A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening

Abstract

Sodium bicarbonate is a well-known antidote for tricyclic antidepressant (TCA) poisoning. It has been used for over half a century to treat toxin-induced sodium channel blockade as evidenced by QRS widening on the electrocardiogram (ECG). The purpose of this review is to describe the literature regarding electrophysiological mechanisms and clinical use of this antidote after poisoning by tricyclic antidepressants and other agents. This article will also address the literature supporting an increased serum sodium concentration, alkalemia, or the combination of both as the responsible mechanism(s) for sodium bicarbonate's antidotal properties. While sodium bicarbonate has been used as a treatment for cardiac sodium channel blockade for multiple other agents including citalopram, cocaine, flecainide, diphenhydramine, propoxyphene, and lamotrigine, it has uncertain efficacy with bupropion, propranolol, and taxine-containing plants.

The use of intralipid emulsion therapy to treat severe cardiotoxicity secondary to lamotrigine ingestion in a dog

“…Lidocaine is a class Ia sodium channel blocker; and is the first line of treatment for VT. It has been used to treat toxicity induced by other sodium channel blockers with the hypothesis that lidocaine's fast kinetics with sodium channel binding reduce the fraction of blocked sodium channels when used with a sodium channel blocker with slower kinetics . The VT exhibited by this patient persisted in spite of an increasing dose of lidocaine, and as such, other treatments were sought.…”

“…It is possible that the increase in sodium concentration, alteration in pH, or a combination thereof reverses the sodium channel blockade. This is evidenced by experimental studies in dogs evaluating the effect of NaHCO 3 on conduction in cases of cocaine and amitryptiline toxicity, and flecainide and mexiletine‐treated purkinje fibers . Twenty percent of patients in the 2018 review of LTG overdose were given NaHCO 3 as part of their treatment, and the effect was variable.…”

Amitriptyline-induced ventricular tachycardia: a case report

“…One guideline recommends it for the treatment of AIVT [36]. The use of sodium bicarbonate in AIVT gives some benefit [33, 37–39].

It provides high sodium load for greater sodium entry into the myocardial cells in the presence of sodium channel blockade by the amitriptyline.

It alkalinizes the blood resulting in reduction of efficacy of the amitriptyline for the sodium channel leading to reduction of TCA binding to sodium channel.

Alkalization of the blood reduces the unbound amitriptyline and increases the protein binding.

…”

Bicarbonate refractory QRS prolongation and left bundle‐branch block following escitalopram and lamotrigine overdose: A case report and literature review of toxic left bundle‐branch block

“…QRS prolongation secondary to sodium channel blockade from tricyclic antidepressants and other classes of medication, which typically manifests with RBBB morphology, responds to bicarbonate therapy . We therefore suggest a left bundle‐branch blockade in overdose may have an alternative toxicological mechanism.…”

“…Possibilities include an increase in ventricular ischaemia or irritability, such as with exercise‐induced LBBB, a phenomenon which is seen in approximately 0.5% of cardiac stress tests . Another possibility could be direct cardiac gap junction inhibition, which is the proposed mechanism for QRS prolongation in bupropion toxicity, and does not appear to respond consistently to bicarbonate therapy …”