ECG Interpretation: ECG Blog #205 — What is Trifascicular Block?

HOW would you interpret the ECG shown in Figure-1? Unfortunately — there is no history available to assist you.

QUESTION: There are 7 ECG findings that should be noted. How many of them did YOU identify?

Figure-1: There are 7 ECG findings that should be noted in this tracing. HOW many of the 7 did you identify?

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NOTE #1: Some readers may prefer at this point to listen to the 7:40 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-23).

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Today’s ECG Media PEARL #23 (7:40 minutes Audio) — A user-friendly Systematic Approach to 12-Lead ECG Interpretation.

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NOTE #2: Written summary of my Systematic Approach to 12-Lead ECG Interpretation appears below in the Addendum (in Figures-2 through Figure-4).

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MY Approach to this Tracing:

The BEST way to avoid overlooking important ECG findings — is to use a Systematic Approach. This is especially true for interpreting tracings when the QRS complex is wide.

PEARL #1: Regardless of the system you use — it’s important to assess intervals at an early point in the process. This is because IF the QRS complex is wide — then criteria for assessing the QTc, Axis, Chamber Enlargement and Ischemia/Infarction will all change! Therefore, as soon as you recognize QRS widening — STOP and Figure Out WHY the QRS is wide before going further in your assessment.

The 6 KEY Parameters in my Systematic Approach:

Rate & Rhythm: The P wave is upright in lead II — so the rhythm in Figure-1 is sinus. Although we are not provided with a long-lead rhythm strip — it should still be apparent that the R-R interval is varying enough to qualify as sinus arrhythmia, here with bradycardia (heart rate varying between ~50-60/minute).
Intervals (PR/QRS/QTc): The PR interval is clearly prolonged (ie, to ~0.32 second) — so there is 1st-Degree AV Block.
Continuing with Intervals — the QRS complex in Figure-1 is wide (I measure between 0.12-0.13 second). As noted in Pearl #1 (above) — as soon as you recognize QRS widening — STOP and Figure Out WHY the QRS is wide before going further in your assessment.

WHY is the QRS Complex Wide?

As discussed in detail in ECG Blog #204 — once you confirm that the rhythm is supraventricular — the reason for QRS widening can be most time-efficiently determined by focusing attention on the 3 KEY Leads (ie, leads I, V1 and V6).

Lead V1 — shows an rSR’ complex that is completely typical for RBBB (Right Bundle Branch Block), in that the initial r wave is small and thin — the S wave that follows descends below the baseline — and the terminal R’ is tall and thin (ie, taller right “rabbit ear”).
Leads I and V6 — confirm the diagnosis of RBBB, because they each manifest a wide terminal S wave.

Returning to our Systematic Approach:

Assessment of the remaining parameters in our Systematic Approach is made with awareness that there is complete RBBB.

QTc: The remaining interval to assess is the QTc. Bundle branch block per se may prolong the QTc. That said — the longest QT that I measure in Figure-1 looks to be less than 450 msec, which considering the bradycardia and conduction defect is not prolonged. (Visually — the QT interval is decidedly less than half the R-R interval, so almost certainly not prolonged in Figure-1).

AXIS — The “meaning” of axis is altered in RBBB. This is because of the zig-zag direction of electrical activity due to this conduction defect. That is — the initial left-to-right vector of septal depolarization is preserved (since the conduction defect with RBBB is on the right side of the septum) — which is followed by depolarization of the unblocked LV (during which time the wave of depolarization travels back to the left)— and finally, return rightward, as the “blocked” RV is the last part of the heart to depolarize.

Clinically — the only thing we care about regarding the axis with RBBB is whether there is: i) RBBB + LAHB; ii) RBBB + LPHB; or, iii) RBBB without any hemiblock. In Figure-1, in addition to RBBB — the QRS complex is predominantly negative in lead II. Therefore — there is bifascicular block (ie, RBBB + LAHB).

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NOTE: For visual review of the Bifascicular Blocks with RBBB — Begin at 9:20 minutes in my Media Pearl #21 in ECG Blog #203).

I have excerpted a written summary from my ECG-2014-ePUb on the ECG diagnosis of the bifascicular blocks. This appears below in the Addendum (in Figure-5 through Figure-7).
To download a PDF of Figures-5, 6, 7 — CLICK HERE.

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Chamber Enlargement: There is no RAA, LAA or RVH. There is LVH.

Criteria for atrial abnormality are unaffected by bundle branch block. However, because RBBB and LBBB alter the sequence of both ventricular depolarization and ventricular repolarization — voltage criteria and ST-T wave changes of LV or RV “strain” will be more difficult to identify.
That said — because the LV depolarizes unopposed with RBBB (since RV depolarization is delayed by this conduction defect) — the effect of RBBB on ECG diagnosis of LVH may not be marked. How much of an effect RBBB may have on ECG diagnosis of LVH may be difficult to predict. So, realizing that data and definitive answers are lacking — the dramatically increased voltage that we see in Figure-1 for the R wave in lead aVL (ie, ~15 mm), in association with an ST-T wave appearance in this lead that looks typical for LV “strain” suggests at least probable LVH.
Figure-4 in the Addendum below shows the voltage criteria I favor for ECG diagnosis of LVH. The caveat — is that voltage criteria in Figure-4 are based on normal QRS duration.
P.S. — LAHB on occasion has also been known to alter QRS amplitude on ECG in a way that may make recognition of LVH problematic. Bottom Line: IF one truly needs to know whether or not there is LVH — an Echo will be needed.

