After seeing this ECG, are there any medications you would consider giving?

Written by Willy Frick

A man in his 50s with COPD presented with dizziness and hypotension. He had worked overnight the night before and presented to the hospital after his shift. His first recorded blood pressure was 88/53 mm Hg.

Here is his presenting ECG:

What do you think?

The ECG shows sinus rhythm. The T waves are suspiciously symmetric, but not hyperacute looking. In contrast to hyperacute T waves which are characteristically broad (Dr. Smith describes them as "puffed full of air"), these T waves have a very narrow base. The concavity is especially pronounced. Altogether, this ECG is suspicious (but probably not diagnostic) for hyperkalemia.

I sent this ECG to Dr. Meyers with no context, and he replied "mild hyperkalemia effect possible." This is an extremely subtle ECG. However, we can make our job a little easier using comparison to a prior ECG.

Here are the leads side by side:

This serial comparison significantly increases our suspicion for hyperkalemia, highlighting how sharply peaked the T waves are relative to prior.

The patient was treated with methylprednisolone, ipratropium-albuterol, and 1 L NS. Forty five minutes later, his blood pressure increased to 157/125 mm Hg, but his heart rate was now in the 30s. Repeat ECG was performed.

This is a very poor quality ECG which limits interpretation. It should have been repeated immediately. However, we can at least make the following observations:

• The QRS has widened

• There are no longer any identifiable P waves

• The ventricular rate is much slower, in the 30s

These are all features of hyperkalemia. If we were suspicious before, it is now certain. The patient needs calcium immediately. Although labs were drawn on arrival to the ED, this hospital apparently has a very slow lab and the results were not back yet (and would not result for another half hour). This ECG was not recognized as showing hyperkalemia.

Instead, the patient received atropine and his heart rate rose to the 80s. The next recorded blood pressure was 211/175 mm Hg, and in response the patient was started on continuous nitroglycerin infusion. His heart rate dropped back into the 30s, and he arrested. He received CPR and was intubated. Repeat ECG is shown:

It looks similar to prior, but with less artifact. At this point, lab called with critical potassium 6.8 mEq/L and the patient finally received 2 g IV. Repeat ECG is shown below.

Much better! Although the QRS has narrowed and the sinus node has gone back to work, there is still subtle upsloping STD in the lateral precordial leads and subtle T wave peaking. The patient's long term outcome is unknown.

Discussion:

This is a case of an initial ECG showing very subtle signs of hyperkalemia. In just 90 minutes from presentation, the patient progressed from that very subtle ECG to cardiac arrest. Dr. McLaren recently wrote an excellent blog post on a similar case. Some advocate that calcium should not be given for "just" peaked T waves, but I disagree. If a patient comes in sick with this ECG, and the cause for illness is not immediately apparent, it is most appropriate to give empiric IV calcium while awaiting the results of further workup. Earlier recognition and administration of treatment may have saved this patient an arrest.

Learning points:

• Identify subtle ECG evidence of hyperkalemia

• When in doubt, give calcium

Here are a couple other cases of hyperkalemia with small, but peaked, T-waves:

A Tragic Case, related to the last post (this one is especially interesting and terrible)

Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)

This is on a previous visit with K = 6.6:

After treatment: 

ST Elevation in I and aVL, with reciprocal ST depression in lead III

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MY Comment, by KEN GRAUER, MD (2/18/2025):

===================================

There are always "lessons to be learned" from the multiple clinical presentations of hyperkalemia. Today's case by Dr. Frick highlights this clinical reality in a patient whose initial ECG could easily pass for "normal". Among the "lessons" from today's case are the following:

