The Dialysis Waterfall (Forget Urea: It’s Fluid That Kills)
Far too much emphasis has been placed on an arbitrary and flawed concept—Kt/Vurea—to the detriment of all else.
Kt/Vurea was developed over 30 years ago after the publication of the NCDS study following 165 patients over 24-48 weeks of 1970's low-flux hemodialysis. None were over 60 and none were diabetic ... not quite a "normal" dialysis population.
Worse, all focus was on one small molecule, urea, thought then to best represent a marker of good clearance. While we now know that it would be hard to find a less representative "toxin" (its trans-compartmental kinetics bear little or no relationship or similarity to the behavioral kinetics of any of Vanholder's vast list of uraemic toxins), Kt/Vurea is still used in the US as the marker of "adequacy." What bunkum!
We now better understand the importance of middle molecules like β2M, homocysteine, and the hydrophilic envelope around tiny phosphate that turns it into a time dependent trans-membrane traveller. Even then, this focus implies that dialysis is all about solute clearance. Another myth. Bunkum again!
Most commonly it is fluid, not solute, that maims and kills the dialysis patient. It is fluid that stifles the breath, stretches the heart past the zenith of Starling's curve, and—when removed—is commonly removed so fast that the blood pressure and circulation collapses, coronary and myocardial perfusion falls, and the heart is stunned. That sequence is not solute-related. Tick that up to fluid!
In the dialysis setting, when fluid is discussed, it is all too often in tones of anger and confrontation. Dialysis staff regularly berate patients over excess fluid gain (the surrogate phrase for non-compliance) without considering why. After all, it is the patients' fault. More bunkum!
A daily scenario in most dialysis units:
A patient arrives for dialysis with excess fluid to remove.
This is what tends to happen:
- A (sometimes ugly) confrontation occurs with: "... you have not adhered to your fluid restriction ..."
- With lots of fluid to remove, a high ultrafiltration rate (UFR) is required and set.
- Surprise: the patient goes "flat" halfway through. Urgent "resuscitation" starts, with N saline (of course). But wait: isn't dialysis meant to be removing excess salt and water?
- After loading up with salt and water, more fluid is taken off, and fast, for time is now short. Even if more flats are avoided, cramp is not and, at the end of dialysis, the patient is as limp as a potted plant at the end of a hot day ... and is grumpy ... and feels like death warmed up.
- Before you is a patient with a maximally contracted circulating volume —to the point of circulatory collapse and hypotension. Before you is a patient with a maximally activated thirst mechanism. Thirst is an irresistible, primal, survival instinct buried deep in the brain stem. The patient is without a hope of suppressing it.
- What, then, does the patient do? He/she drinks! So would you —you would have to! Your brain stem would insist on it! And so this "noncompliant" patient complies with the primal survival drive of thirst, and drinks!
- In 2 days time (or 3, at the staff-convenient weekend), the patient returns, finally revitalized by fluid, but extra kilos "over". More angry berating ensues "You must be more compliant, you are killing yourself ..."
- No ... we are the ones doing the killing.
- Mistake #1:
- The dialysis session is too short. A longer session allows the removal of the same volume over a longer time at a lower UFR.
- Mistake # 2:
- Berating a patient for "non-compliance" is (a) cruel and (b) an abuse of a patient for our own mistake: the 'excess fluid to remove' is fluid that we forced the patient to drink by switching on a primal, irresistible instinct —an instinct we ignited—through far too rapid a contraction of blood volume abetted by further salt loading during the inevitable circulatory resuscitation.
- Mistake # 3:
- It isn't the patient who "doesn't get it." We are the ones that don't get it!
But, there is one last page to the fluid story: the plasma refill rate.
When fluid is rapidly removed, as it is during dialysis, fluid "waterfalls" into the circulation from the extravascular space. Then, in turn, the extravascular space is refilled from the intracellular fluids. A 3-way trans-compartmental fluid shift is set in motion. The contraction of one forces a refilling from the next, and back down the line. But—and here's the key—this re-filling is rate-limited!
While dependent on many factors far too complex to tease out here, the approximate plasma refill rate can be estimated. Kim (1972), Chaigon (1981) and Schneiditz (1992) each estimated the maximal plasma refill rate to lie somewhere in the range of 5-7 ml/kg/hr.
McIntyre has reported that the risk of myocardial stunning (perfusion failure of the myocardium that results from an excess UFR) becomes clinically threatening if the UFR exceeds 10 ml/kg/hr. This is a removal rate of 3-5 ml/kg/hr in excess of the plasma refill rate. In other words, and this is a difficult concept, if contraction of the intravascular volume exceeds the refill rate by just ~3-5 ml/kg/hr, watch out!
I think in 5's. I remember a plasma refill rate of 5 ml/kg/hr. Then I remember the threat-level for myocardial stunning is 5 ml/kg/hr more than the refill rate. Remember this, and you won't be too far out.
For any dialysis patient, multiply their ideal weight x 5 ml/hr for their plasma refill rate. Each ml/min of UFR above that = the approximate rate of plasma volume contraction, remembering that poor hearts poorly tolerate rapid volume contraction. Exceed a contraction rate >2 x the plasma refill rate, and any heart is threatened.
Dialysis should (must) be long enough - at the absolute minimum - to allow for the removal of all required fluid at a UFR that lies within these limits, but any rate in excess of the plasma refill rate will begin to trigger volume driven thirst. Slowing the UFR as closely as possible to the plasma refill rate will prevent thirst-driven volume overload prior to the next dialysis.
The path to compliance – and optimized cardiovascular stability – is not by forcing uncomfortable fluid restriction, but by increasing dialysis frequency to lessen the accumulation of fluid to remove, and by lengthening dialysis sessional duration to a UFR that does not exceed the plasma refill rate (the ideal), or at least to a rate that protects the heart from dialysis-induced 'stunning'.
So ... do we now have a patient who is suddenly "compliant"?
No ... we have a dialysis program that is suddenly thinking!
And, there is one more mistake we make. Subscribe to this blog to be notified when my next post on The Solute Mistake goes live.
- Kim KE, NefT M, Cohen B, Somerstein M, Chinitz J, Onesti G, Swartz C. Blood volume changes and hypotension during hemodialysis. Trans Amer Soc Artif Int Organs 16: 508, 1970
- Chaignon M, Chen WT, Tarazi RC, Bravo EL, Nakamoto S. Effect of hemodialysis on blood volume distribution and cardiac output. Hypertension. 1981;3:327-332
- McIntyre CW, Burton JO, Selby NM, Leccisotti L, Korsheed S, Baker CSR, Camicic PG. Hemodialysis-Induced Cardiac Dysfunction Is Associated with an Acute Reduction in Global and Segmental Myocardial Blood Flow. Clin J Am Soc Nephrol. 2008 January; 3(1): 19–26.