Talk:Hyperventilation

message: :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? AxelBoldt 05:26, 24 Dec 2004 (UTC)
replies: text: 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). Alex.tan 17:48, 25 Dec 2004 (UTC)
replies: text: In 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. AxelBoldt 21:36, 1 Jan 2005 (UTC)
replies: text: 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. Alex.tan 14:36, 6 Jan 2005 (UTC)
thread_title: Heading 1

message: 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!  Ayvah 13:13, 8 June 2006 (UTC)
replies: text: 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... Jay 01:09, 7 April 2007 (UTC)
replies: text: 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).  Cmcnicoll 18:32, 13 April 2007 (UTC)

text: Done.    --209.244.43.122 (talk) 20:41, 5 March 2008 (UTC)
thread_title: Split

message: This section needs both revisions and additions. VodkaJazz 21:59, 28 January 2006 (UTC)
thread_title:  Treatment 

message: 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, 92.108.16.46 (talk) 11:44, 25 February 2009 (UTC)
thread_title:  Treatment (3) 

message: 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... Furrybeagle (talk) 22:46, 26 March 2009 (UTC)
thread_title: "Hyperventilation is not the same as hyperpnoea."

message: 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.
(Artour2006 (talk) 10:41, 23 January 2011 (UTC)
replies: text: The table added appears to be 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 undue weight on the specific conditions noted and not on others. Yobol (talk) 15:40, 23 January 2011 (UTC)
replies: text: Moved this here as per WP:MEDRS
== 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. 
Condition           	Minute ventilation	Number of subjects	Reference
Normal breathing    	6 l/min           	-                 	Medical textbooks: Ganong WF, Review of medical physiology, 15-th ed., 1995, Prentice Hall Int., London. Guyton AC, Physiology of the human body, 6-th ed., 1984, Suanders College Publ., Philadelphia. McArdle W.D., Katch F.I., Katch V.L., Essentials of exercise physiology (2-nd edition); Lippincott, Williams and Wilkins, London 2000. Straub NC, Section V, The Respiratory System, in Physiology, eds. RM Berne & MN Levy, 4-th edition, Mosby, St. Louis, 1998.
Healthy Subjects    	6-7 l/min         	>400              	Douglas NJ, White DP, Pickett CK, Weil JV, Zwillich CW, Respiration during sleep in normal man, Thorax. 1982 Nov; 37(11): p.840-844. Burki NK, Ventilatory effects of doxapram in conscious human subjects, Chest 1984 May; 85(5): p.600-604. 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. 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. 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.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.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. Sherman MS, Lang DM, Matityahu A, Campbell D, Theophylline improves measurements of respiratory muscle efficiency, Chest 1996 Dec; 110(6): p. 437-414.
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.
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. 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. 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.
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.
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.
Normal Subjects     	9-17 l/min        	>400              	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. 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. 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.  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. 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. 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. 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. 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.
Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.
DeLorey DS, Babb TG, Progressive mechanical ventilatory constraints with aging, Am J Respir Crit Care Med 1999 Jul; 160(1): p.169-177. 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.  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. 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. 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. 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.
Asthma              	12 l/min          	101               	McFadden ER & Lyons HA, Arterial-blood gases in asthma, The New Engl J of Med 1968 May 9, 278 (19): 1027-1032.
Asthma              	15 l/min          	8                 	Johnson BD, Scanlon PD, Beck KC, Regulation of ventilatory capacity during exercise in asthmatics, J Appl Physiol. 1995 Sep; 79(3): 892-901.
Asthma              	14.1 (±5.7) l/min 	39                	Bowler SD, Green A, Mitchell CA, Buteyko breathing techniques in asthma: a blinded randomised controlled trial, Med J of Australia 1998; 169: 575-578.
Asthma              	13 (±4) l/min     	17                	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.
Asthma              	13 (±2) l/min     	16                	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.
COPD                	14 (±2) l/min     	12                	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.
COPD                	12 (±2) l/min     	10                	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.
COPD                	14 l/min          	3                 	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.
Heart disease       	14 (±4) l/min     	88                	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.
Heart disease       	12.2 (±3.3) l/min 	132               	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.
Heart disease       	16 (±2) l/min     	11                	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.
Heart disease       	15 (±4) l/min     	22                	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.
Heart disease       	16 (±2) l/min     	11                	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.
Heart disease       	15 (±4) l/min     	55                	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.
Heart disease       	13 (±4) l/min     	15                	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.
Heart disease       	14 (±2) l/min     	30                	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.
Heart disease       	16 (±6) l/min     	20                	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.
Pulm hypertension   	12 (±2) l/min     	11                	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.
Diabetes            	10-20 l/min       	28                	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.
Diabetes            	12-17 l/min       	26                	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.
Diabetes            	15 (±2) l/min     	45                	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.
Diabetes            	12 (±2) l/min     	8                 	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.
Diabetes            	13 (±2) l/min     	20                	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.
Cystic fibrosis     	11-14 l/min       	6                 	Tepper RS, Skatrud B, Dempsey JA, Ventilation and oxygenation changes during sleep in cystic fibrosis, Chest 1983; 84; p. 388-393.
Cystic fibrosis     	13 (±1.8) l/min   	10                	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.
Cystic fibrosis     	15 L/min          	15                	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.
Cystic fibrosis     	10 L/min          	11                	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.
Cystic fibrosis     	10 L/min          	10                	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.
Cystic fibrosis     	16 L/min          	7                 	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.
Cystic fibrosis     	18 L/min          	9                 	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.
Cancer              	12 (±2) l/min     	40                	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.
Sleep apnea         	15 (±3) l/min     	20                	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.
Liver cirrhosis     	11-18 l/min       	24                	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.
Hyperthyroidism     	14.9 (±0.6) l/min 	42                	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.
Epilepsy            	12.8 l/min        	12                	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.
Panic disorder      	12 (±5) l/min     	12                	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.
CHV                 	13 (±2) l/min     	134               	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.
Bipolar disorder    	11 (±2) l/min     	16                	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.
Dystrophia myotonica	16 (±4) l/min     	12                	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.
(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.
Doc James (talk · contribs · email) 13:14, 24 January 2011 (UTC)
thread_title:  Solid Medical Evidence Related to Hyperventilation Is Necessary 

message: 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. :)
NicoSuave (talk) 23:02, 24 May 2011 (UTC)
thread_title:  General Cleanup Tag: Syntax 

message: The treatment sectino as it stands is uselss and should be removed raher than left the way it is108.161.122.195 (talk) 04:20, 30 April 2012 (UTC)
replies: text: I would say it should be left in but expanded and referenced, as it's an important medical condition. Td1wk (talk) 08:49, 30 April 2012 (UTC)
thread_title:  remove treament section 

message: 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 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, when they're unable to generate sufficient energy through purely aerobic respiration, but hyperventilate in an effort to do so. The VO2 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 VO2 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 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 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.
;Treatment
The first step that should be taken is to treat the underlying cause. If 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.
-- Jytdog (talk) 00:49, 30 November 2016 (UTC)
thread_title:  unsourced 

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