EXTRA COPY — ECG Blog #536 — Why 2 Morphologies? — EXTRA COPY

The ECG in Figure-1 was sent to me for my thoughts. Initially I had no clinical information.

QUESTIONS:

• What is the rhythm?  
• Why are there 2 different QRS morphologies?
• What is the likely underlying cause of this rhythm?

Figure-1: The initial ECG in today's case — initially sent to me without clinical information. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The overall rhythm in Figure-1 appears to be regular with obvious QRS widening — and a ventricular rate of just under 100/minute (ie, with an R-R interval just over 3 large boxes in duration).

• There are 2 different QRS morphologies.
• Although the R-R interval varies slightly — I attributed this to uncertainty regarding where the QRS begins in some leads.
• P waves are absent. The only suggestion of atrial activity that I saw is possible retrograde P waves in some chest leads.

PEARL #1: This tracing emphasizes the important concept that, "12 leads are Better than One" — because if you only looked at leads I and V1 (and/or at leads V2,V3,V4) — it would be easy to think the rhythm was simply AIVR (Accelerated IdioVentricular Rhythm). 

• Instead, as shown in Figure-2 — there clearly is an alternating QRS morphology that is seen every-other-beat.

Figure-2: For clarity — I've numbered the beats in the limb leads. 

What is Going On?

Based on what I saw in Figure-2 — I thought the following:

• There is a regular wide QRS rhythm at ~95/minute — but without clear sign of atrial activity. QRS morphology is not consistent with any known form of conduction block — so this most likelly represents a ventricular rhythm.
• Many leads strongly suggest that QRS morphology alternates every-other beat — but without explanation as to why this may be so (ie, There are no P waves that may be conducting — and no significant variation in R-R intervals that might be producing a rate-related effect).
• BOTTOM Line: I was left with the conclusion that the rhythm in Figure-2 most likely represents the rare arrhythmia known as BiDirectional VT.

Semantics:

I've previously reviewed the concept of "AIVR" (Accelerated IdioVentricular Rhythm) — which is a slower form of "VT" (See ECG Blog #108).

• Technically, AIVR is not "VT" — because the ventricular rate is not ≥100/minute. But the ventricular rhythm known as AIVR clearly is faster than the usual ventricular "escape" rate, which normally is between 20-40/minute ==> the designation preferred by many is that AIVR represents a form of "slow VT".
• As emphasized in Blog #108 — the importance of recognizing AIVR depends on the clinical setting in which it occurs (ie, AIVR often occurs as a reperfusion arrhythmia in patients who have had a recent MI).
• PEARL #2: Whenever I see AIVR — I carefully consider the possibility that the patient may have had a recent MI that could have passed undetected.

What is BiDirectional VT?

I presented a case of bidirectional VT in ECG Blog #436:

• As discussed in ECG Blog #231 — bidirectional VT is a special form of VT, in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT is distinguished from PMVT (PolyMorphic VT) and from pleomorphic VT — because a consistent pattern of alternating QRS morphology is seen every-other-beat throughout the VT episode.
• Typically with bidirectional VT — there are alternating longer-then-shorter R-R intervals that correspond to the alternating QRS morphology. That said — as was seen with the case I presented in ECG Blog #436 (as well as with today's case) — QRS widening with uncertainty in some leads as to where the onset of the QRS begins may render it difficult to distinguish subtle alternation in R-R interval duration from what otherwise appears to be a fairly regular ventricular rhythm.
• Technically — this raises the question as to whether today's rhythm might simply represent AIVR with alternating exit sites accounting for the alternating QRS morphology (as I allude to in my discussion of ECG Blog #231). While fully acknowledging these theoretical considerations — My impression of today's rhythm remains unchanged = the most likely explanation for the rhythm in Figure-1 is bidirectional VT.

PEARL #3: There are a limited number of causes of bidirectional VT. As reviewed by Almarzuqi et al (Vasc Health Risk Mgmt 18:397-406, 2022) — Potential Causes of Bidirectional VT include:

• Digitalis toxicity.
• CPVT (Catecholaminergic PolyMorphic VT).
• Acute myocardial ischemia.
• Familial hypokalemic periodic paralysis.
• Cardiac Sarcoidosis.
• Primary Cardiac Tumors and/or Cardiac Metastasis.
• Andersen-Tawil Syndrome ( = Long QT Syndrome, Type 7).
• Acute Myocarditis.
• Certain drug overdoses (Aconitine poisoning, severe caffeine poisoning).

