This ECG was texted to me after the fact with no information. What do you think?

This ECG was texted to me with no other information, with this quote: "You will see this in the Queen of Hearts."  I assumed it was in real time.

Notice this is a photo of the computer screen, and the left half of the EKG is cut off.

This could affect the results.

The Queen's diagnosis based on this inadequate image was "Not OMI", mid confidence:

This was my response: "I am not certain that I agree with the queen on this one. Be careful with it.  Notice that the Queen has low confidence."  

Why am I worried?   The T-waves are quite tall.  Although most hyperacute T-waves are bulky, wide, fat and symmetric in proportion to the QRS (due to longer QT + straightening of ST) — some are only extra tall in proportion to the QRS.  I very much doubt that this is the patient's baseline ECG.  That said, some patients OMI ECGs look like they are normal and you only know for certain if you can compare to old ones or to serial ones (whether the serial ones are progressing or improving).   

There is worrisome T-wave inversion in inferior leads as well, which is another clue to LAD Occlusion

In fact, this ECG meets STEMI criteria!!  There is greater than 1 mm STE in V4 and V5.  Why does the conventional algorithm not diagnose STEMI?

Here is a case in which the ECG looks normal but not when compared to the old one.  (In this case, 4 variable formula was positive and the Queen diagnosed OMI with mid confidence).  

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

The sender asked: "Would you activate the cath lab?"  My response was: "It depends on the patient. How old? What’s the story?"

Here is the history:

62 yo male w 2d of intermittent chest pain, now constant.

Answer: Yes, I would activate the cath lab.

Next best: record frequent serial ECGs.  I always say to get one every 15 minutes.

It turns out that the ECG had been recorded about 3 hours earlier.  Unfortunately, the patient did not get a repeat ECG until after the first troponin I returned at 1100 ng/L.

Here is a more detailed history:

Presented to the emergency department with chest pain. Patient states that he began to develop substernal chest pain two days ago. He was seen in urgent care yesterday after his symptoms persisted, where he was discharged with a presumed diagnosis of GERD after improvement in symptoms with Maalox. He states that his symptoms gradually returned and has now increased in severity.  The intern in the ED was biased by this previous day GERD diagnosis.

Aside: there is only one way to diagnose GERD as a cause of chest discomfort, and that is includes ruling out MI with EKGs and troponins.  Symptoms of acute MI and GERD are identical, and both may or may not resolve with antacids.  There are so many patients who have died with a diagnosis of GERD.

See these 2 cases:

Missed myocardial infarction with subsequent cardiac arrest

Chest pain relieved by Maalox and viscous lidocaine

I had not noticed yet that his image was cut off.

I went into the patient's chart and retrieved a high quality image:

The conventional algorithm said:

 SINUS RHYTHM

ABNORMAL QRS-T ANGLE  [QRS-T AXIS DIFFERENCE > 60]

ABNORMAL ECG 

This time she still said "Not OMI with mid confidence."

Case Continued:

They did not make the diagnosis of OMI. Unfortunately, there was a 150 minute delay to the repeat ECG.

Here is that repeat ECG at 150 minutes:

Here is the first one again:

Here is the Queen's interpretation again:

Here is the 4 variable formula:

This is a very low value

Angio 100% mid LAD occlusion

Next day ECG:

A very bad outcome

Peak hs troponin I was ＞60,000 (too high to measure, very large OMI)

Formal Echo:

The estimated left ventricular ejection fraction is 42%.

Normal LV cavity size with mildly increased wall thickness.

Regional wall motion abnormalities: mid-apical anterior septum, anterior, anterolateral and apical walls hypokinetic.

Given the very high peak troponin (a good measure of infarct size) and the loss of R-waves with persistent STE, there is a low likelihood of substantial recovery ejection fraction.  This patient has a high likelihood of heart failure.

Learning Points:

1. Sometimes OMI ECGs look quite normal

2. Always compare with old ECGs or get frequent serial ECGs

3. NEVER diagnose chest discomfort as due to GERD without a coronary workup.

4. Even the Queen gets it wrong some times.

5. Always consider pretest probability when evaluating the ECG for OMI (or any test for any condition!)

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MY Comment, by KEN GRAUER, MD (10/13/2023):

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The challenge of today's case is to assess the initial ECG without the benefit of any history — precisely as the case was presented to Dr. Smith.

QUESTION:

• How did YOU interpret the initial ECG in today's case — before Dr. Smith revealed the history? 

For clarity in Figure-1 — I've reproduced the initial ECG in the TOP panel — and have labeled my "thought process" in the BOTTOM panel.

Figure-1: The initial ECG in today's case (TOP) — with the sequence of my "thought process" BELOW.

MY Thoughts on the Initial ECG:

Looking first at the TOP panel of Figure-1 — The rhythm is sinus at ~85/minute. All intervals and the axis are normal. Depending on the age and sex of the patient — there may be borderline voltage for LVH (See My Comment re LVH criteria — at the bottom of the page in the August 15, 2022 post in Dr. Smith's ECG Blog). Regarding Q-R-S-T Changes:

• Narrow Q waves are seen in each of the inferior leads (including a fairly deep Q wave in lead III — albeit the q in lead II is tiny).
• R wave progression is normal — in that transition (ie, where height of the R wave becomes taller than the S wave is deep) occurs appropriately between leads V2-to-V4.
• ST-T wave changes — are worthy of special detailed comment (Below).

My Sequential Approach in the BOTTOM Panel:

Like Dr. Smith — I did not know the history prior to interpreting ECG #1 in Figure-1.

