Wednesday, November 21, 2018

Chest Pain and RBBB. What do you think?

An elderly woman presented with 25 minutes of chest pain after working out.

This ECG was texted to me and I viewed it on my phone hurriedly during a meeting:

There was an old ECG with it:
What do you think?

The sender wrote: "I'm thinking proximal LAD or LM.  Your thoughts?"

I wrote: "Agree with cath lab activation.  STE V1 and new RBBB and LAFB.  But I'm only 50% certain on this."

Let's look at it again:
There is sinus rhythm with RBBB. 
There is also an rS in inferior leads, and qR in aVL, consistent with Left anterior fascicular block (LAFB).

The RBBB, however, does not have an rSR', but simply a qR-wave (a very tiny r-wave which is less than 0.5 mm is analogous to a Q-wave).  RBBB in V1-V3 that begins with a Q-wave is a sign of MI, whether new or old.

There is also a bit of ST Elevation in V1.  In RBBB, the ST segment that comes after a large R'-wave in V1-V3 should have slight ST depression (in other words, the ST segment should be discordant to the R'-wave, similar to discordance in LBBB).

Leads V2 and V3 do show appropriate discordant ST depression.

RBBB generally has zero ST elevation anywhere, although there are occasional cases in which a small amount is present without pathology.

If you see STE in RBBB, you should suspect acute MI.

I have not seen an acute MI in the context of RBBB that had STE only in lead V1, which is why I was not entirely convinced by the ECG. 

Cath Result: Large Occlusion of Septal Perforator

This has been reported, but rarely.  Here is one case:

Significance of an isolated new right bundle branch block in a patient with chest pain. BMJ case reports. 2015.


Acute MI with new RBBB and LAFB is usually a very bad combination.  See these cases:

Case 2 of cardiac arrest with unrecognized STEMI, died.

Case 3 with 68 minutes of CPR and good outcome

Case 4 with LAD occlusion, cardiac arrest, could not be resuscitated

Comment by KEN GRAUER, MD (11/22/2018):
Interesting ECG regarding the challenge of assessing tracings with RBBB for acute changes. There are MANY important teaching points to make about this case:
  • Availability of a prior tracing may at times provide definitive evidence that findings on a subsequent ECG are “new”. So it is in this case — as there can be NO DOUBT that the RBBB with LAHB ST elevation in lead V1 Q in V1 are all “new” findings that have occurred since the last tracing was done.
  • The presence of new bifascicular block (RBBB/LAHBST elevation in a patient with new-onset chest pain justifies cath lab activation to define the anatomy. Clearly, an acute coronary syndrome that may benefit from acute reperfusion must be assumed in this case until proven otherwise.
  • The Problem — is that we have NO IDEA of WHEN the prior ECG was done. It could be recent — or, it could have been done years ago. As a result, we simply do not know WHICH of the changes in this patient’s initial ECG are new as a result of this current 25-minute episode of new chest pain (TOP tracing in Figure-1).
  • KEY POINT — For as helpful as availability of the prior tracing in this case is in proving beyond doubt that there have been ECG changes since the prior tracing was done — this prior tracing should not be essential to “justify” the need for prompt cath lab activation. That’s because ample evidence was already present in ECG #1 by itself to justify prompt cath in this elderly patient with new-onset chest pain.
Figure-1: TOP — Initial ECG in this case, obtained from an elderly woman with new-onset chest pain. BOTTOM — Important abnormal ECG findings in this initial ECG are highlighted in RED (See text). 
For clarity — I have highlighted a number of important ECG findings in this patient’s initial ECG in RED in the BOTTOM illustration of Figure-1. Some of these findings are subtle — but I believe they all are real. I also suspect that while ALL of these findings are “new” since the prior ECG was done — that at least some of them may have developed before this current 25-minute episode of chest pain that now brings this patient to the ED. Looking further:
  • RBBB is diagnosed in ECG #1 in Figure-1 by the presence of: iQRS widening; iia QR pattern in lead V1, with predominant positivity of the QRS, and significant widening of this upright R wave (Normally the QRS complex in lead V1 should be predominantly negative in V1 — as was the case in the old ECG of this patient); andiiiWide, terminal S waves in lateral leads I and V6.
  • As emphasized by Dr. Smith — rather than the usual rSR’ pattern expected in lead V1 with uncomplicated RBBB — the initial upright deflection in V1 (r wave) has been lost. Instead, the QRS complex in lead V1 begins with a large and wide Q wave (RED arrow in lead V1). This initial Q wave often indicates that in addition to RBBB — there has also been prior septal infarction.
  • In further support that there has been prior septal infarction — is the presence of a small-but-definitely present initial q wave in lead V2 (RED arrow in lead V2 in the BOTTOM illustration in Figure-1).
  • LAHB is diagnosed in addition to RBBB in Figure-1 — because of the presence of predominant negativity in each of the inferior leads. Note that this predominant negativity was not present in each inferior lead in the old ECG — meaning there is now new bifascicular block.
  • As noted by Dr. Smith — there is also ST elevation in lead V1 (ie, the ST segment clearly appears above the dotted RED baseline in lead V1). While the amount of ST elevation in lead V1 is admittedly subtle — we know this is a real and abnormal finding, because slight ST-T wave depression should normally be expected in anterior leads with uncomplicated RBBB.We need to explain the reason for this ST elevation in lead V1 ...
  • ST elevation is also present in lead aVR of ECG #1 (Note that the ST segment clearly appears above the dotted RED baseline in lead aVR). We also need to explain the reason for this finding in lead aVR.
  • Other subtle-but-real ST-T wave abnormalities are present in multiple other leads in Figure-1. These include ST segment straightening with slight ST depression. While most marked in those leads in which I have drawn a short horizontal RED LINE — I believe these ST-T wave abnormalities are also present in leads I, II and aVF.
  • NOTE — The reason I feel certain the above-mentioned subtle ST-T wave abnormalities are real — is that leads V2 and V3 show definite abnormal findings in ECG #1 that just should not be there with uncomplicated RBBB. Specifically, we should not see coving of the ST segment in lead V3 with uncomplicated RBBB (highlighted by the curved RED line in V3). Instead — a straighter and gradually downsloping ST segment should normally be seen in this lead with uncomplicated RBBB. A similar gradually downsloping ST segment is typically expected in lead V2 when there is uncomplicated RBBB. Thus, the horizontal “straight ledge” ST depression seen here in lead V2 is distinctly uncharacteristic of uncomplicated RBBB (highlighted by the horizontal RED line in V2).
BOTTOM LINE — All of the above-described findings are admittedly subtle! That said, the “theme” (ie, overall “Gestalt” from overview of all12 leads) of the ECG in Figure-1 — is that there is new bifascicular block (including Q waves that shouldn't be there in V1 and V2ST elevation in leads aVR and V1 ST flattening with slight depression in most other leads on this tracing. This suggests that an event (ie, anteroseptal infarction) may have occurred at some point in time since the old ECG was done.
  • Diffuse ST depression with ST elevation in leads aVR and V1 is a common finding with severe but not necessarily acute occlusive coronary disease. And, by History — this patient’s chest pain is only of “25 minutes duration”. Therefore, without additional information — I do not think we can tell for certain WHAT occurred WHEN in this patient who undoubtedly has significant coronary disease ... That is, is the deep and wide septal Q in V1 (and small q in V2) plus the ST elevation isolated to lead V1 the result of new septal infarction from acute occlusion of the septal perforator? — or, might there not also be an element of diffuse subendocardial ischemia from more extensive coronary disease? — or, perhaps both?
  • The above said, regardless of whether all findings in Figure-1 are acute — or whether there has been more than a single event — new, worrisome chest pain in an older woman with bifascicular block and multiple ST-T wave abnormalities including ST elevation in lead V1 is indication to promptly define the anatomy by cardiac catheterization, with the goal of determining IF acute reperfusion may be of benefit for this patient.
Our THANKS to Dr. Smith for presenting this SUPERB case!


