Digoxin

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Mechanism of Action

Digoxin’s inhibits of the Na+/K+ ATPase, in the myocardium causing an increase in intracellular sodium levels, resulting in a reversal of the action of the sodium-calcium exchanger. The exchanger normally imports three extracellular sodium ions into the cardiac myocyte in exchange for one intracellular calcium being exported. By inhibiting the ATPase sodium accumulates intracellularly and is exchanged for Calcium. The reversal of this exchange causes an increase in the intracellular calcium concentration increasing contractility. There is also a lengthening of phase 4 and phase 0 of the cardiac action potential which ultimately decreases heart rate.[1]

General

  • Type:
  • Dosage Forms:
  • Common Trade Names:

Adult Dosing

  • Loading dose = 0.25 mg IV q2hr until effect (max total = 1.5 mg)
  • in acute afib rvr with heart failure = 0.5 mg IV, then 0.25 mg IV q4hr until effect or max 1.5mg

Pediatric Dosing

Special Populations

Indications

  • RVR control in a-fib/flutter, PSVT

Contraindications

  • Allergy to class/drug
  • WPW
    • Increases conduction velocity in atrial tissue

Adverse Reactions

Digoxin toxicity

  • GI: N/V, diarrhea, abd pain
  • CV: Bradycardia, SA/AV block, ventr arrhythmias

Pharmacology

  • Half-life:
  • Metabolism:
  • Excretion:
  • Mechanism of Action:
    • Inhibits NaK pump
      • Positive inotropy
    • Negative chronotropy/dromotropy
      • Indirect vagal stimulator
  • Kinetics
    • Onset of action = 1.5-4hr (IV)

Comments

See Also

References

  1. Gheorghiade M. et al. Digoxin in the Management of Cardiovascular Disorders. Circulation. 2004; 109: 2959-2964