Effect of breath-hold time on DLCO(SB) in patients with airway obstruction

1985 ◽  
Vol 58 (4) ◽  
pp. 1319-1325 ◽  
Author(s):  
B. L. Graham ◽  
J. T. Mink ◽  
D. J. Cotton

The single-breath diffusing capacity of the lung for CO [DLCO(SB)] is considered a measure of the conductance of CO across the alveolar-capillary membrane and its binding with hemoglobin. Although incomplete mixing of inspired gas with alveolar gas could theoretically influence overall diffusion, conventional calculations of DLCO(SB) spuriously overestimate DLCO(SB) during short breath-holding periods when incomplete mixing of gas within the lung might have the greatest effect. Using the three-equation method to calculate DLCO(SB) which analytically accounts for changes in breath-hold time, we found that DLCO(SB) did not change with breath-hold time in control subjects but increased with increasing breath-hold time in both patients with asthma and patients with emphysema. The increase in DLCO(SB) with increasing breath-hold time correlated with the phase III slope of the single-breath N2 washout curve. We suggest that in patients with ventilation maldistribution, DLCO(SB) may be decreased for the shorter breath-hold maneuvers because overall diffusion is limited by the reduced transport of CO from the inspired gas through the alveolar gas prior to alveolar-capillary gas exchange.

1994 ◽  
Vol 76 (4) ◽  
pp. 1494-1501 ◽  
Author(s):  
G. R. Soparkar ◽  
J. T. Mink ◽  
B. L. Graham ◽  
D. J. Cotton

The dynamic changes in CO concentration [CO] during a single breath could be influenced by topographic inhomogeneity in the lung or by peripheral inhomogeneity due to a gas mixing resistance in the gas phase of the lung or to serial gradients in gas diffusion. Ten healthy subjects performed single-breath maneuvers by slowly inhaling test gas from functional residual capacity to one-half inspiratory capacity and slowly exhaling to residual volume with target breath-hold times of 0, 1.5, 3, 6, and 9 s. We calculated the three-equation single-breath diffusing capacity of the lung for CO (DLSBCO-3EQ) from the mean [CO] in both the entire alveolar gas sample and in four successive equal alveolar gas samples. DLSBCO-3EQ from the entire alveolar gas sample was independent of breath-hold time. However, with 0 s of breath holding, from early alveolar gas samples DLSBCO-3EQ was reduced and from late alveolar gas samples it was increased. With increasing breath-hold time, DLSBCO-3EQ from the earliest alveolar gas sample rapidly increased, whereas from the last alveolar gas sample it rapidly decreased such that all values from the small alveolar gas samples approached DLSBCO-3EQ from the entire alveolar sample. These changes correlated with ventilation inhomogeneity, as measured by the phase III He concentration slope and the mixing efficiency, and were larger for maneuvers with inspired volumes to one-half inspiratory capacity vs. total lung capacity.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 80 (4) ◽  
pp. 1126-1132 ◽  
Author(s):  
G. K. Prisk ◽  
A. M. Lauzon ◽  
S. Verbanck ◽  
A. R. Elliot ◽  
H. J. Guy ◽  
...  

We performed single-breath wash-in tests for He and SF6 in four subjects exposed to 14 days of microgravity (microG) during the Spacelab flight Spacelab Life Sciences-2. Subjects inspired a vital capacity breath of 5% He-1.25% SF6-balance O2 and then exhaled to residual volume at 0.5l/s. The tests were also performed with a 10-s breath hold at the end of inspiration. Measurements were also made with the subjects standing and supine in 1 G. Phase III slope was measured after the dead-space washout and before the onset of airway closure. In all subjects in 1 G, whether standing or supine, phase III slope for SF6 was significantly steeper than that for He. However, in microG, the slopes became the same. Furthermore, after breath holding in microG, the SF6 slopes were significantly flatter than those for He. On return to 1 G, the changes were reversed, and there was no difference between preflight and postflight values. Because most of the phase III slope reflects events occurring in the acinar regions of the lung, the results suggest that microG causes conformational changes in the acini or changes in cardiogenic mixing in the lung periphery, but in either case the mechanism is unclear.


