hyperventilation tetany


In medicine, hyperventilation (or overbreathing) is the state of breathing faster and/or deeper than necessary, bringing about lightheadedness and other undesirable symptoms often associated with panic attacks. Counterintuitively, such side effects are not precipitated by the suffer's lack of oxygen or air, but rather, the hyperventilation itself reduces the carbon dioxide concentration of the blood to below its normal level, altering the blood's pH value, initiating constriction of the blood vessels which supply the brain, and preventing the transport of certain electrolytes necessary for the function of the nervous system.

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 and sometimes fainting, particularly when accompanied by the Valsalva maneuver. Sometimes hyperventilation is induced for these same effects.


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 increased acidity of the blood. In the setting of Diabetic Ketoacidosis, this is known as Kussmaul breathing - characterized by long, deep breaths.

Hyperventilation is not the same as hyperpnoea. In hyperpnoea, 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 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 done 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 to carbon dioxide.

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 each breath. Deeper or quicker breaths exchange more of the alveolar gas with air and have the net effect of drawing more carbon dioxide out of 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 held in the blood mostly in the form of carbonic acid, hypocapnia results in the blood becoming alkaline, i.e. the blood pH value rises. (Normally, this alkalosis would automatically be countered by reduced breathing, but for various reasons this doesn't happen when the neural control is not present.)

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 (e.g. from hyperventilation) cause the brain's blood vessels to constrict, resulting in reduced blood flow to the brain and lightheadedness. The alkalinization of blood due to hypocapnia is the mechanism by which vessels constrict; it is theorized that myofibrillar calcium sensitivity is increased in the presence of low hydrogen ion concentration.

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 subsequent parasthesia and lightheadedness. This occurs because alkalinization of the plasma proteins (mainly albumin) increases their calcium binding affinity, thereby reducing free ionized calcium levels.

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 decreased hydrogen ion concentration (respiratory alkalosis), which causes blood vessels to constrict. The other mechanism is that the decrease in hydrogen ions (alkalosis) causes decreased freely ionized blood calcium, thereby causing cell membrane instability and subsequent vasoconstriction.

Although it seems counterintuitive, breathing too much can result in a decrease in the oxygen 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 their breathing. If this cannot be achieved, supplemental oxygen may be given to reduce tissue hypoxia. Oxygen therapy should be continued until a hypoxic episode has been clinically discounted.


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