ECG Blog #231 — A Bizarre, Irregular Tachycardia ...

The 12-lead ECG shown in Figure-1 was obtained from a previously healthy 55-year old man who presented to the ED (Emergency Department) with shortness of breath, altered sensorium and hemodynamic instability.

• WHAT are the diagnostic possibilities for the rhythm?
• What do you feel is the most likely rhythm diagnosis?

 

Figure-1: Presenting ECG from a 55-year old man with shortness of breath, altered sensorium and hemodynamic instability (See text).

 

 

MY THOUGHTS on ECG #1:

My initial impression on looking at the ECG in Figure-1 — was that this irregular, wide rhythm was probably rapid AFib (Atrial Fibrillation), with a mixture of PVCs (Premature Ventricular Contractions) and aberrant conduction of supraventricular impulses.

 

I Changed My Mind on taking a 2nd Look at this tracing:

• I saw no sign of atrial activity.
• I thought all 25 QRS complexes on this tracing were probably ventricular in etiology (Figure-2). Although the QRS does not look overly wide in some leads — as you follow each of these 25 beats down the page from lead I at the top (looking in each of the 11 simultaneously-recorded leads below lead I) — the QRS is revealed to be either definitely wide in other leads — or — to manifest a QRS morphology strongly suggestive of a ventricular etiology (ie, the all-negative, widened complexes in lead V6 for beats #4,5; 8; 11, 12; 14,15; and 21 are ~99% likely to be ventricular in etiology).
• While I can't rule out the possibility that there might be a few supraventricular "capture" beats in Figure-2 — I believe it fair to say that more than 20 of the 25 beats in this tracing are ventricular in etiology.
• Unlike AFib — there does appear to be a "pattern" to the rhythm in Figure-2 (Doesn't the shape and relative timing of beats within the 2 YELLOW and 2 WHITE rectangles in Figure-2 look surprisingly similar?).
• BOTTOM Line: Despite irregularity of the rhythm and variability in QRS morphology — I thought the rhythm in Figure-2 had to represent some form of VT (Ventricular Tachycardia).

 

Figure-2: I have numbered the beats in ECG #1. Doesn't it look like there is some kind of repetitive group pattern in successive beats? (Look within the 2 YELLOW and 2 WHITE rectangles at sequential beats in the long lead V6).

 

 

VT Terminology:

Before going further — it may help to review a number of terms that have been used to describe the morphologic appearance of various forms of VT. These include:

• Monomorphic VT — in which there is a similar (if not identical) QRS appearance throughout the episode of VT.
• PolyMorphic VT (PMVT) — in which QRS morphology and/or axis continuously changes from one beat-to-the-next throughout the episode of VT. PMVT is not a regular rhythm — and it is often quite irregular. When PMVT is associated with a long QT interval — the rhythm is then defined as Torsades de Pointes (See ECG Blog #36 for more on distinction between Torsades vs PMVT).
• Pleomorphic VT — in which more than a single QRS morphology is seen during an episode of VT. Pleomorphic VT differs from PMVT — because QRS morphology is not changing from one beat-to-the-next. Instead, one QRS morphology will be seen for a number of beats — and then another morphology may take over and continue for another series of beats. Several different morphologies may be seen. (For more on Pleomorphic VT — Please SEE My Comment in the June 1, 2020 post in Dr. Smith’s ECG Blog).
• Bidirectional VT — in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT distinguishes itself from PMVT and pleomorphic VT — because a consistent pattern (ie, alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in bidirectional VT — and they alternate every-other-beat. (CLICK HERE — for this case report Review by Femenia et al on BiDirectional VT in a patient with CPVT = Catecholaminergic Polymorphic VT).

 

 

WHY CARE about QRS Morphology with VT?

Classification of the morphologic type of VT may provide clues to etiology, outcome and treatment.

• Monomorphic VT may occur in patients with or without underlying structural heart disease. Because the ventricular activation sequence is constant in monomorphic VT (which is why all beats look the same) — successful treatment (either by medication or cardioversion) is generally easier to accomplish. 
• The occurrence of monomorphic VT in a patient without underlying structural heart disease (and without QT prolongation or metabolic/electrolyte abnormalities) — is known as Idiopathic VT. The “good news” — is that long-term prognosis of patients with idiopathic VT tends to be excellent (See ECG Blog #197 for more on Idiopathic VT).
• As noted earlier — Bidirectional VT is extremely uncommon. Think of digitalis toxicity and catecholaminergic polymorphic VT as potential etiologies in which you are more likely to see bidirectional VT.
• Pleomorphic VT is also uncommon, and less well known than the other morphologic forms of VT. Patients with pleomorphic VT generally have significant underlying structural heart disease. A number of mechanisms have been proposed to explain the pattern of pleomorphic VT, in which there may be one or more runs of VT with a given similar QRS morphology — that is then punctuated by runs of VT with 1 or more other QRS morphologies. Potential mechanisms for explaining pleomorphic VT are complex — and include the possibility of: i) a single VT circuit with more than a single exit site; ii) the presence of more than a single VT circuit; and/or, iii) shifting conduction properties that alter the activation sequence (Liu & Josephson — Circ Arrhythm Electrophyiol 4:2-4 2011). 

