Sunday, April 22, 2018

ECG Blog #151 (WCT - VT - SVT - AV Dissociation - Ashman)

A 47-year old man presented with a history of intermittent dizziness over the previous two days. No chest pain. BP = 110/60 mmHg at the time his initial ECG was obtained (Figure-1).
  • How would you interpret the rhythm?
  • Is this an example of the Ashman phenomenon?
  • Is there any clue to a possible etiology for this patient’s arrhythmia?
Figure-1:Initial 12-lead ECG obtained from a 47-year old man with dizziness for 2 days. What is going on? NOTE — Enlarge by clicking on the Figure.
Interpretation: The ECG in Figure-1 is divided into 2 parts, with each part displaying 6 simultaneously-recorded leads for a monitoring period of 5 seconds. We begin with assessment of the rhythm.

PEARL: When the arrhythmia in front of you is complex, with more than a single element — Look first to see IF there is an underlying rhythm!
  • Question: Is there an underlying rhythm in Figure-1? If so — Can you tell what the rate of this underlying rhythm is?
NOTE: For clarity — we have labeled the beats, and added RED arrows over selected atrial activity (Figure-2).
Figure-2:We have numbered the beats, and added RED arrows to Figure-1, to highlight atrial activity in several leads (See text).
Rhythm Assessment: There are 2 different shapes of QRS complexes in this tracing. The narrower QRS complexes are followed by short runs of wider beats. That said, the underlying rhythmis sinus — as suggested by the presence of an upright P wave with fixed PR interval preceding beats #1 and #6 in lead II.
  • We see 2 sinus beats in a row in lead V1. The R-R interval between beats #1 and 2 in this lead suggests an underlying sinus rate of ~70/minute. NOTE: It is often extremely helpful to determine the underlying sinus rate when looking for clues to the etiology of a complex arrhythmia (as we will see momentarily).
  • In the limb leads (ie, leads I,II,III; aVR,aVL,aVF) — each sinus beat is followed by a run of 4 fairly (but-not-completelyregular wide beats at a rate of ~150/minute.
  • In the chest leads, following 2 sinus beats — there is a run of 8 wide beats. It is more easily apparent that this 8-beat run is not completely regular.
Question: Are the runs of wide beats VT (Ventricular Tachycardia)? Or, do these runs reflect SVT (SupraVentricular Tachycardia) with aberrant conduction?
  • Is this the Ashman phenomenon?
Are the WCT (Wide-ComplexTachycardia) runs VTMany criteria have been described for distinction between WCT rhythms that are due to VT vs SVT with either preexisting BBB (Bundle Branch Block) or aberrant conduction.
  • We summarize the approach we favor for distinction between VT vs SVT with aberrancy or preexisting BBB in our ECG Blog #42. We highlight some key points from Blog #42 in the bullets below.
  • Monomorphic VT is usually a regular (or at least fairly regular) rhythm. That said, there clearly may be some irregularity with VT. Appreciation of the general rule that VT is usually at least fairly regular, is helpful — because the presence of a completely irregular rhythm would strongly suggest AFib (Atrial Fibrillation) rather than VT. QRS widening may be seen with AFib due to preexisting BBB — aberrant conduction — or WPW (Wolff-Parkinson White Syndrome). That said, despite irregularity for portions of the WCT runs in Figure-2 — the overall rhythm for these WCT runs is still regular enough in most places to be consistent with VT. Our feeling is therefore that the regularity of the rhythm in Figure-2 is not helpful for determining its etiology.
  • On the other hand, QRS Morphology for the wide beats in Figure-2 — strongly suggests VT! The WCT run in lead V1 (ie, beats #3-8 in this lead) is consistent with a RBBB (Right Bundle Branch Block) pattern that could be supraventricular. And, there is enough of a wide terminal S wave in both leads I and V6 to also be consistent with RBBB. However, there is extreme axis deviation in the frontal plane (in the form of all negative QRS complexes in each of the inferior leads). Lack of any r wave at all in either lead I or lead aVF qualifies as “extreme” axis deviation — and this finding is highly suggestive of a ventricular etiology. Resemblance in the above noted leads to a RBBB pattern suggests that this is a Fascicular VT, with origin near the left posterior hemifascicle.
  • Statistically, VT is far more common than wide tachycardia due to a supraventricular etiology. Especially in view of extreme axis deviation for the wide beats in this case — the WCT runs in Figure-2 should be assumed VT and treated accordingly until proven otherwise.

