What is the definition of COPD?
a heterogeneous, progressive lung disease state characterised by chronic respiratory symptoms and airflow obstruction that is not fully reversible
What causes obstruction of airflow in COPD?
- Inflammation of the airways:
“chronic bronchitis” - Destruction of the alveolar wall w/ dilation of the airspace:
“emphysema”
(the inflammation + destruction is triggered by):
1. toxic substances
- tobacco smoke
2. Occupational pollutants
- dust and silica
What is chronic bronchitis?
“Productive cough for > 3 months each year for 2+ consecutive years”
An inflammatory process in which:
- there is an increase in mucus production that obstructs the airway
What is the role of elastases in the body?
the integrity and structure of the resp bronchioles and alveolar wall are dependent on the balance between elastases (which destroy elastin) and anti- elastases (which stop elastase)
What is emphysema?
Destruction & enlargement of the alveoli:
1. An inflammatory response usually triggered by tobacco smoke
2. This tips the balance, increasing the amount of elastases in the body (destroy the elastin in alveolar)
3. Leads to excessive destruction of the alveolar wall
4. Elastic recoil is lost
5. Airways collapse
6. Air is trapped in alveoli
7. Gas exchange is impaired leading to hypoxemia and retention of CO2
(can also be caused by alpha-1 antitrypsin deficiency- usually in people under 45 with COPD)
Describe the mechanism of action by which alpha-1 antitrypsin deficiency leads to emphysema
For people < 45 YO with COPD:
- Alpha- 1 antitrypsin deficiency is an autosomal dominant disorder
- Usually alpha-1 antitrypsin is synthesised in the liver and inhibits neutrophil elastase
- With the disorder, this protein is not exported out of the liver; elastase accumulates
- causes damage to the lung parenchyma and liver cirrhosis
onset of symptoms occurs early in smokers vs non-smokers
What are the risk factors for COPD?
- Smoking - predominantly affects upper lobes (as they are better ventilated)
- Air pollution / Environmental toxins (dust, nitrogen dioxide)
- Cadmium, coal, cotton, cement and grain
- Advanced age
- Genetic factors (alpha-1 antitrypsin deficiency)
- Lung growth + development
Summarise the epidemiology of COPD
● VERY COMMON (8% prevalence)
● Presents in middle age or later
● More common in males - this may change because there has been a rise in female smokers
What are the presenting symptoms of COPD?
- Chronic productive cough
- Breathlessness (initially at exercise - reducing exercise tolerance, eventually at rest)
- Fatigue
- Sputum production
- In severe cases, chronic changes in the vascular beds causing pulmonary hypertension –> right sided heart failure (cor pulmonale) –> peripheral oedema
- Pink puffers and blue bloaters
What is meant by “pink puffers and blue bloater”?
this refers to the different symptoms experienced by COPD pts with bronchitis vs emphysema:
BRONCHITIS: “Blue bloater”
- cyanosis
- peripheral oedema
- obesity
- crackles + wheeze
EMPHYSEMA: “Pink puffer”
- Pink skin
- Pursed- lip breathing
- Accessory breathing muscles
- Barrel chest
- Decreased breath sounds
- Cachectic appearance
What symptoms are associated with COPD exaccerbation?
- Upper airway symptoms (colds and sore throats)
- Increased wheeze
- Chest tightness
- Reduced exercise tolerance
- Fluid retention
- Increased fatigue
- Acute confusion
Increased: - Dyspnoea
- Sputum purulence
- Sputum volume
- Cough
What signs of COPD can be found on physical examination?
- Inspection
o Respiratory distress
o Use of accessory muscles – tripod position
o Pursed lip breathing
o Barrel-shaped over-inflated chest
o Decreased cricosternal distance
o Cyanosis
- Tar staining - Palpation
o Reduced expansion - Percussion
o Hyper-resonant chest
o Loss of liver and cardiac dullness - Auscultation
o Quiet breath sounds
o Prolonged expiration
o Wheeze
o Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions
o Sometimes crepitations - Signs of CO2 Retention
o Bounding pulse
o Warm peripheries
o Asterixis - RARE - LATE STAGES: signs of right heart failure (cor pulmonale)
o Right ventricular heave
o Raised JVP
o Ankle oedema
What investigations are used to monitor COPD?
- Pulse oximetry
- Spirometry and Pulmonary Function Tests
- CXR- used to rule out other pathologies:
- May appear NORMAL
- Hyperinflation (> 6 anterior ribs or 10 posterior ribs, flattened diaphragm)
- Reduced peripheral lung markings
- Elongated cardiac silhouette
- Bullae - Bloods :
- FBC
- Increased WCC if infective exacerbation
- increased Hb and haematocrit due to secondary polycythaemia(HAEMATOCRIT >55%)
- ABG - may show hypoxia, normal/raised PCO2 (if acutely unwell) - type 2 respiratory failure
- Inflammatory markers - if evidence of exacerbation - ECG and Echocardiogram- check for cor pulmonale (RBBB & right axis deviation) risk factors for COPD are similar to those for IHD (so co-morbidities common)
- Sputum and Blood Cultures- useful in acute infective exacerbations
- a1antitrypsin levels- useful in young patients (<45) who have never smoked
- reduced DLCO due to emphysema
How is COPD confirmed/ diagnosed?
