History and exam

Key diagnostic factors

common

Usually the initial symptom of COPD.

Frequently a morning cough, but becomes constant as disease progresses.

Usually productive, and sputum quality may change with exacerbations or superimposed infection.

Initially with exercise but may progress to shortness of breath even at rest.

Patients may have difficulty speaking in full sentences.

Any pattern of chronic sputum production may indicate COPD.

Including exposure to tobacco smoke, air pollution, or indoor solid fuel burning; occupational exposure to dusts, chemicals, vapors, fumes, or gases; genetic factors and developmentally abnormal lung.

Other diagnostic factors

common

The anteroposterior diameter of the chest is increased.

This suggests hyperinflation and air trapping secondary to incomplete expiration.

Caused by hyperinflation and air trapping secondary to incomplete expiration.

Caused by barrel chest, hyperinflation, and air trapping.

Secondary to loss of lung elasticity and lung tissue breakdown.

A common finding in exacerbations. The current accepted descriptive word for a continuous musical lung sound.

Is indicative of airway inflammation and resistance.

Expiratory wheeze
Expiratory wheeze

Auscultation sounds: Expiratory wheeze

​​
Polyphonic wheeze
Polyphonic wheeze

Auscultation sounds: Polyphonic wheeze

​

A common finding in exacerbations. A discontinuous sound referring to mucus or sputum in airways.

Indicative of airway inflammation and mucus oversecretion.

Early inspiratory crackles
Early inspiratory crackles

Auscultation sounds: Early inspiratory crackles

​​

uncommon

An increased respiratory rate occurs to compensate for hypoxia and hypoventilation.

May involve use of accessory muscles.

Loss of postural control in outstretched arms (commonly known as a flap) caused by hypercapnia.

This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.

Occurs secondary to increased intrathoracic pressure and cor pulmonale.

Suggests cor pulmonale and secondary pulmonary hypertension as a complication of advanced chronic lung disease.

Occurs because of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and hypercapnia.

May occur secondary to anorexia.

Common in patients with severe or very severe COPD.

May occur due to vasodilation caused by hypercapnia.

Involuntary technique to prolong expiration and decrease air trapping.

Seen in the late stages of COPD, usually with hypoxia, hypercapnia, and cor pulmonale.

Sign of advanced COPD.

Indicates secondary pulmonary hypertension as a complication of cor pulmonale.

Sign of advanced COPD complicated by cor pulmonale.

Sign of advanced COPD complicated by cor pulmonale.

COPD itself does not cause clubbing. The presence of clubbing should alert the clinician to a related condition (e.g., lung cancer or bronchiectasis).

Risk factors

strong

Most important risk factor.[1][12]​​ Tobacco smoking causes over 70% of COPD cases in high-income countries and 30% to 40% of cases in low- and middle-income countries.[22]

Passive exposure to cigarette smoke increases risk of COPD.[39]

There is some evidence that vaping leads to worse pulmonary-related health outcomes in people with or at risk of COPD.[40][41]​​ However, it remains unclear if e-cigarettes are an independent risk factor for COPD.​[1][42]​​

The effect of age may be related to a longer period of cigarette smoking as well as the normal age-related loss of FEV₁.

Airway responsiveness to inhaled insults depends on genetic factors.

Alpha-1 antitrypsin deficiency, a genetic disorder encountered in people of northern European ancestry, causes panacinar emphysema in lower lobes at a young age. One European study estimated that approximately 1 in every 850 patients with COPD has an alpha-1 antitrypsin protease inhibitor ZZ genotype, which is associated with severe disease.[43]

One systematic review and meta-analysis found that the prevalence of COPD in adult offspring of people with COPD is greater than population-based estimates.[44]

The risk of developing COPD can be increased by processes that affect optimal lung growth and therefore lung function.[32] These processes may go back as far as gestation, birth, childhood, and adolescence. For example, there is a positive association between birthweight and FEV₁ in adulthood. Disadvantageous factors in childhood may be as important as heavy smoking in predicting lung function in adulthood.[33][34]​

Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD. History of tuberculosis is associated with increased risk of COPD.[45]

weak

COPD is more common in white people than in black and South Asian people, after adjusting for smoking, age, sex, and socioeconomic status.[46]

Chronic exposure to dust, traffic exhaust fumes, sulfur dioxide, nitrogen dioxide, and particulate matter increases risk of COPD.[12][24][25]

Household exposure to burning coal or biomass fuel increases the risk of COPD.[47]

Approximately 14% of all cases of COPD are attributable to occupational exposure.[26][48]​​

COPD is more common in men, likely due to more smokers being male.[17]​ However, there is a suggestion that women may be more susceptible than men to the effects of tobacco smoke.[49][50][51]​​

The risk for developing COPD is increased in people with lower socioeconomic status.​[10][11]​​​​ However, this may reflect exposure to cigarette smoke, pollutants, or other factors.

Epidemiologic studies indicate an association between risk of COPD and history of rheumatoid arthritis.[45] One meta-analysis showed that, compared with controls, patients with rheumatoid arthritis have a significantly increased risk of incident COPD with a pooled relative risk of 1.82.[52]

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