Can someone explain this?

[Knicks]

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I read that hyponatremia in patients with heart failure indicates that the heart failure is severe.

Why?

 

[ADORE]

Just a guess:

Hyponatremia because your body can't/doesn't want to excrete water due to decreased cardiac output and the body compensating by secreting ADH or renin.

//I haven't started medical school yet. Couple mo' months...

FLAME SUIT ON!!!

 

[KeyzerSoze]

I think it has to do with pathological increased ANP production.

 

[Pansit]

I read that hyponatremia in patients with heart failure indicates that the heart failure is severe.

Why?

anp

 

[jdh71]

effective intravascular volume is low because the pump sucks activating RAAS and ADH, you pull in more water than sodium

 

[dienekes88]

Pre-med got this one.

You have to first realize that sodium concentration is related to water metabolism... not salt metabolism. Nephrologists love it when you drop this one.

The low cardiac output leads to effective arterial underfilling. This leads to both a non-osmotic impetus for ADH secretion and activation of the renin-angiotensin system as a result of decreased pressure at the JGA.

ANP is produced as a result of atrial stretch, but ANP is a diuretic/saliuretic.

ETA: I guess jdh71 already said it.

 

[BigRedder]

Because someone takes one look at them and gives them 80 of Lasix. Then they lose all their sodium and potassium. Hence hyponatremia.

/kidding

 

[MedStudentWanna]

Pre-med got this one.

You have to first realize that sodium concentration is related to water metabolism... not salt metabolism. Nephrologists love it when you drop this one.

The low cardiac output leads to effective arterial underfilling. This leads to both a non-osmotic impetus for ADH secretion and activation of the renin-angiotensin system as a result of decreased pressure at the JGA.

ANP is produced as a result of atrial stretch, but ANP is a diuretic/saliuretic.

Yes, I know that sodium levels refer to its concentration in water. But ANP will reduce sodium levels. The RAAS system will increase sodium levels (aldosterone promotes sodium reabsorption), leading to hypernatremia, not hyponatremia. I see where RAAS would be invoked in heart failure, but doesn't that mean that ANP will then be invoked as well?

 

[jdh71]

Yes, I know that sodium levels refer to its concentration in water. But ANP will reduce sodium levels. The RAAS system will increase sodium levels (aldosterone promotes sodium reabsorption), leading to hypernatremia, not hyponatremia. I see where RAAS would be invoked in heart failure, but doesn't that mean that ANP will then be invoked as well?

Think about aldosterone and ANP as kind of counteracting each other here, and then adding in ADH. The role of the NP's as they contribute to the overall picture in chronic decompensated heart failures is still a little unclear. Extrapolating what they should do from the normal steady state to the chronic decompensated heart failure patient isn't so straight forward, and I think this is backed up by lack of great clinical evidence that nesiritide actually does anything worthwhile in these patients (really only modest short term benefits, if anything).

 

[CaptainSSO]

Diet. A low-sodium, high-water diet can disturb the proper balance between sodium and fluids in the blood. Excessive intake of diuretics, including beer, can have the same effect.

Trying to understand hyponatremia better--wikipedia is saying excessive intake of diuretics can lead to hyponatremia? That seems backwards to me. Would this just be because you're excreting sodium along with the water?

 

[jdh71]

Trying to understand hyponatremia better--wikipedia is saying excessive intake of diuretics can lead to hyponatremia? That seems backwards to me. Would this just be because you're excreting sodium along with the water?

Yes. You move the sodium, the water follows. Thiazide class diuretics are notorious for causing hyponatremias - excreting more salt than water in proportion.

 

[dienekes88]

Yes, I know that sodium levels refer to its concentration in water. But ANP will reduce sodium levels. The RAAS system will increase sodium levels (aldosterone promotes sodium reabsorption), leading to hypernatremia, not hyponatremia. I see where RAAS would be invoked in heart failure, but doesn't that mean that ANP will then be invoked as well?

Whoa whoa whoa. You missed the point. Water metabolism. Sodium concentration is a function of the manner in which water is handled, which is all about the ADH. Increased total body sodium content by virtue of an activated RAAS system will not lead to hypernatremia, because there will be an osmotic impetus for ADH secretion at the hypothalamus. The body will retain water and the patient will gain weight. Sodium concentration will be normal-ish.

