Am. J. Respir. Crit. Care Med., Vol 153, No. 1, Jan 1996, 168-175.
Effects of breathing route, temperature and volume of inspired gas, and airway anesthesia on the response of respiratory output to varying inspiratory flow
D Georgopoulos, I Mitrouska, Z Bshouty, K Webster, NR Anthonisen and M Younes
Section of Respiratory Diseases, University of Manitoba, Winnipeg, Canada.
The determinants of the response of the respiratory output to inspiratory
flow rates (VI) were examined in awake normal subjects. Subjects were
connected to a volume-cycle ventilator in the assist/control mode, and VI
was increased in steps from 30 to 90 L/min and then back to 30 L/min. VI
pattern was square, and all breaths were subject-triggered. In six subjects
the effects of breathing route (nasal or mouth) and temperature and volume
of inspired gas (Protocol A) and in 8 subjects the effects of airway
anesthesia (upper and lower airways; Protocol B) on the response of
respiratory output to varying VI were studied. In Protocol B, in order to
calculate muscle pressure during inspiration (Pmus), respiratory system
mechanics were measured using the interrupter method at end-inspiration.
Independent of conditions studied, breathing frequency increased
significantly and end- tidal concentration of CO2 decreased as VI
increased. The response was graded and reversible and not affected by
breathing route, temperature and volume of inspired gas, and airway
anesthesia. With and without airway anesthesia (Protocol B), neural
inspiratory and expiratory time and neural duty cycle, estimated from Pmus
waveform, decreased significantly as VI increased. At all conditions
studied, the rate of change in airway pressure prior to triggering the
ventilator tended to increase as VI increased. The changes in timing and
drive were nearly complete within the first two breaths after transition,
with no evidence of adaptation during a given VI period. We conclude that
VI exerts an excitatory effect on respiratory output which is independent
of breathing route, temperature and volume of inspirate, and airway
anesthesia. The response most likely is neural in origin, mediated through
receptors not accessible to anesthesia, such as those located in the chest
wall or below the airway mucosa.
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Copyright © 1996 American Thoracic Society
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