This was provided by Mustafa Alwan, an internist from Jordan, on Facebook EKG Club
A 50-something female presented with atypical chest pain described as stabbing, with no radiation
PMHx : DM poorly controlled
VITAL signs stable
Here is the initial ECG with the question "should the cath lab be activated?"
Another ECG was recorded 20 minutes later:
See these cases for the importance of ST segment monitoring:
http://hqmeded-ecg.blogspot.com/search/label/ST%20Segment%20Monitoring
A third ECG was recorded at 45 minutes:
Here are all 3 ECGs, one after another, so you can see the changes:
The cath lab was not activated, but a 4th ECG was recorded at one hour:
There is also new ST elevation in V1. So this is a right ventricular MI also
Echo: Basal inferior wall hypokinetic, pseudonormal LV filling pattern
Initial Troponin T: less than 0.01 ng/mL initial
Troponin T after 2 hours: 0.49 ng/mL
Troponin T after 4 hours: 1.6 ng/mL (this is a large MI)
Cath showed a 100% proximal RCA occlusion.
Learning Points:
1. T-wave inversion in aVL may be the first sign of inferior MI
2. Pay attention to slightly enlarged T-waves
3. When you see these subtle, nonspecific abnormalities, make certain you get serial ECGs!
4. Any patient with ongoing potentially ischemic chest pain should get serial ECGs!
A 50-something female presented with atypical chest pain described as stabbing, with no radiation
PMHx : DM poorly controlled
VITAL signs stable
Here is the initial ECG with the question "should the cath lab be activated?"
 |
| This is suspicious for ischemia because of the T-wave inversion in aVL. However, this is very nonspecific and one would not activate the cath lab! |
Another ECG was recorded 20 minutes later:
 |
| This has more obvious T-waves and T-wave inversion in aVL Here is my response: "This 2nd one is an extraordinarily subtle but real change!!" (i.e., this is diagnostic of MI). "These often resolve with nitro, so I would try that first. It depends on your resources: if activating at night tires out your team for the next day, you try to avoid if possible. But this pain and ECG may not resolve, in which case you must activate." In other words, this is diagnostic of inferior MI, but not of STEMI, and may not need emergent cath lab activation. If the pain and ECG findings resolved with nitroglycerine, it will need at least maximal medical therapy and continuous 12-lead ST segment monitoring |
See these cases for the importance of ST segment monitoring:
http://hqmeded-ecg.blogspot.com/search/label/ST%20Segment%20Monitoring
A third ECG was recorded at 45 minutes:
 |
| Now it is unequivocally diagnostic of inferior MI, even though it does not meet millimeter criteria for inferior STEMI. The cath lab must be activated. |
Here are all 3 ECGs, one after another, so you can see the changes:
The cath lab was not activated, but a 4th ECG was recorded at one hour:
 |
| Now it meets STEMI criteria. Cath lab was activated What else do you notice? |
There is also new ST elevation in V1. So this is a right ventricular MI also
Echo: Basal inferior wall hypokinetic, pseudonormal LV filling pattern
Initial Troponin T: less than 0.01 ng/mL initial
Troponin T after 2 hours: 0.49 ng/mL
Troponin T after 4 hours: 1.6 ng/mL (this is a large MI)
Cath showed a 100% proximal RCA occlusion.
Learning Points:
1. T-wave inversion in aVL may be the first sign of inferior MI
2. Pay attention to slightly enlarged T-waves
3. When you see these subtle, nonspecific abnormalities, make certain you get serial ECGs!
4. Any patient with ongoing potentially ischemic chest pain should get serial ECGs!
I put the first 3 tracings together for clarity (which is the 4th Figure shown here), when this case was first discussed in the EKG Club. KEY points I would add to the discussion here in Dr. Smith’s Blog are the following: i) The history we were provided with is lacking — since we don’t know where the patient presented (to the office or ED?), nor do we know the onset of this patient’s chest discomfort — and, most important — we really are not given insight as to whether her symptoms were or were not worrisome.
