EXTRA COPY: ECG Blog #541: Obvious MI — What is the Culprit? — EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from XXXXX (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

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Figure-5: XXXX

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Figure-6: XXXX

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Acknowledgment: My appreciation to Op. Sanooj (from Calicut, India) — for allowing me to use this case and this tracing.

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ADDENDUM:

I have added this Tab on Technical "Misadventures" — to the Menu at the top of every page in this ECG Blog:

— Where to find this LINK in the Top Menu! — 

All-too-often lead reversals, unsuspected artifact, and other "technical misadventures" go unrecognized — with resultant erroneous diagnostic and therapeutic implications. 

• In the hope of facilitating recognition of these cases — I am developing an ongoing listing on this page with LINKS to examples that I’ve published in this ECG Blog, as well as in Dr. Smith’s ECG Blog where I frequently write commentaries.

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O.p. Sanooj ( 10/10/2023 ) — Facebook Messenger

from Calicut, India — I am from Calicut, India. Myself Dr Sanooj Op

— "Obvious MI but WHAT is the Culprit?"

Sure sir, it is a honour for me if you publish this. 

Your earlier advice of giving   IV betablocker and cordarone helped me to kill VT in this case. And also I gave plenty of fluids suspecting RVMI. Thanks from the bottom of my heart sir.

 

THE CASE:

Hi sir, this patient had arrested in cathlab while doing angioplasty. Given CPR for 30 minutes and multiple shocks for VT. Finally after opening RCA, he became stable. Now he is doing well.

 

There is shelf like ST depression in inferior leads, ST elevation in 1, aVL,V6 indicating infero lateral MI. The absence of ST depression in V1 indicates there is RVMI. Am I right sir?

Sir, this is today's ecg. Patient is stable now. There is no occlusion in Lcx. The culprit artery on cath was RCA. I have confirmed it.

MY 1st REPLY (I was initially fooled !!!! — important to tell why!)

Hi. I put the 2 parts together to get a better 12-lead picture. I see sinus rhythm — with as you say MARKED ST elevation in I,aVL and V3-thru-V6. This picture to me is MUCH MORE SUGGESTIVE of acute LCx (Left CircumfleX) occlusion. One of the 2 QRS complexes in lead V2 has slight ST depression (but neither has the usual slight ST elevation) — which to me suggests there is also posterior MI. I am not quite sure why there appears to be slight ST elevation in lead V1 — but everything else on this tracing suggests that the LCx is the "culprit" artery — and the LCx generally does NOT supply the RV ...

 

Are you sure that the "culprit" artery on cath was the RCA? Did this patient have multi-vessel disease ??? — as if he did, then depending on the pattern of collateralization, you may get a different distribution for the ST elevation and depression.

The massive ST depression in leads II,III,aVF is consistent with reciprocal ST depression — which further supports that the main injury is from LCx occlusion.

 

Let me know if you have any follow-up. How is the patient now doing? Any follow-up ECGs? (the distribution of reperfusion T waves might support our theory for what was the "culprit" artery).

MY 2nd REPLY:

NOW I see what is going on !!!! There was LA-LL Lead Reversal on the initial ECG !!!! The usual "clue to this is that the P wave in lead I is larger than in lead II — but that was not at all obvious here, because P waves are almost of similar size. But your post cath ECG shows DEFINITE reperfusion changes in the inferior leads !!! and that would not make any sense if this was an LCx occlusion.

 

I thought lead V1 (as YOU also said) looked funny for LCx occlusion on the original tracing! — and lead II ALSO looked funny, because I would NOT expect reciprocal ST depression — and the AMOUNT of ST elevation in leads I,aVL is more than I've ever seen for LCx occlusion.

BUT — if you make the adjustments that I've made for LA-LL Reversal — then the original ECG fits PERFECTLY with your clinical scenario ( = marked ST elevation in inferior leads with more recip ST dep in aVL than in lead I — and as YOU said, the subtle ST elevation in V1 IS strongly suggestive of acute RV MI! There is also posterior MI which is "masked" because of all the ST elevation in V1,V2 from the RV MI !!!!

And now the post cath ECG makes perfect sense!!!!

I definitely want to use this as an ECG Blog! It may be a month or so until I get to this (because other cases come before) — but do I have your permission to publish this? Please remind me of the city & country from where you are from — as I will acknowledge you and let you know when I publish this. This is a SUPER CASE!

