Section 2: Scientific Principles
Part D: Physiology and Anesthesia
Chapter 15: Respiratory Physiology and Respiratory Function During Anesthesia

Lung Volumes, Functional Residual Capacity, and Closing Capacity

Lung Volumes and Functional Residual Capacity

The FRC is defined as the volume of gas in the lung at the end of a normal expiration when there is no airflow and PA equals the ambient pressure. Under these conditions, expansive chest wall elastic forces are exactly balanced by retractive lung tissue elastic forces 80  (Fig. 15–15).

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FIGURE 15–15 (A) The resting state of normal lungs when they are removed from the chest cavity; that is, elastic recoil causes total collapse. (B) The resting state of a normal chest wall and diaphragm when the thoracic apex is open to the atmosphere and the thoracic contents are removed. (C) The lung volume that exists at the end of expiration is the functional residual capacity (FRC). At FRC, the elastic forces of lung and chest walls are equal and in opposite directions. The pleural surfaces link these two opposing forces. (Modified from Shapiro et al80 )

The expiratory reserve volume is part of the FRC; it is that additional gas beyond the end-tidal volume that can be consciously exhaled, resulting in the minimum volume of lung possible, known as the residual volume. Thus, the FRC equals the residual volume plus the expiratory reserve volume (Fig. 15–16). With regard to the other lung volumes shown in Figure 15–16, VT, vital capacity, inspiratory capacity, inspiratory reserve volume, and expiratory reserve volume can all be measured by simple spirometry. Total lung volume, FRC, and residual volume all contain a fraction (the residual volume) that cannot be measured by simple spirometry. However, if one of these three volumes is measured, the others can be easily derived because the other lung volumes, which relate these three volumes to one another, can be measured by simple spirometry.

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FIGURE 15–16 The dynamic lung volumes that can be measured by simple spirometry are the tidal volume, inspiratory reserve volume, expiratory reserve volume, inspiratory capacity, and vital capacity. The static lung volumes are the residual volume, functional residual capacity, and total lung capacity. The static lung volumes cannot be measured by observation of a spirometer trace and require separate methods of measurement.

FRC can be measured by one of three techniques. The first method is to wash the nitrogen out of the lungs by several minutes of O2 breathing and to measure the total quantity of nitrogen eliminated. Thus, if 2 L of nitrogen is eliminated and the initial alveolar nitrogen concentration was 80 percent, the initial volume of the lung was 2.5 L. The second method uses the washin of a tracer gas such as helium. If 50 mL of helium is introduced into the lungs and, after equilibration, the helium concentration is found to be 1 percent, the volume of the lung is 5 L. The third method uses Boyle‘s law (i.e., PV = K, where P = pressure, V = volume, and K = a constant). The subject is confined within a gas-tight box (plethysmograph), so that changes in the volume of the body may be readily determined as a change in pressure within the box. Disparity between FRC as measured in the body plethysmograph and by the helium method is often used as a way of detecting large, nonventilating air-trapped blebs. 81  Obviously, there are difficulties in applying the body plethysmograph to anesthetized patients.

Airway Closure and Closing Capacity

As discussed earlier in the section on the distribution of ventilation, Ppl increases from the top to the bottom of the lung and determines regional alveolar size, compliance, and ventilation. Of even greater importance to the anesthesiologist is the recognition that these gradients in Ppl may lead to airway closure and collapse of alveoli.

Airway Closure in Patients with Normal Lungs

Figure 15–17A illustrates the normal resting endexpiratory (FRC) position of the lung-chest wall combination. The distending transpulmonary and the intrathoracic air passage transmural DP are 5 cm H2 O, and the airways remain patent. During the middle of a normal inspiration (Fig. 15–17,B) there is an increase in the transmural DP (to 6.8 cm H2 O), which encourages distention of intrathoracic air passages. During the middle of a normal expiration (Fig. 15–17C), expiration is passive; PA is attributable only to the elastic recoil of the lung (2 cm H2 O), and there is a decrease (to 5.2 cm H2 O) but still a favorable (distending) intraluminal transmural DP. During the middle of a severe forced expiration (Fig. 15–17D), Ppl increases far higher than atmospheric pressure and is communicated to the alveoli, which have a pressure that is higher still owing to the elastic recoil of the alveolar septa (an additional 2 cm H2 O). At high gas flow rates, the pressure drop down the air passage is increased, and there will be a point at which intraluminal pressure equals either surrounding parenchymal pressure or Ppl; that point is termed the equal pressure point (EPP). If the EPP occurs in small intrathoracic air passages (distal to the 11th generation, the airways have no cartilage and are called bronchioles), they may be held open at that particular point by the tethering effect of the elastic recoil of the immediately adjacent or surrounding lung parenchyma. If the EPP occurs in large extrathoracic air passages (proximal to the 11th generation, the airways have cartilage and are called bronchi), they may be held open at that particular point by their cartilage. Downstream of the EPP (in either small or large airways), the transmural DP is reversed (–6 cm H2 O) and results in airway closure. Thus, the patency of airways distal to the 11th generation is a function of lung volume, and the patency of airways proximal to the 11th generation is a function of intrathoracic (pleural) pressure. In extrathoracic bronchi with cartilage, the posterior membranous sheath appears to give first by invaginating into the lumen. 82  If lung volume were abnormally decreased (for example, owing to splinting) and expiration were still forced, the caliber of the airways would be relatively reduced at all times, causing the EPP and point of collapse to move progressively from larger to smaller air passages (closer to the alveolus).

