Saturday, May 27, 2023

ECG Blog #381 — Why was the Troponin Normal?

The ECG in Figure-1 was obtained from a 60-ish year old man with a history of coronary disease (including prior CABG) — who presented to the ED (Emergency Department) with new CP (Chest Pain) of 3 hours duration, diaphoresis and nausea/vomiting. 
  • The patient was hypotensive at the time his initial ECG in Figure-1 was obtained.

The decision was made not to immediately perform cardiac cath — because there is no ST elevation in Figure-1 — and because the initial troponin was negative.
  • Do YOU agree with the decision not to cath at this time?
  • How would you interpret ECG #1

Figure-1: The initial ECG in today's case.

MY Initial Thoughts on Today's CASE:
The clinical scenario presented in today's case is extremely concerning:
  • The patient has a known history of coronary disease.
  • His symptoms of CP are new! These symptoms are associated with diaphoresis, naursea/vomiting — and of special concern, hypotension! Even before looking at the initial ECG — the clinical scenario suggests probable need for prompt cath until proven otherwise!

Interpretation of ECG #1:
Normal sinus rhythm at ~80-85/minute is seen in Figure-1. The PR interval is normal — but the QRS is wide, with QRS morphology consistent with RBBB (Right Bundle Branch Block) and LAHB (Left Anterior HemiBlock). There is no chamber enlargement. 

Regarding Q-R-S-T Changes:
  • There is a Q wave in leads aVL that is "significant" — given its width relative to the R wave in this lead. This may represent high-lateral infarction at some point in time. No other Q waves are present (ie, There is a tiny initial r wave in lead V1).
  • R wave progression — is irrelevant, given the RBBB. 

Regarding ST-T wave Changes:
  • The most "eye-catching" abnormalities are in leads V3 and V4 — both of which show definitely abnormal ST depression. The QRS complex is tiny (as well as fragmented) in lead V3 — with disproportionate J-point ST depression, followed by a coved, downsloping ST segment with an abnormally biphasic terminal T wave. The shelf-like ST depression in lead V4 is never normal, nor is the terminal T wave positivity seen in this lead. The S wave in lead V4 is also fragmented (ie, a sign of prior "scar" and/or infarction).
  • Abnormal ST depression continues in leads V5 and V6, each with prominent (? hyperacute) T waves. The QRST appearance of these 2 lateral chest leads looks very similar to the QRST appearance in each of the inferior leads (albeit there is less J-point depression in the inferior leads).
  • There is ST segment coving and T wave inversion in lead aVL.
  • There is significant ST elevation in lead aVR.
  • Finally, in lead V1 — the ST-T wave depression is expected with RBBB — but the subtle-but-real ST elevation in this lead is not expected with simple RBBB.

Putting It All Together:
Missing from this presentation at this time — is a prior (baseline) ECG on this patient who has a known history of significant coronary disease. As a result — I was not initially sure what was "new" vs "old". That said:
  • There is bifascicular block (RBBB/LAHB) — which if new, would be an extremely worrisome sign.
  • Multiple leads show abnormal ST segment straightening, with ST depression. This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI (Occlusion-based Myocardial Infarction) — most probably with multi-vessel disease (ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1).
  • This patient has new CPand — he is hypotensive.

  • BOTTOM Line: The normal initial troponin — and lack of ST elevation are not reasons for not performing cardiac catheterization. Acute posterior OMI results in ST depression, not ST elevation (with this ST depression typically maximal in leads V2-to-V4). Troponin rise is sometimes delayed. Even if acute coronary occlusion is not present in today's case — the findings of diffuse subendocardial ischemia in a patient with bifascicular block and known coronary disease — who presents with new CP and hypotension — constitute clear indication for immediate cath lab activation at this point in the case.


The CASE Continues:
Another ECG was obtained 54 minutes after ECG #1. Unfortunately — I do not have information on the patient's symptoms and hemodynamics at the time ECG #2 was recorded.

For ease of comparison in Figure-2 — I've put these 2 ECGs together.
  • How would you interpret ECG #2 in light of the initial tracing done 54 minutes earlier?

Figure-2: Comparison between the initial and repeat ECGs.

MY Thoughts on the Repeat ECG:
QRS morphology in the repeat ECG is virtually the same as in the initial tracing — which means that lead-by-lead comparison for subtle differences in ST-T wave morphology will be valid.
  • There are now Q waves in leads V1 and V2 of ECG #2 — that were not previously present.
  • There is more ST elevation in leads aVR and V1.
  • There is more ST depression in virtually all leads compared to what was present in ECG #1.

  • Impression: ECG signs of diffuse subendocardial ischemia have clearly increased. Coronary reperfusion is urgently needed.

