Dyspnea on Exertion (Exertional Dyspnea): Causes and Treatment
Exertional dyspnea and its pathophysiology
Dyspnea on exertion is caused by various factors. However, low body oxygenation is the key parameter, which is always present in people with this symptom. Mouth breathing and chest breathing are among the main additional causes of exertional dyspnea since they reduce body and brain oxygenation and create the sensation of air hunger (shortage of air). People with heart disease, cancer, diabetes, asthma, cystic fibrosis, COPD and many other chronic conditions are most likely to experience this debilitating symptom, as many studies found.
What do we know about their body oxygenation and breathing at rest? Why do people with chronic diseases, but not healthy people, experience exertional dyspnea? What are the main problems with oxygen transport in the sick? Consider this evidence.
Minute ventilation rates (chronic diseases)
| All references or
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Heart disease||15 (~+mn~4) L/min||22||Dimopoulou et al, 2001|
|Heart disease||16 (~+mn~2) L/min||11||Johnson et al, 2000|
|Heart disease||12 (~+mn~3) L/min||132||Fanfulla et al, 1998|
|Heart disease||15 (~+mn~4) L/min||55||Clark et al, 1997|
|Heart disease||13 (~+mn~4) L/min||15||Banning et al, 1995|
|Heart disease||15 (~+mn~4) L/min||88||Clark et al, 1995|
|Heart disease||14 (~+mn~2) L/min||30||Buller et al, 1990|
|Heart disease||16 (~+mn~6) L/min||20||Elborn et al, 1990|
|Pulm hypertension||12 (~+mn~2) L/min||11||D'Alonzo et al, 1987|
|Cancer||12 (~+mn~2) L/min||40||Travers et al, 2008|
|Diabetes||12-17 L/min||26||Bottini et al, 2003|
|Diabetes||15 (~+mn~2) L/min||45||Tantucci et al, 2001|
|Diabetes||12 (~+mn~2) L/min||8||Mancini et al, 1999|
|Diabetes||10-20 L/min||28||Tantucci et al, 1997|
|Diabetes||13 (~+mn~2) L/min||20||Tantucci et al, 1996|
|Asthma||13 (~+mn~2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (~+mn~6) L/min||39||Bowler et al, 1998|
|Asthma||13 (~+mn~4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden, Lyons, 1968|
|COPD||14 (~+mn~2) L/min||12||Palange et al, 2001|
|COPD||12 (~+mn~2) L/min||10||Sinderby et al, 2001|
|COPD||14 L/min||3||Stulbarg et al, 2001|
|Sleep apnea||15 (~+mn~3) L/min||20||Radwan et al, 2001|
|Liver cirrhosis||11-18 L/min||24||Epstein et al, 1998|
|Hyperthyroidism||15 (~+mn~1) L/min||42||Kahaly, 1998|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (~+mn~2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
|Epilepsy||13 L/min||12||Esquivel et al, 1991|
|CHV||13 (~+mn~2) L/min||134||Han et al, 1997|
|Panic disorder||12 (~+mn~5) L/min||12||Pain et al, 1991|
|Bipolar disorder||11 (~+mn~2) L/min||16||MacKinnon et al, 2007|
|Dystrophia myotonica||16 (~+mn~4) L/min||12||Clague et al, 1994|
Note that advanced stages of asthma can lead to lung destruction, ventilation-perfusion mismatch,
and arterial hypercapnia causing further reduction in body oxygen levels.
Chronic hyperventilation (or having an automatic deep-breathing pattern) leads to alveolar hypocapnia (lack of CO2), which causes low oxygen levels in body cells. Therefore, these people have more problems during physical exertion since any forms of exercise require additional oxygen, causing dyspnea on exertion.
Healthy or normal breathing is very small and slow. It is imperceptible or unperceivable (only about 500 ml for tidal volume, and 10-12 breaths/min with 6 L/min for minute ventilation at rest for a 70-kg person). Patients with dyspnea commonly have over 12 L/min (double the norm) for their ventilation rates at rest and over 18 breaths/min for respiratory frequency.
Overbreathing leads to greatly increased work of breathing due to large minute ventilation rates and causes many other adverse effects, apart from exertional dyspnea.
Exacerbating causes in the pathophysiology of exertional dyspnea are:
- oral breathing (due to reduction in NO or nitric oxide absorption and alveolar CO2)
- thoracic breathing (due to reduction in the arterial oxygenation causing hypoxemia)
- presence of chronic inflammation and sputum in airways, causing further narrowing or obstruction of air movement.
Physical exertion, due to anaerobic cell respiration at rest and elevated resting blood lactate, worsens gas exchange and causes further overbreathing and additional losses in alveolar CO2. This leads to acute exertional dyspnea. Acute dyspnea leads to even heavier and faster breathing due to a negative feedback in breathing control caused by a prominent O2 drive (hunger for air), instead of normal CO2-based control of respiration. Respiratory receptors located in the brain sense low brain oxygenation, creating the sensation of air hunger and trying to increase ventilation.
Treatment of dyspnea on exertion
This YouTube video clip "Dyspnea" explains causes and treatment of dyspnea in people with chronic diseases.
Significant reduction in exertional dyspnea has been found in numerous clinical trials after the application of various breathing techniques and respiratory devices that gradually change automatic (basal) breathing patterns at rest, reduce the degree of hyperventilation, and increase body-oxygen levels. Generally, patients with exertional dyspnea need to achieve more than 20 s for the body-oxygen test to prevent dyspnea at rest and on exertion.
Ripamonti C. Management of dyspnea in advanced cancer patients. Support Care
Cancer. 1999; 7: p. 233-243.
"Dyspnea has been defined as an “uncomfortable awareness of breathing"
Coyne PJ, Viswanathan R, Smith TJ, Nebulized fentanyl citrate improves
patients' perception of breathing, respiratory rate, and oxygen saturation in
dyspnea, J Pain Symptom Manage 2002; 23: p. 157–160.
“Dyspnea is exceedingly common. Ruben and Mor found that 70% of 1500 cancer patients suffered dyspnea during their last four weeks of life.”
Reuben DB, Mor V, How much of a problem is dyspnoea in advanced cancer?
Palliat Med 1991; 5: 20–26.
“Introduction. Although a number of articles on dyspnoea in terminal cancer have appeared, [1-8] in terms of publications, this symptom remains a poor relation when compared with pain. Anyone, however, who has looked after dying people will be aware that dyspnoea is a common and often distressing symptom, particularly if severe. In such cases patients may feel that they may die from lack of air - even pain does not have this connotation. This is demonstrated in Comroe’s definition of dyspnoea as ’difficult, laboured, uncomfortable breathing; it is an unpleasant type of breathing, though it is not painful in the usual sense of the word. It is subjective, and, like pain, it involves both perception of the sensation by the patient and his reaction to the sensation.”
Dudgeon DJ, Managing dyspnea and cough, Hematol Oncol Clin North Am 2002
Jun; 16(3): p.557-577.
"Dyspnea, like pain, is a subjective experience that incorporates physical elements and affective components. Management of breathlessness in patients with cancer requires expertise that includes an understanding and assessment of the multidimensional components of the symptom, knowledge of the pathophysiologic mechanisms and clinical syndromes that are common in cancer, and familiarity with the indications and limitations of the available therapeutic approaches. Relief of breathlessness should be the goal of treatment at all stages of cancer. Good control of dyspnea will improve the patient's quality of life."
Reference pages: Breathing norms and the DIY body oxygen test:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in body tissues
- Nerve stabilization: Carbon dioxide has powerful calmative and sedative effects on brain neurons and nerve cells
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