What is this rhythm? And why rhythm problems are easier for the Emergency Physician than acute coronary occlusion (OMI).

Written by Pendell Meyers

Don't miss Ken Grauer's excellent assessment at the bottom.

With no context, what do you think this rhythm is?

Smith comments: Wide complex tachycardia.  The differential diagnosis of WCT is:  

1) Sinus tachycardia with "aberrancy" (in this case RBBB and LAFB), but there are no P-waves and the QRS morphology is not typical of simple RBBB/LAFB.  If you are wondering if there are P-waves that you just can't see, you can use Lewis Leads to magnify the P-waves (or not, if they are not there).  Also, if the rate is constant, not wavering up and down, it is highly unlikely to be sinus tachycardia.  Sinus tach is often misinterpreted as a dysrhythmia.  See this case, for example: A Relatively Narrow Complex Tachycardia at a Rate of 180.  

2) PSVT with "aberrancy" (atypical RBBB+LAFB).  Possible but, again, the QRS morphology is atypical

3) Atrial Flutter with 2:1 conduction and "aberrancy".  I do not see flutter wave baseline, and again the QRS morphology is not typical for a supraventricular rhythm.

4) Antidromic ARVT, which is supported by the slow onset of the QRS. But the superior axis with positive QRS in V1 is difficult to reconcile with an accessory pathway.  Slow onset of QRS is probably the best hallmark of VT.

5) Ventricular Tachycardia: by far most likely, but what kind?

Fortunately, you don't need to make a definite diagnosis.  It is not sinus tachycardia, so you can electrically cardiovert, whether the patient is stable or unstable.

Why are rhythms easier to recognize and manage than OMI for the Emergency Physician?  

First, When you have a rhythm problem, you know you have a problem because the rate is either fast, slow, or irregular.  With OMI, all you know is that your patient has some nonspecific chest pain, SOB, shoulder pain etc. which is probably NOT due to acute MI.  So if you don't recognize the OMI on the ECG immediately, then myocardium is irreversibly lost.  And if you wait for troponin, much myocardium is lost by the time you make the diagnosis. Second, when you have a rhythm problem, you are likely to be able to fix the problem with electricity (cardioversion, defibrillation, pacing).  Third, while you are making a decision about a rhythm, myocardium is not rapidly dying.  Fourth, you can get help from a cardiology colleague; they are very good at this even though they may not be so good at recognizing OMI on the ECG.  Fifth, potential management actions are in your hands; you do not need to request a coronary interventionalist or cath lab team.

Making a specific ECG Diagnosis (less important in the ED)

Without reading the below, I suspected posterior fascicular VT.  There are no P-waves, there is an RBBB + LAFB morphology, with rate slightly over 150, QRS duration is wide but not VERY wide.  This type of VT is often diagnosed in younger patients without any baseline cardiac disease.  They often have good ejection fraction and tolerate the dysrhythmia quite well.  So if the patient is stable, has good LV function on bedside echo, and is relatively young with no history of heart failure or cardiomyopathy, then posterior fascicular VT is likely.  In any case, I would electrically cardiovert.  See Ken's excellent analysis at the end.

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Case continued: Here is the clinical context and all ECGs in order:

An elderly comorbid woman presented with acute respiratory distress. She was critically ill and required noninvasive positive pressure ventilation and ICU admission for suspected infectious respiratory illness.

Smith: now that I know she is "elderly," and in respiratory distress, I am much less confident in that diagnosis.  It would be good to know more about her cardiac history and her ejection fraction on bedside echo.

Case continued

Bedside echo showed a significantly reduced LV ejection fraction (prior echo on file had EF 45%). Here were her first two ECGs:

I believe these two rhythms are supraventricular with LBBB morphology. I think the first one is likely sinus, and the second one is less certain to me, could be sinus or flutter.

Then her rhythm abruptly changed to this:

Regular, monomorphic, just a bit over 120 msec in my estimation. The QRS morphology is completely different than before, and now could be called similar to RBBB and LAFB morphology.

