- David Didlake
Of Twists and Turns
Updated: Apr 29, 2022
David Didlake, NRP, APRN, ACNP-BC
Expert analysis provided by Dr. Ken Grauer
EMS is called to the main reception area of a retirement center where an elderly female is found down, unconscious and unresponsive. She has a palpable pulse at the radial arteries, bilaterally, with shallow respirations. This particular facility is situated for independent living, thus no medical providers are on site to provide pertinent details for medical history, medication intake, or remarkable events prior to the incident at hand. Moreover, front office staff advise that she is a new tenant, and thus have nothing more to offer than a name and assigned apartment number.
Physical exam shows no medical ID badges, or bracelets; no external insulin device; no dialysis fistulas, or grafts; no smell of alcohol; and no evidence of trauma. A prominent vertical scar, however, is noted at the sternum. Initial vital signs include:
HR 150-160 (trend)
RR 10 (spontaneous, but shallow)
SpO2 86 (RA)
The initial rhythm strip is attached:
There is a wide complex tachycardia of varying morphology, amplitude, and R-R cycle length. The rS configuration in Lead I displays a persistent rightward axis.
A 12 Lead ECG was then acquired:
The difficult reality of pre-hospital ECG’s is the absence of continuous telemetry at the bottom of the strip for purposes of discrete morphological juxtaposition in cases such as this. For example, at the end of Leads II and III there is apparent morphological change, which appears to sustain throughout the duration of Leads aVR / aVL / aVF, and most of V1-V3. At the end of the right precordial vicinity, there is another abrupt morphological change that appears to sustain for a few beats, then change – yet again – at the end of V4-V6.
This is clearly a multiform wide complex tachycardia, however any certainty related to the overall persistence of each identifiable morphologic entity is inconclusive – and as such, we’re unable to determine a specific etiology at this time.
As the patient was being prepped for transfer to EMS stretcher, another rhythm strip was captured:
Attending personnel were alarmed by the possibility of a “twisting at the points” (most dramatic in Lead I) eerily reminiscent of Torsade de Pointes, and prepared a Magnesium infusion while simultaneously attempting cardioversion:
100J of synchronized electricity was delivered with restoration to Sinus Rhythm. Unfortunately, a post-conversion 12 Lead was not acquired. The EMS narrative reports that her blood pressure and oxygenation improved modestly with rhythm stability for transport duration. Upon arrival at the receiving emergency department, however, she precipitously degenerated into VF and could not be resuscitated.
This case was originally posted to the EKG Club Facebook page, and Dr. Ken Grauer – the rhythm master – provided the following commentary, which I have reproduced here:
Expert analysis (Dr. Grauer)
Fascinating series of tracings. TRUE — We ALL know that ELECTRICITY was needed to treat this patient — but I still think it insightful (and educational) to work through the process of solving this rhythm.
I’ve reproduced 3 of the 4 parts of the case. ACKNOWLEDGMENT — I was not certain of all aspects of this rhythm until I saw the post-cardioversion tracing … (even though we ALL knew ELECTRICITY woud be needed). What makes this tracing difficult — is the lack of P waves, and not knowing what the baseline supraventricular QRS complex looks like. I initially thought the pointed negative deflection in lead II represented retrograde atrial activity (slanted BLUE lines in A) — though I couldn’t be sure that this wasn’t just part of what the wide QRS in lead II looked like.
A (TOP) = the 12-Lead ECG: I like to start with parts of the tracing that I’m pretty sure about = Beats #20-23 represent a 4-beat run of NSVT — as the all negative QRS in leads V4,5,6 virtually always indicates VT originating from the apex. As a result — beats #24,25,26 which look very different, are probably supraventricular. Working backward — beat #20 is probably a fusion beat (though the leads change right after beat #20 — so we really cannot prove fusion with an intermediate QRS morphology between beats #19 and 21.
