Deterioration of Regional Lung Strain and Inflammation during Early Lung Injury

Ribeiro, Gabriel; Hashimoto, Shinsuke; Winkler, Tilo; Baron, Rebecca M.; Grogg, K. S.; Paula, Luís Felipe; Santos, Arnoldo; Zeng, Cheng; Hibbert, Kathryn A.; Harris, R. Scott; Bajwa, Ednan K.; Melo, Marcos F. Vidal

doi:10.1164/rccm.201710-2038oc

Cited by 57 publications

(66 citation statements)

References 58 publications

(59 reference statements)

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“…More recent studies suggest that the lung pathology compartmentalized by gravity (i.e., normal lung tissue adjacent to acutely injured tissue) is incorrect and that regional lung strain and inflammation throughout the entire lung is the main driver of VILI [16,[31][32][33][34][35][36]. Regional strain is caused with each breath by (1) alveolar and alveolar duct R/D [37][38][39][40][41][42][43] and (2) stress-multiplication (S-M), which cause injury to open lung areas adjacent to collapsed or edema-filled tissue [18,19,[44][45][46][47][48].…”

Section: New Concepts Of Ards Pathophysiologymentioning

confidence: 99%

Prevention and treatment of acute lung injury with time-controlled adaptive ventilation: physiologically informed modification of airway pressure release ventilation

Nieman

Gatto

Andrews

et al. 2020

Ann. Intensive Care

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Mortality in acute respiratory distress syndrome (ARDS) remains unacceptably high at approximately 39%. One of the only treatments is supportive: mechanical ventilation. However, improperly set mechanical ventilation can further increase the risk of death in patients with ARDS. Recent studies suggest that ventilation-induced lung injury (VILI) is caused by exaggerated regional lung strain, particularly in areas of alveolar instability subject to tidal recruitment/ derecruitment and stress-multiplication. Thus, it is reasonable to expect that if a ventilation strategy can maintain stable lung inflation and homogeneity, regional dynamic strain would be reduced and VILI attenuated. A time-controlled adaptive ventilation (TCAV) method was developed to minimize dynamic alveolar strain by adjusting the delivered breath according to the mechanical characteristics of the lung. The goal of this review is to describe how the TCAV method impacts pathophysiology and protects lungs with, or at high risk of, acute lung injury. We present work from our group and others that identifies novel mechanisms of VILI in the alveolar microenvironment and demonstrates that the TCAV method can reduce VILI in translational animal ARDS models and mortality in surgical/trauma patients. Our TCAV method utilizes the airway pressure release ventilation (APRV) mode and is based on opening and collapsing time constants, which reflect the viscoelastic properties of the terminal airspaces. Time-controlled adaptive ventilation uses inspiratory and expiratory time to (1) gradually "nudge" alveoli and alveolar ducts open with an extended inspiratory duration and (2) prevent alveolar collapse using a brief (sub-second) expiratory duration that does not allow time for alveolar collapse. The new paradigm in TCAV is configuring each breath guided by the previous one, which achieves real-time titration of ventilator settings and minimizes instability induced tissue damage. This novel methodology changes the current approach to mechanical ventilation, from arbitrary to personalized and adaptive. The outcome of this approach is an open and stable lung with reduced regional strain and greater lung protection. © The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article' s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article'

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Section: New Concepts Of Ards Pathophysiologymentioning

confidence: 99%

Prevention and treatment of acute lung injury with time-controlled adaptive ventilation: physiologically informed modification of airway pressure release ventilation

Nieman

Gatto

Andrews

et al. 2020

Ann. Intensive Care

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“…High-frequency oscillatory ventilation (HFOV) and lung recruitment maneuvers (LRMs) have been shown ineffective in reducing ARDS mortality (Brower et al, 2004;Meade et al, 2008;Mercat et al, 2008;Ferguson et al, 2013;Young et al, 2013;Cavalcanti et al, 2017;Hodgson et al, 2019). Prone position has been shown effective at reducing mortality (Guerin et al, 2013) by a mechanism of reducing regional alveolar strain and inflammation (Motta-Ribeiro et al, 2018;Xin et al, 2018). VILI, ventilator-induced lung injury; MV, mechanical ventilation; LTV, low tidal volume and inspiratory pressure; PEEP, positive end-expiratory pressure; ECLS, extracorporeal life support; HFOV, high-frequency oscillatory ventilation; LRM, lung recruitment maneuver; Q, perfusion; V A , alveolar ventilation; V A /Q, ventilation/perfusion ratio; baby lung, functional residual capacity (FRC) (Del .…”

