Airway closure, more harmful than atelectasis in intensive care?
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Airway closure, more harmful than atelectasis in intensive care? Göran Hedenstierna1* , Lu Chen2,3 and Laurent Brochard2,3 © 2020 The Author(s)
Since the mid-1980s, atelectasis has been demonstrated during anesthesia in lung healthy subjects [1] and in intensive care patients suffering from acute respiratory failure and requiring ventilator support [2]. In the latter case, there are additional causes of airless lung tissues, such as alveolar fluid filling and consolidation. The airless tissue is still perfused, causing a shunt with impairment of the oxygenation of blood. Moreover, cyclic opening and closing of alveolar units may harm the tissue and trigger an inflammatory reaction [3]. This is well known and has been considered a major morphological disturbance in the mechanically ventilated subject. However, there are indirect observations of another morphological disturbance, some airways that are either continuously closed or cyclically opening and closing during the ventilation. This airway closure is a normal phenomenon, although of small magnitude and seldom continuous, in awake, spontaneously breathing healthy subjects. It begins in dependent lung regions and spreads out to include additional airways during the continuing expiration [4]. However, during anesthesia and in acute respiratory failure airway closure is much more marked and may be of similar importance as alveolar airlessness in impeding lung function, and promoting inflammation [5, 6]. Airway closure was initially demonstrated (or rather suggested) by single breath tracer gas recordings [4]. Recently, airway closure was also visually demonstrated by synchrotron radiation technique (Fig. 1) displaying different patterns of the closure phenomenon [7]. One was complete closure of dependent, peripheral airways, in line with what has been assumed since long. Another *Correspondence: [email protected] 1 Hedenstierna Laboratory, Department of Medical Sciences, University Hospital, Uppsala University, Entr 40:2, 75185 Uppsala, Sweden Full author information is available at the end of the article
was repeated closures of the airway so that gas was trapped within a distance of the airway. This suggests a more complicated background for airway closure, not only trans-airway pressure but also changes in surface tension, liquid distribution within the airway and interdependence between units [7, 8]. Airway closure increases with increasing age, a consequence of loss of elastic tissue in the lung that may produce a positive pleural pressure in dependent regions [4]. Decrease in resting lung volume, functional residual capacity (FRC), promotes airway closure [4]. Factors that in combination reduce FRC, like anesthesia, age, obesity and head down positions for surgery will all increase likelihood for airway closure. Recently, complete airway closure has been suggested in ARDS [6]. In these patients, lung inflation starts when airway pressure reaches a critical level of opening pressure [9]. This has been mistaken i
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