Monday, April 13, 2020

A man in his 60s with chest pain. The ST segments and T waves are ALWAYS interpreted in the context of their QRS.

Written by Pendell Meyers

A man in his 60s with history of CAD, CABG, HTN, DM, and smoking presented with chest pain,and shortness of breath over the past 1 hour, and a mild cough over the past few days, of course asking for COVID testing.

Here is his ECG on presentation (shown to me with no information):

What do you think?

Raw Findings:
 - RBBB (some will also say LPFB)
 - Negative T-waves in V1-V3
 - STD in V1-V6, I, aVL
 - STE in aVR
 - V2 has strange QRS morphology that does not seem to fit in the progression between V1 and V3, possibly lead misplacement

In the context of RBBB, it is normal to have a negative T-wave and small amount of reciprocal STD in leads V1-V4 (this is termed appropriate discordance, where the ST segment and T-wave are deviated discordant to the majority of the abnormally conducted portion of the QRS). But like all appropriate discordance, and like all ECG findings in general, these findings are always proportional.

The STD in V3-4 strikes me as likely too deep for the QRS complex. To me this is excessive discordance, with a maximal vector of acute ST depression in V3-V4. The STD is still present out to V6, but the proportion is maximal in V3-V4.

As we always say on this blog, ST depression maximal in V3-V4 is always considered posterior OMI until proven otherwise.

So what would be your next step if this were your patient?

We confirmed that the patient was having active chest pain, and I looked in the system for the most recent prior ECG:

What does this baseline ECG tell you?

This ECG shows the normal proportions of RBBB, with leads V3 and V4 showing the appropriate discordance of very small STD with shallow negative T-waves. Interestingly, V2 again looks out of place, but multiple ECGs make this unlikely.

Given our extremely high suspicion of OMI, we activated the cath lab despite this ECG obviously not meeting STEMI criteria.

The cardiologists came down and in the meantime we recorded posterior leads:

Leads V4-V6 are actually V7-V9. What do you think?

Two possibilities:
1) the patient has started to reperfuse since the first ECG 10 minutes ago, but this is extremely unlikely because V1-V3 (which have not been moved) remain the same.
2) this posterior ECG shows no signs of posterior OMI, either because
a. posterior leads are not sensitive for posterior OMI (it is extremely common for posterior leads to not show significant STE, and for practitioners to be falsely reassured by seemingly less significant findings in the posterior leads compared to the regular 12 leads)
b. posterior OMI is not present (unlikely)

I was of course not reassured, and the patient continued to complain of 8/10 pain.

We strongly advised the cardiologists to take him to the lab, and due to his history and active chest pain (and the time of day), he was taken emergently for angiogram.

They found that his CABG graft to his posterior descending artery had a total thrombotic occlusion with TIMI 0 flow. They stented it with excellent angiographic result.

Echo showed preserved EF with "hypokinesis of the posterior and inferobasal wall segments."

The first troponin T resulted at 0.03 ng/mL (elevated slightly above upper reference limit of less than 0.01). Subsequent troponins were rising up to 0.16 ng/mL but not trended to peak.

Here is his ECG a day later:

Ratios back to normal in V1-V6. Expected findings and proportions for RBBB.

The patient had an otherwise uneventful course and was discharged to home. COVID results still pending!

Learning Points:

It is worth investing practice seeing many many examples of normal RBBB, LBBB, etc. so that your mind has a clear picture of what normal discordance and normal ratios for various conduction patterns.

ST segments and T-waves are always evaluated in the context of the QRS that generated them. You must understand the principle of appropriate discordance, and how it manifests in various conduction patterns if you wish to diagnose OMI.

In general, acute STD maximal in V1-V4 should be considered posterior OMI until proven otherwise.

Isolated posterior OMI can be thus diagnosed by excessively discordant STD maximal in V1-V4.

Posterior leads are usually a waste of time, often times lead inexperienced readers to be falsely reassured, and very very rarely actually might help decision making. Record them if you have nothing better to do, but never let them reassure you if your gut tells you that there was true STD maximal in V1-V4. Smith comment: The only time I think they are worth recording is when there is no evidence of OMI on the ECG - then maybe you will find something with posterior leads. I say maybe, but I can't think of a case in which I found anything I did not see on the regular 12 leads. Literature from the 90s suggests this happens, but they don't publish the actual ECGs and it may be that, if I looked at them, I would be able to make the diagnosis without the posterior ECG.

This case is yet another example of performance above and beyond the rudimentary STEMI criteria for the diagnosis of Occlusion MI.

See these other relevant cases:

Right Bundle Branch Block and ST Depression in V1-V3. Is that normal? And a complication.

Is This a Simple Right Bundle Branch Block?

MY Comment by KEN GRAUER, MD (4/12/2020):
Insightful case by Dr. Meyers — that highlights a number of important points regarding assessment of ECG changes for ischemic heart disease in the presence of RBBB. Before addressing the specific tracings in this case — I’d like to review a different perspective aimed at rapid assessment (in less than 5 secondsof RBBB, and the presence (or absence) of a hemiblock.
  • By way of review — I suggest taking a look at the July 1, 2019 post by Dr. Smith, in which there are several similarities to the case Dr. Meyers is presenting here.

I’ve reproduced Figure-1 from this July 1, 2019 post. For full discussion — Please CHECK OUT My Comment and the links I provide in this 2019 post — but in brief, the TOP image in Figure-1 shows the expected QRS morphology for RBBB and LBBB in the KEY leads ( = right-sided lead V1 + left-sided leads I and V6).
  • RBBB — is diagnosed by the presence of an rsR’ complex (or its equivalent) in lead V1 + the finding of wide terminal S waves in leads I and V6.
  • LBBB — is diagnosed by the presence of an QS or rS complex in lead V1 + the finding of a monophasic R wave in leads I and V6.

PEARL #1: The series of RED and YELLOW arrows in the schematic TOP image in Figure-1 — which is then applied to an actual 12-lead example of RBBB in the BOTTOM image — illustrate the user-friendly (and surprisingly accurate) concept of “ST Opposition”.
  • That is — the ST segment and T wave should be oppositely directed to the last QRS deflection (RED and YELLOW arrows in Figure-1) in each of the 3 KEY leads (ie, leads I, V1, V6). Deviation from this pattern is not normal — and indicates a primary (1°) ST-T wave change (that should suggest the possibility of ischemia or infarction that may be new or old).

Figure-1: Schematically in the TOP: Assessment of ST-T wave changes expected with typical RBBB or LBBB. BOTTOM: Illustration of these concepts applied to a 12-lead tracing showing ECG findings of typical RBBB. Since the last QRS deflection in lateral leads I and V6 is negative with a “typical” RBBB (RED arrows in these leads) — the T wave in these leads is upright, as expected (YELLOW arrows in I and V6). The last QRS deflection in right-sided lead V1 is the upright R’ (RED arrow in V1) — so the ST segment and T wave in this lead is negative, as expected (YELLOW arrow in V1).

Is there a HEMIBLOCK?
In the case discussed today — the question was raised about the possibility of bifascicular block (ie, RBBB + LPHB). Realizing the lack of consensus among cardiologists about this issue — I’ve developed a simplified approached over the years that accurately distinguishes between RBBB with or without a hemiblock in less than 5 seconds.
  • IF interested in my user-friendly approach on VIDEO to ECG diagnosis of the Hemiblocks  CLICK HERE (this link takes you directly to 26:08 as the point to start watching in this 42-minute video on Axis & Hemiblocks).
  • Alternatively — full discussion of my approach to the Hemiblocks is covered in free download of my Section 7 PDF on Axis/Hemiblocks (from my ECG-2014-ePub).

I summarize the “short answer” to my approach on the Hemiblocks below — and illustrate this in Figure-2:
  • Although the left bundle branch divides into literally millions of fibers — for practical purposes, after the short, common left bundle branch — there are 2 main divisions to the rest of the left bundle branch: i) the left anterior hemifascicle; andii) the left posterior hemifascicle. Impaired conduction down one of these hemifascicles results in a hemiblock. (If there is no conduction at all down both fascicles — the result is complete LBBB).
  • Hemiblocks may occur either alone — or, in association with RBBB (in which case we say there is bifascicular block).
  • LPHB (Left Posterior HemiBlock) is rare — because the left posterior hemifascicle is the much thicker fascicle anatomically, and it has a dual blood supply. When seen — LPHB is almost always associated with RBBB.
  • LAHB (Left Anterior HemiBlock) is common — either as an isolated conduction defect, or in combination with RBBB. PEARL #2: In my experience — up to 98-99% of all hemiblocks are LAHB.
  • Diagnosis of LAHB is easy! Although experts cite various criteria — for practical purposes, there is LAHB if you have a “pathologic” LAD (Left Axis Deviation) — which I define as a left axis more negative than -30 degrees. PEARL #3: If the QRS complex in lead II is clearly more negative than positive — then for practical purposes, there is LAHB!
  • Note: The concept of “axis” makes no sense when there is RBBB. This is because the direction of ventricular activation with RBBB goes first from left-to-right (as the septum is depolarized) — then from right-to-left (as the LV is depolarized) — and finally, back again from left-to-right (as the “blocked” RV is finally depolarized). Thus, vectorial summation (ie, the “axis”) of this zig-zag left-to-right-to-left-to-right effect produced by the continually changing direction of electrical activity during ventricular depolarization with RBBB — does not result in useful clinical information.
  • PEARL #4: ALL that we care about clinically when there is RBBB is whether: i) RBBB is the sole conduction defect; ii) there is RBBB + LAHBoriii) there is RBBB + LPHB.

