Friday, April 16, 2021

A man in his 60s with diaphoresis, vomiting, and inferior STE

Written by Pendell Meyers


A man in his 60s appeared altered and diaphoretic and vomiting to a bystander, who called EMS. EMS personnel agreed that he was altered, possibly intoxicated, and seemed to deny all complaints that EMS inquired about. Vital signs were within normal limits.

EMS performed an ECG:

What do you think?










Raw findings:
 - Sinus rhythm
 - Normal QRS, axis straight down at lead aVF
 - STE in leads II (2.0 mm), III (1.5 mm), aVF (2.0 mm)
 - STD in aVL (1.0 mm)
 - STD in V1 (0.5 mm), STD in aVR (0.5 mm)

Subjective interpretation of those findings:
It is slightly tough to decide whether this is inferior and/or posterior OMI. "Normally", this ECG would trigger the rule that any STE in the inferior leads with any STD and/or TWI in lead aVL (not explained by some other reason, like a QRS abnormality) should be considered inferior OMI until proven otherwise. "Normally", we would teach that STD maximal in V1-V4 (without another explanation e.g. RBBB, juvenile T wave pattern, known prior baseline, etc.) should be considered posterior OMI until proven otherwise. But there is something about this particular ECG and its morphology that matches prior false positives to me. I have a hard time explaining what feature it is, exactly, but I have made lots of mistakes in the past and feel that this one is similar to the last time I saw a false positive like this. One thing I can explain is: Any time there is focal STE in the inferior leads for any reason (whether it is due to acute inferior wall OMI, or whether it is a baseline ECG finding), there MUST BE reciprocal STD in aVL. The fact that there is STD/TWI in aVL does not make the STE in the inferior leads specific for active OMI, it just means that the STE in the inferior leads is indeed focal. If it were diffuse STE on all walls of the LV, it would be very unlikely to have STD in aVL.

Also remember that Dr. Smith's study on STE in the inferior leads and STD/TWI in aVL was only comparing patients with inferior OMI against patients with pericarditis. Normal variants and other reasons for STE in the inferior leads were not in that comparison.





I received this ECG immediately, automatically onto my phone, with no clinical information at all (not even age). I had no idea if the patient had chest pain or any other symptom. I notified the ED that I thought the ECG was likely a false positive, unless the patient has very convincing ACS. But this is a very difficult decision with only this ECG. I was not working at the time, and could not get any more info.

I sent it immediately to Dr. Smith without the outcome or clinical information; he also agreed that he thought it was likely a false positive.  Smith's thoughts: "The ECG is unlikely to represent OMI because it has a combination of 1) high R-wave voltage, 2) J-waves, 3) high STE to T-wave ratio, such that the ST segment is BOTH relatively flat AND upwardly concave, and 4) a "Saddle" appearance, which is usually not due to OMI."




A prior ECG was available in the system:

Does this change your interpretation?






On this prior ECG, we see that the QRS complex is basically the same as the presentation ECG, but with less STE in the inferior leads, isoelectric baseline in aVL, with preexisting but smaller TWI. Some would say that the T waves are smaller in the baseline ECG than the presentation ECG, some would be worried about hyperacute T waves. One of the reasons I think that the inferior T waves in the presentation ECG are not hyperacute is that they are very asymmetric. Hyperacute T waves are usually symmetric. These are not.

Most would say that this prior ECG makes the presentation ECG diagnostic because of a change from baseline. 
Most would say that the inferior STE has gotten larger and therefore is diagnostic. 

This is understandable, and if the patient has ACS clinically then I would call that presentation ECG a STEMI until proven otherwise. However, experienced ECG interpreters know that baseline ECG findings can change, fluctuate, be exaggerated, etc. I always struggle how to teach my residents that baseline ECGs are not always the same day to day, hour to hour. 

All of that said, 

1) if this patient had ACS clinically, I would simply call it STEMI(+) OMI until proven otherwise, and I would have a sneaking suspicion that it would turn out to be a false positive activation. This assumes I do not have access to an emergent high quality contrast enhanced echo (I personally never have this available).

2) if this patient does not have ACS clinically, then I will not be immediately activating the cath lab, but instead will carefully to history, physical, bedside echo, prior ECG checks in system, serial ECGs over the first 10-15 minutes. Then decide. If I still truly think it's a false positive, I could choose to wait for the initial troponin.





Back to the case:

The ED received the ECG, and given the very little information they had at the time of the phone call to discuss the ECG with paramedics, they decided to activate our code STEMI prehospital.

The patient arrived in the ED within about 10 minutes of that phone call, before the cath lab was ready, and so he got evaluated by the ED team. At that point he was able to completely deny any chest pain or shortness of breath, and admitted to large volume alcohol consumption hours prior to his altered behavior and vomiting.

Cardiology arrived, and together ED and cardiology agreed to cancel the cath lab activation.

A repeat ECG was obtained:

In this one, J waves are much more readily apparent in the leads with STE. The same STE and STD is present as before. This one is much easier to identify as normal variant STE in my opinion.



Side note / rant:

All parties involved called this "just J point elevation," which I find to be a term that is almost universal in its usage, but should instead be replaced by describing it as a J wave. A J wave is a discrete wave at the position of the J point. The J point is the point where the QRS ends and the ST segment begins. When there is a wave at the J point, it is a J wave. J waves are frequently seen in benign early repol and benign normal variants. We have a couple examples of clear OMI/STEMI with J waves, but statistically J waves favor benign variants.

It is incorrect to say "J point elevation" in the way that is commonly used. The J point is explicitly where all STE is supposed to be measured (let's talk about whether to use the PR or TP interval as the baseline another day), as stated formally in the Fourth Universal Definition of MI. STE is measured at the J point (unless specified otherwise, such as Dr. Smith's anterior OMI vs. early repol equation), and thus all STE of all the STEMIs you have ever seen are also correctly described by the term "J point elevation." What providers actually mean is "there is a J wave, so I think that is false positive STE."

The distinction is very important because it implies that most physicians do not actually know the formal recommendations for where STE is actually measured (but we already know this is true, as it has been studied: humans cannot agree on how and where to measure STE).

Case continued

The first troponin was negative (less than 6 ng/L).

The second was also negative. No further ECGs were ordered. ED bedside echo was normal

He became sober, without complaints, and was discharged. He did not have ACS in any way.


Learning Points:

In general, if a patient has ACS clinically, then otherwise unexplained STE in the inferior leads with reciprocal STD and/or TWI in aVL is very concerning for inferior OMI. Likewise, ischemic STD maximal in V1-V4 is posterior OMI until proven otherwise in a patient with ACS clinically.

That said, there are always exceptions and false positives to every rule. Experience with cases like this one allow us to build our knowledge of false positive morphology and recognize them better in the future, even if we cannot always express the exact morphology reasons for that suspicion.

"J point elevation" is a widespread term used inappropriately. All providers should know that the Universal Definition of MI recommends the J point is the location to measure STE. All providers should also know the definition of a J wave.



5 comments:

  1. Thank you for the excellent explanations, as usual! Given the appearance of the QT interval in the first tracing and the history of vomit, would you have considered hypocalcemia in the differential diagnosis?
    Thank you for the continuous education in ECG.
    Best regards,

    Aldo Cannata

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    Replies
    1. I don't thinks so. That causes a long ST segment.

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  2. Wow, I was fooled by this one. Thank you for posting false positives. Just when I think I'm gaining cognitive momentum in advanced ECG interpretation I get humbled by cases like this.

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  3. This comment has been removed by the author.

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