Regular Wide Complex Tachycardia. What to do?

A patient in the ICU with significant underlying cardiac disease [HFrEF 30%, non-ischemic cardiomyopathy, LBBB s/p CRT-D (biventricular pacer), AVNRT s/p ablation a few yrs ago, hx sinus tachycardia while on max tolerated BB therapy] went into a regular wide-complex tachycardia after intubation for severe COPD exacerbation. 

Here is the ECG:

Regular Wide Complex Tachycardia at a rate of 166 bpm.  

What do you think?

If the patient is unstable, he should be immediately electrically cardioverted.  Even if he is stable, that is the best course of action.

The majority of regular wide complex tachycardia are due to ventricular tachycardia (VT), and if the patient has a h/o HFrEF with cardiomyopathy, the VAST MAJORITY are VT.

When I first posted this, I thought the initial part of the QRS was wider, and favored AVRT or VT. 

But after receiving a few comments, I looked more closely and magnified it, and measured  the QRS onset (the initial deflection, the first part) of the QRS at about 80 ms.  

This is best seen in V1-V3, where the initial r-wave is very narrow and the rS is about 80 ms.

So this is likely SVT with LBBB.

What is the differential?

1. If it were wider, then VT and antidromic AV reciprocating tachycardia (AVRT) would be likely.  AVRT is due to accessory pathway with the impulse going down the bypass tract and up the AV node.  This results in what is, in effect, a ventricular origin since the ventricle is pre-excited by the accessory pathway.

2. Pacemaker mediated tachycardia (also called endless loop tachycardia).  This is not such a case, as there are no pacer spikes.

What to do?

Electrically cardiovert is always an option.  Adenosine is easiest.  With wide complex and known poor LV function, I would avoid a calcium channel blocker.

The patient was electrically cardioverted several times with 200J without any change!!

So they gave adenosine and the patient cardioverted.

Here is the post cardioversion ECG:

Now there is a ventricular paced rhythm at a rate of 120.

The ventricular pacing makes it impossible to know if there would be delta waves, so we don't know if this was orthodromic AVRT or AVNRT.

It appears that there are P-waves which are triggering the Ventricular pacing, so this post conversion ECG is most likely sinus tach with ventricular paced rhythm. 

Adenosine is safe in regular wide complex tachycardia.  It will not harm VT.  It will likely convert AVRT.  It is absolutely contraindicated in atrial fib with WPW.  

Some say you should not use it is AVRT because the patient might convert to atrial fibrillation.  This seems extremely unlikely to occur during the 10 seconds that adenosine is active.  

See Ken's comment below: most AVRT is orthodromic and is identical in appearance to AVNRT.  You don't have any hesitation to give these patients adenosine, correct?  And yet they have the same probability of converting to atrial fibrillation.  Thus, the argument against using adenosine in antidromic AVRT is fallacious.

Therefore, I use adenosine in regular wide complex tachycardia.

Follow up:

The patient signed out AMA before he could get his pacer interrogated.  We will never know for certain.

Here is a case of antidromic AVRT:

A 30-something with palpitations and lightheadedness

Here is another very complex case of antidromic AVRT:

Young Man with Very Fast Regular Wide Complex Tachycardia

Adenosine will also convert Right Ventricular Outflow Tract Ventricular Tachycardia:

Toothache, incidental Wide Complex Tachycardia

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MY Comment, by KEN GRAUER, MD (6/21/2024):

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Optimal time-efficient management of a regular WCT (Wide-Complex Tachycardia) — is among the most challenging of situations encountered by emergency providers. Seconds count — with the initial KEY decision being "electricity" vs a trial medication deemed most-likely-to-work by the provider at the scene.

• As per Dr. Smith — today's initial tracing shows a regular WCT rhythm at ~170/minute without clear sign of sinus P waves.
• 
  
• Even before looking at this initial ECG — statistical odds in an unselected adult population that this rhythm will turn out to be VT are at least 80%. 
• Given this patient's history of significant underyling heart disease — these odds (even before looking at this ECG) approach at least 90% that this rhythm will turn out to be VT.
• 
  
• Potentially — We can refine our "likely probability" that a regular WCT rhythm is or is not VT after we look at the ECG, with attention to QRS morphology during the WCT (ie, Does QRS morphology resemble any known form of conduction defect — in which case an SVT rhythm becomes at least slightly more likely) — and by comparing QRS morphology during the WCT with prior baseline ECGs on the patient during sinus rhythm (ie, To see if an unusual QRS morphology during the WCT might be identical to the unusual QRS morphology of the patient during sinus rhythm, thereby confirming a supraventricular etiology).
• 
  
• Clinical Reality: In an acute patient in a regular WCT rhythm — it will be rare indeed that we have access at the time to a prior ECG. Instead — we almost always need quickly begin treatment!

