Ventilatory response to CO2 and O2 near eupnea in awake dogs

1988 ◽  
Vol 65 (2) ◽  
pp. 788-796 ◽  
Author(s):  
W. W. Hwang ◽  
S. M. Yamashiro ◽  
D. Sedlock ◽  
F. S. Grodins

The problem faced in determining the ventilatory response to CO2 near eupnea has been the difficulty of unloading metabolically produced CO2 from the subject in the steady state. Previous methods using extracorporeal circuits to unload CO2 are technically difficult and provide a limited number of experimental states per experiment. Using the method of high-frequency ventilation to unload CO2, we were able to obtain a large number of determinations in the same subject under conditions of hypoxia, normoxia, and hyperoxia. Data collected in five awake dogs show that the ventilatory response to CO2 is linear down to apnea during normoxic conditions but exhibits nonlinear behavior dependent on the level of arterial O2 tension. During hyperoxic conditions, the response was concave curvilinear, with a statistically significant decrease in slope near apnea. In contrast, mild hypoxia led to a convex curvilinear response with an increased slope near apnea.

1986 ◽  
Vol 61 (5) ◽  
pp. 1903-1907 ◽  
Author(s):  
Y. Yamada ◽  
C. A. Hales ◽  
J. G. Venegas

It has been suggested that the increase in inspiratory flow rate caused by a decrease in the inspiratory-to-expiratory time ratio (I:E) at a constant tidal volume (VT) could increase the efficiency of ventilation in high-frequency ventilation (HFV). To test this hypothesis, we studied the effect of changing I:E from 1:1 to 1:4 on steady-state alveolar ventilation (VA) at a given VT and frequency (f) and at a constant mean lung volume (VL). In nine anesthetized, paralyzed, supine dogs, HFV was performed at 3, 6, and 9 Hz with a ventilator that delivered constant inspiratory and expiratory flow rates. Mean airway pressure was adjusted so that VL was maintained at a level equivalent to that of resting FRC. At each f and one of the I:E chosen at random, VT was adjusted to obtain a eucapnic steady state [arterial pressure of CO2 (PaCO2) = 37 +/- 3 Torr]. After 10 min of each HFV, PaCO2, arterial pressure of O2 (PaO2), and CO2 production (VCO2) were measured, and I:E was changed before repeating the run with the same f and VT. VA was calculated from the ratio of VCO2 and PaCO2. We found that the change of I:E from 1:1 to 1:4 had no significant effects on PaCO2, PaO2, and VA at any of the frequencies studied. We conclude, therefore, that the mechanism or mechanisms responsible for gas transport during HFV must be insensitive to the changes in inspiratory and expiratory flow rates over the VT-f range covered in our experiments.


1998 ◽  
Vol 74 (5) ◽  
pp. 411-5 ◽  
Author(s):  
Marcus A.J. Oliveira ◽  
Antônio C. P. Ferreira ◽  
João S. Oliveira ◽  
José S. Oliveira ◽  
Yara G. Silva

1982 ◽  
Vol 57 (3) ◽  
pp. A89-A89
Author(s):  
E. L. Owens ◽  
T. S. Lee ◽  
B. D. Wright ◽  
S. Jakobson

1986 ◽  
Vol 26 (3) ◽  
pp. 287-289 ◽  
Author(s):  
DAVID DREYFUSS ◽  
RICHARD S. JACKSON ◽  
LAURENCE H. COFFIN ◽  
ROBERT S. D. DEANE ◽  
TOMATSU SHINOZAKI

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