The Physiology of Respiratory Sensations

The Dyspnea of Asthma: A Model of Multiple Sensations

To this point, we have discussed sensations that arise from or are modified by stimulation of the controller, from receptors in the lungs, and from dissociation between efferent and reafferent neural information. Table 8-1 summarizes some of the most common qualities of breathing discomfort, the disease states or conditions associated with them, and the hypothesized physiological origins of the sensations.

Many cardiopulmonary conditions are associated with several physiological derangements that can lead to multiple sensations and qualitatively distinct types of dyspnea. Attention to the ways that patients describe their respiratory discomfort can provide clues to the underlying physiological problems. Asthma provides an excellent example of the way in which the nature of the physiologic disturbance changes with the severity of the disease process and the associated respiratory symptoms change with the physiology⁸.

Asthma is a disease characterized by inflammation of airways. The inflammatory process leads to swelling or edema of the lining of the airways, increased production of mucus, infiltration of the walls of the airways by white blood cells, and the release of chemicals that cause contraction of smooth muscle surrounding the airways. The inflammatory process and the spasm of the airway muscle, termed bronchospasm, lead to increased airway resistance. Asthma is a type of obstructive lung disease.

In the mildest forms of asthma, or at the very beginning of an asthma attack, you may see bronchoconstriction with minimal, if any, change in airway resistance or lung function as measured by the forced vital capacity (FVC) and the forced expiratory volume in 1 second (FEV₁). At this point, patients complain of a sensation of chest tightness or constriction, presumably caused by stimulation of pulmonary receptors (possibly RARs and C fibers) from the bronchospasm. Clinicians who are unaware of the significance of chest tightness may think that these individuals are malingering (i.e., making up their symptoms) because the “objective” measures of lung function appear to be normal.

As the asthma progresses in severity, the inflammatory process becomes more evident, bronchospasm worsens, and airway resistance increases. The FEV₁ decreases. There is now a more evident problem with the ventilatory pump. The ventilatory muscles must work harder to generate sufficient negative intrathoracic pressure to overcome the resistance and produce flow. Efferent neural output from the controller increases. The person with the asthma attack now perceives a sensation of increased effort or work of breathing. As the FEV₁ decreases further, the sense of effort increases, although chest tightness continues to be present as well (Fig. 8-2).

With more severe asthma, as the FEV₁ decreases even farther, the patient may begin to report a sensation of air hunger, a type of dyspnea that appears to be associated with stimulation of the controller. Hyperventilation, evidence of stimulation of the controller, is typically seen in mild to moderate asthma. In these stages of asthma, increased levels of ventilation may result from afferent feedback from pulmonary receptors (RARs and C fibers) and from behavioral factors (discomfort and anxiety). In moderate to severe asthma, hypoxemia may also develop, typically from ventilation/perfusion mismatch, which further stimulates the respiratory controller.

In one patient, with the progress of a single respiratory problem, we see physiologic changes in the controller, pump, and gas exchanger, each of which contributes to the development of respiratory sensations that are perceived and reported as symptoms of the disease. With knowledge of the relationship between sensations and physiology (Fig. 8-3), the clinician can gain great insights from the patient’s story.

Static Figure 8-3 here

FIGURE 8-3 The physiological pathways of respiratory sensations. The figure summarizes the efferent and afferent pathways that are instrumental in the generation of respiratory sensations. The corollary discharge (see Fig. 8-1) is indicated by the path between the motor and sensory cortex. Output from the brainstem may also contribute to the sense of effort. Manning et al.¹⁴ state: "The sense of air hunger is believed to arise, in part, from increased respiratory activity within the brain stem, and the sensation of chest tightness probably results from stimulation of pulmonary receptors, which transmit information to the brain via the vagus nerve. Although afferent information from airway, lung, and chest-wall receptors most likely passes through the brain stem before reaching the sensory cortex, the dashed lines indicate uncertainty about whether some afferents bypass the brain stem and project directly to the sensory cortex." (Adapted from Manning HL, Schwartzstein RM: Pathophysiology of dyspnea. N Engl J Med 1995, 333:1548).