Thursday, June 17, 2021

Acute Chest pain. All P-waves are not conducting. Is it OMI?

A 50-something male complained of acute onset chest discomfort about 30 minutes PTA while at rest with radiation described as numbness to the back of his neck and both arms.  He denied history of CAD, but he reported that he has history of smoking, hyperlipidemia, and pre-diabetes. He reports some shortness of breath and anxiety.

Here is his first ED ECG, ECG 1:

What is the rhythm?  Are there any signs of OMI?
There is an annotated version below, and Ken Grauer does a laddergram of this one at the bottom of the post.
Peter Hammarlund noticed that there is lead reversal (LA/LL)!!

Notice that there is high degree AV block.  

This is the essential feature.  Acute chest pain with high degree AV block is Occlusion MI (OMI) until proven otherwise.  One much less plausible scenario is that there is supply ischemia -- that is, some other cause of AV block with bradycardia, bradycardia causing hypotension, hypotension causing decreased coronary perfusion which causes chest pain).

In other words, you don't need to have the exact rhythm diagnosis in order to know that there is a need for angiogram +/- coronary intervention.

But here I give more analysis of the rhythm:

Below, the red arrows point out all the P-waves, which are regular.  However, none of them clearly conduct.  Every 2nd P-waves appears to conduct, but if you look closely, the PR interval gradually shortens.  The QRSs are nearly regular.  It may be that some of the P-waves that appear to conduct are actually conducting, in which case it is NOT 3rd degree (complete) AV block.   There is also some variability of QRS morphology, suggesting that there is some degree of fusion (automatic infra-nodal escape fused with conducted beat).

Ken Grauer is the master of rhythms, and he gives a very detailed analysis of this ECG below, with a laddergram.  Even he is not certain of the exact rhythm.

Moreover, the first QRS is of a different morphology that then others, which suggests that it is NOT an escape beat or that the others are fusion beats.

Annotated version of ECG 2

But whether is 2nd degree Mobitz II or 3rd degree does not really matter.

There is acute chest pain and high degree AV block, so this is acute OMI until proven otherwise.

More on this ECG: There is RBBB, but the R'-wave is limited to V1.  Therefore, the ST depression in V2 and V3 cannot be blamed on the RBBB (RBBB only has expected ST depression in V2 and V3 when it is "discordant" to a positive R'-wave)

The cath lab was activated.

While waiting for the cath team, this was recorded at 37 minutes:
2nd Degree Mobitz II
Subtle STE in III with reciprocal STD in aVL.  
These ST-T changes, by themselves, are also diagnostic of inferior OMI.

Here the rhythm is analyzed:

Red arrows point out the somewhat difficult to discern P-waves.
The red line shows the relation between the P-waves in leads V1 and II 
(II is across the bottom, and simultaneous with other leads above.)

Last ECG before cath lab:

What do you see?

There is now STE in V1, and an enlarged T-wave in V2. So this is also a right ventricular MI.

Angiogram: Culprit Lesion (s): Thrombotic occlusion of the proximal RCA.  Proximal confirms that the RV is involved 

(Proximal means proximal to the RV marginal branch, which supplies the RV.  Because most people have some collateral circulation to the RV from the LAD, most proximal occlusions do NOT result in STE in V1 or in right sided leads.  And not all which do have such STE have hemodynamic significance.  This one did not.)

Large MI.  
See how the troponin rose briskly after artery opening!

Formal contrast echo

The estimated left ventricular ejection fraction is 48%.

Regional wall motion abnormality-inferior, and inferolateral.

Right ventricle not optimally visualized, probably normal size/function.

Learning Points:

1. Chest pain and high grade AV block [does not include 2nd degree type I (Wenckebach)] is due to OMI until proven otherwise.

2. As above: Proximal RCA occlusion means proximal to the RV marginal branch, which supplies the RV.  Because most people have some collateral circulation to the RV from the LAD, most proximal occlusions do NOT result in STE in V1 or in right sided leads.  And not even all of them with such STE result in hemodynamic significance.  


Ken Grauer's analysis of ECG 1 

(By the way, this is the only ECG I sent him, so he did not have then benefit of the others -- I don't think they would have helped) 

— Definitely NOT complete AV block because as you note the R-R intervals are NOT all the same. Instead, beats #2 and 3 both clearly occur earlier-than-expected — therefore this is to my eye definite evidence of at least some conduction.

