characterize specific tumors, and testing for genetic mutations may help guide treatment of certain types of lung cancer, as discussed in Chapter 21.
Recently, state-of-the-art molecular biology techniques have been applied to respiratory specimens for diagnosis of certain types of respiratory tract infection. When compared with traditional culture methods, the advantages of molecular techniques include rapid detection and specific identification of pathogens, as well as minimizing the hazard to laboratory personnel of exposure to growing pathogens. Techniques based on nucleic acid amplification can be used directly on respiratory specimens for rapid (3-4 hours) detection of the DNA or RNA of some pathogens. For example, the polymerase chain reaction uses specific synthetic oligonucleotide “primer” sequences and DNA polymerase to amplify DNA unique to a specific organism. If the particular target DNA sequence is present, even if only from a single organism, sequential amplification allows production of millions of copies that can be detected by gel electrophoresis. This technique can be applied to samples such as sputum and BAL, providing an exquisitely sensitive test for identifying organisms such as mycobacteria, P. jirovecii, and cytomegalovirus. In addition, oligonucleotide hybridization probes enable rapid identification of organisms that have been cultured from clinical specimens. These newer molecular techniques are becoming more readily available and have seen increasing clinical use over time.
Assessment on a functional level
Pulmonary evaluation on a macroscopic or microscopic level aims at a diagnosis of lung disease, but neither can determine the extent to which normal lung functions are impaired. This final aspect of evaluation adds an important dimension to overall patient assessment because it reflects how much the disease may limit daily activities. The two most common methods for determining a patient’s functional status are pulmonary function testing and evaluation of gas exchange (using either arterial blood gases or pulse oximetry). In addition, a variety of measurements taken during exercise can help determine how much exercise a patient can perform and what factors contribute to any limitation of exercise.
Pulmonary function tests
Pulmonary function testing provides an objective method for assessing functional changes in a patient with known or suspected lung disease. With the results of tests that are widely available, the physician can answer several questions: (1) Does the patient have significant lung disease sufficient to cause respiratory impairment and account for his or her symptoms? (2) What functional pattern of lung disease does the patient have—restrictive or obstructive disease?
In addition, serial evaluation of pulmonary function enables the physician to quantify any improvement or deterioration in a patient’s functional status. Information obtained from such objective evaluation may be essential in deciding when to treat a patient with lung disease and in assessing whether a patient has responded to therapy. Preoperative evaluation of patients can be useful in predicting which patients are likely to have significant postoperative respiratory problems and which are likely to have adequate pulmonary function after lung resection.
Three main categories of information can be obtained with routine pulmonary function testing:
1.Lung volumes, which provide a measurement of the size of the various compartments within the lung
2.Flow rates, which measure maximal flow within the airways
3.Diffusing capacity, which indicates how readily gas transfer occurs from the alveolus to pulmonary capillary blood
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Before examining how these tests indicate what type of functional lung disease a patient has, we briefly describe the tests themselves and how they are performed.
Lung volumes
Although the lung can be subdivided into compartments in different ways, four volumes are particularly important (Fig. 3.17):
1.Total lung capacity (TLC): total volume of gas within the lungs after a maximal inspiration
2.Residual volume (RV): volume of gas remaining within the lungs after a maximal expiration
3.Vital capacity (VC): volume of gas expired when going from TLC to RV
4.Functional residual capacity (FRC): volume of gas within the lungs at the resting state—that is, at the end of expiration during the normal tidal breathing pattern
FIGURE 3.17 Subcompartments of the lung (lung volumes). Right, Lung volumes
are labeled on spirographic tracing. Left, Block diagrams show two ways in which
total lung capacity can be subdivided. ERV, expiratory reserve volume; FRC,
functional residual capacity; IC, inspiratory capacity; RV, residual volume; TLC,
total lung capacity; VC, vital capacity; VT, tidal volume.
