ECG Blog #409 — Every-Other-Beat ...

 

The ECG in Figure-1 —  was obtained from a patient with palpitations. The patient was hemodynamically stable in association with this rhythm.

QUESTIONS:

• What is the rhythm in Figure-1? 
•   — How certain are you of your answer? 
• 
  
•      —  Why is QRS morphology changing? 

Figure-1: The initial ECG in today's case.

My Interpretation of the ECG in Figure-1:

Since the patient is hemodynamically stable — there is time for systematic assessment of the rhythm. By the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm is fast and QRS complexes are Regular. Since the R-R interval is just under 2 large boxes in duration — I estimate the ventricular Rate to be just over 150/minute.
• 
  
• QRS morphology varies every-other-beat! This is perhaps best seen in lead V1 (but also well seen in leads V3,V4,V6). The QRS is narrow in odd-numbered beats (but the QRS is wide in even-numbered beats).
• 
  
• Sinus P waves appear to be absent — because we do not see a clearly defined upright P wave in lead II. Instead — a negative deflection appears to precede each QRS complex in lead II (and we can see this negative deflection in front of each of the 26 beats in the long lead II rhythm strip).
• 
  
• PEARL #1: Although we know these negative deflections in front of the QRS are not sinus P waves (because, as noted above — these deflections are not upright in lead II) — there does appear to be a fixed interval (distance) between these negative deflections and the QRS complex that follows. This suggests these negative deflections represent some other form of atrial activity (that by the 5th parameter in the Ps,Qs,3R Approach) — is Related to neighboring QRS complexes.

Putting It All Together:

By the Ps, Qs, 3R Approach — We have determined that the rhythm in Figure-1 manifests regular QRS complexes at a rate just over 150/minute — with some form of atrial activity that is related to neighboring QRS complexes.

• But WHY is QRS morphology changing every-other-beat? (ie, being narrow for one beat — and then becoming wide for the next beat)?
•   —  Is the rhythm in Figure-1 supraventricular?
•      — What kind of atrial activity is likely to be present? 

PEARL #2: The obvious initial consideration whenever we see wide beats — is that the etiology of such beats may be ventricular. That said (as per PEARL #1) — the fact that each of the 26 beats in the long lead II rhythm strip in Figure-1 are preceded by a negative deflection with a fixed interval between this negative deflection and the QRS complex that follows (BLUE arrows in the long lead II in Figure-2) — is against these wide beats being ventricular in etiology.

• IF the wide beats were ventricular — we would not expect the interval from the negative deflection preceding each QRS to be equal.
• Instead — the fact that the interval from the negative deflection preceding each of the 26 beats in the long lead II rhythm strip remains constant — suggests that each of these 26 beats are being conducted by whatever form of atrial activity these negative deflections represent.

PEARL #3: QRS morphology of the wide beats strongly supports our presumption that all 26 beats in today's initial ECG are supraventricular! (Figure-2).

• QRS morphology of beats #14,16,18 in lead V1 is consistent with RBBB (Right Bundle Branch Block) conduction — because there is an rsR’ morphology, with S wave descending below the baseline and a taller R’ (right-“rabbit ear” deflection).
• QRS morphology of beats #2,4,6 in lead I — and, beats #8,10,12 in lead aVL support RBBB conduction — because these lateral leads each manifest a slender, upright R wave with wide terminal S wave (RED arrows in these leads).
• 
  
• Finally (as shown in Figure-2) — Note that the wide beats in the inferior leads (especially in lead II) manifest a more marked leftward axis, consistent with LAHB (Left Anterior HemiBlock) aberration — which is yet another suggestion that all wide beats are supraventricular!

Figure-2: I've labeled the initial ECG in today's case.

PEARL #4: As emphasized in ECG Blog #204, in which I review derivation of the bundle branch blocks — RBBB is a terminal conduction delay. By this I mean that the initial vectors of ventricular depolarization occur normally when there is RBBB — and only the last part of ventricular depolarization is altered with this conduction defect.

• As a result — the IVS (InterVentricular Septum) and the LV (Left Ventricle) depolarize normally with RBBB conduction — and it is only after the LV has depolarized that the RV (Right Ventricle) now depolarizes via slow conduction through ventricular myocardium (because of the "block" in the right bundle branch). This results in terminal depolarization moving toward the “blocked” RV — which writes a wide, terminal S wave in left-sided leads (with this S wave being wide with complete RBBB — because conduction through myocardium is slow). 
•  
• KEY Point: Awareness that RBBB is a terminal conduction delay, with the initial vectors of ventricular depolarization being normal — may provide yet another clue that widened QRS complexes are aberrantly-conducted supraventricular beats. This concept is perhaps best illustrated for the wide beats in lead V1 of Figure-2 — in which the shape and slope of the tiny initial r-wave, followed by S wave descent in lead V1 looks identical in shape and slope to the beginning deflections of the narrow beats in this lead. 

