Metabolic Acidosis

what's up ninja nerds in this video today we're going to be talking about metabolic acidosis but before we get started in this video please continue to support us by subscribing hitting that like button and commenting down in the comment section all right engineers let's get into this all right ninja so let's talk about metabolic acidosis which is by far the most significant most important acid-base disorder when we talk about this disorder it is crucial one of the pivotal points in understanding this disorder is really understanding the etiology and the pathophysiology of metabolic acidosis so let's go through these now we're going to go through the diagnostics a little bit later so i want you to trust me but there's two different types of metabolic acidosis there's a elevated anion gap metabolic acidosis and then there is a non-anion gap metabolic acidosis now there's a mnemonic that people love to throw around right for metabolic acidosis that is it has an elevated anion gap and that's called mud piles and that's great but i like to keep it to the most common most important things and easy to remember and that is cult k-u-l-t so the first part of that mnemonic k is keto acidosis this is a very very very important one that i want you guys to remember so keto acidosis now ketoacidosis believe it or not a lot of times we just say oh it's someone's diabetic and that's why they're in dka and that could be the case and that is going to be likely the more common cause but it also could be due to two other reasons one if someone's taking a lot of alcohol they're just guzzling that stuff down that can cause a ketoacidosis or if someone's starving themselves that can also cause a ketoacidosis how let's explain that so start off first with dka if someone has diabetic ketoacidosis usually dka is seen in someone primarily more commonly with type 1 diabetes mellitus which means that they have a deficiency or a lack of insulin now let's make sense of that if someone has decreased insulin what happens to the actual glucose levels within the blood they go up right because if you don't have insulin you can't get the glucose from the blood into the tissue cells and so as a result of that you're not going to be able to utilize the actual glucose and so your body starts tapping into other energy sources so whenever there's this decrease in insulin what happens is your body starts actually tapping into the secondary energy sources what's the secondary one lipids you know within these fat cells this is your adipose tissue right this is your adipose in the adipose you have triglycerides that are packed within these puppies right whenever you have this decreased insulin which means that you can't get glucose into the cells which means that you can't metabolize it to make atp you tap into this lipid source and you start breaking down triglycerides what does this call when you break down triglycerides lipolysis so we're going to start increasing this lipolysis process now when you do that you break down triglycerides into two parts right one is the glycerol we're not super concerned with that part and the other one is the fatty acids now what do the fatty acids do the fatty acids will then start undergoing an extensive amount of metabolism right so if you have a lot of triglycerides you'll break them down into a lot of fatty acids and these generally will go to make acetyl coa and the whole purpose of that acetyl clay is to make atp right but if you have no glucose because you have no insulin to get the glucose into the cells you start breaking down tons of fat you start having lots of fatty acids get converted into acetyl coa that eventually the atp starts going up and this process of going through the krebs cycle decreases and what happens is the fatty acids when they go through this process what is this process when you take fatty acids and make lots of acetyl coa this is called beta oxidation what happens though is that too much acetyl coa accumulates and it can't go into the krebs cycle and make atp so it starts shunting into a different pathway and this forms ketone bodies and the two primary ones that i want you guys to remember are beta hydroxybutyrate and acetoacetate these have the ability to act as acids so beta-hydroxybutyrate and acetyl acetate are actually the conjugate bases of their their corresponding acids beta-hydroxybutyric acid and acetoacetic acid when they give off those protons guess what that does it lowers the ph so these ketone bodies can give off protons and effectively lower the ph within the blood when they lower the ph within the blood and is due to a metabolic issue that is metabolic acidosis okay so that's the dka effect now what if someone is just chug-a-luggin right they're down in those coors lights or whatever it may be and they're consuming lots of alcohol as they start to consume lots of alcohol the mechanism of this is there's two ways one is you actually can make a lot of acetyl coa what's even more interesting with the alcohol is lots of alcohol when it goes through its kind of metabolic pathway it creates a ton of nadhs lots of nadhs have a very interesting mechanism and what they do is this process actually inhibits a process called gluconeogenesis now if you inhibit gluconeogenesis what does that mean that means that you can't actually increase the blood glucose levels okay if you can't increase the blood glucose levels what happens to the glucose levels they're going to drop if your glucose levels drop what does that do you know that actually does a couple things one is it's actually going to stimulate glucagon production and it's also going to stimulate neuroepinephrine release you know what these bad boys are going to do they're going to come act on the adipose tissue stimulate the adipose tissue to increase lipolysis break down fatty acids to make acetyl coa you'll make too many of them they'll start shunting into this pathway making ketone bodies popping off protons and lowering your ph ba-boom so we understand how alcohol does that another way is that if you have lots of alcohol alcohol can actually get converted into acetyl coa too so there can be another way which also if you want to think about it like this alcohol can also be converted into acetyl coa which will also increase that pathway if there's too much acetylcholase it'll shunt into this pathway the last one is starvation and it's kind of a similar mechanism to alcohol if you're actually starving what's the kind of mechanism behind this you're not eating so if you're not eating what's going to happen to your glucose levels they're going to be lower right so you'll have low blood glucose so in this kind of situation we can kind of combine these here you'll have low blood glucose levels low blood glucose levels will trigger the glucagon norepinephrine release that will cause lipolysis that will cause a lot of fatty acids to get converted into acetyl-coa acetyl-coa will get overwhelmed can't go into the krebs cycle shunts into making ketone bodies and drops your ph we now know the three types of ketoacidosis would be dka excessive alcohol use and starvation and that's going to make up one of the primary causes of metabolic acidosis primarily the elevated anion gap type the second one so we remember cult k-u-l-t u is for uremia okay so this is for uremia now uremia is whenever you have elevated levels of metabolic waste products