View source for Talk:Hyperventilation

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==Heading 1==
:''Reduced carbon dioxide concentration causes the blood vessels in the brain to contract, resulting in reduced blood flow to the brain. It also affects the nerves, and can cause heart arrhythmias.''

Why and how does this happen? [[User:AxelBoldt|AxelBoldt]] 05:26, 24 Dec 2004 (UTC)

::Offhand, I don't remember reading that hypocapnea (reduced carbon dioxide concentration) directly causes any blood vessels to constrict. It can affect nerves through a different mechanism, in that hypocapnea causes a shift in pH levels and that causes hypocalcemia which causes nerves to tingle (and I suppose, that that ''can'' cause heart arrhythmias although I would imagine that arrhythmias caused by hyperventilation to be quite rare). [[User:Alex.tan|Alex.tan]] 17:48, 25 Dec 2004 (UTC)

:::In [http://www.euroanesthesia.org/education/rc_vienna/07rc1.HTM this artice] they mention how hypercapnea dilates brain blood vessels, (and hypocapnea accordingly constricts them). They don't clearly say why the body does this though, what the point is. My conjecture: under hypercapnea, the brain vessels "think falsely" that the brain is currently working hard, using up a lot of oxygen and producing a lot of carbon dioxide. So they dilate, to bring more oxygen in. But I haven't read that anywhere. [[User:AxelBoldt|AxelBoldt]] 21:36, 1 Jan 2005 (UTC)

::::Hypercapnea causing increased blood flow to the brain makes sense. It's not "thinking falsely", it's under the assumption (usually correct) that increased carbon dioxide concentration means reduced oxygen concentration. The bottom line is that there are more chemoreceptors measuring carbon dioxide levels than oxygen levels in the body. However, hypocapnea has much less of an effect on blood vessels given that physiological pCO2 levels range from 35-45 or so and you really have to hyperventilate fast for a period of time to get them anywhere near 20 whereas raising pCO2 levels just takes holding your breath for a short lenght of time. I still find it difficult to correlate heart arrhythmias with hypocapnea secondary to hyperventilation. [[User:Alex.tan|Alex.tan]] 14:36, 6 Jan 2005 (UTC)

==Split==
We should either have both tachypnea merged with hyperventilation and bradypnea merged with hypoventilation or we should have neither merged for continuity.  Please look at the bradypnea page and help us decide wheter that should be merged with hypoventilation (and an explanation added like is the case with tachypnea/hyperventilation page) or if the hyperventilation page should be separated from tachypnea.  Thanks!  [[User:Ayvah|Ayvah]] 13:13, 8 June 2006 (UTC)

:I personally think that tachypnea whould be split from hyperventilation because there are enough differences between the two that the information on hyperventilation isn't always useful for someone researching tachypnea (I speak from experience here - I need info on tachypnea and can't find it ''anywhere'' but find hyperventilation information wherever I search).  Also, looking at the dates on this page, I understand that I'm coming in a little after the fact, but I figured that'd be alright with everyone...if I'm wrong about that, feel free to point it out... [[User:Jay Shadow-mage|Jay]] 01:09, 7 April 2007 (UTC)

::Tachypnea, hyperpnea, and hyperventilation are all different from each other.  They all involve breathing fast, but imply slightly different mechanisms.  They should each have their own page. Otherwise, it implies that one is subtype of another (tachypnea is the most general though).  [[User:Cmcnicoll|Cmcnicoll]] 18:32, 13 April 2007 (UTC) 

Hyperpnia should not be used interchangeably with hyperventilation. As I understood it, hyperventilation was the increased alveolar ventilation exceeding the metabolic demand for oxygen, this increases the alveolar partial pressure of oxygen (due to diffusion gradient - Fick's Law).
Hyperpnia on the other hand is the increase in alveolar ventilation with an increased metabolic demand (as seen in excercise).

Definition should be changed with a better reference. Hyperventilation is the process of abnormally prolonged, rapid, and deep breathing (polypnea), resulting in increased alveolar ventilation which reduces carbon dioxide tension leading to alkalosis. (Dorland, W.A., Dorland's Illustrated Medical Dictionary, 2000. W.B. Saunders Company, Philadelphia, USA)  <small>—Preceding [[Wikipedia:Signatures|unsigned]] comment added by [[Special:Contributions/210.49.127.90|210.49.127.90]] ([[User talk:210.49.127.90|talk]]) 08:41, 31 August 2007 (UTC)</small><!-- Template:UnsignedIP --> <!--Autosigned by SineBot-->

*'''Split''' please, these are 3 different terms. --[[User:Stevenfruitsmaak|Steven Fruitsmaak]] <small>([[User_talk:Stevenfruitsmaak|Reply]])</small> 23:26, 28 December 2007 (UTC)

*Agree, '''split'''. [[User:Mr. Absurd|Mr. Absurd]] ([[User talk:Mr. Absurd|talk]]) 05:32, 7 January 2008 (UTC)

:Done. [http://en.wikipedia.org/w/index.php?title=Hyperventilation&diff=prev&oldid=196115859] [http://en.wikipedia.org/w/index.php?title=Hyperpnea&diff=prev&oldid=196115995] [http://en.wikipedia.org/w/index.php?title=Hyperventilation&diff=prev&oldid=196115859] --[[Special:Contributions/209.244.43.122|209.244.43.122]] ([[User talk:209.244.43.122|talk]]) 20:41, 5 March 2008 (UTC)

== Treatment ==

This section needs both revisions and additions. [[User:VodkaJazz|VodkaJazz]] 21:59, 28 January 2006 (UTC)

Treatment for the broad term hyperventilation will be hard to summarise as clinically there are three forms, artificial (mechanical ventilation), chronic (due to disease or syndrome such as chronic generalised anxiety syndrome) and psychogenic of which cause is often undiagnosable but still requires prompt treatment. The whole article would have to be expanded to accurately add a treatment thread.

== Question on Treatment ==

"The common treatment of breathing into a paper bag is no longer recommended by physicians and nurses, as it can cause the carbon dioxide level to rise too rapidly"

Are there any sources to support this?
[[User:Chrisjsaunders|Chrisjsaunders]] 15:18 (BST), 26 July 2006

There are many sources such as cited below by [[User:Alexspence|Alexspence]] that suggest alternatives to the rebreathing treatment or even suggest that rebreathing may do more harm than good.  However article fails to cite such sources. Anyhow the existence of such sources does not really support the assertion that it "is no longer recommended [<i>by anyone</i>]". (Article no longer says "physicians and nurses"). Indeed some time after the first studies that point to the ineffectiveness of the rebreathing treatment I continue to see this treatment recommend in books written or at least reviewed by doctors. (Now I guess I need to add citations here to support that). Anyhow I've tagged the section as needing references.  [[User:nobull67|Brian McCauley]], 8 November 2008 (UTC).

