I am currently taking a dysrhythmia interpretation and management course so this this is all very new to me, forgive me if this sounds too "newbie-ish."
My understanding is that the atrial kick occurs with atrial systole, supplying the ventricles with that last 20-30% of blood before ventricular systole, and that with atrial flutter, this is lost. I'm confused as to why this would be lost as the atria are still contracting. Is it because it is not as much of a coordinated contraction since it is the atrial tissue generating the impulse rather than the SA node, and therefore is not traveling through the normal conduction pathway? I do understand why atrial kick is lost with a-fib, since the atria are not really contracting fully and more so just quivering, but this is not the case with a-flutter so I'm a bit lost.
Looking at an ECG strip with a-flutter, do the flutter waves not signal that the atria are depolarizing just like the P waves do? I'm not quite making the connection as to why this would not also contribute an atrial kick, especially if the ventricular rate is normal and the atria are able to contract a few times before ventricular systole.
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.
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.
murseman24, MSN, CRNA
316 Posts
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.