QuestionSBA
QuestionChoice
This patient has a severe exacerbation of chronic obstructive pulmonary disease (COPD). BiPAP would be indicated in patients with acute respiratory acidosis and would be the most appropriate measure prior to considering intubation and mechanical ventilation
32188
a
Bilevel positive airway pressure (BiPAP) machine
QuestionChoice
In patients with COPD, CPAP would not be preferred as the tidal volume cannot be effectively titrated unlike with BiPAP, hence it is not as suitable for patients with hypercapnia that would require increased alveolar ventilation. CPAP would be indicated in patients with acute cardiogenic pulmonary oedema
32189
b
Continuous positive airway pressure (CPAP) machine
QuestionChoice
Non-rebreather masks can deliver an inspired oxygen concentration of up to 90%, but as it is considered uncontrolled oxygen therapy, it would not be appropriate if the patient is known to retain carbon dioxide, as it may exacerbate hypercapnia and respiratory acidosis
32191
d
High flow oxygen via non-rebreather mask
QuestionChoice
This would be considered only if the patient is clinically deteriorating and has failed a trial of non-invasive ventilation, is unable to tolerate or has contraindications to it
32190
c
Intubation and mechanical ventilation
QuestionChoice
This would be able to provide oxygen of up to 6-10 L per minute, which would likely be insufficient for this patient's current requirements in view of the respiratory acidosis. It is also a form of uncontrolled oxygen therapy which would not be appropriate in carbon dioxide retaining patients
32192
e
Simple face mask
QuestionComment
Does anyone know what the threshold is for when you would prescribe high flow o2 over bipap? I know bipap is given to co2 retainers but when someone is hypoxic they say to give o2 - wondering at which sats you would go non-rebreathe? thanks
24088
QuestionComment
from my understanding high flow is what you would give in a patient first presenting with very low 02 stats + being unstable. This patient most likely wasn't acutely unwell in the beginning so was given ventri mask and after that failed the next step would b BiPAP 

38420
User
subscriber
Embolism Sclerosis
User
subscriber
Odor Myotonia
QuestionComment
literally doesn't say anywhere about COPD
41142
User
subscriber
Fibrosis Ketone
Concept
Chapter
# Summary

Chronic obstructive pulmonary disease (COPD) is a chronic obstructive disease of the airways with the two main components being chronic bronchitis and emphysema. It usually develops due to smoking, with other risk factors including occupation exposures and air pollution. Patients present with breathlessness, a chronic productive cough and wheeze. Key investigations are spirometry (to confirm obstruction), full blood count (to identify anaemia or polycythaemia) and a chest X-ray to exclude lung cancer or other causes of symptoms. Management includes smoking cessation, pulmonary rehabilitation, consideration of long term oxygen therapy, inhaled or nebulised medical treatment and consideration of other medications e.g. mucolytics. Acute exacerbations of COPD may be infective or non-infective, and can be treated by increasing bronchodilator therapy, oral prednisolone and antibiotics (if an infective cause is suspected).

# Definition

Chronic obstructive pulmonary disease (COPD) involves airway obstruction that is usually progressive. It encompasses both emphysema (where alveolar wall destruction leads to enlargement of the distal airspaces) and chronic bronchitis (persistent or recurrent productive cough usually due to mucus hypersecretion). 

# Epidemiology

In the UK 1.2 million people have a diagnosis of COPD, with an estimated 2 million people living with it undiagnosed. It is the 5th commonest cause of death in the UK, causing almost 30,000 deaths per year. 

Around 90% of COPD cases in the UK are caused by smoking, with household pollution being a bigger contributing factor in low and middle income countries.

# Risk Factors

- Tobacco smoking and passive smoke exposure
- Marijuana smoking 
- Occupational exposure to dusts and fumes
- Household air pollution from wood or coal burning
- Alpha-1 antitrypsin deficiency

Prognosis is variable, with the following factors associated with higher morbidity and mortality:

- Poor exercise tolerance
- Smoking
- Low body mass index
- Multi-morbidity and frailty
- Exacerbations requiring admission to hospital or frequent exacerbations
- Severe obstruction on spirometry (as measured by a lower FEV1)
- Chronic hypoxia
- Cor pulmonale

# Pathophysiology

Chronic Bronchitis:

- As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs.
Cilia are not able to remove the excess mucus and so it obstructs the small airways.
Ongoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.

Emphysema:

- Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants. 
- Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.
- This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.

