Titration of mean airway pressure and FiO2 during high frequency oscillatory ventilation in a porcine model of acute lung injury.

BACKGROUND

High frequency oscillatory ventilation (HFOV) is frequently utilized for patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). However, precise criteria to titrate mean airway pressure (mPaw) and FiO(2) as the patient's condition improves are lacking. We hypothesized that reducing mPaw and FiO(2) too quickly after reaching target arterial oxygen saturation levels would promote ventilator induced lung injury (VILI).

MATERIALS AND METHODS

ALI was induced by instilling 3% Tween 20. Pigs were placed supine and received 30 min of nonprotective ventilation. Pigs were separated into two groups: HFOV constant (HFOVC, n = 3) = constant mPaw and FiO(2) for the duration; HFOV titrated (HFOVT, n = 4) = FiO(2) and/or mPaw were reduced every 30 min if the oxygen saturation remained between 88%-95%. Hemodynamic and pulmonary measurements were made at baseline, after lung injury, and every 30 min during the 6-h study. Lung histopathology was determined by quantifying alveolar hyperdistension, fibrin, congestion, atelectasis, and polymorphonuclear leukocyte (PMN) infiltration.

RESULTS

Oxygenation was significantly lower in the HFOVT group compared to the HFOVC group after 6 h. Lung histopathology was significantly increased in the HFOVT group in the following categories: PMN infiltration, alveolar hyperdistension, congestion, and fibrin deposition.

CONCLUSIONS

Rapid reduction of mPaw and FiO(2) in our ALI model significantly reduced oxygenation, but, more importantly, caused VILI as evidenced by increased lung inflammation and alveolar hyperdistension. Specific criteria for titration of mPaw and inspired oxygen are needed to maximize the lung protective effects of HFOV while maintaining adequate gas exchange.