Loop diuretic
Furosemide (Lasix)
Also called Lasix
Indications
- Acute pulmonary edema and decompensated heart failure with congestion (label)
- Edema from heart failure, cirrhosis or kidney disease, including nephrotic syndrome (label)
- Fluid overload in AKI or ARDS; it manages volume but does not treat the AKI (KDIGO 2012)
- Hyperkalemia with working kidneys (off-label)
- Hypercalcemia after volume repletion, on weak evidence (off-label)
- Furosemide stress test to predict AKI progression (off-label)
Dosing
Furosemide drip card and mL/h converterStart: Bolus, then 10–20 mg/h
| Where | Dose |
|---|---|
| Other common pushes | Furosemide: 40–80 mg IV over 1–2 min (double the home oral dose); high doses as an infusion no faster than 4 mg/min (label) |
On the quick cards
Mechanism of action
Furosemide binds the chloride site of NKCC2, the luminal Na⁺-K⁺-2Cl⁻ cotransporter of the thick ascending limb, which reabsorbs about 25% of filtered sodium. Being 91–99% protein-bound, it is barely filtered; organic anion transporters (OAT1, OAT3) secrete it into the proximal tubule, so its effect depends on how much reaches the urine. Blocking NKCC2 abolishes the lumen-positive voltage that drives Ca²⁺ and Mg²⁺ reabsorption, washes out the medullary gradient and sends sodium to the collecting duct, where K⁺ and H⁺ are lost; blocking NKCC1 in the stria vascularis causes ototoxicity.
Pharmacology
- Renal: natriuresis up to about 20–25% of filtered sodium, with a threshold: a weak response needs a higher dose, not a repeat
- Renal: urine loses K⁺, Mg²⁺, Ca²⁺, H⁺ and Cl⁻ and cannot be fully concentrated or diluted
- Cardiovascular: early venodilation may lower preload before diuresis; a bolus can briefly raise renin and SVR in heart failure
- Metabolic: hypokalemia, hypomagnesemia, hyponatremia, contraction alkalosis, hyperuricemia, hyperglycemia
- Other: tinnitus and hearing loss from NKCC1 block in the cochlea, usually reversible
Pharmacokinetics
| Onset | IV within 5 min; oral within 1 h (label) |
|---|---|
| Peak | IV within 30 min; oral 1–2 h (label) |
| Duration | IV about 2 h; oral 6–8 h (label) |
| Half-life | About 2 h (label); 0.8 h in healthy subjects and 14 h in kidney failure (Tilstone 1978) |
| Distribution | Small Vd, about 0.1–0.2 L/kg; enters breast milk (label) |
| Protein binding | 91–99%, mostly albumin; unbound 2.3–4.1% (label) |
| Metabolism | Glucuronidation, largely in the kidney; furosemide glucuronide is the main metabolite (label) |
| Elimination | Mostly unchanged in urine by tubular secretion (label) |
| Bioavailability | Oral 60–64% (label) but 10–100% between patients; 40 mg oral ≈ 20 mg IV |
| Dialysis | Not removed by hemodialysis (label) |
| Organ failure | Kidney failure: uremic acids compete for secretion, so higher doses are needed |
Chemistry
- 4-chloro-N-furfuryl-5-sulfamoylanthranilic acid (C₁₂H₁₁ClN₂O₅S, MW 330.7): an anthranilic acid with a furan ring and a sulfonamide group
- A weak acid (carboxyl pKa about 3.9, PubChem): nearly all ionized at pH 7.4 and poorly lipid-soluble; the free acid barely dissolves in water
- Injection: the sodium salt, 10 mg/mL at pH 8.0–9.3; it precipitates below pH 5.5 and at once with milrinone in the same line (labels)
- Protect from light; do not use discolored solution
- Its sulfonamide lacks the arylamine of sulfonamide antibiotics; cross-allergy appears to reflect a general allergic tendency (Strom 2003), though the label warns
Adverse effects and cautions
In the one-pagers
- Acute Kidney InjuryProtect the kidney, predict progression: Furosemide stress test: 1 mg/kg IV (1.5 if recent loop use) in euvolemic stage 1–2 AKI, urine replaced mL for mL; <200 mL in 2 h predicts stage 3
- Heart FailureDiuretic monitoring: Push usual IV furosemide doses (20–80 mg) over 1–2 min; infuse high doses no faster than 4 mg/min
- CRRT (Continuous Renal Replacement)Daily care, documentation, transport and liberation: Recovery is read from urine: spontaneous output above about 400–500 mL/day without diuretic, rising day over day, and a timed 2–6 h creatinine clearance of 15–20 mL/min or more; a furosemide stress test (1–1.5 mg/kg, urine above 200 mL in 2 h) predicts response. KDIGO 2012 suggests not using diuretics to shorten RRT (2B). Move to intermittent HD
- GI Bleeding, Liver Failure and PancreatitisCirrhosis complications: ascites, SBP, HRS and encephalopathy: Tap new ascites and every admitted patient with ascites (AASLD 2021). A serum–ascites albumin gradient of 1.1 g/dL or more means portal hypertension; ascitic protein below 1.5 g/dL raises SBP risk. Give 2 g sodium a day with spironolactone 100 mg and furosemide 40 mg (up to 400 and 160 mg), and albumin 6–8 g per liter for paracentesis
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In the algorithms
Other loop diuretic drugs
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Sources
- FDA label: Furosemide Injection (Hospira, 2024)
- FDA label: Lasix tablets (Validus, 2025)
- Tilstone 1978 (furosemide in kidney failure)
- PubChem: furosemide
For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow the order, the label and your institution's protocols.