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ARDSnet Ventilatory Protocol and Alveolar Hyperinflation

Role of Positive End-Expiratory Pressure

¹ Dipartimento dell'Emergenza e Trapianti d'Organo (DETO), Sezione di Anestesiologia e Rianimazione; ² Dipartimento di Medicina interna e Medicina Pubblica (DiMIMP), Sezione di Diagnostica per Immagini; and ³ Dipartimento di Medicina Clinica Immunologia e Malattie Infettive, Università degli Studi di Bari, Bari, Italy; ⁴ Azienda Sanitaria Locale Bari-4, Ospedale Di Venere, Servizio di Anestesia e Rianimazione, Bari, Italy; ⁵ Department of Clinical Studies–NBC, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, Pennsylvania; and ⁶ Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California

Correspondence and requests for reprints should be addressed to S. Grasso, M.D., Università di Bari, Dipartimento dell'Emergenza e Trapianti d'Organo (DETO), Sezione di Anestesiologia e Rianimazione, Ospedale Policlinico, Piazza Giulio Cesare 11, Bari 70124, Italy. E-mail: grassos{at}libero.it

Rationale: In patients with acute respiratory distress syndrome (ARDS), 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 (PEEP).

Objectives: We tested the hypothesis that, in this cohort of patients, the table-based PEEP setting criteria of the National Heart, Lung, and Blood Institute's ARDS Network (ARDSnet) low tidal volume ventilatory protocol could induce tidal alveolar hyperinflation.

Methods: In 15 patients, physiologic parameters and plasma inflammatory mediators were measured during two ventilatory strategies, applied randomly: the ARDSnet and the stress index strategy. The latter used the same ARDSnet ventilatory pattern except for the PEEP level, which was adjusted based on the stress index, a monitoring tool intended to quantify tidal alveolar hyperinflation and/or recruiting/derecruiting that occurs during constant-flow ventilation, on a breath-by-breath basis.

Measurements and Main Results: In all patients, the stress index revealed alveolar hyperinflation during application of the ARDSnet strategy, and consequently, PEEP was significantly decreased (P < 0.01) 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 with the ARDSnet strategy–guided ventilation.

Conclusions: Alveolar hyperinflation in patients with focal ARDS ventilated with the ARDSnet protocol is attenuated by a physiologic approach to PEEP setting based on the stress index measurement.

Key Words: acute lung injury • inflammatory response • mechanical ventilation • ventilator-induced lung injury

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Mechanical ventilation may exacerbate lung injury in patients with acute respiratory distress syndrome (ARDS) causing tidal alveolar hyperinflation. The ARDSnet protective ventilatory protocol was intended to minimize hyperinflation by applying low tidal volumes. What This Study Adds to the Field We found evidence of alveolar hyperinflation in patients with focal ARDS ventilated with the ARDSnet protocol. Individual positive end-expiratory pressure titration based on the "stress index" monitoring reduced the risk of alveolar hyperinflation.

 

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