what's up ninja nerds in this video we're going to be talking about hyperkalemia if you guys want to follow along with some awesome comprehensive notes and beautiful illustrations go down the link below in the description box it'll take you to our website go check that out also if you guys benefit from this video it makes sense you enjoy it you have fun please hit that like button comment down in the comment section and please subscribe all right let's start talking about hyperkalemia all right ninja so when we talk about hyperkalemia first off how do we define hyperkalemia it's an elevated potassium level within the blood that's all it is hyperkalemia is an increased level of potassium within the blood now the question that you guys got to be asking is what causes someone to develop elevated potassium within the blood i'm so glad you asked and engineers you're so intuitive it is actually there's a couple different causes there's three particular overall different kind of concepts and within that concept there's multiple tiny little causes but we're going to kind of group them together to help us to remember these causes very easily so the first kind of like overall type of cause is that there is a reduced excretion of potassium so there's a reduced excretion of potassium now let's think very very simply what organ is responsible for excreting or secreting potassium the kidneys has definitely got to be one of them absolutely you know whenever somebody has a condition like acute kidney injury like a very severe acute kidney injury so let's say that they have some type of severe acute kidney injury or they have very severe chronic kidney disease or maybe they have an acute kidney injury that's developed on top of their already present chronic kidney disease in these situations where these patients are severely oligaric what does that mean when you're oligarchic you make very very little urine maybe it's like less than .5 cc's per kg for about at least six or more hours and maybe worst case scenario they could even be a neuric which is they don't make any urine and these patients who are allegoric severely oligarch or aneuric with an acute kidney injury or chronic kidney disease or an acute on chronic kidney injury their ability to be able to excrete potassium decreases you know in the uh different portions of the nephron for example here if we take this tiny little diagram of our nephron here we have the afferent arterial so this would be the afferent arterial this portion here this would be the efferent arterial this right here would be the glomerulus here you would have your bowman's capsule proximal convoluted tubule loop of henle distal convoluted tubule and then the collecting duct right in the distal convoluted tubule that's really where potassium is actually excreted so potassium is primarily excreted into the kidney tubules in the distal convoluted tubule but it depends upon a very specific type of hormone but regardless let's say that the hormones being produced but in a person who has aki or a chronic kidney disease these cells of the distal convoluted tubule are damaged and their ability to respond to that hormone and then excrete potassium is diminished that therefore leads to decreased excretion of potassium so when they're actually supposed to be excreting potassium that function is decreased because of damage to those cells even if the hormone is present here's another thing if a person has some type of severe kidney injury right whether it be an acute whether it be a chronic kidney disease their ability for blood to flow in right via the afferent arterial and then exit out via the efferent arterial you know there's this process when you run through the glomerulus you have to filter things out across the glomerulus that's called the glomerular filtration rate right and patients with an acute kidney injury and a chronic kidney disease or acute on chronic they have a very diminished gfr if they have a reduced gfr that means that there's less of the potassium that's being filtered across the glomerulus that means less potassium would end up in the kidney tubules less potassium is being excreted as a result what does that mean if you have a decreased gfr that means you're not filtering as much of the potassium out so what happens to the potassium then the potassium stays within the bloodstream and so as a result you develop an increased potassium in the blood for two reasons one is because you can't excrete it so it stays in the blood so if you kind of imagine here here's the potassium imagine that these cells or distal convoluted tubular cells pretend these are supposed to be excreting potassium right but because they're damaged that a capability is impaired these are the things that can lead to hyperkalemia so what i want you to remember reduced excretion due to acute kidney injury or chronic kidney disease or acute on chronic kidney disease all right let's come down for a second and the next concept is what else could cause a reduced excretion or diminished excretion of potassium we'll go back what did we say was the hormone that works on a distal convoluted tubule aldosterone where's aldosterone made you know you have an organ called the adrenal and in the adrenal cortex you have these cells that kind of like the top part here called the zona glomerulosa the zona glomerulosa is responsible for making a hormone called aldosterone what does aldosterone do aldosterone normally wants to be able to get inside of cells where again it acts particularly in the distal convoluted tubules so pretend i'm taking a piece of this tubule and i'm zooming in on it okay aldosterone actually is a steroid hormone so it can pass right through the lipid membrane and binds on to little intracellular cytosolic receptors and then activates particular genes now when it activates these genes it activates genes that help to make a couple different types of proteins one of the proteins are these sodium channels we'll we'll have that as maroon and then the other ones here we're going to draw in blue we'll call these the potassium channels okay so it helps to be able to synthesize these and it also makes another channel we can do one more protein here called a sodium potassium atpase and it usually puts that like right here on the basal lateral membrane either way i'm only want you to focus on one of these proteins so as a result of aldosterone stimulating these cells in the distal convoluted tubule it makes all these proteins the overall process here is that when filtrate is coming down through the distal convoluted tubule it should contain sodium and it should contain potassium all right sodium is supposed to be able to move through these channels and then via the sodium potassium atpase get pumped into the bloodstream right so that reabsorbs sodium and then as a process you use the sodium potassium atpases to pump potassium into the cell and then excrete potassium into the filtrate to actually be urinated out well in a person who has hyperkalemia what do you think is the issue what if they had a disorder that caused them to have a decrease in aldosterone that means this process here is actually not going to be happening so little sodium will actually be reabsorbed and this process here where potassium is supposed to be pushed into the cell and then pushed out of the cell is actually going to be impaired and so little potassium is excreted what's the end result then the potassium that you were supposed to push into the cell from the blood and then out into the filtrate isn't happening so the end result is that you increase potassium levels within the blood it's a very simple concept now here's another thing not only going to be hypoaldosteronism