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Background: It is not well understood how different ventilation modes affect the regional distribution of ventilation, particularly within the injured lung.Objectives: We compared respiratory mechanics, lung aeration and regional specific ventilation ((Equation is included in full-text article.)) distributions in healthy and surfactant-depleted rabbits ventilated with pressure-regulated volume control (PRVC) mode with a decelerating inspiratory flow or with volume control (VC) mode.Design: Randomised experimental study.Animals and Interventions: New Zealand white rabbits (n = 8) were anaesthetised, paralysed and mechanically ventilated either with VC or PRVC mode (tidal volume: 7 ml kg; rate: 40 min; positive end-expiratory pressure (PEEP): 3 cmH2O), at baseline and after lung injury induced by lung lavage.Main Outcome Measures: Airway resistance (Raw), respiratory tissue damping (G) and elastance (H) were measured by low-frequency forced oscillations. Synchrotron radiation computed tomography during stable xenon wash-in was used to measure regional lung aeration and specific ventilation and the relative fraction of nonaerated, trapped, normally, poorly and hyperinflated lung regions.Results: Lung lavage significantly elevated peak inspiratory pressure (PIP) (P < 0.001). PIP was lower on PRVC compared with VC mode (-12.7 ± 1.7%, P < 0.001). No significant differences in respiratory mechanics, regional ventilation distribution, strain or blood oxygenation could be detected between the two ventilation modes.Conclusion: A decelerating flow pattern (PRVC) resulted in equivalent regional ventilation distribution, respiratory mechanics and gas exchange, in both normal and mechanically heterogeneous lungs with, however, a significantly lower peak pressure. Our data suggest that the lower PIP on PRVC ventilation was because of the decelerating flow pattern rather than the ventilation distribution. [ABSTRACT FROM AUTHOR]

Background: Ventilator-induced lung injury occurs due to exaggerated local stresses, repeated collapse, and opening of terminal air spaces in poorly aerated dependent lung, and increased stretch in nondependent lung. The aim of this study was to quantify the functional behavior of peripheral lung units in whole-lung lavage-induced surfactant depletion, and to assess the effect of positive end-expiratory pressure. Methods: The authors used synchrotron imaging to measure lung aeration and regional specific ventilation at positive end-expiratory pressure of 3 and 9 cm H2O, before and after whole-lung lavage in rabbits. Respiratory mechanical parameters were measured, and helium-washout was used to assess end-expiratory lung volume. Results: Atelectatic, poorly, normally aerated, hyperinflated, and trapped regions could be identified using the imaging technique used in this study. Surfactant depletion significantly increased atelectasis (6.3 3.3 [mean ± SEM]% total lung area; P = 0.04 vs. control) and poor aeration in dependent lung. Regional ventilation was distributed to poorly aerated regions with high (16.4±4.4%; P < 0.001), normal (20.7±5.9%; P < 0.001 vs. control), and low (5.7 ±1.2%; P < 0.05 vs. control) specific ventilation. Significant redistribution of ventilation to normally aerated nondependent lung regions occurred (41.0 ± 9.6%; P = 0.03 vs. control). Increasing positive end-expiratory pressure level to 9 cm H2O significantly reduced poor aeration and recruited atelectasis, but ventilation redistribution persisted (39.2±9.5%; P< 0.001 vs. control). Conclusions: Ventilation of poorly aerated dependent lung regions, which can promote the local concentration of mechanical stresses, was the predominant functional behav¬ior in surfactant-depleted lung. Potential tidal recruitment of atelectatic lung regions involved a smaller fraction of the imaged lung. Significant ventilation redistribution to aerated lung regions places these at risk of increased stretch injury. [ABSTRACT FROM AUTHOR]

The article presents a study that assessed the effects of positive end-expiratory pressure on regional ventilation distribution in normal lung and after histamine-induced bronchoconstriction. The experiment involved 6 healthy New Zealand rabbits that were tracheostomized, paralyzed, and mechanically ventilated. Results showed that in a mechanically ventilated rabbit with severely heterogeneous bronchoconstriction, a positive end-expiratory pressure of five centimeter (cm) water significantly improves regional ventilation homogeneity.

Objectives: Airway closure is involved in adverse effects of mechanical ventilation under both general anesthesia and in acute respiratory distress syndrome patients. However, direct evidence and characterization of individual airway closure is lacking. Here, we studied the same individual peripheral airways in intact lungs of anesthetized and mechanically ventilated rabbits, at baseline and following lung injury, using high-resolution synchrotron phase-contrast CT., Design: Laboratory animal investigation., Setting: European synchrotron radiation facility., Subjects: Six New-Zealand White rabbits., Interventions: The animals were anesthetized, paralyzed, and mechanically ventilated in pressure-controlled mode (tidal volume, 6 mL/kg; respiratory rate, 40; FIO2, 0.6; inspiratory:expiratory, 1:2; and positive end-expiratory pressure, 3 cm H2O) at baseline. Imaging was performed with a 47.5 × 47.5 × 47.5 μm voxel size, at positive end-expiratory pressure 12, 9, 6, 3, and 0 cm H2O. The imaging sequence was repeated after lung injury induced by whole-lung lavage and injurious ventilation in four rabbits. Cross-sections of the same individual airways were measured., Measurements and Main Results: The airways were measured at baseline (n = 48; radius, 1.7 to 0.21 mm) and after injury (n = 32). Closure was observed at 0 cm H2O in three of 48 airways (6.3%; radius, 0.35 ± 0.08 mm at positive end-expiratory pressure 12) at baseline and five of 32 (15.6%; radius, 0.28 ± 0.09 mm) airways after injury. Cross-section was significantly reduced at 3 and 0 cm H2O, after injury, with a significant relation between the relative change in cross-section and airway radius at 12 cm H2O in injured, but not in normal lung (R = 0.60; p < 0.001)., Conclusions: Airway collapsibility increases in the injured lung with a significant dependence on airway caliber. We identify "compliant collapse" as the main mechanism of airway closure in initially patent airways, which can occur at more than one site in individual airways.