ECG Interpretation: ECG Blog #263

The patient is a middle-aged man with a history of valvular heart disease — who presented to the ED (Emergency Department) with the ECG shown in Figure-1. The patient was hemodynamically stable at the time this tracing was obtained.

HOW would you interpret this tracing?
Is the rhythm VT? — What would YOU do?

Figure-1: Initial ECG obtained in the ED from a middle-aged man with valvular heart disease. He was hemodynamically stable (See text).

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NOTE #1: Some readers may prefer at this point to listen to the 12:20 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-13a).

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Today's ECG Media PEARL #13a (12:20 minutes Audio) — reviews "My Take" on assessing the regular WCT (Wide-Complex Tachycardia) — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

MY Approach to the Rhythm in Figure-1:

We are told that the patient was hemodynamically stable at the time the ECG in Figure-1 was obtained. Therefore, by definition — we have at least a moment-in-time to assess the rhythm before having to decide on treatment. I favor the Ps, Qs & 3R Approach (Reviewed in ECG Blog 185).

Regarding the Ps, Qs & 3Rs: The rhythm in today's tracing is Regular — with a wide QRS — at a Rate of ~180/minute.
Sinus P waves are absent (So regarding the 5th parameter — there are no sinus P waves to be "Related" to the QRS). That said — there may be retrograde atrial activity (See below).
Therefore — There is a regular WCT ( = Wide-Complex Tachycardia) at ~180/minute, without clear sign of sinus P waves.

KEY Points in the Differential Diagnosis:

Once you have taken a quick look at your patient, to ensure that he/she is hemodynamically stable (and not in need of immediate synchronized cardioversion) — it should take NO more than ~10 seconds to work through the answers I provide for the above 3 bullets, with conclusion that the rhythm is a regular WCT.
Statistically — between 80-90% of all regular WCT rhythms without clear sign of sinus P waves will turn out to be VT (Ventricular Tachycardia). As a result — one should always assume the rhythm is VT until proven otherwise. That said — Since the patient in this case is hemodynamically stable, it is reasonable to look closer at the rhythm to see if additional clues might be present to further assist in your differential diagnosis.
IF at any time during the diagnostic process your patient's hemodynamic status deteriorates — Be ready to immediately cardiovert! Clearly, in order to assess this — "Ya gotta be there". But on reading this case as it was presented to me — I wanted to look closer (Please be sure to check out the above Audio Pearl in today's post for a detailed look at the diagnostic process that I favor).

QRS Morphology:

Although true that the great majority of regular WCT rhythms without sinus P waves will turn out to be VT — 10-20% of such rhythms will not be VT. The finding of a QRS morphology that is typical for supraventricular conduction greatly increases the likelihood that either preexisting BBB (Bundle Branch Block) or aberrant conduction is the cause of the wide tachycardia! (See ECG Blog #211 for detailed discussion regarding aberrancy with RBBB conduction).
I've outlined in RED several KEY features of QRS morphology in today's case (Figure-2). The "Bottom Line" (See Figure-5 in the ADDENDUM below!) — is that QRS morphology for the regular WCT rhythm seen in Figure-2 strongly suggests a supraventricular etiology with RBBB (Right Bundle Branch Block) conduction because: i) There is an rSR' complex in lead V1 with small-but-present initial positive deflection (r wave) — and — the S wave in lead V1 descends below the baseline — with terminal, taller right "rabbit ear" positive deflection; ii) There are wide, terminal S waves in lateral leads I and V6, as is consistent with RBBB conduction; iii) There are slender (rapidly rising) and fairly tall initial R waves in each of the lateral leads (ie, leads I, aVL, V4,V5,V6) — whereas VT tends to manifest a slower initial QRS deflection; and, iv) In addition to typical RBBB conduction morphology — the predominantly negative QRS deflection in each of the inferior leads is typical for LAHB (Left Anterior HemiBlock) conduction.
KEY Point: While certainly still posible that the regular WCT rhythm in Figure-2 is the result of Fascicular VT— the above cited morphologic features in favor of supraventricular conduction significantly reduce statistical likelihood of VT from 80-90% — to a much lower figure. MY Thoughts: While I suspected that the rhythm in today's case was not VT — I fully acknowledge that I was not certain.

