In medicine, hyperventilation (or overbreathing) is the state of breathing faster and/or deeper than necessary. It can result from a psychological state such as a panic attack, from a physiological condition such as metabolic acidosis, or can be brought about voluntarily.
Hyperventilation can, but does not necessarily always cause symptoms such as numbness or tingling in the hands, feet and lips, lightheadedness, dizziness, headache, chest pain, 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, 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.
Stress or anxiety commonly are causes of hyperventilation; this is known as hyperventilation syndrome. Hyperventilation can also be brought about voluntarily, by taking many deep breaths. Hyperventilation can also occur as a consequence of various lung diseases, head injury, or stroke (central neurogenic hyperventilation, apneustic respirations, ataxic respiration, Cheyne-Stokes respirations or Biot's respiration). Lastly, 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 his/her VO2 max, when he/she can't transform oxygen into energy beyond a certain level but hyperventilates in an effort to do so.
Hyperventilation is not the same as hyperpnea. In hyperpnea, increased ventilation is appropriate for a metabolic acidotic state, this is also known as respiratory compensation. Whereas in hyperventilation, increased ventilation is inappropriate for the metabolic state of blood plasma.
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.
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 carbonic acid in the blood, hypocapnia results in the blood becoming alkaline, i.e. the blood pH value rises. This is known as a respiratory alkalosis.
This alkalinization of the blood causes vessels to constrict (vasoconstriction); it is theorized that myofibrillar calcium sensitivity is increased in the presence of high pH value.
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 alkalinization of the plasma proteins (mainly albumin) increases their calcium binding affinity, thereby reducing free ionized calcium levels in the blood.
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), which causes 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.
Although it seems counterintuitive, breathing too much can thus result in a decrease in the blood supply to the brain. Doctors sometimes artificially induce hyperventilation after head injury to reduce the pressure in the skull, though the treatment has potential risks.
The first step that should be taken is to treat the underlying cause of the hyperventilation. The patient should be encouraged to control his/her breathing. If this cannot be achieved, supplemental oxygen may be given to reduce tissue hypoxia. For possible behavior therapy see Treatment in Hyperventilation syndrome. Drug management is sometimes necessary. Parenteral drugs may have to be administered to reduce the patients anxiety and to slow the rate of breathing. Diazepam or midazolam are sometimes used.