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.
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
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
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
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
Most important risk factor.[12]Li X, Cao X, Guo M, et al. Trends and risk factors of mortality and disability adjusted life years for chronic respiratory diseases from 1990 to 2017: systematic analysis for the Global Burden of Disease Study 2017. BMJ. 2020 Feb 19;368:m234.
https://www.doi.org/10.1136/bmj.m234
http://www.ncbi.nlm.nih.gov/pubmed/32075787?tool=bestpractice.com
It causes 40% to 70% of cases of COPD.[17]Raherison C, Girodet PO. Epidemiology of COPD. Eur Respir Rev. 2009 Dec;18(114):213-21.
http://err.ersjournals.com/content/18/114/213.long
http://www.ncbi.nlm.nih.gov/pubmed/20956146?tool=bestpractice.com
Passive exposure to cigarette smoke also increases risk of COPD.
Elicits an inflammatory response and causes cilia dysfunction and oxidative injury.
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 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.[32]Blanco I, Diego I, Bueno P, et al. Prevalence of α1-antitrypsin PiZZ genotypes in patients with COPD in Europe: a systematic review. Eur Respir Rev. 2020 Jul 21;29(157):200014.
https://www.doi.org/10.1183/16000617.0014-2020
http://www.ncbi.nlm.nih.gov/pubmed/32699024?tool=bestpractice.com
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.[33]Li LS, Paquet C, Johnston K, et al. "What are my chances of developing COPD if one of my parents has the disease?" A systematic review and meta-analysis of prevalence of co-occurrence of COPD diagnosis in parents and offspring. Int J Chron Obstruct Pulmon Dis. 2017 Jan 24;12:403-15.
https://www.dovepress.com/ldquowhat-are-my-chances-of-developing-copd-if-one-of-my-parents-has-t-peer-reviewed-fulltext-article-COPD
http://www.ncbi.nlm.nih.gov/pubmed/28182144?tool=bestpractice.com
The risk of developing COPD can be increased by processes that affect optimal lung growth and therefore lung function.[26]Lange P, Celli B, Agustí A, et al. Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. N Engl J Med. 2015 Jul 9;373(2):111-22.
https://www.doi.org/10.1056/NEJMoa1411532
http://www.ncbi.nlm.nih.gov/pubmed/26154786?tool=bestpractice.com
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.[27]Lawlor DA, Ebrahim S, Davey Smith G. Association of birth weight with adult lung function: findings from the British Women's Heart and Health Study and a meta-analysis. Thorax. 2005 Oct;60(10):851-8.
https://www.doi.org/10.1136/thx.2005.042408
http://www.ncbi.nlm.nih.gov/pubmed/16055617?tool=bestpractice.com
Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD. History of tuberculosis is associated with increased risk COPD.[34]Bellou V, Belbasis L, Konstantinidis AK, et al. Elucidating the risk factors for chronic obstructive pulmonary disease: an umbrella review of meta-analyses. Int J Tuberc Lung Dis. 2019 Jan 1;23(1):58-66.
http://www.ncbi.nlm.nih.gov/pubmed/30674376?tool=bestpractice.com
COPD is more common in white people than black and South Asian people, after adjusting for smoking, age, sex, and socioeconomic status.[35]Gilkes A, Hull S, Durbaba S, et al. Ethnic differences in smoking intensity and COPD risk: an observational study in primary care. NPJ Prim Care Respir Med. 2017 Sep 4;27(1):50.
https://www.doi.org/10.1038/s41533-017-0052-8
http://www.ncbi.nlm.nih.gov/pubmed/28871087?tool=bestpractice.com
Chronic exposure to dust, traffic exhaust fumes, sulfur dioxide, nitrogen dioxide, and particulate matter increases risk of COPD.[12]Li X, Cao X, Guo M, et al. Trends and risk factors of mortality and disability adjusted life years for chronic respiratory diseases from 1990 to 2017: systematic analysis for the Global Burden of Disease Study 2017. BMJ. 2020 Feb 19;368:m234.
https://www.doi.org/10.1136/bmj.m234
http://www.ncbi.nlm.nih.gov/pubmed/32075787?tool=bestpractice.com
[18]Park J, Kim HJ, Lee CH, et al. Impact of long-term exposure to ambient air pollution on the incidence of chronic obstructive pulmonary disease: A systematic review and meta-analysis. Environ Res. 2021 Mar;194:110703.
