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Chronic obstructive pulmonary disease (COPD) is a leading cause of death in the United States, affecting 16 million persons and many others living with the condition undiagnosed.1 In 2017, the National Institutes of Health (NIH) declared COPD one of the most urgent health care problems facing Americans. Since 1969, the death rate for COPD has doubled; however, that the number of deaths attributed to other chronic conditions has declined.2 Chronic lower respiratory disease, primarily COPD, is projected to be the third leading cause of death by 2020.3

Etiology and Risk Factors

COPD is most commonly due to a history of tobacco use, with approximately 80% of deaths related to smoking.4 Approximately 25% of persons with COPD have no history of smoking but may have been exposed to lung irritants or passive smoke.5 Exposure to cigarette smoke, air pollution, dust, chemicals, or other fumes contribute to the development of COPD. Any factor that affects lung growth during gestation or childhood can also predispose a person to COPD. Persons with alpha-1 antitrypsin deficiency, a rare genetic disorder, are at increased risk for COPD. Many persons with this disorder are young adults for whom the condition is undiagnosed. Approximately 20% of patients with COPD report a history of asthma, which is likely a contributing factor.6 Prevalence of COPD is greater in older age groups (>65 years) and women.7

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Three pathologic conditions within the lungs — chronic bronchitis, emphysema, and hyperreactive airway disease — make up COPD. In chronic bronchitis, the airways become inflamed, and excessive mucus production obstructs air from entering the lungs. Contraction of smooth muscle in the airways causes narrowing that further limits air entry. Difficulty clearing mucus and obstruction of ventilation leads to hypoxia8 and ventilation-perfusion mismatching, in which parts of the lung do not receive oxygenation. This leads to pulmonary arteriole vasoconstriction, which places increased resistance against the right ventricle of the heart (ie, pulmonary hypertension).9[

Increasing pulmonary artery pressure can eventually result in right ventricular failure (ie, cor pulmonale).8

The disease process in chronic bronchitis is different from that in emphysema, in which alveolar membranes lose integrity and become overly distended. Smoking destroys antiproteolytic enzymes and antioxidants in the lungs, which in turn allows proteolytic enzymes and oxidizing agents to weaken alveolar membranes to where they become unable to recoil with exhalation.10 The reduction in elasticity and recoil of lung tissue causes excessive accumulation of CO2, as it is not adequately removed with exhalation. This increases residual volume and blood levels of CO2, potentially disrupting acid-base balance and increasing the risk for respiratory acidosis.8

Hyperreactive airways in COPD are easily triggered by inhaled irritants. Episodic bronchospasms develop, creating an asthmatic component of the disease process.8 With advancing disease, the airway walls thicken and become filled with white blood cells, which secrete inflammatory mediators such as interleukins and tumor necrosis factor-alpha. Epigenetic changes are theorized to cause permanent remodeling of the airways and alveoli.11 Remodeling leads to fibrotic changes in the airways and alveoli that cause progressive ventilatory obstruction.

Clinical Manifestations

Patients with COPD present with symptoms of chronic bronchitis, emphysema, and asthma. Chronic bronchitis causes productive cough, dyspnea, and cyanosis. Due to the stasis of mucus and secretions, patients are at increased risk for pulmonary infection. Many patients with COPD report increased episodes of “winter bronchitis.” Patients often exhibit tachypnea, noisy breathing, open-mouth breathing, clubbing of the nails, and orthopnea.12 With time, findings due to right ventricular failure — such as jugular venous distension, ascites, hepatomegaly, splenomegaly, and ankle or sacral edema — may develop. Air-filled lungs from emphysema can cause an enlarged, barrel-shaped chest to develop. The patient commonly exhales slowly through pursed lips. Wheezing can often be auscultated or heard without a stethoscope. Patients will often report chronic cough and shortness of breath, particularly with exercise.12


The patient history commonly is notable for more than 30 pack-years of smoking. Pulmonary function testing (PFT) is required to make a diagnosis of COPD; it measures the different volumes involved in a patient’s ventilation. Forced expiratory volume and forced vital capacity are the focus in PFT. Forced expiratory volume during 1 second (FEV1) is the amount of air exhaled in the first second of exhalation, and forced vital capacity (FVC) is the volume of air exhaled with maximal effort. The ratio of FEV1 to FVC is measured before and after the patient uses a bronchodilator to maximally open their airways. An FEV1/FVC <70% after using a bronchodilator establishes the presence of airflow limitation, confirming the diagnosis of COPD.13

COPD severity is classified according to criteria established by the Global Strategy for the Diagnosis, Management, and Prevention of COPD, 2019 (Table 1).13

Table 1. Classification of Severity of Airflow Limitation in COPD13

GOLD Classification   Severity PFT Results
GOLD 1 Mild FEV1 ≥80% predicted  
GOLD 2 Moderate 50% ≤FEV1 <80% predicted  
GOLD 3 Severe 30% ≤ FEV1 <50% predicted    
GOLD 4 Very Severe FEV1 <30% predicted    

*In patients who have FEV1 /FVC <70% after use of bronchodilator.