Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung

Pavone, Lucio A.; Albert, Scott P.; DiRocco, Joseph D.; Gatto, Louis A.; Nieman, Gary F.

doi:10.1186/cc6122

Cited by 47 publications

(31 citation statements)

References 31 publications

(35 reference statements)

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“…It is, thus, a method for multi-scale material determination of the lungs in itself. It allows determination of parenchyma properties and alveolar microscopy, which is still the predominant method of determining alveolar behaviour during ventilation (Bickenbach et al, 2009;Mertens et al, 2009;Pavone et al, 2007a).…”

Section: Methods Precisionmentioning

confidence: 99%

In vivo characterization of mechanical tissue properties of internal organs using endoscopic microscopy and inverse finite element analysis

Schwenninger

Schumann

Guttmann

2011

Journal of Biomechanics

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Section: Methods Precisionmentioning

confidence: 99%

In vivo characterization of mechanical tissue properties of internal organs using endoscopic microscopy and inverse finite element analysis

Schwenninger

Schumann

Guttmann

2011

Journal of Biomechanics

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“…[5][6][7] Mechanical ventilation-induced alveolar instability can injure lung tissue. 8,9 Adjustment of the positive end-expiratory pressure (PEEP) level has been used to maintain adequate end-expiratory lung volume at the end of expiration, which protects injury tissue from cyclic tidal opening and closing. Additionally, meta-analyses of clinical studies have shown that higher PEEP values significantly contribute to improved survival in patients with severely hypoxemic ARDS.…”

Section: Critical Care Medicinementioning

confidence: 99%

Higher Frequency Ventilation Attenuates Lung Injury during High-frequency Oscillatory Ventilation in Sheep Models of Acute Respiratory Distress Syndrome

et al. 2013

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Background: High-frequency oscillatory ventilation (HFOV) at higher frequencies minimizes the tidal volume. However, whether increased frequencies during HFOV can reduce ventilator-induced lung injury remains unknown. Methods: After the induction of acute respiratory distress syndrome in the model by repeated lavages, 24 adult sheep were randomly divided into four groups (n = 6): three HFOV groups (3, 6, and 9 Hz) and one conventional mechanical ventilation (CMV) group. Standard lung recruitments were performed in all groups until optimal alveolar recruitment was reached. After lung recruitment, the optimal mean airway pressure or positive end-expiratory pressure was determined with decremental pressure titration, 2 cm H 2 O every 10 min. Animals were ventilated for 4 h. Results: After lung recruitment, sustained improvements in gas exchange and compliance were observed in all groups. Compared with the HFOV-3 Hz and CMV groups, the transpulmonary pressure and tidal volumes were statistically significantly lower in the HFOV-9 Hz group. The lung injury scores and wet/dry weight ratios were significantly reduced in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Expression of interleukin-1β and interleukin-6 in the lung tissue, decreased significantly in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Malondialdehyde expression and myeloperoxidase activity in lung tissues in the HFOV-9 Hz group decreased significantly, compared with the HFOV-3 Hz and CMV groups. Conclusion: The use of HFOV at 9 Hz minimizes lung stress and tidal volumes, resulting in less lung injury and reduced levels of inflammatory mediators compared with the HFOV-3 Hz and CMV conditions. A CUTE respiratory distress syndrome (ARDS) is the most severe manifestation of acute lung injury caused by various direct and indirect factors. Inflammatory pulmonary edema, severe hypoxemia, and diffuse endothelial and epithelial injury are key characteristics of ARDS, which can often lead to multiple organ failure.1,2 Despite being the most widely used approach to treat ARDS, conventional mechanical ventilation (CMV) can induce ventilatorinduced lung injury (VILI) due to alveolar overdistension and the cyclic collapse/reopening of lung units, eliciting inflammatory responses, and worsening the damage. 3,4 Recently, protective CMV has been shown to decrease lung and systemic inflammatory responses and improve What We Already Know about This Topic• High-frequency oscillatory ventilation provides efficient gas exchange using very high frequencies and low tidal volumes, while maintaining a constant mean airway pressure • The effects of frequency in high-frequency oscillatory ventilation on ventilation-induced lung injury are yet to be evaluated What This Article Tells Us That Is New• This study suggests that high-frequency oscillatory ventilation at higher frequencies minimizes lung stress and tidal volume, resulting in less lung injury and reduced local lung inflammation

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“…The endoscopic videos covered only a small area of the surface of the lung that was at the identic anatomical site in all animals. Especially in the case of the lung-injury group it has to be kept in mind that the alveolar damage attributable to the lavage and attributable to ventilatorassociated lung injury is distributed heterogeneously and the latter was shown do develop differently depending on the anatomical site (22). Gas redistribution between slow and fast lung compartments, i.e., the pendelluft phenomenon, is characteristic for the heterogeneously injured lung.…”

Section: Discussionmentioning

confidence: 99%

Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats

Schwenninger

Runck

Schumann

et al. 2012

Journal of Applied Physiology

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Schwenninger D, Runck H, Schumann S, Haberstroh J, Guttmann J. Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats. J Appl Physiol 113: 273-280, 2012. First published May 24, 2012 doi:10.1152/japplphysiol.01620.2011.-This study was aimed at measuring shear moduli in vivo in mechanically ventilated rats and comparing them to global lung mechanics. Wistar rats (n ϭ 28) were anesthetized, tracheally intubated, and mechanically ventilated in supine position. The animals were randomly assigned to the healthy control or the lung injury group where lung injury was induced by bronchoalveolar lavage. The respiratory system elastance Ers was analyzed based on the single compartment resistance/elastance lung model using multiple linear regression analysis. The shear modulus (G) of alveolar parenchyma was studied using a newly developed endoscopic system with adjustable pressure at the tip that was designed to induce local mechanostimulation. The data analysis was then carried out with an inverse finite element method. G was determined at continuous positive airway pressure (CPAP) levels of 15, 17, 20, and 30 mbar. The resulting shear moduli of lungs in healthy animals increased from 3.3 Ϯ 1.4 kPa at 15 mbar CPAP to 5.8 Ϯ 2.4 kPa at 30 mbar CPAP (P ϭ 0.012), whereas G was ϳ2.5 kPa at all CPAP levels for the lung-injured animals. Regression analysis showed a negative correlation between G and relative Ers in the control group (r ϭ Ϫ0.73, P ϭ 0.008 at CPAP ϭ 20 mbar) and no significant correlation in the lung injury group. These results suggest that the locally measured G were inversely associated with the elastance of the respiratory system. Rejecting the study hypothesis the researchers concluded that low global respiratory system elastance is related to high local resistance against tissue deformation.

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Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung

Cited by 47 publications

References 31 publications

In vivo characterization of mechanical tissue properties of internal organs using endoscopic microscopy and inverse finite element analysis

In vivo characterization of mechanical tissue properties of internal organs using endoscopic microscopy and inverse finite element analysis

Higher Frequency Ventilation Attenuates Lung Injury during High-frequency Oscillatory Ventilation in Sheep Models of Acute Respiratory Distress Syndrome

Locally measured shear moduli of pulmonary tissue and global lung mechanics in mechanically ventilated rats

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