected PE → Check vitals: SBP, HR, signs of shock/hypoperfusion
STABLE (SBP ≥90 mmHg)
1
Calculate Wells PE score(or revised Geneva score) to determine pre-test probability
2a
PE Unlikely (Wells ≤4)Send D-dimer (age-adjusted if >50 yrs). Negative → PE excluded, stop. Positive → proceed to CTPA.
2b
PE Likely (Wells >4)Skip D-dimer — proceed directly to CTPA (or V/Q scan if contrast contraindicated/pregnant).
3
Risk-stratify if confirmedTroponin, BNP, echo for RV strain, PESI/sPESI score → guides admission level & need for monitoring.
UNSTABLE (Shock / SBP <90 mmHg)
1
Resuscitate firstO2, IV access, cautious fluids, vasopressors if needed. Do NOT delay treatment for full workup.
2
Skip Wells score and D-dimer entirelyNo role for risk scoring in haemodynamic instability — treat as high-risk PE until proven otherwise.
3a
If stable enough to transport → urgent CTPAFastest definitive confirmation if patient can safely leave the resuscitation area.
3b
If too unstable to transport → bedside echoRV dilation/strain (D-sign, McConnell's sign) supports presumptive diagnosis → treat empirically.
4
Proceed to reperfusion therapySystemic thrombolysis, catheter-directed therapy, or surgical embolectomy — do not wait for full confirmation if imminent arrest.
Key Principles
Stability dictates speed, not just the test ordered — unstable patients need answers in minutes, not the standard stepwise pathway
D-dimer has no role in unstable patients — even if negative, would not change immediate management
Empirical treatment is acceptable in peri-arrest patients with strong clinical suspicion + supportive bedside echo, even without CTPA confirmation
Reassess stability continuously — a stable patient can decompensate mid-workup and require pathway switch
Imaging Choice Notes
CTPA — first-line definitive test in most patients; fast, widely available, also shows RV strain/alternative diagnoses
V/Q scan — alternative if contrast contraindicated (renal impairment, allergy) or in pregnancy (lower breast radiation dose)
Bedside (point-of-care) echo — not diagnostic of PE itself, but RV dysfunction in the right clinical context supports presumptive treatment when CTPA isn't feasible
Compression leg ultrasound — can support diagnosis indirectly by confirming DVT if CTPA unavailable/delayed

Diagnosis

      • 1. Clinical Assessment

        • Symptoms and signs
        • Assessment of risk factors
        • Estimate pretest probability using a clinical prediction rule (e.g., Wells score or Geneva score)

        2. D-dimer

        • Use in patients with low or intermediate clinical probability
        • A negative D-dimer can effectively exclude PE in appropriate patients

        3. CT Pulmonary Angiography (CTPA) — Gold Standard Imaging Test

        • First-line imaging test for most hemodynamically stable patients
        • Demonstrates filling defects within the pulmonary arteries

        4. Ventilation–Perfusion (V/Q) Scan

        Consider when:

        • CTPA is contraindicated
        • Severe contrast allergy
        • Pregnancy (selected patients)
        • Significant renal impairment

        5. Compression Ultrasonography of the Legs

        • Detects deep vein thrombosis (DVT)
        • Supports the diagnosis when CTPA cannot be performed

        6. Echocardiography

        Useful in:

        • Hemodynamically unstable patients
        • Suspected massive Pulmonary Embolism (PE)

        May show:

        • Right ventricular dilation or dysfunction
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Management

Initial Management

  • Oxygen therapy
  • Hemodynamic stabilization
  • Analgesia

Anticoagulation

  • Low-molecular-weight heparin
  • Unfractionated heparin
  • Direct oral anticoagulants (Apixaban, Rivaroxaban)
  • Warfarin (selected patients)

Reperfusion Therapy

  • Systemic thrombolysis (massive Pulmonary Embolism PE)
  • Catheter-directed thrombolysis
  • Surgical embolectomy

Additional Therapy

  • Inferior vena cava (IVC) filter (if anticoagulation is contraindicated)

Complications

    • Acute right ventricular failure
    • Cardiogenic shock
    • Cardiac arrest
    • Recurrent Pulmonary Embolism (PE)
    • Chronic thromboembolic pulmonary hypertension (CTEPH)
    • Death

Prognosis

  • Excellent with early diagnosis and anticoagulation.
  • Massive Pulmonary Embolism (PE) carries a high mortality if untreated.
  • Right ventricular dysfunction is the strongest predictor of poor outcome.

Key Points / Clinical Pearls

  • Most Pulmonary Embolisms (PE) originate from lower-extremity DVT.
  • CT pulmonary angiography is the diagnostic imaging modality of choice.
  • Use the Wells score to assess pretest probability.
  • Start anticoagulation promptly when PE is strongly suspected unless contraindicated.
  • Hemodynamic instability indicates high-risk (massive) Pulmonary Embolism (PE) and may require thrombolysis or embolectomy.
  • Chronic thromboembolic pulmonary hypertension is an important long-term complication.