welcome back to the ninja Nerd video podcast today we're going to be talking about acidbase disorders Zach how pumped are you I am so excited it's going to be amazing it's going to be a lot of fun we're going to have a few cases well five to be exact yeah uh it's going to be what Zach metabolic acidosis but agma nagma yep exactly metabolic alkalosis yep respiratory acidosis some respiratory alkalosis that's you hit it nail on the head Buddy it'll be a little bit of a longer one I think it's going to be long but we're going to make it fun we're going to make it enjoyable and I think that at the end of it you guys will know acidbase disorders hands down 100% we're going to just rock their world exactly so let's get right on into it then we're going to start with case one case one being an Gap metabolic acidosis or really agma so we have here a 45-year-old female presents to the emergency department with severe abdominal pain rapid breathing and confusion a little bit more about the history the patient reports that over the past several days she has experienced a noticeable increase in polyurea polydipsia combined with nausea and intermittent vomiting she has also experienced worsening fatigue and dizziness which has escalated over the last 12 hours her intake has been significantly reduced to nausea leading to decreased fluid consumption amidst her increased urinary output past medical history she has typee 2 diabetes managed with oral hypoglycemics and hypertension her medication list she is only on two medications being metformin and linil uh her review of systems going down we have respiratory rapid breathing no cough or we cardio she reports palpitations and GI she has severe abdominal pain nausea vomiting unable to keep fluids down what do you think so far Zach I mean this is definitely and there's her diabetes is making me think about a lot of stuff the fact that she's has some fast breathing she's peeing a lot she's thirsty she's not eating a lot something's definitely going on respectively with her diabetes so I think I already have an idea but I'll wait for some more information so vitals blood pressure is 100 over 65 heart rate is 120 she's tacky uh respiratory rate is 32 per minute that's teyia yeah her temp is 37.6 celsi or 99 .7 F and her oxygen saturation is 94% room air upon her physical exam her General exam she appears acutely ill and dehydrated her neuro exam confused disoriented to time and place respiratory deep labored breathing we note that this is a cus small respir respiration gotcha cardiovascular to uh like we like we talked about just before tacky cardiac with a regular rhythm no murmurs abdominal is uh diffusely tender on palpation no rebound there's no guarding uh skin dry mucous membranes and decreased skin turer so again kind of more so talking about that dehydration yeah definitely like hypmic in nature okay so getting into some pertinent lab testing here starting off first with serum sodium 138 potassium is 4.5 creatinine is 1.5 bu is 30 glucose is 450 oo mama by carb is 12 and ion gap of 30 not too good so far not too good this is not compatible with Life we we'll make her right though we're going to fix her up I hope ABG so when we got when we got our ABG we have a pH of 7.1 pco2 of 18 and a P2 92 millim of mercury okay her lactate is five heeton bodies sign significantly elevated uh and then we have a calculated serum osmolality 330 osmolar gap of 10 okay tons and tons of things to be thinking about here yeah there's a lot I definitely a lot of things it's pretty clear I think of what's going on with her but we'll talk about if there's is there anything else like any other Imaging or anything else that pops so we do have Imaging we have a couple different images here we have an abdominal x-ray normal gas pattern no evidence of obstruction or free air and then a chess x-ray is a clear lung feels normal cardiac silhouette all right so really just within normal limits all right so Zack based upon all these clinical findings we have vitals we have lab testing Imaging everything that we've gotten so far how would you approach an anap metabolic acidosis yeah so I think you kind of set it up perfect for me is that you know if I got an ABG and I see this patient's ABG pH 7.1 she's definitely acidotic um I would look at her CO2 it's definitely low and it's probably because she's breathing super fast so she's super tnic as you pointed out um the P2 is 92 um her bicarb is what kind of concerns me that it's 12 so being that her bicarb is 12 her pH is low um she has a metabolic acidosis her anine gaps greater than 12 so it's an agma so right away what I want you guys to remember when you think about agmas is to think about the pneumonic cult it's a terrible pneumonic but it works in the sense of keeping things very simple for you so k for keto acidosis U for ureic acidosis L for lactic acidosis and T for your toxic ingestions and the reason why I like that is right off the get-go I can kind of assume look at their history look at potential aspects of their physical exam but then I can order the appropriate Labs or if I need to Imaging to go off of this so let's say that we kind of go down this pathway for this patient she has a lot of features that for me suggest dka diabetic keto acidosis she's a diabetic she's maybe taking her oral anti- hypoglycemia or oral medication or anti-diabetic medications potentially um not sure how consistent or compliant she is with it but she's definitely there's got to be some concern there I I have some concern you have to think that there's some non-compliance going on exactly so you can't get to that point where no to have a sugar of 450 I don't know she's either just not sticking with it or she's just going ham and eating like I don't know cupcakes all the time or something like that but there's definitely concern there for maybe some non-compliance her sugar is pretty high she's got elevated Ketone body IES and then again she's got an acidosis if I have diabetes high glucose and an acidosis with ketones I'm thinking dka the other thing though that's weird with this one is we already know that she has dka but here's something else that she has she has likely a lactic acidosis too and I think the lactic acidosis is a byproduct of her dka so I think what happened is she has diabetes she probably was non-compliant maybe eating lots of sugary Foods or whatever it might be went in to dka started having abdominal pain vomiting nausea peeing a lot and because of that she probably lost a lot of fluids became hypovolemic and then developed lactic acidosis so for this patient her lactate tells me that it's elevated and she probably has a combination of lactic acidosis and on top of that she has diabetic keto acidosis if I look for other things here I could also consider is there any evidence of ureic