Acute inferior STEMI – RCA or LCX?

The revelation that the LCX was the culprit artery in the recent case study made me go back to the peer reviewed literature to see where I went wrong.

Let’s look at the evidence.

From Sgarbossa et al., Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician. Am Heart J. 2001;141:507-17:

“The typical electrocardiographic pattern of inferior infarction consists of ST-segment elevation in leads II, III, and aVF. The occlusion is in the RCA in 80% to 90% of cases and is in the LCX in the remaining patients. Higher ST elevation in lead III than in lead II strongly suggests compromise of the RCA.

A bedside differential diagnosis between culprit arteries can also be attempted by examining additional electrocardiographic leads. Because the only lead that faces the superior part of the left ventricle and directly opposes the inferior wall is aVL, ST depression in lead aVL is almost always determined by RCA occlusion (sensitivity, 94%; specificity, 71%), without indicating concomitant involvement of the posterior wall or the right ventricle. Injury in leads II, III, and aVF without ST depression in aVL indicates proximal LCX occlusion.

Several studies in the 1980s concluded that ST elevation in leads V5 through V6 during inferior injury signaled LCX occlusion. However, because most inferior infarctions are caused by RCA occlusion, the positive predictive value of this sign is poor. The arteries that supply the posterolateral region of the left ventricle are the obtuse marginal branch of the LCX, the posterolateral, and the LAD branches. Thus ST changes in leads V5 and V6 indicate rather posterolateral ischemia triggered by either RCA or LCX occlusion. When this ST elevation is significant (>2 mm), it is probably a sign of “mega-artery-related” (either the RCA or LCX) infarction with a large ischemic burden.”

Let’s look at the 12 lead ECG from the case study:

ST elevation in leads II, III and aVF? Check.

ST elevation lead III > ST elevation lead II?


Close. A virtual tie. (Note that I’m measuring the ST elevation from the TP segment to the J point). There may be slight advantage to lead III with calipers.

Remember this table from Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory – Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004?

It states that when ST elevation in lead II is equal to ST elevation in lead III, you should consider the T wave amplitude!

Well, that’s no help either, since the T wave amplitude in leads II and III are also the same.

Moving on…

ST depression in lead aVL? Check.

ST elevation in leads V5 and V6? Less than 2 mm, but check.

If you had to venture a guess based on these criteria, the smart money would be on the RCA.

Now let’s look at modified leads V4R and V5R.

This created some cognitive dissonance for me. I was surprised not to see ST elevation in these leads, particularly with the clinical correlation of borderline bradycardia and hypotension.

Let’s look at our cheat sheet.


We’re forced to say that lead V4R is inconclusive in this case because the ST segment and T wave are both isoelectric, which supports neither the RCA or the LCX.

In the last analysis, you can’t always identify the culprit artery based on the 12 lead ECG (or in this case, the 14 lead ECG).

Either that, or you have to be smarter than I am (in which case you should leave a comment).

This patient’s unusual coronary anatomy (I’m tempted to call it a mega-LCX) seems to confound the commonly accepted criteria.

It’s still fun to guess! :)

I’ve often said that acute inferior STEMI should be treated as RV infarction until proven otherwise!

I still feel that way. It’s interesting that leads V4R and V5R correctly identified that the patient was not experiencing RV infarction, but with the hypotension, the patient still required a fluid bolus.

Was it worth the paramedic’s time collecting leads V4R and V5R?

I’m not sure it changed anything for the patient, but it is interesting from an academic perspective!

9 Comments

  • I do think that right-sided EKGs are rapidly gaining acceptance in the pre-hospital setting. Do you think the major pre-hospital Monitor companies are going to come up with a 14 lead or 16 lead EKG attachment or an option on the 12-lead acquisition to get a right sided 12 lead? I know such systems exist for the hospital 12-leads, but I've never heard anything on the pre-hospital monitors.

  • Tom B says:

    MIFL – I agree that right sided and posterior chest leads are rapidly gaining acceptance in the pre-hospital setting.I'm not sure what the "Big 3" are going to do, but a simple setting that allows the paramedic to select right sided or posterior chest leads (or both) would be an interesting feature.I personally don't want any additional wires. I just don't think it's necessary.Tom

  • But 12 leads are so yesterday! Why not do a pre-hospital 80 lead EKG? :Dhttp://www.heartscape.com/prod_overview.htmlThe day we see this on the rigs…I think there will probably be a cath lab in there as well.

  • Tom B says:

    MIFL – I take it back! I want my 80 lead ECG! :)Tom

  • Shaggy says:

    While searching for something else a while back, the 80 lead EKG popped up in my search results. It looked like something foreign and experimental, so I only gave it a glance with a shrug of the shoulders.Anyway, Tom, how often are there rules in diagnosing a culprit artery from EKG analysis that are 100% accurate? As you said, the treatment and actions of the medic crew were appropriate for the condition of the patient anyway.

  • Tom B says:

    True, Shaggy! I don't know how often they're accurate. I was completely shocked this was the LCX! Tom

  • Lee says:

    Big inferior STEMI with Sinus brady (30's) with hypotension, if there is ST elevation in V4R would you suspect that the SB is due to SA node ischemia and thus the treatment would only include increasing the preload and reperfusion therapy and not Atropine?

  • The Jarvik 7 says:

    Tom- Outstanding analysis and case presentation. This has been an area of interest for me and you have assembled an unmatched wealth of insight here– very, very helpful. Thank you! 

  • steve says:

    If I identify an inferior MI, I always place V4 on opposite position on chest then repeat ECG making sure to mark it V4R!! To see what side is being effected.

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EMS 12-Lead

Cardiac Rhythm Analysis, 12-Lead ECG Interpretation, Resuscitation
Comments
Mary
“Bad heartburn” – 82 y.o. female without chest pain.
I, for one, would really like to read a response or two, to Dr. Walsh's question to BV about why give atropine at this time. Why give atropin at this time? Thanks.
2014-08-23 13:14:19
“Bad heartburn” – Conclusion | EMS 12 Lead
63 year old male CC: Substernal Chest Pain – Discussion
[…] upright T waves is actually not representative of acute occlusion – for more on this, read this discussion on old versus “new” teaching on recognizing posterior MIs. We do not see ST elevation in aVR or V1 that would suggest a concomitant RV infarct, […]
2014-08-22 16:49:18
Brooks Walsh MD
“Bad heartburn” – 82 y.o. female without chest pain.
Why give atropine at this time?
2014-08-22 15:42:18
Bryan Laviolette
“Bad heartburn” – 82 y.o. female without chest pain.
In addition to the above treatment consensus (ASA, Plavix, judicious NTG, fentanyl, fluid bolus, right sided leads), I would absolutely transport this patient to a PCI centre. Culprit artery is the RCA (STE lead III > II) leading to AV nodal ischemia and junctional bradycardia. In addition to the above treatment I would give 0.5…
2014-08-22 13:14:35
Jared
“Bad heartburn” – 82 y.o. female without chest pain.
Not much to add but my 2 cents...I'd definitely be careful with the nitro, not saying withhold it completely but absolutely use some common sense. I'd have to say probably RCA occlusion, and catch team needs to be activated for a stemi alert immediately. Treat it like a stemi until proven otherwise. If it walks…
2014-08-22 08:49:36

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