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).

============================= 

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.

=============================

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

=============================

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

XXXXXXX

Figure-6: XXX

XXXXXXX

Figure-7: XXX

Figure-8: XXX

Figure-9: XXX

XXXXXXX

Figure-10: XXX

Figure-11: XXX

Figure-12: XXX

Figure-13: XXX

Figure-14: XXX

Figure-15: XXX

XXXXXXXX  

= = = = = = = = = = 

==========================================

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

==========================================

XXXXX 

 

 

==================================

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! — :)

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

 XXXX

XXXXXXX

Figure-1: The initial ECG in today's case — obtained from 60-something year old patient. (To improve visualization — I've digitized the original ECG using PMcardio).

XXXXXXX 

Figure-2: The

XXXXXXX

Figure-3: The

XXXXXXX

Figure-4: The

XXXXXXX

Figure-5: The

XXXXXXX 

XXXXXXX

XXXXXXX

XXXXXXXX

Figure-6: I have adapted this figure from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog. It explains how "polymorphic" VT might arise from a single venricular focus, rather than from multiple sites in the ventricles (See text).

 

 

================================== 

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

==================================

Fardeen Baray — FB Messenger (5/9/2026)

ACKNOWLEDGE: 

Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan)

— I must add possibility of multiple exit sites = Blog #231 !!! —

— "Why 2 Morphologies?" —

NOTE — I think I will only show the initial ECG!

 

THE CASE:

Hello sir Hope this message finds you well This ECG has been sent to me without saying anything about patient symptoms Could please comment on this tracing. The following in my comment The patient history will help us a lot in dx. This is an interesting and electrophysiologically complex ECG. Clinically correlated history and serial ECGs would be very helpful. The ECG appears to show a regular wide-complex rhythm with a bigeminal/alternating pattern and no clearly identifiable sinus P waves. Differential considerations include AIVR, accelerated junctional rhythm with underlying RBBB, or competing junctional and ventricular pacemakers with fusion phenomena. The inferior ST elevations raise concern for acute inferior ischemia/reperfusion, which would support AIVR as a likely mechanism.

MY REPLY:

Hi. Fascinating! Clearly alternating polarity in this fairly slow ventricular rhythm. The only suggestion of atrial activity that I see is possible retrograde P waves in some chest leads. To me — this looks like BiDirectional VT! — a RARE rhythm — but can occur! See my ECG Blog #436

 (https://ecg-interpretation.blogspot.com/2024/06/ecg-blog-436-bigeminy-or-alternans.html ) — Acute ischemia/MI is one possible etiology — and that DOES seem likely with what looks like acute ST elevation and depression that "shouldn't be there" in a number of leads! Let me know what happens! If you can give me follow-up — might be a good one for an ECG Blog! —

 

FARDEEN REPLY:

Thank you very much sir for your valuable comment. I will share patient info once I received. The heart rate in this tracing is less than 100 that’s why we mainly focused on AIVR and specifically competing AIVR and accelerated junctional rhythm. What’s your comment about this competing AIVR and Accelerated junctional rhythm

 

MY REPLY:

Yes the rate of the rhythm is slow for "VT" — and it is mainly because of the differing QRS morphology that I thought this was more of a"BiDirectional Ventricular Rhythm" (whether you call it "VT" vs "bidirectional AIVR" I think is a matter of preference). True bidirectional VT is RARE! — so I don't know that any rate limits have been agreed on — and if that is what this is, the concept differs from the usual "AIVR" which is an escape rhythm (and one that often occurs with reperfusion of an uncomplicated acute MI). So — the R-R interval varies a bit, but not really every-other beat — so I cannot rule out some form of alternating aberrant conduction. But the reason I don't favor that is that QRS morphology really is not consistent with any form of known conduction defection (not truly rbbb + lahb or lphb). Now IF the baseline ECG is very abnormal, then it could be alternating forms of aberrant conduction. As to AIVR + junctional — note the 2 alternating morphology forms (within the dotted RED and dotted GREEN rectangle) — and BOTH show very wide complexes that do not conform to either lahb or lphb morphology ==> I think more like both being of ventricular etiology. I cannot prove this is "bidirectional VT" — and I count on the fingers of my hands how many times I've seen cases of this outside of textbooks — so it is NOT something that is often seen, therefore experience would seem quite limited — but I agree that it looks like there is "extra" ST elevation and "extra ST depression in some complexes, which increases suspicion of recent/ongoing acute MI (as we both noticed) — and perhaps the relatively slow ventricular rate IS a manifestation of "bidirectional AIVR" because of spontaneous reperfusion following an acute MI .... BOTTOM LINE — I think more follow-up, more details, prior and later tracings will be needed to "put all the pieces together" — but the above are my thoughts re what may be going on at this point —

