Saturday, October 1, 2011

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

Before we start, here is another popular post on wide complex tachycardia.
What is the ECG rhythm diagnosis?
Wide complex regular tachycardia at a rate of 209, so it is not atrial fibrillation. 

First, in regular wide complex tachycardia: when in doubt, just use electricity, even in stable patients!  Electricity is safer than medications and will work no matter the diagnosis.   A small dose of propofol is adequate for the patient to be amnestic to the cardioversion.

But even if you can manage it, it may be useful to determine the diagnosis:

Which is it?
1) VT 
2) SVT with aberrancy (usually AV nodal reentry tachycardia with aberrancy)
3) AV reciprocating tachycardia [antidromic, up through AV node and down through bypass tract, (AVRT)]4) What can you do if you don't know? (Does it matter?)

4) I should briefly mention idiopathic VT, which occurs in structurally normal (or nearly normal) hearts, and is therefore not as dangerous as standard VT; this includes adenosine-sensitive VT (RV outflow tract, with LBBB morphology, monomorphic R-wave in inferior leads) and verapamil-sensitive VT (posterior fascicle, RBBB morphology).  I will discuss this in a future post.

Here is the clinical data
26 yo male with chest pain and SOB and no history of structural heart disease.  He was not hypotensive or in shock.

A young person with no cardiac history is likely to have SVT, not VT, but let's consider the ECG alone:

When assessing for the rhythm in wide complex regular tachycardia, these are the assessments I make, though no method is foolproof:

1) Look for hidden p-waves before each QRS.  Don't miss sinus rhythm! Not here.
2) If there is a transition from narrow to wide, is the rate the same?  Then it must be SVT.  Not here.
3) QRS duration: VT usually (but not always) has a QRS duration of at least 140 ms.  A prominent exception is fascicular VT.  The longer the QRS, the more likely it is to be VT.  Here it is 155 ms, so it is plenty long for VT.
4) Is there RBBB or LBBB morphology and is the initial part of that BBB narrow?  Then it is very likely to be SVT.  This one has LBBB morphology with a narrow initial R-wave.
5) Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT.   None here.
6) Do a quick look for concordance (all QRS's in the same direction in precordial leads, not the same as concordance when evaluating ST segments in LBBB).  Concordance means there is no RS.  No concordance here: this is easy to see comparing V4 to V6.
7) Finally, because it is easy to apply, I like a new rule better than Brugada's or Vereckei #1 or Vereckei #2 (aVR).  It is Sasaki's rule (Sasaki K.  Circulation 2009; 120:S671), and it had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia.  It has not been validated; this is important: remember that Brugada's rule was much better in the initial study than in subsequent validation studies.
Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR.  This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.
--If yes, then rhythm is VT. If no, step 2.  Not here.
Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?  See image below.  
--If yes, then rhythm is VT. If no, step 3.  Not here.
Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)
--If yes, then it is VT.   If no, then it is SVT.  "No" here, therefore it is SVT

Treat without a diagnosing
If you don't know what to do, you can always use electricity, but you can also give adenosine.  As long as the rhythm is regular, not irregularly irregular (atrial fibrillation), adenosine is safe.   It will usually (safely) convert SVT with aberrancy and AVRT (antidromic reciprocating tachycardia) without harming a patient in VT, and may convert a patient with fascicular VT.

Obviously, synchronized cardioversion should be undertaken if the patient is unstable.

If it is irregular with a wide QRS, it could be WPW, in which case an AV nodal blocker could be life threatening (see this post).

Diagnosis: SVT with aberrancy; it resolved with adenosine.

Added Oct 22, 2011: many readers thought this was RV outflow tract VT.  The reason that RVOT VT is very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive.  In this case, there is an initial Q-wave in inferior leads.

Here is the post-conversion ECG:
There is slight slurring at the beginning of each QRS, suggestive of delta waves, and the QRS is thus 109 ms (borderline wide).  The PR interval is 138 ms, so WPW is very unlikely.  There is also some ST depression which appears to be secondary to this slightly abnormal QRS, and lends some further credibility to some sort of pre-excitation.

There is no further follow-up at this point.


  1. Given his age and somewhat inferior axis was RVOT considered? It doesn't look typical for RVOT, besides the LBBB and positive complexes in the inferior leads. If it isn't likely, is it because we are looking for broad monomorphic R's in the inferiors with RVOT?

