High cardiac output shock

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leviathan

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Hypothetical scenario: You've got a patient with septic shock. Bedside RN pages you to say their urine output is falling off and their levophed requirements are going up. You determine their cardiac output is actually 10L/min. Is there any role for more IV fluids, even if you determine the patient is fluid responsive?

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When you say the patient is "fluid responsive", is this based on something like pulse pressure variation? Do we know the patient's CVP?
 
Hypothetical scenario: You've got a patient with septic shock. Bedside RN pages you to say their urine output is falling off and their levophed requirements are going up. You determine their cardiac output is actually 10L/min. Is there any role for more IV fluids, even if you determine the patient is fluid responsive?

Is the tank full yet?

So what if the pump is overdrive and doing twice the normal amount of work? That is awesome, if you need to be moving that much fluid to keep perfusing everything. Hope it is sturdy enough to take it. Remember that during periods of high metabolic demand, the average healthy young person's heart can go up to 20L/min. An athlete might be able to push that to 35/min during vigorous exercise. Your sickie is just at 10L. They aren't running a marathon, but their body is stressed by the infection and they have systemic vasodilation from the inflammatory mediators that are causing their shock. It makes sense that they would have a higher output.

But if the tank (SVR) is not adequately juicy, you should probably top it up. Water your patient as long as they are responding to fluid. What are you saving by holding back that IV? What are you harming by giving it? Fill the tank, perfuse the kidneys (and brain and other incidental organs) and save the patient. If you get them too wet, there is an answer for that, too... but one that is a lot easier if the kidneys aren't dead.
 
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Hypothetical scenario: You've got a patient with septic shock. Bedside RN pages you to say their urine output is falling off and their levophed requirements are going up. You determine their cardiac output is actually 10L/min. Is there any role for more IV fluids, even if you determine the patient is fluid responsive?
Fluid-responsive does not mean hypovolemic (that must be the news of the century for some of my non-intensivist colleagues); even a healthy person is fluid-responsive. Also, low urine output probably doesn't mean anything, as long as one has a MAP over 75 (which is what the kidneys like) - higher for chronic hypertensives.

In this case, most likely the SVR is too low (MAP- CVP divided by CO times 80 = ~60/10 * 80 = 480). The solution is probably to add some vasopressin (or phenylephrine), possibly more levo (unless it produces tachycardia in the patient), not fluids. A small degree of hypovolemia is much less dangerous than iatrogenic hypervolemia.

Now if the MAP is not 70 (as assumed) but more like 110, one should maybe also dial down the levo and stop overworking the heart.

Some people (not me, I am too stupid) would also look at the degree of venous congestion in the liver and kidney, and maybe conclude that the patient is fluid overloaded, is developing the beginnings of an abdominal compartment syndrome with secondary AKI, and maybe needs diuresis (with concomitant pressor support).

Anyway, titrating fluids to some imaginary urine output target = bad medicine (especially if the kidneys are already congested). A good urine output is reassuring, but it shouldn't be a resuscitation target at all costs.
 
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But if the tank (SVR) is not adequately juicy, you should probably top it up. Water your patient as long as they are responding to fluid. What are you saving by holding back that IV? What are you harming by giving it? Fill the tank, perfuse the kidneys (and brain and other incidental organs) and save the patient. If you get them too wet, there is an answer for that, too... but one that is a lot easier if the kidneys aren't dead.
I hope you're just a student. Put down grandpa's medical books (e.g. the Surviving Sepsis Campaign) and go read/watch some modern critical care (see below).

 
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I hope you're just a student. Put down grandpa's medical books (aka the Surviving Sepsis Campaign) and go read/watch some modern critical care (see below).



LOL. Indeed, just a student. And I don't mind being schooled. Thank you for the link!
 
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I hope you're just a student. Put down grandpa's medical books (e.g. the Surviving Sepsis Campaign) and go read/watch some modern critical care (see below).



Oh, man... I'm not even 1/2 of the way through and I want to go talk this over with my mentor, because this is definitely not what I've been learning but it is pretty convincing.