due to an underlying kidney disorder now this is important to remember this uremia that we see in elevated anion gap metabolic acidosis is primarily an end-stage renal disease so later renal failure and we actually have to categorize this a little bit more where particularly their gfr is actually less than 20. so if their gfr is less than 20 they have end-stage renal disease that can be a cause now how how what does this actual uremia have anything to do with causing metabolic acidosis we know your kidneys are responsible for filtering out particular types of metabolic waste products you know what those are there's three one is sulfates the other one is phosphates and the last one is urate ions so again remember sulfate is the conjugate base of sulfuric acid phosphate is the conjugate base of phosphoric acid and urate is the the conjugate base of uric acid all of those have the ability to release protons and become these conjugate bases and these have the ability to lower your ph so that's important to remember when you accumulate a lot of these ions and again commonly you kind of correspond these with this is the base the corresponding acid is sulfuric acid you give off that proton it's going to lower the ph either way if your gfr so low that you can't clear and excrete these ions into the urine they'll accumulate in the blood give way to protons and lower the ph so that's the second one the next one is by far going to be the most important type of cause that i really want you guys to remember so we have k u for uremia l so cult k-u-l and this one is going to be lactic acidosis so the next one that i want you to remember is lactic acidosis now lactic acidosis there's actually two types that i really want you to remember the third type i'm not really concerned with you guys knowing first one is type a lactic acidosis now this is due to a problem with oxygenation before we can even talk about that though we have to kind of go through the basic physiology of the kind of the glucose pyruvate lactic acid pathway so you guys know within our cells right you take glucose right here's your glucose your glucose can get taken into particular cells of your body and when it's taken into these particular cells of your body and it goes through the glycolysis process it gets converted into pyruvate then what happens is pyruvate should move into your mitochondria and you know within the mitochondria you have the electron transport chain but either way pyruvate will get converted it'll get taken into the mitochondria and get converted into acetyl coa and then it'll go through your krebs cycle and hopefully the end result out of this is it'll move to the electron transport chain and make atp that's the whole goal of the glycolysis and then the krebs cycle electron transport chain now what's the big thing to remember pyruvate in order for it to be able to become acetyl coa get into the actual mitochondria what does it need it needs oxygen so let's represent that we need oxygen in this process to be able to for this process to occur now if someone does not have the oxygen present to be able to convert the pyruvate into acetyl coa what happens it's a good question i know you guys were asking that right pyruvate will then get converted into a molecule called lactate now lactate again is the conjugate base of corresponding acid lactic acid and again lactic acid will give off a proton that'll lower the ph and again make lactate so it's the corresponding issue there right so again if there is no oxygen let's say low oxygen in this situation there's no oxygen then it's going to get converted into making lactate okay now if that happens then why is the problem what is the problem with this again lactate remember the corresponding issue is that it's related to lactic acid and that lactic acid gives off a proton becomes lactate and then lowers the ph causing a acidosis so that's the big issue here first type of lactic acidosis is called type a and we said the issue is that there is no oxygen so let's write that out then what could be the reasons why someone would have a type a lactic acidosis let's go through these and i want you guys to make it really easy on yourself don't make it hard okay where does what is the path of oxygen first thing is it has to come into your lungs so what if there's an issue where you can't get oxygen into the lungs and into the blood what would that be what would the problem be with that there is a lung issue so first thing i want you guys to think about is is there some type of lung issue think about it simply what if someone has copd what if someone has interstitial lung disease what if someone has a pneumonia that you can't get the oxygen into the alveoli they have fluid in the alveoli like a pulmonary edema or they have a clot in the pulmonary capillaries and you can't actually can't get blood to an alveoli to oxygenate the blood any of those issues are going to cause low oxygen in the blood low oxygen means that if you take a cell for example if i take a tissue cell here here's my tissue cell and i'm zooming in on all the cellular activities i'm zooming in on it here if i'm having a problem being able to deliver oxygen to this tissue it'll start shunting into this pathway one of those issues is that if i have low oxygen because of a lung issue the second thing blood has to go and oxygen has to go into the lungs and then go into the blood and it has to bind on to what thing red blood cells what if you have low red blood cells what's that called anemia so if you have anemia that could also be an issue maybe it's because you're losing blood or maybe you have some type of iron deficiency anemia it could be various causes but either way there's low amounts of red blood cells to carry the oxygen what's the red blood cells moving in to go deliver the actual oxygen to the tissues it's moving in blood so what if you have a low blood volume for some reason or low circulating blood volume so what would that be if you have low we'll put effective arterial blood volume which means the amount of blood that's in the vessel the amount of blood circulating through the vessel is lower what would be reasons for this think about it very simply shock if someone is in shock go through the different types of shock they're losing blood volume maybe they're dehydrated that's decreasing their plasma that's decreasing their effective arterial blood volume maybe they're losing blood that's decreasing their effective arterial blood volume maybe their heart's not pumping well and so they're not actually getting enough blood into the vessels so they're in cardiogenic shock maybe there's something obstructing blood from getting out of the heart like cardiac tamponade or attention pneumothorax or maybe blood is actually getting out of the heart and circulating through the blood vessels but the blood vessels are really leaky and dilated and fluid's leaking out septic shock right so if we think about those reasons that will help us to understand how this can lead to lactic acidosis so a lung issue a red blood cell issue a actual circulating blood volume issue go to the next thing what is the blood should be going to it should be going in the blood vessels and taking this oxygen to the tissues what if there is a obstruction or an occlusion within the blood vessel that the actual red blood cells and blood can't actually pass through that could be a cause so