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- Jan 12, 2015
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Hi!
I'm finding myself stuck on page 275 of (2017) First Aid and can't seem to get past it.
The cardiac and vascular function curve for TPR makes sense to me, in the sense that increased TPR (caused by vasopressors that have a1 adrenergic activity) will ultimately lower venous return. I understand that this is because sympathetic activity is more pronounced in arterioles than in veins, and therefore you have blood essentially stuck on the arterial side of the circulation.
I also understand why increase *venous* tone will increase your venous return, because you are constricting your veins and moving the blood back to the heart.
My question is about "sympathetic activity." Page 275 on FA says that sympathetic activity will increase venous tone.
How can vasopressors (NE, phenylephrine, a1 agonists) increase your TPR to the extent that you get a decrease in venous return and CO, but "sympathetic activity" increases your venous tone so that you get an increase in venous return and CO? I generally understand vasopressors=sympathetic activity, so I'm having trouble understanding how the outcomes are different. Epinephrine preferentially vasodilates--does it have to do with an endogenous norepi-epi combo attenuating the a1 sky-high TPR effect on arterioles so that venous tone can increase CO?
Any help is very appreciated.
I'm finding myself stuck on page 275 of (2017) First Aid and can't seem to get past it.
The cardiac and vascular function curve for TPR makes sense to me, in the sense that increased TPR (caused by vasopressors that have a1 adrenergic activity) will ultimately lower venous return. I understand that this is because sympathetic activity is more pronounced in arterioles than in veins, and therefore you have blood essentially stuck on the arterial side of the circulation.
I also understand why increase *venous* tone will increase your venous return, because you are constricting your veins and moving the blood back to the heart.
My question is about "sympathetic activity." Page 275 on FA says that sympathetic activity will increase venous tone.
How can vasopressors (NE, phenylephrine, a1 agonists) increase your TPR to the extent that you get a decrease in venous return and CO, but "sympathetic activity" increases your venous tone so that you get an increase in venous return and CO? I generally understand vasopressors=sympathetic activity, so I'm having trouble understanding how the outcomes are different. Epinephrine preferentially vasodilates--does it have to do with an endogenous norepi-epi combo attenuating the a1 sky-high TPR effect on arterioles so that venous tone can increase CO?
Any help is very appreciated.