VC can be measured by having the patient exhale into a spirometer from TLC down to RV. By definition, the volume expired in this manner is the VC. However, because RV, FRC, and TLC all include the amount of gas left within the lungs even after a maximal expiration, these volumes cannot be determined simply by having the patient breathe into a spirometer. To quantify these volumes, a variety of methods can measure one of the three volumes, and the other two can then be calculated or derived from the spirometric tracing. Two methods are described here:
1.Dilution tests: A known volume of an inert gas (usually helium) at a known concentration is inhaled into the lungs. This gas is diluted by the volume of gas already present within the lungs, and the concentration of expired gas (relative to inspired), therefore, reflects the initial volume of gas in the lungs.
2.Body plethysmography: The patient, sitting inside an airtight box, performs a maneuver that causes expansion and compression of gas within the thorax. By measuring volume and pressure changes
and by applying Boyle’s law, the volume of gas in the thorax can be calculated.
Lung volumes are determined by spirometry and either gas dilution or body plethysmography.
In many circumstances, dilution methods are adequate for determining lung volumes. However, for patients who have air spaces within the lung that do not communicate with the bronchial tree (e.g., bullae), the inhaled gas is not diluted in these noncommunicating areas, and the measured lung volumes determined by dilution methods are falsely low. In such situations, body plethysmography gives a more accurate reflection of intrathoracic gas volume because it does not depend on ready communication of all peripheral air spaces with the bronchial tree.
Flow rates
Measurement of flow rates on routine pulmonary function testing involves assessing airflow during maximal forced expiration—that is, with the patient blowing out as hard and as fast as possible from TLC down to RV. The volume expired during the first second of such a forced expiratory maneuver is called the forced expiratory volume in 1 second (FEV1) (Fig. 3.18). When pulmonary function tests are interpreted, FEV1 is routinely compared with VC, or with VC specifically measured during the forced expiratory maneuver, called the forced vital capacity (FVC). In interpreting flow rates, the ratio between these two measurements (FEV1/VC or FEV1/FVC) is the most important number used to determine the presence of obstruction to airflow. Another parameter often calculated from the forced expiratory maneuver is the maximal mid-expiratory flow rate (MMFR), which is the rate of airflow during the middle one-half of the expiration (between 25% and 75% of the volume expired during the FVC). MMFR is frequently called the forced expiratory flow (FEF) between 25% and 75% of VC (FEF25%–75%). The MMFR or FEF25%–75% is a relatively sensitive index of airflow obstruction and may be abnormal when the FEV1/FVC ratio is still preserved.
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FIGURE 3.18 Forced expiratory spirogram. Volume is plotted against time while
the patient breathes out as hard and fast as possible from total lung capacity (TLC)
to residual volume (RV). FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity; MMFR, maximal mid-expiratory flow rate (also called forced
expiratory flow from 25%–75% [FEF25%–75%]); VC, vital capacity.
Maximal expiratory airflow is assessed by the FEV1/FVC (or FEV1/VC) ratio and MMFR (FEF25%–
75%).
Diffusing capacity
The diffusing capacity is a measurement of the rate of transfer of gas from the alveolus to hemoglobin within a capillary, measured in relation to the driving pressure of the gas across the alveolar-capillary membrane. Small concentrations of carbon monoxide are generally used for this purpose. Carbon monoxide combines readily with hemoglobin, and the rate of transfer of gas from the alveolus to hemoglobin depends on movement through the alveolar-capillary membrane and the amount of hemoglobin available for binding the carbon monoxide.
The measurement obtained during a diffusing capacity test is primarily dependent on the number of functioning alveolar-capillary units—that is, the surface area available for gas exchange—and the volume of blood (hemoglobin) in the pulmonary capillaries available to bind carbon monoxide. Because the uptake of carbon monoxide by hemoglobin is dependent on the hemoglobin concentration in the blood, patients with anemia may have a depressed diffusing capacity measurement even if the lungs are normal. Therefore, the observed value is generally corrected for the patient’s hemoglobin level.
