What is the volume of air present in the lungs when the lungs are at rest (in between breaths)?

Spirometry—Total Lung Capacity and Subdivisions

The gas volume in the lung after a maximum inspiration is called thetotal lung capacity (TLC; usually 6 to 8 L). TLC can be increased in COPD either by overexpansion of alveoli or by destruction of the alveolar wall, resulting in loss of elastic tissue, as in emphysema (seeFig. 13.4).78 In extreme cases, TLC can be increased to 10 to 12 L. In restrictive lung disease, TLC is reduced, reflecting the degree of fibrosis, and can be as low as 3 to 4 L (seeFig. 13.4).78

Following maximum expiratory effort, some air is left in the lung and constitutes the RV (approximately 2 L). However, usually no region develops collapse because distal airways (<2 mm) close before alveoli collapse,79 trapping gas and preventing further alveolar emptying. In addition, there is a limit to how much the chest wall, rib cage, and diaphragm can be compressed. The importance of preventing collapse of lung tissue was presented earlier (seeFig. 13.6).

The maximum volume that can be inhaled and then exhaled is the vital capacity (VC; 4-6 L), and this is thedifference between TLC and RV. VC is reduced in both restrictive and obstructive lung disease. In restriction, VC reduction reflects the loss of lung volume, such as from the constricting (i.e., shrinking) effects of fibrosis. In obstructive lung disease, long-term trapping of air increases the RV and can occur either by encroaching on (and reducing) the VC or in association with a (proportionally smaller) increase in FVC.78

Tidal volume (VT, usually 0.5 L) is inspired from the resting lung volume reached at end-expiration (FRC, 2.0 L). With increased ventilation, as in exercise, VT is increased and FRC may be reduced by approximately 0.5 L. However, in airway obstruction, exhalation is impeded such that inspiration commences before the usual resting lung volume is reached; thus end-expiratory volume is increased.78 Such air trapping reduces the resistance to gas flow in the narrowed airways, but because the lung tissue is hyperinflated and mechanically disadvantaged, the work of breathing overall is increased.

FRC increases with age as elastic lung tissue is lost; this reduces the lung recoil force countering the outward chest wall force, and the lung assumes a higher volume. The rate of this aging process is accelerated in COPD because of the contributions of chronic air trapping and marked loss of elastic tissue.19 FRC is reduced in fibrotic lung diseases,78 sometimes to 1.5 L (seeFig. 13.4). Lung resection also reduces FRC, but the remaining lung will expand to fill the lung tissue void partially; this is calledcompensatory emphysema (seeChapter 53).

Measurement of Lung Volumes

TLC and its subdivisions (see Fig. 3-19 and the discussion of lung volumes) are measured either with spirometry and the gas dilution technique or with body plethysmography. FRC is commonly measured by the gas dilution technique with rebreathing of a known concentration of helium (10% He in O2). TLC is obtained by adding inspiratory capacity (IC) and FRC. RV is the difference between TLC and VC, the maximum amount of air one can breathe out from TLC. Forced vital capacity (FVC) is the VC obtained during maximum expiratory effort. Normally, FVC and VC in the same healthy person are nearly identical, but in patients with obstructive airway disease, airway closure worsens with effort and FVC may become considerably smaller than VC. VC per se is not a useful indicator for differential diagnosis, because it decreases in both obstructive and restrictive lung disorders such as atelectasis and pulmonary fibrosis. TLC, on the other hand, is decreased in restrictive disease but is increased by air trapping in obstructive disorders.

Gas dilution techniques underestimate TLC in obstructive lung disease, because the test gas molecules (helium) do not sufficiently penetrate into trapped gas compartments. Under these circumstances, body plethysmography should be used to measure FRC more accurately. Measurement of FRC (or thoracic gas volume [TGV]) with body plethysmography is accomplished with a panting (or short, rapid breathing) maneuver against mouth occlusion. TGV is derived from simultaneous changes in lung volume (V) and airway pressure (P) using Boyle's law (P × V = k). When body plethysmography is not available, addition of a low level of end-expiratory positive airway pressure (EPAP) during helium rebreathing increases gas mixing, probably by preventing airway closure or by keeping the collateral channels open. The difference in calculated FRC with and without EPAP correlates well with the degree of air trapping in the lung (Motoyama et al., 1982b). In obstructive lung disease, FRC and in particular RV, in relation to TLC (FRC/TLC, RV/TLC), are markedly increased.

