[Hemodynamic effects of intravenous omeprazole in critically ill children.]

Unidad de Cuidados Intensivos Pediátricos, Hospital General Universitario Gregorio Marañón, Madrid, España.
Anales de Pediatría (Impact Factor: 0.83). 07/2012;
Source: PubMed


INTRODUCTION: Critical patients usually have hemodynamic disturbances which may become worse by the administration of some drugs. Omeprazole is a drug used in the prophylaxis of the gastrointestinal bleeding in these patients, but its cardiovascular effects are unknown. The objective was to study the hemodynamic changes produced by intravenous omeprazole in critically ill children and to find out if there are differences between two different doses of omeprazole. MATERIAL AND METHODS: A randomized prospective observational study was performed on 37 critically ill children aged from 1 month to 14 years of age who required prophylaxis for gastrointestinal bleeding. Of these, 19 received intravenous omeprazole 0.5mg/kg every 12hours, and 18 received intravenous omeprazole 1mg/kg every 12hours. Intravenous omeprazole was administered in 20minutes by continuous infusion pump. Heart rate, systolic, diastolic and mean arterial blood pressure, central venous pressure and ECG were recorded at baseline, and at 15, 30, 60 and 120minutes of the infusion. RESULTS: There were no significant changes in the electrocardiogram, heart rate, blood pressure and central venous pressure. No patients required inotropic therapy modification. There were no differences between the two doses of omeprazole. CONCLUSIONS: Intravenous omeprazole administration of 0.5mg/kg and 1mg/kg is a hemodynamically safe drug in critically ill children.

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    ABSTRACT: Background Pantoprazole has been shown to exert a negative inotropic effect in isolated myocardium. The purpose of this study was to evaluate the hemodynamic effects of pantoprazole in vivo in healthy myocardium and in the setting of heart failure.Methods and ResultsHealthy mice and mice with heart failure 4 weeks after myocardial infarction induced by permanent LAD ligation were instrumented with a Millar Mikrotip conductance catheter to record pressure-volume loops. Pantoprazole was infused at rates of 3 and 10mg/kg/min intravenously and hemodynamic parameters were recorded.Infusion of pantoprazole at increasing rates lead to a significant decline in end systolic LV pressure by decreasing heart rate, myocardial contractility and arterial elastance. These effects were quick, beginning immediately with the infusion and usually reaching a plateau after 2 or 3 minutes of infusion. The effects on blood pressure and heart rate were of comparable size in healthy mice and mice with MI. However in sham-operated mice there was a compensatory increase in stroke volume that sufficed to maintain cardiac output at a constant level, which was missing in mice with MI. In 4 out of 13 mice with MI infusion of 10mg/kg/min pantoprazole lead to pump failure, which was lethal in 2 of these animals.Conclusion At higher infusion rates pantoprazole is able to induce negative hemodynamic responses. Especially in the setting of heart failure these effects can lead to significant impairment of cardiac function. Therefore high infusion rates of pantoprazole should be avoided especially in heart failure patients.This article is protected by copyright. All rights reserved.
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