# Thoughts on this EKG?



## Gurby (Jan 27, 2015)

Sorry about the crummy quality.  Patient basically has no complaints.  Weighs ~300 pounds (which probably accounts for the low voltage).


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## Burritomedic1127 (Jan 27, 2015)

No STEMI, prob some electrolyte imbalance. Hyperkalemia?


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## 9D4 (Jan 27, 2015)

I agree with possible hyperkalemia. Nothing else is really jumping out besides the t waves.


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## Gurby (Jan 27, 2015)

Yep, he had a K of ~8!

The main thing that is catching me up is the rS complexes that extend all the way across - can anybody speak to those?  Maybe part of it is poor lead placement, but it's still kind of puzzling to me.  They aren't quite sine waves that you see in late hyperK, and they aren't QS so not indicative of an old MI or anything like that.  I've seen an identical pattern in a handful of other hyperK ekg's on Google, but I can't figure out why it happens.

Does this guy's EKG look normal once you fix his K?  Or are those rS complexes due to his anatomy and not the hyperK - I know in obese patients the heart can sometimes shift so it's laying more horizontally?  

Would you call the axis indeterminate on this?  Or would you say I is the isoelectric lead and call it a -80 degree extreme left deviation?


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## teedubbyaw (Jan 27, 2015)

Peaked and fairly symmetrical T waves. Though, I don't trust this EKG since the quality is pure crap. His HR is a bit on the slow side for someone of that size.


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## teedubbyaw (Jan 27, 2015)

Gurby said:


> Yep, he had a K of ~8!
> 
> The main thing that is catching me up is the rS complexes that extend all the way across - can anybody speak to those?  Maybe part of it is poor lead placement, but it's still kind of puzzling to me.  They aren't quite sine waves that you see in late hyperK, and they aren't QS so not indicative of an old MI or anything like that.  I've seen an identical pattern in a handful of other hyperK ekg's on Google, but I can't figure out why it happens.
> 
> ...



Things start to widen out and slow down with hyperkalemia. It should return to normal limits if he doesn't have any preexisting cardiac issues. Beyond that, call @Christopher @Brandon O @Remi


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## Gurby (Jan 27, 2015)

teedubbyaw said:


> Peaked and fairly symmetrical T waves. Though, I don't trust this EKG since the quality is pure crap. His HR is a bit on the slow side for someone of that size.



This was taken on a Zoll E-series, and every EKG looked like this (like crap).  Is there a setting I need to play with, or is this just how EKGs look when you take them in the back of a running truck (vibration artifact?) as opposed to a hospital bed?

Also, he's in a rate controlled coarse AFib?  Either that or it's a WAP and a bunch of artifact... Impossible to tell, I suppose.


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## Brandon O (Jan 27, 2015)

Absolutely not typical for hyperkalemia. QRS/T complex should be much more wide and bizarre to match the other features. Is one/both of these post-treatment of some kind?

Very interesting strips. Can you share more about the presentation, medical history, meds, etc?


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## Gurby (Jan 27, 2015)

Brandon O said:


> Absolutely not typical for hyperkalemia. QRS/T complex should be much more wide and bizarre to match the other features. Is one/both of these post-treatment of some kind?
> 
> Very interesting strips. Can you share more about the presentation, medical history, meds, etc?



Dispatched for the "chest pain", on arrival find 60m with CC of peripheral numbness and headache that he developed 1 hour ago (which resolved on its own PTA).  He says his AFib has been acting up for the past week.  He had some sort of kidney surgery about a month ago (there's a clue... wish I could remember what it was), but is not on dialysis.  By the time we get there, he basically has no complaints and is feeling fine, wants to walk to ambulance.  We didn't do anything but transport, so no treatment from us.  Later on in the shift I found out they transferred him out ALS to an ICU at a bigger hospital.

I'm blanking on the rest of the story... I think he was on an ACE inhibitor, metoprolol, might have been diabetic?  You don't really get to be 60 years old and 300 pounds without some medical issues, but I do remember his med list was impressively short with only ~6 things on it.  At the time I was thinking more about a possible TIA than electrolyte/kidney problems, and the EKG didn't jump out at me as being a huge/acute issue.

The strips are from about the same time.  I readjusted leads after the 1st one because I wasn't happy with it, 2nd one was a tiny bit better.


