AUTOMATIC EVALUATION OF CARBON DIOXIDE RESPONSE CURVE SLOPES

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A452 ◽  
Author(s):  
R Dzwonczyk ◽  
I M Minehart ◽  
J S McDonald
1966 ◽  
Vol 275 (3) ◽  
pp. 117-122 ◽  
Author(s):  
C. van Ypersele de Strihou ◽  
L. Brasseur ◽  
J. De Coninck

1970 ◽  
Vol 39 (5) ◽  
pp. 653-662 ◽  
Author(s):  
T. K. C. King ◽  
D. Yu

1. The ventilatory response to carbon dioxide was measured in a group of patients with chronic obstructive airways disease using a rebreathing method. 2. The slope of the carbon dioxide response curve was obtained by plotting the ventilation at successive half minutes against the corresponding mean end tidal Pco2. 3. The slope of the carbon dioxide response curve was positively correlated with (a) the FEV1 and (b) the reciprocal of the resting arterial Pco2, both these correlations being statistically significant. 4. Reference to FEV1 alone could explain more than 80% of the variation in the slope of the CO2 response curve. This explained variation was not significantly improved by the additional consideration of the resting arterial Pco2. 5. It was suggested that whatever the underlying complex mechanisms that determine the response to CO2, the FEV1 can be used as an empirical factor for the prediction of this response in patients with chronic obstructive airways disease.


1965 ◽  
Vol 20 (2) ◽  
pp. 171-174 ◽  
Author(s):  
Bernard Brandstater ◽  
Edmond I. Eger ◽  
Gerald Edelist

Respiratory depression from anesthetic drugs introduces an undefined variable into many experiments. We have produced constant-depth anesthesia in dogs by maintaining an unvarying alveolar concentration of halothane, and we have tested whether such anesthesia can produce a steady state with respect to the respiratory response to CO2. At a constant alveolar halothane concentration, the response to CO2 remained essentially unchanged for up to 8 hr. Carbon dioxide response curves were also obtained at several different alveolar concentrations of halothane. Carbon dioxide response was sensitive to small changes in halothane concentration; the slope of the response curve diminished linearly with increase in alveolar concentration of halothane. With alveolar halothane concentration held constant, a small dose of intravenous thiopental produced a depression of the CO2 response curve that remained for more than 2 hr. carbon dioxide response; control of respiration; depression; respiratory response Submitted on April 29, 1964


1963 ◽  
Vol 1 (2) ◽  
pp. 217-225 ◽  
Author(s):  
J. W. Bellville ◽  
M. C. Gilliland ◽  
H. H. Hara ◽  
W. E. Mower

2000 ◽  
Vol 92 (2) ◽  
pp. 393-393 ◽  
Author(s):  
H. Daniel Babenco ◽  
Pattilyn F. Conard ◽  
Jeffrey B. Gross

Background In doses typically administered during conscious sedation, remifentanil may be associated with ventilatory depression. However, the time course of ventilatory depression after an initial dose of remifentanil has not been determined previously. Methods In eight healthy volunteers, the authors determined the time course of the ventilatory response to carbon dioxide using the dual isohypercapnic technique. Subjects breathed via mask from a to-and-fro circuit with variable carbon dioxide absorption, allowing the authors to maintain end-tidal pressure of carbon dioxide (PET(CO2)) at approximately 46 or 56 mm Hg (alternate subjects). After 6 min of equilibration, subjects received 0.5 microg/kg remifentanil over 5 s, and minute ventilation (V(E)) was recorded during the next 20 min. Two hours later, the study was repeated using the other carbon dioxide tension (56 or 46 mm Hg). The V(E) data were used to construct two-point carbon dioxide response curves at 30-s intervals after remifentanil administration. Using published pharmacokinetic values for remifentanil and the method of collapsing hysteresis loops, the authors estimated the effect-site equilibration rate constant (k(eo)), the effect-site concentration producing 50% respiratory depression (EC50), and the shape parameter of the concentration-response curve (gamma). Results The slope of the carbon dioxide response decreased from 0.99 [95% confidence limits 0.72 to 1.26] to a nadir of 0.27 l x min(-1) x mm Hg(-1) [-0.12 to 0.66] 2 min after remifentanil (P<0.001); within 5 min, it recovered to approximately 0.6 l x min(-1) x mm Hg(-1), and within 15 min of injection, slope returned to baseline. The computed ventilation at PET = 50 mm Hg (VE50) decreased from 12.9 [9.8 to 15.9] to 6.1 l/min [4.8 to 7.4] 2.5 min after remifentanil injection (P<0.001). This was caused primarily by a decrease in tidal volume rather than in respiratory rate. Estimated pharmacodynamic parameters based on computed mean values of VE50 included k(eo) = 0.24 min(-1) (T1/2 = 2.9 min), EC50 = 1.12 ng/ml, and gamma = 1.74. Conclusions After administration of 0.5 microg/kg remifentanil, there was a decrease in slope and downward shift of the carbon dioxide ventilatory response curve. This reached its nadir approximately 2.5 min after injection, consistent with the computed onset half-time of 2.9 min. The onset of respiratory depression appears to be somewhat slower than previously reported for the onset of remifentanil-induced electroencephalographic slowing. Recovery of ventilatory drive after a small dose essentially was complete within 15 min.


1982 ◽  
Vol 47 (3) ◽  
pp. 365-377 ◽  
Author(s):  
C.N. Olievier ◽  
A. Berkenbosch ◽  
J. De Goede

1986 ◽  
Vol 2 (3) ◽  
pp. 198-202 ◽  
Author(s):  
Duane L. Sherrill ◽  
George D. Swanson

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