RL

November 23, 2018

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

February 22, 2018

Kylie & Korbin chime in to the Venous Congestion Issue. #FOAMed, #FOAMcc, #FOAMus

So I think much of the awesomeness of #FOAMed is sparking discussion and exchange, and the many little steps in clinical management besides the initial prescriptions. So I thought I would highlight and exploit a couple of really interesting reader comments:

So first, Kylie (@kyliebaker888):

Great to listen guys, thanks, and very timely. I had just read Tremblay’s paper after coming across a very pulsatile PV in a relatively well elderly patient with bad TR. Two questions – which PV are more likely pulsatile in the first place….Tremblay mentions RVF/TR and very thin folk. What is your experience?
Second Question – what did the GB wall/GB fossa look like after the initial very positive fluid balance? Does everyone blow out their GB wall with fluids, or only some?

It is always important to isolate the patients’ whose physiology may change the clinical signs (in this case PV pulsatility) and make their interpretation different. I agree that massive TR, especially chronic, would likely account for pulsatility. I am not certain about the physiology for the very thin patient, but I have heard the same thing from Andre.  So my personal take on a patient with severe TR and a pulsatile PV would be to look at the IVC variation, TR notwithstanding, if it is fixed and plethoric I would diurese – the organs don’t care what the cause of the congestion is.  

As for the GB, I have also seen edema, and then try to correlate with cholestatic enzyme changes that would be out of proportion to the hepatocellular enzymes if there is a primary GB process. This is certainly an imperfect science. In a critically ill septic patient, I have a low threshold to drain the GB if in doubt.

Then Korbin gives his two cents, and then some! 

Great case, loved it. Thoughtful management, brilliant!

I couldn’t help thinking as I listened, that it is so important to avoid over-resuscitation with fluids in the first place. We all know that the majority of crystalloids given will end up as interstitial edema, so any benefit from the increase in stroke volume is temporary at best (consider carefully what you gain and at what cost). Wet lungs=increased mortality, days on the vent, and ICU stays. Wet kidneys=AKI 2-3 days after initial resuscitation and potential RRT. Congested liver=gut edema and continuation of inflammatory cytokines/sepsis syndrome. Too much fluids–>BNP levels rise, high BNP levels in the presence of LPS=glycocalyx shedding, and more interstitial edema everywhere.

Cannot agree more.

I think there is some decent evidence that an early fluid liberal approach combined with a late fluid restrictive approach can potentially benefit a patient in septic shock, but its clear that an overall positive fluid balance does harm. Perhaps, even the early fluid liberal strategy (in sepsis specifically) should be tempered by a careful consideration of what is really going on.

My take here is that, by using POCUS, there is no need for a “general approach.” POCUS takes essentially no time. In about 5 seconds you can confirm a small IVC that can (initially) take fluid, a medium one (that you need to watch) or a full one (yes, it happens – that gets no fluid). So to me there is no need to have a pre-determined approach…

Sepsis is an entity characterized by venous return being limited by a decrease in mean systemic pressure (MSP) due to an increase in venous capacitance, rather than a decrease in fluids that generates the stressed volume (MSP=fluid filling/venous capacitance). The body compensates with an adrenergic response that maintains (or attempts to maintain) MAP by an increase in a catecholamine driven augmentation in cardiac output/contractility. This adrenergic response likely has more to do with the increase in lactate production observed in sepsis, rather than actual tissue hypo-perfusion and anaerobic metabolism mechanism. Increases in CVP inhibit venous return and congest the kidneys and GI tract (the left atrial pressures are the equivalent problem for the lungs, combined with the fact that pulmonary vascular permeability is increased in sepsis as well). Given this, I think in distributive shock, we should fix the lack of MSP by an earlier vasopressor therapy approach, both to supplement and decrease the crystalloid load to the patient, which is un-natural and contrary to their deranged septic physiology.

Agree.

