Inhaled epoprostenol for management of acute respiratory failure and pulmonary vascular disease
- PMID: 40513981
- PMCID: PMC12261948
- DOI: 10.1016/j.pupt.2025.102374
Inhaled epoprostenol for management of acute respiratory failure and pulmonary vascular disease
Abstract
Inhaled epoprostenol has remained an attractive and viable option for the delivery of prostacyclin to offset abnormalities in ventilation and perfusion mismatch while minimizing the typical adverse effects associated with systemic administration. There is a need to better understand pharmacologic properties of inhaled epoprostenol and its application to diseases affecting the cardiopulmonary system. The goal of this review is to provide an overview of inhaled epoprostenol and outline its use specifically in the medical management of acute hypoxemic respiratory failure and pulmonary vascular disease. Among patients with acute respiratory distress syndrome who ultimately required invasive ventilation, inhaled epoprostenol has not improved ventilator-free days, intensive care unit length of stay, or mortality. However, it may be beneficial in certain select patient populations. In the management of pulmonary hypertension, inhaled epoprostenol has allowed for continued maintenance of chronic pulmonary arterial hypertension-specific therapy and for possibly improving right ventricular function as an attractive option in the critical care management of pulmonary hypertension.
Copyright © 2025 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Nicholas A. Bosch reports financial support was provided by National Heart Lung and Blood Institute. Nicholas A. Bosch reports financial support was provided by Agency for Healthcare Research and Quality. Nicholas A. Bosch reports financial support was provided by American Heart Association. Elizabeth S. Klings reports financial support was provided by National Heart Lung and Blood Institute. Elizabeth S. Klings reports financial support was provided by National Center for Advancing Translational Sciences. Elizabeth S. Klings reports financial support was provided by Health Resources and Services Administration. Elizabeth S. Klings reports financial support was provided by Novo Nordisk. Elizabeth S. Klings reports financial support was provided by Novartis. Elizabeth S. Klings reports financial support was provided by United Therapeutics Corporation. Justin K. Lui reports financial support was provided by American Heart Association. Justin K. Lui reports financial support was provided by National Scleroderma Foundation. Elizabeth S. Klings reports a relationship with Novo Nordisk that includes: board membership and funding grants. Elizabeth S. Klings reports a relationship with Novartis that includes: board membership and funding grants. Elizabeth S. Klings reports a relationship with United Therapeutics Corporation that includes: board membership and funding grants. Justin K. Lui reports a relationship with United Therapeutics Corporation that includes: funding grants within the past 2 years (None currently). If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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