Edwards Clearsite & noninvasive monitoring

[Airlife91]

We have a decently busy ortho trauma service at my shop, and we do a lot of hip fractures on the typical old/frail people falls. Apparently the trauma Service at my hospital has had issues with patients being under-resuscitated while in the hospital (they’ve been trending lactates during their stay to determine this). Now the trauma service has requested we apply the Edwards clearsite on ALL hip Fx surgeries and resuscitate with a goal directed approach using the clearsite SVV as guidance.
My personal experience with this device is poor. Seems to fail frequently and/or give unreliable data. Maybe I’m just cursed and have bad luck. Anyone use it regularly for this, or have any thoughts on mandating it for all hip fix surgeries?

As a CV anesthesiologist, if I’m truly worried about CO, resuscitation, and Hemodynamic monitoring I’ll use a traditional A-line (utilizing SPV, PPV, ABGs, lactates), quick preop/post-op TTEs that I do myself, and Intraop TEE in really fragile patients. But a lot of my partners either aren’t comfortable with that or don’t want to do it, hence this blanket policy to use clearsite.

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[caligas]

We have a decently busy ortho trauma service at my shop, and we do a lot of hip fractures on the typical old/frail people falls. Apparently the trauma Service at my hospital has had issues with patients being under-resuscitated while in the hospital (they’ve been trending lactates during their stay to determine this). Now the trauma service has requested we apply the Edwards clearsite on ALL hip Fx surgeries and resuscitate with a goal directed approach using the clearsite SVV as guidance.
My personal experience with this device is poor. Seems to fail frequently and/or give unreliable data. Maybe I’m just cursed and have bad luck. Anyone use it regularly for this, or have any thoughts on mandating it for all hip fix surgeries?

As a CV anesthesiologist, if I’m truly worried about CO, resuscitation, and Hemodynamic monitoring I’ll use a traditional A-line (utilizing SPV, PPV, ABGs, lactates), quick preop/post-op TTEs that I do myself, and Intraop TEE in really fragile patients. But a lot of my partners either aren’t comfortable with that or don’t want to do it, hence this blanket policy to use clearsite.

it’s a tool, sometimes useful. Blanket use is ridiculous.

 

[nimbus]

Is your trauma service involved in all run of the mill hip fractures? They usually don’t require any resuscitation and are followed by hospitalists where I am.

 

[Endee]

We use these routinely for major abdominal cases and I find them extremely unreliable. I can only get a good waveform like 25% of the time.

 

[MoMoGesiologist]

I think they work pretty well from my N=3.

However, you don’t need a clearsite to resuscitate someone. Sounds like your place is having other issues. Are these pts on the IM or surgery service? Why not just give more fluids? Or maybe just stop measuring lactate? Unless if your place is having issues with pts having MIs, AKI, organ dysfunction from under resuscitation, why go through all this?

 

[Airlife91]

Yes, trauma service manages all hip fx patients, and medicine is consulted if needed.

yes they claim to have been having post-op issues with organ dysfunction, which they’ve attributed to intra-op under-resuscitation. I’m sometimes that is true.

my main point is:
- blanket use is stupid and unnecessary
- my n of 30ish is that the monitor is unreliable at best. Works really well on people who don’t need them (ie healthy people).
- I can assess for adequate resuscitation using many other methods, most of which obviate the need to spend ~$220 on a clearsite probe.

 

[MoMoGesiologist]

Resuscitate based on capillary refill!

Effect on Septic Shock Mortality of Resuscitation Targeting Peripheral Perfusion vs Serum Lactate Levels

This randomized trial compares the effects of resuscitation strategies targeting normalization of capillary refill time vs normalization or decrease of serum lactate levels on 28-day mortality among patients with septic shock.

jamanetwork.com

 

[T-burglar]

Ive always found that people use the term “Under resuscitated” to mean that not enough volume was given.

Please believe that lactate physiology is a little more complex than that and also that there are 1001 things that could be wrong in an elderly trauma patient that won’t be fixed by “giving more resuscitation”.

As a CV anesthesiologist you obviously know all this . Consider the knowledge and skill required to interpret a patient’s physiologic status from a set of TEE images and RHC data and then decide if a device that magically Intuits the cardiac output from some bull**** algorithM should be anywhere but the trash

 

[Ronin786]

Sounds like a setup for disaster. And if I'm the anesthesiologists I'd be incredibly offended that my judgement is being replaced with a bull**** device, but that's the disrespect that comes with the job.