Also, could the type of crystalloid given be important? NS gives a considerable sodium load compared to LR, and this likely promotes/sustains fluid retention that is difficult to remove during de-resuscitation. The high chloride levels of NS will promote an increase afferent arteriolar vasoconstriction and thus decrease GFR, making it more difficult to diuresis the patient later on, and contribute to AKI beyond the iatrogenic interstitial kidney edema caused by the crystalloids we gave.

Absolutely. NS is given by medical peeps only by cultural habit. Most do not know the pH (zero SID due to chloride) of  a solution they give by the buckets. RL is the best option I have available.

If you are involved in the early phase of resuscitation of a shocked patient, consider the downstream consequences of your fluid strategy that you give your patient that may give you a temporary comfort because they will look better in the short term.

Dr. Maitland and the FEAST study corroborates exactly this.

This is not to say that an aggressive and upfront resuscitation is not critical–it surely is. I’m saying resuscitate smarter, not wetter. Look for stop points for crystalloids–E/e’ ratios, consider PVPI, RV dilation/TAPSE, hepatic vein doppler, IVC dynamics, portal vein pulsatility, intra-renal venous Doppler patterns and renal resistive index. Fix the hemodynamics from an approach of the root of their problem, rather than pushing fluids for every hypotensive patient (whether you are taking care of them early, or late in the time frame of their illness). Fluids do have their place, but be careful and cognizant of their real down side. Look at your patient, think it through, and make the best actions for them.

Ok, now I don’t even get to have a punchline. Thanks Korbin!

So if this interests you, tune in to The Great Fluid Debate at H&R2018, and I look forward to meeting both Kylie and Korbin who will be in attendance and, I’m sure, putting us all on the spot!

And yes, there will be a POCUS workshop on portal and hepatic vein POCUS.

click here if you want to take part: H&R2018

cheers!

Philippe

 

December 7, 2017

Fluid Stop Points! More POCUS goodness from Korbin Haycock. #FOAMed, #FOAMcc

I am really enjoying this exchange, and I think it is in the true spirit of #FOAMed to foster these discussions, as we have the opportunity to combine and fine tune our understanding of a topic from several really bright people’s view and experience. 

Korbin:

Jon-Emile, excellent points and insight. I should clarify a couple of my comments. To be specific, by “renal vein flow” I am referring to intra-renal venous flow. Apologies for my imprecision! Thanks for pointing that out.

Yes, a lot of these renal and portal Doppler patterns are surrogates of CVP. But I don’t think any of us would use CVP in isolation these days to make any decision what-so-ever on whether fluids were indicated in our patient.

Also, to clarify, I am not using intra-renal venous flow or renal resistive index as measures of non-fluid responsiveness. Rather, I use these measures as a stop point for attempting to solve the patient’s hemodynamic dysfunction with crystalloid regardless of whether or not my straight leg test tells me the patient is still fluid responsive.

And that is a key re-iteration to me. It is important to set these stop points and not only look at whether the cardiac output can be maximized. This has been tried. And failed. Let’s remember that sepsis is not inherently a disease of low flow. It isn’t cardiogenic or hypovolemic shock at the core.

My rationale for the strategy of using intra-renal Doppler, E/e’, and Lung US (now, I can include portal vein pulsatility) as a stop point for IVF administration is that I think the patient is best served to avoid iatrogenic edema of the upstream organs, primarily the lungs and the kidneys. These are the two organs (maybe you could put the endothelium in this category as well–glycocalyx being a whole other can of worms!) most easily damaged by the chase for optimizing every bit of fluid responsiveness. We have good evidence that getting wet lungs and swollen, congested kidneys is a bad thing, and we have these tools to hopefully warn us when we are pushing things too far.

Absolutely. And the whole glycocalyx is something to keep in mind, even if only to me mindful to disrupt it as little as possible.

