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PEEP titration guided by transpulmonary pressure: lessons from a negative trial
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Hedenstierna laboratory. Hosp Univ Princesa, Dept Crit Care Med, Diego de Leon 62, Madrid 28006, Spain;Inst Salud Carlos III, CIBER Enfermedades Resp, Madrid, Spain.ORCID iD: 0000-0002-7412-2970
Inst Salud Carlos III, CIBER Enfermedades Resp, Madrid, Spain;Inst Invest Biomed August Pi i Sunyer IDIBAPS, Hosp Clin, Dept Anesthesiol & Crit Care, Barcelona, Spain.
Inst Salud Carlos III, CIBER Enfermedades Resp, Madrid, Spain;Hosp Univ Dr Negrin, Res Unit, MODERN, Las Palmas Gran Canaria, Spain;St Michaels Hosp, Li Ka Shing Knowledge Inst, Keenan Res Ctr Biomed Sci, Toronto, ON, Canada.
2019 (English)In: Journal of Thoracic Disease, ISSN 2072-1439, E-ISSN 2077-6624, Vol. 11, p. S1957-S1962Article in journal, Editorial material (Other academic) Published
Abstract [en]

Since the first description of the acute respiratory distress syndrome (ARDS) by the landmark paper of Ashbaugh et al. (1), the adequate use of positive end-expiratory pressure (PEEP) has been surrounded by a vivid controversy. This stems from the fact that its beneficial effects on oxygenation by re-aerating collapsed or flooded airspaces, may be counterbalanced by potential adverse effects on hemodynamics and on the risk of increasing lung tissue mechanical stress. The vast amount of clinical and experimental reports over the last five decades, adequately reflect this “PEEP paradox”: the simultaneous effects of PEEP on gas exchange, lung mechanics and hemodynamics can have competing beneficial or deleterious consequences even in similar clinical or experimental conditions. Thus, the effects of PEEP are complex and difficult to predict, more so in the heterogeneous ARDS lung, and depend not only on the selected level but also on how this level interacts and modifies the lung status. For instance, a high PEEP level may improve oxygenation but if it not associated to significant recruitment of collapsed lung regions can increase non-dependent lung overdistension.

Although in clinical practice the changes in oxygenation remain the main driver for PEEP selection, the progressive awareness that mechanical ventilation can aggravate lung injury has shifted the interest to the potential lung-protective effects of PEEP, already recognized in early experimental studies (2). By preventing end-expiratory lung collapse and increasing end-expiratory lung volume, PEEP can counteract the two major mechanisms related to ventilation-induced lung injury (VILI) (3). On the one hand, it reduces or avoids the strain resulting from cyclic recruitment-derecruitment in boundary-regions of the mid-dependent regions, between collapsed and aerated lung. On the other hand, it promotes a more homogeneous distribution of ventilation by increasing the size of the functional lung thereby reducing the cyclic inflation stress of the non-dependent lung. Lung-protective ventilation (LPV) strategies aimed at reducing the mechanical stress on the lung, are the only therapeutic interventions that have improved ARDS outcome, and although the ultimate contribution of VILI to mortality is not known, it is important to emphasize that only a fifth of ARDS patients die with refractory hypoxemia (4). However, the definitive role of PEEP in lung protection has been difficult to establish in clinical studies (5). Dichotomous high-vs-low PEEP study designs, failure to confirm patient responsiveness to PEEP (6), and absence of proper PEEP individualization are among the reasons behind this lacking evidence.

Place, publisher, year, edition, pages
2019. Vol. 11, p. S1957-S1962
National Category
Respiratory Medicine and Allergy
Identifiers
URN: urn:nbn:se:uu:diva-395998DOI: 10.21037/jtd.2019.08.03ISI: 000488235600037PubMedID: 31632797OAI: oai:DiVA.org:uu-395998DiVA, id: diva2:1366224
Available from: 2019-10-28 Created: 2019-10-28 Last updated: 2019-10-28Bibliographically approved

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