I have this fluid and electrolytes module and I don't get one concept - maybe somebody can explain it to me. We were told that when you have hypervolemic, hypotonic hyponatremia the reason for it is total body sodium excess. So how can you have hyper..., hypo...HYPOnatremia when there is a total body EXCESS of sodium?
Electrolyte question
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Konkan - I'm thinking there is more to your patient than just this, but we'll assume for now you are seeing one moment in time:
A hypervolemic pt - if (a big assumption here) the pt's fluid has been replaced with D5W alone & especially if the pt has some protein issues (ie liver failure in which serum albumin is low) or trauma (losing lots of blood proteins) .....the pt was receiving essentiall free water (which is what D5 is). So within the INTRACELLULAR space...you have lots of fluid, but very few ions & proteins - which determine tonicity...thus....hypervolemic & hypotonic and if you measure the serum Na - it will be low (thus hyponatremic). But...unless the pt has lost Na in the urine...it has gone into the tissues (THE EXTRACELLULAR space) & water (or fluid) will follow the Na which causes the tissues to become edematous (or in the case of liver failure.....the abdomen to enlarge since protein "seep" into the abdominal space causing abdominal edema.
So....you slowly (the key here is slowly) diurese the pt...all the while changing your fluids to something different than D5 - often times they'll use LR when replacing trauma fluids or a colloid...
Does that make sense?
Not really. There is no actual patient here, therefore no other problems like liver damage or anything else. Since Na is mainly extracellular electrolyte, it won't affect IC compartment much. So I understand why we have hypervolemia. But why hypotonicity and hyponatremia? If we introduce Na IV, shouldn't tonicity and natremia rise or fall to the same degree? In other words, shoudn't we also have normotonicity and normonatremia?
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Easy..
Not sure which disease state but here you go. Sodium regulates hydrostasis. Excess Sodium will cause retention of fluid which results in Hypervolemia. And because there is more fluid, the concentration of Sodium will be lower thereby results in Hyponatremia.
Patient needs diuresis.
Hyponatremia can be one of 2 things - dilutional or salt depletion. For both, the net effect is the decrease in effective extracellular osmotically active substances & a relative overhydration of the intracellular space.
Take the CHF pt: cardiac output is decreased which results in decreased perfusion of the kidneys. This APPARENT decrease in intravascular volume sets off the following in the kidney:
1. increased proximal tubular reabsorption of sodium & water resulting in decreased delivery of sodium to the diluting segments of the nephron & impairs the kidney's ability to generate & excrete free water
2. decreased volume which causes a release of renin & an increased secrection of aldosterone which results in an increased reabsorption of sodium & water in the distal tubules
3. decreased cardiac return due to decreased cardiac output. This sets off the secretion of ADH & the net effect of the renal response to the decreased CO in an INCREASED reabsorption of both sodium & water. (the body doesn't realized it doesn't want nor need more Na)
The excess secretion of ADH results in a dilutional hyponatremia even with the presence of an excess total body sodium....as the pt becomes edematous they become more hypervolemic, hyponatremic & hypotonic.
This is in a CHF pt, but it can artifically happen in a trauma pt as well. Introducing IV Na only allows the Na to be in the intravascular space for a moment in time....the body mechanisms controlling fluid & electrolytes take over from there. Altho you want to increase the serum Na...you don't...you restrict Na & give diuretics gently. The reason is...you don't want to damage the kidneys by severely cutting back on their perfusion. The reason their function was altered in the first place, in this pt, is because of an APPARENT decreased perfusion due to the decreased cardiac output which altered the homeostatic mechanisms within the kidney.
Is that any better of an explanation? If not...keep asking.....I'll try to re-explain or someone else will explain it better. Its important you understand fluid & electrolyte balance to understand how many of the drugs function in acute settings (& how to interpret lab tests in a TPN pt!!).
Take the CHF pt: cardiac output is decreased which results in decreased perfusion of the kidneys. This APPARENT decrease in intravascular volume sets off the following in the kidney:
1. increased proximal tubular reabsorption of sodium & water resulting in decreased delivery of sodium to the diluting segments of the nephron & impairs the kidney's ability to generate & excrete free water
2. decreased volume which causes a release of renin & an increased secrection of aldosterone which results in an increased reabsorption of sodium & water in the distal tubules
3. decreased cardiac return due to decreased cardiac output. This sets off the secretion of ADH & the net effect of the renal response to the decreased CO in an INCREASED reabsorption of both sodium & water. (the body doesn't realized it doesn't want nor need more Na)
The excess secretion of ADH results in a dilutional hyponatremia even with the presence of an excess total body sodium....as the pt becomes edematous they become more hypervolemic, hyponatremic & hypotonic.
