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
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.


1991 ◽  
Vol 261 (5) ◽  
pp. R1286-R1293 ◽  
Author(s):  
J. P. Hannon ◽  
C. A. Bossone

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.


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.


1966 ◽  
Vol 1 (3) ◽  
pp. 258-264 ◽  
Author(s):  
P. Cerretelli ◽  
J.C. Cruz ◽  
L.E. Farhi ◽  
H. Rahn

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.


1982 ◽  
Vol 53 (4) ◽  
pp. 1034-1038 ◽  
Author(s):  
H. Chen ◽  
N. P. Silverton ◽  
R. Hainsworth

We have modified the single-breath method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966) for estimating cardiac output and arterial and mixed venous carbon dioxide tensions (PCO2). We assessed this using 30 normal subjects and 23 cardiac patients. The procedure was performed satisfactorily in all but two patients. The random errors, from 60 pairs of estimates of cardiac output in normal subjects and 50 pairs in patients, were +/- 12.8 and +/- 19.6% (95% tolerance limits; i.e., coefficient of variation multiplied by 2 for n greater than 50). The systematic error was assessed in 15 patients from comparisons with results obtained by the direct Fick method. There was no significant difference except in two patients with large intracardiac shunts. Mean values of cardiac output by single-breath and direct Fick estimates were 3.80 and 3.83 l/min. Arterial and mixed venous PCO2 were estimated by the single-breath method with random errors of +/- 1.5 and +/- 1.4 Torr, respectively, and no significant systematic errors. We conclude that our modification of the single-breath method is reliable in humans at rest, although the procedures for delivering the breath and processing the data are of critical importance.


BMJ ◽  
1964 ◽  
Vol 1 (5393) ◽  
pp. 1290-1292
Author(s):  
H. De V. Heese ◽  
C. Freeseman

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