Transcript for:
Overview of Acid-Base Disorders

What's up Ninja Nerds? In this video today we're going to be talking about acid-based disorders. Again this is a part of our clinical medicine section. If you guys like these videos, they really help you, they really support you guys in your studies, please support us. And some simple ways that you can do that is by hitting the like button, commenting down in the comment section, or subscribing.

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All right, without further ado, let's talk about acid-base disorders. So there is four different primary acid-base disorders. There's metabolic acidosis.

alkalosis, respiratory acidosis, and alkalosis, and we'll go through each one of them. We'll talk about the pathophysiology of the causes, but more specifically, kind of get you guys oriented on how to think about these diseases more clinically, pragmatically speaking. So first one is the anion gap metabolic acidosis. This is the subtype, right, of a metabolic acidosis.

Now within these anion gaps, it's really talking about what is the anion gap, why is it elevated. Well, there's your cations in the extracellular fluid, and then there's your anions in the extracellular fluid. fluid.

What I do is I take the cations and I subtract them from the anions. What are there? Well the most abundant one here is going to be sodium.

Then when I talk about it for the anions, I'm talking about chloride, I'm talking about bicarb, and then I have these guys called organic acids and they sometimes have a negative charge after they give off their proton. Now when I look at these, I'm taking and subtracting the cations from the anions and that would give me what's called my anion gap. What I do is I actually take sodium, I subtract it from the anions, and then I subtract the from chloride and subtracted from bicarb and that gives me my anion gap.

When the anion gap is greater than what we call 12, so whenever we actually determine that a patient has an anion gap that is greater than 12, what that tells me is that they have lots of these organic acids, like tons of them. And when you have lots of these organic acids, the problem with these suckers is that whenever you get a lot of them, they give off protons. When they get off protons, they'll soak up some of the bicarb and what they'll do is they'll deplete your bicarb level. And so what you'll see is that these patients will deplete their bicarb level.

All right. Now as I deplete my bicarb level, what happens here? Let's look at this. There's what's called the modified Henderson-Hasselbalch equation. It's pH is equal to bicarb divided by the PCO2.

And in metabolic acidosis, regardless if it's AGMA or NAGMA, the bicarb is dropping. It's just the mechanism by which it precipitates this is different. So in this one, bicarb is dropped. So what's happening here?

What's that going to do to the pH? Drop it. So you have to remember that in a metabolic acidosis, regardless of AGMA or NAGMA, bicarb is depleted, bringing down the pH. What's the reason?

The organic acids. They're driving down the bicarb. Because the concept is, here's an organic acid, just a generic version of it. This guy can give off that proton.

So what it does is it liberates this proton off. And when it liberates this proton off, that is what leads to this depletion in the actual bicarb. binds to bicarb and converts it into carbonic acid.

All right, cool. We'll talk about what these organic acids are when we get in to the causes component. Let's talk about the other one, which is enagma. An enagma, or a non or a normal, you can call it non or normal anti-gap metabolic acidosis. Again, all you're doing is you're taking the cations, which is primarily sodium, and you're subtracting chloride, bicarb and organic acids.

Now what you're noticing is that the organic acids really aren't the bulky one here. It's really what we're noticing is that chloride is going up and that's kind of driving down the bicarb. All right, so I could notice that the chloride could go up and that could drive down the bicarb.

But what I really kind of notice here is that my bicarb is the most significantly diminished. So I have to ask myself the question, okay, I know that in these patients who have enigma, their primary problem is, is that you drop their bicarb. Okay, well how would that affect my ratio?

Well if I go back to it, I think it's a simple concept here, that pH is equal to the bicarb divided by the PCO2. So as I drop down my bicarb, what am I going to see happen to my pH? I want to bring my pH down.

Then we have to generate ourselves the question, what's dropping the bicarb? Well, one is it could be the kidneys dumping bicarb. So there could be a renal loss.

bicarb. Maybe the kidneys are dumping the bicarb into the urine, which is depleting the bicarb within the bloodstream. That could be one reason.

Or it could be a GI loss. bicarb and if I'm losing bicarb from my GIT that could explain why the bicarb in my bloodstream is depleted. Again as the bicarb plummets what happens is that you see the pH drop.

So you have to remember metabolic acidosis the pH is intimately tied to the bicarb and you just have to figure out the reason as why the bicarb dropped. Nagma it's an organic acid I'm sorry agma is an organic acid that's elevated and a nagma it's some type of renal loss of bicarb. or GI loss of bicarb.

All right, cool. Well, we're almost there when we're gonna start talking about what are the causes of increased organic acids, what are the causes of renal losses, what are the causes of GI loss. Before we do that, I want you guys to start asking yourselves a question.

Anytime we have a disease, you should try to have an understanding of why it's bad. What are some of the complications that could arise? One of the first things that metabolic acidosis has three profound effects.

One on your electrolyte system. So, when you think about it, in metabolic acidosis, the pH is low. So, there's also another relationship is that whenever the pH is low, your protons are low.

So, protons and pH are directly proportional in the sense, right? Or inversely proportional in the sense. So, as you have increase in protons, your pH should go down. So, in these patients who have a metabolic acidosis, what I'll notice is they have lots of protons in their bloodstream. Tons of them.

Tons of protons in their bloodstream, whether it's an AGMA or an AGMA. Now, what happens here is that you have cells in your body. And what they love to do is they love to exchange ions sometimes.

So whenever there's lots of protons in your bloodstream, your body tries to say, okay, let me push some of these protons into the cell. That'll get rid of some of the protons and it'll bring the pH back up. That's a way of maintaining homeostasis. But whenever I bring a positive ion into the cell, I have to push a positive ion out of the cell.

And so one of the ions that gets pumped out here... is potassium. And so you know what happens is that potassium starts actually rising in the bloodstream. And if potassium rises in the bloodstream, what do we call this? We call this hyperkalemia.

So when the patient's potassium starts kind of bumping up above five, we start seeing potential complications. You know, one of the biggest complications of hyperkalemia is it can cause muscle weaknesses, but it can cause EKG changes. It can cause arrhythmias.

And that's one of the biggest things that you have to watch out for here with hyperkalemia. is you want to watch out, is the patient at high risk? Are they developing any complications such as? arrhythmias.

Now there is a lot of EKG changes that may also become playful. So in other words, you can see peak T waves. You can see a change in their PR interval.

You could see a flattening of their P wave. You could also see a widening of their QRS complex. And you may even see potential complications such as sine wave patterns that put the patient into VTAC or VFib. So these are all things that we'll talk about more in the actual potassium disorder lecture.

But watch out for hyperkalemia as definitely a possibility as a result of acidosis. The other thing is when a patient has lots of protons, right? So lots of protons built up.

You have to remember that in a patient who has metabolic acidosis, their bicarb depletes, their protons go up, all right? Because as there's less bicarb, there's more protons that are freely available that aren't binding to the bicarb. So when protons go up, what they do is they stimulate these little receptors that are in the periphery called chemoreceptors. These things are present like near the, usually near the carotid artery.

common carotid artery near the bifurcation and also near the aorta. And they're connected to nerves like the vagus nerve and the glossopharyngeal nerve. And what happens is they stimulate these puppies. When they stimulate these chemoreceptors, they send signals to your actual respiratory center and say, hey, man, it's really acidotic in this blood. You need to cause the patient to breathe faster, blow off CO2.

Because if they blow off CO2, they'll blow off some of that carbonic acid, and they'll help to drop down their protons, and that'll bring the pH up. And that's what happens is that what happens is these patients end up stimulating their respiratory center. They send lots of signals to the respiratory center which increases their ventilation.

So what happens is these patients experience an increase in ventilation and when you increase your ventilation, which is your tidal volumes and your respiratory rate, you're gonna blow off CO2. And so what happens is these patients blow their CO2 off and what we'll notice is is that they'll notice that they'll breathe faster. So they may have an increase in their their respiratory rate or an increase in their tidal volumes. So they're taking deep breaths or they're breathing really fast. And what happens is, is they do that to blow their PCO2 down.

And oftentimes we see this as a potential compensation mechanism, is that patients will breathe faster to try to bring their PCO2 down because their hopes is, is if I bring my PCO2 down, what does it do to the equation? It brings the pH up. Because if you remember, from that equation, it will have an inversely proportional relationship to pH. So that's the concept that I want you guys to remember.

All right, so definitely can breathe faster, which creates a compensatory change in the breathing pattern, and at risk for arrhythmias and hyperkalemia. What else? Whenever you have high levels of protons, especially when they're really, really high, causing the pH to get pretty low, this can cause direct inhibition of myocardial contractility. So now the myocardium is all jacked up.

It's not going to contract. If it doesn't contract, you end up with a reduced cardiac output. So that's one of the other complications is now the heart is stinking at being able to pump blood out.

If it struggles to pump blood out, Now what I see is I see a reduction in what's called cardiac output. And so these patients may have a reduction in cardiac output that then precipitates in the form of low blood pressure. So another potential complication from these patients is they could develop hypotension.

But here's the big thing. The acidosis has to be the point where the pH is less than 7.15. It has to be pretty low for you to start actually inhibiting myocardial contractility and sometimes leaving vasodilate the blood vessels. But either way, look for hypotension, tachypnea, and arrhythmia secondary to hyperkalemia in metabolic acidosis. All right, beautiful.

We've talked about metabolic acidosis. We know that the bicarb is low, the pH is low. We know that there's AGMA, anion gap greater than 12, NAGMA, anion gap less than or equal to 12. We know the differences between those pathophysiologically, and we know the hyperkalemia leading to arrhythmias. hypotension and tachypnea are the most common complications or manifestations of metabolic acidosis. Let's now talk about the causes of AGMA.