"Sodium level" isn't the best term to use. You want to talk about sodium concentration or total body sodium. Aldosterone-induced sodium resorption will result in increased total body sodium.

ANP is invoked. BNP is also invoked. That is why we order BNPs on heart failure patients and suspected heart failure patients. If I recall correctly, in a patient with dyspnea, having a BNP <100 is suggestive of another etiology. BNP >400 is very suggestive of dyspnea being secondary to heart failure.

When you're arterially underfilled (or effectively so), the release of ADH leads to an overwhelming resportion of water at the collecting duct. Hyponatremia.

Trying to understand hyponatremia better--wikipedia is saying excessive intake of diuretics can lead to hyponatremia? That seems backwards to me. Would this just be because you're excreting sodium along with the water?

Well, you lose the sodium and water (after giving Lasix, urine is isosmotic)... and then guess what: you're arterially underfilled or effectively arterially underfilled. There's a reason the body was trying to hold onto the water/salt in the first place; you need the volume. You've volume depleted them, and then it's the same story. Being arterially underfilled leads to a non-osmotic impetus for ADH secretion. Hyponatremia.

Sodium concentration is all about the handling of water. Nephrology attendings will hug you if you know this. This is one of 5 or 6 facts I knew on Medicine, and I did well.

 

[Regal Regan]

Whoa whoa whoa. You missed the point. Water metabolism. Sodium concentration is a function of the manner in which water is handled, which is all about the ADH. Increased total body sodium content by virtue of an activated RAAS system will not lead to hypernatremia, because there will be an osmotic impetus for ADH secretion at the hypothalamus. The body will retain water and the patient will gain weight. Sodium concentration will be normal-ish.

Wait a second. I thought sodium is retained, which is why water is retained.

Well, you lose the sodium and water (after giving Lasix, urine is isosmotic)... and then guess what: you're arterially underfilled or effectively arterially underfilled. There's a reason the body was trying to hold onto the water/salt in the first place; you need the volume. You've volume depleted them, and then it's the same story. Being arterially underfilled leads to a non-osmotic impetus for ADH secretion. Hyponatremia.

The poster said that diuretics lead to hyponatremia and you're saying that ADH secretion leads to it. Isn't that a contradiction?

 

[Knicks]

Ok people are starting to bring up 'contraindications', etc....

I KNOW the correct explanation is somewhere in this thread.....

Can someone quote/post the correct explanation in one post so I can just refer to that post? (Again, why does hyponatremia mean that the heart failure is severe?)

 

[jdh71]

Ok people are starting to bring up 'contraindications', etc....

I KNOW the correct explanation is somewhere in this thread.....

Can someone quote/post the correct explanation in one post so I can just refer to that post? (Again, why does hyponatremia mean that the heart failure is severe?)

Because the pump sucks, effective intravascular volume is decreased (even though these patients are most likely fluid overloaded), activating RAAS and ADH, but you bring in more water than sodium leading to hyponatremia.

 

[Knicks]

Because the pump sucks, effective intravascular volume is decreased (even though these patients are most likely fluid overloaded), activating RAAS and ADH, but you bring in more water than sodium leading to hyponatremia.

Pefect.

Thank you 👍

 

[dienekes88]

Wait a second. I thought sodium is retained, which is why water is retained.

If renin-angiotensin is activated with Aldosterone secretion, salt will be retained by virtue of the insertion of the Epithelial Sodium Channel (ENaC). As I understand it, water will not move freely unless the aquaporin is inserted into the apical membrane by virtue of the V2

However, if you take in a lot of salt, and your blood solute concentration goes up, then there will be an osmotic impetus for ADH secretion. That is why you do not become hypernatremic if everything is working relatively normally. I apologize if I was not clear.

The poster said that diuretics lead to hyponatremia and you're saying that ADH secretion leads to it. Isn't that a contradiction?

It's not a contradiction.

Diuresis leads to being arterially underfilled.

Arterial underfilling leads to a non-osmotic impetus for ADH secretion.

That leads to retaining water.

Retaining water leads to suffering. That is the path to the dark side...