Do You Think I'm Having Another Heart Attack?

"It's okay, I don't want to go... Really. [My wife] just got nervous."

"Well man, I think we at least need to check you out. You've been sick enough for your wife to worry, so let's at least give a once over and see where things are - fair?"

"Okay fine... "

"Thank you. I know it's annoying. So you're 74, right? Cool. What kind of medical problems do you have?"

As he answered my partner started getting some vitals. His HR was low, around 45-50, but beyond that, the rest of his vitals were pretty benign. He had a cardiac history with prior MI w/ stents and a CABG, CHF, CAD, HTN, mild COPD, and hypothyroidism. He took all of the usual meds associated with those disorders.

"So everything looks okay, except this HR, it's a bit low. Mind if we get an ECG?"

We got one: https://ecg.bidmc.harvard.edu/.../case223/1350x900.gif.

"So your ECG is concerning to me."

"Do you think I'm having another heart attack? I've been having some mild pain throughout the day... I just figured it was my acid reflux. I had Taco Bell for lunch with my grandson."

Sure. Now he tells me... After I specifically asked about chest pain. Twice.

"No, I don't think you're having one of those. But I'm concerned about some electrolyte issues. Specifically, I think you have too much potassium floating around... Which can go along with your low HR and generally crappy feelings."

At this point, his wife of 50 years was openly gloating... She seems quite pleased that we found something. Oddly pleased. Not central to the story, but noteworthy nonetheless.
"I really think you need to come to the hospital. One, I would like to start an IV and begin fixing this, but also there is probably a reason this is happening (we weren't sure yet) and that needs to be looked into."

"Okay fine... Can I try to pee first? It's been like 2 days and I think I might have to go finally."

... Bro.

Anyway, we got him out to the ambulance and started more of a formal workup and started an IV.
I put an amp of calcium chloride in a 100 mL bag and let that run in. I didn't want to push that too fast and we didn't carry calcium gluconate at the time. Then I started him on an albuterol neb before we headed to the hospital.

The jam with hyperkalemia cardiac toxicity. There are other things affected, yes, but the main issue is with the heart.

The whole +/- thing is really important to the body. Potassium (K+) is positive, and thus a cation. It's the chief intracellular cation more specifically, as most of it lives inside the cells. In hyperkalemia, there is too much potassium outside of the cells. This makes electrical stuff in the body, like the heart, mad because it decreases the intracellular/extracellular +/- ratios.

Remember that whole cardiac action potential thing, paramedics/paramedic students? This relates to that. You have a resting membrane potential and a threshold potential. The cell is at the resting potential, a bunch of positive sodium enters, the cell becomes more positive, hits the threshold potential, everything accelerates, and you get a firing of that cell. Then everything redistributes back to normal, including a bunch of potassium leaving the cell through leak channels. Having more potassium outside of the cell makes the resting membrane potential less negative because less potassium wants to leave the cell. So the cell is "hypercharged" at baseline or "half-cocked" and ready to fire again. It moves the resting potential closer to the threshold potential and makes the heart more excitable or more prone to arrhythmia. At some point though, as the hyperkalemia worsens, you get sorta the opposite effect whereas the resting and threshold potentials get really close together, which makes it so the cell can't sustain an action potential anymore.

You can see all of this represented on an ECG.

Honestly, look up different ECG blogs and stuff like that for this part... You know how there are people who can look at an ECG and be like, "Yes, you can see from this stupid squiggle over here that this patient sneezed 4 hours ago," right? That's not me. Good for those people though!

The big ECG things to remember are tall, peaked T waves, flattening P waves, prolongation of the PR interval, bradycardia, and eventually prolongation of the QRS complex into a wide, gross, mess of a rhythm called a sino-ventricular rhythm (aka sine waves).

Take a look at the ECG I posted below, what do you see?

For me, the trigger to treat is the ECG. Once I see peak T waves with a good story to back them up, I'll usually pull the trigger. So ECG signs + clinical suspicion = treatment.
So what is the treatment?

First and foremost, the initial goal is cardiac stabilization.

This is accomplished with calcium, 99% of the time. Keep in mind, that there are two flavors of this: Calcium chloride and calcium gluconate. There is x3 as much elemental calcium in calcium chloride vs calcium gluconate. You need to give three gluconates for every one chloride. The jam is that because calcium chloride is so concentrated, it can burn, cause IV issues, etc. so it's supposed to be given via a central line. I just dilute it and have had success, personally.

So how does this work?

Calcium raises the threshold potential. It makes the outside of the cell a lot more positive. This re-establishes the difference between the threshold and resting potentials. Basically, in hyperkalemia, the resting potential is getting closer and closer to the threshold potential. Calcium increases the threshold potential and makes them further apart again, making the heart less excitable.

Technically, hypertonic saline can do this too, through a very similar mechanism, so it can be an alternative. The problem is that these effects are short-lived and, while a great bandaid, they don't actually fix the hyperkalemia in any way... So we need to do other things too.

One of those other things is shifting potassium back into the cell where it belongs.
"Shifters" do this. They, through various mechanisms, shift the potassium back into the cell which begins to address the problem a little better. The big two shifters are insulin and albuterol.

Insulin is the main treatment, here. Insulin is really good at this and is really what these patients should get. But in EMS we don't carry insulin (generally) - but we do have albuterol.

Now, when I say "albuterol" what I mean to say is "a lot of albuterol." Not just a quick neb. They need like, 20 mg of albuterol. So stack those nebs! You may remember from EMT class that a side effect of albuterol is HYPOkalemia. That's because albuterol stimulates B2 receptors. These guys work by increasing something called cAMP which ultimately results in the activation of Na/K pumps. So via a side-effect mechanism, albuterol kicks a bunch of potassium back into the cell. However, full disclosure: Technically this only consistently works when synergistically used with insulin.

Albuterol alone is probably not as consistently helpful... but still worth a shot.

A third, kinda shifter is sodium bicarbonate, but it's probably only effective in the setting of hyperkalemia AND acidosis. Really, sodium bicarb may or may not be as helpful as we want it to be... The idea is that by alkalinizing the blood, the body will release H+. H+ and potassium, or K+, like to switch places. So as more H+ is released, more K+ will be taken up.

Now, while albuterol and insulin (and to a lesser extent, sodium bicarb) do start to address the problem, they don't really fix it completely. They shift potassium out, yes, but we need to get rid of it.

This is where "excreters" come into play.

The big excreter is furosemide, a loop diuretic. These work by binding in the area of the loop of Henle and affecting the retention of sodium which ultimately is exchanged with potassium later down the line, causing potassium wasting. This is actually just the mechanism of furosemide, something every paramedic should be familiar with anyway!

Here, it wouldn't work though and we shouldn't give it, why?

Beyond meds, the definite treatment for hyperkalemia is dialysis. Ultimately, if all else fails, dialysis should work. That, and treating the underlying cause!

The patient ended up being fine. He got all the usual hyperkalemia treatment in the ED and dialysis.

He had a new onset renal failure - I'm not actually sure why... I never got a follow-up on it, sorry!

Hope this was helpful! If you have any questions, comment below!

Thanks for reading!

-Dean Stockley

References:

Berberian, JG, BJ Levine, & WJ Brady. Ch. 8: Extra-cardiac Abnormalities, p. 54. EMRA EKG Guide, 1st ed. EMRA, 2017.

How, PP & AH Lau. Ch. 27: Fluid and Electrolyte Disorders. Applied Therapeutics, 12th ed. Wolters Kluwer, 2024.