My Blog #396 (https://tinyurl.com/KG-Blog-396 ) is on a lead reversal — but if you scroll down to the bottom of the page — you'll find links to LOTS of lead reversal cases that I've commented on (including a bunch with LA-LL lead reversal) - FASCINATING! — :)

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ECG Blog #375

https://ecg-interpretation.blogspot.com/2023/04/ecg-blog-375-at-least-3-major-findings.html

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The ECG in Figure-1 was obtained from a 50-year old man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain).

QUESTIONS:

• There are at least 3 principal findings on this ECG — some of which deal with a possible “culprit” artery and/or the location of whatever is going on. How many of these findings can YOU identify?
• 
  
• HINT: Is the rhythm sinus?

Figure-1: The initial ECG in today's case — obtained from a 50-year old man with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always — I like to start my interpretation of 12-lead ECGs with assessment of the rhythm (as per my systematic approach in ECG Blog-205). Since there is no long lead rhythm strip — I focus my attention on the 3 beats that we see in lead II from the 12-lead ECG shown in Figure-1.

• The QRS complex is narrow — so the rhythm is supraventricular.
• Although we lack a long lead rhythm strip — it appears that the overall rhythm in Figure-1 is Regular — at a Rate between ~80-85/minute (ie, with an R-R interval of between 3-4 large boxes in duration).
• Upright P waves are present in lead II — but there is something unusual about these P waves in lead II. Did you notice this unusual finding that is not typically seen with a normal sinus rhythm?

PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as it passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II in the frontal plane (lead II being located at +60 degrees in the frontal axis plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).

• Note in Figure-1 — that the upright P wave in lead II is clearly smaller than the upright P wave in lead I. While possible that this discrepancy in relative P wave size between leads I and II could be seen with either an ectopic atrial rhythm or certain forms of dextrocardia — this P wave size discrepancy should prompt consideration of the most commonly overlooked form of lead reversal, which is a mix-up of the LA (Left Arm) and LL (Left Leg) electrodes.

What Happens with LA-LL Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
• 
  
• By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).
• 
  
• In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal in Figure-2.

Figure-2: LA-LL Lead Reversal (adapted from LITFL).

What Should the Initial ECG in Today's Case Look Like?

For clarity — I've taken the limb leads from the initial ECG in today's case ( = ECG #1) — and inverted lead III — switched leads I and II — and switched leads aVL and aVF. The result is ECG #1a — which is seen in the righthand portion of Figure-3. 

• Note that the chest leads in ECG #1a of Figure-3 — are unchanged from what they were in Figure-1.

QUESTIONS:

Looking at ECG #1a in Figure-3:

• Is the P wave in lead II of ECG #1a now larger than the P wave in lead I (as it should be with a normal sinus rhythm)?
• 
  
• Now that we've established that the 1st KEY finding in today's case is that there was LA-LL Lead Reversal — How would YOU interpret ECG #1a, which shows what today's 12-lead ECG would look like IF lead placement was correct?

MY Interpretation of ECG #1a:

Having accounted for what today's initial tracing would have looked like had lead placement been correct — I see the following in ECG #1a:

• The rhythm is sinus at ~80-85/minute.
• There is dramatic ST elevation in each of the inferior leads. A Q wave is forming in lead II.
• There is equally dramatic reciprocal ST depression in lead aVL (which manifests the mirror-image opposite ST-T wave picture as seen in lead III).
• Significant reciprocal ST depression is also seen in the other high-lateral lead ( = lead I).
• 
  
• In the chest leads — there is significant ST elevation, with a straightened ST segment takeoff in lead V1.
• There is abrupt transition to a surprisingly tall R wave (of ~10 mm) already by lead V2. There is significant ST depression with a positive "Mirror" Test for acute posterior infarction in lead V2. Chest lead ST depression is limited to lead V2.
• There is marked overlap of QRS complexes in virtually all chest leads. The deep anterior S waves and tall lateral chest lead R waves suggest significant LVH.

Putting It All Together: 

After correcting for LA-LL lead reversal — ECG #1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement.

• PEARL #2: The "culprit" artery in today's case — is almost certain to be the proximal RCA (Right Coronary Artery). As discussed in ECG Blog #141 — ECG features in Figure-3 that strongly support the likelihood of the RCA as the "culprit artery" are: i) ST elevation in lead III>II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement. 

