![]() Digoxin is distributed by attaching 20 to 25% of the time to polypeptides (i.e., protein bound) to be delivered to the various receptors for use by the body.The peak serum time of digoxin in oral form is within a 1-3 hour range. ![]() The duration of effectiveness of digoxin lasts for 3 to 4 days. ![]() In the IV form, the initial effect starts within 5 to 30 minutes of administration with a maximum effect of up to 1.5 to 4 hours. The onset of digoxin effects starts within 0.5 to 2 hours initially for oral forms with a 2-6 hour maximal effect.The bioavailability of digoxin is 60 to 80% when in tablet form and 70 to 85% for elixir forms.Explained below are the mechanisms of pharmacokinetics of digoxin (i.e., absorption, distribution, metabolism and elimination). As with all medications, digoxin is processed in the body when administered to achieve the goals of medical therapy. Pharmacokinetics is a body of pharmaceutical knowledge focused on how an organism affects and changes a drug. Furthermore, it permits progressive outflowing of intracellular potassium thereby elevating the serum potassium levels in the body. On higher concentrations, digoxin intensifies sympathetic outflow from the central nervous system (CNS) towards both cardiac and peripheral sympathetic nerves.Because of these, it elevates the sensitivity of baroreceptors, consequently increasing the nerve activity in the carotid sinus, and augmenting sympathetic reaction withdrawal for every elevation in mean arterial pressure. It reduces the uptake of catecholamine (hormones responsible for the “fight or flight” mechanism) at the nerve channels, thereby allowing the body’s blood vessels to have increased sensitivity to endogenous or exogenous catecholamine.Due to these, the drug indirectly causes parasympathetic stimulation of the autonomic nervous system, subsequently affecting the sino-atrial (SA) and atrioventricular nodes (AV) of the heart. Inotropy and automaticity are then consequently raised while conduction rate is diminished. It inhibits Na-K ATPase, which causes increased availability of intracellular calcium in the heart muscle and the conduction system.Finally, calculating for the patient’s lean body weight is ideal when giving to geriatric patients. In addition, a higher dose has no added benefit for patients with heart failure and may even cause increased toxicity. Adult dosing modifications of digoxin should always be guided by assessing for the patients estimated creatinine clearance levels and serum drug levels.However, adjustments are needed and use of lower end dosing is followed for patients with impaired kidney function or low lean body mass. For patients with heart failure, starting the patient on a loading dose of digoxin is not required.When digoxin is administered as an injectable maintenance dose for atrial fibrillation, intravenous (IV) doses are preferred over intramuscular (IM) administration due to the risk of developing severe injection site reaction.When digoxin is administered as an oral maintenance dose for atrial fibrillation, incremental doses of digoxin are only done every 2 weeks and will depend on patient response, serum drug levels and possible toxicity.It is also warranted that careful assessment is done after each dose given to evaluate patient response and possible toxicity. ![]() Incremental increases with ¼ of the loading dose given on a 6-8 hour gap for two succeeding doses should be considered.
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