Friday, February 14, 2020

A man in his 50s with "gas pain"

Written by Pendell Meyers, sent by Anonymous


A man in his 50s with history of type 2 diabetes, HTN, and HLD presented with one day of off and on chest / upper abdominal pain. It had awoken him from sleep earlier, and he described it as "gas pain," located in the upper epigastrium and radiating upwards. Vitals were within normal limits. The patient presented with active pain, diaphoretic and ill appearing.

Here was his triage ECG (sorry for the quality, unable to obtain better images from sender):
Last ECG on file is below for comparison. First try this ECG without the baseline, then with. What do you think?



Previous ECG on file (never just assume its the baseline, but I think this one looks consistent with a baseline).




The presentation ECG shows sinus rhythm at almost 100 bpm. There is STD in V3-V6 (maximal in V4-5) and lead II, aVF, I, and aVL. Because of widespread STD, there is obligatory STE in aVR (the aVerage Reciprocal lead of the rest of the ECG).

This pattern in isolation would signify diffuse supply/demand mismatch without focal complete occlusion, which would be a very large differential of anything causing severe global supply demand mismatch, including ACS and various other processes. However, there is STE in V1 with a large area T-wave which is hyperacute.

This fits the pattern we have described many times including recently, of subtle STE and hyperacute T-wave in V1 with STD in the lateral precordial leads, indicative of LAD occlusion (more specifically, subtotal occlusion, just before the pattern of full occlusion).

I emailed just the presentation ECG to Dr. Smith, without any history, and he replied "LAD. Not totally occluded. 99%. TIMI 1 flow."

If you don't see it, you must use these links below to see many other examples until you can see why it fits the pattern:

A man in his sixties with chest pain, tachypnea, and hypertension





The pain increased within the first 15 minutes and this repeat ECG was obtained:

What is this?



This is classic de Winter pattern in V3 and V4 (depressed ST takeoff with hyperacute T-wave). V1-V4 have hyperacute T-waves. Reciprocal STD in inferior leads. We believe that the transition from the presentation ECG to this signifies the process of going from near total occlusion (~99% ~TIMI1 flow) to complete occlusion.



The cath lab was activated immediately. They presented to bedside and more serial ECGs were obtained:

25 minutes:





While waiting for the cath lab to be ready, another ECG obtained:




At cath they found and opened a complete proximal LAD occlusion (images unavailable). Unfortunately, peak troponins and echo are also unavailable.

The patient was discharged home in good condition several days later.

Learning Points:

You must learn this pattern of near-total LAD occlusion, as well as de Winter's T-wave pattern.  If you can intervene at this early stage, you will salvage a lot of myocardium. Some patients will not progress (or not as quickly) to obvious STEMI, as in this case.  Nevertheless, they also will get enormous benefit from emergent cath due to preemption of progression to full thickness MI.

Even in a case like this, in which OMI evolves into obvious STEMI, expert ECG interpretation at the earliest stage, beyond the STEMI paradigm, leads to faster reperfusion and limits the extent of this patient's infarction.



===================================
MY Comment by KEN GRAUER, MD (2/14/2020):
===================================
I think this case provides an excellent example of how we can learn by retrospective review of serial tracings.
  • CREDIT to Drs. Meyers and Smith, who instantly recognized impending LAD occlusion
  • Although I completely agreed on the need for prompt cardiac cath in this 50s man with risk factors and new symptoms — I did not initially recognize the “culprit artery”.

I thought it might be worthwhile to explore WHY it took me longer than I would have liked to recognize the “culprit artery”.
  • PEARL  One of the best ways to hone your ECG interpretation skills — is by retrospective review of serial tracings on cases in which you know the anatomy. Going back to ECGs in which you may not have recognized all findings the first time you looked — is often humbling, and tremendously insightful (especially when you know “the answer” as revealed by cardiac cath).
  • Cardiac cath in this case confirmed acute proximal LAD occlusion. Correlating evolution of this patient’s symptoms in the ED, with corresponding evolution of serial ECGs tells us (as per Drs. Meyers & Smith) — that the initial ECG in the ED ( = ECG #1 in Figure-1) represented high-grade LAD narrowing, but not yet complete occlusion.
  • It was only later (when ECG #3 was obtained) — that complete occlusion of the proximal LAD occurred.