I showed the strips to a friend who is an EM resident and she said the same thing as you... T waves are pathological (peaked, amplitude, symmetrical) but these are certainly not sine waves and it's pretty atypical.


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## Gurby (Jan 27, 2015)

We know he has some Hx of kidney issues - it's certainly possible he took some med prior to arrival that's affecting the way he's presenting?  I'm not sure what it would be or what it would do... And I suppose I wouldn't remember it from the list because I wouldn't have recognized it.


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## teedubbyaw (Jan 27, 2015)

Possible hyponatremia, but I wouldn't expect EKG changes like that.


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## Ewok Jerky (Jan 27, 2015)

So, basically we don't know his medical hx...

Peaked t waves are reminiscent of hyperK, and possible kidney disease. I agree with brandon though I would expect wider qrs complexes. also, this ekg is pretty poor quality, as is the rest of the scenerio


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## Brandon O (Jan 27, 2015)

Here's what I've got, I guess...

The strip DOES look like A-fib. It DOES look like early hyperkalemia changes, such as peaked but not enlarged T waves. The loss of P waves is probably more attributable to the atrial fibrillation. The QRS/T certainly widened somewhat, but perhaps there's a baseline incomplete LBBB here as well.

It does NOT look like severe hyperkalemia. ECG changes aren't predictably associated with serum K, but you'd certainly expect more than this, and he sounds hardly symptomatic. One wonders whether he's used to a fairly chronically elevated potassium.

The low voltages are a large part of what's confusing, and maybe we can ascribe it to obesity, lung disease, whatever. Or again, baseline cardiomyopathy of whatever kind, which might help us explain the R wave progression too.

Or the punt answer, of course, is that hyperkalemia is the great imitator of the ECG and can do what it wants. But that's no fun.


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## Gurby (Jan 27, 2015)

beano said:


> So, basically we don't know his medical hx...
> 
> Peaked t waves are reminiscent of hyperK, and possible kidney disease. I agree with brandon though I would expect wider qrs complexes. also, this ekg is pretty poor quality, as is the rest of the scenerio



Well, I didn't post it in the scenario forum for a reason 

I didn't pay close enough attention to what apparently was the actual problem.  Dispatched for the chest pain, on scene he complains of TIA-like symptoms and his AFib being somewhat out of control... I did puzzle over the EKG and point out the possible electrolyte problem to hospital staff (who were pretty dismissive of that idea, until the labs came back anyways).  But nothing about the call made me inclined to go down that route of questioning too deeply.  And while the T waves on the EKG are concerning, it really doesn't look like it's as severe as it apparently was (as everyone is pointing out).


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## Ewok Jerky (Jan 28, 2015)

the K could have been an incidental finding.


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## Carlos Danger (Jan 28, 2015)

Hyperkalemia would certainly be on my list of differentials, but as others have said, it's really not a great example of that.

Looks like some AF with some sort of conduction defect....maybe even some sort of antidysthymic toxicity.

Any renal or hepatic impairment?

I'm looking forward to Christopher's wisdom on this.


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## D Brim (Jan 29, 2015)

I would respectfully disagree with those that say this is not typical for hyperkalemia.  In short, it's suggested by the combo of the wide bizarre QRS AND the symmetric abnormal peaked T-waves.  

As the potassium progressively increases T-waves become progressively more peaked (tall relative to QRS volume, and symmetric), QRS widens, and p-wave amplitude decreases.  As the K gets higher and higher, more and more myocytes become unresponsive, because their resting potential never falls back below normal activation levels, e.g. the voltage-gated Na channels never get reset.  As more and more myocytes become unresponsive (or depolarize slowly and ineffectively) it makes sense that the amplitude of QRS and T-waves both will decrease.  

I think this EKG looks very similar to other hyperkalemia EKGs I've seen.  Somewhere between the peaked T-waves and still narrow QRS of the earlier hyperkalemia, and the complete melding of the ever widening QRS and T-waves (sine waves) of very late hyperkalemia.  His numbness and tingling also supports the differential.  Hyperkalemia has complications on depolarization of nerves and muscles, just like it does on myocytes. 

ACE inhibitors decrease urine production, therefore increasing K retention.  Not sure what type of renal surgery the pt may have had, but you can imagine that it may have resulted in impaired renal function. 

