EXTRA COPY- ECG Blog #52i7 — What’s Going On? — EXTRA COPY

The ECG in Figure-1 — was obtained from an older man with CP (Chest Pain).

QUESTION: 

• Should the cath lab be activated?

Figure-1: The initial ECG in today's case.

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Figure-2: I've labeled today's initial ECG.

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Figure-3: Comparison of today's 2 tracings.

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Figure-4: ECG from My Comment in the September 15, 2023 post in Dr. Smith's ECG Blog.

KEY: Why 2 artifacts for each beat with PTA!

An arterial pulse tapping artifact can appear to have 2 separate deflections per heartbeat because the mechanical motion of the artery impacts the ECG electrode twice during the cardiac cycle — typically during systole (contraction) and diastole (relaxation) — or as a result of a sharp movement that creates an oscillatory, biphasic signal. (The artery, when hitting a nearby electrode can create a sharp movement when it expands (systole) — and another artifact when it relaxes (diastole).

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ECG Blog #201 — Reviews the "Culprit Lead" - Roland article!

https://ecg-interpretation.blogspot.com/2021/03/ecg-blog-201-ecg-mp-18-should-cath-lab.html

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PEARL #2: The distribution of the bizarre ST-T wave deflections precisely follows the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle.

• The bizarre ST elevation is approximately equal in 2 of the limb leads (ie, in leads I and II) — and, not seen at all in the 3rd limb lead (ie, no artifact at all is seen in lead III). By Einthoven’s Triangle (See the picture below for today’s ECG Media Pearl — which shows Einthoven’s Triangle in the righthand corner) — the finding of equal ST segment amplitude artifact in Lead I and Lead II, localizes the "culprit" extremity to the RA ( = Right Arm) electrode.
• The absence of any artifact at all in lead III is consistent with this — because, derivation of the standard bipolar limb lead III is determined by the electrical difference between the LL ( = Left Leg) and LA ( = Left Arm) electrodes, which will not be affected if the source of the artifact is the right arm.
• As I discuss in detail in my MP-18 Audio Pearl below — the finding of maximal amplitude artifact in unipolar lead aVR confirms that the right arm is the “culprit” extremity. 

  

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ECG Media PEARL #18 (7:45 minutes Audio) — On recognizing Artifact — and — using Einthoven’s Triangle to determine within seconds the “culprit” extremity causing the Artifact on your ECG.

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NOTE: I reproduce below in Figures 4, 5 and 6 — the 3-page article by Rowlands and Moore (J. Electrocardiology 40: 475-477, 2007) — which is the BEST review I’ve seen on the physiology explaining the relative size of artifact amplitude deflections when the cause of the artifact is a single extremity. These principles are illustrated by the colored deflections in Figure-3:

• As noted by the equations on page 477 in the Rowlands and Moore article: i) The amplitude of the artifact is maximal in the unipolar augmented electrode of the “culprit” extremity — which is lead aVR in Figure-3 (RED outline of the inverted T wave in this lead); and, ii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVL and aVF) is about 1/2 the amplitude of the artifact in lead aVR (GREEN outline of the sharply angled ST-T waves in leads aVL and aVF).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-3 is also significantly reduced from the maximal amplitude seen in leads I, II and aVR (GREEN outline of the sharply angled ST-T waves in each of the 6 chest leads).

 

PEARL #3: A final important clue to artifact as the cause of the bizarre ST-T wave deflections we see in ECG #1 — is provided in the long lead II rhythm strip at the bottom of the tracing!

• Did YOU notice how the artifact comes and goes in this long lead II rhythm strip? Thus, we see maximal artifact in beats #2, 3, 9, 10 and 15 in this long lead II rhythm strip (including that baseline elevation distortion that begins just before the QRS complex of these beats — and which gives false impression of a spiked Helmet Sign).
• In contrast — there is no artifactual ST elevation at all in beats #5, 6, 12, 13 and 17 — and an intermediate amount of artifact distortion in the remaining beats. This changing amount of artifact from one-beat-to-the-next would be consistent with the RA electrode making only intermittent contact with the pulsating artery. I can not think of a physiologic reason other than artifact to explain this beat-to-beat variation in ST-T wave appearance.