PEARL #4: Given how rare bidirectional VT is — the 1st thing to do when contemplating this diagnosis is to consider whether the patient might have one of the above-listed potential causes of this rhythm.

• In years past — Digitalis toxicity used to be the most common cause of bidirectional VT. This no longer appears to be true — given the overall reduced use of Digoxin (and in those cases in which Digoxin is still prescribed — toxicity is much less common nowadays because dosing of this drug is so much less than it used to be). 
• With the exception of myocardial ischemia and myocarditis — the other entities listed as potential causes of bidirectional VT are rare (which explains why bidirectional VT is rare).
• To Emphasize: In my experience — bidirectional VT is not a common manifestation of myocardial ischemia. But the PEARL is that ischemia/infarction should always be considered whenever you contemplate a diagnosis of bidirectional VT.
• Clinically: The BEST treatment of bidirectional VT — is to identify the causative condition in the hope that there may be effective treatment of that condition.

Follow-Up in Today's CASE:

It turns out that today's patient was a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain). The patient's condition rapidly deteriorated with resultant cardiac arrest.

• A complicated course followed, fortunately with successful ROSC (Return Of Spontaneous Circulation) — and, at the earliest opportunity cardiac catheterization was performed.

QUESTION:

• What do you think cardiac cath showed?  

HINT #1: To facilitate assessment of QRST morphology for the 2 "families" of QRS complexes — in Figure-3, I've enclosed beat #3 and beat #6 within the BLUE and RED dotted rectangles. 

Figure-3: To facilitate assessment of QRST morphology — I've enclosed beats #3 and #6 within BLUE and RED dotted rectangles.

HINT #2: To facilitate concentration on ST-T wave morphology even more for the 2 "families" of QRS complexes — I've shaded out the remaining beats in the limb leads.

Figure-4: I've shaded out the remaining limb lead beats.

Answer:

Today's rhythm is bidirectional VT. This means that there are no normally conducted QRS complexes — but instead, all beats on today's tracing are ventricular in etiology.

• PEARL #5: Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.
• That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction. This is precisely what we for the PVCs in ECG Blog #359.
• NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCs — See My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

Applying the advanced concept from PEARL #5 to today's tracing — the shape of ST-T wave morphology in Figure-5 is clearly disproportionate and "off" from what we'd expect for both QRS families. Specifically:

• The QRS family of odd beats in Figure-5 (illustrated by beat #3) — shows inappropriate ST elevation in the inferior leads with reciprocal ST depression in lead aVL (the RED and BLUE arrows in these leads).
• More subtle, but still evident — the QRS family of even beats (illustrated by beat #6) — shows inappropriate ST elevation in each of the inferior leads (which is especially apparent in lead II given tiny size of the QRS in this lead).
• Both families of QRS complexes show a disproportionately increased amount of ST depression in the mid-chest leads of Figure-5 — with the BLUE arrows in leads V2,V3,V4,V5 of the even-numbered beats highlighting the obvious abnormality of this finding by the marked amount of horizontal (ledge-like) ST depression.

CASE Conclusion: 

Today's ECG illustrates a case of bidirectional VT that developed as a result of acute infero-postero OMI. This was confirmed on cardiac catheterization that showed multi-vessel disease with acute total occlusion of the LCx (Left Circumflex) coronary artery.

Figure-5: Both families of QRS complexes suggest that the cause of this bidirectional VT is acute infero-postero OMI. 

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Acknowledgment: My appreciation to Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan) for the case and these tracings.

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EXTRA COPY — ECG Blog #535: A "Fluttering" ECG - EXTRA COPY

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

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Figure-2: XXXXX 

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for allowing me to use this tracing — and to Ahmed Marai (from Anbar, Iraq) for drawing my attention to this case.

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From Ahmed:

Hello Dr. Grauer — I came across this ECG on facebook, which belongs to to a 50-year-old male, hypertensive and diabetic, recorded while he underwent a routine check up.

