A man in his 40s with a highly specific ECG

Case submitted by Charles Harris M.D. and Vitaliy Belyshev M.D., with edits by Pendell Meyers

A 43 year old man with no reported past medical history presented with acute onset chest pain and shortness of breath, as well as a syncopal episode. He stated he was walking into his house when he suddenly started coughing and had a syncopal episode. Over the past few days he had been noticing some intermittent central chest pain described as "burning" with associated shortness of breath. He had no cardiac family history, no drug use, no recent COVID infection. His vitals were normal except for mild tachycardia.

Here is his triage ECG (no prior available):

What do you think?

Meyers' comment: I was on a walk with my wife and new baby daughter in the park when I received a text message with this ECG (see below). In our department we have secure channels to ask each others' opinions on ECGs, echos, etc. You can see that I had no knowledge of the patient, not even age. 

After my interpretation, I was told "burning chest pain." There are certain rare ECGs like this one that are so pathognomonic that clinical context is almost irrelevant, or as in the case of the initial clinical context I got here ("burning chest pain"), can even be misleading in the context of a pathognomonic ECG. There is nothing smart or exceptional about this interpretation, it is simply pattern recognition of squiggly lines. I've seen this exact ECG many times (see below for our other posts on this), have followed up the outcome, and learned from the mimics, to the point that I recognize this ECG instantly and pathognomonically. Anyone can do it, and a computer AI / deep neural network could do it much better than I ever could. I later sent this ECG to Dr. Smith, who instantly said "PE."

ECG Interpretation:

Raw findings:

 - Sinus tachcyardia

 - QRS is narrow with RAD and very poor R wave progression

 - Very slight STE in V2, V3 with convex morphology

 - Terminal T wave inversion in V2 and V3

 - Inferior T wave inversion (III and aVF)

 - S1Q3T3

Subjective Interpretation (Meyers):

 - Pathognomonic for acute severe R heart strain (the most common etiology by far being acute PE)

 - V2-V3 have the most important pathognomonic morphology here, with the small R wave followed by large S wave, then slightly convex ST segment followed by terminal-to-whole T wave inversion

 - paired with the classic simultaneous "inferior and anterior" T wave inversion

 - by the way, sure, there is S1Q3T3, which is by far the least important supportive finding of all the above, because it is the least specific

 - Not consistent with anterior reperfusion (Wellens' morphology), it does not have the right morphology of either the QRS complex or the STT waves. This is hard to describe and can really only be learned by comparison: 

Examples of acute right heart strain from PEs vs. Anterior MI (with reperfusion pattern):

Note that, as Kosuge's study found, ALL cases of PE with precordial T-wave inversion have an inverted T wave in lead III and ALL cases of MI have an upright T wave in lead III:

Examples of anterior reperfusion (Wellens):

Notice that this last one (further along in the reperfusion sequence) has some characteristics in V2-V3 similar to the PE pattern I'm describing, but the differences are easy: PE affects the RV, which should have findings proportionally maximal in V2-V3 and usually not extending leftward beyond V4-5, but this example of Wellens shows the T wave inversions in V2-V6, as well as I, II, aVL. The T waves are upright in III and aVF, whereas they are usually inverted in active right heart strain. 

Back to the case:

A bedside echocardiogram was performed by one of our ultrasound fellowship-trained EM faculty, shown below.

The apical 4 chamber view above was interpreted as having RV dilation and McConnell's sign. Color doppler was applied and showed moderate tricuspid regurgitation.

This was followed by a bedside DVT ultrasound, which shows a non-compressible left popliteal vein as shown below.

Based on all the above information, the patient was given 1mg/kg enoxaparin. The CT pulmonary angiogram was performed approximately 20 minutes later, showing "severe pulmonary thromboembolic disease involving the main pulmonary arteries and lobar supply to all lobes. Imaging evidence of associated right heart strain."

CT images shown below:

The patient was activated as a "Code PE" by our hospital protocol, which facilitates rapid consultation with critical care, interventional radiology, CT surgery, as needed. He continue to have normal oxygen saturation on room air, with no respiratory distress, and BNP 477 and high sensitivity troponin T 55 ng/L (URL = 14 ng/L). He was deemed appropriate for non-ICU status in a medical telemetry bed.

He had an unremarkable 2-day hospital stay on the medical floor, without even requiring any oxygen. He had no obvious coagulopathy discovered, but with further outpatient workup planned. He was discharged on a novel anticoagulant.

Three hours later the ECG was unchanged:

Learning Points:

In a very small subset of PE with at least submassive right heart strain, the ECG can be highly specific or even pathognomonic as detailed by the findings above. The ECG is not at all sensitive for all PE.

Don't forget that severe PE can also present with much more difficult findings on ECG, including RBBB and inferior/RV/anterior STEMI mimics.

Use your bedside echo to correlate ECG findings. 

Wellens (anterior reperfusion) can be differentiated from acute right heart strain as detailed above. 

Consider having a (secure, de-identified, approved) channel for you and your colleagues to help one another recognize and interpret ED-based images for which there is no radiologist or other expert, such as the ECG and bedside ultrasound. It may improve patient care, resident education, and departmental camaraderie.

See some of our prior PE cases:

A crashing patient with an abnormal ECG that you must recognize

Chest pain, ST Elevation, and tachycardia in a 40-something woman

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

A 30-something with 8 hours of chest pain and an elevated troponin

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Primer on the ECG in Pulmonary Embolism:

These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V₁ were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V₁ allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE.