History and Physical Exam for COPD

Your medical history provides important clues that can help your doctor diagnosechronic obstructive pulmonary disease (COPD). In taking your medical history, your doctor will ask questions about:
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Shortness of breath. When were you first short of breath (atexercise or at rest)? How often are you short of breath? How long have you been short of breath? Is it getting worse? How far can you walk, and how many steps can you climb before having to stop because of shortness of breath? Coughing. How often and when do you cough? How long have you been coughing? Is it getting worse? Do you cough up mucus (sputum)? What color is it? Have you ever coughed up blood? Your and any housemate's use of tobacco: whether any of you smoke, how long you've smoked, how many cigarettes a day you smoke, how long ago you quit smoking, whether you feel you can quit smoking, and more. Exposure to airborne irritants, such as dust or chemicals, on the job. Childhood respiratory illnesses. Family history of respiratory disease. Other medical conditions you may have and their treatment. How your condition is affecting your quality of life: missed work, disrupted routines, and depression, for example. The name and dose of all of the medicines you take, including any inhalers you use. What type of family and social support you have. During the physical exam, your doctor will examine your body for other clues that may explain the cause of your symptoms. A physical exam involves:

Taking your temperature, weight, and body mass index (BMI), which measures weight for height and provides a way to estimate the effect of weight on health. Examining your ears, eyes, nose, and throat for signs of infection. Listening to your heart and lungs with a stethoscope. Checking for signs that blood is backing up in your neck veins, which may point to a heart problem such as cor pulmonale. Pressing or tapping on your abdomen (abdominal palpation). Examining your fingers and lips to see whether the skin has a blue tint (cyanosis). Checking your fingers to see if their ends swell and the nails bulge outward (clubbing). Evaluating your legs and feet for swelling (edema). A physical exam is not painful, but parts of it (such as abdominal palpation) may feel slightly uncomfortable.

Why It Is Done A history and physical exam help your doctor make a diagnosis. They are a routine and important part of any visit to a doctor. Results Your history may reveal risk factors that suggest you have COPD or an increased risk for developing COPD, such as: Cigarette smoking. Family history of emphysema. Work-related hazards. Frequent, severe respiratory illnesses. Long-term (chronic) cough with or without mucus. Progressive shortness of breath. Your physical exam may also suggest COPD. Findings indicating COPD include: An expanded chest (barrel chest). Wheezing during normal breathing. Taking longer to exhale fully. Decreased breath sounds or abnormal breath sounds such as crackles or wheezes. Certain physical exam findings will help your doctor assess the severity of your condition. These include: The use of "accessory" muscles, such as the neck muscles, during quiet breathing. Breathing through pursed lips. The inability to complete full sentences without stopping to take a breath. Bluish discoloration of the fingertips or nailbeds (cyanosis). Swelling in the legs or abdomen. Any or all of these findings may suggest severe impairment. A careful history and examination of your heart should also be done to excludeheart disease that can either be associated with or cause symptoms similar to those of COPD. This is especially important, because smoking increases the risk for heart disease as well as for COPD. The heart exam may reveal a rapid heart rate or show signs of heart failure. The liver may be increased in size, which sometimes can occur because of right-sided heart failure (cor pulmonale). The result of the physical exam varies. Not every person will have all the possible symptoms or signs of COPD.
Description

An in-depth report on the causes, diagnosis, treatment, and prevention of COPD -- emphysema and/or chronic bronchitis.
Alternative Names

COPD; Alpha-1 antitrypsin deficiency; Bronchitis - chronic; Chronic bronchitis; Emphysema

Diagnostic Tests:

Despite the widespread incidence and seriousness of COPD, studies strongly suggest that it is underdiagnosed, especially in women. Some experts recommend that any adult smoker who complains of a daily cough should be screened for COPD. In one study, nearly half of patients over age 60 who regularly smoked had COPD. Anyone who has a chronic cough, increased phlegm production, or breathing difficulty that gets worse over time should be checked for the disease.
Medical and Personal History

The doctor will request a history that evaluates the patient's risk factors. Risk factors include:

Past and present smoking Exposure to industrial pollutants at work Family history of alpha-1 antitrypsin deficiency Low exercise capacity (such as trouble climbing stairs or difficulty walking for more than a certain distance) Past and present smoking