The messages that I've received have been "Water the patient until the pneumonia blooms. Now you know where the source was and can tailor the abx. Now you can cope with the ARDS and fluid overload by lasix'ing them back to dehydration." And while that is colloquialized, it is basically in line with Surviving Sepsis, which I'd thought were the prevailing guidelines.

I'm going to need to get my ducks in a row and well supported if I'm going to have a conversation with my guru that the practices that I've seen with a number of ICU patients may not have supported optimal outcomes.

Can I impose on you for any further reading / resources that you might recommend? I'm not asking you to do my homework for me. Obviously, I'm going to make the most of this presentation, but if I've been led this far astray on this matter, I'm hopeful to identify some reliable sources for best practices.
 
Oh, man... I'm not even 1/2 of the way through and I want to go talk this over with my mentor, because this is definitely not what I've been learning but it is pretty convincing.

The messages that I've received have been "Water the patient until the pneumonia blooms. Now you know where the source was and can tailor the abx. Now you can cope with the ARDS and fluid overload by lasix'ing them back to dehydration." And while that is colloquialized, it is basically in line with Surviving Sepsis, which I'd thought were the prevailing guidelines.

I'm going to need to get my ducks in a row and well supported if I'm going to have a conversation with my guru that the practices that I've seen with a number of ICU patients may not have supported optimal outcomes.

Can I impose on you for any further reading / resources that you might recommend? I'm not asking you to do my homework for me. Obviously, I'm going to make the most of this presentation, but if I've been led this far astray on this matter, I'm hopeful to identify some reliable sources for best practices.
Don't feel bad. There is a reason people must do a fellowship for this (and you haven't even been through a residency). But what you describe is really bad medicine in 2018. Fluid overload has been proven again and again to worsen outcomes in sepsis (and many other situations).

All Lasix does is remove fluid from circulation; good luck if the patient has inflammation in his body that's holding the fluid in the interstitium (inflammatory edema). You've just pumped your patient's tissues full of fluid (with the associated hypoperfusion due to venous congestion and compression of capillaries by the edema). Just because you remove fluid from circulation doesn't mean that the body will feel obligated to return the fluids from the interstitium (which is a slow process, mostly through lymphatics, and not at the venous end of the capillaries as old fairy tales suggest).

I'll try to find you some starters and keep posting them here but, as I said, there is an entire fellowship and specialty about this. IV fluids are drugs, and should be given with the same suspicion and vigilance as every other drug.

https://emcrit.org/wp-content/uploads/2015/10/Br.-J.-Anaesth.-2015-Marik-bja_aev349.pdf
iSepsis- "Less is More": The New paradigm in Critical Care
PulmCrit- Killer resuscitation: Abdominal hypertension as an occult driver of multiorgan failure
Fluids in Severe Sepsis 2013
iSepsis - A 30ml/kg bolus: Yes or No -The Results
A Comment on Fluids in Sepsis

For evidence-based critical care, as a resident, if you have free Springerlink at your institution, this is a must: Evidence-Based Critical Care | Paul Ellis Marik | Springer (the link on the right for the ebook should be free). However, as an intern/student, I would recommend starting with the updated version of Marino's ICU book (meaning the updated Inkling ebook that comes for free with the print version of the last edition).

For more fun (I am sure you've seen a lot of lactate hysteria, too):



Or this:



Why the SSC is based on a flawed study, to begin with:



Nota Bene: Marik used to be considered a fanatic years ago, but most recent studies confirm his ideas.
 
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Don't feel bad. There is a reason people must do a fellowship for this (and you haven't even been through a residency). But what you describe is really bad medicine in 2018. Fluid overload has been proven again and again to worsen outcomes in sepsis (and many other situations).

Thank you, thank you, thank you.

I don't expect this to replace a residency/fellowship, but I know very well that the place that I've been learning is using some out-of-date practices. Even my beloved mentor who is on his way to a critical care fellowship has expressed concern about being behind the curve when he goes to "a real hospital..."

And since I've long since blown my anonymity, that is just about all that I ought to say on that matter. I'm just really grateful to get pointed at some resources so that I can get up to speed before I head off to intern year this summer.

