Importance of Appropriately Adjusting Diffusing Capacity of the Lung for Carbon Monoxide and Diffusing Capacity of the Lung for Carbon Monoxide/Alveolar Volume Ratio for Lung Volume

CHEST Journal ◽  
2006 ◽  
Vol 129 (4) ◽  
pp. 1113
Author(s):  
Douglas C. Johnson
Keyword(s):  
Carbon Monoxide ◽  
Lung Volume ◽  
Volume Ratio ◽  
Diffusing Capacity ◽  
Alveolar Volume

The effect of conductive ventilation heterogeneity on diffusing capacity measurement

2008 ◽  
Vol 104 (4) ◽  
pp. 1094-1100 ◽  
Author(s):  
Sylvia Verbanck ◽  
Daniel Schuermans ◽  
Sophie Van Malderen ◽  
Walter Vincken ◽  
Bruce Thompson
Keyword(s):  
Carbon Monoxide ◽  
Vital Capacity ◽  
Experimental Situation ◽  
Normal Subjects ◽  
Diffusing Capacity ◽  
Capacity Measurement ◽  
Alveolar Volume ◽  
Estimation Errors ◽  
Single Breath ◽  
Ventilation Heterogeneity

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.

Effects of altering ventilation on steady-state diffusing capacity for carbon monoxide

1963 ◽  
Vol 18 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Kaye H. Kilburn ◽  
Harry A. Miller ◽  
John E. Burton ◽  
Ronald Rhodes
Keyword(s):  
Carbon Monoxide ◽  
Steady State ◽  
Tidal Volume ◽  
Lung Volume ◽  
Dead Space ◽  
Control Level ◽  
Alveolar Ventilation ◽  
Positive Pressure ◽  
Diffusing Capacity ◽  
Fixed Rate

Alterations in the steady-state diffusing capacity for carbon monoxide (Dco) by the method of Filley, MacIntosh, and Wright, produced by sequential changes in the pattern of breathing were studied in anesthetized, paralyzed, artificially ventilated dogs. The Dco of paralyzed, artificially ventilated control dogs did not differ significantly during 3 hr from values found in conscious and anesthetized controls. A fivefold increase in tidal volume without changing frequency of breathing raised alveolar ventilation and CO uptake 500% and Dco 186%. A high correlation between tidal volume and Dco was noted during reciprocal alterations of tidal volume and rate which maintained minute volume. The Dco appeared to fall when alveolar ventilation was tripled by increments of rate with a fixed-tidal volume, despite a 63% increase in CO uptake. Doubling end-expiratory lung volume by positive pressure breathing without altering tidal volume or rate did not affect Dco. The addition of 100 ml of external dead space with rate and tidal volume constant decreased Dco to 42% of control level, however, stepwise reduction of dead space from 100 ml to 0 in two dogs failed to change Dco. Added dead space equal to frac12 tidal volume (170 ml) reduced Dco to 25% of control in two dogs with a return to control with removal of dead space. Thus, in paralyzed artificially ventilated dogs, tidal volume appears to be the principal ventilatory determinant of steady-state Dco. Dco is minimally affected by increases in alveolar ventilation with a constant tidal volume effected by increasing the frequency of breathing. Prolonged ventilation, at fixed rate and volume, and increased dead space either did not effect, or they reduced Dco, perhaps by rendering less uniform the distribution of gas, and blood in the lungs. Although lung volume was doubled by positive-pressure breathing, pulmonary capillary blood volume was probably reduced to produce opposing effects on diffusing capacity and no net change. Submitted on March 14, 1962

Effects of anemia and hemorrhagic shock on pulmonary diffusion in the dog lung

1963 ◽  
Vol 18 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Benjamin Burrows ◽  
Albert H. Niden
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Blood Cell ◽  
Hemorrhagic Shock ◽  
Red Blood Cell ◽  
Lung Volume ◽  
Diffusing Capacity ◽  
Pulmonary Diffusing Capacity ◽  
Capillary Membrane ◽  
Alveolar Capillary

