Shortness of breath: Looking beyond the usual suspects

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Applied Evidence

Shortness of breath: Looking beyond the usual suspects

J Fam Pract. 2016 August;65(8):526-533

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References

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SIDEBAR
The variable, and subjective, process of dyspnea

The mechanism of action of shortness of breath is a complex and incompletely understood one that involves the central and peripheral nervous systems and neurochemical modulators. In the central nervous system, the medullary respiratory center likely relays increased oxygen demand to the anterior insula. The anterior insula, which is where dyspnea is perceived as unpleasant, then simultaneously disseminates this information to the cerebral cortex and the respiratory muscles to increase respiration and oxygen.^1-3

The peripheral nervous system measures current oxygen flux and lung mechanics through pulmonary stretch mechanoreceptors, pulmonary irritant receptors, and alveolar C fibers. Input from all of these receptors ascends the respiratory pathway and affects how dyspnea is perceived. For example, a patient may complain of shortness of breath because the medullary respiratory center interprets input from activated pulmonary muscular stretch receptors in the setting of discordant oxygen (measured via peripheral chemoreceptors) and carbon dioxide levels (measured by medullary chemoreceptors) as an increased work of breathing.^2,4,5

Neurochemical dissociation, which is the difference between the brain’s desired oxygen level and the amount it gets, is one potential hypothesis to explain why dyspnea is subjective and variable.^2,5 One patient may complain of moderate or severe shortness of breath because he or she has a large dissociation between desired and actual oxygenation despite having only mild to moderate disease severity. However, another patient may report mild dyspnea despite having severe disease because his or her dissociation is small.

Take, for example, a patient who has had an acute myocardial infarction. Such patients often complain of significant difficulty breathing, likely because of the acute and sudden neurochemical dissociation that occurs with the infarction. On the other hand, a patient with gradually worsening moderate heart failure may complain of only mild dyspnea because the change in the patient’s perception of the ability to breathe is slow and small.