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).
• 
  
• 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.
• 
  
• 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).

A 30-something with acute chest pain

This was sent to me from Sam Ghali (@EM_Resus) with no other information.  I assumed it was a patient with acute chest pain.

"What do you think, Steve?  Real or just fake?"

What do YOU think?

It has some inferior ST elevation with some reciprocal ST depression and inverted T in aVL.  This usually indicates inferior OMI.

My answer: "Fake: pretty certain, but not 100% certain."

Sam: "why do you say fake?"

Smith: "Gestalt, but if I must explain: well formed J-waves and high voltage R waves."

Sam: "Yeah I think too the negative QRS in aVL takes away from changes that may be interpreted as “reciprocal”"

Smith: "did the cath lab get activated?"

Sam: "Yes, this case was sent to me.  It was a man in his 30s with chest pain.  Coronaries were clean.  Troponins were all negative -- the patient ruled out for acute MI."

Finally, Sam: "Honestly in addition to expert ECG interpretation I think skilled bedside echo can prevent a lot of these activations."

I agree, however: 

1) I don't think you can get a good enough echo without bubble contrast.  

2) You need to be just as expert at echo as I am at the ECG.

3) Echo is another step that takes time.  Time is myocardium.

So the best course of action:

 Use the PMCardio Queen of Hearts AI in ECG interpretation.

Not OMI with High Confidence

Click here to sign up for Queen of Hearts Access

We showed that the Queen of Hearts decreases false positive cath lab activations:

1) Published recently in Prehospital Emergency Care

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

This showed a decrease of false positive cath lab activations from 69 by medics to 29 by use of the Queen of Hearts, while still identifying all 48 true positive OMI.   I had only 9 false positives but I missed 2 OMI.  The integrated device algorithm had 42 false positives and one missed OMI.

Full text!

2) To be presented at AHA conference in Chicago in 2 weeks: 

Sharkey SW et al.  Performance of Artificial Intelligence Powered ECG Analysis in Suspected ST-Segment Elevation Myocardial Infarction.  This showed a decrease in false positive cath lab activations from 637 out of 2526 (25%) to 403 our of 2526 (16%), a 37% decrease in false positive activations.  Of those with MI and a culprit, 4% were missed (called "Not OMI"), but these were not necessarily occlusions (most MI with an open artery have a culprit), and many were LBBB.

Click here to sign up for Queen of Hearts Access

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MY Comment, by KEN GRAUER, MD (10/3/2024):  

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I looked at the ECG in today’s case knowing only that the patient was a younger male adult with CP (Chest Pain).

• While statistical likelihood of acute OMI is clearly lower in younger adults — nothing is ruled out by age alone (as per My Comment in the January 9, 2023 and December 5, 2023 posts in Dr. Smith's ECG Blog).
• Without knowing more about today’s case — I also thought (as did Dr. Smith) — that this ECG (that I’ve labeled in Figure-1) was likely to be a “fake”. 

ECG Features suggesting "Fake"

As per Dr. Sam Ghali (who sent us today's case) — serial Troponins were clearly indicated since the patient presented to the ED. These were all negative. I'd defer on the question of whether cardiac catheterization was needed by saying, "Ya gotta be there" — but there clearly are ECG features suggesting no OMI.

• The rhythm for the ECG in Figure-1 is sinus — with normal intervals and axis (mean QRS axis about +80 degrees). There is no chamber enlargement.
• One wonders about lead placement, given abrupt transition from the similar-looking predominantly negative QRS complexes in leads V1,V2 — to a nearly all-positive QRS by lead V3.

Regarding ST-T Waves:

• There clearly is ST elevation in each of the inferior leads. 
• I suspect the presence of T wave inversion in lead aVL increased concern about reciprocal ST-T wave changes — which must have been perceived as suggestive of acute inferior OMI, since cardiac catheterization was performed.

There is No Reciprocal ST-T Depression:
We have often referred to the almost "magical" mirror-image relationship for ST-T waves in leads III and aVL when there is acute inferior MI (See My Comment in the September 30, 2019 post in Dr. Smith's ECG Blog, as well as many others). That said — I would not interpret ST-T wave appearance in lead aVL of today's ECG as a "reciprocal" change.

• The T wave vector often follows closely behind the QRS vector. As a result — when the QRS is predominantly negative in lead aVL — then the T wave in this lead may also be negative as a normal finding. This is precisely what we see in ECG #1 — in which the frontal plane axis is +80 degrees (which is most probably the reason for the shallow T wave inversion highlighted by the BLUE arrow in this lead).
• Contrast this normal amount of T wave inversion seen within the BLUE rectangle in ECG #1 — with the disproportionately "bulky" T wave inversion seen within the RED insert of lead aVL that I've excerpted from the initial ECG of a different patient who was having an acute OMI (See My Comment in the September 27, 2024 post).
• Therefore — there is no reciprocal ST-T wave depression in today's case!

