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(Chest. 1996;109:1320-1327.)
© 1996 American College of Chest Physicians

Mechanism of Relief of Tachypnea During Pressure Support Ventilation

Kenneth I. Berger MD1; I. Barry Sorkin RRT1; Robert G. Norman RRT1; David M. Rapoport MD, FCCP1; and Roberta M. Goldring MD1

1 From the Division of Pulmonary and Critical Care Medicine and Bellevue Chest Service, Department of Medicine, New York University Medical Center

Pressure support ventilation (PSV) provides a range of ventilatory support from partial respiratory muscle unloading, where inspiratory work is shared between the patient and the mechanical ventilator, to total respiratory muscle unloading, where inspiratory work is performed solely by the ventilator. This study is designed to determine if minimizing work fully accounts for relief of tachypnea during PSV. We examined respiratory parameters over a range of PSV that includes the crossover from partial to total respiratory muscle unloading. Eight studies were obtained on seven intubated patients in respiratory failure. Ventilation, occlusion pressure (P0.1), and patient inspiratory work (WOBinsp) were measured while PSV was varied. In all patients, WOBinsp decreased as PSV increased. The level of PSV where WOBinsp was minimized was identified; this marked the crossover from partial to total respiratory muscle unloading. Frequency decreased with increasing PSV but remained elevated (range, 22 to 38 breaths/min) at the crossover. Frequency was normalized only at PSV levels 131 to 193% of the levels of pressure at the crossover. Tidal volume (VT) changed little during partial support and averaged 5.9 mL/kg at the crossover. VT increased only on PSV providing total unloading. Six of seven patients exhibited increasing static compliance with increasing VT suggesting alveolar recruitment. P0.1 tracked WOBinsp over the entire range of PSV (r=0.95, p<0.001). The normalization of frequency observed above the crossover coincided with increasing VT rather than decreasing work. These observations suggest that reflexes resulting from increased VT and/or alveolar recruitment may have contributed to the normalization of frequency.

Key Words: occlusion pressure • pressure support ventilation • pulmonary stretch receptors • respiratory insufficiency • work of breathing

Submitted on July 17, 1995
Accepted on November 8, 2007




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