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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
Currently selected section: Mechanical Loads and Sense of Effort
Chemoreceptors
Mechanoreceptors
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: Physiology of Dyspnea: Mechanical Loads and Sense of Effort
        

A detailed discussion of the physiology of dyspnea is not possible here (for more complete analysis see American Thoracic Society, 1999, and Manning and Schwartzstein, 1998). We will highlight the key features of the physiology that must be understood before embarking on research in this field.

Mechanical Loads and the Sense of Effort
Most patients with cardiopulmonary disease and respiratory distress have an increased load on the ventilatory muscles; that is, there is increased stiffness (decreased compliance) of the lungs or chest wall, or increased resistance (airway obstruction). In these circumstances, the ventilatory muscles must work harder compared to the unloaded state to attain the same tidal volume or minute ventilation.

To achieve the increased power output from the ventilatory muscles, the efferent output from the motor cortex to the muscles must increase. This change in neurological activity is perceived as a sense of "effort" or "work" of breathing. This perception is believed to arise from a "corollary discharge," a neurological discharge from the motor to the sensory cortex that occurs simultaneously with the efferent output to the ventilatory muscles (McCloskey, 1981). Muscle strength may alter the perception of respiratory effort. To generate a given tension in a weak muscle, a greater effort is required (Gandevia et al., 1981). Strengthening the diaphragm with an exercise program reduces the intensity of effort associated with a given inspiratory load (Redline et al., 1991). If the intensity of the inspiratory task is expressed as a fraction of the maximal output of the system, however; effort is the same before and after training (Redline et al., 1991).

When asked to rate the intensity of breathlessness and effort, normal subjects breathing at normal and increased lung volumes rated the two sensations in parallel fashion over a range of elastic loads (Killian et al., 1984). This led to the assertion that "breathlessness and effort are identical and are mediated by the same mechanism" (Killian et al., 1984). One might be skeptical of this claim based on the complexity of "breathlessness" as a generic term for the breathing discomfort seen in a wide range of pathophysiological conditions, some of which are not characterized by an increase in the mechanical load on the respiratory system, e.g. pulmonary embolism. In addition, one should consider the fact that the ventilatory muscles receive efferent messages from both the motor cortex (resulting in voluntary contractions) and from the respiratory centers in the brainstem (automatic or involuntary contractions).

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