Magnesium for Sedation in Mechanically Ventilated Patients?

This is cool, really cool. We need more data, but this is a great start. I learned a lot of basic science from reading the introduction as well as discussion on this article and it all makes sense. I don't see myself using this anytime soon until there's a study where they add magnesium to a different agent that's not midazolam because I do not use benzodiazepines in my practice for sedation unless there are extreme cases.

I encourage you read this article yourself as it's interesting and I don't want to divulge too much out of respect for the authors.

-EJ



Link to Abstract

Link to FREE FULL PDF

Altun, Dilek. (2019). Can we use Magnesium for sedation in Intensive Care Unit for critically ill patients; Is it as effective as other sedatives?. Ağrı - The Journal of The Turkish Society of Algology. 31.

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Ketamine Continuous Infusions for Sedation in the ICU

One of the lectures I’m working on is regarding minimizing opioid utilization in the ICU on our critically ill patients on mechanical ventilation.

I honestly do not use ketamine as often as I’d like and I have been reviewing all the data behind continuous infusions over the last two days.

Unfortunately, the data isn’t incredibly robust (small sample sizes, mostly retrospective, heterogenous non-MICU patient populations) and there is a wide variation in the doses used in the different studies. This study published earlier this year used ketamine in conjunction with other agents, mostly propofol or fentanyl. The authors found that using ketamine decreases the doses the other agents with no changes in all the other outcomes. Most clinicians are looking for miracle drugs rather than incremental (albeit small) improvements here and there.

One of the problems I have with ketamine is, depending on how it’s mixed, is the sheer volume of the drip. I try to keep my patients potato chip dry and if the ketamine is basically a maintenance fluid, I’m not going to be as excited about it. 

Do you all use ketamine in your ICU for continuous sedation? Do you use it as monotherapy or with other infusions?



Link to Abstract

Garber, P. M., Droege, C. A., Carter, K. E., Harger, N. J. and Mueller, E. W. (2019), Continuous Infusion Ketamine for Adjunctive Analgosedation in Mechanically Ventilated, Critically Ill Patients. Pharmacotherapy, 39: 288-296.

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Analgesia and Sedation in the ICU

Link to Abstract

Sessler, C. N., Grap, M. J., & Brophy, G. M. (2001). Multidisciplinary Management of Sedation and Analgesia in Critical Care. Seminars in Respiratory and Critical Care Medicine, 22(02), 211–226.

Cardiogenic Shock: NICOM vs. Swan-Ganz Catheter

There are four types of shock: cardiogenic, distributive, obstructive, and hypovolemic.

I routinely make a big deal of volume resuscitation regarding septic shock which obviously falls under the distributive shock type. Part of the problem is that with all these well intentioned "Surviving Sepsis Campaigns", I feel that we are under-recognizing cardiogenic shock which can also present with hypotension and an elevated lactic acid. When you provide 30cc/kg of IVF arbitrarily because the "sepsis screen" pops up on your EMR forcing you to give the fluids, you end up causing harm to your patients.

This is where the history and physical plays a huge role. The physical should include a quick targeted POCUS/bedside echo to make sure you're not missing anything that's staring you in the face. If you see an RVOT on the parasternal long axis that's the size of a tennis ball, you're not dealing with sepsis. If you see an LV on the apical four chamber that is barely moving, you're likely not dealing with sepsis. Remember, if the patient is in septic shock, the systemic vascular resistance (SVR) hits the ground. There's no afterload for the LV to deal with. The LV will be clapping happily like a bodybuilder curling a 10lb weight. The "eyeball test" on POCUS is widely criticized but it has some uses.

But once you make the diagnosis of cardiogenic shock, how do you manage that patient? This is where I feel you may have some value in trending a CVP. I know Swan-Ganz catheters are out of favor, but I feel they're very useful if you know what to do with the numbers. Knowing how to apply the numbers clinically, though, takes some practice. Like everything else, you need to get your reps in. I'm fortunate that I trained at an institution where all the post-op hearts came out with a Swan. It was very helpful in my training and allowed me the opportunity to see the value in it rather than just being a nay-sayer. The Swan does have its limitations, though. It's not the easiest procedure to perform and it comes with some potential cardiac risks that I am not going to list here for the sake of my sanity. Is there something that we can use instead?

