Acid-suppressive therapy with proton-pump inhibitors, such as pantoprazole, significantly increases the risk of hospital-acquired pneumonia, community-acquired pneumonia, and intestinal infections like C-difficile. Histamine-2-receptor antagonists, such as famotidine, did not increase the incidence of hospital-acquired pneumonia in a recent study.
Proton-pump inhibitors decrease stomach acid by blocking the mechanism (pump) that pushes acid into the stomach, thereby decreasing the amount of acid in the stomach and lowering the risk of ulceration. The unwanted side effect of decreasing stomach acid is that gastric contents become less acidic and make the stomach a better place for bacteria to live. Bacteria like C-difficile are not killed by the stomach acid and can reproduce and cause infection. In addition, microaspirations occur in most people (70% have some gastric reflux) and small amounts of gastric secretions migrate up to the trachea and into the lung causing infection.
It is important to prevent your patient from developing gastric ulceration, but it is equally important to know that proton-pump inhibitors increase the risk of pneumonia and to implement interventions to prevent pneumonia. Coughing, deep breathing, and incentive spirometry are part of a plan of great pulmonary hygiene that can help prevent pneumonia. Brushing the patient's teeth every 12 hours is the best intervention for preventing pneumonia.
Pantoprazole is metabolized by the liver and excreted in the urine, but rarely causes damage to either of these organs. Pantoprazole would not cause coronary artery spasm because it does not have vasoactive effects.
From: Herzig, S.J. et al. (2009). Acid-suppressive medication and the risk for hospital-acquired pneumonia. JAMA, May 29; 301:2120.