Wednesday, August 17, 2022

Does this ST Depression Maximal in V3 Represent Posterior OMI?

 I saw this EKG when reading through the system:

What do you think?








This is what I wrote:


ATRIAL FIBRILLATION WITH RAPID VENTRICULAR RESPONSE

RIGHT AXIS DEVIATION  [QRS AXIS > 100]

RIGHT BUNDLE BRANCH BLOCK  

MARKED ST DEPRESSION, CONSIDER SUBENDOCARDIAL INJURY  

"Severe ischemia (STE in I and aVL with reciprocal STD in inferior leads; precordial STD precordial maximal in V3): subendocardial ischemia vs. acute coronary occlusion.  Atrial fib may cause Occlusion mimic."

***ACUTE MI***


(I allowed Acute MI to be in the report because I knew there would be an elevated troponin from ischemia, which is the definition of acute MI -- but in this case it would most likely be a Type 2 MI from tachycardia)


There is also LA-RA lead reversal.


STD Maximal in V1-V4

We have shown in the Journal of the American Medical Association that ST Depression Maximal in V1-V4 (vs. V5, 6) is 97% specific for OMI in a patient population at high risk of ACS.  However, this does NOT apply to patients who have atrial fibrillation, and may not even apply to patients with tachycardia.  


RBBB and STD

ECGs with RBBB have non-ischemic ST depression in V1-V3, discordant to a positive R'-wave; this STD is very moderate, and when "excessive," it represents ischemia, as it does here.  In this case, the ischemia is NOT OMI; it only mimics OMI because of the atrial fib.



I looked into the chart:


Patient was very elderly and had had a fall, was unable to get up and therefore was down on the floor for a long time.  She had some fractures.


It would be possible for acute OMI to initiate such a fall, so it must be on the differential diagnosis.


It is critical to understand that atrial fibrillation can result in ST Depression that mimics posterior OMI.


This was recorded one hour later:

Lead Reversal is no longer present

The ischemia is not as severe (less STD)


High sensitivity troponin I peaked at 82 ng/L (consistent with type 2 MI)

Formal Echo showed hyperdynamic LV function with EF of 78%, no wall motion abnormality.


Next day ECG:

There is sinus rhythm and the ischemia is gone

Learning point:

In the setting of atrial fibrillation with RVR, ST depression maximal in V1-V4 may be due to demand ischemia and not OMI.  This is in contrast to sinus rhythm with a heart rate below 100.



===================================

MY Comment, by KEN GRAUER, MD (8/17/2022):

===================================

I was shown today's ECG without the benefit of any history. Because of an abundance of interesting findings — I focus my comments on this tracing, which I've reproduced in Figure-1. 
  • The rhythm is rapid AFib.
  • The QRS complex is wide and all upright in lead V1, with a wide terminal S wave in lead V6 — so there is complete RBBB.
  • There is lots of ST depression beyond that expected for simple RBBB. This ST depression is maximal in leads V1-thru-V4 — which suggests acute posterior OMI.
  • There also appears to be ST elevation in high lateral leads I and aVL. This would seem to suggest postero-lateral OMI (presumably from acute LCx occlusion).

KEY Points (as per Dr. Smith): It turns out that neither posterior nor lateral OMI were present! These are the "Take-Home" Lessons from today's tracing:
  • As per Dr. Smith — Rapid AFib may sometimes simulate acute posterior OMI. While common to see diffuse ST depression with regular SVT rhythms — ST depression with rapid AFib has a tendency to be maximal in anterior leads (as in Figure-1), in such a way that falsely suggests posterior OMI. This anterior ST depression often resolves (or at least greatly decreases) when AFib is controlled and the heart rate slows.

  • The QRS complex in lead I looks "funny". This lead almost never normally manifests as deep of a Q wave as is seen in Figure-1. Whenever you see an overly large initial negative deflection in lead I — Think of LA-RA Lead Reversal!

Figure-1: The initial ECG in today's case.

QUESTION: 
  • HOW did I know there was LA-RA Lead Reversal?


ANSWER:
My Confession: Initially — I was not at all certain about lead reversal, since ST elevation in high-lateral leads I and aVL seemed to "fit" with a picture of acute LCx occlusion causing postero-lateral OMI — BUT —
  • Rapid AFib is prone to produce transient ST depression that is maximal in the anterior leads, not due to posterior OMI.
  • AND — with LA-RA Lead Reversal, the appearance of leads I and aVR is reversed. That is, the large initial negative deflection in left-sided lead I (ie, the deep Q wave) looks perfectly consistent with what the QRS should normally look in lead aVR — and — the positive R wave with wide terminal S wave in right-sided lead aVR looks perfectly consistent with what the QRS should look like in lead I when there is RBBB.

