Dyspnea, more commonly referred to as shortness of breath, is a symptom of many respiratory diseases and disorders. But, depending on the cause, patients may experience shortness of breath once, or have recurring or prolonged episodes.

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Dyspnea is one of the hallmarks of lung disease but can also be found in cardiac disease and in someone who is very deconditioned (out of shape). It affects as many as half of the patients who are admitted to the hospital and is a complaint of some 25% of patients coming into an ambulatory care center. Emergency departments see between 3 to 4 million visits each year that are linked to dyspnea.1 Respiratory therapists, nurses, and physicians are frequently challenged by their patients, “I am so out of breath—you have to help me.”

The American Thoracic Society has defined dyspnea as “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.”1 Many approaches are used to try and alleviate dyspnea and the research behind these approaches proves some to be effective while others fail to show proof. This article will explore the topic of dyspnea, looking at the causes, assessment, and treatment strategies used relieve this bothersome symptom.

Causes and Assessment

Dyspnea is a major issue in patients with lung or heart disease. For those with advanced COPD, dyspnea is reported in over 90% of the cases; for advanced heart disease, dyspnea is reported in over 60% of the cases.3 Dyspnea is one of the four major symptoms of asthma, along with wheezing, cough, and chest tightness. In the case of asthma, dyspnea may be more episodic and the patient may have periods of no symptoms.4 For patients with COPD, dyspnea is also a major symptom and is described as progressive (chronic and getting worse over time).5 In both asthma and COPD, increasing dyspnea is associated with exacerbation of the condition.

Chronic dyspnea (shortness of breath lasting longer than a month) may be linked to five different organ systems. First on the list is the pulmonary system and its associated diseases (including but not limited to all the obstructive and restrictive diseases, pulmonary hypertension, infections, malignancy, vocal fold issues, and the various pneumoconioses).

Second on the list is the cardiac system (with issues such as cardiovascular disease, heart failure, valve disease, etc). The other systems/physiology include gastrointestinal (issues with gut motility, GERD, etc), neuromuscular (weakness or loss of signal), and psychological (anxiety, depression).6 Poor general health, obesity, and little to no activity can also bring about dyspnea in circumstances that call for robust physical activity.

The pathophysiology of dyspnea is complex and includes multiple areas of consideration. For example, changes in pH, oxygen, and carbon dioxide cause the arterial chemoreceptors to signal the brainstem, and the response is to reset alveolar ventilation (the “supply”) to match the metabolic need (“demand”). An imbalance in this area leads to the sensation of air hunger.

Another area of consideration is in the sensation of work; excessive load or work of breathing may be based on low compliance (a stiff lung) or neuromuscular weakness–all leading to a sensation of increased work and dyspnea. However, if the sensation of work or increased demand is linked to an appropriate action or activity (such as exercise), the feeling of dyspnea may feel appropriate and not be associated with an unpleasant reaction.

A third area of consideration is in the sensation of chest tightness and the level of bronchospasm that may be present. Emotions can drive the sensation of dyspnea and the reverse is also true; anxiety, fear, frustration, or panic may cause a person to feel short of breath while on the other hand, an increase in dyspnea (which may be unexplained or linked to a cause such as exposure to a trigger that brings on bronchospasm) can bring about the emotions of anxiety, fear, frustration, or panic.7,8

Dynamic hyperinflation, often found in patients with COPD, may be involved in the development of dyspnea. Dynamic hyperinflation occurs with exertion. As the body exercises, tidal volume and respiratory rate increase to meet the increased metabolic demand. During exercise in a healthy person, the elastic recoil, the airway diameter, airway patency, the expiratory muscles, and expiratory flow are operating normally and the person can fully exhale all of the inspired volume before taking the next breath.

However, for a person with COPD, loss of elastic recoil, decreased airway diameter (due to bronchospasm and or mucus lining the airway), premature collapse of the airways (due to increased expiratory flow, based on the Venturi effect and Bernoulli’s principle), weaker expiratory muscles, and decreased expiratory flow combine to cause the lungs to fail to reach full exhalation (incomplete exhalation). The next breath is “stacked” on top of the previous breath (airtrapping) and dynamic hyperinflation begins to build. This begins to flatten the diaphragm, the muscle becomes inefficient due to the flattening effect and a vicious cycle begins where breathing becomes more and more limited and labored.9 (See Figure 1.)

