The First Steps Towards Physiological Resuscitation: A Team Effort. #FOAMed, #FOAMcc

(original figure from this old post)

So Rory (@EMnerd) hit us last week with an interesting question that was brought up by David Gordon, a resus fellow working with him, and thought some of us may be willing to belabour his point. A lengthy and really fascinating exchange ensued, which I felt was worth sharing with the #FOAMed community:

 

Rory (Spiegel @EMnerd) find him on emcrit.org

Korbin Haycock (please leave comments to encourage him to get on Twitter)

Segun (Olusanya @iceman_ex) find him on LITFL.com and The Bottom Line

Me (@ThinkingCC) also thinkingcriticalcare.com

David Gordon

My editorial comments!

 

Rory: 

David brought up an interesting question today. Why not do a straight leg raise and use TAPSE to assess the likelihood the pt will be “volume responsive”?

My answer was the following:
“I don’t think the RV increases TAPSE in response to fluid and so the only way TAPSE would be able to assess fluid responsiveness would be if it decreased in response to a a SLR. My contention is this would be a late marker of fluid intolerance and others signs of venous congestion (portal/renal vein doppler) would be seen far earlier. “
In addition I brought up that “volume responsiveness” is a flawed surrogate and we should rather be focusing on volume tolerance.
And that is, in my opinion, the critical concept. 
Anyway David seemed less than satisfied with my answers so I figured I would open the discussion to you physiology nerds…
Korbin: 
That’s an interesting thought, you have brought up.  To clarify, are you asserting that an increase in TAPSE from a volume challenge or SLR could be a indicator of volume responsiveness?  If I missed your meaning, please correct me.
I think Rory is right in his assessment that TAPSE would likely be a more valuable indicator of fluid tolerance (or more importantly , intolerance), rather than fluid responsiveness.  TAPSE, however,  may be (I don’t know) a more sensitive indicator of fluid tolerance than things like IVC collapsibility index, etc.  This might make sense as a decreasing TAPSE (or TAPSV, too for that matter) in response to a fluid challenge might be an earlier indicator that the RV won’t do much with more fluids before it would manifest in things like a non-collapsing, plethoric IVC, decreasing S’/D’ wave ratio on HVD, portal vein pulsitivity, or pulsatile intrarenal venous Doppler.
One problem I’ve had for a long time with fluid responsiveness from the standpoint of the circulation up to the pulmonary valve (IVC collapsibility index being the most common example), is that it doesn’t measure what you really want to know, and that is LV fluid responsiveness.  There is a whole lot going on hemodynamically from when blood leaves the RV to where it finally contributes to LV preload.  I think if you want to know if the patient is fluid responsive, there are quite a few ways to assess this directly, rather than looking at the RV, IVC, etc.
I stopped chasing every bit of volume responsiveness a long time ago, however it does have its place in managing the sick patient, I think.  Usually, my first question is about volume tolerance/intolerance, before I start to think about volume responsiveness.
To investigate the fluid tolerance/intolerance status, I’ll look into a lot of things, usually using a lot of ECHO/US information.  My sonographic considerations are: LV contractility, diastolic function and ventricular compliance, LVEDP, valve pathology, SVR, B-lines (and if B-lines are present, put that into the context of what the LVEDP is because if the pressures are low, but the lungs are wet, pulmonary vascular permeability is high and I’ll think very hard before giving fluids), pulmonary artery pressures, PVR, interventricular septal shifts, RV contractility, IVC, HVD, portal vein, and renal Doppler.
(has anyone ever seen an ED doc do this anywhere??? Wow!!!)
Also, I’m lucky to have some other tools at my place like transpulmonary thermodilution catheters and pulse wave analysis devices to assess things as well.  Sometimes these things make serial assessments more convenient than dragging the US machine over multiple times, and can also give additional information, like EVLW, PVPI, etc.
