EXTRA COPY — ECG Blog #523: Is there a "Culprit"? — EXTRA COPY

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The ECG in Figure-1 was obtained from an older woman — who presents to the ED (Emergency Department) with CP (Chest Pain) that began ~2 hours earlier.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Would you activate the cath lab?

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

MY Thoughts on Today's CASE:

Given the history of new CP — this is an extremely worrisome ECG:

• The  rhythm is sinus at ~80/minute. Regarding intervals — the PR interval and QRS duration are both normal, with the QTc no more than of borderline duration. Regarding chamber enlargement — the S wave of >20 mm in lead V2 is consistent with voltage for LVH (See Figure-7 in the Addendum of ECG Blog #73).

Regarding Q-R-S-T Changes:

• A small and narrow Q wave is seen in lead aVL.
• R wave progression — is normal (Small but definite initial r waves are seen in both leads V1,V2 — with transition occurring normally between leads V3-to-V4).

The remarkable findings relate to ST-T waves:

• My attention was immediately drawn to the ST-T waves in the 3 inferior leads — which show eyecatching straightened and downsloping ST segments (RED arrows in leads II,III,aVF in Figure-2). Each of these leads show terminal T wave positivity (upright YELLOW arrows) — with this down-up T wave appearance in a patient with new CP being an especially worrisome sign of hyperacuity.
• Support for our concern is forthcoming from the hyperacute ST-T wave appearance in lead aVL (with ST segment straightening, subtle-but-real ST elevation given small size of the QRS — and a disproportionately "fattened" T wave with wide base).

In the Chest Leads: 

• Lead V1 is notable for ST segment straightening — which is especially remarkable in light of the distinctly abnormal 1-2 mm of flat ST segment depression in leads V3,V4,V5,V6 (BLUE arrows in these leads). Each of these 4 chest leads show significant terminal T wave positivity — which in this patient with new CP strongly suggests hyperacuity.
• I found lead V2 especially interesting as a "transition" lead — in that it shows neither J-point depression or elevation. This is most probably because lead V2 is situated between lead V1 (which is remarkable for its hyperacute-looking ST segment straightening) — and leads V3,V4,V5,V6 (each of which show unmistakeable ST segment flattening and depression with terminal T wave positivity).
• Finally — there is slight-but-real ST elevation in lead aVR.

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

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Putting It All Together:

• I'd immediately activate the cath lab. The history of new-onset CP in this older woman whose initial ECG shows significant ST-T wave abnormalities in no less than 11/12 leads indicates an acute cardiac event until proven otherwise.

The question arises as to what the "culprit" artery might be? 

• The only lead showing ST elevation is lead aVL. In the absence of ST elevation in other lateral leads — I thought acute LCx (Left Circumflex) occlusion to be less likely.
• ST elevation is commonly seen with proximal LAD (Left Anterior Descending) occlusion — but other than the ST segment straightening in lead V1 — there is no anterior lead ST elevation.
• Instead — the predominant finding in Figure-2 is the very acute-looking ST depression with terminal T wave positivity in 7 leads (leads II,III,aVF; and leads V3,V4,V5,V6) — with transition lead V2 — and with ST elevation in lead aVR.
• 
  
• PEARL #1: The most logical explanation for this series of acute-looking ST-T wave abnormalities without suggestion of a specific "culprit" artery — is that there is severe multi-vessel disease.
• I suspected acute LAD occlusion given findings of ST straightening in V1 + transition lead in V2 with lateral chest lead ST depression suggesting a Precordial "Swirl" pattern (See ECG Blog #380). Supportive findings of ST elevation in aVL with reciprocal inferior lead ST depression is consistent with proximal LAD occlusion — with the diffuseness of the ST depression reflecting impossible-to-account-for attenuation effects from multi-vessel involvement.
• Bottom Line: None of this matters. What counts is simply that prompt cath with PCI is needed. Specific anatomy to be revealed by cardiac cath.

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The CASE Continues:

• Cardiac cath was performed — and revealed severe multi-vessel disease (with an 80% ostial LMain lesion — a 95% "culprit" mid-LAD lesion + RCA disease).
• The initial hs-Troponin-I came back with borderline elevation. The repeat Troponin was clearly elevated.

