1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE [COPD]
By Dr. Zahoor

2. Chronic Obstructive Pulmonary Disease (COPD)
What is COPD ?
A disease state characterized by air flow limitation that is not fully reversible
Air flow limitation is usually progressive and associated with inflammatory response of the lung to the noxious particles or gases
Two conditions come under the term ‘COPD’
1. Chronic Bronchitis
2. Emphysema

3. COPD Epidemiology and Aetiology
In developed countries, cigarette smoking accounts for 90% of cases
In developing countries, only 10-20% of heavy smokers develop COPD, indicating individual susceptibility
COPD is related to the number of cigarette smoked per day
Climate and air pollution are lesser causes of COPD

5. COPD
Pathophysiology
There is increased number of mucous secreting goblet cells in the bronchial mucosa
In advanced cases, bronchi become inflamed and pus is seen in the lumen
Microscopically
- Chronic inflammatory cells are seen in the wall of bronchi, lymphocyte infiltration CD8+ is seen
- Columnar cells are replaced by squamous epithelial cells
- Inflammation is followed by scaring and thickening of the wall which causes narrowing of small air ways

6. Pathological changes in the airways in COPD

7. COPD COPD includes the diagnosis of 1. Chronic Bronchitis 2. Emphysema
Cough with sputum on most days for 3 consecutive months for at least 2 years in a row
There is inflammation of bronchi, it causes narrowing of bronchi, cough, wheezing and chest tightness
Emphysema
Abnormal permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls, without obvious fibrosis

8. Normal Respiratory Tract

9. Chronic Bronchitis

10. Alveoli in healthy lung and in COPD

11. COPD Types of Emphysema 1. Centri Acinar Emphysema
There is distension and damage of lung tissue around respiratory bronchioles, while more distal alveolar ducts and alveoli are well preserved
This type of emphysema may cause substantial air flow limitation

12. COPD Types of Emphysema (cont) 2. Pan Acinar Emphysema
This is less common
There is distension and destruction of whole acinus, there is bullae formation
Ventilation perfusion (VA/Q) mismatch occur
Cause α1 – Antitrypsin deficiency
3. Irregular Emphysema
There is scarring and damage affecting the lung parenchyma which is patchy

13. COPD
Emphysema
Emphysema leads to expiratory air flow limitations and air trapping
Loss of lung elastic recoil results in increase TLC (total lung capacity)
Loss of alveoli decreases capacity for gas transfer
VA/Q ( ventilation/perfusion) mismatch leads to fall in PaO2 and increase work of respiration

14. COPD
Emphysema
CO2 excretion is less affected and many patients have low normal PaCO2 values due to increased alveolar ventilation
Patients are breathless but rarely cyanosed
Heart failure and edema are rare
These patient are called Pink Puffers

15. COPD Chronic Bronchitis
Those patients who have hypoxia and CO2 retention (Chronic Bronchitis), they appear less breathless
NOTE – Increase in CO2 causes stimulation of respiratory center but in high concentration, it causes depression of respiratory center
These patients are often cyanosed, oedematous but not so breathless
These patient have peripheral vasodilatation, bounding pulse, coarse flapping tremor of outstretched hands when PCO2 is increased to 10 KPa ( 75mmHg).

16. COPD Chronic Bronchitis (cont)
Due to renal hypoxia, there is increased RBC production (leading to polycythaemia) and fluid retention
These patient become bloated, plethoric and cyanosed – typical appearance of Blue Bloater

17. COPD Chronic Bronchitis
If we administer O2 to abolish hypoxaemia, by administering O2, it can make situation worse by decreasing respiratory drive as these patients depend on hypoxia to drive their ventilation

18. COPD

20. Pink Puffers (Emphysema) and Blue Bloaters (Chronic Bronchitis)
COPD
Difference between
Pink Puffers (Emphysema) and Blue Bloaters (Chronic Bronchitis)
Pink Puffer
Blue Bloater
Build
Thin
Obese
Cyanosis - +
Breathlessness ++
Hyperinflation of chest
+++
Cor pulmonale
+ (often)

