Tuesday, June 9, 2020

A very fast wide complex tachycardia

A 60-something patient presented by EMS with non-specific symptoms.  He had a very rapid rhythm that was not converted by 6 mg, then 12 mg of adenosine.

On arrival, his BP was 94/75, pulse 127.

A bedside cardiac ultrasound was reported as showing good function, but I just viewed it and there is decreased function.

Here is his 12-lead:

Wide complex, Rate 265
("Pulse" was 127, so many of these beats are not resulting in a strong enough pulse to be palpated.)

What do you think?

Because of the extremely fast rate, the treating physicians thought that this was atrial fib with WPW.  However, this is clearly a misdiagnosis.

When the rate is so fast, it is possible to mistake a regular rhythm for an irregular one.  So one should use calipers (or mark a piece of paper and use it as calipers).  If one does this, one finds that this is perfectly regular.

Atrial fibrillation is ALWAYS irregular. This cannot be atrial fibrillation.

Furthermore, Atrial fibrillation with WPW always has polymorphic QRS complexes.  These complexes are all the same.

What is the morphology of these QRS complexes?

They are perfect LBBB complexes:  a sharp initial r-wave followed by a an S-wave that has a rapid depolarization.  The rS duration is about 55 ms, which is very short (fast) and indicates that this is a supraventricular rhythm.

Here are V2 and V3 magnified:
The initial r-wave is about 30 ms.  If this were VT or antidromic AVRT, the r-wave would be greater than 30 ms.

The rS is about 55 milliseconds.
If VT, it would be greater than 70 ms.

So this is a regular fast non-sinus rhythm with LBBB.  It is thus either:
1) PSVT or
2) atrial flutter with 1:1 conduction, or 
3) as Jerry Jones writes below, is a bundle branch block tachycardia.  This would explain the very rapid rate and also the initial fast depolarization.  Any fascicular or bundle branch VT can look just like SVT because they initiate in the conducting system.  

Pendell wrote a great post on Palpitations of unusual etiology-- all about fascicular and BB tachycardias.

In either of the first 2 situations, the conduction through the AV node is very fast.

PSVT may be AVNRT (re-entrant circuit entirely within the AV node) or may be due to WPW.  In WPW, the circuit can be down the AV node, then up the accessory pathway (orthodromic) or opposite (antidromic); re-entrant regular rhythms using an accessory pathway are called AV reciprocating tachycardia or AVRT.

If the AVRT is orthodromic, the ECG looks like AVNRT.  If antidromic, the initial part of the QRS is wide (analogous to a delta wave), not narrow, and can mimic VT.

Case 1 in this post from May 9, 2011 is a case of antidromic AVRT:

Wide complex tachycardias: 2 cases. What is the diagnosis and management?

Thus, in this case today, even if WPW is present, conduction is not via an accessory pathway; if it were, there would be a wide initial deflection, just as with VT.

Here is the ECG after electrical cardioversion:
Sinus rhythm, perhaps one PAC, nonspecific ST-T wave abnormalities.
There is no delta wave and a normal PR interval, though absence of delta wave does not rule out WPW.

A formal echo showed 37% EF, no wall motion abnormalities, but because of decreased EF, an angiogram was done and showed a 70% LAD lesion but no explanation for the dysrhythmia.


An EP study confirmed atrial flutter with 1:1 block. It was ablated.


Concealed conduction (not present in this case)

When an accessory pathway is present, and is resulting in dysrhythmia but is not seen on the ECG when the patient is in sinus rhythm, it is often called "Concealed conduction." 

Here is a case with Concealed Conduction and a Thorough explanation:

Wide Complex Tachycardia, and What is "Concealed Conduction?"

Adenosine was the appropriate initial therapy, but did not work.

Electrical cardioversion was the appropriate next therapy, and it did work.

But the diagnosis of atrial fibrillation with WPW was not correct, and this could have had consequences for the subsequent inpatient management.

The patient will get an EP study, but this has not been done yet.

MY Comment by KEN GRAUER, MD (6/9/2020):

NOTE (6/13/2020): Both my comment, and Dr. Jones' remarks were made before we knew "the Answer" to this case (that Dr. Smith has just now added near the end of his remarks under, "Outcome"). So please read our remarks keeping in mind that we did not yet know "the Answer" to this case (ie, results of the EP study that was done).

