Electrolyte/fluid balance question

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Ven0m

boop
7+ Year Member
Joined
Jun 11, 2015
Messages
174
Reaction score
42
Why must we, when treating isotonic dehydration, prevent hypokalemia by giving K+ when the urine volume is over 40mL/h? It was a point on our lectures but it wasn't really explained clearly.

One more, lectures state that one of the causes of hypotonic dehydration (where there's more Na+ loss than H2O) is diarrhea. But it doesn't mention diarrhea as a cause of isotonic dehydration. I thought water loss from diarrhea over a couple of days would cause isotonic dehydration though. Any suggestions?

Members don't see this ad.
 
Why must we, when treating isotonic dehydration, prevent hypokalemia by giving K+ when the urine volume is over 40mL/h? It was a point on our lectures but it wasn't really explained clearly.

One more, lectures state that one of the causes of hypotonic dehydration (where there's more Na+ loss than H2O) is diarrhea. But it doesn't mention diarrhea as a cause of isotonic dehydration. I thought water loss from diarrhea over a couple of days would cause isotonic dehydration though. Any suggestions?
@nybgrus
 
Why must we, when treating isotonic dehydration, prevent hypokalemia by giving K+ when the urine volume is over 40mL/h? It was a point on our lectures but it wasn't really explained clearly.

One more, lectures state that one of the causes of hypotonic dehydration (where there's more Na+ loss than H2O) is diarrhea. But it doesn't mention diarrhea as a cause of isotonic dehydration. I thought water loss from diarrhea over a couple of days would cause isotonic dehydration though. Any suggestions?

Caught this one in a more reasonable timeframe @Phloston

Off the top of my head I am not sure where the 40mL/h comes from but I believe the point here is that isotonic dehydration is the removal of equal portions of dissolved solids in plasma (hence isotonic). That means K+ as well. Since the majority of K+ is intracellular the body maintains normokalemia by the efflux of K+ from the cellular compartment. Now, when the process is reversed and you rehydrate it is done (typically) with isotonic fluids like normal saline (308 osm). However that fluid contains only Na+ and Cl- which then raises the Cl- at a greater rate than the Na+ thus leading to some degree of hyperchloremia. Hyperchloremia leads to a non-gap metabolic acidosis since Cl- is a strong base and the Kd is such that it will dynamically shift the equilibrium of H2O dissociation favoring more H+ thus leading to hyperchloremic metabolic acidosis. This is dealt with by the kidneys via excretion of of Cl- as one may imagine. However the normal physiology of the kidney is to re-absorb Cl- in the proximal tubule via a couple means but relevant to here is the potassium-chloride symporter. Start dumping chloride and you no longer re-absorb as much potassium as you normally would. And since in isotonic dehydration you have lost total body K+ and are, in effect, replacing it with extra Cl- that is now needing to be dumped, the kidney is at a minimum hindered in retaining K+ to some degree and when the UOP is high enough in the context of someone already TBK+ depleted it can lead to hypokalemia. There is also an effect of further inducing K+ efflux from the cells from the hyperchloremic acidosis due to the acidosis effect (exchange of extracellular H+ for intracellular K+) which then cannot be as effectively reclaimed further worsening hypokalemia.

I'll add that clinically this is almost a non-issue. Even in the ICU I've almost never had to really contend with or worry overly about such things. I think it matters more in pediatrics for some reason but I don't know anything about kids except that I don't particularly like them.

As for the next question...

My understanding is the diarrheal and vomiting losses are isotonic dehydration. Not sure where the hypotonic dehydration idea comes from. My best guess is that your lecture was in error. Easy enough to mix up these terms since they can get convoluted in regards to frame of reference.

