Thursday, June 25, 2020

Intermittent QRS Widening Without Any History

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MY Comment by KEN GRAUER, MD (6/25/2020):
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I’ve labeled the ECG in Figure-1 as, “The initial ECG in this Case” — as I found this tracing fascinating. Imagine you knew nothing about this patient.
  • HOW would you interpret this tracing?
  • Is there bundle branch block?
  • Are there acute changes?

Figure-1: The initial ECG in this case (See text).



First Impression: The 12-lead ECG and long lead II rhythm strip shown in Figure-1 is difficult to interpret for several reasons:
  • There is much baseline artifact (especially for the first few beats in the tracing).
  • Some beats are wide — and other beats are narrow.
  • Despite marked variation in QRS morphology in several leads — there is only minimal change in QRS morphology in the long lead II rhythm strip.

MY THOUGHTS on ECG #1: To facilitate discussion of the rhythm and 12-lead ECG in Figure-1 — I’ve labeled key findings (Figure-2):
  • The underlying rhythm is sinus at ~85/minute. I believe the slight variation in P wave morphology in the long lead II is the result of artifact. The beauty of simultaneous leads — is that P waves marred by artifact in one lead, will often be clearly visible in other leads. Thus, despite not seeing any atrial activity in the long lead II rhythm strip before beats #1-through-5, and before beat #9 — clear presence of normal sinus P waves is seen for all 14 beats on this tracing in other simultaneously-obtained leads (RED arrows in Figure-2).

Figure-2: I’ve labeled key findings from Figure-1 (See text).



The change that occurs in QRS morphology is easiest to appreciate in lead V1 (Figure-2):
Beat #8 in lead V1 is narrow and sinus-conducted.
  • Beats #9 and 10 in lead V1 manifest a wide QRS complex, consistent with RBBB (Right Bundle Branch Block) morphology. RBBB produces a “terminal delay” in the sequence of ventricular activation — in which the last part of the heart to be activated is the right ventricle. This results in a terminal R’ deflection in the QRS complex in lead V1, due to travel of the depolarizing waveform to the right.
  • Beat #11 in lead V1 is conducted with a normal (narrow) QRS complex.
  • PEARL #1: The reason we know that QRS widening of beats #9 and 10 in lead V1 is the result of intermittent RBBB — is that the PR interval remains the same before all 4 beats in lead V1. We’d expect the PR interval prior to the wide beats to be different if the wide beats were PVCs.

It’s a bit more challenging to identify the beats that conduct with intermittent RBBB in other leads.
  • PEARL #2: I like to look next at lateral leads. Because RBBB produces a “terminal delay” (ie, of the last part of ventricular activation— lateral leads I and V6 should show a wide terminal S wave when there is RBBB. Note that a wide terminal S wave is clearly seen for beats #1, 2 and 3 in lead I. In contrast, despite a virtually identical initial QRS deflection for beat #4 in lead I (ie, tiny initial q wave, followed by a slender upright R wave) — beat #4 has no wide terminal S wave. Therefore — beats #1, 2 and 3 in Figure-2 are conducted with RBBB — but beat #4 is conducted normally.
  • PEARL #3: Awareness that the initial portion of the QRS complex with RBBB is virtually identical to the initial portion of the QRS complex in sinus-conducted beats without RBBB — is the BEST clue I know to confirm that the reason for QRS widening in Figure-2 is intermittent RBBB conduction.
  • Beat #5 is conducted normally. This is easiest to see by looking at lead aVL. Note that the QRS complex of beat #5 in lead aVL is clearly narrow, and lacks a wide terminal S wave. In contrast — the QRS of beats #6 and 7 in lead aVL is wide with a wide terminal S wave — because beats #6 and 7 again conduct with RBBB.
  • Finally — beats #12 and 13 are narrow and conducted normally — whereas the last beat in this tracing ( = beat #14) manifests a subtle-but-widened terminal S wave deflection.
  • BOTTOM LINE: The underlying rhythm in Figure-2 is sinus. There is intermittent RBBB conduction. Beats #4, 5, 8, 11, 12 and 13 all conduct normally (ie, with a narrow QRS complex). In contrast — beats #1, 2, 3, 6, 7, 9, 10 and 14 are all wide, and conduct with RBBB.
  • P.S.: I have seen many cases of intermittent RBBB, in which the conduction defect was seen every-other- or every-third or -forth beat. In such cases, there is a "fixed" interval of time between beats that conduct normally, and those that conduct with RBBB. This allows some predictable amount of time for recovery of right bundle branch conduction properties. In my experience — it is far less common to see random alternation between normal and impaired conduction as we see here (perhaps a result of acute ischemia ...).

