Mechanisms of increased maximum expiratory flow during HeO2 breathing in dogs

1979 ◽  
Vol 47 (3) ◽  
pp. 490-502 ◽  
Author(s):  
S. Mink ◽  
M. Ziesmann ◽  
L. D. Wood
Keyword(s):  
Density Dependence ◽  
Wave Speed ◽  
Flow Limitation ◽  
Elastic Recoil ◽  
Expiratory Flow Limitation ◽  
Pressure Losses ◽  
Peripheral Airways ◽  
Catheter Technique ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

We used the retrograde-catheter technique to investigate the effect of a helium-oxygen gas mixture (HeO2) on resistance to maximum expiratory flow (Vmax) in airways subsegments between alveoli and the equal pressure point (EPP), and between EPP and the flow-limiting segment (FLS). FLS were found at the same site in main-stem bronchi on both air and HeO2 in most dogs studied. Static elastic recoil pressure (Pel = 7 +/- 1 cmH2O) and the lateral pressure at FLS (Ptm' = 11 +/- cmH2O) were not different on the two gases, and delta Vmax averaged 33 +/- 12%. EPP were located on HeO2 in segmental bronchi (7 +/- 2 mm ID), and EPP on air were always located more downstream. There was no density dependence of resistance between alveoli and EPP on HeO2, and delta Vmax was due to the marked density dependence of the pressure losses of convective acceleration in the short airway segment between EPP HeO2 and FLS. Assuming that FLS is the “choke point,” these findings are consistent with wave-speed theory of flow limitation modified to account for viscous pressure losses in peripheral airways. These results and conclusions question previous interpretations of delta Vmax as an index of peripheral airways obstruction, and demonstrate the utility of wave-speed theory in explaining complicated mechanisms of expiratory flow limitation.

Density dependence of maximal flow is lung volume dependent during bronchoconstriction

1987 ◽  
Vol 62 (2) ◽  
pp. 691-705 ◽  
Author(s):  
H. W. Greville ◽  
M. E. Arnup ◽  
S. N. Mink
Keyword(s):  
Airway Obstruction ◽  
Density Dependence ◽  
Lung Volume ◽  
Wave Speed ◽  
Airflow Obstruction ◽  
Phosphate Solution ◽  
Flow Limitation ◽  
Peripheral Airway ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

We examined the changes in maximum expiratory flow (Vmax) and the density dependence of maximum expiratory flow (delta Vmax) during histamine-induced bronchoconstriction in dogs. Histamine acid phosphate solution was nebulized into the airways of six dogs to produce predominantly peripheral airway obstruction. Vmax air, Vmax with the dogs breathing 80% He-20% O2 (delta Vmax), and airway sites of flow limitation (choke points) were examined at four lung volumes (VL), which ranged from 51 to 23% of the control vital capacity (VC). The findings were interpreted in terms of the wave-speed theory of flow limitation. At all VL, Vmax air decreased during bronchoconstriction by approximately 30% compared with the control value. Resistances peripheral to a 0.3-cm-diam airway were increased about threefold with histamine, whereas resistances between 0.6-cm-diam bronchi and main-stem bronchi increased just slightly. Airway diameters were measured in the air-dried lung at 20 cmH2O transpulmonary pressure. Our results showed that only at 44% VC did delta Vmax decrease in all experiments after histamine to indicate peripheral obstruction (mean: 68.5 to 45%). At 23% VC, delta Vmax increased slightly, from 22 to 28%. At 23 and 36% VC, substantial differences in the wave-speed variables between air and HeO2 were present before bronchoconstriction, so that delta Vmax was low in some dogs, although peripheral airway obstruction was not evident. When bronchoconstriction was produced, delta Vmax at 23% VC could not be decreased further and even increased in four of six dogs. Thus changes in delta Vmax at given lung volume may not reflect the predominant site of airflow obstruction during bronchoconstriction.

Influence of airway geometry on expiratory flow limitation and density dependence

1983 ◽  
Vol 52 (1) ◽  
pp. 113-123 ◽  
Author(s):  
Ronald J. Knudson ◽  
Robert C. Schroter ◽  
Dwyn E. Knudson ◽  
Stuart Sugihara
Keyword(s):  
Density Dependence ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Expiratory Flow

Mechanism of reduced maximum expiratory flow in methacholine-induced bronchoconstriction in dogs

1983 ◽  
Vol 55 (3) ◽  
pp. 897-912 ◽  
Author(s):  
S. N. Mink
Keyword(s):  
Wave Speed ◽  
Cross Sectional ◽  
Pressure Losses ◽  
Lung Capacity ◽  
Group I ◽  
Maximum Expiratory Flow ◽  
Pressure Area ◽  
Expiratory Flow ◽  
Group Ii ◽  
Viscous Pressure