• Although many patients follow the "textbook sequence" of ECG changes with their hyperkalemia — a significant percentage of patients do not. As I emphasized in My Comment in the February 27, 2023 post in Dr. Smith's ECG Blog — some patients may develop everything except QRS widening. Others may not show T wave peaking — or may only show this finding as a later change. And despite marked hyperkalemia — some patients may not show any ECG changes at all.
• The above said — today's initial ECG does show T wave peaking in 8/12 leads! As per Drs. Frick and Meyers — it is the composite picture (ie, that 8/12 leads show subtle-but-real T wave peaking) that will prompt the astute clinician to wonder if that isn't 5 or 6 leads too many to show upright, symmetric T waves that are all peaked at their highest point (with another lesson being that peaked hyperkalemic T waves are not necessarily tall).
• Finding a prior ECG on today's patient simplified our diagnostic task — as the comparison of prior with current ECGs provided by Dr. Frick left no doubt that there has been new, diffuse T wave peaking (with the inescapable conclusion of knowing that the serum K+ level needs to be immediately checked).
• The other distinct ECG finding that the astute clinician will appreciate from today's initial ECG — is a uniquely flat ST segment. As I've emphasized in the February 10, 2025 and March 19, 2019 posts — hyperkalemia and hypocalcemia often occur together, and often produce a readily identifiable pattern of flat ST segments ending in peaked T waves that we see in today's case.
• Finally — Today's case shows the consequences of not heeding the ECG signs that are diagnostic of significant hyperkalemia (rapid progression to marked bradycardia — loss of P waves — QRS widening) — demonstrating once more the need to treat with IV Calcium without waiting for the lab to confirm what you already know from arrhythmia progression over the course of 2 ECGs (with the need for IV Calcium being that much more urgent in today's patient whose initial ECG suggests serum Ca++ is already low).
•  =  =  =  =  =  =  =  =  =  =
• P.S.: We are not provided with information in this case as to WHY this patient developed hyperkalemia! So part of the ED evaluation should also consist of evaluating for: i) Renal function (esp. for any potential recent worsening of renal function that might predispose to hyperkalemia); ii) Volume status (ie, hypovolemia may precipitate an increase in serum K+ levels); iii) Any potential K+-retaining medications that the patient might be taking? (ie, K+ supplements? K+-retaining diuretic or ACE-Inhibitor or ARB); — and, iv) Anything else that might potentially predispose to subtle development of unsuspected hyperkalemia.

 

What factor determines final diagnosis of STEMI vs. NSTEMI? Is it ST Elevation? Occlusion? or Something else? What?

The answer is at the bottom, and illustrated by this case.

Written by Willy Frick

A man in his mid 30s with type 1 diabetes presented with two days of midsternal and epigastric pain, described as both "sharp" and squeezing." There was associated nausea, vomiting, and dyspnea. He said the pain was worse with supination and improved with upright posture.

What do you think?

Despite the noisy baseline, this ECG is easily diagnostic for OMI. The Queen of Hearts diagnoses OMI with 0.99 confidence (near maximum). Here is her explainability.

Here are some of the diagnostic findings:

• Very subtle hyperacute T waves (HATW) in lead I

• STE and HATW in II > aVF

• Subtle STD in V1 and V2

• STE and HATW in V5 and V6

Therefore, we have an inferior, posterior, lateral OMI. In fact, even the GE algorithm got this one (partially) right.

The emergency medicine physician documented, "His initial EKG is riddled with artifact and difficult to interpret but does not look like a STEMI." This is a very bold statement in a type 1 diabetic with very concerning sounding chest pain. One wonders why repeat ECG was not immediately performed, if artifact was felt to be a problem. The patient was treated with aspirin and a GI cocktail, which did not help the pain.

Initial hsTnI resulted at 25,994 ng/L (ref. <35 ng/L). At this point, the physician started heparin and gave nitroglycerin, which improved the pain from 7/10 to 3/10. He also obtained repeat ECG.

Once again, easily diagnostic for inferior, posterior, lateral OMI. Getting rid of the artifact increased the Queen's confidence from 0.99 to 1.0 (maximum). The ECG remains positive for STEMI by GE. The emergency physician consulted cardiology. Despite apparently hearing the above history together with two diagnostic ECGs and a troponin compatible with OMI, the cardiologist thought the ECG represented pericarditis and recommended echocardiogram.

