ECG Blog #503 (14,57) — The Cause of the Pause

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NOTE: I’ve decided to update and republish several of my favorite cases from years past. (Today's post is an improved version of ECG Blogs #14,57 — initially published in 2011).

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QUESTIONS: Interpret the rhythm below in right-sided Lead MCL-1.

• There is group beating in Figure-1.  Is this Wenckebach?
• Extra Credit: Why is the PR interval before beat #7 shorter than the PR interval before beat #6 (and also shorter than the PR interval before the other sinus beats in this tracing?).

Figure-1: Is the group beating here due to Wenckebach?

MY Thoughts on the Rhythm in Figure-1:

The rhythm in Figure-1 is not regular, but does manifest a pattern of group beating (with 2 short pauses between beats #2-3 and #6-7). 

• The QRS complex for each of the 9 beats in this tracing is narrow (ie, not more than half a large box in duration = not more than 0.10 second in duration). 
• The underlying rhythm appears to be sinus, with similar-looking P waves showing a fixed PR interval preceding all beats except for beat #7.
• Despite the presence of group beating — there is no evidence of Wenckebach or other form of AV block on this tracing.  Instead, the "cause" of the pause lies partially hidden within the T waves of beats #2 and 6.

PEARL #1: It's important to remember that the most common Cause of a Pause is a blocked PAC. Although most premature supraventricular beats ( = PACs or PJCs) are conducted normally to the ventricles (ie, with a narrow QRS complex that looks like other sinus-conducted beats) — this is not always the case. Instead, PACs (or PJCs) may sometimes occur so early in the cycle as to be "blocked" (non-conducted) because the conduction system is still in an absolute refractory state.

• This is the situation for premature impulse A in Figure-2 — which shows impulse A occurring during the ARP (Absolute Refractory Period).
• At other times — premature (early beats may occur during the RRP (Relative Refractory Period) — in which case aberrant conduction (with a wide and different-looking QRS) occurs. This is the situation for premature impulse B in Figure-2.
• Because impulse B occurs during the RRP — part (but not all) of the ventricular conduction system has recovered. Most often PACs occurring at Point B will conduct with some form of bundle branch block and/or hemiblock (reflecting that part of the conduction system which has not yet recovered).
• Premature impulse C in Figure 2 occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (ie, with a narrow QRS that looks identical to other sinus beats on the tracing).

Figure-2: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

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Returning to the Questions in Today's Case: 

Take another LOOK at Figure-1.

• Is the group beating in Figure-1 due to Wenckebach?
• Why is the PR interval before beat #7 so short?

Figure-1: Taking another look at Figure-1 ...

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ANSWERS:

There is no AV block in Figure-1. The PR interval as one moves from beat #3 to beats #4,5 and 6 is not increasing, as it would if Mobitz I (which is 2nd-degree AV block of the Wenckebach type) was present.

• Instead (as per PEARL #1) — The cause of the pause that we see between beats #6-7 in Figure-1 is a blocked PAC. We show this in Figure-3 — in which the RED arrow in the T wave of beat #6 highlights the "telltale notching" of a PAC buried in this T wave. 
• Note that a similar very early-occurring PAC (corresponding to a PAC occurring at point A in Figure 2) can be seen notching the T wave of beat #2.

PEARL #2: How do we know that the pointed deflection highlighted by the RED arrow in Figure-3 is truly a PAC — and not artifact? The KEY is that none of the normally conducted sinus P waves in this tracing manifest anything resembling an "extra" deflection (ie, The T waves of beats #1; 3,4,5; 7,8,9 are all smooth — and it is only the T waves of beats #2 and 6 that manifest this extra pointed deflection). 

• Thus, we need to first determine what the normal T wave for a sinus-conducted beat looks like — before we can determine if a PAC is partially hidden within the T waves of other beats.

Figure-3: Answer to Figure-1.