This is the link to the poster

https://m.facebook.com/story.php?story_fbid=pfbid0wAJTSLDFuYExamcgrFy3RaR1DzcE6xbef7jf77Pdzy8htmBamYTTG5EJNSM2H13zl&id=61563573262961

This is my interpretation:

A 12 lead ECG, unlabelled calibration and speed, but it looks standard.

Ventricular rate: around 62-66 bpm

Rhythm: regular narrow complex rhythm

Axis: within normal range

No obvious P waves, however, there are regular waves between the QRS complexes, which run at around 273bpm, it appears in all the 12 leads and looks much taller in the chest leads compared to the limb leads.

Regarding QRS complex, it is narrow, with very subtle irregularity. In the chest leads, the QRS is dominantly positive (no obvious S waves), and has high voltage in V2-V5.

 

No obvious ST-T changes, and the QT intervals cannot be determined accurately.

Clinical impression: The regular waves seen between the QRS complexes are probably flutter waves, it runs at around 273bpm, and since ventricles beat at around 66bpm, then it is probably AFlu with 4:1 AV conduction. However, these flutter waves are atypically tall in the chest leads.

The high voltage of R waves in chest leads, is suggestive of possible LVH, the history of hypertension may support the possibility of LVH. The S waves are are not obvious in chest leads, but they are possibly present but are cancelled on the paper by the tall flutter waves. 

However, artifact should be suspected and excluded.

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My thoughts: At the beginning I thought this is an obvious atrial flutter with 4:1 av conduction, however, when I noticed the size of flutter waves in the chest leads, I thought this is unusual. 

I saw many people in the comments say, Artifact !! 

If this was an artifact coming from one limb, then one of these leads ( I, II or III ) should be spared. If the artifact is coming from 2 limbs, then it should be chaotic and not regular like this one.

If this was an artifact, then it is probably coming from the patient torso, maybe the patient was dancing while recording the ECG. This may explain why these waves are taller in the chest leads compared to the limb leads, as they are closer to the torso. Excited to hear your ideas on this ECG — Ahmed

MY REPLY:

Hi. I basically AGREE with you!

I’ve attached what I wrote on the FB site.

I also wrote to Cardiology Notes, asking them for follow-up! (They have great cases — but often don’t tells us what happened unless specifically asked!

: ) Ken

P.S. Another clue should be looked for — which is whether the DISTANCE between the closest deflection and the QRS is equal !!! Be SURE to use your calipers when looking for this. Usually (although not always) — IF the ventricular rhythm is regular — then the distance between the closest deflection and the QRS should be THE SAME! If it is not — and if the R-R interval remains constant — then this implies that NONE of the deflections are conducting!

But in this case — there is a very slight-but-real difference in the “PR” interval across lead II ==> IF the R-R interval would stay precisely equal, then if this was Aflutter — it implies complete AV block (which is possible but not common).

So — We wonder if this patient has a tremor, or perhaps something going on in his chest …

CARDIOLOGY NOTES (on Facebook !!! )

Hello Prof Ken. It was ARTIFACT! The patient is diagnosed with drug-induced Parkinsonism !!!!

EXTRA COPY — ECG Blog #537 — What is the Rhythm? — EXTRA COPY

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

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Figure-2: XXXX

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Figure-3: XXXX

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Figure-4: XXXX

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Figure-5: XXXX

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Acknowledgment: My appreciation to Bashiruddin Sayeem  (from Chittagong, Bangladesh) for the case and this tracing.

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THE CASE: Dear sir, this is an EKG of a 60 years old diabetic lady presenting with SOB. Is this LVH with strain, LAHB, RBBB?

MY REPLY:

Hello Bashiruddin — This is AIVR (or "or slow VT") at ~120/minute!

 

The KEY is to look at the long lead II — and RED arrows show 2 places were we KNOW there are 2 consecutive P waves (which are upright in this long lead II, therefore 2 consecutive sinus P waves. Now set your calipers at this P-P interval (between 2 consecutive RED arrows — and the PINK arrows show partial deflections that we SEE, which we KNOW must be underlying "on time" sinus P waves. The WHITE arrows then show you where additional "on time" sinus P waves lie — telling us there is an underlying sinus tach.

