The Science Journal of the American Association for Respiratory Care
Introduction: In ARDS patients, a biphasic profile characterizes lung volume decay during passive expiration. The inspiratory airway pressure waveform (IAPW) during pressure control ventilation (PCV) is less well studied but is generally thought to approximate a uniexponential washin function. Changes in the IAPW may serve as a marker of lung injury induced by mechanical ventilation. In a model of ventilator induced lung injury (VILI), we examined the IAPW before and after high airway pressure exposure to identify changes that may correlate with the development of VILI.
Methods: Nine New Zealand white rabbits were anesthetized, paralyzed and instrumented to monitor ABGs, FRC and airway pressure. Injury was induced by PCV at Pset = 45 cmH2O for 2 hours, PEEP = 3 cmH2O, f = 23/min, and TI = 1.0 sec (FIO2 = 0.4). On the IAPW, we compared the time to attain 35, 40, 45 cmH2O and goodness of fit of a uniexponential curve between 15 min and 120 min of the experimental period.
Results: Two hours of PCV caused reductions in PaO2 (-159.9 mmHg), FRC (-34%) and compliance (-66%). Consistent changes in IAPW were also seen (example in figure). The mean time to attain 35 cmH2O decreased (p=.048). The mean times to attain 40 and 45 cmH2O increased significantly (p =0.016, p =.001). The uniexponential curve fit worsened as VILI developed.
Conclusions: Change in the IAPW occurred during VILI: the pressure increase period lengthened and became more linear. A change in lung impedance and the reaction of the ventilator's flow metering algorithm may cause the IAPW change. Such alterations in the IAPW might serve as a marker of VILI.
(See Original for Figure)