Brand names: Baking Soda, Neut, Soda Mint
Drug class: Alkalinizing Agents

Medically reviewed by Drugs.com on Apr 10, 2024. Written by ASHP.

Introduction

Alkalinizing agent.^{100 a}

Uses for Sodium Bicarbonate

Acidosis

Treatment of metabolic acidosis associated with many conditions including severe renal disease (e.g., renal tubular acidosis), uncontrolled diabetes (ketoacidosis), extracorporeal circulation of the blood, cardiac arrest, circulatory insufficiency caused by shock or severe dehydration, ureterosigmoidostomy, lactic acidosis, alcoholic ketoacidosis, use of carbonic anhydrase inhibitors, and ammonium chloride administration.^a

Generally considered the alkalinizing agent of choice for oral or parenteral therapy.^a

Diabetic Ketoacidosis

Specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis not established.^a Administration is generally reserved for the treatment of severe acidosis (e.g., arterial pH less than 7–7.15 or serum bicarbonate concentration of 8 mEq/L or less) because of the potential risks of sodium bicarbonate therapy in the treatment of this disorder.^b

Advanced Cardiovascular Life Support

ACLS guidelines state that IV sodium bicarbonate is not recommended for routine use during cardiac arrest; limited data to support such use and potentially associated with detrimental effects.^{400 401} However, may be useful in some resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage).⁴⁰¹

Alkalinization of Urine

Treatment of hemolytic reactions requiring alkalinization of the urine to diminish the nephrotoxic effects of blood pigments; also to increase urinary pH in order to increase the solubility of certain weak acids (e.g., cystine, sulfonamides, uric acid).^a

Sodium Bicarbonate Dosage and Administration

General

• Dosage is determined by severity of the acidosis, appropriate laboratory determinations, and the patient’s age, weight, and clinical condition.^a Frequent laboratory determinations and clinical evaluation of the patient are essential during therapy, especially during prolonged therapy, to monitor changes in fluid and electrolyte and acid-base balance.^a

• Full correction of bicarbonate deficit should not be attempted during the first 24 hours of sodium bicarbonate therapy, since this may result in precipitation of metabolic alkalosis because of delayed physiologic compensatory mechanisms.^a

• Fluid and electrolyte balance of the patient must be carefully monitored during therapy with the drug because of the sodium content of sodium bicarbonate.^a

Administration

Administer orally, by direct IV injection or infusion.^a

May be administered by intraosseous (IO) injection^{† [off-label]} in the setting of pediatric advanced life support (PALS).⁴⁰³

Also has been administered by sub-Q injection if diluted to isotonicity (1.5% sodium bicarbonate solution); avoid extravasation of hypertonic sodium bicarbonate injections.^a

Oral Administration

Administered orally in the treatment of mild to moderately severe acidosis, in conditions (e.g., chronic renal failure) requiring prolonged therapy with an alkalinizing agent, and in conditions in which IV administration of the drug is not necessary (e.g., alkalinization of the urine).

IV Administration

For solution and drug compatibility information, see Compatibility under Stability.

Rate of Administration

Neonates and children <2 years of age: Administer hypertonic sodium bicarbonate injections by slow IV infusion of a 4.2% solution (up to 8 mEq/kg daily).^a

Dosage

Each 84 mg or 1 g of sodium bicarbonate contains 1 or about 12 mEq, respectively, each of sodium and bicarbonate ions.^a

Pediatric Patients

Metabolic Acidosis

IV

Older children: 2–5 mEq/kg as an infusion over 4–8 hours in less urgent forms of metabolic acidosis.^a Subsequent doses should be determined by the response of the patient and appropriate laboratory determinations.^a

Plan sodium bicarbonate therapy in a stepwise manner, since the degree of response following a given dose is not always predictable.^a Reduce dose and frequency of administration after severe symptoms have improved.^a

Pediatric Resuscitation

IV/IO

Infants and children: Some experts recommend 1 mEq/kg administered slowly.⁴⁰³

Ventricular arrhythmias associated with cocaine toxicity: Some experts recommended 1–2 mEq/kg.^{402 403}

Alkalinization of Urine

Oral

1–10 mEq (84–840 mg) per kg daily, adjusted according to response.^a

Adults

Metabolic Acidosis

IV

Initially, administer no more than 33–50% of the calculated bicarbonate requirements when initial, rapid administration of the drug is considered necessary.^a Consult specialized references on fluid and electrolyte and acid-base balance for specific recommendations.^a

2–5 mEq/kg dose as an infusion over 4–8 hours in less urgent forms of metabolic acidosis.^a Subsequent doses should be determined by the response of the patient and appropriate laboratory determinations.^a Therapy should be planned in a stepwise manner, since the degree of response following a given dose is not always predictable.^a Generally, the dose and frequency of administration should be reduced after severe symptoms have improved.^a

Diabetic Ketoacidosis

IV

Partially correct acidosis, generally to an arterial pH of about 7.2, in order to avoid rebound alkalosis.^a

ACLS

IV

If used in certain resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage), usual initial dose is 1 mEq/kg.⁴⁰¹ Whenever possible, dosage should be guided by bicarbonate concentration or by calculated base deficit obtained from blood gas analysis or laboratory measurement.⁴⁰¹ Complete correction of the base deficit not recommended to minimize risk of alkalosis.⁴⁰¹

