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Potassium Disorders | Clinical Medicine — Transcript

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0:08what's up Ninja nerds in this video
0:10today we're going to be talking about
0:11potassium disorders that includes both
0:13hypokalemia and hyperemia again remember
0:17this is a part for our clinical medicine
0:19section if you guys like these videos
0:21they help you they make sense please
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0:30these videos they are very very involved
0:32but if you guys want some great notes to
0:33follow up on some illustrations to kind
0:35of draw along with me or some questions
0:37to test your knowledge or even if you're
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0:49check all that out without further Ado
0:51though let's talk about potassium
0:52disorders so how do we Define
0:54hypokalemia when the potassium is too
0:56low right but we need kind of a number
0:58so like sodium it was like less than 13
1:005 for potassium the range is actually
1:02very quite narrow and so we say when
1:04it's less than 3.5 is hypokalemia and
1:07whenever it's greater than 5.5 we call
1:09that hyperkalemia so when you get a
1:12serum chemistry maybe it's a BMP it's a
1:14CMP it's a renal function panel and you
1:16see that the potassium is less than 3.5
1:19I then want you to start generating a
1:20framework in your head of how to assess
1:23the cause and so the first thing I want
1:25you to ask yourself is the potassium is
1:28it low because I'm shifting potassium
1:31into the cell all right so shifting of
1:34potassium that could be one reason and
1:36we'll talk about some causes of that the
1:38second one is am I having a lot of GI
1:42loss of potassium of some sort and the
1:45third one is are the kidneys in some way
1:48shape or form dumping pottassium into
1:51the urine those are the three Frameworks
1:53in your head to kind of just dig into it
1:56a little bit pathophysiologically what
1:58is this shifting of pottassium mean it's
2:01pretty straightforward often times
2:03potassium is the most abundant cation
2:05inside of the cell right 97% of
2:07potassium is usually in our cells if for
2:10whatever reason let's say the potassium
2:12that we have inside of our bloodstream
2:14more of it
2:16moves into the cell right so let's say
2:20here I have a lot of
2:21potassium that is going to be moving
2:24into the cell if lots of pottassium is
2:27moving into the cell from what we would
2:29say the extracellular fluid or
2:31extracellular space to the intracellular
2:34fluid or intracellular space What
2:35happens to the amount of pottassium
2:37inside of our bloodstream that when we
2:38stab and take some of that blood we see
2:40what the pottassium would be a lot of it
2:42shifted into the cell if that happens
2:44then the potassium inside of the
2:46bloodstream will start going down so we
2:49say What's called our
2:51serum pottassium the potassium inside of
2:53our bloodstream as a result of this
2:55shifting will start to come down it's
2:58pretty straightforward we'll talk about
2:59some of the reasons why the pottassium
3:00shifts into the
3:02cells second one what if I'm losing
3:05potassium from the git this one's
3:06actually very easy thank thankfully what
3:09if I am vomiting like an
3:12exorcist right vomiting is going to be
3:15one way in which I'll be losing
3:17potassium that I'm you know supposed to
3:19be you know usually when you eat
3:20something that potassium will move down
3:22the esophagus move down to the stomach
3:24and then from here it should move down
3:26into your duodenum and then here you
3:28should have some degree of absorption of
3:30potassium into the
3:32circulation but if I'm inhibiting this
3:34because less of this is actually moving
3:36down and being absorbed it's because I'm
3:38vomiting a lot of this out now when you
3:41vomit one of the big things to remember
3:43here is with vomiting yes you will get
3:46rid of potassium but what's another
3:48thing that you actually get rid of here
3:49and this is what I want you guys to
3:50remember I will start seeing that the
3:52potassium can go down but I'll also get
3:54rid of the protons because that's
3:56hydrochloric acid in your stomach right
3:58and so patients who vomit you want to
4:00think about this because if they have
4:01low pottassium and low protons in the
4:04actual bloodstream this will lead to
4:06what type of appearance when you have
4:07less protons it'll lead to an alkalosis
4:10so vomiting leads to hypokalemia and a
4:13metabolic alkalosis history would help
4:15you right away to think about that but
4:17if you got that ABG that may add to the
4:19story and the other scenario what if
4:21it's coming down the other end so in
4:24other words things are supposed to that
4:25you eat run down through the deinum the
4:27ilium all the way downwards and
4:30eventually you're supposed to have some
4:31absorption of that but what if the
4:34transit down through your git is way too
4:38fast that you're not having enough time
4:39to absorb those substances you'll lead
4:42to lots of potassium wasting so if you
4:45got a punami going on here so you're
4:48pooping like a goose and you got a lot
4:50of diarrhea what's going to happen I'm
4:53going to lose pottassium
4:54right but what else will I lose in the
4:57stool well not only will I dump my
5:00potassium but I'm also going to dump my
5:02bicarb because bicarb is supposed to be
5:04absorbed here in the actual the
5:06intestines and so you'll see that as the
5:08potassium goes down so does the bicarb
5:10what happens if you have less base you
5:12become acidotic this is one way that you
5:15can easily think about GI losses the
5:17differentiate between vomiting and
5:21diarrhea the next one and that actually
5:23kind of is easy now we don't really have
5:24to talk about GI losses any further and
5:26we'll really focus our attention when we
5:27get over here to the renal and the
5:29shifting potassium which is actually
5:30nice the renal losses is a little bit
5:33more complicated it's unfortunately a
5:35lot complicated but what I want you to
5:37think about is a couple different things
5:39here pottassium is supposed to be you
5:42know in some way shape or form
5:45reabsorbed in certain parts of the
5:47tubules in other words we should absorb
5:49it reabsorb it in like your proximal
5:51convoluted tubal and even you're
5:53supposed to reabsorb it in parts of your
5:55distal convoluted tubal so technically I
5:57should have some degree of potassium
5:59reabsorption that occurs but what if I
6:02don't reabsorb that potassium for some
6:03reason in the proximal convoluted tubal
6:05and the distal convoluted tubal then
6:07what happens I lose the potassium into
6:10the
6:11urine that's one mechanism that I want
6:13you to think about is
6:16decreased
6:18potassium
6:20reabsorption another mechanism is that
6:23potassium right whenever you're actually
6:25kind of moving down through the tubules
6:27what if and this is really interesting
6:29really really interesting you're
6:30supposed to reabsorb sodium here in the
6:33loop of Henley and you're also supposed
6:35to reabsorb sodium here it's actually do
6:37a blue arrow since we're consistent with
6:39that supposed to reabsorb sodium here in
6:41the ascending Limb and then reabsorb it
6:43here in the distal convoluted tubble but
6:46if you block this what happens is you
6:49end up with a lot of sodium that comes
6:50down here to the distal tubules and what
6:53happens is when you have lots of sodium
6:55that gets delivered down here to your
6:57distal tubul something really
6:58interesting happens so let's say I have
7:00a lot of sodium right
7:02here if I have a lot of
7:04sodium sodium actually tends to move
7:08into the cells and when it moves into
7:10the cells guess who comes out potassium
7:13and so your tubular cells will actually
7:14spit out potassium and dump a lot of
7:18that
7:19potassium into your urine and we call
7:21that increasing distal sodium delivery
7:24and we'll talk about some some drugs
7:26that actually increase distal sodium
7:28delivery so it's either decrease
7:30pottassium
7:31reabsorption or increase
7:35distal sodium
7:37delivery very
7:39interesting the next one is what if I
7:42have low magnesium so magnesium is
7:44actually a really weird one I'm not
7:46going to go too far into because we'll
7:47talk about it down there but whenever
7:49you have low magnesium that also really
7:51really Alters your potassium excretion
7:54so for right now I'm just going to have
7:55you guys be kind of trust me we'll go
7:58into it you just got to trust me will
8:00explain why magnesium when it's low can
8:02lead to a lot of potassium excretion so
8:04increase potassium
8:06excretion the last
8:08one is high
8:10aldosterone so this one's really
8:12interesting when you have super high
8:14aldosterone so hyper
8:16aldosteronism one thing is very
8:18interesting in the sense that when you
8:21have lots of aldosterone you reabsorb
8:23lots of sodium right across your distal
8:26convoluted tubal but what do you excrete
8:30pottassium
8:31so you'll reabsorb a lot of sodium but
8:34you excrete a lot of potassium in the
8:38distal tual so these are the concepts
8:40that I want you guys to understand for
8:42the renal losses of pottassium so in
8:44other words you get a serum chemistry
8:46comes back the potassium is low less
8:48than 3.5 is it shifting a potassium
8:50pottassium is going into the cells we'll
8:52talk about causes or am I losing
8:54potassium from my G am I vomiting it
8:57look for history of vomiting look for
8:58low potassium look for an alkalosis I'm
9:01having diarrhea look for the history
9:03look for low potassium look for an
9:05acidosis renal you have to then form a
9:08framework in your head is it because I'm
9:11not reabsorbing potassium is it because
9:13I'm giving a lot of distal sodium
9:15delivery is it because my magnesium is
9:17low or is it because my aldosterone is
9:20too high and we'll talk about that here
9:23now potassium's low I ask myself the
9:25question do they have vomiting diarrhea
9:28look at the history look at the ABG but
9:30if there's no vomiting no diarrhea then
9:32you can start thinking okay is it renal
9:33losses from the renal losses again what
9:35are the four Frameworks that I want you
9:37to think about the first one was is
9:39there decreased pottassium reabsorption
9:42so that's the first thing I want you to
9:43think about am I not reabsorbing
9:45potassium so decreased potassium
9:49reabsorption now the causes for this is
9:52there is two types
9:54RTA and I know this sounds weird but I'm
9:57going to do it in order of where they
9:58affect the tubal RTA
10:012 and RTA 1 what does the RTA stand for
10:06renal tubular acidosis type one and type
10:09two type two and type one now in renot
10:13tubular acidosis they don't allow for
10:16good potassium
10:17reabsorption now why we'll talk about in
10:21the actual acidosis video but for RTA 2
10:26this one primarily affects and this is
10:28what I want you to remember it causes
10:30proximal convoluted
10:32tubular dysfunction there is many causes
10:36I will not go into that now we'll talk
10:37about that in that video on
10:39acidosis but what happens here is that
10:42you're supposed to reabsorb pottassium
10:44in the proximal convolutive tubal and
10:47guess what else you're supposed to
10:47reabsorb which really really helps in
10:49this scenario
10:51bicarb if you can't reabsorb potassium
10:54and you can't reabsorb bicarbon it's
10:56because this transporter in some way
10:58shape or form is
11:00dysfunctional and again it could be due
11:02to fanone syndrome Carbonic any hydr
11:04Inhibitors like acetazolamide to Pyramid
11:06there's a lot of different things but
11:07the concept here is that you're going to
11:09lose potassium and you're going to lose
11:11bicarbon to the urine if you lose
11:13bicarbon to the urine what happens to
11:15the bicarb in your bloodstream it starts
11:17to go down what happens to your pH it
11:20starts to go down this is interesting
11:24there's not many disorders that where
11:26you have a
11:27hypokalemia and a metabolic acidosis
11:30rtas are one of them so here's what I
11:33want you to remember the proximal conv
11:35tubal yes they'll have low
11:38potassium and they'll have low
11:42bicarb all right that's one really big
11:44thing here you're going to have both of
11:46those Concepts here's where it helps and
11:48will help us to differentiate between
11:50RTA 1 and RTA type 2 in
11:52rta2 you have to remember the proximal
11:54convoluted tubule is damage but the
11:58distal convoluted tu Tu is intact the
12:01distal convoluted tubal guess what it's
12:02supposed to do it's supposed to secrete
12:05protons if the distal tubal is intact
12:07can you secrete protons yes so they have
12:11the capability of secreting protons so
12:14there is a intact we're going to use a
12:16plus sign here an
12:19intact distal convoluted tubal meaning
12:23they can secrete protons meaning they
12:26can
12:27secrete prot protons if I can secrete
12:31protons what happens to the protons in
12:32my urine they go up what happens to my
12:35pH it goes down for these patients one
12:38of the big things to remember is because
12:41they can do this their urine pH can be
12:45low less than
12:465.5 that's really important to remember
12:49so rta2 proximal convolu Tu is damaged
12:52can't reabsorb potassium can't reabsorb
12:54bicarb you lose it in the urine their
12:56distal tubules intact they can secrete
12:58proton so they can acidify their urine
13:01why am I mentioning this so let's bring
13:03rta1 up here so we have some room in
13:08rta1 the area that is injured so we can
13:11actually kind of say it like this like
13:12this one is affecting this one here rta1
13:15is affecting this one here so now we can
13:18kind of add to this in the sense that
13:19this affects the distal convoluted tual
13:23so the distal convoluted tual is
13:26dysfunctional a shoot
13:29why is it dysfunctional it's supposed to
13:31do something very interesting it's
13:33supposed to secrete
13:36protons into the urine and at the same
13:39time it's supposed to bring
13:42potassium into the cell to reabsorb it
13:46but you don't do this because there's
13:47some type of dysfunction there this
13:49could be due to autoimmune diseases
13:51right shogran syndrome rheumatoid
13:54arthritis SLE a lot of those different
13:56types of Concepts but we don't allow for
13:58that to process to
13:59occur if that's the
14:02case what happens is is you lead to less
14:06protons in the bloodstream because
14:08you're going to dump them into the
14:10urine and you're going to have less I'm
14:12sorry less potassium ons in the actual
14:14bloodstream because you're going to dump
14:15it into the urine and you're going to
14:16have less
14:18protons in the bloodstream I'm sorry
14:21you're going to have more protons in the
14:22bloodstream
14:24why because you're not secreting the
14:26protons it's going to retain inside of
14:27the bloodstream so again you're not
14:30going to reabsorb potassium so you dump
14:31that into the urine potassium in the
14:33blood goes down you're not going to
14:35secrete protons so there's less protons
14:37into to the urine the protons in the
14:40bloodstream go up now let's add to the
14:43next component here you'll have an
14:46acidosis acidosis hypokalemia
14:49hypokalemia different areas of the
14:51tubules that are dysfunction different
