Neural tracts of dyspnea

 The sensation appears to have two primary peripheral sensors—chemoreceptors and vagal C fibers; the chemoreceptors probably include the aortic and carotid bodies and/or vagal C fibers. Additional afferent information is provided by chest wall mechanoreceptors and vagal stretch receptors. 

Afferent neural information is conveyed to the NTS in the medulla and from there, probably via the thalamus, to the insular cortex and limbic system, especially the anterior insula, and the sensorimotor cortex. 

Thus, it can be speculated that dyspnea occurs when there is an increase above usual levels of reflex afferent information from the peripheral sensors, which is processed in the insula and cortical network and generates a neural output to the respiratory system; afferent feedback on the effects of this neural output (pulmonary volume change, airflow, and ventilation), is provided by the pulmonary stretch and other receptors innervated by the vagal nerves and by chest wall mechanoreceptors. 

If central neural output does not produce the expected result (airflow or ventilation), either because of muscle paralysis or abnormal lung mechanics (eg, in COPD, asthma or restrictive lung disease), a sensation of dyspnea is generated. 

In asthma and COPD the relationship between inspiratory neural drive and ventilatory output, and therefore dyspnea, may worsen (increased functional residual capacity) on exercise and improves with bronchodilation.

 This assumes that the cortical centers have a pre-existing memory of “normal” afferent input and “normal” respiratory system response, in terms of effort required to achieve a given airflow or ventilation. 

The extent of the mismatch between the new afferent/efferent information and preexisting memory, (“a change in the relationship between central respiratory drive and output, ie, ventilation or effort”) determines the intensity of dyspnea.