ECG

Sodium channel blockade is a potentially life-threatening effect of poisoning. Drugs with potential to cause sodium channel blockade in overdose include:

Tricyclic antidepressants (TCAs) are the most frequently encountered and best studied sodium channel blocking drugs. Good evidence exists for their treatment with serum alkalinisation. Many other drugs can also cause sodium channel blockade; the role of alkalinisation in these exposures is less clear.

Sodium channel blockade results in the typical ECG features of QRS prolongation > 120ms and a dominant terminal R wave in aVR (R’-wave in aVR >3mm or R:S ratio > 0.7).

All patients with evidence of sodium channel blockade on their ECG should remain on cardiac monitoring until the ECG changes have resolved and it is at least 6 hours following an ingestion of an immediate release preparation or 12 hours following an ingestion of a slow-release preparation.

Sodium bicarbonate provides both sodium loading and serum alkalinisation (which reduces the proportion of drug able to interact with the sodium channel). Evidence for the use of sodium bicarbonate for the treatment of cardiotoxicity is largely based on experience with tricyclic antidepressant (TCA) overdoses.

Treat TCA overdose with cardiotoxicity with sodium bicarbonate 1-2 mmol/kg q5min aiming for a pH of 7.50-7.55. Intubation is required to maintain the pH through hyperventilation aiming for a pCO2 of 30-35mmHg.

The role of bicarbonate therapy for sodium channel blockade with non-TCA agents is unclear. A trial of sodium bicarbonate can be given, but if there is no significant response by 3 mmol/kg, it should not be continued.

Excessive use of bicarbonate is harmful and can result in life-threatening hypokalaemia, hypernatraemia, and alkalaemia.

Bruccoleri RE, Burns MM. A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening. J Med Toxicol. 2016 Mar;12(1):121-9. doi: 10.1007/s13181-015-0483-y. PMID: 26159649; PMCID: PMC4781799.