It weighs heavily upon me that I'm about to be the one teaching my to own med students, and I want to be telling them current info.
 
I hope you're just a student. Put down grandpa's medical books (e.g. the Surviving Sepsis Campaign) and go read/watch some modern critical care (see below).



I like this video. It helps that it mirrors my bias and practice.

The only thing I think isn't teased out well by the current literature is if too much fluid given to some patients isn't something that harms them per se but rather merely an indicator of the super sick. A lot in the ICU is like this. Which isn't an argument for or against IV fluids, but rather some commentary that some of the studies noted in the video don't strictly show that IV fluids are harmful, merely they are associated with more "worse outcomes".
 
I like this video. It helps that it mirrors my bias and practice.

The only thing I think isn't teased out well by the current literature is if too much fluid given to some patients isn't something that harms them per se but rather merely an indicator of the super sick. A lot in the ICU is like this. Which isn't an argument for or against IV fluids, but rather some commentary that some of the studies noted in the video don't strictly show that IV fluids are harmful, merely they are associated with more "worse outcomes".

There's some indication that excessive fluids are bad for the glycocalyx and cause increased edema and inflammation. NS is worse than LR although that recent NEJM paper out of vanderbilt seems suspect (why even do a composite outcome except to publish a negative paper?)
 
There's some indication that excessive fluids are bad for the glycocalyx and cause increased edema and inflammation.

Sure. And I'm not arguing an excessive fluid position. Merely pointing out what the "excessive fluids are bad for sick patients" studies can't actually tease out. Or haven't.

It's hard to control for a single variable in any ICU study. But "sicker" patients get more fluids. Is that because they are sicker or is it because they are getting more fluid?
 
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Discussed with Beloved Mentor why the management I'd seen was so very different than what FFP shared. Turns out that there were some very defensible reasons for his approach given limitations of our particular context. (For instance, while watching the Fluid Management video, I kept thinking... "Gosh, it must be nice to have ready access to bedside echo to get realtime stroke volume measurements when you do a passive leg lift. So what to do to get a sense of that here in this foxhole? How valid is the thing I learned about estimating the effect of the maneuver based on change in artline pressure?")

I don't want to get into everything that must be skewed about the setting I learned in for "wrong" to actually make sense, but there was method to the madness and I think that the net effect was to do more good than harm given the circumstances.

Anyhow, it was bewildering to have someone that I look to as my North Star of evidence-based practice having taught me "wrong" things and I was so very grateful that he took the time (on Easter!) to address my crisis of faith. For further reading on the right way to do things, he sent me to:

University of Maryland | CCP Network

I'm probably not even critical care bound. Mentor wishes, but my calling is outpatient FM. Still, I can't deny that there is a certain fascination to unit patients and what we can do to preserve life.
 
Sure. And I'm not arguing an excessive fluid position. Merely pointing out what the "excessive fluids are bad for sick patients" studies can't actually tease out. Or haven't.

It's hard to control for a single variable in any ICU study. But "sicker" patients get more fluids. Is that because they are sicker or is it because they are getting more fluid?
Excessive fluid can lead to abdominal hypertension and ACS, liver and kidney venous congestion, decreased renal perfusion/filtration and AKI, excess lung water and interstitial pulmonary edema, (even more) decreased tissue perfusion in the edematous regions, hemodilution with anemia, coagulopathy and thrombocytopenia etc. I would argue that YES, excess fluids are bad for patients, especially if we look at secondary outcome measures (days of ICU stay, PPV, AKI, transfusions). Plus IV fluids are proinflammatory (hence their gentle action on the glycocalyx).
 
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Excessive fluid can lead to abdominal hypertension and ACS, liver and kidney venous congestion, decreased renal perfusion/filtration and AKI, excess lung water and interstitial pulmonary edema, (even more) decreased tissue perfusion in the edematous regions, hemodilution with anemia, coagulopathy and thrombocytopenia etc. I would argue that YES, excess fluids are bad for patients, especially if we look at secondary outcome measures (days of ICU stay, PPV, AKI, transfusions). Plus IV fluids are proinflammatory (hence their gentle action on the glycocalyx).

Sure. I understand the intuitive argument. I promise. The problem is the studies cited can't actually tease out if it was excess fluids that was detrimental rather than very sick patients that killed them. You may argue that perhaps excess fluids "didn't help" but you can't argue too strongly it's what killed the patients. You don't lose any cool kid points admitting this.
 
Sure. I understand the intuitive argument. I promise. The problem is the studies cited can't actually tease out if it was excess fluids that was detrimental rather than very sick patients that killed them. You may argue that perhaps excess fluids "didn't help" but you can't argue too strongly it's what killed the patients. You don't lose any cool kid points admitting this.
That's why I was talking about secondary outcomes. I care as much about them as about mortality, because one thing leads to another. I want my patients out of the ICU as soon as it's safe. I actively try to avoid doing harm, whenever I can. The enemy of good is better.

And for the kids: Fluids are Drugs (#ISICEM18 #IFAD2018) - The International Fluid Academy
 
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This is my thinking in terms of a theoretical basis to answer your question. Please correct me if I have gone astray at any point.

The only way that fluids work is by increasing cardiac output. Assuming that svo2, sao2 and hb remain constant, the % increase in your cardiac output will equal the % increase in oxygen delivery.

Therefore increasing the index from 1 to 3 is a 200% (and therefore useful) increase in DO2. Such an increase in index from fluids alone I have only ever, albeit in my extremely brief career thus far, seen in someone actively bleeding.

Even if you somehow managed to increase your index from 10 to 12 with fluids (which sounds unlikely) this would only be a 20% increase in DO2.

Therefore there must be a law of diminishing returns with increasing cardiac output and at a certain point the deleterious effects of fluid probably outweigh any gain from being 'fluid responsive'.
 
Thanks for all the feedback so far. I ask this question because I feel like fluid responsiveness is the hot topic at all the ICU conferences and in social media, on rounds with staff ICU docs etc. Give fluids to your patient until your assessment (PPV, SVV, PLR, IVC variability, whatever) shows they're no longer responsive. The problem is, giving fluids until they're on the flat end of the Starling curve is NOT a physiologic state.

So I think we are asking the wrong question. I think the first breakpoint in a resuscitation algorithm should actually be a measurement of cardiac output. If the cardiac output is low, THEN a measurement of fluid responsiveness is appropriate. However if the cardiac output is high, then fixing the vasoplegic state is the answer, not loading them with more fluids.

It's interesting that the first dissenting response I got was from a med student, because that is how a lot of my staff approach septic shock, and how the Surviving sepsis campaign seems to approach it. That said, I'm glad to hear I'm not completely off-base, as some of you seem to be on my side.
 
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That's why I was talking about secondary outcomes. I care as much about them as about mortality, because one thing leads to another. I want my patients out of the ICU as soon as it's safe. I actively try to avoid doing harm, whenever I can. The enemy of good is better.

And for the kids: Fluids are Drugs (#ISICEM18 #IFAD2018) - The International Fluid Academy

You can't even argue its the excess fluid that caused the adverse secondary outcomes. They lack that power.
 
You can't even argue its the excess fluid that caused the adverse secondary outcomes. They lack that power.
Not statistically, but on a case by case basis. Fluid overload by surgical teams does cause problems in my patients, and trying to avoid it is a constant fight. I am with @leviathan.
 
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Great discussion, I agree largely with ffp, it seems that more and more data is coming out to support that over resuscitation is likely more dangerous than under resuscitation and reliance on vasoactives. The mantra should be less “30cc/kg for all” and more “give them what they need and possibly less”.

This is refreshing, I just spent 8 weeks in the SICU where the thought was “gotta swell to get swell”.... it’s nice to be back in realm of reasonableness!


Sent from my iPad using SDN mobile
 
Sure. And I'm not arguing an excessive fluid position. Merely pointing out what the "excessive fluids are bad for sick patients" studies can't actually tease out. Or haven't.

It's hard to control for a single variable in any ICU study. But "sicker" patients get more fluids. Is that because they are sicker or is it because they are getting more fluid?

