Extending inspiratory time in acute respiratory distress syndrome

Objective: To assess the short-term effects of extending inspiratory time b y lengthening end-inspiratory pause (EIP) without inducing a clinically sig nificant increase in intrinsic positive end-expiratory pressure (PEEPi) in patients with acute respiratory distress syndrome (ARDS). Design: Controlled, randomized, crossover study. Setting: Two medical intensive care units of university hospitals. Patients: Sixteen patients with early (less than or equal to 48 hrs) ARDS. Intervention: We applied two durations of EIP (0.2 sees and extended) each for 1 hr while keeping all the following ventilatory parameters constant: F IO2, total PEEP (PEEPtot = applied PEEP + PEEPi), tidal volume, inspiratory flow, and respiratory rate. The duration of extended EIP was titrated to a void an increase of PEEPi of greater than or equal to1 cm H2O. Measurements and Main Results: Despite an increase in mean airway pressure (20.6 +/- 2.3 vs. 17.6 +/- 2.1 cm H2O, p < .01), extended EIP did not signi ficantly improve PaO2 (93 +/- 21 vs. 86 +/- 16 torr [12.40 +/- 2.80 vs. 11. 46 +/- 2.13 kPa] with 0.2 sees EIP, NS). However, although the difference i n PaO2 between the two EIP durations was <20 torr (<2.66 kPa) in 14 patient s, two patients exhibited a >40 torr (>5.33 kPa) increase in PaO2 with exte nded EIP. Extended EIP decreased PaCO2 (62 +/- 13 vs. 67 +/- 13 torr [8.26 +/- 1.73 vs. 8.93 +/- 1.73 kPa] with 0.2 sees EIP, p <.01), which resulted in a higher pH (7.22 +/- 0.10 vs. 7.19 +/- 0.09 with 0.2 sees EIP, p < .01) and contributed to a slight increase in arterial hemoglobin saturation (94 +/- 3 vs. 93 +/- 3% with 0.2 EIP, p < .01). No significant difference in h emodynamics was observed. Conclusion: In patients with ARDS, extending EIP without inducing a clinica lly significant increase in PEEPi does not consistently improve arterial ox ygenation but enhances CO2 elimination.