EXTRA COPY — ECG Blog #550 - Guess the Clinical Setting — EXTRA COPY

XXXXX

XXXX

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

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

XXXXX

Figure-2: XXXX

XXXXXX

Figure-3: XXX

XXXXXX 

Figure-4: XXX

XXXXXX

Figure-5: XXX

XXXXXX

Figure-6: XXX

XXXXXX  

XXXXXX 

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

Acknowledgment: My appreciation to Ali Ibrahim Almfriji (from Tikrit, Iraq) for allowing me to use this case and these tracings. 

================================== 

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

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

Ali ibrahim Almfriji, Interventional cardiologist Tikrit- Iraq (9/16/2026- FB Messenger!)

I need to let Ali know if I publish this! FB Messenger!

“Guess the Clinical Setting!”

 

THE CASE:

Good day dear prof. Ken. 49 male heavy smoker, no HTN, no DM, presented to my cardiac centre (tikrit.iraq) with 8 hours anterior STEMI, LAD totally occluded proximally , primary pci was done with TIMI III flow achieved, this is attached EKG 3 hours after procedure Rhythm analysis please

MY REPLY:

Hi. Interesting tracing! RED arrows are sinus P waves. We do not have a long lead rhythm strip — but the chest leads are the continuation of the limb leads (such that there are a total of 9 beats on this tracing). Beats #8 and 9 are sinus conducted! (RED arrows with a constant and normal PR interval). The PR interval before beat #7 is too short to conduct — so this is an escape beat. There are NO P waves seen before beat #7 — but the YELLOW arrows probably reflect P waves hidden within the QRS. Note that there is NO notching seen within the QRS of beat #1 ==> so the P wave is probably completely hidden within the QRS of beat #1. Putting this all together — Beats #1-thru-6 are ventricular at a rate between 55-60 ==> AIVR (Accelerated IdioVentricular Rhythm). After beat #6 — the SA node begins to wake up and it finally achieves a rate faster than the ventricular escape rate — which is why beats #8 and 9 are sinus-conducted. Beat #7 is a FUSION beat (the PR interval is too short to completely conduct). Note that the QRS is a little smaller than beats #5 and 6 which are ventricular — and a little larger than sinus-conducted beats #8 and 9. AIVR is VERY COMMON as a reperfusion arrhythmia — so that fact that this patient had acute LAD occlusion but was reperfused with PCI means that the expected situation for developing AIVR was present. IF the patient is hemodynamically stable and asymptomatic — then NO treatment is needed! This rhythm is almost always transient (lasting hours to a day or so after reperfusion). If the patient is symptomatic — giving some Atropine may help by speeding up the sinus node. Finally — the ST-T waves in some leads (like leads I and aVL) are abnormal — probably as a result from the recent MI. If you could give me a bit more follow-up on this case — I might want to use it as an ECG Blog (if I could have your permission for this?). I hope the above is helpful — 

 

ALI REPLY: 

This is second day post pci EKG and echo study.

Nice explanation, the patient really developed continuous AIVR immediately after reperfusion on cath lab table, and was stable hemodynamically.

Im pleased if this case used as ECG blog and to mention my name dr. Ali ibrahim Almfriji , Interventional cardiologist Tikrit- Iraq.

 

MY REPLY

Thanks so much for the follow-up! I do plan to write up this case. I’ll focus on the 1sttECG — but will probably also show the 2nd tracing. This 2nd ECG shows loss of R waves in the chest leads with some residual chest lead ST elevation. There is T wave inversion in the limb leads, consistent with “reperfusion T waves”. There is also low voltage (which may be a reflection of the extensive anterior infarction. It may be a little while before I publish this case — but I will let you know when I do. THANK YOU — 

EXTRA COPY — ECG Blog #548 — More than One Family — EXTRA COPY —

XXXXXX

XXXX 

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

XXXX 

Figure-2: XXXX

XXXX

Figure-3: XXXX

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

XXXX  

XXXXXXX

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

Acknowledgment: My appreciation for the anonymous contribution of today's case. 

