ECG Blog #470 — This ECG Tells a Story

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain) that began ~1 hour earlier.

QUESTION:

The title I chose for today’s Blog post is, “This ECG tells a story”.

• What is “the Story” that this initial ECG tells? 

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

MY Thoughts on Today’s CASE:

Unfortunately, there is no long lead rhythm strip in Figure-1. That said — there appears to be a regular, wide-QRS rhythm, at a rate of ~80/minute.

• There appear to be some P waves — but these do not seem to be related to neighboring QRS complexes, as the PR interval continually changes (RED arrows in Figure-2). This suggests there is AV dissociation — which if truly present, suggests a ventricular etiology for the wide-QRS rhythm. 

Figure-2: I've labeled readily visible P waves with RED arrows.

Support that the underlying rhythm in Figure-2 is ventricular — is forthcoming from assessment of QRS morphology (See Figure-3). The following morphologic features are not consistent with any known form of conduction defect:

• The fragmented but all negative QRS complex in lead I.
• The wide and deep Q waves that are seen in each of the 6 chest leads.
• Slow initial depolarization in each of the chest leads (ie, the downslope of virtually all Q waves and QS complexes is “slow” and gradual — whereas depolarization of the initial portion of the QRS tends to be faster with supraventricular rhythms that travel over the specialized conduction system). 
• The predominantly negative and fragmented QRS in lead V6 (The QRS complex in left-sided lead V6 will almost always have more positivity than seen here when the rhythm is supraventricular).
• 
  
• PEARL #1: More than simply suggesting a ventricular etiology for the rhythm in Figure-3 — the wide and deep Q waves (or QS complexes) in 8/12 leads (slanted blue lines) — especially given the fragmentation that we see in several leads (especially in I,V5,V6) — strongly suggests "scar" that most probably is due to prior infarction.

PEARL #2: Despite the challenge of assessing a ventricular rhythm for underlying ischemia and/or infarction — there are primary ST-T wave changes that are seen in Figure-3 that suggest an ongoing acute event.

• Most notable among these “primary” ST-T wave changes in ECG #1 — include coved ST elevation that begins in lead V2 — and continues across the precordial leads until lead V6. Of note — this coved ST elevation is greatest in lateral chest leads V5 and V6 (BLUE arrows in Figure-3).
• To Emphasize: The shape and amount of ST elevation in the chest leads is so pronounced — as to clearly indicate a recent (and potentially ongoing) acute event until proven otherwise.
• Abnormal ST elevation is also seen in the high-lateral limb leads ( = leads I and aVL) — which together with the abnormal (and very large) Q waves and QS complexes in 8/12 leads — suggests that the reason for this ventricular rhythm is a recent and/or ongoing extensive antero-lateral STEMI.

Figure-3: I’ve labeled the abnormal Q waves (and QS complexes) — and the leads showing abnormal ST elevation in this ventricular rhythm.

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The CASE Continues:

• Troponin was positive. This supports the suggestion of ongoing acute infarction.
• The long lead II rhythm strip shown in Figure-4 was obtained.

QUESTIONS:

• What is the rhythm in Figure-4?
• Are we seeing AIVR (Accelerated IdioVentricular Rhythm) — that often appears as a short-lived and usually benign ventricular rhythm that may signal reperfusion in a patient with acute infarction? (See ECG Blog #321 and ECG Blog #108 — for more on AIVR).

Figure-4: Long lead II rhythm seen in today's patient.

ANSWER:

Easy to overlook when assessing the rhythm strip in Figure-4 from today's case — is the finding that although the QRS complex in this long lead II rhythm strip is wide — QRS morphology is very different than the QRS morphology that was seen previously in lead II (Go back and compare the previously positive QRS morphology in lead II of Figure-3 — with the now predominantly negative QRS in Figure-4). 

