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Bench-To-Bedside Review: Permissive Hypercapnia Donall O’ Croinin1, Martina Ni Chonghaile2, Brendan Higgins3 and John G Laffey4

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Bench-To-Bedside Review: Permissive Hypercapnia Donall O’ Croinin1, Martina Ni Chonghaile2, Brendan Higgins3 and John G Laffey4 Available online http://ccforum.com/content/9/1/51 Review Bench-to-bedside review: Permissive hypercapnia Donall O’ Croinin1, Martina Ni Chonghaile2, Brendan Higgins3 and John G Laffey4 1Clinical Research Fellow, Department of Physiology, University College Dublin, Dublin 2Clinical Research Fellow, Department of Anaesthesia, University College Hospital, and Department of Anaesthesia, Clinical Sciences Institute, National University of Ireland, Galway, Ireland 3Postdoctoral Research Fellow, Department of Anaesthesia, Clinical Sciences Institute, National University of Ireland, Galway, Ireland 4Clinical Lecturer, Department of Anaesthesia, University College Hospital, and Department of Anaesthesia, Clinical Sciences Institute, National University of Ireland, Galway, Ireland Corresponding author: John G Laffey, [email protected] Published online: 5 August 2004 Critical Care 2005, 9:51-59 (DOI 10.1186/cc2918) This article is online at http://ccforum.com/content/9/1/51 © 2004 BioMed Central Ltd 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. Keywords acidosis, acute lung injury, acute respiratory distress syndrome, buffering, hypercapnia, mechanical ventilation, ventilation induced lung injury, sepsis Introduction This article reviews the current clinical status of permissive Current protective lung ventilation strategies generally involve hypercapnia, discusses insights gained to date from basic some degree of hypercapnia. This has resulted in a shift in scientific studies of hypercapnia and acidosis, and considers clinical paradigms regarding hypercapnia from avoidance to the potential clinical implications of these findings for the tolerance, with hypercapnia increasingly permitted in order to management of patients with ALI. realize the benefits of low lung stretch. Insights from laboratory models of acute lung injury (ALI) have suggested Permissive hypercapnia: current paradigms that hypercapnia may play an active role in the pathogenesis The potential for mechanical ventilation to potentiate or even of inflammation and tissue injury. This raises the possibility cause lung injury and worsen outcome in acute respiratory that hypercapnia per se may exert direct protective effects in distress syndrome (ARDS) patients is clear [1–3]. Ventilator- ALI states, distinct from the demonstrated benefits of associated lung injury (VALI) may occur via several reduced lung stretch. However, there are no clinical data mechanisms. Mechanotrauma results from repetitive over- evaluating the efficacy of hypercapnia per se, independent of stretching and damage to lung tissue, and cyclic alveolar ventilator strategy, in ALI states. Furthermore, it is unlikely that recruitment and derecruitment [4–9]. Increased mechanical a clinical trial of ‘permissive hypercapnia’ will be carried out, stress may directly activate the cellular and humoral immune at least in the medium term. response in the lung [8–11], although the exact role played κ κ κ κ ALI = acute lung injury; ARDS = acute respiratory distress syndrome; I B = inhibitory protein B; NF- B = nuclear factor B; PaCO2 = arterial carbon dioxide tension; THAM = tris-hydroxymethyl aminomethane; VALI = ventilator-associated lung injury. 51 Critical Care February 2005 Vol 9 No 1 O’ Croinin et al. by this mechanism in the pathogenesis of lung and systemic Because outcome in the intensive care unit might be related organ injury has been disputed [12,13]. In any case, the to systemic injury – as opposed to simply lung injury – it is potential for intrapulmonary prostaglandins [14], cytokines necessary to determine the effects of hypercapnia on [15], endotoxin [16] and bacteria [17] to cross an impaired pathophysiological function in the heart and brain as well as alveolar–capillary barrier following high stretch mechanical the lung. These issues are further underlined by the fact that ventilation is clear. hypercapnia has potentially severe adverse effects in some clinical settings, such as critically elevated intracranial VALI may be limited by instituting protective lung ventilation pressure or pulmonary vascular resistance. strategies