Advanced PEARL #5 ( = Beyond-the-Core): Did YOU notice that there appears to be a technical “misadventure” in today's initial ECG — in that the QRS complex does not look as one should expect with RBBB conduction for the wide beats in lead V6? (ie, for beats #20,22,24,26 in lead V6 of Figure-2).

• To Emphasize — that this technical mishap is an extremely subtle finding that I did not notice when I first looked at the initial ECG in today’s case. But since RBBB conduction is the result of a terminal delay in ventricular repolarization — there should be a wide, terminal S wave for wide beats #20,22,24,26 in lateral chest lead V6. Instead, there is a fragmented, all-positive QRS complex in lead V6 without any terminal S wave.
• 
  
• My Theory: I suspect that the V6 lead connection may have inadvertently been reversed with the lead connection for either V4 or V5.

===================

CONTINUED: Putting It All Together:

Now that we’ve established that all 26 beats in today's initial ECG are supraventricular — We can deduce the following:

• There is RBBB conduction every-other-beat in Figure-2. This is a form of rate-related BBB — in which the rapid ventricular rate may not allow sufficient time between each beat for the right bundle branch to recover.
• Usually, rate-related BBB produces QRS widening with every beat — but on occasion, BBB conduction may only occur every-other or every-third beat.
• 
  
• This means that the rhythm in today's initial tracing — is a regular SVT (SupraVentricular Tachycardia) rhythm at ~150/minute, but without clear sign of sinus P waves. PEARL #6 below reviews the differential diagnosis:

PEARL #6: As discussed in ECG Blog #287 — Recognition that the rhythm in today's initial tracing is a regular SVT without clear sign of sinus P waves (ie, without a definite upright P wave in lead II) — should prompt consideration of the following differential diagnosis LIST:

• i) Sinus Tachycardia (IF there is a possibility that sinus P waves might be hiding within the preceding ST-T wave); 
• ii) A Reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an AP [Accessory Pathway] located outside the AV node is involved); 
• iii) Atrial Tachycardia (ATach);
• iv) Atrial Flutter (AFlutter) with 2:1 AV conduction. 

PEARL #7: By far (!) — the most commonly overlooked entity in the above differential diagnosis LIST is AFlutter (Atrial Flutter) — especially when the ventricular rate is close to ~150/minute (as it is in today's case) — and — when there appear to be negative deflections (rather than upright P waves) in lead II.

• The reason the ventricular rate in untreated AFlutter tends to be close to 150/minute — is that the atrial rate of flutter in patients not on antiarrhythmic medication (that might reduce the flutter rate in the atria) — tends to be very close to 300/minute in adults (ie, usual range ~250-350/minute). 
• Since the most common ventricular response to untreated AFlutter is with 2:1 AV conduction — this results in a ventricular rate HALF as fast as the flutter rate in the atria — and 300 ÷ 2 ~150/minute (usual range ~130-170/minute).
• 
  
• KEY Point: Knowing that the most commonly overlooked arrhythmia is AFlutter — suggests that the BEST way to avoid missing the diagnosis of AFlutter is simply to THINK of AFlutter whenever you have a regular SVT at a rate close to 150/minute (in which you do not clearly see upright sinus P waves in lead II).

PEARL #8: Using calipers facilitates finding the diagnostic "sawtooth" pattern of AFlutter. When looking for AFlutter — I simply set my calipers at precisely HALF the R-R interval — and then look for leads in which I can "walk out" 2:1 conduction.

• I have done this in Figure-3 — in which slanted RED lines in the long lead II rhythm strip highlight negative dips in the baseline that occur at precisely twice the ventricular rate. This corresponds to an atrial rate of ~300/minute (P-P interval ~1 large box in duration).
• The "sawtooth" pattern of the baseline with AFlutter is best appreciated by stepping back a little bit from the rhythm strip. The pattern is best seen in the inferior leads ( = leads II,III,aVF). The other leads that most often manifest readily identifiable 2:1 atrial activity — are leads aVR, V1 and/or V2 — so I favor first checking out these 6 leads whenever looking for AFlutter.
• 
  
• Physiologically — the most commonly observed pattern of AFlutter, known as "Typical" AFlutter — produces 2:1 negative deflections seen in the inferior leads (as seen in Figure-3) — as a result of CCW (CounterClockWise) rotation of a fixed reentrant circuit around the tricuspid valve annulus and through the cavo-tricuspid isthmus. 
• "Atypical" AFlutter patterns may occasionally be seen, in which the rotation direction of the reentrant pathway around the tricuspid valve annulus changes to CW (ClockWise) — in which case smaller positive deflections may be seen.
• Clinically: Initial treatment of AFlutter is the same, regardless of whether the rotation direction is CW or CCW — so this distinction is not important to the emergency provider (Cosio — Arrhythmia & EP Review 6(2):55-62, 2017). The point to remember is that IF you are able to identify regular 2:1 atrial activity at an atrial rate close to 300/minute (with a P-P interval ~1 large box in duration) — then the rhythm is almost certain to be AFlutter.

