ECG Blog #540 — Does it "Fit" the Clinical?

The ECG in Figure-1 was recorded from a 60-ish year old woman who presented via EMS (Emergency Medical Services) to a rural hospital for sudden onset of confusion and seizure activity.

• The patient became agitated and combative during transport. She was non-responsive on arrival in the ED (Emergency Department).
• The patient's medical history was unknown at the time she was seen.

QUESTIONS:

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

 

Figure-1: The initial ECG in today's case — obtained from a 60-ish year old woman who presented with confusion and seizure activity. (To improve visualization — I've digitized the original ECG using PMcardio).

The ECG in Figure-1:

This patient's initial ECG is clearly abnormal:

• The rhythm is sinus tachycardia at a rate of ~130/minute.
• The QRS is narrow and the PR interval is normal.
• While fully acknowledging the difficulty estimating the QTc with marked tachycardia — the QTc is at most "borderline" (Our on-line QTc calculator suggests that the QTc is less than 450 msec.).
• Otherwise — the frontal plane axis is normal, and there is no chamber enlargement.

Regarding Q-R-S-T Wave Changes:

• Q Waves: Considering small size of the QRS in lead aVL — the Q wave in this lead is large in size (deep and wide). In view of the even smaller size of the QRS in lead I — the tiny Q wave in this lead is also likely to be significant.
• R Wave Progression: There is loss of R wave between leads V1 and V2. Although a reasonably sized R wave returns in lead V3 — transition (when the R wave becomes taller than the S wave is deep) is delayed until between leads V5-to-V6.

The above said, the most concerning findings in today's initial ECG are highlighted in Figure-2 (in the 4 leads within the GREEN rectangles). 

• Hyperacute ST elevation is clearly seen in both high-lateral leads ( = leads I and aVL). There is reciprocal ST depression in lead III. 
• In support of this reciprocal change in lead III — ST segment straightening and a lesser degree of ST depression is seen in the other 2 inferior leads ( = leads II and aVF).

In the Chest Leads: 

• Lead V2 is noteworthy because of its slightly elevated and disproportionately enlarged ST-T wave (being both "fatter"-at-its-peak and wider-at-its-base than expected given modest size of the S wave in this V2 lead).
• The picture in this lead V2 stands out in stark contrast to the complete lack of ST-T wave abnormality in the 4 chest leads that follow.

My Impression of ECG #1:

I initially saw today's initial ECG before knowing the history. 

• As suggested by the schematic image that appears above the ECG in Figure-2 — I immediately thought ECG #1 was diagnostic of the South African Flag Sign (See below for review of this important ECG finding). 

Figure-2: Today's ECG "fits" criteria for the South African Flag Sign!

The South African Flag Sign:

The clinical importance of recognizing the South African Flag Sign — is that in a patient with new Chest Pain — this ECG finding strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD (Left Anterior Descending) coronary artery. As per the schematic image above the ECG in Figure-2 — the South African Flag Sign is present when there is: 

• i) ST elevation in leads I, aVL and V2; 
• ii) Reciprocal ST depression in lead III (ST depression is also often seen to a lesser degree in neighboring inferior leads II and aVF);
• iii) No ST elevation in any chest lead except for lead V2.

I previously reviewed the South African Flag sign in ECG Blog #320 (See Pearl #1 in that Blog #320 post) — as well as in My Comment at the bottom of the page in the January 18, 2025 post in Dr.Smith's ECG Blog.

• PEARL #1: Sometimes acute proximal LAD occlusion will initially look like an acute occlusion limited to the 1st or 2nd Diagonal Branch. This is because early on — ST elevation may only be seen lead V2, and not yet in leads V1,V3,V4. A tincture of time (and serial ECGs) will usually clarify the situation.
• PEARL #2: The clinical significance of being aware of a Diagonal Branch "culprit" — is that: i) Since only 1 chest lead shows ST elevation (ie, lead V2) — this pattern will not “fit” the definition of a STEMI, because only 1 chest lead shows ST elevation (and by definition, to satisfy criteria for an anterior STEMI — 2 contiguous chest leads must show ST elevation); — and, ii) Recognizing the S. African Flag Sign alerts the angiographer where to look for the “culprit” artery. We have seen cases in which a capable angiographer initially missed the cath finding of Diagonal Branch occlusion — BUT — seeing this ECG pattern conveyed the need for another LOOK at the cath film, with focus on the expected area for Diagonal Branch takeoff then revealing subtle-but-complete occlusion in one of the Diagonals. 

