The main symptoms of COPD are breathlessness, cough and sputum production.15 Patients often attribute breathlessness to ageing or lack of fitness. A persistent cough, typically worse in the mornings with mucoid sputum, is common in smokers. Other symptoms such as chest tightness, wheezing and airway irritability are common.16 Acute exacerbations, usually infective, occur from time to time and may lead to a sharp deterioration in coping ability. Fatigue, poor appetite and weight loss are more common in advanced disease.

The functional limitation from breathlessness due to COPD can be quantified easily in clinical practice17 (see Box 4).

The sensitivity of physical examination for detecting mild to moderate COPD is poor.18 Wheezing is not an indicator of severity of disease and is often absent in stable, severe COPD. In more advanced disease, physical features commonly found are hyperinflation of the chest, reduced chest expansion, hyperresonance to percussion, soft breath sounds and a prolonged expiratory phase. Right heart failure may complicate severe disease.

During an acute exacerbation, tachypnoea, tachycardia, use of accessory muscles, tracheal tug and cyanosis are common.

The presence and severity of airflow limitation are impossible to determine by clinical signs.18 Objective measurements such as spirometry are strongly recommended. Peak expiratory flow (PEF) is not a sensitive measure of airway function in COPD patients, as it is effort dependent and has a wide range of normal values.19

Spirometry is the gold standard for diagnosing, assessing and monitoring COPD (see Box 5). Most spirometers provide predicted ("normal") values obtained from healthy population studies, and derived from formulas based on height, age, sex and ethnicity.

Airflow limitation is non-reversible when, after administration of bronchodilator medication, the ratio of FEV₁ to forced vital capacity (FVC) is < 70% and the FEV₁ is < 80% of the predicted value. The ratio of FEV₁ to vital capacity (VC) is a sensitive indicator for mild COPD.

Indications for spirometry include:

• breathlessness that seems inappropriate;

• chronic (daily for two months) or intermittent, unusual cough;

• frequent or unusual sputum production;

• relapsing acute infective bronchitis; and

• risk factors such as exposure to tobacco smoke, occupational dusts and chemicals, and a strong family history of COPD.

5: Maximal expiratory flow-volume curves in severe chronic obstructive pulmonary disease (COPD) and chronic asthma

The patient with COPD has reduced peak expiratory flow, and severely decreased flows at 25%, 50% and 75% of vital capacity compared with the normal range (vertical bars), and shows minimal response to bronchodilator (BD). By comparison, the patient with chronic asthma shows incomplete, but substantial, reversibility of expiratory flow limitation across the range of vital capacity. After BD the forced expiratory volume in one second (FEV₁ ) was within the normal range (82% predicted). Absolute and per cent predicted values for FEV₁ and forced vital capacity (FVC) before and after BD are shown for each patient.

Electronic spirometers allow for the simultaneous measurement of flow and volume during maximal expiration. Reduced expiratory flows at mid and low lung volumes are the earliest indicators of airflow limitation in COPD and may be abnormal even when FEV₁ is within the normal range (> 80%).

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.

Measurement of airways resistance, static lung volumes and diffusing capacity of lungs for carbon monoxide assists in the assessment of patients with more complex respiratory disorders.

Cardiopulmonary exercise tests may be useful to differentiate between breathlessness resulting from cardiac or respiratory disease, and may help to identify other causes of exercise limitation (eg, hyperventilation, musculoskeletal disorder).

Specialist referral is recommended for COPD patients suspected of having a coexistent sleep disorder or with hypercapnia or pulmonary hypertension in the absence of daytime hypoxaemia, right heart failure or polycythaemia. Overnight pulse oximetry may be indicated in patients receiving long-term domiciliary oxygen therapy to assess its efficacy.

A plain posteroanterior and lateral chest x-ray helps to exclude other conditions such as lung cancer. The chest x-ray is not sensitive in the diagnosis of COPD, and will not exclude a small carcinoma (< 1cm).

High resolution computed tomography (HRCT) scanning gives precise images of the lung parenchyma and mediastinal structures. The presence of emphysema and the size and number of bullae can be determined. This is necessary if bullectomy or lung reduction surgery is being contemplated. HRCT is also appropriate for detecting bronchiectasis. Vertical reconstructions can provide a virtual bronchogram.

