AHFS Class:

• Alkalinizing Agents 40:08

Generic Name(s):

• Sodium Bicarbonate

Sodium bicarbonate is an alkalinizing agent.100

Overview

Sodium bicarbonate is used as an alkalinizing agent in the treatment of metabolic acidosis. Sodium bicarbonate also is used to increase urinary pH in order to increase the solubility of certain weak acids (e.g., cystine, sulfonamides, uric acid) or in the treatment of hemolytic reactions requiring alkalinization of the urine to diminish the nephrotoxic effects of blood pigments. In addition, the drug is used in the treatment of severe diarrhea accompanied by substantial GI bicarbonate loss.100

Acidosis

Sodium bicarbonate is used in the 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,100 circulatory insufficiency caused by shock or severe dehydration, ureterosigmoidostomy, lactic acidosis, alcoholic ketoacidosis, use of carbonic anhydrase inhibitors, and ammonium chloride administration. In metabolic acidosis, the principal disturbance is a loss of proton acceptors (e.g., loss of bicarbonate during severe diarrhea) or accumulation of an acid load (e.g., ketoacidosis, lactic acidosis, renal tubular acidosis).

Mild acidosis may have minimal clinical importance and require no corrective therapy; physiologic compensatory mechanisms may be adequate to correct the disorder. When the underlying cause can be treated effectively in more severe acidosis, there is often no need to specifically treat the acid-base disorder. Generally, administration of sodium bicarbonate is not necessary unless the acidosis is severe (e.g., arterial pH less than 7.1-7.2 or plasma bicarbonate concentration of 8 mEq/L or less) or the underlying cause of the acidosis cannot be determined and/or corrected.

When specific alkalinizing therapy is necessary, complete correction of the acidosis with an alkalinizing agent is usually not necessary, and may be hazardous, since metabolic alkalosis can be precipitated. Generally, the goal of alkalinizing therapy is to correct the acid-base disturbance toward normal and allow physiologic compensatory mechanisms to complete the correction, if possible. Sodium bicarbonate is generally considered the alkalinizing agent of choice for oral or parenteral therapy. When sodium bicarbonate is used in the treatment of metabolic acidosis, the acid-base status of the patient must be monitored frequently and dosage modified according to response; the bicarbonate deficit can only be estimated, and no more than 50% of the calculated deficit should be replaced initially in patients whose compensatory mechanisms are expected to contribute to correction of the acidosis.

Diabetic Ketoacidosis

The specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established. Because correction of the underlying metabolic disorder generally results in correction of acid-base abnormalities and because of the potential risks of sodium bicarbonate therapy in the treatment of this disorder, administration of sodium bicarbonate 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). Rapid correction of acidosis with sodium bicarbonate in patients with diabetic ketoacidosis may cause hypokalemia, paradoxical acidosis in CSF since carbon dioxide diffuses more rapidly into CSF than does bicarbonate, and lactic acidosis since increased pH increases hemoglobin-oxygen affinity which, when combined with erythrocyte 2,3-diphosphoglycerate (2,3-DPG) deficiency in these patients, results in peripheral tissue hypoxia. However, the benefits and risks of sodium bicarbonate therapy in ketoacidosis have not been fully determined, and additional controlled studies of the safety and efficacy of the drug are necessary. Generally, when sodium bicarbonate is used in the treatment of diabetic ketoacidosis, the acidosis should only be partially corrected (e.g., to an arterial pH of about 7.2) to avoid rebound metabolic alkalosis as ketones are metabolized.

Advanced Cardiovascular Life Support

The American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care state that IV sodium bicarbonate is not recommended for routine use during cardiac arrest.400,401 There are only limited data that support therapy with buffers during cardiac arrest, and routine administration of sodium bicarbonate has not been reported to improve outcomes of resuscitation.401 There is no evidence indicating that sodium bicarbonate improves the likelihood of defibrillation or survival rates in animals with ventricular fibrillation and cardiac arrest.401 In addition, the drug potentially may have detrimental effects (e.g., compromised coronary perfusion pressure [CPP] caused by reduction of systemic vascular resistance; paradoxical intracellular acidosis caused by production of carbon dioxide that freely diffuses into myocardial and cerebral cells and may depress function, especially in ischemic myocardium; shift in the oxyhemoglobin saturation curve, inhibiting release of oxygen; induction of hyperosmolarity and hypernatremia; adverse effects secondary to extracellular alkalosis; exacerbation of central venous acidosis; inactivation of concomitantly administered catecholamines).401