 

Thus there is AV dissociation — with beat #17 being a CAPTURE beat — and beats #6,7 and 16 being FUSION beats — all of which proves that the underlying rhythm is an isorhythmic AV dissociation by "usurpation" by an AIVR at 120/minute that is slightly faster than the underlying sinus tach! (The upright R wave in V1 is not "RBBB" — but indication of the ventricular focus!)

 

Note that the QRS IS actually wide (The tracing is slanted — but the WHITE line that I drew parallel to the heavy grid line shows that what looks like "narrow" beats in the long lead II are actually WIDE (because there is an initial small, upright r wave before the deep S waves)

 

Within the dotted BLUE rectangle we see the capture beat — that shows marked LVH with very deep, symmetric (ischemic) T wave inversion in leads V5,V6 — and also in lead aVF. That said, I don't acute ST elevation in the leads in which I am able to assess — so from what I can see, probably no acute STEMI ...

 

Now this 60 yo woman presented with SOB — so the KEY is to find out WHY she is SOB (ie, heart failure, pneumonia) — and then to treat that — and possibly (hopefully) the underlying "slow VT" will resolve!

 

This would be a SUPERB CASE for an ECG Blog! May I have your permission to use this case! I will acknowledge you as I have in the past (See attached). Let me know what happens! BEST — :) Ken

 

Bashiruddin REPLY:

Thank you sir Please feel free to use it in your ECG Blog.

EXTRA COPY — ECG Blog #538 — An Unusual Finding — EXTRA COPY

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

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Figure-2: XXXX

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Figure-3: XXXX

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With this laddergram — YELLOW arrows are retrograde P waves. Although subtle, the RP' interval is increasing (most easily appreciation by looking at the RP' interval before the retrograde Wenckebach conduction is blocked (darker BLUE double arrows). Note subtle increase in the angle of retrograde p waves that are maximal just before the P wave is dropped (BLUE lines in AV Nodal Tier) — and then the RP' interval shorts again beginning with beat #13.

I must cite the following as PROOF that retrograde Wenckebach confirms VT (with exception of Junctional tach with wide QRS)

— Roig et al — Circulation 153:1171-1173, 2026

https://www.ahajournals.org/doi/epub/10.1161/CIRCULATIONAHA.126.080138

AWAIT Khaled to confirm acknowledgment

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Acknowledgment: My appreciation to Khaled Elashiq, Hasan Al-Qassim and Mahmoud Al-Rahmoun (from Syria) for contributing this case.

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Case from Khaled Ash from Damascus Syria

— "An unusual finding ..." —

— NOTE — This was a very complex case, but I will only give a brief 1-line history — saying this is a young adult complaining of frequent palpitations

— The Dx is Fascicular VT (NOT RBBB aberrancy given atypical features)

— Me to ask, "How certain are you of the diagnosis? HINT: Is there atrial activity? If so — Is there something unusual about atrial activity?"

— Quote article — Retrograde Wenckebach in the setting of a persistently regular WCT is very strongly suggestive of VT (even more so than AV dissociation) — since if the rhythm was supraventricular, it would change the R-R interval!

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Hard to believe this patient was markedly hypothyroid!

That said — I want to make an ECG Blog of this case — and I've spent a few hours fixing up the tracing, since the original was rotated and missing a complex in lead V3. I'll add a laddergram.

It is RARE to see VT with retrograde Wenckebach like this — and as per the attached article, seeing this is diagnostic for VT (with the very rare exception that you could theoretically see retrograde Wenckebach in junctional tach with a wide QRS from BBB).

I'm happy to acknowledge both you and your colleague from who this case comes. That said — I don't feel obligation to necessarily acknowledge your colleage — since I have totally redone the tracing (attached) using PMcardio, and since I will NOT be using clinical details of the case (I'll only give a VERY simple 1-line history). I am HAPPY to acknowledge you if you like (Khaled Ash — from Damascus, Syria) — or I could make the case anonymous, as you prefer.

I've done lots of Fascicular VT cases — so the main reason for doing an ECG Blog is the rare example of retrograde Wenckebach that essentially PROVES this is VT (I suspect many readers won't know what to do with the concept of retrograde Wenckebach.