The History Doesn't "Fit" ...

The problem with today's case — is that the history does not "fit" with the ECG picture that strongly suggests acute occlusion of the 1st or 2nd Diagonal Branch of the LAD.

• Today's patient had no chest pain. Instead — this 60-ish year old woman presented with neurologic symptoms, and arrived at the hospital in a non-responsive state.
• While possible for there to be a "silent" MI (ie, in which chest pain is absent) — the clinical presentation of today's case is contrary to what one would expect for an acute cardiac event. Could something else be going on?

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The CASE Continues:

Given the atypical history for an acute MI (especially in view of this patient's non-responsive state on arrival at the hospital) — the cardiologist on call appropriately opted to explore other etiologies before deciding on where best to transfer this patient (as the capability for cardiac catheterization and/or acute stroke management was not available at the rural hospital where this patient was brought to).

• Complicating assessment — an initial Troponin value was moderately elevated!
• The patient was transferred to a facility with cardiac catheterization and acute stroke management capability.
• Initial imaging suggested a necrotic ring-enhancing mass with significant surrounding edema that was thought to represent a brain tumor.

Figure-3 shows the follow-up ECG that was recorded ~4 hours after ECG #1.

• How do you interpret this repeat tracing? 

Figure-3: Comparison between the follow-up ECG recorded ~4 hours after the initial tracing.

Interpretation of ECG #2:

Compared to ECG #1 — the repeat ECG in Figure-3 shows the following:

• Some slowing of the sinus tachycardia (from ~130/minute — down to a rate of ~110/minute).
• Deflation of virtually all hyperacute ST-T wave changes that had been seen 4 hours earlier.

CASE Conclusion:

• The repeat Troponin was essentially unchanged from its initial value (showing similar moderate elevation).
• Cardiac Cath was performed — and showed completely normal coronary arteries — with an abnormal wall motion abnormality typical for Takotsubo (Stress) Cardiomyopathy.
• Further brain imaging suggested that rather than a brain tumor — the patient's neurologic injury was the result of necrotic transformation from a stroke. Given that the patient's neurologic condition returned to near normal — her longterm prognosis was promising.

Lesson-to-be-Learned:

• As discussed on a number of occasions in this ECG Blog — CNS Catastrophes (from CNS bleeds, stroke, tumor, trauma, undifferentiated coma, etc.) — are notorious for producing some of the most bizarre-looking ECGs that are prone to simulate acute infarction (See ECG Blog #299, among others).
• Today's case illustrates just how close the pseudoinfarction pattern from a "CNS catastrophe" may be! (For all the world — Today's initial ECG suggested acute 1st or 2nd Diagonal occlusion).
• Despite the alarming, seemingly acute ST-T wave changes in today's initial ECG — the clinical scenario did not "fit" for an acute MI. While fully aware that some acute MI patients may not necessarily present with chest pain — it was this "disconnect" between the initial ECG and the patient's history that clued to on call cardiologist into the need to explore other potential diagnoses.
• For other examples in which the unexpected clinical presentation suggested that acute-looking ECG changes represented a pseudoinfarction pattern (and not acute infarction) — Check out the February 20, 2025 post in Dr. Smith's ECG Blog (with My Comment at the bottom of the page in that post).
• A common denominator between these CNS catastrophes and the pseudoinfarction patterns they produce on ECG — is greatly increased endogenous catecholamines! This helps to explain the common finding of Takotsubo Cardiomyopathy (Stress Cardiomyopathy) that so often accompanies these conditions. It also explains many of the abnormal ECG findings, as well as the moderately elevated but non-rising Troponin value (See ECG Blog #456 — for review of the ECG findings in Takotsubo Cardiomyopathy).

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Acknowledgment: My appreciation to Paul Carr and Nataliya Szozda (from Toronto, Canada) for contributing this case.

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ECG Blog #539 — Does SVT cause Hypotension?

The ECG in Figure-1 was obtained from a young adult woman — with a history of recurrent SVT. She was hypotensive with this most recent episode.

