Wide complex tachycardia and hypotension in a 50-something with h/o cardiomyopathy -- what is it?

A 50-something male with unspecified history of cardiomyopathy presented in diabetic ketoacidosis (without significant hyperkalemia) with a wide complex tachycardia and hypotension.

Bedside echo showed "mildly reduced" LV EF.

Here is the ED ECG:

What do you think?

Analysis: there is a wide complex tachycardia. It is regular.  There are no P-waves.  The morphology is of RBBB and LAFB.  The initial part of the QRS is very fast, suggesting that it starts in conducting fibers and not in myocardium.  Thus, it is probably SVT with aberrancy (RBBB + LAFB) or it is posterior fascicular VT (which starts in the posterior fascicle and therefore also has a fast initial depolarization nearly identical to RBBB + LAFB).

The fact that he has a cardiomyopathy argues for a more typical ventricular tachycardia, as does the absence of rSR' in lead V1.  One of the Brugada criteria is RBBB pattern but with the firsr R-wave being larger than the 2nd (true RBBB has rSR' -- that is, the first r- is small and the 2nd R- is large).

The providers for this patient did not spend a lot of time trying to figure this out.  Because the patient was critically ill, they just went ahead and sedated and cardioverted.  

They probably would have had time to give adenosine (after all, they had time to draw up sedatives prior to electrical cardioversion).  Adenosine is safe even if it is VT.  If it is posterior fascicular VT, then verapamil works, but that is very risky in a patient with hypotension.

Here is the difference between VT RBBB and normal RBBB:

In spite of this slightly abnormal morphology, the most important aspect by far that differentiates this from typical VT is that the initial portion of the QRS is fast.  

(The less common atypical VT, otherwise known as idiopathic VT, acts more like SVT with aberrancy because it uses conduction fibers.)

Let's look more closely, magnified:

Click on the image to see it in full size.

I have placed for each lead a line that is at the beginning of the QRS (the left line, with the right side of that line directly at the start of the QRS) and then the 2nd line has its left side at the end of the RS or QR, which is the first part of the QRS.

You can see that that first part of the QRS is about 50 ms.  This is very fast.  

LBBB and RBBB have comparable initial deflection duration.

LBBB has R/S less than 70 ms

RBBB is shorter still.

This was the interpretation I put into the system: 

WIDE COMPLEX TACHYCARDIA.

Has fast early component, with RBBB and LAFB. Thus, possible SVT with RBBB/LAFB or posterior fascicular VT

More typical VT is also possible, as the RBBB is atypical (Brugada criterion): first R-wave is larger than 2nd R-wave in V1

MARKED ST DEPRESSION, SUBENDOCARDIAL ISCHEMIA 

Here is the post cardioversion ECG:

See lead II across the bottom: There are either down-up T-waves, or inverted T-wave followed immediately by a P-wave and prolonged PR interval.  In V1, there is a negative deflection that could be the normal negative component of the P-wave in V1, but it might not be.  I was not certain if this was a fast junctional rhythm or if it was sinus tach, so I wrote: 

UNCERTAIN REGULAR SUPRAVENTRICULAR RHYTHM

RIGHT AXIS DEVIATION  [QRS AXIS > 100]

RIGHT BUNDLE BRANCH BLOCK

The patient had another episode of wide complex tachycardia and was electrically cardioverted again.  He was started on amiodarone and had no more events.

Next day, the cardiologists were convinced (I think correctly) that this was SVT with aberrancy that was triggered by DKA.

The patient later settled into sinus bradycardia.

The amiodarone was discontinued and the patient did well.

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MY Comment, by KEN GRAUER, MD (6/23/2023):

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From an academic standpoint — I love WCT (Wide-Complex Tachycardia) rhythms. That said — from a clinical standpoint regarding initial ED management, the intricacies of determining the etiology of the various WCT rhythms is far less important that "treating the patient" (ie, If the patient is at all hemodynamically unstable or otherwise in precarious clinical condition — immediate synchronized cardioversion will be indicated regardless of whether the rhythm is VT, some type of SVT — and/or a WPW-related tachyarrhythmia).

• The above said — Dr. Smith's approach to today's arrhythmia highlights a number of important points! I focus my comments on some additional thoughts that add to his excellent discussion.

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

Figure-1: I've labeled the 2 ECGs in today's case (See text).

