EXTRA COPY — ECG Blog #548 — More than One Family — EXTRA COPY —

I was sent the ECG shown in Figure-1. I was told that the patient had "palpitations", but was hemodynamically stable. Her admission diagnosis was DKA (Diabetic KetoAcidosis).

QUESTIONS:

• How do you interpret the initial ECG that is shown in Figure-1?
• Can you explain the rhythm?

A

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My "Quick" ( = Initial) Impression:

Unfortunately, the information I was provided on this patient is limited. Nevertheless — I found a number of features in this initial ECG to be fascinating and worthy of discussion. Below my initial "quick thoughts" on Figure-1:

• The QRS is wide with a morphology consistent with RBBB (Right Bundle Branch Block) conduction (ie, predominant positivity in lead V1 — with wide terminal S waves in lateral leads I and V6).
• P waves are present in the long lead II rhythm strip — and without yet measuring, they appear to be at least fairly regular. And at least in front of beats #2,4,6,8 — the PR interval appears to be fixed and normal (therefore indicating at least some sinus conduction, as well as confirming that the rhythm is supraventricular with RBBB conduction).
• PEARL #1: There is group beating! (in the form of repetitive shorter-then-longer R-R intervals). When group beating is seen in association with a regular (or at least almost regular) P wave rhythm in which there is at least some sinus conduction — this suggests some form of Wenckebach conduction.

Turning my attention now back to QRS morphology:

• The QRS complex in leads V1 and V2 begins with a wide Q wave. Whether this Q wave is the result of previous infarction, pulmonary hypertension, or simply represents a less typical RBBB morphology is uncertain. But it’s worthwhile to be aware that the characteristic triphasic rsR’ of RBBB in lead V1 is for whatever reason, not seen in today’s tracing (therefore potentially worthy of follow-up as we learn more about the case).
• The T wave in lead V1, and in other anterior leads is upright in association with RBBB conduction. As reviewed in ECG Blog #204 (See the ECG Video and the Addendum in this ECG Blog #204) — normally with RBBB conduction, the ST-T wave should be oppositely directed to the last QRS deflection in lead V1 (and much of the time, also in other anterior leads).
• Instead — the T waves are surprisingly tall and peaked in leads V2,3,4 in this patient who presents with DKA! 
• PEARL #2: Acute acidosis is notorious for increasing extracellular serum K+ values ==> We need to find out the serum K+ level! (ie, One wonders how tall and peaked the anterior T waves in Figure-1 might really have been if ECG changes of hyperkalemia are not being superimposed on the ST-T wave depression that we would otherwise expect with RBBB conduction).
• PEARL #3: As emphasized in ECG Blog #275 — "All bets are off" regarding arrhythmias (especially forms of AV block) in the presence of hyperkalemia — with the "good news" being that much (most) of the time, these hyperkalemia-induced arrhythmias resolve once serum K+ is corrected. 
• As a result, since today's patient is hemodynamically stable in association with the rhythm in Figure-1 — determining the precise etiology of this fascinating rhythm is far less important than treating the patient's DKA (with treatment of DKA having an excellent chance of restoring a normal sinus rhythm).

The above said — I thought it instructive to explore how to go about assessing today's complex arrhythmia.

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Looking Closer at Today's Rhythm:

As I often emphasize — the simple step of numbering the beats and labeling P waves is often of invaluable assistance for both determining if the atrial rhythm is in fact regular — and for facilitating determination as to whether P waves are (or are not) related to neighboring QRS complexes.

• RED arrows in the long lead II rhythm strip at the bottom of Figure-2 — confirm that an underlying sinus rhythm is present, albeit with a very slight variation in the P-P interval (ie, ventriculophasic sinus arrhythmia — that is so commonly seen in association with 2nd- and 3rd-degree AV blocks).

Figure-2: RED arrows highlight an underlying sinus mechanism, with no more than minimal variat

To facilitate looking even closer at the mechanism of today’s arrhythmia — I’ll focus on the long lead II rhythm strip (See Figure-3 below):

• As noted a moment ago — the P waves in front of beats #2,4,6,8 are all upright and manifest a constant PR interval. This tells us that at least these even-numbered beats — are all sinus-conducted with a normal PR interval.

Figure-3: Focusing on the long lead II rhythm strip …

Surprisingly (as shown in Figure-4) — BLUE arrows highlighting the P waves in front of beats #3,5,7 also manifest a constant (albeit much longer) PR interval.

• This suggests that these BLUE arrow P waves (despite their long PR interval) — are also in some way being conducted!
• Had the rhythm strip in Figure-4 been started a little bit earlier — Presumably, this would have shown another BLUE arrow P wave with a similar prolonged PR interval occurring before beat #1.

Figure-4: Since the PR interval preceding beats #3,5,7 is constant — these QRS complexes must be conducted (albeit with a long PR interval). 

This leaves us with the YELLOW arrow P waves that I highlight in Figure-5 — as the only P waves that have not yet been addressed.

• By the process of elimination (ie, since each of the 8 QRS complexes in Figure-5 have been accounted for) — these YELLOW arrow P waves can not possibly be conducting. 
• This defines today's rhythm as representing some form of 2nd-degree AV block — because some (but not all) of the “on time” sinus P waves are conducting — but others are not.
• That is, there are a total of 15 P waves in Figure-5.
• 8 of these P waves (highlighted by the RED and BLUE arrows) are conducting the 8 QRS complexes in this figure.
• The remaining 7 P waves (highlighted by YELLOW arrows) — are not conducted.

Figure-5: The YELLOW arrow P waves are not conducted.

A Laddergram is needed …

Today’s rhythm is complex! This tracing provides an example of one of the few times in which although I immediately recognized the general mechanism of today’s rhythm — I needed to devise a laddergram in order to prove my theory.

KEY Points: I want you to walk away with the following concepts:

• I review how to read and draw laddergrams in ECG Blog #188-LINK. Although it takes time and practice to become comfortable drawing laddergrams — Learning to read laddergrams is EASY (as I’ll show momentarily).
• It is not necessary to know how to draw laddergrams for optimal clinical management.
• Understanding how to read laddergrams improves our understanding of the mechanism of complex arrhythmias (and this may help in selecting optimal management options in selected cases).
• For interested readers — I provide over 100 examples of laddergrams (many with step-by-step analysis) in ECG Blog #188-LINK.

The “Quick” Answer to Figure-5:

We’ve already established that today’s rhythm manifests a supraventricular rhythm with RBBB conduction, regular P waves and group beating in which a number of “on time” P waves are conducting — but other “on time” P waves are not conducting.

• This establishes the rhythm as some form of 2nd-degree AV block — with the group beating strongly suggesting some form of Wenckebach conduction.
• As implied in the title of this ECG Blog #548 — there is more than a single “family” of PR intervals that are conducting. Specifically — RED arrow P waves are conducting with a normal PR interval — while BLUE arrow P waves are conducting with a much longer PR interval.
• The most logical explanation for why there is this much of a PR interval increment between the normal PR interval of RED arrow P waves vs the much longer PR interval of BLUE arrow P waves — is that there are dual AV Nodal pathways that alternate conduction of sinus impulses.

My proposed Laddergram …

XXXX 

Figure-6: XXXX

Figure-7: XXXX

Figure-8: XXXX

Figure-9: XXXX

Figure-10: XXXX

Figure-11: XXXX

Figure-12: XXXX

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More than One Possibility ...

What follows below goes way beyond-the-Core!

• My purpose in presenting the alternative laddergram that I illustrate in step-by-step fashion below — is solely to illustrate the principle that with complex arrhythmias — there will often be more than a single possible explanation! Without EP (ElectroPhysiologic) study — it will be impossible to know for sure which explanation is correct
• Knowing which explanation is the correct one is not important for optimal clinical management.
• Unless your goal is to "dive in" to the specifics of complex arrhythmia interpretation — Do not concern yourself with the "Hows" and "Whys" of drawing this alternative laddergram.

KEY Point: I want you to walk away with the following concepts:

• With complex arrhythmias — There will often be more than a single possible explanation.
• Knowing which explanation is the correct one is not important for optimal clinical management.
• While it admittedly took me some hours to draw this alternative laddergram — it took me no more than seconds to recognize the likely mechanism of today's arrhythmia — which is that there almost certainly are dual AV Nodal pathways.

Figure-13: XXXX 

Figure-14: XXXX

Figure-15: XXXX

Figure-16: XXXX

Figure-17: XXXX

Figure-18: XXXX

Figure-19: XXXX

XXXXXXX  

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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Sheikh mohsin55er@gmail.com  — 9/5/2026 via E-mail

— “More than one Family?” —

— Make this ANONYMOUS (Let Sheikh know by email when published! )

 

Thanks for your quick response. The patient had a serum K+ of 7.0 at the time of this ecg recording. I would love if you do an ecg blog on this and you have my full permission to do so. You can post it as anonymous without mentioning my name

 

THE CASE:

HyperK with bizarre rhythm:

Hi. I am attaching below this ecg of a 60 year old female who is admitted with DKA and complains of palpitations. Her Vitals are stable and there is no history of presyncope or syncope. Evaluation revealed hyperkalemia and correction of hyperkalemia resulted in the normalization of ecg changes. But i am not able to understand the rhythm here so could you please help figure out the rhythm ?
Thanks’’

MY REPLY:

HI Sheikh. This is very interesting indeed. First — Was this ECG done while the patient was hyperkalemic? If so — do you know how high the serum K+ was at this time?

 

KEY POINT ­— All bets are off when you have an arrhythmia with HyperK+ — because patients “do not obey the rules” when there is HyperK — and much (most) of the time — a normal rhythm resumes once HyperK is corrected (as happened in your case!

 

I spent some time working on this — and from the “pretty” picture I am sending you — You might guess that I’d love to do an ECG Blog of this case. May I have your permission to do so?

 

I like to acknowledge colleagues who send me tracings. I’m happy to put in your name and the city and country from where you are from — OR ­— if you prefer, the case can be anonymous. Just let me know. If you want me to put your name — tell me how to write it (and also send me the city and country from where you are from).

 

There is more than 1 possible solution to this — but the simplest answer to what is going on is if there are dual AV nodal pathways. One of the pathways has faster conduction (a shorter PR interval) which I drew in PINK. 

 

The other pathway is slower = GRAY.

 

In addition to dual AV nodal pathways, there is significant AV block! This may be 4:1 AV block. So you can see from the laddergram how I propose that conduction switches back and forth from one conduction pathway to the other.

 

We KNOW there IS conduction — because we have repetitive PR intervals. And the BEST clue to the presence of dual AV nodal pathways is when there is a big “jump” in PR interval from one beat to the next.

 

Again — this is clearly a result of the HyperK — with the proof of that being how normal sinus rhythm resumed after HyperK resolved.

I hope the above makes sense! Let me know if I can write this up as an ECG Blog!

 

THANKS —  Ken

 

P.S. I’ve included this article on dual AV nodal physiiology — including Table-1 from this article which highlights the need to think of this when you see “2 families” of PR intervals! — :) 

 

P.P.S. I initially thought this was dual-LEVEL AV block out of the AV node ­— but this does not make a “pretty” laddergram. Still could be both dual AV nodal pathways AND dual-level AV block — but that makes for a much more complicated laddergram !!!! — So I tried again to get dual-level AV block to work, but I could not ... I was unable to draw a reasonable laddergram !!!