Fluids and Electrolytes - Episode 57 💦💧🩺
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Hey, what's up everyone? Dr. Zeeshan here. Thank you so much for coming by our YouTube channel. Make sure you subscribe so that way you can know anytime we put out new content. We're always trying to put out new content on all our platforms. So make sure you also subscribe to all our different platforms on Instagram, Facebook, our podcast, TikTok, so on and so forth. The link is below. If you

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Let us help you. We've helped tens of thousands of students pass, and anybody that's going to talk to you has either been in your position and or will be me. So make sure you take advantage of that. And if you have any questions or any comments, please let us know. You can always email us at contact at mclexhighyield.com. So please reach out to us and enjoy the lecture. Take care. Oh, without further ado, let's talk about fluids and electrolytes, but not just fluids and electrolytes. I want to show you

that fluids and electrolytes are a big portion of med-surg. And med-surg is a huge portion of your exam. Not even exam, those of you that are students, I see a lot of students in here as well too. It's a part of your entire schooling.

So when you see that you've got med surge and then a section of fluids, fluids and electrolytes, and now you're moving forward with fluid and electrolytes and med surge into the board exams, I want to show you how medicine is medicine. So get ready to take a lot of notes here and I'm going to go at a decent pace. So if I make this a part one and a part two, don't worry about it. You'll catch part two next week, but again,

make sure you're taking notes. So the basic concept of fluid balance is what? We need it for cellular function. I mean, every single cell has a transport, whether it be sodium, potassium, chloride, magnesium. We've got some sort of an electrolyte going in and out, in and out, and each one of them serves a different purpose. Also responsible for transport of nutrients, waste of excretion. So you can imagine that

that fluid balance is so important in every little minute detail working forward. But what are the kidneys role? The kidneys role is going to determine our fluid volume and electrolytes through filtration. And if you were to go through and look at the loop of Henle, the ascending loop, descending loop, so on and so forth, what the glomeruli does, there's a lot of different moving parts.

Things that get reabsorbed, things that get excreted, things that get put back into the blood. And then comes where we start getting into the med surge and where we get into the actual boards. And it comes into hormonal regulation. This is where I start to teach you how important fluid balance is. The one concept, and I've taught this to my students left and right, and they'll know this,

is the renin-angiotensin-aldosterone system or RAAs. Now I tell my students, the only thing that I want you all to focus on is what part of this is in fact aldosterone. Now everyone thinks renin-angiotensin-aldosterone system, oh, I need to breathe a little bit. But let's simplify things. Aldosterone is going to regulate

Sodium. What follows sodium? Well, water. If I've got sodium and potassium having an inverse relationship through that sodium-potassium pump, if sodium goes up, well, what happens to potassium? Potassium goes down. There's Daniel. I saw it pointing down. I love it. So yes, they go opposite.

So imagine how much we can control with fluid and electrolytes just with aldosterone. Think about it. Just with aldosterone. Now we're taking it a step further. Aldosterone, where are we going to see aldosterone produced? It's going to be where? In the adrenal glands. The adrenal glands.

They sit on top of the kidney. Well, now what system am I going into? I'm talking med-surgeon fluid electrolytes, but I'm already taking you down what path? Taking you down endocrine. Yeah. So now if I have, let's just say I have a tumor in the adrenals, in the portion that increases my aldosterone,

What do I have? If I have a tumor, I'm going to get excess, excess, excess sodium because that tumor is going to produce aldosterone, produce aldosterone, produce aldosterone. I just showed you primary hyperaldosteronism. I just introduced you to Kahn syndrome.

In that situation, in Kahn syndrome or in primary hyperaldosteronism, I've now increased sodium, water is followed, and my blood pressure is through the roof. I'm hypokalemic. You think I got muscle cramps or I'm at risk for dysrhythmia? I am. Do you see how I'm tying in bored questions, signs and symptoms, what I'm freaking out about, potassium, ask, grab?

