Showing posts with label vasopressors. Show all posts
Showing posts with label vasopressors. Show all posts

Monday, September 30, 2019

Vasopressin: Titratable Doses? Monotherapy in Septic shock?

This is what I love about the community in social media. We all just push each other to be better. Rishi posted today about titratable Vasopressin and, me being the data junky that I am wanting to know every study I could possibly know under the sun, had two studies in my back pocket ready to share with everyone. I was planning on sharing this study with you all further down the road but, Rishi indirectly pushed me so here I am sharing this article with you all rather than going out for a run. No, there's no one study where they just looked at titrating vasopressin. What this study does show us, though, is that the authors used vasopressin as a titratable medication as well as a mono therapy medication (that means not just adding it to norephinephrine when it reaches X dose. Studies like this indirectly guide us to what can and can't be done moving forward in medicine. If you get into trouble with a patient, one can justify it by saying "the VANISH study showed that it's safe to use it in this manner". I'm always worried about the lawyers, I'm not going to lie.

The goodies in this article and what I want you to focus on today is not necessarily the conclusions of the article nor all the subgroup analysis, but rather I want you to look at the methods on how they performed the study.

Patients were able to receive titratable doses of vasopressin up to 0.06U/min. That means that they were able to exceed the 0.04U/min you and I use every day.

They also titrated to a MAP of 65 or 75. Note that they did not use a systolic blood pressure. I have covered why you shouldn't do that unless you have an arterial line on youtube and here in the past.

The MAP of 75 is also important because there's data that higher MAP's in patients with chronic hypertension is better for them. I see shops where the MAP goal is 60 and that's just plain stupid and only acceptable on a case by case scenario.

Patients in this study received vasopressin as monotherapy for septic shock and it did not cause issues.

There is much to be said about the methodology of this trial which I am not going to get into today. I'll be here forever. Instead, you can hear me take it apart live in Hawaii in May 2020.

A hat tip to the authors.

- EJ





Link to Abstract

Link to FREE PDF


Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock. JAMA 2016; 316: 509.

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Wednesday, August 14, 2019

Enteral Nutrition Can Be Given to Patients on Vasopressors



Link to Article (Not Free)

I have always been interested in the nutritional status of our patients in the ICU and I don't quite have my mind made up regarding a lot of things. Actually, within the next few months I am going to be asking my registered dietician colleagues here for help with a number of clinical questions.
Truth is that there is a void of solid data regarding nutrition, when to start, how much, how much protein, etc. I understand the ASPEN guidelines have provided some consensus, but much of it is expert opinion rather than actual data. I digress. A topic for another day.
Regarding this article that was published yesterday, the author detailed the vasopressors doses at which one should start feeds (or not start, norepinephrine > 0.3-0.5mcg/kg/min is a no-no), resuscitation markers that should make us feel more comfortable with starting feeds such as decreasing downtrending vasopressor doses.  He also describes the feeding strategy of starting with tropic feeds at 10-20cc/hr.  Lastly, he describes signs of intolerance including residuals > 500cc, note, not 250, not 300... 500.
I have some honest questions for which I personally do not know the answer, though. I need help with this if someone knows the answer. From an evolutionary standpoint, we do not eat when we are ill. Just remember your appetite for a big delicious meal when you last had a significant viral illness. Should we really start to immediately feed these patients? Also, I do not feel that our bodies are accustomed to this whole continuous feeds phenomenon. We normally bolus feed ourselves. Are we shocking the system by doing continuous feeds? See? This is why I need help from some badass registered dietitians.
🎩 tip to the author!

-EJ

Friday, August 2, 2019

Optimal norepinephrine-equivalent dose to initiate epinephrine in patients with septic shock



Link to Abstract

I am quite confused by this article. I was hoping for some answers on how to manage norepinephrine and epinephrine in septic shock but instead I am left scratching my head wondering what in the world happened here. If you're on my page and following along in on this journey, then you know a thing or two about septic shock patients. This article was supposed to provide us with some data regarding when to start epinephrine on these patients once levophed was already running. Instead, you find a retrospective observational study with a statistically significant difference between the optimal dose group and the non-optimal dose group. Within the subgroup analysis, though, you can find that 83.3% of the optimal dose group was also on vasopressin while 62.3% of the non-optimal group was on vasopressin (p=0.001). Does this mean that there's a dose to start epinephrine when a patient is on norepinephrine, or does this mean that before starting epi, you should have vasopressin on board? 

-EJ

Purpose: The specific norepinephrine dose at which epinephrine should be added in septic shock is unclear. This study sought to determine the norepinephrine-equivalent dose at epinephrine initiation that correlated with hemodynamic stability.
Methods: Septic shock patients receiving both norepinephrine and epinephrine were included in this study. Classification and regression tree analysis was conducted to determine breakpoints in norepinephrine- equivalent dose predicting hemodynamic stability, with two cohorts identified. The primary outcome was hemo- dynamic stability, and secondary outcomes were shock-free survival, time to achieve hemodynamic stability, and change in SOFA score.
Results: Optimal dose group was identified as initiating epinephrine when norepinephrine-equivalent dose was between 37 and 133 μg/min. A total of 138 and 61 patients were classified in optimal and non-optimal dose groups, respectively. Baseline characteristics were similar between groups except vasopressin use was more fre- quent in the optimal dose group. More patients in optimal dose group versus non-optimal dose group achieved hemodynamic stability (40 [29%] vs. 9 [14.8%]), absolute risk difference 14.2% [95% CI 2.5–25.9%]; p = .03). On multivariable analysis, initiating epinephrine within the optimal norepinephrine-equivalent dose range was independently associated with higher odds of hemodynamic response (OR 3.06 [95% CI 1.2–7.6]; p = .02). No dif- ferences were observed in other secondary outcomes.

Conclusions: Initiation of epinephrine when patients were receiving norepinephrine-equivalent doses of 37–133 μg/min was associated with a higher rate of hemodynamic stability.

Tuesday, April 2, 2019