PEARL #2: It does not matter what Troponin shows in today's case. This is because regardless of what the 1st and 2nd Troponin assays show — prompt cath with PCI will be needed given the history of new-onset CP and today's initial ECG showing diffuse acute-looking ST-T wave changes in 11/12 leads!

• The initial hs-Troponin may be negative or non-diagnostic in up to 25% of acute STEMI patients (Wereski et al — JAMA Cards 5(11):1302, 2020).
• "Time is Muscle (myocardium)". As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — The most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in 60% more myocardium infarcted).
• Serum Troponin values provide a rear-view mirrow of what has already happened — and not of what is about to happen.
• PEARL #3: The decision to perform cardiac cath in today's case can be made as soon as the initial ECG is seen.

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A 2nd ECG was recorded ~3 hours after ECG #1 (shown in Figure-3):

• ECG #2 was obtained prior to cardiac cath — at a time when the patient's symptoms had decreased. Dual antiplatelet therapy (DAPT) and Heparin were ongoing.

QUESTIONS:

• Given that the patient's CP was less at the time ECG #2 was recorded — How would you interpret this repeat ECG?

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

MY Thoughts on ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows reperfusion changes in virtually all leads that previously looked acute:

• Most remarkable in ECG #2 is the anterior lead ST segment coving, now with deep, symmetric T wave inversion in lead V2.
• The horizontal ST depression previously seen in leads V3,V4,V5,V6 has essentially resolved.
• Reciprocal reperfusion changes are now seen in the inferior leads — in which downsloping ST depression has been replaced by tall, "bulky" positive T waves.
• Deep symmetric T wave inversion is seen in lead aVL.
• PEARL #4: Especially in view of reduced CP — I interpreted the evolutionary changes in ECG #2 as confirming acute LAD occlusion as the "culprit" artery in this patient with underlying multi-vessel disease.

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Acknowledgment: My appreciation to Chun-Hung Chen (from Taichung City, Taiwan) for the case and this tracing.

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EXTRA COPY- ECG Blog #522 — What is the "Other" Diagnosis? — EXTRA COPY

The ECG in Figure-1 is from a middle-aged man who presented to the ED with new-onset severe CP (Chest Pain). His symptoms lasted ~30 minutes — but his CP had totally resolved by the time this ECG was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from middle-aged man with new CP. His CP had resolved by the time this ECG was recorded (To improve visualization — I've digitized the original ECG using PMcardio).

CASE Follow-Up:

Providers on the case interpreted the ECG in Figure-1 as consistent with Brugada Phenocopy (ie, a BrugadaType-1 ECG pattern as a result of "something else" — but not a true Brugada Syndrome).

• Because providers were certain ECG #1 was a manifestation of Brugada Phenocopy — serum Troponin was not ordered.

QUESTION: 

• Do you agree with the above approach?

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NOTE: I review Brugada ECG Patterns in the ADDENDUM below:

• A summary of Brugada Syndrome vs Phenocopy appears in Figure-6 — with more depth exploration in the 2-part ECG Video below (Total view time ~17 minutes).
• For more of an update on Brugada Syndrome — See below!

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MY Thoughts on the CASE:

As is often the case — today's History is KEY ==> a middle-aged man who presents with new CP — but who was asymptomatic by the time today's initial ECG was recorded.

My interpretation of the ECG in Figure-1:

• The rhythm is sinus.
• The QRST complex in lead V1 (within the RED rectangle in Figure-2) — is diagnostic of a Brugada-1 ECG pattern.
• That said — the shape of the ST segment coving in neighboring leads V2,V3,V4 differs from the very steep downsloping ST segment seen in lead V1.  
• Deep, symmetric T wave inversion persists in leads V3 and V4.
• More subtle ST-T wave changes are seen in the limb leads (ST segment straightening in leads I,II,III,aVF — and ST segment coving with slight elevation and T wave inversion in lead aVL). Given small size of the QRS in the limb leads (especially tiny in leads III and aVL) — these changes are subtle indeed!
• 
  
• BOTTOM Line for Figure-2: Although the QRST complex in lead V1 is typical for a Brugada-1 ECG pattern — the other findings described above are not expected with Brugada Phenocopy in the absence of ongoing ischemia. Instead, in this patient who presents for new-onset CP — We have to suspect that in addition to the typical Brugada-1 ECG pattern that we see in lead V1 — the neighboring chest leads also suggest there may be an ongoing acute infarction!

