EXTRA COPY - ECG Blog #545: VT Criteria - EXTRA COPY

The ECG in Figure-1 was obtained from a 60-something year old man — who presented with a history of recurrent palpitations over the past several years. He was hemodynamically stable with this rhythm.

• Prior to the onset of these episodes of palpitations — the patient had been healthy without medical problems.

• Of note — the patient recently developed ankle edema with progressively increasing dyspnea on exertion.

QUESTIONS:

• How would you interpret the rhythm in Figure-1? 
• What clinical entity is suggested by the above history?

  

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today's CASE:

As frequently reviewed on this ECG Blog — I favor the Ps,Qs,3R Approach for assessment of tachycardias (See ECG Blog #185 — for review of this system).

• The rhythm in Figure-1 is Regular at a Rate of ~150/minute.
• The QRS is wide (ie, ≥0.12 second).

Regarding the 4th and 5th parameters of the Ps, Qs and 3Rs:

• P waves are absent — which by definition means there is no Relation between P waves with neighboring QRS complexes (since there are no P waves).

Impression: The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~150/minute.  

• Statistically in an adult of a certain age — We start with the reality that 80-90% of regular WCT rhythms without sinus P waves will turn out to be VT. Therefore — Assume VT until proven otherwise. Treat the patient accordingly.
• That said, since this patient is hemodynamically stable — You have at least a moment in time to look closer at the rhythm for features that might increase (or decrease) your diagnostic likelihood of an 80-90% chance that the rhythm is VT.

As illustrated in last week's ECG Blog #544 — Among the most time-efficient and helpful ECG features that I look for are the following:  

• The frontal plane axis during the WCT rhythm. 
• Other potential signs of atrial activity.
• QRS morphology.

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Looking Closer at Figure-1 ...

In today's case — neither the frontal plane axis nor searching for signs of atrial activity help to provide an answer:

• Although the frontal plane axis during the WCT rhythm is markedly leftward — the axis does not satisfy my definition of an "extreme" axis (because the QRS is not entirely negative in either lead I or lead aVF). Instead — a small-but-definitely-upright initial positive deflection (r wave) is present in lead aVF. As a result — assessment of the frontal plane axis is not sufficiently discriminating to be helpful.
• I see no clear indication of atrial activity in Figure-1. This feature is therefore of no assistance for determining the etiology of today's rhythm.

QRS Morphology during the WCT:

This leaves us with assessing QRS morphology in our hope to increase statistical likelihood beyond the 80-90% likelihood that we start with by simply knowing that today's rhythm is a regular WCT without clear sign of sinus P waves.

• As emphasized in ECG Blog #211 — the chance that a WCT rhythm will turn out to be supraventricular will significantly increase IF — we can demonstrate that QRS morphology is typical for one of the known forms of conduction block (ie, RBBB, LBBB, LAHB or LPHB; or RBBB with one of these hemiblocks).

PEARL #1: The entity of fascicular VT marks an exception to the general rule that when a regular WCT resembles a bifascicular block — that the rhythm is likely to be supraventricular. The reason for this — is that by definition, “fascicular VT” will resemble one of the hemiblock forms (ie, either RBBB/LAHB or RBBB/LPHB). 

• The KEY to recognizing that a regular WCT rhythm that bears a certain resemblance to an rbbb conduction pattern, with either marked left or right axis deviation is unlikely to represent a supraventricular rhythm — is that some features that are atypical for VT are present.
• To Emphasize: QRS morphology is not a perfect science. Even in the best of hands — nothing is perfect (ie, It is always possible that prior scarring from cardiomyopathy or previous infarction will result in a markedly abnormal baseline tracing during sinus rhythm).
• This leaves us with the clinical reality that much of the time — we'll need to begin our treatment of a regular WCT before we know for certain what the etiology of the rhythm is. That said — I find it helpful to be aware of the relative probabilities for VT vs some type of SVT rhythm before I contemplate therapeutic options for treatment.

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Take another LOOK at today’s initial ECG:

I've reproduced today's initial ECG in Figure-2.

• Does QRS morphology during the WCT rhythm in Figure-2 look like one of the known forms of conduction block?

  

Figure-2: I've reproduced today's initial ECG. 

Answer:

YES — Today's initial ECG that is shown in Figure-2 does resemble the RBBB/LAHB form of bifascicular block. That said, as suggested in Figure-3 — there are some atypical features:

• PEARL #2: Although the possibility of rbbb conduction is suggested by the all upright QRS in lead V1 — a triphasic rsR' morphology is lacking (ie, in which there is an s wave that descends below the baseline with a terminal taller right "rabbit ear" R’ wave in lead V1). 
• As discussed in detail in ECG Blog #211 — whereas not all patients with RBBB necessarily manifest a classic triphasic rsR' morphology — the finding of an entirely upright monophasic R wave that we see in lead V1 of Figure-3 could be either the result of supraventricular rbbb conduction or this could be VT. Therefore — the resemblance that we see in lead V1 to rbbb conduction is not helpful in distinguishing between SVT vs VT.
• PEARL #3: The other characteristic feature of rbbb conduction is the presence of a wide terminal s wave in lateral leads I and V6. And although in Figure-3 we do see a terminal s wave in both leads I and V6 (the YELLOW arrows in these leads) — this terminal s wave is narrow in lead I and tiny in lead V6.
• PEARL #4: The typical appearance of lahb conduction — is for there to be rS waves (with predominant negativity) in each of the inferior leads. And although there are initial r waves in leads II,III,aVF — these initial r waves are extremely small in leads II and aVF (YELLOW arrows in these leads) — which is not the typical picture for QRS morphology with lahb conduction.
• PEARL #5: The initial vector of depolarization tends to be fast with supraventricular conduction — because electrical activity begins in the His-Purkinje system. In contrast, with VT — the initial vector of ventricular depolarization tends to be slower, because electrical activity begins away from the conduction system in ventricular myocardium. 
• Instead of a more vertical upslope — the R wave in lead I rises at a slower rate than I'd expect with supraventricular conduction (BLUE arrow in this lead).
• PEARL #6: An insensitive, but highly specific morphologic feature to be aware of when assessing a WCT rhythm — is that IF there is either global positivity or global negativity in all 6 chest leads (ie, Leads V1-thru-V6 being either all positive or all negative) — then the etiology of the rhythm is almost certain to be VT.
• There would be global positivity in leads V1-thru-V6 in Figure-3 — if it were not for tiny intermittent s waves in leads V2,V4,V5,V6. These tiny s waves reduce specificity of this finding — albeit QRS morphology remains suspicious for supraventricular conduction.

Bottom Line: While fully acknowledging that QRS morphology is not definitive for either VT or a supraventricular etiology in today's initial ECG — the above atypical features made me strongly suspect left posterior fascicular VT as the diagnosis.

Figure-3: I've labeled key features regarding QRS morphology.

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The CASE Continues:

The patient was treated for presumed VT with IV Amiodarone, but without success. Electrical cardioversion was applied — which transientlly converted the rhythm, only to result in recurrence of the regular WCT moments later. 

• The patient's condition deteriorated requiring intubation.
• Persistence of the regular WCT led to marked hypotension with cardiogenic shock.
• Finally — overdrive pacing successfully converted the WCT. The resultant rhythm is shown in the bottom tracing in Figure-4.

QUESTIONS:

• Does the repeat ECG recorded after successful overdrive pacing shed light on the etiology of today's initial ECG?
• Going back to the history that we were given at the beginning of today's case (ie, that this 60-something patient had been having recurrent palpitations over a period of years — with recent development of ankle edema and increasing dyspnea on exertion) — What clinical entity is suggested?

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded after successful overdrive pacing.

CASE Conclusion:

The "good news" is that this patient improved greatly after overdrive pacing successfully converted the WCT rhythm.

• The repeat ECG in Figure-4 — shows restoration of sinus rhythm. The remarkable finding is that QRS morphology in sinus rhythm is almost identical during the WCT and during sinus rhythm.
• ECG #2 shows a sinus rhythm at a rate just over 60/minute.
• There is bifascicular block (RBBB/LAHB).
• There is LVH (R wave in lead aVL ≥12 mm; R wave >18 mm in lead V6).
• ST-T waves do not look acute (The inverted T waves in the inferior leads is not necessarily abnormal given the predominantly negative QRS complexes in these leads — and chest lead ST-T wave changes are most likely secondary to the RBBB and to LVH).

• PEARL #8: Cases like today keep us humble! Despite strong suggestion from QRS morphology that today's WCT rhythm was fascicular VT — the finding of nearly identical QRS morphology in the repeat ECG after overdrive pacing tells us that the rhythm in ECG #1 was a reentrant SVT and not fascicular VT. This highlights the importance of being aware that the most "atypical" QRS morphology may occasionally be the result of a markedly abnormal baseine ECG (and not VT).
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• PEARL #9: The patient's history of frequent episodes of recurrent palpitations over a period of years, with recent development of ankle edema and worsening dyspnea on exertion suggest there was TICM (Tachycardia-Induced CardioMyopathy), which over time so depressed LV function as to result in progressively increasing heart failure (See Nerheim et al: — Circulation 110(3):247-252, 2004 — and — Huizar et al: JACC 73(18):2328-2344, 2019 — for more on TICM).
• TICM typically takes weeks or longer to develop after exposure to a persistent tachyarrhythmia — but it has been shown to develop in as quickly as 3 days!
• Fortunately — the depressed LV function that occurs with TICM is usually reversible after rate control (ideally with conversion to sinus rhythm) has been achieved. Most patients recover good LV function within 6 months.

Final Disposition: The patient was referred to EP Cardiology. EP study revealed the etiology to be recurrent AVNRT with dual AV nodal pathways. Ablation of the extra pathway resulted in "cure" of the patient's arrhythmia.

• Normal LV function returned soon after resolution of the arrhythmia. This rapid response to treatment proved that the patient's heart failure was the result of TICM.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Benha City, Egypt) — for allowing me to use this case and this tracing.

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For Additional Review:

• See ECG Blog #489 — for review of another case illustrating the approach to a patient with suspected fascicular VT.