what if they have like an embolus they popped off an embolus so they have an embolism where could these be in the leg you get an acute ischemic limb you get it in the belly you get a mesenteric ischemia right or you get it in the heart you get a myocardial infarction all right so that would be kind of our type a lactic acidosis causes again big thing to remember here if you kind of want to put like a little annotation here is that there is low oxygen or some type of oxygen impairment if you will type lactic acidosis has a couple different kind of types if you will okay the first one for type b is that there's not a problem with oxygen it could be an issue with the clearance of lactate so you need to know what organs are primarily responsible for clearing lactate from the blood so maybe you're making lactate at a normal amount or maybe a slight increased amount if you have normal kidneys normal liver you should be able to clear that lactate but if they're all jacked up what's going to happen it's going to accumulate so in someone who has an associated liver failure so let's say here i put like a liver here i love you with all my liver and that liver is all jacked up that lactate should go to the liver and be cleared but if the liver is impaired and it can't clear that lactate like it wants to be able to it's going to lack it's going to build up within the blood okay lactate builds up lowers the ph causes in acidosis to a lesser degree if the lactate levels are very very high and someone has an associated renal failure the kidneys also do clear lactate but if the kidneys are all jacked up and they're not able to clear that lactate like they want what's going to happen usually the lactate should go to the kidneys and should give it urinated out but if the kidneys are all jacked up what's going to happen that lactate will not get cleared it'll build up lower the ph and cause an acidosis so the other thing to remember here is for type b there's kind of sub categories to the type b if you will so type b the first type is there's no oxygen impairment it's decreased clearance of that lactic acid and the two types that i want you guys to remember here are going to be liver failure and then the second one is going to be renal failure okay the last type or subtype of type b lactic acid is because again remember type a is oxygen impairment type b is there is no oxygen impairment so with the other aspect of this so there's kind of like a subtype of type b where there's actually an increased generation there's an increased production of lactic acid right now this is a couple things okay one is that maybe the pyruvate can't get into the mitochondria because there's some medications that are really jacking up the electron transport chain and so you just can't convert the pyruvate into acetyl coa or you can't undergo the electron transport process of oxidative phosphorylation there's a tons of meds the ones that i really think are important so meds that really what they kind of do is they inhibit oxidative phosphorylation and that really kind of screws up that pyruvate to acetyl-coa process and instead shunts it to lactic acid the big ones that i really want you to remember here is propofol this is very common especially in the icu metformin i can't express how important this one is to remember especially even worse if someone has renal failure so someone has they're taking metformin which can cause an increased production of lactate and you have a jacked up kidney it can even worsen it okay that's important to remember the other one is if someone has um they're taking diazepam or lorazepam for seizures and you know those contain lots of propylene glycol within them so particularly within the benzodiazepines like particularly diazepam lorazepam infusions that can cause it the other thing is if someone has hiv and they're taking nrtis and then last one is if they're taking lynasalid for a mrsa infection okay so just certain medications that you want to keep your eye out on that can cause this type of increased production of lactic acid the other thing that i want you to remember is that maybe it's not just due to medications that are inhibiting this phosphorylation but maybe you're also just having a lot of this glucose undergoing tons of glycolysis so there's so much glycolysis that is going on that because of that naturally this acetyl-coa and krebs cycle pathway gets kind of overloaded that you naturally just kind of shift to making lactate and that's just because you're metabolizing so much glucose so there's an increased glycolytic flux if you will this can be seen whenever there's an increased glycolysis kind of pathway the big thing i want you to remember is seizures and also malignancy particularly in conditions like leukemia lymphoma and multiple myeloma okay so we talked about lactic acidosis this is a very very important one i really want you guys to remember all of these um but this is going to be one of the big big causes of metabolic acidosis remember i told you that there was a third type if you really want to remember it's called type d and it's seen in short bowel syndromes where you're having a problem with the intestinal flora okay so we have so far three parts of our mnemonic k for ketoacidosis u uremia l for lactic acidosis what's the last one t for the last part of the cult mnemonic and that's for toxins right so toxins and this is where that whole mud piles mnemonic really kind of helps but i just like to remember toxins and i like to remember meps so what does meps tell me it tells me the most important kind of toxic ingestions first one is methanol okay second one is ethylene glycol the third one is propylene and the last one is salicylates well methanol actually gets converted into a molecule called formic acid and again formic acid has the ability to release a proton and when it releases the proton it lowers the ph ethylene glycol can actually convert into what's called oxalic acid or another one glycolic acid glycolic acid and again they have the ability to release protons lower the ph problem glycol we already talked about this what does it do it causes the type b lactic acidosis and lactic acid will release a proton become lactate and that will cause a lowering of the ph salicylates what do they do we didn't talk about that but they're also another med that we can actually add into this list of type b's they also can cause lactic acidosis and lower the ph another thing that we talked about before and i know you guys remember this what else does it do it increases your respiratory center and causes respiratory alkalosis so don't forget that one just as a quick reminder but these are your big big toxins that i want you guys to remember as causes of elevated anion gap metabolic acidosis all right so we talked about the etiology and pathophysiology behind the elevated anion gap metabolic acidosis now let's talk about the ones for non-anion got metabolic acidosis right nagmas so we use the mnemonic cult ketoacidosis uremia lactic acidosis and toxic ingestions for the elevated anion gaps for the non-antigut metabolic acidosis i like the mnemonic used cars and then we'll explain how those things cause the acidosis so the first one here you is actually ureteral sigmoid ostomy this is done in patients who have bladder cancer and what they do is they remove the bladder and then divert the ureter into the sigmoid colon and so what