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O' Croinin, Donall Ni Chonghaile, Martina Higgins, Brendan Laffey, John G
O' Croinin, Donall
Ni Chonghaile, Martina
Higgins, Brendan
Laffey, John G
Publication Date
2004-01-01
Keywords
acidosis, acute lung injury, acute respiratory distress syndrome, buffering, hypercapnia, mechanical ventilation, ventilation induced lung injury, sepsis, respiratory-distress-syndrome, acute lung injury, cytoplasmic ph regulation, ischemia-reperfusion injury, activated human-neutrophils, traditional tidal volumes, carbon-dioxide, intracellular ph, mechanical ventilation, nitric-oxide
Type
Article
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Citation
O' Croinin, Donall; Ni Chonghaile, Martina; Higgins, Brendan; Laffey, John G (2004). . Critical Care 9 (1), 51-59
Abstract
Current 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.
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Publisher
Springer Nature
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Attribution-NonCommercial-NoDerivs 3.0 Ireland