• It is a purified cardiac glycoside extracted from the foxglove plant, Digitalis lanata.
  • Its corresponding aglycone is digoxigenin, and its acetyl derivative is acetyldigoxin
  • It is widely used in the treatment of various heart conditions namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication
  • It increases myocardial contractility
  • Heart rate ↓, blood pressure ↑as the stroke volume ↑, leading to increased tissue perfusion 
  • Myocardial efficiency is due to improved hemodynamics, and the ventricular function curve is improved.
  • Initial brief increase in action potential, followed by a decrease as the K+ conductance increases due to an increased intracellular amounts of Ca2+ ions
  • The refractory period of the atria and ventricles is decreased, while it increases in the sinoatrial and AV nodes
  • A less negative resting membrane potential is made, leading to increased excitability 
  • Slight vasodilation is seen in heart failure.
  • It also affects the kidney by increased renal blood flow and increased glomerular filtration rate.
  • A mild diuretic effect is seen only in heart failure .
  • Dose of digoxin in a child 0.04-0.06 mg/kg
  • Theurapetic level: 0.5-1.5 ng/ml.
  • Toxic level > 2.4 ng/ml.
  • Dose of digoxin is altered in Old age,Renal disease & Hypercalcemia
  • About 70 to 80% of an oral dose of digoxin is absorbed, mainly in the proximal part of the small intestine. 
  • The degree of binding to serum albumin is 20 to 30%. 
  • Digoxin is extensively distributed in the tissues, as reflected by the large volume of distribution. 
  • High concentrations are found in the heart and kidneys, but the skeletal muscles form the largest digoxin storage.
  • The half-life of elimination varies between 26 and 45 hours 
  • The time required to establish a new steady-state plasma drug concentration when maintenance doses are changed is approximately four half-lives, the same amount of time required to establish the initial steadystate level. Excreted by kidneys.
  • Congestive Heart Failure
  • Tachyarrhythmias
  • Atrial Fibrillation
  • Atrial Flutter
  • Acute MI
  • Paroximalatrial tachycardia
  • Hypersensitivity
  • Uncontrolled Ventricular Arrhythmias
  • AV block
  • Constrictive Pericarditis
  • Idiopathic Hypertrophic Subaortic Stenosis
  • Diuretics, amphotericin B' and corticosteroids cause hypokalemia can precipitate digitalis induced arrhythmias.
  • Quinidine reduces binding of digoxin to tissue proteins as well as its renal and biliary clearance T Plasma concentration of digoxin toxicity can occur.
  • Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaolin-pectin reduce absorption of digoxin.
  • Dizziness (4.9%)
  • Mental disturbances (4.1%)
  • Diarrhea (3.2%)
  • Headache (3.2%)
  • Nausea (3.2%)
  • Vomiting (1.6%)
  • Maculopapular rash (1.6%)
  • Anorexia
  • Cardiac dysrhythmia:
  1. Associated with digitalis intoxication ventricular premature beats, bigeminy, ventricular tachycardia and rarely ventricular fibrillation. 
  2. AV block and nonparoxysmal atrial tachycardia with variable AV block are characteristic of intoxication.
  • Arrhythmia in children (consider a toxicity)
  • Features: Generally unwell, lethargy, N/V, confusion, yellow-green vision, arrhythmias (e.g. AV block, bradycardia) Common side effects are:
  1. Dizziness
  2. Fainting
  • Precipitating factors:
  1. Renal disease 
  2. Classically: hypokalaemia
  3. Myocardial ischaemia 
  4. Hypomagnesemia 
  5. Hypoalbuminemia
  6. Hypothermia
  7. Hypothyroidism
  8. Hypercalcemia, hypernatremia
  9. Acidosis
  10. Drugs: Amiodarone, quinidine, verapamil, spironolactone,Furosemide,Hydrochlorothiazide (compete for secretion in distal convoluted tubule, therefore reduce excretion)
  • Management
  1. Digibind
  2. Correct arrhythmia by lignocaine
  3. Phenytoin 
  4. Monitor K+
Exam Question
  • On changing maintenance dose of digoxin the new steady state plasma digoxin concentration would be achieved in approximately 1 week 
  • Patient with acute MI developing hypotension & oligouria with bradycardia should be treated with Digoxin & Dopamine
  • Digoxin toxicity may result from the concurrent administration of digoxin with Amiodarone, quinidine, verapamil, spironolactone,Furosemide,Hydrochlorothiazide
  • Digoxin toxicity is increased by Renal impairment, Hypercalcemia hypokalemia & Hypomagnesemia
  • Digoxin induced arrhythmia shows Paroxysmal Atrial Tachycardia with variable AV block, Ventricular Bigeminy & May be used to treat Atrial Fibrillation
  • Most effective method of treatment of Digitalis toxicity is Digoxin Antibody
  • Dose of digoxin is altered in Old age,Renal disease & Hypercalcemia
  • Therapeutic plasma level of digoxin is 0.5-1.5 ng/ml
  • Half Life of Digoxin is 40 hrs(26-45hrs)
  • Diuretics, amphotericin B, corticosteroids , Quinidine, Cholestyramine, sucralfate, neomycin, sulfasalazine, antacids and kaolin-pectin are the drugs showing interaction with digoxin
  • Interaction occurring when quinidine and digoxin are given together Quinidine decreases excretion of digoxin
  • Interaction occurring when quinidine and digoxin are given together Quinidine displaces digoxin from protein binding sites & decreases excretion
  • Digoxin is contraindicated in Hypertrophic obstructive cardiomyopathy
  • Digoxin is useful in Complete heart-block with CHF
  • Digoxin induced arrhythmia can be treated with Lignocaine
  • Dose of digoxin in a child 0.04-0.06 mg/kg
  • Atrial Fibrillation is treated by digoxin
  • Digoxin are distributed in heart , kidney & skeletal muscles
Don't Forget to Solve all the previous Year Question asked on Digoxin