you know there's drugs that affect the renin angiotensin aldosterone adh system you know in the kidneys you have these cool little cells called the juxtaglomerular cells let's just have them like right there there's our there's our jg cells and the jg cells make a hormone called or an enzyme really called renin and what renin does is it works on a molecule called angiotensinogen and converts it into angiotensin one and then angiotensin one goes to the lungs you know there's an enzyme in the lungs there's an enzyme here called angiotensin converting enzyme we call it ace and what ace does is it actually stimulates the conversion of angiotensin one into a molecule called angiotensin ii and then you know what angiotensin ii does it comes over here and stimulates aldosterone production and then aldosterone would work on these channels to be able to regulate increased sodium reabsorption potassium excretion you know there's a drug that we commonly utilize on a daily basis if we're in pain and it's called nsaids nsaids actually have the ability to inhibit renin production and if you decrease renin production you decrease the conversion of angiotensin angiotensinogen into angiotensin one you decrease the activity of angiotensin one forming angiotensin ii and decrease angiotensin two stimulating aldosterone that results in a decreased aldosterone production it's the same kind of process there what if there's another drug that i actually use to inhibit ace what is that drug called ace inhibitors i give an ace inhibitor these ace inhibitors nsaids actually inhibit ace that means less angiotensin one gets converted into less angiotensin too less aldosterone production you know there's another drug we use to block the receptors that angiotensin ii binds to what do we call those angiotensin ii receptor blockers they inhibit this process so they'll block angiotensin 2 binding to the cells of the adrenal cortex and drop the aldosterone production infecting this process why is this important because we prescribe insects for pain we prescribe inhibitors for blood pressure control angiotensin receptor blockers for blood pressure control you know there's one more drug there's another drug so imagine here is actually that little receptor you know there's a receptor here that that's where the aldosterone will bite so here's aldosterone right we'll put it like this aldosterone wants to bind onto this receptor which wants to stimulate this genes to activate those particular channels that we already talked about above we're not going to go that crazy there right there's another drug which are called your potassium it's kind of beautiful when you think about it potassium sparing diuretics like spirenolactone or eplernone these work by blocking aldosterone binding to those receptors if aldosterone isn't able to bind to these receptors it is able to stimulate these genes that cause sodium reabsorption potassium excretion no so therefore sodium isn't reabsorbed and therefore potassium is an excreted what's the overall end result hyperkalemia so that's the overall goal that i want you guys to get out of this so the end result is that if there's a reduced excretion it's due to the kidneys being having an issue a disease of the kidneys aki ckd or there's something wrong with the hormonal system aldosterone whether it's a direct problem or it's an indirect problem through the medications that we commonly prescribe okay now that we covered that let's cover the next overall lump of causes of hyperkalemia all right so the next overall kind of like genre of causes is usually what's called a transcellular shift so this kind of deserves a really quick discussion so there's a trans cellular shift of potassium okay so this is an interesting conversation so potassium is a higher concentration of what part of the body is it in the cell intracellular fluid or is it outside of the cell and the extracellular fluid it's actually 95 of that dang potassium is located inside of our cells they're like bags of potassium so 95 of the potassium is inside of our cells so in order for us to have hyperkalemia increased potassium in the blood the extracellular fluid that means that the potassium is having to go which is 95 of it is in our cells and it has to go out of our cells into the bloodstream that is pretty much what a lot of these are going to be talking about so let's think about things that can actually cause the movement of potassium from inside the cell to outside the cell into the blood the first one is i want you to remember that our pancreas our beautiful pancreas makes a hormone called insulin and insulin works on these particular types of proteins you know what this protein is called this son of a gun is called the sodium potassium atpase and what it loves to do is pump potassium into the cell how many potassium it pumps to potassium into the cell and it pumps three sodium out of the cell that's kind of the function of the sodium potassium atp and it obviously utilizes atp insulin loves to stimulate the sodium potassium etps right so that's what i want you to remember insulin normally wants to stimulate the sodium potassium into pieces so what do you think would be an issue this normally if it's stimulated would put to push potassium into the cell so what would we need in order for the potassium not to be pushed into the cell we would need a decrease in insulin or no insulin so in conditions where patients have a decrease in insulin or the receptors of insulin is very sensitive resistant what is those conditions diabetes so in patients who have diabetes mellitus whether it be type 1 or type 2. you'll see it a little bit more in type 1 because there's very very little insulin but in type 2 if the cells are very very resistant to insulin it's just as the same their ability to activate these pumps are going to be inhibited so if there is a decrease in insulin you inhibit these pumps you don't pump the potassium where it wants to go into the cell instead you're actually going to keep it outside of the cell in the blood or in the extracellular fluid okay there's other things drugs i know it's always coming down but these are important things because we prescribe these medications very often you know there's a drug that we actually give to patients it's called a beta blocker and they're different types of beta blockers right there's beta blockers that are very specific they only work on like beta 1 receptors and then there's ones that are really kind of like they're not they're kind of like happy-go-lucky they'll bind to a beta-1 they'll bind to a beta-2 they're like hey maybe i'll do whatever you want so we got different types of beta blockers they're non-selective beta blockers and that's important because on certain cells that have what's called beta 2 receptors these beta blockers may be able to bind on to these beta 2 receptors and these beta 2 receptors normally stimulate they work to be able to stimulate the sodium potassium atp aces so if i give a beta blocker that's going to inhibit the actual beta 2 receptor and therefore lead to an inhibition of the sodium potassium atpase i don't punch potassium into the cell very simple right so beta blockers within the genre of the beta 2 receptor particularly and then the next thing is we give another drug that we give actually in heart failure or in patients with afib and and one of the benefits of this drug is that it causes like more contractility and it's called digoxin digoxin literally directly affects this channel and so what digoxin actually does is is digoxin actually inhibits we'll put here some dig some digoxin here digoxin actually directly inhibits the sodium potassium atpase and so it doesn't allow potassium