C1. Aetiology and natural history
Cigarette smoking is the most
important cause of COPD.8,9 There is
a close relationship between the
amount of tobacco smoked and the
rate of decline in forced expiratory
flow in one second (FEV1 ), although
individuals vary greatly in
susceptibility.8 Around half of all
smokers develop some airflow
limitation, and 15%–20% will develop
clinically significant disability.8
Smokers are also at risk of
developing lung cancer, and
cardiovascular disease such as ischaemic heart disease and
peripheral vascular disease.
In susceptible smokers cigarette
smoking results in a steady decline
in lung function, with a decrease in
FEV1 of 25–100 mL/year.8
While smoking cessation may lead to
minimal improvements in lung
function, more importantly it will
slow the rate of decline in lung
function and delay the onset of
disablement. At all times smoking
cessation is important to preserve
remaining lung function.8
Impairment increases as the
disease progresses, but may not be
recognised because of the slow pace
of the disease. The time course of
development of COPD and disability
and the influence of smoking
cessation are illustrated in
Box 3.
In addition to cigarette smoking, there are a number of other recognised
risk factors for COPD10 (see
Figure 3-1 below adapted from GOLD
2006). COPD almost always arises from a gene environment interaction. The
best characterised genetic predisposition is alpha1 antitrypsin
deficiency, but multiple other genes each make a small contribution and
further investigation is required. The risk of COPD is related to the total
burden of inhaled particles10 and oxidative stress in the lung.
Occupational dust exposure might be responsible for 20 – 30% of COPD. This
has long been recognised in underground miners, but recently biological dust
has also been identified as a risk factor, particularly in women.11
Fortunately the air quality in most Australian cities is relatively good and
cooking with biomass fuels (wood, dung etc) is uncommon. Failure to achieve
maximum lung function increases the risk of COPD in later life. The role of
gender is uncertain. Beyond the age of 45-50 years, female smokers appear to
experience an accelerated decline in FEV1 compared with male
smokers12 [evidence level II]. Nor is it known whether the increased risk among lower
socioeconomic groups is due to greater exposure to pollution, poorer
nutrition, more respiratory infection or other factors.10
Although FEV1 has long been accepted as the single best
predictor of mortality in population studies in COPD8,13
recent studies have suggested various other indices, which may also predict
mortality. In patients with established COPD, degree of hyperinflation as
measured by inspiratory capacity/ total lung capacity (IC/TLC) ratio was
independently associated with all cause and COPD mortality.14
The 6 minute walk distance (6MWD), peak VO2 during a
cardiopulmonary exercise test, body mass index and dyspnoea score (measured
with the modified Medical Research Council Scale) have all been shown to
predict mortality better than FEV1 in patients with established
disease. Several of these latter indices incorporated together in a single
score, the BODE index (BMI, degree of Obstruction as measured by FEV1,
Dyspnoea score and Exercise capacity measured by 6 minute walk) strongly
predicted mortality15.The single
best predictor of mortality in COPD is FEV1. In one study the five-year
survival rate was only about 10% for those with an FEV1 <20% predicted, 30%
for those with FEV1 of 20%–29% predicted and about 50% for those with an
FEV1 of 30%–39% predicted.
Continued smoking and airway hyperresponsiveness are associated
with accelerated loss of lung
function.16 However, even if
substantial airflow limitation is
present, cessation of smoking may
result in some improvement in lung
function and will slow progression
of disease.16,17
The development of hypoxaemic
respiratory failure is an
independent predictor of mortality,
with a three-year survival of about
40%.18
Long term administration of oxygen
increases survival to about 50% with
nocturnal oxygen18 and to
about 60% with oxygen administration
for more than 15 hours a day19
(see
also section P).
Admission to hospital with an
infective exacerbation of COPD
complicated by hypercapnic
respiratory failure is associated
with a poor prognosis. A mortality
of 11% during admission and 49% at
two years has been reported in
patients with a partial pressure of
carbon dioxide (PCO2) > 50 mmHg.20
For those with chronic carbon
dioxide retention (about 25% of
those admitted with hypercapnic
exacerbations), the five-year
survival was only 11%.20
Patients with an FEV1
<20% predicted and either
homogeneous emphysema on HRCT or a
DLCO <20% predicted are at high risk
for death after LVRS and unlikely to
benefit from the intervention.21
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