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an increased depth and rate of breathing greater than demanded by the body needs; can cause dizziness and tingling of the fingers and toes and chest pain if continued

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/12/27 16:14:20」(JST)

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Hyperventilation occurs when the lawl of alveolar ventilation of carbon dioxide exceeds body's production of carbon dioxide.^[1]^[2] Hyperventilation can be voluntary or involuntary.

When alveolar ventilation is excessive, more carbon dioxide will be removed from the blood stream than the body can produce. This causes the concentration of carbon dioxide in the blood stream to fall and produces a state known as hypocapnia. The body normally attempts to compensate for this metabolically. If excess ventilation cannot be compensated metabolically, it will lead to a rise in blood pH. This rise in blood pH is known as respiratory alkalosis. When hyperventilation leads to respiratory alkalosis, it may cause a number of physical symptoms: dizziness, tingling in the lips, hands or feet, headache, weakness, fainting and seizures. In extreme cases it can cause carpopedal spasms (flapping and contraction of the hands and feet).^[3]

Distinction from other breathing terms

In very general terms, hyperventilation is an increased alveolar ventilation. This is not to be confused with the term hyperpnea which pertains to an increased minute ventilation. In 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.

Hyperventilation should not be confused with tachypnea (fast breathing) or hyperpnea (breathing that is faster or deeper than normal). Both these terms neutrally describe the manner of breathing rather than the impact that breathing has on carbon dioxide levels. 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 CO2 production. Thus hyperpnea in this context is not hyperventilation.

In fact, if the excess CO2 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 deep or fast the person tries to breathe, they cannot expel enough carbon dioxide.

Causes

Hyperventilation can be voluntary or involuntary.

Swimmers sometimes voluntarily hyperventilate in hopes of extending dive time or extending the length of time they can swim underwater without rising to take a breath, though this puts them at risk for shallow water blackout.^[4] Anesthesiologists sometimes recommend that their patients hyperventilate prior to putting them under general anesthesia.^[5] Certain kinds of Yoga, for example, Bhastrika yoga also employ voluntary hyperventilation.

Involuntary hyperventilation can occur in response to both physical and emotional stimuli. These include reduced air pressure at high altitudes,^[6] raised progesterone levels in pregnancy, head injury, stroke, respiratory disorders such as asthma and pneumonia, cardiovascular problems such as pulmonary embolisms, anemia, adverse reactions to certain drugs, physical or emotional stress, fear, pain, and anxiety. Hyperventilation can also be mechanically produced in people on respirators.^[7]

Stress or anxiety commonly are causes of hyperventilation; this is known as hyperventilation syndrome.^[8] Hyperventilation can also be brought about voluntarily, by taking many deep breaths in rapid succession. Hyperventilation can also occur as a consequence of various lung diseases, head injury, or stroke (central neurogenic hyperventilation, apneustic respirations, ataxic respiration, Cheyne–Stokes respiration or Biot's respiration) and various lifestyle causes. In the case of metabolic acidosis, the body uses hyperventilation as a compensatory mechanism to decrease acidity of the blood. In the setting of diabetic ketoacidosis, this is known as Kussmaul breathing – characterized by long, deep breaths.

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 neural (or 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.^[9]

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, counseling (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 carbondioxide released in one's breath. This is traditionally done by breathing into a paper bag.

References

^ [1]
^ yourdictionary.com > hyperventilation Citing: The American Heritage® Dictionary of the English Language, 4th edition Copyright 2010
^ [2]
^ [3]
^ [4]
^ Kenneth Baillie and Alistair Simpson. "Hyperventilation calculator". Apex (Altitude Physiology EXpeditions). Retrieved 2006-08-10. – Online interactive oxygen delivery calculator that mimics hyperventilation
^ [5]
^ Sauty, A; Prosper, M (2008-11-19). "[The hyperventilation syndrome]". Revue medicale suisse 4 (180): 2500, 2502–5. PMID 19127893.
^ Stocchetti N, Maas AI, Chieregato A, van der Plas AA (2005). "Hyperventilation in head injury: a review". Chest 127 (5): 1812–27. doi:10.1378/chest.127.5.1812. PMID 15888864.

UpToDate Contents

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1. 過換気症候群 hyperventilation syndrome
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3. 成人における頭蓋内圧亢進の評価およびマネージメント evaluation and management of elevated intracranial pressure in adults
4. 小児における頭蓋内圧亢進（ICP） elevated intracranial pressure icp in children
5. 動悸を呈する小児に対するアプローチ approach to the child with palpitations

English Journal

Association Between Hypocapnia and Febrile Seizures.

Kilicaslan B1, Erol I, Ozkale Y, Saygi S, Sariturk C.Author information 11Baskent University Faculty of Medicine, Adana Teaching and Medical Research Center, Department of Pediatrics, Adana, Turkey.AbstractThe purpose of this study is to determine whether hyperthermia-induced hyperventilation with subsequent hypocapnia is relevant to febrile seizures in children. This is only the second study to measure pCO2 and pH values in children with febrile seizures. This prospective case-control study enrolled 18 children who presented with febrile seizures and 18 children who presented with a febrile illness without seizures. Venous blood gas analyses were measured both from the febrile seizure and control group. There was no significant difference in mean blood pH between the febrile seizure and control groups but blood pCO2 was significantly lower in the febrile seizure group. Patients with complex febrile seizures exhibited significantly lower pCO2 levels within 1 hour of seizure onset than patients with simplex febrile seizures. These data indicate that febrile seizures may be associated with hyperventilation and that the ensuing hypocapnia may contribute to the development of febrile seizures.
Journal of child neurology.J Child Neurol.2014 May;29(5):599-602. Epub 2014 Jan 5.
The purpose of this study is to determine whether hyperthermia-induced hyperventilation with subsequent hypocapnia is relevant to febrile seizures in children. This is only the second study to measure pCO2 and pH values in children with febrile seizures. This prospective case-control study enrolled
PMID 24396127

Adolescent girls with emotional disorders have a lower end-tidal CO2 and increased respiratory rate compared with healthy controls.