Spiral computed tomography (CT) scans with intravenous contrast should be used in other circumstances, such as for investigating and staging lung cancer.

CT pulmonary angiograms are useful for investigating possible pulmonary embolism, especially when the chest x-ray is abnormal.

The ventilation and perfusion (V/Q) scan may be difficult to interpret in COPD patients, because regional lung ventilation may be compromised leading to matched defects. If pulmonary emboli are suspected, a CT pulmonary angiogram may be more useful. Quantitative regional V/Q scans are helpful in assessing whether patients are suitable for lung resection and lung volume reduction surgery.

Oximeters have an accuracy of plus or minus 2%, which is satisfactory for routine clinical purposes. Oximetry does not provide any information about carbon dioxide status and is inaccurate in the presence of poor peripheral circulation (eg, cold extremities, cardiac failure).

Arterial blood gas analysis should be considered in all patients with severe disease, those being considered for domiciliary oxygen therapy (eg, whose FEV₁ is < 40% predicted or < 1 L, whose oxygen saturation as measured by pulse oximetry [Spo₂ ] is < 92%), those with pulmonary hypertension, and those with breathlessness out of proportion to their clinical status). Respiratory failure is defined as a Pao₂ < 60 mmHg (8 kPa) or Paco2 > 50 mmHg (6.7 kPa).

Routine sputum culture in clinically stable patients with COPD is unhelpful and unnecessary. Sputum culture is recommended when an infection is not responding to antibiotic therapy or when a resistant organism is suspected.

Polycythaemia should be confirmed as being secondary to COPD by blood gas measurement confirming the presence of hypoxaemia. The possibility of sleep apnoea or hypoventilation should be considered if polycythaemia is present, but the oxygen saturation is normal when the patient is awake. Hyperthyroidism and acidosis are associated with breathlessness. Hyperventilation states are associated with respiratory alkalosis. Hypothyroidism aggravates obstructive sleep apnoea.

Multifocal atrial tachycardia is a frequent finding. Atrial fibrillation commonly develops when pulmonary artery pressure rises, leading to increased right atrial pressure.

Echocardiography is useful if cor pulmonale is suspected, when breathlessness is out of proportion to the degree of respiratory impairment or when ischaemic heart disease, pulmonary embolus and left heart failure are suspected.

Patients with COPD are prone to other conditions associated with cigarette smoking, including accelerated cardiovascular, cerebrovascular and peripheral vascular disease, and oropharyngeal, laryngeal and lung carcinoma. Conversely, there is a high prevalence of COPD among patients with ischaemic heart disease, peripheral vascular disease and cerebrovascular disease and smoking-related carcinomas.22 These patients should be screened for symptoms of COPD, and spirometry should be performed.

The two classes of inhaled bronchodilators — selective β-adrenoceptor agonists and anticholinergic agents — target airway smooth muscle contraction, which is one cause of the physiological and functional deficits in COPD.23-25

All bronchodilators have been shown to variably improve exercise capacity.26-29 However, changes in simple measurements of airway function (FEV₁ , FVC) are not closely correlated with symptomatic improvement or changes in measures of quality of life.30,31 The failure to achieve a large therapeutic response should not necessarily trigger the use of higher doses.23,24 Nebulisers are not recommended for routine use in stable disease32 [evidence level C].

The duration of action of short-acting inhaled anticholinergic agents is greater than that of short-acting β-agonists32 [evidence level A]. The combination of β-agonists and anticholinergics may be more effective and better tolerated than higher doses of either agent used alone32-37 [evidence level A].

The use of bronchodilators according to the severity of COPD6 is shown in Box 9. Appendices 1 and 2 list available products, formulations and delivery devices. Patients must be asked to show that they have effective inhaler technique.

Efforts to maintain or regain physical fitness may match or exceed the benefits of bronchodilator use (see the discussion of pulmonary rehabilitation on page S19).6 Use of a short-acting bronchodilator before an exercise session may reduce dynamic hyperinflation and allow better training effects to be achieved.26

Long-acting β-agonists (eg, salmeterol and eformoterol) provide bronchodilation for 12 hours38-41 and are widely used for asthma. They are not currently subsidised under the Pharmaceutical Benefits Scheme for patients with COPD, although they improve exercise endurance, improve health-related quality of life and reduce both the exacerbation rate and number of hospitalisations.

Salmeterol (50 μg twice daily) has a favourable effect on measures of health-related quality of life.41 The dose–response relationship is low, so, compared with the standard dose, the higher dose of 100 μg twice daily does not further improve quality of life41 [evidence level B].

Eformoterol (12 μg twice daily) improves lung function and symptoms.40

Tiotropium (18 μg daily), a new inhaled anticholinergic agent, has a duration of effect of over 24 hours and is used once daily. It is subsidised under the Pharmaceutical Benefits Scheme for use in patients with COPD. Compared with placebo and regular ipratropium, it reduces dyspnoea and exacerbation rate and improves health status42-44 (see Appendix 1).

Theophyllines are rarely used because of their narrow therapeutic index and potential for significant side effects45 [evidence level A]. Some patients with disabling breathlessness may derive benefit from their use.46-48 Theophyllines may have an anti-inflammatory effect or reduce muscle fatigue.49,50 Evidence supports only the slow-release formulation. Dosage should be adjusted according to trough serum levels.51

The long-term use of systemic glucocorticoids in COPD is not recommended52-56 [evidence level A]. Indeed, caution in the long term use of systemic glucocorticoids is necessary because of limited efficacy and potential toxicity in elderly patients.

Some patients with stable COPD show a significant response to oral glucocorticoids (on spirometry or functional assessment). Therefore, a short course (two weeks) of prednisolone (20–50 mg daily) may be tried with appropriate monitoring. A negative bronchodilator response does not predict a negative steroid response.6,57 If there is a response to oral steroids, continued treatment with inhaled glucocorticoids is indicated, but these may fail to maintain the response.57,58 Patients who have a negligible response to glucocorticoids should not use them.

Inhaled glucocorticoids do not influence the rate of decline in FEV₁ in patients with no significant acute reversibility.57-61 Smoking cessation remains the only effective means to affect the decline in lung function for these patients (see Section P).

Patients with clinically significant acute bronchodilator reversibility may benefit from long-term inhaled glucocorticoid therapy. Long term inhaled therapy with glucocorticoids is also indicated in patients with COPD who have significant reversibility of airway function after a more prolonged trial of bronchodilators or glucocorticoids.57-59

In one large RCT of patients with severe non-reversible COPD (mean FEV₁ about 40% predicted), high-dose inhaled glucocorticoid (fluticasone, 1000 μg daily) slowed the rate of decline in quality of life over three years and the rate of acute exacerbations without affecting overall decline in lung function.60 Similar results may be expected from high doses of other inhaled glucocorticoids, but are yet to be documented in RCTs. In another large RCT in patents with milder COPD, medium-dose budesonide had no significant impact.59 Some systemic absorption may occur, so the modest benefits of inhaled glucocorticoids must be weighed against the potential risks of easy bruising, cataract formation and possible contribution to osteoporosis.

The response should be assessed with spirometry and measures of performance status, quality of life or both. They should be trialled for three to six months in patients with moderate to severe COPD, and continued if there is objective benefit.

There is currently insufficient published evidence to determine the role of combination therapy with inhaled glucocorticoid and long-acting bronchodilators.

This operation involves resection of large bullae (larger than 5 cm). The procedure is most successful where there are very large cysts compressing adjacent apparently normal lung.63-65

Lung volume reduction surgery (LVRS) involves resection of the most severely affected areas of emphysematous, non-bullous lung.66 This can improve lung elastic recoil and diaphragmatic function.67 LVRS is still an experimental, palliative, surgical procedure. Several large randomised multicentre studies are under way to investigate the effectiveness and cost–benefit of this procedure.68

Surgery is performed electively after a pulmonary rehabilitation program, to remove about 25% of each lung. Physiological improvement (eg, a 40% improvement in FEV₁ from about 25% predicted to 35% predicted, and six-minute walk from about 300 to 420 metres) takes weeks to months. The duration of the improvement is 2–4 years. These gains should be weighed against risks of operative and postoperative mortality (around 5%–15%), morbidity and cost.68 However, the natural history of patients with COPD of this severity is a progressive decline in function and early mortality.

In patients with COPD, this procedure usually involves replacement of one diseased lung with a normal lung from an organ donor.69,70 Detailed medical and psychological assessment and counselling are required to avoid excessive morbidity and mortality. Malnutrition, severe weakness and steroid and ventilator dependence predict a poor outcome.71,72 The procedure is most successful when lung disease is the recipient's only medical problem and is usually offered to younger patients (eg, those with α₁-antitrypsin deficiency).

Physiological improvement takes weeks to months, and would typically translate to a large improvement in FEV₁ (from about 20% to 60% predicted for a single lung transplant), exercise performance and quality of life.69-72

COPD has adverse effects on sleep quality, resulting in poor sleep efficiency, delayed sleep onset, multiple wakenings with fragmentation of sleep architecture, and a high arousal index. Arousals are caused by hypoxia, hypercapnia, nocturnal cough and the pharmacological effects of methylxanthines and β-adrenergic agents.73 Intranasal oxygen administration has been shown to improve sleep architecture and efficiency, as well as oxygen saturation during sleep.74

Indications for full diagnostic polysomnography in patients with COPD include persistent snoring, witnessed apnoeas, choking episodes and excessive daytime sleepiness. In subjects with daytime hypercapnia, monitoring of nocturnal transcutaneous carbon dioxide levels should be considered to assess nocturnal hypoventilation. Patients with COPD with a stable wakeful Pao₂ of more than 55 mmHg (7.3 kPa) who have pulmonary hypertension, right heart failure or polycythaemia should also be studied. Overnight pulse oximetry is also useful in patients with COPD in whom long-term domiciliary oxygen therapy is indicated (stable Pao₂ < 55 mmHg, or 7.3 kPa) to determine an appropriate oxygen flow rate during sleep.

The overlap syndrome: The combination of COPD and obstructive sleep apnoea (OSA) is known as the "overlap syndrome". The prevalence of COPD in unselected patients with OSA is about 10%, while about 20% of patients with COPD also have OSA.75 Patients with COPD who also have OSA have a higher prevalence of pulmonary hypertension and right ventricular failure than those without OSA.75 There is frequently a history of excessive alcohol intake. While oxygen administration may diminish the degree of oxygen desaturation, it may increase the frequency and severity of hypoventilation and lead to carbon dioxide retention.

As in other patients with OSA, weight reduction, alcohol avoidance and improvement of nasal patency are useful in those with COPD. Nasal continuous positive airway pressure (CPAP) is the best method for maintaining patency of the upper airway and may obviate the need for nocturnal oxygen. If nasal CPAP is not effective, then nocturnal bilevel positive airway pressure ventilation should be considered, although the benefits of this in chronic stable COPD remain to be established. The role of other OSA treatments, such as mandibular advancement splinting, remains to be evaluated in the overlap syndrome.

In patients with COPD, hyperinflation, coughing and the increased negative intrathoracic pressures of inspiration may predispose to reflux, especially during recumbency and sleep. Microaspiration of oesophageal secretions (possibly including refluxed gastric content) is a risk, especially with coexistent snoring or OSA. Reflux and microaspiration exacerbate cough, bronchial inflammation and airway narrowing.

Diagnosis may be confirmed by 24-hour monitoring of oesophageal pH, modified barium swallow or gastroscopy. However, a therapeutic trial of therapy with H₂ -receptor antagonists or a proton-pump inhibitor may obviate the need for invasive investigations. Lifestyle changes, including stopping smoking, reduced intake of caffeine and alcohol, weight loss and exercise, will also help. Elevation of the head of the bed is also recommended.

Aspiration of food and liquid is common in COPD and may be the cause of recurrent exacerbations and complications, such as pneumonia and patchy pulmonary fibrosis.

Diagnosis is usually easy with an adequate history from patients and their partners or carers. Dry biscuits and thin fluids cause the most difficulty. Confirmation rests with assessment by a speech therapist and a modified barium swallow.

Treatment involves retraining in safe swallowing techniques, which may include:

• avoiding talking when eating;

• sitting upright;

• taking small mouthfuls;

• chewing adequately;

• drinking with dry foods;

• using a straw; and

• drinking thickened fluids.

Patients with COPD have impaired gas exchange and an exaggerated fall in Po₂ with recumbency and sleep onset.74,75 Excessive use of alcohol and sedatives exacerbates this and predisposes to sleep-disordered breathing.

