# Scenario: would you call this 12-lead?



## 281mustang (Apr 8, 2015)

49 y/o female with onset of unexplained dyspnea(no hx of copd, asthma, etc.), hx of uncontrolled diabetes(d-stick was 470 which she described as 'low' for her), hypertension, heart murmur, and regurgitation of unknown valve.

Vitals:

HR of 105
156/88
96% sat

Pt is warm and dry and denies any associated chest pain. Pt states her dyspnea is now nearly gone and doesn't want to go to the hospital.

12-lead reveals the following:












What do you do?


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## Underoath87 (Apr 8, 2015)

That looks like a septal MI.  The lack of pain could be explained by her gender and diabetes.
So yeah, I'd call a STEMI alert.


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## Brandon O (Apr 8, 2015)

Meh.


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## chaz90 (Apr 8, 2015)

Not an overly impressive 12 lead. The QRS width isn't overly wide, but V1-V2 are very reminiscent of LBBB patterns...Something to look at and watch, particularly with the QS pattern in V1-V2, but I would not call it at this point.


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## Ewok Jerky (Apr 8, 2015)

Female with dyspnea in the setting of diabetes and HTN? I would bet she is a smoker too. I see ST elevation in V1, V2 and V3 (on my phone, which is bad***). I would call it. She might not get an emergent cath but she is getting a cath soon, on this admission if the CP doesn't resolve.  If it turns out negative I wouldn't feel too bad about it.

Any relief with nitro?


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## Brandon O (Apr 8, 2015)

In the general sense you're right, of course, but acutely, this looks like perfectly proportionate discordance in all leads.


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## Ewok Jerky (Apr 8, 2015)

Just reread the OP. If she is breathing normal and without complaint I would AMA if she has a cardiologist and med control was OK with it after transmitting the 12 lead. Like I said she is getting a cath, just maybe not tonight.

**yes I went from calling a STEMI to AMAing.**


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## 281mustang (Apr 8, 2015)

Ewok Jerky said:


> Female with dyspnea in the setting of diabetes and HTN? I would bet she is a smoker too. I see ST elevation in V1, V2 and V3 (on my phone, which is bad***). I would call it. She might not get an emergent cath but she is getting a cath soon, on this admission if the CP doesn't resolve.  If it turns out negative I wouldn't feel too bad about it.
> 
> Any relief with nitro?


 No CP, which I honestly didn't place too much emphasis on being that she was a female and probably had severe nervous system abnormalities from years of uncontrolled diabetes. I only ran the 12 lead due to the dyspnea.

I didn't WANT to call it in and was fairly certain that based on the presentation of the elevation it was a mimic. I had my EMT run a few additional EKGs and kept looking for reasons not to call it but as a new medic I simply didn't feel confident enough to leave the situation alone.

I honestly wasn't aware that you could go by the proportionate discordance rule outside of the context of a LBBB or paced rhythm. Does anyone have any (preferably online) material that they would recommend for helping identify STEMI mimics? The exchange at the hospital was definitely an embarrassing experience that I would prefer to not repeat again...


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## Brandon O (Apr 8, 2015)

Serial ECGs are always a sound way to resolve dilemmas.

The principle of discordance works pretty good for LVH, RBBB, and some other things. I have a somewhat exhaustive video lecture on this (http://emsbasics.com/2012/10/26/managing-stemi-mimics-in-the-prehospital-environment-video-lecture/), and otherwise I think EMS12lead.com is the best clearinghouse for this stuff out there.


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## captaindepth (Apr 8, 2015)

Does the ST depression in the high lateral leads concern anyone? It does not look to be a strain pattern. With ST elevation in two contiguous leads and reciprocal ST depression with acute onset of SOB I think activation of the cath lab is appropriate. Definitely going to do everything in my power to get her to go.

281mustang, What was the reception at the ED like? why was it embarrassing if you dont mind me asking?


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## Brandon O (Apr 8, 2015)

What about the high laterals looks wrong to you?


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## captaindepth (Apr 8, 2015)

There looks to be symmetrical ST depression in lead I and AvL with at least 1mm of depression in lead I and slightly less in AvL. With the elevation in V1 and V2 and the reciprocal depression doesn't that pretty much confirm that there is an acute myocardial injury/infarction happening?


