The Science of Breathing Well: Difference between revisions

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There is a close relationship between increases in PaCO<sub>2</sub> and alveolar ventilation. While there are individual variations, there is roughly a 1 to 4 L/min increase in minute ventilation for each 1 mmHg increase in PaCO<sub>2</sub>.<ref name=":4" /> However, during times of hyperoxia, CO<sub>2</sub> sensitivity will decrease. Conversely, during periods of hypoxia, it will increase. Thus, when we over-breathe (hyperoxia) the body is less sensitive to hypercapnia and only the central chemoreceptors will respond to increase ventilation.<ref name=":4" />
There is a close relationship between increases in PaCO<sub>2</sub> and alveolar ventilation. While there are individual variations, there is roughly a 1 to 4 L/min increase in minute ventilation for each 1 mmHg increase in PaCO<sub>2</sub>.<ref name=":4" /> However, during times of hyperoxia, CO<sub>2</sub> sensitivity will decrease. Conversely, during periods of hypoxia, it will increase. Thus, when we over-breathe (hyperoxia) the body is less sensitive to hypercapnia and only the central chemoreceptors will respond to increase ventilation.<ref name=":4" />
When hypocapnia is mild, it does not tend to have a significant impact on healthy people, but common signs / symptoms of hypocapnia include:<ref name=":5">Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002;347(1):43-53. </ref>
* paresthesias
* palpitations
* myalgic cramps
* seizures
However, hypocapnia does have the potential to cause various pathological processes:<ref name=":0" /><ref name=":5" />
* The cerebral artery constricts, resulting in signs and symptoms such as dizziness, detachment and reduced clarity of thought.<ref>Yoon S, Zuccarello M, Rapoport RM. pCO(2) and pH regulation of cerebral blood flow. Front Physiol. 2012;3:365. </ref> For every 1mmHG reduction in PaCO<sub>2</sub>, there is a two percent decrease in cerebral blood flow.<ref name=":0" /><ref>Giardino ND, Friedman SD, Dager SR. Anxiety, respiration, and cerebral blood flow: implications for functional brain imaging. Compr Psychiatry. 2007;48(2):103-112. </ref> A decrease of 5mmHG will result in a ten percent reduction of blood flow, which can have a significant impact.<ref name=":0" /> Initially blood flow reduces to the cerebral cortex, which is responsible for planning, logic and thinking. Later, areas that trigger primitive reflexes will be affected, including the amygdala, which plays a key role in fear response and the fight or flight response.<ref>Ressler KJ. Amygdala activity, fear, and anxiety: modulation by stress. Biol Psychiatry. 2010;67(12):1117-1119. </ref><ref name=":0" />
* Uptake of oxygen by haemoglobin is altered. During optimal breathing, oxygen and haemoglobin attach and release readily (known as the Bohr Effect. However, during periods of over-breathing when CO<sub>2</sub> levels decrease, oxygen and haemoglobin attach, but will not readily detach.<ref name=":6">Patel AK, Benner A, Cooper JS. Physiology, Bohr Effect. [Updated 2019 Jul 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK526028/</nowiki></ref> This accounts for readings of 100% saturation shown on pulse oximetry in patients with breathing pattern dysfunctions.
* This increased affinity of oxygen to haemoglobin results in impaired oxygen release to peripheral tissues (brain, heart, liver, kidney).<ref name=":6" /> It will also result in decreased blood flow in the periphery (i.e. hands, feet and mouth) and increased activity of the nervous tissue and nerve synapses.<ref name=":0" />
* A reduction in PaCO<sub>2</sub>, will result in an imbalance of calcium and magnesium, which will increase the likelihood of spasm and fatigue.<ref name=":0" />
* Similarly, low levels of CO<sub>2</sub> in the bloodstream affects lactic acid buffering. This is often present in individuals who have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) chronic fatigue or post-viral fatigue. Lactic acid is the byproduct of exercise and it is usually easily removed due to the bicarbonate buffer. However, in patients with chronic hyperventilation syndrome, the bicarbonate buffer becomes depleted. Thus, they quickly develop a build up of lactic acid, resulting in muscle aches and pains. Thus, patients who have chronic fatigue or post-viral fatigue should be assessed for breathing pattern dysfunction with the aim to restore a good breathing pattern at rest.<ref name=":0" />
All of these symptoms of hypocapnia can be worrisome for patients, resulting in further stress.
The effects of chronic over-breathing with the associated chronic depletion of CO<sub>2</sub>, include:<ref name=":0" />
* Breathlessness disproportionate to actual fitness - if PaCO<sub>2</sub> rises above 42 mmHG or lower than 36/8 mmHg the respiratory reflex will be triggered
* A state of fight or flight with catecholamines released
* Lactic acid build up due to the depletion of the bicarbonate buffer


== References ==
== References ==
<references />
<references />

Revision as of 10:25, 23 August 2020

Introduction[edit | edit source]

Breathing affects all body systems; these systems in turn influence breathing. Optimal breathing patterns help to maintain homeostasis, but when breathing is disrupted, significant issues can arise.

