• Göran Hedenstierna and Lennart Edmark.
• Uppsala University, Dept of Medical Sciences, Clinical Physiology, 751 85 Uppsala, Sweden. goran.hedenstierna@medsci.uu.se
• Best Pract Res Clin Anaesthesiol. 2010 Jun 1; 24 (2): 157-69.

AbstractAtelectasis appears in about 90% of all patients who are anaesthetised. Up to 15-20% of the lung is regularly collapsed at its base during uneventful anaesthesia prior to any surgery being carried out. Atelectasis can persist for several days in the postoperative period. It is likely to be a focus of infection and may contribute to pulmonary complications. A major cause of anaesthesia-induced lung collapse is the use of high oxygen concentration during induction and maintenance of anaesthesia together with the use of anaesthetics that cause loss of muscle tone and fall in functional residual capacity (a common action of almost all anaesthetics). This causes absorption atelectasis behind closed airways. Compression of lung tissue and loss of surfactant or surfactant function are additional potential causes of atelectasis. Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had re-opened a previously collapsed lung tissue results in rapid reappearance of atelectasis. If 40% O2 in nitrogen is used for ventilation of the lungs, atelectasis reappears slowly. A post-oxygenation manoeuvre is regularly performed to reduce the risk of hypoxaemia during awakening. However, a combination of oxygenation and airway suctioning will most likely cause new atelectasis. Recruitment at the end of the anaesthesia followed by ventilation with 100% O2 causes new atelectasis before anaesthesia is terminated but not with ventilation with lower fraction of inspired oxygen (FIO2). Thus, recruitment must be followed by ventilation with moderate FIO2.

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