An Evaluation of Rebreathing Methods for Measuring Mixed Venous Pco2 During Exercise

1972 ◽  
Vol 42 (3) ◽  
pp. 345-353 ◽  
Author(s):  
S. Godfrey ◽  
Eliana Wolf
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Direct Methods ◽  
Extrapolation Method ◽  
Venous Pco2 ◽  
Technical Factors ◽  
End Tidal ◽  
Male Subjects ◽  
Rebreathing Methods ◽  
Mixed Venous

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.

Effect of analyzer on determination of mixed venous PCO2 and cardiac output during exercise

1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands
Keyword(s):  
Cardiac Output ◽  
Gas Mixture ◽  
Arterial Pco2 ◽  
Venous Pco2 ◽  
The Face ◽  
High O2 ◽  
Collision Broadening ◽  
Rebreathing Methods ◽  
Mixed Venous

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.

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
Keyword(s):  
Co2 Concentration ◽  
Arterial Pco2 ◽  
Equilibrium Method ◽  
Venous Pco2 ◽  
Pulmonary Capillary Blood ◽  
Exponential Method ◽  
Power Outputs ◽  
End Tidal ◽  
Rebreathing Methods ◽  
Mixed Venous

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.

Gas-blood CO2 equilibration in parabronchial lungs of birds

1976 ◽  
Vol 41 (3) ◽  
pp. 302-309 ◽  
Author(s):  
M. Meyer ◽  
H. Worth ◽  
P. Scheid
Keyword(s):  
Steady State ◽  
Venous Blood ◽  
Blood Perfusion ◽  
Co2 Exchange ◽  
Mixed Venous Blood ◽  
O2 Uptake ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Mixed Venous ◽  
Haldane Effect

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.

Ventilatory effects of hypoxia and their dependence on PCO2

1975 ◽  
Vol 38 (1) ◽  
pp. 16-19 ◽  
Author(s):  
A. S. Rebuck ◽  
W. E. Woodley
Keyword(s):  
Oxygen Saturation ◽  
Healthy Subjects ◽  
Pulmonary Ventilation ◽  
Response Curves ◽  
Venous Pco2 ◽  
Progressive Hypoxia ◽  
Ventilatory Effects ◽  
Independent Variable ◽  
End Tidal ◽  
Mixed Venous

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.

Cardiovascular and pulmonary effects of morphine in conscious pigs

1991 ◽  
Vol 261 (5) ◽  
pp. R1286-R1293 ◽  
Author(s):  
J. P. Hannon ◽  
C. A. Bossone
Keyword(s):  
Cardiac Output ◽  
Hemoglobin Concentration ◽  
Hemoglobin Saturation ◽  
Morphine Administration ◽  
Venous Pco2 ◽  
Pulmonary Arterial ◽  
Left And Right ◽  
O2 Delivery ◽  
Ventilation Perfusion Ratio ◽  
Mixed Venous

Cardiovascular and pulmonary effects of morphine (1 mg/kg bolus iv) were investigated in conscious chronically instrumented pigs, a species exhibiting an excitable response. Control animals received an equivalent volume (less than 2 ml) of normal saline. Morphine induced an immediate but small increase in cardiac output and substantial increases in heart rate, mean systemic and pulmonary arterial pressure, left and right ventricular work, hematocrit, and hemoglobin concentration, but did not change stroke volume or systemic vascular resistance. Morphine administration also led to a gradual increase in ventilatory rate and rapid increases in tidal volume, expired and alveolar ventilation, ventilation-perfusion ratio, and shunt fraction. In addition, morphine administration produced substantial decrements in arterial and mixed venous PO2, hemoglobin saturation and mixed venous O2 content; no change in arterial O2 content; and a widening of the arteriovenous O2 difference. Arterial O2 transport was increased slightly. Finally, it produced substantial increments in arterial and mixed venous PCO2 and substantial decrements in arterial and mixed venous pH. It was concluded that arterial O2 delivery did not adequately rise to meet tissue O2 demand, in part because an appropriate increase in cardiac output was attenuated by morphine, and in part because morphine impaired pulmonary gas exchange.

