Saturday, July 25, 2026

EXTRA COPY: Obvious MI — What is the Culprit? — EXTRA COPY

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Acknowledgment: My appreciation to Op. Sanooj (from Calicut, India) — for allowing me to use this case and this tracing.

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ADDENDUM:

I have added this Tab on Technical "Misadventures" — to the Menu at the top of every page in this ECG Blog:

— Where to find this LINK in the Top Menu! — 


All-too-often lead reversals, unsuspected artifact, and other "technical misadventures" go unrecognized — with resultant erroneous diagnostic and therapeutic implications. 
  • In the hope of facilitating recognition of these cases — I am developing an ongoing listing on this page with LINKS to examples that I’ve published in this ECG Blog, as well as in Dr. Smith’s ECG Blog where I frequently write commentaries.

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O.p. Sanooj ( 10/10/2023 ) — Facebook Messenger

from Calicut, India — I am from Calicut, India. Myself Dr Sanooj Op

— "Obvious MI but WHAT is the Culprit?"

Sure sir, it is a honour for me if you publish this. 

Your earlier advice of giving   IV betablocker and cordarone helped me to kill VT in this case. And also I gave plenty of fluids suspecting RVMI. Thanks from the bottom of my heart sir.

 

THE CASE:

Hi sir, this patient had arrested in cathlab while doing angioplasty. Given CPR for 30 minutes and multiple shocks for VT. Finally after opening RCA, he became stable. Now he is doing well.

 

There is shelf like ST depression in inferior leads, ST elevation in 1, aVL,V6 indicating infero lateral MI. The absence of ST depression in V1 indicates there is RVMI. Am I right sir?


Sir, this is today's ecg. Patient is stable now. There is no occlusion in Lcx. The culprit artery on cath was RCA. I have confirmed it.


MY 1st REPLY (I was initially fooled !!!! — important to tell why!)

Hi. I put the 2 parts together to get a better 12-lead picture. I see sinus rhythm — with as you say MARKED ST elevation in I,aVL and V3-thru-V6. This picture to me is MUCH MORE SUGGESTIVE of acute LCx (Left CircumfleX) occlusion. One of the 2 QRS complexes in lead V2 has slight ST depression (but neither has the usual slight ST elevation) — which to me suggests there is also posterior MI. I am not quite sure why there appears to be slight ST elevation in lead V1 — but everything else on this tracing suggests that the LCx is the "culprit" artery — and the LCx generally does NOT supply the RV ...

 

Are you sure that the "culprit" artery on cath was the RCA? Did this patient have multi-vessel disease ??? — as if he did, then depending on the pattern of collateralization, you may get a different distribution for the ST elevation and depression.

The massive ST depression in leads II,III,aVF is consistent with reciprocal ST depression — which further supports that the main injury is from LCx occlusion.

 

Let me know if you have any follow-up. How is the patient now doing? Any follow-up ECGs? (the distribution of reperfusion T waves might support our theory for what was the "culprit" artery).


MY 2nd REPLY:

NOW I see what is going on !!!! There was LA-LL Lead Reversal on the initial ECG !!!! The usual "clue to this is that the P wave in lead I is larger than in lead II — but that was not at all obvious here, because P waves are almost of similar size. But your post cath ECG shows DEFINITE reperfusion changes in the inferior leads !!! and that would not make any sense if this was an LCx occlusion.

 

I thought lead V1 (as YOU also said) looked funny for LCx occlusion on the original tracing! — and lead II ALSO looked funny, because I would NOT expect reciprocal ST depression — and the AMOUNT of ST elevation in leads I,aVL is more than I've ever seen for LCx occlusion.



BUT — if you make the adjustments that I've made for LA-LL Reversal — then the original ECG fits PERFECTLY with your clinical scenario ( = marked ST elevation in inferior leads with more recip ST dep in aVL than in lead I — and as YOU said, the subtle ST elevation in V1 IS strongly suggestive of acute RV MI! There is also posterior MI which is "masked" because of all the ST elevation in V1,V2 from the RV MI !!!!

And now the post cath ECG makes perfect sense!!!!



I definitely want to use this as an ECG Blog! It may be a month or so until I get to this (because other cases come before) — but do I have your permission to publish this? Please remind me of the city & country from where you are from — as I will acknowledge you and let you know when I publish this. This is a SUPER CASE!



My Blog #396 (https://tinyurl.com/KG-Blog-396 ) is on a lead reversal — but if you scroll down to the bottom of the page — you'll find links to LOTS of lead reversal cases that I've commented on (including a bunch with LA-LL lead reversal) - FASCINATING! — :)


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ECG Blog #375

https://ecg-interpretation.blogspot.com/2023/04/ecg-blog-375-at-least-3-major-findings.html

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The ECG in Figure-1 was obtained from a 50-year old man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain).



QUESTIONS:
  • There are at least 3 principal findings on this ECG — some of which deal with a possible “culprit” artery and/or the location of whatever is going on. How many of these findings can YOU identify?