Henje Blom E1, Serlachius E, Chesney MA, Olsson EM.Author information 1Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Psychiatry, University of California San Francisco, San Francisco, USA.AbstractHyperventilation has been linked to emotional distress in adults. This study investigates end-tidal carbon dioxide (ETCO2 ), respiratory rate (RR), and heart rate variability (HRV) in adolescent girls with emotional disorders and healthy controls. ETCO2 , RR, HRV, and ratings of emotional symptom severity were collected in adolescent female psychiatric patients with emotional disorders (n = 63) and healthy controls (n = 62). ETCO2 and RR differed significantly between patients and controls. ETCO2 , HR, and HRV were significant independent predictors of group status, that is, clinical or healthy, while RR was not. ETCO2 and RR were significantly related to emotional symptom severity and to HRV in the total group. ETCO2 and RR were not affected by use of selective serotonin reuptake inhibitors. It is concluded that emotional dysregulation is related to hyperventilation in adolescent girls. Respiratory-based treatments may be relevant to investigate in future research.
Psychophysiology.Psychophysiology.2014 May;51(5):412-8. doi: 10.1111/psyp.12188. Epub 2014 Feb 27.
Hyperventilation has been linked to emotional distress in adults. This study investigates end-tidal carbon dioxide (ETCO2 ), respiratory rate (RR), and heart rate variability (HRV) in adolescent girls with emotional disorders and healthy controls. ETCO2 , RR, HRV, and ratings of emotional symptom se
PMID 24571123

The effect of centrally injected CDP-choline on respiratory system; involvement of phospholipase to thromboxane signaling pathway.

Topuz BB1, Altinbas B1, Yilmaz MS2, Saha S3, Batten TF3, Savci V2, Yalcin M4.Author information 1Department of Physiology, Faculty of Veterinary Medicine, Uludag University, Bursa 16059, Turkey.2Department of Pharmacology and Clinical Pharmacology, Faculty of Medicine, Uludag University, Bursa 16059, Turkey.3Division of Cardiovascular and Diabetes Research, Leeds Institute of Genetics, Health and Therapeutics, University of Leeds, Leeds LS2 9JT, UK.4Department of Physiology, Faculty of Veterinary Medicine, Uludag University, Bursa 16059, Turkey. Electronic address: muraty@uludag.edu.tr.AbstractCDP-choline is an endogenous metabolite in phosphatidylcholine biosynthesis. Exogenous administration of CDP-choline has been shown to affect brain metabolism and to exhibit cardiovascular, neuroendocrine neuroprotective actions. On the other hand, little is known regarding its respiratory actions and/or central mechanism of its respiratory effect. Therefore the current study was designed to investigate the possible effects of centrally injected CDP-choline on respiratory system and the mediation of the central cholinergic receptors and phospholipase to thromboxane signaling pathway on CDP-choline-induced respiratory effects in anaesthetized rats. Intracerebroventricularly (i.c.v.) administration of CDP-choline induced dose- and time-dependent increased respiratory rates, tidal volume and minute ventilation of male anaesthetized Spraque Dawley rats. İ.c.v. pretreatment with atropine failed to alter the hyperventilation responses to CDP-choline whereas mecamylamine, cholinergic nicotinic receptor antagonist, mepacrine, phospholipase A2 inhibitor, and neomycin phospholipase C inhibitor, blocked completely the hyperventilation induced by CDP-choline. In addition, central pretreatment with furegrelate, thromboxane A2 synthesis inhibitor, also partially blocked CDP-choline-evoked hyperventilation effects. These data show that centrally administered CDP-choline induces hyperventilation which is mediated by activation of central nicotinic receptors and phospholipase to thromboxane signaling pathway.
Respiratory physiology & neurobiology.Respir Physiol Neurobiol.2014 May 1;195:50-8. doi: 10.1016/j.resp.2014.02.005. Epub 2014 Feb 18.
CDP-choline is an endogenous metabolite in phosphatidylcholine biosynthesis. Exogenous administration of CDP-choline has been shown to affect brain metabolism and to exhibit cardiovascular, neuroendocrine neuroprotective actions. On the other hand, little is known regarding its respiratory actions a
PMID 24560778

Japanese Journal

回腸新膀胱造設術後早期に代謝性アシドーシスおよびテタニーを来たした1例

野村広徳,洪陽子,金城孝則,野々村大地,米田傑,山本致之,鄭則秀,高田晋吾,松宮清美
泌尿器科紀要 59(8), 535-538, 2013-08
… Tetany due to hyperventilation syndrome appeared on postoperative day42. … After re-removal of the urethral catheter, however, hyperventilation syndrome recurred. …
NAID 120005322751

過換気症候群 (特集呼吸器救急対応のコツとピットフォール回避法) -- (救急疾患・病態)

齋藤兄治
救急医学 = The Japanese journal of acute medicine 37(6), 689-693, 2013-06
NAID 40019704558

Low Serum Concentrations of Vitamin B6 and Iron Are Related to Panic Attack and Hyperventilation Attack

Mikawa Yasuhito,Mizobuchi Satoshi,Egi Moritoki,Morita Kiyoshi
Acta Medica Okayama 67(2), 99-104, 2013-04
… Patients undergoing a panic attack (PA) or a hyperventilation attack (HVA) are sometimes admitted to emergency departments (EDs). …
NAID 120005232500