EXTRA COPY — ECG Blog #552 — The Leads were Not Misplaced - EXTRA COPY

The 2 ECGs in Figure-1 were obtained from the same patient. The patient had been admitted to the hospital for evaluation of abdominal pain. The repeat ECG was recorded after admission because of the sudden onset of CP (Chest Pain).

QUESTION:

• How can it be that these 2 ECGs are from the same patient?  
• NOTE: All electrode leads were correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

Figure-1: Comparison between the 2 ECGs in today's case.

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The initial ECG in Figure-1 ...

The patient's admission ECG ( = ECG #1) is not a normal tracing.

• The rhythm in ECG #1 is sinus at a rate of ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal.
• Assuming the patient is over 35 years of age — LVH is probably present (deepest S in lead V2 + tallest R in lead V5 is very close to satisfying the 35 mm criterion, with an R wave in lead V4 that is extremely tall).
• The ST segment is coved in leads V3-thru-V6, with some ST depression and symmetric T wave inversion. There is nonspecific ST-T wave flattening in the limb leads.
• Impression: Sinus rhythm with probable LVH + ST coving and T wave inversion in leads V3-thru-V6 consistent with LV "strain" and/or ischemia. Clinical correlation is needed (and ideally finding a prior tracing for comparison).

The repeat ECG in Figure-1 ...

My 1st impression on seeing the repeat ECG was, "This is bizarre!".

• I wondered how much time had passed between the recording of ECG #1 and ECG #2?
• Seeing both tracings next to each other in Figure-1 — the differences between these 2 ECGs are striking! Not only is QRS amplitude increased in the repeat ECG — but the frontal plane axis has shifted dramatically to the right, and the QRS is now predominantly positive in lead V1 (whereas in the initial ECG — the QRS in V1 was predominantly negative). 
• This is not the result of a conduction defect — because the QRS lacks the widening of RBBB or IVCD.
• Since lead I and lead V6 are both left-sided leads — these 2 leads normally bear some resemblance to each other. Yet lead I is now predominantly negative — and left-sided chest leads V4,V5,V6 are all markedly positive.
• Yet despite this bizarre and drastic change in QRST morphology that we see between the 2 tracings in Figure-1 in both limb and chest leads — we are told that all electrode leads are correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

How Can this Be?

• Thinking "outside the box" and remembering that the reason ECG #2 was recorded was the sudden onset of CP — I wondered about physiologic events that might cause CP, and which have been known to produce bizarre positional shifts in relative cardiac anatomy (ie, abrupt onset of pneumothorax — or since this patient was admitted for abdominal pain, perhaps intestinal perforation?).
• 
  
• OR — Could this still somehow be some manifestation of a technical misadventure?
• 
  
• PEARL #1: If some kind of “lead switch” turns out to be the cause of the bizarre change in appearance between the 2 tracings in Figure-1 — it cannot be a simple extremity electrode switch. This is because mix-up of extremity electrode placement would not affect the chest leads that now show a highly unusual and unexpected predominant R wave in lead V1. 
• Instead — any type of lead mix-up to produce the abrupt change that we see between the 2 tracings in Figure-1 would have to involve misplacement (or misconnection) of electrodes from both limb lead(s) and precordial lead(s). 

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CASE Conclusion:

• 2 hs-Troponins were negative — and another repeat ECG looked the same as ECG #2. Bedside Echo was normal, without any wall motion abnormality ==> the difference between ECG #1 and ECG #2 is not the result of acute infarction.
• Both ECGs are from the same patient.
• The 4 extremity electrodes were verified to all be on the correct extremities.
• The 6 precordial lead electrodes were all correctly placed on the chest.

The Answer:

The lead connections were incorrectly attached at the cable hub ...

• The connecting cables for unipolar lead V1 and the LL (Left Leg) electrode were swapped.
• As shown in Figure-2 — it's easy to understand how the technical misadventure of misconnecting the V1 and LL cables might happen since both cables are color-coded in RED. 
• It turns out that the cable connectors were unplugged during room cleaning — and then misconnected when the cables were reattached.

Figure-2: Magnified view of the ECG cable hub.

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Discussion:

Technical misadventures produced by limb and/or precordial lead misplacement (or misconnection) — are surprisingly common in practice, with an estimated frequency between 0.4-to-4.0% of all ECGs recorded (Sukumaran and Selvaraj — Indian Pacing Electrophysiol J 24(2):119-121, 2024 - and - Rudiger et al — Am J Emerg Med 25:174-178, 2007).

