Vascular function curve

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propofol123

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Hello,

I have a little confusion on Vascular curve. I m reading Costanzo an it says that venoconstriction causes the shift of the unstressed volume to stress volume hence increasing the MFSP--> increase venous return shifting the vascular curve to the right.

Then the increase of total Peripheral resistance (tpr) reduces venous return and shift the vascular curve to the left. And shift the CO curve right (reducing Co) due to the increased afterload. I can understand the CO part... My question is the increase on veno tone is different from increase TPR? Doesnt the increase of TPR increases VR? From my understanding the increase of TPR is increase in arterial tone.

Can anyone clear my confusion?!??

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TPR is on the arterial side. It's cardiac afterload (blood pressure), hence its increase reduces cardiac output. It does not increase venous return because you have the same amount of blood in active circulation, it just doesn't pass through some of the capillaries. The increase in TPR is due to bypassing the capillary system (hence the same blood volume has a smaller container).

The venous side is different than the arterial. It has a much higher volume than the arteries (hence the much lower pressure). A lot of veins don't contribute much to circulation. The blood flow in them is slow, the pressure in them is low due to low venous tone, they contribute very little to the venous return; think about them as blood reservoirs. When those constrict, the blood in them returns to the hemodynamically active (i.e. stressed) volume and increases venous return (hence preload, hence cardiac output).
 
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So, if Tpr is referring to the arterial side, then does the term increase systemic vascular resistance refer to the same thing as tpr? And with sympathetic stimulation, there is increase of Peripheral resistance to increase cardiac output. In this case m assuming its referring to venous side?
 
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So, if Tpr is referring to the arterial side, then does the term increase systemic vascular resistance refer to the same thing as tpr? And with sympathetic stimulation, there is increase of Peripheral resistance to increase cardiac output. In this case m assuming its referring to venous side?
In a simplified description, with sympathetic stimulation, you get increase in both cardiac output (because of increased heart rate and contractility) and blood pressure (because of the increased cardiac output and vasoconstriction - i.e. peripheral vascular resistance). On the venous side, you get venoconstriction that produces increased venous return and contributes to the cardiac output.

You have to read up on the effects of various sympathetic receptors (alpha 1/2, beta 1/2), and also what epinephrine and norepinephrine do respectively. As far as I remember, Costanzo is pretty good at that.
 
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I like FFPs answer. Listen to him. I read your question differently at first.

In say an animal preparation or so forth where you give a venoconstrictor (or mimic cardiac effects of venoconstriction with fluid bolus, DDAVP, etc) a healthy heart receives greater preload/LVEDV, and per frank starling principle, bainbridge reflex, so forth will increase contractility, HR, and maintain ideal LVESV. The increase in CO causes local autoregulatory mechanisms to decrease flow through peripheral tissue, thereby increasing SVR in response to increase CO and local blood flow. The Increased SVR decreases CO, which decreases venous return and homeostasis is somewhat returned (at a higher MAP) until the kidneys do their thing. If natriuresis is impaired, you basically have the underlying pathophysiology of volume-loading HTN.

That's probably not at all what you were after.

I like the way Guyton covers this stuff though
 
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