Shock, perfusion, and systemic vascular pressure

[Daitong]

Thanks for all the help, but here's a quickie:

So I understand that shock is decreased perfusion to the tissues, and this could be caused by vessel dilation, but I'm a bit confused to how the blood vessels respond.

I've read that blood vessels will constrict to increase perfusion, but that also seems counterintuitive since increased SVR would seem like it would decrease perfusion, since the blood vessels are now smaller...

Can someone reconcile the principles of SVR and shock?

Best,

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[DrPicard]

The body will respond to shock with a catecholamine surge, which causes

1. An increase in SVR/TPR, and
2. An increase in the rate and contractility of the heart

Since flow (Q) = P1-P2/R, you're correct in thinking an increase in resistance should decrease organ flow. Except the increase in R isn't uniform across the body, since some areas are auto-regulated and spared the constricting effect of catecholamines. We're talking primarily about the coronary and cerebral circulations. The heart, in overdrive from the catecholamines, is now pumping blood into a body where some areas are vasoconstricted and others aren't. This starts sending blood preferentially down the path of least resistance, ie the coronary and the cerebral circulations. Hence, blood flow to these vital areas is maintained at the cost of decreased blood flow to other areas of the body. The widespread vasoconstriction in the body serves to help maintain the MAP and hence the perfusion pressure for these vital areas.

 

[Daitong]

The body will respond to shock with a catecholamine surge, which causes

1. An increase in SVR/TPR, and
2. An increase in the rate and contractility of the heart

Since flow (Q) = P1-P2/R, you're correct in thinking an increase in resistance should decrease organ flow. Except the increase in R isn't uniform across the body, since some areas are auto-regulated and spared the constricting effect of catecholamines. We're talking primarily about the coronary and cerebral circulations. The heart, in overdrive from the catecholamines, is now pumping blood into a body where some areas are vasoconstricted and others aren't. This starts sending blood preferentially down the path of least resistance, ie the coronary and the cerebral circulations. Hence, blood flow to these vital areas is maintained at the cost of decreased blood flow to other areas of the body. The widespread vasoconstriction in the body serves to help maintain the MAP and hence the perfusion pressure for these vital areas.

Thanks- is this why that increased SVR leads to hypoperfusion of all non-essential organs and is part of the cause of MODS?

 

[DrPicard]

Don't know a lot about that, but hypoperfusion does play a role. But there can be other reasons as well (such as pro-inflammatory cytokines and DIC in septic shock).

 

[worldbeater]

So if you want a time breakdown of how the body responds to shock or any "low volume state", it would be as follows:

0-2 seconds is your carotid reflex - decreased cardiac output goes to carotid, decreases carotid stretch, decreases firing of CN 9, which goes to medulla (nucleus tractus solitarius), decrease firing of CN 10, which goes back to SA node --> the heart rate increases by reflex

2 seconds - 20 min is norepinephrine release from adrenal medulla: increases HR, further alpha 1 veno-vasoconstriction to increase TPR, also increases vasocontriction, which increases TPR further

>20 min (renin from JG apparatus) - JG apparatus recognizes low RBF, renin is released. Renin does its renin-angiotensin-aldosterone pathway buisness. 1 molecule of aldosterone is similar to sodium, pulling in 3 molecules of water, into the vasculature.

Your body has these 3 mechanisms to decrease TPR.

 

[Instatewaiter]

Thanks for all the help, but here's a quickie:

So I understand that shock is decreased perfusion to the tissues, and this could be caused by vessel dilation, but I'm a bit confused to how the blood vessels respond.

I've read that blood vessels will constrict to increase perfusion, but that also seems counterintuitive since increased SVR would seem like it would decrease perfusion, since the blood vessels are now smaller...

Can someone reconcile the principles of SVR and shock?

Best,

Depends on the type of shock:
Septic- The shock cause is due to the vessels being dilated. SVR is low. So despite the vessel trying to constrict it cannot because of the LPS or whatever from the infection. Your cardiac output increases in response but your perfusion pressure remains low because your SVR is so low

Cardiogenic- the root cause is that your cardiac output is too low. In response your SVR increases. Perfusion remains low for a few reasons,- one because the cardiac output cannot increase enough and two because of differential vasoconstriction.

Hypovolemic- you don't have enough fluid to fill the vessels. Your cardiac output drops because venous return is too low to adequately pre-load the heart. In response your SVR rises.

 

[Daitong]

So if you want a time breakdown of how the body responds to shock or any "low volume state", it would be as follows:

0-2 seconds is your carotid reflex - decreased cardiac output goes to carotid, decreases carotid stretch, decreases firing of CN 9, which goes to medulla (nucleus tractus solitarius), decrease firing of CN 10, which goes back to SA node --> the heart rate increases by reflex

2 seconds - 20 min is norepinephrine release from adrenal medulla: increases HR, further alpha 1 veno-vasoconstriction to increase TPR, also increases vasocontriction, which increases TPR further

>20 min (renin from JG apparatus) - JG apparatus recognizes low RBF, renin is released. Renin does its renin-angiotensin-aldosterone pathway buisness. 1 molecule of aldosterone is similar to sodium, pulling in 3 molecules of water, into the vasculature.

Your body has these 3 mechanisms to decrease TPR.

You meant *increase TPR* in your last line right? And the reason for this is to increase BP/MAP by the equation MAP=CO*SVR (SVR~TPR)?

 

[worldbeater]

You meant *increase TPR* in your last line right? And the reason for this is to increase BP/MAP by the equation MAP=CO*SVR (SVR~TPR)?

Yeah, correct, all 3 mechanisms are used to increase TPR at the various timeframes. Haha I wrote out the entire thought process and screwed up the summary. That equation makes sense, there is a page in the PASS Notes that has 3 equations, including this one, and explains everything nicely but I can't find it.

 

[Daitong]

Yeah, correct, all 3 mechanisms are used to increase TPR at the various timeframes. Haha I wrote out the entire thought process and screwed up the summary. That equation makes sense, there is a page in the PASS Notes that has 3 equations, including this one, and explains everything nicely but I can't find it.

Thanks!


What are PASS notes btw?

 

[worldbeater]

It's the lecture notes for The PASS Program, author is Dr. Francis Ihejirika. He is a retired attending who has a background in IM/Peds, trained residents, and also was a Pathology professor. The program is kind of underground, not many people know about it. It's been around for 20 years, but the notes in a textbook form just came out a couple years ago. I like his material because he teaches the very fundamentals of medicine and then works his way upwards to explain the clues and concepts for each individual UWorld question. It makes you understand how certain diseases work/why there are specific protocols in a hospital as opposed to memorizing everything..and the high yield stuff you do have to memorize is embedded in the notes multiple times so you keep getting refreshed.

It's a pre-official 1st edition copy though, so there are some spelling errors here and there. I think you can get it from Amazon and if you want the corresponding audio/video lectures you can get it from their site.