DYSPNEA

DYSPNEA

The American Thoracic Society defines dyspnea as a “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors and may induce secondary physiological and behavioural responses.” Dyspnea, a symptom, must be distinguished from the signs of increased work of breathing.

MECHANISMS OF DYSPNEA

Respiratory sensations are the consequence of interactions between the efferent, or outgoing, motor output from the brain to the ventilatory muscles (feed-forward) and the afferent, or incoming, sensory input from receptors throughout the body (feedback), as well as the integrative processing of this information that we infer must be occurring in the brain. In contrast to painful sensations, which can often be attributed to the stimulation of a single nerve ending, dyspnea sensations are more commonly viewed as holistic, more akin to hunger or thirst. A given disease state may lead to dyspnea by one or more mechanisms, some of which may be operative under some circumstances, e.g., exercise, but not others, e.g., a change in position. 

Motor efferents

Disorders of the ventilatory pump, most commonly increase airway resistance or stiffness (decreased compliance) of the respiratory system, are associated with increased work of breathing or a sense of an increased effort to breathe. When the muscles are weak or fatigued, greater effort is required, even though the mechanics of the system are normal. The increased neural output from the motor cortex is sensed via a corollary discharge, a neural Hypothetical model for the integration of sensory inputs in the production of dyspnea. Afferent information from the receptors throughout the respiratory system projects directly to the sensory cortex to contribute to primary qualitative sensory experiences and provide feedback on the action of the ventilatory pump. Afferents also project to the areas of the brain responsible for the control of ventilation. The motor cortex, responding to input from the control centres, sends neural messages to the ventilatory muscles and a corollary discharge to the sensory cortex (feed-forward with respect to the instructions sent to the muscles). If the feed-forward and feedback messages do not match, an error signal is generated and the intensity of dyspnea increases. Signal that is sent to the sensory cortex at the same time that motor output is directed to the ventilatory muscles.

Sensory afferents

Chemoreceptors in the carotid bodies and medulla are activated by hypoxemia, acute hypercapnia, and acidemia. Stimulation of these receptors, as well as others that lead to an increase in ventilation, produces a sensation of air hunger. Mechanoreceptors in the lungs, when stimulate by bronchospasm, lead to a sensation of chest tightness. J-receptors, sensitive to interstitial oedema, and pulmonary vascular receptors, activated by acute changes in pulmonary artery pressure, appear to contribute to air hunger. Hyperinflation is associated with the sensation of increased work of breathing and an inability to get a deep breath or an unsatisfying breath. Metaboreceptors, located in skeletal muscle, are believed to be activated by changes in the local biochemical milieu of the tissue active during exercise and, when stimulated, contribute to breathing discomfort.

Integration: Efferent-reafferent mismatch A discrepancy or mismatch between the feed-forward message to the ventilatory muscles and the feedback from receptors that monitor the response of the ventilatory pump increases the intensity of dyspnea. This is particularly important when there is a mechanical derangement of the ventilatory pump, such as in asthma or chronic obstructive pulmonary disease (COPD).