Ever since I read this great paper, tend to consider volume status and cardiac filling pressures as 2 separate and equally important concepts that both deserve optimisation in #ICU and #HeartFailure.
Basically, V-p correlation is all over the place! (1/6) journal.chestnet.org/article/S0012-…
What I learned from you all is that #VExUS & especially portal vein flow is a great tool to assess the impact of ⬆️(right-sided) pressure on organ function. This gives you more confidence to diurese patients, even when hypotensive or still hemodynamic unstable. (2/6)
My approach has always been to try and operate at "the lowest comfortable volume or better NaCl status" in ICU (and HF) patients. Therefore, I tend to diurese from the moment I achieve hemodynamic stability. Urine Na concentration helps me to decide how far I can go. (3/6)
My diuretic cocktail is usually bolus acetazolamide+bumetanide (dose~GFR) for balanced diuresis & thiazides in case of diuretic resistance. I only stop to diurese after urine Na <85 mmol/L, which is often AFTER cardiac filling pressures normalize. (4/6) link.springer.com/article/10.100…
Why? Cumulative NaCl overload very common in #ICU from crystalloid administration & intermittent loop diuretics producing hypotonic urine. NaCl determines ECV, is buffered in interstitium & harms the glycocalyx, so NaCl depletion makes sense! (5/6) sciencedirect.com/science/articl…
So this is what I do (below), which means I would consider (slow) diuresis even in patients with normal cardiac filling pressures (but high urinary Na response) that have presumably low #VExUS grade. Get rid of Na overload! Has served me well... Curious about your thoughts! (6/6)
• • •
Missing some Tweet in this thread? You can try to
force a refresh
How is diuretic efficiency changing with severity of #CKD? What is its prognostic relevance?
Read our new paper in CardioRenal Medicine!
@WilsonTangMD@BammensBert
Also thanks to Jeff Testani, Pieter Martens & Dirk Kuypers for their help with the paper...
We used 3 metrics of diuretic efficiency, based on urine output, natriuresis & chloruresis.
Irrespectively of metric, loop diuretic efficiency decreased significantly from KDIGO class IV, while remaining relatively preserved in less advanced CKD.
Patterns were similar for furosemide versus bumetanide (very little patients were on torsemide, which is hardly used in Belgium). Yet, baseline characteristics were strikingly different with bumetanide users older with higher cardiovascular risk.
Key points: 1. Spironolactone = most cost-effective drug in #HFrEF 2. Considering modest diuretic effects with 25-50mg, likely due to pleiotropic effects (Figure) 3. Natriuretic effects increase with dosing up to 600 mg (cirrhosis) 4. Average TOPCAT ~ RALES dose
5. Current study shows marginal (<1%) & short-term (first 8 months) effect on weight loss in TOPCAT Americas.
Spiro patients gradually had lower diuretic need and RAS blockers more frequently withdrawn. 6. Beneficial effects of spironolactone independent of these trends
Why #kidney function does not equal #GFR (and certainly not Cr), making it an elusive target in clinical practice & the latter a poor surrogate outcome, despite its robust correlation with prognosis. Caring for kidneys versus improving Cr/GFR. A thread below:
The kidneys in essence have 3 functions: 1. Glomerular function = Clearance 2. Tubular function = Homeostasis 3. Neurohumoral function
GFR mainly reflects 1. So why do we take GFR (or its estimate Cr) as a surrogate for renal function?
Look at GFR determinants (=N x snGFR).
In stable circumstances, GFR mainly reflects the number of functional nephrons.
Starting from 1 million per kidney at birth, one loses 5,000-10,000 per year with aging: age-related GFR decline <1 mL/min/1.73m²/y