I don't know of any sources, but Buteyko Breathing Therapists use a exercise called the Anti-Hyperventilation Exercise to take the place of a paper bag, this simple breathing exercise puts the gap or pause back in to rapid breathing and helps the breathing to slow down, you can find out more at [[Buteyko Method]] or at [http://www.buteykoscotland.co.uk Buteyko]. [[User:Alexspence|Alexspence]] 11 May 2007

== "Hyperventilation can be self induced..." ==

This (misspelled) line, the last line of the first paragraph, is in direct conflict with the rest of the article. It reads that hyperventilation induces adrenaline rushes (not stated anywhere else in the article) and allows for clearer thought (while the article goes on to state that hyperventilation actually restricts blood flow to the brain). I'm going to remove it.

== Treatment (3) ==

Hi,

The section treatment now both discourages and prescribes the use of paper bags as a treatment for hyperventilation. For the uninformed reader, this will seem very confusing.

Also, the last paragraph above "treatment" begins in a weird way and contains seemingly nonsensical information. I would like to propose to remove it. Cheers, [[Special:Contributions/92.108.16.46|92.108.16.46]] ([[User talk:92.108.16.46|talk]]) 11:44, 25 February 2009 (UTC)

=="Hyperventilation is not the same as hyperpnoea."==

Under Causes, the article talks about how hyperventilation is not the same as [[hyperpnoea]], yet clicking the link for hyperpnoea is just a redirect back to this article. In other words... the article is linking to itself... [[User:Furrybeagle|Furrybeagle]] ([[User talk:Furrybeagle|talk]]) 22:46, 26 March 2009 (UTC)
hi,
i just want to know more about hyperventilation and it's relation to dental office including ( cause-symptoms-mechanism-treatment) thanks

== Solid Medical Evidence Related to Hyperventilation Is Necessary ==

Without specific numbers related to [[minute ventilation]] in healthy subjects, normal subjects, and in diseased states, the article about hyperventilation is nonsense. We should study science and provide public with hard core evidence (as in [[Evidence-based medicine]]), not some fantasies.
([[User:Artour2006|Artour2006]] ([[User talk:Artour2006|talk]]) 10:41, 23 January 2011 (UTC)).

:The table added appears to be [[WP:OR|original research]] synthesizing various minute ventilations from various conditions from disparate primary sources. I would much prefer a secondary source to add this information back in; as created, it isn't encyclopedic in nature anyways - we already describe the conditions that cause hyperventilation; adding a table with the exact minute ventilation from studies appears to place [[WP:UNDUE|undue weight]] on the specific conditions noted and not on others. [[User:Yobol|Yobol]] ([[User talk:Yobol|talk]]) 15:40, 23 January 2011 (UTC)

In order to prove that this Table is "synthesizing various minute ventilations from various conditions from disparate primary sources", you need a small thing: find medical evidence or a single study that confirms that some group of patients with heart disease (of asthma, or diabetes, or CF, etc.) had nearly normal breathing parameters at rest (minute ventilation, or respiratory frequency, etc.). Then you can claim that this table is "synthesizing...". 