14:52causes how do we differentiate them the
14:55distal convol tubal is it intact no so
14:59you have a de uh not intact so you do
15:03not have an
15:05intact distal convol
15:08tubal therefore can they secrete
15:12protons can't secrete protons we see it
15:15right there so they can't secrete
15:17protons therefore can they
15:20acidify their
15:22urine no so the urine pH be able to be
15:25acidic no so in this particular scenario
15:28and we'll bring it down here so we have
15:29room the UR
15:31pH will
15:33be greater than
15:355.5 so that's kind of the ways that we
15:38can differentiate these two rta2
15:40proximal convol tual rta1 distal
15:43convoluted tual both of them lose
15:45potassium into the urine because they're
15:47not reabsorbing it this one loses
15:49bicarbon to the urine if you lose
15:51bicarbon to the urine you have less
15:52bicarbon the blood the acid starts
15:55accumulating and you become acidotic in
15:57rta1 You Don't See protons so the
16:00protons in the bloodstream build up you
16:01become acidotic both of them have an
16:03acidosis both have
16:05hypokalemia this one the proximal convol
16:07tubal is damaged distal is intact they
16:10can secrete protons they can acidify
16:11their urine the urine pH will be acidic
16:14this one the distal tuil is not intact
16:16so therefore it's not able to secrete
16:17protons it cannot acidify the urine the
16:20other thing that you can add on to it
16:21rta1 will cause more acidosis as
16:24compared to rta2 that's it this is the
16:27big thing that I want you guys to
16:28remember for this one and again these
16:30are the Rarities where you'll have a
16:32hypokalemia and an acidosis all right
16:36let's talk about the next one so we said
16:37decrease pottassium reabsorption what
16:38was the other
16:40cause increase distal sodium delivery so
16:43increase
16:45distal sodium delivery could cause this
16:49all right
16:50cool what are things that increase
16:52distal sodium delivery I already kind of
16:53introduced you to it that you're
16:55supposed to reabsorb sodium in the
16:57ascending limb
16:59and you're supposed to reabsorb sodium
17:01in the early distal convoluted tubal
17:04right and if I do not do that thing then
17:10what happens to the amount of sodium
17:11that's remaining with inside of the
17:13Lumen it goes up and so theoretically
17:17what will happen here is that I will
17:19have a higher amount of sodium being
17:21delivered to the distal
17:23tubules if I have a lot of sodium and
17:26this kind of goes off that diagram just
17:27adds a little bit more to it
17:29when there's lots of sodium more than
17:30usual getting delivered to the distal
17:32tubal your distal tubal says hey I got
17:34to take up some of that sodium but when
17:37it takes up a positive ion it has to get
17:40rid of a positive ion and the ones that
17:43it often gets rid of is either potassium
17:47or
17:48protons and so what happens is is you
17:52increase the amount of potassium and the
17:54amount of protons being lost into the
17:55urine so that leads to the question what
17:57the heck is blocking sodium reabsorption
18:00in here and sodium reabsorption here for
18:03this one it would be Loop dicts so what
18:06will we have your Loop diic would block
18:10the ascending limb of the loop of Henley
18:13and what would block the early distal
18:15conval thide diuretics and then you have
18:18your
18:19thide
18:21dtic both of these would block sodium
18:25reabsorption increase disl sodium
18:26delivery they just affect different are
18:29of the loop of Henley or I'm sorry the
18:31nefron and in this particular situation
18:33what's some common features well they
18:36end up doing what secreting protons so
18:40I'd have low protons inside of the I
18:43mean low potassium ions inside of the
18:44bloodstream because I'm secreting them
18:46I'm also going to get rid of protons
18:49into the Ur So what happens to the
18:50protons inside of the bloodstream it
18:52goes down and so I'll have less protons
18:55and less pottassium ions in the
18:57bloodstream what happen if you have less
18:59protons in the bloodstream you become
19:02alkalotic there's going to be more
19:05Alkali so Lop diuretics thid diuretics
19:08cause hypokalemia metabolic alkalosis
19:10RTA is hypokalemia metabolic
19:13acidosis another thing here is that
19:15these are going to be causing you know
19:18what another thing with sodium is is if
19:19I cause if I block sodium reabsorption
19:21guess what Falls sodium water and so
19:24this causes a lot of diuresis so they
19:27get increased diuresis what does that
19:30mean means I pee a lot of stuff out
19:33right which can lead to a
19:35decrease in the blood
19:37volume so I can decrease the
19:40volume of Blood by this diuresis which
19:43can sometimes make patients look a
19:45little hypmic hypotensive Etc so that's
19:48a very very important thing to remember
19:50here there's also Le electrolyte
19:53disturbances to consider but again I
19:54think the big thing here for these
19:55patients is look for Loop Diuretics look
19:58for low potassium metabolic alkalosis
20:01and potentially a hypmic state all right
20:03that's the big things that I want you to
20:05remember for these guys all
20:07right what's another component here okay
20:10so we said we either not reabsorbing it
20:12we're giving a lot of sodium that's
20:13being delivered to the distal tual or
20:16what was the other thing Zach said
20:17hypomagnesemia that I just got to trust
20:18him he's talking about this all right so
20:21in hypo
20:24magnesia this one is really really cool
20:27I see this lot in the ICU and other
20:29patients who have other underline
20:31comorbidities but what's really
20:34important about hypomagnesemia is it has
20:36a couple different things we have a pump
20:39here in the proximal convoluted tubule
20:42and we have this special one here in the
20:44in the distal convoluted tubal this one
20:47here is called a sodium
20:51potassium ATP a right this guy right
20:55here now whenever there is low magnesium
21:00what happens is that low magnesium tends
21:03to stimulate the activity of the sodium
21:07potassium
21:08ATP what do the sodium potassium atpases
21:11do you say they pump potassium into the
21:13cell and pump sodium out of the cell so
21:16three sodium will come out two potassium
21:18will go in so I'm going to pump some
21:21potassium into the cell when I pump the
21:25potassium into the cell and the sodium
21:27out of the cell the potassium will build
21:29up inside of the cell and there's these
21:31little channels that allow for potassium
21:33to do what easily leak out and then I'm
21:38going to dump potassium right into the
21:40tubular system who will then get peed
21:43out so that's one way is I increase the
21:45activity of my sodium potassium pumps in
21:47the proximal tubal what about over here
21:51here's another channel here this pink
21:52one it's called a ROM c
21:56channel and it's supposed to regulate
22:00the outward movement regulate the
22:01outward movement of
22:03potassium now normally when magnesium
22:06levels are normal this ROM K channel is
22:10closed and usually potassium shouldn't
22:12be kind of leaving magnesium is normal
22:16but if magnesium is
22:18low what happen what happens is is you
22:21lose that
22:24regulation and now what happens is the
22:26low magnesium ends up actually keeping
22:29the the actual uh regulator outward
22:31movement of the potassium channels it
22:33keeps it open and now this thing is
22:37open when this puppy is
22:40open now guess what guess what happens
22:43here the potassium can just go ahead and
22:47easily leave the
22:48cell and if it easily leaves this cell
22:52I'm going to dump potassium into the
22:54urine all right so I don't want you to
22:55guys to get too frustrated and focus on
22:57these channels I want you to kind of
22:59think about this clinically in a patient
23:01so when a patient has hypomagnesemia yes
23:04do try your best to remember the
23:06mechanisms by which it causes this but
23:09the patient that you have to think about
23:11this in is a patient who has some type
23:14of chronic alcohol use right they're not
23:17getting enough nutrients within their
23:18diet so they're probably not getting uh
23:20a good amount of
23:22magnesium another one is diuretics
23:24diuretics especially Loop Diuretics and
23:26and th diuretics these can also cause a
23:28lot of magnesium to be lost into the
23:30urine another one would be if you have
23:32some type of bowel disease where you're
23:34not absorbing magnesium so think about a
23:37couple different types of like small
23:39bowel
23:41diseases I think the best ones to
23:44remember here would be things like
23:46Crohn's disease uh maybe some type of
23:48gastric bypass surgery if you had a
23:51reection for some reason these are
23:53altering the activity of where the
23:55Magnesium can be absorbed and there's a
23:57bunch of different drugs that can also
23:58do this as well ppis are a common one
24:00you may see in the vignette either way
24:03look for this history but here's the key
24:06feature here that they'll come up on the
24:08exam is a patient who has
24:11refractory so refractory hypo
24:15calmia what the heck does that mean that
24:19means that you have a patient who has a
24:20low potassium you keep giving them
24:23potassium keep giving them potassium and
24:25their potassium never budges this is the
24:28that you have to think about what do you
24:31do check a magnesium level and see if
24:33it's low so if I have a refractory
24:35hypokalemia that's when you want to
24:37check the magnesium level so then when I
24:39see this a patient who's getting
24:41potassium supplementation constantly and
24:43never budging check of magnesium that
24:45could be the cause all right the last
24:48one that we'll talk about here in a
24:49second again think about this is have we
24:51not reabsorbed it have we delivered too
24:54much sodium to the distal tubal do we
24:56have low magnesium what's the last one
24:58is the aldosterone level high so the
25:00next one we already said is usually due
25:02to a
25:04high
25:06aldosterone state right or hyper
25:09aldosteronism we kind of talked about
25:11how that works in the sense that
25:13aldosterone works the distal convoluted
25:15tubal by helping to reabsorb sodium
25:18excrete potassium and it also helps to
25:19excrete
25:20protons so real quick I want you guys to
25:25think about why aldosterone would be
25:27high right so one concept here is we
25:30could have a primary type of hyper
25:34odinism
25:36meaning the problem exists here at the
25:38kidney you know the kidney they have
25:41this called the JG cells and the JG
25:43cells are supposed to make a molecule
25:45called renin but what if for some reason
25:49that renin production is at a higher
25:52level than
25:53normal there's our problem CU why renin
25:57leads to the formation of what
25:59eventually Angiotensin 2 and then what
26:00does Angiotensin 2 do Angiotensin
26:052 eventually Works
26:08to stimulate our adrenal cortex and our
26:11adrenal cortex will then say okay what
26:15do I make
26:17aldosterone and you'll make lots of
26:23aldosterone so if there's lots of
26:26alstrum production not only could it
26:28come from a prime I mean sorry U not
26:31only could it come because of my kidneys
26:33but it also could come from having too
26:35much production of adone at the what at
26:38the adrenal gland so we call this one I
26:40apologize this one is your primary
26:43hyperaldosteronism so primary hyper
26:45odinism if it's coming from the kidney
26:48where renin production is occurring this
26:50is secondary hyper
26:53odinism we'll talk about some of the
26:55causes of those in a second but I want
26:56you to think about that now if aldoshin
26:59production is high what is it going to
27:01go and do we kind of already introduced
27:03it what it has the capability of doing
27:06is it goes here and it has kind of two
27:09functions if you will one is it'll help
27:12to stimulate the expression of
27:13epithelial sodium channels so that we
27:16can bring sodium into the cell and then
27:19eventually into the bloodstream and it
27:21increases the expression of the
27:23potassium channels and the sodium
27:25potassium or sodium proton pumps on the
27:29uh apical membrane here and so it'll
27:32help to excrete potassium and excrete
27:35protons and so what will I be doing I'll
27:38be bringing in lots of sodium into the
27:41bloodstream and secreting out lots of
27:44pottassium ions and lots of proton ions
27:49now with that concept being said how we
27:53have aldosterone really kind of amping
27:55these processes up what would really be
27:58kind of a highlight of hyper
28:00aldosteronism well hyper aldosterone
28:03patient so if I have high aldosterone
28:06levels let's say what would make me
28:09think that this is the cause in a pot
28:11patient who has low potassium okay first
28:14thing is if you have high sodium that
28:17might be a potential
28:19trigger the other thing is what does
28:21sodium do if I reabsorb sodium
28:23theoretically what may follow water and
28:27what will happen is if you have more
28:28sodium and water inside of the
28:29bloodstream what can happen to your
28:30blood pressure it can go up and so the
28:33other thing I want to know is does the
28:35patient have very very high blood
28:37pressure that's difficult to control in
28:40other words they're on three or maybe
28:42even more anti-hypertensives all right
28:45so high sodium refractory hypertension
28:48and then on top of that yes they
28:51have a low potassium and they're dumping
28:55protons so they're going to have less
28:57protons into the bloodstream so they're
29:00going to have less potassium and less
29:03protons they'll have hypokalemia and
29:06less protons inside of the bloodstream
29:07means metabolic
29:09alkalosis so metabolic alkalosis
29:12hypokalemia hypernia and high blood
29:15pressure that should be making you think
29:17about a hyperaldosterone
29:19patient now coming back here if a
29:22patient has high aldosterone we have to
29:24ask ourselves the question is it primary
29:27or is it secondary
29:28so in a primary patient we know that the
29:32problem is with the adrenal cortex right
29:35and if it's a secondary patient it's a
29:37problem with their what with their
29:39kidneys so in secondary there's a couple
29:42common causes in secondary you want to
29:44think about renal artery stenosis and
29:46like CHF so think about something like
29:49renal artery stenosis maybe a CHF
29:52patient potentially another one to even
29:54think about is your stics so osis and
29:59we'll talk about this more in the Endo
30:01section the primary one is you're
30:04talking about a you know
30:07adrenal kind of like tumor of some sort
30:11right and in this particular scenario I
30:13would be thinking about the disease
30:15called like con syndrome right
30:28there is one
30:29more it's rare but it is something to
30:32think about we have a disease that's
30:34called a parent mineral corticoid excess
30:36it means it kind of is a disease it
30:37looks like you're having lots of aldrum
30:39but you're not really having lots of
30:41alrum this is usually in patients who
30:43have like Cushing syndrome and they have
30:45cortisol in high amounts and the
30:46cortisol can have a little bit of
30:47mineral corticoid activity you think
30:49about that in a Cushing syndrome patient
30:51another one that they like to ask on the
30:53boards and just think about it is what's
