Wednesday, September 9, 2020

Is there Wenckebach? An Elderly Patient with a Fall

MY Arrhythmia Case by KEN GRAUER, MD (9/9/2020):
PREFACE: Recognition of the presence (or absence) of AV block is a common problem in emergency medicine. This case puts beginners, intermediate interpreters and experienced interpreters "to the test" in working through the etiology of this interesting rhythm.

The ECG that is shown in Figure-1 was obtained from an elderly patient, who was admitted to the hospital for a fall. The patient was found to be severely anemic — but was not hemodynamically unstable.
  • In view of this history — HOW would you interpret the ECG in Figure-1?
  • Is there AV block? IF so — HOW would you describe the conduction disturbance? IF not — WHAT is the rhythm? 
  • WHAT treatment is needed for this rhythm?

Figure-1: The initial ECG in this case — obtained from an elderly patient with severe anemia (See text).

My THOUGHTS on ECG #1: This is an challenging tracing — even for experienced providers! I’ll offer a Step-by-Step Approach for assessing this 12-lead ECG and accompanying long-lead rhythm strip. 

PLEASE NOTE: Less experienced providers may not follow all aspects of my explanation. That is fine! — because there is plenty to learn from this case for any level provider. Follow as much as you can. In the 2nd bullet below — I provide a link to review of my user-friendly systematic approach to rhythm interpretation. In any case — Be SURE to read my last section below in which I summarize optimal management for this patient. And for those of you who are more experienced — the challenge is on!
  • Regardless of your experience in ECG interpretation — Look first at the rhythm! This is best done by focusing on the long lead V1 rhythm strip at the bottom of the tracing. (Assessment of the rest of the 12-lead ECG is best deferred till after you’ve looked at the rhythm).
  • I’ve previously reviewed my Systematic Approach to rhythm interpretation (See especially the August 17, 2020 post). But regardless of which of the 5 KEY Parameters (“Watch your Ps, Qs & the 3Rs” that you choose to look at first — there are 3 Observations that should immediately be made: i) The QRS complex in ECG #1 is narrow — which tells us that this is a supraventricular rhythm; ii) There are P wavesandiiiThere is Group Beating (ie, there is a repetitive pattern of 2-beat groups — with alternating short-long R-R intervals, best seen in the long lead V1 rhythm strip).

PEARL #1 — As we’ve emphasized on many occasions — the presence of GROUP beating often means that some sort of Wenckebach phenomenon is present. There are many types of Wenckebach phenomena, of which AV Wenckebach (ie, the Mobitz Type I form of 2nd-degree AV block) is the most common.
  • NOTE: This does not mean that every time you see group beating — that Mobitz I will be the cause. For example, atrial bigeminy or trigeminy will also produce “group” beating. That said — Recognition of group beating in this particular tracing did allow me within seconds to begin focusing attention on the strong possibility that AV Wenckebach might be present!

Is There a Regular P Wave Rhythm?
I find it helpful in sorting out complex arrhythmias to search out P waves at an early point in the process. I like to begin by first identifying deflections that I know are P waves. In Figure-2 — RED arrows show places where we can be certain that there are definite P waves in the long lead V1 rhythm strip that we saw in Figure-1.
  • PINK arrows in Figure-2 highlight deflections that fuse with the end of the T wave in this V1 lead — but which almost certainly also represent P waves, because their size and shape is virtually identical to the definite P waves highlighted by RED arrows.
  • NOTE: Looking at atrial activity in lead II of ECG #1 (in Figure-1) — the P waves that we clearly see in front of beats #3, 5 and 7 in lead II are upright, albeit tiny in amplitude. This suggests that the underlying rhythm is sinus — especially since the PR interval preceding beats #3, 5, 7, 9, 11 and 13 in the long lead V1 rhythm strip is the SAME.
  • NOTE: Since P waves are much easier to see in lead V1 compared to any other lead on the 12-lead tracing — I use lead V1 for each of the remaining Figures in this post.

Figure-2: I’ve labeled P waves that we definitely see with RED arrows, in the long lead V1 rhythm strip (See text).

PEARL #2 — It is sometimes difficult to distinguish 2nd-degree AV block from other causes of group beating (such as atrial bigeminy, SA block, sinus pauses, etc.). For there to be AV block — the atrial rhythm should be regular! (or at least almost regular, if there is sinus arrhythmia). When the atrial rhythm is clearly not regular — then there most probably is not AV block. As a result — I always pay special attention to determine IF some P waves might be hiding. Using calipers greatly facilitates this task!
  • HINT: You’ll never get good at interpreting complex arrhythmia unless you regularly use calipers. Once you begin to use them — you’ll find it takes far less time to work out P wave-QRS complex relationships that you would otherwise never have seen ...
  • Look at Figure-3. If there is an underlying regular atrial rhythm in this tracing — then shouldn’t we expect there to be P waves where I’ve placed BLUE arrows?
  • Now look within the BLUE circles at the onset of beats #8 and 10. Compare what you see — with what appears within the RED circles at the onset of beats #7 and 9. Doesn’t the small pointed notch within the BLUE circles walk out perfectly for where you’d expect regularly-occurring P waves to be?

Figure-3: BLUE arrows have been added where one would expect regular P waves to occur (See text).

Therefore — Using calipers now allows us to walk out regularly-occurring P waves throughout the long lead V1 rhythm strip (RED arrows in Figure-4).

Figure-4: RED arrows indicate the underlying regular atrial rhythm (See text).

PEARL #3 — My suspicion that this rhythm represents some type of Wenckebach block has been further increased because: i) There is definite group beating (ie, groups of 2-beats, with a repetitive long-short R-R interval pattern); ii) The rhythm is supraventricular (ie, the QRS complex is narrow); andiii) There is a regular atrial rhythm. All that remains is to elucidate the mechanism. Drawing a laddergram can help.
  • I list below, at the end of My Comment several links to complex arrhythmias in which I draw step-by-step illustrative laddergrams.
  • In the interest of consolidation — I jump to my proposed answer in Figure-5.

Figure-5: Laddergram illustrating my proposed mechanism for the rhythm in this case (See text).

A Proposed Mechanism: More than 1 mechanism is possible to explain the rhythm in this case. That said — I think the mechanism shown in the Figure-5 laddergram is the most likely.
  • NOTE: Most of the time with AV Wenckebach (ie, Mobitz I, 2nd-degree AV Block) — there is a gradual increase in the PR interval with successive beats until a P wave is non-conducted. However, on occasion — dual AV nodal pathways physiology may be operative (Mani BC & Pavri BB: Dual AV Nodal Pathways Physiology — Indian Pacing Electrophysiol 14[1]:12-25, 2014). When this happens — there may be an abrupt change (increase) in the PR interval from one beat to the next due to sudden change in conduction over the fast pathway (which results in a shorter PR interval) — to conduction over the slow pathway (which results in abrupt PR interval lengthening). I suspect this is what is happening in Figure-5.
  • Beats #1, 3, 5, 7, 9, 11 and 13 in Figure-5 are all conducted with a normal PR interval of ~0.18 second. The BLUE slanted lines in the AV nodal tier illustrate this, by suggesting the P waves labeled “a” and “d” are conducted to the ventricles with a normal PR interval.
  • After normal conduction of the P wave labeled “a” to produce beat #3 (1st BLUE slanted line in the AV Nodal Tier in Figure-5— there is an abrupt increase in the PR interval (to ~0.52 second) for the P wave labeled “b” — that is conducted to the ventricles with 1st-degree AV block to produce beat #4 (illustrated by the GREEN slanted line in the AV Nodal Tier).
  • The next P wave in the cycle (labeled c”) is non-conducted (PURPLE butt end).
  • The cycle then begins again  as conduction shifts back to the faster pathway to conduct the P wave labeled “d” to the ventricles with a normal PR interval to produce beat #5 (illustrated by the 2nd BLUE line in Figure-5).
  • Therefore, in Figure-5 — beats #2, 4, 6, 8, 10, 12 and 14 are all still conducting (since these beats are all preceded an identical PR interval) — but conduction has shifted to the slower AV nodal pathway (which is why conduction of these beats occurs with such a long PR interval).

Putting It All Together — STEP BACK a little bit, and look at the RED lines in the AV Nodal Tier of Figure-5.
  • It should now be much EASIER to appreciate the repetitive pattern of group beating, in which each group consists of 3 P waves and 2 QRS complexes — with an increase in PR interval between the 1st and 2nd beat in each group (seen by the increased slanting within the AV Nodal Tier) until the 3rd P wave in each group is non-conducted. This progressive PR interval lengthening until a beat is dropped defines the conduction disturbance as Mobitz I, 2nd-degree AV Block (AV Wenckebach).
  • KEY Point — The reason it was more difficult to recognize this example of Mobitz I — is that our “eye” is not used to seeing PR intervals as long as we see here conducting — and, we are also not used to seeing such a marked and abrupt increase in PR interval from one beat to-the-next. That said — review of the 3 features cited above in PEARL #3 allowed me to strongly suspect AV Wenckebach within seconds of seeing this tracing (even though it took me much longer to illustrate this with the laddergram I drew in Figure-5).

