Aspiration of dead space allows isocapnic iow tidal volume ventilation in acute lung injury. Relationships to gas exchange and mechanics

Abstract

Objective: In acute lung injury (ALI) mechanical ventilation damages lungs. We hypothesised that aspiration and replacement of dead space during expiration (ASPIDS) allows normocapnic ventilation at higher end-expiratory pressure (PEEP) and reduced tidal volume (VT), peak and plateau pressures (PaWpeak, PaWplat), thus avoiding lung damage. Setting: University Hospital. Patients: Seven consecutive sedated and paralysed ALI patients were studied. Interventions and measurements: Single breath test for CO2 and multiple elastic pressure volume (Pel/V) curves recorded from different end-expiratory pressures guided ventilatory setting at ASPIDS. ASPIDS was studied at respiratory rate (RR) of 14 min-1 and then 20 min-1 with minute ventilation maintaining stable CO2 elimination. Results: Alveolar and airway dead spaces were 24.3% and 31.3% of VT, respectively. Multiple Pel/V curves showed a shift towards lower volume at decreasing PEEP, thus indicating that patients required a higher PEEE At ASPIDS, PEEP was increased from 8.9 cmH2O to 12.6 cmH2O and VT reduced from 11 ml/kg to 8.9 ml/kg at RR 14 min-1 and to 6.9 ml/kg at RR 20 min-1. A significant decrease in Pawpeak (36.7 vs 32 at RR 14 min-1 and 28.7 at RR 20 min-1) and Pawplat (29.9 vs 27.3 at RR 14 min-1 and 24.1 at RR 20 min-1) were observed. PaCO2 remained stable. No intrinsic PEEP developed. No side effects were noticed. Conclusions: ASPIDS allowed the use of higher PEEP at lower VT and inflation pressure and constant PaCO2. Multiple Pel/V curves gave insight into the tendency of lungs to collapse.