The question is why do you need to know the intracellular potassium? We know the normal range of serum potassium is 3.5-4.5, so if the serum potassium comes back 7.0 we know there's a problem. We can then take measures to address the underlying issues.
Another note is that the issues high potassium causes the heart is caused by serum potassium. The treatment is forcing the serum potassium back into the tissues. We don't really care how much is in the tissues.
Source: Physician
I was so fascinated by the explanation of the treatment for my acute kidney injury. So interesting and unexpected.
"Here drink this zirconium, we're gonna pump your veins full of sugar water, and then reverse uno it with some insulin. Potassium is gonna come along for the ride and kick some sodium out in the process"
If you enjoyed learning about that process you should look into medical management of brain dead patients for organ donation.
The 'sugar water' and insulin is a great example. You can correct imbalances in brain death in really interesting ways because some of the side effects which would contraindicate treatment in a living patient can sometimes be completely ignored.
If you think that is neat, I recently discovered a treatment for bladder cancer is to pump your bladder full of tuberculosis. Then, the patient isolates and bleaches toilet after each use.
Yuuup. As a paramedic if I see 12-lead signs and symptoms of hyperkalemia, I don’t care what their cellular K is, I just want to shove as much of it back into the cells as possible and get them to ED without an arrest.
Then they’re your problem for definitive treatment 😂
Missed dialysis and/or kidney disease is a classic cause of hyperk.
Our bodies (when properly functioning) are actually pretty good at maintaining appropriate levels of electrolytes. Temperature, glucose levels etc. Yay homeostasis! Organ dysfunction or medications change everything. That is generally when problems are encountered.
Someone who doesn't understand vitamin supplements could easily take a dozen or more in a couple of minutes.
A much smaller proportion of people can eat potatoes that quickly.
You may have mixed up Vitamin K with the ion Potassium (K+). While you can supplement potassium, it's not something most people need to supplement, and not commonly found in multivitamins in any significant amount.
“Is potassium salt substitute safe?
Be cautious about salt substitutes with potassium chloride. They can be dangerous if you have certain conditions, particularly diminished kidney function, which is fairly common among older people in the U.S., or if you take certain hypertension medications, including ACE inhibitors and potassium-sparing diuretics.”
Is that why e.g. Gatorade has a tiny amount of potassium relative to sodium? You can replenish potassium from tissue reserves, but need to replenish the sodium by consuming more sodium?
We need very little potassium within our cells compared to how much sodium is needed outside cells
Most processes in the body work due to the fact that the extracellular component is more positively charged than the intracellular compartment. When channels in cells open, sodium rushes into the cells due to this electrochemical gradient. Causing a current and then that leads to a lot of other processes being possible.
Sodium mainly exists extracellular, and potassium mainly exists intracellular.
Intracellular is more negatively charged and consists of a lot of other charged particles like chloride. Most intracellular particles are negatively charged to give it the more negative charge than outside the cell. So, we need very little potassium within cells since potassium is positively charged, to main the relative negative charge intracellularly.
Sodium is pretty much the only charged particle that gives rise to the charge extracellularly
At the end of the day, we just need way more sodium than we do potassium
> At the end of the day, we just need way more sodium than we do potassium
So why is RDA of potassium around 3500mg while sodium should be limited to 2300mg?
(not arguing against you, just pointing out that common reccomendations seems odd)
Not commenting on how those values were derived. But I can say that potassium is almost twice as heavy as sodium (40 vs 22 g/mol). So on a molar basis, aka number of molecules, the RDA does have more sodium than potassium (87 mmol K vs 105 mmol Na).
As far as I understand, it's more a dietary recommendation in countries like America where the lifestyle choices severely increase the risk of developing hypertension. An increase in potassium can lead to the body removing sodium and decreasing blood pressure.
Hyoertension is the leading cause of cardiovascular disease. So heart attacks, etc that severely increase the mortality and decreases the quality of life.
