Showing posts with label lactate. Show all posts
Showing posts with label lactate. Show all posts

Thursday, November 14, 2019

Lactate Measurements: Venous or Arterial Samples?

This is a question I remember asking myself quite a bit during my training when I used to check/trend lactate levels more than I do today. Does it really matter whether I check it from an arterial line or from a venous stick?

This study which was a prospective study of 100 patients who had both an arterial line and a central line. The authors compared the values during resuscitation. Short answer is no, there's no statistically significant difference.

Does this reflect the real world? Not really. As much as I would like to have an arterial line in all of my septic shock patients, this does not necessarily happen right away. Arterial lines, even for me who has put in hundreds, is not the easiest of procedures. I actually failed miserably on a patient in 5 different sites several weeks ago. I have excuses but I won't share them ;). Also, it is time consuming and causes the patient discomfort. That being said, when someone is sick sick, they get an arterial line from me or my trusty badass RT's.

The other real-world concern is the central line issue. There's data out there that you don't necessarily need a central line to run vasopressors, some of that data is my own data (my ONLY data out there haha). That being said, these patients will have their venous lactate checked via a peripheral stick, in many cases using a tourniquet. Using a tourniquet has its own problems as that could make the lactate levels unreliable.

Now, let's say that you have both an arterial line and a central line, then you can use this data more appropriately. Sort of. The authors did not specify whether they used the same point-of-care device to check the lactate levels in the venous nor arterial values. You know, some shops use POC for arterial, some have the fancy machine inside the ICU. Some could run the venous blood in that fancy machine, the POC, and some shops have to send it downstairs to the lab. This was not specified. Sigh.

Either way, I need to dissect the data regarding tourniquets for you.

-EJ



Link to Abstract

A. Mahmoodpoor, K. Shadvar, S. Sanaie, et al., Arterial vs venous lactate: Correlation and predictive value of mortality of patients with sepsis du..., Journal of Critical Care, https://doi.org/10.1016/j.jcrc.2019.05.019

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The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.
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Wednesday, November 13, 2019

Lactic Acidosis has a WIDE Differential (not just Sepsis)

There's a pendulum in medicine. Some things are over recognized and aggressively treated, some things are under appreciated (like subtle decreases in serum bicarb showing that the patient is becoming more acidotic and no one notices because the patient has obesity hypoventilation syndrome and their baseline bicarb is 34 and now has a bicarb of 22 and they look like poop).

At this time, all the rage is serum lactate and lactic acidosis. Every time someone says those words, with my biochemistry knowledge lagging far behind, everyone thinks "SEPSIS!! 30cc/kg IVF STAT!!!!" If you all knew how much this upsets me whenever I see it, you'd wonder how I'm still alive because I see it all the time. I bet you see it at your shop, too. It's very common because the pendulum has swung too far.

In order to correct this, I have embarked on discussing this topic ad nauseum in one of my lectures for Hawaii/Portland in 2020. The article linked below from the New England Journal of Medicine has a table that has been reproduced in many different forms. I will not break down the pathophysiology of each one of the etiologies, but I have been called for an ICU transfer for MANY of these.

Here are some examples where I have been called over the years where patients have received 30cc/kg of saline w/stable vital signs:
1. COPD patient receiving albuterol nebs. Lactic acid elevated because they're A. huffing and puffing, and B. receiving beta-2 agonists.
2. s/p seizure patients who are post-ictal
3. hypoglycemic diabetics
4. leukemia patients just watching TV
5. cocaine/chest pain patients in the ED
6. cardiogenic shock patients on an epinephrine gtt
7. HIV pt on Stauvidine (I should have written this one up)

I'm obviously not getting into the different subgroups of lactic acidosis at this time. Let's walk together before we run. Our job is to fix the underlying cause of the lactic acidosis, not dilute the number down with fluids.

-EJ




Link to Abstract

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
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Tuesday, November 12, 2019

Lactate is an Alarm, not a Treatment.

I need to eat my words on this one, because now there's data to show that there's a benefit to rechecking lactate levels in septic patients, but not for the reasons why one would think.

During my rounds over the course of the weekend, I recall telling several nurses that there's no data to suggest that trending lactates changes outcomes. This study, which came out last night, tells me I was wrong in saying that. A close examination of the data will show that it has nothing to do with the lactate itself, but rather the fact that the clinicians are prompted to "do something" in response to a number that makes us uncomfortable.

