Deviation of tracheal pressure from airway opening pressure during high-frequency oscillatory ventilation in a porcine lung model.

Oxygenation during high-frequency oscillatory ventilation is secured by a high level of mean airway pressure. Our objective was to identify a pressure difference between the airway opening of the respiratory circuit and the trachea during application of different oscillatory frequencies. Six female Pietrain pigs (57.1 ± 3.6 kg) were first ventilated in a conventional mechanical ventilation mode. Subsequently, the animals were switched to high-frequency oscillatory ventilation by setting mean airway opening pressure 5 cmH(2)O above the one measured during controlled mechanical ventilation. Measurements at the airway opening and at tracheal levels were performed in healthy lungs and after induction of acute lung injury by surfactant depletion. During high-frequency oscillatory ventilation, the airway opening pressure was set at a constant level. The pressure amplitude was fixed at 90 cmH(2)O. Starting from an oscillatory frequency of 3 Hz, the frequency was increased in steps of 3 Hz to 15 Hz and then decreased accordingly. At each frequency, measurements were performed in the trachea through a side-lumen of the endotracheal tube and the airway opening pressure was recorded. The pressure difference was calculated. At every oscillatory frequency, a pressure loss towards the trachea could be shown. This pressure difference increased with higher oscillatory frequencies (3 Hz 2.2 ± 2.1 cmH(2)O vs. 15 Hz 7.5 ± 1.8 cmH(2)O). The results for healthy and injured lungs were similar. Tracheal pressures decreased with higher oscillatory frequencies. This may lead to pulmonary derecruitment. This has to be taken into consideration when increasing oscillatory frequencies and differentiated pressure settings are mandatory.

Acute respiratory distress induced by repeated saline lavage provides stable experimental conditions for 24 hours in pigs.

Surfactant depletion is most often used to study acute respiratory failure in animal models. Because model stability is often criticized, the authors tested the following hypotheses: Repeated pulmonary lavage with normal saline provides stable experimental conditions for 24 hours with a PaO2/FiO2 ratio < 300 mm Hg. Lung injury was induced by bilateral pulmonary lavages in 8 female pigs (51.5 +/- 4.8 kg). The animals were ventilated for 24 hours (PEEP: 5 cm H2O; tidal volume: 6 mL/kg; respiratory rate: 30/min). After 24 hours the animals were euthanized. For histopathology slides from all pulmonary lobes were obtained. Supernatant of the bronchoalveolar fluid collected before induction of acute respiratory distress syndrome (ARDS) and after 24 hours was analyzed. A total of 19 +/- 6 lavages were needed to induce ARDS. PaO2/FiO2 ratio and pulmonary shunt fraction remained significantly deteriorated compared to baseline values after 24 hours (P < .01). Slight to moderate histopathologic changes were detected. Significant increases of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 were observed after 24 hours (P < .01). The presented surfactant depletion-based lung injury model was associated with increased pulmonary inflammation and fulfilled the criteria of acute ling injury (ALI) for 24 hours.

High-frequency oscillatory ventilation reduces lung inflammation: a large-animal 24-h model of respiratory distress.

OBJECTIVE: High-frequency oscillatory ventilation (HFOV) may reduce ventilator-induced lung injury in experimental neonatal respiratory distress. However, these data permit no conclusions for large animals or adult patients with acute respiratory distress syndrome (ARDS), because in neonates higher frequencies and lower amplitudes can be used, resulting in lower tidal volumes (VT) and airway pressures. The aim of this study was to compare gas exchange, lung histopathology and inflammatory cytokine expression during lung-protective pressure-controlled ventilation (PCV) and HFOV in a long-term large-animal model of ARDS. DESIGN: Prospective, randomized, controlled pilot study. SETTING: University animal laboratory. SUBJECTS: Sixteen female pigs (55.3 +/- 3.9 kg). INTERVENTIONS: After induction of ARDS by repeated lavage, the animals were randomly assigned to PCV (VT = 6 ml/kg) and HFOV (6 Hz). After lung injury, a standardised lung recruitment was performed in both groups, and ventilation was continued for 24 h. MEASUREMENTS AND RESULTS: After lung recruitment sustained improvements in the oxygenation index were observed in both groups. The mean airway pressure (mPaw) was significantly lower in the HFOV group during the experiment (p < 0.01). Histologically, lung inflammation was significantly ameliorated in the HFOV group (p < 0.05). The messenger RNA expression of IL-1-beta in lung tissue was significantly lower in the HFOV-treated animals (p < 0.01). CONCLUSIONS: These data suggest that HFOV compared with conventional lung-protective ventilation can reduce lung inflammation in a large-animal 24-h model of ARDS. Furthermore, it was shown that lung recruitment leads to sustained improvements in gas exchange with a significantly lower mPaw when HFOV is used.

Sustained inflation and incremental mean airway pressure trial during conventional and high-frequency oscillatory ventilation in a large porcine model of acute respiratory distress syndrome.

BACKGROUND: To compare the effect of a sustained inflation followed by an incremental mean airway pressure trial during conventional and high-frequency oscillatory ventilation on oxygenation and hemodynamics in a large porcine model of early acute respiratory distress syndrome. METHODS: Severe lung injury (Ali) was induced in 18 healthy pigs (55.3 +/- 3.9 kg, mean +/- SD) by repeated saline lung lavage until PaO2 decreased to less than 60 mmHg. After a stabilisation period of 60 minutes, the animals were randomly assigned to two groups: Group 1 (Pressure controlled ventilation; PCV): FIO2 = 1.0, PEEP = 5 cmH2O, V(T) = 6 ml/kg, respiratory rate = 30/min, I:E = 1:1; group 2 (High-frequency oscillatory ventilation; HFOV): FIO2 = 1.0, Bias flow = 30 l/min, Amplitude = 60 cmH2O, Frequency = 6 Hz, I:E = 1:1. A sustained inflation (SI; 50 cmH2O for 60s) followed by an incremental mean airway pressure (mPaw) trial (steps of 3 cmH2O every 15 minutes) were performed in both groups until PaO2 no longer increased. This was regarded as full lung inflation. The mPaw was decreased by 3 cmH2O and the animals reached the end of the study protocol. Gas exchange and hemodynamic data were collected at each step. RESULTS: The SI led to a significant improvement of the PaO2/FiO2-Index (HFOV: 200 +/- 100 vs. PCV: 58 +/- 15 and T(Ali): 57 +/- 12; p < 0.001) and PaCO2-reduction (HFOV: 42 +/- 5 vs. PCV: 62 +/- 13 and T(Ali): 55 +/- 9; p < 0.001) during HFOV compared to lung injury and PCV. Augmentation of mPaw improved gas exchange and pulmonary shunt fraction in both groups, but at a significant lower mPaw in the HFOV treated animals. Cardiac output was continuously deteriorating during the recruitment manoeuvre in both study groups (HFOV: T(Ali): 6.1 +/- 1 vs. T(75): 3.4 +/- 0.4; PCV: T(Ali): 6.7 +/- 2.4 vs. T(75): 4 +/- 0.5; p < 0.001). CONCLUSION: A sustained inflation followed by an incremental mean airway pressure trial in HFOV improved oxygenation at a lower mPaw than during conventional lung protective ventilation. HFOV but not PCV resulted in normocapnia, suggesting that during HFOV there are alternatives to tidal ventilation to achieve CO2-elimination in an "open lung" approach.