1984 ◽  
Vol 56 (1) ◽  
pp. 52-56 ◽  
Author(s):  
T. S. Hurst ◽  
B. L. Graham ◽  
D. J. Cotton

We studied 10 symptom-free lifetime non-smokers and 17 smokers all with normal pulmonary function studies. All subjects performed single-breath N2 washout tests by either exhaling slowly (“slow maneuver”) from end inspiration (EI) to residual volume (RV) or exhaling maximally (“fast maneuver”) from EI to RV. After either maneuver, subjects then slowly inhaled 100% O2 to total lung capacity (TLC) and without breath holding, exhaled slowly back to RV. In the nonsmokers seated upright phase III slope of single-breath N2 test (delta N2/l) was lower (P less than 0.01) for the fast vs. the slow maneuver, but this difference disappeared when the subjects repeated the maneuvers in the supine position. In contrast, delta N2/l was higher for the fast vs. the slow maneuver (P less than 0.01) in smokers seated upright. For the slow maneuver, delta N2/l was similar between smokers and nonsmokers but for the fast maneuvers delta N2/l was higher in smokers than nonsmokers (P less than 0.01). We suggest that the fast exhalation to RV decreases delta N2/l in normal subjects by decreasing apex-to-base differences in regional ratio of RV to TLC (RV/TLC) but increases delta N2/l in smokers, because regional RV/TLC increases distal to sites of small airways obstruction when the expiratory flow rate is increased.


1989 ◽  
Vol 76 (6) ◽  
pp. 673-676 ◽  
Author(s):  
A. H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
G. Laszlo

1. Resting pulmonary blood flow (Q.), using the uptake of the soluble inert gas Freon-22 and an indirect estimate of lung tissue volume, has been estimated during breath-holding (Q.c) and compared with direct Fick cardiac output (Q.f) in 16 patients with various cardiac disorders. 2. The effect of breath-hold time was investigated by comparing Q.c estimated using 6 and 10 s of breath-holding in 17 patients. Repeatability was assessed by duplicate measurements of Q.c in the patients and in six normal subjects. 3. Q.c tended to overestimate Q.f, the bias and error being 0.09 l/min and 0.59, respectively. The coefficient of repeatability for Q.c in the patients was 0.75 l/min and in the normal subjects was 0.66 1/min. For Q.f it was 0.72 l/min. There was no significant difference in Q.c measured at the two breath-hold times. 4. The technique is simple to perform, and provides a rapid estimate of Q., monitoring acute and chronic changes in cardiac output in normal subjects and patients with cardiac disease.


1993 ◽  
Vol 75 (2) ◽  
pp. 927-932 ◽  
Author(s):  
D. J. Cotton ◽  
M. B. Prabhu ◽  
J. T. Mink ◽  
B. L. Graham

In normal seated subjects we increased single-breath ventilation inhomogeneity by changing both the preinspiratory lung volume and breath-hold time and examined the ensuing effects on two different techniques of measuring the diffusing capacity of the lung for carbon monoxide (DLCO). We measured the mean single-breath DLCO using the three-equation method (DLCOSB-3EQ) and also measured DLCO over discrete intervals during exhalation by the "intrabreath" method (DLCOexhaled). We assessed the distribution of ventilation using the normalized phase III slope for helium (SN). DLCOSB-3EQ was unaffected by preinspiratory lung volume and breath-hold time. DLCOexhaled increased with increasing preinspiratory lung volume and decreased with increasing breath-hold time. These changes correlated with the simultaneously observed changes in ventilation inhomogeneity as measured by SN (P < 0.01). We conclude that measurements of DLCOexhaled do not accurately reflect the mean DLCO. Intrabreath methods of measuring DLCO are based on the slope of the exhaled CO concentration curve, which is affected by both ventilation and diffusion inhomogeneities. Although DLCOexhaled may theoretically provide information about the distribution of CO uptake, the concomitant effects of ventilation nonuniformity on DLCOexhaled may mimic or mask the effects of diffusion nonuniformity.


1992 ◽  
Vol 73 (6) ◽  
pp. 2623-2630 ◽  
Author(s):  
D. J. Cotton ◽  
M. B. Prabhu ◽  
J. T. Mink ◽  
B. L. Graham

In patients with airflow obstruction, we found that ventilation inhomogeneity during vital capacity single-breath maneuvers was associated with decreases in the three-equation single-breath CO diffusing capacity of the lung (DLcoSB-3EQ) when breath-hold time (tBH) decreased. We postulated that this was due to a significant resistance to diffusive gas mixing within the gas phase of the lung. In this study, we hypothesized that this phenomenon might also occur in normal subjects if the breathing cycle were altered from traditional vital capacity maneuvers to those that increase ventilation inhomogeneity. In 10 normal subjects, we examined the tBH dependence of both DLcoSB-3EQ and the distribution of ventilation, measured by the mixing efficiency and the normalized phase III slope for helium. Preinspiratory lung volume (V0) was increased by keeping the maximum end-inspiratory lung volume (Vmax) constant or by increasing V0 and Vmax. When V0 increased while Vmax was kept constant, we found that the tBH-independent and the tBH-dependent components of ventilation inhomogeneity increased, but DLcoSB-3EQ was independent of V0 and tBH. Increasing V0 and Vmax did not change ventilation inhomogeneity at a tBH of 0 s, but the tBH-dependent component decreased. DLcoSB-3EQ, although independent of tBH, increased slightly with increases in Vmax. We conclude that in normal subjects increases in ventilation inhomogeneity with increases in V0 do not result in DLcoSB-3EQ becoming tBH dependent.


