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doctor712

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Hi All,

Physiology question for anyone who would be willing to provide some insight. I was talking with a doc friend over the phone about a case the other day, and, as usual, we got cut off.
He had a patient who was hypokalemic. I was asking about replacing potassium, and he was saying that since K+ is extracellular, simply replacing with more K+ is like "pissing in the wind." As he described it. Then he had to hop off.

It seems the patient was on Lasix and this was the initial cause...

So, I'm wondering, why wouldn't K+ replacement given in OR or ICU for that matter, not correct the problem? If the Sodium/Potassium pump has ATP to do work, whether there is a gradient or not, shouldn't it be able to overcome any gradient and get K+ into the cell so it can do its job? Is Na+ required to be given at the same time as K+? I recall the doc mentioning another molecule to give with K+ but connection was dicey and I don't think it was Na+... Also, I was told that a diet high in Carbs can also cause Hypokalemia, and I'm sure it's an oversimplification, but wouldn't that provide lots of ATP to get K+ where it belongs? (counterintuitive?)

I was doing some website reading and came across this sentence, "Unlike treatment of hyponatremia, potassium replacement is not a matter of calculating a correction based on serum potassium levels, since these are a poor reflection of the overwhelming proportion of potassium that is intracellular." So, now I'm confused, I thought K+ was extracellular... (3 NA+ out for every 2 K+ that go in, NA/K pump, no?) So a lab value of less K, is not really reflective of what's outside the cell, is that it? Because so much is inside the cell...

So, what do you do, in essence in the OR to treat hypokalemia whose cause is unknown to you during a case? Giving K simply won't do it, so I was told, and you cannot exactly get a history and figure out underlying causes (aside from you yourself giving something that you know may very well cause this condition, presumably that med might be stopped...)

Curiously,
D712

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Hi All,

Physiology question for anyone who would be willing to provide some insight. I was talking with a doc friend over the phone about a case the other day, and, as usual, we got cut off.
He had a patient who was hypokalemic. I was asking about replacing potassium, and he was saying that since K+ is extracellular, simply replacing with more K+ is like "pissing in the wind." As he described it. Then he had to hop off.

It seems the patient was on Lasix and this was the initial cause...

So, I'm wondering, why wouldn't K+ replacement given in OR or ICU for that matter, not correct the problem? If the Sodium/Potassium pump has ATP to do work, whether there is a gradient or not, shouldn't it be able to overcome any gradient and get K+ into the cell so it can do its job? Is Na+ required to be given at the same time as K+? I recall the doc mentioning another molecule to give with K+ but connection was dicey and I don't think it was Na+... Also, I was told that a diet high in Carbs can also cause Hypokalemia, and I'm sure it's an oversimplification, but wouldn't that provide lots of ATP to get K+ where it belongs? (counterintuitive?)

I was doing some website reading and came across this sentence, "Unlike treatment of hyponatremia, potassium replacement is not a matter of calculating a correction based on serum potassium levels, since these are a poor reflection of the overwhelming proportion of potassium that is intracellular." So, now I'm confused, I thought K+ was extracellular... (3 NA+ out for every 2 K+ that go in, NA/K pump, no?) So a lab value of less K, is not really reflective of what's outside the cell, is that it? Because so much is inside the cell...

So, what do you do, in essence in the OR to treat hypokalemia whose cause is unknown to you during a case? Giving K simply won't do it, so I was told, and you cannot exactly get a history and figure out underlying causes (aside from you yourself giving something that you know may very well cause this condition, presumably that med might be stopped...)

Curiously,
D712

Potassium is mainly intracellular, a 1mEQ/L decrease in the serum level usually indicates a net loss of 100-200mEQ. So the serum level does give you some idea of what is going on at the intracellular level, it's just that many people don't appreciate how great the deficit really is. Maybe your attending meant that giving small amounts of potassium is like pissing in the wind because the deficit is much greater than the absolute serum number implies.
Sodium doesn't need to be given with potassium, but maybe your attending mentioned magnesium? Hypokalemia will show less than ideal improvement when repleting in the setting of uncorrected hypomagnesemia. This is thought to be due to the kidney's regulation of magnesium and potassium in the setting of hypomagnesemia where it ends up excreting potassium.
Since potassium is mainly intracellular and sodium mainly extracellular that is why the Na/K pump requires ATP in order to pump those specific ions against their gradient. So the pump sends potassium into the cell and sodium out of the cell.
Hope this helps some
 
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Hypokalemia should always be treated oral potassium intake: hypokalemia is a reflection of total intracellular potassium deficiency so that's 2/3 of body water content @140meq/L.

IV potassium administration is highly limited by the irritation of peripheral vasculature and by it's central effect on the myocardium: typical cardioplegia fluid contains only 20-40meq/l of K+ enough for cadiac arrest!
 
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Potassium is mainly intracellular, a 1mEQ/L decrease in the serum level usually indicates a net loss of 100-200mEQ. So the serum level does give you some idea of what is going on at the intracellular level, it's just that many people don't appreciate how great the deficit really is. Maybe your attending meant that giving small amounts of potassium is like pissing in the wind because the deficit is much greater than the absolute serum number implies.
Sodium doesn't need to be given with potassium, but maybe your attending mentioned magnesium? Hypokalemia will show less than ideal improvement when repleting in the setting of uncorrected hypomagnesemia. This is thought to be due to the kidney's regulation of magnesium and potassium in the setting of hypomagnesemia where it ends up excreting potassium.
Since potassium is mainly intracellular and sodium mainly extracellular that is why the Na/K pump requires ATP in order to pump those specific ions against their gradient. So the pump sends potassium into the cell and sodium out of the cell.
Hope this helps some



Thank you very much, and yes, the patients' Mg was the other molecule discussed, (deficient as well.)

