Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease is a lung disease characterized by airflow limitation due to an obstructive process.  The Global Initiative for Chronic Obstructive Lung disease defines COPD as “a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.  Exacerbations and comorbidities contribute to the overall severity in individual patients.”

COPD is estimated to affect 32 million people in the United States, and is the third leading cause of death in the USA. The most important risk factor for COPD is cigarette smoking.  Alpha1-antitrypsin (whose purpose is to neutralize elastase, thus preventing breakdown) deficiency is the only known genetic risk factor for developing COPD and accounts for less that 1% of all cases in the United States.  

Pathologic changes in COPD occur in the large (central) airways, the smaller bronchioles, and the lung parenchyma.  Most occur as a result of exposure to cigarette smoking.  The pathogenic mechanisms are diverse.  In response to the noxious cigarette smoking stimuli, increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that can’t be counteracted by the antiproteases, leading to lung destruction.  Cigarette smoking also causes neutrophil influx, which secrete matrix metalloproteinases which affect lung parenchyma.

In chronic bronchitis, mucous gland hyperplasia is the histologic hallmark.  The endothelium is also damaged, making the mucociliary response to clear secretions impaired.  Associated with a relatively undamaged pulmonary capillary bed; the body responds by decreasing ventilation and increasing cardiac output.  V/Q mismatch occurs, resulting in rapid circulation in a poorly ventilated lung, leading to hypoxemia.  Eventually hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale.  

Emphysema is a pathologic diagnosis defined by permanent enlargement of the airspaces distal to the terminal bronchioles, leading to a dramatic decline in the alveolar surface available for gas exchange.

    Patients usually present with a combination of symptoms:

• Cough, usually worse in the mornings and productive of a small amount of colorless or whitish sputum
• Dyspnea - The most significant symptom
• Wheezing - may occur in some patients, especially during exacerbations

Physical examination in detecting mild to moderate COPD has relatively poor sensitivity; however for severe disease, sensitivity and specificity of exam increases.  In severe disease, findings include:

•     Tachypnea and respiratory distress with simple activity
•     Use of accessory muscles
•     Cyanosis
•     Elevated jugular venous pulse

Lung examination shows a hyperinflated chest, wheezing, diffusely decreased breath sounds, hyperresonance to percussion, prolonged expiration, and coarse crackles beginning with inspirations in some case.

Formal diagnosis of COPD is made with spirometry, when the ratio of forced expiratory volume in 1 second over forced vital capacity (FEV1/FVC) is less than 70%.

The goal of COPD management is to improve a patient’s functional status and preserving optimal lung function, improving symptoms, and preventing exacerbations.  No treatments apart from lung transplantation have been show to significantly improve lung function or decrease mortality.

Bronchodilator: Combination therapy with beta 2 agonists and anticholingergics have been shown in studies to have greater symptom relief and bronchodilator response.  

Anti-inflammatory - achieved via sytemic and inhaled steroids.  Also azithromycin have been shown to have anti-inflammatory effects in the airways of COPD patients, improving phagocytic function of pulmonary macrophages

COPD is commonly associated with progressive hypoxemia, with oxygen administration being shown to reduce mortality rates in patients with advanced COPD.  Long term therapy is recommended for those with a PaO2 less than 55.

Diligence in preventing pulmonary infections is key to limiting exacerbations.  Vaccinations for influenza and pneumonia are recommended. Smoking cessation is another modality which is strongly encouraged to prevent advancement of disease severity