(I think in the case of Korbin’s hospital, it may be important to bring downstairs care upstairs!)
Secondarily, if I think the patient is volume tolerant and then I have determined that they are volume responsive, and would benefit from volume administration, the next question I ask myself is what’s the best way to do this.
Clinical assessment combined with ECHO comes into play, as if the patient is genuinely volume depleted, volume repletion makes sense.  However, a lot of volume responsiveness is driven by syndromes of high CO and low SVR.  In these cases, I usually give very little volume and opt for a vasopressor to drive venous return instead.  This strategy tends to correct the CO/SVR derangement as well as take care of the volume responsiveness at the same time.  I feel much better if I know that my MAP is being generated by a balanced CO, SVR, and volume status rather than having a “normal” MAP.
I think that is a really, really important cognitive model. The common and traditional approach is to try to maximize CO with fluids and avoid the terrible vasopressors. In a disease where the primary derangement is vasodilatory, it doesn’t seem logical… However finding the right balance is difficult. And with the near-extinction of the PA catheter, we no longer have a low SVR value staring us in the face begging for some pressors.
Sorry to be so long winded, guys.  Hope I didn’t bore you with stuff I’m sure you already know.  These topics are really interesting to me though!  I’d be interested in all of your thoughts on the TAPSE question.
Segun:
I think the RV is more likely to dilate in response to Fluid than change TAPSE, as suggested by a paper or two on RVEDA changes as a predictor of Fluid responsiveness https://ccforum.biomedcentral.com/articles/10.1186/cc3503
(RV dilatation May result in a reduction in TAPSE too?) 
Potentially, yes. SV may not decrease but TAPSE may.
The end result should be a change in stroke volume, so one could argue that rather than TAPSE you could just measure RVOT VTI in response to a passive leg raise. (I don’t really see the difference between M mode and PW doppler, and RVOT VTI is simple enough to measure from a PSAX or RV outflow view)
TAPSE is an Uber-simplified method of looking at RV contractilty rather than volume (overloaded RVs can have excellent TAPSE, for instance). I think it would answer a very different question.
Me:
Interesting question indeed. I can’t agree more with Rory and Korbin. Korbin’s clinical run-through is, as far as I’m concerned, completely on point and, if i weren’t so lazy, and had all the hardware he is fortunate to have, would consider as gold a standard as possible, until  mitochondrial monitoring and trans-capillary flow monitor technology is made.
I think it requires a bit of a paradigm shift away from volume responsiveness, that has been all the rage in the last decade or since the end of the swan age, and instead towards focusing on tolerance. There is significant and building evidence that congestion is end-organ damaging, and evidence that chasing maximal CO is mortality-causing (80’s and 90’s literature supranormal o2 delivery and all that), hence on both fronts focusing on congestion makes more sense.
I think we have to follow the fluid path (venous congestion y/n, rv ok y/n, lungs ok y/n and finally lv ok y/n) and then do a global almost holistic ‘is fluid the best option’ reflection including brain, gut, kidneys, peripheral tissues, etc, with Korbin’s nice little twist on balance of CO, SVR for the BP/perfusion. I don’t think there’s any point of care monitoring tool to unequivocally ascertain the best level of each today.
Rory:
So here is my question, should we be asking “Is this pt likely to benefit from fluids?” rather than “Is this pt likely to augment their CO with fluids?” 
Stop for a moment and think of most of your septic patients (not all, yes, some have cardiomyopathy, some are profoundly hypovolemic), are they actually in a low CO state?  The near-obsession with CO is probably rooted in the common belief that the elevated lactate stems from hypoperfusion, a myth which has been debunked.

