The greatest volume of air that can be expelled with a rapid, forced expiration is the

The reader understands the ventilation of the alveoli.

• Defines alveolar ventilation.
• Defines the standard lung volumes and understands their measurement.
• Predicts the effects of alterations in lung and chest wall mechanics, due to normal or pathologic processes, on the lung volumes.
• Defines anatomic dead space and relates the anatomic dead space and the tidal volume to alveolar ventilation.
• Understands the measurement of the anatomic dead space and the determination of alveolar ventilation.
• Defines physiologic and alveolar dead space and understands their determination.
• Predicts the effects of alterations of alveolar ventilation on alveolar carbon dioxide and oxygen levels.
• Describes the regional differences in alveolar ventilation found in the normal lung and explains these differences.
• Predicts the effects of changes in lung volume, aging, and disease processes on the regional distribution of alveolar ventilation.
• Defines the closing volume and explains how it can be demonstrated.
• Predicts the effects of changes in pulmonary mechanics on the closing volume.

Alveolar ventilation is the exchange of gas between the alveoli and the external environment. It is the process by which oxygen is brought into the lungs from the atmosphere and by which the carbon dioxide carried into the lungs in the mixed venous blood is expelled from the body. Although alveolar ventilation is usually defined as the volume of fresh air entering the alveoli per minute, a similar volume of alveolar air leaving the body per minute is implicit in this definition.

The volume of gas in the lungs at any instant depends on the mechanics of the lungs and chest wall and the activity of the muscles of inspiration and expiration. The lung volume under any specified set of conditions can be altered by pathologic and normal physiologic processes. Standardization of the conditions under which lung volumes are measured allows comparisons to be made among subjects or patients. The size of a person’s lungs depends on his or her height and weight or body surface area, as well as on his or her age and sex. Therefore, the lung volumes for a patient are usually compared with data in a table of “predicted” lung volumes matched to age, sex, and body size. The lung volumes are normally expressed at the Body Temperature and ambient Pressure and Saturated with water vapor (BTPS).

The Standard Lung Volumes and Capacities

There are 4 standard lung volumes (which are not subdivided) and 4 standard lung capacities, which consist of 2 or more standard lung volumes in combination (Figure 3–1).

Figure 3–1.

The standard lung volumes and capacities. Typical values for a 70-kg adult (standing or sitting upright) are shown.

The Tidal Volume

The tidal volume (VT) is the volume of air entering or leaving the nose or mouth per breath. It is determined by the activity of the respiratory control centers in the brain as they affect the respiratory muscles and by the mechanics of the lung and the chest wall. During normal, quiet breathing (eupnea) the VT of a 70-kg adult is about 500 mL per breath, but this volume can increase dramatically, for example, during exercise.

The Residual Volume

The residual volume (RV) is the volume of gas left in the lungs after a maximal forced expiration. It is determined by the force generated by the muscles of expiration and the inward elastic recoil of the lungs as they oppose the outward elastic recoil of the chest wall. Dynamic compression of the airways during the forced expiratory effort may also be an important determinant of the RV as airway collapse occurs, thus trapping gas in the alveoli. The RV of a healthy 70-kg adult is about 1.5 L, but it can be much greater in a disease state such as emphysema, in which inward alveolar elastic recoil is diminished and much airway collapse and gas trapping occur. The RV is important to a healthy person because it prevents the lungs from collapsing at very low lung volumes. The collapsed alveoli would require very great inspiratory efforts to reinflate.

The Expiratory Reserve Volume

The expiratory reserve volume (ERV) is the volume of gas that is expelled from the lungs during a maximal forced expiration that starts at the end of a normal tidal expiration. It is therefore determined by the difference between the functional residual capacity (FRC) and the RV. The ERV is about 1.5 L in a healthy 70-kg adult.

The Inspiratory Reserve Volume

The inspiratory reserve volume (IRV) is the volume of gas that is inhaled into the lungs during a maximal forced inspiration starting at the end of a normal tidal inspiration. It is determined by the strength of contraction of the inspiratory muscles, the inward elastic recoil of the lung and the chest wall, and the starting point, which is the FRC plus the VT. The IRV of a normal 70-kg adult is about 2.5 L.

The Functional Residual Capacity

The FRC is the volume of gas remaining in the lungs at the end of a normal tidal expiration. Because it was traditionally assumed that no muscles of respiration are contracting at the end of a normal tidal expiration, the FRC is usually considered to represent the balance point between the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall, as discussed in Chapter 2.

However, the respiratory muscles may have significant tone at the FRC, and in certain circumstances, the FRC may be greater than or even less than the lung volume of the totally relaxed respiratory system. Thus, the lung volume at which the inward elastic recoil of the lungs is equal and opposite to the outward elastic recoil of the chest wall is sometimes referred to as the relaxation volume of the respiratory system. The FRC may be greater than the relaxation volume if the next inspiration occurs before the relaxation volume is reached, either because of high breathing rates or high resistance to expiratory airflow in the larynx or peripheral airways, or because of active contraction of the inspiratory muscles at end expiration. Either or both of these may occur in babies, who have higher FRCs than would be predicted from the great inward elastic recoil of their lungs and the small outward recoil of their chest walls. During exercise, the FRC may be lower than the relaxation volume because of active contraction of the expiratory muscles.

The FRC, as seen in Figure 3–1, consists of the RV plus the ERV. It is therefore about 3 L in a healthy 70-kg adult.

The Inspiratory Capacity

The inspiratory capacity (IC) is the volume of air that is inhaled into the lungs during a maximal inspiratory effort that begins at the end of a normal tidal expiration (the FRC). It is therefore equal to the VT plus the IRV, as shown in Figure 3–1. The IC of a normal 70-kg adult is about 3 L.

The Total Lung Capacity

The total lung capacity (TLC) is the volume of air in the lungs after a maximal inspiratory effort. It is determined by the strength of contraction of the inspiratory muscles and the inward elastic recoil of the lungs and the chest wall. The TLC consists of all 4 lung volumes: the RV, the VT, the IRV, and the ERV. The TLC is about 6 L in a healthy 70-kg adult.

The Vital Capacity

The vital capacity (VC), discussed in Chapter 2, is the volume of air expelled from the lungs during a maximal forced expiration starting after a maximal forced inspiration. The VC is therefore equal to the TLC minus the RV, or about 4.5 L in a healthy 70-kg adult. The VC is also equal to the sum of the VT and the IRV and ERV. It is determined by the factors that determine the TLC and RV.

Measurement of the lung volumes is important clinically because many pathologic states can alter specific lung volumes or their relationships to one another. The lung volumes, however, can also change for normal physiologic reasons. Changing from a standing to a supine posture decreases the FRC because gravity is no longer pulling the abdominal contents away from the diaphragm. This decreases the outward elastic recoil of the chest wall, as noted in Chapter 2, Figure 2–14. The RV and TLC do not change significantly when a person changes from standing to the supine position. If the FRC is decreased, then the ERV will also decrease (Figure 3–2), and the IRV will increase. The VC, RV, and TLC may decrease slightly because some of the venous blood that collects in the lower extremities and the abdomen when a person is standing returns to the thoracic cavity when that person lies down.

Figure 3–2.

