The conscious awareness of the labored breathing or air hunger in conditions
other than heavy exercise.
Dyspnea is critical to understand because it is common to many of the pulmonary
diseases and is often the predominant and at times an overwhelming symptom which greatly
alters or effects the lifestyle of patients with lung disease.
Breathing is typically an unconscious activity and a common method to induce the
sensation of dyspnea is breathing Breath-holding.
Afferent Signals Involved
The symptom of dyspnea is one that relates to the entire control system of
respiration. In the biggest picture, dyspnea can be related to difficulty getting
mitochondria to undergo oxidative phosphorylation. Both the adequate delivery of oxygen
and adequate removal of carbon dioxide relate to the absence or development of dyspnea.
Both of these chemical drives to breathe may directly and proportionally increase dyspnea.
Mechanoreceptors of the Respiratory Muscles and Chest Wall
These receptors (particularly the muscle spindles) are fairly well known and understood to
- Chest and wall receptors
As a group, these are inversely related to dyspnea. Ex. If the chest is allowed to undergo
respiratory movement (even with no gas exchange) or likewise with swallowing, the
sensation of dyspnea is reduced.
- Muscle spindles
More common in muscles of the rib cage. It is the muscle spindles that have been
recognized to mediate the "length-tension inappropriateness" theory of dyspnea.
In summary, muscle stimulation involves activation of both extrafusal fibers (main fibers)
as well as intrafusal muscle fibers. Under conditions of load on the respiratory muscles,
the inadequate or "inappropriate" shortening of the extrafusal fibers results in
stretching of the muscle spindle and spindle efferent discharge increases. This signal may
then be centrally processed into the sensation of dyspnea.
- Tendon organs
More common in the diaphragm, and act in general as load sensors within a muscle.
- Joint receptors
Provide the center with feedback regarding the movement of the thorax and relative to the
drive to move the thorax (breath) may relate to the development of dyspnea.
- Irritant receptors
- Stretch receptors
Central Processing of these Signals
No simple single physiologic mechanism can account for the various clinical
situations in which dyspnea occurs. In addition, there is a widely varying degree of
dyspnea for similar degrees of lung or heart disease across individuals. It is felt that
both contextual and behavioral influences play an important role in the degree of dyspnea.
- Airway obstruction (Astma, COPD, Tracheal stenosis):
Increased airway resistance
- Diffuse interstitial fibrosis: Stiff lung
- Diffuse alveolar disease
- Acute Pneumonia
- Pulmonary hypertension (PE, Idiopathic, Heart disease,
- Diaphragmatic paralysis: Orthopnea
Anxiety state: Multiple sighs
The optimal therapy is to treat the cause. Often the cause is untreatable and in
that situation the following have been tried
- Breathing techniques which may include pursed-lip or diaphragmatic breathing
- Exercise training: The goal is not to alter the lung disease (usually
untreatable) but rather to maximize the individual's exercise tolerance
- Nutritional manipulations with reduced CO2 production
- Psychologic interventions
- Respiratory muscle training
- Sedative/Narcotic pharmacotherapy
- Supplemental Oxygen to reduce work of breathing