• My attention was first captured by the ST-T wave appearance in lead I (within the RED rectangle). Unfortunately — we only see 3 complexes in lead I, with interpretation complicated by the presence of significant fine baseline undulations (artifact). There is slight variation between ST segment appearance of the 1st and 3rd — vs the 2nd complex that we see in lead I of Figure-1. There is no mistaking that the ST segment of the middle (2nd) complex in lead I is abnormally straight (flat). This is less convincing in the 1st and 3rd QRS complexes.
• In the context of the abnormally straightened ST segment of this middle QRS complex in lead I — I thought the peak of the T wave for each of the 3 complexes in lead I was "fatter"-than-it-should-be (ie, Isn't the peak of each of the T waves in lead I "fatter" than the peak of any other positive T wave in ECG #1?).
• 
  
• To EMPHASIZE: What I describe above for the ST-T wave appearance in lead I is admittedly very subtle — but "my EYE" was immediately drawn to this ST-T wave appearance within the RED rectangle. When I saw this, I THOUGHT: — If the history in today's case was that of new, worrisome CP (Chest Pain) — then perhaps we are seeing hyperacute T waves in lead I?

My attention was next captured by the QRST appearance in inferior leads III and aVF (within the LIGHT BLUE rectangle).

• As noted earlier — We see relatively deep (albeit narrow) Q waves in leads III and aVF.
• Although the ST segments in leads III and aVF are not appreciably elevated — these ST segments are coved, and followed by fairly deep T wave inversion.
• I did not include the 3rd inferior lead ( = lead II) within the light BLUE rectangle — because although there is slight ST elevation in lead II, the overall appearance of the ST-T wave looked relatively benign.
• 
  
• Impression: I thought the QRST appearance in leads III and aVF was non-diagnostic by itself — BUT — If the history was new CP, then the ST coving with fairly deep T inversion might reflect reciprocal changes to a hyperacute T wave in lead I.
• 
  
• NOTE: I did not know how to interpret the ST-T wave appearance in lead aVL. While clearly non-diagnostic — the T wave in lead aVL was relatively tall (almost equaling R wave amplitude in this lead) — such that IF the history was new CP, this T in lead aVL could represent a reciprocal change to the fairly deep T wave inversion in lead III.

Finally — My attention was next captured by the ST-T wave in lead V4 (with the GREEN rectangle).

• Given T wave peaking in multiple chest leads — I would verify that serum K+ is normal (I did not expect this to represent hyperkalemia — because the base of these chest lead T waves is not overly narrow, as it tends to be with hyperkalemia — and we do not see this T wave peaking in the limb leads — but it is worthwhile checking serum K+ nevertheless).
• While R wave progression in the chest leads is normal (with healthy R wave amplitudes attained in leads V2-thru-V5) — and while I did not think the overall shape of the ST-T waves in any of chest leads was abnormal (ie, Normal QTc — upright T waves in V2-thru-V5 without abnormal ST elevation or depression) — I did think that T wave amplitude in lead V4 was disproportionate with respect to height of the R wave and the modest depth of the S wave in this lead. I thought that IF the history was new CP — that this could be the harbinger of a deWinter T wave.
• And — IF the disproportionately tall T wave in lead V4 did represent an early deWinter T wave — then T wave amplitude in neighboring leads V2,V3 and V5 might all also be disproportionately tall, considering R wave amplitude in these leads.

Putting It All Together:

I fully acknowledge that the above description "takes up a lot of words". In brief:

• I thought ECG #1 by itself was non-diagnostic — but potentially suspicious, depending on the history.
• I would not have activated the cath lab based on this single initial ECG in today's case.
• 
  
• Even after learning that the patient was a 62yo man with a 2 day history of "intermittent CP — now constant" — I would not have activated the cath lab. But I would have very soon repeated the ECG (waiting no more than 10-15 minutes, at most).

Unfortunately (as per Dr. Smith) — No repeat ECG was obtained until 2.5 hours after ECG #1 was recorded — at which time the ECG showed an obvious STEMI.

• Even more concerning than not obtaining a repeat ECG until 2.5 hours later — is that there is no mention of what this patient's ECG from the day before looked like (ie, This patient was seen the day before in an urgent care center — and was diagnosed with GERD after improvement of symptoms with Maalox).
• 
  
• IF the diagnosis from the day before visit to the urgent care center was made without doing an ECG — then that would be an essential Learning Point — as symptoms referred to the epigastric area are not uncommon with acute infarction (and as per Dr. Smith — "relief after Maalox" is not at all reliable).
• 
  
• On the other hand, IF an ECG was done in the urgent care center the day before — then there is no excuse for not obtaining a copy of that tracing. Given progression to frank stemi-like ST elevation over the 2.5 hours since ECG #1 was done — it is very likely that a 12-lead ECG from the day before would have looked markedly different, and should have alerted clinicians to the diagnosis of an acute event as soon as ECG #1 was compared with the tracing from a day earlier.

Final Thoughts:

Dr. Smith instantly recognized that today's initial ECG would clearly be suspicious of a possible acute event, depending on the History. 

• From my first look at ECG #1 — I was not certain that an acute event was in progress. But I did know that IF the history was of worrisome, new-onset CP — that the likelihood of an acute event would be significantly increased.
• It's OK not to be "certain" from a single initial ECG about whether or not an acute event is in progress. 
• In a case like today's, even if the initial troponin would have come back "normal" — that would not rule out the possibility of an acute event (because it sometimes takes a little time for troponin to rise).
• So, when you are uncertain from an initial ECG — simple things like seeking out a prior ECG for comparison and repeating the initial ECG soon (ie, within 10-20 minutes at most) — will surprisingly often tell us "the answer" much sooner than occurred in today's unfortunate case.