Thursday, January 30, 2020

How Does Lacate Turn Into Lactic Acid?

You have NO IDEA how much I banged my head against my desk looking for the answer to the question: how does lactate turn into lactic acid? Well, after many hours of searching for an answer, and you can think I'm a dummy for not find the answer sooner or knowing it like a useless fact off of the top of my head, I FOUND IT! It's honestly some information that's not readily available. Many articles play it off and don't mention specifics assuming that "it just happens". I am by no means a biochemist. I'm simply trying to understand all this. In my explanation, I purposefully will be oversimplifying things.


Here's how it works:
In the cytosol, pyruvate turns into lactate (rather than move towards acetyl-CoA) for a number of reasons, again that I'm not going to get into, via lactate dehydrogenase. That lactate (via shuttles) gets to the cytosol of the liver and kidneys where it eventually makes its way into the Cori/Lactic Acid Cycle. The Cori cycle eventually spits out glucose. So far so good, right? Glucose via glycolysis seems to be metabolized into lactate, ATP, and water. Said ATP gets hydrolyzed into ADP and inorganic phosphate which releases that very necessary proton (H+). When conditions get revved up, i.e. septic shock, and an excess of lactate is being produced, then the cell cannot handle the metabolism of lactate and guess what's also being overproduced? Said H+ which tags onto the lactate creating lactic acid.

The articles I've read tend to say that you start running into lactic acidosis territory when you have a lactate 5 with a concurrent acidosis (pH less than 7.35). 


Mad props to Amanda, my pharmacist teammate, for listening to me and helping me work through this while not making too much fun of me. 
<7 .35="" additional="" again.="" and="" any="" are....="" be="" better.="" biochemistry="" br="" can="" definitely="" did="" diving="" going="" help="" here="" i="" into="" knowledge="" me="" nbsp="" never="" of="" or="" others="" pointers="" provide="" think="" this="" to="" understand="" was="" we="" welcome="" you="">
Link to article (NOT FREE)

Fall P, Szerlip H. Lactic acidosis: from sour milk to septic shock. J Intensive Care Med 2005; 20: 255-71.

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.

Wednesday, January 29, 2020

Lactate in IVF Leads to Lactic Acidosis?

"Lactate in fluids, such as Ringer's lactate, causes a lactic acidosis". Ugh. How I cringe every time I hear or read that. You should take into account your patients organ failures since lactate is metabolized approximately 60% in the liver, 30% in the kidneys, and 10% elsewhere (including the heart, muscles, etc depending on your source).

There's no perfect trial to go ahead and prove this concept, but I have linked this study which FREE where they provided patients with a sodium lactate solution versus Hartmann's solution, aka Ringers Lactate. To provide some context, LR provides the patient with Sodium Lactate, 28mmol/L to be exact. The half-molar Sodium Lactate solution described in this article has 504mmol/L of Sodium Lactate. I struggled quite a bit to find that concentration but thankfully I found it in a Spanish (Spain) article.

I have attached the table to illustrate several points. First, if you notice the Sodium Lactate did not create an acidosis in any of the patient groups, on the contrary, they trended more so towards an alkalosis, even a statistically significant alkalosis in the case of the "lactate" group. Overall, there was no increase in lactate whatsoever in the LR group which means that there's no "lactic acidosis" created by LR. It does not make patients acidotic. If you have a functioning liver and kidneys, that lactate is metabolized into bicarbonate. Hope that all makes sense.

A hat tip to the authors.

-EJ

Link to Article

Link to FULL FREE PDF

Nalos, M., Leverve, X.M., Huang, S.J. et al. Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial. Crit Care 18, R48 (2014)


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.

Monday, January 27, 2020

Elevated Lactate Does Not Equal More Fluids

There is a law of diminishing returns when resuscitating patients with bolus after bolus of IV fluids.

Yes, lactate decreased with additional boluses by 1.3% per every 7.5mg/kg increase in fluids making the numbers look pretty, but does that mean we're treating the source of the lactate or are we just diluting it? This study shows that mortality actually increases as we keep providing more fluids.