Determination of Functional Residual Capacity, Residual Volume, and Total Lung Capacity—Helium Dilution Method

The functional residual capacity (FRC), which is the volume of air that remains in the lungs at the end of each normal expiration, is important to lung function. Because its value changes markedly in some types of pulmonary disease, it is often desirable to measure this capacity. The spirometer cannot be used in to measure the FRC directly because the air in the residual volume of the lungs cannot be expired into the spirometer, and this volume constitutes about half of the FRC. To measure FRC, the spirometer must be used in an indirect manner, usually by means of a helium dilution method, as follows.

A spirometer of known volume is filled with air mixed with helium at a known concentration. Before breathing from the spirometer, the person expires normally. At the end of this expiration, the remaining volume in the lungs is equal to the FRC. At this point, the subject immediately begins to breathe from the spirometer, and the gases of the spirometer mix with the gases of the lungs. As a result, the helium becomes diluted by the FRC gases, and the volume of the FRC can be calculated from the degree of dilution of the helium, using the following formula:

FRC=(CiHeCfHe−1)ViSpir

whereFRC is functional residual capacity,CiHe is the initial concentration of helium in the spirometer,CfHe is the final concentration of helium in the spirometer, andViSpir is the initial volume of the spirometer.

Once the FRC has been determined, the residual volume (RV) can be determined by subtracting expiratory reserve volume (ERV), as measured by normal spirometry, from the FRC. Also, the total lung capacity (TLC) can be determined by adding the inspiratory capacity (IC) to the FRC. That is:

RV=FRC−ERV

ALTERATIONS OF LUNG FUNCTION IN NEUROMUSCULAR DISEASE

Total lung capacity (TLC) and vital capacity (VC) may be normal in mild neuromuscular disease but are reduced in moderate to severe disease. The reductions in TLC and VC are caused by inspiratory and expiratory muscle weakness, scoliosis, and decreased lung and chest wall compliance due to a progressive decrease in lung and chest wall expansion.169 RV may be normal or elevated as a result of expiratory muscle weakness. Therefore, an elevated RV/TLC ratio in patients with neuromuscular disease is not usually due to air trapping as is the case in obstructive lung disease.

Maximal expiratory flow rates in patients with neuromuscular disease are usually diminished as a consequence of both low lung volumes and decreased expiratory muscle strength, because both lung volume and driving force can impact maximal flow. Furthermore, patients with neuromuscular disease often have a characteristic shape of the flow-volume curve at low lung volumes, with a precipitous decrease in flows before reaching RV171 rather than a linear decrease through lower lung volumes. This phenomenon is a result of the diminished ability of the expiratory muscles to overcome the outward recoil of the chest wall. As is the case in most restrictive lung disease, the FEV1/FVC ratio is normal in patients with neuromuscular disease.

Lung compliance is reduced in patients with neuromuscular disease,172 whereas specific compliance is usually normal.173 This suggests that the decreased compliance is due to loss of lung units or alveolar number as opposed to an alteration of the tissue properties of the lung.

Total Lung Capacity

Total Lung Capacity

The total lung capacity (TLC) is the maximal volume of gas in the lungs after a maximal inhalation; thus it is the sum of the RV, ERV, VT, and IRV. TLC is approximately 6 L for a healthy 70-kg adult. The vital capacity (VC) is the maximal volume of gas exhaled during a forced exhalation after a forced inhalation. Thus VC is the sum of the VT, IRV, and ERV. The VC is approximately 4.5 L in a healthy 70-kg adult.5

Fig. 5.3 shows a summary of how the standard lung volumes and capacities relate, along with average values for a 70-kg adult.

