Published ahead of print on July 26, 2007, doi:10.1164/rccm.200702-193OC Am. J. Respir. Crit. Care Med., Volume 176, Number 8, October 2007, 761-767 A more recent version of this article appeared on October 15, 2007
Submitted on February 5, 2007 ARDSnet Ventilatory Protocol and Alveolar Hyperinflation: Role of Positive End-Expiratory PressureSalvatore Grasso1*,1 Dipartimento dell'Emergenza e Trapianti d'Organo (DETO), Sezione di Anestesiologia e Rianimazione, Universita degli Studi di Bari, Bari, Italy, 2 Dipartimento di Medicina interna e Medicina Pubblica (DiMIMP), Sezione di Diagnostica per Immagini, Universita degli Studi di Bari, Bari, Italy, 3 Dipartimento di Medicina Clinica Immunologia e Malattie Infettive, Universita degli Studi di Bari, Bari, Italy, 4 Ospedale Di Venere, Servizio di Anestesia e Rianimazione, Azienda Sanitaria Locale Bari-4, Bari, Italy, 5 Department of Clinical Studies-NBC, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA, USA; Department of Anesthesiology, David Geffen School of Medicne at UCLA, Los Angeles, CA, USA * To whom correspondence should be addressed. E-mail: grassos{at}libero.it.
Rationale: In patients with acute respiratory distress syndrome, a focal distribution of loss of aeration in lung computed tomography predicts low potential for alveolar recruitment and susceptibility to alveolar hyperinflation with high levels of positive end-expiratory pressure. Objectives: We tested the hypothesis that in this cohort of patients the table-based positive end-expiratory pressure setting criteria of the National Heart, Lung and Blood Institute ARDS Network (ARDSnet) low tidal volume ventilatory protocol could induce tidal alveolar hyperinflation. Measurements and main results: In 15 patients, physiologic parameters and plasma inflammatory mediators were measured during two ventilatory strategies, randomly applied: the ARDSnet and the stress index strategy. The latter employed the same ARDSnet ventilatory pattern except for the positive end-expiratory pressure level, which was adjusted based on the stress index, a monitoring tool intended to quantify tidal alveolar hyperinflation and/or recruiting/de-recruiting that occurs during constant-flow ventilation, on a breath by breath basis. In all patients the stress index revealed alveolar hyperinflation during application of the ARDSnet strategy and consequently positive end-expiratory pressure was significantly decreased (p < 0.01) in order to normalize the stress index value. Static lung elastance (p = 0.01), plasma concentrations of interleukin-6 (p < 0.01), interleukin-8 (p= 0.031) and soluble tumor necrosis factor receptor I (p = 0.013) were significantly lower during the stress index as compared to the ARDSnet strategy-guided ventilation. Conclusion: Alveolar hyperinflation in patients with focal acute respiratory distress syndrome ventilated with the ARDS Network protocol is attenuated by a physiological approach to positive end expiratory pressure setting based on the stress index measurement. Key words: Acute lung injury; inflammatory response; mechanical ventilation; VILI
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