Potassium acts as an irritant at the neuromuscular junction. Too much and your cells get irritated; not enough and your cells get sluggish. Your heart demands a normal potassium level for its electrical conduction system to work. Too much and you’ll see a peaked T wave; too little and you’ll see ventricular arrhythmias! So, hyperkalemia is a bad thing for your patient’s heart and needs to be treated immediately!
There are so many different ways to treat hyperkalemia, but how do you know what treatment is best and in which situation?
To treat hyperkalemia effectively, you must understand why a patient gets hyperkalemic in the first place and how each treatment option works.
Why is my patient hyperkalemic?
It’s important to understand that you have way more potassium INSIDE the cell than OUTSIDE. Hyperkalemia occurs when the potassium moves from inside the cell to outside. Here are three primary situations when that creates this movement:
The pH of the blood becomes acidic.
Here’s the thing – potassium LOVES to hang out in an acidotic environment. If the pH of the blood starts to drop, as with respiratory or metabolic acidosis, the potassium in side the cell thinks that there’s a party happening outside the cell – and leaves. The result? Hyperkalemia.
Cell wall damage.
Any time you damage the cell wall, the cells will leak their potassium. Cell wall damage occurs with trauma, rhabdo, and trying to draw blood from a patient like a butcher!
If your patient’s kidneys aren't working, they can’t excrete potassium!
Treatment options can be categorized in the following ways:
Temporarily hide the potassium
- Insulin and glucose – as insulin enters the cell, potassium follows. Please note – the ONLY reason you give glucose is to prevent the patient from bottoming out! If the patient’s blood glucose level is high, you may not need to give glucose.
- Sodium bicarbonate – creates an alkaline environment. The potassium that’s partying outside the cell thinks, “party’s over” and goes back into the cell.
- Albuterol – forces potassium back into the cell.
- Kayexelate – binds to potassium and is excreted in the feces. Note – your patient needs to have a functioning intestinal system for this to work. So, don’t ever give to a patient with an ileus!
- Dialysis – removes elemental potassium
- Calcium Gluconate – as mentioned, potassium acts as an irritant at the neuromuscular junction. But calcium acts as a sedative. So, when you see evidence that your patient’s cells are hyperactive and irritated (peaked T wave), giving calcium can counteract this irritation.
What treatment options are best? Here’s an example:
Let’s say your patient is hyperkalemic because she was found down and has rhabdo. A lot of muscle cells are broken causing liberation of potassium into the bloodstream. If you see a peaked T wave, give calcium gluconate, perhaps insulin and maybe some bicarb. However, that might only temporarily hide the potassium and counteract the hyper activity of the cells. You would then need to follow up with some kayexelate and maybe even dialysis to completely remove the extra potassium.
However, if I didn't see a peaked T wave and my patient was stable, I might go straight for the kayexelate - just get rid of the potassium!
The key is to identify the situations that create hyperkalemic states, understand how each treatment option works, and be confident in recommending such treatments when caring for patients.
I hope these tips help. Thanks so much for choosing to become a nurse! I'm cheering for your success.
Take care and stay connected