================================== 

XXXXXXX

Sheikh mohsin55er@gmail.com  — 9/5/2026 via E-mail

— “More than one Family?” —

— Make this ANONYMOUS (Let Sheikh know by email when published! )

 

Thanks for your quick response. The patient had a serum K+ of 7.0 at the time of this ecg recording. I would love if you do an ecg blog on this and you have my full permission to do so. You can post it as anonymous without mentioning my name

 

THE CASE:

HyperK with bizarre rhythm:

Hi. I am attaching below this ecg of a 60 year old female who is admitted with DKA and complains of palpitations. Her Vitals are stable and there is no history of presyncope or syncope. Evaluation revealed hyperkalemia and correction of hyperkalemia resulted in the normalization of ecg changes. But i am not able to understand the rhythm here so could you please help figure out the rhythm ?
Thanks’’

MY REPLY:

HI Sheikh. This is very interesting indeed. First — Was this ECG done while the patient was hyperkalemic? If so — do you know how high the serum K+ was at this time?

 

KEY POINT ­— All bets are off when you have an arrhythmia with HyperK+ — because patients “do not obey the rules” when there is HyperK — and much (most) of the time — a normal rhythm resumes once HyperK is corrected (as happened in your case!

 

I spent some time working on this — and from the “pretty” picture I am sending you — You might guess that I’d love to do an ECG Blog of this case. May I have your permission to do so?

 

I like to acknowledge colleagues who send me tracings. I’m happy to put in your name and the city and country from where you are from — OR ­— if you prefer, the case can be anonymous. Just let me know. If you want me to put your name — tell me how to write it (and also send me the city and country from where you are from).

 

There is more than 1 possible solution to this — but the simplest answer to what is going on is if there are dual AV nodal pathways. One of the pathways has faster conduction (a shorter PR interval) which I drew in PINK. 

 

The other pathway is slower = GRAY.

 

In addition to dual AV nodal pathways, there is significant AV block! This may be 4:1 AV block. So you can see from the laddergram how I propose that conduction switches back and forth from one conduction pathway to the other.

 

We KNOW there IS conduction — because we have repetitive PR intervals. And the BEST clue to the presence of dual AV nodal pathways is when there is a big “jump” in PR interval from one beat to the next.

 

Again — this is clearly a result of the HyperK — with the proof of that being how normal sinus rhythm resumed after HyperK resolved.

I hope the above makes sense! Let me know if I can write this up as an ECG Blog!

 

THANKS —  Ken

 

P.S. I’ve included this article on dual AV nodal physiiology — including Table-1 from this article which highlights the need to think of this when you see “2 families” of PR intervals! — :) 

 

P.P.S. I initially thought this was dual-LEVEL AV block out of the AV node ­— but this does not make a “pretty” laddergram. Still could be both dual AV nodal pathways AND dual-level AV block — but that makes for a much more complicated laddergram !!!!

 

 

EXTRA COPY — ECG Blog #547 — What Happened When? — EXTRA COPY —

The ECG in Figure-1 was obtained from a mid-30s man — who presented with CP (Chest Pain) that began ~1 hour earlier.

• The patient had some risk factors — but no known history of heart disease.
• He reports a similar episode about a week earlier. He did not seek care at that time — because the episode resolved spontaneously. 

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• What happened when?
• What is the “culprit” artery?

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

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

My Thoughts on Today’s CASE:

The challenge in this case is not to diagnose that there is an ongoing acute MI, since that is obvious. Instead — the objective is to figure out what may have happened when?

• The rhythm in Figure-1 is sinus at the relatively fast rate of ~95/minute.
• QRS duration looks to be at the upper limit of normal. The QTc is no more than borderline prolonged. There is no clear sign of chamber enlargement.

The remainder of this tracing is markedly abnormal. I’ve labeled the principal findings in Figure-2: 

