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Chronic obstructive pulmonary disease

Last updated: September 24, 2020

Summary

Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction due to inflammation of the small airways. It is caused predominantly by inhaled toxins, especially via smoking, but air pollution and recurrent respiratory infections can also cause COPD. Some individuals are genetically predisposed to COPD, particularly those with α1-antitrypsin deficiency (AATD). COPD begins with chronic airway inflammation that usually progresses to emphysema, a condition that is characterized by irreversible bronchial narrowing and alveolar hyperinflation. These changes cause a loss of diffusion area, which can lead to inadequate oxygen absorption and CO2 release, resulting in hypoxia and hypercapnia. Most affected individuals present with a combination of dyspnea and chronic cough with expectoration. In later stages, COPD may manifest with more severe symptoms such as tachypnea, tachycardia, and cyanosis. Diagnosis is primarily based on clinical presentation and lung function tests, which typically show a decreased ratio of forced expiratory volume (FEV) to forced vital capacity (FVC). Imaging studies, such as chest x-ray, are helpful in assessing disease severity and the extent of possible complications, but they are not required to confirm the diagnosis. ABG and pulse oximetry are useful for quickly assessing the patient's O2 status. All COPD patients should be staged according to the staging system of the Global Initiative for Chronic Obstructive Lung Disease (GOLD), which considers a variety of factors (e.g., exacerbations, symptom severity, FEV1). Treatment options depend on the GOLD stage and mainly consist of short- and long-acting bronchodilators (beta-agonists and parasympatholytics) and glucocorticoids. Individuals with advanced disease typically require oxygen supplementation, which is the only treatment that decreases mortality. COPD may cause complications such as pulmonary hypertension or respiratory failure. The most significant complication is acute exacerbation of COPD (See AECOPD).

Definition

  • COPD is a chronic pulmonary disease characterized by persistent respiratory symptoms and airflow limitation (postbronchodilator FEV1/FVC < 0.70), which is caused by a mixture of small airway obstruction and parenchymal destruction [1]
  • COPD was formerly subdivided into chronic bronchitis and emphysema. These terms are still widely used to describe patient findings and found as subclasses of COPD in outdated literature. [2]
    • Chronic bronchitis: productive cough (cough with expectoration) for at least 3 months each year for 2 consecutive years
    • Emphysema: permanent dilatation of pulmonary air spaces distal to the terminal bronchioles, caused by the destruction of the alveolar walls and the pulmonary capillaries required for gas exchange

Epidemiology

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Exogenous factors

  • Tobacco use (90% of cases) [2]
    • Smoking is the major risk factor for COPD, but those who have quit ≥ 10 years ago are not at increased risk. [6]
    • Passive smoking
  • Exposure to air pollution or fine dusts [7]
    • Nonorganic dust: such as industrial bronchitis in coal miners [8]
    • Organic dust: incidence of COPD in areas where biomass fuel (e.g., wood, animal dung) is regularly burned indoors

Endogenous factors

Classification

Global initiative for chronic obstructive lung disease (GOLD) classifications [11]

  • GOLD classifies COPD according to the severity of airflow limitation (GOLD 1–4) and the ABCD assessment tool, which takes into account the modified British Medical Research Council (mMRC) dyspnea scale, COPD assessment test (CAT), and risk of exacerbation.
  • Previously, COPD was classified into chronic bronchitis and emphysema based on clinical findings. The use of these terms to classify types of COPD is now considered outdated because most individuals with COPD have a combination of both. However, these terms are still widely used to describe patient findings and found as subclasses of COPD in outdated literature.

Classification based on airflow limitation in patients with FEV1/FVC < 70% [1]

GOLD uses FEV1/FVC (Tiffeneau-Pinelli index) to classify COPD.

