THIS NOTE WILL BE UPDATED SHORTLY TO REFLECT CHANGES IN NICE GUIDELINE NG 115.
COPD is a progressive, obstructive airway disease that is not fully reversible. It results from disease of the airways and parenchyma in the form of chronic bronchitis and emphysema.
3 million people in the UK are diagnosed with COPD and a suspected 2 million more may be undiagnosed. COPD is the fifth most common cause of death in the UK.
Smoking is by far the most important aetiological factor.
90% of cases of COPD are associated with smoking. However, only 10% of smokers will develop it, indicating the presence of a co-factor such as a genetic predisposition.
Emphysema is characteristically centriacinar.
Alpha-1 antitrypsin deficiency is an autosomal codominant condition characterised by a deficiency in alpha-1 antitrypsin. It affects around 1 in 5000 in the UK.
Alpha-1 antitrypsin is a protease inhibitor that is synthesised by the liver. It acts in the lung parenchyma to oppose the action of elastase. Elastase is a protease that causes the breakdown of elastin, a protein important to the structural integrity of the alveoli. This causes emphysema.
Smoking increases the risk of these patients developing emphysema. Emphysema is characteristically panlobular with a lower zone predominance
COPD is a disease of both the airways and the alveoli.
Chronic bronchitis refers to inflammation of the bronchi, defined as a chronic productive cough for three (or more) months in two consecutive years where other causes are excluded.
Chronic bronchitis leads to:
Emphysema is the permanent enlargement of airspaces distal to the terminal bronchiole when interstitial pneumonias are excluded.
Inflammatory processes lead to the production of proteases by inflammatory cells such as macrophages. The protease elastase causes the destruction of elastin, a protein important to the structural integrity of the alveoli.
Loss of elastin has two effects:
Cor pulmonale refers to right ventricular impairment secondary to pulmonary disease. In the developed world COPD is the most common cause.
Clinical features are those of right-sided heart failure.
Chronic productive cough and dyspnea are the hallmarks of COPD.
1. SOB on strenuous exertion
2. SOB on hurrying or slight hill
3. Slower than most on level ground, pause needed after 15 minutes
4. Stops for breath after 100 yards
5. SOB when dressing or unable to leave the house.
An acute exacerbation is a sustained worsening of symptoms that may interrupt a patients stable course.
It may be infective or non-infective.
Spirometry is key to assessing the severity of COPD, it demostrates an obstructive pattern.
Spirometry should be performed at the time of diagnosis to assess airway obstruction.
Spirometry measures the flow and volume of air during inhalation and exhalation:
The following changes are seen in obstructive lung disease (orange line):
Spirometry may be used to categorise COPD. The table below is based on NICE clinical guidance 101.
Beta-2 agonists, muscarinic antagonists and steroids offer symptomatic relief. Smoking cessation and oxygen at home offer decreases in mortality.
Two types of bronchodilators are used in COPD; Beta-2 agonists (BA) and muscarinic antagonists (MA). They may be short-acting (SA) or long-acting (LA) in nature.
In disease in which these inhalers do not control symptoms, inhaled corticosteroids may be prescribed.
Medical management is stepwise. The below diagram is based on NICE clinical guidance 101.
Long-term oxygen therapy (LTOT) is reserved for patient who when stable:
LTOT is required for at least 15 hours a day for a benefit to be seen. Patients who smoke should be explained the dangers of mixing oxygen and cigarettes.
Lifestyle modification and patient education are important in the management of COPD. Patients should understand the benefits of smoking cessation.
The Fletcher and Peto graph shows the effects of smoking cessation. The green line follows the normal trajection of a healthy individuals FEV1 as they age. The red line shows the trajection of a smoker. The orange lines show the effect of smoking cessation - the FEV1 begins to fall at the rate of a non-smoker though existing damage is not reversed.
The annual flu and a one-off pneumococcal vaccination are recommended. Physiotherapy may play an important role.
A decision should be made whether to treat in the community or in a hospital based on the severity of the exacerbation. An ABC approach should be used.
Exacerbations are typically treated with:
Patients with COPD are at risk of developing type II respiratory failure i.e. PaO2 < 8 kPa and PaCO2 > 6.7 kPa. See notes titled ‘Ventilation’ for more details.
Oxygen therapy must be used carefully in patients with COPD, typically saturations of 88-92% are targeted. ABGs may be necessary to monitor for CO2 retention.
Venturi masks are ideal as they allow an exact FiO2 (fraction of inspired oxygen) to be administered.
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