Restoration of oxygen content with appropriate ventilation with oxygen, support of some tissue perfusion and cardiac output with good chest compressions, then rapid return of spontaneous circulation (ROSC), are the mainstays of restoring acid-base balance during cardiac arrest.401 By ensuring adequate alveolar ventilation, a major component of depressed pH (respiratory acidosis) during cardiac arrest generally can be managed without sodium bicarbonate. Sodium bicarbonate may be useful in some resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage).401 In addition, some experts state that sodium bicarbonate may be considered in the treatment of ventricular arrhythmias associated with cocaine toxicity in addition to standard treatments.402,403

It must be kept in mind that administration of sodium bicarbonate is followed by release of carbon dioxide, which requires adequate alveolar ventilation to assure continued excretion of this source of potential acid. Thus, the importance of adequate alveolar ventilation in the control of pH must be emphasized, as well as the need for repeated arterial determination of blood pH and Pa_co2, if possible. Whenever possible, sodium bicarbonate therapy should be guided by the bicarbonate concentration or calculated base deficit obtained from blood gas analysis or laboratory measurement.401 To minimize the risk of iatrogenically induced alkalosis, complete correction of the base deficit should not be attempted.401 Some experts state that other non-carbon dioxide generating buffers (e.g., tromethamine) have shown a potential to minimize some adverse effects of sodium bicarbonate (e.g., carbon dioxide generation, hyperosmolarity, hypernatremia, hypoglycemia, intracellular acidosis, myocardial acidosis, overshoot alkalosis) when used in certain resuscitation situations; however, clinical experience is limited and outcome studies are lacking.401

Antacid Therapy

For the use of sodium bicarbonate as an antacid, see Antacids 56:04.

Administration

Sodium bicarbonate is administered by IV infusion.100 Sodium bicarbonate may be administered by rapid IV injection when initial immediate administration of the drug is considered necessary (e.g., during cardiac arrest).100 The drug also may be 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). The drug has also been administered by subcutaneous injection if diluted to isotonicity (1.5% sodium bicarbonate solution). Extravasation of hypertonic sodium bicarbonate injections must be avoided. (See Cautions: Adverse Effects.) Sodium bicarbonate also has been administered by intraosseous (IO) injection† in the setting of pediatric advanced life support (PALS);403 onset of action and systemic concentrations are comparable to those achieved with venous administration.403 However, acid-base balance analysis may be inaccurate after administration of sodium bicarbonate via the IO cannula.403

In neonates and children younger than 2 years of age, hypertonic sodium bicarbonate injections generally should be administered by slow IV infusion of a 4.2% solution up to 8 mEq/kg daily. (See Cautions: Pediatric Precautions.)

IV Administration

Standardize 4 Safety

Standardized concentrations for sodium bicarbonate have been established through Standardize 4 Safety (S4S), a national patient safety initiative to reduce medication errors, especially during transitions of care.249 Multidisciplinary expert panels were convened to determine recommended standard concentrations.249 Because recommendations from the S4S panels may differ from the manufacturer's prescribing information, caution is advised when using concentrations that differ from labeling, particularly when using rate information from the label.249 For additional information on S4S (including updates that may be available), see [Web].249

Dosage

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. When total carbon dioxide content is returned to normal or beyond within the first day of therapy, substantially alkaline values for blood pH and subsequent adverse effects are likely to occur. When initial, rapid administration of the drug is considered necessary, it is generally recommended that no more than 33-50% of the calculated bicarbonate requirements be administered initially. Several methods for estimating bicarbonate requirements in patients with metabolic acidosis have been suggested; specialized references on fluid and electrolyte and acid-base balance should be consulted for specific recommendations.