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## Brandon O (Apr 8, 2015)

But both those elevations and depressions are deflected opposite the QRS and proportionate in size, which is the expected strain pattern for baseline LVH without acute injury.

(Also, lead I and aVL aren't really reciprocal to the anterior precordials, but rather to the inferior leads.)


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## captaindepth (Apr 8, 2015)

Hmmmm, I am kind of struggling with this one and a few questions.

 If the elevations and depressions are normal for LVH shouldn't the voltage criteria for LVH be met? From my understanding strain pattern is not symmetrical depression but more of a downward slope with a rapid return to baseline (seen typically in lead I and AvL as well as V5 and V6). The only LVH criteria I see met here is the tall R wave AvL. Also the QRS is of normal duration so I would not expect the the ST segment to be pushed the opposite direction of the main of the QRS. To me the EKG changes seem isolated and tied to to a vessel group which leads me to my next question, I thought reciprocal ST depression could be anywhere on the 12 lead not just the anatomical "opposite" of the elevation.


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## Brandon O (Apr 9, 2015)

Great questions. Here's the way I'd recommend looking at it:

The principles of the Sgarbossa criteria (not the specific cutoffs and scoring, but the concept of appropriately discordant ST/T changes) apply to bundle branch blocks, LVH, usually to paced and other ventricular rhythms (e.g. PVCs), and sometimes to pre-excitation like WPW. When it comes to something like LVH, this classic strain pattern is pattern recognition across all 12 leads, and you should immediately switch your brain to thinking discordantly instead of comparing against the isoelectric line. Whether the ECG technically meets electrical criteria for LVH is really neither here nor there, unless you're a cardiologist or PCP trying to diagnose LVH (and then you'd probably want an echo).

Does that make sense? It's a little like wondering if something is an "incomplete" or proper bundle branch block or an IVCD. In other contexts it's worth asking, but when it comes to looking for ischemia the same rules probably apply. If it looks like a duck, the principles work.

Here's another duck by way of example (courtesy LITFL):






As for reciprocal changes, using them anatomically is the only way to go. Primary changes that "go together" matched with the right reciprocal changes that is one of the best clues you're dealing with true myocardial injury. The EMS12lead.com gang have a decent write-up on it.


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## medicaltransient (Apr 9, 2015)

Good conversation guys. I agree with LVH. The elevations and reciprocal changes are concerning. I think I would transmit and maybe call report direct to the md. Punt to the md and no STEMI alert.


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## captaindepth (Apr 9, 2015)

Brandon O - It all made perfect sense and the Sgarbossa Criteria is something I definitely need to become more comfortable with. After reading a few different sources on the subjects we discussed I think Im going to stick to my original thought process on this particular 12 lead. Either way, I love discussing 12 leads and practicing interpretation so the more dialogue better. Thanks for such a solid and detailed response!


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## Brandon O (Apr 9, 2015)

For what it's worth, LVH is probably the #1 most common non-ischemic cause of ST elevation (close tie with LBBB).


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## Handsome Robb (Apr 10, 2015)

I was under the impression that reciprocal changes are anatomically opposite therefore high lateral leads are not reciprocal of septal leads.

Also, where are you comparing the elevation to? What are you using to determine your isoelectric line? A common mistake is comparing the ST segment to the PR segment, which can deviate from the isoelectric line for a few different reasons. I have always been taught to compare the ST segment to the TP segment in order to have a better picture of the true isoelectric line. When you do this in this specific 12-lead I don't personally see enough STE to be worrisome.


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## captaindepth (Apr 10, 2015)

I too was taught to use the TP segment as the guide to where the isoelectric line is. In the original 12 lead of this thread I think its pretty easy to see at least 1mm ST elevation in V1 from the TP segment to the J point of the previous QRS. I also see 1mm ST elevation in V2 using the same TP baseline to the previous J point to measure. As far as I remember reciprocal changes, I remember being taught that they could occur in any anatomical area of the 12 lead that is not in the same lead group as the ST elevation, maybe this was a dumbed down answer we were given, Im not sure why but it stuck with me. I believe with the pts acute onset of SOB and this 12 lead its concerning enough to do everything in my power to get her to the hospital. I don't think I'd necessarily call an alert but I'd let them know my suspicion in my radio report.


