Step 2 CK · Internal Medicine · Pulmonology

Pulmonary Embolism (Clinical)

Name: Pulmonary Embolism (Clinical)
Creator: Veli Bakalov, MD

Risk-stratify, image right, anticoagulate, and know when to lyse

Pulmonology·Pulmonary Vascular & Sleep Disorders·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

Study materialsNo account needed

Card deckActive-recall cards · quick checks · quiz

High-yield

PE usually comes from a leg DVT (Virchow triad: stasis, hypercoagulability, endothelial injury); the most common ECG finding is sinus tachycardia, while S1Q3T3 is classic but uncommon.
A low-risk patient who meets all 8 PERC criteria needs no testing; low or intermediate Wells probability → D-dimer (negative excludes PE); high probability → straight to CT pulmonary angiography.
D-dimer is sensitive but nonspecific: use an age-adjusted cutoff (age × 10 μg/L over 50), and never use a positive result to confirm PE.
CT-PA is the test of choice; use a V/Q scan when contrast is contraindicated (renal failure, contrast allergy, pregnancy).
Massive PE (2026 AHA/ACC category E) = SBP under 90 for ≥15 min or pressors → systemic alteplase if no bleeding contraindication; catheter-directed therapy or embolectomy if lysis fails or is contraindicated.
Submassive PE (category C: normotensive with RV strain or elevated troponin/BNP) → anticoagulate and monitor, lyse only if deteriorating; an sPESI of 0 identifies low-risk PE suitable for outpatient care.
DOACs are first-line (apixaban/rivaroxaban need no heparin lead-in; dabigatran/edoxaban do); treat ≥3 months, stop at 3 months if provoked by a transient factor, extend if unprovoked, recurrent, or ongoing risk.
IVC filter only when anticoagulation is contraindicated or PE recurs despite therapeutic anticoagulation; in massive PE give fluids cautiously and norepinephrine for shock.
In pregnancy: D-dimer is unreliable, start with leg compression ultrasound then V/Q (or CT-PA), and treat with LMWH; avoid warfarin (teratogenic) and DOACs.

Presentation and bedside clues

Source and risk. Most pulmonary emboli start as a lower-extremity deep vein thrombosis (DVT). Risk follows Virchow triad: stasis (surgery, immobility, long travel), hypercoagulability (cancer, estrogen, pregnancy, thrombophilia), and endothelial injury.

Symptoms and signs. Sudden dyspnea, pleuritic chest pain, tachycardia, tachypnea, and hypoxemia. Some patients have hemoptysis, and syncope suggests a large clot. The ABG classically shows hypoxemia with respiratory alkalosis and a widened A–a gradient.

ECG. The most common ECG finding is sinus tachycardia. The textbook S1Q3T3 pattern reflects acute right-heart strain: an S wave in lead I, and a Q wave with an inverted T wave in lead III. It appears only in a minority of patients. A new right bundle branch block or right-axis deviation may also appear.

The chest x-ray is usually normal, which helps separate PE from pneumonia or pneumothorax. The rare classic signs are Westermark sign (regional oligemia) and Hampton hump (a peripheral wedge-shaped infarct).

The diagnostic pathway

Pretest probability comes first. The Wells score counts clinical signs of DVT, PE as the most likely diagnosis, heart rate >100, recent immobilization or surgery, prior DVT/PE, hemoptysis, and cancer. In a patient already judged low risk, PERC can exclude PE with no testing if all 8 criteria are met:

Age <50
Heart rate <100
SaO2 ≥95%
No hemoptysis
No estrogen use
No prior DVT/PE
No unilateral leg swelling
No surgery or trauma needing hospitalization within 4 weeks

A low-risk, PERC-negative patient has a PE risk below 2%, which is lower than the harm of further testing.

Estimate pretest probabilityWells score; apply PERC if the patient is low risk.
Low or intermediate probabilityD-dimer. A negative result excludes PE.
High probability, or D-dimer positiveCT pulmonary angiography.
Contrast contraindicatedV/Q scan (renal failure, contrast allergy, pregnancy).

D-dimer. Sensitive but nonspecific, so it is useful only to rule out PE at low or intermediate pretest probability. Over age 50, use an age-adjusted cutoff (age × 10 μg/L). At high pretest probability, skip the D-dimer and go straight to imaging.

A positive D-dimer never confirms PE. It is also raised after surgery and in pregnancy, cancer, and infection.