Of course renal resistive index, intra-renal venous flow, portal vein pulsativity, and whatever else you like will have limitations and confounders. As long as you understand what can cause abnormalities with these tools, you can make an educated guess as to what’s going on. If our creatinine is off and our RRI is high, but intra-renal venous flow and portal vein flow is normal, perhaps the RRI is caused by something other than renal congestion, like ATN. If the portal vein is pulsatile, but the Doppler patterns of the hepatic vein, kidney and the heart look ok, maybe something else is wrong with the liver. But, if all our modalities are in agreement and pointing to congestion, we should perhaps believe that it’s congestion and stop the fluids. 

That is an awesome approach to integrating RRI. I’ve been toying with it for the last couple of days, and much thanks to Korbin, I think that the limitations of RRI can be overcome by using the rest of our clinical and POCUS data.

It isn’t a hard technique, though in some patients getting a good signal can be tricky.

I think that the kidney, being an encapsulated organ, and the fact that much of our crystalloid ends up as interstitial edema, the kidney will develop sub-optimal flow patterns before CVP would cause congestion. The same is true regarding the lung, except that it’s just related to increased pulmonary permeability due to inflammation. Regardless, the idea is to save organs, and the earlier you can detect the problem, the sonner you can stop battering the more delicate organs with fluid.

As I think we have all mentioned, you really have to look at the whole picture, and put it together to tell the story of what is wrong, so we can logically and thoughtfully treat our patients.

I really appreciate this discussion. Thanks!

 

 

Thanks to Andre, Jon and Korbin for making this very educative for all!

Cheers

 

Philippe

 

ps don’t miss the POCUS Workshops on venous assessment at  !!!

December 3, 2017

Portal Vein POCUS: A Reader’s Case and a Follow-Up to the Denault Discussion

So I’ve been meaning to post a follow up and discussion about portal vein POCUS and how I am integrating it so far, and a few days ago I got a really interesting comment from Dr. Korbin Haycock, and I think it’s got some awesome elements to discuss.

Before we get into it, I would invite anyone reading this to go listen to the original Denault Track here, without which this discussion would be missing some elements.

What we are looking at here is the physiological assessment of venous congestion, and how doppler interrogation of the portal vein may help us. So here is Korbin’s case, and I will interject (in bold) where I think a point can be made, or at least my thoughts on it.

“Awesome post. Awesome website. I had never heard about portal vein pulsatility until reading your blog. I have previously been looking at the renal resistive index and renal vein Doppler pattern in my hypotensive/shock patients (along with doing a bedside ECHO and POCUS pulmonary exam) to guide when to stop fluid resuscitiation.

Very impressive. I have only ever heard of a handful of resuscitationists looking at this (including Andre, and consequently myself) so I’m gonna have to have a chat with this fellow soon! For those who have not tried or are not familiar, some basic info can be found here. I’ll have to review this, but I think one issue with RI is that there is an associated ddx, so that without knowledge of baseline, I would not be certain how to use it. Renal vein doppler seems very interesting to me, as that venous path is the one of the cardiorenal syndrome (forget about all that “low flow” nonsense in CHF – not in shock – patients), and there is clearly bad prognosis associated with abnormal (discontinuous) flow patterns. Here is a really good study (Iida et al)  and its editorial (Tang).

Iida Doppler_CHF Heart Failure JACCHF 2016

Tang Editorial JACCHF 2016

I had a case last night that I think illustrates that fluid administration can be the wrong thing to do in some septic shock patients. Plus, I got to try something new and look at the portal vein for pulsatility.

My case was a gentleman in his late 60’s with a history of HTN, atrial fibrillation and HFrEF who presented with three days for a productive cough and fever. POC lactate was 2.7. His HR was 130-140’s, in atrial fibrillation, febrile, MAP was 50, and he looked a bit shocky and was diaphoretic. The resident had started antibiotics and a fluid bolus of LR, of which not much had gone in (maybe 200cc) when I came to start a night shift and evaluated the patient. I asked that the fluids be stopped until we could have a look at him.

His IVC was about 1.5-2 cm with >50% collapsibility.

So I’m gonna hit the pause button right there for a couple of comments. That’s not a hypovolemic IVC. The RAP may be raised by some of the  It may very well be volume responsive, but I think the first thing to go for is correcting that tachycardia. The antibiotics are definitely the right call, but the fluids should, in my opinion, be held until assessment for volume tolerance is done.

His LV looked to have some mildly decreased EF and was going very fast. RV looked normal. His average SV was 45, CO was 6.1, E/e’ ratio indicated a slightly elevated left atrial pressure. His estimated/calculated SVR by the ECHO numbers was about 550. Lungs were dry anteriorly, without B-lines, but PLAPS view was c/w bilateral lower lobe PNA. Renal vein Doppler was biphasic and the resistive index was very high. I looked at his portal vein and it was pulsatile.

Excellent. So there is pulmonary pathology, which makes fluid tolerance already of concern. The CO is certainly adequate and SVR is low, suggesting a vasodilatory shock etiology. 

In the past, based on the IVC and the way the RV looked, I would have done a straight leg raise or given a given some crystalloid to see if his SV and BP improved, and if it did, give some IVF. Instead, I told the staff to given no more fluids and I gave him 20 mg of diltiazem.

His heart rate decreased from 130-140’s to 90. His averaged SV increased to 65 (probably due to increased LV filling time and better diastolic perfusion time), CO was 5.9, estimated SVR was 570. The renal and portal vein Doppler were unchanged. The MAP didn’t bulge and stayed low at 50-55. At this point I ordered furosemide and but him on a norepinephrine infusion to increase the SVR, first at 5 mcg/min, then 7 mcg/min.

Totally awesome to see. It isn’t unusual for me to diurese patients in vasopressor-dependant shock, as more and more data is emerging on how venous congestion has deleterious effects on the gut and may even contribute to the SIRS-type state. And once a patient is in a euvolemic to hypervolemic state, the only fluid they get from me is the one containing norepinephrine. Maintenance fluid is not for critically ill patients IMO.

The NE gtt increased his MAP to 75 mmHg. His SV was 80, CO 7.1 (I was a little surprised it didn’t go down a bit), estimated SVR was 700. I had his labs back at this point and his creatinine was 1.8 and the last creatinine we had was 1.1 a few months ago. His renal vein pattern was still biphasic and his renal resistive index was also still quite high at 0.89, which would probably predict a significant kidney injury in 2-3 days.

Even though his MAP and hemodynamics looked great, I was worried about the renal resistive index. I ordered a little more furosemide and started him on a little bit of a vasopressin infusion. After things settled down, MAP was 75-80, his average SV was 80, CO 7.3, estimated SVR was about 800, and his renal resistive index (RRI) was 0.75. He looked much better too. The second lactate was 1.3.

Very interesting to see the drop in RRI.  Great case to show how you don’t need to chase lactate with fluids. That is an antiquated knee-jerk reflex hinging on the concept that hyperlactatemia is primarily due to tissue hypoperfusion, which we have learned is not the main cause. 

This morning his creatinine had improved to 1.3 and he is doing well.

South of your border, CMS considers me a bad doctor for not giving 30 cc/kg crystalloid as a knee jerk reaction and instead giving a diuretic and early vasopressors as we did in this patient. Just looking at his IVC would indicate that IVF would be a reasonable strategy. If I had done a SLR or fluid challenge and found him fluid responsive, in the past, I would be temped to chase every bit of fluid response with pushing more fluids, but the renal and portal vein Doppler made me stop fluids in this patient this time. I think this example illustrates the importance of looking at each of your patients on a case by case basis and looking at the whole picture (heart, lungs, kidneys, now portal system too for me!), rather than following protocols.

Kudos. 