MY Thoughts to Today's Initial ECG:

In the BEST of hands — prediction of the etiology of a regular WCT rhythm is less than perfect. Sometimes, it isn't very good at all. But at other times — we can be surprisingly accurate in predicting the etiology of a regular WCT rhythm by considering a number of clinical features.

• I've reviewed "My Take" on distinction between VT vs some form of SVT with either rate-related aberrant conduction or preexisting bundle branch block on many occasions in My Comments at the bottom of the page in Dr. Smith's ECG Blog (ie, in the August 13, 2020 post — the June 25, 2020 post — the April 23, 2019 post — and the April 15, 2020 post, to name just a few).
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• To Emphasize: The fact that today's patient was acutely ill with DKA and hypotensive in association with the initial ECG shown in Figure-1 — meant that immediate synchronized cardioversion (as was done) was the treatment intervention of choice regardless of what the etiology of his regular WCT turned out to be!

Statistics:

• It's important to appreciate that statistical odds that in an unselected population of adults of a certain age — at least 80% of regular WCT rhythms without clear sign of atrial activity will turn out to be VT. This likelihood of VT increases to at least 90% if the patient has documented underlying heart disease. Given the presence of significant diabetes (severe enough to present with DKA) and known cardiomyopathy — this means that even before looking at the ECG, today's patient presented with a ≥90% likelihood that ECG #1 would turn out to be VT.
• As a result — the "onus of proof" is on us to show that the initial ECG is not VT, rather than the other way around. With a patient such as the one in today's case — Assume VT until proven otherwise, and treat accordingly.
• Just because a regular WCT is VT does not necessarily mandate immediate cardioversion — IF the patient is hemodynamically stable and tolerating the arrhythmia. Today's patient was not stable — so cardioversion was immediately undertaken, with successful conversion to a much narrower (presumably supraventricular) rhythm, as shown in ECG #2.

Other Clinical Factors?

• Today's patient presented with a wide tachycardia and DKA. Although his initial ECG does not look like the ECG of a patient with hyperkalemia — serum K+ should be immediately assessed given lack of atrial activity and QRS widening in a patient with DKA.

QRS Morphology:

I interpreted the rhythm in ECG #1 — as a regular WCT at ~170/minute, without clear sign of atrial activity. Based on the appearance of ECG #1 — I initially thought this rhythm was VT. I did so because QRS morphology was not typical of any known form of conduction defection. Although there is superficial resemblance to rbbb/lahb conduction — there are many atypical features. These include: 

• Lack of a triphasic QRS pattern in lead V1, in which there is a distinct S wave that descends below the baseline — that is followed by a terminal "right rabbit ear" in the form of a relatively slender R' that is taller than the initial r wave in this lead. Instead, there is a taller "left rabbit ear" in lead V1 — which if anything, is more suggestive of VT than of supraventricular rbbb conduction.
• Although wide terminal S waves are seen in both lateral leads I and V6 — they are associated with extremely small r waves. This is atypical for supraventricular conduction (which most often manifests significantly taller lateral R wave forces in leads I and V6). 
• All 3 of the standard limb leads (ie, leads I, II and III) — manifest predominant negative deflections. This pattern is much more suggestive of fascicular VT than of supraventricular conduction.
• Small initial q waves are seen in both leads V2 and V3. This suggests either prior infarction — and/or — a ventricular etiology for the WCT rhythm.
• At 1st glance — the QRS complex in lead V1 appears to be extremely wide! This clearly did not look like a supraventricular etiology to me.

How Wide is the QRS in Lead V1?

Although I initially thought the QRS in lead V1 was extremely wide — as I contemplated a 2nd time (admittedly, in the comfort of my office chair in front of my large screen computer) — I thought the vertical RED line (that I drew in simultaneously-recorded leads V1,2,3 — extended downward to intersect in the long lead II rhythm strip) marked the true end of the QRS complex.

• If the vertical RED line that I drew in ECG #1 correctly marks the end of the QRS complex — then the elevated segment to the right of this RED line in lead V1 must represent ST elevation — which is only seen in lead V1. Could this ST elevation in only lead V1 represent Brugada Phenocopy in this patient with a regular WCT rhythm?
• To facilitate assessing where the QRS ends in the other 8 leads — I extended vertical PURPLE lines upward from the same landmark established by the vertical RED line in the long lead II complex under simultaneously-recorded leads V1,2,3.
• To Emphasize: Even if the QRS in lead V1 ends at the vertical RED line in this lead — I still thought overall QRS morphology in ECG #1 was atypical for supraventricular conduction for the other reasons I stated above. So, at this point in the case, on the basis of just ECG #1 — I thought the initial ECG rhythm had to be assumed VT until proven otherwise.

