Flow limitation in a collapsible tube.

1972 ◽  
Vol 33 (1) ◽  
pp. 150-153 ◽  
Author(s):  
R K Lambert ◽  
T A Wilson
2004 ◽  
Vol 106 (6) ◽  
pp. 589-598 ◽  
Author(s):  
Konrad E. BLOCH ◽  
Erich W. RUSSI ◽  
Vladimir KAPLAN

In the present study, our aim was to investigate whether the variability of conductance over the course of inspiration reflects flow limitation. Pressure/flow conditions in the upper airway were modelled by a collapsible tube within a rigid chamber and a pump simulating respiration. Instantaneous conductance was estimated every 20 ms as flow/resistive pressure, and its variability during inspiration expressed as the 90th/50th percentile ratio. Accuracy of this ratio to quantify flow limitation was evaluated by observing whether it changed predictably with adjustments of model parameters. To illustrate the potential of this ratio to quantify flow limitation in a clinical setting, we recorded pneumotachographic airflow and oesophageal pressure in 11 patients with obstructive sleep apnoea during nasal continuous positive airway pressure (CPAP) ventilation, and observed changes in the 90th/50th percentile ratio of inspiratory lung conductance induced by mask pressure titration. Rising pressure surrounding the collapsible tube from subatmospheric to positive values induced progressive inspiratory collapse and increased 90th/50th percentile ratios of inspiratory conductance as predicted. Changes in flow limitation induced by other model modifications were also correctly tracked by the 90th/50th conductance percentile ratio. Increasing mask pressure during CPAP ventilation in sleep apnoea patients from subtherapeutic to therapeutic pressure levels was associated with the expected decrease in the 90th/50th percentile ratio of inspiratory lung conductance from a mean of 6.5±3.1 to 1.6±0.3 (P<0.001). We conclude that variability of inspiratory conductance quantified by the 90th/50th percentile ratio may serve as a measure of flow limitation that is independent of the absolute value of conductance.


1987 ◽  
Vol 174 ◽  
pp. 467-493 ◽  
Author(s):  
J. W. Reyn

Equations for the steady flow of an incompressible, inviscid fluid through a collapsible tube under longitudinal tension are derived by treating the tube longitudinally as a membrane, and taking the collapsibility of the tube into account in an approximate way by replacing in the equation for an axisymmetric membrane a term representing the resistance of the tube to area change by the tube law for collapsible tubes. The flow is assumed to be uniform in a cross-section. A nonlinear differential equation is obtained for the shape of the tube for given values of total pressure p0, flow rate q, longitudinal tension τ and tube law P = P(ρ); where ρ = (A/πR2)½ is the equivalent radius of the tube (A = area of a cross-section, R = radius of the unloaded, then circular tube). The equation can be integrated and analysed in the phase plane. Equilibrium points correspond to uniform flow through cylindrical tubes; saddle points correspond to subcritical flow (S < 1), centrepoints to supercritical (S > 1) and a higher-order point to critical flow (S = 1). Here S is the speed index, the ratio of the flow speed to the speed of long waves. Near centrepoints there are solutions, that represent area-periodic tubes. For a finite tube, held open at the ends, the steady flow is formulated as a two-point boundary-value problem. On the basis of numerical calculations, and a bifurcation analysis using the method of Lyapunov–Schmidt, the existence and multiplicity of the solutions of this problem are discussed and the process of flow limitation studied. For negative total pressures two collapsed solutions are found that disappear at the flow-limitation value of the flow rate. For positive total pressures a distinction is made between subcritical, critical and supercritical total pressures. In all these cases there is a multiplicity, proportional to the ratio of the tube length to [Lscr ]1(0), the wavelength of the collapsed periodic solution for vanishing flow rate, and having maximum radius ρ = 1. For subcritical total pressures increase of the flow rate leads to a gradual loss of all solutions in higher-order flow limitations until final flow limitation occurs by the mergence of two collapsed solutions. For supercritical total pressures increase of the flow rate also leads to a gradual loss of all solutions in higher-order flow limitations in a process which now also depends upon the ratio of the tube length to the wavelength L of periodic solutions with vanishing amplitude and ρ ≡ 1.


2018 ◽  
Vol 125 (2) ◽  
pp. 605-614 ◽  
Author(s):  
Kaixian Zhu ◽  
Ramon Farré ◽  
Ira Katz ◽  
Sébastien Hardy ◽  
Pierre Escourrou