 

FARDEEN REPLY:

Some new info about the patient is that patient has been 47 years old obese patient without significant past history, currently suffering from acute crushing chest pain which ended up to to patient collapse and according to patient’s relatives with low spo2 and undetectable BP most probably cardiogenic shock and pulmonary edema. Patient underwent cor Angio plus pci during which patient collapsed and ended up cardiac arrest. Patient has been resuscitated after giving several shocks according to patient attendance. Patient is currently unconscious under ventilator. By the time patient’s other ECG tracing is sent to me I will share them with you.

 

MY REPLY:

Thanks for the follow-up! Any idea about WHEN this ECG that you sent me was done with respect to the above history. In any case — the scenario to me is consistent with a bidirectional "slow" VT as a result of ischemia/acute MI and shock state ...

 

FARDEEN REPLY:

According to the patient attendance it was taken before PCI.

 

MY REPLY:

That helps — as it goes along with this bidirectional rhythm as an indicator of acute ischemia ...

 

 

FARDEEN REPLY:

Some updates about the patient is that she is still under vent. The above ECG is very first tracing when patient was complaining of chest pain.

 

This last ECG is taken after PCI.

 

MY REPLY:

Hi. THANKS for the follow-up. What did the cath show??? Unfortunately — the very first ECG is too light for PMcardio to improve the image. Can you get a better quality original? It's OK if not since it might be better for the case to just show the tracing you sent me first — and the post-PCI tracing (as I put these 2 tracings together on the attached). So that very first tracing when the patient had CP (Chest Pain) really does NOT show much at all ... The attached figure shows the tracing you sent me + the post-PCI tracing. I think both QRS morphologies on the TOP tracing are different enough from the post-PCI tracing as to confirm that the rhythm you sent me was a bidirectional ventricular rhythm — presumably due to ischemia, and which corrects after PCI. Great case! So I may write this case up. If so — Would you like me to acknowledge you, or leave it anonymous? Could you tell me the city and country from where you are from (as I like to include that information). It may be a while until I publish this, as I have other cases to go before. THANKS again! —

 

FARDEEN REPLY:

Cath showed the lcx to be total and had thromb shift to the lad.

This wasn’t my patient I will get permission from the one who sent me these tracings.

 

MY REPLY:

I can acknowledge your colleague and also you if you like. Just let me know — :)

 

= = = = = = = = =

FARDEEN REPLY on May 11 !!!

ACKNOWLEDGE: 

Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan)

Fardeen — I am an associate professor of Cardiology at Kabul University of Medical Sciences, Hameedullah Ahmadzai is a Cardiologist.

Sir, could AIVR with alternating exit/fusion patterns be considered a possible alternative diagnosis in this case, perhaps to further strengthen the publication? I truly appreciate your hard work and your efforts to share knowledge. I have personally learned a great deal from your insightful comments and, of course, from your weblog as well. I would highly recommend your work to both senior and junior colleagues alike.

= = = =

MY REPLY:

Hi. Thanks for the info. It may be a while ... but I'll let you know when I publish this — and I'll acknowledge Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan).

Good point about about AIVR with alternating exit sites! I review this concept in my ECG Blog #231 

(https://ecg-interpretation.blogspot.com/2021/06/ecg-blog-231-what-is-this-bizarre.html ) from which the attached figure comes from. It would seem impossible to rule out the possibility of different (alternating) exit sites — but I will be sure to add this as a possibility.

GREAT corresponding with you! Take care — :)

==============================

ECG Blog #436

https://ecg-interpretation.blogspot.com/2024/06/ecg-blog-436-bigeminy-or-alternans.html

==============================

The ECG in Figure-1 — was obtained from an older man with known coronary disease. He was on a number of medications — including antiplatelet agents, a statin drug and Digoxin.

