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Bedside Snapshot
  • What it does: Potent loop diuretic for rapid off-loading of excess volume (heart failure, renal/hepatic edema, acute pulmonary edema); strong natriuretic and diuretic effects
  • Onset & Duration:
    • IV: Onset ~5 minutes, peak ~30 minutes, duration ~2 hours
    • Oral: Onset 30–60 minutes, peak 1–2 hours, duration up to ~6 hours; oral bioavailability averages ~50% but is highly variable
  • PO to IV Conversion: 40 mg PO ≈ 20 mg IV furosemide (IV is roughly twice as potent due to incomplete oral absorption)
  • Typical Adult IV Dose: 20–40 mg IV (or 0.5–1 mg/kg) over 1–2 minutes for acute pulmonary edema; if inadequate response after ~1 hour, double the dose (40→80 mg); single IV bolus often capped at ~160–200 mg
  • Chronic Loop Diuretic Users: Common ED/ICU strategy is to give an IV dose equal to, or up to ~2–2.5×, the patient's total home oral loop diuretic dose (as furosemide equivalents), then titrate to urine output
  • Oral Dosing: Typically 20–40 mg PO once or twice daily for chronic edema, titrated by 20–40 mg increments q6–8h as needed; maximum ~600 mg/day in severe edema with close monitoring
  • Continuous Infusion: 40 mg IV loading bolus followed by 10–40 mg/hour infusion may give smoother diuresis in diuretic-resistant heart failure
  • Key Risks: Intravascular volume depletion and prerenal AKI, hypotension, severe hyponatremia/hypokalemia/hypomagnesemia, metabolic alkalosis, ototoxicity (especially with rapid/high-dose IV or in renal impairment), hepatic encephalopathy in cirrhotics
  • Important: Not potassium-sparing—anticipate and proactively manage K⁺/Mg²⁺ loss, especially in patients on digoxin, antiarrhythmics, or with baseline conduction disease
Brand & Generic Names
  • Generic Name: Furosemide
  • Brand Names: Lasix, Furoscix, plus multiple generics (availability is institution- and region-specific)
Medication Class

Loop diuretic (Na⁺-K⁺-2Cl⁻ cotransport inhibitor)

Pharmacology

Mechanism of Action:

  • Site of action: Thick ascending limb of the loop of Henle; competitively inhibits the Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2) on the luminal side of tubular cells
  • Blocking NKCC2 prevents reabsorption of ~20–25% of filtered sodium at this segment and dissipates the hyperosmotic medullary gradient, sharply reducing the kidney's ability to concentrate urine and increasing water excretion
  • Increased delivery of sodium to the distal nephron drives potassium and hydrogen ion secretion in the collecting duct, contributing to hypokalemia and metabolic alkalosis
  • Increases tubular flow and sodium delivery, promoting calciuresis and magnesiuresis (useful in hypercalcemia but predisposes to hypocalcemia/hypomagnesemia)
  • Enhances renal prostaglandin synthesis, causing venodilation and increased venous capacitance → reduces preload and improves pulmonary congestion within minutes, even before significant natriuresis occurs (useful in acute pulmonary edema)
  • Threshold and ceiling-dependent: Minimum concentration must be reached at NKCC2 to trigger diuresis, but beyond a certain dose, higher amounts mainly extend duration rather than increase peak natriuresis (underlies practice of doubling dose when no response)

Pharmacokinetics:

  • Routes: Oral, IV, IM, and subcutaneous (Furoscix); in acute/critical care, IV bolus or continuous infusion preferred; IM generally avoided due to pain and erratic absorption
  • Oral bioavailability: Highly variable but averages ~43–69%; in acute decompensated heart failure or gut edema, oral absorption often significantly reduced, making IV dosing more reliable
  • Onset: IV diuresis begins within ~5 minutes; oral onset typically 30–60 minutes
  • Duration: IV diuretic effect lasts ~2 hours; oral effect up to ~6 hours; after drug effect wanes, kidney tends to retain sodium ("post-diuretic sodium retention")
  • Half-life: About 1.5–2 hours in normal renal function; prolonged in heart failure, hepatic impairment, and renal insufficiency
  • Protein binding: >90% albumin-bound in plasma; must be secreted into proximal tubule (via organic anion transporters) to reach site of action; hypoalbuminemia or competing organic acids can blunt efficacy
  • Elimination: Primarily renal excretion (most of dose appears in urine, much unchanged), with remainder excreted via bile/feces; in advanced kidney failure, higher doses or alternative loop diuretics often required
Indications
  • Acute decompensated heart failure with pulmonary and/or systemic congestion, when blood pressure is adequate to tolerate diuresis
  • Acute pulmonary edema (often with hypertensive emergency), typically combined with nitrates and noninvasive ventilation as appropriate
  • Volume overload/edema due to chronic heart failure, chronic kidney disease, nephrotic syndrome, or cirrhosis with ascites
  • Adjunctive therapy for resistant hypertension in patients with reduced eGFR (not first-line monotherapy)
  • Adjunct in emergent management of life-threatening hyperkalemia or hypermagnesemia (to enhance urinary excretion in patients who make urine)
  • Facilitation of deresuscitation in ICU patients after aggressive fluid resuscitation (ARDS, septic shock survivors, post-operative patients with positive fluid balance)