Several hours passed with no documentation as to the reason for delay. Echocardiogram was finally performed five hours after the first diagnostic ECG. The report indicates LVEF 35-40% with "globally reduced wall motion with regional abnormalities." The cardiologist then recommended emergent transfer to a PCI center.

Upon arrival at the PCI center, he was immediately taken to cath lab. Angiogram showed thrombotic subtotal occlusion of LCx/OM1. Here is an AP caudal view before and after PCI. 

The true AV groove LCx was "jailed" by the stent and appears occluded in the post PCI image. The OM is a much larger vessel.

With the delays and recognition and transit, time from first diagnostic ECG to balloon was 15 hours and 47 minutes. This far out, the benefit of PCI is very attenuated. Troponin peaked above the upper limit of quantitation 60,000 ng/L. Echocardiogram showed LVEF 33% with akinesis of the lateral wall.

Here is the wall motion diagram. The view above is enclosed in a red box.

Final diagnosis written in the chart: NSTEMI

Discussion:

It is hard to understand how this can happen, but unfortunately the blog has innumerable similar cases. If I had to guess, I think some of the cognitive errors that may have contributed to this case are:

• The patient was young, in his mid 30s. But you are never too young to have an OMI. Even if it is not atherosclerotic, young people can have embolic OMIs.
• Here are cases of Young Women

• The ECG was perceived as having diffuse ST elevations. But it is not really diffuse -- it is inferior, posterior, and lateral. The anterior leads clearly show reciprocal change.

• The absolute degree of ST elevation (although enough to meet STEMI criteria), was still relatively small.

We also see that in the end the patient was labeled as NSTEMI, despite meeting STEMI criteria and having acute coronary occlusion. So the diagnosis does not reflect the ECG or the pathology. Instead, the diagnosis reflects how urgently he was treated.

Now, when the data are sent to the National Cardiovascular Data Registry, it will appear that the patient was treated appropriately as an NSTEMI! There is no external auditing of diagnoses selected by treating cardiologists, so missed door-to-balloon time metrics can easily be avoided by simply calling cases NSTEMI.

Smith: We usually talk about OMI that are missed because they do not meet "STEMI criteria".  But in this case, the 2nd ECG definitely meets STEMI criteria, but is nevertheless both missed AND ultimately called "NSTEMI".  We are submitting a paper showing that the most important factor in final diagnosis of STEMI vs. NSTEMI is not whether there is or is not diagnostic ST Elevation, and not whether there is or is not acute coronary occlusion, but rather whether the patient was treated in ＜ 90 minutes vs. ＞ 90 minutes.  This makes it easier to have favorable statistics of course.

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MY Comment, by KEN GRAUER, MD (2/16/2025):  

===================================

Several aphorisms came to mind as I reviewed today's case. These include:

• "Junk in = Junk out ... "
•     — "Common Things are Common."
•         — "If in doubt — Repeat the ECG" (and do it soon! ).

"Junk in = Junk out ... "

Computers are wonderful instruments. But if the data we feed our computer is "junk" — then the answer the computer will give us will inevitably be "junk".

• The application of this 1st aphorism to ECG interpretation is that if your ECG is so full of artifact that assessment of ECG waveforms is unclear — then our interpretation of that ECG will be equally unclear.
• One of the most common errors I've observed over the years — is the tendency of all-too-many providers to accept "junk" on an ECG or rhythm strip when assessing the tracing of an emergency patient. While true that artifact may sometimes be difficult to eliminate (ie, in your shivering or trembling patient) — much (most) of the time the quality of your initial ECG can at least be improved by repeating the ECG with efforts to minimize artifact.
• Today's initial ECG provides a perfect example of this principle (TOP tracing that I have reproduced in Figure-1). Although we can guess at the ECG changes in ECG #1 — because of the small size of the QRS in multiple leads and the amount of baseline undulation — I found it impossible to be confident of my interpretation of this tracing from this patient with 2 days of midsternal CP (Chest Pain). Why guess when the decision of whether or not to immediately activate the cath lab hangs in the balance? Solution: Immediately repeat the ECG!