QUESTIONS:

• How would you interpret the ECG in Figure-1? 
• Does this tracing "fit" with this patient's history?
• Extra Credit: Is there evidence of underlying atrial activity?

Figure-1: The initial ECG in today's case — obtained from a young adult woman with a history of recurrent SVT. (To improve visualization — I've digitized the original ECG using PMcardio).

Review of some Clinical Concepts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~180-190/minute.

• Although in a number of limb leads the QRS does not seem wide — it "looks" wide in most of the chest leads, and measures 0.11-0.12 second in leads V1,V2.
• PEARL #1: I've seen different answers for what constitutes "QRS widening" in an adult. I favor the following 2 guidelines: i) For measuring QRS duration — Use that lead in which you can clearly determine the onset and offset of the QRS complex — and in which the QRS is longest; — and, ii) Because some cases of fascicular VT may only measure 0.11 second in duration — I consider the QRS to be "wide" if in any lead the QRS clearly measures ≥0.11 second in duration. And the easy way to tell if QRS duration is ≥0.11 second — is to determine if QRS duration is clearlly more than 1/2 a large box in duration (ie, Each large box on ECG grid paper = 0.20 second ==> 1/2 a large box = 0.10 second, and if the QRS is more than this — then by my definition it is wide!).
• PEARL #2: Just because a given diagnosis is written in a patient's chart — does not necessarily mean that diagnosis is correct (unless you also find firm objective evidence in that patient's chart to support the diagnosis!). We need to remain open to other possibilities. Therefore, in today's case — I did not fully accept the prior "history of recurrent SVT" — because I was not shown any prior ECG documenting that the known tachycardia was indeed supraventricular.
• PEARL #3: It is still all-too-commonly believed that the cause of the overwhelming majority of regular WCT rhythms in younger adults is some form of SVT (SupraVentricular Tachycardia) — in which QRS widening is explained by either preexisting BBB (Bundle Branch Block) or aberrant conduction. However, as was shown in ECG Blog #489 — Blog #38 — and Blog #464, among others — the idiopathic VTs (which occur in patients without underlying heart disease) are much more common in younger adults than is currently appreciated (More on the idiopathic VTs below in today's ADDENDUM).

PEARL #4: Today's patient was hypotensive in association with the rhythm in Figure-1. Although it is clearly more common for a patient in VT to be hypotensive (than for a patient in an SVT rhythm) — a patient's BP (blood pressure) is not an infallible predictor for distinguishing between VT vs SVT (See ECG Blog #220 — Blog #38 — and Blog #297). For example:

• We've seen a number of patients in sustained VT remain hemodynamically stable not only for hours — but for days!
• In contrast, most otherwise healthy younger adults who present in a sustained SVT rhythm — will remain stable for long periods of time.
• Bottom Line: The fact that today's patient was hypotensive in association with the rhythm in Figure-1 is not reliably predictive of this rhythm's etiology. That said — it is indication of the need for prompt effective therapy (ie, having a lower threshold to proceed with synchronized cardioversion).

The ECG in Figure-1:

As already noted — the rhythm in Figure-1 is a regular WCT at a rate of ~180-190/minute. With regard to atrial activity — there is no consistent sign of upright sinus P waves in lead II, or in any other lead. That said — the negative notching in the terminal portion of the QRS in leads II and aVF suggests there are 1:1 retrograde P waves (YELLOW arrows in Figure-2).

• PEARL #5: Even if the negative notching highlighted by YELLOW arrows in Figure-2 does represent 1:1 retrograde P waves — this does not help in our differentiation of the rhythm because both VT and reentry SVT rhythms may manifest 1:1 VA conduction.

Figure-2: YELLOW arrows highlight what appears to be 1:1 retrograde P waves.

What about QRS Morphology?

Up until this point — We've highlighted this young woman's history, namely of recurrent SVT, with today's episode thought to represent just one more recurrence. That said, because the QRS in Figure-1 is wide — We need to consider the possibility of VT.

• PEARL #6: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #7: As discussed below in the ADDENDUM to today's post — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB/hemiblock conduction!

NOTE: As shown in Figure-3 — QRS morphology is not typical for RBBB with either left anterior or posterior hemiblock.

