fluid responsiveness

October 6, 2014

Fluid Responsiveness: Getting the right answer to the wrong question. #FOAMed, #FOAMcc, #FOAMus

Let me start with a clinical scenario: you have a 68 year old male in front of you who is intubated, has bilateral pleural effusions, pulmonary edema, a bit of ascites, significant peripheral edema, elevated CVP/JVP/large IVC, and a moderately depressed cardiac function.  What is the diagnosis?

If you said CHF, you might be right. If you said post-resuscitation state in a septic patient, you might equally be right. Hmmm….

So as any self-respecting FOAMite knows, there is an ongoing and endless debate about fluid responsiveness, how best to detect it, what exact percentage of some variation represents it – is it 9% or 13% – and everyone has the way they swear by.

Well, I think the entire premise behind this is essentially flawed.

The fact that this is the first question implies that the answer should radically change management (eg giving or not giving fluids “generously” – yes, the quotes imply facetiousness).  Basically, that you should stop giving fluids when your patient is no longer fluid-responsive. The implication is that fluids is a better, safer, healthier, more naturopathic, eco-friendly and politically correct therapy than any other option.

I think we should reflect on that a little.

If you put some faith into normal physiology, you have to acknowledge that the only situations in which our cardiopulmonary system finds itself nearly or no longer fluid responsive are pathological: CHF, renal failure, etc. None of those are healthy. None of those are a bridge to healing.

What do we do when we are hypovolemic?  We vasoconstrict, stop peeing, try to drink a bit (if at all possible) and slowly replete our intravascular space via the portal system. We might build up a little lactic acid (helps feed the heart and brain – yup, nothing toxic about it), but we get over it.  Of course, if we lose too much, the system fails and we head to meet our maker.

Now, having remembered that, why do we feel (and I say feel because the evidence isn’t there to back it up) like we have to get to pathological levels of intravascular venous pressure to fix the problem?  Especially when the problem at hand isn’t primarily hypovolemia, but mostly vasodilation, with possibly a relative hypovolemia in part related to increased venous capacitance.

The real question is: does my patient really, truly need a lot of fluid?

And here is the catch: just because someone is fluid responsive doesn’t mean that they need any, or that it is the best thing for them. Whoa… Heretic… I thought “aggressive fluid resuscitation is the cornerstone of resuscitation in sepsis.”

I think that answer is relatively simple.

No matter which method you are using (mine is IVC ultrasound: -https://thinkingcriticalcare.com/2014/04/01/the-ivc-assessment-by-bedside-ultrasound-lets-apply-some-common-sense-foamed-foamcc/), if you are deciding based on a millimetre of diameter, or a couple of percentage points of variation whether or not to give liters of crystalloids to your patient, there is no truth to that in the individual patient. Trying to figure out the tiniest of differences to decide our therapeutic options is, in my opinion, a huge waste of time with no scientific basis in the one single patient you are treating.   It’s like haggling for a dollar on a hundred dollar item in a flea market: you’re missing the boat.

“85% of patients with a IVC/SVV/SPV/PLR of …. are volume responsive” or something of the sort does NOT apply to the one patient you have in front of you as a recommendation for fluids. You have to make a complete clinical picture of it – feel the belly, look at the inspiratory effort, examine the tissues for edema, etc.

Grey zone it. The best we can do is a gross categorization of truly hypovolemic (need a lot), full (please don’t give me any), and “normal” which may need maybe a little, but probably not “generous” amounts. You’ll end up generously feeding the interstitial space and making things worse – and later maybe saying “oh well, I guess he/she was just so sick…”

Even if my patient is fluid-tolerant, why to we want to push him into near-pathological states? Is it just the old adage of “You have to swell to get well?”  In the light of much of our literature, I’m not sure that old wives’ tale holds a lot of water.

Are vasopressors that bad?  Not according to what we know…

At least, avoid actually reaching the point of no longer being fluid responsive. You can’t tell me you think that CHF is actually a good thing, can you?

 

Love to hear your thoughts!

 

Philippe

PS, if you like to think out of the box and rather be on the cutting edge, make sure to mark your calendar for the coolest conference in Canada: #CCUS2015….http://wp.me/p1avUV-bh

 

 

COMMENTS

SQS Replies:

Philippe,
I think your logic is sound enough, but the moat that makes it currently unassailable is that you are working in an area with no or very little data. There is clearly a reasonably well developed and continuing to develop literature around the mortality effects of excess volume. There is an older literature that suggests that our vasopressors are actually having their effect on the more normally functioning arterioles and may shunt well oxygenated blood from the well functioning cells of a tissue and to the ones that are shocked and can’t use the oxygen, anyway. At this juncture, your guess is as good as mine, as to which of these is the greater evil. Ergo, your argument is as good as any.

