Monday, July 1, 2019

Two patients with RBBB

Case 1.

A 60-something woman presented with dyspnea.  She had a history of chronic respiratory disease and hypoxia, but hypoxia was no worse than normal.

ECG:

There is abnormal ST Elevation in I and aVL.
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this.

Therefore, I went to find an old ECG and it looked the same.







The patient ruled out for acute MI with all negative troponins.
She had a completely normal formal echo.
All previous ECGs were identical.

This was her baseline ST elevation, and I have seen this many times.




Case 2: sent by Dr. James Alva

A man in his 50s with diabetes, hypertension, and hyperlipidemia presented to the ED with chest pain and shortness of breath off and on over the past three days, with associated vomiting. He was slightly tachycardic, otherwise normal vital signs.

Here is his initial ECG (no prior available):


What do you think?


I sent this ECG with no clinical context to Dr. Smith. He commented: "by every measure, this would be RBBB with inferior and lateral STE appearing to be STEMI," but he also noted that there are several features that appear similar to false positives (like the first case above). For example, he noted a lot of what looks like STE in inferior leads in this EKG is really just the end of the QRS complex. "Nevertheless, lead II really does have STE that looks ischemic, and aVR has STD that looks ischemic." There is also much STE in V3-V6, especially V4-V6, that must be considered to be STEMI.

The first troponin (contemporary troponin T) returned at 2.00 ng/mL.

The patient was taken to the cath lab where a 100% occluded OM2 was opened.

Peak troponin was 3.21 ng/mL.

Here is his ECG just after cath:
This is minimally different from the pre-cath ECG. If the ECG findings are truly new compared to a baseline (unavailable), this could suggest persistent ECG findings of ischemia, meaning poor downstream perfusion ("no reflow" phenomenon). Or it may be simply too early after cath, and subsequent ECGs may show resolution of ischemic findings.

Learning Points:

It can be difficult to distinguish true positive vs. false positive ECG findings in RBBB in some cases like these. As a general rule, there is usually no STE in any lead in most normal RBBB. However, some baseline cases of RBBB may sometimes have STE in leads with especially large, slurred S-wave of RBBB (such as V5-6, I, and aVL). When in doubt, these findings should be assumed new until proven otherwise.


Here is an old post with some similar relevant cases:

PseudoSTEMI and True ST elevation in Right Bundle Branch Block (RBBB). Don't miss case 4 at the bottom.



===================================
Comment by KEN GRAUER, MD (7/1/2019):
===================================
The ECG diagnosis of BBB (Bundle Branch Blockhas long been a source of potential confusion for many interpreters. The challenge is magnified when trying to assess BBB tracings for acute ischemia. This blog post highlights a number of pearls and pitfalls in assessment of RBBB in patients who present to the ED.
  • ECG diagnosis of BBB can be simplified. The method I favor allows accurate diagnosis of the type of BBB in less than 5 seconds. CLICK HERE — if interested in my user-friendly approach on VIDEO to ECG diagnosis of BBB (This link takes you directly to 3:16 as the point to start watching in this 17-minute video).
  • The 2 reasons you can diagnose the type of BBB so quickly are: iThat once we’ve ruled out VT and WPW conduction as the cause of QRS widening — for practical purposes, we only have to concern ourselves with 3 Types of Supraventricular Conduction Defects (RBBB — LBBB — IVCD)andiiTo distinguish between these 3 conduction defect types, we only need to look at 3 of the 12 leads ( lead I — lead V1 — lead V6). I’ll emphasize that I always look at all 12 leads — but, accurate distinction between RBBB, LBBB or IVCD is most easily and most time-efficiently achieved by simply focusing on leads right-sided lead V— and — left-sided leads and V6.
Details of my approach to ECG diagnosis of BBB are beyond the scope of this blog post — but are discussed at the above link in my ECG Video (or in free download of my Section 5 PDF on BBB  from my ECG-2014-ePub).


Let’s return to today’s topic = Assessment of 2 ECGs showing RBBB. But first — Consider the 2 parts of Figure-1:
Figure-1: TOP — Assessment of ST-T wave changes expected with typical RBBB or LBBB. BOTTOM — Illustration of these concepts in a 12-lead showing typical RBBB (See text).

