Lung Volumes and Airway Resistance

Author(s):  
Joseph Feher
2008 ◽  
pp. 91-97 ◽  
Author(s):  
G. A. Lyubimov ◽  
I. M. Skobeleva ◽  
G. M. Sakharova ◽  
A. V. Suvorov

This report introduces a mathematical model of forced expiration to analyze pulmonary function. Results of 3-year lung function monitoring of an ex-smoker have been shown in the paper. Actual values of lung volumes and airway resistance were used for modeling. The computerized data were compared to the flow-volume curve parameters and lung volumes measured during the forced expiration. Weak correlation between the "flow-volume" curve parameters and the time after quitting smoking together with significant change in the lung volumes and the airway resistance seen in the study could be due to some processes which have not been followed in this study (lung compliance, airway resistance at forced expiration, and elastic properties of airway walls).The results demonstrated that mathematical models could increase informative value of pulmonary functional tests. In addition, the model could emphasize additional functional tests for better diagnostic usefulness of functional investigations.


2021 ◽  
pp. 57-61
Author(s):  
M. I. Chushkin ◽  
L. A. Popova ◽  
E. A. Shergina ◽  
N. L. Karpina

Interpretation of bronchodilator (BD) test based on reaction of forced expiratory in one second (FEV 1). For assessing bronchodilator responsiveness of lung volumes, airway resistance remains largely unexplored. Therefore, we assessed the response of pulmonary function parameters to BD to reveal the most responsive parameter. 90 patients with chronic airway obstruction (61 male and 29 female; aged 55±11; post-  BD FEV 1 was 63.1+18.3 % predicted) performed spirometry and static lung volume measurements before and after inhalation of BD. We calculated effect size (ES) for each parameter from the difference between two means divided by the standard deviation of baseline score. There was a significant increase both FVC and FEV 1by 8.2 and 12.3 % from baseline (p<0.001). ES were 0.34 for FEV1 and 0.26 for FVC. The ES for lung volumes were from -0.07 (total lung capacity) to -0.31 (residual volume). The ES for sRtot (specific airway resistance) was -0.5 and ES for sGeff (specific effective airway conductance) was 0.95. The parameters of airway resistance and conductance were more responsive for the assessment of pulmonary function changes than spirometry and lung volumes parameters in patients with chronic airway obstruction.


1989 ◽  
Vol 66 (2) ◽  
pp. 977-982 ◽  
Author(s):  
S. T. Kariya ◽  
L. M. Thompson ◽  
E. P. Ingenito ◽  
R. H. Ingram

We examined the effects of lung volume change and volume history on lung resistance (RL) and its components before and during induced constriction. Eleven subjects, including three current and four former asthmatics, were studied. RL, airway resistance (Raw), and, by subtraction, tissue viscance (Vtis) were measured at different lung volumes before and after a deep inhalation and were repeated after methacholine (MCh) aerosols up to maximal levels of constriction. Vtis, which average 9% of RL at base line, was unchanged by MCh and was not changed after deep inhalation but increased directly with lung volume. MCh aerosols induced constriction by increasing Raw, which was reversed by deep inhalation in inverse proportion to responsiveness. such that the more responsive subjects reversed less after a deep breath. Responsiveness correlated directly with the degree of maximal constriction, as more responsive subjects constricted to a greater degree. These results indicate that in humans Vtis comprises a small fraction of overall RL, which is clearly volume-dependent but unchanged by MCh-induced constriction and unrelated to the degree of responsiveness of the subject.


1982 ◽  
Vol 53 (3) ◽  
pp. 698-702 ◽  
Author(s):  
P. Helms

In 57 infants and very young children, less than 2 yr of age and with a variety of cardiopulmonary illnesses, problems were encountered in the estimation of lung volume with the plethysmographic technique. In 19 subjects calculated thoracic gas volume (TGV) was found to be consistently larger when airway occlusions were performed at low lung volumes than when performed at higher lung volumes. In 13 infants, changes in intraesophageal pressure (Pes) during airway occlusions were found to be larger than simultaneous changes in mouth pressure. In 25 subjects in whom none of the above changes were observed, total pulmonary resistance (TPR) and airway resistance (Raw) did not differ significantly [mean TPR, 50.1 +/- 27.5 cmH2O X l-1; mean Raw, 48.1 +/- 26.5 (P greater than 0.5)]. In the 13 subjects in whom the delta Pes-to-delta Pm occlusion ratio exceeded 1.05, closest agreement with specific resistance (sRaw) and TPR derived lung volume was found when TGV was calculated with delta Pes rather than mouth pressure change (delta Pm). A similar close agreement with the sRaw TPR derived volume was obtained when TGV was calculated during airway occlusions at the higher lung volume. Two separate lung models are proposed to explain these observations, one with a segmental airway closure and the other with more a generalized airway closure. If plethysmographic techniques are to be used in these young subjects for the estimation of lung volume and airway resistance, possible errors may be reduced by performing airway occlusions at lung volumes above functional residual capacity and noting the delta Pes-to-delta Pm ratio obtained during the occlusion.