Category

Symptoms

FEV1% of the predicted value
GOLD 1 (Class I)
  • Mild
  • ≥ 80%
GOLD 2 (Class II)
  • Moderate
  • 50% ≤ FEV1 < 80%
GOLD 3 (Class III)
  • Severe
  • 30% ≤ FEV1 < 50%
GOLD 4 (Class IV)
  • Very severe
  • < 30%

For GOLD categories according to the FEV1%, remember that 30 + 50 = 80.

Classification using combined assessment tools

Patient group Degree of severity Exacerbations per year Symptoms mMRC Dyspnea Scale CAT score
A
  • ≤ 1 (with no hospital admission)
  • Mild symptoms
  • < 2
  • < 10
B
  • Severe symptoms
  • ≥ 2
  • ≥ 10
C
  • ≥ 2
  • ≥ 1 leading to hospital admission
  • Mild symptoms
  • < 2
  • < 10
D
  • Severe symptoms
  • ≥ 2
  • ≥ 10

Classification based on underlying morphological changes

Emphysema is divided into the following subtypes: [12]

  • Centrilobular emphysema (centriacinar emphysema)
    • Most common type of emphysema
    • Classically seen in smokers
    • Characterized by the destruction of the respiratory bronchiole (central portion of the acinus); spares distal alveoli
    • Usually affects the upper lobes
  • Panlobular emphysema (panacinar emphysema)
    • Rare type of emphysema
    • Associated with α1-antitrypsin deficiency
    • Characterized by the destruction of the entire acinus (respiratory bronchiole and alveoli)
    • Usually affects the lower lobes
  • Other subtypes
    • Cicatricial emphysema
      • Mainly caused by exposure to quartz dust
      • Results in chronic inflammation and nodular scar formation
    • Giant bullous emphysema
      • Characterized by large bullae (congenital or acquired) that extrude into the surrounding tissue
      • Bullae may rupture, leading to pneumothorax.
      • Depending on the shape of the bullae, resection should be considered.
    • Senile emphysema
      • Loss of pulmonary elasticity with age may lead to an emphysematous lung.
      • Not considered pathological but a normal consequence of aging

To remember that centriacinar emphysema is associated with smoking and that it primarily involves the upper lobes of the lungs, think of: Smoke rising up.

Pathophysiology

COPD is characterized by chronic airway inflammation and tissue destruction. [2][13]

Chronic inflammation

It results from significant exposure to noxious stimuli, increased oxidative stress (most commonly due to cigarette smoke) as well as by increased release of reactive oxygen species by inflammatory cells.

Tissue destruction [15]

Clinical features

Symptoms are minimal or nonspecific until the disease reaches an advanced stage.

Presenting findings [2]

  • Chronic cough with expectoration (expectoration typically occurs in the morning)
  • Dyspnea and tachypnea
    • Initial stages: only on exertion
    • Advanced stages: continuously
  • Pursed lip breathing
    • The patient breathes in through the nose and breathes out slowly through pursed lips.
    • This style of breathing increases airway pressure and prevents bronchial collapse during the last phase of expiration.
    • More commonly seen in patients with emphysema
  • Prolonged expiratory phase, end-expiratory wheezing, crackles, muffled breath sounds, and/or coarse rhonchi on auscultation
  • Cyanosis due to hypoxemia
  • Tachycardia

Features of advanced COPD [16]

Nail clubbing is not a finding specific to COPD; its presence usually suggests comorbidities such as bronchiectasis, pulmonary fibrosis, or lung cancer.

Pink puffer and blue bloater [16]

According to their clinical appearance, patients with COPD are often categorized as either “Pink Puffer” or “Blue Bloater”.

