Antacids neutralize the acidity of gastric fluid by providing a base (usually hydroxide, carbonate, bicarbonate, citrate, or trisilicate) that reacts with hydrogen ions to form water.
Common uses of antacids include the treatment of gastric and duodenal ulcers, GERD, and Zollinger– Ellison syndrome. In anesthesiology, antacids provide protection against the harmful effects of aspiration pneumonia by raising the pH of gastric contents. Unlike H 2-receptor antagonists, antac-ids have an immediate effect. Unfortunately, they increase intragastric volume. Aspiration of particu-late antacids (aluminum or magnesium hydroxide) produces abnormalities in lung function compa-rable to those that occur following acid aspiration. Nonparticulate antacids (sodium citrate or sodium bicarbonate) are much less damaging to lung alveoli if aspirated. Furthermore, nonparticulate antacids mix with gastric contents better than particulate solutions. Timing is critical, as nonparticulate antac-ids lose their effectiveness 30–60 min after ingestion.
The usual adult dose of a 0.3 M solution of sodium citrate—Bicitra (sodium citrate and citric acid) or Polycitra (sodium citrate, potassium citrate, and citric acid)—is 15–30 mL orally, 15–30 min prior to induction.
Because antacids alter gastric and urinary pH, they change the absorption and elimination of many drugs. The rate of absorption of digoxin, cimetidine, and ranitidine is slowed, whereas the rate of pheno-barbital elimination is quickened.
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