Figure-1: The first 3 ECGs that were shown above in this case. (See text).



MRETROSPECTIVE THOUGHTS on this Case  I encourage review of the 7 cases that Dr. Meyers provides links to above — each showing ECGs with acute LAD occlusion. NO 2 ECGs are ever the same — so the more one’s eye reviews patterns in which we “know” the answer — the better (and faster) one gets at recognizing these KEY patterns of acute LAD occlusion.

That said — I had an easier time recognizing the “culprit artery” in each of these 7 cases, than I did for ECG #1. ECG findings that helped me to recognize LAD OMI in these 7 cases included:
  • In addition to inferior lead ST depression — some of these 7 tracings showed ST elevation in lead aVL (which is often a great clue to proximal LAD occlusion). Note that there is no ST elevation in lead aVL of ECG #1 in Figure-1.
  • Some of these 7 tracings showed subtle-but-definite ST segment straightening and/or elevation in at least 2 (if not all 3) anterior leads. Note that there is no ST elevation in leads V2, V3 or V4 in ECG #1.
  • The shape of the abnormal ST elevation in lead V1 in some of these 7 tracings was clearly coved (ie, “frowny”-configuration). The ST segment in lead V1 of ECG #1 is not coved (ie, it is upward-sloping = a “smiley” configuration). Dr. Meyers astutely noted that there is indeed ST elevation in lead V1 of ECG #1 with a large-area T wave that looks hyperacute”PITFALL  Perhaps because amplitude of the QRS complex in lead V1 of ECG #1 is so small, it is easy to overlook that the J-point in this lead is indeed 1 mm elevated above the PR segment baseline. Normally, the T wave in lead V1 may be positive — but it should not be as disproportionally large as it is in ECG #1 (and the T wave in lead V6 should normally be larger than the T wave in lead V1 — and this is not the case in ECG #1!).
  • Some of these 7 tracings showed at least one (or more) anterior T waves that were more obviously fatter-at-their-peak and/or wider-at-their-base than what we see in ECG #1. Clearly, the T wave in lead V3 of ECG #1 is taller and more pointed than is usually seen — but it is narrow at its peak, and relatively narrow at its base.


THOUGHTS on ECG #(the Baseline Tracing): As per Dr. Meyers — the diagnosis of impending LAD occlusion in this patient with new symptoms can (and should) be made on the basis of ECG #1 alone. That said — having access to a Baseline tracing (that is shown in ECG #2) confirms that the ECG findings in ECG #1 are acute:
  • The diffuse ST depression seen in ECG #1 was not seen in the earlier tracing!
  • The ST-T wave in lead V1 of ECG #2 was completely flat. This confirms that the hyperacute appearance of the ST-T wave in lead V1 of ECG #1 is new!
  • The disproportionally tall and remarkably pointed T waves in leads V2, V3 and V4 of ECG #1 are all new!


THOUGHTS on ECG #3: The reason ECG #3 was obtained just 15 minutes after ECG #1 — was because of an increase in the patient’s chest pain. As per Dr. Meyers — ECG #3 now shows a classic de Winter wave pattern. Note the following:
  • Starting from several millimeters of J-point depression (most marked in leads V3 and V4 of ECG #3) — an upward-sloping ST segment rises to very prominent T waves (with a giant T wave in lead V3). Note how fat-at-their-peak and wide-at-their-base the T waves in most chest leads have become compared to what they were in ECG #1.
  • DID YOU SEE the marked loss of R wave in the anterior leads of ECG #3? R waves in leads V2, V3 and V4 were tall in ECG #1. The fragmented initial part of the QRS complex in leads V2 and V3 (with initial Q in V2) + the classic de Winter T wave pattern — tells us that the high-grade proximal LAD narrowing is now completely occluded.