acidosis I'd want to look at the kidney function and the serum creatinine's 1.5 the bu's 30 it's a little bit elevated but it's not that significantly elevated to where I would actually be concerned that the urei was contributing to this at all I would really be looking for a very high bu and I'd be looking for a very elevated creatinine for me to be even considering ureic acidosis and then you wouldn't be thinking at all toxic alcohol ingestion right because that osmolar Gap is not quite where you would need to be exactly yeah you're you're on the money there usually I like it greater than than 10 to even start considering that she was right at 10 yeah and so greater than 10 and then also history would usually kind of like lend to itself some concern here and I don't see any worries for a toxic alcohol ingestion of any sort so for me right off the get-go I think you know metabolic acidosis agma ketones are elevated and she has diabetes dka lactates elevated usually if your lactates greater than to we can consider it somewhat of lactic acidosis I don't think her renal function suggests ureic acidosis and she doesn't have an osmolar Gap that's greater than 10 and I don't see anything in her history to suggest that so that's how I would approach this patient's acma okay all right so I'm just trying to think about this patient overall what would you say Zach is the most concerning of her acidosis and What complications is she most at risk for so for me I worry about her breathing so the fact that she's like breathing I forget what it was 32 yeah 32 that's kind of concerning she's T cardic she exactly so I think the TAC cardia the tipia and even she's borderline her blood pressure is a little bit soft but she's not technically hypotensive and then the confusion the disorientation that kind of confus that that concerns me so I think there's a couple different things that I worry about uh for her but I would say the biggest thing is definitely the respiratory comp compensation so whenever you're acidotic naturally what it does is it triggers your chemo receptors tells them hey I'm acidotic can you tell the actual lungs to breathe at a deeper rate a deeper and breathe faster to blow off CO2 and her ABG suggest that cuz her CO2 is catastrophically low electrolyte imbalances is something I get super concerned with with acidosis though Rob especially if they get really acidotic it changes the movement of protons and potassium in and out of the cell so what happens is if you're more acidotic protons move into the cell and potassium moves out and you can develop hyperemia which can increase the risk of arhythmia so I don't see that on her uh BMP yet but I'll be watching out for that the scariest thing that I notice in an ICU setting though is refractory hypotension and arrhythmias one thing about really really bad acidosis is it can really wreak a lot of havoc on the heart and the blood vessels so when the pH gets really really low your your heart stops Contracting very well so contractility drops and then your blood vessels dilate and so it can actually make a patient a little bit more hypotensive something I noticed working in the ICU is that vasopressor stop working as well so norepinephrine epinephrine all those things that we're supposed to put people on to push their blood pressure up they stop working as well so those are some things that I would really be careful of and I would especially watch the potassium and watch closely on her ECG to make sure she doesn't get any kind of like weird like Peak T waves or prolong Pier interval or widening of the QRS sine wave all of those things so that's something that I would be watching out for but for her it's really the respiratory cons compensation that I'm concerned about as well as the volume depletion as the result of her dka so her hypovolemia is also concerning to me so there's a lot of things we're watching out for especially that hyperemia ECG changes things that could really cause the patient some pretty pretty bad things to happen yeah exactly yeah I mean we're talking about possibly death so a lot of things are concerning but what do we do now at this point we we figured out what's going on we have a really good history all of our tests are in we're we're following this patient closely yeah what do we do now to treat this patient yeah so for this patient it's all about that's one of the nice things about acidbase disorders it's all about treating the underlying cause so you have to just figure out what the underlying cause is and once you diagnose that you treat that for her it's dka so the Frontline treatment for dka is insulin so for her what I would do is I would start by giving her insulin um probably put her on like an insulin infusion um insulin infusion is going to be more closely titrated and then what I would do is I would closely monitor her Ann Gap and so for example if I put her on insulin and I give her fluids to repet the volume that she's lost the fluid will help with improving her volume status it'll help to improve her blood pressure impove improve some of her Tacho cardia and then when I give her insulin the insulin will help to shuttle glucose into the cells and stop producing Ketone bodies and so what I'll notice is I monitor her an Gap it'll start getting smaller and smaller and smaller and smaller to the point where it closes and in other words it gets less than 12 and once that happens I can shut the insulin off I've done everything I need to do so that's the first thing I would do for this patient get her on insulin give her some fluids closely monitor her pottassium and her other electrolytes and then watch her an Gap to see when it closes um a lot of the times people will see oh it's a metabolic acidosis pH is 7.1 give them bicarbonate not necessarily unless vasopressors aren't working and if a patient's on multiple vasopressors sure you can give them sodium bicarbonate but it's never the answer for a diabetic keto acidosis and it's really never the answer for lactic acidosis unless the pH is less than like 7.15 it's just not worth it and you have to treat the underlying cause um and I that would be the big thing for her I would say like a lot of the times after you said you treat the cause you give them sodium bicarb only when it's less than 7.15 people say oh what about dialysis the only indications that you would do for a dialysis is if a patient has refractory acidosis that you treat the underlying cause you've given them bicarbonate and they're still not improving for this patient dka lactic acidosis you give them insulin you give them fluids they'll improve their anti Gap will drop their lactate will close and they will start to steadily improve and you won't have to give them any bicarbonate or do any other kinds of like intervention for this patient so with this patient