Influence of panting frequency on plethysmographic measurements of thoracic gas volume

1982 ◽  
Vol 52 (3) ◽  
pp. 739-747 ◽  
Author(s):  
A. B. Bohadana ◽  
R. Peslin ◽  
B. Hannhart ◽  
D. Teculescu

Using an integrated flow pressure-corrected body plethysmograph we obtained total lung capacities (TLC) derived from thoracic gas volumes measured at low, medium, and high panting frequencies in 10 healthy men and in 13 patients with chronic airflow obstruction before and after an aerosol of albuterol. Using a gastric balloon we also assessed gastric-to-mouth pressure ratios (delta Pga/delta Pm). In patients before albuterol, estimated TLC remained unchanged from low to medium and increased (not significantly) from medium to high frequency. Healthy subjects and patients after albuterol showed a significant decrease in TLC from low to medium panting frequencies, which persisted after correcting the data for abdominal gas compression using observed delta Pga/delta Pm. In patients after albuterol the results may be explained, at least in part, by intrathoracic airway compliance and mechanical inhomogeneity of the lung. In healthy subjects a remote possibility is the association of mechanical inhomogeneity and nonuniform pleural pressure.

1984 ◽  
Vol 57 (6) ◽  
pp. 1865-1871 ◽  
Author(s):  
R. Brown ◽  
A. S. Slutsky

With airways obstruction, panting frequency affects plethysmographically determined thoracic gas volume (Vtg) because the extrathoracic airway acts as a shunt capacitor. Stanescu et al. (19) suggested that in the calculation of Vtg, use of esophageal (delta Pes) rather than mouth pressure (delta Pm) swings might eliminate the problem. We measured total lung capacity (TLC) plethysmographically in 10 subjects with chronic airways obstruction (CAO) and in four normal subjects. TLC (using delta Pm) was derived from Vtg obtained from slow-(approximately 1 Hz) and fast- (approximately 4 Hz) panting frequencies. In the normal subjects and four subjects with CAO, TLC was also obtained using delta Pes. In these subjects abdominal gas compression and decompression did not contribute significantly to the frequency dependence of TLC. In CAO, TLC was frequency dependent in direct proportion to the severity of obstruction. Although the frequency dependence was greater using delta Pm to calculate Vtg, it also occurred using delta Pes. Thus it could not be explained entirely by the shunt capacitor effect of the extrathoracic airways. The residual and significant overestimations of TLC (reflected by frequency dependency of TLC derived from Vtg calculated from delta Pes) may be explained by interregional nonhomogeneities during the panting maneuver.


1985 ◽  
Vol 58 (6) ◽  
pp. 1783-1787 ◽  
Author(s):  
L. J. Folinsbee ◽  
J. F. Bedi ◽  
S. M. Horvath

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25–75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25–75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.


1995 ◽  
Vol 78 (3) ◽  
pp. 938-947 ◽  
Author(s):  
M. Rotger ◽  
R. Farre ◽  
R. Peslin ◽  
D. Navajas

The aim of this work was to demonstrate that the three compartments of the lung T network and the chest wall impedance (Zcw) can be identified from input and transfer impedances of the respiratory system if the pleural pressure is recorded during the measurements. The method was tested in six healthy volunteers in the range of 8–32 Hz. The impedances resulting from the decomposition confirm the adequacy of the monoalveolar structure commonly used in healthy subjects. Indeed, the T shunt impedance is well modeled by a purely compliant element, the mean compliance [0.038 +/- 0.081 (SD) l/kPa], which coincides within 9.5 +/- 6.3% of the alveolar gas compressibility derived from thoracic gas volume (0.036 +/- 0.011 l/kPa). The results obtained provide experimental evidence that the alveolar gas compression is predominantly isothermal and that lung tissue impedance is negligible throughout the whole frequency range. The shape of Zcw is consistent with a low compliance-low inertance pathway in parallel with a high compliance-high inertance pathway. We conclude that the proposed method is able to reliably identify the T network featuring the lung and Zcw.


1998 ◽  
Vol 84 (2) ◽  
pp. 553-561 ◽  
Author(s):  
R. Peslin ◽  
C. Duvivier

Peslin, R., and C. Duvivier. Partitioning of airway and respiratory tissue mechanical impedances by body plethysmography. J. Appl. Physiol. 84(2): 553–561, 1998.—We have tested the feasibility of separating the airway (Zaw) and tissue (Zti) components of total respiratory input impedance (Zrs,in) in healthy subjects by measuring alveolar gas compression by body plethysmography (Vpl) during pressure oscillations at the airway opening. The forced oscillation setup was placed inside a body plethysmograph, and the subjects rebreathedbtps gas. Zrs,in and the relationship between Vpl and airway flow (Hpl) were measured from 4 to 29 Hz. Zaw and Zti were computed from Zrs,in and Hpl by using the monoalveolar T-network model and alveolar gas compliance derived from thoracic gas volume. The data were in good agreement with previous observations: airway and tissue resistance exhibited some positive and negative frequency dependences, respectively; airway reactance was consistent with an inertance of 0.015 ± 0.003 hPa ⋅ s2 ⋅ l−1and tissue reactance with an elastance of 36 ± 8 hPa/l. The changes seen with varying lung volume, during elastic loading of the chest and during bronchoconstriction, were mostly in agreement with the expected effects. The data, as well as computer simulation, suggest that the partitioning is unaffected by mechanical inhomogeneity and only moderately affected by airway wall shunting.


1982 ◽  
Vol 52 (3) ◽  
pp. 798-801 ◽  
Author(s):  
A. Harf ◽  
H. Lorino ◽  
G. Atlan ◽  
A. M. Lorino ◽  
D. Laurent

To improve the computer determination of thoracic gas volume (TGV), two new approaches were worked out. 1) A new program was designed, which overcomes the difficulties encountered in the time recognition of the panting maneuver and rules out the artifacts. Such a procedure is based on the data analysis in the pressure-volume time derivatives plane. 2) A hyperbolic fitting of the signals recorded during the panting maneuver was introduced. This last procedure, lying on Boyle's law, has proved to be useful in case of large mouth pressure changes. In fact the error induced by the conventional linear fitting may reach 500 ml (9% of the TGV value).


1980 ◽  
Vol 48 (5) ◽  
pp. 911-916 ◽  
Author(s):  
H. Lorino ◽  
A. Harf ◽  
G. Atlan ◽  
Y. Brault ◽  
A. M. Lorino ◽  
...  

Plotting a line to the variables obtained during a panting maneuver, i.e. thoracic volume and mouth pressure, is the conventional way of computing plethysmographic thoracic gas volume (TGV). This procedure is reliable if the magnitude of the thoracic volume changes is large compared to the drift on the signal; this is one of the major problems in volumetric plethysmography. We propose replacing the thoracic volume signal (Vt) by its time derivative (Vt) and similarly mouth pressure (Pm) with its time derivative (Pm). Drift is thus ruled out, and the magnitude of Vt is preserved when the subject fails to carry out noticeable changes in thoracic volume during the panting, since even then the speed of these changes in thoracic volume remains high. The use of Vt and Pm appeared to be necessary when a minicomputer was connected to a pressure-compensated flow plethysmograph to obtain an automatic calculation of TGV. A regression-line technique applied to signals obtained during the panting was used to find the slope of the relation and thus TGV. However, this slope can only be predicted with less than 5% error if the correlation coefficient is very high (i.e., above 0.99). The analysis of 121 recordings from patients showed that the mean r was only 0.954 when Vt and Pm were used. It increased to 0.993 with Vt and Pm. For the same recordings the comparison of hand-calculated TGV and computer-derived TGV showed a much better agreement for the Vt-Pm method (standard error of the estimate (SEE) = 0.14 liter) than for the Vt-Pm method (SEE = 0.34 liter). These results emphasize that, in contrast to the manual technique, the computer does not adequately handle even a small drift of the thoracic signal. The proposed time-derivative method is therefore useful for a hand calculation, but essential to a reliable computer determination of thoracic gas volume.


1983 ◽  
Vol 55 (2) ◽  
pp. 368-376 ◽  
Author(s):  
T. Y. Sullivan ◽  
P. L. Yu

Minute ventilation (VE) and breathing pattern during an abrupt increase in fractional CO2 were compared in 10 normal subjects before and after airway anesthesia. Subjects breathed 7% CO2-93% O2 for 5 min before and after inhaling aerosolized lidocaine. As a result of airway anesthesia, VE and tidal volume (VT) were greater during hypercapnia, but there was no effect on inspiratory time (TI). Therefore, airway anesthesia produced an increase in mean inspiratory flow (VT/TI) during hypercapnia. The increase in VT/TI was compatible with an increase in neuromuscular output. There was no effect of airway anesthesia on the inspiratory timing ratio or the shape and position of the curve relating VT and TI. We also compared airway resistance (Raw), thoracic gas volume, forced vital capacity, forced expired volume at 1s, and maximum midexpiratory flow rate before and after airway anesthesia. A small (0.18 cmH2O X l-1 X s) decrease in Raw occurred after airway anesthesia that did not correlate with the effect of airway anesthesia on VT/TI. We conclude that airway receptors accessible to airway anesthesia play a role in hypercapnic VE.


1979 ◽  
Vol 56 (3) ◽  
pp. 215-221 ◽  
Author(s):  
C. S. Garrard ◽  
D. J. Lane

1. The pattern of breathing in 12 patients with severe irreversible airflow obstruction has been studied during ventilatory stimulation by rebreathing CO2. Mean maximum tidal volume response was only 1·23 ± 0·30 litres (mean ± sd); this represented 65% of mean measured vital capacity and 82% of mean measured inspiratory capacity. During the course of rebreathing mean total breath duration was reduced from 3·48 ± 0·93 to 2·44 ± 0·48 s. 2. End-expiratory thoracic gas volume (FRC) was elevated at rest in all subjects and increased significantly by a further 0·50–1·90 litres during ventilatory stimulation in 10 of the 12 subjects. The maximum increase in FRC was proportional to the degree of airflow obstruction afforded by the airways in each subject. 3. It is suggested that the increase in FRC during ventilatory stimulation is responsible for the diminished tidal volume response and is an important determinant of breathing pattern and symptomatology in patients with airflow obstruction.


1961 ◽  
Vol 16 (4) ◽  
pp. 717-719 ◽  
Author(s):  
Jay A. Nadel ◽  
Donald F. Tierney

We measured airway resistance and thoracic gas volume by the body plethysmograph technique, and transpulmonary pressure in seven healthy, adult subjects, before and after induction of bronchoconstriction. A deep inspiration never altered airway resistance, measured at functional residual capacity in the control state, but always reduced it for 1—2 min when bronchoconstriction was present. Discrepancies in data published on airway resistance may be due to use of methods which require a deep inspiration, or to occurrence of a spontaneous deep inspiration shortly before the test. Submitted on January 13, 1961


1990 ◽  
Vol 68 (6) ◽  
pp. 2403-2412 ◽  
Author(s):  
K. R. Lutchen ◽  
C. A. Giurdanella ◽  
A. C. Jackson

Respiratory input impedance (Zrs) from 2.5 to 320 Hz displays a high-frequency resonance, the location of which depends on the density of the resident gas in the lungs (J. Appl. Physiol. 67: 2323-2330, 1989). A previously used six-element model has suggested that the resonance is due to alveolar gas compression (Cg) resonating with tissue inertance (Iti). However, the density dependence of the resonance indicates that is associated with the first airway acoustic resonance. The goal of this study was to determine whether unique properties for tissues and airways can be extracted from Zrs data by use of models that incorporate airway acoustic phenomena. We applied several models incorporating airway acoustics to the 2.5- to 320-Hz data from nine healthy adult humans during room air (RA) and 20% He-80% O2 (HeO2) breathing. A model consisting of a single open-ended rigid tube produced a resonance far sharper than that seen in the data. To dampen the resonance features, we used a model of multiple open-ended rigid tubes in parallel. This model fit the data very well for both RA and HeO2 but required fewer and longer tubes with HeO2. Another way to dampen the resonance was to use a single rigid tube terminated with an alveolar-tissue unit. This model also fit the data well, but the alveolar Cg estimates were far smaller than those expected based on the subject's thoracic gas volume. If Cg was fixed based on the thoracic gas volume, a large number of tubes were again required. These results along with additional simulations show that from input Zrs alone one cannot uniquely identify features indigenous to alveolar Cg or to the respiratory tissues.


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