Monday, August 17, 2026

EXTRA COPY — ECG Blog #546: I was sent this Tracing ...— EXTRA COPY

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Figure-1: XXXX (To improve visualization — I've digitized the original ECG using PMcardio).


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Acknowledgment: My appreciation to 林柏志 (from Taiwan) and M Shah (from Srinagar, India) — for allowing me to use this case and this tracing.
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THE CASE:

60Y man with CKD history, feels dizziness. A challenging ECG tracing shared for discusson. Thanks to M Shah asking me this one.

 

GREAT case! I don't have time now to draw a laddergram — but I walk thru step-by-step laddergrams in a similar case in my ECG Blog #256 (https://tinyurl.com/KG-Blog-256 ). The mechanism is almost certain to be ESCAPE-CAPTURE with Echo beats that for the most part conduct.

So I will ask 林柏志 and M Shah both for PERMISSION for me to use this case as a future ECG Blog (on which I will draw laddergrams. PLEASE LET ME KNOW if I can use this case!

Otherwise — I'd LOVE to know clinical follow-up — because this 60yo with dizziness DOES have subtle ST segment flattening with taller-than-expected T waves in leads V2,V3 + deeper-than-expected T inversion for simple RBBB conduction in V1 — so I wonder IF recent/acute posterior OMI may be responsible for the bradycardia here with junctional escape?

So — the KEY to this fascinating rhythm is the single sinus conducted beat ( = beat #2 — with the point marked "X" telling us what a "normal" T wave should look like. And while I cannot rule out the possibility of multiple PACs — this looks much more like ALL YELLOW arrows indicate retrograde conduction from junctional escape beats #1,3,6,8,9 and 11).

Beats #3, 4, 6 and 9 then "turn around" such that these "echo beats" on the way back to the atrium are able to ALSO conduct forward to produce echo beats #4,5,7 and 10 (with beat #7 conducting with incomplete rbbb and beat #10 with complete rbbb aberration).

So the underlying rhythm here is sinus bradycardia — which leads to junctional escape — which leads to the retrograde P wave conduction — with my suspicion of need to rule out recent/acute post. OMI as the cause.

Isn't this fascinating? — :)





















Saturday, August 15, 2026

EXTRA COPY - VT Criteria - EXTRA COPY

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Figure-1: XXXX (To improve visualization — I've digitized the original ECG using PMcardio).




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Acknowledgment: My appreciation to Mohammed Elsisi (from Benha City, Egypt) — for allowing me to use this case and this tracing.

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Mohammed Elsisi <mohammedelsisi18@gmail.com>  (EMAIL on 7/14/2026)

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   ­VT Criteria ... ­—

 

 

Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

 

This tracing was obtained from a 60 y male pt with free medical hx apart from recurrent palpitation over last 5y, who recently become short of breath & exoerience progreesive ll swelling & presented to the ER. 

Pt was received 2 amp amiodarone with no effect, sync dc shocks also convert rhythm transiently on monitor then rapidly return to this tachy. 

My differential is : 

1)LPF VT

2)Aberrant AFL rhythm is strictly ~150bpm

3)aberrant svt 

Woth this incessant rhythm causes tachycardia induced cardiomyopathy. 

What do u think? 


MY REPLY:

Hi Mohammed.

 

I agree that this regular WCT ( = Wide-Complex Tachycardia) looks like LPF VT!

  • The QRS is wide; the rhythm is regular without clear sign of sinus P waves.
  • This does NOT look like aberrant conduction.Lead V1 does not show the triphasic rsR’ that characterizes aberrant conduction — and note that the QRS stays predominantly positive for ALL 6 chest leads (which does not generally happen when there is RBBB conduction). In the limb leads — the R in lead I is slow rising, and there is no more than a tiny r wave in the inferior leads — so QRS morphology is atypical for rbbb/lahb conuction.
  • Verapamil (not Amiodarone) is the drug of choice for a hemodynamically stable patient with Fascicular VT. Given frequent recurrence of this rhythm — I’d refer to EP for confirmation and then ablation.
  • See ECG Blog #489 — for review of a case.

 

Hope the above is helpful! Let me know if you get follow-up!

