Pharmacology
Summary
Digoxin, a cardiac glycoside primarily utilized in symptom management of chronic heart failure, derives its therapeutic benefit from its ability to inhibit Na+/K+ ATPase on the cell membrane. This inhibition results in elevated intracellular sodium levels, subsequently hindering calcium from leaving the cell via the Na+/Ca2+ exchanger. The accumulation of calcium in the sarcoplasm enhances cardiac contractility, thereby offering symptomatic relief. Additionally, digoxin directly stimulates the vagus nerve, giving it the capability to treat specific arrhythmias
Despite its utility in heart failure and treating certain arrhythmias, digoxin is limited by a narrow therapeutic index, necessitating vigilant monitoring of its serum levels. Notable side effects include hyperkalemia, heart block, GI side effects and visual anomalies (xanthopsia). Other contributing factors like renal dysfunction or the concurrent use of antiarrhythmic agents can increase the risk of digoxin toxicity, emphasizing the importance of meticulous dosing. In situations of pronounced arrhythmias due to digoxin toxicity, digoxin immune fab can be used as an antidote.
Lesson Outline
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FAQs
Digoxin, a cardiac glycoside, exerts its effects by reversibly inhibiting the Na+/K+ ATPase enzyme. This inhibition results in elevated intracellular sodium levels, subsequently hindering calcium from leaving the cell via the Na+/Ca2+ exchanger. The accumulation of calcium in the sarcoplasm enhances cardiac contractility, thereby offering symptomatic relief in chronic systolic heart failure. Additionally, digoxin directly stimulates the vagus nerve, giving it the capability to treat specific arrhythmias.
Digoxin is associated with several side effects. Due to its inhibitory affect on the Na+/K+ pump, digoxin use can lead to hyperkalemia; hence, regular potassium monitoring is imperative. The drug can induce bradycardia due to augmented parasympathetic activity at both the SA and AV nodes, potentially progressing to heart block. Chronic administration might manifest as 'scooped' concave ST segments on ECG readings. Patients might also experience GI symptoms and xanthopsia, a distinctive effect of digoxin that causes a yellowish tint in visual perception. Given these potential side effects, vigilant monitoring of heart rate and rhythm is essential.
Patients with heart block are advised against using digoxin due to its amplification of the parasympathetic activity at the AV node. This can lead to further deceleration of heart rhythm, exacerbating the heart block.
Both renal insufficiency and numerous antiarrhythmics can diminish the renal clearance of digoxin. This impediment leads to a prolonged serum half-life, amplifying the risk of digoxin toxicity. Thus, when prescribing digoxin, clinicians must exercise caution, especially in the presence of renal dysfunction or concurrent antiarrhythmic therapy.
Digoxin immune Fab serves as an antidote for digoxin toxicity. Digoxin immune Fab operates by binding to digoxin, forming a complex that is then safely excreted via the kidneys, consequently decreasing the circulating toxic digoxin levels.
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