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Chronic Obstructive Pulmonary Disease

Title

Ñ    Chronic Obstructive Pulmonary Disease

Definition

Ñ    The term chronic obstructive pulmonary disease

Ñ    Encompasses a number of syndromes

Associated with:

Ñ    Destruction of lung tissue

And:

Ñ    Airflow obstruction

Chronic bronchitis

Ñ    Refers to production of increased amounts of mucoid sputum

It is defined as:

Ñ    Production of sputum

Ñ    On most days

Ñ    For 3 months of each year

Ñ    In more than one consecutive year

Emphysema

Defined as:

Ñ    Dilatation and destruction of lung tissue

Ñ    Distal to the terminal bronchiole

Pathogenesis

Risk Factors

Ñ    Cigarette smoking

Ñ    Atmospheric pollution

Ñ    Alpha₁ antitrypsin deficiency

Pathological Process

Chronic Bronchitis

Irritation of the airways by inhaled substances (e.g. cigarette smoke) causes:

Ñ    Hypersecretion of mucous

Ñ    Hypertrophy of mucous glands

Ñ    Goblet cell metaplasia

Ñ    Bronchiolitis

Ñ    Secondary infections maintain and promote this injury

Resulting in:

Ñ    Hyperaemia and oedema of the mucous membranes

Ñ    Mucinous secretions or casts filling airways

Ñ    Increase in size of mucous glands

Ñ    Mucous plugging

Ñ    Inflammation and fibrosis

Ñ    Squamous metaplasia or dysplasia of bronchial epithelium

Emphysema

Ñ    Destruction of alveolar walls is thought to be the result of an imbalance between proteases in the lungs and their inhibitors

Cigarette smoking contributes to this process by:

Ñ    Activating alveolar macrophages

Ñ    Activated macrophages release substances which attract neutrophils

Ñ    Neutrophils release elastase

Ñ    Smoking also enhances macrophage elastase activity

Ñ    Tobacco smoke or free radicals released by activated neutrophils inactivate alpha ₁ antitrypsin (proteinase inhibitor)

The result of the above process is:

Ñ    Destruction of the walls of the airspaces

Ñ    Abnormal enlargement of the airspaces

·          Distal to the terminal bronchioles

Clinical Features

History

RS

Ñ    Cough with production of sputum

Ñ    Wheeze

Ñ    Dyspnoea

Examination

CVS

Ñ    Tachycardia

Ñ    Raised JVP:

“a “ wave in pulmonary hypertension

“V” wave in tricuspid regurgitation

Ñ    Left parasternal heave

Ñ    Loud single P₂

Ñ    Pan systolic murmur left sternal edge:

Tricuspid regurgitation

RS

Ñ    Pursed lip breathing

Ñ    Use of accessory muscles of respiration

Ñ    Reduced cricosternal distance

Ñ    Tachypnoea

Ñ    Hyperinflated chest

Ñ    Poor chest expansion

Ñ    Decreased cardiac and liver dullness on percussion

Ñ    Auscultation:

Usually clear

There may be scattered rhonchi and crepitations

GIT

Ñ    Hepatomegaly:

Cor pulmonale

CNS

Ñ    Confusion:

Hypercapnoea

Ñ    Drowsiness:

Hypercapnoea

Ñ    Papilloedema:

Hypercapnoea

Ñ    Flapping tremor:

Hypercapnoea

E&M

Ñ    Weight loss:

Advanced emphysema

Complications

CVS

Ñ    Pulmonary hypertension

Ñ    Cor pulmonale

HS

Ñ    Polycythaemia

Investigations

Fluids

Haematology

Ñ    Polycythaemia

Biochemistry

Ñ    Blood Gases:

Normal initially

Later hypoxia and hypercapnoea

Ñ    Alpha one antitrypsin levels:

May be low

Sputum

Microbiology

Not necessary to culture sputum as the usual organisms are:

Ñ    Streptococcus pneumoniae

Ñ    Haemophilus influenzae

Ñ    Moraxella catarrhalis

Imaging

Chest X-ray

Ñ    Normal:

Often

Ñ    Hyperinflated lungs

Ñ    Flattened diaphragms

Ñ    Large retrosternal air space on lateral film

Ñ    Bullae

Ñ    Peripheral cut off of blood vessels

Electrophysiology

ECG

Ñ    P pulmonale

Ñ    Right bundle branch block (RBBB)

Ñ    Right ventricular hypertrophy (RVH)

Physiological studies

Pulmonary Function Tests

Ñ    FEV₁: FVC ratio low

Ñ    PEFR low

Ñ    Lung volumes normal or increased

Ñ    Carbon monoxide gas transfer:

·          Low:

Significant emphysema

Management

Control

Drugs

Ñ    Oxygen 24%-28%

Ñ    Beta-adrenergic agonists:

Salbutamol

Ñ    Antimuscarinic agents:

 Ipratropium, oxitropium

Ñ    Corticosteroids:

Trial of prednisolone 30 mgs daily for 2 weeks, if lung function improves use inhaled corticosteroids

Ñ    Antibiotics:

Infective exacerbations

Ñ    Diuretics:

In all oedematous patients

Ñ    Alpha one antitrypsin replacement:

Weekly or monthly infusion if serum levels are low

Ñ    Respiratory stimulants:

Doxapram, not used much now

Ñ    Pulmonary hypertension:

Oral beta-adrenergic    

Lifestyle Adjustments

Ñ    Smoking cessation

Ñ    Exercise:

Pulmonary rehabilitation

Support

Biological Agents

Venesection

Ñ    Reduce polycythaemia if haematocrit >0.60:

Reduce to 0.5

Surgery

Ñ    Bullectomy

Ñ    Lung volume reduction surgery

Ñ    Single lung transplantation:

End stage emphysema

Staffing

Ñ    Physiotherapy:

Clear excessive secretions

Equipment

Ñ    Bilevel Positive Airway Pressure (BiPAP):

Respiratory failure

Ñ    Domiciliary Oxygen:

Fall in pulmonary artery pressure is achieved if oxygen is administered for 19 hours a day

Indications:

·          COPD with FEV₁ < 1.5L

·          P_aO₂ on air less than 7.3 kPa with or without hypercapnoea:

2 occasions 3 weeks apart after bronchodilator therapy

·          Carboxyhaemoglobin < 3%:

Indicates that patients have stopped smoking

Ñ    NIPPV (Non-Invasive Positive-Pressure Ventilation):

Nocturnal NIPPV improves chronic respiratory failure

Symptom Relief

Ñ    Breathlessness:

Sensation of breathlessness may be reduced by using:

·          Promethazine

·          Dihydrocodeine

Prognosis

Ñ    50 % of patients with severe breathlessness will die within 5 years

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