30:55called licorice ingestion licorice which
30:58is really weird black licorice if you
31:00ingest enough of it it contains a really
31:01weird like acid molecule that helps to
31:04it basically what it does inhibits one
31:06of these enzymes that is supposed to
31:08help cortisol be broken down into its
31:10metabolite and if you can't break the
31:12cortisol down cortisol builds up like a
31:14Cushing syndrome patient and has that
31:15Minal cord cord activity so if you get
31:18this Ren ostrin level and they're normal
31:22or if even like worst case scenario they
31:24are high levels of renin
31:26Ostrum um it in these patients what you
31:28would want to uh do is you'd actually
31:30want to say like okay if I have normal
31:31renin normal osone it's not really kind
31:33of consistent with the primary secondary
31:36think about the apparent Minal corticoid
31:37exess that's when you start working them
31:39up for Cushing syndrome working them up
31:41for licorice ingestion all right because
31:43those are drugs are going to act like
31:45aldosterone somewhat so they will
31:47suppress renin and they will suppress
31:49aldosterone so you can think about that
31:50in low renin low aldosterone or normal
31:53renin normal aldosterone States think
31:55about the apparent Minal corticoid
31:56excess all right
31:58at this point we've now talked about the
32:00renal causes that can lead to
32:02hypokalemia either you're not
32:03reabsorbing it rta1 rta2 you're
32:06delivering too much sodium to the distal
32:07tubal Loop Diuretics thid diuretics your
32:09magnesium is low or your lostone is too
32:11high in the scenario of primary
32:13secondary or apparent mineral corticoid
32:16excess the one I talked about was
32:18shifting of potassium too much potassium
32:20is getting shifted into the cell all
32:24right let's talk about this there's a
32:26pump here this pump pump is called the
32:29sodium pottassium
32:32ATP a pump right and what it's supposed
32:35to be doing is doing what it's supposed
32:37to move potassium into the cell and move
32:42sodium out of the cell technically three
32:45sodium right if we really want to be
32:46particular here supposed to move three
32:48sodium out and then two potassium in all
32:52right
32:53cool if I'm stimulating this pump right
32:56if I'm really really stimulating this
32:58pump then I'm going to pump a lot of
33:00potassium into the cell right and I'm
33:03going to pump a lot of sodium out of the
33:04cell so the end game here is that what
33:07will happen is is I'm going to have
33:09increased
33:13potassium
33:15move
33:17into the cell and that's the cause of
33:19the hypokalemia that's how we explained
33:21that over there my question is is what
33:24in the heck is increasing the sodium
33:27potassium ATP activity that would lead
33:30to this type of effect that's a great
33:32question that you guys asked there one
33:35is because the patient has too much
33:39insulin running through their
33:41bloodstream now if there's lots of
33:43insulin insulin acts on its insulin
33:45receptors and helps to
33:48activate these
33:50pumps all right helps to activate these
33:53pumps and you stimulate the sodium atp's
33:56activity what are some St
33:58in which you would have lots of insulin
34:00it's when you're giving a patient
34:01insulin so usually we see this and this
34:04is why it's a perfect scenario let's say
34:06a patient has diabetes like dka HHS and
34:09they're getting treated for their dka or
34:11HHS and we're giving them insulin if you
34:13give them high amounts of insulin it's
34:15high amounts of insulin in the
34:16bloodstream it's going to shift the
34:18potassium into the cells it's often
34:20times used in the treatment of dka or
34:22HHS or it's using the treatment of
34:25hyperkalemia and so we can see whenever
34:27we're we're giving insulin in the
34:28treatment of hyperemia or the treatment
34:30of dka and HHS we can see hypokalemia
34:33start to arise so think about that all
34:36right High insulin another
34:40one is it could be due to increased
34:44beta beta 2 Agonist activity so beta
34:492 Agonist you're like what the what the
34:53heck is a beta 2
34:55Agonist these will stimulate the beta 2
34:57receptors and the beta 2 receptors have
34:59the capability of stimulating this pump
35:03this sodium potassium pump this would be
35:06things like albuterol right albuterol
35:08guess what we use that for asthma guess
35:10what else we use it for the treatment of
35:12hyperkalemia so sometimes when you're
35:14treating a patient who has hyperemia
35:15high potassium they can end up with low
35:18potassium because you give them a little
35:20bit too much alol so look at this for an
35:22asthma patient look at this for a
35:23patient who's getting treated for
35:24hyperemia another one is any kind of
35:28like drug that has a sympathic function
35:30epinephrine norepinephrine it can have
35:33that type of activity all right
35:35cool so this is the scenario here so
35:38again High insulin think about the
35:39patient being treated for dka HHS or
35:42getting treated for hyperemia albuterol
35:44think about a patient who has asthma or
35:46COPD and getting albuterol or think
35:49about those patients who are get treat
35:51for hyperemia and they just
35:53overshot another reason you shift
35:55potassium is acidbase disorders you have
35:58a pump here and this pump is called the
36:01pottassium
36:03proton pump and what it's supposed to do
36:06is it's supposed to allow for potassium
36:10to move out of the cell and protons to
36:12move into the cell so let's say here I
36:15have some
36:16protons and I want to move the protons
36:18into the cell and I have potassium ions
36:21here and I want to move them out of the
36:23cell in situations where a patient has
36:26guess what they have a we're going to
36:28write it here a alkalosis if they have a
36:32alkalosis what does that mean their pH
36:34is too high when you have that what this
36:37does is this actually
36:41inhibits this potassium proton pump if
36:45this potassium proton pump is inhibited
36:47are you going to be able to pump the
36:50protons into the cell and pump the
36:52potassium ions out of the cell no and so
36:56what happens is Pro less uh protons come
37:00in and less potassium ions go out so
37:05that's the concept is that there's less
37:08potassium
37:09moving less
37:12potassium moves out and then over here
37:17again
37:20less
37:22protons are moving in I won't write that
37:24down but I think that's you know
37:26acceptable in the concept again again
37:27you're having an alkalosis inhibiting
37:29this pump less protons are coming into
37:31the cell less potassium ions are leaving
37:34the cell so that means that less
37:35potassiums are coming out here into the
37:38bloodstream what's happening to the
37:39potassium in the blood it's decreasing
37:42what kind of conditions would cause
37:43alkalosis metabolic alkalosis of any
37:46sort of cause as well as what
37:48else respiratory alkalosis so think
37:51about any kind of alkalic state now
37:53that's interesting because we know that
37:55patients who have hypokalemia can also
37:57have metabolic alkalosis but that also
38:00means that alkalosis can cause
38:01hypokalemia and that's a really really
38:03important thing is that they have a nice
38:05reversible relationship okay shifting
38:08potassium insulin's too high increased
38:10beta 2 activity like albuterol or
38:13alkalic state these are the causes of
38:17hypokalemia what about hyperkalemia all
38:19right so now we move into the next part
38:21when the potassium is just too high
38:23right potassium is high how high again
38:26we say it's usually when it's greater
38:27than 5.5 mil equivalents
38:30now when a potassium is high again you
38:33get a serum chemistry all right BMP CMP
38:36renal function panel of any sort and you
38:38see that and it comes back with the
38:39potassium is greater than 5.5 build a
38:41framework same thing for hypocam you
38:43said okay I'm sh shifting pottassium
38:44into the
38:45cell or I'm losing potassium from the
38:48kidneys or I'm losing potassium from the
38:50git in this one it's just only two seps
38:54am I shifting potassium out of the cell
38:57right
38:58or am I retaining potassium via the
39:01kidneys so those are the two concepts to
39:03think about am I shifting potassium and
39:06in this case am I shifting
39:09it out of the cell and the second one is
39:14are the kidneys retaining potassium so
39:17is there a renal
39:21retention of potassium and that's the
39:24concepts now when you retain
39:27pottassium via the kidneys there's two
39:30mechanisms one is we have our Glarus is
39:34supposed to filter certain things across
39:37this into the uh Bowman's capsule and
39:39then down into the proximal convoluted
39:41tubule where it's supposed to be
39:42reabsorbed at different
39:44points now if my filtration is reduced
39:49right so I have something like I have
39:51what's called a
39:52low
39:54GFR then if I have a low GFR I'm not
39:57going to filter off as much potassium
39:59across the Glarus and into the Bowman's
40:01capsule and so that potassium will stay
40:03within the bloodstream that's one
40:06potential mechanism so one mechanism
40:08could be low GFR and thankfully there's
40:12only one other
40:13scenario
40:15one is it could also be due to a low
40:19aldosterone state so in a patient has
40:22either a low GFR
40:28or a low aldosterone State these are the
40:32things to think about the reason why is
40:33when you have less aldosterone guess
40:34what you're not doing you're not
40:37allowing for the proper movement of
40:40sodium across to be reabsorbed so you're
40:43not going to be able to reabsorb the
40:45sodium and on top of that you're not
40:47secreting pottassium and you're not
40:49secreting protons so this
40:53process is not occurring this is being
40:56inhibited
40:57and therefore you're retaining
40:59pottassium retaining protons and losing
41:01sodium into the
41:03urine this is the concept is either that
41:06my GFR is way too low or my aldosterone
41:09is too low and therefore I'm not
41:11secreting potassium or filtering
41:13potassium and therefore my kidneys are
41:15retaining on them and that's going to
41:17build up in the
41:19bloodstream same thing for this scenario
41:21here potassium 97% of the pottassium
41:23stays inside of the cells now what if
41:26for some reason pottassium was being
41:30shifted so there's an increased movement
41:33let's say so increased
41:37potassium
41:40moves out of the cell and so now the
41:44potassium is going to move out of the
41:45cell into the bloodstream that means
41:49that you're going to have increased
41:50potassium increase serum potassium so
41:54more potassium that builds up
41:58inside of the bloodstream because again
42:00what happens is the potassium is moving
42:02from the intracellular fluid or space
42:04into the extracellular fluid or space
42:07and so we just have to figure out why is
42:09potassium moving out of the cells
42:11excessively and then why is the GFR low
42:14why is the aldosterone low that's the
42:17question let's move in now to talking
42:19about the renal retention aspect now
42:21you're probably like okay wait what
42:22about the GI thing is there any GI
42:24problem no thankfully there's no GI
42:25problem here that we have to talk about
42:27the ability to increase the absorption
42:29of potassium is like somewhat relatively
42:31impossible unless you have some
42:32underlying renal disease but generally
42:34the most common cause of hyperkalemia is
42:37going to be a renal retention problem so
42:39let's talk about that all right so let's
42:40talk about the causes of renal retention
42:42of potassium so we already kind of
42:43introduced the pathophysiological
42:45concept potassium's high is it because
42:47the kidneys are retaining or are we
42:48shifting it out of the cell if the
42:50kidneys are retaining it's actually not
42:52that bad in the sense that if a patient
42:55has a really high potassium you really
42:56want look at the renal uh function and
42:59so we said one is that the GFR is
43:02ridiculously low and when I say like
43:04ridiculously low I am talking about like
43:06you have a patient who their GFR is like
43:09near the point of classifying them as a
43:11severe acute kidney injury where they're
43:13not really making much urine um or like
43:17a CKD patient who's at least like stage
43:19four or greater at that point their GFR
43:22is like almost like less than 20 and
43:24they're just not generating enough
43:25filtration across the GL Ulus now the
43:28concept behind this is that if your GFR
43:30is ridiculously low you're not filtering
43:32potassium so potassium is going to be
43:34running through the aeren arterial not
43:37being filtered across the Glarus and
43:39you're leaving the aeren arterial I me
43:41eerin arterial with a high potassium
43:44because the concept is that you're just
43:45not going to be filtering the potassium
43:48across the glara so the potassium is
43:49supposed to be coming here that process
43:52is just not occurring because the GFR is
43:54so dang low now
43:57if the GFR is low what are some causes
44:01of a really really reduced
44:03GFR now one is it could be an acute
44:07onset so let's say that a patient has a
44:10normal renal function all of a sudden
44:13they injure their kidneys for whatever
44:15reason and their creatinine starts to
44:17rise their bu starts to rise and their
44:20GFR starts to tank that's an Aki so one
44:23of these is it could be due to an acute
44:25kidney injury
44:27or it could be due to a patient who we
44:30would kind of classify as like an
44:31endstage renal disease so there's ckd4
44:34or there ckd5 and they're almost at the
44:36point where they need dialysis and these
44:38patients that's the likely
44:41cause the other thing is to really think
44:43about this patient not only will they
44:45have a low GFR but look at the other
44:47parameters will they have an elevated bu
44:50so they're having some evidence of
44:52potentially ureia will they have an
44:54elevation as well not just in their bu
44:58but in their creatinine so their C CR
45:01which is we're going to abbreviate for
45:02creatinine is that elevated are they
45:05making very little urine which can also
45:07tell me that they're having poor
45:09filtration across the actual G uh the
45:11Glarus so is there a decrease in the
45:14urine output what do we call that
45:17oliguria or are they making no urine
45:20anuria and these patients they'll have a
45:23very severe high potassium level so
45:27that's one thing to think about is the
45:28GFR really really low at least getting
45:30to the point where they're like less
45:31than 20 within their GFR that's the
45:34likely cause of their acute their their
45:37hyperemia the other scenario is let's
45:39say that the GFR isn't like low this may
45:42be normal or just mildly low that's when
45:45you think about the low aldosterone
45:46States so in patients who have like a
45:49really really
45:50low aldosterone State um this is where I
45:54really want to be thinking okay do they
45:56have like a normal GFR their GFR is
45:58mildly reduced how in the heck would
46:01this cause this all right again we
46:05already kind of introduced this a little
46:06bit but we said that whenever you have
46:07low aldosterone what happens here is
46:10it's not going to allow for a good
46:11function to bring
46:13sodium across the enac channels and