Lets say we use Korbin’s gold standard I think we still have to ask what is the benefits of giving this pt fluids? There are many patients I see who would meet all the criteria outlined by Korbin in whom I still don’t administer fluids because whatever increase in cardiac output I get will be transient at best. I am inclined to sit tight allow my antibiotics to take effect and let the pt correct their own vasoplegia. After an initial small aliquot of fluid in the ED I like to see obvious signs of hypovolemia before I give additional boluses. I do like the CLASSIC trials criteria:

(1) Lactate of at least 4 mmol/L
(2) MAP below 50 mmHg in spite of the infusion of norepinephrine
(3) Mottling beyond the edge of the kneecap (mottling score greater than 2)

(4) Oliguria 

All this from the perspective of a decongested venous system and a under-filled heart on US
Korbin:
To Rory’s point, I agree that just because there is a lack of fluid intolerance and the presence of fluid responsiveness, it doesn’t necessarily mean fluids are indicated.
If I have a clinical story that supports a likely lack of hydration plus I’m looking at a high SVR, low CO, and a low SV, I will usually give some fluids.  Mottling, especially if pressors are on board, to me is a clue that some sort of volume might be indicated.
That’s actually quite interesting.  The pathophysiology of mottling isn’t clear (click here for an interesting read), but definitely a space to earmark, when trying to find the optimal balance between vasopressors and CO augmentation.
As far as the lactate goes, as everyone here knows, there’s a whole lot of reasons to have a hyperlactatemia.  It’s drives me a little crazy when I see a lactate come back elevated and the first thing someone wants to do is give fluids, especially if they haven’t considered any of the stuff we’ve been talking about.
I think if you have a patient with a high lactate, the first thing to do is ask yourself why they have a high lactate, rather than trying to correct the number.
Rory:
Agreed, most of the time in a septic pt I view a rising lactate as a sign I don’t have source control rather than a signal to give additional fluids.
Philippe:
So in terms of fine tuning, here is one thing I like to do with tissue saturation – SctO2 (cerebral)  and peripheral:   if it drops with vasopressors I favor augmenting CO (fluids if not too congested, inotropes to consider) if it rises or stays flat with pressors i stay the course. This is definitely not evidence-based, but to me, if tissue saturation decreases while increasing vasopressor dose, it seems logical that the perfusion is dropping, and not a course worth pursuing. I like to think of it as an example of MBE (medicine-based evidence) in the patient in which it is occurring.
David:
It seems to me the feeling is that we shouldn’t be chasing any single indicator of fluid status/tolerance/response/optimization evaluation and the key is to ask the clinical questions and pair that with our sonographic assessment.   RV functional assessment may have a role in that discussion, but TAPSE may not be the best indicator as RVOT VTI may be a better answer to the initial question.
The study that Segun sent out seems to indicate that LVEDA may be a better predictor of SVI.  The septal interdependence plays a larger role than I initially thought and perhaps using M mode to look at changes in septal motion gives you more information about the ability of the heart as a whole to manage the fluids…
That’s an excellent point, because even if the RV can handle the fluid, if the LV cannot, it’s gonna end up in the lungs.
Philippe, what kind of time course do you allow for your lactate to change, other than just response to your initial resuscitation?
Lactate should improve over hours. As Rory says, if a day later it’s still hovering above 4, and you don’t have impaired hepatic clearance, you might be missing something…
Korbin:
That’s something that certainly something to consider, Rory.   I think a lactate that is suddenly rising is most likely driven by a catecholamine surge driven by something going the wrong way.  But not always.
The important thing is to stop and think about what’s going on.
Case in point:  Last week I had a patient that had cardiac arrest due to an asthma exacerbation.  I had put a TEE probe down during he resuscitation, and a little bit afterward based on what I was seeing on the TEE, I felt she needed a pressor.  I used epinephrine because the beta-2 agonism might help with bronchodilation.  Everything hemodynamically look pretty good, except the lactate came up.  The ICU resident saw the lactate and ordered a liter of LR.  I called them and explained that the epinephrine was likely the cause of the lactate and it probably wasn’t anything to worry about.
Rory:
Just the other day I was called to the floor to assess a pt because the treating team was concerned he was septic when his lactate came back at 6.5. I walked in the rm as they were hanging the 30cc/kg fluid bolus. A brief assessment revealed he was in florid CHF. Once I convinced them to stop giving fluids and instead use an aggressively dose of diuretics he did just fine and cleared his lactate without issue.