Physiotherapists are well placed to assess and treat breathing pattern disorders. It is, however, important to understand the science behind optimal breathing in order to understand the relationship between breathing and the quite varied symptoms that occur with dysfunctional breathing. The science of breathing can essentially be broken down into three subcategories:

  • The mechanics of breathing well (ie biomechanics)
  • The physiology of breathing well (ie biochemistry)
  • The psychophysiology of breathing well (or psychology)

The Mechanics of Breathing Well[edit | edit source]

Brief Anatomy Review[edit | edit source]

For more information on the anatomy of breathing, click here, but in brief the respiratory conduction zone consists of the:[1]

  • Nasal cavity
  • Pharynx
  • Larynx
  • Trachea
  • Bronchi and bronchioles

The nose plays an important role in nitric oxide production, which impacts latency and dilation of blood vessels. It is also involved in sterilisation of air in the airways.[2][3] The larynx transports air down to the lungs.

The respiratory muscles are:[4]

  • Diaphragm, which acts as a vital pump
  • Rib cage muscles
  • Abdominal muscles

The thoracic and abdominal cavities essentially form a canister with the larynx and vocal cords on top, diaphragm in the middle and the pelvic floor at the base. All work together to ensure optimal respiration, as well as to maintain / modulate intrathoracic and intra-abdominal pressure.[3]

How Do the Biomechanics of Breathing Influence Other Systems and Organs?[edit | edit source]

Heart[edit | edit source]

Other organs and systems are influenced by the biomechanics of breath, including the heart. The heart is encased in, and moves with, the diaphragm, which influences heart tone.[3] Similarly,  when the diaphragm descends and ascends, the heart is essentially “micro-massaged”, which affects its baroreceptors.[3][5] Baroreceptors are a type of mechanoreceptor which enable information about blood pressure to be sent to the autonomic nervous system.[6]

Heart rate variability (HRV) is also influenced by breathing.[7] HRV refers to the variation in time intervals between heart beats.[7] HRV is an important indicator of health, as well as mood and our ability to adapt. A number of physiological systems influence heart rhythm. Higher HRV generally is a marker of good physiological functioning whereas lower HRV predicts morbidity and mortality. Low HRV is also more common in individuals who have depression, anxiety and chronic stress.[7]

Intra-abdominal and Intra-thoracic Pressure[edit | edit source]

The diaphragm works with the anterior abdominal wall muscles to increase intra-abdominal pressure, enhancing processes such as gut motility, defecation, micturition (urination) and parturition (giving birth).[8]

As mentioned above, the diaphragm acts as a vital pump.[3] On inhalation, its descent decreases intrathoracic pressure and increases intra-abdominal pressure. This acts on the inferior vena cava, helping to push deoxygenated blood into the right atrium. It also compresses the abdominal lymph vessels, which aids lymphatic movement.[8] Similarly, cerebrospinal fluid is pumped into the brain on inhalation and pumped back down on exhalation.[9]

Continence and Voice Quality[edit | edit source]

Continence and vocal quality are also affected as they make up the base and top of the canister.[3]

Contraction of the pelvic floor muscles and diaphragmatic motion correlate with breathing. Moreover, breathing is more effective when the pelvic floor contracts.[10].

