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Hyperventilation

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Hyperventilation

Hyperventilation or overbreathing is the act of breathing faster or deeper than normal (hyperpnoea),[1] causing excessive expulsion of circulating carbon dioxide. This causes the arterial concentration of carbon dioxide (PaCO2) to fall below normal (35–45 mmHg), raising blood pH and resulting in alkalosis.[2] It can result from a psychological state such as a panic attack or cold shock, from a physiological condition such as metabolic acidosis, lifestyle risk factors or voluntarily as in the yogic practice of Bhastrika. Distinct from labored breathing when that is a natural response to higher than normal carbon dioxide levels. Chronic obstructive pulmonary disease, (COPD), asthma and multiple panic disorders have also been identified.

Hyperventilation can sometimes cause symptoms such as numbness or tingling in the hands, feet and lips, lightheadedness, dizziness, headache, chest pain, flexor spasm of hands and feet (carpopedal spasm),[3] slurred speech, nervous laughter, and sometimes fainting, particularly when accompanied by the Valsalva maneuver.

Counterintuitively, such effects are not precipitated by the sufferer's lack of oxygen or air. Rather, the hyperventilation itself reduces the carbon dioxide concentration of the blood to below its normal level because one is expiring more carbon dioxide than what is being produced in the body, thereby raising the blood's pH value (making it more alkaline), initiating constriction of the blood vessels which supply the brain, and preventing the transport of oxygen and other molecules necessary for the function of the nervous system.[4] At the same time, hypocapnia causes a higher affinity of oxygen to haemoglobin, known as the Bohr effect, further reducing the amount of oxygen that is made available to the brain.

Causes

Stress or anxiety commonly are causes of hyperventilation; this is known as hyperventilation syndrome.[5] 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 polisaccharide 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.

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.

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, parasthesia, 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 parasthesia.

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.[6]

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, a few days of benzodiazepines and psychological referral for cognitive behavioral therapy may be useful.

References

  1. ^ Martin, Elizabeth A (ed.) (2003). Oxford concise medical dictionary (6th ed. w. corrections & new cover). Oxford University Press. p. 334. ISBN 10:0-19-860753-9
  2. ^ yourdictionary.com > hyperventilation Citing: The American Heritage® Dictionary of the English Language, 4th edition Copyright 2010
  3. ^ http://www.ncemi.org/cse/cse0102.htm
  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 (2008-11-19). "[The hyperventilation syndrome]". Revue medicale suisse. 4 (180): 2500, 2502–5. PMID 19127893. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  6. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)

See also