Dawn's picture

This 92-year-old patient was diagnosed with left bundle branch block on ECG, and left ventricular hypertrophy on echocardiogram.  The two conditions are very often seen together, in fact, a majority of LBBB patients have LVH.  Since the two conditions can have similar ECG changes, it is difficult from the ECG alone to determine the presence of LVH when LBBB is present.  If the ECG criteria for LVH are present, it can be assumed that LVH is present, even in the presence of LBBB.  For determining LVH by ECG criteria, the Sokolov-Lyon criteria are commonly used ( S wave in V1 + R wave in V5 or V6 > 35 mm). 

The common criteria for left bundle branch block include:  wide QRS complex, frontal plane axis normal or leftward, negative QRS in V1, and positive QRS in leads I and V6.   LBBB is only found in supraventricular rhythms (not ventricular rhythms).  The ST segment and T wave will be negative in leads with positive QRS complexes, and positive in leads with negative QRSs (discordant).

Left ventricular hypertrophy also widens the QRS, although not often as much as LBBB does.  There will be discordant ST segments and T waves, which is called the "strain" pattern.  It also is easier to diagnose in supraventricular rhythms, because ventricular rhythms usually have large QRS complexes due to the depolarization wave being in one direction across the heart.

For confirmation of LVH, an echocardiogram is recommended.

This ECG also has an interesting rhythm.  The first beat appears normal, the second beat is a PAC.  The third beat appears to arise from a different focus, which would make it an escape beat, but it is very difficult to determine this due to the very tiny P waves.  After a pause, a regular sinus rhythm resumes.  To see the P waves, look at the right chest leads:  V1, V2, V3.  Since left bundle branch block only occurs in SUPRAVENTRICULAR rhythms, it is important to determine the rhythm, and P waves are a definite sign of SV rhythm.  We wish the P waves here were taller.

References:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC482258/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC482000/, http://journal.publications.chestnet.org/article.aspx?articleid=1058580, http://lifeinthefastlane.com/ecg-library/basics/left-ventricular-hypertrophy/

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ekgpress@mac.com's picture

     The clinical significance of any conduction block depends upon the company it keeps. Complete RBBB may be seen in patients without any underlying heart disease. In contrast — Complete LBBB Is almost always accompanied by significant underlying heart disease. Statistically  the odds that LVH will be present in a patient who has complete LBBB on ECG approach 80%. This goes up to at least 90% if in addition: i) there are very deep S waves (>25-30mm) in lead(s) V1,V2 or V3 and/or ii) ECG evidence of LAE is also present (ie, wide notched P wave in lead II; deep negative component to the P wave in lead V1). 

The ECG in this example certainly qualifies (even without LAE) — as the S wave in lead V2 is almost 45mm !!!
Assessment of ST-T wave abnormalities in the setting of complete LBBB is challenging. The findings seen on this example (significant J-point depression in multiple leads; asymmetric ST depression in lateral leads and also in lead II; and J-point ST elevation with peaked T waves in V1,V2,V3) are all consistent with LBBB. The amount of J-point ST elevation in the anterior leads is not excessive in view of the marked increase in QRS amplitude. Thus, I'd interpret this ECG as showing sinus rhythm, a PAC, complete LBBB with probable LVH — but no acute ST-T wave changes.
As per Dawn — Echo is by far the most sensitive and specific way to determining if there is true chamber enlargement. That said — I wouldn't need an Echo to tell me that this patient has LVH given the dramatic anterior S wave deepening that we see.
P.S. We'll also point out that despite "poor r wave progression" (ie, no more than a tiny r wave in leads V2,V3) — this is not at all unexpected with complete LBBB, such that it is impossible from this ECG if there has been prior infarction.

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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