Sunday, March 19, 2023

ECG Blog #369 — 10 Minutes Later ...

The ECG in Figure-1 was obtained from a man in his mid-60s — who presented with new chest pain.
  • Should the cath lab be activated?

Figure-1: The initial ECG in today’s case. Should the cath lab be activated?

MY Thoughts on the Initial ECG:
The rhythm in ECG #1 — is sinus at ~70/minute. All intervals (PR, QRS, QTc) are normal. There is no chamber enlargement.
  • There is significant LAD (Left Axis Deviation) — as the QRS is predominantly negative not only in lead aVF, but also in lead II. This results in a frontal plane axis of at least -40 degrees — which is consistent with LAHB (Left Anterior HemiBlock).

Regarding Q-R-S-T Changes:
  • There are no Q waves (ie, There is a tiny-but-present initial positive deflection [r wave] — in both leads III and aVF).
  • R Wave Progression overall is appropriate — in that Transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V3-to-V4.

  • PEARL #1: Although the zone of transition in the chest leads is appropriate — Note that the R wave in lead V2 increases abruptly in height (attaining 5 mm already by lead V2). This is relevant to today’s case (!) — as we will see momentarily.

Regarding ST-T wave abnormalities: 
  • PEARL #2: It's most time-efficient to assess ST segment and T wave abnormalities together — and to do so at the same time for all leads in a given anatomic area. For example, in Figure-1 — My “eye” was drawn first to the inferior leads (II,III,aVF) each of which show ST segment coving, followed by symmetric T wave inversion (BLUE lines that I've added to these leads in Figure-2).
  • KEY Point: It is important to note that while inferior lead ST-T wave changes are clearly more marked in leads III and aVF — they are also present in the 3rd inferior lead ( = lead II). It is far less likely for a notable ST-T wave finding in leads III and aVF to be the result of a normal repolarization variant — IF a similar ST-T wave appearance is also seen in the 3rd inferior lead ( = lead II). 

  • PEARL #3: Confirmation that the abnormal inferior lead ST-T wave findings just described are “real” (and indicative of a recent or acute cardiac event) — is immediately forthcoming from assessment of lead aVL — which shows the mirror-image opposite ST-T wave picture as is seen in lead III (ie, not only scooped ST depression — but also terminal T wave positivity in lead aVL — as seen in Figure-2). 
  • Further support that the picture in lead aVL represents true reciprocal ST-T wave changes to the abnormal inferior lead findings — is forthcoming from the similar ST-T wave shape (albeit a little less marked) for the ST-T wave depression in lead I.

  • To EMPHASIZE: My above description is intentionally made in “slow motion”. The total time it should take for you to arrive at this point in your interpretation (in which we already know that the cath lab needs to be activated)should be less than 10 seconds.

Figure-2: I've labeled significant ST-T wave findings in the limb leads of ECG #1.

Assessment of ST-T Wave Changes in the Chest Leads:
  • There is ST depression in leads V2-thru-V6 (See Figure-3). Leads V2 and V3 show terminal T wave positivity. The magnitude of ST-T wave change is maximal in lead V2 — with the insert in this lead showing a positive "Mirror" Test — that in this patient who presents with new chest pain, is diagnostic of acute posterior OMI — until proven otherwise.

  • PEARL #4: Normally, when there is acute posterior OMI — there is ST depression that is maximal in one or more of the leads between V2-to-V4. This ST depression sometimes extends more laterally (ie, to leads V5,V6 — as it does in Figure-3). That said — There should also be at least some ST depression in lead V1 with acute posterior OMI — unless something else is going on that results in ST elevation. The fact that instead of ST depression in lead V1, there is slight-but-real ST elevation (RED arrow in this lead in Figure-3) — strongly suggests that in addition to acute posterior OMI — there is also acute RV (Right Ventricular) involvement! (For more on this Pearl #4 — See the Audio Pearl and Figures-5 and -6 in the ADDENDUM below).

Putting It All Together:
In view of the history in today's case (ie, A man in his mid-60s who presents with new chest pain) — the ECG in Figure-1 is diagnostic of recent or ongoing acute infero-postero OMI.
  • The fact that the amount of ST elevation in the inferior leads of ECG #1 is minimal (and associated with more impressive T wave inversion in leads III and aVF) — suggests that we are seeing reperfusion T waves from spontaneous reopening of the "culprit" artery.
  • Consistent with the presence of reperfusion T waves in the inferior leads — is the modest amount of J-point ST depression in leads V2-thru-V4. The surprisingly tall terminal T wave positivity that we see in lead V2 almost certainly represents reperfusion in the posterior wall distribution.