"Common Things are Common."

The consulting cardiologist in today's case further delayed the decision to perform cardiac catheterization because this cardiologist interpreted the 2 serial ECGs in today's case as consistent with acute pericarditis — despite an initial Troponin value over 25,000 ng/L. 

• Acute coronary syndromes are common in patients who present to an ED with new CP. In contrast — acute pericarditis is rare among chest pain patients who present to the ED (a point we have emphasized on numerous occasions in Dr. Smith's ECG Blog — including My Comment in the May 16, 2023 post — and the December 13, 2019 post, among others).
• KEY Point: Since it is rare to see true acute pericarditis among patients who present with new CP to an ED — that diagnosis should only be made after confidently ruling out an acute OMI (and not after an initial Troponin over 25,000 ng/L and 2 serial ECGs that should be interpreted as strongly suggestive of acute OMI until proven otherwise).
• Solution: The easiest way to avoid the misdiagnosis of acute pericarditis — is to remind yourself that most of the time the patient presenting to the ED with new CP will either have an acute coronary syndrome or "something else", but not acute pericarditis.
• P.S.: I saw no mention of having listened for a pericardial friction rub in the description of today's case. Not carefully listening for a rub when contemplating the diagnosis of acute pericarditis is not understanding that a pericardial friction rub is the single finding that could potentially be diagnostic of acute pericarditis. In my experience over 4+ decades of Attending and consulting on cases of other providers — not mentioning (and documenting in the chart) whether or not a rub was listened for in cases of suspected pericarditis is the most common oversight I've encountered. Not mentioning as a positive or negative finding whether a pericardial friction rub was or was not heard in my experience means that the provider did not listen for this.

"IF in Doubt — Repeat the ECG (and Do It Soon! )."

We are not told how much time passed in between the recording of ECG #1 and ECG #2 (beyond knowing that at least enough time passed for Troponin results to return).

• Regardless of how much time passed between the recording of these 2 tracings — it was too much time — since the artifact-laden initial ECG should have been immediately repeated by the "Junk in = Junk out" principle.

Figure-1: I've labeled the 2 ECGs in today's case.

ECG Findings in Today's CASE:

Despite the technical problems with ECG #1 — there are a number of insightful findings. As per Dr. Frick — there are subtle hyperacute T waves in multiple leads (upward arrows that I have added in).

• I enclosed lead V2 within a RED rectangle — because this is the lead that immediately caught my "eye". This lead eliminated acute pericarditis from my differential diagnosis. Among the ECG findings of acute pericarditis that I review in My Comment in the May 16, 2023 post — there should not be ST depression in lead V2 (RED arrow in this lead).
• Instead, in this patient with persistent CP and a markedly elevated Troponin — the ST depression seen in lead V2 is diagnostic of acute posterior OMI. This diagnosis is supported by the lack of any ST elevation in neighboring lead V3 (since there should normally be a slight amount of gently upward sloping ST elevation in leads V2,V3).
• The question marks and +/- label that I added in ECG #1 also negate consideration of acute pericardits, which would not show more ST elevation in lead V6 than in leads V3,V4,V5. Instead (and despite the artifact) — the unmistakable ST elevation in lead V6 confirms (until proven otherwise) that there is ongoing acute lateral OMI.
• Limb lead findings consistent with acute infero-lateral OMI are the subtly elevated ST segments in leads I,II,III,aVF — and especially the T wave inversion in lead aVL (BLUE arrow in this lead). Abnormal straightening of the ST segment takeoff in leads II and aVF is seen through the artifact — but before clinical decisions are made, this tracing should be repeated.
• Finally — there is low voltage in the limb leads. While many entities may cause low voltage — this is potentially a worrisome sign when seen in association with acute MI, as it may be an indicator of extensive infarction with myocardial "stunning" (See My Comments in the November 12, 2020 post and the January 24, 2020 post).