to push into the cell stays outside the cell there's one more cause you know in conditions where we have lots and lots of protons whether this proton be due to an increase in co2 because you know co2 when it combines with water it makes carbonic acid which breaks down into protons and bicarb well that's one way if you have a lot of co2 you can make protons what's that called respiratory acidosis right if it's primarily a lung disorder or it could be due to things like organic acids right so lactate you know or lactic acid you know sulfuric acid phosphoric acid different things like that so different organic acids keto acids all of those things so whenever there's an increase in protons there's an acidic environment you know whenever there's lots of acidic environment in the extracellular fluid what we want to do naturally you know there's a channel there's like a channel here imagine there's like a channel here on on the cell so here's this channel normally what we want to do is if the the protons are really really increasing what does that do to the ph it reduces the ph right so what we try to do is let's say if we kind of hide it in a way we say let's put the protons somewhere else besides the blood and then we can kind of pretend like the ph is kind of normal so we'll shift the proton somewhere else well if i'm going to shift a proton into the cell this is a positive charge i need something else that's positive charge so i can maintain an electro neutrality in this cell that i can push out what can i push out potassium and so what i'll do is i'll push potassium out in exchange for that proton the more protons there are the more you're going to push in the more proto potassium lines you're going to push out so in severe acidosis whether it be respiratory whether it be metabolic acidosis this can really cause a lot of potassium to get pushed out of the cell because you're trying to push protons into the cell to mediate that acidic environment okay beautiful that covers that part what else is another way that we can actually shift potassium you know not only does diabetes directly affect it through the insulin process but you know whenever there's high amounts of glucose kind of in the blood what do we call that whenever the the blood is really really kind of rich in solutes and very little fluid what do we call that it's called hyperosmolar right so we call it hyper osmolar so in a hyperosmolar state right what's a disease which causes a hyperosmolar state related to glucose there's a condition called h s hyperglycemic hyperosmolar state this can happen to patients with diabetes where they have very very high glucose levels and those situations where there's really really high glucose levels it kind of does what to the water which is inside of our cells the water like looks at it and there's like [Music] lots of glucose idea i'm going to go out there and so the water will then say all right i'm going to leave out of this cell to come to where all of this actual sugar molecules are because it's going to draw it like an osmotic gradient therefore the hyperoz molar term that pulls water out of our cells and into the blood when you pull water out of the cell water helps to kind of be able to maintain somewhat of a concentration gradient so for example when you take potassium the more water there is in that cell it kind of affects the potassium gradient but when water leaves there's less water in the cell and so that kind of affects the potassium gradient and now whenever water leaves the cell so let's say that there's actually as a result of water leaving there's decreased water in the cell this results in kind of a higher potassium concentration inside the cell in comparison to the potassium concentration outside the cell and what that does is that high concentration gradient yanks the potassium out of the cells and into the blood and then as a result the potassium levels in the blood will increase because you're pulling potassium out of the cells because of this hyperosmolar state or hyperosmotic gradient what's another condition that not only can cause this what if you're super super dehydrated so sometimes in conditions where there is significant dehydration you can cause the actual body to become a little bit more hyperoz molar because there's less fluid right less fluid within the extracellular space so in the same way you're going to cause lots of solutes lots of salt right that can actually build up within the bloodstream because you're actually pulling off fluid in the sense of dehydration or excessive diuretics so excess diuresis you know in patients who get lots of like loop diuretics of some form it may pull off a lot of fluid a lot of dilute fluid water and then lower the actual amount of water in the vasculature and because of that it makes it a little bit more hyperoz molar in the sense of maybe there's more sugar molecules or more salt molecules there and so these are things that you want to think about and that can create a pool of water into the actual tissue spaces and into the blood but as a result it changes the concentration gradient potassium which pulls more potassium out as well okay all right so we finished up talking about these causes of trans cellular shift let's come down and talk about a couple more causes of a trans-cellular shift so you have patients who you know maybe they have some type of seizure right or maybe they have a severe crush injury and this causes a lot of damage to their skeletal muscles and their skeletal muscles as a result of maybe like extreme exertion seizure activity crush injuries it causes the skeletal muscle damage and scale skeletal muscles are cells right they're containing cells and what are cells made up of cells are just bags of potassium and so these cells start popping open releasing things like potassium resin releasing things like creatinine kinase releasing things like myoglobin right and this can be a process what's one of those things potassium so that could be one way that could lead to increased potassium levels in the blood you know and a condition called tumor lysis syndrome tumor lysis syndrome you know tumor cells particularly like you know whenever you're like leukemia lymphoma they get chemotherapy and these cells start getting damaged from the chemotherapy they start popping open releasing tons and tons of molecules inside of their actual cells one of them is potassium or they start releasing phosphate or they start releasing other types of molecules like uric acid right so tons of different things start kind of increasing inside of the actual bloodstream and this could be a sign of tumor lysis syndrome the other thing that you want to be thinking about is if someone has some type of damage to their red blood cells what does this call whenever you lyse open or pop open their red blood cells it's called homolysis and whenever this happens for whatever the hemolytic cause is you pop open these cells and you start releasing what's one of the components potassium you also start releasing hemoglobin and then there's also going to be kind of an increase in bilirubin so there's a lot of different things that can happen as a result of this right so this would be particular things that you have to be able to think about all right so i wanted to take a quick second to fix up these roman numerals so that we have the third and then the fourth kind of causes kind of categories of causes of hyperkalemia so this next one it's not super common it'd be pretty hard to do but it can happen especially if you're taking medication for like hypokalemia when you take too much of it or you decide i don't know to go ham and eat tons of bananas or you're getting a lot of potassium