COPY of ECG Blog #509 — Computer said, "Acute MI" - COPY of 599

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

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Figure-2: XXX

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Figure-3: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. (B) Brugada-2 ECG pattern (the “Saddleback” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave. (C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: the ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum R’ rise point — the base of the triangle formed is ≥4 mm — as this ensures a ß-angle ≥58°).

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MUBARAK AL-HATEMI <mubarakhatmi88@gmail.com>

— The computer says "Acute MI"—

Good Afternoon Prof. Ken. 9/25/2025 —

I send you this nice case of Brugada syndrome.

This ECG belongs to a 35 years old male from southeast Asia.

No past medical history
 witnessed cardiac arrest in the hotel , initiated CPR by security personnel for nearly 5 minutes , when EMS arrived he was in ventricular fibrillation with successful one DC shock and ROSC achieved. Fully recovered.

Plan: ICD insertion.

 

— Me to check QTc to see if this is SHORT QTc Syndrome? —

NOTE: Mubarak is from Doha, Qatar —

MY REPLY:

Hi. GREAT case that I most probably will use for an ECG Blog — THANK YOU!

I will acknowledge you and let you know when I publish this (may be a little while …).

 

QUESTION — Was cardiac cath done on this patient? If so — WHEN with respect to his cardiac arrest? (ie, Was it emergent or done after a couple of days).

 

Again — Excellent teaching case — and very fortunate for this 35yo that he had his arrest where others witnessed it and were able to promptly shock him! — : ) Ken

 

MY THOUGHTS — Note the ST elevation in V3 and ST coving in aVL — so this patient should have cardiac cath, since acute MI is one of the causes of a Brugada-1 Phenocopy!

 

REFERENCES:

Batchvarov — Eur Cardiol 9(2):82-87, 2014

https://pmc.ncbi.nlm.nih.gov/articles/PMC6159405/

 

Netsere et al — BMC Cardiovasc Dis 25, 638, 2025

https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-025-05102-y

 

Nakano and Shimizu — JACC Asia 19:2(4):412-421, 2022

https://pmc.ncbi.nlm.nih.gov/articles/PMC9627855/

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

Acknowledgment: My appreciation to Mubarak Al-Hatemi  (from Qatar) for making me aware of this case and allowing me to use this tracing.

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

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

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

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

Figure-5: 2-page Summary of the essentials of Brugada Syndrome (from my ECG-2014-ePub).

 

Figure-6: 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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

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

BELOW is FROM ECG Blog #238

https://ecg-interpretation.blogspot.com/2021/07/ecg-blog-238-53-what-is-phenocopy.html

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The ECG shown in Figure-1 was obtained from an elderly woman, who presented to the ED (Emergency Department) with an acute febrile illness (40°C).

• How would you interpret her initial ECG?
• Clinically — Could this be an early acute antero-septal STEMI?

 

Figure-1: ECG obtained from an elderly woman with an acute febrile illness (See text).

 

 

The Case Continues:

The ECG was repeated (Figure-2) — this time with anterior leads placed 1 interspace higher.

 

Figure-2: Repeat ECG of the tracing shown in Figure-1, with anterior leads placed 1 interspace higher (See text).

 

QUESTION:

• Do these serial tracings suggest an acute evolving anterior STEMI?

 

 

 

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

NOTE: Some readers may prefer at this point to refer to ECG Media PEARL #53 before reading My Thoughts regarding the ECGs in Figure-2. This 2-part ECG Video (9 minutes and 8 minutes) — reviews the ECG recognition and clinical significance of Brugada-1 and Brugada-2 ECG patterns + it clarifies the concept of Brugada Phenocopy.

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018).
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• For brief summary of this material — Please refer to Figures-5, -6 and -7 in the Addendum below.

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

In Part 1 of today's ECG Media Pearl #53 (9:00 minutes Video) — the essentials of Brugada Syndrome are reviewed.

Int Part 2 of today's ECG Media Pearl #53 (8:00 minutes Video) — these essentials are applied clinically.

My THOUGHTS on this Case:

Looking first at the ECG in Figure-1 — The rhythm is sinus — all intervals (PR, QRS, QTc) and the axis are normal — and there is no chamber enlargement.