There is No Sign of Posterior OMI:
It is common to see indication of posterior OMI when (if) there is inferior OMI. Posterior OMI is typically diagnosed by the finding of chest lead ST depression that is maximal in leads V2, V3 and/or V4. We do not see this in ECG #1.

• As noted above — the similar-appearing QRST complex in leads V1,V2 — followed by abrupt transition to a predominantly positive QRS by lead V3 — suggests there may be an error with precordial electrode lead placement.
• That said — None of the chest leads show ST depression.
• While the absence of indication of posterior OMI does not rule out the possibility of acute inferior OMI — it does make this less likely.

There ARE Signs of a Repolarization Variant:

Among the many posts in which we've reviewed cases of repolarization variants — is the May 23, 2022 post. From this post:

• Among the most suggestive ECG features of a repolarization variant — is the presence of an end-QRS notch (J wave) — and/or — a "slur" on the downslope of a prominent R wave.
• Although subtle — J-point notching is seen in leads V4 and V5 of ECG #1 (within the dotted PURPLE circles in these leads).
• A "slur" is seen on the downslope of the R waves in leads II,III,aVF and V6 (GREEN arrows in these leads).
• 
  
• Finally — Not only are reciprocal changes absent in ECG #1 — but a similar shape to the ST segments is seen in multiple leads (ie, leads I,II,III; aVF; V3,4,5,6) — which is more characteristic of a repolarization variant (as opposed to the ST-T wave changes of acute OMI that more often localize).

BOTTOM Line in Today's CASE: While fully acknowledging that in a patient who presents to the ED with CP — "Ya gotta be there" to best determine how much evaluation is needed to rule an OMI in or out. That said — I thought the ECG in Figure-1 looked more like a "fake" than like an acute OMI.

• Negative serial Troponins were needed to rule out an acute event.
• Serial ECGs would be expected to show no evolution.
• A normal Echo obtained during CP would support this being a repolarization variant.
• If a final test was perceived as "needed" — perhaps a normal coronary CT angiogram could have helped to avoid cardiac catheterization.

Figure-1: I’ve labeled the initial ECG in today's case. The RED Insert for lead aVL is excerpted from My Comment in the September 27, 2024 post in Dr. Smith's ECG Blog (taken from the initial ECG in that Sept. 27 post).

 

What do you think of these 2 ECGs in patients with chest pain? How to approach these?

What do you think of these 2 ECGs in patients with chest pain?  How to approach these?

ECG 1 (sent to my by Sam Ghali @EM_resus)

ECG 2

ECG 1 

This was sent to me with no clinical information and the question "what do you think?"  

My answer was: "sinus rhythm with right atrial enlargement, probable right ventricular hypertrophy, and old inferior MI with inferior LV aneurysm."  The T-wave inversion in I and aVL is reciprocal to the Old inferior aneurysm.

After I sent my answer, I received this history:

66 yo man presented with chest pain

History of CAD [unclear details out of state, stent(s)?]

STEMI alerted pre-hospital

Found to have very elevated lactate

Significant AKI

Aortic thrombus (chronic) on CT

hS Trop T:   1609->2471->1929 ng/L

Cards was planning on  cath when metabolic situation settled

Angiogram: no culprit and all open arteries.

Final diagnosis: type II MI due to illness

The Queen of Hearts said "OMI with mid confidence."  Version 1 of the Queen does not do a good job of recognizing LV aneurysm morphology, whether it is anterior (which for an expert is not too difficult because they almost always have QS-waves) or inferior (which is even very difficult much of the time for me, because inferior aneurysm frequently has QR-waves)

How to approach?  --when the diagnosis could be "ST Elevation due to Old MI" or "LV Aneurysm Morphology", it is essential to look into the old charts and old ECGs, if available.  It is also essential to assess for other etiologies of the symptoms, and in this case the patient had physiological derangement, with elevated lactate and AKI.  This points to another inciting etiology rather than ACS as the primary mover.  

These physiological derangements do not rule out ACS, but make it much more likely that the patients illness was incited by another factor.

ECG 2

I was reading ECGs on the system and came across ECG 2 and said out loud: "This is a fake."  A colleague sitting next to me asked "why?", and I answered that there is a "saddleback" in lead III and well-formed Q-wave.  Saddleback ST elevation is rarely due to OMI. 

However, on very few occasions Saddleback STE actually is due to OMI.