replacement therapy and you're getting just more than you actually should have and you have chronic kidney disease or acute kidney injury whatever it may be it's the last cause that i want you guys to kind of the last kind of big one to think about here is some type of increased potassium intake whether this be in certain foods whether this be in the medications that you're taking you're taking potassium you're getting potassium replacement therapy if there is an increase in the amount of potassium that you're taking in whether it be via the gut or whether you're getting potassium iv because you're in the hospital for some reason and you're getting just a little bit too much potassium this maybe leads to an increased absorption of potassium across the gut or an increased delivery of potassium into the actual venous circulation and either way that may lead to hyperkalemia it's not super common but it is one to think about it's one of the easiest ones probably to think remember right as you give potassium it's going to cause hyperkalemia now the last one and believe it or not probably one that you'll see more often than not and you definitely want to remember is what's called pseudo hyperkalemia where you actually think that it's hyperkalemia the potassium levels will show up elevated greater than 5 because generally like 3.5 to 5 is like the normal range for potassium so what happens is you can order labs right and you know when patients get venipunctures and they use like the tourniquet or maybe they're using like some type of like smaller iv whatever it is when they're drawing blood and especially with very intense tourniquet use or it's staying on for a long period of time some of the red blood cells when it gets taken up during the blood draw they lyse what does red blood cells contain potassium so if they lyse and pop open what can they release into that actual blood sample when you're taking it potassium and so whenever they run that test that bmp to give you your potassium value it can be falsely elevated because a lot of the cells actually rupture during the venipuncture so during venipuncture sometimes you may have these elevated potassium levels and what what you have to do is usually the the tech will actually look at the actual blood sample under the actual microscope and look to see oh there was a lot of hemolysis so you know the specimen's not actually super correct because it was hemolyzed and so that's a big thing to think about another thing that can actually kind of present like pseudo hypercholine does not do a hemolyzed venipuncture is sometimes if people have very high platelets what is that called thrombo so they have what's called thrombo cytosis sometimes in high levels of platelets platelets actually contain granules that have potassium so you have tons and tons and tons of platelets and they pop open and they release their potassium that also can cause hyperkalemia so in these two situations just remember that pseudohyperkalemia is a very common cause one of the most common is the venipuncture process where it gets a hemolyze sample another one could be thrombocytosis all right that covers all the causes of hyperkalemia let's now talk about the pathophys all right ninjas let's talk about how hyperkalemia leads to the particular clinical manifestations and certain types of electro cardiographic features that we may see in a patient who presents with hyperkalemia so really quickly to kind of go through the path of fist so we have a basic understanding of it you have to have a basic understanding of the membrane physiology if you guys want a little bit more understanding on that go watch our video on resting membrane potential greater potential action potentials it'll really help you to understand this we're going to kind of briefly go through it though so quickly understanding is that you have a cell that has what's called a resting membrane potential so really quickly if i were to have something like this here this kind of graphical representation you have a cell that has what's called a resting membrane potential what's that normal resting membrane potential in cells usually it's like negative 70 millivolts right that's about what it is now the resting membrane is kind of carried out by a couple different types of channels the big ones that i want you guys to remember is you have what's called the sodium potassium atpases right but normally they function to pump potassium two potassium into the cell and they pump three sodium into the cell that's one of the things that contributes to the resting membrane potential but the more important thing that contributes to the resting membrane potential of excitable cells what are excitable cells cells that are cardiac muscle smooth muscle skeletal muscle and neurons those are kind of your excitable cells and those types of cells they have these things called potassium leakage channels and what they normally do is they allow for potassium to move out of the cell because you know normally potassium is in high concentration inside of our cells and low concentration out of the cells and so potassium will leave and that if you have a positive ion leaving that makes the inside of the cell negative so that's why the resting membrane potential should be relatively negative now what happens is is this is what contributes primarily to what's called your resting membrane potential right and and you know whenever a cell becomes like excited whenever you have an excitable cell you have to have something like some kind of stimulus right like there's there's a stimulus that you have to have to be able to reach something called a threshold potential so normally cells at rest and it has to get to a point of what's called a threshold potential to be able to have like an action potential and so that's where you need something called greater potential something that stimulates the cell brings it up to that threshold and then it can have what's called an action potential so it would look kind of something like this right you'd get up to threshold potential through that graded get up here come down you'd overshoot a little bit and then it would go back into that resting state ready to be stimulated again and and what happens in this this kind of effect here is that in order for you to have this point here which is above called the action potential you have to have these things called your voltage-gated sodium channels open you know what happens is in these kind of phases is that whenever you hit threshold potential let's say that this is the sodium channel at the threshold potential whenever you hit that threshold potential normally before you hit it this is what it looks like before so let's actually say right before let's actually be more specific right before threshold potential this is what it should look like this is called your activation gate and this is called your inactivation gate normally this one's closed and this one's open but what happens is once you hit threshold potential and you get to the you know the action potential like the peak part of the action potential it should look like this where the activation gate should be nice and open and the inactivation gauge should be slowly starting to close and what happens in this phase is this where sodium is just loading into the cell right it's making the cell super positive and then after that you kind of go back down to this original state that you had here so this right here is at the resting membrane potential state right where your activation gate is closed and your inactivation gate is open but sodium can't get into the cell here it's blocked this is kind of the normal cycle of your sodium channels well guess what