The relationship to the diaphragm and vocal quality has been studied most extensively in singing, but it has been found that co-activation of the diaphragm during phonation may impact voice quality.[11][12]

Musculoskeletal System[edit | edit source]

The diaphragm also has a significant impact on our musculoskeletal system. Breathing mechanics affect posture and spinal stabilisation; breathing pattern disorders contribute to pain and motor control deficits and can result in muscular imbalance, changes in motor control and physiological adaptations which result in modified movement patterns.[13]

For instance, a significant correlation between low back pain and breathing pattern disorders has been demonstrated[3] and a recent study by Finta and colleagues found that diaphragm strengthening combined with other training may be beneficial in the management of chronic nonspecific low back pain.[14] A link between chronic ankle instability and altered diaphragm contractility has also been established.[15]

The Physiology of Breathing Well[edit | edit source]

The main purpose of breathing is to maintain homeostasis, which is achieved by the inspiration of oxygen and the exhalation of carbon dioxide (CO2). This process stabilises pH. The normal range of pH in the human body is 7.35-7.45, with an average of 7.4.[16] Every organ system in the body depends on this pH balance. pH is modulated by both the respiratory and renal systems[16]

When breathing does not match the level required by the body, homeostasis is disrupted. As it is essential that pH remains stable, the level of CO2 in the bloodstream (PaCO2) will increase or decrease based on requirements.[3]

  • NB When assessing breathing patterns, it is important to first assess a patient at rest and then move on to dynamic breathing and movement as there will often be greater mismatch during breathing at rest [3]
  • Often patients will report feelings of air hunger, or that they cannot get enough air. Using pulse oximetry can be useful as patients with breathing pattern disorders will often have readings above normal levels of 96-98% saturation. This result will help to demonstrate that they are over-breathing at rest and not in need of more oxygen. If saturation readings are low (less than 94%) then other causes must be considered with respect to lung function[3]

PaCO2 level plays a key role in our breathing. Normal resting levels of PaCO2 is 40 milligrams of mercury (mmHg). PaCO2 is the main driver of the rate and depth of breathing.[3]

Typically, large changes in PaCO2 and the resultant changes in pH are controlled by the hydrogen ion buffering system. Without this system, even brief periods of apnea would cause death due to hypercapnia.[17] However, the respiratory centre is more sensitive to CO2 levels than oxygen levels. If pH becomes more acidic (i.e. PaCO2 decreases), the central and peripheral chemoreceptors will stimulate respiratory drive through bronchodilation and hypoxic vasoconstriction. This will increase CO2 clearance and improve ventilation / perfusion matching.[17]

There is a close relationship between increases in PaCO2 and alveolar ventilation. While there are individual variations, there is roughly a 1 to 4 L/min increase in minute ventilation for each 1 mmHg increase in PaCO2.[17] However, during times of hyperoxia, CO2 sensitivity will decrease. Conversely, during periods of hypoxia, it will increase. Thus, when we over-breathe (hyperoxia) the body is less sensitive to hypercapnia and only the central chemoreceptors will respond to increase ventilation.[17]

When hypocapnia is mild, it does not tend to have a significant impact on healthy people, but common signs / symptoms of hypocapnia include:[18]

  • paresthesias
  • palpitations
  • myalgic cramps
  • seizures

However, hypocapnia does have the potential to cause various pathological processes:[3][18]

  • The cerebral artery constricts, resulting in signs and symptoms such as dizziness, detachment and reduced clarity of thought.[19] For every 1mmHG reduction in PaCO2, there is a two percent decrease in cerebral blood flow.[3][20] A decrease of 5mmHG will result in a ten percent reduction of blood flow, which can have a significant impact.[3] Initially blood flow reduces to the cerebral cortex, which is responsible for planning, logic and thinking. Later, areas that trigger primitive reflexes will be affected, including the amygdala, which plays a key role in fear response and the fight or flight response.[21][3]
  • Uptake of oxygen by haemoglobin is altered. During optimal breathing, oxygen and haemoglobin attach and release readily (known as the Bohr Effect. However, during periods of over-breathing when CO2 levels decrease, oxygen and haemoglobin attach, but will not readily detach.[22] This accounts for readings of 100% saturation shown on pulse oximetry in patients with breathing pattern dysfunctions.
  • This increased affinity of oxygen to haemoglobin results in impaired oxygen release to peripheral tissues (brain, heart, liver, kidney).[22] It will also result in decreased blood flow in the periphery (i.e. hands, feet and mouth) and increased activity of the nervous tissue and nerve synapses.[3]
  • A reduction in PaCO2, will result in an imbalance of calcium and magnesium, which will increase the likelihood of spasm and fatigue.[3]
  • Similarly, low levels of CO2 in the bloodstream affects lactic acid buffering. This is often present in individuals who have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) chronic fatigue or post-viral fatigue. Lactic acid is the byproduct of exercise and it is usually easily removed due to the bicarbonate buffer. However, in patients with chronic hyperventilation syndrome, the bicarbonate buffer becomes depleted. Thus, they quickly develop a build up of lactic acid, resulting in muscle aches and pains. Thus, patients who have chronic fatigue or post-viral fatigue should be assessed for breathing pattern dysfunction with the aim to restore a good breathing pattern at rest.[3]

All of these symptoms of hypocapnia can be worrisome for patients, resulting in further stress.