Okay, so the lactic acid is elevated. You're going to do one or two or all three of the following:
a. start vasopressors
b. start antibiotics
c. give more fluids

That's the kicker, we don't know which of those interventions, or combination of which, are what decreased mortality. Maybe it just means that someone gave these patients more attention. It certainly just wasn't the "checking the lactate" part. Lactate is just an alarm of sorts, we still need to be clinicians. I will suggest, though, that earlier initiation of antibiotics plays the most important role in decreasing mortality as there's already data suggesting that earlier antibiotics leads to improved outcomes. I personally start vasopressors pretty early and will share data in the upcoming weeks as to why I do that in my practice. Giving more fluids is only useful if the patients is fluid responsive, you know, if you can prove that giving that fluid will increase the cardiac index/output or increase the stroke volume. Giving fluids just to make the blood pressure go up arbitrarily is just plain dumb. It's 2019. We're better than that.

Ultimately, early lactate measurement did not improve outcomes, nurses relaying the information to the doctors, ARNP's, or PA's did.

-EJ



Link to FULL FREE PDF

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works.

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work!
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Monday, September 2, 2019

Lactic Acidosis: Does it really mean Hypoperfusion?

Understanding lactatemia in human sepsis: potential impact for early management

Having an elevated lactate in septic acid on admission is bad. Trending it, as studies that I have shown on this page does not change mortality. Seeing the numbers downtrend do give us that warm and fuzzy feeling inside, though. We give off a sigh of relief when that number becomes "euboxic". This article was published in April 2019 and authors explained the different mechanisms by which lactic acid is elevated in septic patients.
1. a deficit in oxygen delivery or extraction
2. shunting
3. stress
4. increased adrenergic stimulation

Notice that none of these mean that we have to drown the lactates with a bunch of fluids thereby diluting the value. We need to go after the etiology of it in a more specific manner. The authors of this study looked at the patients enrolled in the ALBIOS study (you know, the 2014 study where they sorted out that giving patients in septic shock albumin was good for depleting hospital resources but not a survival benefit? I guess I need to cover that trial on here) and used more than 1700 patients in whom lactate and central venous oxygen saturation were measured. They did a bunch of calculations and statistics that I am not going to cover here but you can click on the link for the article and go to town on it if you so wish.

Something really interesting was found in this study. The authors found that 1017 patients had a lactic acidosis but 57% of those patients had a normal serum pH. I would've thought that the number would have been lower. And it's not because these patients were on bicarbonate drip band-aids either.

The Early Goal Directed Therapy trial made us infatuated with checking central venous oxygen sats and our target was to get that to be over 70%. This study showed us that only 35% of that patients they looked at had a value less than 70%. 65% of patients with an elevated lactic acid had a normal or high ScVO2. Strange. We do know that the extremes of ScVO2 are bad and that ultimately ScVO2 has a number of limitations within itself. Anyway, I'm not going to dive too deep into all that, I'll leave it for the authors to explain.

All in all their main conclusion in this study, and the important takeaway is that lactate is not primarily created in sepsis by of the cells not receiving enough oxygen, but rather by impaired tissue oxygen utilization. This is a game changer. In my opinion, it doesn't mean that fluids are the answer, but rather, to find a way to help the tissues use said oxygen. Now let's all change our practice.

Don't take my word as gospel on all this, I could be wrong. Read the article for yourself. A hat tip to the authors.

-EJ



Link to Abstract

Gattinoni, L., Vasques, F., Camporota, L., Meessen, J., Romitti, F., Pasticci, I., … Marini, J. J. (2019). Understanding Lactatemia in Human Sepsis: Potential Impact for Early Management. American Journal of Respiratory and Critical Care Medicine.

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

The primary source of compensation I receive for this page and Instagram work is via Amazon Affiliates. All this free education you receive is much out of the kindness of my heart but I also like to receive a check every month from Affiliate Marketing. No one likes to work for free. The best part is that it's of no cost to you. Here's how it works. 

You click on the link for Will Owens' awesome ventilator book here: https://amzn.to/2myFxYm and whether or not you purchase the book I receive a small commission for whatever you buy on Amazon for the next 24 hours at no cost to you. For every copy of the Ventilator book people have bought off of my affiliate links, for example, I have earned $0.85. I know it's not big money but it helps motivate me to keep on plugging along doing this heavy lifting in Critical Care. Thank you for supporting my work! 

My Amazon Store