Dyspnea is a condition characterized by shortness of breath or difficult or labored breathing. The intensity of the condition varies from mild to severe, as does the number of episodes a person with dyspnea may experience. The condition can be extremely frightening for patients, though it is typically not life-threatening.
A number of different physiological path way may lead to shortness of breath including via chemoreceptors, mechanoreceptors, and lung receptors.
It is currently thought that there are three main components that contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed that the central processing in the brain compares the afferent and efferent signals, and that a "mismatch" results in the sensation of dyspnea. In other words, dyspnea may result when the need for ventilation (afferent signaling) is not being met by the physical breathing that is occurring (efferent signaling). Afferent signals are sensory neuronal signals that ascend to the brain. Afferent neurons significant in dyspnea arise from a large number of sources including the carotid bodies, medulla, lungs, and chest wall. Chemoreceptors in the carotid bodies and medulla supply information regarding the blood gas levels of O2, CO2 and H+. In the lungs, juxtacapillary (J) receptors are sensitive to pulmonary interstitial edema, while stretch receptors signal bronchoconstriction. Muscle spindles in the chest wall signal the stretch and tension of the respiratory muscles. Thus, poor ventilation leading to hypercapnia, left heart failure leading to interstitial edema (impairing gas exchange), asthma causing bronchoconstriction (limiting airflow) and muscle fatigue leading to ineffective respiratory muscle action could all contribute to a feeling of dyspnea.
Efferent signals are the motor neuronal signals descending to the respiratory muscles. The most important respiratory muscle is the diaphragm. Other respiratory muscles include the external and internal intercostal muscles, the abdominal muscles and the accessory breathing muscles.
As the brain receives its plentiful supply of afferent information relating to ventilation, it is able to compare it to the current level of respiration as determined by the efferent signals. If the level of respiration is inappropriate for the body's status then dyspnea might occur. It is worth noting that there is a psychological component of dyspnea as well, as some people may become aware of their breathing in such circumstances but not experience the distress typical of dyspnea.
What causes dyspnea and its pathophysiology
Dyspnea is caused by various factors. Mouth breathing and chest breathing are among the causes of dyspnea since they reduce brain oxygenation and create the sensation of air hunger. However, the main cause of dyspnea and low body oxygenation is obvious from this Table.
[Courtsey of http://www.normalbreathing.com]
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Chronic hyperventilation (or automatic deep breathing pattern) leads to alveolar hypocapnia (lack of CO2) which is normal in people with heart disease, asthma, COPD, cancer, cystic fibrosis, diabetes, pregnancy and many other conditions.
Healthy, normal breathing is imperceptible or unperceivable, since it is very small (500 ml for tidal volume, 10-12 breaths/min, and 6 L/min for minute ventilation at rest for a 70-kg person). In contrast, dyspneic patients have over 12 L/min (double the norm) for their ventilation rates and over 18 breaths/min for respiratory frequency at rest.
Hyperventilation leads to greatly increased work of breathing due to large minute ventilation rates. But there are other effects as well. For example, alveolar hyperventilation always leads to cell hypoxia (regardless of ventilation-perfusion ratio).
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| [Courtsey of http://www.normalbreathing.com] |
The main physiological factors (causes of dyspnea) that increase the work of breathing (often several fold) are:
- constriction of airways due to alveolar hypocapnia
- reduced oxygen tension in the diaphragm and chest muscles due to worsened oxygen transport
- tense states of the diaphragm and chest muscles due to arterial hypocapnia.
- reduced oxygen tension in the diaphragm and chest muscles due to worsened oxygen transport
- tense states of the diaphragm and chest muscles due to arterial hypocapnia.
Exacerbating causes in the pathophysiology of dyspnea are:
- mouth breathing (due to reduction in nitric oxide absorption and alveolar CO2)
- chest breathing (due to reduction in the arterial oxygenation)
- presence of inflammation and mucus in airways causing further narrowing or obstruction of air flow.
Exertion, exercise (with mouth breathing), meals (or eating and especially overeating), overheating, stress, anxiety, attempts to breathe deeply, deep breathing exercises, night sleep and being in the horizontal position (especially supine sleep), poor posture, pregnancy and many other factors are all known causes of hyperventilation. Therefore, they also worsen breathlessness.
- mouth breathing (due to reduction in nitric oxide absorption and alveolar CO2)
- chest breathing (due to reduction in the arterial oxygenation)
- presence of inflammation and mucus in airways causing further narrowing or obstruction of air flow.
Exertion, exercise (with mouth breathing), meals (or eating and especially overeating), overheating, stress, anxiety, attempts to breathe deeply, deep breathing exercises, night sleep and being in the horizontal position (especially supine sleep), poor posture, pregnancy and many other factors are all known causes of hyperventilation. Therefore, they also worsen breathlessness.
For example, physical exertion, due to anaerobic cell respiration at rest and elevated resting blood lactate, worsens gas exchange and causes overbreathing. This leads to acute exertional dyspnea. Acute dyspnea leads to even heavier breathing due to a negative feedback in breathing control caused by a prominent oxygen drive (hunger for air), instead of normal CO2-based regulation of respiration. Respiratory receptors located in the brain sense low brain oxygenation creating the sensation of air hunger and trying to increase ventilation.
