Sunday, January 14, 2018

ECG Blog #146 – (BBB – Primary ST-T Changes)

The ECG in Figure-1 was obtained from a patient with new-onset chest pain. It was interpreted as showing LBBB (Left Bundle Branch Block). As a result, the provider thought — “impossible to tell if anything acute is going on because there is LBBB”.
  • Do you agree with that assessment?
Figure-1: 12-lead ECG from a patient with chest pain. How do you interpret this tracing? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
Clinical NOTE: In the past, it was thought that one could not diagnose an acute STEMI (ST Elevation Myocardial Infarction) in the presence of LBBB. This notion has been completely refuted. Although it will often be more difficult to diagnose acute ischemia/infarction in a patient with chest pain who presents in complete LBBB — in a surprising number of such patients, there will be at least strong suggestion on the initial ECG of acute STEMI despite the presence of underlying LBBB.
  • When acute ECG changes in a patient with LBBB are subtle — diagnostic aids such as Smith-modified-Sgarbossa criteria may be helpful. At other times (such as for the ECG in Figure-1) — the diagnosis of acute STEMI is obvious without need to invoke modified Smith-Sgarbossa criteria. (NOTE: Search of Dr. Stephen Smith’s web site at the above link will provide numerous examples of how his criteria can be applied to clinical cases).
Interpretation of the ECG in Figure-1: The rhythm is sinus. The QRS complex is wide (≥0.12 second) — and QRS morphology is consistent with complete LBBB because there is a predominantly positive complex in lateral leads I and V6 — and, a predominantly negative QRS in lead V1. (For review of the Basics of BBB — Please see my ECG Blog #11). That said, there are a number of features that are distinctly atypical for simple LBBB. These include:
  • i) The presence of septal Q waves in lateral leads I and aVL. Because the presence of LBBB alters the direction of initial septal activation (which can no longer proceed from left-to-right) — there should never normally be a septal q wave in a lateral lead when there is uncomplicated LBBB. The prominent Q waves in leads I and aVL of this tracing leave little doubt that infarction has occurred at some point in time.
  • Beyond-the-Core: The presence of one or more lateral Q waves in association with LBBB do not indicate “lateral” infarction. Instead, they indicate septal and/or anteroseptal infarction — since the reason for their occurrence is that the LBBB has altered the direction of initial septal activation.
  • ii) There is ST segment coving and primary ST elevation in lead aVL. This just shouldn’t be seen with typical LBBB. The most reliable way to recognize acute STEMI that occurs in association with LBBB is by the presence of frank ST elevation in a lead that should not show ST elevation. So, while it is admittedly challenging to determine if the anterior ST elevation that is seen in Figure-1 is a result of LBBB or acute anterior STEMI (because there is often some normal ST elevation in anterior leads with simple LBBB) — there should not be ST elevation in lateral or inferior leads.
  • iii) There are reciprocal ST-T wave changes in each of the inferior leads. We know the inferior ST-T wave changes that are seen here are likely to be both real and acute — because these inferior ST-T wave changes are a “mirror-image” reflection of the ST-T wave in lead aVL. This reciprocal change picture shouldn’t be seen with uncomplicated LBBB.
  • iv) The final abnormality occurs in the chest leads, and is indeed subtle — but it supports the above limb lead findings. That is, the ST segments in leads V5 and V6 are coved — and manifest a disproportionate amount of J-point ST depression (considering the modest amplitude of the R wave in these leads). This abnormal shape of the ST-T wave extends to lead V4. (We think there are also tiny-but-real q waves in lateral leads V5 and V6).
Clinical Impression: In a patient with new-onset chest pain — the combination of the above findings should suggest an acute evolving STEMI until proven otherwise despite the presence of underlying LBBB.
  • NOTE: Access to a prior ECG on this patient would clarify whether the LBBB in Figure-1 was new — and, would help to establish that the above noted changes are acute. But in the absence of a comparison tracing — the history (of new-onset chest pain) in this patient whose ECG shows LBBB with inappropriate lateral Q waves and primary ST-T wave changes despite the LBBB, should strongly suggest acute STEMI with need for immediate evaluation and reperfusion therapy until proven otherwise.
Follow-up: Unfortunately, the cardiac catheterization lab was not immediately activated for this patient. The patient coded in the hospital, and could not be resuscitated.
Acknowledgment: My thanks to Casey Caldwell for allowing me to use this tracing and clinical case.
Additional Material: For Review on ECG Diagnosis of the Bundle Branch Blocks — See my 17-minute ECG Video on this subject at
  • Please note that if you click on SHOW MORE on the You-Tube page under where this video appears — You’ll see a detailed linked Contents that will allow you to immediately find whatever key points you are looking for in this video.


  1. Insightful discussion on diagnosis of STEMI in the presence of LBBB. It makes me think how many appropriate therapies have been omitted just on the myth according to which it is impossible to diagnose ongoing acute ischemia in the presence of LBBB. In regard to the present ECG, together with PR interval at the upper limit of normal, I noticed very likely LAA (biphid and wide P wave in lead II) but I would like to know your opinion about the coved ST in lead I: to say the truth, it is visible only in the second beat but in this context is very suspicious (along with redundant given the clear STE in aVL...). Thanks for reinforcing and emphasizing (and cancelling a false myth) once again that LBBB often does not prevent us to diagnose STEMI!

  2. Thanks (as always!) for your comments Mario. Qualitatively — the ST segment in lead I is also clearly abnormal — but this is much more subtle than the changes seen in lead aVL. That is, one usually expects more of a downsloping with the mid-point of the ST segment lying a bit BELOW the baseline (rather than touching the baseline, as it does here in lead I). And the fact that lead aVL is obviously abnormal, makes it that much MORE likely that these subtle changes in lead I are also abnormal. In addition, the shape of the J-point in leads V1 and V2 to me ( = my opinion) is not typical for the shape of an anterior ST segment in association with simple LBBB). That said, it is because these ST-T wave changes in leads I, V1 and V2 are all extremely subtle that I chose NOT to mention them. They aren’t needed for diagnosis of acute STEMI in this case — and I didn’t want to confuse less seasoned interpreters with subtle changes that by themselves were not definitive ... Instead, my emphasis was on the Q wave and ST elevation in lead aVL plus the reciprocal mirror-image changes in each of the inferior leads — because THOSE are qualitative changes that I feel ALL providers should become facile in rapidly recognizing. Regarding the bifid P wave in lead II — I don’t feel this tells us much, given the very poor sensitivity and specificity of the ECG for detecting atrial chamber enlargement. Add to that the entity of intra-atrial conduction defects — which I have always found very difficult to distinguish from P wave changes suggestive of atrial chamber enlargement. So in the context of LBBB — I don’t think that bifid P wave in lead II tells me anything that I would use clinically. THANKS again for your comments.