Shortness of Breath Causes: Chest Breathing, Low Body O2
What Causes Shortness of Breath?
Shortness of breath causes related to those factors of mechanics of breathing that relate to ineffective breathing patterns. Ineffective breathing reduce oxygen delivery to body tissues. Among the common breathing abnormalities are mouth breathing (e.g., on exertion or during sleep) and thoracic (of chest) breathing. Both causes of shortness of breath drastically reduce oxygen transport to cells. Chest breathing does not provide oxygen for lower parts of the lungs that get about 6-7 times more blood than the top portions of the lungs due to gravity.
However, the main cellular cause of shortness of breath is
due to the predominant hypoxic drive (oxygen drive) caused by tissue hypoxia
(low oxygen levels in cells). Breathing of healthy people is mainly controlled
by CO2 levels in the blood and brain. Oxygen drive is about 50-100 times weaker.
For example, if the surrounding air composition changes to 100% O2, the person
would not notice that. However, in CO2 levels in air is increased just by 1%,
there is an immediate increase in minute ventilation that is noticeable for the
person and surrounding people.
In sick people, the situation is different. Due to low levels of oxygen in the brain (see the image on the left), oxygen drive becomes the main factor that controls breathing. Why do sick people have low brain oxygenation? This table explains why the main causes of shortness of breath relate to tissue hypoxia.
Minute ventilation rates (chronic diseases)
| Condition | Minute ventilation |
Number of people |
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 |
We see that all these groups of patients suffer from chronic hyperventilation or alveolar hypocapnia (CO2 deficiency) in the lungs. Normal breathing in healthy people is imperceptible: it is small and light (500 ml for tidal volume and 6 L/min for minute ventilation at rest for a 70-kg person). Hyperventilation leads to tissue hypoxia (or low cell oxygen levels) regardless of arterial CO2 changes and the presence of the ventilation-perfusion mismatch.

Secondary causes of shortness of breath
Overheating, meals (or overeating), anxiety, and exertion all lead to
hyperventilation (and alveolar hypocapnia). Therefore, these are other lifestyle-related
shortness of
breath causes. The factors that increase the work of breathing are constriction of airways due to alveolar hypocapnia,
chest breathing (due to spasmodic
diaphragm), obstruction of airways due to
mucus and inflammation and increased blood viscosity. Mouth breathing worsens breathlessness due to reduction in
NO (nitric oxide) absorption and reduced alveolar CO2.
Numerous medical studies have found that exertion (or physical exercise), stress, anxiety, meals (or eating), overheating, attempts to breathe deeply, deep breathing exercises, night sleep, poor posture, pregnancy and many other factors causes shortness of breath. All these factors also intensify breathing and reduce alveolar CO2 levels through overbreathing. Therefore, it is logical that these factors cause shortness of breath.
People with shortness of breath generally have less than 10-14 seconds for the body oxygen test. These are very poor results since the normal result is about 40 seconds. The main symptoms of shortness of breath disappear, when they get about 20-25 seconds for the body oxygen test. This is based on experience of thousands of people, as well as results of the published Ukrainian clinical trial on cancer (see Cancer Section). Hence, both physiological and clinical considerations clearly demonstrate that low cell oxygenation, due to chest breathing, possible mouth breathing and hyperventilation are the causes of shortness of breath.
Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and
Body Oxygen in Healthy, Normal and Sick People
Breathing
norms Parameters, graph, and description of the normal
breathing pattern
6 breathing myths 6
myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of
hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the
Sick. Table
1. Western scientific evidence about prevalence of CHV
(chronic hyperventilation) in patients with various chronic conditions
(34 medical studies)
Normal Minute Ventilation in
Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of
Normal People (24 medical publications)
HV and hypoxia
How and why deep breathing reduces oxygenation of cells and tissues of
all vital organs
Body oxygen test
How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy
Table 4. CP (body oxygen level) in healthy people (27 medical
studies)
Body oxygen in sick Table 5.
CP (body oxygen level) in sick people (14 medical studies)
Buteyko
Table of Health Zones with clinical description of most common zones
Morning HV Morning
hyperventilation effect or how and why critically ill people are most
likely to die during early morning hours
References: CO2 Effects Web Pages
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 tissues
Cell Oxygen Levels and oxygen transport are controlled by
alveolar CO2 and breathing
Oxygen Transport depends on
breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr
effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2
content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes
place due to anaerobic cell respiration caused by cell hypoxia. Hence,
antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by
breathing since hypoxia leads to or intensifies chronic inflammation through over-expression
of the hypoxia-inducible factor 1, while normal
breathing reduces these processes
Nerve stabilization takes place due to calmative or
sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells
is normal at high CO2, while hypocapnia causes muscular tension, poor posture
and, sometimes, aggression and violence
Brochodilation - dilation of
airways (bronchi and bronchioles) by carbon dioxide, and their constriction due
to hypocapnia
Blood
pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon
dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine
in the Brain, CO2 fixation, and other chemical reactions
CO2 myth
"CO2 is a toxic waste gas" myth
Breathing control
How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic
References (shortness of breath or breathlessness)
Thorax. 2011 Mar;66(3):240-6.
Neural respiratory drive, pulmonary mechanics and breathlessness in patients
with cystic fibrosis.
Reilly CC, Ward K, Jolley CJ, Lunt AC, Steier J, Elston C, Polkey MI, Rafferty
GF, Moxham J.
Rev Esp Cardiol. 2005 Oct;58(10):1142-4.
[The circulating NTproBNP level, a new biomarker for the diagnosis of heart
failure in patients with acute shortness of breath].
[Article in Spanish]
Aust Fam Physician. 2005 Jul;34(7):541-5.
Shortness of breath - is it chronic obstructive pulmonary disease?
McDonald CF.
Institute for Breathing and Sleep, Austin Hospital, Heidelberg, Victoria,
Australia.
Int J Cardiol. 2002 Sep;85(1):133-9.
Origin of symptoms in patients with cachexia with special reference to weakness
and shortness of breath.
Coats AJ.
Medsurg Nurs. 2000 Aug;9(4):178-82.
Helping patients with COPD manage episodes of acute shortness of breath.
Truesdell S.
Division of Pulmonary and Critical Care Medicine, Henry Ford Hospital, Detroit,
MI, USA.
The most disabling and frightening symptom experienced by patients with COPD is
dyspnea. Even with the use of bronchodilators, the symptom may not be completely
relieved. Patients often develop their own strategies for managing shortness of
breath, including the use of a breathing technique called pursed-lip breathing.
Although most nurses are familiar with this breathing technique, they often have
difficulty assisting patients to use it during acute episodes of shortness of
breath. A strategy is described which nurses can use to assist patients in
implementing pursed-lip breathing effectively during episodes of acute dyspnea.
Go back to Breathing Techniques
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