Figure-2: I've labeled KEY findings in ECG #1 (and added an insert with illustration of Brugada-1 and Brugada-2 ECG patterns).

The CASE Continues:

As noted above — serum Troponins were not obtained because the provider attributed all ECG findings in Figure-2 to Brugada "Phenocopy".

• A short while later — the ECG in Figure-3 was recorded. 

HINT: The changes in the chest leads of ECG #2 are extremely subtle.

• Do you see them?

Figure-3: Repeat ECG done a short while after ECG #1.

Comparison of the ECGs in Figure-3:

As noted above — the changes between the 2 ECGs in Figure-3 are extremely subtle:

• The R' that was seen in ECG #1 has thinned out — with subtle-but-real reduction in the ß-angle in ECG #2 (See the insert in the upper right of Figure-2 regarding calculation of the ß-angle).
• In neighboring leads V2,V3,V4 of ECG #2 — the ST segment coving is less pronounced, and there is narrowing with slight reduction in the depth of T wave inversion that was seen in the initial ECG.
• Bottom Line: Although subtle indeed — ECG #2 suggests ongoing evolution of reperfusion T waves.

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Figure-4 shows the final ECG done the next day ( = ECG #3):

• Unfortunately — I lack details on this case beyond knowing that the patient had no more chest pain — that Troponins were never done — and that there was no cardiac catheterization.

QUESTION:

• How would you explain the ECG changes seen in Figure-4?

Figure-4: Comparison between the initial and the final ECGs that were recorded in today's case. How best to explain these changes?

MY Thoughts on the ECGs in Figure-4:

Whereas the changes in Figure-3 (between ECGs #1 and #2) were extremely subtle — the changes now seen in Figure-4 (between ECGs #1 and the final ECG #3) are obvious.

• The Brugada-1 ECG pattern in lead V1 of ECG #1 has now almost completely resolved in ECG #3.
• ST segment coving without ST elevation persists in neighboring chest leads of ECG #3 — with marked deepening of symmetric T wave inversion.
• In the limb leads of ECG #3 — there has been slight axis shift, with marked increase in the now widened and tall inferior T waves (essentially the reciprocal opposite ST-T wave picture that is now seen for leads V2 and V3 in ECG #3).
• Deep, widened T wave inversion is now seen in leads I and aVL of ECG #3.
• Bottom Line: Even without Troponin values and without cardiac catheterization — the ECG evolution that is now obvious in ECG #3 confirms reperfusion changes following extensive infero-antero MI (presumably following acute LAD occlusion in a patient with multi-vessel disease).

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Final Editorial NOTE:

I initially hesitated using today's case because I lacked follow-up. Efforts to contact today's patient were unsuccessful. He lived remotely, away from health care facilities — and apparently flew back to the island where he lived without returning calls.

• Today's case is insightful — because it illustrates that among the causes of a transient Brugada-1 ECG pattern are acute LAD occlusion, which may superimpose the ST-T wave changes of acute infarction.
• In my experience — the most common precipitants of a Brugada-1 ECG pattern in patients who do not have Brugada Syndrome (ie, Brugada "Phenocopy" ) — are acute febrile illness and hyperkalemia. I've seen cases in which there is complete resolution of the Brugada-1 ECG pattern after resolution of the febrile illness and hyperkalemia.
• But — acute ischemia and/or infarction and/or S/P cardiac arrest may also be causes of a Brugada-1 ECG pattern, as was seen in today's patient whose presenting complaint was new chest pain.

 

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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 (3/13/2026): 

I've added below material relating to Brugada ECG Patterns — beginning with my 2-part ECG Video:

• NOTE: Although I recorded this 2-part ECG Video in 2021 ( = 5 years ago) — with the exception of a few changes in approach (that I highlight below) — this 2-part video remains current, and hopefully facilitates recall of Brugada ECG patterns.
• I introduced the concept of Brugada Phenocopy in my ECG Blog #238 (published in July, 2021). This distinction between true Brugada Syndrome — vs a transient Brugada ECG pattern attributable to some other precipitating condition (ie, febrile illness; hyperkalemia; acute ischemia/MI, etc.) with resolution of the ECG pattern once the precipitating condition resolves — remains critical for risk assessment, as well as for optimal management (Adytia and Sutanto — Current Prob in Card 49(6), 2024).  