Regarding Today's Case:

Dr. Smith's approach that is (that is succinctly detailed above) — conveys the ideal approach to today's case (NOTE: We have presented numerous decision-making cases regarding WCT rhythms on Dr. Smith's Blog. Among others — "My Take" is reviewed in the May 5, 2020 post).

• As per Dr. Smith — VT needs to be assumed as the etiology of todays' initial ECG until proven otherwise. The safest treatment is clearly immediate electrical cardioversion.
• It turns out that today's patient was cardioverted "several times with 200J without any change". At this point Adenosine was given — and the patient converted (with what appears to be sinus P waves, immediately followed by ventricular pacing — as shown above at ~120/minute).

MY Thoughts on Today's CASE:

The "good news" — is that the patient was successfully treated, with return to a paced rhythm. In the interest of providing some additional thoughts — I'll offer the following:

• Electrical cardioversion is almost always successful in converting regular tachycardias to sinus rhythm — at least immediately after the electrical discharge is released. What sometimes (often) happens — is within seconds of this electrical discharge, the WCT rhythm returns. This is especially common following administration of Adenosine for a reentry SVT rhythm, since the half-life of Adenosine is measured in seconds.
• KEY Point: Always record the initial short-term period during and after interventions such as cardioversion and Adenosine administration. Things happen quickly! It is extremely difficult to know if your intervention was initially successful — but that the WCT then quickly returned unless you have hard copy of the rhythm during and immediately after the cardioversion or Adenosine administration. 
• Clinically — a hard copy recording during this period is important — because the ANSWER as to what the etiology of the WCT rhythm was will often be revealed during those initial seconds after cardioversion (or Adenosine) — and your subsequent treatment may vary depending on whether your intervention did not work at all — or — was effective for a few seconds, before recurrence of the WCT. Unless you have hard copy to show — We can not know if those "several times" that today's patient was cardioverted worked for a few seconds, or did not work at all.
• 
  
• Returning to "probability assessment" of today's WCT rhythm — QRS morphology of today's initial ECG looks very much like LBBB conduction (ie, all upright in left-sided lead V6 — and predominantly negative in the first 4 chest leads). Admittedly — the rsR' in lead I, with predominantly negative QRS in lead aVL is not typical of LBBB conduction — although in a patient with severe underlying heart disease, LBBB conduction will often look different than the "textbook" picture — so I thought QRS morphology was not helpful in my assessment of today's WCT rhythm.
• 
  
• BUT — I did think that there probably was retrograde atrial activity in today's initial ECG (RED arrows in Figure-1). While fully acknowledging that I could not be 100% certain — I thought that small-but-consistent pointed deflections (negative in leads II and aVF — and positive in leads aVR and V1) — were likely to represent retrograde P waves with a relatively longer RP' interval. IF I was correct in this interpretation — then the rhythm was likely to be antidromic AVRT (which I believe is supported by the fact that the sinus P waves seen just before pacer spikes in the post-conversion tracing are indeed pointed).
• 
  
• Final POINT: I completely support Dr. Smith's approach of using Adenosine to treat AVRT. In fact — this is done all the time, despite most providers being unaware they are doing so! I say this — because a significant percentage of patients with reentry SVTs thought to be "AVNRT" actually have "concealed conduction" over an AP (Accessory Pathway) that can only conduct retrograde. As such — these narrow QRS reentry SVT rhythms are in fact orthodromic AVRT with the reentry circuit including passage outside of the AV node over an AP. And, adverse effects are so rarely encounted from Adenosine administered countless times to these unsuspected orthodromic AVRT rhythms with "concealed" conduction over an AP. BOTTOM Line: As per Dr. Smith — Adenosine almost always works to safely convert orthodromic AVRT.
• 
  