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FIGURE 15–17 Pressure gradients across the airways. The airways consist of a thin-walled intrathoracic portion (near the alveoli) and a more rigid (cartilaginous) intrathoracic and extrathoracic portion. During expiration, the pressure due to elastic recoil is assumed to be +2 cm H2O in normal lungs (A–D) and +1 cm H2O in abnormal lungs (E and F). The total pressure inside the alveolus is pleural pressure plus the elastic recoil. The arrows indicate direction of airflow. EPP, equal pressure point. See text for explanation. (Modified from Benumof189 )

In patients with normal lungs, airway closure may still occur even if exhalation is not forced, provided residual volume is approached closely enough. Even in patients with normal lungs, as lung volume decreases toward residual volume during expiration, the small airways (0.5–0.9 mm in diameter) show a progressive tendency to close, whereas larger airways remain patent. 83, 84  Airway closure occurs first in the dependent lung regions (as directly observed by computed tomography [CT]), 85  because the distending transpulmonary pressure is less and the volume change during expiration is greater. The airway closure is most likely to occur in the dependent regions of the lung whether the patient is in the supine or lateral decubitus position, 85  and whether ventilation is spontaneous or positive-pressure ventilation. 86, 87 

Airway Closure in Patients with Abnormal Lungs

Airway closure occurs with milder active expiration, lower gas flow rates, and higher lung volumes and occurs closer to the alveolus in patients with emphysema, bronchitis, asthma, and pulmonary interstitial edema. In all four conditions, airway resistance is increased, causing a larger pressure decrease from the alveoli to the larger bronchi, thereby creating the potential for negative intrathoracic transmural DP and narrowed and collapsed airways. In addition, the structural integrity of the conducting airways may be diminished owing to inflammation and scarring, and therefore these airways may close more readily for any given lung volume or transluminal DP.

In emphysema, the elastic recoil of the lung is reduced (to 1 cm H2 O in Fig. 15–17E), the air passages are poorly supported by the lung parenchyma, the point of airway resistance is close to the alveolus, and the transmural DP can become negative quickly. Therefore, during only a mild forced expiration in an emphysematous patient, the EPP and the point of collapse are near the alveolus (see Fig. 15–17E). Use of pursed lip or grunting expiration (the equivalents of partly closing the larynx during expiration), PEEP, and a continuous positive airway pressure in an emphysematous patient restores a favorable (distending) intrathoracic transmural air DP (Fig. 15–17F). In bronchitis, the airways are structurally weakened and may close when only a small negative transmural DP is present (as with a mild forced expiration). In asthma, the middle-size airways are narrowed by bronchospasm, and if expiration is forced, they are further narrowed by a negative transmural DP. Finally, with pulmonary interstitial edema, perialveolar interstitial edema compresses alveoli and acutely decreases FRC; the peribronchial edema fluid cuffs (within the connective tissue sheaths around the larger arteries and bronchi) compress the bronchi and acutely increase closing volume. 88, 89, 90 

Measurement of Closing Capacity

Closing capacity (CC) is a sensitive test of early smallairway disease and is performed by having the patient exhale to residual volume 91  (Fig. 15–18). An inhalation from residual volume toward total lung capacity is begun, and at the beginning of the inhalation a bolus of tracer gas (xenon-133 [133 Xe], helium) is injected into the inspired gas. During the initial part of this inhalation from residual volume, the first gas to enter the alveolus is the VD gas and the tracer bolus. The tracer gas will only enter alveoli that are already open (presumably the apices of the lung; see hatched lines, Fig. 15–18). and does not enter alveoli that are already closed (presumably the bases of the lung; see no hatched lines, Fig. 15–18) As the inhalation continues, apical alveoli complete filling and basilar alveoli begin to open and fill, but with gas that does not contain any tracer gas.

