O7. Aggravating factors

O7.1 Aspiration

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/ pathologist and videofluoroscopy.

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.

O7.2 Gastro-oesophageal reflux

In patients with COPD, hyperinflation, coughing and the increased negative intrathoracic pressures of inspiration may predispose to reflux, especially during recumbency and sleep. A cross-sectional questionnaire-based study found an increased rate of gastro-oesophageal reflux was associated with increased COPD exacerbations¹¹² but this finding has not been addressed prospectively. 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, limiting food intake within 4 hours of bed-time, reduced intake of caffeine and alcohol, weight loss and exercise, will also help. Elevation of the head of the bed is also recommended.

O7.3 Alcohol and sedatives

Patients with COPD have impaired gas exchange and an exaggerated fall in PO₂ with recumbency and sleep onset.^113,114 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.

O7.4 Sleep related breathing disorders

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 beta-adrenergic agents.¹¹⁵ Intranasal oxygen administration has been shown to improve sleep architecture and efficiency, as well as oxygen saturation during sleep.¹¹³

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.¹¹⁴  Patients with COPD who also have OSA have a higher prevalence of pulmonary hypertension and right ventricular failure than those without OSA.¹¹⁴ 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.