An elderly male with acute altered mental status and huge ST Elevation

Written by Bobby Nicholson

What do you think of this “STEMI”?

A man in his 90s with a history of HTN, CKD, COPD, and OSA presented to the emergency department after being found unresponsive at home. With EMS, patient had a GCS of 3 and was saturating 60% on room air. He improved to 100% with the addition of non-rebreather, however remained altered and was intubated by EMS with ketamine and succinylcholine. Vital signs were within normal limits on arrival to the Emergency Department. Blood glucose was not low at 162 mg/dL. CTA head and neck were obtained and showed no evidence of intracranial hemorrhage, large vessel occlusion stroke (what a helpful and apt name for an acute arterial occlusion paradigm, by the way...), or basilar ischemia. 

EKG on arrival to the ED is shown below:

What do you think?

On my initial interpretation, the patient has normal sinus rhythm with a narrow QRS complex, and LVH.  However, T waves do not appear to be hyperacute or hyperkalemic. There are J waves and and STE in leads V2-V6, however there is no evidence of terminal QRS distortion as V2 and V3 have clear S waves and V4-V6 have J waves. There is also an important limb lead reversal (RA-RL), see Ken Grauer's detailed explanation below.

Smith: 

First, the clinical situation is has a low pretest probability of OMI. The patient is unconscious and hypoxic.

Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching).  There is high QRS voltage.  The T-waves are very assymetric, typical of early repol.  

All of this tells us that this ST Elevation is not ischemic ST Elevation.

Here is the Queen of Hearts interpretation with explainability:

Notice that she highlights the large R-waves, the J-waves and the upward concavity.
Version 1 model output = 0.0373.  Version 2 = 0.0272.  Both highly negative.

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Given the lack of intracranial hemorrhage, the patient was administered aspirin for suspected ACS and cardiology was consulted. The providers documented concern for ST elevation in the precordial and lateral leads as well as a concern for hyperkalemic T waves in the setting of succinylcholine administration. Potassium resulted as 4.9, initial troponin I 0.05 ng/mL (consistent with prior baseline), and a repeat EKG was obtained 1 hour after the initial EKG.

What do you think? Any changes? (limb lead reversal is now resolved)

Unfortunately, QOH V1 got tricked by this second ECG! V1 output 0.667 (which is actually mid to high confidence), but thankfully the new and improved version 2 was not tricked at all, correctly sees No OMI with extremely low output of 0.0053.

Repeat EKG was noted to have persistent ST elevation in the precordial leads, thus the patient was treated with heparin and ticagrelor, and taken for cardiac catheterization. Preliminary findings documented in the cath lab were “Anterior STEMI and no significant coronary artery disease.” (!!!)

Following PCI, the patient ruled out by troponins: troponin increased to 0.08 ng/mL and 0.10 ng/mL before returning to 0.05 ng/mL. Echocardiogram was obtained and showed mild LVH without regional wall motion abnormality.


The conclusion after cardiac catheterization was that this case represents benign early repolarization, or normal variant STE. I think this is actually clear on the initial EKG, but we can check our suspicion with the 4 variable formula which was 16.7, supporting a diagnosis of benign early repolarization (BER) instead of LAD occlusion.(1)

Both the old formula and Queen of Hearts got this right.

But overall, Queen of Hearts is more reliable than the formula.

In considering a differential diagnosis of BER vs LAD OMI, it is important to remember the importance of terminal QRS distortion in V2 and V3. This is defined as the absence of either an S wave or a J wave in V2 and V3. In cases where terminal QRS distortion is present in V2 or V3, it has been 100% specific for LAD OMI.(2)  There was no terminal QRS distortion on these ECGs.


1. Driver BE, Khalil A, Henry T, Kazmi F, Adil A, Smith SW. A new 4-variable formula to differentiate normal variant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion - Adding QRS amplitude of V2 improves the model. J Electrocardiol. 2017 Sep-Oct;50(5):561-569. doi: 10.1016/j.jelectrocard.2017.04.005. Epub 2017 Apr 19. PMID: 28460689.

2. Lee DH, Walsh B, Smith SW. Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. Am J Emerg Med. 2016 Nov;34(11):2182-2185. doi: 10.1016/j.ajem.2016.08.053. Epub 2016 Aug 27. PMID: 27658331.

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MY Comment, by KEN GRAUER, MD (10/12/2024):  

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I found today’s 2 ECGs remarkable for a number interesting findings — including the reasons why I thought acute OMI unlikely.

• For ease of comparison in Figure-1 — I’ve put both tracings in today’s case together.