 

: ) Ken

 

MOHAMMED REPLY:

Thanks ken, as i mentioned  before pt was admitted to ccu d was intubated due to cardiogenic shock d respiratory distress rhythm was incessant & resistant to dc shock. 

D over drive pacing done with succeessful conversion to sinus rhythm with morphology strictly the same during tacharrhythmia. 

Pt hemodynamics improvwd d was successfully weaned from mech

Ventilation then underwent an EP study d a dual av nodal pathway was found with reproduction of avnrt 

Finally succeessful ablation of the pathway done. 

Case finally considered tyical AVNRT. 

With tachy induced cardiomyopathy. 

MOHAMMED (7/14/2026) 

Yes, dramatic improvement after maintenance of sinus rhythm — proves this was tachycardia-induced cardiomyopathy — because EF improved after the WCT was treated !!!!

Of course u can use this case as a blog — Thanks ken. 


MY REPLY:

GREAT case! I want to use this for an ECG Blog — it may be a while — but I'll let you know when I publish this. So LV function improved once AVNRT was ablated? If so — then YES, this was a tachycardia-induced cardiomyopathy!

 

Always good to consider the possibility of an underlying abnormal ECG with similar morphology as during the WCT — which sometimes you just don't know when you first see the patient!

 

GREAT WORK on your part! 

Tha






Friday, August 14, 2026

EXTRA COPY — ECG Blog #542 — Why is the Rhythm Irregular? — EXTRA COPY


The ECG in Figure-1 was obtained from a man in his 60s — who is aware of his "irregular heart beat".

Relevant history: 
  • The patient is overall healthy — with the exception of some "kidney issues" for which he periodically has "low potassium" and sees a nephrologist.
  • The patient notes that his "skipped beats" tend to increase when he is lying down — and generally go away when he stands up.
 
QUESTIONS:
  • How to interpret the rhythm in Figure-1?
    • What is your differential diagnosis for the irregularity?
    • How does the 12-lead ECG help in diagnosing the rhythm?

Figure-1: The initial ECG in today's case. 


ANSWER:
By the PsQs, 3R Approach to systematic rhythm interpretation (See ECG Blog #185) — I note the following:
  • The QRS is narrow everywhere. This tells us that the rhythm is supraventricular.
  • The Rate is controlled, averaging ~60/minute — but the rhythm is not Regular. Instead, there is a bigeminal rhythm (ie, Every-other-beat occurs early — such that we see a repetitive pattern with groups of 2 beats followed by a short pause). See ECG Blog #232 for more on the types of bigeminal rhythms.
  • P waves are present. These P waves precede each of the 9 beats in the long lead II (as per the RED arrows in the long lead II rhythm strip in Figure-2).
  • These P waves are "Related" to neighboring QRS complexes — because the PR interval before each QRS complex is constant (as well as being normal = not more than 1 large box in duration).

Figure-2: I've added RED arrows to highlight regularly occurring P waves that precede each QRS with a constant (conducting) PR interval.


Our Differential Diagnosis:
We've arrived at a relatively common situation in that there is a bigeminal rhythm — in which all QRS complexes are preceded by P waves that appear to be conducting because they have a constant PR interval. At this point — my diagnostic considerations were the following:
  • Atrial bigeminy (in which every other beat is a PAC). I thought this to be unlikely — because as I look at all 12 leads in the simultaneously-recorded ECG above the long lead rhythm strip — P wave morphology looks to be identical for the early beats ( = beats #1,3,5,7,9) — and for the normal sinus-conducted beats ( = beats #2,4,6,8). Because PACs arise from a different place in the atria — P wave morphology of PACs should differ from the P wave morphology of normal sinus-conducted P waves.
  • Atrial trigeminy with blocked PACs (ie, in which every 3rd beat is a non-conducted PAC). This is also unlikely, because as I look at all 12 leads in the ECG above the long lead II — the T waves of beats #1,3,5,7,9 do not manifest any notching or extra peaking that would alert to hidden, non-conducted P waves.
  • 2nd-degree AV block of the Mobitz I Type (which is the same thing as AV Wenckebach) is not present because: i) The  PR interval is not increasing within each of the 2-beat groups; — andii) The P-P interval is not regular (or at least almost regular) — as it should be if AV block was present.
  • 2nd-degree AV block of the Mobitz II Type is not present. This is because the P-P interval is not regular (or at least almost regular) — as it should be if there was some form of AV block.
  • Sinus arrhythmia is unlikely to be present here. This is because the rhythm in Figure-2 represents a fixed pattern of group beating, in which the duration of each of the longer, and each of the shorter R-R intervals is remarkably consistent. In contrast — the duration of R-R interval variation is generally longer with sinus arrhythmia, and manifests much more variability than what we see in Figure-2.

