Sunday, January 15, 2023

OMI can be very subtle and easy to miss, but be a very large infarction.

I was reading ECGs on the system and came across this one.  

There is minimal STE in II, III, with an inverted T-wave in aVL.
There is a very flat ST segment in V2, with 0.5 mm of STD, highly suspicious for posterior OMI.
We showed in this paper that ANY amount of STD maximal in V1-V4 (especially in V2) in a patient with chest symptoms is posterior OMI until proven otherwise

I knew that if this is a patient with chest discomfort, that it is an infero-posterior OMI.

So I went to the chart and found that it was from a 50-something woman with CP of a couple hours duration.

Unfortunately, the OMI was not seen.

When the first troponin returned slightly elevated, this ECG was recorded 100 minutes later (too long to wait for a repeat ECG!!):

Now it is not subtle: there is clear, obvious inferior posterior OMI.

At this point, the cath lab was activated.  Angiography showed:

100% Distal RCA occlusion. Pre-procedure TIMI 0 flow was noted. Stent placed.  Post Procedure TIMI III flow was present. 

ECG recorded after PCI:

Large upright T-waves in V2, V3 indicated posterior reperfusion.

Later after PCI:

Trop went over 50,000 ng/L very quickly


The estimated left ventricular ejection fraction is 58 %.

Regional wall motion abnormality basal-inferior (this is the posterior wall), akinetic.

Regional wall motion abnormality basal inferoseptum, akinetic.

Learning Points:

1. Acute 100% coronary occlusion can be VERY subtle on the ECG.

2. Record serial ECGs every 15 minutes!!  Even if you don't see the OMI, you can usually prevent such a long delay to reperfusion by recording serial ECGs every 15 minutes for a patient with persistent chest pain.  Hillinger et al. showed that ST Elevation criteria are 21% sensitive for OMI on the first ECG, and 30% sensitive on serial ECGs.  

My Comment by KEN GRAUER, MD (1/15/2023):
For many reasons — I thought today's post by Dr. Smith to be highly insightful and extremely useful to any provider charged with interpreting emergency ECGs. These reasons include:
  • Recognition of the importance of having someone "overread" ECGs in the clinical setting in which you work.
  • The initial tracing in today's case — serves as an excellent test to see how good YOU are at recognizing a subtle OMI that should not be missed!
  • The serial tracings in today's case provide a superb review of the ECG evolution of an acute OMI with subsequent reperfusion.
  • Finally — today's case provides a challenge to see IF you recognize some subtle-but-important lead placement issues that appear on serial tracings?

Having Someone "Overread" ECGs in Your Clinical Setting:
Today's case arose by chance — as Dr. Smith was simply reading ECGs posted on his hospital system (without the benefit of any clinical history).
  • I performed this function for 30 years in our primary care residency clinic — where I overread all tracings for our 35 medical providers. My experience was similar to that described in today's post — in that I would often see things on an ECG which I thought might not have been noticed by the provider(s) caring for the patient. This would lead me to pull the chart and/or directly call the medical care provider to find out happened clinically.
  • This experience served as a "quality control" — in that I learned to appreciate the ECG interpretation skills of our providers. It would also pick up a small but important percentage of cases in which an important ECG finding potentially having a direct impact on patient care would have been missed had I not been overreading ECGs. 

  • QUESTION: Is there an expert interpreter overreading the ECGs in the clinical setting where YOU practice? If not — Do you think this would be helpful? In today's case — it enabled providing feedback to the clinician who missed the subtle-but-important ECG signs of acute OMI.

