to treat. There is a dissenting view on the full extent how and when a person reaches a stage of permanent injury, but it is agreed that pressure on the vagus nerve causes changes to pulse rate and blood pressure and is dangerous in cases of carotid sinus hypersensitivity. Increased breathing The second mechanism requires hyperventilation (forced overbreathing) until symptoms of hypocapnia such as tingling, light-headedness or dizziness are felt, followed by a breath-hold. This alone is enough to cause a blackout, but it is widely believed that the effect is enhanced if lung air pressure is increased by holding the breath "hard" or "bearing down" (tightening the diaphragm as in a forced exhalation while allowing no air to escape or having an assistant apply a bear-hug). These latter actions may augment the effects of hypoxia by approximating the Valsalva maneuver, causing vagal stimulation. The hyperventilation leads to an excessive elimination of carbon dioxide (CO2) whereas no significant additional amounts of oxygen can be stocked in the body. As only carbon dioxide is responsible for the breathing stimulus, after hyperventilation, breath can be held longer until cerebral hypoxia occurs. The blood also becomes abnormally alkaline as a result of the excessive elimination of carbon dioxide; this subsequent rise in blood pH is termed alkalosis. Alkalosis interferes with normal oxygen utilization by the brain. The symptoms of alkalosis are neuromuscular irritability, muscular spasms, tingling and numbness of the extremities and around the mouth, and a dizziness, or giddiness, often interpreted as a sense of euphoria. In the body alkalosis generally induces vasodilation (widening of the blood vessels) but in the brain alone it causes vasoconstriction (narrowing of the blood vessels). This vasoconstriction appears to be made even worse by a sudden increase in blood pressure caused by squeezing or holding the breath "hard". The alkalosis-induced euphoria can be followed rapidly by hypoxia-induced unconsciousness. The sequence of events leading to unconsciousness from hyperventilation is as follows: Decrease in partial pressure of alveolar CO2. Decrease in partial pressure of arterial CO2. Increase in blood pH, (respiratory alkalosis). Vasoconstriction of blood vessels supplying brain. Pooling of the blood present in the brain at the time. Brain rapidly uses up oxygen (O2) available in the pooled blood. O2 concentration in the brain drops. Unconsciousness from hypoxia of cerebral tissue. Because the brain cannot store reserves of oxygen and, unlike other organs, has an exceedingly low