ReplyDeleteii) Although The ST segment is coved and the T wave inverted in lead aVL — I was more concerned in ECG #1 by the appearance of the T wave in lead III, which looks disproportionately tall compared to the QRS complex in this lead. Together with lead aVL — these 2 leads (IF onset of symptoms was new and of concern) would make me highly suspicious of early evolving inferior stemi, albeit they are not yet diagnostic.
iii) As per Dr. Smith, the 2nd ECG shown here is subtle but diagnostic of acute evolving inferior MI. Inferior leads often manifest low amplitude QRST complexes — so the changes seen are often quite subtle, as they are here. But compared to ECG #1 — the T waves in both leads III and aVF clearly look more prominent relative to the QRS complexes in these leads. This change can be more readily appreciated by also looking at the ST segment preceding the T waves in these leads — which shows ST segment flattening before abrupt rise to the disproportionately tall T waves. The ST-T wave in lead aVL clearly shows “mirror-image” ST-T depression, as is typical with acute inferior infarction. IF onset of this patient’s symptoms was new and her chest pain history was concerning — then I’d be on the phone with the Cardiologist-on-Call at this point in the case. If one wanted further confirmation of an acute evolving event — doing the Echo at this point would provide that.
iv) The diagnosis is obvious on review of ECG #3. The point I would stress would be that IF the history was new and of concern — that the diagnosis of acute inferior STEMI should be made on seeing ECG #2.
THANKS to Dr. Smith for enriching the previous discussion we had about this case on the EKG Club!
thanks, Ken!
DeleteDr. Smith, could you please explain a little more about the difference between ECGs #2 and #3 from this case, concerning why can we try to avoid emergent cath lab activation in #2 but not #3. To the long time readers, #2 is diagnostic of an occluded RCA, especially in context of #1, as you explained above. So the RCA is occluded during both #2 and #3 (and #4 obviously). If the changes resolve with medications after #2, then it was transient occlusion. I think I've learned previously on this blog that transient occlusion should go emergently to the cath lab. So how can I conceptualize this difference? Unless I can hawk over the patient until the morning and ensure that she gets emergent cath if her symptoms/ECG changes come back overnight, when and why shouldn't transient occlusion go to the lab emergently? Thanks for this great case!
ReplyDeletePendell,
DeleteGood question. I think it is a matter of degree and of judgment. Not a lot of data to guide one in either direction. Very early in thrombus formation, aspirin and antithrombotics. along with endogenous tPA, have a good chance of lysing the clot. The longer the thrombus is present, the less likely it is to resolved spontaneously. The longer the clot is there, the higher risk.
Not sure I can explain better than that.
STeve
In your institution, who typically gets serial EKG's? Is it the ER? I'm a hospitalist at a large academic institution, and the ER typically does 1 EKG and admits patients to the floor. Just wondering, because the idea of serial EKG's is great but impractical once they are on the floor overnight.
ReplyDeleteThese should be done in the ED, or ICU. There should be no chance of further evolution once a patient goes to an non-ICU setting.
DeleteVery interesting post showing, one again, the value of serial ECGs.
ReplyDeleteIn ECG #1 could TV1>TV6 be useful? Thank you.
Mario
Good question and I was going to comment on it, but decided not to.
DeleteThat is sometimes useful, but nonspecific. We studied it for anterior MI and it was of no added value to the formula I use. For inferior MI, it may be useful only for RV MI, as in this case. Note that on the first ECG, the TW V1 is smaller than V6, but as time goes on it gets larger. But the inferior leads with aVL show it all anyway. So does it add any value? Maybe a little.
Dr. Smith,
ReplyDeleteYou recommended NTG after the second EKG. But this patient ended up having an RV involvement. So should NTG be held? And what are your thoughts of NTG in inferior MI? Thanks
-Eric Abrams, MD
The RV MI was not evident at that time. Only became clear on the subsequent ECG.
DeleteWhy PCI for ecg3 no obvious elevation!
ReplyDeletethere is definite, and diagnostic, ST elevation in inferior leads. look closely.
Delete