Chronic obstructive pulmonary disease

COPD is a progressive obstructive airway disease that is mostly irreversible. It encompasses 2 diseases:

1. Chronic bronchitis
2. Emphysema

The main risk factor for COPD is smoking. Other risk factors include occupational and environmental exposures to irritants.

Pathophysiology

Let’s first take a look at restrictive vs obstructive airway disorders and what this means and how it is represented on our flow-volume loop charts with spirometry:

• Restrictive airway disorders are disorders that restrict expansion of the lungs. If the lungs are unable to expand then the volume of inhaled air is below normal. Some examples include pulmonary fibrosis, sarcoidosis, muscular dystrophy.
• Obstructive airway disorders are disorders when there is an obstruction or narrowing of the airways. So the patient is able to able to inhale normally but have difficulty exhaling all the air out completely. Some examples include asthma, COPD, cystic fibrosis.

🌬 Spirometry

Spirometry is used to assess lung function by measuring the volume of that is able to be exhaled after maximal inspiration. It is good at differentiating between obstructive disorders and restrictive diseases. It is also useful at monitoring disease severity.

First let us review some important volumes and ratios:

• Forced expiratory volume in 1s (FEV1) - the volume exhaled in the first second after deep inspiration and forced expiration. Normal is >80% of predicted score.
• Forced vital capacity (FVC) - total volume of air that the patient can forcibly exhale in one breath. Normal is >80% of predicted score.
• FEV1/FVC - ratio of the 2 volumes. Normal is >0.7 (70%).

The predicted score is based on the patient’s sex, age and height.

Features of an obstructive spirometry pattern include:

1. Reduced FEV1 (<80% of predicted)
2. Reduced FVC but to a lesser extent then the reduced FVC
3. Reduced FEV1/FVC ratio

The curve tends to continue further and the patient is able to continue to exhale slowly as they still have air in their lungs, so no plateau is reached early.

Features of a restrictive spirometry pattern include:

1. Reduced FEV1 (<80% of predicted)
2. Reduced FVC (more than that seen in obstructive patterns)
3. Normal FEV1/FVC ratio

The curve looks similar to normal but it plateaus with a reduced volume as there is less air in the lungs to exhale so the plateau is reached quickly.

Flow-volume loops

Flow volume loops show a graphical analysis of inspiratory and expiratory flow. In this procedure, patients inhale to their total lung capacity (TLC) then perform a forced expiration and then rapidly inhale back.

Below the X-axis we see our inspiratory limb and above the X-axis we see our expiratory limb of the test.

Here are some important interpretations to remember:

🫁

Emphysema:

Emphysema means to inflate/swell. It refers to the damage or destruction of alveolar sacs which results which causes abnormal air exchange. The alveolar sacs become enlarged due to septal destruction and fusion of the alveoli. This forms bullae which are air bubbles that may burst and can lead to a pneumothorax.

Exposure to irritants/dust/smoke the release of inflammatory markers in the lungs → release of leukotrienes & mediators such as elastase and collagenases → destruction of elastin and collagen, causing them to lose elasticity.

Low pressure during expiration causes collapse of non-elastic alveoli → air-trapping distal to the collapse → septal breakdown + fusion of neighbouring alveoli → decreased surface area for lung exchange.

Alpha-1 antitrypsin (AAT) deficiency is a genetic factor that can lead to emphysema. AAT protects elastin from being broken down by elastase, so a deficiency leads to increased elastin activity and alveolar breakdown which causes alveolar collapse and ultimately emphysema.

😷 Presentation

• Dyspnoea
• Shortness of breath
• Productive cough with sputum

🔍 Investigations

NICE says diagnosis should be suspected if there are risk factors present along with >1 or more of the following:

• Persistent progressive breathlessness that worsens on exertion.
• Recurrent cough
• Recurrent sputum production
• Wheeze
• Frequent LRTI

🔢 Classification

The most common classification is the GOLD classification which grades COPD according to reduction in FEV1 compared to the predicted scores for the appropriate age, sex height, ethnicity etc.

We can also use the MRC dyspnoea scale to grade the patient’s dyspnoea:

🧰 Management

💊

Medical management:

1. The following are given via inhalers or via spacers:

• SABA (short acting B2 agonist)
• Salbutamol

OR

• SAMA (short acting muscarinic antagonist)
• Ipratropium

These are taken as needed (PRN- pro re nata).

2. If this fails to control the COPD, we can give:

• Asthmatic/steroid responsive features: SABA + LABA + inhaled corticosteroid (ICS)
• LABA - salmeterol/formoterol
• If on a SAMA switch to → SABA
• Non-asthmatic: SABA + LABA + LAMA
• ICS - fluticasone/beclamethasone/budesonide
• LAMA - tiotropium

3. If still not controlled:

• LABA + LAMA + ICS

Additional therapies to consider include:

1. Mucolytic therapy if a person with stable COPD develops chronic productive cough of sputum.
2. Specialist decisions:
1. Oral theophylline - after a trial of SABA/LABA or for patients who cannot use inhaled therapies.
2. Prophylactic antibiotic therapy in the form of azithromycin but be wary as azithromycin can cause QT-prolongation (ECG to be done first).
3. Oral PDE4 inhibitors (phosphodiesterase) for severe disease with persistent symptoms and exacerbations despite optimal inhaled and non-pharmacological therapy.
3. Surgical management - if refractory to all treatments.
1. Lung volume-reduction - to remove bullae which compress functional lung tissue.
2. Lung transplantation

ACUTE EXACERBATIONS OF COPD

Acute exacerbations of COPD is a common finding in A&E. It is a sustained deterioration in a patient’s respiratory systems beyond their normal day-to-day variability.

😷 Presentation

• URTI in the past 5 days.
• Worsening breathlessness
• Increased sputum volume and purulence - suggest infective cause.
• Cough
• Wheeze
• Fever without obvious source
• Increased RR and HR

🦠 Causative agents

🔍 Investigations

🧰 Management

AECOPD management:

1. Oxygen therapy as our greatest concern is hypoxia.

We need to be careful as COPD patients who have CO2 retention become insensitive to CO2 and therefore their breathing is not driven by hypercapnia, but rather by hypoxia. As a result if we give too much oxygen, they will decrease their respiratory rate and have hypercapnia that can lead to respiratory arrest.

As a result we start off with 24-28% O2.

That being said, any critically ill patient should be started on high-flow oxygen (15L via a non-rebreather mask) and then titrate it down.

Aim to keep SpO2 between 88-92%.

2. Nebulised bronchodilators:
1. SABA - salbutamol 5mg. Repeat every 15-30 mins.

+

SAMA - ipratropium 500mcg every 6 hours if the SABA is not enough.

3. Steroids
1. Oral prednisolone - 30mg OD for 5 days.
4. Antibiotics - if there is evidence of infection. NICE only recommend oral antibiotics 'if sputum is purulent or there are clinical signs of pneumonia’.
1. Amoxicillin - 500mg every 8 hours, OR
2. Clarithromycin, OR
3. Doxycycline
5. If no response with nebulisers consider IV aminophylline.
6. If there is still no response, provide non-invasive ventilation. This is typically used when there is respiratory acidosis (pH of 7.25-7.35). BiPAP is typically used if there is type 2 respiratory failure while CPAP is often used with type 1 respiratory failure.
1. If the pH drops <7.25 → consider intubation.
7. A respiratory stimulant such as doxapram if they are unsuitable for ventilation. However doxapram is a full CNS stimulant and may cause seizures and should be avoided if possible.

🚨 Complications