Clinical review: Ventilator-induced diaphragmatic dysfunction - human studies confirm animal model findings!
1 Department of Critical Care and Anesthesiology (DAR B), CHU Montpellier, Hôpital Saint Eloi, 80 avenue Augustin Fliche, 34295 Montpellier Cedex 5, France
2 Intensive Care Unit, Anesthesia and Critical Care Department B, Saint Eloi Teaching Hospital, Equipe soutenue par la Région et l'Institut National de la Santé et de la Recherche Médicale 25, Université Montpellier 1, Centre Hospitalier Universitaire Montpellier, Montpellier 34000, France
3 Clinical Physiology Center, Arnaud de Villeneuve Teaching Hospital, Equipe soutenue par la Région et l'Institut National de la Santé et de la Recherche Médicale 25, Université Montpellier 1, Centre Hospitalier Universitaire Montpellier, Montpellier 34000, France
4 Meakins-Christie Laboratories and Respiratory Division, McGill University Health Center and Research Institute, Montreal, Quebec H2X 2P2, Canada
Critical Care 2011, 15:206 doi:10.1186/cc10023Published: 11 March 2011
Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation. However, the use of controlled mechanical ventilation in animal models results in a major reduction of diaphragmatic force-generating capacity together with structural injury and atrophy of diaphragm muscle fibers, a condition termed ventilator-induced diaphragmatic dysfunction (VIDD). Increased oxidative stress and exaggerated proteolysis in the diaphragm have been linked to the development of VIDD in animal models, but much less is known about the extent to which these phenomena occur in humans undergoing mechanical ventilation in the ICU. In the present review, we first briefly summarize the large body of evidence demonstrating the existence of VIDD in animal models, and outline the major cellular mechanisms that have been implicated in this process. We then relate these findings to very recently published data in critically ill patients, which have thus far been found to exhibit a remarkable degree of similarity with the animal model data. Hence, the human studies to date have indicated that mechanical ventilation is associated with increased oxidative stress, atrophy, and injury of diaphragmatic muscle fibers along with a rapid loss of diaphragmatic force production. These changes are, to a large extent, directly proportional to the duration of mechanical ventilation. In the context of these human data, we also review the methods that can be used in the clinical setting to diagnose and/or monitor the development of VIDD in critically ill patients. Finally, we discuss the potential for using different mechanical ventilation strategies and pharmacological approaches to prevent and/or to treat VIDD and suggest promising avenues for future research in this area.