— QRS morphology is definitely within the conduction system, given the picture-perfect rSR’ in lead V1 with terminal S waves in lateral leads I, V6. I don’t know the history … but if there was recent chest pain — then the ST segment in lead V1 is abnormal (should be slightly depressed) and those T waves in leads V2,V3 look taller-than-they-should be with RBBB conduction — so could represent possible hyperacute T waves … (T waves in leads III and aVF for beats #2, 3,4 also look abnormal, even accounting for fusion … ).

— Unfortunately, we don’t see what happened before beat #1 …. so I’m just guessing on this beat — but it is notable that we KNOW the P wave before beat #1 is NOT conducting (1st RED arrow in the long lead II showing an ultra-short PR interval) — and QRS morphology shows LAHB morphology not seen for the 2nd beat in leads II and III. I interpreted this different morphology in leads I, II, III (in view of the P wave too short to be conducting at all) as indicative of a fascicular escape beat from the left posterior hemifascicle.

— The P waves before beats #2 and 3 are definitely conducting (2nd and 4th RED arrows in the long lead II). I believe these beats are manifesting Wenckebach periodicity. Marriott always emphasized that in addition to progressively increasing PR interval until  a beat is dropped — AV Wenckebach manifests “PR/RP reciprocity”. By this, he meant that the shorter the RP’ interval — the longer the next PR interval — and vice versa. So as a result of beat #1 presumably being a left posterior hemifascicular escape beat — the 2nd P wave ( = 2nd RED arrow) has a shorter RP’ interval (measured from beat #1) — than we see for the RP’ interval between beat #2 and the 4th P wave — which is why the PR interval preceding conducted beat #2 is LONGER than the PR interval preceding beat #3.

— The R-R interval between ALL OTHER BEATS in this tracing is the same ( = 1100 msec) — therefore, I propose these are all escape beats arising from the left posterior hemifascicle — and that the reason for slightly varying QRS morphology between these beats, is that they are ALL manifesting slightly different degrees of fusion.

— I wasn’t quite sure how to represent a left posterior hemifascicular escape focus on a laddergram (never did that before … ) — because it is BELOW the AV nodal tier — yet not arising from ventricular myocardium … so after several trials, I decided on showing the RED circle arising from the bottom of the ventricular tier — as this is the easiest way to show variable degrees of fusion.

— I have NO IDEA of what a “pure” sinus-conducted QRS would look like — but I think beat #3 comes closest to pure sinus conduction — which is why you see the shortest distance traveling upward from the RED circle of beat #3.

— Although subtle — Note that the distance between the QRS and the closest P wave IS changing for each beat on this tracing. Therefore, I believe we have 2nd-degree AV Block with 2:1 AV conduction — showing potention for AV Wenckebach (that PR/RP reciprocity), therefore making this Mobitz I despite the wide QRS — with an accelerated left posterior hemifascicular escape rhythm and variable degrees of fusion — and, as mentioned earlier — the possibility of hyperacute T waves IF the history at all suggests a possible recent event.

— If you make a blog post on this, feel free to use this laddergram.

Again — I am NOT certain of the above … but that’s my best guess.

Take care — :) Ken

ADDENDUM (Added on 6/18/2021 by Ken Grauer): Peter Hammarlund questioned whether this 1st ECG might represent LA/LL Reversal. As per Dr. Smith — I did not know the history, and my focus was purely on the fascinating cardiac rhythm ( = My OVERSIGHT! ).

Yes — this DOES look like LA/LL reversal (as per Peter). I’ve reproduced the Learning Points from the November 19, 2020 post in Dr. Smith’s ECG Blog — in which I presented another case of LA/LL reversal (See Figure-1 below). This 1st ECG in today’s case is consistent with LA/LL reversal because:

  • Those dissociated P waves in lead I are larger than the P waves in lead II.
  • The QRS is surprisingly negative in lead III.
  • In the 2 follow-up ECGs in today’s case (these ECGs are shown above in Dr. Smith's discussion) — the QRS is positive in lead III, and the P wave returns to being larger in lead II than in lead I (as is expected with normal sinus rhythm).

NOTE: For additional details regarding the changes to expect when there is LA/LL reversal — Please check out my discussion at the above link in the Nov. 19, 2020 post.

Figure-1: Learning Points from the November 19, 2020 post in Dr. Smith’s ECG Blog — taken from another case of LA/LL lead reversal.

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