happens is you you know your urine you actually get rid of a lot of chloride and you get rid of a lot of sodium well the chloride is the one that's actually the more pertinent one and the reason why is the chloride when it actually gets into the bowel it actually gets absorbed across the gi tract and when it gets absorbed across the gi tract guess what actually moves into the bowel and then gets excreted from the bowels so from the blood into the bowels bicarb so you're going to lose some of that bicarb in the stool because of this ureterosigmoidostomy and what happens if you get rid of the bicarb from the blood so now think about this decreased bicarb within the blood right what's going to happen there that you're not going to have as many bicarb ions to counteract the protons so now the protons are going to increase if the protons increase what does that do to the ph that will lower the ph and cause an underlying acidosis okay so that's the first one so you ureterosigmoidoscopy the next one s saline infusions this is very common okay i see this a ton in the icu is you're giving someone too much normal saline infusions or even more significant is you're giving them hypertonic saline infusions why is this a problem so i like to remember s so saline infusions now the two big ones are going to be your normal saline and then the second one is going to be your hypertonic saline either way both of these contain large amounts of chloride when you increase the amount of chloride what happens is you actually kind of effectively decrease the bicarb okay so whenever you increase the bot the chloride you effectively decrease the bicarb and that decrease in bicarb there's less of those protons to be counteracted right by this bicarb and so that's going to do what to the ph lower the ph okay so you see this in normal saline infusions and hypertonic saline infusions the next one so used e is renal failure but here is early renal failure in the elevated anion gap one it was late renal failure in stage renal disease so it's important to remember that particularly in early renal failure this would be a cause of enagma now how is this one different well this situation is primarily because the kidneys have a decreased ability to generate bicarb so there's decreased bicarb production if there is a decrease in biocarb production from the kidneys what happens there then you can't actually counteract the protons if you can't counteract all those protons that lowers the ph you guys are starting to get the point here right okay use d diarrhea so if someone is just painting the town brown if they're uh restocking the lake with brown trout if they got the hershey squirts and they're blasting this out they're losing what you know within the intestinal secretions what is the primary thing within the intestinal secretions it's bicarb you know your intestinal cells they make lots of bicarb to counteract the acidic environment of the stomach that could be one reason if you're having diarrhea you're losing a lot of that bicarb from those intestinal secretions but there's one other thing you know the pancreas right the exocrine proportion of it the ascendant cells they're helping to make bicarb and so sometimes if someone has a pancreatic fistula that's having a direct connection between the pancreas and the actual intestines that can just dump a lot of bicarb from those pancreatic acinar cells or the ductal cells there and they can also lose a ton of bicarb that way so two ways upon which you can actually have a metabolic acidosis from this associated gi tract problem here is if they have primary one d diarrhea okay and the whole mechanism behind is that you're losing bicarb so if there's a decrease in bicarb in the blood what's going to happen that's going to decrease the ph but the other associated issue to not forget about just because they like to throw it in there sometimes is you can also if you want to add in their pancreatic fistula especially if someone had a history of pancreatitis okay so we have used now we've got to go to the cars portion so c is actually if someone was on a particular medication that causes you to get rid of um bicarbonate in the urine you know what this condition is where you actually get rid of bicarb in the urine so tons of bicarb is going to get lost in the urine this isn't whenever someone is taking carbonic anhydrase inhibitors what is the primary one here acetazolamide so if someone is taking acetazolamide that actually works by acting on the renal tubular cells and causing them to lose bicarb if you lose bicarbonate the urine what happens to the bicarb in the blood then you have decreased bicarb in the blood less of this bicarb to counteract the protons in the blood and that'll lower the ph okay so we've gone through used c so now we have r's right the next one is kind of a double whammy okay so i'm going to combine a and r because they're kind of together so the next group of conditions that i'm going to combine with the a and the r is called renal tubular acidosis okay to make it easy though okay to make it easy i'm just going to put over here on the side the a just to be you know consistent here the a is for addison's disease and it is a type of renal tubular acidosis particularly type 4. and then the r to the cars is going to be the renal tubular acidosis so that's why i'm combining them is because addison's disease is actually one of the types of renal tubular acidosis so they go together so let's go through these renal tubular acidosis there's four types type three is not that big of a deal and it's actually very rare so we're not even gonna talk about it we're gonna talk about type one two and four so let's start off with kind of the types based upon their location within the kidney tubes i think it makes most sense and it's easier to remember so here you have this two symbol so we're talking about renal tubular acidosis type 2 renal tubular acidosis primarily is a problem where there is an issue in the proximal convoluted tubule so let's write that down so type 2 renal tubular acidosis the issue is in the proximal convoluted tubule but what is the problem in the proximal complex tubule i'm so glad you guys asked what happens is the pct is responsible for reabsorbing tons and tons of molecules but one of the big ones that causes this issue is bicarb they can't reabsorb bicarb for some reason so because of that there is a decreased reabsorption of bicarb and so instead of actually reabsorbing the bicarb here what do you do you lose all of that bicarb into the actual kidney tubules and you'll urinate that bicarb out so where's the bicarb actually gonna end up it's gonna end up in the urine and you're getting rid of the bicarb so if you decrease your reabsorption of bicarb what does that do to the bicarb in the blood it decreases the bicarb in the blood what does that do to the ph well you don't have enough bicarb to counteract the increased protons and what is that going to do to the ph it's going to lower the ph okay one other thing you guys need to remember this is a really interesting one whenever you have a lot of bicarb that's kind of getting pulled through the kidney tubules it does have an osmotic gradient with it so whenever it moves through the kidney tubules down like the descending limb the ascending limb so on and so forth and then gets down here to the urine you're also going to lose a lot of stuff with