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Welcome to the lesson on potassium. We’re going to be talking about what potassium is, what role it plays in the body, then what you’re going to see if the patient has hypokalemia and hyperkalemia, and how we’re going to treat those different disorders.
So first, I want you to understand that the normal value for potassium is about 3.5-5. You might see slightly different values within the facility that you work. Don’t worry about it too much. The one we want you to keep in mind is 3.5-5 with below 3.5 being hypokalemia, above 5 being hyperkalemia. If you write your labs out in a lab value skeleton, and you see somebody writing out a lab value skeleton, this is where you’re going to see potassium, is in this lower left corner. So what is potassium? Well, potassium is the most abundant intracellular cation. Cation means positively charged ion. Here’s our cell. So inside our cell, we’re going to have all this potassium. Now, 98 percent of the body’s potassium is located inside the cell. So here’s our cell, here’s our blood vessel. We’re gonna use this diagram several times today, so here’s our intracellular potassium, and then here’s the potassium floating through the blood vessel. Remember, most of it is inside the cell. Now potassium plays a big role in transmission of electrical impulses, so it really helps move impulses smoothly. Without potassium, things start to slow down. Now too much and we get to a state of hyperactivity. It plays a very big role in our heart muscle, and in our skeletal muscle.
In the heart, everything in the heart is controlled electrically, and potassium has a huge component in these impulses, and we’ll talk about that in just a minute. Now it also plays a big role in acid base balance. Hydrogen is also positively charged. Potassium is positively charged, and so they kind of swap with each other inside the cell. If we have a lot of potassium in the cell, hydrogen is going to move out. If we have a lot of hydrogen in the cell, potassium is going to move out. So they really kind of balance each other, and we’re going to talk about that as we get into some of the hypo and hyper different things going on. Now one interesting fact to keep in mind is that a 0.1 decrease in pH will result in a 0.5 increase in potassium, so you can see even just a slight decrease in pH will lead to a much bigger increase in our potassium. So it’s important to understand that these two kind of balance each other, out and what that relationship looks like.
So for a patient who has hypokalemia, that’s going to be a potassium level less than 3.5. What are some of the causes of this? Well, one of the main causes of this is excess insulin. So here’s our cell. Here’s this potassium. One of insulin’s roles is to bring potassium into the cell. So here’s our blood vessel. If we have a bunch of insulin here inside our blood vessel, what it’s gonna do is it’s going to start bringing this potassium into the cell. If potassium leaves our blood vessel, goes into the cell, we’re going to end up with hypokalemia.
Another cause is going to be alkalosis. Let’s draw our blood vessel again. There’s our blood vessel, there’s our cell. So inside our cell, we got some hydrogen, we got some potassium. In alkalosis, what do we see inside our blood vessel? Well, we don’t have much hydrogen. So what’s gonna happen is this hydrogen inside the cell is going to start moving out to balance the hydrogen inside our blood vessel. As that happens, as this positively charged hydrogen comes into the blood vessel, the potassium inside the blood vessel is going to move out and into the cell. As that happens, we start to see our potassium levels in our blood draws decrease. Another cause is going to be vomiting and diarrhea. Whenever your patient is having vomiting and diarrhea, it’s never a bad idea to just check their potassium levels, because a lot of potassium is lost through vomiting and diarrhea.
And then there’s diuretics. You guys probably know of diuretics. A lot of diuretics are potassium wasting, and the main ones you’re going to see that are potassium wasting our loop diuretics and thiazide diuretics. So keep that in mind as you have your patient on these potassium wasting diuretics that we need to be monitoring their potassium levels very closely. The last one I want to talk to you about with hypokalemia, the last cause I want to talk to you about, is increased adrenal activity. Here’s our kidney. Here’s our adrenal gland, sits on top of the kidney. Now what happens with this is if we have hyperaldosteronism, aldosterone plays a role. So then here comes your bladder. So aldosterone plays a role in potassium excretion, so getting rid of potassium through the urine. So if we have hyperaldosteronism, if we have increased levels of aldosterone, we’re going to see more potassium leaving the body via the urine.
