Estimation of mixed venous Pco2 by rebreathing for one minute

1967 ◽  
Vol 61 (3) ◽  
pp. 131-135
Author(s):  
L.H. Capel ◽  
H. Zeitlin ◽  
E.C. Fletcher
Keyword(s):  
1976 ◽  
Vol 41 (3) ◽  
pp. 302-309 ◽  
Author(s):  
M. Meyer ◽  
H. Worth ◽  
P. Scheid

We have conducted two experimental series in the chicken in order to study CO2 exchange in the parabronchial lungs of birds.In the first series, the animals were artifically ventilated and end-expired PCO2, PE'CO2,was measured and compared with mixed venous PCO2, PVCO2. On the average, PECO2 exceeded PVCO2 by 2.8 Torr. In the second series, rebreathing was used to investigate the mechanism of this positive (PE'-PV)CO2 difference.Lung gas PCO2 was found to equilibrate with PVCO2 if both CO2 and O2 exchange in the lung was abolished during rebreathing. Only if O2 uptake continued, we observed a positive gas-to-mixed venous blood PCO2 difference. The results suggest that positive gas-blood PCO2 differences both during rebreathing and steady-state ventilation are brought about by the Haldane effect.Model calculations show that in the homogeneous avian lung, unlike in the alveolar lung, the Haldane effect can produce positive (PE'-PV)CO2 differences during steady-state breathing due to the peculiarities of the crosscurrent arrangement and parabronchial ventilation and blood perfusion.


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.


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.


BMJ ◽  
1963 ◽  
Vol 2 (5365) ◽  
pp. 1096-1097 ◽  
Author(s):  
N. J. Gross ◽  
J. D. Hamilton
Keyword(s):  

1990 ◽  
Vol 68 (1) ◽  
pp. 369-373 ◽  
Author(s):  
J. A. Estavillo

The effects of elevated venous PCO2 and denervation of the cardiac ventricles on ventilation were studied in 20 anesthetized open-chest unidirectionally ventilated White Leghorn cockerels. Venous PCO2 was increased by insufflating the gut with high CO2 while recording changes in the amplitude of the sternal movements. Arterial blood gases were held constant by unidirectionally ventilating the lungs with gas flows approximately five times the animal's resting minute volume. Insufflating the gut with 90% N2-10% O2 did not change the level of ventilation, whereas with 90% CO2-10% O2 the amplitude of sternal movement increased 500% above that with no gut gas flow. Exchange of N2 for the CO2 was followed by a rapid reduction of ventilatory movements to control levels. Arterial blood gases remained constant during gut gas insufflation, whereas mixed venous PCO2 increased and mixed venous pH decreased when high CO2 was given to the gut. Cutting the middle cardiac nerves, which primarily innervate the ventricles of the heart, reduced the ventilatory response to CO2 gut insufflation by 67%. Sympathetic denervation of the thoracic viscera did not change the responses. It appears that, in the chicken, increasing the mixed venous PCO2 while holding the arterial blood gases constant alters ventilation by an afferent system located in the venous circulation or in the right ventricle which is sensitive to changes in PCO2.


1987 ◽  
Vol 62 (6) ◽  
pp. 2467-2476 ◽  
Author(s):  
J. Gronlund ◽  
E. R. Swenson ◽  
J. Ohlsson ◽  
M. P. Hlastala

Changes in PCO2 and PO2 during expiration have been ascribed to simultaneous gas exchange, but other factors such as ventilation-perfusion inhomogeneity in combination with sequential emptying may also contribute. An experimental and model approach was used to study the relationship between gas exchange and changes in expired PCO2 and PO2 in anesthetized dogs during prolonged high tidal volume expirations. Changes in PCO2 and PO2 were quantified by taking the area bounded by the sloping exhalation curve and a line drawn horizontally from a point where the Fowler dead space plus 250 ml had been expired. This procedure is similar to using the slope of the exhalation curve but it circumvents problems caused by nonlinearity of the PCO2 and PO2 curves. The gas exchange components of the CO2 and O2 areas were calculated using a single-alveolus lung model whose input parameters were measured in connection with each prolonged expiration. The relationship between changes in experimental CO2 areas caused by sudden reductions in mixed venous PCO2 (produced by right atrial infusions of NaOH) and those calculated by the model was also studied. In seven dogs, calculated CO2 and O2 areas were 13% higher and 25% lower than the respective experimental areas, but interindividual variations were large. Changes in experimental CO2 areas caused by step changes in mixed venous PCO2 were almost identical to changes in the calculated areas. We conclude that the changes in PCO2 and PO2 during expiration cannot be explained solely by gas exchange. However, the single-alveolus lung model accurately predicts changes in the CO2 exhalation curve caused by alterations in the alveolar CO2 flow.


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.


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