Melissa, some day it will be revealed that high dose diuretics for ADHF is the frontal lobotomy of cardiology. What is even more shocking is that it is happening 70 years after blood letting became passe. It is well documented that high dose diuretics (> 160 mg/day):  a) are routinely prescribed for ADHF, b) Don't work, and c) are directly linked with worsning renal function (WRF) during the ADHF hospitalization. It is also extremely well documented that WRF is a death sentence. If you want to shine the light of day into this medical black hole and save these patients lives consider a RCT comparing high dose diuretics to Aquapheresis....Please do something.

Dear "Just a thought",

Appreciate your commentary and it's well taken. By doing these blogs, I want you to know that I really am trying "to do something".  Getting a dialogue going on these issues really helps and lays the ground work sometimes for other trials, changes in daily practice, etc.  Though we have to be careful with aquaphoresis , the same way we must be with diuretics, I do think it's a good option for refractory endstage CHF'ers. 

Melissa

I am a family physician frequently tasked with caring for ADHF.  I have never used Lasix at a dose of 160 mg per day, but I had no idea exceeding that dose did not work and was harmful.  Any reference for me to read?  Is 160 mg / day the max for chronic compensated CHF as well?  Thanks. I enjoy your blog.

Great evidence. I like the DOSE study and wonder when/where it will be published. Any takers?

We see the DOSE-like patient every day and night in our ER. I never believed in furosemide infusions, and now it seems to be that high dose furosemide is better than low dose furosemide. I think if anything, we have been underdosing our patients, and could probably get them out of failure and out of hospital much faster with short-term, high dosing. As to aquaphoresis, hasn't that been disproved in the setting of ARF/sepsis?

High dose bolus Furosemide is potentially ototoxic. Physicians should be mindful of this when giving Furosemide in the acute setting. Starting low with the option of additional doses as required upon early review would be preferable.

The DOSE Study is a great concept and I look forward to it being published.  However, the sample size may be too small.  There were 308 patients, divided into 4 arms.  The stated power was 88% to detect a difference in Creatinine of 0.2mg/dl and VAS AUC of 600 points.  However, the Change in Creatinine at 72 hours was 0.05 vs 0.07 for Q12 vs Continuous; and 0.04 vs 0.08 for Low vs High Intensification.  The Patient Global Assessment VAS AUC was 4236 vs 4373 for Q12 vs Continuous; and 4171 vs 4430 for Low vs High Intensification.  Thus it is not surprising there was no statistically significant difference.

Dear Dr Walton-Shirley:

Pre-med student who does frequent shadowing of a local cardiologist responding (I hope I don't look like an idiot to you!):

Why don't you use a Primacor drip, and a Bumex bolus followed by a maintence drip for your severe ADHF patients? That should reduce their PCWP and increase their CO and decrease their SVR quickly and effectively. And it only requires two meds, rather than the four you use.  Also, the cardiologist I shadow, as well as my pharmacist, says that Bumex is more consistent and predictable, and works when Lasix doesn't.

Maybe the reason is that every doc has their own remedy-of-choice for certain conditions.

And what was the Zofran for? Isn't that an anti-nausea drug?

Thanks so much for responding to my comment, Doctor!

Doug Pereira  

A couple of reasons Doug.

1)  Since 1989, trials of milrinone as a routine HF therapy have shown three things.  1:  Improved quality of life by both subjective and objective indices.  2:  Improved NYHA functionality.  3:  Increased mortality.  At 6 months, I think the rates were 30% vs 24% on milrinone therapy.  This is why we use it for palliative reasons or as bridge-to-transplant, but not as a routine adjuvent.  Many stage IV class D HF patients would rather die than live in their current state and are willing to accept an increased risk of death for an improved quality of life.  This is not something you'd want to do on a population-basis.

2)  The DOSE trial which is awaiting publication now shows that bolus dosing of loop diuretics is at least as safe and effective as IV drip in most of the domains that matter, maybe with a trend toward less harm to kidneys, though I suspect that's just because you got less urine out in the same amount of time.  A small creatinine "bump" is often how you know you've hit mild hypovolemia in these folks.  Regardless, drips add cost and complexity to the care and are unnecessary.

3)  Acute Decomp HF (ADHF) responds beautifully to mild afterload reductions.  The reasons for this are complex and are best visualized by flow-volume loops of normal and systolically dysfunctional hearts.  I won't try to describe that in words, but suffice to say that when the Emax is substantially diminished (as is the case with systolic HF), a small drop in afterload produces a profound increase in stroke volume, which is directly related to cardiac output assuming HR stays constant.  Thus, standard management is often considered to be bolus diuresis and afterload reduction provided the patient is not in hemodynamic shock and is in the "warm" phase of the illness.

4)  Finally, many decompensations of HF are initiated by patient behavior, true, but the final straw is often that when they need it most, many patients find their Lasix stops providing necessary diuresis.  This is part urban legend and part truism, but furosemide has a bioavailability of 5-95%, sometimes even within the same patient.  This has been ascribed to "gut edema" which I will not comment on here; you can check out the literature and decide for yourself whether you believe that explanation.  What works in reality, however, is the administration of a dose of something like torsemide (Demadex) at 50-100mg PO x1.   With a 10-12 hour duration of action and a reliable 85-95% bioavailability even in decompensation, this can often have  the effect of IV furosemide and has the potential to abort the admit outright.

That's an incomplete answer to your question, but I hope it helps.

Thanks!

-John

(Some cardiologist somewhere)