it you know what you lose with it it actually pulls sodium and water if you pull off sodium and water what do you think that's going to do to your blood volume it decreases the blood volume what does that do to your kidneys you know what it stimulates your jg cells what do they do they love whenever you have low blood volume they make renin renin then does what you stimulate the renin angiotensin aldosterone system aldosterone does what acts on the distal kidney tubules and causes you to get rid of potassium so what else will be a result out of this if you stimulate this pathway you'll have low potassium can't express how important that is so in type 2 you'll have decreased reabsorption of bicarbonate in the pct and loss of potassium ions okay the next one type 1 renal tubular acidosis let's do a different color just to be interesting and purdy right so type 1 renal tubular acidosis primarily affects the distal tubules right so more like your distal convoluted tubule and you're collecting duct areas okay but particularly what cells of the distal tubules is what i want you to remember i want you to remember the alpha inter-collated cells you know the alpha intercalated cells are responsible for secreting protons guess what these guys do they don't excrete protons so because these are all jacked up there is a decreased proton excretion from these alpha intercalated cells if you don't excrete protons into the urine what happens to the proton concentration in the blood it's going to go up so there's going to be an increase in proton retention in what the blood and if you increase the proton retention within the blood what does that do to the ph it drops your ph here's something very interesting though you have two types of kind of pumps at the alpha intercalated cells one is a proton atpase pump and the other one is a proton potassium pump so for example if i had like a cell here and here was that portion of the cell here's going to be one pump that pumps out the proton into the filtrate and the other one will pump the proton out and bring the potassium in both of these pumps aren't working so if i can't pump the proton out guess what i also can't pump in potassium and so guess what else happens as a result of this there's also going to be potassium excretion so increased potassium excretion and what does that do to the serum potassium that lowers the blood potassium that causes hypokalemia so same thing low potassium in the blood for type 2 and low potassium in the blood for type 1. okay the last one which is going to be this addison's disease type is type 4. let's do another purdy color here let's do this red one here type 4 renal tubular acidosis this one is a problem again with the distal tubules so those distal tubules are all jacked up and primarily it's both so we're going to actually kind of abbreviate these so if it's the alpha intercalated cells and the principal cells are jacked up okay we already kind of know what happens with the alpha intercalated cells right with the alpha intercalated cells what are you going to do you're going to decrease your proton excretion and we already know what that does it leads to a lower ph by retention of protons so that part's already done that's one way that it contributes to the acidosis something else happens though whenever you work on the principal cells what does it do to the principal cells aldosterone normally should do what it should actually cause what process it should act on the principal cells and increase the reabsorption of sodium and excrete potassium in addison's disease guess what the problem is you have low aldosterone and maybe even other it's a the primary the the the failure of the entire adrenal cortex but aldosterone's also one of those hormones that's going to be whacked off right so because of that you're going to have low aldosterone okay if you have low aldosterone think about what it'll do to the principal cells you're going to have less sodium reabsorption so what's going to happen to the sodium then if there's decreased sodium reabsorption there's decreased sodium in the blood and what else it's normally supposed to cause potassium excretion but you're not getting rid of the potassium so if you don't get rid of the potassium what happens it accumulates in the blood so the potassium will rise in the blood and this will cause hyperkalemia okay so with this combination of effects and type 4 renal tubular acidosis you affect the distal tubules you decrease potassium excretion causes proton retention lowers the ph you also don't reabsorb sodium into the blood and you get rid of potassium and so potassium will rise within the blood okay so these are the different types of renal tubular acidosis which can help to finish the a and the r portion of our mnemonic of used cars there's one last one and this one is kind of like the lower end of the list but just to throw it in there for you it's supplementation so used cars the s part is supplementation so supplements and the primary ones that i want you to remember is tpn so total parenteral nutrition this is happening in patients that you need to feed and what happens is whenever you're kind of giving them these calories if there's too much chloride or there's too much acetate these can cause problems right because whenever you have an increase in chloride you're going to be getting rid of bicarb so there's a loss of bicarb right so this decreases your bicarb and what does that do when you decrease bicarb you have less bicarb to interact with the protons and that lowers the ph so again whenever someone is getting hyper elementation or their tpn is containing lots of chloride lots of acetate that can also cause enagma this pretty much gives us all the etiologies and pathophysiologies of both nagma and agmas let's talk about the workup and diagnosis all right so now that we've really kind of built the foundation for understanding metabolic acidosis we talked tons about etiology and pathophys it's really going to make diagnosis and kind of work up uh portion of this very very straightforward simple and understanding so how do we kind of go through our diagnosis or work up of acidosis well first thing we need is an abg because it's going to help us to determine what type is it a nagmar agma and then we can kind of go down those lists so first thing is let's look at our abg here we have a low ph right why how do i know that well normally it's 7.35 to 7.45 that's way less than that that's down pco2 well normal is 35 to 45 that's less than 35 that's down bicarb is 22 to 26 it's less than 22 that's down and then o2 is within normal range 80 to 100 millimeters of mercury right so no hypoxia so with that being said remember what we told you whenever s'more right whenever the ph is moving in the same direction it's metabolic it's a primary metabolic acidosis let's write that down this is definitely a primary metabolic acidosis but let's try to make sense of this co2 thing right let's be consistent with what we've learned so far if this is an acidosis what does that mean that means that the ph is low what does that do to your respiratory system what tells the respiratory system hey ph is really low let's try to breathe off some of that co2 why because let's make sense of this if i take co2 right and i use my equation co2 plus water yields carbonic acid and that breaks down into protons and into bicarb let's make sense of this if i