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Open lung approach ventilation abolishes the negative effects of respiratory rate in experimental lung injury
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. Pontificia Univ Catolica Chile, Dept Med Intens, Santiago, Chile.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Hedenstierna laboratory. Univ Sao Paulo, Cardiopulm Dept, Pulm Div, Heart Inst Incor, Sao Paulo, Brazil.
Pontificia Univ Catolica Chile, Dept Med Intens, Santiago, Chile.
Natl Vet Inst, Dept Pathol & Wildlife Dis, Uppsala, Sweden.
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2016 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 60, no 8, 1131-1141 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: We recently reported that a high respiratory rate was associated with less inflammation than a low respiratory rate, but caused more pulmonary edema in a model of ARDS when an ARDSNet ventilatory strategy was used. We hypothesized that an open lung approach (OLA) strategy would neutralize the independent effects of respiratory rate on lung inflammation and edema. This hypothesis was tested in an ARDS model using two clinically relevant respiratory rates during OLA strategy.

METHODS: Twelve piglets were subjected to an experimental model of ARDS and randomized into two groups: LRR (20 breaths/min) and HRR (40 breaths/min). They were mechanically ventilated for 6 h according to an OLA strategy. We assessed respiratory mechanics, hemodynamics, and extravascular lung water (EVLW). At the end of the experiment, wet/dry ratio, regional histology, and cytokines were evaluated.

RESULTS: After the ARDS model was established, Cdyn,rs decreased from 21 ± 3.3 to 9.0 ± 1.8 ml/cmH2 O (P < 0.0001). After the lung recruitment maneuver, Cdyn,rs increased to the pre-injury value. During OLA ventilation, no differences in respiratory mechanics, hemodynamics, or EVLW were observed between groups. Wet/dry ratio and histological scores were not different between groups. Cytokine quantification was similar and showed a homogeneous distribution throughout the lung in both groups.

CONCLUSION: Contrary to previous findings with the ARDSNet strategy, respiratory rate did not influence lung inflammatory response or pulmonary edema during OLA ventilation in experimental ARDS. This indicates that changing the respiratory rate when OLA ventilation is used will not exacerbate lung injury.

Place, publisher, year, edition, pages
2016. Vol. 60, no 8, 1131-1141 p.
National Category
Anesthesiology and Intensive Care
Identifiers
URN: urn:nbn:se:uu:diva-296932DOI: 10.1111/aas.12735ISI: 000380960400012PubMedID: 27110871OAI: oai:DiVA.org:uu-296932DiVA: diva2:940186
Funder
Swedish Heart Lung FoundationSwedish Research Council, K2015-99X-22731-01-4
Available from: 2016-06-20 Created: 2016-06-20 Last updated: 2016-09-15Bibliographically approved
In thesis
1. Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome
Open this publication in new window or tab >>Aspects on ventilation induced stress and strain on regional and global inflammation in experimental acute respiratory distress syndrome
2016 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Mechanical ventilation (MV) is a life-saving therapy in acute respiratory distress syndrome (ARDS), a condition that affects 3000 patients/year in Sweden with a mortality rate of about 40%. However, MV may induce or worsen lung injury causing “ventilator-induced lung injury (VILI)”. From a mechanical perspective strain (deformation, or relative change in lung volume) and stress (tension) have been postulated as main determinants of VILI. High respiratory rate is potentially another factor that may exacerbate VILI by amplifying the total energy transmitted to the lungs during MV. In this thesis in animal ARDS models the hypotheses were that 1) lung parenchyma inhomogeneities concentrate stress and amplify lung damage and inflammation, 2) higher respiratory rates increase lung inflammation and lung edema in heterogeneous ARDS, and 3) local lung deformation is related to local inflammation.

First, in a rat model the effect on inflammation and structural damage of regional lung collapse on the healthy surrounding lung tissue was assessed. Second, in porcine models the effect of respiratory rate on lung edema and inflammation was studied during two ventilatory modes; a) a permissive collapse mode and b) a homogenized lung parenchyma mode. Finally, lung deformation was correlated with lung inflammation assessed by positron emission tomography using 18F-FDG uptake.

It was found that; 1) local inhomogeneities can act as stress amplifiers, increasing lung tissue inflammation and damage in the healthy surrounded lung. 2) high respiratory rate increases lung edema but decreases lung inflammation when permissive lung collapse is used and that these effects are prevented with lung parenchyma homogenization; 3) local lung deformation and inflammation are well correlated.

In conclusion, lung inhomogeneities may aggravate VILI, respiratory rate may affect in different ways VILI progression depending on the ventilatory strategy, and finally, lung deformation is closely related to lung inflammation. With the caveat that the studies are performed in animal models, the results suggest that using ventilator strategies that homogenize the lungs, i.e., open collapsed lung regions and prevent re-collapse in ARDS will reduce VILI and in the end may decrease morbidity and the high mortality in this condition.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2016. 64 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1235
Keyword
ARDS, VILI, respiratory rate, strain, PET
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:uu:diva-296952 (URN)978-91-554-9612-8 (ISBN)
Public defence
2016-09-06, Hedstrandsalen, Akademiska sjukhuset, Ing 70, 751 85 Uppsala, UPPSALA, 09:00 (English)
Opponent
Supervisors
Funder
Swedish Heart Lung Foundation, K2015-99X-22731-01-4
Available from: 2016-08-16 Created: 2016-06-20 Last updated: 2016-08-16

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Retamal Montes, JaimeBorges, João BatistaHedenstierna, GöranSuarez-Sipmann, FernandoLarsson, Anders
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