Cardiac and Vascular Function curve question

[GomerPyle]

Hey guys,

So on page 269 of first aid, there are the 3 graphs. The third graph shows how an increase in TPR causes a decreased CO (makes sense as you're increasing afterload) and then a decrease in venous return (which makes sense as you're constricting the arterioles and there's less blood flowing through to the veins to get to the heart).

Now it says this happens because of vasopressors (epinephrine, norepinephrine, etc). I thought these drugs increase venous return to the heart by constricting veins...but according to this, vasopressors decrease the venous return. Can someone please clarify this for me?

I appreciate it, thanks!

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[zhopv10]

Now you are probably right in the short term but these curves are kind of an "averaged" look of what is going on. So ya if you have a vasopressor you would increase return in the short term but the idea here is that TPR is mostly influenced by the arterioles. So you constrict those then conceptually you could have less blood getting to the veins, since it is restricted and blood is getting held in the arterioles, thereby decreasing venous return. Likewise, vasodilating you get increased venous return. All this is exactly what you said, basically the answer lies I believe in the overall averaged picture. Yes you will increase the construction at the veins but you will increase it at the arterioles more so the relationship still holds after equilibration. Hope that makes sense. Guyton has great explanations for these curves and the experimental process behind them and costanzo has an ok explanation of them.


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[zhopv10]

I should note, so guyton derived these curves from experiments that were looking at the relationship of cardiac regulation, i.e do the tissues or the heart regulate CO? These are the culmination of a series of experiments showing how that system is integrated. The model was thought of basically as a high pressure low compliance artery side, capillaries and then low pressure high capacity side (veins) and a pump running them. The calculations are based on series circuit/ohms law and so the model is pretty simplistic, as such I find it good when looking at these graphs to not think too much about nuance and just general principle. In reality it's more nuanced for example an increase in TPR would have a decrease in CO which would actually decrease RAP and at the same time it would decrease venous return which would decrease RAP and the actual magnitude of those could be variable in real life but for the graphs it shows an averaged compromised position (I.e CO Is decreased to the same degree that venous return is and this RAP stays the same). Anyway hope that helps a little bit, these charts are really fairly complex in their derivation so if there's confusion the constanzo or guyton stuff is pretty clear and makes for a quick read.


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[zhopv10]

*edit: shortened better concept behind curves. Guyton was showing that CO was dependent on venous return. Also the RAP is on the x-axis because it can help predict either CO or venous return (increasing RAP decreased venous return and increases cadiac output). So you can look at the interaction between the two given a RAP (the intersection of the CO and venous return curve represents the true value for the situations of the CO, venous return and RAP. ). That is the idea behind the curves which can help frame it.


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[Entadus]

Hey guys,

So on page 269 of first aid, there are the 3 graphs. The third graph shows how an increase in TPR causes a decreased CO (makes sense as you're increasing afterload) and then a decrease in venous return (which makes sense as you're constricting the arterioles and there's less blood flowing through to the veins to get to the heart).

Now it says this happens because of vasopressors (epinephrine, norepinephrine, etc). I thought these drugs increase venous return to the heart by constricting veins...but according to this, vasopressors decrease the venous return. Can someone please clarify this for me?

I appreciate it, thanks!

Pressors are primarily effective on the Arterial side. Remember your sympathetic Adrenergic receptor types: Alpha 1 (constriction) > Alpha 2 >> Beta 2 (vasodilation)

From a pharmacology standpoint, the primary effect of Epi or other "pressors" will be in the arteriOles, increasing afterload... but there will be little effect on the veins.

From a physio standpoint, remember that most of the variation in peripheral vascular resistance comes from the arterioles, which provide fine control of the perfusion of organs and tissues.

For drugs affecting veins, you'd be thinking more about vasodilators like Nitrites/NO, along with Ca++ channel blockers like Nifedipine.