Expiratory flow limitation and dynamic pulmonary hyperinflation during high-frequency ventilation

1986 ◽  
Vol 60 (6) ◽  
pp. 2071-2078 ◽  
Author(s):  
J. Solway ◽  
T. H. Rossing ◽  
A. F. Saari ◽  
J. M. Drazen
Keyword(s):  
High Frequency ◽  
Progressive Increase ◽  
High Frequency Ventilation ◽  
Dynamic Hyperinflation ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Pulmonary Hyperinflation ◽  
Residual Capacity ◽  
Frequency Ventilation ◽  
Expiratory Flow

Dynamic hyperinflation of the lungs occurs during high-frequency oscillatory ventilation (HFOV) and has been attributed to asymmetry of inspiratory and expiratory impedances. To identify the nature of this asymmetry, we compared changes in lung volume (VL) observed during HFOV in ventilator-dependent patients with predictions of VL changes from electrical analogs of three potential modes of impedance asymmetry. In the patients, when a fixed oscillatory tidal volume was applied at a low mean airway opening pressure (Pao), which resulted in little increase in functional residual capacity, progressively greater dynamic hyperinflation was observed as HFOV frequency, (f) was increased. When mean Pao was raised so that resting VL increased, VL remained at this level during HFOV as f was increased until a critical f was reached; above this value, VL increased further with f in a fashion nearly parallel to that observed when low mean Pao was used. Three modes of asymmetric inspiratory and expiratory impedance were modeled as electrical circuits: 1) fixed asymmetric resistance [Rexp greater than Rinsp]; 2) variable asymmetric resistance [Rexp(VL) greater than Rinsp, with Rexp(VL) decreasing as VL increased]; and 3) equal Rinsp and Rexp, but with superimposed expiratory flow limitation, the latter simulated using a bipolar transistor as a descriptive model of this phenomenon. The fixed and the variable asymmetric resistance models displayed a progressive increase of mean VL with f at either low or high mean Pao. Only the expiratory flow limitation model displayed a dependence of dynamic hyperinflation on mean Pao and f similar to that observed in our patients. We conclude that expiratory flow limitation can account for dynamic pulmonary hyperinflation during HFOV.

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.

scholarly journals Expiratory Flow Limitation Definition, Mechanisms, Methods, and Significance

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Claudio Tantucci
Keyword(s):  
Work Of Breathing ◽  
Chronic Obstructive ◽  
Dynamic Hyperinflation ◽  
Flow Limitation ◽  
Negative Consequences ◽  
Expiratory Flow Limitation ◽  
Obstructive Pulmonary Disease ◽  
Inspiratory Muscles ◽  
Copd Patients ◽  
Expiratory Flow

When expiratory flow is maximal during tidal breathing and cannot be increased unless operative lung volumes move towards total lung capacity, tidal expiratory flow limitation (EFL) is said to occur. EFL represents a severe mechanical constraint caused by different mechanisms and observed in different conditions, but it is more relevant in terms of prevalence and negative consequences in obstructive lung diseases and particularly in chronic obstructive pulmonary disease (COPD). Although in COPD patients EFL more commonly develops during exercise, in more advanced disorder it can be present at rest, before in supine position, and then in seated-sitting position. In any circumstances EFL predisposes to pulmonary dynamic hyperinflation and its unfavorable effects such as increased elastic work of breathing, inspiratory muscles dysfunction, and progressive neuroventilatory dissociation, leading to reduced exercise tolerance, marked breathlessness during effort, and severe chronic dyspnea.

Dynamic pulmonary hyperinflation occurs without expiratory flow limitation in chronic heart failure during exercise

2013 ◽  
Vol 189 (1) ◽  
pp. 34-41 ◽  
Author(s):  
Stefania Chiari ◽  
Chiara Torregiani ◽  
Enrico Boni ◽  
Sonia Bassini ◽  
Enrico Vizzardi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Pulmonary Hyperinflation ◽  
Expiratory Flow

Relationship for gas transport during high-frequency ventilation in dogs

1985 ◽  
Vol 59 (5) ◽  
pp. 1539-1547 ◽  
Author(s):  
J. G. Venegas ◽  
J. Custer ◽  
R. D. Kamm ◽  
C. A. Hales
Keyword(s):  
Body Weight ◽  
Functional Residual Capacity ◽  
Lung Volume ◽  
High Frequency ◽  
Alveolar Ventilation ◽  
High Frequency Ventilation ◽  
Arterial Pco2 ◽  
Expiration Time ◽  
Residual Capacity ◽  
Frequency Ventilation

