Our first episode dedicated to a class of medications. This episode we explore the autonomic nervous system and medications that can affect it called Adrenergic and Cholinergic Medications.
Hey friends and welcome to nursing with Dr. Hobbick. Today I am thinking about electrolytes. Still thinking a little bit about that fluid balance. These two concepts are pretty interwoven. And in a later episode I'll get into acid base. Today I want to talk about electrolytes and how they can be imbalanced. The first thing I want you to think about is intake, absorption, distribution, and output. Electrolytes can be imbalanced through intake if they're not taking in enough or they're taking in too much. Absorption can affect your electrolyte balance by not absorbing electrolytes appropriately, we could end up with low levels distribution. This is big when we're talking about things like potassium, calcium and magnesium, especially potassium. Because the levels of these electrolytes inside the cells in the intracellular compartment are much higher than they are in the extracellular compartment. Remember that when we're testing the levels of these electrolytes, we're testing the levels in the bloodstream in the serum in the extracellular space, the difference between the levels is pretty dramatic. Sodium is the most abundant can ion in the extracellular compartment. Potassium is the most abundant cat ion in the intracellular compartment. And you'll see the huge difference when you look at the levels that we would see a normal level. Now I want you to understand that you will see some variants in reference ranges, don't let that worry you too much. Just memorize some set that you're using in your current program. And you'll get through just fine. So if I use reference ranges that are different than what you're used to, they shouldn't be way off. If they are Gosh, send me a message on one of my platforms. You can find me on Facebook, Instagram, YouTube, Tik Tok, where else I'm everywhere, let's say potassium, the normal range for potassium is 3.5 to five. Now that's the serum level, the normal range for sodium is 135 to 145, you may see 136 to 145, it doesn't matter that much. Obviously, there's a huge difference between the number or the amount rather of sodium then potassium, consider this if my patient has blunt force, trauma, or burns, or something that is going to cause a lot of cells to burst, those cells will release all of their intracellular contents, including their high concentrations of these other electrolytes, that's going to really mess up my balance of electrolytes in the bloodstream in the extra cellular space. That would be a imbalance of distribution, we can have an output. If there is too much output or not enough output of electrolytes that can also cause imbalance output, we normally lose electrolytes through urine, feces a little bit through sweat abnormally we could lose it through vomiting, wound drainage. Now we're talking about a lot of drainage not like that little paper cut, we also need to talk about other GI losses gastric suction, if you put an end G tube into your patient and it's to suction, you might want to think about their electrolyte balance. Just like if they were vomiting, it's the same thing. And if your patient has diarrhea, they could be losing electrolytes. The functions of the large intestine are really to absorb water and electrolytes. If we have diarrhea, that stuff's moving through there so fast, he can't do its job, we're going to lose fluid. And electrolytes that way, remember that fluid is water with things dissolved in it. In that case, we're losing both electrolytes and water, let's just get an idea of plasma versus intracellular concentration. So I told you that the plasma volumes for potassium is 3.5 to five for sodium it's 135 or 136 to 145. inside the cell, we have about 14 mil equivalents per liter of sodium only 14 When outside the cell we have 135 to 145. inside the cell, we have 140 Millet equivalents per liter of potassium were outside the cell we have 3.5 to five, you can see that the concentrations of these are very different on either side. The reason for that has to do with how the body creates energy, how the body creates nerve and muscle contraction. That's really what our electrolytes do for us besides also contributing to osmolarity like we talked about last week. So we'll talk briefly about these different electrolytes, sodium in some textbooks is really described as an osmolarity imbalance. In other words, it's a concentration issue in the bloodstream, the patient could have too much sodium or too little water, or they could have a water excess or too little sodium. If you need to go back and refresh on some of the anatomy of the rest system ADH hormone metric peptide, I recommend the Khan Academy videos they are fantastic on review for pathophysiology. These are important concepts for you to understand if you're going to understand sodium and fluid balance despite potential variations in diet, our kidneys really manage our sodium pretty well. Low serum sodium levels are going to inhibit the secretion of ADH and NP and trigger the RAS system. This will increase sodium levels by increasing the reabsorption of sodium and enhancing the loss of water. If your patient has high serum sodium that's going to inhibit aldosterone secretion and stimulate secretion of ADH and NP. So these hormones and the kidneys all together are going to maintain that water and sodium balance. I know that you all had an instructor who told you if you take a cell and drop it into a hypotonic