CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
[COPD]
By Dr. Zahoor
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Chronic Obstructive
Pulmonary Disease (COPD)
What is COPD ?
 A disease state characterized by air flow limitation that is not
fully reversible
 Air flow obstruction 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
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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
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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
- Inflammatory cells( Neutrophil and Macrophage) 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
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Pathological changes in the airways in COPD
COPD
COPD includes the diagnosis of
1. Chronic Bronchitis
2. Emphysema
1.


2.

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Chronic Bronchitis
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 alveolar walls, without
obvious fibrosis
Normal
Respiratory Tract
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Chronic Bronchitis
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Alveoli in healthy lung and in COPD
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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
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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
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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
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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
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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).
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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
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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
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COPD
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COPD
Difference between
Pink Puffers (Emphysema) and Blue Bloaters (Chronic Bronchitis)
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Pink Puffer
Blue Bloater
Build
Thin
Obese
Cyanosis
-
+
Breathlessness
++
+
Hyperinflation of
chest
+++
+
Cor pulmonale
-
+ (often)
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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
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COPD
Clinical Features ( cont)
 Systemic effects of COPD include
- Hypertension
- Osteoporosis
- Depression
-Weight loss
- Reduced muscle mass
- General weakness
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Pulmonary and Systemic Features of COPD
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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
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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
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Type 2: PaO2 is low & PaCO2 is high
Cause : COPD, Respiratory center depression e.g. drugs
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)
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COPD
Diagnosis - Spirometry
 FEV1 is reduced in COPD
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COPD
FEV1 %
Mild
70%
[60-70%]
Moderate
60%
[50-60%]
Severe
< 50%
Very severe
< 30 %
FEV1 curve
b
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Flow volume loop
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
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X-ray Chest COPD
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
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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
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COPD
Oxygen Therapy
 Continuous O2 2L/minute via nasal prongs to achieve O2
saturation of greater than 90%
 O2 is given 15-19 hours daily at home
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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
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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
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COPD
Pulmonary Rehabilitation
 Exercise training e.g. walking
 Physiotherapy
 Stop smoking
 Nutritional advice
 Vaccine – Pneumococcal, Influenza
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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
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Thank you
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