Then I take it a step further. What if in this situation I have no aldosterone? What if I go the opposite way? Which means I've got adrenal insufficiency. Adrenal insufficiency. Adrenal, A-D-I. How about Addison's? So now in this situation, I just knocked out sodium. So if I knocked out sodium, water went with it. So my blood pressure dropped.

And guess what just went up? My potassium. I'm hyperkalemic. So you see fluid balance or fluid and electrolytes and med-surg and now endocrine, but that is all, it's all the same. It all ties in. It all ties in. And when you start to understand that if you sectionalize medicine, it's never going to help pass the boards.

If you sectionalize it, it's going to make everything harder for you. When you start tying in, oh, this subject is fluid electrolytes, but medicine is medicine. Now we move on to, because in this situation, all we are regulating, what electrolyte were we regulating? We're just focused on one electrolyte. And by default, the other one followed or went the opposite way. By default, water followed or it went with it. The next one is ADH, which is antidiuretic hormone.

anti-diuretic hormone. And not to get too much into this, but what is anti-diuretic? Well, diuretic means I'm going to pee. Diuretic means I'm going to pee. If it's anti-diuretic, it's anti-peeing. I'm not going to pee. So for me, when I had to think about diabetes insipidus, or I had to think about SIADH, the way that I think about it, I had to dumb it down for myself.

And I thought about it in terms of peeing because it made sense to me. Instead of worrying about a hormone, I just thought about, okay, well, a diuretic makes me pee. This is anti-diuretic, so I'm not going to pee, which means I'm going to retain water if I have too much of it, which is SIADH, where we have inappropriate amounts of anti-diuretic hormone.

So I'm not going to pee. Now let's take this a step further. Let's think boards. Let's think school. Let's go back. Let's think real life. In general, in general, not SIADH, in general, if I don't pee, what is that called? If I don't pee, I'm probably what? I'm probably dehydrated, right?

And I've said to everyone that dehydration is a concept that is presented in so many different ways. So not peeing. Do you think this is something that's going to happen in real life? Now, my students that have been in my course know the story. I'm an MA. I mean, I'm an MA. I was an MA before I went to medical school.

So I was a medical assistant and I would take the pee out of the little cabinet and sometimes it was dark, it was concentrated, and it was pungent and smelled tea color, cola color, signs and symptoms of dehydration. Select all that applied. I did a urine dipstick and guess what? It showed me that the specific gravity was elevated above 1.030.

That the urine osmolality, the urine concentration was elevated. That's not even talking about ADH. That's just talking about dehydration in general. So you can see that fluids in that situation or a lack of in dehydration throws off our fluid balance. But we must know our balance.

signs and symptoms, our lab values, how the boards are going to ask it. And that's what I'm trying to tie together. So you understand, not only is this a fluid and electrolyte med surge, look at how many other things I'm going to tie in today. That's why I want you to take so many notes. Really pay attention today. That's why I was so excited about this lecture. I was like, I'm super stoked about this. This is just a little definition, nothing to take away from this, nothing that's going to be tested.

So it's just more definitions. What intracellular fluid is, what extracellular fluid is, interstitial and intravascular fluid as well too. But we can take it a step further and get into our electrolytes. The ones that I'm going to focus on are the ones that I feel, and I'm going to focus on ones a little more heavy than the other ones because I feel there's more to it. Now, sodium...

Our normal range, should we know it? Absolutely. Why? We're getting case studies now. And guess what case studies are throwing in? They're throwing in lab values. Now, they're going to give you the normal range. But guess what? If you kind of know it off the top of your head, it makes life easier. All I'm trying to do is make you prepared more for your exam and for real life. But the extremes on each electrolyte is what we're concerned about, whether we're high or whether we're low and what they entail.