 

Regarding Q-R-S-T Changes in Figure-1:

• There are no Q waves.
• R Wave Progression is normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
• Regarding ST segments and T waves — the most striking abnormality is the ST elevation in leads V1, V2 and V3, with "double-hump" upward concavity in lead V3.
• ST segments are noticeably flattened in several limb leads — as well as in lateral chest leads (that also show slight ST depression).

 

My Impression of ECG #1: There is no denying the presence of anterior ST elevation with ST segment flattening and slight ST depression in other leads.

• That said — Against these ST-T wave changes in ECG #1 representing an acute cardiac event — is the clinical history of acute febrile illness in this elderly woman, with no mention in the history of associated chest pain.

 

QUESTION:

What happened in ECG #2 (bottom tracing in Figure-2)?

 

 

ANSWER:

The main difference between ECG #1 and ECG #2 is the appearance of the ST-T waves in leads V1, V2 and V3:

• The R' peak in leads V1 and V2 is higher in ECG #2, with sharp downsloping that leads into a more noticeably inverted T wave.
• The "double-hump" upward ST segment concavity that was seen in lead V2 of ECG #1 — is now seen in lead V3 of ECG #2.

 

My Impression of ECG #2: The ECG picture in Figure-2 stongly suggests we are seeing Brugada ECG patterns.

• The "double-hump" upward ST segment concavity in lead V2 of ECG #1 — is consistent with a Brugada-2 (ie, "Saddleback" ) pattern.
• The higher-rising, steeper downsloping ST-T wave appearance in leads V1 and V2 of ECG #2 — now meets criteria for a Brugada-1 ECG pattern, with a Brugada-2 pattern now seen in lead V3.
• In view of the clinical history — this is unlikely to represent an acute anteroseptal STEMI.

 

PEARL #1: It turns out that ECG #2 was repeated soon after ECG #1. This illustrates how the simple measure of placing anterior leads 1 or 2 interspaces higher on the chest may serve to bring out a Brugada ECG pattern!

 

 

The Case Continues:

The patient was treated for her acute febrile illness. Her ECG was repeated after her fever had resolved (Figure-3).

Figure-3: Repeat ECG following resolution of this patient's fever — compared to the initial ECG in this case (See text).

 

QUESTION:

Does the patient in today's case have Brugada Syndrome?

 

 

 

WHAT is Brugada Syndrome?

First described in 1992 — the Brugada Syndrome is important to recognize because of an associated very high risk of sudden death in otherwise healthy young or middle-aged adults who have structurally normal hearts.

• The prevalence of Brugada Syndrome in the general population is ~1/2,000. The syndrome has become a leading cause of sudden death in young adults (under 40 years of age).
• PEARL #2: Brugada Syndrome is much more common in Southeast Asia compared to the rest of the world. When considering the possibility of this syndrome — demographics of the patient are important! (See Figure-6 in the Addendum below).
• PEARL #3: Although the genetics of Brugada Syndrome are complicated — the gender of the patient is also important. There is a distinct male predominance to this syndrome.

Personal Reflection: I never learned about Brugada Syndrome in medical school (the syndrome had not yet been described). But especially during the past 10 years, in which I've closely followed numerous international ECG internet forums — I've seen countless cases, especially of transient Brugada ECG patterns similar to today's case. 

• Once a clinical entity is "discovered" — it begins to get noticed with increasing frequency.

 

 

Regarding BRUGADA Syndrome vs Phenocopy: 

I reference an excellent state-of-the-art Review article on Brugada Syndrome (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). I've synthesized key aspects of this article:

• A Brugada Type-1 ECG pattern is diagnosed by the finding of ST elevation of ≥2 mm in one or more of the right precordial leads (ie, V1, V2, V3) — followed by an r’ wave and a coved or straight ST segment — in which the ST segment crosses the isoelectric line and ends in a negative T wave (See Panel A in Figure-4).
• A Brugada-1 pattern may either be observed spontaneously (with leads V1 and/or V2 positioned normally — or — positioned 1 or 2 interspaces higher than usual) — or — a Brugada-1 pattern may be observed as a response to provocative drug testing after IV administration of a sodium-channel blocking agent such as ajmaline, flecainide or procainamide.
• NOTE: In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. This definition was changed following an expert consensus panel in 2013 — so that at the present time, all that is needed to diagnose Brugada Syndrome is a spontaneous or induced Brugada-1 ECG pattern (without need for additional criteria).
• Panel B in Figure-2 illustrates the Brugada Type-2 or "Saddleback" ECG pattern. This pattern may be suggestive — but by itself, it is not diagnostic of Brugada Syndrome (See Figure-4).

