Tuesday, April 30, 2019

What do you think about this Left Bundle Branch Block?

I was reading through a stack of ECGs and saw this one:
The Veritas computer algorithm called it Left Bundle Branch Block without ischemia.
What do you think?

The computer has a hard time with these.  This is WPW.  Note the very short PR interval.  The upstroke of the QRS is delayed (delta wave).  It looks like LBBB because the accessory pathway is on the right side of the heart, so the right heart is pre-excited and then depolarizes the left heart from right to left, just like in LBBB.   All of the repolarization abnormalities are due to the depolarization abnormality of WPW.

I looked into the chart to find more information: it turns out that this patient had a known diagnosis of WPW and had never had it ablated.  He had had episodes of tachycardia in the past, so he has clinical WPW.

Not all WPW manifests on the ECG.  When it does not, it has sometimes been called "concealed conduction".  See this case: Wide Complex Tachycardia

Not all patients with WPW manifesting on the ECG have clinical WPW.

This patient has both.

Diagnosis: WPW

Comment by KEN GRAUER, MD (4/30/2019):
As per Dr. Smith — We can quickly recognize that this ECG (found “in a stack of tracings” that were to be overread) is not an example of LBBB — because the PR interval is extremely short! Instead, this patient has WPW (Wolff-Parkinson-Whiteby ECG. This brings up a series of issues regarding the entity of WPW:

ECG Manifestations of WPW:
In addition to a short PR interval, there are 2 other features that are characteristic of WPW: iDelta waves (usually present in at least several leads)andiiQRS widening.
  • The reason for the short Pinterval is that travel from the atria to the ventricles is much faster over the AP (Accessory Pathway), compared to relatively slow conduction of the impulse through the normal AV nodal pathway.
  • After arriving in the ventricles — conduction then slows down, as the impulse moves through unspecialized myocardial fibers. It is this slowed conduction that produces slurring of the initial portion of the QRS, which is the delta wave. Ultimately, the impulse hooks up with the terminal portion of the conduction system as the last part of the QRS is produced.
  • The QRS complex with WPW is widened due to fusion of the initial QRS slurring (delta wave) with the last portion of ventricular depolarization.

It should be appreciated that patients with WPW may conduct in any of the following manners:
  • Entirely over the AP — in which case all 3 features (short PR interval; delta waves; QRS widening) will be seen on the ECG.
  • Entirely over the normal AV nodal pathway — in which case the PR interval is normal, and the QRS complex is not widened.
  • Partially over the AP, and partially over the normal AV nodal pathway — in which case, depending on the relative amount of preexcitation — the PR interval may be only slightly (or more than that) shortened — and the QRS complex only slightly (or more than that) widened. This explains why sometimes it may be extremely difficult to recognize WPW in a patient who is manifesting only partial preexcitation.
  • The relative amount of preexcitation may vary from one occasion to another — such that a patient’s ECG may look entirely normal on one day — and may manifest classic WPW on another.
  • Some patients may only be able to conduct over the AP in retrograde fashion. As a result, the ECG in sinus rhythm will look normal — BUT — because there is an AP present capable of conducting retrograde — a ready-made “reentry pathway” exists — and the patient may be predisposed to developing the reentry SVT rhythm known as AVRT (AtrioVentricular Reentrant Tachycardia). If the AP in such a patient never conducts anterograde (ie, in the forward direction) — then this is said to be an “occult” AP.
  • It is the presence of one (and sometimes of more than one) AP — and, the ability of the AP to conduct rapidly either anterograde (forward) to the ventricles or retrograde (backward) to the atria or both — that predisposes to development of certain tachyarrhythmias. For example, excessively rapid anterograde conduction predisposes to development of AFib rates that may attain ≥220-250/minute (CLICK HERE for Review of WPW-associated arrhythmias).

ECG Diagnosis of LBBB:
The ECG picture of typical”  LBBB consists of the following:
  • QRS widening to at least 0.12 second.
  • An entirely upright (monophasic) QRS complex in left-sided leads I and V6 (that may or may not be notched ).
  • A predominantly negative QRS complex in right-sided lead V1. There may (or may not) be a small and narrow initial r wave in lead V1 (ie, lead V1 may show either a QS or an rS complex).
NOTE: The presence of “other conditions” (ie, infarction, marked hypertrophy, cardiomyopathy, etc) may alter the ECG appearance of a patient with LBBB — but the above features are what should be seen if there is uncomplicated LBBB.
  • For illustrative purposes — I show derivation of these waveforms that comprise the ECG picture of “typical” LBBB in Figure-1:
Figure-1: Schematic representation of normal ventricular depolarization (TOP) — and the changes in ventricular depolarization that occur when there is LBBB (BOTTOM). (Excerpted from pages 101 & 106 of Grauer K: Practical Guide to ECG Interpretation [2nd Edition], Mosby, 1998).
Why the ECG in this Case is Not LBBB:
When I first looked at the ECG in this case — I initially thought this was LBBB. But, in addition to the short PR interval — the following features were distinctly atypical for LBBB (Figure-2):
  • Lead aVL usually looks similar to left-sided leads I and V6 (ie, with a monophasic = all upright R wave). The GREEN arrow in Figure-2 shows a most unusual QRS morphology in lead aVL, with a terminal, fragmented s wave that is totally uncharacteristic.
  • Leads V1V2 and V3 should all be predominantly negative with typical LBBB, with no more than a very small and thin initial r wave (if there is any r wave at all). Instead, these 3 leads each manifest a surprisingly wide initial R wave (within the dotted BLUE oval).
  • Lead V4 usually looks similar to leads V1-V3 with typical LBBB (ie, predominantly negative). It is generally not all upright and notched as we see in Figure-2 when there is typical LBBB.
  • BOTTOM LINE: The initial slurring (ie, slow upslope) of entirely upright QRS complexes in Figure-2 represents delta waves that are seen in multiple leads. The initial wider-than-expected positive deflections (r waves) in leads V1, V2 and V3 are also delta waves!
Figure-2: The ECG in this case (See text).
WHO with WPW should bAblated?
The patient in this case apparently had known WPW on ECG, as well as a history of arrhythmias — but was never ablated. This raises the question of WHO with WPW should be ablated? In my opinion — the answer depends! Clearly, if the patient is referred to an EP cardiologist — there is a much greater chance that ablation will be recommended. And, in the hands of a skilled EP cardiologist with high-volume experience — the chance of "curing" WPW-associated arrhythmias is high, and the risk of complications from this invasive procedure is usually very low. That said, risk of complications still exists — and for that older patient with incidental WPW (or with uncommonly-occurring arrhythmias that are satisfactorily controlled with medication) — the "balance" may not necessarily favor intervention. Historical Factors to consider when contemplating whether or not to suggest ablative treatment include the following:
  • How old is this patient? (never stated in the history here …).
  • At what age did the patient become symptomatic? (Risk of developing malignant arrhythmias is significantly less for patients who do not develop symptoms until after 35-40 years of age).
  • How often do symptomatic episodes occur? How severe are the symptoms? Do antiarrhythmic medications control episodes?
  • Importantly — What does the patient want to do?
  • CLICK HERE — For more specific info on which patients to refer.