And this increased adrenal activity, you might also see a patient with Cushing’s syndrome. So a patient with Cushing’s syndrome is going to also see increased potassium excretion, which will lead to hypokalemia. So what are we going to see in our patient? We talked about what’s going to cause it. Let’s talk about what we’re going to see. Remember we’re talking hypokalemia, so we’re gonna be talking hyporeactivity, so we’re going to see shallow breaths. Now this typically has to do with the body trying to correct this alkalosis. If we have this alkalosis, our respirations might become shallow, and that alkalosis is also going to cause that hypokalemia, and so we just start seeing that kind of cycle happening there. Now, musculoskeletal wise, you’re gonna see hyporeflexia, you’re going to see weakness, and we’re going to see slower muscle responses happening. Cardiovascular wise, you’re going to see weak pulses, you’re going to see dysrhythmias, you might also see orthostatic hypotension.
Now think again about having these weaker electrical impulses. So as we have these weaker electrical impulses, it’s going to affect our body all around. Neural wise, you might see AMS. What does that stand for? That stands for altered mental status. You might see lethargy, you might see a decreased level of consciousness. Again, we’re thinking slower. Hypokalemia, hypoactivity, slowing down, and that again carries over to the GI system. We’re going to see a hypoactive GI system, hypoactive bowel sounds, constipation, ileus, distention, nausea, vomiting. These slower like impulses means slower motility. So every time you think about hypokalemia, think about slower electrical impulses, slower movements, and slower reactivity. Think hypo equals hypo.
How are we going to treat these patients? What are we going to do for a patient with hypokalemia? The first thing is we obviously want to treat the cause. We want to find the cause. We want to treat the cause. If it’s nausea, vomiting, and if it’s diarrhea, we can treat that quickly. If it’s alkalosis, we start to treat that, and then we want to prevent more of loss. Find the cause, treat the cause, prevent further loss from occurring. We can also replace potassium, but we want to replace potassium very slowly. KCL, potassium chloride, is a lethal injection, so we need to be very careful as we’re giving this potassium that we’re not just pushing it too fast back on this patient and then causing further problems.
So we might want to change our patient to a potassium sparing diuretic. The main one you’re going to see what that is actually called spironolactone. Maybe you’ve heard of that. If you haven’t heard of that, write that one down on your paper right now. Spironolactone is the potassium sparing diuretic that you’re going to see tested and given more often than anything else. We can switch our patient to some potassium rich foods. Foods like bananas, you probably already knew that one before you started nursing school. Foods like kale, that’s become more popular, avocados. And switching our patients to those potassium rich foods that can kind of naturally start to replace that potassium. Then cardiovascular wise and respiratory function, these are so important. I want you to, this is what you’re going to see this, what you’re going to do this, how you need to talk, take care of your patient.
We really want to be monitoring our patient’s cardiovascular status, especially when we’re putting them on potassium replacements and monitoring their respiratory drive, their respiratory functions as much as possible. Now let’s talk about hyperkalemia. Hyperkalemia is a potassium level greater than five. The main reasons you’re going to see this are if the patient is in renal failure. If they’re in renal failure, they’re not able to excrete that potassium, and we start seeing that potassium go up. Then acidosis. Let’s draw a blood vessel. Let’s start our cell. In acidosis, we have a bunch of hydrogen in ourselves or in our blood vessel. We got a little bit of hydrogen in here, we got our potassium all going on in here. All this hydrogen is going to start trying to move into the cell. As that happens, this potassium starts to switch places with it. So our potassium in our blood vessels starts to go up, and we end up with hyperkalemia as that hydrogen is trying to move into the cell. I hope that makes sense. I think that makes sense, guys.
Then we have diabetes and DKA. Like we talked about, insulin plays such a big role in getting potassium into the cell. If we don’t have enough insulin, this potassium can’t get back into the cell, so we start seeing this buildup of this potassium, this hyperkalemia. Then on top of that, we’re also in an acidotic state. So if all this hydrogen moving in and all this potassium moving out, while there’s not enough insulin to get the potassium into the cell, so our patient ends up in this diabetic ketoacidosis. And then our body starts burning these ketones. Really fascinating process, really fascinating disease to see with your patients. Then we also have burn and tissue injuries. Burn and tissue injuries are going to cause potassium issues, dehydration and infection. Any kind of dying tissue or cell will release potassium into the bloodstream. And then decreased adrenal activity, the exact opposite of what we talked about with hypokalemia and increased adrenal activity. So if you have hypoaldosteronism or Addison’s disease, we’re going to see potassium levels start to climb because this aldosterone isn’t able to excrete all that potassium.