22. COPD Clinical Features of COPD Productive cough with white sputum
Wheeze and breathlessness usually after many years of smoker’s cough
Cold causes frequent infective exacerbation with purulent sputum
Other precipitating factors – foggy weather, atmospheric pollution

23. COPD Clinical Features ( cont) Systemic effects of COPD include
- Hypertension
- Osteoporosis
- Depression
- Weight loss
- Reduced muscle mass
- General weakness

24. Pulmonary and Systemic Features of COPD

25. COPD Signs Wheezes in the chest
Tachypnea in severe disease with prolonged expiration
Accessory muscles of respiration are used, there may be intercostal indrawing on inspiration and pursing of lips on expiration
Chest expansion is poor
Lungs are hyper inflated
Severe Hypercapnia causes confusion, drowsiness
Papilloedema may be present

26. COPD Respiratory failure
In COPD, respiratory failure occurs when there is PaO2 < 8 kPa (60 mmHg) or PaCO2 > 7 kPa (55 mmHg)
Chronic alveolar hypoxia and Hypercapnia leads to constriction of pulmonary arterioles and pulmonary hypertension
Note: Respiratory failure is type 1 and type 2
Type 1: PaO2 is low & PaCO2 is normal or low
Cause : Pneumonia
Type 2: PaO2 is low & PaCO2 is high
Cause : COPD, Respiratory center depression e.g. drugs

27. COPD Pulmonary Hypertension (Corpulmonale) What is Corpulmonale ?
It is right ventricular hypertrophy (failure) secondary to lung disease (pulmonary hypertension)
On examination, patient is centrally cyanosed due to lung disease
Left para sternal heave is felt due to right ventricular hypertrophy
Loud P2 (Pulmonary second sound)
Signs of right ventricular failure (increase JVP, Ascites, liver enlargement, peripheral oedema)

28. COPD Diagnosis FEV1 is reduced in COPD COPD FEV1 % Mild 70% [60-70%]
70% [60-70%]
Moderate
60% [50-60%]
Severe
< 50%
Very severe
< 30 %

29. FEV1 curve
Flow volume loop b

30. COPD Other investigations CO gas transfer factor is low in emphysema
X-ray chest – shows signs of hyperinflation of lungs with low flattened diaphragm
High resolution CT- scan
Hemoglobin and PCV (Packed cell volume) may be increased due to secondary polycythaemia

31. X-ray Chest COPD

32. COPD Other investigations (cont)
Blood gases show hypoxaemia and Hypercapnia
Sputum examination – strept pneumoniae and H.Influenzae produced acute exacerbations
ECG – right ventricular hypertrophy, tall P-wave (pulmonary hypertension)
Echo cardiography – to assess cardiac function
α1 Antitrypsin level

33. COPD Management Smoking should be stopped
Drug therapy – it is used for Short term management of exacerbations and Long term management
Bronchodilators – β2 agonist e.g. salbutamol
– Anti muscarinic drugs e.g. Ipratropium
– Theophyllines
– Corticosteroids
– Anti biotic
– Diuretic therapy
– Oxygen therapy

34. COPD
Oxygen Therapy
Continuous O2 2L/minute via nasal prongs to achieve O2 saturation of greater than 90%
O2 is given hours daily at home

35. COPD Nocturnal Hypoxia
COPD patients get severe arterial hypoximia during REM sleep and PaO2 may fall very low 2.5 kPa (19 mmHg)
Most COPD death occur at night possibly due to cardiac arrhythmias due to hypoxaemia

36. COPD Treatment for Nocturnal Hypoxaemia
Patient should not be given sleeping tablets as they will depress respiratory drive
Give O2 at night and ventilatory support
BIPAP – Bi-level Positive Airway Pressure
It is non invasive positive pressure ventilation given by tight fitting nasal mask
It provides inspiratory and expiratory assistance

37. COPD Pulmonary Rehabilitation Exercise training e.g. walking
Physiotherapy
Stop smoking
Nutritional advice
Vaccine – Pneumococcal, Influenza

38. COPD
Important
In Type 2 respiratory failure PaCO2 is elevated and the patient is dependent on hypoxic drive. Therefore, O2 therapy is given with care so that PaCO2 should not rise and pH should not be allowed to fall below 7.25

39. Thank you