Q.why inc VR,inc CO & dec TPR in shock? - USMLE Forums
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Old 08-27-2015
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Default Q.why inc VR,inc CO & dec TPR in shock?

Q. In distributive shock (septic/anaphylactic), why there is increased venous return ,increased CO & decreased TPR? In septic shock, there is systemic peripheral vasodilation which should decrease venous return and if venous return is decreased cardiac output will also decrease , this is how I think about the process. May be I am not relating the phenomenon systematically.Can anybody pls help me to organise these 3 parameters correctly.Thanks.(From FA 2014, pg.222, under pathology>inflammation>shock)
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Normally when we dialate the venous system the blood returning to the heart(venous return) decreases but here and I am quoting Sir Edward Goljan from his audio lectures,

In case of septic shock the arterioles dialate and the blood moves through them fast and the tissues are unable to use the o2 from this increased arterial blood flow! Since the circuit is dialating the resistance falls and the flow increases resulting into increased cardiac output and since venous dilation remains unchanged so venous return or blood returning to heart is not affected!

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Originally Posted by Aumsai View Post
Q. In distributive shock (septic/anaphylactic), why there is increased venous return ,increased CO & decreased TPR? In septic shock, there is systemic peripheral vasodilation which should decrease venous return and if venous return is decreased cardiac output will also decrease , this is how I think about the process. May be I am not relating the phenomenon systematically.Can anybody pls help me to organise these 3 parameters correctly.Thanks.(From FA 2014, pg.222, under pathology>inflammation>shock)

Decreasing the peripheral resistance increases flow downstream which will increase venous return and therefore CO. Also decreased TPR it will will be easier for the heart to pump as there is less resistance through the aorta.

CO = MAP/ TPR

basically q= p/r which means more resistance less flow inorder to maintain pressure.. On the other hand septic shock causes vasodilation = decreased resistance = more flow to heart.

Maybe someone else can explain better because i also have a few questions i dont understand

1. In hemorrage there is increased total peripheral resistance according to the co/ VR chart in fa : is that a compensation to maintain blood pressure?? But that will decrease CO
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Also aumsai: its when you constrict the veins you get increased venous return but if you constrict arterioles you are just decrease flow down stream.
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Hey! I find a contrasting information about this topic. FA2014,p.222 says there is increased venous return in septic shock while FA2015,p.297 says there is decreased preload (which is almost same as venous return, right?).Which one to follow?What do u think is more acceptable?

Next, I found it interesting to know what cleverfox mentioned from Goljan audio that septic shock only dilates arterial system and the venous system remains unchanged. I didn't find this fact anywhere when I was googling about septic shock.Most of the articles have simply mentioned that "septic shock causes massive vasodilation", and since they are not specifically mentioning venodiation or arterial dilation, I was thinking it dilates both venous and arterial system.BUT, there is twist in this story too when we compare this fact from Goljan with FA 2015 which on the contrary is mentioning Venous return/preload decreases in septic shock, not increases.

Now,the following is my explanation/understandig in response to the question of mk09. Yes, increased afterload causes decreased cardiac output which is not what we want in this condition.

I think the only way to get rid of this confusion is to interpret these parameters step-by-step.What happens 1st in hemorrhagic shock (dec. preload), what happens next (dec. cardiac output), and what happens as a result of dec CO (inc TPR, as a compensation to increase BP).But,like u said, increased TPR in turn contribute to dec CO .In this case, may be, body is more concerned in increasing BP to maintain perfusion to vital organs (by increasing TPR), rather than concerning about additional decrease in CO.

And, guys also pls think over what I mentioned about septic shock above and share your thoughts too.Thanks.
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I would request you to check Goljan Ed 4,Pg 124...

It clearly states the following for Septic Shock:

1>Increased CO(due to dilated arterioles,causing increased Venous return to right heart)
2>Decreased compliance of the Left Ventricle
3>Decreased Peripheral vascular resistance(dialation of arterioles)
4>Increased MVO2 since the tissues are unable to extract oxygen(mixed venous O2 content)

So FA2015 is wrong if it mentions that! I trust Goljan more
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ok, I will see goljan.
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These types of opposite explanations really creates chaos.If we analyse from their point of view, both explanations seems to be logical and correct. But, still we can choose more authentic one (here, I too like to prefer Goljan).
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Here is another explanation, which says that there can be both increase or decrease in preload depending on the stage of septic shock.Have a look.



initial phase. endotoxins cause large scale vasodilatation(arteriolar), leading to initial FALL IN PRELOAD>>>>>compensatory INCREASE cardiac contractility and stroke volume>>>>>>AFTERLOAD maintained.

Intermediate phase has INCREASE volume of vascular compartment(normal response to any shock)>>>>>preload normal>>>>cardiac contraction and SV tries to normalize(doesnt last too long in septic shock)>>>>after load normal.

Later phase....in septic shock>>>myocard depress factors leaked into circulation and suppresses cardiac contractility and compromises both SV and rate>>>> relative increase in preload and afterload increases due to the action of endotoxins on arterioles.


From- http://www.prep4usmle.com/forum/thread/92023/
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