scholarly journals Viscoelasticity of the trachea and its effects on flow limitation

2006 ◽  
Vol 100 (2) ◽  
pp. 384-389 ◽  
Author(s):  
Nikolai Aljuri ◽  
Jose G. Venegas ◽  
Lutz Freitag

To test the hypothesis that peak expiratory flow is determined by the wave-speed-limiting mechanism, we studied the time dependency of the trachea and its effects on flow limitation. For this purpose, we assessed the relationship between transmural pressure and cross-sectional area [the tube law (TL)] of six excised human tracheae under controlled conditions of static (no flow) and forced expiratory flow. We found that TLs of isolated human tracheae followed quite well the mathematical representation proposed by Shapiro (Shapiro AH. J Biomech Eng 99: 126–147, 1977) for elastic tubes. Furthermore, we found that the TL measured at the onset of forced expiratory flow was significantly stiffer than the static TL. As a result, the stiffer TL measured at the onset of forced expiratory flow predicted theoretical maximal expiratory flows far greater than those predicted by the more compliant static TL, which in all cases studied failed to explain peak expiratory flows measured at the onset of forced expiration. We conclude that the observed viscoelasticity of the tracheal walls can account for the measured differences between maximal and “supramaximal” expiratory flows seen at the onset of forced expiration.

1999 ◽  
Vol 87 (5) ◽  
pp. 1973-1980 ◽  
Author(s):  
Nikolai Aljuri ◽  
Lutz Freitag ◽  
José G. Venegas

Flow limitation during forced exhalation and gas trapping during high-frequency ventilation are affected by upstream viscous losses and by the relationship between transmural pressure (Ptm) and cross-sectional area ( A tr) of the airways, i.e., tube law (TL). Our objective was to test the validity of a simple lumped-parameter model of expiratory flow limitation, including the measured TL, static pressure recovery, and upstream viscous losses. To accomplish this objective, we assessed the TLs of various excised animal tracheae in controlled conditions of quasi-static (no flow) and steady forced expiratory flow. A tr was measured from digitized images of inner tracheal walls delineated by transillumination at an axial location defining the minimal area during forced expiratory flow. Tracheal TLs followed closely the exponential form proposed by Shapiro (A. H. Shapiro. J. Biomech. Eng. 99: 126–147, 1977) for elastic tubes: Ptm = K p[( A tr/ A tr0)− n − 1], where A tr0 is A tr at Ptm = 0 and K p is a parametric factor related to the stiffness of the tube wall. Using these TLs, we found that the simple model of expiratory flow limitation described well the experimental data. Independent of upstream resistance, all tracheae with an exponent n < 2 experienced flow limitation, whereas a trachea with n > 2 did not. Upstream viscous losses, as expected, reduced maximal expiratory flow. The TL measured under steady-flow conditions was stiffer than that measured under expiratory no-flow conditions, only if a significant static pressure recovery from the choke point to atmosphere was assumed in the measurement.


1986 ◽  
Vol 60 (2) ◽  
pp. 441-448 ◽  
Author(s):  
H. W. Greville ◽  
M. E. Arnup ◽  
S. N. Mink ◽  
L. Oppenheimer ◽  
N. R. Anthonisen

We examined the mechanism of the reduced maximum expiratory flow rates (Vmax) in a dog model of postpneumonectomy compensatory lung growth. During forced expiration, a Pitot-static tube was used to locate the airway site of flow limitation, or choke point, and to measure dynamic intrabronchial pressures. The factors determining Vmax were calculated and the results analyzed in terms of the wave-speed theory of flow limitation. Measurements were made at multiple lung volumes and during ventilation both with air and with HeO2. Five of the puppies had undergone a left pneumonectomy at 10 wk of age, and 5 littermate controls had undergone a sham operation. All dogs were studied at 26 wk of age, at which time compensatory lung growth had occurred in the postpneumonectomy group. Vmax was markedly decreased in the postpneumonectomy group compared with control, averaging 42% of the control flow rates from 58 to 35% of the vital capacity (VC). At 23% of the VC, Vmax was 15% less than control. Choke points were more peripheral in the postpneumonectomy dogs compared with controls at all volumes. The total airway pressure was the same at the choke-point airway in the postpneumonectomy dogs as that in the same airway in the control dogs, suggesting that the airways of the postpneumonectomy dogs displayed different bronchial area-pressure behavior from the control dogs. Despite the decreased Vmax on both air and HeO2, the density dependence of flow was high in the postpneumonectomy dogs and the same as controls at all lung volumes examined.


