COPD

Notes

Definition & classification

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.

Aetiology

Smoking is by far the most important aetiological factor.

Smoking

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

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

Pathophysiology

COPD is a disease of both the airways and the alveoli.

Airways

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:

  • Goblet cell hyperplasia
  • Mucus hypersecretion
  • Chronic inflammation and fibrosis
  • Narrowing of small airways

Alveoli

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:

  • Collapse: the alveoli are prone to collapse.
  • Dilation and bullae formation: alveoli dilate and may eventually join with neighbouring alveoli forming bullae. 

Cor pulmonale

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.

Clinical features

Chronic productive cough and dyspnea are the hallmarks of COPD.

Symptoms

  • Productive cough
  • SOB
  • Orthopnea

Signs

  • Dyspnea
  • Pursed lip breathing (prevents alveolar collapse by increasing the positive end expiratory pressure)
  • Wheeze
  • Coarse crackles
  • Loss of cardiac dullness
  • Downward displacement of liver
  • Signs of C02 retention
    • Drowsy
    • Asterixis
    • Confusion
  • Signs of cor pulmonale
    • Peripheral oedema
    • Left parasternal heave (caused by right ventricular hypertrophy)
    • Raised JVP
    • Hepatomegaly 

MRC dyspnoea scale

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.

Acute exacerbation

An acute exacerbation is a sustained worsening of symptoms that may interrupt a patients stable course.

It may be infective or non-infective.

Spirometry

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:

  • FVC: the forced (expiratory) vital capacity is a persons maximal expiration following full inspiration.
  • FEV1: the forced expiratory volume in one second, i.e the volume of FVC expelled after one second.

The following changes are seen in obstructive lung disease (orange line):

  • FVC: may be normal but often reduced due to air trapping.
  • FEV1: reduced
  • FEV1/FVC: < 70%

Spirometry may be used to categorise COPD. The table below is based on NICE clinical guidance 101.

Investigations & Diagnosis

Bedside

  • Observations
  • BMI
  • Sputum culture (if purulent)
  • Pulse oximetry
  • Arterial blood gas (if hypoxia or hypercapnia is suspected)
  • ECG (if cor pulmonale suspected)

Bloods

  • Full blood count 
    • Anaemia
    • Polycythaemia 

Imaging

  • Chest x-ray (CXR):
    • Hyperexpanded
    • Flattened hemidiaphragms
    • Hypodense
    • Saber-sheath trachea
  • CT scan: if symptoms disproportionate to spirometric assessment.
  • Echocardiogram: if cor pulmonale suspected.

Management

Beta-2 agonists, muscarinic antagonists and steroids offer symptomatic relief. Smoking cessation and oxygen at home offer decreases in mortality.

Medical management 

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:

  • Have Pa02 < 7.3 kPa. or
  • Have Pa02 < 8 kPa with any of:
    • Pulmonary hypertension
    • Peripheral oedema
    • Nocturnal hypoxaemia
    • Secondary polycythaemia

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.

Modifiable factors and physiotherapy

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.

Acute exacerbation

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:

  • Bronchodilators: may be delivered by handheld devices or nebuliser.
  • Prednisolone: 30mg for 7-14 days.
  • Antibiotics: often tetracyclines, used when an infective cause is suspected.

Type II (hypercapnic) respiratory failure

Patients with COPD are at risk of developing type II respiratory failure i.e. PaO< 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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