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  • Type: Cardiac glycoside; CHF medications
  • Mechanism of action- Inhibits Na+/K+ ATPase, leading to an increase in intracellular sodium that can increase cardiac contractility
  • Dosage Forms: PO, IV, IM
  • Common Trade Names: Digitek, Digox, Lanoxin

Adult Dosing

  • Loading dose = 0.25mg IV q2hr until effect (max total = 1.5mg)
  • in acute atrial fibrillation with RVR with heart failure = 0.5mg IV, then 0.25mg IV q4hr until effect or max 1.5mg

Pediatric Dosing

Special Populations


  • RVR control in a-fib/flutter, PSVT


  • Allergy to class/drug
  • WPW
    • Increases conduction velocity in atrial tissue

Adverse Reactions

Digoxin toxicity

  • GI: nausea and vomiting, diarrhea, abdominal pain
  • CV: Bradycardia, SA/AV block, ventr arrhythmias
  • Neuro: altered mental status, visual disturbances (yellow-tinted vision)


  • Onset of action
    • IV = 5-30 minutes
    • PO = 0.5-2 hours
  • Half-life: 36-48 hours (may be increased with renal impairment)
  • Absorption: 60-80% absorption after oral administration
  • Metabolism: ~16% is converted to metabolites
  • Excretion: Almost entirely by the kidneys

Mechanism of Action

  • Inhibits Na+/K+ ATPase in the myocardium[1]
    • Causes increase in intracellular sodium levels
    • Results in reversal of sodium-calcium exchanger
      • Normally imports three extracellular sodium ions into the cardiac myocyte in exchange for one intracellular calcium being exported
    • Sodium accumulates intracellularly and is exchanged for Calcium.
    • Causes an increase in the intracellular calcium concentration increasing contractility
      • Also a lengthening of phase 4 and phase 0 of the cardiac action potential which ultimately decreases heart rate
  • Summary
    • Inhibits NaK pump
      • Positive inotropy
    • Negative chronotropy/dromotropy
      • Indirect vagal stimulator


See Also


  1. Gheorghiade M. et al. Digoxin in the Management of Cardiovascular Disorders. Circulation. 2004; 109: 2959-2964