46:17you're not going to be able to secrete
46:19pottassium
46:20and you're not going to be able to
46:22secrete
46:25protons into the Y
46:27so you'll have
46:28decreased
46:30sodium that's being reabsorbed and
46:33decreased potassium and protons that are
46:35being excreted
46:37now the concept behind this is actually
46:40quite interesting because you have to
46:41then ask yourself why in the heck is
46:43aldosterone low so it kind of comes back
46:45to the diagram we talked about with
46:47hyber aldosteronism we know that the JG
46:50cells are responsible for making a
46:53molecule called renin and then what we
46:56know is
46:57is that renin eventually leads to the
46:59formation of angiotensin
47:02to now whenever renin levels are reduced
47:06you'll have less Angiotensin 2 now less
47:09Angiotensin 2 means that you may not be
47:11able to stimulate the Angiotensin 2
47:13receptors on the adrenal
47:15cortex and that means that the adrenal
47:18cortex may not be pushing out a very
47:21particular hormone called aldosterone so
47:25here's the way I want you guys to think
47:26about about this in a particular path
47:29all right let's say that I have diseases
47:33that can actually reduce renin so let's
47:35say that their cause is a low renin
47:38production so we say that it's low renin
47:43production if we have low renin right
47:47what will happen less Angiotensin too
47:50less stimulation of the adrenal cortex
47:52making less aldosterone less aldosterone
47:54means that you're going to have less of
47:56this guy coming coming over here and
47:58acting on the kidney
48:00tubule to help to reabsorb sodium
48:04secrete potassium and protons and so if
48:06you don't have that you'll end up with
48:07this complication that we see
48:09here what are some diseases that can
48:11actually work to
48:14inhibit Rand of production well one is
48:19it could be due to diabetes and another
48:22one is ineds so diabetes militis and
48:25ineds are very common offenders here all
48:28right that's one thing all right that's
48:29not too bad so think about that do they
48:31have diabetes really bad diabetes or are
48:33they taking
48:34inets what if I have something that
48:38decreases aldrum production so that's
48:41the next thing so the next one is what
48:43if I decrease so it's now here
48:47decrease so I'll kind of do it like this
48:49I'll inhibit aldosterone production so
48:53what if I have a problem where I'm
48:55decreasing
48:57testosterone
49:00production I want you to think of three
49:03causes
49:04one is the adrenal gland failing two are
49:08they taking something that is blocking
49:10Angiotensin 2 or blocking the renin
49:13Angiotensin aldosterone system and so
49:15here's the way I want you to think about
49:16it is it a decreased production from the
49:18adrenal gland or something blocking the
49:20renin Angiotensin aldosterone system if
49:22it's blocking the Ren and Angiotensin
49:24aldosterone system there's a couple
49:26drugs
49:27one is your ACE inhibitors another one
49:30could be your arbs and another one
49:32that's kind of derivative is the A and I
49:36which we use in heart failure these are
49:37very common offenders of blocking the
49:40Ren otens and ostrin system so they'll
49:41lead to decreased Angiotensin 2 and
49:43decrease ostrin production the last one
49:46is adrenal failure so Addison's
49:50disease or any kind of adrenal failure
49:52itself could lead to
49:55this now that's going to lead to a
49:58decreased adrone right and then your Ren
50:02in production actually will increase as
50:03a response to
50:05this the last one is what if I have
50:08something that blocks aldosterone here
50:10so pretend this black dot here is
50:13aldosterone aldosterone is supposed to
50:16go and bind onto these intracellular
50:18receptors but what if I have something
50:20that blocks the interaction of alstone
50:23on the distal convoluted tubal so in
50:26other words I decrease the aldosterone
50:29effect or
50:30response all right if that's the case
50:33what are some potential causes there
50:36that would mean I have to have a drug
50:37that's blocking the aldosterone receptor
50:40site there's two potential offenders
50:42here
50:43one is the potassium
50:46sparing
50:48diuretics this is your
50:50spirolactone the Epler known very common
50:53offenders here and the last one is a
50:55drug that's utilized for infections this
50:58is often times Baum or trimethoprim suam
51:01methoxy use for UTI we use it a lot in U
51:05um it can be used in a lot of other
51:06scenarios as well maybe soft tissue
51:08infections like
51:09cellulitis if I have these particular
51:12scenarios you have to then ask yourself
51:14the question okay what could be the
51:15potential cause if a patient has a
51:17normal or just a mildly low GFR are they
51:20taking inets do they have diabetes are
51:22they taking an a inhibitor are is there
51:23adrenal insufficiency or are they on a
51:25pottassium spare IC or trith suth oxisol
51:29either way often times the low
51:32aldosterone
51:34picture here's what I want you to think
51:38about does the patient
51:41have a low
51:44sodium that could be one potential
51:46offender the other thing is that
51:48sometimes their blood pressure may be a
51:49little bit on the Lower Side that's not
51:52always perfect though the other thing is
51:54their potassium they're going to be
51:56having less potassium secreted inside of
51:59the urine so they'll have a high
52:02potassium and on top of that they'll
52:04also retain protons because they're not
52:06going to secrete protons so they'll have
52:08high protons so they'll have a high
52:10potassium in the bloodstream and they'll
52:12have high protons in the blood so they
52:13have a metabolic acidosis so a metabolic
52:15acidosis hyponatremia
52:18hyperemia these are potential things to
52:20be considering now a lot of the times
52:23here again think about this patient do
52:25they have like a normal GFR or just a
52:30very mildly low GFR this is the other
52:33patient population to think about this
52:36in and then look through their
52:38medication list and think about
52:40potential diseases like diabetes or
52:42Addison's disease and in Addison's
52:45disease you would have not just low
52:47aldosterone you would have low cortisol
52:50so in these patients you would have
52:51other features that would make you think
52:52about Addison's disease all right my
52:55friends that's how we would talk about
52:56the renal retention problem so we talked
52:59either really really low GFR or normal
53:01SL mildly low GFR with a hyperstone
53:03state let's now talk about the next
53:06scenario no problems with Ostrum no
53:09problems with GFR we think it's a
53:11shifting of potassium out of the cell
53:13let's talk about those all right my
53:14friends so now we come to the next
53:15aspect which is we think that there's a
53:16lot of Shifting of pottassium this one's
53:18kind of more of a historical concept if
53:21I have a patient who really has no
53:23underlying renal dysfunction right so
53:25there there really no AK I CKD I've
53:28looked through it and I try to analyze
53:30is there any kind of drugs ACE
53:32inhibitors arbs Arnis pottassium
53:34diuretics ineds trith suth oxisol that
53:37could really contribute to a
53:38hypoaldosterone state and I haven't
53:40found that then I started thinking about
53:42shifting now when we have this it's the
53:45exact opposite of hypokalemia so in this
53:48particular scenario here we have a a
53:50sodium potassium pump we have a
53:52decreased activity of the sodium
53:55potassium ATP
53:57activity sodium potassium
54:00atpa now if this is inhibited or
54:03decreased in some way shape or form
54:05what's going to happen well in this
54:07scenario I'm going to
54:10have less movement of what well in some
54:14particular scenarios here what I'm going
54:16to have is I'm going to have less
54:17movement of potassium into the cell and
54:21I'm going to have less sodium ions
54:22coming out of the cell so there's going
54:25to be less sodium
54:27that is coming out of the cell and you
54:29know in this case three and there's
54:31going to be less potassium ions that are
54:34moving into the cell so if I have less
54:37pottassium ions moving in then what
54:40happens to the potassium inside of the
54:42bloodstream it builds up because they're
54:44not pushing the pottassium into the
54:45cells if that happens what happens to
54:48the serum potassium then what I notice
54:51is that my serum potassium starts kind
54:53of going up
54:56well then I have to ask myself the
54:58question bro what's decreasing my sodium
55:01potassium ATP
55:03bases one is it's the exact opposite in
55:06the other situation of hypocam was high
55:08insulin what if I have a patient who has
55:12decreased insulin you're like decrease
55:14insulin ain't that just the
55:17diabetics yeah pretty much so in a
55:19patient who has diabetes but let's be
55:21really kind of a little bit more
55:22specific I have a patient who has
55:24diabetes metis but more more likely
55:26they're like a dka or an HHS patient so
55:30in other words they have really bad
55:32production of glucose so in other words
55:34their glucose level is super super high
55:37right if I have a patient who has
55:39diabetes their glucose level is really
55:40high they have acidosis and they're just
55:43again they're not just having enough
55:44insulin production that's going to lead
55:46to this potential problem all right so
55:48then what will happen is this insulin
55:51receptor will become no longer
55:53stimulated and therefore there's going
55:55to be less stimulation of the sodium
55:57potassium ETP Aces and in that effect we
55:59can say it is inhibiting these pumps so
56:02think about a patient who has a really
56:04bad diabetic they have high glucose
56:06levels maybe they're in a dka or an HHS
56:09State the other scenario is we have some
56:13type of drug that has a beta 2
56:16antagonist activity and then there's
56:19another scenario here so what if it's
56:21due to a
56:23beta blocker and there's one other drug
56:28dexin think about this in a patient who
56:30has atrial fibrillation all right and
56:33they're being treated for their rapid
56:34ventricular rate and preventing them
56:36from having taco cardia and they have
56:38just too much of their beta block or too
56:40much of their dexin what that will do is
56:43is that'll lead to the inhibition of the
56:45beta 2 receptor and less stimulation to
56:48the sodium potassium pumps if there's
56:50less stimulation to the sodium potassium
56:53pumps in that effect you are inhibiting
56:55it leading to less potassium coming in
56:58less sodium going out all right so it's
57:01either a beta blocker too much of it or
57:04too much dexin so too much of a beta
57:07blocker or too much of dejin so like a
57:11dejin toxicity or excessive amounts of
57:12beta
57:13blockade with this being said this one
57:16is the really really important one to
57:18think about and here's why the other
57:21concept is that in hypokalemia there was
57:24also this activity of the
57:28potassium proton pump right here's what
57:32I want you to think about again we said
57:33that the potassium I mean the proton
57:35ions will move in and potassium ions
57:38will move
57:40out if I have a patient who has
57:43something
57:44called acidosis so I have an
57:47acidosis and guess what's a disease that
57:50can cause acidosis
57:52dka this is interesting because dka if
57:54you have a patient who has dka not only
57:56will they have low insulin they'll have
57:58acidosis and also hypoglycemia
58:00hypoglycemia can actually cause
58:02hyperosmolarity and cause solute drag uh
58:05to pull potassium out of the cells along
58:07with water and so that's kind of an
58:08interesting concept here but acidosis
58:11will actually work and what it'll do is
58:14it'll increase the activity of these
58:16potassium proton pumps and so what will
58:19happen is you'll have more protons
58:21moving into the cell and more potassium
58:24ions moving out
58:27now watch what
58:28happens if more protons move into the
58:32cell and more potassiums move out of the
58:34cell what happens
58:37effectively to the potassium in the
58:39blood it goes up and you get what's
58:41called an
58:42increase in your serum potassium so
58:45here's the kind of thing that I want you
58:46to think about as a very common scenario
58:48in a vignette a patient who has acidosis
58:51due to dka they have decreased insulin
58:54due to their underlying diabetes and has
58:56hypoglycemia hypoglycemia increases
58:58osmolarity of the blood which then
58:59creates a solu drag to pull water and
59:01potassium out of the cells that's a very
59:03common offender and if you don't have
59:05that scenario then think about the
59:07patient who has a beta blockade or dexin
59:10and again this doesn't have to be just
59:12dka it could be any kind of metabolic
59:14acidosis ureic lactic acidosis any kind
59:18of toxic related acidosis and it also
59:20can be respiratory acidosis so that's
59:22really important to remember here guys
59:24so think about that especially with an
59:26ABG and an appropriate clinical history
59:29here's the last
59:30scenario the last one's kind of tough
59:34this one is more you have to really
59:37listen to the patient's history and you
59:39have to look for historical features
59:41that suggest that they are busting open
59:42cells and what did I tell you what's the
59:44most abundant cation inside the cells
59:46potassium 97% of potassium is sitting
59:48inside the cells if I bust them open I'm
59:50putting out tons of pottassium into the
59:52blood if I listen to their history and I
59:55hear here that they have a new onset
1:00:00anemia or maybe
1:00:03jaundice then I'm going to start
1:00:05thinking about a type of cell liis
1:00:09called
1:00:10hemolysis the problem with
1:00:12homolysis is that with homolysis you're
1:00:15going to dump not only potassium into
1:00:17the bloodstream but you're going to
1:00:19decrease your hemoglobin and your
1:00:20hematocrite you're going to increase
1:00:22your LDH you're going to decrease your
1:00:24haptoglobin and so one of the ways that
1:00:26think about this is you think about yes
1:00:27anemia you think about jaundice but you
1:00:30look and say oh they have high potassium
1:00:33inside of the
1:00:34bloodstream but I also notied that they
1:00:37have a low hemoglobin a low hematocrite
1:00:40suggesting their
1:00:41anemia they have a high
1:00:44LDH because this is another enzyme that
1:00:47sits inside of the cells and they have a
1:00:49low haptoglobin which is a protein that
1:00:51binds up hemoglobin and so if it's
1:00:54binding up hemoglobin there's less free
1:00:56apoglobin
1:00:58this would be suggestive of
1:01:01homolysis if I look at the patient's
1:01:03history and it says oh they just had a
1:01:05very severe seizure like a really really
1:01:07bad seizure or they had some type of
1:01:10like Crush
1:01:12injury and they had like a compartment
1:01:14syndrome in that scenario I think about
1:01:18busting open of skeletal muscle cells
1:01:20which is
1:01:22called
1:01:24rabdo myo
1:01:26Lis in this scenario not only will they
1:01:30have muscle pain along with the history
1:01:32that suggests that they've kind of bust
1:01:34open some of these muscle cells they'll
1:01:35have a high potassium they'll have a
1:01:37high CK and their urine
1:01:40myoglobin tends to be positive so I'll
1:01:42see a high potassium a high CK and a