start breathing faster and deeper i'm blowing off the co2 the co2 levels within the blood will drop what does le chatelier's principle say you have to move things to keep the the reaction kind of stable or in equilibrium so if it's lower on this side the reaction is going to have to shift towards the left when you do that you use more bicarbon protons to combine and make carbonic acid and then help to convert and make more co2 in water so what does that do to the amount of protons then if you're shifting this towards the left it decreases the amount of protons and that's trying to help to help to compensate for that low ph so there's definitely some respiratory compensation here because you're trying to breathe that co2 off so we would say this is a partial respiratory compensation okay next thing i determined that it's metabolic acidosis right there is some respiratory compensation the next thing is i need to know is this this an elevated anion gap or normal anion gap how do i determine that i got to get my bmp so from my bmp what am i going to take from my bmp i'm going to take my sodium and i'm going to take my chloride because i have my bicarb for my abg so let's say that um sodium from this bmp is 129. okay your chloride is 100. so if i take and what's my equation for the anion gap so the equation if you guys remember is anion gap is equal to sodium minus chloride plus bicarb so if i take this and utilize this equation then anion gap all my numbers is equal to what sodium is 129 minus the chloride here which in this case is 100 plus my bicarb which is 11 what does that give me that gives me an anion gap of 18. okay now what is a normal anion gap usually it's less than 12. if this anion gap is greater than 12 it's considered to be elevated so in this case this is definitely a agma elevated anion got metabolic acidosis right but if there was an anion gap that was less than 12 in this situation that would definitely be a nagma but if it's greater than 12 that would be a agma okay so in this example we knew it's a primary metabolic acidosis we used our anion gap to determine that in this case it's definitely an agma if it was less than 12 it would be enagma the next thing we want to determine is this a pure agma a mixed agma or is there some other concomitant condition there present do you guys remember your delta ratio delta ratio you'd have to calculate out you know you take your you take the anion gap that you actually calculated minus the normal divided by the normal bicarb minus the bicarb that they have and get a ratio generally if the ratio is you have a couple options here less than one you have one to two and you have greater than two if it's less than one it's an agma and nagma if it's one to two it's just an agma and if it is greater than two it's an agma and a metabolic alkalosis so if we were to actually calculate all of this out you take for example 18 minus 12 divide that by 24 minus 11 it's gonna be less than one okay so this person has a agma and enagma in this example here so we figured out so far kind of how we would go about doing this so first step get your abg determine the primary condition if it is a metabolic acidosis determine the anion gap if it's elevated you go on to determine the delta ratio okay and now so far we've kind of determined that there's a mixture either way once we've got up to this point of the anion gap that's pretty much all i really need to start my algorithm all right so i know this wasn't here before but i wanted to draw this kind of like flow diagram algorithm process that we're going to go through to make it look pretty so it doesn't get too messy when we're kind of going through it on the fly but i really think that this algorithm is really going to make sense of everything that we talked about over here trying to figure out the cause in the etiology so let's go through this we suspect someone has metabolic acidosis based upon their abg we get our bmp we calculate our anion gap if the anion gap is elevated what do i mean by that by its greater than 12 then that means that the person probably has an anion gap metabolic acidosis which has the differentials that we talked about before and what were those differentials k-u-l-t ketoacidosis uremia lactic acidosis are toxic ingestions if the anion gap was low or normal meaning that's less than 12 that may be associated with a non-anion gap metabolic acidosis and then again we have our used cars as the particular type of mnemonic to remember all those let's go through the labs and different types of things that we would go to figure this out first one k for the colt part what do i think of ketones so ketoacidosis so i'm going to check the ketones and you can do this by checking the serum ketones you can check the urinary ketones either way if the ketones are positive within the serum or urine you can suspect potentially this is a diabetic ketoacidosis an alcoholic ketoacidosis or maybe even a starvation type of ketoacidosis again go through their underlying cause they may be they're hyperglycemic they have diabetes they've been drinking alcohol or they've been on a special diet lately okay if the ketones are negative maybe then it's not a keto acidosis instead it's one of the other parts so uremia lactic acidosis or toxic ingestions okay so i think i think of lactic acidosis as the next one i'm going to send off a lactate level if the lactate is elevated and we'll just put positive in that sense greater than like four uh like mille equivalence then i would say oh actually it's a little elevated maybe they have a underlying lactic acidosis and again with lactic acidosis you have to figure out the type is this a type a issue where there's an impairment in oxygen or is this a type b issue meaning that there is no impairment in oxygen and there's some type of increased production or decreased clearance of that lactate okay so once i've done that okay that could be the cause there now go through the next one maybe uremia so we did ketoacidosis we've done lactic acidosis what about uremia as a potential cause well again if i have my bmp i can use the creatinine and the bun from that right so if they have like an elevated bun if they have an elevated creatinine and maybe their baseline gfr is low like less than 20. what can i associate that with maybe there's a renal failure and so if there's some type of renal failure again if it's kind of like late end-stage renal disease where the gfr is less than 20 it's more likely to be end stage and cause the agma but if it's early where there's an impairment in bicarbonate production maybe it could be a magma and we'll talk about that a little bit later so because this can actually have kind of a side pathway all right next thing i could also assess what if this person has had a toxic ingestion so i go to the last part of my mnemonic toxins so i run a tox screen if i do a toxic screen and it comes back positive maybe i think that they have an ingestion if i suspect an ingestion what do i do oh well what do i think zac do i order every single one that i think about no what you can do is you can order what's called an osmolar gap now this isn't always the best but it's helpful to think about osmolar gaps is a particular calculation you base it upon the person's bun their sodium uh they're also their glucose their alcohol level and you basically form a calculation we're not going to go through all of it but