Sodiumbicarbonate is a buffering agent that reacts with hydrogen ions tocorrect acidemia and produce alkalemia. Urinary alkalinization fromrenally excreted bicarbonate ions enhances the renal elimination ofcertain acidic drugs (eg, salicylate, chlorpropamide, chlorophenoxyherbicides, fluoride, and phenobarbital) and helps prevent renaltubular damage from deposition of myoglobin in patients withrhabdomyolysis as well as from precipitation (by enhancing solubility)of methotrexate with high-dose therapy. In addition, maintenance of anormal or high serum pH may prevent intracellular distribution ofsalicylate and formate (a toxic metabolite of methanol).

Thesodium ion load and alkalemia produced by hypertonic sodium bicarbonatereverse the sodium channel–dependent membrane-depressant(“quinidine-like”) effects of several drugs (eg, tricyclicantidepressants, type Ia and type Ic antiarrhythmic agents,propranolol, propoxyphene, cocaine, and diphenhydramine).

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

Sodiumbicarbonate given orally or by gastric lavage forms an insoluble saltwith iron and theoretically may help prevent absorption of ingestediron tablets (unproved).

E.Neutralization of acidic substances to prevent caustic injury usuallyis not recommended because of the potential for an exothermic reaction,generation of gas, and lack of evidence that tissue injury is minimized.

F.Case series of organophosphate (OP) poisonings in regions lackingsufficient access to traditional antidotes (oximes, atropine) havesuggested beneficial outcomes from high-dose IV bicarbonate therapy (5mEq/kg over 60 minutes, then 5–6 mEq/kg/day). The authors of thosestudies theorize that alkalinization may enhance degradation of OPs. Itmay also enhance the efficacy of 2-PAM (rat model).

Drug Indications ::

Indications

Severemetabolic acidosis resulting from intoxication by methanol, ethyleneglycol, or salicylates or from excessive lactic acid production (eg,resulting from status epilepticus or shock).

Toproduce urinary alkalinization, enhance elimination of certain acidicdrugs (salicylate, phenobarbital, chlorpropamide, chlorophenoxyherbicides-2,4-D), and to prevent nephrotoxicity from the renaldeposition of myoglobin after severe rhabdomyolysis or precipitation ofmethotrexate. (Although enhanced elimination may be achieved, it isuncertain if clinical outcomes are improved with this therapy.) Alsorecommended by REAC/TS for internal contamination of uranium fromradiation emergencies to prevent acute tubular necrosis (see Radiation[Ionizing]).

Cardiotoxicitywith impaired ventricular depolarization (as evidenced by a prolongedQRS interval) caused by tricyclic antidepressants, type Ia or type Icantiarrhythmics, and other membrane-depressant drugs (see Table II–7). Note: Not effective for dysrhythmias associated with abnormal repolarization (prolonged QT interval and torsade de pointes).

Drug Contra-Indications ::

III. Contraindications. The following contraindications are relative:

Significant metabolic or respiratory alkalemia or hypernatremia.

Severe pulmonary edema associated with volume overload.

Intolerance to sodium load (renal failure, CHF).

Drug Adverse Effects ::

IV. Adverse effects

Excessivealkalemia: impaired oxygen release from hemoglobin, hypocalcemictetany, and paradoxic intracellular acidosis (from elevated pCO2 concentrations) and hypokalemia.

Hypernatremia and hyperosmolality. Caution with rapid infusion of hypertonic solutions in neonates and young children.

Aggravation of CHF and pulmonary edema.

Extravasation leading to tissue inflammation and necrosis (product is hypertonic).

E. Mayexacerbate QT prolongation and associated dysrhythmias (eg, torsade depointes) as a result of electrolyte shifts (hypokalemia).

F. Use in pregnancy. FDAcategory C (indeterminate). However, this does not preclude its acute,short-term use for a seriously symptomatic patient (see Table III–1).

Drug Lab Interactions ::

Drug or laboratory interactions. Do not mix with other parenteral drugs because of the possibility of drug inactivation or precipitation.

Drug Dose Management ::

Dosage and method of administration (adults and children)

Metabolic acidemia. Give0.5–1 mEq/kg IV bolus; repeat as needed to correct serum pH to at least7.2. For salicylates, methanol, or ethylene glycol, raise the pH to atleast 7.4–7.5.

Urinary alkalinization. Give44–100 mEq in 1 L of 5% dextrose in 0.25% normal saline or 88–150 mEqin 1 L of 5% dextrose at 2–3 mL/kg/h (adults 150–200 mL/h). Check urinepH frequently and adjust flow rate to maintain urine pH level at 7–8.5.Note: Hypokalemia and fluid depletion prevent effectiveurinary alkalinization; add 20–40 mEq of potassium to each liter unlessrenal failure is present. Prevent excessive systemic alkalemia (keepblood pH < 7.55) and hypernatremia. Monitor urine pH and serumelectrolytes hourly.

Cardiotoxic (“membrane-stabilizing”) drug intoxication. Give1–2 mEq/kg IV bolus over 1–2 minutes; repeat as needed to improvecardiotoxic manifestations (eg, prolonged QRS interval, wide-complextachycardia, hypotension) and maintain serum pH at 7.45–7.55. There isno evidence that constant infusions are as effective as boluses givenas needed.

Drug Chemical Formulations ::

Formulations

Severalproducts are available, ranging from 4.2% (0.5 mEq/mL preferred forneonates and young children) to 7.5% (0.89 mEq/mL) to 8.4% (1 mEq/mL)in volumes of 10–500 mL. The most commonly used formulation availablein most emergency “crash carts” is 8.4% (“hypertonic”) sodiumbicarbonate, 1 mEq/mL, in 50-mL ampules or prefilled syringes.

The suggested minimum stocking level to treat a 70-kg adult for the first 24 hours is 10 ampules or syringes (approximately 500 mEq).

Disclaimer ::

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