• The most “eyecatching” findings are in anterior leads V1,V2,V3 (within the RED rectangle in Figure-2).
• Deep QS complexes are seen in these first 3 anterior leads (YELLOW arrows in leads V1,V2,V3).
• The T waves in leads V2,V3 are hyperacute — in that they are huge (taller than the S waves are deep in these leads) — with symmetric rise-and-fall, with a “fattened” peak and widened base. We instantly know that the cath lab needs to be activated! That said — I found it impossible to identify the J-point defining the amount of ST elevation, because the ascending limb of these hyperacute T waves is so smooth (I suspect there is at least 2-3 mm of ST elevation — but can’t prove this on the basis of this initial tracing).
• It’s insightful to recognize that the ST-T wave in lead V1 is clearly abnormal! The coved shape with ≥1 mm J-point ST elevation is not normal in lead V1 — and provides an important clue regarding the “culprit” artery.
• In contrast to the hyperacute anterior T waves in Figure-2 — is the scooped ST depression in lateral chest leads V5,V6 (BLUE arrows in these leads).
• I interpreted lead V4 as a “transition” lead — in that it shows an “intermediate” pattern with less hyperacuity than its neighboring anterior leads, and less ST depression than its neighboring lateral chest leads.

There are comparable ST-T wave abnormalities in the limb leads:

• There is marked reciprocal ST depression in the inferior leads (BLUE arrows in leads II,III,aVF).
• Lead aVL is especially abnormal — with a deep and wide Q wave in its fragmented QRS, followed by an obvious hyperacute ST-T wave (showing ST segment straightening, ≥1 mm of J-point ST elevation with “fattened” T wave peak and widened T wave base).
• The other high-lateral lead ( = lead I ) shows less marked, but still hyperacute ST-T wave changes.

Figure-2: I've labeled today's ECG. What do you see?

=============================  

Putting It All Together:

Despite the younger age and seemingly been prior history of today’s 30-ish year old man — determining the “culprit” artery, as well as “What happened when?” does not change the obvious need for prompt cath as soon as this can be done. Virtually all leads on this tracing show marked ST-T wave abnormalities! 

• Q waves have been documented to develop in as short a time period as 1-2 hours. That said — it would seem highly unlikely for Q waves as large XXXX

XXXXX

Cath Findings:

• Left-dominant coronary system.
• 100% proximal LAD occlusion.
• 80% distal LCx stenosis.
• 95% left PDA stenosis.

Cath Intervention:

• Aggrastat (Tirofiban) bolus administered.
• Proximal LAD — Thrombectomy performed; PCI with drug-eluting stent.
• Distal LCx/Left PDA — PCI performed with drug-eluting stent.
• Post-procedure Ejection Fraction preserved!

 

XXXXX 

XXXXXXX

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

Acknowledgment: My appreciation for the anonymous contribution of today's case. 

================================== 

Jennifer Carlquist — FB Messenger (8-19-2026)

 “What happened when?” — Hi! David said this is also a precordial swirl The case is a 36 yo male with cp x 1 hour. Hx: pre dm He had unrealized fh and his cath showed lad circ

EXTRA COPY — ECG Blog #549 — Why CP? — EXTRA COPY —

 XXXXThe ECG in Figure-1 is from a middle aged woman who presented with palpitations and dizziness of 2 hours duration. No chest pain. BP ~120/70 mm Hg.

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

QUESTIONS: 

• How would you interpret the ECG in Figure-1?
• Is this NSVT (NSVT) or aberrant conduction? (How certain are you of your answer?)
• What would you do?
• Does this ECG show anything else?

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

DISCLAIMER:

My follow-up of the above case is unfortunately limited. That said — What counts is the approach. This matches the clinical reality that we often encounter patients for whom we need to initiate management before we know with certainty what the diagnosis is from the initial tracing.

Take another look - now with beats numbered

What are the hints to the likelihood of VT vs aberrant?

Figure-2: XXXX

MY APPROACH:

XXXXX 

underlying rhythm = AFib

despite AFib - constant C (coupling interval)

post-ectopic pauses

atypical lbbb morphology (transition by V3 !!!

Figure-3: XXXX

Why VT?

XXXXX 

Always good to go back to the 12-lead

Although I don't have follow-up - note ST dep = ? post OMI

You'll have to repeat the ECG after treatment of VT to see if ST persists?

Figure-4: XXXX

XXXXXX

XXXXXX

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

Acknowledgment: My appreciation for the anonymous contribution of today's case. 

================================== 

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

THE CASE (from Ahmed Abbas — Anonymous! 

Dear Dr.Grauer. I hope you are doing well.

Today i present to you a case of a 49 year old woman,pre DM, presented to our urgent care center with dizziness and palpitations for the past 2 hours.

 

she denies and chest pain, shortness of breath , or syncope.

