fluid resuscitation

August 5, 2016

Tom Woodcock: The Revised Starling Principle and The Glycocalyx! #FOAMed, #FOAMcc

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So today, I had the chance of having a private tutorial with Dr. Thomas Woodcock (@thomaswoodcock) about the glycocalyx and the revised Starling principles.  For anyone interested in fluid resuscitation, this is an area you have to delve into. The basic principles we all learned (which are still being taught) are basically the physiological equivalent of the stick man we all started drawing as toddlers: overly simplified and far from an accurate representation of reality.

Now my first disclaimer is that I have been a colloid supporter for many years. My physiological logic for that had been to minimize the crystalloid spillover into inflamed/septic areas, particularly the lungs and abdomen, when those are the septic sources. However, I was likely misled by my education and lack of knowledge about the endothelium.

So I stumbled upon the whole glycocalyx thing a couple years ago, and this prompted me to try more enteral fluids – the only way fluids normally ever enter the vasculature – but little else. Aware that it’s there, but unsure what to do about it.

Now a year and a half ago, Andre Denault, my closest thing to a mentor, casually dropped the line to me about albumin not working. “Don’t use it. It doesn’t act the way we think it does.”  But it was a brief chat, and I didn’t get to pick his brain about it.  Just a few weeks ago, I discuss with Jon Emile (Kenny), and he’s coming to the same conclusion.  Damn. I’m finding it a bit harder to hang on to my albumin use, which is beginning to look a bit dogmatic and religious.

Here is Jon-Emile’s take on it – a must-read.

Here is Tom Woodcock’s site and article – another must-read.

And here is my discussion (in two parts) with Tom (to skip the silence, skip forward to about 30 seconds into each – sorry my editing skills are limited!)

 

Bottom line?

Probably stick to isotonic crystalloids, and some hypertonics.

 

Love to hear some thoughts!

Cheers

 

Philippe

 

 

August 3, 2016

The NYC Tracks with Jon-Emile: The Glycocalyx – The Next Frontier. #FOAMed, #FOAMcc

I was really psyched when Jon-Emile mentioned he would like to talk about the glycocalyx.  I first blogged about it here, basically when I stumbled on the extensive literature on this huge organ we have been completely ignoring in terms of physiology and therapeutics. It lines our entire endothelium, which is where most of our therapeutic interventions go, and we only heard of it in passing, possibly in histology class as med 1’s.   Hmmm.  Anyhow, here, Jon-Emile and I talk about it a little, discuss possible clinical implications, but more importantly Jon mentions the relatively new blog of Dr. Thomas Woodcock (@thomaswoodcock), http://www.fluidtherapy.org, who is one of the pioneer clinicians who have studied the glycocalyx, and who is now trying to bridge the bench to the bedside.

I’ve been fortunate enough to get in touch with him and we’re planning to record some discussions soon.

So, in my view, the glycocalyx is a formidable force we have been ignoring, and have been damaging often with our interventions. I’m hoping to see some developments allowing glycocalyx assessment outside of the labs in order to give us the tools to reassess every fluid in terms of the relative damage it does to what is essentially the gatekeeper between the blood and the tissues.

Love to hear some comments!

Here is the chat with Jon:

 

cheers

 

Philippe

July 9, 2016

The NYC Tracks with Jon-Emile: Paracentesis and Volume Status. #FOAMed, #FOAMcc, #FOAMus

So I was in NYC last week and met up with my buddy Jon-Emile Kenny, (@heart_lung), intensivist-physiologist extraordinaire, and we recorded a few discussions on practical matters.

I always love to debunk myths and avoid dogmatic guesswork, and, more often than not, Jon, with his encyclopedic knowledge of the physiology literature, but more importantly a cutting edge understanding of it, can back up my vague ideas and empirically derived ideas, so that the next time someone asks me why this is so, I can have a semi-enlightened answer!

So here is the first, where we discuss the common question about the need (or not) of intravascular volume repletion during or following large volume paracentesis. Yes, there are some formulas out there as to how much albumin or crystalloid one should give, due to the worry of subsequent hypovolemia. Note how those formulas use no data about your patient’s volume status at the time of paracentesis, so as far as I’m concerned, they have no value whatsoever in an era where we can assess this. Yes, ultrasound is the base as far as I’m concerned.