Pink Puffer Blue Bloater
Main pathomechanism
Clinical features
  • Noncyanotic
  • Cachectic
  • Pursed-lip breathing
  • Mild cough
PaO2
  • Slightly reduced
  • Markedly reduced
PaCO2

Features of COPD due to AATD

  • Age of onset is generally younger (< 60 years)
  • Also, often have hepatic signs and symptoms (jaundice) related to hepatitis or cirrhosis

Diagnostics

Pulmonary function test (PFT) [2]

Spirometry and/or body plethysmography

Postbronchodilator test

  • Objective: assesses reversibility of bronchoconstriction
  • Procedure
    1. Spirometry to establish a baseline
    2. Inhalation (e.g., salbutamol)
    3. Perform spirometry again after ∼10–15 min.
  • Results: FEV1/FVC < 0.7 is diagnostic of COPD (in patients with typical clinical features and exposure to noxious stimuli).
    • Delta FEV1 < 12% (irreversible bronchoconstriction): COPD is more likely than asthma.
    • Delta FEV1 > 12% (reversible bronchoconstriction): Asthma is more likely than COPD.
    • If spirometry is normal, COPD can be excluded.

To remember FEV1 for COPD patients, imagine a COP with low FEVer.

Blood gas analysis and pulse oximetry

  • Pulse oximetry: assesses O2 saturation
  • ABG: only indicated when O2 is < 92% or if the patient is severely ill (e.g., altered mental status, acute exacerbation)
    • Hypoxemia and hypercapnia are expected findings in patients with acute or chronic respiratory acidosis.
      • Decreased pO2: partial respiratory failure
      • Decreased pO2 and increased pCO2: global respiratory failure
      • Many individuals with severe COPD have chronic hypercapnia due to CO2 trapping from hyperinflation and progressive loss of pulmonary elasticity.

Imaging

Other tests

Consider AATD in patients with COPD who are < 60 years of age, have no smoking history, and/or have basilar-predominant COPD. However, testing for AATD is recommended for all new patients with COPD.

Differential diagnoses

The differential diagnoses listed here are not exhaustive.

Treatment

General treatment [1][2]

Medical treatment according to GOLD [1]

Medical treatment in COPD reduces the severity of symptoms, improves overall health status, and lowers the frequency and severity of exacerbation. The first-line treatment of COPD consists of bronchodilators, inhaled corticosteroids, and phosphodiesterase (PDE) type 4 inhibitors.

Patient group Exacerbations per year Symptoms Initial treatment Subsequent escalation
A
  • ≤ 1 (with no hospital admission)
  • Mild symptoms
B
  • Severe symptoms
C
  • ≥ 2
  • ≥ 1 leading to hospital admission
  • Mild symptoms
D
  • Severe symptoms

Other treatment options [1]

Complications

Chronic respiratory failure [2]

  • Description: occurs in the advanced stages of COPD due to progressive emphysematous changes and loss of diffusion surface area
  • Criteria
    • Long-standing partial respiratory failure (pO2 at rest < 60 mm Hg)
    • Global respiratory insufficiency failure (pO2 changes at rest < 60 mm Hg and pCO2 > 45 mm Hg)
  • Management: depends on the severity and etiology [1]
    • Long-term oxygen therapy (LTOT): 16 hours oxygen administration per day (minimum dosage) is associated with lower mortality rates.
      • Indication: patients with COPD GOLD D and severe respiratory insufficiency failure that exhibit long-standing pO2 < 55 mm Hg, despite administration of optimal medication
      • Oxygen administration is regulated in a way that the pO2 value rises and pCO2 drops to a level of 60–70 mm Hg. Hypercapnia would lead to respiratory acidosis and disorientation and should be prevented. [21]
    • Portable respiration
      • Principle: a type of non-invasive respiration done overnight when the patient is asleep
      • Goal: This allows recovery of the respiratory muscles and in turn permits better respiratory function during the day.
    • Lung volume reduction surgery
    • Lung transplantation: considered the last resort in patients with emphysema associated with advanced COPD and severe diffusion dysfunction

Other complications [2]

We list the most important complications. The selection is not exhaustive.

