Tuesday, April 23, 2019

What is this tachycardia that alternates from wide to narrow to wide?

This is 50-something who presented after a seizure and was unconscious and tachycardic:

There is a wide complex, followed by a narrow complex, followed by a wide complex.
What is the diagnosis?

The rate is 174.  The rhythm alternates between a wide complex (first 4 beats, and beats 16-28) and narrow complex (beats 5-15).  There are no P-waves.

Are the wide complexes due to a supraventricular rhythm (AVNRT or Atrial flutter or atrial fib) with aberrancy?  Or are they due to ventricular tachycardia (VT).

Favoring VT:  They are VERY wide, and the initial part of the QRS is quite wide in places.  For instance, in V4 the onset of the R-wave to the nadir of the S-wave is 90 ms.  This would normally imply VT.

However, there is one feature that is diagnostic for SVT with aberrancy.   What is it??

Answer: If you use a caliper, the rate of the 2 different morphologies is the same.  It would be a nearly impossible coincidence that a rhythm of SVT would have the exact same rate as a VT rhythm.

What was done?

Amiodarone 150 mg bolus was given and this was the result:
Now there is atrial fib with RVR, and the same QRS morphology as the narrow complex rhythm above.

What was the first rhythm?  If you take the time to measure every RR interval, as Ken Grauer did (see below), you will find that there is slight variation in all of them.  So it appears that the initial rhythm was atrial fib with aberrancy.

The amiodarone will slow AV conduction and lead to a slower ventricular rate, make it slow enough that there is no aberrancy, and make it obviously irregular.

Within about an hour, he spontaneously converted to sinus rhythm:

Comment by KEN GRAUER, MD (4/23/2019):
Interesting rhythm — in which the tachycardia alternates from a wide to narrow QRS complex. I agree with Dr. Smith — that the mechanism of the initial rhythm is supraventricular — though my approach was a bit different. Rhythms like this are great subjects for discussion, and there will often be more than a single viewpoint.
  • For clarity — I’ve reproduced and labeled the initial ECG in this case (Figure-1).
Figure-1: The initial ECG in this case. BLACK numbers in the long lead II rhythm strip indicated selected R-R interval measurements — with the thin RED vertical lines showing the consistent spot at the beginning of QRS complexes from where I measured (See text).
As per Dr. Smith — there is a tachycardia at ~170/minute with alternating wide and narrow complexes.
  • Sinus P waves are absent. Although there is some notching seen after the QRS complexes in leads II and III when the QRS complex is wide — I do not think this represents retrograde atrial activity. Instead — my hunch is that this notching is simply part of the QRS complex.
  • Although not specifically mentioned — we can assume that this patient was hemodynamically stable, because he/she was treated medically with Amiodarone. One benefit of this medication — is that it may be effective for both ventricular and supraventricular tachyarrhythmias.
A KEY to rhythm analysis at this point — is to determine IF the rhythm is regular or not, especially just before and just after QRS width changes.
  • CONFESSION: I spent no less than half an hour measuring and comparing R-R interval duration throughout this tracing. Reasons that this was so challenging include the rapid rate throughout the tracing — the less than distinct onset in the long lead II of beats with QRS widening — and the overlap with the exceedingly deep S waves in lead V3 that coincided with that elusive onset of widened QRS complexes that began again with beat #16.
  • BOTTOM Line: To my measurement — the R-R interval does not stay constant throughout the tracing! So as not to overly “clutter” the tracing — I limited millisecond measurements to just those needed to demonstrate that there is some variability. Most R-R intervals in this tracing measure 360 msec (ie, beats #1-thru-4; and then virtually all beats after beat #17).
  • The first 4 beats in this tracing are wide. Beats #5-thru-15 are narrow. QRS widening resumes with beat #16 — and persists until the end of the tracing. But the R-R interval preceding the first narrow beat ( = the R-R interval between beats #4-5) is slightly longer ( = 390 msec) than the 360 msec R-R interval for the preceding 4 wide beats. This suggests that the reason that the QRS narrows beginning with beat #5 might be a rate-related type of aberrant conduction. Admittedly — the R-R interval then shortens (ie, to 310 and 320 msec) — but it may happen with aberrant conduction that shortening after a longer R-R interval might not necessarily immediately alter QRS morphology.
  • There seems to be some variability in R-R interval duration for a number of beats in the narrow run. That this is true is easiest to see near the top of the tracing in leads aVR and V1. Even without caliper measurement — it should be evident that there is a difference in R-R intervals for the lettered durations A — B — C — D — and E. So, at least during this part of the tracing — since there is some irregular irregularity to this rhythm, but no P waves — which suggests this is probably rapid AFib! The PEARL — is that when AFib is rapid, parts of the tracing often look regular — but are not truly regular when measured with calipers.
  • In support of a rate-related relationship for aberrant conduction in this tracing — note that QRS widening resumes with beat #16 — and the R-R interval just preceding beat #16 (labeled D) is the shortest R-R interval on the entire tracing!
Additional findings in favor of aberrant conduction rather than VT in this tracing include the following:
  • QRS morphology is completely typical for LBBB aberration because: iThere is a monophasic R wave in lateral leads I and V6; andiiThere is predominant negativity in lead V1 (as well as in other anterior leads).
  • Although the rate of wide and narrow tachycardias is not identical throughout the entire tracing — the rates are very similar and, there is no post-ectopic pause when QRS morphology changes from wide-to-narrow, and then back from narrow-to-wide. VT is much more likely to manifest at least a slight pause when runs stop.
  • There is a reason for aberrant conduction! That is, a rate-related relationship is suggested — because the longest R-R interval (390 msec between beats #4-5) precedes the switch-over to a narrow QRS — and the shortest R-R interval (labeled D, between beats #15-16) precedes the switch back to a wide QRS complex.
CLINICAL NOTE: Obviously, in “real life” — there is not time with a sick, tachycardic patient like this one to say, “Stop while I pull out my calipers”. Fortunately — There is NO need to!
  • Even without making measurements — I suspected very quickly that a supraventricular mechanism was likely because: iQRS morphology in the 3 KEY leads (leads I, V1 and V6) is so very typical for LBBB — and although not impossible, VT is much less likely to look so typical for LBBB; — iiThe observation of narrow and wide tachycardias having such similar rates without any post-ectopic pause favors a supraventricular mechanism; — andiiiSince this patient was hemodynamically stable with this tachycardia — treatment with an agent such as Amiodarone that may be effective for both VT and supraventricular rhythms is appropriate even before you know a definitive diagnosis.
  • P.S. — I believe parts of this tracing represent rapid AFib. Other parts looked to be regular — so I wasn’t sure if there might not be some transition between a regular reentry SVT rhythm and AFib. Clinically though, this uncertainty wouldn’t alter the initial treatment approach.
  • P.P.S. It is of interest that the reason why there is so much overlapping of S waves from leads V2 and V3 in Figure-1 — is that this patient has marked LVH! In general — it is clearly more difficult to assess for LVH in the presence of LBBB — because this conduction disturbance alters the sequence of both depolarization and repolarization. As a result — both voltage criteria and ST-T wave changes of LV "strain" are different when evaluating a patient with LBBB. That said — the finding of VERY deep anterior S waves (ie, ≥25-30mm in any one or more of the anterior leads V1,V2,V3) is predictive of LVH despite the presence of LBBB. In further support of LVH in Figure-1 — note increased voltage, as well as repolarization changes consistent with "strain" (or a "strain"-equivalent) on the 2 ECGs done after QRS widening resolved. And, the fact that this patient has such marked LVH perhaps accounts for slight delay in the descent of those anterior S waves in Figure-1 during the run of wide QRS beats ( = beats #16-22 — with a thicker ventricle requiring more time for the impulse to pass, therefore a less steep initial descent for the QRS in anterior leads).
  • For more on the phenomenon of Rate-Related Aberrant Conduction — CLICK HERE.


