Acute Chest pain in a 50-something, and a "Normal" ECG

Chris Mondie of the Newark Beth Israel Emergency Medicine Residency sent this case

A 50-something man presented with acute chest pain.

Here is his ECG:

As you can see, the computer called it completely normal
What do you think?

This was the Marquette 12 SL GE algorithm

The computer did not even mention the ST elevation.  It could at least say: "ST Elevation, consistent with normal variant," or "consistent with ischemia or normal variant," or "consistent with early repolarization."  But it simply says "normal."

An interpretation of "normal" could, of course, deceive many providers.

Analysis

This could be normal variant ST Elevation in V2 and V3.  There is 1.5 mm STE in at the J-point in lead V2 (relative to QRS onset, otherwise known as PQ junction).  There is 1.0 mm in V3.

So this is a normal amount of STE in V2 and V3, defined by Universal Definition of MI as up to 2.0 mm in men over age 40.  So there is definitely no STEMI, and the STE is normal.  So the computer is correct in calling it normal.

But after reading this blog, you all know that most OMI do NOT meet STEMI criteria.  Some patient's baseline ECG has zero STE.  Some patient's baseline has normal variant STE.  You don't know which kind of patient this is.

Some normal STE is actually due to OMI.  Some normal STE is not due to ischemia at all.

It is your responsibility to determine if STE is ischemic or not.

How do we do so?

Use the formula.

QTc = 385
STE60V3 is at least 4.0 mm, maybe more
RAV4 = 6
QRSV2 = 18

Formula value = 19.94 (very high, indicating LAD occlusion).

Any value greater than 18.2 is likely to be LAD occlusion.

For graphs of sensitivity, specificity, and accuracy at various cutoffs, see this post:

More precise interpretation of the results of the 4-variable formula.

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

Let's see how the Queen of Hearts does:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  

For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

Chris Mondie's note:

"My read: Acute proximal LAD occlusion. Hyperacute T waves which tower above the preceding R waves, poor precordial R wave progression. Large T in V1.  Smith subtle LAD equation indicative of acute LAD occlusion. 

"Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI. 

"Cardiology agreed to take the pt to the lab but thought it would likely be negative. 

"100% proximal LAD successfully stented. 

Defibrillated out of v fib in the cath lab. 

Initial TnI was negative. 

"I thank you for constantly updating your blog and allowing free open access education on EKG interpretation. I recognized this as a STEMI immediately and I was only able to do so solely because of your blog."

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MY Comment by KEN GRAUER, MD (8/18/2019):

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Our thanks to Dr. Chris Mondie for providing this case. Credit to him for performing stat Echo in the ED — which, with the finding of anteroseptal wall motion abnormality immediately confirmed the need for prompt cath, even before a 2nd tracing was done.

• For clarity — I’ve labeled a number of KEY findings in the initial ECG performed in the ED ( = ECG #1 in Figure-1).

Figure-1: The initial ECG done in the ED (See text).

MY THOUGHTS on ECG #1: This is not a normal tracing. The remarkable ECG findings are multiple:

• There are small-but-definite Q waves in each of the inferior leads (RED arrows). These Q waves in leads III and aVF are surprisingly wide — and to me are suggestive of inferior infarction at some point in time (possibly acute).
• It is difficult to assess ST-T waves in the inferior leads — because we only have 2 QRST complexes in each lead — and, there is baseline wander in lead aVF + obvious artifact with a different appearance of the ST-T wave for each of the 2 beats in leads II, III and aVF. IF clarification of these findings was important (as to whether something acute was ongoing in the inferior leads) — I would immediately repeat this ECG. That’s because despite lack of reciprocal ST-T wave changes in lead aVL — it looks like there may be slight-but-real ST elevation with slightly fatter-than-they-should-be T waves (probably hyperacute) in each of the 3 inferior leads (Compare the elevated J-point to the horizontal RED baseline in each of these leads).

That said, there is NO urgency for clarifying what is going on in the inferior leads — because clear indication for immediate cath is already forthcoming solely from the appearance of the chest leads in this patient with new-onset worrisome chest pain. Among the remarkable chest lead ECG findings include:

• As per Dr. Mondie — the T waves in leads V2 and especially in V3 “tower over” the respective R waves in these leads. These are hyperacute T waves.
• Whereas the base of these T waves in leads V2 and V3 does not seem all that wide — the base of the overly tall T wave (compared to its respective R wave) in lead V4 is wide. So, until proven otherwise — we need to assume hyperacute T waves in at least leads V2-thru-V4.
• There are Q waves in leads V4, V5 and V6 (RED arrows in these leads). Although these lateral chest lead Q waves are not that deep — the do appear to be wider-than-expected for “septal Q waves”.
• Two other reasons to suspect that these are not “normal septal Q waves” in leads V4-thru-V6 are: i) Although normal septal Q waves may occasionally be seen in lead V4 — they are generally not as large in lead V4 as the septal Q waves in leads V5 and V6. However, the Q wave that we see in lead V4 of ECG #1 IS equally large and wide as the Q waves in V5 and V6. This most probably is not normal; and, ii) Instead of the usual progressive increase in R wave amplitude as we move from lead V2-to-V3 — there is slight decrease in R wave amplitude. While I can’t rule out lead placement as the reason for this slight decrease in lead V3 R wave amplitude — the finding of a larger-than-expected Q wave in neighboring lead V4 makes me suspect that this is a real phenomenon related to ongoing anterior OMI.
• There appears to be slight-but-real ST elevation in leads V4 and V5 (I’m uncertain about V6). The amount of ST elevation in lead V4 (even if it doesn’t satisfy stemi criteria) looks more than what I’d normally expect in this lead (Compare the elevated J-point to the horizontal RED baseline in these 2 leads).
• Of the 2 QRST complexes that we see in lead V1 — the T wave of the 1st complex is taller-than-normally-expected for an upright T wave in lead V1 (V1 usually does not have tall T waves). Once again, due to technical issues — we do not know which of the 2 QRST complexes that we see in lead V1 is accurate ...

BOTTOM LINE: Some of the above abnormalities I mention are subtle. Individually — they probably would not mean much. BUT:

• In a patient with new-onset worrisome chest pain — the potentially hyperacute T waves in leads V2, V3 and V4 should be more-than-enough to merit prompt cath.
• Once determined that stat Echo shows an anterior wall motion abnormality — the diagnosis of acute ongoing OMI is confirmed!
• The possibility of something acute ongoing in the inferior leads is real. Support for the likelihood of acute ECG changes is then strengthened by identifying the additional subtle ECG abnormalities that I describe above in other leads on this tracing.

Once again — our THANKS to Dr. Chris Mondie for presenting this case!