PEARL #3 — is related to PEARL #1: 

• Because the most common cause of a pause is a blocked PAC, it turns out that in clinical practice — blocked PACs are much more common than any form of AV block.
• That said — blocked PACs are often subtle and difficult to detect. As a result — they are often overlooked. But — blocked PACs will be found IF looked for (they'll often be hiding and/or notching a part of the preceding T wave — as seen above in Figure-3).

NOTE: The occurrence of a PAC depolarizes the rest of the atria — and therefore resets the SA Node. As a result — a brief pause usually follows after a premature P wave. These relationships are schematically illustrated in the laddergram shown in Figure-4:

• The rhythm in Figure-4 begins with 2 normally sinus-conducted beats (beats #1 and 2).
• The PINK circles in the Atrial Tier of the laddergram represent the 2 PACs that are not conducted to the ventricles, because they occur so early as to fall within the ARP (corresponding to impulse A, as was shown in Figure-2).
• Note the brief pause that follows each of these blocked PACs (ie, the pauses that occur between beats #2-3 and between #6-7).
• Unlike AV Wenckebach (in which the underlying P wave rhythm remains regular) — We can see that the sinus P wave before beat #3 ( = the 3rd RED circle in Figure-4) is delayed. When this 3rd RED arrow sinus P wave finally occurs — this P wave is conducted to the ventricles with a normal PR interval.
• There follow 3 more on-time sinus P waves (producing sinus-conducted beats #4,5,6) — until the next very early-appearing PAC occurs (the RED arrow highlighting this 2nd blocked PAC that notches the T wave of beat #6).
• Once again — a brief pause is seen after this 2nd blocked PAC. But note that when the next sinus P wave finally occurs — the PR interval before beat #7 is shorter than all other PR intervals on this tracing! (as per the open RED circle showing this very short PR interval before beat #7).

PEARL #4: The PR interval before beat #7 is too short to conduct. But since the QRS of beat #7 is narrow and virtually identical in morphlogy to all of the other sinus-conducted beats on this tracing — beat #7 must be a junctional escape beat! (schematically represented by the BLUE circle within the AV Nodal Tier).

• Normal sinus rhythm then resumes for the last 2 beats in Figure-4 ( = beats #8 and 9).
• To Emphasize: The occurrence of a junctional escape beat in Figure-4 is perfectly appropriate. The R-R interval preceding beat #7 is slightly more than 6 large boxes in duration, which corresponds to a junctional escape rate of slightly less than 50/minute — which means that the AV node is doing what it is "supposed to do" — namely, putting out an escape beat at the appropriate junctional escape rate of between 40-60/minute if and when the next sinus P wave is delayed.
• 
  
• Beyond-the-Core for a Very Advanced Point: Extra credit to any readers who used calipers, and on carefully measuring the R-R intervals of both pauses in Figure-4 — detected that the R-R interval for the 1st pause (between beats #2-3) — is actually slightly longer than the R-R interval for the 2nd pause. Since most of the time — the junctional escape rate is quite regular, I would have expected the junctional escape beat in this tracing ( = beat #7) to be preceded by a longer pause than the pause that precedes beat #3 which is sinus-conducted — but the opposite occurs. I attribute this unexpected finding to the slight variation in regularity that may occasionally be seen with escape rhythms.

Figure-4: Laddergram illustration of the rhythm from Figure-1. The cause of the 2 brief pauses (between beats #2-3 and #6-7) are blocked PACs. The PR interval preceding beat #7 is too short to conduct — which tells us that beat #7 is a junctional escape beat.  

Part 2 in Today's CASE: 

To emphasize the clinical importance of today's case — I present another challenging rhythm that I show in Figure-5.

QUESTIONS: 

Interpret the rhythm below in right-sided Lead MCL-1:

• What kind of AV block is present?
• Is a pacemaker likely to be needed?

