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Atrial kick and A-flutter

CCU   (427 Views 14 Comments)
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On 1/27/2019 at 11:17 AM, offlabel said:

A fall in renal perfusion (fall in CO) causes a fall in sodium and water retention, right? That results in volume retention which acts to overcome the impediment to right heart return, or the right atrial pressure. ANP and BNP, as I noted in my post,  act to counter act that fluid retention and inhibit systems which increase vasomotor tone. But it isn't a 1:1 relationship. Fluid retention even in the presence of the ANP activity pushes volume through the heart in a compensatory mechanism that maintains cardiac output. It works the same way with any congestive heart failure scenario.

If this is confusing, look at some material dealing with "mean systemic filling pressure/venous return". 

Sorry, I didn't get a "notice" that you replied b/c I wasn't quoted in your response.  So let me know if I'm interpreting this correctly.  CO is maintained by increased preload (from the RAAS system).  I thought you were making the case that it was maintained through ANP secretion.  I understand that ANP is secreted as the atria stretches in response to the increased preload, but it is not a contributing factor to the maintenance of the CO (It is maintained through fluid retention via aldosterone/ADH), correct?  I'm confused as to the significance of ANP in this scenario.

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3 hours ago, murseman24 said:

Sorry, I didn't get a "notice" that you replied b/c I wasn't quoted in your response.  So let me know if I'm interpreting this correctly.  CO is maintained by increased preload (from the RAAS system).  I thought you were making the case that it was maintained through ANP secretion.  I understand that ANP is secreted as the atria stretches in response to the increased preload, but it is not a contributing factor to the maintenance of the CO (It is maintained through fluid retention via aldosterone/ADH), correct?  I'm confused as to the significance of ANP in this scenario.

We're talking about 2 compensatory responses to heart failure that result in  "congestion", which is what keeps forward flow occuring, at least in the compensatory phase. 

1. Fall in renal perfusion causes volume retention and increased mean systemic filling pressure which is the entity required to push blood past the right atrial pressure into the RV.

2. ANP/BNP (among other things) create a fall in afterload, facilitating LV stroke volume. They do antagonize the fluid retention (see #1) as well to some degree, but not enough to prevent it altogether.

Instead of thinking of it as "congestive heart failure" think of it as "congestive heart success" because CO is being maintained (temporarily) in a failing heart. 

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