Pharmacology NOT taught in Medic School - Lasix edition

I love the anecdotal stories from senior medics, stories enriched in tradition and history. All too often I hear the same story when it comes to Furosemide (Lasix) – “We used to give this all the time for CHF and it worked so well, I’m not sure why it fell out of favor”. And it is true, Lasix has really fallen out of favor for the treatment of CHF. However, I think the senior medics who helped bring me up were on to something that has been overlooked about Lasix.

And it is not all about diuresis….

I. The Pharmacology of Furosemide

Traditionally we are taught that Lasix is a loop diuretic that inhibits the reabsorption of sodium and chloride and as a result blocks the reabsorption of water from the tubules of the kidneys. If water is not being reabsorbed then it is staying within the tubules and eventually making its way out in the form of urine. Furosemide is highly protein-bound -about 95% to albumin in the blood- and as a result, tends to “stick around” for longer. Read more about the importance of plasma protein binding here. Furosemide has a total duration of 6-8 hours and an initial onset of 1-2 hours (Khan et al., 2019). This is a contributing factor as to why Lasix has fallen out of favor, the onset time is too long, and we do not get the immediate effects to manage the sick CHF patient in the back of the truck (or rig or whatever you call it).

There are two sides to this Lasix coin though. One side is the diuresis we are familiar with, but the flip side is a very different mechanism of action that has been overlooked by many.

Lasix is a potent venodilator, and this mechanism of action has a relatively quick onset of action.

In this study, researchers looked at the immediate cardiovascular effects of giving Lasix to acute CHF patients secondary to an acute MI. They dosed Furosemide at 0.5 – 1.0 mg/kg and waited to see its effects on left ventricular filling pressure and venous capacitance.

After Furosemide administration they saw a steady decline in left ventricular filling pressure over the 60 minutes with a peak decline in 5-10 minutes.

This was directly correlated to a rise in venous capacitance within the first 5 minutes of administration. As a review, venous capacitance refers to the ability of the venous system to engorge and “re-distribute” the volume overload from the heart and lungs into our peripheral veins. Our veins can essentially act as reservoirs to hold our blood volume, thereby taking the stress off the heart and lungs (Dikshit et al., 1973).

II. Who gets the Furosemide?

Without getting too complex there exist two forms, or phenotypes, of CHF. We have our chronic exacerbation of CHF wherein patients exhibit peripheral edema, have a known history, and display the classic “rales” and can hear them from the front door. Sometimes these patients may be on chronic Lasix and typically matching their daily dose or doubling it can be beneficial. But this patient relies on the true diuretic effect of Lasix. Disclaimer here, follow your local guidelines or protocols!

On the other hand, we have our acute CHF presentation otherwise known as SCAPE. This stands for Sympathetic Acute Crashing Pulmonary Edema. This occurs when the patient has a profound sympathetic response causing peripheral vasoconstriction and a re-distribution of blood flow from the periphery to the heart and lungs. It can be analogous to squeezing a water bottle, when you squeeze the bottom of the water bottle the water re-distributes to the top where the heart and lungs are located. This is the physiological basis for SCAPE.

The main point to take away is that the acute SCAPE version of CHF is not a volume overload but rather a volume re-distribution problem. And unfortunately, this is commonly missed. Patients present with acute dyspnea, tachycardia, and notable hypertension with a low room air Spo2. These patients may not even have a history of CHF! When it comes to Furosemide, SCAPE responds very well to Lasix administration because we get that immediate venodilation and increase in venous capacitance to “re-distribute” the blood off the heart and lungs. We essentially release our hand from the water bottle, as well as with the help of other dilators like NTG to allow the blood to settle back into the peripheries. And as a result, we reduce LV filling pressures (aka preload).

III. How is this practice-changing?

With the addition of POCUS in our shop, it is incredibly easy to identify if the patient has fluid in their lungs with the presence of B lines. I have encountered far more patients experiencing SCAPE-type CHF than I have the chronic exacerbation form.

So, if I find that patient with acute dyspnea, hypertension, & tachycardia indicative of increased sympathetic outflow I like to start them on an NRB while transitioning to the truck. Hit them with NTG (typically their BP is sky high and can tolerate aggressive sublingual doses). Once in the truck I transition to NIV with BiPap, get my IV, and hit them with a 40 mg dose of Furosemide to try and augment that venodilation I started with NTG. Remember, these SCAPE patients are suffering not from fluid overload but from fluid re-distribution!

IV. Final Take-home Points

Furosemide has an additional mechanism of action that is hardly talked about. In addition to its diuresis, it is a potent venodilator and acts to reduce preload and increased venous capacitance.

Furosemide is a great weapon when it comes to the SCAPE patient. It directly helps in allowing for a re-distribution of blood off the heart and lungs along with other medications like NTG.


Dikshit, K., Vyden, J. K., Forrester, J. S., Chatterjee, K., Prakash, R., & Swan, H. J. C. (1973). Renal and Extrarenal Hemodynamic Effects of Furosemide in Congestive Heart Failure after Acute Myocardial Infarction. New England Journal of Medicine, 288(21), 1087–1090.

Furosemide action on LVFP & venous capacitance

Khan, T. M., Roshan Patel, & Siddiqui, A. H. (2019, September 16). Furosemide.; StatPearls Publishing.

Lasix mechanism of action