I will admit that I personally do not have any experience with the NICOM device. I look forward to playing with the technology one day. I like non-invasive things for my patients. I typically use another device which I will not name but I feel it is very helpful when used appropriately. No technology is perfect, not even the Swan. I was excited when I read this article because I was hoping for an out to not have to float Swans in this patient population. I also very much enjoyed how the authors conducted the study. Simultaneous measurements on the same patient was definitely the way to go and I applaud them on that.

Without boring you all with the details, the authors found that the NICOM correlates poorly with indirect Fick and therm-dilution measurements of cardiac output. The authors attribute it to the biorreactance technology being interfered with by pulmonary and interstitial edema. Makes sense to me. They also listed other factors as well which are on the full article. Nonetheless, what method do you use at your institution to manage cardiogenic shock?

-EJ



Link to Abstract

Rali, A. S., Buechler, T., Van Gotten, B., Waters, A., Shah, Z., Haglund, N., & Sauer, A. (2019). Non-Invasive Cardiac Output Monitoring in Cardiogenic Shock – The NICOMTM Study. Journal of Cardiac Failure.

Great article for indirect Fick
De Maria AN, Raisinghani A. Comparative overview of cardiac output measurement methods: Has impedance cardiography come of age? Congestive Heart Failure. 2000;6:60–73.

Indirect Fick Abstract

Indirect Fick PDF

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17 years from research evidence to clinical practice

Link to Abstract

Link to PDF

Morris ZS, Wooding S, Grant J. The answer is 17 years, what is the question: understanding time lags in translational research. J Roy Soc Med. 2011;104:510–20.

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Awake Intubation Guidelines

Link to Article

Link to PDF

Ahmad, I. , El‐Boghdadly, K. , Bhagrath, R. , Hodzovic, I. , McNarry, A. F., Mir, F. , O'Sullivan, E. P., Patel, A. , Stacey, M. and Vaughan, D. (2019), Difficult Airway Society guidelines for awake tracheal intubation (ATI) in adults. Anaesthesia. doi:10.1111/anae.14904

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Spontaneous Breathing Trials: How Does Your Shop Handle This?

There has been quite a bit of variation regarding pressure support trials, spontaneous breathing trials, liberation trials, whatever you want to call it.
I recently looked at the data for my academic curiosity and would like your input as to how you do it at your shop. I’d like to apologize in advance if I don’t write back to each of you in a timely fashion. I’ll try my best.

Here’s how I like to approach it (in the ideal world).
1. Patient isn’t deteriorating and they’ve done well on their spontaneous awakening trial (SAT).
2. RT goes ahead and places them on pressure support (PS or PSV are the lingo)
3. PS for 30 minutes and the RT flips them back into their prior setting on the vent if they don’t fly.
4. If they do fly, I eyeball the patient and have my RT teammate pull the tube.

I usually have HFNC or NIPPV at the bedside in case they have a high likelihood of needing reintubation.

I know many clinicians check ABGs prior to extubating their patients. I very rarely do. I think I’ve checked maybe 2 or 3 prior to extubating in the almost 2.5 years that I’ve been out of training.

A 🎩 tip to the authors.

Let’s reduce the mechanical ventilation days with this! 💪🏼




Link to Abstract

Link to FULL FREE Article

Ouellette DR, Patel S, Girard TD, Morris PE, Schmidt GA, Truwit JD, et al. Liberation From Mechanical Ventilation in Critically Ill Adults: An Official American College of Chest Physicians/American Thoracic Society Clinical Practice Guideline: Inspiratory Pressure Augmentation During Spontaneous Breathing Trials, Protocols Minimizing Sedation, and Noninvasive Ventilation Immediately After Extubation. Chest. 2017;151:166–180.

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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

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.

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

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Stress dose steroids for septic shock: bolus dosing or continuous infusion

This study published just this month, November 2019, suggests that providing bolus dosing of hydrocortisone, 50mg IV every 6 hours shortens the time a patient needs to be on vasopressors compared to 200mg IV through a continuous infusion every day.

