8AM- Manoach- Hemodynamic Monitoring
9AM- Wright- ACLS
10AM- Mallemat- The slowly crashing tamponade pt
Part 2- Who really needs a central line?
11AM- Walalce- Part 1- Emergency Medicine Health Services Research
Part 2- Regional Critical Care Supply and Demand
This week hit a lot of great critical care issues. In my opinion the most thought provoking and controversial lecture was Dr. Mallemat’s lecture on who really needs a central line. He included a lot of literature by the powerhouses of sepsis management.
The biggest controversy is what you use to monitor patient’s response to therapy, i.e. fluids, ScvO2 versus lactate. I think as a residency we are already sold on US for hemodynamic monitoring and we all know CVC is not the way to go for large amount of fluids. I think we are a little biased in the lactate department due to being a PROCESS center.
In the study shown by Dr. Mallemat in the JAMA commentary by Dr. Jones about lactate he discusses his RCT showing lactate to be non-inferior to ScvO2. The mortality was not significantly different and he says lactate is a more accurate picture of global tissue hypoxia. And of course it is easier to obtain with no central venous access needed. Article can be seen here:
http://journal.publications.chestnet.org/article.aspx?articleid=1148995
Dr. Rivers’ counterpoint to this discusses lactate as being a lot more complicated than Dr. Jones claims. That lactate clearance and levels are affected by too many factors such as liver failure. He also states lactate level does not address specific issues such as inotropy and oxygen carrying capacity the same way ScvO2 does. His final point about lactate precluding CVC access is that it may cause people to place lines too late in patients who really need them. This article can be found here:
http://journal.publications.chestnet.org/article.aspx?articleid=1148996
I would like to hear your guys opinions on this debate. I think a lot of people should have something to say. This is something we will see and deal with for the rest of careers. Let’s here some responses from all our future critical care docs!
jwillis
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This was really an excellent lecture. Just my opinion but I think both ScvO2 and lactate clearance are about equally flawed but the best we have to use for this purpose so far. I don’t think there is strong evidence to use one over the other. I probably wouldn’t put in a CVC just to get the ScvO2, but agree with Dr. Mallemat’s sentiments that if you have a sick hypotensive septic patient, you need a CVC for pressors (dopamine is really not safer through a peripheral line than norepi!).
Great lecture both content and from a didactic point of view.
EMS in NYC, by protocol, give peripheral Dopamin for cardiogenic shock/hypotension. Granted they are not putting in central lines in the field and its a last ditch resort but is there evidence/case reports that it extravasates and is harmful? Thanks, Baruch
Yes, indeed this was a nice lecture. 2 mainly analytical studies which support lactate clearance as a predictor of survival:
Shock. 2009 Jul;32(1):35-9. (Prospective, observational)
Crit Care. 2011 Sep 27;15(5):R229. (Prospective, cohort)
I think at this time, we should use both ScvO2 and lactate levels, if possible, to guide resuscitation and management. For me, the main thing to remember is to FOLLOW SOMETHING – perform serial blood gases and look at these markers. If either ScvO2 or lactate clearance is concerning, re-evaluate your patient more closely.
Also, I agree that we should be a bit more aggressive about placing CVLs in presumably septic patients with mild hypotension or even borderline BP after initial fluid bolus. (This bolus recommendation is going to be changed to 30ml/kg over 30 min.)
My last point is to remember that dopamine may be dangerous, outside of its risk of extravasation when administered through a PVL. Remember there was a recent study possibly showing increased mortality when used in patients with cardiogenic shock (dysrhythmogenic). Some suggest one should use combinations of norepinephrine and dobutamine rather than dopamine (De Backer D – N Engl J Med 2010;362:779-89).