 

BOTTOM LINE: You will see artifact frequently in real-life practice. With a little practice, you can immediately KNOW with 100% certainty that the bizarre deflections on a tracing like this one are the result of artifact, and are related to arterial pulsations in one of the extremities. 

• Nothing else shows fixed relation to the QRS complex in the mathematical relationships described above, in which there is equal maximal artifact deflection in 2 of the 3 limb leads (with no artifact at all in the 3rd limb lead) — in which maximal artifact in the unipolar augmented lead will be seen in the extremity electrode that shares the 2 limb leads that show maximal artifact (as according to Einthoven’s Triangle).

 

Figure-4: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-5: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-6: Page 477 from the Rowlands and Moore article referenced above (See text).

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From the 1/17/2023 post in SSmith Blog

https://drsmithsecgblog.com/a-60-year-old-with-chest-pain-2/

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KEY Point: As emphasized by Samaniego et al (Emerg Med J 20: 356-357, 2003) — there are 2 main sources of artifact — which are “physiologic” vs “non-physiologic” sources:

• Non-Physiologic Artifact Sources — include 60 hertz cycle interference (from AC current devices in the area) — and/or cable or electrode malfunction (ie, loose or broken wire, loose electrode lead connection, etc.).
• Physiologic Artifact Sources — include patient movement and/or voluntary or involuntary muscular activity (ie, tremor, shivering, scratching, coughing, hiccups, distressed breathing, etc.).

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From the 9/15/2023 post in SSmith Blog

https://drsmithsecgblog.com/a-60-year-old-diabetic-with-chest-pain/

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The 1st time that I saw APTA (Arterial Pulse Tap Artifact) — I did not know what it was. Since then (as we have shown on already many cases of Dr. Smith’s ECG Blog) — this is actually a surprisingly common phenomenon that all-too-often goes unrecognized (as per the unnecessary cardiac catheterization that was done in today’s case).

• As per Dr. Smith — I review in detail the mathematical relationships seen when there is APTA in one of the extremities in My Comment in the January 17, 2023 post of Dr. Smith’s ECG Blog.
• Awareness of the mathematical relationships discussed in this Jan. 17, 2023 post — allows you within seconds to recognize with certainty that the unusual deflections in the ECG in front of you is the result of APTA. This is wonderfully illustrated in today’s case.

Take another LOOK at today’s ECG (which I’ve reproduced and labeled in Figure-1):

Figure-4: ECG from My Comment in the September 15, 2023 post in Dr. Smith's ECG Blog.

How to Recognize APTA within SECONDS!

As per Dr. Smith — You should suspect APTA in today’s ECG immediately on seeing that despite unusual (if not frankly bizarre) deflections in multiple leads — one of the 3 standard limb leads (ie, leads I,II,III) looks normal — as lead I does in Figure-1 (within the RED rectangle).

• As per my discussion in the January 17, 2023 post, when there is APTA — maximal artifact will be seen in the other 2 standard limb leads ( = leads II and III) — as well as in that augmented lead that is common to both of these maximal artifactual limb leads (in this case lead aVF — with these 3 leads showing maximal artifact being within the BLUE rectangles).
• NOTE: It is that augmented lead that shows maximal artifact — that identifies the “culprit“ extremity (ie, the Left Foot in today’s case).
• The other 2 augmented leads ( = leads aVR and aVL — within the GREEN rectangles) — show approximately half the amount of artifact, compared to maximal artifact leads II,III,aVF.
• Final confirmation that the only thing that can produce these mathematical relationships is APTA — is forthcoming from seeing approximately 1/3 the amount of artifact in each of the chest leads (within the YELLOW rectangles).
• In Conclusion: It literally took me no more than seconds to recognize APTA in today’s tracing because: i) I saw a normal-looking lead I — despite bizarre deflections elsewhere; — ii) With maximal artifact in leads II,III,aVF — and about half that artifact amount in aVR,aVL; — and, iii) A lesser amount of artifact in each of the chest leads. 