treating the underlying cause you really can't go wrong and most likely you're going to fix it right away exactly yep yep that's the key that's the key well there's case one we nailed it not too bad I don't think that was too bad right no not too bad let's keep moving through we got the next Case Case two is still part of a metabolic acidosis but this one is a normal an Gap metabolic acidosis anagama all right so we have a 62-year-old male presented to the emergency department with Progressive weakness and difficulty breathing his hisory the patient reports feeling increasingly weak over the past few days accompanied by significant muscle cramps shortness of breath on exertion he also mentions a recent increase in the frequency of urination and thirst which he initially attributed to the hot weather the patient admits to consuming large amounts of anti acids due to Chronic heartburn his past medical history is a chronic kidney disease he's in stage three gird and hypertension medications are calcium carbonate which his Anta acid lenil and mapine review of systems we have respiratory increased work of breathing no cough for we GI frequent heartb managed with over-the-counter meds the the ant acids um msk is muscle weakness and cramps he's experiencing some vitals we have for this gentleman blood pressure is 145 over 89 little elevated heart rate is 88 uh respiratory rate is 24 again a little elevated temperature is 37.1 C or 98.8 F and his oxygen saturation is 96% on R physical exam General we have an elderly male appearing fatigued overall respiratory mild teyia no audible wheezes or crackles cardio regular rate and Rhythm no murmur and msk like we talked about generalized muscle weakness in cramping okay so overall Zack any thoughts so far for this this gentleman I mean nothing's really popping out right away there is some I think again concerns here something's really kind of off with the frequent urination and thirst and I'm not sure this is kind of trying to distract me but the large amount of anas is due to Chronic harpon and I'm not sure what to make of that yet but yeah but yeah hit me with some more let's keep going so some Laboratory Testing we get back we have in order here serum sodium is 138 pottassium is four serum chloride is 112 serum creatinine is 1.8 his bu is 29 serum bicarbonate 16 calcium is uh 10.2 magnesium is 2.1 you get an ABG you get the following of a pH of 7.28 pco2 of 38 and a P2 of 90 uh his serum an Gap is 10 it's within normal limits okay uh hence the name yeah and urine an ion Gap is 20 okay all right so indicative of a decreased ability to excrete ammonium suggesting a renal cause yeah this one's definitely there's more kind of coming to me now with this once I got some of the labs so that was a big red flag right there yeah yeah the uran UR yeah okay uh Imaging we just get a chess X-ray and there's no no issues at all with that okay so Zack let's go ahead and try let's dissect this case let's go through it we have all of the pertinent findings we have the history a lot of things are popping out some red flags how would you go ahead and approach this patient with anagama yeah so a lot of this stuff it's great but I think one thing that I like to look at um based upon a lot of the literature is the urine anion gap so for example if I looked at this patient's ABG it suggests they have an acidosis so the pH is 7.28 the bicarb 16 so that's low so they have a metabolic acidosis but they're an gaps 10 so it's a nagma as Rob pointed out so then for me the next test that is suggested is to look at the urine anion gap the reason why is it tells you is the patients nag ma renally related or is it EXT renally related and that helps me a lot and that's what is important to me because nothing came up in the patient's history that suggested that this was extra renal and that's what was kind of weird for me so when I look at here and I see the urine anine Gap is positive and that's what you want to remember is if it's positive that tells me it's a renal cause I remember uh there's a kind of from one of the books that if the urine anine Gap is negative so you can remember negtive so the gut tells you that it's probably from a GI source of of sorts so that's right away the big answer for me urine anig gaps positive it's likely a renal cause so then I got to think about this okay if it's a renal cause there's three potential differentials one is chronic kidney disease two is a renot tubular acidosis type one and three is a renot tubular acidosis type four these are not easy diagnoses to to make um so what I like to do is I like to look at their GF far kind of get an idea or that or some degree of their renal function and then what I like to look at is I like to look at their um their potassium and lastly I'd like to look at their urine pH those three things can give me somewhat of an idea of what's going on with the patient so for example this patient here I'm looking at what's going on I see a positive urine anion gap I see a potassium that's kind of like on the normal range though and I see a creatinine that's kind of just a little bit elevated and a Buu in that's a little bit elevated so for this one right away I'm kind of thinking hey this this could be potentially CKD I don't have a GFR that's listed but for me it could be CKD the other thing is I would have to look at the uh if it's rta1 or RTA 4 rta1 will usually have to have a low potassium so usually the patient would have hypokalemia I don't see any hypokalemia here so that's one thing and then I wasn't given a UR pH so I don't think that this is leading me towards a direction because the UR pH it would actually have to be for rta1 it would have to be greater than 5.5 so they look for a higher urine pH I don't think this is an rta1 I don't think it's an rt4 because rt4 usually has hyperemia so being that being that this patient has a past medical history of CKD type 3 can we just like pretty much assume that yeah so here's that's a good I don't want to ever assume something but like it's pretty much right there in front of you that's the whole thing so you got to Rob made a perfect Point here it's almost impossible to make a diagnosis of rta1 and RTA 4 like he said if a patient has abnormal renal function and that's what Rob kind of hit the nail on the head there that if the GFR is normal you could consider that the patient could have an rta1 or RTA 4 you could entertain that idea but if they have a a diminished or reduced GFR or some abnormal renal function you cannot definitively make a diagnosis of rta1 and RTA 4 so boom nailed it that's what makes me think that this is likely a degree of her underlying CKD that's making me think this if the urine anine Gap was negative you can think negative that would make me think about a GI Source are they having like profuse uh