digitalis
Summary
Digitalis refers to cardiac glycosides (e.g., digoxin) derived from the foxglove plant, used primarily for heart failure with reduced ejection fraction and rate control in atrial fibrillation. It works by inhibiting the Na+/K+-ATPase pump, increasing intracellular calcium and myocardial contractility, while also increasing vagal tone to slow AV conduction. It has a narrow therapeutic index and is prone to toxicity, especially with hypokalemia or renal impairment.
Detail
Mechanism: Digitalis glycosides inhibit the Na+/K+-ATPase on cardiac myocytes, leading to increased intracellular Na+, which reduces the activity of the Na+/Ca2+ exchanger. This results in increased intracellular Ca2+ and enhanced myocardial contractility (positive inotropy). Digitalis also increases vagal tone, which slows conduction through the AV node, making it useful for rate control in atrial fibrillation/flutter. It has a narrow therapeutic index (0.5-2.0 ng/mL), and toxicity risk is increased by hypokalemia (which potentiates digoxin binding to the Na+/K+-ATPase), hypomagnesemia, hypercalcemia, and renal failure (since digoxin is renally excreted).
Clinical Use: Heart failure with reduced ejection fraction (improves symptoms but not mortality), rate control in atrial fibrillation/flutter.
Toxicity: Signs include GI symptoms (nausea, vomiting, anorexia), visual disturbances (blurry vision, yellow-green halos - xanthopsia, associated with Van Gogh's paintings), cardiac arrhythmias (can cause almost any arrhythmia, but classically causes AV block with accelerated junctional rhythms, and bidirectional ventricular tachycardia is highly specific for digoxin toxicity), and CNS effects (confusion, delirium). ECG can show a 'scooped' ST segment.
Treatment of toxicity: Digoxin-specific antibody fragments (digoxin immune Fab), correction of potassium levels (avoid giving calcium in setting of digoxin toxicity/hyperkalemia as it can worsen cardiac toxicity), and supportive care.
Drug interactions: Quinidine, verapamil, amiodarone, and other drugs can displace digoxin from tissue-binding sites and increase serum digoxin levels, increasing toxicity risk.
Pharmacokinetics: Renal excretion, long half-life (36-48 hours), narrow therapeutic index requiring monitoring of levels, especially in renal impairment.
Sources
- Katzung's Basic and Clinical Pharmacology
- First Aid for the USMLE Step 1
- Goodman & Gilman's The Pharmacological Basis of Therapeutics
- Harrison's Principles of Internal Medicine
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