Metabolism – minimal hepatic metabolism.Distribution – 30% protein bound, Vd 10L/kg (higher in the elderly and obese).Absorption – good oral absorption with oral bioavailability of 80% and peak levels at 6 hours.Increased vagal tone (vagomimetic effect) > calcium-mediated inotropy and increased automaticity, as well as negative dromotropy due to decreased intracellular K+ > increased intracellular Ca2+ due to Na+/Ca2+ antiporter > increased intracellular Na+ and increased extracellular K+ Inhibition of Na/K ATPase on the cell surface negative dromotropy (slowing of AV conduction).supplies of digibind should be available on site in the emergency department, and in severe toxicities early steps to source more may be necessaryĭirect and indirect effects resulting in:.digoxin levels cannot be accurately measured for about 3 weeks after administration of digibind, as they will be artefactually high given that most serum digoxin assays measure both free and digibind-bound digoxin in the circulation (some laboratories may be able to measure free digoxin levels specifically).there is often a reluctance to give the digibind antidote due to cost and underestimating the mortality associated with digoxin toxicity, however it is prudent to administer digibind based on a considered risk assessment and before the life-threatening manifestations of digoxin toxicity develop.Digoxin-specific Fab fragments (digibind) is the definitive treatment, toxicity is refractory standard dysrhythmia treatments. Chronic digoxin toxicity varies in severity but is associated with a mortality at one week of 15-30% (!).Digoxin has a narrow therapeutic index and chronic toxicity is more likely in the elderly and those with renal impairment.Digoxin toxicity is characterised by gastrointestinal distress, hyperkalemia and life-threatening dysryhthmias, including increased automaticity and AV nodal blockade.
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