• P.S.: To confirm whether my supposition of retrograde P waves with a long RP' interval was correct — We'd need to see a repeat ECG in sinus rhythm with WPW conduction, perhaps showing a similar LBBB conduction pattern but without those notches that I highlight with RED arrows in Figure-1. Since today's patient signed out AMA — We'll never know. 
• P.P.S.: Alternatively (given what I think are retrograde P waves with a longer RP' interval) — this still could be orthodromic AVRT in which either the RBB (Right Bundle Branch) was participating in association with an AP to form a reentry circuit with lbbb-like conduction — or — the LBBB conduction was simply a rate-related aberrancy result due to the rapid rate during the wide SVT rhythm.
• 
  
• NOTE: I review clinical utility of assessment of the retrograde RP' interval in My Comment at the bottom of the page in the October 25, 2022 post of Dr. Smith's ECG Blog.

Figure-1: I’ve labeled the initial ECG in today's case.

A young lady with wide complex tachycardia. My first time actually making this diagnosis de novo in real life in the ED!

 Written by Pendell Meyers

A woman in her 30s with minimal past medical history presented simply stating she was "feeling unwell." Her symptoms started suddenly about 48 hours ago, but had continued to worsen, including epigastric discomfort, nausea, cough, and dyspnea and lightheadedness on exertion. She denied chest pain and denied feeling any palpitations, even during her triage ECG:

What do you think?

Despite otherwise normal vital signs, she was appropriately triaged to the critical care area of the ED.

She was awake, alert, well perfused, with normal mental status and overall unremarkable physical exam except for a regular tachycardia, possible rales at both bases, some mild RUQ abdominal tenderness. My bedside ultrasound was of insufficient quality, but showed somewhat reduced overall EF, distended IVC without respiratory variation, no pericardial effusion, and diffuse bilateral B lines.

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

What do you think of her ECG?

There is clearly a wide complex tachcyardia (although the QRS duration is not far above 120msec). There is some movement artifact here and there, so the next determination of whether it is regular or irregularly irregular is slightly complicated, but I believe movement artifact is the only reason this rhythm is not regular. At beside, looking at the monitor during periods without movement artifact, this rhythm seemed perfectly regular and monomorphic. 

Thus, I believe it is a regular, monomorphic, wide complex tachycardia. The differential thus includes classic VT, idiopathic VT, and ST/SVT/Flutter + aberrancy. 

In general, most rhythms in this category will turn out to be (classic) VT. With increasing age, comorbidities, cardiac history, QRS duration, and sickness, the chances of VT increase further among this differential. 

But this was a young lady with no history, who has seemingly been in VT for at least 48 hours, with otherwise normal vitals and no signs of distress, with not-terribly-wide QRS complex, 

AND:

The QRS complex morphology has LBBB + inferior axis. This particular QRS complex morphology may be consistent with Right Ventricular Outflow Tract Ventricular Tachycardia (RVOT VT), which involves underlying RV dysplasia. 

Or it could simply still be classic VT. Or still could be ST/SVT/Flutter with aberrancy.

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Typically, my most common approaches to likely VT would be sedation and elective cardioversion, or amiodarone/procainamide.

But I remembered / recognized this pattern from this review of idiopathic VT I wrote years ago. I wondered if this might be RVOT VT.

RVOT VT is reported to be sometimes responsive to adenosine. It was a young person who was very stable. Adenosine does not cause harm in classic VT.

So we gave 12 mg adenosine rapid IV push.

Nothing happened, no break in the rhythm, no effect, no change in heart rate, nothing.

So we proceeded with etomidate sedation and synchronized cardioversion, with successful cardioversion on first attempt. 

Here is her 12 lead after cardioversion:

What do you think of this one?

I thought to myself: No way! Is this the day I actually found epsilon waves for the first time as a new diagnosis? It is so rare, that I was still unsure.

There is sinus rhythm with an initially normal QRS complex, but there is a very unusual looking wave at the end of the QRS complex, seen in basically all leads. It is especially unusual looking in leads V2 and V3, where it is clear that this is not a routine J wave, or incomplete RBBB.

When I teach important syncope ECG patterns to my residents, I have always had to find case reports and review articles to show them the rare epsilon waves in the past. They are rare and hard to find in normal practice in the ED.

