1 What is chronic obstructive pulmonary disease (COPD)?

COPD is characterized by airflow limitation that is not fully reversible. Chronic airflow limitation results from a combination of small-airway disease and parenchymal destruction due to inflammatory processes. These inflammatory processes are often caused by exposure to noxious particles or gases.

2 How many people are affected by COPD?

COPD is the fourth leading cause of mortality and morbidity in the United States. The number of people affected by COPD worldwide continues to increase because of exposure to tobacco smoke and aging of the population. Historically the prevalence of disease was higher in men, but, with changing patterns of exposure to tobacco, women are now affected as frequently as men. Worldwide, exposure to indoor pollution from heating and cooking fuels substantially contributes to COPD in women.

3 What processes are involved in the pathogenesis of COPD?

COPD is characterized by chronic inflammation throughout the lung, with increased neutrophils, macrophages, and CD8⁺ T lymphocytes. An imbalance between proteinase-antiproteinase activity and oxidative stress also contributes to the pathogenesis of this disease. Oxidative stress and proteinase-antiproteinase imbalance can be related to a combination of factors, including the inflammation itself, environmental exposures (e.g., oxidative substances in cigarette smoke), and genetics (e.g., α₁-antitrypsin deficiency).

4 What are the major pathologic changes in COPD?

All structures of the lung are subjected to pathologic changes in COPD. In the central airways, inflammatory cells infiltrate the surface epithelium, edema is present, mucus-secreting glands are enlarged, and the number of goblet cells increases with mucus hypersecretion. In the peripheral airways (small bronchi and bronchioles with an internal diameter < 2 mm), chronic inflammation leads to repeated injury and repair of the airway wall. In emphysema, destruction of alveolar septa leads to confluence of adjacent alveoli and enlarged terminal air spaces. Vascular changes include thickening of the vessel wall with increased smooth muscle, proteoglycans, and collagen deposition.

5 How is severity graded in COPD?

The staging system should be regarded as an educational tool and a guide to management (Table 22-1).

^{Table 22-1} Classification of Copd by Severity

FEV₁ < 30% predicted or FEV₁ < 50% predicted plus chronic respiratory failure.

FEV₁, Forced expiratory volume in 1 second; FVC, forced vital capacity.

From the Global Initiative for Chronic Obstructive Lung Disease.

6 What are the benefits of smoking cessation for a patient with COPD?

Smoking cessation is the most important intervention. It is the most effective intervention to decelerate the decline in lung function characteristic of this disease. In addition to the modest improvement in forced expiratory volume in 1 second (FEV₁) seen with smoking cessation, the rate of decline in FEV₁ may be reduced, in some cases even to the rate found in healthy nonsmokers (± 30 mL/yr).

7 Why are bronchodilators used in the treatment of COPD?

Bronchodilators treat airway obstruction in patients with COPD. By reducing bronchomotor tone, they decrease airway resistance, which can improve airflow. This will improve emptying of the lungs and tends to reduce dynamic hyperinflation during rest and exercise and thus improve exercise performance. Spirometric changes after bronchodilator therapy may be minimal, despite significant clinical benefit, as quantified by changes in quality-of-life measures and exercise tolerance (e.g., 6-minute walk).

8 Which bronchodilators should be used in the treatment of COPD?

9 Are inhaled corticosteroids beneficial in COPD?

Although regular use of inhaled corticosteroids does not prevent loss of lung function in patients with COPD, inhaled corticosteroids in combination with long-acting bronchodilators are recommended for patients with severe disease (FEV₁ < 50% predicted) and recurrent exacerbations. Data indicate that inhaled corticosteroids in combination with long-acting bronchodilators decrease the risk of exacerbations in patients with COPD. However, treatment with inhaled corticosteroids alone may increase the risk of pneumonia and does not reduce mortality.

10 What other pharmacologic treatments may benefit patients with COPD?

11 Who should get pulmonary rehabilitation?

Patients with all levels of COPD can benefit from exercise training programs. Pulmonary rehabilitation has been shown to improve functional status, decrease dyspnea, and reduce health care use. Pulmonary rehabilitation is currently recommended as part of the treatment plan for patients with moderate, severe, and very severe COPD.

12 What are the indications for long-term oxygen therapy in patients with COPD?

For a patient at rest breathing room air in a stable condition:

or

and one of the following:

13 What level of oxygen should be prescribed for patients with the indications listed in question 12?

Oxygen should be prescribed in a dose sufficient to raise the PaO₂ to 65 to 80 mm Hg at rest during wakefulness. This PaO₂ usually is achieved with a 1- to 4-L/min oxygen flow through nasal prongs. The dose of O₂ should be increased by 1 L/min during sleep or exercise to prevent hypoxemic episodes. Oxygen should be given continuously at least 19 hours per day.