1:01:47positive urine myoglobin high potassium
1:01:50High CK High urine myoglobin this is a
1:01:55very common an offender of acute kidney
1:01:58injuries the last one's kind of like the
1:02:00most interesting one if I have a patient
1:02:03who has an underlying hematological
1:02:04malignancy like non- hodkin lymphoma Al
1:02:09or
1:02:10AML and recent
1:02:15chemo I want to think about a disease
1:02:18called
1:02:20tumor Lis syndrome now in tumor Lis
1:02:25syndrome what happens is the chemo kills
1:02:28multiple tumor cells and what happens is
1:02:30is they will have high potassium inside
1:02:32of the bloodstream they'll also leak out
1:02:35this enzyme LDH they'll also have lots
1:02:38of uric acid and they'll have lots of
1:02:41phosphorus inside of the bloodstream and
1:02:44so we see a high potassium we see a high
1:02:47LDH a high uric acid and a high
1:02:50phosphorus and sometimes a low
1:02:52calcium so with that being said high
1:02:55potassium
1:02:56high uric
1:02:58acid High LDH and high
1:03:03phosphate this would help me to think
1:03:05about a patient's historical features
1:03:08really in combination with these other
1:03:10lab values to make me think about
1:03:12hyperkalemia all right so this one's a
1:03:15tough one but look at their clinical
1:03:16history it'll give you so much
1:03:18information and if you think about the
1:03:19other labs that will help out again
1:03:21we'll talk about more of these disorders
1:03:23in the respective systems but this kind
1:03:25of introduces the concept of how they
1:03:27may cause hyperemia all right my friends
1:03:29that covers the causes the
1:03:31pathophysiology the introduction to the
1:03:33material now let's go into why is
1:03:35hypokalemia and hyperemia so dangerous
1:03:38all right my friends let's talk about
1:03:39the complications of pottassium
1:03:40disorders all right so why is it so bad
1:03:42to have hypokalemia and hyperemia
1:03:44essentially what are the
1:03:46complications often times the
1:03:48presentation could be completely
1:03:50asymptomatic but it is important it is
1:03:52imperative for us to understand the
1:03:54effect that potassium has across
1:03:56excitable cells for example what kind of
1:03:58effect does it have across cardiac
1:03:59muscle skeletal muscle even smooth
1:04:01muscle and neurons because it does play
1:04:04a very important role with our membrane
1:04:06potential here's what's
1:04:08interesting with respect to excitability
1:04:11when we look at the cardiac
1:04:13myocytes and we look at the activity of
1:04:15them versus the activity of their
1:04:17skeletal muscle
1:04:19cells or our smooth muscle cells or our
1:04:23neurons there is a degree of excited
1:04:25ility that is different what do I mean
1:04:28hypokalemia when the pottassium level
1:04:30inside of the serum or the blood is
1:04:31lower than normal we find that the
1:04:33excitability of our cardiac myocytes go
1:04:36up and the
1:04:38excitability of the smooth muscle the
1:04:40skeletal muscle and the neurons go down
1:04:42I'll explain why in a second but I I
1:04:45want you to trust me all right and the
1:04:46reason why this is important is when we
1:04:49talk about excitability this is the one
1:04:51that actually carries the higher risk of
1:04:52mortality is the increased excitability
1:04:54of the cardiac monocytes it can lead to
1:04:56a lot of Tachi arrhythmias and a lot of
1:04:58EKG changes that is important for us to
1:05:00be able to identify very quickly in the
1:05:01clinical world this is not as common but
1:05:04it is important for us to be able to be
1:05:06cognizant of that it can cause a
1:05:08decreased contraction of our skeletal
1:05:10muscles leading to weakness um and
1:05:12fatigue of the muscles it can also lead
1:05:15to decreased contractility of the smooth
1:05:16muscle within our git and so that could
1:05:18lead to ilas and constipation um it also
1:05:21can lead to decreased firing of
1:05:23particular neurons and so it may cause
1:05:25some typ of decreased deep tendon
1:05:26reflexes in the worst case scenario
1:05:28potentially even paralysis but these are
1:05:31you know some of the the presentations
1:05:33that you want to be considered of for
1:05:35the uh smooth muscle skeletal muscle and
1:05:37neuron involvement for the cardiac
1:05:39muscle it can have a wide range of
1:05:40activity and I'll talk about that in a
1:05:42little bit but what I want you to
1:05:44understand is is why is the excitability
1:05:46decreased particularly in skeletal
1:05:48muscle smooth muscle and neurons and
1:05:51then we'll talk about why is the
1:05:52excitability in cardiac tissue increased
1:05:55and then what would that look like in a
1:05:57patient so let's take a second here
1:05:59let's look at some cells here I'm going
1:06:00to zoom in on these cardiac myocytes and
1:06:02as we zoom in on these cardiac myocytes
1:06:03what I want you to notice is is that
1:06:05there is a gradient for potassium so
1:06:08when we look at the pottassium basically
1:06:10the concentration of potassium inside
1:06:12the cell versus the potassium
1:06:15concentration outside the cell we know
1:06:18that our our cells are bags of potassium
1:06:2196 97% of the potassium inside of our
1:06:23body is found inside of our cells so
1:06:25there's natural a gradient where
1:06:27potassium will want to move from inside
1:06:28the cell to outside the cell because
1:06:31it's going to move down its
1:06:32concentration gradient but what if and a
1:06:35patient who has hypokalemia the
1:06:37potassium outside the cell is just much
1:06:40much lower than normal now the
1:06:41concentration gradient is insane and so
1:06:44what will happen is is pottassium
1:06:47will naturally efux out of the cell more
1:06:51intensely now as pottassium leaves our
1:06:54cells more significantly what happens to
1:06:58the inside of the cell you're losing
1:07:00positive ions and so the inside of the
1:07:02cell starts to become more
1:07:05electronegative over time and what is
1:07:08the difference here is that in our cells
1:07:11we often times when you look at this
1:07:13graph this is going to be time which we
1:07:14can say is like in milliseconds and then
1:07:16on the Y AIS you're going to have Mill
1:07:18volts
1:07:19right every excitable cell has a
1:07:21threshold but when when you hit that
1:07:23threshold you open up voltage gated ion
1:07:25channels like calcium or sodium and then
1:07:27that causes depolarization of that cell
1:07:30that's our threshold potential I'm going
1:07:31to represent that as
1:07:34TP the cell also has a membrane
1:07:37potential that when this cell is not
1:07:39being stimulated or it's not in the
1:07:41point where it's in a depolarization
1:07:43state it is resting it is ready to be
1:07:44excited again that's called our resting
1:07:46membrane potential so I'm going to say
1:07:48that this is our resting membrane
1:07:51potential when you have a patient like
1:07:53this this is normal so they would go
1:07:55resting membrane potential to threshold
1:07:57potential and they would trigger an
1:07:59action potential right here so normally
1:08:00it would go you have some type of
1:08:02resting you go here to threshold you
1:08:04open up voltage gated and then you come
1:08:06back down right that's our normal
1:08:08process now add in this problem when the
1:08:11potassium is much lower outside the
1:08:13cells lots and lots of pottassium will
1:08:15leave which makes the cell more
1:08:18electronegative essentially what this
1:08:20will
1:08:21do and this will precipitate what's
1:08:23called
1:08:27hyperpolarization so this will induce
1:08:28what's called
1:08:32hyper polarization essentially bringing
1:08:36the resting membrane potential even
1:08:38lower so now this is our resting
1:08:40membrane potential what I'm going to do
1:08:42is I'm going to create a new
1:08:44one now look where it is it's much more
1:08:48negative we're going to call this
1:08:49resting membrane potential we're going
1:08:51to give a little Dash now do you see
1:08:53what happened here how the resting membr
1:08:55potential decreased it went from here to
1:08:59here the problem with this is is in a
1:09:03normal cell I only had to go from this
1:09:04baby blue line to the threshold
1:09:06potential to trigger an action potential
1:09:08now in a skeletal muscle cell a smooth
1:09:10muscle cell a neuron I have to go from
1:09:13this resting membrane potential slash
1:09:17all the way up to threshold potential
1:09:20that's a longer that's a much larger
1:09:23distance I'm going to need a stronger
1:09:24stimulus I'm going to need more cationic
1:09:26influx in order for this to occur and so
1:09:29because of this this will reduce the
1:09:32excitability of these cells and it will
1:09:34reduce the the intensity of their
1:09:36depolarization so that is the big thing
1:09:38to remember is that what happens is is
1:09:41with this hyperpolarization we will see
1:09:43a resting membrane potential that will
1:09:46be reduced and when you reduce the
1:09:48resting membrane potential it requires a
1:09:50very stronger degree of stimulus and
1:09:52it's going to take a harder stimulus for
1:09:54you to be able to get from this new rest
1:09:55memory potential to threshold potential
1:09:57to trigger an action
1:09:59potential okay I hope that makes sense
1:10:02for that part now we get into the tricky
1:10:04one which is how does this cause
1:10:06increased excitability in our cardiac
1:10:08tissue well initially it is important to
1:10:11remember initially with hypokalemia it
1:10:14may cause some degree of decreased
1:10:17excitability but over time as the
1:10:20potassium continues to become lower or
1:10:22it persistently stays lower what happens
1:10:25is a couple interesting Concepts let's
1:10:28say here I take a look at two different
1:10:29cells this is what's called a
1:10:30ventricular myosite so it's going to be
1:10:31like one of our contractile
1:10:33cells in this cell it has a pump here
1:10:36called a sodium pottassium atps and so
1:10:40naturally it's exchanging different ions
1:10:42here right it's supposed to exchange
1:10:45three sodium ions for two potassium ions
1:10:51when potassium levels are really really
1:10:53low guess what they do to this pump they
1:10:55inhibit this pump now this pump is going
1:10:58to be inhibited because of the low
1:11:00potassium what happens to the sodium
1:11:02concentration inside the cell it builds
1:11:05up why is that important the reason why
1:11:08that's important is in order for us to
1:11:10be able to get
1:11:12calcium out of the cell so in order for
1:11:15calcium to be able to move out of the
1:11:17cell it needs sodium present outside the
1:11:20cell but guess what you just messed up
1:11:23you messed up the sodium ATP and so
1:11:27because I don't have as much sodium out
1:11:29here I'm going to have less calcium
1:11:32leaving the cell so there's going to be
1:11:33less sodium coming into the cell less
1:11:36calcium going out of the cell so what
1:11:38ends up effectively Happening Here is I
1:11:40get a lot of intracellular sodium and a
1:11:42lot of intracellular calcium because
1:11:45there's going to be less movement
1:11:46outwards and so what happens is if
1:11:48there's less calcium leaving what
1:11:51happens is that the calcium builds up
1:11:54inside the cell
1:11:57and as the calcium starts building up
1:11:59inside of the cell it makes the cells a
1:12:00little bit more agitated it increases
1:12:04the risk of them forming what's called
1:12:06early after
1:12:07depolarizations so what happens is let's
1:12:09say here I have a ventricular Mite and
1:12:11it shows its kind of action potential
1:12:13right as we're going into the
1:12:14repolarization phase so you see how it's
1:12:16plateauing and then it goes into the
1:12:17repolarization what happens is because
1:12:21hypokalemia leads to an inhibition of
1:12:22the sodium pottassium pumps sodium
1:12:25builds up in the cell there's less of it
1:12:26outside the cell it can't come in
1:12:28calcium can't come out so calcium builds
1:12:30up sodium builds up makes the cell super
1:12:32positive and increases the risk
1:12:36of what's called early after
1:12:39depolarizations so now I have an
1:12:40increase
1:12:42risk of what's called
1:12:45Eads and this is going to increase the
1:12:47risk of forming Tachi arhythmia that's
1:12:49one reason why the cell is a little bit
1:12:51more excitable is because you led to an
1:12:54increased interest C sodium and an
1:12:56increased intracellular calcium by
1:12:57inhibiting the sodium potassium pump and
1:12:59thereby inhibiting the sodium calcium
1:13:02exchange the other concept here is that
1:13:05whenever the potassium level is low
1:13:08there's these weird channels up to date
1:13:10says that they're called the K2 P1 other
1:13:14literature suggest that they're actually
1:13:15so funny sodium channels but the
1:13:17literature suggests that these are
1:13:18channels that are more specifically for
1:13:20potassium and what potassium is supposed
1:13:23to do is it's only going to be moving
1:13:24through these ch channels but when
1:13:26pottassium is really low guess what
1:13:28happens pottassium doesn't move through
1:13:30these channels guess what does move
1:13:31through the channels sodium ions so now
1:13:36sodium will
1:13:38influx into some of these pacemaker
1:13:40cells and when the sodium influxes into
1:13:43the pacemaker cells it makes the cells
1:13:45more
1:13:46electropositive and by doing that it
1:13:49increases the rate of their phase 4
1:13:53depolarization so you know how here we
1:13:55have phase four which is this UPS
1:13:57sloping which is kind of like the
1:13:58pacemaker potentials because potassium
1:14:01is so low you lose the regulation of
1:14:03this K2 P1 Channel and what happens is
1:14:06you have increased sodium influx and so
1:14:09now look what happens to the rate it
1:14:10goes Boop boom Boop boom Boop boom so
1:14:16you see what's happening here is the
1:14:17rate of of phase four depolarization is
1:14:20faster and it increases the risk of
1:14:23having tacky arrhythmias
1:14:25this is the concept that I want you to
1:14:27understand so again hypokalemia will
1:14:30reduce the resting membrane potential by
1:14:32hyperpolarizing our cells yes that
1:14:35reduces the citability of skeletal uh
1:14:37smooth muscle and neurons so you can
1:14:40present with weakness fatigue ilas
1:14:42constipation and decreased deep tinon
1:14:45reflexes initially it'll decrease the
1:14:47excitability of cardiac tissue but over
1:14:49time as the hypokalemia persists it
1:14:52shuts down the sodium pottassium pumps
1:14:54which leads to a buildup of
1:14:55intracellular sodium that prevents the
1:14:57proper sodium calcium exchange calcium
1:15:00builds up sodium builds up early after
1:15:02depolarizations ensue and the the actual
1:15:05myocytes the pacemaker cells like your
1:15:07peni system or other types of pacemaker
1:15:11cells they have normally on them K2 P1
1:15:15channels but whenever potassium is low
1:15:17you lose the regulation of this Channel
1:15:19and sodium starts moving in instead of
1:15:21potassium and what happens is this
1:15:23causes the cell to become a little bit
1:15:24more more positive and increases the
1:15:26phase four so it does what's called
1:15:30increases the
1:15:33rate of what's called your
1:15:35phase
1:15:37for
1:15:39depolarization in these pacemaker cells
1:15:43and by doing that that'll increase the
1:15:45rate of the heart all right so we have