 

So then, Andre decides to chime in as well:

Very interesting but be careful about the interpretation of portal pulsatility because it can be falsely positive particularly in hyperdynamic young patient, which was may be not the case. We published an algorithm in order to identify the true portal pulsatility associated with right heart failure and fluid overload and a normal portal vein with pulsatility:

Tremblay Portal pulsatility Flolan Mil AACR 2017

(Tremblay 2017 A&A care report) A & A Case Reports. 9(8):219–223, OCT 2017 DOI: 10.1213/XAA.0000000000000572 , PMID: 28604468)

The latter will be associated with normal RV even hyperdynamic, normal hepatic venous and renal flow, normal IVC. We still need to explore the significance of portal hypertension outside the area of cardiac surgery where we are finalizing our studies.

Always tell my residents and fellow, treat the patient and not the number or the image. That being said, the patient got better so cannot argue with success.

So I think this is a really important point, that it can become dangerous in POCUS to look for a simple, single-factor “recipe” with which to manage the patient, when in fact you can have many factors which, integrated, can give you a much better understanding about your patient’s pathophysiology.

My take on portal vein POCUS so far is that it is a marker of critical venous congestion, beyond simply a plethoric IVC. I think it is wise to stop fluids before the plethoric IVC, but a plethoric IVC with a pulsatile PV should bring fluids to a screeching halt and some decongestive therapy started. The data for this?  Andre is cooking it up, but in the meantime, there is plenty of evidence that congestion is plenty bad, and NO evidence that maximizing CO works at all, so I am very comfortable in witholding fluids and diuresing these patients. 

For fun, here is a little figure from Tang et al about the doppler patterns discussed.

Love to hear everyone’s thoughts!

and for those interested, there will be a workshop run by Andre and myself on this at :

more to come on this soon…

cheers

 

Philippe

August 5, 2016

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

Screen Shot 2016-08-05 at 11.57.11 PM

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

 

 

March 24, 2015

Physician, know thy fluids! #FOAMed, #FOAMcc, #FOAMer

So I posted a quick poll on http://www.therounds.com, a really upcoming physician site, with the intent of getting an idea of what people use as fluids and what they know about them.

 

The first question was “What is your fluid of choice for resuscitation?”

Screen Shot 2015-03-24 at 10.58.56 AM

…no big surprise, 61% choose NS.  Despite the evidence of increased renal dysfunction (JAMA 2012 – I posted about this here: https://thinkingcriticalcare.com/2013/11/18/enough-with-the-normal-saline-foamed-foamcc/)

Well, at least this is chosen with good knowledge of its pharmacological properties, right?

Screen Shot 2015-03-24 at 10.59.12 AM

Hmmm… 57% peg it as physiological or basic.  Only 9% get it right. The pH is 5.6 or so.

So here we have favorite medication used by a lot of people, who use a lot of it, usually in quite ill patients, often acidotic, and who are not aware that the pH is in fact also quite acidotic.

I think it just is an important example on how we need to treat fluids as medications, and not think of them as benign interventions, and by doing so, we’d feel much more obliged to look at what we are giving in terms of composition and quantity, rather than the debonair attitude we have mostly grown up with.

 

cheers!

 

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

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…

Screen Shot 2015-02-09 at 12.05.58 PM

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.

Screen Shot 2015-02-09 at 12.06.26 PM

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

November 8, 2014

Limited EGDT in Zambia Study: Salt Water Drowning Syndrome… #FOAMed, #FOAMcc

So in this month’s issue of Critical Care Medicine, an interesting article was published, where investigators took a (necessarily) simplified version of EGDT to Zambia and applied it to septic patients. It turned out they had to stop it early due to an excessive number of cases of respiratory failure in the treatment group.  The difference was – you guessed it – they got “aggressive” volume resuscitation – up to 4l in the first 6 hours – guided by JVP assessment, and blood and dopamine if needed.

Simplified_Severe_Sepsis_Protocol___A_Randomized.1

The amounts received by 6, 24 and 72h were 2.9, 3.9 and 5.6 l for the treatment group vs 1.6, 3.0 and 4.3 l.