• This change that we see in QRS morphology in lead II — suggests that the site of the ventricular rhythm we are now looking at in Figure-4, has changed from what it was previously. This can occur, and in today's case — was not felt to represent a change in the overall ongoing rhythm, since the changing relationship between P waves and neighboring QRS complexes over the course of the next few hours (and as it turned out, ensuing days) on telemetry monitoring remained the same.
• Throughout this time period — the patient remained hemodynamically stable and surprisingly without symptoms!
• The patient refused cardiac catheterization. Instead — he felt well, and ultimately decided to go home a few days later. The patient left before a final ECG could be done — so we do not know what the rhythm was at the time the patient left the hospital.

What Then is the Rhythm in Figure-4?

I find the easiest way to assess rhythms such as the one in Figure-4 — is by labeling P waves. Doing so facilitates assessment of the relationship (if any) of P waves with neighboring QRS complexes. I have labeled P waves in Figure-5.

• RED arrows in Figure-5 highlight those P waves that we can readily identify.
• PINK arrows highlight where my calipers suggest on-time P waves are probably hiding (with subtle peaking or "extra bulging" in a number of T waves, thus supporting my suspicion of on-time sinus P waves below these arrows).
• Note that the PR interval in front of the 13 QRS complexes in Figure-5 is constantly changing, Thus we have a fairly regular wide-QRS (ventricular) rhythm at ~80-85/minute — and an independent, fairly regular underlying sinus rhythm, but with no relationship between on-time sinus P waves and neighboring QRS complexes (ie, there is complete AV dissociation).
• Technically — the diagnosis of complete (3rd-degree) AV block is difficult to make in the absence of a ventricular escape rhythm below ~50-55/minute (because of the difficulty demonstrating at ventricular rates that are over 55-60/minute that all P waves have adequate opportunity to conduct — yet still fail to do so). That said — today's patient maintained this same rhythm over time — so this rhythm was thought to represent 3rd-Degree AV Block.
• PEARL #3: Another point in support of this rhythm being complete AV block — is that the atrial rhythm is faster than the ventricular rhythm. Under normal circumstances — this should enable the more rapidly occurring sinus P waves at some point to regain control of the rhythm IF there is not complete AV block. Instead, none of the sinus P waves are able to conduct to the ventricles.

Figure-5: I've labeled with colored arrows what appears to represent an underlying sinus rhythm for the tracing in Figure-4.

Laddergram of Figure-5:

As opposed to AIVR, in which there is an accelerated ventricular rhythm with either no P waves or with retrograde P waves — the rhythm in Figure-5 appears to be complete AV block. 

• I represent this in the laddergam shown in Figure-6. The Atrial Tier shows fairly regular sinus P waves (slight ventriculophasic sinus arrhythmia) — and a fairly regular accelerated ventricular "escape" rhythm — but without any of the on-time sinus P waves being able to conduct to the ventricles as a result of complete AV block (double dotted lines in the AV Nodal Tier depicting the barrier preventing conduction of any sinus impulses to the ventricles).

Figure-6: Complete AV dissociation. The double dotted line suggests this is the result of complete AV block.

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CASE Conclusion: The Story Told in Today's Case ...

Putting the "story" together in today's case:

• In Figure-7 — are 2 additional 12-lead ECGs that were obtained during the course of this patient's hospitalization. Although difficult to assess the rhythm in these 2 tracings without the benefit of any accompanying long lead rhythm strips — intermittent P waves with variable PR intervals appear to be present in both tracings, suggesting persistence of the same rhythm that we saw in Figure-6.
• If we review the serial ECGs in today's case (that I've put together in Figure-7) — there is clear evolution of an extensive antero-lateral STEMI (ie, increased ST elevation, especially in leads V4,V5,V6 in ECG #2 — followed by a fall in ST elevation with more pronounced T wave inversion, especially in the inferior leads of ECG #3). 
• PEARL #4: Today's case therefore provides an excellent example of how serial ST-T wave morphology changes in ventricular beats may at times provide insight to the evolutionary changes of acute infarction. The reduction in ST elevation with deepening T wave inversion in ECG #3 suggests there has been some amount of reperfusion.

