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Dyspnea: Definition, Causes, and Proven Treatment

Man with dyspnea and chest painDyspnea (pronounced as "disp-neŽah") is characterized as being unable to take a satisfying deep inspiration. This weird definition was likely invented by proponents of breathing more air (as if breathing more than the medical norm provides health benefits). Even large official websites promote this implication related to goodness of breathing more air at rest.

What causes dyspnea and its pathophysiology

Brain oxygen levels for normal breathing and after hyperventilationThe deep cause of dyspnea is in changes in air composition during last 2 millions of years. When first prototypes of lungs were evolving, air had about 7-12% CO2 and less than 1% O2. This was before advance of green life. As a result, overbreathing was beneficial for increased tissue oxygenation. Now the situation is reversed, but humans still possess this ancient pathological reflex called "dyspnea". In modern conditions, overbreathing reduces body oxygenation, and this intensifies the desire to breathe creating a vicious circle.

Dyspnea is caused by overbreathing (deep breathing), mouth breathing and chest breathing. All these activities reduce brain and body oxygenation and create the sensation of air hunger. Let us start with evidence related to chronic deep breathing in people with dyspnea. Think of the feeling you would get waiting on test results or a call back from you Dallas DWI attorney and it may be similar to the shortness of breathe you'd have with dyspnea.

Minute ventilation rates (chronic diseases)

Condition Minute
Number of
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 (±4) L/min 22 Dimopoulou et al, 2001
Heart disease 16 (±2) L/min 11 Johnson et al, 2000
Heart disease 12 (±3) L/min 132 Fanfulla et al, 1998
Heart disease 15 (±4) L/min 55 Clark et al, 1997
Heart disease 13 (±4) L/min 15 Banning et al, 1995
Heart disease 15 (±4) L/min 88 Clark et al, 1995
Heart disease  14 (±2) L/min 30 Buller et al, 1990
Heart disease 16 (±6) L/min 20 Elborn et al, 1990
Pulm hypertension 12 (±2) L/min 11 D'Alonzo et al, 1987
Cancer 12 (±2) L/min 40 Travers et al, 2008
Diabetes 12-17 L/min 26 Bottini et al, 2003
Diabetes 15 (±2) L/min 45 Tantucci et al, 2001
Diabetes 12 (±2) L/min 8 Mancini et al, 1999
Diabetes 10-20 L/min 28 Tantucci et al, 1997
Diabetes 13 (±2) L/min 20 Tantucci et al, 1996
Asthma 13 (±2) L/min 16 Chalupa et al, 2004
Asthma 15 L/min 8 Johnson et al, 1995
Asthma 14 (±6) L/min 39 Bowler et al, 1998
Asthma 13 (±4) L/min 17 Kassabian et al, 1982
Asthma 12 L/min 101 McFadden, Lyons, 1968
COPD 14 (±2) L/min 12 Palange et al, 2001
COPD 12 (±2) L/min 10 Sinderby et al, 2001
COPD 14 L/min 3 Stulbarg et al, 2001
Sleep apnea 15 (±3) L/min 20 Radwan et al, 2001
Liver cirrhosis 11-18 L/min 24 Epstein et al, 1998
Hyperthyroidism 15 (±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 (±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 (±2) L/min 134 Han et al, 1997
Panic disorder 12 (±5) L/min 12 Pain et al, 1991
Bipolar disorder 11 (±2) L/min 16 MacKinnon et al, 2007
Dystrophia myotonica 16 (±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 overbreathing) leads to alveolar hypocapnia (CO2 deficiency) which is normal in people with heart disease, asthma, COPD, cancer, cystic fibrosis, diabetes,  pregnancy and many other conditions. Low brain oxygenation (see the brain image above) is the known effect of overbreathing.

Healthy, normal breathing is imperceptible or unperceivable since it is very small (500 ml for tidal volume, 10-12 breaths/min, and 6 L/min for minute ventilation at rest for a 70-kg person). In contrast, dyspneic patients have over 12 L/min (double the norm) for their ventilation rates and over 18 breaths/min for respiratory frequency at rest. This simple ideas are unknown to most doctors. This is reflected in the Wikipedia article devoted to dyspnea: click here.

Cause of dyspnea

Hyperventilation leads to greatly increased work of breathing due to large minute ventilation rates. But there are other effects as well. For example, alveolar hyperventilation always leads to cell hypoxia (regardless of ventilation-perfusion ratio).

Causes of dyspnea

Medical peopleThe main physiological factors (causes of dyspnea) that increase the work of breathing (often several-fold) are:
- constriction of airways due to alveolar hypocapnia
- reduced oxygen tension in the diaphragm and chest muscles due to worsened oxygen transport
- tense states of the diaphragm and chest muscles due to arterial hypocapnia.

Older man with exertional dyspnea due to exercise Exacerbating causes in the pathophysiology of dyspnea are:
- mouth breathing (due to reduction in nitric oxide absorption and alveolar CO2)
- chest breathing (due to reduction in the arterial oxygenation)
- presence of inflammation and mucus in airways causing further narrowing or obstruction of air flow.

Exertion, exercise (with mouth breathing), meals (or eating, and especially overeating), overheating, stress, anxiety, attempts to breathe deeply, deep breathing exercises, night sleep and being in the horizontal position (especially supine sleep), poor posture, pregnancy and many other factors are all known causes of hyperventilation. Therefore, these lifestyle factors exacerbate the problem with breathlessness.

For example, physical exertion, due to anaerobic cell respiration at rest and elevated-resting-blood lactate, worsens gas exchange and causes overbreathing. This leads to acute exertional dyspnea.

Acute dyspnea leads to even heavier breathing due to a negative feedback in breathing control caused by a prominent oxygen drive (hunger for air), instead of normal CO2-based regulation of respiration. Respiratory receptors located in the brain sense low-brain oxygenation creating the sensation of air hunger and trying to increase ventilation.

This short YouTube video "Shortness of Breath (Dyspnea)" explains development of dyspnea due to hyperventilation in people with chronic diseases.

Get flash player to play to this file

Treatment of dyspnea

Dyspnea disappears when a person gets more than 20 s for the body-oxygen test. This number is still 2 times less than the medical norm (40 seconds), but is sufficient to solve problems with shortness of breath at rest. More information: Hyperventilation treatment.

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

Or go back to Hyperventilation Symptoms

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