She woke up uneventfully from her sedation and seemed to feel slightly better. Her labs were remarkable for slight transaminitis without hyperbilirubinemia, elevated BNP (1,226 mg/dL), and elevated troponin (73 ng/L), all of which seemed reasonably attributable to the possible 48 hours of ventricular tachycardia, congestive hepatopathy, etc. CXR confirmed bilateral pulmonary edema and bilateral small effusions.

I admitted her to cardiology with these concerns, and we agreed that cardiac MRI may help us confirm possible ARVC.

A small sample of MRI images are shown below, and the formal read included:

LVEF 44%, normal LV cavity size. LV systolic function is regionally impaired with wall thinning and akinesis of the mid inferior wall, mid inferoseptum and mid inferolateral wall. The basal anterior wall and basal septum are hypokinetic. 

RVEF 34%, RV is mildly enlarged. RV systolic function is severely decreased globally. There is focal dyskinesis of the RVOT region. There is mild-moderate tricuspid valve regurgitation.

Late Gadolinium enhancement: Multifocal scarring of the septum (including RV septum), basal anterior wall and transmural mid inferior region scarring - a non-CAD hyperenhacement pattern.

Overall CMR findings are consistent with arrhythmogenic cardiomyopathy. Two major CMR task force criteria for ARVC are present: 1. RVEF <40% with RV regional wall motion abnormality. 2. RV cavity dilation with RVEDVI>100 ml/m2.

She was formally diagnosed with ARVC. She received an AICD. She was given some intense exercise restrictions and offered genetic testing.

Long-term follow up is unavailable.

See similar or relevant cases here:

Regular Wide Complex Tachycardia. What is the Diagnosis?

Syncope in a young man

Young man with syncope while riding a bike [Arrhythmogenic Right Ventricular Dysplasia (ARVD)]

See my review of idiopathic VTs here:

Idiopathic Ventricular Tachycardias for the EM Physician

See our brief review of ARVD here:

ARVD Review below, reproduced from this post: 

Young man with syncope while riding a bike [Arrhythmogenic Right Ventricular Dysplasia (ARVD)]

ARVD, also known as arrhythmogenic RV cardiomyopathy, is estimated to have a prevalence of 1 in 5000 adults and is responsible for approximately 11% of sudden death in young adults and 22% in a study of athletes in northern Italy.  The diagnosis is not easy (see below).

Here is a 2017 review article on ARVD in the New England Journal

  

There is a 2010 publication by the Task Force in Diagnosis of ARVD: Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. 

Free full text: https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.108.840827 

There are 6 categories of criteria: 

1) Imaging

2) Pathologic

3) ECG Repolarization

4) ECG Depolarization

5) Arrhythmias

6) Family History.  

ECG and historical Highlights of this publication are (Suspect ARVD with):

1) High risk syncope with no other etiology; Family History

2) Depolarization abnormalities (Major criteria):

        a) Epsilon Waves

        b) Localized prolongation (greater than 110 ms) of the QRS complex in right precordial leads (V1-V3)

3) Repolarization abnormalities in patients of age at least 14 years (because younger patients often have juvenile T-waves)

        a) Minor: Inverted T-waves in right precordial leads V1-V2 

        b) Major: Inverted T-waves in right precordial leads V1-V3 or beyond (major criteria) 

4) Arrhythmias

        a) Major criterion:

                i) VT of LBBB morphology with superior axis (negative or indeterminate QRS in leads II, III, aVF and positive in lead aVL) (major criteria)

        b) Minor criteria:

                i) VT of LBBB morphology with inferior axis (positive QRS in leads II, III, aVF and negative in lead aVL) (minor criteria)

                ii) More than 500 PVCs per hour

5) Finally, it is a progressive disease and patients without ECG abnormalities may develop them over time.

Here is an example of an epsilon wave (image C).  And another example.  Here are some great examples from the post on RV dysplasia (translated by Google translate!) on Pierre Taboulet's great French site:  #1, #2, #3

Here's a great example on Wave Maven.

Here is an explanation of the importance of leads V1 and V2.

Here is another nice example. 

