Digoxin: Difference between revisions

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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.<ref>Gheorghiade M. et al. Digoxin in the Management of Cardiovascular Disorders. Circulation. 2004; 109: 2959-2964</ref>
==General==
==General==
*Type:  
*Type: Cardiac glycoside; [[CHF medications]]
*Dosage Forms:
*Mechanism of action- Inhibits Na+/K+ ATPase, leading to an increase in intracellular sodium that can increase cardiac contractility
*Common Trade Names:  
*Dosage Forms: PO, IV, IM
*Common Trade Names: Digitek, Digox, Lanoxin


==Adult Dosing==
==Adult Dosing==
*Loading dose = 0.25 mg IV q2hr until effect (max total = 1.5 mg)
*Loading dose = 0.25mg IV q2hr until effect (max total = 1.5mg)
*in acute afib rvr with heart failure = 0.5 mg IV, then 0.25 mg IV q4hr until effect or max 1.5mg
*in acute [[atrial fibrillation with RVR]] with heart failure = 0.5mg IV, then 0.25mg IV q4hr until effect or max 1.5mg


==Pediatric Dosing==
==Pediatric Dosing==


==Special Populations==
==Special Populations==
*[[Drug Ratings in Pregnancy|Pregnancy Rating]]:
*[[Drug Ratings in Pregnancy|Pregnancy Rating]]: C
*[[Lactation risk categories|Lactation risk]]:
*[[Lactation risk categories|Lactation risk]]:
*Renal Dosing
*Renal Dosing
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**Pediatric
**Pediatric


== Indications ==
==Indications==
*RVR control in a-fib/flutter, PSVT
*RVR control in a-fib/flutter, PSVT


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==Adverse Reactions==
==Adverse Reactions==
''[[Digoxin toxicity]]''
''[[Digoxin toxicity]]''
*GI: N/V, diarrhea, abd pain
*GI: nausea and vomiting, diarrhea, abdominal pain
*CV: Bradycardia, SA/AV block, ventr arrhythmias
*CV: Bradycardia, SA/AV block, ventr arrhythmias
*Neuro: [[altered mental status]], visual disturbances (yellow-tinted vision)


==Pharmacology==
==Pharmacology==
*Half-life:  
*Onset of action
*Metabolism:  
**IV = 5-30 minutes
*Excretion:  
**PO = 0.5-2 hours
*Mechanism of Action:
*Half-life: 36-48 hours (may be increased with renal impairment)
**Inhibits NaK pump
*Absorption: 60-80% absorption after oral administration
***Positive inotropy
*Metabolism: ~16% is converted to metabolites
**Negative chronotropy/dromotropy
*Excretion: Almost entirely by the kidneys
***Indirect vagal stimulator
 
*Kinetics
==Mechanism of Action==
**Onset of action = 1.5-4hr (IV)
{{Digoxin mechanism}}


==Comments==
==Comments==
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==References==
==References==
<references/>
<references/>
[[Category:Drugs]]
[[Category:Pharmacology]]
[[Category:Cardiology]]

Latest revision as of 21:17, 6 January 2022

General

  • Type: Cardiac glycoside; CHF medications
  • Mechanism of action- Inhibits Na+/K+ ATPase, leading to an increase in intracellular sodium that can increase cardiac contractility
  • Dosage Forms: PO, IV, IM
  • Common Trade Names: Digitek, Digox, Lanoxin

Adult Dosing

  • Loading dose = 0.25mg IV q2hr until effect (max total = 1.5mg)
  • in acute atrial fibrillation with RVR with heart failure = 0.5mg IV, then 0.25mg 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: nausea and vomiting, diarrhea, abdominal pain
  • CV: Bradycardia, SA/AV block, ventr arrhythmias
  • Neuro: altered mental status, visual disturbances (yellow-tinted vision)

Pharmacology

  • Onset of action
    • IV = 5-30 minutes
    • PO = 0.5-2 hours
  • Half-life: 36-48 hours (may be increased with renal impairment)
  • Absorption: 60-80% absorption after oral administration
  • Metabolism: ~16% is converted to metabolites
  • Excretion: Almost entirely by the kidneys

Mechanism of Action

  • Inhibits Na+/K+ ATPase in the myocardium[1]
    • Causes increase in intracellular sodium levels
    • Results in reversal of sodium-calcium exchanger
      • Normally imports three extracellular sodium ions into the cardiac myocyte in exchange for one intracellular calcium being exported
    • Sodium accumulates intracellularly and is exchanged for Calcium.
    • Causes an increase in the intracellular calcium concentration increasing contractility
      • Also a lengthening of phase 4 and phase 0 of the cardiac action potential which ultimately decreases heart rate
  • Summary
    • Inhibits NaK pump
      • Positive inotropy
    • Negative chronotropy/dromotropy
      • Indirect vagal stimulator

Comments

See Also

References

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