Rationale: Clinicians usually perceive pleural effusion (PLEF) as a restrictive condition that compresses the lung. However the influences of PLEF on ventilator monitoring and management remain uncertain. Methods: Unilateral PLEF was produced by right hemithorax saline instillations of 13 ml/kg (PLEF Mod), and 26 ml/kg (PLEF-Large) into five anesthetized pigs mechanically ventilated with tidal volume 9 ml/kg. Low (1 cmH20, P1) and moderate (10 cmH20, P10) PEEP were consecutively applied under three conditions: baseline (BSL), PLEF-Mod and PLEF-Large. Thus, six stages were studied: BSL-P1, BSL-P10, PLEF-Mod-P1, PLEF-Mod-P10, PLEF-Large-P1 and PLEF-Large-P10. Whole-lung computed tomography (CT) scans were acquired during end-inspiration and end-expiration at each stage. Inspiratory plateau pressure (Pplat) and static tidal compliance of the respiratory system (Cst) were recorded. End expiratory gas lung volume (EELV) and collapse-volume were computed by quantitative CT analysis of the whole lung at end-expiration. PEEP-associated lung recruitment was defined as the difference of collapse-volume between P1 and P10 at end-expiration. Tidal recruitment was calculated as the difference between percent collapse-volume at end-expiration and end-inspiration. Chest wall (Cw) expansion from BSL-P1 was calculated as EELV under PLEF, plus the PLEF volume, minus EELV at BSL-P1. Pplat increased with PLEF additions at P1, but did not change at P10. Cst decreased with PLEF additions more sharply at P1 than at P10. EELV decreased and collapse-volume increased with PLEF additions at both PEEP levels. The left lung contained 30.3±4.2% and 38.5±2.3% of the collapse-volume at PLEF-Mod-P1 and PLEF-Large-P1, respectively. PEEP increase always increased EELV, but effects on Cst and recruitment were different: at BSL, PEEP increase induced little recruitment and worsened Cst; at PLEF-Large, PEEP increase induced extensive recruitment and improved Cst. Tidal recruitment increased with PLEF additions at P1 and was minimized by P10. Cw expansion accommodated approximately 50% of PLEF-Mod and 60% of PLEF-Large at P1. At P10 Cw expansion was equivalent to PLEF-High and 1.5 times PLEF-Mod, allowing full restoration of BSL-P1 EELV. CONCLUSIONS: 1) Although unilateral PLEF produces substantial bilateral lung
collapse at end-exhalation, it imposes little restriction to overall lung inflation and recruitment if the Cw is otherwise normal. 2) PLEF-induced lung collapse and tidal recruitment are effectively abrogated by moderate PEEP. 3) A similar Pplat under the same ventilatory settings may result from different combinations of lung inflation, recruitment, Cw expansion and hydrostatic pressure. In the presence of PLEF, Pplat should be interpreted with caution.