Monday, February 16, 2015

Wide Complex Tachycardia in a 20 something.

This was sent by a former resident.  He will remain anonymous because his identity could compromise patient confidentiality.

Case

A 20-something female presented with palpitations and lightheadedness.  She had no previous medical history except for some "in utero tachycardia" which was treated until a very early age.  She has had no problems since and takes no medications.  She has no specific conduction abnormality diagnosis.

Her mother states she is not thinking clearly ("acting as if she is intoxicated").  The patient reports exertional syncope and was syncopal on the way to the triage desk.

Exam: Very large, at 5' 10" (178 cm) tall and 346 lbs. (156 kg).
Pulse: 235
BP: 121/67
SpO2: 98% on room air

Otherwise unremarkable.

EKG:
There is a regular wide complex tachycardia at a rate of 231. 
There is no recognizable morphology, such as RBBB or LBBB.
The complexes are very wide
The initial portion of the QRS represents prolonged depolarization, arguing strongly against SVT.
So it must be VT or antidromic AV reciprocating tachycardia (AVRT)
There are small waves in lead II across the bottom.  Are these retrograde P-waves?










The rhythm strips, which unfortunately were not recorded, reportedly showed irregularity, with a rate varying from 180-250.

Because of this irregularity, the treating physician was worried about Atrial fibrillation and WPW, and therefore was reluctant to give adenosine.

See here for a discussion of Atrial fib and WPW, and the danger of adenosine and of other AV nodal blockers, and of the safety of these medications if it is NOT atrial fibrillation.

What would cause this rhythm but have some irregularity on the rhythm strip?  Could this be atrial fibrillation?  Is adenosine really contraindicated?

It is very important that you recognized that the ECG shown CANNOT be Atrial fibrillation with WPW.  
1) it is perfectly regular (I even used calipers)
2) When you have atrial fibrillation with WPW, there are multiform QRS complexes.



Clinical Course:

Procainamide was administered.  There was no response.

Labs were normal.  K was 3.5 mEq/L.

Electrical Cardioversion was the next step.  As the BP was stable after some fluids, low dose propofol  (60 mg) was used for sedation.

Synchronization was turned on; here it is:
Are the sync arrows pointing to a T-wave?  Or QRS?  If the point to the T-wave, synchronized cardioversion could result in ventricular fibrillation.
See this post demonstrating dangerous and erroneous identification of the QRS.

Cardioversion was done at 200J biphasic.

Here is the result:
The cardioversion occurs almost halfway through the strip. There is conversion to Polymorphic VT or Ventricular Fibrillation.

There was a pulse, so it must be Polymorphic VT.  The BP was 70 systolic.  She was given 2 g of Mg, and defibrillated at 200 J biphasic.  Here is the result:
Polymorphic VT has deteriorated into Ventricular Fibrillation

After a couple defibrillations, there was conversion back to a wide complex tachycardia:


Color and BP were improving and she was awakening.

Consultant recommends amiodarone and repeat cardioversion.

This was done without success.

She reverted to V Fib again:



Chest compressions were started.  She was given an Esmolol bolus and infusion and then defibrillated again, all during chest compressions:

She is defibrillated into an organized wide complex rhythm, which then becomes a narrow complex tachycardia with occasional wide complexes.

Continued monitor strips:
Finally stabilizes in sinus rhythm

12-lead:
Sinus rhythm.  There is no good indication of underlying pathology.

She remained on the esmolol drip and had no more dysrhythmias.  Cardiac MRI was normal.  Echo was normal.  EP study was done.  See below.




What happened?

Was there an irregular rhythm?  We must take the word of the physician.

Was it atrial fibrillation?  On the initial ECG, it certainly is not atrial fibrillation.   Therefore, if the irregular rhythm was atrial fib, then the patient was flipping back and forth between a rapid atrial fib and a regular wide complex tachycardia.  This is very improbable.  

What else could it be?

It could be what it was proven to be on EP testing: Dual AV nodal pathways and WPW (there is no delta wave, and thus there is 'concealed conduction'.  Read this to understand concealed conduction.

In this scenario, the dysrhythmia is antidromic AV reciprocating tachycardia (AVRT) that goes down the accessory pathway and up either one of two AV node pathways.  The resulting rate depends on which pathway is used.

