Comparison of Two Rebreathing Methods for the Determination of Mixed Venous Partial Pressure of Carbon Dioxide during Exercise

1979 ◽  
Vol 56 (5) ◽  
pp. 433-437 ◽  
Author(s):  
G. J. F. Heigenhauser ◽  
N. L. Jones

1. Duplicate measurements were made of mixed venous Pco2 (Pv̄, co2) by two rebreathing methods during steady-state exercise at three power outputs in seven subjects. One method employed a high initial bag CO2 concentration to obtain equilibrium of CO2 in the lung—bag system before recirculation (equilibrium method); in the other, a low initial bag CO2 concentration was used and a statistical method was applied to alveolar Pco2 measurements before recirculation, to obtain the asymptote from the exponential rise in end-tidal Pco2 during rebreathing (exponential method). 2. The reproducibility was similar; sd of duplicate determinations of Pv̄, co2 was 0·15 kPa (1·1 mmHg) for the equilibrium method and 0·20 kPa (1·5 mmHg) for the exponential method. Measurements of Pv̄, co2 by the exponential method were systematically lower than the equilibrium method. When the equilibrium Pv̄, co2 was corrected for the alveolar—arterial (‘downstream’) Pco2 difference, using published values, Pv̄, co2 was similar for both methods. 3. As an alveolar to arterial Pco2 difference did not appear to exist with the exponential method, it is concluded that the previously described disequilibrium between alveolar and arterial Pco2 during rebreathing in exercise is mainly related to prevention of net CO2 movement from the pulmonary capillary blood in the equilibrium method, and is not present when continuous CO2 evolution occurs in the exponential method.

1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands

Cardiac output (CO) during exercise can be determined noninvasively by using the indirect Fick CO2-rebreathing technique. CO2 measurements for this technique are usually performed with an infrared analyzer (IA) or mass spectrometer (MS). However, IA CO2 measurements are susceptible to underreading in the face of high O2 concentrations because of collision broadening. We compared an IA (Ametek model CD-3A) with a MS (Marquette model MGA-1100) to see the effect this would have on mixed venous PCO2 (PVCO2) and CO measurements. After calibration with room air and a gas mixture of 5% CO2–12% O2–83% N2, both devices were tested with three different gas mixtures of CO2 in O2. For each gas mixture, IA gave lower CO2 values than did the MS (4.1% CO2: IA, 3.85 +/- 0.01% and MS, 4.13 +/- 0.01%; 9.2% CO2: IA, 8.44 +/- 0.07% and MS, 9.19 +/- 0.01%; 13.8% CO2: IA, 12.57 +/- 0.15% and MS, 13.82 +/- 0.01%). Warming and humidifying the gases did not alter the results. The IA gave lower values than did the MS for eight other medical gases in lower concentrations of O2 (40–50%). Equilibrium and exponential rebreathing procedures were performed. Values determined by the IA were > 10% higher than those determined by the MS for both rebreathing methods. We conclude that all IAs must be checked for collision broadening if they are to be used in environments where the concentration of O2 is > 21%. If collision broadening is present, then either a special high O2-CO2 calibration curve must be constructed, or the IA should not be used for both arterial PCO2 and PVCO2 estimates because it may produce erroneously low PVCO2 values, with resultant overestimation of CO.


1972 ◽  
Vol 42 (3) ◽  
pp. 345-353 ◽  
Author(s):  
S. Godfrey ◽  
Eliana Wolf

1. Measurements have been made of mixed venous Pco2 (PV̄co2) by two methods during exercise at 50 and 100 W in five adult male subjects. 2. The equilibration (plateau) method and the extrapolation (Defares) method were performed alternately, five times each, during the steady-state exercise. 3. The coefficient of variation of PV̄,co2 by the extrapolation method was much higher than that of the plateau method. The PV̄,co2 can be estimated to within ± 1 mmHg by the plateau method, and the derived cardiac output to within ± 0·5 1/min in most cases. The cardiac output calculated by this method agrees closely with that found by direct methods in other studies, whereas the extrapolation method usually overestimates the cardiac output in adults. 4. It is suggested that the degree of variation in the extrapolation method is due to technical factors in construction of the line and to the difficulty of deciding what constitutes the end-tidal Pco2.


