Effects of Recruiting Maneuvers in Patients with Acute Respiratory Distress Syndrome Ventilated with Protective Ventilatory Strategy

Background: A lung-protective ventilatory strategy with low tidal volume (VT) has been proposed for use in acute respiratory distress syndrome (ARDS). Alveolar derecruitment may occur during the use of a lung-protective ventilatory strategy and may be prevented by recruiting maneuvers. This study examined the hypothesis that the effectiveness of a recruiting maneuver to improve oxygenation in patients with ARDS would be influenced by the elastic properties of the lung and chest wall.

Methods: Twenty-two patients with ARDS were studied during use of the ARDSNet lung-protective ventilatory strategy: VT was set at 6 ml/kg predicted body weight and positive end-expiratory pressure (PEEP) and inspiratory oxygen fraction (Fio2) were set to obtain an arterial oxygen saturation of 90-95% and/or an arterial oxygen partial pressure (Pao2) of 60- 80 mmHg (baseline). Measurements of Pao2/Fio2, static volume-pressure curve, recruited volume (vertical shift of the volume-pressure curve), and chest wall and lung elastance (EstW and EstL: esophageal pressure) were obtained on zero end-expiratory pressure, at baseline, and at 2 and 20 min after application of a recruiting maneuver (40 cm H2O of continuous positive airway pressure for 40 s). Cardiac output (transesophageal Doppler) and mean arterial pressure were measured immediately before, during, and immediately after the recruiting maneuver. Patients were classified a priori as responders and nonresponders on the basis of the occurrence or nonoccurrence of a 50% increase in Pao2/Fio2 after the recruiting maneuver.

Results: Recruiting maneuvers increased Pao2/Fio2 by 20 +/- 3% in nonresponders (n = 11) and by 175 +/- 23% (n = 11; mean +/- standard deviation) in responders. On zero end-expiratory pressure, EstL (28.4 +/- 2.2 vs. 24.2 +/- 2.9 cm H2O/l) and EstW (10.4 +/- 1.8 vs. 5.6 +/- 0.8 cm H2O/l) were higher in nonresponders than in responders (P < 0.01). Nonresponders had been ventilated for a longer period of time than responders (7 +/- 1 vs. 1 +/- 0.3 days;P < 0.001). Cardiac output and mean arterial pressure decreased by 31 +/- 2 and 19 +/- 3% in nonresponders and by 2 +/- 1 and 2 +/- 1% in responders (P < 0.01).