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Drug Reference

digoxin

Cardiac glycosides· Brands: LanoxinIVPO

Mechanism of action
Digoxin inhibits the sodium-potassium ATPase on cardiac myocytes, increasing intracellular sodium and subsequently reducing the sodium-calcium exchanger activity, which raises intracellular calcium and enhances myocardial contractility. It also increases vagal tone, slowing atrioventricular conduction and reducing heart rate. This dual action provides positive inotropy and negative chronotropy.
Pharmacokinetics
Digoxin is well absorbed from the gastrointestinal tract with a bioavailability of about 70-80% for the tablet formulation. It has a large volume of distribution and is widely distributed to tissues. Protein binding is approximately 25%. A small portion is metabolised in the liver, but the majority is excreted unchanged in the urine via glomerular filtration and tubular secretion. The elimination half-life is approximately 36-48 hours in patients with normal renal function, and is prolonged in renal impairment. Steady state is reached in about 5-7 days. It is not significantly removed by haemodialysis.
Indications & dosing

Atrial fibrillation (rate control)

Renal impairment: reduce dose or use lower dose; monitor serum digoxin levels.

  • adult · PO: 0.125–0.25 mg once daily · Renal impairment: reduce dose or use lower dose; monitor serum digoxin levels.

Chronic heart failure (HFrEF)

Used as an adjunct to standard therapy; dose depends on renal function.

