Shock Macro and Micro-circulation: Piecing things together. (Part 1) #FOAMed, #FOAMcc

 

So I have really, really enjoyed the discussions I had with these bright people on shock circulation:

Segun Olusanya (@iceman_ex) Resus Track 2

Rory Spiegel (@EMnerd) Resus Track 3

Korbin Haycock (tell him to get on twitter) Resus Track 4

Jon Emile (@heart-lung)  Resus Track 5

 

Some take home points so far:

I think that more questions than answers truthfully came out of this, and that is really the best part. But lets see what the common agreed upon thoughts were:

a. the relationship between the MAP and tissue perfusion it quite complex, and definitely not linear. So scrap that idea that more MAP is more perfusion. Could be more, same, or less…

b. you can definitely over-vasoconstrict with vasopressors such that a increasing MAP, at some point, can decrease tissue perfusion. Clinically, we have all seen this.

c. no matter what you are doing theorizing about physiology and resuscitation, THE MOST IMPORTANT IS TO CONTROL THE SOURCE!

 

Some of the interesting possibilities:

a. Korbin sometimes sees decreasing renal resistive indices with resuscitation, particularly with the addition of vasopressin.

b. the Pmsa – can this be used to assess our stressed volume and affect our fluid/vasopressor balance?

c. trending the end-diastolic velocity as a surrogate for the Pcc and trending the effect of hemodynamic interventions on tissue perfusion.

This stuff is fascinating, as we have essentially no bedside ability to track and measure perfusion at the tissue level. This is definitely a space to watch, and we’ll be digging further into this topic.

 

Jon-Emile added a really good clinical breakdown:

I think one way to think of it is by an example. Imagine 3 patient’s MAPs are 55 mmHg. You start or increase the norepi dose. You could have three different responses as you interrogate the renal artery with quantitative Doppler:

patient 1: MAP increases to 65 mmHg, and renal artery end-diastolic velocity drops from 30 cm/s to 15 cm/s
patient 2: MAP increases to 65 mmHg and renal artery end-diastolic velocity remains unchanged.
patient 3: MAP increases to 65 mmHg and renal artery EDV rises from 10 cm/s to 25 cm/s

in the first situation, you are probably raising the critical closing pressure [i know i kept saying collapse in the recording] relative to the MAP. the pressure gradient falls and therefore velocity falls at end diastole. one would also expect flow to fall in this case, if you did VTI and calculated area of renal artery. in this situation you are raising arteriolar pressure, but primarily by constriction of downstream vessels and perfusion may be impaired. ***the effects on GFR are complicated and would depend on relative afferent versus efferent constriction***

in the second situation, you have raised MAP, and probably not changed the closing pressure because the velocity at the end of diastole is the same. if you look at figure 2 in the paper linked to above, you can see that increasing *flow* to the arterioles will increase MAP relative to the Pcc [closing pressure]. the increase in flow raises the volume of the arteriole which [as a function of arteriolar compliance] increases the pressure without changing the downstream resistance. increasing flow could be from beta-effects on the heart, or increased venous return from NE effects on the venous side activating the starling mechanism. another mechanism to increase flow and therefore arteriolar pressure relative to the closing pressure is the provision of IV fluids.

in the third situation, MAP rises, and EDV rises which suggests that the closing pressure has also fallen – thus the gradient from MAP to closing pressure rises throughout the cycle. how might this happen? its possible that raising the MAP decreases stimulus for renin release in afferent arteriole, less renin leads to less angiotensin and less efferent constriction. thus, paradoxically, the closing pressure falls with NE! another possibility is opening shunts between afferent and efferent arterioles [per Bellomo]. as above ***the effects on GFR are complicated and would depend on relative afferent versus efferent resistance changes***

 

This is really, really interesting stuff. So in theory, the MAP-Pcc gradient would be proportional to flow, so if we can estimate the direction of this gradient in response to our interventions, we may be able to decrease iatrogenism. I’ll have to discuss with Jon and Korbin which arterial level we should be ideally interrogating…

More to come, and next up will be Josh Farkas (@Pulmcrit), and I’m sure anyone following this discussion is looking forward to what he has to say. I know I am.

cheers!

 

Philippe

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