Since you've been talking to a wall - I wonder the same thing as you about all the studies that show harm. Some of the things I know are out there which seem to support the idea of fluids being bad.

1. The two African RCTs that have now come out showing harm with more fluids. Of course the external validity is argued as being extremely poor.

2. There are a few studies that used dynamic assessment of fluid status to guide resuscitation, and I think they tended to give less fluid, and in turn the outcomes were better.

3. There's one study that showed a correlation between mortality and higher CVPs. Again, maybe the patients with higher CVPs were just sicker and had more RV dysfunction (rather than being reflective of more volume), but it at least tells us the RIvers mantra of resuscitating to a CVP of 8 seems to be harmful.

4. There's one study of a conservative fluid strategy (weird protocol to bolus only if there was mottling beyond the kneecap) vs usual care, and outcomes were better in the conservative fluid arm.
 
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I feel like I'm talking to a wall a little bit.
I'm sorry. I must have missed something. I didn't mean to suggest you were wrong or to debate you, just the idea of primary "outcomes" (i.e. mortality)-based care.

Yes, one can always argue that association doesn't mean causation, but that's for mortality purposes. I don't need statistics to "prove" that fluid overload will cause pulmonary edema, increased oxygen requirements, hence intubation, VAP etc., or abdominal organ congestion and decreased tissue perfusion, hence AKI, hence bowel ischemia, or hemodilution hence unnecessary transfusions, or cardiac strain hence ischemia and heart failure, hence more hypotension and organ ischemia, hence central lines with more of their complications etc. etc. etc. And this is just the tip of the hypervolemia iceberg.

It's known pathophysiology (i.e. it's been proven before). And it's much easier to prevent than to treat. Even Hippocrates knew this. First do no harm.

Of course I am not talking about the super sick patient on 3 pressors, where the physiology is already a big mess. That ship has probably sailed. I am talking about the patient who is still salvageable, who still has time for therapeutic trials that don't involve fluids. Why fluid overload him, instead of trying pressors first? Just because it's more convenient? Why chase numbers that have been proven to mean nothing, e.g. urine output? Why not try to understand the physiology, instead of jumping on some knee-jerk protocol?

It drives me nuts when people who don't KNOW critical care and/or physiology are allowed to play fluid resuscitation. Fluid responsive does not mean hypovolemic, it only means that a fluid bolus will increase the stroke volume. So what? It does the same in healthy individuals and we don't drown them in fluids because of that. It's STUPID to treat vasodilation with fluids. If a shock is secondary to low SVR (as in OP's example), there is no reason to give fluids. IV fluids should be given only to replace loss of intravascular fluid, not for basically any hypotension (that's just PGY-1 level, no offense). People should learn how to use simple things such as a peripheral phenylephrine infusion or bolus (both SAFE peripherally), fix the MAP faster than it takes to bolus salted or lactated crap, which can't be always diuresed as easily as people think; and not wait till the patient is fluid overloaded, still hypotensive, and still needing pressors. People should learn to use a bedside echo and calculate a VTI or cardiac output, and derive a SVR (or drop a Swan for CO/SVR monitoring if TTE is too much to ask), or just use some imprecise fancy bioimpedance or waveform monitoring or whatever toy (anything is better than guessing). People should stop guesstimating fluid overload based on archaic jokes such as a chest X-ray, and learn to do a lung ultrasound, and see the increase in lung water before it's obvious clinically. And some people should start by reading Marik's EB Critical Care book (since all those great and free CCM blogs are too much for the "busy professional" anyway), and would probably become 3 times better intensivists overnight, because critical care has changed tremendously in those 10 years since they last read current literature. And some people should definitely stop TEACHING others. End of rant.
 
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I'm sorry. I must have missed something. I didn't mean to suggest you were wrong or to debate you, just the idea of primary "outcomes" (i.e. mortality)-based care.