PEARL #3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx (Left Circumflex) coronary occlusion. The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the culprit artery. 

• ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI. That said — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. 
• Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changess due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement. This is precisely what we see in lead V1 of ECG #1a.

Figure-3: Comparison of the limb leads from the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal. (To improve visualization — I've digitized the original ECG using PMcardio).

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Acknowledgment: My appreciation to Adem Ahmed (from Nouakchott, Mauritania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• 
  
• ECG Blog #190 — When to suspect acute RV Infarction?
• ECG Blog #141 — On acute RCA Occlusion (with RV MI).
• ECG Blog #80 — More on the "culprit" artery.
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
• 
  
• ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis). 
• ECG Blog #317 — reviews use (or not) of Posterior Leads.
• 
  
• ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
• 
  
• 
  
• ECG Blog #264 — For review of another limb lead reversal (ie, LA-RA lead reversal in a patient with an acute MI).

OTHER Examples of Lead Reversal (from Dr. Smith's ECG Blog):

Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — it's important to familiarize ourselves with how best to recognize the various forms of these "misadventures". For review — Check Out My Comment — at the bottom of the page in the following posts on Dr. Smith's ECG Blog:

• The June 4, 2018 post (LA-LL reversal).
• The July 29, 2018 post (LA-RA reversal).
• The November 4, 2018 post (Leads V1,V2 misplacement).
• The February 11, 2020 post (LA-RA reversal).
• The March 18, 2020 post (LA-RA reversal).
• The August 28, 2020 post (LA-LL reversal).
• The November 19, 2020 post (LA-LL reversal).
• The November 27, 2021 post (LA-RA reversal).
• The April 17, 2022 post (Leads V1,V2 misplacement).
• The May 24, 2022 post (LA-LL reversal).
• The May 26, 2022 post (LA-LL reversal).
• The August 17, 2022 post (LA-RA reversal).

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EXTRA COPY — ECG Blog #540: It Doesn't "Fit" ...- EXTRA COPY

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

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Figure-2: XXX

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Figure-3: XXX

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Acknowledgment: My appreciation to Paul Carr and Nataliya Szozda (from Toronto, Canada) for contributing this case.

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From Paul Carr

Paul Carr <paul.carr@medportal.ca>  (7/13/2026)

TITLE: — It Does Not "Fit" Clinical —

ME TO ACKNOWLEDGE: — Paul Carr and Dr. Nataliya Szozda (both from Toronto, Canada) 

 

This case is from a rural hospital with no cath lab or stroke thrombolysis capacity.

A 59 year old female was brought by ambulance to the emergency department. She was at a spa and while getting out of the hot tub suddenly became confused and unable to speak. She subsequently had clonic movements and profuse diaphoresis. She was placed in a position of safety.

 

On EMS arrival patient was confused and "post ictal" with ongoing diaphoresis. During transportation she became agitated and combative requiring sedation with midazolam. During transport the monitor showed ECG changes concerning for "STEMI" and so they diverted to my local hospital rather than preceding directly to the nearest stroke centre. On arrival patient was not responsive.

 

The nearest interventional cardiologist was paged and his concern was that with the story not fitting occlusion MI, it was important to work up for other etiologies before considering any medical intervention for possible acute MI.

 

The nearest stroke centre also had interventional cardiology and the stroke team there agreed to take the patient emergently "code stroke".

 

While patient was in transit the initial high sensitivity troponin was 400 (upper limit of normal for our assay is 20).

 

At the stroke centre the patient was found unfortunately to have a necrotic ring enhancing mass with significant surrounding edema favoured to represent a tumour. I do not have a follow-up ECG but my understanding is these ST elevations normalized over 1-2 hours.

 

Paul Follow-Up !!!!

Survived neurologically intact. Now they think might be necrotic transformation of previous stroke rather than tumour. Cardiologist opined may be Takotsubo. Repeat troponin was unchanged.

 

Just saw that they did do a Cath and pristine coronaries with mid-type typical Takotsubo wall motion abnormality.

SSmith! "Clinical does not "fit" OMI. These cases tell you everything you need to know to interpret your case!

