Controversy exists whether high frequency oscillatory ventilation with an active expiratory phase (HFO-A) should be used at low ventilator pressures or high alveolar volumes to minimize lung injury in the atelectasis-prone lung. We therefore ventilated 20 anesthetized, tracheostomized rabbits made surfactant-deficient by lung lavage in 1 of 3 ways: HFO-A at a high lung volume (HFO-A/HI), HFO-A at a low lung volume (HFO-A/LO), or conventional mechanical ventilation (CMV); all received 100% oxygen for 7 h. We examined oxygenation, lung mechanics, and lung pathology. Arterial oxygenation in the HFO-A/HI rabbits was kept greater than 350 mm Hg. Mean lung volume above FRC in these animals was 23.4 ml/kg. In rabbits ventilated with HFO-A/LO and CMV, arterial oxygen tensions were 70 to 100 mm Hg. Mean lung volumes were 7.8 and 4.3 ml/kg, respectively. Total respiratory system pressure-volume curves (P-V curves) showed no change from baseline in the HFO-A/HI group after 7 h of ventilation. The low lung volume groups (HFO-A/LO and CMV) showed a diminution in hysteresis of their P-V curves, lower total respiratory system compliance, more hyaline membranes and severe airway epithelial damage. (All changes significant with p less than 0.05). We conclude that maintenance of alveolar volume is a key mechanism in the prevention of lung injury during mechanical ventilation of the atelectasis-prone lung. For optimal outcome using high frequency oscillatory ventilation, alveoli must be actively reexpanded and then kept expanded using appropriate mean airway pressures.

We evaluated four ventilator patterns after the administration of 80 mg/kg bovine lipid extract surfactant (LES) to anesthetized, paralyzed, saline-lavaged New Zealand white rabbits. Two ventilator types were compared: high frequency oscillatory ventilation (HFO) versus conventional mechanical ventilation (CMV), each at high (HI) and low (LO) end-expiratory lung volumes (EELV); n = 6, each group; treatment duration = 4 h. Target PaO2 ranges were > 350 mm Hg for groups with high EELV (i.e., HFO-HI and CMV-HI) and 70 to 100 mm Hg for those with low EELV (i.e., HFO-LO and CMV-LO). Ventilator pressures were limited to < or = 39/9 cm H2O in the CMV-HI group. Five of six CMV-HI-treated animals did not maintain target PaO2 levels. Both ventilator type and strategy influenced outcome significantly. Animals managed with HFO had higher mean arterial pressures (p = 0.004), lower mean airway pressures (Paw) (p < 0.00008) and HCO3- requirements (p < 0.02), larger inflation (p = 0.003) and deflation (p < 0.00001) respiratory system volumes at 10 cm inflation pressure, and higher lung lamellar body (p = 0.0006) and lavage fluid (p = 0.003) phospholipid quantities than did CMV-treated animals. The deflation P-V curve (p = 0.0004), lamellar body (p < 0.00001) and lavage fluid (p = 0.0002) phospholipid levels were superior after the high EELV strategy. We conclude that ventilator pattern strongly influences exogenous surfactant efficacy. Benefits arise from keeping EELV high enough to prevent atelectasis and using small (approximately 2 ml/kg) tidal volumes to prevent overdistension.(ABSTRACT TRUNCATED AT 250 WORDS)

Both ventilator pattern and neutrophil activation influence lung injury in adult respiratory distress syndrome (ARDS). We therefore questioned whether ventilator pattern independently affects neutrophil accumulation and function in early ARDS. Thirty-five New Zealand White rabbits were anesthetized, paralyzed, and prepared using sterile techniques. Fifteen surfactant-depleted animals were randomized and ventilated for 4 h using high-frequency oscillatory ventilation (HFO) at 15 Hz with an inspired O2 fraction = 1.0 and arterial PO2 (PaO2) > 400 Torr (a pattern known to reverse atelectasis) or conventional mechanical ventilation (CMV) with PaO2 = 80-100 Torr (a pattern with some atelectasis despite positive end-expiratory pressure). Eight normal animals on CMV with PaO2 > 400 Torr served as a reference group (NorCMV). NorCMV animals progressively increased circulating polymorphonuclear neutrophil (PMN) numbers and had minor pressure-volume curve alterations but no other significant changes. Lavaged CMV animals developed the characteristic gas exchange and marked pressure-volume curve abnormalities of ARDS. Circulating PMNs remained constant but developed decreased chemotactic activity, whereas lung neutrophil numbers increased significantly (P = 0.0002) and had substantially enhanced chemiluminescence (P = 0.0003 vs. NorCMV animals). Although lavaged HFO animals accumulated an intermediate number of lung neutrophils (lung myeloperoxidase > NorCMV animals; P = 0.003), the chemiluminescence and chemotaxis of these PMNs were the same as in cells from NorCMV animals. We concluded that both the degree of neutrophil activation and lung injury can be minimized by preventing cyclic alveolar/airway expansion and collapse in the surfactant-deficient lung by use of appropriate ventilator patterns.

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