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Dear sir, please forgive me for sending two EKG at the same time. Ist EKG ( Top one) is of a 60 years old diabetic gentleman with chest pain. Some of my colleagues thought about " Spike Helmet " sign involving inferior leads. But because the Lead 1 was normal, the thought of artifacts came to my mind. So i repeated the EKG. Repeat EKG is the 2nd EKG here ( Bottom one). It's within normal limit. So 1st EKG had artifacts. Can you please tell me the clues to dete ct artifacts (vs Spike Helmet) from 1st EKG.

MY REPLY:

Hi. This is PTA = "Pulse-Tap Artifact". YOU correctly told me how it is detected — because despite marked deflections, there is a NORMAL lead = lead I !!!

You can see LOTS of examples of artifact (and many PTA cases). Simply click on this tab in the top menu on ANY page in my ECG Blog! See my ECG Blog #201 for full details! 

With your permission — I'd like to use this case for an ECG Blog. I'll be glad to acknowledge you — and I will let you know when the case is  published. It will be a while, as I have a bunch of others to go before, but I'll let you know. Let me know if you still have questions after reviewing ECG Blog #201 ! — :)

P.S.: GOOD question! As I take another look — I see 2 artifact deflections for each R-R interval — and that is confusing, because typically there should only be 1 artifact deflection that occurs with a fixed relation to the QRS ... I am not sure why there is the 2nd deflection ... But as per the attached Einthoven Triangle diagram — it should be the LL electrode that is producing the artifact (because leads II and III both use the LL electrode — but lead I does is not affected). I'll have to look up to see if there might be a reason for why we are getting 2 artifact deflections! But we KNOW this is artifact because lead I is normal — and because it all went away with the repat ECG — :)

NOTE: Look what I found! So the arterial pulse can have 2 deflections for each R-R interval! I've seen a good 20 or so cases of this — and NONE of the others had 2 deflections for each R-R interval. So we all learn something new each day !!! — :)

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Acknowledgment: My appreciation to Bashiruddin Sayeem (from Chittagong, Bangladesh) 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.
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ADDENDUM (4/XXX/2026):

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EXTRA COPY — ECG Blog #528 — What's the Rhythm? Why? — EXTRA COPY

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

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Figure-2: I've labeled today's ECG.

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Figure-3: Laddergram of today's rhythm.

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GREAT post on FB from Cardiology Notes (on Facebook !!! )
—  YES — I can acknowledge them as “Cardiology Notes” — and perhaps I should give the link to this post on FB?
— Also to acknowledge — Omar Hassan and Khaled Ash (both from FB !!! )
 
TITLE of MY BLOG POST —
 — “The Patient just left … “
 
THIS IS THE CASE from Cardiology Notes:
https://www.facebook.com/good.job.692776/posts/pfbid0gY4XyPWXBYniYjdLoifq7oPJji2sMU8V7G3d1jAgd5nmUbyuRa8LRZitH7RZqCArl
 
A 54 year old female patient with history of ischemic heart disease complaining of palpitations and dyspnea
MY 1stt REPLY:
FASCINATING rhythm! I've taken the figure posted by Khaled Ash (above) — and have added light BLUE arrows that to me suggest 1:1 retrograde V-A conduction (in addition to the suggestion of 3:2 Wenckebach conduction!
Possibilities are several — in addition to AIVR with 3:2 Wenckebach conduction out of the ventricular focus — this could be junctional with a baseline ECG showing MBBB ( = Masquerading Bundle Branch Block), again with 1:1 VA conduction backward and 3:2 Wenckebach out of the AV node.
My PLEA to Cardiology Notes — PLEASE GIVE US FOLLOW-UP of this fascinating case! Surely YOU have some follow-up!
— What does the baseline ECG look like?
— Is this patient on Digoxin? (if so — likely Dig Toxicity)
— What happened? (Recent acute MI? Electrolyte abnormalities?)

