Body plethysmographic measurement of thoracic gas volume without panting against a shutter

1996 ◽  
Vol 81 (2) ◽  
pp. 1007-1011 ◽  
Author(s):  
A. Agrawal ◽  
K. P. Agrawal

When a subject breathes through a pneumotachograph in a body box, the measured value of specific airway resistance (sRaw1) is equal to the product of thoracic gas volume (TGV) and the sum of the airway resistance (Raw) and the instrument resistance (Rins). If an additional resistance (Radd) is put in the breathing path, the measured specific, airway resistance (sRaw2) exceeds sRaw1 by the product of TGV and Radd and can be used for determining TGV. With the use of a device increasing Rins by a known amount (Radd) during normal breathing, sRaw1 and sRaw2 were measured in 3 normal subjects, 16 asthmatic patients, 2 patients with chronic obstructive pulmonary disease, and 1 patient with restrictive lung disease from the slopes of the x-y plots of airflow vs. box signals obtained before and after adding Radd. TGV was calculated by dividing (sRaw2-sRaw1) bu Radd. We also determined subjects' TGV by the panting method of A. B. DuBois, S. Y. Botelho, G. N. Bedell, and J. H. Comroe, Jr. (J. Clin. Invest. 35: 322–326, 1956) and functional residual capacity by the helium-dilution method. The results of the new method were quite reproducible (coefficient of variation = 5.6) and equivalent to those obtained by the other two methods.

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.


2000 ◽  
Vol 89 (1) ◽  
pp. 283-290 ◽  
Author(s):  
Martin R. Miller ◽  
Ole F. Pedersen

Previous studies have shown that the added resistance of a mini-Wright peak expiratory flow (PEF) meter reduced PEF by ∼8% in normal subjects because of gas compression reducing thoracic gas volume at PEF and thus driving elastic recoil pressure. We undertook a body plethysmographic study in 15 patients with chronic obstructive pulmonary disease (COPD), age 65.9 ± 6.3 yr (mean ± SD, range 53–75 yr), to examine whether their recorded PEF was also limited by the added resistance of a PEF meter. The PEF meter increased alveolar pressure at PEF (Ppeak) from 3.7 ± 1.4 to 4.7 ± 1.5 kPa ( P = 0.01), and PEF was reduced from 3.6 ± 1.3 l/s to 3.2 ± 0.9 l/s ( P = 0.01). The influence of flow limitation on PEF and Ppeak was evaluated by a simple four-parameter model based on the wave-speed concept. We conclude that added external resistance in patients with COPD reduced PEF by the same mechanisms as in healthy subjects. Furthermore, the much lower Ppeak in COPD patients is a consequence of more severe flow limitation than in healthy subjects and not of deficient muscle strength.


1980 ◽  
Vol 49 (3) ◽  
pp. 398-402 ◽  
Author(s):  
R. Brown ◽  
S. Scharf ◽  
R. H. Ingram

When thoracic gas volume (TGV) is determined plethysmographically, it is assumed that the alveolar pressure swings are homogeneous and are appropriately represented by pressure swings at the mouth. However, recent studies have demonstrated differences in total lung capacities derived from TGV measurements made at different levels in the vital capacity. These differences suggested that, in the presence of airway closure, alveolar pressure swings may be nonhomogeneous during a TGV determination. This possibility was tested in six dogs. Pressure at the airway opening (ao) was measured from an endotracheal catheter. A balloon-tipped catheter was passed into the right lower lobe (RLL) bronchus for measurement of RLL pressure. delta PRLL -- delta Pao was monitored during inspiratory efforts with the airway opening occluded. With the RLL balloon inflated, delta PRLL always exceeded delta Pao by an amount averaging 8.2%. Induction of a pneumothorax eliminated all differences between delta PRLL and delta Pao. Thus, during a TGV measurement, the chest wall may apply to the lungs nonhomogeneous forces that, in the presence of airway closure (e.g., chronic obstructive pulmonary disease and asthma) would result in nonhomogeneous alveolar pressure swings and potentially significant errors in the plethysmographic determination of TGV.


1983 ◽  
Vol 54 (1) ◽  
pp. 159-165 ◽  
Author(s):  
D. O. Rodenstein ◽  
D. C. Stanescu

In airway obstruction, thoracic gas volume derived from mouth pressure vs. plethysmographic volume changes (TGVm) is overestimated, whereas TGVes, derived from esophageal pressure vs. plethysmographic volume changes, is not (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 52: 939–954, 1982). The reason appears to be that mouth pressure swings are less than alveolar pressure swings. We measured TGVm and TGVes in six normal subjects and in nine asthmatic patients before and during bronchospasm, while panting at the same lung volume at 0.8 Hz (low), 2–2.5 Hz (medium), and 4.5–5 Hz (high). No difference was observed between TGVm and TGVes (P greater than 0.05) at any frequency (f) in normal subjects or asthmatics before bronchospasm. During bronchospasm, TGVm and TGVes were similar at low f. However, TGVm increased from 5.66 +/- 1.16 (SD) liters at low f to 6.50 +/- 1.71 liters at medium f (P less than 0.01), resulting in a TGVm 1.16 +/- 0.95 liters higher than TGVes (P less than 0.01). In three asthmatics during bronchospasm, mean TGVm-TGVes difference was 0.01 liter at low f, 0.26 liter at medium f, and 0.73 liter at high f. Surprisingly TGVes was in average 5% higher at low f than at medium or high f, both in normal subjects and asthmatics. A similar pattern was observed for TGVm, except in asthmatics during bronchospasm. We conclude that in airway obstruction overestimation of TGVm is frequency dependent and can be avoided by panting at low f. However, at this f TGV is 5% larger than at higher f, difference which is not related to airway obstruction.


