Sodium Bicarbonate

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. 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.

Antacid, Electrolyte replacement

Sodium bicarbonate

Neut, many generic; OTC oral: Alka-Seltzer (with aspirin/citric acid), baking soda

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Summary

Classes

Antacid, Electrolyte replacement

Common uses

Severe metabolic acidosis▲0▼, Hyperkalemia with ECG changes▲0▼, Tricyclic-antidepressant overdose with QRS widening▲0▼, Urinary alkalinization (salicylate or methotrexate toxicity, uric-acid stones)▲0▼, Symptomatic antacid (oral)▲0▼

Pharmacy

Starting dose

IV: 1 mEq/kg bolus in arrest indication, then titrated to ABG and clinical status; PO: 325-2000 mg up to QID as antacid

Preparations

4.2%, 7.5%, 8.4% IV (1 mEq/mL at 8.4%); 325, 650 mg oral tablets; bulk powder

US FDA Max

No fixed maximum; titrated to pH and bicarbonate level; chronic high oral doses cause metabolic alkalosis and volume overload

Pharmacology

Routes

IV, oral

Onset

Immediate (IV); within minutes (oral antacid)

Duration

IV: hours, dependent on ongoing acid load; oral antacid: ~30 minutes

Half-life

Not applicable (electrolyte and buffer)

Bioavailability

100% (IV); rapidly neutralized by gastric acid (oral)

Pregnancy

Routine antacid and acidosis correction acceptable

Legal status

Rx-only for IV formulations; OTC for oral

Purported mechanism

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.