I'd start off by providing the trauma service with literature regarding the relationship of lactate with resuscitation and other causes of hyperlactemia, but I'd be surprised if they listened since old habits die hard. Then I'd find the Edwards rep and murder them in their sleep for peddling their little box of lies.

Seriously, there is zero evidence that these devices do what they say and even more data to suggest that more numbers does not equal to better outcomes. But there's money to be made and pretty reps shaking their tail, so hospitals bite.

 

[MoMoGesiologist]

Sounds like a setup for disaster. And if I'm the anesthesiologists I'd be incredibly offended that my judgement is being replaced with a bull**** device, but that's the disrespect that comes with the job.

I'd start off by providing the trauma service with literature regarding the relationship of lactate with resuscitation and other causes of hyperlactemia, but I'd be surprised if they listened since old habits die hard. Then I'd find the Edwards rep and murder them in their sleep for peddling their little box of lies.

Seriously, there is zero evidence that these devices do what they say and even more data to suggest that more numbers does not equal to better outcomes. But there's money to be made and pretty reps shaking their tail, so hospitals bite.

To play devils advocate: if the MDAs judgements are so good, why are the trauma pts being so under resuscitated in the OR and having bad postop outcomes (according to them)?

 

[T-burglar]

To play devils advocate: if the MDAs judgements are so good, why are the trauma pts being so under resuscitated in the OR and having bad postop outcomes (according to them)?

Out of curiosity , what does “under resuscitated” mean to you. How do you decide how many liters of resuscitation to give ?

 

[dchz]

The only thing more unbelievable about being forced to use ClearSight is that trauma is basing their decision making on Lactate rather than Base Deficit...

Sounds like a setup for disaster. And if I'm the anesthesiologists I'd be incredibly offended that my judgement is being replaced with a bull**** device, but that's the disrespect that comes with the job.

I'd start off by providing the trauma service with literature regarding the relationship of lactate with resuscitation and other causes of hyperlactemia, but I'd be surprised if they listened since old habits die hard. Then I'd find the Edwards rep and murder them in their sleep for peddling their little box of lies.

Seriously, there is zero evidence that these devices do what they say and even more data to suggest that more numbers does not equal to better outcomes. But there's money to be made and pretty reps shaking their tail, so hospitals bite.

At least they are not using base deficits? I think this is a step forward by trauma.

OP, there are so many assumptions here it's ridiculous to make it apply to everyone:

Increased lactate is due to lactic acidosis.
Lactatic acidosis is due to hypoperfusion.
Hypoperfusion is due to low CO.
Low CO is due to hypovolemia.
Pt's heart is working at the point where increase pre load actually increases contractility, not the other way around.
Clearsight correlates with A line near 100% of the time.
You are venting with TV of 8-10cc/kg of ideal body weight.
The pt is NSR.

if and only if all the above is true should you use clear sight (btw it's spelld SIGHT) to calculate the SVV.

Last time i checked the sensor is $200ish per use, no? what if you just paid every anesthesiologist in your shop $200 everytime the lactate is below 3 at the end of the case?

 

[deleted875186]

Out of curiosity , what does “under resuscitated” mean to you. How do you decide how many liters of resuscitation to give ?

I could play devils advocate and say some people had bad outcomes because they are sick frail old people that broke a hip.

 

[MoMoGesiologist]

Out of curiosity , what does “under resuscitated” mean to you. How do you decide how many liters of resuscitation to give ?

In the words of someone smarter than me on this forum (I forget who), “gotta swell to get well!”

 

[T-burglar]

Hyperlactatemia isn’t due to hypoperfusion. It’s a marker of major stress and sympathetic activation and can occur in any situation that fits that description. Give an otherwise healthy or well compensated person moderate to high dose epinephrine by infusion and measure lactate some time if you’re bored.

And momo I was making fun of you for equating resuscitation with “more fluid” . There are Lots of resuscitative interventions that don’t involve fluid administration. A patient is “resuscitated” when you’ve stabilized them from whatever ails them. How do you resuscitate a tension pneumothorax? 500 ml or 1 liter of resuscitation ?

 

[Ronin786]

The only thing more unbelievable about being forced to use ClearSight is that trauma is basing their decision making on Lactate rather than Base Deficit...



At least they are not using base deficits? I think this is a step forward by trauma.

