Mechanism of paracetamol-induced hypotension in critically ill patients: A prospective observational cross-over study
| Autor: | František Duška, Adéla Krajčová, Vojtěch Matoušek |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Male
Mean arterial pressure Cardiac output Antipyretics Critical Illness Cardiac index Emergency Nursing Critical Care Nursing Body Temperature law.invention law medicine Humans Prospective Studies Antipyretic Infusions Intravenous Acetaminophen Aged Cross-Over Studies business.industry organic chemicals digestive oral and skin physiology Hemodynamics Middle Aged Intensive care unit Crossover study medicine.anatomical_structure Anesthesia Vascular resistance Female Hypotension business medicine.drug |
| Zdroj: | Australian Critical Care. 26:136-141 |
| ISSN: | 1036-7314 |
| DOI: | 10.1016/j.aucc.2012.02.002 |
| Popis: | Summary Objective To elucidate the mechanism of hypotension following intravenous administration of paracetamol (acetaminophen) to patients on the Intensive Care Unit. Design Prospective observational cross-over study. Setting Intensive Care Unit, University Hospital Kralovske Vinohrady, Prague, Czech Republic. Methods Ventilated critically ill patients monitored by PiCCO and administered intravenous paracetamol at the same time were eligible for the study. We recorded haemodynamic indices, as well as core and peripheral temperatures, continuously for 3 h after the dose of paracetamol. Ranitidine was then used as a control drug known not to influence haemodynamics. Results We included 6 subjects, and recorded 48 cycles of observations after administration of paracetamol, and 35 cycles after administration of the control drug. Haemodynamic parameters were not different at the baseline and administration of control drug did not result in any change in haemodynamics. After intravenous paracetamol, mean arterial pressure (MAP) dropped by 7% (p 15% reduction in MAP with paracetamol. Analysis of these cycles suggests that hypotension with paracetamol can be caused by reduction of both cardiac index and systemic vascular resistance. In febrile cycles paracetamol caused narrowing of the gradient between central and peripheral temperatures suggesting skin vasodilation. These changes were not correlated to a change of systemic vascular resistance at any time point. Conclusion Hypotension with intravenous paracetamol in critically ill patients is caused by a reduction of both cardiac output and systemic vascular resistance. We did not demonstrate any relation between haemodynamic changes and antipyretic action of paracetamol. A possibility that cardiac output is reduced with paracetamol might be clinically important. |
| Databáze: | OpenAIRE |
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