Figure 5: Lead MCL-1 rhythm strip. Is this Mobitz I or Mobitz II? 

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ANSWER:

Hopefully you did not fall into the trap. There is no AV block in Figure-5. 

• As always — I find it easiest to be systematic. I favor the Ps,Qs,3Rs Approach (See ECG Blog #185).
• 
  
• The ventricular rhythm in Figure-5 is quite Regular at a Rate of ~50/minute for the first 6 beats. I'll defer attention to beat #7 for the moment.
• The QRS for these first 6 beats is narrow in this single lead rhythm strip. Assuming the other 11 leads in a 12-lead tracing confirm that the QRS is narrow — this would tells us that the rhythm is supraventricular.
• P waves are present! (ie, the colored arrows in Figure-6).
• The 5th parameter in the Ps,Qs,3R Approach addresses whether P waves are Related to neighboring QRS complexes — which they are for the first 6 beats, because the PR interval preceding beats #1-thru-6 is constant (RED arrow P waves in Figure-6). Thus, there is sinus conduction!
• But — every-other-P-wave is not conducted (No QRS follows the BLUE arrow P waves in Figure-6).

PEARL #5: The rhythm in Figure-6 is not a form of AV block! There are several reasons why we know this:

• The shape of the P waves highighted by the RED and BLUE arrows is different! (RED arrow P waves have an initial pointed positive deflection, followed by a wider, rounded negative deflection — vs — BLUE arrow P waves that have a triphasic negative-positive-negative morphology). This is consistent with atrial bigeminy (every-other-P-wave being a PAC) — because P wave morphology will be different when P waves arise from different atrial sites.
• The P-P interval is irregular! While true that 2nd- and 3rd-degree AV blocks often manifest slight P-P interval variation — the degree of P-P interval variation with this type of "ventriculophasic sinus arrhythmia" is generally not nearly as marked as the variation in P-P intervals seen in Figure-6.
• Beat #7 is a PAC that is conducted to the ventricles, here with a wider QRS complex due to aberrant conduction. P wave morphology of this last premature P wave is identical to the P wave morphology of each of the preceding BLUE arrow P waves — suggesting that all of these P waves are PACs.
• 
  
• CONCLUSION: The commonest cause of a pause is a blocked PAC, and not some form of AV block. There is no AV block in Figure-6. Instead — the rhythm is atrial bigeminy (every-other-P-wave is a PAC) — with the first 4 BLUE arrow P waves highlighting blocked PACs — and the last BLUE arrow representing a PAC that conducts with aberration (similar to impulse B in Figure-2).

Figure 6: Colored arrows highlight each P wave in Figure 5.

ECG Blog #502 (Video): Is this Wellens' Syndrome?

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 — Today's case is an ECG Video!

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The ECG in Figure-1 is from an older patient who was awakened by severe CP (Chest Pain) in the middle of the night. The CP was intermittent throughout the night — with her again awakened by very severe CP that morning.

• The patient called EMS that morning — but her CP had almost disappeared by the time the paramedics arrived (which is when the ECG in Figure-1 was recorded).

QUESTIONS:

• Is this Wellens' Syndrome? 
• — or — Is it something else?

Figure-1: The ECG in today's Case.

Below is the Video presentation of today's case (6 minutes):

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

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
• 
  
• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
• 
  
• ECG Blog #350 — another case of Wellens' Syndrome.
• ECG Blog #326 — Reviews a case that was missed.
• 
  
• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
• 
  
• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).

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ADDENDUM (10/25/2025): I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog).

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The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published over 40 years ago! I thought it insightful to return to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):

• The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
• I've reproduced (and adapted) in Figure-2 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
• Most patients also showed characteristic changes in lead V4.
• Most patients showed some (but less) ST-T wave change in lead V1.
• In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.
• 
  
• Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after hospital admission.
• Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:

The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-2:

• Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
• Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep.

