Hyponatremia Question

[JasonE]

Little confused here, maybe someone can help me out.

If you have a patient with a pitting edema state, lets say CHF, the kidneys are going to see low effecive arterial blood volume. The kidneys will retain a net hypotonic fluid (due to action of Aldo and ADH).

Thus the patient will have an increased total body sodium and an even more increased total body water. Thus we have hyponatremia and pitting edema.


WHY would a diuretic help? Take a loop diuretic for example. Doesn't this cause a net loss of Na in excess of water (it says this in rapid review path). Thus you would lose a hypertonic urine and therefore be MORE hyponatremic?

Pretty confused. If anyone can help me out I'd really appreciate it!

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[jfgavina]

I don't think your fluid becomes more hypotonic in CHF because ADH doesn't play a big role there, it is secreted when your plasma is with high osmolality, which doesn't happen in CHF but does happen in dehydration.

 

[Tig2575]

A volume overloaded state decreases the heart's ability to pump blood effectively, which the kidney "perceives" as low blood volume. Using a diuretic decreases the volume overload, which allows the heart to pump more effectively, which increases perfusion of the kidneys to a normal state and stops them from excessively reabsorbing hypotonic fluid. That results in a correction of the hyponatremia.

The base problem is that in a volume overloaded state, the kidneys aren't perfused well enough due to heart failure. Giving a diuretic fixes the heart failure and allows the kidneys to function normally.

I don't think your fluid becomes more hypotonic in CHF because ADH doesn't play a big role there, it is secreted when your plasma is with high osmolality, which doesn't happen in CHF but does happen in dehydration.

This is incorrect. While ADH is normally secreted only in response to changes in serum osmolarity, in a state with severely decreased effective arterial blood volume (EABV), the body basically says "screw it, I'll take anything I can get to replenish my blood volume, even free water" and secretes ADH in response to low EABV.

 

[JasonE]

so the diuretic doesn't really address the electrolyte problem directly?

Is it true that diuretics (whether loop or thiazide) make a hypertonic urine?

 

[jfgavina]

thanks tig!

 

[Tig2575]

^^ my pleasure!

so the diuretic doesn't really address the electrolyte problem directly?

Is it true that diuretics (whether loop or thiazide) make a hypertonic urine?

The diuretic does not address the electrolyte problem directly.

From what I recall, thiazide diuretics inhibit the NaCl cotransporter that is iso-osmotic (doesn't generate free water), so they simply increase the volume of urine without impacting serum osmolarity. Loop diuretics poison the medullary concentration gradient and prevent the kidney from concentrating the urine (in addition to preventing sodium reabsorption).

 

[Phlame217]

I don't think your fluid becomes more hypotonic in CHF because ADH doesn't play a big role there, it is secreted when your plasma is with high osmolality, which doesn't happen in CHF but does happen in dehydration.

ADH will be active. The only way you get a hypotonic resorption is ADH, every other respiration mechanism in the kidney is ~isotonic.

Dr. Goljan has spoke, therefore it is the law....

 

[OveractiveBrain]

so the diuretic doesn't really address the electrolyte problem directly?

Is it true that diuretics (whether loop or thiazide) make a hypertonic urine?

A fundamental error in thought processes that is perpetuated throughout medical school.

Disorders or sodium are NOT disorder of electrolytes (i.e. sodium). Yes. That is correct. Disorders of sodium are not disorders of sodium. Sodium is a surrogate for water.

Disorders of sodium are actually disorders of water.

In hypervolemic states the intravascular volume is deplete, and ADH kicks in, creating a hypotonic serum.

Diuretics likely improve renal function by improving cardiac function. A telological way of looking at is that as diuretics move fluid off the body, they "pull" the fluid from the interstitium into the intravascular volume.

Tig has hit everything correctly. Well explained, Tig.

 

[stillthinking]

Hi, I'm encountering a similar issue but this is in the context of cirrhosis.

ADH and RAAS are implicated due to peripheral vasodilation, resulting in an increase in total body sodium but an even greater increase in total body water and eventual dilutional hyponatremia

What do we do to solve the hyponatremia? Would it not be worsened by the advice to the patients to restrict sodium intake? Would diuretics be effective here if the cause is not a pump failure as in CCF, but rather an increase in the production of splanchnic vasoconstrictors leading to splanchnic vasoconstriction which incited the release of peripheral vasodilator as the inciting event for RAAS/ ADH activation?

 

[cbrons]

Hi, I'm encountering a similar issue but this is in the context of cirrhosis.

ADH and RAAS are implicated due to peripheral vasodilation, resulting in an increase in total body sodium but an even greater increase in total body water and eventual dilutional hyponatremia

What do we do to solve the hyponatremia? Would it not be worsened by the advice to the patients to restrict sodium intake? Would diuretics be effective here if the cause is not a pump failure as in CCF, but rather an increase in the production of splanchnic vasoconstrictors leading to splanchnic vasoconstriction which incited the release of peripheral vasodilator as the inciting event for RAAS/ ADH activation?

Ascites is due to portal hypertension (increased extrahepatic production of vasoDILATORY substances i.e. NO synthase) = vasodilation of the splanchnic circulation & pooling of blood and a decrease in the EABV.

 

[stillthinking]

Thanks for the reply; error on my part.

If ascites is due to portal hypertension, will diuretics used to treat the ascites resolve the hyponatremia?

If it doesn't, will sodium restriction worsen the hyponatremia in cirrhotic patients?