I’m not saying that patients who are in septic shock do not need fluids. On the contrary, they need judicious use of IV fluids and 30cc/kg initial resuscitation is okay with me in the vast majority of patients. I had to read many articles to finally fall in line with that. Of course there are several patient populations where I’m against it. For example, severe pulmonary hypertension patients with right hearts living on a tight rope. I digress. But tagging along with my prior post discussing giving fluid boluses reflexively, this study shows that fluids don’t really “clear” lactate in the way we all hope and want them to. The correlation of having an elevated lactate to mortality is there. The correlation with more fluids making lactate decrease isn’t. The pathophysiology behind where lactate comes from explains why not. And as we all should know, fluids are not benign. The more fluids we give patients the higher the mortality per the 9000 that were assessed in this study.
A 🎩 tip to the authors. .


Liu V, Morehouse JW, Soule J, Whippy A, Escobar GJ. Fluid volume, lactate values, and mortality in sepsis patients with intermediate lactate values. Ann Am Thorac Soc. 2013;10:466–73.



FREE FULL ARTICLE

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.

Sunday, January 26, 2020

Albumin in the Initial Resuscitation of Sepsis and Septic Shock.

Several days ago I posted a comment on @iculaughingrn's page when the cited meme was posted. I guess I need to be extremely careful with my wording because I wrote "Looks like $30 of not much evidence to support its routine use in resuscitation". 


We live in a world now where every word counts and some people in the comments section let me have it. I am under a microscope and therefore this post clarifies my thought process with guidelines to support. It's also important to recognize why we do what we do or don't do. I'm not going to dissect the different albumin studies at this juncture. Maybe later. 


Healthcare as a whole in the US at this time is not sustainable. This is why I am hopeful that the HAT cocktail which is extremely cheap is successful versus one of these -NIB or -MAB drugs that costs tens of thousands of dollars. Albumin, relative to crystalloids, is extremely expensive. We need to be cognizant of these things. 

I should have written "routine use in sepsis resuscitation". The CVICU population is a completely different beast although I would LOVE to see data for albumin being beneficial in that population. I have not seen it. The burn population is one that terrifies me so kudos to all of you practicing there. I do not know your literature. 
Many of you know I am not a big fan of guidelines but this is something I can agree with. Earlier in my career I routinely used albumin. Now, I rarely use it. During my entire fellowship, albumin was not a word that was uttered in the MICU unless you were referencing the lab value.
Ultimately, the guidelines state: "The absence of any clear benefit following the administration of colloid compared with crystalloid solutions in the combined subgroups of sepsis, in conjunction with the expense of albumin, supports a strong recommendation for the use of crystalloid solutions in the initial resuscitation of patients with sepsis and septic shock."

After the initial resuscitation, the clinician needs to be the clinician. Giving fluids arbitrarily to make the BP look pretty is not something I am a fan of. Some patients may need albumin, some may not. I rarely use it in my practice, though. Use your best clinical judgement. A hat tip to the authors. 

Levy, M. M., Evans, L. E.; Rhodes, A. The surviving sepsis campaign bundle: 2018 update. Crit. Care Med. 46, 997–1000 (2018).

- EJ




Link to Article

Link to FULL FREE PDF

Levy, M. M., Evans, L. E.; Rhodes, A. The surviving sepsis campaign bundle: 2018 update. Crit. Care Med. 46, 997–1000 (2018).



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.

Saturday, January 25, 2020

Bicarbonate in Lactic Acidosis?

I would like to make this perfectly clear, this article has many nuisances to it. Many limitations and different components that need to be dissected carefully. Too carefully for what I can do on IG. Please attempt to obtain it and read it for yourself as it does not provide a black and white response to the question: can we treat lactic acidosis with bicarb?
The slides presented here are preliminary slides from my lectures that I am actively working on. I plan on explaining things in far more detail to my audience than what is on the slides. Is that enough of a disclaimer? Well then let's let it rip!
There exists a pendulum in many things medicine and providing bicarb in lactic acidosis patients is one of them. There's always been the question of whether it's beneficial, ineffective or harmful. If you look at the data pre-2000, it is almost entirely supportive of not providing bicarb for these patients. The data after 2001 is more lenient to where it is discussed in one paper that "bicarbonate might prolong survival sufficiently to allow treatment of the underlying cause of lactic acidosis". This is why I use the term "bicarb band-aid" whenever I put someone on a bicarb drip to buy some time to figure things out. 
Like everything in medicine, bicarb drips have their drawbacks. I know people LOVE to give amps of bicarb during ALCS but there's no data to do so. Much more to that than what I'm going to discuss here. Very broad topic. 
Getting back to the article. They took almost 400pts in France who were very sick, with a lactic acidosis, and randomized them to get either nothing or 4.2% bicarb gtt. They had some very strange outcomes which are a conversation for another day but ultimately, patients who had acute kidney injury did better, and this is even considering that 24% of the control group got bicarb. Nonetheless, the numbers are explained in the slides. 
Again, is this black and white? Nope. But it's the first large RCT in this patient population looking at this intervention and major hat tips to the authors. 

