Sunday, March 31, 2019

Three EKGs shown to me - which if any need emergent reperfusion?

Written by Pendell Meyers

We commonly get feedback from readers who are skeptical that we can pick out the subtle NSTEMI occlusions from the endless onslaught of triage/EMS EKGs. Some believe that one cannot learn to pick out subtle true positive STE or hyperacute T-waves without sacrificing specificity.

We see countless EKGs constantly (as do all EM physicians) plus more because other providers constantly send us EKGs in addition. I see countless abnormal-looking EKGs to which I respond "I don't see any evidence of occlusion", and only a tiny percentage of diagnostic EKGs among those shown to me.

So take a look at these three EKGs I was shown during a single shift the other day. Imagine how you would handle these and see if you think it's impossible to differentiate the few OMIs from the countless abnormal but meaningless EKGs.

The only information I had in all three cases was a middle aged patient with chest pain. I could not see or evaluate the patient at the time of making the EMS/triage decisions (to activate the cath lab or not). 

Here they are:




What would you say in each of these cases brought to you in the middle of your shift?

My responses: 

#1 I suspect false positive ST elevation, do not activate the lab, and please get a 12-lead on a machine that does not cut off the QRS voltage so we can see the true ratios of QRS and ST deviations. Clear J-waves and typical morphology make BER extremely likely.

#2 STEMI equivalent because of hyperacute T-waves which are diagnostic in anterior leads. This patient was headed for a nearby hospital via ambulance, so I called them and told them my concerns because we are not able to activate their cath lab. If this patient were coming to my hospital, I would not activate the cath lab but instead we have a "heart alert" for situations that are deemed STEMI equivalents which do not meet formal criteria, in which we discuss immediately with the interventionalist, then decide the best course of action. I would have called a heart alert and argued strongly for emergent cath on arrival.

#3 False positive ST elevation, although technically this does meet "STEMI criteria" it is false positive because of the Q waves, abnormal and high voltage QRS, and ST morphology which is very unlike acute ischemic STE. The fact that there is indeed STD in aVL does not mean that it has to be acute ischemia - any process which causes focal STE must cause reciprocal STD. This case was brought to me after other providers had already activated the cath lab, so the patient was already proceeding emergently for cath.

So what happened?

Patient #1:


The patient (turned out to be 38 years old) was brought into the ED (not my zone) and had this EKG on arrival:

This is perhaps the lowest score I've ever heard of!

The providers were worried by the STE and activated the cath lab. Coronaries were completely normal (no CAD whatsoever), 3 troponins were undetectable, and the EKG remained unchanged (did not evolve).

Patient #2:


Although we lack V3, we can see Q-waves from V1-V4, with slight STE and very large symmetric T-waves which are hyperacute compared to their QRS complexes. There is STD in I and aVL. The forumula is contraindicated due to Q-waves because normal ST elevation never had Q-wave in V2-V4.

I called the receiving hospital and explained my concern about these EKG findings.

On arrival there, this was his EKG:

Findings may have improved slightly, however V3 still has diagnostic Q-wave, STE, and hyperacute T-wave. There is slight STD in V6, I, and aVL.

Days later I called to find out what happened to him.

Luckily, despite no STEMI criteria being met, the patient was taken fairly quickly to the cath lab where he was found to have a 99% thrombotic stenosis (TIMI-1 flow) of the mid-LAD, in the setting of severe three vessel disease. PCI was technically difficult, and the patient went for emergent CABG the next day. Peak trop and echo were not available unfortunately.

Patient #3: 

Triage EKG:

I found out later that this patient was a 57 yo M with history of CAD s/p CABG (LIMA-LAD), multiple PCI to LM, LAD, LCX, presenting with intermittent chest pain for the past 2 days. Just before arrival, he had an episode with associated diaphoresis. He was having chest pain during this ECG on arrival.

The providers activated the cath lab. He was of course found to have his previously known three vessel disease, and his LIMA-LAD was patent. He was found to have a 90% stenosis (TIMI 3 flow) of his ramus intermedius which was stented, however it does not seem to have been an acute culprit. 

Four serial troponins were undetectable, and this was the only repeat ECG on file (5 hours after cath):

Despite the difference in the QRS complex, there is still STE in the inferior leads (this morphology is actually closer to ischemic changes than the initial EKG). Thus, the ECG has not evolved down the progression of ischemia. Troponins remained undetectable during this persistent STE and during pain. Echo showed no wall motion abnormalities, no LVH, and EF 65%. This is all strong evidence that there was no acute culprit and no ACS. 

Learning Points:

Some EMS 12-leads have software which cut off the QRS complexes to avoid overlap on the display. This is important to know because all findings on EKG are proportional, and so you must be able to see the full QRS complex in order to interpret the ST segments and T-waves correctly.