Striking Features and Technical “Misadventures” in ECG #1:

Among the findings in today's initial ECG that caught my "eye" — are the following:

• P wave morphology in ECG #1 is “off”. By this I mean that: i) The largest P wave is not in lead II (as it almost always is when the rhythm is sinus). Instead, the largest P wave is in lead III (BLUE arrow); — and, ii) The P wave is negative in lead I (PINK arrow) — which usually suggests either an ectopic atrial rhythm or some type of lead misplacement.
• There is extreme low voltage in the limb leads of ECG #1. More than this — there is almost a null vector in lead II, which when present — essentially guarantees lead reversal.
• There is significant baseline artifact in the limb leads (short vertical BLUE lines, especially in lead aVL).
• There is huge biphasic amplitude for the QRS complex in lead V3.
• There are giant T waves in leads V2,V3,V4 (T wave amplitude attaining 19 mm in lead V3! ).
• There is ST elevation in each of the chest leads (being especially marked in leads V2,V3,V4) — this being the reason that cardiac cath was done.
• There are large J waves (Osborn waves) — which are especially large in leads V4 and V5 (within the dotted RED ovals in these leads).

Figure-1: Comparison of the initial ECG — with the repeat ECG done 1 hour later. (To improve visualization — I've digitized the original ECG using PMcardio).

Not a STEMI:

Reasons I did not think ECG #1 represented an acute STEMI — included the following:

• There was no history of chest pain. Admittedly — this 91-year old man with underlying comorbidities was not clinically in condition to provide a history — but I thought the case sounded more the result of hypoxemia and/or neurological insult.
• The shape of the elevated ST segments in leads V2-thru-V5 is consistently upsloping (ie, "smiley"-configuration) — with a similar morphology in most chest leads. 
• There is no reciprocal ST depression.
• As per Dr. Nicholson — there is no T-QRS-D (Terminal QRS Distortion). Rather than loss of both a J wave and S wave — there is a "slur" (J-point equivalent) in lead V2 of ECG #2 (See My Comment in the November 14, 2019 post for illustration of T-QRS-D).
• Although the T waves are huge in leads V2,V3,V4 — considering greatly increased QRS amplitude in these same leads (with overlapping R waves and S waves) — I was not convinced these T waves were disproportionate.
• I thought the ST-T waves in the chest leads "looked" more like a repolarization variant than like an acute MI.
• And there are prominent J waves ...

About the J Waves:

We periodically review the occurrence and clinical significance of Osborn waves (See My Comment in the February 2, 2024 post of Dr. Smith's ECG Blog for more on this topic — with illustration in that post of huge, diffuse Osborn waves).

• By way of review — the Osborn wave has been described as a deflection with a dome or hump that occurs at the point where the end of the QRS complex joins with the beginning of the ST segment. This is the J-Point (ie, it Joins the end of the QRS with the beginning of the ST segment) — so Osborn waves are really exaggerated J waves.
• Although commonly associated with hypothermia — other conditions have also been associated with Osborn waves, including CNS disorders and severe cardiac ischemia (potentially relevant considerations — given the impaired mental status and the ST elevation in today's case).

QUESTION: When do J waves become "large enough" to be called Osborn waves in a non-hypothermic patient?

• While fully acknowledging that I continue to wonder about the answer to this question — I thought the J waves in leads V4,V5 (within the dotted RED ovals in ECG #1) qualified for Osborn wave designation.
• Looking ahead, at the bottom tracing in Figure-1 — the J waves within the dotted RED ovals in ECG #2 looked even larger than those in ECG #1 (in further support of Osborn wave designation).
• Qualitatively — I thought the prominent J-point notching, as well as the "slur" of the terminal QRS in lead V6 supported my impression of a repolarization variant rather than an acute MI (the "slur" serving as a J-point equivalent — as recently described in My Comment in the October 3, 2024 post).

Did YOU Recognize the Lead Reversal?

As alluded to earlier — the clues to lead reversal in ECG #1 include: i) P wave morphology is "off"; — and, ii) There is almost a null vector in lead II.

• My favorite on-line "Quick GO-TO" reference for the most common types of lead reversal comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.
• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict. (For a list of lead reversal cases we've discussed in Dr. Smith's ECG Blog — GO TO the bottom of the page in My Comment from the January 6, 2024 post).
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• As described on the LITFL site — the type of lead reversal in ECG #1 of today's case is RA-RL Reversal. The result of this lead reversal is that Einthoven's Triangle is reduced to a very narrow triangle, with the practical result that the neutral electrode is moved in space and limb lead orientations are distorted. 

NOTE: 

I have excerpted from the LITFL site the effect RA-RL reversal will have on each of the limb leads (Look toward the bottom of Figure-1).

• Take another LOOK at Figure-1. 
• ECG #2 was recorded ~1 hour after ECG #1. If each of the effects listed for RA-RL reversal were to occur on the 6 limb leads in ECG #2 — Wouldn't the result look like the limb leads in ECG #1?
• Therefore — we can suspect that IF the limb lead electrodes had been correctly placed at the time that ECG #1 was recorded — that the largest upright P wave would have been seen in lead II — and that there would not have been a null vector in lead II.
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• As a final point — LITFL notes that because the neutral electrode has been "moved" when there is RA-RL reversal — that precordial voltages may also be distorted. I believe this is the reason we see such an unusually large amplitude biphasic complex in lead V3 of ECG #1 (that is no longer seen in lead V3 of ECG #2).