https://www.doi.org/10.1016/j.envres.2020.110703
http://www.ncbi.nlm.nih.gov/pubmed/33417909?tool=bestpractice.com
[19]Zhu RX, Nie XH, Chen YH, et al. Relationship between particulate matter (PM2.5) and hospitalizations and mortality of chronic obstructive pulmonary disease patients: a meta-analysis. Am J Med Sci. 2020 Jun;359(6):354-64.
http://www.ncbi.nlm.nih.gov/pubmed/32498942?tool=bestpractice.com
Household exposure to burning coal or biomass fuel increases the risk of COPD.[36]Chan KH, Kurmi OP, Bennett DA, et al. Solid fuel use and risks of respiratory diseases. A cohort study of 280,000 Chinese never-smokers. Am J Respir Crit Care Med. 2019 Feb 1;199(3):352-61.
https://www.doi.org/10.1164/rccm.201803-0432OC
http://www.ncbi.nlm.nih.gov/pubmed/30235936?tool=bestpractice.com
Approximately 14% of all cases of COPD are attributable to occupational exposure.[37]Blanc PD, Annesi-Maesano I, Balmes JR, et al. The occupational burden of nonmalignant respiratory diseases. An official American Thoracic Society and European Respiratory Society statement. Am J Respir Crit Care Med. 2019 Jun 1;199(11):1312-34.
https://www.doi.org/10.1164/rccm.201904-0717ST
http://www.ncbi.nlm.nih.gov/pubmed/31149852?tool=bestpractice.com
[20]Peng C, Yan Y, Li Z, et al. Chronic obstructive pulmonary disease caused by inhalation of dust: A meta-analysis. Medicine (Baltimore). 2020 Aug 21;99(34):e21908.
https://www.doi.org/10.1097/MD.0000000000021908
http://www.ncbi.nlm.nih.gov/pubmed/32846856?tool=bestpractice.com
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.[38]Xu X, Weiss ST, Rijcken B, et al. Smoking, changes in smoking habits, and rate of decline in FEV1: new insight into gender differences. Eur Respir J. 1994 Jun;7(6):1056-61.
http://erj.ersjournals.com/content/erj/7/6/1056.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/7925873?tool=bestpractice.com
[39]Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. 1994 Nov 16;272(19):1497-505.
http://www.ncbi.nlm.nih.gov/pubmed/7966841?tool=bestpractice.com
[40]Silverman EK, Weiss ST, Drazen JM, et al. Gender-related differences in severe, early-onset chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2000 Dec;162(6):2152-8.
https://www.atsjournals.org/doi/full/10.1164/ajrccm.162.6.2003112
http://www.ncbi.nlm.nih.gov/pubmed/11112130?tool=bestpractice.com
[41]Calverley PM, Anderson JA, Celli B. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med. 2007 Feb 22;356(8):775-89.
https://www.nejm.org/doi/full/10.1056/NEJMoa063070
http://www.ncbi.nlm.nih.gov/pubmed/17314337?tool=bestpractice.com
The risk for developing COPD is increased in people with lower socioeconomic status.[42]Prescott E, Lange P, Vestbo J. Socioeconomic status, lung function and admission to hospital for COPD: results from the Copenhagen City Heart Study. Eur Respir J. 1999 May;13(5):1109-14.
http://erj.ersjournals.com/content/erj/13/5/1109.full.pdf
http://www.ncbi.nlm.nih.gov/pubmed/10414412?tool=bestpractice.com
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.[34]Bellou V, Belbasis L, Konstantinidis AK, et al. Elucidating the risk factors for chronic obstructive pulmonary disease: an umbrella review of meta-analyses. Int J Tuberc Lung Dis. 2019 Jan 1;23(1):58-66.
http://www.ncbi.nlm.nih.gov/pubmed/30674376?tool=bestpractice.com
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.[43]Ma Y, Tong H, Zhang X, et al. Chronic obstructive pulmonary disease in rheumatoid arthritis: a systematic review and meta-analysis. Respir Res. 2019 Jul 9;20(1):144.
https://www.doi.org/10.1186/s12931-019-1123-x
http://www.ncbi.nlm.nih.gov/pubmed/31288799?tool=bestpractice.com