By Dr. Zahoor

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

[COPD]

Chronic Obstructive Pulmonary Disease (COPD)

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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

COPD

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Epidemiology and Aetiology In developed countries, cigarette smoking

accounts for 90% of casesIn 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

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PathophysiologyThere is increased number of mucous secreting goblet

cells in the bronchial mucosaIn 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

COPD

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COPD includes the diagnosis of 1. Chronic Bronchitis 2. Emphysema

1. 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

2. Emphysema Abnormal permanent enlargement of air spaces distal to

terminal bronchioles, accompanied by destruction of their walls, without obvious fibrosis

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Normal Respiratory Tract

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Chronic Bronchitis

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Alveoli in healthy lung and in COPD

COPD

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Types of Emphysema

1. Centri Acinar EmphysemaThere 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

COPD

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Types of Emphysema (cont)

2. Pan Acinar EmphysemaThis is less commonThere is distension and destruction of whole acinus,

there is bullae formation Ventilation perfusion (VA/Q) mismatch occur

Cause α1 – Antitrypsin deficiency

3. Irregular EmphysemaThere is scarring and damage affecting the lung

parenchyma which is patchy

COPD

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EmphysemaEmphysema 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

COPD

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EmphysemaCO2 excretion is less affected and many

patients have low normal PaCO2 values due to increased alveolar ventilation

Patients are breathless but rarely cyanosedHeart failure and edema are rare These patient are called Pink Puffers

COPD

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Chronic BronchitisThose 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).

COPD

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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

COPD

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Chronic BronchitisIf 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

18COPD

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COPD

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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)

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COPD

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Clinical Features of COPDProductive cough with white sputumWheeze and breathlessness usually after

many years of smoker’s coughCold causes frequent infective exacerbation

with purulent sputumOther precipitating factors – foggy weather,

atmospheric pollution

COPD

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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

COPD

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SignsWheezes in the chest Tachypnea in severe disease with prolonged

expirationAccessory 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

COPD

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Respiratory failureIn 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

COPD

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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)

COPD

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DiagnosisFEV1 is reduced in COPD

COPD FEV1 %

Mild 70% [60-70%]

Moderate 60% [50-60%]

Severe < 50%

Very severe < 30 %

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FEV1 curve Flow volume loop

b

COPD

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Other investigationsCO gas transfer factor is low in emphysemaX-ray chest – shows signs of hyperinflation

of lungs with low flattened diaphragm High resolution CT- scanHemoglobin and PCV (Packed cell volume)

may be increased due to secondary polycythaemia

31 X-ray Chest COPD

COPD

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Other investigations (cont)Blood gases show hypoxaemia and

HypercapniaSputum 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

COPD

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ManagementSmoking 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

COPD

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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

COPD

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Nocturnal HypoxiaCOPD 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

COPD

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Treatment for Nocturnal HypoxaemiaPatient should not be given sleeping tablets

as they will depress respiratory driveGive 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

COPD

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Pulmonary RehabilitationExercise training e.g. walking Physiotherapy Stop smokingNutritional adviceVaccine – Pneumococcal, Influenza

COPD

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ImportantIn 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

Thank you

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