solution, the cells gonna swell. My instructor said Hi, Bo, oh, you can imagine me spreading my arms out as I exaggerate the cell swelling. If a sodium imbalance is a osmolality imbalance, that means that it's a concentration imbalance. If my patient is hyponatremia check, their blood essentially becomes hypotonic. What will happen to the cells let's think about the brain, that water is going to leave the bloodstream because there's too much water and not enough salt in there. And it's going to go into the cells so the brain cells could swell. Most of the problems that we see related to hyponatremia are because of reduced excitability of membrane depolarization and cellular swelling. One of the most common causes of low sodium levels is the overuse of diuretics. We could also experience a relative sodium deficit meaning too much water when actually because by drinking too much water in a very short period of time, Kidney Failure syndrome of inappropriate antidiuretic hormone secretion or si d h heart failure, a too much hypotonic fluid administration. Anytime we add water, we could be diluting that blood one of the most obvious things that we're going to see in a patient with hyponatremia is that cellular swelling which is going to lead to altered mental status, or changes in level of consciousness. If you see your patient develop, sudden worsening of confusion, especially if they're elderly or on diuretics, you could suspect a sodium problem, we'll see some other changes, maybe general muscle weakness, because neuromuscular changes will see an increase in intestinal motility that will cause nausea, diarrhea, abdominal cramping and hyperactive bowel sounds. Any cardiovascular changes that we see are typically related to the volume rather than the hyponatremia itself. If our patient has hyponatremia with hypovolemia, we're gonna have a rapid weak thready pulse, we will have decreased blood pressure and orthostatic hypotension. Again, that is related to the hypovolemia more than hyponatremia. If our patient has hyponatremia that occurs with hyperbole, Mia, we will see full or bounding pulses, maybe a normal or a high blood pressure, those symptoms are going to be more related to that volume than they are the concentration of the sodium itself. These are going to be treated by addressing both the sodium and the volume imbalance. If the patient is hypovolemic and hyponatremia, you might expect to give them and hypertonic IV solution like 3% normal saline if the patient has hyponatremia that's accompanied by hyperkalemia. Then medications are going to be used to get rid of water but not sodium. Next, let's talk about hypernatremia. Too much sodium. This can actually also occur with a volume imbalance. But if we have too much sodium we're going to have this condition called irritability. The sodium is moving rapidly across cell membranes during depolarization. And this makes excitable tissues even more easily excited. They over respond to stimuli, water is going to move into the extracellular compartment in order to dilute that hyper azmol or hypertonic extracellular fluid. And so if we have high sodium levels, we can see cellular dehydration. Remember that your anatomy and physiology teacher told you if you drop the cell into a hypertonic solution, it's going to shrink up. Always think about the Wicked Witch of the West, right? She was either a cell being dumped into a hypertonic solution or she was a slug. I'm not sure which kidney failure is one of the most common reasons you're going to see high sodium levels. Of course, if we administer too much sodium containing IV fluid, we could see too much sodium in the bloodstream. A patient who takes in too much sodium, corticosteroids and Cushing syndrome, which are going to cause similar problems. We'll address those in some other episodes and hyperaldosteronism. If we have hypernatremia, as a result of not having enough water that causing us to have too concentrated a blood or too much sodium. This might be because your patient is not taking in anything by mouth. Maybe they have a fever, a fever is going to increase those insensible losses of just water hyperventilating, again, an increase of water loss that's insensible, excessive diuresis if they have watery diarrhea, and this is often something that we'll see in dehydration, thinking about those brain cells in this now hypertonic solution, they're going to shrivel up, they're going to become dehydrated, we're going to have altered cerebral function, this patient will have mental status changes, changes in cognitive function. This patient may have a very short attention span be agitated or confused. If the patient has overload also, they could be lethargic or superest, or comatose. The most frequent treatments are going to be 0.9%, isotonic, or often called normal saline. You might also see dextrose 5% in 0.4, or 5% Sodium chloride. This is often called half normal saline. If the patient's problem is excretion of sodium they may use medications like furosemide, a loop diuretic to facilitate excretion of sodium through the kidneys. Let's now talk about another major player. Let's talk about potassium. low potassium. Minor changes can cause major changes in cell excitability and can be life threatening because every body system is affected by potassium. Some common reasons that we lose too much potassium would be inappropriate or excessive use of diuretics or corticosteroids increased secretion of aldosterone, Cushing syndrome, especially diarrhea, vomiting, wound drainage, particularly gi drainage, prolonged nasal gastric