Study objective: To study the hemodynamic effects of famotidine administered undiluted intravenously over 2 minutes.
Design: Nonblinded, nonrandomized.
Setting: Medical/surgical intensive care unit in a university-affiliated, tertiary care, teaching hospital.
Patients: Eleven consecutive critically ill patients receiving famotidine for stress ulcer prophylaxis. Seven of these patients were also receiving vasopressors or inotropes.
Interventions: Famotidine 20 mg/2 ml was administered intravenously undiluted through a peripheral line over 2 minutes. All other medications, including vasopressors and inotropes, were held constant.
Measurements and main results: No clinically important (> 20 variations from baseline) or statistically significant (p < 0.05) changes were seen in heart rate, mean pulmonary arterial pressure, cardiac output, systolic/diastolic blood pressure, systemic vascular resistance, or central venous pressure. Mean arterial pressure (MAP) was elevated at 8 minutes following famotidine (91.2 mm Hg [22.4 SD]) versus baseline (86.7 mm Hg [19.6 SD]). Pulmonary capillary wedge pressure (PCWP) was elevated at 8 minutes (17.2 mm Hg [6 SD]), 12 minutes (17.9 mm Hg [5.68 SD]), and 16 minutes (17.8 mm Hg [6.08 SD]), versus baseline (14.8 mm Hg [7.14 SD]). These changes in MAP and PCWP achieved statistical significance, but were not thought to be of clinical significance.
Conclusions: Famotidine given undiluted intravenously over 2 minutes produced no adverse hemodynamic effects in critically ill patients. Administration in this manner should be safe even in patients requiring supportive cardiovascular drug therapy.