One of the most common and important acute arrhythmias that the emergency care provider encounters is assessment of the patient who presents with a regular WCT ( = Wide-Complex Tachycardia) rhythm. This is the focus of today’s case. I’ll add a few points to the concise explanation by Dr. Smith:
  • We are not told the patient’s age, nor his previous medical history. All we know is that the patient in this case presented with non-specific symptoms — and the ECG that I’ve reproduced in Figure-1. To our knowledge — the patient was not on antiarrhythmic medication at the time ECG #1 was done.
  • The rhythm in ECG #1 failed to respond to 6mg, followed by 12mg of adenosine. The patient’s BP was reported at 94/75 mm Hg. The pulse rate of 127/minute that was obtained on arrival in the ED clearly did not reflect the rapidity of his heart rate (Perhaps only every-other-heart beat produced a palpable pulse ...?).

Figure-1: The initial ECG in today’s case (See text).

My THOUGHTS on ECG #1: I’ve previously reviewed my approach to the regular WCT (ie, My Comment in the April 15, 2020 post on Dr. Smith’s ECG Blog— as well as to the regular SVT rhythm (ie, My Comment in the October 16, 2019 post). The KEY to time-efficient diagnosis and management of these regular tachycardias is to systematically apply the principles emphasized in those 2 prior posts:
  • 1st Priority — is to always determine IF the patient is hemodynamically stable. This is because IF the patient is not stable — then it no longer matters what the rhythm is, because immediate electricity is the treatment of choice for a tachycardia that produces symptoms as a direct result of the rapid rate. Despite the extremely rapid rate in ECG #1 — there presumably was at least a “moment of time” to contemplate the rhythm, because the patient was still maintaining a systolic BP of 94 mm Hg (which is a low but not critical BP), and the description of having “non-specific symptoms” sounded like he was probably still tolerating the rhythm. That said, this is clearly a situation in which, “Ya gotta be there” — as the BEST way for ongoing assessment of whether immediate cardioversion is or is not needed.
  • As per Dr. Smith — Adenosine was the appropriate initial therapy, but it did not work. Given the extremely rapid rate and suboptimal BP — electrical cardioversion then became the next appropriate therapy, and it did work!

Back to the Rhythm for ECG #1: As per My Comment in the 10/16/2019 and 4/15/2020 posts — I find it easiest to assess any cardiac rhythm for the 5 KEY parameters by remembering the saying, Watch your Ps, Qand the 3 Rs”. I like to alter the sequence in which I assess these parameters depending on which parameter(s) is easiest to detect:
  • In ECG #1 — the rhythm is regular — extremely fast — the QRS complex is extremely wide (ie, ~0.15 second) — and sinus P waves are absent. This defines the rhythm as a regular WCT.

Looking closer at the 5 KEY parameters:
  • It is challenging to determine QRS width for this tracing. I thought the limits of the QRS complex in ECG #1 were best defined in simultaneous leads V1, V2 and V3. The vertical RED line in these leads shows what I took for the onset of the QRS complex. The vertical BLUE line shows my take for the end of the QRS. Continuing these vertical lines straight down to the simultaneously-obtained long lead II rhythm strip shows these limits for onset and offset of the QRS complex in lead II. This allowed me to define the onset and offset of the QRS in simultaneous leads I, II and III (vertical RED and BLUE lines drawn in those leads). I measured QRS duration as ~0.15 second.
  • Sinus P waves are clearly absent in ECG #1. Several deflections that might be construed as representing some form of atrial activity are seen in a number of leads (RED, PURPLE and BLACK arrowheads in Figure-1). The purpose of my drawing those RED and BLUE vertical lines in leads I, II and III is to show that each of those arrowhead deflections falls within the QRS complex. I therefore thought those deflections were part of the QRS. I did not think there was evidence of atrial activity in ECG #1.
  • One KEY to assessing the rhythm in ECG #1 — is to accurately determine the heart rateWhen the rhythm is fast and regular — the Every-Other (or Every-Third or Fourth) Beat Method allows rapid and accurate rate estimation. Find a part of the QRS complex that begins on a heavy line. In ECG #1 — I chose the little spiked deflection in lead aVF (See the 1st short RED line in this lead, that appears just above the spike). Using the Every-Fourth Beat Method — the amount of time that it takes to record 4 beats (RED numbers in lead aVF) is just over 4 1/2 large boxes (BLUE numbers in this Figure). Therefore — ONE FOURTH the rate is a bit faster than 300/5 — or in this case, 1/4 the rate is ~67/minute.
  • The actual rate for the rhythm in ECG #1 is therefore ~67 X 4 ~268/minute. Knowing the actual rate of the WCT rhythm in ECG #1 is relevant to this case — as we will see below.
  • CLICK HERE if interested in brief video review of this Every-Other-Beat Method.

