Digoxin Flashcards
What is the primary mechanism of action of digoxin?
Increased intracellular calcium via increased intracellular sodium. Digoxin inhibits the sodium-potassium ATPase pump, increasing intracellular sodium, which indirectly increases intracellular calcium via the sodium-calcium exchanger, leading to increased cardiac contractility.
What are the indications for digoxin use?
- Rate control in atrial fibrillation (especially in patients with systolic heart failure).
- Symptomatic heart failure with reduced ejection fraction (HFrEF) to improve symptoms.
Why does digoxin increase vagal tone?
Digoxin sensitizes arterial baroreceptors and enhances parasympathetic ganglionic transmission, leading to increased vagal output and slowed AV node conduction.
What are the key clinical effects of digoxin?
- Positive inotropic effect (increased contractility) useful in heart failure.
- Negative chronotropic effect (slows heart rate) useful in atrial fibrillation.
How does digoxin affect heart rate in atrial fibrillation?
Digoxin increases parasympathetic (vagal) tone, slowing conduction through the atrioventricular (AV) node and improving rate control.
Why is digoxin not typically used as monotherapy for rate control in atrial fibrillation?
Digoxin is less effective during exercise or high sympathetic tone; it is usually combined with beta blockers or nondihydropyridine calcium channel blockers.
What ECG changes are associated with digoxin use?
Characteristic ‘scooped’ ST depression (reverse tick sign), T-wave flattening, and possible bradyarrhythmias or AV block.
What are the prodromal symptoms of digoxin toxicity?
Nausea, vomiting, diarrhea, abdominal pain, visual disturbances (xanthopsia; yellow-green vision, halos), and fatigue.
What happens to potassium levels in digoxin toxicity?
Potassium becomes markedly elevated, therefore requires routine monitoring.
How does digoxin toxicity affect the atria and ventricles?
Toxic levels can cause increased automaticity and decreased refractory periods, leading to bradycardia, atrial tachyarrhythmias, ventricular tachycardia, or ventricular fibrillation.
How does digoxin affect Purkinje fibers at toxic levels?
Toxic levels increase Purkinje fiber automaticity, which can lead to ventricular arrhythmias such as ventricular tachycardia.
What electrolyte imbalances increase the risk of digoxin toxicity?
Hypokalemia, hypomagnesemia, and hypercalcemia increase the risk of digoxin toxicity.
What are the contraindications for digoxin use?
Digoxin is contraindicated in patients with Wolff-Parkinson-White syndrome and pre-excitation atrial fibrillation, patients with heart blocks without a pacer, and patients with renal failure.
How does digoxin interact with renal function?
Digoxin is primarily renally excreted; impaired renal function increases the risk of toxicity.
What is the therapeutic serum level of digoxin?
0.5-2.0 ng/mL, with levels >2 ng/mL associated with toxicity.
What is the reversal agent used in digoxin toxicity?
Digoxin Fab.
What is the treatment for digoxin toxicity?
- Stop digoxin. 2. Correct electrolyte imbalances (e.g., potassium, magnesium). 3. Administer digoxin-specific antibody fragments (Digibind) in severe cases.
