How bolus infusions of NaCl may affect low sodium levels...?

Nurses General Nursing

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So, the other day in clinical I had an elderly patient who had low sodium levels and low blood pressure. They gave the pt two bolus infusions of NaCl to help get his/her bp back up, and afterward my instructor asked me a few questions about the effects of giving boluses of NS NaCl to someone who already has low sodium levels. The instructor said that giving those boluses would dilute the sodium levels in the pt even further, causing his/her [Na+] ratios to drop. For some reason, I'm having a really hard time believing that. My reasoning:

1) NS NaCl concentrations are based on regular sodium levels. So, if you have a pt who has lower-than-normal sodium in his/her system, then the NS solutions are hypertonic to the pt's Na+ solutes, and that should cause there to be an increase in [Na+] ratio levels, right?

2) Also, even if the pt's Na+ levels were average, shouldn't the 0.9% NaCl solution not dilute the sodium in the pt's system?

I'm just having issues with this because to me it does not logically follow. What do you all say? Am I mistaken or is my instructor?

btw, that 2006 in the reference is supposed to be 2005.

Me still likey this thread.

That is all.

:)

of course from a chemistry standpoint, saline literally is sodium+chloride+water. however, for clinical purposes, saline pretty much sicks together as saline, and does not, for purposes of fluid management, dissociate. that was the point i was trying to make. if someone is confused about how serum sodium and water are related and how iv water vs iv saline works, it is much more functional to think of saline as an entity, not as salt and water. thus, "water moves, saline stays." sorry i didn't make that clear enough.

although i must say that in all the years i've been teaching this, you are the very first person to ask me this question! thanks for the opportunity to clarify, and i hope that helps.

Right, 140, because that measurement is a measurement of CONCENTRATION, not a count of the absolute number of sodium molecules. Got that? If not, work on it, because you have to "get" it.

If you have a concentration (140 meq/L) and a volume (blood volume, body weight, etc.) then you have a total count of sodium molecules. This is why you can estimate TB sodium and sodium deficit. Get it?

As a matter of fact, you can pour quite a bit of NS into a body and not really influence the serum sodium that much at all. The way you change the serum sodium is by changing the amt of WATER.

This is just not true. By this thought process, to bring up a patient's sodium you would water restrict them? No. You administer sodium containing fluid in order to increase TBS. YOU DON'T WANT the sodium to change very much very quickly. Slow is good.

Saline is not sodium and water.

Last I checked it was.

Saline pretty much stays in its vascular place (unless you cut a blood vessel and spill some out).

I think you need to review Na/K pump physiology and active transport. Sodium is the primary extracellular ion, but it doesn't "stay in the vascular space".

OK. You are walking down the street with a perfectly good crit of 40 and a serum sodium of 140 (and normal other lytes). You are accosted by someone with a sharp thing and before you know it, a whole lot of your circulating volume is running into the storm drain. Fortunately, you are whisked into a nearby ER immediately, having had your bleeding stopped by a nearby Boy Scout with good First Aid Merit Badge training (ummmm, I teach that too). The ER nurse draws a baseline crit and lytes. What are they?

OK, crit is still 40...because hct is a *percentage of the blood that is red cells*, not a count of the absolute number of red cells you have. So even if you lose a lot of your blood, your crit is unchanged. Until they start fluid-resuscitating you with.... normal (not half-normal) saline (or RL, which acts like it for purposes of this discussion).

Na+ is still 140, because you have lost saline (serum counts as saline) but not water.

This depends on how long before presentation to ED where crit and sodium are analyzed. RAS kicks in and body retains sodium, so serum sodium will increase. Why?

The body is trying to autoresuscitate by raising serum sodium in an effort to draw fluid from EC space to IV space. This is why the crit drops, though not immediately. This is why if a GSW patient comes in you don't just administer WB or component therapy; you administer NS as well to resuscitate the ECF as well.

But what happens to the crit of a tube of blood if you add water-- like D5W? Answer: Nothing. Why? Because the crit is a % of volume....and when you add water, the water travels into the cells too. So they swell up, and their %age size change means no change in the crit of the tube. They still take up (in this example) 40% of the volume. What happens if, instead of adding water to your original tube of hct=40 blood, you evaporate half of the water out of it? (The answer is NOT, "Make gravy." Shame on you.) No, the hct stays the same, because the cells lose water too, and they shrink as much as the liquidy part did. Same percentage of red cells in the resulting volume = no change in hematocrit.

