Cite this post as:
Scott Weingart, MD FCCM. An Uproar about the IVC. EMCrit Blog. Published on July 8, 2017. Accessed on April 20th 2024. Available at [https://emcrit.org/emcrit/an-uproar-about-the-ivc/ ].
Financial Disclosures:
Dr. Scott Weingart, Course Director, reports no relevant financial relationships with ineligible companies.
This episode’s speaker(s), (listed above), report no relevant financial relationships with ineligible companies.
CME Review
Original Release: July 8, 2017
Date of Most Recent Review: Jan 1, 2022
Termination Date: Jan 1, 2025
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1. The concept of fluid responsiveness and the idea that the only benefit of fluid administration is to increase cardiac output are not evidence based, and I would even argue they are likely an oversimplification. As Marik himself points out, there is a wide range of cardiac outputs in critically ill patients, and it’s been shown that artificially increasing this with inotropes does not seem to have any benefit. 2. Having used the NICOM, which seems to be a random number generator, I am extremely skeptical of a paper using it as a gold standard. 3. Putting aside the first… Read more »
#3 is the money–it’s why i really don’t even think about fluid responsiveness anymore
Explain further, please. Sorry; getting caught up.
My 2 cents worth (if its worth that much). #3 is the answer. The fact that a patient is a fluid responder does not imply that the patient will benefit from fluid. Furthermore, in the responders the hemodynamic benefit is usually very small and short lived (in the septic patient); the net result is minimal hemodynamic benefit with severe tissue edema. A very important point that is often neglected is: “what’s wrong with the patient and where do you want the fluid to go.” The approach to a patient with DKA (or severe diarrhoea) and sepsis (the very patients included… Read more »
” The fact that a patient is a fluid responder does not imply that the patient will benefit from fluid.” – Totally agree. Would love to see this studied, with a randomized controlled trial of size adequate to give us meaningful data. The reality is, that hasn’t happened. so w’re left debating physiology. I love physiology. Believe me, I make it a point to teach residents physiology all the time, it’s the basis of how we should think about medicine and pretest probabilities of therapies.Physiology is the best possible starting point for us to launch our journeys into science. But…… Read more »
There’s also a distinct possibility that Marik is physiologically correct about IVC ultrasound and yet operationally wrong. Maybe IVC ultrasound is a random number generator, just as I think the NICOM device is. But a random number generator will tell you not to give fluid half the time, while most physicians treating sick patients always think more fluid is the answer. So maybe even a worthless test is indeed better than our “judgement” here.
Dear Prof. Theyyyunni,
Physiology is a fact, how to use or interpret it is the matter of discussion.
Unfortunately, physiology is not a fact. It’s a collection of hypotheses based on experimental data, attempting to simplify the behavior of an extremely complex system. When we attempt to create therapies based on physiologic reasoning, we find that they are usually ineffective, suggesting that our understanding of physiology was inadequate to begin with.
Very nice explanation and I fully agree with it. This makes even more complex the connection between the physiological phenomenon and how we interpret and use this in our therapies. As you mentioned, very often our inadequate understanding of physiology is the main problem with ineffective therapies based on “normalizing” physiological end-points. Just take as an example, CVP in hemodynamic resuscitaiton, the central oxygen saturation, or supranormal DO2 in septic patients. I think we cannot say that ” in the absence of empiric data to validate it, physiology remains a fairy tale”, as Dr Theyyyunni suggested in his comment.
The problem with both CVP and cIVC is that they do a poor job of reflecting vascular capacitance unless that capacitance is at an extreme (high/low). This, I think is the black box of all of this. If we figure where on the pressure volume curve the capacitance of the vascular system lies we can better understand the IVCs or CVPs ability to reflect a response to a fluid bolus. Im curious if this could be quantified by calculating the IVC changes in response to fluid bolus i.e. as the volume change begins to drop with subsequent boluses then capacitance… Read more »
This should be good… looking forward to the ensuing podcast and Rory’s post. Fluid responsiveness is an interesting surrogate, but I don’t believe that it has been proven to improve outcomes. Most of the crystalloid that we give to septic/inflamed patients will eventually end up in the tissues. Even if this fluid is able to cause a transient increase in cardiac output prior to transuding into the tissues (“fluid responsiveness”), eventually it’s still probably harming the patient. Off the top of my head I can only think of a few RCTs evaluating fluid: – FEAST (fluid boluses in African children… Read more »
We can definitely argue about whether or not fluid responsiveness is the right question – but until they’re actual randomized data on this people are going to ask the question. As it is, large volume vs not large volume resuscitation isn’t a well studied topic. Totally worth looking into, maybe one of the PETAL network trials will do this soon, would be awesome if it was well designed. I have some issues with you’re references here though: FEAST: african children, with no ICU resources, esp vents, no guidance to the resuscitation at all (which is the whole point of talking… Read more »
The main utility of IVC US in my practice is around fluid safety. We use a nearly completely non-invasive system to monitor (some art lines). IVC gives some data – which needs to be interpreted in the specific context of the individual patient. A flat / near 100% collapsed IVC is probably useful to know about? However, if giving vasopressors achieves the same “plumping” of the IVC as a gallon of fluid – then I don’t need to know if they are “fluid responsive”. To me a flat ivc just means something needs doing. The “what” depends on the other… Read more »
More Reflections. I believe that the study by Cori et al is fatally flawed primarily as the patient population consisted of patients with sepsis (44%) COMBINED with those with DKA/HHS (38%). These are two clearly distinct disorders and from a fluid management perspective are managed completely differently. The management of DKA/HHS is not controversial with well-established universally accepted treatment guidelines. [1] Conversely, the fluid treatment strategy in patients with sepsis is more controversial with no universally recognized approach. The primary inclusion criteria for this study was “acute circulatory failure”. Having treated patients with DKA/HHS for over 30 years in both… Read more »
Hi all. As someone who has never posted to a medical blog before today I must say that I am both simultaneously flattered and surprised that our manuscript has stimulated a debate. I’d like to make a few statements in response to a number of comments so far. #1 I’m in 100% agreement with the statement that just because a patient is fluid responsive, that doesn’t mean you should continue to give them IVF. The question of does fluid responsiveness (aka tailored resuscitation) matter needs to be examined in a prospective RCT with hard patient oriented outcomes. #2 The most… Read more »
Keith: At least we have “some agreement” and that is good. The post did generate a Twitter storm; which in itself is also a good thing (although I am not a Twitter fan); if the post and Twitter result in folks critically thinking about the issues and engaging in meaningful dialogue then our Dear Friend Scott has achieved an important goal. Regards, Paul