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FORUMS > EKG CHALLENGE [ REFRESH ]
Thread Title: It's been a while, so...
Created On Tue Apr 28, 2009 10:34 AM


ncmedic309
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Tue Apr 28, 2009 10:34 AM

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...here's another strip to ponder over!

Very briefly, 65 y/o male with acute onset of substernal chest pain, sharp in nature, radiating through his left chest. He also reports left arm tingling and some nausea. He rates the pain a 6 on 10 but states that the pain increases to a 10 and then eases off intermittently.

The Strip...

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PARAMEDICMIKE
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Tue Apr 28, 2009 11:29 AM

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Looks antero-septal to me with some inferior wall ischemia.

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IntermediateEMT
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Tue Apr 28, 2009 5:46 PM

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Quote

Originally posted by: PARAMEDICMIKE
Looks antero-septal to me with some inferior wall ischemia.


Agree

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ncmedic309
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Thu Apr 30, 2009 5:25 PM

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I guess nobody finds interpreting 12-Leads interesting anymore? I'm sure some folks on here could really benefit from participating in these cases. Oh well, I try - thanks to those of you that do (even though the majority of the cases won't leave you scratching your heads... )

Edited: Thu Apr 30, 2009 at 5:26 PM by ncmedic309

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roblanious
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Thu Apr 30, 2009 7:55 PM

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What are you talking about? This one looks fairly easy. We seem to agree. Is there something occult we are missing? Do you disagree? I would not expect TomB to jump in because I think he is too busy with his blogspot, though he seems to pick out some crazy stuff. Anyway, it looks to me like it is a slight right axis deviation between +90-+120 degrees to the right. Was this patient a COPDer? I thought there might be a LBBB but lead 1 is not monophasic. The ischemia in the inferior leads I do not consider reciprocal changes as the inferior leads are not reciprocal to the anterior and septal leads.
Treatment: MONA, cath lab activation.

Is there a catch we are missing? What is your two cents, NC?

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Edited: Thu Apr 30, 2009 at 7:56 PM by roblanious

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ncmedic309
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Fri May 01, 2009 4:02 PM

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I think you misinterpreted my post Rob, I'm only referring to the lack of participation in these cases, not any one individual case. I guess in all reality, it's not only here - it's all across the boards as of late. We just don't have as much participation these days...

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TomB
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I'm busy all right! But not with my blog.

Besides, I'm never too busy for one of ncmedic309's ECGs.

This ECG looks like a strain pattern from LVH. Don't get me wrong, it's ugly! I'd definitely perform serial ECGs and look for dynamic changes. However, the really ugly ST/T waves are discordant with the main deflection of the QRS complex, and the lead with the most ST segment elevation (V3) has the deepest S wave.

If I'm right, then this is an amazing STE-mimic that is truly worthy of being in a textbook.

Great case, as always!

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ncmedic309
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Fri May 01, 2009 6:35 PM

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Tom:

When are you ever wrong? This ECG is most impressive, but as usual Tom nailed it - it is an STE-mimic!

I worked this guy up for a STEMI - providing the ECG abnormalities and the symptoms. He was very uncomfortable during transport, even with nitrates and morphine. I continued to obtain serial ECGs during the transport but there were no changes noted. He remained stable throughout transport with no significant changes in vital signs. He was evaluated very briefly in the ED and sent up to the cath lab. The cath was negative - go figure - no STEMI. It was another interesting case nonetheless.

We really can't do anything different in the field, we have to treat it as so and go with the worst case scenario. I'm glad things turned out well for the patient, but I have to admit, I was a little disappointed that it wasn't as I suspected...

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TomB
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Fri May 01, 2009 6:43 PM

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Just out of curiosity, did it fool the interpretive algorithm?

Anyone interested in learning how to identify a "strain pattern" (the new terminology is repolarization abnormality) with left ventricular hypertrophy should pay close attention to this case and the previous case posted by ncmedic309.

They are different looking ECGs, but they have a few things in common, the most important of which is the discordant relationship between the ST/T abnormalities and the main deflection of the QRS complex.