PEARL #4 — Suspect that dual AV nodal pathways may be operative whenever you see AV Wenckebach in which there is an unexpectedly marked increase in PR interval from 1 conducted beat to the next.
  • P.S.: I fully acknowledge that my proposed mechanism for the laddergram in Figure-5 is not the only possible theory. For example, rather than beat #3 — beat #2 could be the first conducted beat in this initial grouping (with a very long PR interval). Or, there could be an associated accelerated junctional rhythm that serves as the reason consecutive P waves are not conducted. Sometimes the only way to prove what the true mechanism for a complex arrhythmia is — is through additional ECG monitoring and/or by EP (ElectroPhysiologic) Study. That said — I believe the mechanism I postulate in Figure-5 provides the most logical explanation for the rhythm we see. And, in any case — AV Wenckebach is almost certainly responsible for the group beating we see in this tracing!

RETURN to Figure-1: Now that we’ve determined the cardiac rhythm — we need to assess the rest of the 12-lead ECG.
  • As presented at the beginning of this post — the elderly patient in today’s case was admitted to the hospital following a fall. The patient was severely anemic, but was not hemodynamically unstable.
  • Regarding interpretation of the 12-lead tracing in Figure-1 — there is low voltage in the limb leads. The axis is leftward — but not leftward enough to qualify as LAHB. There is no chamber enlargement. There is some nonspecific ST-T wave flattening, with perhaps some mild ST depression — but these changes do not appear to be acute.
  • Clinical MANAGEMENT: This symptomatic, severely anemic elderly patient does not manifest acute ST-T wave changes. Despite Mobitz I, 2nd-degree AV block — the overall ventricular rate is more than adequate (an average ventricular rate in Figure-1 of ~80-90/minute) — and there is no evidence of “high-grade” AV block. As a result — all that may be needed is consideration of blood transfusion + efforts to determine (and correct) the cause of anemia. No treatment of AV block would seem indicated at this time.

For Additional Practice with Step-by-Step Laddergrams:
  • SEE My Comment in the May 16, 2020 post on Dr. Smith’s ECG Blog.
  • SEE My Comment in the May 28, 2019 post.
  • SEE My Comment in the August 17, 2020 post.
  • For those of you who would like a Video Review of the Basics of AV Block — Please CLICK HERE. And, if you click on SHOW MORE (under the video on the You-Tube page) — you’ll find a detailed linked Contents that will allow you to jump to whichever part on AV Blocks you are interested in.
NOTE: My sincere THANKS to Drs. Giovanni Serafini & Viola Tallarico (of Italy) for sharing the tracings and this case with us!

ADDENDUM (9/9/2020):

I am gratified by commentary on this post from 2 international arrhythmia experts, in the names of Dr. Adrian Baranchuk (through personal correspondence to me) and Dr. Jerry Jones (See the comment from “Double Down” = Jerry Jones below).  Both of these renowned experts suggest additional potential mechanisms for today’s fascinating rhythm.

  • I like to quote Rosenbaum, who said, “Every self-respecting arrhythmia has at least 3 possible interpretations.”
  • In contemplating my decision on how I would write up this case — I decided not to “overcomplicate” my explanation with additional laddergrams. But please NOTE in the “P.S.” of my PEARL #4 (above) — that I alluded to other potential mechanisms for this rhythm.
  • I went so far as to draw 2 additional laddergrams — but I decided not to publish those initially, for fear of overcomplicating the subject. Given astute commentary by Drs. Baranchuk and Jones — I am adding to this Addendum my Figure-6 — in which I show these 2 laddergrams that I had previously drawn, but chose not to previously publish. I believe these 2 additional laddergrams address their concerns. Perhaps there are even more possibilities to explain this rhythm ... 
  • Sometimes the only way to prove what the true mechanism for a complex arrhythmia is — is through additional ECG monitoring on the patient or by EP (ElectroPhysiologic) Study.
  • That said — regardless of whichever of the proposed mechanisms is the “real one” — the POINT I want readers of any level of ECG expertise to walk away with from this case — is that there is AV block here — the group beating suggests some type of Wenckebach mechanism — and, as I emphasize in my last bullet entitled, “Clinical Management” — there is no evidence of high-grade AV block, such that optimal treatment in this case is consideration of blood transfusion + efforts to determine (and correct) the cause of anemia — with no specific treatment needed at this time for the AV block!