Most important thing to keep in mind, the EKG is almost never 100% diagnostic on its own.  It's certainly helpful to suggest a differential (I believe it does suggest hyperkalemia) but you never know for sure until you get those labs back (K 8.0).  I wonder what was the underlying cause of his hyperkalemia.


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## Brandon O (Jan 30, 2015)

Well, I think we can all agree that it looks like hyperkalemia, it's just that it doesn't look like such advanced hyperkalemia as the labs suggested. Which happens (K is funny), but is still worth pondering on. It's also just a bit odd in that some features seem more advanced than others; in particular, although you're correct that your QRS/T amplitude will be lost eventually in hyperkalemia, it is usually quite a late finding, whereas the other features here are not so dramatic. I think that's the main incongruity.

All pretty academic though. There's probably no takeaway here except to remember that hyperkalemia is the syphilis of the ECG.


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## BlueJayMedic (Jan 30, 2015)

We just did an inservice on hyperK and from the looks of that 12 those T waves are not large enough for us to treat this patient as per our protocol.  The sine wave you are thinking of is such a late progression that you would have noticed the massive peak on the T wave well before it progressed to that. The large peak in II is up there but being a limb lead I wouldn't really consider that in the Dx.  This a-fib, LBBB or borderline LBBB and Q waves are the only things that pop out to me in regards to this strip. Personally I do not look at axis in my pre-hospital 12's, the electrodes we use are too big and honestly I am not hitting the EXACT placement 100% of the time which you need in order to accurately determine totally accurate deviation.  Also a moving pt and truck definitely do not help that either on Zoll or LifePak. Also taking into consideration his weight like you said... Without the lab value I would need some serious convincing in order to treat this guy. 

All that being said, if this guy was on some form of K sparing diuretic like spironolactone mixed with the ACEI and kidney Hx at his size and weight I would be calling for ventolin and ca gluconate provided Dig wasn't in the med list.


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## Brandon O (Jan 30, 2015)

For what it's worth, it's hard to go wrong with a little calcium (unless you infiltrate it, I suppose). Rapidly therapeutic, albeit in a temporizing fashion, and helpful diagnostically too. The dig thing has been shown to be largely unfounded. I'd have a low threshold for trying it if K is a consideration.


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## BlueJayMedic (Jan 30, 2015)

I have never used it. Because it is a new directive for us they are scaring us into believing that if you give it either too rapidly or to someone who is in dig toxicity their heart will turn into a contracted stone. I wonder if you follow the calcium in that case with the old school cardiac thump if it would then crumble into dust...


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## Carlos Danger (Jan 30, 2015)

THE EFFECTS OF INTRAVENOUS CALCIUM IN PATIENTS WITH DIGOXIN TOXICITY 

http://medicineforresidents.blogspot.com/2011/03/calcium-gluconate-in-digitalised-heart.html


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## BlueJayMedic (Jan 30, 2015)

Thanks for that info, good read.


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## Christopher (Jan 30, 2015)

BlueJayMedic said:


> Thanks for that info, good read.


Indeed, withholding calcium during hyperK+ due to the possibility of an interaction with digoxin is probably negligent these days. I lobbied (successfully) to have it removed from our protocols many years ago.


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## BlueJayMedic (Jan 30, 2015)

Negligent? Quite the term.  I understand what your saying for sure though.  Our educators have made an over the top point to withhold calcium if they're showing signs of dig toxicity.  It almost seems like a scare tactic, right along with bolusing it any faster than 2-3 suggested minutes, haha.  I would assume because it is brand new for not only our service or base hospital group but province in general.  This is all super interesting. Appreciate the feedback here.


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## Christopher (Jan 30, 2015)

Calcium chloride can be pushed, calcium gluconate needs to be given over a longer period of time.

I use the term because an "old" protocol is no excuse for a service to hide behind (not directed at you in any way). Services love to hide behind, "well that is what our protocol is."


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## SandpitMedic (Jan 30, 2015)

The sine wave is way late in the game usually. Without knowing the lab value... 

Who is giving the CaCl here? 

Hands?

And Bicarb and Albuterol? That's our hyper K protocol.

Glucose is no longer in my local protocol. 

Got to be unstable and have renal issues.


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## Carlos Danger (Jan 30, 2015)

CaGl is safer to push simply because it's more "dilute", but if CaCl is all you have, you can push that, in a running IV line, very slowly. 