 

Figure-4: Review of ECG Patterns in Brugada Syndrome (adapted from the above cited article by Brugada et al in JACC: Vol 72, Issue 9) — (A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. (B) Brugada-2 ECG pattern (the “Saddleback” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave. (C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: the ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum R’ rise point — the base of the triangle formed is ≥4 mm — as this ensures a ß-angle ≥58°).

 

PEARL #4: A number of conditions other than Brugada Syndrome may temporarily produce a Brugada-1 ECG pattern. A partial list includes the following:

• Certain drugs (antiarrhythmics; calcium channel blockers; ß-blockers; antianginals; psychotropic medications; alcohol; cocaine; other drugs).
• Acute febrile illness.
• Variations in autonomic tone.
• Hypothermia.
• Electrolyte imbalance (hypokalemia; hyperkalemia).
• Ischemia/infarction.
• Cardioversion/defibrillation.
• Bradycardia.

 

KEY Point: Development of a Brugada-1 or Brugada-2 ECG pattern as a result of one or more of the above factors — with resolution of this Brugada ECG pattern after correction of the precipitating factor(s) is known as Brugada Phenocopy.

• The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition (ie, the acute febrile illness in today’s case) may result in resolution of the Brugada-1 ECG pattern — with a much better longterm prognosis compared to patients with true Brugada Syndrome (ie, an ICD may not be needed, as it probably would be if true Brugada Syndrome was present!).
• NOTE: To ensure a diagnosis of Brugada Phenocopy — the patient should have: i) A negative family history of sudden death; ii) Lack of a Brugada-1 ECG pattern in 1st-degree relatives; iii) No history of syncope, serous arrhythmias, seizures or nocturnal agonal respiration; and, iv) A negative sodium channel-blocker challenge test.

 

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

Final Comment on Today's Case:

Assuming the elderly woman in today's case had otherwise been healthy (without a personal history of syncope, serious arrhythmias, seizures or nocturnal agonal respiration) — the fact that the Brugada-1 ECG pattern we initially saw completely resolved so soon after fever resolution, strongly suggests she has Brugada Phenocopy (and not Brugada Syndrome) — and that her longterm prognosis is likely to be good.

• Whether she needs to undergo a negative sodium channel-blocker challenge test at her advanced age (and what impact her family history might have at her age) — are issues for her informed consent and medical providers to decide.

 

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

Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.

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

 

References & Related ECG Blog Posts to Today’s Case: 

• For an excellent state-of-the-art Review article on Brugada Syndrome — CLICK HERE (Brugada J et al: J Am Coll Cardiol 72(9) 1046-1059, 2018). 
• For a Review on the entity of Brugada Phenocopy — CLICK HERE (Anselm D et al: World  Cardiol 6(3) 81-86-2014).
• For a study documenting the inability of experts to distinguish between a Brugada-1 ECG pattern from Brugada Syndrome vs Brugada Phenocopy — CLICK HERE (Gottschalk et al: Europace 18, 1095-1100, 2016).
• 
  
• ECG Blog #50 — For a case of Brugada Syndrome.
• 
  
• The September 5, 2020 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case shows an example of Brugada Phenocopy as a result of Hyperkalemia. 
• The May 6, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to seeMy Comment). This case reviews an example in which it was difficult to distinguish between Brugada Phenocopy vs an ongoing acute STEMI. 
• The September 8, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case reviews another example of Brugada Phenocopy as a result of Hyperkalemia.

 

 

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

ADDENDUM (7/1/2021): Summarizing material on Brugada Syndrome:

 

 

Figure-5: 2-page Summary of the essentials of Brugada Syndrome (from my ECG-2014-ePub).

 

Figure-6: 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 timesmore common than in North America). The country with highest prevalence of Brugada Syndrome is Thailand, with ~15 times higher prevalence thn 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-7: Summarizing Figure of KEY concepts reviewed in the above ECG Videos (ECG MP-53).

COPY of Blog #507 — Teenager with Palpitations- EXTRA COPY

The ECG in Figure-1 — was obtained from an otherwise healthy male teenager with palpitations.

• How would you interpret this tracing?

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

MY Thoughts on the ECG in Figure-1:

This is a complex tracing. I thought it best to break it down into parts.

• Beginning right after beat #6 — is a continuous run of a regular tachycardia which is wide until beat #21, when the QRS complex suddenly narrows!

NOTE: Although there is no single long lead rhythm strip — limb leads and chest leads are continuous, such that there are 30 consecutive beats on this tracing. In all — there is just under 10 seconds of monitoring.

• By the Every-other-Beat Method — the rate of the tachycardia is ~200/minute (See the ADDENDUM below for a brief ECG Video that reviews application of this concept).
• In Figure-2 — I have chosen the R wave of beat #8 in lead I as my "starting point" — because this begins precisely on a heavy grid line.
• We can see that the time it takes to record 2 beats (PINK numbers 1 and 2) — is 3 large boxes on ECG grid paper (BLUE numbers 1,2,3). This tells us that HALF of the rate = 300 ÷ 3 large boxes = 100/minute.
• Therefore, the actual rate = 100 X 2 = 200/minute.

Figure-2: Illustration of the Every-other-Beat Method for rapid estimation of fast rates. The rate of the regular tachycardia that begins after beat #6 is ~200/minute.

Today's Fast Rhythm is Supraventricular:

Although the QRS complex is wide from beat #7 through to beat #20 — the QRS then suddenly becomes narrow (ie, beginning with beat #21). This is best seen by focusing on the top row of beats in Figure-2 (ie, I suggest focusing on the 30 consecutive beats in leads I and V1 for my description below):

• PEARL #1: The facts that the last 10 beats in today's tracing clearly represent a regular SVT rhythm ( = narrow-complex tachycardia) — and that the transition from the wide tachycardia ( = beats #8-thru-20) — to the regular SVT that begins with beat #21 occurs without any pause or acceleration — suggests that this entire tachycardia is all supraventricular! (ie, If the wide beats represented VT — then it would be exceedingly unlikely for precise regularity of the rhythm to continue as the QRS narrows)!
• PEARL #2: QRS morphology during the wide tachycardia is consistent with RBBB aberrancy! (ie, The all positive QRS in lead V1 for beats #14-thru-20 — with slender initial R wave and wide terminal S wave in lead V6 for these beats — is completely consistent with RBBB conduction — as is the slender initial R wave with wide terminal S wave in lead I for beats #8-thru-13).
• PEARL #3: Putting together what we've established from PEARLS #1 and 2 — the tachycardia that begins after beat #6 is a regular SVT (albeit with a changing QRS morphology) at a rate of ~200/minute, but without sinus P waves. As I review in ECG Blog #240 — the rate of ~200/minute would be faster-than-expected for sinus tachycardia in a teenager — and unusual for AFlutter (since 2:1 AV conduction for untreated AFlutter typically results in a ventricular response close to 150/minute). Given that Atrial Tachycardia is an uncommon arrhythmia in an otherwise healthy teenager — this leaves a reentry SVT rhythm (either AVNRT or AVRT) as the most likely diagnosis for today's tachycardia, especially given the abrupt onset of this SVT rhythm.

================================ 

How Does Today's SVT Begin?

Now that we've established our "working diagnosis" as most probably being a reentry SVT rhythm — We can focus our attention on HOW this arrhythmia begins (See Figure-3):

• Beats #1,2,3 in Figure-3 — appear to be the last 3 beats in a previous SVT run at ~200/minute (that is probably of the same SVT mechanism with normal [narrow] QRS conduction as is seen in the chest leads for beats #21-thru-30).
• Beat #4 is sinus-conducted! (the 1st RED arrow in Figure-3 highlighting the sinus P wave).
• Beat #5 occurs early, and is preceded by a PAC (the 1st BLUE arrow that peaks the T wave of beat #4).
• Beat #6 is another sinus-conducted beat.
• Beat #7 is another PAC (2nd BLUE arrow in Figure-3). Note that this 2nd PAC produces a QRS complex that is wider than the normally-conducted QRS of beat #5.

Figure-3: Focusing on how the regular SVT begins.

================================ 

QUESTION:
Can you explain WHY in Figure-3 — the QRS complex of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

• HINT: The measurements (in milliseconds) that I’ve added under beats #3-thru-7 in lead II of Figure-4 provide an important clue to the Answer!

ANSWER:

As I explain in the ADDENDUM below — the concept of "cycle-sequence" comparison (as it relates to aberrant conduction) — and — the Ashman Phenomenon — explain why beat #7 is wider and looks different than beats #1-thru-6 in Figure-4 (See ECG Blog #70 — for detailed illustration of the Ashman Phenomenon).

• PEARL #4: My user-friendly way to synthesize the Ashman Phenomenon is simply to recall, “The funniest-looking beat follows the longest pause”. 
• The physiologic reason for this phenomenon — is that the longer the R-R interval preceding a given beat is — the longer the RP (Refractory Period) after that beat will be (with the RP consisting of both an absolute and relative refractory period — as in ECG Blog #70).
• In Figure-4 — the R-R interval preceding beat #6 is 740 msec. — which is longer than the 720 msec. R-R interval that precedes beat #4. Therefore, by the Ashman Phenomenon — the PAC that follows beat #6 will be more likely to conduct with aberration.

PEARL #5: The other component of cycle-sequence comparison — relates to the coupling interval, which is the distance from the onset of a QRS complex until the onset of the PAC that follows it. 

• It makes sense that the shorter the coupling interval — the greater the chance that a PAC will fall within the RRP (Relative Refractory Period), and therefore be conducted with aberration.
• In Figure-4 — it is the coupling interval of the 2nd PAC that is shorter (ie, 180 msec. vs 220 msec.) — therefore explaining why beat #7 is aberrantly conducted, but beat #5 is not.
• KEY Point: There is an "art" to applying the dual concepts of "cycle-sequence" comparison — in that both a longer preceding R-R interval and a shorter coupling interval may not be present, as they are for beat #7 in Figure-4.
• PEARL #6: Given the need for preciseness when applying cycle-sequence comparison for determining the likelihood of aberrant conduction — it should be obvious that use of calipers is a must to apply this concept!

PEARL #7: The ECG Video and content in Figures-7,-8,-9 in the ADDENDUM below — review the basics of aberrant conduction. As emphasized in this review — aberrantly conducted beats most often manifest some known form of conduction block (ie, RBBB, LBBB, and/or left anterior or posterior hemiblock).

• The predominantly positive R wave in lead I — with predominant negativity of the QRS in each of the inferior leads — suggest that beat #7 in Figure-4 is conducted with LAHB (Left Anterior HemiBlock) aberration.

Figure-4: How do the measurements that I’ve added under beats #3-thru-7 in lead II explain why the QRS of beat #7 is wider and looks different than the QRS of beats #1-thru-6?

PEARL #8: It is important to appreciate that the run of reentry SVT that begins with beat #7 in Figure-4 — is initiated by a PAC! 

• In contrast to ATach (ie, an ectopic Atrial Tachycardia) that usually begins with gradual acceleration of the ectopic atrial focus ("warm-up" phenomenon) — SVT reentry rhythms often start abruptly after a PAC — because this early beat arrives at the AV Node when the faster AV Nodal pathway is still refractory.
• This may serve to set up a reentry circuit — IF as a result of the PAC, the impulse starts down the other pathway, and is then able to complete the formation of a reentry circuit (ie, IF the faster AV Nodal pathway that was blocked has recovered in time to allow return of the impulse via retrograde conduction — as shown in Figure-5). 