Stress dose steroids are clearly in my armamentarium in the treatment of septic shock. I tend to reach for them when I’m starting my second vasopressors, usually Vasopressin when the norepinephrine hits around 10-15mcg. I also ready for the vitamin C and thiamine at that point, too. Actually, I have a quick little bundle in the EMR where I just check off all these goodies. Sometimes I stray in different directions, of course. Every patient is different and this is not a recommendation on how you should practice. I haven’t gotten on the fludrocortisone train yet, have you?

Either way, the shock reversal is faster with the bolus dosing. This should make all my nurse followers happy as they won’t have a channel and lumen bogged down with this medication and all the compatibility questions that arise with it. Whether bolus or continuous dosing you won’t see a difference in mortality, ventilator days, adverse effects, length of stay, etc.

Also not yet another study where they don’t check cortisol levels before initiating this treatment. I’m not a fan of checking cortisol levels myself. I see it done and I ask, why?

A 🎩 tip to the authors.

-EJ

Link to FULL FREE Article

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Inferior Vena Cava Assessments with US

Ultrasound assessment of the inferior vena cava for fluid responsiveness: easy, fun, but unlikely to be helpful

This is where I stand on the matter today, November 3rd, 2020. I am open to changing my mind with new data. Guiding fluid responsiveness, as I’ve covered here, is a huge pain in the butt. But giving patients either too little fluids or too much fluids increases mortality. That little feeling inside of “just doing something” isn’t the best thing.

When I was going to through fellowship, I was trained to perform this assessment of placing the US probe on the patients subxiphoid area and digging around until the IVC was found. I got pretty good at it, but I have to admit that I also haven’t used it in 2 years. I never found it to be as useful or reliable as I initially thought it would be. It’s a tool but it has many caveats. I remember reading this article and got some confirmation bias to how I already felt about the scan.

Fortunately, this article is free and you can download it on my website, eddyjoemd.com. The article illustrates the many caveats which any clinician developing the skill to perform this scan NEEDS to know. He discusses the technical limitations, confounding factors, and reviews the evidence in both patients who are spontaneously breathing and in those who are on the vent.

I’ll repeat again, if you are a medical student, emergency medicine resident, internal medicine resident, or any clinician learning and managing patients based on this scan, you need to know the limitations of it. At least until we find the holy grail of Critical Care where we find a way to know the correct amount of fluids to give our patients. Not a drop more or a drop less.



Link to Abstract

Link to FREE FULL PDF

Millington, S.J. Can J Anesth/J Can Anesth (2019) 66: 633. https://doi.org/10.1007/s12630-019-01357-0

Incorporating Dynamic Assessment of Fluid Responsiveness Into Goal-Directed Therapy: A Systematic Review and Meta-Analysis.

Incorporating Dynamic Assessment of Fluid Responsiveness Into Goal-Directed Therapy: A Systematic Review and Meta-Analysis.

Let’s talk a little bit about resuscitation. I chose to go down this path to start off the weekend bc I frequently see patients receiving arbitrary fluid boluses for SBP less than x (we all know how o feel about using systolics on oscillometric machines), MAP less than 65, or decreased urine output. It makes us feel like we are doing something but we are actually causing harm. At the end of the day, giving fluid just to make the blood pressure pretty does not indicate fluid responsiveness. If I were to give you a liter of fluid, definitely not saline, your BP would go up. That doesn’t mean you’re fluid responsive. Using the technologies listed in this article from 2017 are a step in the right direction. If you read the validation studies for them you’ll learn that they leave much to be desired but they’re amongst the best tools we have today. I’m going to go much deeper down this rabbit hole in the upcoming months.

What do you use at your shop to measure fluid responsiveness?

Link to Abstract

Link to FULL FREE PDF

Bednarczyk JM, Fridfinnson JA, Kumar A, et al. Incorporating Dynamic Assessment of Fluid Responsiveness Into Goal-Directed Therapy: A Systematic Review and Meta-Analysis. Crit Care Med. 2017;45(9):1538–1545. doi:10.1097/CCM.0000000000002554

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