So I just finished reading the CHAISE study, which compared Parm as a surrogate for Pmsf as a surrogate for “volume status.”
It is a really cool study for anyone who loves physiology, which I definitely do, and there may be some interesting elements that can be clinically used.
But let’s first set the record straight. I do not believe that “volume status” is a medical and especially not a scientific term. It is a vague reference to intravascular fluid and can be interpreted in a lot of different ways, making it essentially useless. There is such a thing as the status of your flight (on time, delayed, cancelled), your reservation (confirmed, cancelled), your postal delivery (returned, delivered, in-transit), etc. But there are no such clear strata for “volume status.”
So what are the true scientific terms that can be measured? Blood volume. So if we had a bedside radiolabelled substance test that could give us our true blood volume, that could give us a real measure of “volume status.”
On the other hand, that would be of marginal use clinically, in all likelihood.
Why? Because there are only three questions that the savvy clinician is trying to answer, in order of importance:
1. Does my patient need fluid?
2. Is my patient volume tolerant?
3. Is my patient volume responsive?
The answer to the first question is mysterious, outside of the obvious extremes, and in my opinion, anyone who feels they can clearly answer correctly is deluding themselves.
The answer to the second question is complex and multi-factorial and includes echographic findings (venous congestion/hypertension, B lines, effusions, ascites) as well as physical examination findings (tight abdomen, edema) and clinical findings (respiratory failure, intracranial pathology) and more. But this is a critical one, because if the answer is no, then you need some really compelling evidence to even consider trying to answer the third question.
The answer to the third question is, outside of the extremes, a bit of a quagmire of assessments and technology with generally poor evidence, particularly in terms of duration of effect. The most fearsome aspect of this third question is that it is usually the first question asked instead of the last, and thus has the side effect of creating volume-responsiveness terminators who, 500cc shot after 500cc shot end up satisfied that they have blasted responsiveness into oblivion.
But that’s probably bad news for the patient, that they have now pushed into venous congestion or salt-water drowning. Unless, of course, they just look for volume-responsiveness in the same way that bird-watchers do, for the sake of scientific satisfaction, and do no more than look, or maybe snap a picture at most.
So sure, echocardiographic parameters for volume status should be under fire, as all other parameters should. The authors in this paper themselves state two critical assumptions in the Parm/msf logic:
(1) that the fluid stay intravascular in the 10 minutes (ok, I’ll buy that)
(2) that the compliance is linear (nope, I don’t buy that, especially not in sick patients on vasopressors – as opposed to the normal cardiopulmonary and hemodynamic patients this study was done on).
Essentially, what should be under fire is the obsession with a measurable variable to assess intravascular volume. Too many factors in play, and the answer is useless clinically anyway.
On the other hand, this study is fascinating in terms of what might be done using dynamic Parm… Maybe individualizing pressor response, unstressed volume recruit-ability? I’ll let @iceman_ex tell us about that at H&R2019!
So what is important is stop points. And reverse points. And yes, these can be looked at using POCUS, and also CVP, and CVP tracings. And yes, there is good data that venous hypertension is a bad state. And this is what you should be looking at, to make sure you have not pushed your patient into a universally pathological state of non-volume-responsiveness.
So Kylie (@kyliebaker888) had some comments and questions:
Hi Philippe, I just had to read the article after your blog. Most is a bit above my head (yeah right Kylie)– but I am perplexed by three things that I did understand -perhaps you can help me with….
1. Is P(arm) a useful measure? – it went up in 19 patients and down in 8 patients after a 500ml bolus yet they claim it went up (after statistical repeated measures or something)..if P(arm) is confounded by something else – I think they suggest sympathetic tone – shouldn’t we sort that before we start using P(arm) as a reference test.
I don’t think we can consider it to be a reference at all. I think it is an interesting physiological measure and that it might have some application in phenotyping vascular tone/compliance and possibly helping in vasopressor fine tuning. In my opinion for fluids it adds little to what we have.
2. What do you think of their IVC measure – 0.5cm below junction with RA?
As I do for all IVC diameter measures, I think it is inherently mathematically flawed to try to assess a volume using a diameter. Eyeball the whole IVC. A recent study finally looked at this. 3D IVC assessment and (of course) found it better.
3. What do you think of the fact that E changed, but e prime and E/e prime didn’t….That seems like there may not be enough precision in some of those measurements.
I also have another savvy-clinician question to add to yours
Q4: Is my patient leaking?