Illustration of alterations in the lung volumes and capacities that occur when a subject changes from the standing to the supine position. IC = inspiratory capacity; TLC = total lung capacity; FRC = functional residual capacity; IRV = inspiratory reserve volume; VT = tidal volume; ERV = expiratory reserve volume; RV = residual volume; VC = vital capacity.

Determination of the lung volumes can be useful diagnostically in differentiating between 2 major types of pulmonary disorders—the restrictive diseases and the obstructive diseases. Restrictive diseases like alveolar fibrosis, which reduce the compliance of the lungs, lead to compressed lung volumes (Figure 3–3). The increased elastic recoil of the lungs leads to a lower FRC, a lower TLC, a lower VC, and lower IRV and ERV, and it may even decrease the RV. The VT may also be decreased, with a corresponding increase in breathing frequency, to minimize the work of breathing.

Figure 3–3.

Illustration of typical alterations in the lung volumes and capacities in restrictive and obstructive diseases. The pattern shown for obstructive diseases is more characteristic for emphysema and asthma than for chronic bronchitis. IC = inspiratory capacity; TLC = total lung capacity; FRC = functional residual capacity; IRV = inspiratory reserve volume; VT = tidal volume; ERV = expiratory reserve volume; RV = residual volume; VC = vital capacity.

Obstructive diseases such as emphysema and chronic bronchitis cause increased resistance to airflow. Airways may become completely obstructed because of mucus plugs as well as because of the high intrapleural pressures generated to overcome the elevated airways resistance during a forced expiration. This is especially a problem in emphysema, in which destruction of alveolar septa leads to decreased elastic recoil of the alveoli and less radial traction, which normally help hold small airways open. For these reasons, the RV, the FRC, and the TLC may be greatly increased in obstructive diseases, as seen in Figure 3–3. The VC and ERV are usually decreased. The breathing frequency may be decreased to reduce the work expended overcoming the airways resistance, with a corresponding increase in the VT.

Spirometry

The spirometer is a simple device for measuring gas volumes. The traditionally used water sealed spirometer, shown in Figure 3–4, consists of an inverted canister, or “bell,” floating in a water-filled space between 2 concentrically arranged cylinders. The space inside the inner drum, which is closed off from the atmosphere by the bell, is connected to tubing that extends to a mouthpiece into which the person breathes. As the person breathes in and out, gas enters and leaves the spirometer, and the bell then floats higher (during expiration) and lower (during inspiration). The top of the bell is connected by a pulley to a pen that writes on a rotating drum, thus tracing the person’s breathing pattern.

Figure 3–4.

Determination of lung volumes and capacities with a spirometer. A: Schematic representation of a water-sealed spirometer. B: Determination of the tidal volume, vital capacity, inspiratory capacity, inspiratory reserve volume, and expiratory reserve volume from a spirometer trace.

As is evident from Figure 3–4, the spirometer can measure only the lung volumes that the subject can exchange with it. As is the case with many pulmonary function tests, the subject must be conscious and cooperative and understand the instructions for performing the test. The VT, IRV, ERV, IC, and VC can all be measured with a spirometer (as can the forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and forced expiratory flow [FEF25%–75%], as discussed in Chapter 2). The RV, the FRC, and the TLC, however, cannot be determined with a spirometer because the subject cannot exhale all the gas in the lungs. The gas in a spirometer is at Ambient Temperature, Pressure, and water vapor Saturation (ATPS), and the volumes of gas collected in a spirometer must be converted to equivalent volumes in the body. Other kinds of spirometers include rolling seal and bellows spirometers. These spirometers are not water-filled and are more portable.

Measurement of Lung Volumes Not Measurable with Spirometry

The lung volumes not measurable with spirometry can be determined by the nitrogen-washout technique, by the helium-dilution technique, and by body plethysmography. The FRC is usually determined, and RV (which is equal to FRC minus ERV) and the TLC (which is equal to VC plus RV) are then calculated from volumes obtained by spirometry.

Nitrogen-Washout Technique

In the nitrogen-washout technique, the person breathes 100% oxygen through a 1-way valve so that all the expired gas is collected. The concentration of nitrogen in the expired air is monitored with a nitrogen analyzer until it reaches zero. At this point, all the nitrogen is theoretically washed out of the person’s lungs. The total volume of all the gas the person expired is determined, and this amount is multiplied by the percentage of nitrogen in the mixed expired air, which can be determined with the nitrogen analyzer. The total volume of nitrogen in the person’s lungs at the beginning of the test can thus be determined. Nitrogen constitutes about 80% of the person’s initial lung volume, and so multiplying the initial nitrogen volume by 1.25 gives the person’s initial lung volume. If the test is begun at the end of a normal tidal expiration, the volume determined is the FRC:

Total volume expired × % N2 = original volume of N2 in lungs

Original volume of N2 in lungs × 1.25 = original lung volume

Helium-Dilution Technique

The helium-dilution technique, like other indicator dilution techniques, makes use of the following relationship: If the total amount of a substance dissolved in a volume is known and its concentration can be measured, the volume in which it is dissolved can be determined. For example, if a known amount of a solute is dissolved in an unknown volume of solvent, and the concentration of the solute can be determined, then the volume of solvent can be calculated:

Amount of solute (mg) = concentration of solute (mg/mL) × volume of solvent (mL)

In the helium-dilution technique, helium is dissolved in the gas in the lungs and its concentration is determined with a helium meter, allowing calculation of the lung volume. Helium is used for this test because it is not taken up by the pulmonary capillary blood and because it does not diffuse out of the blood, and so the total amount of helium does not change during the test. The person breathes in and out of a spirometer filled with a mixture of helium and oxygen, as shown in Figure 3–5. The helium concentration is monitored continuously with a helium meter until its concentration in the inspired air equals its concentration in the person’s expired air. At this point, the concentration of helium is the same in the person’s lungs as it is in the spirometer, and the test is stopped at the end of a normal tidal expiration, in other words, at the FRC.

Figure 3–5.

The helium-dilution technique for the determination of the functional residual capacity. A: Before the test, the spirometer is filled with a mixture of helium (denoted by the dots) and oxygen. The concentration of helium is determined by the helium meter. B: The subject breathes from the spirometer until the helium concentration in the lungs equilibrates with that in the spirometer. During the equilibration period, the subject’s expired carbon dioxide is absorbed and oxygen is added to the spirometer at the subject’s oxygen consumption rate. The helium concentration and spirometer volume are determined after equilibration, when the subject is at functional residual capacity.

The FRC can then be determined by the following formula (total amount of He before test = total amount of He at end of test):

FHEi Vspi = FHEf (Vspf + VLf)

That is, the total amount of helium in the system initially is equal to its initial fractional concentration (Fhei) times the initial volume of the spirometer (Vspi). This must be equal to the total amount of helium in the lungs and the spirometer at the end of the test, which is equal to the final (lower) fractional concentration of helium (Fhef) times the final volume of the spirometer (Vspf) and the volume of the lungs at the end of the test (Vlf). Since it may take several minutes for the helium concentration to equilibrate between the lungs and the spirometer, in practice, CO2 is absorbed from the system and oxygen is added to the spirometer at the rate at which it is consumed by the person. A correction factor is used to account for the small amount of helium that does dissolve in the blood during the test. Both the nitrogen-washout and helium-dilution methods can be used on unconscious patients.