This is in a CHF pt, but it can artifically happen in a trauma pt as well. Introducing IV Na only allows the Na to be in the intravascular space for a moment in time....the body mechanisms controlling fluid & electrolytes take over from there. Altho you want to increase the serum Na...you don't...you restrict Na & give diuretics gently. The reason is...you don't want to damage the kidneys by severely cutting back on their perfusion. The reason their function was altered in the first place, in this pt, is because of an APPARENT decreased perfusion due to the decreased cardiac output which altered the homeostatic mechanisms within the kidney.
Is that any better of an explanation? If not...keep asking.....I'll try to re-explain or someone else will explain it better. Its important you understand fluid & electrolyte balance to understand how many of the drugs function in acute settings (& how to interpret lab tests in a TPN pt!!).
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When I have a salty meal, my fingers get fat.. (hypervolemic/hyponatremic).. I go drink a couple of bottles of water..and take a long pee.. then I'm all good.👍
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Typical UCSF answer... can't you explain it in 2 sentences so us USC grads can understand??
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That's what the OP wanted... and what I summed up in 2 sentences... like a typical USC grad..
That's what the OP wanted... and what I summed up in 2 sentences... like a typical USC grad..
hmmm....not so much what you explained....but it works for you I'm sure & doesn't involve the use of Xopenex at all - so you're all good!😀
(btw....he was confused about why there was a total body excess of sodium - which, unless you're not a very healthy guy....won't happen because your kidneys function fine.)😉
bingo....you eat too many chips with those beers while watching football...then you stay up all night in the bathroom & your beautiful bride fumes (for all sorts of reasons - believe me!!!!).
the ops point was....there is a total body excess of sodium, in spite of hypervolemic, hyponatremic & hypotonic....when you eat chips & drink beer...you are temporarily hypernatremic & hypervolemic...a different situation entirely.
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Not to beat a dead horse with a stick (is that the saying?), but maybe this variation will help you:
Here, the body has retained (gained) both sodium and water, but not at equal/comparable levels. More water than sodium was retained. More water was absorbed than was needed to make the retained sodium isotonic, so the solution is now hypotonic. The XS water makes the pt hypervolemic, and the XS water diluting out the smaller gain of sodium makes the pt hyponatremic. Hyponatremia refers to the concentration of sodium, not the absolute amount (grams) of sodium in the body.
Now, if you reverse the situation and retain both sodium and water, but retain more sodium than you do water, you will become:
Here, the body has retained (gained) both sodium and water, but not at equal/comparable levels. More water than sodium was retained. More water was absorbed than was needed to make the retained sodium isotonic, so the solution is now hypotonic. The XS water makes the pt hypervolemic, and the XS water diluting out the smaller gain of sodium makes the pt hyponatremic. Hyponatremia refers to the concentration of sodium, not the absolute amount (grams) of sodium in the body.
Now, if you reverse the situation and retain both sodium and water, but retain more sodium than you do water, you will become:
- hypervolemic: because you gained water volume!
- hypertonic: not enough water was retained to dilute the retained sodium out to isotonicity
- and hypernatremic: hypernatremia is a disease of hypertonicity. Again, you have not gained enough water to dilute out that sodium, so the sodium is more concentrated than normal. Hypernatremia refers to concentration, not absolute levels, because you can also lose sodium and be hypernatremic if you do not lose an equal volume of water.
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👍 drug dealer. i followed every word.
Thanks for your time, but I guess you didn't read carefully what I've written. You are expaining the problem from the point where more water than sodium was retained. That's NOT what I was trying to find out. If you get both Na and H20, but relatively more H20 then sure it's very easy - you are hypervolemic because of the volume gain and hyponatremic because of relative lesser Na gain.
I, on the other hand, asked how you get hypervolemic hypotonic hyponatremia when you have a total Na excess (which means either you gain both H20 and Na, but MORE Na or you just gain plain Na).
still don't get why we would have hyponatremia. we will have more fluid, but also more Na, so why not normonatremia?
I think your explanation was from the point of total Na loss which is not what I am trying to find out. In addition, "your patient" got D5W and other things which has nothing to do with my case. I will repeat - the is a total Na GAIN which means either H20 and Na gain with relatively bigger Na gain or just plain Na gain. So how come HYPOnatremia?