Within AGMA, we have to talk about those organic acids. What's building them puppies up? One of the biggest causes is diabetic ketoacidosis.

You need to have a patient who has diabetes. They need to have a very high glucose level. And they need to have elevated ketone bodies in their bloodstream.

So most of the time it's diabetic type 1. And you want to see elevated glucose levels. And you want to see elevated ketone bodies. How does this happen? You know, diabetes, they got a jacked up pancreas.

It's not doing a good job. Reduction of insulin production, usually. And what happens is whenever the insulin is reduced in its production, it doesn't allow for the cells to take glucose up. And so glucose uptake is inhibited. And that's what leads to the increase in blood glucose levels.

Well, how does the ketone bodies come into play? Insulin, whenever you can't get the glucose into the cells, says, hey, I've got to tap into an alternative source. I need to generate ATP because I'm not using glucose to make ATP. So what it does is. it tells your liver to take fatty acids and break them down.

So it undergoes a process called beta oxidation. So you increase your beta oxidation and when you increase your beta oxidation you increase the formation of free fatty acids and then they get broken down eventually into ketone bodies because there's too much acetyl CoA you take free fatty acid make it acetyl CoA not enough of that to actually get into the electron transport I'm sorry into the Krebs cycle. So a lot of it gets shunted into making ketone bodies. That's what happens and these patients get heavy amounts of ketones in their bloodstream.

Now what kind of ketone bodies are there? Well one is called beta hydroxybutyrate and the other one is called acetoacetate. Usually the one that we measure in the bloodstream is beta hydroxybutyrate but both of these can actually be excreted into the urine, you can get that off the urinalysis. All right, beautiful. That's the concept there.

All right, what's another cause? Another one is uremic acidosis. Uremic acidosis you can see in two particular diseases. One is a severe AKI, to the point where they pretty much need dialysis.

getting ready to go on dialysis, or severe end-stage renal disease where they're on dialysis and they haven't gotten dialysis recently, or they're almost at the point of needing dialysis. Now, differences in the pathophysiology slightly here is that in a severe AKI, what you're going to want to look at here is they're just profound, elevated creatinine, and usually a reduction in the urine output. In end-stage renal disease, you may also see this, but what you're looking for more specifically is their significantly reduced GFR over the years. Either way, in both of these scenarios, what ends up happening is the kidneys are losing the ability to excrete metabolic waste products, whether it be indicative of them having a very high creatinine or a very poor GFR. What happens is they build up nasty metabolic waste products like sulfuric acid and phosphoric acid.

acid. These things are building up. Now... The concept behind this is that the kidneys are damaged.

They've had profound injury, especially to the portions of the proximal convoluted tubule where you're supposed to excrete a lot of things. And they have injury to their glomerulus where you're supposed to filter things. So these patients not only struggle with filtration via their GFR, they also struggle with intact tubular function to secrete things from the blood into the tubular lumen. So what happens is these patients lose the capacity to be able to excrete these waste products.

products into the bloodstream. And that's usually the problem here, my friends. So we're struggling to excrete waste products, whether it be via filtration or tubular secretion, into the bloodstream, I'm sorry, into the urine.

That's the concept. So in these patients, you really want to see a poor renal function. In this one, you want to see high glucose and lots of ketone bodies.

All right, what about this next one here? Lactic acidosis. So with lactic acidosis, the problem with this one is there's two particular etiologies here.

One is you want to see very poor. perfusion. So you want to see a patient who's likely critically ill.

They're likely in shock. That's usually the most common etiology here is a patient who is in shock. What kind of shock am I talking about? We'll go through the different types of shock, any type.

It could be cardiogenic shock, could be obstructive shock, could be distributive shock. So again they could have cardiogenic septic, obstructive shock, hypovolemic shock, any of the types. Either way within the concept of this, when you have poor perfusion you struggle to get blood out of the left heart. heart, you struggle to get blood to the tissues and deliver oxygen to the tissues.

If I do not deliver oxygen to these tissues, so there's decreased oxygen delivery to the tissues, what happens is they say, well, I'm not going to undergo cellular respiration aerobically. And so because of that, what they do is, is they say, all right, I'm not going to convert pyruvate into acetyl-CoA. Instead, I'm going to undergo anaerobic glycolysis, and I'm going to make a crap ton of lactogy.

acid and they build up lactic acid within the bloodstream to the point where this thing starts relieving protons and start causing acidity within the bloodstream. So one problem could be poor perfusion. Again, think about any type of shock. The other thing is there could be a clot.

What if there's like some type of like clot or embolus here that's obstructing the flow? That could definitely be another one. So not only do you want to think about shock, you want to think about some type of the most common cause is what's called acute mesenteric ischemia where there's a clot.

inside of the actual mesenteric vessels, blocking the blood flow to the entire small intestine. Thing becomes ischemic and then infarcts. The other one is maybe it's not a problem with perfusion. Maybe it's a problem with oxidative phosphorylation.

There's many diseases that do this, but you really want to think, could the patient be having something like some type of decreased electron transport chain activity? Because even electron transport chain is supposed to be able to help make ATP from having oxygen. So what if you're having good but something's interfering with this.

There's so many different drugs that actually could do this. I think that's important to remember some of the drugs. One of them is metformin.

So metformin, especially in patients who have very, very significant chronic kidney disease can cause this. They can uncouple the oxidative phosphorylation. Another one is isoniazid. So look for a patient who is on this because they have TB. Another one that I really think is important to remember is whenever you have a very deficient level of thymine, so thymine deficiency.

And another one is isoniazid. one could be aspirin toxicity. So patients who have aspirin toxicity, B1 deficiency, isoniazid or metformin, these have all been shown that they potentially could inhibit the ATP formation.

So they not necessarily decrease oxygen levels, oxygen like perfusion to the tissue could be completely normal, but they uncouple it and lead to lots of lactic acid production. Okay, so one of the big things is poor perfusion or uncoupling. Sometimes we actually call this, if you want to call it a want to remember it like this, we call this one type A.

So lactic acidosis type A. And this one we call lactic acidosis type B. Because this one is a perfusion problem or a oxygenation problem.

And this one is a uncoupling of electron transport activity problem. Either way, in both of these, lactate levels should be elevated. So look for the patient who's in shock, who has abdominal pain, or think about these particular drugs. All right. Next one's actually pretty easy.

there's not too much to remember about this, think about incidental ingestions. So the two most common ones are going to be methanol and ethylene glycol. Now with these two particular toxins, what we notice is that whenever they're ingested, they do have the ability to liberate lots of hydrogen ions and cause an acidosis. But the other thing is that they change the osmolality. And so one of the things that we don't really look at, so you've noticed a trend here.

This one we're looking at problematic issues with like renal function, more particular issues with ketone body. Lactate levels. This one there's not really a specific like level and this one it's more looking at something called the osmolar gap. And so we'll talk about this a little bit later.

What it does it actually changes the osmolar gap and increases the serum osmolality and causes a big gap between the normal and expected. And so you'll see that this level will go up and that's something to think about. We'll talk about that later in the diagnostic section. Think about these particularly in antifreeze.

Usually that's the classic example of a child who consumed some type of antifreeze or pain thinner. Next concept here is we're gonna move on to number three. non-anti-gap or normal anti-gap metabolic acid dose, because we've talked about all the agmas at this point.

So, Zach, okay, I know that it's an agma, meaning that the anti-gap has to be less than or equal to 12. I know it's a renal loss problem, or I know it's a GI loss problem. All right, let's go through the renal loss problems. In this particular scenario, there is a couple of them that I want you to think about. First one that we can easily get off the board is CKD. First thing I want you to look at in any patient is, do they have a diminished renal function?

Not to the point of what we call for... uremic acidosis, but it's mild. I'm talking that their GFRs may be reduced. It's less than 60, but it's not to the point where they're almost on dialysis. So you want to look.

Do they have a reduction in their GFR? If they have a reduction in their GFR, you're done. You don't really have to go any further.

okay this is a patient who likely is gonna have CKD and again they're just their problem is that they struggle to excrete protons or reabsorb bicarb but most commonly is they struggle to they have a decreased ability to excrete protons so they decreased they struggle to excrete protons that's their big problem these you only look at when you say oh the GFR is normal so across the Across the board, the only way that you can think about these is if the patient truly has to have a normal GFR. So normal GFR because you can't exclude this. You see what I'm saying? You can't exclude it.

And then it makes these tests a lot more complicated and also kind of alters their sensitivity and specificity. So we'll go through these now. RTAs 1, 2, and 4. You're like, where's 3? I don't know. We don't really talk about it.

So we're going to pretend like it's never there. Within each one of these, they have a very specific mechanism that's important to remember for your exams. RTA1, the primary disease process is in the distal tubule.

That's what I want you to remember. Their distal tubule is all jacked up. So that's where their dysfunction exists.

Okay, so what do I mean? Well, I'm on the distal tubule. What happens is you take and you excrete protons, right? So you excrete protons into the urine, and then you're also supposed to take potassium ions and then reabsorb the potassium ions. That's what you're supposed to do.

So you're supposed to take potassium ions in, and you're supposed to excrete protons. You know what happens in these patients? all jacked up. They don't do this. They do not reabsorb potassium ions and they don't excrete proton ions.

If they don't excrete protons, what happens to the proton ions within the bloodstream? Goes up. If proton ions go up, what happens to your bicarb, my friends? The bicarb will go down. Yes.

So this will cause the bicarb to go down and if bicarb goes down, what happens to the pH? The pH goes down. So we see how that happens, right?

