Sodium bicarbonate is an oral and parenteral alkalinizing agent indicated for 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; for the treatment of certain drug intoxications, including barbiturates, salicylates, or methyl alcohol; for the treatment of hemolytic reactions requiring urine alkalinization to diminish nephrotoxicity of blood pigments; for the treatment of severe diarrhea accompanied by a significant loss of bicarbonate; and for the treatment of heartburn or dyspepsia. Routine administration of sodium bicarbonate is not recommended during adult cardiac arrest or during pediatric cardiac arrest in the absence of hyperkalemia or sodium channel blocker toxicity. Overly aggressive therapy with sodium bicarbonate can result in metabolic alkalosis and hypernatremia. Inadvertent extravasation of intravenously administered hypertonic solutions of sodium bicarbonate have been reported to cause chemical cellulitis, with tissue necrosis, ulceration, or sloughing at the site of infiltration.
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)
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.
Overdosage of IV sodium bicarbonate can result in metabolic alkalosis and/or hypernatremia. Metabolic alkalosis is a greater risk in patients with impaired renal function, and the reaction is accompanied by hyperirritability or tetany. The rapid administration of sodium bicarbonate to patients with ketoacidosis can result in clouding of consciousness, obtundation, tremor, seizures, cerebral dysfunction, and lactic acidosis.
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 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. Sodium bicarbonate-induced peripheral edema can exacerbate heart failure.
Large oral doses of sodium bicarbonate can cause flatulence, gastric distension, and/or abdominal pain. Spontaneous rupture of the stomach after ingestion of oral sodium bicarbonate has been reported in case reports.
In patients with nonlife-threatening metabolic acidosis, the desired dose of sodium bicarbonate should not be administered as a single, IV injection. Administration over 8 hours via IV infusion or oral administration is preferable.
Long-term administration of 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 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 be detrimental in these patients.
Sodium bicarbonate injection should be administered to children with caution. Parenteral formulations are hypertonic and should be diluted before injection.
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.
Sodium bicarbonate should not be used for prolonged therapy because of the risk of causing hypernatremia. Rapid injection of hypertonic sodium bicarbonate can cause hypernatremia in neonates, infants, and children under the age of 2; the drug should be administered cautiously to these patients. Sodium bicarbonate therapy should be used with caution in patients receiving corticotropin or corticosteroids, in patients with renal disease or insufficiency, or in patients with congestive heart failure or other condition in which sodium retention could be detrimental.
Sodium bicarbonate is contraindicated in patients with hypocalcemia because of the risk of developing alkalosis-induced tetany.
Although no untoward effects have been observed in humans, chronic use of sodium bicarbonate may lead to metabolic alkalosis, which may threaten maternal-fetal health. Increased sodium intake can produce edema and weight gain from fluid retention. Guidelines consider sodium bicarbonate-containing antacids unsafe for use during pregnancy due to these side effect risks; there are many other antacids, such as the occasional use of calcium carbonate, that are considered appropriate for occasional use for dyspepsia, heartburn and gastroesophageal reflux disease (GERD). Sodium bicarbonate may be used intravenously when critical for the health of the mother.
Sodium bicarbonate has no specific precautions for use during breast-feeding. The American Gastroenterological Association states that sodium bicarbonate antacids represent a low risk to the infant when used during breast-feeding. According to guidelines, if heartburn/gastroesophageal reflux (GERD) symptoms persist after delivery, antacids are safe to use during lactation because they are not concentrated in breast milk.
For the treatment of metabolic acidosis, including renal tubular acidosis (RTA):
-for metabolic acidosis NOT associated with cardiopulmonary arrest:
Intravenous dosage:
Adults: 1 to 2 mEq/kg/dose IV over 5 to 30 minutes or as a slow IV infusion (i.e., 100 to 150 mEq in 1 L IV 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). The FDA-approved dose is 2 to 5 mEq/kg/dose IV over 4 to 8 hours.
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.
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).
-for metabolic acidosis in chronic renal failure:
Oral dosage:
Adults: 0.5 to 1 mEq/kg/day (42 to 84 mg/kg/day) PO in 2 to 3 divided doses. Alternately, 650 or 1,300 mg PO twice daily for a serum bicarbonate concentration of 19 to 21 mEq/L or 18 mEq/L or less, respectively. Titrate dose up to 1,950 mg PO 3 times daily to target serum bicarbonate concentration (22 mEq/L or more).
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:
Adults: 1 to 2 mEq/kg/day (84 to 168 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.
Infants: 5 to 8 mEq/kg/day (420 to 672 mg/kg/day) PO in 2 to 3 divided doses.
Neonates: 5 to 8 mEq/kg/day (420 to 672 mg/kg/day) PO in 2 to 3 divided doses.
-for metabolic acidosis due to proximal renal tubular acidosis:
Oral dosage:
Adults: 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.
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.
For the treatment of hyperkalemia, including during cardiac arrest (cardiopulmonary resuscitation):
Intravenous or Intraosseus* dosage:
Adults: 50 to 100 mEq (approximately 1 to 2 mEq/kg/dose) IV/IO every 5 to 10 minutes as needed. Routine administration of sodium bicarbonate is not recommended during adult cardiac arrest.
