Dyspnea: Definition, Causes, and Proven Treatment
Dyspnea (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
The 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)
| 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).
The 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.
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.
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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