Dec. 20, 2021 CASE

https://drsmithsecgblog.com/collapse-ventricular-tachycardia/

 

Feb. 20, 2025 CASE

https://drsmithsecgblog.com/acute-coma-then-sudden-pea-arrest-in-2/

MY REPLY to PAUL — I wrote Steve back the following: THANKS Steve! My Comment on the 2nd case you sent (from Feb. 20, 2025) relates to a subarachnoid hemorrhage causing the pseudo-MI pattern. I hadn’t been aware of brain tumor doing the same, but as per your 1st case — a simple MI should not result in a non-responsive patient — and no flow to the heart as well as the brain + greatly increased catecholamines might raise Troponin and produce bizarre ECG changes that in a patient with CP would say S. Afr. Flag .. — but which in a comatose patient say CNS catastrophe and NO MI. THANK YOU = “Clinical does not fit OMI!” —

 

PAUL — So yes, I DO want to write up this case! I like to acknowledge people — so should I say that the case is from Paul Carr from Toronto, Canada? — or if you prefer, the case can be anonymous — JUST LET ME KNOW! It may be a little while before I publish it as I have other cases to go in front of it.

Otherwise — My wife and I just went on a Tauck tour to Canada's eastern "Capital Cities" and Toronto was our first stop. GREAT CITY! I love the unique skyline! We went up the CN Tower and toured the city. Other stops on the tour were Niagara Falls (Canadian side) — Ottawa, Montréal, Québec — GREAT country, wonderful and friendly people who amazingly still like us Americans after all the mess that our current administration continues to cause (very embarrassing to me!)

Let me know if you find out anything else? Did the patient survive?
I'll let you know when I publish this — :)

 

Paul Follow-Up !!!!

Survived neurologically intact. Now they think might be necrotic transformation of previous stroke rather than tumour. Cardiologist opined may be Takotsubo. Repeat troponin was unchanged.

 

Just saw that they did do a Cath and pristine coronaries with mid-type typical Takotsubo wall motion abnormality.

 

 

MY REPLY (7/14/2026):

Thanks for the clinical & ECG follow-up! Cath very helpful that it ruled out coronary disease and confirmed Takotsubo. That said — although Takotsubo can definitely mimic an acute MI (!) — as Takotsubo evolves, you'll usually see a more prolonged QTc than what we see here ... so would be GREAT if you could find out #1) How much time passed between these 2 ECGs that you have sent me — and #2) Any chance you could check to see if a final ECG was done? (looking to see if the T wave inversion with long QTc finally developed .... GREAT CASE with review of Takotsubo here. THANKS again! — :) Ken

https://ecg-interpretation.blogspot.com/2024/10/ecg-blog-456-woman-with-chest-pain-from.html

 

P.S. You say "Ontario, Canada" — but for "symmetry", is it OK if I say both you and Dr. Szozda are from Toronto, Canada? 

 

P.P.S. It may be a little while until I publish this as I have other cases to go before — but I'll definitely let you know when I do publish it — :)

 

PAUL REPLY (on 7/16/2026):

Thanks as always. Yes Toronto Canada for both is great. There was only about 4 hours between ECGs I believe and I will look for a discharge ECG for completeness. Probably best to have some time before publication to help with anonymity of the case anyway. All the best, Paul

PAUL's COMPLETE CASE !!!!
Hi, Ken, This is Paul Carr writing. Had a very interesting case yesterday I wanted to share in case you wanted to use for the blog.

 

This case is from a rural hospital with no cath lab or stroke thrombolysis capacity.

 

A 59 year old female was brought by ambulance to the emergency department. She was at a spa and while getting out of the hot tub suddenly became confused and unable to speak. She subsequently had clonic movements and profuse diaphoresis. She was placed in a position of safety.

 

On EMS arrival patient was confused and "post ictal" with ongoing diaphoresis. During transportation she became agitated and combative requiring sedation with midazolam. During transport the monitor showed ECG changes concerning for "STEMI" and so they diverted to my local hospital rather than preceding directly to the nearest stroke centre.

 

On arrival patient was not responsive. She was met in the ambulance bay where a formal ECG showed concerning elevation in I and aVL, disproportionately large T waves in I, and reciprocal depression maximal in lead III.

 

The nearest interventional cardiologist was paged and his concern was that with the story not fitting occlusion MI it was important to work up for other etiologies before considering any medical intervention for possible acute MI.

 

The nearest stroke centre also had interventional cardiology and the stroke team there agreed to take the patient emergently "code stroke".

