Simple methods to predict the effect of lung recruitment maneuvers (LRMs) in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are lacking. It has previously been found that a static pressure-volume (PV) loop could indicate the increase in lung volume induced by positive end-expiratory pressure (PEEP) in ARDS. The purpose of this study was to test the hypothesis that in ALI (1) the difference in lung volume (DeltaV) at a specific airway pressure (10 cmH2O was chosen in this test) obtained from the limbs of a PV loop agree with the increase in end-expiratory lung volume (DeltaEELV) by an LRM at a specific PEEP (10 cmH2O), and (2) the maximal relative vertical (volume) difference between the limbs (maximal hysteresis/total lung capacity (MH/TLC)) could predict the changes in respiratory compliance (Crs), EELV and partial pressures of arterial O2 and CO2 (PaO2 and PaCO2, respectively) by an LRM.
In eight ventilated pigs PV loops were obtained (1) before lung injury, (2) after lung injury induced by lung lavage, and (3) after additional injurious ventilation. DeltaV and MH/TLC were determined from the PV loops. At all stages Crs, EELV, PaCO2 and PaO2 were registered at 0 cmH2O and at 10 cmH2O before and after LRM, and DeltaEELV was calculated. Statistics: Wilcoxon's signed rank, Pearson's product moment correlation, Bland-Altman plot, and receiver operating characteristics curve. Medians and 25th and 75th centiles are reported.
DeltaV was 270 (220, 320) ml and DeltaEELV was 227 (177, 306) ml (P < 0.047). The bias was 39 ml and the limits of agreement were - 49 ml to +127 ml. The R2 for relative changes in EELV, Crs, PaCO2 and PaO2 against MH/TLC were 0.55, 0.57, 0.36 and 0.05, respectively. The sensitivity and specificity for MH/TLC of 0.3 to predict improvement (>75th centile of what was found in uninjured lungs) were for EELV 1.0 and 0.85, Crs 0.88 and 1.0, PaCO2 0.78 and 0.60, and PaO2 1.0 and 0.69.
A PV-loop-derived parameter, MH/TLC of 0.3, predicted changes in lung mechanics better than changes in gas exchange in this lung injury model.
2008. Vol. 12, no 1, R7- p.