GOLD COPD Guideline 2024 Flashcards
Definition and diagnostic criteria of COPD
Heterogenous lung condition with (symptoms + structural damage + outcome):
1. Chronic respiratory symptoms (dyspnoea, cough, sputum production, exacerbation)
2. Due to airway abnormalities (bronchitis, bronchiolitis) and/or alveoli (emphysema)
3. Causing persistent, progressive airflow obstruction
Spirometry - non-fully reversible airway obstruction post-bronchodilation
- FEV1 / FVC < 0.7
Special considerations to patients not fulfilling criteria:
A. Pre-COPD or PRISM (preserved ratio impaired spirometry)
- Normal FEV1/FVC ratio but with other abnormal spirometry results (low FEV1, low DCO)
Causes and risk factors of COPD
Genetics (G) + Environment (E) + lifetime (T) exposure (GETnomics)
- Tobacco smoking
- Toxic particles and gases, pollution
- Abnormal lung development/accelerating lung aging
- Alpha-1-antitrypsin deficiency (SERPINA-1 gene)
Clinical presentation of COPD
- Asymptomatic
- Dyspnoea and wheeze, chest tightness, fatigue
- Progressive activity limitations
- Sputum production
- Acute exacerbation due to illness or exposure
Spirometry - FEV1 in adulthood
- Predisposing: birthweight, growth failure (abnormal lung growth)
- Precipitating: accelerated decline
- Birthweight and childhood disadvantage factor
- Lower birthweight leads to lesser FEV1 since childhood
- Higher birthweight can achieve supranormal FEV1 - Growth failure and abnormal lung growth
- Growth failure and failure of lung to reach maturity and full FEV1
- Adolescents with catch up growth may achieve full lung growth, maturity and FEV1
–> 50% develop COPD due to abnormal lung growth and development - Accelerated decline - due to environment exposure (50%)
Pathobiology of COPD
- Exaggerated response to chronic irritants increases inflammatory cells and mediators
- Macrophages, neutrophils, lymphocytes (+/- eosinophils and IL-2) release mediators that perpetuate inflammation, oxidative stress and drive structural changes - Imbalance between protease and anti-protease leads to destruction of elastin
- Muscle proliferation, fibrosis of airways
- Inflammation persist even after smoking cessation due to autoantigens and changes in lung microbiome
Outline the pathophysiology of COPD
A. Air trapping and hyperinflation
B. Pulmonary gas exchange abnormalities
C. Pulmonary hypertension
D. Exacerbations and multimorbidities
A. Air trapping and hyperinflation in COPD
- Chronic inflammation leads to:
- Narrowing of small airways
- Luminal exudates (mucous)
- Destruction of lung parenchyma (emphysema)
- Mucociliary dysfunction - Resultant changes
- Reduced elastic recoil
- Loss of alveolar attachments decrease ability of airways to remain open during expiration - Airflow obstruction and limiting lung emptying during forced expiration
- Reduced FEV1 and FEV1/FVC ratio
- Static hyperinflation: increased volume at rest due to loss of elastic recoil
- Dynamic hyperventilation: increased volume during exercise due to obstruction when demands increase and expiratory time reduced
B. Pulmonary Gas Exchange Abnormalities
- Structural changes in airways, alveoli and pulmonary circulation result in ventilation perfusion (V/Q) mismatch and hypoxaemia
- Reduced ventilatory drive cause hypercapnic respiratory failure
- Parenchymal destruction from emphysema reduces DLCO
C. Pulmonary hypertension in COPD
- Intimal hyperplasia, smooth muscle hyperplasia of pulmonary circulation causing hypoxic vasoconstriction
- Eventual loss of pulmonary capillary bed from emphysema
- RVH, right sided failure
Diameter of pulmonary artery on CT scan correlates with risk and severity of exacerbations
D. Exacerbations and multimorbiditis of COPD
Triggers
1. Infections (bacterial or viral)
2. Environmental pollutants
Multimorbidities
1. Ischaemic heart disease and heart failure
2. Osteoporosis
3. Anaemia
4. Diabetes and metabolic syndrome
Triggers increase airway and systemic inflammation, leading to worsened gas trapping, reduced expiratory flow, worsened dyspnoea, V/Q mismatch, hypercapnia
Clinical indicators to suspect COPD
- Dyspnoea - progressively worsens over time, worse with exercise or persistent
- Recurrent wheeze
- Chronic cough
- Recurrent lower respiratory tract infection
- History of risk factors
- Tobacco smoking
- Smoke from home cooking, heating fuels
- Occupational (dust, vapors, fumes, gases, chemicals)
- Host factors (genetics, development abnormalities, low birthweight, prematurity, childhood respiratory infections)
Confirmatory test: spirometry
Clinical presentation of patients with COPD
- Chronic dyspnoea (40%)
