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Assess severity

C3. Assessing the severity of COPD

Spirometry is the most reproducible, standardised and objective way of measuring airflow limitation, and FEV1 is the variable most closely associated with prognosis.13 The grades of severity according to FEV1 and the likely symptoms and complications are shown in Box 6. However, it should be noted that patients with an FEV1 > 80% predicted, although within the normal range, may have airflow limitation (FEV1/FVC ratio < 70%).
 

Box 6. of chronic obstructive pulmonary disease (COPD)7
  COPD Severity
Factor Mild Moderate Severe
Spirometry findings - postbronchodilator FEV1%
 		 60-80% predicted 40-59% predicted <40% predicted
Functional assessment (Activities of daily living) Few symptoms
No effect on daily activities
Breathless on moderate exertion
 		 Increasing dyspnoea
Breathless on the flat
Increasing limitation of daily activities 		Dyspnoea on minimal exertion
Daily activities severely curtailed
Complications No  Exclude complications;
consider sleep apnoea if there is pulmonary hypertension		 Severe hypoxaemia (PaO2 <60mm Hg or 8kPa)
Hypercapnia (PaCO2 >45mm Hg or 6kPa)
Pulmonary hypertension
Heart Failure Polycythaemia
FEV1  = forced expiratory volume in one second. PaO2  = partial pressure of oxygen, arterial. PaCO2  = partial pressure of carbon dioxide, arterial.
 

C4. Assessing acute response to bronchodilators

The response to bronchodilators is determined to:

  • assign a level of severity of airflow obstruction (post-bronchodilator); and

  • help confirm or exclude asthma.

The details for this assessment are outlined in Box 7.

The change in FEV1 after an acute bronchodilator reversibility test indicates the degree of reversibility of airflow limitation. This is often expressed as a percentage of the baseline measurement (eg, 12% increase). An increase in FEV1 of more than 12% and 200 mL is greater than average day-to-day variability and is unlikely to occur by chance.29,30 However, this degree of reversibility is not diagnostic of asthma and is frequently seen in patients with COPD (eg, the FEV1 increases from 0.8 L to 1.0 L when the predicted value is, say, 3.5 L). The diagnosis of asthma relies on an appropriate history and complete, or at least substantial, reversibility of airflow limitation (see also below).
 

Box 7: Assessment of acute response to inhaled beta-agonist at diagnosis

Preparation
  • Patients should be clinically stable and free of respiratory infection.
  • Withhold inhaled short-acting bronchodilators in the previous six hours, long-acting beta-agonists in the previous 12 hours, or sustained-release theophyllines in the previous 24 hours.

Spirometry

  • Measure baseline spirometry (pre-bronchodilator). An FEV1 < 80% predicted and FEV1/FVC ratio < 0.70 shows airflow limitation.
  • Give the bronchodilator by metered dose inhaler (MDI) through a spacer device or by nebuliser.
  • Give short-acting beta-agonist, at a dose selected to be high on the dose–response curve (eg, 200–400 mcg salbutamol from MDI and spacer).
  • Repeat spirometry 15–30 minutes after bronchodilator is given and calculate responsiveness. 
FEV1 = forced expiratory flow in one second.
FVC = forced vital capacity.
 

C4.1 Confirm or exclude asthma

 
If airflow limitation is fully or substantially reversible, the patient should be treated as for asthma 
 

Asthma and COPD are usually easy to differentiate. Asthma usually runs a more variable course and dates back to a younger age. Atopy is more common and the smoking history is often relatively light (eg, less than 15 pack-years). Airflow limitation in asthma is substantially, if not completely, reversible, either spontaneously or in response to treatment. By contrast, COPD tends to be progressive, with a late onset of symptoms and a moderately heavy smoking history (usually >15 pack-years) and the airflow obstruction is not completely reversible.

However, there are some patients in whom it is difficult to distinguish between asthma and COPD as the primary cause of their chronic airflow limitation. Long-standing or poorly controlled asthma can lead to chronic, irreversible airway narrowing even in non-smokers, thought to be due to airway remodelling resulting from uncontrolled airway wall inflammation with release of cytokines and mediators.

Furthermore, asthma and COPD are both common conditions, and it must be expected that the two can coexist as least as often as the background prevalence of asthma in adults.

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