An open-circuit method for determining lung diffusing capacity during exercise: comparison to rebreathe

2005 ◽  
Vol 99 (5) ◽  
pp. 1985-1991 ◽  
Author(s):  
Eric M. Snyder ◽  
Bruce D. Johnson ◽  
Kenneth C. Beck

To avoid limitations associated with the use of single-breath and rebreathe methods for assessing the lung diffusing capacity for carbon monoxide (DlCO) during exercise, we developed an open-circuit technique. This method does not require rebreathing or alterations in breathing pattern and can be performed with little cognition on the part of the patient. To determine how this technique compared with the traditional rebreathe (DlCO,RB) method, we performed both the open-circuit (DlCO,OC) and the DlCO,RB methods at rest and during exercise (25, 50, and 75% of peak work) in 11 healthy subjects [mean age = 34 yr (SD 11)]. Both DlCO,OC and DlCO,RB increased linearly with cardiac output and external work. There was a good correlation between DlCO,OC and DlCO,RB for rest and exercise (mean of individual r2 = 0.88, overall r2 = 0.69, slope = 0.97). DlCO,OC and DlCO,RB were similar at rest and during exercise [e.g., rest = 27.2 (SD 5.8) vs. 29.3 (SD 5.2), and 75% peak work = 44.0 (SD 7.0) vs. 41.2 ml·min−1·mmHg−1 (SD 6.7) for DlCO,OC vs. DlCO,RB]. The coefficient of variation for repeat measurements of DlCO,OC was 7.9% at rest and averaged 3.9% during exercise. These data suggest that the DlCO,OC method is a reproducible, well-tolerated alternative for determining DlCO, particularly during exercise. The method is linearly associated with cardiac output, suggesting increased alveolar-capillary recruitment, and values were similar to the traditional rebreathe method.

1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.


1999 ◽  
Vol 87 (4) ◽  
pp. 1506-1512 ◽  
Author(s):  
Rebecca C. Barker ◽  
Susan R. Hopkins ◽  
Nancy Kellogg ◽  
I. Mark Olfert ◽  
Tom D. Brutsaert ◽  
...  

Noninvasive measurement of cardiac output (Q˙t) is problematic during heavy exercise. We report a new approach that avoids unpleasant rebreathing and resultant changes in alveolar[Formula: see text] or[Formula: see text] by measuring short-term acetylene (C2H2) uptake by an open-circuit technique, with application of mass balance for the calculation ofQ˙t. The method assumes that alveolar and arterial C2H2pressures are the same, and we account for C2H2recirculation by extrapolating end-tidal C2H2back to breath 1 of the maneuver. We correct for incomplete gas mixing by using He in the inspired mixture. The maneuver involves switching the subject to air containing trace amounts of C2H2and He; ventilation and pressures of He, C2H2, and CO2 are measured continuously (the latter by mass spectrometer) for 20–25 breaths. Data from three subjects for whom multiple Fick O2 measurements ofQ˙t were available showed that measurement ofQ˙t by the Fick method and by the C2H2technique was statistically similar from rest to 90% of maximal O2 consumption (V˙o 2 max). Data from 12 active women and 12 elite male athletes at rest and 90% ofV˙o 2 max fell on a single linear relationship, with O2 consumption (V˙o 2) predictingQ˙t values of 9.13, 15.9, 22.6, and 29.4 l/min atV˙o 2 of 1, 2, 3, and 4 l/min. Mixed venous [Formula: see text] predicted from C2H2-determinedQ˙t, measuredV˙o 2, and arterial O2 concentration was ∼20–25 Torr at 90% ofV˙o 2 max during air breathing and 10–15 Torr during 13% O2 breathing. This modification of previous gas uptake methods, to avoid rebreathing, produces reasonable data from rest to heavy exercise in normal subjects.


1987 ◽  
Vol 72 (4) ◽  
pp. 437-441 ◽  
Author(s):  
Y. M. H. Al-Shamma ◽  
R. Hainsworth ◽  
N. P. Silverton

1. This study was undertaken to determine the accuracy of a modification of a single breath method for estimation of cardiac output. The technique incorporated a single rebreathing stage followed by a prolonged expiration. Cardiac output was determined from the O2 uptake and the instantaneous changes in O2 and CO2 in the expired gas during the prolonged expiration. 2. The mean values and the random errors (determined from the differences between pairs of estimates) of cardiac outputs in normal subjects at rest and exercise were 5.42 and ± 0.60 litres/min (2 sd, 60 pairs) and 14.1 and ±1.8 litres/min (40 pairs). 3. Larger random errors were obtained in a group of cardiac patients but, except in hypoxic patients, the mean values obtained by the single breath and the direct (Fick) methods were almost identical. 4. We conclude that our modification of the single breath method is simple to use and sufficiently reliable for use in humans both at rest and during steady states of light exercise.