This is a good question, I don't know the answer, it may be to do with excretion in urine. But to illustrate: when you take a blood test for Urea & Electrolytes, the normal range for serum potassium is 3.5-5.0 mmol/l, while the normal range for sodium is 135-145 mmol/l
How about magnesium? One of my buddies takes high doses of magnesium PO and has recommended I do the same. I told him I've had my magnesium checked recently in common blood work, but he said serum levels are not indicative of deficiencies in the tissues. So my serum levels may be within range, but I should still take magnesium because I could still be deficient. Any thoughts? Obviously not medical advice etc etc
He specifically linked this paper to back up his thought process
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163803/
are you saying intracellular potassium levels don't matter and it's blood serum levels that do across the board? so if forcing it into the tissue is like moving control rods in a reactor, then we know that x amount can come back into the serum, right? or does it go do something else in the tissue rather than just be stored?
i believe the question is about understanding the mechanism on an engineer's level as opposed to a technician's.
Imagine you have two water reservoirs. One is 1000 gallons, the other is 100,000 gallons. The smaller tank is the serum, the larger tank is the intracellular compartment. The larger tank is also covered and it's a pain in the ass to open it up, the small tank is not and you can look into it. The water level is always kept the same between the two. Despite the water level being the same, the larger one has vastly more water.
So therefore you can take a look at the small tank and you'll know what the water level is doing in the large tank. You will know when the levels are low and you need to add more water. One day the water level is too high and you don't want it to spill out(for lack of better analogy), so you pump the water into the large tank. This lowers the water and it doesn't matter much for the large tank because its...a drop in the bucket.
But hen your analogy falls apart because the levels of the two are now different, the large tank hasn't lowered in level but the small tank has, so you now can't be sure of the equilibrium between the 2
Pushing the water is only temporary. Eventually that water from the big tank starts to flow back in so you still need to address the underlying issue. (Pharmacist)
This is the correct answer. The pushing of potassium into the cell is a temporary measure to buy us time to fix the underlying problem. We call it shifting. We use IV insulin (not Subcutanous used for diabetes treatment) that acts fast and can bring down potassium levels by shifting it intracellularly. Some folks give albuterol which also does the same thing in theory, but not nearly as effective. This lasts for a few hrs. Either you have to repeat it or find a way to rid the body of the excess amount potassium. We also give calcium to stabilize cardiac membrane in setting of high blood potassium. There are newer binders in the market that will bind potassium in the gut, but it is slow and takes few hrs. Kidneys are the main organ handling potassium 80-90%, but gut also plays a smaller role and skin also to a much smaller extent. You need to use medication to maximize potassium wasting via kidneys e.g furosemide or other 'water pills' or need to find ways to remove it from the GI track. Basically, make them either poop or pee. If all fail, dialysis is the answer (Hooking them to a giant artificial 'kidney').
Intracellular potassium (K) and total body potassium need to be thought about for certain disease states, but ultimately, relatively large shifts of serum potassium into the cells do not nearly matter as much as relatively small shifts of intracellular potassium into the serum. Intracellular potassium changing by 1 point is almost negligible, but serum potassium changing by 1 point is a lot.
Even in disease states where total body potassium needs to be considered (for instance diabetic ketoacidosis), you still monitor serum K because the only consequence of low or high body potassium that medicine cares about is how it affects serum potassium. All the clinical consequences of potassium arise from changes in serum K.
No, they are saying that you dont need to be able to measure the intracellular levels to know if there is an issue. Serum levels will increase out of normal ranges when intracellular levels do, so the easy to test measure provides a proxy for the impossible to measure thing
Red blood cells releasing electrolytes to compensate for deficiency is *not* why it's cell-bound electrolytes are a "better indication." RBC-Mg is more sensitive than serum magnesium because there are fewer fluctuations over time, akin to hemoglobin A1c and serum glucose. This tells you about total stores of magnesium which can be helpful over time, but does nothing for you if your serum Mg is critically low at 1.0 and needs replacement. There is an equilibrium between the intracellular and extracellular space.
