Saturday, September 26, 2020

40 Something Man with Palpitations and Grouped Beating: Is it Wenckebach?

From Dr. Smith: A 40 something male complained of palpitations.  See the ECG below and how Ken Grauer dissects this grouped beating.

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MY Comment by KEN GRAUER, MD (9/26/2020):

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The 12-lead ECG and accompanying long lead II rhythm shown in Figure-1 was obtained from a 40-something year old man who was found to have a fairly slow and irregular heart rate. He was hemodynamically stable at the time this tracing was done. Imagine this is the only history available.

  • What is the rhythm? Is this Wenckebach?
  • Clinically — WHY might it matter?


Figure-1: 12-lead ECG and rhythm strip from a 40-something year old man with an irregular heart rate (See text).




MY Thoughts on ECG #1: This is a challenging tracing. My purpose in discussing this case is to highlight distinction between AV block vs mimics of AV block. Treatment indications for being able to quickly make this distinction are obvious = A pacemaker may be needed for more severe, symptomatic forms of AV block — whereas a pacemaker will usually not be needed for most AV block “mimics”.


As always — I favor beginning with the cardiac rhythm (in the long lead rhythm strip) before assessing the rest of the 12-lead ECG. By the 5 Parameter Ps, Qs & 3R Approach — I noted the following:

  • P waves are present. However, it is not immediately apparent how consistent atrial activity is (More on this below).
  • The QRS complex is narrow in all 12 leads. Therefore, this is a supraventricular rhythm.
  • The Rhythm is not regular. That said — there appears to be group beating (ie, 4 groups of 3 beats each, with a similar pattern of spacing throughout the long lead II rhythm strip).
  • Since the ventricular rhythm is not regular — the Rate is changing! The longest R-R intervals are approximately 7 large boxes in duration (corresponding to a rate in the low 40s). The shortest R-R intervals are about 3 large boxes in duration (corresponding to a rate of ~100/minute).
  • We can estimate the overall heart rate by the fact that the entire rhythm strip is 50 large boxes in duration (ie, ~10 seconds) — during which time 11 beats occur. Therefore — 11 beats X 6 = 66/minute as the average overall rate.
  • The 5th Parameter is the 3rd R — which stands for Related (ie, Are P waves related to neighboring QRS complexes?). We can tell at a glance that at least some of the P waves are related to neighboring QRS complexes — because the PR interval preceding each of the QRS complexes that terminate each of the short pauses is equal (ie, a normal PR interval ~0.15 second precedes the QRS complex of beats #4, 7 and 10).
  • NOTE: For those interested in more on “My Take” on the Ps, Qs & 3R Approach for Systematic Rhythm interpretation — CLICK HERE.


PEARL #1: I have emphasized on a number of occasions in Dr. Smith’s ECG Blog, that whenever group beating is seen — one should immediately consider the possibility of some type of Wenckebach conduction. Clearly — Not all group beating will turn out to be the result of Wenckebach conduction (ie, atrial bigeminy or trigeminy, among other rhythms — may manifest “group beating” that is not the result of Wenckebach). That said — Keeping in mind this concept of group beating has allowed me to recognize literally hundreds of Wenckebach cases in record time!

  • The most common form of Wenckebach conduction is 2nd-degree AV block, Mobitz Type I (also known as AV Wenckebach) — and this is the type of Wenckebach conduction that I will consider here. KEY Point: For there to be 2nd-degree AV block of the Mobitz I type — the atrial rhythm (ie, P-P interval) should be regular (or at least almost regular, if there is underlying sinus arrhythmia).
  • The utility of this PEARL — is that simple use of calipers allows you within seconds to establish that regardless of what you interpret as P waves in the long lead II rhythm strip in Figure-1  the atrial rhythm is not regular. Therefore, despite group beating — 2nd-degree AV block of the Mobitz I type is not present in ECG #1!
  • NOTE: For those interested in my video on ECG recognition of the AV Blocks — CLICK HERE. (If you click on SHOW MORE under the video on the YouTube page — you’ll see a detailed linked Contents to key topics in the video).


PEARL #2: The following truism has served as my arrhythmia “mantra” over the past 4 decades — “The commonest cause of a pause is a blocked PAC” (taught to me by the incomparable Henry J. L. Marriott).

  • Statistically — Blocked PACs are a far more common cause of pauses than any form of AV block. By repeating this truism to myself whenever I see a short pause (such as for the 3 short pauses in ECG #1) — I avoid overdiagnosis of AV block, and, I tremendously increase my ability to quickly spot even the most subtle of blocked PACs.


Figure-2: I’ve labeled key points from Figure-1 (See text).




PEARL #3: In my experience, the 2 simple steps of labeling P waves and numbering the beats in a complex arrhythmia have proved invaluable for facilitating recognition of the mechanism of the arrhythmia — and, for being able to communicate your thoughts to colleagues (ie, It’s impossible to do this with any time efficiency unless you number the beats). I illustrate my approach in Figure-2.

