Furosemide is a loop diuretic that is used to alleviate the symptoms of breathlessness and oedema. It is the standard first line therapy for treatment of symptomatic fluid overload in congestive heart failure.
Loop diuretics inhibit sodium and water reabsorption from the ascending limb of the loop of Henle in the renal tubule and are powerful diuretics. Loop diuretics are potent and act rapidly.
Bioavailability: 60-70% orally but may be reduced by gastrointestinal oedema in heart failure. The bioavailability of subcutaneous furosemide (compared to IV) is noted to be 100%, with equivalent diuresis to the intravenous route.
Onset of action: 30-60 minutes when administered orally, 30 minutes when administered subcutaneously.
Peak effect: 1-2 hours when administered orally.
Plasma half-life: 50 min- 6 hours in heart failure, 10 hours in end stage renal failure.
Duration of action: 4-6 hours when administered orally, 4 hours when administered subcutaneously.
Increased risk of hypokalaemia with steroids or B-adrenergic receptor agonists (such as Salbutamol, Salmeterol and Terbutaline)
Diuretic effect may be antagonised by corticosteroids or non-steroidal anti-inflammatory drugs (NSAIDS), increased risk of nephrotoxicity with NSAIDS. Furosemide-induced hypokalaemia can increase the risk of cardiac arrhythmias with drugs known to prolong the QT interval, such as citalopram and methadone, and concurrent use alongside risperidone in patients with dementia is associated with an increased risk of death. Furosemide is unlikely to be involved in significant drug interactions when used via CSCI for end of life care.
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Some of the management strategies describe the use of drugs outside their licensed indications. They are, however, established and accepted good practice. Please refer to the current BNF for further guidance.
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