NOTE: There is 1 more clue in Figure-2 that virtually confirms our impression. 
  • HINT: Look at the RED arrows …
ADissociation: AV Dissociation is said to occur when “on time” P waves are not related to neighboring QRS complexes. This phenomenon may be transient (occurring for as little as a single beat) — or persistent (as occurs when there is complete AV block). The diagnostic value of recognizing AV dissociation in a WCT rhythm — is that it virtually proves the rhythm to be VT, since if “on time” P waves are not being conducted to produce the regularly-occurring wide complexes, then these wide beats must be arising from below the AV node (See ECG Blog #133).
  • The problem is that most of the time when confronted with a WCT rhythm of uncertain etiology — the rateof the WCT will be too fast to allow us to reliably detect underlying sinus P waves. Therefore, you will not often see AV Dissociation in faster VTs, which are the VTs that challenge our diagnostic abilities.
  • In our experience — AV Dissociation is overdiagnosed. There is a tendency to think AV dissociation is present whenever one sees “extra deflections” in a WCT rhythm. The clinical reality, is that artifact rather than true AV dissociation is the usual cause of these deflections. As a result — we favor undercalling AV dissociation — and reserve use of this criterion for those cases in which we are convinced of its veracity.
We believe AV Dissociation is present in Figure-2. If so, this proves that the WCT runs are VT.
  • Recall how we emphasized the importance of identifying 2 sinus-conducted beats in a row — as we see for the first 2 beats in lead V1 (first 2 RED arrows in this lead). This tells us that the P-P interval for sinus P waves is just over 4 large boxes, which corresponds to an underlying sinus rate ~70/minute.
  • Setting our calipers to precisely this P-P interval — the notch that is highlighted by the 3rd RED arrow in lead V1 occurs right on time! This 3rd P wave in lead V1 therefore manifests AV dissociation.
  • That this is not due to chance can be seen in leads I and aVL in the limb leads, where on-time notching occurs after sinus P waves (RED arrows). Admittedly, we cannot “walk out” underlying atrial activity throughout the entire rhythm strip (You often will not with VT rhythms be able to “march out” underlying sinus P waves throughout the entire tracing) — but we feel the occurrence of on-time notching highlighted by the RED arrows is not due to chance.
  • NOTE: You are unlikely to ever pick up AV dissociation in a WCT rhythm unless you use calipers
Is the Ashman Phenomenon present in Figure-2? The Ashman Phenomenon is based on the fact that the refractory period (and therefore, also the relative refractory period) is dependent upon the preceding R-R interval. Slowing of the rate by a relative pause in the rhythm will therefore lengthen the relative refractory period of the next beat. This makes it most likely that the 1st beat after a relative pause will conduct with aberration (See ECG Blog #70).
  • In our experience — the Ashman Phenomenon is often misused. This phenomenon may be invaluable in the context of other clues that support a diagnosis of aberrant conduction. But it should not be used alone. In Figure-2, despite onset of WCT runs following a relative pause in the rhythm — the finding of extreme axis deviation + AV dissociation + lack of a premature P wave initiating the wide runs, combine to overwhelmingly favor VT as the diagnosis.
Finally: There is 1 more component of Figure-2 that we have not yet analyzed. What is it?

Answer: After assessing the cardiac rhythm — we need to evaluate sinus-conducted beats on this 12-lead ECG for possible acute changes. We therefore discipline our eye to focus on QRST morphology for beats #1 and 6 in the limb leads — and for beats #1 and 2 in the chest leads.
  • All 3 inferior leads (II, III, aVF) show Q Waves, ST segment coving with slight elevation, and T wave inversion. Although lead aVL does not show reciprocal ST depression — it does show ST segment flattening, which is not quite normal. Our impression is that recent (possibly acute) inferior STEMI is likely. 
  • In the chest leads — the very deep S wave in lead V2 (nearly 25mm deep) suggests voltage for LVH.
  • The takeoff of the ST segment in lead V3 is straight. It becomes coved in lead V4. Moderate-to-deep T wave inversion is seen in leads V3-thru-V6. This picture clearly suggests ischemia, which could be acute.
  • NOTE: The above ECG findings that strongly suggest a recent or acute cardiac event provide yet another reason in favor of the WCT runs being VT — as VT is much more likely to occur than aberrant SVT in the setting of acute ischemia or infarction.
FOLLOW-UP: It turned out that this patient had severe underlying coronary disease. The inferior infarction was found to be old — though there was no way to know this from assessment of this patient’s initial ECG that we saw in Figure-2. The runs of VT responded to medical therapy with amiodarone.
Acknowledgment: My thanks to MG for his permission allowing me to use this tracing and clinical case.
NOTE: The following blogs provide more information on topics mentioned in this case.
  • Our approach for distinction between VT vs SVT with either aberrant conduction or preexisting BBB — See ECG Blog #42.
  • For review of the Ashman Phenomenon  See ECG Blog #70.
  • For review of AV Dissociation  See ECG Blog #133.
  • For review of Fusion Beats  See ECG Blog #128.

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