COPD Flashcards
What characterises COPD?
Progressive disease
airway obstruction little or no reversibility
FEV1/FVC ratio <0.7. inc. chronic bronchitis and emphysema
What is chronic bronchitis?
clinically as cough, sputum production on most days for 3 months of two successive years.
What is emphysema?
defined histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls. It is classified according to the site of damage:
• centri-acinar - commonest; distension and damage is around resp bronchioles whilst distal alveolar ducts are preserved
• pan-acinar - less common; destruction involves whole acinus
• irregular - patchy scarring and damage; no regard for acinar damage
What are pink puffers?
- SOB/ cyanosed
- ventilation
- PaO2 and PaCO2
- Failure type?
- Could develop?
breathless but not cyanosed
increased alveolar ventilation, are only slightly hypoxic and have a normal or low PaCO2
may progress to type 1 respiratory failure.
What are blue bloaters?
- SOB/ cyanosed
- ventilation
- PaO2 and PaCO2
- Failure type?
- Could develop?
cyanosed but not breathless
decreased alveolar ventilation with low PaO2 and high PaCO2
may progress to type 2 respiratory failure. rely on their hypoxic drive to keep breathing
could develop cor pulmonale.
What age does it mainly affect?
> 40’s
How common cause of death?
Predicted to become 3rd most common cause of death and 5th most common disability worldwide by 2020
90% of COPD patients are smokers
What are 3 mechanisms have been suggested for this limitation of airflow in small airways?
- Loss of elasticity and alveolar attachments of airways due to emphysema. This reduces the elastic recoil and the airways collapse during expiration.
o emphysema leads to expiratory airflow limitation and air trapping. The loss of lung elastic recoil = ↑ TLC and premature closure of airways limits expiratory flow, and loss of alveoli = decreased surface area for gas exchange
• Chronic bronchitis – cough, sputum production on most days for 3 months of 2 successive years
• Emphysema – enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls - Inflammation and scarring cause the small airways to narrow.
o Microscopically: infiltration with acute and chronic inflammatory cells.
o Epithelial layer may become ulcerated, with squamous cells replacing the columnar cells on healing of the ulcer
o Inflammation leads to scarring and thickening of the walls => narrowing of the small airways
o Small airways especially affected in early disease (w/o any breathlessness); accounts for improvement in lung function if smoking is stopped early enough. Inflammation continues in later stages so smoking cessation not as effective. - Mucus secretion which blocks the airways.
o Increased number of mucus-secreting goblet cells in bronchial mucosa; bronchi may become inflamed and covered in pus.
Explain the FEV1 and FVC ratio?
In obstructive respiratory disease the FEV1 is decreased due to airway obstruction, the FVC remains normal as the lung capacity is unaffected. Therefore the FEV1:FVC ratio is decreased (<0.7). Normaly 75-80% of the FVC comes out in the first second hence the cut-off limit of 0.7 for the ratio. Common progressive disorder characterized by airflow obstruction (FEV1 <80% predicted; FEV1:FVC ratio <0.7) with little or no reversibility
What are the risk factors?
- Smoking
- Age
- a-1-antitrypsin deficiency
- Air polluaiton
- Infections often lead to exacerbations
Why is a-1-antitrypsin deficiency a problem?
accounts for 2% emphysema cases; major anti-protease. Alpha 1 antitrypsin is a protease I that inhibits enzymes able to destroy alveolar wall .
Smoking = inhibits a-1-antitrypsin
What are the symptoms?
- Chronic cough
- Sputum – white/clear; purulent during infective exacerbation
- SOB
- Wheeze
- Recurrent chest infections
- Dyspnea
- Weight loss
When is SOB worse?
Worse in cold weather/pollution. Minimal diurnal variation
What signs should you look out for?
