Sodium Bicarbonate Injection

Sodium bicarbonate is a systemic alkalinizing agent. It most often is administered IV in the treatment of metabolic and respiratory acidosis. Sodium bicarbonate is also used in the acute treatment of hyperkalemia, although it should be kept in mind that this represents palliative treatment for this condition. Sodium bicarbonate is sometimes used for urinary alkalinization. Despite being a highly effective antacid, sodium bicarbonate is rarely used for the chronic treatment of peptic ulcer disease because it can be absorbed and can affect systemic acid-base balance. Sodium bicarbonate was in use prior to 1938 and approved by the FDA at its inception.

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

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

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

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

Sodium bicarbonate pharmaceutical products (e.g., oral tablets, injectable solution) are classified as FDA pregnancy risk category C. Although no untoward effects have been observed in humans, chronic use sodium bicarbonate may lead to systemic alkalosis, which may threaten maternal-fetal health. Increased sodium intake can produce edema and weight increase from fluid retention. The American Gastroenterological Association considers sodium bicarbonate-containing antacids unsafe in pregnancy; there are many other antacids, such as occasional use of calcium carbonate, that are considered appropriate for occasional use for dyspepsia. Sodium bicarbonate may be used parenterally when critical for the health of the mother. Due to radiographic use, Baros effervescent granules for imaging studies would not be indicated in pregnancy.

Sodium bicarbonate has no specific precautions for use in breastfeeding women. The American Gastroenterological Association states that sodium bicarbonate antacids represent a low risk to the infant when used during breastfeeding. Chronic or indiscriminate use may result in metabolic alkalosis or sodium and fluid retention in the mother. In general, there are other antacids (e.g., calcium carbonate, magnesium hydroxide) that are generally preferred for antacid use due to wider safety margins. Consider the benefits of breastfeeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breastfeeding infant experiences an adverse effect related to a maternally administered drug, healthcare providers are encouraged to report the adverse effect to the FDA.

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.

Store this medication at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.

Learn how to prepare medication for self-administered injection.

1.Mahadevan U, Kane S. American Gastroenterological Association Institute technical review on the use of gastrointestinal medications in pregnancy. Gastroenterology 2006;131:283-311.
2.Sodium bicarbonate package insert. Lake Forest, IL: Hospira Inc; 2012 October.