Chronic Obstructive Pulmonary Disease
Sean O’Reilly
Deirdre L. Kathman
I. GENERAL PRINCIPLES
A. Chronic obstructive pulmonary disease (COPD): a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.
B. COPD frequently results in significant activity limitation, permanent disability, and frequent utilization of costly medical resources.
II. ETIOLOGY
A. Cigarette smoking is the major risk factor. Age at initiation and total number of pack years are associated with the diagnosis.
B. Homozygous α1-antitrypsin deficiency.
C. Other factors that may increase risk include significant childhood respiratory illnesses, outdoor and indoor air pollution (especially cooking with coal, wood, and charcoal), uncontrolled asthma, and occupational dust and chemical exposure.
III. PATHOPHYSIOLOGY
A. Structural (excessive mucus production, mucus gland hypertrophy, and inflammatory edema) and functional airway narrowing (bronchoconstriction, loss of elastic recoil, and destruction of alveoli) causes expiratory airflow limitation.
B. Consequences of severe, chronic airflow obstruction.
1. Reduced flow rates, limiting minute ventilation.
2. Ventilation/perfusion ([V with dot above]/[Q with dot above]) mismatch.
3. Air trapping, hyperinflation, and increased airway resistance place elevated workloads on the respiratory muscles and can result in muscle fatigue.
4. CO2 retention due to increased dead space and a shift of the hemoglobin-oxygen binding curve.
IV. DIAGNOSIS
A. History.
1. Cardinal symptoms are chronic productive cough and dyspnea on exertion.
2. The diagnosis is unlikely without history of smoking; however, it develops in a minority of smokers, suggesting some role of host susceptibility.
B. Physical examination.
1. Rarely diagnostic; may include pursed lip breathing, accessory muscle use, decreased breath sounds, prolonged expiration, wheezing, and hyperinflation.
C. Radiology.
1. Chest roentgenogram findings are not sensitive for the diagnosis of COPD.
2. Chest computed tomography (CT) scan is more sensitive for COPD and can demonstrate emphysematous changes, when present, and the nature and extent of disease. It can also be used to screen for patients who might benefit from lung volume reduction techniques.
D. Pulmonary function tests (PFTs).
1. Expiratory airflow obstruction on spirometry that is not fully reversible, as measured by a postbronchodilator ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC).
2. FEV1/FVC of <0.7 is required to make the diagnosis of COPD.
3. Postbronchodilator FEV1 correlates with clinical outcome and mortality; not entirely predictive of disease progression and may not correlate with functional status.
4. Hypercapnic respiratory failure in COPD is not usually seen until FEV1 is <1 L.
5. Increased total lung capacity and residual volume, suggesting air trapping, and/or a reduction in carbon monoxide diffusing capacity may occur.
6. Arterial blood gases (ABGs) diagnose and quantitate the severity of respiratory failure; consider if peripheral oxygen saturation <92% or if concern for hypercapnia.
7. Pulse oximetry should be performed in all stable patients with FEV1 < 35% predicted or with clinical signs of respiratory or right heart failure to assess need for supplemental oxygen.
E. Global Initiative for Chronic Obstructive Lung Disease (GOLD).
1. Consensus workshop report with strategy for diagnosis, management, and prevention of COPD.
2. GOLD guidelines describe a spirometric classification of disease severity. In patients with FEV1/FVC < 0.7, based upon postbronchodilator FEV1.
a. Stage I (mild): FEV1 ≥ 80% predicted.
b. Stage II (moderate): 50% ≤ FEV1 < 80% predicted.
c. Stage III (severe): 30% ≤ FEV1 < 50% predicted.
d. Stage IV (very severe): FEV1 < 30% predicted.
3. GOLD guidelines also describe a combined assessment of COPD severity that is based on symptoms, spirometric classification, and frequency of exacerbations. The combined assessment is designed to improve management.
F. Acute exacerbation of COPD.
1. Classically marked by one or more of the following:
a. Increase in severity or frequency of cough.
b. Increased sputum production or purulence.
c. Worsening dyspnea.
2. Nearly 70% to 80% of exacerbations are related to upper or lower respiratory infections.
3. Exacerbation frequency varies greatly between patients; tends to increase with worsening airflow limitation.
V. TREATMENT
A. Acute exacerbations.
1. Oxygen therapy is required in all hypoxemic patients (PaO2 < 60 mm Hg) with an acute exacerbation. Correction of hypoxemia is of prime importance, although the change in PaCO2 with FIO2