SODIUM BICARBONATE-WATER

General Administration Information
For storage information, see the specific product information within the How Supplied section.

Route-Specific Administration

Oral Administration
Oral Solid Formulations
-Oral tablets: May be swallowed whole or dissolved in water prior to use.
-Effervescent or soluble tablets: Dissolve in water completely before administering.

Other Oral Formulations
-Powder: Dissolve in 4 ounces of water completely before administering.



Injectable Administration
-Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
Intravenous Administration
-Flush IV line before and after administering to prevent any incompatibilities.
-Do not mix with vasoactive amines or calcium.

IV bolus
-Use prefilled syringes or premeasured ampules to ensure accurate dosing.
-In neonates and infants, use only the 0.5 mEq/mL (4.2%) solution for direct IV administration. Alternatively, the 1 mEq/mL (8.4%) solution may be diluted 1:1 with Sterile Water for Injection to a final concentration of 0.5 mEq/mL.
-Inject as a bolus over several minutes. A slow infusion time of 30 minutes is recommended in preterm neonates to minimize fluctuations in cerebral hemodynamics. The rate of administration should not exceed 10 mEq/minute.
-In neonates, may administer via the umbilical vein.

Intermittent IV Infusion
-Dilute to a maximum concentration of 0.5 mEq/mL in a compatible injection solution.
-Administer over 4 to 8 hours in patients with nonlife-threatening metabolic acidosis.
-Infusion rates should generally not exceed 1 mEq/kg/hour.

Continuous IV Infusion
-ASHP Recommended Standard Concentrations for Pediatric Continuous Infusions: 0.5 mEq/mL or 1 mEq/mL.



Other Administration Route(s)
Extemporaneous Compounding-Other
Intraosseous Administration
NOTE: Sodium bicarbonate is not FDA-approved for intraosseous administration.
-During cardiopulmonary resuscitation, the same dosage may be given via the intraosseous route if IV access is unsuccessful or not feasible.

Overly aggressive therapy with IV sodium bicarbonate can result in metabolic alkalosis and/or hypernatremia. Metabolic alkalosis can be accompanied by hyperirritability or tetany. If these symptoms occur, stop the bicarbonate infusion and administer calcium gluconate; administer potassium chloride if there is hypokalemia. Depending on the severity of alkalosis, an acidifying agent may be administered. In neonates, infants, and children under the age of 2, rapid injection (10 ml/min) of hypertonic sodium bicarbonate can cause hypernatremia, a decrease in cerebrospinal fluid pressure, and possible intracranial hemorrhage. Administer sodium bicarbonate cautiously to these patients using a 4.2% solution at a rate not to exceed 8 mEq/kg/day.

Extravasation of hypertonic solutions of sodium bicarbonate can cause an injection site reaction manifested as tissue necrosis, sloughing, and ulceration. Extravasation may be treated with prompt elevation, warm compresses, and local injection of lidocaine or hyaluronidase into the affected area.

Sodium and fluid retention can occur in patients receiving sodium bicarbonate therapy and is especially likely when large doses are administered or when the patient has renal impairment. Fluid and/or solute overload can result in dilution of serum electrolyte concentrations, overhydration, congestion, and pulmonary edema. Sodium bicarbonate-induced peripheral edema can exacerbate heart failure.

Large oral doses of sodium bicarbonate can cause flatulence, gastric distension, and/or abdominal pain.

Sodium bicarbonate is contraindicated for use in patients with preexisting metabolic alkalosis. Sodium bicarbonate is contraindicated in patients with hypochloremic alkalosis secondary to vomiting, diuretics, or nasogastric suction. The acid-base status of a patient should be assessed periodically during sodium bicarbonate administration to minimize the possibility of overdosage or metabolic alkalosis. Other causes of metabolic alkalosis include Cushing's syndrome, primary hyperaldosteronism, and Bartter's syndrome, so sodium bicarbonate should be used cautiously in patients with these conditions.

Sodium bicarbonate therapy should be used cautiously in patients with preexisting respiratory acidosis. Although sodium bicarbonate may successfully correct the acidosis associated with respiratory insufficiency, hypercapnia can worsen. It is important that patients be able to handle the excess carbon dioxide load as a result of sodium bicarbonate administration. Because sodium bicarbonate can worsen preexisting respiratory alkalosis, it should not be used in patients with this condition.

Sodium bicarbonate therapy should be used cautiously in patients with preexisting hypokalemia. Alkalosis can increase the risk of developing arrhythmias in these patients due to a rapid shift of potassium ions from the extracellular space into the intracellular space. Sodium bicarbonate therapy can worsen hypokalemia. In some patients, sodium bicarbonate is used to treat hyperkalemia. If hypocalcemia is also present then patients are at risk of carpopedal spasm (alkalosis-induced tetany) as the plasma pH rises. Correct electrolyte imbalances prior to, or concomitantly with, sodium bicarbonate infusion.