1998 ◽  
Vol 274 (5) ◽  
pp. R1496-R1499
Author(s):  
Hartmut Heller ◽  
Klaus-Dieter Schuster

The single-breath diffusing capacities for singly and doubly 18O-labeled CO2,[Formula: see text]and[Formula: see text], as well as for NO, were determined in seven anesthetized rabbits to investigate whether the theoretically predicted ratio of specific blood uptake rates of both isotopic CO2species,[Formula: see text]/[Formula: see text]= 2.0, can be derived from the measured values of[Formula: see text]and[Formula: see text]. Data of Dl were obtained by inflating the lungs with gas mixtures containing 0.35% C16O18O or 0.8% C18O2or 0.05% NO in nitrogen, with breath-holding periods of 0.05–0.5 s and 2–12 s for the CO2 and NO tests, respectively.[Formula: see text]/[Formula: see text]was calculated by applying the double-reciprocal Roughton-Forster equation to Dl values obtained in each animal and by assuming that NO diffusing capacity represents the gas conductance of the alveolar-capillary membrane. The measured ratio was[Formula: see text]/[Formula: see text]= 1.9 ± 0.2 (mean ± SD), thus comparing reasonably with the predicted one. Therefore, our findings provide evidence that the greater value of[Formula: see text]is mainly due to the twofold higher probability (or theta value) for C18O2than for C16O18O to disappear within red blood cells via isotopic exchange reactions.


1987 ◽  
Vol 63 (6) ◽  
pp. 2438-2449 ◽  
Author(s):  
G. M. Saidel ◽  
M. Modarreszadeh

A model has been developed to quantify the effectiveness of alveolar-capillary transport in the presence of ventilation inhomogeneity. The exhalation dynamics of carbon monoxide (CO), argon (Ar), and lung volume from a single-breath experiment are analyzed simultaneously. A membrane transport coefficient (MTCO) that does not vary with lung volume is evaluated by a two-stage optimization procedure and related to diffusing capacity. Also, the model allows for a decrease in membrane transport rate associated with reduced lung volume. The model is tested by simulation studies and experiments with human subjects having normal or diseased (mainly obstructed) lungs. The MTCO provides a clear distinction between normal and obstructed lungs with respect to alveolar-capillary transport, whereas the semilog slope of the Ar alveolar plateau characterizes the ventilation inhomogeneity. Only when the diffusing capacity is corrected by the Ar slope, DLCO(Ar), do the breathing maneuvers performed from different preinflation volumes (residual volume or functional residual capacity) yield the same results for lungs with ventilation inhomogeneity. The uncorrected DLCO overestimates the effectiveness of alveolar-capillary transport in the presence of ventilation inhomogeneity.


1997 ◽  
Vol 273 (6) ◽  
pp. R2055-R2058
Author(s):  
Hartmut Heller ◽  
Klaus-Dieter Schuster

Pulmonary diffusing capacity of NO (Dl NO) was determined by performing single-breath experiments on six anesthetized paralyzed supine rabbits, applying inspiratory concentrations of NO (Fi NO) within a range of 10 parts per million (ppm) ≤ Fi NO ≤ 800 ppm. Starting from residual volume, the rabbit lungs were inflated by 50 ml of a NO-nitrogen-containing indicator gas mixture. Breath-holding time was set at 0.1, 1, 3, 5, and 7 s. Alveolar partial pressure of NO was determined by analyzing the end-tidal portion from expirates, with the use of respiratory mass spectrometry. In the six animals, pulmonary diffusing capacity of NO averaged Dl NO = 1.92 ± 0.21 ml ⋅ mmHg−1 ⋅ min−1(mean ± SD value). Despite extreme variations in Fi NO, we found very similar Dl NOvalues, and in three rabbits we found identical values even at such different Fi NO levels of 80 ppm or 500, 20, or 200 ppm as well as 10 or 800 ppm. There was also no dependence of Dl NO on the respective duration of the single-breath maneuvers. In addition, the time course of NO removal from alveolar space was independent of applied Fi NOlevels. These results suggest that Dl NOdeterminations are neither affected by chemical reactions of NO in alveolar gas phase as well as in lung tissue nor biased by endogenous release of NO from pulmonary tissue. It is our conclusion that the single-breath diffusing capacity of NO is able to provide a measure of alveolar-capillary gas conductance that is not influenced by the biochemical reactions of NO.


Sign in / Sign up

Export Citation Format

Share Document