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 ingested a handful of the drug about 1 hour ago. Since then, he states having abdominal pain, nausea, and vomiting. He also discloses 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 administered 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