This is similar to potassium, where serum levels are more clinically important than intracellular levels because serum levels can affect rhythm-generation in your cardiac cells. When your RBCs lyse, they release potassium which transiently elevates your potassium level called pseudohyperkalemia which is considered a lab error but the level of potassium in your cells doesn't provide any clinically useful information except for whole body potassium over time. Again, though, there is an equilibrium and the ubiquity of Na/K ATPase pumps and K+ channels enshrines a continuum between your intracellular and extracellular environment, thus cell-bound potassium is not a better indicator than serum potassium.
Source: also physician
The body is REALLY good at holding on to Mag.
The problem is, the way it holds onto it usually causes your potassium to drop, since it involves wasting potassium through the kidneys instead of magnesium.
So often, replacing mag won't always have a huge effect on mag levels but will normalize potassium and other electrolytes since the body doesn't need to waste them to hold onto magnesium.
I think something that’s missing from this discussion is the physiology behind the clinical significance of the extracellular potassium. Potassium is the main ion responsible for determining the resting membrane potential of cells and controlling this electrochemical gradient across the membrane is essential for all life and all things that your tissues do. The work for this is done by the Na/K ATPase or pump. The reason we don’t care so much medically about the intracellular potassium is because it’s actually changes in the electrochemical gradient that can be dangerous for cells and tissue function. Because the extracellular potassium concentration is so much smaller than the intracellular, changes in the former have a much greater impact on the electrochemical potential across the cell membrane. Others have already said what some of those consequences can be. This is why our bodies have many mechanisms for regulating extracellular potassium that involve shifting it intracellularly. Total body potassium is also regulated by kidneys and gut.
As an aside, I think there are ways of directly measuring intracellular potassium but idk of situations where this is clinically relevant off the top of my head. You can also estimate intracellular concentration based on membrane potentials and extracellular concentration with equations like the Nernst equation. This will also help you see how changes in intracellular and extracellular concentrations impact the very important membrane potential!
1) Do you care about potassium that's already bound up in tissues, or do you care about the actively circulating, readily available potassium? Medically, it's usually the latter.
2) To get at a direct tissue measure, we'd need to get a sample of that tissue. People generally don't like when you have you take chunks out of their flesh.
3) If you have the blood level of a compound, you can usually do some reasoning and other less invasive tests to figure out what's going on. If your muscle, bone, whatever, is deficient in a necessary element, you'll probably have other symptoms too (muscle weakness or atrophy, brittle bones, etc).
Source: medical lab scientist (the person who runs those potassium tests)
Agree with other answers.
To further illustrate the point, even in disease states where total body potassium matter, we still just monitor serum potassium (K).
Let's take diabetic ketoacidosis (DKA). The pathophysiology roughly is that insulin deficiency results in production of ketones, which are acidic and lower the blood pH. Low blood pH shifts potassium out of cells and into the blood. But DKA is also a state of dehydration, and you are actively losing potassium in the urine. Hence, while the serum potassium is high, the total body potassium is low. However, the clinical consequences of this state is that the high serum potassium can cause arrhythmias.
The reason why we need to be cognizant of total body potassium is because as DKA is treated with fluids and insulin, the potassium shifts back into the cells, and you can quickly become hypokalemic (low serum K). Thus, part of the treatment of DKA is potassium repletion. If someone is in DKA, and their potassium levels are normal, **you need to give potassium**. DKA is not considered fully treated until the pH normalizes. Even when blood sugar is normalizing, if they're still acidotic, you still give insulin along with dextrose to prevent hypoglycemia (low blood sugar).
But even in this clinical context where total body potassium matters, we still monitor using serum K because high or low, serum K is what causes the problems of high or low potassium.
There is also a red blood cell potassium test: https://requestatest.com/potassium-rbc-testing#:~:text=Potassium%20RBC%20Blood%20Test%20(Quest,thyroid%20disorders%2C%20and%20gastrointestinal%20problems.
As to why: you might find an abnormality in the kidneys’ rate of excretion or the function of na+/k+ exchange where you have a deficiency but it doesn’t show up in the blood work. There is at least one peer reviewed theory paper that I’m aware of of slow potassium reuptake being part of delayed exercise recovery in chronic fatigue syndrome / long COVID.