Typically with LVH, the larger the QRS, the more pronounced the ST/T abnormality in the opposite direction.

Tom

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Edited: Fri May 01, 2009 at 6:57 PM by TomB

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roblanious
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Fri May 01, 2009 7:15 PM

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You are friggin' amazing! You make me sick!

Anyway, the EKG obviously fooled the ED attending and most likely the interventional cardiologist or the patient would not have been accepted to the cath lab.

When I think of ventricular hypertrophy I tend to think of very tall R waves, but it appears there are more precise criteria I need to review.

EDIT:
Alright, now that I went back and looked at it again, I don't see how I could have missed the hypertrophy. I still would be fooled into thinking it was an MI.

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Edited: Fri May 01, 2009 at 7:39 PM by roblanious

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roblanious
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Quote

Originally posted by: ncmedic309
I'm only referring to the lack of participation in these cases, not any one individual case. I guess in all reality, it's not only here - it's all across the boards as of late. We just don't have as much participation these days...


I actually was thinking the same thing recently.

Hell, I cannot even get Hewitt to get into a heated argument with me anymore. I miss those days.

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Greatness is not standing above our fellows and ordering them around, it is standing with them and helping them to be all they can be.
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Edited: Fri May 01, 2009 at 8:07 PM by roblanious

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ncmedic309
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The interpretation did call it an ACUTE MI on each and every 12-Lead that was obtained. I noted the LVH on the initial interpretation and actually thought about the fact that it was likely causing the elevation that we were seeing and once again fooling the interpretive algorithm. It seems I have had several of these cases lately.

The ED doc had a chance to glance at it and the interventional cardiologist reviewed the prehospital ECGs and determined that it warranted a further look up in the cath lab.

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jsadin
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Another hint at LVH is the diphasic p-wave in V1. You need to blow up the image a bit, but it is there.

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jsadin
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One other thing I just noticed that might steer you away from an MI....no Q waves.

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roblanious
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Do you mean no Q waves with the LVH or in the presence of MI period? I never looked for Q waves in an acute MI. If I saw prominent Q waves, it means the MI is already too old.

I will admit, as much as I read about LVH, as I never had it in medic class or formally, I am still a little weak with it. I do know it is an MI-mimick (thanks TomB for discussing it in your bogsite).

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jsadin
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I'm just finishing up with Dubin's "Rapid Interpretation of EKG's" and he's very insistent about looking for Q waves as a sign that you have a real MI happening. Acute anterior infarctions produce Q waves/ST elevation in V1/V2, Q waves in I/AVL point to a lateral infarction, etc. Depolarization moving away from a positive electrode records a negative wave on the EKG. Think of the infarcted area as a blank spot in the heart. You're seeing the depolarization wave on the opposite side of the heart and it's moving away from the associated lead producing a negative deflection. If there was no infarcted area the two healthy depolarizating areas would cancel each other out and you'd have no Q wave.

At least that's the way I'm interpreting it. Please correct me if I'm mistaken!

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roblanious
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No are you trying to say Q waves, period, or prominent Q waves. If you are saying prominent Q waves, you are mistaken as that is a late sign of infarcted tissue. Now to say that if you have ST elevevation in an acute infarct, you must have at least a normal Q wave as opposed to just an R wave, then that is something I never considered or saw as making a difference. That might be one of those little quirks I never new. I have never been taught that or seen it, but then again, everytime TomB chimes in on something, I scratch my head and wonder...

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jsadin
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Here is a direct quote from Dubin's book:

"The diagnosis of myocardial infarction is usually based on the presence of significant Q waves produced by an area of necrosis in the wall of the left ventricle."

"A significant Q wave is 0.04 sec wide or 1/3 the amplitude of the QRS."

"An infarct is necrotic; it cannot depolarize and has no vectors. So, the positive electrode nearest the infarct detects no "toward" vectors, it sees only the "away" vectors from the opposite wall (through the necrotic void). Therefore, a Q wave is inscribed on EKG in the leads which use that positive electrode for recording."

