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.


METHODS
An intensive care unit of a university hospital.


METHODS
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.


METHODS
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).


CONCLUSIONS
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.
Medical Intensive Care Unit, University Hospital Ambroise Paré, Assistance Publique Hôpitaux de Paris, Boulogne Cedex, France.
Antoine
A
Vieillard-Baron
Sebastien
S
Prin
Roch
R
Augarde
Pierre
P
Desfonds
Bernard
B
Page
Alain
A
Beauchet
François
F
Jardin
D000208:Acute Disease; D000328:Adult; D000368:Aged; D002245:Carbon Dioxide / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012121:Respiration, Artificial / Q000379:methods*; D012131:Respiratory Insufficiency / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D016278:Ventricular Function, Right
D002245:Carbon Dioxide