Hyperventilation

Hyperventilation or overbreathing is the state of increased respiratory rate in a person, being inappropriately high in regard to the respiratory drive from carbon dioxide, or causing inappropriate decrease of it. It can result from a psychological state such as a panic attack, from a physiological condition such as metabolic acidosis, can be brought about by lifestyle risk factors or voluntarily as in the yogic practice of Bhastrika. It often occurs together with labored breathing, which, in contrast, can also be a response to increased carbon dioxide levels.

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 because one is expiring more carbon dioxide than 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. 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 however is a diagnosis of exclusion. 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 respirations or Biot's respiration) and various lifestyle causes. 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 their VO2 max, when they're unable to transform oxygen into energy beyond a certain level but hyperventilates in an effort to do so.

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

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.

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, 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, 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), 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.

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, benzodiazepines may be useful.