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Today’s expert is Dr. Jerry W. Jones, MD, FACEP, FAAEM

Jerry W. Jones, MD FACEP FAAEM is a diplomate of the American Board of Emergency Medicine who has practiced internal medicine and emergency medicine for 35 years. Dr. Jerry JonesDr. Jones has been on the teaching faculties of the University of Oklahoma and The University of Texas Medical Branch in Galveston. He is a published author who has also been featured in the New York Times and the Annals of Emergency Medicine for his work in the developing field of telemedicine. He is also a Fellow of the American College of Emergency Physicians and a Fellow of the American Academy of Emergency Medicine and, in addition, a member of the European Society of Emergency Medicine. 

 Dr. Jones is the CEO of Medicus of Houston and the principal instructor for the Advanced ECG Interpretation Boot Camp and the Advanced Dysrhythmia Boot Camp. 

QUESTION:  How can I explain to students that injury from an M.I. “localizes” on the ECG, but subendocardial ischemia/injury does not?

ANSWER:                 Allegory of Subendocardial Ischemia

 For many years we have misunderstood the concept of subendocardial ischemia as it manifests on the 12-lead ECG.  Previously, if one saw ST depression in leads II, III, and aVF, it would be labelled "inferior subendocardial ischemia" and, if the patient were momentarily having little or no chest pain, the patiet would be sent home.  The same thing happened with ST depression in leads V4 - V6; "anterolateral subendocardial ischemia," probably chronic and again, the patient may be sent home.  And of course, ST depression in leads V1-V4: "anteroseptal subendocardial ischemia" and often the patient was sent home.

Then a number of years ago, some disturbing information began to surface in various medical journals around the globe.  Sometimes ST depression that was limited to just leads II, III, and aVF, for example, did not reveal any actual subendocardial ischemia in the inferior wall of the left ventricle.  In some cases, subendocardial ischemia was indeed present but very little involved the inferior wall and most of the ischemia was elsewhere; but... the only ST depression present was in the inferior leads.  Some articles began mentioning the same findings regarding ST depression in other leads as well.

What we have learned is that when ST depression indicates subendocardial ischemia, IT DOES NOT LOCALIZE!  Just because there is ST depression in leads II, III, and aVF does NOT necessarily mean that the ischemia is located in the inferior wall of the left ventricle.  It MAY be there, or there may be SOME ischemia there but most of it elsewhere, or there may be NO ISCHEMIA AT ALL there.

Some people still have difficulty conceptualizing this, so I developed an allegory of subendocardial ischemia using the concept of a vacant house at night.


Imagine you have gone out for a walk one pleasant evening in your neighborhood.  As you stroll down the street, you come upon a vacant house.  You know it is vacant because the family that lived there moved out recently.  However, you can see light coming from some of the windows of the house. You wonder what's going on, so you walk up to the house and look through a window into the living room.  The room is illuminated but you don't actually see a light on there.  You move around to another window and look into the dining room.  Again, there is enough light for you to see everything in the room but you don't actually see any light fixture that is on. Finally, you move around to the window that looks into the kitchen.  It's illuminated as well and you can see everything but, once again, the source of the light is not there.  Is the light in a room that you cannot see or is it perhaps a closet light that has been left on somewhere in the house?

That - in essence - is subendocardial ischemia.  Just because you see ischemia through the "windows" of leads II, III or aVF or the "windows" of leads V4 - V6 doesn't mean that the "source of the ischemia is in those "rooms."

Subendocardial ischemia manifested by ST depression does NOT localize reliably.  So how should you report such ischemia?  This is what I would say if I saw (for instance) ST depression in leads V4 - V6:  "There is subendocardial ischemia present indicated by ST depression in leads V4 - V6."  I would NOT call it "anterolateral ischemia."

Actually, this information has been available for a number of years.  So, if you are reading textbooks, journal articles or posts on websites that still refer to "inferior ischemia", "high lateral ischemia", "anteriorlateral ischemia" etc., then you are reading information that is OUTDATED. If it was recently written, then you are reading information from someone who is NOT staying current with advances in electrocardiography.



ekgpress@mac.com's picture


Our THANKS to Dr. Jones for his provocative discussion regarding non-localization of ischemia on ECG. One KEY concept I’ve found — is suboptimal appreciation by many clinicians of the difference between the 2 Essential Steps in ECG Interpretation = i) “Descriptive Analysis” of ECG findings (in which the interpreter merely DESCRIBES what is seen, without attaching any “meaning” to the findings detected) — and, ii) “Clinical Interpretation”, in which based on history, exam, risk factors, etc + one, or ideally more than a single ECG on the patient — the interpreter renders a synthesized clinical interpretation in which concern for possible acute, less acute, or non-acute ECG issues (ie, ischemia, infarction, etc.) is expressed. As Dr. Jones emphasizes — ST segment depression, even if present in a number of leads — might not even be cardiac in nature (ie, drugs, electrolyte disturbance, emotions, hyperventilation, “sick patient” are just a few of the numerous non-cardiac conditions that might produce ST-T wave abnormalities). On the other hand — a history of new-onset worrisome chest discomfort may render even “minimal” ST-T abnormalities significant and acute (especially if availability of a prior ECG on the patient shows such subtle changes to be new).

One problem I have with brief survey I just now made of internet tracings purporting “non-localization” of ischemia — is that subtle findings in other leads are often missed by less-than-expert interpreters. Designing a truly objective, double-blind, randomized clinical trial proving zero value for ever being able to localize ischemia on a 12-lead tracing I predict would be a Herculean task.

What We KNOW: i) ST depression on exercise testing does not correlate with location of ischemia. ii) Diffuse ST-T changes (depression, some T inversion in ≥6-7 leads) + ST elevation in aVR correlates with diffuse subendocardial ischemia that may be due to severe coronary disease (LMain, proximal LAD, multi-vessel disease) OR, sometimes to some other non-cardiac disorder (ie, tachycardia, anemia, etc.). iii) Ischemia in patients with multi-vessel disease (+ collateralization) defies localization; and, iv) Truly localized ST depression to the inferior leads does not necessarily mean coronary narrowing in the RCA; and truly localized ST depression in lateral leads does not necessarily mean coronary narrowing in the left circumflex.

The above said — for the example provided by Dr. Jones, I’ll offer an alternative description for what I still report on my written interpretations = ST depression (adding shape and amount of these ST-T wave changes) in LATERAL precordial leads V4-V6 in my “Descriptive Analysis” — with my “Clinical Interpretation” then stating EITHER “possibly ischemic” — “consistent with ischemia” — or “probably ischemic” + “SUGGEST (or urge) Clinical Correlation”, based on whatever history I’m able to obtain + comparison of any prior or serial ECGs available on the patient. What we REALLY care about in interpreting an ECG that shows ST depression is whether this is likely or not to be an acute or recent indication of ischemia or other acutely ongoing cardiac process. I believe there is universal agreement that “Location” of such ischemia is not clinically important.

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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