In my mind lactate in and of itself uninterruptible. In a pt who is otherwise improving and the lactate is not clearing as fast as I would like I tend to just stop checking it. The one I find troublesome is in the post resus pt who doesn’t look great, I don’t have an obvious source, their pressor requirements are slowly rising and the lactate is hovering in the 4-5 range. That’s the pt that tends to do poorly if you don’t identify and establish source control

Korbin:
Agree with that Rory.
If I have those patient with a persistent lactate elevation, and they look like they could be malnourished, I’ll give them some thiamine, too.
Segun:
My two cents- there’s data soon to be released that compared echocardiographic dimensions (RV/LVEDA, IVC etc) to mean systemic pressure- showing no correlation with ANY echocardiographic parameters.
It would seem that going purely by dimensions, you cannot predict volume state on echo… so at the moment we can detect hypERvolaemia with lung, portal vein, and renal vein POCUS (and to a degree IVC), and profound hypOvolaemia by looking at doppler patterns (although the patient is more likely to tell you).
The other side of things, which has been clearly elucidated by everyone in this thread, is the concept of “permissive responsiveness”. Ruthlessly thrashing every heart to its maximum myocardial stretch doesn’t necessarily seem to be the best idea, to my mind.
I agree with everyone’s thoughts. Beyond the initial LLS/Shocked AF stage, you need a very good reason to give a fluid bolus!
And don’t get me started on lactate…
Korbin
I would only comment that the magic of Doppler probably is far more valuable than cardiac dimensions when dealing with hemodynamics.  Dimensions give anatomic values that can be extrapolated to hemodynamics, but PW and CW Doppler interrogation infers pressure differentials, which can directly be applied to things like flow and resistance.  Tissue Doppler has the added informative value of cardiac compliance, so that a comprehensive picture can be painted in light of filling pressures and the relationship to preloading.
When I look at all this together, I really feel that in most cases, a quite accurate picture of what’s going on is within grasp.
To emphasize again, something like B-lines with a compliant, low LVEDP LV, tells me valuable information about pulmonary vascular permeability.  Tread carefully about fluids here.
David:

How does the RV respond to a fluid bolus?

To answer this question first we must understand the role of the right heart in the circulatory system. Often the right ventricle (RV) is compared to the left ventricle, in reality it serves an entirely different function. The left ventricle generates the necessary pressures required to maintain systemic perfusion. The right ventricle’s job is to enable venous return, which is generated by the gradient between the mean systemic filling pressure and the right atrial pressure (RAP). The role of the RV is to maximize that gradient by keeping the RAP as low possible. 

With this in mind let us examine the RV’s response to a fluid bolus. As the RV becomes filled, conformational changes occur within the RV that allow it to increase its stroke volume without increasing the distending pressure.Under normal circumstances, the RV end diastolic distending pressure does not increase in response to fluid loading. Therefore, if the RV is functioning appropriately, RAP does not accurately reflect RV preload. But in pathological states, when the RV is hypertrophied, diseased, or overdistended there is an inverse relationship between RVEDV and RV stroke volume. Any fluid, or increased RV pressure beyond this point results in an increase in RAP, decreasing venous return.1

1. Pinsky MR. The right ventricle: interaction with the pulmonary circulation. Critical care (London, England). 2016;20:266.

So that was the discussion. I certainly thought it was very interesting. Following this, we decided we’d band together and try to hammer out what we think should be the optimal management of shock, trying to tie in physiology, the scant evidence that is out there about resuscitation, and the pitfalls of venous congestion. Finding the sweet spot in the balance between vasopressors, inotropes and fluids is a very real challenge that all resuscitationists face regularly, and it is very unlikely that, given the complexity of such a protocol, looking at tolerance, responsiveness and perfusion, that an RCT would be done anytime soon.

We’ll be sure to share when we come to a consensus, but certainly the broad strokes can be seen here, and I’d love to hear anyone’s take on this!