Figure-2: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:

I've reproduced (and adapted) in Figure-3 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose serial ECGs are shown in Figure-3 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
•  
• Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-3 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
• 
  
• Not shown in Figure-3 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-3). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
• 
  
• Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-3: Representative sequential ECGs from one of the patients in the original 1982 article. 
— Panel A: The initial ECG on admission to the hospital; 
— Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing). 
— Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

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Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described over 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.

• One of the 2 ECG Patterns shown in Figure-3, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
• Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remained normal, or were no more than minimally elevated.
• Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.

• We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.
•  The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).
• BUT: What spontaneously occludes, and then spontaneously reopens — may continue with this cycle of occlusion — reopening — reocclusion — reopening — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
• 
  
• Clinically: We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example — resolution of chest pain in association with reduction of ST elevation suggests that the "culprit" vessel has spontaneously reopened. And, if this is followed by return of chest pain in association with renewed ST elevation — the "culprit" artery has probably reclosed.
• The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
• Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
• It is not "Wellens' Syndrome" — IF the patient is having CP (Chest Pain) at the time one of the ECG patterns in Figure-2 are seen. Active CP suggests that the "culprit" artery is still occluded.
• Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.

A final word about the 2 ECG Patterns in Figure-2. 

• As suggested from data in the original 1982 manuscript, Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
• Unlike Pattern A in Figure-2 — Pattern B may be limited to symmetric T wave inversion in a number of chest leads without an initially positive T wave, that then steeply descends into terminal negativity. The diagnostic problem — is that deep, symmetric T wave inversion may be seen in a number of other conditions, and is therefore much less specific for Wellens' Syndrome.

In Conclusion: The 145 patients studied by de Zwaan, Bär & Wellens in 1982 continue to this day to provide clinical insight into the nature of Wellens' Syndrome.

 

ECG Blog #501 (15) — Is this a Run of VT?

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NOTE: I’ve decided to update and republish several of my favorite cases from years past. (Today's post is an improved version of ECG Blog #15 — first published in 2011).

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The rhythm in Figure-1 — is from a right-sided MCL-1 monitoring lead.

• Does a run of VT (Ventricular Tachycardia) begin with beat #6?
• How certain are you of your diagnosis?

Figure-1: Does a run of VT begin with beat #6?

MY Thoughts on the Rhythm in Figure-1:

The underlying rhythm (as suggested by the first 5 beats) — is sinus tachycardia at ~105/minute (ie, The QRS is narrow and regular, with an R-R interval for the first 5 beats of just under 3 large boxes — and with P waves showing a fixed PR interval before each QRS for beats #1-5). 

• After beat #5 — Sinus rhythm is interrupted by a run of a regular WCT rhythm (Wide-ComplexTachycardia).  
• The rate of this regular WCT rhythm is ~200/minute (the R-R interval of every-other-beat for the WCT run is ~3 large boxes — so half the rate = 300÷3 =100 X 2 ~200/minute).
• We don't know for how long this run lasts — since it is still ongoing as the rhythm strip ends after beat #14.
• Sinus P waves are absent during the WCT, but — Doesn't it look like some form of atrial activity is present?

PEARL #1: The finding of atrial activity during a run of a regular WCT rhythm does not necessarily mean that the rhythm is supraventricular. This is because both reentry SVT rhythms, as well as VT may conduct retrograde with 1:1 VA conduction.

• Whereas retrograde P waves are generally negative in the inferior leads — they are usually positive in a right-sided lead such as aVR, V1 or MCL-1. Therefore — the small, upright pointed deflections that we seem to see occurring in the middle of the R-R interval during the WCT (ie, starting after beat #6) — do not tell us the answer.

PEARL #2: The width of QRS complexes during the tachycardia that begins with beat #6 clearly looks wider than it is for the first 5 sinus-conducted beats. That said — it does not look "very" wide.