Q-R-S-T Changes:

Q Waves are seen in both high lateral leads in Figure-1 (ie, in leads I and aVL). Although the Q in lead I is small — the Q wave in lead aVL is both deeper and wider than expected for a normal septal q wave. This abnormal Q wave should be noted in the written interpretation — and, it should be noted that this Q wave in lead aVL may reflect prior lateral infarction.
R Wave Progression — is less relevant in this tracing, since the presence of RBBB by definition results in a predominant R wave in lead V1.

PEARL #2: There are primary ST-T Wave Changes in at least leads V1 and V2. As discussed in detail in ECG Blog #204 — the normal response of ST-T waves in the 3 KEY lead with BBB is to be oppositely directed to the last QRS deflection.

If anything — the ST segment in lead V1 may be slightly elevated. It normally should be depressed (ie, opposite to the last QRS deflection, which is the positive R’ in this lead). The T wave in lead V1 is clearly abnormal — as the normal ST-T wave response with RBBB in lead V1 should be at least some ST depression.
It is difficult to predict for “how many leads” the expected ST depression with RBBB should last — but the surprisingly tall and peaked T wave in lead V2 is clearly not a normal response.
We’ve already noted the shape of the ST-T wave depression in lead aVL — which looks very much like LV “strain”. Other leads in Figure-1 show nonspecific flattening of the ST segment and reduced T wave amplitude. Therefore — the 2 leads in this tracing of most concern regarding ST-T wave appearance are leads V1 and V2.

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ANSWER to the Question We Posed at the Beginning of this Case:

The 7 ECG Findings that should be noted in Today’s Tracing are:

Sinus bradycardia and arrhythmia.
RBBB.
LAHB.
1st-Degree AV Block.
LVH (with ST-T wave changes consistent with LV “strain”).
An abnormal Q wave in lead aVL (with a smaller Q in lead I).
Primary ST-T wave changes, at least in leads V1 and V2.

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Putting It All Together: It is always challenging to have to interpret ECGs in the absence of any clinical history. That said — I was often confronted with this situation as the faculty member charged with official interpretation of ECGs for multiple providers in our clinic, regarding numerous patients I knew nothing about.

It should be obvious that the patient in today’s case has significant underlying heart disease, given probable LVH (with LV “strain”) — possible prior infarction (the abnormal Q in lead aVL) — and bradycardia + 3 additional indicators of conduction system disease (ie, 1st-degree AV block — RBBB — LAHB).
That said — despite the primary T wave abnormalities in leads V1 and V2 — my “hunch” is that the changes we see are probably not acute (since other than the changes in leads V1 and V2 — ST-T wave changes in the other 10 leads do not look new).
BOTTOM LINE: Clinical correlation on this patient will be needed for deciding appropriate management. Finding a prior tracing on this patient would be invaluable for determining which of the above ECG findings are likely to be new vs old. And, IF there was a history of syncope or presyncope — this would be especially concerning given bradycardia + 3 conduction system defects. A recent history of chest pain would also be of great concern — since the ECG findings on today's tracing could be consistent with recent infarction. Clinical correlation is essential.

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Is There Tri-Fascicular Block?

The term, “trifascicular” block — implies impaired conduction in all 3 of the major conduction fascicles: i) the right bundle branch; ii) the left anterior hemifascicle; and, iii) the left posterior hemifascicle.

The term, “trifascicular block” is no longer recommended (Surawicz et al, JACC: Vol. 53, No. 11, pp 976-981, 2009). This is because of “the great variation in anatomy and pathology producing this pattern” — as well as the fact that one will usually not be able to make a definitive diagnosis of trifascicular block from the surface ECG. We simply can not tell IF PR interval prolongation in a patient with bifascicular block (as occurs in Figure-1) is due to AV nodal disease or disease in the remaining conducting fascicle.
Rarely, one may be able to diagnose involvement in all 3 conduction fascicles — if for example, there is RBBB and LAHB that alternates with LPHB. But even in this circumstance — current recommendations favor clarity in description by avoiding the term “trifascicular block”, and instead noting each of the conduction defects that are present (ie, in Figure-1 — this is 1st-degree AV block + RBBB + LAHB).

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Relevant ECG Blog Posts to Today’s Case:

ECG Blog #203 — Reviews the ECG diagnosis of Axis and Hemiblocks.
ECG Blog #204 — Review of my user-friendly Approach to the ECG diagnosis of BBB.
ECG Blog #73 — “My Take” on the ECG diagnosis of LVH.
ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation.

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ADDENDUM (3/18/2021): In the following 3 Figures — I outline the Systematic Approach that I favor (in Figures-2 and -3) — and my preferred criteria for the ECG diagnosis of LVH (Figure-4).

Figure-2: The Systematic Approach that I favor. Review of the first 4 parameters in Descriptive Analysis (Rate; Rhythm; Intervals; Axis). NOTE: IF the QRS complex is wide — then STOP and find out WHY the QRS is wide before proceding to assessment of Axis, Chamber Enlargement and QRST Changes. This is because IF the QRS is wide because of BBB (Bundle Branch Block) — criteria for axis, hypertrophy, and ST-T wave changes will be different when there is BBB or IVCD! To emphasize, IF the QRS is wide — this is the ONE time that I depart from the sequence in Figures-2 and -3 (P.S. IF the QRS is wide — Make sure that the rhythm is not VT. If the rhythm is sinus — ECG Blog #204 reviews how to determine if RBBB, LBBB or IVCD is present).

Figure-3: The Systematic Approach that I favor (Continued). Review of the last 2 parameters in Descriptive Analysis (Chamber Enlargement; Looking for Q-R-S-T Changes) — and then formulating your Clinical Impression.