Hyperosmolar sodium bicarbonate solutions are widely used in clinical toxicology both as an antidote to drugs that impair fast sodium channel function and as an alkalinising agent to manipulate drug distribution and excretion (salicylate and phenobarbitone). It is also used in profound metabolic acidosis with cyanide, isoniazid and toxic alcohol toxicity. Finally, it can also increase the urinary solubility of methotrexate toxicity and drug-induced rhabdomyolysis
Cardiotoxicity secondary to TCA poisoning:
- Sodium bicarbonate is a wonderful antidote for classic TCA overdoses but too much can be fatal and not all sodium channel blocking drugs respond the same.
- Bear in mind the 3 end goals of sodium loading and perform 30-minute repeat arterial blood gases to ensure you are not over target:
- Narrowing the QRS to normal for the patient or less than 140ms (toxicologists have varied opinions but between 120-140ms is safer than too much sodium bicarbonate). Normalisation in large overdose may not occur until 24-48 hours later.
- Maximum Sodium of 155 mmol/L
- pH aim of 7.5 to 7.55
- EXCESS Sodium Bicarbonate can kill. You risk severe alkalaemia, hypernatraemia and hypokalemia. Don’t go over a maximum of 6mmol/kg or raise pH >7.5-7.55 without discussion with a clinical toxicologist.
- If repeated doses are required it is easier and safer to intubate and hyperventilate to maintain a pH >7.5 – 7.55 than repeated boluses of sodium bicarbonate or an infusion (debatable efficacy).
- See our TCA post for other drug choices if sodium bicarbonate is not working but at this point, you should be talking to a clinical toxicologist. Remember, “everything is poison, it just depends on the dose” (Paracelsus – paraphrased). Sodium bicarbonate is no exception.
Cardiotoxicity secondary to a non-TCA poisoning (e.g. lamotrigine, flecanide and propranolol):
- Give 1 mmol/Kg or 100 mmol bolus every 3-5 minutes PRN to a maximum total of 3 mmol/kg and gently hyperventilate (aim for pCO2 35-45) until a normal pH target range of 7.35 – 7.45 is reached on ABG.
- The QRS interval often remains unchanged.
- If hypotension persists, add inotropic or vasopressor therapy guided by bedside echo.
Prevention of redistribution of salicylate to CNS:
- The pH must be maintained above 7.4 at all times. If the patient is critically ill with a severe metabolic acidosis they are usually intubated and the pH is maintained via hyperventilation. If they are not….
- Give sodium bicarbonate 2 mmol/kg IV bolus.
- Intubate, hyperventilate and recheck the VBG/ABG.
- Serum alkalinisation is maintained until definitive care with haemodialysis is achieved.
- Correct hypokalaemia.
- Give 1-2 mmol/kg sodium bicarbonate IV bolus.
- Commence an infusion of 150 mmol sodium bicarbonate in 850 ml of 5% dextrose at 250 ml/hour.
- 20 mol of KCl may be added to maintain normokalaemia.
- Aim for a urinary pH > 7.5.
- Monitor serum bicarbonate and potassium every 4 hours.
- Bradberry SM, Thanacoody HK, Watt BE et al. Management of the cardiovascular complications of tricyclic antidepressant poisoning: role of sodium bicarbonate. Toxicological Reviews 2005; 24(3):195-204.
- Isoardi KZ and Chiew AL. Too much of a good thing: Bicarbonate toxicity following treatment of sodium channel blocker overdose. Emergency Medicine Australia. 2022 Apr 26. doi: 10.1111/1742-6723.13995.
- Proudfoot AT, Krenzelok EP, Brent J et al. Does urine alkalinization increase salicylate elimination? If so, why? Toxicological Reviews 2003; 22(3):129-136.
Dr Neil Long BMBS FACEM FRCEM FRCPC. Emergency Physician at Kelowna hospital, British Columbia. Loves the misery of alpine climbing and working in austere environments (namely tertiary trauma centres). Supporter of FOAMed, lifelong education and trying to find that elusive peak performance.