Influence of age on pulmonary diffusing capacity

1959 ◽  
Vol 14 (4) ◽  
pp. 483-492 ◽  
Author(s):  
R. E. Donevan ◽  
W. H. Palmer ◽  
C. J. Varvis ◽  
D. V. Bates

The pulmonary function of 24 normal subjects ranging in age from 20 to 50 years has been studied at rest and during exercise. At rest there is a significant decrease with age in the pulmonary diffusing capacity and the level of diffusing capacity attained on exercise at any particular oxygen uptake decreases with increasing age. Simultaneous measurements of O2 uptake, ventilation, end tidal O2 and CO2 concentration and calculated alveolar CO2 concentration, using the Bohr equation, show no evidence that any of these measurements are significantly influenced by age. The predicted maximal O2 diffusing capacity ( J. Appl. Physiol. 6: 588, 1954) predicts with fair accuracy the diffusing capacity for carbon monoxide that will be found in any given individual at an O2 uptake of about 2.8 l/min. It correctly predicts the change in CO diffusing capacity with increasing age. Reasons are given for suggesting that the decrease in pulmonary diffusing capacity observed may be explained by a diminution in cardiac output with increasing age. Submitted on November 21, 1958

1990 ◽  
Vol 68 (4) ◽  
pp. 1443-1452 ◽  
Author(s):  
M. C. Kallay ◽  
R. W. Hyde ◽  
R. J. Smith

We investigated sources of error in estimating steady-state O2 consumption (VO2ss) by calculating O2 uptake from an anesthesia bag containing O2, He, and N2 during 10-20 s of rebreathing (VO2rb). In 11 normal resting subjects, VO2rb calculated with end-tidal sampling overestimated VO2ss by 16 +/- 15% (SD) (P less than 0.003). This error was proportional to the increase in pulse rate during rebreathing, so that pulse-corrected VO2rb slightly underestimated VO2ss by 2.1 +/- 12.2% (P = 0.66) in the six subjects who rebreathed 28% O2 in the rebreathing bag but significantly underestimated VO2ss by 7.5 +/- 6.7% (P less than 0.04) in the six subjects who rebreathed 21% O2 in the rebreathing bag. During exercise, VO2rb underestimated VO2ss by 4 +/- 12% (P less than 0.001) and by 7 +/- 6% at O2 consumptions greater than 2,000 ml/min if O2 in the rebreathing bag was kept above 20% throughout rebreathing. We found that VO2rb calculated with end-tidal gas concentrations underestimated VO2ss by 1-43% in patients with moderate-to-severe obstructive lung disease, with even greater errors when mixed expired samples were used. The magnitude of the discrepancy correlated poorly with abnormalities in standard pulmonary function tests. Based on these data, VO2rb closely approximates VO2ss in normal subjects, provided hypoxia during rebreathing is avoided and cardiac acceleration from rebreathing is taken into account during resting measurement.


2004 ◽  
Vol 16 (4) ◽  
pp. 378-390 ◽  
Author(s):  
Frédéric Lemaître ◽  
Mario Bedu ◽  
Jean Coudert

Pulmonary function was measured in 48 air divers (age range: 8–38 yr) and 56 control participants (age range: 8–34 yr). Static lung volumes, dynamic lung volumes and flows, and the pulmonary diffusing capacity for carbon monoxide were measured twice, 29 months apart. At both times the adult divers (>18 yr) had higher forced vital capacity, forced expiratory volume in 1 s and maximal expiratory flow rate at 50%, as well as lower pulmonary diffusing capacity for carbon monoxide, than did the adult controls. Whatever the age, mean annual changes in these parameters did not differ between groups. Our results indicate that there were no significant changes in pulmonary function in the young (8–12 yr), adolescent, or adult divers compared with healthy controls over the 29-month period. The mean annual changes in forced expiratory flow and volume, however, were negatively correlated with number of years of diving experience in adult divers and with maximal diving depth in adolescent (13–18 yr) divers (p < .05 and p < .001, respectively). Deep diving during the teenage years coupled with years of recreational diving might increase the risk of airway obstruction.