Some excellent references on ARVD:

This is a case report with lots of good info, from 2019, but you can only read it if you have a subscription to American J Cardiol:

Holshouser JW and Littmann L.  Usefulness of the Electrocardiogram in Establishing the Diagnosis and Prognosis of Arrhythmogenic Right Ventricular Cardiomyopathy

Other References, from the above article:

1

FI MarcusEpsilon waves aid in the prognosis and risk stratification of patients with ARVC/D

J Cardiovasc Electrophysiol, 26 (2015), pp. 1211-1212

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2

FI Marcus, W ZarebaThe electrocardiogram in right ventricular cardiomyopathy/dysplasia. How can the electrocardiogram assist in understanding the pathologic and functional changes of the heart in this disease?

J Electrocardiol, 42 (2009), pp. 136.e1-136.e5

Article

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3

RNW Hauer, MGPJ Cox, JA GroenewegImpact of new electrocardiographic criteria in arrhythmogenic cardiomyopathy

Front Physiol, 3 (2012), p. 352

eCollection 2012

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FI Marcus, WJ McKenna, D Sherrill, C Basso, B Bauce, DA Bluemke, H Calkins, D Corrado, MG Cox, JP Daubert, G Fontaine, K Gear, R Hauer, A Nava, MH Picard, N Protonotarios, JE Saffitz, DM Sanborn, JS Steinberg, H Tandri, G Thiene, JA Towbin, A Tsatsopoulou, T Wichter, W ZarebaDiagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria

Circulation, 121 (2010), pp. 1533-1541

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WC Roberts, N Kondapalli, SA HallUsefulness of total 12-lead QRS voltage for the diagnosis of arrhythmogenic right ventricular cardiomyopathy in patients with heart failure severe enough to warrant orthotopic heart transplantation and morphologic illustration of its cardiac diversity

Am J Cardiol, 122 (2018), pp. 1051-1061

Article

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6

JE Madias, R Bazaz, H Agarwal, M Win, L MedepalliAnasarca-mediated attenuation of the amplitude of electrocardiogram complexes: a description of a heretofore unrecognized phenomenon

J Am Coll Cardiol, 38 (2011), pp. 756-764

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MY Comment, by KEN GRAUER, MD (6/3/2023):

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Today's case is gratifying — in that it illustrates an uncommon phenomenon that Dr. Meyers picked up with potential life-saving implications. As per Dr. Meyers — I had not previously seen epsilon waves as a new diagnosis! I focus my comments on some other aspects of ARVC/D (Arrhythmogenic Right Ventricular Cardiomyopathy-Dysplasia) in the hope of adding to Dr. Meyers' excellent discussion.

• For clarity in Figure-1 — I've reproduced the 2 ECGs in today's case.

Figure-1: The 2 ECGs in today's case. Vertical BLUE lines mark timing of epsilon waves in all leads (with respect to the BLUE arrow marking the epsilon wave in lead V3).

The History in Today's Case:

Today's patient was a previously healthy young adult (ie, a woman in her 30s) — apparently presenting for the 1st time to medical attention for an arrhythmia episode related to her condition. 

• Of Note: This patient was hemodynamically stable without palpitations at the time ECG #1 was recorded. Given that her symptoms of "feeling unwell" had begun 48 hours earlier — it is likely that she was in this arrhythmia for a considerable period of time before coming to the ED (and that perhaps she had previous arrhythmia episodes that spontaneously resolved without her ever seeking medical attention). 
• Therefore: This case proved insightful for me as illustration that: i) Patients with ARVC may remain relatively asymptomatic for an extended period of time; and, ii) Although uncommon — We may encounter patients in their 30s (or potentially older) who present for the 1st time with ARVC.

The Initial ECG:

Today's patient presented in a hemodynamically stable regular WCT ( = Wide-Complex Tachycardia) rhythm at ~180/minute, without clear sign of atrial activity. As per Dr. Meyers — the differential diagnosis includes: i) VT in a patient with coronary disease, or other structural heart disease; ii) Idiopathic VT — in which there is no underlying structural heart disease; and, iii) SVT with preexisting bundle branch block or aberrant conduction.

