Digoxin toxicity

Background

• Mechanism of action
  • Positive inotropic effect
    • Inhibits Na-K pump -> incr extracelluar K, incr intracellular Na -> incr intracellular Ca
  • Increases vagal tone
    • Can lead to bradyarrhythmias (esp in young)
  • Increases automaticity
    • Can lead to tachyarrhythmias (esp in elderly)
• Renally cleared
• Hemodialysis does not work

Risk Factors

1. Electrolyte Imbalance
   1. Hypokalemia, Hypomagnesemia, Hypercalcemia
2. Hypovolemia
3. Renal insufficiency
4. Cardiac ischemia
5. Hypothyroidism
6. Meds
   1. CCBs, amiodarone

DDX

1. CCB/BB toxicity
2. Clonidine toxicity
3. Organophosphate poisoning
4. Sick sinus syndrome

Clinical Manifestations

Cardiac

1. Syncope
2. Dysrhythmias
   1. PVCs
   2. Bradycardia
   3. SVT w/ AV block
   4. Junctional escape
   5. Ventricular dysrhythmia (esp in chronic toxicity)
3. Digitalis Effect (seen with therapeutic levels; not indicative of toxicity)
   1. T wave changes (flattening or inversion)
   2. QT interval shortening
   3. Scooped ST segments with depression in lateral leads
   4. Increased U-wave amplitude

GI

1. Often the earliest manifestation of toxicity
   1. Nausea/vomiting
   2. Abdominal pain

Neuro

1. Confusion
2. Weakness
3. Visual disturbances
   1. Yellow halos
   2. Scotomas
4. Delirium

Diagnosis

1. Must use H&P and labs in combination; no single element excludes or confirms the dx
2. Digoxin level
   1. Normal = 0.5-2 ng/mL (ideal = 0.7-1.1)
      1. May have toxicity even with "therapeutic" levels (esp w/ chronic toxicity)
   2. Measure at least 6hr after acute ingestion (if stable); immediately for chronic ingestion
      1. If measure before this may be falsely elevated due to incomplete drug distribution
3. Potassium level
   1. Acute toxicity: Degree of hyperkalemia correlates w/ degree of toxicity
   2. Chronic toxicity: K+ may be normal/low (concomitant diuretic use) or high (renal failure)

Work-Up

1. Dig level
2. Chemistry
3. Urine output
4. ECG (serial)

Treatment

1. Digoxin Immune Fab
2. Activated Charcoal
   1. Questionable efficacy
   2. Only an adjunctive tx; NOT an alternative to fab fragment therapy
   3. Consider only if present within 1 hr of ingestion
   4. 1g/kg (max 50g)

Dysrhythmias

1. Fab fragments is the agent of choice for all dysrhythmias!
2. Cardioversion should only be used as a last resort (may precipitate V-Fib)
   1. Consider lower energy settings (25-50J)
3. Bradyarrhythmias (symptomatic)
   1. Atropine 0.5mg IV
   2. Pacing
4. Ventricular dysrhythmias
   1. Phenytoin
      1. Enhances AV conduction
      2. Infuse at 25-50 mg/min to a loading dose of 10-15mg/kg
   2. Lidocaine
      1. Decreases ventricular automaticity
      2. 1-3mg/kg over several minutes; follow by 1-4mg/min

Hyperkalemia

1. Treat with Fab, not with usual meds
   1. Once Fab is given hyperkalemia will rapidly correct
2. If Fab unavailable and hyperkalemia is life-threatening then treat with:
   1. Glucose-insulin
   2. Sodium bicarb
   3. Kayexelate
   4. Dialsysis
   5. Calcium (controversial: some say dangerous, others say not)

Hypokalemia

1. Chronic intoxication
   1. Raise level to 3.5-4
2. Acute intoxication
   1. Do not treat (likely that potassium level is rapidly rising)

Hypomagnesemia

1. Treat with 1-2g over 10-20 min
   1. Monitor for resp depresion
   2. Avoid in pts with:
      1. Renal failure
      2. Bradydysrhythmias/conduction blocks

See Also

• Digoxin Immune Fab
• Toxidromes
• Digoxin

Source

• Rosen's
• Tintinalli