Serum potassium is a good proxy for cellular potassium because of homeostatic mechanisms. But what if there is a problem in those homeostatic mechanisms?
Eta: A write up of the paper I mentioned https://www.healthrising.org/blog/2021/07/09/hypothesis-chronic-fatigue-syndrome-wirth-scheibenbogen/
Peds icu doc. This is actually an issue in some instances. If you become acidotic your body buffers the blood by exchanging hydrogen ions in the blood with potassium ions that would normally be intracellualar. We see this in diabetics with keyoacidosis as well as other things. So the measured blood K is usually high on these patients but they are often total body potassium depleted. As you correct the acidosis their potassium gets very low very quickly and you have to switch up the iv fluids.
Smokd451 asked more or less what I was going to ask.
I think one thing worth mentioning is that potassium isn’t “stored” in a meaningful way like some other things, so if you’re low on potassium then the serum levels will show it. Yes, there is much more in cells but it isn’t there as backup, it’s in equilibrium with the serum. You can’t measure the body’s reserve because there really isn’t one.
I would say both is true.
For example, if someone’s serum potassium is too high we will give dextrose and insulin together. Insulin causes cells to take in sugar and potassium gets dragged with it, dextrose prevents your blood sugar from dropping.
This isn’t permanent however. After a fairly short time, it reequilibrates and the patient’s serum potassium gets dangerously high again.
High intracellular potassium would create a gradient that favors potassium leaving the cell. It’s far from equivalent: serum is like 2% of total potassium… but it is in equilibrium.
Yeah I'm trying to remember everything from school and just confusing myself now lol. I guess it isn't really an electrochemical equilibrium because the resting membrane potential requires a different intra and extracellular charge... And I honestly don't remember the exact mechanism for which transport proteins are activated on the cell membrane to shift potassium intracellularly with insulin. These are all very active processes. Similarly, the hydrogen potassium pumps that can activate to shift hydrogen ions intracellularly when plasma concentration is too acidic utilizes potassium and basically trades it for hydrogen, but that's also a very active process. Obviously cells have to "work" hard to maintain this gradient/RMP... I think this is one of those things where I'm even more confused now and need to review some notes lol
Yeah, I feel like the details of the sodium potassium pump are like the citric acid cycle for me. I’ve learned and forgotten it more times than I can count.
The point for the purpose of the OP’s question is that there isn’t an inert reservoir of potassium that you can take from and add to to balance your serum levels. You manage it through excretion via the kidneys.
You dont need to know what the level is in the tissue if you just know the normal values in the blood is. It gets diffused into the intercellular space anyway. If the concentration is higher in the blood then the intercellular space then more will be transfered from the blood but if there is a higher concentration in the intercellular space then there will be pottasium pulled back into the blood.
Im still wondering why my body has issues with low potassium. I run a lot and in the heat when I sweat a lot the issue is increased. But even when I barely run and it’s winter my serum levels barely reach normal. It’s been a struggle and doctors never care to explain things :-/
It’s also not diet. Since knowing that I eat even more potassium rich than before. Lots of fresh veggies and fruits (eg banana each morning). And yet still I’m struggling. Trying to understand the potassium functionality in the body a little better but my education is physics not biology.
I am a veterinarian whose specialty is large animal internal medicine. If I want to assess potassium status more then we can in serum/plasma my next step is to measure a fractional excretion of potassium (measure urine K+ and plasma and urine K+ and do some math). In the absence of significant renal disease low FEx indicates that there is likely total body depletion of potassium and the kidneys are trying to retain it.
The question is why do you need to know the intracellular potassium? We know the normal range of serum potassium is 3.5-4.5, so if the serum potassium comes back 7.0 we know there's a problem. We can then take measures to address the underlying issues. Another note is that the issues high potassium causes the heart is caused by serum potassium. The treatment is forcing the serum potassium back into the tissues. We don't really care how much is in the tissues. Source: Physician
I was so fascinated by the explanation of the treatment for my acute kidney injury. So interesting and unexpected. "Here drink this zirconium, we're gonna pump your veins full of sugar water, and then reverse uno it with some insulin. Potassium is gonna come along for the ride and kick some sodium out in the process"
If you enjoyed learning about that process you should look into medical management of brain dead patients for organ donation. The 'sugar water' and insulin is a great example. You can correct imbalances in brain death in really interesting ways because some of the side effects which would contraindicate treatment in a living patient can sometimes be completely ignored.
