Randomized Feasibility Trial of a Low Tidal Volume-Airway Pressure Release Ventilation Protocol Compared With Traditional Airway Pressure Release Ventilation and Volume Control Ventilation Protocols

Hirshberg, Eliotte L.; Lanspa, Michael J.; Peterson, Juhee; Carpenter, Lori; Wilson, Emily L.; Brown, Samuel M.; Dean, Nathan C.; Orme, James F.; Grissom, Colin K.

doi:10.1097/ccm.0000000000003437

Cited by 33 publications

(51 citation statements)

References 61 publications

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“…5b). In addition, there was no evidence that the Vt of 12 ml/kg caused VILI since there were no significant differences in PaO 2 /FiO 2 (P/F) ratio, sedation, vasoactive medications, pneumothorax, or outcome between groups [95]. Lastly, the T Low was not set to a strict E FP × 75% = E FT .…”

Section: Analysis Of Recent Rcts Using the Aprv Modementioning

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: Analysis Of Recent Rcts Using the Aprv Modementioning

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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“…Thus, one of the critical protective mechanisms of the TCAV method, the ability to fully open the lung, was not incorporated into the APRV setting in either the Hirshberg or Ganesan study. The conclusion from these clinical studies should not be that "APRV is not lung protective" but rather that the Zhou (Zhou et al, 2017) and TCAV methods (Andrews et al, 2013) are superior to the Ganesan (Lalgudi Ganesan et al, 2018) and Hirshberg (Hirshberg et al, 2018) methods for lung protection. Two recent statistical reviews and meta-analyses of RCTs have shown the APRV mode is associated with a mortality benefit, improved oxygenation, and a greater number of ventilator-free days when compared with conventional ventilation strategies, FIGURE 13 | Chest X-rays (CXRs) and blood gases in a patient with respiratory failure on extracorporeal membrane oxygenation (ECMO).…”

Section: The Tcav Methods To Open and Stabilize The Acutely Injured Lungmentioning

confidence: 98%

“…We postulate that this is also the reason for the failed RCTs using an RM and titrated PEEP (Brower et al, 2004;Meade et al, 2008;Mercat et al, 2008;Cavalcanti et al, 2017). Hirshberg et al (2018) conducted an RCT in adults, and similarly to the Ganesan study, targeted a Vt at ∼6 mL/kg. The study was stopped early, in part because the Vt often exceeded 12 mL/kg, even though there were no significant differences between groups in pneumothorax, sedation, vasoactive medications, P/F ratio, or outcome (Hirshberg et al, 2018).…”

Section: The Tcav Methods To Open and Stabilize The Acutely Injured Lungmentioning

confidence: 99%

“…Hirshberg et al (2018) conducted an RCT in adults, and similarly to the Ganesan study, targeted a Vt at ∼6 mL/kg. The study was stopped early, in part because the Vt often exceeded 12 mL/kg, even though there were no significant differences between groups in pneumothorax, sedation, vasoactive medications, P/F ratio, or outcome (Hirshberg et al, 2018). As stated above, when the TCAV method is used, an increase in Vt is indicative of lung recruitment and is a positive effect.…”

Section: The Tcav Methods To Open and Stabilize The Acutely Injured Lungmentioning

confidence: 99%

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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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“…One randomised controlled trial [99] sought to impose LVT (6-7 cc•kg −1 ) to patients on APRV (APRV-LVT) and found that there was a higher mortality as compared with standard LVT ventilation Another three-armed study [100] aimed at comparing LVT with APRV-LVT and TCAV revealed no significant difference between the three groups in terms of oxygenation or mortality, with the main flaw of the study being that it was limited by power. In addition, the authors reported concerns regarding measured release volumes of >8 cc•kg −1 in the APRV and APRV-LVT groups, but made no mention of the driving pressure or compliance [100]. In an open, compliant lung, this VT is probably affiliated with a low driving pressure and will be distributed across a set of open homogenous alveoli reflecting small alveolar VT [22].…”

Section: Aprv Critiquementioning

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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Randomized Feasibility Trial of a Low Tidal Volume-Airway Pressure Release Ventilation Protocol Compared With Traditional Airway Pressure Release Ventilation and Volume Control Ventilation Protocols

Abstract: Supplemental Digital Content is available in the text.

Cited by 33 publications

References 61 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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