• The patient presented to the ED (Emergency Department) for an episode of syncope. He developed cardiac arrest shortly after the ECG in Figure-1 was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
•   What is the most likely cause of this arrhythmia?

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

MY Thoughts on the ECG in Figure-1:

A repetitive bigeminal pattern is seen in Figure-1 — in which QRS morphology alternates with each beat. 

• There are 2 different QRS morphologies — both of which clearly manifest a wide QRS complex when this rhythm is viewed in certain leads. Thus, although one of these QRS morphologies looks narrow in lead V3 — a glance at leads III, aVR, aVL, V1 and V2 confirms that the QRS is wide!
• NOTE: Although QRS morphology from one-beat-to-the-next looks similar in certain leads (ie, in leads aVR, V4,V5,V6) — there can be no doubt about the presence of 2 distinct QRS morphologies when one looks at leads I, III, aVL, aVF — and leads V1,V2,V3.
• 
  
• The overall rate of the rhythm in Figure-1 is fast (at least 150/minute).
• There are no P waves.
• 
  
• And, the patient is older (ie, prone to reduced renal function) — and he is taking Digoxin.

IMPRESSION: Given the presence of a wide tachycardia — with 2 distinct QRS morphologies, and no sign of P waves — a presumed diagnosis of BiDirectional Ventricular Tachycardia has to be made.

• 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 (ie, alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in bidirectional VT — and they alternate every-other-beat (CLICK HERE — for this case report Review by Femenia et al on Bidirectional VT in a patient with CPVT = Catecholaminergic Polymorphic VT).
• 
  
• KEY Point: There are a limited number of causes of Bidirectional VT — with the 2 most common causes being Digoxin toxicity and CPVT. Given that today's patient was taking Digoxin — Digoxin Toxicity was immediately suspected as the most likely cause. 
• Since Digoxin is primarily renally excreted — older age, that is commonly associated with reduced renal function, would predispose to developing Digoxin toxicity.

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).

To Emphasize: Bidirectional VT is rare. That said, it does occur — and awareness of the entities associated with this diagnosis may be important in evaluation and treatment.

==============================

CASE Conclusion:

As noted above — today's patient developed cardiac arrest shortly after arrival in the ED. Despite prolonged resuscitation with multiple defibrillation attempts — the patient could not be saved.

==================================

Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

==================================

 

=======================

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #36 — Reviews irregular wide tachycardias (with distinction between Torsades de Pointes vs Polymorphic VT discussed in Figure-3 in this post). 
• See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — for review of Pleomorphic VT.
• ECG Blog #231 — for review on the types of VT (including monomorphic — polymorphic — pleomorphic — and bidirectional VT).
• 
  
• Bidirectional VT: Challenges and Solutions (Almarzuqi et al — Vasc Health Risk Mgmt 18:3997-406, 2022). 
• 
  
• Pleomorphic VT and Sudden Cardiac Death — Editorial by Liu and Josephson on potential mechanisms to explain the ECG appearance of Pleomorphic VT. 
• Case Report on BiDirectional VT — by Femenia et al on this patient with BiDirectional VT from CPVT (Catecholaminergic Polymorphic VT).
• ECG Blog #197 — Reviews the concept of Idiopathic VT (including recognition and treatment of Fascicular VT and RVOT VT).
• Multifocal vs Polymorphic VT — September 23, 2011 post from Dr. S. Venkatesan's insightful and user-friendly Cardiology Blog (from which I adapted his figures to derive my Figure-3).

==============================

ECG #231

https://ecg-interpretation.blogspot.com/2021/06/ecg-blog-231-what-is-this-bizarre.html

==============================

The 12-lead ECG shown in Figure-1 was obtained from a previously healthy 55-year old man who presented to the ED (Emergency Department) with shortness of breath, altered sensorium and hemodynamic instability.

• WHAT are the diagnostic possibilities for the rhythm?
• What do you feel is the most likely rhythm diagnosis?

 

Figure-1: Presenting ECG from a 55-year old man with shortness of breath, altered sensorium and hemodynamic instability (See text).

 

 

MY THOUGHTS on ECG #1:

My initial impression on looking at the ECG in Figure-1 — was that this irregular, wide rhythm was probably rapid AFib (Atrial Fibrillation), with a mixture of PVCs (Premature Ventricular Contractions) and aberrant conduction of supraventricular impulses.

