EMS Expo had several excellent presentations and a lot of good company. One of my favorite topics was covered by one of my favorite doctors, Keith Wesley. Attend his presentations if you have the opportunity.
For emergency treatment of CHF (Congestive Heart Failure), furosemide (Lasix – frusemide in Commonwealth countries) is a bad drug.
If we use Lasix, are we killers?
How much follow up do we get on our patients?
How would we know if we dehydrate a patient and alter his electrolytes to the point of killing him?
How would we know that the increase in blood pressure from Lasix is not making the CHF worse?
What if we give Lasix to someone with asthma, or pneumonia, or a PE (Pulmonary Embolus), are we shortening the lives of these patients?
How many of these patients die and how many might not die if they never received Lasix from EMS or from the ED?
We do not know, but we would have to be insane to think that the number is zero – or even close to zero.
Where does Lasix work?
In the kidneys, when there is good circulation to the kidneys – not in the patient who is pale, cool, and sweaty, because that is an indication of catecholamine release.
Some claim that Lasix will cause vasodilation and that this will improve outcomes.
Lasix causes vasoconstriction.
Vasoconstriction is what kills CHF patients.
Does Lasix kill?
Yes. Lasix kills.
In patients with chronic heart failure and especially in the presence of generalized edema, prior investigations have demonstrated either increases in intravascular volume17-19 or no consistent changes.20 During acute cardiogenic pulmonary edema, however, blood volume is more frequently reduced. In 16 of the 21 patients herein reported, the initial volume measured or calculated after onset of acute dyspnea demonstrated a lower than normal intravascular volume. To this extent, volume changes during acute pulmonary edema differ from those which were observed during chronic congestive heart failure.
Chronic CHF and Acute CHF are not the same and should not be treated as if they are the same.
Lasix is safe for chronic CHF.
Lasix is not safe for acute CHF.
We need to lower the blood pressure, but Lasix raises the blood pressure.
Two patients became noticeably shorter of breath by 10 to 20 minutes after furosemide administration.
We need to lower the heart rate, lower the blood pressure, and decrease the amount of work being done by the heart. Heart failure means that the heart is already having trouble.
The solution is not to make the heart work harder.
Activation of the sympathetic nervous system by intravenous furosemide treatment in patients with congestive heart failure is a new finding.
The paper was written in 1985, but we keep hearing that Lasix is a vasodilator.
Lasix raises blood pressure in emergency treatment of CHF.
Lasix raises heart rate in emergency treatment of CHF.
Lasix decreases cardiac output in emergency treatment of CHF.
Lasix makes acute CHF worse.
For the first hour, or more, the effects of Lasix are dangerous to the patient.
Lasix is a stress test that kills.
We should listen to Dr. Wesley and stop killing our patients.
What should we use?
NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries) does the opposite of what Lasix does. Higher doses of NTG produce better outcomes.
Also read NTG and the Hero Medic at Street Watch: Notes of a Paramedic, for a perspective on high dose NTG for acute CHF.
Would half a bottle of NTG tabs kill an acute CHF patient? No, and that is still much safer than giving Lasix to acute CHF patients.
This lecture examines our better understanding of the pathophysiology of congestive heart failure and the history of its treatment. Old theories result in old therapies, and current research should guide us in providing better prehospital therapy for this deadly condition. We will explore the role of pharmacologic agents such as diuretics and nitrates, as well as the value of continuous positive airway pressure (CPAP) support.
 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]
 Nitroglycerin for Treatment of Acute, Hypertensive Heart Failure – Bolus, Drip or Both?
Wed, 17 Oct 2012
Article with links to plenty of studies on high dose NTG