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 was 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?

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

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Figure-2: XXXX

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Figure-3: XXXX

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

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THE CASE:

Challenging for interpretation, rarely happened..

67 M with DM, HTN, HLP, was admitted for abdominal pain 4 days ago. Acute onset of chest pain at midnight, ECG followed by duty resident, he was sure that ECG leads were not misplaced. F/U TnT twice both negative. What cause the limb leads and precordial leads QRS morphology quite different ?

MY INITIAL COMMENT:

Bizarre tracing. @ 林柏志 — Just wondering how much time passed between these 2 tracings and IF the patient was still having CP when the 2nd (bottom) ECG was recorded?

So the bottom ECG is MUCH more plausible than the bizarre top ECG. Assuming the resident verified lead placement AND repeated the ECG after doing so — We then have to consider what might cause this bizarre and drastic change in QRST morphology in both limb and chest leads. Could the patient's sudden chest pain be the result of a PNEUMOTHORAX? (or since the patient had abdominal pain — could it be an abdominal perforation?). I'll eagerly await the answer to this mystery!

 

THE ANSWER:

To Ken Grauer and all responsed folks, it tooks a while to unravel the puzzle. In this case, the lead connections were incorrect at the cable hub: V1 and LL were swapped, as were V2 and LA. Note that both V1 and LL utilize red color-coding; errors can occur if the connectors are unplugged during room cleaning and subsequently reattached incorrectly. Based solely on the ECG, V1 and V2 showed tall R waves compared to the admission tracing. While a posterior MI was initially suspected clinically, this was ruled out following serial ECG follow-ups and an echocardiogram that showed no regional wall motion abnormalities (RWMA). Additionally, an abnormally tall R wave in aVR—a finding typically associated with sodium channel blocker toxicity—was observed; however, the patient was not tachycardic, the QRS complex was not widened, and a medication review ruled out toxicity. A shift in the QRS axis from normal to "right superior axis" (also known as "No-man’s land") was noted, raising suspicion of lead misplacement. Deep S waves in leads I, aVL, and II provided further clues that the leads were misplaced, altering the apparent QRS morphology. Combined with the suspicion of V1–V2 misplacement, it appeared that the V1 and V2 leads had been swapped with the limb leads. After confirming correct electrode placement and re-checking the setup, the error was traced back to incorrect connections at the cable hub.

 

I have unravelled the puzzle of this ECG , hope you enjory it. Never see this kind of misplacement before.

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MY REPLY:

Thanks for the explanation. The ECG is totally bizarre and does not look "anatomic". I should have mentioned that part of verifying that all was done correctly entails checking the cable connections. I "assumed" that was done — and that was my mistake. GREAT case — mystery solved! 

 

PAUL MATERA Comment:

Ken Grauer , as you know we have discussed this issue a few times ie the old bad info in bad info out routine , patient position, lead placement, lead input, calibration all have to be “standard” .. supine (or notation that they were not able to) , leads and inputs correct , 10mm/mV , 25mm/sec (except for Nordic colleagues 50mm/sec) or a “standard” interpretation can’t be done . I have also had situations where the computer was reading something other than the ECG printout was showing .. because the paper feed was slipping making it look like bizarre dysrhythmia , my position is that a seasoned ECG interpreter can read through any non-standard ECG .. as long as the interpreter is aware of each lead positive and negative and which chest leads were misplaced , nod to Einthoven and Vector , great case

 

MY REPLY to Paul:

Paul Matera — Agree entirely with you Paul! The "hint" is how bizarre the change in these tracings is. Simple lead misplacement won't alter the chest leads (and certainly not like this). "Ya gotta be there" — but we need to routinely "add to the checklist" looking at the lead connectors.

林柏志 has kindly granted me permission to write this case up as an ECG Blog — which I will entitle, "The leads were not misplaced!" — 

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Sukumaran and Selvaraj — Indian Pacing Electrophysiol J 24(2):119-121, 2024

https://pmc.ncbi.nlm.nih.gov/articles/PMC11010442/

 

Rudiger et al — Am J Emerg Med 25:174-178, 2007

https://www.sciencedirect.com/science/article/abs/pii/S0735675706003822?via%3Dihub

 

Lead reversals are surprisingly common in practice — estimated to make up between 0.4%-to-4% of all ECGs recorded. It is crucial to recognize electrocardiographic lead reversal because it can lead to a false diagnosis of myocardial ischemia or infarction. The most commonly encountered reversals involve misplacement of the limb electrodes, with right arm–left arm misplacement accounting for 20% of all lead reversals. ECG findings due to limb lead reversal produce characteristic patterns which can help identify them.

 

In contrast, when limb and precordial electrodes are interchanged (Fig. 4), the Wilson Central Terminal is altered, producing bizarre ECGs that are difficult to interpret. These are less common and usually happen because of the misconnection of the electrodes. Electrode misplacement due to faulty cable connections is much less common. Most modern ECG machines have a single cable attaching all the electrodes to the machine. However, a few machines have two separate cables with an identical attachment providing an opportunity for reversal of the cables.

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Paul and Jacob — Indian Pacing Electrophysiol 23(6):205-213, 2023

https://pmc.ncbi.nlm.nih.gov/articles/PMC10685096/

 

— This is an amazingly complete article that details virtually all possibilities of limb lead and precordial lead misplacements. In general — misplacements contained within limb leads (without interchange in any of the chest leads) — and those contained within the chest leads (without interchange in any of the limb leads) — are easier to recognize because the are likely to produce predictable lead reversal patterns (Reference my technical misadventure page). But reversals involving misplacement/interchange of limb and chest leads may produce any number of bizarre possibilities with a unique resultant ECG impossible to predict. The clinical implications are clear: #1) Realize that bizarre ECGs that seem impossible to explain by physiology do occur. When you see such a tracing in a patient in whom the clinical history does not suggest any medical condition likely to produce such a bizarre ECG — especially if other parameters (ie, CxR, Echo) look normal — then suspect some unusual “technical misadventure”. If limb lead electrodes are all on the correct extremity and chest lead electrodes seem appropriately placed — then look at the electrode lead hub connections!

 

Interchange of a precordial electrode with a limb electrode can occur due to the matching colours of the two electrodes [23], or the incorrect attachment of the cable connectors to the junction box of the ECG machine [24]. This distorts the Wilson's central terminal, and results in distortion of the tracings of multiple leads, with augmented precordial-like amplitudes in some of the limb leads and altered morphology in the concerned precordial leads. It could lead to ST elevation/depression in some of the leads, raising the possibility of erroneous diagnosis of myocardial ischaemia/infarction  [24]. This distorts the Wilson's central terminal, and results in distortion of the tracings of multiple leads, with augmented precordial-like amplitudes in some of the limb leads and altered morphology in the concerned precordial leads. It could lead to ST elevation/depression in some of the leads, raising the possibility of erroneous diagnosis of myocardial ischaemia/infarction 

 

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I’ll close with this primer on terminology by “lub dub medical” on ECG Cables: The Complete Guide to Types, Connectors, Lead Configurations and Compatibility ( https://www.lubdub.com/ecg-cables-the-complete-guide-to-types-connectors-lead-configurations-and-compatibility/ ) that 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.

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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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Figure-2: XXXX

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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 —