Physical Examination

Appearance. There are usually no changes in physical appearance in people with mild-to-moderate COPD. In advanced COPD, patients with emphysema may be wasted and thin, with normal-colored pink skin. Those with chronic bronchitis may have bluish lips and fingers, be obese, and may have swollen feet and legs. Breathing may be rapid and shallow, done through pursed lips, and it may take longer to breathe out. The patient will be asked to cough and produce phlegm, if possible. Chest Examination. The physician will next perform a simple examination of the chest area with a stethoscope to listen for:

Crepitations, a noise resembling a paper bag being rumpled Reduced or distant breath sounds Signs of pulmonary hypertension Wheezing or gurgling sounds

Other findings may include:

Breathlessness when the patient lies flat Increased pressure in the veins

Pulmonary Function Tests (Spirometry)

The best tests for diagnosing COPD and seeing how well it responds to treatment are pulmonary function tests. The gold-standard test for patients with respiratory symptoms such as shortness of breath is spirometry. Spirometry measures the volume and force of air as it is exhaled from the lungs. It measures airway obstruction, can identify COPD early, and the results are standardized so they are always consistent. The patient is asked to breathe in and breathe out forcefully into an instrument. This is repeated several times. The force of the air is then measured. From the results, the physician determines two important values: The forced vital capacity (FVC). FVC is the maximum volume of air that a patient can breathe out with force. It indicates lung size, elasticity, and how well the air passages open and close. The forced expiratory volume in one second (FEV1). FEV1 is the maximum volume of air that a patient can breathe out in 1 second after breathing in fully. Airflow is considered to be limited if the forced breath out stays low over 1 second. People with COPD have a decline in FEV1 over time. FEV1 is measured as "percent of predicted:"

Moderate COPD is an FEV1 50 - 80% of predicted. Severe COPD is an FEV1 30 - 50% of predicted. The ratio of FEV1 to FVC (FEV1/FVC) is less than 70% of normal, regardless of whether the patient has an FEV1 greater than 80% or less than 50%.

Spirometry is a painless study of air volume and flow rate in the lungs. Spirometry is frequently used to evaluate lung function in people with diseases such as asthma or cystic fibrosis.

Tests for Measuring the Ability of the Lung to Exchange Oxygen and Carbon Dioxide

Arterial Blood Gas. The physician may request an arterial blood gas test to determine the amount of oxygen and carbon dioxide in the blood (its saturation). Low oxygen (hypoxia) and high carbon dioxide (hypercapnia) levels often indicate chronic bronchitis, but not always emphysema. A blood gas analysis that shows very low oxygen levels is useful for determining which patients would benefit from oxygen therapy (see below). This procedure typically involves drawing blood from an artery in the wrist.

Click the icon to see a depiction of arterial blood gas sampling. Pulse Oximetry Test. A safe and painless test for measuring oxygen in the blood is called pulse oximetry, which involves placing a probe on the finger or ear lobe. The probe emits two different lights. The amount of each light the blood absorbs is related to how much oxygen the red blood cells carry. This test measures only oxygen in the blood, however, and not carbon dioxide. Results should be taken together with other tests to determine the need for medication or oxygen therapy.

Carbon Monoxide Diffusing Capacity. The lung carbon monoxide diffusing capacity (DLCO) test determines how effectively gases are exchanged between the blood and airways in the lungs. Patients should not eat or exercise before the test, and they should not have smoked for 24 hours. The patient inhales a mixture of carbon monoxide, helium, and oxygen and holds his or her breath for about 10 seconds. The gas levels are then analyzed from the exhaled breath. Results can help physicians differentiate emphysema from chronic bronchitis and asthma. Patients with emphysema have lower DLCO results (a reduced ability to take up oxygen). Such results are also important in helping to determine appropriate candidates for lung reduction surgery. Carbon monoxide levels that are 20% or less than predicted values pose a very high risk for poor survival. Exhaled Breath. The measurement of nitric oxide (NO) in exhaled breath can be a simple method of diagnosing COPD and monitoring the effects of treatment. In most patients with COPD, no levels are below normal. Levels above normal in a patient with COPD indicate that the person also has asthma.

Click the icon to see an image of lung diffusion testing.