• Instead of the expected triphasic rsR' complex in lead V1 (with taller right "rabbit ear" and a distinct S wave that descends below the baseline) — a qR pattern is seen in this lead. While SVT rhythms do not always show "typical" QRS morphology — it's important to appreciate that atypical conduction features may be a hint of a ventricular etiology (See Figure-9 in the ADDENDUM below).
• Typical RBBB conduction should manifest a wide terminal S wave in left-sided leads I and V6. While we do see a wide terminal S wave in lead I — this feature is missing in lead V6 (ie, the deep S wave in lead V6 in Figure-3 is narrow and followed by a small positive deflection = an RSr' in lead V6).
• With RBBB conduction — left-sided lead I typically manifests predominant positivity prior to the wide terminal S wave. However, the R wave in lead I in Figure-3 is relatively small.
• QRS morphology in leads II and III is not typical for either LAHB or LPHB conduction (ie, leads II and III lack the predominant positivity of LPHB — and the rSr' pattern in lead III is not the expected rS pattern typical of LAHB conduction).

BOTTOM Line: While the above subtle morphologic features do not rule out the possibility of an SVT rhythm for today's tracing — they should increase our suspicion that the rhythm in Figure-3 may represent fascicular VT.

• PEARL #8: Assessment of QRS morphology on the surface ECG is not definitive for distinguishing between SVT vs VT. Sometimes the only way to determine the true etiology of a regular WCT rhythm is by EP testing. That said — especially given the history in today's case of recurrent episodes — these atypical morphologic features made me highly suspicious that the rhythm in Figure-3 was probably fascicular VT.

PEARL #9: As has been emphasized on many posts in this ECG Blog — the treatment of choice for a hemodynamically stable patient in fascicular VT is IV Verapamil (or IV Diltiazem).

• Although Adenosine may convert some cases of fascicular VT — it is much less effective than IV Verapamil in this group of patients.
• IV Verapamil or IV Diltiazem should not be given to patients with ischemic VT (ie, in patients with underlying structural heart disease). This is because the negatively inotropic and vasodilating effects of these drugs may lead to hemodynamic decompensation. However, these drugs are safe in patients with idiopathic VT who do not have underlying heart disease.
• The extra advantage of using IV Verapamil to treat an otherwise healthy younger adult with suspected fascicular VT — is that this drug is likely to be effective regardless of whether the rhythm is fascicular VT or a reentry SVT rhythm!
• The above said, since today's patient was hypotensive in association with the rhythm in Figure-1 — the treatment of choice is synchronized cardioversion.

Figure-3: QRS morphology in today's tracing is not typical for RBBB/hemiblock conduction.

One More Clue to Today's Rhythm!

Take another LOOK at today's rhythm in Figure-4.

• Could the slanted RED lines in Figure-4 represent atrial activity?

Figure-4: What do the slanted RED lines indicate?

Answer:

Overall — there is very little artifact in Figure-4. As a result — I was struck by the consistent disturbance in the baseline in lead II that has to be "real" (ie, slanted RED lines in Figure-4) — with similar disturbance of the baseline in lead lead aVF (slanted BLUE lines) — albeit not in the other inferior lead ( = lead III), and not in other leads.

• I wondered IF the slanted RED lines in lead II might represent underlying AV dissociation?

To explore this possibility — I've isolated and enlarged in Figure-5 the 15 beats that we were seeing in Figure-4.

Figure-5: A closer look at the 15 beats in lead II.

As suggested earlier in Figure-2 — YELLOW arrows pointing to the terminal negative notching in Figure-6 highlight retrograde P waves. 

• But did YOU previously notice when you first examined this tracing, that this negative terminal notching is not present after beats #3 and 10? Why might this be so?

Figure-6: Retrograde P waves are not seen after beats #3 and 10.

Calipers are needed to answer this question.

• I thought the 2 consecutive RED arrows in Figure-7 looked to be highlighting 2 consecutive sinus P waves (ie, upright in this lead II rhythm strip).
• Setting my calipers to the P-P interval between these 2 consecutive RED arrows — I then looked for additional deflections likely to represent more sinus P waves, keeping in mind that slight variation in this P-P interval would be possible if there was an underlying sinus arrhythmia. This led me to the deflections highlighted by the PINK arrows in Figure-7.
• This left me to postulate the likely presence of "on time" sinus P waves directly over the QRS of beats #3 and 10 (the 2 WHITE arrows).
• NOTE: Beats #3 and 10 are the only QRS complexes in Figure-7 that lack retrograde conduction (ie, No YELLOW arrow is seen at the end of the QRS of beats #3 and 10).