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.

scholarly journals Effect of expiratory flow limitation on respiratory mechanical impedance: a model study

1996 ◽  
Vol 81 (6) ◽  
pp. 2399-2406 ◽  
Author(s):  
R. Peslin ◽  
R. Farré ◽  
M. Rotger ◽  
D. Navajas
Keyword(s):  
Respiratory System ◽  
Input Impedance ◽  
Wave Speed ◽  
Mechanical Impedance ◽  
Flow Limitation ◽  
Maximal Flow ◽  
Expiratory Flow Limitation ◽  
Rubber Tubing ◽  
Model Study ◽  
Expiratory Flow

Peslin, R., R. Farré, M. Rotger, and D. Navajas.Effect of expiratory flow limitation on respiratory mechanical impedance: a model study. J. Appl. Physiol. 81(6): 2399–2406, 1996.—Large phasic variations of respiratory mechanical impedance (Zrs) have been observed during induced expiratory flow limitation (EFL) (M. Vassiliou, R. Peslin, C. Saunier, and C. Duvivier. Eur. Respir. J. 9: 779–786, 1996). To clarify the meaning of Zrs during EFL, we have measured from 5 to 30 Hz the input impedance (Zin) of mechanical analogues of the respiratory system, including flow-limiting elements (FLE) made of easily collapsible rubber tubing. The pressures upstream (Pus) and downstream (Pds) from the FLE were controlled and systematically varied. Maximal flow (V˙max) increased linearly with Pus, was close to the value predicted from wave-speed theory, and was obtained for Pus-Pds of 4–6 hPa. The real part of Zin started increasing abruptly with flow (V˙) >85%V˙max and either further increased or suddenly decreased in the vicinity of V˙max. The imaginary part of Zin decreased markedly and suddenly above 95%V˙max. Similar variations of Zin during EFL were seen with an analogue that mimicked the changes of airway transmural pressure during breathing. After pressure andV˙ measurements upstream and downstream from the FLE were combined, the latter was analyzed in terms of a serial (Zs) and a shunt (Zp) compartment. Zs was consistent with a large resistance and inertance, and Zp with a mainly elastic element having an elastance close to that of the tube walls. We conclude that Zrs data during EFL mainly reflect the properties of the FLE.

scholarly journals Ventilation distribution and density dependence of expiratory flow in asthmatic children

1983 ◽  
Vol 54 (4) ◽  
pp. 1125-1130 ◽  
Author(s):  
D. M. Cooper ◽  
R. B. Mellins ◽  
A. L. Mansell
Keyword(s):  
Density Dependence ◽  
Dead Space ◽  
Time Constants ◽  
Asthmatic Children ◽  
Peripheral Airways ◽  
Single Breath ◽  
Maximum Expiratory Flow ◽  
Anatomical Dead Space ◽  
Expiratory Flow ◽  
Steep Slopes

Of 114 asthmatic children, 21% had abnormally steep phase III slopes from a modified single-breath oxygen (SBO2) procedure. We hypothesized that the steep slopes reflect inequality of time constants caused by obstruction of peripheral airways and tested this by using a bronchodilator to reduce overall time constants in subgroups of 10 children with steep slopes (SS) and 20 children with normal slopes (NS). Maximum expiratory flow increased by equivalent degrees (0.65–0.70 l/s) in both groups, but slope decreased significantly only in the SS group. Moreover, the single-breath mixing efficiency of inspired oxygen with resident nitrogen was normal in the NS group but significantly low in the SS group. Density dependence of maximum expiratory flow (DD) was abnormally small in the SS group [15 +/- 6% (SD) increase compared with 57 +/- 13% increase in a separate group of normal children] and was independent of the anatomical dead space. In contrast, DD was normal and varied inversely with anatomical dead space (r = 0.62, P less than 0.01) in the NS group. These results indicate that 1) steep SBO2 slopes found in asthmatic children between acute episodes reflect unequal time constants caused by obstruction of peripheral airways and 2) part of the variation in DD among asthmatic children is caused by variation in convective accelerative pressure losses in major airways.