PEARL #5: Distinction between infarction-related AIVR (which is usually a transient and benign ventricular rhythm that often occurs in association with acute MI) — vs — development of complete AV block (as occurred in today's case) — has important clinical implications:

• In most instances — No treatment is needed for AIVR.
• In contrast — emergency (and/or longterm) pacing may be needed when complete AV block is the result of acute infarction. This is especially true when AV block arises as the result of an extensive anterior STEMI, as in today's case (as opposed to AV block that occurs in association with acute inferior MI, which is much more likely to be transient — and much less likely to need pacing).

Optimal Management of today's CASE — would therefore include prompt cardiac catheterization with PCI as the best chance for resolving the 3rd-degree block. 

• If 3rd-degree AV block persists despite PCI (especially if associated with hemodynamic instability) — then emergency pacing will be needed, at least temporarily (ie, Guidelines suggest not to implant a permanent pacemaker for at least a few days following PCI — in the event of spontaneous recovery of AV conduction).
• 
  
• The above said — Today's patient had other ideas. He remained remarkably stable despite the above conduction disorder. He ultimately decided to leave the hospital at some point after ECG #3, after which he was lost to follow-up.
• What then is "the Story?" — The "story" that I quickly derived on seeing today's initial ECG — is that the regular wide-QRS rhythm in Figure-1, with apparent AV dissociation — represents complete AV block, most likely resulting from recent (and/or ongoing) extensive antero-lateral STEMI.

Figure-7: Serial ECGs in today's case. 

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Potential Final Outcomes: Today's patient amazingly became asymptomatic after a day or so in the hospital. He refused cardiac cath and PCI — and — since he was feeling well, decided to go home.

• It's obvious from the serial ECGs shown in Figure-7 — that significant myocardium was lost from extensive infarction. That said, despite complete AV block — the normal ventricular rate (of ~80/minute) provided by this patient's accelerated ventricular "escape" rhythm was apparently maintaining sufficient cardiac output to render him "asymptomatic".
• In the Best Case Scenario — this patient's 3rd-degree AV block will spontaneously resolve. In this case, despite significant functional loss from his extensive infarction — he may be able to continue sufficient daily activity acceptable for his lifestyle. We wish for this best case scenario outcome!
• In a Less Optimal Case Scenario — this patient's 3rd-degree AV block might not only become permanent, but the ventricular "escape" rhythm will probably slow down at some point to the the usual 20-40/minute idioventricular escape rate. In this less optimal case scenario — the patient will hopefully remain alive long enough to return for permanent pacing.

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Acknowledgment: My appreciation to Fardeen Baray a (from Kabul, Afghanistan) for the case and this tracing.

• Special THANKS to Dr. Willy Frick — for his Cardiology insights on this case.

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For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-8: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

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• For more on AIVR — See ECG Blog #108 — and ECG Blog #321 —

ECG Blog #469 — Epigastric Pain with Dinner

The ECG in Figure-1 was obtained from a middle-aged woman — who presented to the ED (Emergency Department) for epigastric pain that had begun ~1 hour earlier.

• The epigastric pain began during dinner. She was diagnosed in the ED as having gastritis.
• The 1st Troponin was not elevated. 

QUESTIONS:

• How would you interpret the initial ECG in Figure-1?
•    Does the negative initial Troponin rule out an acute event?

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

ANSWERS:

• A negative initial Troponin value does not rule out an acute cardiac event. This is true even if a "hs" ( = high sensitivity) Troponin assay is used.
• Instances in which an initial Troponin value may be negative despite an acute, ongoing infarction — include IF the period of coronary occlusion is short (ie, because there has been spontaneous reperfusion of the "culprit" artery).
• 
  
• The ECG in Figure-1 is not normal. Rather than gastritis — this initial ECG suggests an acute OMI (Occlusion-based MI) in progress.

QUESTION:

• Did you pick up all of the findings highlighted in Figure-2?

Figure-2: I've labeled abnormal findings on the initial ECG. How many of these findings did you identify?

My Interpretation of the ECG in Figure-2:

The rhythm in Figure-2 is sinus, perhaps with some sinus arrhythmia given variability of the R-R interval in the chest leads. Intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q waves — Narrow Q waves of uncertain significance are seen in each of the inferior leads. Tiny (probably septal) q waves are seen in lateral chest leads V5,V6.
• R Wave Progression — shows a somewhat abrupt, early increase in R wave amplitude between leads V1-to-V2 — although transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V3-to-V4.