Body Plethysmography

A problem common to both the nitrogen-washout technique and the helium-dilution technique is that neither can measure trapped gas: the nitrogen trapped in alveoli supplied by closed airways cannot be washed out and the helium cannot enter alveoli supplied by closed airways. Furthermore, if the patient’s lungs have many alveoli served by airways with high resistance to airflow (the “slow alveoli” discussed at the end of Chapter 2), it may take a very long time for all the nitrogen to wash out of the patient’s lungs or for the inspired and expired helium concentrations to equilibrate. In such patients, measurements of the lung volumes with a body plethysmograph are much more accurate because they do include trapped gas.

The body plethysmograph makes use of Boyle’s law, which states that for a closed container at a constant temperature, the pressure times the volume is constant. The body plethysmograph, an expensive piece of equipment, is shown schematically in Figure 3–6.

Figure 3–6.

The use of the body plethysmograph for the determination of the functional residual capacity. The subject is seated in the small airtight chamber and breathes through the apparatus shown. By monitoring the subject’s airflow with a pneumotachograph, the operator can briefly occlude the subject’s airway at end expiration. As the subject makes an inspiratory effort against the closed airway, the pressure in the chamber (Pbox) increases and the pressure at the subject’s mouth (Pm) decreases. The subject’s functional residual capacity can then be calculated.

As can be seen from the figure, the body plethysmograph is an airtight chamber large enough so that the patient can sit inside it. The patient sits in the closed plethysmograph, or “box,” and breathes through a mouthpiece and tubing. The tubing contains a sidearm connected to a pressure transducer (“mouth pressure”), an electrically controlled shutter that can occlude the airway when activated by the person conducting the test, and a pneumotachograph to measure airflow, allowing the operator to follow the subject’s breathing pattern. A second pressure transducer, which must be very sensitive, monitors the pressure in the plethysmograph (“box pressure”).

After the subject breathes through the open tube for a while to establish a normal breathing pattern, the operator closes the shutter in the airway at the end of a normal tidal expiration. At this point, the subject breathes in for an instant against a closed airway. As the subject breathes in against the closed airway, the chest continues to expand and the pressure measured by the transducer in the plethysmograph (Pbox) increases because the volume of air in the plethysmograph (Vbox) decreases by the amount the patient’s chest volume increased (ΔV):

Pboxi × Vboxi = Pboxf × (Vboxi − ΔV) (1)

where (Vboxi – ΔV) = Vboxf

That is, the product of the initial box pressure times the initial box volume must equal the final box pressure times the final box volume (the initial box volume minus a change in volume), according to Boyle’s law. Of course, direct measurement of box volume, which is really equal to the volume of the plethysmograph minus the volume occupied by the patient, is impossible, and so the plethysmograph is calibrated by injecting known volumes of air into the plethysmograph and determining the increase in pressure. After such a graph of pressure changes with known changes in volume has been constructed, the ΔV in Equation (1) can be determined.

The product of the pressure measured at the mouth (Pm) times the volume of the patient’s lungs (Vl) must also be constant during the inspiration against a closed airway. As the patient breathes in, the volume of the lungs increases by the same amount as the decrease in the volume of the box determined in Equation (1) above (ΔV). As the lung volume increases, the pressure measured at the mouth decreases, as predicted by Boyle’s law:

PMi × VLi = PMf × (VLi + ΔV) (2)

where (Vli + ΔV) = Vlf

The ΔV in Equation (2) is equal to that solved for in Equation (1) and Vli is now solved for. It is the FRC, since the airway was occluded at the end of a normal tidal expiration. In current practice, the patient makes several panting inspiratory efforts against the closed airway, and all the calculations described above are made automatically by a computer receiving inputs from the pressure transducers.

The volume of air entering and leaving the nose or mouth per minute, the minute volume, is not equal to the volume of air entering and leaving the alveoli per minute. Alveolar ventilation is less than the minute volume because the last part of each inspiration remains in the conducting airways and does not reach the alveoli. Similarly, the last part of each expiration remains in the conducting airways and is not expelled from the body. No gas exchange occurs in the conducting airways for anatomic reasons: The walls of the conducting airways are too thick for much diffusion to take place; mixed venous blood does not come into contact with the air. The conducting airways are therefore referred to as the anatomic dead space. They correspond to the conducting zone in Figure 1–2.

The anatomic dead space is illustrated in Figure 3–7. A subject breathes in from a balloon filled with 500 mL of a test gas such as helium (mixed with oxygen) that is not taken up by or liberated from the pulmonary capillary blood. Initially (Figure 3–7A), there is no test gas in the subject’s airways or lungs. The subject then (Figure 3–7B) breathes in all 500 mL of the gas. However, not all the gas reaches the alveoli. The final portion of the inspired gas remains in the conducting airways, completely filling them. The volume of the test gas reaching the alveoli is equal to the volume breathed in from the balloon minus the volume of the anatomic dead space, in this case 500 mL – 150 mL, or 350 mL. The 350 mL of test gas mixes with the air already in the alveoli and is diluted. During expiration (Figure 3–7C) the first gas breathed back into the balloon is the undiluted test gas that remained in the anatomic dead space. Following the undiluted test gas is part of the gas that reached the alveoli and was diluted by the alveolar air. The last 150 mL of alveolar gas breathed out remains in the anatomic dead space. The concentration of test gas collected in the balloon after expiration is lower than it was before the breath but higher than the concentration left in the alveoli and conducting airways because it is composed of pure test gas from the anatomic dead space and diluted test gas from the alveoli.

Figure 3–7.

Illustration of the anatomic dead space. A: The subject inspires 500 mL from a balloon filled with a high concentration of a test gas (denoted by the dots). B: At the end of the inspiration, only 350 mL of the test gas has reached the alveoli. This 350 mL is added to the 2 to 3 L of alveolar gas already in the lungs at the functional residual capacity, and so its concentration is diluted. The other 150 mL of test gas remains virtually unchanged in the subject’s anatomic dead space. C: At end expiration, diluted test gas remains virtually unchanged in the subject’s anatomic dead space, and it remains equally concentrated in alveolar air and in the anatomic dead space. The test gas in the balloon is a mixture of undiluted gas from the dead space and diluted alveolar gas.

Therefore, for any respiratory cycle, not all the VT reaches the alveoli because the last part of each inspiration and each expiration remains in the dead space. The relationship among the VT breathed in and out through the nose or mouth, the dead space volume (Vd), and the volume of gas entering and leaving the alveoli per breath (Va) is:

Thus, if a person with an anatomic dead space of 150 mL has a VT of 500 mL per breath, then only 350 mL of gas enters and leaves the alveoli per breath.

The alveolar ventilation (per minute) can be determined by multiplying both sides of the above equation by the breathing frequency (n) in breaths per minute:

Thus, if n = 12 breaths per minute in the example above:

The alveolar ventilation

in liters per minute is equal to the minute volume (

) minus the volume wasted ventilating the dead space per minute (

):

The dot over the letter V indicates per minute. The symbol

is used because expired gas is usually collected. There is a difference between the volume of gas inspired and the volume of gas expired because as air is inspired, it is heated to body temperature and humidified and also because normally less carbon dioxide is produced than oxygen is consumed. (See the alveolar air equation on pages below.)

Alveolar ventilation cannot be measured directly but must be determined from the VT, the breathing frequency, and the dead-space ventilation, as noted in the previous section.