Now lets keep in mind that the patients, for the most part, did not have access to critical care, so the limited resources for ventilatory support made stopping the trial a bit early the only reasonable thing to do. Mortality in the treatment group was 64% and control 60%. High numbers, but this is explained in part by the prevalence of HIV (80%) and TB (37% of the HIV positive patients), so this data can’t necessarily be extrapolated to all populations, but to me, this is physiological support for the concept that aggressive fluid resuscitation – as I have stated in prior posts/podcasts – is most dangerous in those patients where the septic source – presumably “leaky” is ill-equipped to handle extra-physiological fluid.  In these patients, as Myburgh states in a sepsis talk, “noradrenaline is the fluid of choice,” and although perhaps a bit tongue in cheek, this certainly speaks to my beliefs of resuscitating to euvolemia rather than to the lack of volume responsiveness (http://intensivecarenetwork.com/myburgh-john-beta-blockers-and-sepsis/).

Additionally, these patients were not hypotensive, and lactate was not available – local limitations of medical system. Hence the definition of severe sepsis triggering aggressive fluid resuscitation was based  on SIRS type criteria, rather than some form of volume assessment.

 

Bottom line?

Be cautious in aggressive fluid administration in pulmonary sepsis. What, I really dislike when people say “be careful” or “be cautious,” because let’s face it, that doesn’t really mean anything, does it?  It doesn’t tell you what to actually do… We are frontline clinicians, so I’ll say to limit fluid resuscitation in pulmonary sepsis.  2 litres up front?  Probably ok so long as I have a varying, mid-size IVC (maybe 10-15mm – arbitrary and chronic pulmonary disease and hypertension have to be factored in) and a decent heart, but I don’t want to get to the point of no longer being fluid-responsive. Rather, go to pressors a bit earlier, perhaps, and no need for ongoing “maintenance” fluids at 100-150 cc’s an hour – remember that 80% of this wonderful therapy ends up where we don’t want it to.

 

cheers!

 

Philippe

PS for awesome talks by amazing speakers, don’t forget to register for CCUS 2015!!! For more info: http://wp.me/p1avUV-aU and register at http://www.ccusinstitute.org! 

October 6, 2014

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

Let me start with a clinical scenario: you have a 68 year old male in front of you who is intubated, has bilateral pleural effusions, pulmonary edema, a bit of ascites, significant peripheral edema, elevated CVP/JVP/large IVC, and a moderately depressed cardiac function.  What is the diagnosis?

If you said CHF, you might be right. If you said post-resuscitation state in a septic patient, you might equally be right. Hmmm….

So as any self-respecting FOAMite knows, there is an ongoing and endless debate about fluid responsiveness, how best to detect it, what exact percentage of some variation represents it – is it 9% or 13% – and everyone has the way they swear by.

Well, I think the entire premise behind this is essentially flawed.

The fact that this is the first question implies that the answer should radically change management (eg giving or not giving fluids “generously” – yes, the quotes imply facetiousness).  Basically, that you should stop giving fluids when your patient is no longer fluid-responsive. The implication is that fluids is a better, safer, healthier, more naturopathic, eco-friendly and politically correct therapy than any other option.

I think we should reflect on that a little.

If you put some faith into normal physiology, you have to acknowledge that the only situations in which our cardiopulmonary system finds itself nearly or no longer fluid responsive are pathological: CHF, renal failure, etc. None of those are healthy. None of those are a bridge to healing.

What do we do when we are hypovolemic?  We vasoconstrict, stop peeing, try to drink a bit (if at all possible) and slowly replete our intravascular space via the portal system. We might build up a little lactic acid (helps feed the heart and brain – yup, nothing toxic about it), but we get over it.  Of course, if we lose too much, the system fails and we head to meet our maker.

Now, having remembered that, why do we feel (and I say feel because the evidence isn’t there to back it up) like we have to get to pathological levels of intravascular venous pressure to fix the problem?  Especially when the problem at hand isn’t primarily hypovolemia, but mostly vasodilation, with possibly a relative hypovolemia in part related to increased venous capacitance.

