CHF, what initial diuretic?

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MLT2MT2DO

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I have had 3 different sources tell me 3 different answers, I'm just curious if anyone has any insight. Also there were no modifiers in the question ie nobody was G6PD, or acoholic, or hyopkalemic.

Foursemide
Ace inhib
Spironolactone

Seriously the only thing I've learned with diuretics and CHF is you don't give them mannitol.
 
You use all of them depending on the NYHA failure scale. Furosemide is the big gun to get fluids off the lungs but you'd give ace inhibitors and spironolactone chronically to lower mortality.
 
You use all of them depending on the NYHA failure scale. Furosemide is the big gun to get fluids off the lungs but you'd give ace inhibitors and spironolactone chronically to lower mortality.

So I should assume that "What is the initial diuretic you would use in CHF" is not black and white and probably shouldn't have been asked that way? Otherwise the answer is basically fouresemide?
 
Start treatment with ACE for HT
If cant tolerate ACE then ARBs
Loops and Thiazides for Sx relief (no decrease in mort)
 
Start treatment with ACE for HT
If cant tolerate ACE then ARBs
Loops and Thiazides for Sx relief (no decrease in mort)

If Thiazides are the preferred diurectic for Essential HTN why would I use an ACE inhibitor for the HTN in CHF?

I've always wondered why would an ACE inhib in CHF. Wouldn't the increase in bradykinin give you issues?
 
If Thiazides are the preferred diurectic for Essential HTN why would I use an ACE inhibitor for the HTN in CHF?

I've always wondered why would an ACE inhib in CHF. Wouldn't the increase in bradykinin give you issues?

Because ACE decrase Mortality
 
Start treatment with ACE for HT
If cant tolerate ACE then ARBs
Loops and Thiazides for Sx relief (no decrease in mort)

Yes. I'm pretty sure ACEi or ARB is standard of care in CHF. That would be my go to. If neither of those are there, spironolactone, metoprolol, or carvedilol would be my next choice as they all also increase longevity. Doubt you'd have to make a choice between those
 
You give ace and beta blocker as baseline treatment for CHF. Once they reach stage III then you add spironolactone and may place an implantable defibrillator. The order of this **** isn't important for Step 1 - worry about it for clerkship exams or the hospital floor. Knowing which drugs/interventions lower mortality (ace, ARB, beta blocker, spironolactone, defibrillator) and which provide merely symtompatic relief (furosemide, thiazides, digoxin, CCBs, etc.) is what the Step 1 guys want you to know.
 
You give ace and beta blocker as baseline treatment for CHF. Once they reach stage III then you add spironolactone and may place an implantable defibrillator. The order of this **** isn't important for Step 1 - worry about it for clerkship exams or the hospital floor. Knowing which drugs/interventions lower mortality (ace, ARB, beta blocker, spironolactone, defibrillator) and which provide merely symtompatic relief (furosemide, thiazides, digoxin, CCBs, etc.) is what the Step 1 guys want you to know.

As mentioned I've had this exact question once on two different Qbanks (different answer on each). Pretty much why I came here to ask, as I felt I was missing some sort of basic science thing.

It seems that I'm not, pretty much a we give ACE inhibs because studies have been done that confirm they reduce mortality by an unknown mechanism. First time I picked fouresemide because "it's a big water dump" and the bradykinin affect seems counterintuitive to me in CHF
 
You give ace and beta blocker as baseline treatment for CHF. Once they reach stage III then you add spironolactone and may place an implantable defibrillator. The order of this **** isn't important for Step 1 - worry about it for clerkship exams or the hospital floor. Knowing which drugs/interventions lower mortality (ace, ARB, beta blocker, spironolactone, defibrillator) and which provide merely symtompatic relief (furosemide, thiazides, digoxin, CCBs, etc.) is what the Step 1 guys want you to know.

Good, the less to know the better, gracias

As mentioned I've had this exact question once on two different Qbanks (different answer on each). Pretty much why I came here to ask, as I felt I was missing some sort of basic science thing.

It seems that I'm not, pretty much a we give ACE inhibs because studies have been done that confirm they reduce mortality by an unknown mechanism. First time I picked fouresemide because "it's a big water dump" and the bradykinin affect seems counterintuitive to me in CHF

The mechanism is known - it prevents aldosterone-mediated remodeling of the heart
 
The mechanism is known - it prevents aldosterone-mediated remodeling of the heart

And Spirinolactone has been shown to reduce mortality by 30%, and foursemide allows a large fluid dump. I understand why ACE inhibitors are now used, but again not anymore than why over the other 2 as a first line. Additionally it seems like magic to me that bradykinin never becomes an issue.

Though this discussion may have become beyond the scope of step one (not my intention originally as it was from qbanks), I SAW the "aldosterone remodeling" sentence for the first time even though I've read this in FA at least 3x.

All the input was much appreciated. Thanks!
 
Out of laziness, I'm going to go off my memory of class lecture and not search uptodate or something, but I don't think the choice of ACEi as the go to is based on greater efficacy. It's a better 1st choice than ARB's based on cost and spironolactone based on side effect profile

And oh yes, the all too familiar feeling of reading something 10x only to really read it once
 
Isn't spironolactone chosen basically just for the anti-aldosterone effect?

I feel like I've read that its usually given in doses that are too low to appreciably diurese the patient but that are high enough to bind and inhibit aldosterone receptors.
 
As everybody has mentioned ACE-I. Here's the summary from Goljan's RR that talks about it. The yellow is just the search feature when I typed in "ace inhibitors" into the search box...lol

qUWnfxI.png
 
I could be remembering wrong. Aldosterone makes more intuitive sense to me though give that it's a steroid and given the efficacy of spironolactone (with aldosterone being downstream of ATII)
 
Interesting, thanks for digging that up. I guess that would be another reason spironolactone isn't the 1st go to, but still helpful (or at least a BS reason to make it stick)
 
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