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Pulmonary Embolism (PE): Complete Clinical Overview

Autopsy Specimen

Autopsy showing massive PE occluding the right ventricular outflow system

Autopsy photograph showing a massive pulmonary embolism completely occluding the right ventricular outflow system - Rosen's Emergency Medicine

1. Causes and Risk Factors

PE is almost always caused by deep vein thrombosis (DVT) that dislodges and travels to the pulmonary vasculature. The pathophysiology is explained by Virchow's Triad - three predisposing factors that together promote thrombus formation:

Factor	Examples
Hypercoagulability	Factor V Leiden, prothrombin G20210A mutation, antiphospholipid syndrome, protein C/S/antithrombin III deficiency, cancer, pregnancy, oral contraceptives, HRT
Venous Stasis	Prolonged immobility, long-haul travel, bed rest, obesity, CHF, paralysis
Endothelial Injury	Surgery (especially hip/knee arthroplasty), trauma, central venous catheters, IV drug use

Major acquired risk factors include:

Recent surgery or immobilization (within 4 weeks)
Active malignancy (especially adenocarcinomas - lung, GI, GU)
Prior DVT/PE history
Pregnancy and postpartum state (5x increased risk vs. non-pregnant age-matched women)
Oral contraceptive pills / hormone replacement therapy
Obesity, age >65
Long-distance air travel
COVID-19 infection

The most common source of PE is thrombus from the proximal deep veins of the lower extremities (popliteal, femoral, iliac veins). Rarely, PE arises from upper extremity DVT or cardiac thrombus.

Rosen's Emergency Medicine, p. 1200-1202

Miller's Review of Orthopaedics, p. 5382

Murray & Nadel's Respiratory Medicine, p. 1558

2. Clinical Presentation

Symptoms range from asymptomatic to sudden cardiovascular collapse.

Symptom	Frequency
Dyspnea	75-80% (most common)
Chest pain (pleuritic or non-pleuritic)	~65%
Cough	~40%
Hemoptysis	~10% (peripheral/infarction-type PE)
Unilateral leg swelling	<30%
Syncope	<5% (but high mortality when present)

Signs: tachycardia, tachypnea, hypoxemia (SpO2 <95%), loud P2, right heart failure signs (elevated JVP, RV heave). Fever may occur but is typically low-grade; temperature >38.6°C suggests infection.

3. Diagnostics

A. Risk Stratification First

Wells Score (most common):

Feature	Points
Prior PE/DVT	1.5
HR >100 bpm	1.5
Surgery/immobilization within 4 weeks	1.5
Clinical signs of DVT	3
Hemoptysis	1
Active cancer	1
PE is most likely diagnosis	3

Score <2 = low probability; 2-6 = intermediate; >6 = high

Revised Geneva Score: uses only objective criteria (age >65, prior PE/DVT, recent surgery, active cancer, unilateral leg pain, hemoptysis, heart rate, leg edema on palpation).

PERC Rule (to rule out PE in low-pretest-probability patients without any testing):

Age <50, HR <100, SpO2 >94%, no leg swelling, no hemoptysis, no trauma/surgery, no prior PE/DVT, no hormone use

B. Laboratory

Test	Use
D-Dimer	95-98% sensitive; 40-55% specific. Negative D-dimer in non-high pretest probability excludes PE (NPV 99-100%). Not useful in high-PTP patients
Troponin	Elevated with RV myocardial injury; indicates worse prognosis
BNP/NT-proBNP	RV strain marker; helps risk stratify intermediate-PE
ABG	Hypoxemia, hypocapnia, respiratory alkalosis
CBC, CMP	Baseline; help exclude other diagnoses

C. Imaging

CT Pulmonary Angiography (CTPA) - Gold Standard

Sensitivity/specificity 90-95% on modern multidetector scanners
Shows filling defects in pulmonary arteries; a clot straddling both main pulmonary arteries = saddle embolus
Requires >200 HU contrast opacification in main pulmonary artery and absence of motion artifact

V/Q Scan - for patients with iodinated contrast allergy or renal impairment

High probability scan confirms PE; normal scan excludes PE
Only ~1/3 of scans are clearly high-probability or normal

Bedside Ultrasound

DVT on venous ultrasound (86-96% sensitive) in symptomatic patient = sufficient to treat
Echo showing RV:LV ratio >1 raises suspicion for PE