But there's other things that we can gain from this. If we don't reabsorb potassium, what happens to potassium? It ends up in the urine. So you get lots of potassium into the urine. That's actually helpful because then I dump my potassium, my potassium in the bloodstream should theoretically go down because I'm supposed to absorb this.

That's helpful. So having a low serum potassium level could help aiding in the diagnosis here. Cool.

What else? Well, the other concept is that I don't actually acidify the urine. This distal tubule is responsible for acidifying the urine.

If it's not intact, you can't acidify the urine. the urine. So what happens to the urine pH?

Is it going to be acidic? No, it's going to go up. It's going to be greater than 5.5. So we consider that less acidic. So we'll say that the urine pH, theoretically, is going to be higher, greater than 5.5 at least.

Okay. Beautiful. So that's how we establish the diagnosis of RTA1. Now you're probably like, okay, what causes RTA1? There's a lot of things that may cause this.

I think it's important to remember that usually it can be in the scenario of lithium. So lithium has actually been shown to cause this. Sometimes even autoimmune diseases.

So like as SLE, RA, make it because there are things like that. But oftentimes, it's maybe like autoimmune diseases or lithium use that's been shown to be associated with RTA1. Again, this is RTA1, this diagram here.

Okay, what about the next concept, RTA2? Got to have a normal GFR. Where's the problem?

Proximal tubule. So now this proximal tubular dysfunction. If the proximal tubule is jacked up, what is the problem here? Alright, well, it's supposed to take bicarb, and it's supposed to take potassium, and it's supposed to reabsorb these in the proximal tubule. But, it's all jacked up.

Can't do it. Alright, so then you lose bicarb. What happens if you... lose bicarb you plummet the pH pretty simple one here right all right but I'd also don't reabsorb bicarb I mean potassium what happens to potassium shoot right in the peepee right in the peepee it goes so potassium there'll be a lot of in the urine So what happens to the amount of the blood?

Tanks. So oftentimes these patients will have hypokalemia. Pretty bad actually too.

Now here's the interesting concept and RTA1 distal tubules jacked up. RTA2, RTA4 distal tubule is intact. It's pristine and it's secreting protons.

It's secreting protons. So because of that, you're beautifully secreting protons in this distal tubule that's not regulated by aldosterone. Because of that, am I able to acidify the urine?

Yeah. So since this is okay, My urine pH should be low for both of these and that actually helps in differentiating these from one another. Alright, cool.

So low urine pH less than 5.5, low urine pH less than 5.5. Alright, cool. So that's RTA2.

Well, what's causing proximal tubular dysfunction? There's a lot of things that have been theoretically associated with this. Could be multiple...

myeloma right there's also anti-seizure drugs to pyramids also been associated with this one and there's another weird disease it's called Fanconi syndrome this is usually some type of like genetic disorder and then another one is acetazolamide Which we actually use in certain patients. We're trying to diurese them and get rid of some of their actual bicarb. So we don't actually bring their bicarb up pretty high.

So it's usually used in metabolic alkalosis when you want to diurese people. Or we also use it in idiopathic intracranial hypertension as well. All right, so these are the particular things that you want to associate with RTA2. All right, beautiful.

All right, we're going to the next concept here, RTA4. In RTA4, the problem is the distal tubule. But you're probably like, oh.

Okay, Zach, I'm confused. You said distal tubule and now distal tubule. But Zach, you said the distal tubule is intact here.

It is. It's just there's a part of the distal tubule that we say is actually altered, but it's more particular than the distal tubule that is aldosterone regulated. Let's actually kind of parenthesy that right there.

So it's aldosterone regulated. Alright, so this is the one that's jacked up. So we're going to kind of bring it just a little bit further for simplicity's sake.

Alright, in this particular scenario you now have to say, okay this is aldosterone regulated. Alright, cool, cool, cool. Well, in this RTA4, aldosterone levels are depleted.

Aldosterone levels are depleted. What aldosterone is supposed to do, is normally you'll actually secrete two different things. One is to secrete protons.

The other one you'll secrete potassium. That's what it's supposed to do. If it's intact, there's a transporter there. Aldosterone will help to increase the expression of it and push these ions out. If aldosterone is not present or it's depleted, it's not going to be able to do this.

And therefore, this process will be inhibited. Will you be able to secrete protons into the urine? No.

If I have less protons, protons being excreted, what happens to my proton levels in the blood? They go up. If proton levels in the blood go up, what happens to my bicarb levels? Well, it's going to bind to the bicarb and then deplete the bicarb levels. So that should deplete.

What happens to my pH if my bicarb goes down? It goes down. So we see how that causes that, right?

But here's where it gets a little bit cooler. It's supposed to secrete potassium, but it's not going to secrete potassium. What happens to the potassium in the urine? It's low. Potassium in the urine is low.

If potassium in the urine is low, that means the potassium is likely going to be high in the bloodstream. You see how there is a difference between all of these. Now, you're also like, okay, Zach, I see that they're not secreting protons here. So wouldn't they not be able to acidify the urine? Again, the one that's more specifically constant, it's not like aldosterone dependent, is this part of the distal tubule.

It's secreting protons properly. So therefore, the urine should be appropriately acidified. This is the big differences that I want you to remember.

Now, hypoaldosteronism. There's different. types. So there's primary, right, and in primary usually this is an adrenal problem, so actually just put this in parentheses.

So primary is some type of adrenal issue, maybe like a tumor or an adrenal adenoma of some sort, all right. Secondary, a little bit more different though, there's a lot of different like things here that we can say with secondary hypohidrosis, and some of these things that maybe are worth remembering could be things like diabetes. It's actually been pretty common, this is a pretty common board exam question. NSAIDs.

and then any kind of drug that actually blocks like the angiotensin, like renin-angiotensin on the diastereo system. So you can think about that like your ACE inhibitors, your ARBs. And I'm going to abbreviate these MRAs, your mineral corticoid receptor antagonists, your aldosterone blockers. Anything like this can block the effect of aldosterone and exhibit the same type of effect. So either you don't release it or you block its actual activity somewhere in the renin-angiotensin aldosterone system activity.

Okay, we talked about the renal causes. We come down to the last one, and thank goodness this is the so easy one. It's the GI losses.

Now, your GI loss of bicarb is primarily dependent upon movement of bicarb through the intestines. If it's moving fast and it's not getting a lot of time to to be reabsorbed, then you're not going to have an appropriate amount of bicarb to be able to be absorbed. So the concept here is that whenever you're losing a lot of bicarb, because the absorption of bicarb is being inhibited, then you're going to deplete your serum bicarb levels.

So diarrhea is going to be a big one. I think the concept that you have to think about is what's the trigger. Oftentimes this is usually associated with something like gastroenteritis. You may see this.

The other concept here is that usually these patients are significantly dehydrated. So you really also want to look for a significant volume depletion. So they're significantly volume depleted in comparison to the etiologies up above. Alright.

Same thing with the pancreatic fistula. Usually this is like some type of recent abdominal surgery. So they probably have had some, look for a history of like an underlying abdominal surgery. And if they've had that, they probably had something that caused like a leak between their pancreas and their intestines.

And what happens is their pancreas is responsible for making a lot of the basic bicarbonate. And what happens is if there's an opening connection between one of the ducts and the intestines, it'll dump bicarb right into the actual intestines. And then what happens is you load your bicarb into your intestines, and then if there's lots of bicarb, you're going to saturate a lot of the opportunities to be able to allow for the absorption of bicarb.

And then what happens is the bicarb in your bloodstream gets depleted. Abdominal surgery, big one. Usually volume is not a significant issue here, so there's not usually a problem with volume here.

All right. So with this being said, this is by far going to be the most common cause of GI losses. This would be the least common cause of GI losses.

All right. All right, we talked a lot about metabolic acidosis, right? Now what we have to do is we have to move into the other concept, which is metabolic alkalosis, and then we're going to talk about the respiratory disorders, so acidosis and alkalosis.

All right, my friends, so now we're going to talk about metabolic alkalosis. So in this particular scenario, I think it's really important to try to be able to, again, think about what's really happening in this process. So really what's kind of occurring in this process is the patient is having a renal loss, particularly of protons.

That's really one of the big things is that they really lose a lot of protons in their urine. This is definitely, I'd say, one of the more common etiologies to definitely remember. So whenever you pee out tons of protons, right, what happens is it drops the number of protons inside of the bloodstream. So if you're peeing out tons of protons, that means less protons that are present in your serum. Right?

That's definitely the way we could look at this, is if you're losing lots of protons from your urine, this is definitely the less protons in the serum. What will happen is, is when there's less protons, That means that there's less of these protons binding to bicarb. And so technically, there'll be more free bicarbonate that'll be present. Less of it will be bound in this particular scenario to protons. And so bicarb will kind of go up.

And then what we know is that pH is basically equivalent to bicarb concentration divided by the partial pressure of CO2. And so what we can surmise here is that as bicarb goes up, pH will also go up. We just have to ask the reason as to why the bicarb is going up.

up, it's going up because the kidneys are dumping out protons. If they have lots of protons in the urine, then what will happen is theoretically in this scenario is that if you dump protons in the urine, you'll have less of these protons that will be available in the serum. And then you'll increase your bicarb because less of the protons will be bound to the bicarb.

All right, what else? Another cause could be GI losses. So you could lose a lot of these protons from your actual GIT. All right.

Now, whenever you're losing a lot of these protons from the particularly the GIT, as this starts to occur, again, you're going to have lots of these protons lost within your feces and maybe unfortunately, or I should not, I'm sorry, you're going to have lots of these protons lost in your gastric acid. That's usually the example here. And what happens is, is as I have more of the protons being lost from the body, lost from the body, what happens is, is I lead to less protons that are present within the serum. And again, as there's less protons, so as I lose more protons from the body, I'll have less protons present in the serum.

