Snapshot A 50-year-old man with a past medical history of renal failure and dilated cardiomyopathy presents to the emergency room for nausea, vomiting, and blurry vision. He noticed that previously white objects now look yellow. He was recently started on digoxin. An echocardiogram reveals an atrioventricular block. He is found to be hyperkalemic. He is given an antidote for suspected digoxin toxicity. Introduction Drug a cardiac glycoside derived from the foxglove plant, digitalis purpurea Mechanism of action direct reversible inhibition 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 login to view 2 more bullets 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 hyperkalemia arrhythmias atrial ectopy and atrial tachycardia Risk factors for severe toxicity renal failure chronic conditions login to view 2 more bullets medications login to view 5 more bullets 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