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.
Neonates: 1 mEq/kg/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 (tablets):
Adults 60 years and older: 650 to 1,300 mg PO every 4 hours as needed. Max: 7.8 g/day.
Adults 18 to 59 years: 650 to 2,600 mg PO every 4 hours as needed. Max: 15.6 g/day.
Oral dosage (powder):
Adults 60 years and older: 2,616 mg PO every 2 hours as needed. Max: 7.8 g/day.
Adults 18 to 59 years: 2,616 mg PO every 2 hours as needed. Max: 15.6 g/day.
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:
Adults: 1 mEq/kg/dose IV as needed to increase arterial pH to 7.4. Follow with sodium bicarbonate 132 to 150 mEq (and potassium chloride 20 to 40 mEq) in 1,000 mL 5% Dextrose Injection continuous IV infusion to induce urine output of 2 to 3 mL/kg/hour and 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.
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.
-for the treatment of sodium channel blocker toxicity:
Intravenous dosage:
Adults: 50 to 100 mEq (approximately 1 to 2 mEq/kg/dose) IV/IO every 5 to 10 minutes as needed. Routine administration of sodium bicarbonate is not recommended during adult cardiac arrest.
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.
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.
Maximum Dosage Limits:
Specific maximum dosage information is not available. Individualize dosage based on careful monitoring of arterial blood gas and other clinical parameters in all patient populations.
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
Acalabrutinib: (Moderate) Separate the administration of acalabrutinib capsules and antacids by at least 2 hours if these agents are used together. Acalabrutinib capsule solubility decreases with increasing pH values; therefore, coadministration may result in decreased acalabrutinib exposure and effectiveness. In healthy subjects, the AUC of acalabrutinib was decreased by 53% when acalabrutinib capsules were coadministered with another antacid.
Acetaminophen: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid. (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid. (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Aspirin: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid. (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid. (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Caffeine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Caffeine; Dihydrocodeine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Caffeine; Pyrilamine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Chlorpheniramine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Chlorpheniramine; Dextromethorphan: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Chlorpheniramine; Dextromethorphan; Phenylephrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Chlorpheniramine; Phenylephrine : (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Codeine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Dextromethorphan: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Dextromethorphan; Doxylamine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Dextromethorphan; Guaifenesin; Phenylephrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Dextromethorphan; Guaifenesin; Pseudoephedrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Dextromethorphan; Phenylephrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Dextromethorphan; Pseudoephedrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Diphenhydramine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Guaifenesin; Phenylephrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Hydrocodone: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Ibuprofen: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Oxycodone: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Pamabrom; Pyrilamine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Phenylephrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Acetaminophen; Pseudoephedrine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetazolamide: (Minor) Acetazolamide and sodium bicarbonate used concurrently increases the risk of renal calculus formation via calcium phosphate supersaturation.
Acrivastine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Albuterol; Budesonide: (Major) Enteric-coated budesonide granules dissolve at a pH > 5.5. Likewise, the dissolution of the coating of extended-release budesonide tablets (Uceris) is pH dependent. Concomitant use of oral budesonide and antacids, milk, or other drugs that increase gastric pH levels can cause the coating of the granules to dissolve prematurely, possibly affecting release properties and absorption of the drug in the duodenum. In general, it may be prudent to avoid drugs such as antacids in combination with enteric-coated budesonide.
Alendronate: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Alendronate; Cholecalciferol: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Amlodipine; Atorvastatin: (Moderate) Concomitant administration of atorvastatin with antacids reduced the plasma concentrations of atorvastatin by approximately 35 percent. However, LDL-cholesterol reduction was not altered.
Amphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Amphetamine; Dextroamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Amphetamines: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Ascorbic Acid, Vitamin C: (Minor) Because antacids can alkalinize the urine, they can interact with urinary acidifiers, such as ascorbic acid. Frequent use of high doses of antacids should be avoided by patients receiving urinary acidifiers.
Aspirin, ASA: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Butalbital; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid. (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Dipyridamole: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Omeprazole: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Oxycodone: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Atazanavir: (Major) It is recommended that antacids not be given at the some time as atazanavir because of potential interference with absorption of atazanavir. Separate the administration of atazanavir and antacids to avoid the potential for interaction; give atazanavir 2 hours before or 1 hour after the antacid.
Atazanavir; Cobicistat: (Major) It is recommended that antacids not be given at the some time as atazanavir because of potential interference with absorption of atazanavir. Separate the administration of atazanavir and antacids to avoid the potential for interaction; give atazanavir 2 hours before or 1 hour after the antacid.
Atorvastatin: (Moderate) Concomitant administration of atorvastatin with antacids reduced the plasma concentrations of atorvastatin by approximately 35 percent. However, LDL-cholesterol reduction was not altered.
Bempedoic Acid; Ezetimibe: (Minor) Antacids may decrease the peak plasma concentration (Cmax) of total ezetimibe by 30%. The effect of the antacids in this regard is not expected to have a significant effect on the ability of ezetimibe to lower cholesterol. However, to limit any potential interaction, it would be prudent to administer ezetimibe at least 1 hour before or 2 hours after administering antacids.