The Baseline ECG was Found:
A prior ECG on today's patient, done ~9 months earlier — was found. For ease of comparison in Figure-3 — I've put this baseline tracing together with the initial ECG in today's case. 
  • What do we learn from the baseline ECG? 

Figure-3: Comparison between the initial ECG in today's case — with a prior tracing recorded ~9 months earlier. What does this baseline ECG tell us?

MY Thoughts on the Baseline ECG:
Although I lack information regarding when the baseline ECG was obtained with respect to this patient's bypass surgery — 9 months earlier, the QRS was narrow without evidence of any conduction defect. With the exception of minimal, nonspecific inferior lead ST-T wave flattening — ECG #3 is essentially a normal tracing!
  • Impression: The baseline tracing confirms that all of the above-described findings in ECG #1 are acute!


CASE Conclusion:
A final 12-lead ECG was obtained on today's patient — which for ease of comparison in Figure-4, I have put together with ECG #2.
  • Unfortunately — I do not have information on the sequence of treatment interventions, nor on correlation between patient symptoms, hemodynamics and specific timing with each of these serial ECGs.

  • At some point ~1-2 hours after the initial ECG — the patient developed runs of VT, leading to cardiac arrest. He could not be resuscitated.

There are lessons to be learned from this case. I include the final 12-lead that was done in Figure-4 — as I found it instructive to compare this last tracing with ECG #2 done 52 minutes earlier.
  • How would you interpret ECG #4?

Figure-4: Comparison between the last ECG and ECG #2.

MY Thoughts on the Final ECG:
I am not certain what the rhythm in ECG #4 is.
  • We see runs of rapid beats that I initially thought represented an irregular VT. However, the long lead II rhythm strip at the bottom of the tracing shows these runs to be punctuated by a number of pauses (ie, between beats #3-4; 5-6; 7-8; and 15-16) — and that an upright sinus P wave is clearly seen to be present at the end of each pause before beats #1, 4, 6, 8 and 16.
  • Looking at each of the 18 beats in this long lead rhythm strip — the QRS morphology of sinus beats #1,4,6,8,16 is similar to QRS morphology of the rapid, irregular beats that follow these sinus-conducted beats in virtually each of the simultaneously-recorded leads of the 12-lead tracing (with possible exception of beats #14,15) — which makes me wonder if the rhythm in the long lead II is sinus with multiple successive PACs (perhaps a short run of AFib from beats #9-thru-15?) — vs — sinus rhythm with very frequent PVCs manifesting a QRS morphology very similar to the morphology of sinus beats.

  • What is certain — is the continued marked ST depression in the mid-chest leads, consistent with an ongoing, extensive infarction in this patient with severe symptoms and hypotension.


Acknowledgment: My appreciation to 張三毛 = JJ (from Taiwan) for the case and this tracing.



Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.

  • ECG Blog #271 — Reviews the concept of diffuse Subendocardial Ischemia.

  • ECG Blog #316 — The patient died. Was the LMain coronary artery the "culprit"?

Additional Relevant ECG Blog Posts

  • ECG Blog #193 — Reviews a case with a dominant LCx as the "culprit" artery (with ECG AUDIO Pearl on the concept of "OMI" and on Predicting the "Culprit" Artery).

  • ECG Blog #184  That magical inverse relationship between leads III and aVL.
  • ECG Blog #167 — More on that "magical" lead III-aVL relationship.
  • ECG Blog #183 — deWinter-like T waves.
  • ECG Blog #374Acute LMain Occlusion.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( Occlusion-based MI) as an improvement from the outdated STEMI paradigm.

  • ECG Blog #56 — Posterior MI; Mirror Test.
  • ECG Blog #80 — What's the Culprit Artery (and the Mirror Test).
  • ECG Blog #82 — What’s the Culprit Artery?
  • ECG Blog #162 — What’s the Culprit Artery?
  • ECG Blog #193 — What's the Culprit Artery? 
  • ECG Blog #222 — What's the Culprit Artery? 

  • ECG Blog #367 — for another example of acute LCx OMI

  • ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
  • ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

  • The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.

  • ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamicST-T wave changes
  • ECG Blog #230 — How to compare serial ECGs.

  • ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...

  • ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
  • ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post)
  • ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.


  1. I enjoyed reading this tremendously. Any new RBBB in ACS setting is "concerning", and you show us more than that. What a feast for the mind!! Thank you.

  2. So this patient was likely having a multi-vessel OMI, why were his troponins normal?

    1. Thanks for your question. Surprisingly — the initial troponin can be negative! Dr. Smith's informal study showed more than 25% of initial troponin values in patients with acute OMI ( = occlusion-based MI) had a normal initial troponin. Serial troponins will turn positive (unless the period of occlusion is very brief — and followed by spontaneous reopening). Note in today's case — that the patient presented relatively "early" (within 3 hours of CP onset) — so not so surprising that initial troponin might be negative ...