 

I had a broad differential and agreed with the consultant recommendations. Near the top for me was acute aortic syndrome involving the left main coronary with embolic stroke so we did not give any antiplatelet or anticoagulation.

 

While patient was in transit the initial high sensitivity troponin was 400 (upper limit of normal for our assay is 20).

 

At the stroke centre the patient was found unfortunately to have a necrotic ring enhancing mass with significant surrounding edema favoured to represent a tumour. I do not have a follow-up ECG but my understanding is these ST elevations normalized over 1-2 hours.

 

It is important to remember that history is just as important as the ECG itself and that we need to keep an open mind and at least consider a thorough differential for all cases.

 

I'm curious to see what QOH would make of that ECG and also for your expert opinion on the case.

 

Best wishes,

Paul

EXTRA COPY — ECG Blog #539: Does SVT cause Hypotension? — EXTRA COPY

The ECG in Figure-1 was obtained from a young adult woman — with a history of recurrent SVT. She was hypotensive with this most recent episode.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Does this tracing "fit" with this patient's history?
• Extra Credit: Is there evidence of underlying atrial activity?

Figure-1: The initial ECG in today's case — obtained from a young adult woman with a history of recurrent SVT. (To improve visualization — I've digitized the original ECG using PMcardio).

Review of some Clinical Concepts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~180-190/minute.

• Although in a number of limb leads the QRS does not seem wide — it "looks" wide in most of the chest leads, and measures 0.11-0.12 second in leads V1,V2.
• PEARL #1: I've seen different answers for what constitutes "QRS widening" in an adult. I favor the following 2 guidelines: i) For measuring QRS duration — Use that lead in which you can clearly determine the onset and offset of the QRS complex — and in which the QRS is longest; — and, ii) Because some cases of fascicular VT may only measure 0.11 second in duration — I consider the QRS to be "wide" if in any lead the QRS clearly measures ≥0.11 second in duration. And the easy way to tell if QRS duration is ≥0.11 second — is to determine if QRS duration is clearly more than 1/2 a large box in duration (ie, Each large box on ECG grid paper = 0.20 second ==> 1/2 a large box = 0.10 second, and if the QRS is more than this — then by my definition it is wide!). 
• PEARL #2: Just because a given diagnosis is written in a patient's chart — does not necessarily mean that diagnosis is correct (unless you also find firm objective evidence in that patient's chart to support the diagnosis!). Make this sentence BOLD! We need to remain open to other possibilities. BOLD & ITALICS! Therefore, in today’s case — I did not fully accept the prior “history of recurrent SVT” — because I was not shown any prior ECG documenting that the known tachycardia was indeed supraventricular.
• PEARL #3: It is still all-too-commonly believed that the cause of the overwhelming majority of regular WCT rhythms in younger adults is some form of SVT (SupraVentricular Tachycardia) — in which QRS widening is explained by either preexisting BBB (Bundle Branch Block) or aberrant conduction. However, as was shown in ECG Blog #489 — Blog #38 — and Blog #464, among others — the idiopathic VTs (which occur in patients without underlying heart disease) are much more common in younger adults than is currently appreciated (More on the idiopathic VTs below in today's ADDENDUM).

PEARL #4: Today's patient was hypotensive in association with the rhythm in Figure-1. Although it is clearly more common for a patient in VT to be hypotensive (than for a patient in an SVT rhythm) — a patient's BP (blood pressure) is not an infallible predictor for distinguishing between VT vs SVT (See ECG Blog #220 — Blog #38 — and Blog #297). For example:

• We've seen a number of patients in sustained VT remain hemodynamically stable not only for hours — but for days!
• In contrast, most otherwise healthy younger adults who present in a sustained SVT rhythm — will remain stable for long periods of time.
• Bottom Line: The fact that today's patient was hypotensive in association with the rhythm in Figure-1 is not reliably predictive of this rhythm's etiology. That said — it is indication of the need for prompt effective therapy (ie, having a lower threshold to proceed with synchronized cardioversion).

The ECG in Figure-1:

As already noted — the rhythm in Figure-1 is a regular WCT at a rate of ~180-190/minute. With regard to atrial activity — there is no consistent sign of upright sinus P waves in lead II, or in any other lead. That said — the negative notching in the terminal portion of the QRS in leads II and aVF suggests there are 1:1 retrograde P waves (YELLOW arrows in Figure-2).

