Wednesday, March 8, 2023

ECG Blog #367 — Recognize The KEY Finding?

You are given this ECG to review. No history is provided — except knowing that this patient was seen in the ED (Emergency Department).

  • Is there a potential problem with this ECG?

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

NOTE: Many of us are charged with reviewing ECGs that have been interpreted by other clinicians — often without the benefit of much (or any) history. I did this for 30 years — overseeing (that is "overreading") the ECGs of 35 clinician colleagues. 
  • Given a "pile" of ECGs to review without benefit of the history — I had to "strike a balance" between pulling the chart (or calling the clinician) for each tracing (to see if the ECG was correctly interpreted) — and — my time constraints to finish "the pile" as time efficiently as possible, so that I could get on to my "normal" daily tasks. As a result — I had to be selective about which ECGs I needed to find out more about.
  • This is relevant to today's case — because the ECG in Figure-1 is a tracing that mandates: i) Finding out what the history is (which since we know the patient was seen in the ED — most probably entails chest pain that may be new); and, ii) Pulling the chart or calling the clinician to find out what was done clinically.

MY Thoughts on the ECG in Figure-1:
Today's case highlights a subtle-but-critical ECG finding that all-too-often is missed. It was missed in today' case. As a result — cardiac cath (and reperfusion of an acutely occluded LCx [ = Left Circumflex ]) artery — was delayed for 9 hours, until markedly elevated troponin values finally brought attention to this case.
  • The rhythm in ECG #1 is sinus. Intervals (PR, QRS, QTc) and the mean QRS axis are normal. There is no chamber enlargement (Not shown in Figure-1 is indication of the normal 10 mm = 1 mV standardization mark).
  • Assessment of ST-T wave appearance in the limb leads of ECG #1 is essentially normal.
  • In the chest leads — R wave progression is appropriate, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.

KEY Point: The abnormal leads in today's tracing are leads V2, V3 and V4.
  • Normally — there is a small amount of gentle-upsloping ST elevation in leads V2 and V3. This is not what we see in ECG #1. Instead — there is no ST elevation at all in V2,V3 — and there is straightening of the ST segments in leads V2,V3,V4 (RED lines in leads V2,V3,V4 in Figure-2).

  • In addition — the T waves in leads V2,V3 look taller-than-expected (given height of the R wave in these respective leads). In addition — these T waves look "fatter"-at-their-peak and wider-at-their-base than they should be given QRS amplitude in these leads.

  • To EMPHASIZE: These are subtle findings. But, in a patient who presents to the ED for new chest pain — seeing these subtle findings that are localized to leads V2-thru-V4 should at the least make you consider acute posterior OMI (Occlusion-based MI) — until you prove otherwise. The increased amplitude and volume of the T waves in leads V2,V3 may represent "reperfusion" T waves.

Figure-2: I've labeled the ECG from Figure-1 — to highlight the subtle-but-real ST segment flattening in leads V2,3,4 of ECG #1. If this patient was having new chest pain — the T waves in leads V2 and V3 may be hyperacute (See text).

Today's CASE Continues:
Some time after ECG #1 — a repeat ECG was obtained ( = ECG #2 in Figure-3).
  • What do YOU think?

Figure-3: The repeat ECG — done a bit after ECG #1.

MY Thoughts on the Repeat ECG:
It is difficult to assess the limb leads in ECG #2. This is because there are artifactual undulations in the baseline that result in some variation of ST-T wave morphology from one-beat-to-the-next. That said — I thought there were some definite changes in the chest leads.
  • To EMPHASIZE: The ST-T wave changes in ECG #2 (compared to ECG #1) — are subtle and EASY to overlook unless one compares ST-T wave appearance by looking lead-to-lead, one lead at a time. To facilitate this comparison — I have put the chest leads from ECG #1 and ECG #2 side-by-side in Figure-4.

Figure-4: Comparison of the chest leads from ECG #1 and ECG #2. Do you appreciate the changes that I've labeled in the repeat ECG?

Lead-by-Lead Comparison of Chest Leads in Figure-4:
For optimal lead-by-lead comparison — QRS morphology for the 2 tracings you are comparing should be as similar as possible. This is because significant change in QRS morphology would suggest some variation in lead placement that may clearly affect ST-T wave appearance.
  • Apart from slight increase in R wave amplitude in leads V4 and V5 of ECG #2 — there is no significant difference in QRS morphology between the 2 tracings shown in Figure-4. This suggests that any difference in ST-T wave morphology between these 2 tracings is likely to represent a "real" difference due to an ongoing ischemic process.

  • Compare ST-T wave appearance of the 2 leads within the RED-GREEN rectangle in ECG #2 — with ST-T wave appearance of leads V2,V3 in ECG #1. Don't the ST segments in leads V2,V3 of ECG #2 look straighter, with more distinct angulation between the end of the ST segment and the start of the T wave ascent?
  • Isn't the ST segment takeoff in leads V5,V6 of ECG #2 straighter than it was — compared to its appearance in leads V5,V6 of ECG #1? (comparison of RED vs BLUE lines in these leads). 
  • Isn't there also now some J-point ST elevation in leads V5,V6 of ECG #2? (RED arrows in these leads).

