Metabolic Alkalosis

what's up ninja nerds in this video today we're going to be talking about metabolic alkalosis before we get started though please continue to support us by subscribing hitting that like button and commenting down in the comment section all right ninja nerds let's get into it all right ninjas let's talk about the etiology and pathophysiology of metabolic alkalosis so i like to the easy way i like to remember them in my head is is the person volume down and if i give them some fluid they're going to respond to that and improve or are they kind of normal volume or volume up and if i give them fluid it's not really going to make a difference it's not going to help them at all so that's kind of the way i hel it helps me to separate my etiologies so if the person is volume down they're losing some type of volume somewhere and the first one i like to think about are they vomiting if someone's vomiting you're losing a lot of volume and they'd be pretty responsive to fluid bolus so why would vomiting first off be a cause of metabolic alkalosis it's actually relatively simple right when you vomit what are you getting rid of from your gi tract protons right because in your actual stomach you have tons and tons of hydrochloric acid and so you're spilling out tons of protons from the gi tract as you spill out a lot of these protons what happens then as a result of the ph within the the body well the ph will then start to increase there's also some other mechanisms in here you actually kind of reabsorb a little bit more bicarb as a response to this i don't want to go crazy into detail but you do actually reabsorb a little bit more bicarb in response to this getting rid of a lot of protons but that's one way if we increase the ph that's causing an alkalosis and the problem is due to an underlying issue with a metabolic change in this case vomiting so vomiting consistent vomiting profuse vomiting exorcist like level vomiting right that could be one potent potential cause but also it could be a way that we're we're doing it where we are actually vomiting for them we're actually pulling that vomit off in situations where maybe they have a bowel obstruction or they have some issue like pancreatitis or they're not able to get that hydro or that food chyme all of that stuff stomach contents moving forward and we have to suction that off what's that called suctioning via an ng tube so we call that ng suction so nasogastric tube suction and this can happen in conditions generally where there's a lot of inflammation right or an obstruction somewhere within the upper part of the gi tract okay so these are two easy causes to automatically think about are they vomiting are you suctioning them a lot via their nasogastric tube the next one that i like to think about is okay if they're not losing a lot of volume from their gi tract are they losing a lot of volume from their urinary system so i go to the renal things and generally one of the most common causes that you see a lot of is that someone is on a loop diuretic or thiazide diuretic so if you have them on a diuretic more commonly loops but we'll say diuretic use so you just gave them a diuretic okay what do diuretics do they pull off tons of fluid right they're going to get rid of sodium they're going to get rid of potassium they're going to pull with it water but if you guys remember from our video on loop diuretics their mechanism of action one of the other issues is not only does it pull water sodium and potassium with it what else does it pull with it protons so guess what else you lose of a lot of in the urinary system particularly in the urine protons and then guess what else they do they actually reabsorb a little bit more bicarb so they excrete sodium potassium water get rid of protons and reabsorb a teensy bit of bicarb what does that do then if you're getting rid of protons you're decreasing your proton concentration you're increasing your bicarb what's that going to do to your ph it's going to shoot that ph up right it's going to cause that alkalosis so diuretic use could be a very potential cause of this more particularly loops less commonly thiazide diuretics the next one is kind of like a a weird one it's there for the sake of being thorough and this is actually a very interesting one so sometimes in people who have chronic respiratory acidosis copd as an example here and people who have chronic respiratory acidosis what is one of the things that they usually just kind of live with as their baseline they have an acidosis they retain a lot of co2 so they don't get a lot of that co2 out of the body because of their underlying obstructive disease and again this is most common in what kind of conditions copders so they naturally get rid of very little co2 and you guys remember your equation that co2 plus water yields carbonic acid carbonic acid disassociates into protons and into bicarb what happens if you actually don't get rid of a lot of co2 and if i were to draw like a blood vessel because they're not getting rid of the co2 what happens as a result of this in the blood you build up a lot of co2 so what happens in this reaction if we use le chatelier's principle if you get a lot of co2 in here we'll just represent like this lots of co2 what happens well then if you increase this it has to shift to the right if you shift it to the right what happens as a result of that you make a lot of protons now you guys are like whoa zach i thought this was metabolic alkalosis believe me it is i'll explain what happens they get a lot of protons that's going to do what a lot of protons will decrease the ph now as a response to that acidosis what does the body do it triggers the kidneys over time right it's a long term kind of compensation but eventually your kidneys will kick in they'll say oh peach is really low i'm going to start