 
MY 2nd REPLY:
NOTE: Cardiology Notes and Omar Hassan, Khaled Ash and myself have all been corresponding about this fascinating case. The patient is on Respiridone (See attached — as this psychotropic medication IS associated with a number of adverse effects that may have contributed to this unusual cardiac arrhythmia !!!
Otherwise — Cardiology Notes has shared with us that this patient signed out of the hospital on his own, refusing further evaluation. Pt was not cooperative !!! — but at least he felt well enough to sign out AMA on his own !!!
I would have loved to see a copy of his previous ECG to help determine if today's rhythm is supraventricular (with MBBB) vs ventricular in etiology as a possible adverse effect from Respiridone ...
 
Respiridone — high risk of sudden death
Ray et al — N Engl J Med 360(3):225-235, 2009
https://pmc.ncbi.nlm.nih.gov/articles/PMC2713724/
 
Users of typical antipsychotics have increased risk of serious ventricular arrhythmias and sudden cardiac death. However, less is known regarding the cardiac safety of the atypical antipsychotic drugs, which have largely replaced the older agents in clinical practice.
 
At present, less is known regarding the cardiac safety of the atypical antipsychotic drugs, which have largely replaced the older agents in clinical practice. Several atypical antipsychotics block repolarizing potassium currents² and prolong ventricular repolarization,^1,13 and the electrophysiologic effects of some drugs are comparable to those of the older agents. However, although torsade de pointes has been reported with atypical antipsychotics,^14–16 whether these drugs increase the risk of sudden cardiac death to the same extent as the older medications is unknown. We thus conducted a large retrospective cohort study designed to compare the risk of sudden cardiac death for the two classes of antipsychotic drugs.
 
Our study did not assess the mechanisms by which either class of antipsychotics increased risk of sudden cardiac death. Although antipsychotics have chronic adverse cardiovascular effects,¹² the risk of sudden death was elevated in an analysis excluding long-term users, which suggests that acute drug effects are involved. We believe the most plausible explanation is that antipsychotic drugs increase the risk of serious ventricular arrhythmias, probably through blockade of potassium channels and prolongation of cardiac repolarization. However, other mechanisms may be involved, including autonomic effects, inhibition of other ion channels, or other acute cardiotoxicities, such as the myocarditis associated with clozapine use.³⁸
In conclusion, current users of both typical and atypical antipsychotics in the study cohort had a similar dose-related increased risk of sudden cardiac death. This suggests that with regard to this adverse effect, the atypical antipsychotics are no safer than the older drugs.
Respiridone does prolong the QTc — but unless there is an overdose, usually by not enough to cause Torsades — it may cause bradycardia — it may cause av block (although this is less common at lower doses.

EXTRA COPY — ECG Blog #526: Epigastric Pain — EXTRA COPY

The ECG in Figure-1 — was obtained from a younger adult male who presented to the ED (Emergency Department) with new epigastric pain. The patient had a history of prior PCI (Percutaneous Coronary Intervention).

• The cardiology team was consulted — but felt there was no indication of a STEMI, and that the tall chest lead T waves represented a repolarization variant in this patient whose presenting symptom was abdominal pain.