Prognosis

  • 40–70% of all COPD patients survive the first 5 years after diagnosis. [22]
  • Survival rates vary significantly depending on the severity of the disease. [22]
  • Measures that improve survival
  • COPD is the third most common cause of death worldwide. [23]

References

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  2. Barnes PJ, Drazen JM, Rennard SI. Asthma and COPD. Academic Press ; 2009
  3. Sarkar M, Mahesh D, Madabhavi I. Digital clubbing. Lung India. 2012; 29 (4): p.354. doi: 10.4103/0970-2113.102824 . | Open in Read by QxMD
  4. Sandhaus RA, Turino G, Brantly ML, et al. The Diagnosis and Management of Alpha-1 Antitrypsin Deficiency in the Adult. Chronic Obstructive Pulmonary Diseases: Journal of the COPD Foundation. 2016; 3 (3): p.668-682. doi: 10.15326/jcopdf.3.3.2015.0182 . | Open in Read by QxMD
  5. Harrigan RA. ABC of clinical electrocardiography: Conditions affecting the right side of the heart. BMJ. 2002; 324 (7347): p.1201-1204. doi: 10.1136/bmj.324.7347.1201 . | Open in Read by QxMD
  6. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease Report 2018. http://goldcopd.org/wp-content/uploads/2017/11/GOLD-2018-v6.0-FINAL-revised-20-Nov_WMS.pdf. Updated: January 1, 2018. Accessed: March 27, 2018.
  7. Martineau AR, James WY, Hooper RL, et al. Vitamin D 3 supplementation in patients with chronic obstructive pulmonary disease (ViDiCO): a multicentre, double-blind, randomised controlled trial. Lancet Respir Med. 2015; 3 (2): p.120-130. doi: 10.1016/s2213-2600(14)70255-3 . | Open in Read by QxMD
  8. Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012; 16 (5): p.323. doi: 10.1186/cc11475 . | Open in Read by QxMD
  9. Nishimura K, Tsukino M. Clinical course and prognosis of patients with chronic obstructive pulmonary disease. Curr Opin Pulm Med. 2000; 6 (2): p.127-132. doi: 10.1097/00063198-200003000-00008 . | Open in Read by QxMD
  10. The top 10 causes of death. http://www.who.int/mediacentre/factsheets/fs310/en/. Updated: January 1, 2017. Accessed: March 27, 2018.
  11. Peter J. Barnes. Sex Differences in Chronic Obstructive Pulmonary Disease Mechanisms. American Journal of Respiratory and Critical Care Medicine. 2016 .
  12. Georgios Ntritsos, Jacob Franek, Evangelos Evangelou, et al.. Gender-specific estimates of COPD prevalence: a systematic review and meta-analysis. International Journal of Chronic Obstructive Pulmonary Disease. 2018 .
  13. Wheaton AG, Cunningham TJ, Ford ES, Croft JB, Centers for Disease Control and Prevention (CDC).. Employment and activity limitations among adults with chronic obstructive pulmonary disease--United States, 2013.. MMWR Morb Mortal Wkly Rep. 2015; 64 (11): p.289-95.
  14. Liu Y, Pleasants R, Croft J, et al. Smoking duration, respiratory symptoms, and COPD in adults aged ≥45 years with a smoking history. International Journal of Chronic Obstructive Pulmonary Disease. 2015 : p.1409. doi: 10.2147/copd.s82259 . | Open in Read by QxMD
  15. Household air pollution and health. http://www.who.int/mediacentre/factsheets/fs292/en/. Updated: February 1, 2016. Accessed: February 27, 2017.
  16. Occupational and work-related diseases. http://www.who.int/occupational_health/activities/occupational_work_diseases/en/. Updated: February 27, 2017. Accessed: February 27, 2017.
  17. Singh D, Agusti A, Anzueto A, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. European Respiratory Journal. 2019; 53 (5): p.1900164. doi: 10.1183/13993003.00164-2019 . | Open in Read by QxMD
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