• Potential consequences of errors in lead misplacement (or misconnection) are obvious — including over- and/or under-diagnosing acute coronary occlusion.
• The most common form of lead misplacement (or lead reversal) — occurs with mix-up of 2 of the 4 limb lead electrodes. By far, the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes — but any lead reversal combination is possible (See ECG Blog #479 — for a growing list of lead reversals and other technical misadventures).
• PEARL #2: Lead reversals of any 2 of the 4 limb lead electrodes are usually readily recognizable once you become familiar with the possibilities — because they generally produce characteristic patterns (as described in detail in ECG Blog #479). 
• In contrast — mix-up between limb lead electrodes and one or more of the chest lead electrodes are often unique, producing unpredictable ECG changes that complicate ECG recognition (as in today's case! ). This is because the Wilson Central Terminal is altered when there is mix-up between limb lead and chest lead electrodes.
• There is tremendous variation among ECG machines that are used worldwide. As a result — hub connections are not "standard". Fortunately — most modern ECG machines have a single cable attaching all electrodes to the machine. But some machines have 2 separate cables, providing more opportunity for lead misconnection (as seen in Figure-2).

I found the article by Paul and Jacob amazingly complete for detailing the numerous possibilities of limb lead and chest lead misplacements (Ind Pacing Electrophysiol 23(6):205-213, 2023).

• PEARL #3: Realize that although uncommon — combined mix-up between limb lead and chest lead electrodes can occur, and when it does — the resultant ECG may look bizarre with an impossible-to-explain appearance by the rules of physiology. Voltage amplitudes may be greatly increased or decreased in various leads — and unpredictable ST-T wave deviations (elevation or depression) may be seen.
• Suspect some unusual form of technical misadventure when you encounter such a bizarre tracing in a patient in whom the clinical history is not consistent with any condition likely to produce such changes (ie, normal CxR and normal Echo — especially if after verifying lead placement and repeating the ECG, the same bizarre findings are present).
• Don't forget to add checking hub lead connections to the checklist!

PEARL #4: I’ll close with reference to the primer by Lub Dub Admin — which reviews the essentials of ECG cables, including types, connectors, lead configurations and compatibility (Figure-4).

• This primer provides insight into the many ways the technical components of what goes into an ECG machine may vary. ECG machines are not all made the same. When you encounter a truly bizarre-looking ECG that does not comply with the usual predictable patterns of lead reversal — we need to put on our “detective hats” and look for unusual forms of technical misadventures.    

—  — 

Figure-3: What can go wrong with ECG Cables (by Lub Dub Admin).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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EXTRA COPY — ECG Blog #553: What Happened? — EXTRA COPY —

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

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Acknowledgment: My appreciation to Kashif Aleem (from Lahore, Pakistan) for allowing me to use this case and these tracings. 

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Kashif Aleem <rock2hawk@gmail.com>  (on Feb. 10, 2026)

You can address me as 

Kashif Aleem — PIC Lahore, Pakistan. (from Lahore, Pakistan)

 

Hi, I hope this email finds you well. 

I'd really appreciate your input on this one which will help many of my colleagues understand this ecg pattern...

76 years old female with Typical chest pain lasting 2 hours which settled accompanied by unsettling st elevations. 

 

What could be the culprit vessel and what territory infarct/STEMI it can be labeled for documentation purpose. 

I take it as significant and mostly LMCA significant disease. 

I'll follow up on angiogram and share when available. 

Thanking you in advance! 

Stay blessed. 

MY REPLY:

Hi. I agree with you — I strongly suspect this is one of those rare cases of acute LMain occlusion in which the patient survives long enough to do the ECG.

 

I refer you to the December 18, 2025 post in Dr. Smith’s ECG Blog. Check out my comment at the bottom of the page — in which I updated Dr. Smith’s collection, now of 9 cases of documented acute LMain occlusion — as to what you might see on the ECG of a patient with acute LMain occlusion.

 

In a word — you might see ANYTHING! Simply because you have multiple different vectors of ST elevation from varied contributions of all major coronary arteries. Some give ST elevation vectors — other give reciprocal ST depression — and impossible to predict which of these multiple vectors will dominate with ST elevation not cancelled out by opposing ST depression …

In your case — we see marked ST elevation in the antero-lateral area, with reciprocal ST dep in the inferior leads.

 

Hopefully your patient survives.

 

With your permission — I would definitely want to publish an ECG Blog of your case once you have cardiac cath result.

• May I have your permission to publish this case?
• I would be glad to acknowledge you — Please confirm how you would want your name to read = Kashif Aleem? — I also like to add the city and country from where you are from — OR — your contribution could be anonymous. JUST LET ME KNOW.

