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Flashcards in Digoxin Deck (12)
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1
Q

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

A
  • 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)
2
Q

Describe the pharmacodynamics of digoxin.

A
  • 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
3
Q

How does digoxin achieve its inotropic effects?

A

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
4
Q

How does digoxin achieve its anti-arrhythmic effects?

A

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
5
Q

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

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

*increased automaticity, AV block

6
Q

What are the clinical uses of digoxin?

A
  • 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”)
7
Q

What are major drug-drug interactions with digoxin?

A
  • 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)
8
Q

What is the therapeutic range of digoxin?

A

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

9
Q

What contraindications are associated with digoxin?

A
  • 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
10
Q

Describe the pharmacokinetics of digoxin.

A
  • 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).
11
Q

What are the major indications for digoxin?

A

Congestive heart failure

Arrhythmia (rate control)

12
Q

What should be done if digoxin related arrhythmia occurs?

A

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