ECG Blog #512 — Important Details ...

The ECG in Figure-1 was obtained from a middle-aged adult — who presented "acutely ill" with septicemia — but no chest pain.

• How would you interpret this ECG?
• Should you activate the cath lab? 
• If not — Why not?

Figure-1: The initial ECG in today's case — obtained from a middle-aged patient with septicemia, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on this CASE:

The rhythm is sinus, at a rate just under 100/minute (ie, The R-R interval is just over 3 large boxes in duration). Intervals (PR,QRS,QTc) and the axis look normal. No chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q Waves — are seen in each of the inferior leads. At least in lead III — the Q wave looks somewhat wider than is usually seen (which suggests this may be an "infarction Q wave" from an MI that occurred at some point in time).
• R Wave Progression — The R wave in lead V2 looks slightly taller than is generally seen in this lead. That said, the point for transition (ie, where the R wave becomes taller than the S wave is deep) — is normal (seen here to occur between lead V2-to-V3).

Regarding ST-T Wave Changes: 

• The 3 inferior leads (seen in Figure-2 within the RED rectangles) — each show slight-but-real ST elevation, with ST segment straightening in leads II and III.
• PEARL #1: Viewed in isolation — it would be difficult to know if the Q waves and slight-but-real ST elevation that we see in leads II,III,aVF indicate an acute (or recent) OMI, especially given the absence of CP (Chest Pain). But in the context of lead aVL (that manifests a nearly perfect, mirror-image opposite picture to what we see in lead III) — we have to at least consider a recent or acute event until proven otherwise (Note the slight ST depression with terminal T wave positivity seen within the BLUE rectangle in Figure-2). 
• KEY Point: As shown in ECG Blog #171 — Blog #158 and Blog #474 (among others) — one of the most helpful clues for determining whether subtle ST elevation in the inferior leads represents acute or recent OMI — is the presence of a mirror-image opposite ST-T wave picture between leads III and aVL. I find this reciprocal relationship almost "magical" in its reliability for suggesting an acute OMI (Occlusion-based Myocardial Infarction) based on the nearly opposite anatomical location in the frontal plane of lead III (at +120 degrees) and lead aVL (at -30 degrees). 

Figure-2: I've labeled key findings in the initial ECG.

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• NOTE #1: See my ADDENDUM below for review of the concept of what is an "OMI" (vs the outdated concept by clinicians "stuck" on insisting on STEMI criteria before they consider thrombolytic therapy or cath with PCI).
• NOTE #2: In today's case — Assessment as to whether STEMI criteria are met is difficult (ie, Seeing whether ≥1 mm of ST elevation is attained in at least 2 inferior leads). This is because there is PR segment depression in the inferior leads in Figure-2. Clinically, this should not matter — because what really counts is whether or not there is acute coronary occlusion — and PEARLS #1 and 2 suggest that an OMI is present regardless of whether or not STEMI criteria are satisfied!

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PEARL #2: Additional support regarding our concern for an ongoing acute inferior OMI — is forthcoming from the appearance of lead V2 (BLUE arrow in this lead in Figure-2).

• Because of the common blood supply in most patients between the inferior and posterior walls of the left ventricle — seeing a suggestion of acute posterior OMI adds support that uncertain limb lead findings are likely to be "real".
• This is precisely what we see in Figure-2. As is often emphasized in this ECG Blog — there normally is slight, upward sloping ST elevation in leads V2 and V3. However, the BLUE arrow in lead V2 highlights ST-T wave flattening with slight ST depression in this lead that is clearly abnormal.
• KEY Point: When inferior OMI is suspected — the presence of ST depression that is maximal in leads V2, V3 and/or V4 suggests associated posterior OMI. And, in today's case — it is this ST-T wave flattening and depression in lead V2 that tells us we have to consider the inferior lead ST elevation as recent until proven otherwise.
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• PEARL #3: In addition to suspected recent infero-postero OMI — there may also be RV involvement in Figure-2. This is because, rather than ST depression — the ST segment in lead V1 is coved and not at all depressed (as would be expected with a posterior OMI). 
• If there is simultaneous posterior OMI and acute RV involvement — then ST elevation in right-sided lead V1 from the RV MI may attenuate the amount of ST depression that we would otherwise see in lead V1 from posterior OMI. For this reason — an ECG with right-sided chest leads would ideally have been recorded as the best way to quickly determine if there is (or is not) RV involvement (See ECG Blog #190 for more on ECG recognition and management concerns regarding acute RV involvement).
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• PEARL #4: More than the ST-T wave flattening and depression that we see in lead V2 — the remaining leads in Figure-2 are also abnormal (ie, leads I; V3,V4,V5,V6 all manifest either ST-T wave flattening and/or a lack of clearly upright T waves). In the context of suspected recent or acute infero-postero OMI — these nonspecific ST-T wave findings suggest that in addition to the acute event, the patient may have significant underlying multi-vessel disease.