BEST — Ken

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KASHIF REPLY:

I'd try my best to trace her angiogram. 

I was interested in explanation of these aberrant vectors. Especially st elevation lead 2. Broadly, we have predominant st elevation in left sided leads and st depression in right sided vectors. 

I also acknowledge that I have seen such cases in which this pattern transiently appears like during stress testing and signifies Supply demand mismatch of significant LMCA lesion rather than total occlusion. 

Our patient was hemodynamically stable and chest pain free when presented to our setup. ECG changes and pain had settled completely. Cath operators didn't oblige our request for angiogram on priority basis. 

 

Yeah I would definitely want others to learn from this case...

You can address me as 

Kashif Aleem 

PIC Lahore, Pakistan. 

 

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MY REPLY:

Thanks for your reply.

 

Hard to imagine WHY the interventionists decided not to promptly catheterize this patient ==> this is a KEY factor for others to learn form. The process of acute coronary occlusion is often marked by intermittent “spontaneous reperfusion” of the “culprit” artery, which in this case, most probably is the LMain coronary artery.

What spontaneously reopens — may just as easily (and at any time) spontaneously reclose — and given likely LMain location, this patient would be a high risk of VFib and dying at that time.

• The fact that this patient’s CP resolved and “his ECG changes settled” at that time is telling us that his acute occlusion did spontaneously open. But this patient is at very high risk of spontaneous reclosure that may occur at any time.

 

As to “explaining” the reason for the location of findings — I think Dr. Smith’s collection of 9 cases (that I put together in the attached table) tells the story. The KEY points are:

• We have NO IDEA as to what the “culprit’ artery looked like at the time that cath was done! (ie, We know there was spontaneous reopening shortly after because CP resolved and the ST elevation was much less) —  so we just don’t know if the culprit artery was completely or partially closed at that time …
• There could have been subtotal (but not complete) LMain occlusion with some unpredictable pattern of collateral flow.
• Instead of LMain occlusion — there could be underlying multivessel disease with occlusion of one or more of the major arteries (ie, acute occlusion of the proximal LAD and LCx …).

 

All I know is that we see a huge vector of anterolateral ST elevation here with reciprocal ST dep in “right-sided” areas ( = leads IIII, aVR and V1).

 

Would be GREAT if you could get a copy of that ECG at the time CP resolved and the ECG improved. The fact that operators decided not to immediately cath the patient because CP resolved and the ECG improved is the KEY learning point.

 

Hopefully the patient survives …

 

Ken

 

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Thank you Kashif.

 

I’ll await cath results from you. I’ll try to publish this within a month or so after I receive cath results (I have a few other cases to go before — and it also will be good to give this a little time before I publish the case).

• Let me know how much time passes until cardiac cath is done ...

I will acknowledge you = Kashif Aleem (from PIC Lahore, Pakistan) — and I will let you know once the case is published.

 

There is a lot for others to learn from this case! — Ken

EXTRA COPY — ECG Blog #554: What is Unusual Here? — EXTRA COPY

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Acknowledgment: My appreciation to M Athar Sadiq (from Muscat, Oman) for the case and this tracing.

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Athar Sadiq matharsadiq@gmail.com   — 10/15/2026

— “What is unusual here?” —

 

Dear Respected Prof. Grauer. I hope you are doing well.

I would greatly appreciate your expert opinion on the attached ECG, particularly regarding the underlying rhythm.

The patient has diabetes mellitus, hypertension, and known coronary artery disease, with previous PCI involving three drug-eluting stents in 2022 and 2024. LV systolic function is preserved, with Grade II diastolic dysfunction. The patient is clinically stable without heart failure symptoms but has limited mobility. The referral to me was for preoperative cardiac assessment before knee replacement and radiofrequency ablation for knee pain.

ECG showed right axis deviation consistent with left posterior fascicular block (LPFB), associated with poor R-wave progression.

My main concern is the rhythm, which is difficult to interpret, and the underlying conduction pattern is unclear.

I would be grateful for your interpretation, particularly regarding the atrioventricular conduction pattern.

Please feel free to discuss this ECG on your ECG blog if you find it interesting.

Thank you very much for your time and expertise.

 

Kind regards — M Athar Sadiq

 Consultant Interventional Cardiologist

Sultan Qaboos University Hospital, Muscat, Oman 

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MY THOUGHTS and REPLY to M Athar Sadiq:

This is a very challenging tracing — that I definitely want to use as a case for my ECG Blog. I will probably publish it in about a month. I’ll be happy to acknowledge you — as M Athar Sadiq (from Muscat, Oman) if you like — or the case can be anonymous. JUST LET ME KNOW. In any case — I’ll let you know when I publish it!