Lower extremity duplex ultrasound

First-line in pregnant patients before CT

Rosen's Emergency Medicine, p. 1203-1207

4. Chest X-Ray Findings

The chest X-ray is most often normal or shows only nonspecific changes. It is primarily useful to exclude other diagnoses (pneumothorax, pneumonia, aortic dissection). Key findings:

Sign	Description	Significance
Normal CXR	Most common - a normal CXR in a hypoxic, tachypneic patient should raise PE suspicion	Important negative finding
Westermark Sign	Focal oligemia (hyperlucency/decreased vascular markings) distal to occluded vessel	Suggests occlusion of a major pulmonary artery
Hampton's Hump	Peripheral, pleural-based, wedge-shaped opacity (base toward pleura)	Indicates pulmonary infarction
Fleischner Sign	Enlarged, prominent central pulmonary artery	Indicates large proximal PE
Atelectasis / elevation of hemidiaphragm	Most common radiographic finding	Nonspecific
Pleural effusion	Small, typically unilateral; seen in ~50%	Nonspecific; usually exudative
Pulmonary infiltrate	Patchy opacity, usually peripheral	From infarction/atelectasis
Cardiomegaly	RV enlargement in massive PE	Nonspecific

X-Ray Images from Murray & Nadel's Respiratory Medicine:

Hampton's Humps (bilateral basal wedge-shaped opacities):

Hampton's Humps - bilateral basal subpleural wedge-shaped opacities in a 36-year-old with acute PE

eFigure 81.7 - Frontal CXR in a 36-year-old with acute PE showing bilateral, basal subpleural wedge-shaped opacities (Hampton's Humps), representing pulmonary infarction

Westermark Sign (right lung hyperlucency):

Westermark Sign - hyperlucency of right thorax showing oligemia

eFigure 81.6 - Frontal CXR showing hyperlucency of the right thorax compared with left, consistent with oligemia (Westermark Sign)

Fleischner Sign + Westermark Sign (enlarged left pulmonary artery):

Fleischner Sign and Westermark Sign - enlarged left pulmonary artery with relative hyperlucency of left thorax

eFigure 81.8 - Frontal CXR showing enlargement of the left pulmonary artery (Fleischner Sign) and relative hyperlucency of the left thorax (Westermark Sign)

Murray & Nadel's Respiratory Medicine, eFigures 81.6-81.8

5. ECG Findings

The ECG is nonspecific but helps exclude other diagnoses (ACS, pericarditis) and can indicate RV strain. Most common finding in PE is sinus tachycardia (present in ~40% of cases).

ECG Finding	Significance
Sinus tachycardia	Most common (40%); reflects sympathetic activation
S1Q3T3 pattern	S wave in lead I, Q wave + T-wave inversion in lead III; classic but only seen in minority; suggests RV strain
T-wave inversions V1-V4	Most specific sign for PE; represents RV ischemia/strain. Simultaneous inversion in V1-4 AND inferior leads (II, III, aVF) has specificity up to 99%
Right bundle branch block (RBBB)	Complete or incomplete; indicates RV outflow obstruction
Right axis deviation	RV pressure overload
P pulmonale	Peaked P waves >2.5 mm in II, III, aVF from right atrial enlargement
Atrial fibrillation/flutter	Especially with underlying cardiopulmonary disease
Sinus bradycardia / PEA	Ominous - indicates impending cardiac arrest in massive PE

Clinical pearl: Negative T waves in both lead III and V1 were seen in only 1% of ACS patients vs. 88% of acute PE patients - this combination is highly specific for PE (specificity 99%).

Important: The presence of S1Q3T3, RBBB, or T-wave inversions V1-V3 all suggest RV dysfunction and are associated with increased mortality.