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Could the patient have SIADH?
OK....Try this to see if you can see it this way:
Hyponatremia can be associated with hypovolemia, euvolemia (SIADH fits here) & hypervolumia. We're only going to try to explain the third one - hypervolemia.
Hypervolemic hyponatremia is found in edematous disorders like CHF, cirrhosis (sometimes nephrotic syndrome). The underlying thing in all of them is a decrease in effective circulating volume.
This decreased volume results in the release of ADH & angiotensin II. The hyponatremia results from the antidiuretic effect of ADH on the kidney & the direct impairment of renal water excretion by angiotensin II. The kidney is being told to hold onto more Na & H2O.....there is just a relatively greater increase in total body water.
Decreased GFR & stimulation of thirst by angiotensin II also potentiate the development of hyponatremia. Urine excretion of NA is usually <10mEq/L & urine osmolality is high relative to plasma olmolality.
So, because of the Kidney......& how the Kidney works to conserve both Na & H2O.....you get an increase in total body Na with a relatively greater increase in total body water. The Kidney is holding onto more Na than it should if the body (the blood circulation) were functioning normally.
Do you understand the renin-angiotensin system of sodium & water regulation by the kidney??? Thats the basis of this. You need to know what stimulates renin release. Then what is angiotensin II, how does it come about & what does it do? What does aldosterone do to Na reabsorption? If you understand the renin-angiotensin-aldosterone axis - you'll understand the mechanism of Na balance (thus water balance since Na is the major osmotically active ion in the ECF).
So....your last question to me - why HYPONATREMIA? Because, altho there is an increase in total body Na (thus ECF volume) and total body water, there is a relatively greater increase in total body water. Remember - serum Na concentration does not necessarily reflect total body Na.
Good luck - come back if you still don't get it & we'll try again...but review that renin-angiotensin system.
Hyponatremia can be associated with hypovolemia, euvolemia (SIADH fits here) & hypervolumia. We're only going to try to explain the third one - hypervolemia.
Hypervolemic hyponatremia is found in edematous disorders like CHF, cirrhosis (sometimes nephrotic syndrome). The underlying thing in all of them is a decrease in effective circulating volume.
This decreased volume results in the release of ADH & angiotensin II. The hyponatremia results from the antidiuretic effect of ADH on the kidney & the direct impairment of renal water excretion by angiotensin II. The kidney is being told to hold onto more Na & H2O.....there is just a relatively greater increase in total body water.
Decreased GFR & stimulation of thirst by angiotensin II also potentiate the development of hyponatremia. Urine excretion of NA is usually <10mEq/L & urine osmolality is high relative to plasma olmolality.
So, because of the Kidney......& how the Kidney works to conserve both Na & H2O.....you get an increase in total body Na with a relatively greater increase in total body water. The Kidney is holding onto more Na than it should if the body (the blood circulation) were functioning normally.
Do you understand the renin-angiotensin system of sodium & water regulation by the kidney??? Thats the basis of this. You need to know what stimulates renin release. Then what is angiotensin II, how does it come about & what does it do? What does aldosterone do to Na reabsorption? If you understand the renin-angiotensin-aldosterone axis - you'll understand the mechanism of Na balance (thus water balance since Na is the major osmotically active ion in the ECF).
So....your last question to me - why HYPONATREMIA? Because, altho there is an increase in total body Na (thus ECF volume) and total body water, there is a relatively greater increase in total body water. Remember - serum Na concentration does not necessarily reflect total body Na.
Good luck - come back if you still don't get it & we'll try again...but review that renin-angiotensin system.
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even if you have NA GAIN you can have MORE H20 GAIN. So you have higher than normal sodium, but you also have higher than normal water. IN RELATION TO WATER, there is less sodium (hyponatremia). b/c there is lots more water: HYPERVOLEMIA. b/c the electrolyte conc. is far less than the water conc (even though lots of NA, lots more H20) you get hypotonicity. I am pretty sure this is how it is.
Yep....in a nutshell, this is it - good job!😀
Now...if you can understand WHY it is that way...you understand why certain drugs are chosen &/or where certain drugs work.
Ok so finally I was able to figure it out. Total Na excess leads to (at first) shift of H20 from IC to IV (hypervolemia), but the most important part is that after some time kidneys kick in and they start to secrete ADH to retain H20 even though H20 shift from IC has already apeared (kidneys are too slow to react to that). That's why we have hyponatremia.