Benzhydrocodone; Acetaminophen: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form. (Moderate) Separate the time of administration of oral hyoscyamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral hyoscyamine absorption and reduce efficacy.
Benzphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with antacids can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid antacids within 1 hour before or after the bisacodyl dosage.
Bismuth Subcitrate Potassium; Metronidazole; Tetracycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Bismuth Subsalicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy. (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Bisphosphonates: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Bosutinib: (Moderate) Bosutinib displays pH-dependent aqueous solubility; therefore, concomitant use of bosutinib and antacids may result in decreased plasma exposure of bosutinib. Separate the administration of bosutinib and antacids by more than 2 hours.
Brompheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Brompheniramine; Pseudoephedrine; Dextromethorphan: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Budesonide: (Major) Enteric-coated budesonide granules dissolve at a pH > 5.5. Likewise, the dissolution of the coating of extended-release budesonide tablets (Uceris) is pH dependent. Concomitant use of oral budesonide and antacids, milk, or other drugs that increase gastric pH levels can cause the coating of the granules to dissolve prematurely, possibly affecting release properties and absorption of the drug in the duodenum. In general, it may be prudent to avoid drugs such as antacids in combination with enteric-coated budesonide.
Budesonide; Formoterol: (Major) Enteric-coated budesonide granules dissolve at a pH > 5.5. Likewise, the dissolution of the coating of extended-release budesonide tablets (Uceris) is pH dependent. Concomitant use of oral budesonide and antacids, milk, or other drugs that increase gastric pH levels can cause the coating of the granules to dissolve prematurely, possibly affecting release properties and absorption of the drug in the duodenum. In general, it may be prudent to avoid drugs such as antacids in combination with enteric-coated budesonide.
Budesonide; Glycopyrrolate; Formoterol: (Major) Enteric-coated budesonide granules dissolve at a pH > 5.5. Likewise, the dissolution of the coating of extended-release budesonide tablets (Uceris) is pH dependent. Concomitant use of oral budesonide and antacids, milk, or other drugs that increase gastric pH levels can cause the coating of the granules to dissolve prematurely, possibly affecting release properties and absorption of the drug in the duodenum. In general, it may be prudent to avoid drugs such as antacids in combination with enteric-coated budesonide.
Butalbital; Acetaminophen: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Butalbital; Acetaminophen; Caffeine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Butalbital; Acetaminophen; Caffeine; Codeine: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Butalbital; Aspirin; Caffeine; Codeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Cabotegravir; Rilpivirine: (Moderate) Concurrent administration of rilpivirine and antacids may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of antacids for at least 2 hours before and at least 4 hours after administering rilpivirine.
Cefpodoxime: (Moderate) Because cefpodoxime proxetil requires a low gastric pH for dissolution, drugs which increase gastric pH, such as antacids, can decrease the bioavailability of cefpodoxime.
Cefuroxime: (Moderate) Antacids can interfere with the oral absorption of cefuroxime axetil and may result in reduced antibiotic efficacy. If an antacid must be used while a patient is taking cefuroxime, administer the oral dosage of cefuroxime at least 1 hour before or 2 hours after the antacid.
Cetirizine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlophedianol; Dexchlorpheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chloroquine: (Major) Chloroquine absorption may be reduced by antacids. Administer chloroquine and antacids at least 4 hours apart.
Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpheniramine; Ibuprofen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Choline Salicylate; Magnesium Salicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Ciprofloxacin: (Moderate) Crystalluria related to ciprofloxacin has been reported only rarely in humans because human urine is usually acidic. Avoid alkalinity of the urine in patients receiving ciprofloxacin when possible. A large proportion of ciprofloxacin is normally excreted unchanged in the urine. If sodium bicarbonate is used concomitantly, the solubility of ciprofloxacin might be decreased because of alkaline urine. Patients should be monitored for crystalluria, proper urination,and altered kidney function. Hydrate patients well to prevent the formation of highly concentrated urine.
Codeine; Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Cysteamine: (Major) In general, cysteamine may be administered with electrolyte and mineral replacements necessary for managing Fanconi syndrome, as well as with vitamin D and thyroid hormone. However, delayed-release cysteamine (Procysbi) should be administered at least 1 hour before or 1 after medications that increase gastric pH, including those containing bicarbonate or carbonate (i.e., sodium bicarbonate). Drugs that increase the gastric pH, such as bicarbonate and carbonate, may cause the premature release of cysteamine from delayed-release capsules, leading to an increase in WBC cystine concentration.
Dasatinib: (Moderate) Separate the administration of dasatinib and sodium bicarbonate by at least 2 hours if these agents are used together. The simultaneous administration of an antacid with dasatinib decreased the Cmax and AUC of dasatinib by 58% and 55%, respectively.
Delavirdine: (Major) Coadministration of delavirdine with antacids results in decreased absorption of delavirdine. Administration of delavirdine and antacids should be separated by at least 1 hour.
Demeclocycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Desloratadine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dexbrompheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dexchlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dextroamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Dextromethorphan; Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dextromethorphan; Quinidine: (Major) Urinary alkalinization increases the renal tubular reabsorption of quinidine, resulting in higher quinidine serum concentrations which may lead to toxicity. Avoid citric acid; potassium citrate; sodium citrate administration to any patient receiving treatment with quinidine.
Diazepam: (Moderate) The coadministration of diazepam with antacids results in delayed diazepam absorption due to the fact that antacids delay gastric emptying. It may be prudent to separate dosing by 2 hours to limit any potential interaction.
Dicyclomine: (Moderate) Separate the time of administration of oral dicyclomine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral dicyclomine absorption and reduce efficacy.
Diflunisal: (Moderate) Concurrent use of diflunisal with antacids, such as sodium bicarbonate, may reduce plasma diflunisal concentrations. The effect may be clinically significant if antacids are used on a continuous schedule.
Diphenhydramine; Naproxen: (Minor) Concomitant administration of antacids can delay the absorption of naproxen. Periodic antacid use should not be problematic as long as the antacid and enteric-coated naproxen administration are separated by at least 2 hours.
Dolutegravir; Rilpivirine: (Moderate) Concurrent administration of rilpivirine and antacids may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of antacids for at least 2 hours before and at least 4 hours after administering rilpivirine.
Donepezil; Memantine: (Moderate) Urinary alkalinizing agents may decrease the elimination of memantine, resulting in drug accumulation and potential toxicity. The clearance of memantine is reduced by about 80% under alkaline urine conditions at pH 8. Memantine should be used with caution with drugs known to increase urinary pH.
Doxycycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Eltrombopag: (Major) Eltrombopag chelates polyvalent cations (e.g., antacids) in food, mineral supplements, and antacids. In a clinical study, systemic exposure to eltrombopag was decreased by 70% when it was administered with a polyvalent cation-containing antacid. Administer eltrombopag at least 2 hours before or 4 hours after any oral products containing polyvalent cations, such as magaldrate.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Alafenamide: (Moderate) Separate administration of elvitegravir and antacids by at least 2 hours. Due to the formation of ionic complexes in the gastrointestinal tract, simultaneous administration results in lower elvitegravir plasma concentrations.
Elvitegravir; Cobicistat; Emtricitabine; Tenofovir Disoproxil Fumarate: (Moderate) Separate administration of elvitegravir and antacids by at least 2 hours. Due to the formation of ionic complexes in the gastrointestinal tract, simultaneous administration results in lower elvitegravir plasma concentrations.
Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Moderate) Concurrent administration of rilpivirine and antacids may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of antacids for at least 2 hours before and at least 4 hours after administering rilpivirine.
Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Moderate) Concurrent administration of rilpivirine and antacids may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of antacids for at least 2 hours before and at least 4 hours after administering rilpivirine.
Ephedrine: (Moderate) Sodium bicarbonate-induced urinary alkalization can increase the half-life of ephedrine.
Ephedrine; Guaifenesin: (Moderate) Sodium bicarbonate-induced urinary alkalization can increase the half-life of ephedrine.
Erlotinib: (Major) Separate administration by several hours if concomitant use of erlotinib with sodium bicarbonate is necessary. Erlotinib displays pH-dependent solubility with decreased solubility at a higher pH; the increased gastric pH resulting from sodium bicarbonate therapy may reduce the bioavailability of erlotinib. Increasing the dose of erlotinib without modifying the administration schedule is unlikely to compensate for loss of exposure. The effects of antacids on erlotinib pharmacokinetics has not been evaluated.
Ethotoin: (Major) The oral absorption of ethotoin may be reduced by antacids. Separating the administration of ethotoin and antacids by at least 2 hours will help minimize the possibility of interaction.
Etidronate: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Ezetimibe: (Minor) Antacids may decrease the peak plasma concentration (Cmax) of total ezetimibe by 30%. The effect of the antacids in this regard is not expected to have a significant effect on the ability of ezetimibe to lower cholesterol. However, to limit any potential interaction, it would be prudent to administer ezetimibe at least 1 hour before or 2 hours after administering antacids.
Ezetimibe; Simvastatin: (Minor) Antacids may decrease the peak plasma concentration (Cmax) of total ezetimibe by 30%. The effect of the antacids in this regard is not expected to have a significant effect on the ability of ezetimibe to lower cholesterol. However, to limit any potential interaction, it would be prudent to administer ezetimibe at least 1 hour before or 2 hours after administering antacids.
Ferric Maltol: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Fexofenadine: (Major) Co-administration with antacids within 15 minutes decreases the AUC and Cmax of fexofenadine. Separate administration is recommended.
Fexofenadine; Pseudoephedrine: (Major) Co-administration with antacids within 15 minutes decreases the AUC and Cmax of fexofenadine. Separate administration is recommended. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Flecainide: (Moderate) Urinary alkalinization can decrease the renal clearance of flecainide, resulting in an increased elimination half-life and AUC for flecainide.
Food: (Moderate) Food or medicines containing a high sodium content (e.g., tomato juice) could increase the risk of complications of sodium excess when given with sodium bicarbonate. Patients and clinicians should be aware of the amount of sodium intake in medications and foods.