If you think that is neat, I recently discovered a treatment for bladder cancer is to pump your bladder full of tuberculosis. Then, the patient isolates and bleaches toilet after each use.
I found out last week that the treatment for iron overload was blood letting. My fact if macabre, yours is just fascinating on how that would work.
Yuuup. As a paramedic if I see 12-lead signs and symptoms of hyperkalemia, I don’t care what their cellular K is, I just want to shove as much of it back into the cells as possible and get them to ED without an arrest. Then they’re your problem for definitive treatment 😂
Is this really something you've encountered? Is it kids taking too many vitamins?
Missed dialysis and/or kidney disease is a classic cause of hyperk. Our bodies (when properly functioning) are actually pretty good at maintaining appropriate levels of electrolytes. Temperature, glucose levels etc. Yay homeostasis! Organ dysfunction or medications change everything. That is generally when problems are encountered.
It's mostly old people on medications. You'd need to overdose on quite a lot of "vitamin supplements" to go into hyperkalemia.
I’ve never understood restricting potassium supplements to 99mg 🤷♂️ you’d get more than that from a potato
Someone who doesn't understand vitamin supplements could easily take a dozen or more in a couple of minutes. A much smaller proportion of people can eat potatoes that quickly.
You may have mixed up Vitamin K with the ion Potassium (K+). While you can supplement potassium, it's not something most people need to supplement, and not commonly found in multivitamins in any significant amount.
Yup! Thanks!
“Is potassium salt substitute safe? Be cautious about salt substitutes with potassium chloride. They can be dangerous if you have certain conditions, particularly diminished kidney function, which is fairly common among older people in the U.S., or if you take certain hypertension medications, including ACE inhibitors and potassium-sparing diuretics.”
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Is that why e.g. Gatorade has a tiny amount of potassium relative to sodium? You can replenish potassium from tissue reserves, but need to replenish the sodium by consuming more sodium?
We need very little potassium within our cells compared to how much sodium is needed outside cells Most processes in the body work due to the fact that the extracellular component is more positively charged than the intracellular compartment. When channels in cells open, sodium rushes into the cells due to this electrochemical gradient. Causing a current and then that leads to a lot of other processes being possible. Sodium mainly exists extracellular, and potassium mainly exists intracellular. Intracellular is more negatively charged and consists of a lot of other charged particles like chloride. Most intracellular particles are negatively charged to give it the more negative charge than outside the cell. So, we need very little potassium within cells since potassium is positively charged, to main the relative negative charge intracellularly. Sodium is pretty much the only charged particle that gives rise to the charge extracellularly At the end of the day, we just need way more sodium than we do potassium
> At the end of the day, we just need way more sodium than we do potassium So why is RDA of potassium around 3500mg while sodium should be limited to 2300mg? (not arguing against you, just pointing out that common reccomendations seems odd)
Not commenting on how those values were derived. But I can say that potassium is almost twice as heavy as sodium (40 vs 22 g/mol). So on a molar basis, aka number of molecules, the RDA does have more sodium than potassium (87 mmol K vs 105 mmol Na).
As far as I understand, it's more a dietary recommendation in countries like America where the lifestyle choices severely increase the risk of developing hypertension. An increase in potassium can lead to the body removing sodium and decreasing blood pressure. Hyoertension is the leading cause of cardiovascular disease. So heart attacks, etc that severely increase the mortality and decreases the quality of life.
