Aortic stenosis: Why is this

[rsweeney]

In aortic stenosis, you get a decrease in stroke volume and cardiac output, thus you eject less blood and thus have a larger end systolic volume [increased residual volume]. But WHY does end diastolic volume and pressure increase? According to texts, the NORMAL venous return adds to the increased residual volume thus increasing preload or end diastolic volume and pressure. But why is this? If you eject less then shouldn't that smaller stroke volume return to the heart thus maintaining end diastolic volume? Since the circulatory system is a closed system, then cardiac output has to equal venous return. Thus, if you have a decreased cardiac output, which you do with aortic stenoisis, then you should have a reduce venous return, thus maintaining your end diastlic volume and pressure [preload].

So, when texts say that the normal venous return adds to the increased residual volume causing an increase in end diastolic pressure and volume [preload] isn't that wrong? Shouldn't the end diastolic pressure and volume [preload] stay the same since the previous stroke volume was less?

Following is the link which shows the PV-loop for aortic senosis for your reference:
http://www.oucom.ohiou.edu/cvphysiology/HD009.htm

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[LuckyMD2b]

Wow, good question... I thought I was pretty solid on my CV-phys.

I'm not sure about the answer to your question, so I can only respond with another question: Isn't it an over symplification to view the circulatory system as a closed system?

If it was completely closed then you wouldn't get peripheral edema or hypovolumic.

-- So aortic stenosis leads to decreased SV and i think it would initially lead to decreased systolic BP {increased pressure drop across the aortic valve} Wouldn't this then lead to deacres renal perfussion and activation of the Renin-Angiotensin-Aldosterone System. Resuling in Water retension and Vasoconstriction. As a result there would be an increase in water load and venous return to the heart.

Eventually I think that there would be Left ventricular hypertrophy and dilation --> increased end diastolic volume.

So i don't think that Stroke volume and venous return necessarily must change by the same amount over a large enough period of time.

But I'm only a first year, so I'm not completely sure,

just my 2cents

 

[Kalel]

Preload is derived by end-systolic volume and whatever volume from the venous system that is emptied into the right atrium. As explained in that link, with aortic stenosis, end systolic volume is increased because stroke volume decreases. However, stroke volume does not necessarily correlate with venous return, as venous return can be increased or maintained through compensatory systemic mechanisms like sympathetic activation with increases in systemic and venous tone and retention of fluid. Eventually, these compensatory mechanisms lead to heart failure.

 

[CYP2E1]

This is a great question because it shows a couple of things.

Firstly you are correct that a ?normal functioning CVS? is a closed system. The key to your question is the difference between the functioning of the CVS in normal and pathological situations. Secondly in understanding the abnormal and normal functioning it is important to understand the regulation of CO by local vascular beds as the primary controller of blood flow. This concept of autoregulation sees the heart as a responder to the needs of metabolising tissue rather than the driver of the CVS.

In the normal CVS the heart behaves as you describe, beat to beat variability in SV will lead to beat to beat variations in VR, EDV, ESV etc. Changes in intravascular volume will lead to alterations in VR, SV etc however in the normal situation the CVS compensates and these changes are ?evened out?. Changes in ESV lead to an increased force of contraction (anrep effect), however the metabolic needs of the tissues drive (remember ficks principle) the VR and therefore CO and all is harmonious.

Now in the case of Aortic Stenosis these regulatory mechanisms are unable to overcome the pathology that has afflicted the aortic value, as a consequence the metabolic needs of the tissues are poorly met (they may be adequate at rest or even with some degree of activity but at some point they will fail). So the tissues cry out for more and then body responds with all the systems it has to increase CO. This may be increased autonomic activity, renin-angiotensin-aldosterone activation, intrinsic heart mechanisms to overcome the increased afterload (Starlings law) etc ?

The point is that in a pathological state the pathophysiology is different from the normal physiology. The body then seeks to rectify this imbalance.

 

[rsweeney]

I feel like a dope--end diastolic volume and pressure do increase, even in the absence of compensatory mechanisms.

Since the text in the link says,

"These changes just described do not include cardiac and systemic compensatory mechanisms that attempt to maintain cardiac output and arterial pressure."

there has to be another reason end diastolic volume and pressure are up, and here it is. It really helped once I drew a picture of the heart as a closed pump.