1:15:46an understanding now of how whenever the
1:15:48potassium is low the effect it has on
1:15:50excitable tissue cells right again the
1:15:52one that I want to stress on is the
1:15:54cardiac
1:15:55high risk of mortality so we know
1:15:58essentially that low pottassium right
1:16:00what can we assume here that whenever
1:16:02you have a very low potassium level this
1:16:05essentially puts the heart into a state
1:16:08of increased risk of Eads and increased
1:16:11race rate of phase four depolarization
1:16:13within pacemaker
1:16:14cells essentially what will this do to
1:16:16the heart you kind of just turn this
1:16:19puppy on hyperdrive so it'll really try
1:16:21to you know lead to an increased risk of
1:16:23tacky arhythmia
1:16:25and what would that look like well
1:16:27there's a couple different types of
1:16:28tachmes that I would want you to be
1:16:29aware
1:16:30of one is it really increases the risk
1:16:34of what's called paroxysmal super
1:16:37ventricular tacac cardia that's
1:16:39one another one is there's very high
1:16:42risk of things like PVCs so PVCs are you
1:16:45know premature ventricular
1:16:47complexes it also can increase the risk
1:16:50of what's called ventricular tacac
1:16:51cardia or vtac we'll put
1:16:55but here's the big
1:16:57one whenever you have this increased
1:16:59risk of Eads the other thing that
1:17:01happens is is the combination of these
1:17:04you can have a a a prolonged action
1:17:06potential duration when you have a
1:17:09prolonged action potential duration one
1:17:11of the issues that comes about here is
1:17:14you can do something to the QT interval
1:17:16you can prolong the QT interval as the
1:17:19QT interval starts to kind of get a
1:17:21little bit longer and longer it
1:17:24increases is the risk of a disease which
1:17:26we're going to abbreviate here called
1:17:28torsades depont and this is even higher
1:17:32risk in patients who have
1:17:33hypomagnesemia so that's the big thing
1:17:35that I want you to remember hypokalemia
1:17:37increases the risk of tach rmias uh
1:17:39super ventricular pvc's vtac and
1:17:42torsades dep points there is other ones
1:17:45but these are the big ones so that is
1:17:48the big thing to take away from
1:17:49hypokalemia and its effects on excitable
1:17:51tissue cells right decreasing
1:17:53excitability of skeletal smooth and
1:17:54neurons initially decrease the
1:17:56excitability of the cardiac tissue but
1:17:58over time it becomes hyp excitable and
1:18:00we see how not every patient will be
1:18:04tacac cardic they won't all present with
1:18:07super ventricular tacac cardia vtac
1:18:08torsades to points some of them may not
1:18:11even present with any kind of skeletal
1:18:12smooth muscle or neuron presentation so
1:18:14it's important for you to be able to
1:18:15recognize vague ECG changes in these
1:18:18patients so if you get an ECG it's
1:18:20important for you to see some potential
1:18:22changes when we look at a a patient who
1:18:25hypokalemia one of the first things that
1:18:27we like to look at here is the t-wave
1:18:30what do you notice dang thing ain't
1:18:32there so sometimes what happens is the
1:18:34t-wave starts to flatten that's often
1:18:37times a very common presentation is
1:18:39what's called t-wave
1:18:43flattening now this isn't always perfect
1:18:46you can't say that as the potassium
1:18:47levels get lower and lower and lower
1:18:49these ECG changes also become more
1:18:51common that's not a perfect thing but in
1:18:56theory as the potassium gets lower and
1:18:58lower and lower you may see some other
1:19:00potential changes one is look at the ST
1:19:03segment do you notice What's Happening
1:19:05Here in comparison to the isoelectric
1:19:07line what happened it depressed and so
1:19:10what you may notice here is you may
1:19:13appreciate some
1:19:14depression within the ST segment so ST
1:19:18segment
1:19:19depression is also another potential
1:19:22finding that you would want to be
1:19:24considerate of enough all right so look
1:19:26for t-wave flattening ST depression the
1:19:29biggest one that they love to ask about
1:19:31on the boards and do not miss this
1:19:33one is when you look here you see a
1:19:36p-wave you see your your um QRS complex
1:19:39and we see something else here you see
1:19:41there's a little t-wave but there's a
1:19:42little
1:19:43blip off of the t-wave what's that
1:19:45called that's a uwave so that's the
1:19:48other type of presentation that you want
1:19:51to be able to notice is a uwave and then
1:19:53again with this you could also notice
1:19:55that the QT interval tends to become
1:19:57longer and longer and longer so you may
1:19:59even notice a prolonged QT interval
1:20:01before the patient goes into the deadly
1:20:02arhythmia known as torsa points all
1:20:05right so we see here the effects that
1:20:08potassium has on the cardiac tissue both
1:20:10with non-specific ECG changes as well as
1:20:13the higher risk of Tachi arhythmia and
1:20:15we should understand the path of Fizz
1:20:16there let's now move into hyperia all
1:20:19right my friends now let's talk about
1:20:20hyperemia when the pottassium be too
1:20:21dang high now when the potassium is too
1:20:23high again the concept behind this is
1:20:25that it plays a role in the membrane
1:20:27potential now here's where you're going
1:20:28to be like dang it Zach why do you do
1:20:30this to me the excitability is actually
1:20:33consistent across all of these you're
1:20:35like okay so I got to remember that the
1:20:36excitability is decreased for the
1:20:37skeletal and smooth and neurons for hypo
1:20:40and then it's increase for cardiac okay
1:20:42cool for cardiac skeletal smooth and
1:20:45neurons and hyperkalemia they relatively
1:20:47all of them have a decreased
1:20:48excitability at least it makes it a
1:20:50little bit easier but I know that in the
1:20:53grand scheme of things you you probably
1:20:55wish it was like oh man I just I wish it
1:20:57was just a flip of everything but it's
1:20:59not unfortunately in this particular
1:21:02scenario the excitability across all of
1:21:04these tissues is reduced
1:21:07now the concept behind this is somewhat
1:21:12very straightforward with a slight
1:21:14Nuance that will add into this again
1:21:17here we're taking a myocardial cell
1:21:20because here's the thing in hyperkalemia
1:21:23again it can affect skeletal muscle
1:21:25cells they could be weak you could have
1:21:27fatigue it can affect the actual smooth
1:21:30muscle slightly not as much with like
1:21:33ilas and constipation and it can affect
1:21:36our neurons and so it can lead to
1:21:37reduced deep tendon reflexes and
1:21:39sometimes even paralysis in worst case
1:21:41scenario but the high degree of
1:21:43morbidity and mortality lies within its
1:21:45effect on the cardiac tissue and so it
1:21:47is of imperative nature that we
1:21:50understand the effect of high Potassium
1:21:51on the cardiac tissue because we already
1:21:53understand that low potassium and the
1:21:55cardiac tissue increases the risk of
1:21:56Tachi arhythmia right via increased Eads
1:22:01via the uh k2p one channels and
1:22:03increasing the sodium influx and causing
1:22:04a lot of increased phase four
1:22:06depolarization so we get
1:22:08that with potassium on the heart
1:22:12particularly when it's high it actually
1:22:13slows things down and it increases the
1:22:16risk of heart blocks and so we'll talk a
1:22:18little bit about that let's say we take
1:22:20a piece of the cardiac tissue and again
1:22:22we look at the current or the gradient
1:22:24so here's our potassium concentration
1:22:26inside the cell and we look at the
1:22:28potassium
1:22:30concentration outside the cell now again
1:22:33our cells are bags of potassium they're
1:22:35filled to the gills with potassium but
1:22:38what if the potassium concentration
1:22:39outside the cell increase a little bit
1:22:41more there's still going to be a
1:22:42gradient because there's so much
1:22:44potassium inside of our cells but the
1:22:46gradient is going to be much less and so
1:22:48the amount of potassium that is moving
1:22:52out of these cells is significant L
1:22:54reduced in compared to the norm right
1:22:57and so because of that potassiums will
1:23:00start to build up inside of these cells
1:23:03because they won't leave as easily
1:23:06because of the gradient bring altered
1:23:08there is a reduced concentration
1:23:10gradient for
1:23:11potassium so now because of that the
1:23:13cell will become a little bit more
1:23:16positive now if you look at this let's
1:23:19say here is your resting membrane
1:23:21potential here is your threshold
1:23:23potential and we're looking at a graph
1:23:24again where on the x-axis is time
1:23:27particularly in a milliseconds and then
1:23:29here is voltage in Mill volts right we
1:23:32know that a normal cell when it's at
1:23:34rest maybe - 70 molts if you have it
1:23:38give a little stimulus it'll get it up
1:23:40the threshold once you get threshold
1:23:41voltage gated sodium channels will open
1:23:43and allow for cation to influx in and
1:23:45cause the cell to
1:23:47depolarize now in this particular
1:23:50situation of hyperemia less pottassium
1:23:52is moving out of the cell right right so
1:23:55if what happens in this particular
1:23:56situation is less potassium is moving
1:23:58outside of the cell what this does
1:24:01is is this makes the inside of the cell
1:24:03a little bit more positive and it
1:24:06actually can lead to a slight
1:24:08depolarization of the cell so it kind of
1:24:10causes a
1:24:12slight depolarization of the cell makes
1:24:16the inside of the cell a little bit more
1:24:18positive even at rest so now look at the
1:24:22new resting membrane potential get this
1:24:24dotted line so here's our resting
1:24:27membrane potential with our Dash that's
1:24:28the new one where did the resting
1:24:30membrane potential go it went from here
1:24:33to
1:24:34here
1:24:36now what you would look at is you would
1:24:38be like okay well Zach wouldn't this
1:24:42Zach wouldn't this increase the
1:24:43excitability because look my resting
1:24:45membrane potential is so much closer to
1:24:47my threshold so all I would have to do
1:24:50is go from this tiny little difference
1:24:52here maybe I was at70 now I'm at like
1:24:55I don't know let's just say that I'm at
1:24:56like -60 and all I have to do is go from
1:25:00-60 to 55 wouldn't that be easier Zach
1:25:02that would make sense yes that's true
1:25:05you are correct that whenever the
1:25:08resting membrane potential is increased
1:25:12initially initially the excitability
1:25:15will increase but over time as the
1:25:19pottassium levels within the serum
1:25:20continue to rise and rise and Rise we
1:25:23see that that excitability start to
1:25:26decrease the question that you want to
1:25:28ask me is why over time as the potassium
1:25:32Rises and Rises Rises does the
1:25:34excitability decrease because Zach right
1:25:36now I don't get it I'm closer to
1:25:39threshold let me explain
1:25:41now when we slightly depolarize the
1:25:45cell what happens is is you bring it
1:25:48closer to threshold now we have these
1:25:51channels on our cardiac tissue and
1:25:54they're called voltage gated sodium
1:25:56channels right so I'm going to put here
1:25:58a voltage these are voltage
1:26:02gated sodium channels
1:26:05now whenever you have this
1:26:09tissue and you look at it and you look
1:26:12at the amount of voltage gated sodium
1:26:15channels let's say we have here a
1:26:17resting membrane potential that is
1:26:20normal and then over here we're going to
1:26:21say this is resting membrane potential
1:26:24Prime resting membrane potential Prime
1:26:26so this is the new
1:26:28one let's say on this cell when it's at
1:26:31rest your voltage sodium channels the
1:26:33amount of active voltage gate of sodium
1:26:35channels the amount of channels that are
1:26:36open for sodium to flow in are
1:26:39three but then as the potassium levels
1:26:42go higher and higher and higher what you
1:26:44notice is is that the as the cell
1:26:46becomes slightly depolarized the number
1:26:48of voltage gated sodium channels active
1:26:51ones start to decrease so look at what
1:26:54happens here as I go in this direction
1:26:58in this particular direction here the
1:27:00amount of voltage at sodium channels
1:27:02decrease so here I have a decent number
1:27:05but as I go this way the
1:27:08number of
1:27:10active
1:27:14channels
1:27:15decrease why is that a
1:27:18problem the reason why that's a problem
1:27:20is is because these voltage gated sodium
1:27:22channels are supposed to allow for
1:27:24sodium ions to do what to rush into the
1:27:29cell once you have threshold potential
1:27:32the sodium should rush into the
1:27:34cell make the cell super
1:27:36positive and as it makes the cell super
1:27:39positive it'll help with the rising
1:27:41phase of the depolarization
1:27:43right but as you have less voltage gated
1:27:47sodium channels because as the
1:27:48pottassium is coming up the number of
1:27:50voltage sodium channels that are active
1:27:52are decreasing
1:27:54so now what happens is you have less
1:27:56sodium rushing in and so what happens is
1:27:59now look at my phase 4
1:28:01depolarization it's much longer so I
1:28:05have a slower rate of my phase 4
1:28:09depolarization does that make sense so
1:28:11what I will do is I will
1:28:14decrease the
1:28:17rate of the phase
1:28:204
1:28:22depolarization in p maker
1:28:28cells and the thing that that will do is
1:28:32is that it will actually reduce the
1:28:33heart rate
1:28:34significantly so now the patient has a
1:28:37higher uh risk of Brady cardia or Brady
1:28:41arrhythmias that is the big
1:28:43understanding that I want you to have so
1:28:44again yes it is correct that in
1:28:47hyperemia initially because there's less
1:28:50movement of potassium outside of the
1:28:53cell going from inside the cell to the
1:28:54outside of the cell the cell will become
1:28:56a little bit more positive because it
1:28:57has more potassium staying there so it
1:28:59will slightly depolarize bring the
1:29:01resting membrane potential closer to
1:29:02threshold so initially you only need a
1:29:04little stimulus boom you can have
1:29:05increased excitability over time though
1:29:09as the resting membrane potential
1:29:10continues to climb because the potassium
1:29:12is going up you'll get closer to
1:29:14threshold the problem is is that in
1:29:17order for voltage gated sodium channels
1:29:19to go from a inactive to an active State
1:29:22they have to kind of go back to a
1:29:24resting membrane potential and so as the
1:29:26potassium levels get higher you get them
1:29:29closer to threshold you have less active
1:29:32voltage sodium channels that are
1:29:34available to open that is the problem
1:29:37and that's why you'll have a reduced
1:29:39rate of phase4 depolarization now you're
1:29:42like okay Zack that's a lot of patho
1:29:43Fizz just give me the the you know nuts
1:29:46and bolts how will they present well if
1:29:49you think about it if they're decreasing
1:29:51the rate of pH phase 4 depolarization
1:29:54then theoretically we would expect some
1:29:56kind of like reduced heart rate
1:29:58essentially correct so that's what I
1:30:01want you to think about here is that
1:30:04whenever you have a what color did I do
1:30:06I did Black over there whenever you have
1:30:08a very high potassium
1:30:10level the effect that this has
