Emily mentioned in her recent post on the Rule of 6s that potassium administration needs to be taken into account when correcting the plasma sodium in cases of hyponatremia. Why is this the case?
When potassium is given most of it will move into to cells (remember that 98% of total body potassium resides here.) As this occurs, electroneutrality is maintained in three ways, all of which act to raise the plasma sodium concentration.
1. Intracellular sodium exits cells directly increasing the plasma sodium concentration.
2. Extracellular Cl will enter cells along with potassium. The addition of intracellular KCl raises intracellular osmolality causing water to move into cells. The loss of extracellular water causes the plasma sodium concentration to rise.
3. Intracellular protons exit cells as potassium enters. Proton movement is osmotically neutral as they combine both intra and extracellularly with buffers. This is in contrast to potassium, which raises intracellular osmolality and causes water to move into cells. This loss of extracellular water again causes the plasma sodium concentration to rise.
The Practical Point: If solute is part of your hyponatremia treatment plan and you need to additionally replete potassium remember that each mEq of potassium given will act on the plasma sodium like a mEq of sodium.
2 comments:
My understanding was that chloride is relatively impermeable into cells. This is the reason commonly given for why non-gap (hyperchloremic) metabolic acidosis causes hyperkalemia via a shift, whereas anion-gap acidosis, in general, does not cause hyperkalemia to the same extent. That is, since Cl- is impermeable into cells, the entry of H+ must be accompanied by the exit of a cation (K+) to maintain electroneutrality, in the case of hyperchloremic met acidosis. The same is not true for organic acidosis, in which case the anion (ketones, lactate, etc) follow the H+ into the cells.
Thanks for your comments David.
The reasoning in the post is what is given in Rose (pages 727 and 728 in the 5th edition for the bookish).
I'm guessing the Cl movement is a minor player out of the three due to the relative impermeability issue that you nicely point out.
Great explanation of potassium shift in gap vs no-gap acidosis. Rose does backtrack bit on the issue stating "alternatively experimental studies suggest that organic anions may act as substrates for the pancreatic beta cell, leading to the release of insulin. Insulin then drives K into the cells, counteracting the direct effect of acidemia. However, the applicability of these findings remains to be proven, especially in DKA, where insulin deficiency is the primary abnormality." Page 380 for this one.
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