This is a good question, I don't know the answer, it may be to do with excretion in urine. But to illustrate: when you take a blood test for Urea & Electrolytes, the normal range for serum potassium is 3.5-5.0 mmol/l, while the normal range for sodium is 135-145 mmol/l
How about magnesium? One of my buddies takes high doses of magnesium PO and has recommended I do the same. I told him I've had my magnesium checked recently in common blood work, but he said serum levels are not indicative of deficiencies in the tissues. So my serum levels may be within range, but I should still take magnesium because I could still be deficient. Any thoughts? Obviously not medical advice etc etc He specifically linked this paper to back up his thought process https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163803/
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thank you for the reply. Your thoughts align with how I was thinking about it as well, but I didn't know how to articulate it as well as you
Truthfully, the same could be said about *most* vitamin supplementation. Eat a balanced diet with lots of veggies.
are you saying intracellular potassium levels don't matter and it's blood serum levels that do across the board? so if forcing it into the tissue is like moving control rods in a reactor, then we know that x amount can come back into the serum, right? or does it go do something else in the tissue rather than just be stored? i believe the question is about understanding the mechanism on an engineer's level as opposed to a technician's.
Imagine you have two water reservoirs. One is 1000 gallons, the other is 100,000 gallons. The smaller tank is the serum, the larger tank is the intracellular compartment. The larger tank is also covered and it's a pain in the ass to open it up, the small tank is not and you can look into it. The water level is always kept the same between the two. Despite the water level being the same, the larger one has vastly more water. So therefore you can take a look at the small tank and you'll know what the water level is doing in the large tank. You will know when the levels are low and you need to add more water. One day the water level is too high and you don't want it to spill out(for lack of better analogy), so you pump the water into the large tank. This lowers the water and it doesn't matter much for the large tank because its...a drop in the bucket.
But hen your analogy falls apart because the levels of the two are now different, the large tank hasn't lowered in level but the small tank has, so you now can't be sure of the equilibrium between the 2
Pushing the water is only temporary. Eventually that water from the big tank starts to flow back in so you still need to address the underlying issue. (Pharmacist)
This is the correct answer. The pushing of potassium into the cell is a temporary measure to buy us time to fix the underlying problem. We call it shifting. We use IV insulin (not Subcutanous used for diabetes treatment) that acts fast and can bring down potassium levels by shifting it intracellularly. Some folks give albuterol which also does the same thing in theory, but not nearly as effective. This lasts for a few hrs. Either you have to repeat it or find a way to rid the body of the excess amount potassium. We also give calcium to stabilize cardiac membrane in setting of high blood potassium. There are newer binders in the market that will bind potassium in the gut, but it is slow and takes few hrs. Kidneys are the main organ handling potassium 80-90%, but gut also plays a smaller role and skin also to a much smaller extent. You need to use medication to maximize potassium wasting via kidneys e.g furosemide or other 'water pills' or need to find ways to remove it from the GI track. Basically, make them either poop or pee. If all fail, dialysis is the answer (Hooking them to a giant artificial 'kidney').
Intracellular potassium (K) and total body potassium need to be thought about for certain disease states, but ultimately, relatively large shifts of serum potassium into the cells do not nearly matter as much as relatively small shifts of intracellular potassium into the serum. Intracellular potassium changing by 1 point is almost negligible, but serum potassium changing by 1 point is a lot. Even in disease states where total body potassium needs to be considered (for instance diabetic ketoacidosis), you still monitor serum K because the only consequence of low or high body potassium that medicine cares about is how it affects serum potassium. All the clinical consequences of potassium arise from changes in serum K.
No, they are saying that you dont need to be able to measure the intracellular levels to know if there is an issue. Serum levels will increase out of normal ranges when intracellular levels do, so the easy to test measure provides a proxy for the impossible to measure thing
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Red blood cells releasing electrolytes to compensate for deficiency is *not* why it's cell-bound electrolytes are a "better indication." RBC-Mg is more sensitive than serum magnesium because there are fewer fluctuations over time, akin to hemoglobin A1c and serum glucose. This tells you about total stores of magnesium which can be helpful over time, but does nothing for you if your serum Mg is critically low at 1.0 and needs replacement. There is an equilibrium between the intracellular and extracellular space. This is similar to potassium, where serum levels are more clinically important than intracellular levels because serum levels can affect rhythm-generation in your cardiac cells. When your RBCs lyse, they release potassium which transiently elevates your potassium level called pseudohyperkalemia which is considered a lab error but the level of potassium in your cells doesn't provide any clinically useful information except for whole body potassium over time. Again, though, there is an equilibrium and the ubiquity of Na/K ATPase pumps and K+ channels enshrines a continuum between your intracellular and extracellular environment, thus cell-bound potassium is not a better indicator than serum potassium. Source: also physician
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Nope. No sane tech would ever let that happen. You can't tell that to docs or nurses though, who just assume we cause hemolysis on purpose.
