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.

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.

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.

scholarly journals Estimation of Mixed Venous Pco2 for Determination of Cardiac Output in Children

CHEST Journal ◽  
1997 ◽  
Vol 111 (2) ◽  
pp. 474-480 ◽  
Author(s):  
Sheila V. Jacob ◽  
Laura Hornby ◽  
Larry C. Lands
Keyword(s):  
Cardiac Output ◽  
Venous Pco2 ◽  
Mixed Venous

Gas-blood PCO2 gradients during avian gas exchange

1975 ◽  
Vol 39 (3) ◽  
pp. 405-410 ◽  
Author(s):  
D. G. Davies ◽  
R. E. Dutton
Keyword(s):  
Gas Exchange ◽  
Exchange System ◽  
Arterial Pco2 ◽  
Charged Membrane ◽  
Venous Pco2 ◽  
Avian Lung ◽  
Gas Exchange System ◽  
Spontaneously Breathing ◽  
Membrane Mechanism ◽  
Mixed Venous

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.

Relationship between cardiac output and mixed venous-arterial Pco2 gradient in sodium bicarbonate-treated dogs

Resuscitation ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 266
Author(s):  
K Okamoto ◽  
H Kishi ◽  
H Choi ◽  
M Kurose ◽  
T Sato ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Bicarbonate ◽  
Arterial Pco2 ◽  
Mixed Venous

Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema

1985 ◽  
Vol 59 (6) ◽  
pp. 1698-1703 ◽  
Author(s):  
J. R. Catterall ◽  
P. M. Calverley ◽  
W. MacNee ◽  
P. M. Warren ◽  
C. M. Shapiro ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Chronic Bronchitis ◽  
Rem Sleep ◽  
Normal Subjects ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Nocturnal Hypoxemia ◽  
Voluntary Hypoventilation ◽  
Arterial Po2 ◽  
Mixed Venous

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

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.

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