I was texted this ECG by a former resident, who just just graduated (there are 2 images of the same ECG, as they are not of high quality):
It came with the message: "Thanks for the good training, Steve!"
I responded: "Sweet! This would have been missed by almost anyone." It is diagnostic of LAD OMI (but not STEMI!). OMI = Occlusion Myocardial Infarction.
This physician said he had been handed the ECG just before starting a shift, while being told it is a woman with chest pain, and he immediately activated the cath lab based on just that information + the ECG.
As all emergency physicians know, most chest pain is not due to OMI or even to any acute MI; most is due to a benign condition such as chest wall and esophageal pain. (And then of course there are serious etiologies such as pulmonary embolism, aortic dissection, pericarditis, pneumothorax, pneumonia, and more.) In fact, depending on the population studied, only about 2-5% of patients who present to the ED with chest pain have OMI. Anywhere from 5-18% have any MI (OMI + Non-OMI). This means that ECG interpretation is CRITICAL to making the diagnosis.
After activating the cath lab, the physician began to get nervous and worried that he had made a rash decision, and had a false positive on his hands. But when he did a bedside echo, there was an obvious anterior wall motion abnormality.
The angiogram showed a 100% mid LAD occlusion.
If we applied the formula for differentiating normal ST Elevation from LAD occlusion, this is the result (there must be at least one lead with at least 1 mm of STE):
QTc = 434, R-wave amplitude in V4 = 9, QRS amplitude in V2 = 8, ST Elevation at 60 ms after the J-point in lead V3 = 1.5. Value = 20.54 (very high and all but diagnostic of LAD occlusion). If you don't know what the formula is, see this post: 12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion
You don't have to be a graduate of an EM residency to recognize a case like this. Anyone can learn it if they are interested and curious. See this case:
Was the intern correct?
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MY Comment by KEN GRAUER, MD (11/8/2020):
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Today’s case illustrates a number of important points. These include the following.
- As per Dr. Smith — any emergency provider can learn to recognize many (most) OMIs — even when millimeter-criteria for STEMI are absent. This is true even when ECG images are of suboptimal quality (as was the case for the 2 ECG images above that were texted to Dr. Smith). The diagnosis of acute LAD OMI even in these suboptimal images is there to be made — despite the poor resolution.
- Dr. Smith’s 4-Variable Formula can be invaluable for facilitating the diagnosis of OMI. As per Dr. Smith — the value of 20.54 is “very high, and all but diagnostic of LAD occlusion” in today’s case.
- A Qualitative Approach can be equally valuable for recognizing the need to activate the cath lab within seconds.
For illustrative purposes — I have made a number of technical adjustments to enhance the quality of the initial ECG that was texted to Dr. Smith in today's case (Figure-1).
QUESTIONS regarding ECG #1:
- WHY is the history so important in this case?
- By the qualitative approach — HOW MANY of the 12 leads in ECG #1 manifest ECG findings that are suspicious and/or supportive of OMI?
- WHICH of the 12 leads in ECG #1 is the most abnormal?
MY Thoughts regarding this Case and ECG #1:
Adequate appreciation of the importance of the History is sometimes overlooked. We are told that the provider in today’s case “was handed ECG #1 just before starting a shift — while being told that the tracing was from a woman with chest pain."
- POINT #1: Simply knowing that the patient in today’s case presented to an ED with new-onset chest pain — automatically places this patient in a “higher-prevalence” group. This means that we need to pay special attention for even subtle abnormalities that appear, while we look for "patterns of leads".
Regarding specifics of the initial tracing itself:
- The mechanism of the rhythm in ECG #1 is sinus. There is slight variability in the rate between 55-60/minute (ie, It’s probably academic whether you simply call this sinus rhythm vs sinus bradycardia and arrhythmia).
- The PR interval and QRS duration are normal. The QTc is upper normal at ~440 msec. The frontal plane axis is normal at about +20 degrees. There is no chamber enlargement.
Regarding Q-R-S-T Changes:
- It is difficult to assess for Q waves in the inferior leads of ECG #1. It looks like tiny Q waves are probably present in leads II and aVF. A small initial positive deflection is seen for the initial QRS complex in lead III — but wide and deep Q waves do appear to be present in the 2nd and 3rd QRS complexes in this lead. Given the tiny size of the Q waves (and QRS complexes) in leads II and aVF — and the extremely small and predominantly negative QRS in lead III — it may well be that none of these Q waves are clinically significant.
- POINT #2: It is important to note that R wave progression is not normal! That is — the R wave remains extremely small in each of the first 3 anterior leads (V1, V2 and V3). Although the reason for “slow R wave progression” is very often due to faulty chest lead electrode placement — this is not the reason for poor R wave progression in today’s case (as becomes instantly clear below, with assessment of ST-T wave changes).
Regarding ST-T Waves:
- POINT #3: The 1 lead in ECG #1 that immediately caught my eye as being indisputably abnormal in this patient who presented to the ED with new-onset chest pain — is lead V3. After taking into account the history, the 1st KEY principle of qualitative ECG assessment — is to look for one or more leads that NO matter how you spin it — are clearly abnormal! Given the lack of R wave progression (ie, no more than a tiny r wave is seen by lead V3), and the modest depth of the S wave in V3 — the T wave in lead V3 is clearly hyperacute because: i) This T wave is much taller-than-expected considering modest depth of the S in V3; ii) The T in V3 is much fatter-than-expected at its peak; and, iii) The T in V3 is much wider-than-expected at its base. Stated another way — the T wave in lead V3 is “much more voluminous” than it should be, and therefore hyperacute in this patient who present with new-onset chest pain.