urinating out a lot of what protons i'm going to get rid of a lot of protons in the urine and then what i'm going to do is i'm going to try to reabsorb some bicarb and by doing that what happens as a result of this you try to increase the ph to compensate for this chronic respiratory acidosis now here's where it gets interesting and this is why this is a little weird kind of condition but it's something to remember especially if you work in an icu if someone has chronic respiratory acidosis it's compensatory they have that increase in bicarb now you put them on a ventilator you put them on a ventilator and treat their copd once you put them on a ventilator and let's say that you're breathing properly for them that you get rid of some of that excess co2 a little bit better now than they can on their own so now they're on the ventilator and you remove [Music] their co2 what happens if there was a lot of co2 you put them on a ventilator you dropped their co2 levels a little bit what's going to happen now the reaction will shift to the left and now because of that they may normalize or they may go in the opposite direction a little bit but either way the protons now in the blood are going to start to decrease if the protons in the blood start to decrease now the ph will kind of go up and let's just say that there's a resolution of their respiratory acidosis but what's left over what's left over lots of bicarb so their kidneys compensated for them they increased their bicarb you put them on a ventilator got rid of their respiratory acidosis now what do they have left over they have a compensatory metabolic alkalosis that's left over we call this a post hypercapnic metabolic alkalosis that's the cause this is called post hypercapnia metabolic alkalosis and this is a unique case that you see in people with chronic copd you put them on a ventilator get rid of their co2 and then they still have this bicarb from their kidneys compensating so very very interesting situation here okay so we covered for the most part the saline response of etiologies now what i want to do is talk about some of the saline resistant etiologies all right so we have the saline responsive etiologies all right vomiting into tube suction right current actually prior diuretic use and then post hydrocapnic metabolic alkalosis saline resistant ones are less common the saline responses are going to be by far the more common etiologies that you guys really need to remember but we'll still mention some of these so saline resistant the first one is probably on the higher yield but not as common is when someone has a lot of a particular type of mineral corticoid you know your adrenal cortex it makes a very special mineral corticoid you know what that's called it's called aldosterone so aldosterone is a steroid hormone and what do we know about this hormone well we know that this acts on the kidneys right particularly around that distal convoluted tubule collecting duct area and what's the overall response of it the overall response is that you reabsorb sodium okay which pulls water with it so that would be kind of the mechanism here is that you would pull sodium into the blood you pull water into the blood and that may kind of increase your blood volume and as a response increase your blood pressure right the other thing is you get rid of a couple things you get rid of potassium you get rid of bio protons and so because of that you're getting rid of some of these acid molecules and the other thing is there's a teensy bit not a ton but there's a teensy bit of bicarb reabsorption so if you have a combined effect where you're getting rid of a lot of protons that's going to decrease the protons within the blood what will that do to the ph that'll increase your ph right you're increasing a little bit of your bicarb reabsorption what's that going to do that's also going to increase your ph okay but this is more pronounced because this can be relatively normal whenever there's normal aldosterone levels but what happens if i jack up my aldosterone levels i jacked that sucker up now and i got blasting aldosterone levels all over the place now what's going to happen i'm going to reabsorb more sodium more water have more higher blood volume higher blood pressures i'm going to reabsorb a little bit more bicarb than usual i'm going to increase that ph and i'm just going to start urinating out like a crazy man tons of these protons which is also going to increase my ph that could be a potential ethiology not super common but still something to remember so what would this be called here when you have tons of aldosterone well here's what we've got to be a little bit careful right because you can have what's called hyper aldosteronism and this can be due to many different things so the the first thing to remember is is it primary so is it an issue with the adrenal cortex and so if it is an issue with the adrenal cortex we give that a particular name it's called conn syndrome and it's important to remember that this is a primary cause it's an issue with the adrenal cortex most likely just a big old goombach or tumor here that's just blasting out aldosterone okay the second thing is you want to remember is this a secondary cause is there something that's eventually leading to higher aldosterone levels these ones are a teensy bit more common but secondary issues would be something like renal artery stenosis and i'll explain why the third one could be if someone has chf or maybe even cirrhosis will kind of combine these two and explain the mechanism really really briefly so think about this very very simply your kidneys they depend upon a lot of you know decent amount of blood flow they need blood flow in order for them to function right so what happens is what if somebody has an issue where they have renal artery stenosis or they just don't have