At least that's my best understanding off the top of my head. Hope that helps
 
  • Like
Reactions: 1 users
Members don't see this ad :)
T
Caught this one in a more reasonable timeframe @Phloston

Off the top of my head I am not sure where the 40mL/h comes from but I believe the point here is that isotonic dehydration is the removal of equal portions of dissolved solids in plasma (hence isotonic). That means K+ as well. Since the majority of K+ is intracellular the body maintains normokalemia by the efflux of K+ from the cellular compartment. Now, when the process is reversed and you rehydrate it is done (typically) with isotonic fluids like normal saline (308 osm). However that fluid contains only Na+ and Cl- which then raises the Cl- at a greater rate than the Na+ thus leading to some degree of hyperchloremia. Hyperchloremia leads to a non-gap metabolic acidosis since Cl- is a strong base and the Kd is such that it will dynamically shift the equilibrium of H2O dissociation favoring more H+ thus leading to hyperchloremic metabolic acidosis. This is dealt with by the kidneys via excretion of of Cl- as one may imagine. However the normal physiology of the kidney is to re-absorb Cl- in the proximal tubule via a couple means but relevant to here is the potassium-chloride symporter. Start dumping chloride and you no longer re-absorb as much potassium as you normally would. And since in isotonic dehydration you have lost total body K+ and are, in effect, replacing it with extra Cl- that is now needing to be dumped, the kidney is at a minimum hindered in retaining K+ to some degree and when the UOP is high enough in the context of someone already TBK+ depleted it can lead to hypokalemia. There is also an effect of further inducing K+ efflux from the cells from the hyperchloremic acidosis due to the acidosis effect (exchange of extracellular H+ for intracellular K+) which then cannot be as effectively reclaimed further worsening hypokalemia.

I'll add that clinically this is almost a non-issue. Even in the ICU I've almost never had to really contend with or worry overly about such things. I think it matters more in pediatrics for some reason but I don't know anything about kids except that I don't particularly like them.

As for the next question...

My understanding is the diarrheal and vomiting losses are isotonic dehydration. Not sure where the hypotonic dehydration idea comes from. My best guess is that your lecture was in error. Easy enough to mix up these terms since they can get convoluted in regards to frame of reference.

At least that's my best understanding off the top of my head. Hope that helps
Wow thanks for putting together a detailed response for me. I guess I'll just understand that isotonic dehydration can result in K+ losses, so the patient's K+ levels should be monitored for hypokalemia. Thanks man
 
  • Like
Reactions: 1 user
Caught this one in a more reasonable timeframe @Phloston

Off the top of my head I am not sure where the 40mL/h comes from but I believe the point here is that isotonic dehydration is the removal of equal portions of dissolved solids in plasma (hence isotonic). That means K+ as well. Since the majority of K+ is intracellular the body maintains normokalemia by the efflux of K+ from the cellular compartment. Now, when the process is reversed and you rehydrate it is done (typically) with isotonic fluids like normal saline (308 osm). However that fluid contains only Na+ and Cl- which then raises the Cl- at a greater rate than the Na+ thus leading to some degree of hyperchloremia. Hyperchloremia leads to a non-gap metabolic acidosis since Cl- is a strong base and the Kd is such that it will dynamically shift the equilibrium of H2O dissociation favoring more H+ thus leading to hyperchloremic metabolic acidosis. This is dealt with by the kidneys via excretion of of Cl- as one may imagine. However the normal physiology of the kidney is to re-absorb Cl- in the proximal tubule via a couple means but relevant to here is the potassium-chloride symporter. Start dumping chloride and you no longer re-absorb as much potassium as you normally would. And since in isotonic dehydration you have lost total body K+ and are, in effect, replacing it with extra Cl- that is now needing to be dumped, the kidney is at a minimum hindered in retaining K+ to some degree and when the UOP is high enough in the context of someone already TBK+ depleted it can lead to hypokalemia. There is also an effect of further inducing K+ efflux from the cells from the hyperchloremic acidosis due to the acidosis effect (exchange of extracellular H+ for intracellular K+) which then cannot be as effectively reclaimed further worsening hypokalemia.

I'll add that clinically this is almost a non-issue. Even in the ICU I've almost never had to really contend with or worry overly about such things. I think it matters more in pediatrics for some reason but I don't know anything about kids except that I don't particularly like them.

As for the next question...

My understanding is the diarrheal and vomiting losses are isotonic dehydration. Not sure where the hypotonic dehydration idea comes from. My best guess is that your lecture was in error. Easy enough to mix up these terms since they can get convoluted in regards to frame of reference.

At least that's my best understanding off the top of my head. Hope that helps
Thank u for this great response nybgrus. Very helpful as always!
 
  • Like
Reactions: 1 user
Top