Sodium bicarbonate is not recommended for routine use in advanced cardiovascular life support (ACLS) during cardiac arrest (see Uses: Advanced Cardiovascular Life Support); however, if the drug is used in certain resuscitation situations (e.g., preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdosage), an IV dose of 1 mEq/kg is usually given initially in adults.401 Whenever possible, dosage of sodium bicarbonate should be guided by the bicarbonate concentration or by the calculated base deficit obtained from blood gas analysis or laboratory measurement.401 Complete correction of the base deficit is not recommended to minimize the risk of alkalosis.401 For the management of cardiac arrest due to hyperkalemia in adults, 50 mEq of sodium bicarbonate has been administered IV over 5 minutes as adjunctive therapy to other standard ACLS measures.196

If sodium bicarbonate is used for pediatric resuscitation, the guidelines for pediatric advanced life support (PALS) recommend a pediatric dose of 1 mEq/kg, administered slowly by IV or IO† injection.403 If blood gas tensions and pH measurements are available, subsequent doses should be determined by the following equation:

mEq NaHCO₃ = 0.3 × bodyweight (in kg) × base deficit (in mEq/L)

In less urgent forms of metabolic acidosis, a 2-5 mEq/kg dose of sodium bicarbonate may be administered to older children or adults as a 4- to 8-hour IV infusion. Subsequent doses should be determined by the response of the patient and appropriate laboratory determinations. Sodium bicarbonate therapy should be planned in a stepwise manner, since the degree of response following a given dose is not always predictable. Generally, the dose and frequency of administration should be reduced after severe symptoms have improved.

For the treatment of ventricular arrhythmias associated with cocaine toxicity in pediatric patients, 1-2 mEq/kg of IV sodium bicarbonate has been administered.402,403

Although the specific role of sodium bicarbonate therapy in the treatment of diabetic ketoacidosis has not been established (see Uses: Diabetic Ketoacidosis), when IV sodium bicarbonate is administered, the acidosis should only partially be corrected, generally to an arterial pH of about 7.2, in order to avoid rebound alkalosis.

For the treatment of acidosis associated with chronic renal failure, oral sodium bicarbonate therapy is generally initiated when plasma bicarbonate concentration is less than 15 mEq/L. Therapy is usually initiated in adults with an oral sodium bicarbonate dosage of 20-36 mEq daily, given in divided doses. Dosage is then titrated to provide a plasma bicarbonate concentration of about 18-20 mEq/L. Because of the sodium content of sodium bicarbonate, the fluid and electrolyte balance of the patient must be carefully monitored during therapy with the drug. To relieve symptoms and prevent or stabilize renal failure and osteomalacia in patients with renal tubular acidosis, higher dosages of sodium bicarbonate are necessary. In adults with distal (type 1) renal tubular acidosis, an initial oral dosage of 0.5-2 mEq/kg daily, given in 4 or 5 divided doses, has been suggested. Dosage is titrated until hypercalciuria and acidosis are controlled, and according to the response and tolerance of the patient. Alternatively, an adult dosage of 48-72 mEq (about 4-6 g) daily has been suggested. Higher dosages are generally required in patients with proximal (type 2) renal tubular acidosis; oral dosages of 4-10 mEq/kg daily, given in divided doses, have been suggested.

The usual oral dosage of sodium bicarbonate for alkalinization of urine in adults is 48 mEq (4 g) initially, followed by 12-24 mEq (1-2 g) every 4 hours. 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. Dosage should be individually titrated to maintain the desired urinary pH. For alkalinization of urine in children, an oral dosage of 1-10 mEq (84-840 mg) per kg daily, adjusted according to response, has been suggested.

Adverse Effects

Gastric distention and flatulence may occur when sodium bicarbonate is administered orally. Inadvertent extravasation of hypertonic solutions of sodium bicarbonate has reportedly caused chemical cellulitis because of their alkalinity, subsequently resulting in tissue necrosis, ulceration, and/or sloughing at the site of injection. One manufacturer recommends that extravasation be treated by elevating the affected area, applying warm compresses to the site, and locally injecting lidocaine or hyaluronidase.

Sodium bicarbonate, 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. The manufacturers recommend that severe bicarbonate-induced alkalosis be treated with a parenteral calcium salt (e.g., calcium gluconate) and/or an acidifying agent (e.g., ammonium chloride). In patients with ketoacidosis, rapid alkalinization with sodium bicarbonate may reportedly result in clouding of consciousness, cerebral dysfunction, obtundation, seizures, and peripheral tissue hypoxia and lactic acidosis.

