A Functional and Morphologic Analysis of Pressure-Controlled Inverse Ratio Ventilation in Oleic Acid-Induced Lung Injury: Alveolar Recruitment and Aeration of Lung Tissue

As expected, VCV ZEEP resulted in poorer expiratory aeration in comparison to VCV PEEP and PCIRV. However, no difference in expiratory aeration between the two latter ventilatory modes could be found. The FRC measurements were in agreement with the CT data. These findings indicate that the mechanism for creation of end-expiratory pressure (ie, extrinsic or intrinsic PEEP) is unimportant with respect to the size of increase in end-expiratory lung volume as measured by CT lung density or FRC.
Mean inspiratory lung densities were equal among the three ventilatory modes despite peak airway pressures that were significantly lower with VCV ZEEP and PCIRV than with VCV PEEP.
VCV PEEP and PCIRV gave similar effects on alveolar recruitment measured as difference in density between end-expiration and end-inspiration. However, with PCIRV, the decrease in end-inspiratory density was reached with a smaller airway pressure difference between end-inspiration and end-expiration (peak airway pressure-end-expiratory airway pressure) of 23 cm H2O than that observed with VCV PEEP (33 cm H20). The significance of this finding is unclear but may be of importance with regard to structural damage to the lung caused by high peak airway pressure levels. In an animal study, less morphologic damage was caused by I:E ratios of 4:1 than by I:E ratios of 1:2.
The difference between end-expiratory and end-inspiratory attenuation was greatest with VCV ZEEP website inhalers for asthma. This finding suggests that the absolute magnitude of attenuation increase between expiration and inspiration is not important with regard to oxygenation of the blood.
A well-known negative effect of externally applied PEEP is an increase in nondependent regional lung volume accompanied by an increased risk of barotrauma. It may be postulated that the increase in end-expiratory pressure generated by PCIRV leads to a more physiologic distribution of the lung volume increase, thereby avoiding regional overdistention.

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