Thanks
D712
 
Hypokalemia should always be treated oral potassium intake: hypokalemia is a reflection of total intracellular potassium deficiency so that's 2/3 of body water content @140meq/L.

Except in the OR or in patients that cannot take PO for other reasons. Sometimes you still have to treat it and IV is the only route available.
 
Sodium doesn't need to be given with potassium, but maybe your attending mentioned magnesium? Hypokalemia will show less than ideal improvement when repleting in the setting of uncorrected hypomagnesemia. This is thought to be due to the kidney's regulation of magnesium and potassium in the setting of hypomagnesemia where it ends up excreting potassium.
Since potassium is mainly intracellular and sodium mainly extracellular that is why the Na/K pump requires ATP in order to pump those specific ions against their gradient. So the pump sends potassium into the cell and sodium out of the cell.
Hope this helps some

Regardless of the renal effect of hypomagnesemia, every ATP based reaction requires Mg2+ as a cofactor. The NaK-ATPase pump obviously uses ATP and requires Mg2+ to function properly and move the potassium into the intracellular space.
 
Regardless of the renal effect of hypomagnesemia, every ATP based reaction requires Mg2+ as a cofactor. The NaK-ATPase pump obviously uses ATP and requires Mg2+ to function properly and move the potassium into the intracellular space.

not really related, as patients rarely are hyperkalemic due to excess magnesium but are frequently hypokalemic in conjunction with magnesium depletion as described above. that is why magnesium administration should be considered when replacing potassium, even in a patient with normal magnesium levels (we frequently dont even check mag levels before giving in patients with intact renal function)
 
also there are K+ channels (leak channels) that allow it to more or less flow freely. It's kind of the lubricant of the cell that balances concentration gradients and transmembrane voltage gradients.
 
not really related, as patients rarely are hyperkalemic due to excess magnesium but are frequently hypokalemic in conjunction with magnesium depletion as described above. that is why magnesium administration should be considered when replacing potassium, even in a patient with normal magnesium levels (we frequently dont even check mag levels before giving in patients with intact renal function)

Absolutely related. Cofactors, by definition, don't regulate their enzymes, so a supraphysiologic magnesium level shouldn't influence the flux of the NaK-ATPase. The channels used by the kidney to resorb K are ATPase pumps and require Mg too.

To answer the original question: hypokalemia is much better tolerated by patients compared to hyperkalemia, which is why anesthesiologists infrequently will replete K. Except in my patient population where they will fibrillate at the drop of a hat plus the insulin I end up using will produce profound hypokalemia. In cardiac surgery patients, I'll replete K slowly if it's <3.6.
 
I can count the number of times I have replaced K in the OR on one hand. In patients in which it is absolutely necessary to avoid arrhythmias like critical AS, K+ replacement can give peace of mind.

I will never forget the 23 year old CF patient that had just been extubated after his double lung transplant. The K was 3.1, and according to the protocol this required 40 mEQ IV. The nurse hung the bag as we were rounding. As I was leaving to go home post call, I wanted to go tell the kid how happy I was for him. Right in front of my eyes, he went into pulseless V tach. The 40 mEQ bag had gone in over 10 minutes. After a few minutes of ACLS, he came right out of it. I've had a healthy fear of IV K+ since then.
 
Regardless of the renal effect of hypomagnesemia, every ATP based reaction requires Mg2+ as a cofactor. The NaK-ATPase pump obviously uses ATP and requires Mg2+ to function properly and move the potassium into the intracellular space.

I agree with you that the role of Magnesium as a co-factor in the ATPase pump plays a key role, but the kidneys end up being where the party is at.

In terms of your Na/K/ATPase pump with hypomagnesemia you will have a decrease of potassium being pumped into the intracellular space leading to an initial increase in your serum potassium. Therefore, there still needs to be some wasting mechanism of that potassium, either GI or renal. If it were purely based off the Magnesium level and Na/K/ATPase pump we would actually see hyperkalemia in response to hypomagnesemia.

So the best explanation I can find seems to include the renal outer medullary potassium channel (ROMK) which is partially regulated by magnesium levels, however it's really only one factor as it can't explain everything. ROMK can both conduct potassium in and out of the cell, and magnesium plays a role in inhibiting the outward flux of potassium at physiological levels(limiting secretion).

The problem is there are disease processes with hypomagnesemia without hypokalemia. The only thing I can find that help explain this are:

1. Hypokalemia -> Cell Memebrane to Hyperpolarize -> Opposing potassium flow down its concentration gradient and resisting wasting
2. Like you stated channels in the kidney use Na/K/ATPase and require Magnesium, these channels take up the potassium into the intraceullar level and are then excreted thru the ROMK channels -> wasting. Therefore, by lacking a factor in the uptake of potassium, the kidneys are unable to excrete it on the other side.

The final piece of the puzzle seems to be distal sodium delivery and/or the role of Aldosterone, when one of these two factors is combined with hypomagnesemia it seems that hypokalemia will occur(see the original post, pt was on diuretic therapy and fits the picture).
 
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