So if I'm low, I'm hyponatremic, hyponatremic below 135. When we get to below 120, we get very scared and we have to be careful how we correct it. I'm going to talk about that here in a little bit. But when we're hyponatremic, what are we worried about? We're worried about one of ASK graph. Which one of ASK graph are we worried about?

altered mental status by way of seizures, by way of seizures. So what are some ways that we can develop that? Well, hyponatremia, if I'm retaining fluid, didn't we just talk about SIADH? Sure, we did. What about in infants? We talk about diluting what? Milk, water intoxication, right? Hypernatremia, if we're losing water, we're losing water, we become hypernatremic, we develop thirst.

high sodium intake, so on and so forth. Not really the one that I'm concerned about. The one I'm freaking out about is seizures because that is ASK graph. But potassium, do we have a lot of room for error with potassium? 3.5 to 5 milliequivalents? No, we don't. And it is part of ASK graph. And I don't say hypo or hyperkalemia, do I? I say changes in potassium, changes in potassium.

And as we realize this, we're going to see that whether we're hypo or hyperkalemic, hypo or hyperkalemic, we can develop arrhythmias. What part of the heart does potassium predominantly control? It is, in fact, the ventricle. So now we just took it from fluid and electrolytes into EKGs. Do you see how we're not jumping all over the place? We're making sense of things, right?

And in my EKG, I've got my QRST, which is going to signify what's happening with the ventricle. So can I get, now look at these terms and what they really mean, okay? So pay attention to these terms. The term widened QRS complex. How many times do you see a medication and it says widened QRS complex?

Or you see that term and you're like, wait a minute, what does that mean? Well, ultimately, if it widens and widens and widens and widens, can it not turn into a dysrhythmia like that? Yeah. And what are we worried about the most? Ventricular fibrillation. With hyperkalemia, you may see, and this is exaggerated, a peaked T wave, but it's still affecting the ventricle. So you see how potassium and those dysrhythmias are so dangerous. So dangerous. Calcium.

With calcium, we may be hypocalcemic or hypercalcemic. Now, with hypocalcemia, what is the most popular way to develop hypocalcemia on the boards is a thyroidectomy where we get rid of the parathyroids, incidentally. Yeah. So we get rid of the parathyroids, which regulate calcium.

And now we've got hypocalcemia. Now I ask the question, how will it present and how will you more than likely see it? So we've got two different tests that you can see. You can see Trousseau's and you can see Chostek. So Trousseau's is going to be the most common one because you're probably going to go get a blood pressure on this patient and they're going to start to have this carpal spasm and that tetany. Whereas hypercalcemia, we're going to see lethargy. With magnesium,

And I just talked about this yesterday, as a matter of fact, with magnesium, you're starting to see a lot of studies that talk about nerve conduction, nerve transmission, and how magnesium is now helped with mood, with sleep to calm people down. So you can see that nerve transmission, and I talked about this, those of you that have ever drank and been hung over the next day, you deplete your magnesium and guess what happens? You get one of these, you get tremors.

And you're like, wait, what's going on? That's nerve instability because your loss of magnesium. So hypomagnesemia, look at the tremors, look at the anxiety. And then again, with too much magnesium, they're going to get somnolent. They're going to get lethargic. Chloride, not something I'm too big on. The only thing I do want to show you is that chloride

It interacts with bicarb. So chloride will kind of get in the way of bicarb. So if you have too much chloride, it's going to interfere with bicarb absorption, which means that I'm going to start to lose my bicarb if chloride goes up, which means if I get rid of bicarb, what do I develop? Acidosis. If I'm dealing with chloride, I'm getting rid of bicarb. What type of acidosis am I talking about?

I'm talking about metabolic acidosis. So we just went into renal and ABGs. We're in like 15 minutes. Look at how much we've covered and how much of medicine we've covered. So we talked about this hyponatremia and hypernatremia. And the takeaway that I want to do on this part is the hyponatremia. And the one thing, and as we get into fluids,

I want to show you is that at 120 milliequivalents per liter and below, we need to correct this. And we're going to talk about the different types of solutions here, different types of IV fluids. We're going to give them 3% sodium chloride. The thing about this solution is it is in fact hyper tonic, meaning it is more dense than

than our normal blood. It's packed with sodium chloride compared to our blood because our objective is to bring that sodium up. But what are we concerned about when we're bringing our sodium up? Are we trying to bring it up as fast as we can because this patient's at risk for seizures? Absolutely not. Absolutely not. What we're going to do is we're going to increase this

only by four to six milliequivalents per liter in the first 24 hours. That's it. So you're telling me if we're at 120, 119, we're only going to get to 123, 124, give or take? Yeah, that's it. That's it. And then moving forward, we're only going to go up to eight milliequivalents per day. Why? We can develop what's called