In practice, the diffusing capacity is commonly decreased in three categories of disease in which surface area for gas exchange is lost, pulmonary capillary blood volume is decreased, or both: (1)
emphysema, (2) diffuse parenchymal lung disease, and (3) pulmonary vascular disease. In disorders that affect only the airways and not pulmonary parenchymal tissue (e.g., asthma, chronic bronchitis), diffusing capacity is generally preserved. On the other hand, the diffusing capacity may be elevated in cases of recent intrapulmonary hemorrhage as a result of uptake of carbon monoxide by hemoglobin in the erythrocytes within the alveolar spaces.
Diffusing capacity of carbon monoxide depends largely on the surface area for gas exchange and the pulmonary capillary blood volume.
Interpretation of normality in pulmonary function testing
Interpretation of pulmonary function tests necessarily involves a qualitative judgment about normality or abnormality on the basis of quantitative data obtained from these tests. To arrive at a relatively objective judgment, the patient’s values are compared with normal standards established for each test, based on measurements in large numbers of asymptomatic nonsmoking control subjects without known cardiopulmonary disease. Separate regression equations for men and women have been constructed to fit the data obtained from these normal control subjects. A “normal” or predicted value for a test in a given patient can be determined by inputting the patient’s age and height into the appropriate regression equation. Separate race-/ethnicity-specific equations may be used because of population data showing slight differences in pulmonary function in normal individuals of different races and ethnicities. Although the intent is to ensure comparison of each individual to a relevant normal standard, previous studies have not clearly accounted for the contribution of social determinants of health. Therefore, the utility of race- /ethnicity-specific equations is controversial.
The standards for determining what constitutes the “lower limits of normal” for a particular test vary among laboratories. Most laboratories now consider values below the bottom 5th percentile of a normal reference group (also called the “95% confidence interval”) to be abnormal, whereas others consider an observed value to be abnormal if it is less than 80% of the predicted value. No matter which criteria are used, all the data must be considered to determine whether certain patterns are consistently present.
Interpretation of any test in isolation, with the assumption that a patient with a value of 79% has lung disease, but a patient with a value of 81% is disease-free, is obviously dangerous.
As a general rule, the normal FEV1/VC or FEV1/FVC ratio is 0.70 or greater. This means that an individual without obstructive lung disease should, during the first second of a maximal exhalation, be able to exhale at least 70% of the total volume exhaled. However, because the normal ratio can decrease with age, the actual value ideally should be considered abnormal if it is less than the 95% confidence interval for that patient’s age.
Patterns of pulmonary function impairment
In the analysis of pulmonary function tests, abnormalities are usually categorized as one of two patterns (or a combination of the two): (1) an obstructive pattern, characterized mainly by obstruction to airflow, and (2) a restrictive pattern, with evidence of decreased lung volumes but no airflow obstruction.
An obstructive pattern, as seen in patients with asthma, chronic bronchitis, and emphysema, consists of a decrease in rates of expiratory airflow and usually manifests as a decrease in FEV1/FVC ratio,
accompanied by a decrease in MMFR (FEF25%–75%) (Fig. 3.19). There is generally a high RV and an increased RV/TLC ratio, indicating air trapping due to closure of airways during forced expiration (Fig. 3.20). Hyperinflation, reflected by an increased TLC, is often found in patients with emphysema. Diffusing capacity is decreased in patients who have loss of alveolar-capillary bed (as seen in emphysema) but not in those without loss of available surface area for gas exchange (as in chronic
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bronchitis and asthma).
FIGURE 3.19 Forced expiratory spirograms in a normal individual and a patient with airflow obstruction. Note the prolonged expiration and changes in forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) in a patient with obstructive disease. MMFR, maximal mid-expiratory flow rate.
FIGURE 3.20 Diagram of lung volumes (total lung capacity [TLC] and its
subcompartments, vital capacity [VC] and residual volume [RV]) in a normal
individual and patients with obstructive and restrictive disease.
