Cardiovascular responses to high-frequency oscillatory ventilation during acute lung injury in sheep
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The present study was designed to evaluate pulmonary and systemic hemodynamics and blood gas changes on switching from conventional mechanical ventilation (CMV) to high-frequency oscillatory ventilation (HFOV) in a large animal model of acute lung injury.
Eleven anesthetised sheep chronically instrumented with vascular monitoring were prepared. Animals received oleic acid (0.08 ml·kg−1) intravenously and were ventilated for 4 h h after the administration of oleic acid. The animals were then randomized into the two following different ventilation modes: CMV (tidal volume [VT], 6 ml·kg−1; respiratory rate [RR], 25 · min−1) with positive end-expiratory pressure (PEEP) of 12 cmH2O; or CMV under the same settings without PEEP. HFOV was then switched. The setting of mean airway pressure with a fixed stroke volume was changed between 25, 18, and 12 cmH2O every 20 min. Mean pulmonary artery pressure, pulmonary artery occlusive pressure (Paop), left atrium pressure, systemic arterial pressure, cardiac output (CO), and blood gas composition under each setting were measured before and after HFOV.
Switching to HFOV, from without PEEP, resulted in significant increases in Paop and PaO2 and a decrease in CO at higher (25, 18 cmH2O) mean airway pressure. However, when changed from low VT and PEEP, HFOV produced further improvements in oxygenation without any deterioration of cardiovascular depression. Thus, switching to HFOV from CMV with low VT and high PEEP may have little influence on pulmonary or systemic hemodynamics in acute lung injury.
We conclude that hemodynamic responses are dependent on the predefined setting of PEEP during CMV, and on applied mean airway pressure during HFOV.
Key wordsAcute lung injury Open lung strategy Ventilation-induced lung injury
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