The Case
A 40-year-old male with no significant past medical history presents to the ED via EMS with 2 weeks of progressive chest pain and dyspnea on exertion that worsened today while at work. While at work (as a cook) on the day of his ER presentation, he experienced 9/10 retrosternal pain and increased difficulty breathing, which prompted calling 911. Initial vital signs: BP 136/72, HR 72 bpm, RR 18, Temp 98.2 F, SpO2 95% on RA
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EKG Characteristics
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Rate
95 BMP
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Rhythm
Normal Sinus Rhythm
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Intervals
Normal PR and QRS; Prolonged QTc at 512ms
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Axis
Normal
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ST Segments
No ST-segment elevations or depressions
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Additional Features
TWI in leads V1, V2, V3, V4, III, aVR, aVF Absent/flattened T waves in lead II, v5 Prominent S-wave in lead I, Q-wave in lead III
Diagnosis
Diagnosis: Acute saddle pulmonary embolism with acute cor pulmonale (Submassive PE)
Questions
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What are some differential diagnoses for this patient?
Most likely diagnoses: Acute Coronary Syndrome (ACS), Pericarditis/Myopericarditis, Pulmonary embolism (PE), Pneumonia/Pleuritis Not to miss diagnoses: Aortic Dissection, Tension pneumothorax, Esophageal rupture
Discussion
Case Discussion:
- In this case, the patient presented with suspected new T-wave changes in the setting of chest pain and shortness of breath. In the emergency department, his vitals were overall reassuring, and the patient was never in any significant distress. The ED workup revealed an elevated troponin level of 148 ng/L and a BNP of 487 pg/mL. Due to these findings, the patient received a dose of aspirin, was started on a heparin infusion, and was admitted to the medicine floor with concerns for a non-ST elevation myocardial infarction (NSTEMI).
- Considering the patient’s relative hypoxia at 93%, elevated troponin and BNP levels, and EKG findings suggestive of either ischemia or right heart strain, the inpatient team initiated a workup for pulmonary embolism. The d-dimer was significantly elevated at 2,168 ng/mL DDU (normal < 230), and a CT angiography of the chest confirmed bilateral acute pulmonary embolism, including a saddle embolus with evidence of right heart strain.
Pathophysiology behind the diagnosis / EKG Changes
- In a submissive PE, the defining feature is right ventricle (RV) dysfunction without systemic hypotension. The dysfunction comes from an acute obstruction of the pulmonary arterial tree that results in increased afterload of the RV. The strain from increased pulmonary vascular resistance and RV afterload causes RV dilation, hypokinesis, and interventricular septal shift, which can in turn produce electrical changes detectable on an electrocardiogram.
- Sinus Tachycardia
- This is the most common ECG abnormality seen in almost 50% of patients with a PE. This happens due to the compensatory activation of the sympathetic nervous system in response to impaired cardiac output. Not a specific finding, but an early clinical sign that could clue providers into the diagnosis.
- T-wave inversions in the right precordial leads (V1-V4) and/or the inferior leads (II, III, aVF)
- This ECG pattern is associated with high pulmonary artery pressure. The embolic obstruction generates higher RV pressures than normal, which results in myocardial oxygen supply-demand mismatch and ischemia, particularly in the RV free wall and interventricular septum. These alter repolarization currents and manifest as T-wave inversions.
- “S1-Q3-T3”
- Another ECG pattern suggestive of RV strain, this is neither sensitive nor specific for PE. It corresponds to an S wave in lead I (rightward shift of the QRS vector), a Q wave in lead III (due to altered depolarization), and T-wave inversion in leads III (from RV subendocardial ischemia).
- Complete or Incomplete RBBB
- Acute RV enlargement stretches the right bundle branch, impairing its conduction and resulting in delayed right ventricular depolarization.
Management of the patient
- Low-Risk PE: managed with anticoagulation therapy
- If there are contraindications to anticoagulation (e.g. recent intracranial hemorrhage), an inferior vena cava filter is an option
- Intermediate-Risk PE: management includes anticoagulation, expert evaluation for potential thrombolysis vs thrombectomy
- High-Risk PE (unstable): Patients have a high risk of death and should be considered for thrombolytic therapy vs catheter-directed embolectomy
This case: Critical Care, Cardiology, and Vascular Interventional Radiology teams were consulted for further management. The patient was categorized as “Intermediate High Risk”. He was enrolled in the intervention arm of an ongoing clinical trial and underwent catheter-directed therapy and continued on the heparin infusion. His hospital course was complicated by peri-procedure hypertension requiring a Nicardipine drip and rising troponin that were monitored closely in the intensive care unit. Follow-up EKGs, however, were reassuring in the absence of new ischemic changes. The rest of his hospital course was unremarkable, and he was eventually discharged on Eliquis.
Pearls
- Sinus tachycardia is the most common ECG abnormality seen in patients with pulmonary embolism.
- Other ECG findings include T wave inversion in right precordial leads, S1Q3T3, RBBB.
- Elevated troponin and BNP levels can indicate right heart strain and are important in the assessment of PE severity. These biomarkers, along with EKG changes, can guide further diagnostic workup and management.
Sources
- Weekes, A. J., Raper, J. D., Thomas, A. M., Lupez, K., Cox, C. A., Esener, D., Boyd, J. S., Nomura, J. T., Davison, J., Ockerse, P. M., Leech, S., Abrams, E., Kelly, C., & O’Connell, N. S. (2022). Electrocardiographic findings associated with early clinical deterioration in acute pulmonary embolism. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 29(10), 1185–1196. https://doi.org/10.1111/acem.14554
- Ullman, E., Brady, W. J., Perron, A. D., Chan, T., & Mattu, A. (2001). Electrocardiographic manifestations of pulmonary embolism. The American journal of emergency medicine, 19(6), 514–519. https://doi.org/10.1053/ajem.2001.27172
- Piazza, G. (2013). Submassive pulmonary embolism. Jama, 309(2), 171-180.
- Stein, P. D., Dalen, J. E., McIntyre, K. M., Sasahara, A. A., Wenger, N. K., & Willis, P. W., 3rd (1975). The electrocardiogram in acute pulmonary embolism. Progress in cardiovascular diseases, 17(4), 247–257. https://doi.org/10.1016/s0033-0620(75)80016-8
- Thomson, D., Kourounis, G., Trenear, R., Messow, C. M., Hrobar, P., Mackay, A., & Isles, C. (2019). ECG in suspected pulmonary embolism. Postgraduate medical journal, 95(1119), 12–17. https://doi.org/10.1136/postgradmedj-2018-136178
- Weinberg, A. S., & Rali, P. (2023). Acute pulmonary embolism in adults: Treatment overview and prognosis. In J. E. Dalen (Ed.), UpToDate. Retrieved July 13, 2025.