  1. Hi Dr. Smith,

    I can also see a slight widespread STD (even in th presence of RBBB + LAFB) and a slight STE in avR, which is what clued me in suspecting OMI from the start. Plus, noneof these findings were present in the previous baseline ECG and thus must be assumed to be meaningful from OMI untie othwerwise proven.

    Am I right?

    1. Luca,
      Yes, you are right in your description of the leftward ST depression and STE in aVR!
      And these are all due to transmural septal ischemia (STEMI)
      The leftward ST elevation vector of the septum shows as STE in V1 and aVR, and STD in lateral leads.

  2. Very interesting and pedagogical case, as usual.
    But, Dr Smith, when you look again at the ECG 1, you comment there's LAFB because there's rS pattern in inferior leads and qR in aVL. I just don't see the latter.
    I do agree there's LAFB due to axis deviation and inferior rS, but I just can't see the lateral qR criteria in this ECG. In my short experience, I have rarely seen the 'perfect' LAFB, and I have concluded that we have to assume it by clinical context and some of the criteria but rarely the three of them (axis smaller than -45, rS in inferior leads and qR in aVL/D1).
    Am I wrong with this assumption? Is there really a 'micro' q wave in aVL and should I thus arrange a visit at the ophtalmologist's?
    Thanks a lot.

    1. Fernando,
      I think I see a micro q-wave, but perhaps I have a vivid imagination!

    2. Fernando, maybe I am wrong in saying this (and I am more than willing to admit it), but, according to what I learnt, while in a LBBB QRS morphology you don't necessarily have to see a letward axis deviation to make that diagnosis, QRS vector MUST be deviated rightward in the presence of RBBB. Thus,if you see a RBBB morphology AND a leftward axis, there must be a RBBB +LAFB regardless of the presence of Q waves in high lateral leads!

      I'm asking other people, way more expert than me in ECG interpretation, to confirm or deny this!

    3. I believe this to be true, but don't know of any formal studies to prove it. Try searching the medical literature and see what you find.

  3. As RBBB usually has discordant ST segment changes;its a bit confusing whether to expect STe or STd in the setting of RBBB in v3 to V6, because relative to NET QRS deflection it becomes STd and relative to last direction of deflection of QRS (S wave in this case)it becomes STe

    1. RBBB only has discordant ST changes in V1-V3: the ST is almost always negative, discordant to a positive R'-wave. In leads with deep wide S-wave (lateral), there is only rarely baseline discordant STE.


DEAR READER: We welcome your Comments! Unfortunately — due to a recent marked increase in SPAM — we have had to restrict commenting to Users with a GOOGLE Account. If you do not yet have a Google account — it should not take long to register. Comments give US feedback on how well Dr. Smith’s ECG Blog is addressing your needs — and they help to clarify concepts of interest to all readers. THANK YOU for your continued support!

Recommended Resources