On left—normal healthy individual; on right—individual with COPD. Exercise is in the shaded area. Note that during normal breathing, the TLC is the same for both persons but the RV and FRC are elevated in the COPD side (indicates static airtrapping and no hyperinflation). As exercise begins, Vt and respiratory rate increase with both individuals. During exercise in the healthy person, FRC begins to decrease as Vt increases. During exercise in the COPD person, FRC begins to increase as Vt increases, and the TLC also begins to increase which indicates dynamic hyperinflation along with increased air trapping.[9]

On left—normal healthy individual; on right—individual with COPD. Exercise is in the shaded area. Note that during normal breathing, the TLC is the same for both persons but the RV and FRC are elevated in the COPD side (indicates static airtrapping and no hyperinflation). As exercise begins, Vt and respiratory rate increase with both individuals. During exercise in the healthy person, FRC begins to decrease as Vt increases. During exercise in the COPD person, FRC begins to increase as Vt increases, and the TLC also begins to increase which indicates dynamic hyperinflation along with increased air trapping.[9]

The American Thoracic Society (ATS) has recommended that assessment of dyspnea should be classified in three domains:

  • Sensory-perceptual measures (what does breathing “feel like”) using tools such as a Likert scale;
  • Affective distress measures (examining levels of immediate distress or assessing the possible consequences of the perception);
  • Symptom impact or burden measures (how breathing affects functional ability, capability to work, quality of life) 1,10

Also in the process of assessing dyspnea, patients are placed in one of two categories. They either have new onset of discomfort and the underlying cause has not been uncovered, or they have some known cause (for pulmonary, cardiac, neuromuscular).

For patients with a new onset of dyspnea, the foundational assessment rests on the history and physical examination with particular emphasis on the cardiac and pulmonary systems since these two systems account for most of the causes. Laboratory studies (for example results from an ABG or cardiac enzymes) and radiographic findings (chest x-ray, CT, MRI) may also help assess dyspnea and uncover the cause.

Finally, examining the words or phrases used by the patient to describe their breathing may give insights as to the cause and point to treatment. Feelings of chest tightness are often linked to bronchospasm. Descriptions of air hunger and not being able to “get a deep breath” may point to dynamic hyperinflation or some restrictive cause such as pulmonary fibrosis.

Dyspnea assessment has been accomplished by validated tools such as the Modified Medical Research Council Dyspnea Scale (mMRC, see Figure 2), which measures perceived dyspnea,11 and the St George Respiratory Questionnaire (SGRQ), which includes several questions out of the 16 total questions that are related to breathlessness.12 Pulmonary function testing and FEV1 may give some insight into the pulmonary status and aid in diagnosis (but the correlation to quality of life is not strong).11

Treatment

A recent article in Chest tells us, “As breathing difficulty is the primary reason that most patients with cardiorespiratory disease seek medical care, it is reasonable to expect that relief of dyspnea would be a major treatment goal.”10 Treatment of dyspnea falls into several approaches—the following deals primarily with pulmonary causes of dyspnea.

Inhaled bronchodilators. Inhaled bronchodilators are the first-line agents in most strategies to relieve dyspnea from pulmonary causes. Several categories of medications are included in the inhaled bronchodilator choices; short-acting ?2 agonists (SABAs), short-acting muscarinic antagonist (SAMA), long-acting ?2 agonists (LABAs), long-acting muscarinic antagonist (LAMAs).

Inhaled corticosteroids. Inhaled corticosteroids (ICS) are also included in the medications to fight dyspnea; they are useful to reduce airway inflammation and help improve airflow. Recent releases of new LABA, LAMA, and ICS medications are changing the strategies for administering inhaled bronchodilators as these new drugs are once-daily medications.

Oxygen therapy. Oxygen therapy is often used in severe COPD, cancer, and heart failure based on proof of hypoxia. Oxygen has been shown to improve exercise distance and exercise time as well as improving the level of dyspnea. There are some patients who don’t meet the criteria for home oxygen therapy but have had it ordered under palliative care. Interestingly, some studies have looked at administration of medical air as a placebo versus oxygen (in both hypoxic and non-hypoxic patients) and have found that a substantial number of patients responded to air in terms of reduced levels of dyspnea.13

Pulmonary rehabilitation. Pulmonary rehabilitation has proven to be significant in improving symptoms including dyspnea for COPD patients.10