Putting It All Together:
  • The rhythm in ECG #1 is therefore a regular WCT rhythm at ~268/minute, without clear sign of atrial activity. Statistically — at least 80-90% of the time, this description for the rhythm will turn out to be VT (Ventricular Tachycardia). That said — QRS morphology in ECG #1 (as per Dr. Smith) is perfectly consistent with LBBB (monophasic R wave in lateral leads I and V6; predominant negativity in each of the anterior leads).
  • Although hemodynamics are far from infallible (ie, I’ve seen cases of VT with systolic BPs approaching 200 mm Hg) — the fact that this patient remained surprisingly stable despite a heart rate ~268/minute adds support to the QRS morphology appearance that this regular WCT is likely to be supraventricular.
  • So — IF the rhythm in ECG #1 is supraventricular — What kinds of SVT rhythms attain heart rates this fast? Das & Zipes (Electrocardiography of Arrhythmias; Elsevier, Philadelphia, PA, 2012) say that reentry SVT rhythms (ie, AVNRT and AVRTmost commonly do not exceed ~250/minute in adults — BUT — on occasion they can attain SVT rates as fast as 280/minute. Another possibility could be AFlutter with 1:1 AV conduction (as in a patient with WPW).

BOTTOM Line: Realistically — it’s not possible to be certain of the etiology of the regular WCT rhythm in ECG #1 from this initial ED tracing (especially given the lack of historical information about this patient). My "hunch" — is that the rhythm in ECG #1 was AFlutter with 1:1 AV conduction because: i) The ventricular rate of 268/minute is within the usual expected atrial rate range for untreated flutter (which is ~250-to-350/minute) — whereas 268/minute is faster than the rate usually seen with AVNRT or AVRT; and, ii) We are told there was no response to 2 doses of Adenosine — and both AVNRT and AVRT usually respond to this drug. On the other hand — AFlutter won't be converted with Adenosine. That Said we can not be certain which of the above possibilities is the true etiology of ECG #1 (AVNRT or orthodromic AVRT with lbbb aberration; antidromic AVRT; antidromic AFlutter with 1:1 AV conduction, presumably with WPW — or even VT with a morphology simulating lbbb).
  • What can be said (as per Dr. Smith) — is that the absolute regularity (and consistent QRS morphology) for the rhythm in ECG #1 rules out very fast AFib with WPW.
  • What can also be said — is that initial use of Adenosine as a diagnostic/therapeutic trial was appropriate, especially given our suspicion that the rhythm is likely to be supraventricular. Even if the rhythm turned out to be VT — the ultra-short half-life of Adenosine (which is less than 10 seconds) makes it unlikely that the drug will be harmful.
  • P.S.: We are told that the rapid rhythm in this case "was not converted by 6mg, then 12mg of Adenosine". Although it is implied by this wording that administration of Adenosine had NO EFFECT at ALL — that is not explicitly stated. I've learned the "hard way" — that one should go back to precisely what happened (in this case, ongoing monitoring strips of the inital fast rhythm during and immediately after administration of Adenosine) — to see IF there was any slowing at all — or perhaps "telltale" momentary conversion to sinus rhythm, with rapid resumption of the WCT rhythm. Even when Adenosine does not convert an SVT rhythm — it can often provide much diagnostic information by revealing hidden atrial activity during the brief period of temporary slowing after giving the drug.

ADDENDUM (June 9, 2020 @ 5pm)After writing My Comment above — I pondered this case some more. At the time I wrote My Comment yesterday — the post-conversion tracing was not available to me.
  • As per Dr. Smith — the post-conversion tracing showed sinus rhythm with a narrow QRS complex; early transition (R=S for the tiny QRS complex in lead V1); and nonspecific ST-T wave abnormalities that did not look acute. There were NO delta waves. While this does not entirely rule out the possibility of WPW — it does make anterograde AFlutter with 1:1 AV conduction in a patient with WPW far less likely.

