Experimental intra-abdominal hypertension attenuates the benefit of positive end-expiratory pressure in ventilating effusion-compressed lungs*.

OBJECTIVE: To test the ability of positive end-expiratory pressure to offset the reduction of resting lung volume caused by intra abdominal hypertension, unilateral pleural effusion, and their combination.
DESIGN: : Controlled application of intrapleural fluid, raised abdominal pressure and their combination before and after positive end-expiratory pressure in an anesthetized porcine model of controlled ventilation.
SETTING: Large animal laboratory of a university-affiliated hospital.
SUBJECTS: Fourteen deeply anesthetized swine (weight 30-35 kg).
INTERVENTIONS: Unilateral pleural effusion instillation (13 mL/kg), intra-abdominal hypertension (15 mm Hg), and simultaneous pleural effusion/intra abdominal hypertension. MEASUREMENTS: Tidal compliance, end-expiratory lung aeration by gas dilution functional residual capacity, and quantitative analyses of computerized tomograms of the lungs at the extremes of the tidal cycle. MAIN
RESULTS: Positive end-expiratory pressure of 10 cm H2O (positive end-expiratory pressure 10) increased mean functional residual capacity by 368 mL when pleural effusion was present and by 184 mL when intra-abdominal hypertension was present. When pleural effusion and intra-abdominal hypertension were simultaneously applied, positive end-expiratory pressure 10 failed to improve tidal compliance and increased functional residual capacity by only 77 mL, whereastidal recruitment during ventilation remained substantial.
CONCLUSIONS: The presence of intra-abdominal hypertension negates most of the positive end-expiratory pressure 10 benefit in reversing pleural effusion-induced de-recruitment. Relief of intra-abdominal hypertension may be instrumental to the treatment of pleural effusion-associated lung restriction and cyclical tidal collapse and reopening.