Furthermore, we got here 4 medical doctors, who claim that this table 
{| class="wikitable" border="1"
|-
!Condition
!Minute ventilation (± standard deviation)
!Number of patients
!Reference
|-
|Normal breathing
|6 l/min
|None
|Medical textbooks: <ref name=Ganong>Ganong WF, Review of medical physiology, 15-th ed., 1995, Prentice Hall Int., London.</ref> <ref name=Guyton>Guyton AC, Physiology of the human body, 6-th ed., 1984, Suanders College Publ., Philadelphia.</ref> <ref name=McArdle>McArdle W.D., Katch F.I., Katch V.L., Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000.</ref> <ref name=Straub>Straub NC, Section V, The Respiratory System, in Physiology, eds. RM Berne & MN Levy, 4-th edition, Mosby, St. Louis, 1998.</ref>
|-
|Healthy Subjects
|6-7 l/min
|>400
|<ref name=Douglas>Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich CW, Respiration during sleep in normal man, Thorax. 1982 Nov; 37(11): p.840-844.</ref>
<ref name=Burki>Burki NK, Ventilatory effects of doxapram in conscious human subjects, Chest 1984 May; 85(5): p.600-604.</ref>
<ref name=Smits>Smits P, Schouten J, Thien T, Respiratory stimulant effects of adenosine in man after caffeine and enprofylline, Br J Clin Pharmacol. 1987 Dec; 24(6): p.816-819.</ref>
<ref name=Fuller>Fuller RW, Maxwell DL, Conradson TB, Dixon CM, Barnes PJ, Circulatory and respiratory effects of infused adenosine in conscious man, Br J Clin Pharmacol 1987 Sep; 24(3): p.306-317.</ref>
<ref name=Tanaka>Tanaka Y, Morikawa T, Honda Y, An assessment of nasal functions in control of breathing, J of Appl Physiol 1988, 65 (4); p.1520-1524.</ref>
<ref name=Turkey>Turley KR,McBride PJ, Wilmore LH,  Resting metabolic rate measured after subjects spent the night at home vs at a clinic, Am J of Clin Nutr 1993, 58, p.141-144.</ref>
<ref name=Bengtsson>Bengtsson J, Bengtsson A, Stenqvist O, Bengtsson JP, Effects of hyperventilation on the inspiratory to end-tidal oxygen difference, British J of Anaesthesia 1994; 73: p. 140-144.</ref>
<ref name=Sherman>Sherman MS, Lang DM, Matityahu A, Campbell D, Theophylline improves measurements of respiratory muscle efficiency, Chest 1996 Dec; 110(6): p. 437-414.</ref>
<ref name=Bell>Bell SC, Saunders MJ, Elborn JS, Shale DJ, Resting energy expenditure and oxygen cost of breathing in patients with cystic fibrosis, Thorax 1996 Feb; 51(2): 126-131.</ref>
<ref name=Parreira>Parreira VF, Delguste P, Jounieaux V, Aubert G, Dury M, Rodenstein DO, Effectiveness of controlled and spontaneous modes in nasal two-level positive pressure ventilation in awake and asleep normal subjects, Chest 1997 Nov 5; 112(5): p.1267-1277.</ref>
<ref name=Mancini>Mancini M, Filippelli M, Seghieri G, Iandelli I, Innocenti F, Duranti R, Scano G, Respiratory Muscle Function and Hypoxic Ventilatory Control in Patients With Type I Diabetes, Chest 1999; 115; p.1553-1562.</ref><ref name=></ref>
<ref name=Pinna>Pinna GD, Maestri R, La Rovere MT, Gobbi E, Fanfulla F, Effect of paced breathing on ventilatory and cardiovascular variability parameters during short-term investigations of autonomic function, Am J Physiol Heart Circ Physiol. 2006 Jan; 290(1): p.H424-433.</ref>
<ref name=Pathak>Pathak A, Velez-Roa S, Xhaët O, Najem B, van de Borne P, Dose-dependent effect of dobutamine on chemoreflex activity in healthy volunteers, Br J Clin Pharmacol. 2006 Sep; 62(3): p.272-279.</ref>
<ref name=Gujic>Gujic M, Houssière A, Xhaët O, Argacha JF, Denewet N, Noseda A, Jespers P, Melot C, Naeije R, van de Borne P, Does endothelin play a role in chemoreception during acute hypoxia in normal men? Chest. 2007 May; 131(5): p.1467-1472.</ref>
|-
|Normal Subjects
|9-17 l/min
|>400
|<ref name=clague>Clague JE, Carter J, Coakley J, Edwards RH, Calverley PM, Respiratory effort perception at rest and during carbon dioxide rebreathing in patients with dystrophia myotonica, Thorax 1994 Mar; 49(3): p.240-244.</ref>
<ref name=Dahan>Dahan A, van den Elsen MJ, Berkenbosch A, DeGoede J, Olievier IC, van Kleef JW, Halothane affects ventilatory afterdischarge in humans, Br J Anaesth 1995 May; 74(5): p.544-548.</ref>
<ref name=Clark>Clark AL, Chua TP, Coats AJ, Anatomical dead space, ventilatory pattern, and exercise capacity in chronic heart failure, Br Heart J 1995 Oct; 74(4): 377-380. </ref>
<ref name=Tant-96>Tantucci C, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Scionti L, Sorbini CA, Ventilatory response to exercise in diabetic subjects with autonomic neuropathy, J Appl Physiol 1996, 81(5): p.1978–1986.</ref>
<ref name=clark97>Clark AL, Volterrani M, Swan JW, Coats AJS, The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology, Heart 1997; 77: p.138-146.</ref>
<ref name=han>Han JN, Stegen K, Simkens K, Cauberghs M, Schepers R, Van den Bergh O, Clément J, Van de Woestijne KP, Unsteadiness of breathing in patients with hyperventilation syndrome and anxiety disorders, Eur Respir J 1997; 10: p. 167–176.</ref>
<ref name=Tantucci>Tantucci C, Scionti L, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Sorbini CA, Influence of autonomic neuropathy of different severities on the hypercapnic drive to breathing in diabetic patients, Chest. 1997 Jul; 112(1): 145-153.</ref>
<ref name=Epstein>Epstein SK, Zilberberg MD; Facoby C, Ciubotaru RL, Kaplan LM, Response to symptom-limited exercise in patients with the hepatopulmonary syndrome, Chest 1998; 114; p. 736-741.</ref>
<ref name=Bowler>Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.</ref>
<ref name=DeLorey>DeLorey DS, Babb TG, Progressive mechanical ventilatory constraints with aging, Am J Respir Crit Care Med 1999 Jul; 160(1): p.169-177.</ref>
<ref name=Tantuc-2001>Tantucci C, Bottini P, Fiorani C, Dottorini ML, Santeusanio F, Provinciali L, Sorbini CA, Casucci G, Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy, J Appl Physiol 2001, 90: p. 889–896. </ref>
<ref name=Bell2>Bell HJ, Feenstra W, Duffin J, The initial phase of exercise hyperpnoea in humans is depressed during a cognitive task, Experimental Physiology 2005 May; 90(3): p.357-365.</ref>
<ref name=Narkiew>Narkiewicz K, van de Borne P, Montano N, Hering D, Kara T, Somers VK, Sympathetic neural outflow and chemoreflex sensitivity are related to spontaneous breathing rate in normal men, Hypertension 2006 Jan; 47(1): p.51-55.</ref>
<ref name=Ahuja>Ahuja D, Mateika JH, Diamond MP, Badr MS, Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone, J Appl Physiol. 2007 May; 102(5): p.1832-1838.</ref>
<ref name=Travers>Travers J, Dudgeon DJ, Amjadi K, McBride I, Dillon K, Laveneziana P, Ofir D, Webb KA, O'Donnell DE, Mechanisms of exertional dyspnea in patients with cancer, J Appl Physiol 2008 Jan; 104(1): p.57-66.</ref>
|-
|Asthma	
|12 l/min
|101
|<ref name=McFadden>McFadden ER & Lyons HA, Arterial-blood gases in asthma, The New Engl J of Med 1968 May 9, 278 (19): 1027-1032.</ref>
|-
|Asthma
|15 l/min
|8
|<ref name=JohnsonBD1>Johnson BD, Scanlon PD, Beck KC, Regulation of ventilatory capacity during exercise in asthmatics, J Appl Physiol. 1995 Sep; 79(3): 892-901.</ref>
|-
|Asthma
|14.1 (±5.7) l/min
|39
|<ref name=Bowler>Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.</ref>
|-
|Asthma
|13 (±4) l/min
|17
|<ref name=Kassab>Kassabian J, Miller KD, Lavietes MH, Respiratory center output and ventilatory timing in patients with acute airway (asthma) and alveolar (pneumonia) disease, Chest 1982 May; 81(5): p.536-543.</ref>
|-
|Asthma
|13 (±2) l/min
|16
|<ref name=Chalupa>Chalupa DC, Morrow PE, Oberdörster G, Utell MJ, Frampton MW, Ultrafine particle deposition in subjects with asthma, Environmental Health Perspectives 2004 Jun; 112(8): p.879-882.</ref>
|-
|COPD
|14 (±2) l/min
|12
|<ref name=Palange>Palange P, Valli G, Onorati P, Antonucci R, Paoletti P, Rosato A, Manfredi F, Serra P, Effect of heliox on lung dynamic hyperinflation, dyspnea, and exercise endurance capacity in COPD patients, J Appl Physiol. 2004 Nov; 97(5): p.1637-1642. </ref>
|-
|COPD
|12 (±2) l/min
|10
|<ref name=Sinder>Sinderby C, Spahija J, Beck J, Kaminski D, Yan S, Comtois N, Sliwinski P, Diaphragm activation during exercise in chronic obstructive pulmonary disease, Am J Respir Crit Care Med 2001 Jun; 163(7): 1637-1641.</ref>
|-
|COPD
|14 l/min
|3
|<ref name=Stulbarg> Stulbarg MS, Winn WR, Kellett LE, Bilateral Carotid Body Resection for the Relief of Dyspnea in Severe Chronic Obstructive Pulmonary Disease, Chest 1989; 95 (5): p.1123-1128. </ref>
|-
|Heart disease
|14 (±4) l/min
|88
|<ref name=Clark>Clark AL, Chua TP, Coats AJ, Anatomical dead space, ventilatory pattern, and exercise capacity in chronic heart failure, Br Heart J 1995 Oct; 74(4): 377-380. </ref>
|-
|Heart disease
|12.2 (±3.3) l/min
|132
|<ref name=Fanfulla>Fanfulla F, Mortara , Maestri R, Pinna GD, Bruschi C, Cobelli F, Rampulla C, The development of hyperventilation in patients with chronic heart failure and Cheyne-Stokes respiration, Chest 1998; 114; p. 1083-1090.</ref>
|-
|... and about 25 more lines with a similar content
|}
are "from disparate primary sources" with "synthesizing" intentions. You, Yabol, in fact, claim that, for example, 3 doctors from Department of Cardiac Medicine, National Heart and Lung Institute, London, UK ""synthesized"" 88 patients with minute ventilation 15 (±4) L/min instead of normal 5-8 (or 6-7) L/min and then these medical ""synthesizers"
published their [[original research]] in British Heart Journal (1995 Oct; 74(4): 377-380.)

