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.

Wave-speed-determined flow limitation at peak flow in normal and asthmatic subjects

1997 ◽  
Vol 83 (5) ◽  
pp. 1721-1732 ◽  
Author(s):  
O. F. Pedersen ◽  
H. J. L. Brackel ◽  
J. M. Bogaard ◽  
K. F. Kerrebijn
Keyword(s):  
Wave Speed ◽  
Peak Flow ◽  
Lower Lobe ◽  
Flow Limitation ◽  
Alveolar Pressure ◽  
Cross Sectional ◽  
Peripheral Airways ◽  
Speed Flow ◽  
Esophageal Balloon ◽  
The Right

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.

Maximum expiratory flow and transpulmonary pressure in the hamster

1978 ◽  
Vol 45 (6) ◽  
pp. 840-845 ◽  
Author(s):  
E. C. Lucey ◽  
B. R. Celli ◽  
G. L. Snider
Keyword(s):  
Vital Capacity ◽  
Simple Technique ◽  
Transpulmonary Pressure ◽  
Esophageal Pressure ◽  
Flow Limitation ◽  
Flow Volume ◽  
System Pressure ◽  
Pleural Surface ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

Maximum expiratory flow was measured in 19 normal, anesthetized, tracheostomized, supine hamsters from records of forced deflation produced by the application of varying degrees of negative pressure to the tracheostomies of animals whose lungs had been previously inflated to a transpulmonary pressure (PL) of 25 cmH2O. Flow was measured with a pneumotachograph, volume with a constant-volume pressure plethysmograph and pleural surface pressure (Ppl) with a water-filled esophageal catheter. The esophageal pressure measurement overestimated Ppl and a simple technique was based on an estimate of the resting volume of the chest wall. This volume, at which the Ppl is zero, was calculated for anesthetized supine hamsters from the measurement of respiratory-system pressure and PL made independently of esophageal pressure and was found to be about 30% of vital capacity (VC). Flow limitation was present below 70% of VC with a tracheal deflation pressure of -30cmH2O. Negative effort dependence of flow was seen in small segments of the flow-volume curves. Mean +/- SD maximum expiratory flow at 50% VC was 52 +/- 9.5 ml/s or 9.1 VC/s. Upstream resistance was 0.09 +/- 0.03 cmH2O/ml per s.

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.

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.

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
Keyword(s):  
Wave Speed ◽  
Mathematical Representation ◽  
Forced Expiration ◽  
Flow Limitation ◽  
Time Dependency ◽  
Cross Sectional ◽  
Elastic Tubes ◽  
Forced Expiratory Flow ◽  
Expiratory Flow ◽  
The Relationship

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.

Mechanism of reduced maximum expiratory flow in dogs with compensatory lung growth

1986 ◽  
Vol 60 (2) ◽  
pp. 441-448 ◽  
Author(s):  
H. W. Greville ◽  
M. E. Arnup ◽  
S. N. Mink ◽  
L. Oppenheimer ◽  
N. R. Anthonisen
Keyword(s):  
Control Flow ◽  
Sham Operation ◽  
Forced Expiration ◽  
Flow Limitation ◽  
Lung Growth ◽  
Lung Volumes ◽  
Flow Rates ◽  
Compensatory Lung Growth ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

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.

Variability of the configuration of maximum expiratory flow-volume curves

1979 ◽  
Vol 46 (3) ◽  
pp. 565-570 ◽  
Author(s):  
Y. K. Tien ◽  
E. A. Elliott ◽  
J. Mead
Keyword(s):  
Normal Subjects ◽  
Flow Limitation ◽  
Residual Volume ◽  
Flow Volume ◽  
Maximum Difference ◽  
Slope Ratio ◽  
Computer Technique ◽  
Volume Increment ◽  
Maximum Expiratory Flow ◽  
Expiratory Flow

With a computer technique variability of the configuration of maximum expiratory flow-volume (MEFV) curves was studied in terms of slope ratio, SR. SR = dV/dV divided by V/V, where V is the instantaneous flow and V is the volume increment above residual volume.) Approximately four SR-V curves, each based on three to five smoothed and averaged MEFV curves, were derived for each of 20 normal subjects (aged 23–55 yr) on a single occasion, and again at least 1 wk later. Individual curves were largely reproducible, the maximum difference in SR at most volumes being 0.3–1 U, but frequently showed substantial yet reproducible fluctuations with volume. These corresponeded to hitherto unrecognized irregularities of maximum expiratory flow that may reflect sudden changes in the location of flow limitation.