Diseases & Conditions Treated:

  • Acute and chronic decompensated heart failure with volume overload
  • Cardiogenic pulmonary edema, including hypertensive pulmonary edema
  • Chronic kidney disease and acute kidney injury with volume overload and preserved urine output
  • Cirrhosis with ascites and peripheral edema (often combined with spironolactone)
  • Nephrotic syndrome with edema
  • Resistant hypertension in patients with reduced kidney function
  • Hypercalcemia (adjunctive, with isotonic saline) and hypermagnesemia
  • Life-threatening hyperkalemia with adequate renal function and urine output
Dosing & Administration

Available Forms:

  • IV injection: 10 mg/mL furosemide solution in vials or ampoules (e.g., 20 mg/2 mL, 40 mg/4 mL, 100 mg/10 mL)
  • Oral tablets: Commonly 20 mg, 40 mg, and 80 mg strengths
  • Oral solutions: Typically 10 mg/mL (other strengths vary by manufacturer)
  • Subcutaneous on-body infusor (Furoscix): Delivers 80 mg furosemide over several hours for outpatient management of chronic heart failure congestion (generally not used in emergent/critical care)

IV Dosing (Always Follow Local Protocols):

Indication / Population Initial IV Bolus Repeat / Titration Typical Maximum
Adult edema / acute decompensated HF (loop-naïve or low home dose) 20–40 mg IV (0.5–1 mg/kg) over 1–2 min If inadequate response in ~1 hr, double dose (40→80 mg); reassess; dose q6–8 hr based on urine output, symptoms Single bolus often limited to 160–200 mg; total daily dose commonly ≤600 mg (rarely higher with close monitoring)
Adult decompensated HF on chronic loop diuretic IV dose ≥1–2.5× patient's total daily home PO loop dose, given as IV furosemide equivalent Adjust q6–12 hr or transition to continuous infusion; titrate to weight change, urine output, decongestion targets Similar daily limits (often ≤600 mg furosemide equivalent), individualized to renal function and response
Pediatric edema (general) 1 mg/kg IV given slowly over 1–2 min (max ~20 mg for many non-chronic-loop patients) May increase by 1 mg/kg not sooner than 2 hr after previous dose if inadequate; max 6 mg/kg per dose Weight-based and age-dependent; follow pediatric-specific protocols

Administration Guidelines:

  • Push rate: Administer IV boluses slowly (commonly over 1–2 minutes), with maximum rate of ~4 mg/min recommended to reduce ototoxicity risk; very large doses (160–200 mg) may be given over longer periods or as short infusions
  • Continuous IV infusion (adults): Common regimen is 40 mg IV loading bolus followed by 10–40 mg/hour, titrated to urine output and congestion; some protocols double infusion rate every 2 hours (up to 80–160 mg/hour) if urine output inadequate
  • In severe renal impairment, higher bolus doses or infusion rates may be necessary, but true diuretic resistance often requires combination strategies rather than endlessly escalating furosemide
  • In cirrhosis or marginal blood pressure, start with lower doses and escalate cautiously

Oral Dosing (Adults – Outpatient / Non-ICU):

  • Starting dose: 20–40 mg PO once or twice daily for edema or hypertension
  • Titration: Increase by 20–40 mg per dose every 6–8 hours until desired weight loss, edema reduction achieved
  • Maximum: Up to ~600 mg/day in severe edematous states with careful monitoring
  • Frequency: Due to short duration and post-diuretic sodium retention, twice-daily dosing (morning and early afternoon) usually more effective than once-daily for edema control

Loop Diuretic Equivalence (Approximate):

Drug Approx. PO Equivalent Approx. IV Equivalent
Furosemide 40 mg PO 20 mg IV
Torsemide 20 mg PO ~20 mg IV (where available)
Bumetanide 1 mg PO 1 mg IV

These are rough estimates; individual response varies widely. Clinical response and urinary sodium/output should guide dose.