Or a group of 7 Italian doctors from the Respiratory Function Laboratory, IRCCS, S. Maugeri Foundation, Montescano Medical Center, Pavia specially selected 132 patients with minute ventilation 12 (±3) l/min and published their synthesis in Chest (1998; 114; p. 1083-1090.)

All together, you are now blaming about 150 authors of over 50 peer-reviewed published medical studies that they deliberately selected sick patients with abnormally large minute ventilation and healthy subjects with normal minute volumes. 

You are allowing yourself very strong claims, Yabol. ([[User:Artour2006|Artour2006]] ([[User talk:Artour2006|talk]]) 10:21, 24 January 2011 (UTC)).
([[User:Artour2006|Artour2006]] ([[User talk:Artour2006|talk]]) 10:19, 24 January 2011 (UTC)).

::Moved this here as per [[WP:MEDRS]]

<blockquote>== Prevalence of hyperventilation ==
[[Minute ventilation]] or [[respiratory minute volume]] is the volume of air which is inhaled (inhaled minute volume) or exhaled (exhaled minute volume) from a person's lungs in one minute. Medical evidence suggests that hyperventilation is a common clinical finding for a variety of chronic health problems. 
{| class="wikitable" border="1"
|-
!Condition
!Minute ventilation
!Number of subjects
!Reference
|-
|Normal breathing
|6 l/min
| - 
|Medical textbooks: <ref name=Ganong>Ganong WF, Review of medical physiology, 15-th ed., 1995, Prentice Hall Int., London.</ref> <ref name=Guyton>Guyton AC, Physiology of the human body, 6-th ed., 1984, Suanders College Publ., Philadelphia.</ref> <ref name=McArdle>McArdle W.D., Katch F.I., Katch V.L., Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000.</ref> <ref name=Straub>Straub NC, Section V, The Respiratory System, in Physiology, eds. RM Berne & MN Levy, 4-th edition, Mosby, St. Louis, 1998.</ref>
|-
|Healthy Subjects
|6-7 l/min
|>400
|<ref name=Douglas>Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich CW, Respiration during sleep in normal man, Thorax. 1982 Nov; 37(11): p.840-844.</ref> <ref name=Burki>Burki NK, Ventilatory effects of doxapram in conscious human subjects, Chest 1984 May; 85(5): p.600-604.</ref> <ref name=Smits>Smits P, Schouten J, Thien T, Respiratory stimulant effects of adenosine in man after caffeine and enprofylline, Br J Clin Pharmacol. 1987 Dec; 24(6): p.816-819.</ref> <ref name=Fuller>Fuller RW, Maxwell DL, Conradson TB, Dixon CM, Barnes PJ, Circulatory and respiratory effects of infused adenosine in conscious man, Br J Clin Pharmacol 1987 Sep; 24(3): p.306-317.</ref> <ref name=Tanaka>Tanaka Y, Morikawa T, Honda Y, An assessment of nasal functions in control of breathing, J of Appl Physiol 1988, 65 (4); p.1520-1524.</ref><ref name=Turkey>Turley KR,McBride PJ, Wilmore LH,  Resting metabolic rate measured after subjects spent the night at home vs at a clinic, Am J of Clin Nutr 1993, 58, p.141-144.</ref><ref name=Bengtsson>Bengtsson J, Bengtsson A, Stenqvist O, Bengtsson JP, Effects of hyperventilation on the inspiratory to end-tidal oxygen difference, British J of Anaesthesia 1994; 73: p. 140-144.</ref> <ref name=Sherman>Sherman MS, Lang DM, Matityahu A, Campbell D, Theophylline improves measurements of respiratory muscle efficiency, Chest 1996 Dec; 110(6): p. 437-414.</ref>
<ref name=Bell>Bell SC, Saunders MJ, Elborn JS, Shale DJ, Resting energy expenditure and oxygen cost of breathing in patients with cystic fibrosis, Thorax 1996 Feb; 51(2): 126-131.</ref>
<ref name=Parreira>Parreira VF, Delguste P, Jounieaux V, Aubert G, Dury M, Rodenstein DO, Effectiveness of controlled and spontaneous modes in nasal two-level positive pressure ventilation in awake and asleep normal subjects, Chest 1997 Nov 5; 112(5): p.1267-1277.</ref> <ref name=Mancini>Mancini M, Filippelli M, Seghieri G, Iandelli I, Innocenti F, Duranti R, Scano G, Respiratory Muscle Function and Hypoxic Ventilatory Control in Patients With Type I Diabetes, Chest 1999; 115; p.1553-1562.</ref> <ref name=Pinna>Pinna GD, Maestri R, La Rovere MT, Gobbi E, Fanfulla F, Effect of paced breathing on ventilatory and cardiovascular variability parameters during short-term investigations of autonomic function, Am J Physiol Heart Circ Physiol. 2006 Jan; 290(1): p.H424-433.</ref>
<ref name=Pathak>Pathak A, Velez-Roa S, Xhaët O, Najem B, van de Borne P, Dose-dependent effect of dobutamine on chemoreflex activity in healthy volunteers, Br J Clin Pharmacol. 2006 Sep; 62(3): p.272-279.</ref>
<ref name=Gujic>Gujic M, Houssière A, Xhaët O, Argacha JF, Denewet N, Noseda A, Jespers P, Melot C, Naeije R, van de Borne P, Does endothelin play a role in chemoreception during acute hypoxia in normal men? Chest. 2007 May; 131(5): p.1467-1472.</ref>
|-
|Normal Subjects
|9-17 l/min
|>400
|<ref name=clague>Clague JE, Carter J, Coakley J, Edwards RH, Calverley PM, Respiratory effort perception at rest and during carbon dioxide rebreathing in patients with dystrophia myotonica, Thorax 1994 Mar; 49(3): p.240-244.</ref> <ref name=Dahan>Dahan A, van den Elsen MJ, Berkenbosch A, DeGoede J, Olievier IC, van Kleef JW, Halothane affects ventilatory afterdischarge in humans, Br J Anaesth 1995 May; 74(5): p.544-548.</ref> <ref name=Clark>Clark AL, Chua TP, Coats AJ, Anatomical dead space, ventilatory pattern, and exercise capacity in chronic heart failure, Br Heart J 1995 Oct; 74(4): 377-380. </ref> <ref name=Tant-96>Tantucci C, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Scionti L, Sorbini CA, Ventilatory response to exercise in diabetic subjects with autonomic neuropathy, J Appl Physiol 1996, 81(5): p.1978–1986.</ref> <ref name=clark97>Clark AL, Volterrani M, Swan JW, Coats AJS, The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology, Heart 1997; 77: p.138-146.</ref> <ref name=han>Han JN, Stegen K, Simkens K, Cauberghs M, Schepers R, Van den Bergh O, Clément J, Van de Woestijne KP, Unsteadiness of breathing in patients with hyperventilation syndrome and anxiety disorders, Eur Respir J 1997; 10: p. 167–176.</ref> <ref name=Tantucci>Tantucci C, Scionti L, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Sorbini CA, Influence of autonomic neuropathy of different severities on the hypercapnic drive to breathing in diabetic patients, Chest. 1997 Jul; 112(1): 145-153.</ref> <ref name=Epstein>Epstein SK, Zilberberg MD; Facoby C, Ciubotaru RL, Kaplan LM, Response to symptom-limited exercise in patients with the hepatopulmonary syndrome, Chest 1998; 114; p. 736-741.</ref>
<ref name=Bowler>Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.</ref>
<ref name=DeLorey>DeLorey DS, Babb TG, Progressive mechanical ventilatory constraints with aging, Am J Respir Crit Care Med 1999 Jul; 160(1): p.169-177.</ref> <ref name=Tantuc-2001>Tantucci C, Bottini P, Fiorani C, Dottorini ML, Santeusanio F, Provinciali L, Sorbini CA, Casucci G, Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy, J Appl Physiol 2001, 90: p. 889–896. </ref> <ref name=Bell2>Bell HJ, Feenstra W, Duffin J, The initial phase of exercise hyperpnoea in humans is depressed during a cognitive task, Experimental Physiology 2005 May; 90(3): p.357-365.</ref> <ref name=Narkiew>Narkiewicz K, van de Borne P, Montano N, Hering D, Kara T, Somers VK, Sympathetic neural outflow and chemoreflex sensitivity are related to spontaneous breathing rate in normal men, Hypertension 2006 Jan; 47(1): p.51-55.</ref> <ref name=Ahuja>Ahuja D, Mateika JH, Diamond MP, Badr MS, Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone, J Appl Physiol. 2007 May; 102(5): p.1832-1838.</ref> <ref name=Travers>Travers J, Dudgeon DJ, Amjadi K, McBride I, Dillon K, Laveneziana P, Ofir D, Webb KA, O'Donnell DE, Mechanisms of exertional dyspnea in patients with cancer, J Appl Physiol 2008 Jan; 104(1): p.57-66.</ref>
|-
|Asthma	
|12 l/min
|101
|<ref name=McFadden>McFadden ER & Lyons HA, Arterial-blood gases in asthma, The New Engl J of Med 1968 May 9, 278 (19): 1027-1032.</ref>
|-
|Asthma
|15 l/min
|8
|<ref name=JohnsonBD1>Johnson BD, Scanlon PD, Beck KC, Regulation of ventilatory capacity during exercise in asthmatics, J Appl Physiol. 1995 Sep; 79(3): 892-901.</ref>
|-
|Asthma
|14.1 (±5.7) l/min
|39
|<ref name=Bowler>Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.</ref>
|-
|Asthma
|13 (±4) l/min
|17
|<ref name=Kassab>Kassabian J, Miller KD, Lavietes MH, Respiratory center output and ventilatory timing in patients with acute airway (asthma) and alveolar (pneumonia) disease, Chest 1982 May; 81(5): p.536-543.</ref>
|-
|Asthma
|13 (±2) l/min
|16
|<ref name=Chalupa>Chalupa DC, Morrow PE, Oberdörster G, Utell MJ, Frampton MW, Ultrafine particle deposition in subjects with asthma, Environmental Health Perspectives 2004 Jun; 112(8): p.879-882.</ref>
|-
|COPD
|14 (±2) l/min
|12
|<ref name=Palange>Palange P, Valli G, Onorati P, Antonucci R, Paoletti P, Rosato A, Manfredi F, Serra P, Effect of heliox on lung dynamic hyperinflation, dyspnea, and exercise endurance capacity in COPD patients, J Appl Physiol. 2004 Nov; 97(5): p.1637-1642. </ref>
|-
|COPD
|12 (±2) l/min
|10
|<ref name=Sinder>Sinderby C, Spahija J, Beck J, Kaminski D, Yan S, Comtois N, Sliwinski P, Diaphragm activation during exercise in chronic obstructive pulmonary disease, Am J Respir Crit Care Med 2001 Jun; 163(7): 1637-1641.</ref>
|-
|COPD
|14 l/min
|3
|<ref name=Stulbarg> Stulbarg MS, Winn WR, Kellett LE, Bilateral Carotid Body Resection for the Relief of Dyspnea in Severe Chronic Obstructive Pulmonary Disease, Chest 1989; 95 (5): p.1123-1128. </ref>
|-
|Heart disease
|14 (±4) l/min
|88
|<ref name=Clark>Clark AL, Chua TP, Coats AJ, Anatomical dead space, ventilatory pattern, and exercise capacity in chronic heart failure, Br Heart J 1995 Oct; 74(4): 377-380. </ref>
|-
|Heart disease
|12.2 (±3.3) l/min
|132
|<ref name=Fanfulla>Fanfulla F, Mortara , Maestri R, Pinna GD, Bruschi C, Cobelli F, Rampulla C, The development of hyperventilation in patients with chronic heart failure and Cheyne-Stokes respiration, Chest 1998; 114; p. 1083-1090.</ref>
|-
|Heart disease
|16 (±2) l/min
|11
|<ref name=JohnsonBD2>Johnson BD, Beck KC, Olson LJ, O'Malley KA, Allison TG, Squires RW, Gau GT, Ventilatory constraints during exercise in patients with chronic heart failure, Chest 2000 Feb; 117(2): 321-332.</ref>
|-
|Heart disease
|15 (±4) l/min
|22
|<ref name=Dimopoulou>Dimopoulou I, Tsintzas OK, Alivizatos PA, Tzelepis GE, Pattern of breathing during progressive exercise in chronic heart failure, Int J Cardiol. 2001 Dec; 81(2-3): 117-121.</ref>
|-
|Heart disease
|16 (±2) l/min
|11
|<ref name=Johnson1>Johnson BD, Beck KC, Olson LJ, O'Malley KA, Allison TG, Squires RW, Gau GT, Ventilatory constraints during exercise in patients with chronic heart failure, Chest 2000 Feb; 117(2): p. 321-332.</ref>
|-
|Heart disease
|15 (±4) l/min
|55
|<ref name=clark97>Clark AL, Volterrani M, Swan JW, Coats AJS, The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology, Heart 1997; 77: p.138-146.</ref>
|-
|Heart disease
|13 (±4) l/min
|15
|<ref name=banning>Banning AP, Lewis NP, Northridge DB, Elbom JS, Henderson AH, Perfusion/ventilation mismatch during exercise in chronic heart failure: an investigation of circulatory determinants, Br Heart J 1995; 74: p.27-33. </ref>
|-
|Heart disease
|14 (±2) l/min
|30
|<ref name=Buller>Buller NP, Poole-Wilson PA, Mechanism of the increased ventilatory response to exercise in patients with chronic heart failure, Heart 1990; 63; p.281-283.</ref>
|-
|Heart disease
|16 (±6) l/min
|20