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.

Expiratory flow limitation and intrinsic positive end-expiratory pressure in obesity

1998 ◽  
Vol 85 (4) ◽  
pp. 1236-1243 ◽  
Author(s):  
W. Pankow ◽  
T. Podszus ◽  
T. Gutheil ◽  
T. Penzel ◽  
J.-H. Peter ◽  
...  
Keyword(s):  
Supine Position ◽  
Lateral Position ◽  
Normal Weight ◽  
Upright Position ◽  
Flow Limitation ◽  
Positive End Expiratory Pressure ◽  
Expiratory Flow Limitation ◽  
Transdiaphragmatic Pressure ◽  
Expiratory Flow ◽  
The Right

Breathing at very low lung volumes might be affected by decreased expiratory airflow and air trapping. Our purpose was to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure (PEEPi) in grossly obese subjects (OS). Eight OS with a mean body mass index (BMI) of 44 ± 5 kg/m2 and six age-matched normal-weight control subjects (CS) were studied in different body positions. Negative expiratory pressure (NEP) was used to determine EFL. In contrast to CS, EFL was found in two of eight OS in the upright position and in seven of eight OS in the supine position. Dynamic PEEPi and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS. In OS, PEEPi increased from 0.14 ± 0.06 (SD) kPa in the upright position to 0.41 ± 0.11 kPa in the supine position ( P < 0.05) and decreased to 0.20 ± 0.08 kPa in the right lateral position ( P < 0.05, compared with supine), whereas, in CS, PEEPi was significantly smaller (<0.05 kPa) in each position. In OS, mean Pdi in each position was significantly larger compared with CS. Mean Pdi increased from 1.02 ± 0.32 kPa in the upright position to 1.26 ± 0.17 kPa in the supine position (not significant) and decreased to 1.06 ± 0.26 kPa in the right lateral position ( P < 0.05, compared with supine), whereas there were no significant changes in CS. We conclude that in OS 1) tidal breathing can be affected by EFL and PEEPi; 2) EFL and PEEPi are promoted by the supine posture; and 3) the increased diaphragmatic load in the supine position is, in part, related to PEEPi.

Expiratory flow limitation in dogs with regional changes in lung mechanical properties

1988 ◽  
Vol 64 (1) ◽  
pp. 162-173 ◽  
Author(s):  
S. N. Mink ◽  
H. Greville ◽  
A. Gomez ◽  
J. Eng
Keyword(s):  
Mechanical Properties ◽  
Wave Speed ◽  
Main Stem ◽  
Left Main ◽  
Main Stem Bronchus ◽  
Left Main Stem ◽  
In Series ◽  
Left Main Stem Bronchus ◽  
Expiratory Flow ◽  
The Right

We examined maximum expiratory flow (Vmax) in two canine preparations in which regional changes in lung mechanical properties were produced. In one experiment serial bronchial obstructions were made to determine whether flow-limiting sites (choke points, CP) would occur in series. With the right lung tied off, constrictions were placed at the left lower lobar bronchus (LLL) and left main-stem bronchus. On deflation from total lung capacity, the obstructed LLL and nonobstructed left upper lobe (LUL) emptied into the obstructed left main-stem bronchus. Although a CP common to both lobes was identified at the main-stem obstruction, which limited total Vmax, we questioned whether there was also a CP at the lobar obstruction that fixed LLL flow. In that case the rate of LLL emptying would not be dependent on the presence of the common (i.e., central) CP and thus the flow contribution of the LUL. We found that when the LUL was removed, the LLL increased its rate of emptying. Thus a lobar CP did not fix LLL flow and CP did not occur in series. In a second experiment emphysema was produced in the left lung to reduce lung recoil, whereas the right lung was normal. CP were identified at approximately lobar bronchi of each lung, and the lungs were emptied at different rates. A CP common to both lungs was not identified. Our results indicate that in localized lung disease, if flows from the different regions are high enough, then wave speed is reached in proximal airways, and a CP occurs centrally rather than peripherally. On the other hand, if flows are low, then wave speed is reached peripherally and a CP common to all lung regions does not occur.

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