GOING BACK to ECG #1: In view of what the baseline tracing on this patient looked like — and, now knowing what the ECG will look like in 15 minutes (ie, in ECG #3— it becomes much easier to see:
  • That the subtle-but-real ST elevation with disproportionately large T wave (considering small size of the QRS) in lead V1 of ECG #1 provides early indication of the more obvious hyperacute ST straightening and T wave fattening that we see in lead V1 of ECG #3.
  • That in retrospect, the T waves in leads V2, V3 and V4 of ECG #1 are all clearly hyperacute — and together with clearly abnormal J-point depression in leads V3, V4 of ECG #1 — we are seeing early indication of the frank de Winter T wave pattern that is about to evolve. BOTTOM LINE: Rather than non-localized diffuse ST depression with ST elevation in lead aVR — the overall picture in ECG #1 provides clear indication of impending proximal LAD occlusion. This case is highly insightful as to HOW the pattern of de Winter T waves may develop.
  • NOTE: For more on the pattern of de Winter T waves (including the Figure of various ECG patterns, excerpted from the original 2008 Letter to NEJM by de Winter et al) — Please SEE My Comment in the May 2, 2019 post).

Our THANKS to Dr. Meyers for presenting this instructive case!



6 comments:

  1. is the T wave in V3 of thhe first ECG representative of a De Winter ???

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    Replies
    1. GREAT Question you ask! — and your question is precisely the reason I wrote My Comment (above, at the bottom of the post). In my experience — there are MULTIPLE “variants” on the theme of de Winter T waves. I was not used to seeing T waves like the one in lead V3 of ECG #1, with as THIN of a base as we see here in de Winter. BUT — as we follow this case, we see just 15 minutes AFTER ECG #1 was done (ie, in ECG #3) — that a frank de Winter T wave pattern has indeed evolved. So, “retrospective review of serial tracings” ( = the point of My Comment) tells us that YES, the appearance of the T wave in lead V3 of ECG #1 was an EARLY sign of the frank de Winter T wave pattern that followed soon thereafter! — :)

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  2. Thanks a lots for an great case with several teaching points! I have one question:The ECG #1 couldn't to be a posterior OMI or diffuse supply/demand mismatch ischemia? There are STD in leads V3-V6 and STE in aVR with R wave transition have occured earlier(R>S in V2) and this had taken me to think in posterior OMI and diffuse supply/demand mismatch ischemia.
    Anderson Santos, medical student from Brazil

    ReplyDelete
    Replies
    1. @ Anderson — Muito boa pergunta! (Very good question!) — and IF you read through My Comment above (on the bottom of this post) — this was precisely why I initially did not recognize that the “culprit artery” was the proximal LAD! It is true that early transition (as seen in ECG #1) is a finding in posterior MI — but if you follow the Step-by-Step analysis in My Comment (above), I believe you’ll see why Drs. Meyers and Smith INSTANTLY recognized that the only pattern that explains all findings on ECG #1 is acute proximal LAD occlusion. Then ECG #3 (done just 15 minutes later) confirms their astute diagnosis! Obrigado mais uma vez por sua pergunta! (Thanks again for your question — :)

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  3. Thank you for the usual outstanding case and explanations. Considering the first ecg only (deep S waves in precordial leads, S in I-II-III, neg T in III), what allows to exclude right ventricular strain (eg secondary to pulmonary TE)?
    Best regards

    Aldo Cannata, MD
    Milan, Italy

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    Replies
    1. Thanks for your question Aldo. Acute RV strain typically produces ST-T inversion in the anterior leads — and we have the opposite picture here. Other acute RV “strain” findings (ie, right axis, RAA) are also missing. S waves DO persist through through to V6 — but there really aren’t deep in lateral chest leads. So I didn’t think ECG #1 (by itself) was particularly suggestive of acute RV strain. And then when we compare this to ECG #2 — we confirm that the multiple S waves are not a new finding.

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