Adverse Effects and Monitoring of Sodium Bicarbonate Therapy

Metabolic and Electrolyte Disturbances

Hypokalemia is a major concern because alkalemia drives potassium into cells, which can prolong the QT interval and precipitate torsade de pointes, especially in poisonings with mixed sodium‑ and potassium‑channel drugs (e.g., hydroxychloroquine, flecainide). Expert recommendation to monitor and treat potassium during alkalemia therapy. 3
Hypernatremia can develop with excessive dosing; serum sodium concentrations should be kept below 150–155 mEq/L to avoid iatrogenic harm. Expert consensus recommends limiting the dose to ≤ 6 mmol/kg of hypertonic sodium bicarbonate. 3, 4
Hyperosmolality results from the high sodium load delivered with bicarbonate infusions. 1, 2

Impaired cardiac function and a decreased ventricular fibrillation threshold occur with excessive sodium bicarbonate administration. 1, 2
Impaired tissue oxygen delivery is mediated by a leftward shift of the oxygen‑hemoglobin dissociation curve after bicarbonate therapy. 1, 2

Excessive metabolic alkalosis may develop if serum pH exceeds 7.50–7.55; clinicians should avoid over‑alkalinization, particularly when bicarbonate is given until QRS duration normalizes in sodium‑channel blocker poisoning. Expert recommendation to target pH < 7.50. 3, 4

In cardiac arrest or severe shock, arterial blood‑gas analysis may not accurately reflect tissue or venous acidosis, increasing the risk of inappropriate sodium bicarbonate dosing. 1, 2

Serial electrolyte monitoring (especially potassium, sodium, and ionized calcium) is essential during therapy. 3
Frequent arterial blood‑gas and pH measurements should be performed to guide dosing and detect over‑alkalinization. 3