Increasing respiratory rate to improve CO2 clearance during mechanical ventilation is not a panacea in acute respiratory failure.

BACKGROUND

Increasing respiratory rate has recently been proposed to improve CO2 clearance in patients with acute respiratory failure who are receiving mechanical ventilation. However, the efficacy of this strategy may be limited by deadspace ventilation, and it might induce adverse hemodynamic effects related to dynamic hyperinflation.

SETTING

An intensive care unit of a university hospital.

PATIENTS: We studied 14 patients with acute respiratory failure during the adjustment of ventilator settings on the first day of mechanical ventilation in volume-controlled mode.

MEASUREMENTS: After determining the positive end-expiratory pressure that suppresses any intrinsic positive end-expiratory pressure at a respiratory rate of 15 breaths/min, we compared blood gas analysis, respiratory measurements, and Doppler evaluation of right ventricular systolic function by using two different respiratory strategies with the same airway pressure limitation (plateau pressure, < or =25 cm H2O), a low-rate conventional respiratory strategy with a respiratory rate of 15 breaths/min, and a high-rate strategy with a respiratory rate of 30 breaths/min.

RESULTS

Compared with the low-rate strategy, the high-rate strategy neither significantly reduced PaCO2 (47 +/- 8 vs. 51 +/- 7 mm Hg with the low-rate strategy) nor significantly improved PaO2 (99 +/- 40 vs. 95 +/- 35 mm Hg with the low-rate strategy). It significantly increased alveolar deadspace to tidal volume ratio (21% +/- 8%, vs. 14% +/- 6% with the low-rate strategy) and produced dynamic hyperinflation, resulting in a substantial intrinsic positive end-expiratory pressure (6.4 +/- 2.7 cm H2O). Right ventricular outflow impedance was increased, resulting in a significant drop in the cardiac index (2.9 +/- 0.6 vs. 3.3 +/- 0.7 L/min/m with the low-rate strategy).

CONCLUSION

We conclude that a high respiratory rate strategy during mechanical ventilation in patients with acute respiratory failure did not improve CO2 clearance, produced dynamic hyperinflation, and impaired right ventricular ejection.