It will be a while before I publish this — but in any case, I'll let you know when I do. Just LET ME KNOW what you prefer. THANKS — :)

EXTRA COPY — ECG Blog #534: What is or is not Conducting? — EXTRA COPY

I was sent this ECG with the question, "What is or is not conducting?" Unfortunately — no clinical information was available. 

QUESTIONS:

• What is the rhythm?
• There are multiple interesting ECG findings on this tracing with regard both to the rhythm, as well as to the 12-lead ECG. How many of these findings can you identify?
• Do you need to draw a laddergram in order to interpret this tracing?

Figure-1: Today's ECG that was sent to me. (To improve visualization — I've digitized the original ECG using PMcardio).

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NOTE: This is an extremely challenging ECG. Regardless of how far you got with your interpretation — there is much to learn for providers of all experience levels.

• Confession: My initial impression for the rhythm was wrong.
• PEARL #1: I can figure out 90-95% of complex rhythms within seconds without the need to draw a laddergram. That said — it's important to appreciate that there will always be some rhythms for which even arrhythmia specialists may not be able to determine a precise etiology without aid of a laddergram. Today's case is one of those rhythms.
• That said — You do not need a laddergram in today's case in order to make a time-efficient diagnosis of the essentials needed for appropriate initial management. As a result — I divide my discussion into 2 Parts: i) Detailed discussion of multiple interesting findings in today's ECG (including my proposed laddergram for the etiology of the rhym); — and, ii) The steps I used to expedite time-efficient assessment sufficient for appropriate clinical decision-making.

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Part 1: Details of the many Interesting Findings:

As always, I like to start with assessment of the rhythm — for which I favor the Ps, Q's, 3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3Rs).

• NOTE: It does not matter in what sequence we assess the Ps, Qs and 3Rs. As a result — I do not always look first for P waves. Instead — I often start with whichever of the 5 KEY parameters is easiest to assess.
• Focusing on the long lead II rhythm strip at the bottom of the tracing — We should be able to appreciate that the rhythm is not Regular. But because of the relatively small difference between R-R intervals — it could be easy to mistake this tracing for a regular rhythm. Instead, there is a regular irregularity to the rhythm ( = group beating in the form of alternating longer-then-shorter R-R intervals).

PEARL #2: Use of calipers is essential for interpretation of complex rhythms such as this one. The simple fact is that with minimal practice — Use of calipers greatly speeds up and increases the accuracy of your interpretation.

• In Figure-1 — Longer R-R intervals ( = R-R intervals between beats #1-2; 3-4; 5-6; and 7-8) — alternate with shorter R-R intervals ( = R-R intervals between beats #2-3; 4-5; and 6-7).
• PEARL #3: Practically speaking — this finding of alternating longer-then-shorter R-R intervals is too consistent in Figure-1 to be due to chance. This means there is "group" beating — which should always suggest the possibility of some form of Wenckebach conduction (ie, There are other causes of group beating not due to Wenckebach, such as atrial bigeminy with either blocked or conducted PACs. That said — it is helpful clinically to always consider Wenckebach conduction whenever you realize that there is a repetitive pattern of beats).

Continuing with the Ps, Qs and 3Rs ... 

• The QRS in Figure-1 is intermittently wide. Depending on which lead(s) you used to assess QRS width — it could be EASY to overlook the fact that some QRS complexes are wide, while others are narrow.
• PEARL #4: 12 leads are better than one! Appreciation that some QRS complexes are wide while others are not is best seen in lead V1 — in which beat #5 (which corresponds to the 1st beat seen in lead V1) is wide with  the appearance of RBBB conduction. On the other hand — beat #6 ( = the 2nd beat in lead V1) is narrow! (See Figure-2).
• Armed with the knowledge that beat #5 in Figure-2 is wide, but beat #6 is not wide — We can see that in the long lead II rhythm strip, a terminal S wave is present at the end of every-other-QRS complex (ie, a terminal wide S wave is seen at the end of the QRS of each odd-numbered beat = beats #1,3,5 and 7).
• PEARL #5: The fact that the QRS of each of the even-numbered beats is narrow — suggests that the longer preceding R-R interval before beats #2,4,6,8 allowed enough additional time for recovery of right bundle branch conduction (ie, that the reason for intermittent QRS widening is a form of rate-related RBBB block).