Here are some schematics that were nicely drawn by the physician:

Dual AV nodal pathways:
Fast pathway: conducts quickly, longer refractory period
Slow pathway: shorter refractory period


Add an Accessory pathway to the mix:


Ablation of the Bypass tract (Accessory Pathway) was completed.


How would I have managed this?

I would have attempted adenosine.  It is not atrial fib with WPW.  If it is VT, adenosine will be safe.   It might work.  If adenosine does not work, then cardiovert.

I believe adenosine would have worked here.

I have talked with Ken Grauer about his comments below.

We are now agreed that this was indeed a wide complex tachycardia due to antidromic WPW.


 

===================================

MY Comment by KEN GRAUER, MD (5/30/2018):

===================================

Fascinating case — that was first published back in February, 2015 — and which Dr. Smith is reposting today because of its “timeless nature”. I find it always interesting to review tracings previously interpreted — since sometimes what we said earlier might not be what we think now. There are 2 reasons for this: i) Intra-observer variability (in which the same interpreter when given the same tracing at a later time says something different …). The literature suggests this occurs ~10-20% of the time in expert interpreters; and, ii) We may have learned something since the time that we first interpreted the tracing! So it is humbling for me to see how my interpretation today ( = May 30, 2018) differs from what I said in my 2 February, 2015 comments ...
  • In 2018 — I see a regular tachycardia at ~240/minute that on first glance looks to be wide — but which I suspect is actually not wide. Leads V4,V5,V6 in particular suggest a narrow QRS complex. The vertical RED line I’ve drawn in Figure-1 shows where I think the limits of the QRS complex lie in the long lead II rhythm strip about the bottom. Looking at this precise point in the long lead II in leads I, II, III; and aVR; aVL, aVF — the vertical GREEN line suggests where I think the limits of the QRS complex may lie. Could this really be a narrow QRS with marked ST-T wave abnormality secondary to the marked tachycardia? What do YOU think? There may be some aberration — but perhaps the QRS is not nearly as wide as it first appears to be ...
Figure-1: Combining the initial tachycardia tracing with the post-conversion 12-lead ECG (See text for discussion).
  • Even if the QRS complex was wide — my interpretation in an otherwise presumably healthy 20-year old woman who presents hemodynamically stable in a regular wide tachycardia at this fast a rate (~240/minute) — would be that this may well be AVRT conducting anterograde (ie, first down an AP). In either case (ie, whether the QRS was narrow or wide) — I completely agree with Dr. Smith that Adenosine would seem the clear drug of choice! (ie, low chance of significant lasting adverse effect — and excellent likelihood of converting AVRT with either anterograde or orthodromic conduction).
  • The final clinical point I’d make relates to how to rapidly and accurately estimate the rate when the rhythm is regular and fast. I use either the “every-other-beat” or “every-third-beat” Method. I used the “every-third-beat” Method in this case. Find a part of a QRS complex that begins or ends on a heavy line. Count the number of large boxes that it takes to record 3 beats. This allows you to calculate 1/3 of the rate. In this case — it takes just under 4 large boxes (BLACK numbers) to record 3 beats (RED letters). Therefore 1/3 the rate ~80/minute X = ~240/minute for the heart rate in this case. This is VERY helpful, because while AVNRT may record at this rapid a rate — one begins to think more of AVRT at a rate this fast ...
  • Note that I’ve attached the post-conversion 12-lead ECG to the bottom of Figure-1. Doesn’t the narrow QRS in the post conversion tracing resemble  what I suggested above might reflect a narrow QRS during the tachycardia (vertical RED and GREEN lines)?
  • We are told that EP testing revealed, “Dual AV nodal pathways and an Accessory Pathway, but no Delta wave” — therefore AVRT in which conduction is orthodromic (ie, first going down the normal AV nodal pathway [which is why the QRS may be narrow] — and then coming back up the AP). Given that delta waves are not seen in either the tachycardia or post-conversion tracing — isn’t my theory plausible (if not probable) that the QRS in the initial tracing (TOP in Figure-1) is actually narrow because this is orthodromic AVRT with marked ST-T wave changes?
  •  
 

 

23 comments:

  1. The differential diagnosis of the wide complex tachycardia is VT or a *preexcited tachycardia*. Antidromic AVRT is only one mechanism of preexcited tachycardia. Others include ventricular activation via a bystander accessory pathway of atrial tachycardia, atrial flutter, or AVNRT. Rarely, pathway-to-pathway circus movement tachycardia can cause a preexcited tachycardia.

