ECG Blog #541 — Obvious MI; WHAT is the Culprit?

The ECG in Figure-1 was obtained from a patient with chest pain.

• NOTE: The challenge in today's case is not to recognize that prompt cath is needed — because that is obvious.

• The challenge is to determine the culprit artery?

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

Why Care about the "Culprit" Artery?

In addition to the intellectual challenge of trying to predict the "culprit" artery from the initial ECG of a patient with chest pain — there are times when awareness of the likely "culprit" artery is clinically invaluable.

• We are aware of cases in which recognizing the culprit artery on ECG has clued the angiographer into looking especially closely during cath at a specific coronary artery for a subtle but important acute occlusion that might not otherwise be obvious (this being particularly relevant for subtle occlusion of the 1st or 2nd LAD Diagonal branch of the LAD that may not always be obvious on initial inspection).
• Another example for which awareness of the culprit artery may prove invaluble — involves distinction between the RCA (Right Coronary Artery) vs the LCx (Left Circumflex). This is because management decisions may be impacted depending on whether or not RV involvement is likely, which is common when there is a proximal RCA culprit (and extremely rare when the LCx is the culprit artery).
• Knowing there is significant acute RV involvement mandates careful attention to volume hemodynamics (ie, emphasis on prompt cath with PCI, avoidance of sublingual NTG, cautious fluid management of likely hypovolemia) — See Shams and Parks: StatPearls, 2026 and ECG Blog #190 for more on RV MI.

Today's Initial ECG:

I initially thought the "culprit" artery for the obvious acute STEMI in Figure-1 had to be the LCx because: 

• i) Q waves with dramatic hyperacute ST elevation are seen in both high-lateral leads ( = leads I and aVL); 
• ii) Equally marked reciprocal ST depression is present in all 3 inferior leads ( = leads II,III,aVF); — and, 
• iii) A lesser degree of hyperacute ST elevation is also seen in lateral chest leads V5,V6 (and to a lesser extent in antero-lateral leads V3,V4 — which show subtle ST segment straightening, with disproportionately increased size of the overly "bulky" ST-T waves in these leads).

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The CASE Continues:

The obvious acute STEMI was immediately recognized — and the cath lab was activated.

• This patient's course was complicated. During angioplasty — sustained VT (Ventricular Tachycardia) occurred and the patient arrested. Multiple shocks were required during the extended resuscitation effort. 
• Finally, after successfully opening the acutely occluded RCA — the patient stabilized.
• There was no occlusion in the LCx.

The repeat ECG after successful PCI of the RCA is shown in Figure-2 — placed below the initial ECG.

QUESTIONS:

Take another LOOK at today's initial ECG in Figure-2. Compare it to the repeat ECG recorded after successful PCI of the RCA.

• In today's case — Can YOU explain the cath findings of acute RCA occlusion in the face of a non-occluded LCx?
• Is the repeat ECG consistent with these cath findings?
• 
  
• What clues to identifying the correct "culprit" vessel did I miss in my above description of the findings in ECG #1?

Figure-2: Comparison between today's initial ECG — and the repeat ECG recorded after successful PCI of the RCA.

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What did the post-PCI ECG show?

In Figure-3 — I highlight findings in the post-PCI ECG consistent with reperfusion following an acute inferior STEMI:

• Large Q waves are seen in each of the inferior leads (YELLOW arrows in leads II,III,aVF).
• The amount of residual ST elevation in the inferior leads is modest in ECG #2 — and there is inferior lead T wave inversion consistent with post-PCI reperfusion.
• Remarkably absent in ECG #2 — are the Q waves that were present in the high-lateral leads in ECG #1 (RED arrows in leads I,aVL).
• The hyperacute ST-T wave changes that had previously been seen in the anterolateral chest leads of ECG #1 — are no longer present in ECG #2. Instead — chest lead T waves are tiny with, if anything — slight J-point ST depression.

Figure-3: I highlight key findings in the post-PCI ECG.

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The Answer:

The reason I mistakenly thought that the "culprit" artery in today's case was the LCx — is that I did not initially recognize LA-LL Lead Reversal!

• In my experience — the most easily overlooked lead reversal is the failure to recognize when the LA (Left Arm) and LL (Left Leg) electrodes are interchanged (See ECG Blog #375 — for another example of this).

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 much more difficult to predict from a single ECG.
• 
  
• 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 in Figure-4 — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal.

Figure-4: LA-LL Lead Reversal (adapted from LITFL).

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The "Tip-Off" to LA-LL Reversal:

As suggested in Figure-4 under the "Quick Guide" to spotting LA-LL Reversal — it is the relative size of the P wave in lead I compared to the size of the P wave in lead II that provides the KEY clue.

• PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as the impulse passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II (lead II being located at +60 degrees in the frontal 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).
• PEARL #2: As stated a moment ago — it is often EASY to overlook LA-LL reversal because the changes in QRST morphology that this lead reversal produce often do not look "off" enough to arose suspicion of some form of lead misplacement. This is especially true if P wave size in the limb leads is relatively small — as it is in today's case.
• In addition, if instead of sinus rhythm an ectopic atrial rhythm is present — then it is possible that an upright P wave in lead II might not necessarily be larger in size than the upright P waves in other limb leads.

What today's ECG should look like ...

Take a look in Figure-5 below — at ECG #1 and ECG #1a, in which I have reproduced today's initial ECG — and compare it to what today's initial ECG would have looked like if the LA and LL electrodes would have been correctly placed.

• Note in Figure-5 that QRST morphology with LA-LL reversal does not change the appearance of complexes in the chest leads — because misplacement of the LA and LL electrodes has nothing to do with the appearance of complexes in the 6 unipolar chest leads.
• Note also in ECG #1 — the overall low amplitude of P waves in each of the 12 leads. As a result — I still interpreted the rhythm in today's initial tracing as sinus, because even though the P wave in lead II is tiny — this tiny P wave in lead II is upright.
• That said — I did notice that the amount of ST elevation in high-lateral leads I and aVL seemed excessive (I rarely see this much ST elevation in leads I and aVL). However, this excessive ST elevation in leads I and aVL did not prompt me to consider LA-LL reversal — because I attributed these changes to acute occlusion of a dominant LCx vessel (with this also accounting for the hyperacute ST-T wave appearance in leads V3-thru-V6 in ECG #1).

Now look at the schematic bottom tracing in Figure 5.

• After accounting for the changes expected when there is LA-LL reversal — Doesn't the limb lead appearance in ECG #1a now look like a large inferior STEMI?

Figure-5: Comparison of 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.

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Taking another LOOK at the post-PCI ECG:

I conclude today's case with Figure-6 that combines ECG #1a (which is what today's initial tracing would have looked like had the LA and LL electrodes been correctly placed) — with the repeat ECG that was recorded following successful PCI to the "culprit" RCA.

Concluding Question:

• Does the evolution of QRST changes between the 2 serial ECGs in Figure-6 now make sense?

Figure-6: Comparison between what today's initial ECG would have looked like (if LA and LL electrodes had been correctly placed) — with the repeat ECG following successful PCI to the "culprit" RCA.

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CASE Conclusion:

We now see a completely logical conclusion to today's case — with the evolutionary ECG changes in Figure-6 that one would expect following successful PCI reperfusion of the "culprit" RCA.

• ECG #1a — shows the occurrence of ongoing extensive acute inferior infarction, with developing Q waves and marked hyperacute ST elevation in leads II,III,aVF — and with equally marked reciprocal ST depression in high-lateral leads I and aVL.
• Hyperacute (ie, disproportionately "bulky") ST-T waves in chest leads V3-thru-V6 — reflect acute lateral involvement. It is not uncommon to see this in association with acute occlusion of a dominant RCA, in which posterolateral branches wrap around the LV to supply the posterolateral wall (albeit acute lateral wall ST-T wave changes are usually limited to leads V5,V6).
• ECG #1a is also consistent with posterior involvement — because lead V2 lacks the usual slight amount of upward sloping ST elevation that is normally seen with posterior OMI in this lead (ie, I suspect that the ST depression usually seen in leads V2, V3 with posterior OMI — was attenuated by hyperacute changes occurring elsewhere). 
• For example, the slightly coved ST elevation in lead V1 in association with acute RCA occlusion — may be indication of acute RV involvement. Attenuation of anterior lead ST depression by right-sided ST elevation from RV MI may also account for the lack of frank ST depression in lead V2 (although right-sided leads would be needed for confirmation of RV MI).

Following successful PCI of the RCA — the expected evolutionary ST-T wave changes are now seen:

• ECG #2 — shows progression to larger infarction Q waves in each of the inferior leads. The "good news" — is that this is accompanied by deflation of the marked ST-T wave deviations that were seen in the initial tracing:
• Minimal residual ST elevation persists in the inferior leads, that now manifest reperfusion T waves in leads II,III,aVF.
• The prominant reciprocal ST depression that had been seen in leads I and aVL has almost completely resolved.
• The hyperacute ST-T waves previously seen in leads V3-thru-V6 are no longer present.
• The ST segment in lead V1 remains coved — but the subtle ST elevation is no longer seen.

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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.