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.
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• 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.
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• 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).
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• 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.
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• 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.
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• 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).
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• 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.
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• 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.
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• 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.