Sodium and water retention and edema may occur during sodium bicarbonate therapy, especially when the drug is given in large doses or to patients with renal insufficiency, congestive heart failure, or those predisposed to sodium retention and edema. Sodium and water overload may result in hypernatremia and hyperosmolality.401 Severe hyperosmolal states may develop during cardiopulmonary resuscitation when excessive doses of sodium bicarbonate are administered. (See Pharmacology.)

Precautions and Contraindications

Generally, the goal of alkalinizing therapy is to correct the acid-base disturbance while avoiding overdosage and resultant metabolic alkalosis.

Sodium bicarbonate should be used with extreme caution in patients with congestive heart failure or other edematous or sodium-retaining conditions; in patients with renal insufficiency, especially those with severe insufficiency such as oliguria or anuria; and in patients receiving corticosteroids or corticotropin, since each gram of sodium bicarbonate contains about 12 mEq of sodium. (For the sodium content of commercially available injections, see Chemistry and Stability: Chemistry.) IV administration of sodium bicarbonate may cause fluid and/or solute overload resulting in dilution of serum electrolytes, overhydration, congestive conditions, or pulmonary edema. The risk of dilutional conditions is inversely proportional to the electrolyte concentration administered, and the risk of solute overload and resultant congestive conditions with peripheral and/or pulmonary edema is directly proportional to the electrolyte concentration administered.

Potassium depletion may predispose to metabolic alkalosis and coexistent hypocalcemia may result in tetany and carpopedal spasm as the plasma pH increases. To minimize the risks of preexisting hypokalemia and/or hypocalcemia, these electrolyte disturbances should be corrected prior to initiation of, or concomitantly with, sodium bicarbonate therapy.

Sodium bicarbonate is generally contraindicated in patients with metabolic or respiratory alkalosis, in patients with hypocalcemia in whom alkalosis may induce tetany, in patients with excessive chloride loss from vomiting or continuous GI suctioning, and in patients at risk of developing diuretic-induced hypochloremic alkalosis. Sodium bicarbonate should not be used orally as an antidote in the treatment of acute ingestion of strong mineral acids, since carbon dioxide gas forms during neutralization and may cause gastric distention and possible rupture. Some experts state that non-lipid soluble drugs (e.g., sodium bicarbonate) may injure the airway and should not be administered via the endotracheal route.403

Pediatric Precautions

One manufacturer cautions that rapid injection (10 mL/minute) of hypertonic sodium bicarbonate solutions in neonates and children younger than 2 years of age may produce hypernatremia, decreased CSF pressure, and possible intracranial hemorrhage. It is recommended that the rate of IV administration in these children not exceed 8 mEq/kg daily and that slow IV administration of a 4.2% solution may be preferred. In emergencies such as cardiac arrest, the risk of rapid infusion of the drug in these children must be weighed against the potential for death from acidosis.

Pregnancy

Pregnancy

Animal reproduction studies have not been performed with sodium bicarbonate. It is also not known whether sodium bicarbonate can cause fetal harm when administered to pregnant women. Sodium bicarbonate should be used during pregnancy only when clearly needed.

Pharmacology

Sodium bicarbonate is an alkalinizing agent which dissociates to provide bicarbonate ion.

Bicarbonate is the conjugate base component of the principal extracellular buffer in the body, the bicarbonate:carbonic acid buffer. Various metabolic processes in the body either generate or consume hydrogen ions. Despite the dynamic nature of these processes, the hydrogen ion concentration in plasma and interstitial fluid is maintained at an almost constant level between 38-42 nmole/L (pH 7.37-7.42). The acid-base balance is maintained by 3 interacting mechanisms: buffers, regulation of carbonic acid concentration by the pulmonary system, and renal excretion of acid or base.