Figure-5: The mechanism of a reentry SVT rhythm can be seen from this schematic figure — in that each time the impulse completes its path over the reentry circuit — retrograde conduction (back to the atria) as well as forward conduction to the ventricles (through the His-Purkinje system) occurs. As discussed below (as well as in ECG Blog #240) — this retrograde conduction back to the atria can sometimes be seen on the ECG during the tachycardia in the form of retrograde P waves.
= = = = =
KEY Point: With a reentry SVT — the impulse continues to circulate over the reentry circuit until this circuit is either interrupted (ie, by AV nodal blocking drugs or a vagal maneuver or another PAC or a PVC) — or — until the reentry SVT stops spontaneously.
= = = = =
NOTE: The reentry circuit shown here in Figure-5 depicts the mechanism for AVNRT (in which the reentry circuit is completely contained within the AV Node). This differs from the situation with AVRT — in which the reentry circuit extends outside of the AV Node via participation of an AP = Accessory Pathway (See PEARL #9).

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NOTE: What follows below goes Beyond-the-Core. As an emergency provider — it is more than enough to recognize that the teenager in today's case is highly symptomatic with recurrent, rapid runs of a reentry SVT rhythm that merits referral to an EP cardiologist for EP study and probable ablation treatment.

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Beyond-the-Core:  Is there more Atrial Activity?

Take Another LOOK at Figure-4 that I've reproduced below ...

• Is there any evidence of atrial activity after beat #7?
• If so — What does this atrial activity suggest?

Figure-4: Take Another LOOK at Figure-4. Is there more atrial activity?

ANSWER:

There are a number of signs suggesting additional atrial activity that are seen after beat #7. I highlight some of these below in Figure-5:

• To Emphasize — I am not certain about all potential signs of additional atrial activity. That said — I thought this to be of less clinical importance, since this symptomatic teenager with recurrent runs of reentry SVT will need EP study regardless — to clarify the nature of his arrhythmia (and most likely for curative ablation).

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PEARL #9: Sinus P waves are upright in lead II (as well as in the other inferior leads). In contrast — retrograde P waves will be negative in the inferior leads. Other leads that commonly show retrograde atrial activity are leads aVR and V1 — in which retrograde P waves tend to be positive in these right-sided leads.

• As discussed in ECG Blog #240 — the 2 major types of reentry SVT rhythms are AVNRT (if the reentry circuit is completely contained within the AV Node) — and — AVRT (if an AP located outside of the AV Node is present and participating as the retrograde limb of the reentry circuit).
• The very sharp, negative deflections that are seen at the very end of the widened QRS complex for beats #8-thru-13 (highlighted by YELLOW arrows in Figure-6) look like retrograde P waves.
• I added yellow question marks highlighting possible retrograde P waves in the ST segment of beats #1 and 2, which are the last few beats of the narrow SVT rhythm that ends after beat #3.
• Perhaps the BLUE arrow that I added over the ST segment of beat #3 — represents another PAC that occurs with a very short coupling interval (180 msec.) but without a long preceding R-R interval, such that this PAC is blocked (therefore ending the SVT at the beginning of this tracing?).
• Perhaps the sharp, negative deflections seen in other leads during the widened SVT (ie, in lead aVF for beats #8-thru-13 — and at the very end of the QRS in leads V5,V6 for beats #14-thru-20) also represent retrograde P waves?

PEARL #10: I thought the above suggestions of retrograde atrial activity during the runs of reentry SVT in Figure-6 were occurring relatively late in the cycle — which, as illustrated in ECG Blog #240 — suggests participation of an AP (Accessory Pathway) in the reentry circuit (therefore defining the rhythm as orthodromic AVRT). 

• NOTE: The presence and participation of an AP in the reentry circuit will result in a longer reentry circuit than what occurs with AVNRT, in which the reentry circuit is completely contained within the AV Node. This is why the RP' interval tends to be longer with orthodromic AVRT compared to AVNRT (in which the reentry circuit is shorter, given that it is completely contained within the AV Node).

Figure-6: I've highlighted some indications of retrograde atrial activity.

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More about AVRT (AtrioVentricular Reciprocating Tachycardia):

A nice review of AVRT by Jabbour et al appears in StatPearls, 2024.