Here we go:

Please share your thoughts!

cheers

 

Philippe

May 31, 2016

Fluids in Sepsis: An EmCrit Webinar! #FOAMed, #FOAMcc

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So a few weeks ago Scott (@EmCrit) asked me to be part of a pretty cool webinar organized by the Greater New York Hospital Association about fluids in sepsis. The gang consisted of David Gaiesky, Emmanuel Rivers and moderated by Scott himself. And for some obscure reason, he asked me to be part of it – much to my honour (terror, also), naturally.  It was only afterwards that he told me it was to help stir the pot and be controversial, challenge the “old school” etc… He seemed to have overlooked that I am Canadian, and inherently and perhaps overly polite and considerate – at least live and in “person”!

We talk about a bunch of stuff around fluids, which, how much, how to assess, etc.

Anyhow, I hope I got a few ideas across, but it was really cool to hear that these gurus do use ultrasound – don’t necessarily strictly adhere to, for instance, EGDT, and also advocate that guidelines are guidelines and not necessarily gold standards.

Here is the link to the webinar for those interested:

 

https://t.co/dbL03Vuqlj

 

And here is the figure for the section where I refer to fluid responsiveness/tolerance:

Screen Shot 2016-02-21 at 9.25.50 AM

I further talk about this in a previous post here.

Scott and I also recorded a debrief which should be coming up in the next weeks on EmCrit – link to follow!

cheers!

 

Philippe

March 19, 2016

Cerebral & Somatic NIRS (Near InfraRed Spectroscopy) in shock states: tailoring therapy. (PART 1) #FOAMed, #FOAMcc

So I’d mentioned using NIRS to monitor and tailor therapy a few months ago, and promised a more in-depth discussion to come, so here we go.

For this not familiar with the technology or the concept, NIRS measures tissue saturation, predominantly venous. Hence physiologically it is akin to central/mixed venous gases, but localized. Cerebral NIRS found its foothold in the OR with carotid and cardiac surgery, but its use is now expanding. Given typical knowledge translation time of a decade, it should end up joining ETCO2 as a routine vital in monitored units, but probably not soon enough.

So in our unit at Santa Cabrini Hospital in Montreal, we’ve had this technology for about a year (the INVOS system), and have been studying its uses. In this time, three applications have stood out:

  1. Finding the “Sweet Spot” for vasopressors.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate.
  3. Cardiac arrest: CPR adequacy, prognostication and detecting ROSC.

 

  1. Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion.  With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure.  So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP.  However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point.  For example,  a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen.  Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate – I feel this is really important. When a patient’s life is literally on the line, and knowing that our interventions are seldom without potential nefarious side effects, it is poor medicine to be introducing a therapy without having some form of monitoring – preferably multiple – that we are headed in the right direction, or at least not making things worse. Of course, we already do this – with BP, sat, lactate, CCO, ultrasound, ETCO2 – but I think using a realtime measure of tissue saturation adds to this. It is also my firm opinion that integrated, multimodality monitoring is necessary – at least until someone develops some form of mitochondrial monitoring which tells us that the cytoenergetics are sufficient to survive. Until then we are stuck with surrogate markers and many of them (e.g. lactate) are the result of complex processes that preclude them being a simple indicator of perfusion adequacy. For instance, when giving a fluid bolus/infusion – after having determined that the patient is likely fluid responsive AND tolerant – one should expect to see an increase in ETCO2 (other parameters being constant), an increase in CO, an increase in NIRS values. The absence of such response should make one reconsider the intervention, because without benefit, we are left only with side effects.

Here is a patient’s cerebral (top) and and somatic (thigh – bottom) and CO values. This patient had an RV infarct and was in shock.

IMG_7948IMG_7946

 

Following initiation of dobutamine, this is what occurred:

IMG_7951IMG_7949

Given that we cannot always predict the response to an inotrope – depending on the amount of recruitable myocardium, it is reassuring to see an improving trend. This enabled us to decrease the vasopressor dose significantly.

Note that, so far, and unless some good evidence comes out, I don’t use a goal value, and so far, I have not identified a value that is predictive of prognosis. However, downward trends usually bode very poorly. For instance, I had a severe chronic cardiomyopathy patient whose cerebral saturation was 15%!!!  But more surprisingly, she was awake, alert and hemodynamically stable. Adaptation.

Part 2 and the stuff on cardiac arrest coming soon!

Please, anyone using NIRS in shock, share your experience!