- Spirometry and Pulmonary Function Tests :
Reduced FEV1/FVC <70% & - After PFTs, give inhaled bronchodilator (COPD is irreversible so the bronchodilator SHOULD NOT change PFTs)
- Repeat PFTs, if FEV1 has not increased by at least 12%-> COPD
- In COPD there is also an increased total lung capacity and residual volume (due to air trapping)
How is COPD managed generally- to achieve stable COPD?
General:
o Stop smoking
o Encourage exercise
o Treat poor nutrition or obesity
o Influenza and pneumococcal vaccination
o Pulmonary rehabilitation/palliative care
o PRN short-acting antimuscarinic (ipratropium) or short acting b2 agonist (salbutamol)
How are acute exacerbations of COPD managed?
Acute Exacerbations (most commonly due to haemophilus influenzae) →
1. should have the same initial target saturations as other critically ill patients (15 L/min via non-rebreathe mask) pending the results of blood gas results after which these patients may need controlled oxygen therapy:
(24% Oxygen (blue venturi mask)), Nebulised Bronchodilators (salbutamol + ipratropium bromide nebulisers),
2. Corticosteroids (oral prednisolone for 5 days or IV hydrocortisone),
3. Antibiotics (only if evidence of infection such as green sputum - amoxicillin/doxycycline/clarithromycin),
4. IV Theophyllines (bronchodilators)
- NIV (BIPAP) if respiratory acidosis with high CO2 despite maximum medical treatment
- Antibiotics (for infective exacerbation) ⇒ amoxicillin, clarithromycin or doxycycline
- If meet criteria due to recurrent exacerbations ⇒ prophylactic azithromycin (need to monitor QT interval)
How would you manage chronic COPD?
- Initiate short-acting b2-agonist (SABA)/short-acting muscarinic antagonist (SAMA)
- Then:
▪ If FEV1>50%: long-acting b2-antagonist (LABA) + long-acting muscarinic antagonist (LAMA)
If worsens: add inhaled corticosteroids (ICS)
▪ If FEV1 <50%: LABA + inhaled corticosteroid (ICS) in combined inhaler or LAMA
If worsens: add ICS
● SABA example: salbutamol
● SAMA: ipratropium
● LABA: salmeterol
● LAMA: tiotropium
● Inhaled corticosteroids: beclomethasone
● Symbicort – budeonside + formotrel
- If remain symptomatic:
o Refer to specialist
o Consider steroid trial, home nebulisers, theophylline - Regular oral steroids should be avoided if possible
- Surgery
- Pulmonary rehabilitation
o Oxygen therapy (LTOT)
When should you consider surgery for a COPD pt?
● Indications for surgery: recurrent pneumothoraces, isolated bullous disease, lung volume reduction surgery
What is the criteria for Long Term Oxygen Therapy (LTOT) for COPD?
- Supplemental O2 for at least15 hrs/day
- ABG measured on 2 separate occasions
- Assess need for oxygen if: ”HOPPC”
- High JVP
- O2 stats <92%
- Polycythaemia
- Peripheral oedema
- Cyanosis
- FEV1 <30% predicted
Indicated if non-smoker AND:
1. PaO2 < 7.3 kPa on air
2. PaO2 7.3-8 kPa and 1 of the following:
- Polycythaemia (secondary)
- Peripheral oedema
- Pulmonary HTN
- Nocturnal hypoxaemia
Can’t offer long term oxygen therapy to a COPD patient if they are smoking
Identify the possible complications of COPD
● Acute respiratory failure
● Infections
● Pulmonary hypertension
● Right heart failure
● Pneumothorax (secondary to bullae rupture)
● Secondary polycythaemia
Summarise the prognosis for patients with COPD
● High morbidity
● 3-year survival of 90% if < 60 yrs, FEV1 > 50% predicted
● 3-year survival of 75% if > 60 yrs, FEV1: 40-49% predicted
Why is it so important to choose the appropriate oxygen therapy for patients with COPD?
When using oxygen in any circumstance you should remember that it is a drug that can have potential negative effects and so should be used only when needed, and with care. This is even more important in COPD patients who have the potential to become carbon dioxide retainers - this can result in them transitioning from being reliant on their hypercapnic drive for respiration, into a hypoxic drive for respiration. This means if they are over-oxygenated this can prompt respiratory arrest as they lose their hypoxia that was previous driving respiration - to reduce this risk it is always best to use a controlled method of oxygen delivery such as a Venturi mask in COPD patients. This is so you can be specific and certain about how much oxygen you are administering and make small changes to this by titrating through the different colours Venturi masks, corresponding to different oxygen concentrations when used at specific given flow rates. This helps to avoid over-oxygenation, in addition to lower oxygen saturation targets for these patients of 88-92%, as opposed to the usual target of 94-98%.
What ECG changes are suggestive of COPD?
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
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Asthma36
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COPD23
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Respiratory Arrest10
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Respiratory Failure54
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Pneumothorax15
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Pneumonia23
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Tuberculosis15
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Acute bronchitis6
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Allergic disorder11
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Asbestos- related lung disease9
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Bronchiectasis14
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COVID-194
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Fibrotic lung disease10
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Influenza7
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Lower Respiratory Tract Infection9
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Upper respiratory tract infection8
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Occupational lung disease11
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Lung cancer11
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Sarcoidosis6
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Asthma COPD overlap syndrome6
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Developmental delay24
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Toddler Diarrhoea5
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Constipation16
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Cerebral Palsy16