I sent the tracing and my questions to Dr. Jerry Jones, an internationally known and widely published clinician-educator, who is a frequent commenter on Dr. Smith’s ECG Blog. I think Dr. Jones’ impression, that the rhythm in ECG #1 is BBR VT (Bundle Branch Reentrant Ventricular Tachycardia) makes the most sense for the particulars of this case.
  • BBR VT is an uncommon form of VT. CLICK HERE for an excellent review of this topic.
  • Dr. Smith indicates that an EP study is pending. I look forward to seeing the results!

Dr. JONES Wrote the Following to Me:

What a really interesting WCT! Here are my thoughts ...
  • First, the rate — while not too fast for SOME ventricular tachycardias — it is simply too fast for MOST of those arising in the ventricles (but not ALL — more of that in a moment). I usually expect to see VTs between 160 and 180/minute — and, in my experience, most are. The rhythm is mathematically regular, so atrial fib is out of the equation. Personally, I think 268/minute is too fast for anything involving the AV node except in babies and possibly young, very healthy people. Again, we don't know the age or patient's overall condition here.
  • I think a blood pressure of 94/75 mm Hg, with pulses that are only palpable about every second beat is very worrisome. A systolic BP of 94 may be OK for a woman who weighs about 90 lbs — but I am guessing that wasn't the case here. And if the patient's “normal” BP was closer to 160 — then this is a very significant drop. Again, as you say Ken: "You gotta be there!" I probably would have been inclined to go directly to cardioversion unless the patient looked exceptionally good (but again, I wasn't there). I've treated patients who have had both adenosine and sedation/cardioversion — and they ALL preferred the sedation/cardioversion!
  • Regarding the issue of the smooth, straight downslope of the S wave in lead V1 — I remember a number of years ago when I first came across Marriott's famous article on how to differentiate ectopy from aberrancy, and learned about the straight, smooth downslope in V1. I was very impressed with that information, and promptly misdiagnosed a number of VTs using that finding. I found out that a VT can present with the same smooth slope — as I feel it does in this particular case. I now consider this finding supportive — but I would be very, very careful basing a diagnosis on that alone. That's like the "rabbit ears" in RBBB. Most people know that if the left ear is taller, then that represents ectopy. What they DON'T know is that the discussion ends right there — because a taller right rabbit ear can be seen in BOTH aberrancy AND ectopy.
  • Finally — If the WCT in today’s case was due to antidromic conduction in a patient with an accessory pathway — then I’d expect to see evidence of ventricular preexcitation on the post-conversion ECG. But it’s not there ...

In Summary — I think the rhythm in today’s case is most likely a Bundle Branch Reentrant Tachycardia. That's why it did not respond to the adenosine — but responded immediately to the electrical cardioversion. Bundle branch reentrant tachycardias can present with a LBBB or RBBB morphology.
  • In my experience, LBBB is much more common and looks often (though not always) exactly like LBBB in V1. When it begins in the right ventricle, it begins within the conduction system, coming DOWN the right bundle branch (just like in LBBB) — then crosses the septum (just like in LBBB) — and then travels back up the left bundle branch. Therefore, it is quite possible for a BBRT with LBBB morphology to have a smooth, straight downward slope of the S wave in lead V1.
  • BBRTs are also well-known for their rapidity — sometimes in the upper 200's and approaching 300/minute! Hence, their lethality.

Again, I think this is most likely a BBRT with LBBB morphology. I congratulate the ER team on saving this man's life!

Jerry W. Jones, MD, FACEP, FAAEM


  1. Great post Steve. Had a similar ddx but also thought about RVOT VT given LBBB and inferior axis. Any reason why this cant be RVOT VT?

    1. Hi. Outflow Tract VTs (most commonly RVOT VT, but occasionally LVOT VT) generally manifest an inferior frontal plane axis — because the rhythm originates from “above” (where the outflow tract lies) — and travels downward. In my Figure-1 above — I’ve drawn in a RED vertical line in leads I,II,III to indicate the onset of the QRS — and a BLUE vertical line to indicate the end of the QRS. It can be seen in lead III of Figure-1 (with a similar picture being seen in lead aVF) that the QRS complex is predominantly negative within these 2 vertical lines — therefore, the frontal plane axis for ECG #1 is leftward and superior. One does not expect a superior axis with Outflow Tract VT. For an example of RVOT VT (with a LBBB pattern in the chest leads and inferior frontal plane axis) — Please CHECK OUT the Feb. 5, 2013 post — http://hqmeded-ecg.blogspot.com/2013/02/regular-wide-complex-tachycardia-what.html — :)