One thing I will say is that the patients who concern us are those in whom endotoxin, blood loss, or other factors have resulted in a shock state wherein cells and even large parts of tissues have both inadequate oxygen supply and inadequate ability to use whatever oxygen is supplied them. Any tool we have to alter this pathological state is blunt. Blood pressure? CVP? IVC size and behavior? SVI? What do any of these say about how well we are doing at the tissue and cellular level? Even the interesting markers of lactate, ScvO2, CV CO2, etc. are blunt instruments. As is our bag of fluid and as are our vasopressors. And think about our end result – “hemodynamic stability”, “better mental functioning”, “good urine output”, “feeling better”, “walking around”, “able to go back to work”. Things that are important to us and to our patient, but barely even measurable. How blunt are they?

My own approach, which I suspect to be yours, too, is to recognize that the new onset shock patient is momentarily different from the chronic CHF patient/”chronic” shock patient you describe above. We know there is an oxygen deficit, and it behooves us to correctly that as quickly as we can. We believe, with some data to back us up, that rapid correction of that deficit, to the extent that we can, can prevent the ugly chronic state. I use the blunt measures of fluid responsiveness in the first hour or two of resuscitation to ensure that the CO component of oxygen delivery is not deficient, and then I stop giving fluid. Early in the course, I am prone to rechecking “volume responsiveness” in some hours, because I know that fluid is leaching out of the vascular space and the patient has not stabilized, yet. All the while, I am highly aware that I am hoping this makes a difference, not knowing that it does. I am aware that it is rather circular to check SVI or IVC, give fluid, see a change and say, “See? Volume responsive.” And all the while knowing that every patient has his or her own line, beyond which more fluid will not be helpful but harmful. And all the while knowing that I can’t see that line, nor measure it with any tool that currently exists.

I think perhaps that we are like Phoenicians, navigating our way across the ocean by the North Star and trying to keep land in sight. We do a pretty good job of getting where we’re going a lot of the time. But won’t it be nice when we come up with GPS? Or even the astrolabe?

SQS

 

Fantastic points!

I can’t agree more. I do check for fluid responsiveness, and I do believe in rapid intervention – just perhaps not quite a vigorous and generous as medical marketing would have us buy. There isn’t more data for that than for a somewhat more conservative approach, in my opinion. Even the rate of administration is rarely looked at, just the totals. There is good animal data showing that, for instance, a more rapid rate of albumin infusion results in greater leak and less intravascular albumin at 6, 12 and 24 hours.  Little reason to think it would be any different in humans.  There is also data showing that the oxygen deficit in sepsis is not as ubiquitous as we think.

Our understanding of the septic disease state is minimal at best, and our tools exceedingly blunt, as you point out.  

GPS or astrolabe would be amazing. I’ve had a few discussions with people working on cytochrome spectroscopy – a possibility to assess mitochondrial “happiness,” which could give us an oxygenation endpoint. Then we could have a trial that might end up showing which degree of mitochondrial oxygenation is optimal, if any.

I know I am playing a bit of a devil’s advocate and that, in strict numbers, I probably don’t give a lot less fluid or a lot slower than most, but I think it is important to keep our minds open to change rather than keep a clenched fist around the ideas we have. 

When we have two docs debating whether IVC, SVV, carotid flow time (I do like Vicki’s stuff a lot) or something else, I think we are mostly in the grey zone, and the good thing is that either way, we are dealing with two docs who are aware and conscientious and doing the rest of the right things. But keep in mind there are a lot of docs out there who are in the acute care front lines who believe that bicarb “buffers” lactate. And by buffers they understand “neutralizes.”

I just hope that when the GPS comes along, we don’t lose ten years of knowledge translation time because we are still clinging to (at that point) outdated ideas like the IVC ultrasound… 😉

cheers and thanks so much for contributing fantastic material!

Philippe

Marco says:

Philippe, I really feel like being on your same wavelength when I read your posts about fluid responsiveness. I think it’s obviously easy to agree that a bleeding hypovolemic patient is fluid responsive AND needs fluids, but the more accurately I think about the physiology of fluid resuscitation when a nurse is asking me “should we give him some fluids?” the more I realise that the “grey zone” is large and its upper limit is not easily detectable. Probably if you fill your patients to the point where they are no more fluid responsive, you are sure that no more fluid is needed, but you should be able to stop a bit earlier.
Blunt instruments and measures are an issue, and integration of the data is a possible solution (at least until a GPS comes along), but critical thinking is always a valuable resource.
The more I grow old the more I become minimalist in my approach to the “chronic acute ill” patient (90% of the patients on an ordinary day in my ICU). If a patient is in the grey zone, with a reasonably good hemodynamic stability, some vasopressor support, low dose diuretics and his urine output decreases, probably the decision of giving him fluids OR diuretics would be equally harmful. When a patient is in the grey zone and your instruments are not so accurate, it’s better to keep him safely in the grey zone. When you are in the mountains, you are caught in a snowstorm and cannot find your tracks, the safest decision is to stop and wait.. or follow your GPS 😉

Marco

thanks!