Assessment of ST-T Wave Appearance:

• Considering the history of new epigastric pain (which can sometimes be a chest pain equivalent) — My “eye” was immediately drawn to the 3 inferior leads (within the RED rectangles in Figure-2).
• Each of the inferior leads show slight-but-real J-point ST elevation — with straightening of the ST segment takeoff — and — a wider-than-expected T wave base. In this patient with new symptoms — these ST-T wave changes have the look of hyperacute ST-T waves.
• Strong support that these inferior lead changes are “real” and indicative of inferior OMI — is provided by the reciprocal ST-T wave depression in lead aVL, with a biphasic terminal T wave (BLUE arrow within the BLUE rectangle in Figure-2).

KEY Point: Given how common it is for inferior OMI to be associated with posterior lead involvement — extra attention is focused on leads V2,V3,V4, looking for abnormal ST depression.

• Normally — there should be slight, gently upsloping ST elevation in leads V2 and V3. This is absent in leads V2 and V3 in Figure-2 — in which this normal, upsloping ST elevation has been replaced by ST segment flattening (with a hint of J-point depression in lead V2).
• Lead V4 serves as a "transition" lead — showing nonspecific ST-T wave flattening. This is followed in lead V5 by ST segment straightening, with a hint of ST elevation and a hint of terminal T wave inversion.
• There is too much artifact in lead V6 to tell much.

Impression of ECG #1:

I interpreted this initial ECG in Figure-2, as highly suggestive of acute infero-postero-lateral OMI until proven otherwise.

• If providers were to have any doubt about the diagnosis — the ECG should be repeated within 15-to-20 minutes (or even sooner if there is a change in symptom severity).
• Additional Troponins should be drawn (sometimes it takes 2 or 3 samples with acute OMI until Troponin levels rise).
• Stat Echo at the bedside may be helpful if it reveals a localized wall motion abnormality (Remembering that a normal Echo is only helpful for making OMI less likely if obtained during symptoms).

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The CASE Continues:

• A 2nd Troponin assay was also negative.
• The patient's epigastric pain continued.
• The ECG was repeated ~2 hours after the initial tracing.

To facilitate comparison in Figure-3 — I've put both ECGs together.

• QUESTION: Has there been any change?

Figure-3: Comparison between the initial ECG — and the repeat ECG that was done ~2 hours later. The patient continued to have epigastric pain.

KEY Point: Comparison between serial ECGs is best accomplished by putting both tracings together and looking at them lead-by-lead (as is easily done in Figure-3).

• I did not see any significant change in the limb leads.
• In the chest leads — the ST segment straightening in lead V2 now clearly shows ST depression in ECG #2.
• Leads V3 and V4 now show a hint of shallow T wave inversion.
• Lead V5 continues to show ST segment coving with slight ST elevation.
• The artifact that was seen in lead V6 of ECG #1 has disappeared. This now allows us in ECG #2 to appreciate comparable ST segment coving, if not slightly more ST elevation in lead V6 compared to lead V5.

Impression of ECG #2:

The patient continues to have epigastric pain — which given the findings in these 2 serial ECGs, is clearly a CP (Chest Pain) "equivalent" symptom.

• I interpreted the comparison between ECGs #1 and #2 as confirmation of ongoing acute evolutionary changes of infero-postero-lateral OMI.

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The CASE Continues:

• A 3rd Troponin was positive.
• The patient's epigastric pain decreased.
• A 3rd ECG was done (recorded ~2 hours after ECG #2).

To facilitate comparison in Figure-4 — I've put the 2nd and 3rd ECGs next to each other.

• QUESTION: Considering that ECG #3 was done ~2 hours after ECG #2 (and that the patient's epigastric pain is now less) — How would you interpret this 3rd ECG? 

Figure-4: Comparison between the ECG #2 — and ECG #3 that was recorded ~2 hours later. The patient's epigastric pain had decreased at the time ECG #3 was done.