Imaging Tests

Chest X-Rays. Chest x-rays are often performed, but they are not very useful for detecting early COPD. By the time an x-ray reveals COPD, the patient is already well aware of the condition. X-rays can look for growths in the lungs to rule out other diseases, however. Clear signs of COPD on x-ray include the following:

Abnormally large amounts of air spaces in the lung A flattened diaphragm A smaller heart (however, if the person has heart failure, the heart becomes enlarged and there may not be signs of overinflated lungs) Exaggerated lung inflation in upper areas Larger amounts of air in the lower lungs in patients with emphysema related to alpha-1 antitrypsin deficiency

Chest x-rays are rarely useful for diagnosing chronic bronchitis, although they sometimes show mild scarring and thickened airway walls. Computed Tomography. Computed tomography (CT) scans can accurately assess the severity of COPD and may be used to determine the size of the air pockets (bullae) in the lungs.
Other Tests for COPD

Noninvasive Methods for Determining Severity. Questionnaires and short exercise tests are very useful for determining the severity of COPD. Test for alpha-1 antitrypsin deficiency. Physicians will typically test for the enzyme alpha-1 antitrypsin in COPD patients who are nonsmokers and who develop emphysema in their 30s. Additional Blood and Sputum Tests. Additional tests may be required if the physician suspects other medical problems. If the person has pneumonia, for instance, blood and sputum tests and cultures may be performed to determine the cause of infection. Bronchodilator Challenge. Using a bronchodilator can usually relieve the symptoms of asthma. However, patients with COPD typically have a limited response to bronchodilation. A bronchodilator challenge test may help distinguish between the two diseases. Some patients with COPD experience limited and temporary improvement in FEV1 30 - 45 minutes after inhaling medication from a metered dose inhaler. However, their airflow remains poor. Definitions
Asthma In the recent Global Initiative for Asthma (GINA) Guidelines 1 asthma is defined as follows: a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation causes an associated increase in airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment. Chronic obstructive pulmonary disease In the recent Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines 2, COPD is defined as follows: a disease state characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal response of the lungs to noxious particles or gases. Previous SectionNext Section

Similarities and differences

Asthma and COPD have important similarities and differences 3. Both are chronic inflammatory diseases that involve the small airways and cause airflow limitation49, both result from gene-environment interactions and both are usually characterised by mucus and bronchoconstriction.

The similarities are striking, but the differences are also striking. For example, different anatomical sites are involved 8; COPD affects both the airways and the parenchyma, whilst asthma affects only the airways. Both asthma and COPD involve the small airways and the structural changes in the small airways are responsible for much of the physiological impairment that occurs in these diseases 1012. Perhaps the most important difference between asthma and COPD is the nature of inflammation, which is primarily eosinophilic and CD4-driven in asthma, and neutrophilic and CD8-driven in COPD 1, 2, 1315. This is a very important distinction because the nature of the inflammation affects the response to pharmacological agents. There is now ample evidence that inhaled corticosteroids are effective against the eosinophilic inflammation in asthma but largely ineffective against the primarily neutrophilic inflammation seen in COPD 1618. One fact not acknowledged in the definitions is that airway remodelling can occur in long-standing asthma 13, 1922 and results in partially reversible airflow obstruction. Therefore, in many (but not all) patients with long-standing asthma there is a component of chronic irreversible airflow obstruction with reduced lung function and incomplete response to a short-acting bronchodilator or to an oral or inhaled corticosteroid. This makes the diagnosis of asthma sometimes challenging in older adults and it requires the adjustment of the goals of treatment with respect to the patient's age, as maintenance of normal lung function can no longer be a realistic goal. It is also not often acknowledged that both diseases often co-exist in an individual, so it is not uncommon to see the characteristics of both diseases. It is therefore often challenging for the clinician to know which disease a patient has or what mix of diseases, since COPD is not one disease but rather a spectrum of diseases involving both the airways and parenchyma 2, 23. Because of the differences in the cells involved in asthma and COPD, and the relative lack of efficacy of pharmaceutical agents that can alter the progression of COPD (disease-modifying), the approach to the treatment of asthma and COPD is different. The essential difference is that the treatment of asthma is driven by the need to suppress the chronic inflammation, whereas in COPD, treatment is driven by the need to reduce symptoms. The treatment algorithm is based on severity for both asthma and COPD. For asthma, severity is based on symptom frequency and severity, lung function and healthcare utilisation 1. For COPD, the stages of severity are defined by lung function 2.

Before a specific comparison can be made between COPD and asthma, it is important to acknowledge the variations in structure and physiology observed within each disease. Such differences in disease structure and function are not only found between individuals but may evolve within a given individual over time. The dominant classification paradigm for COPD identifies the extreme categories of chronic bronchitis vs emphysema but acknowledges that there are often components of each process present in any individual. This common classification, however, fails to emphasize the substantial literature suggesting an important, potentially independent contribution of the small peripheral conducting airways to the increased airways resistance, resulting in airflow obstruction in patients with advanced disease.56789 Significantly, individuals exhibit considerable variability in the degree of small airway involvement relative to the severity of emphysema and large airway bronchitis.1011 Detailed morphologic evaluations11 have revealed that 79% of patients with COPD had evidence of parenchymal emphysema, while 85% had significant airway involvement including mucosal hyperplasia (75%) and bronchiolitis (47%). Of note, 11% had evidence of bronchiolitis but no mucosal hypertrophy consistent with chronic bronchitis. Such observations provide an explanation for apparent discrepancies in anatomy and physiology between certain individuals (Fig 1 ). The patient in Figure 1, left, A, has had 66% of his lung destroyed by emphysema (FEV 1, 25% of predicted), whereas the patient in Figure 1, right, B, is an individual with minimal emphysema but a lower FEV 1 (23% of predicted). Both patients had a similar history of tobacco use, and neither had symptomatic bronchitis or bronchodilator reversibility, thus indirectly supporting the disproportionate contribution of small airways disease in the second patient. Advances in quantitative CT scanning may allow us to more accurately separate subjects into unique subgroups using noninvasive techniques.1213 Such CT scanning techniques have been validated by comparison with tissue histology for both emphysema volume and airway wall thickness measurements. 1415 By quantifying the percentage of low-attenuation area (LAA%), that is, emphysema, and the percentage of airway wall thickness relative to airway perimeter (WA%) using quantitative CT scanning, we can stratify patients into airway-dominant phenotype, parenchyma-dominant phenotype, or combined phenotypes (Fig 2 ). In fact, such measurements of LAA% and WA% are independent predictors of expiratory flow rates. Although asthma has traditionally been described as a reversible disease of the large airways, an increasing body of knowledge describes an often progressive process with an incompletely reversible component that often involves the

small peripheral airways as well as the large airways.161718 CT scan studies19performed in asthma populations have identified increases in airway wall thickness that are similar to those found in the airway-dominant subgroup of COPD subjects. While early studies in patients with milder asthma suggested that airway luminal diameter was preserved in patients with asthma compared to those with COPD, studies 1920 evaluating more severe asthma demonstrate decreased airway luminal diameter associated with the airway-wall thickening as is found in COPD. Furthermore, increases in LAA% that are consistent with emphysema are observed in nonsmoking asthmatic patients. The volume of lung in the density range that is consistent with emphysema is associated with increasing asthma severity and age. One study21 found 5.1% of the lung volume in the emphysema density range in patients with mild asthma, and 23% in those with severe disease. The higher percentage of emphysema found in patients with more severe asthma is more than would be expected simply from the hyperinflation of healthy lung tissue. Importantly, studies2122 have shown a significantly greater percentage of CT scan-detected emphysema in asthmatic patients who are smokers compared with nonsmokers. Consistent with these observations, high-resolution CT scans that have been interpreted by expert observers have been shown to have poor discriminative value between clinical asthma and COPD.23 Previous SectionNext Section

