| ICD-10 | R06.0 |
|---|---|
| ICD-9 | 786.0 |
| DiseasesDB | 15892 |
| MedlinePlus | 003075 |
| MeSH | D004417 |
Dyspnea or dyspnoea (pronounced /dɪspˈniːə/ disp-NEE-ə), (from Latin dyspnoea, from Greek dyspnoia from dyspnoos, shortness of breath), also called shortness of breath (SOB) or air hunger[1], is a debilitating symptom that is the experience of unpleasant or uncomfortable respiratory sensations.[2] It is a common symptom of numerous medical disorders, particularly those involving the cardiovascular and respiratory systems; dyspnea on exertion (or exertional dyspnea) is the most common presenting complaint for people with respiratory impairment.[3]
Contents |
|
Lungs and breathing activity |
| Eupnea - normal breathing |
| Dyspnea or shortness of breath - sensation of respiratory distress |
| Bradypnea - decreased breathing rate |
| Hyperaeration/Hyperinflation - increased lung volume |
| Hyperpnea - faster and/or deeper breathing |
| Hyperventilation - increased breathing that causes CO2 loss |
| Labored breathing - physical presentation of respiratory distress |
| Tachypnea - increased breathing rate |
Dyspnea has been more specifically defined by the American Thoracic Society as the "subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses."[2]
Importantly, dyspnea is a symptom experienced by the individual, rather than a noticeable or measurable sign.
Still, many[4] simply define dyspnea as difficulty in breathing without further specification, which may confuse it with e.g. labored breathing or tachypnea (rapid breathing).[5] Labored breathing has occasionally been included in the definition as well.[6] However, in the standard definition, these related signs may be present at the same time, but don't necessarily have to be. For instance, in respiratory arrest by a primary failure in respiratory muscles the patient, if conscious, may experience dyspnea, yet without having any labored breathing or tachypnea. The other way around, labored breathing or tachypnea can voluntarily be performed even when there is no dyspnea.
In general, dyspnea signals that there is inadequate ventilation.[3] This happens when the body is unable to ventilate enough to sufficiently meet the body's needs. This situation may occur when there is increased ventilatory demand (e.g. during exercise) or reduced ability to ventilate enough (e.g. due to respiratory muscle weakness).[5]
Although the exact mechanisms of dyspnea are not fully understood, some general details have been found. 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).[9]
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.[9]
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.[9]
Dyspnea can be a worrying and disabling symptom for the patient. In order to assess the level of dyspnea, the doctor might ask the patient to rank the severity from 1 to 10. Alternatively a scale such as the MRC Breathlessness Scale might be used - it suggests five different grades of dyspnea based on the circumstances in which it arises.[10]
| 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 | dyspnea with minimal activity such as getting dressed, too dyspneic to leave the house |
Some studies have suggested that up to 27% of people suffer dyspnea,[3] while in dying patients 75% will experience it.[9]
Intravenous or oral immediate-release opioids have a strong level of evidence supporting their use in causing a reduction of breathlessness. There is a lack of evidence to recommend extended-release morphine, midazolam combined with morphine, nebulised opioids, the use of gas mixtures, and cognitive-behavioral therapy. There is evidence to support the use of oxygen in hypoxic cancer patients.[11]
People with SOB make up about 7% of people who present to the emergency department in the United States. Of these approximately 51% are admitted to hospital and 13% are dead within a year.[12]
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