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## Burritomedic1127 (Apr 10, 2015)

Don't know the exact QRS duration but I'm saying incomplete LBBB, which would naturally make the morphology of the "depressions" in the high lateral leads the op mentioned earlier. 

If it truly were depressions (which this is not) in the high lateral leads, you would see reciprocal changes in the inferior leads (II, III, aVF). Usually these (inferior STEMI) have more parasympathetic tone and would have slower heart rate, the rate on the original 12 is around 90-100ish


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## Brandon O (Apr 10, 2015)

Reciprocal changes are absolutely just as localized as primary ischemic changes.

For anybody still worried about these ST/T changes, here's an absolutely, completely normal LVH ECG that'll really alarm you (courtesy LITFL):


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## Underoath87 (Apr 10, 2015)

So Brandon, considering what you're showing us, what would we need to see in someone with LVH or LBB to actually suspect a STEMI?  An actual "tombstone" shaped S-T/T wave?


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## Brandon O (Apr 10, 2015)

Use Sgarbossa (the principles, not the numbers)! Concordant changes (same direction as the QRS) are bad. So are discordant changes that are too big compared to the QRS.

Dr. Smith at Hennepin has come up with a modification that helps compare the proportionality with the very large waves of LVH. Basically, if your elevation/depression is more than about 1/4 to 1/5 (he keeps tinkering with the formula) the size of the QRS, that's too much, even if it's discordant as it should be. Get a sense for what "normal LVH" (or normal LBBB, or any of these mimics) looks like so you can recognize 1) that it's different from STEMI, and 2) what it looks like when there's a STEMI on top of that.

Here's a true STEMI in the setting of LVH:


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## Brandon O (Apr 10, 2015)

The morphology of the ST elevation and other clues can also be helpful, but this is one of the most universally valuable tools to understand. Notice the numerous ST changes in the same direction (not opposite) the last deflection of the QRS complex. And notice, for instance, aVL, where the ST segment is depressed, which is discordant to the QRS... but it's nearly as deep as the QRS is tall, which is far too much (disproportionate).

Compare against the precordial leads in my PREVIOUS strip, where there is over 5mm of ST elevation, but it's discordant to the QRS, and if you could measure that huge S wave the amount of ST elevation (while objectively large) would only equal a fraction of it, relatively speaking. That's all normal.


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## Underoath87 (Apr 11, 2015)

Thanks!  I'll reread all that when I'm fully sober and rested...


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## medic6676 (Apr 11, 2015)

I'm going to throw in here the AMA RMA point here, seeing as everyone is talking about the 12 lead, which I see elevations in V1-V2, and would def consider that a septal STEMI.

That being said I read a recent article in JEMS in regards to refusals. It spoke about how you need to be sure that the patient is fully competent in self and mind to refuse any further care. It then went on to explain that this goes beyond "acceptable vitals" and the patient is CAOx3, and that if the patient doesn't fully comprehend the fact that they may likely be choosing to die, the legally you as a provider have the right to deny a refusal, and seek ways to transport the patient against their wishes.

In this case, based on the 12 lead, I would be concerned for the patients future safety, and would clarify that they could likely die if they do not seek immediate care. If they still refuse but don't seem aware, or just don't seem to care, you can always contact MedCon for assistance. Sometimes getting a doctor on the phone to convince a patient that they should be in the ER does the trick, and if it doesn't and the MD agrees with you, they can give orders to detain the patient, whether through PD assistance or some other legal method as deemed by agreed upon local laws and protocols.

1800-MEDCON is my favorite number when on duty. I don't always call them, but I definitely an not afraid to call. They are always available to aid you in any way possible, even if you just want to bounce ideas off of them.


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## captaindepth (Apr 11, 2015)

So i was just rereading through the thread and I'm curious, What are we using to confirm LVH in the original 12 lead? The Sgarbossa criteria has been very helpful and makes a lot more sense but Im still not quite sold on the LVH.