Alveolar ventilation during high-frequency ventilation (HFV) was estimated from the washout of the positron-emitting isotope (nitrogen-13-labeled N2) from the lungs of anesthetized paralyzed supine dogs by use of a positron camera. HFV was delivered at a mean lung volume (VL) equal to the resting functional residual capacity with a ventilator that generated tidal volumes (VT) between 30 and 120 ml, independent of the animal's lung impedance, at frequencies (f) from 2 to 25 Hz, with constant inspiratory and expiratory flows and an inspiration-to-expiration time ratio of unity. Specific ventilation (SPV), which is equivalent to ventilation per unit of compartment volume, was found to follow closely the relation: SPV = 1.9(VT/VL)2.1 X f. From this relation and from arterial PCO2 measurements we found an expression for the normocapnic settings of VT and f, given VL and body weight (W). We found that the VL was an important normalizing parameter in the sense that VT/VL yielded a better correlation (r = 0.91) with SPV/f than VT/W (r = 0.62) or VT alone (r = 0.8).

Expiratory Flow Limitation, Dynamic Hyperinflation, and Inspiratory Muscle Fatigue during Exercise in Asthmatic Subjects

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S342
Author(s):  
Louise A. Turner ◽  
Sandra Tecklenburg ◽  
Timothy D. Mickleborough ◽  
Alison McConnell ◽  
Joel M. Stager ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Inspiratory Muscle ◽  
Dynamic Hyperinflation ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Expiratory Flow ◽  
Inspiratory Muscle Fatigue

High-frequency ventilation-induced apnea: interaction of frequency, volume, FRC, and CO2

1989 ◽  
Vol 66 (5) ◽  
pp. 2462-2467 ◽  
Author(s):  
P. W. Davenport ◽  
D. J. Dalziel
Keyword(s):  
High Frequency ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
High Frequency Ventilation ◽  
Emg Activity ◽  
Bipolar Electrodes ◽  
Residual Capacity ◽  
Frequency Ventilation ◽  
Anesthetized Dogs ◽  
End Tidal

Apnea is often observed during high-frequency oscillatory ventilation (HFOV). This study on anesthetized dogs varied the oscillator frequency (f) and determined the stroke volume (SV) at which apnea occurred. Relaxation functional residual capacity (FRC) and the eupneic breathing end-tidal CO2 level were held constant. Airway pressure and CO2 were measured from a side port of the tracheostomy cannula. An arterial cannula was inserted for blood gas analysis. Diaphragm electromyogram (EMG) was recorded with bipolar electrodes. Apnea was defined as the absence of phasic diaphragm EMG activity for a minimum of 60 s. During HFOV, SV was increased at each f (5–40 Hz) until apnea occurred. The apnea inducing SV decreased as f increased. SV was minimal at 25–30 Hz. Frequencies greater than 30 Hz required increased SV to produce apnea. The f-SV curve was defined as the apneic threshold. Increased FRC resulted in a downward shift (less SV at the same f) in the apneic threshold. Elevated CO2 caused an upward shift (more SV at the same f) in the apneic threshold. These results demonstrate that the apnea elicited by HFOV is dependent on the interaction of oscillator f and SV, the FRC, and CO2.

Mean airway pressure and alveolar pressure during high-frequency ventilation

1984 ◽  
Vol 57 (4) ◽  
pp. 1069-1078 ◽  
Author(s):  
B. A. Simon ◽  
G. G. Weinmann ◽  
W. Mitzner
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
High Frequency ◽  
Airway Pressure ◽  
High Frequency Ventilation ◽  
Alveolar Pressure ◽  
Mean Flow ◽  
Mean Airway Pressure ◽  
Expiratory Flow Limitation ◽  
Frequency Ventilation

Studies and applications of high-frequency ventilation (HFV) are often performed under conditions of controlled mean airway pressure (Paw). In the present study we tested the assumption that controlling Paw adequately controls lung volume during HFV by investigating the relationship between a reliably measured Paw and the mean alveolar pressure (Palv) of the lungs during HFV of healthy dogs. We minimized the errors of Paw measurement due to the Bernoulli effect and various technical factors by appropriate choice of transducers, amplifiers, and measurement site. Palv was estimated by clamping the ventilator tube during oscillation and measuring the equilibration pressure of the lung and airways. Paw and Palv were determined as functions of frequency (8–25 Hz), tidal volume (60–90 ml), Paw (-5 to 12 cmH2O), and position of the animal (supine vs. lateral). We found that Paw could significantly underestimate Palv and that the degree of underestimation increased at higher frequencies, larger tidal volumes, and lower Paw. Shifting the animal from the supine to the lateral position greatly accentuated this effect. The elevation of Palv above Paw was seen to be a function of mean flow and largely independent of the frequency-tidal volume combination which produced the flow. A possible explanation of this pressure difference is that it results from differences in inspiratory and expiratory airway impedances, which in turn depend on airway geometry, compliance, lung volume, and expiratory flow limitation.

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