For management of cardiac arrest due to hyperkalemia, 50 mEq has been administered IV over 5 minutes as adjunctive therapy to other standard ACLS measures.¹⁹⁶

Acidosis Associated with Chronic Renal Failure

Oral

Initially, 20–36 mEq daily, given in divided doses when plasma bicarbonate concentration is less than 15 mEq/L.^a Titrate dosage to provide a plasma bicarbonate concentration of about 18–20 mEq/L.^a To relieve symptoms and prevent or stabilize renal failure and osteomalacia in patients with renal tubular acidosis, higher dosages of sodium bicarbonate are necessary.^a

Distal (type 1) renal tubular acidosis: Initially, 0.5–2 mEq/kg daily, given in 4 or 5 divided doses.^a Titrate dosage until hypercalciuria and acidosis are controlled, and according to the response and tolerance of the patient.^a Alternatively, 48–72 mEq (about 4–6 g) daily.^a

Proximal (type 2) renal tubular acidosis: 4–10 mEq/kg daily, given in divided doses.^a

Alkalinization of Urine

Oral

Initially, 48 mEq (4 g), followed by 12–24 mEq (1–2 g) every 4 hours.^a Dosages of 30–48 mEq (2.5–4 g) every 4 hours, up to 192 mEq (16 g) daily, may be required in some patients.^a Titrate dosage to maintain the desired urinary pH.^a

Cautions for Sodium Bicarbonate

Contraindications

• Metabolic or respiratory alkalosis.^a

• Hypocalcemia in which alkalosis may induce tetany.^a

• Excessive chloride loss from vomiting or continuous GI suctioning.^a

• Risk of developing diuretic-induced hypochloremic alkalosis.^a

• Oral administration as an antidote in the treatment of acute ingestion of strong mineral acids, since formation of carbon dioxide gas during neutralization may cause gastric distention and possible rupture.^a

Warnings/Precautions

Warnings

CHF

Use with extreme caution in patients with CHF.^a

Fluid and/or Solute Overload

Possible fluid and/or solute overload following IV administration resulting in dilution of serum electrolytes, overhydration, congestive conditions, or pulmonary edema.^a Risk of dilutional conditions is inversely proportional to the electrolyte concentration administered.^a Risk of solute overload and resultant congestive conditions with peripheral and/or pulmonary edema is directly proportional to the electrolyte concentration administered.^a

Major Toxicities

Electrolyte Disturbances

Potassium depletion may predispose to metabolic alkalosis and coexistent hypocalcemia may result in tetany and carpopedal spasm as the plasma pH increases.^a Correct electrolyte disturbances prior to or concomitantly with administration of sodium bicarbonate therapy to minimize the risks of preexisting hypokalemia and/or hypocalcemia.^a

General Precautions

Dosing Considerations

Generally, the goal of alkalinizing therapy is to correct the acid-base disturbance while avoiding overdosage and resultant metabolic alkalosis.^a Frequent laboratory determinations and clinical evaluation of the patient are essential to monitor changes in fluid and electrolyte and acid-base balance.^a

Extravasation

Chemical cellulitis with inadvertent extravasation of hypertonic solutions, subsequently resulting in tissue necrosis, ulceration, and/or sloughing at the site of injection.^a Treat extravasation by elevating the affected area, applying warm compresses to the site, and locally injecting lidocaine or hyaluronidase.^a

Specific Populations

Pregnancy

Category C.^b

Pediatric Use

Neonates and children < 2 years of age: Rapid injection (10 mL/minute) of hypertonic sodium bicarbonate solutions may produce hypernatremia, decreased CSF pressure, and possible intracranial hemorrhage.^a

Renal Impairment

Use with extreme caution in patients with renal insufficiency, especially those with severe insufficiency such as oliguria or anuria.^a

When given in large doses or to patients with renal insufficiency, may cause metabolic alkalosis.^{100 401} Metabolic alkalosis may be accompanied by hyperirritability or tetany.^a

Common Adverse Effects

Gastric distention and flatulence with oral administration.^a

Drug Interactions

Specific Drugs

Stability

Storage

Oral

Tablets

Tight containers at 15–30°C.^a

Parenteral

Injection

15–30°C.^a Avoid freezing and extreme heat.^b

Compatibility

Parenteral

Solution CompatibilityHID

Drug Compatibility

Actions

• Dissociates to provide bicarbonate ion; bicarbonate is the conjugate base component of the principal extracellular buffer in the body, the bicarbonate:carbonic acid buffer.^a Changes in the concentration of either component of the buffer can cause a decrease or increase in pH.^a

• Administration of sodium bicarbonate, by decreasing pH, can cause a redistribution of potassium ions into cells in patients with acidosis.^a

• Provides bicarbonate, which is readily excreted in urine; administration of the drug will increase urinary pH in patients with normal renal function.^a Alkalinizing the urine can increase the solubility of certain weak acids (e.g., cystine, uric acid) and can increase the ionization and urinary excretion of lipid-soluble organic acids (e.g., phenobarbital, salicylates) that are reabsorbed in the kidney via diffusion of the un-ionized species.^a

• Potent antacid action; each gram of sodium bicarbonate has an in vitro neutralizing capacity of about 12 mEq of acid.^a

Advice to Patients

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs as well as any concomitant illnesses.^b

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.^b

• Importance of informing patients of other important precautionary information. (See Cautions.)^b

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.

Preparations

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