|<ref name=Elborn>Elborn JS, Riley M, Stanford CF, Nicholls DP, The effects of flosequinan on submaximal exercise in patients with chronic cardiac failure, Br J Clin Pharmacol. 1990 May; 29(5): p.519-524.</ref>
|-
|Pulm hypertension
|12 (±2) l/min
|11
|<ref name=alonzo>D'Alonzo GE, Gianotti LA, Pohil RL, Reagle RR, DuRee SL, Fuentes F, Dantzker DR, Comparison of progressive exercise performance of normal subjects and patients with primary pulmonary hypertension, Chest 1987 Jul; 92(1): p.57-62. </ref>
|-
|Diabetes
|10-20 l/min
|28
|<ref name=Tantucci>Tantucci C, Scionti L, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Sorbini CA, Influence of autonomic neuropathy of different severities on the hypercapnic drive to breathing in diabetic patients, Chest. 1997 Jul; 112(1): 145-153.</ref>
|-
|Diabetes
|12-17 l/min
|26
|<ref name=Bottini>Bottini P, Dottorini ML, M. Cordoni MC, Casucci G, Tantucci C, Sleep-disordered breathing in nonobese diabetic subjects with autonomic neuropathy, Eur Respir J 2003; 22: p. 654–660.</ref>
|-
|Diabetes
|15 (±2) l/min
|45
|<ref name=Tantuc-2001>Tantucci C, Bottini P, Fiorani C, Dottorini ML, Santeusanio F, Provinciali L, Sorbini CA, Casucci G, Cerebrovascular reactivity and hypercapnic respiratory drive in diabetic autonomic neuropathy, J Appl Physiol 2001, 90: p. 889–896. </ref>
|-
|Diabetes
|12 (±2) l/min
|8
|<ref name=Mancini>Mancini M, Filippelli M, Seghieri G, Iandelli I, Innocenti F, Duranti R, Scano G, Respiratory Muscle Function and Hypoxic Ventilatory Control in Patients With Type I Diabetes, Chest 1999; 115; p.1553-1562.</ref>
|-
|Diabetes
|13 (±2) l/min
|20
|<ref name=Tant-96>Tantucci C, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Scionti L, Sorbini CA, Ventilatory response to exercise in diabetic subjects with autonomic neuropathy, J Appl Physiol 1996, 81(5): p.1978–1986.</ref>
|-
|Cystic fibrosis
|11-14 l/min
|6
|<ref name=Tepper>Tepper RS, Skatrud B, Dempsey JA, Ventilation and oxygenation changes during sleep in cystic fibrosis, Chest 1983; 84; p. 388-393. </ref>
|-
|Cystic fibrosis
|13 (±1.8) l/min
|10
|<ref name=Bell>Bell SC, Saunders MJ, Elborn JS, Shale DJ, Resting energy expenditure and oxygen cost of breathing in patients with cystic fibrosis, Thorax 1996 Feb; 51(2): 126-131.</ref>
|-
|Cystic fibrosis
|15 L/min
|15
|<ref name=Bell>Ward SA, Tomezsko JL, Holsclaw DS, Paolone AM, Energy expenditure and substrate utilization in adults with cystic fibrosis and diabetes mellitus, Am J Clin Nutr 1999;69:913–9.</ref>
|-
|Cystic fibrosis
|10 L/min
|11
|<ref name=Browning>Browning IB, D'Alonzo GE, Tobin MJ, Importance of respiratory rate as an indicator of respiratory dysfunction in patients with cystic fibrosis, Chest. 1990 Jun;97(6):1317-21.</ref>
|-
|Cystic fibrosis
|10 L/min
|10
|<ref name=Ward>Ward SA, Tomezsko JL, Holsclaw DS, Paolone AM, Energy expenditure and substrate utilization in adults with cystic fibrosis and diabetes mellitus, Am J Clin Nutr 1999;69:913–9.</ref>
|-
|Cystic fibrosis
|16 L/min
|7
|<ref name=Dodd>Dodd JD, Barry SC, Gallagher CG, Respiratory factors do not limit maximal symptom-limited exercise in patients with mild cystic fibrosis lung disease, Respiratory Physiology & Neurobiology 152 (2006) 176–185. </ref>
|-
|Cystic fibrosis
|18 L/min
|9
|<ref name=McKone>McKone, E.F., Barry, S.C., Fitzgerald, M.X., Gallagher, C.G., The role of arterial hypoxemia and pulmonary mechanics in exercise limitation in adults with cystic fibrosis, J Appl Physiol. 2005 Sep; 99(3): 1012-8.</ref>
|-
|Cancer
|12 (±2) l/min
|40
|<ref name=Travers>Travers J, Dudgeon DJ, Amjadi K, McBride I, Dillon K, Laveneziana P, Ofir D, Webb KA, O'Donnell DE, Mechanisms of exertional dyspnea in patients with cancer, J Appl Physiol 2008 Jan; 104(1): p.57-66.</ref>
|-
|Sleep apnea
|15 (±3) l/min
|20
|<ref name=radwan>Radwan L, Maszczyk Z, Koziorowski A, Koziej M, Cieslicki J, Sliwinski P, Zielinski J, Control of breathing in obstructive sleep apnea and in patients with the overlap syndrome, Eur Respir J. 1995 Apr; 8(4): p.542-545. </ref>
|-
|Liver cirrhosis
|11-18 l/min
|24
|<ref name=Epstein>Epstein SK, Zilberberg MD; Facoby C, Ciubotaru RL, Kaplan LM, Response to symptom-limited exercise in patients with the hepatopulmonary syndrome, Chest 1998; 114; p. 736-741.</ref>
|-
|Hyperthyroidism
|14.9 (±0.6) l/min
|42
|<ref name=Kahaly>Kahaly GJ, Nieswandt J, Wagner S, Schlegel J, Mohr-Kahaly S, Hommel G, Ineffective cardiorespiratory function in hyperthyroidism, J Clin Endocrinol Metab 1998 Nov; 83(11): 4075-4078.</ref>
|-
|Epilepsy
|12.8 l/min
|12
|<ref name=Esquivel>Esquivel E, Chaussain M, Plouin P, Ponsot G, Arthuis M, Physical exercise and voluntary hyperventilation in childhood absence epilepsy, Electroencephalogr Clin Neurophysiol 1991 Aug; 79(2): 127-132.</ref>
|-
|Panic disorder
|12 (±5) l/min
|12
|<ref name=pain>Pain MC, Biddle N, Tiller JW, Panic disorder, the ventilatory response to carbon dioxide and respiratory variables, Psychosom Med 1988 Sep-Oct; 50(5): p. 541-548. </ref>
|-
|CHV
|13 (±2) l/min
|134
|<ref name=han>Han JN, Stegen K, Simkens K, Cauberghs M, Schepers R, Van den Bergh O, Clément J, Van de Woestijne KP, Unsteadiness of breathing in patients with hyperventilation syndrome and anxiety disorders, Eur Respir J 1997; 10: p. 167–176.</ref>
|-
|Bipolar disorder
|11 (±2) l/min
|16
|<ref name=mackin>MacKinnon DF, Craighead B, Hoehn-Saric R, Carbon dioxide provocation of anxiety and respiratory response in bipolar disorder, J Affect Disord 2007 Apr; 99(1-3): p.45-49.</ref>
|-
|Dystrophia myotonica
|16 (±4) l/min
|12
|<ref name=clague>Clague JE, Carter J, Coakley J, Edwards RH, Calverley PM, Respiratory effort perception at rest and during carbon dioxide rebreathing in patients with dystrophia myotonica, Thorax 1994 Mar; 49(3): p.240-244.</ref>
|}

