Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 146-154

Respiratory Response to CO₂ during Pressure-support Ventilation in Conscious Normal Humans

DIMITRIS GEORGOPOULOS, IOANNA MITROUSKA, ZOHEIR BSHOUTY, KIMBERLY WEBSTER, DIMITRIS PATAKAS, and MAGDY YOUNES

Respiratory and Critical Care Section, General Hospital "G. Papanicolaou," Aristotle University of Thessaloniki, Thessaloniki, Greece; and Section of Respiratory Diseases, Health Sciences Center, University of Manitoba, Winnipeg, Manitoba, Canada

The respiratory response to CO₂ during pressure-support ventilation (PSV) was studied in 16 conscious normal humans. The subjects breathed through a mouthpiece connected to a ventilator in PSV mode, with pressure set to the highest comfortable level for each subject (10.1 ± 0.6 cm H₂O, mean  ± SE). Compared with breathing spontaneously through the ventilator (CPAP mode with zero positive end-expiratory pressure), with PSV, tidal volume (VT) increased significantly (1.16 ± 0.1 versus 0.85 ± 0.04 L), whereas breathing frequency (f ) remained stable (16.0 ± 0.9 versus 15.6 ± 1.1 breaths/min). As a result, the subjects hyperventilated, decreasing significantly end-tidal PCO₂ (PET_CO2, 23.5 ± 1.2 versus 35.5 ± 1.1 mm Hg). Fraction of inspired CO₂ (FI_CO2) was then increased in steps, and changes in respiratory motor output were quantitated from changes in f, VT, ventilation (. V I), peak inspiratory flow (. Vpeak), and muscle pressure (Pmus). Pmus was calculated by the equation of motion, based on respiratory system mechanics, which were measured previously by airway occlusion at end-inspiration. V T, . V I, and Pmus increased significantly with increasing PET_CO2, and the response was detectable even below eupneic levels; f remained relatively stable over a wide range of PET_CO2 (23 to 45 mm Hg) and increased significantly only when PET_CO2 approached 50 mm Hg. These results indicate that in conscious normal humans during PSV, CO₂ responsiveness extends well into hypocapnia and is expressed principally as an increase in intensity of respiratory motor output with little change in respiratory rate.

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