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Focus on Chronic obstructive pulmonary disease

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VOL: 98, ISSUE: 35, PAGE NO: 41

JUDITH McALLISTER, MA, RN, Respiratory Specialist Nurse, North Peterborough Primary Care Trust; Regional Trainer, Asthma and COPD, National Respiratory Training Centre, Warwick

Sponsored by Pfizer.


Chronic obstructive pulmonary disease (COPD) is a common condition predominantly caused by smoking. Most nurses will have cared for COPD patients at some point in their nursing career. The British Thoracic Society in its recent report into lung disease in Britain (BTS, 2001) estimates that COPD is responsible for a quarter of medical admissions to district general hospitals and that it is the 6th most common cause of death in England and Wales, accounting for 20% of respiratory mortality (Office for National Statistics, 2000).

Estimates of prevalence suggest that 6% of men and 4% of women over the age of 45 suffer from COPD, much of it undiagnosed (Renwick and Connolly, 1996). A more recent study in general practice by Dickinson et al. (1999) found a prevalence rate of 9.9% among 60 to 75- year-olds. Ten-year survival rate from the point of diagnosis is approximately 50% (Ferguson and Cherniack, 1993), while an audit from general practice undertaken before the publication of the COPD guidelines (BTS, 1997) suggested that more than a third of patients aged over 40 labelled as ‘asthmatic’ may really have COPD (Boehringer Ingleheim, 1994).

There is currently no national service framework for respiratory disease and no prospect of such a framework in the foreseeable future (Partridge, 2002). Consequently, despite its high prevalence, mortality and morbidity levels, COPD management is rarely viewed as a priority in healthcare and patients are all too often under-treated or ignored.

The disease process and anatomy and physiology

COPD is not a single disease entity. A number of different disease processes are involved, all of which lead to irreversible airflow obstruction, characterised by a reduced forced expiratory volume in one second (FEV1) and a reduced ratio of FEV1 to forced vital capacity (FVC) that changes little over time. It is slowly progressive, with little respite from symptoms, particularly shortness of breath on exertion, but also wheeze and cough (BTS, 1997).

Three different disease processes are involved: chronic bronchitis, emphysema and, in some cases, asthma, although they often overlap (Fig 1). While it is rarely possible to identify which disease process (or processes) are involved in the individual patient, it is helpful to have some understanding of the underlying pathophysiology, as treatment may differ, particularly if there is an asthmatic element present.

Chronic bronchitis

The increased sputum production that characterises chronic bronchitis results from an increase in the size and number of goblet cells in the bronchi and bronchioles and enlargement of sub-mucosal glands in the bronchi (Jeffery, 2001). While chronic bronchitis is often regarded as being synonymous with COPD, it is important to remember that while most smokers have evidence of increased sputum production, not all smokers develop the irreversible airflow obstruction that characterises COPD: only 15 % of smokers will develop COPD (Fletcher and Peto, 1977).

In the majority of smokers, smoking cessation leads to resolution of increased sputum production and ‘early morning cough’. In those smokers who develop COPD, mucus hypersecretion is accompanied by inflammatory changes, which lead to scarring, fibrosis, narrowing and distortion of the small peripheral airway. Extensive damage can occur in these airways before symptoms arise (Sandford et al., 1997).


Emphysema affects the parenchyma of the lung through destruction of the alveolar walls, leading to permanent enlargement of air spaces distal to the terminal bronchioles (Sandford et al., 1997) (Fig 2). The exact causative mechanism has not been identified, but it is thought that an imbalance occurs in favour of destructive (proteolytic) enzymes in the lungs, normally kept in check by restorative (antiproteolytic) enzymes (Barnes, 2000). Destruction of the alveolar walls increases narrowing in the small airways by loosening the attachments that help keep these airways open. During normal inspiration, the diaphragm moves downwards while the rib cage moves outwards, and air is drawn into the lungs by the negative pressure that is created. As the rib cage and diaphragm relax (expiration) the elastic recoil of the lung parenchyma (alveolar driving pressure) pushes air upwards and outwards. Destruction of the lung parenchyma and loss of alveolar attachments reduces alveolar driving pressure, leading to small airway collapse and air-trapping, with consequent hyperinflation of the lungs. Hyperinflation flattens the diaphragm, resulting in less efficient contraction, reduced alveolar driving pressure and more air-trapping (Fig 3).

While substantial alveolar surface area can be destroyed without noticeable symptoms, destruction of the alveolar walls eventually leads to disruption in the exchange of blood gases. The principal function of the lungs - gas exchange - cannot be efficiently maintained if there is either obstruction to the flow of air into the alveoli or insufficient alveolar surface for gas exchange, both of which occur in COPD. Eventually this leads to respiratory failure.

Think Point: Revise the anatomy and physi-ology of the respiratory system.


While asthma is commonly recognised as ‘reversible’ airflow obstruction, some people with asthma do develop irreversible obstruction, particularly if the asthma is untreated, either because it is unrecognised or incorrectly managed, or if it is particularly severe. Children with asthma have a one in 10 chance of developing irreversible disease (Rasmussen et al., 2002), while the risk for adult onset asthmatics is one in four (Ulrik and Lange, 1994). Studies from the early 1990s by Agertoft and Pedersen (1994) and Haahtela et al. (1991) in both adults and children clearly demonstrated how asthma can quickly lead to irreversible changes in lung function if it is not treated with appropriate anti-inflammatory therapy (inhaled corticosteroids).

The airway inflammation which underlies even the mildest asthma, can lead to remodelling of the airways through increased smooth muscle, disruption of surface epithelium, increased fibrotic tissue and collagen deposition and thickening of the basement membrane (Reed, 1999). While many older patients with a long history of asthma do develop fixed airflow obstruction, the asthmatic inflammation is ongoing and needs to be effectively treated.

Think Point: If you care for any older people who have had asthma most of their lives, think about how their treatment might have changed over the past 30 years. As inhaled steroids were developed only in the late 1970s, what might be the consequences of late access to anti-inflammatory treatment?

Risk factors for COPD

Fletcher and Peto (1977) identified smoking as the most significant cause of the airflow obstruction that characterises COPD. Their study highlighted the accelerated loss of lung function that some smokers develop (Fig 4). A smoking history of the equivalent of at least 20 pack years (20 cigarettes a day for 1 year = 1 pack year) is usual (BTS, 1997). There is a long time lag between exposure to smoking and presentation: only when a considerable amount of lung function is lost does the patient notice significant symptoms.

If the patient manages to stop smoking, the rate of lung function decline reverts to normal, although lost lung function is not regained. Although smoking causes 85-90% of COPD, some patients do not have a significant smoking history. Why only 15% of smokers and some non-or light smokers develop COPD is not well understood, but several other risk factors have been associated:

- Air pollution and occupational exposure

- Maternal and passive smoking

- Infections

- Social class

- Genetic risk.

Today, COPD is more common in men, reflecting smoking habits of the past 40 years, and presenting when they are in their 50s and 60s. The increased risk of COPD in these age groups reflects the cumulative effects of smoking and the decline in lung function with age. COPD in younger age groups is rare, and such patients should be referred to a respiratory physician, as they may have the rare inherited condition, alpha1 anti-trypsin deficiency, which causes 1% of cases of COPD (BTS, 1997).

Some occupations where workers are exposed to coal, silica and cotton, such as miners, textile workers and cement workers are associated with an increased risk of COPD, while exposure to cadmium, a heavy metal, has been recognised as a cause of emphysema since the 1950s (Burge, 1994). Generally, dust exposure is more hazardous than exposure to gas or fumes, but shipyard welders and caulkers also have an increased risk (Hendrick, 1996). Both authors note the confounding effect of smoking and suggest that occupational exposure may simply promote its destructive effects. Air pollution is frequently cited, particularly by the general public, as a cause of respiratory disease. While there is no firm evidence to link air pollution alone as a causative factor in COPD, increased exacerbation rates have been associated with increases in pollution levels, as has cardiovascular and respiratory mortality (Anderson et al., 1996, Atkinson et al., 2001).

Other risk factors relate to insults to the developing lung and to maintaining lung health. The respiratory system is not fully developed at birth: the airways are complete in number but increase their size until maximum growth is attained in the 3rd decade. Alveoli numbers are not complete at birth, however, and increase from birth, particularly in the first three years of life, until lung growth ends in early adult life (Stick, 2000). If developing lungs are damaged, maximum potential lung function may never be achieved, resulting in lung function levels that produce symptoms at an earlier age. Evidence from a review of health visitor records for men born in Hertfordshire between 1911 and 1930 showed lower levels of lung function in adult life among those who had bronchitis, pneumonia or whooping cough during infancy, and among those who had lower birth weights (Barker et al., 1991). Impaired lung growth in utero, possibly through maternal smoking and malnutrition, appears to have a long-term effect on lung function and structure (Stick, 2000).

High intakes of antioxidant vitamins (Dow et al., 1996) and increased fish consumption (Sharp et al., 1994) seem to preserve lung function in adults, although the effects on children are unknown. The association between lower socioeconomic grouping and COPD suggests that poor nutrition may play a role. Prescott and Vestbo (1999) suggest that such links are multifactorial, involving poor housing, poor diet, exposure to passive smoking, increased lower respiratory tract infections in childhood, manual occupation and active smoking.

Think Point: How might the different risk factors interrelate? Think about a patient you have known with COPD and how these factors related to them.

Think Point: Why might a patient who is just beginning to develop symptoms of COPD be reluctant to seek help?

Signs and symptoms

Symptoms in COPD increase with severity of airflow obstruction. COPD is classified as mild, moderate or severe depending on the level of FEV1 compared to what would be expected for a person of a similar age, sex, height and race (Fig 5).

Fig 5. Classification of COPD (BTS, 1997)

Mild: FEV1 60-80% predicted

Moderate: FEV1 40-59% predicted

Severe: FEV1<40% predicted

Most patients complain initially of increasing breathlessness on exertion. While airflow obstruction is mild this may be the only symptom, and examination of the chest and measurements of peak flow may be normal. Typically, patients with mild disease complain of getting more breathless than they used to going upstairs, walking uphill or walking quickly. Many patients associate such breathlessness with age, and the associated ‘smoker’s cough’ as a natural consequence of smoking. These patients have few contacts with general practice, except perhaps during winter when they may present with a ‘chest infection’. They will be able to carry out all their normal activities and may be unaware of their worsening lung function.

Moderate COPD is associated with an increased range of symptoms, as lung function is now approaching half of normal. Exertional activities will make these patients breathless, and possibly wheezy, while cough with or without sputum production will be a normal part of everyday life. Regular winter visits to the doctor will be needed for ‘chest infections’. Some patients may have abnormal blood gases at this stage, although this is highly unlikely to be identified unless the patient is unwell enough to be admitted to hospital. These patients are a target group for proactive intervention.

Patients with severe COPD are familiar to nurses in secondary care. As the disease progresses, these patients are breathless on even the slightest exertion until finally they become breathless at rest. Hyperinflation of the lungs is very common, and a barrel shaped chest with an increased anterior-posterior chest diameter can be seen. Respiratory rate is increased to more than 16 per minute, even at rest, and use of accessory muscles, particularly the sternomastoids can be seen. Patients often develop ‘pursed lip’ breathing during expiration: this is thought to reduce small airway collapse by controlling the outflow of air. Cardiovascular involvement is common at this stage, with pitting oedema and an elevated venous jugular pressure suggesting the presence of pulmonary hypertension.

Pulmonary capillaries become narrowed in the presence of chronic low oxygen levels. This leads to increases in pulmonary pressures and to the eventual development of right ventricular hypertrophy and right ventricular failure. However, oedema in COPD may not be cardiac in origin: it has been suggested by Palange (1998) that hypercapnia and possibly hypoxaemia induce renal and hormonal abnormalities that lead to the development of oedema.

Blood gas abnormalities will be present before cyanosis is noticeable. Some patients are able to compensate for falling oxygen levels by increasing their breathing rate; these patients are very breathless but pink, as they manage to maintain oxygen levels until very late in the disease process. Others are unable to keep increasing their breathing rate, and begin to tolerate high levels of carbon dioxide, relying on low levels of oxygen to maintain their respiratory drive. These patients are less breathless but may be blue.

Patients who are hypoxic and have severely reduced FEV1 may fit the criteria for long-term oxygen therapy. Great care needs to be taken with these patients, as increasing their oxygen level with supplemental oxygen can stop their respiratory drive completely.

Exacerbations of the underlying disease cause frequent admissions to hospital, and when at home patients may be almost completely housebound. Weight loss is common, as is sleep disturbance and, unsurprisingly, a high level of depression and anxiety has been noted among these patients (Van Manen et al., 2002).

Think Point: Think of a patient you have nursed who has severe COPD. What do you recollect about his/her symptoms and care? How much support did the patient need?


COPD is a common condition that affects a substantial proportion of the population. Late presentation is common, as symptoms do not appear until patients have lost almost half their lung function. Patients with severe disease are frequently admitted to hospital, while those with mild disease have few contacts with healthcare professionals. As the disease progresses, symptoms increase, so that eventually breathlessness is present even at rest. Smoking is the main cause of COPD, although why only some 15- 20 % of smokers are affected is not well understood.

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