ECG Blog #426 — Are STEMI Criteria Met?

The ECG in Figure-1 — was obtained from a 70-ish year old man with episodic CP (Chest Pain) over the previous 2-3 days, being awakened from sleep now for a more severe CP episode.

QUESTIONS:

• In view of this history — How would YOU interpret this ECG?
• Should you activate the cath lab?

Figure-1: The initial ECG in today's case.

MY Initial Thoughts on Today's CASE:

Although it is difficult from the brief history we are given, to determine the true onset of whatever might be happening — the patient's age, persistence and severity of CP are clearly cause for concern.

• Which lead(s) immediately "caught YOUR eye"?

ANSWER:

The ST-T waves in 5 leads immediately captured my attention. I have labeled these leads in Figure-2 with RED and BLUE rectangles.

• WHY did these leads capture my attention?

Figure-2: I've labeled with RED and BLUE rectangles the 5 leads that immediately "caught" my eye.

The Most Abnormal Leads in Figure-1:

When assessing a patient for a possible acute OMI — I like to begin with leads that I know are definitey abnormal.

• PEARL #1: If when assessing a patient with new CP — you see 1 or 2 leads in which you know the ST-T waves are definitely abnormal — it then becomes much easier to identify more subtle changes in neighboring leads that support your impression of an acute ongoing event.

Applying PEARL #1 to Today’s CASE:

The initial ECG in today’s case shows sinus rhythm at ~80/minute— normal intervals (PR-QRS-QTc) — normal axis — and no chamber enlargement. Although there are QS complexes in leads V1,V2 — this is not necessarily abnormal, and R wave progression is appropriate (with transition where the R wave becomes taller than the S wave is deep — occurring normally, here between leads V2-to-V3). 

• Lead III and Lead V3 (within the RED rectangles in Figure-2) — are the 2 leads in ECG #1 that I absolutely knew were abnormal.
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• The QRS complex in lead III is tiny (ie, the R wave in lead III is at most 2 mm tall). And, although the T wave in this lead is not “tall” in terms of its absolute height — this T wave in lead III is clearly disproportionate in size, with respect to its QRS complex (ie, The T wave in lead III is almost twice as tall as the R in this lead — with this T wave being “fatter”-at-its-peak and much wider-at-its-base than-it-should-be, given the dimensions of the QRS in lead III). 
• Once we recognize in this patient with new CP, that the ST-T wave in lead III is clearly hyperacute — it becomes much EASIER to recognize that the T wave in neighboring lead aVF is also disproportionately taller and “fatter”-at-its-peak than it should be, given modest height of the R wave in this lead aVF.
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• PEARL #2: It’s important to appreciate by the above principles — that even though by itself, I would not necessarily interpret the ST-T wave in neighboring lead II as “abnormal” — in the context of new CP, in which we have just identified hyperacute T waves in the other 2 inferior leads ( = leads III and aVF) — Doesn’t the T wave in this 3rd inferior lead ( = lead II) also look “fatter”-at-its-peak and wider-at-its-base than it should, especially given modest amplitude of the R wave in this lead?  
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• PEARL #3: In my experience, the EASIEST way to convince myself that ST-T wave changes in leads III and/or aVF are acute — is to LOOK FOR the “magical” mirror-image opposite relationship that almost always exists between the ST-T waves in leads III and aVL when there is acute inferior OMI (See ECG Blog #167 and Blog #184, among many other posts). 
• KEY Point: It is rare with acute inferior OMI not to see reciprocal ST-T wave changes in lead aVL. This is an important distinguishing point between inferior lead ST elevation that is normally seen with a benign repolarization variant (in which you will not see reciprocal ST-T wave changes in lead aVL) — vs with acute inferior OMI, in which you will!
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• Clearly, in Figure-1 — the ST-T wave flattening, with shallow T wave inversion that we see in lead aVL is a subtle finding (within the BLUE rectangle in aVL) — BUT — in the context of a patient with new CP and hyperacute T waves in the inferior leads — I interpreted the ST segment flattening with shallow T wave inversion in lead aVL as being consistent with a reciprocal change.