What Happens with LA-RA 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 is the mix-up that occurred in today’s case. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-2.

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



What Should the Initial ECG Look Like?
For clarity — I've taken the initial ECG in today's case ( = ECG #1A) — and inverted lead I — switched leads II and III — and switched leads aVL and aVR ( = ECG #1B, which is the lower tracing in Figure-3).
  • Doesn't ECG #1B now look perfectly consistent with what we might expect for this initial ECG with rapid AFib and RBBB? Note that there is now: i) A positive R wave and wide terminal S wave in leads I and aVL; ii) A deep initial negative deflection in lead aVR; and, iii) An rSR' complex in lead III (instead of lead II) — as is commonly seen when there is RBBB.

  • KEY Point: Note that there is no longer any suggestion of high-lateral OMI — because with the leads correctly placed (as in ECG #1B) — there would be no ST elevation in leads I and aVL!

Figure-3: Applying the manipulations specified in Figure-2 for LA-RA Lead Reversal — reveals in ECG #1B what the initial tracing should have looked like if the LA and RA electrodes had been properly placed.


There was No Posterior OMI
Finally — I've placed the "corrected" initial tracing ( = ECG #1B) together with the repeat ECG recorded 1 hour later (Figure-4).
  • Note how this comparison confirms that there was LA-RA Lead Reversal in the initial ECG from Figure-1 — as QRS morphology in ECG #1B and ECG #2 is virtually identical!
  • As per Dr. Smith — the repeat ECG showed significantly less ST depression. The modest HS troponin elevation with lack of wall motion abnormality and excellent ejection fraction on Echo were consistent with Type-2 MI — confirming that the initial ECG did indeed give the false impression of acute coronary occlusion.

Figure-4: Comparison of the "corrected" initial tracing — with the repeat ECG done 1 hour later. The virtually identical QRS morphology between the 2 tracings confirms that there was LA-RA Lead Reversal in Figure-1. Note the amount of ST depression has decreased considerably in ECG #2 (See text).



ADDENDUM on Lead Reversal:
What has helped me over the years to rapidly recognize most cases of lead misplacement is attention to the following parameters:
  • Lead I — usually manifests a predominantly positive QRS complex, because this left-sided lead normally sees the heart’s electrical activity as traveling toward lead I. It is of course possible to have right axis deviation — but you will virtually never see an all-negative (ie, QS) complex in lead I unless there is: i) lead reversal; or ii) dextrocardia.
  • It is also extremely uncommon for there to be a very deep and wide Q wave in lead I in the presence of a QR complex in this lead. Of course, there are exceptions (ie, a large lateral MI) — but I always consider the possibility of lead misplacement whenever there is a predominant initial negative deflection (ie, a large and wide Q wave in the presence of a QR complex) in lead I.
  • IF there is “global negativity” (ie, negative P wave, QRS complex and T wave) in lead I — then the diagnosis of either lead reversal or dextrocardia is virtually assured! (ie, IF lead I looks like you expect aVR to look — and aVR looks like you expect lead I to look — then suspect LA-RA lead reversal!)
  • Lead aVR — usually manifests a predominantly negative QRS complex, because this right-sided lead normally views the heart’s electrical activity as traveling away from the remote (looking down from the right shoulder) viewpoint of lead aVR. Clearly, there are instances in which the QRS manifests positive activity in lead aVR — but the finding of an all negative QRS in lead I with an all positive QRS in lead aVR is virtually diagnostic of either lead reversal or dextrocardia!
  • The P wave should always be upright in lead II when there is sinus rhythm. The only 2 exceptions (ie, when there may be sinus rhythm without the P in lead II being upright) — is when there is either lead reversal or dextrocardia.
  • Finally — the way to distinguish between lead reversal vs dextrocardia on ECG is to look at R wave progression. When there is dextrocardia — there will be reverse R wave progression (ie, a modest R wave in lead V1 will quickly become smaller and disappear as you move across left-sided chest leads). Repeating the ECG with right-sided leads when the patient has dextrocardia will normalize R wave progression.

OTHER Examples of Lead Reversal on Dr. Smith's Blog:
Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — we'll continue to periodically publish clinical examples of lead misplacement. For review — GO TO:


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