 

I Changed My Mind on taking a 2nd Look at this tracing:

• I saw no sign of atrial activity.
• I thought all 25 QRS complexes on this tracing were probably ventricular in etiology (Figure-2). Although the QRS does not look overly wide in some leads — as you follow each of these 25 beats down the page from lead I at the top (looking in each of the 11 simultaneously-recorded leads below lead I) — the QRS is revealed to be either definitely wide in other leads — or — to manifest a QRS morphology strongly suggestive of a ventricular etiology (ie, the all-negative, widened complexes in lead V6 for beats #4,5; 8; 11, 12; 14,15; and 21 are ~99% likely to be ventricular in etiology).
• While I can't rule out the possibility that there might be a few supraventricular "capture" beats in Figure-2 — I believe it fair to say that more than 20 of the 25 beats in this tracing are ventricular in etiology.
• Unlike AFib — there does appear to be a "pattern" to the rhythm in Figure-2 (Doesn't the shape and relative timing of beats within the 2 YELLOW and 2 WHITE rectangles in Figure-2 look surprisingly similar?).
• BOTTOM Line: Despite irregularity of the rhythm and variability in QRS morphology — I thought the rhythm in Figure-2 had to represent some form of VT (Ventricular Tachycardia).

 

Figure-2: I have numbered the beats in ECG #1. Doesn't it look like there is some kind of repetitive group pattern in successive beats? (Look within the 2 YELLOW and 2 WHITE rectangles at sequential beats in the long lead V6).

 

 

VT Terminology:

Before going further — it may help to review a number of terms that have been used to describe the morphologic appearance of various forms of VT. These include:

• Monomorphic VT — in which there is a similar (if not identical) QRS appearance throughout the episode of VT.
• PolyMorphic VT (PMVT) — in which QRS morphology and/or axis continuously changes from one beat-to-the-next throughout the episode of VT. PMVT is not a regular rhythm — and it is often quite irregular. When PMVT is associated with a long QT interval — the rhythm is then defined as Torsades de Pointes (See ECG Blog #36 for more on distinction between Torsades vs PMVT).
• Pleomorphic VT — in which more than a single QRS morphology is seen during an episode of VT. Pleomorphic VT differs from PMVT — because QRS morphology is not changing from one beat-to-the-next. Instead, one QRS morphology will be seen for a number of beats — and then another morphology may take over and continue for another series of beats. Several different morphologies may be seen. (For more on Pleomorphic VT — Please SEE My Comment in the June 1, 2020 post in Dr. Smith’s ECG Blog).
• Bidirectional VT — in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT distinguishes itself from PMVT and pleomorphic VT — because a consistent pattern (ie, alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in bidirectional VT — and they alternate every-other-beat. (CLICK HERE — for this case report Review by Femenia et al on BiDirectional VT in a patient with CPVT = Catecholaminergic Polymorphic VT).

 

 

WHY CARE about QRS Morphology with VT?

Classification of the morphologic type of VT may provide clues to etiology, outcome and treatment.

• Monomorphic VT may occur in patients with or without underlying structural heart disease. Because the ventricular activation sequence is constant in monomorphic VT (which is why all beats look the same) — successful treatment (either by medication or cardioversion) is generally easier to accomplish. 
• The occurrence of monomorphic VT in a patient without underlying structural heart disease (and without QT prolongation or metabolic/electrolyte abnormalities) — is known as Idiopathic VT. The “good news” — is that long-term prognosis of patients with idiopathic VT tends to be excellent (See ECG Blog #197 for more on Idiopathic VT).
• As noted earlier — Bidirectional VT is extremely uncommon. Think of digitalis toxicity and catecholaminergic polymorphic VT as potential etiologies in which you are more likely to see bidirectional VT.
• Pleomorphic VT is also uncommon, and less well known than the other morphologic forms of VT. Patients with pleomorphic VT generally have significant underlying structural heart disease. A number of mechanisms have been proposed to explain the pattern of pleomorphic VT, in which there may be one or more runs of VT with a given similar QRS morphology — that is then punctuated by runs of VT with 1 or more other QRS morphologies. Potential mechanisms for explaining pleomorphic VT are complex — and include the possibility of: i) a single VT circuit with more than a single exit site; ii) the presence of more than a single VT circuit; and/or, iii) shifting conduction properties that alter the activation sequence (Liu & Josephson — Circ Arrhythm Electrophyiol 4:2-4 2011). 

