• Progressive disorder of airway obstruction with little or no reversibility
  • Usually patients have either COPD or asthma not both
  • Diagnosis of COPD is favoured by;
  • Age of onset >35
  • Smoking related
  • Chronic dyspnoea
  • Sputum production
  • No marked diurnal or day to day variation

 

  • Chronic bronchitis is defined clinically as having a productive cough on most days for 3 months of 2 successive years
  • Emphysema is a histological diagnosis with enlarged airspaces distal to the terminal bronchioles with destruction of the alveolar walls

 

Pink puffers

  • Have increased alveolar ventilation, a near normal PaO2 and a normal or low PaCO2
  • They are breathless but not cyanosed
  • They may progress to type I respiratory failure

Blue Bloaters

  • Have decreased alveolar ventilation with a low PaO2 and a high PaCO2
  • They are cyanosed but not breathless and may go on to develop cor pulmonale
  • Rely on hypoxic drive to maintain respiratory effort

 

Clinical features

  • Symptoms
    • Cough, sputum, dyspnoea, wheeze
  • Signs
    • Tachypnoea, use of accessory muscles of respiration, hyperinflation, decreased cricosternal distance (<3cm), decreased expansion, resonant or hyperresonant percussion note, quite breath sounds (over bullae), wheeze, cyanosis, cor pulmonale
  • Complications
    • Acute exacerbations
    • Polycythaemia
    • Respiratory failure
    • Cor pulmonale (raised JVP, oedema)
    • Pneumothorax (rupture of bullae)
    • Lung carcinoma

 

Tests

  • FBC – increased PCV
  • CXR – hyperinflation (greater than 6 anterior ribs seen above diaphragm in the midclavicular line), flat hemidiaphrams, large central pulmonary arteries, decreased vascular markings, bullae
  • ECG – RA and RV hypertrophy
  • ABG
  • Lung function – FEV1 <80% of predicted, FEV1/FVC <70%

 

Severity of COPD

  • Mild – FEV1 50-80% predicted
  • Moderate – FEV1 30-49% predicted
  • Severe – FEV1 <30% predicted

 

Treatment

  • Chronic stable
  • Non pharmacological
    • Stop smoking, exercise, treat poor nutrition or obesity, influenza and pneumococcal vaccination, pulmonary rehabilitation, palliative care
  • Pharmacological;
    • Mild – antimuscarinic e.g. ipratropium or ?2 agonist PRN
    • Moderate – regular ipratropium or long acting ?2 agonist plus inhaled steroid (Seretide provides these)
    • Severe – combination therapy with regular short acting ?2 agonist and anticholinergic. Refer to specialist, consider steroid trial, assess for home nebulisers
  • Mucolytics may help chronic productive cough
  • Treat any depression

 

Long term O2 therapy

  • An MRC trial showed that if a PaO2 was maintained > or equal to 8kPa for 15hr a day, 3yr survival improved by 50%
  • UK guidelines suggest LTOT showed be given for;
  • Clinically stable non-smokers with a PaO2 <7.3kPA despite maximum therapy (these values should be taken on 2 separate occasions 3wk apart
  • If PaO2 is 7.3-8 kPa and pulmonary hypertension

 

Management of acute exacerbation of COPD

  • History – ask about usually/recent treatments (home oxygen?), smoking, exercise capacity

 

DDX

  • Asthma
  • PE
  • URT obstruction
  • Pulmonary oedema
  • Anaphylaxis

 

Investigations

  • PEF
  • ABG
  • CXR – exclude pneumothorax and infection
  • FBC, U&Es, CRP
  • ECG
  • Blood cultures is pyrexial
  • Sputum culture

 

Management

  • Oxygen start at 24-28% vary according to ABG. Aim for a PaO2 >8kPA with a rise in PaCO2 <1.5kPa
  • Give nebulised bronchodilators – salbutamol 5mg/24hr and ipratropium 500?g/6hr
  • Steroids – IV hydrocortisone 200mg and oral prednisolone 30-40mg
  • Antibiotics if evidence of infection e.g. amoxicillin 500mg/8hr
  • Physiotherapy to aid sputum expectoration
  • If no response repeat nebulisers and considered IV aminophylline
  • If no response consider nasal intermittent positive pressure ventilation if RR >30 or pH <7.35
  • Consider intubation and ventilation if pH <7.26 and PaCO2 is rising
  • Consider a respiratory stimulant drug e.g. doxapram 1.5 – 4mg (SE agitation, confusion, tachycardia, nausea). Only for patients not suitable for mechanical ventilation – use short term

 

Prior to discharge

  • Liaise with GP regarding steroid reduction, home oxygen, smoking and pneumoccal and flu vaccinations

 

Surgery can be considered if;

  • Recurrent pneumothoracese
  • Isolated bullous disease
  • Lung volume reduction (selected patients only)

 

  • Air travel may be hazardous if PaO2 is <6.7kPa
 

One Response to COPD

  1. Chris Wigley says:

    Diagnosis should be primarily by spirometry if COPD is a possible cause of symptoms, but remember that about 20% of people with COPD have never smoked, so do not ignore this possibility.
    The theory of Blue bloaters ( or anyone with COPD) relying on “hypoxic drive” is one of those “medical myths” that is totally without any scientific proof. I am on LTOT and fly regularly but really have to watch my SaO2 as there is no sensation of any increased desire to breathe when O2 sats drop to 80% virtually all the desire to breath comes from the need to feel air moving (just dunk someone in a swimming poll and watch them panic NOW) and from increased CO2 levels FROM the LEVEL WE ARE ACCUSTOMED TO.
    But watch out for pH dropping too low! You might check out http://tinyurl.com/7sv4jf 1

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