QUESTIONS:

• Do YOU agree with the cardiology consultant's opinion?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from a younger adult male with epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

It’s always challenging when you disagree with your consultant and the patient’s well-being is dependent on a timely correct diagnosis. There are many reasons why the Cardiology Team’s opinion is not correct. These include: 

• i) The “focus” is wrong. In a patient who presents to the ED for new-onset of a potential “CP (Chest Pain) Equivalent” symptom — the onus is on medical providers to rule out an acute event, rather than having to “rule it in”. (This is especially true in a patient with known coronary disease, given prior PCI).
• ii) The diagnosis of a “repolarization variant” — is a diagnosis of exclusion (ie, to only be made after you have ruled out the possibility of an acute event). While I have seen very tall, peaked, non-hyperkalemic T waves represent a benign repolarization variant — this is rare! Instead — the presence of overly tall, peaked chest lead T waves in a patient who presents to the ED with new symptoms should be suspected as representing a form of deWinter-like T waves until proven otherwise (See the ADDENDUM below).  
• 
  
• iii) The morphology of the chest lead ST-T waves is diagnostic! As shown below in Figure-2 — these T waves are symmetric (Benign repolarization variants tend to be asymmetric — with slower rising and more rapid downsloping of the ascending and descending T wave limbs). In addition — the T wave peaks become “fatter”-than-they-should-be” as one more toward chest leads more lateral than lead V3. Finally — straightening of the ST segment takeoff in lead V6 indicates hyperacuity in a patient with new symptoms.
• iv) STEMI Criteria are satisfied in Figure-2 (ie, the dotted RED lines in leads V4,V5 show 2 mm of J-point ST elevation). To Emphasize: STEMI criteria are not needed to justify the need for prompt cath in today’s patient — but these criteria are nevertheless satisfied.
• v) Limb lead findings confirm that today’s ECG is not a repolarization variant! This is because: a) There is clearly abnormal ST segment straightening with angulation of the T wave onset in leads III and aVF (These represent subtle “reciprocal” changes to the chest lead T wave peaking); — and, b) There is equally subtle-but-real ST elevation in lead aVL — and — a “bulky” (hyperacute) T wave in lateral lead I.

Bottom Line: In a patient who presents to the ED with new symptoms — today’s ECG is strongly suggestive of acute LAD occlusion (LAD OMI) until proven otherwise! 

Figure-2: I've labeled today's ECG.

What to Do?

If your cardiology consultant does not agree with your interpretation — Consider the following:

• Repeat the ECG within 10-20 minutes! Especially in the presence of ongoing symptoms — it is often surprising how quickly acute ECG finding may evolve. Seeing “dynamic” ST-T wave changes in a patient with new symptoms should serve to convince the most skeptical of interventionists of an acute evolving event in need of prompt cath.
• And, if your 1st repeat ECG fails to show significant changes — Continue to order timely additional repeat tracings (which in a patient with ongoing symptoms will usually show changes).
• Find a prior ECG for comparison! Given the history of previous PCI — We know that this patient has previous ECGs. If the ECG in Figure-2 represents a new acute event — there is no way that a previous ECG will show such overly tall, peaked T waves (ie, You can immediately prove that the ST-T wave changes in Figure-2 are new if these findings are not seen on a previous tracing).
• Perform bedside Echo. If your patient who shows the extensive ECG abnormalities seen in Figure-2 continues to have ongoing symptoms — a bedside Echo will almost always show a localized wall motion abnormality that is diagnostic of an acute event.
• Realize that any elevation in Troponin is significant in a patient with persistent new symptoms. 

To Emphasize: Waiting for serum Troponin to rise takes longer than the time it should take to repeat the ECG, find a prior tracing (if PCI was done in the same hospital) — and/or do bedside Echo. 

• CAVEAT #1: As noted in ECG Blog #508 — Although one may be momentarily comforted by an initial normal hs-Troponin value — this in no way rules out an acute cardiac event. Wereski et al (JAMA Cardiology, 2020) — found that 14% of patients with an acute STEMI had a normal initial hs-Troponin (and ~25% had hs-Troponin levels below the infarction “rule-in” level). 
• Therefore — IF serial ECGs show "dynamic" ST-T wave changes — or, a prior ECG looks different — or, bedside Echo shows a localized wall motion abnormality — then waiting for an elevated Troponin wastes precious time (and precious myocardium).
• 
  
• CAVEAT #2: Bedside Echo is only helpful in lowering the likelihood of an acute event IF: a) LV contractility is completely normal; and, b) The patient is having symptoms at the time the Echo is done (Nothing is ruled out if the patient is pain-free at the time the Echo is done).

