Hardened arteries = high systolic/lower diastolic

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engineeredout

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THought I'd be done with this forum forever, but a friend of mine studying for the mcat asked me a bio question and I couldn't provide the answer, and the more I think about it the more its driving me crazy.

Arteriosclerosis is the arteries becoming less flexible. This leads to a rise in systolic pressure and a lowering of diastolic pressure.


Why? Conceptually I'm not getting this. Wouldn't an inflexible artery lead to a lesser contraction, therefore lower BP?

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I think the reason the arteries are less flexible is because of plaque so there's less room in the vessel for blood flow. If the same volume of blood is pumped but it has a much more narrow vessel to go through, the force is going to be greater to get all that blood through the vessel.

If I'm wrong, someone please correct me.
 
I think the reason the arteries are less flexible is because of plaque so there's less room in the vessel for blood flow. If the same volume of blood is pumped but it has a much more narrow vessel to go through, the force is going to be greater to get all that blood through the vessel.

I believe this is correct. As a consequence of arterial hardening higher systolic pressures are needed to maintain stroke volume (like with a garden hose - the narrower the hose is, the higher the pressure you need to get the same volume out). This accounts for the higher systolic pressures.

Now to the diastolic pressure. What creates the diastolic blood pressure? It is the elasticity of the vessel walls pushing on the blood inside. So if you have less elastic vessels due to sclerosis, the pressure exerted on the blood during diastole is lower.
 
Well my BP's been 135/65 and 2 doctors both said the lower diastolic was because I had ELASTIC vessels and the arteries were not hardened so...
 
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If only there were some doctors around to explain it to us ... :laugh:

Well- I think you guys are def. right in that context. I looked it up and found some stuff on mayo clinic..http://www.mayoclinic.com/health/pulse-pressure/AN00968

Now I'm scared about my BP...135/70 is the average. I don't know how I could have ateriosclerosis at my age with perfect cholesterol, homocysteine, and C-reactive protein all being optimal. I am nervous a lot so I'm hoping thats the cause...going to the doc next week actually for a check up so I'll ask :|
 
I believe this is correct. As a consequence of arterial hardening higher systolic pressures are needed to maintain stroke volume (like with a garden hose - the narrower the hose is, the higher the pressure you need to get the same volume out). This accounts for the higher systolic pressures.

Now to the diastolic pressure. What creates the diastolic blood pressure? It is the elasticity of the vessel walls pushing on the blood inside. So if you have less elastic vessels due to sclerosis, the pressure exerted on the blood during diastole is lower.


Still seems counterintuitive that less flexible would lead to higher systolic BP. Does it always have to be less available arterial volume to do this?
 
Does it always have to be less available arterial volume to do this?

I'm not quite sure what you mean by this.

The more I look into this the more unsure I get of the mechanism behind this. I think what this whole issue comes down to is the compliance of the vessels (Compliance = Volume / Pressure). There are two types of compliance: dynamic and static. Dynamic would be that measured during flow (and takes into account the resistance of the vessel), and static, which is measured during non flow (diastole).

Assuming that arteriosclerosis causes a DECREASE in compliance, we can look at this in two ways: 1) It takes more pressure to force the same volume into a vessel; or 2) For the same pressure you get less volume into a vessel. In an attempt to maintain stroke volume, it would make sense that the heart would increase its systolic pressure. Notice that the pressure would be even higher due to the resistance of the vessels.

During diastole, however, the resistance of the vessels is not an issue. So while there is still a decreased compliance, it does not cause nearly the same increase in pressure as during systole.

I wrote this really quick because I'm in a hurry. I hope it makes some sense at least. Can anyone else support/refute this?
 
Still seems counterintuitive that less flexible would lead to higher systolic BP. Does it always have to be less available arterial volume to do this?

Think about it like this -- you have a vessel that needs the same volume of blood it's always gotten, but it's more narrow now thanks to the plaque that formed because of arteriosclerosis. There's less room and the vessel is incapable of stretching to accommodate the blood so the force to get the blood in has to be greater.

It might seem counterintuitive because it's the opposite of what it is for ideal fluids in physics because blood isn't an ideal fluid.
 
I'm not quite sure what you mean by this.

The more I look into this the more unsure I get of the mechanism behind this. I think what this whole issue comes down to is the compliance of the vessels (Compliance = Volume / Pressure). There are two types of compliance: dynamic and static. Dynamic would be that measured during flow (and takes into account the resistance of the vessel), and static, which is measured during non flow (diastole).

Assuming that arteriosclerosis causes a DECREASE in compliance, we can look at this in two ways: 1) It takes more pressure to force the same volume into a vessel; or 2) For the same pressure you get less volume into a vessel. In an attempt to maintain stroke volume, it would make sense that the heart would increase its systolic pressure. Notice that the pressure would be even higher due to the resistance of the vessels.

During diastole, however, the resistance of the vessels is not an issue. So while there is still a decreased compliance, it does not cause nearly the same increase in pressure as during systole.

I wrote this really quick because I'm in a hurry. I hope it makes some sense at least. Can anyone else support/refute this?