The upper airway (UA) in humans is commonly modeled as a Starling resistor. However, negative effort dependence (NED) observed in some patients with obstructive sleep apnea (OSA) contradicts predictions based on the Starling resistor model in which inspiratory flow is independent of inspiratory driving pressure when flow is limited. In a respiratory bench model consisting of a collapsible tube and an active lung model (ASL5000), inspiratory flow characteristics were investigated in relation to upstream, downstream, and extra-luminal pressures (denoted as Pus, Pds, and Pout, respectively) by varying inspiratory effort (muscle pressure) from −1 to −20 cmH2O in the active lung. Pus was provided by a constant airway pressure device and varied from 4 to 20 cmH2O, and Pout was set at 10 and 15 cmH2O. Upstream resistance at onset of flow limitation and critical transmural pressure (Ptm) corresponding to opening of the UA were found to be independent of Pus, Pds, and Pout. With fixed Ptm, when Pds fell below a specific value (Pds′), inspiratory peak flow became constant and independent of Pds. NED plateau flow patterns at mid-inspiration (V̇n) were produced within the current bench setting when Pds fell below Pds′. V̇n was proportional to Pds, and the slope (ΔV̇n/ΔPds) increased linearly with Ptm. Ptm and Pds were the two final independent determinants of inspiratory flow. Our bench model closely mimics a flow-limited human UA, and the findings have implications for OSA treatment and research, especially for bench-testing auto-titrating devices in a more physiological way. NEW & NOTEWORTHY A respiratory model consisting of a collapsible tube was used to mimic a flow-limited human upper airway. Flow-limited breathing patterns including negative effort dependence were produced. Transmural and downstream pressures acting on the tube are the two independent determinants of the resulting inspiratory flow during flow limitation. The findings have implications for obstructive sleep apnea treatment and research, especially for bench-testing auto-titrating devices in a more physiological way.


Thorax ◽  
2001 ◽  
Vol 56 (9) ◽  
pp. 713-720
Author(s):  
J Hadcroft ◽  
P M A Calverley

BACKGROUNDBronchodilator reversibility testing is recommended in all patients with chronic obstructive pulmonary disease (COPD) but does not predict improvements in breathlessness or exercise performance. Two alternative ways of assessing lung mechanics—measurement of end expiratory lung volume (EELV) using the inspiratory capacity manoeuvre and application of negative expiratory pressure (NEP) during tidal breathing to detect tidal airflow limitation—do relate to the degree of breathlessness in COPD. Their usefulness as end points in bronchodilator reversibility testing has not been examined.METHODSWe studied 20 patients with clinically stable COPD (mean age 69.9 (1.5) years, 15 men, forced expiratory volume in one second (FEV1) 29.5 (1.6)% predicted) with tidal flow limitation as assessed by their maximum flow-volume loop. Spirometric parameters, slow vital capacity (SVC), inspiratory capacity (IC), and NEP were measured seated, before and after nebulised saline, and at intervals after 5 mg nebulised salbutamol and 500 μg nebulised ipratropium bromide. The patients attended twice and the treatment order was randomised.RESULTSMean FEV1, FVC, SVC, and IC were unchanged after saline but the degree of tidal flow limitation varied. FEV1 improved significantly after salbutamol and ipratropium (0.11 (0.02) l and 0.09 (0.02) l, respectively) as did the other lung volumes with further significant increases after the combination. Tidal volume and mean expiratory flow increased significantly after all bronchodilators but breathlessness fell significantly only after the combination treatment. The initial NEP score was unrelated to subsequent changes in lung volume.CONCLUSIONSNEP is not an appropriate measurement of acute bronchodilator responsiveness. Changes in IC were significantly larger than those in FEV1and may be more easily detected. However, our data showed no evidence for separation of “reversible” and “irreversible” groups whatever outcome measure was adopted.


2019 ◽  
Vol 48 (10) ◽  
pp. 402-406
Author(s):  
Matthias Leschke

ZUSAMMENFASSUNGDie Diagnose einer koronaren Herzkrankheit (KHK) bei Patienten mit COPD (chronisch obstruktive Lungenerkrankung) wird häufig verspätet gestellt, da Symptome wie Dyspnoe, thorakale Schmerzen und Palpitationen sowie Herzrhythmusstörungen auf die zugrunde liegende COPD bezogen werden. Nach verschiedenen Studien ist die COPD durch ein bis zu 3-fach erhöhtes Mortalitätsrisiko gegenüber Nicht-COPD-Patienten belastet. Nach einer aktuellen Studie sind 69 % der COPD-Patienten kardiovaskulär erkrankt. So fand sich eine um 2,33 höhere Wahrscheinlichkeit einer stationären Aufnahme wegen einer kardiovaskulären Genese gegenüber Nicht-COPD-Patienten. Wesentlich dürfte dafür eine systemische Inflammation sein, die in Beziehung mit dem Ausmaß der bronchialen Obstruktion und der Air-Flow-Limitation steht und sich laborchemisch durch einen Anstieg des hochsensitiven CRP (C-reaktives Protein), aber auch der Fibrinogenkonzentration insbesondere bei akuten Exazerbationen zeigt. COPD-Patienten haben signifikant erhöhte Troponinkonzentrationen infolge eines Typ-2-Myokardinfarktes aufgrund von Hypoxie und Tachykardie, einer damit sekundären stressbedingten Myokardischämie. Demnach müssen COPD-Patienten sorgfältig bezüglich kardiovaskulärer Risikofaktoren untersucht und kardiale Komorbiditäten diagnostiziert werden.


Respiration ◽  
2007 ◽  
Vol 75 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Katrien B. Hertegonne ◽  
Bart Rombaut ◽  
Philippe Houtmeyers ◽  
Georges Van Maele ◽  
Dirk A. Pevernagie

2001 ◽  
Vol 163 (2) ◽  
pp. 494-497 ◽  
Author(s):  
RAMON FARRÉ ◽  
JORDI RIGAU ◽  
JOSEP M. MONTSERRAT ◽  
EUGENI BALLESTER ◽  
DANIEL NAVAJAS
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