1:30:13particularly on the heart especially
1:30:15right here this guy right here this is
1:30:16our friend our av node is it tends to
1:30:20inhibit the AV node so what would this
1:30:23look like
1:30:24often times these patients can present
1:30:26with AV
1:30:29blocks and these AV blocks could be a
1:30:32first degree could be a second degree
1:30:34mobitz one second degree mobitz two
1:30:36chances of third degree is lower but
1:30:38it's a
1:30:40possibility one other thing with
1:30:43hyperkalemia when patients have these
1:30:45weird EKG changes which we will talk
1:30:47about they have a risk high risk of
1:30:49what's called high
1:30:52risk of leading to something something
1:30:54called a sine
1:30:56wave and the the the problem with a sine
1:30:59wave is it's this weird wave that
1:31:02whenever it potentially progresses it
1:31:05can cause the patient to go into
1:31:07something referred to
1:31:10as ventricular
1:31:12fibrillation
1:31:13or they could then break down completely
1:31:16to no electrical Rhythm whatsoever known
1:31:18as asy so hyperemia is very very high
1:31:22risk of developing Cardiac Arrest but it
1:31:26is important for the P for you to
1:31:28understand that these types of events
1:31:30when they occur it is due to a rapid or
1:31:34acute rise in potassium more so than a
1:31:36chronic slow rise in
1:31:38potassium all right hyperemia can cause
1:31:42AV blockade so bradicardia it can
1:31:44increase the risk of asy V FIB is the
1:31:47pottassium levels rise very high and
1:31:49acutely we know now it does this by
1:31:53again
1:31:54A reduced movement to potassium outside
1:31:56of the cell so yes it will bring the
1:31:58resting membrane potential up because
1:32:00you keep more potassium in the problem
1:32:02in is is as you move the resting
1:32:04membrane potential closer to threshold
1:32:06you have
1:32:07less available active voltage gated
1:32:11sodium channel so you can't generate a
1:32:13very strong
1:32:15depolarization now the question that you
1:32:17should ask is okay do all hyperemic
1:32:19patients present with weakness do all
1:32:21hyperic patients present with some type
1:32:24of decreased deep tendon reflexes or
1:32:27with AV blockade or increased risk of
1:32:30cardiac arrest no sometimes they present
1:32:32with these non-specific EKG changes that
1:32:35you have to be able to identify so when
1:32:37you see a potassium level is as high get
1:32:38an
1:32:39EKG one of the first
1:32:41signs is this as you see this heck of a
1:32:43wave here about the size of a a QRS
1:32:46complex right heck of a thing there so
1:32:49this right here is called a
1:32:51peak t-wave
1:32:54and a peak t-wave is very characteristic
1:32:57you hear this as a buzzword term as it
1:32:59indicates hyperkalemia all right not all
1:33:02patients will present with this but this
1:33:03is one same concept I told you that
1:33:05hypokalemia as the pottassium levels get
1:33:07lower and lower and lower and lower they
1:33:08don't always progress this way same
1:33:11thing as the potassium levels get higher
1:33:13and higher and higher and higher they
1:33:15may progress this way but it's not
1:33:17always a perfect science well what could
1:33:19they do so I like to remember it like
1:33:21this I like to go like this I go up I go
1:33:25left I go down and I go this way and I
1:33:28remembered in this order I go one 2
1:33:31three
1:33:33four up is the peak t wve two I'm going
1:33:37back and when I go back I'm going to go
1:33:39back to my PR interval and look what
1:33:42happens to this puppy right here it
1:33:45prolongs and that makes sense because if
1:33:47you prolong your PR interval it
1:33:50increases the risk of Av blockade does
1:33:52that make sense so what I'll notice here
1:33:55is that my PR
1:33:57interval I can have an increase in my PR
1:34:00interval here all right what else go
1:34:04down so I'm back at the PR interval area
1:34:07look what happened p-wave
1:34:09go if the p-wave disappears that again
1:34:12also supports the increased risk of Av
1:34:15disassociation too and so the absence of
1:34:18the p-wave is very concerning so I'm
1:34:20going to put here no p-wave you you lose
1:34:24that p-wave or p-wave flattening if you
1:34:26will then notice one other thing go
1:34:30right now what I do is I'm going to go
1:34:32right I'm going to widen out my QRS
1:34:35complex so look at here from when I go
1:34:37from here all the way over here what
1:34:40happened to my curus complex it
1:34:41increases and so I notice a
1:34:46wide
1:34:48Qs this is often times the presentation
1:34:52that you want to remember is a t-wave a
1:34:55prolong PR interval dropping of the
1:34:57p-wave widening QRS and then what's the
1:34:59thing that usually follows this the sine
1:35:02wave what follows the sine wave viib or
1:35:06asy so these are the things that I want
1:35:08you guys to remember when it comes to
1:35:10hyperemia and then overall the things to
1:35:12remember when it comes to complications
1:35:13of pottassium disorders let's now move
1:35:15on to how to diagnose the potential
1:35:18causes and concerning features on the
1:35:20EKG of pottassium disorders we've talked
1:35:23a lot about the patho Fizz we've talked
1:35:25a lot about the complications how do we
1:35:27actually diagnose the reason why a
1:35:29patient is developing hypokalemia that's
1:35:31really important right so first thing
1:35:34let's say the patient comes back they
1:35:35have a potassium that's less than 3.5
1:35:37I'd like to send off a urine potassium
1:35:40if I send off the urine potassium the
1:35:42reason for this is if it's high it's
1:35:44renal if it's low it's GI right that's
1:35:47often times the case so if it's high
1:35:49meaning it's greater than 20 it's a
1:35:51renal cause if it's low less than 20
1:35:54it's likely a GI cause now if it's a
1:35:58renal cause what I need to do is then
1:36:00obtain a blood pressure oh you're like
1:36:02wait what the reason why is if you
1:36:05remember in patients who have this they
1:36:07can have
1:36:09hyperaldosteronism so hyperaldosteronism
1:36:11was one hypomagnesemia was one diuretics
1:36:13was another one as well right and so
1:36:16these are the big things to be thinking
1:36:18about here in the rtas so if I get a
1:36:21blood pressure it's the only one that'll
1:36:23really cause
1:36:24hypertension so if I get a blood
1:36:25pressure and it's high I then want to
1:36:27think about o hyper aldosteronism but I
1:36:29should get the renin and alone levels
1:36:32because if the renin is low and aldon's
1:36:34high oh I know that this is the primary
1:36:36problem negative feedback to shut this
1:36:38one down that's
1:36:40primary if they are both high oh that's
1:36:43secondary that means the JG cells are
1:36:45driving the random production which is
1:36:46driving ostron and there is one more I
1:36:49don't want you to go too crazy but if
1:36:50the renan and aldron are low you can
1:36:52think about an app mineral corticoid
1:36:54excess sometimes we can see this in
1:36:56other
1:36:57diseases especially like licorice
1:37:00ingestions all right that's going to be
1:37:02a big one here so this would kind of
1:37:04give away your hyper Aldo if the BP is
1:37:07normal or low then it rules these out
1:37:09for the most part another big thing is
1:37:11that these patients will have
1:37:13hypernia right and metabolic
1:37:17alkalosis for this one if you have
1:37:19normal or low BP check a magnesium in an
1:37:22AGG all right right ABG will tell if you
1:37:25have any kind of renot tubular acidosis
1:37:28it'll also tell you if you have a
1:37:29metabolic alkalosis and the Magnesium
1:37:31will tell you you have
1:37:32hypomagnesemia if I check a magnesium
1:37:34and it's the only thing that's low
1:37:36everything else is normal that's
1:37:37hypomagnesemia and often times you'll
1:37:39see in the vignette how the patient's
1:37:40getting uh potassium and they're not
1:37:42improving if the Magnesium is low that's
1:37:44likely the
1:37:45cause if you see a metabolic alkalosis
1:37:48okay which diseases were metabolic
1:37:50alkalosis that was diuretics diuretics
1:37:53were the the biggest one for this one
1:37:55because they cause potassium and proton
1:37:57loss and the last one is if I see
1:38:00metabolic acidosis there's only two that
1:38:02was rta1 and rta2 done that's not too
1:38:05bad right if I have a GI loss of
1:38:08pottassium then I should just get an ABG
1:38:10because if it was vomiting they're
1:38:12losing proton so they'll become an
1:38:14alkalotic right and if they're having
1:38:16diarrhea they're losing lots of B uh
1:38:19bicarbon their stool so they're going to
1:38:21become acidotic so this is a simple easy
1:38:24way by which we can classically and
1:38:26diagnostically think about
1:38:28hypokalemia lastly don't forget about
1:38:30your shifting often times history can
1:38:32elucidate this so you have to think have
1:38:35they gotten any recent insulin use
1:38:36because that's a very common cause
1:38:38recent albuterol use and lastly is there
1:38:41an alkalosis in general present that
1:38:44could also be the
1:38:45cause we come to the very feared
1:38:47hyperemia now what's the reason for this
1:38:50one well first thing you have to make
1:38:52sure that it's actually real sometimes
1:38:54in patients who have very tight
1:38:56tourniquets or um they have a hemol lied
1:39:00sample sometimes what can happen is is
1:39:03they can
1:39:04have uh their bloodstream not
1:39:06necessarily has a high potassium it's
1:39:08when the blood runs through the actual
1:39:10veny puncture tube or around that vessel
1:39:12that they rupture open and it can cause
1:39:14hemolysis and a hemolly sample is a very
1:39:17common cause of pseudo hyperkalemia so
1:39:20what you always want to do is if you
1:39:22check a patient's potass it's greater
1:39:24than five recheck it if it's normal it's
1:39:26pseudo hyperemia and then that's usually
1:39:30it no further workup but if you recheck
1:39:32it and the potassium is still high
1:39:34greater than five you should then look
1:39:36at their GFR in other words off their
1:39:39BMP their basic metabolic panel which is
1:39:41like a chemistry um it's going to give
1:39:43you their renal function if their GFR is
1:39:45really low or if it's really uh if it's
1:39:48low or it's normal so let's say mildly
1:39:50low or normal that's usually the hypo
1:39:54aldosteronism in this particular
1:39:56scenario what could you do get a Ren and
1:39:58aldosterone level the reason why is is
1:40:01if I really think about each scenario
1:40:03let's say for example low renin low
1:40:05aldosterone this is diabetes ineds most
1:40:07likely this isn't always the case but
1:40:09this will help you to think about it uh
1:40:12pathophysiologically right if I said
1:40:14that the patient has a high renin but
1:40:16they're outron low this means I'm
1:40:18shutting something down at the
1:40:20Angiotensin 2 or adrenal cortex level so
1:40:23this has to be ACE inhibitors arbs Arnis
1:40:26or Addison's disease and then lastly if
1:40:28the renin is high and aldosterone's high
1:40:31but something's blocking it something's
1:40:33blocking it at its actual site that has
1:40:36got to be the TMP uh trith sulam oxisol
1:40:40and potassium sparing diuretics this
1:40:41will just help you to think about it
1:40:43more pathophysiologically but in true
1:40:45reality often times it's about
1:40:48discontinuing the ineds discontinuing
1:40:50these drugs and seeing if the patient's
1:40:52potassium start to come
1:40:54down often times these causes of hypo
1:40:57odinism especially drug related it is
1:41:00worsened if a patient has any dimunitive
1:41:03or decreased GFR because they lose their
1:41:06clearance now now if the GFR is really
1:41:08low all right really low let's go with
1:41:11the you know concept of that they're at
1:41:13least ckd3 or worse so if they're
1:41:15getting to like less than 60 then I
1:41:18would start being a little bit more kind
1:41:19of
1:41:20concerned now this is usually going to
1:41:23be a CKD or an acute kidney injury in
1:41:26this particular scenario before you even
1:41:28say okay that's it I guess it's just
1:41:30either this or this think about trans
1:41:33cellular shifting causes so you have to
1:41:35really think about history to depend
1:41:37upon these has the patient had recent
1:41:39beta blocker or deox in use have they
1:41:41had a recent seizure or Crush injury
1:41:43check their CK level if that's elevated
1:41:46that could suggest potentially a rabdo
1:41:49if they had recent chemotherapy for any
1:41:51kind of hematological malignancy okay
1:41:53cool check the uric acid check their
1:41:56phosphate and LDH and see if those are
1:41:58elevated and then lastly do they have
1:42:00recent anemia or jaundice okay check
1:42:03their LDH their haptoglobin and a CBC
1:42:06and a smear to look to see if there's
1:42:08any schistocytes and reduced hemoglobin
1:42:10hematocrite those can help you with the
1:42:12shifting causes but basically look at
1:42:15their GFR if they have a severe kidney
1:42:17injury it's likely this if it's mild or
1:42:20normal think about your hypo aerone
1:42:22states and and then don't forget to rule
1:42:24out the transcellular
1:42:26shifting last thing is if a patient has
1:42:28an acidosis present any kind of acidosis
1:42:31that is a very common trigger for
1:42:33hyperemia all right let's now treat the
1:42:36patients low potassium and high
1:42:38potassium if a patient has a low
1:42:40potassium how do we go about treating
1:42:42these patients often times oral
1:42:44potassium potassium chloride potassium
1:42:46bicarbonate are very very common
1:42:48anything through the gut is great
1:42:51however there is specific times where I
1:42:52would maybe supplement with IV over oral
1:42:56the reason for oral is when the
1:42:57potassium is greater than three so it's
1:43:00less than 3.5 but it's at least greater
1:43:02than three or at least they have no ECG
1:43:05changes and that's really important
1:43:07because then you have time to allow for
1:43:09that to get properly absorbed and again
1:43:11the purpose of this is just to replace
1:43:12the pottassium that's being lost that is
1:43:15key you're just rep replacing the
1:43:16pottassium that's lost you're not
1:43:18treating the underlying cause of hypoa
1:43:21you always have to treat the underlying
1:43:23cause to prevent
1:43:25recurrence now one really high yield tip
1:43:29is that if a patient has a potassium
1:43:31let's say of
1:43:323.2 and you give them 40 mil equivalents
1:43:36of potassium you're going to increase
1:43:38their potassium by
1:43:400.4 so every 10 Mill equivalent will
1:43:43increase their potassium by .1 mil
1:43:45equivalent that's very important you
1:43:47could get a question on that in your
1:43:49exam now that's oral when do I go to IV
1:43:52IV is when the pottassium is less than
1:43:54three or they have ECG changes what are
1:43:57the ECG changes any kind of like super
1:43:59ventricular tacac cardia sinus acoc
1:44:01cardia vtac or they have ECG changes
1:44:04such as What U waves flattening of the
1:44:07t-wave sometimes even inverti waves SD
1:44:09depressions give them IV
1:44:12potassium now the other thing that's
1:44:14really important is you can give them
1:44:16potassium but if they have
1:44:18hypomagnesemia you have to give them
1:44:20magnesium so you give them magnesium
1:44:23because it's going to continue to occur
1:44:25where they keep dumping potassium into