- Increased effort, chest tightness, air hunger or gasping - Chronic cough (30%)
- Intermittent, or persistent
- Dry cough or with sputum production
- Cough until rib fracture
- Cough syncope - Wheeze
- Fatigue
- Anorexia, weight and muscle loss
- Ankle swelling (right heart failure)
- Depression and anxiety
Differential diagnosis of chronic cough
Intrathoracic
1. Asthma and COPD
2. Lung cancer
3. Tuberculosis
4. Bronchiectasis
5. Left heart failure
6. Interstitial lung disease
7. Cystic fibrosis
8. Idiopathic cough
Extrathoracic
1. GERD
2. Chronic allergic rhinitis
3. Post nasal drip syndrome (PNDS)
4. Upper airway cough syndrome (UACS)
5. Medications (ACE inhibitors)
History taking in COPD
- Ascertain presenting complaints
- Chronic dyspnoea, chronic cough
- Wheeze
- Fatigue, anorexia, weight and muscle loss
- Ankle swelling (right heart failure)
- Symptoms development: onset, duration - Exposure to risk factors
- Smoking: pack years, current status
- Environment: occupational, housing
- Cessation attempts - Past medical history
- Early life events: prem, low birthweight, maternal smoking, childhood respi infections
- HIV, tuberculosis, lung diseases
- Family history of COPD - Exacerbations and hospitalisation
- Frequency, severity, triggers, ICU admissions - Comorbidities
- Impact on daily life
- Activity limitations, work impact
- Social and family life
- Psychological wellbeing: depression, anxiety
- Sexual dysfunction
- Social support available
What is the single best predictor of future exacerbation frequencies?
What are other predictors of future exacerbations?
- Best: past exacerbation frequency - exacerbations contribute to disease progression
Other predictors (not sensitive):
2. Smoking status - active smoker > stop smoking
3. Older age
4. FEV1 predicted% when stable
5. Sputum eosinophilia - susceptibility to viral infection and positive steroid responsiveness
What are the criterias for LTOT in COPD?
What are the effects of LTOT in qualified COPD patients?
Criterias for LTOT in COPD
Chronic hypoxaemia patients
1. PaO2 ≤ 55 mmHg (7.33kPA) or SaO2 ≤ 88% (at rest on RA) after receiving optimal medical regimen for at least 30 days
2. PaO2 55 to 59 mmHg (8.0kPA) or SaO2 ≤ 89% (at rest on RA) with cor pulmonale or erythrocytosis (> 55%)
3. Consider for nocturnal desaturation, exercise desaturation or severe dyspnea
(this criteria shows no improvement in survival or hospitalization)
4. Stopped smoking - oxygen is a fire hazard
Effects of LTOT in COPD
1. Reduces polycythaemia
2. Reduces pulmonary vascular resistance (reduces vasoconstriction and increases blood flow)
3. Corrects alveolar hypoxaemia
mMRC (modified Medical Research Council) dyspnea scale
Assess degree of breathlessness and impact on daily activities
0 - Not troubled by breathlessness except on strenuous exercise
1 - Short of breath when hurrying on the level or walking up a slight hill
2 - Walks slower than people of the same age on level ground because of breathlessness, or have to stop for breath when walking at own pace
3 - Stop to breathe after walking about 100 yards (100 metres) on the level or after a few minutes on level ground
4 - Too dyspneic to leave house or breathless when dressing
What is the COPD mMRC scale with best evidence for pulmonary rehabilitation?
mmRC 2-4 (or MRC 3-5) - Grade A evidence
Contrary:
mmRC 0-1 (or MRC 2 or less) - Grade D evidence
What is the NNT for pulmonary rehabilitation?
Role of pulmonary rehabilitation in COPD
Number needed to treat (NNT): 4
- Reduces risk of hospitalisation for COPD exacerbation
- Reduces anxiety and panic disorder
- Increases exercise tolerance and self management ability
- Improves quality of life
Contrary to popular belief, PR does not:
1. No overall improvement in spirometry
2. No reduction in mortality (majority studies are underpowered)
Contraindications:
1. Unstable ischaemic heart disease
2. Unable to mobilise (significant arthritis, immobility)
What intervention has the greatest impact on morbidity and mortality in COPD?
Smoking cessation
(While adding long acting inhalers confers improvement in symptoms, they do not reduce mortality)
NICE / GOLD COPD staging
Staging based on FEV1
Special consideration for stage 3 (FEV1 30–50% predicted) with respiratory failure:
Upgraded from severe stage 3 to very severe stage 4
Macrolides (azithromycin, clarithromycin) drug interactions
Cessation:
1. Statin - inhibits CYP3A4, high risk for myopathy
Dose adjustment/monitoring
2. Hydrochlorothiazide - increases QTc
3. Digoxin - increases concentration
4. Carbamazepine - increases concentration
5. Warfarin - increases INR
Step ladder approach to COPD (????)
