Saturday, August 23, 2014

A Very Fast Regular Narrow Complex, Followed by an Equally Fast Regular Wide Complex

This case was sent to me by for analysis by Scott Flannagan in Australia.  I am by no means a rhythm master like Dr. K. Wang, but I think I was able to figure this one out.  If anyone has a better idea, let me know.  He will be able to get me the electrophysiology results in a few weeks, but I couldn't wait to post it now.

Case

A young woman in otherwise excellent health presented with one year history of intermittent palpitations.  She was alert but not well perfused: she had cool skin but she had no chest pain and was not diaphoretic.  Her BP was 110/90.

Here was her 12-lead:
There is a narrow complex, regular tachycardia that is very fast, at 259 BPM.   Computerized QRS duration in 94 ms. 


No matter what is causing this, the rate is extremely fast and suggests remarkably fast AV nodal conduction.  Children and infants can normally conduct this fast through the AV node, but not adults.

ECG Differential Diagnosis includes: 
Paroxysmal SVT 
        --AV nodal re-entrant tachycardia vs. 
        --Orthodromic re-entrant tachycardia through a bypass tract (accessory pathway)
        --If there are P-waves: Very fast Atrial Tachycardia with Very Fast AV conduction
Slow atrial flutter (rate 259) with 1:1 conduction through a fast conducting AV node

Every possibility includes very fast AV node conduction.


Pads were placed and the patient was given 6 mg of adenosine.  Here is the subsequent 12-lead ECG:
Now there is a wide complex rhythm with a rate of 257 (essentially the same rate).  Computerized QRS duration is 112 ms.  Lead V4 gives the suggestion that there is no wide complex, but rather a narrow complex that mimics a wide complex  because of ST depression (the link takes you to such a case).
But all other leads confirm that this is wide complex.

There were no atrial flutter waves uncovered during the pause induced by adenosine, so this is not atrial flutter.

Turns out the patient had asthma, and adenosine can trigger asthma. [An increase in intracellular cAMP in bronchial smoothe muscle cells relaxes them and improves asthma.  Adenosine decreases intracellular cyclic AMP; Xanthines such as theophylline increase intracellular cAMP]

She became distressed and SOB, and had a vigorous spasm of coughing, then converted!!

Here is her post conversion ECG:
Sinus tachycardia at a rate of about 130, with a very short PR interval.  Computerized QRS duration is 80 ms.

Her respiratory distress subsided and she did well.

Analysis

We knew there would be a short PR interval because, by the extremely fast rate of the narrow complex, we knew that the AV node must conduct fast.

What is the diagnosis here?  Here is what I wrote to Scott:

--So, there are two abnormalities here:
       1) Accelerated AV conduction
       2) An accessory pathway (WPW), in which the conduction down the AV node occurs before it can get to the accessory pathway (thus, no delta wave on baseline ECG).

--I believe that the first rhythm was a re-entrant rhythm that went down through that fast AV Node, then up through an accessory pathway (which is equally fast, as they often are).

--After adenosine, the re-entry reversed: it went down through the accessory pathway (Atrioventricular reciprocating tachycardia, or AVRT), with a wide QRS because the accessory pathway activates the ventricle first, and then up through the very fast AV node.  See Case 2 of this post for more on AVRT.

--Thus, both rhythms have identical rates, but are going in opposite directions.

--The problem with this explanation is that the beginning of the QRS in both tachycardias is fast.  If it were through an accessory pathway, then the beginning of the antidromic rhythm should be wider, and it does not appear to be so.

--The baseline ECG does NOT have any delta wave: the impulse travels down through the AV node too fast for it to make it down the accessory pathway.  This is often called "concealed conduction."  See this post for an explanation of Concealed Conduction.--the explanation starts halfway down the page.

--Since the wide complex rhythm has an LBBB configuration, the accessory pathway must be on the right side.

--Alternative explanations:
Dual AV nodal pathways (but why is one tachycardia wide?)
AV nodal pathway with "slow-fast" component (I don't see how this explains that the latter part of the QRS in the wide complex is slow)

The EP results are back, and:

1. Accelerated AV conduction
2. Left lateral accessary pathway


18 comments:

  1. This is avnrt with slow fast component and should be treated with calcium channel blocker.

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    1. you might be rght. I'm certainly getting a variety of opinions on this.

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    2. very interesting dr. Smith! Can'T wait to see the results!!

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  2. Abberrancy. AVNRT->adenosine->patient fells bad with more simpatetic activity ->little faster AVNRT with aberrancy

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  3. are you sure there is no delta wave in the third ECG (I see one in DII, V3-4-5). The different morphology of the qrs in the 2nd ECG looks like a "superwolf", no?