Fosamprenavir: (Moderate) Administer fosamprenavir at least 1 hour before or 1 hour after oral sodium bicarbonate. Coadministration of antacids, such as sodium bicarbonate, may decrease the exposure of fosamprenavir and impair its efficacy.
Gabapentin: (Moderate) Antacids have been shown to reduce the oral bioavailability of gabapentin by roughly 20%. This decrease in bioavailability was about 5% when gabapentin was administered 2 hours after the antacid. It is recommended that gabapentin be taken at least 2 hours following the administration of antacids in order to avoid a significant interaction.
Gastrointestinal Enzymes: (Major) The effectiveness of gastrointestinal enzymes can be diminished with concurrent administration of antacids. In-vitro studies suggest that calcium and magnesum cations exert their deleterious effect on replacement enzyme therapy by formation of poorly soluble calcium or magnesium soaps and precipitation of glycine conjugated bile salts.
Gefitinib: (Major) Avoid coadministration of sodium bicarbonate with gefitinib if possible due to decreased exposure to gefitinib, which may lead to reduced efficacy. If concomitant use is unavoidable, take gefitinib 6 hours after the last dose or 6 hours before the next dose of sodium bicarbonate. Gefitinib exposure is affected by gastric pH. Coadministration with high doses of ranitidine with sodium bicarbonate to maintain gastric pH above 5 decreased gefitinib exposure by 47%.
Glipizide: (Moderate) Monitor blood glucose concentrations closely during coadministration of glipizide and sodium bicarbonate. Antacids have been reported to increase the absorption of glipizide, enhancing its hypoglycemic effects. Although the exact mechanism is not known, theoretically it may be due to alterations in gastric pH.
Glipizide; Metformin: (Moderate) Monitor blood glucose concentrations closely during coadministration of glipizide and sodium bicarbonate. Antacids have been reported to increase the absorption of glipizide, enhancing its hypoglycemic effects. Although the exact mechanism is not known, theoretically it may be due to alterations in gastric pH.
Glyburide: (Moderate) Antacids have been reported to increase the absorption of non-micronized glyburide, enhancing their hypoglycemic effects. Although the exact mechanism is not known, theoretically it may be due to alterations in gastric pH. Consider closely monitoring blood glucose concentrations.
Glyburide; Metformin: (Moderate) Antacids have been reported to increase the absorption of non-micronized glyburide, enhancing their hypoglycemic effects. Although the exact mechanism is not known, theoretically it may be due to alterations in gastric pH. Consider closely monitoring blood glucose concentrations.
Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Hydroxychloroquine: (Major) Hydroxychloroquine absorption may be reduced by antacids as has been observed with the structurally similar chloroquine. Administer hydroxychloroquine and antacids at least 4 hours apart. Of note, a study demonstrated no significant difference in hydroxychloroquine serum concentration in patients taking concomitant antacids (n = 14) compared to those not taking antacids (n = 495).
Hyoscyamine: (Moderate) Separate the time of administration of oral hyoscyamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral hyoscyamine absorption and reduce efficacy.
Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form. (Moderate) Separate the time of administration of oral hyoscyamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral hyoscyamine absorption and reduce efficacy.
Ibandronate: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Ibuprofen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Indomethacin: (Moderate) Antacids may inhibit the oral absorption of indomethacin. Simultaneous administration should be avoided; separate dosing by at least 2 hours to limit an interaction.
Iron Salts: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Iron: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Moderate) Concomitant use of sodium bicarbonate and rifampin may decrease the absorption of rifampin. Daily doses of rifampin should be given at least 1 hour before the ingestion of sodium bicarbonate.
Isoniazid, INH; Rifampin: (Moderate) Concomitant use of sodium bicarbonate and rifampin may decrease the absorption of rifampin. Daily doses of rifampin should be given at least 1 hour before the ingestion of sodium bicarbonate.
Itraconazole: (Moderate) Administer antacids at least 2 hours before or 2 hours after oral itraconazole to minimize the potential for an interaction. Because itraconazole oral bioavailability requires an acidic environment for solubility, its absorption may be decreased with concomitant administration of antacids.
Ketoconazole: (Major) Ketoconazole requires an acidic pH for absorption. Medications that increase gastric pH or decrease acid output can cause a notable decrease in the bioavailability of ketoconazole. Medications that have this effect are antacids, antimuscarinics, histamine H2-blockers, and proton pump inhibitors (PPIs). Except for antacids, these medications have a prolonged duration of action, and staggering their time of administration with ketoconazole by several hours may not prevent the drug interaction; ketoconazole should be administered at least 2 hours before or 1 hour after antacids. An alternative imidazole antifungal should be chosen if any of these gastrointestinal medications are required. If these drugs must be coadministered, administer ketoconazole tablets with an acidic beverage and closely monitor for breakthrough infection.
Lactulose: (Minor) Oral, nonabsorbable antacids may interfere with the decrease in colon pH necessary for lactulose's action.
Ledipasvir; Sofosbuvir: (Moderate) Separate administration of ledipasvir and antacids by at least 4 hours. Solubility of ledipasvir decreases as gastric pH increases; thus, simultaneous administration of these drugs may result in lower ledipasvir plasma concentrations.
