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
In: 1
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.
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.
I’m not sure if your premise is correct. In hypovolemic shock, central venous pressure (which I think is a [useful proxy](https://www.medintensiva.org/en-why-should-we-continue-measuring-articulo-S2173572717301777) 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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