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CASE Follow-Up:

• Bedside Echo showed reduced contractility.
• The patient continued to have severe pain.
• As a result — cardiac cath was performed and showed a "culprit" lesion in the LAD (Left Anterior Descending) coronary artery. The patient's pain was relieved following PCI — and he has done well in follow-up.

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Acknowledgment: My appreciation to Nirdosh Rassani (from Quetta, Pakistan) for the case and this tracing.

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ADDENDUM (4/4/2026): 

• See ECG Blog #183 for review of the original 2008 NEJM manuscript by deWinter and colleagues.
• ECG Blog #341 is equally insightful (There are many other examples of deWinter-like T waves on this Blog).

MY Observations regarding De Winter T Waves: 

Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

• Many (most) of these cases do not fit strict definition of “de Winter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, giant T waves are limited.
• ECG changes in many of these cases are not “static” until reperfusion, as was initially reported in 2008 by de Winter et al. Nevertheless, cath follow-up routinely confirms LAD occlusion.
• 
  
• MY "Take": I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. What will be seen on the ECG depends greatly on when during the process the ECG was obtained. While many of these patients do not manifest “true de Winter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I don’t feel ( = my opinion) that it matters whether a “true” de Winter T wave pattern vs simple “hyperacute” T waves (that are deWinter-like) is present.

 

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TODAY’s ECG Media PEARL #1 (3:00 minutes Audio): — relates to the phenomenon of deWinter-like T waves.

EXTRA COPY- ECG Blog #525- Another Wide Tachycardia- EXTRA COPY

The ECG in Figure-1 was obtained from an older woman who presented with new-onset palpitations. She was hemodynamically stable in association with this tracing.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How specific can you be with your interpretation?
• What is the treatment of choice? 

Figure-1: The initial ECG in today's case.

MY Thoughts on this Tracing:

The ECG in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~185/minute without clear sign of atrial activity.

• QRS morphology is consistent with LBBB conduction in the chest leads (ie, predominantly negative QRS in the anterior leads — with an all-positive QRS in lateral chest leads) — with an inferior frontal plane axis (as determined by the all-positive QRS in inferior leads — with an equiphasic QRS in lead I).

Impression:

The above description is virtually diagnostic of RVOT VT (Right Ventricular Outflow Track Ventricular Tachycardia).

• PEARL #1: Once you are familiar with the entity of RVOT VT — You should be able to make this diagnosis with high accuracy within seconds of seeing an ECG that looks like today’s tracing. 
• As we’ve shown on multiple posts on this ECG Blog — RVOT VT is one of the two most common forms of idiopathic VT (See ECG Blog #489 — Blog #346 — Blog #323 — among many others). This term “idiopathic” VT simply refers to the ~10% of patients who present with VT without underlying heart disease.

I review the KEY distinguishing points of the idiopathic VTs in the ADDENDUM to today’s post (See my summary info sheet in Figure-4 — and my 8-minute Audio Pearl below).

• Many (admittedly not all) of the idiopathic VTs are readily recognizable by their QRS morphology (described in Figure-4).
• Because the QRS complex in idioventricular VT is typically not overly wide — and because of the resemblance to QRS morphologic features of known conduction blocks (ie, RBBB + Hemiblock for fasicular VTs — and LBBB for outflow track VTs) — there is a tendency to misdiagnose the idiopathic VTs as some form of reentry SVT with aberrant conduction (instead of recognizing them as VT).