  • To EMPHASIZE: Despite there not being "enough" ST elevation to satisfy millimeter-based criteria for an acute "STEMI" in ECG #1 — this initial ECG is absolutely diagnostic of OMI. The fact that spontaneous reopening of the occluded vessel has occurred in no way eliminates the risk that spontaneous reocclusion might at any time reoccur. Prompt cardiac cath is clearly indicated!

  • PEARL #5: We could probably get a better idea of the sequence of events in today's case with some additional history that correlates the timing of ECG #1 — with the timing of symptom onsetand — with the presence (as well as relative severity) of chest pain at the time the initial tracing in Figure-1 was done.

  • PEARL #6: The finding of slight-but-real ST elevation in lead V1 (RED arrow in this lead in Figure-3) — localizes the "culprit" artery to RCA (since the LCx does not supply the right ventricle).

Figure-3: Significant ST-T wave findings in the chest leads of Figure-1. The insert in lead V2 shows a positive "Mirror" Test indicative of acute posterior OMI

Today's CASE Continues: 
Approximately 10 minutes after ECG #1 was recorded — an ECG with right-sided chest leads was obtained ( = ECG #2).
  • For clarity in Figure-4 — I've put the repeat ECG together with the initial tracing.

  • How do YOU interpret the repeat ECG?

Figure-4: Comparison of the initial ECG — with the repeat tracing obtained 10 minutes later using right-sided leads.

MY Thoughts on the ECGs in Figure-4:
  • Although difficult to assess (because of artifact in lead V2R — and very low QRST amplitude in leads V3R-thru-V6R) — there is ST elevation in these last 4 right-sided leads. This confirms the acute RV involvement that we strongly suspected from the ST elevation in lead V1 of ECG #1.
Ideally, in addition to right-sided leads — a complete repeat 12-lead ECG with normal electrode lead placement would also have been done. Instead — we have no idea about what normally-placed leads V3-thru-V6 look like.
  • Keeping in mind that ECG #2 was obtained just 10 minutes after ECG #1 — We now see dramatic ST elevation in each of the inferior leads in ECG #2, in association with comparable reciprocal ST depression in lead aVL. Even without knowing if the patient's chest pain was increased at the time ECG #2 was recorded — the inescapable conclusion is that just 10 minutes after seeing reperfusion T waves in the infero-postero leads — there has now been spontaneous reocclusion of the "culprit" RCA!

  • PEARL #7: It is good to remember that lead V1R corresponds to a normally-placed lead V2 (and lead V2R corresponds to a normally-placed lead V1). As a result — We can compare lead V2 in ECG #1with lead V1R in ECG #2. When we do — it should be obvious that a comparable amount of acute ST-T wave change as is seen in the limb leads — has also occurred in the posterior wall distribution (further supporting the inescapable conclusion of spontaneous reocclusion of the RCA).

CASE Conclusion:
On seeing ECG #2 — cardiac cath was expedited. The RCA was confirmed as the culprit artery — and PCI was promptly performed with good result. There was insignificant disease in the LAD and LCx.


Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.


ADDENDUM (3/19/2023):

ECG Media PEARL #7 (4:50 minutes audio) — reviews the ECG findings of acute RV MI — as well as other pearls for determining the likely “culprit” artery.

FOR Other Examples of Acute RV MI:

Figure-5 (together with Figure-6): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).



Figure-6 (continued from Figure-5): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).


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 #190 — Reviews the concept of RV MI.

  • 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 (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

  • ECG Blog #184 and ECG Blog #167 — illustrate the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL
  • The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
  • The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 

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

  • ECG Blog #266 — Reviews distinction between Posterior MI vs deWinter T waves (with anterior terminal T wave positivity reflecting "Reperfusion" T waves).

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

  • ECG Blog #262 — Potential significance of Low Voltage with acute MI.
  • ECG Blog #272 — Significance of Low Voltage with acute MI.



  1. Great Interpretation, as usual! Emeritus Prof Ken Grauer has once again demonstrated the thrombosis is always dynamic. Occlusion occurs, then spontaneous lysis of clot, reperfusion and in the twinkling of an eye, a second OMI happens again, We see this sequence of events in patients very often, I am reminded of my own patient whose initial ECG showed obvious OMI and enroute to Hospital, she reperfused but minutes later when the doctor in the ED was doing the posterior leads, a second occlusion occurs. This Post is a "MUST READ" for all physicians. Here is KG, ECG Guru par excellence at his scintillating best.

    1. THANK YOU so much for the supportive comments! — :)