Dyspnea is a complex sensation that involves both objective and subjective elements. Unlike other noxious sensations, dyspnea does not have a defined neural pathway, and the perceived difficulty probably arises from several pathophysiologic mechanisms.2 The following processes are involved in the sensation of dyspnea:
1. A sense of voluntary skeletal muscular effort occurs with increased work of breathing. Muscle spindle receptors found in the muscles of respiration, as well as the associated Golgi tendon organ receptors, contribute to the sense of dyspnea when stimulated.
2. Hypercapnic chemoreceptors in the central medulla are stimulated.
3. Hypoxic chemoreceptors, primarily in the carotid body in concert with those in the aortic arch, are stimulated. However, there is a poor correlation between hypoxia and dyspnea, and dyspneic patients with hypoxia often have little improvement after correction of hypoxia.
4. Upper-airway mechanical and thermal receptors are stimulated.
5. A variety of lung receptors respond to various stimuli. They include intraparenchymal pulmonary stretch receptors, airway irritant receptors, and unmyelinated receptors that respond to interstitial edema or a change in compliance. Afferent signals from these receptors reach the brainstem by way of the vagus nerve and supply the majority of neurologic input that results in dyspnea.
6. Peripheral vascular receptors, including the right atrial and left atrial mechanoreceptor and the pulmonary artery baroreceptor, contribute to dyspnea in a poorly defined way.
Input from any or all of these receptors is integrated in a complex manner in the central nervous system (CNS) at both the subcortical and cortical level. Many authors believe that dyspnea results from afferent mismatch, when feedback from these peripheral receptors indicates that the work of breathing is greater than would be expected by the patient's level of activity.3
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