2018 ◽  
Vol 52 (1) ◽  
pp. 1500677 ◽  
Author(s):  
Mathias Munkholm ◽  
Jacob Louis Marott ◽  
Lars Bjerre-Kristensen ◽  
Flemming Madsen ◽  
Ole Find Pedersen ◽  
...  

The aim of this study was to determine reference equations for the combined measurement of diffusing capacity of the lung for carbon monoxide (CO) and nitric oxide (NO) (DLCONO). In addition, we wanted to appeal for consensus regarding methodology of the measurement including calculation of diffusing capacity of the alveolo-capillary membrane (Dm) and pulmonary capillary volume (Vc).DLCONO was measured in 282 healthy individuals aged 18–97 years using the single-breath technique and a breath-hold time of 5 s (true apnoea period). The following values were used: 1) specific conductance of nitric oxide (θNO)=4.5 mLNO·mLblood−1·min−1·mmHg−1; 2) ratio of diffusing capacity of the membrane for NO and CO (DmNO/DmCO)=1.97; and 3) 1/red cell CO conductance (1/θCO)=(1.30+0.0041·mean capillary oxygen pressure)·(14.6/Hb concentration in g·dL−1).Reference equations were established for the outcomes of DLCONO, including DLCO and DLNO and the calculated values Dm and Vc. Independent variables were age, sex, height and age squared.By providing new reference equations and by appealing for consensus regarding the methodology, we hope to provide a basis for future studies and clinical use of this novel and interesting method.


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.


2017 ◽  
Vol 49 (2) ◽  
pp. 1600962 ◽  
Author(s):  
Gerald S. Zavorsky ◽  
Connie C.W. Hsia ◽  
J. Michael B. Hughes ◽  
Colin D.R. Borland ◽  
Hervé Guénard ◽  
...  

Diffusing capacity of the lung for nitric oxide (DLNO), otherwise known as the transfer factor, was first measured in 1983. This document standardises the technique and application of single-breathDLNO. This panel agrees that 1) pulmonary function systems should allow for mixing and measurement of both nitric oxide (NO) and carbon monoxide (CO) gases directly from an inspiratory reservoir just before use, with expired concentrations measured from an alveolar “collection” or continuously sampledviarapid gas analysers; 2) breath-hold time should be 10 s with chemiluminescence NO analysers, or 4–6 s to accommodate the smaller detection range of the NO electrochemical cell; 3) inspired NO and oxygen concentrations should be 40–60 ppm and close to 21%, respectively; 4) the alveolar oxygen tension (PAO2) should be measured by sampling the expired gas; 5) a finite specific conductance in the blood for NO (θNO) should be assumed as 4.5 mL·min-1·mmHg-1·mL-1of blood; 6) the equation for 1/θCO should be (0.0062·PAO2+1.16)·(ideal haemoglobin/measured haemoglobin) based on breath-holdingPAO2and adjusted to an average haemoglobin concentration (male 14.6 g·dL−1, female 13.4 g·dL−1); 7) a membrane diffusing capacity ratio (DMNO/DMCO) should be 1.97, based on tissue diffusivity.


1987 ◽  
Vol 62 (5) ◽  
pp. 1962-1969 ◽  
Author(s):  
W. A. Whitelaw ◽  
B. McBride ◽  
G. T. Ford

The mechanism by which large lung volume lessens the discomfort of breath holding and prolongs breath-hold time was studied by analyzing the pressure waves made by diaphragm contractions during breath holds at various lung volumes. Subjects rebreathed a mixture of 8% CO2–92% O2 and commenced breath holding after reaching an alveolar plateau. At all volumes, regular rhythmic contractions of inspiratory muscles, followed by means of gastric and pleural pressures, increased in amplitude and frequency until the breakpoint. Expiratory muscle activity was more prominent in some subjects than others, and increased through each breath hold. Increasing lung volume caused a delay in onset and a decrease in frequency of contractions with no consistent change in duty cycle and a decline in magnitude of esophageal pressure swings that could be accounted for by force-length and geometric properties. The effect of lung volume on the timing of contractions most resembled that of a chest wall reflex and is consistent with the hypothesis that the contractions are a major source of dyspnea in breath holding.


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