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FIGURE 15–18 Measurement of closing capacity by the use of a tracer gas such as xenon-133 (133Xe). The bolus of tracer gas is inhaled near residual volume and, owing to airway closure in the dependent lung, is distributed only to those nondependent alveoli whose air passages are still open (shown crosshatched in diagram). During expiration, the concentration of the tracer gas becomes constant after the dead space is washed out. This plateau (phase 3) gives way to a rising concentration of tracer gas (phase 4) when there is once again closure of the dependent airways because the only contribution made to the expired gas is by the nondependent alveoli with a high 133Xe concentration. (Modified from Nunn91 )

A differential tracer gas concentration is thus established; the gas in the apices has a higher tracer concentration (see Fig. 15–18, hatched lines) than that in the bases (see Fig. 15–18, no hatched lines). As the subject exhales and the diaphragm ascends, a point is reached at which the small airways just above the diaphragm start to close, limiting airflow from these areas. The airflow now comes more from the upper lung fields, where the alveolar gas has a much higher tracer concentration, which results in a sudden increase in the tracer gas concentration toward the end of exhalation (phase 4)

The closing volume (CV) is the difference between the onset of phase 4 and residual volume; because it represents part of a vital capacity maneuver, it is expressed as a percentage of the vital lung capacity. The CV plus the residual volume is known as the CC and is expressed as a percentage of total lung capacity. Smoking, obesity, aging, and the supine position increase the CC. 92  In healthy individuals at a mean age of 44 years, CC = FRC in the supine position, and at a mean age of 66 years, CC = FRC in the upright position. 93 

Relationship Between Functional Residual Capacity and Closing Capacity

The relationship between FRC and CC is far more important than consideration of the FRC or CC alone because it is this relationship that determines whether a given respiratory unit is normal or atelectatic or has a low ratio. The relationship between FRC and CC is as follows. When the volume of lung at which some airways close is greater than the whole of the VT, lung volume never increases enough during tidal inspiration to open any of these airways. Thus, these airways stay closed during the entire tidal respiration. Airways that are closed all the time are equivalent to atelectasis (Fig. 15–19). If the CV of some airways lies within the VT, then as lung volume increases during inspiration, some previously closed airways will open for a short time until lung volume recedes once again below the CV of these airways. Because these opening and closing airways are open for a shorter time than normal airways, they have less chance or time to participate in fresh gas exchange, a circumstance equivalent to a low region. If the CV of the lung is below the whole of tidal respiration, no airways are closed at any time during tidal respiration; this is a normal circumstance. Anything that decreases FRC relative to CC or increases CC relative to FRC will convert normal areas to low and atelectatic areas, 94  which causes hypoxemia.

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FIGURE 15–19 Relationship between the functional residual capacity (FRC), which is the percentage of total lung capacity that exists at the end of exhalation, shown by the level of each trough of the sine wave tidal volume, and the closing capacity (CC) of the lung (three different closing capacities are indicated by the three different straight lines). See text for explanation of why the three different FRC to CC relationships depicted result in normal or low ventilation/perfusion relationships (VA/Q) or atelectasis. The abscissa is time. (From Benumof189 )

Mechanical intermittent positive-pressure breathing (IPPB) may be efficacious because it can take a previously spontaneously breathing patient with a low relationship (in which CC is greater than FRC but still within the tidal volume, as depicted in Fig. 15–20, right panel) and increase the amount of inspiratory time that some previously closed (at end exhalation) airways spend in fresh gas exchange and thereby increase the relationship (Fig. 15–20, middle panel). However, if PEEP is added to the IPPB, the PEEP increases FRC to or above a lung volume greater than CC, thereby restoring a normal FRC to CC relationship, so that no airways are closed at any time during the tidal respiration depicted in Figure 15–20 (left panel) (IPPB + PEEP). Thus, anesthesia-induced atelectasis (CT scan shows crescent-shaped densities) in the dependent regions of patients‘ lungs has not been reversed with IPPB alone but has been reversed with IPPB plus PEEP (5–10 cm H2 O). 85

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FIGURE 15–20 The functional residual capacity to closing capacity relationship during spontaneous ventilation (SPON), intermittent positive-pressure breathing (IPPB), and intermittent positive-pressure breathing and positive end-expiratory pressure (IPPB + PEEP). See text for explanation of the effect of the two ventilatory maneuvers (IPPB and PEEP) on the functional residual capacity to closing capacity relationship. TLC, total lung capacity.