[The effect of PEEP-ventilation on gas exchange and airway closure in experimental pulmonary emphysema]. / Der Einfluss der PEEP-Beatmung auf Gasaustausch und Atemwegsverschluss im experimentellen Lungenemphysem.

The benefits of mechanical ventilation with positive end-expiratory pressure (PEEP) are well documented, especially for patients with acute respiratory failure. PEEP increases functional residual capacity (FRC) and reduces closing volume (CV) and ventilation-perfusion mismatching. Little is known about the effects of PEEP in patients with chronic obstructive pulmonary disease, where closing volume and ventilation-perfusion mismatching are increased. We investigated the effects of PEEP in a canine model of panlobular emphysema (PLE). METHODS. After completion of control-period measurements, PLE was induced in eight dogs by intratracheal application of 20 ml aerosolized 16% papain solution. Three weeks later the effects of continuous positive-pressure ventilation (CPPV, PEEP 10 cmH2O) on gas exchange, FRC, and CV were investigated. Conventional intermittent positive-pressure ventilation (IPPV) served as reference. Measurements of CV were done using both the foreign gas bolus method and the single-breath oxygen test. FRC was determined by the nitrogen dilution technique. RESULTS. The papain-induced emphysema produced a deteriation in oxygenation, enlargement of FRC and CV, and an increase in quasi-static lung compliance. CPPV led to a further increase of FRC, but gas exchange was not improved nor was CV reduced. In the PLE period, mean pulmonary arterial pressures (MPAP) were higher during both modes of ventilation. CPPV tended to increase MPAP and pulmonary capillary wedge pressure when compared with IPPV. Systemic hemodynamic conditions were stable throughout the experiment. CONCLUSIONS. The application of PEEP to emphysematous lungs seemed to enlarge FRC, predominantly in the nondependent rather than in the dependent lung regions, which are prone to airway closure. In patients with emphysema, ventilation with PEEP may further deteriorate the impaired distribution of ventilation and thus counteract any improvement of gas exchange.

Single breath N2 washout in papain-induced pulmonary emphysema.

Single breath nitrogen washout tests were analyzed in dogs (n = 8) with healthy lungs and after development of emphysema. The animals were in the supine position and studied during anaesthesia and mechanical ventilation (FiO2 = 0.4, FiN2 = 0.6). During controlled expiration with constant flow (VE = 0.15 l/s) onset of phase IV of the alveolar plateau was related to airway closure of dependent lung regions (closing volume CV). In the control state, CV accounted for 6.2 +/- 1.5% VC, and closing capacity (CC) was lower than functional residual capacity (FRC). Likewise, gas exchange was normal in all animals (PaO2 = 24.7 +/- 3.32 kPa, PaCO2 = 5.18 +/- 0.53 kPa, PA-aO2 = 2.6 +/- 0.3 kPa). Panlobular emphysema (PLE) was induced by inhalation of papain (100 mg/kg). After three weeks development of PLE was documented by measurements of lung volumes (functional residual capacity (FRC), expired vital capacity (EVC), total lung capacity (TLC), residual volume (RV], pulmonary mechanics (dynamic and static compliance (Cdyn, Cstat), mean airway resistance (Raw], gas exchange (PaO2, PaCO2, PA-aO2), and by radiomorphological analysis. In the PLE-group, FRC and RV (p less than or equal to 0.05), and Cstat (p less than or equal to 0.01) were significantly elevated. CV increased to 16.2 +/- 2.7% VC (p less than or equal to 0.01) and CC exceeded FRC by 80 ml, indicating that tidal volume breathing took place within the range of closing volume. Oxygenation was significantly impaired (PaO2 = 18.6 +/- 3.72 kPa, PA-aO2 = 6.5 +/- 1.1 kPa, p less than or equal to 0.05), but not CO2-elimination. Pathological analysis by radiomorphological means showed dissiminate parenchymal lesions compatible with emphysema of grade II severity located predominantly in subpleural areas. In dogs with papain-induced PLE, premature closure of dependent airways is enhanced, which is due to structural changes and a loss of elastic recoil in the lungs.