In cardiorenal syndrome with diuretic resistance, how high can we drive the creatinine level before stopping the use of furosemide?
- submitted by Juana Gonzalez
The problem with experts is that they do not know what they do not know. NNT.
In cardiorenal syndrome with diuretic resistance, how high can we drive the creatinine level before stopping the use of furosemide?
- submitted by Juana Gonzalez
I read three reviews of diuretic resistance and none of them mentioned a Cr cut-off for stopping furosemide diuresis. But to address the concept of diuretic resistance, I found this:
Canadian Cardiovascular Society Consensus Conference recs on HF update 2007:
In HF patients not responding to >240mg IV furosemide [per day], treatment options include:
-More frequent or higher doses of IV boluses of furosemide (Class 2B, Level C)
-Combination with thiazide diuretics (HTCZ or metolazone) (Class 2A, Level B)
-Continuous IV furosemide infusion (Class 2A, Level B) (1)
The "braking phenomenon," or short term tolerance to lasix, may be the reason a drip works better than boluses. (2)
Another suggestion was to administer salt-poor albumen with lasix to increase UOP. The mechanism is increased renal perfusion and amount of lasix getting to the kidneys.(2)
Also, diuretics do not have a smooth dose response curve. A drug excretion threshold has to be reached and then they start working. So, when a patient does not respond to 20mg IV lasix, a 40mg IV dose of lasix will work better than 20mg IV BID (2)
Refferences:
1) Can J Cardiol Vol 23 No1 January 2007 p21-45
2) Exp Clin Cardiol Vol 13 No 4 2008 p165-170
First, creatinine at higher levels is associated with smaller incremental declines in GFR which is represented as a rectangular hyperbola here.
Next, the the use of diuretics in the cardiorenal syndrome needs to be understood before the use of loop diuretics is undertaken.
In the cardiorenal syndrome, some have suggested that it is a prerenal syndrome. However, worsening renal failure more commonly occurs when the patient is fluid overloaded (J Card Fail 2002; 8: 136). The reason is that volume overload is a high catecholamine state and causes a resultant decline in cardiac output. Ljung-man showed that renal blood flow does not decrease until cardiac index is less than 1.5L/m2 (Drugs 1990; 39: 10).
The kidneys, which use 25% of the cardiac output, are affected by MAP and CVP; the difference is the renal perfusion pressure.