If there's less protons present within the serum, that will lead to an increase in your bicarb. Because again, there's going to be less protons binding to the bicarb. So again, This is the particular scenarios. You're either losing protons from the GIT or losing protons from the kidneys.

We'll talk about the etiologies here in a little bit, but that's the concept of metabolic alkalosis is bicarb is going up, pH is going up. It's either because you're losing protons from the GIT or from the kidneys. Alright, simple as that. complications of metabolic alkalosis? Whenever the pH is really high, what are some of the downstream negative consequences that can arise?

One of the things here I think that's important to remember, if you guys remember from the metabolic acidosis, is again, whenever protons are present in the bloodstream, there's a nice exchange, particularly potassium. ions. So in other words, in patients when they have less protons with inside of the bloodstream, there'll be less exchange. So less protons will be available to move into the cell and therefore less potassium ions will move out of the cell.

If less potassium ions move out of the cell, then the potassium levels with inside of the bloodstream will decrease and the patient can experience hypokalemia, usually when the potassium levels drop to less than 3. When potassium levels drop to less than 3, than three, the patient is at risk for arrhythmias. So you can start experiencing an increased risk of arrhythmias. What are some of these particular arrhythmias you may ask?

Well, I think one of them is to remember that it can lead to something called torsades de points because the concept behind this one is it can actually drop your T waves. So it can cause T wave inversion. It also can cause U waves to form, especially when the potassium gets low.

But then when it gets really, really low, it prolongs the QT interval, which increases the risk of things like torsades de points. We'll talk about that more again in the potassium potassium disorder lecture though. All right, so that's one big thing is hypokalemia.

You really wanna watch out for that. You know what's really interesting? In patients who have hypokalemia, that can actually cause metabolic alkalosis and metabolic alkalosis can also cause hypokalemia. So there is a bit of like back and forth and it's usually due to this particular activity here.

All right, beautiful. Next concept, this is actually kind of rare, but sometimes they will kind of test this for you in the vignette. And it's kind of related to calcium a little bit too, which is kind of nice because we're in the renal system, is that we're- And whenever you have less of these protons, right, so less protons technically, because again in these particular scenarios you're dumping these protons in your vomit or you're dumping them in the urine. What happens is the chemoreceptors in the carotids or in the aorta are responsible for sensing that. And whenever this happens, the chemoreceptors, they're normally responsive to whenever you have like really high levels of protons.

In this case, they're kind of going to be inhibited. They're not really responding to this like low pH. So they send less signals, if you will, via the vagus nerve, the glossopharyngeal nerve, to the respiratory system. So the respiratory center inside of the brainstem will be kind of inhibited, and it'll send less signals down to your diaphragm, into your intercostal muscles. So the rate of breathing will kind of actually kind of drop.

So these patients will experience something called hypoventilation. Now whenever the patient hypoventilates, what do you think actually happens here? Yeah. So the hypoventilation.

Hypoventilation will lead to, in this particular scenario, less gas exchange. Whenever there's less gas exchange in this particular event here, the patient will try to build up their CO2. And so what will happen is in this hypoventilation, you'll see that the patient's partial pressure of CO2 in these attempts will try to go up.

And they'll try to generate a weird respiratory acidosis in this particular scenario. And that's also important. However, this is not as common. I think it's important to remember that in comparison to a patient who has metabolic acidosis and they develop a respiratory alkalosis, extremely common. Patients with metabolic alkalosis and developing a respiratory acidosis, it is less common.

All right. The other thing that I think is important to remember here is that in patients who have metabolic alkalosis, they may also have one other kind of effect, and that is that they can cause tetany and they can cause neuromuscular irritability. So I will write this down.

I'm not going to go crazy into the mechanism. But it is important and it's kind of prudent to know that as proton levels kind of deplete, what happens is, is you have more freed up spots from albumin. I'm going to call it like a free albumin.

And I'm going to kind of put that in parentheses, meaning it has more like sites where ions, positive ions can bind onto. So whenever you have low protons, you now increase the amount of like free sites for albumin. And what happens is, is this binds up calcium. So then you get this calcium albumin complex. complex.

And whenever you bind up calcium, what happens to the amount of free calcium? Well, then the amount of free calcium goes down. And so as I form more of this complex, I deplete my free calcium.

And as I deplete my free calcium, I can start to experience weird things like tetany. And I think it's important to remember this is more pertinent in the hypocalcemia lecture. What does tetany look like?

Perioral, paresthesias. You can also get the carpal-pedal spasm, right, which is particularly when you inflate the blood pressure cuff, the Tresor's sign, and you also may get the Shavstak sign whenever you tap over the facial nerve. So these could be things that you see in metabolic alkalosis that can worsen tetany findings.

Alright, cool. So tetany, kind of maybe something to think about. Hypoventilation, something to think about, but I think hypokalemia is a really big one to remember in metabolic alkalosis. The next concept here is like, okay, well, I know metabolic alkalosis.

I know that the patient is, they're getting rid of, in this particular situation, they're dumping out protons in their urine or they're dumping out protons from their vomit. They deplete their protons inside the bloodstream and as a result, bicarb goes up. All right, let's think about the renal losses of protons. There's usually two etiologies, one diuretics and the other one is hyperaldosteronism.

There is another one, it's called Barter and Gittleman syndrome. It's more in the pediatrics kind of system. It's very rare, so we're not gonna talk too much about it.

We're gonna focus on the more common things. Diuretics is the big one. There's two types. Loops is going to be more common. Thiazide is going to be another one that's utilized.

This one's more in hypertension. This one's more in like, you know, volume overload states, CHF patients. Now, what happens with these is that they particularly work. So, you know, here's our loop of Henle, or our nephron, I apologize.

So, Bowman's proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct. And the ascending limb of the loop of Henle What happens is these loop diuretics, they're specifically working at this part here. So what they're supposed to do is, is they're supposed to play a role in kind of like sodium and chloride. You know, generally this helps to reabsorb sodium, reabsorb chloride, particularly into like the, like this medullary interstitium to create a nice gradient, which allows for water to get pulled out in the descending limb.

So it's really important that countercurrent multiplier mechanism we talked about in physiology. Well, Lupov-Henley... particularly loop diuretics, they'll inhibit this.

And so you're not going to be able to reabsorb the sodium and the chloride and put it into the interstitium. So it kind of keeps water in the tubule and then kind of pulls a lot of volume out from the patients. That's actually one thing to remember, is that in this particular state, you aren't able to, so it's supposed to pull water. So we'll kind of represent this as water.

But you're not going to be able to do that because you're not going to be able to pull the sodium and the chloride out here in the interstitium to drag the water out. So another really important thing to remember is that whenever patients use diuretics, they can kind of get relatively volume depleted. So I think a really important thing to remember, so when patients are taking diuretics, they may use it because they're volume overloaded or they may use it for other situations, but sometimes with excessive or overzealous use, you may deplete the patient's blood volume. All right, cool.

Question is, how the heck does this lead to acidosis? Okay. Whenever you have this inhibition of reabsorption, you're kind of causing a lot of sodium to get to the distal tubule.

So now, whenever there's lots of sodium in the distal tubule, like more than usual, locking this off, what happens is that there's supposed to be like a little transporter right here. And what it does is it brings sodium in and pushes protons out. And the more sodium there is present here, the more protons it pushes out. So if you have lots of distal sodium delivery, you're going to have lots of protons that are being pumped out here into the tubule and then out into the urine.

That's how this happens. So the mechanism by which it actually triggers this is it increases distal sodium delivery. And by increasing that distal sodium delivery, you cause more exchange for protons in the actual distal tubules or the collecting duct, leading to loss of protons in the urine. But on top of that, they also lose a lot of volume, and they also sometimes deplete their potassium. So I think it's also important to remember that these patients will have a volume depletion and a depletion in their potassium.

And that could be helpful, believe it or not, in the diagnostic algorithms. All right, cool. So we now know that loop diuretics are acting here. for completeness sake, the thiazide diuretics would actually work.

Here. So they're supposed to be pulling the sodium and the chloride at this level. And if you are inhibiting this with the thiazide diuretics, it'll cause a lot of sodium distal delivery there, leading to protons being lost.

Alright, beautiful. So think about that, my friends. Hyperaldosteronism, on the other hand. What's happening here? Well, in this one...

It's actually affecting the distal tubule. So it's more particularly going to be two types We'll talk about these one. There is a primary type and the other one is a secondary type, but we will discuss these.

I think one of the big things to remember here is that with hyperoptic For aldosteronism, is it primarily, regardless of the primary or secondary, it is going to hit the distal tubule. So let's remember that it's going to be working on the distal tubule in comparison to the loop of Henle or the distal convoluted tubule, the early part for thiazide heretics. Now when it works here, what happens is, let's kind of go through this mechanism. You know the adrenal cortex?

The adrenal cortex is good at making a hormone called aldosterone. But what if for some reason, and we'll talk about the different reasons why this could happen which comes into the primary and secondary in a second, what if it's producing too much aldosterone? Well, you guys remember metabolic acidosis that what was the distal tubule which is aldosterone regulated doing?

Secreting what? Come on, I'm yelling out. Protons and potassium.

So if aldosterone is present in high amounts, what do you think it's going to do? That sucker is going to be amped up. And it is going to really hike up the activity of this.

And it's going to cause a lot of protons and a lot of potassium ions to be dumped into the urine. That's one of the big things here to remember. The other concept is it actually will cause a lot of sodium reabsorption as well. So what I see here is I see that the patient is definitely losing a lot of potassium. But here's the other concept.

