COPD Flashcards
(18 cards)
Explain what is meant by the term Chronic Obstructive Pulmonary Disease (COPD)
COPD is an umbrella term used to describe airway obstruction in the conducting airways (from the mouth/nose to the terminal bronchioles) as a result of the presence of an obstructive respiratory disease such as chronic bronchitis, emphysema or chronic asthma.
It results in decreased pulmonary function tests such as FEV1 and PEFR. Risk factors of this disease include smoking, air pollution, chemicals, dust and genetics.
Explain the pathological changes seen in Chronic Bronchitis
Irritants/chemicals enter the lungs through inhalation, leads to:
Inflammatory changes - vasodilation, inflammatory mediators etc etc.
Thickening of the mucous membrane - obstruction, decreased sol layer.
Size and number of Goblet cells increases, resulting in overproduction of sputum - muco-ciliary escalator impairment, retained secretions = ?infection
Airway fibrosis due to chronic inflammation, release of elastase from inflammation.
Macrophage activity decreases - increased risk of infection.
Results in airway obstruction, decreased pulmonary function tests.
How does the pathological changes seen in Chronic Bronchitis relate to the normal structure of the lungs?
Inflammation - normal response to injury/infection, formation of pulmonary oedema through increased permeability of capillaries.
Mucous membrane thickening - through goblet cell mucous secretion,
Increased size/no. of goblet cells - affects muco-ciliary escalator, impairment
Airway fibrosis - elastase released in inflammation, floppy, less elastic recoil - obstruction
Dec. macrophage activity
Explain the pathological changes seen in Emphysema
Emphysema is the dilation of the terminal air spaces distal to the terminal bronchioles, resulting in inflammation and destruction of the alveoli.
2 types of emphysema:
- Centriacinar - affects the upper lobes and respiratory bronchioles
- Panacinar - affects the alveoli
Causes: Smoking, air pollution, chemicals, dust, genetics and more.
Panacinar emphysema is caused by an alpha-one anti trypsin enzyme deficiency. This enzyme breaks down elastase, which breaks down elastin which maintain the elastic recoil of the lungs, which helps with airflow modulation and expiration under pressure changes. The enzyme deficiency means that the elastase levels increase so the elastin levels decrease.
Elastase is also released when the irritants trigger an acute inflammatory response.
This results in less, bigger alveoli = decreased surface for gaseous exchange = hypoxaemia, cyanosis, hypercapnia etc.
Alveoli and airways become floppy and collapse on expiration; airway obstruction.
How does the pathological changes seen in Emphysema relate to the normal structure of the lungs?
Dec elastic recoil - obstruction
Dec surface area of the lungs for gaseous exhange due to bigger, less alveoli - hypoxaemia
List the 8 causes of airway obstruction
Sputum Inflammation Fibrosis Airway hypertrophy Bronchospasm Foreign body e.g. peanut Tumour Decreased elasticity
How does increases sputum production affect the normal structure of the lungs?
Obstruction within the airways = increased airway resistance
Impaired muco-ciliary escalator, increased risk of infection.
How does airway fibrosis affect the normal structure of the lungs?
Decreased elastic recoil, reduced lung compliance - airway collapse and obstruction = V/Q mismatch
How does the presence of a foreign body affect the normal structure of the lungs?
Increased airway resistance
Narrowed lumen = obstruction - V/Q mismatch
How does a tumour affect the normal structure of the lungs?
Increased airway resistance
Narrowed lumen = obstruction - V/Q mismatch
How does decreased elastin affect the normal structure of the lungs?
Decreased elastic recoil so airways collapse on expiration = barrel shaped chest, gas trapping, dec lung compliance.
How does airway inflammation affect the normal structure of the lungs?
Cause fibrosis, decreased elastin, increased airway resistance, = V/Q mismatch
How does airway hypertrophy affect the normal structure of the lungs?
Impairs muco-ciliary escalator, increased airway resistance, = V/Q mismatch
How does bronchospasm affect the normal structure of the lungs?
Increased airway resistance, = V/Q mismatch
A man with mild COPD has the following results from his dynamic (time/volume) lung function tests
Patient’s values Predicted values
FVC = 4.0L FVC = 4.0 L
FEV1 = 2.3L FEV1 = 3.3 L
PEFR = 285 L/min PEFR = 459 L/min
Explain the significance of these results with reference to the pathological changes of COPD
Obstructive disease:
Decreased FEV1 - Forced expiratory volume in the 1st second of expiration - decreased due to increased air resistance as lumen size has decreased. Airways close quicker
Decreased PEFR - ^ due to mucous, inflammation, fibrosis, decreased elastin.
FVC remains the same as this is an obstructive disorder, not a restrictive disorder, therefore lung volumes have not dramatically decreased - the same volume of air is entering the lungs, it takes longer to enter the airways and dec. surface area.
Explain the signs and symptoms of COPD
Decreased pulmonary function tests of PEFR and FEV1
Increased WOB due to airway resistance, decreased lung compliance, pain
SOB due to V/Q mismatch, less air entering lungs, gas trapping so pt has to inspire before fully expired
Hypoxaemia - V/Q mismatch, less Hb saturated with O2, beware cor pulminale
Cyanosis and clubbing - due to V/Q mismatch
Decreased exercise tolerance due to fatigue, hypoxaemia = dec aerobic respiration, respiratory muscle fatigue and atrophy.
Abnormal pattern of breathing - using accessory muscles of inspiration, not nice diaphragmatic breathing encouraging basal distribution
Chronic cough with purulent sputum production
Potential chest infection e.g. lobar pneumonia due to retained secretions
Abnormalities shown on CXR
Barrel shaped chest due to gas trapping and dec. elastin
Mucous plug resulting in lung collapse and atelectasis (lower lobe alveolar collapse)
List five possible problems that a patient with COPD might present and suggest one appropriate physiotherapy treatment/management approach for each problem listed
Excess sputum production - ACBT, postural drainage, vibs and percussion, shaking, nebs, mucolytics
Decreased exercise tolerance - NIV, O2 therapy e.g. SBOT, LBOT, AOT, mobility to decreased cycle of breathlessness.
Abnormal breathing techniques - relaxed breathing, promote diaphragmatic breathing
Gas trapping, blue bloaters - pursed lip breathing, bronchodilators, nebs.
Dyspnoea (breathlessness) - positions of ease, O2 therapy, bronchodilators, mobilisation, relaxed breathing, reassurance.
Outline how the physiotherapist may contribute in the management of the signs and symptoms of airways obstruction
Sputum clearance techniques e.g. ACBT, vibs, percussion, postural drainage, shaking, mucolytics, cough assist, nebs.
IPPB
IPAP, EPAP
Mobility - increases the respiraory demand - increasing the FRC, TV = greater differentiation of Hb, basal distribution of air, greater thoracic movement and inspiration aiding with sputum clearance too.
Education re painkillers, inhalers (reinforce good technique, when to use), exercise, breathlessness
Positions of ease
Sustained inspiration, sniffs
Mobilise stiff joints