in order to reduce mechanical trauma and the resulting inflammatory effects. These strategies invariably It is not currently practicable or feasible to examine the direct involve a reduction in the tidal volume and/or transalveolar effects of hypercapnic acidosis, independent of ventilator pressure, which generally leads to an elevation in arterial strategy, in humans. This has necessitated a return to the carbon dioxide tension (PaCO2), an approach that has been laboratory bench, and an examination of the potential for termed ‘permissive hypercapnia’. These protective lung induced hypercapnia to modulate the severity of ALI and ventilation strategies have been demonstrated to improve systemic organ injury in animal models. survival in patients with ARDS [1,18,19]. The reported levels Hypercapnia and acidosis: insights from the of PaCO2 and pH (mean maximum PaCO2 67 mmHg, mean pH 7.2) in the study conducted Hickling and coworkers [18] bench reflect typical levels observed with institution of this There is a growing body of evidence suggesting that technique. Accordingly, there has been a shift toward greater hypercapnia and acidosis exert biologically important clinical acceptability of hypercapnia in ALI and ARDS. beneficial effects in experimental ALI and systemic organ Current paradigms attribute the protective effect of these injury. The mechanisms that underlie these protective effects ventilatory strategies solely to reductions in lung stretch, with of hypercapnia are increasingly well characterized. hypercapnia permitted in order to achieve this goal. However, the potential exists for hypercapnia to modulate the Acute lung injury pathogenesis of VALI. Direct administration of inspired carbon dioxide has been demonstrated to attenuate ALI in several ex vivo and in vivo ‘Bedside-to-bench’: rationale for laboratory laboratory models. In the isolated perfused rabbit lung, studies hypercapnic acidosis was demonstrated to attenuate the Protective ventilatory strategies that involve hypoventilation increases in lung permeability seen following free radical [24], result in both limitation of tidal volume and elevation in ischaemia/reperfusion [24,25] and ventilator-induced [26] ALI. systemic carbon dioxide tension. Lung stretch is distinct from Hypercapnic acidosis directly attenuates indices of ALI such elevated carbon dioxide tension, and by manipulation of as oxygenation, lung mechanics and lung permeability, respiratory parameters (frequency, tidal volume, dead-space, following in vivo pulmonary [27] and mesenteric [28] inspired carbon dioxide) it can, at least to some extent, be ischaemia/reperfusion. Hypercapnic acidosis also directly separately controlled. The ARDSnet investigators reported a protects against endotoxin-induced lung injury, a model of 25% reduction in mortality with a complex ventilation strategy sterile sepsis-induced ARDS [29]. Hypercapnic acidosis [20] involving limitation of mean tidal volume to 6 ml/kg, as attenuates pulmonary apoptosis, a mechanism of compared with a more traditional tidal volume of 12 ml/kg [2]. programmed cell death, following pulmonary ischaemia/ That study minimized the potential for hypercapnia in the low reperfusion [27]. tidal volume group, and instead permitted increased respiratory rates (respiratory frequency of 29 breaths/min). In In most clinical scenarios, therapeutic intervention is only fact, the need to reduce tidal volumes substantially to improve possible after initiation of the injury process. The therapeutic outcome in ARDS patients was recently questioned [21,22], potential of hypercapnic acidosis is underlined by the finding and it is increasingly clear that most clinicians seldom use that it was effective when instituted after initiation of the lung very low tidal volumes in practice [23]. These findings raise injury process, in the settings of both mesenteric ischaemia/ questions regarding the need for – and indeed the clinical reperfusion and endotoxin-induced ALI models [28,29]. This acceptability of – permissive hypercapnia. contrasts with many other initially promising experimental strategies, which demonstrate potential when used before These issues underscore the need to determine the effects of the injury process but lose their effectiveness when utilized hypercapnia in isolation. If hypercapnia were proven to have after the development of organ injury. independent benefit, then deliberately
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