Overall, it would be best to assume VT until proven otherwise. It might not be "classic" VT, but instead Posterior Papillary Muscle VT, or Posterior Fascicle VT. Both of these types of VT access the left posterior fascicle, thereby creating VT with RBBB/LAFB morphology and thus QRS duration shorter than "classic" VT.

Smith: Now that we see the preceding ECGs and the clinical story, Posterior Fascicular VT is far less likely than standard monomorphic VT arising from a sick left ventricle, though Pendell's assessment may be correct

Case Continued

Thanks to several colleagues for this interpretation, including Pierre Taboulet and Nanashi and Willy Frick.

Amiodarone was chosen as an "antidysrhythmic", and it was later attributed temporally to cessation of the rhythm.

(Ever since Dr. Nils Johnson told me that he calls them "rhythm modifying drugs", I also prefer this term, as we all know that any of these medications in general can be both "anti-dysrhythmic" and "pro-dysrhythmic.")

Later in her hospital course, here is another ECG:

Sinus rhythm with bigeminal PVCs. In my opinion, the PVCs match the likely VT from the prior ECG. This increases the confidence that the prior rhythm was VT.  I believe this makes Posterior Papillary Muscle VT more likely, but these cases are still a bit rare and esoteric to me, especially when they are likely caused by (and resolve with) a critical illness. There is no evidence that this elderly patient has suffered from VT or other primary dysrhythmias in the past.

Unfortunately, the patient continued to worsen, was intubated and admitted to the ICU, where she ultimately expired days later, with an overall impression of multifactorial respiratory failure.

Here is an article about PPM VT

Here are some other relevant cases:

A 12 year old with Wide Complex Tachycardia

Incessant Regular Wide Complex Tachycardia

Wide complex tachycardia in a 36 year old

Also see my prior post with EM-focused teaching on Fascicular VTs:

Idiopathic Ventricular Tachycardias for the EM Physician

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MY Comment, by KEN GRAUER, MD (3/6/2025):

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Among the greatest challenges faced by emergency care providers — is assessment of the regular WCT (Wide-Complex Tachycardia). Today's case presented by Dr. Meyers amplifies this challenge by presenting us with not one, but 3 serial WCT rhythms. 

• While fully agreeing with the key concepts conveyed above by Dr. Meyers — I'll offer an additional perspective to these 3 serial rhythms.
• For those wanting Quick Review of my approach to the regular WCT — Please See my May 5, 2020 post in Dr. Smith's ECG Blog.

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— ECG #1 — (The initial ECG shown by Dr. Meyers):

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From an educational standpoint — I thought Dr. Meyers' choice was excellent, to begin today's case by first showing the 3rd ECG that was recorded (even though this ECG that I have labeled in Figure-1 — was recorded after ECG #2 and ECG #3 that appear in Figure-2 below). 

Emergency providers need to attain high confidence that ECG #1 is all-but-certain to represent VT.