diarrhea because when you have diarrhea you lose a lot of bicarbonate nothing in our history suggest that she's having any type of diarrhea and then if that's the case I could even look at another one called r rta2 and rta2 you would have to have first a negative an Gap but you would have to have hypokalemia and you would have to have an acidic urine urine pH less than 5.5 those things aren't listed here but that's something that I would have to think about so the perfect way you lined it up I check the year Gap it's positive from there renal function does she have diminished yes it's CKD you can't really go any further and say rta1 or RTA 4 and the fact that the earning Gap is positive it can't be diarrhea and it can't be RTA to and and not to mention ta they're pretty freaking rare right they're tough they're tough to make a diagnosis on they're not super common uh they're one of those that are great for your board exam but in real life you're not going to see them too often awesome all right so let's keep moving on with this case then we're almost done with this one we have to now figure out we we figured out all the complications everything we know so far how do we treat this patient for this patient honestly bicarbonate this is kind of the patient where you can probably put them on bicarbonate obviously ideally every disease you have to treat the under disease so improving her renal function if possible but with CKD the damage has already been done so unfortunately when patients have CKD you can't really reverse what's already been done you can just hopefully prevent recurrent injury so if they have hypertension treat that if she has diabetes treat those things um but for her honestly it would just be putting her on some sodium bicarbonate tablets and that would be it if her renal function started going up and up and up and I couldn't get her to improve off the sodium bicarbonate that's when I could consider something like dialysis but often times this is a super straightforward one give her some sodium bicarbonate and treat her underlying disease normalize the ph and you're good to go I think our uh I think our patient suddenly became a a female oh jeez I'm so sorry yep yep yep no that was honestly funny let's move right into case three metabolic alkalosis we have a 48-year-old female presents the emergency department with complaints of persistent nausea repeated episodes of vomiting and generalized weakness history the patient reports that she has been experiencing nausea and vomiting for the past week which she has initially attributed to a stomach bug she also admits to using over-the-counter diuretics recently to help her lose some weight maybe I should try the I should do this I was I think I think she's on to something there buddy all that water weight's gone but now she's in the hospital so who knows I don't know maybe not a great idea the vomiting has been severe with up to 5 to six episodes per day and she has been unable to keep down any food or fluids since yesterday past medical history hypertension and no previous episodes of similar symptoms like this ever before medications she's on hydrochlorizide self-administered she was not prescribed that uh mline for hypertension her uh review of systems GI like we talked about she has severe nausea vomiting unable to tolerate anything oral uh cardio no chest pain no palpitations neuro she does report dizney especially Pawn standing her vitals we have blood pressure 100 over 60 that's a bit soft right there heart rate is 110 she's tacky respiratory rate is 18 her temp is 36.8 celsius oxygen saturation is 97% on room air uh going a little bit further her physical exam uh General appears dehydrated and lethargic cardio Tachi cardic no normal Rhythm no murmurs abdominal is soft non-distended no rebound no guarding but she does have diffuse mild tenderness on palpation uh skin dry mucous membranes decrease skin terer as we talked about she's overall overall dehydrated yeah so we're going to go ahead and get some lab testing now same thing we've been getting for each patient so far sodium is at 140 potassium is at three chloride is 90 bicarb is 36 that's elevated serum creatinine is 1.1 bu is 25 urine chloride is 15 okay what is that Zack low I've never ordered one but yeah usually it indicates that it's low it's usually kind of like a we call it a saline or volume responsive so just it's just not a normal test to get yeah I don't I've never really ordered it but I they did something off the board exams that if you check the eron chloride it tells you if they're going to respond to normal saline or if they're not going to respond to normal saling all right and then the last thing we do is we order an AVG which is a pH of 7.52 pco2 of 44 and the O2 of 98 okay so we have everything we need now to kind of pour through this patient's History exam everything and let's talk complications what is she going through yeah so with her definitely as you said from the ABG 7.5 it's elevated her byy carb is elevated so both of them are going up metabolic alkalosis I think right off the get-go I look at her situation and her history kind of told me everything that's why I don't think a urine chloride is always super helpful but the fact that she's kind of like a little bit tacac cardic she has a softish kind of blood pressure she has physical exam findings that she appears dehydrated like the decreased skin turer and the dry mucous membranes and those kinds of findings that makes me think that she's probably kind of like what's called a hypovolemic metabolic alkalosis and the reason why that's important is because right off the get-go then I kind of think okay where is she losing the volume from where is this chloride Rich fluid coming from and from her it's likely coming from her git not from her kidneys and so it's not Direct itics related there's a rare diseases called barter and gittleman syndrome we see it in kids it's unlikely that so then it kind of just comes down to it's likely GI related and in her it's likely vomiting or if she had like a ball obstruction and she had an NG tube in and they were suctioning out tons of hydrochloric acid that could be another way but for her it's likely all vomiting that's where when you brought up the exam or the uh urine chloride sometimes we can look at the urine chloride and if the urine chloride is kind of low it indicates that they would respond bond to normal saline and these are patients who usually are going to be more particularly on the hypovolemic side so those extrenal ones like vomiting or if they potentially had a recent like a prior diuretic use that could be patients who are going to be a little bit more volume responsive so for her um uh or I'm sorry for yeah her last patient was a him and I called him a her uh so for her this one again it's really