Yes, one can always argue that association doesn't mean causation, but that's for mortality purposes. I don't need statistics to "prove" that fluid overload will cause pulmonary edema, increased oxygen requirements, hence intubation, VAP etc., or abdominal organ congestion and decreased tissue perfusion, hence AKI, hence bowel ischemia, or hemodilution hence unnecessary transfusions, or cardiac strain hence ischemia and heart failure, hence more hypotension and organ ischemia, hence central lines with more of their complications etc. etc. etc. And this is just the tip of the hypervolemia iceberg.

It's known pathophysiology (i.e. it's been proven before). And it's much easier to prevent than to treat. Even Hippocrates knew this. First do no harm.

Of course I am not talking about the super sick patient on 3 pressors, where the physiology is already a big mess. That ship has probably sailed. I am talking about the patient who is still salvageable, who still has time for therapeutic trials that don't involve fluids. Why fluid overload him, instead of trying pressors first? Just because it's more convenient? Why chase numbers that have been proven to mean nothing, e.g. urine output? Why not try to understand the physiology, instead of jumping on some knee-jerk protocol?

It drives me nuts when people who don't KNOW critical care and/or physiology are allowed to play fluid resuscitation. Fluid responsive does not mean hypovolemic, it only means that a fluid bolus will increase the stroke volume. So what? It does the same in healthy individuals and we don't drown them in fluids because of that. It's STUPID to treat vasodilation with fluids. If a shock is secondary to low SVR (as in OP's example), there is no reason to give fluids. IV fluids should be given only to replace loss of intravascular fluid, not for basically any hypotension (that's just PGY-1 level, no offense). People should learn how to use simple things such as a peripheral phenylephrine infusion or bolus (both SAFE peripherally), fix the MAP faster than it takes to bolus salted or lactated crap, which can't be always diuresed as easily as people think; and not wait till the patient is fluid overloaded, still hypotensive, and still needing pressors. People should learn to use a bedside echo and calculate a VTI or cardiac output, and derive a SVR (or drop a Swan for CO/SVR monitoring if TTE is too much to ask), or just use some imprecise fancy bioimpedance or waveform monitoring or whatever toy (anything is better than guessing). People should stop guesstimating fluid overload based on archaic jokes such as a chest X-ray, and learn to do a lung ultrasound, and see the increase in lung water before it's obvious clinically. And some people should start by reading Marik's EB Critical Care book (since all those great and free CCM blogs are too much for the "busy professional" anyway), and would probably become 3 times better intensivists overnight, because critical care has changed tremendously in those 10 years since they last read current literature. And some people should definitely stop TEACHING others. End of rant.

Ok. Though I think your soap box is misplaced time and energy in response to my simple point.
 
Ok. Though I think your soap box is misplaced time and energy in response to my simple point.
It wasn't in response to YOU. I have nothing but respect for you (and for most frequent posters on this subforum).

It was in response to the idea that just because some stuff hasn't been proven yet, we should continue harming patients. Yes, when a patient needs to be treated because of iatrogenic hypervolemia it's harm, even if it's just with Lasix (it's usually much more than that). People have forgotten to avoid hurting patients, before anything else. When unsure, we should just watch and think, not do "something". That's what the rant was about.

It was also about this: PulmCrit- Chasing mortality endpoints is a fool's errand

"As critical care evolves, our goals mature beyond merely keeping patients alive. For example, if a patient with septic shock survives but develops end-stage renal failure, that's not a great outcome. The family may be thrilled that the patient survived, but I'm not – my goal is return of all organ functions. With ongoing progress, there will be a greater focus on “soft” outcomes such as:

  • Avoidance of chronic renal insufficiency, heart failure, or pulmonary limitation
  • Avoidance of delirium, depression, PTSD, or long-term cognitive dysfunction
  • Improved strength, increased discharge to home, increased return to work
  • More vent-free days and ICU-free days (surrogates for ICU-related morbidity)
These outcomes are hugely important to patients. None of them involves mortality. A narrow-minded focus solely on mortality ignores the benefits that we can offer our patients by improving these outcomes." - Josh Farkas
 
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This is my thinking in terms of a theoretical basis to answer your question. Please correct me if I have gone astray at any point.

