USMLE

Digoxin/Digitalis

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Cardiovascular Pharm
  1. Adenosine
  2. Magnesium
  3. Nitroprusside
  4. Nitrates
  5. Ivabradine
  6. Digoxin/Digitalis
  7. Class IA Antiarrhythmics
  8. Class IB Antiarrhythmics
  9. Class IC Antiarrhythmics
  10. Class II Antiarrhythmics
  11. Class III Antiarrhythmics - Amiodarone
  12. Class III Antiarrythmics - Sotalol
  13. Class III Antiarrhythmics - Ibutilide, Dofetilide
  14. Class IV Antiarrhythmics - Verapamil, Diltiazem
  15. HMG-CoA Reductase Inhibitors (Statins)
  16. Ezetimibe
  17. Fibrates
  18. PCSK9 Inhibitors (Alirocumab, Evolocumab)
  19. Fish Oil and Omega-3s
  20. Milrinone
  21. Aliskiren
  22. Hydralazine
  23. Ranolazine
  24. Sacubitril

Summary

Cardiac glycosides including digoxin, digitalis, and digitoxin are drugs that work in two ways.

First, they can inhibit the sodium/potassium pump in the heart, causing sodium levels to rise. The increased sodium levels inside the cell indirectly activate a sodium/calcium exchanger to bring more calcium into the cell. More calcium causes more contractility in cardiac muscle. This increased contractility is useful in the treatment of heart failure.

Second, digoxin can increase vagal tone, which acts mainly on the pacemaker SA and AV nodes to slow conduction. By slowing conduction down the AV node, digoxin is a useful drug in rate control for atrial fibrillation.

Note that these drugs are rarely administered first-line, mainly due to their narrow therapeutic windows. Patients taking these drugs often experience toxicity, which includes symptoms like disturbed color vision, AV heart block, as well as non-specific GI and neurological symptoms.

Key Points

  • Digoxin and Digitoxin
    • Also known as the cardiac glycosides
      • Derived from the foxglove plant, digitalis purpurea
      • Digitoxin is a more stable form of digoxin with a longer half-life
    • Mechanism
      • Inhibition of Na+/K+ ATPase
        • Reversible block of Na+/K+ ATPase leads to increased intracellular Na+
          • Increased Na+ stimulates increased Na+/Ca2+ exchange → increased Ca2+ influx → ↑ cardiac contractility
      • Increased vagal tone (CN X)
        • Slows conduction at SA and AV node
        • Decreases heart rate
    • Clinical Use
      • Heart Failure
        • Due to increased calcium influx leading to positive inotropic effect (increased contractility)
      • Atrial fibrillation
        • Due to slowed conduction at AV node (reduces ventricular rate) and depression of SA node
        • 2nd line after metoprolol/diltiazem (due to side effect profile)
    • Adverse Effects
      • Narrow therapeutic window (toxicity is common)
        • Especially in hypokalemia (increased drug binding since potassium competes with digoxin), hypovolemia, and renal failure (decreased clearance)
      • Visual disturbances
        • May see yellow halos around objects
      • AV block
        • Due to conduction blockade at AV node
      • Hyperkalemia
      • Nonspecific GI (nausea, vomiting, diarrhea) and nervous (fatigue, confusion, weakness) side effects
    • Reversal
      • Anti-digoxin Fab fragments
        • Can reverse both digoxin and digitoxin