He goes on for many pages describing where to look for Q waves so that you can pinpoint where the infarct is. I don't believe I'm misreading what he's stating, but are you disagreeing with his assertion?

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sheerin
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Tue May 05, 2009 8:59 AM

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Originally posted by: jsadin
Here is a direct quote from Dubin's book:

"The diagnosis of myocardial infarction is usually based on the presence of significant Q waves produced by an area of necrosis in the wall of the left ventricle."

"A significant Q wave is 0.04 sec wide or 1/3 the amplitude of the QRS."

"An infarct is necrotic; it cannot depolarize and has no vectors. So, the positive electrode nearest the infarct detects no "toward" vectors, it sees only the "away" vectors from the opposite wall (through the necrotic void). Therefore, a Q wave is inscribed on EKG in the leads which use that positive electrode for recording."

He goes on for many pages describing where to look for Q waves so that you can pinpoint where the infarct is. I don't believe I'm misreading what he's stating, but are you disagreeing with his assertion?


I got the same interpretation from Dubin when I read it (in fact I often find myself going back to his book and rereading certain sections - I really want to get the latest edition. My current edition is the second I believe. It's actually quite comical to read some of the passages in it as it was clearly written at a different time...).

When I did my 12-lead training, it was taught that ST elevation is a sign of injury, and that the presence of a pathological Q wave indicates that there is an actual infarct.
Essentially what I took from that (and Dubin) was that you can have ST elevation without actually having infarcted tissue, but that if there if treatment is delayed or is non-existent, the injury site will become an infarcted area, which will then produce pathological Q waves. But I was also taught that Q-waves may not show up for a significant amount of time after the event.


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roblanious
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Tanks Sheerin. Then pathological Q waves are present, it usually means the tissue is already infarcted and opening up the vessel through PCI will not reperfuse the tissue, or should I say, will not "bring it back to life". When you look at someone's EKG and you see those Q waves, you can ask your patient not "if" they had an MI in the past, but "when". That is if they know they had one.

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jsadin
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I see what you're getting at Rob. Is there any kind of a timeframe from the time ST elevations are seen until a true infarction has occured (Q waves present)? I would think this window would be very small.

I find it interesting that we call in ST elevations as a STEMI (ST elevation myocardial infarction) when in fact, without the Q waves present, it really isn't an infarction yet...just an injury pattern really.

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roblanious
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Um, yup. That is why it is a big deal to get 12 leads early, and get the patient to a cath lab. I believe I have seen somewhere recently that if a patient can get PCI within the first 2 hours of the MI, there is the chance of "aborting" the MI in 25% of cases-meaning it is as if there was never an MI. But reperfusing the tissue to salvage what muscle is very important and that is why the goal of arrival at the ED to the cath is 90 min.

As far as how long does it take for Q waves to develop is a good question I cannot answer in certainty, but I believe it is different for everyone and depends on many factors. Either way, the best I can say is anywhere from hours to days.

Oh, and the reason they call an STEMI an "MI", is because it is an MI in progress, and why we need to act quickly to counteract its progress. Make sense?

Maybe Graham can shed some light on this, but I am not sure if anyone can say for sure.

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Edited: Fri May 08, 2009 at 2:07 AM by roblanious

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TomB
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Gents -

The "reperfusion era" changed everything!

The emphasis is no longer on "Q-wave" or "non-Q-wave" MI.

In the first place, we now know that "Q-wave" does not necessarily mean "transmural". But more importantly, Q-waves do not help with risk stratification and treatment decisions during the acute event.

That's the reason behind the paradigm shift to "ST-elevation". That's the key to identifying patients who are candidates for immediate reperfusion therapy. Patients with STEMI may or may not develop pathological Q waves.

By the way, I have seen Q-waves show up within minutes of the hyperacute phase!

Tom

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ncmedic309
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Fri May 08, 2009 9:27 PM

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Wow, great discussion everyone - I'm glad this one is staying alive!

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jsadin
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Thanks Rob and Tom. Great info.

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FORUMS > EKG CHALLENGE [ REFRESH ]

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