The Queen of Hearts had stated "Not OMI with low confidence"

There was a previous ECG available:

This confirmed my opinion.

I found out later that the patient had gone to the cath lab.  And I found out that the cath lab activation was a result of this follow up ECG:

I find this to be a negative ECG, except that there is now new ST Depression in V4-V6.

However, there is new tachycardia, and that new ST depression could be a result of supply-demand ischemia from tachycardia.

This time, the Queen of Hearts diagnosed this as "OMI with High Confidence."

This Queen interpretation led to a false positive cath lab activation.

Alternative Management: Always look into the patient's chart!! (including the old ECG above, which was not seen)

In fact, I found that I had blogged this patient before (!!!) due to the ECG that looked like inferior aneurysm.  There were many previous similar ECGs.  Here is that post: 

A Patient with Vertigo

Angiogram 3 months ago:

Severe three vessel native CAD with occlusion of the mid-Cx, mid-LAD, and mid-RCA including several areas of in-stent stenosis or occlusion.  4/4 patent bypass grafts (RIMA > dLAD, LIMA > OM, SVG > rPDA, and free radial > rPLA1) with severe native vessel stenosis just beyond the anastomosis in the dLAD, OM, and rPDA

Previous coronary disease and h/o CABG tells you that there probably is an old infarct and that the baseline ECG is likely to be abnormal and that you should read the present ECG in that context.

Previous Echo:

Normal left ventricular cavity size, mildly increased wall thickness and moderate LV systolic dysfunction.

The estimated left ventricular ejection fraction is 35-40 %.

Regional wall motion abnormality- basal inferior akinetic.

Regional wall motion abnormality- basal inferolateral, akinetic.

Regional wall motion abnormality-apex small .

An Akinetic wall can have the same "LV aneurysm" Morphology as a Dyskinetic wall ("diastolic dyskinesis" is the echo definition of aneurysm.)

The cath lab was activated and there was no acute OMI.  False Positive.

Discussion:

These are very complex cases in which there could be OMI or there could be old MI.  These are the kind of cases in which you want to consult your friendly cardiologist and have a discussion.  But that is only if your cardiologists accept the idea of OMI (Acute Coronary Occlusion in the Absence of ST Elevation criteria).  To make such a consultation,  there must be mutual trust that the consultant will not dismiss your concerns or say "Nah, couldn't be."

It can take years to build such trust.

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MY Comment, by KEN GRAUER, MD (7/30/2024):

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The "theme" of My Comment in today's case is — Shape is KEY!

• For clarity and ease of comparison in Figure-1 — I've labeled and put together the initial 2 ECGs in today's case.

MY Thoughts on ECG #1:

This is a complex tracing. I saw the following:

• There is significant baseline artifact. This is relevant to our interpretation given the difficulty it poses for assessment of ST-T wave changes in multiple leads.
• That said — the rhythm is clearly sinus with a normal PR interval.
• QRS morphology is not normal. That said — the QRS is really not wide (ie, not more than 0.10 second). Given the all upright QRS complex in lead V1, with narrow but definite terminal S waves in lateral leads I and V6 — this QRS morphology is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• The QTc is prolonged (I measure the QT at ~0.44 second — which corrected for the rate of ~80/minute, comes out to a QTc ~0.49 second).
• There is marked LAD (Left Axis Deviation) — with entirely negative QRS complexes in each of the inferior leads. This is consistent with LAHB (Left Anterior HemiBlock).
• There is RAA (Right Atrial Abnormality) — as determined by the presence of tall, peaked and pointed P waves in the inferior leads (ie, P waves ≥2.5 mm in amplitude).
• There may be RVH (Right Ventricular Hypertrophy) — which always needs to be considered if there is true right atrial enlargement. Because of the artifiact — we can not tell if QRS morphology in lead V1 is triphasic (rsR') or represents a qR pattern, which could be consistent with pulmonary hypertension (for more on RAA, RVH — See My Comment in the February 12, 2023 post).
• There may be LVH by Peguero criteria (See My Comment in the June 20, 2020 post) — as suggested by the very deep S waves in leads V3 and V4 (with the PURPLE arrow in lead V3 showing that S wave amplitude is cut off in this lead).

