Why is residual volume provided as a theoretical value

What's the total lung, inspiratory, and vital capacity formula? What's the vital capacity equation? Choose whether you're male or female - the vital capacity equation differs slightly, depending on the given sex.

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Definition Clinical assessment of lung function is aided by the determination of several parameters derived from usage of a spirometer. This device allows for accurate measurement of the rate and volume of air flowing into and out of a patient's lungs during particular maneuvers. Lung Volumes Tidal Volume The Tidal Volume is the volume of air breathed in and out by a person during normal breathing at rest.

Residual Volume The Residual Volume is the volume of gas remaining in the lung after a person has breathed out to his or her maximum capacity. Naturally, the residual volume cannot be determined directly using spirometry since it is not possible to measure the remaining air volume after maximum expiration. Consequently, more advanced techniques must be used to determine this parameter. Lung Volumes The above graph shows the volume of air inspired and expired by an individual over time using a spirometer.

After a period of initial quite breathing the individual takes a maximal inspiration and a maximal expiration. Lung volumes can be calculated from the graph above. Restrictive lung diseases RLD are associated with decreased compliance of the lungs, chest wall or both. This results in rightward shift of static PVC of the lungs, chest wall or both [ 15 ].

In RLD, the rightward shift of dynamic lung compliance curves increases the elastic work of breathing required for inspiration, which is usually compensated by rapid shallow breathing [ 16 ]. Causes of RLD may be intrinsic or extrinsic to the lung parenchyma. Examples of intrinsic causes are interstitial lung diseases, pneumonia and surfactant deficiency e.

Alternatively, respiratory muscles weakness, chest deformities, cardiomegaly, hemothorax, pneumothorax, empyema, pleural effusion or thickening are examples of extrinsic causes. In obstructive lung diseases OLD , the pulmonary compliance is normal or increased especially if emphysematous lung changes co-exist. No extra-negative P Pl is needed as dynamic lung compliance curves are either not displaced or shifted leftward if emphysematous lung changes developed Fig.

The main defect in OLD is increased airways resistance, especially during expiration. Normally, expiration is a passive process as the energy needed to overcome expiratory resistive work of breathing is stored in the elastic fibers of the lung during inspiration. Famous examples of obstructive pulmonary diseases include bronchial asthma, emphysema, chronic bronchitis and bronchiectasis.

The lung volumes increase steadily from birth to adulthood. The lungs mature at the age of 20—25 years, yet only minimal changes occur in the lung volumes over the following 10 years [ 17 ]. After 35 years, aging is associated with gradual changes in the lung volumes and other pulmonary functions [ 18 ]. These changes include enhanced static lung compliance due to diminished alveolar elastic recoil and depressed chest wall compliance due to stiffening and increased outward recoil of the thoracic cage [ 19 , 20 ].

As a result of these changes in the lung and chest wall compliances, the inward recoil of the lung balances the outward recoil of the chest at higher FRC as age progress [ 12 , 13 ]. These variations in lung and chest wall compliances act synergistically to cause early closure of small airways upon forced expiration and hence explain increased RV in elder people [ 19 ].

As shown in Fig. It is also apparent from Fig. This results in a reduction of the difference between these two capacities i. Standard morphometric methods confirmed that males had larger lung size, more respiratory bronchioles and wider airways diameters compared with females with the same age and stature [ 21 , 22 ]. These anatomical lung differences between males and females explain the gender variations in static lung volumes and capacities. Males tend to have larger anthropometric measurements and are, therefore, more likely to have increased static lung volumes and capacities [ 23 ].

Tall stature is typically associated with higher static lung volumes and capacities [ 24 ]. Increased body weight is associated with lower lung volumes in obese subjects [ 25 ]. Waist-to-hip ratio could be a better predictor for fat distribution than BMI [ 27 ].

In athletes, repeated muscular exercise increases muscle mass and consequently body weight. In such condition, the static lung volumes and capacities are expected to increase with weight [ 29 — 32 ]. Increased total body fat content, therefore, seems better than high BMI as an indicator of obesity as well as predictor for decreased static lung volumes and capacities [ 33 ].

Such variations were largely attributed to anthropometric differences between different ethnic groups. Recently, GLI Global Lung Initiative offered spirometric prediction equations, that also considered ethnic differences, to be used worldwide [ 38 ].

Lung volumes correlate well with the level of physical activity [ 39 ], regular exercise, especially swimming and endurance training [ 32 ]. Alternatively, ascending to high altitude may decrease lung volumes probably due to increased pulmonary blood flow, pulmonary edema or premature small airways closure [ 40 ].