B (MIDDLE) = 1st Rhythm Strip — is helpful. Beats #1-thru-7 manifest the same morphology as we saw in the 12-lead tracing (A) for leads I and II. The QRS is wide in B — but the rhythm is irregularly irregular with no sinus P waves — so this most probably represents rapid AFib with an atypical RBBB/LPHB morphology. Beat #8 in B is a FUSION beat — as both QRS and T wave morphology of beat #8 is intermediate between supraventricular beat #7 — and ventricular beats #9-11 (this is best seen in lead II of B). Then beat #12 at the end of the run is again of intermediate morphology, therefore another FUSION beat. Beat #18 is also a fusion beat.
Proof of the above is seen in the post-cardioversion tracing ( = C = BOTTOM) — as RED arrows confirm conversion to sinus rhythm. We now see that QRS morphology in lead II during sinus rhythm is similar to the QRS morphology in lead II during rapid AFib (beats #1-5 in lead II in A). The QRS is now narrower in C post-cardioversion — because the rate-related LPHB (deep S in beats #1-5 in A) has resolved at the slower rate. I think (but can’t be sure without see a lead V1 post-cardioversion) that the RBBB is still present. So, the rhythm initially was rapid AFib with an atypical RBBB/LPHB conduction pattern — that was interrupted by runs of NSVT.
Additional analysis (Didlake)
I would like to add a few observations from the Figure 3 telemetry strip, specifically, reproduced here with markings:
As already discussed by Dr. Grauer, the initial portion is most likely rapid AFib with conduction delay in the left posterior fascicle to account for rightward frontal plane axis. What corroborates an initial supraventricular mechanism is the narrow, and sharply deflected, r-wave (first green arrow) in Lead I, suggesting rapid initial antegrade spread through the natural conduction system. This r-wave then becomes much wider (second green arrow, Lead I) to suggest a slower activation sequence – specifically, cell-to-cell electrical transmission consistent with ventricular origin.
In Lead II the horizontal blue line isolates a certain morphology, followed by an orange arrow of demonstrable configuration transition. The black line then shows a completely different sustained morphology (most apparent in Lead I). As previously mentioned, the attending EMS crews interpreted this to be a Torsades-like “twisting of the points,” but closer inspection at the granular level will manifest a certain nuance to potentially suggest something different.
In general, monomorphic VT has a single, stable QRS morphology. Polymorphic, or multiform, VT has a changing QRS morphology. The polymorphic category of VT can be further subdivided into Torsades de Pointes (TdP), Polymorphic VT (PVT, i.e. Non-Torsades), Bidirectional, and Pleomorphic. 
Concerning TdP versus PVT
Josephson reports that Torsades is a unique term usually reserved for clinical syndromes of polymorphic VT attributed to reversible causes of QT prolongation, including 1) medication use, 2) electrolyte depletion [e.g. hypokalemia, hypomagnesemia], and/or 3) CNS dysfunction. Critical to diagnosis is a baseline 12 Lead ECG recorded during Sinus Rhythm that confirms QT prolongation when adjusted for heart rate – otherwise known as the QTc. Unfortunately, today’s case is lacking any such diagnostics, thus I cannot say with certainty that the QT interval is, or is not, culpable in arrhythmogenesis. 
The morphology of PVT closely mirrors that of TdP but the underlying mechanism differs from reversible QT prolongation. In most cases, rather, the culprit is gross ischemia due to myocardial infarction, cardiomyopathy, or advanced coronary artery disease. A unique subset of PVT is induction via inherited channelopathy – sodium channel dysfunction in Brugada Syndrome, calcium mishandling at ryanodine receptors within the myocyte sarcoplasmic reticulum in cases of catecholamingeric PVT, or irreversible QT prolongation (e.g. genes implicated in congenital Long QT syndrome, such as SCN5A and KCNQ1). [1-3, 5]
As an aside, recall that a horizontal scar was identified on the patient’s sternum during rapid physical exam, thus eluding to prior corrective open thoracic surgery of some magnitude, to potentially include coronary artery bypass grafting, or valve replacement, for example. This finding might favor a diagnosis of ischemic-driven PVT.
