ECG Interpretation: ECG Blog #293 — What Diagnoses to Suspect?

You are given the ECG in Figure-1 — but without the benefit of any history.

How would YOU interpret this tracing?
What clinical diagnoses do you suspect?

Figure-1: ECG you are given without the benefit of any history.

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NOTE #1: I'm repeating Video PEARL-22, that is relevant to today's case. Some readers may prefer at this point to watch to this Video Pearl before reading My Thoughts that appear below, regarding the ECG in today's case.

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Today’s ECG Media Pearl #22 (13:15 minutes Video) — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds.

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NOTE #2: I have excerpted a written summary of today's Video Pearl in the Addendum below (in Figure-2 through Figure-7).

CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).

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My THOUGHTS on the ECG in Figure-1:

It would be extremely helpful to know the clinical history in today's case. That said — sometimes we are asked to interpret ECGs without the benefit of any history, as we are in Figure-1. My thoughts on today's tracing were as follows:

The rhythm in ECG #1 is rapid, irregular — and with a QRS complex that is obviously wide.
Although small-amplitude deflections in the baseline are seen in lead II during the short pause at the beginning of the tracing — there are no clearly defined P waves in any of the 12 leads.
More than simply being irregular — the rhythm in Figure-1 is irregularly irregular. That is, despite looking “almost regular” in certain parts of this tracing — careful observation confirms slight-but-definite differences in the R-R interval from one-beat-to-the-next throughout the ECG.
IMPRESSION: The above description defines the rhythm in Figure-1 as AFib (Atrial Fibrillation), here with a rapid ventricular response (average rate well over 120/minute). Although VT (Ventricular Tachycardia) is not always regular — VT is rarely as irregularly irregular as we see here when QRS morphology is constant throughout the tracing. Thus, the rhythm in Figure-1 is AFib with QRS widening and not VT.

Continuing with My Systematic Approach:

Since the rhythm in Figure-1 is supraventricular and the QRS complex is wide — we next need to determine WHY the QRS is wide before proceeding further with our systematic approach. This is because ECG crtieria for axis, chamber enlargement and ischemia/infarction will all be different, depending on the type of conduction defect (See Figures-2 thru -7 in the Addendum below).

QRS morphology for the ECG in Figure-1 is most consistent with complete LBBB (Left Bundle Branch Block). This is because: i) The QRS is ≥0.12 second in duration; ii) The QRS complex in lateral leads I and V6 manifests a monophasic (all upright) R wave; and, iii) There is predominant negativity for the QRS in right-sided lead V1 — and — the angle of descent for anterior S waves is extremely steep. Although most of the time with LBBB, the initial R wave in other anterior leads (ie, leads V2, V3) is not as large as is seen in ECG #1 — QRS morphology is otherwise extremely typical, such that best description of the conduction defect for this tracing is complete LBBB.

Regarding other features of the ECG in Figure-1:

Chamber Enlargement: Criteria for the ECG diagnosis of LVH are different when there is complete LBBB. This is because this conduction defect alters the sequence of electrical depolarization — such that the usual voltage criteria for assessing LVH are no longer valid when there is LBBB. That said — the finding of extremely deep anterior S waves (ie, greater than 25-30 mm in V1, V2 and/or V3) is highly correlated with LVH in patients with this conduction defect.
Axis: Calculation of the frontal plane axis is of little use in patients with LBBB. This is because the left bundle branch is an extensive conduction fascicle — which when damaged, may result in development of LBBB from a variety of anatomic lesions (depending on where in the common left bundle branch and/or in the left anterior or posterior hemidivisions the conduction block occurs). As a result — a variety of axis deviations are possible with LBBB.
R Wave Progression: By definition — IF there is true LBBB — then R wave progression will be delayed in the chest leads. This explains the delay in Transition that is seen in Figure-1 — in which the R wave does not become taller than the S wave is deep until between leads V5-to-V6.
ST-T Wave Changes: It follows that since LBBB alters the sequence of electrical depolarization — the sequence of repolarization will also be changed. As a result — the appearance of ST-T waves in a patient with complete LBBB will look different than what one would otherwise expect. Thus, ST-T wave depression that may be seen in lateral leads with LBBB (ie, in leads I, aVL, V6) — will not necessarily reflect LV "strain" or ischemia — but may instead simply be the result of secondary ST-T wave changes that are to be expected in lateral leads with LBBB. Similarly, some ST elevation with T wave peaking in anterior leads in association with LBBB will often simply reflect an expected reciprocal finding from the conduction defect.

Final Interpretation:

The ECG in Figure-1 shows rapid AFib + complete LBBB + probable LVH. I suspect that there are no acute ST-T wave abnormalities in this tracing. Instead — the ST-T wave depression in lateral leads I, aVL and V6 probably reflects normal repolarization changes of LBBB. The modest amount of J-point ST elevation and T wave peaking in leads V1-thru-V4 is most probably the result a combination of factors including: i) The tachycardia (which may often produce some transient ST elevation that resolves when the rate slows); ii) The LBBB itself; and, iii) The tremendous increase in QRS amplitude in leads V1-thru-V4 (such that the height of anterior T wave peaking is probably not disproportionate given how deep S waves in leads V1-thru-V4 are).

Clinical correlation will be essential in order to know what to do with this tracing.

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Acknowledgment: My appreciation to M Shah (from Srinagar, India) for the case and this tracing.

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Relevant ECG Blog Posts to Today’s Post:

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
ECG Blog #282 — for a case that reviews the application of modified Smith-Sgarbossa Criteria in the setting of a patient with LBBB and acute symptoms.
ECG Blog #198 — An Irregular WCT (LBBB or IVCD).
ECG Blog #162 — LBBB with obvious STEMI.
ECG Blog #146 — LBBB with Acute ST-T Wave Changes.
ECG Blog #145 — RBBB with Diffuse Subendocardial Ischemia.
The January 31, 2022 post in Dr. Smith's ECG Blog — Reviews subtle signs of acute OMI in a patient with LBBB (Please see My Comment at the bottom of the page).

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ADDENDUM (3/26/2022): In the following 6 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of BBB.

CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).