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    1. Olivier,
      It's not a delta wave. If it were, it would be registered as a wide QRS. The QRS is only 80 ms.
      If there were a delta wave, the remainder of the QRS would have to be impossibly short, around 50-60 ms.
      Steve

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  4. No delta waves? There is something subtle delta-like in V5 and V6, maybe also in V4. It could be seen better at 50 or 100 mm/s.

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    1. It's not a delta wave. If it were, it would be registered as a wide QRS. The QRS is only 80 ms.

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  5. Did the adenosine terminate the initial tach followed by reinitiation or did the axis change mid tach

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    1. The adenosine terminated it and then it restarted.

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  6. The first narrow complex tachy looks like AVRT with retro p and St depressions. The wide complex tachy looks like anti dromic tachy but with fast initial component which can be explained if the pathway was atrio fascicular with distal insertion in rbb. However usually such pathways would have decremental properties which is not seen here.

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    1. Gautam,
      That is the best explanation I have seen yet!
      Are you an electrophysiologist?
      Steve Smith

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    2. Thank you Dr Smith. I am a general and interventional cardiologist. I have been following your blog with keen interest for the past few months and found it extremely informative.
      Gautam

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    3. Thank you Gautam. Keep the great comments coming!
      Steve

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  7. VERY interesting case - and I do not know "the Answer" - but I'll make a couple of comments:

    After reading the case and before reading comments I wanted to give Adenosine - so I'm glad that treatment worked, even though we don't yet know for sure why it did ...

    The PR interval in the post-conversion tracing isn't necessarily that short. So I'm wondering how old this "young woman" is (PR intervals tending toward shorter in younger adults). In addition - the post conversion tracing shows sinus rhythm at a rate ~120/minute and PR intervals tend to shorten with tachycardia. There is a lot of artifact - but I measure the PR ~ 0.11-0.12 second (most of it P wave) - which isn't necessarily so "short" if this is a young adult with a rate ~ 120/minute ....

    I think you still may have a differential between AVNRT vs AVRT (no delta; PR not necessarily short) - though I definitely would not be surprised if this patient had an AP (Accessory Pathway). AVNRT on occasion may attain 260/minute.

    To my calipers - the rate = 260/minute and is identical for ECG #1 and #2 - which would seem to be too much to be chance .... I'd imagine/expect some short transient break in the rhythm if conduction shifted from orthodromic to antidromic down an AP (but I totally defer to Dr. Wang and others as to whether such immediate shift in direction can occur).

    As much as the fast rate makes me think about flutter - as you say, you'd then have to explain conversion post-adenosine which is highly unlikely. So my bet is on reentry. I imagine there could be functional/rate-related lbbb aberration vs Steve's theory of changing directions .... I do think the QRS is wide in ECG #2 (despite V4's appearance - the limb leads look quite different - and leads I,aVL and V6 to me look legitimately wide).

    But after going back-and-forth-and-back again with the above theories in my mind - I just don't know and eagerly await EP results by Dr. Wang.

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  8. There are case reports of atrial flutter termination with adenosine (not suggesting this occurred), or possibly the flutter waves during the AVN blockade were subtle enough to go unnoticed. Strips from the conversion could rule this out as a possibility. V4 in ECG #2 sure looks "fluttery"...

    That being said...I think the first ECG strongly suggests orthodromic AVRT and the second ECG (given the first) strongly suggests antidromic AVRT. I'm with Ken that aberrancy can be considered as well given the marked change in both frontal axis and Z-axis (perhaps this leans more to AVRT?).

    Looking forward to the EP study results!

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  9. Hi Dr.Smith,
    and really great case, once again.

    I think it would have been very interesting to look at the ECG while (or just after) giving Adenosine, because I think it could also prove your theory: assuming there were a concealed conduction with a fast AV-Node, thus not developing Delta-Waves on the baseline ECG (3rd one), if we block completely the AV-Node with Adenosine than we should expect some P-Waves followed by a very large QRS (though the accessory pathway). This phenomenon is practically what we fear when giving Adenosine bei Aflutter+WPW (thus contraindicated).

    Isn´t it?

    Looking forward for the definitive diagnosis.

    Greets from Germany

    Aldo

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    1. Aldo,
      Thanks! I wasn't there and so don't have that data. That might have shown it, but that does presuppose that the sinus node would have recovered from the adenosine faster than the AV node, which is not a given.
      Steve Smith

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