ECG Images:

ECG from Harrison's Principles - S1Q3T3 pattern:

ECG showing S1Q3T3 pattern in pulmonary embolism

Harrison's Fig. 290-11 - ECG showing the S1Q3T3 sign and T-wave inversions in right precordial leads in acute PE

ECG from Fishman's Pulmonary Diseases - S1Q3T3 pattern (annotated):

S1Q3T3 pattern ECG in right ventricular dysfunction from PE

Fishman's Fig. 73-7 - S1Q3T3 pattern seen in RV dysfunction such as acute PE (blue circle = S wave in I; red circle = Q wave in III; yellow box = inverted T in III)

Rosen's Emergency Medicine, p. 1204; Fishman's Pulmonary Diseases, p. 1295-1296; LITFL ECG Library

6. Treatment

Treatment is guided by risk stratification into three categories:

Risk Categories

Category	Criteria	Mortality
Low-risk PE	Hemodynamically stable, no RV dysfunction	<1%
Intermediate-risk PE	Stable but RV dysfunction on echo/CT and/or elevated troponin or BNP	3-15%
High-risk (massive) PE	Hemodynamic instability (SBP <90 or drop >40 mmHg for >15 min not due to other cause)	>15-30%

Treatment Algorithm

Step 1 - Immediate Supportive Care (all patients):

Supplemental O2 targeting SpO2 >90%
Avoid intubation if possible (increases intrathoracic pressure, reduces preload, can precipitate RV failure)
Small IV fluid boluses (250-500 mL) for hypotension - avoid fluid overload
Vasopressors if fluids fail: norepinephrine first-line; dobutamine as adjunct

Step 2 - Anticoagulation (cornerstone of treatment):

Drug	Use	Notes
DOACs (rivaroxaban, apixaban)	Low- and intermediate-risk PE, hemodynamically stable	Preferred; rivaroxaban/apixaban can be started directly without heparin bridge
Unfractionated Heparin (UFH)	When thrombolysis or surgical intervention planned	IV infusion, weight-based dosing
LMWH (enoxaparin)	Intermediate-risk, subcutaneous, predictable dosing	Preferred in pregnancy (does not cross placenta)
Warfarin	Long-term therapy	Needs heparin bridge until INR therapeutic (2-3)

Step 3 - Advanced Therapies for High-Risk/Selected Intermediate-Risk PE:

Intervention	Indication	Notes
Systemic Thrombolysis (tPA 100 mg IV over 2 hrs)	High-risk PE with hemodynamic instability; no absolute contraindications	Contraindicated with recent surgery, stroke, active bleeding
Catheter-Directed Thrombolysis (CDT)	Intermediate-high risk; contraindication to systemic lysis	Lower dose thrombolytic directly into clot via catheter
Mechanical Thrombectomy	Intermediate/high-risk; contraindication to thrombolysis	Percutaneous catheter-based suction/fragmentation
Surgical Embolectomy	Massive PE with failed thrombolysis or absolute contraindication	High-volume centers; may include ECMO
IVC Filter	Recurrent PE despite anticoagulation, or absolute contraindication to anticoagulation	Retrievable preferred
ECMO	Refractory hemodynamic collapse	Bridge to definitive intervention

Pulmonary Embolism Response Team (PERT): Multidisciplinary teams at major centers that guide management of intermediate/high-risk PE, coordinating hematology, pulmonology, cardiology, IR, and cardiac surgery.

Duration of Anticoagulation

Scenario	Duration
Provoked PE (reversible risk factor)	3 months
Unprovoked PE, first episode	At least 3-6 months; consider indefinite if low bleeding risk
Recurrent unprovoked PE	Indefinite anticoagulation
Cancer-associated PE	LMWH or DOAC (edoxaban/rivaroxaban) - continue as long as cancer active

Rosen's Emergency Medicine, p. 1208-1215

Braunwald's Heart Disease, p. 3342

Murray & Nadel's Respiratory Medicine

7. Quick Memory Aid

CAUSES:   Virchow's Triad (Stasis + Hypercoagulability + Endothelial injury)
CXR:      Usually NORMAL → Westermark + Hampton's hump + Fleischner sign
ECG:      Sinus tachycardia (most common) → S1Q3T3 + T inversions V1-4 + RBBB
Dx:       PERC → D-Dimer → CTPA
Tx:       Anticoagulate (DOAC preferred) → Thrombolysis for massive PE

Recent Evidence Note: A 2026 meta-analysis (PMID 41865356) showed mechanical thrombectomy vs. anticoagulation alone in intermediate-risk PE is an area of active investigation - specific center expertise should guide this decision. A 2025 paper (PMID 40586314) also found that classical ECG findings including S1Q3T3 have minimal diagnostic value in isolation for PE diagnosis and should not be used in isolation to confirm or exclude PE.

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