Respiratory JC019: Cough In A Chronic Smoker: COPD, Smoking Cessation Flashcards
Chronic Obstructive Pulmonary Disease (COPD)
- Progressive
- Not fully reversible airflow obstruction (Reversible: Asthma)
- ∵ Inflammatory response to toxic particles / gases in **Airways (Chronic bronchitis) + **Alveoli (Emphysema)
Chronic bronchitis (Defined clinically (CPRS57))
- **Bronchoconstriction
- **Inflammation
- ***↑ Mucus
—> Chronic cough + Sputum
Emphysema (Defined pathologically (CPRS57))
—> Progressive SOB (∵ Alveoli volume ↓)
Epidemiology
- 10% >70yo
- ↑ in incidence ∵ smoking, air pollution
Risk factors of COPD
Environmental:
1. ***Smoking (>85%)
2. Air pollution
3. Passive smoking
4. Indoor biomass combustion e.g. wood, occupational exposure
Host:
1. ***α1-antitrypsin deficiency (rare, only consider in young patients, <45yo, Caucasians)
Clinical presentations of COPD
- Middle age / elderly
- Man > Women
- History of chronic smoking
- Chronic cough and sputum (i.e. Chronic bronchitis)
- for **years
- **whitish, mucoid (unless exacerbation) - ***Progressive SOB (i.e. Emphysema)
- Complications requiring ***hospitalisation (ask about frequency of hospitalisation)
Physical examination of COPD
- Cyanotic
- High RR
- Pitting edema
- ↑ JVP
- Parasternal heave
- ***Hyperinflation of lungs
- ***↓ Air entry + Prolongation of expiratory phase with rhonchi (wheeze) (NB: wheeze often absent in COPD (Davidson, Talley))
- ***Coarse inspiratory crackles
***Complications of COPD
- Acute exacerbation
- **Pneumothorax
- ↑ Airflow obstruction
- **Infection
- ***Respiratory failure (acute) - Chronic respiratory failure
- ***Cor pulmonale (heart disease due to lung disease)
- chronic hypoxaemia —> pulmonary HT —> RVH —> RVF - Pulmonary thromboembolism
***Investigations of COPD
- Lung function test
- Spirometry: FEV1/FVC **<70% —> **Airflow obstruction
- Lung volumes: ↑ RV + ↑ TLC —> **Hyperinflation of lung
- **↓ DLCO —> Emphysema with destroyed alveoli - CBC
- ***CXR
- Hyperinflation
- Hypertranslucency
- Cardiomegaly
- Prominent pulmonary arteries - ***Arterial blood gases —> Respiratory failure
- Sputum examination —> Infections
- ECG +/- Echocardiogram —> Cor pulmonale
***Diagnosis of COPD (GOLD guideline)
- Considered in any patient who has dyspnea, chronic cough or sputum production, and / or a history of exposure to risk factors for the disease (e.g. tobacco smoke, smoke from home cooking / heating fuels, occupational dusts, host factors e.g. genetic, low birthweight, prematurity, childhood respiratory infections)
- Forced spirometry demonstrates the presence of a post-bronchodilator FEV1/FVC <0.7 is ***mandatory to establish the diagnosis of COPD
***Management of COPD
- Assess and monitor disease
- Reduce risk factors
- Stop smoking - Manage exacerbation (account for most hospitalisations + mortality)
- **Antibiotics (infection)
- **Inhaled BD
- **Systemic steroid
- **Controlled O2 therapy
- ***Non-invasive ventilation (NIV) - Manage stable COPD (in OPD settings)
- **Bronchodilator
- **ICS
- ***Long term O2 therapy (LTOT)
- Rehabilitation - End stage COPD
- Lung volume reduction surgery (breathe more comfortably (↓ effect of hyperinflation))
- Lung transplant
3 main principles in COPD management
- Stop smoking
- Bronchodilators (Inhaled preferred)
- Anticholinergics
- β2 agonists - Anti-inflammatory treatment (when frequent exacerbations)
- ICS
- Roflumilast (oral)
β2 agonists
- Salbutamol (Ventolin)
- Terbutaline (Bricanyl)
- Salmeterol (Serevent)
- Formoterol (Oxis)
Anti-cholinergics
- Ipratropium (Atrovent)
- Tiotropium (Spiriva)
Anti-inflammatory
ICS:
1. Beclomethasone (Becotide, Becloforte)
2. Budesonide (Pulmicort)
3. Fluticasone (Flixotide)
Roflumilast (Daxas):
- new oral ***non-steroid anti-inflammatory therapy specific for COPD (a PDE4 inhibitor with anti-inflammatory effect)
Management of complications
- Acute exacerbation
- **Exclude + Treat pneumothorax
- **Antibiotics
- **↑ Inhaled BD
- **Systemic steroids
- **Controlled O2 therapy
- **Non-invasive ventilation (NIV) for acute type 2 respiratory failure - Cor pulmonale
- Diuretics
- Salt + Fluid restriction
Controlled O2 therapy
Aim:
- Use O2 in controlled manner to achieve target PaO2 of **8 kPa (SaO2 **90%) without significant PaCO2 retention + acidosis
—> X 100% O2
∵
1. Respiratory drive in COPD patients is O2 dependent (rather than CO2)
Chronic hypoxia
—> respiratory alkalosis
—> renal compensation by HCO3 excretion
—> reset central chemoreceptors towards a lower PCO2
—> any PCO2 changes become important
—> O2 lack becomes ***important respiratory stimulus
Chronic CO2 retention
—> respiratory acidosis
—> renal compensation by HCO3 retention
—> reset central chemoreceptors towards a higher PCO2
—> buffer any PCO2 changes
—> CO2 becomes ***less important in respiratory drive
- V/Q mismatch (∵ inhibition of hypoxic pulmonary vasoconstriction —> poorly ventilated alveoli are now well perfused)
- Haldane effect (↑ O2 —> ↓ Hb ability to carry CO2 —> ↑ CO2 unloading but cannot be exhaled since poor ventilation in COPD —> CO2 retention)
結論: 唔能夠淨係比O2 —> 要比Ventilation
Modes:
- Nasal cannula (1-2 L/min)
- Venturi masks (24%, 28%)
Monitor:
- Clinical
- **Pulse oximeter
- **Arterial blood gases