What's NEW?

I'll preface the 2-part Video below with select updates from the following comprehensive newer references:

• Xu et al — Brugada Syndrome Update- 2025 —
• Krahn et al — JACC: Clinical EP 8(3):386-405, 2022 —

Brugada ECG Patterns: 

• As per the above JACC Review — for practical purposes, the only ECG pattern that is diagnostic of BrS (Brugada Syndrome) is Type-1 (as shown below for A in Figure-5 — when this ECG pattern is present in ≥1 of the anterior leads = V1,V2,V3).
• I had not been distinguishing between a Type-2 vs Type-3 pattern (as per my illustration in Figure-2 above). For investigators who do favor distinction between Type-2 ( = B in Figure-5) and Type-3 ( = C in Figure-5) — the shape of the ST-T wave is similar, with the difference being that with Type-3, there is <2mm of ST elevation. 
• My Preference: I still favor use of only 2 Types ( = Brugada Types-1 and -2) — but whatever your preference, it’s good to be aware that some investigators employ the use of 3 Types (as shown below in Figure-5).
• Neither Type-2 nor Type-3 Brugada ECG patterns alone are diagnostic of BrS. That said — BrS can be diagnosed in these patients IF provocative testing with a SCB (Sodium Channel Blocker) converts a Type-2 or Type-3 pattern into a Brugada-1 ECG. 

Figure-5: The 3 Brugada ECG Patterns (Adapted from Krahn et al — JACC: Clin Electrophys 8(3):386-405, 2022).

Additional Considerations:

The KEY to optimal management of BrS lies with Risk Assessment (To Emphasize: Risk assessment is best performed by cardiologists well versed in the many manifestations of BrS — with current accepted concepts explored in the above 2 references).

• SAEs (Serious Arrhythmic Events) — are rarely the 1st symptom in patients with BrS (which emphasizes the importance of identifying Brugada ECG Patterns — and determining which of these patients are at highest risk for SAEs, and therefore in need of preventive treatment).
• Aside from a malignant arrhythmia — highest risk of SAEs are in: i) Patients with a history of cardiogenic syncope; — ii) The presence of a spontaneous Brugada-1 ECG; — and/or, iii) Association with Other Factors (ie, Excessive alcohol consumption — hypo-/hyperKalemia — Acidosis — Febrile Illness — have all been shown to facilitate Brugada-1-induced SAEs).
• 
  
• The sensitivity for ECG recognition of a Brugada-1 pattern is increased by ~50% including high-lead positions (ie, Recording of leads V1 and V2 not only in the 4th IC space — but also in the 2nd and 3rd IC spaces, so as to account for anatomic variation in the position of the vulnerable RV Outflow Track).
• Be aware of intermittent, spontaneous fluctuations in the presence and potential sudden resolution of a Brugada-1 ECG pattern, especially in response to potential precipitating factors such as febrile illness, hyperkalemia, and/or certain drugs. As a result — Provocative Testing with a SCB (Sodium-Channel Blocking agent), is an important adjunct in risk assessment of the patient with a Brugada-1 ECG pattern (NOTE: Not all SCBs used in provocative testing are created equal — but this concept extends well beyond the scope of this ECG Blog).
• Genetic Testing is an important part of Brugada-1 risk assessment (especially since such testing may facilitate identifying family members at risk).

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In Part 1 of this ECG Video (9 minutes) — the essentials of Brugada Syndrome are reviewed.

Int Part 2 (8:00 minutes) — these essentials are applied clinically. 

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Figure-6: 2-page Summary of the essentials of Brugada Syndrome (from Grauer K: ECG-2014-ePub, KG/EKG Press, 2014).

 

Figure-7: World prevalence map of Brugada Syndrome. The overall worldwide prevalence of Brugada Syndrome is ~0.5/1,000 in the population. This prevalence is highest in Southeast Asia (at least 5 times more common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence than for the worldwide average. Brugada-2 patterns (ie, "Saddleback") are also much more prevalent in Southeast Asia than elsewhere in the world. (Excerpted from Vutthikraivit et al: Acta Cardiol Sin 34:267-277, 2018).

 

Figure-8: Summary of KEY concepts reviewed in the above ECG Video.

 

 

 

EXTRA COPY — ECG Blog #520 — How Certain Are You? - EXTRA

You are asked to interpret the ECG in Figure-1. Which of the following choices provides the best answer?