In a patient with evidence of airflow obstruction, additional testing is often performed to assess whether the obstruction is at least partially reversible with an inhaled bronchodilator, typically an inhaled β-agonist. Clinically significant improvement or reversibility with bronchodilators is said to be present if either the FEV1 or FVC improves over baseline by at least 10% of the predicted value.
A restrictive pattern is defined by a low TLC, and the hallmark of restrictive disease is a reduction in lung volumes, although expiratory airflow is normal (see Fig. 3.20). Therefore, in addition to TLC, other volumes (RV, VC, and FRC) all tend to be reduced, whereas MMFR and FEV1/FVC are preserved. In some patients with significant loss of volume resulting from restrictive disease, MMFR is decreased because less volume is available to generate a high flow rate. Interpreting a low MMFR in the face of significant restrictive disease is difficult unless MMFR is clearly decreased out of proportion to the decrease in lung volumes.
Patterns of impairment:
1.Obstructive: diminished rates of expiratory airflow (↓ FEV1/FVC, ↓ MMFR)
2.Restrictive: diminished lung volumes (↓ TLC and often other volumes) and preserved expiratory airflow
A wide variety of parenchymal, pleural, neuromuscular, and chest wall diseases can demonstrate a
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restrictive pattern. Certain clues are useful in distinguishing among these causes of restriction. For example, a decrease in the diffusing capacity for carbon monoxide suggests loss of alveolar-capillary units and points toward diffuse parenchymal lung disease as the cause of the restrictive pattern. The finding of a relatively high RV can indicate either expiratory muscle weakness or a chest wall abnormality that makes the thoracic cage particularly stiff (noncompliant) at low volumes.
Although lung diseases often occur with one or the other of these patterns, a mixed picture of obstructive and restrictive disease can be present, making interpretation of the tests much more complex. These tests do not directly reflect a patient’s overall capability for O2 and CO2 exchange, which is assessed by measurement of arterial blood gases.
A simplified guide to the interpretation of pulmonary function tests is presented along with several sample problems in Appendix B.
Other tests
A significant amount of work was performed in the past to develop tests that detect early obstruction to airflow, particularly when it is due to small or peripheral airway obstruction. Such tests include maximal expiratory flow-volume loops, analysis of closing volume, and frequency-dependent dynamic compliance. Unfortunately, pathologic studies have shown that the correlation between tests of “small airway function” and the actual presence of disease in small airways (as demonstrated by histopathologic specimens) is inconsistent, making the value of these tests unclear. Despite this limitation, the maximal expiratory flowvolume loop is a test with sufficient routine clinical applicability to warrant a short discussion here.
The flow-volume loop is a graphic record of maximal inspiratory and maximal expiratory maneuvers. However, rather than the graph of volume versus time that is given with usual spirometric testing, the flow-volume loop has a plot of flow (on the Y-axis) versus volume (on the X-axis). Although the initial flows obtained during the early part of a forced expiratory maneuver are effort dependent, the flows during the latter part of the maneuver are effort independent and primarily reflect the mechanical properties of the lungs and the resistance to airflow.
In patients with evidence of airflow obstruction, flow rates at a given volume are decreased, often giving the curve a “scooped out” or coved appearance. The flow data obtained from maximal expiratory flow-volume loops can be interpreted quantitatively (comparing observed flow rates at specified volumes with predicted values) or qualitatively (visually analyzing the shape and concavity of the expiratory portion of the curve). When routine spirometric parameters reflecting airflow obstruction (FEV1/FVC, MMFR) are abnormal, the flow-volume loop is generally abnormal. However, in patients with early airflow obstruction, perhaps localized to small airways, the contour of the terminal part of the expiratory curve may be abnormal even when the FEV1/FVC ratio is normal. Examples of flow-volume loops in a normal patient and in a patient with obstructive lung disease are shown in Fig. 3.21.
In obstructive lung disease, the expiratory portion of the flow-volume curve typically has a “scooped out” or coved appearance.
Another important application of flow-volume loops is for diagnosing and localizing upper airway obstruction. By analyzing the contour of the inspiratory and expiratory portions of the curve, the obstruction can be categorized as fixed or variable, as well as intrathoracic or extrathoracic. In a fixed lesion, changes in pleural pressure do not affect the degree of obstruction, and a limitation in peak airflow (a plateau) is seen on both the inspiratory and expiratory portions of the curve. In a variable lesion, the amount of obstruction is determined by the location of the lesion and the effect of alterations in pleural and airway pressure with inspiration and expiration (Fig. 3.22). A variable intrathoracic lesion is
characterized by expiratory limitation of airflow and a plateau on the expiratory portion of the flowvolume curve, whereas a variable extrathoracic lesion demonstrates inspiratory limitation of airflow and a plateau on the inspiratory portion of the flow-volume curve (Fig. 3.23).
FIGURE 3.21 Flow-volume loops in a normal individual and a patient with
airflow obstruction. Expiratory “coving” is apparent on tracing of a patient with
airflow obstruction. RV(N), residual volume in normal individual; RV(O), residual
volume in a patient with obstructive disease; TLC, total lung capacity.
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FIGURE 3.22 Effect of phase of respiration on upper airway obstruction. A,
Variable extrathoracic obstruction. During forced inspiration, airway or tracheal pressure (Ptr) becomes more negative than surrounding atmospheric pressure (Patm), and airway diameter decreases. During forced expiration, more positive intratracheal pressure distends the airway and decreases the magnitude of obstruction. B, Variable intrathoracic obstruction. Pleural pressure (Ppl) surrounds and acts on large intrathoracic airways, affecting the airway diameter. During forced expiration, pleural pressure is markedly positive, and airway diameter is decreased. During forced inspiration, negative pleural pressure causes intrathoracic airways to be increased in size, and obstruction is decreased. Source: (From Kryger, M., Bode, F., Antic, R., & Anthonisen, N. (1976). Diagnosis of obstruction of the upper and lower airways. American Journal of Medicine, 61, 85–93, with permission from Excerpta Medica Inc.)
FIGURE 3.23 Maximal inspiratory and expiratory flow-volume curves in three
types of upper airway obstruction. A, Fixed obstruction, either intrathoracic or
extrathoracic. Obstruction is equivalent during inspiration and expiration, so
maximal inspiratory and expiratory flows are limited to the same extent. B, Variable
extrathoracic obstruction. Obstruction is more marked during inspiration, and only
the inspiratory part of the curve demonstrates a plateau. C, Variable intrathoracic
obstruction. Obstruction is more marked during expiration, and only the expiratory
part of the curve demonstrates a plateau. Dashed line represents higher initial flow
occasionally observed before the plateau in intrathoracic obstruction.
Source: (From Kryger, M., Bode, F., Antic, R., & Anthonisen, N. (1976). Diagnosis
of obstruction of the upper and lower airways. American Journal of Medicine, 61,
85–93, with permission from Excerpta Medica Inc.)
Upper airway obstruction can be evaluated and characterized by maximal inspiratory and expiratory flow-volume curves.
An easy and inexpensive test of airflow that is commonly used in clinical practice, particularly in patients with asthma as a method to follow severity of disease, is the peak expiratory flow rate. In performing this test, the patient blows out from TLC as hard and rapidly as possible into a simple, readily available device that records the maximal (or peak) expiratory flow rate achieved. Patients with asthma frequently perform and record serial measurements of the test at home as a way of self-monitoring their disease. A significant drop in the peak flow rate from the usual baseline often indicates an exacerbation of the disease and the need for escalating or intensifying the therapeutic regimen.