The only way that fluids work is by increasing cardiac output. Assuming that svo2, sao2 and hb remain constant, the % increase in your cardiac output will equal the % increase in oxygen delivery.

Therefore increasing the index from 1 to 3 is a 200% (and therefore useful) increase in DO2. Such an increase in index from fluids alone I have only ever, albeit in my extremely brief career thus far, seen in someone actively bleeding.

Even if you somehow managed to increase your index from 10 to 12 with fluids (which sounds unlikely) this would only be a 20% increase in DO2.

Therefore there must be a law of diminishing returns with increasing cardiac output and at a certain point the deleterious effects of fluid probably outweigh any gain from being 'fluid responsive'.
Especially in sepsis, the problem is not as much the DO2, but the fact that the body is not able to use it. That's why the Rivers EGDT with all his inotropes and ScvO2 monitoring and transfusions failed. Beyond a certain level, there is no benefit in increasing oxygen delivery. And it kind of makes sense. We see all kinds of studies that show that the enemy of good is better, that the body doesn't like O2 that much, that a saturation of 92-94% is less toxic than 100%.

Also, increasing cardiac output or volemia do not necessarily lead to a better tissue perfusion; I would argue that tissue edema from fluid overload will actually decrease peripheral perfusion, simply by compressing those capillaries and by creating venous congestion. Perfusion pressure is always pressure at the arterial end minus the higher between tissue compartment pressure and pressure at the venous end. We tend to focus so much on the arterial end (MAP), but forget about the rest.

If we create venous congestion and tissue edema by giving too much fluid, the increase in MAP may not improve much, because capillary perfusion may actually worsen.

Soapbox over.
 
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Especially in sepsis, the problem is not as much the DO2, but the fact that the body is not able to use it. That's why the Rivers EGDT with all his inotropes and ScvO2 monitoring and transfusions failed. Beyond a certain level, there is no benefit in increasing oxygen delivery. And it kind of makes sense. We see all kinds of studies that show that the enemy of good is better, that the body doesn't like O2 that much, that a saturation of 92-94% is less toxic than 100%.

Also, increasing cardiac output or volemia do not necessarily lead to a better tissue perfusion; I would argue that tissue edema from fluid overload will actually decrease peripheral perfusion, simply by compressing those capillaries and by creating venous congestion. Perfusion pressure is always pressure at the arterial end minus the higher between tissue compartment pressure and pressure at the venous end. We tend to focus so much on the arterial end (MAP), but forget about the rest.

If we create venous congestion and tissue edema by giving too much fluid, the increase in MAP may not improve much, because capillary perfusion may actually worsen.

Soapbox over.

No disagreement from me there. I was just pointing out that even if you just focus on overly simplistic DO2 alone, driving an already high cardiac output higher probably doesn't even add much theoretical benefit.
 
You can't even argue its the excess fluid that caused the adverse secondary outcomes. They lack that power.

Lets start to not give epinephrine in cardiac arrest situations because those studies lack power and only have Class IIB recommendations. We can't even argue that its the epinephrine that caused ROSC. :unsure:
 
Lets start to not give epinephrine in cardiac arrest situations because those studies lack power and only have Class IIB recommendations. We can't even argue that its the epinephrine that caused ROSC. :unsure:

You are missing the point.

Of course too much of anything is bad. And perhaps none of something (pressors) is bad.

The topic being discussed and in particular addressed by me per my point regarding Marik's presentation was about *how much* fluid was particularly detrimental. The difference here between treatment groups was literally a few liters in the studies cited. Is this what *caused* the patients to be sicker and do worse? Marik's intuitive argument is "yes" but the studies he uses to support this don't actually say this as they don't tease out how sick the patients were who got the additional fluid.

This is not an argument for simply dumping crystalloid into patients.

I can always count on you to not get it and or try for a cheap shot. Keep it classy.
 
Lets start to not give epinephrine in cardiac arrest situations because those studies lack power and only have Class IIB recommendations. We can't even argue that its the epinephrine that caused ROSC. :unsure:

Is that really your argument?? If so, there is some signal in some of the data that epi may be harmful. Your analogy is truly awful.
 
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