    Adenosine would terminate antidromic AVRT and AVNRT using a bystander bypass tract for AV conduction because the AVN is involved in the mechanism of both of these arrhythmias. Adenosine would not be expected to terminate VT, or AT/AFL using a bystander bypass tract, nor would it be expected to terminate pathway-to-pathway circus movement tachycardia. In any of these situations, adenosine could cause atrial fibrillation, which could represent a medical emergency if the bypass tract has a short enough refractory period to permit a very rapid preexcited ventricular response to AF.

    A concealed bypass tract only conducts retrogradely (from ventricle to atrium). Accordingly, these bypass tracts can participate in *orthodromic* AVRT.

    You are describing a *latent* bypass tract - one that is not apparent in sinus rhythm because conduction over the normal AV conduction system preempts ventricular activation over the bypass tract.

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  2. Superb case with step-by-step analysis! My understanding is that Adenosine may shorten atrial tissue refractory period - so that this might predispose conversion of a reentry SVT to AFib, which is of course problematic when there is WPW. So IF you KNOW you have very rapid AFib + WPW (which you should know if you have an irregularly irregular very rapid rhythm, in parts over 220-250/minute with QRS widening) - then don't use Adenosine (which has no chance to convert AFib - and which may cause further deterioration to VFib). While there is a theoretical chance that Adenosine might predispose a patient with antidromic AVRT to develop AFib - it may (as per Dr. Smith) alter conduction properties in part of the reentry circuit and thereby convert the rhythm. Onset & offset of action of Adenosine is ultra-fast - so it should in most instances be safe and worth a try. As occurred in this case - if the drug you select causes deterioration of the rhythm - you are right on the scene and should be able to successfully cardiovert. Glad the ending was positive in this case. I presume the patient subsequently underwent ablation therapy? THANKS for presenting!

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  3. Could the conversion to polymorphic VT have been due to the electric shock coinciding with the T wave? and what should we do in case we are not sure if the sync arrows are pointing to the QRS complex or not? thank you

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    1. Yes! That is what happened. Good question. I do not know how to avoid it in this situation. In the case from a week ago that I link to, one can see that it is not detecting the QRS correctly and one can change the lead that it monitors. But in this case, it is not obvious where the T or QRS are and whether the machine is correctly detecting them.

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    2. My impression has always been that if YOU are unable to clearly distinguish between QRS & ST-T wave - that the machine (defibrillator) may also not be able to do so ... in which case synchronized cardioversion runs the real risk of delivering the energy at the wrong point in time (ie, during the "vulnerable period") - which might predispose to precipitating VFib (or the PMVT that occurred here). Choices are: i) "Chance it" (ie, hope that the machine is selecting the correct time interval to deliver the shock) and Synch anyway; and/or ii) Turn off Sych and deliver an unsynchronized shock ( = defibrillation) that will probably work. And if you select Option i) and you get the wrong result - then do as was done here = immediate unsynchronized shock, and you'll probably convert the rhythm (given that you are right on the scene, so immediate defibrillation should convert the rhythm).

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    3. But first one should change the monitor leads and see if the QRS and T are more obviously differentiated. Right?

      thanks, Ken,

      Steve

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    4. I of course agree Steve - though in your original 12-lead - I think it difficult to be certain as to what is QRS vs ST-T wave in many of the leads - so there may be times when it may not be easy to find another monitoring lead that clearly distinguishes between the two ...

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  4. Quick question as to timing. After cardioversion the rhythm went to polymorphic VT. Mag was given and PT was defibrillated. In this case the PT required multiple defib attempts. Should these be done in back to back succession of each other? I imagine this would correct the issue, instead of defib, 2 minutes CPR, defib?

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    Replies
    1. I don't have all the details, but you have a reasonable idea there.

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  5. Great case, thanks for posting that. I am a practicing cardiologist for 15 years and always learn something here! I wonder what Esmolol did in this equation? I don’t think it has influence on an accessory pathway ?