• PEARL #5: Even if the negative notching highlighted by YELLOW arrows in Figure-2 does represent 1:1 retrograde P waves — this does not help in our differentiation of the rhythm because both VT and and reentry SVT rhythms may manifest 1:1 VA conduction.

Figure-2: YELLOW arrows highlight what appears to be 1:1 retrograde P waves.

What about QRS Morphology?

Up until this point — We've highlighted this young woman's history, namely of recurrent SVT, with today's episode thought to represent just one more recurrence. That said, because the QRS in Figure-1 is wide — We need to consider the possibility of VT.

• PEARL #6: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #7: As discussed below in the ADDENDUM to today's post — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB/hemiblock conduction!

NOTE: As shown in Figure-3 — QRS morphology is not typical for RBBB with either left anterior or posterior hemiblock.

• Instead of the expected triphasic rsR' complex in lead V1 (with taller right "rabbit ear" and a distinct S wave that descends below the baseline) — a qR pattern is seen in this lead. While SVT rhythms do not always show "typical" QRS morphology — it's important to appreciate that atypical conduction features may be a hint of a ventricular etiology (See Figure-9 in the ADDENDUM below).
• Typical RBBB conduction should manifest a wide terminal S wave in left-sided leads I and V6. While we do see a wide terminal S wave in lead I — this feature is missing in lead V6 (ie, the deep S wave in lead V6 in Figure-3 is narrow and followed by a small positive deflection = an RSr' in lead V6).
• With RBBB conduction — left-sided lead I typically manifests predominant positivity prior to the wide terminal S wave. However, the R wave in lead I in Figure-3 is relatively small.
• QRS morphology in leads II and III is not typical for either LAHB or LPHB conduction (ie, leads II and III lack the predominant positivity of LPHB — and the rSr' pattern in lead III is not the expected rS pattern typical of LAHB conduction).

BOTTOM Line: While the above subtle morphologic features do not rule out the possibility of an SVT rhythm for today's tracing — they should increase our suspicion that the rhythm in Figure-3 may represent fascicular VT.

• PEARL #8: Assessment of QRS morphology on the surface ECG is not definitive for distinguishing between SVT vs VT. Sometimes the only way to determine the true etiology of a regular WCT rhythm is by EP testing. That said — especially given the history in today's case of recurrent episodes — these atypical morphologic features made me highly suspicious that the rhythm in Figure-3 was probably fascicular VT.

PEARL #9: As has been emphasized on many posts in this ECG Blog — the treatment of choice for a hemodynamically stable patient in fascicular VT is IV Verapamil (or IV Diltiazem).

• Although Adenosine may convert some cases of fascicular VT — it is much less effective than IV Verapamil in this group of patients.
• IV Verapamil or IV Diltiazem should not be given to patients with ischemic VT (ie, in patients with underlying structural heart disease). This is because the negatively inotropic and vasodilating effects of these drugs may lead to hemodynamic decompensation. However, these drugs are safe in patients with idiopathic VT who do not have underlying heart disease.
• The extra advantage of using IV Verapamil to treat an otherwise healthy younger adult with suspected fascicular VT — is that this drug is likely to be effective regardless of whether the rhythm is fascicular VT or a reentry SVT rhythm!
• The above said, since today's patient was hypotensive in association with the rhythm in Figure-1 — the treatment of choice is synchronized cardioversion.

Figure-3: QRS morphology in today's tracing is not typical for RBBB/hemiblock conduction.

One More Clue to Today's Rhythm!

Take another LOOK at today's rhythm in Figure-4.

• Could the slanted RED lines in Figure-4 represent atrial activity?

Figure-4: What do the slanted RED lines indicate?

Answer:

Overall — there is very little artifact in Figure-4. As a result — I was struck by the consistent disturbance in the baseline in lead II that has to be "real" (ie, slanted RED lines in Figure-4) — with similar disturbance of the baseline in lead lead aVF (slanted BLUE lines) — albeit not in the other inferior lead ( = lead III), and not in other leads.

• I wondered IF the slanted RED lines in lead II might represent underlying AV dissociation?

To explore this possibility — I've isolated and enlarged in Figure-5 the 15 beats that we were seeing in Figure-4.

Figure-5: A closer look at the 15 beats in lead II.

As suggested earlier in Figure-2 — YELLOW arrows pointing to the terminal negative notching in Figure-6 highlight retrograde P waves. 

