Tidal changes on CT and progression of ARDS

Cereda, Maurizio; Xin, Yi; Hamedani, Hooman; Bellani, Giacomo; Kadlecek, Stephen; Clapp, Justin T.; Guerra, Luca; Meeder, Natalie; Rajaei, Jennia; Tustison, Nicholas J.; Gee, James C.; Kavanagh, Brian P.; Rizi, Rahim R.

doi:10.1136/thoraxjnl-2016-209833

Cited by 41 publications

(49 citation statements)

References 41 publications

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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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“…CT scans can show regional atelectasis, edema and changes in tissue density to suggest unstable inflation (Cereda et al, 2016a(Cereda et al, , 2017Xin et al, 2018) but is not specific enough to detect the immediate response of the alveoli and alveolar ducts to changes in mechanical ventilation (Cereda et al, 2016a(Cereda et al, , 2019. Electrical impedance tomography has demonstrated usefulness as a potential bedside tool to demonstrate changes in regional ventilation but may not be sensitive enough to detect subtle changes (Kaczka et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Mechanical Ventilation Lessons Learned From Alveolar Micromechanics

et al. 2020

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Morbidity and mortality associated with lung injury remains disappointingly unchanged over the last two decades, in part due to the current reliance on lung macro-parameters set on the ventilator instead of considering the micro-environment and the response of the alveoli and alveolar ducts to ventilator adjustments. The response of alveoli and alveolar ducts to mechanical ventilation modes cannot be predicted with current bedside methods of assessment including lung compliance, oxygenation, and pressurevolume curves. Alveolar tidal volumes (Vt) are less determined by the Vt set on the mechanical ventilator and more dependent on the number of recruited alveoli available to accommodate that Vt and their heterogeneous mechanical properties, such that high lung Vt can lead to a low alveolar Vt and low Vt can lead to high alveolar Vt. The degree of alveolar heterogeneity that exists cannot be predicted based on lung calculations that average the individual alveolar Vt and compliance. Finally, the importance of time in promoting alveolar stability, specifically the inspiratory and expiratory times set on the ventilator, are currently under-appreciated. In order to improve outcomes related to lung injury, the respiratory physiology of the individual patient, specifically at the level of the alveolus, must be targeted. With experimental data, this review highlights some of the known mechanical ventilation adjustments that are helpful or harmful at the level of the alveolus.

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“…Thus, lowering Vt and Pplat to reduce overdistension in the open lung tissue, which is surrounded by a large volume of collapsed and unstable tissue of very low compliance, may not reduce VILI. Regional instability and inflammation occur throughout the entire lung, including in tissue that appears to be normal on computed tomography (CT) scan or chest X-ray, and serve as pathologic focal points from which VILI-induced tissue damage expands (Wellman et al, 2014(Wellman et al, , 2016Cereda et al, 2016bCereda et al, , 2017. This suggests that to protect the normal lung tissue regional instability must be eliminated.…”

Section: Problems With Protecting the Baby Lungmentioning

confidence: 99%

“…There is no consensus on how best to set PEEP to effectively stabilize lung tissue (Coruh and Luks, 2014;Gattinoni et al, 2017;Nieman et al, 2017a;Bergez et al, 2019). The current ARDSnet method for setting PEEP uses a sliding scale of oxygenation (Acute Respiratory Distress Syndrome Network, 2000), but increased oxygenation does not correlate well with an increase in alveolar stability (Andrews et al, 2015), a key VILI mechanism (Wellman et al, 2014(Wellman et al, , 2016Cereda et al, 2016bCereda et al, , 2017. Many methods have been used in an attempt to titrate the PEEP to stabilize lung tissue.…”

Section: Problems With Stabilizing the 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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Tidal changes on CT and progression of ARDS

Cited by 41 publications

References 41 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

Mechanical Ventilation Lessons Learned From Alveolar Micromechanics

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

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