1.5 mEq/min I think is considered safe.  

FWIW, CaCl has about 3x the elemental calcium that CaGl has; 13.5 mEq/270mg per gram vs. 4.5 mEq/90 mEq per gram.


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## Christopher (Jan 30, 2015)

SandpitMedic said:


> The sine wave is way late in the game usually. Without knowing the lab value...
> 
> Who is giving the CaCl here?
> 
> ...


I give CaCl without labs. I usually do not give bicarb, but if we are lucky enough (hello horrible vascular access patients) to have a second line I will. I rarely get to Albuterol.


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## SandpitMedic (Jan 30, 2015)

Christopher said:


> I give CaCl without labs. I usually do not give bicarb, but if we are lucky enough (hello horrible vascular access patients) to have a second line I will. I rarely get to Albuterol.


I like that. 
We have to give all 3 here. Not a lot of wiggle room. We base it on EKG, history, and presentation.


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## SandpitMedic (Jan 30, 2015)

I did it once last year.


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## BlueJayMedic (Jan 30, 2015)

SandpitMedic said:


> I did it once last year.


Our protocol is 1G calgl slow IV push and 1600mcg salbutamol. We have been advised to steer clear of bicarb for the time being unless ordered by doc via patch.


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## triemal04 (Feb 2, 2015)

Brandon O said:


> ECG changes aren't predictably associated with serum K.


Most important part to remember.  There are lots of ecg changes associated with hyperkalemia; widening of the QRS, av dissociation, peaked t-waves, bradycardia, sine wave, and just overall bizarre morphology.  But you can't reliably predict the K level off of that.

Hell, the OP's patient had a K of 8.  That's high to put it mildly.  And yet there weren't any major changes in the ecg that would be associated with hyperkalemia.  Some sure, but not a lot.  The last 2 hyperkalemic patient's I treated had K levels of 8 and 7; both had fairly similar ecg's to the ones above, maybe even less noticeable.


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## zzyzx (Feb 2, 2015)

You guys are still giving bicarb for hyperK? Why? Even if they are acidotic, bicarb has fallen out of favor.


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## SandpitMedic (Feb 3, 2015)

zzyzx said:


> You guys are still giving bicarb for hyperK? Why? Even if they are acidotic, bicarb has fallen out of favor.



Because I want to be like John and  Roy, dude.


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## MackTheKnife (Feb 11, 2015)

Gurby said:


> Sorry about the crummy quality.  Patient basically has no complaints.  Weighs ~300 pounds (which probably accounts for the low voltage).
> 
> 
> View attachment 1720


Looks likewhat we used to call AV Dissociation. Looks like there are some P waves in some of the leads.


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## Sunburn (Feb 19, 2015)

There aren't, you are more than likely seeing artifacts from van jumping on the road. He is in partial/incomplete LBBB almost certainly. His axis is way off, he has either AF or atrial undulation (latter is more likely).
Also, with high K, LBBB and history of AH he is a prime candidate for nSTEMI AIM, which LBBB does a splendid job of hiding.
What meds was he on?


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## Schwartz42 (Apr 6, 2022)

Gurby said:


> Sorry about the crummy quality.  Patient basically has no complaints.  Weighs ~300 pounds (which probably accounts for the low voltage).
> 
> 
> View attachment 1720


The inverted t's and the breaks predict Coronary slow flow phenomenon. Weight does not effect the voltage through the heart cavities. Small calcifications build up in the vessels and find their way to the heart. They are small enough that they don't cause a total and complete blockage however they can fill with blood and break loose as blood clots. A coronary angiography with TIMI is used to definitively diagnose. Diseases of the lymphatic system (beta cells in particular) would account for the CSFP and the weight.


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## Schwartz42 (Apr 6, 2022)

The TIA symptoms would be consistent with CSFP as posted above. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6050810/
It most likely would have been a losing fight with the ER staff either way. They probably dismissed his symptoms. You should get called back to his location for a midbrain stroke within 6 months. 