14 Is lung volume reduction surgery effective in the treatment of COPD?

In lung volume reduction surgery, part of the lungs is resected to reduce hyperinflation. This has beneficial effects on the mechanical action of the respiratory muscles and improves elastic recoil, which facilitates emptying of the lungs. Lung volume reduction surgery does not improve long-term survival in COPD but does improve exercise capacity in a select group of patients. Patients who benefit from lung volume reduction surgery are those with predominantly upper lobe emphysema and a low exercise capacity.

15 What factors predict death in patients with COPD?

Long-term prognosis is hard to predict in patients with COPD. Factors that have been shown to predict mortality include low body mass index, degree of airflow obstruction, dyspnea, and exercise capacity as measured by the 6-minute walk test.

16 Are antibiotics useful in treating COPD exacerbations?

Giving antibiotics for COPD exacerbations is indicated when patients are seen with increased sputum purulence associated with increased sputum volume and/or dyspnea. For patients receiving mechanical ventilation for a COPD exacerbation, withholding antibiotics has been associated with increased mortality and hospital-acquired pneumonia.

17 What organisms cause COPD exacerbations?

Bacteria and viruses cause COPD exacerbations. In mild exacerbations Streptococcus pneumoniae is common. As severity of COPD increases, Haemophilus influenzae and Moraxella catarrhalis become more common, and, in severe COPD, Pseudomonas aeruginosa may occur.

18 What is the role of steroids in the treatment of COPD exacerbations?

Systemic glucocorticoids shorten the duration of the exacerbation and lead to faster improvements in lung function. A recent study suggested that nebulized budesonide may be an alternative to oral glucocorticoids in nonacidotic exacerbations but is likely to be more expensive.

19 What are the causes of acute respiratory failure in patients with COPD?

Causes include bronchial infection, pulmonary emboli, cardiac failure, pneumonia, pneumothorax, respiratory depression (usually by the injudicious use of sedatives or narcotic analgesic drugs), surgery (especially of chest and upper abdomen), stopping of medications, or occasionally malnutrition. In general, the criteria for the diagnosis of acute respiratory failure in patients with COPD include the following:

20 What is the initial treatment of a severe COPD exacerbation?

Assess the patient’s symptoms and signs, and obtain a chest radiograph and arterial blood gas analysis. Administer adequate oxygen: Death or irreversible brain damage results within minutes when severe hypoxemia is present, whereas hypercapnia may be well tolerated. The appropriate amount of oxygen is that which satisfies tissue oxygen needs: usually a PaO₂ > 60 mm Hg, without worsening the respiratory acidosis and/or further depressing sensorium. Administer β₂-agonist and anticholinergic bronchodilators. Add glucocorticoids and antibiotics. Consider noninvasive ventilation.

21 What is the role of noninvasive ventilation in the treatment of COPD exacerbations?

Noninvasive ventilation has been used for patients with moderate to severe dyspnea and moderate to severe acidosis from a COPD exacerbation. A number of trials report improvements in acid-base balance, reduced PaCO₂, and decreased length of stay. Intubation rates are also reduced by noninvasive ventilation. Box 22-1 summarizes the indications and contraindications for noninvasive ventilation in COPD exacerbations; Box 22-2 summarizes indications for intubation and invasive mechanical ventilation in COPD exacerbation.

22 What is the prognosis for a patient requiring mechanical ventilation?

Many studies report reasonable short-term mortality rates (25%-30%) for patients with an endotracheal tube in place for a COPD exacerbation rate, and mortality is lower than among patients with an endotracheal tube for non-COPD causes. High mortality rates in the long term occur in patients with poor lung function (FEV₁ < 30%) before intubation and those with significant other comorbidities.

23 What is the role of positive end-expiratory pressure (PEEP) in mechanical ventilation during a COPD exacerbation?

The presence of positive alveolar pressure at the end of exhalation (intrinsic PEEP) may prevent the patient from triggering the ventilator. The level of external PEEP should be set just below the level of intrinsic PEEP to allow the patient to trigger the ventilator with minimal effort.

24 What is the preferred mode of mechanical ventilation in a COPD exacerbation?

No mode of mechanical ventilation has been shown to be superior to another during a COPD exacerbation. In general, the principles of ventilation are to minimize hyperinflation by allowing adequate expiratory time and avoiding high tidal volumes. Oxygen should be titrated to maintain an arterial partial pressure of approximately 60 mm Hg. Overventilation should be avoided: These patients frequently have hypercapnia and a compensatory metabolic alkalosis at baseline.