Fig. 2.
Changes induced by central obesity in supine position during spontaneous breathing, sedation and paralysis, and mechanical ventilation. (A) The patient is actively breathing. Displacement of the diaphragm by a high abdominal load (horizontal red arrows) leads to high pleural pressure and lung volumes reduction with consequent narrowing of the small airways (red arrows in subpanel a, representing a partially collapsed airway-alveolar unit). Airway collapse at low lung volume is partially counteracted by the contraction of the inspiratory muscles (green arrows), which lowers pleural pressure, at the cost of a high work of breathing produced by the patient (work of breathing [WOB] patient). (B) The patient is sedated and paralyzed, with suboptimal manual intermittent positive pressure ventilation (IPPV). Paralysis prevents inspiratory muscular contraction (red crosses on the green arrows) and pronounced total collapse of the small airways predominates (subpanel b). Concomitant administration of a high fraction of inspired oxygen (Fio2) results in reabsorption atelectasis in underventilated alveolar units (subpanel c), with further reductions in expiratory lung volumes, deterioration of compliance, and shunting leading to hypoxemia. (C) Mechanical ventilation with a titrated level of positive end-expiratory pressure (PEEP) counteracts small airways collapse (subpanel d), restoring lung volumes and, consequently, lung mechanics and oxygenation.