  2. What about adenosine-sensitive VT? Doesn't that muddy the diagnostic waters for you?

    Also, I was taught to consider WPW (not necessarily with antidromic conduction) in any arrhythmia with a rate over 200 in an adult. A fair statement?

  3. Graham,
    1) That is true. There are some unusual causes of VT such as adenosine-sensitive right ventricular outflow tract VT (with an LBBB morphology), and verapamil sensitive fascicular VT from the left posterior fascicle. As VT goes, however, these are relatively unimportant because the heart is structurally normal or nearly normal and so they are not nearly as dangerous, and so for practical purposes are not so different from SVT with aberrancy. This is especially true for adenosine sensitive VT, of course, because it terminates with adenosine! I will post more on this in the future.

    2) I think you mean that you were taught to think of WPW and Atrial fib when the rate is so fast, and this is true: you should certainly think of it. However, atrial fib with WPW is not only fast and wide, but irregular and bizarre. If it is clearly regular, and the QRS morphology is the same for every beat, it is not atrial fib with WPW. If you have any doubt as to whether the rhythm is irregular, it may be atrial fib with WPW. However, when it is dangerous WPW, the shortest R-R interval is usually < 250 ms, and < 270 should be safe. Here all R-R intervals are around 287 ms (60 divided by rate of 209, since it is regular).

    Steve Smith

  4. RVOT, adenosine sensitive VT should have a completely inferior axis, to my knowledge. Here there is an initial negative deflection in inferior leads, with impulse going superior, then inferior. So, yes, there should be broad monomorphic R-waves in RVOT. Any more thoughts on this?

  5. Dr Smith,

    It sounds like you are saying that WPW can't exist in a tachyarrhythmia unless it is atrial fibrillation. I agree with you regarding the fast, broad, and irregular appearance of a-fib with WPW. However, I like Graham, have read to consider WPW, with any tachycardia greater than 200; irregular or not. For instance, a 1:1 a-flutter. I was under the impression that this is why AHA initially took a stance to treat all wide complex tachycardias as VT, because they felt Amiodarone was safe with WPW. I know they have since added Adenosine as an option when treating WCT, but isn't the fear of WPW still a realistic concern?

  6. Adam,

    First, I hope I didn't imply that it can't be WPW. I'm saying it is not WPW with atrial fib, which is the ONLY time that AV nodal blockers are contraindicated.

    As for flutter, it almost never has a rate < 230 in the absence of anti-dysrhythmic drugs such as procainamide.

    As for amiodarone, I don't think it is proven safe in WPW with atrial fib and could do harm because of its beta blocking effects. Theoretically, anyway.

    The only way you're going to run into trouble giving adenosine (if it is not atrial fib) is if the patient converts to atrial fib during treatment with adenosine (which can happen on occasion) AND has accelerated conduction resulting in v fib during the few seconds that the adenosine is still active. Sounds pretty unlikely, and it does not worry me. Apparently it does not worry the ACC/AHA either. Right?

    Steve Smith

    1. Dr. Smith,

      Can you explain why AV nodal agents would be okay in atrial flutter with WPW? or correct me if that is inaccurate

    2. Dr. Smith,
      I may be mistaken, but it seems you are saying that it would be safe to give AV nodal agents to a patient with WPW in Atrial Flutter. Is that correct? If so, could you please explain why this would not cause AP conduction at 300/min to ventricle?

    3. I would not use them. However, in atrial flutter with 1:1 block, you cannot make things worse. The conduction through the bypass tract cannot be faster than the flutter atrial rate. If it is 2:1 conduction, you can make things worse. Any time you have 1:1 conduction, you will have a ventricular rate matching the atrial rate, which will not be less than 230. It will never be 209, such as in this case. Therefore, unless the rate is extreme, you don't have to worry about atrial flutter with 1:1 conduction and therefore adenosine will be safe.

  7. Adding to above, of course any PSVT, even narrow complex, can be WPW. In fact, 30% of unknown PSVT is WPW. So this case could indeed have been a paroxysmal reentrant WPW. But it is ok to give adenosine in these cases.