Although Subtle — this OMI Should Be Recognized!
I agree with Dr. Smith — that the acute OMI evident on today's initial tracing is subtle. That said, in my opinion — the experienced emergency care provider should within seconds — recognize that if ECG #1 (that I have reproduced in Figure-1) is obtained from a patient with new chest pain — that this tracing is diagnostic of acute OMI until proven otherwise!
  • The rhythm in ECG #1 is sinus bradycardia and arrhythmia. The lead that immediately caught my eye —  is lead aVL. Although the T wave in lead aVL will often normally be negative when the QRS in this lead is predominantly negative — the inverted T wave (at least for the 1st QRS complex in this lead) — is disproportionately hypervoluminous.
  • Support that this abnormal ST-T wave finding in lead aVL is "real" — is forthcoming from the abnormal appearance of the abnormally straightened ST segment in lead I.
  • NOTE: I fully acknowledge that there are baseline artifactual undulations in the limb leads of ECG #1 — and that there is beat-to-beat variation in QRST appearance, raising the question as to which beat is the "real" one. That said — the ST segment straightening in lead I is seen in all 3 of the QRS complexes present in this lead. This confirms that this ST segment straightening is a real change — and it supports our concern about the hypervoluminously inverted T wave in lead aVL.

  • In lead III of ECG #1 — the ST-T wave is not normal. While fully aware that the ST-T wave appearance for each of the 3 beats in lead III varies — there does appear to be straightening of the ST segment takeoff, with at least a slight amount of abnormal ST elevation. In association with the reciprocal changes suggested in high-lateral leads I and aVL — this should raise concern for acute inferior OMI.

 that the above subtle limb lead changes are real — is forthcoming from the definitely abnormal ST-T waves in leads V2-thru-V6
  • As we have often emphasized regarding the normal appearance of the ST-T wave in lead V2 and lead V3 — there is normally slight ST elevation, with a gradually upsloping shape of the ST segment, as it imperceptively blends into a normally upright T wave.
  • Instead — the ST segment in leads V2 and V3 of ECG #1 is unmistakably flat, if not slightly depressed. As per Dr. Smith — this abnormal ST segment appearance in these anterior suggests posterior OMI — especially in association with the limb lead changes just described that suggest inferior OMI.
  • Abnormal ST segment straightening continues in leads V4,V5,V6 of ECG #1. While fully aware of the difficulty of knowing which of the 2 QRST complexes in these lateral chest leads is the "real" one — there is at the least, abnormal ST flattening with slight ST depression.

  • PEARL #1: Dr. Smith instantly recognized that if ECG #1 was from a patient with new chest pain — that this tracing represents acute ongoing infero-postero OMI until proven otherwise. The words that I use to describe the abnormal ST-T wave findings do not do justice to this ECG diagnosis. Instead — it is the "picture" of the hypervoluminously inverted T wave in lead aVL — in association with the straight takeoff and ST elevation in lead III — in association with the "shape" of the ST flattening and depression in multiple anterior leads — that tells the experienced interpreter within seconds that there is acute infero-postero OMI.

  • PEARL #2: When asking myself IF the ST-T wave changes I am contemplating are "real" — I look first for those 1, 2 or 3 leads that I know show abnormal changes. In a patient with new chest pain — there is no way that the inverted T wave in lead aVL and the ST flattening with slight depression in anterior leads is "normal". Once I've identified a few definitely abnormal leads — it becomes easier to recognize less marked ST-T wave abnormalities in neighboring leads.

  • PEARL #3: Because the acute OMI was not recognized in ECG #1 of today's case — a 2nd ECG was not done for well over an hour. As per Dr. Smith — by the time ECG #2 was recorded (ie, 1:37 after ECG #1) — the diagnosis of acute infero-postero OMI had become obvious. KEY Point: Even if one was uncertain about an acute OMI from assessment of ECG #1 — at the very least, the abnormal ST segment flattening in multiple leads of this initial tracing should have been recognized. IF ever in doubt about whether an acute event may be ongoing — Repeat the ECG within 10-to-15 minutes (since dynamic ST-T wave changes during an actively evolving event may occur with surprising rapidity)
Figure-1: The first 3 ECGs in today's case.

The Evolution of ECG Changes with Acute OMI:
It's instructive to review the serial tracings recorded during the evolution of an acute OMI. Doing so is a great way to hone skills for recognizing subtle findings on the initial tracing — that rapidly evolve into "tell-tale" abnormalities.
  • Note that what seemed to be very subtle ST-T wave changes in lead aVL and lead III in ECG #1 — has blossomed into obvious abnormalities in ECG #2. The volume of the inverted T wave in lead aVL has deepened — and — the ST segment takeoff straightening with J-point ST elevation has clearly accentuated in the repeat ECG.
  • The evolution of serial ECG changes between ECG #1 and ECG #2 — is even more marked in the chest leads. Increased J-point ST depression, with downslope sagging ST segments and terminal T wave positivity (ie, markedly positive "Mirror" Test — as per My Comment in the September 21, 2022 post of Dr. Smith's ECG Blog — confirms acute posterior OMI.

