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Digoxin

Digoxin is a cardiac glycoside that inhibits the Na⁺/K⁺-ATPase enzyme, leading to increased intracellular calcium and enhanced myocardial contraction. It is used to treat heart failure, atrial fibrillation, atrial flutter, and certain supraventricular tachyarrhythmias, with a bioavailability of 70-80% and a half-life of 36-48 hours. Side effects include bradycardia, gastrointestinal disturbances, central nervous system effects, and visual disturbances, with contraindications for conditions like ventricular fibrillation and severe renal impairment.

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5 views3 pages

Digoxin

Digoxin is a cardiac glycoside that inhibits the Na⁺/K⁺-ATPase enzyme, leading to increased intracellular calcium and enhanced myocardial contraction. It is used to treat heart failure, atrial fibrillation, atrial flutter, and certain supraventricular tachyarrhythmias, with a bioavailability of 70-80% and a half-life of 36-48 hours. Side effects include bradycardia, gastrointestinal disturbances, central nervous system effects, and visual disturbances, with contraindications for conditions like ventricular fibrillation and severe renal impairment.

Uploaded by

aminahaslam2004
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Digoxin

Mechanism of Action (MOA)


Digoxin is a cardiac glycoside that produces its effect by inhibiting the Na⁺/K⁺-ATPase enzyme
present on the cardiac cell membrane.

Mechanism:
1. Digoxin inhibits Na⁺/K⁺-ATPase pump.
2. Intracellular sodium concentration increases.
3. Increased intracellular sodium decreases the activity of Na⁺/Ca²⁺ exchanger.
4. Intracellular calcium concentration increases.
5. Increased calcium is stored in the sarcoplasmic reticulum.
6. During depolarization, more calcium becomes available for myocardial contraction.
7. This results in increased force of cardiac contraction (positive inotropic effect).
Additional actions:
• Increases vagal tone
• Decreases sympathetic activity
• Slows AV nodal conduction
• Decreases heart rate

Pharmacokinetics
Absorption
• Digoxin is well absorbed after oral administration.
• Oral bioavailability is approximately 70–80%.

Distribution
• Widely distributed throughout body tissues, particularly the heart, skeletal muscles, liver, and
kidneys.
• Plasma protein binding is approximately 20–30%.
• Has a large volume of distribution.

Metabolism
• Only a small amount undergoes hepatic metabolism.

Elimination
• Primarily excreted unchanged by the kidneys.
Half-life
• Approximately 36–48 hours in patients with normal renal function.
• Half-life is prolonged in renal impairment.

Therapeutic Uses
1. Heart failure
• Used in symptomatic heart failure, especially heart failure with reduced ejection
fraction.
• Improves cardiac output and reduces symptoms.
2. Atrial fibrillation
• Controls ventricular rate by slowing AV nodal conduction.
3. Atrial flutter
• Used for ventricular rate control.
4. Supraventricular tachyarrhythmias
• Useful in selected supraventricular arrhythmias.

Side Effects
Cardiac effects
• Bradycardia
• Atrioventricular (AV) block
• Ventricular arrhythmias
• Palpitations

Gastrointestinal effects
• Nausea
• Vomiting
• Anorexia
• Diarrhea

Central nervous system effects


• Headache
• Fatigue
• Dizziness
• Confusion

Visual disturbances
• Blurred vision
• Yellow-green discoloration of vision (xanthopsia)
• Halos around objects

Contraindications
• Ventricular fibrillation
• Severe bradycardia
• Second- or third-degree AV block
• Hypertrophic obstructive cardiomyopathy
• Hypersensitivity to digoxin
• Severe renal impairment (requires caution and dose adjustment

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