• Of the SVT rhythms — a rate of ~180/minute makes both sinus tachycardia and AFlutter unlikely (albeit not impossible). It's not common to see sinus tachycardia over 160-170/minute in supine (non-exercising) patients — and 2:1 conduction with AFlutter would result in a rate of 360/minute, which is faster than the usual atrial range for AFlutter.
• Overall — I thought an SVT rhythm to be unlikely in today's case. Although QRS morphology of ECG #1 superficially resembles LBBB conduction — there are atypical features. These include: i) Right axis deviation in the frontal plane (ie, the predominantly negative QRS in lead I); and, ii) Earlier-than-expected transition for LBBB (ie, with a tiny isoelectrical complex in lead V3 and predominant positivity of the QRS already in lead V4 — whereas transition should be delayed at least until lead V5 with typical LBBB conduction).
• Especially in a previously healthy, younger adult — a QRS morphology that is not typical for a known conduction defect (ie, LBBB, RBBB, LAHB, LPHB) — significantly increases the odds that a regular WCT will turn out to be VT.
• 
  
• NOTE #1: I initially thought that there might be AV dissociation in ECG #1 — which if true, would prove that the rhythm is VT. That said — after careful study (in the comfort of my home study) — I came to the conclusion that my calipers would simply not walk out any consistent atrial activity (I fully acknowledge how much more challenging it is to try and identify AV dissociation at the bedside of a crashing patient!).
• 
  
• NOTE #2: While antidromic AVRT in a patient with WPW can not be ruled on the basis of this single ECG — over 95% of regular WCT rhythms that are not supraventricular will turn out to be VT. Clinically, distinction between antidromic AVRT and VT is usually not essential in the ED — since appropriate initial management is usually similar (ie, both rhythms will respond to electrical cardioversion).

This leaves us with the strong likelihood that ECG #1 is some form of VT.

• Although in a general population — VT in association with underlying structural heart disease is the predominant form of VT (comprising up to 90% of VT cases) — idopathic VT becomes significantly more common in younger adults without known heart disease (Please see my ADDENDUM below if interested in more about the idiopathic VTs).
• 
  
• As per Dr. Meyers — QRS morphology of ECG #1 showing right axis in the frontal plane — with LBBB features in the chest leads would be consistent in this young adult patient with RVOT VT (Right Ventricular Outflow Track VT), which is the most common form of idiopathic VT.
• 
  
• As per my ADDENDUM below — initial treatment with Adenosine (as given by Dr. Meyers) was perfectly appropriate in this hemodynamically stable patient — since RVOT VT may be an adenosine-responsive form of VT. When this did not work — synchronized cardioversion was the clear treatment of choice. 

Can You Distinguish Between RVOT vs ARVC VT?

From my review of the subject — distinction between RVOT VT vs VT in a patient with ARVC can not be reliably accomplished on the basis of a single ECG recorded during the regular WCT rhythm.

• Hoffmayer et al studied this question (JACC 58(8):831-838, 2011) — and while these authors concluded that certain ECG features do provide insight as to the likelihood of RVOT VT vs ARVC for the regular WCT tracing with LBBB/inferior axis morphology — I came to the opposite conclusion after reviewing their study.
• The problem with using QRS duration >120 msec. in lead I and delayed chest lead transition to at least lead V5 or V6 — is highlighted by our case, in which today's patient was found to have ARVC despite showing uninterpretable QRS duration in lead I and an earlier transition.
• I did think the criterion of fragmentation (ie, excessive notching in one or more QRS complexes) to be potentially helpful — since otherwise healthy young adults with RVOT VT would seem less likely to manifest fragmentation (that typically indicates underlying "scar"). But sensitivity and specificity of all criteria put forth by the authors was imperfect — with overlap of criteria between patients with RVOT vs ARVC VT.
• 
  
• P.S.: Despite the artifact in ECG #1 — there clearly is fragmentation in a number of leads (best seen in V3,V4). That said — in a previously healthy younger adult — RVOT VT is so much more common than encountering a new case of ARVC — that I had no expectation today's patient would turn out to have that diagnosis!
• 
  
• P.P.S.: Clinically — there is no need to labor over trying to determine if a regular WCT tracing is more likely to be RVOT VT vs VT from ARVC. This is because initial management decision-making is essentially the same. Dr. Meyers tried IV Adenosine — but this didn't work. He then sedated the patient and successfully cardioverted to return of sinus rhythm. Suspicion of ARVC was strongly suggested by the post-conversion 12-lead tracing — but even if the post-conversion 12-lead would have been unremarkable, cardiac MRI would still be recommended for virtually any patient with RVOT VT to rule out mimics of severe underlying cardiac pathology such as ARVC or cardiac sarcoidosis (Macias et al — JAFIB 7(4):106-111,2015). Cardiac MRI will tell you if ARVC is or is not present.

