Assessment and management of dyspnoea

The terms ‘dyspnoea’ or ‘breathlessness’ refer to an individual's subjective awareness of discomfort related to the act of breathing. Elevations in CO 2 above normal levels have been shown to cause breathlessness although it is unlikely to be the sole cause of breathlessness in a clinical setting. Several studies suggest that supplemental O 2 during exercise will diminish the sensation of breathlessness although not all work has confirmed this finding. Much about the role of gas exchange in dyspnogenesis remains controversial. Phrenic blockade can abolish dyspnoea in response to breath‐holding, while work in quadriplegics suggests that the intercostal muscles are not involved. A separate and direct pathway from the respiratory centre to the sensory cortex has also be implicated. Threshold discrimination has established that patients with chronic airflow limitation (CAL) have a blunted response to the addition of resistive loads to breathing, while category scaling methods (e.g. the Borg scale) have added descriptive terms to these physiological measures. Questionnaires often appear limited by their subjectivity and lack of correlation with physiological changes, but remain a useful tool in the clinical setting. In regard to therapy of dyspnoea high fat diets have a theoretical advantage in the CAL group but are generally not well tolerated. Resistive training devices and exercise training in CAL have been widely researched but in general, measures of lung remain unaltered and many of the studies would suggest that they have little, if any, inpact on functional status. Beta‐agonists have been widely shown to be useful in CAL patients, despite the fact that bronchodilatation is not always demonstrable. Anticholinergics have be shown to be effective bronchodilators, but whether there is an improvement in dyspnoea above that expected from improvement in lung function is unclear. Animal studies and work in normal individuals would suggest that methylxanthines have a theoretical role in CAL possibly by increasing diaphragmatic muscle strength and decaying fatigue, but toxicity and lack of clear benefit in this group suggest that they should not be used as monotherapy. There is little evidence to support the use of opioids in chronic CAL although their role in the acute dyspnoea of end‐stage CAL remains defined. The use of benzodiazepines has also been disappointing. Bullectomy remains widely accepted in clinical practice. New techniques such as ‘reduction surgery’ for diffuse emphysema are showing promise, although still in need of further testing and validation.