  2. Although adenosine did not convert the arrhythmia, a recording of ecg during adenosine administration would be helpful to look for unmasking of flutter waves.
    Atrial flutter with 1:1 av conduction is possible without a bypass tract also especially when patient is on chronic oral Flecainide without a beta blocker or rate limiting ccb.
    Since patient is relatively stable iv Flecainide could have been tried as it works both in atrial flutter and svt.
    The width of qrs and failure of adenosine notwithstanding ,is outflow tract VT (lbbb morphology ) a possibility?

    1. @ Subhasish — THANKS for your comment. I agree entirely with you that it would help for us to see the period of ECG monitoring during and immediately after adenosine administration (Plese see the “P.S.” in My Comment above, which is the very last paragraph that I wrote).

      YES — We include the possibility of AFlutter with 1:1 AV conduction without a bypass tract (in which case, QRS widening would be the result of rate-related LBBB aberration — since no BBB is seen on the post-conversion tracing). There is no mention of ongoing antiarrhythmic use in this case (I assumed the patient was not on Flecainide — but I don’t know details of the history).

      As to treatment with Flecainide — YES, it can be effective in converting AFlutter — but “Ya gotta be there” if you choose to opt for additional antiarrhythmics (such as IV Flecainide) in a patient with a wide tachycardia at 268/minute with a lowish BP, who failed to respond to adenosine. I’d favor cardioversion — which was done and which was successful.

      As per my answer to the question just above you — the frontal plane axis in ECG #1 is not inferiorly directed (it is instead a superior axis, the QRS being predominantly negative in leads III and aVF) — therefore not manifesting a QRS morphology suggestive of RVOT VT — :)

  3. Ken...

    Regarding my comment about expecting to see delta waves in the post-cardioversion tracing, it is true that some people with pre-excitation do not normally manifest any delta waves on their ECGs. However, that is due to the fact that in those cases the AP either conducts only in a retrograde manner (concealed pathway) OR that the AP conducts in an antegrade direction but only very slowly - more slowly than the AV node (not every AP is superfast!). In those cases, the patient will not be at risk for rapid, destabilizing wide complex tachycardias. The AV node will dominate the depolarization of the ventricles.

    1. @ Jerry — CORRECT. I think this is precisely why you so very carefully worded your statement (last bullet before your Summary in my Addendum above): “If the WCT in today’s case was due to antidromic conduction in a patient with an accessory pathway — then I’d expect to see evidence of ventricular preexcitation on the post-conversion ECG. But it’s not there ... “. The fact that no delta wave is seen after conversion to sinus rhythm only means that at this normal heart rate, conduction goes through the normal AV nodal pathway. This of course says nothing about the possibility of there being a “concealed” AP that is not going to be seen during sinus rhythm — because conduction only occurs retrograde in that “concealed” AP. But since the most dangerous tachyarrhythmias in patients with WPW are the very rapid AFib and AFlutter rhythms because they conduct anterograde (with risk of conducting very fast rates to the ventricles) — lack of a delta wave in the post-conversion tracing IS indeed reassuring that risk to the patient is less. THANKS so much for your insights! — :)

  4. A very challenging diagnosis with excellent management (=synchronized cardioversion).
    As to the diagnosis of this very fast WCT in this 60-year old patient, I initially disregarded the diagnosis of VT due the presence of the typical LBBB morphology (importantly with fast initial ventricular activation, a finding favouring a SVT rhythm and thus against VT). But, without excluding VT at all, I would immediately contemplate also the Bundle Branch Reentry tachycardia (this arrhytmia fits well with the severe LV disfunction): this is my second diagnostic choise, though I would have expected a beseline ECG with much more significant abnormalities (namely, conduction defects).
    While aknowledging that there is not any certainty, my first diagnostic choise is 1:1 atrial flutter caused by 1C-drug (Propafenone, Flecainide) effects; this is based just on the above my considerations and on my experience since I have seen a few those cases in patients treated with 1C-drugs and without taking beta-blockers.
    Great case!

    1. Thanks for your comment. To my knowledge this patient was NOT on a 1C drug prior to coming to the ED. Clearly, AFlutter with 1:1 AV conduction would have risen to the top of our differential if he had been on a 1C drug! — :)


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