The Mechanism of Lung Volume Change during  Mechanical Ventilation

Carney, David E.; Bredenberg, Carl E.; Schiller, Henry J.; Picone, Anthony; McCann, Ulysse G.; Gatto, Louis A.; Bailey, Graeme; Fillinger, Mark F.; Nieman, Gary F.

doi:10.1164/ajrccm.160.5.9812031

Cited by 127 publications

(92 citation statements)

References 23 publications

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“…In the supine position, gravity causes the heart to be suspended from the sternum, occupying a larger space in the anterior compartment, whereas in the prone position, the heart is resting on the sternum, allowing more anterior lung expansion. Our EIT data set will provide a valuable comparison for future studies in subjects with lung disease or during mechanical ventilation, where alveolar recruitment and derecruitment during tidal breathing can occur [26,[28][29][30].…”

Section: Image Analysismentioning

confidence: 99%

Regional ventilation distribution in the first 6 months of life

Pham

Yuill²,

Dakin³

et al. 2010

Eur Respir J

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Electrical impedance tomography (EIT) has been used to study regional ventilation distribution in neonatal and paediatric lung disease; however, little information has been obtained in healthy newborns and infants.Data on regional ventilation distribution and regional filling characteristics were obtained using EIT in the neonatal period, at 3 and 6 months of age, in spontaneously breathing infants during non-rapid eye movement sleep. Regional ventilation distribution was described using regional end-expiratory and end-inspiratory impedance amplitudes, and geometric centre of ventilation. Regional filling characteristics were described with the phase lag or lead of the regional impedance change in comparison to global impedance change.32 infants were measured in the supine position. Regional impedance amplitudes increased with age but regional ventilation distribution remained unchanged in all infants at any age, with the dependent (posterior) lung always better ventilated. Regional filling characteristics showed that the dependent lung filled during inspiration before the nondependent lung during all followup measurements.Regional ventilation distribution and regional filling characteristics remained unchanged over the first 6 months of life, and the results obtained on regional ventilation distribution are very similar to those in adult subjects.

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Section: Image Analysismentioning

confidence: 99%

Regional ventilation distribution in the first 6 months of life

Pham

Yuill²,

Dakin³

et al. 2010

Eur Respir J

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“…Because most fixatives affect tissue hydration and surface tension and thereby distort lung architecture relative to its in vivo state, the current models of alveolar micromechanics await morphometric confirmation on living, unfixed specimens (48). Microscopic imaging of canine subpleural alveoli through a pleural window suggested that alveolar volume changes little during normal breathing (49) and that the acinus expands nonuniformly (43). Because the mechanics of subpleural alveoli may be dominated by their coupling to a relatively inelastic pleural membrane, which in these experiments had to be immobilized to generate a focused image, the amplitude of alveolar volume change during quiet breathing is likely to remain a topic of active investigation.…”

Section: Alveolar Micromechanics Of the Normal Lungmentioning

confidence: 99%

Cellular Stress Failure in Ventilator-injured Lungs

Vlahakis

Hubmayr

2005

Am J Respir Crit Care Med

189

120

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The clinical and experimental literature has unequivocally established that mechanical ventilation with large tidal volumes is injurious to the lung. However, uncertainty about the micromechanics of injured lungs and the numerous degrees of freedom in ventilator settings leave many unanswered questions about the biophysical determinants of lung injury. In this review we focus on experimental evidence for lung cells as injury targets and the relevance of these studies for human ventilator-associated lung injury. In vitro, the stress-induced mechanical interactions between matrix and adherent cells are important for cellular remodeling as a means for preventing compromise of cell structure and ultimately cell injury or death. In vivo, these same principles apply. Large tidal volume mechanical ventilation results in physical breaks in alveolar epithelial and endothelial plasma membrane integrity and subsequent triggering of proinflammatory signaling cascades resulting in the cytokine milieu and pathologic and physiologic findings of ventilatorassociated lung injury. Importantly, though, alveolar cells possess cellular repair and remodeling mechanisms that in addition to protecting the stressed cell provide potential molecular targets for the prevention and treatment of ventilator-associated lung injury in the future.

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“…Intravital microscopy has been used to visualize alveolar structures (11)(12)(13)(14)(15)(16), but these techniques are also limited by the ability to visualize only subpleural structures and the invasive nature of the technique. As pointed out by Hubmayr (17), there is relatively little consensus about alveolar deformation during breathing.…”

mentioning

confidence: 99%

Airway Strain during Mechanical Ventilation in an Intact Animal Model

Sinclair

Molthen

Haworth

et al. 2007

Am J Respir Crit Care Med

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Rationale: Mechanical ventilation with large tidal volumes causes ventilator-induced lung injury in animal models. Little direct evidence exists regarding the deformation of airways in vivo during mechanical ventilation, or in the presence of positive end-expiratory pressure (PEEP). Objectives: To measure airway strain and to estimate airway wall tension during mechanical ventilation in an intact animal model. Methods: Sprague-Dawley rats were anesthetized and mechanically ventilated with tidal volumes of 6, 12, and 25 cm 3 /kg with and without 10-cm H 2 O PEEP. Real-time tantalum bronchograms were obtained for each condition, using microfocal X-ray imaging. Images were used to calculate circumferential and longitudinal airway strains, and on the basis of a simplified mathematical model we estimated airway wall tensions. Measurements and Main Results: Circumferential and longitudinal airway strains increased with increasing tidal volume. Levels of mechanical strain were heterogeneous throughout the bronchial tree. Circumferential strains were higher in smaller airways (less than 800 mm). Airway size did not influence longitudinal strain. When PEEP was applied, wall tensions increased more rapidly than did strain levels, suggesting that a ''strain limit'' had been reached. Airway collapse was not observed under any experimental condition. Conclusions: Mechanical ventilation results in significant airway mechanical strain that is heterogeneously distributed in the uninjured lung. The magnitude of circumferential but not axial strain varies with airway diameter. Airways exhibit a ''strain limit'' above which an abrupt dramatic rise in wall tension is observed.

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The Mechanism of Lung Volume Change during Mechanical Ventilation

Cited by 127 publications

References 23 publications

Regional ventilation distribution in the first 6 months of life

Regional ventilation distribution in the first 6 months of life

Cellular Stress Failure in Ventilator-injured Lungs

Airway Strain during Mechanical Ventilation in an Intact Animal Model

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