Opioids. The perception of dyspnea can be reduced by the administration of opioids by decreasing the respiratory drive. When given with care, use of opioids has not brought on significant decreases in oxygenation. Much like pain management, response to opioids to relieve dyspnea is variable and dosage/response must be monitored accordingly.10,14,15

Inotropes and diuretics. Inotropes and diuretics have been effective in treating dyspnea in patients with underlying cardiovascular disease as the cause.15

NIV and other approaches. Noninvasive ventilatory support has been used to reduce dyspnea, delay buildup of lactic acid, and improve exercise performance. Other approaches have been utilized with varying results including acupuncture, bronchoscopic volume reduction, deep brain stimulation, positioning, pursed-lip breathing, and meditation.10,15,16

Dyspnea is a major symptom in many patients and the underlying cause links to many diseases and organ systems. Relief from dyspnea should be a primary goal when caring for these patients and can sometimes be as simple as repositioning and using meditative or calming words of comfort—but often relief involves administration of various medications, oxygen therapy, or non-invasive ventilatory support. Being aware of this symptom and knowing how to effectively reduce the sensation of dyspnea is a vital part of providing quality care. RT

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Bill Pruitt, MBA, RRT, CPFT, AE-C, FAARC, is a senior instructor and director of clinical education in the department of Cardiorespiratory Sciences, College of Allied Health Sciences, at the University of South Alabama in Mobile. For further information, contact RTmagazine@allied360.com.

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References

  1. Parshall MB, Schwartzstein RM, Adams L, Banzett RB, Manning HL, et.al. An Official American Thoracic Society Statement: Update on the Mechanisms, Assessment, and Management of Dyspnea. 2012. Am J Respir Crit Care Med 185(4): 435–452.

  2. Mourik YV, Rutten FH, Moons KG, Bertens LC, Hoes AW, Reitsma JB. Prevalence and underlying causes of dyspnea in older people: a systematic review. 2014. Age Ageing 43: 319–326

  3. Mahler DA, Selecky PA, Harrod CG, Benditt JO, Carrieri-Kohlman V, et. al. American College of Chest Physicians consensus statement on the management of dyspnea in patients with advanced lung or heart disease. 2010. Chest 137(3): 674-691.

  4. Patadia MO, Murrill LL, Corey J. Asthma: symptoms and presentation. 2014. Otolaryng Clin N Am. 47(1):23-32.

  5. From the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2015 update. http://www.goldcopd.com/. Accessed 6/28/15

  6. Wahls SA. Causes and evaluation of chronic dyspnea. 2012. Am Fam Physician. 86(2):173-82.

  7. Gilman SA, Banzett RB. Physiologic changes and clinical correlates of advanced dyspnea. 2009. Curr Opin Support Palliat Care. 3:93–97.

  8. Scano G, Gigliotti F, Stendardi L, Gagliardi E. Dyspnea and emotional states in health and disease. 2013. Resp Med. 107(5): 649-655

  9. Gagnon P, Guenette JA, Langer D, Laviolette L, Mainguy V, et al. Pathogenesis of hyperinflation in chronic obstructive pulmonary disease. 2014. Int J COPD. 9: 187–201

  10. Mahler DA, O’Donnell DE. Recent Advances in Dyspnea. 2015. Chest 147(1):232-241.

  11. van der Molen T, Miravitlles M, Kocks JW. COPD management: role of symptom assessment in routine clinical practice. 2013. Int J COPD. 8: 461-471

  12. Jones PW, Quirk FH, Baveystock CM, Littlejohns P. A self-complete measure of health status for chronic airflow limitation. The St. George’s Respiratory Questionnaire. 1992. Am Rev Respir Dis. 145(6):1321-1327.

  13. Uronisa HE, Abernethy AP. Oxygen for relief of dyspnea: what is the evidence? 2008. Current Opin in Support Palliative Care 2(2):89–94.

  14. 14 . Horton R, Rocker G, Currow D. 2010. The dyspnea target: can we zero in on opioid responsiveness in advanced chronic obstructive pulmonary disease?. Current Opin in Support Palliative Care, 4(2), 92-96.

  15. Puntillo K, Nelson JE, Weissman D, Curtis R, Weiss S, et al. Palliative care in the ICU: relief of pain, dyspnea, and thirst—a report from the IPAL-ICU Advisory Board. 2014. Intens Care Med, 40(2), 235-248.

  16. Yates P, Zhao I. Update on complex nonpharmacological interventions for breathlessness. 2012. Current Opin in Support Palliative Care, 6(2), 144-152.