Alterations in lung volumes associated with high altitude are usually temporal and resolve after returning to the sea level [ 41 ]. The position of the subject is important while measuring lung volumes and capacities [ 42 ].

Compared with the standing position, the effect of gravity on abdominal viscera is less at sitting position and least if lying supine [ 43 ]. The supine position, therefore, compromises diaphragmatic movement and chest wall recoil during breathing. The measurement of the lung volumes is not an easy task and requires cooperative patients and qualified technicians. Special attention should be given to the accuracy of the method used for estimation of the static lung volumes and capacities. Plethysmography was claimed to overestimate while dilutional techniques may underestimate the true measurements of the lung volumes and capacities [ 5 ].

The normal lung volumes and capacities can be predicted based on gender, age, weight, height and ethnicity of the subject [ 47 ]. Although authorized spirometric reference values are available for most populations, normal ranges of lung volumes and capacities were not established in others yet.

However, the use of these cut-off points may be misleading in characterizing ventilatory defects in some pulmonary diseases if only simple spirometry is performed [ 48 , 49 ]. Simultaneous increase of RV with VC reduction is indicative of obstructive lung disease because of small airway closure or expiratory flow limitation [ 53 ]. Therefore, decreased VC readings are better interpreted in conjunction with other clinical and spirometric indicators of OLD, especially if measurements of RV and TLC are not available [ 54 ].

According to Aaron et al. This hypothesis is further supported by Vandevoorde et al. If thoracic cage expansion is restricted, rightward displacement of the chest wall static PVC takes place.

This readjusts the point where the inward recoil of the lung equalizes the outward recoil of the chest wall at a lower FRC level. According to Jones et al. Marked reduction of FRC and ERV in such cases may induce premature formation of flow limiting segments during quiet breathing, especially in the lower regions of the lungs [ 57 ].

This implication is further supported by the studies that confirm an inverse relationship between FRC and airway resistance in obese patients [ 58 , 59 ]. Taking into consideration the variations in airways resistance between inspiration and expiration, it is easy to conclude that different types of VC are not equal. The differences between the four types of VC are minimal in those with no ventilatory defect [ 61 ].

In OLD, formation of flow limiting segments occurs early due to narrowing of airways. IC can directly be measured by spirometry, which is advantageous in places where there are no facilities to measure RV and TLC.

There are accumulating evidences that indices derived from IC are helpful to assess severity, prognosis and response to treatment of many OLD [ 66 — 69 ]. This fact is further supported by the finding of French et al. Likewise, lung hyperinflation secondary to air trapping can be estimated by calculating the difference between lung volumes measured by plethysmography and dilutional techniques.

This assumption was validated by Tantucci et al. The results confirmed that comparing FRC pl with FRC He was helpful in identifying asthmatic patients at risk of tidal airway closure induced by methacholine.

In addition, Tantucci et al. Typical changes in the static lung volumes and capacities in OLD are summarized in Fig. In a recent study involving asthmatic patients during methacholine challenge, FEV 1-Sp overestimated bronchoconstrictor response in those with larger lung volume [ 73 ].

FEV 1-Sp also overestimated bronchodilator response following administration of salbutamol to the same patients. In another study, FEV 1-Sp and FEV 1-Pl were simultaneously measured in 47 and 51 subjects with dominant emphysema and dominant chronic bronchitis, respectively [ 74 ]. The results confirmed larger lung volumes and lower FEV 1-Sp in emphysematous patients compared with those with dominant chronic bronchitis.

When FEV 1-Pl was used instead of FEV 1-Sp , the disease severity was less in classes with dominant emphysema than those with dominant chronic bronchitis. Decreased TLC in patients with spirometric evidence of airways obstruction e.

This fact explains the findings of Balfe et al. According to Balfe et al. However, NSP was also demonstrated in patients with restrictive ventilatory defects [ 80 ]. Possible explanation for NSP in patients with restrictive ventilatory defects remains for further investigations and researches.

Simultaneous increase in RV with VC reduction is indicative of obstructive lung disease. Therefore, decreased VC readings are better interpreted in conjunction with other clinical and spirometric indicators of OLD. In RLD like central obesity, decreased chest wall compliance reduces FRC and ERV, which may induce premature formation of flow limiting segments during quiet breathing. NSP was also demonstrated in patients with restrictive ventilatory defects, which needs further investigations and researches.

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