Pathophysiology of Dyspnea


Dyspnea is actually a common form of uncomfortable sensation in breathing. It is actually a common symptom which is found in several respiratory diseases. 1 Thus, it is commonly found in patients with cardiopulmonary disorders. However, it should be noted that dyspnea is not often a problem to be complained until the FEV1 has decreased below about 60% of the predicted value. 2

To understand more about the etiology or the cause of dyspnea, we should understand clearly about the pathophysiology of dyspnea itself. Hence, in this opportunity, we are going to discuss about pathophysiology of dyspnea.



Dyspnea is a subjective experience of breathing discomfort which is felt qualitatively in varying intensity. This sensation might derive from interactions of several aspects including physiological, psychological, social, and environmental factors. 3


Sense of Respiratory Effort

Respiratory sensations are actually the consequences of interactions between efferent – motor neuron, afferent – sensory neuron, and integrating neuron which processed the information in central nervous system; in respiratory cases, brain. These interactions influence the sense of respiratory effort. 3

Sense of respiratory effort is related with the ratio of pressure generated by respiratory muscles (Pbreath) to the maximum pressure generating capacity of the muscles (Pimax). 1

Hence, we can conclude that the sense of respiratory effort will increase when respiratory muscles exert higher pressure, such as when there is an increased in elasticity, resistive or threshold load. Similar thing happens when the pressure generating capacity of the muscles is decreased such as in weakened muscles due to fatigue or when the muscles experience mechanical disadvantage in increased lung volume. 1


Interactions between Sensory, Motoric, and Integrating Center

It has been mentioned previously that respiratory sensations are actually caused by the interactions of both motoric and sensory neurons with its integration center. All of these aspects can influence respiratory sensations variably. Interactions between these aspects will be explained by the figure below. 3 [Figure 1]

Figure 1. Algorithm for the inputs in dyspnea production 3



Motor efferent

When muscles are weak or fatigued, neural output from the motor cortex will increase via a corollary discharge. Thus, the neural signal will be sent to sensory cortex simultaneously with the transfer of motor output to ventilator muscles. 3

Sensory afferent

Sensory afferent functions to transfer information from chemoreceptors, mechanoreceptors, J-receptors, pulmonary vascular receptors, and metaboreceptors to be analyzed in central nervous system. 3

  • Chemoreceptors

Both peripheral and central chemoreceptors 1 such as chemoreceptors in carotid bodies and medulla will be activated in hypoxemia, acute hypercapnia, and acidemia condition. Activations of chemoreceptor will increase ventilation and may lead to a sensation in which the body is hungry of air. 1,3,4

  • Mechanoreceptors

These receptors are stimulated by bronchospasm and leads to chest tightness. Mechanoreceptors are spread throughout the respiratory system and are in charged for giving respond to mechanical stimuli. 1,3

  • Metaboreceptors

Metaboreceptors are richly found in skeletal muscles. When there are changes in local biochemical milieu of tissue active during exercise, it will be activated and lead to breathing discomfort. 3

  • Other sensory receptors

J-receptors are sensitive to interstitial edema. Meanwhile, when there are acute changes in pulmonary artery pressure, pulmonary vascular receptors will be activated and thus, lead to further air hunger. Hyperinflation might also lead to increase work of breathing, inability to get a deep breath, and unsatisfying breath. 3

Furthermore, Manning HL and Mahler DA said that there are classifications of receptors based on its location, which are upper airway receptors, chest wall receptors, and lung receptors. 1,4

  • Upper airway receptors

Based on the experiment, upper airway receptors will make the subject has a tendency to decrease their breathlessness intensity when sitting by a fan or open window. Thus, we can conclude that in normal subjects, the intensity of dyspnea or breathlessness can also be influenced by the receptors which are the distribution of trigeminal nerve. 4

  • Chest wall receptors

Chest wall is innervated by neuron receptors. Thus, joints, tendons, and muscles of the chest might influence ventilation and affect breathlessness sensations. For example, it has been found that such mechanical stimuli as vibration in the parasternal intercostal muscles will decrease dyspnea in both normal and COPD patients. 4

  • Lung receptors

Receptors in the lung will transmit signal gotten from the lung to central nervous system. These receptors include pulmonary stretch receptors – mechanoreceptors, chemoreceptors, irritant receptors, C-fibers (unmyelinated nerve endings) which is located in the alveolar wall and blood vessels – in charge of detecting interstitial congestion. Furthermore, vagal receptors are also reported to influence dyspnea depending on the activated receptors. For example, vagal irritant receptors will increase breathlessness and induce chest tightness or constriction. 1,4

Integration: efferent-reafferent mismatch

Intensity of dyspnea may increase when there is mistmatch between the feed-forward message to the ventilator muscles and feedback from receptors which monitor ventilator pump responses. This discrepancy is specifically related to mechanical derangement of ventilator pump, such as in asthma or chronic obstructive pulmonary disease (COPD). 3

Other factors influencing dyspnea

There are several factors such as emotional or affective factors which may contribute to dyspnea. For example, fear and acute anxiety might cause the worsening of dyspnea by resulting hyperinflation, increased breathing effort, and sense of unsatisfying breath. This is due to the alteration of sensory data interpretation or by leading breathing patterns which increase the physiologic abnormalities in the respiratory system. 3


Mechanism of Dyspnea in Common Respiratory Diseases

Dyspnea is a common symptom arisen in respiratory diseases. Each respiratory disease has different mechanism in inducing dyspnea. Details about mechanism of dyspnea in correlation with common respiratory diseases can be seen in the tabel below. 3 [Tabel 1]

Tabel 1. Mechanism of Dyspnea in Common Diseases 3




Dyspnea is a respiratory symptom which is characterized by discomfort or difficulty in breathing. 1,4 Dyspnea is common to be found in cardiorespiratory disorders, for example: dyspnea due to pneumonia arisen by Measles infection. Pneumonia caused by Measles infection can cause dyspnea by: 3

  • Increasing the work of breathing
  • Increasing drive to breathe
  • Stimulation of chemoreceptors due to hypoxemia and acute hypercapnia
  • Stimulation of pulmonary receptors





  1. Manning HL, Mahler DA. Pathophysiology of dyspnea. Monaldi Arch Chest Dis. 2001; 56(4):325-30.
  2. Grippi MA, Elias JA, Fishman JA, et al. Fishman’s pulmonary diseases and disorders. 5th New York: McGraw-Hill Education; 2015: 620.
  3. Longo DL, Fauci AS. Harrison’s gastroenterology and hepatology. NewYork: The McGraw-Hill; 2010:47e1-5.
  4. Epstein FH. Mechanism of Disease. N Engl J Med. 1995; 333(23):1547-53.

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