Levoketoconazole: (Major) Ketoconazole requires an acidic pH for absorption. Medications that increase gastric pH or decrease acid output can cause a notable decrease in the bioavailability of ketoconazole. Medications that have this effect are antacids, antimuscarinics, histamine H2-blockers, and proton pump inhibitors (PPIs). Except for antacids, these medications have a prolonged duration of action, and staggering their time of administration with ketoconazole by several hours may not prevent the drug interaction; ketoconazole should be administered at least 2 hours before or 1 hour after antacids. An alternative imidazole antifungal should be chosen if any of these gastrointestinal medications are required. If these drugs must be coadministered, administer ketoconazole tablets with an acidic beverage and closely monitor for breakthrough infection.
Levonorgestrel; Ethinyl Estradiol; Ferrous Bisglycinate: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Levonorgestrel; Ethinyl Estradiol; Ferrous Fumarate: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Lisdexamfetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Lithium: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with lithium, especially patients who are stabilized on lithium, as urinary alkalinization increases the renal clearance of lithium. If coadministration can not be avoided, monitor lithium serum concentrations and patient clinical response very closely. Also of note, lithium clearance is increased if hypernatremia occurs.
Lopinavir; Ritonavir: (Moderate) Concurrent administration of tipranavir and ritonavir with antacids results in decreased tipranavir concentrations. Administer tipranavir and ritonavir 2 hours before or 1 hour after antacids.
Loratadine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Magnesium Salicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Mefenamic Acid: (Moderate) Ingestion of mefenamic acid with antacids is not recommended. Administration with an antacid containing 1.7 grams of magnesium hydroxide resulted in a 36 percent increase in the area under the time versus concentration curve of mefenamic acid.
Mefloquine: (Moderate) Antacids may increase plasma concentrations of mefloquine. Patients on chronic mefloquine therapy might be at increased risk of adverse reactions, especially patients with a neurological or psychiatric history.
Memantine: (Moderate) Urinary alkalinizing agents may decrease the elimination of memantine, resulting in drug accumulation and potential toxicity. The clearance of memantine is reduced by about 80% under alkaline urine conditions at pH 8. Memantine should be used with caution with drugs known to increase urinary pH.
Mesalamine, 5-ASA: (Moderate) Do not coadminister mesalamine extended-release capsules (Apriso) with antacids. Apriso is a pH-dependent, delayed-release capsule product with an enteric coating that dissolves at a pH of at least 6. Other mesalamine products do not have an interaction with antacids.
Methamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Methenamine: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form. (Moderate) Separate the time of administration of oral hyoscyamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral hyoscyamine absorption and reduce efficacy.
Methenamine; Sodium Salicylate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Methscopolamine: (Moderate) Separate the time of administration of oral methscopolamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral methscopolamine absorption and reduce efficacy.
Mexiletine: (Major) If alkalinizing agents, such as sodium bicarbonate, are administered concomitantly with mexiletine, urinary excretion and plasma half-life of the antiarrhythmic can be altered. Elimination of mexiletine is decreased when the urine is alkaline and increased when it is acidic. Dosage adjustments should be made as necessary.
Minocycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Mycophenolate: (Major) Coadministration of mycophenolate mofetil with antacids decreases the bioavailability of mycophenolate mofetil. Aluminum or magnesium hydroxide antacids decrease AUC of mycophenolic acid by about 17%. Avoid administration of mycophenolate mofetil with agents that may decrease its absorption.
Naproxen: (Minor) Concomitant administration of antacids can delay the absorption of naproxen. Periodic antacid use should not be problematic as long as the antacid and enteric-coated naproxen administration are separated by at least 2 hours.
Naproxen; Esomeprazole: (Minor) Concomitant administration of antacids can delay the absorption of naproxen. Periodic antacid use should not be problematic as long as the antacid and enteric-coated naproxen administration are separated by at least 2 hours.
Naproxen; Pseudoephedrine: (Minor) Concomitant administration of antacids can delay the absorption of naproxen. Periodic antacid use should not be problematic as long as the antacid and enteric-coated naproxen administration are separated by at least 2 hours. (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Neratinib: (Major) Administer neratinib at least 3 hours after administration of sodium bicarbonate if concomitant use is necessary due to decreased absorption and systemic exposure of neratinib; the solubility of neratinib decreases with increasing pH of the GI tract.
Nilotinib: (Moderate) If concomitant use of these agents is necessary, administer the antacid approximately 2 hours before or approximately 2 hours after the nilotinib dose. Nilotinib displays pH-dependent solubility with decreased solubility at a higher pH; therefore, concomitant use of nilotinib and antacids may result in decreased bioavailability of nilotinib. In a study in healthy subjects, there was no significant change in nilotinib pharmacokinetics when an antacid (aluminum hydroxide/magnesium hydroxide/simethicone) was administered approximately 2 hours before or approximately 2 hours after a single 400-mg nilotinib dose.
Nirmatrelvir; Ritonavir: (Moderate) Concurrent administration of tipranavir and ritonavir with antacids results in decreased tipranavir concentrations. Administer tipranavir and ritonavir 2 hours before or 1 hour after antacids.
