BACKGROUND AND OBJECTIVE: This prospective observational study analyses cardiovascular changes in adult patients with acute respiratory distress syndrome (ARDS) during transition from pressure-controlled ventilation to high-frequency oscillatory ventilation (HFOV), using transoesophageal echocardiography (TOE) and invasive haemodynamic monitoring. METHODS: Nine patients (median age 65 years; range 42-70) with ARDS were studied. HFOV was started and maintained with an adjusted mean airway pressure of 5 cmH2O above the last measured mean airway pressure during pressure-controlled ventilation. Haemodynamic and TOE measurements were performed in end-expiration during baseline pressure-controlled ventilation, and again 5 and 30 min after the start of during uninterrupted HFOV. RESULTS: Right atrial pressure increased immediately (P = 0.004). After 30 min, pulmonary arterial occlusion pressure increased (P = 0.008), cardiac index decreased (P = 0.01), stroke volume index decreased (P = 0.02) and both left ventricular end-diastolic and end-systolic area indices decreased (P = 0.02). Fractional area change, left ventricular end-systolic wall stress, heart rate, mean arterial pressure and mean pulmonary artery pressure remained unchanged. CONCLUSIONS: Transition to HFOV at a mean airway pressure of 5 cmH2O above that during pressure-controlled ventilation induced significant, but clinically minor, haemodynamic effects, which are most probably due to airway pressure-related preload reduction.
BACKGROUND AND OBJECTIVE: This prospective observational study analyses cardiovascular changes in adult patients with acute respiratory distress syndrome (ARDS) during transition from pressure-controlled ventilation to high-frequency oscillatory ventilation (HFOV), using transoesophageal echocardiography (TOE) and invasive haemodynamic monitoring. METHODS: Nine patients (median age 65 years; range 42-70) with ARDS were studied. HFOV was started and maintained with an adjusted mean airway pressure of 5 cmH2O above the last measured mean airway pressure during pressure-controlled ventilation. Haemodynamic and TOE measurements were performed in end-expiration during baseline pressure-controlled ventilation, and again 5 and 30 min after the start of during uninterrupted HFOV. RESULTS: Right atrial pressure increased immediately (P = 0.004). After 30 min, pulmonary arterial occlusion pressure increased (P = 0.008), cardiac index decreased (P = 0.01), stroke volume index decreased (P = 0.02) and both left ventricular end-diastolic and end-systolic area indices decreased (P = 0.02). Fractional area change, left ventricular end-systolic wall stress, heart rate, mean arterial pressure and mean pulmonary artery pressure remained unchanged. CONCLUSIONS: Transition to HFOV at a mean airway pressure of 5 cmH2O above that during pressure-controlled ventilation induced significant, but clinically minor, haemodynamic effects, which are most probably due to airway pressure-related preload reduction.
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