Bicarbonate Therapy for Arrhythmias
Bicarbonate is specifically indicated for ventricular arrhythmias caused by tricyclic antidepressant (TCA) overdose and other sodium channel blocker toxicity, particularly when QRS prolongation exceeds 120 milliseconds. 1, 2
Primary Indication: Sodium Channel Blocker-Induced Arrhythmias
Bicarbonate works by reversing cardiac conduction delays and ventricular arrhythmias caused by sodium channel blockade, not by correcting acidosis per se. The mechanism involves increasing extracellular sodium concentration and raising serum pH, which enhances sodium channel availability and reverses the cardiotoxic effects. 1, 3
Tricyclic Antidepressant Toxicity
- Administer 1-2 mEq/kg IV bolus of hypertonic sodium bicarbonate (8.4% solution) for life-threatening cardiotoxicity with QRS widening >120 ms 2, 4
- Target arterial pH of 7.45-7.55, which is deliberately alkalemic 2
- Follow with continuous infusion of 150 mEq/L solution at 1-3 mL/kg/hour to maintain alkalosis 2
- Bicarbonate is effective even in the presence of pre-existing alkalosis, as demonstrated in case reports where ventricular tachycardia responded immediately to bicarbonate despite alkalemia 3
Other Sodium Channel Blockers
- Give 50-150 mEq bolus using hypertonic solution (1000 mEq/L), titrated to resolution of QRS prolongation and hypotension 2
- Continue infusion to maintain pH ≥7.30 until QRS duration normalizes 2
- This includes cocaine-induced ventricular arrhythmias, where 1-2 mEq/kg sodium bicarbonate is recommended 2
Secondary Indication: Hyperkalemia-Associated Arrhythmias
Bicarbonate serves as a temporizing measure for life-threatening arrhythmias caused by severe hyperkalemia by shifting potassium intracellularly. 1, 2
- Administer 50-100 mEq (50-100 mL of 8.4% solution) IV over 5-10 minutes 2
- Combine with glucose/insulin for synergistic effect 2
- This buys time while definitive therapies (dialysis, calcium, insulin/glucose) are initiated 2
Arrhythmias Where Bicarbonate is NOT Indicated
Ventricular Fibrillation/Cardiac Arrest
Routine bicarbonate administration during cardiac arrest is NOT recommended and may be harmful. 1
- Multiple studies show no improvement in ROSC, hospital admission, or survival to discharge with routine bicarbonate use in VF arrest 1
- Bicarbonate may compromise coronary perfusion pressure by reducing systemic vascular resistance 1
- Consider bicarbonate only after first epinephrine dose fails AND in specific circumstances: documented severe acidosis (pH <7.1), hyperkalemia, or TCA/sodium channel blocker overdose 1, 2
Torsades de Pointes
Magnesium sulfate 1-2 g IV, NOT bicarbonate, is the treatment for torsades de pointes. 1
- Temporary pacing or isoproterenol are alternatives if magnesium fails 1
- Potassium repletion to 4.5-5 mEq/L is essential 1
Critical Monitoring During Bicarbonate Therapy for Arrhythmias
- Monitor serum sodium every 2-4 hours, avoiding levels >150-155 mEq/L 2
- Monitor arterial pH every 2-4 hours, avoiding pH >7.50-7.55 (except in TCA toxicity where target is 7.45-7.55) 2
- Monitor serum potassium closely, as bicarbonate causes intracellular shift and can precipitate severe hypokalemia 2
- Monitor QRS duration continuously in sodium channel blocker toxicity, stopping bicarbonate when QRS normalizes 2
Common Pitfalls to Avoid
- Never mix bicarbonate with calcium-containing solutions or vasoactive amines (causes precipitation/inactivation) 1, 2
- Flush IV line with normal saline before and after bicarbonate administration 2
- Do not withhold bicarbonate in TCA toxicity due to concerns about alkalosis—deliberate alkalemia is therapeutic 3
- Ensure adequate ventilation before giving bicarbonate, as it produces CO2 that must be eliminated to prevent paradoxical intracellular acidosis 1, 2