- Inc. resp rate/tachypnoea
- Accessory muscles of respiration
- Pursed lips
- Peripheral/central cyanosis – when more severe
- CO2 flap – due to hypercapnia due to CO2 retention; usually when more severe and in respiratory failure
- Decreased expansion
- Resonant/hyper resonant to percussion – due to hyperinflation
- Wheeze
- Decreased vesicular breath sounds – over bullae
- Peripheral oedema – when severe
- Hyperinflation
- Decreased cricosternal distance <3cm
- Cyanosis
- Cor pulmonale
What investigations would you request?
CXR Spirometry FBC ABG ECG
What are looking for on a CXR?
o Hyperinflated lungs (>6 ant ribs seen above diaphragm in clavicular line) o Flat hemi-diaphragms o Large central pulmonary arteries o Decreased peripheral vascular markings o Bullae
What are you looking for in spirometry results?
o Patient sat down, breathes in fully, then breathes out as fast and hard as possible and keeps going until nothing left
o FEV1 <80% of predicted – predicted normal for a person of same sex, age and height
o FEV1:FVC <0.7
o Flow volume loop: decreased peak expiratory flow, decline in airflow to complete exhalation creating concave curve
What is the GOLD/NICE staging on COPD?
> = 80 Stage 1 (mild)*
50-79 Stage 2 (moderate)
30-49 Stage 3 (severe)
<30 Stage 4 (very severe)**
What are you looking for in blood results?
o Secondary polycythaemia
o Incr. PCV
What are you looking or in ABG results?
o To check for respiratory failure if sats drop
o To monitor oxygen
o Decreased PaO2
o +/- Hypercapnia
What are you looking for in ECG results?
o Cor pulmonale in advanced disease
o Right atrial and ventricular hypertrophy
What management would you suggest?
- Smoking cessation
- Pulmonary rehab
3 .Diet advice and supplementation - Vaccination and antiviral therapy
- Drug therapy (mucolytics)
- Oxygen therapy
- Surgery
- Palliative care
What is pulmonary rehab?
Programme of physical training, disease education, nutritional assessment and advice, and psychological, social, and behavioural intervention.
What vaccination do you offer?
Pneumococcal and annual flu vaccination
Antivirals recommended for influenza infections (zanamivir and oseltamivir)
What are the surgical options?
o Bullectomy if single large bulla present on CT scan
o Lung transplant if remain breathless despite maximal medical therapy
What palliative care do you consider?
o For people with end-stage COPD unresponsive to other medical therapy
o Opioids should be used as pain relief
o Use benzodiazepines, tricyclic antidepressants, major tranquillisers and oxygen to treat breathlessness
When do you use short-acting b-agonist?
e.g. salbutamol, turbutaline – as needed, mild COPD
Example and when do you use Short-acting muscarinic antagonist?
e.g. ipratropium – as needed
Example and when do you use Long-acting beta agonist?
e.g. salmeterol, formoterol – more severe COPD, maintenance therapy
Example and when do you use Long-acting muscarinic antagonist?
e.g. tiotropium – equally as effective as LABA
When do you use Inhaled corticosteroids?
– if LABA/LAMA insufficient in severe COPD
When do you give antibiotics?
acute exacerbations and sometimes long-term
When do you give oral corticosteroids?
to decrease acute exacerbations in moderate to severe COPD
When do we use theophylline?
use not encouraged; used only when corticosteroids and other medication have not helped
When do you use mucolytics? How are they administered?
e.g. carbocisteine – chronic productive cough
Oral
Acute Oxygen Therapy
o SaO2 aim 88-92%
o ABGs required to monitor changes to PaO2 and O2
o If PaO2 rises and PaCO2 drops then continue to give
o If pH drops and PaCO2 rises then consider non-invasive ventilation (NIV) instead – in hypercapnia patients lose their respiratory drive from low CO2 and so require hypoxia to keep them breathing
Describe LTOT
o At least 15 hours a day
o Given at night if arterial hypoxaemia worsens overnight
o Considered for patients with FEV1 <30% predicted, cyanosis, polycythaemia, peripheral oedema, raised JVP, sats <92% on air
o Ambulatory oxygen can also be given to those already o LTOT who want to use it outside the house
o Hypercapnic patients should be considered for long-term NIV
When do we consider short-burst oxygen therapy?
o Should be considered for patients not eligible for LTOT but who remain breathless after minimal exertion
How do we treat mild COPD?