Figure-7: Using calipers allows us to identify the likely presence of an underlying sinus rhythm (ie, AV dissociation).

My Proposed Laddergram:

Normally — I would never expect to see the simultaneous presence of AV dissociation from an underlying sinus rhythm in a patient with VT that produces 1:1 VA conduction. That said — this is what appears to be happening.

• I drew my proposed laddergram in Figure-8 — as my attempt to explain how these findings might reasonably account for the failure of retrograde conduction for only 2 out of 15 QRS complexes in this tracing.
• It is because the 2 "on time" underlying sinus P waves highlighted by the WHITE arrows in Figure-8 occur at precisely the time when ventricular beats #3 and #10 are conducting retrograde through the AV Node — that completion of retrograde conduction is rendered impossible by downward conduction from these 2 "on time" WHITE arrow P waves.
• PEARL #10 (Beyond-the-Core): This failure of retrograde conduction from ventricular beats #3 and 10 proves that today's rhythm is VT (and not SVT with aberrant conduction) even more convincingly than the finding of AV dissociation — because the reentry circuit of a supraventricular reentry rhythm could not be maintained if retrograde conduction was intermittent. (See Figures-5 and -6 and the accompanying text in ECG Blog #538 — for  explanation and illusration of the advanced concept of WHY intermittent retrograde conduction in association with a regular WCT rhythm  rules out a reentry SVT rhythm).
• Editorial Comment (Beyond-the-Core): I don't believe I have ever encountered the sequence of events portrayed in Figure-8. That said — the "beauty" of this rare occurrence is that: i) It provides a wonderful example of the concept known as "concealed" conduction — in which we are able to predict an electrophysiologic happening (in this case, failure of retrograde conduction after ventricular beats #3 and 10) despite not seeing the reason why this occurs on the surface ECG; — and, ii) It absolutely proves that today's ECG (and presumably most, if not all of the recurrent arrhythmia episodes this young woman has had) were the result of fascicular VT, and not of a reentry SVT.

Figure-8: My proposed laddergram.

CASE Conclusion:

I subsequently learned that this patient's recurrent ED visits for "palpitations" in association with a regular WCT rhythm (similar to the rhythm shown in today's case) — were resistent on several occasions to initial treatment with Adenosine, but responsive to IV Verapamil.

• This new historical information (ie, that several previous episodes responded to IV Verapamil, but not to IV Adenosine) — provides further support that this young woman's recurrent WCT episodes most likely were all the result of fascicular VT.
• And, now that the correct diagnosis of fascicular VT has been made — the patient was referred for EP study, most probably to be followed by ablation that hopefully will be curative.
• In the interim (awaiting scheduling for her EP appointment) — I'd consider oral Verapamil in hope of minimizing (eliminating) episodes.
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• P.S.: To answer the question posed by my title — Yes, some patients may become hypotensive with a reentry SVT rhythm (ie, If they have significant other problems that lower the BP — or if they have poor LV function — or if they fatigue after a prolonged period in a sustained SVT rhythm) — but many (most) patients maintain sufficient perfusion for even extended periods of time in a reentry SVT.

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Acknowledgment: My appreciation to Hamdallah Naser (from AL-Najaf, Iraq) — for allowing me to use this case and this tracing.

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ADDENDUM:

I've added below relevant materials in support of today's diagnosis. 

Figure-9: QRS morphology in lead V1 suggestive of either aberrant conduction vs VT (Figure 08.25-1, excerpted from my ACLS Pocket Brain-2013).

Figure-10: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minute Audio): What is Idiopathic VT? — with special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

ECG Blog #538 — An Unusual Finding

The ECG in Figure-1 was obtained from an adult who complained of frequent “palpitations”.  Imagine no history is available.

Choose the BEST Answer regarding the rhythm in Figure-1:

• a) The probability of VT is ~50%.
• b) The probability of VT is ~75%.
• c) The probability of VT is virtually 100%.
• d) The rhythm is a reentry SVT (ie, AVNRT or AVRT) with aberrant conduction.
• e) The rhythm is AFlutter with 2:1 AV conduction. 