Figure-2 schematically summarizes what to look for when the KEY leads (I, V1, V6) establish the diagnosis of RBBB. One of these 3 entities will be present:
  • There is RBBB/LAHB — if in addition to RBBB, the QRS complex in lead II is clearly more negative than positive (Left Panel in Figure-2).
  • There is RBBB/LPHB — if in addition to RBBB, the straight portion of S wave descent in lead I is obviously predominantly negative (Right Panel in Figure-2).
  • If in association with RBBB the QRS complex in lead II is not predominantly negative — and, the straight part of the S wave in lead I is not clearly much more negative than positive — then all that there is, is RBBB (This was the case for the bottom tracing in Figure-1).

Figure-2: Schematic representation of bifascicular block from RBBB + either LAHB or LPHB (See text).

Let’s Return to TODAY’s CASE:
For illustrative purposes — I’ve reproduced and labeled some key findings from the 3 12-lead tracings pertinent to this case in Figure-3. (Note that I’ve omitted ECG #3 [the tracing with posterior leads] from Figure-3 — which as per Dr. Meyers’ discussion, did not contribute to this case).

Figure-3: The initial ECG in this case ( = ECG #1) — a prior tracing for comparison ( = ECG #2) — and a follow-up ECG done the next day after PCI ( = ECG #4).

MY THOUGHTS on ECG #1: I completely agree with Dr. Meyers that even in the absence of any clinical information about the patient in this case — ECG #1 has to be interpreted as highly suggestive of acute coronary disease until proven otherwise.
  • The rhythm in ECG #1 is sinus at a regular rate of ~85/minute. The PR interval is normal — but the QRS complex is wide as the result of complete RBBB (diagnosed by the presence of a typical rSR’ complex in lead V1, with taller right rabbit ear + wide terminal S waves in lateral leads I and V6).
  • Completing systematic assessment — the QTc appears slightly prolonged — there is RAA (tall, pointed P wave in lead II ≥2.5mm tall) — there are small, narrow q waves of uncertain significance in inferolateral leads — and there are markedly abnormal ST-T wave changes (to be described in detail momentarily).
  • As per Dr. Meyers — lead V2 looks “off” (it just doesn’t make physiologic sense to see a QRS complex with predominant negativity in lead V2, sandwiched between the rSR’ complex in V1, and the predominantly positive QRS complex we see in lead V3).
  • As to the question of whether there is bifascicular block (RBBB + LPHB) in ECG #1 — the initial straight portion of S wave descent in lead I is clearly not more negative than positive. By the criteria I favor (discussed above in Figure-2) — the straight portion of S wave descent in lead I must not only be more negative than positive, but predominantly negative — and this criterion is clearly not met. Therefore, I’d say there is RBBB in ECG #1 — but not LPHB.

HOW Do We KNOW that ECG #1 is Clearly Abnormal?
Even without the benefit of any clinical information — there are a number of findings in ECG #1 that clearly suggest acute coronary syndrome until you prove otherwise. Arriving at the same answer as did Dr. Meyers — I approached the issue from a slightly different perspective:
  • By the concept of ST Opposition (See Pearl #1 and Figure-1 above) — the T waves in lateral leads I and V6 of ECG #1 should be oppositely directed to the last QRS deflection in these leads, which is the wide terminal S wave (PINK arrows in I and V6). But instead of being opposite (ie, an all-positive T wave) — the T waves in leads I and V6 of ECG #1 are biphasic (PURPLE arrows down; BLUE arrows up). This is not normal. Instead, it constitutes a primary T wave change — that in a clinical context of new chest pain may indicate ischemia or infarction that could be acute.
  • By this same principle of ST Opposition — both the ST segment and the T wave in lead V1 should be oppositely directly to the last QRS deflection ( = the R’) in this lead. But instead of showing slight ST depression — the ST segment in lead V1 is isoelectric (horizontal dotted RED line in lead V1). This is not normal!
  • Dr. Meyers emphasized that the amount of J-point ST depression in leads V3 and V4 of ECG #1 was out of proportion to what should be expected for simple RBBB. The easy way to remember this — is to consider that since RBBB is expected to produce some ST depression in lead V1 (by the concept of ST Opposition) — the amount of J-point ST depression tends to be maximal in lead V1 (and perhaps also in V2) if the only thing going on is simple RBBB (since lead V1 is the lead in which you see the rsR' complex). This is not what we see in ECG #1 — in that the amount of J-point ST depression becomes greater as we move across to the mid-chest leads.
  • Finally — the shape of the ST-T wave is “off”. Instead of a relatively straight, gently downsloping ST segment as expected in response to simple RBBB — there is ST segment coving (curved RED lines in leads V3, V4, V5 of ECG #1) — and this clearly is not normal. The ledge-like (straight) ST segment depression in leads II and V6 is also not normal.
  • Bottom Line: While impossible to know without seeing a prior ECG if the above findings in ECG #1 are acute or longstanding — the coved shape and disproportional amount of ST depression we see in this tracing is way beyond that expected simply from RBBB — and has to be interpreted as acute until proven otherwise!
  • P.S.: Did you note the excessive fragmentation in the S waves of leads I, aVL, V2, V4, V5 — and in the R’ component in lead V3? This degree of fragmentation is not expected with simple RBBB — and strongly suggests this to be a patient with underlying structural heart disease (ie, scar, likely from previous infarction).