PEARL #2: One of the most helpful clues that a regular WCT without P waves is likely to be idiopathic VT (and not some form of reentry SVT with aberrant conduction) — is that there are subtle atypical features that are not consistent with any known form of conduction block. For example — in Figure-1:

• Although the predominant negativity of the QRS complex in leads V1,V2 is consistent with LBBB conduction — with typical LBBB, transition tends to occur later than what is seen in Figure-1 (ie, with simple LBBB — no more than a tiny r wave usually persists past lead V3 — and this R wave does not become predominant until at least lead V5). Instead, as we look at Figure-1 — the R wave is already enlarging in lead V3, and it is predominant in lead V4.
• With LBBB — septal depolarization moves right-to-left (instead of left-to-right) — followed by slow, progressive leftward depolarization of the left ventricle (that overwhelms electrical activity arising from the much smaller right ventricle). As a result — the QRS vector in left-sided leads V6 and in lead 1 manifest an all-positive widened R wave. The small, isoelectric QRS complex in lead I of Figure-1 should not be seen with LBBB (unless there has been prior infarction and/or extensive scarring or myocardial infiltration). The fact that this small isoelectric complex in lead I begins with a negative deflection — and the finding of an all negative QRS in high-lateral lead aVL are especially atypical for LBBB conduction.
• To Emphasize: It’s impossible from Figure-1 alone to be 100% certain that this ECG represents VT. But the findings of LBBB-like conduction in the chest leads with an inferior frontal plane axis are completely typical for RVOT VT — and — the atypical QRS morphology features described in this PEARL #2 strongly suggest VT until proven otherwise.

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The CASE Continues:

Today's patient was successfully cardioverted — but the WCT rhythm in Figure-1 returned. Lasting conversion to sinus rhythm was finally achieved after a 2nd cardioversion (as shown in Figure-2).

QUESTIONS:

• Does the ECG in Figure-2 solidify the diagnosis of VT for the initial ECG that was seen in Figure-1?
• What other interventions might have been considered?

Figure-2: The repeat ECG, recorded after the 2nd cardioversion.

My Thoughts:

The repeat ECG in Figure-2 shows restoration of a normal sinus rhythm (RED arrows in Figure-3 highlighting upright sinus P waves in the long lead II) — with the exception of a single early wide beat toward the end of the tracing ( = beat "X").

• PEARL #3: We know with 100% certainty from Figure-3 that beat X is a PVC (Premature Ventricular Contraction) and not an aberrantly conducted supraventricular beat — because underlying "on time" sinus P waves continue thoughout this long lead II rhythm strip (ie, The PINK arrow P wave shows continuation of these "on time" sinus P waves — and this can only happen if the wide beat originates "from below", since a supraventricular beat would have delayed the next sinus P wave).
• 
  
• PEARL #4: Note that QRS morphology in Figure-3 of the PVC is identical in simultaneously-recorded leads V4,V5,V6 (within the BLUE rectangle) — to QRS morphology in leads II,V4,V5,V6 during the WCT rhythm in ECG #1. This finding highlights the utility of the post-conversion ECG for retrospectively making a definitive diagnosis of the etiology of a WCT rhythm if one or more similar QRS morphology PVCs are seen.

Figure-3: Comparison between the 2 ECGs in today's case.

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Final Thought: Regarding treatment of the WCT rhythm in ECG #1: 

• There is no single "correct" answer for how best to treat the regular WCT rhythm that today's patient presented with. And, the treatment path chosen in today's case was successful.
• Synchronized cardioversion is clearly the intervention of choice if there is any concern about hemodynamic stability in association with a WCT rhythm. Sometimes, "Ya just gotta be there" to judge when to go ahead with synchronized cardioversion.
• That said — today's patient was stable on presentation, so options are available. As noted below in Figure-4 — RVOT VT often responds to Adenosine, which could have been tried.
• Recurrence of the WCT after the 1st synchronized cardioversion in today's case was a signal that a longer-acting intervention (ie, perhaps IV Amiodarone) might be needed to maintain sinus rhythm, rather than repeat cardioversion.
• I do not have further follow-up as to whether or not this patient was referred for EP evaluation. 

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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Johore, Malaysia) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (3/XXX/2026):

• Below — More on idiopathic VT:

Figure-4: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? 

— WHY do we care? Special attention to the 2 most common forms 

= RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

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