Heavy cigarette smoking is associated with misuse of other substances in many individuals. Nicotine, caffeine and alcohol also predispose to gastro-oesophageal reflux.

Treat underlying lung disease: The logical first step is to optimise lung function and treat all potential aggravating conditions.

Oxygen therapy: Long term, continuous (> 15 h/day) oxygen therapy to treat chronic hypoxaemia prolongs survival of patients with COPD, presumably by reducing pulmonary hypertension.12,13,80-82 (For a detailed description of oxygen therapy in COPD see Section P, page S21).

Ventilatory support: For patients with COPD who also have sleep apnoea or hypoventilation, ventilatory support with continuous positive airway pressure (CPAP) or non-invasive positive pressure ventilation (NIPPV) may be more appropriate than oxygen therapy (for more details see Section X, page S29). The efficacy of NIPPV for long-term treatment has not yet been proven.74,83-85

Diuretics: Diuretics may reduce right ventricular filling pressure and oedema, but excessive volume depletion must be avoided. Volume status can be monitored by measuring serum creatinine and urea levels. Diuretics may cause metabolic alkalosis resulting in suppression of ventilatory drive.

Digoxin: Digoxin is not indicated in the treatment of cor pulmonale and may increase the risk of arrhythmia when hypoxaemia is present.6 It may be used to control the rate of atrial fibrillation.

Vasodilators: Vasodilators (hydralazine, nitrates, nifedipine, verapamil, diltiazem, angiotensin-converting enzyme [ACE] inhibitors) do not produce sustained relief of pulmonary hypertension in patients with COPD.86,87 They can worsen oxygenation (by increasing blood flow through poorly ventilated lung) and result in systemic hypotension. However, a cautious trial may be used in patients with severe or persistent pulmonary hypertension not responsive to oxygen therapy. Some vasodilators (eg, calcium antagonists) have been shown to reduce right ventricular pressure with minimal side effects and increased well-being, at least in the short term. Nitric oxide worsens V/Q mismatching and is therefore contraindicated in patients with COPD.86,87

Pulmonary rehabilitation is one of the most effective interventions in COPD89-93 and has been shown to reduce symptoms, disability and handicap and to improve functioning by:

• improving cardiovascular fitness, muscle function and exercise endurance;89,90,93-99

• enhancing the patient's self-confidence and coping strategies, and improving medication adherence and use of respiratory treatment devices;89-91,95,100-103

• improving mood by controlling anxiety and panic, decreasing depression, and reducing social impediments.89,90,104

Pulmonary rehabilitation should be offered to patients with moderate to severe COPD, but can be relevant for people with any long-term respiratory disorder characterised by dyspnoea.101,102 Exercise programs alone have clear benefits,103 while the benefits of education or psychosocial support without exercise training are less well documented.101,104-106 Comprehensive programs incorporating all three interventions have the greatest benefits (see below).

Most research has been undertaken with hospital-based programs, but there is increasing evidence of benefit from rehabilitation in the community.95,100

Numerous randomised controlled trials in moderate to severe COPD have shown decreased symptoms (breathlessness and fatigue) and improved cardiovascular fitness, exercise endurance, health-related quality of life and mood following exercise conditioning alone103 [evidence level A]. Improvements in muscle strength and self-efficacy have also been reported.89-100,103

The evidence for benefit from high-intensity training of the respiratory muscles is less convincing.101,103,104 Some very disabled patients are shown how to reduce unnecessary energy expenditure for activities of daily living.101 Some patients may benefit from portable oxygen (see section P, page S21).

Maintenance of activities is essential for continuing the benefits from the initial training program. Home- or community-based exercise should be encouraged6,105 [evidence level D].

There is limited evidence that education alone can improve self-management skills, mood and health-related quality of life105-107 [evidence level C]. Providing information and tools to enhance self-management in an interactive session is more effective than didactic teaching.105,108

The single most important intervention is assistance with smoking cessation.6 Good nutrition; task optimisation for more severely disabled patients; access to community resources; help with control of anxiety, panic or depression; instruction on effective use of medications and therapeutic devices (including oxygen where necessary); relationships; end-of-life issues; continence; safety for flying; and other issues may be addressed.6,101,102

Improved exercise tolerance, mood, self-efficacy and health-related quality of life have been reported from cognitive behavioural therapy alone102,105 [evidence level C]. Depression, anxiety and panic are frequent complications of chronic disabling breathlessness, with dependence and social isolation being common.109 General support, specific behavioural training and the use of appropriate antidepressant medications may enhance quality of life for the patient, and for the spouse or carer.