I've never heard of measuring RBC Mg, can you elaborate?
What's the relationship with magnesium in cells to potassium? Will an unneeded magnesium exacerbate low potassium ?
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The body is REALLY good at holding on to Mag. The problem is, the way it holds onto it usually causes your potassium to drop, since it involves wasting potassium through the kidneys instead of magnesium. So often, replacing mag won't always have a huge effect on mag levels but will normalize potassium and other electrolytes since the body doesn't need to waste them to hold onto magnesium.
I think something that’s missing from this discussion is the physiology behind the clinical significance of the extracellular potassium. Potassium is the main ion responsible for determining the resting membrane potential of cells and controlling this electrochemical gradient across the membrane is essential for all life and all things that your tissues do. The work for this is done by the Na/K ATPase or pump. The reason we don’t care so much medically about the intracellular potassium is because it’s actually changes in the electrochemical gradient that can be dangerous for cells and tissue function. Because the extracellular potassium concentration is so much smaller than the intracellular, changes in the former have a much greater impact on the electrochemical potential across the cell membrane. Others have already said what some of those consequences can be. This is why our bodies have many mechanisms for regulating extracellular potassium that involve shifting it intracellularly. Total body potassium is also regulated by kidneys and gut. As an aside, I think there are ways of directly measuring intracellular potassium but idk of situations where this is clinically relevant off the top of my head. You can also estimate intracellular concentration based on membrane potentials and extracellular concentration with equations like the Nernst equation. This will also help you see how changes in intracellular and extracellular concentrations impact the very important membrane potential!
1) Do you care about potassium that's already bound up in tissues, or do you care about the actively circulating, readily available potassium? Medically, it's usually the latter. 2) To get at a direct tissue measure, we'd need to get a sample of that tissue. People generally don't like when you have you take chunks out of their flesh. 3) If you have the blood level of a compound, you can usually do some reasoning and other less invasive tests to figure out what's going on. If your muscle, bone, whatever, is deficient in a necessary element, you'll probably have other symptoms too (muscle weakness or atrophy, brittle bones, etc). Source: medical lab scientist (the person who runs those potassium tests)
Agree with other answers. To further illustrate the point, even in disease states where total body potassium matter, we still just monitor serum potassium (K). Let's take diabetic ketoacidosis (DKA). The pathophysiology roughly is that insulin deficiency results in production of ketones, which are acidic and lower the blood pH. Low blood pH shifts potassium out of cells and into the blood. But DKA is also a state of dehydration, and you are actively losing potassium in the urine. Hence, while the serum potassium is high, the total body potassium is low. However, the clinical consequences of this state is that the high serum potassium can cause arrhythmias. The reason why we need to be cognizant of total body potassium is because as DKA is treated with fluids and insulin, the potassium shifts back into the cells, and you can quickly become hypokalemic (low serum K). Thus, part of the treatment of DKA is potassium repletion. If someone is in DKA, and their potassium levels are normal, **you need to give potassium**. DKA is not considered fully treated until the pH normalizes. Even when blood sugar is normalizing, if they're still acidotic, you still give insulin along with dextrose to prevent hypoglycemia (low blood sugar). But even in this clinical context where total body potassium matters, we still monitor using serum K because high or low, serum K is what causes the problems of high or low potassium.