And of course, we’ll definitely be discussing this further with smarter people at H&R2019 – think Jon-Emile Kenny (@heart_lung), Andre Denault and Sheldon Magder!

Cheers

Philippe

H&R2019! Final Programme. Register Now! Montreal, May 22-24, 2019! #HR2019

 

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Registration is open and we have said goodbye to the snail mail process. Fortunately, we are a lot more cutting edge in medicine than in non-medical technology.

We are really excited about this programme, and a lot of it comes from the energy and passion coming from the faculty, who are all really passionate about every topic we have come up with.

The hidden gem in this conference is the 4 x 40 minutes of meet the faculty time that is open to all. Personally I’ve always felt that I learn so much from the 5 minute discussions with these really awesome thinkers and innovators, so wanted to make it a priority that every participant should get to come up to someone and say ‘hey, I had this case, what would you have done?’   Don’t miss it!

Scientific Programme

Wednesday May 22 – PreCongress courses

NOTE DUE TO LIMITED SPACE AND UNTIL JANUARY 1ST REGISTRATION FOR THESE IS RESERVED FOR H&R2019 ATTENDEES, FOLLOWING WHICH REMAINING SPOTS WILL BE OPENED TO ALL-COMERS. H&R2019 REGISTRANTS SHOULD RECIEVE A CODE ENABLING REGISTRATION. FOR ANY QUESTIONS CONTACT HOSPRESUSCONFERENCE@GMAIL.COM.

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(for more details on these pre-conference courses please see here)

 

Thursday May 23 – Day 1

0800-0820 – Respiratory failure on the wards – MALLEMAT

0820-0840 – Phenotyping Cardiac Arrest – SPIEGEL

0840-0900 – Help! my patient is bleeding! AJJAMADA

0900-0920 – Perioperative basics. KAUD

0920-0940 – Advanced POCUS-based management of CHF – ROLA

0940-1020 – MEET THE FACULTY OPEN DISCUSSION

1020-1040 – Pharmacology Pearls – VINCENT

1040-1100 – Green Medicine: Can We Help Save the Planet? ZIGBY

1120-1140 – A Free Upgrade to your WBC: The NLR! FARKAS

Critical Care track

1240-1300 – pH-guided fluid resuscitation – FARKAS

1300-1320 – the Great EPI debate – SPIEGEL

1320-1340 – Revisiting CPR physiology: What do we know? – TERAN

1340-1400 – Cardiogenic Shock 2019 – OLUSANYA

1400-1420 – Late Breaker TBA – MALLEMAT

1420-1440 –  Intra-Arrest Hemodynamics: One Size Doesn’t Fit All – TERAN

Hospitalist track

1240-1310 EKG Pearls – MULLIE

1310-1330 Nutrition in the Hospitalized Patient – RUBINO

1330-1400 The Best Neuro Exam Ever! – TBA

1400-1420 Dermatology 101 – SKINNER

1420-1500 MEET THE FACULTY OPEN DISCUSSION

Workshops (1500-1700) 

Workshops will have an open format where you can attend as many or as few as you would like, and spend as much time as you choose. This will enable you to focus on the areas you want to gain the most from:

Basic Hospitalist POCUS (IVC, lungs, heart, renovascular and GI, US-guided venous access),

Pharmacology Cases 

EKG Cases 

Nuts & Bolts: Troubleshooting Thoracic Drainage

Mid-Line Catheter Insertion  

KENNY’s Cardio-Pulmonary Physiology Workshop 

SPIEGEL’s The Art of the Bougie – Airway Workshop 

 

Meet the Faculty cocktail! 1900 – Location TBA

 