Comprehensive pulmonary rehabilitation,89-103,110-116 which includes all the components discussed above, enhances health-related quality of life and self-efficacy, improves exercise performance, and reduces breathlessness and healthcare use [evidence level A]. It is possible to provide these comprehensive programs in the community,95,100-102 as well as in larger hospitals.114

Lung support groups may provide patients and carers with emotional support, social interaction, and other social outlets, and help them gain new knowledge and coping strategies. More than 80 groups throughout Australia can be contacted via LungNet (toll-free phone number, 1800 654 301; Internet address, http://www.lungnet.com.au. In New Zealand, contact the Asthma and Respiratory Foundation of New Zealand (phone (04) 499 4592; Internet address, http://www.asthmanz.co.nz).

A systematic review in COPD and bronchiectasis showed a significant increase in sputum clearance with no change in lung function or health status117 [evidence level B].

The aims of chest physiotherapy are to assist sputum removal and improve ventilation without increasing the distress of the patient.117 Auscultation plus chest x-ray findings help determine the regions of the lung to be treated. Bronchodilator therapy before treatment may result in a more effective treatment. If patients are hypoxaemic (Spo₂ , < 88%), supplemental oxygen is given during treatment.

Various techniques and devices are available to aid sputum removal. The choice of technique depends on the volume of sputum, the patient's condition (eg, extent of airflow limitation, severity of breathlessness), patient preference and the cognitive status of the patient.

In patients with COPD, both excess and low weight are associated with increased morbidity. Excessive weight increases the work of breathing and predisposes to sleep apnoea — both central hypoventilation and upper-airway obstruction. Progressive weight loss (body mass index < 20) is an important prognostic factor for poor survival118,119 [evidence level A]. This may be the result of a relative catabolic state (related to high energy demands of increased work of breathing) added to disturbance of nutritional intake (related to breathlessness while eating). Deleterious consequences include combined protein–energy malnutrition,119 and possibly mineral or essential vitamin and antioxidant deficiencies.119

Randomised controlled trials of nutritional support in COPD have not shown significant improvements in nutrition, exercise capacity or other outcomes [evidence level B]. Patients with COPD should not eat large meals, as this can increase dyspnoea. Several small nutritious (high energy, high protein) meals are better tolerated. Snacks may provide a useful addition to energy and nutrient intake. Referral to a dietitian for individual advice may be beneficial.

A successful smoking cessation strategy involves integration of public policy, information dissemination programs and health education through the media and schools.6

Smoking prevention and cessation programs should be implemented and be made readily available6,120 [evidence level A].

Smoking cessation (see Box 3) has been shown to halt the accelerated decline in lung function seen with COPD6,7 [evidence level A]. People who continue to smoke despite having pulmonary disease are highly nicotine dependent and may require treatment with pharmacological agents to help them quit.121,122

Smoking cessation interventions have been shown to be effective in both sexes, in all racial and ethnic groups tested, and in pregnant women.6 International data show that smoking cessation strategies are cost effective, but with a 10-fold range in cost per life-year gained depending on the intensity of the program and the use of pharmacological therapies.6

Brief counselling is effective [evidence level A] and every smoker should be offered at least this intervention at every visit.6 Currently accepted best practice is summarised in the 5-A strategy: 6

• Ask and identify smokers.

• Advise smokers about the risks of smoking and benefits of quitting and discuss options.

• Assess the degree of nicotine dependence and motivation or readiness to quit.

• Assist cessation — this may include specific advice about pharmacological interventions or referral to a formal cessation program if available.

• Arrange follow-up to reinforce messages.

Cessation of smoking is a process rather than a single event, and smokers cycle through the stages of being not ready, unsure, ready, quitting and relapsing before achieving long-term success. The aim of initial intervention is to advance one stage in the cessation cycle. The most strenuous efforts should be made with those smokers ready to quit or quitting. Cessation rates increase with the amount of support and intervention, including practical counselling and social support arranged outside of treatment.