• A) AFib with a rapid ventricular response.
• B) SVT with RBBB aberration.
• C) The rhythm could be VT.
• D) The rhythm is VT.

Figure-1: Which of the above choices is the best answer? 
= = = = = = =
[ Abbreviations: AFib (Atrial Fibrillation) — SVT (SupraVentricular Tachycardia) — RBBB (Right Bundle Branch Block) — VT (Ventricular Tachycardia)].

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MY Approach to Today's Tracing:

As much as we always want at least a brief history (including at least the age of the patient — and the reason why the ECG was recorded) — we are not provided with one. Nevertheless, there is enough information to select the right answer.

• Take another LOOK at today's tracing in Figure-2. For clarity — I've numbered the beats in the long lead II rhythm strip.

Figure-2: I've numbered the beats in today's tracing.

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MY Thoughts:

By the P's, Q's, 3R Approach (See ECG Blog #185) — the rhythm in Figure-2 is a regular WCT (Wide-Complex Tachycardia):

• The overall rhythm appears to be Regular. This is best assessed in simultaneously recorded leads I and III, in which it is easier to see the consistency in the R-R interval (and more difficult to appreciate in lead II — where there is more artifact distortion).
• The Rate of the rhythm is slightly more than 150/minute (ie, with an R-R interval of slightly less than 2 large boxes in duration).
• The QRS is wide (at least 3 small boxes in duration — therefore ≥0.12 second).
• 
  
• Are there P waves?

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What Can We Already Rule Out?

• The fact that the R-R interval in Figure-2 is regular effectively rules out AFib (and if we can confirm that P waves are truly present — this would definitively rule out AFib).

What We Know:

• The rhythm in Figure-2 is a regular WCT (Wide Complex Tachycardia).
• The rate of the rhythm is slightly more than 150/minute. 
• There is no clear sign of sinus P waves (ie, There is no consistent upright P wave with constant PR interval preceding each QRS complex in the long lead II rhythm strip).
• The above said — a number of small upright deflections in the baseline do appear to be present throughout the long lead II. These could be P waves.
• PEARL #1: Assuming today's patient is an adult — by far, the most common cause of a regular WCT rhythm without clear sign of sinus P waves is VT. Therefore — We need to assume VT until proven otherwise!

PEARL #2: We can go 1 step further in our differential diagnosis by looking at QRS morphology. 

• Although the predominantly upright QRS complex in lead V1, in association with wide terminal S waves in lateral lead V6 could be consistent with RBBB conduction — you should virtually never see an all negative QRS complex in lead I with a supraventricular rhythm. 
• Based on QRS morphology then — this strongly suggests that the rhythm in Figure-2 is VT (which means we can effectively rule out SVT with RBBB aberration). 

QUESTION:

• But — Are we 100% certain that today's rhythm is VT?

My Next Thoughts:

At this point in my interpretation — I would estimate the statistical likelihood that the rhythm in today’s case is VT at over 95%! (based on the fact that sinus P waves are absent in this regular WCT rhythm — and the finding that QRS morphology in lead I is all negative). That said — I prefer to increase the accuracy of my interpreatation as much as possible — and — there is a way we can increase this statistical likelihood to 100%

• To Emphasize: IF we were at the bedside with this patient — the 1st thing we would do is determine if the patient is hemodynamically stable! That's because if the patient is not stable with this rhythm — then it would no longer matter what the rhythm is, because synchronized cardioversion would then be immediately indicated.
• But assuming that this patient is hemodynamically stable — we would then have a moment in time to quickly look a little closer.
• 
  
• Please NOTE: I have described my above thoughts in slow motion. With practice and experience — You should be able to arrive at this point in the process in no more than 10-to-15 seconds!

The Next Step: So — Are there P waves in Today’s ECG?

Take another LOOK at the ECG in Figure-2.

• Is there an EASY way to determine with certainty whether P waves are (or are not) present in today’s ECG?

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ANSWER: Are there P waves in Today’s ECG?

The KEY to optimizing the accuracy of our interpretation — is to determine IF underlying regular sinus P waves are present!