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## Brandon O (Apr 11, 2015)

captaindepth said:


> So i was just rereading through the thread and I'm curious, What are we using to confirm LVH in the original 12 lead? The Sgarbossa criteria has been very helpful and makes a lot more sense but Im still not quite sold on the LVH.



That's my point. It doesn't matter. At least not for the question of STEMI. (If you're into cardiology you can worry about diagnosing LVH.)


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## captaindepth (Apr 11, 2015)

Brandon O said:


> But both those elevations and depressions are deflected opposite the QRS and proportionate in size, which is the expected strain pattern for baseline LVH without acute injury.




Here you attribute the elevation and depression to LVH and where the entire discussion turned to the Sgarbossa criteria. Now you are saying it doesn't matter, and totally lost me. . Sorry to be stubborn but I still see an acute event happening with the original OP.


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## chaz90 (Apr 11, 2015)

captaindepth said:


> Here you attribute the elevation and depression to LVH and where the entire discussion turned to the Sgarbossa criteria. Now you are saying it doesn't matter, and totally lost me. . Sorry to be stubborn but I still see an acute event happening with the original OP.



Proportionally appropriate discordance doesn't only apply to LVH. Whether the original EKG exhibits criteria that allow diagnosis of LVH (which isn't the gold standard anyway) isn't really relevant. The minor ST segment elevation we're noticing is not overly shocking based on the massive preceding negative QRS deflection. The similarly negative ST segment depressions are also appropriately discordant with significant positive QRS deflections. 

One of my favorite quotes from several medical blogs from people who know far more about electrocardiography than I: "Novices read ST segment changes as numbers alone; Professionals read the entire EKG."  

Sgarbossa criteria are numbers to determine what is appropriate and what isn't most of the time, but the general principle still applies that when you see huge QRS deflections, small and discordant ST changes simply don't matter as much. Look at it, then move on to serial EKGs and continued assessment in light of the patient's condition and clinical signs.


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## Nova1300 (Apr 11, 2015)

Guys, we may be missing the forest here. 

The EKG is interesting.  But this a female patient with years of uncontrolled diabetes and hypertension.  Her acute coronary syndrome can be expected to be atypical.  And with routine glucose in that range, she should be presumed to have coronary disease.

She is presently hypertensive and has a HR of 106.  That is a heart under strain.  Granted she may have autonomic dysfunction from her terrible diabetes, but that's not a call to make in the field. 

Even the sats are a little worrisome. A lady with no pre-existing lung disease shouldn't have sats in the mid 90's.  That is a ventilation perfusion mismatch.  Was she morbidly obese? 

Not only could this be an NSTEMI, but this is frequently how diastolic heart failure presents. 

I do my best to talk this lady into a trip downtown.  Maybe not a cath lab alert, but certainly for troponins and an echo.  We do this same workup on BS patients all the time.  This is a lady who actually deserves it.


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## chaz90 (Apr 11, 2015)

@281mustang

To help validate our opinions on this EKG, what was the diagnosis for this patient at the hospital? Did cardiac enzymes show much of anything? Did she get taken for a cath? If not, do you know if she received a cardiology consult or if the ED physician handled it?


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## Brandon O (Apr 11, 2015)

captaindepth said:


> Here you attribute the elevation and depression to LVH and where the entire discussion turned to the Sgarbossa criteria. Now you are saying it doesn't matter, and totally lost me. . Sorry to be stubborn but I still see an acute event happening with the original OP.



chaz said it pretty well already, but here's my best shot:

If you see an ECG like the OP posted, it should instantly send you back like Proust's cookies to thoughts of LVH... a whiff of LBBB... even a dash of early repolarization. Although these are distinct disorders, for the matter at hand, they have the same relevance, because what we're doing is pattern recognition based upon the shapes, widths, and sizes of the QRS-T complexes. And as soon as you start thinking that way -- realizing this strip fits into that family -- you should stop trying to compare ST segments against the isoelectric line and start using the different "baseline" you've learned is normal for those syndromes. Looking for a STEMI will always be one of our top priorities in emergency medicine, and this method is how you do it with an ECG that looks this way.