important to remember history suggests that it's likely vomiting her exam suggests that she's hypovolemic so from there I'm going to put her into the camp of saying that her likely caus the metabolic alkalosis is the profuse vomiting like an exorcist and that's what I would say her cause is if there was an example let's say they she came in she had a elevated bicarb an elevated pH her blood pressure is up um she has also features of hyperemia maybe some edema maybe like pulmonary edema peripheral edema aites things like that things that are making me think that she's more on the hyperic side that's when I would think about a disease like hyperaldosteronism so that's when I would check the renin levels and aldosterone levels but for her she doesn't have any of those features I think it's a dead giveaway plus patients with hyperaldosteronism they often times have like their pottassium definitely does tank and their sodium often times will go up and so she would have highy bernia and she would also have hypokalemia so for this one I don't think that's likely the case hers definitely suggest it's a hyp ofic and I would think her cause is likely from vomiting is that your way of delineating basically if it's a GI or renal cause so for a GI renal cause you can do it just off history like if a patient says hey I've been on diuretics and I've been using them pretty consistently that would likely be the cause and for this patient was she using oh she was using diuretics wasn't she so for her she actually has a double whammy now that I'm looking at it's almost uh she's losing a lot exactly yeah so for her she actually has two reasons as to why she would have a metabolic alkalosis it's because of the prior diuretic use and on top of that the excessive vomiting so her history would definitely tell me that um and that's what's going to be more important but if you look at the urine chloride the urine chloride is actually pretty low and that suggests that she had some prior diuretics that what she was using or she's been excessively vomiting or having things suctioned from her stomach via an NG tube so I think there's two ways that you can look at if the urine chloride is low it's likely prior diuretics vomiting in tube suction if it was elevated it could be hyperaldosteronism or it could be are they actively using diuretics that is pumping chloride on the urine at that moment and so for this scenario her history gives it away and I think this is definitely a combination of diuretics from the hydrochloride as well as the profuse vomiting okay biggest complications what are you most concerned about hypokalemia I would say be the big one um so so electrolyte imbalances is pretty common with acidbase disorders but pottassium is the most sensitive so in patients who have metabolic alkalosis less protons are being shunted into the cell and L potassium ons are coming out of the cell into the blood so hypokalemia can start to occur so I'd watch those t- waves make sure that they're not inverting or flattening make sure you're watching out for U waves those are some big things respiratory compensation wise I wouldn't say it's a super common one but they could slow down their breathing it's not something I would say that would be all too common one thing I would be careful of is and I just now thought about that is tetany so whenever a patient becomes alkalotic what happens is abum is a negatively charged protein and so it likes to have protons binding onto it if you get rid of a lot of these protons because you're becoming alkalic you have lots of negative charges that are exposed calcium will bind on to all that alumen and calcium levels in the blood will start to deplete and if you have hypocalcemia you can actually start developing tetany so perioral paresthesias the uh what is this called when you tap on the cheek the the CH sign and soine when you pump up the blood pressure cuff and they start developing the carpopedal spasms so those are things I would I would watch out for as well all right so we have a pretty good idea then all we have left is treatment what do we have to do to make sure that we take care of this patient and get her back to to Really her Baseline so that's why was when I was saying before is when you look at the patient if they look volume depleted oftentimes the answer is just to give them like normal saline okay um so I would give them normal saline preferably for this patient she's having like vomiting she's not feeling too well she can't eat or drink appropriately so first thing I would disc continue the diuretics she's she doesn't have hypertension she doesn't need to be on them so I would discontinue that um second thing is I would give her maybe like a liter of like normal saline keep an eye on that see if it improves her blood pressure if it improves her tach of cardia see if she's making good urine maybe check a BMP see if the chloride is starting to kind of come up and the bicarb starting to come down and you can even do a repeat ABG as well if you need to but oft times it's just going to be giving them fluids there is one time where I would be super super careful of giving fluids so let's say that you have a patient this is the only exception let's say that I have a patient who has CHF right or therosis and they're naturally they have lots of edema in that patient if you give them fluids you're going to worsen their edema and so I would have to be very very careful with that that's the only time whereas if I have a patient who a CHF or curosis and I'm continuing to dires them so I'm giving them like Loop Diuretics to get rid of some of their edema what happens is with Loop Diuretics is it gets rid of a a lot of your you know your protons and so it makes you alkalotic but helps to get rid of excessive volume in this situation I would add on acetazolamide to the patient's diuretic regimen if they're hyperemic and they need to get rid of that fluid so I put them on like for example feros amide 40 milligrams and then I would also add on acetazolamide maybe 500 milligrams give that to them and what it would do is it help them to pee out a lot of that basic bicarbonate so it bring the bicarb down but also help them to get rid of the excess fluid and so that's the one kind of scenario where acetazolamide may be helpful another little trick that I've learned is giving them potassium chloride why because what's the most common complication of metabolic alcalosis hypokalemia if you get the pottassium chloride you replate the pottassium you give them chloride it brings the bicarb down so those are two options but most of the time hypmic cases give them fluids back normal saline and then if they're not hypmic they're hyper acetazolamide or potassium chloride would be the answer all right case four respiratory acidosis so only only two left oh baby so