Abstract

Positive-pressure ventilation during general anesthesia is a prerequisite for numerous surgical conditions. Mechanical ventilation is non-physiological and can induce lung injury, although ventilator-induced lung injury may be of minor clinical importance during anesthesia for most patients with healthy lungs. However, growing evidence suggests that lung injury can be initiated by mechanical ventilation with a low tidal volume as well as with a high tidal volume in animal models of healthy lungs [1-4]. These recent data suggest that ventilation strategies to minimize lung stress (e.g., prevention of repeated closure and opening) improve oxygenation and can reduce lung injury during general anesthesia. A previous study demonstrated that atelectasis rapidly develops after the induction of anesthesia with a high oxygen fraction, which can be effectively resolved by a lung recruitment maneuver and subsequent application of a substantial level of positive end-expiratory pressure (PEEP) [5]. Increase in shunt and low ventilation to perfusion after the induction of general anesthesia are due to alterations in the shape and dimension of the thoracic cage, which result in reductions in the functional residual capacity (FRC) and pulmonary compliance and an increase in airway resistance [6,7]. The cephalad movement and reduced activity of the diaphragm in the supine position promote the formation of compression atelectasis in the dependent portion of the lung. In addition, the decreased lung volume increases the ratio of the closing capacity to FRC during general anesthesia, which may increase cyclic alveolar closure and reopening during mechanical ventilation. In particular, the increase in abdominal pressure caused by pneumoperitoneum and the head-down body position during laparoscopic surgery causes an additional cranial shift in the end-expiratory position of the diaphragm and enhances airway

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