So. When you have someone dehyrated (as evidenced by their elevated serum Na+), you give him water (or D5W). This dilutes his serum Na+ back towards normal and allows his shrunken dehydrated cells to regain their girlish plumpness. Normal saline will not help, as it will not change the serum sodium level ("Saline is not sodium and water") and will not move into cells to restore their lost water content ("Saline stays, water travels.")

Thankfully there is a huge difference between in vitro an in vivo. D5W will change the crit of a patient depending on water balance.

Just because you have an elevated sodium doesn't mean you are dehydrated.

NS WILL rehydrate a patient, and is the fluid of choice during hypovolemic hyponatremia.

you give him saline, which goes into his vascular space where you want it for circulating volume but doesn't go anywhere else. D5W will not do the job, as it will travel into cells (not just RBC's, but all cells, and most of it will thus not be available in the vascular space to make blood pressure).

Wow. OK. Saline does leave the IV space with only about 20-30% still remaining in the IV space after 1 hour. With D5W, even less remains, but some does remain in the IV space, as it equilibrates with the interstitium and the ICF.

) Serum Na+ 140, Hct 25, BP 110/60. OK, so this guy is relatively anemic, but his circulating volume is OK (as evidenced by an adequate BP) and his water balance is fine (as evidenced by his normal Na+).

Just because you have a normal ABP doesn't mean you have adequate circulating volume (think compensatory shock-you need to lose 1/3 of blood volume before you see a drop in ABP), and just because you have normal sodium levels doesn't mean you have normal water balance (think DKA).

Well, anemia can have many causes, but if he comes in with a hx of a recent bleed with fluid resuscitation, you could guess that he had a perfectly good crit until he lost some red cells out his GI bleed or stab wound or bloody ortho surgery or something, and we were stingy and just gave him NS back. His crit is called "dilutional," as in, "His red cells are floating in saline."

This patient could present with these vitals and blood results before administration of any IVF, due to compensatory shock and autoresuscitation, which dilutes the crit in the same way (robbing the ICF and interstitium.

2) Serum Na+ 118, Hct 40, BP 110/60. This guy has 'way too much water on board, as evidenced by his Na+ that's 'way low ("dilutional" too). We call him hyponatremic, but it's not that he has lost sodium (in most cases), it's that he retained too much water. He hasn't lost saline, as evidenced by his decent BP

This is so far off the mark. Just because you have a low sodium doesn't mean you are hypervolemic. You need to take into account pertinent history, other diesease processes, etc. There are 3 different types of hyponatremia, and this could be any of those 3. The patient MAY (probably does) have a decreased TBS.

Again, ABP is not a reliable indicator of circulating volume, or "saline" as you say.

"Syndrome of inappropriate antidiuretic hormone"? Lessee.... inappropriate, ummm, too much. Antidiuretic, ummmm, doesn't allow diuresis, holds onto water.... Bingo.

Condescending much?

However, for clinical purposes, saline pretty much sicks together as saline, and does not, for purposes of fluid management, dissociate.

Yes, yes it does.

That was the point I was trying to make. If someone is confused about how serum sodium and water are related and how IV water vs IV saline works, it is much more functional to think of saline as an entity, not as salt and water. Thus, "water moves, saline stays." Sorry I didn't make that clear enough.

That is the WRONG way to think of saline, as it does redistribute in the body (large volume of distribution duh).

Although I must say that in all the years I've been teaching this, you are the very first person to ask me this question! Thanks for the opportunity to clarify, and I hope that helps.

I am so glad I wasn't a student of yours. I would go back and review basic fluid therapy and electrolyte homeostasis if I was you...

Seriously. Still enjoying this tennis match...

:)

However, for clinical purposes, saline pretty much sicks together as saline, and does not, for purposes of fluid management, dissociate.

Yes, yes it does.

Seconded

What happens if the body begins to produce aldosterone during a hyponatremic phase that's being treated with NS? I may only be a student nurse right now, but I would almost bet money that the kidneys would separate out the Na+ from the water in the saline solution.

It's not so much that the kidneys separate Na, Cl, and H2O, but that it is an aqueous solution. NaCl does dissociate when in solution. It's just basic chemistry.

Yes, it does. I completely agree :) I was just giving an example of a scenario someone couldn't counter by talking about membrane permeability and the creation of osmotic pressure differentials that can be used to reestablish the NS's original [Na+] and have something random like "systemic dispersion of the saline volume acting as a single, well-stuck-together unit" be a part of their rebuttal...or something lol.

i think this discussion has taken an interesting turn, and it reminds me of two anecdotes:

1) little girl runs into the kitchen. "mommy! mommy! where did i come from?" mother gulps, wonders how her little girl grew up so fast, and begins the explanation she's been hoping she could put off awhile longer. "no, mommy, sarah says she came from brooklyn, where did i come from?"