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

My Initial Thoughts:

The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~160/minute, without clear sign of sinus P waves.

• As always, the diagnosis of VT must be considered until you prove otherwise — whenever you encounter a regular WCT rhythm without clear sign of sinus P waves.

Additional factors in favor of VT include the following:

• The frontal plane axis during the WCT rhythm is indeterminate (predominantly, but not completely negative in both leads I and aVF). This degree of frontal axis deviation favors VT — because it is not consistent with either LAHB (Left Anterior HemiBlock) or LPHB (Left Posterior HemiBlock) conduction. That said, because the frontal plane axis is not “extreme” (ie, not completely negative in either lead I or aVF) — this degree of axis deviation is suggestive but not diagnostic of VT (See Rule #1 and Table-2 in ECG Blog #42-bis, among many other examples throughout my ECG Blog of "extreme" axis deviation as a sign of VT).
• QRS morphology in lead V1 is all positive, but amorphous (ie, completely lacking in the triphasic rsR’ morphology characteristic of RBBB conduction). Although this lead V1 appearance does not completely rule out RBBB conduction (from either preexisting bundle branch block or rate-related aberrant conduction) — this QRS morphology does somewhat favor VT (as per Figure-2 in ECG Blog #42-bis). That said, wide terminal S waves are seen in left-sided leads I and V6 — and there is enough of a positive r wave in lead V6 such that RBBB conduction is still possible (ie, QRS morphology in Figure-1 is suggestive but not diagnostic of VT).
• 
  
• BOTTOM Line: At this point in our assessment — We lack a definitive answer. Without knowledge of this patient’s age, awareness of his/her prior medical history (ie, Any history of underlying heart disease?) — and without the benefit of a prior ECG that might reveal similar QRS widening during sinus rhythm — We are left with the statistical reality that the clear majority of regular WCT rhythms with atypical morphologic features and without clear sign of sinus P waves (as is the case in Figure-1) — are likely to be VT (although some of these regular WCT rhythms will turn out to be supraventricular).
• Looking again at the answer choices provided at the beginning of today’s post — the BEST choice would seem to be b) The probability of VT is ~75%.

BUT — There is One More Important Clue!

• HINT #1: This KEY clue that I have not yet mentioned tells us that the answer is not choice "b" — but something else. This KEY clue is related to atrial activity.

Take another LOOK at Today's Tracing in Figure-2:

• HINT #2: Why have I numbered the beats in Figure-2?

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

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Answer: The Clue provided by Atrial Activity ...

It turns out that atrial activity is present in today's tracing — in the form retrograde P waves (highlighted by YELLOW arrows in Figure-3).

Figure-3: YELLOW arrows highlight retrograde P waves.

Retrograde P Waves:

Retrograde P waves typically appear as a negative notch or a negative deflection that occurs after the QRS in one or more of the inferior leads (ie, P wave negativity in the inferior leads being an indication that atrial depolarization is moving away instead of toward the AV Node).

• PEARL #1: The finding of AV dissociation during a regular WCT rhythm is an important clue that a regular WCT rhythm is the result of VT (as was shown in ECG Blog #133). But the finding of consistent 1:1 VA (retrograde) conduction is not AV "dissociation" — because in this case, each QRS complex is related to each neighboring QRS complex (ie, by a constant RP' interval). Both VT and reentry SVT rhythms may manifest consistent 1:1 VA conduction — such that the finding of 1:1 VA conduction during a regular WCT rhythm is of no assistance for distinguishing between VT vs an SVT rhythm (See ECG Blog #240 — for full discussion of the role that consistent 1:1 retrograde atrial activity may play in sustaining the reentry SVT rhythms of AVRT and AVNRT).
• 
  
• PEARL #2: In Figure-3, we do not see consistent 1:1 VA conduction — because retrograde P waves are not seen after each QRS complex (ie, There is no retrograde P wave seen after the QRS of beats #6, 12, 18 and 21 in Figure-3).

Looking Closer at Today's Retrograde Activity ...

To better visualize the nature of retrograde atrial activity in today's tracing — I've magnified in Figure-4 an excerpt of of beats #5-thru-15 from Figure-3.

• Can you appreciate what's happening to the RP' interval following beats #7-thru-12?

Figure-4: I've magnified beats #5-thru-15 from Figure-3. What's happening to the RP' interval following beats #7-thru-12?

