Friday, December 16, 2022

Right Bundle Branch Block and Posterior OMI????

 This 39 year old patient presents with syncope.

What do you think?
















There appears to be RBBB with excessively discordant ST depression (2-2.5 mm) in V2 and V3, suggestive of RBBB with posterior OMI

Whenever you see abnormal ST-T (ST elevation, ST depression, hyperacute T-waves), you MUST look at the entire ECG (rhythm, rate, P-waves, intervals, and QRS) to see if there is some abnormality among these which can explain the ST-T.  

One's first impression is that this is RBBB (tall R-wave in V1).  But that is ONLY if you don't look at it closely, and don't look at the intervals.

Differential of a Tall R-wave in V1: 
1. RVH
2. RBBB
3. WPW
4. Old "posterior" infarct
5. Lead placement
6. Septal hypertrophy (HOCM)
7. Normal Variant

There is a short PR interval. There are several Q-waves which have a slow downslope (Negative delta waves).  There are clear positive delta waves in many leads.

WPW has abnormal depolarization, with pre-excitation, through an accessory pathway.  And this abnormal depolarization (QRS) usually leads to abnormal repolarization (ST-T).

Diagnosis: 
WPW with repolarization abnormalities.  
Superimposed OMI cannot be ruled out, but the patient has syncope, not chest pain.

Here are many more examples of this:

See this recent post: 

Chest pain and anterior ST depression. What’s the cause(s)?


See this post: 






==================================
My Comment by KEN GRAUER, MD (12/16/2022):
==================================
Fascinating case — for which we unfortunately have no follow-up. That said — I still thought it worthwhile to explore this case further.


My Initial THOUGHTS on Today’s Tracing:
Clearly, I noticed the short PR interval with initial slurring of the QRS in multiple leads — so, like Dr. Smith, my 1st impression was to wonder if this was all WPW. That said — I have never seen delta waves this large (ie, 7 mm deep — and ~0.09 second wide in lead I).
  • If this was all WPW — then I wondered about the boundaries of the delta wave. The vertical RED time lines that I’ve dropped in Figure-1 — suggest that IF delta waves comprised everything to the left of these vertical RED time lines, then this would mean that there was a biphasic appearance to the delta waves in leads like IIIaVL, and V6 (ie, an initial large negative component to the delta wave — with a much shorter terminal positive component as the delta wave returned to the baseline). This was also something that I was not used to seeing — since most (albeit not all) of the time, delta waves in most leads tend to blend in with the initial direction of the QRS complex



PEARL: In patients with WPW — preexcitation can be: 

  • i) Total (ie, all impulses traveling first down the AP [Accesory Pathway]) — in which case the QRS will probably be very wide — the PR interval will be obviously short — and prominent delta waves will be present in multiple leads.
  • ii) Occult (in which case there are no delta waves, the QRS is not wide, and the PR interval is not short — because all impulses travel down the normal AV nodal pathway) — OR — 
  • iii) Partial (ie, a certain relative percentage of impulses simultaneously travel down the AP and the normal AV nodal pathway). Depending on the relative amount of impulses traveling down the AP (compared to down the normal AV nodal pathway) — the QRS may not be overly wide, and delta waves may be extremely subtle and only seen in a limited number of leads.



Can You EVER Diagnose Acute OMI with WPW?
Because significant preexcitation will alter both the QRS complex and the resulting ST-T wave in unpredictable fashion — it becomes much more difficult to recognize acute OMI in such patients. I suspect that most acute OMIs in patients with WPW are overlooked (See My Comment at the bottom of the page in the October 13, 2022 post in Dr. Smith's ECG Blog). That said — there are times when despite WPW, you can suspect acute OMI on ECG:
  • CLICK HERE — for a case of a patient with WPW and new-onset chest pain. Would you have recognized the acute posterior OMI?
  • CLICK HERE — for an example of acute OMI in a patient with intermittent preexcitation (occurring every-other-beat)!


What About Today's Tracing?
I admittedly was not sure about the reasons for the strange appearance of the ECG in Figure-1.
  • IF everything to the left of the vertical RED time line is delta wave — and IF everything to the right of this RED line is the underlying QRS — then this would make for huge, biphasic delta waves in multiple leads with a surprisingly narrow QRS (looking to the right of the RED line in leads V1,V2,V3).

I asked David Richley (who is truly an expert in this area — as former Cardiac Physiologist at NHS — UK) — for his opinion as to whether the ECG in Figure-1 was all WPW? Dave completely agreed with Dr. Smith — and wrote me the following:
  • Hi Ken. 100% WPW. It is the initial part of the QRS that is broadened — not the terminal part. Nice negative delta waves in the inferolateral leads, mimicking Q waves.
  • The delta waves are certainly huge! This suggests to me that the ventricles are almost completely pre-excited. The T wave vector is almost opposite the delta wave vector — which might be expected given the probably large mass of muscle that’s pre-excited. I really do not know whether there is any evidence of a superimposed acute event.

  • I think everything to the left of the RED line is delta wave — and the narrow bit to the right is probably mainly due to normal ventricular activation (although there is bound to be some overlap!). Maybe the narrow bit is of low amplitude because most of the myocardium has already been depolarised. 
  • In the limb leads the pre-excitation and normal conduction vectors are about 180 degrees from each other — hence the biphasic complexes. I suspect there is less of a difference in the horizontal plane, so most of the complexes in the chest leads are not biphasic — and the broad R waves in the anterior leads are probably a combination of pre-excitation and normal conduction. That said — of course, we can not prove the above ...


Is There Evidence of Acute OMI in Figure-1?
With full acceptance of expert commentary from Stephen Smith and David Richley — the ECG in Figure-1 almost certainly represents WPW with virtually complete preexcitation and pseudo-Q waves formed by the huge negative delta waves in no less than 5/12 leads. That said — given the clinical presentation of syncope, I still wondered if despite WPW — we might be seeing suggestion of acute OMI because:
  • The T waves in leads I and aVL look like they may be hyperacute.
  • There is ST segment coving, significant J-point depression — and surprisingly deep T wave inversion in leads V2-thru-V4 (with the amount of T wave inversion increasing in leads V2 and V3 compared to what it was in lead V1).
  • The T wave in lead V6 looks similar to what we saw in leads I and aVL (ie, possibly hyperacute).

  • To EMPHASIZE: Because of WPW (especially given near total preexcitation in today's tracing) — there is no way to know if the above ST-T wave changes are simply part of this patient's WPW appearance — OR — if they might represent superimposed acute ischemia/OMI?

How I wish we had follow-up on this case ... 


Figure-1: I've added time lines to today's tracing — in order to better appreciate the likely boundaries of the delta waves (See text).



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