- POINT #4: The next KEY principle of qualitative ECG assessment — is to look for “patterns of leads”. Given the definite hyperacute T wave appearance in lead V3 — it should be easier to appreciate that neighboring leads V2 and V4 also manifest hyperacute T waves which look overly “voluminous” (ie, disproportionately tall + fatter-at-their-peak + wider-at-their-base than expected, especially given relative amplitude of the QRS complex in these leads).
- Recognition of poor R wave progression with hyperacute T waves in anterior leads V2, V3 and V4 in this patient with new chest pain is by itself sufficient to suggest anterior OMI until proven otherwise. Knowing this — I strongly suspect that the next set of “neighboring leads” ( = leads V1 and V5) are also manifesting more subtle, yet still hyperacute changes.
- POINT #5: My initial “Go To” limb lead when assessing a tracing for acute anterior OMI is lead aVL. Detection of ST elevation in lead aVL strongly supports the diagnosis of anterior OMI. Though subtle — there is slight ST elevation in lead aVL in ECG #1 (as well as slight ST elevation in lead I, which is the other high lateral lead).
- Finally — I look at the inferior leads. In the context of this patient with new chest pain and acute ST-T wave abnormalities as described above in 7 of the 8 leads we have looked at — I interpreted the subtle ST segment flattening (albeit without ST depression) in leads II and aVF — and — the relatively broad T wave inversion in lead III — as consistent with subtle reciprocal changes.
BOTTOM LINE:
- Justification for immediate activation of the cath lab by the emergency provider in today’s case was forthcoming from: i) Knowing the history (ie, new-onset chest pain leading to an emergency ED visit); in association with — ii) Definite hyperacute T waves in leads V2, V3 and V4 + subtle-but-real ST elevation in lead aVL + poor R wave progression (with no more than a tiny r wave in lead V3).
- Additional scrutiny of ECG #1 then suggested no less than 10/12 leads showing potentially acute ST-T wave abnormalities.
With interest and practice — I believe any emergency provider can attain efficiency in Systematic ECG Interpretation — and, in qualitative assessment of acute ST-T wave abnormalities.
very excellent. thank you Steve and Ken, and the recently graduated EM doc. another great example of OMI without STEMI, and saving myocardium, and perhaps a life, with rapid recognition and and appropriate action. thank you all.
ReplyDeletetom
THANKS as always Tom! — :)
DeleteExcellent ECG and wonderful explanation by Dr KG. Thanks Alot . Can u kindly elaborate How much R wave u normally expect in lead V3?
ReplyDelete@ ECG Life — Excellent question you ask (!) — but one for which there is no single “correct” answer. It all depends …. (I would need to see the ACTUAL tracing to tell you if R wave amplitude in lead V3 was abnormal … ). That said — some of the things that it depends on are the following: i) Is there LVH? If so — often you will see unexpectedly deep S waves in the anterior leads (due to increased leftward forces that oppose the normal “development” of R waves as one moves across the precordium. As a result — r waves may be quite small in leads V1, V2 and V3 — BUT — usually there is at least SOME initial positive deflection (r wave) by the time you get to leads V2 and V3. If instead you see NO r wave at all in leads V1, V2 and V3 — then statistically, this is not a “normal” finding, and it increases the odds that there has at some point in time been anterior infarction. But those odds don’t attain 100% — so it depends (ie, I’d have to see the actual tracing).
Deleteii) If there is LBBB — then ALL bets are off! That’s because when there is complete LBBB, initial deflection of the interventricular septum cannot move in the normal left-to-right direction (because the left bundle branch is blocked!) — so initial ventricular depolarization has to go right-to-left. This means that electrical activity begins, and then continues (as the bulk of the LV is depolarized) going right-to-left. As a result, it is EXPECTED with LBBB that there will be no more than tiny initial anterior r waves (if there are any initial r waves at all).
iii) With marked RVH in adults, there tends to be increased rightward forces (leading to a tall R wave in lead V1) — but NOT necessarily with COPD (chronic pulmonary disease, emphysema). Instead, with emphysema there is often “clockwise rotation” of the heart’s electrical axis — which leads to delayed transition in the chest leads (with persistence of fairly deep S waves through to lateral chest leads V5, V6) — BUT — you still should see at least SOME initial r wave in anterior leads. So even though the amplitude of the r wave in lead V3 with emphysema may be small — by looking at the rest of the ECG (ie, maybe seeing RAA and a rightward or indeterminate axis with low voltage) — you can usually tell that even though small, that you still have a “normal-considering-COPD” height of the r in lead V3.
iv) Chest wall abnormalities — can alter what is “normal” for R wave progression.
v) Conduction defects — so with LAHB, since the left anterior hemifascicle is placed a little bit anterior to the posterior hemifascicle — a small (but STILL PRESENT) r wave in lead V3 might be acceptable when there is LAHB (ie, NOT indicative of anterior infarction).
vi) Lead Placement problems — malposition of chest lead electrodes is SURPRISINGLY COMMON (even by skilled ECG techs, according to our observations on the internet!)
vii) OTHER causes ….