Determination of Anatomic Dead Space

For a normal, healthy subject, the anatomic dead space can be estimated by referring to a table of standard values matched to sex, age, height, and weight or body surface area. A reasonable estimate of anatomic dead space is 1 mL of dead space per pound of ideal body weight. The anatomic dead space can be determined by using Fowler’s method. This method uses a nitrogen meter to analyze the expired nitrogen concentration after a single inspiration of 100% oxygen. The expired gas volume is measured simultaneously. Fowler’s method is summarized in Figure 3–8.

Figure 3–8.

Fowler’s method for the determination of anatomic dead space. A: The subject takes a single breath of 100% oxygen, holds his or her breath for a second, and then exhales. Nitrogen concentration is monitored along with the volume of gas expired, in this case by integrating with time the airflow (L/s) determined by a pneumotachograph-differential air pressure transducer system. B: The volume of gas expired between the beginning of the exhalation and the midpoint of the rising phase of the expired nitrogen concentration trace is the anatomic dead space. (The midpoint is determined such that the 2 shaded areas are equal.)

The subject breathes in a single breath of 100% oxygen through a 1-way valve, holds it in for a second, and then exhales through the 1-way valve. Nitrogen concentration at the mouth and the volume expired are monitored simultaneously.

Initially, the nitrogen concentration at the mouth is 80%, the same as that of the ambient atmosphere. As the stopcock is turned and the subject begins to inspire 100% oxygen, the nitrogen concentration at the mouth falls to zero. The subject holds his or her breath for a second or so and then exhales through the valve into a spirometer or pneumotachograph. The first part of the expired gas registers 0% nitrogen because it is undiluted 100% oxygen from the anatomic dead space. In the transitional period that follows, the expired gas registers a slowly rising nitrogen concentration. During this time, the expired gas is a mixture of dead-space gas and alveolar gas because of a gradual transition between the conducting pathways and the respiratory bronchioles, as was seen in Figure 1–2. The final portion of expired gas comes solely from the alveoli and is called the alveolar plateau. Its nitrogen concentration is less than 80% because some of the inspired breath of 100% oxygen reached the alveoli and diluted the alveolar nitrogen concentration, as shown in Figure 3–7. The volume of the anatomic dead space is the volume expired between the beginning of the expiration and the midpoint of the transitional phase, as shown in Figure 3–8. Fowler’s method is rarely used clinically.

Physiologic Dead Space: The Bohr Equation

Fowler’s method can be used to determine the anatomic dead space. It does not, however, permit the calculation of another form of wasted ventilation in the lung—the alveolar dead space.

The alveolar dead space is the volume of gas that enters unperfused alveoli per breath. Alveolar dead space is therefore alveoli that are ventilated but not perfused with venous blood. No gas exchange occurs in these alveoli for physiologic, rather than anatomic, reasons. A healthy young person has little or no alveolar dead space, but a person with a low cardiac output might have a great deal of alveolar dead space, for reasons explained in the next chapter.

The Bohr equation permits the determination of the sum of the anatomic and the alveolar dead space. The anatomic dead space plus the alveolar dead space is known as the physiologic dead space:

Physiologic dead space = anatomic dead space + alveolar dead space

The Bohr equation makes use of a simple concept: Any measurable volume of carbon dioxide found in the mixed expired gas must come from alveoli that are both ventilated and perfused because there are negligible amounts of carbon dioxide in inspired air. Inspired air remaining in the anatomic dead space or entering unperfused alveoli will leave the body as it entered (except for having been heated to body temperature and humidified), contributing little or no carbon dioxide to the mixed expired air:

The

of the collected mixed expired gas can be determined with a CO2 meter. The CO2 meter is often also used to estimate the alveolar

by analyzing the gas expelled at the end of a normal tidal expiration, the “end-tidal CO2” (Figure 3–9). But in a person with significant alveolar dead space, the estimated alveolar

obtained in this fashion may not reflect the

of alveoli that are ventilated and perfused because some of this mixed end-tidal gas comes from unperfused alveoli. This gas dilutes the CO2 coming from alveoli that are both ventilated and perfused. There is, however, an equilibrium between the

of perfused alveoli and their end-capillary

(see Chapter 6 for detailed discussion), so that in patients without significant venous-to-arterial shunts, the arterial

represents the mean

of the perfused alveoli. Therefore, the Bohr equation should be rewritten as:

Figure 3–9.

A normal capnograph: Partial pressure of carbon dioxide at the mouth as determined by an infrared carbon dioxide meter or mass spectrometer. During inspiration the

rapidly decreases to near zero (0.3 mm Hg). The first expired gas comes from the anatomic dead space, and therefore also has a

near zero. After exhalation of a mixture of gas from alveoli and anatomic dead space, the gas expired is a mixture from all ventilated alveoli. The slope of the alveolar plateau normally rises slightly because the alveolar

increases a few mm Hg between inspirations. The last alveolar gas expired before inspiration is called end-tidal.

The VT is determined with a spirometer, and the physiologic dead space is then calculated.

If the arterial

is greater than the mixed alveolar

determined by sampling the end-tidal CO2, then the physiologic dead space is probably greater than the anatomic dead space; that is, a significant arterial-alveolar CO2 difference means that there is significant alveolar dead space. As already noted, this difference is determined from the

from an arterial blood gas sample and from the end-tidal

. Situations in which alveoli are ventilated but not perfused include those in which portions of the pulmonary vasculature have been occluded by blood clots from the venous blood (pulmonary emboli), situations in which there is low venous return leading to low right ventricular output (hemorrhage), and situations in which alveolar pressure is high (positive-pressure ventilation with positive end-expiratory pressure).

The anatomic dead space can be altered by bronchoconstriction, which decreases Vd; bronchodilation, which increases Vd; or traction or compression of the airways, which increases and decreases Vd, respectively.

The levels of oxygen and carbon dioxide in the alveolar gas are determined by the alveolar ventilation, the oxygen consumption (

o2) of the body, and the carbon dioxide production of the body (

). Each inspiration brings into the 3 L of gas already in the lungs approximately 350 mL of fresh air containing about 21% oxygen, and each expiration removes about 350 mL of air containing about 5% to 6% carbon dioxide. Meanwhile, about 250 mL of carbon dioxide per minute diffuses from the pulmonary capillary blood into the alveoli, and about 300 mL of oxygen per minute diffuses from the alveolar air into the pulmonary capillary blood.

Partial Pressures of Respiratory Gases

According to Dalton law, in a gas mixture, the pressure exerted by each individual gas is independent of the pressures of other gases in the mixture. The partial pressure of a particular gas is equal to its fractional concentration times the total pressure of all the gases in the mixture. Thus, for any gas in a mixture (gas1) its partial pressure is

Oxygen constitutes 20.93% of dry atmospheric air. At a standard barometric pressure of 760 mm Hg,

(The unit mm Hg is also expressed as torr, in honor of Evangelista Torricelli, the inventor of the barometer.) Carbon dioxide constitutes only about 0.04% of dry atmospheric air, and so,

As air is inspired through the upper airways, it is heated and humidified, as will be discussed in Chapter 10. The partial pressure of water vapor is a relatively constant 47 mm Hg at body temperature, and so the humidification of 1 L of dry gas in a closed container at 760 mm Hg would increase its total pressure to 760 mm Hg + 47 mm Hg = 807 mm Hg. In the body, the gas will simply expand, according to Boyle’s law, so that 1 L of gas at 760 mm Hg is diluted by the added water vapor. The

of inspired air, or

(saturated with water vapor at a standard barometric pressure), then is equal to the fractional concentration of inspired oxygen (the

) times the barometric pressure minus the water vapor pressure:

where PB = barometric pressure and Ph2o = the water vapor pressure

0.2093 (760 – 47) mm Hg = 149 mm Hg

The

of inspired air (the

) is equal to the Fico2 (Pb –Ph2o) or 0.0004 (760 – 47) mm Hg = 0.29 mm Hg. This rounds back up to 0.3 mm Hg.

