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  1. Pharmacology

    1. Sodium bicarbonate is a buffering agent that reacts with hydrogen ions to correct acidemia and produce alkalemia. Urinary alkalinization from renally excreted bicarbonate ions enhances the renal elimination of certain acidic drugs.

    2. It also may help prevent renal tubular damage from deposition of myoglobin in patients with rhabdomyolysis; precipitation (by enhancing solubility) of methotrexate; and dissociation of BAL-metal complex; and it may prevent contrast-induced nephropathy (by slowing free radical production). In addition, maintenance of a normal or high serum pH may prevent intracellular distribution of weak acids such as salicylate.

    3. The sodium ion load and alkalemia produced by hypertonic sodium bicarbonate reverse the sodium channel-dependent membrane-depressant ("quinidinelike") effects of several drugs (eg, tricyclic antidepressants, type Ia and type Ic antiarrhythmic agents, propranolol, propoxyphene, cocaine, diphenhydramine).

    4. Alkalinization causes an intracellular shift of potassium and is used for the acute treatment of hyperkalemia.

    5. Sodium bicarbonate given orally or by gastric lavage forms an insoluble salt with iron and theoretically may help prevent absorption of ingested iron tablets (unproven).

    6. Neutralization of acidic substances to prevent caustic injury usually is not recommended because of the potential for an exothermic reaction, generation of gas, and lack of evidence that tissue injury is minimized. Nebulized sodium bicarbonate has been used to neutralize the hydrochloric acid formed on mucosal surfaces from chlorine gas exposures (efficacy uncertain).

    7. Early animal studies and human case series of organophosphate (OP) poisonings in regions lacking sufficient access to traditional antidotes (oximes, atropine) have suggested beneficial outcomes from high-dose IV bicarbonate therapy (5 mEq/kg over 60 minutes, then 5–6 mEq/kg/d). The authors of those studies theorize that alkalinization may enhance degradation or elimination of OPs, improve tissue perfusion with volume expansion, and enhance the efficacy of 2-PAM. Systematic reviews of human trials have failed to show differences in mortality but have demonstrated a trend toward improved outcomes (lower atropine requirements and shorter length of hospital stay).

  2. Indications

    1. Severe metabolic acidosis resulting from intoxication by methanol, ethylene glycol, or salicylates or from excessive lactic acid production (eg, resulting from status epilepticus or shock, mitochondrial toxins or chemical asphyxiants, cyanide, carbon monoxide, metformin).

    2. To produce urinary alkalinization, enhance elimination of certain acidic drugs (salicylate, phenobarbital, chlorpropamide, chlorophenoxy herbicide 2,4-D [dichlorophenoxyacetic acid]). Note: Although enhanced elimination may be achieved, it is uncertain whether clinical outcomes are improved with this therapy.

    3. To prevent nephrotoxicity resulting from the renal deposition of myoglobin after severe rhabdomyolysis; the precipitation of methotrexate; dissociation of BAL-metal complex; and to prevent contrast-induced nephropathy.

    4. Also recommended for internal contamination of uranium from radiation emergencies to prevent acute tubular necrosis (see "Radiation").

    5. Cardiotoxicity with impaired ventricular depolarization (as evidenced by a prolonged QRS interval) caused by tricyclic antidepressants, type Ia or type Ic antiarrhythmics, and other membrane-depressant drugs. Note: Not effective for dysrhythmias associated with abnormal repolarization (prolonged QT interval and torsade de pointes). Wide-complex dysrhythmias associated with yew berries (Taxus spp) and bupropion intoxications may not be responsive to sodium ...

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