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dc.contributor.authorAndrews, P.
dc.contributor.authorMadden, M.
dc.contributor.authorHabashi, N.M.
dc.date.accessioned2020-04-14T14:28:49Z
dc.date.available2020-04-14T14:28:49Z
dc.date.issued2020
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85082666803&doi=10.3389%2ffphys.2020.00227&partnerID=40&md5=b75aa05fb33a122cb212eb91b234dfdc
dc.identifier.urihttp://hdl.handle.net/10713/12546
dc.description.abstractAcute 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 ventilator-induced 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. Copyright The Authorsen_US
dc.description.sponsorshipNational Institutes of Health, NIH: R01 HL142702en_US
dc.description.urihttps://doi.org/10.3389/fphys.2020.00227en_US
dc.language.isoen_USen_US
dc.publisherFrontiers Media S.A.en_US
dc.relation.ispartofFrontiers in Physiology
dc.subjectalveolar mechanicsen_US
dc.subjectAPRVen_US
dc.subjectARDSen_US
dc.subjectmechanical ventilalionen_US
dc.subjectVILI (ventilator induced lung injury)en_US
dc.titleA Physiologically Informed Strategy to Effectively Open, Stabilize, and Protect the Acutely Injured Lungen_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fphys.2020.00227


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