Whether the patient actually _has_ LVH, LBBB, etc is a totally different question. But who cares? Are you trying to code in a new ICD-9 diagnosis? In some cases those questions are worth asking, in others not. For instance, newly diagnosing a patient with LVH has some significance as to their cardiac risk. Diagnosing them with benign early repolarization does not. In both cases, however, this is not a very important task for paramedics except as a hobby, because it bears very little upon prehospital care. (The old idea that "new or presumed new" LBBB should be a STEMI equivalent has been roundly disproven.)

I understand what you're asking, which is: "How can we know whether to apply a Sgarbossa-type analysis if we don't know whether there truly is [LBBB or whatever]?" My answer is: "The _general pattern_ of secondary changes consistent with these electrical abnormalities is what leads you to apply that approach, not their definite, confirmed diagnosis."

Does that make sense? The important dilemma is whether the original ECG here shows a STEMI. Now, it looks a little like it has LBBB morphologies, but I'm not going to add up the boxes to see if it's >.120ms or not, because that's not the question. It also looks a little like LVH, but I'm not going to add up R and S amplitudes to see if they exceed one of the numerous ECG criteria for LVH, because that's not the question either. But irrespective of those distinctions, I DO know that the patterns I'm seeing cause secondary ST/T changes, and after I take those into account, I see no evidence of any ischemic changes superimposed onto that baseline.

Sorry if this isn't very clear. Sometimes I give good explanations. This isn't one of those days.


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## Handsome Robb (Apr 12, 2015)

medic6676 said:


> I'm going to throw in here the AMA RMA point here, seeing as everyone is talking about the 12 lead, which I see elevations in V1-V2, and would def consider that a septal STEMI.
> 
> That being said I read a recent article in JEMS in regards to refusals. It spoke about how you need to be sure that the patient is fully competent in self and mind to refuse any further care. It then went on to explain that this goes beyond "acceptable vitals" and the patient is CAOx3, and that if the patient doesn't fully comprehend the fact that they may likely be choosing to die, the legally you as a provider have the right to deny a refusal, and seek ways to transport the patient against their wishes.
> 
> ...



A physician cannot order you to transport someone against their will unless they are a danger to themselves or others. With that said, being awake, alert, oriented, not intoxicated and able to reiterate the risks you explain back to them and still refusing transport for a potentially life threatening illness does not equal suicidal intentions/ideations, which is about the only time we can transport someone against their will. People have the right to make decisions about their healthcare, even if they are bad decisions. It is not our place to decide wether patients go to the hospital or not. I've AMAd STEMI and CVA patients. That's not saying I didn't spend an extended period of time on scene reasoning with them and contacting the hospital to have a physician speak with them and explain to them the risks in order to have another person in my corner trying to convince them they need to go but at the end of the day if they are awake, alert, oriented and competent they can refuse care. I'd tread carefully forcing patients to go to the ER against their will and treating them against their will. That is kidnapping, assault and potentially battery if you perform invasive treatments on them during transport. 



Nova1300 said:


> Even the sats are a little worrisome. A lady with no pre-existing lung disease shouldn't have sats in the mid 90's.  That is a ventilation perfusion mismatch.



I live at altitude, I run at 95-96% at my baseline without any pre-existing lung pathologies outside of exercise induced bronchospasm. While I agree with what you're saying a SpO2% in the mid 90s without a history of respiratory disease does not equal a V/Q mismatch.


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## Nova1300 (Apr 12, 2015)

Yes, it is correct that in an environment with decreased partial pressure of oxygen, the sats will decrease.  And this does not represent a VQ mismatch.  So, I guess I stand corrected.  If this call took place on a mountaintop, it is possible her hypoxemia is from altitude.  

However, in the absence of some confounding factor like altitude or an underlying disorder shifting the oxy-hgb curve, she has mismatch.  

Was this fine specimen mountain climbing at the time of her presentation?


