Thoughts on this EKG?

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...
 
Thanks for that info, good read.
 
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.
 
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.
 
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."
 
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.
 
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.
 
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.
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 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.
 
I did it once last year.
 
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.
 
You guys are still giving bicarb for hyperK? Why? Even if they are acidotic, bicarb has fallen out of favor.
 
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.

;)
 
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.
 
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?
 
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.
 
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.
Well, I didn't post it in the scenario forum for a reason :p

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).
 
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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