Breathlessness/Dyspnoea/Shortness of breath (SOB)/Air hunger

Definition: It can be defined as the feeling of an uncomfortable need to breath.

Or,

The American Thoracic Society defines dyspnea as: "A subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity."Other definitions describe it as "difficulty in breathing"," disordered or inadequate breathing", "uncomfortable awareness of breathing", and as the experience of "breathlessness" (which may be either acute or chronic). 
Dyspnea is distinct from labored breathing, which is a common physical presentation of respiratory distress.
Grading:

MRC Breathlessness Scale:

Grade Degree of dyspnea
0 no dyspnea except with strenuous exercise
1 dyspnea when walking up an incline or hurrying on the level
2 walks slower than most on the level, or stops after 15 minutes of walking on the level
3 stops after a few minutes of walking on the level
4 with minimal activity such as getting dressed, too dyspneic to leave the house

Pathophysiology: Physiological pathways may lead to shortness of breath including via chemoreceptors, mechanoreceptors, and lung receptors. It is thought that three main components contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed the central processing in the brain compares the afferent and efferent signals; and dyspnea results when a "mismatch" occurs between the two: such as when the need for ventilation (afferent signaling) is not being met by physical breathing (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. There is also a psychological component to dyspnea, as some people may become aware of their breathing in such circumstances but not experience the distress typical of dyspnea.

Causes:
[A]Cardiovascular:

1. Acute dysponea:
• Acute pulmonary oedema.
• Myocardial ischaemia(angina equivalent)
2. Chronic exertional dyspnoea:
• Chronic heart failure.
• Myocardial ischaemia(angina equivalent)
[B]Respiratory cause:

1. Acute dysponea at rest:
• Acute severe asthma.
• Acute exacerbation of COPD.
• Pneumothorax.
• Pneumonia.
• Pulmonary embolism.
• ARDS(acute respiratory distress syndrome)
• Lobar collapse.
• Laryngeal oedema(e.g anaphylaxis)

2. Chronic exertional dysponea:
• COPD.
• Chronic asthma.
• Bronchial carainoma.
• Interstitial lung disease: e.g. Sarcoidosis.
• Chronic pulmonary thromboembolism.
• Lymphatic carcinomatosis.
• Large pleural effusion.

[C]Others cause:

1. Acute:
• Metabolic acidosis (e.g. diabetic ketoacidosis, lactic acidosis, uraemia, overdose of salicylates).
• Psychogenic hyperventilation(anxiety/panic related)
2. Chronic: Sever anaemia, obesity.
Differential diagnosis:

1. Acute coronary syndrome
2. Congestive heart failure
3. Chronic obstructive pulmonary disease
4. Asthma
5. Pneumothorax
6. Pneumonia
7. Pulmonary embolism
8. Anaemia
Treatment: In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause. Extra oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations, even in those who are palliative. 
Physiotherapy: Individuals can benefit from a variety of physical therapy interventions. Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation. Some physical therapy interventions for this population include active assisted cough techniques, volume augmentation such as breath stacking, education about body position and ventilation patterns and movement strategies to facilitate breathing. 
Palliative: Along with the measure above, systemic immediate release opioids are beneficial in reducing the symptom of shortness of breath due to both cancer and non cancer causes. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy. 

Reference:

1. Davidson’s Principle and Practice of Medicine,21st edition
2. Wikipedia the free encyclopedia.

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