Physiologic Comparison of Asthma and COPD

The Physiologic Dogma: Asthma vs COPD The most common working definitions of COPD and asthma in most clinical and research settings consistently incorporate the following physiologic attributes. While, on average, populations separate based on these characteristics, as will be discussed below, frequent exceptions occur to these classic patterns in individual patients. Degree of Variability and Reversibility of Spirometry: Both asthma and COPD are defined by decreases in the FEV1/FVC ratio. FEV1 in asthma patients is considered to be at least partially (12% change in FEV1) or completely reversible and to vary significantly throughout the day.24 COPD, by definition, is never completely reversible, and significant reversibility often leads to exclusion from clinical trials. Both chemically induced and exercise-induced hyperresponsiveness are defining characteristics of asthma but are not traditionally associated with COPD. Diffusing Capacity: Measurements of the diffusing capacity of the lung for carbon monoxide (D LCO) are typically normal or increased in asthma patients. In COPD patients, they are typically decreased. The decreases are thought to be directly related to the loss of alveolar-capillary surface area that is associated with emphysema. Hyperinflation: COPD is typically associated with more severe increases in resting lung volume that are accentuated during exertion. Asthma is conventionally thought to be associated with resting hyperinflation only during attacks. Lung Elastic Recoil/Lung Compliance: Increased lung elastic recoil (ie, decreased compliance) is characteristic of COPD and is considered to be normal in asthma. Simple Measures of Pulmonary Function in Asthma and COPD The excessive rate of decline in expiratory flow rates in susceptible smokers has been welldescribed. 25 Long-term results from the Lung Health Study25 have demonstrated a decline of 66 mL per year in men and 54 mL per year in women compared with the expected normal decline of 20 to 30 mL per year. Given that the Lung Health Study only included subjects with known pulmonary dysfunction, the rate of decline in all smokers is expected to be significantly less than these values. The impact of asthma on the rate of decline in FEV 1 is more controversial, ranging between 0 and 95 mL per year, and depends on disease definition, concomitant smoking, age, and severity of disease in the populations studied.262728 It is clear, however, that asthma in a significant subgroup of patients evolves into incompletely reversible disease, thus becoming more difficult to distinguish from subgroups of patients with tobacco-related COPD. Three articles1229 have compared the spirometry, lung volume, and D LCO of COPD patients to subjects who had never smoked and had incompletely reversible asthma. All three studies compared patients with similar FEV1 severity. These studies demonstrated significantly lower DLCO and significantly greater residual volume (RV), functional residual capacity, and total lung capacity (TLC) in the COPD subgroup compared with the asthma

subgroup. There was, however, significant overlap between groups. The D LCO was the single best physiologic discriminator between the two groups, with values in COPD patients ranging from 58 to 67% predicted and those in patients with incompletely reversible asthma ranging from 85 to 99% predicted. Unfortunately, even D LCO was inadequate as a discriminator in individual subjects. A DLCO value of 80% predicted was only 77% sensitive and 71% specific in discriminating COPD from asthma. Bronchodilator Reversibility and AHR The acute improvement in expiratory flow rates, such as FEV 1 following bronchodilator use, is on average greater in asthma patients than in COPD patients (16% vs 11%, respectively). However, despite the common use of bronchodilator reversibility in the clinical and research setting to distinguish asthma from COPD, the diagnostic effectiveness of this parameter is poor in unselected patients. 3031 One large study,32 using a threshold bronchodilator FEV1 change of 15%, determined only a 44% sensitivity for detecting asthma and a 72% specificity in distinguishing asthma from COPD. Increasing the minimum FEV 1 threshold change to 20% increased the specificity to 84% but dramatically decreased the sensitivity. 31 A large population-based analysis32 found that 30% of individuals with fixed airflow obstruction have a history of asthma. While there is a correlation between bronchodilator reversibility and AHR to methacholine, the relationship is not strong.33 Tests of AHR are useful in distinguishing patients with asthma from healthy persons.343536 A 20% reduction in expiratory flow rates in response to 8 mg/mL methacholine occurs in nearly all patients with active asthma and in < 5% of healthy individuals. On the other hand, these tests are not useful in distinguishing asthma from COPD, since 68% of patients with COPD (85% of women and 59% of men) also exhibit AHR. In fact, in COPD patients, poorer pulmonary function is associated with a greater magnitude of AHR, and increasing severity of AHR is associated with greater rates of decline in lung function in continuing smokers. 37 Twenty-seven percent of patients with 1-antitrypsin deficiency who are enrolled in the National Heart, Lung, and Blood Institute registry have significant bronchodilator reversibility, although the prevalence of AHR in one series39 (16%) was not significantly different from that of the control group (11%). 3839