Saturday, May 26, 2018

RBBB and inverted hyperacute T-wave in V3. Do not let negative posterior leads dissuade you!

An elderly male with history of MI 10 years prior called 911 for chest pain.

Here is the prehospital ECG:
What do you think?
Computer only noted RBBB.

There is sinus rhythm with RBBB.  There is a bit of ST elevation in III and aVF, with reciprocal ST depression in aVL.  This is a subtle inferior MI. 

Is there more?

In RBBB, there should be some ST depression in V1-V3, discordant to (in the opposite direction of) the R'-wave.  But unless there is a huge R'-wave (as in RVH), this ST depression should not exceed 1 mm.  And the inverted T-wave should be proportional.

Here there is more than 1 mm of ST depression in lead V2, and the inverted T-wave in V3 is hyperacute.  This is posterior STEMI.

Moreover, look at V6.  There is ST elevation with a hyperacute T-wave (there should never be STE in RBBB!).  This is lateral STEMI, which supports the diagnosis of posterior STEMI.

Frequently, in posterior STEMI, one can see subtle STE in lead V6.

I knew this was an inferior posterior MI, so I activated the cath lab.

We recorded an ED ECG:
There is now more STE in inferior leads.
The inverted hyperacute T-wave in V3 is more pronounced.
The ST depression in V2 and V3 is more profound.
Interestingly, the STE and hyperacute T-wave in V6 are not evident. 

Just for my own interest, I recorded posterior leads.  Unfortunately, that ECG was lost.

But what I want to share with you is that there was no ST elevation in posterior leads!  And this cannot be blamed on reperfusion, because leads V1-V3 were recorded simultaneously with V7-V9,  and they were identical to the above ECG.

Once you have made the diagnosis of posterior MI (with or without associated inferior or lateral MI), you should not believe negative posterior leads.  They are often falsely negative!


Posterior leads are recorded through a lot of impedance of the intervening lungs, and the voltage simply many not be adequate.  It is true that the QRS is also very small in posterior leads, so (as always), proportion is the most important element.  That is why the "criteria" for posterior leads is only 0.5 mm.  However, in this case, there was not even 0.5 mm of STE.

Another ECG was recorded:
It is looking somewhat better.
The T-waves are not as deep in V2 and V3
There is some terminal upright of the T-waves in V2 and V3, typical of reperfusion.

Angiogram report:

Culprit Lesion (s):
99% thrombotic occlusion of the mid-circumflex, which is the culprit lesion for the patient's acute chest pain syndrome
70% in-stent restenosis of the pRCA

Severe disease of the distal/apical LAD

Echo report:

The estimated left ventricular ejection fraction is 40-45 %.
Regional wall motion abnormality - inferior.

Regional wall motion abnormality - lateral.  (remember that posterior (inferobasal) is now called "lateral" in echocardiography)

Post reperfusion ECG:
This is a normal RBBB.

More posts:

Beware confusing the diagnosis of posterior STEMI by using posterior leads...


  1. Superb illustration by Dr. Smith of the subtleties of acute posterior MI in the setting of complete RBBB. I’d add the following points to Dr. Smith’s excellent commentary: i) All 3 of the inferior leads show consistent acute abnormalities. The amount of ST elevation is clearly more in leads III and aVF than in lead II — but SHAPE is often more important than AMOUNT — and especially in view of the tiny-amplitude QRS in lead II — the ST segment coving in this lead is unmistakeable; ii) One looks at “Patterns of Leads” — ie, the experienced ECG interpreter takes in the QRST appearance of ALL leads in a given lead area together. Thus, one looks at leads II, III and aVF simultaneously. Of these 3 leads, lead II most often is the one that shows the most subtle changes — and that is the case here — but given the context of the ST elevation and beginning T wave inversion in leads III and aVF — lead II is clearly abnormal; iii) There is a deep Q wave in lead aVF. One can debate if there is or is not a tiny initial r in lead III. The patient has a history of prior MI, so without a baseline comparison tracing, we have no idea if this Q in aVF is new or old; iv) In the setting of complete RBBB — it is often challenging to determine if the amount and nature of ST-T depression in anterior leads is simply the result of the RBBB, vs ischemia, vs a combination of the two. Perhaps the best clue in this case is that the AMOUNT of J-point ST depression (as well as the depth of the ST-T wave) is MORE in lead V3 than it is in lead V1 (whereas with typical ST-T wave changes that are purely secondary to RBBB but without ischemia — ST-T wave depression should be more prominent in lead V1 and not in V3); v) In addition to the coved ST segment appearance in lead V6 — the S wave expected with complete RBBB (and which IS seen in left-sided limb leads I and aVL) is lost here in lead V6. This is due to lateral chest lead ST elevation — and is further indication of the abnormal ST-T wave in V6; vi) Following through with the concept of “Patterns of Leads” that I introduced in ii) — the ST-T wave in lead V5 is also abnormal. Lead V6 is the “neighboring lead” of V5 — and in the context of obvious ST-T wave abnormality in V6 — the subtle-but-real ST segment coving we see in V5 is part of this process; vii) It’s fine to get posterior leads — but they are not needed for definitive diagnosis in this case, given clear abnormality in virtually all leads on the initial standard 12-lead tracing.

  2. very interesting.
    i can hear a voice of a cardiologist saying " yes, but there are deep Q's in III, and aVF. this is old, fiero. no cath lab now".
    although perhaps he might agree that the changes in V2, V3 and V6 are very concerning. but if he goes by the "STEMI" criteria, he still might refuse, which is why the " old" STEMI criteria are not nearly as good as the broader evidence for acute occlusive MI. (am i incorrect here?)


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