Advanced ECG interpretation involves improvement in sensitivity and specificity over the current STEMI vs. NSTEMI paradigm. With practice you can diagnose hyperacute T-waves and all the other subtle OMI findings without overcalling the majority of cases.

Comment by KEN GRAUER, MD (4/2/2019):
Instructive post by Dr. Pendell Meyers — regarding 3 ECGs shown to him during a routine shift in the ED. The only clinical information known about each case — was that the patient was “middle-aged”, and that they had “chest pain”.
  • For clarity — I’ve reproduced these 3 ECGs in Figure-1.
  • My “bottom line” impressions about each tracing (regarding whether or not to activate the cath lab) — were the same as those of Dr. Meyers.
  • I did have a few additional thoughts ...
Figure-1: The 3 ECGs reviewed by Dr. Meyers in this case (See text).
ECG #1: Great point by Dr. Meyers (!), regarding the importance of using a 12-lead ECG machine that does not cut off QRS voltage. Without this — we have no idea of either S wave depth or R wave height in 5 (if not all 6) of the chest leads (RED arrows).
  • The ST-T wave appearance in leads V4-6 clearly suggests a repolarization variant (concave-up = “smiley”-configuration shape to the ST segment, with very prominent J-point notching in V4, V5). Determining whether or not T wave amplitude looks taller-than-it-should-be in leads V2 and V3 would be greatly facilitated by knowing how deep the S waves are in these leads — which we unfortunately are unable to do from this tracing alone.
  • Even without being able to see true QRS amplitudes — I suspected this was most probably a repolarization variant because of: igeneralization of the ST elevation and its shape in virtually all chest leads (a stemi would be more likely to localize); andiithe unremarkable ST-T wave appearance in the limb leads.
  • That said, although I would not activate the cath lab on the basis of ECG #1 — I would want more information — and, I’d want to see a follow-up ECG, done with a machine allowing full visualization of QRS amplitude before making my final decision. (As discussed by Dr. Meyers in follow-up of this case — the 2nd ECG done on this patient did confirm that actual QRS amplitude in chest leads was dramatically increased).
  • I have no doubt that the ST-T wave appearance in leads V4 and V5 of this tracing represents a repolarization variant. But, if anterior S waves were no deeper in ECG #1 than what we see here — my concern regarding the ST-T wave appearance in leads V2 and V3, would be to ensure that we are not looking at new changes superimposed on a repolarization variant.
ECG #2: It’s hard to imagine not promptly performing cardiac cath on this patient, given a history of “chest pain” and the appearance of ECG #2. As per Dr. Meyers — there are large Q waves in leads V1-thru-V4 and dramatic, hyperacute T waves in leads V2-thru-V6. Although J-point ST depression is lacking — this T wave pattern otherwise evokes the image of DeWinter T waves, in how disproportionately tall most chest lead T wave are in relation to R wave amplitude in their respective lead.
  • Without more information (and ideally, a prior ECG for comparison) — it would be difficult to “date” the occurrence of LAD occlusion — but regardless of whether the “millimeter amount” of ST elevation in the “stemi definition” is met — the cardiologist-on-call needs to immediately evaluate this patient.
There are 2 additional findings that concerned me about ECG #2:
  • There is incomplete RBBB (Qr’ pattern in both leads V1 and V2 + terminal S waves in both leads I and V6LAHB (rS pattern, with predominant negativity in all 3 inferior leads). Is this bifascicular conduction disturbance a new finding? — related to a large acutely evolving anterior STEMI?
  • The ST-T wave appearance in lead II of ECG #2 is remarkable! The image of the tiny QRS complex in this lead — with strikingly flat ST segment — and obviously fat-at-its-peak and disproportionately tall T wave — is one that should be embedded in memory as saying, “I am acute until you prove otherwise”.
ECG #3: I found ECG #3 the most interesting — and the most challenging of these 3 tracings! Rather than a “yes” or “no” determination, I wondered — What was going on? My thoughts, as I systematically assessed ECG #3 without the benefit of any clinical information other than that the patient was “middle-aged with chest pain”:
  • There is sinus tachycardia — which is a finding of concern.
  • The intervals (PR, QRS, QT) and mean QRS axis both seem to be normal.
  • Chamber enlargement: This is a bit more difficult to assess than at first might appear. There is no sign of LVH. There is a predominant R wave in lead V1 — which should always make one consider the possibility of RVH (See LINK provided below). That said — I did not think there was RVH here. But P wave morphology is clearly abnormal! It is rare in my experience to see notched inferior P waves with an initial negative (not positive) component. Rather than atrial enlargement — I interpreted this as an intra-atrial conduction defect — which is relevant, in suggesting underlying coronary disease.
  • Beyond-the-Core: There appear to be PTa deviations (elevation or depression of the T wave component of the preceding P wave, during which time atrial repolarization takes place = “PTa” wave). Specifically, the PTa segment in leads III, aVF and aVR appears to be elevated. It appears to be depressed in other leads. Given our concern in assessing this patient with chest pain and sinus tachycardia for a possible acute event — I contemplated whether these PTa deviations might be acute (Please see Figure-2 below — for thoughts on recognizing the usually ignored entity of acute atrial infarction).
Assessment of QRST Changes — is complex:
  • Q waves (big and smallare seen in multiple leads (ie, leads II, III, aVF; V1 — and small q waves in V3, V4, V5, V6). The surprisingly wide (relatively speaking) Q wave in lead V1, as well as the q waves in V3 and V4 raise the question of prior anterior infarction (the Q in V1 is not normal; and normal septal q waves shouldn’t go as far anterior as lead V3).
  • R Wave Progression — As noted earlier, the R wave is predominant (albeit with a qRs complex) in lead V1. This is followed by a very large R wave in lead V2. This raises the possibility of prior posterior infarction. 
  • Consistent with the idea of prior posterior infarction — is the virtual certainty of prior inferior infarction. The question I had was whether these large and wide inferior Q waves with associated ST elevation were “old” — vs recent — vs “new-on-top-of” old? The huge Q in III with modest ST elevation looked “old” to me, as did the minimal reciprocal changes in lead aVL. But I was not at all sure about the ST elevation in leads II and aVF — which to me looked like they certainly might reflect new injury.
  • BOTTOM Line about ECG #3: I would not immediately activate the cath lab for this patient based on the appearance of ECG #3. That said — the multiple ECG abnormalities noted tell us this patient has significant underlying coronary disease. I thought that although the changes on ECG #3 most likely were not the result of acute coronary occlusion — that with a history of new chest pain, the cardiologist-on-call should be seeing this patient sooner-rather-than-later — that more information was needed — and, that another cath might be in this patient’s “near future”.