Density dependence of maximum expiratory flow in the dog

1982 ◽  
Vol 53 (2) ◽  
pp. 397-404 ◽  
Author(s):  
O. F. Pedersen ◽  
R. G. Castile ◽  
J. M. Drazen ◽  
R. H. Ingram
Keyword(s):  
Density Dependence ◽  
Maximum Flow ◽  
Transmural Pressure ◽  
Expiratory Flow Limitation ◽  
Frictional Loss ◽  
Frictional Losses ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow ◽  
Dependent Flow ◽  
Density Dependent Flow

Airway lateral and impaction pressures were measured during expiratory flow limitation in six anesthetized, vagotomized, tracheally intubated, open-chest dogs with the lungs filled with air or a mixture of 80% helium-20% oxygen (HeO2). Pressures were measured in the vicinity of equal pressure points (EPP) and choke points (CP). Maximum flow (Vmax) was ensured by demonstrating no increase in flow with a 50% increase of driving pressure. At 50% vital capacity, mean density dependence (VmaxHeO2/Vmaxair) was 1.58, which was less than 1.69 predicted for fully density-dependent flow. Transmural pressure and airway area at CP and EPP (located on air) were significantly less with HeO2 than with air. Frictional losses between the alveoli and CP were 40% greater with HeO2 than with air. These enhanced losses were mostly peripheral to the EPP. Frictional loss upstream from the EPP was 47% of the total pressure loss on air and increased to 70% on HeO2. The data at 50% VC suggest that these higher frictional losses with HeO2 resulted in decreased density dependence of Vmax due to different pressure distribution along the airway with a lower transmural pressure and smaller area at the CP.

Insensitivity of maximum expiratory flow to bronchodilation in normal dogs

1990 ◽  
Vol 68 (5) ◽  
pp. 2006-2012 ◽  
Author(s):  
J. Eng ◽  
A. Gomez ◽  
S. Mink
Keyword(s):  
Wave Speed ◽  
Vital Capacity ◽  
Lower Lobe ◽  
Pressure Head ◽  
Complex Interaction ◽  
Base Line ◽  
Flow Limitation ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow ◽  
The Right

We examined the effects of the inhaled parasympatholytic agent atropine and the sympathomimetic agent salbutamol on partitioned frictional pressure (Pfr) losses to the site of flow limitation (choke point, CP) in dogs to see how changes brought about by these agents would affect maximum expiratory flow (Vmax) and response to breathing 80% He-20% O2 (delta Vmax) in terms of wave-speed theory of flow limitation. In open-chest dogs, a Pitot-static tube was advanced down the right lower lobe to locate CP, to determine CP lateral and end-on pressures (PE), and to partition the airway into peripheral (alveoli to sublobar) and central (sublobar to CP) segments. Measurements were obtained at approximately 50% vital capacity. After inhalation, CP locations were unchanged with both bronchodilating agents. After atropine inhalation, Pfr central was decreased by one-half compared with base line. Despite the decrease in Pfr central, however, Vmax failed to increase after atropine because of altered bronchial area pressure (BAP) behavior at the CP site. After salbutamol inhalation, Pfr peripheral was reduced by about one-half compared with base line. However, Vmax failed to increase, because this reduction was too small to significantly increase the CP pressure head (i.e., PE). delta Vmax was also insensitive to these agents. Our results show mechanisms by which small changes in Pfr, as well as the complex interaction of changes in Pfr and BAP, may limit the use of Vmax in detecting bronchodilation at different airway sites.

Expiratory flow limitation

1983 ◽  
Vol 55 (1) ◽  
pp. 1-7 ◽  
Author(s):  
R. E. Hyatt
Keyword(s):  
Wave Speed ◽  
Signal To Noise Ratio ◽  
Major Advance ◽  
Flow Limitation ◽  
Flow Volume ◽  
Expiratory Flow Limitation ◽  
Flow Curves ◽  
Maximal Expiratory Flow ◽  
Airway Mechanics ◽  
Expiratory Flow

The first major advance in understanding expiratory flow limitation of the lungs came with the description of isovolume pressure-flow curves. These curves documented the existence of a volume-dependent limit to maximal expiratory flow and led directly to the description of the maximal expiratory flow-volume (MEFV) curve. Definitive modeling of flow limitation awaited the description of a localized mechanism that dominated the flow-limiting process. The phenomenon of wave speed limitation of flow was shown to apply to the airways and provided the needed localized mechanism. Using this concept and recent data on airway mechanics and the frictional losses in the flow, a computational model of the MEFV curve has been developed. Further progress will require modeling of inhomogeneous emptying in diseased lungs, perfecting noninvasive techniques of estimating pertinent airway characteristics, and improving techniques for increasing the signal-to-noise ratio in MEFV curves.

Modeling expiratory flow from excised tracheal tube laws

1999 ◽  
Vol 87 (5) ◽  
pp. 1973-1980 ◽  
Author(s):  
Nikolai Aljuri ◽  
Lutz Freitag ◽  
José G. Venegas
Keyword(s):  
Static Pressure ◽  
Pressure Recovery ◽  
High Frequency Ventilation ◽  
Flow Limitation ◽  
Flow Conditions ◽  
Expiratory Flow Limitation ◽  
Elastic Tubes ◽  
Viscous Losses ◽  
Forced Expiratory Flow ◽  
Expiratory Flow

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.

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