Pathophysiology of
Chronic Airflow Limitation
Chronic Obstructive Lung Disease
Emphysema
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Abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and
without obvious fibrosis
Risk Factors:
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Cigarette Smoking
Irritation - > 4,000 chemicals inhaled
 Hyperplasia – reduces airway diameter
 Abnormal dilatation of distal airspaces
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Destruction of alveolar walls
Chronic Obstructive Lung Disease
Emphysema
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Risk Factors (cont’d):
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Recurring respiratory tract infections
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Heredity – alpha 1 –Antitrypsin (ATT) deficiency
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H. flu, Strep pneumoniae, Moraxella catarrhalis
Accounts for <1% of COPD in US
AAT is a serum protein produced by the liver and normally found in
the lungs
IV or nebulized AAT (Prolastin) slows COPD progression
Aging – Changes in lung structure
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Gradual loss of elastic recoil – thin alveolar wall – thoracic cage
changes from osteoporosis & calcification
COPD
Pulmonary Blebs & Bullae
Pathophysiology of Chronic
Bronchitis and Emphysema
Interferences with Ventilation
Collaborative Care Goals
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Improve ventilation
Promote removal of secretions
Prevent complications & progression
of symptoms
Promote patient comfort &
participation in care
Improve quality of life as much as
possible
Interferences with Ventilation
Collaborative Treatment
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Patients are treated primarily as
outpatients
Hospitalizations
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Acute exacerbations
Complications
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Respiratory failure, pneumonia, congestive
heart failure
Interferences with Ventilation
Collaborative Management
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Smoking cessation
Treatment of respiratory infections
Bronchodilator therapy
 Beta2-adrenergic agonists
 Anticholinergic agents
 Long-acting theophylline
Corticosteroids
PEFR monitoring (peak expiratory flow rate)
Chest physiotherapy / Breathing exercises & retraining
Hydration 3L/day (unless contraindicated)
Rest - Progressive plan of exercise
Patient & family education
Influenza / Pneumovax immunization
Low flow oxygen rate (if indicated)
Pulmonary rehabilitation program