• We are told that the rhythm in Figure-1 is from an acutely ill elderly woman with underlying comorbid conditions. This rhythm is a regular WCT at ~160/minute, without clear sign of atrial activity. Knowing this — before we even begin to look at specific features in this ECG, we need to remember that statistical likelihood  that this rhythm is VT approach 90%. As a result — our mindset is not to determine if this rhythm "might be" VT — but rather that we need to assume VT (and treat accordingly) unless we can conclusively prove otherwise.
• Although it may be tempting to interpret the small negative deflections marked by BLUE arrows in the long lead V5 rhythm strip as P waves — these are not P waves. As shown by the double RED arrows — the QRS complex in each of the limb leads begins with subtle slurring. Thus, the parallel BLUE time lines show this initial negative deflection in lead V5 to be part of the QRS. 
• KEY Point: When you see deflections that "look" like sinus P waves in one or 2 leads, but you do not see anything resembling a sinus P wave in either lead II or lead V1 — then those deflections you are seeing in those other leads (like the negative deflections here in lead V5) are not sinus P waves!
• "12 leads are better than one" — and skillful use of simultaneously recorded leads can be invaluable. For example — the parallel GREEN timeline tells us that a similar small negative deflection also appears at the onset of the QRS complex in leads V4 and V6. This negative deflection is a Q wave — and it is surprisingly wide for its tiny size, and followed by a notched (fragmented) r'rS wave in lead V6. In my experience, seeing surprisingly wide, successive Q waves in a series of chest leads (as we do in leads V4,V5,V6) — is a "tip-off" that the rhythm is almost certain to be VT.
• Returning to the limb leads in Figure-1 — there is extreme frontal plane axis deviation during this WCT (which we easily recognize by the finding of all negative QRS complexes in each of the inferior leads). This is another "tip-off" to 98+% likelihood that the rhythm is VT (barring the rare exception of a markedly distorted baseline tracing with identical morphology). 
• To Emphasize: The criterion of "extreme" frontal plane axis deviation during a WCT is not valid unless the QRS is entirely negative in either lead I or lead aVF. But especially given the initial slurred descent of the inferior lead QS complexes in Figure-1 — the "picture" that we see here is almost never seen with supraventricular rhythms.
• Is there relative “delay” in the initial QRS deflection? SVT rhythms tend to manifest more rapid initial depolarization vectors — because supraventricular depolarization generally begins its path toward the ventricles by travel over established conduction pathways. A notable exception to this generality is when there is an AP (accessory pathway) that bypasses the AV node (ie, in a patient with WPW). That said — “relative delay” in the initial portion of the QRS complex in multiple leads favors VT. And — in no lead in Figure-1 is there rapid initial depolarization of the QRS complex, thus one more feature pointing to VT. (Remember this criterion! — as we will apply momentarily when we take another look below at Figure-2).

But before moving on to Figure-2 — Consider this last criterion: Is there resemblance to any known form of conduction block?

• In ECG #1 — it might initially seem that the QRS complex in lead V1 resembles RBBB morphology. But does it? As highlighted within the dotted GREEN oval — QRS morphology in lead V1 is that of an rsR'R'' — or, a truly bizarre morphology not anything like the typical triphasic rSR' that characterizes RBBB conduction. And while patients with underlying heart disease often manifest variations on that typical triphasic scheme — this is a truly bizarre QRS morphology that we see in lead V1.
• If anything — the limb leads resemble lbbb conduction (and not rbbb conduction). Therefore — QRS morphology in Figure-1 does not come close to resembling any known form of conduction defect.

BOTTOM Line: I have reviewed the above features of ECG #1 in "slow motion". That said, with practice in applying these features — a conclusion of 98+% likelihood of VT should be arrived at for this tracing within seconds!

Figure-1: This is the 1st ECG shown by Dr. Meyers in today's case. How certain were YOU that this is VT?

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— ECG #2 and ECG #3 — (The first 2 ECGs recorded in Today's Case):

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I agree with Dr. Meyers that ECG #2 and ECG #3 (that I have reproduced in Figure-2) — most likely both represent supraventricular rhythms with LBBB-like morphology.

• That said — I also agree with Dr. Meyers that a definitive diagnosis of the specific type of SVT rhythm is difficult (if not impossible) to make on the sole basis of these 2 ECGs.

Again — the clinical history is helpful. While admittedly not certain of the specific etiology of ECG #2 ( = the 1st ECG recorded in the ED in today's case) — Several features immediately suggest a supraventricular etiology to me:

• The rate of the rhythm is fast (a bit over 120/minute) — but not as fast as the VT in Figure-1. We often need to begin treatment of our patient before we know for certain what the rhythm is. So, given that this patient presents with an acute infectious respiratory illness — IF she is hemodynamically stable, it would be reasonable to continue to treat her acute pulmonary illness as we look further at this ECG.
• Sinus P waves in lead V1 with tachycardia often manifest as subtle negative deflections. While admittedly not certain — I suspect that the vertical RED lines in lead V1 of ECG #2 represent sinus P waves.
• Clearly, baseline artifact in the limb leads prevents identification of atrial activity. That said — some extra "width" to the terminal T wave peak in lead II (RED arrow) could represent a hidden sinus P wave with similar PR interval as for the RED arrow I drew in lead V1. Admittedly — I am not at all certain about these suppositions from this difficult-to-interpret tracing — but I suspect (like Dr. Meyers) that ECG #2 represents sinus tachycardia.
• QRS morphology in ECG #2 is consistent with LBBB conduction (wide, all upright QRS in lateral leads I and aVL — with minimal positivity and very rapidly descending S waves in leads V1,V2,V3 — transitioning to predominant positivity by lead V6).
• And — there is a very narrow initial deflection of the QRS in leads V1-thru-V5 (within the dotted BLUE ovals in these leads). This is in marked contrast to the wide initial QRS deflections seen in Figure-1 with VT.
• BOTTOM Line: While I am in no way certain that ECG #1 represents sinus tach with LBBB accounting for QRS widening — as long as this patient was hemodynamically stable, I'd continue for the moment with treatment of her acute pulmonary condition.

What happens in ECG #3?

• The heart rate has significantly increased in ECG #3 (now ~150/minute). I no longer see the negative deflection that I had perceived as a probable sinus P wave in lead V1 of ECG #2.
• As per Dr. Meyers — at the rate of ~150/minute, we need to consider AFlutter with 2:1 AV conduction. But despite careful caliper review (Something impossible for providers at the bedside to do! ) — I can not get 2:1 atrial activity to march out, so I do not believe this is AFlutter. 
• On the contrary — vertical GREEN lines in the inferior leads suggest possible retrograde conduction — but I clearly would not be expecting sudden onset of a reentry SVT given the clinical situation.
• BUT — LBBB-like morphology persists (wide, upright QRS in lateral leads I,aVL — minimal positivity in anterior leads with very narrow initial upright deflections followed by steeply descending S waves — transitioning to predominant positivity by lead V6).
• BOTTOM Line: While I am again in no way certain — I agree with Dr. Meyers that ECG #3 most probably still represents a supraventricular rhythm. Clinically — this means that as long as the patient remains hemodynamically stable — We can continue with treatment of her acute pulmonary condition.

NOTE: At this point in the case, the VT rhythm shown in Figure-1 abruptly developed. This patient was apparently treated with Amiodarone — and some time thereafter, the rhythm shown in Figure-1 stopped.

• My Thought: Abrupt change in the rhythm from what we see in ECG #3 — to the virtually certain VT that we saw in Figure-1 would have prompted me to use synchronized cardioversion. 

Figure-2: The 2 ECGs shown above were recorded before the ECG shown in Figure-1. Did YOU think one or both of these ECGs were VT?

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— ECG #4 — (An ECG obtained later in this patient's hospital course):

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I wanted to review the final tracing in today's case — because I believe it resolves any doubt that may have existed about the etiology of ECG #1.

• As noted — ECG #4 was obtained later in this patient's hospital course. It shows ventricular bigeminy ( = sinus rhythm, with every-other-beat a PVC).
• We know with 100% certainty that all odd-numbered beats in Figure-3 are PVCs — because the subtle, variable distortion of the T wave of each PVC walks out perfectly for demonstrating an underlying regular sinus rhythm at ~80/minute (PINK arrows in the long lead II of Figure-3). This means that the wide, very different-looking QRS complex of beats #1,3,5,7,9,11,13 has to be coming from below the AV node ==> PVCs.
• A PEARL for retrospective confirmation of VT after conversion to sinus rhythm — is if you can demonstrate the same QRS morphology for post-conversion PVCs as was seen for the QRS during the WCT rhythm. While not all QRS complexes during ECG #1 are exactly the same — the all-negative QS complexes in each of the inferior leads with initial slurred descent of the S wave (within the dotted RED rectangles in ECG #4) look identical to QRS morphology in the inferior leads during ECG #1 — and QRS morphology in the other 9 leads looks close enough to confirm that ECG #1 was indeed VT.

Figure-3: Comparison of QRS morphology of the WCT rhythm in ECG #1 with the PVCs in the post-conversion tracing.