Esophageal pressure as an estimate of average pleural pressure with lung or chest distortion in rats

Pressure-volume curves of the lungs and chest wall require knowledge of an effective \u2018average\u2019 pleural pressure (Pplav), and are usually estimated using esophageal pressure as PLes-V and PWes-V curves. Such estimates could be misleading when Ppl becomes spatially non-uniform with lung lavage or shape distortion of the chest. We therefore measured PLes-V and PWes-V curves in conditions causing spatial non-uniformity of Ppl in rats. PLes-V curves of normal lungs were unchanged by chest removal. Lung lavage depressed PLes-V but not PWes-V curves to lower volumes, and chest removal after lavage increased volumes at PL 6515 cmH2O by relieving distortion of the mechanically heterogeneous lungs. Chest wall distortion by ribcage compression or abdominal distension depressed PWes-V curves and PLes-V curves of normal lungs only at PL 653 cmH2O. In conclusion, Pes reflects Pplav with normal and mechanically heterogeneous lungs. With chest wall distortion and dependent deformation of the normal lung, changes of PLes-V curves are qualitatively consistent with greater work of inflatio

Friction and lubrication of pleural tissues

The frictional behaviour of rabbit\u2019s visceral pleura sliding against parietal pleura was assessed in vitro while oscillating at physiological velocities and amplitudes under physiological normal forces. For sliding velocities up to 3 cm s 121 and normal compressive loads up to 12 cm H2O, the average value of the coefficient of kinetic friction (\u3bc) was constant at 0.019\ub10.002 (S.E.) with pleural liquid as lubricant. With Ringer-bicarbonate solution, \u3bc was still constant, but significantly increased (\u394\u3bc=0.008\ub10.001; P < 0.001). Under these conditions, no damage of the sliding pleural surfaces was found on light and electron microscopy. Additional measurements, performed also on peritoneum, showed that changes in nominal contact area or strain of the mesothelia, temperature in the range 19\u201339 \ub0C, and prolonged sliding did not affect \u3bc. Gentle application of filter paper increased \u3bc 10-fold and irreversibly, suggesting alteration of the mesothelia. With packed the red blood cells (RBC) between the sliding mesothelia, \u3bc increased appreciably but reversibly on removal of RBC suspension, whilst no ruptures of RBC occurred. In conclusion, the results indicate a low value of sliding friction in pleural tissues, partly related to the characteristics of the pleural liquid, and show that friction is independent of velocity, normal load, and nominal contact area, consistent with boundary lubrication

A fixed correction of absolute transpulmonary pressure may not be ideal for clinical use: Discussion on “Accuracy of esophageal pressure to assess transpulmonary pressure during mechanical ventilation”

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Maintaining end-expiratory transpulmonary pressure prevents worsening of ventilator-induced lung injury caused by chest wall constriction in surfactant-depleted rats

Objective: To see whether in acute lung injury 1) compression of the lungs caused by thoracoabdominal constriction degrades lung function and worsens ventilator-induced lung injury; and 2) maintaining end-expiratory transpulmonary pressure by increasing positive end-expiratory pressure reduces the deleterious effects of chest wall constriction. Design: Experimental study in rats. Setting: Physiology laboratory. Interventions: Acute lung injury was induced in three groups of nine rats by saline lavage. Nine animals immediately killed served as a control group. Group L had lavage only, group LC had the chest wall constricted with an elastic binder, and group LCP had the same chest constriction but with positive end-expiratory pressure raised to maintain end-expiratory transpulmonary pressure. After lavage, all groups were ventilated with the same pattern for 1(1)/(2) hrs. Measurements and Main Results: Transpulmonary pressure, measured with an esophageal balloon catheter, lung volume changes, arterial blood gasses, and pH were assessed during mechanical ventilation. Lung wet-to-dry ratio, albumin, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-10, and macrophage inflammatory protein-2 in serum and bronchoalveolar lavage fluid and serum E-selectin and von Willebrand Factor were measured at the end of mechanical ventilation. Lavage caused hypoxemia and acidemia, increased lung resistance and elastance, and decreased end-expiratory lung volume. With prolonged mechanical ventilation, lung mechanics, hypoxemia, and wet-to-dry ratio were significantly worse in group LC. Proinflammatory cytokines except E-selectin were elevated in serum and bronchoalveolar lavage fluid in all groups with significantly greater levels of tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 in group LC, which also exhibited significantly worse bronchiolar injury and greater heterogeneity of airspace expansion at a fixed transpulmonary pressure than other groups. Conclusions: Chest wall constriction in acute lung injury reduces lung volume, worsens hypoxemia, and increases pulmonary edema, mechanical abnormalities, proinflammatory mediator release, and histologic signs of ventilator-induced lung injury. Maintaining end-expiratory transpulmonary pressure at preconstriction levels by adding positive end-expiratory pressure prevents these deleterious effects