Gurby said:


> Well, I didn't post it in the scenario forum for a reason
> 
> I didn't pay close enough attention to what apparently was the actual problem.  Dispatched for the chest pain, on scene he complains of TIA-like symptoms and his AFib being somewhat out of control... I did puzzle over the EKG and point out the possible electrolyte problem to hospital staff (who were pretty dismissive of that idea, until the labs came back anyways).  But nothing about the call made me inclined to go down that route of questioning too deeply.  And while the T waves on the EKG are concerning, it really doesn't look like it's as severe as it apparently was (as everyone is pointing out).


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## ffemt8978 (Apr 6, 2022)

Schwartz42 said:


> You should get called back to his location for a midbrain stroke within 6 months.


This thread had been dead for 7 years so I don't think a 6 month call back is still in play.


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## Gurby (Apr 6, 2022)




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## coolidge (Apr 18, 2022)

Pardon me for several basic questions.  
Can someone circle the part of the image that they mean by spiked T waves?
Can someone circle the QRS and explain the possible reasons for its appearance?
Thanks


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## Aprz (Apr 18, 2022)

coolidge said:


> Pardon me for several basic questions.
> Can someone circle the part of the image that they mean by spiked T waves?
> Can someone circle the QRS and explain the possible reasons for its appearance?
> Thanks


I don't know your level or ability to interpret, if you are experienced and trying to understand how people came to their conclusions, but if you are a student or new, this is not a great ECG example to learn from. It looks like there are some artifacts (outside interference causing the ECG to be distorted), a lot of it is small and questionable.





This is how I broke it down or saw it. Like I said, some of it is questionable.

For any QRS complex, the size of the letter is based on the size of the QRS complex. For example, a big R wave is written as R and a little r wave is written as r. rS means it has a small r wave followed by a big S wave. qrS means it has a small q wave, small r wave, and a big S wave. I think the only weird thing is that usually an S wave is not written by itself, if there is no R or r wave with the S wave, it is written as QS or qs. You'd include any small deflection so sometimes you might see an initial small r wave at the beginning with a big S wave following it. Like in lead II here, it is questionable if that is due to artifact or if there is an initial r wave at the beginning. That could be a QS wave or it could be an rS wave. It's questionable. Lead V2 is an excellent example of an rS wave where there is definitely an r wave in the beginning even though it is small. Anytime there are extra waves, you put an apostrophe after it and it is called "prime". A common example is right bundle branch blocks (RBBB) will have rsR' wave.





(RBBB is meant to stand for right bundle branch block, there are no B waves.. not a thing)

You can also write something like RR' or something like that, if the deflection is small before the second prime wave. This is somewhat subjective and up to the interpreter. I think for the most part, it's kind of moot and not that important, in my opinion. I am okay with people just saying or writing "QRS complex" instead of breaking it down by wave. You could call all these "QRS" and I'd be totally happy with that. Trying to figure out size or what is what is kind of subjective, kind of. Like the inferior leads II, III, aVF, and then lead V1, are examples of that subjectiveness, are those showing initial r waves or not? To me, it kinda looks like it, but it could be argued that these are QS waves. Who knows?

Any part of the QRS is going to be based on what has more negative and positively charged cells I guess you'd say? I like to imagine it like a football field or soccer field where there is a line in the middle and you are comparing the two. Hopefully I don't get these charges mixed up (I reverse them sometimes, haha), but it goes something like this.






How it is normally taught in books is not by thinking of individual cells, but rather as a mean or average of all of them combined and what is becoming more positive. If the positive is headed towards the negative lead, it creates a downward deflection. If it heads more towards the positive lead, it creates a upward deflection. If it is perpendicular to the positive and negative lead, because both sides have an equal or near equal amount of positive and negatively charged cells, it is isoelectric or flat. Because books tend to tend to primarily teach using the mean QRS vector, it can be someone tricky to comprehend how you can have so many deflection or waves. This mean is looking at everything at once, but in reality, there might be depolarization in different parts of the heart and slightly different timing. There is a little bit overlap.

So for example, the inferior leads II, III, and aVF (aVFoot), the positive electrode (labeled LL for left leg, put sideways... looks like an F for Foot, good way to learn this). All this means is that the mean QRS vector is going away from the foot/LL leg lead. That's all. I would say for the most part, at leas for me, it doesn't really mean much. It's more of a fun fact and maybe help me determine a block name (eg left anterior fascicular blocks are going to have "extreme" left axis deviation* and the inferior leads are going to be negative or the mean QRS vector is going to be going away from the foot). Note: it's not normal for people to say extreme left axis deviation, but when I look for left anterior fascicular block (LAFB) (or Dale Dubin's book and how some people learned it, they say left anterior hemiblock (LAH)), you are usually looking for a lot of left axis deviation, greater than 30 or 45 degrees (Thomas Garcia book on 12-lead) says >45 degrees looking for an S wave in lead II that is deeper than the r wave , but I am not sure if that is a hard rule or not (I personally look for poor R wave progression along with left axis deviation when I commit to saying LAFB).