PEARL #1: It's important to appreciate the clinical reality that you often will not know with certainty the etiology of a wide tachycardia at the time that you need to begin treatment. This is OK. In such cases — Begin treatment based on your best hunch as to what you think the rhythm is.

PEARL #2: It is difficult to "second guess" any of a number of potential therapeutic options that might be selected for today's case. Simply stated — there is more than a single potentially appropriate medication that might be initially tried. That said — IF your principal differential diagnosis is between Fascicular VT vs an SVT with either preexisting BBB or aberrant conduction — Realize that IV Verapamil (and/or IV Diltiazem) has a good chance for being effective in controlling either of these diagnostic possibilities (See ECG Blog #197 for detailed discussion of this topic).

Figure-2: I've labeled key features from Figure-1 regarding today's case (See text).

Rapid Estimation of the Heart Rate:

How close did YOU come to 180/minute as your rate estimation for the WCT rhythm shown in Figure-2? The reason accurate estimation of the heart rate is important — is that the etiology of various SVT rhythms will often be suggested by the heart rate (See ECG Blog #240 for review of this concept).

Figure-2 illustrates use of the Every-Third-Beat Method for rapid estimation of heart rate (this method discussed in full in ECG Blog #210). It takes approximately 5 large boxes (BLUE numbers in lead V1 of Figure-2) — to record 3 beats (RED numbers). Therefore — 1/3 of the rate is ~300 ÷ 5 = 60/minute X 3 ~180/minute. NOTE: With practice — you can accurately estimate the rate of tachycardias in less than 5 seconds!

Is there Atrial Activity in Figure-2?

Normal sinus P waves are not seen in Figure-2 — because we do not see any clearly defined upright P wave in lead II. But there is suggestion of possible retrograde P waves in several leads (light BLUE arrows in leads III, aVL and aVF in Figure-2). The fact that the deflections in question appear to be negative in 2 inferior leads is consistent with retrograde conduction.

As interesting as the possibility of retrograde atrial conduction is — I was not certain this was a "real" finding. This is because several of the other leads that usually show retrograde atrial activity do not manifest any deflection consistent with this hypothesis (ie, I saw nothing suggestive of retrograde P waves in leads II, aVR and V1).
PEARL #3: Even IF the light BLUE arrows in Figure-2 do represent retrograde atrial conduction — this does not help with our differential diagnosis because both VT and reentry SVT rhythms may manifest 1:1 retrograde conduction. VT is favored by identifying atrial activity during a WCT rhythm only when there is AV dissociation (See ECG Blog #151).

WHY is QRS Morphology Changing in the Long Lead II?

Did YOU notice continual change in QRS morphology in the long lead II rhythm strip in Figure-2? Although other leads show much less variation in QRS morphology — there is no denying the beat-to-beat variation in QRS morphology that we see in the long lead II rhythm strip! There are several possible explanations for this change:

The variation in QRS morphology could be the result of respiratory variation — which is commonly seen in acutely ill patients (especially if they are tachycardic and/or short of breath).
The primary difference in QRS morphology that we see in the long lead II rhythm strip relates to the depth of the S wave. Perhaps there is intermittent LAHB conduction?
The change in QRS morphology might reflect electrical alternans! (See ECG Blog #83 for full discussion of this phenomenon). In support of this theory — is the finding that T waves also vary in morphology throughout the long lead II rhythm strip. Although most cases of electrical alternans that I have seen manifest 2:1 beat-to-beat variation — other recurring ratios are possible (ie, 3:1, 4:1, etc) — and this seems to be the case in Figure-2.
BOTTOM LINE: Without additional ECG monitoring (especially in the moments during and immediately after conversion to sinus rhythm) — it is difficult to prove that the variation in QRS and T wave morphology evident in the long lead II of Figure-2 represents electrical alternans. The reason recognition of electrical alternans may be helpful in the diagnosis of tachyarrhythmias — is that this finding favors AV nodal reentry as the mechanism (especially AV nodal reentry involving an accessory pathway). That said — a number of other (non-arrhythmia related) clinical conditions have been associated with electrical alternans — and — among arrhythmias, electrical alternans has been seen on occasion with monomorphic VT — so this phenomenon is not necessarily diagnostic of an SVT etiology.