PEARL #4: Because of the common blood supply of the RCA (Right Coronary Artery) — and the LCx (Left Circumflex) artery (ie, both of these coronary arteries usually supply both the inferior and posterior walls of the left ventricle) — it is very common when you see ECG evidence of acute OMI in one of these anatomic areas, to also see it in the other anatomic area (See ECG Blog #193 — and Blog #351, among many others).

• Applying this PEARL #4 to the initial ECG in today’s case — I was hoping to find further support that the subtle ST-T wave changes in 4 of the limb leads were real — by also finding ST-T wave changes in the chest leads suggestive of acute or recent posterior OMI.
• In a patient with new CP — there should be no doubt that the ST-T wave in lead V3 in Figure-2 (within the RED rectangle in lead V3) is abnormal! Given the tiny amplitude of the QRS complex in this lead — the T wave in lead V3 is at least equally tall as the R in lead V3, with this T wave being “fatter”-at-its-peak and wider-at-its-base than it should be, given small size of this R wave.
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• PEARL #5: Normally — there should be slight ST elevation with a gently upsloping ST segment in leads V2,V3. Thus, the ST-T wave in neighboring lead V2 is also abnormal — in that the ST segment in this lead is flat without any ST elevation (ie, within the BLUE rectangle in V2).

Putting It All Together:

In view of the history of new CP — today’s initial ECG is diagnostic of an acute OMI ( = an MI with acute coronary Occlusion).

• While additional assessment can certainly be undertaken — the point to emphasize is that the ECG in Figure-1, in association with the history of new, severe CP that awakened this patient from sleep — is all that is needed to know that prompt cath with PCI should be done as soon as this is possible.
• There is no need to wait for Troponin results to come back before the patient is taken to cath. This is because even if the initial Troponin came back normal — this rules out nothing! (ie, An initial hs-Troponin may occasionally be normal with acute OMI). Therefore — there is no need to wait for Troponin results, because these results will not alter the need for prompt cath.
• Serial ECGs should of course be obtained — but, there is no need to wait for a 2nd ECG before the patient is taken to cath — since given the history of new, severe CP and hyperacute ST-T waves in multiple leads — regardless of whether a 2nd ECG looks better or worse — prompt cath is needed.
• Assuming arrangements are made for prompt cath — there will almost always be "a moment" before cath is done that a repeat ECG can be obtained, which will be helpful in assessment. But the point to emphasize, is that the decision to perform prompt cath need not wait until that 2nd ECG is done.
• As is also emphasized often in this ECG Blog — spontaneous reperfusion of the "culprit" artery is common — and, IF this occurs before a 2nd ECG is done, ST-T wave changes may "look better" (See References to related Blog posts below). But — What spontaneously opens — may just as easily spontaneously reclose — which is why even if a 2nd ECG "looks better" — prompt cath with PCI is still needed to prevent spontaneous reocclusion of the "culprit" artery at a later point.
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• Finally — this is not be called a NSTEMI (because this term would falsely imply that there has not been acute coronary occlusion — and that PCI will not be of benefit). The term "NSTEMI" has been overused, and is often applied by "default" (ie, because millimeter-based criteria for a STEMI are not seen on any of the ECGs that have been done). Instead, we know from discussion above and the pathophysiology involved, that acute coronary occlusion (ie, an OMI) is by far the most likely explanation for events in today's case.

KEY Point: All extra testing in today's case would serve to do is delay — with resultant risk of losing more myocardium that might be saved by PCI from prompt intervention. Therefore — as soon as you know there has been acute OMI — cardiac cath with PCI is indicated (without further need to "confirm" what you have already confirmed).

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Acknowledgment: My appreciation to Si Cocksey (from Manchester, UK) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).