for this patient Chief complaint we have a 68-year-old male presents the Ed with increased shortness of breath coughing and wheezing the patient a long standing smoker with COPD reports that his respiratory symptoms have progressively worsened over the past 3 days he mentions increased wheezing a productive cough greenish sputum and marked shortness of breath that has become significantly worse than the day prior okay he uses supplemental O2 at home but has been using it more frequently over the last few days so past medical history COPD diagnosed 10 years ago hypertension in a former smoker 30 pack years however he did quit 5 years ago good for him medications tiotropium cerol and linil for his hypertension upon his review of systems we find respiratory reports increased cough that that green sput production and wheezing cardio no chest pain reports palpitations though and for his neuro no headache dizziness but there is increased fatigue vitals his blood pressure is 145 over 85 heart rate is 102 respiratory rate is 26 which is we're we're we're up there yeah temperature is 37.8 and his oxygen saturation is 88% on two liters of nasal canula oxygen for his physical exam we have an elderly male in respirate distress uh Audible wheezes and coarse crackles on oscilation really noticing some use of accessory muscles upon Him breathing cardio tacky cardic normal Rhythm no murmur and his for his abdominal um exam it's soft non- tender non-distended for some pertinent lab testing we have sodium is 142 potassium is 4.2 chloride is 100 bicarb is 32 bu is 9 19 creatinine is one for our ABG we have a pH of 7.3 pco2 of 60 hello P2 55 Mill 55 millimeters of mercury on 2 liters of oxygen nasal canula all right Zach so a lot of things going on but I think in the history we we've pretty much spelled it all out yeah yeah big time COPD exactly previous smoker accessory muscle use yep what do you think you're seeing here and how do you kind of approach this case I think you kind of said it is it's always for your respiratory problems a lot of acid Bas dis are really any disease itself you require a good history and physical exam but often times for acid-based disorders a history and physical will do you better than any other kind of test would um for this patient I kind of look particularly for example I kind of make a diverging kind of thought process where do they have like an altered mental status is there any underlying neuro deficits or weakness if there is not then I ask myself the question are they having any kind of wheezing or course crackles or Ron ey anything that suggests truly a limited air flow so Airway obstruction of sorts this patient has wheezing as Rob said they're a persistent smoker they've been diagnosed with COPD they're having difficulty with their breathing this tells me it's likely a limited limitation in air flow especially expiratory it's likely an airway obstruction another thing I like to look at is do these patients improve with Bronco dilators and steroids because if they do for example let's say they have asthma they have COPD you give them a chunk of steroids you give them some albuterol as well as some eper Tropi and bromides which are short acting ones that are going to dilate the bronchials if their wheezing improves if their breathing improves and their CO2 starts coming down that could also suggest that this is a lot of Airway obstruction in this patient so that's the way I would look at it this patient is super obvious now let's say they weren't obvious there wasn't anything on their ex physical exam that suggested that there was air flow limitation instead instead the patient was maybe less arousable if you're trying to stimulate them to wake up hey Mr Smith open your eyes hey M Mr Smith look at me hey can you talk to me and they're not really talking to you and they're really really lethargic or obtunded that's what I'm thinking okay something's suppressing their respiratory system that's when I would look at kind of possibilities of drug overdoses so especially if they're not taking any breath so if they're apnic um I would start thinking is this an opioid overdose maybe reverse them with mexone is this a benzo dipene overdose reverse them with flumazenil if they boom wake up and all of a sudden they're breathing normally you've kind of established a diagnosis of an opioid or benzodiazapine overdose but if they're having let's say example you're talking to them and they're less arousable but on top of that they're having neuro like focal deficits weakness on one side of the body then I'm thinking oh shoot could they have some type of like stroke or bleed or something in the vicinity of the respiratory Center that's suppress ing that drive that's when I would say oh they're not improving when I gave them the lockone they're not improving when I gave them flumazenil this is probably not a drug overdose this could actually be something structural in the brain so that's the way I would kind of like form these differentials in my head this one it's a grand slam with as you already suspected the COPD exacerbation with this patient is there anything you're very concerned about I know it's not as scary as like a metabolic concern but is there anything that you're like we have to make sure that we identify it and and figure out what complications are they at risk for yeah I think one thing that I have noticed is that it can cause for example let's say that a patient has COPD they've probably lived at like that Co this patient's probably lived at that CO2 of 60 for a while so they've compensated but in patients who their CO2 really really starts to rise and it gets up there it actually can suppress the um the brain and actually can cause kind of a decreasing level of arousal we call it CO2 Narcosis and so it can cause and so the patient can actually start to become sleepier and more difficult to arouse which is kind of a scary thing but one thing I think that's really important is with respiratory acidosis it actually has been shown to uh to actually kind of cause vasod dilation of the blood vessels and so if you kind of cause that Vaso dilation it can increase blood flow to the brain so if a patient let's say has a bleed or a stroke or some kind of like tumor inside of their brain and their ICP is already elevated and they're acidotic it'll dilate the the blood vessels push more blood into the brain it'll increase their ICP even more so those are one thing I'd say having an intracranial disease and having respiratory acidosis is not a good thing for high for ICP issues so that's one thing the other thing I also like to look at for respiratory acidosis their kidneys so for metabolic problems we either breathe faster or slower depending if we're acidotic or alkalotic so acido you breathe faster alkalis you bre slower for a respiratory