based upon this you take whatever you calculate and you actually use a particular equation from the the actual measured serum osmolality and you subtract the difference between them if the difference between the calculated and the measured is greater than 10 then it's most likely indicative of toxins of that mep part right so we had meps this is the first part mep so methanol could be one ethylene glycol could be the other and propylene glycol could be that last one if the osmolar gap is greater than 10. okay if the osmolar gap is less than 10 right so the calculation between the serum and the measured osmos is less than 10 then you start thinking about salicylates okay and that's how we would kind of go through that whole list that we did with the elevated anion gap we've done that now we go through the non-anion metabolic acidosis so the first thing i like to do is i like to think about this is is the person getting rid of particular types of molecules like protons or bicarb and it's it's affecting their urine are they having issues with their urine or is it a gi or other miscellaneous issue that's the first thing i want to know is that a renal cause or some other extra renal cause so the first thing i do is i order a urine anion gap so if i check the urine anion gap and it's kind of like the same thing you take sodium urinary sodium plus the urinary potassium and you subtract the urinary chloride all urine anion gap tells you is if the person is getting rid of so here's what i want you guys remember you're an anion gap i want you to kind of associate this with the amount of ammonium that is being excreted by the kidneys if the amount of ammonium that is being excreted by the kidneys is decreased the urine anion gap will go up okay and this means that this is a renal issue okay so if the urine anion gap is positive that means that it is what greater than zero elevated that means that you're not getting rid of ammonium okay so this makes me think of renal causes okay if the urine anion gap is negative or less than zero that means that there is ammonium being so a low urine align gap that means that the ammonium is being excreted and the kidneys are working fine there's probably some other extra renal issue that's a cause so we can put here that there's maybe an extra renal causes okay so now that i've done that i thought start thinking about the renal causes the first one that i can go right into check their bu in check their creatinine check their gfr if the bu and create needs bumped up if the gfr is low it could be renal failure so that was one of them the other part as you think about all those renal tubular acidosis right there was a bunch of those so if i think that this is a renal tubular acidosis the next thing i do is i check the potassium because that was one of the big things that i talked about with you guys what if i check the potassium and the potassium is elevated so i checked the potassium and they have high potassium if there's high potassium they have a nagma i may want to start thinking about a type 4 renal tubular acidosis and i can go and confirm that by looking to see if they have maybe low aldosterone levels low cortisol levels so on and so forth right but again that's one of the big things here if i check and their potassium is low then i have type 1 or type 2. how do i differentiate those do you guys remember so let's go back to type 2. type 2 renal tubular acidosis what was the issue it was with the pct and what were you not able to do you weren't able to reabsorb bicarb so you lose bicarb in the urine so what do you think the fractional excretion of bicarb in the urine is going to be it's going to be high it's actually going to be elevated sometimes we say greater than 15 not super important but it's going to be high the other thing is the urine ph where's the problem okay you're not able to reabsorb bicarb is the alpha intercalated cells working though in the distal tubule yes those are still working you didn't damage those you only damaged the proximal convoluted tubule so your alpha intercalated cells can still make protons and release those protons so your urine ph will still be relatively normal so maybe like less than 5.3 so the urine ph it can vary but it's usually kind of less than 5.3 compare that with the type 1 renal tubular acidosis what's the issue the problem is that you have an issue being able to excrete protons in the urine if you're probably excreting protons into the urine what do you think the urine ph is going to be well i'm not putting a lot of protons into the urine is it going to be less than 5.3 or greater than 5.3 it's going to be greater than 5.3 because i'm not putting a lot of that protons into the urine and then am i getting rid of a lot of bicarb no so my fractional excretion of bicarb is going to be low you see how those can differ they both have hypokalemia both have enagma but their urine ph's differ and their fractional excretion of bicarbs differ okay we figured out a renal tubular acidosis right now we come over here we have our urine anion gap it's negative we got to think about extra renal causes this is where you just have to dig into their clinical history right dig into the clinical history so go through some of the issues that go through some of them that mnemonic let's see if we can figure out which ones we have left over first one used cars uretero sigmoidostomy do they have that that's a simple thing right look into their surgical history so first thing is do they have a uretero sigmoidostomy that's the first one second thing we go down s are they getting saline infusions next one e or do they have any early renal failure we already hit that part okay d do they have any diarrhea or a pancreatic fistula okay c are they on any kind of carbonic antihydrous inhibitors are they taking acetazolamide r do they have renal tubular acidosis we already talked about all of those and addison's disease we talked about that one and then the last one here is what else supplements are they getting any type of tpn once i figure out all of these other things it's just kind of going through my mnemonic and filling in any like parts that i missed and that'll cover your entire workup for being able to figure out and pinpoint the cause or the etiology of metabolic acidosis let's finish it up with talking about the treatments all right engineers we have drilled home how to really figure out the differential diagnosis how to work it up let's talk about the treatment now we're not going to go ham bone because each of these individuals like you have to treat the underlying cause so to treat the underlying cause you have to figure out what that cause is we're not going to go crazy into each treatment of every single thing i just want you to know the basic points what's the overall treatment goal for these patients so the most important ones that are relatively reversible and that you should try to take care of first i want us to focus on ketoacidosis is one of those so in ketoacidosis it depends upon the cause right so if they have diabetic ketoacidosis what's the mainstay of treatment for that it's primarily three things that i want you guys to remember iv fluids insulin and then check you know their potassium you got to give them back potassium especially if you're giving them insulin because there's shifts of potassium there if they're having alcoholic ketoacidosis you want to give