Wide Complex Tachycardia with Fusion and Capture Beats. Not what you think.

This late middle-aged patient presented with acute hypoxic respiratory failure, with chest discomfort and apparent pulmonary edema, with a decrease in systolic function.

Here is her 12-lead ECG:

There is LBBB with sinus rhythm at a rate of about 100. This was new LBBB.
There is no concordant ST elevation or excessively discordant STE.
Notice the morphology of the P-waves and QRS in lead II

She was appropriately taken to the cath lab because of ischemic symptoms and pulmonary edema with new decrease in LV function.  At angiogram, no evidence of ACS was found.

While in the ICU, she remained tachycardic and had this rhythm strip recorded:

Wide complex tachycardia.
What is the rhythm?  Is it still sinus?

Perhaps it will help if I circle a couple complexes:

It is a wide complex.
Note two different narrower complex beats (circled). 

1. The third QRS complex (second of the two circled) is "narrow," preceded by a P-wave.  

If this were an unknown WCT, it could easily be interpreted a as "capture beat"  and be "diagnostic" of VT. 

2. The second QRS complex (first of the two circled) is wider than the third beat, but narrower than the other wide-complex beats. 

If this were an unknown WCT, it could easily be interpreted a as "fusion beat" and be "diagnostic" of VT. 

Such beats, which are fusion or capture beats, are said to always indicate that the wide complex tachycardia is VT.

But this is clearly sinus tachycardia. How can there be capture and fusion beats?

These are "pseudo" fusion and capture beats. 

Here is the explanation and learning points:

First, a couple definitions (of fusion beat and capture beat): Both typically occur in cases of VT with AV dissociation.  In fact, it is generally said that in wide complex tachycardia, the presence of a fusion beat or a capture beat implies VT with nearly 100% specificity.  

Capture beat: A sinus impulse reaches the atrioventricular node and the ventricle in a nonrefractory phase between the wide QRS complexes, and produces a beat with a normal QRS duration. 

Fusion beat:  A sinus impulse reaches the atrioventricular node and the ventricle during a ventricular beat (ectopic beat or VT beat) and they coincide to produce a hybrid complex. 

The below was written by our electrophysiologist, Dr. Rehan Karim:

Explanation of Mechanism:

-  If you measure the sinus rate (and march-out P-P interval), it stays fairly constant before and after those "fusion" and "capture" beats.

-  However, if you measure the ventricular rate (R-R interval), the "fusion beat" comes in early. This essentially would occur if there is a PVC originating from the ventricle that is ipsilateral to the bundle-branch block (e.g., LV PVC in the setting of LBBB).  In standard LBBB, the LV activation is delayed, and if a PVC originates from LV at the right time, it can activate the LV at the same time that the RV is being activated by the right bundle.  In other words, the right and left ventricles get activated simultaneously which, compared to the LBBB, shortens the QRS!  This thus results in a relatively narrow beat (AKA "fusion" beat).

- If you closely look at the PR interval on the third beat ("capture beat"), it is slightly longer than the other PR intervals during the wide-complex beats.

- The PVC from the second beat (1st of the two beats in question) has some degree of "retrograde concealment" into the Right bundle, therefore, slightly prolonging refractoriness of the Right bundle. Important concept here is, when we call bundle branch "block" - it is not always a "true block", but rather a "delay". If Right-bundle has faster conduction than Left-bundle, then it will give rise to LBBB type pattern on EKG. In this situation, both the RBB and LBB get delayed so now the QRS complex looks narrow ("capture") beat, but with a slightly prolonged PR interval.

I remained a bit confused by this, so Rehan wrote this:

-  The second of those two narrower beats ("capture" beat) does NOT have a PVC in it.

-  Here is how delaying in both RB and LB can shorten the QRS:  If two people are racing and one of them is slow (delayed), then the faster one will win (BBB). However, if for some reason, you slow down the fast person (trip him over to make him fall so he becomes slow too) - then both will reach at the same time, but the finish line will be reached later (hence longer PR).

-  The PVC from the blocked (slow) side goes trans-septal and collides with the opposite bundle. This prolongs the refractory period of the bundle so the faster bundle also becomes slow for the next beat. So now, both the bundles conduct slow and you have narrow (capture)beat after a slightly prolonged PR interval.

Similar situation can occur with any WCT. Therefore, the statement "Presence of fusion and capture beats are diagnostic of VT" is not always true.

Learning points:

1. Bundle-branch "block" is not always a "block" but rather a "delay"

2. PVC from the side where bundle branch conduction is delayed or "blocked" would result in fusion complex that would be narrower than the wide-complex tachycardia.

3. Similar delay in both bundle branches would result in a narrow QRS complex, but with a relatively longer PR interval.

4. Presence of "fusion" and "capture" beats would favor VT, but are not "diagnostic" of VT, as they could occur in SVT with aberrancy.
5. Supraventricular tachycardia with aberrancy (sinus tachycardia is a type of SVT) can have capture and fusion beats!

I guess your readers may need a cup of coffee before they read this :)

Rehan.