ICU Primary Snippet – Furosemide Vs Acetazolamide

Dr Swapnil Pawar April 11, 2024 31 1

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    ICU Primary Snippet – Furosemide Vs Acetazolamide
    Dr Swapnil Pawar


Compare and contrast the pharmacology of Furosemide and Acetazolamide

Written by Dr Madhuri Anupindi


  Furosemide Acetazolamide
Class Loop diuretic Carbonic anhydrase inhibitor
Formulations Tablets: 20mg, 40mg

Oral solution: 10mg/ml

Injection: 10mg/ml available in 20mg, 50mg or 250mg vials.

Tablets: 250mg

Injection: 500mg

Administration PO or IV, can be given IM

IV doses should be given no faster than 4mg/min to avoid ototoxicity

PO or IV

IV requires reconstitution with water before use

Absorption 60-69% bioavailability in healthy patients

Reduces to 43-46% in patients with end stage renal failure.

Onset of action 30 – 60 minutes after PO and 5 minutes after IV administration.

Bioavailability of 90%

Onset of action 1-2 hours after PO and 2 minutes after IV administration

Distribution Highly protein bound 91-99%, mainly to albumin

Crosses the placenta

Highly protein bound: approximately 90-98%

Tightly bound to carbonic anhydrase and accumulates in tissues containing this enzyme especially red blood cells and renal cortex

Metabolism Minimal hepatic and renal metabolism – main metabolite is furosemide glucuronide. Nil metabolism
Elimination Half-life of about 2 hours in patients with normal renal function (prolonged in patients with renal or hepatic failure)

80% of an IV or IM dose is excreted in the urine within 24 hours by both glomerular filtration and proximal tubular secretion. Remainder excreted in faeces.

Half life 4- 9 hours

Excreted unchanged by tubular secretion in the urine – this is enhanced in alkaline urine

Target in kidney Thick ascending limb loop of Henle Proximal tubule
Mechanism of action Blocks the Na-K-2Cl transporter à reduces reabsorption of these ions à increases amount of solute delivered to distal nephron which increases water excretion and also disrupts the counter-current multiplier system by decreasing the reabsorption of these ions into the medullary interstitium due to decreased osmotic gradient between the duct and inner medulla Inhibits carbonic anhydrase à blocks conversion of carbonic acid into co2 and h20 in the tubular lumen and its conversion back into carbonic acid in the proximal tubule cellsà normally the c02 + h20 diffuses into the proximal tubule cells and is converted back into carbonic acid by carbonic anhydrase. The hydrogen ions can then be exchanged with sodium from the tubular lumen. Acetazolamide therefore decreases sodium and bicarbonate resorption.
Indications Oedema: CCF, liver cirrhosis, renal disease


Metabolic alkalosis

Oedema: adjunctive with other diuretics

Prevention of acute mountain sickness

High altitude cerebral oedema

Elevated intra-ocular pressure associated with acute angle closure glaucoma

Chronic open angle glaucoma

Idiopathic intracranial hypertension

Contraindications/precautions Allergy to furosemide or sulfonamides

Prostatic obstruction (can precipitate urinary retention)


Severe hypovolemia

Treatment with other ototoxic medication

Hyperchloraemic acidosis



Renal failure GFR < 10ml/min

Hypersensitivity to acetazolamide, sulphonamide or sulphonamide derivatives

Severe hepatic impairment or Hepatic failure (decreases ammonia clearance à can precipitate hepatic encephalopathy)

Long term administration in patients with chronic non-congestive angle-closure glaucoma

Use in pregnancy and breastfeeding Category C: can cause electrolyte disturbances in neonate and thrombocytopenia

Passes into breastmilk and inhibits lactation

Category B3: shown to be teratogenic in animals at very high doses. No well controlled human studies – avoid use especially in first trimester.

Passes into breastmilk: use caution

Adverse effects Ototoxicity



Electrolyte imbalances (see below)

Anorexia, nausea

Pancreatitis, transaminitis (rare)

Increased triglycerides and cholesterol

Aplastic anaemia, thrombocytopenia, haemolytic anaemia, leukopenia

TENs, SJS, erythema multiforme, drug rash, pruritis, urticaria



Fatigue and drowsiness

Hypersensitivity reactions

Nausea, vomiting, diarrhoea

Electrolyte imbalances (see below)

Aplastic anaemia, thrombocytopenia, agranulocytosis, neutropenia



Electrolyte effects Metabolic alkalosis Hypernatremia







Metabolic acidosis




Significant drug interactions Aminoglycosides, cephalorodine: cisplatin: increases risk of ototoxicity

Chloral hydrate: flushing, hypertension, tachycardia

Lithium: decreases excretion of lithium

ACEI: may cause hypotension or deterioration in renal function

Theophylline: IV furosemide increases theophylline levels

Salicylates: decreases protein binding and renal clearance of acetazolamide à can result in severe metabolic acidosis

Lithium: increases lithium excretion

Phenytoin: increases phenytoin levels, accelerates osteomalacia

Cyclosporine: increases cyclosporine levels

Amphetamines: reduces urinary excretion of amphetamine




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