The Repeat ECG in Today's CASE:

Artifact was virtually eliminated in the repeat ECG. As noted — we are not told how much time passed between the recording of ECG #1 and ECG #2. There have been some serial changes between these 2 tracings. These are best appreciated by putting both ECGs side-by-side (as in Figure-1).

• QRS amplitude remains tiny in the limb leads. Considering the small size of QRS complexes in all 6 limb leads — the ST-T wave shape and the amount of ST elevation relative to the QRS is extreme.
• Why is there now ST depression in lead III? Presumably the increase in ST elevation in lateral leads I,aVL; V5,V6 from acute LCx/OM-1 occlusion attenuated the ST elevation from associated inferior infarction as it is seen in oppositely-directed lead III (lead III being the most distant of the inferior leads from lateral leads I and aVL).
• Chest lead findings in ECG #2 that further support acutely evolving posterior OMI include: i) Development of a tall R wave in lead V2; and, ii) Subtle increase in the amount of J-point ST depression in leads V1,V2,V3.

Conclusion: There is much to be learned from today's case ...  

 

A man in his 30s with epigastric pain and chest pressure

Written by Pendell Meyers

A man in his 30s presented with acute upper midline abdominal pain and nausea. He described it as radiating into his chest, like "pressure", and "burning". 

Vitals were within normal limits except bradycardia. Here is his triage ECG:

What do you think?

Sinus bradycardia, normal QRS. There is STE in several leads including I, aVL, and V2, with STD in II and aVF. The question is whether this is due to OMI, or not. If it were due to OMI, it would fulfill the "South African Flag" pattern.

Unfortunately, presence of reciprocal depression does not ensure that STE is due to OMI. 

I sent this ECG with zero other information to Dr. Smith and Dr. Frick, both said it was an OMI mimic (meaning they do not think that the STE in I, aVL, V2, etc, is due to acute coronary occlusion, but rather a normal variant). I agreed, there is something about the morphology (including the J waves, but not limited to that) that doesn't match prior OMIs in my experience, and does match prior normal variants. 

PM Cardio QOH says No signs of OMI.

The ECG meets STEMI criteria objectively.

The ED physician did not think the ECG represented OMI.

Two serial high sensitivity troponin T levels were undetectably low (less than 6ng/L). AMI was ruled out.

One other ECG was obtained during the ED stay:

The patient was discharged home. No further follow up is available.

Compare this case with similar OMIs and OMI mimics:

Quiz post - which of these, if any, are OMI? What is the South African Flag Sign? Will you activate the cath lab? Can you tell the difference on ECG?

Quiz post: do either or both of these patients have high lateral OMI / South African flag sign?

Abdominal Pain in a middle-aged patient

True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

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MY Comment, by KEN GRAUER, MD (2/14/2025):

===================================

I find cases like today's challenging. My answers usually take 1 of 3 forms: i) That the initial ECG is diagnostic or strongly suspicious of acute OMI until proven otherwise; — ii) That the initial ECG is simply not suggestive of anything acute; — or — iii) That I do not think the initial ECG represents an acute OMI — but I would not send the patient home on the basis of this single ECG.

• For me, today's initial tracing best fits in Category iii) — in that I did not think this tracing represents an acute OMI — but that I would want more information before sending the patient home.

For clarity in Figure-1 — I've labeled today's initial ECG to highlight the findings that "caught my eye".

Figure-1: I've labeled the initial ECG in today's case.

Today's Initial ECG:

For an otherwise presumably healthy 30-year old man — there are some unusual findings in ECG #1. These include the following:

• A fairly marked sinus arrhythmia with bradycardia, and almost the pattern of "group" beating in the long lead rhythm strip. P wave amplitude is reduced in virtually all leads — with comparable small size of the upright P waves in lead I as in lead II, making me question whether this truly is a sinus rhythm? — vs a low atrial rhythm? — vs the possibility of LA-LL Reversal? (See My Comment in the June 25, 2024 post for changes with LA-LL reversal). The above said — this is not necessarily an abnormal rhythm in a young adult.
• A 4-component rSR's' complex in lead V1. This is not a simple incomplete RBBB pattern, which should only consist of 3 components without a terminal s' deflection.
• A slender, but unusually deep Q wave in lead III (that is over 5 mm deep). Narrow Q waves are also seen in leads aVF and V6.
• Prominent J-point notching in leads I and aVL. These look a bit unusual, because we are not accustomed to seeing such deep S waves in these high-lateral leads. That said — this notching is usually a benign feature of repolarization variants, especially when associated with no more than modest ST elevation associated with an upward concavity (ie, "smiley" configuration), as seen here.
• From the perspective of a patient presenting to the ED with abdominal pain radiating to the chest — I found the flat (shelf-like) ST depression in lead aVF to be the most concerning feature in this tracing.
• J-point depression with a downsloping ST segment and biphasic T wave in lead III would have added to my concern if this ST-T wave picture in lead III was not the exact mirror-image opposite of what I perceived to be a benign picture of prominent J-point with smooth, upsloping ST elevation in lead aVL.
• Finally, though not more than minimally depressed — the flattened ST segment in lead V6 could be complementary to the ST depression seen in lead III.

Putting It All Together: 

I thought the initial ECG in today's case was not "normal" for a man in his 30s.

• I did not think this initial tracing represented an acute OMI — because of the benign-looking appearance of J-point notching with upward sloping ST elevation in leads I,aVL.
• I wondered if some of the unusual QRS features in the limb leads could be the result of LA-LL reversal — so I would verify lead placement.
• That said — a form of limb lead reversal would not alter the 4-component rSR's' complex in lead V1, so the leads may be correctly placed.
• I'd want to know about the patient's body habitus (as possible explanation for some of the less usual ECG features).
• And then, I am left with that shelf-like ST segment depression in lead aVF — that is not usually part of the picture of a repolarization variant. And this patient did present to an ED with new symptoms of a "pressure" that radiates to the chest. Primarily for this reason — I was less than 100% certain about the diagnosis.
• BOTTOM LINE: I did not think ECG #1 represented an acute OMI. That said — I was less than 100% certain of that on the basis of the single initial ECG. As a result — I would: i) Repeat the ECG after verifying lead placement; — ii) Rule out acute OMI with 2 serial Troponins, as was done; — and, iii) Get an Echo to rule out any unexpected underlying structural disease (I find it insightful to always try to better understand why a non-OMI ECG may have unexpected features). 

 

** **ACUTE MI/STEMI** **: Activate the cath lab if the patient has chest pain?

Written by Willy Frick

I was reviewing our institutional PMcardio account which we are using to improve early identification of patients with electrocardiographically subtle OMI. 

I came across this ECG:

What do you think?

Even before we have clinical context, this ECG simply does not appear concerning for OMI, notwithstanding the machine's interpretation ** ** ACUTE MI / STEMI ** **. 

I sent this ECG to Dr. Smith with no clinical context, and he immediately replied "Fake." 

I suspect most blog readers did not struggle with this one. But in the world of STEMI, this is a challenging ECG to most.

Furthermore, how many clinicians are truly comfortable setting aside the machine interpretation and sticking with their gut that this ECG does not look ischemic. Fortunately, the physicians seeing the patient were using the Queen of Hearts PM Cardio AI ECG OMI Model, and she had absolutely no concerns.

When the Queen has some suspicion of OMI, she asks if the patient has ACS Symptoms.  She did not even need to ask in this case, because even if the patient presented with chest pain, she would call it NEGATIVE.

When I reviewed the chart, I learned that the patient had presented with syncope. The emergency physician does cautiously (correctly) note that the ECG meets STEMI criteria in V3 and V4, but goes on to document absence of ACS symptoms. The patient ruled out for MI with serial troponin testing.

Most impressively, cardiology was never consulted! This reassuring assistance from AI improved the patient's care by preventing unneeded additional testing and involvement of specialists.