Some Final Thoughts on Epsilon Waves:

As I fully acknowledged earlier — My prior exposure to epsilon waves was limited to previously diagnosed cases. Why is it so difficult to pick up epsilon waves on a standard 12-lead ECG?

• There are several reasons ... 

Reason #1: The Wrong Filter Setting is Used ...

All too often — filter settings are ignored. Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. Greater filtering is generally used in monitor mode, with a common setting beting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) is recommended for diagnostic mode, where more accurate ST segment analysis is essential.

• I've taken Figure-2 from the illustration by García-Niebla et al (Rev Esp Cardiol 69(4):438, 2016) — to show how selection of a 40 Hz cutoff frequency (that is commonly chosen in clinical practice in an attempt to "improve" tracing appearance) may result in disappearance of fine ECG features such as the epsilon wave, that is only optimally seen in Figure-2 at a cutoff high-pass filter setting of 150 Hz (BLUE arrows).

 

Figure 2: Illustration of the effect of filter settings on the likelihood of seeing epsilon waves on a standard 12-lead ECG.

Reason #2: The Wrong Lead System is Used ...

I strongly recommend the section by Drs. Buttner and Cadogan in Life-In-The-Fast-Lane on the Fontaine Lead — https://litfl.com/fontaine-lead/ — as this concise review outlines what to know for optimizing your chance of identifying an epsilon wave in a patient with ARVC on ECG. I highlight below a few KEY points from this LITFL Review:

• Identification of epsilon waves is the most specific ECG sign of ARVC. These small deflections may be seen as a "blip" or "wiggle" either at the end, or just after the QRS complex. They are best seen in leads V1,V2 — and a bit less well seen in V3,V4.
• LITFL cites a figure of 23% for the frequency of visualizing epsilon waves on a standard ECG. The filter settings used in association with this figure are not mentioned — so given the tendency of all-too-often selecting a 40 Hz high-pass setting (instead of the optimal 150 Hz setting) — an even lower likelihood of finding epsilon waves might be expected on the ECGs sent our way in search of epsilon waves.
• In contrast — use of special placement of standard ECG machine electrodes called Fontaine Lead Placement — allowed detection of epsilon waves in up to 75% of patients! Rather than reproducing the user-friendly instructions on the LITFL site — I'll refer interested readers directly to their site — https://litfl.com/fontaine-lead/ —
• 
  
• Finally —There are a variety of potential epsilon wave shapes! These include: i) "Wiggle" waves; ii) Small upward spikes; iii) Small downward spikes; and/or, iv) Smooth potential waves at the end of the QRS (which result in prolongation of the QRS in lead V1 exceeding duration of the QRS in lead V3 by ≥25 msec.).

We See LOTS of Epsilon Waves in Today's Case!

Return for a moment to Figure-1 above — in which ECG #2 ( = the post-cardioversion tracing) provides the most convincing example I've yet seen of ARVC.

• There is anterior lead T wave inversion (here in leads V1-thru-V4) despite the lack of a clear RBBB pattern. PEARL: It is unlikely that your patient has ARVC if you do not see anterior lead T wave inversion!
• Despite the artifact — there is QRS fragmentation.
• 
  
• I thought the epsilon wave in lead V3 was the easiest to recognize (BLUE arrow in lead V3 of ECG #2). To clarify the timing of deflections seen in other leads — I drew a vertical DARK BLUE line through this most easily identifiable positive epsilon wave deflection in lead V3. This tells us where to look for the epsilon wave in the simultaneously-recorded long lead II rhythm strip.
• Epsilon waves dip into a negative deflection after slight prolongation of the QRS in leads V1, V2.
• The vertical LIGHT BLUE lines that I extended upward from the long lead II rhythm strip identify what appear to be smaller positive epsilon wave deflections just after the QRS in multiple other leads!

ADDENDUM: 

• In Figure-3 — I summarize key features of Idiopathic VT.
• For review of a case of RVOT VT — Please see My Comment at the bottom of the page in the February 14, 2022 post in Dr. Smith's ECG Blog.
• Please see My Comment in the May 14, 2022 post for a regular WCT that turned out to be antidromic AVRT.

  

Figure 3: Key features of idiopathic VT.