  • SA (SinoAtrial) block . . .

Conclusion: Having ruled out my top 5 diagnostic considerations that I list above — We are left with the last consideration on my list = SA Block!
  • The reason I put SA block last on my list — is that true SA block is the least common of the above entities that I encounter. That said — it "fits best" for the characteristics of today's ECG.
  • My proposed laddergram in Figure-3 illustrates what appears to be the mechanism of this patient's SA block. 

Figure-3: My proposed laddergram for today's rhythm.


Laddergram Illustration:
I review how to read laddergrams (as well as presenting a primer for how to draw them) — with numerous examples of laddergrams in ECG Blog #188.
  • As I illustrate in Blog #188 — it's EASY to read laddergrams that have already been drawn for you. All the laddergram does — is follow the electrical impulse as it records the cardiac rhythm, showing the path of electrical activity as it makes its way through the Atria — then the A-V Node — and finally through the Ventricles.
  • In today's case, since the mechanism of the rhythm is SA Block — the problem arises from within the SA Node.

We show this schematically in Figure-3:
  • Beginning with beat #2 — We see that only 2 out of every 3 SA nodal impulses ( = the RED circles at the very top of the laddergram) — are able to make it through the SA Node to arrive in the Atria.
  • Keeping in mind that time is recorded horizontally — We can see that once an impulse arrives in the atria, that conduction speeds up. We schematically depict this by drawing the lines that pass through the Atrial Tier vertically (representing fast conduction through specialized atrial fibers).
  • Conduction of each impulse then slows down as the impulse passes through the AV Nodal Tier (which is why there is slight increase in angulation of the RED lines within the AV Nodal Tier).
  • On arrival in the ventricles — conduction again speeds up due to fast conduction through specialized His-Purkinje fibers (less angulation of the RED lines within the Ventricular Tier).
Return for a moment to the SA Nodal Tier at the top of the laddergram: 
  • Note the increase in angulation between the 1st and 2nd RED circles in each group — with the 3rd RED circle being blocked — after which the sequence begins again. This is Wenckebach conduction! (ie, There is 3:2 SA block of the Wenckebach Type).
  • For more on SA Block — See the ADDENDUM below!

Clinical Correlation in Today's CASE:
Going back to the brief history presented at the beginning of this case — We were told that today's patient has a history of hypokalemia — and that he noticed a tendency for his "skipped beats" to increase when lying down, and to go away when standing up.
  • In my experience of having looked for true examples of SA block over decades — this phenomenon is not common in the general population.
  • At times I've observed incidental SA block, seemingly without clinical consequence (almost like a normal variant).
  • At other times, this rhythm is clearly pathologic — accompanying inferior infarction with 2nd-degree AV block of the Wenckebach (Mobitz I) Type — or — as a component of the arrhythmias seen with SSS (Sick Sinus Syndrome).
  • In today's case — I suspect that this patient's periodic hypokalemia was at least contributing to development of his SA block, if not frankly causative.
  • Holter monitoring showed this patient's SA block to be without hemodynamic consequence, although persistent through much of the day that the Holter was done. I lack the follow-up to know if the rhythm resolved once serum K+ normalized.
  • Otherwise — selected patients with cardiac arrhythmias have been known to observe a change in the frequency of certain rhythm disorders depending on body posture. This effect is highly individualized — with literature on the subject scarce, and the mechanism uncertain. Theories include variation in vagal tone, which tends to increase when resting supine. Other theories involve changes in intrathoracic pressure occurring with changes in body position — and/or increased "stretch" on cardiac tissue seemingly being more likely when supine.
  • Bottom Line: It's hard to know what to do with a history that the patient notes of a change in arrhythmia frequency depending on body position — other than to accept that in some selected patients, there is evidence that arrhythmias may increase or decrease depending on body position.

