We like to give treatments that produce results that we can see and logically attribute to the treatments we gave.
We like to give IV (IntaVenous) furosemide (Lasix – frusemide in Commonwealth countries) for CHF (Congestive Heart Failure).
1. The patient had CHF.
2. I gave IV furosemide.
3. The patient produced urine.
4. The patient improved.
Anecdotes like this can lead us to the conclusion that the furosemide produced the improvement, even if we have been giving many other treatments along with the Lasix.
We can use logic to back up that conclusion.
1. CHF is fluid in the lungs.
2. CHF is too much fluid.
3. Getting rid of the fluid gets rid of the problem.
4. The patient improved, so the logic must be sound.
But is the logic sound? Is the conclusion justified or are we seeing what we want to see?
The way we find out is by studying patients with similar enough presentations that they are treated the same way, except that not all patients are given Lasix.
When we study the results of furosemide on CHF, we see that the things we have been told about IV Lasix are not true.
Hypothesis #1. Acute CHF patients are overloaded with fluid. We have to remove the fluid to save them.
CHF = Pee or die!
This hypothesis was tested – all the way back in 1978, but the myth continues.
The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema.
The normal patients had 22% more total plasma volume.
The normal patients had 21% more total blood volume.
The need to remove fluids is based on what?
It is interesting that this study was of patients treated with oxygen, morphine, and furosemide. Only oxygen is still important in the acute treatment of CHF/ADHF.
Hypothesis #2. IV Lasix almost immediately causes vasodilation.
IV Lasix almost immediately causes vasoconstriction.
This hypothesis was tested – in 1985, but this myth also continues.
The use of intravenous furosemide in patients with chronic congestive heart failure, although well established, can promote further clinical hemodynamic deterioration during the first 20 minutes.
Lasix raises blood pressure in emergency treatment of CHF.
Hypothesis #3. IV Lasix improves outcomes for acute CHF patients.
IV Lasix does not improve outcomes for acute CHF patients.
This hypothesis was also tested a long time ago (in 1987), and at other times, but the myth persists longer than the patients treated with Lasix.
If we can eliminate a treatment and the outcomes of patients do not get worse, where is the benefit from the treatment?
Why expose the patient to the side effects of a treatment, if the patient is not expected to benefit from the treatment?
 Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Activation of the neurohumoral axis.
Francis GS, Siegel RM, Goldsmith SR, Olivari MT, Levine TB, Cohn JN.
Ann Intern Med. 1985 Jul;103(1):1-6.
PMID: 2860833 [PubMed – indexed for MEDLINE]
 Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema.
Hoffman JR, Reynolds S.
Chest. 1987 Oct;92(4):586-93.
PMID: 3115687 [PubMed – indexed for MEDLINE]
Figueras J, & Weil MH (1978). Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. Circulation, 57 (2), 349-55 PMID: 618625
Francis GS, Siegel RM, Goldsmith SR, Olivari MT, Levine TB, & Cohn JN (1985). Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Activation of the neurohumoral axis. Annals of internal medicine, 103 (1), 1-6 PMID: 2860833
Hoffman JR, & Reynolds S (1987). Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema. Chest, 92 (4), 586-93 PMID: 3115687