 

I’ll add that I shared this tracing with Dr. Willy Frick — who is a cardiologist who also often writes for Dr. Smith’s ECG Blog (as I do). I believe he shares my opinion of this tracing — which I describe below.

 

I agree with your interpretation of the 12-lead in this patient with known coronary disease, as well as evidence of impaired conduction with the LPHB. I see no acute ST-T wave changes.

 

What is so interesting about this case — is the total variability and unpredictability of PR and R-R intervals! I have seen cases of “vagotonic block” (See my ECG Blog #61) — in which because of intense vagal tone (from vomiting, pain, exertion) — there can be surprising variability in PR, R-R intervals, as well as variable forms of AV block. But as I understand — this was a preop ECG in a patient not under any specific stressors.

 

https://www.ekgblog.com/2013/02/ecg-interpretation-review-61-av-block.html

 

I see NO repetition of PR intervals on your patient’s ECG! This is unusual. Almost always with simple AV Wenckebach — the 1st beat in most groups is preceded by a constant PR interval. But as you can see from the measurement figure that I have attached — ALL PR intervals are different! And all R-R intervals are different — which is NOT what I’d expect if there were junctional escape beats (typically — the preceding R-R interval of junctional escape beats is constant! (but it is totally variable here).

 

The most logical way for me to explain this — is that there is autonomic influence occurring throughout the tracing despite no obvious vasovagal stimulus! Although impossible to know for certain (because of the complete variability in PR and R-R intervals) — I think it most logical to postulate that there is AV Wenckebach (as I show on my attached laddergram) — with the variation in PR and R-R intervals being caused by alteration of underlying autonomic tone. Given this patient’s known history of significant coronary disease and conduction defect ( = the LPHB) — and perhaps older age? (How OLD is this patient?) — these factors may predispose to variation (instability) of underlying vasovagal tone. That said — I cannot recall seeing any other case showing this much unpredictable variability in intervals.

 

Bottom Line — I believe the reason there are more “on time” P waves than QRS complexes — is that there is 2nd-degree AV block of the AV Wenckebach (Mobitz I) type plus underlying coronary and conduction system disease producing the variation in autonomic tone. That said — there seems to be NO higher-grade AV block, so it should be fine to go ahead with the surgery.

 

I hope the above is helpful to you! — : ) Ken

 

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MY QUESTIONS TO WILLY FRICK

Hi Willy. I’ve just spent the past hour-plus “playing” with your ECG Toolkit. I’ve saved 2 tracings on a VERY interesting case (that I’ll also pick your brain on) — sent to me from an interventional cardiologist from Oman. I was going to use this as a case on my ECG Blog.

 

Here is the history: The patient has diabetes mellitus, hypertension, and known coronary artery disease, with previous PCI involving three drug-eluting stents in 2022 and 2024. LV systolic function is preserved, with Grade II diastolic dysfunction. The patient is clinically stable without heart failure symptoms but has limited mobility. The referral to me was for preoperative cardiac assessment before knee replacement. ECG showed right axis deviation consistent with left posterior fascicular block (LPFB), associated with poor R-wave progression. My main concern is the rhythm, which is difficult to interpret, and the underlying conduction pattern is unclear.

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My “Take” (as per the attached laddergram) — is that this is some kind of 2nd-degree Mobitz I ( = AV Wenckebach) tracing, as the P wave rhythm is fairly (not completely) regular — and there are more QRS complexes than P waves ==> 2nd-degree AV block. The fascinating part is that ALL of the PR intervals and all of the R-R intervals vary! (sometimes not by much — but I believe the variability phenomenon is real! The only way I can explain this is that there must be variation in autonomic tone! The patient presumably is an older adult (age not given) — with a history of coronary disease and assuming no RVH … what looks like LPHB on his 12-lead (therefore conduction baseline conduction system abnormalities).

 

There are of course a bunch of other potential laddergram explanations for this … (ie, Could be some form of dual level AV block — there could be junctional escape beats — although against this as a sole explanation is the fact that those P waves with a real long interval that look like they are not conducting are NOT associated with a constant R-R interval as is usually seen with junctional escape. And the reason I really think all QRS complexes are more likely to be conducted — is that despite “on time” P waves — R-R intervals are occurring “earlier-than-expected. What do you think?  (I will write you now my feedback on using your EKG Toolkit for this case —