  1. Steve and Ken...

    Thanks! This is a great tracing for illustrating rate-related aberrant conduction. I would like to add a few more points here...

    1. In teaching this concept, I find that many of my students look for a very obvious - even dramatic - rate change. Don't! The incremental change in rate required to cause the aberrant conduction can be very, very small - even a few milliseconds - and certainly not amenable to visual detection without the use of calipers (maybe even digital calipers).

    2. There is an apparent "paradox" present in this tracing. As Ken pointed out, the R-R interval that initiates the aberrancy is the shortest on the tracing and the R-R interval that terminates the aberrant conduction is the longest. However, the "seeming" paradox lies in the fact that there are some R-R intervals during the aberrant conduction that are longer than some R-R intervals during the normal conduction. But there is an explanation (and there really is no paradox at all)...

    If you really want to get into the specific cause of the aberrancy, just looking at the R-R intervals is not sufficient and actually provides only a partial explanation. The aberrancy is not caused by a problem throughout the conduction system - it is caused by a problem in one bundle branch. In this case, it's the left bundle branch and that makes this a bit unusual and ominous. Usually aberrancy is due to the fact that the refractory period of the right bundle branch is longer than that of the left bundle. So, it takes only a minimal amount of extra delay to initiate aberrant conduction with an RBBB morphology. This is why most aberrancy has an RBBB morphology. Aberrancy caused by LBBB usually implies more extensive heart disease. The bottom line is that it is not so much the R-R intervals we should be looking at but rather the activation of the individual bundle branches.

    In this particular case, the delay is in the left bundle which allowed the right bundle to activate the right ventricle first and then the left ventricle after traveling across the interventricular septum from right-to-left. During the next beat, the right bundle again conducts normally but - even if the left bundle had had a chance to repolarize sufficiently, the transseptal impulse conduction from the right ventricle during the previous beat has ensured that the left bundle would remain refractory... and so the aberrancy continues. This explains how an R-R interval during aberrant conduction can be a bit longer than some R-R intervals during normal conduction. In fact, this "paradox" was illustrated by Ken himself when he indicated that the R-R interval terminating the aberrancy was the longest on the tracing. It has been known for years that the heart rate must often slow well below the rate at which the aberrancy began before it converts back to normal. That's because the heart rate recorded on the ECG is based on the functioning bundle branch. It will have to slow down more in order to allow the non-functioning bundle branch to begin repolarizing sufficiently to conduct normally.

    Jerry W. Jones, MD FACEP FAAEM

  2. Totally how many types of ecg disorders present

  3. I don't understand the question


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