ASSESSMENT OF ALVEOLAR VENTILATION, CARDIAC OUTPUT AND TISSUE O2 SUPPLY UTILISING ESTIMATION OF MIXED VENOUS PCO2 BY A REBERATHING TECHNIQUE

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.

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Cardiovascular and pulmonary effects of morphine in conscious pigs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.261.5.r1286 ◽

1991 ◽

Vol 261 (5) ◽

pp. R1286-R1293 ◽

Cited By ~ 1

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

Clinical Science ◽

10.1042/cs0420345 ◽

1972 ◽

Vol 42 (3) ◽

pp. 345-353 ◽

Cited By ~ 13

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.

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Estimation of Cardiac Output from the Rate of Change of Alveolar Carbon Dioxide Pressure during Rebreathing

Clinical Science ◽

10.1042/cs0580263 ◽

1980 ◽

Vol 58 (4) ◽

pp. 263-270 ◽

Cited By ~ 6

Author(s):

Mary Winsborough ◽

J. N. Miller ◽

D. W. Burgess ◽

G. Laszlo

Keyword(s):

Cardiac Output ◽

Co2 Concentration ◽

Co2 Exchange ◽

Rate Of Change ◽

Venous Pco2 ◽

The Difference ◽

Dissociation Curves ◽

Mixed Venous

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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Evaluation of a method for estimating cardiac output from a single breath in humans

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.4.1034 ◽

1982 ◽

Vol 53 (4) ◽

pp. 1034-1038 ◽

Cited By ~ 8

Author(s):

H. Chen ◽

N. P. Silverton ◽

R. Hainsworth

Keyword(s):

Cardiac Output ◽

Normal Subjects ◽

Random Errors ◽

Tolerance Limits ◽

Mean Values ◽

Single Breath ◽

Significant Difference ◽

Venous Pco2 ◽

Mixed Venous ◽

Single Breath Method

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.

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

CHEST Journal ◽

10.1378/chest.111.2.474 ◽

1997 ◽

Vol 111 (2) ◽

pp. 474-480 ◽

Cited By ~ 9

Author(s):

Sheila V. Jacob ◽

Laura Hornby ◽

Larry C. Lands

Keyword(s):

Cardiac Output ◽

Venous Pco2 ◽

Mixed Venous

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Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1977.42.2.228 ◽

1977 ◽

Vol 42 (2) ◽

pp. 228-234 ◽

Cited By ~ 316

Author(s):

S. M. Cain

Keyword(s):

Cardiac Output ◽

Critical Value ◽

Hypoxic Hypoxia ◽

Gas Mixture ◽

O2 Uptake ◽

The Third ◽

Diffusion Limited ◽

O2 Supply ◽

O2 Delivery ◽

Mixed Venous

Three groups of dogs were anesthetized, paralyzed, and ventilated at constant rates with the spleen clamped. Two groups were isovolemically hemodiluted with warm dextran and plasma to hematocrits just above and below that at which O2 uptake (VO2) could not be maintained at preanemic levels. One of these groups was given propranolol to reduce the cardiac output response to anemia. The third group was ventilated on a low O2 gas mixture to decrease oxygen uptake. VO2 was thus limited at a high-delivery O2 pressure (PO2) in anemia and a low-delivery PO2 in hypoxic hypoxia. VO2 was reduced at a mixed venous PO2 of 45 Torr in anemia and at 17 Torr in hypoxic hypoxia. VO2, mixed venous PO2, and O2 delivery decreased precipitously at hematocrits below 10%. Once VO2 was limited by O2 availability, a single linear relationship (r = 0.91) was found for percent VO2 as a function of total O2 delivery (cardiac output X arterial O2 content) during both anemic and hypoxic hypoxia. The critical value for O2 delivery was 9.8 ml/kg-min. When O2 supply became limiting, VO2 apparently was not diffusion limited because it was more dependent on volume delivery rates than on delivery PO2.

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Estimation of mixed venous Pco2 by rebreathing for one minute

British Journal of Diseases of the Chest ◽

10.1016/s0007-0971(67)80038-x ◽

1967 ◽

Vol 61 (3) ◽

pp. 131-135

Author(s):

L.H. Capel ◽

H. Zeitlin ◽

E.C. Fletcher

Keyword(s):

Venous Pco2 ◽

Mixed Venous

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Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

Journal of Applied Physiology ◽

10.1152/japplphysiol.00002.2006 ◽

2007 ◽

Vol 102 (1) ◽

pp. 331-339 ◽

Cited By ~ 27

Author(s):

Rebecca S. Syring ◽

Cynthia M. Otto ◽

Rebecca E. Spivack ◽

Klaus Markstaller ◽

James E. Baumgardner

Keyword(s):

Cardiac Output ◽

Lung Injury ◽

Respiratory Rate ◽

Pressure Control ◽

Plateau Pressure ◽

Control Mode ◽

Intrinsic Peep ◽

Mixed Venous Saturation ◽

Mixed Venous ◽

Saline Lavage

Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared with PEEPe. In seven New Zealand White rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with a fraction of inspired O2 (FiO2) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH2O, and either 1) high RR ( 24 ) and low PEEPe (3.5) or 2) low RR ( 7 ) and high PEEPe ( 14 ). We assessed cyclical lung recruitment with a fast arterial Po2 probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared with the high PEEPe group ( P < 0.001), and mixed venous saturation was consistently greater in the high RR group ( P < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.

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Respiratory measurements of cardiac output: from elegant idea to useful test

Journal of Applied Physiology ◽

10.1152/japplphysiol.01074.2001 ◽

2004 ◽

Vol 96 (2) ◽

pp. 428-437 ◽

Cited By ~ 41

Author(s):

Gabriel Laszlo

Keyword(s):

Cardiac Output ◽

Human Subjects ◽

Venous Blood ◽

The Body ◽

Mixed Venous Blood ◽

Indirect Determination ◽

Arterial Blood ◽

Pulmonary Capillary ◽

Pulmonary Arterial ◽

Mixed Venous

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.

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