• But did YOU previously notice when you first examined this tracing, that this negative terminal notching is not present after beats #3 and 10? Why might this be so?

Figure-6: Retrograde P waves are not seen after beats #3 and 10.

Calipers are needed to answer this question.

• I thought the 2 consecutive RED arrows in Figure-7 looked to be highlighting 2 consecutive sinus P waves (ie, upright in this lead II rhythm strip).
• Setting my calipers to the P-P interval between these 2 consecutive RED arrows — I then looked for additional deflections likely to represent more sinus P waves, keeping in mind that slight variation in this P-P interval would be possible if there was an underlying sinus arrhythmia. This led me to the deflections highlighted by the PINK arrows in Figure-7.
• This left me to postulate the likely presence of "on time" sinus P waves directly over the QRS of beats #3 and 10 (the 2 WHITE arrows).
• NOTE: Beats #3 and 10 are the only QRS complexes in Figure-7 that lack retrograde conduction (ie, No YELLOW arrow is seen at the end of the QRS of beats #3 and 10).

Figure-7: Using calipers allows us to identify the likely presence of an underlying sinus rhythm (ie, AV dissociation).

My Proposed Laddergram:

Normally — I would never expect to see the simultaneous presence of AV dissociation from an underlying sinus rhythm in a patient with VT that produces 1:1 VA conduction. That said — this is what appears to be happening.

• I drew my proposed laddergram in Figure-8 — as my attempt to explain how these findings might reasonably account for the failure of retrograde conduction for only 2 out of 15 QRS complexes in this tracing.
• It is because the 2 "on time" underlying sinus P waves highlighted by the WHITE arrows in Figure-8 occur at precisely the time when ventricular beats #3 and #10 are conducting retrograde through the AV Node — that completion of retrograde conduction is rendered impossible by downward conduction from these 2 "on time" WHITE arrow P waves.
• PEARL #10 (Beyond-the-Core): This failure of retrograde conduction from ventricular beats #3 and 10 proves that today's rhythm is VT (and not SVT with aberrant conduction) even more convincingly than the finding of AV dissociation — because the reentry circuit of a supraventricular reentry rhythm could not be maintained if retrograde conduction was intermittent. (See Figures-5 and -6 and the accompanying text in ECG Blog #538 — for explanation and illustration of the advanced concept of WHY intermittent retrograde conduction in association with a regular WCT rhythm rules out a reentry SVT rhythm).
• Editorial Comment (Beyond-the-Cord Core): I don't believe I have ever encountered the sequence of events portrayed in Figure-8. That said — the "beauty" of this rare occurrence is that: i) It provides a wonderful example of the concept known as "concealed" conduction — in which we are able to predict an electrophysiologic happening (in this case, failure of retrograde conduction after ventricular beats #3 and 10) despite not seeing the reason why this occurs is happening on the surface ECG; — and, ii) It absolutely proves that today's ECG (and presumably most, if not all of the recurrent arrhythmia episodes this young woman has had) were the result of fascicular VT, and not not of a reentry SVT.

Figure-8: My proposed laddergram.

CASE Conclusion:

I subsequently learned that this patient's recurrent ED visits for "palpitations" in association with a regular WCT rhythm (similar to the rhythm shown in today's case) — were resistent on several occasions to initial treatment with Adenosine, but responsive to IV Verapamil.

• This new historical information (ie, that several previous episodes responded to IV Verapamil, but not to IV Adenosine) — provides further support that this young woman’s recurrent WCT episodes most likely were all the result of fascicular VT.
• Now And, now that the correct diagnosis of fascicular VT has been made — the patient was referred for EP study, most probably to be followed by ablation that hopefully will be curative.
• In the interim (awaiting scheduling for her EP appointment) — I'd consider oral Verapamil in hope of minimizing (eliminating) episodes.

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Acknowledgment: My appreciation to Hamdallah Naser (from AL-Najaf, Iraq) — for allowing me to use this case and this tracing.

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ADDENDUM:

I've added below relevant materials in support of today's diagnosis. 

Figure-9: QRS morphology in lead V1 suggestive of either aberrant conduction vs VT (Figure 08.25-1, excerpted from my ACLS Pocket Brain-2013).

Figure-10: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minute Audio): What is Idiopathic VT? — with special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT.