Clinical Scenarios—Do These Patients Have Airflow Limitation?
In each of the following cases, the clinician needs to decide whether the patient has airflow limitation. In case 1, a 63-year-old man who has smoked 2 packs of cigarettes per day for the past 47 years presents with decreased exercise tolerance caused by shortness of breath. In case 2, a 35-year-old woman complains of coughing, wheezing, and shortness of breath every autumn. In case 3, an 18-year-old man is brought to an emergency department, with extreme difficulty breathing that began earlier that evening.
Why Is It Important to Detect Airflow Limitation by Clinical Examination?
Airflow limitation is a disorder known by many names, including airway obstruction and obstructive airways disease. Recognizing airflow limitation can lead to appropriate treatment and can yield important prognostic information. Patients with symptomatic airflow limitation may benefit by treatment with oral or inhaled bronchodilators, oral or inhaled glucocorticoids, or antibiotics. Recognition of this disorder also triggers environmental controls and preventive services, such as vaccination against pneumococcus and influenza.
Screening is advocated for target disorders in which early intervention favorably affects patient outcomes. Physicians do not screen for airflow limitation because early intervention has not been shown to alter the disease course. Therefore, clinicians are likely to want to confirm or rule out disease in patients presenting with pulmonary symptoms, such as cough or dyspnea, rather than screen for unrecognized disease in asymptomatic individuals.
The 3 clinical scenarios illustrate cases in which recognizing airflow limitation by the clinical examination is important. In the first case, recognizing airflow limitation might lead to the diagnosis of pulmonary emphysema, more intensive counseling on smoking cessation, vaccination against influenza and pneumococcal infection, and bronchodilator therapy to improve exercise tolerance. In the second case, recognizing airflow limitation might lead to the identification of environmental irritants or allergens responsible for symptoms. In the third case, recognizing airflow limitation would lead to the diagnosis of asthma and to acute, potentially lifesaving therapy with bronchodilators and systemic glucocorticoids. Recognizing airflow limitation clinically may have time, cost, and convenience advantages compared to routine pulmonary function testing.
Spirometry is the test of choice for confirming a diagnosis of airflow limitation. Both the forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) values are reduced in patients with airflow limitation; because the FEV1 is affected more than the FVC, the ratio of FEV1 to FVC (FEV1/FVC) also decreases. The reduced FEV1/FVC is the hallmark of airflow limitation. Although emphysema and chronic bronchitis represent permanent reductions in airflow, asthma is a disorder characterized by increased responsiveness of the bronchial tree to a variety of stimuli, leading to intermittent airflow limitation.1 In patients with asthma, provocative testing, such as methacholine challenge, may be necessary to bring about airflow limitation between symptomatic episodes.
The reference standard for airflow limitation is the measurement of the FEV1 and the FVC by spirometry. An FEV1/FVC lower than the fifth percentile for age, height, and sex is considered abnormal.2 However, a normal FEV1/FVC during an asymptomatic period does not rule out intermittent airflow limitation. For most patients, the fifth percentile of FEV1/FVC is approximately 70%, but using this single value to diagnose airflow limitation is discouraged.2
We performed an English-language MEDLINE search, using the following Medical Subject Headings: (EXP Medical History Taking OR EXP Physical Examination) AND (EXP Lung Diseases, Obstructive). The titles and abstracts of the 1022 articles retrieved from the above MEDLINE search were reviewed independently by the 2 authors. If either reviewer chose an article as possibly useful, the article was reviewed for content. The authors had excellent agreement (κ = 0.85) on the 158 articles chosen for full review. If the article contained results of the clinical examination predicting airflow limitation, the article was reviewed for quality. References from appropriate articles were reviewed for additional references. Nineteen articles evaluating the clinical examination for airflow limitation3-21 used the accepted definition or a similar spirometric definition of disease. Others used a variety of definitions, including FEV1 only22-27 or other, less-accepted or unclear definitions.28-37 We chose to include articles using reference standards that are not currently accepted because they were otherwise methodologically sound or they provided the only data available for some of the clinical examination findings. The reference standards used in studies evaluating operating characteristics for individual clinical examination items are listed in Table 13-1. Because all studies used reference standards of current airflow limitation, the results in this review can be used only to predict airflow limitation at the evaluation. Patients with asthma may be overlooked if examined between attacks.
Table 13-1Reference Standards Used in Studies Yielding Operating Characteristics for Individual Clinical Examination Items |Favorite Table|Download (.pdf) Table 13-1 Reference Standards Used in Studies Yielding Operating Characteristics for Individual Clinical Examination Items
|Reference Standard ||References |
|FEV1 < fifth percentile and FEV1/FVC < fifth percentilea ||14 |
|FEV1/FVC < fifth percentile ||11 |
|FEV1/FVC < 0.70 ||5-8, 16, 18, 22 |
|FEV1/FVC < 0.75 and FVC < 80% of predicted ||9 |
|FEV1 < 75% of predicted and FEV1/FVC < 0.80 ||20 |
|FEV1 < 70% of predicted ||23, 24 |
|FEV1 < 2 L ||25, 26 |
|FEV1 < fifth percentile ||37 |
|FEV1 < 60% of predicted or FEV1/FVC < 0.60 ||17 |
|Roentgenography, total lung capacity, and residual capacity ||33 |
|FEV1/FVC < 0.6 or history ||31 |
|Diagnosis of asthma ||32 |
|Normal spirometry ||30 |
Pathophysiologic Characteristics of Airflow Limitation
Understanding the physiologic characteristics of pulmonary airflow helps to explain the clinical examination findings in airflow limitation. The airways are a branching system of tubes that link the outside atmosphere with the lung parenchyma. During inspiration, the thoracic cavity actively expands. As the chest volume increases, the intrathoracic pressure decreases. Because the airways are open to the atmosphere, air flows into the airways to equalize the intrathoracic pressure with the atmospheric pressure. Therefore, during inspiration, the pressure inside the airways is greater than the pressure in the surrounding lung. This pressure exerts a force on the inner wall of the airway, increasing the airway diameter during inspiration.
At end inspiration, the chest no longer expands, and the intrathoracic-to-atmospheric pressure difference disappears. During expiration, the thoracic cavity passively contracts. As the chest volume decreases, the intrathoracic pressure increases and exceeds the atmospheric pressure. Because the airways communicate with the atmosphere, the pressure inside the airways is lower than the pressure in the surrounding lung. This pressure difference exerts a force on the outer wall of the airway, decreasing the airway diameter during expiration. The resistance to airflow is inversely and exponentially related to the diameter of the airway, so small decreases in airway diameter lead to large increases in resistance.
During inspiration and expiration, the diameter of the airway varies around its static, resting diameter. In airflow limitation, the resting airway diameter is abnormally small. In emphysema, the lung parenchyma is destroyed. This leads to a decrease in the tethering forces that maintain airway diameter, resulting in decreased resting airway diameter. In asthma, the smooth muscle that surrounds the airway is hyperreactive to various stimuli. When one of these stimuli is present, the smooth muscle contracts. This leads to decreased resting diameter of the airway. In chronic bronchitis, there is increased mucus production in the airways. There may also be decreased mucus clearance caused by ciliary dysfunction. The resulting increased intra-airway mucus coats the inner wall of the airway. This leads to decreased resting diameter of the airway. Thus, in airflow limitation syndromes, the resistance to airflow is increased throughout the respiratory phase. Because of the further physiologic decrease in airway diameter during expiration, it is significantly more difficult to empty the lungs than to fill them. This leads to air trapping and to lung hyperinflation that can be demonstrated by an abnormally large residual volume on pulmonary function testing.
The touted physical examination findings for airflow limitation arise either from the difficulty in emptying the lungs or from the resulting hyperinflation. The prolonged expiratory phase, wheezing, rhonchi, and match test are signs of abnormally high resistance to airflow during expiration. Decreased breath sounds, barrel chest, hyperresonance, decreased cardiac and hepatic dullness, absent or subxiphoid cardiac apical impulse, decreased chest expansion, and decreased diaphragmatic movement are signs of hyperinflation. Use of accessory muscles results from both the increased work of expiration and pulmonary hyperinflation.
How to Elicit Symptoms and Signs of Airflow Limitation
A concise evaluation for airflow limitation includes a focused medical history and physical examination.
The history should elicit background features and specific symptoms.
The most important background features are exposure to cigarette smoke and to occupational or environmental pollutants. The duration of cigarette exposure can most easily be elicited by asking at what age the patient started smoking and in what year he or she quit. Although pack-years is the traditional measure of cigarette exposure, quantifying years of exposure works at least as well.13 The patient's personal and family history of atopic diseases is also associated with increased likelihood of asthma.
The most important symptoms to elicit from patients with suspected airflow limitation are wheezing, coughing, and sputum production. In fact, chronic bronchitis is defined by sputum production for at least 3 consecutive months in at least 2 consecutive years.1
The physical examination for airflow limitation should include inspection, measuring vital signs, palpation, percussion, auscultation, and expiratory airflow.
While assessing the patient's overall appearance, the clinician should observe for the presence of a barrel chest. If the anteroposterior diameter appears greater than normal, the patient has a barrel chest deformity. This finding may be more an illusion than a true deformity because the anteroposterior dimensions have not been shown to be increased in patients with clinically defined barrel chests.38
While measuring blood pressure, the clinician can determine whether there is pulsus paradoxus. This maneuver may be most helpful in patients with suspected acute airflow limitation. During tidal breathing, the sphygmomanometer is inflated to above the systolic blood pressure. The cuff pressure is slowly released until the first Korotkoff sound is heard only during expiration; this systolic blood pressure value is noted. The cuff pressure is further reduced until the first Korotkoff sound is heard throughout inspiration; the systolic blood pressure at this point is also noted. The systolic blood pressure is normally lower during inspiration than during expiration. The normal difference is accentuated when the patient has airflow limitation. If the difference between these 2 pressures is at least 15 mm Hg, the patient has pulsus paradoxus.
Palpation should include locating the cardiac apical impulse. Chest palpation should be performed with the patient supine and disrobed from the waist up. A sheet or gown should be used to maintain patient comfort and privacy; however, palpation should be performed with the hand directly on the chest wall. When the chest volume is increased because of hyperinflation, the cardiac apex shifts to a more central location and either may not be palpable or may be palpable in the subxiphoid area.
The chest should be percussed to determine the quality of the sound that resonates. Percussion of the chest wall should be performed by placing a digit (usually the second or third) of the nondominant hand firmly against the chest wall parallel to and between the ribs. The second and third digits of the dominant hand are flexed slightly at the metacarpophalangeal and proximal and distal interphalangeal joints to form a slight arch with the 2 fingertips even. The fingertips of the dominant hand tap the distal interphalangeal joint of the nondominant hand with a firm pecking motion. If the sound is more hollow than normal, the chest is hyperresonant.
Clinicians should auscultate the chest for wheezes, rhonchi, and breath sound intensity. Chest auscultation should be performed in a quiet room with the patient disrobed from the waist up. The warmed stethoscope diaphragm should be placed with moderate pressure on the patient's chest to ensure good sound transmission. The chest should be auscultated bilaterally over the lower, middle, and upper lung fields posteriorly, anteriorly, and along the midaxillary line. Patients should be breathing heavily, but not forcefully. Wheezing will be heard as high-pitched musical tones especially during expiration. Rhonchi are lower-pitched wheezes.39 The intensity of breath sounds should be observed. Although elaborate scoring systems for breath sound intensity9, 26 and for wheezing16 have been developed, they are not clearly better than the customary normal vs abnormal dichotomization.
Measures of expiratory airflow include the forced expiratory time13, 17 and the match test.16, 24, 25 To perform a forced expiratory time test, the patient must take a deep breath and forcefully exhale until no more air can be expelled. During this maneuver, the patient must keep mouth and glottis fully open as if the patient were yawning. While the patient is performing the forced expiration, the clinician listens over the larynx or lower trachea with a stethoscope and times the duration of audible airflow. To obtain the best results, the forced expiratory time should be measured with a stopwatch and recorded to the nearest 0.1 second. An alternative maneuver is the match test. During this test, the patient performs a forced expiration exactly as in the forced expiratory time maneuver. However, the clinician holds a burning match 10 cm from the patient's widely open mouth. If the match is still burning after the forced expiration, the test result is positive. Others have used a candle for this test. However, one needs a match to light a candle, and we can find no benefit in carrying around both except for those who frequently practice in the dark. Also, to avoid malpractice claims and personal injury, we do not recommend this test in patients receiving supplemental oxygen!
Precision of History and Symptoms for Airflow Limitation
The observer agreement for smoking history, dyspnea, coughing, wheezing, chronic bronchitis, and orthopnea has been described with the κ statistic.13 Two physicians almost always agree on the smoking history (κ = 0.95). Physicians agree frequently on the presence or absence of wheezing (κ = 0.61), chronic bronchitis (κ = 0.55), dyspnea (κ = 0.44-0.48), and coughing (κ = 0.46).
Accuracy of Medical History and Symptoms for Airflow Limitation
Table 13-2 summarizes the operating characteristic estimates for airflow limitation, obtained for each historical item and symptom, after pooling data from referenced studies.
Table 13-2Composite Operating Characteristics of History Items Predicting Airflow Limitation |Favorite Table|Download (.pdf) Table 13-2 Composite Operating Characteristics of History Items Predicting Airflow Limitation
|Item ||Grade of Recommendationa ||References ||Sensitivity, % ||Specificity, % ||LR+ ||LR– |
|Smoking history |
|≥70 vs <70 pack-years ||B ||17 ||40 ||95 ||8.0 ||0.63 |
|Ever vs never ||A ||6, 7, 14 ||92 ||49 ||1.8 ||0.16 |
|Sputum production ≥ 1/4 cup ||B ||17 ||20 ||95 ||4 ||0.84 |
|Symptoms of chronic bronchitis ||A ||14, 20 ||30 ||90 ||3.0 ||0.78 |
|Wheezing ||B ||14 ||51 ||84 ||3.8 ||0.66 |
|Exertional dyspnea |
|Grade 4 vs 3 or less ||A ||20 ||03 ||99 ||3.0 ||0.98 |
|Any vs none ||A ||20 ||27 ||88 ||2.2 ||0.83 |
|Coughing ||B ||14 ||51 ||71 ||1.8 ||0.69 |
|Any dyspnea ||B ||14 ||82 ||33 ||1.2 ||0.55 |
The best background information for diagnosing airflow limitation is exposure to cigarette smoke. Although patients who have smoked are only slightly more likely to have airflow limitation,5, 6, 13 never having smoked cigarettes is moderately well associated with decreased likelihood of disease.5, 6, 13 Perhaps more useful is the fact that the number of years the patient has smoked correlates well with the likelihood of disease (Figure 13-1).13 Patients with at least a 70-pack-year history of smoking are much more likely to have airflow limitation.16
Predicting Probability of Airflow Obstruction at the Bedside
Choose the number of years the patient smoked cigarettes under the “Smoking History” heading; use scale A if the patient reports no symptoms of wheezing or scale B if the patient reports symptoms of wheezing. Under “Wheezing on Examination,” select “No” if wheezing was absent or “Yes” if wheezing was present (alternatively, the best of 3 peak expiratory flow [PEF] rates could be chosen under the “PEF” heading). With a straightedge, connect the points chosen on the “Smoking History” and “Wheezing on Examination” lines. Read the probability of airflow limitation where the straightedge intersects the line under the “Probability of Airflow Obstruction” heading.
Reprinted from Holleman et al,13 with the permission of the Journal of General Internal Medicine.
Age is related to airflow limitation. Asthma is more common in the young, whereas chronic bronchitis and emphysema are more common in older patients. The prevalence of airflow limitation appears to be lowest between ages 10 and 30 years.40 The higher prevalence at younger ages is due to asthma, which frequently remits after childhood. The higher prevalence in the older age group is probably due to 2 factors. First, age is a proxy for exposure to toxins, especially cigarette smoke. When smokers and nonsmokers are analyzed separately, the prevalence of airflow limitation does not appear to increase significantly with age in nonsmokers.41 Second, in adults, most airflow limitation is a chronic disease, so new incident cases are added faster than attrition from mortality, except in the very old. Therefore, advancing age is associated with increased likelihood of airflow limitation in adult smokers, but airflow limitation should not be considered a normal process of aging.