Vital capacity

At TLC inspiratory muscle forces are counterbalanced by elastic recoil of the lung and chest wall. Both these parameters and the size of the lung, which varies with body size and gender (Box 38.1), determine TLC. Vital capacity, the difference between TLC and FRC, is also reduced by factors that reduce FRC, e.g. increased abdominal chest wall elastance and premature airway closure in COPD. The normal VC is ∼70 mL/kg; although reduction to 12–15 mL/kg has been suggested as an indication for mechanical ventilation, many other factors need to be considered including the patient's general condition, the strength of the expiratory muscles, glottic function, and the response to non-invasive ventilation. Indeed, many chronically weak patients are able to manage at home with extremely low VC with the assistance of non-invasive ventilation.

CT Assessment of Lung Ventilation

TLC, full inspiration, supine CT imaging of the lungs has been used to assess airway geometry of large airway diseases and tissue destruction by emphysema, and FRC and RV, or partial and full expiration, supine chest imaging of the lungs has been used to assess small conducting airway disease by the assessment of air trapping. The quantitative assessment of air trapping using chest CT scans obtained at either FRC or RV represent a very effective means of assessing air trapping produced by small airway disease in at risk subjects. The success of expiratory CT scanning in assessing air trapping and the presence of small airway disease is the simplest form of “functional lung imaging” [13,16,94,95]. The question that remains is how might more sophisticated CT measures of imaging normal and abnormal ventilation in the human lung add to our ability to understand, diagnose, and treat patients with airway disease.

Static Lung Volumes

Total lung capacity is the volume of air present in the chest after full inspiration (Fig. 13-2). During quiet ventilation, the volume of air inspired and expired in one breath is the tidal volume, normally 500 to 750 mL. The vital capacity (VC) is perhaps the most commonly measured bedside volume. It is the amount of air that can be moved into or out of the lungs on a single breath, normally about 65 mg/kg. The forced vital capacity (FVC) is the volume of air that can be exhaled forcefully after a maximal inspiration. The volume of air left in the lungs at the end of quiet expiration is the functional residual capacity (FRC), and the amount remaining at the end of maximal expiration is the residual volume (RV). Unlike the other lungs volumes defined earlier, RV and FRC cannot be measured by spirometry. Gas dilution techniques or body plethysmography are needed. RV, but not FRC, depends on expiratory muscle strength in addition to the elastic recoil of the chest wall and airway closure.

It is useful to follow lung volumes, especially the FVC, in patients with neuromuscular diseases that may affect respiration because improvement in the FVC may parallel clinical improvement and reflect successful therapy; a falling FVC can warn the clinician of impending respiratory failure.

Pathology

Total lung volume is not decreased in hyaline membrane disease. Postmortem examination of human infants dying during the acute phase of this disorder reveals lungs that are described as full2 or even voluminous.3 They are often compared with liver to emphasize their appearance as a solid, airless organ that is congested and dark purplish red. Microscopic examination reveals marked capillary and venous congestion. Interstitial edema is widespread and is especially prominent in the adventitia surrounding small arterioles, which are markedly constricted early in the disease. Dilated lymphatic spaces are frequently seen adjacent to respiratory bronchioles and arterioles. Hyaline membrane formation, which represents a coagulum of sloughed cell debris in a protein matrix, occurs characteristically at the junction of respiratory bronchioles and alveolar ducts. Hyaline membranes are visible evidence that this disease involves a massive exudation of plasma proteins occurring in association with a destructive injury of the epithelial lining of the terminal conducting airways. The fully formed membrane often has the appearance of an eschar plastered against the denuded epithelial basement membrane. The respiratory bronchioles and alveolar ducts are frequently dilated and may be filled with protein-rich edema fluid in association with membrane formation early in the course of the disease.

The pathologic appearance of the lung of infants dying early in the course of hyaline membrane disease presents a picture of lung injury characterized by vascular engorgement and interstitial edema in association with terminal airways filled with protein-containing fluid. These features are consistent with physiologic findings that include delayed clearance of fetal lung liquid,4-7 increased permeability of both epithelial4,8,9 and endothelial barriers,6 delayed lung lymph protein clearance,5,6 and a grossly increased pulmonary blood volume.10 These physiologic observations confirm that the pathologic appearance of the lung in hyaline membrane disease results from disruption of the normal segregation of gas and liquid compartments.