happens potassium is in higher concentrations now outside the cell so now your potassium level that you have inside of the cell so you should normally have high potassium inside the cell and low potassium outside the cell but now in a patient who has hyperkalemia the potassium outside the cell's a little bit higher than it should be and that affects the concentration gradient and so as a result less potassium leaves so if less potassium leaves the cell that makes instead of the resting membrane potential being like like slightly like more negative negative 70 it actually can make the resting membrane potential less negative and if i make the resting membrane potential less negative let's pretend for a second that now the new resting membrane potential is actually like right here so let's actually call this the resting membrane potential prime that's the new one well guess what if because of that hyperkalemia does that let's say that you get a stimulation that you happened here before right so you have hyperkalemia you get like this action potential that occurs but then what happens is normally your actual cell will go through this phase of you hit threshold you cause an action potential and then should go back to a resting membrane potential and the only way that it rests it's in this state is if you hit negative 70 millivolts that's the only way well if my new resting membrane potential is not negative 70 it's actually like more positive now will i ever be able to get these sodium channels that are stuck in inactivation open again no and so because of that the sodium channels and hyperkalemia the sodium the voltage gated sodium channels become locked in the inactivation state in activation state and that means you can't stimulate this cell if i can't stimulate the cell because it's stuck in this inactivation state that means that the cells become less excitable and their activity of cardiac muscle smooth muscle and skeletal muscle neurons all declines what can that present as i'm so glad you asked if you affect skeletal muscle let's just say skeletal muscle like the limbs what would happen if you have less excitable muscle cells skeletal muscle cells they're not contracting if they're not contracting what will that present as weakness if your neurons are less excitable if they're less excitable because they're locked in this inactivation state and they can't be brought to their true resting membrane potential what happens to the actual action potentials of neurons there's decreased action potentials of neurons and this may lead to again neuromuscular weakness right because neurons actually serve muscles so that can also kind of lead to weakness but also you know when you check reflexes those are supposed to be a response of electrical activity if there's a decreased responsiveness of the neurons decrease excitability you tap a reflex what do you think is going to happen they're going to have decreased reflexes so this can lead to what's called decreased deep tendon reflexes what about the smooth muscle of the git it's supposed to be able to contract and move stuff through the actual git and poop it out what's going to happen if you can't do that you can develop constipation sometimes maybe even an ileus and you know what else if things aren't moving through the actual gi tract they start backing up and you aren't able to get it out it's going to come through one hole it might start leading to nausea and vomiting okay if it's affecting the cardiac muscle so now the cardiac muscle is less excitable it's normally supposed to be able to be excited be stimulated and want to contract and if that doesn't happen what will that result in it result in a decreased contractility of the heart if there's decreased contractility of the heart what does that do to the cardiac output that decreases cardiac output what does that do to the blood pressure it may reduce the blood pressure so there may be a decreased contractility of the heart but also it can lead to a lot of nasty kind of ekg changes we'll put here changes there a lot of arrhythmias particularly it would lead to a decreased type of heart rate right because if you have less excitability it's not going to want to be able to be stimulated as much and so it'll be a slower conduction so that may present as bradycardias maybe heart blocks maybe sinus bradycardia and we'll talk about some other things prolongation of the pr interval what about the muscles the skeletal muscles that are also important for breathing the diaphragm the intercostal muscles they're all jacked up now what about those poor guys in this situation this can lead to difficulty breathing like respiratory distress and one of the other key things to think about is in someone who has hyperkalemia what may be the most common cause acute kidney injury chronic kidney disease and what happens in those kinds of patients and those patients who have acute kidney injury and chronic kidney disease which is usually the most common cause of someone having hyperkalemia they may have a decrease in urine output or worst case scenario no urine output what's the call when you have to decrease your output i'll agree what's it called when you have no urine output a neuria so these may be some of the clinical features that we see in a patient who has hyperkalemia all right let's do a mnemonic to help you guys to remember it all right so we talked a lot about a lot of the clinical features and decreased excitability of cells but let's try to have a nice little way of remembering hyperkalemia for your exams you know how you can remember it there's been a murder in savannah if you know you know but the whole mnemonic here for murder is that m is for muscle weakness so decrease skeletal muscle excitability low urine output oliguria aneurya right or no urine output for a area this would be a situation where someone has acute kidney injury chronic kidney disease respiratory distress due to the diaphragm intercostal muscles decreased cardiac contractility decreased cardiac activity ekg changes due to the effect on the cardiac muscle and decreased reflexes due to the decreased activity of the neurons and if you wanted to add in another one in there you could add in that gi activity as well but that is going to how that's going to be how you guys remember the basic clinical features are signs of hyperkalemia now let's talk about the diagnosis all right so how do we go about diagnosing hyperkalemia it's actually a relatively simple diagnosis right in order for you to have hyperkalemia what does the potassium have to be greater than that's to be greater than five right so really you have to start off kind of saying okay we have to have a potassium level that is greater than five and that's kind of the the average range is about 3.5 to a five so if i have greater than five i know that it's actually hyperkalemia but to be really really careful one of the first things you have to do is go back to remember your closet we spend so much time on causes because it's actually important for the diagnosis right you can easily diagnose hyperkalemia but finding the cause of hyperkalemia is important so the first thing is you have to rule out pseudo hyperkalemia and again what did we say was the two particular causes behind that was a hemolyze sample so usually the lab will actually write down if you have a hemolyze sample or what could you do if it was a hemolyzed sample send another one send a repeat one maybe grab it from an arterial line or something and see what it happens if you actually get it from a different line or you try another stick that's our try it from an arterial line see what happens if it comes back and it's actually still elevated potassium it