(Source: www.normalbreathing.com) There are many more medical studies that found 100% prevalence of chronic hyperventilation in patients with various chronic diseases and modern normal subjects.
{{reflist-talk}}
</blockquote>[[User:Jmh649|<span style="color:#0000f1">'''Doc James'''</span>]] ([[User talk:Jmh649|talk]] · [[Special:Contributions/Jmh649|contribs]] · [[Special:EmailUser/Jmh649|email]]) 13:14, 24 January 2011 (UTC)

== General Cleanup Tag: Syntax ==

Hi - This is just a quick note to say that I put the General Cleanup tag instead of making the change to the first sentence myself because the language is so convoluted that I can't quite make out what it means and am afraid I'd edit it incorrectly. Thanks! Sorry if I did anything incorrectly -- this is my first edit. :)
[[User:NicoSuave|NicoSuave]] ([[User talk:NicoSuave|talk]]) 23:02, 24 May 2011 (UTC)

== remove treament section ==

The treatment sectino as it stands is uselss and should be removed raher than left the way it is[[Special:Contributions/108.161.122.195|108.161.122.195]] ([[User talk:108.161.122.195|talk]]) 04:20, 30 April 2012 (UTC)
:I would say it should be left in but expanded and referenced, as it's an important medical condition. [[User:Td1wk|Td1wk]] ([[User talk:Td1wk|talk]]) 08:49, 30 April 2012 (UTC)

== unsourced ==

Moved the content here per [[WP:PRESERVE]] as it is unsourced -- what is sourced i also moved as leavning it would be UNDUE:

;Terminology

In very general terms, hyperventilation is an increased [[alveolar ventilation]]. Hyperventilation should not be confused with tachypnea (fast breathing) or [[hyperpnea]] (breathing that is faster or deeper than normal with an increased [[minute ventilation]]). Both of these terms neutrally describe the manner of breathing rather than the impact that breathing has on carbon dioxide levels. In tachypnea and hyperpnea, increased ventilation is appropriate for a metabolic acidotic state (also known as respiratory compensation) whereas in hyperventilation, increased ventilation is inappropriate for the metabolic state of blood plasma.

Exercise, fever, shivering, and other disorders can cause the body to produce more carbon dioxide than normal. The body attempts to correct for this by breathing more rapidly and deeply. This corrective behavior does not lead to excess ventilation. Rather, it brings the body into balance by compensating for excess [[carbon dioxide]] production. Thus, hyperpnea in this context is not hyperventilation. In fact, if the excess carbon dioxide production cannot be completely cast off via hyperpnea, then a person will in fact be [[hypoventilation|hypoventilating]] even though they are breathing faster or more deeply than normal. For example, in certain respiratory disorders, the transfer of carbon dioxide from the blood to the alveoli may be blocked. No matter how deeply or rapidly the person tries to breathe, they cannot expel enough carbon dioxide.