Noninvasive diffusing capacity and cardiac output in exercising dogs

1988 ◽  
Vol 65 (2) ◽  
pp. 669-674 ◽  
Author(s):  
J. I. Carlin ◽  
S. S. Cassidy ◽  
U. Rajagopal ◽  
P. S. Clifford ◽  
R. L. Johnson
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Cardiac Output ◽  
Steady State ◽  
Pulmonary Blood Flow ◽  
Maximal Exercise ◽  
O2 Consumption ◽  
Diffusing Capacity ◽  
Metabolic Capacity ◽  
End Tidal

We have developed a rebreathing procedure to determine diffusing capacity (DLCO) and pulmonary blood flow (Qc) in the awake, exercising dog. A low dead space, leak-free respiratory mask with an incorporated mouthpiece was utilized to achieve mixing between the rebreathing bag and the dog's lung. The rebreathing bag was initially filled with approximately 1.0 liter of gas containing 0.6% C2H2, 0.3% C18O, 9% He, and 35-40% O2. End-tidal gas concentrations were measured with a respiratory mass spectrometer. The disappearance of C2H2 and C18O was measured with respect to He to calculate Qc and DLCO. Values for DLCO in dogs, expressed per kilogram of body weight, were much larger than those reported in humans. However, at a given level of absolute O2 consumption, measurements of absolute DLCO in dogs were comparable to those reported in humans by both rebreathing and steady-state methods at rest and near-maximal exercise. These results suggest that DLCO is more closely matched to the metabolic capacity (i.e., maximal O2 consumption) than to body size between these two species.

Role of the larynx in control of pattern of breathing during CO2 inhalation in humans

1983 ◽  
Vol 54 (6) ◽  
pp. 1726-1735 ◽  
Author(s):  
W. N. Gardner
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Breathing Pattern ◽  
Matched Control ◽  
Quantitative Comparison ◽  
Inspiratory Time ◽  
End Tidal ◽  
Laryngeal Resistance ◽  
Male Subjects

To determine whether change of laryngeal resistance causes shortening of expiratory time (TE) and hence increase of respiratory frequency with CO2 inhalation in conscious humans, 11 fit male subjects with permanent tracheostomies after laryngectomy for cancer (L group) and 8 matched control subjects (C group) inhaled CO2 in mild hyperoxia to produce various levels of steady-state hyperpnea within “nonvagal” range 1. Breathing pattern was averaged at the end of each steady state and behaved similarly in both groups. As end-tidal PCO2 (PACO2) increased, TE significantly shortened in both groups, whereas inspiratory time (TI) remained roughly constant (slightly increasing in the L group), suggesting that the larynx, at least in range 1, has no major role in determining this pattern. Quantitative comparison between the two groups showed that in the L group TE was significantly longer, whereas expiratory flow peaked and declined significantly earlier, resulting in a greater tendency to form end-expiratory pauses. All differences were greatest in eucapnia and decreased as PACO2 increased. Despite matched mean PACO2 values, mean tidal volume (VT) ventilation and mean inspiratory flow (VT/TI) were significantly less in the L group, and the slope of VT/TI vs. PACO2 was significantly depressed.

Effect of water immersion on cardiopulmonary physiology at high gravity (+Gz)

1986 ◽  
Vol 61 (5) ◽  
pp. 1686-1692 ◽  
Author(s):  
R. Arieli ◽  
U. Boutellier ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Functional Residual Capacity ◽  
Water Immersion ◽  
Systemic Circulation ◽  
Co2 Production ◽  
Arterial Pco2 ◽  
Residual Capacity ◽  
Gravitational Influence ◽  
End Tidal ◽  
Mixed Venous

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.

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