-EJ

PS: Can I take credit for the term "bicarb band-aid"? I'd like to but I feel that I'm not original enough to have come up with it. 





Link to Article

Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. Lancet 2018; 392:31.

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.

Wednesday, January 22, 2020

Don't give fluids just because the lactate is elevated.

Lactate is elevated? (without assessing the patient) Give a fluid bolus.

Wait, WHAT?!?!? Whyyyy? 😫

This is something I routinely see today. I routinely saw it at the Ivory Tower where I trained in fellowship. I routinely did it myself when I was a young whipper snapper of a resident and didn't know any better. Now, I'm here to tell you that you can do better.

I don't blame you for doing this, though. You've seen other clinicians do it. You were likely trained this way. The nurses have been trained this way. When the lactate is elevated, page the doctor and expect an order for a fluid bolus. It makes one feel all warm and fuzzy inside like "I did something". Everyone pats themselves on the back. Well I'm here to tell you that from now on, every time you do that, you're more likely to be wrong in your management that right.

This article which describes the "lacto-bolus reflex", i.e. to give a bolus of fluid for every elevated lactate. The authors are just as fed up about it as I am. IV fluid boluses are not benign. Fortunately, this article is completely free (I like finding you all full free articles) and it describes why the whole idea of patients developing a lactic acidosis due to cells not getting oxygen hypoperfusion is silly to the point where many of us need to be re-educated. I will admit, I had to be re-educated myself. I was not born knowing this stuff. I used to do it wrong. Now I'm trying to do it right.

The article is easy to read, for those of you who choose to dive further into it. Ultimately, they conclude that, although lactate levels are helpful for prognosis (plenty of data on that), and lactate not going away is helpful to know whether you have control of your patient or not, it ultimately does not help in any way, shape, or form, to guide fluid resuscitation. A 🎩 tip to the authors.


-EJ



Link to Article

Link to FULL FREE PDF

Spiegel R, Gordon D, Marik PE. The origins of the Lacto-Bolo reflex: the mythology of lactate in sepsis. J Thorac Dis 2020;12(Suppl 1):S48-S53.


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.

Vitamin C Should Help Decrease Vasopressor Doses and Duration

The VITAMINS trial didn’t pan out was not a positive study as it was conducted. I’ve already provided my take on that with my main argument being that they took too long to initiate the study drug (median time >25 hours, not including the time to arrive in the ICU). Sepsis management is expedient, you and I see it every day. Waiting over a day is not being expedient.

I’m seeing a benefit in my clinical practice, as admittedly worthless as my opinion is on the grand scheme of evidence. But when something doesn’t make sense from a results standpoint, you need to go back to the basics and wonder what happened.

Here are some things we absolutely know: 88% of patients in septic shock have hypovitaminosis C and 38% of septic shock patients have severe vitamin C deficiency. What many of you may not know, and I’m here to help you understand why I’m so surprised by the findings of the VITAMINS trial, is that vitamin c is a co-factor to the creation of endogenous catecholamines. That means that without vitamin c, your body isn’t going to produce the appropriate amounts of dopamine, norepinephrine, and epinephrine. It also is necessary for the production of vasopressin. It’s as simple as that. 38% of people will not produce appropriate endogenous catecholamines. The fact that administering exogenous vitamin c did not decrease time that the patients were receiving vasopressors in the study makes me wonder why. I am aware that there was a delay of >24 hours to start the therapies in the study but is there more I'm missing. Hopefully you can take some basic biochem away from this post as to why it should work (although it didn't in the study).

A 🎩 tip to the authors.

-EJ




Link to Article

Link to FULL FREE PDF

Carr, A.C.; Shaw, G.M.; Fowler, A.A.; Natarajan, R. Ascorbate-dependent vasopressor synthesis: A rationale for vitamin C administration in severe sepsis and septic shock? Crit. Care 2015, 19, e418.