a lot of blood flow coming to the kidney right in chf cirrhosis something like that if there's decreased blood flow whether it be due to a blockage or just not enough blood how do your kidneys usually respond to that decrease in blood flow what's that hormone that they release renin so the kidneys will then release a particular hormone here called renin and what does renin do we're not going to go through this entire cascade but you know that it eventually leads to angiotensin ii production what does angiotensin ii do stimulates the adrenal cortex to make aldosterone if i make more aldosterone than the usual what's going to happen i'm going to produce the same effect over here just secondarily it's not the adrenal cortex that's the problem it's a secondary issue that's causing the adrenal cortex to make a lot of aldosterone and that's usually due to these are two relatively common causes okay so either way increase in renin increase in angiotensin ii increase in your aldosterone production okay so what i want you to remember here is that these are what's called secondary causes and these are kind of a little bit more of those common ones that you guys want to remember the last one and i really don't want you guys to get too crazy on this one get bogged down on it but there's actually what's called a pseudo hyperaldosteronism it seems like there's a similar issue where there's a lot of aldosterone but actually it's an underlying issue related to something else let me explain what i mean sometimes if people have very high levels of cortisol you know there's a condition called cushing syndrome they have cushing's syndrome whenever there's high levels of cortisol cortisol can act similar to aldosterone and it can other mechanisms as well we're not going to get too crazy into the into the weeds here but it can act similar to aldosterone and cause an increase in the ph by absorbing some bicarb and getting rid of protons in the urine so cushing's syndrome can kind of look like aldosterone but there's no increase in aldosterone it's an increase in cortisol and that increase in cortisol is kind of mimicking that effect so that's the overall thing and the last one here is if you could put someone on a drug that is like aldosterone like fluids or cortisone so that's the kind of medication that you give to people whenever they're kind of hypotensive but either way these are the big big ones that i really want you guys to remember primary con secondary renal artery stenosis chf cirrhosis and then pseudo-hyperaldosteronism cushing's syndrome i think that's good enough all right the next saline resistant kind of etiology i don't want you guys to get bogged down in the details but i want you to know the conditions and then how they kind of basically work these two are called barter syndrome and the other one is called gittleman syndrome you probably need to know this probably because someone's got a name on it that's why but the basic thing i want you guys to remember is that barter syndrome acts as if someone's kind of like on a loop diuretic so if you guys remember loop diuretics do what you get rid of a lot of sodium you get rid of a lot of potassium you get rid of a lot of water but what else do you get rid of a lot of protons and a little bit of bicarb reabsorption and either way if you're getting rid of protons and you're reabsorbing bicarb what's the overall effect you're increasing ph all i want you to know is that this is if someone's on a loop diuretic so bl gittleman syndrome is if someone's on a thiazide directive but the overall effects the same they get rid of sodium they get rid of a little bit of potassium they get rid of water they get rid of protons and they reabsorb a teensy bit of bicarb and this is if someone was on a thiazide diuretic okay that's really all i want you guys to know the big takeaway is that bl barter acts like if someone's on a loop gt gettlemen acts like someone's on a thiazidiretic either way they can cause metabolic alkalosis all right so the next etiology here is that i want you guys to remember hypokalemia so hypokalemia basically there's just kind of this like shifting of potassium and usually protons so what happens is is whenever there a patient has hypokalemia this can happen in the proximal convoluted tubular cells this can happen in other cells in the body but in the pct particularly when someone has hypokalemia what happens is they spit a lot of these protons out into the urine from that shifting of this potassium proton exchanger and then they bring in some of these potassium ions and so in hypokalemia it's people can get rid of a lot of protons in their urine if you get rid of a lot of protons in their urine what happens to the proton level in the blood well the proton level in the blood is going to decrease and so because of that if you decrease the amount of protons present within the blood that's going to cause the ph to kind of jack up there right so this can cause a metabolic alkalosis and this can happen kind of as other cells in the body where there's shifting of potassium and protons as well so these are that's the big one the last one i want you to remember again not a super common one but again to be thorough here sometimes if someone is receiving some type of alkalitic material or alkalotic material exogenously and one of the big ones that sometimes is given for multiple different reasons especially if someone is in acidosis they have kidney failure a couple other reasons high icps you can give them what's called sodium bicarb and if you give someone a lot of this sodium bicarb what are you giving them you're giving them bicarbonate and if you give a lot of bicarbonate what's that going to do to the ph it's going to jack that ph up right and so sometimes whenever people are getting sodium bicarbonate infusions like a lot of what's called