might actually be real but ask the lab is there any signs of hemolysis or draw it from another line or an arterial line okay the other thing is make sure that they don't have any elevated platelets how can i check to see if they have any significant thrombocytosis i can get a cbc a cbc will tell me if i have any thrombocytosis if there's a really really a large number of them okay that's the easy way right the next thing is let's say okay we definitely have a diagnosis of hyperkalemia what are these other particular causes that may be responsible so now we know that there is a true diagnosis of hyperkalemia which means that it's greater than five milli equivalents per liter now how do i actually figure out what is the underlying cause of that we'll go back and think about all of them what were one of them aki ckd look at their history do they have a history of ckd what was their gfr if they have a history of ckd and they don't have an acute kidney injury it's their baseline you can check their gfr it's not good in acute kidney injuries but it's good in chronic kidney disease so if they have a low gfr that may be a good idea right what else check their bu in if it's elevated check to see if their creatinine is elevated but make sure that again is it their baseline is it beyond their baseline because if it's greater than 1.5 times their baseline it's greater than 0.3 within the past 48 hours it may be an acute kidney injury so looking at that looking at their urine output have they had a decreased urine output or no urine output these may be ways that you can kind of lead to this being the cause of their hyperkalemia what was the other one hypoaldosteronism right how do i check for hypoaldosteronism you check the dang aldosterone level so in a patient who has hypo aldosteronism check to see if they have a low aldosterone level usually if they have a low aldosterone level they'll also have a high renin level so that's one of the ways to determine if it's actually coming from the adrenal cortex and it's not something else what was the other things that kind of affected aldosterone indirectly and you can just go ahead and either hey do you take this medication or you look through their medication list and see if they take it so what were some of those drugs do they take any nsaids discontinue them see what happens do they take an ace inhibitor do you see what happens if you discontinue do they take an arb do they take a potassium sparing diuretic like spironolactone if that's the case look through their actual medical history of their medication list maybe discontinue that and see what happens at the potassium level when you draw it another day what else the other things that you have to be thinking about is what if it was a hyper osmolar cause and they have diabetes how do i determine that oh i don't know maybe i'll just check a blood glucose right so what i could do is i could actually check a bmp oh real quickly what would i get a lot of this stuff from what can i get a gfr bu and the creatinine from i could get that from a bmp correct yeah so i can get that from a bmp but nonetheless let's say that we just check what's called a point of care glucose or we just check what their glucose is off the bmp as well because the bmp gives you their glucose as well if they have a super high glucose or their bmp is really having a high glucose maybe they have a hyper osmolar state also check to see if they're dehydrated look at their volume status have they been taking tons of diuretics recently that might be another sign you know what else you can do what was the other cause acidosis right how can i determine if someone has acidosis i could if i really want to be accurate if i really want to be accurate i can get an avg so if i got an abg of a patient and i look to see oh wow their ph is really low and then from there i can determine oh it was because they had a high co2 so they have respiratory acids oh it's actually because they have a low bicarb ah so it's a metabolic acidosis that can kind of give me an idea of what was the cause of the acidosis but the acidosis may be the very thing that's driving their hyperkalemia and if i fix the acidosis i may fix their hyperkalemia what about other drugs that we talked about that cause trans cellular shifting what about beta blockers right so beta blockers do they have a history of any kind of heart failure or anything that requires beta blockers and they've taken it before have they gotten any digoxin leaks lately and again maybe trying a discontinuation and seeing what happens might be the way to go about this what if it's not just these things but it was we actually know that they had another condition where they were popping cells open like left and right what if they were popping open some muscle cells and they had something called rhabdo well maybe they have pain in their legs right maybe they have pain in their arms they have a lot of like sore muscles what's something else i can check in the blood that we kind of mentioned over there they may have a lot of ck they may also have what's called myoglobin in their urine myoglobin area which may make the urine really like darkish kind of colored right so that may be a sign and what else what if there's what's called tumor lysis syndrome we're going to abbreviate that tls tumor lysis syndrome well not only were you popping open cells that had lots of potassium but you're also going to be popping open cells that have lots of phosphate you have lots of uric acid and there can even be other different things that are also being popped out of these cells so whenever they have a high potassium high phosphate high uric acid these may be particular signs what else what if you have another cell red blood cells that are actually lysine so you have signs of hemolysis what could i check to look to see if my hemolysis is leading to anemia i can check a cbc but i can also check other levels that make me think of hemolysis whenever these cells pop open it actually causes the release of ldh it can cause an increase in your bilirubin what kind of bilirubin though let's be very specific is it unconjugated or conjugated it's unconjugated so here we'll put we call that indirect bilirubin or unconjugated bilirubin and then what protein made by the liver sops up a lot of that hemoglobin haptoglobin so there is a decrease in the free haptoglobin levels so these could be ways that you could say oh it's a hemolysis is the cause so these are the ways that we can go about determining if it's true hyperkalemia once we've determined it's true hyperkalemia figure out the cause once you figure out what it is you treat that you fix it now the last thing is sometimes a patient may not come in with any of these clinical manifestations and all you may see is you get a 12-lead ekg and you get a 12-lead ekg and you see some particular really weird abnormal ekg changes what are some things that i really want you guys to take away from this and not to forget okay the first one that i want you guys to remember here is that this leads to again decreased cardiac excitability and contractility one of the things that happens it causes repolarization abnormalities right because again whenever you have the action potential it has to go down all the way to hit resting phase but do you actually truly ever hit the resting phase the true resting phase no because the hyperkalemia created a new resting membrane potential and so it affects the repolarization of the ventricles what what is this this wave here that represents ventricular repolarization the t wave it produces what's called peaked t waves so that's one sign here okay then it may get a little bit now this is not always the case in the