  • KEY Point: Unfortunately, we lack important information about clinical correlation in today's case: i) We do not know how much time passed between recording the 2 tracings in Figure-4; ii) We do not know about the presence (and relative severity) of chest pain at the time each tracing was recorded (ie, Was chest pain increased when ECG #2 was recorded?).

  • BOTTOM Line: What we do know — is that this patient presented to the ED presumably for new symptoms — and that the subtle-but-real ST-T wave abnormalities seen in ECG #1 have increased in ECG #2. This qualifies as "dynamic" ST-T wave change — and in a patient with new chest pain, this is indication for prompt cath to define the anatomy and ensure reperfusion. 
  • The ST-T wave changes we describe above localize to the posterior wall (ie, the ST-T wave changes in leads V2-V4) — and to the lateral wall (the ST-T wave changes in leads V5,V6 of ECG #2) — which suggest acute LCx (Left Circumflex) occlusion until proven otherwise.

CONCLUSION of Today's Case:
The subtle-but-real ST-T wave changes in today's initial tracing — as well as the equally subtle-but-real "dynamic" ST-T wave changes seen in the repeat tracing — went unrecognized for 9 hours. Maximum Troponin I elevation attained 30,000. Cardiac cath revealed acute LCx occlusion.
  • Fortunately — this patient did well, and was discharged with surprisingly good LV function. But there are important lessons to be learned from this case!


Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) 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 #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 #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 #260 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-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 #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).

  • 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.

  • ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).

  • 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.


ADDENDUM (3/8/2023):
The original tracing in today's case was recorded using the Cabrera lead format. This ECG recording format is favored in Norway, Sweden, Germany — and in a number of other countries. 
  • Given the ever expanding use of the internet — virtually all clinicians everywhere are likely to encounter this format at the very least, from time to time. As a result — I show in Figure-5, the initial ECG in today's case as it was originally recorded using the Cabrera format (Please see my Editorial Note near the top of the page in ECG Blog #365 for review of the basics of the Cabrera recording system)

  • For comparison — I've reproduced in Figure-6 the initial ECG shown in today's case, in which I've simulated the standard recording format used in the U.S. and most other countries (ie, I inverted lead aVR — and moved the location of various limb leads).

Figure-5: The initial ECG in today's case — as it was originally recorded using the Cabrera format. (Given ever expanding use of the internet — it's good to become familiar with this recording format, that in many ways is more logical than the standard format we are used to).

Figure-6: For comparison purposes — I've reproduced the initial ECG in today's case that was shown in Figure-1.

Included below are a series of links and other material relevant to detection of the “culprit” artery — and my thoughts for making the case to replace the term “STEMI” with OMI” (in the hope of substantially increasing detection of acute coronary occlusion).

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

  • PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
  • PDF File: Posterior MI and the “Mirror Test” —  

Figure-7: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post


NOTE: This Editorial just published by Drs. Steven Smith and Pendell Meyers details use of Hyperacute T-Waves in the diagnosis of acute OMI — "Hyperacute T-waves Can Be a Useful Sign of Occlusion MI IF Appropriately Defined" (Ann Emerg Med — March 3, 2023).

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MIshould replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.


  1. Thank you for introducing great case. In addition to the lead V2~V4 mentioned above about initial ECG, I think the T wave morphology of V1("down-up" T wave pattern) is also obviously abnormal. (In fact, the abnormal finding I discovered firstly was V1, followed by V2 and V3).
    And for the second ECG, although very accurate analysis is somewhat limited due to baseline artifacts, don't you think that reciprocal ST depression and flattening in lead III are clearly more prominent than the initial ECG?
    Similarly, ST segment elevation of lead aVL and reciprocal depression of lead aVF are slightly more prominent in my opinion, but it's so subtle that they appear rather indeterminant in the presence of baseline artifacts. However, since the abnormality of lead III mentioned above is relatively clear, it is thought that ST-T waves of lead aVL and aVF have also changed.

  2. THANK YOU for your astute comments. This is what I wrote in my above description — "It is difficult to assess the limb leads in ECG #2. This is because there are artifactual undulations in the baseline that result in some variation of ST-T wave morphology from one-beat-to-the-next. That said — I thought there were some definite changes in the chest leads."

    I agree with you that lead III does appear to have acute changes (leads II, aVL, aVF just have too much artifact and baseline movement for me to tell). That said — I didn't think the increased ST flattening and depression isolated to lead III in ECG #2 really added to defining the problem (or "culprit" vessel) — whereas I thought the changes in the chest leads DID (and supported the LCx as the culprit vessel).

    I'm happy to "agree to disagree" with you if your opinion still differs from mine — but I think we DO both agree on the subtle-but-real chest lead changes consistent with acute LCx OMI.

    THANK AGAIN for your astute comments! — :)