• That said — We only see 1/12 of the ECG in Figure-1. Part of the QRS may lie on the baseline. When it does — then the QRS may "look" narrow in some leads, whereas in reality — the QRS may be very wide in other leads. 
• "12 leads are better than one!" (ie, When possible, if your patient is hemodynamically stable — Try to get a 12-lead ECG during the tachycardia! ).
• The above said, we might suspect that the rhythm in Figure-1 is supraventricular — because the initial deflection of QRS complexes during the WCT run is upright and narrow (very much like it is for the first 5 sinus-conducted beats). 
• In addition — S waves of the QRS during the run are steeply (rapidly) descending. This suggests supraventricular conduction — whereas with VT, the initial QRS deflection tends to be wider (because the impulse is not arising from within the ventricular conduction system — and is therefore is slower to depolarize the ventricles). 
• The above said — exceptions exist — and "12 leads are better than one" for determining IF the QRS is (or is not) truly wide during a tachycardia.

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KEY Point: How does the WCT run begin in Figure-1? 

(ie, What do we see just before beat #6?).

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ANSWER:

Note the RED arrow that I've added in Figure-2!

• This red arrow notches the T wave that precedes the run of widened beats ( = the T wave of beat #5). This is the "tell-tale" notching of a PAC (Premature Atrial Contraction) — that in Figure-2, precipitates a reentry SVT ( = AVNRT or AVRT).
• In contrast — the onset of VT is not preceded by a PAC.

Figure-2: Answer to Figure-1.

PEARL #3: To Emphasize: The most common cause of a regular WCT rhythm is ventricular tachycardia! That said — there are times when we can definitely exclude VT from consideration.  The rhythm in Figure-2 is one of those times. 

• QRS widening during a tachycardia may occur because of rate-related aberrant conduction (See below). The best way to diagnose aberrant conduction — is by identifying a premature P wave at the onset of the tachycardia. The RED arrow in Figure-2 does just that.
• PACs are sometimes difficult to identify — because they may be partially (or totally) hidden within the preceding T wave. But not in Figure-2. The way that we can be sure that the notching highlighted by the RED arrow is "real" (and not the result of artifact) — is that none of the 4 preceding T waves of the sinus-conducted beats show any hint of notching.
• And, as previously noted — 2 additional findings consistent (albeit not diagnostic) of a supraventricular etiology for beats #6-thru-#14 are: i) that the amount of QRS widening during the run appears to be minimal — and, ii) that the initial deflection (both the small, slender r wave and the steep downslope of the S wave) is similar in morphology to the initial part of the QRS of sinus beats.

Laddergram Illustration:

Appreciation of the mechanism of a reentry SVT is best conveyed by laddergram (as shown in Figure-3):

• Beats #1-thru-5 are sinus conducted.
• Beat #6 is a PAC. This starts the sequence — with retrograde conduction back to the atria (dotted lines that arise from within the AV nodal tier). 
• When "the timing is just right" — the mechanism by which a PAC may initiate a run of a reentry SVT — is if this early beat arrives at the AV node and finds the fast pathway still to be refractory, such that conduction to the ventricles occurs over the slow pathway — whereby a self-sustaining reentry loop is potentially established.

Figure-3: Laddergram illustration of a reentry SVT — in which a PAC precipitates establishment of a self-sustaining reentry loop.

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NOTE: Please check out my ADDENDUM #2 below regarding the insightful comment that I have just received from WB Ren.

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So Why is the QRS Wide in Figure-2?