You hit the nail on the head with “integration is key.”

Philippe

April 1, 2014

The IVC Assessment by bedside ultrasound: Let’s apply some common sense! #FOAMed, #FOAMcc

So I have a huge issue the IVC and its ultrasound assessment. For the most part, neither the yay-sayers or the nay-sayers are applying much sound physical principles, as far as I’m concerned.

To assess a patient’s volume status, it may be practical to begin with the sub-xiphoid view of the IVC, since the decision to give fluids or not – especially in emergency situations – can then be taken within the first few seconds of examining the patient. The physiological rationale behind assessing the IVC as a marker for volume responsiveness is simple and solid. As the venous compartment fills, the size of the IVC will gradually increase until it reaches a maximal size of about 20-25mm or even 30mm, depending on physical size and chronicity.

Concomitantly, the phasic respiratory variation will decrease as the venous pressure increases and the effect of varying intrathoracic pressure is no longer felt. At this point, the flat part of the Starling curve of the right ventricle is approaching, and there is little response to volume, and little physiological rationale to support giving more.

Currently, many use a variation of about 20% or more to suggest a volume responsive state in ventilated patients or an inspiratory collapse “sniff test” of 50% or more in spontaneously breathing patients.

There remains controversy around using IVC assessment for volume responsiveness, and with good reason! There are a few important reasons why:

a. technique – First of all, there is the manner in which IVC measurement has been taught: the M-mode measurement of the antero-posterior (AP) diameter during breathing (usually of ventilated patients) about 3 cm below the diaphragm. Although highly practical and reproducible, it has many shortcomings. If we look at the physiology, what changes with cycles of respiration is the volume of blood entering the chest/right atrium. Hence the key variable we are trying to assess is the transient variation in IVC size – which is a volume, not a linear dimension (I’m getting painful flashbacks of using pressure  to determine volume!)Hence the use of a single linear measure on one point along the length of the IVC to assess this is inherently flawed. For instance, the figure to the left shows how, if this IVC were to be measured in its AP diameter, the variability may not be that great. In the short axis, however, one can clearly see the significant change in surface area, and hence volume between phases of mechanical ventilation. Also, the IVC is rarely perfectly circular, but often ovoid, and occasionally with the greatest diameter in an anteroposterior axis, making that single AP measurement even less relevant.

b. intrathoracic pressure – Secondly, the variation in intrathoracic or intrapleural pressure (Pip) must be measured, as, for instance, a young and fit patient can generate large changes, which would result in more significant IVC variation, as compared to a frail elderly patient, even if they are on the same point of their Starling curve, invalidating the IVC measurement. All “sniffs” are not created equal.

c. intra-abdominal pressure – Finally, the intra-abdominal pressure (IAP) must also be assessed, since an elevated pressure would decrease the size of the IVC and make that measure no less accurate, but less relevant in terms of representing venous filling.

So what should we do?

Instead, a more global assessment of the IVC volume, measuring short axis area measurements and variation at several points along the IVC would give a much more accurate estimate of IVC volume variation. This is currently being studied by our group.

“Eyeballing the IVC” Attempting to link evidence and physiology, some bedside sonographers’ approach is to take a global look at the IVC in both long and short axis during respiration, while clinically assessing the respiratory effort and the abdominal pressure. This approach is analogous to the “eyeballing” of LV function – versus more formal measurements such as Simpson’s disk method, etc – which has been proven just as accurate with sufficient clinical experience.

The figure below shows an IVC that is about 10-12mm along most of its intrahepatic segment on expiration, and collapses almost completely on inspiration. If this belongs to a patient breathing with little effort and with a soft abdomen to palpation, it is physiologically quite clear that this patient would be fluid responsive. It also shows how impressive the collapse is in the short axis.

IVC insp dual

For instance, let’s say Patient A is in respiratory distress and using accessory muscles and presents to the ER with a respiratory rate of 35 and a systolic BP of 80. His IVC measures approximately 21 mm in diameter at several points along its axis, and has a brief collapse to about 10 mm with strong inspiratory efforts. His abdomen is soft during inspiration but firm during a prolonged expiratory phase.

Patient B is brought to the ER somnolent with a respiratory rate of 10 and a systolic BP of 80. His IVC measures 15 mm with minimal respiratory variation. His respirations are shallow and his abdomen soft. These two patients show how the IVC assessment needs to be taken in clinical context.

