a. Disorders. There are four major obstructive lung diseases:
ii. Chronic obstructive pulmonary disease (COPD)
iv. Cystic fibrosis
b. Definitions. All obstructive diseases are marked by airflow limitation, characterized by a low forced expiratory volume in 1 second (FEV1) and a low FEV1/forced vital capacity (FVC) ratio. Asthma and COPD are by far the most common obstructive lung diseases; therefore, these two disorders are the focus of this chapter. Please note that there is increasing recognition that an overlap exists between these phenotypes.
i. Asthma is characterized by reversible narrowing of the distal airways as a result of chronic inflammation and airway hyperreactivity. Over time, pathologic changes, including smooth muscle hypertrophy, mucosal edema, excessive mucus secretion, and mucus plugging, develop. Initially, the airflow limitation is reversible with bronchodilators. Because of reversibility, the FVC and FEV1 may be normal between exacerbations. A methacholine provocation test showing a drop in FEV1 of ≥20% supports a clinical diagnosis of asthma.
ii. COPD is characterized by persistent and progressive airflow limitation. Like asthma, it is associated with a heightened inflammatory response to noxious particles and gases in the airways and lungs. Most patients have some combination of chronic bronchitis and emphysema.
1. Chronic bronchitis is clinically defined by productive cough for >3 months for >2 consecutive years. This results from chronic large and small airway inflammation with hyperproduction of mucus.
2. Emphysema is pathologically defined by permanent enlargement of the airspaces distal to the terminal bronchioles with parenchymal destruction.
iii. Asthma-COPD overlap syndrome (ACOS). Although the distinct phenotypes of asthma and COPD have been well studied, it is estimated that ACOS is present in 15%–45% of patients with obstructive lung disease. This entity represents a convergence of the two phenotypes of disease and is more prevalent with increased age.
B. Clinical Manifestations of Asthma and Chronic Obstructive Pulmonary Disease
a. Asthma is usually seen in children and young adults. Clinical manifestations include:
i. Episodic wheezing, chest tightness, and dyspnea
ii. Chronic cough
iii. Tachypnea, use of accessory muscles, and intercostal retraction
iv. A prolonged expiration phase and hyperresonance to percussion
v. Pulsus paradoxus
i. Chronic and progressive dyspnea
iii. Sputum production
iv. Wheezing during an exacerbation
v. Hypoxemia is common in early stages of the disease. As the condition progresses, hypercarbia develops and is a hallmark of chronicity
C. Diagnosis. Asthma and COPD are diagnosed on the basis of history, physical examination findings, and abnormal pulmonary function tests.
a. Asthma. Patients with asthma are usually diagnosed based on history, pulmonary function testing, and responsiveness to therapy. When the diagnosis is in question, specialized testing can be performed (e.g., methacholine provocation, exercise spirometry) to aid in the diagnosis. Remember, “not all that wheezes is asthma,” and assessment of the degree of asthma control is particularly relevant to prevent complications (Table 19.1).
Table 19.1 Assessment of Asthma Control
Asthma Symptom Control
Level of Asthma Symptom Control
In the past 4 weeks, has the patient had:
Daytime asthma symptoms more than twice/week?
None of these
1–2 of these
3–4 of these
Any night waking due to asthma?
Reliever needed for symptoms more than twice/week?
Any activity limitation due to asthma?
b. COPD. Patients with COPD often have a history of chronic cough, sputum production, and dyspnea for many years. Besides identification of the most common risk factor, cigarette smoking, recognizing other risk factors such as secondhand smoke, occupational exposures to organic and inorganic dusts, and indoor pollution from biomass cooking in poorly ventilated areas is important. α1-Antitrypsin deficiency should be suspected in patients who are younger than 40 years, especially if they have predominantly basilar emphysema. Use the Global Initiative for Chronic Obstructive Lung Disease (GOLD) system to grade the severity of COPD by spirometry (Table 19.2).
Table 19.2 GOLD Classification of Chronic Obstructive Pulmonary Disease
Degree of Severity
Forced Expiratory Volume in 1 Second (FEV1)
D. Treatment. Treatments of asthma and COPD and their acute exacerbations share common approaches. Exacerbations of disease are characterized by worsening of the patient’s respiratory symptoms beyond normal daily variation.
a. Risk factor modification. Encourage smoking cessation and reduce other identified occupational and home exposures. Smoking cessation should be assessed at every opportunity in both the outpatient and inpatient settings.
b. Management strategy
i. COPD. Grade the severity of disease by using a combination of GOLD stage, frequency of exacerbations, and validated scales such as the COPD assessment test or asthma control test to guide therapy. Level of dyspnea can be assessed by the modified Medical Research Council Scale. Tables 19.3 and 19.4 show how these features are used to help guide therapy in stable disease.
ii. Asthma. After assessing level of control (see Table 19.2), prescribe therapy in a stepwise fashion as shown in Table 19.5. Review response to therapy to determine escalation. The severity of asthma can be defined by the regimen, or step, required to maintain the patient in a well-controlled state.
Table 19.3 Grading Severity of Chronic Obstructive Pulmonary Disease by Symptoms and Exacerbation Risk
Exacerbations per Year
Low risk, less symptoms
Low risk, more symptoms
High risk, less symptoms
High risk, more symptoms
GOLD = Global Initiative for Obstructive Lung Disease; CAT = COPD Assessment Test; mMRC = modified Medical Research Council.