Arterial blood gases
Despite the extensive information provided by pulmonary function tests, they do not show the net effect of lung disease on gas exchange, which is easily assessed by studies performed on arterial blood. Arterial blood is usually sampled by needle puncture of a radial artery or, less commonly and with more potential risk, of a brachial or femoral artery. The blood is collected into a heparinized syringe (to prevent
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clotting), and care is taken to expel air bubbles from the syringe and analyze the sample quickly (or to keep it on ice until analyzed). Three measurements are routinely obtained: arterial PO2, PCO2, and pH.
Arterial PO2 is normally between 80 and 100 mm Hg, but the expected value depends significantly on the patient’s age and the simultaneous level of PCO2 (reflecting alveolar ventilation, an important determinant of alveolar and, secondarily, arterial PO2). From the arterial blood gases, the alveolararterial oxygen gradient (AaDO2) can be calculated, as discussed in Chapter 1. Normally, the difference between alveolar and arterial PO2 is less than 10 to 15 mm Hg in a healthy young person, and this difference increases with patient age. The oxygen content of the blood does not begin to fall significantly until the arterial PO2 drops below approximately 60 mm Hg (see Chapter 1). Therefore, an abnormally low PO2 generally does not affect O2 transport to the tissues until it drops below this level and the saturation falls.
The range of normal arterial PCO2 is approximately 36 to 44 mm Hg, with a corresponding pH between 7.44 and 7.36. Respiratory and metabolic factors interact closely in determining these numbers and a patient’s acid-base status. PCO2 and pH should be interpreted simultaneously because both pieces of information are necessary to distinguish respiratory from metabolic abnormalities.
When PCO2 rises acutely, carbonic acid is formed and the concentration of H+ also rises; therefore pH falls. As a general rule, pH falls approximately 0.08 for each 10 mm Hg increase in PCO2. Such a rise in PCO2 with an appropriate decrease in pH indicates an acute respiratory acidosis. Conversely, a drop in PCO2 resulting from hyperventilation, with the attendant increase in pH, indicates an acute respiratory alkalosis. With time (hours to days), the kidneys attempt to compensate for a prolonged respiratory acidosis by retaining bicarbonate (HCO3−), or by excreting bicarbonate in the case of a prolonged respiratory alkalosis. In either case, the compensation returns the pH value toward but not entirely to normal, and the disturbance is termed a chronic (i.e., compensated) respiratory acidosis or alkalosis.
On the other hand, a patient who is producing too much (or excreting too little) acid has a primary metabolic acidosis. Conversely, an excess of HCO3− (equivalent to a decrease in H+) defines a primary metabolic alkalosis. In the same way the kidneys attempt to compensate for a primary respiratory acidbase disturbance, respiratory elimination of CO2 is adjusted to compensate for metabolic acid-base disturbances. Hence, metabolic acidosis stimulates ventilation, CO2 elimination, and a rise in the pH toward the normal level, whereas metabolic alkalosis suppresses ventilation and CO2 elimination, and the pH falls toward the normal range.
Arterial PCO2 and pH together determine the nature of an acid-base disorder and the presence or absence of compensation.
In practice, the clinician considers three fundamental questions in defining all acid-base disturbances:
(1) Is there an acidosis or alkalosis? (2) Is the primary disorder of respiratory or metabolic origin? (3) Is there evidence for respiratory or metabolic compensation? Table 3.2 summarizes the findings in the major types of acid-base disturbances. Unfortunately, matters are not always so simple in clinical practice, and it is quite common to see complex mixtures of acid-base disturbances in patients who have several diseases and are receiving a variety of medications.
