With CHF, is there decreased extracellular fluid volume causing sodium retention

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str8flexed

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Just curious. This question was one on the NBME4. I knew there was volume overload and higher hydrostatic pressure causing transudation of intravascular fluid into the interstitium, but ..

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Nevermind, I'm stupid, the decrease in cardiac output increases sympathetic activity that acts on the kidneys to release aldosterone!

I guess my other question is, does low CO stimulate renin release directly? I know low blood volume would, but does low CO also...
 
CHF is a volume overload state (like cirrhosis) but only in the venous system. the arterial system, one the other hand, is volume depleted. the same reasoning applies for decrease in CO, you're venous overloaded, but the arterial tree is depleted, so you would activated renin/ANII/etc.
 
CHF is a volume overload state (like cirrhosis) but only in the venous system. the arterial system, one the other hand, is volume depleted. the same reasoning applies for decrease in CO, you're venous overloaded, but the arterial tree is depleted, so you would activated renin/ANII/etc.

That's very good, I never thought about it that way. I guess the backup because of right heart failure affects your veins mostly and since your total body blood/water is the same, you have less in your arteries.

However, why does arterial and not venous blood volume activate renin/angiotensin?
 
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The macula densa cells that produce renin detect volume status in the distal tubule. Since the tubular fluid is filtered at the glomerulus from arterial blood, that's what is going to affect it.
 
CHF, cirrhosis, and ARF/CRF are hypervolemic states that can result in hyponatremia because the body senses reduced arterial volume or pressure since the fluid is elsewhere. So the actual sodium concentration the body sees is low and the body secretes too much ADH (causing water retention) even when they are fluid overloaded.
 
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