Is there a Preexisting ECG for Comparison?

When confronted with an acutely ill, hemodynamically unstable patient who presents with a regular WCT rhythm — there rarely is time to "pause" for search of a prior (baseline) ECG on the patient. But it is helpful to do so at the earliest reasonable opportunity — since on occasion, availability of a prior tracing on the patient may provide the answer!

• All bets are off when assessing a regular WCT rhythm in a patient with a markedly abnormal baseline ECG during sinus rhythm. In such cases — none of the "general rules" for QRS morphology used for distinction between SVT vs VT may hold.
• Unfortunately — NO prior tracing is provided in today's case. Instead — all we have is the post-conversion ECG ( = ECG #2 in Figure-1) — which shows that the QRS has narrowed (to between 0.10-to-0.11 second) compared to ECG #1 — but which (as per Dr. Smith) — fails to clearly show sinus P waves. 
• Presumably — ECG #2 is a supraventricular rhythm (either junctional tachycardia or sinus tachycardia with a long 1st-degree AV block) — in which the atypical features of incomplete RBBB conduction are the result of scar from prior infarction (ie, producing overall low voltage — Q waves in leads V2,V3 — and QRS fragmentation in a number of leads).

WHY Did the Post-Conversion Tracing Change My Mind?

After seeing ECG #2 — my impression of the initial ECG changed.

• As per Dr. Smith — the initial portion of the QRS complex in ECG #1 is relatively narrow (implying fast initial conduction — that is typical of a supraventricular etiology). More than this — the shape of the initial QRS deflection is virtually the same in most leads for ECGs #1 and #2.
• I've drawn vertical BLUE lines in both of today's tracings that define the initial portion of the QRS deflection that I am referring to. For example — the direction and slope to the LEFT of the vertical BLUE line in simultaneously-recorded leads I,II,III in both ECGs #1 and #2 show a similar tiny R wave in lead I — and a small, thin initial r with deep and steep S wave downslope in leads II and III.
• Similarity in the portion of the QRS to the LEFT of the vertical BLUE line in the other 9 leads in both tracings is likewise present. This high degree of similarity in the initial deflections of so many leads would be highly unlikely if ECG #1 was VT.

Learning Points:

• The accuracy of ECG criteria for prediction of VT vs SVT with either aberrant conduction or preexisting BBB is imperfect. Certain predictive criteria can be highly accurate. That said — today's case was especially challenging because: i) QRS morphology in the initial ECG was not optimally consistent with any known conduction defect; and, ii) The post-conversion tracing still showed atypical QRS morphology (ie, completely positive QRS in lead V1 — anterior Q waves — marked fragmentation).
• Initial management of an unstable patient in a regular WCT rhythm is the same regardless of whether the etiology of the rhythm is VT or an SVT = immediate cardioversion!
• Even though initial management of the unstable patient in a WCT is the same for both SVT and VT — determining the etiology of the initial rhythm may be extremely helpful for deciding on further management (ie, For deciding which medication to continue the patient on after successful cardioversion, so as to prevent recurrence? — and at times for deciding whether or not to refer the patient to EP cardiology, which may depend on what the diagnosis of what the WCT was).
• Finding a prior ECG on the patient may prove invaluable — especially for comparaing QRS morphology during the WCT rhythm compared to the patient's baseline ECG during sinus rhythm.
• RBBB conduction produces a terminal delay in QRS morphology. The fact that the initial QRS deflection in virtually all leads of today's tracing was both narrow and virtually identical in direction and slope (ie, the deflections to the LEFT of the vertical BLUE lines) — supports a supraventricular etiology for the WCT in today's case.
• Other factors may alter QRS morphology of a supraventricular rhythm (ie, hyperkalemia, transient development of a Brugada Phenocopy pattern).
• Certain fascicular VTs may manifest a QRS morphology that is consistent with rbbb/lahb conduction. That said — I agree with Dr. Smith that the initial ecg in today's case more likely than not was supraventricular in etiology.
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• I wish we could find a baseline tracing on today's patient for comparison ...