Tops (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.

Antacids are administered orally. The dose of antacids should be expressed in terms of mEq of acid neutralizing capacity. Dose and frequency of administration depend on the acid secretory rate of the stomach, gastric emptying time, and the disorder being treated. The duration of action of antacids is determined principally by gastric emptying time. In fasting subjects, antacids have a duration of action of 20-60 minutes. However, if the drugs are administered 1 hour after meals, acid neutralizing effects may persist up to 3 hours. Sodium bicarbonate generally has a shorter duration of action than other antacids. Antacids should be used for longer than 2-week periods only under the management of a physician and as part of a carefully planned therapeutic regimen.

There is considerable variation in in vivo acid neutralizing capacity of equal volumes of different antacids and antacid products. Since suspensions are more rapidly and effectively solubilized than powders or tablets, antacid suspensions have a greater ability to react with and neutralize gastric acid. Antacid suspensions have a smaller particle size than do tablets and drying of antacid suspensions to prepare powders and tablets causes substantial loss of ability to neutralize acid. In general, an antacid suspension is preferable to a tablet or powder; tablets should be reserved for chronic use in patients who refuse suspensions because they are inconvenient or unpalatable. Tablets should be thoroughly chewed before swallowing.

The US Food and Drug Administration (FDA) requires that antacids have a minimum in vitro acid neutralizing capacity of 5 mEq per dose and that antacid labeling contain the in vitro acid neutralizing capacity; however, this FDA in vitro test does not correlate with in vivo acid neutralizing capacity.

For peptic ulcer disease, dosages of antacids are empirical and various antacid dosages have been used. In patients with uncomplicated duodenal ulcers or gastric ulcers, an antacid is administered 1 and 3 hours postprandially and at bedtime. In patients with duodenal ulcers, antacids are usually given for 4-6 weeks, and in patients with gastric ulcers, antacids are administered until healing is complete. If symptoms of duodenal ulcer recur, some clinicians recommend that antacids be administered 1 and 3 hours postprandially and at bedtime for 1 week and, if pain is relieved, less frequently for an additional 1-2 weeks; these patients should consult their physicians if pain worsens or is not relieved after the first week of therapy. Additional doses of antacids may be administered to relieve ulcer pain which occurs between regularly scheduled doses.

For the acute management of moderate or severe esophageal reflux, an antacid suspension is administered every hour; if symptoms persist, antacids may be given every 30 minutes. For long-term therapy of esophageal reflux, antacids are administered 1 and 3 hours postprandially and at bedtime and whenever symptoms recur.

In the management of GI bleeding and stress ulceration, antacids are usually administered every hour and, for GI bleeding, the antacid dosage should be titrated to maintain the nasogastric aspirate above pH 3.5. For severe symptoms, antacid suspensions may be diluted with water or milk and given by continuous intragastric infusion.

To reduce the risk of anesthesia-induced gastric acid aspiration, an antacid suspension has been given 30 minutes before anesthesia.

In conjunction with dietary phosphate restriction in the management of hyperphosphatemia, 30-40 mL of aluminum hydroxide or aluminum carbonate suspension is administered 3 or 4 times daily.

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All antacids potentially may increase or decrease the rate and/or extent of absorption of concomitantly administered oral drugs by changing GI transit time or by binding or chelating the drug. In vitro studies indicate that magnesium hydroxide or trisilicate has the greatest potential for drug binding and aluminum hydroxide and calcium carbonate are intermediate. Antacid-induced increases in GI pH may affect the disintegration, dissolution, solubility, or ionization of enteric-coated preparations and weakly acidic or basic drugs.

Simultaneous administration of aluminum-, calcium-, or magnesium-containing antacids with orally administered tetracyclines reduces the absorption of the tetracycline, probably because of chelation of these antacids by the tetracycline. Therefore, doses of tetracyclines should be spaced 1-2 hours from doses of antacids.

Concurrent administration of antacids and orally administered digoxin, indomethacin, or iron salts may decrease the absorption of these drugs. Doses of these drugs should be spaced as far apart as possible from doses of antacids. Concurrent administration of isoniazid and aluminum hydroxide gel may decrease the absorption of isoniazid; therefore, isoniazid should be administered at least 1 hour before aluminum-containing antacids. Absorption of buffered or enteric-coated aspirin is increased by simultaneous administration of antacids. Antacid-induced changes in urine pH increase urinary excretion and decrease blood concentrations of salicylates. Concurrent administration of dicumarol and an aluminum and magnesium hydroxides preparation reportedly increases the absorption of dicumarol; patients receiving antacids and oral anticoagulants should probably use warfarin rather than dicumarol. Concurrent administration of aluminum hydroxide and pseudoephedrine or diazepam increases the rate of absorption of the latter drugs. Administration of a magnesium and aluminum hydroxide preparation with chlordiazepoxide decreases the rate of chlordiazepoxide absorption. Administration of sodium bicarbonate with naproxen increases the rate of naproxen absorption, while concurrent administration of magnesium oxide or aluminum hydroxide with naproxen decreases the rate of naproxen absorption.

Antacid-induced increases in urine pH may decrease excretion of weakly basic drugs and increase excretion of weakly acidic drugs. Urinary excretion of amphetamines and quinidine are markedly decreased in patients whose urine is alkalinized with sodium bicarbonate and patients receiving these drugs concomitantly may have increased amphetamine or quinidine effects.

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

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

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

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

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.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

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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.