Sodium Bicarbonate (sodium bicarbonate)

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

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

Generally, full correction of bicarbonate deficit should not be attempted during the first 24 hours of sodium bicarbonate therapy, since this may result in precipitation of metabolic alkalosis because of delayed physiologic compensatory mechanisms. Due to this delay, reaching a total CO2 content of approximately 20 mEq/liter by the end of the first day of treatment is typically linked to a normal blood pH. Further correction of the acidosis to fully normal levels usually happens if the kidney function is normal and if and when the underlying cause of the acidosis can be controlled. If total CO2 levels are normalized or brought above normal within the first day, this may likely result in an excessively high (alkaline) blood pH, which can lead to undesired side effects.

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

No dosing information is available for this tab.

No dosing information is available for this tab.

No dosing information is available for this tab.

There is no enhanced messaging for this drug.

Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

Urinary Alkalinizers/Methenamine

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Urinary alkalinizers may elevate urinary ph preventing the conversion of methenamine to formaldehyde and mandelic acid.(1)

CLINICAL EFFECTS: Concurrent administration may result in alkalinization of the urine causing methenamine to be less effective.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The Australian and UK manufacturers of methenamine state that concurrent use with agents that make urine alkaline or urine alkalinizing agents should be avoided.(2,3) Patients receiving concurrent therapy should be monitored for urinary ph and any worsening symptoms of their infection, including dysuria, flank pain, or fever.(1)

DISCUSSION: Administration of urinary alkalinizers may result in alkalinization of the urine resulting in therapeutic failure of methenamine. Formaldehyde is released by acid hydrolysis from methenamine resulting in bactericidal concentrations at urinary ph 5.0 to 5.5. Above urinary ph 6.0 there is insufficient quantities of formaldehyde and methenamine released to achieve a therapeutic response.(1) An in vitro study showed that methenamine efficacy is achieved when the urine pH is less than 5.7 to 5.85.(4)

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Urinary Alkalinizers/Dextroamphetamine Transdermal

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Urinary alkalinizers decrease the renal elimination of dextroamphetamine.(1)

CLINICAL EFFECTS: Concurrent use of dextroamphetamine and urinary alkalinizers may result in increased dextroamphetamine levels and side effects.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Coadministration of dextroamphetamine with urinary alkalinizing agents should be avoided.(1)

DISCUSSION: Concurrent use of alkalinizing agents with dextroamphetamine decreases the renal elimination of dextroamphetamine. Co-administration of these should be avoided because of the potential of increased actions of dextroamphetamine.(1)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Urinary Alkalinizers/Memantine; Amantadine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Memantine and amantadine elimination is impaired by urinary alkalinization.(1,2)

CLINICAL EFFECTS: Potentiation of memantine or amantadine effects may be observed.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitor patient for adverse reactions such as dizziness, headache, or confusion if a urinary alkalinizer is required. The memantine or amantadine dose may need to be adjusted when a urinary alkalinizer is started or stopped.(1,2)

DISCUSSION: The clearance of memantine was reduced by about 80% under alkaline urine conditions at pH 8. Urine alkalinization may lead to an accumulation of memantine with a possible increase in adverse effects. Urine pH is also altered by diet and clinical state of the patient (e.g., renal tubular acidosis or severe infections of the urinary tract). Hence, memantine should be used with caution under these conditions.(1) A study in rats showed that concomitant administration of sodium bicarbonate with amantadine caused a decrease in amantadine renal clearance (1.16 vs. 0.76). Amantadine's area-under-the-curve (AUC) was increased approximately 78%.(3) A study in 12 healthy subjects showed that plasma concentrations of memantine are dependent on urine pH. Alkaline urine pH caused a 79% reduction in renal clearance.(4)

Urinary Alkalinizers/Quinidine

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Quinidine elimination is impaired by urinary alkalinization.

CLINICAL EFFECTS: Potentiation of quinidine effects may be observed.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitoring quinidine levels and cardiac function may be indicated. The quinidine dose may need to be adjusted when a urinary alkalinizer is started or stopped.

DISCUSSION: Additional documentation is necessary to confirm this potential interaction.

Urinary Alkalinizers/Sympathomimetics

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Unionized sympathomimetic amines will be reabsorbed into systemic circulation from the distal tubules of the kidneys.

CLINICAL EFFECTS: Enhanced sympathomimetic activity and increased risk of sympathomimetic toxicity.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Watch patient for enhanced sympathomimetic side effects when urinary alkalinizers are concomitantly used. A lower dose of certain sympathomimetics may be required.

DISCUSSION: Signs and symptoms of sympathomimetic toxicity include euphoria, confusion, delirium, hallucinations and nervousness.

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

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

• Hypochloremia
• Metabolic alkalosis

• Anuria
• Chronic heart failure
• Edema
• Hypocalcemia
• Hypokalemia
• Severe renal impairment

• Oliguria

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

Rare or Very Rare

• Hypocalcemia
• Hypokalemia
• Metabolic alkalosis

Rare or Very Rare

• Cellulitis
• Edema

No enhanced messaging available.

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

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

The manufacturer provides no specific information for use of sodium bicarbonate during breast-feeding.

The manufacturer makes no specific dosage recommendations for geriatric patients. In general, dosage selection for geriatric patients should be cautious, usually starting at the low end of the dosing range, reflecting the higher incidence of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy.

Clinical studies of sodium bicarbonate did not include sufficient numbers of patients >=65 years of age to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between geriatric and younger patients.

In general, dosage selection for geriatric patients should be cautious, usually starting at the low end of the dosing range, reflecting the higher incidence of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy.