Respiratory tissue properties derived from flow transfer function in healthy humans

1997 ◽  
Vol 82 (4) ◽  
pp. 1098-1106 ◽  
Author(s):  
W. Tomalak ◽  
R. Peslin ◽  
C. Duvivier

Tomalak, W., R. Peslin, and C. Duvivier. Respiratory tissue properties derived from flow transfer function in healthy humans. J. Appl. Physiol. 82(4): 1098–1106, 1997.—Assuming homogeneity of alveolar pressure, the relationship between airway flow and flow at the chest during forced oscillation at the airway opening [flow transfer function (FTF)] is related to lung and chest wall tissue impedance (Zti): FTF = 1 + Zti/Zg, where Zg is alveolar gas impedance, which is inversely proportional to thoracic gas volume. By using a flow-type body plethysmograph to obtain flow rate at body surface, FTF has been measured at oscillation frequencies ( f os) of 10, 20, 30 and 40 Hz in eight healthy subjects during both quiet and deep breathing. The data were corrected for the flow shunted through upper airway walls and analyzed in terms of tissue resistance (Rti) and effective elastance (Eti,eff) by using plethysmographically measured thoracic gas volume values. In most subjects, Rti was seen to decrease with increasing f os and Eti,eff to vary curvilinearly with f os 2, which is suggestive of mechanical inhomogeneity. Rti presented a weak volume dependence during breathing, variable in sign according to f os and among subjects. In contrast, Eti,eff usually exhibited a U-shaped pattern with a minimum located a little above or below functional residual capacity and a steep increase with decreasing or increasing volume (30–80 hPa/l2) on either side. These variations are in excess of those expected from the sigmoid shape of the static pressure-volume curve and may reflect the effect of respiratory muscle activity. We conclude that FTF measurement is an interesting tool to study Rti and Eti,eff and that these parameters have probably different physiological determinants.

1995 ◽  
Vol 78 (3) ◽  
pp. 938-947 ◽  
Author(s):  
M. Rotger ◽  
R. Farre ◽  
R. Peslin ◽  
D. Navajas

The aim of this work was to demonstrate that the three compartments of the lung T network and the chest wall impedance (Zcw) can be identified from input and transfer impedances of the respiratory system if the pleural pressure is recorded during the measurements. The method was tested in six healthy volunteers in the range of 8–32 Hz. The impedances resulting from the decomposition confirm the adequacy of the monoalveolar structure commonly used in healthy subjects. Indeed, the T shunt impedance is well modeled by a purely compliant element, the mean compliance [0.038 +/- 0.081 (SD) l/kPa], which coincides within 9.5 +/- 6.3% of the alveolar gas compressibility derived from thoracic gas volume (0.036 +/- 0.011 l/kPa). The results obtained provide experimental evidence that the alveolar gas compression is predominantly isothermal and that lung tissue impedance is negligible throughout the whole frequency range. The shape of Zcw is consistent with a low compliance-low inertance pathway in parallel with a high compliance-high inertance pathway. We conclude that the proposed method is able to reliably identify the T network featuring the lung and Zcw.


1998 ◽  
Vol 84 (2) ◽  
pp. 553-561 ◽  
Author(s):  
R. Peslin ◽  
C. Duvivier

Peslin, R., and C. Duvivier. Partitioning of airway and respiratory tissue mechanical impedances by body plethysmography. J. Appl. Physiol. 84(2): 553–561, 1998.—We have tested the feasibility of separating the airway (Zaw) and tissue (Zti) components of total respiratory input impedance (Zrs,in) in healthy subjects by measuring alveolar gas compression by body plethysmography (Vpl) during pressure oscillations at the airway opening. The forced oscillation setup was placed inside a body plethysmograph, and the subjects rebreathedbtps gas. Zrs,in and the relationship between Vpl and airway flow (Hpl) were measured from 4 to 29 Hz. Zaw and Zti were computed from Zrs,in and Hpl by using the monoalveolar T-network model and alveolar gas compliance derived from thoracic gas volume. The data were in good agreement with previous observations: airway and tissue resistance exhibited some positive and negative frequency dependences, respectively; airway reactance was consistent with an inertance of 0.015 ± 0.003 hPa ⋅ s2 ⋅ l−1and tissue reactance with an elastance of 36 ± 8 hPa/l. The changes seen with varying lung volume, during elastic loading of the chest and during bronchoconstriction, were mostly in agreement with the expected effects. The data, as well as computer simulation, suggest that the partitioning is unaffected by mechanical inhomogeneity and only moderately affected by airway wall shunting.


