Mechanism of Action
As a systemic antacid, sodium bicarbonate directly reacts chemically with hydrochloric acid ($HCl$) in the stomach, rapidly neutralizing it. However, this process is accompanied by vigorous carbon dioxide ($CO_2$) gas evolution.
As an agent affecting excretion, intravenous administration of the drug causes urinary alkalinization (increasing the pH of the renal filtrate). According to the ion trapping principle, in an alkaline environment weak acids (e.g., barbiturates, acetylsalicylic acid, sulfonamides) become ionized. The ionized (polar) form cannot cross the lipid membranes of the renal tubules, loses the ability to undergo passive reabsorption, and is actively eliminated from the body.
Pharmacological Effects
The drug provides an immediate, albeit short-lived, reduction in gastric acidity. Upon systemic absorption, sodium bicarbonate shifts the acid-base balance toward alkalinity, causing systemic alkalosis. When excreted via the kidneys, urinary alkalinization accelerates the elimination of weak acids, which is utilized to speed up drug clearance during overdoses and poisonings.
Indications
Sodium bicarbonate is indicated for:
- Hyperacidity and heartburn (as symptomatic therapy to relieve pain during peptic ulcer disease exacerbations);
- Poisoning and overdoses with weak acid medications (for forced elimination via urinary alkalinization);
- Metabolic acidosis.
Adverse Effects and Contraindications
Adverse Effects:
- Gastric distension caused by evolving carbon dioxide, which provokes secondary gastric acid hypersecretion (the "rebound" effect);
- Development of systemic alkalosis with frequent and uncontrolled use.
Contraindications:
- Alkalosis of any etiology.
Clinical Administration
The drug is available as 0.3 g and 0.5 g tablets. The standard oral dosage is 0.5–1.0 g per dose. In forced diuresis and acute poisoning settings, it is administered parenterally (intravenously) to rapidly alter the pH of the renal filtrate.