OP, there are so many assumptions here it's ridiculous to make it apply to everyone:

Increased lactate is due to lactic acidosis.
Lactatic acidosis is due to hypoperfusion.
Hypoperfusion is due to low CO.
Low CO is due to hypovolemia.
Pt's heart is working at the point where increase pre load actually increases contractility, not the other way around.
Clearsight correlates with A line near 100% of the time.
You are venting with TV of 8-10cc/kg of ideal body weight.
The pt is NSR.

if and only if all the above is true should you use clear sight (btw it's spelld SIGHT) to calculate the SVV.

Last time i checked the sensor is $200ish per use, no? what if you just paid every anesthesiologist in your shop $200 everytime the lactate is below 3 at the end of the case?

I disagree. Lactate and base deficit are both equally terrible markers of resuscitation. So many factors go into either number that making any judgement as a result is foolhardy.

They're both highly non-specific numbers that result in knee-jerk administration of potentially deleterious crystalloids. Stupid line of thought that the Edwards folks are certainly happy to take advantage of with their murky sight bull****.

 

[deleted697535]

Id fight the carpenters on this.

Yeah they're sick old people that die periop. Ain't no way in **** anyone can convincingly prove that's down to getting a couple litres of ringers intraop or no

Lactate? The ****? Who's 'research' is this? An r1 in ortho?

I think you should use cvp instead

 

[T-burglar]

Persistently elevated lactate in a fresh post op trauma patient needs to be investigated , not just thrown more fluid

 

[DocVapor]

My gut reaction is that it sounds like they should take better care of their patients.

 

[dchz]

I disagree. Lactate and base deficit are both equally terrible markers of resuscitation. So many factors go into either number that making any judgement as a result is foolhardy.

They're both highly non-specific numbers that result in knee-jerk administration of potentially deleterious crystalloids. Stupid line of thought that the Edwards folks are certainly happy to take advantage of with their murky sight bull****.

Correct me if i'm wrong: trauma lit used to be littered with base deficit because it was a good surrogate marker for lactate. the thought is that lactate could be the result of hypoperfusion (type A lactic acidosis, but there are other causes of lactic acidosis), using lactate to predict lactate is better than using base deficit to predict lactate.

With regards to them being non-specific, I agree it's not specific. Hence the first two assumptions in my post you quoted. However, your beef is in the misinterpretation of the data, not the data itself.

DDx for a high lactate is much narrower for hypoperfusion than the DDx for a high base deficit. Therefore, lactate is better.

Blaming the lactate for the knee jerk reaction is like blaming the helicopter instead of the pilot.

 

[Ronin786]

Correct me if i'm wrong: trauma lit used to be littered with base deficit because it was a good surrogate marker for lactate. the thought is that lactate could be the result of hypoperfusion (type A lactic acidosis, but there are other causes of lactic acidosis), using lactate to predict lactate is better than using base deficit to predict lactate.

With regards to them being non-specific, I agree it's not specific. Hence the first two assumptions in my post you quoted. However, your beef is in the misinterpretation of the data, not the data itself.

DDx for a high lactate is much narrower for hypoperfusion than the DDx for a high base deficit. Therefore, lactate is better.

Blaming the lactate for the knee jerk reaction is like blaming the helicopter instead of the pilot.

The whole premise is that base deficit = acidosis = hypoperfusion. The lactate is irrelevant to that discussion.

This becomes a needlessly academic discussion, but I would suggest that in a trauma patient, acidosis (and indirectly base deficit) is more indicative of hypoperfusion than hyperlactemia. The lactate can be elevated simply because of pain! It can't get any more non-specific than that.

They both ****ing suck.

 

[dannyboy1]

If a patient is normotensive under a full MAC of GA w/o the need for pressors they are adequately resuscitated. No need for the stupid clearsight.

 

[dchz]

The lactate can be elevated simply because of pain! It can't get any more non-specific than that.

Not to the degree of bad hypoperfusion. Most cardiologists would agree that epi induced lactate elevation is very minimal compared to hypo perfusion. And yes it can get more nonspecific than that, you can have it go up due to pain and due to NS infusion (base deficit).

Regardless, lactate is more specific than Base Deficit, so it is a better test for ruling in certain things. The discussion is academic, but not needless. Because we would do others a disservice if we made them think lactate and base deficit are the same ****ty test. That's like saying chest x-ray and TTE are both ****ty tests for PE because they are both nonspecific. TTE is way more specific than CXR and lactate is way more specific than base deficit.