1979 ◽  
Vol 46 (2) ◽  
pp. 399-406 ◽  
Author(s):  
B. E. Pennock ◽  
C. P. Cox ◽  
R. M. Rogers ◽  
W. A. Cain ◽  
J. H. Wells

A simple noninvasive technique for measuring specific airway resistance (airway resistance X thoracic gas volume) in unanesthetized guinea pigs is described. Specific airway resistances measured by this technique correlated well (r = 0.81) with the resistances obtained using a pleural catheter pressure measurement over a wide range of airway resistances. This range of resistances was generated by exposing the pigs to an aerosolized histamine bronchial challenge. The average specific airways resistance in unchallenged pigs was 1.24 +/- 3.47 cmH2O/s, somewhat lower than found by others, probably reflecting in part our larger pigs and in part some uncertainty in the absolute value of resistance inherent in our measurement technique. This technique is particularly useful in bronchial challenge experiments because of its sensitivity to acute changes in airway resistance.


1999 ◽  
Vol 87 (3) ◽  
pp. 920-927 ◽  
Author(s):  
Kirby L. Zeman ◽  
Gerhard Scheuch ◽  
Knut Sommerer ◽  
James S. Brown ◽  
William D. Bennett

Effective airway dimensions (EADs) were determined in vivo by aerosol-derived airway morphometry as a function of volumetric lung depth (VLD) to identify and characterize, noninvasively, the caliber of the transitional bronchiole region of the human lung and to compare the EADs by age, gender, and disease. By logarithmically plotting EAD vs. VLD, two distinct regions of the lung emerged that were identified by characteristic line slopes. The intersection of proximal and distal segments was defined as VLDtransand associated EADtrans. In our normal subjects ( n = 20), VLDtrans [345 ± 83 (SD) ml] correlated significantly with anatomic dead space (224 ± 34 ml) and end of phase II of single-breath nitrogen washout (360 ± 53 ml). The corresponding EADtranswas 0.42 ± 0.07 mm, in agreement with other ex vivo measurements of the transitional bronchioles. VLDtrans was smaller (216 ± 64 ml) and EADtrans was larger (0.83 ± 0.04 mm) in our patients with chronic obstructive pulmonary disease ( n = 13). VLDtrans increased with age for children (age 8–18 yr; P = 0.006, n = 26) and with total lung capacity for age 8–81 yr ( P < 0.001, n = 61). This study extends the usefulness of aerosol-derived airway morphometry to in vivo measurements of the transitional bronchioles.


1991 ◽  
Vol 71 (1) ◽  
pp. 259-270 ◽  
Author(s):  
M. Mishima ◽  
K. Kawakami ◽  
K. Higashiya ◽  
T. Fukunaga ◽  
T. Ooka ◽  
...  

We measured the frequency characteristics (at 10–40 Hz) of airway (Za) and tissue (Zt) impedances in cases of chronic obstructive pulmonary disease [asthmatic bronchitis (AB), chronic pulmonary emphysema (CPE)] and interstitial pneumonitis (IP) by use of an improved random noise oscillation and body box method. The results were then compared with those obtained for normal subjects. The real part of Za was markedly elevated in patients with AB but only slightly elevated in those with CPE. To interpret these data we used an electromechanical analogue including serial inhomogeneity with shunt impedance. From this model we concluded that AB causes both the central and peripheral airway resistances to increase, while CPE brings about a rise mainly in peripheral resistance. In IP patients, only the imaginary part of Zt decreased, which might reflect the decrease in both lung and chest wall compliance. In CPE patients, but not in AB patients, the real part of Zt fell. These data were consistent with the assumption that the decrease in mass per unit volume of lung tissue and hyperinflation of the chest wall in CPE patients might lower the tissue resistances.


2004 ◽  
Vol 11 (6) ◽  
pp. 427-433 ◽  
Author(s):  
Pierre Lajoie ◽  
Andrée Laberge ◽  
Germain Lebel ◽  
Louis-Philippe Boulet ◽  
Marie Demers ◽  
...  

BACKGROUND:Asthma education should be offered with priority to populations with the highest asthma-related morbidity. In the present study, the aim was to identify populations with high-morbidity for asthma from the Quebec Health Insurance Board Registry, a large administrative database, to help the Quebec Asthma and Chronic Obstructive Pulmonary Disease Network target its interventions.METHODS:All emergency department (ED) visits for asthma were analyzed over a one-year period, considering individual and medical variables. Age- and sex-adjusted rates, as well as standardized rate ratios related to the overall Quebec rate, among persons zero to four years of age and five to 44 years of age were determined for 15 regions and 163 areas served by Centres Locaux de Services Communautaires (CLSC). The areas with rates 50% to 300% higher (P<0.01) than the provincial rate were defined as high-morbidity areas. Maps of all CLSC areas were generated for the above parameters.RESULTS:There were 102,551 ED visits recorded for asthma, of which more than 40% were revisits. Twenty-one CLSCs and 32 CLSCs were high-morbidity areas for the zero to four years age group and five to 44 years age group, respectively. For the most part, the high-morbidity areas were located in the south-central region of Quebec. Only 47% of asthmatic patients seen in ED had also seen a physician in ambulatory care.CONCLUSION:The data suggest that a significant portion of the population seeking care at the ED is undiagnosed and undertreated. A map of high-morbidity areas that could help target interventions to improve asthma care and outcomes is proposed.


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