Chronic Obstructive Pulmonary Disease
Roger D. Yusen
Chronic obstructive pulmonary disease (COPD) is a common, preventable, treatable, and usually progressive condition characterized by persistent airflow limitation (i.e., not fully reversible) and an enhanced chronic inflammatory response to noxious particles or gases.
Patients with COPD have emphysema and/or airways disease (e.g., chronic bronchitis).
Emphysema, defined pathologically, consists of nonuniform distal airway enlargement associated with destruction of the acini, loss of lung elasticity, and absence of significant parenchymal fibrosis.
Chronic bronchitis is defined clinically as cough productive of (e.g., at least 2 tablespoons of) sputum on most days of 3 consecutive months in 2 consecutive years, in the absence of other lung diseases.
COPD has characteristics that overlap with asthma, and both conditions may occur in the same patient (asthma copd overlap syndrome, ACOS).
Although asthma, bronchiectasis, obliterative bronchiolitis, and sarcoidosis often have associated expiratory airflow obstruction, they do not fall within the classification of COPD.
The Global Obstructive Lung Disease 2015 (GOLD) classification of COPD bases its assessment on the patient’s level of symptoms, exacerbation history, spirometric abnormality, and identification of comorbidities.1
Inhaled particles that cause lung inflammation may induce parenchymal tissue destruction (e.g., emphysema) and cause airway disease (e.g., airway fibrosis) through the disruption of normal repair and defense mechanisms.
Increased mucus production from goblet cell hyperplasia.
Genetic disorders may create a predisposition to developing COPD.
Role of airway infections in COPD:
Defective innate immune responses promote persistent airway bacterial colonization and recurrent airway infections.
Acute airway infections often lead to acute exacerbations and subsequently worsened lung function.
Viral infections (e.g., influenza, rhinovirus, and adenovirus) and bacterial infection (e.g., Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Mycoplasma pneumoniae) cause most exacerbations.
TABLE 10-1 2016 GOLD SEVERITY GRADE OF AIRFLOW LIMITATION FOR PATIENTS THAT HAVE COPDa
The risk of developing COPD correlates with the total lifetime burden of exposure of inhaled toxins.
The most important risk factor for the development of COPD is cigarette smoking, which is associated with the majority of cases. However, only a minority of smokers develop clinically significant COPD, suggesting that genetic predisposition and other environmental factors may be required for its development.
Cigar and pipe smokers are also at increased risk of developing COPD.
Occupational exposures and indoor air pollution may lead to COPD.
Genetic disorders may lead to the development of COPD. α1-Antitrypsin deficiency (A1ATD) contributes to <1% of COPD cases.
α1-Antitrypsin inhibits neutrophil-derived elastase, an enzyme responsible for the destruction of lung parenchyma in emphysema.
Patients with A1ATD carry a genetic polymorphism that leads to decreased α1-antitrypsin serum levels.
A1ATD should be considered in a patient with emphysema who has:
A number of extrapulmonary comorbidities have been identified in those with COPD such as cardiovascular disease, lung cancer, osteoporosis, skeletal muscle dysfunction, depression, and metabolic syndrome.
Symptoms of dyspnea or chronic cough should lead to an evaluation.
History of heavy smoking should prompt further evaluation in the appropriate clinical setting.
Spirometry is required to make the diagnosis of COPD.
Symptoms of COPD typically consist of increased dyspnea with exertion, decreased exercise tolerance, and increased sputum production.
Chronic cough and sputum production may precede the development of COPD by many years.
COPD may develop without chronic cough or sputum production.
Dyspnea from COPD typically develops after the FEV1 has significantly decreased (e.g., <60% of the predicted normal value) over many years.
Clinicians should perform a thorough medical history assessment, and question patients regarding symptoms, risk factors, clinical course, comorbidities, medications, and family history.
Physical examination findings suggestive of COPD do not become apparent until after COPD has significantly progressed, and include:
Accessory muscle use, pursed lip breathing, and Hoover sign.
Hyperinflation of the lungs associated with hyperresonant chest percussion.
Decreased breath and heart sounds.
Expiratory wheezes variably occur.
Clubbing of the fingers not expected.
Symptoms of cor pulmonale occur less commonly:
Lower extremity edema.
Right ventricular precordial heave, increased S2 and P2 strength, right-sided S3, and tricuspid regurgitation.
Spirometry is used to diagnose COPD, and the FEV1 determines the severity of the expiratory airflow obstruction based on the GOLD stages, see Table 10-1 for classification schema.1
Peak expiratory flow measurement has high sensitivity but low specificity.
Symptoms and examination findings assist with diagnosis.
Imaging studies provide evidence of the presence or absence of emphysema.
Reactive airways dysfunction syndrome
Langerhans cell histiocytosis
Fixed or variable airway obstruction in the upper airways
Vocal cord dysfunction
Congestive heart failure (will not cause expiratory airflow obstruction)
We suggest obtaining an arterial blood gas (ABG) if the patient has a low SpO2 (e.g., <92%), FEV1 very low (e.g., <35%), or signs of respiratory or right heart failure occur.
CBC, to look for polycythemia.
Complete metabolic panel, to look for elevated bicarbonate level.
CXR posterioranterior and lateral to assess for emphysema or other conditions that could produce similar signs or symptoms.
Pulmonary function tests:
Spirometry: pre- and postbronchodilator (FEV1/FVC <0.70 and scooping of the expiratory limb of the flow–volume curve).
Lung volumes (e.g., air trapping [elevated residual volume (RV)] and thoracic hyperinflation [e.g., elevated total lung capacity (TLC)]).
Diffusing capacity (e.g., reduced diffusing capacity of the lung for carbon monoxide [DLCO]).
Pulse oximetry assessment at rest, with exercise, and possibly during sleep.
Cardiac testing, when appropriate, to assist with a dyspnea evaluation.
COPD exacerbations are diagnosed clinically based on a worsening in respiratory symptoms beyond the expected day-to-day variation.
COPD exacerbations typically increase (compared to baseline) one or more of the following:
Cough and sputum production
The first step taken when encountering a patient with an acute exacerbation should be a quick assessment to determine the need for hospitalization or intensive care unit (ICU) admission for impending respiratory failure (Table 10-2).
TABLE 10-2 INDICATIONS FOR ICU ADMISSION
Severe dyspnea that does not adequately respond to initial therapy
Mental status deterioration (e.g., confusion, coma, lethargy)
Persistently worse or worsening hypercapnia or respiratory acidosis
Persistently worse or worsening hypoxemia
Lack of adequate response to supplemental oxygen and/or noninvasive positive pressure ventilation
Indications for inpatient admission include
New physical findings such as cyanosis or peripheral edema
New or worsened hypoxemia/hypercapnia
Lack of adequate response to initial medical management
Consider hospital admission for those with advanced age or significant comorbidities
ABG, CBC, chemistry panel, brain natriuretic peptide (BNP), and cardiac enzymes.
ABG provides important information about alveolar gas exchange and acid–base status not obtained by pulse oximetry.
ABGs can differentiate between acute and chronic respiratory acidosis, and may indicate a need for assisted ventilation and ICU admission.
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