1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.


1977 ◽  
Vol 52 (4) ◽  
pp. 423-428
Author(s):  
A. R. Rubinfeld ◽  
M. C. F. Pain

1. Lung volumes, airway resistance and flow/volume curves were measured in ten asthmatic subjects at times when tightness in the chest was just sensed (threshold symptom). 2. These measurements when the threshold symptom was induced by methacholine inhalation were compared with those when a similar symptom occurred spontaneously, in the same subjects. 3. Values during the methacholine-induced thresholds were very similar to those observed when threshold symptoms developed spontaneously. 4. Controlled bronchial provocation mimics spontaneous asthma sufficiently well to allow this technique to be used in the study of sensations associated with breathing. This has some advantages over the already established models utilizing external hindrances to breathing.


2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Bill Brashier ◽  
Sundeep Salvi

Obesity induces some pertinent physiological changes which are conducive to either development of asthma or cause of poorly controlled asthma state. Obesity related mechanical stress forces induced by abdominal and thoracic fat generate stiffening of the lungs and diaphragmatic movements to result in reduction of resting lung volumes such as functional residual capacity (FRC). Reduced FRC is primarily an outcome of decreased expiratory reserve volume, which pushes the tidal breathing more towards smaller high resistance airways, and consequentially results in expiratory flow limitation during normal breathing in obesity. Reduced FRC also induces plastic alteration in the small collapsible airways, which may generate smooth muscle contraction resulting in increased small airway resistance, which, however, is not picked up by spirometric lung volumes. There is also a possibility that chronically reduced FRC may generate permanent adaptation in the very small airways; therefore, the airway calibres may not change despite weight reduction. Obesity may also induce bronchodilator reversibility and diurnal lung functional variability. Obesity is also associated with airway hyperresponsiveness; however, the mechanism of this is not clear. Thus, obesity has effects on lung function that can generate respiratory distress similar to asthma and may also exaggerate the effects of preexisting asthma.


Author(s):  
Mark Harrison

This chapter describes respiratory physiology as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of lung volumes and pressures, lung epithelium, lung compliance, surfactant, airway resistance, gas transfer, gas transport within circulation, control of respiration, and ventilation–perfusion relationship. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.


Author(s):  
Isha Garg ◽  
K.C. Agarwal ◽  
Gopal Purohit ◽  
C.R. Choudhary ◽  
Naveen Dutt ◽  
...  

1990 ◽  
Vol 68 (5) ◽  
pp. 1875-1882 ◽  
Author(s):  
C. M. Hesser ◽  
F. Lind ◽  
D. Linnarsson

The effects of increased airway resistance on lung volumes and pattern of breathing were studied in eight subjects performing leg exercise on a cycle ergometer. Airway resistance was changed 1) by increasing the density (D) of the respired gas by a factor of 4.2 and changing the inspired gas from O2 at 1.3 bar to air at 6 bar and 2) by increasing airway flow rates by exposing the subjects to incremental work loads of 0-200 W. Increased gas D caused a slower and deeper respiration at rest and during exercise and, at work loads greater than 120 W, depressed the responses of ventilation and mean inspiratory flow. Raised airway resistance induced by increases in D and/or airway flow rates altered respiratory timing by increasing the ratio of inspiratory time (TI) to total breath duration. Furthermore, analyses of the relationships between tidal volume and TI and between end-inspiratory volume and TI revealed elevation of Hering-Breuer inspiratory volume thresholds. We propose that this elevation, and hence exercise-induced increases of tidal volume, can largely be explained by previous observations that the threshold of the inspiratory off-switch mechanisms depends on central inspiratory activity (cf. C. von Euler, J. Appl. Physiol. 55: 1647-1659, 1983), which in turn increases with airway resistance (Acta Physiol. Scand. 120: 557-565, 1984).


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