• L Beydon, L Uttman, R Rawal, and B Jonson.
• Department of Anaesthesia, University Hospital, 49033 Angers Cedex 01, France. lbeydon.angers@invivo.edu
• Intensive Care Med. 2002 Sep 1;28(9):1239-45.

ObjectiveA large tidal volume (VT) and lung collapse and re-expansion may cause ventilator-induced lung injury (VILI) in acute lung injury (ALI). A low VT and a positive end-expiratory pressure (PEEP) can prevent VILI, but the more VT is reduced, the more dead space (VD) compromises gas exchange. We investigated how physiological, airway and alveolar VD varied with PEEP and analysed possible links to respiratory mechanics.SettingMedical and surgical intensive care unit (ICU) in a university hospital.DesignProspective, non-randomised comparative trial. PATIENTS. Ten consecutive ALI patients.InterventionStepwise increases in PEEP from zero to 15 cm H2O.Measurements And ResultsLung mechanics and VD were measured at each PEEP level. Physiological VD was 41-64% of VT at zero PEEP and increased slightly with PEEP due to a rise in airway VD. Alveolar VD was 11-38% of VT and did not vary systematically with PEEP. However, in individual patients a decrease and increase of alveolar VD paralleled a positive or negative response to PEEP with respect to oxygenation (shunt), respectively. VD fractions were independent of respiratory resistance and compliance.ConclusionsAlveolar VD is large and does not vary systematically with PEEP in patients with various degrees of ALI. Individual measurements show a diverse response to PEEP. Respiratory mechanics were of no help in optimising PEEP with regard to gas exchange.

18 keywords...

hide…