Hyperkalemia and hyperosmolarity, etc.

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sideways

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Can anyone explain why hyperosmolarity would cause K+ to shift out of the cell? It seems like it'd be the other way around.

(I'm assuming First Aid means that the plasma is hyperosmotic with respect to the cell. If it's the cell that's hyperosmotic, then it makes sense to me.)
 
Can anyone explain why hyperosmolarity would cause K+ to shift out of the cell? It seems like it'd be the other way around.

(I'm assuming First Aid means that the plasma is hyperosmotic with respect to the cell. If it's the cell that's hyperosmotic, then it makes sense to me.)

The only reason I could think of is that as the water moves out of cells via osmosis, it would carry potassium ions along with it.
 
Can anyone explain why hyperosmolarity would cause K+ to shift out of the cell? It seems like it'd be the other way around.

(I'm assuming First Aid means that the plasma is hyperosmotic with respect to the cell. If it's the cell that's hyperosmotic, then it makes sense to me.)

It does seem like it:

Increased plasma osmolarity > Water shift from the cell into the extracellular compartment > Decreased water content of cell > Increased intracellular K concentration

But the story doesn't end here. This increase in K concentration will create a gradient, resulting in potassium movement from the cell (where K concentration is high) into the extracellular fluid (where K concentration is low). So, the net effect is hyperkalemia.
 
I guess you guys are right. I hate situations like this though, because it uses one concept to explain something, but ignores the same concept when it could explain the exact opposite. In this case, why wouldn't water just move back into the cell, and stop at some isotonic balance point?

In other words, in the situation you describe, once the water leaves the cell and the cell becomes hyperkalemic...well, if we saw that situation in isolation, wouldn't we predict an influx of water rather than an efflux of K+?

Or like the poster above you noted, maybe it just passively goes along for the ride with water. That makes more sense to me.
 
I guess you guys are right. I hate situations like this though, because it uses one concept to explain something, but ignores the same concept when it could explain the exact opposite. In this case, why wouldn't water just move back into the cell, and stop at some isotonic balance point?

In other words, in the situation you describe, once the water leaves the cell and the cell becomes hyperkalemic...well, if we saw that situation in isolation, wouldn't we predict an influx of water rather than an efflux of K+?

Or like the poster above you noted, maybe it just passively goes along for the ride with water. That makes more sense to me.

Because the overall effect of K on osmolarity is negligible.

Remember the formula: Posm= 2 (Na+K) + Glucose/18 + BUN/2.8 + (other osmotic substances)

Na is normally between 135-145 mEq, K is 3.5-5.5 mEq. This is also why it's sometimes omitted from the formula, as shown in this website: http://www.mdcalc.com/serum-osmolality-osmolarity
 
Going to go out on an interpretive limb here and suggest that the hyperosmolarity of the plasma FA is mentioning, could be due to glucose excess --> could lead to acidosis --> extracellular shift. It would take awhile for the action of the insulin released to move the K+ back into the cells.

The other common cause of hyperosmolarity is hypernatremia... no idea what the pathogenesis would be of a K+ shift in this scenario
 
The earlier posters were correct. Hyperosmolarity causes water to shift out of the cell into the plasma, and K+ diffuses with it leading to hyperkalemia.
 
Was just wondering this myself the other day. If one water went out and one K+ followed it would negate the purpose of the original water shift. I guess more H2O moves out of the cell than K+...
 
It is also important to remember that most cells contain K leak channels (out) and Na/K exchangers (Na out to K in) and intracellular K concentration is usually maintained very high and Na very low. intravascular osmolarity is determined almost completely by Na, Glucose and albumin. In situations where extracellular osmolarity is high it will inhibit the Na/K exchange but still allow K to leak due to the relative high intracellular concentration, contributing to net flow of K out of cell during hyperosmolar states.
 
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