exogenous alkali that could also be a potential etiology here for someone developing a metabolic alkalosis all right so this covers our etiologies our pathophysiologies now let's kind of do like a little diagnostic workup of metabolic alkalosis all right so metabolic alkalosis it's it's really a straightforward diagnosis i mean you can pretty much say okay let's say i order an abg on a patient i could right but what would make me want to order an abg well let's say that i got a bmp on somebody a basic metabolic panel right and when i got their basic metabolic panel it came back and i saw that their bicarb was abnormal right so you know when you get a bmp it kind of should give you a couple different things right so it should give you someone's sodium it should give you someone's potassium it should give you their bun their blood urea nitrogen their glucose should give you their creatinine it should give you their bicarb and it should also give you their their chloride levels okay so what i want to do is is let's say that i look at this and i see that the bicarb is off a little bit right maybe their bicarb is elevated okay if i see that their bicarb is elevated that may make me say okay maybe there's something going on maybe they have an acid-base disorder let me get an abg all right so we get the abg when we get the abg this is what we get back here right our ph we see it's going up right why because it's greater than 7.45 our pco2 is what well normally that's 35 to 45 that's within a normal range right so normal range bicarb is what that's like 22 to 26 this is above 26. that's high that's going in a different dirt it's going way higher than it should be and then oxygen is within its normal range 80 to 100 millimeters of mercury so it's normal oxia so if i see that the ph and the bicarb are moving in the same direction what does that tell me then that tells me that there's a primary metabolic alkalosis so in this case here i can already tell that this person has a primary metabolic alkalosis and i don't really see much of the respiratory compensation present here because usually what would happen well if the ph is going up what would you want to do to your co2 well you'd want your co2 to do what you kind of want that to start kind of going up right because you want that to compensate you want there to be more co2 to make the environment a little bit more acidic but i don't really see much respiratory compensation here okay so we went through that we've gotten our bmp we saw that there was kind of an abnormality within the bicarb we got our abg it showed primary metabolic alkalosis no true respiratory compensation we're trying to figure out now okay what's the cause this is where i go to that next thing volume status are they saline responsive are saline unresponsive and you know resistant in this case so the saline and responsive are going to be your more common causes remember i told you that and what do you what can you do it's a something that's very very simple if someone's in the hospital or you're just asking them maybe you look at their eyes and o's their eyes and noses their intake their output it gives you a good idea of their overall volume status in the hospital sometimes it's a simple thing as asking them as well if i looked let's say on my chart and i saw oh geez here's my output and this brown is representing vomiting or gastric residual that they've been suctioning off of the patient if that's the case and they're pulling off a lot of there's a lot of vomit or there's a lot of ng ng-tube suction here that they're pulling off a ton of residual oh that could be explaining why there's more output than there is input their volume status is down that could be one of the etiologies there the next thing is i could say okay what's their urine output looking like or i could ask them how's your urine output have you been peeing a lot i look here and i say oh dang they're putting out a lot of urine you're urinating all the time if there's way more urine output than there is intake that's definitely going to lead to a volume depletion so there's an increase in the volume of urine right and what could that make me think are they on a diuretic or is there some other thing that's causing them to get rid of a lot of this urine and that's something i got to think about but one of the things that i talked about with the etiologies is what diuretic use so that could be one way i could look at this and then here's your kind of your example where it's relatively normal right there's nothing abnormal there maybe they have that post hypercapnic metabolic alkalosis and you just gotta look do they have a history of copd and are we putting them on a ventilator and correcting their co2 so it could be something as simple as that so volume status will help you a little bit the next thing that also can help you a little bit with those saline responsive and resistant etiologies is to check a urine chloride so i look at their volume status their eyes and o's or ask them the questions simply and then i check a urine chloride the urine chloride is pretty good because if the urine chloride comes back and let's say that it is less than 20 that is usually more indicative of a saline responsive etiology if i check their urine chloride and their urine chloride is greater than 20 that usually is indicative of more of a saline resistant etiology okay so that's the other way i could go about doing this i check their volume status i check their urine chloride and you can check volume status in a bunch of other ways right you could check their mucous membranes you could check their skin turgor you could do an ultrasound of their inferior vena cava there's a lot of different ways of doing it but you just want to know are they having a decreased volume what's their urine chloride that'll help me to figure