suction, I mentioned that earlier, it's the same as that vomiting. If the patient has kidney disease that impairs the reabsorption of potassium, or being nothing by mouth, meaning not taking in anything in the mouth, we can also end up with relative potassium deficits with alkalosis hypokalemia can be associated with alkalosis. If the patient has too much insulin, insulin likes to take potassium out of the bloodstream and into the cell with glucose. So if the patient has too much insulin, then it can cause that potassium to go out of the bloodstream. It's the same way if you give the patient too much insulin IV, you can cause that same thing to happen. If the patient's on TPN, or total parenteral nutrition, that's where they're getting all their nutrition through an IV that can cause this. And if we give patients IV therapy that has not very much potassium in it, we're constantly losing potassium out of our kidneys. Normally, if we don't replace it, then we can end up in this potassium deficit. When we talk about potassium, most of us are going to think about the heart but we also need to think about the lungs, we can end up with this respiratory muscle weakness, resulting in shallow respirations that can actually result in respiratory insufficiency. So two big things you want to monitor with your patients who are hypokalemic are their respiratory rate and rhythm and depth and their cardiovascular function without that potassium The GI tract slows down. This can lead to hypoactive bowel sounds, nausea, vomiting constipation, which can lead to abdominal distension. We want to monitor for that with our patient auscultate their bowel sounds, and you can see ECG changes like ST segment depression, flat or inverted T waves. There's a hint in hyperkalemia, we'll see tall peaked T waves in hypokalemia, we'll see flat or inverted T waves. And we might see some increase in new waves. A star point, older patients who are taking digoxin are particularly at risk for dysrhythmias. To replace potassium, we can give it by mouth, we can give it IV, a couple more star points for you. Number one, potassium should never be mixed on the floor, it should only be done by a pharmacist or registered pharmacist, you should not have a dilution greater than one mil equivalent of potassium per 10 milliliters of solution. And it should never be given IV push. When we're giving potassium IV you should use a pump. And you should never exceed the recommended rate of infusion is somewhere around five to 10 mil equivalents per hour, but should never exceed 20 mil equivalents per hour. Last star point for this one, if your patient is not making urine. And I'm not talking about urinary retention, I'm talking about a patient whose kidneys are not making urine, you should reconsider administering potassium, that patient may not have any way to get extra potassium out of their body. And so we could cause them to become hyperkalemic. high potassium levels or hyperkalemia are really going to affect your heart. When we think about sodium we kind of think about the brain and the swelling or shrinking of brain cells. When we think about potassium, we often think about the heart, it's really sensitive to increases in potassium. And that hyperkalemia is going to interfere with conduction, which could lead to heart block or V fib, which has been tricular fibrillation. Some common reasons that people end up with too much potassium would be over ingestion. salt substitutes, if you look at the bottle may be potassium. And that could be one way that you end up with too much potassium transfusion of whole blood or packed red blood cells. This can be an issue if those cells burst or if they have burst inside the bag, then they're going to release that potassium in the intracellular compartment which is going to raise Tassie and level kidney failure is going to be a big one kidneys put out potassium. If they're not working, they can't put it out. And a patient who's taking potassium sparing diuretics, the one that comes to mind is Spironolactone. These encourage the kidneys to hold on to potassium, which can lead to high levels of potassium, especially if your patient doesn't know that they shouldn't be eating salt substitutes with that particular medication. Too much potassium can also be caused by tissue damage, like I talked about earlier. Anything that causes cells to break open and spill their contents acidosis and hyperkalemia go together and uncontrolled diabetes. The reason is the patient with uncontrolled diabetes does not have that insulin to move the sugar and the potassium into themselves from the bloodstream. This is going to be relatively rare in people who have normal kidney function. The people who may experience high potassium levels are those who are going to be taking a potassium sparing diuretic, or people who have certain chronic illnesses. We could see those tall peaked T waves as far as cardiovascular changes, we might see some changes in our P or QRS complex, this patient could end up with bradycardia or hypotension. We want to be monitoring that ECG to correct high potassium levels, they're either going to try to use a medication that's going to increase secretion, or they're going to try to move potassium from the extracellular to the intracellular space. medications that excrete potassium would be those loop diuretics we talked about earlier. Or they might prescribe a solution, an IV solution that includes glucose and insulin, right? I mentioned that that insulin will take the glucose and the potassium into the cells. But we want to make sure that