 

cheers

 

Philippe

February 21, 2016

Volume responsiveness and volume tolerance: a conceptual diagram. #FOAMed, #FOAMcc, #FOAMus

So I know I’ve belaboured the point about the difference between volume responsiveness (i.e. will there be significant increase in cardiac output with volume infusion) and volume tolerance (is the volume I am considering giving going to have nefarious consequences), because in my opinion, the focus has been – rightly so to some degree – to look for an accurate way of discerning responsive patients from non. Of course this is absolutely necessary, as one does not want to give volume if it will not have any benefit, but the too-common corollary to that is to automatically give volume to those who are responsive.  Here is an earlier post about this:

Fluid Responsiveness: Getting the right answer to the wrong question. #FOAMed, #FOAMcc, #FOAMus

So in discussing with a bright young colleague yesterday, Dr. St-Arnaud (@phil_star_sail), I realized that there may be a common conception that physiologically, the relationship between the two may be the following:

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This would mean that it is safe to give volume until a patient is no longer volume responsive, and even perhaps a bit more. Alternately, the two may be closer:

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This would mean that once can go just till the point where the patient is no longer volume responsive.

Either one of these scenarios would be awesome. That would mean that by using any of the flow or volume variation techniques, arterial or venous, we could pretty much remain safe.

However…

While the above may hold true for healthy subjects, I would contend that in sick people (which is who I tend to deal with, especially when resuscitating shock), that the more likely physiological relationship is the following:

Screen Shot 2016-02-21 at 9.03.28 AM

Hmmm… That would mean that assessing for volume responsiveness would only tell you that there would be an increase in cardiac output, but absolutely nothing about whether it would be safe to do so.

This concept is not a new one by any stretch of the imagination. It’s inferred in the diagnosis of “non-cardiogenic pulmonary oedema.” So what causes this shift? Here:

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So, how do we figure out where the point is? Sorry to say there is no answer that I know of. My friend Daniel Lichtenstein uses the FALLS Protocol (identifying the appearance of B lines during resuscitation) which is the least we should do, but I suspect that at that point, we have already overshot the mark. My adopted mentor Dr. Andre Denault (@Ad12andre, in addition to IVC, has identified portal vein characteristics including pulsatility (lots of stuff in press) to show that the viscera are at risk, but as of yet there is no simple answer. CVP value? Please. CVP tracing morphology? Maybe.

No simple answer. No one-size-fits-all velue to look for. Clinical integration.

In my opinion, one should not, in sick patients, seek to volume resuscitate until the point of no-volume-responsiveness. The old adage of “you have to swell to get well” likely kills a few additional patients along the way, just as much as under-resuscitation. I plead guilty for over-resuscitating patients for years before realizing that being on the flat part of Frank-Starling is 100% a pathological state.

Love to hear your ideas and comments!

 

Jon-Emile Kenny says:

I like your graphics, it makes the concepts tangible. I think we should try to integrate ‘volume status’ into this framework as well. A physiological purist might say that as soon as you are ‘hypervolemic’, you are volume intolerant, because hypervolemia is an abnormal state which should always be avoided. A functionalist might say that you become volume intolerant as soon as you have physiological embarrassment of any organ system – but how is this determined? My gut is that by the time there are B-lines in the lung, you’ve gone too far. By the time there is abnormality of splanchnic venous return, you’ve already gone too far. I am more of a purist, so in my perfect ICU, I would perform q4-6 hour radio-labeled albumin studies to determine the patient’s true plasma volume. In health, the normal blood volume is about 80 mL/kg [thus, once you’ve given a 70kg man 5 L of NS, you’ve almost certainly replenished his vascular volume]. The moment that the blood volume becomes > 95% the norm, I would call the patient volume intolerant and stop volume expansion and focus on venous tone with pressors, cardiac function with inotropes, etc. To me, this makes the most sense in the pure Guytonian world; if you keep flogging a patient with litre after litre of fluid and the patient’s BP remains low, you are missing something – volume is not the answer – regardless of what an ultrasound shows you:
1. trouble shoot the venous return curve [i.e. too little blood volume, too little venous tone, too high resistance to venous return]
2. trouble shoot the cardiac function [i.e. poor rate, rhythm, contractility, valve function, biventricular afterload]
If you need some objective measure of blood volume before you can call volume status optimized before moving onto the next problem to fix – that’s a radio-labeled albumin.
Maybe I’m crazy.cheers

Jon

Thanks for commenting Jon!