out their etiology because then once i do that and i say their volume down they have a urine chloride less than 20 i go in i say what's going on are they vomiting lots of suction or are they on a diuretic or do we have them on a ventilator and they have chronic copd and i figure out their issue and i address that issue and treat it the next one's a little bit more complicated and this is the less common causes i told you right the ones that it's not going to be like you find you find an abg and it cracks the case and you're like oh this person has a problem with their their you know their aldosterone system no they're not going to do that it's not going to bust open the case maybe who knows but the whole thing is let's say that you do this you run through it you get the abg you find a metabolic alkalosis their volume status is relatively normal they're urine chlorides greater than 20. they don't have any of these problems here then what you do is you check and say okay what's their blood pressure i want to know that so i check their blood pressure if the blood pressure is high they have high bp okay high blood pressure that's going to make me kind of like a little interested like maybe they do have this like weird aldosterone problem because remember what aldosterone does it increases sodium water reabsorption increases blood volume increases your bp so i may start being a little curious in saying okay let me look at other things so it would make me before i start going into the plasma aldosterone renin ratio here a plasma renal adoption ratio let's say this i did think that there was an aldosterone problem what is something i told you i can get from the bmp and start having a little bit more suspicion if i think that this is an aldosterone issue what else does aldosterone do besides increase your sodium and your water reabsorption one of the things i may say is they have high bp their urine chloride is greater than 20 normal volume status but they have high sodium in the blood they have hypernatremia what else does aldosterone do it gets rid of potassium so all their potassium be on the bmp it'd be low so they may have a low potassium and then also we would get their abg showing metabolic alkalosis and their blood pressure is high if i do that so i have a high blood pressure high serum sodium low potassium urine chloride greater than 20 i start thinking about potentially an issue with the aldosterone system how do i go about this it's very very straightforward remember we said that there was a primary type a secondary type and then a pseudotype and these are the only ones that i really wanted you to remember primary was conn syndrome the problem was the adrenal cortex was making a lot of aldosterone so what would the aldosterone be the aldosterone levels would be high now remember when you have lots of aldosterone you reabsorb lots of sodium you reabsorb lots of water so what happens to the blood volume so now think about it like this think about your diagram here you get a lot of sodium you get a lot of water what happens to the blood volume that you have now that would be going to the kidneys would it be a lot or would it be a little we have a lot more sodium and water so your blood flow is going to increase does blood flow increasing blood flow does that stimulate wren and release or inhibit red and release it's not going to cause rendering to be released because you have normal blood flow so what will happen to the renin levels they'll be normal or they'll be lower so because of this the renin levels you won't be making a lot of renting so we'll just say to make this easy they'll be low random levels straightforward right secondary what was the problems it was a renal artery stenosis that was blocking the blood flow or it was the the the heart was failing or the liver was failing and you just didn't have enough circulating blood going to the kidney either way there was decreased blood flow if that's the case then what did we say that did a decreasing blood flow to the kidney did what it caused rain and release right so use your diagram here caused random release so there was a decrease in blood flow that's going to lead to an increase in the renin production okay so renin production will increase what does renin do activates angiotensin 2 angiotensin 2 activates what aldosterone so what will happen to the aldosterone levels they'll go up right so it'll signal your adrenal cortex and say hey buddy start popping out some aldosterone and the aldosterone levels will go up difference in the ratio okay this last one though it had nothing to do with the person having a problem with their aldosterone system right so it wasn't an issue with aldosterone it wasn't an issue with a renin what was the problem that i told you the main one i wanted really wanted you to remember cushing syndrome so in cushing's syndrome how do you work this one up you order a what a cortisol right you check their cortisol levels so you check an am cortisol level and usually in this situation what is it it's high and then you can also to figure out where the cause of it is is it pituitary is it like a tumor in the lung or is it an adrenal problem you can also check out their acth levels to see if the acth is high coming from the pituitary if it's low it's coming from the adrenal cortex right so that's the next thing you could do to isolate if it is a cushing's but i think this really gives you an idea of how to go about figuring out that those rare causes okay so that covers that and helps us to really understand these etiologies now let's talk about the treatments of these issues all right so let's talk about treatment treatment of metabolic alkalosis is relatively straightforward because again that's why this condition is in a lot of the acid-base disorders it's really primarily dependent upon what is the