Regarding Q-R-S-T Changes:

• More than inferior Q waves — there is marked fragmentation on each downslope of the S wave in the inferior leads (RED arrows in these leads). It is because of this marked fragmentation that the “attempt” to form a positive deflection in each inferior lead never makes it back to the baseline before being overtaken by resumption of S wave negativity. In my experience — this fragmented QRS shape in any one (let alone all 3) of the inferior leads strongly suggests inferior infarction at some point in time.
• Regarding R wave progression — I interpreted the seemingly multi-phasic upright complex in lead V1 as the result of IRBBB rather than RVH because: i) There is marked LAD with no more than modest depth of the S wave in lead I; and, ii) I thought the overall ECG picture more suggestive of coronary disease rather than RVH. Yet predominant positivity never occurs in the lateral chest leads — and I could not rule out the possibility of RVH on this ECG alone.
• The shape of the S-T segments in the inferior leads is coved, of relatively long duration, and shows slight ST elevation. This shape forms a “picture to remember” — that does not look acute. That this inferior lead ST-T wave appearance is unlikely to be acute — is further supported by a lack of reciprocal ST depression in high-lateral leads I and aVL. Instead (as per Dr. Smith) — this “picture” strongly suggests inferior wall aneurysm, especially given the inferior lead S wave fragmentation marker of prior inferior MI described above.
• Finally — there is ST segment straightening and depression beginning in lead V3 beyond that expected for simple IRBBB (BLUE arrows in the chest leads).

BOTTOM Line: Like Dr. Smith — as a single ECG that I interpreted knowing only that the patient had "chest pain" — I thought ECG #1 did not look acute. But there are multiple complexities that beg further explanation.

• I suspected prior inferior MI with IRBBB/LAHB — and now with inferior wall aneurysm. There is ST depression in leads V3-thru-V5 that I thought likely to reflect multi-vessel disease — but with need to explain the reason for RAA, probable LVH, and possible RVH. But – not an OMI.
• As per Dr. Smith — this patient turned out to have Troponin elevation due to Type-2 MI (clean coronaries on cath). Instead — his clinical presentation was dominated by acute renal failure with severe acidosis. We are left with more questions than answers (ie, How severe is his underlying coronary disease? Any RVH or pulmonary hypertension?) — but this is not the ECG of acute coronary conclusion.
• Personal NOTE: I have been fooled more than once by chest pain in the setting of severe underlying disease (ie, acidosis, sepsis). The KEY is to recognize that ECG #1 is unlikely to represent an acute OMI — with clinical priority to treat underlying conditions, and to then reassess symptoms and repeat ECGs as needed.

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

MY Thoughts on ECG #2:

I found today’s 2nd tracing easier to interpret — in that there were far fewer complicating findings.

• The rhythm is sinus — with normal intervals (PR-QRS-QTc). There is LAD (negative QRS in lead aVF) — but an axis not leftward enough to qualify as LAHB (predominant positivity in lead II).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are very large and wide Q waves in leads III and aVF — with a small-but-present Q wave in lead II (RED arrows in these leads). This patient has had inferior infarction at some point in time.
• R wave progression shows slight delay in transition (the R wave only becomes taller than the S wave is deep between lead V4-to-V5).
• S-T elevation is seen in each of the inferior leads, followed by a prominent upright T wave. That said — the shape of the elevated inferior lead ST segments manifests an upward concavity (ie, "smiley" configuration). As per Dr. Smith — this shape is less likely to represent an acute cardiac event.
• Although both high-lateral leads ( = leads I and aVL) manifest ST depression — the precise mirror-image opposite ST-T wave picture from lead III — is seen in lead aVL (within the BLUE rectangle, in which I merely inverted one QRST complex from lead III). This to me suggested a similar acuity (or lack thereof) for both lead aVL and the inferior leads.
• There is slight, nonspecific ST-T wave flattening in leads V1,V2 and V6.

BOTTOM Line: Once again, as a single ECG that I interpreted knowing only that the patient had “chest pain” — I thought ECG #2 did not look acute. 

• The deep, wide Q waves in leads III and aVF (with small-but-present Q in lead II) — strongly suggest prior infarction. This patient almost certainly does have underlying coronary disease. Clinically, if I was managing this patient — more information would clearly be needed (ie, specifics of the history; repeat ECG; troponins; comparison with prior tracings, etc.). But as a single ECG without the benefit of more information — the shape of these inferior lead ST segments — and the lack in the chest leads of any suggestion of associated acute posterior involvement — suggest this is not the result of acute coronary conclusion.
• As per Dr. Smith — review of this patient's chart told the story. Not surprisingly — the patient had very severe underlying coronary disease — but no acute OMI.

 

Quiz post: two patients with chest pain. Do either, both, or neither have OMI?

Written by Pendell Meyers

Two patients with acute chest pain. 

Do either, neither, or both have OMI and need reperfusion?

Patient 1:

Patient 2:

Patient 1:

A man in his 40s with minimal medical history presented with acute chest pain radiating to his R shoulder.

