History and exam
Key diagnostic factors
common
cough
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
common
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.
Auscultation sounds: Expiratory 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.
Auscultation sounds: Early inspiratory crackles
uncommon
tachypnea
An increased respiratory rate occurs to compensate for hypoxia and hypoventilation.
May involve use of accessory muscles.
asterixis
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.
fatigue
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.
headache
May occur due to vasodilation caused by hypercapnia.
pursed lip breathing
Involuntary technique to prolong expiration and decrease air trapping.
cyanosis
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.
hepatosplenomegaly
Sign of advanced COPD complicated by cor pulmonale.
clubbing
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
cigarette smoking
Most important risk factor.[1][13] It causes 40% to 70% of cases of COPD.[23] 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.[39][40] However, it remains unclear if e-cigarettes are an independent risk factor for COPD.[1]
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.[41] 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.[42]
lung growth and development
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] 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.[43]
weak
white ancestry
COPD is more common in white people than in black and South Asian people, after adjusting for smoking, age, sex, and socioeconomic status.[44]
exposure to air pollution
exposure to burning solid or biomass fuel
Household exposure to burning coal or biomass fuel increases the risk of COPD.[45]
occupational exposure to dusts, chemicals, pesticides, vapors, fumes, or gases
male sex
low socioeconomic status
rheumatoid arthritis
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