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dc.contributor.authorO' Croinin, Donall
dc.contributor.authorNi Chonghaile, Martina
dc.contributor.authorHiggins, Brendan
dc.contributor.authorLaffey, John G
dc.date.accessioned2018-08-24T08:25:53Z
dc.date.available2018-08-24T08:25:53Z
dc.date.issued2004-01-01
dc.identifier.citationO' Croinin, Donall; Ni Chonghaile, Martina; Higgins, Brendan; Laffey, John G (2004). . Critical Care 9 (1), 51-59
dc.identifier.issn1364-8535
dc.identifier.urihttp://hdl.handle.net/10379/9638
dc.description.abstractCurrent protective lung ventilation strategies commonly involve hypercapnia. This approach has resulted in an increase in the clinical acceptability of elevated carbon dioxide tension, with hypoventilation and hypercapnia 'permitted' in order to avoid the deleterious effects of high lung stretch. Advances in our understanding of the biology of hypercapnia have prompted consideration of the potential for hypercapnia to play an active role in the pathogenesis of inflammation and tissue injury. In fact, hypercapnia may protect against lung and systemic organ injury independently of ventilator strategy. However, there are no clinical data evaluating the direct effects of hypercapnia per se in acute lung injury. This article reviews the current clinical status of permissive hypercapnia, discusses insights gained to date from basic scientific studies of hypercapnia and acidosis, identifies key unresolved concerns regarding hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
dc.publisherSpringer Nature
dc.relation.ispartofCritical Care
dc.subjectacidosis
dc.subjectacute lung injury
dc.subjectacute respiratory distress syndrome
dc.subjectbuffering
dc.subjecthypercapnia
dc.subjectmechanical ventilation
dc.subjectventilation induced lung injury
dc.subjectsepsis
dc.subjectrespiratory-distress-syndrome
dc.subjectacute lung injury
dc.subjectcytoplasmic ph regulation
dc.subjectischemia-reperfusion injury
dc.subjectactivated human-neutrophils
dc.subjecttraditional tidal volumes
dc.subjectcarbon-dioxide
dc.subjectintracellular ph
dc.subjectmechanical ventilation
dc.subjectnitric-oxide
dc.title
dc.typeArticle
dc.identifier.doi10.1186/cc2918
dc.local.publishedsourcehttps://ccforum.biomedcentral.com/track/pdf/10.1186/cc2918?site=ccforum.biomedcentral.com
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