Skip to Content
Interactive Textbook on Clinical Symptom Research Logo


Home Button

Clinical Research on Dyspnea
Author Bios
What is Dyspnea?
What Provokes Dyspnea?
The Nature of Dyspnea
Language of Dyspnea
Clinical Application
Research Application
Variability in Sensations
Challenges in Study
Mechanical Loads and Sense of Effort
Chemoreceptors
Currently selected section: Mechanoreceptors
Currently selected section: Neuro-Mechanical Dissociation
Phase of Respiration and Dyspnea
Physiology of Dyspnea
Respiratory System
Cardiovascular System
Measuring Dyspnea
Scaling Issues
Qualitative Aspects
Reliability and Validity Overview
Reliability and Validity
Sensitivity and Specificity
Scales
Sensation vs. Perception vs. Symptom
Treating Dyspnea
Why Measure?
Cluster Analysis
Statistical vs. Clinical Significance
Standard Error of Measurement
Measuring Fatigue
Measuring Depression
Measuring Anxiety and Hyperventilation
Measuring Quality of Life
Conclusion

 

Chapter 23: Dyspnea: Neuro-Mechanical Dissociation
        

You Answered:

Selection AIntensified

Correct

Figure 12.1: Relationship between Dyspnea (Breathlessness) Score and Ventilation Index (V IND) Plotted for Ten Subjects
Graphic depiction of relation between dyspnea score and ventilation index, described in text.
Official Journal of the American Thoracic Society. © American Lung Association.
Reprinted with permission.

The data illustrated here are from a study in which normal subjects were made hypercapnic and their breathing was targeted at different levels of ventilation. Dyspnea intensity is plotted as a function of the ventilation index (the ratio of the targeted ventilation to that of the ventilation that would have resulted from the hypercapnia without targeting). Despite the fact that the chemical drive to breathe is constant throughout, that is, the stimulation of the chemoreceptors is constant, at levels of ventilation below that dictated by the chemical drive, the intensity of dyspnea increased. At levels of ventilation above the chemically determined ventilation, approximately half of the subjects had an increase in dyspnea while the remainder had a plateau in their ratings. Similar results were obtained by Chonan et al. (1990) and are compatible with the hypothesis that dissociation between the neural output to the ventilatory muscles and the mechanical consequences of muscle stimulation intensifies dyspnea. We believe the brain assesses this dissociation by monitoring the afferent feedback from mechanoreceptors throughout the respiratory system.

Back to Question