There's multiple terms. I'm going to use one of them. Osmotic demyelination syndrome or CPM. I'll take that as well too. Central pontine myelinosis or I'll take another term, locked-in syndrome. Osmotic demyelination syndrome, central pontine myelinosis or locked-in syndrome. I'll take any three of those terms.

as a side effect of overcorrecting sodium too fast. Because now we're destroying their nervous system. We're getting the cellular swelling because sodium is going intracellularly. And guess what's following it? Water. You think those cells are going to expand, expand, expand, and burst? That's exactly what's going to happen. So we're going to get

This locked-in syndrome. And why is that scary? Why are we so concerned? Why do we do this in the ICU, monitoring them every two to four hours, minimum two hours? Because locked-in syndrome, they can see, they can hear, and they can't move, period. And it's permanent. There is no reversing it. So again, very important to understand that we're going to give them that hypertonic solution in severe hyponatremia.

severe hyponatremia, below that 120. Otherwise, we can use normal saline to try to correct it. And we'll talk about this a little bit more. Hypernatremia, again, we just talked about that. Again, I want to talk about the ones that I feel are going to be more tested. Hypernatremia, if we're talking about dehydration, I just want to say with dehydration, diabetes insipidus, give them what they don't have, right? That's my common saying. If diabetes insipidus, they don't have ADH, then give it to them. And what is ADH?

And what is ADH? How do we give it to them? Desmopressin, right? Give them what they don't have. Dehydration, give them normal saline. Hydrate them. Cool. The next one is hypokalemia and hyperkalemia. And the reason why I wanted to talk about this one is, again, we're worried about ASKGRAPH. So what do we give them in a situation where they're hypokalemic? Give them what they don't have.

So give them potassium supplements. What do we know about IV supplements for potassium? How does it feel? Anybody know? Anybody ever gotten one? Anybody ever given one? Is it pleasant for the patient? It burns. Yeah, it burns. It's not pleasant at all. So educate them. They sting a little bit. A little bit. Burning sensation is expected. But the next one I wanted to talk about because you will see potentially on the boards, you'll see this.

So on the boards, you may see sodium polystyrene sulfonate, which is K-exolate, but again, we're going to go generic. You may see an option as IV calcium, or you may see insulin with glucose, or you may say dialysis. When we talk about hyperkalemia, if we're hovering around that 5.5 milliequivalents,

We're okay to give the sodium polystyrene sulfonate because it's not an emergency. If they don't have any other symptoms, if they don't have any type of palpitations or anything that we can see on an EKG strip or an ECG strip, I'm not too concerned about it. So I can take my time and I can give them sodium polystyrene sulfonate. But what do we see in this? We see sulfa. So we have to be careful. We must monitor this.

But what if we start to get up at that 6.5 milliequivalents per liter? What if we start to see those peaked T waves or widened QRS? Now we've got to do something more aggressive. This becomes life-threatening hyperkalemia. It becomes life-threatening hyperkalemia. So now we must do an immediate intervention

And your options could be IV calcium, insulin with glucose, or dialysis. Sometimes you can use combination and throw in maybe sodium polystyrene sulfonate in conjunction with these. But in severe hyperkalemia, select all that apply.

Or a patient presents with a sodium level of 6.5 with peak T waves. That's the one you're going to see first initial priority, urging most concerning immediate report to HCP. So when we see this, and I'm sure we've seen these on QBanks. I know I've written questions about this. And a lot of people tend to trend towards going with sodium polystyrene sulfonate, and they disregard IV calcium insulin with glucose dialysis, or you get confused.

But there is a fine line of where we are able to do something a little bit slower, where we're not in trouble versus where we are in trouble and we're seeing EKG changes or we have an elevated 6.5 and above potassium level and we are freaking out about it. We are freaking out about it. Cool.