Use of recruitment maneuvers to reopen collapsed lung and the application of positive end- expiratory pressure (PEEP) to prevent collapse have been analyzed by comparing different single and multicenter studies. The current review focuses on atelectasis and how to prevent it. 6, 7 Large tidal volume and high airway pressure increase lung stress and strain with a potential impact on inflammation, at least in the intensive care setting. 5 Atelectasis may promote bacterial translocation and trigger inflammation. Gas trapped behind a continuously closed airway will be absorbed and eventually result in atelectasis. So, what have we learned from these studies? A consistent finding in general anesthesia is the loss of muscle tone with a subsequent decrease in resting lung volume, that is, functional residual capacity. The advance in knowledge has followed two main tracks: studies that identify mechanisms of impairment and large multicenter trials that test these new findings in the clinical environment. However, increased knowledge about how the lung is affected by mechanical ventilation may help us improve methods of ventilator support used during anesthesia and intensive care. 4 in the current issue of A nesthesiology begins with a summary of potential mechanisms of lung damage in the anesthetized, mechanically ventilated, surgical patient. The comprehensive review on intraoperative protective mechanical ventilation by Güldner et al. Can it be harmful also when ventilating the “lung-healthy” patient during anesthesia? Probably not during anesthesia alone, as suggested by animal experiments on prolonged mechanical ventilation, 1, 2 but inflammatory events, 3 such as those associated with surgery, may trigger adverse effects. Mechanical ventilation may cause harm to the lung, at least if the lung is already hurt as is the case in intensive care.
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