Today I had the pleasure to interview Dr. Paul Marik, Professor and Division Chief of Pulmonary Critical Care at Eastern Virginia Medical Center. We got to speak on the topic of fluid responsiveness–one of the toughest questions in critical care.
Fluid Responsiveness
The definition we are using for fluid responsiveness is an increase of stroke volume of 10-15% after the patient receives 500 ml of crystalloid over 10-15 minutes
Dr. Marik’s Path through the Morass
this is a modification of the algorithm from Dr. Marik’s upcoming paper
* if using passive leg raise, give a 500 ml bolus if the response is positive
What is Passive Leg Raising?
For a brief period of time, a bolus of fluid is sent to the heart, allowing you to test fluid responsiveness without doing anything permanent to the patient’s fluid status.
What is the Monitor that Dr. Marik mentioned?
The NICOM Monitor by Cheetah Med uses bio-reactance to yield cardiac output/stroke volume non-invasively. I have been trialing the monitor and have been very impressed so far. It is inexpensive and correlates with my echocardiograms.
Articles of Interest
- This systematic review basically was the end of using CVP in the ICU for fluid responsiveness: Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares
- Marik’s review of hemodynamic parameters to guide fluid therapy
- An even better review by Dr. Marik will be published in the journal Resuscitation, as soon as it is published, I’ll put it up on the site
- If using Pulse Pressure Variation, probably only helpful if <9 or >13: Assessing the diagnostic accuracy of pulse pressure variations for the prediction of fluid responsiveness: a “gray zone” approach. by Maxime Cannesson (Anesthesiology. 2011 Aug;115(2):231-41.)
Neither Dr. Marik nor I have any Conflicts of Interest!
Update 6-10-12
Here is an amazing review article by Dr. Marik on this topic
and Now to the Podcast…
Podcast: Play in new window | Download (22.1MB) | Embed
Hi, my name is Scott Weingart. 
I noticed the technology used in the NICOM product runs a small current through the patient at radio frequencies (not sure if it is low-frequency or high-frequency). Does this interfere with the surface ECGs or do the standard monitor-mode filters work fine?
Never noticed a whit of interference thus far
Thanks Scott and Dr Marik
Profound stuff! Keep it up. My service looked into one of these non invasive CO monitors using doppler USS. a few years ago and nothing ever came of it as the evidence at the time was not so convincing. It seems things have matured. prehospital CO measurement…now thats an exciting concept!will chase this up again with my retrieval colleagues!
Hi Scott. Sounds like there has been a lot of movement in this area in just the last 12 months or so.
I have been trialling the arterial line based SVV CO monitor and found it has limitations as discussed in the talk with Dr Marik
Probably the single biggest limitation is the reliance on the staff to run the machine / calibrate, interpret and “trust” the numbers. There is a lot of fiddle and training required for the device we are using at the moment – and it does rely on a patient being ventilated – so only the super sick in Broome.
For me, the need to stick an A-line into somebody where you may or may not great data out is tough, and my colleagues are not convinced either – so a completley non-invasive device that costs nothing in terms of harm to the patient is a winner in my shop. I think it will be the next device I trial – it will be nice to have a device you can use on the medium-sick patients, to learn the ropes and get a feel – it always seems unfair to “play and learn” on a patient who is really in trouble. With limited resources in terms of manpower – fiddling can be doing harm to the patient!
Will have to get me one of those!
Casey
Hi Casey,
What monitors do you guys run?
The Phillips MP line does PPV (aka SVV) out of the box (at least the MP50, 70 and 90′s I play with, not sure about the MP30), so if you have a medium sick patient who you don’t feel like putting a Vigeleo on (I assume it’s a Vigeleo), you can set it up and it spits out a number at you, no fiddling with another machine or otherwise interrupting your workflow; enable it, wait ~30 seconds, and get a number.
I use PiCCO and Vigeleo a fair bit, but it can be tough convincing other people that they improve outcomes given there doesn’t appear to be much evidence at all when it comes to ICU patients.
The NICOM monitor looks very interesting, although I think it could be tough to convince people it gives real numbers; a lot of people still scoff at the numbers that a PiCCO thermodilution gives you.
(I swear I don’t represent any of these companies, I just love me some technology!)
Shaun
Got a bit worried when he started talking noninvasive! We trialled a bioimpedance device about 7-8 years ago and were way less than impressed. I’ve often wondered why more people don’t use the simplest tests, 500cc bolus or passive leg raise. Dr. Marik shows remarkable common sense.
Scott, thank you for this amazing blog. Besides tons of useful information it’s a great source of inspiration.