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Acknowledgment: My appreciation to Stewart (from Los Angeles, USA) — for allowing me to use this case and this tracing.

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ADDENDUM:



Figure-4: Essentials of SA Block (Modified from Grauer: ACLS-2013-ePub).


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Related ECG Blog Posts to Today’s Case: 









Monday, August 3, 2026

EXTRA COPY — ECG Blog #543: A 24-Hour Holter was Done- EXTRA COPY

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Figure-1: The initial ECG in today's case.



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Acknowledgment: My appreciation to ANONYMOUS? OR Passang Jinpa (from Guayaquil, Ecuador) — for allowing me to use this case and this tracing.

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Passang Jinpa — Guayaquil, Ecuador (Cardiologist at a free clinic! ) – 7/31/2026


THE CASE — Passang Jinpa

An 80-year-old woman presented with mild dizziness and fatigue, denying chest pain or dyspnea. Resting12-lead ECG showed marked sinus bradycardia with biphasic T-wave changes in anterior precordial leads, suggestive of a Wellens pattern. Ambulatory heart rate response was preserved. Echocardiography revealed regional wall motion abnormalities in the basal and mid-anteroseptal segments with sinus bradycardia throughout. A 24-hour Holter monitor was ordered.

 

Clinical Timeline: Day 1: Resting 12-lead ECG. Day 2: 24-hour Holter monitoring initiated. Day 3: Patient found deceased while wearing the Holter monitor. Retrospective review of the Holter recording captured the entire electrocardiographic evolution of the acute myocardial infarction, from initial ischemic changes through ST-segment elevation to the terminal arrhythmia.

 

What should I've done at first? Cath lab activation?

On Day-2 when she came to clinic no chest pain, absolutely fine.

 

MY REPLY:

Be sure to carefully review my ECG Blog #350 (https://ecg-interpretation.blogspot.com/2022/12/ecg-blog-350-severe-cp-not-much-on-ecg.html ) that reviews what Wellens' Syndrome truly is. Be sure to also review material in the Addendum (including the 8 minute Audio Pearl). So your patient did not have a true "Wellens' Syndrome" — because there was no history of chest pain that then went away. But it's important to remember the pathophysiology of Wellens' Syndrome (which I review in Blog #350) — as well as the fact that an IDENTICAL ECG may be seen AFTER an infarction. And in older patients — a "silent" MI (ie, an MI but without any chest pain) is the probable explanation for the T wave inversions that we see in your patient's ECG. So my main questions would relate as to WHEN the patient had those symptoms of mild dizziness and fatigue. It is a very fine line as to which older patient who you strongly suspect has had a "silent MI" needs to be hospitalized until you can be comfortable that their condition has stabilized. So — IF this patient's symptoms were in the last day or two — and especially since the heart rate on this ECG is SLOW (about 50/minute) — a period of monitoring in the hospital would seem warranted. Were Troponins done? If so — and if still elevated, that's another clue that this patient's MI was recent — and if this is a fully functioning 80-year old — cardiac cath should probably have been done before sending the patient home. P.S. Again, the history here is very subtle — but serial Troponins and serial ECGs may have provided insight as to WHEN the MI occurred (and the need for cath). Finally — Before I'd want to send this patient home — I would want to see if she is able to walk at a level comparable to doing her everyday activities. Ideally she is monitored when you do that. The point is that many patients don't want to stay in the hospital — but if this 80 yo woman normally is able to walk everywhere — and now she gets fatigued on much less activity — that's one more sign that she has had a recent MI that may not yet have "completed" (such that cath may be indicated before she goes home). TOUGH case. I hope the above is 

helpful ...