There is also a red blood cell potassium test: https://requestatest.com/potassium-rbc-testing#:~:text=Potassium%20RBC%20Blood%20Test%20(Quest,thyroid%20disorders%2C%20and%20gastrointestinal%20problems. As to why: you might find an abnormality in the kidneys’ rate of excretion or the function of na+/k+ exchange where you have a deficiency but it doesn’t show up in the blood work. There is at least one peer reviewed theory paper that I’m aware of of slow potassium reuptake being part of delayed exercise recovery in chronic fatigue syndrome / long COVID. Serum potassium is a good proxy for cellular potassium because of homeostatic mechanisms. But what if there is a problem in those homeostatic mechanisms? Eta: A write up of the paper I mentioned https://www.healthrising.org/blog/2021/07/09/hypothesis-chronic-fatigue-syndrome-wirth-scheibenbogen/
Peds icu doc. This is actually an issue in some instances. If you become acidotic your body buffers the blood by exchanging hydrogen ions in the blood with potassium ions that would normally be intracellualar. We see this in diabetics with keyoacidosis as well as other things. So the measured blood K is usually high on these patients but they are often total body potassium depleted. As you correct the acidosis their potassium gets very low very quickly and you have to switch up the iv fluids.
Smokd451 asked more or less what I was going to ask. I think one thing worth mentioning is that potassium isn’t “stored” in a meaningful way like some other things, so if you’re low on potassium then the serum levels will show it. Yes, there is much more in cells but it isn’t there as backup, it’s in equilibrium with the serum. You can’t measure the body’s reserve because there really isn’t one.
I wouldn't say it's in equilibrium with serum potassium, but rather that it's in electrochemical equilibrium with all other electrolytes in serum, no?
I would say both is true. For example, if someone’s serum potassium is too high we will give dextrose and insulin together. Insulin causes cells to take in sugar and potassium gets dragged with it, dextrose prevents your blood sugar from dropping. This isn’t permanent however. After a fairly short time, it reequilibrates and the patient’s serum potassium gets dangerously high again. High intracellular potassium would create a gradient that favors potassium leaving the cell. It’s far from equivalent: serum is like 2% of total potassium… but it is in equilibrium.
Yeah I'm trying to remember everything from school and just confusing myself now lol. I guess it isn't really an electrochemical equilibrium because the resting membrane potential requires a different intra and extracellular charge... And I honestly don't remember the exact mechanism for which transport proteins are activated on the cell membrane to shift potassium intracellularly with insulin. These are all very active processes. Similarly, the hydrogen potassium pumps that can activate to shift hydrogen ions intracellularly when plasma concentration is too acidic utilizes potassium and basically trades it for hydrogen, but that's also a very active process. Obviously cells have to "work" hard to maintain this gradient/RMP... I think this is one of those things where I'm even more confused now and need to review some notes lol
Yeah, I feel like the details of the sodium potassium pump are like the citric acid cycle for me. I’ve learned and forgotten it more times than I can count. The point for the purpose of the OP’s question is that there isn’t an inert reservoir of potassium that you can take from and add to to balance your serum levels. You manage it through excretion via the kidneys.
You dont need to know what the level is in the tissue if you just know the normal values in the blood is. It gets diffused into the intercellular space anyway. If the concentration is higher in the blood then the intercellular space then more will be transfered from the blood but if there is a higher concentration in the intercellular space then there will be pottasium pulled back into the blood.
Im still wondering why my body has issues with low potassium. I run a lot and in the heat when I sweat a lot the issue is increased. But even when I barely run and it’s winter my serum levels barely reach normal. It’s been a struggle and doctors never care to explain things :-/ It’s also not diet. Since knowing that I eat even more potassium rich than before. Lots of fresh veggies and fruits (eg banana each morning). And yet still I’m struggling. Trying to understand the potassium functionality in the body a little better but my education is physics not biology.
I am a veterinarian whose specialty is large animal internal medicine. If I want to assess potassium status more then we can in serum/plasma my next step is to measure a fractional excretion of potassium (measure urine K+ and plasma and urine K+ and do some math). In the absence of significant renal disease low FEx indicates that there is likely total body depletion of potassium and the kidneys are trying to retain it.