EXTRA COPY — ECG Blog #544: Caused by an Acute MI? — EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from a patient with "palpitations". (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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Memory T Waves

Gunaseelan et al — J Emerg, Trauma, Shock 13(4), 2020

https://pmc.ncbi.nlm.nih.gov/articles/PMC8047955/

Viskin et al — Circulation 146:1170-1181, 2022

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.061259

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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> (3/11/2026)

— from Mohammed Elsisi (Benha City, Egypt) —

— "Caused by an Acute MI? "

 

NOTE — I wrote Mohammed via email on 6/27, asking if EP Study was done?

— Mohammed wrote back that "unfortunately there is no follow-up! "

 

These ecgs :Obtained from a 60 y old male patient free past history apart from a psychoatric illness & was on quitapine, valproate & riperidone

. Heavy smoker 

Presents with acute onset palpitations 

Ecg during episode as shown 

Pt was stable but the er physician shocked him & reverted to sinus brady as shown 

Echo reveals a mid range EF ~ 45 _50% with rhin hypokinetic apex proper d adjoining apical segments 

Troponin serialy negative 

My interpretation is :

Regular WCT ~110ms or slightly above 

With lbbb morphology & rt axis 

May be RVOT VT

With retrograde va conduction in a 1: 1 fashion evident in inf leads

The other ECG show sinus bradycardia with rbbb & std TWI  in v1 v5

May be ischemic changes but no evolutionary changes on serial ecg 

Thoughts??

In this case also pt should be referred to EPS study & possible ablation for this vt 

No indication for icd here 

What do you think?

MY REPLY:

Hi. I'd LOVE to use this case for an ECG Blog — if I can have your permission. Would help if you are able to get follow-up — but even if  you can't, it is an excellent teaching case.

 

So I agree with you — I think this is RVOT VT for the reasons you state = there is a regular WCT ( Wide-ComplexTachycardia) at ~170/minute without sinus P waves. Instead (as you say) — it looks like there is 1:1 VA (retrograde) conduction in the inferior leads. QRS morphology is consistent with RVOT VT given all neg QRS complexes in the anterior leads — that then become positive by V6 — with a right axis in the limb leads.

 

I agree that I would refer the patient for EP testing — as this may be a rhythm that can (and should) be ablated.

 

I would repeat the Echo in a day or two, as the impaired LV function may be a result of being in the VT for a period of time.

 

As to the repeat ECG after cardioversion — the T wave inversion may be "Memory" — which is the name given to ST-T wave changes that are sometimes transiently seen after a patient has been in a sustained tachycardia for a period of time. Usually this goes away within hours or a day or two — and it is NOT indicative of coronary disease. Of course, you always have to rule out coronary disease, which it sounds like you did because there were no serial ECG changes. Were Troponins drawn to rule out an MI as the cause of the VT?

Let me know if you get follow-up (and IF I can use this case) — THANKS — :) Ken

Mohammed REPLY:

Of course can use it as teaching case in a blog

Troponin was drawn & serially negative 

Patient was referred for an eps study 

 

MY REPLY:

Thanks for your quick reply. Good that Troponin was negative! — which means that this IS most likely "Memory" — and not related to heart disease (especially if this T wave inversion goes away over the next 24-48 hours!).

 

Let me know what the EP Study shows!

 

Otherwise — I like to acknowledge people who send me tracings — so Please tell me how you would like me to write your name AND also the city and country you are from — OR — if you prefer, I can make this an "anonymous" case — Just let me know! THANKS — :)   

 

It may be a while — but I will let you know when I do publish this! — :)

 

Mohammed Reply: — YES — To Acknowledge him !!!!

Mohammed elsisi

From benha city egypt 

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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Figure-2: XXXX

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Figure-3: XXXX

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Figure-4: XXXX

Figure-5: XXXX

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Figure-6: XXXX

Figure-7: XXXX

Figure-8: XXXX

Figure-9: XXXX

Figure-10: XXXX

Figure-11: XXXX

Figure-12: XXXX

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Figure-13: XXXX

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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? — :)

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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Figure-2: XXXX

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Figure-3: XXXX

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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

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 Ps, Qs, 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; — and, ii) 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: 

• ECG Blog #312 and ECG Blog #488 — for additional examples of SA block. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

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

The ECG in Figure-1 was obtained from a previously healthy elderly woman — who presented with dizzyness and fatigue, but no CP (Chest Pain).

• Details of the timing of this patient's symptoms with respect to when the ECG in Figure-1 was recorded are uncertain.

QUESTIONS:

With the above history in mind: 

• How do YOU interpret today's initial ECG?
• Clinically — What would you do?

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

My Thoughts:

The ECG in Figure-1 shows sinus bradycardia at a rate of ~50/minute.

• The QRS is narrow — the PR interval is normal — and the QTc is probably not increased given the slow rate. 
• There may be small U waves in the mid-chest leads (which sometimes occurs in association with bradycardia).
• There is a slight leftward axis — though not negative enough to qualify as LAHB (The QRS is slightly more negative than positive in lead aVF — but mainly positive in lead aVL — which puts the axis at about -15 degrees).
• There may be voltage for LVH (Hard to say for sure if the R in aVL ≥12 mm — given overlap of this R wave with the S wave in lead aVR).

Regarding Q-R-S-T Wave Changes:

• The narrow Q waves in leads I,aVL are probably not abnormal given fairly tall R wave amplitude in these leads.
• R wave progression — looks normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally beween leads V2-V3.
• There are subtle ST-T wave abnormalities in a number of leads. As shown in lead III and in leads V1,V2,V3 — there is ST segment coving but really no elevation, followed by T wave inversion (the RED arrows in these leads).
• BLUE question marks in a number of other leads highlight ST-T wave segments of uncertain significance — especially given the different ST-T wave appearance between the only 2 complexes that we see in leads aVL and aVL — and our inability to fully see the ST-T wave of the 2nd complex in leads V4,V5,V6 (? what is real vs artifact). That said — there appears to at least be ST segment flattening in lead II, with slight ST depression in leads V4,V5,V6.

