Circulation physiology question (sympathetic stimulation and CO)

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Grurik

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Just have a question regarding sympathetic stimulation of heart regarding cardiac output. Cardiac output is basically controlled by everything that affects blood flow and ultimately venous return.

Venous return can be calculated as:
VR = (Psf-PRA)/RVR where Psf: mean systemic filling pressure; PRA: right atrial pressure; RVR: resistance to venous return.

Sympathetic stimulation makes the heart pump stronger. The other part it affects is the systemic circulation where it increases the mean systemic filling pressure because of vasoconstriction of peripheral vessels (especially the veins), and this increases the resistance to venous return. So basically, one factor that increases VR (Psf increase) and one that decreases (RVR increases).

What factors makes the venous return, and thereby CO, increase so much when maximally sympathetic stimulated?
Will the resistance to venous return be overdriven by the mean systemic filling pressure? And the heart's stronger beat keep the pressure difference?
Is this increase in resistance to venous return just a necessary "brake"?

Additionally, the pressure in right atria will increase and also decrease the VR looking at the forumula. Even though I get that if Psf would be like 14mmHg and right atrial pressure 12 mmHg it would be a pressure difference that would keep the blood flowing into the heart, no matter the volume.

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Just have a question regarding sympathetic stimulation of heart regarding cardiac output. Cardiac output is basically controlled by everything that affects blood flow and ultimately venous return.

Venous return can be calculated as:
VR = (Psf-PRA)/RVR where Psf: mean systemic filling pressure; PRA: right atrial pressure; RVR: resistance to venous return.

Sympathetic stimulation makes the heart pump stronger. The other part it affects is the systemic circulation where it increases the mean systemic filling pressure because of vasoconstriction of peripheral vessels (especially the veins), and this increases the resistance to venous return. So basically, one factor that increases VR (Psf increase) and one that decreases (RVR increases).

What factors makes the venous return, and thereby CO, increase so much when maximally sympathetic stimulated?
Will the resistance to venous return be overdriven by the mean systemic filling pressure? And the heart's stronger beat keep the pressure difference?
Is this increase in resistance to venous return just a necessary "brake"?

Additionally, the pressure in right atria will increase and also decrease the VR looking at the forumula. Even though I get that if Psf would be like 14mmHg and right atrial pressure 12 mmHg it would be a pressure difference that would keep the blood flowing into the heart, no matter the volume.

Sympathetics are active during "fight and flight" or generally, states in which more flow is needed systemically. Overall, sympathetics send more blood to the heart and skeletal muscle than elsewhere. This is due to different adrenergic receptors (beta-2 receptors in vessels of the heart and skeletal muscle, which cause vasodilation around these organs. Alpha receptors, located elsewhere, lead to vasoconstriction).

Increased vasodilation in vessels (arteries) leading away from the heart increases venous return. Afterload will probably be reduced in the aorta beta-2 (or beta-1???) is dominant here. The net effect is increased cardiac output. Beta-2 is also in bronchiolar smooth muscle and induces vasodilation in the lungs. Beta-1 receptors in the heart also increase myocontractility leading to more blood flow. This makes sense-->reserve more blood flow for, and increase oxygen supply to, heart, muscles, and the airway, especially during exercise.
 
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You're thinking about the venous system incorrectly if I understand your post. A good model for the circulatory is a closed fluid circuit containing a pump, arteries, a resistance bed, and a venous return system. The circulatory system can be modeled in this way. Vasoconstriction of veins increases venous return. Catecholamines released during exercise increase both heart rate and contractility and stimulation of alpha 1 cause vasoconstriction. If the veins are dilated fluid pools on them because there is not much pressure to push the blood back to the heart. Think about our model. The size of the venous pipe has increased and less blood is able to return to the heart. While exercising this pipe constricts. The heart is pumping more now as well. Remember it is a closed circuit. The arteries are opening up due to vasodilation by the beta2 , so more blood is traveling through the arterial system and this increased blood flow must then pass through the resistance vessels and then into the venous system. The venous system pipe is now smaller. This blood does not back up as a result this constriction. It now shoots through the venous system much faster and thus returns to the heart more quickly. Think about it conceptually rather than mathematically.
 
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You're thinking about the venous system incorrectly if I understand your post. A good model for the circulatory is a closed fluid circuit containing a pump, arteries, a resistance bed, and a venous return system. The circulatory system can be modeled in this way. Vasoconstriction of veins increases venous return. Catecholamines released during exercise increase both heart rate and contractility and stimulation of alpha 1 cause vasoconstriction. If the veins are dilated fluid pools on them because there is not much pressure to push the blood back to the heart. Think about our model. The size of the venous pipe has increased and less blood is able to return to the heart. While exercising this pipe constricts. The heart is pumping more now as well. Remember it is a closed circuit. The arteries are opening up due to vasodilation by the beta2 , so more blood is traveling through the arterial system and this increased blood flow must then pass through the resistance vessels and then into the venous system. The venous system pipe is now smaller. This blood does not back up as a result this constriction. It now shoots through the venous system much faster and thus returns to the heart more quickly. Think about it conceptually rather than mathematically.

You brought out a good point, which I missed. That is, venoconstriction increases venous return. So, to keep it simple, heart contracts more, arteries dilate (esp to heart and muscle), and smooth muscle in veins contract more (increased venous return) .
 
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Thank you very much for your responses. I was aware of the fact that it increased venous return by increasing the mean systemic filling pressure, that is, blood is pushed into the heart. However, by increasing the mean systemic filling pressure, resistance to venous return also increases, this is a "force" against the systemic pressure towards the heart. And I though these two increased proportional, and hence would diminish some of the effect, which does not seem to be the case.

Anyway, the model you proposed madchemist89 is real nice. Sometimes you just mess things up when looking at specific formula without thinking about it conceptually, so thanks very much for that!
 
sympathetics --> constriction of all vessels --> increased VR --> increased CO --> increased TPR (in both arteries + veins due to constriction + increased CO) --> increased pressure gradient --> increased flow --> increased VR
 
sympathetics --> constriction of all vessels --> increased VR --> increased CO --> increased TPR (in both arteries + veins due to constriction + increased CO) --> increased pressure gradient --> increased flow --> increased VR

This part is not always true. It depends on the receptor intrinsic to the blood vessel. .
 
This part is not always true. It depends on the receptor intrinsic to the blood vessel. .

VEINS + ARTERIES. Got it? And I believe he's trying to get the concept down.
 
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