Finally, I still maintain your problem is with the operator and not the test. To which I 100% agree.

 

[vector2]

Not to the degree of bad hypoperfusion. Most cardiologists would agree that epi induced lactate elevation is very minimal compared to hypo perfusion. And yes it can get more nonspecific than that, you can have it go up due to pain and due to NS infusion (base deficit).

Regardless, lactate is more specific than Base Deficit, so it is a better test for ruling in certain things. The discussion is academic, but not needless. Because we would do others a disservice if we made them think lactate and base deficit are the same ****ty test. That's like saying chest x-ray and TTE are both ****ty tests for PE because they are both nonspecific. TTE is way more specific than CXR and lactate is way more specific than base deficit.

Finally, I still maintain your problem is with the operator and not the test. To which I 100% agree.

I see a dime a dozen young patients involved in some non- life threatening, no major organ damage trauma who get a trauma panel sent in the ED. They're normotensive, normal HR, Hgb 15, but the lactate is 2 and the CO2 is mildly decreased on BMP. These people were fine 30 min ago and now the only change is that they have a bruise on their shoulder. My hypothesis is that the catecholamine surge can elevate lactate to a more significant level than one thinks.

 

[wanttoreadforum]

Lactate, like every test or imaging study, needs to be correlated to the clinical picture. But to say that it is somehow a worthless marker of hypoperfusion is silly. It can absolutely be indicative of an under-resuscitated patient. Equally silly is to point to a lactate of 2 in a hemodynamically stable patient awake and use that as your sole determining factor that they are under-resuscitated. In fact, I'd say it's a great investigative tool in lieu of a PAC or TEE, as long as you use other data available to you.

What else is the patient telling you? Are they tachycardic? Are they hypotensive requiring a vasopressor? What's the CVP? What's the urine output? How much blood have they lost? Are their extremities warm or cool to the touch? None of these are particularly useful independently, but together you will start to get an idea of how the patient is doing.

If they have sinus tachycardia, have made 20 cc of urine in the last 3 hours, the orthopedists are covered in blood, you're on 80 mcg/min of phenylephrine, your lactate is 5, and you've given 500 cc of LR during the case then yes, you're probably under-resuscitated.

To throw the test (and base deficit) in the trash just because it's non-specific is ridiculous. To force anesthesiologists to use a Clear Sight for every case is also ridiculous.

 

[vector2]

If they have sinus tachycardia, have made 20 cc of urine in the last 3 hours, the orthopedists are covered in blood, you're on 80 mcg/min of phenylephrine, your lactate is 5, and you've given 500 cc of LR during the case then yes, you're probably under-resuscitated.

This is obviously not a scenario where a clear sight is needed. And similarly as you point out neither is the totally hemodynamically stable pt whose only lab derangement is a mildly elevated lactate. The OP is describing one of those equivocal spots where I'm sure they were competent enough to resus the hip fx pts to the traditional measures you describe, but yet the lactate remained elevated.

 

[wanttoreadforum]

I think we agree. It's difficult to take a single measurement of lactate and make any determination.

But OP stated they are trending the lactates. I would posit that if your lactate is still increasing (with soft blood pressures and other clinical signs as noted above, in the absence of major cardiac/hepatic disease), you're probably behind. If it's decreasing, then no one should be reaching for more crystalloid to treat a lactate of 3.

 

[T-burglar]

THERE ARE OTHER REASONS FOR HYPERLACTATEMIA IN A TRAUMA PATIENT BESIDES “BEING BEHIND”

 

[dchz]

But OP stated they are trending the lactates. I would posit that if your lactate is still increasing (with soft blood pressures and other clinical signs as noted above, in the absence of major cardiac/hepatic disease), you're probably behind. If it's decreasing, then no one should be reaching for more crystalloid to treat a lactate of 3.

You're taking for granted the assumption that the pt is volume responsive. Which is a big assumption in the 80 years old population.

 

[wanttoreadforum]

THERE ARE OTHER REASONS FOR HYPERLACTATEMIA IN A TRAUMA PATIENT BESIDES “BEING BEHIND”

No kidding. I don't think anyone would argue to the contrary. To do so would be to disregard the fundamentals of what an elevated serum lactate represents. Like all things in medicine, there is nuance here, which is why an elevated lactate needs to be taken into account with the entire clinical picture. If a service is arguing that a single elevated lactate should trigger a reflexive administration of crystalloid, I agree that is absurd. What it should trigger is an investigation into why and trending the value.

But in a general sense, if the patient's injuries are addressed, there was an appreciable degree of blood loss, their cardiac function is intact, their liver isn't dysfunctional, they don't have a massive thiamine deficiency, you're titrating up vasopressors, and your lactates are increasing it can certainly be an indicator that you are, in fact, behind.

Don't you think?

 

[deleted162650]

You're taking for granted the assumption that the pt is volume responsive. Which is a big assumption in the 80 years old population.

Hence the Clear****e.

(Pun intended)

 

[IlDestriero]

I can’t remember if this is the one that the PICU wants to trial for some patients or if it’s the one they trialed and referred to as a random number generator?
They’re pushing to trial these things in peds but from our experience, too many things have to be perfect for them to give good data and the patients that really need something like this the most are never perfect.

 

[Ronin786]

The lactate epidemic is very frustrating. This is why it's a terrible marker of anything. It induces knee-jerk responses. The level of "behind ness" you have to be to get a lactate elevation is absurdly high. Sure there are people who can appreciate the nuance of what a lactate means, but clearly the kind of folks trying to rely on the clearsite are not the type.

Identification of the critical oxygen delivery for anaerobic metabolism in critically ill septic and nonseptic humans - PubMed

The critical O2 delivery for anaerobic metabolism was identified from the biphasic relationship between O2 delivery and O2 consumption in individual humans. The critical O2 delivery is considerably lower than previously reported in humans with the use of pooled group data. Sepsis does not alter...

www.ncbi.nlm.nih.gov

"In adults this translates into a hemoglobin of 4g/dl and a cardiac index of just over 1 L/minM2."

iSepsis - The Lactate Myths

Lactate the Myths. Lactate is good for the patient and not bad.

emcrit.org

It's a terrible marker of hypo perfusion and just as useless as the base deficit or whatever other single number that anybody wants to hang their hat on.

 

[nimbus]

Relevant editorial

PulmCCM | Substack

Life, death and the ICU. Click to read PulmCCM, a Substack publication with tens of thousands of subscribers.

pulmccm.org

 

[dchz]

It's a terrible marker of hypo perfusion and just as useless as the base deficit or whatever other single number that anybody wants to hang their hat on.

The article has many fallacies and assumption. Specifically this is in regards to septic patients, not the patients with traumatic join surgeries. But let's say I grant you the article is 100% true. It still does not support the bolded portion of your post.

Lactate is more specific than base deficit. To categorize them both as the same is to ignore science and facts.

 

[Ronin786]

The article has many fallacies and assumption. Specifically this is in regards to septic patients, not the patients with traumatic join surgeries. But let's say I grant you the article is 100% true. It still does not support the bolded portion of your post.

Lactate is more specific than base deficit. To categorize them both as the same is to ignore science and facts.

And you have yet to provide any evidence for that assumption...

 

[dchz]

And you have yet to provide any evidence for that assumption...

Quoting from the same EM crit website:

https://emcrit.org/wp-content/uploads/2016/05/27140683_-Stewart-Acid-Base_-A-Simplified-Bedside-Approach.pdf

The whole premise is that base deficit = acidosis = hypoperfusion. The lactate is irrelevant to that discussion.

I disagree. The whole premise is base-excess ~ lactate = acidosis = hypoperfusion.

"Base-excess = Na-Cl effect + lactate effect + albumin effect + OI effect." from the article quoted.

The classic dogmatic use in trauma literature is that assuming Na-Cl effect, Albumin effect, and Other Ion Effect are all stable in the trauma population, the base excess is used to approximate the lactate:

Base-excess = lactate effect ONLY when Na-Cl, albumin, and other ions are all constant.

Assuming lactate is a marker of poor perfusion, base excess was essentially a means to guestimate a (not-so-perfect marker) of poor perfusion. With modern point of care blood gases, the lactate no longer needs to be approximated. You no longer have to worry about NaCl effect, which is huge because this trauma population are getting random boluses of crystalloids.

Lactate directly measures the marker of poor perfusion, where as base-excess is convoluted by Na-Cl effect, Albumin effect, and Other Ion effect. Therefore lactate is way more specific than base-excess. Lactate is not a perfect marker by any means. But it's better than the base-excess. To say they are the same is to be misleading people for the sake of hyperbole.

