Eli5, how do contracted Blood Vessels lead to Increased Cardiac Preload?

Submitted by WebW3b t3_z7tfmb in explainlikeimfive

in hypovolemic shock, there is a deficiency in blood cells (hence the name, Hypo.Vol.Emic) thus the blood vessels react to this by contracting in hopes of increasing cardiac preload by increasing blood pressure (So Blood Vessels contract > blood pressure increases > preload increases.) but how does this lead to an increased preload? Isn’t the heart just receiving the same quantity of blood but throughout a longer period? (So small amounts throughout a longer period instead of a big amount throughout a short period)

I think I’ve got this whole thing tangled up

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shaokim t1_iy8trca wrote

I'm not sure if your premise is correct. In hypovolemic shock, central venous pressure (which I think is a useful proxy for preload) will decrease or remain equal because of lower circulating blood volume. I'm not sure if your reference to "blood cells" is of relevance in this particular bit of physiology.

Total intravascular volume goes down, therefore preload goes down. I think it's roughly as straightforward as that, in any case I don't think it would increase.

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WebW3b OP t1_iy9bui1 wrote

That’s what had me confused, this is what I was able to understand. Circulating blood volume does indeed decrease hence blood pressure drops hence preload is decreased. the body apparently reacts to this by undergoing vasoconstriction which pushes/squeezes the red blood cells forward to the heart (blood pressure isn’t sufficient so vasoconstriction is like an additional booster to help “maintain” things) thus the blood pressure increases as the heart has just received blood (that wasn’t able to make it back before vasoconstriction) and preload increases as again heart has just received blood.

Now of course by saying “blood pressure increases” & “preload increases” it’s definitely a minuscule amount and the rate of increase is still far below than average and not enough to suffice for the body

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shaokim t1_iy9dq7p wrote

I have it like this:

There is bleeding. At a certain point, blood pressure measured in the aortic arch and carotid body baroreceptors drops. The body compensates by triggering a release of circulating adrenaline as well as noradrenaline signaling to the sinus node. This will briefly increase contractility of the heart and heart rate, as well as induce peripheral vasoconstriction through signaling at alpha receptors.

All this would serve to compensate for blood pressure loss that goes with blood loss. So if I have that right, in this initial stage of bleeding blood pressure and venous return (preload) could be kept relatively constant by this compensation mechanism.

Over time, the bleeding overwhelms this compensation mechanism, and as intravascular volume drops, blood pressure drops and central venous pressure drops.

At no point, I think, will any of these parameters be significantly increased over baseline: blood pressure and venous return will be compensated (equal) at best, initially, before dropping.

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WebW3b OP t1_iy9fy7n wrote

You’re correct but what I was asking/confused about in the post was about your first paragraph. I had trouble understanding how the vasoconstriction increases/keepsConstant preload (before getting overwhelmed)

It’s true that preload & BP ultimately decreases due to overwhelming blood loss, I just couldn’t comprehend the first part about how the body tries to maintain/increase the initial drop before the overwhelming fall

Your reply is immensely insightful and much appreciated!!

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shaokim t1_iy9jasw wrote

This great page shows factors affecting central venous pressure.

It isn't the arterial vasoconstriction that affects preload, but venous vasoconstriction, that would also occur in the compensation by sympathetic factors (such as circulating adrenaline).

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WebW3b OP t1_iyc4fxg wrote

This proves to be very useful, Lots of Thanks!

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Fellainis_Elbows t1_iy832rq wrote

Most of your total vasculature is in the peripheries / not in the great vessels.

Widespread vasoconstriction therefore preferentially forces blood away from the peripheries and towards the heart.

This results in increased preload.

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WebW3b OP t1_iy89npn wrote

I see, so vasoconstriction squeezes the blood cells that was initially unable to reach the heart due to low blood pressure and Thereby increasing preload?

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Fellainis_Elbows t1_iy8elyj wrote

Mostly right. The more technical explanation is that blood is squeezed from the arterial space into the venous space. Veins return blood to the heart -> therefore increased preload

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betterman74 t1_iy87x5t wrote

Turns a low pressure low volume system into a high pressure high volume system. Delivering more blood (preload) therefore hopefully (if EF preserved) increased cardiac output etc. I agree it's a bit tough sometimes to get it right in the head. Brings back days as a cardiothoracic jnr Dr.

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WebW3b OP t1_iy899cp wrote

Well yes but how does increasing blood pressure and vasoconstriction lead to increased preload? Isn’t it just receiving the same amount of blood?

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