Overview
ECG findings in PE are neither sensitive nor specific (18-24% have no ECG changes), but in the dyspneic, hypoxic, or unstable patient, they can raise clinical suspicion of acute right heart strain. Findings are most valuable when new or when interpreted with clinical context.
ECG Findings in PE
Basic Physiology: Clot burden → ↑ RV afterload → dilation → septal shift → ↓ CO
- There is ↑ catecholamine response to maintain CO.
- ↑ RV afterload/ RV dilation can lead to axis changes and conduction abnormalities
- RV stretch → RV specific ischemia or ↑ oxygen demand/supply mismatch can cause global subendocardial ischemia
ECG Finding |
Sinus tachycardia |
ECG Finding | |
Right axis deviation (RAD) | Dominant R in V1 |
S1Q3T3 | RAE (P pulmonale) |
Incomplete or complete RBBB | Clockwise rotation (persistent S wave in V6) |
ECG Finding | |
T wave inversions (V1–V4 ± II, III, aVF) | QTc prolongation |
T wave flattening | Inferior/RV STEMI (rare) |
ECG PE Examples
- ECG #1: Sinus rhythm, diffuse TWI
- ECG #2: Sinus rhythm, TWI in V1-V3 with prolonged QTc
- ECG #3: Sinus tachycardia, classic S1Q3T3, RAD
- ECG #4: Sinus tachycardia, TWI in V1-V2, TWF V3
Case details: Clot in transit
Case details: Massive PE with clot in transit
- ECG #5: Sinus tachycardia, RBBB, RAD
- ECG #6: Sinus bradycardia w/ 1st degree av block, RV/Inferior/Anterior STEMI (rare), RBBB, RAD
Case details: ED Presentation
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Case details: After thrombectomy
Case details: Post-ROSC after cardiac arrest
Repeat ECG after further resus: sinus tachycardia, persistent inferior-septal, STE
Dynamic ECG Changes in PE
Co et al., Journal of Emergency Medicine 2017 retrospectively compared ECGs at the time of PE diagnosis to prior ECGs in 352 patients to identify newly developed electrocardiographic changes associated with acute PE and the most common new ECG changes were T wave inversions and flattening while the classic S1Q3T3 pattern appeared in only 3.7%. The study also suggests that the presence of sinus tachycardia in PE may be overstated, with a frequency of only 27% among confirmed cases.
New ECG Change | % of Patients |
T wave inversion | 34.4% |
T wave flattening | 29.5% |
Sinus tachycardia | 27.3% |
ST depression | 9.1% |
RAD | 11.1% |
New RBBB | 5.7% |
S1Q3T3 | 3.7% |
No changes | 24.1% |
Pearl: Inferior/lateral changes were more common than anterior in this series. Always compare to prior ECGs when available
Pitfalls & Mimics
- Wellens Syndrome presents with deep, symmetric T wave inversions in V2–V4 (or biphasic waves), usually after chest pain resolves, and indicates critical proximal LAD stenosis
Case detail: Chest pain
Case detail: Chest pain free (Wellens)
- Posterior MI classically shows horizontal ST depression with upright T waves in V1–V3, reflecting reciprocal changes from posterior ST elevation, often accompanied by tall R waves. PE, on the other hand, more commonly presents with T wave inversions in V1–V3 and III/aVF, sometimes with ST depression but usually in a more diffuse or inferior pattern and paired with RV strain signs described previously.
- Hypertrophic Obstructive Cardiomyopathy (HOCM) can present with deep symmetric T wave inversions, especially in the anterolateral leads (V4–V6), but may also show LVH voltage, septal Q waves, or pseudoinfarct patterns and often occurring in younger patients.
- CNS T Waves Inversions (e.g., from SAH, stroke) are typically deep, symmetric, diffuse T wave inversions, often with QT prolongation and a clinical context of coma, seizure, or neuro catastrophe.
- Right Ventricular Hypertrophy (RVH), in contrast to PE, shows persistent ECG changes due to chronic pressure overload, including dominant R in V1, deep S in V6, RAD, and possible RV strain pattern — but typically no acute T wave evolution.
- Normal Variant especially in young, healthy patients, may show TWI in V1–V3, but these are asymptomatic, stable over time, and often occur with normal axis and no strain signs.
Case detail: history of COPD and pulmonary HTN on home O2
Summary
PE Mimic | How to Distinguish |
Wellens Syndrome | Deep, symmetric inversions or biphasic in V2-V4 |
Posterior MI | Tall R in V1 + upright T + deep STD in anterior leads |
HOCM | Deep symmetric TWI + LVH pattern |
CNS T waves | Deep, diffuse TWI |
RVH | RAD, no acute TWI, dominant R in V1 |
Normal variant | RAD or R > S in V1 in thin adults without other findings |
Clinical Context
When to Suspect PE:
- Onset of dyspnea chest pain, weakness or syncope especially when accompanied by:
- Sinus tachycardia
- Anterior-inferior T wave inversions
- S1Q3T3, new RBBB, or dominant R in V1
- Subtle T wave flattening or inversion in inferior leads
Suggested Workup Strategy:
- POCUS: Evaluate for RV dilation, septal flattening, and IVC plethora
- D-dimer: If low or moderate pretest probability
- CT pulmonary angiography: If hemodynamically stable and high-risk features are present
- Systemic thrombolytics: If hemodynamically unstable / signs of massive PE
Conclusion
Although ECG findings in PE lack sensitivity and specificity, they remain clinically valuable when interpreted in the context of chest pain, dyspnea, hypoxia, syncope, or hemodynamic instability. Patterns such as anterior-inferior T wave inversions, RAD, RBBB, and S1Q3T3 can suggest acute RV strain, particularly when new or dynamic. However, ACS, posterior MI, neurologic T wave patterns, HOCM, and even normal variants can mimic these findings—making clinical context, comparison to prior ECGs, and bedside imaging essential for accurate diagnosis.
References
- Co I et al. New ECG Changes in PE. J Emerg Med. 2017
- Burns E, Buttner R. Pulmonary Embolism – LITFL ECG Library. 2024
- Kosuge M et al. Am J Cardiol, 2007 – specificity of TWI in III and V1
- Chou B. Electrocardiography in Clinical Practice, 6th ed.
- Garcia TB. 12-Lead ECG: The Art of Interpretation
- Mattu A. ECGs for the Emergency Physician
- The ECG – Davila 2025
- Rosen’s Emergency Medicine, 8th ed.
- Tintinalli’s Emergency Medicine, 9th ed.