 

[T-burglar]

As someone else said, you have to lose a ton of volume to start seeing lactate in the blood. And the lactate is not from anaerobic metabolism, it’s a marker of stress.

Global hypoperfusion to the point of inadequate oxygen delivery for basic functions and anaerobic metabolism kills you in minutes. You don’t languish in the ICU for a couple days if you’re truly into global anaerobic metabolism territory

 

[Ronin786]

Quoting from the same EM crit website:

https://emcrit.org/wp-content/uploads/2016/05/27140683_-Stewart-Acid-Base_-A-Simplified-Bedside-Approach.pdf

I disagree. The whole premise is base-excess ~ lactate = acidosis = hypoperfusion.

"Base-excess = Na-Cl effect + lactate effect + albumin effect + OI effect." from the article quoted.

The classic dogmatic use in trauma literature is that assuming Na-Cl effect, Albumin effect, and Other Ion Effect are all stable in the trauma population, the base excess is used to approximate the lactate:

Base-excess = lactate effect ONLY when Na-Cl, albumin, and other ions are all constant.

Assuming lactate is a marker of poor perfusion, base excess was essentially a means to guestimate a (not-so-perfect marker) of poor perfusion. With modern point of care blood gases, the lactate no longer needs to be approximated. You no longer have to worry about NaCl effect, which is huge because this trauma population are getting random boluses of crystalloids.

Lactate directly measures the marker of poor perfusion, where as base-excess is convoluted by Na-Cl effect, Albumin effect, and Other Ion effect. Therefore lactate is way more specific than base-excess. Lactate is not a perfect marker by any means. But it's better than the base-excess. To say they are the same is to be misleading people for the sake of hyperbole.

So you introduce NaCl and ions as a confounder for base deficit and neglect stress, catecholamine surge and clearance as confounders for lactate. Gotcha.

Acidosis occurs independent of lactate production. Until you can show me a non-dogmatic piece of evidence that lactate production occurs as a result of global hypoperfusion at non-critical levels of ischemia, then it is no better than the base deficit.

It is a meaningless marker of perfusion.

 

[dchz]

So you introduce NaCl and ions as a confounder for base deficit and neglect stress, catecholamine surge and clearance as confounders for lactate. Gotcha.

Not sure if you're trolling being dense on purpose or truly don't understand the difference between base excess and lactate. I am going to give you the benefit of the doubt and answer non-sarcastically: I did not neglect anything. stress, catecholamine surge, and decreased clearance are confounders for BOTH lactate and base excess. But lactate is more specific because it is not confounded by NaCl, albumin, or other ions. You keep saying it is no better than base excess over and over again despite me giving you evidence to the contrary. It clearly is better because it has less confounders. It is not perfect. But it is better.

Acidosis occurs independent of lactate production.

Yes acidosis can occur independently, some ways include respiratory acidosis, lowering strong ion difference by NaCl, albumin, or other ion (entire mudpiles DDx). I fail to see how this contributes to your argument that lactate is no better than base excess.

Until you can show me a non-dogmatic piece of evidence that lactate production occurs as a result of global hypoperfusion at non-critical levels of ischemia, then it is no better than the base deficit.

I honestly don't know how else to tell you that lactate is more specific. It's very easy to label chemistry as "dogmatic" but i assure you that it's not dogma and many chemists smarter than you and I have spent their lives contributing to that science:

Base-excess = [Na-Cl-35] + [1-lactate] + [.25x (42-albumin)] +other ions.

Are you disagreeing that above equation is true?

Are you asking me to show you that type A lactic acidosis occurs? Are you asking me to show you in my own chemistry lab how the green arrow occurs, otherwise you wouldn't believe me?!?

No one has argued that blind reflex of seeing blind lactate and then bolusing the patient is optimal treatment. Also no one is arguing that all lactate increases results from hypoperfusion. Hence my previous outline of assumptions starts with:

Increased lactate is due to lactic acidosis.
Lactatic acidosis is due to hypoperfusion.

Finally, I feel like you keep changing my assertions just so you can disagree with me. I have made 0 claims that lactate is a perfect marker of hypoperfusion. I simply said over and over again that it is better and more specific than base excess. To which you keep showing me evidence that lactate is not a great marker of hypoperfusion (which wasn't my argument in the first place), and somehow that proves lactate and base excess are the same. I have to tell ya, I feel like i'm having an argument on facebook with an anti-vaxxer here.