Imagine the pump is turned off until all blood inside is at a stand-still. Now, at stand-still, let's say hypothetically you have 5L in the right ventricle, 5L in the left ventricle, and nothing in the veins or arteries. Now you decide to turn the pump on. Since there is nothing prohibiting ejection from the right heart, a normal 3L will be pumped out and 2L will stay in [residual volume]. But, the aortic stenois in the left heart will only permit 2L to be ejected and 3L remains [residual volume]. Therefore, at the end of the first right- left heart cycle after the pump was turned on, the normal 3L that was ejected from the right will build up on the abnormal 3L that remained in the left heart, thus you will have 6L as your end diasotlic volume. Also, the 2L that was ejected from the left heart will add to the 2L that remained in the right heart leaving the right heart with an end diastolic volume of 4L.

Then, since the left heart now has more blood in it than before [6L], it will eject say 3L instead of 2L thus bringing the end diastolic volume in the right heart back to normal--to 5L. Also, since the right heart had only 4L in it, it only ejected 2L [b/c end systolic volume won't change due to the Frank-Starling relationship and because nothing is wrong with the right heart], thus that 2L added to the 3L that remained in the left heart bringing its end diastolic volume back to 5L.

Then, I believe, that whole cycle will start all over again. I would imagine that the end diastolic volume does not increase indefinatlely because of my hypothetical situation [right heat ejects more and left heart ejects less then right heart ejects less and left hear ejects more--Since the CVS is a closed system that is. Even with aortic stenosis, a higher end diastolic volume will still result in a greater stroke volume --right?

-Thanks everyone!

-Richard

 

[Goofyone]

Originally posted by rsweeney
According to texts, the NORMAL venous return adds to the increased residual volume thus increasing preload or end diastolic volume and pressure. But why is this? If you eject less then shouldn't that smaller stroke volume return to the heart thus maintaining end diastolic volume?

CO=SV x HR

If the SV decreases, the CO (ie venous return) can remain "normal" by simply increasing the HR.

I don't know if that's indeed what happens, but that would certainly explain it--I think.


[edit] I reread your question--I think I misunderstood.

So, when texts say that the normal venous return adds to the increased residual volume causing an increase in end diastolic pressure and volume [preload] isn't that wrong? Shouldn't the end diastolic pressure and volume [preload] stay the same since the previous stroke volume was less?

I think the end-diastolic pressure could be higher even with the same venous return. I assume they mean only the pressure in the heart, not the diastolic blood pressure. In other words, I don't think the ventricular pressure is due to just preload, but, me thinks, could be simply due to more internal resistance within the heart itself from hypertrophy.

Man I hope this makes sense.

 

[Mossjoh]

Hmm...not sure if this is as simple as it sounds.

The aortic stenosis causes an increased afterload and will cause concentric left ventricular hypertrophy. This reduces the size of the left ventricle. Filling pressures into this hypertrophied ventricle are increased, and eventually blood can back up into the left atrium causing left atrial dilation. This can lead to eventual atrial fibrillation and an even worse filling of the left ventricle because of loss of the Left atrial "kick" of contraction.
The elevated pressures in the left atrium eventually go retrograde into the pulmonary circulation causing pulmonary congestion and heart failure. Remember though, heart failure is also defined as a decreased systemic flow.
This decreased systemic flow does several things. It causes decreased renal perfusion, which is sensed by the juxtaglomerular cells causing them to increase synthesis of renin, eventually causing vasoconstriction via Angiotensin II, as well as salt and water retention via the actions of aldosterone.
The initial decreased systemic flow and pressures can also causes a reflex tachycardia, helping to increase the cardiac output.

Heart failure will eventually become global (closed circuit) as pulmonary resistance increases and the right heart fails, causing peripheral edema, hepatomegaly, splenomegaly ect.

Its helpful to think of the heart as a pump...and increased pressures in one chamber have to effect all other chambers.

Hope this helps....

Mossjoh

"Future Cardiologist"

 

[CYP2E1]

There are some inaccuracies in previous posters statements.

Firstly Goofyone said

?CO=SV x HR

If the SV decreases, the CO (ie venous return) can remain "normal" by simply increasing the HR.

I don't know if that's indeed what happens, but that would certainly explain it--I think?

This is nonsense and fails to understand CO and its control. The statement CO = HR * SV, is not like an equation from school where all the variables can be altered independently of one another. You cannot simply increase the HR and maintain a normal CO, the increased HR means that less time is spent in diastole and hence there is less filling (EDV) and hence SV is reduced. This is not new Kumada et al showed this clearly in 1967 and along with this the constancy of CO with varying HR.