  • As per Dr. Smith — cardiac cath revealed 100% distal RCA occlusion. ECG #3 (performed just after successful PCI) — provides the classic picture of posterior wall reperfusion T waves in leads V1-thru-V5 (ie, resolution of the ST depression seen in ECG #2 — with evolution to tall, now completely positive T waves).

Subtle-but-Important Lead Placement Issues:
In Figure-2 — there are 2 subtle-but-important lead placement issues evident over the course of the 3 serial tracings in this figure. Can YOU identify them?

Figure-2: Comparison of the 2nd, 3rd and 4th tracings in today's case. Can you identify the subtle-but-important lead placement issues raised over the course of these serial tracings?

Its essential when comparing serial tracings to make sure that technical aspects of the ECG recording remain constant. By this I mean — that the frontal plane axis does not significantly shift from one tracing to the next — and that precordial electrode lead placement does not significantly vary. Even change in the angle of the patient's bed may affect QRST appearance in a number of leads.
  • Did YOU notice that there has been a marked leftward shift of the frontal plane axis in ECG #3? By chance — Did you also notice that the P wave in lead I of ECG #3 is now larger than the P wave in lead II?

  • Did YOU notice that leads V1 and V2 of ECG #4 were placed too high on the chest?

LA-LL Lead Reversal:
We periodically show cases with technical mishaps that often go unnoticed (Please see My Comment at the bottom of the page of the August 17, 2022 post in Dr. Smith's ECG Blog for a series of links with illustrative cases).
  • The reason for the surprising marked shift in frontal plane axis seen in ECG #3 of Figure-2 — is that there is LA-LL Lead Reversal! This is relevant — because QRST morphology in the limb leads of this tracing obtained shortly after PCI is otherwise confusing!
  • I review in detail the approach to recognizing LA-LL Lead Reversal in My Comment in the May 26, 2022 post of Dr. Smith's ECG Blog. PEARL #4: In addition to the unexplained marked frontal plane axis shift — the "tipoff" to LA-LL Reversal — is that the P wave in lead I of ECG #3 is clearly larger than the P wave in lead II (and this is distinctly unusual when there is sinus rhythm).

  • In Figure-3 — I account for correction of the changes produced by LA-LL Lead Reversal. Note in ECG #3a — that the frontal plane axis and QRS morphology in each of the limb leads now looks very similar (as it should be) to QRS morphology in the limb leads of ECGs #1, 2, and 4. Note also in ECG #3a — that the P wave in lead II is once again clearly larger than the P wave in lead I (as it should be with sinus rhythm).
  • Finally, in ECG #3a — Note the presence of the expected ST-T wave reperfusion waves in the limb leads for this patient with infero-postero OMI (ie, T waves now positive in lateral leads I and aVL — and T wave inversion in lead III).

Figure-3: Comparison of ECG #3 before and after correction for LA-LL Lead Reversal.

Too High Lead V1,V2 Placement in ECG #4:
Last but not least — it's clinically important to recognize that leads V1 and V2 in ECG #4 (from Figure-2) were placed too high on the chest. As I review in detail My Comment in the April 17, 2022 post in Dr. Smith's ECG Blog — the ECG findings that define this lead placement error are:
  • Clue #1: There is an rSr' in leads V1 and V2, in the absence of incomplete RBBB (ie, no terminal s wave in lateral leads I and V6).
  • Clue #2: There is a deep, negative component to the P wave in leads V1 and V2.
  • Clue #3: The appearance of the QRS complex and the ST-T wave in leads V1 and V2 very much resembles the appearance in lead aVR.

  • NOTE: The clinical relevance of immediately recognizing too high placement of leads V1,V2 — is that we lose the evolutionary reperfusion T wave findings that we were expecting to see in this post-PCI tracing. 

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