How to Localize the AP from the ECG:
EP study will localize the AP. That said, it’s fun (and may provide some initial important clinical insight) to try to localize the AP from the appearance of delta waves on ECG. Having studied multiple proposed algorithms for doing so — I synthesized the data I found into a user-friendly approach — CLICK HERE for full details & references. Using the system I describe at this link leads to the following:
  • Since the QRS complex is not all upright in lead V1 — Begin with Step B-1: Since the QRS is predominantly negative in lead V1 and transition occurs after lead V2 — there is a RIGHT-sided AP.
  • Go to Step B-2Transition in Figure-2 occurs between lead V3-to-V4 — which takes us to Step B-4.
  • Step B-4Delta wave amplitude in lead II appears to be >10 mm (ie, there appears to be a very steep upslope to the initial positive deflection in lead II) — which implies a Right-sided Septal AP — which takes us to Step B-3.
  • Step B-3Delta waves are upright (positive) in all 3 inferior leads — so the sum = +3 — which makes us suspect there is a Right-sided AnteroSeptal AP.

  • Regarding ECG Diagnosis of WPW + “My Take” on What To Do When theWPW Patient is Asymptomatic + WPW vs “WPW Syndrome” — CLICK HERE.
  • For “My Approach”  to Localization of the A— CLICK HERE.
  • For Review of WPW-associated Arrhythmias — CLICK HERE.


  1. This comment has been removed by a blog administrator.

  2. Tricky case, Steve!

    The narrow PR interval is the main factor alerting us to the diagnosis. The widened QRS actually looks a lot like an LBBB with typical notching.

    Thanks for not dwelling on the repolarization abnormality. With ventricular pre-excitation the repolarization abnormality, in my experience, is actually quite variable and sometimes very unnoticeable. It is supposed to be opposite the delta wave but I've come to the conclusion that it can be in any direction. As you (I'm sure) noticed, the T wave vectors in this case are about 180 degrees from the ST segment vectors - which one would NOT expect of a classic repolarization abnormality in the absence of ischemia.

    Steve, I would like your opinion on this observation: with a right-sided pathway, the delta wave in V1 should be negative, but in this tracing there is a small (but definite) r wave in V1 before it descends into a notched S wave. The delta wave must be the first deflection of the QRS (by definition). What do you think is happening here? Could it be that there is a pathway other than a Kent bundle causing this? Perhaps with an IVCD that simply doesn't result in the repol abnormality typical of an LBBB?

    Jerry W. Jones, MD FACEP FAAEM

    1. Jerry,
      First, I think the repolarization abnormalities are often particular to WPW. In fact, the first thing that struck me and alerted me to WPW when I saw this were the rounded repolarization, with scooped ST segments. I have found this to be fairly unique to WPW.
      Second, I agree it is very difficult to localize the AP. The delta wave is left to right in V1, and is right to left in lateral leads. Why is it both right to left and left to right. V1 is also anterior, so it is not wholly left to right. Therefore, it is both anterior and leftward -- perhaps it is in the posterior septum?
      Thanks as always for the great comments.

  3. In this patient, the delta waves are so tall (almost as tall as the R wave in leads I and II), no wonder the computer is confused with LBBB.
    Additional points about WPW ECG findings:
    1) The delta wave can be upright in some leads, inverted in other leads simulating the Q wave of an infarction, or isoelectric in still other leads.
    2) Preexcitation can be intermittent; how intermittent? only every other beat is preexcited, several beats at a time, or several days at a time. If only every other beat is preexcited, it may simulate electrical alternans.
    K. Wang.

    1. Here is a nice example of intermittent WPW: https://hqmeded-ecg.blogspot.com/2018/06/a-wide-complex-rhythm-in-intoxicated.html

  4. I've never seen so tall delta waves. Isn't there also a conduction abnormality along the normal pathway?

    1. I see what you mean, but I think it is all due to delta waves. No EP study, no ablation to prove it though.


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