Table 19.4 Treatment of Stable Chronic Obstructive Pulmonary Disease
SABA/SAMA as needed
LABA or LAMA (consider both if severe dyspnea)
ICS + LABA or LAMA combination; or add-on PDE-4 instead of ICS as alternative
ICS + LABA and/or LAMA combination; add-on PDE-4 to ICS/LABA or LAMA
SABA = short-acting β-agonist; SAMA = short-acting muscarinic antagonist; ICS = inhaled corticosteroid, LABA = long-acting β-agonist; LAMA = long-acting muscarinic antagonist; PDE-4 = phosphodiesterase-4 inhibitor.
Table 19.5 Management of Asthma in a Stepwise Fashion
Refer for add-on (immunologic therapy)
Other controller options
Consider low-dose ICS
LTRA or low-dose theophylline
Med/high dose ICS + LTRA
Add tiotropium High-dose ICS + LTRA
Add low-dose OCS
As-needed SABA or low-dose ICS/formoterol
MILD, if well controlled at steps 1–2
MODERATE, if well controlled at step 3
SEVERE, if well controlled at steps 5–6
SABA = short-acting β-agonist; SAMA = short-acting muscarinic antagonist; ICS = inhaled corticosteroid, LABA = long-acting β-agonist; LTRA = leukotriene receptor antagonist; OCS = oral corticosteroid.
c. Bronchodilators are first-line agents in the management of both stable disease and acute exacerbations. There are short- and long-acting β-agonists (SABA and LABA, respectively), as well as short- and long-acting muscarinic agonists (SAMA and LAMA, respectively) to choose from. Patients must use proper technique with drug delivery devices (i.e., inhalers) for therapy to be effective. Therefore, careful patient coaching along with the use of a spacer with the inhaler is paramount. A common SAMA, ipratropium, may be more effective in COPD than asthma. SABAs, such as albuterol, appear to have a more rapid onset of action and can be nebulized if patients are too distressed to use metered-dose inhalers effectively.
d. Steroids are critical agents in the management of acute asthma exacerbations and are also of benefit in patients hospitalized with COPD exacerbations. Inhaled corticosteroids are used early in the management of asthma, whereas they are reserved for more severe disease in COPD. Oral or intravenous steroids can be used to treat acute exacerbations of both diseases. Length of steroid therapy is generally 5 days but may be longer in select patients who do not respond to initial therapy. Oral therapy is as efficacious as parenteral therapy and should be used if patients can tolerate it.
e. Theophylline is now uncommonly used to treat asthma and COPD because of concerns regarding toxicity. If used, levels should be checked carefully and doses modified accordingly. More recently, a new phosphodiesterase-4 inhibitor, roflumilast, has been shown to reduce exacerbations in patients with moderate or severe exacerbations of COPD when used in addition to a LABA.
f. Oxygen supplementation should be used in all patients who are hypoxemic. Long-term oxygen therapy in patients with COPD with chronic hypoxemia (SpO2 ≤88% or Pao2 ≤55 mm Hg) improves survival. Flow rate that achieves an SpO2 of 90%–92% should be prescribed so as to avoid deleterious effects of oxygen toxicity. Caution is needed in patients susceptible to carbon dioxide retention because high blood levels of oxygen can blunt the normal physiologic hypoxemic vasoconstrictive response and worsen V/Q match (increase dead space due to redirection of blood flow to areas not participating in gas exchange).
g. Heliox, a mixture of oxygen and helium, improves laminar air flow to decrease airway resistance. Although there is no role for its use in routine care of asthma or COPD, it may be considered in severe exacerbation of asthma (not COPD), with airflow limitation not responding to routine modalities.
h. Intravenous magnesium, although controversial, may be beneficial in patients with severe asthma by inducing smooth muscle relaxation.
i. Antibiotics should be given to patients with COPD exacerbation who have an increase in all of the following symptoms: dyspnea, sputum volume, and sputum purulence or two symptoms if increased sputum purulence is present. Antibiotics should otherwise be reserved in treating acute exacerbations of asthma, unless a bacterial infection is specifically suspected.
j. Noninvasive positive pressure ventilation (NPPV) should be considered in patients with COPD exacerbation with severe dyspnea without a diminished level of consciousness. NPPV decreases work of breathing, improves ventilation and oxygenation, and has been shown to improve outcomes in patients with COPD exacerbation. The evidence for NPPV in severe asthma exacerbations is weak. Therefore, NPPV should only be tried in asthmatic patients in a closely monitored setting.
k. Mechanical ventilation may be necessary for definitive respiratory support in patients who fail NPPV or are too unstable to tolerate NPPV.
Suggested Further Readings
Global Initiative for Asthma. Global strategy for asthma management and prevention: National Institutes of Health, and National Heart, Lung, and Blood Institute; 2006.Find this resource:
Postma DS, van den Berge M. The different faces of the asthma-COPD overlap syndrome. Eur Respir J 2015;46:587–90.Find this resource:
Qaseem A, Wilt TJ, Weinberger SE, et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med 2011;155:179–91.Find this resource:
Rabe KF, Hurd S, Anzueto A, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med 2007;176:532–55.Find this resource: