Respiratory - COPD Flashcards
What is COPD?
WHO definition of COPD is:
- preventable and treatable disease with some significant extrapulmonary effects
- airflow limitation that is not fully reversible
- airflow limitation is progressive and associated with an abnormal inflammatory response of the lungs
Patients with COPD have chronic bronchitis and emphysema in varying degrees.
What is emphysema?
Emphysema is enlargement of the airspaces distal to the terminal bronchioles with destructive changes in the alveolar wall.
There are a number of different types of emphysema depending on the pattern of airspace enlargement. In centrolobular emphysema, damage is limited to the central part of the lobule around the respiratory bronchiole. In panacinar emphysema there is distruction and distension of the whole lobule.
What is chronic bronchitis?
This is the second disease that forms COPD. It is defined as a daily cough with sputum production for at least 3 months a year for at least 2 consecutive years.
Notice that emphysema is an anatomical definition, whereas chronic bronchitis is a clinical one.
Is COPD the only disease where poorly reversible airflow limitation occurs?
No. All obstructive diseases can have an element of airflow limitation - e.g. bronchiectasis, CF, TB and some cases of chronic asthma.
Asthma is really the exception because it is characterised by reversible (rather than progressive) airflow obstruction.
What is the pathogenesis of emphysema?
1) Imbalance between protease/ anti-protease system
2) Cigarette smoking results in release of neutrophil elastase (and increased neutrophil margination/ holding up in capillaries)
3) Elastase cleaves elastin AND type IV collagen
4) Type IV collagen in the blood gas barrier may be a particularly critical structure - loss affects gas diffusion
What are the pathological features of chronic bronchitis?
There is mucus gland hypertrophy in chronic bronchitis which extends into the lumen.
Hypertrophic glands secrete large amounts of mucus in response to inhaled pollutants which overwhelms the muco-ciliary escalator.
There are also small airway changes that are likely to be the first changes seen in chronic bronchitis. These include:
- inflammation
- wall oedema
- narrowing
- cellular infiltration
- peribronchial fibrosis
What reduction in FEV1 and FEV1/FVC is required to diagnose airflow obstruction?
On spirometry a reduction in FEV1 to <80% of predicted and an FEV1/FVC of <0.7 suggests airflow obstruction. The key in COPD is that this is poorly reversible.
What are some important aetiologies for COPD?
1) Age - rarely clinically significant in patients less than 50 years of age due to its natural long history
2) Cigarette smoking - most important; severity of clinical disease is related to the number of cigarettes smoked
3) Environmental - morbidity and mortality related to the degree of general atmospheric pollution, but this effect is only significant in smokers
4) Infection - viral and bacterial infections are important in acute exacerbations of COPD; not causative
5) Allergic predisposition - allergic factors may have a minor role in the aetiology of persistent airflow limitation
6) Hereditary factors - alpha 1 antitrypsin is a rare but important predisposition to the development of emphysema
7) Individual susceptibility - not ALL smokers develop COPD
What are the signs and symptoms of COPD?
Symptoms - cough, sputum, dyspnoea, wheeze
Signs - tachypnoea, use of accessory muscles of respiration, hyperinflation, decr. cricosternal distance, decr. expansion, resonant or hyper-resonant percussion note, cyanosis, cor pulmonale, wheeze
What are pink puffers and blue bloaters? Which group are in danger of hypercapnic respiratory failure?
The clinical presentation of COPD is varied as patients have a variable degree of chronic bronchitis and emphysema. Pink puffers and blue bloaters are at the ends of spectrum of presentation.
Pink puffers: have increased alveolar ventilation, a near normal PaO2 and a normal or low PaCO2 (due to hyperventilation). They are breathless but not cyanosed. They may progress to type 1 respiratory failure.
Blue bloaters: have decreased alveolar ventilation, with low PaO2 and high PaCO2. They are cyanosed but are not breathless and may go onto develop cor pulmonale. There respiratory centres are relatively insensitive to carbon dioxide and they rely on hypoxic drive to maintain respiratory effort - give supplementary oxygen with caution.
What are the complications of COPD?
- acute exacerbation +/- infection
- polycythaemia (due to hypoxia)
- respiratory failure
- cor pulonale (oedema, raised JVP, palpable liver)
- pneumothorax (ruptured bullae)
- carcinoma (due to smoke exposure)
Why do patients with COPD have hyperinflated chests?
This correlates with the degree of emphysema. There is loss of elastic recoil from loss of alveolar walls, air trapping and a reflex reaction where the patient breathes at a higher FRC to maintain small airway patency*.
- Lung volume alters airway resistance because of radial traction exerted on the airways by the surrounding lung tissue. High lung volumes are associated with lower resistance because of increased traction on airways. Patients with increased airway resistance due to obstruction “learn” to breathe at higher lung volumes to offset the high airway resistance associated with their disease.
Why do patients with COPD have impaired maximal respiratory airflow?
FEV1 is reduced because of airway obstruction (from distortion, fibrosis and mucus production).
FVC is reduced because of premature airway closure towards the end of expiration. This is caused by dynamic compression of the airways. Loss of elastic recoil from loss of alveolar wall support leads to increased or earlier airways closure for any expiratory pressure.
How is gas exchange affected in COPD?
COPD is associated with V/Q inequality which caused hypoxaemia, CO2 retention, increased A-a difference, increased physiologic dead space, increased physiologic shunt.
Distribution of V/Q inequalities is slightly different for type A (pink puffers) and type B (blue bloaters) patients:
- Type A patient: large amount of ventilation to regions of lung with high V/Q ratios (i.e. large ventilation with low blood flow); capillaries destroyed by emphysematous process –> physiologic dead space; no hypoxia because blood diverted by hypoxic pulmonary vasocontriction
- Type B patient: large blood flow to poorly ventilated regions (low V/Q ratios) leading to cyanosis
What investigations are used to diagnose COPD?
1) CXR: hyperinflation (>6 anterior ribs visible), flat hemidiaphragms, large central pulmonary arteries, decr peripheral vascular markings, bullae
2) FBC: polycythaemia
3) ECG: right atrial and ventricular hypertrophy
4) ABG: hypoxia +/- hypercapnia
5) Lung function: FEV1 <80% predicted, FEV1/FVC <0.7, incr. TLC, RV and decr DLCO
NB - alpha 1 anti-trypsin deficiency tends to affect the lung bases rather than smoking related COPD which affects the whole lung