Friday May 24 – Day 2

0800-0820 Metabolic Resuscitation: is is for real? FARKAS

0820-0840 Acid-Base in 3 Parts – SPIEGEL

0840-0900 Late-Breaker TBA

0900-0920 Gut POCUS – BAKER

0920-0940 Diastology for Intensivists – CHEN

0940-1020 MEET THE FACULTY OPEN DISCUSSION

1020-1040 The Art of the Bougie – SPIEGEL

1040-1100 Renal Doppler in Acute Care. HAYCOCK

1100-1120  The IVC don’t Lie: Ask the Right Question! KENNY

1120-1140 Blood Pressure: a Closer Look. MAGDER

Trauma track

1240-1300 Permissive Hypotension: Permissive Death?  NEMETH

1300-1320 Thoracic Trauma – HAYCOCK

1320-1340 Massive transfusion – MALLEMAT

1340-1400 To REBOA or Not To REBOA – HAYCOCK

1400-1440 Traumatic Cardiac Arrest: How To Avoid Killing the Dead! NEMETH

Critical Care Track

1240-1300 Inhalation Therapy for acute RV Failure – DENAULT

1300-1320 Advanced Doppler for the Intensivist – KENNY

1320-1340 Pmsa: Is There a Clinical Use? OLUSANYA

1340-1400 Got ROSC! Now What? TERAN

1400-1420 – Insights on Delirium Using POCUS – DENAULT

1420-1500 – MEET THE FACULTY OPEN DISCUSSION

Workshops (1500-1700)

Advanced POCUS (venous, shock, advanced CHF, GI, neuroPOCUS)

TERAN’s Intro to Resus TEE

HAYCOCK’s Intro to REBOA

Intro to ECMO

POCUS-SIM

KENNY’s Advanced Physiology Workshop

 

Register here!

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The Resus Tracks 06: Farkas (@Pulmcrit) on Shock Perfusion and Infrared Tech! #FOAMed, #FOAMcc

So I had the chance to catch my friend Josh today, and, as always, he had some unique insights to contribute.

 

I really like the IR idea from the standpoint of objectivity and reproducibility. At first it sounded like a fancy (and fun, of course) way to check skin temperature as I routinely do, but the ability to objectify from doc to doc could be really interesting. Will get on that with my colleagues in my unit. We’ll see what we can come up with in the next months!

 

Love to hear from some others trying to tweak and optimize their resus!

 

cheers

 

Philippe

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

The Resus Tracks 05: Kenny (@heart_lung) Tackles Shock Perfusion! #FOAMed, #FOAMcc, #FOAMus

So finally got around to corralling Physiology Jedi Master Jon-Emile Kenny for a chat, which is always a tremendous learning opportunity. And this time was no different. Jon breaks down some of the mysteries around arteriolo-capillary coupling and shock flow, and brings up some really interesting potential uses of the critical collapse pressure of small arterioles, and hints at how we may be able to use some POCUS techniques to clinically assess tissue perfusion.

Here you go:

Please leave comments and questions!

The article we refer in the beginning to is here:

MAP in sepsis review

And the article on critical closing pressure in the neurocirculation that Jon refers to is here:

CrCP Brain

cheers!

 

Philippe

The Resus Tracks 04: Shock Circulation & Renal Perfusion with Korbin Haycock. #FOAMed, #FOAMer, #FOAMus

 

So I got to have a chat with ER doc extraordinaire Korbin Haycock today, reasserting my belief that tissue perfusion is not proportional to blood pressure.  I am again including the article discussed, and here is the graph in question:

Here is our talk:

And the paper – which is definitely worth a read, as it clearly supports individualizing therapy!

MAP in sepsis review

 

cheers and please jump into the discussion!

 

Philippe

The Resus Tracks 03 – Shock Circulation with @EMnerd! #FOAMed, #FOAMcc, #FOAMer

Here we go!

 

Discussing with Rory is always awesome, because he manages to distill things to the most important stuff. In this one he basically says sure Phil, it’s fun to think up all kinds of semi-theoretico-imaginary hemodynamic stuff, but you gotta make sure you control the source!

Thanks!

 

Love to hear comments and criticisms!

 

Philippe

 

Here is the open access paper I was talking about, graph on page 2.

MAP in sepsis review