: from Causes
Hyperventilation can also occur when someone exercises over their [[VO2 max|VO<sub>2</sub> max]], when they're unable to generate sufficient energy through purely aerobic respiration, but hyperventilate in an effort to do so. The VO<sub>2</sub> max is a representation of an individual's aerobic capacity during exercise of large duration and low intensity (from 30 minutes to hours), for example the marathon. It is the highest rate of oxygen consumption reached during maximum exertion in long duration exercises. If the intensity of exercise increases past an individual's VO<sub>2</sub> max the consumption of oxygen will be relatively stabilized and the body will utilize anaerobic energy substrates, e.g. hepatic glycogen (a polysaccharide which stores glucose in the liver) through [[glycolysis]], also known as passing the [[anaerobic threshold]]. As the result of the above-mentioned process there is an increase of lactic acid and carbon dioxide in the blood and therefore a decrease of the pH of the blood. Carbon dioxide is transported as bicarbonate ion through the blood during the gaseous exchange of oxygen and carbon dioxide between alveoli and blood capillaries through the respiratory membrane. The increase of the level of carbon dioxide in the blood reflects the more anaerobic metabolism past the anaerobic threshold by (Wasserman and Mclllory) and hence provokes the hyperventilation.

;Mechanism 
In normal breathing, both the depth and frequency of breaths are varied by the nervous system, primarily in order to maintain normal amounts of carbon dioxide but also to supply appropriate levels of oxygen to the body's tissues. This is mainly achieved by measuring the carbon dioxide content of the blood; normally, a high carbon dioxide concentration signals a low oxygen concentration, as we breathe in oxygen and breathe out carbon dioxide at the same time, and the body's cells use oxygen to burn fuel molecules, making carbon dioxide as a by-product. Normal [[minute ventilation]] is generally 5–8 liters of air per minute at rest for a 70&nbsp;kg man.

If carbon dioxide levels are high, the body assumes that oxygen levels are low, and accordingly, the brain's blood vessels dilate to assure sufficient blood flow and supply of oxygen. Conversely, low carbon dioxide levels cause the brain's blood vessels to constrict, resulting in reduced blood flow to the brain and lightheadedness. The gases in the [[alveoli]] of the lungs are nearly in equilibrium with the gases in the [[blood]]. Normally, less than 10% of the gas in the alveoli is replaced with each breath taken. Deeper or quicker breaths as in hyperventilation exchange more of the alveolar gas with ambient air and have the net effect of expelling more carbon dioxide from the body, since the carbon dioxide concentration in normal air is very low. The resulting low concentration of carbon dioxide in the blood is known as [[hypocapnia]]. Since carbon dioxide is carried as [[bicarbonate]] in the blood, the loss of carbon dioxide will drive bicarbonate to combine with hydrogen ions (protons) to form more carbon dioxide. The loss of hydrogen ions results in the blood becoming [[alkaline]], i.e. the blood [[pH value]] rises. This is known as a [[respiratory alkalosis]].

This alkalization of the blood causes vessels to constrict ([[vasoconstriction]]). The high pH value resulting from hyperventilation also reduces the level of available [[calcium]] ([[hypocalcemia]]), which affects the nerves and muscles, causing constriction of blood vessels and tingling. This occurs because alkalization of the plasma proteins (mainly [[albumin]]) increases their calcium binding affinity, thereby reducing free ionized calcium levels in the blood. Therefore, low levels of carbon dioxide can cause [[Tetany (medical sign)|tetany]] by altering the albumin binding of calcium such that the ionised (physiologically influencing) fraction of calcium is reduced.

Therefore, there are two main mechanisms that contribute to the cerebral vasoconstriction that is responsible for the [[lightheadedness]], [[paresthesia]], and [[fainting]] often seen with hyperventilation. One mechanism is that low carbon dioxide ([[hypocapnia]]) causes increased blood pH level ([[respiratory alkalosis]]), causing blood vessels to constrict. The other mechanism is that the alkalosis causes decreased freely ionized blood calcium, thereby causing cell membrane instability and subsequent vasoconstriction and paresthesia.

Hyperventilation can be useful in the management of head trauma.  After head injuries, fluids can leak into the cranial vault, thus elevating intracranial pressure.  Since the total cranial volume is relatively fixed, and the brain is much more compressible than the skull, in settings of increased intracranial pressure, the brain is preferentially compressed and damaged.  Hyperventilation, and the resultant cerebral vasoconstriction, is useful in this situation, since it decreases the volume of blood in the brain.  Less blood volume in the cranial cavity results in less pressure compressing the brain.  However, this vasoconstriction comes at the cost of reducing blood flow to the brain, which can potentially result in ischemic damage.<ref>{{cite journal |vauthors=Stocchetti N, Maas AI, Chieregato A, van der Plas AA |title=Hyperventilation in head injury: a review |journal=Chest |volume=127 |issue=5 |pages=1812–27 |year=2005 |pmid=15888864 |doi=10.1378/chest.127.5.1812}}</ref>

;Treatment
{{Unreferenced section|date=November 2008}}
The first step that should be taken is to treat the underlying cause. If [[Hypoxia (medical)|hypoxia]] is present supplemental [[oxygen]] may be useful. If it is due to [[anxiety]] as the cause of [[hyperventilation syndrome]], counselling (such as [[cognitive behavioral therapy]]) to identify and address triggers may be useful, possibly supported by a few days of [[benzodiazepines]].
Mild hyperventilation can be treated by recycling some of the carbon dioxide released in one's breath.  This is traditionally done by breathing into a paper bag.
	
The [[Buteyko method]] will also reduce [[respiratory alkalosis]] in the short term and also claims to correct chronic hyperventilation by retraining the breathing pattern through repetitive breathing exercises although this is disputed.

{{reflist-talk}}
-- [[User:Jytdog|Jytdog]] ([[User talk:Jytdog|talk]]) 00:49, 30 November 2016 (UTC)

== Technique vs Condition ==

There is not enough balance in the article between the Technique vs Condition, for the moment it is 0% vs 100%. --[[User:TudorTulok|TudorTulok]] ([[User talk:TudorTulok|talk]]) 12:17, 13 May 2017 (UTC)