Alveolar gas is composed of the 2.5 to 3 L of gas already in the lungs at the FRC and the approximately 350 mL per breath entering and leaving the alveoli. About 300 mL of oxygen is continuously diffusing from the alveoli into the pulmonary capillary blood per minute at rest and is being replaced by alveolar ventilation. Similarly, about 250 mL of carbon dioxide is diffusing from the mixed venous blood in the pulmonary capillaries into the alveoli per minute and is then removed by alveolar ventilation. (The

and

of mixed venous blood are about 40 mm Hg and 45 to 46 mm Hg, respectively.) Because of these processes, the partial pressures of oxygen and carbon dioxide in the alveolar air are determined by the alveolar ventilation, the pulmonary capillary perfusion, the oxygen consumption, and the carbon dioxide production. Alveolar ventilation is normally adjusted by the respiratory control center in the brain to keep mean arterial and alveolar

at about 40 mm Hg (see Chapter 9). Mean alveolar

is about 104 mm Hg.

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Alveolar Gas at Standard Barometric Pressure

	104 mm Hg
Paco2	40 mm Hg
Pan2	569 mm Hg
Pah2o	47 mm Hg

The alveolar

increases by 2 to 4 mm Hg with each normal tidal inspiration and falls slowly until the next inspiration. Similarly, the alveolar

falls 2 to 4 mm Hg with each inspiration and increases slowly until the next inspiration. Expired air is a mixture of about 350 mL of alveolar air and 150 mL of air from the dead space. Therefore, the

of mixed expired air is greater than alveolar

and lower than the inspired

, or approximately 120 mm Hg. Similarly, the

of mixed expired air is much greater than the inspired

but lower than the alveolar

, or about 27 mm Hg.

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Mixed Expired Air at Standard Barometric Pressure

Peo2	120 mm Hg
Peco2	27 mm Hg
Pen2	566 mm Hg
Peh2o	47 mm Hg

Alveolar Ventilation and Carbon Dioxide

The concentration of carbon dioxide in the alveolar gas is, as already discussed, dependent on the alveolar ventilation and on the rate of carbon dioxide production by the body (and its delivery to the lung in the mixed venous blood). The volume of carbon dioxide expired per unit of time (

) is equal to the alveolar ventilation

times the alveolar fractional concentration of CO2

. No carbon dioxide comes from the dead space:

Similarly, the fractional concentration of carbon dioxide in the alveoli is directly proportional to the carbon dioxide production by the body (

) and inversely proportional to the alveolar ventilation:

In healthy people, alveolar

is in equilibrium with arterial

(Paco2). Thus, if alveolar ventilation is doubled (and carbon dioxide production is unchanged), then the alveolar and arterial

are reduced by one-half. If alveolar ventilation is cut in half, near 40 mm Hg, then alveolar and arterial

will double. This can be seen in the upper part of Figure 3–10.

Figure 3–10.

Predicted alveolar gas tensions for different levels of alveolar ventilation. (Reprinted by permission of Elsevier Science Limited from Nunn JF. Applied Respiratory Physiology. 4th ed. Elsevier Science; 1993.)

Alveolar Ventilation and Oxygen

It is evident that as alveolar ventilation increases, the alveolar

will also increase. Doubling alveolar ventilation, however, cannot double

in a person whose alveolar

is already approximately 104 mm Hg because the highest

one could possibly achieve (breathing air at sea level) is the inspired

of about 149 mm Hg. The alveolar

can be calculated by using the alveolar air equation. (The derivation of this formula is outside the scope of this book.)

As alveolar ventilation increases, the alveolar

decreases, bringing the alveolar

closer to the inspired

, as can be seen in the lower part of Figure 3–10. Note that the alveolar

obtained using the alveolar air equation is a calculated idealized average alveolar

. It represents what alveolar

should be, not necessarily what it is.

The respiratory exchange ratio, R, represents the whole body carbon dioxide produced per time divided by the whole body oxygen consumption per time. It is primarily dependent on the foodstuffs metabolized by the cells of the body. In a person with a typical mixed diet, it is approximately 0.8; a person consuming a diet consisting of mainly carbohydrates or proteins would have an R of approximately 1.0; a person consuming a diet consisting of mainly fat would have an R of approximately 0.7.

As previously discussed, a 70-kg person has about 2.5 to 3 L of gas in the lungs at the FRC. Each eupneic breath brings about 350 mL of fresh gas into the alveoli and removes about 350 mL of alveolar air from the lung. Although it is reasonable to assume that the alveolar ventilation is distributed fairly evenly to alveoli throughout the lungs, this is not the case. Studies performed on normal subjects seated upright have shown that alveoli in the lower regions of the lungs receive more ventilation per unit volume than do those in the upper regions of the lung.

Demonstration of Differences between Dependent and Nondependent Regions

If a normal subject, seated in the upright posture and breathing normally (inspiring from the FRC), takes a single breath of a mixture of oxygen and radioactive Xe, the relative ventilation of various regions of the lung can be determined by placing scintillation counters over appropriate areas of the thorax, as shown in Figure 3–11.

Figure 3–11.

Regional distribution of alveolar ventilation as determined by a breath of a mixture of Xe and O2. (Reproduced with permission, Data of Bryan, 1964.)

It is assumed that if the oxygen and Xe are well mixed, then the amount of radioactivity measured by the scintillation counters in each region will be directly proportional to the relative ventilation (the ventilation per unit volume) in each region.

The results of a series of such experiments are shown on the graph on the right side of Figure 3–11. In a subject seated in the upright posture and breathing normally from the FRC, the lower regions of the lung are relatively better ventilated than the upper regions of the lung.

If a similar study is done on a subject lying on his or her left side, the regional differences in ventilation between the anatomic upper, middle, and lower regions of the lung disappear, although there is better relative ventilation of the left lung than of the right lung. The regional differences in ventilation thus appear to be influenced by gravity, with regions of the lung lower with respect to gravity (the “dependent” regions) relatively better ventilated than those regions above them (the “nondependent” regions).

Explanation for Differences in Regional Alveolar Ventilation

In Chapter 2, the intrapleural surface pressure was discussed as if it were uniform throughout the thorax. Precise measurements made of the intrapleural surface pressures of intact chests in the upright position have shown that this is not the case: The intrapleural surface pressure is less negative in the lower, gravity-dependent regions of the thorax than it is in the upper, nondependent regions. There is a gradient of the intrapleural surface pressure such that for every centimeter of vertical displacement down the lung (from nondependent to dependent regions) the intrapleural surface pressure increases by about +0.2 to +0.5 cm H2O. This gradient is apparently caused by gravity and by mechanical interactions between the lung and the chest wall.

The influence of this gradient of intrapleural surface pressure on regional alveolar ventilation can be explained by predicting its effect on the transpulmonary pressure gradients in upper and lower regions of the lung. The left side of Figure 3–12 shows that alveolar pressure is zero in both regions of the lung at the FRC. Since the intrapleural pressure is more negative in upper regions of the lung than it is in lower regions of the lung, the transpulmonary pressure (alveolar minus intrapleural) is greater in upper regions of the lung than it is in lower regions of the lung. Because the alveoli in upper regions of the lung are subjected to greater distending pressures than those in more dependent regions of the lung, they have greater volumes than the alveoli in more dependent regions.

Figure 3–12.

Effect of the pleural surface pressure gradient on the distribution of inspired gas at the functional residual capacity (FRC). (Reproduced with permission from Milic-Emili, 1977.)

It is this difference in volume that leads to the difference in ventilation between alveoli located in dependent and nondependent regions of the lung. This can be seen on the hypothetical pressure-volume curve shown on the right side of Figure 3–12. This curve is similar to the pressure-volume curve for a whole lung shown in Figure 2–6, except that this curve is drawn with the pressure-volume characteristics of single alveoli in mind. The abscissa is the transpulmonary pressure (alveolar pressure minus intrapleural pressure). The ordinate is the volume of the alveolus expressed as a percent of its maximum.

The alveolus in the upper, nondependent region of the lung has a larger transpulmonary pressure than does the alveolus in a more dependent region because the intrapleural pressure in the upper, nondependent regions of the lung is more negative than it is in more dependent regions. Because of this greater transpulmonary pressure, the alveolus in the upper region of the lung has a greater volume than the alveolus in a more gravity-dependent region of the lung. At the FRC, the alveolus in the upper part of the lung is on a less steep portion of the alveolar pressure-volume curve (ie, it is less compliant) in Figure 3–12 than is the more compliant alveolus in the lower region of the lung. Therefore, any change in the transpulmonary pressure during a normal respiratory cycle will cause a greater change in volume in the alveolus in the lower, gravity-dependent region of the lung than it will in the alveolus in the nondependent region of the lung, as shown by the arrows in the figure. Because the alveoli in the lower parts of the lung have a greater change in volume per inspiration and per expiration, they are better ventilated than those alveoli in nondependent regions (during eupneic breathing from the FRC).

A second effect of the intrapleural pressure gradient in a person seated upright is on regional static lung volume, as is evident from the above discussion. At the FRC, most of the alveolar air is in upper regions of the lung because those alveoli have larger volumes. Most of the ERV is also in upper portions of the lung. On the other hand, most of the IRV and IC (the ability to take air into the alveoli) are in lower regions of the lung.

Alterations of Distribution at Different Lung Volumes

As discussed in the previous section, most of the air inspired during a tidal breath begun at the FRC enters the dependent alveoli. If a slow inspiration is begun at the RV, however, the initial part of the breath (inspiratory volume less than the ERV) enters the nondependent upper alveoli, and dependent alveoli begin to fill later in the breath. The intrapleural pressure gradient from the upper parts of the lung to the lower parts of the lung is also the cause of this preferential ventilation of nondependent alveoli at low lung volumes.

Positive intrapleural pressures are generated by the expiratory muscles during a forced expiration to the RV. This results in dynamic compression of small airways, as described in Chapter 2. At the highest intrapleural pressures these airways close, and gas is trapped in their alveoli. Because of the gradient of intrapleural pressure found in the upright lung, at low lung volumes the pleural surface pressure is more positive in lower regions of the lung than it is in upper regions. Also, alveoli in lower lung regions have less alveolar elastic recoil to help hold small airways open because they have smaller volumes than do the alveoli in upper regions. This means that airway closure will occur first in airways in lower regions of the lung, as can be seen in the hypothetical alveolar pressure-volume curve at the RV shown in Figure 3–13. The expiratory effort has ended and the inspiratory effort has just begun. Airways in the lowest regions of the lung are still closed, and the local pleural surface pressure is still slightly positive. No air enters these alveoli during the first part of the inspiratory effort (as indicated by the horizontal arrow) until sufficient negative pressure is generated to open these closed airways.

Figure 3–13.

Effect of the pleural surface pressure gradient on the distribution of inspired gas at the residual volume (RV). (Reproduced with permission from Milic-Emili, 1977.)

In contrast to the situation at the FRC, at the RV the alveoli in the upper regions of the lungs are now on a much steeper portion of the pressure-volume curve. They now have a much greater change in volume per change in transpulmonary pressure—they are more compliant at this lower lung volume. Therefore, they receive more of the air initially inspired from the RV.

It has already been noted that even at low lung volumes the upper alveoli are larger in volume than are the lower gravity-dependent alveoli. They therefore constitute most of the RV.

Patients with emphysema have greatly decreased alveolar elastic recoil, leading to high FRCs, extremely high RVs, and airway closure in dependent parts of the lung even at high lung volumes. They therefore have relatively more ventilation of nondependent alveoli.

The lung volume at which airway closure begins to occur is known as the closing volume. It can be demonstrated by utilizing the same equipment used in Fowler’s method for the quantification of the anatomic dead space seen in Figure 3–8. This method can also demonstrate some maldistributions of alveolar ventilation.

The subject, seated upright, starts from the RV and inspires a single breath of 100% oxygen all the way up to the TLC. The person then exhales all the way back down to the RV. Nitrogen concentration at the mouth and the volume of gas expired are monitored simultaneously throughout the second expiration.

Consider what occurs during the first expiration to the RV. Because of the gradient of intrapleural pressure from the top of the lung to the bottom of the lung, the alveoli in upper parts of the lung are larger than those in lower regions of the lung. Any gas left in the lungs at the end of this initial forced expiration to the RV is about 80% nitrogen, and so most of the nitrogen (and most of the RV) is in upper parts of the lung. Alveoli in lower portions of the lung have smaller volumes, and thus contain less nitrogen. At the bottom part of the lung, airways are closed, trapping whatever small volume of gas remains in these alveoli.

The subject then inspires 100% oxygen to the TLC. Although the initial part of this breath will probably enter the upper alveoli, as described previously, most of the 100% oxygen will enter the more dependent alveoli. (The very first part, which does enter the upper alveoli, is dead-space gas, which is 80% nitrogen anyway.) If the nitrogen concentration of alveoli in different parts of the lung could be measured at this point, the nitrogen concentration would be highest in the upper regions of the lung and the lowest in the lower regions of the lung.

The subject then exhales to the RV as the expired nitrogen concentration and gas volume are monitored. The expired nitrogen concentration trace is shown in Figure 3–14.

Figure 3–14.

Expired nitrogen concentration after inhalation of a single breath of 100% oxygen from the residual volume to the total lung capacity. Subject exhales to the residual volume. Phase I: 0% nitrogen from anatomic dead space. Phase II: mixture of gas from anatomic dead space and alveoli. Phase III: “alveolar plateau” gas from alveoli. A steep slope of phase III indicates nonuniform distribution of alveolar gas. Phase IV: closing volume. Takeoff point (closing capacity) of phase IV denotes beginning of airway closure in dependent portions of the lung.

The first gas the subject exhales (phase I) is gas from the anatomic dead space. It is still virtually 100% oxygen or 0% nitrogen. The second portion of gas exhaled by the subject (phase II) is a mixture of dead-space gas and alveolar gas. The third portion of gas expired by the subject is mixed alveolar gas from the upper and lower regions (phase III, or the “alveolar plateau”).