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## medic6676 (Apr 12, 2015)

Handsome Robb said:


> A physician cannot order you to transport someone against their will unless they are a danger to themselves or others. With that said, being awake, alert, oriented, not intoxicated and able to reiterate the risks you explain back to them and still refusing transport for a potentially life threatening illness does not equal suicidal intentions/ideations, which is about the only time we can transport someone against their will. People have the right to make decisions about their healthcare, even if they are bad decisions. It is not our place to decide wether patients go to the hospital or not. I've AMAd STEMI and CVA patients. That's not saying I didn't spend an extended period of time on scene reasoning with them and contacting the hospital to have a physician speak with them and explain to them the risks in order to have another person in my corner trying to convince them they need to go but at the end of the day if they are awake, alert, oriented and competent they can refuse care. I'd tread carefully forcing patients to go to the ER against their will and treating them against their will. That is kidnapping, assault and potentially battery if you perform invasive treatments on them during transport.



That was kind of my point, I guess I should have elaborated that there needs to be extenuating circumstances that make an MD agree with you.


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## 281mustang (Apr 16, 2015)

chaz90 said:


> @281mustang
> 
> To help validate our opinions on this EKG, what was the diagnosis for this patient at the hospital? Did cardiac enzymes show much of anything? Did she get taken for a cath? If not, do you know if she received a cardiology consult or if the ED physician handled it?


 No idea if they even drew labs, I don't typically work in that area and this is the only transport I've done at that specific hospital.

The doc's rational was that the deep Q waves were pathological from a previous septal MI which was causing repolarization abnormalities/elevation. Don't know if he got a consult but I doubt it, he didn't seem concerned about the situation whatsoever.


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## Brandon O (Apr 16, 2015)

281mustang said:


> The doc's rational was that the deep Q waves were pathological from a previous septal MI which was causing repolarization abnormalities/elevation. Don't know if he got a consult but I doubt it, he didn't seem concerned about the situation whatsoever.



This is what we often call "left ventricular aneurysm," or LVA. Bit of a misnomer since there may or may not be any anatomical aneurysm, but it just refers to persistent ST changes from prior MI. The changes look more or less like this, although I might quibble a little since it's debateable whether some of these are truly Q waves. (No question the R progression is pretty abused, though.)


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## jwk (Apr 22, 2015)

Sorry - still trying to get past the BS of 470 which is "low for her".


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## D Brim (May 4, 2015)

Tough EKG to do anything with 100% certainty.  I for one would never blame someone for talking a poorly controlled diabetic with a complaint of shortness of breath and an ugly looking 12-lead into going in for further evaluation.  For that matter, I would personally try to talk anyone with a blood sugar of 450 into seeking out immediate care regardless of other complaints!  Peripheral nerves and vasculature are being turned into those little cubes of sugar with ever passing minute!

That being said, I'm in the LVH with normally discordant ST deviations camp.  It was mentioned that the 12-lead doesn't immediately appear to meet criteria for LVH.  I presume that's referring to the the strongest EKG criteria, the ole' adding up S waves and R waves.  Bottom line about LVH is that you can't count on EKG criteria to diagnose it, you really only know for sure based on echo (to the best of my knowledge, not a Doc here!).  However, there are other, less convincing but still legit, EKG criteria for LVH.  One of these criteria is a tall (> 11 mm) R wave in  aVL, which the EKG demonstrates. 

The other thing to keep in mind is AHA criteria for STEMI make allowances for a little STE in V2-V3, 2 mm in men, and 1.5 mm in women.  The baseline is a little tricky in the septal anterior leads, but by my best estimate, you've got  at most 2 mm in V1 and 1.5 mm in V2.   So, you've got one of your two congruent leads that is bad enough to be concerned about, the other is very borderline.  They don't really add up to warrant a text book defined STEMI.


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## D Brim (May 4, 2015)

Brandon O said:


> This is what we often call "left ventricular aneurysm," or LVA. Bit of a misnomer since there may or may not be any anatomical aneurysm, but it just refers to persistent ST changes from prior MI. The changes look more or less like this, although I might quibble a little since it's debateable whether some of these are truly Q waves. (No question the R progression is pretty abused, though.)



Yep, my post was already getting too long. . . . but seems like some ugly looking combination of past pathology.  A little LVH, a little pathological Q. . . all equals one really ugly looking, but not acute, 12-lead


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