I totally agree, if we knew each patient’s normal blood volume, that would be a starting point.  And of course, that would prevent the over resuscitation of a very dilated and compliant venous system (small IVC on ultrasound). Let us know if you figure out a practical way to do that!

It’s too bad that extravascular lung water doesn’t seem to have panned out – not sure why exactly.

 

 

Philippe

March 15, 2015

Musings with Jon-Emile & Philippe – Fluid Resuscitation: Physiology and Philosophy! #FOAMed, #FOAMcc, #FOAMer

So here, Jon-Emile and I explore a topic I’ve posted about before (http://wp.me/p1avUV-bd) so I can see if a master physiologist agrees with my rationale (…not just my rationale but supported by a ton of literature many choose to overlook!).

Please visit http://www.heart-lung.org for Jon’s awesome physiology tutorials!

Love to hear listeners’ thoughts!

cheers

 

Philippe

March 3, 2015

Musings with Jon-Emile & Philippe 2: Putting Jon on the Spot!!! #FOAMed, #FOAMcc, #FOAMer

So in this second instalment, I put Jon-Emile on the spot about some common clinical scenarios which, to me, contain a bit of dogma. Let’s see if physiology will give us the bottom line!

 

I think these are actually really important, because just too many times, I hear people automatically saying that in RV infarct, the patients need a lot of fluids, and in PE and tamponade as well.  I’m not so sure that’s always true, so I thought it would be a good idea to review this physiology with s real pro!

 

enjoy, and love to hear some comments!

 

cheers

 

Philippe

 

February 9, 2015

Enteral Fluid Resuscitation? The WHO to the rescue in the ED/ICU? (ORT part 1) #FOAMed, #FOAMcc, #FOAMer

So something has been trotting around my head for a few months, and it actually stems from a small and not-so-proud moment I experienced during a conversation with my wife, while she was still a resident.

She was telling me some of the stories of the day, and how one of her supervisors who had a mixed outpatient and ED practice, always pushed them to use PO fluids, get rid of IVs and get the patients home.  I kind of scoffed, in a sadly typical acute care physician mode, saying how you had to be a bit more aggressive and give them IV fluids to revert their dehydration a bit faster.

Then I caught myself. Hmmm. What exactly am I saying this (con brio) on the basis of. Knowledge, or belief?    I tried to find knowledge but came up woefully short. It seems I’m doing this out of habit, what I’ve seen/learned/believed in the two decades since someone handed me an MD degree. Damn.

So, I do believe in evolution. We have evolved platelets to stop bleeding, fibroblasts and osteoblasts that can fix bones, white cells that go mop up the messes, and all kinds of other good stuff.  One thing we do NOT have is small openings in vascular structures that allow unprocessed, man-made fluids directly into the bloodstream. We make these. We insert tubing into normally sterile environment and infuse a vast number of medications directly into this fragile matrix of cells and organic colloid – with the best of intentions.

In our physiology, however, the ONLY way fluid ever enters the vascular spaces is by diffusion from the outside of the endothelial cell into the lumen, molecule by molecule and ion by ion.

So let me seemingly diverge for a bit…

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Prior to the 1970’s, restricting oral intake was a “cornerstone” therapy of diarrheal illness, due to the pervasive belief that the GI tract needed time to heal and recover before resuming normal function. This was felt to be crucial. Hence, only IV therapy was used (in developed countries), and in the underdeveloped world, the death toll was appalling – especially among children.   In the 40’s, Dr. Darrow of Yale started actually studying the GI tract fluid and electrolyte issue, and advocating oral rehydration with mixed fluids. He was able to bring infant mortality radically down in his practice, but it would take over twenty years before a groups started to formally look at this in the 60’s.  Finally, in the late 70’s, the WHO pushed this out into the field, and the childhood worldwide mortality from acute diarrheal illness dropped by over 70%, from over 5 million deaths a year to a bit over 1 million – at that time.

Oral Rehydration Therapy (ORT) is now felt to be one of the most significant advances in modern medicine. Compared to that impact, all the critical care and cardiology trials are about as significant as a drop in a bucket. We’re not talking about composite end points and subgroup odds ratios of 0.85…

For a great review on this check out The History of Oral Rehydration Therapy by Joshua Nalibow Ruxin (google it).  A great story of science and humanity, good and bad.

So, back to 2015 ED/ICU’s.