The Queen of Hearts not only is extremely sensitive for subtle OMI, but is also great at recognizing false positive ECGs.

The Queen decreases false positive cath lab activations.

We published this study, showing that false positive prehospital cath lab activations would be decreased by 58% if they used the Queen:

https://www.tandfonline.com/doi/abs/10.1080/10903127.2024.2399218

Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study

Peter O. Baker

,

Shifa R. Karim

,

Stephen W. Smith

,

H. Pendell Meyers

,

Aaron E. Robinson

,

Ishmam Ibtida

,

Rehan M. Karim

,

Gabriel A. Keller

,

Kristie A. Royce

 &

Michael A. Puskarich

Abstract

Objectives

Data suggest patients suffering acute coronary occlusion myocardial infarction (OMI) benefit from prompt primary percutaneous intervention (PPCI). Many emergency medical services (EMS) activate catheterization labs to reduce time to PPCI, but suffer a high burden of inappropriate activations. Artificial intelligence (AI) algorithms show promise to improve electrocardiogram (ECG) interpretation. The primary objective was to evaluate the potential of AI to reduce false positive activations without missing OMI.

Methods

Electrocardiograms were categorized by (1) STEMI criteria, (2) ECG integrated device software and (3) a proprietary AI algorithm (Queen of Hearts (QOH), Powerful Medical). If multiple ECGs were obtained and any one tracing was positive for a given method, that diagnostic method was considered positive. The primary outcome was OMI defined as an angiographic culprit lesion with either TIMI 0–2 flow; or TIMI 3 flow with either peak high sensitivity troponin-I > 5000 ng/L or new wall motion abnormality. The primary analysis was per-patient proportion of false positives.

Results

A total of 140 patients were screened and 117 met criteria. Of these, 48 met the primary outcome criteria of OMI. There were 80 positives by STEMI criteria, 88 by device algorithm, and 77 by AI software. All approaches reduced false positives, 27% for STEMI, 22% for device software, and 34% for AI (p < 0.01 for all). The reduction in false positives did not significantly differ between STEMI criteria and AI software (p = 0.19) but STEMI criteria missed 6 (5%) OMIs, while AI missed none (p = 0.01).

Conclusions

In this single-center retrospective study, an AI-driven algorithm reduced false positive diagnoses of OMI compared to EMS clinician gestalt. Compared to AI (which missed no OMI), STEMI criteria also reduced false positives but missed 6 true OMI. External validation of these findings in prospective cohorts is indicated.

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MY Comment, by KEN GRAUER, MD (2/12/2025):  

===================================

As per Dr. Frick — the ST elevation and T wave inversion in today's ECG is not the result of an acute OMI. Instead — it is almost certain to be a longstanding finding in this patient with marked LVH.

• As I emphasized in My Comment at the bottom of the page in the December 14, 2022 post — We have reviewed many cases that illustrate the challenge posed by distinguishing between marked LVH — vs LVH + superimposed acute OMI.
• PEARL #1: In general, it is rare to see both marked LVH and acute OMI in the same tracing. It is for this reason — that we can get a "head start" in our interpretation of a patient with symptoms in which there is obvious LVH. This is because statistically (supported by our experience) — in the vast majority of cases, such tracings may mimic acute OMI, but acute coronary occlusion will rarely be seen.
• PEARL #2: The above said — Remember the rule of "N = 1". By this I mean that even though it is rare to see an acute anterior OMI in a patient with marked LVH — this can occur — so that we want to be prudent and avoid overlooking the rare OMI in a patient with marked LVH (See the above mentioned December 14, 2022 post for a case in which marked LVH and acute OMI coexist).
• BOTTOM Line: Awareness of the criteria for ECG diagnosis of LVH goes a long way toward facilitating interpretation. Toward this end — we've conveniently added a LINK for "LVH Criteria" in the Menu at the top of every page in Dr. Smith's ECG Blog. This link takes you to My Comment in the June 20, 2020 post — in which I review a user-friendly approach to ECG recognition of LVH and "Strain".