Symptoms of chronic bronchitis,13, 19 sputum production of at least one-fourth of a cup when present,16 or wheezing13, 36 are associated with a moderate increase in the likelihood of airflow limitation. However, symptoms of cough5, 13 or exertional dyspnea13, 36 are associated with only a slight increase in the likelihood of airflow limitation. Orthopnea is not useful in diagnosing airflow limitation, because its positive likelihood ratio (LR+) and negative likelihood ratio (LR–) are not significantly different from 1.13 No single symptom effectively rules out airflow limitation. The absence of dyspnea5, 13, 36 or of exertional dyspnea13, 36 is only moderately useful in ruling out disease.
Precision of the Signs of Airflow Limitation
Precision has not been studied for most inspection items, and physicians agree only part of the time that a patient has a cough (κ = 0.29),13 which can probably be explained largely by patients having paroxysms of coughing. They may cough during one, but not the other, examination.
The precision of pulsus paradoxus has not been well studied.
Physicians agree only part of the time on the results of palpating for an absent apical impulse (κ = 0.39).34 Physician agreement on whether a patient has a subxiphoid apical impulse may be no greater than chance (κ = 0-0.3).13, 16 However, the low prevalence of this finding may lead to underestimating the chance-corrected agreement.
Physicians appear to agree infrequently on the results of chest percussion. However, only hyperresonance (κ = 0-0.42)16, 37 and diaphragmatic excursion (κ = –0.04; r = 0.24) have been studied.16, 35
Physicians agree frequently on the results of auscultation for wheezing (κ = 0.43-0.93),13, 16, 37 whereas they agree less frequently on breath sound intensity (κ = 0.23-0.47)13, 16, 28, 37 and crackles (κ = 0.30-0.63).37
Physicians frequently obtain the same results when measuring forced expiratory time (intraclass correlation, 0.81; κ = 0.7)13, 17 or interpreting the match test (κ = 0.39).16 Agreement on the forced expiratory time is better if a stopwatch is used instead of a second hand.
Accuracy of The Signs of Airflow Limitation
Table 13-3 summarizes the operating characteristic estimates for airflow limitation, obtained for each sign, after pooling data from referenced studies.
Table 13-3Composite Operating Characteristics of Physical Examination Items Predicting Airflow Limitation |Favorite Table|Download (.pdf) Table 13-3 Composite Operating Characteristics of Physical Examination Items Predicting Airflow Limitation
|Itema ||Grade of Recommendationb ||References ||Sensitivity, % ||Specificity, % ||LR+ ||LR– |
|Wheezing ||A ||14, 17, 34 ||15 ||99.6 ||36 ||0.85 |
| ||Bc ||32 ||10 ||99 ||10 ||0.90 |
|Decreased cardiac dullness ||B ||17 ||13 ||99 ||10 ||0.88 |
|Match test ||B ||17, 25, 26 ||61 ||91 ||7.1 ||0.43 |
|Rhonchi ||B ||31, 32 ||8 ||99 ||5.9 ||0.95 |
|Hyperresonance ||B ||17 ||32 ||94 ||4.8 ||0.73 |
|Forced expiratory time, sd ||A ||14, 18 || || || || |
|>9 || || || || ||4.8 || |
|6-9 || || || || ||2.7 || |
|<6 || || || || ||0.45 || |
|Subxiphoid cardiac apical impulse ||B ||14, 17 ||8 ||98 ||4.6 ||0.94 |
|Pulsus paradoxus (>15 mm Hg) ||C ||8, 23, 24 ||45 ||88 ||3.7 ||0.62 |
|Decreased breath sounds ||B ||14, 17 ||37 ||90 ||3.7 ||0.70 |
|Accessory muscle use ||C ||33, 37 ||24 ||100 ||e ||0.70 |
|Excavated supraclavicular fossae ||C ||37 ||31 ||100 ||e ||0.69 |
A barrel chest 31, 32 predicts airflow limitation. However, the evidence for this association comes largely from one study in asthmatic children. Recent studies using currently accepted reference standards have failed to include this finding. Therefore, the value of the barrel chest sign in adults is not well supported. Other inspection items (accessory muscle use, excavated supraclavicular fossae, and coughing) have not been studied in a large enough sample of patients to determine the extent of their usefulness in diagnosing airflow limitation.13, 32, 36 In other words, their likelihood ratio confidence intervals are wide and include 1.42 Decreased chest expansion and kyphosis have been studied only in patients with known disease,32 so their usefulness has not yet been determined. Patients who do not use accessory muscles32, 36 or who do not have excavated supraclavicular fossae are only slightly less likely to have airflow limitation.36 Patients without a barrel chest31, 32 or who do not cough13 are significantly less likely to have airflow limitation but the clinical importance of the absence of these findings is negligible. Therefore, the only inspection item we can recommend is looking for a barrel chest. The presence of this finding, especially in children, virtually rules in airflow limitation.
The presence of pulsus paradoxus of at least 15 mm Hg is associated with only a moderate increase in the likelihood of airflow limitation, and the absence of this sign is associated with only a slight reduction in the likelihood of disease.7, 22, 23 Other vital signs have not been studied and cannot be recommended for use in determining the likelihood of airflow limitation.
Palpating a subxiphoid cardiac apical impulse is associated with a moderate increase in the likelihood of airflow limitation. However, the absence of this finding is not useful.13, 16 Absent apical impulse has been studied only in patients with known disease,32 so its usefulness has not yet been determined. Therefore, according to current evidence, we recommend palpating the subxiphoid region for the cardiac apical impulse. We recommend this despite the reportedly low observer agreement because the low prevalence of this finding may lead to underestimates of the chance-corrected agreement.
Chest hyperresonance on percussion is associated with a moderate increase in the likelihood of disease.16, 32 Neither decreased cardiac dullness nor decreased diaphragmatic movement has been studied in enough patients to determine definitively the extent of usefulness.16 However, patients with decreased cardiac dullness are more likely to have airflow limitation. Decreased liver dullness has been studied only in patients with known disease,32 so its usefulness has not yet been determined. Patients without chest hyperresonance are only slightly less likely to have airflow limitation.16, 32 Normal cardiac dullness and normal diaphragmatic movement are likely not useful for decreasing the likelihood of airflow limitation.16 We recommend percussing the chest for the resonance sound. Hyperresonance over the precordium may be particularly useful for increasing the likelihood of airflow limitation.
Objective wheezing, or wheezing observed on physical examination, is the most potent predictor of airflow limitation. Patients with wheezing almost certainly have airflow limitation.13, 15, 16, 37 However, this is true only of wheezing on unforced expiration. Forced expiration is associated with increased sensitivity of wheezing, and with decreased specificity. The current literature suggests that the presence or absence of wheezing on forced expiration is of no value in diagnosing or ruling out airflow limitation.15, 20 Additionally, the sensitivity of wheezing increases with the severity of airflow limitation.13 Studies that recruited patients referred for spirometry15, 36 yielded sensitivities greater than those found in unreferred populations.13, 16 Although the sensitivity of wheezing varies greatly (10%-50%) by study population, the LR+ and LR– change little. Rhonchi were associated with a moderate increase in the likelihood of airflow limitation in 2 studies30, 31; however, because neither study explicitly defined rhonchi and because there is significant variability in how physicians define rhonchi,43 this result must be interpreted cautiously. Decreased breath sounds are associated with only a moderate increase in the likelihood of disease.13, 16, 32 Absent wheezing,13, 15, 16, 36 normal breath sound intensity,13, 16, 32 or absent rhonchi30, 31 are associated with only a moderate decrease in the likelihood of disease. We recommend auscultating the chest for wheezes and for breath sound intensity. Patients with wheezing should be considered to have airflow limitation, and patients with decreased breath sound intensity should be considered somewhat more likely to have airflow limitation. Patients without wheezing or with normal breath sound intensity should be considered somewhat less likely to have this disorder. Neither the presence nor absence of crackles (rales) helps with the diagnosis of airflow limitation.8, 13, 29
Patients who are unable to extinguish a lighted match held 10 cm from the open mouth are significantly more likely to have airflow limitation than patients who are able to extinguish a match. The ability to extinguish a match is associated with a moderate decrease in the likelihood of disease.16, 24, 25 The forced expiratory time4, 5, 10, 11, 13, 16-18 is a continuous variable that can range from a few tenths of a second to more than 20 seconds. Unfortunately, each of the 4 best studies of forced expiratory time10, 13, 16, 17 used different methods. Two studies10, 16 used average expiratory time, which makes bedside use cumbersome. Of the other 2 studies, one used the shortest expiratory time of 3 trials;13 the other, the longest expiratory time of 2 trials.17 Because the ability to discriminate between patients with and without airflow limitation is the same regardless of whether the shortest or longest time is used,13 there is no clear advantage to one method over the other. To allow pooling of results, one of the studies13 was reanalyzed with the longest rather than the shortest time. When the longest expiratory time is chosen, a result less than 6 seconds was associated with a modest decrease in the likelihood of airflow limitation; a result between 6 and 9 seconds was associated with a modest increase in the likelihood of airflow limitation; and a result greater than 9 seconds was associated with a great increase in the likelihood of airflow limitation. A forced expiratory time of approximately 9 seconds predicts an FEV1/FVC of 70%,8 a level suggesting the diagnosis of airflow limitation.
Peak expiratory flow rates predict airflow limitation (Figure 13-1).13 However, 2 studies have shown that peak expiratory flow adds little to the clinical examination for airflow limitation.13, 16 In one study,16 peak expiratory results improved the accuracy of the clinical examination for only 1 of the 4 physicians studied. In the other study,13 peak expiratory flow was equivalent to auscultating for wheeze, but more difficult to assess. Therefore, we cannot recommend routine peak flow measurements in the diagnosis of airflow limitation. Peak flow measurements may be useful in assessing benefit from therapy, especially for asthma.
Can the Clinical Examination Predict Severity of Airflow Limitation?
Stubbing et al3 found that the number of positive findings (tracheal descent during inspiration, sternomastoid contraction, scalene contraction, supraclavicular fossae excavation, supraclavicular fossae recession, intercostal recession, or costal margin movement) predicted the severity of airflow limitation in patients with known disease. These findings tended to be present only if the FEV1 was less than 50% of the predicted value. The American Thoracic Society1, 2 found that the number of positive findings (barrel chest, low diaphragm, decreased diaphragmatic excursion, decreased breath sounds, prolonged expiratory phase, wheezing, noisy inspiration, or crackles) predicted the severity of airflow limitation (r = 0.6). The literature suggests that, as airflow becomes more limited, more physical examination findings become apparent.
Accuracy of the Overall Clinical Impression for Predicting Airflow Limitation
Three studies 14, 17, 33 evaluated the accuracy of the overall clinical impression or a clinician's ability to integrate all aspects of the clinical examination in forming an impression about the likelihood of airflow limitation. Clinicians’ overall impressions13 (graded as moderate to severe limitation [LR+ = 4.2], mild [LR+ = 0.82], or none [LR+ = 0.42]), predicted any airflow limitation only moderately well. However, Badgett et al16 found that clinicians’ impressions (blinded to medical history but not physical examination) predicted moderate to severe airflow limitation somewhat better (LR+ = 7.3; LR– = 0.53) and about as well as some of the individual findings in Table 13-3. On the other hand, Fletcher32 evaluated the clinical impressions of 6 physicians and found sensitivities ranging from 15% to 95% for airflow limitation. Therefore, clinicians’ ability to diagnose airflow limitation clinically is variable, but accuracy seems to improve as the severity of airflow limitation increases.