Patient A has some 50% inspiratory collapse of a large IVC in the context of large variations in Pip, whereas Patient B has little variation of a mid-sized IVC in the context of very small variations in Pip. In all likelihood, Patient A is not very volume responsive, while Patient B probably is.

Volume Responsiveness vs. Volume Tolerance – it is critically important to distinguish the difference between these two concepts as they are often misused interchangeably: Volume responsiveness refers to an increase in cardiac output (CO) to a fluid challenge. This is a purely hemodynamic concept. Volume Tolerance refers to whether or not a patient can tolerate volume without clinically significant side effects. This is a complex clinical assessment that should include: -the patient’s plasma oncotic pressure (serum albumin) and level of capillary leak, if present, -the patient’s pathology – is there risk of capillary leak in critical tissues such as lung, brain, abdomen? -the type of fluid being considered (isotonic crystalloid vs hypertonics or colloids/blood products). It is important to distinguish that not all patients who are volume responsive are necessarily volume tolerant.

Volume assessment summary – this issue remains a difficult one, even with the use of bedside ultrasound, because the optimal point for any one patient to be on his or her Starling curve at any one time in different clinical conditions remains elusive. Despite considerable study and several proposed management algorithms, there is no means by which to determine exactly how much of any given fluid is enough, without being too much.

In my opinion… – no direct evidence – keeping an IVC below 20mm and probably below 15mm with significant respiratory variation, if hemodynamics allow, is probably ideal. However, bedside ultrasound allows to clearly identify the cases where fluid is clearly needed and those where fluid is unlikely to benefit. Both of these scenarios are easily and routinely missed by traditional examination. Additionally, when the IVC assessment is done in conjunction with lung ultrasound, it becomes possible to detect early development of pulmonary edema and halt aggressive fluid resuscitation (FALLS Protocol, Daniel Lichtenstein).

 

Technical Pearl: the part of the IVC we generally assess being the intrahepatic segment, it is possible to find it almost by scanning through any part of the liver, which happens to provide a great acoustic window. This may be particularly useful when the epigastric area is difficult to access (incision/bandage, drains, in the OR, etc…) or when there is bowel gas in the epigastrium. The figures below show the same IVC, first in a “traditional” epigastric view, then in a view approximately along the plane of the red arrow on the CT scan.

2 views IVC std:liver

CT liver IVC views

 

Bottom line?

When assessing volume status, it is absolutely essential to keep the clinical question in mind. It is a great minority of patients who are volume responsive who actually need volume. Normal, healthy humans are very much fluid responsive and fluid tolerant but certainly not in need of any. Much of the current studies and literature focus on assessing volume responsiveness in the setting of shock, which, although arguably the most important, is not the only type of information that can be obtained from the IVC. For instance, as will be discussed in the chapter on congestive heart failure, knowing that your patient is very “full” should prompt further diuresis. If you are dealing with managing severe anasarca, knowing that a patient’s intravascular volume is low may prompt the use of albumin or hypertonics prior to further diuresis to help resorb some of the interstitial fluid. Another critical question to which there is currently no answer is just how much fluid to give to patients in shock. There are many opinions but no certainty. It is common practice to fill a patient in shock until they are no longer fluid responsive, in an effort to avoid or minimize the use or dose of vasopressor medications. There is no study to date that compares a “moderate fluid/early vasopressors” vs “aggressive fluid/avoid-vasopressors-if-possible” approach.

Hopefully this will be answered soon. In light of the clear evidence linking positive fluid balance and mortality, it would seem wise to fill to a “moderate fullness” where some respiratory variation remains, rather than to the point of no longer being fluid responsive. After all, physiologically, the only time humans are really full (>20mm IVC with little or no variation) is in pathological states of congestive heart failure or obstructive shock. So again, when assessing an IVC, keep in mind what your clinical question is and interpret the sonographic data accordingly.

 

cheers!

 

Comments:

Marco says:

Thanks Philippe, very interesting post.
Using your great categorization, I think that the worst scenario is represented by a patient who is volume responsive but poorly volume tolerant. In that case, it is important to have clear in mind which is our target: cerebral perfusion, oxygenation and lung extravascular fluid, ventilatory weaning, renal function, avoiding vasopressors or mechanical ventilation, etc…
Very often, maintaining a brain dead heart beating donor, every organ would require a different volemic status, and if all of them are suitable for transplantation you have to compromise.
Just a last thought: as well as “all sniffs are not created equal”, also tidal volumes are very variable. Assessing respiratory variations during protective (low TV) ventilation requires a thoughtful interpretation of the results.

 

Absolutely. Interpretation of the findings in each individual case is key. 

Philippe