The real question is: does my patient really, truly need a lot of fluid?

And here is the catch: just because someone is fluid responsive doesn’t mean that they need any, or that it is the best thing for them. Whoa… Heretic… I thought “aggressive fluid resuscitation is the cornerstone of resuscitation in sepsis.”

I think that answer is relatively simple.

No matter which method you are using (mine is IVC ultrasound: -https://thinkingcriticalcare.com/2014/04/01/the-ivc-assessment-by-bedside-ultrasound-lets-apply-some-common-sense-foamed-foamcc/), if you are deciding based on a millimetre of diameter, or a couple of percentage points of variation whether or not to give liters of crystalloids to your patient, there is no truth to that in the individual patient. Trying to figure out the tiniest of differences to decide our therapeutic options is, in my opinion, a huge waste of time with no scientific basis in the one single patient you are treating.   It’s like haggling for a dollar on a hundred dollar item in a flea market: you’re missing the boat.

“85% of patients with a IVC/SVV/SPV/PLR of …. are volume responsive” or something of the sort does NOT apply to the one patient you have in front of you as a recommendation for fluids. You have to make a complete clinical picture of it – feel the belly, look at the inspiratory effort, examine the tissues for edema, etc.

Grey zone it. The best we can do is a gross categorization of truly hypovolemic (need a lot), full (please don’t give me any), and “normal” which may need maybe a little, but probably not “generous” amounts. You’ll end up generously feeding the interstitial space and making things worse – and later maybe saying “oh well, I guess he/she was just so sick…”

Even if my patient is fluid-tolerant, why to we want to push him into near-pathological states? Is it just the old adage of “You have to swell to get well?”  In the light of much of our literature, I’m not sure that old wives’ tale holds a lot of water.

Are vasopressors that bad?  Not according to what we know…

At least, avoid actually reaching the point of no longer being fluid responsive. You can’t tell me you think that CHF is actually a good thing, can you?

 

Love to hear your thoughts!

 

Philippe

PS, if you like to think out of the box and rather be on the cutting edge, make sure to mark your calendar for the coolest conference in Canada: #CCUS2015….http://wp.me/p1avUV-bh

 

 

COMMENTS

SQS Replies:

Philippe,
I think your logic is sound enough, but the moat that makes it currently unassailable is that you are working in an area with no or very little data. There is clearly a reasonably well developed and continuing to develop literature around the mortality effects of excess volume. There is an older literature that suggests that our vasopressors are actually having their effect on the more normally functioning arterioles and may shunt well oxygenated blood from the well functioning cells of a tissue and to the ones that are shocked and can’t use the oxygen, anyway. At this juncture, your guess is as good as mine, as to which of these is the greater evil. Ergo, your argument is as good as any.

One thing I will say is that the patients who concern us are those in whom endotoxin, blood loss, or other factors have resulted in a shock state wherein cells and even large parts of tissues have both inadequate oxygen supply and inadequate ability to use whatever oxygen is supplied them. Any tool we have to alter this pathological state is blunt. Blood pressure? CVP? IVC size and behavior? SVI? What do any of these say about how well we are doing at the tissue and cellular level? Even the interesting markers of lactate, ScvO2, CV CO2, etc. are blunt instruments. As is our bag of fluid and as are our vasopressors. And think about our end result – “hemodynamic stability”, “better mental functioning”, “good urine output”, “feeling better”, “walking around”, “able to go back to work”. Things that are important to us and to our patient, but barely even measurable. How blunt are they?

My own approach, which I suspect to be yours, too, is to recognize that the new onset shock patient is momentarily different from the chronic CHF patient/”chronic” shock patient you describe above. We know there is an oxygen deficit, and it behooves us to correctly that as quickly as we can. We believe, with some data to back us up, that rapid correction of that deficit, to the extent that we can, can prevent the ugly chronic state. I use the blunt measures of fluid responsiveness in the first hour or two of resuscitation to ensure that the CO component of oxygen delivery is not deficient, and then I stop giving fluid. Early in the course, I am prone to rechecking “volume responsiveness” in some hours, because I know that fluid is leaching out of the vascular space and the patient has not stabilized, yet. All the while, I am highly aware that I am hoping this makes a difference, not knowing that it does. I am aware that it is rather circular to check SVI or IVC, give fluid, see a change and say, “See? Volume responsive.” And all the while knowing that every patient has his or her own line, beyond which more fluid will not be helpful but harmful. And all the while knowing that I can’t see that line, nor measure it with any tool that currently exists.

I think perhaps that we are like Phoenicians, navigating our way across the ocean by the North Star and trying to keep land in sight. We do a pretty good job of getting where we’re going a lot of the time. But won’t it be nice when we come up with GPS? Or even the astrolabe?

SQS

 

Fantastic points!

I can’t agree more. I do check for fluid responsiveness, and I do believe in rapid intervention – just perhaps not quite a vigorous and generous as medical marketing would have us buy. There isn’t more data for that than for a somewhat more conservative approach, in my opinion. Even the rate of administration is rarely looked at, just the totals. There is good animal data showing that, for instance, a more rapid rate of albumin infusion results in greater leak and less intravascular albumin at 6, 12 and 24 hours.  Little reason to think it would be any different in humans.  There is also data showing that the oxygen deficit in sepsis is not as ubiquitous as we think.

Our understanding of the septic disease state is minimal at best, and our tools exceedingly blunt, as you point out.  

GPS or astrolabe would be amazing. I’ve had a few discussions with people working on cytochrome spectroscopy – a possibility to assess mitochondrial “happiness,” which could give us an oxygenation endpoint. Then we could have a trial that might end up showing which degree of mitochondrial oxygenation is optimal, if any.

I know I am playing a bit of a devil’s advocate and that, in strict numbers, I probably don’t give a lot less fluid or a lot slower than most, but I think it is important to keep our minds open to change rather than keep a clenched fist around the ideas we have. 

When we have two docs debating whether IVC, SVV, carotid flow time (I do like Vicki’s stuff a lot) or something else, I think we are mostly in the grey zone, and the good thing is that either way, we are dealing with two docs who are aware and conscientious and doing the rest of the right things. But keep in mind there are a lot of docs out there who are in the acute care front lines who believe that bicarb “buffers” lactate. And by buffers they understand “neutralizes.”

I just hope that when the GPS comes along, we don’t lose ten years of knowledge translation time because we are still clinging to (at that point) outdated ideas like the IVC ultrasound… 😉

cheers and thanks so much for contributing fantastic material!

Philippe

Marco says:

Philippe, I really feel like being on your same wavelength when I read your posts about fluid responsiveness. I think it’s obviously easy to agree that a bleeding hypovolemic patient is fluid responsive AND needs fluids, but the more accurately I think about the physiology of fluid resuscitation when a nurse is asking me “should we give him some fluids?” the more I realise that the “grey zone” is large and its upper limit is not easily detectable. Probably if you fill your patients to the point where they are no more fluid responsive, you are sure that no more fluid is needed, but you should be able to stop a bit earlier.
Blunt instruments and measures are an issue, and integration of the data is a possible solution (at least until a GPS comes along), but critical thinking is always a valuable resource.
The more I grow old the more I become minimalist in my approach to the “chronic acute ill” patient (90% of the patients on an ordinary day in my ICU). If a patient is in the grey zone, with a reasonably good hemodynamic stability, some vasopressor support, low dose diuretics and his urine output decreases, probably the decision of giving him fluids OR diuretics would be equally harmful. When a patient is in the grey zone and your instruments are not so accurate, it’s better to keep him safely in the grey zone. When you are in the mountains, you are caught in a snowstorm and cannot find your tracks, the safest decision is to stop and wait.. or follow your GPS 😉

Marco

thanks!

You hit the nail on the head with “integration is key.”

Philippe