Note that in a healthy person the slope of phase III is nearly horizontal. In patients with certain types of airways-resistance maldistribution, the phase III slope rises rapidly. This is because those alveoli that are supplied by high-resistance airways fill more slowly than those supplied by the normal airways during the 100% oxygen inspiration. Thus, they have a relatively higher nitrogen concentration. During expiration they empty more slowly, and when they do, the expired nitrogen concentration rises.

As the expiration to the RV continues, the positive pleural surface pressure causes dynamic compression and ultimately airway closure. Because of the intrapleural pressure gradient from the upper parts of the lung to the lower parts of the lung and because the smaller alveoli in lower parts of the lung have less elastic recoil, the airway closure first occurs in lower regions of the lung where the nitrogen concentration is the lowest. Thus, as airway closure begins, the expired nitrogen concentration rises abruptly because more and more of the expired gas is coming from alveoli in upper regions of the lung. These alveoli have the highest nitrogen concentration. The point at which the expired nitrogen concentration trace rises abruptly is the volume at which airway closure in dependent parts of the lung begins. At this point, the subject is at his or her closing capacity, which is equal to the RV plus the volume expired between the beginning of airway closure and the RV. This volume is called the closing volume. (Unfortunately, many people, the author included, commonly use the terms closing volume and closing capacity interchangeably.) The problem with the closing volume test is that patients with increased airways resistance have rapidly increasing nitrogen concentrations during phase III because the units that have normal low resistance to airflow get most of the oxygen. They fill first on inspiration and empty first on expiration. As more gas comes from the high resistance units, the expired nitrogen concentration increases, so the rapid upstroke in phase IV nitrogen concentration may not occur.

Aging causes important changes in the structure and function of the respiratory system. These include a loss of alveolar elastic recoil, alterations in chest wall structure causing it to have increased outward elastic recoil, decreased respiratory muscle strength, and a loss of alveolar surface area and pulmonary capillary blood volume.

The progressive loss of alveolar elastic recoil, combined with calcification of costal cartilages, decreased spaces between the spinal vertebrae, and a greater degree of spinal curvature, leads to increased static lung compliance and decreased chest wall compliance. This usually leads to an increase in the FRC with aging, as shown in Figure 3–15. The TLC, if adjusted for the decrease in height seen in older people, stays fairly constant with age.

Figure 3–15.

Illustration of the alterations in the standard lung volumes and capacities occurring with age. TLC = total lung capacity; FRC = functional residual capacity; ERV = expiratory reserve volume; RV = residual volume; IC = inspiratory capacity; VC = vital capacity; CC = closing capacity. (Reproduced with permission from Levitzky, 1984.)

Loss of alveolar elastic recoil results in decreased traction on small airways to oppose dynamic compression during forced expirations, as well as decreased driving pressures for airflow. This leads to airway closure at higher lung volumes, as shown by the rising closing capacity illustrated in Figure 3–15, and, combined with a decrease in the strength of the expiratory muscles, leads to an increase in the RV and decreased maximal expiratory airflow rates such as the FEF25%–75% and FEV1. As shown in Figure 3–15, airway closure may occur in dependent airways of the elderly even at lung volumes above the FRC. Such older persons may therefore have relatively more ventilation of upper airways than do younger individuals. If blood flow to these poorly ventilated dependent regions is not reduced, this will lead to decreased arterial oxygen tension, which will be discussed in Chapter 5. The loss of alveolar surface area and decreased pulmonary capillary blood volume result in a decreased pulmonary diffusing capacity, which will be discussed in Chapter 6. This can also contribute to a progressive decrease in arterial oxygen tension with aging.

Alveolar ventilation is less than the volume of air entering or leaving the nose or mouth per minute (the minute volume) because the last part of each inspiration remains in the conducting airways (the anatomic dead space).

Alveoli that are ventilated but not perfused constitute alveolar dead space.

The physiologic dead space is the sum of the anatomic dead space and the alveolar dead space.

At constant carbon dioxide production, alveolar

is approximately inversely proportional to alveolar ventilation; alveolar

must be calculated with the alveolar air equation.

At or near the functional residual capacity, alveoli in lower regions of the upright lung are relatively better ventilated than those in upper regions of the lung.

What is the effect on each of the following standard lung volumes and capacities of changing from a supine to an upright position?

a. Functional residual capacity (FRC)

c. Expiratory reserve volume (ERV)

d. Total lung capacity (TLC)

f. Inspiratory reserve volume (IRV)

g. Inspiratory capacity (IC)

As a person stands up, the effects of gravity alter the mechanics of breathing (and also decrease venous return). The contents of the abdomen are pulled away from the diaphragm, thus increasing the outward elastic recoil of the chest wall. The inward recoil of the lungs is not affected, and so the functional residual capacity (FRC) is increased. The residual volume (RV) is relatively unaffected. The expiratory reserve volume (ERV) increases because the FRC is increased and the RV is relatively unchanged. The total lung capacity (TLC) may increase slightly because of the slightly decreased inward elastic recoil of the chest wall at high lung volumes and because the abdominal contents are pulled away from the diaphragm. The tidal volume (VT) is probably unchanged. The higher FRC and similar TLC and VT lead to a decrease in the inspiratory reserve volume (IRV) and a decrease in the inspiratory capacity (IC). The vital capacity (VC) is also relatively unchanged, although it may be slightly increased because of the slight increase in TLC and the decreased intrathoracic blood volume.

How would the predicted values for the standard lung volumes and capacities and the closing capacity of a healthy elderly person differ from those of a young healthy person?

Assuming general good health and normal weight, the main changes seen with age are a loss of pulmonary elastic recoil and a slight increase of the elastic recoil of the chest wall, especially at higher volumes. The loss of pulmonary elastic recoil has the secondary effect of increasing airway closure in dependent areas of the lung at the lower lung volumes. For these reasons, the FRC will be increased and the RV may be greatly increased, with the TLC slightly decreased. The VT should be unchanged or may be either slightly increased or decreased, depending on whether the increased lung compliance, increased airways resistance, or decreased chest wall compliance predominates. The ERV will decrease because the increase in RV due to airway closure is greater than the increase in FRC. IRV and IC are decreased, as is the VC. The closing volume is also increased.

A volume of 1 L of gas is measured in a spirometer at 23°C (296 K; Ph2o is 21 mm Hg), and barometric pressure is 770 mm Hg.

a. What would the volume be under STPD conditions?

b. What would the volume be under BTPS conditions?

V2 = V1 × temperature correction × pressure correction

Pressure correction = P1V1 = P2V2

Combining the two, we get

Note that temperatures must be expressed in degrees Kelvin (K) when these corrections are made.

A subject starts at her FRC and breathes 100% O2 through a 1-way valve. The expired air is collected in a very large spirometer (called a Tissot spirometer). The test is continued until the expired N2 concentration, as measured by a nitrogen analyzer, is virtually zero. At this time, there are 36 L of gas in the spirometer, of which 5.6% is N2. What is the subject’s FRC?

The volume of N2 in the spirometer is 0.056 × 36 L, or 2.0 L. This is the volume of N2 in the subject's lungs when the test began (at her FRC). Since N2 constituted 80% of her FRC, her FRC is equal to 100 ÷ 80 × 2.0 L, or 1.25 × 2.0 L, which is equal to 2.5 L.

