Saturday, December 27, 2014

Very Fast Very Wide Complex Tachycardia

A male in his 60's called 911 for dizziness and chest pain, onset with exertion.  He was pale and diaphoretic (in shock) with a thready radial pulse.

Here is his initial rhythm strip (it is not a full 10 seconds):
Wide complex tachycardia, rate 235
This is a very wide complex regular tachycardia at a rate of 235.  It should be considered to be Ventricular Tachycardia and treated as such.

Here is the 12-lead:

By any analysis, it is most likely VT: There is slow depolarization of the initial deflections of the QRS.  However, this is a very fast VT.

The patient should be safely sedated and electrically cardioverted.

The paramedic instead gave adenosine, which is not contraindicated, and will not harm a patient in VT.  It is now part of the ACLS protocol.

If it is VT, as suspected, it will not work (RV outflow, adenosine sensitive VT is likely to respond, but this is NOT such a benign VT as it is too wide and does not have the right morphology).

If it is SVT with aberrancy, it is likely to work.

If it is AV reciprocating (antidromic WPW), adenosine is likely to work.

If it is slow Atrial flutter with 1:1 conduction, it should slow the conduction and reveal the flutter waves.  This is the exact rate one expects with slow atrial flutter and it is why slow atrial flutter can be so dangerous: it conducts 1:1, with fast ventricular rates.

Here are the monitor leads during and after adenosine:

During adenosine:
Lead II is monitored.  The rate starts at 222 with a wide complex.  It is uncertain to me why the initial rate is slower than the rate above; it is clear though that it is the same rhythm because lead II has the same morphology.  In the middle of the second strip, there is a minimal pause, after which the complexes are narrow, and after which there are visible flutter waves at a rate of 228.  There is mostly 2:1 conduction, but some 1:1  

After adenosine:

The strip continues: now the flutter waves are easily seen at a rate of 240 (almost exactly the same rate it started with) with 2:1 conduction and a relatively narrow complex QRS (less than 120 ms).

2 12-lead ECGs were recorded within the next 3 minutes:
Rate 118, flutter rate 236: One can see the flutter waves in lead II, and an upright P-wave in V1 confirms that this is flutter.  Some of the ST depression is due to flutter waves, but there is also significant subendocardial "demand" ischemia.  ACS is of course possible.

Rate 120, flutter rate 240.  Still more ST depression.

So what happened?

One might speculate that the patient co-incidentally converted from VT to atrial flutter at the time of the adenosine.  But I think that this atrial flutter was just slow enough to conduct through the AV node but too fast to use the conducting system, so if conducted through the ventricles VERY aberrantly and, the first time that there was AV conduction delay (2nd line of rhythm strip during adenosine), the conducting system recovered (was no longer refractory) and was able to conduct such that the QRS is a relatively narrow complex.  

How do I know (or think I know) it was atrial flutter with aberrancy?

Because the rates before and after the change in conduction are nearly exactly the same.  Again, see line 2 of rhythm strip during adenosine.  It is clearly atrial flutter after, so it must have been atrial flutter before

Did adenosine convert anything?  

No, but it appears to be associated here with a slight increase in atrial flutter rate and thus subsequent 2:1 conduction with slower ventricular response (atrial flutter 240, faster, but ventricle at 120, slower).

Learning points:

1.  Sometimes it is better to be lucky than right.
2.  Generally, adenosine is safe in VT
3.  If it looks like VT, treat it like VT.  Don't count on being lucky.
4.  Slow atrial flutter can produce VERY FAST ventricular rates.
5.  Very fast ventricular rates may conduct very aberrantly and be very wide.
6.  Sometimes what appears to unequivocally be VT is not

Comments appreciated.


  1. SUPERB Case Study! I would also have called the initial tracing VT and treated it as such with immediate cardioversion (without stopping to try Adenosine) - though I love it when I am "lucky" - and I'm humble enough to be happy with lucky results. Follow-up tracings I believe show exactly what you describe = slow AFlutter with 1:1 AV conduction initially.

    To me - QRS morphology during the wide tachycardia does not resemble a pattern suggestive of aberrant conduction. As a result - my bet is on AFlutter with anterograde ( = forward) conduction down an AP ( = Accessory Pathway) during the tachycardia. WPW is said to "never" produce pure negative QRS complexes in V4,V5,V6 (since there are no APs originating from the apex) - but I believe the QRS complex in lead V6 is not negative. I had to print out the 1st ECG and drop vertical lines with a straight edge to determine that the negative deflection in lead V6 is offset from the negative deflection that is the QRS in lead V4. BOTTOM LINE - is of course ALL of the learning points you highlight plus need for referral to EP for definitive diagnosis. I'd love to hear follow-up on this case. THANK YOU for posting - fascinating!

  2. Dear Dr. Smith,
    I was more focused on a ventricular tachycardia and given the instability of the patient would immediately opted for a concersione electric synchronized.
    Atrial flutter with aberrant conduction can result in treatment with antiarrhythmic drugs class Ic propafenone, flecainide.
    In history there was use of these drugs?
    Very interesting case.
    Thank you.

    1. Vittorio,
      I don't have any other history. But it is likely, as slow atrial flutter is often caused by presence of such drugs.

  3. Had a very similar patient once. Cardioverted him at 200J. Then he went sinus brady with a pressure of about 70. Fluid bolused 500 and gave a total of 1 mg of atropine. Transported him emergent to Oklahoma Heart Hospital where he did fine and was later discharged.

