Digoxin and digoxin toxicity

Digoxin and digoxin toxicity

Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure

positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure

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.

Mechanism of action

• decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
• increases the force of cardiac muscle contraction due to inhibition of the Na⁺/K⁺ ATPase pump
  Digoxin - inhibits the Na⁺/K⁺ ATPase pump
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  Importance: 56
  . Also stimulates vagus nerve
• digoxin has a narrow therapeutic index
  digoxin has a narrow therapeutic index
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Monitoring

• digoxin level is not monitored routinely, except in suspected toxicity
  digoxin level is not monitored routinely, except in suspected toxicity
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• if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose
  If toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose
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  Importance: 100

Digoxin toxicity

Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range

Toxicity may occur even when the concentration is within the therapeutic range

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. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.

Features

• generally unwell, lethargy, nausea & vomiting, anorexia
  anorexia
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  , confusion
  Digoxin may cause confusion
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  Importance: 18
  , yellow-green vision
  Digoxin may cause yellow-green vision
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  Importance: 46
• arrhythmias (e.g. AV block
  AV block
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  , bradycardia
  Digoxin may cause bradycardia
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  Importance: 26
  )
• gynaecomastia
  Gynaecomastia is a recognised side effect of digoxin
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  Importance: 23

Precipitating factors

• classically: hypokalaemia
  hypokalaemia
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  • digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
    Digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia --> digoxin more easily bind to the ATPase pump --> increased inhibitory effects
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    Importance: 61
• increasing age
  • due to reduced GFR
    Digoxin toxicity is more common in elderly patients due to reduced GFR
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    Importance: 31
• renal failure
  renal failure
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• dehydration
• myocardial ischaemia
• hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
• hypoalbuminaemia
• hypothermia
• hypothyroidism
• drugs: amiodarone
  Amiodarone may cause precipitation of digoxin toxicity - if starting amiodarone on a patient taking digoxin the dose should be reduced
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  Importance: 39
  , quinidine
  Type 1 diabetes often presents with the triad of weight loss, polyuria and polydipsia
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  Importance: 20
  , verapamil
  Verapamil may cause precipitation of digoxin toxicity
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  Importance: 51
  , diltiazem
  Diltiazem may cause precipitation of digoxin toxicity
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  Importance: 45
  , spironolactone
  Spironolactone may cause precipitation of digoxin toxicity
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  Importance: 33
  (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin
  Ciclosporin may cause precipitation of digoxin toxicity
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  Importance: 28
  . Also drugs which cause hypokalaemia e.g. thiazides
  Thiazides may cause precipitation of digoxin toxicity
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  Importance: 38
  and loop diuretics
  Loop diuretics may cause precipitation of digoxin toxicity
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  Importance: 3

Management

• Digibind
  Digibind
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• correct arrhythmias
• monitor potassium

+PassMedicine Notes

Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.

Mechanism of action

• decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
• increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
• digoxin has a narrow therapeutic index

Monitoring

• digoxin level is not monitored routinely, except in suspected toxicity
• if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose

Digoxin toxicity

Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.

Features

• generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
• arrhythmias (e.g. AV block, bradycardia)
• gynaecomastia

Precipitating factors

• classically: hypokalaemia
• digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia --> digoxin more easily bind to the ATPase pump --> increased inhibitory effects
• increasing age
• due to reduced GFR
• renal failure
• dehydration
• myocardial ischaemia
• hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
• hypoalbuminaemia
• hypothermia
• hypothyroidism
• drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

Management

• Digibind
• correct arrhythmias
• monitor potassium