So let’s talk about what we’re going to see with our patient who has hyperkalemia. Again, the main things I want you to think about is in hyper, we’re gonna see hyper activity. And ones I want you to focus on our cardiovascular changes and EKG changes. The big one we’re going to talk about here are the EKG changes. We talked about how in the heart, everything is electrical activity in the heart. This is the electrical graph of the heart. You’ve probably covered this. You might cover this a little bit later on. Don’t worry about it too much, but what I want to tell you is this is the point of depolarization. It’s usually at about negative 90. If we have all this potassium in the cell that’s leaving more slowly because we have hyperkalemia, then our cell becomes more positive, and the heart becomes more excitable. Okay, so then we start seeing all these weird EKG changes going on. We start seeing tall peaked T waves, we start seeing a prolonged PR. We start seeing a wide QRS, and then we might also see heart blocks, asystole, V-fib.
This is a major priority with our hyperkalemic patients, and we really want to be monitoring their heart rhythms. We want to be putting them on an EKG, monitoring that as closely as we can, especially as their potassium starts to climb higher and higher because we’re going to start seeing all these cardiovascular changes. Now, muscle wise, you’re going to see twitching, numbness, weakness. Think hyperactivity. GI, again, hyperkalemia, hyperactivity. Messy, spastic colon, diarrhea, things are moving more quickly, and we’re going to be wanna watching that. Now, how are we going to treat this patient who has hyperkalemia? Well, let’s give potassium decreasing medications. There’s a couple things we can do. We can give kayexelate, which is going to help us get rid of potassium in the stool. Another one we can give is potassium wasting diuretics. This is going to help us get rid of potassium in the urine. So we’re getting rid of it in the stool, getting rid of it in the urine.
Other things we can do for temporary help are giving things like insulin, plus D50, and that’s going to get a lot of this potassium to go back into the cell. We can give Albuterol, which actually drives potassium into the cell temporarily, and that’s also why when you give your beta blockers, you need to be watching your patient’s potassium levels. Then we can give bicarb. This counteracts all the acidosis that’s going on and allows potassium to get back in the cell. Another really cool medicine that we can give is something called calcium gluconate. Now what calcium gluconate does, it actually prevents, it actually helps protect the heart from these high potassium levels.
So this is really cardioprotective, and that’s why we’re giving that medication. Now we’re going to want to monitor our patient. This is top priority. Like I said, I’ve been saying that, but I really want you to keep in mind with your patient having potassium levels greater than 5, 5.5. 6, get your patient on a monitor and then we can get them on a potassium restricted diet. The main thing I want you to keep in mind here is we want to be careful with salt substitutes because a lot of those salt substitutes are potassium versus sodium chloride or potassium chloride. So we don’t want to be getting all this extra potassium unintentionally. So be really careful with that, and then dialysis. Dialysis is going to help us clean up the blood, get rid of all that extra potassium, and get us back to a homeostatic state.
Now, key points. Remember, normal potassium levels are 3.5 to 5. That might vary slightly from facility to facility. We really want to watch the electrical impulses, or this is what potassium does for us. It helps with the electrical impulses, acid base balance, and it’s the main intracellular cation, or positively charged ion hypokalemia is less than 3.5. Think hypokalemia, hypoactive, and we really want to replace our potassium. Hyperkalemia is greater than 5. Think hyperkalemia, hyperactive. We want to restrict and reduce our potassium. Top priorities, we want to treat the cause and protect the heart. Watch the heart, protect the heart.
Alright guys, that is really a summary of potassium, hyper, hypo, what it does in the body, how it works. I hope that’s helped. And like we always say here, it’s time to go out and be your best selves today. Happy nursing.