exams it says this but it's not always like concentration of potassium in the blood dependent you can have any of these ekg changes at different levels of potassium in the textbook definition it says that these kind of ekg changes occur as the potassium levels increase but that's not always the case okay so just remember that in true clinical experience now what else can happen not only can you have peak t waves but if it gets a little bit worse what's oh what the heck look at this qrs wave that's a big mama that's wide that's a wide qrs so you may start seeing signs of a wide qrs and maybe still a little bit of a peak t wave okay what oh my gosh look at that pr interval there that pr interval is gargantuan that's a long pr interval so if i have a prolonged pr interval that may lead to some bradycardia okay so i'm starting to see some signs of some bradycardia there can be like a heart block kind of sign here oh my gosh the p wave's gone so i start seeing flattening of the p wave so not only is there a prolonged pr interval but where the heck is my p wave so i got flat or absent and sometimes absent p waves what is it called because this is sometimes one of the findings that i see a lot um in the icu is that you know what this is called when you don't have a p wave and there's no actual sinus rhythm there what is it called whenever the av node is now the one that's taking over it's a junctional rhythm sometimes one of the most common signs of a patient in hyperkalemia is a junctional rhythm believe it or not so think about that oh my gosh what is this this is called a sine wave so sometimes hyperkalemia leads to this really weird looking type of sine wave or sinusoidal type of pattern and when you see this it's usually a precursor for some type of ominous thing which is usually when they start going into something like v-fib or worst-case scenario they go into cardiac arrest and they have a systole okay so these are the ekg changes that i want you to remember so quick quick quick reminder peak t waves to yqrs to prolonged pr to flat pr the flat p wave to a sine wave to cardiac arrest whether it be v fiber asystole that covers the diagnostics let's talk about treatment all right so let's talk about the treatment of hyperkalemia now it's actually not that bad it's really straightforward okay so the first thing that you want to do in a patient with hyperkalemia generally if you start seeing some signs of some ekg changes so any signs that we talked about before right peak t waves you start seeing some yqrs some prolonged pr intervals you start seeing signs of some flattening of the p waves a sine wave pattern v fib cardiac arrest anything like that signs of cardiac toxicity due to hyperkalemia you have to stabilize those cardiac membranes so not only is the ekg changes but if the potassium levels getting really really high it's getting really really high you got to start considering potentially giving them something to stabilize their cardiac membranes so stabilizing they're cardiac membranes now for a long time i was like what does that mean to stabilize cardiac membranes and you just kind of assume it's like oh it just stabilizes it the real actual mechanism is isn't completely understood it's actually kind of difficult um to elucidate but what we've been able to so for the most part assume is that when you give somebody what's called calcium gluconate so you can give them what's called calcium gluconate and sometimes if that isn't the best situation you may try something called calcium chloride but either way you want the calcium part of that when you give them these substances what it does is imagine remember go back to that graphic appearance that we had before okay in the graphic appearance before you had something here called your resting membrane potential and then you had this thing here which was called your threshold potential and due to hyperkalemia what happened hyperkalemia created this new resting membrane potential resting membrane potential prime right so this was the old one and then what happened is when you had action potentials it should normally look something like this right it should go here trigger this action potential come back down have a little shoot there now let's say that we have this person who has hyperkalemia now they'll actually go here same thing hit that threshold potential come up but now guess what their new resting membrane potential is right there guess what i'm going to do i'm going to give them calcium glucage and calcium chloride and i'm going to make the inside of the cell a little bit more positive to the point where i bring my threshold potential i bring it up i increase my threshold potential now i have a new threshold potential which is above the new resting membrane potential and so because of that these cells may actually go into this rested state and actually have the ability to somewhat be excitable and so that is what kind of happens in these patients you start having signs of cardiac toxicity so the first thing that you want to do if any signs of ekg changes or is the potassium starts kind of getting greater than six is you might want to start stabilizing those cardiac membranes calcium glucanate calcium chloride the second thing that we want to do is is we want to control a lot of that shifting between cells so then we have to control the shift of potassium all right so in other words we're not going to be able to actually excrete potassium this is stabilizing the cardiac membranes the next thing is can we push potassium like back into cells by some way and get it out of the blood can we do that somehow and guess what we can what was i taught what did i tell you was one of the things that actually stimulates sodium potassium atp aces insulin so you know what i can actually do i can give a patient a little hefty dose of insulin and if i give them a hefty dose of insulin like regular insulin that's going to stimulate these sodium potassium pumps if i stimulate the sodium potassium atpases what will that do it'll push two potassium into the cell and push three sodium out of the cell but if effectively i got potassium that was high in the blood into the cell i i just transferred it i shifted it sometimes if you give a hefty dose of insulin it may cause hypoglycemia so what can we do from preventing that hyperglycemia hypoglycemia we can give something called dextrose and usually in the form of like d50 okay to be able to give them some type of sugar to prevent that insulin dropping their sugar levels if they're if they're close to the verge of having normal glycemia or eu glycemia you don't want to give them a bunch of insulin and drop their insulin of their glucose down to like zero so insulin and d50 will shift the potassium into the cells by stimulating the sodium potassium atpases guess what i'll stimulate the sodium potassium atpases what i said the beta2 receptors right beta2 receptors and then whenever they respond to epinephrine norepinephrine or some type of agonist like that it stimulates the sodium potassium pumps what if i give something that's a beta2 stimulator or a beta2 agonist guess what we can give beta2 agonists we can give a drug called albuterol pretty hefty doses of albuterol because albuterol is a beta 2 agonist and so what it's going to do is it's going to bind onto these beta 2 receptors and then increase or stimulate the activity via the cyclic amp kind of process stimulate the sodium potassium atp aces and what's that going to do that's going to shift the potassium into the cell right particularly you're going to put two potassium ions into the cell and then you're going to get rid of three sodium ions but i shifted the potassium in that's one way