How the HISTORY Helps?
Neither Dr. Meyers nor I knew any clinical information at the time we first interpreted ECG #1. Then we learned the patient is a man in his 60s with a history of coronary disease, who is S/P CABG — and who presented with new chest pain.
  • Learning this clinical information in the context of the tracing seen in ECG #1 solidifies the need for prompt cardiac catheterization.

Other than RBBB — Was the Prior ECG as Expected for RBBB?
I interpreted the prior ECG ( = ECG #2) as showing sinus rhythm with complete RBBB. I noted a number of additional findings:
  • Excessive fragmentation for RBBB (in leads I, aVL, V3) — suggesting the patient has underlying heart disease.
  • The T wave in lead I of ECG #2 is negative (PURPLE arrow) instead of upright, as would be expected if there was simply RBBB.
  • The ST segment in lead V1 of ECG #2 is not depressed (as we’d expect) — and the T wave in this lead is upright (BLUE arrow) instead of oppositely directed to the last QRS deflection (the R’) in this lead (PINK arrow in V1).
  • The coved shape of the ST segment in lead V2 is not normal (instead, there should be a straighter, more gently sloping depressed ST segment in this lead).
  • Bottom Line: While impossible to tell if these abnormal findings in the prior ECG ( = ECG #2) are new or old (my guess is that they are old) — these findings in ECG #2 are more than what should be expected from simple, isolated RBBB.
  • That said — comparison of ECG #1 with ECG #2 clearly shows that a series of worrisome, ischemic-looking changes have now developed in ECG #1!

What do you See on the Final ECG (done after PCI)?
The final ECG in this case ( = ECG #4) done the next day after PCI again shows sinus rhythm with RBBB.
  • Compared to the initial ECG ( = ECG #1) — the amount of ST depression (especially in the mid-chest leads) is clearly less in ECG #4.
  • That said — there are still a number of longstanding abnormal ECG findings in ECG #4 beyond those expected with simple RBBB. These include shelf-like (flat) ST depression with biphasic T waves in leads I and V6 — and ST segment coving, with more J-point ST depression in leads like V4 than should be expected with simple RBBB.

Our THANKS to Dr. Meyers for presenting this case!
  • IF You'd Like Another Example — in applying the above concepts regarding recognition of RBBB + hemiblock + acute coronary disease — CHECK OUT the November 21, 2018 post on Dr. Smith’s ECG Blog!


  1. Nice case. Covid results still pending ?

    1. @ Felipe — I don't know the answer to your question, as it wasn't my case. I've passed your question on to Dr. Meyers to see if he has any follow-up on this.

    2. Looks like it came back negative, came back after I wrote the post. Of course, there are false negatives. and anecdotally we are seeing so many patients with covid who have all kinds of thrombotic complications that seem to be related.

  2. Interesting ECG.

    Between the previous and the first ECG there appears to have been a pseudonormalization of the T waves in Leads I and aVL.