Sodium bicarbonate therapy should be used with caution in patients receiving corticotropin or corticosteroids and in patients with renal impairment, congestive heart failure, pre-existing hypernatremia, or other condition in which sodium retention could be detrimental. Additionally, long-term administration of absorable alkali orally (such as sodium bicarbonate) with calcium or milk can cause the milk-alkali syndrome, which is manifested by hypercalcemia, metabolic acidosis, renal insufficiency, mental confusion, anorexia, nausea, vomiting, and headache. Patients with certain renal disease, such as a salt-losing nephropathy, are at an increased risk of developing the milk-alkali syndrome, so sodium bicarbonate should be used extremely cautiously in these patients. Although patients with renal failure often develop metabolic acidosis and sodium bicarbonate is often used for this condition, the increased sodium load could also be detrimental in these patients.

The use of sodium bicarbonate during neonatal resuscitation is controversial. If given early during a resuscitation, sodium bicarbonate can be harmful. Resuscitation guidelines for neonates state that sodium bicarbonate may be beneficial in prolonged cardiac arrest. In a randomized controlled trial, 55 asphyxiated neonates received either sodium bicarbonate (n = 18) or placebo (n = 19) within the first 5 minutes of life. The administration of sodium bicarbonate did not change survival or neurological outcomes. Sodium bicarbonate should not be used for prolonged therapy because of the risk of causing hypernatremia. In neonates, infants, and children under the age of 2, rapid injection (10 mL/minute) of hypertonic sodium bicarbonate can cause hypernatremia, a decrease in cerebrospinal fluid pressure, and possible intracranial hemorrhage. The drug should be administered cautiously to these patients using a 4.2% solution at a rate not to exceed 8 mEq/kg/day.

Description: Sodium bicarbonate is a systemic alkalinizing agent. It most often is administered IV in the treatment of metabolic and respiratory acidosis. Sodium bicarbonate is used for urinary alkalinization, particularly after certain drug overdoses (i.e. salicylate poisoning, tricyclic overdose). It is used for the replacement of bicarbonate for ongoing renal losses. Sodium bicarbonate has also been used off-label as a component of cardioplegia solutions. The routine use of sodium bicarbonate in cardiac arrest is not recommended, however, it may be used in cases with documented metabolic acidosis after establishment of effective ventilation. Sodium bicarbonate use is also reasonable during situations such as severe metabolic acidosis with myocardial dysfunction or pacemaker noncapture and hyperkalemic cardiac arrest. Despite being a highly effective antacid, sodium bicarbonate is rarely used for the chronic treatment of peptic ulcer disease because it can be absorbed and can affect systemic acid-base balance. Sodium bicarbonate is approved in pediatric patients, as young as neonates.

-Do not administer sodium bicarbonate via the endotracheal tube. It is caustic and may injure the airway.

For the treatment of metabolic acidosis, including renal tubular acidosis (RTA):
-for metabolic acidosis NOT associated with cardiac arrest:
Intravenous dosage:
Neonates: 0.5 to 1 mEq/kg/dose IV over 5 to 30 minutes or as a slow IV infusion over several hours. Individualize continued dosage based on the acid-base status of the patient, as derived from the patient's blood CO2 content, pH, and clinical condition. Alternatively, calculate the dose using 1 of the following formulas: Dose (mEq) = [bicarbonate desired - bicarbonate actual] x weight (kg) x 0.4 or Dose (mEq) = 0.3 x weight (kg) x base deficit (mEq/L).
Infants, Children, and Adolescents: 0.5 to 1 mEq/kg/dose (Max: 50 mEq/dose) IV over 5 to 30 minutes or as a slow IV infusion over several hours. Individualize continued dosage based on the acid-base status of the patient, as derived from the patient's blood CO2 content, pH, and clinical condition. Alternatively, calculate the dose using 1 of the following formulas: Dose (mEq) = [bicarbonate desired - bicarbonate actual] x weight (kg) x 0.4 or Dose (mEq) = 0.3 x weight (kg) x base deficit (mEq/L). For older children, the FDA-approved dose is 2 to 5 mEq/kg/dose IV over a 4 to 8 hours.
-for metabolic acidosis in chronic renal failure:
Oral dosage:
Infants, Children, and Adolescents: 1 to 2 mEq/kg/day (84 to 168 mg/kg/day) PO in 2 to 3 divided doses. Titrate dose to target serum bicarbonate concentration. To prevent growth failure, guidelines recommend correcting serum bicarbonate concentrations less than 20 mEq/L in infants and children 2 years or younger and less than 22 mEq/L in children and adolescents 2 to 17 years.
-for metabolic acidosis due to distal renal tubular acidosis:
Oral dosage:
Neonates: 5 to 8 mEq/kg/day (420 to 672 mg/kg/day) PO in 2 to 3 divided doses.
Infants: 5 to 8 mEq/kg/day (420 to 672 mg/kg/day) PO in 2 to 3 divided doses.
Children and Adolescents: 3 to 4 mEq/kg/day (252 to 336 mg/kg/day) PO in 2 to 3 divided doses.
-for metabolic acidosis due to proximal renal tubular acidosis:
Oral dosage:
Neonates: 5 to 20 mEq/kg/day (420 to 1,680 mg/kg/day) PO in 2 to 3 divided doses. Titrate dose to target serum bicarbonate concentration.
Infants, Children, and Adolescents: 5 to 20 mEq/kg/day (420 to 1,680 mg/kg/day) PO in 2 to 3 divided doses. Titrate dose to target serum bicarbonate concentration.

