Why does Blood pressure important in low TPR?

[AlexBest96]

This is the example: we have vasodilation (decrease TPR) in septic shock, the MAP will decrease despite of CO will increase (MAP=TPR*CO). So, we have high perfusion of tissues, because of arteriolodilation. So what is the problem? Why if we have decreased pressure (due to decreased TPR) it will cause problems like: syncope, low perfusion of tissues and etc? I really want to UNDERSTAND the importance of blood pressure in this situation (in the cases of low TPR=>high CO, low MAP). This my thought: if MAP decreases (despite we have high CO and so we have high EQUAL Flow(Q) in all system it will be less pressure in aorta and in some vessels of tissues (brain) that haven't vasodilate will come less blood, because all the flow everytime go to vasodilated arterioles, so some tissues overperfused, i.e. that tissue that was vasodilated, and some not, because even the CO (flow Q) is high it will all go to the regions with low TPR, thus pressure GRADIENT will be not enough to maintain the perfusion (in the brain for example, or some others) ..??????) What the main concept is here? I really kind of exhausted then I am thinking about it. Thanks for answer!

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[donovank730]

Your body tightly regulates pressure by opening and closing arterioles as needed. You have a set amount of blood in your body obviously, so if you were to suddenly dilate every arteriole in your body, you would have a massive decrease in blood pressure.

Think about a dam, a dam slowly lets water through and therefor there is a large pressure gradient between the two sides. If you were to suddenly open every channel in the dam, you would quickly drain all the water from the dammed side and the pressure and flow would be equalized.

I think the main principal you need to grasp is that the septic vasodialation causes all the pressure/energy stored up in your blood vessels to be released suddenly, and that your body under normal conditions would never let that many arterioles dilate at once.

 

[cbrons]

You need a certain MAP to maintain organ perfusion.

There is also the fact that septic shock often causes a not insignificant amount of capillary leak and microvascular damage. Hence why half of septic patients are not responsive to IV fluids at all

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[takeurmeds02]

There is also the fact that septic shock often causes a not insignificant amount of capillary leak and microvascular damage. Hence why half of septic patients are not responsive to IV fluids at all
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Above is what's described as "third spacing." Google it, know it, love it. Basically, Because your body is in a global inflammatory state with increased cytokine action, you have robust vasodilation and permeability. Now protein are able to fall into the interstitial space from systemic circulation and with that brings fluid to maintain osmolality. You then become hypovolemic. This decreases overall resistance and perfusion to tissues.

 

[Levo]

I think all of the answers here are great! The mildly hand-wavey explanation for this question that I got when I first asked a resident about it was that given a fixed blood volume, there needs to be some degree of vascular tone to make sure that blood is preferentially routed to the tissues that have the highest demand and the highest "priority," like the brain and kidneys. The inflammatory processes in sepsis causes maximal vasodilation in all tissues regardless of their metabolic demands, so tissues that can get by with less blood, like skin and inactive skeletal muscles, receive more of the blood supply at the expense of "hungrier" tissues like the brain and kidneys. It's a miss-allocation of resources. That's why MVO2 goes up in septic shock, more oxygenated blood goes to tissues with lower O2 demands, so less O2 is extracted.

 

[mppcc]

You need a certain MAP to maintain organ perfusion.

There is also the fact that septic shock often causes a not insignificant amount of capillary leak and microvascular damage. Hence why half of septic patients are not responsive to IV fluids at all

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What can be even more interesting is asking the question of what responsive to ivf means. Often individuals use CO as a measure of response. However if CO increases without map by definition svr has to decrease which is the base hemodynamics issue in sepsis. So should responsive mean that a patient has a reduced svr? There is very little solid evidence based medicine studying the effect of fluid administration in sepsis. PROSPECT was intriguing as the ivf protocol group had similar mortality with increase renal failed as compared to standard care.
The more I look at this question the more I ponder how many people really are "fluid responders".

 

[CherryRedDracul]

Piggybacking onto the "fluid responsiveness" discussion, I was perusing through EMCrit and found out Dr. Paul Marik has a Youtube channel. He's put out a video on fluids in critical care.

Fair Warning: this is beyond what med school teaches and this area of research is still contentious. Marik is considered a maverick physician of sorts, flying in the face of the Surviving Sepsis Campaign.