History and exam

Key diagnostic factors



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.

shortness of breath

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

Patients may have difficulty speaking in full sentences.

sputum production

Any pattern of chronic sputum production may indicate COPD.

exposure to risk factors

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


barrel chest

The anteroposterior diameter of the chest is increased.

This suggests hyperinflation and air trapping secondary to incomplete expiration.

hyperresonance on percussion

Caused by hyperinflation and air trapping secondary to incomplete expiration.

distant breath sounds on auscultation

Caused by barrel chest, hyperinflation, and air trapping.

poor air movement on auscultation

Secondary to loss of lung elasticity and lung tissue breakdown.

wheezing on auscultation

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

coarse crackles

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




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.

distended neck veins

Occurs secondary to increased intrathoracic pressure and cor pulmonale.

lower-extremity swelling

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.

weight loss

May occur secondary to anorexia.

muscle loss

Common in patients with severe or very severe COPD.


May occur due to vasodilation caused by hypercapnia.

pursed lip breathing

Involuntary technique to prolong expiration and decrease air trapping.


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

loud P2

Sign of advanced COPD.

Indicates secondary pulmonary hypertension as a complication of cor pulmonale.

hepatojugular reflux

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


cigarette smoking

Most important risk factor.[12] It causes 40% to 70% of cases of COPD.[18] Passive exposure to cigarette smoke also increases risk of COPD.

Elicits an inflammatory response and causes cilia dysfunction and oxidative injury.

There is some evidence that vaping leads to worse pulmonary-related health outcomes in people with or at risk of COPD.[33]

advanced age

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

genetic factors

Airway responsiveness to inhaled insults depends on genetic factors. Alpha-1 antitrypsin deficiency is a genetic disorder, mostly encountered in people of northern European ancestry, which 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.[34] A systematic review and meta-analysis has shown that the prevalence of COPD in adult offspring of people with COPD is greater than population-based estimates.[35]

lung growth and development

The risk of developing COPD can be increased by processes that affect optimal lung growth and therefore lung function.[27] 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.[28] Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD. History of tuberculosis is associated with increased risk COPD.[36]


white ancestry

COPD is more common in white people than black and South Asian people, after adjusting for smoking, age, sex, and socioeconomic status.[37]

exposure to air pollution

Chronic exposure to dust, traffic exhaust fumes, sulfur dioxide, nitrogen dioxide, and particulate matter increases risk of COPD.[12][19][20]

exposure to burning solid or biomass fuel

Household exposure to burning coal or biomass fuel increases the risk of COPD.[38]

occupational exposure to dusts, chemicals, pesticides, vapors, fumes, or gases

Approximately 14% of all cases of COPD are attributable to occupational exposure.[21][39]​​

male sex

COPD is more common in men, likely due to more smokers being male. However, there is a suggestion that women may be more susceptible than men to the effects of tobacco smoke.[40][41][42][43]

low socioeconomic status

The risk for developing COPD is increased in people with lower socioeconomic status.[44] However, this may reflect exposure to cigarette smoke, pollutants, or other factors.

rheumatoid arthritis

Epidemiologic studies indicate an association between risk of COPD and history of rheumatoid arthritis.[36] A 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.[45]

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