RBBB and LAFB: Is there a "concordance" of the ST segment in inferior leads? Is the ST depression in V3 due to RBBB only?

This ECG was texted to me.  

I later received this clinical history: The patient in his 60s with h/o COPD had presented with 2 days of dyspnea without any chest pain.  He was not hypoxic.  He also had abdominal discomfort and vomiting.

What do you think?

There is a very atypical RBBB + LAFB.  It lacks the typical rSR' in V1-V3.  The first R-wave is taller than the 2nd R-wave in V1 (abnormal).  There is no R'-wave in V2 and V3.  

The providers thought that there was "concordant ST depression" in inferior leads -- however, this apparent inferior STD is a mimic!  What may appear to be ST depression is really a negative notch in the QRS.   Below I have indicated the end of the QRS by drawing lines at the end of the QRS in all leads:

The lines mark the end of the QRS

Notice that the "concordant ST depression" is really a negative notch at the end of the QRS.

My response was that it is "not an ischemic ECG."  

I was convinced by the RBBB + LAFB with very high voltage that the repolarization abnormalities were all secondary to the abnormal depolarization.  There is only 1 mm of ST depression in lead V3, and that is an acceptable amount of ST depression when it is discordant to the R'-wave.  

The problem is that there is no R'wave!!  So this was a mistake on my part.

The ST depression in V3 comes after a single upright R-wave, NOT after an R'-wave.  

See this typical RBBB here, in which there is ST depression in V1-V3 but it follows an R'-wave:

Notice that there is up to 1 mm of normal ST depression following the R'-wave in V1-V3

Unbeknownst to me, there was a previous ECG in the chart from 9 months prior:

A definite change in the ST segment in V3 and T-waves in V4-V6 is now obvious

Case Progression

Cardiology was contacted.  The initial troponin returned at 9,800 ng/L, consistent with subacute MI.  The patient was treated for Non-OMI (Non-STEMI with open artery).

Serial troponins downtrended.

Next AM, this was recorded. 

ST depression in V3 persists.  There is some change in T-waves

It is very similar.  Here are precordial leads side-by-side:

                                 First ECG                                                                    Next AM

There is new T-wave inversion in V5 and V6, suggesting reperfusion of a lateral OMI

An formal echo was done:

Normal left ventricular sized and function; estimated LVEF is 56%.

Basal inferolateral and inferior segments are akinetic.

This is a new wall motion abnormality; a previous echo was normal

Translation: there is a new posterior wall motion abnormality.  This ST depression in V3 represented a subacute OMI supplying the posterior wall.

At 36 hours, this was recorded:

ST segment in V3 mostly normalized

T-wave is more upright in V2, and more inverted in V4-V6.

An angiogram was done on day 3:

--Severe distal small (one vessel) disease involving the small LPL1 with an apparent filling defect.

--Vessel is less than 1 mm in diameter and flow improved with IC TNG.

--Otherwise, mild Plaque no angiographically significant obstructive coronary artery disease 

--Based on lesion of filling defect there is high suspicion for thromboembolic occlusion secondary to a proximal atrial fibrillation versus proximal coronary plaque rupture, thought to be less likely.

This confirms OMI to the posterior wall

Conclusion:

There was indeed OMI of a very small vessel.  It may have been due to an embolism.  No matter the etiology, it did manifest on the ECG and was easily, but mistakenly, attributed to RBBB and high voltage.

Learning Points:

1.  ST depression is only normal following an R'-wave in V1-V3.  If there is no R'-wave, then ST depression should be considered ischemic.

2.  Make sure you identify the end of the QRS in any BBB before attributing deviations to the ST segment.

3.  Always compare with a previous ECG if one is available.

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Comment by KEN GRAUER, MD (4/26/2022):

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Interesting case for discussion — regarding the ECG that was sent to Dr. Smith for his interpretation. I wanted to present another perspective regarding how I approached this initial ECG in today’s case.

I have previously reviewed my approach to the ECG diagnosis of RBBB (See My Comment at the bottom of the page in the July 1, 2019 post in Dr. Smith’s ECG Blog). The reasons this approach allows me to diagnose the type of conduction defect in less than 5 seconds are that: i) You only have to look at 3 leads (ie, left-sided leads I and V6 — and right-sided lead V1); and, ii) Assuming you've ruled out VT, WPW, hyperkalemia and other toxicity as the cause of QRS widening — there are for practical purposes, only 3 possible answers (ie, RBBB, LBBB or IVCD).

• RBBB (Right Bundle Branch Block) — is defined as a supraventricular rhythm in which the QRS complex is wide — and — QRS morphology in the 3 KEY leads is consistent with RBBB (ie, an rsR' pattern or it's "equivalent" in right-sided lead V1 — and an R wave with a wide terminal S wave in left-sided leads I and V6).
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• NOTE: For those interested in my user-friendly approach that allows ECG diagnosis of the type of conduction defect within seconds — Please check out my 13-minute ECG Video and downloadable PDF at the bottom of this page.

I focus my comments on the initial ECG in today's case. For clarity — I have reproduced this tracing in the bottom panel of Figure-1. 

• As per Dr. Smith — ECG #1 (Bottom panel in Figure-1) — manifests a sinus rhythm with QRS widening due to a bifascicular block ( = RBBB/LAHB). 
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• With a “typical” RBBB pattern (in which there are no other potentially confounding factors) — QRS morphology in right-sided lead V1 should manifest a triphasic rsR’ or rSR’ pattern, in which: i) There is an initial positive deflection, in the form of a small, slender r wave; ii) This initial r wave deflection is then followed by an S wave that descends below the baseline; and, iii) There is a terminal R’ (taller right “rabbit ear” deflection) — in which this R’ is slender and taller than initial positive r deflection.

The above said — it is common to see other QRS morphologies in lead V1 that are still consistent with RBBB despite not manifesting the typical triphasic rsR' or rSR' pattern.

• In a normal ECG — the QRS complex in an adult will be predominantly negative in right-sided lead V1. This is because left ventricular mass predominates over right ventricular mass in an adult — such that the depolarization vector is primarily directed to the left (or away from lead V1 — which is why a deep S wave is normally seen in lead V1).
• IF the rhythm is supraventricular — and — the QRS complex is wide and predominantly positive in right-sided lead V1 (ie, similar to any of the QRS patterns shown in the upper panel of Figure-1) — then RBBB may still be present despite the absence of a triphasic rsR' or rSR' pattern in lead V1 — as long as a wide terminal S wave is present in left-sided leads (ie, in leads I and V6).
• Reasons why the typical triphasic (rsR'; taller right rabbit ear) complex in lead V1 may be lost in some patients with RBBB include scarring (cardiomyopathy) and/or infarction (which will often be suggested by a qR in lead V1 and/or V2).

MY Thoughts on Today's Initial ECG:

The rhythm in ECG #1 is sinus. The PR interval is normal. The QRS complex is wide. The diagnosis of RBBB is confirmed by the finding of a predominantly positive QRS complex in lead V1 (consistent with one of the RBBB "Equivalent" Patterns shown in Figure-1) — in association with the presence of wide terminal S waves in both leads I and V6.

• LAHB (Left Anterior HemiBlock) is diagnosed in addition to RBBB — by the predominant negativity in the initial descent of the S wave in each of the inferior leads.
• There is excessive fragmentation in a number of QRS complexes in this tracing (ie, in the upslope of the S wave in leads II, III, aVF — and in the slurred R waves in leads aVR and V1). This amount of fragmentation often implies "scar" and/or prior infarction.
• Q waves are present in leads aVL and V2. The Q wave in lead V2 is definitely not normal (RED arrow in this lead in Figure-1) — since as described above, an initial positive deflection is normally seen in lead V1 (and usually also in lead V2) with a "typical" RBBB. While not definitive — this small Q wave in lead V2 may be a marker of anterior infarction having occurred at some point in time.
• The Q wave in lead aVL may or may not be significant (RED arrow in this lead). While true that normal septal q waves are commonly seen in one or more lateral leads (due to the left-to-right vector of septal depolarization, that does not change direction with RBBB) — I thought the Q wave in lead aVL in ECG #1 was slightly more prominent than expected for a septal q wave.
• As I reviewed in My Comment in the July 1, 2019 post — typical RBBB or LBBB both alter the sequence of ventricular depolarization and repolarization in a predictable fashion in the 3 KEY leads. With regard to the expected ST-T wave changes with simple RBBB — we should expect to see the ST segment and T wave in leads I, V1 and V6 oppositely directed to the last QRS deflection in that lead. This is precisely what we see in ECG #1 — in that the upright T wave in leads I and V6 is oppositely directed to the wide terminal S wave — and the depressed ST-T wave in lead V1 is oppositely directed to the all positive RR' complex that we see in lead V1.

KEY Point: In Figure-1 — there are other chest leads in ECG #1 that do not manifest the ST-T wave appearance expected if the only thing going on is simple RBBB.

• Lead V2 is indeed unusual in manifesting a huge positive R wave (over 30 mm tall). Assuming the chest lead V2 electrode is correctly placed — the small Q wave in this lead is abnormal. The ST segment in this lead is also unusual and probably abnormal — in that rather than initial downsloping (as is seen for the ST segment in lead V1) — the slightly depressed ST segment in lead V2 is upsloping!
• As emphasized earlier — there may normally be some ST-T wave depression in right-sided lead V1 with RBBB. But when the only thing going on is RBBB — then the relative amount of this ST-T wave depression should progressively decrease as one moves across the precordium. This is not what we see in lead V3 — in which the amount of J-point ST depression has again increased (relative to lead V2) — and the shape of the ST segment is now clearly coved (similar to the curved RED line in this lead) — followed by a deepening of symmetric T wave inversion. This is not what should be seen with simple RBBB.
• The T wave remains inverted in lead V4 (BLUE arrow) — which again should not be expected with simple RBBB.

In the Limb Leads:

It is common to see some T wave inversion in leads III and aVF when the QRS is predominantly negative. The T wave in lead II is less likely to be inverted unless there is ischemia.

• That said — the shape of the ST segment prior to developing symmetric T wave inversion in not only leads III and aVF — but also in lead II — is coved (similar to the curved RED lines in these leads). This is not a normal appearance for the ST-T wave in the inferior leads with simple LAHB.

BOTTOM LINE: No history was provided at the time I first saw the initial tracing in today's case. The ECG shows sinus rhythm with bifascicular block (ie, RBBB/LAHB) of uncertain age.

• I did not think the above-described ST-T wave changes suggested acute coronary occlusion.
• Depending on the prior ECG and the past and present medical History — I thought ECG #1 could reflect ischemia and/or recent infarction.
• Given the bifascicular block — the QRS fragmentation in no less than 5 leads —the potentially significant Q waves in leads aVL and V2 — and ST-T wave abnormalities in multiple leads that looked to be more than just RBBB and LAHB — I suspected that at the least, this patient had significant underlying heart disease.

Figure-1: TOP — QRS morphology of RBBB "Equivalent" Patterns. BOTTOM — I've labeled the initial ECG in today's case.

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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.

• CLICK HERE to download a PDF of this 12-page file on the ECG diagnosis of BBB (from Grauer K: ECG-2014-ePub).