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Snapshot
  • A 28-year-old man presents to the emergency room after ingesting an unknown amount of his grandfather’s digoxin medication. He reports feeling depressed and ingesting a handful of the drug about 1 hour ago. Since then, he reports having abdominal pain, nausea, and vomiting. He also says that his vision is becoming blurry, with yellow halos around objects. He is found to have a K+ of 6.5 mEq/L. He is quickly given activated charcoal, given the recent ingestion, and started on digoxin antibodies. (Digoxin poisoning)
Introduction
  • Drug
    • a cardiac glycoside derived from the foxglove plant, digitalis purpurea
  • Mechanism of action
    • direct reversible inhibitor of Na+/K+ ATPase
      • causing ↑ in intracellular Na+ and ↓ in intracellular K+
    • indirectly inhibits Na+/Ca2+ exchanger
      • the increased intracellular Na+ prevents expulsion of Ca2+ from the cell and increases intracellular Ca2+
    • this results in
      • ↑ free Ca2+ ions
      • ↑ inotropy and contractility
      • ↑ vagal tone
        • ↓ conduction through sinoatrial and atrioventricular nodes
        • ↓ heart rate
  • Clinical use
    • heart failure
    • left ventricular dysfunction
    • atrial fibrillation
Toxicity
  • Toxicity can be fatal
  • Clinical manifestations
    • gastrointestinal symptoms (most common)
      • nausea
      • vomiting
      • abdominal pain
      • diarrhea
    • vision changes
      • yellow halos around objects
      • blurry vision
    • arrhythmias
    • hyperkalemia
  • Risk factors for severe toxicity
    • renal failure
    • hypokalemia
      • K+ competes with digoxin for binding sites and excretion
      • low K+ allows digoxin to bind at K+ binding sites on Na+/K+ ATPase 
  • Evaluation
    • serum digoxin concentration
    • serum potassium
    • serial electrocardiograms
  • Treatment
    • digoxin antibodies (anti-digoxin Fab fragments)
    • Mg2+
    • activated charcoal
      • for those who present within 1-2 hours of ingestion

 


 

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