Lung Recruitment Guided by Ultrasonography in Unilateral Lung Injury

Lung recruitment and derecruitment contribute significantly to variations in the elastance of the respiratory system during mechanical ventilation. However, the decreases in elastance that occur with deep inflation are transient, especially in acute lung injury. Bates and Irvin ( 8 ) proposed a model of the lung that recreates time-varying changes in elastance as a result of progressive recruitment and derecruitment of lung units. The model is characterized by distributions of critical opening and closing pressures throughout the lung and by distributions of speeds with which the processes of opening and closing take place once the critical pressures have been achieved. In the present study, we adapted this model to represent a mechanically ventilated mouse. We fit the model to data collected in a previous study from control mice and mice in various stages of acid-induced acute lung injury ( 3 ). Excellent fits to the data were obtained when the normally distributed critical opening pressures were about 5 cmH2O above the closing pressures and when the hyperbolically distributed opening velocities were about an order of magnitude greater than the closing velocities. We also found that, compared with controls, the injured mice had markedly increased opening and closing pressures but no change in the velocities, suggesting that the key biophysical change wrought by acid injury is dysfunction of surface tension at the air-liquid interface. Our computational model of lung recruitment and derecruitment dynamics is thus capable of accurately mimicking data from mice with acute lung injury and may provide insight into the altered biophysics of the injured lung.

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Noninvasive quantification of macrophagic lung recruitment during experimental ventilation-induced lung injury

Journal of Applied Physiology ◽

10.1152/japplphysiol.00825.2018 ◽

2019 ◽

Vol 127 (2) ◽

pp. 546-558

Author(s):

Laurent Bitker ◽

Nicolas Costes ◽

Didier Le Bars ◽

Franck Lavenne ◽

Maciej Orkisz ◽

...

Keyword(s):

Lung Injury ◽

Protective Ventilation ◽

Lung Recruitment ◽

Translocator Protein ◽

Emission Tomography ◽

Dynamic Strain ◽

Lung Uptake ◽

Positron Emission ◽

Ventilation Induced Lung Injury

Macrophagic lung infiltration is pivotal in the development of lung biotrauma because of ventilation-induced lung injury (VILI). We assessed the performance of [11C](R)-PK11195, a positron emission tomography (PET) radiotracer binding the translocator protein, to quantify macrophage lung recruitment during experimental VILI. Pigs ( n = 6) were mechanically ventilated under general anesthesia, using protective ventilation settings (baseline). Experimental VILI was performed by titrating tidal volume to reach a transpulmonary end-inspiratory pressure (∆PL) of 35–40 cmH2O. We acquired PET/computed tomography (CT) lung images at baseline and after 4 h of VILI. Lung macrophages were quantified in vivo by the standardized uptake value (SUV) of [11C](R)-PK11195 measured in PET on the whole lung and in six lung regions and ex vivo on lung pathology at the end of experiment. Lung mechanics were extracted from CT images to assess their association with the PET signal. ∆PL increased from 9 ± 1 cmH2O under protective ventilation, to 36 ± 6 cmH2O during experimental VILI. Compared with baseline, whole-lung [11C](R)-PK11195 SUV significantly increased from 1.8 ± 0.5 to 2.9 ± 0.5 after experimental VILI. Regional [11C](R)-PK11195 SUV was positively associated with the magnitude of macrophage recruitment in pathology ( P = 0.03). Compared with baseline, whole-lung CT-derived dynamic strain and tidal hyperinflation increased significantly after experimental VILI, from 0.6 ± 0 to 2.0 ± 0.4, and 1 ± 1 to 43 ± 19%, respectively. On multivariate analysis, both were significantly associated with regional [11C](R)-PK11195 SUV. [11C](R)-PK11195 lung uptake (a proxy of lung inflammation) was increased by experimental VILI and was associated with the magnitude of dynamic strain and tidal hyperinflation. NEW & NOTEWORTHY We assessed the performance of [11C](R)-PK11195, a translocator protein-specific positron emission tomography (PET) radiotracer, to quantify macrophage lung recruitment during experimental ventilation-induced lung injury (VILI). In this proof-of-concept study, we showed that the in vivo quantification of [11C](R)-PK11195 lung uptake in PET reflected the magnitude of macrophage lung recruitment after VILI. Furthermore, increased [11C](R)-PK11195 lung uptake was associated with harmful levels of dynamic strain and tidal hyperinflation applied to the lungs.

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Lung aeration changes after lung recruitment in children with acute lung injury: A feasibility study

Pediatric Pulmonology ◽

10.1002/ppul.22508 ◽

2012 ◽

Vol 47 (8) ◽

pp. 771-779 ◽

Cited By ~ 8

Author(s):

Juan P. Boriosi ◽

Ronald A. Cohen ◽

Evan Summers ◽

Anil Sapru ◽

James H. Hanson ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Feasibility Study ◽

Lung Recruitment ◽

Lung Aeration

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Lung recruitment during small tidal volume ventilation allows minimal positive end-expiratory pressure without augmenting lung injury

Critical Care Medicine ◽

10.1097/00003246-199909000-00037 ◽

1999 ◽

Vol 27 (9) ◽

pp. 1940-1945 ◽

Cited By ~ 108

Author(s):

Peter C. Rimensberger ◽

Gorsev Pristine ◽

J. Brendan M. Mullen ◽

Peter N. Cox ◽

Arthur S. Slutsky

Keyword(s):

Lung Injury ◽

Tidal Volume ◽

Lung Recruitment ◽

Positive End Expiratory Pressure ◽

Volume Ventilation

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

Anesthesiology ◽

10.1097/aln.0b013e31829419a6 ◽

2013 ◽

Vol 119 (2) ◽

pp. 398-411 ◽

Cited By ~ 14

Author(s):

Songqiao Liu ◽

Yang Yi ◽

Maohua Wang ◽

Qiuhua Chen ◽

Yingzi Huang ◽

...

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Lung Injury ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

High Frequency ◽

Distress Syndrome ◽

High Frequency Oscillatory Ventilation ◽

Lung Recruitment ◽

Oscillatory Ventilation ◽

High Frequency Oscillatory

Abstract 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 H2O 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.

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