With aldosterone, I'm going to bring it over here. Aldosterone has also been known to... increase sodium and water reabsorption.

So it increases sodium, it increases water reabsorption. What does that do to your blood volume, my friends? it increases your blood volume. What would that do to your blood pressure?

It would pump up your blood pressure. So oftentimes their blood volume may actually become a little bit elevated. And then on top of that, their blood pressure may be elevated.

And that is actually very helpful to differentiate between these two, is that sometimes these patients may be mildly hypervolemic. They usually don't become profoundly hypervolemic because of something called aldosterone escape. We're not going to go into that, but it actually is important to remember that can happen. But it is also common that we're dumping potassium. So potassium will also be low.

But you're going to notice a slight difference here between a volume overloaded or hypervolemic state and a hypovolemic state with excessive diuresis. Okay, so we got a concept of that. And again, it's important to remember that this is all based on aldosterone regulation.

That is important to remember. So the mechanism between this is aldosterone regulation, whereas distal sodium delivery. Now, let's briefly talk about primary and secondary, just real quick.

In a patient who has what's called primary hyperaldosteronism, the problem exists here in their adrenal cortex. Usually there's a tumor here. There's a tumor that's just pumping out aldosterone.

Usually it's something called Kahn syndrome. So it may be worth remembering Kahn syndrome, which is usually some type of adenoma. That's something worth remembering. The other one is usually secondary.

Now secondary. is usually a little bit more interesting. This is usually things like a renal artery stenosis.

It could be CHF. It could be cirrhosis. I think the common thread along all of these is that all of these lead to a reduced renal perfusion. In renal artery stenosis, there's a plaque in the renal artery, right? In CHF, they are having a lot of fluid leaking in their interstitial spaces.

Same thing with cirrhosis. And so they have... have a reduced effective arterial blood volume.

Because of that, they have less perfusion to the glomerulus. What's the hormone that's released whenever there's low-breeding perfusion? Renin.

So, whenever there's high levels of renin, This is the big difference here. Renin will then stimulate the actual adrenal cortex to make lots of aldosterone. So that's the difference between these patients.

Patients with secondary usually have high renin and high aldosterone. Patients with primary... have high aldosterone and usually get negative feedback they shut down their renin.

So that's actually kind of helpful to remember when we get to the diagnostic portion. Okay my friends we've talked now about this point pretty good about the renal pathophysiologies behind metabolic alkalosis. What about the GI? With GI it's pretty straightforward. Your GIT is just, you know, dumping out protons.

And usually another one is chloride. So they're dumping out protons and then another ion that they may be dumping out is chloride. Now when you dump out tons of protons and tons of chloride, you'll see that these patients will lose their protons, they'll end up causing an increase in their bicarb, and as a result, they'll end up with a metabolic alkalosis. So with this one, you really want to think about a loss of hydrochloric acid from the stomach.

What are the etiologies behind this? A patient is vomiting, or they have an NG tube. Maybe they have a bowel obstruction of some sort. When you have a bowel obstruction, sometimes they put an NG tube down into your actual stomach, to help to decompress it.

Maybe there's lots of fluid there, and they're having to suction and suction and suction a lot of that out so that the patient doesn't have consistent abdominal pain. That could be a very, very, very common pathophysiological process here. The thing that you have to remember is that in these patients, they're losing lots of protons, hydrochloric acid, but guess what else they're losing? They're losing volume.

So oftentimes, these patients are pretty commonly volume depleted. So they will have maybe a low volume. The other concept here that's actually important to remember is that these patients, Whenever they're kind of in this state of metabolic alkalosis, they'll try to tell their kidneys to kind of try to respond to that. And what the kidneys will try to do is maybe it'll change the chloride kind of states. And so another thing important to remember here is that in vomiting and NG tube suction, they have a urine chloride level.

And what we've seen with these urine chloride levels is that they're often like relatively low. And what it tells me is that these patients probably have some type of non-renal source of proton and chloride loss. It really has.

helps to add to the diagnostic utility of this and saying if the urine chloride is low, it maybe is more of a saline responsive state like excessive volume losses and vomiting, NG tube suction, or like a remote prior history of diuretics. Because diuretics will lead to direct chloride losses when they're being actively used. We'll get more into the diagnostics.

It may seem confusing. It'll become more apparent when we talk about the diagnostics. That covers metabolic alkalosis.

We now have to move into the respiratories and finish this off. about them and then go into the diagnostic section. Alright my friends so now we're gonna move on to the respiratory acidosis and alkalosis. This will finish off the pathophys that causes the complications and then we'll move into the diagnostics. So let's go through these.

When we talk about respiratory acidosis the problem here is the lungs. They're having difficulty with being able to properly ventilate. So the primary pathophysiological process that explains all of this is usually that the patient is undergoing what's called ventilation.

Now the problem with hypoventilation is that the they're not allowing for proper gas exchange. There's not enough movement of CO2 from the blood into the alveoli. If that happens, then you're not getting rid of CO2.

All right. So the problem here is with hypoventilation is that there is a inability to clear CO2, right? So we're going to put down that there's what's called decreased CO2 clearance, right? When there's decreased CO2 clearance, what happens is that the partial pressure of CO2 in the bloodstream starts rising.

So if the partial pressure of CO2 in the bloodstream starts to rise, what happens to the pH, my friends? Come on. The pH will do what?

It'll decrease. And the reason why is we can figure that out from the formula here is that the sense of this is that there's pH is equal to bicarb divided by the PCO2. And if PCO2 rises in the setting of hypoventilation, then the pH should drop. And that's what drives the acidosis. The question that helps us.

us here is what's driving the increase in pco2 hypoventilation now to dig in a little bit more all right hypoventilation is whenever the patient is not taking in a deep breath or they're not breathing at a fast enough rate so it's poor respiratory rate and poor deep breathing so with that being said there's three particular ways that you can look at that one is there is a respiratory problem or a respiratory center problem so you know inside of the brainstem this is the area that's supposed to send information to the nerves to the muscles contract take a deep breath breath in or breathe at a good rate. If there is a dysfunction of the respiratory center, can you send the signals down to the muscles, I mean via the nerves to the muscles and cause them to contract? No, that'll drive hypoventilation. The other concept is What if there's damage to the spinal cord or to the nerves or the muscles that are supposed to be contracting? If they're not sending signals or they're not receiving the signals to contract, will they contract properly and take a deep breath in?

No. And then lastly, what if there's an obstruction in the airway or there's an inability to take a breath in because there's an underlying airway obstruction process that would also limit CO2 clearance. So there's three particular ways that I want you to remember it.

Respiratory-centered depression, neuromuscular disease, and airway obstruction. That can drive hypoventilation. and drive up the pCO2. So what we've seen here, it doesn't usually cause very prolonged effects. It's usually whenever you're at these high levels for a long period of time that it can be kind of detrimental.

But what we see is, is when a patient has very high high partial pressure of CO2, it kind of has an interesting effect on the cerebral blood vessels. All right? So what it can actually do is it can actually promote what's called cerebral vasodilation.

So it's going to cause these vessels to undergo a very expansional process. So they'll have what's going to go what's called cerebral vasodilation. Whenever you dilate these blood vessels, that allows for kind of an increase in blood volume or blood flow to the brain.

So as a result, these patients will get what's called an increase in cerebral blood flow. We kind of usually abbreviate that CBF. When you increase the amount of blood flowing into the brain, the brain is inside of a skull, right?

So the skull is a fixed space. Whenever you have more brain, more blood, more CSF, the pressure inside of that skull increases, and that's called intracranial pressure. And so oftentimes these patients may have an increase in their intracranial pressure, the pressure inside of the skull. And this could lead to cognitive deficits or actually I would say more specifically arousal problems. So what could that potentially look like?

These patients may kind of experience states of lethargy, right? So they may have lethargy, maybe super, super tired. Maybe they become obtunded.

And they require... a lot of painful stimuli to arouse. Or they may even go to a comatose state.

This is usually in severe, severe ICP elevations. All right. This is definitely something to consider. All right.

Now, I think why this is really important is in patients who have underlying intracranial pressure, you want to avoid respiratory acidosis. I think that's the big thing to remember is if you have already an intracranial pressure problem, the ICP is high. If you add respiratory acidosis into the mix, it can... can potentially worsen their intracranial pressure. That's where you want to add this in.

So remember, if there is a intracranial disease, for example, let's say like an ICH or a subarachnoid hemorrhage, and then you add, and you have the problem here that you add respiratory acidosis, This will definitely be a recipe for disaster because this combination, my friends, could lead to the very thing of where ICP can kind of boost up. And that's where I really would want you guys to remember is that respiratory. acidosis in itself is not going to be capable of producing a massive ICP elevation to cause these kinds of effects. It'd be more likely if they have some other type of intracranial disease that it could precipitate this.

Okay, that's one concept. The other concept here is How does the body compensate when a patient is chronically acidotic? Because you know the process whenever a patient's metabolically acidotic or alkalotic, your respiratory system responds quickly.

When patients are chronically acidotic or chronically alkalotic from a respiratory process, the kidneys take time to do this. And so it's really important to remember that when a patient has a very high partial pressure of CO2, and I'd say the most common cause of this is going to be something like COPD. Super, super common cause.

It causes the PCO2 to rise. When the PCO2 rises, it will cause what to do, what happens to the pH? Let's actually go there first. What happens to the pH?

The pH will drop. When the pH drops, this tells the kidneys, hey, pH is, you know, kind of struggling here, dude. You got to change something. And what the kidney does is says, all right, hold my beer. I'm going to go ahead and reabsorb more bicarbonate.