Looking at Figure-1:
  • BOTTOM — This 12-lead ECG shows a supraventricular rhythm with QRS widening (probably a low atrial rhythm — given the negative P wave in lead II, but positive P wave in leads I and aVL). Looking at the KEY leads (I-V1-V6— the presence of a typical rSR’ complex in lead V1 — with upright QRS showing a wide terminal S wave in both leads I and V6 — defines QRS morphology for the tracing in Figure-1 as a typical RBBB pattern.
  • TOP of Figure-1  Typical RBBB and typical LBBB both alter the sequence of ventricular depolarization in a predictable fashion. As a direct result of this altered sequence of ventricular activation — these conduction defects also alter the sequence of ventricular repolarization, which leads to development of expected secondary (ST-wave changes — which are shown in the TOP part of Figure-1.
  • These ST-T wave changes shown in the TOP of Figure-1 are called “secondary” — because they are the direct result of (ie, they are secondary to) the conduction defect itself. That is, we expect to see this pattern of ST-T wave response as a normal part of RBBB or LBBB. This expected pattern for either typical RBBB or typical LBBB is Sopposition”. That is — the ST segment and T wave should be oppositely directed to the last QRS deflection (RED and YELLOW arrows in the TOP of Figure-1in each of the 3 KEY leads (I,V1,V6). Deviation from this pattern is abnormal — and indicates a primary (ST-wave change (that should suggest the possibility of ischemia or infarction).
  • PEARL: The beauty of the ST opposition rule — is that it allows you to concentrate your assessment of ST-T morphology with BBB to the 3 KEY leads. Clearly, we’ll next need to look at neighboring leads to assess ST-T wave changes — but focusing attention on ST-T wave appearance in leads I, V1 and V6 often provides key insight within seconds on the presence of ischemia in patients with typical RBBB or LBBB.
  • NOTE #1: The “ST opposition” rule works for RBBB and LBBB — but not for IVCD (which is why it is often more difficult to assess for acute changes with IVCD).
  • NOTE #2: In my experience — the “ST opposition” rule is reliable for RBBB and LBBB in the 3 KEY leads (I,V1,V6) — but not necessarily in other leads. That said — you’ll be amazed at how often this simple rule provides helpful insight within a matter of seconds!
  • NOTE #3: In addition to “ST opposition” — the presence of primary Selevation in leads that should not show ST elevation is often the best indicator of acute STEMI in a patient with BBB.
BOTTOM of Figure-1 — As already stated, there is a low atrial rhythm with typical RBBB (rSR’ in V1; wide terminal S waves in I & V6).
  • Focus on the ST-T waves in leads IV1 and V6. The upright T waves in left-sided leads I and V6 (YELLOW arrows in these leads) is an expected response ( = normal secondary ST-T wave change) — because it is opposite to the last QRS deflection in these leads (which is the wide-terminal S wave = RED arrows in I and V6).
  • In right-sided lead V1 — the negative ST-T wave in V1 (YELLOW arrow in this lead) is an expected response to RBBB — because it is opposite to the last QRS deflection in lead V1 (which is the upright R’ deflection = RED arrow in V1).



Regarding the 2 ECGs in today’s blog post (Figure-2):

Figure-2: The 2 ECGs in today’s blog post (See text).