 

PolyMorphic VT (PMVT) — is divided into 2 groups, depending on whether the preexisting QT interval is prolonged. 

• The occurrence of PMVT in association with baseline QTc prolongation — is defined as Torsades de Pointes. Torsades often has a multifactorial etiology (ie, drug-induced, electrolyte depletion, CNS disturbance and/or other underlying disorder that may predispose to QT lengthening). KEY aspects of treatment include IV Mg++ (often at high dose) + finding and “fixing” the cause of the long QTc.
• In contrast — PMVT without QT lengthening most often has an ischemic etiology. Although IV Mg++ is also indicated as initial treatment of PMVT with a normal QT — it is clearly less likely to respond to IV Mg++, than when the QT interval is prolonged. Instead, antiarrhythmic drugs such as amiodarone or ß-blockers may be needed — and/or treatment targeted to correcting ischemia.

 

COMMENT on Today's Case:

What I found especially interesting about the rhythm in Figure-2, is that unlike the complete variability in QRS morphology and R-R intervals that is usually seen with PMVT — there seemed to be a distinct, repetitive pattern in several parts of this tracing.

• That said, given lack of atrial activity and numerous different ventricular QRS morphologies — I thought the rhythm in today's case to be most consistent with Polymorphic VT.
• Clinical details on this patient were scarce — but there was no history of medication use or toxic ingestion.

 

My thoughts as to why there may be a repetitive pattern in parts of the rhythm in from today's case — are illustrated in Figure-3, which I adapted from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog.

• Although one might expect PMVT to originate from multiple sites in the ventricles — much (if not most) of the time — this is not what happens. Instead — it is more common for PMVT to originate from a single ventricular focus (despite significant variation in QRS morphology that may sometimes be seen from one beat-to-the-next).
• As suggested in Figure-3 — the physiologic explanation for why this may happen, is that the polymorphic VT focus may travel over a different path in its exit from the myocardium.
• Irregularity of PMVT may be explained by variation in conduction times for the various exit paths.
• The "repetitive pattern" that I suggest is present (within the YELLOW and WHITE rectangles drawn in Figure-2) — may be the result of a somewhat organized "rotation" over a series of potential exit paths.
• PEARL: As one might imagine — most PMVT rhythms are hemodynamically unstable, with tendency toward rapid deterioration to VFib. That said — Dr. Venkatesan makes the clinically important point that on occasion — some PMVT rhythms are surprisingly well tolerated! This could be the result of a "competition" between the different foci and/or exit sites that serve to prevent any one malignant focus from predominating and precipitating deterioration to VFib. To paraphrase Dr. Venkatesan, "One VT focus may act like a natural anti-tachycardia pacing device, that serves to terminate a VT from another focus".

 

Figure-3: I have adapted this figure from the September 23, 2011 post in Dr. Venkatesan's Cardiology Blog. It explains how "polymorphic" VT might arise from a single venricular focus, rather than from multiple sites in the ventricles (See text).

 

FOLLOW-UP to Today's Case:

Unfortunately — the rhythm in Figure-2 deteriorated, and cardiac arrest was called. The patient could not be resuscitated. I believe this unfortunate clinical course supports our presumption of PMVT as the etiology of the rhythm in today's case. Further information on the case was not available — so we never learned the cause of this malignant rhythm.

 

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Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #36 — Reviews some irregular wide tachycardia rhythms (with distinction between Torsades de Pointes vs Polymorphic VT discussed in Figure-3 on this post). 
• See My Comment in the June 1, 2020 post in Dr. Smith's ECG Blog — for review of Pleomorphic VT.
• Pleomorphic VT and Sudden Cardiac Death — Editorial by Liu and Josephson on potential mechanisms to explain the ECG appearance of Pleomorphic VT. 
• Case Report on BiDirectional VT — by Femenia et al on this patient with BiDirectional VT from CPVT (Catecholaminergic Polymorphic VT).
• ECG Blog #197 — Reviews the concept of Idiopathic VT (including recognition and treatment of Fascicular VT and RVOT VT).
• Multifocal vs Polymorphic VT — September 23, 2011 post from Dr. S. Venkatesan's insightful and user-friendly Cardiology Blog (from which I adapted his figures to derive my Figure-3).

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ADDENDUM (6/5/2021 - 8pm):

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Today’s ECG Media PEARL #48 (5:00 minutes Audio) — Reviews the ECG and clinical distinction between PolyMorphic VT (PMVT) vs Torsades de Pointes.