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Sodium bicarbonate is a systemic alkalinizing agent and antacid, used intravenously in severe metabolic acidosis, hyperkalemia with cardiotoxicity, tricyclic-antidepressant overdose with QRS widening, and (historically) cardiac arrest; orally as an antacid and urinary alkalinizer; and as the carrier base for many effervescent formulations[1]. Routine bicarbonate administration in cardiac arrest was removed from ACLS algorithms because it did not improve survival and worsened intracellular acidosis; the remaining strong indications are narrow and physiology-driven.
Sodium bicarbonate raises serum pH directly via the carbonic acid / bicarbonate buffer system; in TCA overdose its benefit is partly pH-driven (reducing the free unbound fraction) and partly sodium-driven (overcoming TCA sodium-channel blockade), which is why hypertonic 8.4% is preferred over isotonic.0 Bicarbonate is not benign: high-volume use produces hypernatremia, metabolic alkalosis, hypokalemia, and (in arrest) paradoxical intracellular acidosis[1].