etiology what's the path of fizz what's the cause if you figure that out you just treat the underlying cause it's straightforward right if someone's vomiting a ton what can i do i can give them an antimatter but i should try to figure out what's causing them to vomit but if they're having a ton of vomiting and i want to treat that vomiting i can give them an antimatter okay to try to reduce the vomiting that will reduce the amount of protons that they're getting rid of from their gi tract and help to prevent some of that that alkalosis the other thing i could do is that maybe we can't control that maybe it's the suctioning part right so you're having somebody who you're trying you're having to suction them a ton and you're pulling off a lot of their hydrochloric acid it's simple decrease the ng tube suctioning frequency if possible or the amounts that you're having to pull off that may decrease some of the alkalosis the last thing is let's say that you can't really do you know these things aren't working sometimes what you can do is you can actually decrease the amount of hydrochloric acid that you're actually producing so if the person is vomiting or you are suctioning off a lot at least you're not pulling off a ton of protons from their gi tract so the last thing that you could do is you could actually give them a proton pump inhibitor to try to decrease the hydrochloric acid production in the stomach and if you decrease the hydrochloric acid production in the stomach even if they do vomit or they suction you're not pulling off a lot of protons so it's a simple way of going about that so that's the saline responsive one right the next saline responsive one kind of comes down to this diuretic problem right we said if we have someone on a diuretic they're on a loop primarily loop sometimes thiazide you're pulling off a lot of volume you're pulling off protons and because of that you're causing this alkalosis what could i do maybe if you do need to direct them and you do need to pull off fluid because they have pulmonary edema for some reason you just have to decrease the dose maybe a little bit so the first thing you should try to do before discontinuing it is decrease the dose maybe that'll work the next thing is so decrease dose of particularly we'll put a loop diuretic that's the more common one the next one is you might just have to stop the actual diuretic so stopping the loop diuretic because maybe it's just pulling off too much of those protons and you're just reabsorbing too much bicarb now here's the next thing what if you have somebody that you you have to you've directed them okay you've dropped their volume down and you've caused this out this alkalosis what could i do to try to fix these situations here well one thing i could honestly do is just give them fluid back so i could actually give them fluid just like in this situation if someone's vomiting or they're having a lot of suctioning i should give them fluid back so that's one thing we could do here but also with someone who's on a diuretic or they're losing a lot of fluid give them sodium chloride back how do i give them that i give them saline infusions so maybe what i'll do is i'll just have to give them iv saline infusions right so i'll give them a couple boluses of fluids particularly what like your normal saline right so your 0.9 normal saline infusions and by giving them back what that's going to do is it's going to give them back volume and also normal saline has a little bit of an acidotic property to it so it actually may reverse a little bit of that alkalosis here's the problem though and this is what i really really want you guys to remember if someone has you've diuresed them for whatever reason maybe you were diuresing them because they had pulmonary edema and their cause for the pulmonary edema was this they had some type of cardiopulmonary disease of some kind right so maybe they had chf and that chf was causing some of that fluid to back up into the lungs causing pulmonary edema or maybe they have underlying cirrhosis maybe they have some problems with their liver so they have some underlying cirrhosis and maybe because of that they less common but in cirrhosis there's a decrease in the level of albumin remember that albumin maintains oncotic pressure or osmotic pressure within the blood vessels if there's less of that more of that fluid is going to leak into the interstitial spaces causing pulmonary edema either way here's the problem in these people if you have to direct them to pull off the fluid because it's causing their pulmonary edema right and then you have to give them fluid back maybe they're volume they're intravascularly depleted because they're third spacing a lot of that fluid but you have to figure out a way to give them some type of volume what could i do well i could do a couple things one thing i could do is in these kinds of conditions so if someone has chf or they have cirrhosis and i diurese them but i want to give them back fluid because they're intravascularly depleted i don't want to give them a lot i can do two things one is i can give them small boluses of fluid okay so maybe 250 ccs to 500 ccs at a time because i don't want to fluid overload them and cause pulmonary edema again the other thing that's become a little bit more utilized in some way shape or form is actually giving them other types of diuretics so potassium sparing diuretics so potassium sparing diuretics have been seen to be somewhat beneficial like spirinolactone is one and the other one that's also utilized because it doesn't pull off as much fluid is acetazolamide so acetozolamide and sometimes with the potassium sparing duratix they like to give this with potassium chloride as well so like chlor-con tablets and stuff like that so again what could you do if you need to kind of they have a person who has