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Difficult or labored breathing; shortness of breath.

Dyspnea is a feeling of difficult breathing from a patient and subjectively varies from
severities. It is more of a symptom rather than a disease since its a sensation and can be caused
by a lot of things. (Manning and Schwartzstein, 1995; Ashton and Raman, 2015)
Dyspnea occurs when the respiratory drive is increased by any means, the respiratory system
undergo some mechanical load or the whole respiratory system have some abnormalities will result
in air hunger thus difficult breathing. Another concept of dyspnea is Afferent mismatch,
meaning theres somewhat unsynchronized between outgoing motor signal and the resulting
breathing information such as the amount of O2 in the body. This also makes the body feeling need
of more air, creating the sense of dyspnea. (Manning and Schwartzstein, 1995; Ashton and Raman,

Diseases such as pulmonary fibrosis affect the alveolar membrane as well as lung compliance,
causing dyspnea through impairment of gas exchange and increased work of breathing to expand
stiff lung tissue. Chronic obstructive pulmonary disease (COPD) and asthma causing dyspnea
through increased work of breathing due to airflow obstruction. These diseases of airflow
obstruction also lead to air trapping and hyperinflation of the lungs, altering respiratory mechanics
and further increasing the work of breathing. Some disease may overlap the mechanism of dyspnea
when it occurs, such as deconditioning and neuromuscular diseases. For instance, in amyotrophic
lateral sclerosis, the respiratory muscles become weak, which results in impaired ventilation due
to failure of the respiratory pump. In obesity, the pump itself may require more energy to move air
in and out, and yet still be unable to meet the demands of the body due to general deconditioning.
The nervous system can be impaired by many disease states or sometimes by medications, leading
to decreased respiratory drive or action, or even central apnea, which leads to the feeling of
dyspnea. The central nervous system also detects changes in body pH, which can be a powerful
stimulus for a patient's dyspnea, such as in acidosis, even if its not related to any respiratory

Cardiovascular disease is an important cause of dyspnea. Many of these mechanisms overlap

with those of the respiratory system. For example, in low cardiac output states such as systolic
heart failure, the low output is unable to meet the oxygen demands of the body causing ischemia
due to inadequate tissue perfusion, resulting in lactate generation and acidemia. Patients with
cardiac insufficiency often have pulmonary edema that impairs gas exchange as well as increasing
the work of breathing, both of which add to the feeling of shortness of breath. Besides ischemic
heart disease, other broad classes of cardiac disease can impair oxygen delivery by decreasing
cardiac output, including arrhythmias, valvular insufficiency or stenosis, congenital structural
heart disease or remodeling from infarction. or chronic heart failure. A commonly recognized
anginal equivalent in patients with acute coronary syndromes is dyspnea, which may be the only
symptom present.

Defects in the oxygen carrying capacity are also important causes of dyspnea. The typical
example would be anemia due to iron deficiency or other causes. This again is primarily due to a
mismatch in oxygen supply capacity and demand. There is considerable overlap with other
mechanisms here as well. When patients with severe anemia develop a high output state, cardiac
failure can ensue causing them to have shortness of breath from cardiac causes as well.

Diseases in other organs, such as the kidneys and the liver, may cause dyspnea by a
combination of the interactions we have discussed. In end stage renal disease, for example,
dyspnea can be due to metabolic acidosis, volume overload causing pulmonary edema, and/or
pleural effusions impairing lung expansion.

Although the above pathophysiological model can help explain the interaction between organ
systems and dyspnea, the real mechanism of dyspnea is much more nebulous and has to do with
conscious perception and the how the signals produced by these mechanistic abnormalities are
conveyed to the brain. Many of these sensations originate in various receptors throughout the
respiratory system. Mechanoreceptors sense stretch or strain of lung tissue and have been linked
to the cause of chest tightness in bronchoconstriction and lung fibrosis. Vascular
mechanoreceptors convey a sense of dyspnea in diseases like pulmonary hypertension. Pulmonary
edema activates J receptors which are sensitive to structural changes in the lung interstitium. Chest
wall expansion and stretch, especially when combined with respiratory muscle fatigue, can give a
sense of hyperinflation seen in emphysema. These peripheral receptors constitute the afferent limb
of the central nervous system's interpretation of dyspnea. Chemoreceptors which detect changes
in pH are also part of the afferent limb and contribute to the interpretation of dyspnea by the patient.

The efferent limb of the central nervous system is also important in the sensation of dyspnea,
linking the motor cortex and the muscles of the respiratory system. An increase in efferent neural
discharge to meet ventilatory needs increases the work of the respiratory muscles and is perceived
as dyspnea due to increased work of breathing. If the increased stimulation cannot result in an
adequate increase in ventilation, the feeling of air hunger will persist and may become worse.

Mismatch of the afferent and efferent signals may result in dyspnea. For example, in COPD,
the cortex may be instructing the pump to work harder to increase ventilation. The rise in
respiratory rate increases the work of breathing, and the obstructed outflow of air in COPD leads
to worsening hyperinflation and heightened stimulation of mechanoreceptors. This results in more
dyspnea, which may make the patient breath faster and worsen the hyperinflation still more.
An exhaustive list of signs and symptoms is beyond the scope of this discussion although these
often provide clues to the underlying organ system involved. In many respiratory disorders cough
may be a common symptom, alerting to airway inflammation or irritation. Presence of fever may
often point towards an infectious disease also contributing to dyspnea. Patients may misinterpret
pleuritic chest pain as dyspnea, and this should be clarified in the history.

Ashton, R. and Raman, D. (2015). Dyspnea. [online] Clevelandclinicmeded.com. Available at:

[Accessed 4 Dec. 2016].

Manning, H. and Schwartzstein, R. (1995). Pathophysiology of dyspnea. Mechanisms of Disease,

333(23), pp.1547-1553.