Sodium Bicarbonate (sodium bicarbonate)

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Last reviewed · Source: First Databank (FDB) drug data

Overview

Sodium bicarbonate is an alkalinizing agent.

Sodium bicarbonate is a systemic alkalizer and electrolyte replenisher. IV administration of sodium bicarbonate elevates plasma bicarbonate concentrations, buffers excess hydrogen ions, increases systemic pH, and reverses the clinical manifestations of acidosis.

In aqueous solution, sodium bicarbonate dissociates into sodium (Na+) and bicarbonate (HCO3-) ions. Sodium, the predominant extracellular cation, plays a critical role in the management of fluid and electrolyte disturbances. Bicarbonate is an endogenous constituent of body fluids, with normal plasma concentrations ranging from 24-31 mEq/L.

Plasma concentrations are maintained by renal mechanisms, through urinary acidification in states of deficit or urinary alkalinization in states of excess.

Sodium bicarbonate solution has an approximate pH of 8.0 (7.0-8.5). Sodium bicarbonate solutions contain equal amounts (mEq/mL) each of sodium and bicarbonate ions. The 8.4, 7.5, and 4.2% concentration solutions contain 1 mEq/mL, 0.892 mEq/mL, and 0.5 mEq/mL, respectively, of each ion.

These solutions are very hyperosmolar-- 2000 mOsm/L for the 8.4% concentration and 1786 mOsm/L for the 7.5% concentration.

The bicarbonate anion is considered chemically labile, as it may combine with hydrogen ions to form carbonic acid (H2CO3), which subsequently converts to its volatile form, carbon dioxide (CO2), which is excreted by the lungs. Under physiologic conditions, the extracellular fluid maintains a 1:20 ratio of carbonic acid to bicarbonate. In adults with normal renal function, virtually all bicarbonate filtered at the glomerulus is reabsorbed, with urinary excretion typically accounting for <1%.

Oral administration of sodium bicarbonate leads to systemic absorption of excess bicarbonate, which induces metabolic alkalosis and promotes urinary alkalinization. IV administration achieves complete bioavailability. The onset of action after an IV push is rapid, with a mean onset of 8-10 minutes.

Sodium bicarbonate is extensively distributed within the extracellular fluid compartment. The elimination half-life of sodium bicarbonate is unknown.

Sodium bicarbonate is used parenterally as an alkalinizing agent in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest, and severe primary lactic acidosis. Sodium bicarbonate is also used parenterally for the treatment of certain drug intoxications, including barbiturates, salicylate or methyl alcohol poisoning, and in the treatment of hemolytic reactions requiring alkalinization of the urine to diminish the nephrotoxic effects of blood pigments. In addition, sodium bicarbonate is used parenterally in the treatment of severe diarrhea accompanied by substantial GI bicarbonate loss.

Generic name: sodium bicarbonate

Reference product & biosimilars

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Indications

The following indications are listed for Sodium Bicarbonate:

  • Metabolic Acidosis
  • Salicylate Intoxication
  • Severe Diarrhea
  • Toxic Phenobarbital Serum Level
  • Tricyclic Antidepressant Overdose
  • Urine Alkalinization

Also known as: Alkalinize The Urine, Aspirin Overdose, Overdose Of Phenobarbital, Phenobarbital Intoxication, Profuse Diarrhea, Salicylate Overdose, Secretory Diarrhea, Toxic Phenobarbital Concentration, Tricyclic Antidepressant Drug Intoxication, Tricyclic Antidepressant Drug Overdose.

Dosing

Sodium bicarbonate 42 mg is equal to 0.5 mEq each of sodium (Na+) and bicarbonate (HCO3-). Sodium bicarbonate 75 mg is equal to 0.892 mEq each of Na+ and HCO3-. Sodium bicarbonate 84 mg is equal to 1 mEq each of Na+ and HCO3-.

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

Generally, 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. Due to this delay, reaching a total CO2 content of approximately 20 mEq/liter by the end of the first day of treatment is typically linked to a normal blood pH. Further correction of the acidosis to fully normal levels usually happens if the kidney function is normal and if and when the underlying cause of the acidosis can be controlled. If total CO2 levels are normalized or brought above normal within the first day, this may likely result in an excessively high (alkaline) blood pH, which can lead to undesired side effects.

In cases of metabolic acidosis associated with shock, monitor therapy by assessing blood gases, plasma osmolarity, arterial blood lactate, hemodynamic status, and cardiac rhythm. Bicarbonate therapy should always be administered gradually and in stages since the degree of response from a specific dose is not precisely predictable.

Drug interactions

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Contraindications

*Patients with excessive chloride loss from vomiting or continuous GI suctioning.

*Patients at risk of developing diuretic-induced hypochloremic alkalosis.

Adverse reactions

Adverse effects from IV sodium bicarbonate treatment include manifestations of metabolic alkalosis (muscular twitching, irritability, and tetany); hypernatremia; and chemical cellulitis with tissue necrosis, ulceration or sloughing at the site of infiltration from extravasation.

Precautions

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ICD codes

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Formulary status

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Last reviewed · Source: First Databank (FDB) drug data