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Discussion Starter · #1 ·
FA says decrease in contractility in hemorrhage (p-282 2012 edition) while kaplan says increase in contractility in hemorrhage due to reflex sympathetic (p-76 kaplan green physio). Which one is correct??
 

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Hemorrhage would lead to decrease in blood volume and therefore venous return. Both of these would lead to hypotension (decreased TPR) and a reflex increase in HR. That's my understanding of it.
 

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Discussion Starter · #3 ·
Hemorrhage would lead to decrease in blood volume and therefore venous return. Both of these would lead to hypotension (decreased TPR) and a reflex increase in HR. That's my understanding of it.
In hemorrhage TPR increases (not decreases) due to reflex sympathetic nervous system.
And at one place on net i saw that increased TPR decreases heart contractility. Don't know how.
 

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In hemorrhage TPR increases (not decreases) due to reflex sympathetic nervous system.
And at one place on net i saw that increased TPR decreases heart contractility. Don't know how.
Yes you're right .. it increases TPR.

PNS is decreased and SNS is increased. I think that's why the HR increases.

Although when TPR is increased, it causes reflex decrease in HR.

Not sure.
 

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FA says decrease in contractility in hemorrhage (p-282 2012 edition) while kaplan says increase in contractility in hemorrhage due to reflex sympathetic (p-76 kaplan green physio). Which one is correct??
hemorrhage > decreased BP > reflex tachycardia and systemic vasoconstriction > restores BP.

So increased contractility after hemorrage makes sense to me.

my FA (2011 edition) doesnt say anything about contractility decreasing in hemorrhage.
 

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Discussion Starter · #6 ·
hemorrhage > decreased BP > reflex tachycardia and systemic vasoconstriction > restores BP.

So increased contractility after hemorrage makes sense to me.

my FA (2011 edition) doesnt say anything about contractility decreasing in hemorrhage.
Its there. Just see in the cardiac and vascular function curve. No 3 is hemorrhage. And the reason is increase in TPR. I don't understand the mechanism.
 

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Its there. Just see in the cardiac and vascular function curve. No 3 is hemorrhage. And the reason is increase in TPR. I don't understand the mechanism.
yes, it says increased TPR, not decreased contractility.
increased TPR is the reflex action.
baroreceptors notice the decreased BP and that causes decreased firing to the ummm medulla(?), which causes less PSNS firing and more SNS firing.
This results in an increased HR and contractility and vasoconstriction of the vessels, which means increased TPR.

look under the section named "maintenance of mean arterial pressure", and it describes this feedback loop.

however, your original comment said decreased contractility, which makes no sense and i dont know where you are seeing that.
But just now you said increased TPR, which makes perfect sense and is the way it is because of what I descrived above.
 

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Discussion Starter · #8 ·
yes, it says increased TPR, not decreased contractility.
increased TPR is the reflex action.
baroreceptors notice the decreased BP and that causes decreased firing to the ummm medulla(?), which causes less PSNS firing and more SNS firing.
This results in an increased HR and contractility and vasoconstriction of the vessels, which means increased TPR.

look under the section named "maintenance of mean arterial pressure", and it describes this feedback loop.

however, your original comment said decreased contractility, which makes no sense and i dont know where you are seeing that.
But just now you said increased TPR, which makes perfect sense and is the way it is because of what I descrived above.
http://www.usmle-forums.com/usmle-s...iac-output-venous-return-curves-question.html

see in that post. both decrease in contractility and venous return occur with increased TPR.
 

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http://www.usmle-forums.com/usmle-s...iac-output-venous-return-curves-question.html

see in that post. both decrease in contractility and venous return occur with increased TPR.
I think you are NOT talking in the same page here ,however , I really got benefit from this conversation.
this post talking about the effect of hemorrhage on contractility , and it make sense that hemorrhage cause inc. in contractility due to inc. in sympathatic ref. and in turn increase in catecholamine and contractilityand aslo venous constriction (inc. preload) and inc. in TPR ( increase afterload) ---> return BP to normal. THE ^ in TPR here is in case of heamorrhage not a close system.

in the other post that talking about increase on TPR in close system on contractility, which cause derrease in contractilty and that make sense cause the heart will pump against high blood pressure and lead to decrease in contractility .
anyway , I was looking for answers for this difficult graf and now have some idea about it :D
 

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To my knowledge if u hemorrhage you will decrease preload ( by reducing volume --> Reduces MSFP --> Reduces Preload ) Reduced Preload leads to reduced CO , the BP sensors in carotid see it --> Increase sympathetic tone
--> Increase contractility and vaso/venoconstriction --> Gets preload towards normal and Increase contractility --> Kinda normal CO and increased TPR from vasoconstriction ---> BP gets normal/maintained until you lose enough volume to decompensate--> Hypovolemic shock--> Death

Increased HR is also a result of sympathetic tone and just helps a little with CO
 
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