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The question now becomes the following: why – in the presence of a functional gut – do I choose to entirely rely on non-physiological IV fluid resuscitation?

I can already hear the roars and the outrage and the cries of heresy.  And heresy is certainly what this is (Heresy is any provocative belief or theory that is strongly at variance with established beliefs or customs – Wikipedia). But that doesn’t make it wrong.

So I would ask everyone – particularly the naysayers, to examine their knowledge and see if they actually have any at all that supports the strong conviction that IV fluids are the way to go in ALL cases (my N=1  principle precludes going for the one-size-fits-all therapeutic approach).

Now everyone agrees that, once patients are better, they should be on feeds with little maintenance fluids. I don’t think many will debate that. So that should be the basis to wonder whether, in the presence of a functional gut, a variable proportion of fluid resuscitation in acute illness should be enteral…

I’ll let everyone digest that.

Comments more than welcome.

More to come in Part 2.

 

 

cheers!

Philippe

January 1, 2015

Post-Arrest BP Study by Young et al (Resuscitation) – interesting & important, but not yet an N=1 answer! #FOAMed, #FOAMcc

Happy New Year to all!

So trying to catch up on some reading, here is an interesting paper I came across. Young et al did a retrospective study on post-arrest BP, in an attempt to answer the very pertinent and important question as to whether or not a higher MAP may confer better neurological recovery, which is a very sensical hypothesis. After all, a brain with potential swelling, both of tissue and endothelium, may “need” a higher BP. Some societies have advocated for a higher MAP than is usually targeted (i.e. 65) and in studies this has been anywhere from 60 to 100. In their particular institution (Vanderbilt) the protocol aimed for 80-90.

Here it is:

Young et al RESUS

So what did they find?

Basically, they were unable to demonstrate that a higher MAP – in this case defined as achieving 80 mmhm – improved anything, with a follow up to 3 months. There was also no increased mortality related to the use of vasopressors.

So, why might this be? Well, I think there are a couple of important principles to review, especially for the novices reading this.

1. Pressure does not equal flow. The relationship between pressure and flow is a complex one and depends on the interaction between the pump (CO) and the circuit resistance (SVR). Pressure rises when resistance is increased, output is increased, or both. If resistance is increased without increasing output – or by a disproportionate increase in resistance vs output, flow decreases. The effect of vasopressors such as norepinephrine is complex, with both vasoconstriction and increased cardiac output (both via beta stimulation and via increased venous return), and depends on volume status, alpha sensitivity and the recruitable cardiac reserve.

So…? This means that on the surface, a BP number tells you little about flow. The same MAP may represent a highly vasoconstrictor, low-flow state, or a normal flow state. Obviously, a certain minimum pressure is required, to drive the flow from artery down thru the capillaries, but what that number is is unclear. So when looking at any study using simply MAP without another assessment of flow, one cannot draw a conclusion that improving hemodynamics may not help the situation.  How does one assess this – in all likelihood  an integrated approach using ultrasound (volume status, cardiac function), tissue saturation (cerebral/somatic oximetry) and possibly other technologies, including simple physical exam looking at skin mottling.  This type of information could categorize patients into flow categories and make results much more interesting and applicable.

Note that this isn’t really criticism on the authors – it would be impossible to do this on a retrospective study, but simply food for thought for further studies to come.

2. The N=1 principle: remember that we are never treating hundreds of patients at once, and we do not have to decide what is best for most (which is what an RCT generally answers) but what is best for the one patient we are treating.  Hence, looking at any one patient and saying that the target BP should be 65 vs 80 based on this study is incorrect.  What we should be saying is that aiming for a higher MAP may not be necessary if we feel that the patient is well perfused at 65. How each of us figures that out will depend on individual skills and available technologies, but to simply aim for 65 without further thought and assessment is relinquishing your MD in favour of the printed word, essentially what any paper protocol could do.

In the next post I’ll discuss the use of tissue oximetry and how it can be used as part of a strategy to optimize vasopressor use and MAP targets.

 

Thanks and love to hear your opinions!

 

Oh, and don’t forget to register for CCUS 2015 at http://www.ccusinstitute.org, and for more info at http://wp.me/p1avUV-bh.  In those couple of days, Paul Marik, Scott Weingart (@emcrit), Josh Farkas (@pulmcrit), and a bunch of other totally amazing speakers will be talking about this stuff, and more!

Philippe