Antimuscuarinic eg ipratropium or B2 agonist inhaled PRN
How do we treat moderate COPD?
Regular anticholinergic eg ipratropium or tiotropium or long acting B 2 agonist eg salmetrol + inhaled corticosteroid eg beclomethasone esp if FEV1 <50% and >2 exacerbations/yr eg seretide. May consider oral theophylline
How do we treat severe COPD?
Long acting B2 agonist + inhaled steroid + anticholinergic
Refer to specialist
Consider steroid trial or home nebs
How do we deal with pulmonary hypertension?
Assess need for long term O2 therapy
UK DoH guidelines suggest LTOT for:
1.) Clinically stable non smokers with PaO2 <7.3kPa despite max Rx
2.) If PaO2 7.3-8.0 AND pul HTN (eg RHV; loud S2) + cor pulmonale
3.) Terminally ill patients
Treat oedema with diuretics
What are the indications for surgery?
Recurrent pneumothoraces
Isolated bullous disease
Lung vol reducing surgery (selected pts)
How do we deal with an acute exacerbation of COPD?
Increasing cough, breathlessness, wheeze. Decr exercise capacity
Look for cause eg infection, pneumothorax
Controlled O2 therapy (start 24-48%; vary according to ABG. Aim for PaO2 >8.0kPa with prise in PaCO2 <1.5kPa
Nebulised bronchodilators – salbutamol 5mg/4hr and ipratropium 500mcg/6hr
Steroids – IV hydrocortisone (200mg) and oral prednisolone 30-40mg for 7-14d
Antibiotics – if evidence of infection – amoxicillin 500mg/8hr PO or clarithromycin or doxycycline
Physio to aid sputum expectoration
If no response – repeat nebs and consider IV aminophylline
If still no response, consider NIPPV if RR >30 or pH <7.35
Consider intubation and ventilation if pH <7.26 and PaCO2 is rising
Consider a resp stimulant drug eg doxapram 1.5-4mg/min IV. SE: agitation, confusion, tachycardia, nausea. In pt who not suitable for mechanical ventilation. Short term measure and rarely sued now NIPPV available.
Are symptoms common in <35yrs?
Uncommon
Is a chronic productive cough common or uncommon?
Common
White/clear/grey sputum
Is night time waking with SOB common or uncommon?
Uncommon
Is significant diurnal/day-to-day variation common or uncommon?
Uncommon
How do you differentiate between COPD and Asthma?
Asthma – does not usually coincide with COPD; no sputum; presents earlier; reversible airway obstruction
How do you differentiate between COPD and Bronchictasis?
Bronchiectasis – purulent sputum; presents earlier; absence of smoking Hx
How do you differentiate between COPD and congestive heart failure?
Congestive heart failure – no cough;
How do you differentiate between COPD and Pneumonia?
Pneumonia - acute; consolidation on CXR
What is the prognosis?
Five-year survival from diagnosis is 78% in men and 72% in women with clinically mild disease (defined as not requiring continuous drug therapy), but falls to 30% in men and 24% in women with severe disease defined as requiring oxygen or nebulised therapy.
What are the complications?
- Acute exacerbations/infections
- Respiratory failure
- Secondary polycythaemia – hypoxia stimulates erythropoietin increasing number of red blood cells
- Cor pulmonale – hypoxia leads to vasoconstriction of lulmonary vessels in order to improve ventilation-perfusion; leads to right-heart strain resulting in right-sided hypertrophy
- Pneumothorax – bullae; thin, brittle alveolar walls; prone to rupture