acidosis what you'll actually do is is your kidneys will say okay okay I need to do what okay well my pH right now is too low I need to retain bicarb and so what you'll notice is in patients who have chronic respiratory acidosis is their bicarb will be higher and higher and higher as a way to compensate for their respiratory acidosis so that's something that I also like to look for in these patients if I see a high bicarb and respiratory acidosis it probably tells me that they've been dealing with this for a long time but I'd say the big thing is ICP all right so let's wrap it up here we have to figure out how do we go about Tre treating this patient with respiratory acidosis so I think we kind of lended to that that topic and that discussion within the Diagnostics right in the sense that if a patient has COPD or asthma exacerbation their problem is Bronco constriction what do you have to do Bronco dilate them best thing to do is to give them steroids so methyl pricon is a good one especially if they're having a hard time breathing you don't want them to be trying to take a pill like prazone orally so methyl pricon IV give them a good slug of that 60 to 125 milligrams is usually the the goats we'll talk about that more in pulmonary though but you'll hit them with something like that and you'll put them on uh dubs which is Al butol and epot tropial bromide and you'll do that pretty consistently so you'll do it frequently to dilate the bronchioles now the thing is is when you do this right it takes a time for these drugs to work so there's something that we can hook these patients up to like a little Darth Vader mask and we can help them to breathe better while those medications are kicking in boom BiPAP oh baby my man exactly so BiPAP is kind of like the best thing it's actually evidence-based for patients with COPD put them on BiPAP you control their inspiratory positive airway pressure and their expiratory positive airway pressure basically in layman's term what you're doing is when you're pushing this air in you're keeping their airways kind of stented open so that they can allow for air to leave their lungs and so they're not hyperinflated feeling like they have to work really hard to take a deep breath so it improves their breathing and then gives time for those medications to start opening up the bronchioles improving CO2 to exhalation and release so that's the the big thing for this patient there's nothing else that you really have to do you don't have to give them like any byy carb or anything like that for this disease all right then we only have one more left to go and that would be case five respiratory alkalosis okay so we have a 42-year-old male presents to the post anesthesia Care Unit the PAC you with complaints of severe pain feeling extremely anxious following elective hernia repair HPI the patient underwent an uncomplicated El hernia repair under general anesthesia posttop he started experiencing significant pain at the surgical site which he rised as an eight out of 10 he also feels very anxious describing a feeling of breathlessness and inability to get enough air in leading to Rapid breathing his past medical history no real pertinent medical history um but he does have an anxiety disorder managed intermittently with medication that medication he does take as needed is Al praam uh review of systems he reports for resp reports rapid breathing and unable to feel like he can catch his breath cardio no chest no chest pain at all does report palpitations neuro anxiety no confusion or focal deficits so his vitals upon presentation to the pack view uh blood pressure is 145 over 90 heart rate is 102 respiratory rate is 28 his temp is 36.7 de C and his oxygen saturation is 96% on room air for his exam uh General patient appears restless and in acute distress he's pretty anxious respiratory rapid and shallow breathing clear to oscilation bilaterally cardio he is tacky cardic with a regular rhythm no murmur present when we inspect the surgical site it's appropriate there's no signs of hematoma or infection at all the Laboratory Testing the serum sodium is 140 pottassium is 4.1 chloride is 104 bicarb is 22 bu is 14 his creatinine is 0.9 and then upon getting an ABG he has a pH of 7.49 pco2 of 30 and a po2 of 98 um again that's on R A all right Zach so we have an idea of the case we know what's going on with this patient what do you think you have to do to break this down and kind of approach this patient yeah so this is where like when you talk about acidbase disorders a lot of the times the history will kind of give you more than even sometimes the ABG will but nonetheless looking at abgs and trying to interpret them the ABG is pretty obvious right in the sense that he has alkalosis via the pH his CO2 is low which means that he's likely having a respiratory driver of this his bicarbs fine so again we can confirm that this is a respiratory alkalosis a primary disorder here's the thing though this is a kind of healthy dude I don't I don't really see any history of diseases right so for me one of the biggest things that I like to think about is a reason why patients are breathing fast faster primarily is what's triggering the respiratory Center to fire faster often times hypoxemia is the big trigger and you kind of hit on this that his oxygen saturation is 96 right so he doesn't have any hypoxemia so that's unlikely driving his underlying Topia that would be something that would be concerning to me does he have pneumonia does he have maybe an exacerbation of an obstructive airway disease does he have pulmonary edema did he go ex you know hiking Mount Everest and he had high altitude kind of like a related respiratory alosis but nothing pulmonary seems like that's the driving factor and so if that's the case I can divert all pulmonary pathology away it's unlikely the cause the other thing that I would think about is is this patient in a lot of pain or are they super anxious and based upon their history they don't really have any underlying diseases that would suggest anything except for anxiety yeah that's that's just the one that's stearing you down and so they just had a surgery so they got got cut into so they're probably having pain and they're anxious so often times in this scenario if you've ever had kind of like a panic attack and you start breathing really really fast it's because that anxiety is driving your lyic system it's making your actual respiratory sensor breathe at a faster rate and that's why sometimes when patients get super super anxious and they're breathing really really fast what's the one thing that you were always taught to do if you're kind of having a panic attack breathing into a bag yeah and the reason why is when you're breathing really really fast you're blowing off your CO2 and sometimes patients will have a Syncopy