Imaging. CT pulmonary angiography (CT-PA) is the confirmatory test of choice. A V/Q scan is the alternative when contrast is contraindicated by renal failure, contrast allergy, or pregnancy (it gives less breast radiation). Lower-extremity compression ultrasound can confirm PE indirectly: finding a DVT in a patient with PE symptoms justifies treatment. If suspicion is high and bleeding risk is low, start empiric anticoagulation while imaging is pending.

Risk stratification

PE severity tiers

Tier	Definition	Management
Massive (high risk)	Sustained hypotension: SBP <90 mmHg for ≥15 min, or needing pressors; high mortality	Systemic thrombolysis if no contraindication
Submassive (intermediate risk)	Normotensive, but RV dysfunction on echo/CT or elevated troponin/BNP	Anticoagulate and monitor closely; lyse if deteriorating
Low risk	Normotensive, normal RV, normal biomarkers	Anticoagulation; possibly outpatient treatment

2026 AHA/ACC categories. The 2026 guideline replaces these labels with clinical categories A to E: A, subclinical (incidental) PE; B, symptomatic PE without RV dysfunction or biomarker elevation; C, normotensive PE with RV dysfunction or elevated troponin or BNP (formerly submassive); D, incipient cardiopulmonary failure (transient hypotension or normotensive hypoperfusion such as a rising lactate); and E, cardiopulmonary failure with sustained hypotension, shock, or arrest (formerly massive).

PESI and sPESI. These scores predict 30-day mortality from age, cancer, chronic cardiopulmonary disease, heart rate ≥110, SBP <100, and SaO2 <90%. The simplified sPESI gives one point each (age counts only if >80). An sPESI of 0 marks low risk: the patient is a candidate for outpatient or early-discharge management.

Anticoagulation: agent and duration

Anticoagulate most stable PEs immediately. Direct oral anticoagulants (DOACs) are first-line.

Choosing the anticoagulant

Situation	Agent	Note
Most stable PE	Apixaban or rivaroxaban	No parenteral lead-in needed
Dabigatran or edoxaban	Start with LMWH first	These two require a parenteral lead-in
Warfarin	Bridge with LMWH	Overlap until the INR is therapeutic
Possible thrombolysis, severe renal failure, high bleeding risk	IV unfractionated heparin	Short-acting and reversible with protamine
Cancer-associated VTE	LMWH or a DOAC (edoxaban, apixaban, rivaroxaban)	Ongoing risk: continue while cancer is active
Pregnancy	LMWH	Warfarin is teratogenic; DOACs are avoided

Duration. Every course lasts at least 3 months.

Provoked by a transient, reversible factor (such as surgery): stop at 3 months
Unprovoked or recurrent PE: extended or indefinite therapy
Ongoing risk (active cancer, thrombophilia): extended or indefinite therapy

Unprovoked proximal PE increasingly gets indefinite anticoagulation when bleeding risk is low. After the first 6 months, extended therapy can use a reduced DOAC dose (apixaban 2.5 mg twice daily or rivaroxaban 10 mg daily).

Massive PE: reperfusion and support

SBP <90 mmHgfor ≥15 min, or needing pressors, defines massive PE

Thrombolysis. Systemic thrombolysis (alteplase, tPA) is indicated for massive PE with hemodynamic instability, unless there is a major bleeding contraindication (prior intracranial hemorrhage, recent stroke or neurosurgery, active bleeding). If systemic lysis fails or is contraindicated, use catheter-directed thrombolysis or surgical/catheter embolectomy. Submassive PE is not lysed routinely; lyse only if the patient deteriorates.

Supporting the right ventricle. Give oxygen, cautious IV fluids, and norepinephrine for shock. The RV is preload-sensitive, but overload makes it worse.

Aggressive fluid loading overdistends the failing RV, bows the septum into the LV, and lowers cardiac output. Give fluids cautiously.

IVC filter. Place one only if anticoagulation is contraindicated or PE recurs despite therapeutic anticoagulation. A filter does not treat the existing clot.

PE in pregnancy

Diagnosis. Pregnancy is prothrombotic and physiologically raises D-dimer, so a D-dimer is unreliable. Start with leg compression ultrasound: a DVT justifies treatment without chest imaging. If the ultrasound is negative, get a V/Q scan (or CT-PA).

Treatment. LMWH is the anticoagulant of choice throughout pregnancy because it does not cross the placenta. Avoid warfarin (teratogenic) and DOACs. After delivery, warfarin can be used and is compatible with breastfeeding.