Tuesday, March 24, 2026

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

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

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Clinical setting - 67yo woman
Sudden onset of palpitations - presented - 30 minutes - stable BP - had recurrence of 4 episodes before she checked into the ED 
Needed 2 cardioversions before she converted to sinus rhythm. 


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Figure-2: XXXX




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Figure-3: 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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Another Regular WCT = VT- from Kianseng (3/21/2026)

Klanseng Ng- Aequanimitas <plusultra.ng@gmail.com>


Hi Kianseng. This is RVOT VT! (This is your corrected Power Point — :)

  • Regular WCT at ~185/minute without atrial activity.
  • LBBB-like configuration in the chest leads with marked right axis in the limb leads.
  • As per the attached review on Idiopathic VT — the less common LVOT is unlikely given transition between V3-to-V4. (My Audio-Pearl on this topic in the Addendum of ECG Blog #489 —
  • Cardiology assessment (in light blue on page 3) — in my opinion takes longer to consider, includes (as you note) some errors — and is not needed (again = my opinion) —because it should take seconds to recognize that this regular WCT with LBBB-like configuration in the chest leads and right axis without P waves is almost certain to be RVOT VT.
  • LBBB does not have a right axis with this type of fragmented lead I — and LBBB conduction typically continues with smaller R waves than we see by V3 — and almost always (unless there is “something else” = prior infarction, cardiomyopathy) almost alway has a later transition than we see here.
  • The post-conversion ECG proves VT — because of the obvious PVC that shows identical QRS morphology in leads V4,5,6 as seen during the WCT.

 

The most popular Blog posts are the WCT rhythms — so I want to use this case for an ECG Blog. I’ll let you know when I publish this case! — BEST — :) Ken

 

P.S.: Just wondering why Adenosine was not tried? Why Amiodarone was not started after the 2nd cardioversion? If the patient was referred for EP testing? There are of course many ways to manage patients — but the above would be my thoughts — :)





Friday, March 20, 2026

EXTRA COPY — ECG Blog #524: A little bit of Jadwar — EXTRA COPY


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NOTE: Today's post is from our publication in JACC Case Reports — 
(Nirdosh Rassani, MBBS & Ken Grauer, MD — Jan, 2026) (https://www.jacc.org/doi/10.1016/j.jaccas.2026.107164)
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The patient in today's case is a man in his late 20s — who presented to the ED about 6 hours after ingesting a finger-breadth piece of Jadwar (Figure-1).

Figure-1: Photograph of Delphinium denudatum (Jadwar). 


Details of today's case can be found in our JACC Case Reports article (available at the above link)
  • Suffice it to say that the patient's symptoms at the time of presentation were limited to mild flushing, increased sweating and palpitations
  • He was alert — with stable vital signs.

On seeing this patient's initial ECG (that I've reproduced in Figure-2) — it is easy to understand his chief complaint of "palpitations".


QUESTION:
  • How would you interpret this initial ECG?

Figure-2: The initial ECG in today's case — obtained from a man in his 20's who ingested Jadwar. (To improve visualization — I've digitized the original ECG using PMcardio).



MY Thoughts on the ECG in Figure-2:
This patient's initial ECG is extremely worrisome. That's because there is a constantly changing QRS morphology. It's hard to tell if there any "normal" beats.
  • To facilitate assessment in Figure-3 — I've numbered the beats in the long lead II rhythm strip.
    • Can you tell what is going on? (See below).

Figure-3: I've numbered the beats in today's initial ECG.


= = = = = = = = = = = = = = = = = = = = =

The Long-Lead II Rhythm Strip:
This is a complicated rhythm strip. I outline my stepwise "thought process" for assessment below:
  • The rhythm is irregularly irregular.
  • As noted — QRS morphology is constantly changing throughout the long lead II rhythm strip. Many of the beats are wide.
  • There are some narrow beats. Three of these narrow beats look similar and are upright in the long lead II (ie, beats #5,12,18). Presumably these 3 beats are supraventricular!
  • A short pause precedes beats #5 and 18 — but I see no sign of atrial activity. If P waves were present — I would expect to see them in the short pause that precedes beats #5 and 18. Given the overall irregularity with occasional narrow beats but no sign of P waves — I suspect that the underlying rhythm is AFib (Atrial Fibrillation).
  • There are multiple wide beats in the long lead II. Other than beats #5,12,18 — all of the other positive QRS complexes are clearly wide (ie, beats #1,2,3,4; #6; #9,10,11; #14; #19). Each of these beats look to be of ventricular etiology.
  • Fortunately — the long lead II rhythm strip is simultaneously recorded with the 12-lead tracing above it. The reason this is so helpful in this tracing — is that this allows us to view the QRS complexes that are negative in the long lead II in other simultaneously-recorded leads. For example — although beat #13 looks fairly narrow in the long lead II — it is actually a wide (presumably ventricular) beat when viewed in simultaneously-recorded leads V2,V3.
  • Beat #16 is all negative and appears to be slightly widened in the long lead II — but it looks much wider, and clearly of ventricular etiology in simultaneously-recorded leads V1,V2,V3.
  • Beat #15 in the long lead II looks intermediate in QRS morphology between beats #14 and #16Is the intermediate QRS shape of beat #15 the result of fusion between beats arising from 2 different ventricular sites?
  • On the other hand — not only is beat #21 narrow in the long lead II — but it appears to also be narrow in simultaneously-recorded leads V4,V5,V6. This suggests that beat #21 may be supraventricular, with its negative QRS morphology in the long lead II explained by aberrant conduction. Perhaps other fairly narrow, negative complexes in the long lead II are also supraventricular with aberrant conduction?