event and so you're breathing into the paper bag to retain some of that CO2 back into the bloodstream so I think this is a lot of this is anxiety and pain ridden and if you treat their anxiety and you treat the patients's pain I think that their teyia will start to settle down so being that he has increased pain anxiety induced this is both stemming from heightened Lim lyic system activity exactly and I think if we treat that we'll kind of shut that down a little bit and we'll start to see that the respiration will decrease if it was hypoxemia driven I would say oo I got to take a look and maybe get a chest x-ray CT scan figure out what's going on in the chest that driving their hypoxemia and then fix that but I don't see any of those things that would be the spo2 yeah exactly if that was really low or you know there was other concerning signs that they had significant work of breathing or whatever it may be then I would be a little bit more concerned but for this one it doesn't seem like that there's a super rare one out there they always add this into the exams aspirin toxicity or salic toxicity it's one of those weird disease or one those weird types of situations where a patient can have a mixed disorder they can have respiratory alkalosis and an anap metabolic acidosis and so usually with this when you're seeing a young child who has tentis they're having headaches and they have fast breathing and an elevated lactate level I don't see any concerning signs here of aspirin toxicity if I wanted to I could check an aspirin level if I was really concerned but I don't see that being the case at all and So based upon history physical exam and then just looking at the patient I think that this is likely anxiety pain induced give them that medication so something to kind of make them a little bit less anxious treat their pain and then hopefully we can Trend down and watch the respiratory rate go go go go go it is pretty neat to see the overall theme of all these acid base disorders it's like if you get a really good history you have a really good exam you're pretty much understanding exactly what's going on yeah Labs prior to get one lab labs are great but I think that they come with certain limitations right and I think often times being a clinician is really being able to pull information from your patient a lot of the time yeah that's pretty cool all right so we have an idea we we've gone through a lot of that pathophysiology and and clinical findings what about complications are you are you concerned with anything going on in this patient yeah like I said before I think one of the big things is respiratory acidosis can increase ICP because it increases cerebal blood flow with respiratory alkalosis especially if it's kind of transient it can cerebral vasil constrict so it can reduce blood flow to the brain and they could syncopize so that's one thing I would watch out for for often times in the neurological ICU uh we use this technique to reduce patients ICP so for example if they have an ICP of like 35 sometimes what we'll do is we'll actually if they're on the ventilator we'll turn the rate up on their ventilator and we'll make them breathe faster to blow their CO2 off so it constricts the cerebral vessels reduces blood flow and reduces the ICP but that's more of a therapeutic usage the complications of inadvertent respiratory alosis often times could be Syncopy otherwise there's nothing really else that I would be super concerned about off the off the GetGo well hey let's keep it simple for the viewers right yeah exactly you don't have to go too crazy here let's move into treatment how do we treat this patient I think that was kind of like one of the big things where it was kind of treat the underlying cause right so for this patient it's pain and anxiety I'm going to give them some type of pain medication maybe start off with Tylenol maybe ineds if that's not working you can always escalate upwards if you need to to opioids um but obviously those should be ones of your last resort if if necessary um and then analis so treat putting them on something that they maybe take it home potentially could be helpful to provide some short-term analysis that would be the thing that I would do for this patient if they had hypoxemia I would give them oxygen because that oxygen will improve their spo2 or improve their pao2 and it'll shut down the respiratory center from breathing so fast um and then I'd have to treat their underlying disease if it was aspirin toxicity then usually for those patients we have to give them something to actually treat that aspir toxicity often times though we usually have to dialyze them if it's really bad but that's kind of the big treatment for this patient is just pain control analis if they had hypoxemia oxygen otherwise this patient's straightforward we're going to treat them underlying cause and they're going to get better awesome cool well there you have it we have five cases done yeah we killed this man that was pretty awesome I really really like this one yeah this was a good one I think a lot of really good cases I think they were very very helpful yeah I think so I that's my kind of idea for you guys is that whenever you're looking at any patient who has an acid-based disorder again it's great to look at the ABG to figure out the primary disorder it's great to have a good overall understanding of their Labs Etc but a good history and physical will lend to you pretty much more than any kind of lab could so really lend into that lean into that HPI lean into their physical exam and I think that that'll give you a lot of valuable information to nail this on your exams and to nail it on the Ws when you're treating your patients we're to keep trying to do podcasts like this again we we have complete and and total intentions to keep making them as much as we can just bear with us in the beginning here as we kind of get things going we're still trying to you know get a little traction but I promise things are ramping up absolutely and we're having a lot of fun with these this is great I love this and I really hope that this stuff makes sense and I hope that at the end of the day whatever way that you learn I hope that we here at ninjer are able to provide that for you if you like to watch videos we got it if you like to look at notes and practice on illustrations we got you if you want to listen to case series and go along with us as we try to solve a case we got you and if you want podcast we got you so come here check out all the things that we have to offer because our ultimate goal is to help you out in your academic Endeavors so yeah thanks so much Robie this was a fun one all right let's give him the send off all right Niners well I love you guys I thank you guys and as always until next time [Music] [Music] for [Music]