2009 ◽  
Vol 169 (5) ◽  
pp. 583-594 ◽  
Author(s):  
Haruo Kanagami ◽  
Toshiki Katsura ◽  
Koichiro Shiroishi ◽  
Kenji Baba ◽  
Toshiaki Ebina

2008 ◽  
Vol 104 (4) ◽  
pp. 1094-1100 ◽  
Author(s):  
Sylvia Verbanck ◽  
Daniel Schuermans ◽  
Sophie Van Malderen ◽  
Walter Vincken ◽  
Bruce Thompson

It has long been assumed that the ventilation heterogeneity associated with lung disease could, in itself, affect the measurement of carbon monoxide transfer factor. The aim of this study was to investigate the potential estimation errors of carbon monoxide diffusing capacity (DlCO) measurement that are specifically due to conductive ventilation heterogeneity, i.e., due to a combination of ventilation heterogeneity and flow asynchrony between lung units larger than acini. We induced conductive airway ventilation heterogeneity in 35 never-smoker normal subjects by histamine provocation and related the resulting changes in conductive ventilation heterogeneity (derived from the multiple-breath washout test) to corresponding changes in diffusing capacity, alveolar volume, and inspired vital capacity (derived from the single-breath DlCO method). Average conductive ventilation heterogeneity doubled ( P < 0.001), whereas DlCO decreased by 6% ( P < 0.001), with no correlation between individual data ( P > 0.1). Average inspired vital capacity and alveolar volume both decreased significantly by, respectively, 6 and 3%, and the individual changes in alveolar volume and in conductive ventilation heterogeneity were correlated ( r = −0.46; P = 0.006). These findings can be brought in agreement with recent modeling work, where specific ventilation heterogeneity resulting from different distributions of either inspired volume or end-expiratory lung volume have been shown to affect DlCO estimation errors in opposite ways. Even in the presence of flow asynchrony, these errors appear to largely cancel out in our experimental situation of histamine-induced conductive ventilation heterogeneity. Finally, we also predicted which alternative combination of specific ventilation heterogeneity and flow asynchrony could affect DlCO estimate in a more substantial fashion in diseased lungs, irrespective of any diffusion-dependent effects.


1985 ◽  
Vol 58 (5) ◽  
pp. 1654-1658 ◽  
Author(s):  
J. A. Loeppky ◽  
P. Scotto ◽  
H. Rieke ◽  
M. Meyer ◽  
J. Piiper

Arterial-alveolar equilibration of CO2 during exercise was studied by normoxic CO2 rebreathing in six dogs prepared with a chronic tracheostomy and exteriorized carotid loop and trained to run on a treadmill. In 153 simultaneous measurements of PCO2 in arterial blood (PaCO2) and end-tidal gas (PE'CO2) obtained in 46 rebreathing periods at three levels of mild-to-moderate steady-state exercise, the mean PCO2 difference (PaCO2-PE'CO2) was -1.0 +/- 1.0 (SD) Torr and was not related to O2 uptake or to the level of PaCO2 (30–68 Torr). The small negative PaCO2-PE'CO2 is attributed to the lung-to-carotid artery transit time delay which must be taken into account when both PaCO2 and PE'CO2 are continuously rising during rebreathing (average rate 0.22 Torr/s). Assuming that blood-gas equilibrium for CO2 was complete, a lung-to-carotid artery circulation time of 4.6 s accounts for the observed uncorrected PaCO2-PE'CO2 of -1.0 Torr. The results are interpreted to indicate that in rebreathing equilibrium PCO2 in arterial blood and alveolar gas are essentially identical. This conclusion is at variance with previous studies in exercising humans during rebreathing but is in full agreement with our recent findings in resting dogs.


1982 ◽  
Vol 52 (1) ◽  
pp. 109-113 ◽  
Author(s):  
H. A. Jones ◽  
J. C. Clark ◽  
E. E. Davies ◽  
R. E. Forster ◽  
J. M. Hughes

The rate of uptake of carbon monoxide (CO) in the lungs of normal subjects were measured at inspired concentrations of less than 1, 300, and 3,000 ppm (less than 0.0001–0.3%) using radioactive CO (11CO). In nine subjects the rate of uptake was monitored at the mouth during rebreathing. At inspired CO concentrations of approximately 1, 300, and 3,000 ppm and a mean alveolar O2 fraction of 0.15, the mean lung diffusing capacity was 25.8, 26.4, and 25.3 ml . min-1. Torr-1, respectively. In seven subjects the measurements were repeated after a period of O2 breathing, giving a mean alveolar O2 fraction of 0.78. The calculated membrane diffusing capacity was 31.9, 33.7, and 32.0 ml . min-1. Torr-1 at less than 1, 300, and 3,000 ppm inspired CO. We conclude that there is no difference in the rate of uptake of CO over the range of concentrations studied in these experiments. No evidence for the presence of a facilitated transport system for CO in the normal human lung was found.


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