1975 ◽  
Vol 39 (3) ◽  
pp. 405-410 ◽  
Author(s):  
D. G. Davies ◽  
R. E. Dutton

The avian respiratory system is a crosscurrent gas exchange system. One of the aspects of this type of gas exchange system is that end-expired PCO2 is greater than arterial PCO2, the highest possible value being equal to mixed venous PCO2. We made steady-state measurements of arterial, mixed venous, and end-expired PCO2 in anesthetized, spontaneously breathing chickens during inhalation of room air or 4–8% CO2. We found end-expired PCO2 to be higher than both arterial and mixed venous PCO2, the sign of the differences being such as to oppose passive diffusion. The observation that end-expired PCO2 was higher than arterial PCO2 can be explained on the basis of crosscurrent gas exchange. However, the observation that end-expired PCO2 exceeded mixed venous PCO2 must be accounted for by some other mechanism. The positive end-expired to mixed venous PCO2 gradients can be explained if it is postulated that the charged membrane mechanism suggested by Gurtner et al. (Respiration Physiol. 7: 173–187, 1969) is present in the avian lung.


1975 ◽  
Vol 38 (1) ◽  
pp. 16-19 ◽  
Author(s):  
A. S. Rebuck ◽  
W. E. Woodley

In 11 healthy subjects the effect of progressive hypoxia on pulmonary ventilation at various alveolar carbon dioxide pressures was studied. A rebreathing technique was used to produce hypoxia, CO2 was held constant and oxygen saturation was taken as the independent variable. We found a linear relationship between ventilation and falls in oxygen saturation when Pco2 was held at the resting mixed venous, end-tidal, or any intermediate level. Within this range of Pco2, a family of ventilation-So2 response curves was obtained for each subject. The effect of altering the isocapnic level was to change the slope and position of the ventilation-So2 response curve, the amount by which the slope changed being related to the slope for that subject at their mixed venous Pco2.


1995 ◽  
Vol 79 (6) ◽  
pp. 2086-2093 ◽  
Author(s):  
C. M. St Croix ◽  
D. A. Cunningham ◽  
J. M. Kowalchuk ◽  
A. K. McConnell ◽  
A. S. Kirby ◽  
...  

Arterial PCO2 (PaCO2), determined directly in the radial artery, was compared with indirect estimates of PCO2 in six elderly men (mean age 73.8 yr). Estimates of PaCO2 included arterialized venous PCO2 (PavCO2); end-tidal PCO2; mean alveolar PCO2, calculated by using a reconstruction of the alveolar oscillation in PCO2 and accounting for the presence of dead space (time-weighted mean for PCO2 throughout the respiratory cycle); and values calculated by using the empirical formula developed by Jones et al. (N. L. Jones, D. G. Robertson, and J. W. Kane. J. Appl. Physiol. 47: 954–960, 1979), which incorporates end-tidal PCO2 and tidal volume (PaCO2 derived from end-tidal PCO2 and VT). Measurements were made at rest and during cycle ergometry at 25 and 50 W while the subjects breathed various gas mixtures (euoxic-eucapnic, hypoxic-eucapnic, hyperoxic-eucapnic, and hyperoxic-hypercapnic). The mean differences between the estimates and the actual PaCO2 at rest and in 25- and 50-W exercise were as follows: PavCO2, 0.3 +/- 0.7 (SD), -0.1 +/- 0.7, and 1.8 +/- 1.2 Torr; end-tidal PCO2, 2.9 +/- 1.7, 4.0 +/- 3.1, and 3.7 +/- 3.2 Torr; time-weighted mean of alveolar PCO2, 2.6 +/- 1.9, 3.3 +/- 3.1, and 3.6 +/- 3.8 Torr; and PaCO2 derived from end-tidal PCO2 and VT, 2.4 +/- 1.3, 1.3 +/- 3.0, and 0.6 +/- 2.9 Torr. It is concluded that mean PavCO2 agreed most closely with mean PaCO2 both at rest and in exercise. All methods of deriving PaCO2 using measurements from the respired gases overestimated arterial values at rest. Of the noninvasive techniques, mean estimates calculated using the regression equation developed by Jones et al. corresponded most closely with PaCO2 in exercise.