  • I start with what I know. As mentioned earlier — the QRS complex that terminates each of the 3 pauses in ECG #1 is preceded by a sinus P wave with a constant (and normal) PR interval. RED arrows highlight these 3 sinus beats (ie, beats #4, 7 and 10).
  • Similar events regarding additional atrial activity seem to be occurring within each of the groups. In Figure-2 — I focus on the group that consists of beats #4, 5 and 6 — and have labeled the atrial activity that I believe is occurring.
  • The P wave labeled “a” is the sinus P wave of beat #4 that begins the cycle.
  • The next P wave in this group of 3 beats appears to be added on to the end of the T wave of beat #4 (labeled “b”). The fact that “b” occurs at the very end of the T wave of beat #4 allows us to see what a “normal T wave” looks like ( = the 1st BLUE T in the long lead II — that is contained within the BLUE rectangle).
  • Compare the shape of the T waves of beats #5 and 6 (labeled with a PURPLE T’ ) — with the shape of the “normal” T wave that follows beat #4. Aren’t these T waves of beats #5 and #6 more peaked than the normal T wave? This extra peaking is the result of premature P waves “c” and “e” that are hidden within these T waves.
  • One more P wave occurs in this 3-beat group (labeled “d”  which precedes beat #6 with a longer PR interval than the PR interval for sinus beat #4).
  • The P waves that are hidden within the T waves of beats #5 and #6 (labeled “c” and “e”) are both blocked. That neither of these P waves are conducted makes sense — because these P waves occur very early in the cycle, presumably during the absolute refractory period.


BOTTOM Line: The above findings make for a repetitive sequence, in which a short pause is terminated by a sinus-conducted beat — which is then followed by 4 successive P waves (PINK arrows highlighting b, c, d and e) — and then the cycle repeats (ie, similar events occurring within the next group consisting of beats #7, 8, 9 — and one more time with the last 3-beat group = beats #10, 11, 12).

  • It is admittedly difficult to distinguish between a single sinus beat followed by repetitive PACs vs being followed by short runs of ATach (Atrial Tachycardia). I favor the former because: i) The P-P intervals between a, b, c and d are not all the same (ie, the P-P interval between c-to-d is noticeably shorter than the other P-P intervals); andii) P wave morphology seems to vary during these successive P waves — whereas I’d expect a similar P wave morphology if these were runs of ATach (Note different shapes for P waves in several leads highlighted by the small YELLOW vs BLUE arrows).


The Rest of the 12-Lead ECG: The remainder of the 12-lead tracing for ECG #1 is fairly unremarkable.

  • There is a leftward axis — though not negative enough to qualify for LAHB (since the QRS in lead II is isoelectric and not predominantly negative). The QTc is not prolonged. There is no chamber enlargement. Blocked PACs (within many of the T waves) account for much of the extra T wave peaking. ST-T wave changes do not appear to be acute.


Putting It Together: The underlying rhythm is sinus. The primary rhythm disturbance appears to be repetitive sequences of successive PACs. These terminate with a blocked PAC that results in a brief pause (of <1.4 second) — and then the cycle resumes.

  • The rhythm disturbance is not AV Wenckebach. No pacemaker is needed.
  • Management will depend on symptoms — frequency of PAC episodes over time, and whether longer runs of PACs are sustained (whether this develops into runs of ATach) — and, the presence or absence of underlying heart disease or other predisposing factors. Unfortunately — additional follow-up was unavailable on this case.
  • P.S. Re-entry SVT rhythms (such as AVNRT) often begin with multiple PACs. Whether to begin a trial of empiric therapy (ie, with a ß-blocker or other agent) — or to assess with a longer period of monitoring would be a decision for the treating clinician.


ADDENDUM (9/26 pm): Dr. Smith wrote me just as today’s post was published, asking me, “Could I add a laddergram?”. The reason I did not do this initially — is that there are several potential explanations for the atrial activity we see, and I did not feel there was enough monitoring to delineate an exact answer.

  • As is often the case with complex arrhythmias (especially when the amount of monitoring recordings is limited) — there may be more than a single plausible theory for the mechanism of an arrhythmia. I illustrate 3 possibilities in the Laddergram that I’ve just derived (Figure-3). I still do not think we can know for certain what is going on — but it may be instructive to contemplate possibilities:
  • For the 1st Grouping ( = beats #4,5,6) — The initial beat in this grouping is sinus-conducted (beat #4). There follows 4 successive PACs. I used different colors to suggest origin from different sites in the atria — but one or more of these PACs could be coming from the same site. Reasons why the PR intervals preceding beats #5 and #6 are longer than the PR interval for sinus-conducted beat #4 could be: i) These PACs originate from an atrial site further away from the AV node; or, ii) There could be some partial retrograde conduction (dotted butt ends traveling backward) that delays forward conduction. The last PAC (labeled “e” — and the GREEN circle in the laddergram) presumably occurs during the absolute refractory period, and is therefore blocked (non-conducted).
  • For the 2nd Grouping ( = beats #7,8,9) — The laddergram depiction is similar to my proposed mechanism for the 1st Grouping — with the exception that beat #9 might be sinus-conducted (albeit with a prolonged PR interval due to delay caused by partial retrograde conduction from the previous PAC that is shown in YELLOW).
  • For the 3rd Grouping ( = beats #10,11,12) — There could simply be atrial tachycardia (ie, all P waves after sinus-conducted beat #10 arise from the same atrial focus — shown in GREEN). NOTE #1: Given the frequent prolonged PR intervals we see in this tracing — it seems likely that if ATach ever became established and sustained — that this ATach would manifest Wenckebach conduction. NOTE #2: ATach is not always a perfectly regular arrhythmia — as could be the case in this last Grouping.