 

 

PASSANG Reply:

Dear Guru KEN, Thank you very much for your thoughtful comments and for taking the time to review my case. I really appreciate your insights. This was actually the patient's first medical evaluation. She had never previously seen a physician. I work in a charitable foundation that provides free outpatient cardiology consultations. Although it functions as a private clinic, patients are responsible for any additional investigations or hospital care, and many have significant financial limitations. Clinically, she looked remarkably well. She was an active 80-year-old woman who came with a friend in her 90s. They were both independent, regularly went shopping together, and she denied chest pain or dyspnea. She only mentioned mild fatigue. Because she appeared so functional and stable, I did not initially suspect an acute coronary syndrome. On the first day, I obtained a 12-lead ECG and observed an abnormal T-wave pattern. I ordered routine laboratory tests, but unfortunately I did not obtain troponin levels. Immediate coronary angiography was also not a realistic option because of the patient's financial situation. What makes this case particularly fascinating is what happened afterward. A 24-hour Holter monitor had been placed, and sadly, the patient was found deceased the following day before returning to have it removed. During my retrospective analysis of the Holter recording, I was able to observe the complete electrical evolution—from the initial ischemic T-wave abnormalities, through progressive ST-segment elevation, and ultimately to the terminal rhythm. The transition began at approximately 11:00 PM. To my knowledge, it is uncommon to have continuous Holter documentation of the entire evolution of an untreated myocardial infarction ending in sudden death. I believe this provides a unique opportunity to correlate the initial 12-lead ECG with the continuous ischemic progression. Do you think this case would be suitable for publication as a case report? If so, I would greatly appreciate any suggestions regarding the best way to present it or which aspects should be emphasized.

 

MY REPLY:

Hi. I can totally relate to ALL that you describe. Knowing more of the details — I may have done what you did.

My training is in family medicine. I was faculty in a Family Medicine Residency for 30 years — so we would see ambulatory patients and on occasion we'd get a history similar to what you describe, in which you suspect that an MI occurred days earlier. So the question then arises as to HOW MUCH to do for a "completed MI?" in an older patient who doesn't want to come into the hospital.

I am also familiar with free clinics as you describe (but for which funding is lacking if additional investigations are needed. You deserve CREDIT for providing care to people who otherwise have NO care .... but situations like this one are clearly frustrating!

In retrospect — the only thing I could say is that subtle change in symptoms (ie, development of some new "fatigue" in recent days in an older person with the initial ECG that you show is suggestive that a recent MI may have occurred, and that we are now seeing reperfusion T waves. What to do with this IF the patient otherwise "seems well" is a difficult question and "Ya gotta be there!" because there is NO certain answer.

In my capacity as hospital Attending for 3-4 months each year — I would read all of our service ECGs and I'd see the Holter Monitors. I will NEVER forget reading ECGs one day — and seeing a Holter monitor of a hospitalized patient, when I suddenly saw on the Holter that the rhythm was getting slower and slower — and then stopped. So I ran up to the floor where this patient was — only to find everyone at the bedside treating her cardiac arrest. It was an EERIE feeling seeing that Holter, and then seeing the patient (just like the eerie feeling that I'm sure you have when you saw these tracings!).

The above said — YES, this is rare to catch this — but I'm not sure you have best exposure by writing an article. Instead — I propose that you let me write an ECG Blog Case that I will publish within a couple weeks. I will show the 12 lead ECG that you sent me and ask the reader how they will interpret this?

I will write up the case giving enough basic info to "set the scene" — but I will not give specific details that may identify the patient. And then I will show the sequential tracings you sent me (that I put into a PDF here).

When I was on faculty — I would "collect" code tracings and later went thru them for insight while I was writing my books on ACLS. So these sequential tracings that you sent me show a similar sequence of events as this unfortunate woman evolved her huge extensive LAD occlusion.

These are TOUGH cases. Given age, vague symptoms (!!!) and lack of resources — there is no right or wrong answer — but the fact that you are soul searching events is sign that YOU are truly a good, caring physician doing the best you can given limited resources for the best you can do for your patients. Many clinicians would not give this case a second thought ....

Is it OK with you that I write this case up as an ECG Blog? I would be happy to acknowledge you if you like? — or the case can be anonymous — JUST LET ME KNOW. It will be published as a Blog post on-line, so it can be referenced by a link to my Blog.

Let me know what you prefer. THANK YOU for sharing this very difficult case with me. I believe it IS worthwhile to soul search events and think IF there is anything for you to learn from this OR if in fact you considered everything and from the information you had simply thought this was a completed MI with not much to gain by hospital admission in an older, minimally symptomatic patient. Putting older patients in a hospital is NOT benign, as "things happen" in the hospital ...

Should I acknowledge you as Passang Jinpa from Guayaquil, Ecuador — Dejame saber lo que quieres que hago por este caso — Ken