history and physical exam for copd

7/31/2019 History and Physical Exam for COPD

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History and Physical Exam for COPDYour medical history provides important clues that can help your doctor diagnosechronic obstructivepulmonary disease (COPD).

In taking your medical history, your doctor will ask questions about:

Recommended Related to COPD

Pulmonary Rehabilitation for COPD

Shortness of breath often limits what people with COPD can do. When ordinary activities like walking or climbing stairsbecome difficult, everyday life with COPD gets harder. Pulmonary rehabilitation for COPD includes a program ofexercises that helps people with COPD build their physical fitness. Many pulmonary rehab centers also teach peoplebreathing techniques and strategies for living better with COPD.

Read the Pulmonary Rehabilitation for COPD article > >

Shortness of breath.

o When were you first short of breath (atexerciseor at rest)?

o How often are you short of breath?

o How long have you been short of breath? Is it getting worse?

o How far can you walk, and how many steps can you climb before having to stop because of shortness ofbreath?

Coughing.

o How often and when do you cough?

o How long have you been coughing? Is it getting worse?

o Do you cough upmucus(sputum)? What color is it?o Have you ever coughed upblood?

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 youquit smoking, whether you feel you canquitsmoking, 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, anddepression, forexample.

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 thephysical exam, your doctor will examine your body for other clues that may explain the causeof your symptoms. A physical exam involves:

Taking your temperature,weight, andbody mass index (BMI), which measures weight for height and

provides a way to estimate the effect of weight on health.

Examining yourears,eyes, nose, and throat for signs of infection.

Listening to yourheartandlungswith a stethoscope.

Checking for signs that blood is backing up in your neck veins, which may point to a heart problem suchascor pulmonale.

Pressing or tapping on yourabdomen(abdominal palpation).

Examining your fingers and lips to see whether theskinhas a blue tint (cyanosis).

Checking your fingers to see if their ends swell and the nails bulge outward (clubbing).

Evaluating your legs andfeetfor swelling (edema).

A physical exam is not painful, but parts of it (such as abdominal palpation) may feel slightlyuncomfortable.
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Why It Is Done

A history and physical exam help your doctor make a diagnosis. They are a routine and important part ofany visit to a doctor.

Results

Your history may reveal risk factors that suggest you have COPD or an increased risk for developingCOPD, such as:

Cigarette smoking.

Family history ofemphysema.

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).

Wheezingduring 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 diseasethat caneither 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 arapid heart rate or show signs ofheart failure.

Thelivermay be increased in size, which sometimes can occur because of right-sidedheart failure(corpulmonale).

The result of the physical exam varies. Not every person will have all the possible symptoms or signs ofCOPD.

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of

COPD -- emphysema and/or chronic bronchitis.

Alternative Names
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COPD; Alpha-1 antitrypsin deficiency; Bronchitis - chronic; Chronic

bronchitis; Emphysema

Diagnostic Tests:

Despite the widespread incidence and seriousness of COPD, studies stronglysuggest that it is underdiagnosed, especially in women. Some experts

recommend that any adult smoker who complains of a daily cough should bescreened for COPD. In one study, nearly half of patients over age 60 who

regularly smoked had COPD. Anyone who has a chronic cough, increasedphlegm 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 peoplewith mild-to-moderate COPD. In advanced COPD, patients with emphysemamay be wasted and thin, with normal-colored pink skin. Those with chronic

bronchitis may have bluish lips and fingers, be obese, and may have swollenfeet 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:


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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 totreatment 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 theresults 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 thenmeasured. From the results, the physician determines two important values:

The forced vital capacity (FVC). FVC is the maximum volume of airthat apatient 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 maximumvolume of airthat 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 ismeasured 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% orless 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.


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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 todetermine 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 oxygentherapy(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 theblood is called pulse oximetry, which involves placing a probe on the fingeror 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 carbondioxide. Results should be taken together with other tests to determine the

need for medication or oxygen therapy.
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Carbon Monoxide Diffusing Capacity. The lung carbon monoxide diffusing

capacity (DLCO) test determines how effectively gases are exchangedbetween 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 andholds his or her breath for about 10 seconds. The gas levels are then

analyzed from the exhaled breath. Results can help physicians differentiateemphysema from chronic bronchitis and asthma. Patients with emphysema

have lower DLCO results (a reduced ability to take up oxygen). Such resultsare 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 canbe a simple method of diagnosing COPD and monitoring the effects of

treatment. In most patients with COPD, no levels are below normal. Levelsabove 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 veryuseful 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 inthe 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
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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 accuratelyassess 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 shortexercise tests are very useful for determining the severity of COPD.

Test for alpha-1 antitrypsin deficiency. Physicians will typically test for theenzyme 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 thephysician suspects other medical problems. If the person has pneumonia, forinstance, blood and sputum tests and cultures may be performed todetermine the cause of infection.

Bronchodilator Challenge. Using a bronchodilator can usually relieve thesymptoms of asthma. However, patients with COPD typically have a limited

response to bronchodilation. A bronchodilator challenge test may helpdistinguish 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 remainspoor.

Definitions

AsthmaIn the recent Global Initiative for Asthma (GINA) Guidelines1asthma 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) Guidelines2, COPD is defined asfollows: 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 differences3. 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.
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The similarities are striking, but the differences are also striking. For example, different anatomical sites are

involved8; 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 diseases1012.

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 COPD1,2,1315. 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 COPD1618. One fact not acknowledged

in the definitions is that airway remodelling can occur in long-standing asthma13,1922and 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 parenchyma2,23.

Because of the differences in the cells involved in asthma and COPD, and the relative lack of efficacy ofpharmaceutical 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 utilisation1. For COPD, the stages of severity are defined by

lung function2.

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 thatthere 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.56789Significantly, individuals exhibit considerable variability in the degree of small airway

involvement relative to the severity of emphysema and large airway bronchitis .1011Detailed morphologic

evaluations11have 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 inFigure 1,left, A, has had 66% of his lung destroyed by emphysema (FEV1, 25% of predicted), whereas the

patient inFigure 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.1213Such CT scanning techniques have been validated by comparison with tissue

histology for both emphysema volume and airway wall thickness measurements.1415By 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
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small peripheral airways as well as the large airways.161718CT 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, studies1920evaluating 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 study21found 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, studies2122have 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 consistentlyincorporate 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.24COPD, 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 (DLCO) 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 COPDThe excessive rate of decline in expiratory flow rates in susceptible smokers has been welldescribed.25Long-term

results from the Lung Health Study25have 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.262728It 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 articles1229have compared the spirometry, lung volume, and DLCO 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
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subgroup. There was, however, significant overlap between groups. The DLCO 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 DLCO 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 AHRThe 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.3031One large study,32using 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 FEV1 threshold change to 20% increased the

specificity to 84% but dramatically decreased the sensitivity.31A large population-based analysis32found 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.33Tests of AHR are useful in distinguishing patients with asthma from healthy persons.343536A 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.37Twenty-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
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history and physical exam for copd

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