1983 ◽  
Vol 55 (3) ◽  
pp. 897-912 ◽  
Author(s):  
S. N. Mink

Airway sites of flow limitation [“choke points” (CP)] were identified during forced deflation in open-chest dogs before (C) and after (B) bronchoconstriction was produced by nebulizing a solution of methacholine chloride into their airways. CP were identified in two respective groups. In group I (n = 8) a retrograde catheter was used to locate CP and in the other a Pitot static tube (group II, n = 5), CP were identified at multiple lung volumes (VL) over the lower one-half of total lung capacity. Both groups showed similar findings at each condition. At B, corresponding values of maximum expiratory flow (Vmax) at each VL decreased to about 10% of those at C. Movement of CP relative to their original location varied at each VL and, especially at the lower VL, showed little peripheral movement. In group I, equal pressure points were also measured and were found to move peripherally at all the measured VL. In group II, cross-sectional area (A*) and airway compliance (K) at CP were estimated. During bronchoconstriction, A* decreased at the respective VL, and airways became less compliant. The reduction in Vmax could be explained in terms of changes in A* and K as described by wave-speed theory, and Vmax decreased because A* decreased. The decrease in A* was related in part to an increase in viscous pressure losses that reduced total pressure at CP and also in part to a change in the pressure-area behavior of bronchi at CP. Their relative effects on reducing A* and Vmax were examined.


2000 ◽  
Vol 88 (5) ◽  
pp. 1870-1879 ◽  
Author(s):  
Laurent L. Couëtil ◽  
Frank S. Rosenthal ◽  
Chris M. Simpson

The purpose of this study was to assess whether our method of inducing forced expiration detects small airway obstruction in horses. Parameters derived from forced expiratory flow-volume (FEFV) curves were compared with lung mechanics data obtained during spontaneous breathing in nine healthy horses, in three after histamine challenge, and in two with chronic obstructive pulmonary disease (COPD) pre- and posttherapy with prednisone. Parameters measured in the healthy horses included forced vital capacity (FVC = 41.6 ± 5.8 liters; means ± SD) and forced expiratory flow (FEF) at various percentages of FVC (range of 20.4–29.7 l/s). Histamine challenge induced a dose-dependent decrease in FVC and FEF at low lung volume. After therapy, lung function of the two COPD horses improved to a point where one horse had normal lung mechanics during tidal breathing; however, FEF at 95% of FVC (4.9 l/s) was still decreased. We concluded that FEFV curve analysis allowed the detection of induced or naturally occurring airway obstruction.


1984 ◽  
Vol 56 (6) ◽  
pp. 1655-1658 ◽  
Author(s):  
I. S. Davey ◽  
J. E. Cotes ◽  
J. W. Reed

The results of divers' annual medical examinations were used to assess the effects of diving exposure independent of age, stature, and smoking on forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). Cross-sectional analysis of records for 858 men showed a significant positive association between the maximal depth that subjects had experienced and FVC but not FEV1. There was a significant negative association for FEV1/FVC%, and this index was also positively correlated with years of diving exposure. Among a subsample of 81 men the forced expiratory flow rate at low lung volume was reduced relative to that of control subjects similarly assessed; the extent of the reduction from the reference value was significantly correlated with the diving exposure. Longitudinal analysis of results for 255 men over a minimum of 5 yr showed that the change in FVC per annum (positive or negative) was correlated with the change in maximal depth; there were no similar associations for FEV1 or FEV1/FVC%. Thus diving exposure affects the vital capacity and the forced expiratory flow rate at small lung volumes. The latter is evidence for narrowing of airways that might be secondary to diving-induced loss of lung elastic tissue; this hypothesis merits further investigation.


1977 ◽  
Vol 43 (3) ◽  
pp. 498-515 ◽  
Author(s):  
S. V. Dawson ◽  
E. A. Elliott

The mechanism limiting forced expiratory flow is explained on the basis that a local flow velocity reaches the local speed of wave propagation at a point, called the choke point, in intrathoracic airways. This theoretical approach to the “waterfall effect” leads to selection of the analogy of constricted open-channel flow to apply to the elastic network of airway tubes. Quantitative results are derived for the case of negligible friction by use of the Bernoulli principle. Shapes predicted for the maximum-flow static recoil curves depend only upon the nature of the pressure-area curve at the choke point in the case of negligible friction; and the magnitude of the critical rate of flow depends on reference values of cross-sectional area and elastic modulus at the choke point, on gas density, and on the static recoil pressure. The present theoretical results are used to interpret previous experiments, but quantitative applicability is limited because of frictional effects and lack of knowledge of choke point conditions.


