I was sent the ECG in Figure-1 with the information that this man in his 60s presented to the ED (Emergency Department) — for flank pain of several days duration (that he thought was from a kidney stone) and an intermittent "heartburn" sensation over the past few weeks.
QUESTIONS:
- Given the above history — How would YOU interpret this patient's initial ECG, that was obtained on arrival in the ED?
- Should you activate the cath lab?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
Would YOU Activate the Cath Lab?
Many providers would look at the initial ECG shown in Figure-1 — and say, "This is not a STEMI — therefore there is no need to activate the cath lab at this time".
- STEMI Criteria are not satisfied in ECG #1 — because in this man ≥40 years old, ≥2 mm of ST elevation is not attained in consecutive anterior leads V2 and V3.
- Unfortunately, following the outdated, millimeter-based STEMI Paradigm in today's case — would result in needless delay in reperfusion of acute coronary Occlusion, with potential loss of a significant amount of salvageable myocardium.
- KEY Point: To interpret ECG #1 in the absence of awareness of the newer, superior OMI Paradigm is to risk missing at least 30% of all acute OMIs (acute MIs resulting from acute coronary Occlusion) — as discussed in detail in our ECG Video Blog series in Blog #406 — Blog #407 — and Blog #408.
MY Thoughts on Today's Initial ECG:
The initial ECG in today's case (as shown in Figure-1) — is not "normal".
- The rhythm is sinus at ~75/minute (with upright P waves and a constant PR interval in lead II). All intervals (PR, QRS, QTc) and the frontal plane axis are normal (ie, The isoelectric QRS complex in lead aVF, with maximal net R wave amplitude in lead I — suggests a frontal plane axis near 0 degrees). There is no chamber enlargement.
Regarding Q-R-S-T Wave Changes:
- Q waves: Tiny (normal) septal q waves are seen in lateral leads I, aVL and V6. It is hard to determine if a tiny initial positive deflection (r wave) is or is not seen in lead III — but neither of the other 2 inferior leads ( = leads II,aVF) manifest a Q wave.
- R wave progression: Normal-sized R waves are seen in anterior leads V1,V2 — with normal transition (Height of the R wave becomes greater than depth of the S wave between leads V2-to-V3, which is normal).
The ECG findings of potential concern relate to the ST-T Wave Changes — that I highlight in Figure-2.
- Did YOU See these areas that raised my concern?
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| Figure-2: I've labeled the initial ECG in today's case. |
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To Emphasize: The History in today's case is not typical for acute MI, in that this patient did not present with CP (Chest Pain). Instead — today's patient presented with a potential "CP-equivalent" symptom (ie, a "heartburn" sensation), albeit this sensation of "heartburn" was of uncertain duration.
- PEARL #1: As emphasized in ECG Blog #228 — Not all patients with acute MI have chest pain. Instead, the estimated incidence of "Silent" MI may be as high as between 20-40% of all MIs (depending on the definition used). As a result — lack of chest pain in today's case does not rule out the possibility of acute MI given the patient's age (in his 60s) — and given the description of "a heartburn sensation", as this symptom is commonly confused with cardiac CP.
- PEARL #2: One of my favorite history questions to ask is, "What happened today (instead of yesterday, or the day before) — that led you to come to the ED?" To emphasize that we do not know the answer to this question from the brief history provided above at the beginning of this case.
- IF the reason this patient presented to the ED today is that his "heartburn" got significantly worse — this would be important imformation that would greatly increase the likelihood that even subtle ECG changes may be an important clue to an ongoing acute cardiac event.
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The ECG Changes of Concern in Today's Case:
I was concerned by the appearance of 6/12 leads in Figure-2:
- For me in Figure-2 — the most "eye-catching" ST-T wave abnormality is in lead V2 (within the RED rectangle).
- PEARL #3: Normally, there should be a small amount of gradually-upsloping ST elevation in anterior leads V2,V3. Instead — the amount of J-point ST elevation in lead V2 is excessive (ie, as per the PURPLE arrow in this lead). In addition — the gently upsloping shape of the ST segment in lead V2 has been replaced by the abnormally straightened ST segment "takeoff" (straightening of the RED line in this lead).