TABLE 3.2
Acid-Base Disturbances
Condition |
Pco2 |
pH |
HCO3− |
Normal |
36–44 torr |
7.36–7.44 |
23–30 mEq/L |
|
|
|
|
Respiratory Acidosis |
|
|
|
|
|
|
|
No metabolic compensation |
↑ |
↓ |
Normal (or ↑) |
|
|
|
|
With metabolic compensation |
↑ |
Lesser ↓ |
↑ |
|
|
|
|
Respiratory Alkalosis |
|
|
|
|
|
|
|
No metabolic compensation |
↓ |
↑ |
Normal (or ↓) |
|
|
|
|
With metabolic compensation |
↓ |
Lesser ↑ |
↓ |
|
|
|
|
Metabolic Acidosis |
|
|
|
|
|
|
|
No respiratory compensation |
Normal |
↓ |
↓ |
|
|
|
|
With respiratory compensation |
↓ |
Lesser ↓ |
↓ |
|
|
|
|
Metabolic Alkalosis |
|
|
|
|
|
|
|
No respiratory compensation |
Normal |
↑ |
↑ |
|
|
|
|
With respiratory compensation |
↑ |
Lesser ↑ |
↑ |
|
|
|
|
Because of the discomfort and small risk of vessel injury with arterial puncture, a venous blood sample is sometimes used as a surrogate for arterial blood gas analysis. The PCO2 in venous blood is typically slightly higher than in arterial blood, whereas the venous pH is slightly lower than arterial pH. Because venous PO2 is largely dependent on how much O2 has been extracted at the local tissue level, it does not reflect arterial PO2 and therefore is not clinically useful.
A simplified guide to the interpretation of arterial blood gases is presented along with several sample problems in Appendix C.
Pulse oximetry
Although direct measurement of arterial blood gases provides the best method for assessing gas exchange, it requires collection of blood by arterial puncture. As already noted, sampling of arterial blood is uncomfortable for patients, and a small but finite risk of complications is associated with arterial puncture. As a result, pulse oximetry, a noninvasive method for assessing arterial oxygen saturation of hemoglobin, has come into widespread use, particularly for hospitalized patients. The pulse oximeter is clipped onto a patient’s finger, and specific wavelengths of light are passed through the finger (Fig. 3.24). Oxygenated and deoxygenated hemoglobin have different patterns of light absorption, and measurement of the pulsatile absorption of light by arteriolar blood passing through the finger allows quantifying the two forms of hemoglobin. However, certain limitations are inherent in pulse oximetry: (1) the oximeter measures O2 saturation rather than PO2, (2) no information is provided about CO2 elimination and acidbase status, and (3) the results are typically inaccurate in the presence of an abnormal hemoglobin such as
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carboxyhemoglobin, as seen in carbon monoxide poisoning. Theoretically, skin pigmentation should not affect pulse oximetry because it measures the difference in absorption of oxygenated and deoxygenated hemoglobin for an individual patient. However, recent studies have suggested that pulse oximetry is less accurate in patients with darker skin as opposed to lighter skin. Thus, for all the reasons outlined above, pulse oximetry values must be considered as only part of the clinical picture.
FIGURE 3.24 Pulse oximeter. The two numbers shown on the digital display
represent the oxygen saturation and the heart rate.
Exercise testing
Because limited exercise tolerance is frequently the most prominent symptom of patients with a variety of pulmonary problems, study of patients during exercise may provide valuable information about how much these patients are limited and why. Adding measurements of arterial blood gases during exercise provides an additional dimension and shows whether gas exchange problems (either hypoxemia or hypercapnia) contribute to the impairment. Pulse oximetry commonly is also used during exercise, particularly because it is noninvasive, but it provides less information than direct measurement of arterial blood gases.
Although any form of exercise is theoretically possible for the testing procedure, the patient usually is studied while exercising on a treadmill or stationary bicycle. Measurements that can be made at various points during exercise include work output, heart rate, ventilation, O2 consumption, CO2 production, expired gas tensions, and arterial blood gases. Analysis of these data can often distinguish whether ventilation, cardiac output, or problems with gas exchange (particularly hypoxemia) provide the major limitation to exercise tolerance. The results can guide the physician to specific therapy on the basis of the type of limitation found.
A simpler form of exercise often used to assess functional limitation is the 6-minute walk test. This test measures the distance a patient is able to walk (not jog or run) in 6 minutes and whether there is a change