And that's what it does. It increases the bicarbonate. When it increases the bicarbonate, what that does is that causes the pH to do what?

Go up. And that's the compensatory process. That's why patients who have chronic respiratory acidosis, they may often live with an elevated baseline bicarbonate to compensate and increase their pH so that they can live appropriately.

So that's really, I think, something to remember more appropriately in patients who have underlying COPD. So again, you can see elevation. elevated intracranial pressure.

I just think it's more important to remember in this particular scenario. And you can see a compensatory process here. It's just way more common and appropriate to see it in a COPD state.

We understand the complications now. Now we move on to the next step here, which is okay. What is causing hypoventilation? I told you three things, respiratory depression, neuromuscular disease, airway obstruction. With respiratory depression, it's all here.

Something is depressing this puppy. The respiratory center within the pons medulla area. It's not sending signals down to the nerves and so because of that the patient will undergo a reduced respiratory rate.

And that's usually the big thing. Sometimes we even say that this is so bad that they may even they may even progress to kind of an apneic state. Sometimes even worst case scenario they may develop apnea.

So they're not really breathing at all. Okay? This is usually because of drugs or some type of pathological process that is depressing the center.

Usually for drug overdoses it's going to be opioids or it could be Benzodiazepines. These are usually going to be the most common kind of triggers here. I would say opioids are going to be the big one with the opioid kind of like pandemic that we have.

And this is usually the problems. One of the big things I think is important to remember with these is that they oftentimes present with an altered mental status. In combination, with their reduced respiratory rate and apnea. But here's the big thing.

They oftentimes respond or improve with a reversal agent. And we'll talk about those in the treatment section or even in the diagnostic section. So improve with an antidote.

So watch out for a degree of altered mental status and on top of that an improvement with an antidote. With a stroke this is usually some type of like brainstem pathology. Alright so some type of brainstem disease maybe a brainstem stroke, brainstem bleed, something to that effect and what happens is is that these patients oftentimes not only have an altered mental status, maybe they have an altered mental status, but they also have neuro deficits. They may have dysarthria, dysphasia, contralateral weakness, so things like that effect that you really need to remember. And these will...

have no change with an antidote. So no change with an antidote. So sometimes these patients may come in not breathing. You think, oh, man, I wonder if they're altered.

You don't really notice the neuro deficits at that moment. You give them an antidote like flumazenil for benzos or naloxone for the opioids, and they don't improve. And maybe you think of that as a stroke pathology. And then you show it to the CT scan or an MRI. All right.

That covers respiratory depression. Not too bad, right? But basically, the concept is that they're not breathing. They're not ventilating, so they're not going to.

clear the CO2. What about neuromuscular diseases? I don't want to spend a ton of time on these because they're actually kind of difficult to diagnose in the acute setting.

This is more kind of applicable to the actual neuromuscular disease that we'll talk about individually. But in this particular scenario, the respiratory center is intact. There's something wrong with maybe the spinal cord, the nerves themselves, or the neuromuscular junction.

There's a lot of different diseases here. I don't want to go stir crazy on this. I think it's important to remember, think about things like ALS with respect to the spinal cord. Think about something like Guillain-Barre syndrome. particularly with the nerves because it causes demyelination.

Think about maybe even a patient who has like a myasthenia gravis. All of these things could be potentially etiologic because of the neuromuscular junction. I think one of the big things here is that these patients again they have dysfunctional nerves or neuromuscular junctions.

The muscles don't contract. So if there's an impairment and contraction this will therefore lead to very shallow tidal volumes. So the big kind of problem here is that these patients take in very little.

decrease tidal volumes or they have what's called shallow breathing. So it's not that they're not breathing, they're breathing, they're just not breathing very well. So they take in very poor tidal volumes or in other words quotation shallow breathing and sometimes they compensate and breathe faster to help themselves with that. So think about that and the patient has ALS you'll expect more significant like deficits and like especially weakness. Can't brace injury, maybe the ascending paralysis with areflexia, myasthenia gravis you may expect, more particularly the bulbar symptoms, the dysarthria, the diplopia, the ptosis, the dysphagia in combination with the kind of shallow breathing.

So again, ALS, GBS, and then make sure that this is clear, myasthenia gravis. Okay. What about the last one?

This is the one that I really want you to remember because respiratory depression is a big one and airway obstruction is a big one. For airway obstruction, it's usually COPD and asthma exacerbation. There can't be upper airway stuff like a foreign body, but these are the big ones that I think you'll experience in the exam. So first thing is the primary problem with this is that the patient has an airway obstruction that is leading to something called dynamic hyperinflation. We talk about this more in the pulmonary system, but the concept is pretty like relatively simple.

And patients who have COPD and asthma, their airways are obstructed. When they're obstructed, it's hard for them to get air out. Their lungs inflate. So they kind of like hold on to a lot more air. They have more residual volume.

Their total lung capacity is bigger. Because of that, it makes it harder for them to take a deep breath in. So imagine this is where their lungs are in the solid blue line.

The dotted blue line is the place where they can go. That's not a lot. So their ability to take a deep breath in is very poor. So they have kind of a similar scenario to the neuromuscular diseases where their tidal volumes are really, really poor.

In other words, they have that shallow, shallow breathing. And so sometimes you'll be like, oh, okay, well, how do I differentiate these two? What if I don't have like an obvious neuro exam that helps me out or neuromuscular exam that kind of makes it obvious that it's a neuromuscular disease? One of the big things with this one. is that oftentimes these patients will also have like profound wheezing because it's more of an airway obstruction.

So you really want to be looking for that. That's one big thing. But here's the other concept. It actually improves when you give them bronchodilators. So if you give them something like a bronchodilator or you give them a steroid, it'll open up their airways.

It'll reduce the airway obstruction. It'll help to be able to allow air to leave. It'll reduce dynamic hyperinflation and allow for them to take a deep breath in and clear their CO2.

So that's some things to remember. For COPD exacerbation, please do not forget that. That's respiratory acidosis, baby. Let's talk about respiratory alkalosis.

This one's actually not too bad, and I won't spend a lot of time on it. I think there's a couple of things that are important to take away from it, but it's not the most important acid based disorder, and unlikely the one that you'll get tested on a lot. With respiratory alkalosis, the primary concept behind this one is the respiratory center and that pons medulla junction is on fire.

That thing is hyperactive, sending tons of signals down to the spinal cord, down to the nerves, down to the muscles, and causing the patient to hyperventilate. That's the concept here, my friends. They are hyperventilating.

When you hyperventilate, you're breathing deeper and maybe even faster. If you're breathing faster and you're breathing deeper, you're going to clear your CO2. Pretty good. So now if I'm increasing my CO2 clearance by ventilating faster or better, what's going to happen to my partial pressure of CO2?

My partial pressure of CO2 will dip. If it dips, what's going to happen to my underlying pH? Well, use the equation here. pH is equal to bicarb divided by the PCO2. As my PCO2 dips, my pH will go up.

Because again, these are inversely proportional. So that's how I get the alkalosis. The concept of how my CO2 drops is I'm hyperventilating. So there has to be some type of respiratory center hyperactivity. We'll talk about what those are in a second.

When a patient has respiratory alkalosis, what could be? be the complications. Well remember I told you before that it was actually more affecting the cerebral vessels so whenever a patient has a particularly their pco2 is kind of low so let's say that pco2 is really low When the pCO2 is relatively low, what it'll do is it'll cause the cerebral vessels to undergo vasoconstriction, right? So now I got a low pCO2, really low, it'll cause cerebral vasoconstriction. Those things will squeeze down.

When I vasoconstrict these vessels, my cerebral blood flow, common abbreviated like this, is reduced. If my cerebral blood flow is reduced, again, brain, blood, CSF, inside of the fixed space of the skull. If brain decreases, blood decreases, CSF decreases, what happens to the pressure inside of the skull? It decreases. And so theoretically, what can happen is the intracranial pressure could decrease.

Now you're like, well, that actually sounds like kind of a good thing. Wouldn't it be? Well, it could be. One of the concepts here is that whenever you have a reduced cerebral blood flow, one of the concepts that these patients may have reduced cerebral blood flow really quickly and they could pass out.

And so one of the concepts that we can kind of see here, especially with the reduced cerebral blood flow, is you can get that transient loss of consciousness. And so one of the things is that you could experience what's called syncope, or at least even presyncope. That's one manifestation.

Imagine breathing really, really fast and deep. You ever hyperventilated before? You got anxious? Sometimes you can syncopize.

That's kind of common with this effect. With the ICP, it's actually a therapeutic. tactic.

Let's say that a patient has an intracranial disease. All right. So something like an ICH, something like a subarachnoid hemorrhage.

And because of this disease, they've increased their intracranial pressure. They've increased blood. They've increased the amount of CSF or things inside of their brain.

Because of that, when you you increase their ICP, what could you do in effect to lower their ICP? Hyperventilate them. We do this in patients on the ventilator. So what we'll do is, is we'll actually undergo hyperventilation on the ventilator.

We'll make the ventilator cause them to breathe faster and deeper. Doing that will drop their PCO2, and when we drop their PCO2, we'll cerebrovasoconstrict them and drop their ICP. This is a therapeutic tactic.

It's usually only going to transiently drop it down during an ICP crisis. That's what it's used for. It shouldn't be used all that often because there has been some literature that says that it could actually cause them to vasoconstrict too much that they could get a stroke. So you want to be careful with this.

All right, that's the concept I really want you to remember is them using an intracranial disease is to drop the ICP. What can it do to the kidneys? It's actually pretty interesting. With this, what do we see? We see the PCO2 is low, and that's going to cause the pH to go up, right?

So PCO2 low, pH goes up. That's going to tell the kidneys, all right, pH is up, all right. I should probably dump bicarb, right? I should probably dump the bicarb.

So I'm going to do that. I'm going to pee out a ton of bicarb in my urine. And if I... pee out a ton of bicarb in my urine, then I'll leave less bicarb in the serum.

And if there's less bicarb in the serum, my pH will do what? What's going to happen? It's going to go down.

So again, I'm going to have this process where the PCO2 is low because I'm hyperventilating. pH goes down, tells the kidneys, the kidneys say, okay, I'm going to go ahead and dump lots of bicarb into the urine. If I dump bicarb into the urine, theoretically, The bicarb in the bloodstream now will drop. If the bicarb in the bloodstream drops, that means, again, what's going to happen?

You're going to have lots of protons that are available here. What's it going to do to the pH? It's going to drop the pH. So this is the compensation mechanism.

I would say that this is relatively rare. You don't see this a lot, but it is something to consider. All right, my friends. Now, the last part here is what's triggering the respiratory center to be hyperactive?

I don't want you to go too crazy with these. I want you to make it pretty simple. The limbic system has a pretty profound effect on our medulla. So things like pain and anxiety can definitely increase the stimulation of the respiratory center.

It's pretty straightforward. Usually this improves. So one of the ways we can determine if this is the cause, it is improves with the appropriate treatment. In other words, you give someone analgesia, anxiolysis, their respiratory rate will kind of come down, their deep breathing will come down.

With hypoxemia, there's so many different types of diseases. Oh my gosh. It could be high altitude. I think that's an easy one to be able to pick up, especially off of the patient's kind of history. So if they're kind of at a high altitude and they come down and during the descent they improved with their respiratory rate and tidal volumes, that could be the etiology.

But it could have to be other pulmonary diseases, pneumonia, PE, ARDS, so many different things that causes like chalked up lungs. When the lungs get all jacked up, they aren't able to oxygenate. When you don't oxygenate, what happens? It tells the chemoreceptors, bro, I ain't oxygenating.

You better breathe faster and deeper and get some more oxygen in me. And that's the common thread here is that oxygen, when it's low, tells the respiratory center, breathe faster. So usually the key with this one is that you treat them with oxygen, treating the underlying disease. But oftentimes when you give them oxygen, it improves when you give them what they're deficient in.

So give them what they're deficient in, they should improve. Alright, what else? Metabolic toxicity. This one's actually so many different things.

I don't want you to go too crazy because there could be a lot of other things that are hard to kind of differentiate, but oftentimes, aspirin toxicity seems to be kind of a common one that gets tested on. There can be other ones if you want to remember them. Think about things like...

early sepsis, think about liver disease, think about pregnancy. There's been some kind of literature that suggests that maybe even hyperthyroidism can do this as well. But I want you to remember aspirin toxicity. What happens with this one is that I think it's important to remember that this is one of the disorders where you can get a metabolic acidosis and a primary respiratory alkalosis.

This is a rare one. So sometimes it's it'd be mean but they could do it and in this particular situation they could actually have you use what's called the Winters formula and that could help you to calculate determine the changes in the pCO2 in a metabolic acidotic patient, but also think about patients with aspirin toxicity they oftentimes present with tinnitus so sometimes tinnitus and acidosis and tachypnea or respiratory alkalosis could really seal the diagnosis of an incidental or purposeful ingestion of aspirin toxicity all right my friends that covers the path of pathophys, the causes, the complications of the acid-based disorders. Now, let's move into the diagnostics.

Now, we've gone through the patho, we've gone through the complications. I think the important thing to remember is how do we really diagnose the primary acid-based disorder? And once we've diagnosed that primary acid-based disorder, how do we determine what the actual type or etiology is of that specific acid-based disorder? Let's go through that.

First thing you're going to need is an arterial blood gas. From the arterial blood gas, you're going to be able to get your pH. It If it's less than 7.35, it suggests an acidosis. From here, you then need to determine, is it metabolic or respiratory?

So for respiratory, the CO2 is the problem. It's greater than 45. That's respiratory acidosis. In this situation, bicarb, if this is low, that's the primary problem.

This is metabolic. Then from here, you need to look at the anion gap. Why?

Because the anion gap tells me which type of metabolic acidosis. So from here, I need to calculate it. Sodium minus chloride minus bicarb. If it's less than or equal to 12, oh, that was nagma.

And if it's greater than 12, that's agma. So right away, I've already determined if it's an acidosis, then I think respiratory depression, neuromuscular, obstruction. Antiongap, NAGMA, CKD, RTAs, and diarrhea. Here, aniongap is at the cult mnemonic. There is other things.

I don't want you to go too crazy, but the aniongap metabolic acidosis, you can further go forward and check what's called the delta-delta ratio because sometimes people can have an agma as well as mixed diseases. When you check the delta-delta ratio, you're basically checking the difference in the aniongap over the difference in the bicarb. And based upon that, you get a ratio.

than 0.4, it's a pure NAGMA. If it's 0.4 to 1, it can be an AGMA and a NAGMA combined. If it's 1 to 2, it's a pure AGMA.

And if it's greater than 2, it is an AGMA and a metabolic alkalosis. This is more step one, particularly pertaining. But now we've gotten a good idea of at least these primary.

Let's go over here and talk about the other primaries. Greater than 7.45, it's an alkalosis. Check the CO2 and the bicarb.

If the bicarb is high, it's metabolic. If the CO2 is low, it's respiratory alkalosis. Done. We've generated our primary diagnoses and then gone a little bit further to determine the NAGMA and NAGMA.

Now we just have to go through each one of these and figure out how do we determine the actual cause. So let's go through these. Respiratory acidosis, history, and physical. Do they have an altered mental status? You've got to suspect respiratory depression.

This could be drug overdose or stroke. Does it improve with naloxone? Oh, that was opioid overdose. Does it improve with LAPF?

flumazenil, oh, that was the benzodiazepine overdose. And if it doesn't improve with any of them, you probably should suspect some type of brainstem disease or stroke. Is there wheezing? Oh, that probably means that there's a COPD or asthma exacerbation by an airway obstruction. Given bronchodilators and steroid, does it get any better?

Oh, that's probably a COPD or asthma exacerbation. If you've done these and you've ruled these out, then you can potentially start considering a neuromuscular disease. All right, my friends, now let's move on to the diagnostic approach to figuring out the cause behind menopause.

metabolic acidosis. So when you look at this patient, if they have an anion gap greater than 12, it's an AGMA, right? Now from an AGMA, you then get to think about, okay, what were the particular causes?

Oh, Zach said it was cult, right? It was a ketoacidosis, uremic acidosis, lactic acidosis, and toxic congestions. Well, how the heck do I figure that out?

Well, I would check ketones. I would check a BMP to look at the renal function. And then on top of that, I would check a lactate and an osmolar gap. By doing that, you're giving yourself enough information, figure out what the underlying cause is. For example, if the ketones come back elevated and they have diabetes and their glucose is high, it's probably DKA.

If their urea, their BUN, their creatinine, their GFR is all jacked up, then I would be thinking potentially about AKI or CKD as a potential etiology behind uremic acidosis. If their lactate level came back elevated, it could be a lactic acidosis. You then just have to do a little bit more digging behind their lactic acidosis.

Look at their history. Are they hypotensive? Have they recently been in shock, like circulatory shock of sorts, septic, cardiogenic, obstructive, hypovolemic?

That could be their cause. Could it be that they have abdominal pain out of proportion? Could be acute mesenteric ischemia.

Or could it be due to none of those? Their blood pressure is normal. Their perfusion is good. It's just that they've been taking metformin, isoniazid, thymine, or aspirin toxicity that's causing this decoupling of the electron transport chain. And then lastly, check their osmolar gap.

So you check, calculate, their serum osmolality, and you compare that to what the osmolality that was generated from a lab, and then looking at that, is it greater than 10? If it is, then it's likely a toxic alcohol ingestion, so methanol or ethylene glycol. Now, from here, you've generated your AGMA differential.

What about the NAGMAs? Well, if it's less than or equal to 12, okay, then I'm suspecting a NAGMA. What do I do? Here's where you check the urine anion gap. The urine anion gap is very, very helpful, and what you're looking at is the NAGMA.

looking at is you're looking at the ability to secrete ammonium chloride into the urine. That is the basic concept. You're looking at the ability to secrete ammonium chloride into the urine. If the urine anion gap is positive, positive, this is most likely telling you that the problem is existing at the kidneys. All right.

So usually this is your CKD, your RTA1 or your RTA4. From here, how do I differentiate these three? Check a GFR, check potentially a potassium from the BMP and check a urine pH. For example, if I do that and the GFR is really low, It's probably CKD.

If the GFR is normal, their serum potassium is low, and their urine pH is high, this is probably RTA1. And if their GFR is normal, their serum potassium is high and their urine pH is low, that's probably an RTA4. If the urine anion gap is negative, so negative, remember gut, that can tell you that it's possibly a GI cause.

Now, there is one other renal cause that can kind of get mixed in there with the GI causes, and that's RTA2. So now you're thinking, is it RTA2 or is it? a gut cause, diarrhea pancreatic fistula.

If there's no diarrhea, no abdominal surgeries, nothing that suggests the pancreatic fistula, then get a GFR, a BMP, and a urine pH. The reason why is that the GFR is normal. The BMP suggests that they have a low potassium and their urine pH is going to be low. That's an RTA2.

And then boom, you've gotten the nagmas and you're done. Let's now move into the respiratory alkalosis. This one's, again, a little bit more like schematic.

You have to think about it clinically. If you get a history and physical and it suggests, okay, I think that there's concerns for aspirin toxicity. They have tinnitus.

They have a headache. They have metabolic acidosis and respiratory alkalosis. Get an aspirin level to rule out aspirin toxicity.

But oftentimes, pain or anxiety that improves with a proper treatment regimen, that could be suspected increased limbic system activity. And again, if you give them analgesia and it improves, it's probably pain-induced. If you give them anxiolysis and it improves, it's probably anxiety-induced.

If they have hypoxemia from pneumonia, ARDS, or from potentially a pulmonary embolism or high altitude, and you give them oxygen supplementation and they improve, that could, again, support a hypoxemia-driven etiology. But then you have to ask yourself the question right off the get-go. Do they have exposure to high altitude? If it's yes, it's high altitude induced respiratory alkalosis.

If that answer is no, then it's probably all the other ones. Pneumonia, ARDS, or maybe a pulmonary embolism. In that particular situation, maybe get a chest x-ray or a CT scan of the chest and look to see for those particular pulmonary pathologies that would suggest this. For metabolic alkalosis, this was actually pretty straightforward in the sense that you just want to look at their volume status. The reason why is I want to know if it's renal or GI, right?

But I want to know, okay, renal, I know it was diuretics. That was the big one. And it was also going to be a problem with aldosterone, right? So in this particular situation, it was hyperaldosteronism.

If I look at these patients and I say, okay, either they're having lots of vomiting or they're peeing out lots of protons or they have hyperaldosteronism. I know that the diuretics and the vomiting and the injury tube suction, that caused hypovolemia. I know that. But hypervolemia was the hyperaldosteronism.

So right away I can create a bifurcation. For example, if I have a patient who has decreased skin turgor, dry mucous membranes, as you can see here, they have increased heart rate. So so tachycardia and hypotension suggesting hypovolemia. And they have flat jugular veins.

They have no evidence of edema. This suggests hypovolemia and particularly what we refer to as a contraction alkalosis. If I look and their membranes are moist, they have normal skin turgor, their BP is maybe even a little bit elevated. They're a little hypertensive. They have distended jugular veins.

They have maybe some evidence of peripheral and pulmonary edema. That's a hypervolemic related. elevated alkalosis. Right away, this makes our lives so much easier. Because in a hypovolemic, you just need to look at the urine and to see which one is more rich in chloride.

If the chloride is really, really rich in the urine, or if it's low in the urine, you get an answer. So low urine chloride tells you that this is not really coming necessarily from the kidneys. It's coming from the GIT, vomiting, increased energy tube suction. And this one's interesting.

It's prior diuretic use. So their kidneys had the opportunity. after they stopped diuresing to go into a retention mode and so they stopped actually excreting chloride if they're actively using diuretics they're going to be peeing out chloride with their sodium and in this situation that would be their potential etiology. All right.

Now, hypervolemic is pretty straightforward because it's probably just hyperaldosteronism. And you then have to evaluate if it's a primary or secondary by checking their renin and aldosterone levels. If the renin is low and aldosterone is high, it's an adrenal problem.

All right. So this is primary. And if it's high renin, high aldosterone, this is a secondary problem.

And boom, we've gone through a metabolic alkalosis. Now the question that comes about here is how do we really treat these? And it really depends upon the underlying cause. For all of these, treatment of the underlying cause is of the utmost importance. So for example, in metabolic acidosis for DKA patients, you need to give them insulin because if a patient has very decreased insulin, they're not going to get glucose into their actual cells.

So it builds up and they develop hyperglycemia. If they don't have insulin, they undergo lots of lipolysis and they make lots of fatty acids that they take into the liver. They undergo a lot of ketogenesis and make ketone bodies. So your job is to come in there and say, how can I help? Let me give insulin.

If I give insulin, I'll shuttle the glucose into the cells and drop their glucose. If I give them insulin, I shut down lipolysis and ketogenesis and I decrease their ketone bodies. One of the best ways of being able to see if a patient's acid anion gap is improved. improving and their acidosis is improving, especially DKA, is look to make sure that their anion gap normalizes as you give them insulin. If it's not, you need to give them more.

For lactic acidosis, you have to treat the underlying cause. For example, if a patient's hypovolemic, give them more fluid. You'll increase their blood volume, their stroke volume, their cardiac output.

You'll perfuse their tissues more, give them more oxygen, shut down the lactate formation, and decrease their lactate level. If they have distributive shock, meaning that their vessels are super dilated, you give them vasopressors to squeeze the vessels. This increases their resistance, increases their mean arterial pressure, perfuses their tissues better, gives them less anaerobic glycolysis, and decreases their lactate level.

And if they have cardiogenic shock, you give them inotropes to squeeze the heart and pump more blood out of the heart. If you pump more blood out of the heart, you'll perfuse the tissues better, drop their anaerobic glycolysis, and decrease their lactate levels. So again, you're treating the underlying trigger. And if it's a drug, discontinue or remove the offending drug.

Now, the next one's uremic acidosis. This one, you have to treat the underlying disease, but this is the only time where sodium bicarb really is kind of like the primary treatment here. In uremic acidosis, the problem is that they're having difficulty retaining bicarb.

And so because of that, their pH is dropping. And so what you do is you give them bicarbonate. And by giving them bicarbonate, you're replenishing the bicarbonate levels in their blood.

And this is going to bring their pH up. And a patient who has uremic acidosis, who you give them sodium bicarbonate, and they still become refractory to that and maintain an acidosis. this is where I would obtain some type of access via fistula, a graft, or a central venous catheter, and perform dialysis to remove a lot of the excess acid. Now, toxic alcohol ingestion, if they are taking methanol and ethylene glycol, you can give them a drug to shut down a lot of the metabolites that are being formed.

When methanol and ethylene glycol are ingested, they tell the liver to make a lot of this particular molecules of toxic metabolites via an enzyme alcohol dehydrogenase. If you give fomepazole, it inhibits this enzyme, inhibits the breakdown, and reduces the toxic metabolites that are formed here. Now, if a patient has a toxic ingestion and they're continuing to undergo the unfortunate effects of that ingestion, you can then bridge them to dialysis to remove those actual toxic ingestions. Lastly, in a patient who has a nagma.

and non-anti-gap metabolic acidosis, this is the time where sodium bicarbonate is helpful. So in patients with mild CKD, any of the RTAs, particularly RTA1 and RTA2, not so much RTA4, and any of the particular causes due to diarrhea or pancreatic fistulas could even be considered here as well. The next thing is a metabolic alkalosis. It depends upon which type.

So is it hypovolemic or is it hypervolemic? So in hypovolemic, you've gotten rid of too much fluid. Either you've gotten rid of a lot of chloride-rich fluid from them vomiting and G-tube suction or peeing out a lot of sodium.

chloride. Give them back that fluid. So normal saline, which is going to be 0.9% sodium chloride with fluid and water is going to improve their volume and improve their chloride lobe, which is going to bring down their bicarb and bring down their pH. All right. So that's the mechanism here is replacing what they're losing, and that's going to replace their volume, and it's going to drop their bicarb, because as you increase chloride, bicarb will drop, and as a result, pH will drop.

If it's hypervolemic metabolic alkalosis, acetazolamide may be the potential option here, and this is good in patients who have underlying CHF, or they have a contraindication to getting lots of fluids. And this... particular situation, acetazolamide inhibits sodium and it also inhibits bicarbonate reabsorption.

And so because of that, you're going to lose a lot of the bicarbonate and volume in the urine. And by doing that, if you lose bicarbonate in the urine, you have less bicarb present within the bloodstream. And this is going to therefore cause the pH to start to come down. All right. Again, this is usually given to patients who have, let's say, CHF, and they have a metabolic alkalosis, but you have to continue to keep diuresing them.

So you're giving them loop diuretics and thiazide diuretics, which causes metabolic alkalosis. and it's continuing and you don't want that metabolic alkalosis to continue, you give them acetazolamide. Another option is you can give them potassium chloride tablets.

Because as you diurese, you also get rid of potassium. So you give them potassium chloride tablets, you'll replete their potassium, but you'll give them... them chloride and chloride naturally will drop their bicarb levels and that will also decrease their pH. Now that's how we would treat the acidosis and alkalosis for metabolic.

What about respiratory? Again, it's treating the underlying cause. So if they have a drug overdose, for example, naloxone would be the best for an opiate overdose. Flumazenil would be the best for a benzodiazepine overdose.

You restore the activation to the center and boom, breathing ensues. And that's how you treat the acidosis. That's going to be important to remember there. For a COPD and asthma exacerbation, the best thing to do is to bronchodilate and reduce inflammation.

So steroids, bronchodilators. And you know what else is very, very helpful? BiPAP.

BiPAP has been shown to be beneficial because it gives time for those anti-inflammatories and bronchodilators to kick in. The concept behind this is that patients who have COPD or asthma exacerbations, they air trap. They trap a lot of air and they build up their CO2 within the lungs, within the bloodstream. So what you need to do is institute BiPAP.

BiPAP keep the airways stented open and maintain that patency to deflate and get rid of their co2 if you get rid of that co2 you're going to now improve their actual respiratory acidosis and also reduce that need for constantly having to breathe faster and deeper so you'll reduce their worker breathing significantly respiratory alkalosis it's actually pretty straightforward we talked about a lot pain anxiety give them pain medication or anxiolysis hypoxemia give them oxygen but treat the specific cause and based upon this we have now effectively, and completely talked about acid-based disorders. That was a tough one. I hope that you guys stuck in there. I hope that you guys enjoyed it and it makes sense to you.

And I hope that you're able to nail these questions really easily. All right, engineers, love you, thank you. And as always, until next time.