ECG Blog #488 — 5 ECG Findings Say the Same

The ECG in Figure-1 was obtained from a previously healthy older man — who presented to the ED (Emergency Department) with new CP (Chest Pain).

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Challenge: What 5 ECG findings on this tracing all point to the same diagnosis? Explain your answer.

Figure-1: The initial ECG in today's case — obtained from a previously healthy older man who presents with new CP. (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

Given the history of new CP in today’s case — at least 5 ECG findings all point to (and/or are consistent with) the same clinical diagnosis. This diagnosis is an acute OMI (Occlusion-based MI) of the proximal RCA (Right Coronary Artery) as the “culprit” artery. As I highlight below in Figure-2 — pertinent ECG findings include:

• Q waves and ST elevation in inferior leads III and aVF, followed by T wave inversion in both of these leads (within the RED rectangles in Figure-2).
• Reciprocal ST segment flattening, with a hint of ST depression in high-lateral leads I and aVL — with terminal T wave positivity in both of these leads (within the BLUE rectangle in lead aVL). Together with the changes in leads III and aVF — these limb lead findings are diagnostic of recent (if not ongoing) inferior OMI.
• QRST changes in leads V2,V3,V4 — that are diagnostic of posterior OMI. These include: i) Early transition (with a surprisingly tall R wave already in lead V2); — ii) Shelf-like ST depression that is maximal in leads V2,V3,V4 compared to other chest leads (within the BLUE rectangle in these 3 leads); — and, iii) Surprisingly tall terminal wave positivity in V2,V3,V4.
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• PEARL #1: There is ST segment coving in lead V1. Given the clinical scenario of new CP and the above ECG evidence of infero-postero OMI — this suggests acute RV involvement (ie, Normally with posterior OMI — we would expect to see similar ST-T wave changes in lead V1 as we see in lead V2 — unless there is RV MI producing ST elevation in V1 that attenuates ST depression from the posterior OMI).
• PEARL #2: Statistically — over 80% of patients have a right-dominant circulation, which is why the RCA (rather than a LCx = Left Circumflex artery) is by far the most common "culprit" artery with inferior MI. And, since the proximal RCA almost always provides blood supply to the RV (Right Ventricle) — the fact that ECG #1 suggests an infero-postero-RV MI points to the proximal RCA as the "culprit artery.
• PEARL #3: The way to confirm RV infarction — is by recording right-sided leads (See ECG Blog #190 — for more on right-sided leads and RV MI).
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• PEARL #4: Although details of this patient's history are not known (all we are told is that the patient presented with "new" CP) — the findings of large infarction Q waves in leads III and aVF — a tall initial R wave in lead V2 ( = the mirror-image opposite picture of a Q wave with posterior OMI) — and a relatively modest amount of ST elevation and ST depression with terminal T wave inversion in leads III,aVF — and — terminal T wave positivity in leads I,aVL and V2,V3,V4 — all combine to suggest that there may be some spontaneous reperfusion (and that the MI may have occurred hours ago or longer).
• PEARL #5: Learning more details about the history in today's case may help to explain the above ECG findings. For example — if the history of this patient's CP was "stuttering" (ie, off-and-on for a day or more before the severe CP that brought him to the hospital) — this may suggest a scenario of some spontaneous reperfusion of the "culprit" artery — especially if the severity of the patient's CP had decreased some time before ECG #1 was recorded (ie, This could account for the relatively modest amount of ST segment elevation and depression — and the inferior lead T wave inversion with terminal T wave positivity in other leads, which are often ECG findings suggesting some reperfusion).
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• PEARL #6: There is group beating in the long lead II (ie, alternating shorter-then-longer R-R intervals — as highlighted by the double BLUE arrows in the long lead rhythm strip). This suggests there may be SA Block — and since the sinoatrial nodal artery is usually supplied by the proximal RCA, this is yet one more ECG finding consistent with a proximal RCA "culprit" (See below).

Figure-2: I've labeled the initial ECG in today's case.

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Looking Closer at Today's Rhythm:

As suggested in Figure-2 by the double BLUE arrows in the long lead II rhythm strip — there is group beating. Although the presence of group beating in association with inferior MI most often suggests the possibility of AV Wenckebach ( = 2nd-degree AV Block of the Mobitz I Type) — this is not what we see in today's tracing because:

• As shown by the RED arrows in Figure-3 — the P-P interval is not constant (whereas the atrial rhythm is usually regular with Mobitz I — or at least fairly regular if there is some sinus arrhythmia).
• The PR interval is not increasing within groups as it should be if the rhythm was Mobitz I.
• There is no dropped P wave, as there would be with Mobitz I.

Figure-3: Focusing on the long lead II rhythm strip.

A Bigeminal Rhythm:

The presence of alternating shorter-then-longer R-R intervals that we see in Figure-3 — defines this as a bigeminal rhythm. As discussed in ECG Blog #312 — there are a number of causes of a bigeminal rhythm:

• Statistically — SA Block is not a common rhythm. That said — the consistent P wave morphology in Figure-3 rules out atrial bigeminy — the narrow QRS makes Mobitz II highly unlikely — and we have already ruled out Mobitz I.
• By the process of elimination — this leaves SA Block as the most likely rhythm diagnosis. This diagnosis makes sense — since the probability of a proximal RCA "culprit" for today's infero-posterio OMI may compromise flow to the sinoatrial nodal artery.

Laddergram Illustration:

As discussed in ECG Blog #312 — the concept of SA Block is that there is some type of "exit" block that limits the number sinus impulses that are able to make it out of the SA node.

• Beyond-the-Core: The presence of group beating, in which the pause is not some direct multiple of the shorter R-R interval — suggests this is the Wenckebach (Type I) form of SA Block.
• In contrast, with the Type II form of SA Block — the pause without any P wave should be some multiple of the shorter R-R interval.
• As shown in my proposed laddergram in Figure-4 — there is progressive delay of sinus node impulses trying to get out of the SA node, with every 3rd impulse failing to do so.
• Once out of the SA node — conduction to the AV node, and from there to the ventricles proceeds normally. 

Figure-4: My proposed laddergram of today's rhythm.

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CASE Conclusion:

• Timely cardiac cath was performed on this patient — and revealed total RCA occlusion.

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Acknowledgment: My appreciation to Ahmed Badyan (from Sana'a, Yemen) for allowing me to use this case and these tracings.

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ADDENDUM (7/19/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
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• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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