Figure-2: Recognition of Atrial Infarction (Excerpted from Grauer K: ECG-2014-ePub).

Our THANKS to Dr. Meyers for this highly insightful case!
  • Regarding ST segment Shape (ie, “smiley” vs “frowny” configuration— CLICK HERE (Please see My Comment at the bottom of the page).
  • For more on the Tall R Wave in Lead V1 — CLICK HERE.


  1. Regarding patient #1, the "concave-upward" ST elevation in V4 with notching at the junction is pathognomonic of early repolarization pattern as a normal variant as Dr. Smith mentioned above. Nothing else will do it; not ischemia, not infarction, not hypothermia, no nothing. If that patient was indeed sent to the cath lab because of the findings in V4, I can not believe it!!
    K. Wang.

    1. Agreed! But I'm afraid it happens around the world. Thanks Dr. Wang

  2. ECG 1 has QRS distortion ie no S wave in V4,V5 so i thought it is suspicious for OMI. Thoughts?

    1. There are 2 reasons that this is not terminal QRS distortion:
      1) Terminal QRS distortion only applies to V2, V3
      2) V4 does NOT have terminal QRS distortion: it is defined as absence of BOTH an S-wave and a J-wave in V2 or V3. V4 has a very prominent J-wave

  3. Thank you for the great post. I made the same diagnosis in case of ECG 1 and 2 as you did. I never knew that ECG program can cut off QRS complex. I thought the machine record them in Auto 0.5 mV in case of high qrs voltage. For ECG 3 I indeed thought it was acute. And I still cant see why it is not acute. Maybe Dr. Ken will explain this with details.

    1. Smith opinion: EKG 3 does not look acute for a couple reasons: 1) there is a very deep and wide Q-wave in III 2) there is a very tall R-wave in III 3) the T-waves are not large enough. My ECG diagnosis when I saw this was: inferior LV aneurysm (persistent STE after old MI). However, echo showed no WMA, so this was not the case. Furthermore, the next ECG was so different that it looks as if it came from a different patient. Unexplained.

    2. Can LV aneurysms have reciprocal STd as seen in lead aVL of ECG3?

    3. Grauer opinion: I also thought that ECG #3 was probably not acute — but I was not completely sure for the reasons I discuss in detail above (I added My Comment a day after Swagata asked this question — :)

    4. Yes. Inferior LV aneurysm has STE in III and reciprocal STD in aVL.

  4. @ Swagata — To me ( = my opinion), the amount of reciprocal ST-T wave deviation in lead aVL of ECG #3 is modest compared to what is seen in lead III — and the inverted T wave in aVL is not nearly as deep as the T in III is tall = > the ST-T wave in aVL is NOT really a “mirror-image” of the ST-T wave in lead III. As a result, these changes in aVL look “less acute” (if not old) — therefore potentially consistent with LV aneurysm, and less likely to reflect acute occlusion.

  5. Thank you for the detailed explanation. Dr. Ken pointed out few topics like intra atrial conduction defect or PTa deviations which I didnt know about before. And its always nice to learn something new.


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