So if i'm unclear let me state my stance very clearly one last time before you show me more evidence that argues against something I didn't claim:

Lactate elevation does not equal hypoperfusion, it has the same DDx as tachycardia.
Lactate elevation is more specific for hypoperfusion than base excess.

That is all. Why did i just spend the last 30 mins typing this... i've already waste too much of my time. This is all i'm contributing to this boards understanding of basic biochemistry.

 

[Ronin786]

Lactate elevation does not equal hypoperfusion, it has the same DDx as tachycardia.
Lactate elevation is more specific for hypoperfusion than base excess.

I am not being dense. I am challenging the basic premise that everybody takes as gospel with absolutely nothing to prove it. And thank you for the biochemistry lesson, none of it is new.

Cut off blood supply to an organ and you will have a lactic acidosis. Provide critical levels of hypo perfusion and you will induce a lactic acidosis.

Sans an insanely low cardiac index and hemoglobin concentration, there is absolutely nothing in the literature to prove that lactate production correlates in ANY way with hypoperfusion.

DO2 outmatches VO2 at baseline 5 times to 1. Hyoperfusion (at levels that are not insanely low) does not lead to lactate production in the classical way you are taught in medical school. Correlation does not equal causation. Same patients have a lactate of 10 and no acidosis. Others have severe acidosis and no lactate.

If anything, I have no idea why I need to sit here and prove that two numbers are equally stupid. One is just newer and fancier than the other.

 

[dchz]

I am ending this argument as I ended all my convos with anti vaxxers.

But for those people that are willing to at least understand the chemistry, this stuff matters. It's basic science, but it matters.

The reason I spent all the time typing out and quoting the boring chemistry:

This is what makes us different from a nurse.

 

[Ronin786]

Great. So now that you can't provide any convincing literature you resort to hyperbole and comparison with anti-vaxxers or pretend that I'm ignoring biochemistry. It's actually quite offensive when I've been trying to actually have a discussion with you and have provided evidence to the contrary.

This isn't me being obtuse or uneducated. It's a topic I've spent time researching during my ICU fellowship. I dont even care about the base deficit. Lactate's association with mild hypo perfusion is something that has no real basis in basic science or biochemistry. Look into Paul Marik's work on lactate.

This video is a great start:

Understanding Lactate - Paul Marik - Intensive Care Network

Lactate is the Critical Care physician’s North Star in the treatment of shock. Paul Marik overhauls traditional thinking in this scintillating talk.

intensivecarenetwork.com

The article I linked above is another:

iSepsis - The Lactate Myths

Lactate the Myths. Lactate is good for the patient and not bad.

emcrit.org

This here is also another, that goes through the same biochemical pathways you mentioned (Lactate, a useful marker for disease mortality and severity but an unreliable marker of tissue hypoxia/hypoperfusion in critically ill patients) Lactate production in most situations we see is almost always secondary to an increase in pyruvate rather than a switch into anaerobic production.

Just look at the ANDROMEDA-SHOCK trial (Effect on Septic Shock Mortality of Resuscitation Targeting Peripheral Perfusion vs Serum Lactate Levels)

Lactate was no better than a capillary refill based resuscitation strategy. Capillary Refill!

Manipulation of oxygen delivery has failed multiple times in the past. Using solo markers to indicate hyoperfusion has proved unsuccessful time and again. That should tell us something about how bad things have to be for you to become anaerobic. The newest in a long line of markers is renin (Renin as a Marker of Tissue-Perfusion and Prognosis in... : Critical Care Medicine).

Until we start thinking outside of the box, we're going to continue to harm our patients with reflex reactions to baseless numbers.

 

[deleted162650]

Oh get a room you two.

 

[Shimmy8]

Anyone seen this and had their institution/Edwards try to push this on you?

Acumen Hypotension Prediction Index software

www.edwards.com

Hypotension Prediction Index software for management of hypotension during moderate- to high-risk noncardiac surgery: protocol for a randomized trial - Trials

Background Hypotension is associated with serious complications, including myocardial infarction, acute kidney injury, and mortality. Consequently, predicting and preventing hypotension may improve outcomes. We will therefore determine if use of a novel hypotension prediction tool reduces the...

trialsjournal.biomedcentral.com