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Published ahead of print on October 12, 2006, doi:10.1164/rccm.200607-915OC
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American Journal of Respiratory and Critical Care Medicine Vol 175. pp. 160-166, (2007)
© 2007 American Thoracic Society
doi: 10.1164/rccm.200607-915OC


Original Article

Tidal Hyperinflation during Low Tidal Volume Ventilation in Acute Respiratory Distress Syndrome

Pier Paolo Terragni, Giulio Rosboch, Andrea Tealdi, Eleonora Corno, Eleonora Menaldo, Ottavio Davini, Giovanni Gandini, Peter Herrmann, Luciana Mascia, Michel Quintel, Arthur S. Slutsky, Luciano Gattinoni and V. Marco Ranieri

Dipartimento di Anestesiologia e Rianimazione, and Dipartimento di Radiologia, Università di Torino, Ospedale S. Giovanni Battista-Molinette, Turin; Istituto di Anestesia e Rianimazione, Fondazione Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale Maggiore Policlinico, Mangiagalli, Regina Elena di Milano, Milan; Università degli Studi di Milano, Milan, Italy; Department of Anesthesiology, University of Göttingen, Göttingen, Germany; and Interdepartmental Division of Critical Care, Division of Respiratory Medicine, University of Toronto, St. Michael's Hospital, Toronto, Ontario, Canada

Correspondence and requests for reprints should be addressed to V. Marco Ranieri, M.D., Università di Torino, Dipartimento di Anestesiologia e Rianimazione, Ospedale S. Giovanni Battista-Molinette, Corso Dogliotti 14, 10126 Turin, Italy. E-mail: marco.ranieri{at}unito.it

Rationale: Tidal volume and plateau pressure limitation decreases mortality in acute respiratory distress syndrome. Computed tomography demonstrated a small, normally aerated compartment on the top of poorly aerated and nonaerated compartments that may be hyperinflated by tidal inflation.

Objectives: We hypothesized that despite tidal volume and plateau pressure limitation, patients with a larger nonaerated compartment are exposed to tidal hyperinflation of the normally aerated compartment.

Measurements and Main Results: Pulmonary computed tomography at end-expiration and end-inspiration was obtained in 30 patients ventilated with a low tidal volume (6 ml/kg predicted body weight). Cluster analysis identified 20 patients in whom tidal inflation occurred largely in the normally aerated compartment (69.9 ± 6.9%; "more protected"), and 10 patients in whom tidal inflation occurred largely within the hyperinflated compartments (63.0 ± 12.7%; "less protected"). The nonaerated compartment was smaller and the normally aerated compartment was larger in the more protected patients than in the less protected patients (p = 0.01). Pulmonary cytokines were lower in the more protected patients than in the less protected patients (p < 0.05). Ventilator-free days were 7 ± 8 and 1 ± 2 d in the more protected and less protected patients, respectively (p = 0.01). Plateau pressure ranged between 25 and 26 cm H2O in the more protected patients and between 28 and 30 cm H2O in the less protected patients (p = 0.006).

Conclusions: Limiting tidal volume to 6 ml/kg predicted body weight and plateau pressure to 30 cm H2O may not be sufficient in patients characterized by a larger nonaerated compartment.

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


AT A GLANCE COMMENTARY

Scientific Knowledge on the Subject
Limiting tidal volume to 6 ml/kg and plateau pressure to 30 cm H2O protects the lungs of patients with acute respiratory distress syndrome from ventilator-induced lung injury (VILI).

What This Study Adds to the Field
Patients characterized by a larger amount of collapsed lung may be exposed to VILI despite tidal volume and pressure limitation; plateau pressure should be limited to 28 cm H2O to guarantee lung protection.

 



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