# Classification

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) classifies COPD severity using airflow limitation (as measured by FEV1), severity of symptoms and frequency of exacerbations. 

| GOLD Grade | Severity                | Post-Bronchodilator FEV₁ (% Predicted) |
|------------|--------------------------|----------------------------------------|
| 1          | Mild                     | ≥ 80%                                 |
| 2          | Moderate                 | 50-79%                                |
| 3          | Severe                   | 30-49%                                |
| 4          | Very Severe              | < 30%                                 |


The two measures used to quantify symptom severity are the CAT (COPD Assessment Test) and the mMRC (modified Medical Research Council) dyspnoea scale which is given below:

| Grade | Description |
|-------|----------------------------------------------------------------------------------------------------|
| 0 | I only get breathless with strenuous exercise. |
| 1 | I get short of breath when hurrying on level ground or walking up a slight hill. |
| 2 | On level ground, I walk slower than people of the same age because of breathlessness, or I have to stop for breath when walking at my own pace. |
| 3 | I stop for breath after walking about 100 yards or after a few minutes on level ground. |
| 4 | I am too breathless to leave the house, or I am breathless when dressing or undressing. |

# Signs and symptoms

- Shortness of breath that worsens with exertion
- Reduced exercise tolerance
- Chronic productive cough
- Recurrent lower respiratory tract infections
- Wheeze
- In more advanced cases, systemic symptoms such as weight loss and fatigue may be present

Examination may be normal, though signs may include:

- Wheeze or crackles on auscultation
- Accessory muscle usage
- Pursed lip breathing (this creates a small amount of positive end expiratory pressure to prevent the alveoli from collapsing)
- Cyanosis 
- Hyperinflation of the chest
- Cachexia
- Raised JVP and peripheral oedema (indicating cor pulmonale has developed)

# Investigations

- **Spirometry** - the diagnostic investigation for COPD and key to classification of severity, may be used to monitor progression of the disease. A FEV1/FVC ratio <0.7 confirms obstruction.

- **Bloods** - Full blood count looking for polycythaemia (resulting from chronic hypoxaemia) or anaemia (usually anaemia of chronic disease), consider BNP to assess for heart failure (with an **echocardiogram** if suspected, alpha-1 antitrypsin in young patients/minimal smoking history/strong family history
- **ECG** - the following ECG changes are often seen in advanced COPD with features of e.g. cor pulmonale, and include:
	- Right axis deviation
	- Prominent P waves in inferior leads
	- Inverted P waves in high lateral leads (I, aVL)
	- Low voltage QRS
	- Delayed R/S transition in leads V1-V6
	- P pulmonale
	- Right ventricular strain pattern
	- RBBB
	- Multifocal atrial tachycardia

- **Chest X-ray** - used to rule out other causes of symptoms (e.g. lung cancer, bronchiectasis), may show features of COPD including hyperinflation of the chest with flattening of the hemidiaphragms and bullae.

[lightgallery1]

- **Sputum culture** - during exacerbations to target antibiotic therapy

# Differential diagnosis

- **Asthma:** may coexist with COPD, suspect if onset of symptoms <35, history of atopy, non-smoker, variable or nocturnal symptoms.
- **Bronchiectasis:** copious secretions and coarse crepitations on examination, triggering factors include severe childhood respiratory tract infections.
- **Heart Failure:** suspect in patients with ischaemic heart disease, may have orthopnoea and paroxysmal nocturnal dyspnoea.
- **Interstitial Lung Disease:** dry rather than a productive cough, fine crackles on examination.
- **Lung cancer:** patients with COPD are usually at higher risk due to smoking history, need to investigate for malignancy in cases with a persistent cough/haemoptysis/weight loss.
- **Tuberculosis:** similar symptoms, systemic manifestations include fevers and weight loss, consider in at-risk groups.

# Management of Chronic COPD

**Conservative:**

- Patient education, ensure all patients have a personalised self-management plan
- Smoking cessation support
- Nutritional support and dietician referral if malnourished
- Annual influenza and one-off pneumococcal vaccination
- Pulmonary rehabilitation (refer if grade 3 and above on mMRC dyspnoea scale or a recent admission for an acute exacerbation)
- Consider referral for respiratory physiotherapy to help with sputum clearance and breathing techniques

**Medical:**


- For patients whose activities are limited by breathlessness, start a short-acting beta-2 agonist (SABA, e.g. salbutamol) or short-acting muscarinic antagonist (SAMA, e.g. ipratropium) inhaler
- The next step depends on if they have features of asthma or steroid responsiveness: if these are present then add a long-acting beta-2 agonist (LABA, e.g. formoterol) and an inhaled corticosteroid (ICS, e.g. beclomethasone). If these are not present then add a LABA and a long-acting muscarinic antagonist (LAMA, e.g. tiotropium). 
- If patients do not respond adequately to this, the third inhaler can then be trialled (i.e. all patients would be on a SABA/SAMA + LABA + LAMA + ICS).

Patients who require further therapy should be referred to a specialist for ongoing management which may include oral steroids, oral theophylline or oral phosphodiesterase-4 inhibitors (e.g. roflumilast).

Management of stable COPD is can be tailored according to the patient’s clinical phenotype. The following groups are defined according to 2024 NICE guidance:

**Group A**
 
- **Definition**: Patients with minimal symptoms (mMRC grade 0–1 or CAT score <10) and no history of exacerbations requiring hospitalisation or oral corticosteroids in the last year.  
- **Management**:
  - Start with a **short-acting bronchodilator (SABA or SAMA)** as needed for symptom relief.
  - If symptoms are not controlled, consider switching to a long-acting bronchodilator:  
    - **LAMA** or **LABA**, depending on individual tolerance and symptom profile.  

**Group B**
 
- **Definition**: Patients with significant symptoms (mMRC grade ≥2 or CAT score ≥10) but no exacerbations requiring hospitalisation or oral corticosteroids in the last year.  
- **Management**:  
  - Initiate treatment with a **LAMA** or **LABA** as maintenance therapy.  
  - If symptoms persist despite monotherapy, escalate to **dual therapy (LABA + LAMA)**.  

**Group E**
  
- **Definition**: Patients with frequent exacerbations (≥2 per year or ≥1 requiring hospitalisation) regardless of symptom burden.  
- **Management**:  
  - First-line therapy is **LAMA** for exacerbation prevention.  
  - If exacerbations persist, escalate to:  
	    - **Dual therapy (LABA + LAMA)**.  
	    - If asthmatic features or steroid responsiveness are present (e.g., eosinophilia or a history of asthma), consider **LABA + ICS**.  
  - For patients who continue to experience exacerbations despite dual therapy, switch to **triple therapy (LABA + LAMA + ICS)**.  



| **Group**   | **Phenotype**                  | **Initial Therapy**          | **Escalation Therapy**             |  
|-------------|--------------------------------|------------------------------|------------------------------------|  
| **Group A** | 0 or 1 moderate exacerbation not leading to hospitalisation | SABA or SAMA as needed       | LAMA or LABA                      |  
| **Group B** | 0 or 1 moderate exacerbation not leading to hospitalisation| LAMA or LABA                 | LABA + LAMA                       |  
| **Group E** | 2 or more moderate exacerbations or 1 or more exacerbations leading to hospitalisation	     | LAMA                         | LABA + LAMA or LABA + LAMA + ICS  |  


Other medical treatments that may be considered include:

- Oral mucolytic therapy - for patients with a chronic cough productive of sputum.
- Prophylactic antibiotics - in cases of frequent infective exacerbations, should be discussed with a specialist, a common choice would be azithromycin 3x per week.
- Nebuliser therapy - for patients with disabling breathlessness despite optimised use of inhalers.
- Long-term oxygen therapy (LTOT) - see below for more details


**Surgical:**

- In certain cases of severe COPD when patients have not responded to maximal medical therapies, surgical intervention may be considered. 
- Both the NICE recommended options involve lung volume reduction (which involves removing emphysematous areas of the lung so that the healthy lung can expand) - this can be done either by surgical resection or using bronchoscopy to site a one-way valve in one of the larger airways to collapse the diseased lung.  

### Long term oxygen therapy (LTOT)

**The following patients should be referred for assessment for LTOT:**

- Oxygen saturations <92% in air or cyanosis
- FEV1 <30% predicted (consider referring if <49%)
- Polycythaemia
- Peripheral oedema or raised jugular venous pressure (suggesting cor pulmonale)

This assessment involves ensuring that patients are medically optimised and their COPD is stable (i.e. they’re not recovering from a recent exacerbation). Patients who are current smokers cannot be offered LTOT because of the risk of burns and fires. 

Patients then have two ABGs in air at least 3 weeks apart and the following patients should be offered LTOT (with the advice to use the oxygen for at least 15 hours per day):

- PaO2 below 7.3kPa
- PaO2 7.3-8kPa with any of secondary polycythaemia, peripheral oedema or pulmonary hypertension

# Complications

## Acute exacerbations

- These present with worsening breathlessness, productive cough and wheeze, and patients may be febrile, tachycardic and tachypnoeic. 
- Patients who are clinically well may be treated at home with an increase in their usual inhalers, a short course of oral steroids (usually 30mg prednisolone for 5 days) and oral antibiotics if bacterial infection is suspected. 
- Those who have frequent exacerbations may be given a “rescue pack” of steroids and antibiotics to keep at home and start using in case of an exacerbation (alongside seeking medical help).

- Patients requiring hospital admission should also receive steroids and antibiotics if indicated. 
- They may require nebulised bronchodilators, supplementary oxygen and in case of deterioration respiratory support with non-invasive ventilation may be required. 
- Advanced care planning and ensuring that escalation status is discussed with patients is therefore key, so that if they deteriorate to the point of needing intensive care support it is established whether or not this is appropriate and in line with their wishes.

## Polycythaemia

- Chronic tissue hypoxia as seen in COPD leads to a compensatory overproduction of erythropoietin, which leads to increased red blood cell production (i.e. secondary polycythaemia). 
- This causes an increase in blood viscosity that in turns increases risk of both arterial and venous thrombosis. 


## Cor Pulmonale

Cor pulmonale refers to right ventricular dilation or hypertrophy in response to pulmonary hypertension caused by chronic lung disease - COPD is not the only cause of this but it is the most common.

The pathophysiology is as follows:

- Changes in the lungs and chronic hypoxaemia cause the walls of the pulmonary arteries to thicken.
- This increases vascular resistance in the lungs.
- The right ventricle then has to pump against greater resistance, which causes it to either dilate or hypertrophy.
- Ultimately this leads to right heart failure, with resulting peripheral oedema, hepatomegaly and elevated jugular venous pressure (JVP).

Peripheral oedema may be treated symptomatically with diuretics and long-term oxygen therapy has been shown to reduce morbidity and mortality. All patients with suspected cor pulmonale should be referred to secondary care.

## Pneumothorax

- COPD is a common cause of secondary pneumothoraces (i.e. a pneumothorax secondary to underlying lung disease). These occur when a bulla ruptures, releasing air into the pleural cavity. 
- Investigations and treatment are as per the BTS guidelines (see Pneumothorax chapter for more details).

## Depression and anxiety
- Over 1 in 3 people with COPD report symptoms of depression and anxiety so screening for this is important during patient reviews. 
- The COPD Assessment Test (CAT) can be used to assess the impact of COPD on everyday life. 
- Referral to psychological services for support may be appropriate, as well as holistic assessment and management.

# NICE Guidelines

[Click here for the NICE Guidelines](https://www.nice.org.uk/guidance/ng115)

[NICE CKS - COPD](https://cks.nice.org.uk/topics/chronic-obstructive-pulmonary-disease/)

# References

[Patient UK - COPD](https://patient.info/doctor/chronic-obstructive-pulmonary-disease-pro)

[GOLD report 2023](https://goldcopd.org/2023-gold-report-2/)

[Radiopaedia - COPD](https://radiopaedia.org/articles/chronic-obstructive-pulmonary-disease-1?lang=gb)

[Patient UK - Cor Pulmonale](https://patient.info/doctor/cor-pulmonale)
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COPD Management (NICE).png
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A chest x-ray showing hyperinflated lungs and a flattened diaphragm in an individual with COPD.
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Chronic obstructive pulmonary disease (COPD)
Topic
20
Respiratory Physiology
6438
A 75-year-old man is admitted to the general medical ward with a 3 day history of worsening shortness of breath and a productive cough with green sputum. He has a past medical history of COPD.


On examination, he has visible accessory muscle use and has widespread coarse crepitations with an expiratory wheeze.


Observations:


 - Temperature 38.5°C
 - pulse 105
 - BP 140/70
 - SpO<sub>2</sub> 89% on 40% O<sub>2</sub> via Venturi mask


Arterial blood gas:

||||
|--------------|:-------:|------------------|
|pH|7.27|7.35 - 7.45|
|PaO₂|8 kPa|11 - 15|
|PaCO₂|7.1 kPa|4.6 - 6.4|
|Bicarbonate|15 mmol/L|22 - 30|



Which is the next most appropriate management?
a