• PEARL #3: As I have often emphasized in this ECG Blog — the simple step of labeling P waves is incredibly helpful for determining the presence and nature of underlying atrial activity.
• In Figure-3 — I’ve labeled with RED arrows those small upright deflections in the long lead II rhythm strip that look like they may represent P waves.
• If these RED arrows in Figure-3 are in fact highlighting the presence of underlying P waves — Does this suggest what the P-P interval might be?
• 
  
• PEARL #4: If we can demonstrate that the small upright deflections in Figure-3 remain consistently regular throughout the long lead II — this would prove that these small upright deflections do represent an underlying rhythm of regular P waves. 
• To do this — I look to see what the shortest distance between 2 consecutive RED arrows might be. Doesn't it look like this shortest distance repeats between the 4th and 5th RED arrows — and between the 7th and 8th RED arrows?

Figure-3: I've highlighted with RED arrows the small upright deflections in the long lead II rhythm strip that I can clearly see.

PEARL #5: To determine within seconds if an underlying rhythm of regular P waves may be present in the long lead II — You have to use calipers!

• To Emphasize: I am not encouraging the use of calipers if your patient is unstable. A hemodynamically unstable patient in a WCT rhythm should be immediately cardioverted!
• But IF the patient whose rhythm is shown in Figure-3 is hemodynamically stable — it takes no more than seconds to walk out the rhythm that I've highlighted with colored arrows in Figure-4.

Figure-4: I've added WHITE and PINK arrows to Figure-3.

Breaking Down Figure-4: 

All that I've done to get from Figure-3 to Figure-4 — is to set my calipers to the P-P interval suggested by the distance between the 4th and 5th RED arrows in Figure-4 (which equals the distance between the 7th and 8th RED arrows) — and then to "walk out" this presumed P-P interval with your calipers throughout the remainder of the long lead II.

• Although on-time regular wide QRS complexes prevent us from seeing P waves under the WHITE arrows that I've added to Figure-4 — a definite underlying upright deflection can be seen under each of the 2 PINK arrows!
• This tells us that the colored arrows in Figure-4 represent an underlying rhythm of regular P waves occurring at an atrial rate of ~90/minute!

PEARL #6: Since the P waves represented by the colored arrows in Figure-4 are completely unrelated to neighboring QRS complexes — this tells us there is AV dissociation throughout the long lead II rhythm strip. The finding of AV dissociation within a regular WCT rhythm proves that the rhythm is VT!

• In my experience — AV dissociation is greatly overdiagnosed! This is because of the tendency to assume there is AV dissociation whenever clinicians see any suggestion of underlying baseline deflections. In my decades of following up on regular WCT rhythms — most cases of WCT rhythms labeled as showing "AV dissociation" do not truly represent this finding.
• It is because true AV dissociation proves that a WCT rhythm is VT — that I feel it best to avoid the diagnosis of AV dissociation unless you can clearly demonstrate the presence of underlying regular P waves throughout a significant portion of the rhythm. Doing so can only be done by use of calipers.
• Unfortunately — the clinical reality is that it is rare to see AV dissociation in faster WCT rhythms. This is because when a WCT occurs at a faster rate — the wide QRS complexes and often large-sized ST-T waves are highly efficient at "hiding" underlying P waves.
• 
  
• BOTTOM Line: The colored arrows in Figure-4 do demonstrate AV dissociation. This proves beyond doubt that today's WCT rhythm is VT!

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NOTE: For readers wanting more regarding the concepts and clinical utility of AV dissociation in assessing a regular WCT rhythm — Review of ECG Blog #335 may prove insightful.

• Additional examples of "My Take" on assessing the regular WCT rhythm can be found in ECG Blog #196 — Blog #220 — Blog #263 — and Blog #283 — among many others.

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Today's CASE Continues:

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Figure-5: XXX

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Figure-6: XXX

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Figure-7: XXX

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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) for the case and this tracing.

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ADDENDUM (2/XXX/2026):

I refer the reader to my ECG Blog #196 — in which I walk through a similar problem-solving process for another regular WCT rhythm. 

• I've excerpted from that post my Audio PEARL on assessing the regular WCT — as well as Figures on my "3 Simple Rules" and on QRS morphology in lead V1.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

Figure-8: Use of the “3 Simple Rules” for distinction between SVT vs VT (excerpted from my ACLS-2013-ePub).

Figure-9: Use of lead V1 for assessing QRS morphology during a WCT rhythm (excerpted from my ACLS-2013-ePub).