In body fluids, there are many buffers, including hemoglobin, proteins, and phosphates; however, the principal extracellular buffer is the bicarbonate:carbonic acid buffer. At a given pH, the ratio of bicarbonate:carbonic acid is constant. At pH 7.4, the bicarbonate:carbonic acid ratio is 20:1. Although buffers are most efficient when the ratio is 1, the unique characteristics of the bicarbonate:carbonic acid buffer make it highly effective even at a ratio of 20:1. In a solution such as plasma, all buffers are in equilibrium with the same hydrogen ion concentration and with each other. Thus, assessment of any one of these buffers (e.g., bicarbonate:carbonic acid) is reflective of the hydrogen ion concentration of the entire solution and the ratios of conjugate base to undissociated acid for all buffers. The bicarbonate:carbonic acid buffer is the only buffer in the body whose component concentrations can be varied independently by physiologic regulatory mechanisms. The bicarbonate buffer is extremely effective in buffering fixed acids and bases since changes in its components can be compensated by physiologic mechanisms such as formation and excretion of high concentrations of carbon dioxide, regulation by the pulmonary system of carbon dioxide concentration in body fluids, and generation or excretion by the kidney of substantial amounts of bicarbonate. Since carbonic acid is readily converted to or from carbon dioxide gas, its concentration is responsive to changes in alveolar Pco₂ and can be readily altered by changes in pulmonary ventilation.

Carbonic acid and dissolved carbon dioxide constitute the weak acid component and bicarbonate is the conjugate base component in the bicarbonate:carbonic acid buffer. The bicarbonate:carbonic acid buffer can be expressed as the following form of the Henderson-Hasselbalch equation:

pH = 6.1 + log (HCO₃ ^- / (H₂CO₃ + dissolved CO₂))

At equilibrium, the amount of dissolved carbon dioxide in plasma greatly exceeds that of carbonic acid. Thus, measurement of carbon dioxide is used to determine the concentration of the weak acid component of the buffer. Since the concentration of dissolved carbon dioxide in plasma (liquid phase) is in equilibrium with alveolar carbon dioxide (gas phase), the concentration of carbon dioxide in plasma can be calculated from the partial pressure of carbon dioxide using the following equation:

CO₂ (mmol/L) = 0.03 × Pco₂ (mm Hg)

and the Henderson-Hasselbalch equation can be expressed as follows:

pH = 6.1 + log (HCO₃ ^- / (0.03 × Pco₂))

Changes in the concentration of either component of the buffer can cause a decrease or increase in pH. Administration of sodium bicarbonate will increase the plasma bicarbonate concentration and possibly increase plasma pH; however, pH is usually maintained within the normal range, since compensatory mechanisms such as increased glomerular filtration and decreased tubular reabsorption of bicarbonate in the kidneys will rapidly decrease the plasma concentration of bicarbonate and restore the bicarbonate:carbonic acid ratio. Although metabolic alkalosis may result from IV infusion or ingestion of large amounts of sodium bicarbonate, renal mechanisms for increasing bicarbonate excretion are usually adequate to compensate for the acid-base imbalance. Primary acid-base disturbances (i.e., respiratory acidosis or alkalosis and metabolic acidosis or alkalosis) result from an initial change in one of the components of the bicarbonate:carbonic acid buffer. Generally, compensatory physiologic mechanisms and correction of the underlying cause of the disturbance are sufficient to restore acid-base balance. Occasionally, when acidemia is severe or plasma bicarbonate concentration is severely depleted, administration of sodium bicarbonate may be necessary to restore acid-base balance in patients with metabolic or respiratory acidosis. However, administration of sodium bicarbonate in these patients may result in metabolic alkalosis.

Changes in acid-base balance also stimulate compensatory ion-exchange mechanisms. Cations such as potassium and sodium can exchange for extracellular hydrogen ions. When the extracellular hydrogen ion concentration increases, as in acidosis, there is a redistribution of potassium ions from intracellular to extracellular fluid. Administration of sodium bicarbonate, by decreasing pH, can cause a redistribution of potassium ions into cells in patients with acidosis.

Since sodium bicarbonate provides bicarbonate which is readily excreted in urine, administration of the drug will increase urinary pH in patients with normal renal function. 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.

Sodium bicarbonate has a potent antacid action. Each gram of sodium bicarbonate has an in vitro neutralizing capacity of about 12 mEq of acid. For a discussion on sodium bicarbonate's antacid action, see Antacids 56:04.