1990 ◽  
Vol 68 (6) ◽  
pp. 2403-2412 ◽  
Author(s):  
K. R. Lutchen ◽  
C. A. Giurdanella ◽  
A. C. Jackson

Respiratory input impedance (Zrs) from 2.5 to 320 Hz displays a high-frequency resonance, the location of which depends on the density of the resident gas in the lungs (J. Appl. Physiol. 67: 2323-2330, 1989). A previously used six-element model has suggested that the resonance is due to alveolar gas compression (Cg) resonating with tissue inertance (Iti). However, the density dependence of the resonance indicates that is associated with the first airway acoustic resonance. The goal of this study was to determine whether unique properties for tissues and airways can be extracted from Zrs data by use of models that incorporate airway acoustic phenomena. We applied several models incorporating airway acoustics to the 2.5- to 320-Hz data from nine healthy adult humans during room air (RA) and 20% He-80% O2 (HeO2) breathing. A model consisting of a single open-ended rigid tube produced a resonance far sharper than that seen in the data. To dampen the resonance features, we used a model of multiple open-ended rigid tubes in parallel. This model fit the data very well for both RA and HeO2 but required fewer and longer tubes with HeO2. Another way to dampen the resonance was to use a single rigid tube terminated with an alveolar-tissue unit. This model also fit the data well, but the alveolar Cg estimates were far smaller than those expected based on the subject's thoracic gas volume. If Cg was fixed based on the thoracic gas volume, a large number of tubes were again required. These results along with additional simulations show that from input Zrs alone one cannot uniquely identify features indigenous to alveolar Cg or to the respiratory tissues.


1985 ◽  
Vol 58 (2) ◽  
pp. 346-351 ◽  
Author(s):  
P. Begin ◽  
R. Peslin ◽  
B. Hannhart ◽  
C. Gallina

We investigated two methods of decreasing the error on plethysmographic determinations of thoracic gas volume (TGV) related to cheeks movements during panting maneuvers: lowering gas density in the airways with an 80% He-20% O2 mixture and computing TGV from the in-phase component of the plethysmographic signal (TGVr). The methods were tested by measuring how TGV estimates varied when panting frequency was raised from 0.8 to 2.5 Hz during the same occlusion. The measurements were performed in 6 normal subjects and 12 patients with chronic bronchitis with and without cheeks support and when the airway was connected to an external device simulating an increased cheeks compliance. A small negative frequency dependence of TGV (delta TGV/delta f = -1.2 +/- 0.8%/Hz with cheeks support), most probably unrelated to upper airway walls, was found in normal subjects. Delta TGV/delta f was positive and algebraically larger in patients than in normals, reaching 2.2 +/- 3.4%/Hz without cheeks support and 11.8 +/- 8.0%/Hz with the additional cheeks. The latter value was only 20% smaller when computed on the basis of TGVr, demonstrating the limited usefulness of the phase-based correction. In contrast, breathing He-O2 decreased delta TGV/delta f to approximately 50% of its air value (P less than 0.01) and appears as an effective way to diminish the error in obstructive patients.


2016 ◽  
Vol 48 (5) ◽  
pp. 1340-1350 ◽  
Author(s):  
Luigi Taranto-Montemurro ◽  
Scott A. Sands ◽  
Bradley A. Edwards ◽  
Ali Azarbarzin ◽  
Melania Marques ◽  
...  