    1. Thanks Jerry. Both the prior tracing ( = ECG #2) — and the 1st ECG ( = ECG #1) are abnormal by my interpretation. The change that you note (the inverted high lateral T waves from the prior tracing on their way to becoming positive (ie, “pseudonormalizing”) is definitely occurring — but the points I’d emphasize are: i) Viewed by itself, the downsloping ST segment leading to a biphasic T wave with terminal positivity in leads I and aVL is clearly abnormal (and part of the overall picture of acute coronary syndrome); - AND - ii) There definitely are evolving dynamic ST-T wave changes ongoing — given clear difference between ST-T wave appearance in leads I and aVL between the 2 tracings. THANKS (as always!) for your comment! — :)

  3. Thanks Ken...

    From my perspective, I don't accept that every ST segment depression followed by an upright T wave implies a -/+ biphasic T wave. I do not see any evidence of T wave inversion in the first ECG done in the ER in Leads I and aVL. There is definitely a down-sloping ST depression followed by an upright T wave. I do NOT see any inverted T wave in Leads I and aVL in that particular tracing. Can anyone show me where the ST segment ends and the inverted T wave begins with any assurance?

    1. Jerry — I don’t think we are far apart regarding interpretation of this tracing. The clearly inverted T waves in leads I and aVL were seen in my ECG #2 ( = the prior tracing), which appears above in my Figure-3. I think that the T wave in ECG #1 is biphasic in leads I and aVL. We agree that the terminal portion of the T wave in these leads of ECG #1 is positive. I could be wrong (!) — but to me, considering the timing and duration of the clearly negative T wave we see in lead V2 of ECG #1 — the positive component of the T wave in leads I and aVL is too short-lived to comprise the entire T wave — and the slope of the downward slanting ST segment in these leads (given this timing of the last and most negative point of the ST segment) suggests to me that these T waves are biphasic. Again — I fully acknowledge that I could be wrong and you could be correct. That said, I’d emphasize: i) that it is often difficult with certainty to define the “end” of the ST segment and the beginning of the “T wave” — AND, most importantly — ii) regardless of whether you or I is correct — the SHAPE of the ST-T wave in leads I and aVL of ECG #1 is clearly abnormal for a patient with RBBB (ie, the ST segment should not be downsloping in these lateral leads …) — so in the context of the clinical scenario for this case + other abnormal ST-T wave findings on this tracing — I think we both agree that the ST-T wave appearance in leads I and aVL of ECG #1 is fully consistent with acute ischemic heart disease. I hope the above makes sense? THANKS as always for your wonderful insights! — :)

  4. Ken...

    Thank you for clarifying what you see for me. I was primarily referring to the ECG recorded in the ED and not the old ECG. I DO see your point regarding the biphasic T waves on the old tracing. And I agree - they ARE biphasic in I and aVL. And they ARE obvious. I still feel the ECG recorded in the ED is not so clear cut. However, this is getting to be like the parable of the 7 blind men describing an elephant. We are looking at the same thing from different perspectives - except in our case we arrive at the same conclusion.

    I appreciate the time you've taken to clarify things.

    1. Thanks Jerry. I think the important point is that we reached a similar conclusion. I always welcome (and I learn) from your comments! — :)

  5. thank you Pendell.
    it is interesting that we have had a significant decrease in daily ED patient volume overall, but i suspect that the overall acuity has risen. Also, as in this case, public awareness, and concern, has brought patients who "just aren't feeling well" (chest pain, shortness of breath, fatigue, gi complaints, even neuro complaints, to the ER requesting COVID 19 testing.
    and... many of these have serious cardiac, pulmonary, or neurologic pathology with no COVID19. and what is worse, is that we know that COVID 19 is a multi-faceted disease, with various presentations, and also a hyper-coagulable state, with d-dimers of several thousands, and so a covid 19 patient might present with severe disease of heart (myocarditis, cardiomyopathy), lung (ARDS, pulmonary embolism) neurologic (seizures, stroke, headache) in addition to, or even without, the "typical" fever, cough, infiltrates.

    thank you Pendell for a good case of PWMI. and kenny g and jerry jones, thank you too. i shall never look at leads I and aVL ever the same. keep well and safe in long island, florida, and texas. these are terrible times.

    1. THANKS for your comments Tom! LOTS for us all still to learn about COVID-19 — with in particular the complicating factor of it being a multi-faceted disease, with potential serious end-organ damage NOT limited just to the lungs ...

  6. thanks for lucid explaination
    one thing willing to confirm is regarding Biphasic T wave : What i learnt is Biphasic T wave with terminal negativity is more specific for ischemia, whereas Biphasic T wave with terminal Positivity is more specific in hypokalemia.
    Is that applies to all leads or only in precordial leads.
    I agree that these subtle abnormalities from baseline ECG and atypical findings from usual RBBB can indicate underlying acute Ischemia

    1. Terminal positivity may be reciprocal to a lead with terminal negtivity. One sees this in III when there is reperfusion in aVL, in aVL when there is reperfusion in III, and in V2 when there is reperfusion of the posterior wall.


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