Hemorrhagic shock induced a marked fall in the pulmonary diffusing capacity for carbon monoxide in the dog (Dl) and produced marked nonuniformity of Dl/Va ratios throughout the lung as assessed by the “equilibration technique”. Difficulties in calculating over-all Dl under these conditions are discussed. Induced anemia also produced a fall in Dl, but little change in the uniformity of Dl/Va ratios was noted. In isolated perfused dog lungs where blood flow, pulmonary vascular pressures, lung volume, and ventilation were maintained constant, Dl was found to be proportional to hematocrit, suggesting either: 1) that virtually all resistance to CO diffusion is in the erythrocyte or 2) that the apparent diffusing capacity of the alveolar-capillary membrane is dependent upon hematocrit, carbon monoxide transfer being reduced across portions of membrane which are some distance from a red blood cell. Submitted on January 12, 1962

scholarly journals Epigenome-wide association study on diffusing capacity of the lung (DLCO)

2020 ◽  
pp. 00567-2020
Author(s):  
Natalie Terzikhan ◽  
Hanfei Xu ◽  
Ahmed Edris ◽  
Ken R. Bracke ◽  
Fien M. Verhamme ◽  
...  
Keyword(s):  
Gene Expression ◽  
Carbon Monoxide ◽  
Gas Exchange ◽  
Association Study ◽  
Lung Tissue ◽  
Whole Blood ◽  
Positive Association ◽  
Specific Gene ◽  
Diffusing Capacity ◽  
Alveolar Volume

BackgroundEpigenetics may play an important role in pathogenesis of lung diseases. However, little is known about the epigenetic factors that influence impaired gas exchange at the lungs.AimTo identify the epigenetic signatures of the diffusing capacity of the lung measured by carbon monoxide uptake.MethodsEpigenome-Wide Association Study (EWAS) was performed on diffusing capacity, measured by carbon monoxide uptake (DLCO) and per alveolar volume (DLCO /VA) using the single-breath technique in 2674 individuals from two population-based cohort studies, the Rotterdam Study (the discovery panel) and the Framingham Heart Study (the replication panel). We assessed the clinical relevance of our findings by investigating the identified sites in whole blood and lung tissue specific gene expression.ResultsWe identified and replicated two CpG sites (cg05575921 and cg05951221) that were significantly associated with DLCO /VA and one (cg05575921) suggestively associated with DLCO. Furthermore, we found a positive association between AHRR (cg05575921) hypomethylation and gene expression of EXOC3 in whole blood. We confirmed that the expression of EXOC3 in lung tissue is positively associated with DLCO/VA and DLCO.ConclusionsWe report on epigenome wide associations with diffusing capacity in the general population. Our results suggest EXOC3 to be an excellent candidate through which smoking induced hypomethylation of AHRR might affect pulmonary gas exchange.

Diffusing Lung Capacity of Carbon Monoxide/Alveolar Volume as an Index for Evaluating Diffusing Capacity of the Acromegalic Lung

2009 ◽  
Vol 19 (6) ◽  
pp. 288-290 ◽  
Author(s):  
Tayyibe Saler ◽  
Sema Ucak ◽  
Tijen Yesim ◽  
Gulfidan Cakmak ◽  
Yuksel Altuntas
Keyword(s):  
Carbon Monoxide ◽  
Diffusing Capacity ◽  
Alveolar Volume ◽  
Lung Capacity

Measurement of lung diffusing capacity by means of C14O in a closed system

1964 ◽  
Vol 19 (1) ◽  
pp. 59-74 ◽  
Author(s):  
Paul S⊘lvsteen
Keyword(s):  
Carbon Monoxide ◽  
Uniform Distribution ◽  
Lung Volume ◽  
Closed System ◽  
Normal Subjects ◽  
Alveolar Ventilation ◽  
Diffusing Capacity ◽  
Mathematical Equations ◽  
Experimental Findings ◽  
Better Than

A method of measuring the lung diffusing capacity (Dl) with radioactive carbon monoxide (C14O) and nonuniformity of ventilation with nonabsorbable gas in a closed system is described. Treating ventilation as a continuous phenomenon and disregarding dead space, the mathematical equations for uniform and nonuniform ventilation (two lung regions ventilated in parallel) are derived. It is proved that sooner or later the curve for carbon monoxide, plotted on semilogarithmic paper, will be rectilinear. Experiments in six normal subjects and eight patients with chronic lung disease are described. Determinations of the distribution of the ventilation and the Dl are made in separate experiments. Since the method is unreliable at high Dl values, many of the Dl estimations are performed at high oxygen tension, which reduces the apparent Dl. It is shown that the assumption of a uniform distribution of Dl to lung volume explains the experimental findings better than the assumption of a uniform distribution of Dl to alveolar ventilation. Dl was decreased in four of the eight patients. mathematics of uniform and nonuniform ventilation; distribution of lung diffusing capacity in relation to lung volume and alveolar ventilation; N2 curve for use in calculating alveolar ventilation and regional lung volumes; CO curve for use in calculating lung diffusing capacity; diffusing capacity of lung determined with a closed system Submitted on October 15, 1962

