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Flashcards in Digoxin Deck (12):

What is the structure of cardiac glycosides (i.e. digoxin)? (Don't memorize)

- Steroid nucleus (necessary for activity)
- 5-member lactone ring at C17 (necessary for activity)
- Series of sugar groups at C3 (affects pharmacokinetic properties)
- Lack of ionizing group(s)


Describe the pharmacodynamics of digoxin.

- Inotropic effects (increase myocardial contractility)
- Na/K pump inhibited => more sodium inside the cell; less K pumped into the cell
- Increase Ca++ flux into sarcomere
- Anti-arrhythmic effects
-Therapeutic levels cause a vagotonic effect that is useful in slowing AV conduction in patients with atrial fibrillation


How does digoxin achieve its inotropic effects?

Primary action: inhibits the Na, K-ATPase enzyme/pump in cell membrane
- This inhibition increases the intensity of the interaction of actin and myosin filaments in the sarcomere => Increases [Ca++]
- This leads to increased myocardial contractility
- Causes increased sympathetic tone


How does digoxin achieve its anti-arrhythmic effects?

Primary action=> slow conduction through the AV node/rate control (vagotonic effect)
- Slows ventricular response rate to atrial fibrillation (but doesn't fix a-fib)
- Can have pro-arrhythmogenic (tachyarrhythmic) effects


In what ways does digoxin work on other organ systems (ie toxicities)?

- GI: Anorexia, nausea and vomiting, abdominal pain, diarrhea
- CNS effects: Disorientation, nightmares, hallucinations, vision (green -yellow color, blurring)

*increased automaticity, AV block


What are the clinical uses of digoxin?

- CHF with normal sinus rhythm
- Patients with large, dilated hearts, JVD, S3 gallop rhythm
*Diuretics, ACE inhibitors also effective, probably safer over years

- Use in patients with atrial fibrillation to slow AV conduction (“rate control”)


What are major drug-drug interactions with digoxin?

- Absorption reduced by oral antacids (e.g. Mg, Al hydroxides)
- Will bind digoxin in the GI, lower the bioavailability
- Quinidine (reduces renal clearance of digoxin by about 50%!!!)
- Digoxin plasma level increases => possible digoxin toxicity
- Amiodarone (additive effects on A-V node conduction)
- Ventricular rate decreases
- Verapamil, propranolol (additive effects on A-V node conduction blockages)
- Again, excessively slow ventricular response/ventricular asystole (with one another and with digoxin)


What is the therapeutic range of digoxin?

Therapeutic range: 0.5 - 2.5 ng/ml (narrow)


What contraindications are associated with digoxin?

- Ventricular tachycardia, VF
- May cause or worsen
- Wolff-Parkinson-White syndrome
- May encourage conduction down accessory pathway (V-tach)
- 1st, 2nd and 3rd degree AV or SA block
- May worsen any AV block
- Hypertrophic cardiomyopathy (Idiopathic hypertrophic sub aortic stenosis)
- May worsen degree of functional obstruction.

*Relative contraindications: hypoxia, hypokalemia (ie with hydrochlorothiazide/furosemide)

*Toxic levels increase automaticity of all areas of the heart except the SA node


Describe the pharmacokinetics of digoxin.

- Bioavailability 60-95% (best with capsule)
- Can be given slowly IV
- Redistribution over about 8 hours
- Clearance 80% renal, t1/2 30-40 hours (normal GFR)
- Markedly high Vd (approx. 6-7 L/kg).


What are the major indications for digoxin?

Congestive heart failure
Arrhythmia (rate control)


What should be done if digoxin related arrhythmia occurs?

1) Correct hypoxia, electrolyte, and acid/base abnormalities
2) Treat arrhythmias
3) Consider anti-digoxin Fab fragments (Digibind) in severe cases