we don't take all of the sugar out of the bloodstream. So we're going to give them a little bit extra facilitate that movement. We're going to talk about calcium, low calcium can be caused by a couple of things you'll want to think about the thyroid particularly The parathyroid hypocalcemia and hyperparathyroidism will go together. If the patient doesn't take in enough calcium, or say that they're lactose intolerant, they may not take in enough calcium. We could have patients without absorption problems. This would be someone with celiac disease or Crohn's disease, if they don't take in enough vitamin D either through diet or through sudden end stage kidney disease, diarrhea sanatoria, which is fatty stools, and wound drainage. But we can also have alkalosis, we could have medications that bind to calcium. If the calcium is bound to albumin, it's not free to help with muscle and nerve conduction in the body. If we have acute pancreatitis, or immobility, we can end up with this symptoms for hypocalcemia. A lot of these are going to be neuro muscular, so we might see paraesthesia as a paraesthesia is a numbness or tingling sensation. It usually starts in the hands and feet and can progress to the lips, nose and ears. If it gets that far, we could start to see neuromuscular overstimulation, that can lead to tetany. Two tests that you can do to look for this as nurses. One is true SOS and one is Fostex, you'll need to look these up, it's going to be pretty visual, true SOS is where I'm going to apply a blood pressure cuff around the arm and inflate it higher than the patient's systolic pressure, this is going to cause a little bit of a hypoxic condition. And what we're going to see is the hand and fingers go into a spasm in Palmer flexion. So they're going to the fingers are going to come together, and a lot of times the hand will supinate a little bit. Szostak sign is where you tap the face just below and in front of the ear and this is going to trigger facial twitching. A patient who has chronic hypocalcemia can see it in their bones, they're not going to have the bone density that we would expect they might have unexplained bone pain, something we'll focus on for them is going to be injury prevention. If they have thin, brittle bones, and we're going to replace calcium. It could be replaced orally, or it could be replaced IV depending on what the provider wants to do. High levels of calcium or hypercalcemia can affect excitable tissues. Those that we're going to see here are the heart that skeletal muscle nerves, intestinal smooth muscles, we're going to see depending on the severity and how fast the imbalance occurs, an increase in heart rate and blood pressure, confusion, lethargy, maybe some decrease in peristalsis, which will lead to constipation, anorexia, nausea, vomiting and abdominal distension. Bowel sounds will be hypo active. Too much calcium can be caused by too much intake of calcium, too much intake of vitamin D. We want to talk to our patients about some over the counter products that include calcium like Tums, which are calcium carbonate, kidney failure. Again, if we can't excrete these electrolytes they can end up too high and our thiazide diuretics, hyperparathyroidism and hypercalcemia go together. malignancy, especially the bones, hyperthyroidism, immobility can cause high calcium levels use of glucocorticoids and dehydration. The next major electrolyte to discuss is magnesium. low magnesium levels are typically caused by too much excretion of magnesium often because of a thiazide diuretic, or not enough intake. Simple nursing does my very favorite video on this week, he does Magnum magnesium, the sheriff in town, I love the way that he does that, and allows you to remember that when magnesium is around when there's more magnesium, we're going to have a decrease in a lot of things. And if we have low magnesium, you know, the shares out of town we're going to have high wild and crazy stuff happening. We can have hypertension, we can have atrial or ventricular fibrillation, premature contractions of either atria or ventricles, increased nerve impulse transmission because normally magnesium inhibits that. At the synapse, we'll see hyperactive deep tendon reflexes, our patient can end up with too much magnesium through intake maybe an IV replacement of magnesium or magnesium containing antacids or laxatives, like milk of magnesia. Or once again, kidney failure or decreased kidney excretion of magnesium. Now we're going to have depressed nerve impulse transmission, the patient might be drowsy or lethargic, they could end up in a coma, where patients going to have absent deep tendon reflexes. And we need to think about cardiac changes like bradycardia, peripheral vasodilation, which is going to lead to hypotension and we're going to want to monitor their respiratory status because if the magnesium is decreasing nerve impulses to the lungs, though it doesn't directly affect the lungs, it can cause the patient to have respiratory insufficiency. Thank you for hanging out with me for an extra long episode. I hope that this helps you. I'm going to leave you with just a couple of things to keep in mind. Sodium affects the brain. Potassium affects the heart. Calcium affects the musculoskeletal system, and magnesium affects the nerves slash deep tendon reflexes. That's all I've got for you for today. Reach out if you have some topics you'd like to hear about or to let me know that you enjoy this podcast. Please leave a review. Hopefully it'll be a good one. And I'll see you next time on nursing with Dr. Hobbick.