Nirogacestat: (Moderate) Separate the administration of nirogacestat and antacids by at least 2 hours. Simultaneous coadministration may impair nirogacestat absorption resulting in reduced exposure and efficacy.
Nitrofurantoin: (Major) Antacids can delay both the rate and the extent of GI absorption of nitrofurantoin. This interaction may be due to surface absorption of the antibacterial onto the antacid. Separate administration by at least 1 hour.
Norethindrone Acetate; Ethinyl Estradiol; Ferrous fumarate: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Norethindrone; Ethinyl Estradiol; Ferrous fumarate: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Octreotide: (Moderate) Coadministration of oral octreotide with antacids may require increased doses of octreotide. Coadministration of oral octreotide with drugs that alter the pH of the upper GI tract, including antacids, may alter the absorption of octreotide and lead to a reduction in bioavailability.
Omadacycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Pamidronate: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Pancrelipase: (Major) The effectiveness of gastrointestinal enzymes can be diminished with concurrent administration of antacids. In-vitro studies suggest that calcium and magnesum cations exert their deleterious effect on replacement enzyme therapy by formation of poorly soluble calcium or magnesium soaps and precipitation of glycine conjugated bile salts.
Pazopanib: (Moderate) Separate administration of pazopanib and antacids by several hours if coadministration is necessary in order to avoid a reduction in pazopanib exposure, which may decrease efficacy.
Penicillamine: (Moderate) Because penicillamine chelates heavy metals, it is possible that antacids could reduce penicillamine bioavailability, which can decrease the therapeutic effects of penicillamine. Simultaneous administration should be avoided; separate dosing by at least 2 hours to limit an interaction.
Phenobarbital; Hyoscyamine; Atropine; Scopolamine: (Moderate) Separate the time of administration of oral hyoscyamine and oral sodium bicarbonate by at least 2 hours. Simultaneous coadministration may decrease oral hyoscyamine absorption and reduce efficacy.
Phenytoin: (Moderate) Because the absorption of phenytoin suspension can be reduced by antacids containing magnesium, aluminum, or calcium, administration at the same time of day should be avoided when possible. Ingestion times of phenytoin capsules and calcium antacids should be staggered in patients with low serum phenytoin levels to prevent absorption difficulties. Studies evaluating the effects of magnesium-aluminium antacids on the absorption of phenytoin capsules or tablets have yielded conflicting results. Nevertheless, serum phenytoin levels and clinical response should be closely monitored if these agents are co-administered. The mechanisms by which antacids reduce phenytoin absorption may involve increased gastric transit time, chelation, adsorption, and/or altered solubility. The oral absorption of phenytoin may be reduced by calcium carbonate (e.g., as found in antacids) or other calcium salts. Calcium products may form complexes with phenytoin that are nonabsorbable. Although the magnitude of the interaction is not great, an occasional patient may be affected and the interaction may lead to subtherapeutic phenytoin concentrations. Separating the administration of phenytoin and antacids or calcium salts by at least 2 hours will help minimize the possibility of interaction.
Polyethylene Glycol; Electrolytes; Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with antacids can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid antacids within 1 hour before or after the bisacodyl dosage.
Polysaccharide-Iron Complex: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Propranolol: (Major) Antacids may reduce the absorption of propranolol. The need to stagger doses of propranolol has not been established, but may be prudent. Monitor clinical response, and adjust propranolol dosage if needed to attain therapeutic goals.
Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Pseudoephedrine; Triprolidine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Quinidine: (Major) Urinary alkalinization increases the renal tubular reabsorption of quinidine, resulting in higher quinidine serum concentrations which may lead to toxicity. Avoid citric acid; potassium citrate; sodium citrate administration to any patient receiving treatment with quinidine.
Quinine: (Moderate) Use caution if using citric acid and quinine concomitantly. Urinary alkalinizing agents may increase plasma quinine concentrations because quinine is reabsorbed when the urine is alkaline. (Moderate) Use caution if using sodium bicarbonate and quinine concomitantly. Urinary alkalinizing agents may increase plasma quinine concentrations because quinine is reabsorbed when the urine is alkaline.
Rifampin: (Moderate) Concomitant use of sodium bicarbonate and rifampin may decrease the absorption of rifampin. Daily doses of rifampin should be given at least 1 hour before the ingestion of sodium bicarbonate.
Rilpivirine: (Moderate) Concurrent administration of rilpivirine and antacids may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of antacids for at least 2 hours before and at least 4 hours after administering rilpivirine.
Risedronate: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
Ritonavir: (Moderate) Concurrent administration of tipranavir and ritonavir with antacids results in decreased tipranavir concentrations. Administer tipranavir and ritonavir 2 hours before or 1 hour after antacids.
Rosuvastatin: (Major) Coadministration of rosuvastatin with antacids has reduced rosuvastatin plasma concentrations by 54%. When the antacid is given 2 hours after rosuvastatin, no significant change in rosuvastatin plasma concentrations is observed.