metabolic alkalosis and you've given them diuretics for these conditions they're volume depleted and you have to give them volume back small boluses potassium sparinderetics and acetozolamide the last really really it's very weird but sometimes not joking you can actually give people hydrochloric acid infusions and sometimes that may be somewhat beneficial so these are kind of the big things that you can utilize in these scenarios okay a big thing though for the diuretic is just either decreasing it stopping it and giving them some fluid back if you can't give them the fluid back because they have an underlying condition give them small boluses or try these methods let's talk about these last et treatments for these underlying ethiologies all right so now let's talk about the treatments for issues with the aldosterone system right the saline resistant type so with this one the whole problem regardless if it's a primary or secondary type of issue is that there's a lot of aldosterone right and the causes of these are something that we need to know because if we know what it is we can treat it if it's a tumor if it's a big old goombak there that's sitting there what can we do with that well just cut that sucker out right so what would that be called you could either do a tumor section sometimes they may even just remove the entire entire adrenal glands or doing like an adrenalectomy or some type of tumor resection sometimes you try medical management so you're giving drugs that are going to basically oppose aldosterone and so what are drugs that oppose adoption are basically block its effect of the peripheral tissues one is going to be spironolactone and the other one is a pleurinone okay these basically are blockers of adoption so they're going to block the peripheral tissue effect of it okay so now that we know that this could be for like particularly for primary hyperaldosteronism what about for secondary hyperedonism so if someone has like a renal artery stenosis or they have chf or they have some type of cirrhosis or some kind of problem like that you treat the underlying issue if it's renal artery stenosis what do you go you go in there and you kind of angioplasty a balloon or put a stent into that renal artery to improve the perfusion to the kidney or treat the underlying chf if they have a cardiac disorder treat their cirrhosis and that should improve their underlying secondary hyperaldosteronism all right the next one that i want you guys to know here is like you know not super super important to remember but just to be thorough here is barter and gittleman syndrome right these ones uh it's very very interesting kind of the way that they work how you treat them it's very interesting so barter syndrome gilman syndrome either way this one acts like there's like someone's taking a loop diuretic this one's that someone's taking a thiazide diuretic either way those what happens is they cause you to waste sodium in the urine low sodium is a stimulus for aldosterone production aldosterone is going to do what was going to absorb more sodium more water and then you're going to excrete potassium and excrete protons and have a little bit of bicarb reabsorption as a result of that that's going to be kind of a secondary hyper aldosteronism in a way right so give them drugs that block aldosterone like spraying a lactone or a plarinone right so we can give them spirinolactone or we can give them a polarinone to just basically oppose that secondary hyperaldosteronism now the next thing here is that if someone has uh high cortisol levels we said that this could be like a pseudo hyperaldosteronism right so sometimes like a pseudohyper hyperaldosteronism that it's not actually a lot of aldosterone is what we said it's cushing's syndrome related right like cortisol high levels of cortisol well high levels of cortisol this isn't meant to be an endocrinology lecture but basically where's the problem with that it could be a problem with the pituitary gland right so the pituitary's making too much acth and if you're doing that what is it going to do it's going to cause the adrenal gland to make a lot of cortisol cortisol is going to act like aldosterone and have that metabolic alkalosis effect what do you do you get rid of the pituitary gland right so you can do what's called a trans sphenoidal resection of the pituitary particularly that adenoma that may be causing it what if it's an adrenal problem so if it's an adrenal problem what do you do you just maybe you have to cut out that adrenal lesion maybe they have an adrenal tumor so there could be some type of adrenal tumor resection and then the last thing is that sometimes this could even be related to what sometimes it could be someone's taking a lot of corticosteroids if they're taking a lot of corticosteroids you may just have to decrease the dose so this could be what's called an exogenous type of effect from taking tons and tons of exogenous corticosteroids decrease the dose of their exogenous steroids and the last thing is sometimes you can give medical therapy to basically block the effect of cortisol in the peripheral tissues and this could be things like ketoconazole or another one which is called meteropone and these basically just basically block the effect of cortisone in the peripheral tissues either way you fix the underlying issue that's going to help to resolve the metabolic alkalosis so this gives us everything that we need to know about metabolic alkalosis all right engineers so in this video we talk about metabolic alkalosis i hope it made sense and i truly hope that you guys did enjoy it alright engineers as always until next time [Music] so [Music] you

Channel: Ninja Nerd

Views: 25,955

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science

Id: rgLvalw-bqM

Length: 40min 29sec (2429 seconds)

Published: Mon Jun 07 2021