• A significant percentage of patients with a reentry SVT rhythm will have a "silent" AP (Accessory Pathway) that only allows retrograde conduction — which is why delta waves are never seen on a 12-lead ECG in these patients.
• Sinus P waves in these patients are preferentially conducted in the forward direction over the normal AV Nodal pathway — which is why the QRS complex is narrow.
• If a PAC occurs in such patients — it will be conducted over the normal AV Nodal pathway and, if it occurs "at just the right moment" — it may find that the AP has recovered its ability to conduct retrograde, thereby completing the formation of a reentry circuit. If the "right timing" persists (ie, with recovery of AP ability to conduct retrograde each time an impulse conducted over the normal AV Nodal pathway arrives at the His-Purkinje junction) — this may perpetuate a run of orthodromic AVRT (as appears to be happening in Figure-6).

Miscellaneous additional notes re AVRT rhythms:

• Rarely (in only ~5% of AVRT episodes) — conduction of a supraventricular impulse may arrive in the ventricles via forward conduction over the AP — with retrograde conduction to complete the reentry circuit occurring over the AV Nodal pathway (ie, antidromic AVRT). In such cases, since the forward limb of the reentry circuit passes directly to the ventricles over the AP — the QRS complex will be wide, and antidromic AVRT may look identical to VT.
• On occasion — a patient may have more than a single AP (with this consideration relevant to the conclusion of today's case — as I discuss below).
• The ability of an AP to conduct retrograde (and participate in the reentry circuit of an AVRT rhythm) is not necessarily lifelong. Especially in children — the ability of a "silent" AP to conduct retrograde often resolves as the child becomes older.
• The abrupt switch of a reentry SVT that begins with QRS widening (ie, with either RBBB or LBBB conduction) — but then suddenly normalizes QRS duration without appreciable change in the R-R interval between wide vs narrow beats — suggests that an AP may be participating in the reentry cycle (This is seen beginning with beat #21 in Figure-6). 
• 
  
• Coumel's law may then help to predict localization of the AP:
• IF the R-R interval is slightly longer during the SVT with RBBB conduction than when the QRS is narrow — then the AP is right-sided. 
• IF the R-R interval is slightly longer during the SVT with LBBB conduction than when the QRS is narrow — then the AP is left-sided.

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CASE Follow-Up:

EP study was done on today's patient — and verified the presence of a participating AP in the reentry circuit (thereby confirming orthodromic AVRT as the mechanism of the arrhythmia).

• Noted in the EP report was that atrial stimulation induced orthodromic AVRT mediated by a concealed left lateral AP.
• Intermittent tachycardia was seen with RBBB conduction while maintaining the same cycle length — and with LBBB conduction manifesting a longer cycle length. This confirmed left-sided localization of the AP ( = Coumel's sign).
• The pathway was ablated — after which it was no longer inducible on EP study.

Unfortunately — Holter monitoring following ablation showed some recurrence of the SVT rhythm.

• I do not have further follow-up at this time.
• As I noted earlier — it is known that on occasion more than a single AP may be present. I suspect this may be the case with today's patient — as alternating participation by more than a single AP would seem the most logical explanation for recurrence of this patient's reentry SVT rhythm after ablation of only one of the APs.
• I suspect a 2nd EP study may be needed to identify one or more additional APs that may need to be ablated.

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Acknowledgment: My appreciation to Amelia Aria (from Bucharest, Romania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #240 — and ECG Blog #345 — Atrial activity in reentry SVT Rhythms.

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ADDENDUM #1 (11/XXXX/2025): Included below is the following:

• The Every-other-Beat Method for rapid estimation of fast rates.
• More on aberrant conduction.

ECG Media Pearl #27 (3:00 minutes Video) — ECG Blog #210 — Reviews the Rule of 300 for estimating heart rate — and — @ 1:25 minutes in the video, the Every-Other-Beat Method for Estimating Rate with fast rhythms (4/2/2021).

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ECG Media PEARL #28 (4:45 minutes Video) — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why the most common form of aberrant conduction manifests RBBB morphology).

• NOTE: I have excerpted a 6-page written summary regarding Aberrant Conduction from my ACLS-2013-ePub. This appears below in Figures-7, -8, and -9).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

Figure-7: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-8: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-9: Aberrant Conduction (Continued) — Example/Summary.