The CASE Continues:

The patient was treated with IV Amiodarone — which (as shown in Figure-3) successfully converted the AFlutter into normal sinus rhythm.

• Although significant baseline artifact is seen in ECG #2 — regular upright sinus P waves can be seen in the long lead II rhythm strip.
• RBBB is no longer seen after conversion to sinus rhythm — which supports our suspicion that the intermittent RBBB conduction seen every-other-beat during the tachycardia (in Figure-1) was rate-related.
• Note that QRS morphology after conversion to sinus rhythm is very similar to QRS morphology of odd-numbered beats during the tachycardia.
• Note also that modest T wave inversion persists after conversion to sinus rhythm (seen in leads III; and in V1-thru-V4). This most likely reflects a transient and benign "Memory" effect (ie, Not uncommonly — non-ischemic ST-T wave abnormalities may be seen for hours or even days following a sustained tachycardia).

Figure-3: Slanted RED lines in the long lead II rhythm strip of ECG #1 — highlight the "sawtooth" pattern of AFlutter.

And a Final Tracing ...

As a final advanced concept — I add one more tracing in Figure-4.

• ECG #3 was obtained during treatment of this patient's AFlutter — at approximately the same time that ECG #1 was obtained.
• 
  
• As I noted earlier in advanced PEARL #5 — lack of a wide terminal S wave for the wide beats in lead V6 of ECG #1 did not make physiologic sense, given that beats #20,22,24,26 were conducted with RBBB aberration (within the RED rectangle in Figure-4). I suspected some type of lead connection "technical misadventure".
• 
  
• I believe ECG #3, which was obtained during the treatment process — supports my theory. Note that rather than every-other-beat RBBB conduction — rate-realted RBBB aberrancy is seen every beat in ECG #3 — and, a terminal S wave (albeit a notched deflection) is indeed seen in lead V6. As expected — wide terminal S waves are seen in the other lateral leads in ECG #3 ( = in leads I and aVL).

Figure-4: Confirmation of the "technical misadventure" I described earlier in advanced PEARL #5 (See text).

==================================

Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.

==================================

Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
• 
  
• See ECG Blog #240 — for Review on the ECG assessment of the patient with a regular SVT rhythm (including distinction between the various types of SVT reentry).
• 
  
• ECG Blog #287 — for a regular SVT that was AFlutter.
• See ECG Blog #250 — for a regular SVT with ST depression.
• 
  
• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.
• 
  
• ECG Blog #210 — reviews the Every-Other-Beat Method for estimation of heart rate when the rhythm is very fast.
• 
  
• ECG Blog #220 — reviews my LIST #1: Causes of a regular WCT (and how to assess hemodynamic stability).
• 
  
• ECG Blog #242 — Reviews rate-related BBB.
• ECG Blog #32 — More on rate-related BBB.
• 
  
• The August 17, 2020 post by me in Dr. Smith's ECG Blog — in which I review the phenomenon of Bradycardia-dependent BBB (sometimes called "Phase 4" or "paradoxical" block).
• 
  
• ECG Blog #211 — Reviews WHY some early beats and some SVT rhythms are conducted with Aberration (and why aberrant beats usually look like some form of conduction block).
• 
  
• ECG Blog #203 — reviews ECG recognition of the Hemiblocks.
• ECG Blog #204 and ECG Blog #282 — reviews ECG recognition of the Bundle Branch Blocks.

 

ADDENDUM (12/23/2023):

I've presented this material before — but it bears repeating for reference. These concepts should be automatic for assessment of the patient who presents with a regular SVT rhythm.

—  —

ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.

===================================

—  —

ECG Media PEARL #45 (10:00 minutes Audio) — Why is Atrial FIutter so commonly overlooked? Reviews PEARLS regarding the ECG diagnosis of AFlutter — and — What's "New"? in the field, regarding distinction between AFlutter vs Atrial Tachycardia (5/29/2021).

—  —

ECG Media PEARL #57 (8:00 minutes Audio) — What is rate-related Bundle Branch Block? How does this differ from "aberrant" conduction.