I think you explained it well!
 
I'm not quite sure what you mean by this.

The more I look into this the more unsure I get of the mechanism behind this. I think what this whole issue comes down to is the compliance of the vessels (Compliance = Volume / Pressure). There are two types of compliance: dynamic and static. Dynamic would be that measured during flow (and takes into account the resistance of the vessel), and static, which is measured during non flow (diastole).

Assuming that arteriosclerosis causes a DECREASE in compliance, we can look at this in two ways: 1) It takes more pressure to force the same volume into a vessel; or 2) For the same pressure you get less volume into a vessel. In an attempt to maintain stroke volume, it would make sense that the heart would increase its systolic pressure. Notice that the pressure would be even higher due to the resistance of the vessels.

During diastole, however, the resistance of the vessels is not an issue. So while there is still a decreased compliance, it does not cause nearly the same increase in pressure as during systole.

I wrote this really quick because I'm in a hurry. I hope it makes some sense at least. Can anyone else support/refute this?

Yea, you're right about the increase in systolic pressure. The decrease in diastolic pressure is because the walls aren't elastic anymore, due to hardening. In normal arteries, when blood is pumped from the heart, the arteries expand (increase in diameter) due to elasticity and "store" some blood and during diastole, the recoil of the arteries pushes the stored blood through the circulatory tree to give the diastolic pressure. When arteries harden, this capacity to store blood decreases and thus, the diastolic pressure decreases also. So what basically happens in atherosclerosis is the systolic pressure rises to high levels while the diastolic pressure drops to low levels due to the hardening of the arteries.


This is how I learned it in my physiology class and it makes sense me; let me know what you guys think.
 
Yea, you're right about the increase in systolic pressure. The decrease in diastolic pressure is because the walls aren't elastic anymore, due to hardening. In normal arteries, when blood is pumped from the heart, the arteries expand (increase in diameter) due to elasticity and "store" some blood and during diastole, the recoil of the arteries pushes the stored blood through the circulatory tree to give the diastolic pressure. When arteries harden, this capacity to store blood decreases and thus, the diastolic pressure decreases also. So what basically happens in atherosclerosis is the systolic pressure rises to high levels while the diastolic pressure drops to low levels due to the hardening of the arteries.


This is how I learned it in my physiology class and it makes sense me; let me know what you guys think.

Beautiful. It's how we learned it too. I knew why the systolic increased, less room, =more pressure. However, diastolic bothered me and I knew it had something to do with less stretching. Well done.
 
I'm not quite sure what you mean by this.

The more I look into this the more unsure I get of the mechanism behind this. I think what this whole issue comes down to is the compliance of the vessels (Compliance = Volume / Pressure). There are two types of compliance: dynamic and static. Dynamic would be that measured during flow (and takes into account the resistance of the vessel), and static, which is measured during non flow (diastole).

Assuming that arteriosclerosis causes a DECREASE in compliance, we can look at this in two ways: 1) It takes more pressure to force the same volume into a vessel; or 2) For the same pressure you get less volume into a vessel. In an attempt to maintain stroke volume, it would make sense that the heart would increase its systolic pressure. Notice that the pressure would be even higher due to the resistance of the vessels.

During diastole, however, the resistance of the vessels is not an issue. So while there is still a decreased compliance, it does not cause nearly the same increase in pressure as during systole.

I wrote this really quick because I'm in a hurry. I hope it makes some sense at least. Can anyone else support/refute this?

Yea, you're right about the increase in systolic pressure. The decrease in diastolic pressure is because the walls aren't elastic anymore, due to hardening. In normal arteries, when blood is pumped from the heart, the arteries expand (increase in diameter) due to elasticity and "store" some blood and during diastole, the recoil of the arteries pushes the stored blood through the circulatory tree to give the diastolic pressure. When arteries harden, this capacity to store blood decreases and thus, the diastolic pressure decreases also. So what basically happens in atherosclerosis is the systolic pressure rises to high levels while the diastolic pressure drops to low levels due to the hardening of the arteries.


This is how I learned it in my physiology class and it makes sense me; let me know what you guys think.


Love it! Thanks guys I get it now.

This whole discussion makes me wanna go out to white castle and start pounding down burgers to see the effects firsthand.
 
I'm having just a little bit of trouble with this concept. I get everything in the last few posts and I think alot of it has been clarified for me and I appreciate that.

One question I have is why in aortic stenosis, there is a really narrow pulse pressure if untreated?

And a second more fundamental question, in hypertension since elevation of diastolic pressures is enough to be diagnostic, what causes that elevation of diastolic pressures if those previous explanations talk about atherosclerosis elevating systolic and decreasing diastolic?
 
Well my BP's been 135/65 and 2 doctors both said the lower diastolic was because I had ELASTIC vessels and the arteries were not hardened so...

This does not seem correct. Hypertension with normal arteries would have narrow pulse pressures, and is considered lower risk with medical intervention. Hypertension with atherosclerosis would have wide pulse pressures and more difficult to manage.

e.g., A patient with a 180/70 b.p. has a WORSE prognosis than a patient with a 180/100 b.p.
 
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