Literature review yields noteworthy descriptors of TdP and PVT behavior on the ECG. There is uniform agreement on the pattern of shifting QRS axis (aka, twisting of the points) with undulations of varying amplitude. More interestingly, however, is the repetitious mention of grossly irregular cadence and an overall configuration that is uncharacteristic of classic QRS, or T wave, morphology. Said differently, in both TdP and PVT it is often difficult to reliably distinguish the QRS, or T waves. This begets morphology that is “ugly” and changes dramatically from one beat to the next. [4-6]
In figures 1-4, specifically during the episodes of NSVT, there is a mostly regular cadence with preserved definition of both QRS and T.
A case for pleomorphism
Josephson elucidated the concept of pleomorphism during electrophysiological study of patients with recurrent, sustained ventricular tachycardia. This is a circumstance in which there exists a single focus of arrhythmogensis, yet conducts through multiple exit sites and/or experiences shifting conduction properties for arrhythmia duration. This manifests on the ECG as morphological alternations between RBBB and LBBB, as well as dramatic swings in frontal plane axis, while maintaining overall regularity and cadence. It was postulated that such an ECG feature is associated with advanced myocardial dysfunction, to include left ventricular aneurysm, as the cause of arrhythmia. 
Liu later proposed that a favorable suggestion of pleomorphic VT from a single exit site – as opposed to interplay between two distinct circuits – is a relatively consistent cycle length during morphological change. This is in stark contrast to TdP, or PVT, which has been reported to be grossly irregular. 
In Figure 3, there is an overall consistency in R-R cycle length despite morphological change, and thus satisfying the Liu proposal for pleomorphism.
By process of elimination, we can deduce that this episodic VT is not monomorphic, or bidirectional, in nature. It fails to satisfy criteria for TdP, or PVT, for reasons already posited. I favor a diagnosis of Pleomorphic VT with multiple exit sites from a single focus, or alternating conduction properties for arrhythmia duration, because there is surprising QRS regularity with only gradual change in morphology – as opposed to a grossly irregular pattern (with constant morphology change) that would be expected in TdP, or PVT.
Be sure to check out this post from Dr. Grauer on the Smith ECG Blog:
Take a deep dive into the management of TdP versus PVT with Dr. Smith:
 Callans, D. J. (2021). Josephson’s Clinical Cardiac Electrophysiology: Techniques and Interpretations (6th ed). Chapter 10: Recurrent Ventricular Tachycardia (pg. 451-651). Wolters-Kluwer: Philadelphia, PA.
 Viskin, S., et al. (2021). Polymorphic ventricular tachycardia: Terminology, mechanism, diagnosis, and emergency therapy. Circulation, 144; 823-839.
 Murphy, M. A., et al. (2017). The athlete with catecholaminergic polymorphic ventricular tachycardia. American College of Cardiology: Expert Analysis.
 Surawicz, B. & Knilans, T. K. (2008). Chou’s Electrocardiography in Clinical Practice (6th ed). Chapter 17: Ventricular Arrhythmias (pg. 405-439). Elsevier-Saunders: Philadelphia, PA.
 Strauss, D. G. & Schocken, D. D. (2021). Marriott’s Practical Electrocardiography (13th ed). Chapter 17: Ventricular Arrhythmias (pg. 370-390). Wolters-Kluwer: Philadelphia, PA.
 Goldberger, A. L., et al. (2018). Goldberger’s Clinical Electrocardiography: A Simplified Approach (9th ed). Chapter 16: Ventricular Arrhythmias (pg. 156-171). Elsevier: Philadelphia, PA.
 Josephson, M. E., et al. (1979). Recurrent sustained ventricular tachycardia: Pleomorphism. Circulation, 59(3); 459-468.
 Liu, E., et al. (2011). Pleomorphic ventricular tachycardia and risk for sudden cardiac death. Circulation: Arrhythmia and Electrophysiology, 4; 2-4.