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.

Tuesday, January 21, 2020

Melatonin for Sepsis

You’re following along on my page bc you know I’m trying to find the most cutting-edge treatments and therapies for my critically ill patients. I hope to keep on pumping out eye catching content such as this article on melatonin. Please share with you’re nerdy friends who would also find this nerdy content I put out interesting.

Yes, melatonin. I finished my lecture today on metabolic resuscitation and this article was published just a few days ago. It’s actually free and you can download it from my website, eddyjoemd.com. I have learned a ton of fascinating facts regarding melatonin as to why is SHOULD work. I can see the eyes rolling already. No, there aren’t any double blind, randomized controlled trials on this but one is in the works.

It definitely makes me curious as this is yet another therapy that many of us take during the day to sleep while on night shifts and is benign (based on years and years of studies listed in this article).

Fascinating stuff, right? Did you know that melatonin did all these cool things? I surely didn’t. Now I do... and that’s why I read as much as I do. A 🎩 tip to the authors!

-EJ

Link to article

Link to full free PDF

Colunga Biancatelli, R., Berrill, M., Mohammed, Y., & Marik, P. (2020). Melatonin for the treatment of sepsis: the scientific rationale. Journal Of Thoracic Disease, 12(S1), S54-S65.


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.

















Monday, January 20, 2020

Sepsis Killed Approx 11 million people in 2017.

This data was published on January 18th, 2020. Hot and fresh stuff! This represents the most recent estimate of sepsis-related deaths globally. We're doing better from a mortality perspective in the developed world with the mortality, but 11 million people is the, per census data, the entire population of New York City and Chicago combined per year. That's a lot of people. 20% of worldwide deaths. Many of these occur in our own ICU's. We could and need to do better. I understand we are all going to die of something one day, but this is mostly treatable with quick identification, source control, and appropriate and timely antibiotics.

People ask me all the time why I spend so much time and energy on social media educating about the critically ill when I could instead be doing other things. At the time of this writing there are 26,122 people following along in my insanity on Instagram (thank you all, btw). As the number grows, and I may be an idealist on this, we may be able to put a dent into those 11 million deaths by keeping our practices in line with the best evidence available.

Hope you all have a great day!

- EJ



Link to FULL FREE PDF

Rudd, Kristina E et al. Global, regional, and national sepsis incidence and mortality, 1990–2017: analysis for the Global Burden of Disease Study. The Lancet, Volume 395, Issue 10219, 200 - 211.



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.

Saturday, January 18, 2020

VITAMINS Trial: Timing was overlooked

You all know my bias. It shouldn't be a surprise given my body of work: I wanted this to be a positive study. I wanted patients to benefit from this therapy and SURVIVE. I cannot understand the vitriol I have received in my direct messages when I shared my initial take on the study. I’m prepared to deal with more. Bring it!

Ultimately, there's no difference in the the endpoints, whether primary or secondary. No need to go through them in depth. That’s what the data says, that’s what the study concluded. Hat tip to the authors. It is what it is. I can agree with their conclusions based on the study conducted. But clinicians should not take the study as the end of HAT therapy. It would be scientifically irresponsible to do so. The study had a fatal flaw that doomed it from the beginning. Let me explain why. I practice real world medicine. I am not a trialist. I do the best I can every day with what I have.

Here's a take on how I care for septic shock patients for some perspective. There are plenty of nurses and physicians who work with me currently and have worked with me in the past following along on IG who can vouch for my style of practicing medicine.

This is NOT MEDICAL ADVICE. Do not do what I do because I say so. This post is not all 100% all inclusive for every nuisance. Every pt is different. That is your disclaimer.

1. I get a call from a colleague: ED physician, hospitalist, or surgeon regarding a patient who is in septic shock. At this point they have already gotten antibiotics and fluids bc everyone is excellent at this.
2. I go see the patient IMMEDIATELY
3. I assess, as quickly as possible with my limited tools a guesstimate on their fluid status
4. I start vasopressors EARLY while fluid resuscitating
5. pt arrives in the ICU, central line placed, arterial line placed, EV1000 hooked up.
6. I camp out at the nurses station next to the patient with them in my line of sight.
7. I watch how the patient behaves to my interventions, how the vasopressors go up, if they go up
8. As the vasopressor requirement increases, says NE around 10mcg, I start feeling uneasy. Especially how quickly their requirement increases.
9. I pull the trigger after 10-15mcg of NE to start vasopressin, hydrocortisone 50mg IV q6h, vitamin C 1500mg IV q6h and thiamine 200mg IV q12hours. I hit click, click, click, click, on an order set I created for myself on my EMR.
10. I keep on monitoring the patient closely to assess their response and provide additional fluids and learn more about their physiology.
Thing I do on the side: airway, bedside echo, talk to family and patient, management of other sick patients happen in this time period as needed. This post is not all-inclusive.