Chemistry and Stability

Chemistry

Sodium bicarbonate is an alkalinizing agent.100 Sodium bicarbonate occurs as a white, crystalline powder which has a saline and slightly alkaline taste. The drug is soluble in water and insoluble in alcohol. Aqueous solutions of sodium bicarbonate, when freshly prepared, are alkaline to litmus; alkalinity increases as the solutions stand, are agitated, or are heated. Each 84 mg or 1 g of sodium bicarbonate contains 1 or about 12 mEq, respectively, each of sodium and bicarbonate ions.

Sodium bicarbonate injections are sterile solutions of the drug in water for injection. Carbon dioxide may be added during the manufacture of the injection to adjust the pH to 7-8.5. An 8.4% solution contains 1 mEq each of sodium and bicarbonate ions per mL and has a calculated osmolarity of 2000 mOsm/L. A 7.5% solution contains 0.892 mEq/mL each of sodium and bicarbonate ions and has a calculated osmolarity of 1786 mOsm/L. A 5% solution contains 0.595 mEq each of sodium and bicarbonate ions per mL and has a calculated osmolarity of 1190-1203 mOsm/L. A 4.2% solution contains 0.5 mEq each of sodium and bicarbonate ions per mL and has a calculated osmolarity of 1000 mOsm/L. Sodium bicarbonate is also available as a 4% small volume parenteral additive solution (Neut^®) which provides 2.4 mEq each of sodium and bicarbonate ions per 5 mL and is used to increase the pH of acidic infusion solutions.

A 1.5% solution of sodium bicarbonate is isotonic. A 1.5% sodium bicarbonate solution can be prepared by diluting each mL of an 8.4, 7.5, or 4.2% solution of the drug with 4.6, 4, or 1.8 mL of sterile water for injection, respectively.

Stability

Sodium bicarbonate tablets and effervescent tablets should be stored in tightly closed containers at a temperature less than 40°C, preferably between 15-30°C. Sodium bicarbonate injection should be stored at a temperature less than 40°C, preferably between 15-30°C; freezing should be avoided.

Sodium bicarbonate is stable in dry air, but slowly decomposes into sodium carbonate, carbon dioxide, and water in moist air. When heated, sodium bicarbonate loses water and carbon dioxide and is converted into sodium carbonate. Solutions of sodium carbonate are much more alkaline than sodium bicarbonate; since sodium carbonate may be formed when the dry salt or its solutions are sterilized with heat, the pH of heat-sterilized solutions or of solutions prepared from heat-sterilized powder should be determined prior to use. When sodium bicarbonate is combined with acids in aqueous solutions, a vigorous evolution of carbon dioxide gas occurs; the liberated carbon dioxide bubbles through the solution resulting in effervescence. In the dry state, sodium bicarbonate and acids do not react.

Sodium bicarbonate is physically and/or chemically incompatible with many drugs including acids, acidic salts, and many alkaloidal salts, but the compatibility depends on several factors (e.g., concentrations of the drugs, specific diluent used, resulting pH, temperature). Sodium bicarbonate injection should not be admixed with solutions containing calcium salts, except where compatibility has been specifically established, since haze formation or precipitation may result from such combinations. Also, sodium bicarbonate should not be admixed with or administered in the same IV line as catecholamines (e.g., epinephrine) because sodium bicarbonate may inactivate simultaneously administered catecholamines.403 Specialized references should be consulted for specific compatibility information.

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.

Only references cited for selected revisions after 1984 are available electronically.

100. Hospira, Inc. Sodium bicarbonate injection prescribing information. Lake Forest, IL; 2005.

249. ASHP. Standardize 4 Safety: pediatric continuous infusion standard. Updated 2024 Mar. From ASHP website. Updates may be available at ASHP website. [Web]

196. Vanden Hoek TL, Morrison LJ, Shuster M et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation . 2010; 122(18 Suppl 3):S829-61.

400. Link MS, Berkow LC, Kudenchuk PJ et al. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation . 2015; 132(18 Suppl 2):S444-64.

401. Neumar RW, Otto CW, Link MS et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation . 2010; 122(18 Suppl 3):S729-67.

402. de Caen AR, Berg MD, Chameides L et al. Part 12: Pediatric Advanced Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation . 2015; 132(18 Suppl 2):S526-42. [PubMed 26473000]

403. Kleinman ME, Chameides L, Schexnayder SM et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation . 2010; 122(18 Suppl 3):S876-908.