- PEARL #4: I favor looking for 1 or more leads that I know are abnormal. Once found — then more subtle findings in neighboring leads become much more likely to be supportive of an acutely evolving cardiac event. For example, in Figure-2 — the amount of J-point ST elevation in lead V3 is not excessive — but in the context of the definitely abnormal amount and shape of the elevated ST segment in lead V2 — the ST segment straightening that we also see in lead V3 is also abnormal!
- Each of the 3 inferior leads in Figure-2 manifest reciprocal ST segment depression (within the BLUE rectangles in leads II,III,aVF).
- By far — lead aVF manifests the most abnormal ST depression, given how small amplitude of the QRS complex is in this lead. There is therefore no doubt that the scooped, downsloping ST segment with terminal T wave positivity in lead aVF has to be assumed acute until proven otherwise!
- In the context of knowing that the ST-T wave in lead aVF is abnormal — the more subtle-but-real ST segment straightening with slight depression in leads II and III adds further support to our impression that there is reciprocal inferior lead ST depression.
- KEY Point: Any doubt that I may have had about whether ST-T waves in anterior leads V2 and V3 were truly abnormal — was eliminated the moment I saw the definitely abnormal ST-T wave in lead aVF!
- PEARL #6: The isolated finding of T wave inversion in either lead III and/or lead aVF in association with a predominantly (or entirely) negative QRS — is not necessarily abnormal. BUT — the finding of ST segment straightening with some amount of ST depression in lead III, instead of just T wave inversion (as highlighted by the BLUE arrow in Figure-2) — is clearly not normal. And, ST flattening with some ST depression in lead III is even more definitely abnormal when it occurs in association with ST-T wave depression in the other 2 inferior leads! (as it does in today's case).
- PEARL #7: My "Go-To" Lead when I find myself contemplating the possibility of an acute anterior OMI — is lead aVL. The presence of even subtle ST elevation (as highlighted by the BLUE arrow in Figure-2) solidifies our suspicion of an acute cardiac event in today's case.
- Note that there is fulfillment of the "magical" reciprocal (ie, mirror-image opposite) shape of the ST-T wave for the subtle ST depression in lead III — and the equally subtle ST elevation in lead aVL. This provides yet one more indication that despite the lack of new CP in today's case — the collective abnormal ST-T wave findings in the 6 leads highlighted in Figure-2 strongly suggest an acute evolving cardiac event!
- PEARL #8: The distribution of ST-T wave changes in today's case suggests the ECG pattern known as Precordial Swirl — in that there is ST segment straightening and elevation in leads V1,V2 with some coved ST depression in lead V6. The clinical significance of recognizing the pattern is that it suggests a very proximal occlusion of the LAD involving the interventricular septum (See ECG Blog #380).
- PEARL #9: Among the actions to undertake at this point in today's case are the following: i) Go back and carefully question the patient — trying to get a better "feel" for the likelihood that his "sensation of heartburn" may or may not represent a "CP equivalent" symptom — with focus on how much this sensation increased today, and how severe it was at the time the initial ECG was done; and, ii) Assuming at least 10 minutes have passed since ECG #1 was recorded — Repeat the ECG.
- To Emphasize — In the absence of acute symptoms, immediate activation of the cath lab may not yet be indicated on the sole basis of ECG #1. That said — IF an acute cardiac event is indeed ongoing — then serial ECGs (repeated as soon as between 10-30 minutes after the initial ECG) — in conjunction with clinical information (ie, initial troponin values, correlation with the presence and ongoing severity of symptoms with each serial ECG that is done) — are actions likely to quickly confirm the need for prompt cardiac catheterization.
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Today's CASE Continues:
A prior ECG on today's patient was found. For clarity in Figure-3 — I have put this previous ECG together with today's initial tracing:
QUESTION:
- What do we learn from this prior tracing?
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| Figure-3: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
What We Learn from the Prior ECG:
While the ST-T wave changes in today's initial ECG are subtle and do not satisfy millimeter-based STEMI criteria — there can be no doubt from comparison with the prior tracing shown in Figure-3 — that ST-T wave findings highlighted in the initial ECG are new!