  • HINT: Is the rhythm sinus?

Figure-1: The initial ECG in today's case — obtained from a 50-year old man with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on the ECG in Figure-1:
As always — I like to start my interpretation of 12-lead ECGs with assessment of the rhythm (as per my systematic approach in ECG Blog-205). Since there is no long lead rhythm strip — I focus my attention on the 3 beats that we see in lead II from the 12-lead ECG shown in Figure-1.
  • The QRS complex is narrow — so the rhythm is supraventricular.
  • Although we lack a long lead rhythm strip — it appears that the overall rhythm in Figure-1 is Regular — at a Rate between ~80-85/minute (ie, with an R-R interval of between 3-4 large boxes in duration).
  • Upright P waves are present in lead II — but there is something unusual about these P waves in lead II. Did you notice this unusual finding that is not typically seen with a normal sinus rhythm?


PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as it passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II in the frontal plane (lead II being located at +60 degrees in the frontal axis plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).
  • Note in Figure-1 — that the upright P wave in lead II is clearly smaller than the upright P wave in lead I. While possible that this discrepancy in relative P wave size between leads I and II could be seen with either an ectopic atrial rhythm or certain forms of dextrocardia — this P wave size discrepancy should prompt consideration of the most commonly overlooked form of lead reversal, which is a mix-up of the LA (Left Arm) and LL (Left Leg) electrodes.


What Happens with LA-LL Lead Reversal?
My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.
  • This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.

  • By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).

  • In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal in Figure-2.


Figure-2: LA-LL Lead Reversal (adapted from LITFL).


What Should the Initial ECG in Today's Case Look Like?
For clarity — I've taken the limb leads from the initial ECG in today's case ( = ECG #1) — and inverted lead III — switched leads I and II — and switched leads aVL and aVF. The result is ECG #1a — which is seen in the righthand portion of Figure-3. 
  • Note that the chest leads in ECG #1a of Figure-3 — are unchanged from what they were in Figure-1.


QUESTIONS:
Looking at ECG #1a in Figure-3:
  • Is the P wave in lead II of ECG #1a now larger than the P wave in lead I (as it should be with a normal sinus rhythm)?

  • Now that we've established that the 1st KEY finding in today's case is that there was LA-LL Lead Reversal — How would YOU interpret ECG #1a, which shows what today's 12-lead ECG would look like IF lead placement was correct?


MY Interpretation of ECG #1a:
Having accounted for what today's initial tracing would have looked like had lead placement been correct — I see the following in ECG #1a:
  • The rhythm is sinus at ~80-85/minute.
  • There is dramatic ST elevation in each of the inferior leads. A Q wave is forming in lead II.
  • There is equally dramatic reciprocal ST depression in lead aVL (which manifests the mirror-image opposite ST-T wave picture as seen in lead III).
  • Significant reciprocal ST depression is also seen in the other high-lateral lead ( = lead I).

  • In the chest leads — there is significant ST elevation, with a straightened ST segment takeoff in lead V1.
  • There is abrupt transition to a surprisingly tall R wave (of ~10 mm) already by lead V2. There is significant ST depression with a positive "Mirror" Test for acute posterior infarction in lead V2. Chest lead ST depression is limited to lead V2.
  • There is marked overlap of QRS complexes in virtually all chest leads. The deep anterior S waves and tall lateral chest lead R waves suggest significant LVH.

Putting It All Together: 
After correcting for LA-LL lead reversal — ECG #1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement.
  • PEARL #2: The "culprit" artery in today's case — is almost certain to be the proximal RCA (Right Coronary Artery). As discussed in ECG Blog #141 — ECG features in Figure-3 that strongly support the likelihood of the RCA as the "culprit artery" are: i) ST elevation in lead III>II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement. 

PEARL #3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx (Left Circumflex) coronary occlusion. The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the culprit artery. 
  • ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI. That said — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. 
  • Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changess due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement. This is precisely what we see in lead V1 of ECG #1a.


Figure-3: Comparison of the limb leads from the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal. (To improve visualization — I've digitized the original ECG using PMcardio).



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Acknowledgment: My appreciation to Adem Ahmed (from Nouakchott, Mauritania) 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.
  • ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.

  • ECG Blog #190 — When to suspect acute RV Infarction?
  • ECG Blog #141 — On acute RCA Occlusion (with RV MI).
  • ECG Blog #80 — More on the "culprit" artery.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).

  • ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis). 
  • ECG Blog #317 — reviews use (or not) of Posterior Leads.

  • ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.


  • ECG Blog #264 — For review of another limb lead reversal (ie, LA-RA lead reversal in a patient with an acute MI).

OTHER Examples of Lead Reversal (from Dr. Smith's ECG Blog):
Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — it's important to familiarize ourselves with how best to recognize the various forms of these "misadventures". For review — Check Out My Comment — at the bottom of the page in the following posts on Dr. Smith's ECG Blog:
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