1993 ◽  
Vol 74 (5) ◽  
pp. 2552-2558 ◽  
Author(s):  
R. Pellegrino ◽  
V. Brusasco ◽  
J. R. Rodarte ◽  
T. G. Babb

To investigate the impact of expiratory flow limitation (FL) on breathing pattern and end-expiratory lung volume (EELV), we imposed a small expiratory threshold load for a few breaths during exercise in nine volunteers (29–62 yr): six were healthy and three had mild-to-moderate airflow obstruction (67–71% predicted forced expiratory volume in 1 s). Six subjects showed evidence of FL, i.e., tidal expiratory flow impinging on maximal forced expiratory flow, at one or more exercise levels. Whenever an expiratory threshold load was imposed, mean expiratory flow decreased (P < 0.02) in association with an increased expiratory time (TE; P < 0.05). When the load was imposed during non-FL conditions, TE increased less than expiratory flow decreased and EELV tended to increase. In contrast, during FL, with the load, TE increased more than expiratory flow decreased, subjects did not achieve maximal expiratory flow until a lower volume, and EELV decreased (P < 0.001). Under both FL and no-FL conditions, unloading reversed the changes associated with loading. These data indicate that the increase in EELV during exercise is linked to the occurrence of FL. We suggest that compression of airways downstream from the flow-limiting segment may elicit a reflex mechanism that influences breathing pattern by terminating expiration prematurely, thus increasing EELV.


2021 ◽  
Vol 12 (7) ◽  
pp. 100-106
Author(s):  
Sujata Biswas ◽  
Nisha Bharti ◽  
Gandhari Basu

Background: Beedi workers are more prone to develop chronic respiratory diseases over time. Aims and Objectives: The present research aimed to investigate and compare the respiratory health profile and the factors associated among the beedi workers and non-beedi workers. Materials and Methods: An analytical, community based, cross sectional study was conducted among 60 female beedi and non-beedi workers. Multistage sampling was used to select three wards out of twenty wards under a municipality of the study district. After interview with a pre-designed structured questionnaire, the respondents were examined clinically and pulmonary function test was done using a portable spirometer. Results: All beedi workers were married and 23.3% were illiterate. Most of them had 1to 10 years exposure. Half of them initiated their work between 11 to 20 years. Rate of tobacco smoking, obesity, hypertension, asthma, diabetes was high among beedi workers. Forced Vital Capacity, Forced Expiratory Flow 25-75 and Peak Expiratory Flow Rate were significantly more among non-beedi workers. Forced Expiratory Volume in 1st second was more among non-beedi workers but FEV1/FVC ratio was same for both the group. Conclusion: Significantly better respiratory health profile of non-beedi workers have reflected beedi binding as a reason behind chronic respiratory disease. Therefore, awareness generation session regarding occupation based adverse effects and safety measures must be conducted at regular interval to make the working condition favorable.


1997 ◽  
Vol 83 (5) ◽  
pp. 1721-1732 ◽  
Author(s):  
O. F. Pedersen ◽  
H. J. L. Brackel ◽  
J. M. Bogaard ◽  
K. F. Kerrebijn

Pedersen, O. F., H. J. L. Brackel, J. M. Bogaard, and K. F. Kerrebijn. Wave-speed-determined flow limitation at peak flow in normal and asthmatic subjects. J. Appl. Physiol. 83(5): 1721–1732, 1997.—The purpose of this study was to examine whether peak expiratory flow is determined by the wave-speed flow-limiting mechanism. We examined 17 healthy subjects and 11 subjects with stable asthma, the latter treated with inhaled bronchodilators and corticosteroids. We used an esophageal balloon and a Pitot-static probe positioned at five locations between the right lower lobe and midtrachea to obtain dynamic area-transmural pressure ( A-Ptm) curves as described (O. F. Pedersen, B. Thiessen, and S. Lyager. J. Appl. Physiol. 52: 357–369, 1982). From these curves we obtained cross-sectional area ( A) and airway compliance (Caw = d A/dPtm) at PEF, calculated flow at wave speed {V˙ws = A[ A/(Caw∗ρ)0.5], where ρ is density} and speed index is (SI =V˙/V˙ws). In 13 of 15 healthy and in 4 of 10 asthmatic subjects, who could produce satisfactory curves, SI at PEF was >0.9 at one or more measured positions. Alveolar pressure continued to increase after PEF was achieved, suggesting flow limitation somewhere in the airway in all of these subjects. We conclude that wave speed is reached in central airways at PEF in most subjects, but it cannot be excluded that wave speed is also reached in more peripheral airways.


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