Laddergram Illustration:

My laddergram in Figure-5 schematically shows that the RP' interval is progressively increasing as we move from beat #7 to beat #11 (dotted RED lines after these beats) — until we see that there is no retrograde P wave after beat #12.

• Retrograde conduction resumes after the brief pause between beats #12-13 — albeit once again with a shorter retrograde RP' interval after beat #13.
• PEARL #3: With this laddergram in Figure-5 — the YELLOW arrows represent retrograde P waves. Although subtle, the RP' interval is increasing. This is most easily appreciated by looking at the RP' interval before the retrograde Wenckebach conduction is blocked (darker BLUE double arrows seen in the rhythm strip after beat #11). Note subtle increase in the AV Nodal Tier in the angle of retrograde P wave conduction, that becomes maximal just before the P wave is dropped (dotted BLUE line in the AV Nodal Tier). And then, following the brief pause between beats #12-13 — the Wenckebach cycle begins again with the RP' interval shortening after beat #13. 

Figure-5: Laddergram showing retrograde Wenckebach conduction for magnified beats #5-thru-15 from Figure-4.

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Significance of Intermittent Retrograde Conduction

In Figure-6 — I've drawn theoretical laddergrams to illustrate why the presence of intermittent retrograde conduction that does not disturb the regularity of a WCT rhythm is virtually diagnostic of VT (Roig et al — Circulation 153(15):1171-1173, 2026 — and — Pilecky et al — Eur Heart J 7:1-2, 2023).

• Panel A (Top laddergram in Figure-6) — A PAC (beat #3) is seen after 2 normal sinus beats. If the timing is "just right" — this PAC may initiate a reentry SVT rhythm (usually either AVNRT or AVRT). But because reentry SVT rhythms are dependent on continued retrograde conduction (dotted lines during the SVT run from beat #3-thru-11) — the reentry SVT will abruptly end if for any reason retrograde conduction fails (as it does here in this theoretical laddergram after beat #11).
• Panel B (Bottom laddergram in Figure-6) — Following 2 sinus beats, a run of VT begins with beat #3. I've drawn in some different possibilities for different VA conduction ratios. It should be apparent in Panel B that regardless if 1:1 VA conduction persists (as it does from beats #4-to-9) — or is intermittent with a 2:1 VA conduction ratio (as it is from beats #9-to-12) — or manifests retrograde Wenckebach conduction with progressive RP' prolongation until retrograde conduction fails (as occurs from beats #13-to-17) — the regularity of the VT rhythm is unaffected! This proves that ventricular activation is independent of atrial activity — thereby essentially confirming VT by eliminating the possibility of a reentry SVT that is dependent on persistence of retrograde conduction with a reentry circuit.

Figure-6: Theoretical laddergrams illustrating the expected effect of intermittent retrograde conduction on a reentry SVT vs the effect on VT.

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Final Thoughts on Today’s CASE:

Intermittent block of retrograde conduction during a regular WCT rhythm (be this by retrograde Wenckebach or other intermittent VA conduction phenomenon) — is not a common occurrence. This is an advanced concept that you will not often see. But it does occur (as in today's case) — and you can detect it if looked for.

• Going back to Figure-1 (and to Figure-3) — the fact that the WCT rhythm in today's case maintains a regular ventricular rate despite the failure to conduct retrograde with every beat essentially proves that this WCT rhythm is sustained VT (with the only rare exception being the possibility of a wide junctional tachycardia that conducts retrograde).

Clinically — this subtle informative clue of intermittent retrograde conduction during a regular WCT rhythm will usually not be needed to determine optimal initial management. 

• This is because IF your patient in a regular WCT rhythm without sinus P waves is hemodynamically unstable — then electrical cardioversion will be needed regardless of whether the rhythm is VT or an SVT.
• IF on the other hand, your patient in a regular WCT is stable — then a trial of medical therapy is reasonable. And, if you do recognize intermittent retrograde conduction despite maintenance of the regular WCT rhythm — then I'd skip a trial of Adenosine, because we would then know that the WCT rhythm is VT.

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Acknowledgment: My appreciation to Khaled Elashiq, Hasan Al-Qassim and Mahmoud Al-Rahmoun (from Syria) for contributing this case.

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