Regional diffusing capacity in normal lungs during a slow exhalation

1982 ◽  
Vol 52 (6) ◽  
pp. 1487-1492 ◽  
Author(s):  
N. R. MacIntyre ◽  
J. A. Nadel
Keyword(s):  
Carbon Monoxide ◽  
Lung Volume ◽  
Vital Capacity ◽  
Normal Subjects ◽  
Lower Half ◽  
Diffusing Capacity ◽  
Lung Volumes ◽  
Lower Volume ◽  
Xenon 133 ◽  
Normal Lungs

From an analysis of carbon monoxide uptake and xenon-133 distribution after two bolus inhalations of these gases, we calculated regional diffusing capacity in the upper and lower volume halves of the lungs during the middle 60% of an exhaled vital capacity in five seated normal subjects. We found that the regional diffusing capacity of the upper half of the lungs was 11.6 +/- 4.2 (mean +/- SD) ml.min-1.Torr-1 and that the regional diffusing capacity of the lower half of the lungs was 24.4 +/- 2.4 ml.min-1.Torr-1 after 25% of the vital capacity had been exhaled. These values remained relatively constant as lung volume decreased from 25 to 75% of the exhaled vital capacity. Diffusing capacity in the upper half of the lungs ranged from 9.4 to 12.4 ml.min-1.Torr-1 during exhalation, and in the lower half of the lungs from 21.0 to 28.6 ml.min-1.Torr-1 during exhalation. These results suggest that total lung diffusing capacity remains relatively constant over this midrange of lung volumes and that this occurs because the regional diffusing capacities in both the upper and lower halves of the lungs remain relatively constant.

Effect of lung volume and positional changes on pulmonary diffusing capacity and its components

1991 ◽  
Vol 71 (4) ◽  
pp. 1477-1488 ◽  
Author(s):  
H. Stam ◽  
F. J. Kreuzer ◽  
A. Versprille
Keyword(s):  
Lung Volume ◽  
Supine Position ◽  
Body Position ◽  
Membrane Conductance ◽  
Normal Subjects ◽  
Negative Slope ◽  
Sitting Position ◽  
Diffusing Capacity ◽  
Alveolar Volume ◽  
Residual Capacity

Normal subjects have a larger diffusing capacity normalized per liter alveolar volume (DL/VA) in the supine than in the sitting position. Body position changes total lung diffusing capacity (DL), DL/VA, membrane conductance (Dm), and effective pulmonary capillary blood volume (Qc) as a function of alveolar volume (VA). These functions were studied in 37 healthy volunteers. DL/VA vs. VA yields a linear relationship in sitting as well as in supine position. Both have a negative slope but usually do not run parallel. In normal subjects up to 50 yr old DL/VA and DL increased significantly when subjects moved from a sitting to a supine posture at volumes between 50 and 100% of total lung capacity (TLC). In subjects greater than 50 yr old the responses of DL/VA and DL to change in body position were not significant at TLC. Functional residual capacity (FRC) decreases and DL/VA increases in all normal subjects when they change position from sitting to supine. When DL/VA increases more than predicted from the DL/VA vs. VA relationship in a sitting position, we may infer an increase in effective Qc in the supine position. In 56% of the volunteers, supine DL was smaller than sitting DL despite a higher DL/VA at FRC in the supine position because of the relatively larger decrease in FRC. When the positional response at TLC is studied, an estimation obtained accidentally at a volume lower than TLC may influence results. Above 80% of TLC, Dm decreased significantly from sitting to supine. Below this lung volume the decrease was not significant. The relationship between Qc and VA was best described by a second-order polynomial characterized by a maximum Qc at a VA greater than 60% of TLC. Qc was significantly higher in the supine position than in the sitting position, but the difference became smaller with increasing age. In observing the sitting and supine positions, we saw a decrease in maximum Qc normalized per square meter of body surface area with age.

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