  8. Even though AHA still endorses amiodarone for Afib with WPW I disagree. It has beta and calcium channel blocking activities and so would be contraindicated in Afib with WPW

  9. Dr. Smith,

    Thanks for the reply. I completely agree with you regarding the potential for negative effects following Amiodarone administration to a patient with WPW, however AHA is not on board with this; unless something has changed I believe they advocate Amiodarone administration for a-fib w/WPW. I understand procainamide would be a much better choice if cardioversion is contraindicated.

    I was not aware that AV nodal slowing agents are safe with WPW outside of a-fib. Is there no fear of stimulating an antidromic or ventricular re-entry?

    Sorry if this is off topic, but you have peeked my interest.

  10. Thanks for this post. I hope you post more like this.

    Why would you diagnose SVT while you just said that QRS of 155 ms is >140 ms favoring VT?

    In step 2 of Sasaki, I see 4 small squares which is 160ms on V6.

    BTW, I have given type 1c flecainide IV (not FDA approved) for Af with WPW, and it worked beautifully.

  11. Adam,

    Indeed AV nodal blocking agents are just fine in WPW as long as there is no atrial fib. You should read this post:


  12. Iatrophobic,

    Almost all VT is > 140 ms, but I didn't say that all SVT with aberrancy is < 140 ms. It is not. So 140 ms has a high sensitivity for VT, but not a high specificity.

    Aha. This is difficult. V6 has no S-wave; it is a monomorphic R-wave. The negative part is the ST segment and T-wave! I should have explained this better; maybe will go back and do so.

    Yes, Flecainide, propafenone, and ibutilide have the highest acute conversion rates for atrial fib. I would like to hear more: how much flecainide did you give, how fast did it convert?

  13. Adenosine is perfectly safe in these instances. The initial forces of the QRS are very sharp, so either this is aberrancy – most likely – in the setting of AVNRT/AT/CMT (concealed BT) or else the BT inserts into the conduction system (e.g. atriofascicular BT). There are no signs of the latter on the resting ECG (rS in III, absence of septal q waves in aVL/I).

    I would bet for AVRT with a concealed BT; differential AVRNT.

  14. i really appreciate the way you approach wide-complex tachycardia. too often people are stuck in the "either a or b" mindset and they feel that they MUST pick one, not realizing that there could be c or d or e or f or g and even h and i at the same time.

  15. THank you.
    Flecainide 1.5mg/kg over 15 minutes, we're about to give another dose over an hour when it converted to sinus.

    In a narrow complex tachycardia, how would you differentiate AVNRT vs orthodromic AVRT based on ECG? Or does it matter on ED therapeutic standpoint?

  16. I will soon put up a post showing how one must be flexible in the approach to wide complex tachycardia!

  17. Iatrophobic,
    You can't tell the difference between AVNRT and orthodromic AVRT, and you're right, it does not make a difference. All you need to do is block the AV node for a few seconds (adenosine) and the reentrant loop will be interrupted, allowing sinus rhythm to re-establish.

  18. one question.. if there's retrograde atrial activity visible..wouldn't there be a difference in the RP interval for AVNRT typical and atypical and orthodromic AVRT?

    I remember reading in an old books omewhere that, if RP is less than 70ms its some form of AVNRT. And whether its typical or atypical can be differentiated further depending if the RPi is longer or shorter than the PRi. This was an old sweedish EKG book, may have been discredited. An orthodromic AVNRT should have RP over 120ms.. right?

  19. In general, if the RP is longer than 70 ms, it is probably AVNRT vs. AVRT. Or, if the RP is longer than the PR, it is AVNRT vs. AVRT. This is because the AV nodal conduction is shorter in AVRT (fast bypass tract) than without a bypass tract. In some cases, the bypass tract is slowly conducting and then this rule doesn't work.

    See here:

  20. thank you for your answer DR Smith! from the text i found, if no visible p-waves, most likely AVNRT. if retrograde p-waves distorts terminal qrs also AVNRT. i understand this. What i dont get is why the AV nodal conduction is faster in AVRT than in AVNRT? the orthodromic AVRT takes the same atrial to ventricular pathway right? is it because AVNRTs have A-V conduction down the slow limb of the AV-node and V-A re-entry up the fast limb and that orthodromic AVRT in thesetting of WPW usually conducts down the fast limb? or could i be getting confused just from not specifying that i meant AVRT in the setting of WPW.. by fast bypass tract you mean mahaim fibers or fast pathway in AV node..

  21. You have me stumped. I think you better ask an electrophysiologist!


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