Figure-1: I've labeled today's ECG.

Regarding Today's CASE:

For clarity in Figure-1 — I've labeled today's tracing. 

• The diagnosis of marked LVH should be obvious in Figure-1. That said — overlap of R waves with S waves in multiple leads (especially with the long lead rhythm strips at the bottom of the tracing) — complicates accurate determination of QRS amplitudes (See my color-coding in Figure-1 for my best effort at calculating R wave and S wave amplitudes in the various leads).
• PEARL #3: The easiest way to avoid confusing lead overlap — is simply to repeat the ECG at half standardization. This was not done in today's tracing.
• The most difficult beats to assess QRS amplitude on are beats #7,8,9 — because there is overlap with each of the 3 simultaneously-recorded long lead rhythm strips (of leads V1,II,V5). For example — true amplitude of the S wave in lead V3 is almost entirely concealed by overlap of both the lead V1 and lead II rhythm strips below it. In such cases of multiple lead overlap — I look elsewhere for leads with less overlap (ie, in leads II and V1, which are outlined in YELLOW and PINK) to determine the true amplitude of the S and R waves in these leads. This allowed me to determine that the S wave in lead V3 (in light BLUE) measures 36 mm deep!
• PEARL #4: The KEY for determining that rather than "fulfilling STEMI millimeter-based criteria" for the amount of ST elevation in lead V3 — given the 36 mm deep S wave in this lead — this is in no way an "abnormal" amount of ST elevation (ie, the principle of "proportionality" reigns supreme for qualitative assessment of ST-T wave changes in a patient with marked LVH).
• As to the straightened shape of the ST segment takeoff in lead V3 — this shape is completely consistent with the appearance of LV "strain" in an anterior lead in a patient with extremely deep anterior S waves (See My Comment in the February 6, 2020 post).

What About ST-T Wave Changes in Other Leads in Figure-1?

At 1st glance — the ST segment coving with seemingly "deep", symmetric T wave inversion in lead V5 might be of concern. That said — there are several reasons why I felt this ST-T wave appearance in lead V5 was not of concern:

• Again, by the principle of "proportionality" — the 38mm tall R wave in lead V5 suggests the relative size of the inverted T wave in this lead is not as deep as one might initially think.
• The slow downsloping, more rapid upsloping ST depression seen in lead V6 is absolutely typical for LV "strain" in this left-sided lead in which R wave amplitude is significantly increased (measuring 22 mm).
• Patients with marked LVH (especially those with longstanding hypertension) often manifest not only ST-T wave changes that are typical for LV "strain" — but also symmetric T wave inversion as seen here in lead V5.
• Finally — I interpreted the ST-T wave appearance in lead V5 as a "transition" lead that lies in between the ST coving and elevation seen in lead V4 — and the "strain"-like ST depression seen in lead V6. This ST-T wave pattern in lead V5 is not seen in other leads, as would be expected if this was truly a change of acute ischemia.

What about the R = S Phenomenon in the Inferior Leads?

I found the surprisingly tall R = S Waves in each of the inferior leads an interesting and unusual feature (R waves and S waves each ≥15 mm in leads II,III and aVF). I cannot remember the last time I saw this pattern in each of the 3 inferior leads.

• This R=S pattern of tall RS complexes brings to mind the Katz-Wachtel phenomenon described in pediatric patients — in which the finding of biphasic RS complexes of ≥50 mm in mid-chest leads V2, V3 or V4 suggests biventricular hypertrophy, especially in children with VSD (Ventricular Septal Defect).
• Clearly, the R=S waves in today's tracing are not as deep as occurs with the Katz-Wachtel phenomenon. That said, given the association of these inferior lead R=S waves with marked increase in chest lead amplitude — I would love to see an Echo on this patient, so as to correlate Echo findings with today's interesting ECG.

Conclusion:

The ECG in today's case is notable for marked LVH. As per Dr. Frick — this ECG is not suggestive of acute OMI. I attributed the diffuse ST-T wave changes to LV "strain" and not ischemia.