2) although there are at least eight ways for a man to reach first base (really-- you can count them if you've a mind to), as they said to the rookies in the classic bull durham, "it's a simple game. you throw the ball, you hit the ball, you catch the ball."

while i would be happy to start tossing in aldosterone, angiotensin, ace inhibitors, the stretch receptors in lungs, vasopressin and the pituitary axis, the role of protein in oncotic pressure, how loop diuretics work, osmoreceptors, and all manner of other things renal and homeostasis (and have no doubt, i can do it :D), let us remember that the original simple question i attempted to address was, does normal saline have much of an effect on hyponatremia.

the answer is still that hyponatremia is much, much more often to be a water-excess problem than a sodium-deficit problem, and the treatment is much more likely to be free water restriction and, only if necessary, judicious addition of a more concentrated saline solution.

further, hypovolemia with hyponatremia is still a multifactorial problem with two solutions (as it were:d) involved in its resolution.

last, hypovolemia with normal lytes is most likely to be successfully treated, at least in the short run, with normal saline (maybe blood or albumin, if indicated), and this will not increase serum na+ to any clinically significant degree, although hypovelemia with a normal crit if treated with ns alone will result in a lower (dilutional) crit.

over to you, guttercat.:D

i think this discussion has taken an interesting turn, and it reminds me of two anecdotes:

1) little girl runs into the kitchen. "mommy! mommy! where did i come from?" mother gulps, wonders how her little girl grew up so fast, and begins the explanation she's been hoping she could put off awhile longer. "no, mommy, sarah says she came from brooklyn, where did i come from?"

2) although there are at least eight ways for a man to reach first base (really-- you can count them if you've a mind to), as they said to the rookies in the classic bull durham, "it's a simple game. you throw the ball, you hit the ball, you catch the ball."

while i would be happy to start tossing in aldosterone, angiotensin, ace inhibitors, the stretch receptors in lungs, vasopressin and the pituitary axis, the role of protein in oncotic pressure, how loop diuretics work, osmoreceptors, and all manner of other things renal and homeostasis (and have no doubt, i can do it :D), let us remember that the original simple question i attempted to address was, does normal saline have much of an effect on hyponatremia.

the answer is still that hyponatremia is much, much more often to be a water-excess problem than a sodium-deficit problem, and the treatment is much more likely to be free water restriction and, only if necessary, judicious addition of a more concentrated saline solution.

further, hypovolemia with hyponatremia is still a multifactorial problem with two solutions (as it were:d) involved in its resolution.

last, hypovolemia with normal lytes is most likely to be successfully treated, at least in the short run, with normal saline (maybe blood or albumin, if indicated), and this will not increase serum na+ to any clinically significant degree, although hypovelemia with a normal crit if treated with ns alone will result in a lower (dilutional) crit.

over to you, guttercat.:D

the problem here is that your answer to the op "original simple question" contains fundamentally incorrect material (see post 39 above).

i'd be interested to see the clinician's reaction when you attempt to water/fluid restrict a hypovolemic patient (which is the case with the op patient).

whether or not the patient has a low tbs depends on the underlying disease. if the patient is voiding sodium, but not taking in sodium (the body doesn't just "make" sodium), there will be a decrease in tbs. i'm having trouble thinking of a way a patient could be hypovolemic and hyponatremic, but not have a decreased tbs (if you can give me one i would love to be enlightened). these patients are unlikely to benefit from hypertonic saline, as there is not interstitial fluid to pull from to increase blood volume. treatment would be (is) ns or balanced solution (lrs, etc.) in order to raise the sodium ~1 meq/l/hr.

in the case of hypervolemic hyponatremia, there may or may not be a decrease in tbs. then your logic is more likely to be applicable (hypertonic saline, water restriction, loop diuretics, etc.). (see post 18 above)

back to the original issue...

op- i believe that ns was a correct choice for treating your hypovolemic hyponatremic patient.

Btw, update...

I asked another instructor about the hypovolemic hyponatremia scenario, and she was as confused as I as to why the other instructor would say that the NS would dilute the Na+ even further. "Forgiving any underlying causes you've not told me about," she said, "then that just fundamentally does not make sense to me." So, yeah. Just thought that I'd share. :)

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