Triage ECG:

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Three serial troponins were all undetectable.

Here is a later ECG during the visit:

Slightly different, with less TWI in inferior leads this time.

He was discharged home.

Patient 2

A man in his 50s with history of CAD and prior PCI, diabetes, presented with acute constant chest pain for the past few hours. Described as a dull ache, 6/10 in severity.

Triage ECG:

It was interpreted as lateral STEMI, and he was sent to the cath lab, where the angiogram showed unchanged CAD from known prior, with no acute culprit.

His disease included 70% prox LAD, 80% distal LAD, 10% in-stent stenosis in the distal LCX, 70% OM1, 70% OM2, and 60% prox RCA.

Three troponins were undetectable.

Here is another ECG later in his stay:

A prior ECG was found:

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Compare the ECGs above with two cases of true high lateral OMIs:

The Queen identifies both of these accurately as OMI with high confidence and explains why:

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How can we identify the top 2 above as false positives?

1) Use the Queen of Hearts

2) It is very difficult to explain and requires a lot of pattern recognition experience and skill.  Dr. Smith identified both correctly, and so did the Queen.

3) Dr. Smith explanation: all I can say is that there is plenty of QRS voltage and that the ST segments, though elevated, have a lot of upward concavity or reciprocal downward concavity.  The ST depression in V4-V6 makes this particularly difficult and hard to ascertain that it is a mimic!

4) Compare with the bottom 2 cases: 

 Top: small voltage QRS and straight ST segments

Bottom: ischemic appearing ST Depression in V2-V6 

See these other relevant cases:

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

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

Even when the story is obvious, with intractable pain, the STEMI paradigm can cause preventable delays

Man in his 60's with very subtle ECG and pain not controlled with medical therapy

Pericarditis vs. MI #2

See other "Quiz Posts":

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?

Two patients with chest pain. Do either of them need emergent reperfusion? Both? Neither?

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

MY Comment, by KEN GRAUER, MD (5/29/2024):

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The expertise of Drs. Smith & Meyers in assessing ECGs for the likelihood of “OMI or no OMI” is truly impressive — and it is through their programming that QOH has obtained “her expertise”. Ongoing updates by Drs. Smith & Meyers will result in ever increasing accuracy of QOH.

• For clarity in Figure-1 — I've reproduced the initial ECGs from Patients #1 and #2 in today's case. 

Figure-1: The initial ECGs for Patients #1 and #2 in today's case.

The above said — I’ll offer the following perspective:

• What really “counts” in a patient who presents to the ED with new CP is whether or not there is an acute, ongoing OMI for which prompt cath with reperfusion will save myocardium (and potentially save a life). This means that some of the patients who present with new CP may have underlying coronary disease from prior events (ie, the multi-vessel disease of Patient #2 in today’s case).
• While I was skeptical after seeing the ECGs in Figure-1 that the 2 patients in today’s case were having an acute OMI (for reasons similar to those highlighted by Dr. Smith above) — I fully acknowledge that I was not 100% certain there was no OMI after seeing the initial tracings. And, we want to get as close to 100% certainty as possible — so additional evaluation (ie, troponins, serial tracings, comparison with prior tracings — and at times, cardiac catheterization) — are all at times appropriate until you can be more certain.
• Although not perfect — the QOH application can be reassuring. Together with the illustration of numerous cases on Dr. Smith’s ECG Blog — our hope is to facilitate rapid identification when acute OMI can be immediately diagnosed by history and the initial ECG. And, although prudence is advised until one attains that greater certainty that an acute event is not ongoing — our hope is that some diagnostic cardiac catheterizations that are not needed can be avoided by the tips and insights provided on this ECG Blog
• 
  
• That said, today’s cases are tough — because both initial ECGs manifest ST elevation with ST depression in oppositely-directed leads — and both manifest taller-than-expected T waves in lead V2 — as well as some unexpected ST depression.
• LVH may further complicate assessment for OMI. As per Dr. Smith — criteria for LVH are satisfied in Patient #2 (ie, R > 20 mm in lead II). Although voltage criteria may fall a bit short for LVH in Patient #1 — the ST-T wave in lead V6 looks typical for LV “strain”. (For more on LVH — See My Comment in the June 20, 2020 post in Dr. Smith’s ECG Blog). 
• 
  
• Bottom Line for Me: Were I in the ED — I would not have been certain from just the initial ECG that there was no OMI, until I obtained more information. I learn from knowing Drs. Smith, Meyers & QOH were certain sooner than I was.

Our thanks to Dr. Meyers for presenting today’s case. It’s always helpful to be “put to the test” — and then provided with insightful follow-up.