My Impression of Figure-3: 
This is an extremely complicated tracing. My assessment:
  • The underlying rhythm appears to be AFib.
  • There are multiple wide beat QRS morphologies that most-likely represent non-sustained runs of PMVT (PolyMorphic Ventricular Tachycardia).
  • Those beats that are narrower in the long lead II exhibit beat-to-beat variation in QRS morphology, suggestive of aberrant conduction and/or fusion with ventricular ectopy.

  • PEARL #1: What counts in assessment of Figure-3 is the overall "Gestalt" of what is likely to be happening. It simply is not worth spending excessive time trying to "dissect" the etiology of every beat in this tracing — as this is a thankless, if not impossible task. Instead, our goal for interpreting the rhythm is to arrive at an overall assessment — and this appears to be underlying AFib with non-sustained runs of PMVT.

  • PEARL #2: As noted above — beat #21 is probably supraventricular with aberrant conduction. As a result, I looked closely at ST-T wave morphology and the QT interval for this beat. Note within the RED rectangle in Figure-3 — that there appears to be marked ST depression in leads V5,V6 for beat #21 (BLUE arrow) — as well as QT prolongation considering the overall rapid rate.

  • PEARL #3: The unusual rhythm in Figure-3 is best interpreted in light of the clinical situation. This clinical situation is that today's patient ingested Jadwar prior to the onset of his symptoms! 
= = = = = = = = = = = = = = = = = = = = =

About Jadwar:
Jadwar (Delphinium denudatum) is a traditional medicinal herb widely used in South Asia as a "universal antidote" for treating a wide variety of neurologic, analgesic and gastrointestinal conditions. Among its attributed actions include pain relief, an anti-inflammatory effect, reduced fatigue, antidote properties (for snake or scorpion bites), addiction recovery (to help manage narcotic dependency) — as well as for treatment of URIs and other common infections.
  • Although Jadwar itself is generally considered safe and of low toxicity when used appropriately — Jadwar may sometimes be adulterated with aconite (which can occur if/when herbal medicines are improperly prepared).
  • Aconite ingestion may be highly toxic and even fatal. The mechanism stems from binding to and persistently activating voltage-sensitive sodium channels in excitable cells (including myocardial, nerve and muscular tissue). This results in sustained sodium influx with persistent sodium channel activation (Chan — Clin Toxicol 47(4):279-285, 2009).
  • Patients with aconite ingestion may present with a combination of neurologic features (paresthesias with facial or limb numbness) — motor effects (muscle weakness) — and cardiovascular effects that may be severe (hypotension, chest pain, palpitations from a variety of arrhythmias including refractory ventricular tachycardia and ventricular fibrillation).
  • Management of aconite poisoning is largely supportive until effects of ingestion have worn off. IV Lidocaine was successfully used in our case for its sodium-channel blocking effect that counteracts aconitine toxicity.
= = = = = = = = = = = = = = = = = = = = =

CASE Follow-Up:
Detailed description of today's presentation is covered in our JACC Case Reports article. In brief — laboratory evaluation of this patient was largely normal, with exception of low-normal serum Mg++ (treated with IV Mg++ replacement). Serum Troponins were negative and Echo showed surprisingly normal LV function despite the arrhythmia.
  • Within 30 minutes of administering IV Lidocaine (IV bolus followed by IV infusion) — there was a dramatic reduction in the frequency and duration of PMVT episodes — with complete suppression of ventricular ectopy achieved by 6 hours.
  • IV Lidocaine infusion was continued for 24 hours — followed by observation on telemetry for an additional 24 hours, after which the patient was discharged from the hospital.

To facilitate comparison in Figure-4 — I've added the discharge ECG below this patient's initial tracing. This discharge tracing reflects what was seen on telemetry during the last 40+ hours of observation.
  • Note return of normal sinus rhythm (RED arrow P waves in the long lead II of ECG #2) — and the complete absence of ventricular ectopy!
  • The lateral chest lead ST depression in ECG #2 is now minimal — with normalization of the QT interval.
  • PEARL #4: In support of my suspicion that beat #21 in the initial tracing was indeed a supraventricular beat — is the finding of similar QRS morphology for this beat in leads V5,V6 of ECG #1 — with QRS morphology in leads V5,V6 after restoration of sinus rhythm in ECG #2. This suggests that the reason beat #21 was negative in the long lead II of ECG #1 was indeed aberrant conduction.
  • The "PEARL" — is that sometimes the etiology of certain beats or rhythms of uncertain etiology in an initial tracing may become clear by careful comparison of morphology on subsequent tracings.

Figure-4: Comparison of today's initial ECG — with the discharge ECG recorded 48 hours later.


FINAL Thoughts:
Today's case proved satisfying by the complete recovery made by this patient who had ingested a potentially lethal dose of medicinal herb.

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Related Material:





Monday, March 16, 2026

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 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 "transitionlead — 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 IAll 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 "culpritartery 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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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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Sunday, March 8, 2026

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:

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/oriii) 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.