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Константин Тихонов <dropattack03@icloud.com>  (2/11/2026)

I just can't seem to fully explain a certain point to myself

I had a patient on call today. This is a 45-year-old man with a history of hypertrophic cardiomyopathy (without obstruction of the outflow tract of the left ventricle) and thyrotoxicosis. In January of this year, he had two similar episodes, and he was hospitalized twice by an ambulance team. Both times, the rhythm was restored with the help of electric pulse therapy. The diagnosis was ventricular tachycardia. He called an ambulance for a rapid heartbeat. During our examination, the patient was not pale, and there was no diaphoresis. His blood pressure was 125/70, compared to his normal blood pressure of 130/80. His oxygen saturation was 97%. His respiratory rate was 16.

 

 ECG No. 1 was recorded first. After that, there was a short episode of sinus rhythm recovery with premature ventricular complexes, after which the tachycardia with wide QRS complexes recurred (ECG No. 2).

ECG No. 3 was recorded after 150 mg of amiodarone, after which the patient felt a significant improvement in his well-being.

 

My opinion:

I believe that ECG No. 1 shows ventricular tachycardia.

 

1. There is an almost regular rhythm with small differences in RR intervals in some places. (Black lines)

2. The electrical axis on ECG No. 1, in my opinion, is approximately +120 degrees, while on ECG No. 3 it is about +60 degrees.

3. I have marked with red arrows on ECG No. 1 the possible presence of atrioventricular dissociation, which I believe is present.

4. The R nadir time in lead II is more than 50 ms.

5. The QRS complexes in tachycardia are similar in morphology to the premature ventricular complexes on ECG No. 3.

 

 ECG No. 3 raises special questions. It seems to me that there are regular P waves, the first of which are conducted, while the second are not and are hidden in the ST-T of the ventricular extrasystoles. These P waves are very similar in morphology to the sinus waves, as can be seen by comparing their morphology, which I have indicated with blue arrows on ECG No. 3. Also, these possible P's are not premature, so they are probably not blocked atrial extrasystoles. Is it possible that after a sinus contraction, a ventricular extrasystole occurs that retrogradely depolarizes the AV node, but the next sinus P finds the AV node in the absolute refractory period and is not conducted to the ventricles?

MY REPLY:

Hi Konstantin.Yes — VERY interesting case. I would like to do an ECG Blog on this case. Because the tracings are so long, I will need to reduce them — and I probably will only show the 1st and 3rd tracings together with the laddergram that I’ve drawn below. If OK by you — I will acknowledge  you — and I’ll let you know when I publish this (it may be a little while — as I have other cases to go before this).

 

MUCH better to show this tracing when you ask the question about retrograde P waves — because I can now directly refer to this ECG.

• There are NO retrograde P waves. You did a GREAT job highlighting the P waves. There is often some underlying sinus arrhythmia — which is the reason for slight change in P-P intervals.
• You PROVE beyond doubt (100%) that this rhytm is VT. Assuming no lead misplacement — you virtually NEVER see an all negative QRS in lead I.
• You very nicely highlight the on-time sinus P waves. This establishes AV dissociation, which especially given the abnormal QRS morphology tells us 100% that this rhythm is VT.
• Your ECG #3 shows ventricular bigeminy. The attached laddergram shows what is happening = on-time sinus P waves that are unable to conduct because the ventricular beats do conduct retrograde and therefore prevent every-other on-time P wave from being conducted down to the ventricles.
• This is a NICE PEARL — the fact that on-time sinus P waves continue throughout the tracing proves that beats #2,4,6,8,10,12 can not possibly be supraventricular (because if they were supraventricular, they would have reset the SA node)

 

I hope this makes sense. You did a GREAT job mapping out the P waves and the AV dissociation — and this PROVES this rhythm is VT. 

 

Do you have any more follow-up on this patient!

 

Take care.

 

: )  Ken

 

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KONSTANTIN Reply:

Thanks a lot, Ken. I am very glad that my version turned out to be correct, because I am now trying to learn to understand complex rhythms in more detail. 

 

On account of this patient. Later that night, the patient called an ambulance twice more and had two more recurrences of ventricular tachycardia. As a result, he was admitted to the hospital. He has been assigned to conduct an electrophysiological examination and the issue of installing a cardioverter-defibrillator will be considered.