Needless to say, all of this happens WITHIN 6 HOURS. One has a general idea, within 6 hours of the patient being in septic shock, a pathology that has a 25-40% mortality rate depending on the study, what is the likelihood of the patient turning the corner.

What can we all agree on regarding management for sepsis: early antibiotics make a difference. Early source control makes a difference. Early fluids are better than late fluids. Early vasopressor administration is showing to be better than late (data for that coming soon).

Here’s my main problem with the study:
- Time for patients to get randomized: I CAN'T FIND THIS DATA
- Time from ICU admission to randomization: 13.7 hours (IQR 7.1-19.3 hrs).
- Median time for patients to receive study study from randomization: 12.1 hours (IQR, 5.7-19 hours).
13.7 + 12.1 = 25.8 hours PLUS time for patients to get randomized!
For those who don't know what IQR means: click here

Why in the world did they take so long to start the study drugs?

That's my problem with the study. My larger problem with the study is the fact that, since it was published in JAMA, a very high impact factor journal, clinicians are going to take it as gospel and dismiss the therapy entirely. If they would have provided the study drugs appropriately, there may have been a difference in outcomes. Since they didn't, patients who could have potentially benefitted will not.
Or maybe I'm just wrong.


-EJ



Link to FULL FREE ARTICLE


Fujii T, Luethi N, Young PJ, et al. Effect of Vitamin C, Hydrocortisone, and Thiamine vs Hydrocortisone Alone on Time Alive and Free of Vasopressor Support Among Patients With Septic Shock: The VITAMINS Randomized Clinical Trial. JAMA. Published online January 17, 2020.


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.

Sunday, January 12, 2020

ACLS in the CVICU

Yesterday, @yournursingeducator created a great post on Code Blue tips. @fobiesme asked a very legitimate question regarding how to proceed in patients who are s/p bypass or any open chest situation in the CVICU. This was something I wondered about myself even as someone who taught ACLS for the AHA at a point in my life. It was hard to find a solid answer. Fortunately, as of 2017, the Society of Thoracic Surgeons put forth this consensus statement and algorithm on how to handle cardiac arrest situations in the CVICU population. Since this is relatively new data (only 2 years ago), I understand that the CVICU nurses out there may not be familiar with nor using this particular algorithm. What we did in my shop is that we printed this out with all its pretty colors, laminated it, and placed it on the code carts. Fortunately, this is entirely FREE!

-EJ



Link to full FREE PDF

Dunning J, Levine A, Ley J; STS Task Force. The Society of Thoracic Surgeons expert consensus for the resuscitation of patients who arrest after cardiac surgery. Ann Thorac Surg 2017;103:1005–20.

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.

Saturday, January 11, 2020

Vitamin C and "Fictitious Hyperglycemia"

I’m plenty fired up for the VITAMINS trial that’s going to be published on the 17th. That’s the first large RCT looking at Vitamin C, Thiamine, and Hydrocortisone in Septic Shock. If the trial turns out to be positive, which I really hope it does, then we will really need to know about this limitation as our utilization will definitely increase worldwide.

From burn data and providing high dose vitamin C in that population, and I’m taking about doses >50gm/day, they have noted a cross reactivity in certain point of care blood glucose monitors where the ascorbic acid, due to having to do with glucose having a similar molecular structure to ascorbic acid with six-carbon molecules.

This seems to confuse the POC machine and the readings could be falsely >30%. Ultimately, those designing the studies for 1.5gm IV q6 hours have known this and have been checking to see if there’s a difference between the lab numbers and the POC numbers. As of the time of publication, they found no significant difference. We still need to keep this in mind, though. In the burn population someone died of iatrogenic hypoglycemia 😔. A 🎩 tip to the authors and those who answered the questions.