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    1. THANKS for your question! I thought this case fascinating, because despite what appeared to be marked QRS widening — the QRS complex was almost certainly narrow during the SVT rhythm (See My Comment at the bottom of the page). As to the effect of Esmolol (beta-blockers) — my understanding is that it is not complete certain how this class of drugs with affect the relative interaction between normal AV nodal pathway and AP (accessory pathway). Clearly, if the patient was in WPW with very rapid AFib — then beta-blockers (as well as Verapamil, Diltiazem) would be contraindicated. My impression is that there is relatively LESS potential of Esmolol to accelerate anterograde conduction down the AP than there is for Verapamil/Diltiazem — but that some potential for this nonetheless exists … Reference to the 2015 ACC/AHA/HRS SVT Guideline by Page et al (SEE page e175 — https://www.heartrhythmjournal.com/article/S1547-5271(15)01189-3/pdf ) — says IV beta-blockers “might be considered for acute treatment in patients with orthodromic AVRT who have pre-excitation on their resting ECG and have NOT responded to other therapies” So while this patient does NOT have WPW on his resting tracing — she DOES have an EP-proved AP, and therefore it WOULD seem to me reasonable to try the IV beta-blocker in the hope that Esmolol might be effective for this orthodromic AVRT rhythm. In addition, given several instances of VFib during the management phase — the IV beta-blocker might exert a beneficial protective effect in this regard (ie, despite the patient’s young age — Polymorphic VT might well be ischemic, given failure to respond to Mg++, and given those huge ST-T wave deviations during the SVT). Bottom Line — I am NOT certain of the answer to your question — but the above is my best guess based on my experience and what I glean from the literature. THANKS again for your question — :)

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    2. Thanks for your responds. Regarding the polymorphic VT, I was thinking the same thing, the most likely aetiology was actual demand ischemia

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  6. Thanks, great case! But why was given 200 j, rather than 360 j at cardioversion?

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    1. @ Anonymous — To my reading of the literature — the energies suggested for cardioversion or defibrillation are dependent greatly on preferences and experiences of the user. There are some generalities (ie, lower energies usually all that is needed to successfully cardiovert AFlutter; higher energies often needed to cardiovert AFib). As “ugly” as the rhythm in this tracing looked — if the thought was that this was monophasic VT, then VT often DOES successfully cardiovert at less than maximal energy — so 200 joules initially was perfectly appropriate. And if the thought was that this was AVRT (and therefore an SVT) — then less-than-maximal energy is also appropriate. And, you can always go up within seconds if the first 200j attempt was not successful. In this case, 200j was all it took to precipitate polymorphic VT/VFib. Maximal energy would of course have done the same — :)

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    2. This is biphasic cardioversion. 200J is maximum in biphasic.

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    3. Thank you for correcting Steve! I missed in my reading of the case that a biphasic defibrillator was used (as is now standard practice). As you say, 200J is maximum in biphasic! — :)

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  7. Great case. There is however one detail that botthers me: It is not possible for any accessory pathway tachycardia to have a negative QRS in V6.

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    1. @ Hiago — What you are referring to is that IF the QRS complex during a wide tachycardia is ALL NEGATIVE in leads V4, V5 and V6 — that the cause of this won’t be anterogrde conduction down an AP (Accessory Pathway) — because ALL neg QRS in V4-6 would imply an apical location — and APs are not found at the apex. But that is NOT what we have here. Instead we have orthodromic AVRT (ie, no delta wave). We also don’t have an all neg QRS in V6 (and we definitely don’t have a neg QRS in V4 and V5) — so I see nothing on this tracing that rules out the possibility of an AP. Hope that helps. THANKS again for your comment — :)

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  8. Great case. I agree with Hiago that the initial QS in V6 is bothering me. Even in orthodromic AVRT you should not get the initial Q in V6. If you postulate a orthodromic AVRT with RBBB, then have to account LAFB as well because of superior axis change. In that case, the initial V6 has to be positive deflection. Also the much positive AVR tell us not likely orthodromic in nature.
    There are several differentials to this kind of morphology tachycardia
    Idiopathic: Posterior fascicular VT, papillary muscle VT
    Structural: Epicardial VT (usually would have scar on CMR)
    Very rarely: Antidromic AVRT with decremental accessory pathway that inserts near the LV apex.

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    1. @ andykkw — THANKS so much for your comments! This was not my case. All I can say is that this is what was found on EP testing: "Dual AV nodal pathways and WPW."

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  9. Understood. You guys are doing excellent job. It’s a very good practice to decipher analyze the ECGs, and share with others. I always tell my electrophysiology fellow that 12-lead ecg is a EP study itself with 12 EGM information. Putting EP catheters add in additional 4 “leads”. Interpreting ECGs should not be a lost skill.

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