albuterol sometimes we call this a saba short acting bronchodilator right which is a beta2 agonist what else could i do another thing we can do is we can control the acidotic environment so we said that before whenever there was lots of protons right whenever there was lots of protons this was basically causing that problem of pushing potassium where out of the cells what if i give something to counteract those protons so i give something that can bind with the protons and when if i combine them together i'll get something called carbonic acid which is less acidic this is way less acidic what's that bicarb simple so i can administer bicarbonate and if i give them bicarbonate what will this effectively try to do this will effectively try to reduce the amount of protons it's going to reduce the amount of protons that's being pumped into the cell and reduce the amount of potassium ions that's being pushed out of the cell so it's effectively leading to this shift change we're having less of the potassium leaving out of the cell usually we give bicarb if it's getting to the point where the patient has severe uremia or their ph is very very very low sometimes if it's approaching like less than 7.2 it's not always given for all patients okay but we stabilize the cardiac membranes with the calcium gluconate we shift the potassium back into cells or at least prevent the potassium from exiting via insulin give d50 to prevent over correction causing hypoglycemia hefty dose of albuterol and bicarb in the situations of uremic acidosis or very very low ph to where it's getting less than 7.2 all right so we've already controlled stabilizing the cardiac membranes and hyperkalemia we shifted some of the potassium back into the cells what about trying to just eliminate potassium through the ppe or the poopoo that's the way that we can try to do it and so what we can try to do is eliminate or excrete potassium if the kidneys and the bowels have the ability to do that now what can we give that can actually get rid of potassium diuretics right so diuretics are going to be kind of your go-to so when i talk about diuretics the best one to consider is something called furosemide furosemide also known as lasix works particularly how you can use thiazide you can actually add them as an adjunct you can do like a plus or minus hydrochlorothiazide or some type of thiazide like diuretic you can consider those but generally furosemide is going to be the best situation here and the reason why is this works in the loop of henle and a good chunk of potassium is actually supposed to be reabsorbed in the loop of henle but when you give furosemide it inhibits this channel you're probably like oh my gosh this is that beast one isn't it yeah it inhibits what's called the sodium potassium two chloride co transporter okay now if it inhibits this channel this channel is responsible for bringing sodium reabsorbing sodium it's actually helpful for reabsorbing chloride and it's helpful for reabsorbing potassium but if you inhibit this channel are you able to reabsorb potassium are you able to reabsorb sodium and chloride no and so because of that all of this stuff stays within the kidney tubules and because it can't be resorbed at this point here this is dependent upon aldosterone and if aldosterone isn't going to be able to control enough of that guess what happens that goes right into the pp and you get tons of potassium that should be excreted this is called calyuresis right and you may have to give sometimes some pretty hefty doses in a patient who has a pretty significant kidney injury so this is what we would try something like furosemide now the other option is let's say that they can't be diurese for whatever reason maybe they're in chronic they have chronic kidney disease or maybe they aren't able to make any urine they're anuric and so putting them on that actually may not work or maybe they're just a little bit dry they're actually a little bit dry and you don't want to direct them and make them actually even more dry and you actually have to give them a little bit of fluids instead of lasix then maybe you might go to another option here which is called chiaxillate so another drug here it's it's it's kind of a sodium polystyrene so it's actually sodium polystream and it's actually called chiaxillate it's kind of like the the brand name of it and what this does is kayak slate or sodium polystream is it it's responsible for actually kind of so imagine here you have that kiaxial molecule one of the things that it does is it actually can release sodium ions out and the sodium ions actually get across the enterocytes and when it crosses the enterocytes a positive ions going into the cell so something has to be able to come out of the cell that's also positive and guess what actually gets kind of pushed out here potassium you know what else the sodium polystyrene does it actually kind of binds up any potassium that may be present with inside of the actual gi lumen so it kind of acts like a potassium binder so it releases sodium ions that actually cause sodium to get exchanged and processed for potassium and it also binds on to the potassium and tries to bring that potassium out into the poo poo the only downside of this one is that there has been actual risk of intestinal necrosis due to it maybe causing some compaction in certain patients okay last but not least here for effective art treatments is if a patient is completely refractory to all of the actual measures that we've employed they're completely aneuric we don't want to give them any calculator we don't think it's actually going to make much of a difference we may have to use something called dialysis so at this point in time when it gets to this level we may need to do what's called dialysis and depending upon the patient's hemodynamic stability they may need something like continuous renal replacement therapy or if they're pretty hemodynamically robust intermittent hemodialysis of some type okay and that's going to be responsible for taking all you basically have like these catheters in the actual venous circulation you have an arterial side and a venous side basically here's the arterial side here's the venous side it's just the circuits but it's all coming from a vein any of the potassium that's all kind of accumulated here in the blood gets sucked up through this kind of catheter taken through this kind of colander here and the potassium gets kind of pushed out of the actual blood plasma into this colander and then we remove the potassium through this actual filter and put it back into the bloodstream effectively removing potassium so that's going to be the kind of the last line treatment but here's what i want you to leave you guys with remember there's a cause for the hyperkalemia and if there is a cause for the hyperkalemia what do you need to do you have to treat the underlying cause you have to figure out what is the underlying cause if it's a kidney injury then you have to be able to unfortunately maybe only dialysis is the best option for these patients and trying other therapies that may help in preventing the continuous progression of kidney injury right but if it's all the other things that we talked about those require particular medical therapies discontinuing of a lot of medications that may be the thing to fix the person's hyperkalemia so go back in those causes and start thinking about things that you can actually fix and that's what you would do to actually treat hyperkalemia and that covers the final discussion on hyperkalemia all right engineers in this video we talk about hyperkalemia i hope it made sense i hope that you guys enjoyed it as always ninja nerds until next time [Music] you