- Despite no significant change in chest lead QRS morphology — the ST segment straightening in leads V2 and V3 was not previously present! In addition — there previously was no ST elevation in lead V2 — and there was even a hint of ST depression in lead V3.
- In the limb leads — inferior lead ST depression was far less than in today's initial ECG — and there previously was no ST elevation in lead aVL.
- BOTTOM Line: While questions remain from brevity of the history as to when the ECG findings noted in ECG #1 may have developed — there is no doubt that the above-noted ST-T wave findings in today's initial ECG are new since the prior tracing from ~1 year ago was done. As a result — an acute and/or recent LAD (Left Anterior Descending) OMI must be assumed until proven otherwise.
- Cardiac Cath was ultimately performed in today's case — almost 7 hours after arrival in the ED. It revealed multi-vessel disease, with "culprit" lesions in both the proximal LAD, as well as in the 1st Diagonal Branch of the LAD. Reperfusion with PCI was successful.
- Among the actions undertaken during the hours until cardiac cath was performed, were: i) Return of 3 abnormal troponin assays, with progressively increasing values; ii) Several repeat ECGs, including one in which the acute ECG findings highlighted in Figure-2 had greatly improved (albeit no notation was made regarding the presence and/or relative severity of the patient's symptoms at this time); and, iii) Coronary CT scan — showing subtotal occlusion of the proximal LAD.
Final COMMENT: Cardiac catheterization in today's case should not have been delayed for nearly 7 hours.
- Although assessment of today's case was understandably made more difficult by the lack of chest pain — the possibility that the patient's "heartburn" might be an acute "CP equivalent" was apparently not explored.
- Even without a history of "new CP-equivalent symptoms" — the abnormal findings in the initial ECG (as detailed in discussion of Figure-2) — place the onus on medical providers to assume acute OMI until proven otherwise.
- As soon as the prior ECG was found — it should have been obvious that the ST-T wave changes in the initial ECG were definitely acute. In this context — any troponin elevation is a mandate for prompt cath.
- "Dynamic" ST-T wave changes (ie, the improvement of ECG findings on a serial tracing) — should have served as additional indication for prompt cath.
- In the context of the above events — further delay to perform coronary CT scan serves no useful purpose. The above described ECG findings (especially in association with any even minimally elevated troponin value) — defines today's case as an acute OMI in need of prompt cath. This need for prompt cath would not be changed regardless of coronary CT scan results (ie, Spontaneous reperfusion is suggested in today's case by the "improvement" in abnormal ECG findings — which could have shown up as a "non-critical stenosis" = "negative" result on coronary CT scan).
- As emphasized often in this ECG Blog — prompt cath with PCI is still indicated after spontaneous reperfusion because of the high risk in ensuing hours of spontaneous reocclusion (See ECG Blog #326 — Blog #337 — and Blog #320, among many others).
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Acknowledgment: My appreciation to Hans Helseth (from Minneapolis, Minnesota, USA) for the case and this tracing.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
- ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (and review of why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).
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- CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
- CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
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- Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
- Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog — as well as ECG Blog #380.
- ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
- ECG Blog #230 — Reviews how to compare serial ECGs.
- ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
- ECG Blog #268 — Shows an example of reperfusion T waves.
- ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
- ECG Blog #387 — Dynamic change in 2 minutes.
- ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
- ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
- 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).
- 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.
- For review on when despite acute OMI — the initial hs-troponin may come back normal — See the March 24, 2023 post in Dr. Smith’s ECG Blog.
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ADDENDUM (3/31/2024):
- I've added a series of Audio Pearls relevant to today's case.
ECG Media PEARL #1 (3:00 minutes Audio) — Reviews the concept of deWinter T waves (and the many variations on this "theme" ).
ECG Media PEARL #35a (4:50 minutes Audio) — WHEN is a T Wave Hyperacute vs a Repolarization variant?
ECG Media PEARL #39a (4:50 minutes Audio) — Reviews the concept of dynamic ST-T Wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).
ECG Media PEARL #46a (6:35 minutes Audio) — How to compare serial ECGs (ie, Are you comparing "Apples with Apples" — or — with Oranges?).
ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should 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.
Pearl 7 is great!! Thank you Prof for your labor of love
ReplyDeleteMy pleasure! — :)
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