Impression: In view of the brief history we were given, but without "being there" — it's hard to know what to think of the above described ECG changes shown in Figure-2.

• It is clearly possible that this elderly woman at some point in time (possibly recently) — had inferior and anterior infarction. That said — the lack of a history of preceding chest pain (and uncertainty about the time of this elderly patient's "dizzyness and fatigue" ) — make it difficult to know whether she may have had a "silent" MI with "chest pain equivalent" symptoms? And if so — when this may have happened? (See ECG Blog #228 — for more on "Silent" MI).
• Without a preceding history of CP that then resolved — this case does not fit criteria for "Wellens' Syndrome". That said — ECG #1 certainly could be the result of infero-antero infarction at some point in time, possibly recent (See ECG Blog #320 and ECG Blog #350 — for more on what Wellens Syndrome is, and what it is not).

Figure-2: I've labeled ECG findings in the initial ECG.

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The CASE Continues:

This elderly woman up until now had not sought out medical care. She lived alone and functioned completely independently. Although she reported dizziness and fatigue as the reason for her ED (Emergency Department) visit — the medical care provider who treated the patient thought she looked remarkably well. As a result — ACS (Acute Coronary Syndrome) was not considered:

• Of note, the patient did not have medical insurance, and she had financial limitation. As a result — she did not want an extensive diagnostic work-up, especially given that she felt good enough to return to her independent living situation at home. 
• Troponin was not ordered.
• Instead, a 24-hour ambulatory Holter monitor was placed — and the patient went home. Follow-up was scheduled for her to return the next day.

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The Patient's Holter Monitor . . .

As you think about the challenging limitations for managing this case — what follows below in Figures-3 -thru-9 are non-sequential rhythm strips from this patient's 24-hour ambulatory Holter moniter that was reviewed the next day.

• NOTE: Each of the 6 non-sequential Holter rhythm strips that are shown below manifest 6 leads — including 1 limb lead (lead aVR) — and 5 chest leads (leads V1-thru-V5).
• As you review these 6-lead rhythm strips — Keep in mind that the only symptoms this elderly woman reported when she was seen several hours earlier, were some "dizzyness" and "mild fatigue" — but no chest pain.
• For ease of comparison in Figure-3 — I've reproduced this patient's initial ECG that was shown above in Figure-2.

Figure-3: Comparison between the initial ECG — and Holter-A, recorded several hours later after the patient had returned home (at 11:16 pm — while the patient was sleeping).

My Thoughts on Holter-A:

Keeping in mind the inevitable slight differences in lead placement with 6-lead Holter monitoring vs the patient's 12-lead — I did not perceive any significant different between these 2 tracings in Figure-3.

13 Minutes Later ...

Figure-4: Holter-B — recorded 13 minutes later (at 11:29 pm) while the patient was still sleeping.

Subsequent Recordings during Sleep ...

Figure-5: Holter-C — recorded ~2 hours later (at 1:23 am).

Figure-6: Holter-D — recorded at 7:30 am the next morning.

Figure-7: A closer look at Holter-D — in which I've labeled regular-occurring P waves that are no longer upright in lead aVF. The vertical RED line marks the end point of the now widened QRS complex in these 6 simultaneously-recorded leads — with the ST segment beginning to the right of this vertical RED line.

Figure-8: 10 minutes after Holter D — We now see a markedly widened agonal rhythm without atrial activity.

Figure-9: 12 minutes later a flat line is seen ...

Editorial Comment:

Today's case is difficult. This elderly woman who lived alone, died at home in her sleep. These Holter tracings were only retrieved afterward.

• Presumably — the initial ECG in Figure-2 did represent recent LAD occlusion and infarction in the form of a "silent" MI in this elderly woman with minimal "CP-equivalent" symptoms, who otherwise looked good — and who wanted to go home.
• Presumably, the reason this patient's initial ECG did not show acute ST elevation — is that there was spontaneous reperfusion of her recent MI, with resolution of what must have been ST elevation several hours earlier. The RED arrows in leads III; V1,V2,V3 — as well as the Blue question marks in her initial ECG represented reperfusion T waves.
• 
  
• I have "been there". As a family medicine Attending and faculty physician for 30 years — we would periodically see elderly patients present a day or more later after some form of symptoms with ECGs similar to that seen in Figure-2. While clearly — hospitalization for a day or two to ensure nothing active is still ongoing would be ideally recommended (and depending on case specifics — serial tracings, Troponins and potentially cardiac catheterization) — but with full informed consent, that is not always the path chosen.

I have also "been there" in the eerie situation of interpreting a Holter monitor on one of our serivce patients who was admitted to the hospital and seemingly doing well on a telemetry-monitored floor. I was downstairs in the hospital ECG station, reviewing the patient's 24-hour Holter recording that had just been placed into my in-box for interpretation. XXXXXXX

I have been there. I'll never forget

Editorial Note:

I have had this same experience myself — that I'll never forget 

Watanabe et al — Heart Rhythm 8:18-25, 2014
https://pubmed.ncbi.nlm.nih.gov/24793460/

Nikolic et al — Circulation 66(1):218-225, 1982
https://www.ahajournals.org/doi/10.1161/01.CIR.66.1.218?doi=10.1161/01.CIR.66.1.218

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

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pful ...

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?

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.