Combinations of Individual Findings
Six studies (Table 13-4) assessed the usefulness of combining clinical examination items to predict airflow limitation. Unfortunately, as with individual findings, combinations of findings do not effectively rule out airflow limitation. The best combination is never having smoked, no reported wheezing, and no wheezing on examination (Figure 13-1; LR–, 0.18).13 Other combinations have LR– values ranging from 0.33 to 0.77. Even the best combination is no better than smoking history alone (LR–, 0.16). Therefore, combinations of findings are more helpful for ruling in than for ruling out this disorder. In fact, a patient with any combination of 2 findings (≥70-pack-year history of smoking, history of chronic obstructive pulmonary disorder, or decreased breath sounds) can be considered to have airflow limitation.16
Table 13-4Combinations of Clinical Examination Items Predicting Airflow Limitation |Favorite Table|Download (.pdf) Table 13-4 Combinations of Clinical Examination Items Predicting Airflow Limitation
|Clinical Examination Item ||Interpretation ||Relation to Airflow Limitation ||Reference Standard |
|Years of cigarette exposure, patient-reported wheezing, objective wheezing13 ||See Figure 13-1 ||LR+ varies (see Figure 13-1) LR– = 0.18 ||FEV1/FVC and FEV1 < fifth percentile |
|Patient-reported chronic obstructive pulmonary disease, ≥ 70 pack-years of cigarette smoking, decreased breath sounds16 ||≥2 Findings present ||LR+ = 34 ||FEV1 < 60% of predicted or FEV1/FVC < 0.60 |
|<2 Findings present ||LR– = 0.34 |
|Dyspnea, subjective wheezing, objective wheezing, accessory muscle use, excavation of supraclavicular fossae, and distention of external jugular veins36 ||No. of findings present ||r = –0.64 ||Ratio of FEV1 to predicted FEV1 |
|Breath sound intensity, use of scalene muscle, objective wheezing, and rales during cough27 ||No. of findings present ||Negatively correlated with FEV1 ||FEV1 |
|Decreased breath sounds, objective wheezing, rales, and prolonged expiratory time33 ||All 4 findings present ||LR+ = 3.3 ||Abnormal FVC, FEV1, or maximal midexpiratory flow |
|<4 Findings present ||LR– = 0.44 |
|History by questionnaire, standardized physical examination21 ||Any abnormal finding ||LR+ = 1.4 ||FEV1/FVC < 0.70 |
|No abnormal findings ||LR– = 0.77 |
In case 1, the patient reported a 47-year smoking history but no other environmental or occupational exposures. He complained of episodes of wheezing but had no wheezing on examination. According to Figure 13-1, he has a 65% chance of having airflow limitation.
In case 2, the patient was asymptomatic during the office visit. She had never smoked cigarettes and had no exposure to environmental or occupational pollutants. She did not have a barrel chest, her apical impulse was normally located, and her chest was not hyperresonant. Her breath sounds were normal in intensity, without wheezing or rhonchi. Her forced expiratory time was 2 seconds. Because of clinical examination findings, you conclude that she does not have airflow limitation at the office visit. However, because of her medical history, you suspect that she has intermittent airflow limitation secondary to environmental allergens.
In case 3, the patient had no smoking history or previous episodes of dyspnea. His chest was hyperresonant, and he had diffuse expiratory wheezes. His forced expiratory time was 12 seconds, and he had pulsus paradoxus of 32 mm Hg. You diagnose acute bronchospasm and begin appropriate bronchodilator and glucocorticoid therapy.
No single item or combination of items from the clinical examination rules out airflow limitation. However, the best finding associated with decreased likelihood of airflow limitation is a history of never having smoked cigarettes (especially in patients without a history of wheezing and without wheezing on examination).
The best findings associated with increased likelihood of airflow limitation are objective wheezing, barrel chest, positive match test result, rhonchi, hyperresonance, forced expiratory time greater than 9 seconds, and subxiphoid apical impulse.
A finding of a barrel chest (in children) or wheezing virtually rules in airflow limitation.
Any 2 of the following virtually rule in airflow limitation: 70 pack-years or more of smoking, decreased breath sounds, or history of chronic obstructive pulmonary disorder.
Three findings predict the likelihood of airflow limitation in men (Figure 13-1): years of cigarette smoking, subjective wheezing, and either objective wheezing or peak expiratory flow rate.
Author Affiliations at the Time of the Original Publication
Medical Service, Lexington Veterans Affairs Medical Center and Department of Medicine, University of Kentucky, Lexington (Dr Holleman); and the Center for Health Services Research in Primary Care, Durham Veterans Affairs Medical Center, and Department of Medicine and Center for Health Care Policy Research and Education, Duke University, Durham, North Carolina (Dr Simel).
This study was supported in part by the Andrew W. Mellon Foundation, New York, New York.
We thank Marilyn Schapira, MD, and Bob Badgett, MD, for providing raw data from their studies that allowed us to calculate composite operating characteristics. We also thank Bob Badgett, MD, and Joseph Govert, MD, for their careful reviews.
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