Rosuvastatin; Ezetimibe: (Major) Coadministration of rosuvastatin with antacids has reduced rosuvastatin plasma concentrations by 54%. When the antacid is given 2 hours after rosuvastatin, no significant change in rosuvastatin plasma concentrations is observed. (Minor) Antacids may decrease the peak plasma concentration (Cmax) of total ezetimibe by 30%. The effect of the antacids in this regard is not expected to have a significant effect on the ability of ezetimibe to lower cholesterol. However, to limit any potential interaction, it would be prudent to administer ezetimibe at least 1 hour before or 2 hours after administering antacids.
Salsalate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Sarecycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Sodium Ferric Gluconate Complex; ferric pyrophosphate citrate: (Moderate) Doses of antacids and iron should be taken as far apart as possible to minimize the potential for interaction. Antacids may decrease the absorption of oral iron preparations. At higher pH values, iron is more readily ionized to its ferric state and is more poorly absorbed.
Sodium Fluoride: (Moderate) Absorption of sodium fluoride may be reduced by concomitant use of antacids. An interval of at least 2 hours is advisable between administration of sodium fluoride and antacids.
Sodium Polystyrene Sulfonate: (Moderate) Sodium polystyrene sulfonate should be used cautiously with other agents that can induce hypokalemia such as loop diuretics, insulins, or intravenous sodium bicarbonate. Because of differences in onset of action, sodium polystyrene sulfonate is often used with these agents. With appropriate monitoring, hypokalemia can be avoided.
Sotalol: (Major) Coadministration of antacids with sotalol reduces the Cmax and AUC of sotalol by 26% and 20%, respectively. This interaction results in a 25% reduction in the bradycardic effect of sotalol (measured at rest). Administer magnesium hydroxide two hours after the sotalol dose to avoid altering sotalol pharmacokinetics or pharmacodynamics.
Sparsentan: (Moderate) Administer sparsentan 2 hours before or after antacids. Simultaneous coadministration may decrease sparsentan exposure and efficacy. Medications that affect gastric pH may reduce sparsentan absorption.
Sucralfate: (Major) Antacids can interfere with the binding capacity of sucralfate to the GI mucosa, decreasing its effectiveness. Antacids should not be administered within 30 minutes of sucralfate.
Sumatriptan; Naproxen: (Minor) Concomitant administration of antacids can delay the absorption of naproxen. Periodic antacid use should not be problematic as long as the antacid and enteric-coated naproxen administration are separated by at least 2 hours.
Tacrolimus: (Moderate) Administration of oral tacrolimus at the same time as sodium bicarbonate may result in pH-dependent degradation of tacrolimus. Administer oral Tacrolimus 1 hour before or 2 hours after the Sodium Bicarbonate dose to help limit an interaction. Separation of the oral tacrolimus and sodium bicarbonate doses by at least 2 hours may not be necessary, but more data are needed. Tacrolimus concentrations can be maintained with appropriate monitoring and dosage adjustment. Intravenous and topical forms of tacrolimus do not interact.
Tetracycline: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Tetracyclines: (Major) Early reports noted an increase in the excretion of tetracyclines during coadministration with sodium bicarbonate, and that the oral absorption of tetracyclines is reduced by sodium bicarbonate via increased gastric pH. However, conflicting data have been reported, and further study is needed. Two recent studies show no effect of oral sodium bicarbonate administration on tetracycline oral bioavailability. In one of these trials, coadministration with sodium bicarbonate was reported to have no effect on tetracycline urinary excretion, Cmax, or AUC. Until more information is available, avoid simultaneous administration of sodium bicarbonate and tetracyclines. When concurrent therapy is needed, stagger administration times by several hours to minimize the potential for interaction, and monitor for antimicrobial efficacy.
Thiothixene: (Major) Antacids may reduce the oral availablility of thiothixene. To avoid this, administer thiothixene at least 1 hour before or 2 hours after the antacid.
Tolmetin: (Major) The bioavailability of tolmetin is decreased by sodium bicarbonate. Do not use a sodium bicarbonate containing antacid concurrently with tolmetin.
Tramadol; Acetaminophen: (Minor) Antacids can delay the oral absorption of acetaminophen, but the interactions are not likely to be clinically significant as the extent of acetaminophen absorption is not appreciably affected.
Trospium: (Moderate) Antacids may inhibit the oral absorption of antimuscarinics. Simultaneous oral administration should be avoided when feasible; separate dosing by at least 2 hours to limit an interaction.
Valproic Acid, Divalproex Sodium: (Minor) Sodium bicarbonate may increase valproic acid AUC. Patients should be monitored for adverse effects in this situation.
Zoledronic Acid: (Moderate) Sodium bicarbonate can reduce the absorption of the oral bisphosphonates. Wait at least 30 minutes after oral alendronate, 1 hour after ibandronate, and 2 hours after oral etidronate, risedronate, or tiludronate before taking a sodium bicarbonatecontaining product.
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.
Sodium bicarbonate is administered orally and intravenously. Sodium bicarbonate is not metabolized, and bicarbonate ions are filtered and reabsorbed by the kidneys.
-Route-Specific Pharmacokinetics
Oral Route
Sodium bicarbonate is rapidly absorbed following an oral dose, entering the blood as bicarbonate and sodium ions.