Just want to ask what you think of dr Lichtenstein’s protocol where you give fluid till you get the “wet” pattern on lung ultrasound (predominant B-lines)? It’s extremely simple so nice in the ED/non-ICU ward, and you get to see what actually happens in the organ most sensitive to fluid overload. Even SV must be a surrogate parameter in a sense?
in performing the passive leg raise—how long do you wait before rechecking the blood pressure? what are you using as your stroke volume surrogate?–systolic, diastolic, or MAP? I assume we are looking at a greater than 10% increase as being indicative of “fluid responsive”. This seems imprecise without an A-line but you say simple non-invasive BP measurement can work?
Intermittent blood pressure will not work. For an a-line I think a 10% increase in MAP or SBP is a reasonable positive. But if negative, it doesn’t mean the patient is not fluid responsive.
If the result is negative durante the PLR.. should that repeated.. or give the patients medication (inotropics, etc)?
If negative, use pressors or inotropes; recheck for fluid responsiveness in a bit.
Scott -
I appreciate the perspective of Dr. Marik, and it was an interesting discussion. It was somewhat frustrating to hear, though, to hear the empiric data for septic shock dismissed out of hand.
I would tend to agree about the accuracy of CVP as an isolated measurement of fluid responsiveness, no argument there. However, whatever the limitations of the Rivers trial, it gave us actual outcomes, an NNT for mortality. You can’t ignore the fact that it did so, in part, by using the CVP to guide therapy.
Sure, there may have been some clinicians who applied the results of EGDT in a rote, unthinking fashion – “6 liters in the first 6 hours” – but it seems like Dr. Marik used that characterization to invalidate the application of the study’s results, setting up a “straw-man” argument.
Is there any comparable outcomes-based research using the NICCOM or similar) devices?
Thanks for the podcast!
Brooks, Thanks for the comment. I can’t say I agree with you. One thing the EGDT trial did not show at all is any value to CVP per se. Both groups got CVP monitoring and both groups had the same CVP goal.
I believe Dr. Marik’s comment re: empiric fluid admin was less a commentary on Rivers’ trial than the ongoing PROCESS trial in which empiric fluid admin without a marker is considered a good idea.
Dr. Weingart, I want to congratulate you for this podcast, it is excelent, for me, the best of the best. I work in Laredo, Tx Doctors Hospital ER and I use a lot of your concepts to take care of my patients. Again congratulations and I hope you
keep on with this cast.
Best wishes
Carlos F Crespo, MD
Much thanks for the feedback, Carlos
Fantastic podcast! I’ve been waiting a while for this one. I have a couple of quick questions though. First, is there any data out there on whether sonographic parameters like IVC collapse or LV diastolic function (like the ultrasound podcast guys suggest) correlate w/ fluid responsiveness vs just static measures like CVP OR PAOP?
Second, and this is just a random thought I had, but what about using a continuous ScVO2 monitor in lieu of the SV monitor in the algorithm above to see if DO2 is increased w/ the fluid challenge?
Thanks!
IVC with mech vent has shown fluid responsiveness; spont resp–nope.
ScvO2 and SvO2 has been used for this purpose (and to decide who needs blood transfusions as well). It is a bit downstream though, and doesn’t measure regional improvements in perfusion.
Does anyone have any experience with the NICOM in the pediatric population? Are there any studies supporting the use of this monitor in pediatrics?
haven’t seen any peds stuff yet
Hi Scott, Loved this podcast. Totally agree with the best measure being actually giving a volume challenge via fluid or passive leg raise and evaluating the results. However, given the infrequency of CO monitoring in my ICU – I do also find myself using a gross assessment of PPV or Systolic pressure variation and IVC distensibility as well as the chart etc in my assessment of whether a patient will be fluid responsive. My question is:
Given that we have established that there is poor correlation between CVP and fluid responsiveness, what is the physiological rationale behind why IVC distensibility works. I understand that it is a dynamic test however, surely it is simply proportional to the relationship between the airway driving pressure (Pinsp-PEEP) and CVP. As such it does not really represent the preload to the LV and it is affected by all the same variables as CVP such as RV dysfunction, changes in pulmonary vascular resistance etc that occur in critical illness.
Or am I missing something. Perhaps the original studies were in a healthier population with good lungs and good RV function. Any help with thinking this through would be great – as I really think IVC ultrasound is a neat test but can’t get past the above theoretical problems.
Cheers, Mike
ED/ICU registrar Australia
How can the CVP be a the devil and the IVC be wonderful. They are looking at the same vessels! I know CVP is pressure and IVC is volume. Is it possible to have a high CVP with a full collapse and possitve IVC exam? Please explain!