A 63-year-old woman who is 5 ft 5 in. tall and weighs 100 lb complains of dyspnea. During the determination of her lung volumes, she rebreathes the gas in a 20-L-capacity spirometer that originally contained 10 L of 15% helium. After a number of breaths, the concentration of helium in her lungs is equal to that now in the spirometer, which is 11% helium. (During the equilibration period, the expired CO2 was absorbed by an absorbent chemical in the spirometer and O2 was added to the spirometer at the subject’s

.) At the end of a normal expiration, the spirometer contains 10.64 L when corrected to BTPS. What is her FRC?

Because helium is not absorbed or given off by the lung, the initial amount of helium in the system must equal the final amount of helium in the system. The amount is equal to the fractional concentration times the volume:

FHEi × Vspi = FHEf (Vspf + VLf)

where F = fractional concentration

• V = volume
• sp = spirometer
• L = lungs
• i = initial
• f = final (after equilibration)

Because the test was ended at the end of a normal expiration, VLf equals the subject's FRC.

The same patient discussed in the previous problem, now in a body plethysmograph, breathes normally through a mouthpiece. At the end of a normal expiration, a valve in the mouthpiece is closed. The next inspiratory effort is made against the closed valve. Additional air cannot enter the lungs; instead, the inspiratory effort lowers the pressure at the mouth by 10 mm Hg and expands the gas in the lungs by 50 mL, as determined by the increase in the plethysmograph pressure and its calibration curve with the subject in the box. What is the patient’s FRC measured with this technique?

PMi × VLi = PMf × (VLi + Δ V)

• V = volume
• M = mouth
• L = lung
• i = initial
• f = final

Because the valve was closed at the end of a normal expiration, VLi equals the subject's FRC.

How do you explain the difference between the 2 FRCs obtained for this patient?

Assuming that the 2 tests have been done correctly, this patient has approximately 750 mL of trapped gas at her FRC.

A patient on a ventilator has a rate of 10 breaths per minute and a tidal volume (VT) of 500 mL.

a. What is the patient’s

?

b. If the patient’s anatomic dead space is estimated to be 150 mL, what is his

?

c. If his rate is increased to 15 breaths per minute with VT remaining at 500 mL, what will his new

and

be?

d. If his VT is increased to 750 mL, with his rate remaining at 10 breaths per minute, what will his new

and

be?

a.

is

b.

is

c. The new

and

are

d. The new

and

are

The following measurements were made on a patient when the barometric pressure was 747 mm Hg:

where F

co2 = fractional concentration of CO2 in the subject’s mixed expired air.

What is the patient’s Vd/VT? What is the patient’s physiologic dead space? Assuming the patient’s anatomic dead space is 100 mL, what is her alveolar dead space? Is this patient’s arterial

likely to be lower than, greater than, or equal to her end-tidal

?

Since

= anatomic dead space + alveolar dead space, the alveolar dead space = 50 mL. The presence of alveolar dead space results in an arterial end-tidal

difference, so arterial

should exceed end-tidal.

A person with a

of 40 mm Hg, a

of 104 mm Hg, and a respiratory exchange ratio of 0.8 breathing room air at a barometric pressure of 760 mm Hg doubles alveolar ventilation. What will this person’s new steady-state

and

be (assuming no change in oxygen consumption and carbon dioxide production and assuming that the correction factor [F] = 0)?

If alveolar ventilation doubles, alveolar

is cut in half:

From Raff H, Levitzky MG, eds. Medical Physiology: A Systems Approach. New York: McGraw-Hill; 2011:339–340.

A 38-year-old man with an obvious curvature of the spine in the coronal and sagittal planes is seen by a pulmonologist because of dyspnea that has gotten worse during the last few months. He is 163 cm (5 ft 4 in.) tall and weighs 61.2 kg (135 lb). Blood pressure is 135/95 mm Hg, heart rate is 80/min, and his respiratory rate is tachypnic at 25 breaths/min. His respiratory muscle strength appears to be normal. The pulmonologist orders pulmonary function tests and an arterial blood gas (with reference ranges in parenthesis) with the following results:

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Total Lung Capacity (TLC):	45% predicted
Vital Capacity (VC):	40% predicted
Residual Volume (RV):	75% predicted
Functional Residual Capacity (FRC):	50% predicted
Forced Expiratory Volume in 1 second (FEV1):	40% predicted
Forced Vital Capacity (FVC):	40% predicted
FEV1/FVC:	80% (100% of predicted)
Arterial Po2	75 mm Hg (80–100 mm Hg)
Arterial Pco2	46 mm Hg (35–45 mm Hg)
Arterial pH	7.38 (7.35–7.45)

The patient has kyphoscoliosis, which is a lateral curvature of the spine (scoliosis), as well as a sagittal curvature (kyphosis). It can be congenital; secondary to many disorders, including muscular dystrophy, poliomyelitis, spina bifida, and cerebral palsy; or it may be idiopathic (of unknown cause). Kyphoscoliosis results in decreased compliance of the rib cage with much less outward recoil of the chest wall at low thoracic volumes and much greater inward recoil at higher volumes. Kyphoscoliosis is therefore a restrictive disease.

It is difficult for the patient to breathe in and, as a result, his inspiratory work of breathing is increased. It explains his increased resting respiratory rate (normally 12–15 breaths/min) because taking smaller tidal volumes at an increased breathing frequency decreases his work of breathing. The effects of the changes in the mechanics of his thorax can be seen in the lung volumes and capacities determined in this patient (see Figure 3–3). His FRC is low because, with less outward recoil of his chest wall, the balance point between the outward recoil of the chest wall and the inward recoil of his lungs occurs at a lower lung volume. His TLC is low because his ability to inhale maximally is severely impaired. His RV is also lower than predicted, but not as much as the TLC, because his ability to exhale is not as impaired. His VC, FVC, and FEV1 are all lower than predicted because his TLC is very low—he cannot exhale very much because he is unable to inhale very much. On the other hand, this patient does not have airway obstruction. Although both his FEV1 and FVC are low, the FEV1/FVC is within the normal range. The blood gases demonstrate that the increased work of breathing has resulted in decreased alveolar ventilation. His arterial

is high and his arterial

is low.

Treatment of patients with kyphoscoliosis is aimed at improving alveolar ventilation, for example, with noninvasive mechanical ventilation at night. Orthopedic surgery to help correct the problem may be effective in some patients.

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Cotes JE. Lung Function: Assessment and Application in Medicine. 4th ed. Oxford: Blackwell; 1979.

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Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. London: Churchill Livingstone; 2011:83–98, 119–123.

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Milic-Emili J. Pulmonary statics. In: Widdicombe JG, ed. MTP International Review of Sciences: Respiratory Physiology. London, England: Butterworth; 1974:105–137.

Milic-Emili J. Static distribution of lung volumes. In: Macklem PT, Mead J, eds. Mechanics of Breathing, part 2, Handbook of Physiology, sec 3: The Respiratory System. Bethesda, MD: American Physiological Society; 1986;3:561–574.

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Which peak flow zone indicates that large airways are beginning to narrow?

What is a patient's peak expiratory flow rate quizlet?

Which of the following measures and evaluates a patient's lung capacity and volume?

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