Figure-2: I've added BLUE arrows to highlight that every-other beat is wide (as per the wide terminal S wave in beats #1,3,5,7).

P waves are present!

I've highlighted with RED arrows in Figure-3 that an underlying regular atrial rhythm is present.

• You may or may not have initially seen P waves in all of the places where I've added RED arrows — because some of the P waves are partially hidden within the end of the QRS or within peaked T waves.
• PEARL #6: Use of calipers allows us to very quickly verify where all of the P waves lie. For example — we definitely see P waves under the 3rd and 4th RED arrows — and if we set our calipers to the P-P interval between these 3rd and 4th red arrows, we can "walk out" where the partially hidden P waves lie throughout the rest of the tracing.
• PEARL #7: I find the simple steps of numbering the beats and labeling the P waves (with arrows) — tremendously facilitates the next step in our assessment of the rhythm, which is to determine if P waves are Related to neighboring QRS complexes?
• NOTE (Beyond-the-Core): If you carefully measured the P-P interval in Figure-3 — You may have noted slight variation. Technically, this is the result of a slight ventriculophasic sinus arrhythmia — which is a common phenomenon when there are more P waves than QRS complexes. But for practical purposes — We can say that the underlying atrial rhythm is essentially regular.

Figure-3: I've added RED arrows to highlight the regular atrial rhythm.

Are P Waves Related to Neighboring QRS Complexes?

The KEY step for determining if some form of AV block is present — is to determine if at least some P waves are Related to neighboring QRS complex?

• To do this — I survey the entire rhythm strip, looking to see if any PR intervals repeat? Once again — calipers greatly facilitate (and expedite) this step, since calipers enable us to immediately tell if PR intervals are or are not varying in duration.
• In Figure-4 — the PINK arrows highlight identical (albeit prolonged) PR intervals in front of beats #1,3,5,7.
• PEARL #8: The fact that at least some of the PR intervals in today's tracing repeat tells us that at least some beats are being conducted to the ventricles!

Figure-4: Pink arrows highlight P waves with identical (albeit prolonged) PR intervals that repetitively occur throughout the long lead II rhythm strip (ie, before beats #1,3,5,7).

Are Any More P Waves Conducting?

At this point — we know from Figure-4 that beats #1,3,5,7 are all being conducted with a long PR interval.

• As we continue to look at the PR intervals preceding the remaining beats — it turns out that the shorter PR intervals highlighted by RED arrows in Figure-5 are also all identical (equal to 0.16 second). 
• This tells us that each of these RED arrow P waves are also conducting to the ventricles.

Figure-5: RED arrows highlight P waves identical PR intervals

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Part 2: Putting What We Know Together ...

In Figure-6 — I've put together what we've worked out so far in the context of the 12-lead ECG.

• There is group beating in the form of a regularly irregular rhythm with alternating shorter-then-long R-R intervals.
• There is an underlying regular atrial rhythm (the colored arrows in Figure-6).
• Many of the P waves are conducting — albeit with 2 different PR intervals (highlighted by RED and PINK arrow P waves).
• But there are many more P waves than QRS complexes — so lots of P waves are not conducting ( = the YELLOW arrow P waves are not conducting).
• There are 4 places in the long lead rhythm strip where consecutive P waves are not conducting ( = consecutive YELLOW arrows between beats #1-2; 3-4; 5-6; and 7-8).

Impression:

• There is AV block — because we have a regular atrial rhythm, but not all of the on-time P waves are being conducted.
• This is not complete AV block because: i) The ventricular rhythm is not regular (whereas with complete AV block — there usually will be a regular ventricular escape rhythm); and, ii) The fact that the RED and PINK arrow P waves are conducting means that AV block can not be complete.
• Since there is AV block that is not "complete" — the rhythm must be some form of 2nd-degree AV block. And since there are consecutive on-time P waves that fail to conduct — this is a high-grade form of 2nd-degree AV block.
• The 2nd-degree AV blocks are divided into the Mobitz I and Mobitz II forms. Detailed review of these concepts can be found in ECG Blog #62 and ECG Blog #465 (with Video Review of these concepts in the Addendum). Reasons why today's AV block is almost certain to be some form of Mobitz I ( = AV Wenckebach) are: i) Mobitz I is much more common than Mobitz II; — ii) The QRS complex of conducting beats is intermittently narrow — whereas the QRS is almost always consistently wide with the more severe Mobitz II form of 2nd-degree AV block; — and, iii) There is group beating — and as noted earlier in PEARL #3 — the presence of group beating in association with a regular atrial rhythm with some beats being conducted, but others not conducted is often the result of AV Wenckebach ( = Mobitz I).
• BEGIN- why Wencke = ? recent inf-post MI? on 12 lead, inverted T waves!

the above conclusions i reached in just a few minutes .... 

now the laddergram discussion

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Acknowledgment: My appreciation to Omar Hassan Seddik (from Mansoura City, Egypt) for submission of today's case with these tracings.

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Omar Hassen — FB Messenger (5/3/2026)

This ECG was sent to me by a friend he was asking about the rhythm unfortunately he provided no information.

— "What is or is not Conducting?" —

My impression Sinus rhythm/tachycardia (black arrows) DDX AT, RAA alternating Wenchebach periodicity (multi-level AVB> 3:2Wenchebach+2:1 AVB, intermittent RBBB (red arrows), probable posterior wall OMI (blue arrows), LQRSV in V4 thru V6 (probably due to large posterior infarction/myocardial stunning). What is your impression?

Hello Omar. You have made EXCELLENT progress in assessing this tracing — and your conclusions are good ones! That said — My thoughts are the following. Again, to emphasize that you are doing VERY GOOD in recognizing important findings — but if you want to get into complex rhythms such as multi-level AV block — then you will never get beyond the "guessing game" until you begin to do the following. To emphasize — it takes a good while to get beyond the level where you are — but you need to understand WHY this is multi-level block (and I do not see that yet explained).

— So, now that you are getting sophisticated in your rhythm interpretation: i) You should ALWAYS send me a copy of the ORIGINAL tracing before you mark it up with lines. Always SAVE a copy of the original.

— You need to ALWAYS number the beats. Otherwise there is NO intelligent way to talk about which beat is doing what.

— You need to use CALIPERS. Maybe you did — but I do not see you mentioning WHY this is multi-level AV block. The ANSWER is that the PR interval for ALL of the RED arrow P waves is the SAME! So the underlying rhythm is ATach — and we have group beating with definite conduction of the RED arrow P waves = Wenckebach conduction.

— You make a GREAT diagnosis recognizing dual level Wenckebach with 3:2 and 2:1 conduction !!! — but the reason you KNOW this is that all the PINK arrow P waves also have a constant PR interval (that is longer than the RED arrow P waves).

— BOTTOM LINE — I also suspected dual-level AV block — but the reality is that IF you really want to get good at recognizing complex AV blocks like this — then you NEED to begin to draw laddergrams. I could NOT be certain of the mechanism of this complex rhythm UNTIL I was able to draw a laddergram that made sense.

So if you want to learn how to draw laddergrams — GO TO — https://ecg-interpretation.blogspot.com/ — Power Point is BY FAR the best program to use, and I give you a STENCIL for laddergrams, as well as 100+ examples, many with step-by-step instructions. Now it takes time to get good at drawing laddergrams — but that's the ONLY way to really get good at figuring out the precise mechanisms.

Otherwise — You can get better than most at recognizing complex mechanisms — but without drawing a laddergram that is reasonable — you need to number beats, and measure intervals and know WHY certain beats are conducting (ie, the RED and PINK arrow P waves) — and then you can figure out why certain beats are not conducting (the WHITE and YELLOW arrow P waves) even if you do not take the time to draw a laddergram (which is MUCH BETTER than most cardiologists do!)

As to the 12-lead — I am less sure of the "culprit" — and I'm not sure if there is post. vs ant. MI as the cause. There is RBBB (as you say) — but the T wave inversion in V1-thru-V4 is MORE than I'd expect for simple RBBB! If the T wave inversion in the inf. leads was due to recent Inf. MI, now with reperfusion — then I'd expect upright T waves in the anterior leads if this was also a post. MI, now with reperfusion. Instead we see deeper anterior T wave inversion, and also ST elevation in aVL — so I suspect an LAD culprit — with the ST flattening in V5,V6 suggesting multi-vessel disease — BUT I AM NOT AT ALL CERTAIN of this. With multi-vessel disease — you can get unusual findings (due to different hard-to-predict collateralization patterns).