WHY is this tracing so challenging to interpret?
As alluded to earlier — QRS morphology in the long lead II rhythm strip does not appreciably change from one beat-to-the-next. The reason for this, is that RBBB is a terminal delay in ventricular conduction — and the terminal portion of the QRS complex in the long lead II rhythm strip is isoelectric!
  • The thin, vertical BLUE line in Figure-2 marks the onset of the QRS complex in simultaneously-obtained leads V1, V2, V3 — and in the long lead II rhythm strip below the 12-lead.
  • The thin, vertical RED line in Figure-2 marks the end of the QRS complex in these leads. Note in the long lead II rhythm strip how the last part of the QRS complex of beat #10 lies on the baseline. We simply can not reliably determine by looking at lead II alone which beats are narrow and which beats are wide!
  • PEARL #4: Comfort in using simultaneously-obtained leads is of invaluable assistance for assessing complex arrhythmias!

Are there any Acute Changes on this ECG?
I thought assessment of QRS morphology of the narrow beats in Figure-2 was unimpressive — and not indicative of acute coronary disease.
  • In contrast — the ST segments in leads V2 and V3 are clearly more coved than should be expected with simple RBBB (curved PURPLE lines in these leads). The J-point after the wide S wave in lead I for beats #1, 2 and 3 that conduct with RBBB also appears elevated. This patient had positive troponin values — with high-grade stenosis of the proximal LAD, as well as significant circumflex disease. I thought it of interest that the most suspicious ECG findings for acute coronary disease were found in beats that conducted with RBBB — but not in normally conducted beats.
  • NOTE: If interested in review on assessing RBBB for potential ischemic changes — Please check out My Comment in the April 13, 2020 post in Dr. Smith's ECG Blog.
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ACKNOWLEDGMENT: My sincere THANKS to 유영준 (from Seoul, South Korea) for sharing this case with us!
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4 comments:

  1. No r wave in V1, V2 with ST-elevation during normal ventricular conduction. No r in V1 during RBBB.

    ReplyDelete
    Replies
    1. Yes, you are correct (!) that lead V1 does not show an initial small r wave in the RBBB-conducted beats. I'm not sure about lead V2 — in which the 3rd complex shows a tiny initial r, but the 2nd complex does not. That said — I'm not sure what to do with this finding, given we only have 2 beats in lead V1 to look at, and the non-rbbb conducted beats also do not manifest any initial r wave.

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  2. Are there hyperacute T-waves in lead 2?

    ReplyDelete
    Replies
    1. We have the advantages that with lead II, there is a long lead rhythm strip — which gives us 14 “looks” at the ST-T wave in this lead. There is a LOT of baseline wander/artifact in the first 4 beats — so I would not look at those. For the other beats — we need to remember that there is intermittent RBBB conduction (ie, beats #6,7; 9,10; and 14 all conduct with RBBB — so while not impossible to see hyperacute changes — the “look” will be different for beats in lead II that are vs are not conducting with RBBB. All of that said — I was not impressed by the ST-T wave appearance in lead II. As discussed in the last section of My Comment above — I thought leads I, V2 and V3 were the 3 leads showing ST-T waves of most concern.

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