My sincere THANKS to Drs. Baranchuk and Jones for adding additional intrigue to this case!

Figure-6: Two additional potential mechanisms for the fascinating arrythmia in today's case!


  1. Ken...

    An excellent case and great discussion. But I think there is still some a problem that needs to be addressed:

    First, while I DO agree wholeheartedly that this is a 3:2 Mobitz I block, I don't think it is formed the way you have indicated. With any type of Wenckebach conduction through the AV node (i.e., a Mobitz I block), a shortened PR interval should be followed by a lengthened RP interval and a lengthened PR interval should be followed by a shortened RP interval. In your diagram, you've indicated just the opposite: a short PR interval is followed by a short RP interval and a longer PR interval is followed by a longer RP interval. That is the opposite of what should be happening with a Wenckebach conduction and is a finding that is actually used to exclude Wenckebach conduction.

    However, if you consider the possibility of a "skipped P wave" phenomenon, it will follow the rules. The P wave that initiates the long PR interval ("B" in Fig. 4) - even though another P wave ("C" in Fig. 4) is starting to appear just BEFORE the QRS (hence, the "skipped P wave"), is likely the true PR interval for this patient. If you measure from the beginning of the partially hidden P wave ("C") to the next QRS, there will be another increase in the PR interval. Now we have a longer PR interval followed by a shorter RP interval in each case. The P wave that fails to conduct is the P wave that "appears" to initiate the "normal" PR interval ("D"). So, referring to your Fig. 4, P waves "B" and "C" conducted while P wave "D" did not.

    A severely anemic, elderly person could very well be experiencing ischemia of the artery to the AV node. Also, the LAD (which also contributes to the blood supply of the AV node) may be suffering from some occlusive disease which could contribute to AV nodal ischemia and a marked 1st degree AV block. What better set-up for a Mobitz I conduction than an already prolonged PR interval?

    The most disconcerting thing about the "skipped P wave phenomenon" is that the non-conducted P wave is often the P wave with the most "normal PR interval."

    Jerry W. Jones, MD FACEP FAAEM

    1. THANKS so much Jerry. I DID think of the mechanism you suggest previously. I’m not sure that the PR/RP reciprocity relationship that you note (which Barney Marriott emphasized to me! — as I bet he also did to you) necessarily holds, given my proposed dual AV nodal pathway mechanism ...

      Please look at the ADDENDUM ( + additional laddergrams) that I have just added to better address your astute comment! — :)

    2. Ken...

      I understand what you are saying, but this is how Mobitz himself defined the Mobitz I AV conduction. I think it holds. That being said, the impulse still arises in the SA node and still manages to enter the ventricles in a 3:2 ratio - however we look at it.

      Jerry W. Jones, MD FACEP FAAEM

  2. Can you help me with this one, Ken? I do not understand . How is beat B not conducted when it's so close to a QRS? I thought beat A would be the one not conducted, and beat B would be the start of a new cycle, it would still be a Mobitz I Weckenback.

    1. @ Hiago — Excellent question you ask — and NO definitive answer is possible unless an EP study is done! This is what makes it so fascinating to study this case. There are a number of features that I discuss above which may result in conduction that is actually different than what one might think. These include “concealed conduction” — with which physiologic events occur that can NOT be deduced from simply looking at the ECG. For example — each of the impulses from the underlying atrial tachycardia may conduct partially backward — so as to prevent conduct of the next atrial impulse downward. This phenomenon of “concealed conduction” is VERY COMMON in AFlutter, in which it is RARE that the flutter P wave closest to the QRS is the one that conducts. The AV node receives so many impulses — that it cannot normally conduct them all.

      In addition — there can be DUAL AV Nodal Patways — in which conduction properties are DIFFERENT from one to the other. One of the pathways may conduct better (faster) than the other — and there can be beat-to-beat switching on occasion from one pathway to the other. I suspect this whenever their is an abrupt change in PR interval from one beat-to-the-next, as we see here.

      So, in this case — please note in Figures 5 & 6 that I’ve drawn out 3 possible answers. Sometimes with complex rhythms — there may be MORE than a single possible answer. This depends on conduction properties happening at DIFFERENT LEVELS WITHIN the AV node — and we can always predict this without EP study simply based on the ECG.

      That said — I try to emphasize in my discussion that despite how complex this arrhythmia is — the regular atrial rhythm and resultant group beat in ALL 3 of my proposed laddergrams shows WENCKEBACH-type conduction — and THAT is the important “take home point.

      I hope the above makes sense! — THANKS again for your question! — :)


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