Her vitals were BP 118/63, sat 99 on RA, pulse 182.

 

Here ECG showed atrial fibrillation with runs of nonsustained Vtach,her troponin was negative , received 150mg of amiodarone  then transported to hospital.

 

kindly help us interpreting the ECG with the details you usualy provide.

my questions:

1. were those runs of psvt or appatently conducted atrial fibrillation?

2. the widw complex qrs after narrow ,is it ashman?

3. what causes the re-entry if there is one?

 

Your insights are always helpful and appreciated.

Best Regards — Ahmed

MY REPLY:

Very interesting case — so much that I’d like to use it for an ECG Blog if you can give me follow-up.

 

I received 2 ECGs. The 1st one has the date of October 9 @ 7:23 on it — so it is a current (and not a previous tracing). But I have NO idea as to when this 1st ECG occurred with respect to the 2nd ECG that shows NSVT. Was the patient initially in sinus rhythm when she presented with “dizziness and palpitations” but no CP (chest pain)? Or was this after receiving Amiodarone. WHEN did she develop AFib?

 

ECG #2 shows as you say AFib with runs of NSVT (although since beats #1-thru-6 at the beginning of the tracing are all ventricular — we have no idea as to HOW LONG this first run was? (ie, it could have been sustained VT).

 

The few narrow (supraventricular) beats that we do see are irregularly irregular. So despite what looks like a “sinus P wave” in front of beat #23 in lead V3 — this is almost certainly a “fib wave” for a rhythm of underlying AFib.

 

The runs of WCT (wide-complex tachycardia) are fairly but not completely regular. There is a somewhat rightward frontal plane axis (more positive in II,III than in lead I) — and with lbbb-like conduction in the chest leads — BUT this is not “typical” lbbb conduction because there is already a predominantly positive QRS for the wide beats as early as lead V3 (and with true lbbb conduction, transition occurs later, typically by V5 or V6).

In addition — there is a “post-ectopic pause” after beats #6 and after #22 — and that is much more commonly seen following VT.

Finally — there is NO reason for aberrant conduction. Ashman occurs when you have a wide beat occurring after a relative pause ... See ECG Blog #70 and ECG Blog #71 for details about Ashman. But there is no preceding pause to set up conditions for aberrancy — and the same shape wide beat occurs for beats #10 and 14 despite different preceding coupling intervals. These are ventricular beats!

QRS morphology of these wide beats is consistent with RVOT VT (ie, lbbb-like in the chest leads; right frontal plane axis).

 

But GO BACK to ECG #1 — and note the flat (abnormal!) shape of the ST segment in lead V2 (should normally show a gently upsloping ST segment with slight ST elevation) and the clearly FLAT ST segments in V3,4,5 (and definite slight ST depression in V3). So if you only did a single normal Troponin — MORE troponin values should have been done since the 1st Troponin can sometimes be normal despite acute coronary occlusion.

Bottom Line — I am missing details as to what happened when ... but ECG #1 is not normal in a patient who develops runs of VT (and if this was the initial ECG before ECG #2, then I wonder if she had a silent acute posterior OMI?

 

ECG #2 shows AFib with runs of NSVT with RVOT VT morphology.

 

What happened? As I mentioned — I’d love to use this as an ECG Blog if you can answer some of my questions. I’d be happy to acknowledge you (a number of years ago I had you as from Amman, Jordan when you sent me a tracing that I published as a blog. Is that the way you would want me to acknowledge you? Or do you prefer for this case to be anonymous. Just let me know.

 

Hope the above is helpful — 

 

ABBAS REPLY:

Dear Dr grauer

Thank you for your reply. 

The ecg showing nsvt is the initial rhythm at presentation. Only complaining of dizziness, she came to the clinic at 16:45.

 

ECG with sinus rhythm was after we administered amiodarone and transported the patient, it was recorder at the receiving facility at 19:23. 

 

I am not sure if they gave something else in the hospital, I will check tomorrow and let you know. 

 

As for publishing, that would great but as anonymous, because I was not directly involved in the management of the patient,it is recorded in my new job in UAE,I am still new to the place and I don't want colleagues to accuse me of stealing there efforts. 

 

Best regards — Ahmed Abbas