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.

Saturday, April 27, 2019

Is this terminal QRS distortion? Is there LVH?

This ECG of a patient was sent to me with the question, "Just LVH, no?"

What do you think?

First, is there Terminal QRS distortion?  We defined terminal QRS distortion as absence of BOTH a J-wave and S-wave in EITHER of V2 or V3, and found that zero of 171 patients with normal variant ST elevation in V2-V4 had this finding.  In other words, it is very specific for LAD occlusion (vs. early repol), though not sensitive.  We found that there was an S-wave in V2 100%, and an S-wave in V3 in 90%.  In the 10% that had no S-wave in V3, all had a J-wave of at least 0.5 mm.

This ECG has no S-wave in V3, but it has a definite J-wave.  Therefore this is NOT TQRSD.

Citation: Lee DH.  Walsh B.  Smith SW.  Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarizationThe American Journal of Emergency Medicine 34 (11): 2182–85. https://doi.org/10.1016/j.ajem.2016.08.053.

Left ventricular hypertrophy?  There is certainly high voltage.  There are new LVH criteria which say that to add the sum of the deepest S-wave in any lead plus the amplitude of the S-wave in V4.  If the deepest S-wave is in V4, then double that value. If the total is greater than 28 mm for men or 23 for women, then LVH is diagnosed.  I think the S-wave in V2 is 28 mm, so it would qualify for the new criteria.

Citation: Peguero, Julio G., Saberio Lo Presti, Jorge Perez, Omar Issa, Juan C. Brenes, and Alfonso Tolentino. 2017. “Electrocardiographic Criteria for the Diagnosis of Left Ventricular Hypertrophy.” Journal of the American College of Cardiology 69 (13): 1694–1703. https://doi.org/10.1016/j.jacc.2017.01.037.

But LVH can especially be mimicked by young healthy athletic subjects, especially with thin walls. Furthermore, when high voltage is not accompanied by discordant ST depression and T-wave inversion (the typical repolarization abnormalities associated with LVH, formerly called "strain"), the likelihood of clinically significant LVH is much less and the prognosis is much better, especially in patients without hypertension.

This is what I texted back:

"Actually, probably not even LVH. Probably early repolarization in a young person with a thin chest wall. Probably African-American.  But definitely not ischemia."

It turned out he was an otherwise healthy, thin, African American male.  He ruled out for MI.

Comment by KEN GRAUER, MD (4/27/2019):
Before I began corresponding with Dr. Stephen Smith — the concept of Terminal QRS Distortion (T-QRS-Dwas unknown to me. It’s a beautiful concept that on occasion may provide invaluable assistance for distinguishing between early repolarization vs acute OMI. This case adds insight to what is, and what isn’t TQRSD.
  • T-QRS-— is defined as the absence of both J-wave and an S-wave in either lead Vor lead V3. Although simple to define — it’s taken me a bit of practice to become comfortable and confident in its recognition.
  • The ECG in this case does not demonstrate T-QRS-D for the reasons stated by Dr. Smith above ( = a well-defined J-wave [notch] is seen in lead V3).
There are an increasing number of other examples of what T-QRS-D is, and what it is not on Dr. Smith’s Blog. For easy reference — Consider these 2 links:

The other theme addressed in this post that I’d like to comment on regards ECG criteria for LVH. For MTake” on a user-friendly method for ECG diagnosis of LVH — CLICK HERE. KEY points to emphasize include the following:
  • More than 50 criteria for ECG diagnosis of LVH have been described in the literature. The fact that there have been so many attempts at defining criteria — simply means that none of these criteria are optimally accurate. All criteria suffer from imperfect sensitivity (generally well under 55%).
  • Despite suboptimal sensitivity for ECG diagnosis of LVH — specificity can be much higher (ie, >90%) — IF several specific features are present.
  • The 2017 Peguero criteria cited above by Dr. Smith now offer an additional ECG option for assessment of LVH — with purported increased sensitivity (up to 62%) compared to previously used criteria. However, their criteria were based on a small (<100 patients) retrospective cohort with limited variability in their patient selection (patients with LVH all had hypertensive crisis) — so in my opinion, their data can be considered, but should not yet replace other criteria.
  • Rather than dependence on any one single voltage criterion — I’ve found ( = my experience) that assessment of likelihood of LVH is best based on a series of factors including: iPatient age (young adults <35 tend to have increased QRS amplitude, not necessarily related to true chamber enlargement); iiPresence of other cardiovascular disease + demographics (ie, LVH is statistically much more likely before you even look at the ECG if the patient is an adult African-American male with longstanding hypertension)iiiAwareness of different criteria that may assist when certain ECG findings are present (ie, I’ve found voltage criteria of an R≥12mm in lead aVL especially helpful when there is left axis deviation — in which case chest lead voltage criteria may not detect LVH); andivFigure-1 = Presence of LV “Strain” and/or Strain Equivalent” pattern (which if either is present in association of clinical features consistent with LVH — likelihood of true chamber enlargement is greatly increased).
Figure-1: The importance of recognizing LV “strain” and/or a “Strain Equivalent” in the ECG diagnosis of LVH (Excerpted from HERE).

Regarding LVH or Not in this Case:
For clarity — I’ve reproduced the ECG in this case in Figure-2. Assessment is somewhat challenging given the angling distortion, so I’ve counted voltage in several key leads.
Figure-2: The ECG in this case (See text).

  • As per Dr. Smith — the 28mm S wave in lead V2 satisfies Peguero Criteria [deepest S in any lead + SV4 ≥28 (men) or ≥23 (women)].
  • Numerous other voltage criteria would be met in Figure-2 (CLICK HERE), given the very deep S wave in lead V2 (28mm) — and, the very tall R waves in V5 (30mm) and V6 (21mm) — IF this patient was ≥35 years of age. Much greater QRS amplitude increase should be seen for true chamber enlargement in younger adults (ie, I’ve used the reverse of 35mm = 53mm for deepest S in V1,2 + tallest R in V5,6 as my voltage criterion in young adults). NOTE — Peguero criteria did not assess QRS amplitudes in their study for adults <35 years of age.
  • NOTE — Neither LV “strain” nor a “strain equivalent” are seen in any of the lateral leads in Figure-2. IF this patient was older (say in his 40s or 50s) — then voltage criteria for LVH would be easily met, but without “strain” or a “strain equivalent”. In this situation, I favor the term Voltage for LVH” — which is an easy way of conveying that despite increased QRS amplitude — specificity for true chamber enlargement is limited (ie, under 50%, and possibly much less depending on other clinical factors).
  • As per Dr. Smith, given that the patient in this case turned out to be a young, thin, and otherwise healthy African-American male — the likelihood of true chamber enlargement is minimal.
  • BOTTOM LINE: Assessment of age, clinical factors + demographics and the presence or absence of LV “strain” and/or a “strain equivalent” (as discussed in Figure-1) — may be of invaluable assistance for refining your assessment of the likelihood of true LV chamber enlargement.

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