-EJ



Link to Website

Flannery AH, Bastin MLT, Magee CA, Bensadoun ES. Vitamin C in sepsis: when it seems too sweet, it might (literally) be. Chest. 2017;152(2):450–1.


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.

Saturday, January 4, 2020

Vasopressors have immunologic activity

This is a post I’m 90% sure you’re going to learn something from because I had NO IDEA this was a thing until I was doing all my research on vasopressors. I’m sure it’s not going to get many likes nor any shares, but it’s cool stuff like this that really gets me excited. Not many know what tumor necrosis factor is and what interleukins are, but they all play a huge role in inflammation and the overresponse of the body in sepsis. I’m going to stay far away from the specifics on this one. We give catecholamines and Vasopressin to our patients almost daily, might as well know the intricacies of these treatments. Cool stuff, right? A 🎩 tip to the authors.

Thanks for following along in my insanity.

-EJ




Link to Abstract

Link to FULL FREE ARTICLE (maybe)

Stolk RF, van der Poll T, Angus DC, van der Hoeven JG, Pickkers P, Kox M (2016) Potentially inadvertent immunomodulation: norepinephrine use in sepsis. Am J Respir Crit Care Med 194(5):550–558

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.

Angiotensin II/ Giapreza

I’ve said this on numerous occasions and I’ll repeat it again. I do not do research. I have one study published and that’s because I needed to do it to complete fellowship. Outside of that, I’m a boot on the ground doc. I feel bad criticizing but here we are.

Now that that’s out of the way, I can’t believe that so many huge names in critical care research are listed on this study that has sooooo many issues.

I’m always excited at the prospects of a new vasopressor or anything to help out my patients in shock, but at $1500 a vial, we better be seeing some serious benefits.

Here’s my take and I’m over simplifying: they took real shock patients who were on norepinephrine and gave them either the study drug, known since the 1930’s to cause an increase in BP, or a placebo. Basically giving a hungry person food or air and seeing which one made them feel full. Obviously the delicious meal group felt full. Oddly enough, 23.4% of the pts who received placebo had an increase in their BP. And then people try to tell me this is good data? Want to have some air?

There was also a change in their CV SOFA score. I had to look this up but it means the patients had a decrease in pressor requirement. Well, isn’t that the point? How about having the patient on NE and adding Vasopressin in one group and adding Giapreza in the next? Wouldn’t that world out better? Oh, yeah, this study was sponsored by La Jolla. They created softball endpoints. That’s lame. So you mean to tell me that a $6 dose of vitamin c is garbage but have no qualms with this study? Get out of here.

Ultimately, you should check out @pulmcrit (Josh Farkas) post on this from two years ago. It’s much better than mine: https://emcrit.org/pulmcrit/angiotensin-ii/

- EJ



Link to Article

Link to FULL FREE PDF

Khanna A et al. "Angiotensin II for the Treatment of Vasodilatory Shock". New Engl J Med. 2017. 377:419-30.

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.

Wednesday, January 1, 2020

Keep the Dopamine at the bottom of the shelf


Does your friendly neighborhood cardiologist or intensivist start your Cardiogenic Shock patient on dopamine? Do you ever ask them when was the last time they read a study? I don’t mean to be harsh but this data is now almost a decade old.

This study placed dopamine far down on the vasopressor selection totem pole. They looked at patients who were in all types of shock, hypovolemic, septic, and cardiogenic on norepinephrine or dopamine and checked a bunch of outcomes.

What did they find? Well, no difference in mortality EXCEPT in those patients in Cardiogenic Shock. (p=0.03). Also, dopamine caused more severe arrhythmias than norepinephrine: 6.1% vs. 1.6%.

24.1% of the dopamine patients had arrhythmias and 12.4% in the norepinephrine group. That’s a lot of time managing side effects. No thank you.

Also, I need to find more data on this “renal dose dopamine” nonsense. This study showed an increase in urine output in the first 24 hours but then it evened out. They had an equal fluid balance when all was said and done. Although there was no statistically significant difference (p=0.07) in renal function and the norepinephrine group trended towards having better renal function. I know seeing urine makes us feel all warm and fuzzy inside but if it’s providing false reassurance than what is it worth?

Still want to use dopamine? I hope not.

-EJ

Link to Article


De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779–789. doi:10.1056/NEJMoa0907118

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.