Question on Physiology RE: Decompensated Cardiac Failure

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docelh

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This question may be too advanced for the MCAT forum.

In decompensated cardiac failure, the heart fails to pump enough blood which leads to sympathetic discharge, fluid retention, higher mean systemic filling pressure, and potentially peripheral edema. Possible therapy includes digitalis to strengthen the heart and/or a diuretic to reduce the pressure on the right atrium.

Q: Wouldn't the conditions that lead to fluid retention and edema also expand renal artery and promote excretion?
 
So one of the issues in heart failure is that the Renin, Angiotensin, Aldosterone pathway is activated which is the pathway to conserve Na and thus water. The extra fluid migrates out of the blood vessels (which is why it is edema). So that fluid is not being "seen" by the kidney at all. Only fluid in your vasculature can be filtered by the kidney. Furthermore the heart is failing so its output is dropping. Thus the kidneys are seeing even less blood to filter.
 
Here's my thought process based on everything including your response.

The bulk of the blood volume and pressure would be in the veins since the heart (being the weak link) is damming up the blood. This, in turn, would reduce blood flow through the arteries despite peripheral vasodilation. In a chronic case, arterial pressure would still need to be greater than venuous pressure; otherwise, blood would not circulate.

While fluid is being retained, much of it is being diverted to edema and a great portion of the remainder is getting parked in the veins.

At the same time, I suspect both the mean circulatory and systemic filling pressure are increasing since the blood volume is rising. This rise is probably unequal, with the bulk of the increase in the veins. In a chronic case, at some point, equilibration of the blood pressure would not happen until the heart stops beating completely.

If I left out something or mis-stated another thing, please let me know. Just trying to wrap my head around a rather difficult topic. Thank you for your reply.
 
Well, two things. First, this is not something you need to understand for the MCAT, so I wouldn't be worrying about it. Second, you're not going to have the background knowledge to fully understand it yet, but the basics of it are as follows:

In heart failure (of which there are different flavors) you generally have both left and right sided failure. The definition is basically that the heart is not pumping enough blood to meet the metabolic needs of the body. With left-sided failure, the heart is unable to pump enough blood due to an infarct or some other derangement. Right-sided failure often follows left-sided failure because of volume overload of the right ventricle following pulmonary edema. This leads to backup of blood in the venous circulation.

One of the important results of all this, as Instatwaiter mentioned, is congestion that builds in the kidney. This leads to activation of the renin-angiotensin-aldosterone axis. Aldosterone causes the kidney to reabsorb more sodium and thus more water causing an increase in blood volume. With Angiotensin II there is also an increase in the systemic vascular resistance. Accompanying all this is also a spike in sympathetic outflow, which contributes to the increase in resistance and also tries to augment the action of the heart.

The problem is in most cases the heart can no longer compensate through the Frank-Starling mechanism so the increase in fluid retention does not augment the cardiac output enough to meet the metabolic needs of the body, so you just keep retaining more fluid and keep sympathetic outflow high. The increase in fluid along with the higher hydrostatic pressure due to backup of blood leads to the edema (peripheral and pulmonary).

The simple answer to your first question is no, the extra volume does not "expand the renal artery and promote excretion." There is congestion of the kidney and this leads to renin-AII-aldosterone activation which leads to further fluid retention.
 
Well, two things. First, this is not something you need to understand for the MCAT, so I wouldn't be worrying about it. Second, you're not going to have the background knowledge to fully understand it yet, but the basics of it are as follows:

In heart failure (of which there are different flavors) you generally have both left and right sided failure. The definition is basically that the heart is not pumping enough blood to meet the metabolic needs of the body. With left-sided failure, the heart is unable to pump enough blood due to an infarct or some other derangement. Right-sided failure often follows left-sided failure because of volume overload of the right ventricle following pulmonary edema. This leads to backup of blood in the venous circulation.

One of the important results of all this, as Instatwaiter mentioned, is congestion that builds in the kidney. This leads to activation of the renin-angiotensin-aldosterone axis. Aldosterone causes the kidney to reabsorb more sodium and thus more water causing an increase in blood volume. With Angiotensin II there is also an increase in the systemic vascular resistance. Accompanying all this is also a spike in sympathetic outflow, which contributes to the increase in resistance and also tries to augment the action of the heart.

The problem is in most cases the heart can no longer compensate through the Frank-Starling mechanism so the increase in fluid retention does not augment the cardiac output enough to meet the metabolic needs of the body, so you just keep retaining more fluid and keep sympathetic outflow high. The increase in fluid along with the higher hydrostatic pressure due to backup of blood leads to the edema (peripheral and pulmonary).

The simple answer to your first question is no, the extra volume does not "expand the renal artery and promote excretion." There is congestion of the kidney and this leads to renin-AII-aldosterone activation which leads to further fluid retention.

i'm impressed that you even care enough to post and look this up - im pretty sure all i cared about in undergrad was getting drunk.
 
Think about "autoregulation". The mechanisms that organs use to make sure they get constant blood flow in the setting of a wide range of blood pressure.
 
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