For the treatment of hyperkalemia, including during cardiac arrest:
Intravenous dosage:
Neonates: 1 mEq/kg/dose IV/IO. Routine administration of sodium bicarbonate is not recommended during pediatric cardiac arrest in the absence of hyperkalemia.
Infants, Children, and Adolescents: 1 mEq/kg/dose (Max: 50 mEq/dose) IV/IO. Routine administration of sodium bicarbonate is not recommended during pediatric cardiac arrest in the absence of hyperkalemia.

For the treatment of dyspepsia or pyrosis (heartburn):
Oral dosage (powder):
Children and Adolescents 12 to 17 years: 2,616 mg PO every 2 hours as needed. Max: 15.6 g/day.

For the treatment of certain drug intoxications, such as salicylate toxicity including urinary alkalinization and sodium channel blocker toxicity:
-for the treatment of salicylate toxicity including urinary alkalinization:
Intravenous dosage:
Neonates: 1 mEq/kg/dose IV as needed to increase arterial pH to 7.4. Follow with sodium bicarbonate 1 mEq/kg (and potassium chloride 1 mEq/kg) in 10 mL/kg 5% Dextrose Injection continuous IV infusion at 2 mL/kg/hour to induce urine pH of 7.5 to 8.
Infants, Children, and Adolescents: 1 mEq/kg/dose IV as needed to increase arterial pH to 7.4. Follow with sodium bicarbonate 1 mEq/kg (and potassium chloride 1 mEq/kg) in 10 mL/kg 5% Dextrose Injection continuous IV infusion at 2 mL/kg/hour to induce urine pH of 7.5 to 8.
-for the treatment of sodium channel blocker toxicity:
Intravenous dosage:
Neonates: 1 to 2 mEq/kg/dose IV/IO every 3 to 5 minutes as needed. Follow with sodium bicarbonate 150 mEq in 1,000 mL 5% Dextrose Injection continuous IV infusion to maintain alkalosis. Routine administration of sodium bicarbonate is not recommended during pediatric cardiac arrest in the absence of sodium channel blocker toxicity.
Infants, Children, and Adolescents: 1 to 2 mEq/kg/dose IV/IO every 3 to 5 minutes as needed. Follow with sodium bicarbonate 150 mEq in 1,000 mL 5% Dextrose Injection continuous IV infusion to maintain alkalosis. Routine administration of sodium bicarbonate is not recommended during pediatric cardiac arrest in the absence of sodium channel blocker toxicity.

Maximum Dosage Limits:
Specific maximum dosage information is not available. Individualize dosage based on careful monitoring of arterial blood gas and other clinical parameters.

Patients with Hepatic Impairment Dosing
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.

Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

*non-FDA-approved indication

Monograph content under development

Mechanism of Action: After oral administration, sodium bicarbonate neutralizes hydrochloric acid in the stomach, forming sodium chloride, carbon dioxide, and water. Excess bicarbonate ions are absorbed in the small intestine. Thus, all of a dose of exogenous sodium bicarbonate eventually reaches the extracellular fluid, and a mild alkalosis can result. This usually is corrected quickly by the renal system in patients with normal renal function. After IV administration, sodium bicarbonate dissociates to bicarbonate ions, which constitute the conjugate base portion of the body's extracellular buffer system (bicarbonate/carbonic acid buffer). Administration of sodium bicarbonate will restore acid-base balance in patients with metabolic or respiratory acidosis; however, metabolic alkalosis can result from the use of sodium bicarbonate.

Excess bicarbonate ions that result from the administration of sodium bicarbonate are excreted in the urine, alkalizing the urine. This alkalization decreases renal absorption and increases the clearance of certain drugs, intoxicants, weak acids, and blood pigments.

Pharmacokinetics: Sodium bicarbonate is administered orally and intravenously. Sodium bicarbonate is not metabolized, and bicarbonate ions are filtered and reabsorbed by the kidneys; less than 1% is excreted in the urine.

Affected cytochrome P450 isoenzymes: none


-Route-Specific Pharmacokinetics
Oral Route
Sodium bicarbonate is rapidly absorbed after an oral dose, entering the blood as bicarbonate and sodium ions.