Section: Problems With Protecting the Baby Lungmentioning

confidence: 99%

A Physiologically Informed Strategy to Effectively Open, Stabilize, and Protect the Acutely Injured Lung

et al. 2020

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Acute respiratory distress syndrome (ARDS) causes a heterogeneous lung injury and remains a serious medical problem, with one of the only treatments being supportive care in the form of mechanical ventilation. It is very difficult, however, to mechanically ventilate the heterogeneously damaged lung without causing secondary ventilatorinduced lung injury (VILI). The acutely injured lung becomes time and pressure dependent, meaning that it takes more time and pressure to open the lung, and it recollapses more quickly and at higher pressure. Current protective ventilation strategies, ARDSnet low tidal volume (LVt) and the open lung approach (OLA), have been unsuccessful at further reducing ARDS mortality. We postulate that this is because the LVt strategy is constrained to ventilating a lung with a heterogeneous mix of normal and focalized injured tissue, and the OLA, although designed to fully open and stabilize the lung, is often unsuccessful at doing so. In this review we analyzed the pathophysiology of ARDS that renders the lung susceptible to VILI. We also analyzed the alterations in alveolar and alveolar duct mechanics that occur in the acutely injured lung and discussed how these alterations are a key mechanism driving VILI. Our analysis suggests that the time component of each mechanical breath, at both inspiration and expiration, is critical to normalize alveolar mechanics and protect the lung from VILI. Animal studies and a meta-analysis have suggested that the time-controlled adaptive ventilation (TCAV) method, using the airway pressure release ventilation mode, eliminates the constraints of ventilating a lung with heterogeneous injury, since it is highly effective at opening and stabilizing the time-and pressure-dependent lung. In animal studies it has been shown that by "casting open" the acutely injured lung with TCAV we can (1) reestablish normal expiratory lung volume as assessed by direct observation of subpleural alveoli; (2) return normal parenchymal microanatomical structural support, known as alveolar interdependence and parenchymal tethering, as assessed by morphometric analysis of lung histology; (3) facilitate regeneration of normal surfactant function measured as increases in surfactant proteins A and B; and (4) significantly increase lung compliance, which reduces the pathologic impact of driving pressure and mechanical power at any given tidal volume.

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“…This improvement in oxygenation is in part due to alveolar recruitment from the increased PTI [11,22,26]. However, alveolar recruitment itself may not be sufficient to maintain oxygenation and prevent lung injury without sustained time-dependent alveolar stabilisation, preventing recurring collapse and cyclic recruitment/derecruitment (R/D), ultimately inducing a durable homogenous lung that decreases stress-risers [27][28][29]. The homogeneity induced with the extended PTI at Pplat permits persistent alveolar recruitment with less energy transfer as compared to PEEP recruitment methods [30].…”

Section: Figurementioning

confidence: 99%

The time-controlled adaptive ventilation protocol: mechanistic approach to reducing ventilator-induced lung injury

et al. 2019

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Airway pressure release ventilation (APRV) is a ventilator mode that has previously been considered a rescue mode, but has gained acceptance as a primary mode of ventilation. In clinical series and experimental animal models of extrapulmonary acute respiratory distress syndrome (ARDS), the early application of APRV was able to prevent the development of ARDS. Recent experimental evidence has suggested mechanisms by which APRV, using the time-controlled adaptive ventilation (TCAV) protocol, may reduce lung injury, including: 1) an improvement in alveolar recruitment and homogeneity; 2) reduction in alveolar and alveolar duct micro-strain and stress-risers; 3) reduction in alveolar tidal volumes; and 4) recruitment of the chest wall by combating increased intra-abdominal pressure. This review examines these studies and discusses our current understanding of the pleiotropic mechanisms by which TCAV protects the lung. APRV set according to the TCAV protocol has been misunderstood and this review serves to highlight the various protective physiological and mechanical effects it has on the lung, so that its clinical application may be broadened.

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Deterioration of Regional Lung Strain and Inflammation during Early Lung Injury

Cited by 57 publications

References 58 publications

Prevention and treatment of acute lung injury with time-controlled adaptive ventilation: physiologically informed modification of airway pressure release ventilation

Prevention and treatment of acute lung injury with time-controlled adaptive ventilation: physiologically informed modification of airway pressure release ventilation

A Physiologically Informed Strategy to Effectively Open, Stabilize, and Protect the Acutely Injured Lung

The time-controlled adaptive ventilation protocol: mechanistic approach to reducing ventilator-induced lung injury

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