  • adult · PO: 0.125–0.25 mg once daily · Used as an adjunct to standard therapy; dose depends on renal function.
Contraindications & precautions
  • Ventricular fibrillation · Digoxin can exacerbate or precipitate ventricular arrhythmias in this setting.
  • Second or third degree atrioventricular block · Avoid unless a pacemaker is present; digoxin can worsen conduction delay.
  • Hypertrophic obstructive cardiomyopathy · Digoxin may increase contractility and worsen outflow obstruction.
  • Hypokalaemia · Hypokalaemia increases digoxin sensitivity and risk of toxicity; correct before use.
  • Hypercalcaemia · Hypercalcaemia can precipitate digoxin toxicity.
  • Monitor renal function and serum electrolytes (potassium, magnesium, calcium) regularly.
  • Monitor digoxin levels, especially in patients with renal impairment or on interacting drugs.
  • Use caution in elderly and in patients with hypothyroidism, as they are more sensitive to digoxin.
  • Adjust dose in renal impairment, as digoxin clearance is reduced.
  • Consider drug interactions, especially with amiodarone, verapamil, diltiazem, quinidine, and diuretics that cause hypokalaemia.
  • Ensure adequate potassium levels, as hypokalaemia increases the risk of toxicity.
Adverse effects
  • Nausea
  • Vomiting
  • Visual disturbances (e.g. yellow/green halos)serious
  • Confusionserious
  • Arrhythmias (bradycardia, heart block, ventricular ectopics)serious
  • Diarrhoea
Interactions
  • bisoprololmoderateCo-prescription is often intentional in heart failure and atrial fibrillation, but requires caution. Monitor heart rate and blood pressure before and after initiating therapy or dose changes. Consider ECG monitoring for patients with underlying conduction disease or at risk of hypokalaemia. Adjust doses as needed; avoid in patients with marked bradycardia or high-degree AV block without a pacemaker. Monitor digoxin levels if renal function changes or signs of toxicity appear.
  • metoprololmoderateCo-prescription is acceptable but requires monitoring. Check heart rate and ECG before and during treatment, particularly when introducing or adjusting doses. Monitor for signs of bradycardia or heart block. Consider reducing doses of one or both agents if the heart rate is too low. Digoxin levels should be monitored if renal function changes.
  • carvedilolmoderateMonitor serum digoxin concentrations and electrocardiogram (heart rate and PR interval) after initiation or dose changes of carvedilol. Adjust the digoxin dose as needed. Advise patients to report symptoms of toxicity or bradycardia.
  • amiodaronemajorIf co-prescription is necessary, consider reducing the digoxin maintenance dose by approximately 50% (or use a lower starting dose) and monitor serum digoxin concentrations, renal function, and ECG. Monitor for signs of digoxin toxicity. Adjust digoxin dose based on levels and clinical response. Alternative antiarrhythmics may be considered to avoid the interaction.
  • salbutamolmoderateMonitor serum potassium levels before and during concurrent therapy, especially in patients at risk of hypokalemia (e.g., those on diuretics). Correct hypokalemia promptly. Consider ECG monitoring in patients with symptoms of digoxin toxicity or if potassium falls below 3.5 mmol/L. Avoid excessive salbutamol doses in patients with digoxin toxicity.
  • prednisolonemajorMonitor serum potassium, digoxin levels, and ECG at baseline and periodically during concurrent therapy. Correct any hypokalemia promptly. Consider potassium-sparing diuretics or potassium supplementation if needed. Adjust digoxin dose based on clinical response and levels. In patients with hypokalemia, digoxin toxicity may occur even at therapeutic digoxin levels.
  • clarithromycinmajorAvoid co-prescription when possible. If use is necessary, consider reducing the digoxin dose and closely monitoring serum digoxin concentrations and renal function before and during therapy. Monitor the patient for signs of digoxin toxicity, including heart rate and rhythm. Consider alternative antibiotics that do not inhibit P-glycoprotein (e.g., azithromycin has a less pronounced effect) where appropriate.
  • ibuprofenmajorAvoid co-prescribing digoxin and ibuprofen when possible, especially in patients with renal impairment or heart failure. If the combination is necessary, monitor serum digoxin concentrations, renal function (e.g., creatinine, eGFR), serum potassium, and signs of digoxin toxicity. Consider alternative analgesics such as paracetamol or tramadol. Adjust the digoxin dose based on monitoring.
  • furosemidemajorMonitor serum potassium, magnesium, renal function, and digoxin levels before and during co-administration. Correct hypokalaemia with potassium supplementation or potassium-sparing diuretics as appropriate. Adjust digoxin dose if renal function deteriorates. Advise patients to report symptoms of toxicity promptly. Consider ECG monitoring in high-risk patients.
  • hydrochlorothiazidemajorMonitor serum potassium and renal function at baseline, within 1-2 weeks after starting or changing doses, and periodically thereafter. Consider potassium supplementation or use of potassium-sparing diuretics if hypokalemia develops. Adjust digoxin dose if renal function deteriorates. In patients with concurrent hypokalemia, correct the potassium deficit and reassess digoxin levels. Consider digoxin level monitoring in patients with symptoms of toxicity or if potassium is persistently low.
  • spironolactonemajorMonitor serum digoxin concentrations, serum potassium and renal function before starting spironolactone and at regular intervals thereafter. Adjust the digoxin dose as needed to maintain therapeutic levels. Consider alternative diuretics if the patient is at high risk of hyperkalaemia or digoxin toxicity. Advise patients to report symptoms of toxicity such as nausea or palpitations.
  • verapamilmajorMonitor digoxin plasma concentrations before and after starting verapamil, and adjust the digoxin dose downwards (often by 25-50%) as guided by levels. Monitor ECG and heart rate. Consider using a different calcium channel blocker (e.g., amlodipine) if appropriate, and avoid combination in patients with significant conduction abnormalities or heart block.
  • quininemajorAvoid concurrent use if possible. If co-prescription is necessary, monitor serum digoxin concentrations, renal function, and electrocardiogram closely. Reduce the digoxin dose empirically (e.g., by 25% to 50%) and adjust based on digoxin levels and clinical response. Monitor for signs of digoxin toxicity.
  • erythromycinmajorMonitor serum digoxin concentrations and renal function before and after starting erythromycin. Watch for signs of digoxin toxicity. A digoxin dose reduction may be needed, and alternative antibiotics should be considered if possible. If erythromycin is used, adjust the digoxin dose according to the measured levels.
  • diltiazemmajorIf co-prescription is necessary, monitor serum digoxin concentrations and clinical response closely, especially after starting or stopping diltiazem. Consider a lower digoxin dose and adjust based on levels and renal function. Monitor heart rate, blood pressure, and ECG for signs of toxicity.
Renal & hepatic adjustment
  • eGFR 30+: No dose adjustment normally required. Monitor serum digoxin and renal function.
  • eGFR 15–29: Reduce maintenance dose by 25-50%. Consider lower loading dose if needed. Monitor serum digoxin closely.
  • eGFR 0–14: Use reduced dose (e.g., 62.5 micrograms on alternate days) with close monitoring. Avoid if possible.
Monitoring, pregnancy & toxicity
  • Serum digoxin concentration · At steady state, usually 5-7 days after starting or dose change; also in renal impairment, suspected toxicity, or poor response.
  • Renal function (eGFR/creatinine) · Before starting, then regularly (e.g., every 3-6 months) depending on patient stability.
  • Electrolytes: potassium, magnesium, calcium · Before starting and regularly, especially in patients on diuretics or with renal impairment.
  • Heart rate and rhythm · Before and during treatment, especially when used for atrial fibrillation.
  • Signs of toxicity (e.g., nausea, visual changes, confusion) · At each review.
  • Pregnancy: Digoxin is indicated during pregnancy when required for maternal or fetal cardiac conditions. Use the lowest effective dose and monitor maternal heart rate, renal function, and serum digoxin levels. Crosses the placenta but is generally considered compatible with pregnancy.
  • Toxicity: Bradycardia, heart block, atrial or ventricular arrhythmias · Stop digoxin. Correct potassium and magnesium. Establish IV access. Give digoxin-specific antibody fragments (Digibind) for severe toxicity. Monitor ECG and electrolytes.
  • Toxicity: Nausea, vomiting, anorexia · Stop digoxin. Supportive care. Monitor electrolytes and renal function. Review dose and toxicity.
  • Toxicity: Visual disturbances (e.g., blurred vision, halos), confusion, fatigue · Stop digoxin. Consider digoxin-specific antibody fragments for significant toxicity. Monitor for other signs.
  • Toxicity: Hyperkalaemia in acute overdose; hypokalaemia in chronic toxicity · Monitor serum potassium. Correct electrolyte imbalances. Give digoxin-specific antibodies if severe hyperkalaemia with renal impairment.
Antidotes & reversal
  • Digoxin immune Fab (DigiFab) · For life-threatening arrhythmia, hyperkalaemia >5 mmol/L, or severe toxicity; dose by load ingested or level.
Clinical notes
Digoxin has a narrow therapeutic index, so monitoring of serum levels is essential, especially in elderly patients, renal impairment, and with interacting drugs. Usual maintenance doses are 0.125 to 0.25 mg daily. It is used for heart failure with reduced ejection fraction and for rate control in atrial fibrillation. Signs of toxicity include nausea, visual disturbances, arrhythmias, and confusion. Hypokalaemia increases toxicity risk. Monitor electrolytes, renal function, and digoxin levels.

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BNF; local formulary