Effect of tidal volume and positive end-expiratory pressure on expiratory time constants in experimental lung injury

Henderson, William R.; Dominelli, Paolo B.; Molgat‐Seon, Yannick; Lipson, Rachel; Griesdale, Donald; Sekhon, Mypinder S.; Ayas, Najib; Sheel, A. William

doi:10.14814/phy2.12737

Cited by 10 publications

(5 citation statements)

References 31 publications

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“…The lung becomes time and pressure dependent when acutely injured, such that it will quickly collapse at atmospheric pressure [67,[84][85][86]. In animal ARDS models, the majority of lung collapse occurred in the first 4 s of exhalation with collapse as fast as 0.6 s [72].…”

Section: Expiratory Time and Lung Collapsementioning

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: Expiratory Time and Lung Collapsementioning

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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“…Increasing PEEP irrespective of resistance increases the time constant too. In healthy lungs this increase is not confined to early or late time constant segments but is constant throughout the expiratory phase [153]. In injured lungs the PEEP increase changes the mechanical properties of the respiratory system fast-emptying compartments [57].…”

Section: Discussionmentioning

confidence: 99%

Transpulmonary driving pressure during mechanical ventilation–validation of a non‐invasive measurement method

Gudmundsson

Persson

Perchiazzi

et al. 2019

Acta Anaesthesiol Scand

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Background: One of the most common diagnoses in the intensive care unit is acute respiratory failure. In its most severe form it is called acute respiratory distress syndrome and often requires mechanical ventilation. The main challenge for physicians is to provide mechanical ventilation that treats the patient´s hypoxia, which can be due to a variety of causes, without damaging the lung. Method:In paper I computed tomography scans were acquired in ten anesthetized surfactant depleted pigs. The volume of gas and atelectasis were correlated with transpulmonary pressure as the pressure support and PEEP were lowered. In paper II a non-invasive method for measuring transpulmonary driving pressure was validated in 31 mechanically ventilated intensive care patients. In paper III external expiratory resistors were added to the expiratory limb of the ventilator while calculating expiratory time constant, respiratory compliance, driving pressure and intrinsic PEEP in 12 anesthetized pigs. In paper IV transpulmonary pressure was calculated from esophageal pressure in supine and prone position in 10 anesthetized lung healthy patients.Results: Gradual decrease in transpulmonary pressure causes a proportional increase in atelectasis and decrease in gas content while the work of breathing increases. There is a good statistical agreement between the conventional and the non-invasive method for measuring transpulmonary driving pressure. Increasing the expiratory resistance increases the expiratory time constant and increases intrinsic PEEP in healthy lungs. There is a great variability in esophageal pressure in the part of the esophagus 22 -44cm from the nostrils in both supine and prone position. Depending on method the transpulmonary pressure either increases or decreases when patients are turned in prone position. Conclusion:There is no transpulmonary pressure threshold, where atelectasis with desaturation or cyclic collapse suddenly occurs during gradual decrease in the ventilator support. The PEEP-step method is comparable to the traditional esophageal balloon method for measuring transpulmonary driving pressure. The application of expiratory resistors could be useful during weaning from mechanical ventilation. The mean end-expiratory esophageal pressure changes which affect the calculation of transpulmonary pressure but uncertainties about the use of absolute esophageal pressure remains.

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“…The tendency for ongoing lung collapse is increased in ARDS [87,91,92]. In animal models of ARDS, loss of aeration during exhalation can occur as quickly as 0.6 s, with the majority of aeration loss occurring within the first 4 s of exhalation [93,94].…”

Section: Time-dependent Alveolar Collapsementioning

confidence: 99%

First Stabilize and then Gradually Recruit: A Paradigm Shift in Protective Mechanical Ventilation for Acute Lung Injury

Nieman

Kaczka

Andrews

et al. 2023

JCM

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Acute respiratory distress syndrome (ARDS) is associated with a heterogeneous pattern of injury throughout the lung parenchyma that alters regional alveolar opening and collapse time constants. Such heterogeneity leads to atelectasis and repetitive alveolar collapse and expansion (RACE). The net effect is a progressive loss of lung volume with secondary ventilator-induced lung injury (VILI). Previous concepts of ARDS pathophysiology envisioned a two-compartment system: a small amount of normally aerated lung tissue in the non-dependent regions (termed “baby lung”); and a collapsed and edematous tissue in dependent regions. Based on such compartmentalization, two protective ventilation strategies have been developed: (1) a “protective lung approach” (PLA), designed to reduce overdistension in the remaining aerated compartment using a low tidal volume; and (2) an “open lung approach” (OLA), which first attempts to open the collapsed lung tissue over a short time frame (seconds or minutes) with an initial recruitment maneuver, and then stabilize newly recruited tissue using titrated positive end-expiratory pressure (PEEP). A more recent understanding of ARDS pathophysiology identifies regional alveolar instability and collapse (i.e., hidden micro-atelectasis) in both lung compartments as a primary VILI mechanism. Based on this understanding, we propose an alternative strategy to ventilating the injured lung, which we term a “stabilize lung approach” (SLA). The SLA is designed to immediately stabilize the lung and reduce RACE while gradually reopening collapsed tissue over hours or days. At the core of SLA is time-controlled adaptive ventilation (TCAV), a method to adjust the parameters of the airway pressure release ventilation (APRV) modality. Since the acutely injured lung at any given airway pressure requires more time for alveolar recruitment and less time for alveolar collapse, SLA adjusts inspiratory and expiratory durations and inflation pressure levels. The TCAV method SLA reverses the open first and stabilize second OLA method by: (i) immediately stabilizing lung tissue using a very brief exhalation time (≤0.5 s), so that alveoli simply do not have sufficient time to collapse. The exhalation duration is personalized and adaptive to individual respiratory mechanical properties (i.e., elastic recoil); and (ii) gradually recruiting collapsed lung tissue using an inflate and brake ratchet combined with an extended inspiratory duration (4–6 s) method. Translational animal studies, clinical statistical analysis, and case reports support the use of TCAV as an efficacious lung protective strategy.

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Effect of tidal volume and positive end-expiratory pressure on expiratory time constants in experimental lung injury

Cited by 10 publications

References 31 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

Transpulmonary driving pressure during mechanical ventilation–validation of a non‐invasive measurement method

First Stabilize and then Gradually Recruit: A Paradigm Shift in Protective Mechanical Ventilation for Acute Lung Injury

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