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Follow-Up in Today's Case:

The clinical course of today's case was challenging — and included trial of a number of medications (ie, Adenosine, Amiodarone, Diltiazem, Propafenone). Ultimately — the rhythm was controlled. A post-conversion ECG is shown in Figure-3.

QUESTION: What conclusions can be made from Figure-3 about the etiology of the regular WCT rhythm in the initial ED tracing?

Figure-3: Comparison of the initial ED tracing ( = ECG #1) — with the post-conversion tracing ( = ECG #2).

ANSWERS & DISCUSSION:

The post-conversion tracing in Figure-3 shows sinus bradycardia with a prolonged PR interval (of ~0.34 second), most likely secondary to antiarrhythmic medication needed to control the tachycardia.

The marked amount of PR interval prolongation will need to be carefully monitored as longterm antiarrhythmic medication decisions are made.
QRS morphology in sinus rhythm (ie, in ECG #2) is identical to QRS morphology during the wide tachycardia (in ECG #1). Specifically — there is an rSR' (with descent of the S wave below the baseline — and taller right "rabbit ear" terminal deflection) in lead V1 — with wide terminal S waves in lateral leads I and V6 — and — predominantly negative QRS complexes in each of the inferior leads. This QRS morphology is completely consistent with RBBB/LAHB conduction. The fact that QRS morphology during the WCT and after conversion to sinus rhythm is identical proves that the etiology of the regular WCT in today's case was supraventricular!
NOTE #1: The reason the QRS was wide in the initial ED tracing was preexisting BBB (ie, RBBB/LAHB) — and not "aberrant conduction". Aberrant conduction is a rate-related phenomenon that should only be invoked as the cause of QRS widening if the QRS becomes narrow once the tachycardia resolves.
NOTE #2: In the post-conversion tracing in Figure-3 — We no longer see the deflections that occurred just after the QRS in Figure-2 (highlighted by light BLUE arrows in that figure). This suggests that these deflections did in fact represent retrograde atrial conduction during the tachycardia — in this case, as a result of a reentry SVT rhythm (either AVNRT or orthodromic AVRT).
NOTE #3: The beat-to-beat variation in QRS morphology that was seen in the long lead II rhythm strip during the tachycardia is no longer evident in the post-conversion tracing. IF this beat-to-beat variation in QRS morphology resolved promptly after conversion to sinus rhythm — it would confirm my suspicion that this represented electrical alternans — in today's case, as a result of the reentry SVT.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
ECG Blog #211 — WHY does Aberrant Conduction occur? (And why the most common form of abverrant conduction manifests RBBB morphology — with an ECG Video on this topic in this post).
ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm.
ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types.
ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD).
ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Video Pearl #21 in this blog post.
ECG Blog #220 — Reviews My List for the Causes of a Regular WCT Rhythm (with Audio Pearl on assessing for hemodynamic stability).
ECG Blog #240 — Reviews the Case of a Regular SVT (SupraVentricular Tachycardia) Rhythm — with emphasis on how Rate of the rhythm may help in SVT diagnosis.
ECG Blog #151 — Reviews a Case of a wide tachycardia in which identification of AV Dissociation facilitated the diagnosis of VT!
ECG Blog #83 — Reviews ECG recognition and clinical significance of Electrical Alternans.