The reason QRS complexes are wide in the run of SVT that begins with beat #6 — is that the fast heart rate precipitates a run of rate-related aberrant conduction. As shown in Figure-4 — Depending on when during the period of repolarization a PAC occurs — there are 3 possibilities for conduction:

• Possibility #1: Premature Impulse A — occurs so early as to fall within the ARP (Absolute Refractory Period). Because the entire conduction system is still in an abolute refractory state — premature impulse A is "blocked" (ie, non-conducted to the ventricles).
• Possibility #2: Premature Impulse C — occurs after the refractory period is over.  As a result — a PAC occurring at Point C will conduct normally (with a narrow QRS that looks identical to other sinus beats on the tracing).
• Possibility #3: Premature Impulse B occurs at an intermediate point during the RRP (Relative Refractory Period). A PAC occurring at Point B will therefore conduct aberrantly (ie, with QRS widening) — because only part (but not all) of the ventricular conduction system has recovered.
• 
  
• PEARL #4: Most often PACs that occur during the RRP will conduct with some form of bundle branch block and/or hemiblock pattern (reflecting that part of the cnduction system which has not yet recovered).

Figure-4: Absolute and Relative Refractory Periods (ARP & RRP) — explaining why beat A is blocked — and beat B is conducted with aberration.

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Putting It All Together:

The MCL-1 rhythm in today's case begins with 5 sinus-conducted beats. This is followed by a regular WCT run of at least 9 beats, until the rhythm strip ends.

• The WCT manifests a rate of ~200/minute. This rate is faster than usual for sinus tachycardia in an adult — and "off" for untreated AFlutter with 2:1 AV conduction (untreated AFlutter most often manifesting a ventricular rate close to 150/minute). This strongly suggests that the differential diagnosis is between a reentry SVT rhythm (ie, AVNRT or orthodromic AVRT) with QRS widening as a result of rate-related aberrant conudction — vs — VT.
• As shown by the RED arrow in Figure-2 — a "tell-tale" PAC initiates the run of wide beats. This virtually confirms that the WCT is supraventricular due to a reentry SVT (as per the laddergram in Figure-3).

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ADDENDUM #1 (10/19/2025):

• Included below is more on aberrant conduction.

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-5, -6, and -7).
• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction. 

Figure-5: Aberrant Conduction — Refractory periods/Coupling intervals (from my ACLS-2013-ePub).

 

Figure-6: Aberrant Conduction (Continued) — QRS morphology/Rabbit Ears.

 

Figure-7: Aberrant Conduction (Continued) — Example/Summary.

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ADDENDUM #2 (10/21/2025):

My appreciation goes out to WB Ren, an EP cardiologist — who has just left me the following comment on the CCRG (Critical Care Recent Guidelines) Facebook ECG forum:

Dr. Ren wrote the following: "Thank you for this case. It is very interesting. As I agree with everything you say, may I point you to a subtlety that caught my eye… During the “WCT” (which as you pointed out, is not that wide) — there is a recurring pattern. 

• P waves 7,9,11,13 are preceded by QRS with slightly different slurring of the end of the S wave. As well as these P waves have a lower amplitude. If this was a classic typical AVNRT, everything would be uniform. 
• As there is beat-to-beat variation in the end-upstroke of the S and P waves — this makes me consider an orthodromic-conducting AP (Accessory Pathway) concomitant to dual AV nodal physiology. 
• Now this can only be proven on an EP study but this is not out of the realm of possibility, as I have seen 2 in the past month or so."

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On review of today's tracing — I completely agree with Dr. Ren!

• What I had initially taken as random variation — is very clearly a recurring pattern — as I show in my amended Figure-2a. This is too consistent to be by chance.

Figure-2a: As per WB Ren — there clearly is a recurring pattern of alternating retrograde P wave morphology (alternating RED and YELLOW ovals). There is also some alternation of S wave morphology.

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I've also amended my laddergram in Figure 3a: 

• As per Dr. Ren — specifics of the reentry circuit in today's case can only be proven via EP study — but I greatly appreciate his observation that makes perfect sense.
• Final thought: RP' intervals of both retrograde P wave morphologies manifest a fairly long RP' interval, which is consistent with conduction over an AP.

Figure-3a: My amended laddergram — in which RED and YELLOW dotted lines show alternating pathways for the retrograde limb of the reentry circuit.