1:44:27their urine you are basically trying to
1:44:30prevent excessive potassium loss from
1:44:32the kidney because by giving the
1:44:34Magnesium you basically shut down the
1:44:37sodium potassium pump and shut down
1:44:38potassium loss in the proximal conf
1:44:40tubal and you close the ROM K channels
1:44:43and reduce the excretion of potassium
1:44:46there the last thing that you can
1:44:48consider in patients who have chronic
1:44:50hypokalemia especially with an
1:44:52underlying
1:44:53uh adrenal insufficiency uh adrenal um
1:44:56hyperactivity hyper aldosteronism is you
1:44:59can give them aldosterone antagonist
1:45:01because we know that when aldosterone
1:45:02levels are really really high they tend
1:45:04to stimulate sodium reabsorption and
1:45:06potassium excretion if you block that
1:45:09effect you're going to prevent the
1:45:10potassium loss in the DCT so the concept
1:45:13behind this is that here a patient has
1:45:15high aldosterone they're going to
1:45:16continue to reabsorb sodium secrete
1:45:17potassium and protons if you give them
1:45:20spinal lactone or epone you're
1:45:21inhibiting this and therefore you're
1:45:23going to block sodium reabsorption and
1:45:25you're going to block the potassium and
1:45:27proton secretion so potassium will start
1:45:29to build up in the bloodstream so this
1:45:30is good for patients with chronic
1:45:32hypokalemia and hyperaldosteronism all
1:45:35right now let's move on to kind of like
1:45:36looking at this as an approach to how we
1:45:38would treat a patient with hypoa when we
1:45:40have a patient with hypoc cemia if the
1:45:42pottassium is less than three no ECG
1:45:43changes oral pottassium will be fine you
1:45:46may be asked a question how do I know
1:45:47when to give pottassium chloride versus
1:45:49potassium bicarb really it's just the
1:45:51difference of if they have an acidosis
1:45:52or you know an alkalosis that's really
1:45:55it if for example if they have an
1:45:56alkalosis uh I give them pottassium
1:45:58chloride if they have an acidosis give
1:46:00them pottassium bicarb if the pottassium
1:46:02is less than three and they have ECG
1:46:04changes oh that's IV baby now when you
1:46:08give IV potassium you can give ivid
1:46:10pottassium in two forms one is via a
1:46:12peripheral IV problem is if you give it
1:46:15via peripheral IV this can burn and
1:46:17cause fitis so you can only give it at a
1:46:19very slow rate 10 Mill equivalents per
1:46:21liter per hour all right so you can't
1:46:23give a lot of it too fast if you want to
1:46:26give some uh potassium faster then you
1:46:29have to get put in what's called a
1:46:30central Venus catheter and Via this you
1:46:33can now avoid some of that fitis because
1:46:35you're putting this into larger veins
1:46:37you can now push it up to 20 mil
1:46:39equivalents per liter per hour and
1:46:41that's the only time you can push it up
1:46:42this High all right and you're doing
1:46:44this because you want to try to replete
1:46:45their potassium relatively quickly maybe
1:46:47because it's really low or they're
1:46:48having ECG
1:46:50changes if the potassium is still low
1:46:52but the repleting their pottassium
1:46:54what's the trigger to think about what's
1:46:55the Magnesium is it low if it is give
1:46:58them magnesium if they have normal
1:47:01magnesium but they have a hyper Aldo
1:47:03State what do you think about my friends
1:47:06that's when you think about the
1:47:07aldosterone antagonist all right all
1:47:11right what about
1:47:12hyperkalemia in this patient we want to
1:47:14give them calcium gluconate oh okay
1:47:17calcium gluconate for what because their
1:47:19potassium is really high but more
1:47:21specifically they have ECG changes they
1:47:23have Peak T waves they have a prolong PR
1:47:26interval they have a flatten P wve they
1:47:28have a wide QRS complex they're
1:47:30developing some type of concerning sine
1:47:32wave pattern in those situations you
1:47:35need to give them calcium the whole
1:47:36point is you're trying to stabilize the
1:47:38cardiac membrane and reduce the risk of
1:47:40disastrous uh cardiac
1:47:43arrhythmias the concept behind this is
1:47:44actually kind of interesting so let's
1:47:45say here we have a patient with hyperia
1:47:47we know that they are basically going to
1:47:49do what increase the resting membrane
1:47:51potential all right
1:47:53now here's the thing here's the
1:47:56threshold and the reason why this is
1:47:59interesting is in a patient has
1:48:01hyperemia they're never able to kind of
1:48:03completely reactivate their sodium
1:48:05channels what if I give them calcium and
1:48:08when I give them calcium what it might
1:48:10do is is it may take and increase my
1:48:14threshold voltage farther away from my
1:48:17resting membrane potential by doing that
1:48:20I may allow for a better repolarization
1:48:23and then a reactivation of some of my
1:48:25voltage gated sodium channels and if I
1:48:27increase the activity of them I'll
1:48:29reduce the risk of braic cardia Av
1:48:32blocks as well as V fibon
1:48:34ayti that's the concept of calcium
1:48:37gluconate so if they have a high
1:48:38potassium but more specifically ECG
1:48:40changes this is a rapid drug that you
1:48:43have to give it's first
1:48:44line another thing is if they have ECG
1:48:47changes it's actually going to be nice
1:48:48to shift potassium into the cells so
1:48:51calcium will stay stabilize the membrane
1:48:54but you got to start reducing the
1:48:55pottassium in the bloodstream and doing
1:48:56it quickly shifting of potassium is a
1:48:59very quick and efficient way to do this
1:49:02one is we can give them insulin plus or
1:49:04minus D50 why do I say plus or minus if
1:49:06they're hyperglycemic you don't have to
1:49:08give them D50 if they're normal or ug
1:49:11glycemic or hypoglycemic give them the
1:49:13D50 because if you give them insulin
1:49:15they're possibly going to become
1:49:17hypoglycemic why do I give
1:49:20insulin and why do I give albuterol oh
1:49:23wow this is interesting Zach didn't you
1:49:24say that this can cause hypokalemia yeah
1:49:28but in hyperemia wouldn't this be great
1:49:30because why because what these guys are
1:49:32going to do is they're going to help to
1:49:34do what shift potassium from the extal
1:49:37space to the inalar space the concept
1:49:40behind this is that Albuterol and
1:49:41Insulin are going to stimulate the
1:49:43sodium potassium atpases so they're
1:49:45going to pump sodium out in pottassium
1:49:46in and that's going to lower the serum
1:49:49potassium now you see over here there's
1:49:51a little guy here called Ivy by
1:49:52carbonate the only reason we would give
1:49:55this is if they have a pottassium
1:49:56greater than six ECG changes and they
1:49:59have to have an acidosis if they do not
1:50:02have an acidosis you do not give
1:50:04bicarbonate the concept behind giving
1:50:06bicarbonate is that you're giving bicarb
1:50:08to reduce the amount of protons that
1:50:10they have in the bloodstream and if they
1:50:12reduce the amount of protons they have
1:50:13in the bloodstream less protons are
1:50:14moving in less potassium is moving out
1:50:18if less potassium is moving out less
1:50:19potassium will be in the bloodstream and
1:50:22therefore we will have less hyperkalemia
1:50:24so again ECG changes with hyperkalemia
1:50:29calcium insulin albuterol only by carb
1:50:33if they have an
1:50:34acidosis okay that's immediate
1:50:37interventions what about getting rid of
1:50:39the potassium so now that I've done this
1:50:41patient who's come in they have maybe
1:50:43they have a potassium of 6.5 they have
1:50:45some ECG changes I give them calcium I
1:50:47give them insulin I give them Albuterol
1:50:49and then I even give them uh bicarb if
1:50:51their pH is 7.2
1:50:53good but now I got to get rid of the
1:50:55excess
1:50:56potassium so in this situation you have
1:50:58two options one is Loop Diuretics feride
1:51:01torside banide these are great drugs
1:51:04what they can do is is they can use the
1:51:06kidneys to excrete potassium now how do
1:51:09they do that well Loop Diuretics work by
1:51:11basically blocking the sodium pottassium
1:51:13to Chloride Cod transporter but
1:51:15basically they increase distal sodium
1:51:17delivery thide diuretics will block
1:51:20again uh the sodium chloride absorption
1:51:23which will increase distal sodium
1:51:24delivery if you increase distal sodium
1:51:27delivery at the collecting duct guess
1:51:28what happens sodium rushes in and
1:51:30pottassium rushes out and guess what you
1:51:32excrete into the urine tons of potassium
1:51:35so this is a really important thing to
1:51:37think about for diuretics is if a
1:51:38patient has
1:51:39hyperemia maybe they have ECG or maybe
1:51:42they don't have ECG changes doesn't
1:51:44really matter you have a patient with
1:51:46Hyper calmia you have to excrete that
1:51:48potassium from the body you give them
1:51:51this drug ESP especially when their
1:51:54volume overloaded that's a really good
1:51:56reason you don't want to give this to a
1:51:58patient who is a nuic because they don't
1:52:00have the ability to make urine so you're
1:52:01us utilizing a drug for no reason you
1:52:05have to be able to produce urine in this
1:52:06scenario now here's a caveat because uh
1:52:10we actually can use this it's good in
1:52:12patients who have volume overload but
1:52:14what if a patient's uvalic or
1:52:16hypovolemic you give them the diuretic
1:52:19and you follow it up with fluids because
1:52:20you're using the diuretic to excrete the
1:52:23potassium but unfortunately it will
1:52:24cause volume depletion you give them
1:52:27back the fluid to replete the volume
1:52:29that you're excreting out and that's the
1:52:31mechanism there now what if you have a
1:52:35patient who is a nuic um and they're not
1:52:37able to utilize such drug like a Lube
1:52:40diuretic well then you can give them
1:52:41potassium binding resins so sodium
1:52:43polyan sulfonate or SPS sodium zirconium
1:52:47and pomor now these drugs are
1:52:49interesting because again you can give
1:52:51them the same particular scen scario
1:52:53except you can give them patients who
1:52:54don't really have functioning kidneys
1:52:56you can also give it to patients who do
1:52:57have functioning kidneys but you don't
1:52:59want to give them a diuretic um
1:53:01diuretics are going to be more like
1:53:03effective than a pottassium binding
1:53:05resin though now the concept behind this
1:53:08is that you're excreting the potassium
1:53:09via the gut you're having them poop it
1:53:11out so the mechanism is kind of
1:53:13interesting here's your pottassium
1:53:14binding resin often times they'll have
1:53:17sodium and calcium they have catons on
1:53:19them that they liberate these will get
1:53:21absorbed and then potassium ions will
1:53:23kind of beit kind of push into the Lumin
1:53:24here and then bind onto that resin and
1:53:27now you have potassium binding resin
1:53:29here that gets lost into the school
1:53:31stool and then again there's how we kind
1:53:33of drop the potassium inside of the
1:53:35bloodstream so this is one particular
1:53:37mechanism again I would do this in a
1:53:39patient who know as hyperemia maybe it's
1:53:41kind of a mild hyperemia and they are
1:53:43not a or they a are aeric or you don't
1:53:46want to give them a loop diuretic and
1:53:48what do I mean by aerk they uh don't
1:53:50have the ability to produce urine
1:53:53if they do not have the ability to
1:53:55produce urine you're not going to give
1:53:57them a loop diuretic so therefore you
1:53:59can give them one of these drugs and
1:54:01often times it's to bridge them to
1:54:03hemodialysis last case is hemodialysis
1:54:05and we do this in patients who we've
1:54:06tried every type of management possible
1:54:08and they're not getting any better and
1:54:10we're not getting the pottassium out I'm
1:54:11going to remove it from the circulation
1:54:13often times you need access to do this
1:54:15like an AV Fula a graft or a central
1:54:18Venus
1:54:19catheter now this is a lot right there's
1:54:22one other kind of little small little
1:54:25add-on drug that you sometimes can
1:54:27utilize to your advantage especially in
1:54:30patients who have uh particular reasons
1:54:32like
1:54:33hypoaldosteronism if a patient has
1:54:35adrenal insufficiency along with
1:54:37hyperemia you could consider this drug
1:54:40the concept behind is that you're giving
1:54:42them basically aldosterone and
1:54:44aldosterone is going to help to reabsorb
1:54:46sodium and secrete potassium and protons
1:54:48so you're going to turn the kidneys into
1:54:49potassium dumping machines will which
1:54:51will drop the pot potassium now I know
1:54:53this is a lot let's kind of put this
1:54:55together piece by piece you have a
1:54:57patient who comes in the pottassium is
1:54:58greater than six do they have ECG
1:55:00changes okay they do stabilize the
1:55:03cardiac membrane give them calcium
1:55:05gluconate okay you've done that you want
1:55:07to shift the potassium into the cells to
1:55:09get the potassium down quickly give them
1:55:12insulin plus or minus sugar D50 if
1:55:15they're hypo or ug glycemic give them
1:55:18inhaled OB uteral really high doses for
1:55:20these like 20 milligrams um and then on
1:55:22top of that bicarbonate only if they are
1:55:26acidotic after you've done this you can
1:55:28then secrete the potassium out of the
1:55:31body via a potassium binding resin like
1:55:34those drugs that we talked about this
1:55:35SPS the
1:55:37Pomer and then Loop Diuretics is an
1:55:40alternative here often times potassium
1:55:43binding resins is when it's mild or the
1:55:44patient isn't capable of producing urine
1:55:46so use the the colon if they are able to
1:55:49make urine and their their potassium is
1:55:51a little bit higher and on top of that
1:55:53they have hypervolemia this is a great
1:55:56candidate to give a loop
1:55:58diuretic now if they have no ECG changes
1:56:00you don't have to stabilize their
1:56:02cardiac membrane and quickly shift you
1:56:04just need to go ahead and get the
1:56:06potassium out of their body and this
1:56:08would be the mechanism if all of this
1:56:10fails and you still have this particular
1:56:13issue then you can go to hemodialysis
1:56:15another question that happens here is
1:56:17how do I prevent recurrent hyperkalemia
1:56:20because obviously the important thing
1:56:22for every disease is to treat the
1:56:24underlying cause in a patient who has
1:56:26recurrent hyperemia look for particular
1:56:29drugs or inciting agents ineds ACE
1:56:32inhibitors arbs potassium sportics trith
1:56:35suth oxisol if a patient has a kidney
1:56:37injury and they're taking these you
1:56:39should hold these for a little bit and
1:56:41restart them when the kidneys have
1:56:44improved again lastly if a patient has
1:56:46refractory hyperemia their kidneys are
1:56:48really really badly injured and they're
1:56:50not able to produce any urine and so
1:56:52none of these mechanisms are working or
1:56:54the potassium binding resin isn't
1:56:55cutting it that's when you're going to
1:56:57have to go to
1:56:58hemodialysis all right my friends that
1:57:00was a monster of a lecture I really hope
1:57:02it made sense I hope that you guys
1:57:03enjoyed it love you thank you and as
1:57:05always until next time
1:57:10[Music]

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