MTHOUGHTS on ECG #1  The patient in Case #1 was a 60-something woman with acute dyspnea, but no chest pain.
  • The rhythm is sinus tachycardia at ~105/minute.
  • The PR interval is normal — but the QRS is wide. QRS morphology is consistent with RBBB because: ithere is an rSR’ pattern (with taller right rabbit-ear) in lead V1; andiithere are wide terminal S waves in both leads I and V6.
  • NOTE: There is marked fragmentation of the QRS in this tracing beyond the simple triphasic rSR’ in lead leads V1 and V2. Specifically — note that profound notching of the QRS continues in leads V3-thru-V6. And, rather than the very typical monophasic negative deflection S wave that we do see in lead I — the QRS in lead V6 manifests a multiphasic RSR’S’ pattern. This degree of fragmentation that we see in so many leads in ECG #1 suggests scarring from some underlying structural defect — be it from prior infarction or cardiomyopathy.
  • The ST-T wave in lead V1 of ECG #1 is perfectly appropriate = opposite to the last QRS deflection in this lead, which is the positive R’ (oppositely directed RED and YELLOW arrows in ECG #1).
  • The T wave in lead I is appropriately upright — but as Dr. Smith has emphasized, there is J-point ST elevation in both leads I and aVL — which is not always normal.
  • The ST-wave in lead Vof ECG #1 is definitely not normal! This ST segment in lead V6 is straight (ledge-like) — if not coved. It is followed by a T wave that appears to be biphasic (small initial negative deflection, followed by a larger positive deflection). Neighboring lead V— and next to it, lead V— support the finding that the ST-T waves in these lateral chest leads are not normal (the ST segment in these leads is coved, if not slightly depressed — and the T waves look biphasic). Finally — the BLUE arrow in lead Vhighlights J-point depression that leads into a sagging ST-T wave. With “typical” RBBB — ST-T wave depression should be maximal in lead V1 — and not in lead V3, as it is in ECG #1.
  • There is also J-point depression in each of the 3 inferior leads in ECG #1 — with a straightened, almost shelf-like ST segment in lead II. In the context of the abnormal ST-T waves in leads V3-thru-V6 — this inferior lead J-point ST depression high lateral lead (in I, aVL) J-point ST elevation should raise the concern that it did in this case!
  • BOTTOM Line: As per Dr. Smith — the patient in Case #1 ruled out for acute MI with all negative troponins. Formal echo was completely normal — and ECG #1 was unchanged from all prior tracings in her chart. That said — the Take-Home” Points from Case #1 are: ithat there was sinus tachycardia with complete RBBB; iithat there was marked fragmentation of the QRS beyond that expected for simple RBBB (which should suggest high probability of underlying heart disease); andiiithat in addition to J-point ST elevation in high lateral leads I and aVL — there was abnormal ST-T wave depression in no less than 7 of the 12 leads. These findings on an initial ECG clearly suggest ischemia that may be acute. Further evaluation was necessary until an acute event can be ruled out.

MTHOUGHTS on ECG #2  The patient in Case #2 was a man in his 50s with dyspnea and chest pain over the prior 3 days.
  • The rhythm is sinus tachycardia at ~115/minute.
  • The PR interval is normal — but the QRS is wide. QRS morphology is consistent with RBBB because: ithere is an RBBB-equivalent pattern (monophasic, notched R wave) in lead V1; andiithere are wide terminal S waves in both leads I and V6.
Assessment of ST-T wave changes in ECG #2 is challenging in parts of this tracing because of the difficulty determining where the QRS complex ends. To facilitate this — I selected lead V1 as one lead in which I could clearly delineate the end of the QRS complex and the end of the T wave (parallel vertical RED lines in ECG #2).
  • I’ve added parallel vertical BLUE lines that delineate the end of the QRS and end of the T wave in the other groups of simultaneously-recorded leads in ECG #2. This facilitates identifying the ST segment — which lies between each set of vertical lines.
  • RED arrows in leads IV4V5 and V6 clearly show J-point Selevation in each of these lateral leads. There is no such J-point ST elevation in lead aVL.
  • Using the set of vertical BLUE lines to delineate ST segments in the inferior leads — we clearly see a small-but-definite amount of coved ST elevation in leads II and aVF (RED arrows in these leads). Considering how small the QRS complex is in these leads — this inferior lead ST elevation is significant. In contrast, the ST segment within the vertical BLUE lines in lead III is much more equivocal.
  • There are large Q waves in each of the inferior leads.
  • I don’t see reciprocal ST depression in ECG #2.
  • BOTTOM Line: The ECG in Case #2 shows sinus tachycardia, RBBB — and a very steep S wave descent in lead I that might indicate LPHB. In this patient with several days of ongoing chest pain — the inferior Q waves ST elevation in infero-lateral leads is diagnostic of acute STEMI until proven otherwise.



3 comments:

  1. Hello Dr. Smith,

    I totally share your considerations about these ECGs. But, regarding the second one, I think that (similarly to aVR) lead V1 maybe holds an excessively discordant STD, so I was worried about a posterior AMI too, especially in the setting of inferior STE.

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    Replies
    1. That is very likely, thanks for noticing!

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    2. @ Anonymous — Interesting possibility that you raise — though given the exceedingly wide, all upright complex we see in lead V1 — and the lack of the usual ST depression that we generally are still able to see in lead V2 with RBBB and posterior MI — I think it’s difficult to distinguish between an “appropriate” amount of ST-T wave depression in V1 due to RBBB vs disproportionate ST-T depression in this lead due to associated posterior involvement. Thanks again for your comment! — :)

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