Sodium bicarbonate (antidote)

#completed #carded

Related FACEM curriculum (2022) learning objectives:

• ME 3.8.1.6(e) Principles of management of toxicological presentations including: Indications for antidotes
• ME 3.8.2.4 Identify the appropriate antidote or antivenom.

Toxicological Indications

• Cardiotoxicity due to fast sodium channel blockade:
  • Tricyclic antidepressants, bupropion, chloroquine/hydroxychloroquine, dextropropoxyphene, propranolol, Type 1a/1c antidysrhythmics (flecainide, quinidine, quinine).
• Prevention of CNS drug redistribution: Severe salicylate poisoning.
• Correction of life-threatening metabolic acidosis: Cyanide poisoning, isoniazid overdose, toxic alcohol poisoning (ethylene glycol, methanol).
• Enhanced urinary drug elimination: Salicylates, phenobarbitone.
• Increased urinary solubility: Methotrexate toxicity, drug-induced rhabdomyolysis.

Contraindications

• Acute pulmonary oedema.
• Hypokalaemia.
• Metabolic/respiratory alkalosis.
• Uncontrolled congestive cardiac failure.
• Renal failure.
• Severe hypernatraemia.

Mechanism of Action

• Bicarbonate load: Buffers hydrogen ions, raises serum pH, promotes urinary alkalinisation.
• Improved sodium channel function:
  • Elevation of serum pH (maximal benefit at pH 7.50–7.55) improves sodium channel function, mitigating drug-induced cardiotoxicity.
  • Sodium load enhances sodium channel function.
• Alteration of drug distribution: Alkalosis reduces drug ionisation, limiting CNS distribution.
• Acidosis correction: Life-threatening metabolic acidosis impairs cardiovascular function; rapid correction stabilises physiology.
• Urinary alkalinisation: Promotes ion trapping and water solubility of certain drugs (e.g., salicylates, myoglobin), enhancing elimination and preventing renal injury.

Administration

Cardiotoxicity (Fast Sodium Channel Blockade)

• Resuscitation:
  • Bolus 2 mmol/kg IV; repeat until cardiovascular stability.
  • Post-stabilisation: Monitor ABGs; maintain pH 7.50–7.55.
• Infusion:
  • 150 mmol sodium bicarbonate in 850 mL normal saline at 250 mL/hour.
  • Cease infusion when cardiovascular toxicity resolves (clinical and ECG criteria).

Prevention of CNS Salicylate Redistribution

• Maintain pH >7.4 via hyperventilation (if intubated).
• For unwell, unintubated patients: 2 mmol/kg IV bolus, followed by intubation and hyperventilation.

Urinary Alkalinisation

• Correct hypokalaemia before starting.
• Bolus 1–2 mmol/kg IV, followed by infusion (150 mmol bicarbonate in 850 mL 5% dextrose at 250 mL/hour).
• Add 20 mmol KCl if needed to maintain normokalaemia.
• Monitor bicarbonate and potassium levels every 4 hours; aim for urine pH >7.5.

Adverse Reactions

• Alkalosis (pH >7.6 impairs cardiovascular function).
• Hypernatraemia and hyperosmolarity.
• Fluid overload and pulmonary oedema.
• Hypokalaemia.
• Local tissue inflammation from extravasation.

Specific Considerations

• Pregnancy/Lactation: No restrictions.
• Paediatrics: Use same mmol/kg doses with reduced fluid volumes.

Handy Tips

• Rapid correction of acidosis is critical in tricyclic antidepressant poisoning.
• Frail elderly or cardiac patients may poorly tolerate fluid and osmotic loads.

Pitfalls

• Insufficient bicarbonate doses in severe tricyclic antidepressant toxicity.
• Failure to correct hypokalaemia in urinary alkalinisation.
• Delayed recognition/treatment of acidaemia in severe salicylate poisoning.

Controversies

• Role of urinary alkalinisation in toxic rhabdomyolysis.
• Prophylactic alkalinisation in tricyclic antidepressant poisoning.
• Hyperventilation vs sodium bicarbonate in tricyclic toxicity.
• Mechanism of urinary alkalinisation enhancing salicylate elimination.