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

The ECG in Figure-1 was obtained from a man in his 60s — who presented to the ED (Emergency Department) for "palpitations". He was hemodynamically stable with this rhythm.

• The patient overall had previously been healthy without a known cardiac history.
• The above said — he is a heavy smoker, and has been on a number of psychoactive medications.

QUESTIONS:

• How would you interpret the rhythm in Figure-1? 
• How certain are you of your diagnosis?
• How should you treat the patient?

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

My Thoughts:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, without clear sign of sinus P waves. As per the many cases of regular WCT rhythms that we've seen in this ECG Blog:

• Statistically — 80-90% of regular WCT rhythms without sinus P waves will turn out to be VT. Therefore — Assume VT until proven otherwise. Treat the patient accordingly.
• That said, since this patient is hemodynamically stable — You have at least a moment in time to look closer at the rhythm for features that might increase (or decrease) your diagnostic certainty from an initial statistical likelihood of 80-90% VT.

Among the ECG features I look for are:  

• The frontal plane axis.
• Signs of atrial activity.
• QRS morphology during the WCT rhythm.

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

The Frontal Plane Axis:

The finding of an extreme frontal plane axis during a WCT is highly predictive of VT. The KEY is how we define "extreme". The definition I favor is driven by seeking a highly specific diagnostic criterion, which if satisfied — will strongly predict VT as the etiology.

• My definition of an "extreme" frontal plane axis — is that the QRS complex must be entirely negative in either lead I and/or in lead aVF.
• As highlighted in Figure-2 — there is indeed a marked right axis in ECG #1, as the small-amplitude QRS in lead I is predominantly negative.
• That said — the QRS in lead I is not all negative, because a small-but-definitely-present initial positive deflection (r wave) is seen in this lead.
• Bottom Line: The marked right axis in Figure-2 favors VT. However, because the QRS is not all negative in lead I — the descriminatory value of a right-but-not-extreme axis is significantly reduced. Therefore, the rightward axis in ECG #1 is of limited diagnostic value, and does not prove VT.

Signs of Atrial Activity:

Although we don't see sinus P waves in ECG #1 — there do appear to be retrograde P waves, as highlighted in Figure-2 by the YELLOW arrows that produce a notching seen just after the QRS complex in each of the 3 inferior leads.

• That said — these retrograde P waves appear to occur after each QRS complex in the inferior leads. Since both reentry SVT rhythms (AVNRT, AVRT) and VT may manifest 1:1 VA conduction as we see here — the finding of retrograde P waves in ECG #1 does not prove VT.

QRS Morphology during the WCT:

Assessment of QRS morphology may help greatly to narrow down the likelihood that a given WCT rhythm is either VT or an SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block) or aberrant conduction (See ECG Blog #196 for details).

• As emphasized in ECG Blog #211 — the chances of a WCT rhythm being supraventricular increase significantly IF — QRS morphology is consistent with one of the known forms of conduction block (ie, RBBB, LBBB, LAHB or LPHB; or RBBB with one of these hemiblocks).

Take another LOOK at today’s initial ECG:

• Does QRS morphology during the WCT rhythm look like one of the known forms of conduction block?

Figure-2: I've labeled key features from Figure-1.

ANSWER:

• As seen in Figure-2 — QRS morphology during the WCT rhythm in today’s initial ECG does not in the least resemble RBBB conduction. This is because the QRS is all negative in lead V1, as well as in other anterior leads.
• QRS morphology also does not resemble LBBB conduction — because the QRS is predominantly negative in the lateral limb leads ( = leads I and aVL).
• As shown in Figure-2 — the frontal plane axis is rightward (ie, as seen by the predominant negativity in lead I). This immediately rules out LAHB conduction which requires a markedly leftward frontal plane axis. LPHB conduction is also unlikely — because the typical qR morphology in the inferior leads is lacking (ie, monophasic R waves without an initial q wave are seen in leads II,III,aVF).

Instead, if anything — QRS morphology is most consistent with RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia):

• As noted in ECG Blog #525 — QRS morphology of RVOT is characterized by a pattern resembling LBBB conduction in the chest leads — with a rightward axis in the frontal plane.
• There clearly is a rightward frontal plane axis in Figure-2.
• Most cases of RVOT VT manifest a QRS with predominant negativity for the first 3 or 4 chest leads — after which a predominantly positive R wave develops. Although transition to a predominantly positive R wave is delayed in Figure-2 — it does finally develop by lead V6. Thus, although R wave progression is a bit atypical for RVOT VT — the QRS morphology that we see in Figure-2 still could be consistent with RVOT VT if an all positive R wave develops by lead V7 or V8.
• Bottom Line: QRS morphology in Figure-2 is most consistent with some form of VT. As discussed in the ADDENDUM in ECG Blog #525 — the clinical relevance of determining whether or not an ischemic VT form is present vs RVOT VT — is that initial treatment considerations will differ. That said, because QRS morphology does not resemble any known form of conduction block — the odds are strongly in favor of some form of VT.

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

Today's CASE Continues . . .

XXXX

Figure-3: XXXX

XXXXXXX 

Note diffuse T wave inversion in this repeat ECG recorded after successful cardioversion. Instead of ischemia — I suspected this diffuse T wave inversion most likely represents a “memory” effect (that is commonly observed for hours up to a few days following a sustained tachyarrhythmia). 

PEARL: Cardiac catheterization would not necessarily be needed to prove a “memory” effect if T wave inversion resolves in timely fashion, Troponins are negative, normal LV function resumes and the patient returns to his pre-arrhythmia asymptomatic state.

XXXXXXX

Drug-Induced Arrhythmias

isdale et al — Circulation 142(15):e214-e233, 2020

https://www.ahajournals.org/doi/10.1161/CIR.0000000000000905

Very complete guide on drug-induced arrhythmias

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

XXXXXXX

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

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

================================== 

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:

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!

 

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

XXXXX

 XXXXXX

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

XXXXXX

Figure-2: XXXX

XXXXXX

Figure-3: XXXX

XXXXXX

Figure-4: XXXX

Figure-5: XXXX

'

Figure-6: XXXX

Figure-7: XXXX

Figure-8: XXXX

Figure-9: XXXX

Figure-10: XXXX

Figure-11: XXXX

Figure-12: XXXX

XXXXXXX 

Figure-13: XXXX

XXXXX

XXXXXX

XXXXXXX

XXXXXXX

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

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.
================================== 

XXXXXXX

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

 XXXXXX

XXXXXXX  

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

XXXXXXX

Figure-2: XXXX

XXXXXXX 

Figure-3: XXXX

XXXXXXX

XXXXXXX

XXXXXXX

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

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

================================== 

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

XXXXXXXX

—   ­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.

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

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

================================== 

 

ADDENDUM:

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

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

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.