Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD)  Permanent reduction in airflow in the lung  Caused by smoking, air pollution, dust, lack of alpha 1 -antitripsien

COPD Patho physiology  Loss in elasticity due to changes in collagen and elastin on alveolar level  Narrowing of airways

COPD

COPD Chronic bronchitis  Productive cough for more than 3 months of 2 consecutive years (other conditions excluded)

Chronic bronchitis Pathology  ↑ mucous production  Hypertrophy of mucous glands  Thickening of the airway  ↑ number of goblet cells  Thus narrowing of the lumen of the airways and airway obstruction.  Infection caused by accumulated secretions.

Chronic bronchitis

COPD Emphysema  Permanent enlargement in the normal size of the air spaces distal to the terminal bronchioles due to destruction of alveolar tissue.

Anatomy

Emphysema Pathology  Lack of alpha 1 -antitripsien causes uncontrolled breakdown of collagen and elastin, damaging the alveolar framework

What’s in a cigarette?

Emphysema Classification  “Blue-bloater”  Moderately severe airflow impairment  Stimulus for breathing ↓ PO 2

Emphysema Classification  “Pink puffer”  Little sputum production, dyspnoea gr.IV  Right heart failure and peripheral oedema

Emphysema and Chronic bronchitis Clinical signs  Use of accessory muscles  Drawing in of supraclavicular fossae and intercostal space  ↓ chest expansion  ↓ lung sounds (breath sounds)  Dyspnoea with or without productive cough

Emphysema and Chronic bronchitis X-rays  Hyperinflation  Flattened diaphragms  Lengthening of heart shadow  Prominent hilar vessels

Emphysema X-ray

Emphysema Lung functions  ↓ FEV 1  ↓ forced vital capacity  ↓ peak flow  ↑ total lung capacity and residual volume

Emphysema Course of disease  Airflow impairment develops over long time  Productive smoker’s cough  Acute bronchitis  Cannot go to work – severe bronchitis  Attacks occur repeatedly – lose jobs

Emphysema Complications  Cor pulmonale – pulmonary hypertension causes right ventricular failure  Bullae – alveolar walls burst and form large air-filled spaces with thin walls

Cor Pulmonale

Bullae

COPD rehabilitation Dyspnoea  Overactivity of accessory muscles inhitis diaphragm  Patient must be taught to breathe with lower part of his chest

COPD rehabilitation Dyspnoea  Relaxation positions and breathing control  “Pursed lip breathing”

“Pursed lip breathing”  Maintains airway pressure in lungs, prevents airways from collapsing  ↑ airflow

Ontspanningsposisies

COPD rehabilitation Bronchodilators  Relieves bronchospasm  Anti-cholinergic drugs (atrovent) and not B 2 -stimulants  If stimulus for breathing is ↓ PO 2 – do not nebulise with 100% O 2

COPD rehabilitation Improve exercise tolerance  Improve physical activity to highest functional level  Improve quality of life  6 minute walking test  Exercise programme

COPD rehabilitation Remove secretions  Nebulise with mucoliticum  Percuss, shake and vibrate  Precaution – patients on korticosteroids develop osteoperosis. Shaking and vibrating can cause rib fracture.  “Huffing”

“Huffing”  Forced expiratory technique  Just as effective as coughing, less effort  Medium-sized breath, mouth and glottis open, force air out using chest wall and abdominal muscles.

References  Pryor, J.A. and Prasad, S.A Physiotherapy for respiratory and cardiac problems. Adult and paediatrics. Edinburgh: Churchill Livingstone  FTB 309 Dictate  Images courtesy of Google search engine