ANSWER: 

There are subtle-but-real changes between ECG #3 and ECG #4:

• The limb leads in ECG #3 — all show nonspecific ST-T wave flattening. Complared to ECG #2 — this represents a reduction in the hyperacute changes in virtually all limb leads.
• In the chest leads — the ST depression in lead V2 from ECG #2 has resolved. The hyperacute ST-T waves in leads V5,V6 are much improved, now without any ST elevation. Shallow T wave inversion is seen in leads V3-thru-V6. 
• Impression: Especially given the reduction in epigastric pain — there has been significant improvement in the acute ST-T wave changes seen earlier, with T wave inversion in leads V3-thru-V6 representing reperfusion T waves.
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• Cardiac Cath was performed — which confirmed LCx (Left Circumflex) occlusion, with involvement of 2 obtuse marginal branches. The patient was stented. 

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Acknowledgment: My appreciation to Tayfun Anil Demir and Emine Karakaya (from Antalya, Turkey) for the case and this tracing.

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For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

 

ECG Blog #468 — Aberrant or VT?

I was sent the ECG in Figure-1 — without the benefit of any clinical information.

QUESTIONS:

• What is the rhythm?
•      — How certain are you of your answer?

Figure-1: The ECG I was sent ... (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Making the Diagnosis:

Rather than a "Yes-No" answer (ie, Rather than saying the rhythm is VT vs SVT) — it is preferable to simply describe what you see.

• PEARL #1: There is a tendency for many providers to think only about 2 possible answers for the first question that I ask above — that is: i) That the rhythm is either VT (Ventricular Tachycardia); — or — ii) That the rhythm is an SVT (SupraVentricular Tachycardia) with aberrant conduction.
• This thinking is erroneous — because rather than the rhythm being either VT or an SVT with aberrant conduction, I think of a 3rd (very common) possibility, namely: iii) That the answer is a probability statement, in that we realize we can not be 100% certain what the etiology of the rhythm is, based on the single ECG that we have in front of us. In this case, depending on a series of factors (ie, the clinical history — frontal plane axis — QRS morphology, etc.) — we may only 30-to-50% confident, or perhaps 80-to-90% (but not 100%) confident of our diagnosis.
• PEARL #2: Thinking about our answer in terms of a probability statement is important for optimal treatment — since the clinical reality is that much of the time, we need to begin our treatment before we are 100% certain of the rhythm diagnosis. Awareness of our relative certainty about whether we are dealing with ischemic or idiopathic VT vs some form of SVT vs a WPW-related tachycardia — can guide us for deciding when to try vagal maneuvers, electrical cardioversion, or some form of medical therapy (ie, Adenosine, Amiodarone, Verapamil, ß-Blocker, or other).
• PEARL #3: As a result of the above 2 Pearls — rather than saying, "VT" or "SVT with aberrancy" — it is BEST to simply describe what you see. For example, in Figure-1 — the rhyhm is a regular WCT (Wide-Complex Tachycardia) at ~160/minute, without clear sign of atrial activity.

PEARL #4: I provide numerous links in the references below illustrating my approach to a series of WCT rhythms. That said — it is well to remember the literature-based Statistics, which suggest that even before you look at the ECG — about 80% of regular WCT rhythms without clear sign of atrial activity will turn out to be VT.

• This figure goes up to ~90% if the patient is an adult of a certain age (say, over 50-60 years old) — and if the patient has some form of underlying heart disease.
• Assessment of the frontal plane axis and QRS morphology can help in selected cases to further increase your probability estimate of the likely diagnosis (See my ADDENDUM below for my "user-friendly" approach to WCT diagnosis).

PEARL #5: Many providers limit their considerations to a differential between VT vs SVT with aberrancy. But as I show below in Figure-2 in my ADDENDUM — rather than aberrant conduction, the QRS complex may be wide in a supraventricular rhythm due to: i) Preexisting bundle branch block; — or, ii) Something else! (ie, a WPW-related tachyarrhythmia, hyperkalemia, some other toxicity).

PEARL #6: There are 2 insensitive (ie, uncommonly found) findings that I always look for when assessing WCT rhythms — because IF seen — you can approach 99% likelihood that the rhythm is VT:

• Finding #1: Is there AV Dissociation during the WCT rhythm? IF so — this is virtually diagnostic of VT. That said — most of the time, AV dissociation will not be seen unless the rate of VT is relatively slow. Therefore — the absence of AV dissociation is nondiagnostic. However, its presence may be confirmatory.
• NOTE: Many providers "think" they are seeing AV dissociation when in fact it is not present. Unless you can walk out regular underlying P waves through much (most) of the tracing — it is unlikely that AV dissociation is present (See ECG Blog #133 — and — ECG Blog #151 for examples of AV dissociation with VT).
• 
  
• Finding #2: Is there Concordance of the QRS in all chest leads? IF ever all QRS complexes in leads V1-thru-V6 are either all positive or all negative (ie, if there is "global positivity" or "global negativity" ) — this is virtually diagnostic of VT. That said — since the sensitivity of this finding is so low (probably less than 10% of cases) — the lack of chest lead concordance is not helpful.

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Back to Today's CASE:

As stated earlier — the rhythm in Figure-1 (that I reproduce again below) — is a regular WCT at ~160/minute without clear sign of P waves.

Figure-1: The ECG I was sent. No history.

MY Approach to Figure-1:

We do not have the benefit of any history in today's rhythm — so we do not know the age of this patient, nor whether there is any underlying heart disease. That said, by PEARL #4 — Statistical likelihood that the regular WCT in Figure-1 is VT is ~80% even before we look closer at the ECG.

• By the 3 Simple Rules (shown in Figure-3 in the Addendum below) — there is an "extreme" frontal plane axis, because the QRS is all negative in each of the inferior leads. This finding significantly increases statistical likelihood of VT!
• Also by the 3 Simple Rules — the wide QRS does not look like any known form of bundle branch block (ie, QRS morphology could be consistent with LBBB in the limb leads — but the all positive QRS in lead V1 looks more like RBBB, albeit none of the lateral leads have wide terminal S waves). Not resembling any known conduction defect makes VT more likely.
• Looking for AV dissociation — Although there are some intermittent undulations in the baseline, I do not see a regular underlying atrial rhythm. There is no sign of AV dissociation (but we know that most of the time with a faster VT — we will not see AV dissociation — so not seeing it here does not alter our prediction of the rhythm).
• PEARL #7: But there is global positivity (ie, QRS Concordance) in all 6 chest leads! Although the QRS in lead V6 is tiny — it is all positive! All other chest leads are decisively positive.

BOTTOM Line: Even without knowing the patient's age or the history in today's case — I'd estimate ~99% likelihood that the regular WCT rhythm in Figure-1 is VT because: i) There is an "extreme" frontal plane axis; ii) QRS morphology does not resemble any known form of conduction defect; — and, especially iii) Today's rhythm is one of the rare cases in which we do see QRS concordance (global positivity) in all 6 chest leads!

• About the only exception for which an SVT rhythm might produce the unusual QRS morphology that we see here in Figure-1 — would be in a patient with severe underlying heart disease, who during sinus rhythm has an identical QRS morphology as we see in Figure-1 as a result of previous infarction(s) and unusual conduction defects.
• 
  
• To Emphasize: My above discussion is in "slow motion". It literally took me no more than seconds to look at today's rhythm and know there was a 99+% likelihood that this was VT.
• 
  
• CASE Follow-Up: The patient was treated and converted to sinus rhythm. Today's rhythm was proven to be VT.

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Acknowledgment: My appreciation to Adem Ahmed (from Nouakchott, Mauritania) for the case and this tracing. 

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
• 
  
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT.
• ECG Blog #263 and Blog #283 — Blog #361 — Blog #384 — and Blog #460 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
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• ECG Blog #211 — WHY does Aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 and Blog #361 — Another regular WCT rhythm ...
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• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
• 
  
• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

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ADDENDUM (2/8/2025):

• I've reproduced below from ECG Blog #361 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

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

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).

• CLICK HERE — to download a PDF of this 6-page file on Aberrant Conduction.