P.S.: I’ll emphasize that regardless of whatever the precise mechanism for this arrhythmia turned out to be — my initial approach to management would be the same.



Figure-3: I’ve added a laddergram to Figure-2, showing 3 possible theories for the mechanism of atrial activity in this arrhythmia (See text).



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  • NOTE: My sincere THANKS to Feroz Haroon (from Srinagar, India) for sharing this tracing with us!

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ADDENDUM #2 — by David Richley (9/28/2020): Dave has followed up on his 9/26 comment with his own laddergram (Figure-4). Although we still do not know for certain what the correct answer is — I think it instructive to show how sometimes a number of possibilities exist.

  • I’ll once again emphasize that even though we are not certain of the mechanism of this interesting rhythm — my initial approach to management would still be the same.


David Richley said the Following: I think this could simply be sinus rhythm with an atrial bigeminy, in which the atrial premature beats (APBs) are alternately conducted and non-conducted, as illustrated in this laddergram (Figure-4). According to my theory, beats #1, 3, 4, 6, 7, 9, 10 and 12 are sinus beats; beats #2, 5, 8 and 11 are conducted APBs — and immediately following beats #3, 6 and 9 is a non-conducted APB.

  • The reason every other APB does not conduct is because it has a slightly shorter coupling interval than the conducted APBs, something that is most clearly seen in lead V1.
  • The sinus beat at the end of each group of 3 beats has a longer PR interval than the one at the start of the group — because the AV node, having had less time to recover, is still partially refractory and conducts more slowly.
  • The big weakness with my explanation is that the 2nd beat in each group has a taller T wave than the first. This is easily explained by Ken’s theories because he proposes that there is a premature P wave on top of this T wave, whereas I don’t think there is. My best explanation for the tall T wave of the 2nd beat, is that this QRS has a taller R wave and greater overall positivity than the 1st beat, particularly in some of the chest leads — and that a taller T wave might therefore be expected.
  • The big weakness of Ken’s theories – in my opinion – is that there is absolutely no evidence of a P wave on the T wave of the 2nd beat in each group in V1. Ken thinks that there is a P wave here, and I think there isn’t — and this is the main difference between us in how we see the ECG and therefore interpret it.


Figure-4: David Richley’s laddergram (See Addendum #2).



7 comments:

  1. This is a great case! I have scratched my head at similar rhythms in the past. What causes the prolonged PR interval in PAC's b and d specifically?

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    1. Thanks for your comment. Hopefully I’ve answered your question with the Addendum that I just now wrote — :)

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    2. Thank you very much. You have definitely answered my question with your thorough addendum.

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  2. I’d like to offer an alternative explanation! I think this could be sinus rhythm with atrial bigeminy throughout, but with every other APB not conducting and this may be because of alternating long and short coupling intervals. I think this evident in V1, where it looks like there is a non-conducted P wave on the end of the T wave of the 3rd QRS. Do you think this is plausible, Ken?

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    1. Hi Dave! What complex arrhythmia would be complete without theory for an additional plausible mechanism from David Richley? — :) That said — I just now spent over an hour adding my Addendum for some thoughts about what might be going on (this was before I saw your comment …). I’m afraid I just don’t visualize what you are describing Dave … Feel free to design your own laddergram and then email it to me — and I’ll be glad to publish as Addendum #2 (with your laddergram) from David Richley! THANKS as always for your astute comments that ALWAYS force me to “rethink” my theories. Great way to continue learning from each other! — :)

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    2. Unlikely because in each cluster of grouped beats, the 2nd and 3rd t waves have similar morphology.if there is a nonconducted p only in the t wave preceding the pause ,it should have a unique morphology

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    3. @ Subhasish Singh — THANKS for your comments. I agree completely with you — as I believe (as you do) that there has to be a non-conducted P wave hidden within the peaked T waves of beats #2, 5, 8, and 11 (just as there has to be a blocked PAC within the peaked T waves of beats #3, 6 and 9). I am in ongoing correspondence with David Richley on this question. Wish we had some additional monitoring on this patient, so that we could determine the “true” answer.

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