The pathophysiology of dyspnoea is poorly understood. Normal breathing is controlled by respiratory centres in the brain stem. The vagus nerve carries efferent and afferent components and provides the pathway for the neurological input resulting in the sensation of dyspnoea.

Intrapulmonary parenchymal stretch receptors, carotid body and central medullary chemoreceptors, peripheral vascular receptors and pulmonary artery baroreceptors all contribute to the pathways leading to dyspnoea. Input from these receptors is integrated in the cortical and subcortical respiratory centres.


Hypercapnia is well recognised as a cause of dyspnoea; however the relationship between hypercapnia and dyspnoea is not straightforward – patients with chronic hypercapnia (e.g. COPD, neuromuscular disease) may not be breathless at rest. This is because the mechanism is mediated by changes in pH measured in chemoreceptors which can be compensated (e.g. by retention of bicarbonate) in chronic disease.

There is uncertainty over the role of hypoxia as a cause for dyspnoea [1]. Few studies have evaluated the relationship between hypoxia and breathlessness; in one study, patients with COPD had improvement in their breathlessness when given oxygen [2]. Despite this, the relationship between dyspnoea and hypoxia is, as with hypercapnia, not straightforward – we all have seen patients who are relatively hypoxic and comfortable and also patients who are dyspnoeic but not hypoxic.


Afferent information from pulmonary baroreceptors is transmitted in the vagus nerve to the respiratory centres. Pulmonary stretch receptors, for example, are stimulated during lung inflation and provide feedback to terminate inspiration. Stimulation of pulmonary stretch receptors [3] and of mechanoreceptors in the chest wall [4], both of which provide afferent information to the respiratory centres, has been shown to influence the intensity of dyspnoea.

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