Contraindications

Absolute Contraindications:

  • Anuria (no urine output), where increasing diuretic dose will not improve kidney function and may worsen toxicity
  • Known hypersensitivity to furosemide or any component of the formulation (including sulfonamide-type hypersensitivity)
  • Hepatic coma or severe electrolyte depletion until volume status and electrolytes have been corrected

Major Precautions:

  • Severe hyponatremia, hypokalemia, hypomagnesemia, or hypovolemia: Correct before or while using furosemide; the drug can worsen all of these derangements
  • Hypotension or hemodynamic instability: Aggressive diuresis can precipitate shock or worsen renal perfusion—ensure adequate perfusion pressure
  • Advanced renal impairment: Furosemide may require much higher doses; lack of response despite adequate dosing suggests diuretic resistance
  • Cirrhosis and portal hypertension: Rapid intravascular volume shifts can precipitate hepatorenal syndrome or worsen hepatic encephalopathy; combination with spironolactone standard
  • Diabetes mellitus and gout: May cause mild hyperglycemia and frequently raises uric acid, precipitating gout flares
  • Concurrent ototoxic agents: High-dose IV aminoglycosides, cisplatin markedly increase hearing loss risk—avoid rapid/high-dose IV furosemide
  • Pregnancy and lactation: Generally avoided unless benefit of treating significant maternal edema or heart failure clearly outweighs risks
Ototoxicity Risk: Rapid high-dose IV administration, underlying renal failure, or concomitant ototoxic medications significantly increase risk of tinnitus, hearing loss, and vertigo. Administer slowly (≤4 mg/min) and monitor for auditory symptoms.
Adverse Effects

Common:

  • Increased urine output, urinary frequency, and nocturia
  • Dizziness, orthostatic hypotension, and lightheadedness (especially after large IV boluses)
  • Electrolyte disturbances: hypokalemia, hyponatremia, hypomagnesemia, mild hypocalcemia
  • Metabolic alkalosis due to increased distal sodium delivery and RAAS activation
  • Mild increases in blood glucose and uric acid; potential to worsen gout or glucose intolerance
  • Muscle cramps, thirst, dry mouth, and fatigue related to volume and electrolyte changes

Serious:

  • Profound volume depletion leading to prerenal azotemia, acute kidney injury, or shock
  • Severe electrolyte abnormalities (marked hyponatremia, hypokalemia, hypomagnesemia) causing delirium, seizures, arrhythmias, or neuromuscular instability
  • Ventricular or supraventricular arrhythmias precipitated by electrolyte shifts, particularly in patients with structural heart disease or on QT-prolonging drugs
  • Ototoxicity (tinnitus, hearing loss, vertigo), especially with rapid high-dose IV administration, underlying renal failure, or concomitant ototoxic medications
  • Hepatic encephalopathy in cirrhosis from aggressive volume and electrolyte shifts
  • Rare but serious hypersensitivity reactions, including Stevens–Johnson syndrome, toxic epidermal necrolysis, agranulocytosis, or aplastic anemia
Special Populations

Renal Impairment:

  • In advanced kidney failure, higher doses often needed to achieve tubular concentrations
  • True diuretic resistance may require alternative loop diuretics (bumetanide, torsemide) or sequential nephron blockade
  • Monitor closely for volume depletion and electrolyte abnormalities

Hepatic Impairment:

  • Half-life prolonged in liver disease
  • Use cautiously; rapid volume shifts can precipitate hepatorenal syndrome or encephalopathy
  • Often combined with spironolactone for cirrhotic ascites

Pregnancy & Lactation:

  • Pregnancy: Category C; use only if benefit justifies potential fetal risk
  • Can decrease placental perfusion and cause fetal electrolyte abnormalities
  • Lactation: Excreted in breast milk; may suppress lactation; use with caution

Pediatric Considerations:

  • Dosing: 1 mg/kg IV initial dose (max 6 mg/kg per dose)
  • Monitor electrolytes closely
  • Follow pediatric-specific protocols for titration

Geriatric Considerations:

  • Higher risk of volume depletion, orthostatic hypotension, and falls
  • More susceptible to electrolyte abnormalities
  • Often have reduced renal function requiring dose adjustment
  • Start at lower doses and titrate carefully
Monitoring

Clinical Monitoring:

  • Strict intake and output (I/O) with hourly urine output in unstable or ICU patients; track net fluid balance and daily weights when feasible
  • Vital signs and hemodynamics: blood pressure (including orthostatics when appropriate), heart rate, and invasive pressures where available
  • Signs of over-diuresis: tachycardia, hypotension, rising creatinine, dizziness, confusion, poor skin turgor, excessive weight loss
  • In high-dose or rapid IV use, monitor for auditory changes (tinnitus, hearing difficulties) and vestibular symptoms
  • In cirrhotics, monitor for mental status changes (encephalopathy) and signs of hepatorenal syndrome

Laboratory Monitoring:

  • Serum electrolytes: sodium, potassium, magnesium, chloride, and bicarbonate—check at least daily in stable inpatients, more frequently in high-risk or aggressively diuresed patients
  • Renal function: BUN, serum creatinine, and when available, urine sodium or fractional excretion indices to assess diuretic response and perfusion
  • Perfusion markers: lactate, ScvO₂ where available
Clinical Pearls
Threshold Drug: If a reasonable furosemide dose produces no diuretic response, repeating the same dose is usually less effective than doubling the dose (up to a sensible ceiling) or switching to a continuous infusion.
"LASIX Lasts Six Hours": This is mostly true for oral dosing; with IV bolus, the strong diuretic window may be only ~2 hours. After that, the kidney tends to retain sodium. For true fluid off-loading, schedule dosing q6–8 hours or use an infusion, rather than a single daily IV bolus.
Oral Absorption Issues: Oral furosemide's erratic bioavailability means that poor response to high-dose PO often reflects absorption issues rather than receptor-level resistance. Consider switching to IV, bumetanide, or torsemide in patients with gut edema or severe heart failure.
Sequential Nephron Blockade: Adding metolazone or IV chlorothiazide can dramatically augment natriuresis in diuretic resistance, but it's a high-risk maneuver for profound electrolyte derangements and AKI—reserve for monitored settings with robust lab support.
Furosemide Stress Test: A 1–1.5 mg/kg IV bolus with measurement of 2-hour urine output can help stratify risk of progression to severe AKI in ICU populations; strong diuretic response suggests more salvageable kidney function.
Equivalence Tables Are Starting Points: Loop diuretic equivalence tables are helpful, but the only real test is urine output and natriuresis. Titrate to effect and reassess frequently rather than making large, unmonitored dose changes.
Coordinate with Overall Resuscitation: Align diuresis strategy with overall resuscitation/deresuscitation goals: in septic or cardiogenic shock, coordinate diuretic use with vasopressors, inotropes, and mechanical ventilation strategies so that decongestion does not undermine perfusion.
References
  • 1. Drugs.com. (2024, June 11). Furosemide dosage guide with max dose, adjustments. Drugs.com. https://www.drugs.com/dosage/furosemide.html
  • 2. DrugBank Online. (n.d.). Furosemide (DB00695). DrugBank. https://go.drugbank.com/drugs/DB00695
  • 3. Felker, G. M., Lee, K. L., Bull, D. A., et al. (2011). Diuretic strategies in patients with acute decompensated heart failure. New England Journal of Medicine, 364(9), 797–805. https://doi.org/10.1056/NEJMoa1005419
  • 4. Khan, T. M., & colleagues. (2023). Furosemide. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK499921/
  • 5. Konerman, M. C., Bozaan, D., Adie, S., et al. (2022). Michigan Medicine inpatient diuretic guideline for patients with acute decompensated heart failure. Michigan Medicine/NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK589894/
  • 6. Medscape. (2025). Lasix, Furoscix (furosemide) dosing, indications, interactions, adverse effects, and more. Medscape Reference. https://reference.medscape.com/drug/lasix-furoscix-furosemide-342423
  • 7. StatPearls. (2023). Loop diuretics. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK546656/
  • 8. U.S. Food and Drug Administration. (2024). Furosemide injection prescribing information. FDA Drug Label. https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/018267s029lbl.pdf
  • 9. Weingart, S. (2024). Diuretics & deresuscitation (IBCC). EMCrit Project. https://emcrit.org/ibcc/diurese/