LABA
LAMA
Trial ICS
Roflumilast
BODE index for prognostication
Probability of survival in each quartiles
What is the limitation of BODE index?
B: Body mass index (+1 point in anorexia BMI < 21)
O: Obstruction (FEV1)
D: Dyspnoea (mMRC score)
E: Exercise limitation (6-minute walk test distance)
Probability of survival at 52 months (4 years+):
- Quartile 1 (0-2): 0.8
- Quartile 2 (3-4): 0.7
- Quartile 3 (5-6): 0.6
- Quartile 4 (7-10): 0.2
Limitations:
1. Does not factor in age
2. Does not use modern statistical techniques during its development
What are the commonest mortality (cause of death) in COPD patients? (based on 2010 statistics)
- Commonest: cardiovascular disease
- Lung cancer
- Respiratory failure and pneumonia
British Thoracic Society Oxygen Guideline for critically ill COPD patients
Critical illness: including major trauma, sepsis, shock and anaphylaxis, REGARDLESS of hypercapnic status
- Initiated on NRM 15 L/min
- Titrated oxygen support to a target saturation range of 94–98% (no role in hyperoxia)
- DO NOT remove oxygen to perform ABG
Patients with hypercapnic respiratory failure should have
- Reduce supplementary oxygen to VM 28% aim for saturations of 88–92%
- If persistent hypercapnia, to start on NIV
- Oxygen alert card
Bronchoscopic lung volume reduction with endobronchial valve trial for chronic emphysema
Met all criterias:
1. Maximal medical therapy
2. Completed pulmonary rehabilitation
3. Stopped smoking for 6 months
Suitable candidates (potential to gain most benefit):
1. Heterogenous emphysema with significant hyperinflation
2. Intact fissures with minimal collateral ventilation
3. RV > 150% (some suggest >175%)
4. RV/TLC ratio >55%
Required investigations
1. CT thorax
2. VQ scan
3. Chartis system - designed balloon catheter with a flow sensor
Post-op complications
1. Tension pneumothorax
2. Massive haemoptysis
3. Exacerbation of COPD
4. Pneumonia
5. Valve expectoration, aspiration, or migration (first 90 days)
Lung volume reduction surgery (LVRS)
Criteria:
1. Hyperinflation
- Residual volume >150% predicted (more in >200%)
- Total lung capacity >100% predicted
2. Heterogenous upper lobe emphysema benefits more than homogenous
(NETT trial: 5 year survival benefit)
Contraindications:
1. Bronchiectasis
2. Co-existent tumour
3. Respiratory failure
Benefits:
1. Increases exercise tolerance
2. Reduces breathlessness
3. Enhances quality of life
Complications:
1. Peri-operative death
2. Air-leak
3. Pneumonia
HIV and COPD
HIV who smoke has:
- Increased 20–30% risk of COPD compared to non-HIV patients
- Earlier onset of COPD
Antiretroviral protease inhibitor (ritonavir, atazanavir) interaction with inhalers (CYP450 inhibition)
Fluticasone and budesonide - Cushing’s syndrome
(Relvar, Seretide, Symbicort)
(requires significant dose adjustment)
Safe: beclomethasone (no need dose adjustment)
(Fostair)
Beta blockers improve prognosis in patients with COPD and IHD
COPD =/= asthma
- Risk NOT apparent in COPD
- Caution in asthma
Benefits:
1. Improves prognosis of COPD
2. Survival benefits in myocardial infarct
3. Reduces admission rates
Hyperoxaemia use
- Carbon monoxide and cyanide poisoning (histotoxic hypoxia)
- Spontaneous pneumothorax
- Some postoperative complications (e.g. surgical site infection and anastomotic problems in gastrointestinal surgery)
- Cluster headache
Nebulisers vs MDI in treatment of exacerbations
Both nebulisation and MDI with space chamber are equally effective
Some studies suggest MDI with space chamber is superior and requires lesser dose
Nebulizer: preferred for acute exacerbation
- 10-15% reaches lungs, with 40-60% bioavailability
1. Pro: More consistent and continuous drug delivery.
2. Pro: bypasses poor MDI technique, not requiring coordination during exacerbation
3. Con: takes longer and requires a power source.
MDI with space chamber:
- 30–50% reaches lungs, with 40-60% bioavailability
1. Pro: convenient and portable
2. Pro: quicker to use
3. Con: requires coordination (can be improved with spacer)