 

PolyMorphic VT (PMVT) — is divided into 2 groups, depending on whether the preexisting QT interval is prolonged. 

• The occurrence of PMVT in association with baseline QTc prolongation — is defined as Torsades de Pointes. Torsades often has a multifactorial etiology (ie, drug-induced, electrolyte depletion, CNS disturbance and/or other underlying disorder that may predispose to QT lengthening). KEY aspects of treatment include IV Mg++ (often at high dose) + finding and “fixing” the cause of the long QTc.
• In contrast — PMVT without QT lengthening most often has an ischemic etiology. Although IV Mg++ is also indicated as initial treatment of PMVT with a normal QT — it is clearly less likely to respond to IV Mg++, than when the QT interval is prolonged. Instead, antiarrhythmic drugs such as amiodarone or ß-blockers may be needed — and/or treatment targeted to correcting ischemia.

 

COMMENT on Today's Case:

What I found especially interesting about the rhythm in Figure-2, is that unlike the complete variability in QRS morphology and R-R intervals that is usually seen with PMVT — there seemed to be a distinct, repetitive pattern in several parts of this tracing.

• That said, given lack of atrial activity and numerous different ventricular QRS morphologies — I thought the rhythm in today's case to be most consistent with Polymorphic VT.
• Clinical details on this patient were scarce — but there was no history of medication use or toxic ingestion.

 

My thoughts as to why there may be a repetitive pattern in parts of the rhythm in from today's case — are illustrated in Figure-3, which I adapted from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog.

• Although one might expect PMVT to originate from multiple sites in the ventricles — much (if not most) of the time — this is not what happens. Instead — it is more common for PMVT to originate from a single ventricular focus (despite significant variation in QRS morphology that may sometimes be seen from one beat-to-the-next).
• As suggested in Figure-3 — the physiologic explanation for why this may happen, is that the polymorphic VT focus may travel over a different path in its exit from the myocardium.
• Irregularity of PMVT may be explained by variation in conduction times for the various exit paths.
• The "repetitive pattern" that I suggest is present (within the YELLOW and WHITE rectangles drawn in Figure-2) — may be the result of a somewhat organized "rotation" over a series of potential exit paths.
• PEARL: As one might imagine — most PMVT rhythms are hemodynamically unstable, with tendency toward rapid deterioration to VFib. That said — Dr. Venkatesan makes the clinically important point that on occasion — some PMVT rhythms are surprisingly well tolerated! This could be the result of a "competition" between the different foci and/or exit sites that serve to prevent any one malignant focus from predominating and precipitating deterioration to VFib. To paraphrase Dr. Venkatesan, "One VT focus may act like a natural anti-tachycardia pacing device, that serves to terminate a VT from another focus".

 

Figure-3: I have adapted this figure from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog. It explains how "polymorphic" VT might arise from a single venricular focus, rather than from multiple sites in the ventricles (See text).

 

FOLLOW-UP to Today's Case:

Unfortunately — the rhythm in Figure-2 deteriorated, and cardiac arrest was called. The patient could not be resuscitated. I believe this unfortunate clinical course supports our presumption of PMVT as the etiology of the rhythm in today's case. Further information on the case was not available — so we never learned the cause of this malignant rhythm.

 

==================================

Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

==================================

 

======================= 

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #36 — Reviews some irregular wide tachycardia rhythms (with distinction between Torsades de Pointes vs Polymorphic VT discussed in Figure-3 on this post). 
• See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — for review of Pleomorphic VT.
• Pleomorphic VT and Sudden Cardiac Death — Editorial by Liu and Josephson on potential mechanisms to explain the ECG appearance of Pleomorphic VT. 
• Case Report on BiDirectional VT — by Femenia et al on this patient with BiDirectional VT from CPVT (Catecholaminergic Polymorphic VT).
• ECG Blog #197 — Reviews the concept of Idiopathic VT (including recognition and treatment of Fascicular VT and RVOT VT).
• Multifocal vs Polymorphic VT — September 23, 2011 post from Dr. S. Venkatesan's insightful and user-friendly Cardiology Blog (from which I adapted his figures to derive my Figure-3).