  4. Interesting case, as always. How concerned are we with the STE in aVR with ST depressions in anterolatetal leads in this scenario? Was the cath lab activated? If so, what were the results?

    1. In a case of dysrhythmia as the primary insult, any ischemia is probably due to demand, not ACS. So the first step is to shock the patient out of atrial flutter. Then, when in sinus as a reasonable ventricular rate, give it 15 minutes for the ischemia to subside and get another 12-lead. Only then, if ischemia persists, should you pursue treatment for ACS.
      Steve Smith

  5. I thought adenosine was not safe in case of SVT with WPW in the aspect of Super Wolff ? as digoxin, calcium channel blocker and even now amiodarone (as seen in 2014 AHA/ACC guidelines).

    1. Tom,
      That is a very common misconception. It only applies to WPW with atrial fibrillation, which will be an irregularly irregular rhythm with bizarre multiform complexes. See this post:
      Steve Smith

  6. Hi Steve,
    Great case. It suffices to say we all agree re: management; but the rhythm & Adenosine sequence=intriguing. I think we clearly see A-Flutter 2:1 after Adenosine and on the latter EKGs, but I also agree rhythm strips & EKG’s all point towards a prior slow A-Flutter as well. Adenosine-converted V-tac (or even a re-entry tachycardia) that converted to A-Flutter seems far-fetched. I doubt we are dealing with an accessory pathway. It seems Adenosine administration in A-Flutter w/WPW wouldn’t impact the ventricular response at all, assuming all the flutter impulses would come down the accessory pathway. There also didn’t appear to be an indication of accessory pathway on the ultimately slowed 2:1 EKG.

    I think the key, as well as the most puzzling part, is the peri-Adenosine rhythm strip. There is an interesting pattern of 2’s which evolves to a pattern of 4’s w/ regard to the QRS. We ultimately see a repeating pattern of narrow-narrow(pause)-narrow-WIDE. (these all march out). Not sure exactly how to explain do think this except that it is probably best explained by refractoriness of the distal conducting system.

    It makes sense that when the flutter rate went up to 240, it became too fast for 1:1 & the AV Node yielded a 2:1 block at that point. But it is unclear to me why Adenosine would have had a lasting effect on the atrial rate? As you noted, there also seemed to be some variation in the atrial rate prior to Adenosine administration.

    Super interesting case. Thanks for sharing.


    1. Sam, I did not mean to imply that there was a direct causal relationsh between the adenosine and the flutter rate. I think that it coincided with an increase in sympathetic tone (which may be due to the stress of adenosine), slightly increasing the atrial rate and thus changing conduction to 2:1.
      Sorry for any confusion.

    2. Thanks, Steve. Wouldn't expect an ectopic focus to be directly susceptible to influences of sympathetic/parasympathetic tone, in terms of altering fire rate? Having said that- don't have a good explanation for why these rates ever fluctuate..

    3. Sam, given this paper, you're probably right about sympathetic/parasympathetic tone, but other variables such as volume do alter flutter rate:

  7. If this is flutter with accessory pathway, wouldnt you expect the conduction through the pathway to be enhanced rather than decreased when giving adenosine resulting in even wider qrs? Also, how do you explain the abscense of delta waves in the last ecgs if you have a pathway with anterograde conduction? Intermittent conduction?

    1. For these reasons I do not think it is WPW. However, it could be. Absence of delta waves could be due to "concealed conduction." This is when the conduction gets to the AV node much faster than it gets to the bypass tract, and thus conducts down the AV node before it can conduct down the bypass tract. Many SVTs that are due to WPW have absence of delta waves after conversion to sinus. In this case, atrial flutter waves are in the right atrium. The bypass tract would be in the far left of the heart and the impulse from the right atrium (from flutter wave) would arrive at the AV node very quickly. On the other hand, I don't believe we would ever see 2:1 conduction if there were a bypass tract. One would go down the conducting system, the next would be blocked at the AV node but then make it down the bypass tract, alternating.
      Make sense?

      Steve Smith

  8. Hi Steve,
    very valuable website for the never ending tacit learning in ecg
    you refer early on in this post about the slow initial conduction of the QRS being indicative of VT and Ive read that in other posts, could you point out what you mean by that on an ecg pls,
    and possibly also expand on why it is that the ST elevation / depression is often exagerated in PVCs?

    1. Thomas,
      The initial part of the QRS in SVT will be nearly vertical because the voltage change happens over a very short time period. In VT, the slope is a slow upward (or downward) stroke because the voltage changes slowly over time. Look at all the complexes in the first ECG: they are not vertical, but rather rise (or fall) comparatively slowly.
      The ST elevation is not exaggerated in PVCs any more than in pacing or LBBB. If it is (and is concordant, or excessively discordant, to the majority of the QRS), then ST elevation (or depression) should be suspected.
      Steve Smith

  9. Dr Smith,
    on the initial ecg, it looks like there is notchings in teh QRS complexes suggesting P waves at a rate just under 300. Does this not suggest a supraventricular origin, the wide complex being then a rate dependent aberrancy? Or is there a retroactive p wave in cases of VT that matches the ventricular rate?

    1. If the notches are atrial activity, then they are flutter waves, not P-waves. But I am not at all certain that what you see is atrial activity.


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