Secondly Mossjoh said

??aortic stenosis causes an increased afterload and will cause concentric left ventricular hypertrophy. This reduces the size of the left ventricle??

What Mossjoh meant to say was that due to the extension of the Law of laplace where

(S) Wall Stress = P (transmural pressure) * r(Radius) / w (wall thickness)

When pressure overload causes concentric hypertrophy the thicker wall, but similar lumen (r) means that wall tension (s) is reduced. However this compensation does mean that ventricular wall compliance is reduced which leads to the complications Mossjoh discussed.

 

[Goofyone]

Originally posted by CYP2E1
You cannot simply increase the HR and maintain a normal CO, the increased HR means that less time is spent in diastole and hence there is less filling (EDV) and hence SV is reduced. This is not new Kumada et al showed this clearly in 1967 and along with this the constancy of CO with varying HR.

I understand that the variables are not totally independent, but I disagree that increasing heart rate will not increase cardiac output (to a point, until like you said that the decreased filling time outweighs the higher rate). However, I thought that was only at higher heart rates. Care to help me out?

By the way, I don't know if you intended to or not, and I mean no disrespect, but your post sounded a little condescending. I don't appreciate being called nonsensical. We're all just trying to learn here.

 

[Kalel]

Originally posted by Goofyone
I understand that the variables are not totally independent, but I disagree that increasing heart rate will not increase cardiac output (to a point, until like you said that the decreased filling time outweighs the higher rate). However, I thought that was only at higher heart rates. Care to help me out?

I agree with you. Unless we are talking about some sort of tachyarrhythmia, increasing heart rate is part of how people who exercise increase their cardiac output. Pace makers can actually improve a CHF patient with a bradyarrhythmia's cardiac output and therefore CHF status. If we are wrong, then a *lot* of physiology text books need to be corrected.


http://www.merck.com/mrkshared/mmanual/section16/chapter213/213a.jsp
http://www.cvphysiology.com/Cardiac Function/CF001.htm

 

[CYP2E1]

Try berne and levy?s Cardio vascular physiology pp 217 this should help you out, between approx 100-200 bpm changes in HR do not affect CO due to the corresponding decrease in filling time.

?increasing heart rate is part of how people who exercise increase their cardiac output?
This statement is not true the increase in HR plays a permissive role in augmenting CO it is not the cause (increased VR is). I disagree with Kalel that ?If we are wrong, then a *lot* of physiology text books need to be corrected.? B&L and ?The Heart? by Page et al (APS) both state this fact clearly.

No offense intended Goofyone, just tired at the time, and I have had this discussion lots of times, so I get kinda ?raw? and my comment was not that you are nonsensical rather this notion of HR being the ?driver? of increase CO.

 

[Goofyone]

Originally posted by CYP2E1
Try berne and levy?s Cardio vascular physiology pp 217 this should help you out, between approx 100-200 bpm changes in HR do not affect CO due to the corresponding decrease in filling time.

?increasing heart rate is part of how people who exercise increase their cardiac output?
This statement is not true the increase in HR plays a permissive role in augmenting CO it is not the cause (increased VR is). I disagree with Kalel that ?If we are wrong, then a *lot* of physiology text books need to be corrected.? B&L and ?The Heart? by Page et al (APS) both state this fact clearly.

No offense intended Goofyone, just tired at the time, and I have had this discussion lots of times, so I get kinda ?raw? and my comment was not that you are nonsensical rather this notion of HR being the ?driver? of increase CO.

That's cool CYP. Maybe I'm just too touchy You sound like you know what you're talking about. I didn't realize that there was no effect over 100bpm. Thanks for the info.

 

[deleted29780]

I must admit, we are all a bunch of future medics who really understand their physiology. Thats gr8 . I agree with all the contributors. Lets continue to develop our limbic systems.

 

[deleted29780]

Originally posted by Goofyone
That's cool CYP. Maybe I'm just too touchy You sound like you know what you're talking about. I didn't realize that there was no effect over 100bpm. Thanks for the info.

i know for a fact that, increased HR greater than 150 bpm... Paroxysmal tachycardia. results in a decreased cardiac output, simply because fast filling is compromised - fast filling accounts for 70 % of EDV. The reduced EDV, by starlings law, reduces the contractililty of the heart, thus reducing SV and thus CO.

Desculpe