# Hypovolemia and systemic resistance.

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#### veganbythefjord

##### Full Member
What is the advantage in increasing systemic vascular resistance in hypovolemia? Would it not be easier for blood to flow into different organs if it had to flow into lesser resistance ? Thanks in advance.☺

diverts blood from periphery in systole so it can be used to feed coronary arteries in diastole

Maintains mean arterial pressure and thus vital organ perfusion

diverts blood from periphery in systole so it can be used to feed coronary arteries in diastole

Thanks you for the reply, So when it's referred to as systemic vasoconstriction, it is mainly the peripheral organs not in imminent danger from which blood is being shuttled to coronary and other important organs?

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Maintains mean arterial pressure and thus vital organ perfusion

Thank you, would you mind explaining that a wee further please? Thank you.

Thank you, would you mind explaining that a wee further please? Thank you.

From the flow equation, Q = (P1 - P2)/R, where Q is flow, P1 is the upstream pressure, P2 is the downstream pressure and R is the resistance.

MAP which basically represents the perfusion pressure of each organ equals to 2/3 x DBP+ 1/3 x SBP. MAP is the pressure in the aorta using the above equation and corresponds to P1 (upstream pressure) from the flow equation.

As MAP is determined by BP, it is basically affected by CO and TPR. Cardiac output is severely diminished in hypovolemic shock due to decreased preload. So as MAP decreases, P1 drops enough to approach the P2, basically nullifying the pressure gradient and without a pressure gradient, there is no flow.

Underactivation of the baroreceptors stimulates increased sympathetic output, increasing HR and thus CO as well as TPR. By increasing TPR, flow is reduced resulting in increased MAP which functions to maintain perfusion to vital organs.

The balance between maintaining flow and a perfusion pressure is delicate and overactivation of the SANS can eventually increase afterload so much that flow is reduced enough that multi-organ failure occurs from underperfusion.

In all forms of shock, low MAP is what basically causes underperfusion, whether that is a result of decreased CO (either due to decreased preload in hypovolemic and obstructive or decreased contractility in cardiogenic) or decreased TPR in anaphylactic and neurogenic.

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From the flow equation, Q = (P1 - P2)/R, where Q is flow, P1 is the upstream pressure, P2 is the downstream pressure and R is the resistance.

MAP which basically represents the perfusion pressure of each organ equals to 2/3 x DBP+ 1/3 x SBP. MAP is the pressure in the aorta using the above equation and corresponds to P1 (upstream pressure) from the flow equation.

As MAP is determined by BP, it is basically affected by CO and TPR. Cardiac output is severely diminished in hypovolemic shock due to decreased preload. So as MAP decreases, P1 drops enough to approach the P2, basically nullifying the pressure gradient and without a pressure gradient, there is no flow.

Underactivation of the baroreceptors stimulates increased sympathetic output, increasing HR and thus CO as well as TPR. By increasing TPR, flow is reduced resulting in increased MAP which functions to maintain perfusion to vital organs.

The balance between maintaining flow and a perfusion pressure is delicate and overactivation of the SANS can eventually increase afterload so much that flow is reduced enough that multi-organ failure occurs from underperfusion.

In all forms of shock, low MAP is what basically causes underperfusion, whether that is a result of decreased CO (either due to decreased preload in hypovolemic and obstructive or decreased contractility in cardiogenic) or decreased TPR in anaphylactic and neurogenic.

That was brilliantly worded, cleared up a few concepts for me. Thank you so much for your patience and efforts to educate.

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