Digoxin
Digoxin is a cardiac glycoside which increases contractility of the myocardium by direct activity. Its primary action is through inhibition of adenosine triphosphatase, and thus sodium-potassium exchange activity. This results in augmentation of calcium ion influx allowing for increased calcium availability at the time of excitation-contraction coupling. A similar effect is exerted on the autonomic nervous system which results in reduced sympathetic tone thereby reducing ventricular rate. If rapid digitalisation is required, intravenous (IV) administration of a loading dose of digoxin produces a pharmacological effect within 5-30 minutes, whilst the oral route occurs in 0.5-2 hours.
Routine monitoring of digoxin levels is not usually indicated unless there is suspicion of toxicity, change in renal function, or there is a possible lack of compliance. Digoxin levels should be taken at least 6 hours post dose. There are no set guidelines stating what range of serum digoxin levels is most efficacious but analysis by the Digitalis Investigation Group trial suggested that levels between. 0.5-1 nanogram/mL could be efficacious.
Digoxin toxicity can occur at low digoxin concentrations, but it is more commonly associated with levels above 2 nanogram/mL. The signs of digoxin toxicity are often non-specific and include nausea, vomiting, diarrhoea, lethargy, confusion, visual disturbance, and arrhythmias. Cardiac arrhythmias account for many deaths due to digoxin toxicity. In case of suspected or known life-threatening digoxin toxicity Digibind antidote can be administered.
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