them fluids back that's definitely important you actually want to give them glucose so you give them dextrose because they're going to be hypoglycemic you also want to give them b1 and b9 so thymine and folate because that's they also lose that because they're not getting it from their diet and the other thing that you want to give an alcoholic ketoacidosis is you want to replace a lot of their electrolytes so potassium magnesium and then the phosphates you got to replace those and then also be careful if someone is a very dependent alcohol user they can go through the dts the limit delirium tremens so you may have to give them some benzos to prevent that as well but either way that's uh not at the pinpoint thing that i want to focus on and the last one is starvation ketoacidosis it's pretty much iv fluids and giving them back some sugar because they haven't really eaten anything okay and you may have to also replace some of their electrolytes as well renal failure with this one you can try to again figure out the underlying cause if it's kind of an early renal failure there's like an acute kidney injury and you can try to treat the underlying cause of that acute kidney injury like if it's a pre-renal giving them fluids treating their chf trading their cirrhosis whatever it may be if you can fix those things fix it but usually if it's very severe at this point when someone has severe let's actually put severe renal failure sometimes this may lead to the person having to be on continuous renal replacement therapy usually this is very important in patients who are like hemodynamically unstable or you can do what's called intermittent hemodialysis and this is better in patients who are hemodynamically stable because you pull off a lot of fluid on those okay so again if you can try to figure out the cause of the renal failure and it's early try to fix that but if not and if it's a little bit later it might lead to these kinds of unfortunate things like hemodialysis or renal replacement therapies if someone has lactic acidosis again there's there's too many things to go through we're not going to go through all of them i just want you to go back and think we're going to kind of quickly recap it if it's type a fix the issue so is it a lung issue if it's chf give them diuretics if it's pneumonia give them antibiotics if it's some type of copd exacerbation treat the copd with steroids and do a neb so on and so forth right if it's an embolism a pe give them heparin or tpa it's the simple thing right if they're anemic so if they have anemia give them a transfusion if they have a decreased effective arterial blood volume figure out the cause of that are they hypovalemic give them fluids are they losing blood give them blood is their heart not working give them inotropic agents is there a tension pneumo or cardiac tamponade do a pericardiocentesis or a chest tube is there septic shock give them antibiotics impressers right is there an imbalus somewhere maybe you have to go and do an embolectomy so once you've figured that out you treat the underlying cause it should help hopefully resolve the other one is your type b right and for this one you got to think about it right what was the big thing there's an increased generation maybe you have to discontinue all those terrible offending medications that were causing it the nrtis the nasal the propofol the propylene glycol right the metformin all of those things get rid of them or maybe at least decrease the effective dose of them and then the other one is if someone is having seizures and they're having a lot of glycolytic flux that may also be a reason so maybe you have to give them some benzodiazepines and if they have some type of underlying malignancy like leukemia lymphoma or multiple myeloma you may have to treat that as well so a lot of stuff within this category we're not going to go through every single treatment just think about the cause and treat the underlying cause toxic ingestions and these ones actually do want you to remember because these are relatively high yield so toxic ingestions the big ones that i want you to remember is methanol and ethylene glycol these you actually do give um phamepazol there's a drug called phamepazol but this is primarily if it's early so if someone has really just recently taken a lot of methanol or ingested ethylene glycol you can give them femepozole but if it's late it's usually hemodialysis to pull that stuff off okay the other one is since we did these we'll just mention the other one propylene glycol remember i told you about this one it was within the infusions if someone's getting like diazepam lorazepam or like a phenobarbital or something like that like an infusion you just discontinue it stop taking it okay and if it's really bad then you might even have to do hemodialysis and the last one is salicylates and this one you give sodium bicarb to them and then sometimes if that doesn't work you may even have to do hemodialysis so again this one doesn't work hemodialysis all righty the last thing that i want to talk about which is a very controversial topic with respect to metabolic acidosis is do you give them sodium bicarb right it's very controversial and the reason why is that there's actually not been a lot of good research like evidence that shows that sodium bicarb can help to treat acidosis especially ketoacidosis and lactic acidosis there actually hasn't been much benefit for it however still some people believe in it right so again sodium bicarb can be one of those that can be utilized and it can be given in two ways if it's acute acidosis sometimes they'll give this as an iv kind of like infusion and we're not going to go through all the calculations that's not necessary here if it's chronic it may be given in like tablets so sodium bicarb tablets okay that's one thing to think about the big thing to remember with sodium bicarb is that whenever you give sodium bicarb the problems why people are very like worrisome about it is that if you give this you're giving a lot of sodium so it can cause hypernatremia you can also lower someone's calcium cause hypocalcemia and increase their co2 and this can cause a lot of cardiovascular problems so again when someone gives sodium bicarb there is a lot of complications and there hasn't been much benefit in the literature to see its actual its effect in lactic acidosis and diabetic ketoacidosis but still sometimes it can be utilized the last one that also can be sometimes utilized especially in a person who has metabolic acidosis and respiratory acidosis is a drug called tro methamine abbreviated tham so thiam is basically kind of a proton acceptor and so it picks up any protons from this synthetic environment within the blood and this again is particularly beneficial in patients who have metabolic acidosis and associated respiratory acidosis so you give this to people who have very high partial pressure of co2 levels in the blood okay this is actually seen to be a little bit more beneficial in those scenarios so this covers the treatment of metabolic acidosis and finishes our lecture on metabolic acidosis all right ninja nerds in this video we talk about metabolic acidosis i hope it made sense i hope that you guys enjoyed it and as always ninja nerds until next time [Music] you

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Length: 65min 41sec (3941 seconds)

Published: Thu Jun 10 2021