1979 ◽  
Vol 47 (5) ◽  
pp. 954-960 ◽  
Author(s):  
N. L. Jones ◽  
D. G. Robertson ◽  
J. W. Kane

The relation between end-tidal carbon dioxide tension (PETCO2) measured by infrared analysis and arterial carbon dioxide tension (PaCO2) during exercise was systematically examined in five healthy adults at two power outputs (25 and 50% VO2max) and at three frequencies of breathing (15, 30, and 45 breaths/min). PETCO2-PaCO2 varied between -2.5 and +9.1 Torr, was inversely related to the frequency of breathing (r = 0.475), and directly related to tidal volume (VT; r = 0.791) and CO2 output (r = 0.627). An equation was obtained by multiple regression analysis, to predict PaCO2 from PETCO2: PaCO2 = 5.5 +0.90 PETCO2 -0.0021 VT (r = 0.915). The equation was applied to measurements of PETCO2 obtained in two previous studies in 10 subjects in which PaCO2 had been measured, and was found to predict PaCO2 to within 1.04 Torr (+/- SD) for PaCO2 between 25 and 58 Torr (n = 56; r = 0.962). The effect of the response characteristics of the CO2 analyzer on the measurement of PETCO2 was also systematically examined by comparison with a fast-responding respiratory mass spectrometer.


1986 ◽  
Vol 61 (5) ◽  
pp. 1686-1692 ◽  
Author(s):  
R. Arieli ◽  
U. Boutellier ◽  
L. E. Farhi

We compared the cardiopulmonary physiology of eight subjects exposed to 1, 2, and 3 Gz during immersion (35 degrees C) to the heart level with control dry rides. Immersion should almost cancel the effects of gravity on systemic circulation and should leave the lung alone to gravitational influence. During steady-state breathing we measured ventilation, O2 consumption (VO2), CO2 production, end-tidal PCO2 (PACO2), and heart frequency (fH). Using CO2 rebreathing techniques, we measured cardiac output, functional residual capacity, equivalent lung tissue volume, and mixed venous O2 content, and we calculated arterial PCO2 (PaCO2). As Gz increased, ventilation, fH, and VO2 rose markedly, and PACO2 and PaCO2 decreased greatly in dry ride, but during immersion these variables changed very little in the same direction. Functional residual capacity was lower during immersion and decreased in both the dry and immersed states as Gz increased, probably reflecting closure effects. Cardiac output decreased as Gz increased in dry rides and was elevated and unaffected by Gz during immersion. We conclude that most of the changes we observed during acceleration are due to the effect on the systemic circulation, rather than to the effect on the lung itself.


1977 ◽  
Vol 52 (4) ◽  
pp. 377-382 ◽  
Author(s):  
Reiah Al-Dulymi ◽  
R. Hainsworth

1. A new open-circuit respiratory method was developed to estimate mixed venous Pco2 more rapidly and accurately than is possible with rebreathing techniques. 2. The subject breathes a mixture of CO2 in air from an open circuit. Carbon dioxide is added to the air flowing through the circuit at a rate such that the Pco2 in the inspired and expired gases (recorded continuously with a CO2 analyser) are almost identical. 3. Results from respiratory and cardiac patients showed that equilibrium occurred in less than 10 s. There was good agreement between the tensions of CO2 in the respiratory plateaux and in mixed venous and arterial blood withdrawn during equilibrium. 4. During exercise, the tensions of CO2 of the plateaux and arterial blood at equilibrium also showed good agreement. 5. It is suggested that the new method represents an improvement over rebreathing methods as equilibrium is achieved rapidly before the mixed venous tension rises from recirculation.


1980 ◽  
Vol 58 (4) ◽  
pp. 263-270 ◽  
Author(s):  
Mary Winsborough ◽  
J. N. Miller ◽  
D. W. Burgess ◽  
G. Laszlo

1. A new CO2-rebreathing method for estimating cardiac output is described, and compared with a method employing N2O performed at the same time. 2. The subject inhales from a reservoir of 30% O2 in N2 and rebreathes into and out of an empty bag for 10s. 3. Oxygenated mixed venous Pco2 is then determined by rebreathing 7–15% CO2 in O2, the mixture being selected to obtain a plateau of CO2 concentration. 4. Pco2 rises exponentially towards the plateau value during the rebreathing of 30% O2. Cardiac output is calculated from the rate of change of the alveolar—mixed venous Pco2 difference by a differential version of the Fick equation employing published CO2 dissociation curves for whole blood in vitro. 5. The slope of the regression of cardiac output on V̇o2 is similar to that obtained in other studies employing direct Fick measurements. The slope is some 15% greater than obtained with N2O but the difference is significant only when Oz consumption is greater than 2 litres/min. 6. The CO2 dissociation slope of blood does not differ during pulmonary gas exchange in vivo from that determined at equilibrium in vitro. 7. The volume of pulmonary blood available for CO2 exchange may rise to about 1 litre in heavy exercise, with a transit time of 1–2 s in the lungs. 8. The method can be employed for estimating pulmonary blood flow during physiological studies in subjects with normal lungs.


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