Table of contents · 10 sections
In a nutshell. PE is the occlusion of the pulmonary artery by an embolus, most commonly originating from the deep veins of the lower extremities. The underlying mechanism is Virchow's triad: stasis, endothelial injury, and hypercoagulability. The key to diagnosis is clinical probability assessed via the Wells or Geneva score + D-dimer + CT pulmonary angiography. Treatment: anticoagulation for all, thrombolysis for high risk.
1. Definition and epidemiology
Pulmonary embolism (PE) is an acute occlusion of the main pulmonary artery trunk or its branches by a thrombus, predominantly dislodged from the deep veins of the lower extremities or pelvis. Together with deep vein thrombosis (DVT), PE constitutes a single clinical entity known as venous thromboembolism (VTE).
Incidence is 100–200 per 100,000 population per year; untreated mortality is 30%, dropping to 2–8% with timely therapy. Following an acute PE, 2–4% of patients develop chronic thromboembolic pulmonary hypertension (CTEPH).
2. Etiology and pathogenesis
Virchow's triad — the basis of thrombus formation
- Stasis: immobilization, long-haul flight, postoperative period.
- Endothelial injury: trauma, sepsis, catheters, chemotherapy.
- Hypercoagulability: hereditary thrombophilias (Factor V Leiden mutation, prothrombin G20210A mutation, antithrombin III, protein C/S deficiency), acquired conditions (malignancy, pregnancy, nephrotic syndrome, SLE with antiphospholipid syndrome).
VTE risk factors
- High: major surgery (orthopedic, oncological), trauma, active malignancy, prior VTE episode.
- Moderate: immobilization > 3 days, heart failure, pregnancy/postpartum period, estrogen-containing contraceptives.
- Low: long flights, obesity, varicose veins, age > 60 years.
3. Pathophysiology of hemodynamic disorders
Occlusion of > 30–50% of the pulmonary vascular bed → ↑ pulmonary vascular resistance → right ventricular (RV) overload. As RV pressure rises, it dilates, the interventricular septum shifts to the left, ↓ left ventricular filling → ↓ cardiac output → arterial hypotension, shock. Concurrently, hypoxemia develops due to ventilation-perfusion mismatch and shunting.
4. Clinical presentation
- Sudden dyspnea (the most frequent symptom, 75%).
- Pleuritic chest pain aggravated by inspiration.
- Cough, sometimes with hemoptysis (in pulmonary infarction).
- Tachycardia, tachypnea.
- In massive PE — syncope, arterial hypotension, shock, cyanosis.
- Signs of DVT: unilateral leg swelling, calf tenderness.
There are no pathognomonic symptoms; PE is referred to as the "great masquerader." The key is assessment of pretest probability.
5. Clinical probability scores
Wells Score
| Sign | Score |
|---|---|
| Clinical signs of DVT | 3,0 |
| Alternative diagnosis less likely than PE | 3,0 |
| Heart rate > 100 bpm | 1,5 |
| Immobilization or surgery within the past 4 weeks | 1,5 |
| Previous VTE episode | 1,5 |
| Hemoptysis | 1,0 |
| Active malignancy | 1,0 |
Two-tier interpretation (ESC 2019): PE unlikely ≤ 4, likely > 4. A three-tier version also exists: low (0–1), intermediate (2–6), high (≥ 7). Use the online calculator: Wells for PE.
Revised Geneva Score
An alternative, more objective scale (does not require "alternative diagnosis less likely"). Evaluates age > 65, previous VTE, surgery/fractures, heart rate, unilateral leg pain/swelling, hemoptysis, active malignancy.
6. Diagnostic algorithm
- Assess probability using the Wells/Geneva score.
- Low/intermediate: D-dimer. Negative (< 500 ng/mL, age-adjusted formula = age × 10 for patients > 50 years) — PE is excluded. Positive — CT pulmonary angiography.
- High: proceed directly to CT pulmonary angiography (bypassing D-dimer).
- Unstable patient (hypotension, shock): bedside echocardiography — RV dilation, reduced TAPSE, LV "D-shape"; if feasible, CT or immediate empirical therapy.
Additional tests: ECG (classic — S1Q3T3, right bundle branch block, RV strain), BNP/NT-proBNP, troponin (for risk stratification).
7. Classification by early mortality risk
| Risk | Hemodynamics | RV dysfunction | Troponin |
|---|---|---|---|
| High | Shock / hypotension | Present | +/− |
| Intermediate-high | Stable | Present | Elevated |
| Intermediate-low | Stable | Present or elevated troponin | ± |
| Low | Stable | No | Normal |
8. Treatment
High risk (shock)
- Immediate systemic thrombolytic therapy: alteplase 100 mg over 2 hours (or 0.6 mg/kg over 15 min, max 50 mg).
- If thrombolysis is contraindicated — endovascular thrombectomy.
- Simultaneously, unfractionated heparin IV (bolus 80 IU/kg, infusion 18 IU/kg/h targeting aPTT ×1.5–2.5).
- Hemodynamic support: norepinephrine, fluid challenge with caution (risk of RV overload), oxygen therapy.
Intermediate risk
- Anticoagulation (LMWH or DOAC) is standard.
- Thrombolysis is not routine, considered in case of clinical deterioration.
- Monitoring in the cardiac care unit for the first 24–72 h.
Low risk
- Direct oral anticoagulants: rivaroxaban (15 mg bid for 3 weeks → 20 mg/day) or apixaban (10 mg bid for 7 days → 5 mg bid).
- Alternative: LMWH → warfarin with bridging (INR 2.0–3.0).
- Duration: at least 3 months; for an irreversible risk factor — up to 6 months; for unprovoked PE and cancer — indefinitely.
9. In-hospital VTE prophylaxis
- Early patient mobilization.
- Mechanical methods: compression stockings, intermittent pneumatic compression.
- Pharmacological prophylaxis: enoxaparin 40 mg once daily or fondaparinux 2.5 mg once daily in moderate/high-risk patients (Padua score for medical patients, Caprini score for surgical patients).
10. FAQ
Is CT angiography always necessary?
No. With low/intermediate Wells probability and a negative D-dimer, CT is not indicated — the probability of PE is < 1%.
What is age-adjusted D-dimer?
For patients > 50 years, the cutoff is calculated as age × 10 ng/mL. This increases specificity and reduces the number of false-positive results.
When is an IVC filter indicated?
In case of absolute contraindications to anticoagulation (active bleeding) or recurrent PE despite adequate therapy.
Can PE be diagnosed by ECG?
No, ECG is an ancillary method. The classic S1Q3T3 pattern occurs in < 25% of patients. Sinus tachycardia is registered much more frequently.
How soon after PE is flying permitted?
Once fully anticoagulated and in a stable condition — after 4–6 weeks, with flight-time thrombosis prophylaxis (compression stockings, hydration).
See also: Myocardial infarction · CHF · Anticoagulants · Pneumonia · Wells score · sPESI · Cardiology catalog