BOTTOM LINE — Nice interpretation by YOU! I might want to use this for an ECG blog if you can: i) Send me a copy of the ECG without your markings; ii) Find out WHERE your friend saw this tracing? (His case? or from the internet? and if from the internet — what is the SPECIFIC LINK on the internet? And can I have his approval to use the case? And I'm happy to acknowledge you and/or him if I publish this).

Please NOTE — I have taken a lot of time to draw the laddergram and suggest to you the next steps to really get good at interpreting complex arrhythmias — because you seem to be very interested in many of these ECGs that you continue to send me. But if I do not see you numbering beats and describing specific measurements of various intervals in the future — I will be much briefer in the future with my descriptions. It's up to you as to how good you want to get. I'm happy to take the time to explain details — but only if you take equal time in applying the measurements I describe. Otherwise — I'll always answer your queries — but I'll be much briefer in my explanations.

OMAR REPLY:

I really appreciate your efforts and your time Professor. And next time with such rhythm I'll draw laddergram. And i will ask him where he got this ECG whether from internet or it is one of his cases . Thank you again Sir.

MY REPLY: 

My pleasure Omar! And now that I take another look at this — I need to REDRAW my laddergram! I initially did not think that the YELLOW arrows were conducting because the PR interval before beat #8 in the long lead II looked too short — BUT when you look at the 12-lead — beat #6 (in lead V1) IS conducting with a NORMAL QRS (the longer pause before beat #6 allowed recovery, so that we no longer see the RBBB that was present for beat #5 in lead V1 — so this is still Wenckebach — and probably still dual level — but I need to relook at this tracing and "play" with another laddergram! It's a GREAT case that I'd LOVE to write up as a BLOG. I'll let you know what I come up with.

 

Overall — I can figure out 90+% of rhythms — but occasionally, I need a laddergram to figure out the most plausible mechanism for some complex rhythms — and that is why it will be GREAT for YOU to get good with laddergrams! — :)

 

MY NEW REPLY - after REDOING LADDERGRAM:

Hello Omar. I touched up the 12-lead and redid the laddergram. My oversight with the 1st laddergram that I sent you — perhaps the artifact threw me off?  

 

— So — the PR interval for the RED arrow P waves is NOT too short. It is 0.16 second — and as you can see, the PR interval in front of beats #2,4,6 and 8 are all the same (0.16 second = RED arrow P waves).

 

— The PR interval for the PINK arrow P waves are all the same ( = 0.32 second).

— Note that every other QRS is a little bit narrower! This is easiest to see in lead V1 for beats #5 and #6 — in which beat #5 in V1 conducts with RBBB aberration. Because there is a slighty longer R-R interval before beat #6 — there is time to recover, and beat #6 is narrow (again easiest to see this in lead V1 — but the SAME thing occurs for beats #2,4 and 6, all of which are conducted normally — vs beats #1,3,5 which all conduct with RBBB aberration. (I don't see much of a difference in QRS morphology for beats #7 and 8 ...).

 

— So for the laddergram — it is the same conduction ratios as for the earlier version that I made = Dual-level Wenckebach conduction with 3:2 and 2:1 conduction — but I think this new laddergram looks much better than my 1st version (much smoother and more gradual development of Wenckebach which looks much more realistic). Sometimes it just takes a little extra time to put everything together.

 

So it is OK if you cannot get ahold of your friend. As you can see — the tracing looks completely DIFFERENT than the original after my "touch-ups" — and since there is "No history", I am not infringing on anyone's case. So I do NOT need any more information about what happened!

 

So I plan to write this up as an ECG Blog (it may be ~2 months before I publish it). I'll be glad to acknowledge you if you like ( = Omar Hassan Seddik from Mansoura City, Egypt) — or the case could be anonymous — JUST LET ME KNOW! I plan to show step-by-step development of my laddergram (so there will be over 10 Figures in all) — but I'm attaching the 2 key ones to explain the above.

 

Great case! — :)