MY Clinical Impression: This is a difficult case — that is clearly complicated by the following: i) This patient is acutely ill with septicemia; — and, ii) The patient is not having chest pain! That said — my thoughts when this case was sent to me were the following:

• There most likely has been a recent infero-postero OMI. Whether this represents an ongoing acute event is impossible to determine from this single ECG without the benefit of additional clinical information (ie, a more complete history; comparison with a previous "baseline" ECG to see if the above-described ECG changes are "new"; serial Troponins; Echo at the bedside looking for a localized wall motion abnormality; etc.).
• Right-sided chest leads would have ideally been obtained to assess for the possibility of associated RV MI.
• Apart from any acute event — this patient may have multi-vessel disease with an unknown pattern of collateralization.
• Cardiac catheterization (sooner rather than later) may be needed to determine if an acute event is ongoing. That said — the timing for when to perform cardiac cath is complicated by the patient's other acute illness ( = septicemia). Ideally, at least some degree of stabilization would be achieved before beginning to contemplate acute intervention from this patient's presumed OMI. Admittedly — determining the optimal moment for intervention is a "juggling" act.

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The CASE Continues:

• The patient responded positively to initial treatment of his septicemia.
• Additional history was obtained — indicating that the patient did have chest pain prior to coming to the hospital!
• Initial Troponin was moderately elevated.
• As shown in Figure-3 — a repeat ECG was obtained. The patient's CP was "less" at the time of this repeat ECG.

QUESTIONS regarding Figure-3:

• How would you interpret the repeat ECG?
• Does Figure-3 confirm the diagnosis of an acute OMI?

Figure-3: Comparison between the 2 ECGs in today's case.

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MY Answers:

Clinically, the most useful way to interpret the repeat ECG shown at the bottom in Figure-3 — is to compare this tracing with today's initial ECG.

• First — Note how much easier it is compare serial ECGs when the 2 tracings you are looking at are placed side-by-side (as they are in Figure-3).
• My overall impression — is that the repeat ECG is clearly improved compared to the initial ECG that appears at the top of Figure-3.
• Of note — QRS amplitude is reduced in many leads in the repeat ECG. This is of uncertain significance. However, the frontal plane axis and R wave progression in the chest leads are similar in both tracings — such that lead-by-lead comparison should be valid.
• Accounting for the reduced QRS amplitude in ECG #2 — ST elevation is less in each of the inferior leads, and the reciprocal ST depression that had been seen in lead aVL (and to a lesser extent in lead I) on the initial ECG is no longer present. 
• In the chest leads — ST coving in lead V1 is less. 
• ST depression is no longer seen in lead V2, now with some return of a T wave in this lead.
• Lateral chest lead ST-T waves now look less abnormal.

BOTTOM Line:  The moderately elevated Troponin confirms infarction. Given reduction in the severity of this patient's CP in association with the above subtle-but-real improvement in ST-T wave appearance — I interpreted the repeat ECG in Figure-3 as suggestive of "dynamic" ST-T wave changes, providing further support of an evolving acute event.

• Cardiac catheterization was performed — and revealed severe triple-vessel disease!
• Unfortunately, I lack further details regarding follow-up.

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Final PEARL:

Figuring out what happened when with respect to acute coronary occlusion is challenging at best — and nearly impossible to do in the absence of timely documentation during the process.

• In my experience — correlation between the presence and relative severity of CP and the timing of each ECG obtained — can rarely be determined by retrospective review of the patient's chart.
• That said — Wouldn't it be EASY to document this correlation between CP severity with each serial ECG if this was done at the time that the patient is being evaluated in the ED? (ie, Medical providers can simply write ON each actual ECG [as well as in the chart] the severity of CP at the time each ECG is recorded).
• Doing so would then give us a "story" — that we can then piece together into the most reasonable clinical scenario (that should tell us if the "culprit" vessel is open or closed at the time of each tracing).
• Doing so would also clue us into the "pseudo-normalization" period that may occur following spontaneous reperfusion with reduction in CP (ie, No more than minimal if any ECG abnormalities may be seen if the initial tracing occurs in between the period of ST elevation on the way to reperfusion T wave inversion).
• For example, in today's case — knowing that the patient's CP had decreased in association with the timing of the repeat ECG allowed us to appreciate that relatively modest improvements in ECG findings are consistent with "dynamic" ST-T wave changes.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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ADDENDUM (1/3/2026): 

For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):

• Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
• Consider the 2 Audio Pearls at the bottom of this page.
• Consider Figure-4 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-4 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!). Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ] ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).

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How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association), ACC (American College of Cardiology), ESC (European Society of Cardiology), and the WHF (World Heart Federation):

• New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).
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• In leads V2 and V3:
• ST elevation ≥2 mm for men >40 years of age.
• ST elevation ≥2.5 for men ≤40 years of age.
• ST elevation ≥1.5 mm for women.

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—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.

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ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.