These electrical rules apply to other waves in 12-leads as well, including P wave and T waves. You can actually calculate the mean vector of these waves and a lot of 12-lead machines automatically do this for us. So when a T wave is small or near isoelectric, it's likely because the mean T wave vector is perpendicular to the lead. So in lead aVL in this 12-lead, we don't see the T wave really and that means the mean T wave vector is perpendicular to it. The T wave is positive in all the other frontal leads except lead aVR so the T wave mean vector is about +60 degrees I believe.

Anyways, what we see here is the high lateral leads I and aVL are near isoelectric. That means on our imaginary football or soccer field where you are drawing a line in the middle, the positive and negative sides have about the same amount of positive and negatively charged cells, which means the mean QRS vector is perpendicular to them. The inferior leads II, III, and aVFoot here are all mostly negative downward deflection. That means the mean QRS vector is pointing up, away from the foot, and it is either pointing straight up away from the foot towards the patient head around -90 degrees OR it is pointing slightly upward and to the right about -120 degrees. For me personally, it is kind of hard to tell further or to what degree because the QRS complexes are so small here and a lot of them are close in size that it is hard to tell a different.

Um, something to point out is the size of the T waves in here. These T waves by themselves are not very big. Again, this I wouldn't consider very classic personally. The reason these are big is when you compare them to the size of the QRS complexes they are associated with. A lot of these QRS complexes are very small, yet have T waves that are as big or bigger than them. Considering that normally the T waves are half or less the size of the QRS wit them, these are big. Electrolyte imbalances can change wave size, obesity/fat can make the waves smaller, pregnancy, pericardial tamponade and myxedema coma come to mind. In general, I don't feel like there is any real significance to trying to figure out what is causing small complexes usually because I am usually comparing them size of each wave to each other.

Amal Mattu calls hyperkalemia the syphilis of ECGs. It will create a lot of weird patterns. "Classic" patterns for hyperkalemia are tall, peaked, narrow, symmetrical T waves early on when the hyperkalemia isn't as severe. I feel like this is usually most appreciated in the precodial leads (even in normal 12-lead, the T waves in those leads are usually the biggest), which is something we see here. This is usually an early finding. As the hyperkalemia worsens (more and more potassium outside of the cell, normal lab value is between 3.5-5.3 mEq/L or mmol/L, whatever unit you like to use, sometimes people use slightly different lab range like 3.5-5.0, not a big deal), typically the P-waves will become smaller (cannot appreciate any P waves in these 12-leads), the QRS complexes will become more wide and merge with the T wave creating a sine wave or z-fold appearance. You sometimes cannot even tell what is the T wave or QRS. A lot of people are used to looking at either extremes, tall peaked T waves, symmetrical, T waves you wouldn't want to sit on unless you are into BDSM or sine waves or Z folds. Most 12-leads I see with hyperkalemia are going to be somewhere in between... they are not going to have classical findings that are taught. They are going to have intraventricular conduction delay (IVCD) where they might not follow typical bundle branch block patterns. Thomas Garcia teaches that in his book, Art of Interptation:12-lead, that the #1 cause of IVCD is hyperkalemia so consider that when you don't see a typical pattern.

In a lot of cases, I would say axis, rhythm, STEMI, it's pointless to really try to diagnose these I feel like with hyperkalemia. Correct the hyperkalemia first, redo the 12-lead, and move on. Treat hyperkalemia almost like an artifact where it is not really important to interpret the 12-lead beyond hyperkalemia. Correct that "artifact" and then make an interpretation.


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## sdadam (Jun 12, 2022)

BlueJayMedic said:


> This a-fib, LBBB or borderline LBBB and Q waves are the only things that pop out to me in regards to this strip.


That's my read on it too. Interesting EKG though.

The rate, especially early on in the first 12 is a bit concerning, especially considering he was just symptomatic.


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