We recently demonstrated that desipramine reduces the sleep-related loss of upper airway dilator muscle activity and reduces pharyngeal collapsibility in healthy humans without obstructive sleep apnoea (OSA). The aim of the present physiological study was to determine the effects of desipramine on upper airway collapsibility and apnoea–hypopnea index (AHI) in OSA patients.A placebo-controlled, double-blind, randomised crossover trial in 14 OSA patients was performed. Participants received treatment or placebo in randomised order before sleep. Pharyngeal collapsibility (critical collapsing pressure of the upper airway (Pcrit)) and ventilation under both passive (V′0,passive) and active (V′0,active) upper airway muscle conditions were evaluated with continuous positive airway pressure (CPAP) manipulation. AHI was quantified off CPAP.Desipramine reduced activePcrit(median (interquartile range) −5.2 (4.3) cmH2O on desipramineversus−1.9 (2.7) cmH2O on placebo; p=0.049) but not passivePcrit(−2.2 (3.4)versus−0.7 (2.1) cmH2O; p=0.135). A greater reduction in AHI occurred in those with minimal muscle compensation (defined asV′0,active−V′0,passive) on placebo (r=0.71, p=0.009). The reduction in AHI was driven by the improvement in muscle compensation (r=0.72, p=0.009).In OSA patients, noradrenergic stimulation with desipramine improves pharyngeal collapsibility and may be an effective treatment in patients with minimal upper airway muscle compensation.


1990 ◽  
Vol 9 (4) ◽  
pp. 220-223 ◽  
Author(s):  
Celia J. Lanteri ◽  
Joan M. Raven ◽  
Peter D. Sly

1988 ◽  
Vol 64 (2) ◽  
pp. 823-831 ◽  
Author(s):  
H. L. Dorkin ◽  
K. R. Lutchen ◽  
A. C. Jackson

Recent studies on respiratory impedance (Zrs) have predicted that at frequencies greater than 64 Hz a second resonance will occur. Furthermore, if one intends to fit a model more complicated than the simple series combination of a resistance, inertance, and compliance to Zrs data, the only way to ensure statistically reliable parameter estimates is to include data surrounding this second resonance. An additional question, however, is whether the resulting parameters are physiologically meaningful. We obtained input impedance data from eight healthy adult humans using discrete frequency forced oscillations from 4 to 200 Hz. Three resonant frequencies were seen: 8 +/- 2, 151 +/- 10, and 182 +/- 16 Hz. A seven-parameter lumped element model provided an excellent fit to the data in all subjects. This model consists of an airway resistance (Raw), which is linearly dependent on frequency, and airway inertance separated from a tissue resistance, inertance, and compliance by a shunt compliance (Cg) thought to represent gas compressibility. Model estimates of Raw and Cg were compared with those suggested by measurement of Raw and thoracic gas volume using a plethysmograph. In all subjects the model Raw and Cg were significantly lower than and not correlated with the corresponding plethysmographic measurement. We hypothesize that the statistically reliable but physiologically inconsistent parameters are a consequence of the distorting influence of airway wall compliance and/or airway quarter-wave resonance. Such factors are not inherent to the seven-parameter model.


1985 ◽  
Vol 58 (6) ◽  
pp. 1783-1787 ◽  
Author(s):  
L. J. Folinsbee ◽  
J. F. Bedi ◽  
S. M. Horvath

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25–75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25–75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.


2008 ◽  
Vol 105 (6) ◽  
pp. 1864-1872 ◽  
Author(s):  
Z. Hantos ◽  
Á. Adamicza ◽  
T. Z. Jánosi ◽  
M. V. Szabari ◽  
J. Tolnai ◽  
...  

Absolute lung volumes such as functional residual capacity, residual volume (RV), and total lung capacity (TLC) are used to characterize emphysema in patients, whereas in animal models of emphysema, the mechanical parameters are invariably obtained as a function of transrespiratory pressure (Prs). The aim of the present study was to establish a link between the mechanical parameters including tissue elastance (H) and airway resistance (Raw), and thoracic gas volume (TGV) in addition to Prs in a mouse model of emphysema. Using low-frequency forced oscillations during slow deep inflation, we tracked H and Raw as functions of TGV and Prs in normal mice and mice treated with porcine pancreatic elastase. The presence of emphysema was confirmed by morphometric analysis of histological slices. The treatment resulted in an increase in TGV by 51 and 44% and a decrease in H by 57 and 27%, respectively, at 0 and 20 cmH2O of Prs. The Raw did not differ between the groups at any value of Prs, but it was significantly higher in the treated mice at comparable TGV values. In further groups of mice, tracheal sounds were recorded during inflations from RV to TLC. All lung volumes but RV were significantly elevated in the treated mice, whereas the numbers and size distributions of inspiratory crackles were not different, suggesting that the airways were not affected by the elastase treatment. These findings emphasize the importance of absolute lung volumes and indicate that tissue destruction was not associated with airway dysfunction in this mouse model of emphysema.


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