The effects of chronic over-breathing with the associated chronic depletion of CO2, include:[3]

  • Breathlessness disproportionate to actual fitness - if PaCO2 rises above 42 mmHG or lower than 36/8 mmHg the respiratory reflex will be triggered
  • A state of fight or flight with catecholamines released
  • Lactic acid build up due to the depletion of the bicarbonate buffer

References[edit | edit source]

  1. Cedar SH. Every breath you take: the process of breathing explained. Nursing Times [online]. 2018; 114(1): 47-50.
  2. Lundberg JO, Settergren G, Gelinder S, Lundberg JM, Alving K, Weitzberg E. Inhalation of nasally derived nitric oxide modulates pulmonary function in humans. Acta Physiol Scand. 1996;158(4): 343-347.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 Clifton-Smith T. The Science of Breathing Well Course. Physioplus. 2020.
  4. Aliverti A. The respiratory muscles during exercise. Breathe (Sheff). 2016; 12(2):165-168.
  5. Baekey DM, Molkov YI, Paton JF, Rybak IA, Dick TE. Effect of baroreceptor stimulation on the respiratory pattern: insights into respiratory-sympathetic interactions. Respir Physiol Neurobiol. 2010;174(1-2):135-145.
  6. Armstrong M, Kerndt CC, Moore RA. Physiology, Baroreceptors. [Updated 2020 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538172/
  7. 7.0 7.1 7.2 Steffen PR, Austin T, DeBarros A, Brown T. The Impact of Resonance Frequency Breathing on Measures of Heart Rate Variability, Blood Pressure, and Mood. Front Public Health. 2017;5: 222.
  8. 8.0 8.1 Bains KNS, Kashyap S, Lappin SL. Anatomy, Thorax, Diaphragm. [Updated 2020 Apr 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519558/
  9. Clifton-Smith T. How We Breathe Course. Physioplus. 2020.
  10. Park H, Han D. The effect of the correlation between the contraction of the pelvic floor muscles and diaphragmatic motion during breathing. J Phys Ther Sci. 2015;27(7):2113-2115.
  11. Leanderson R, Sundberg J, von Euler C. Role of diaphragmatic activity during singing: a study of transdiaphragmatic pressures. J Appl Physiol (1985). 1987;62(1):259-270.
  12. Salomoni S, van den Hoorn W, Hodges P. Breathing and Singing: Objective Characterization of Breathing Patterns in Classical Singers. PLoS One. 2016;11(5):e0155084.
  13. Bradley H, Esformes J. Breathing pattern disorders and functional movement. Int J Sports Phys Ther. 2014; 9(1): 28-39.
  14. Finta R, Nagy E, Bender T. The effect of diaphragm training on lumbar stabilizer muscles: a new concept for improving segmental stability in the case of low back pain. J Pain Res. 2018;11:3031-3045.
  15. Terada M, Kosik KB, McCann RS, Gribble PA. Diaphragm Contractility in Individuals with Chronic Ankle Instability. Med Sci Sports Exerc. 2016;48(10):2040-2045.
  16. 16.0 16.1 Hopkins E, Sharma S. Physiology, Acid Base Balance. [Updated 2020 Aug 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507807/
  17. 17.0 17.1 17.2 17.3 Benner A, Sharma S. Physiology, Carbon Dioxide Response Curve. [Updated 2020 Apr 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538146/
  18. 18.0 18.1 Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002;347(1):43-53.
  19. Yoon S, Zuccarello M, Rapoport RM. pCO(2) and pH regulation of cerebral blood flow. Front Physiol. 2012;3:365.
  20. Giardino ND, Friedman SD, Dager SR. Anxiety, respiration, and cerebral blood flow: implications for functional brain imaging. Compr Psychiatry. 2007;48(2):103-112.
  21. Ressler KJ. Amygdala activity, fear, and anxiety: modulation by stress. Biol Psychiatry. 2010;67(12):1117-1119.
  22. 22.0 22.1 Patel AK, Benner A, Cooper JS. Physiology, Bohr Effect. [Updated 2019 Jul 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526028/