question: Why exactly happens that makes brain damage permanent after three minutes of oxygen deprivation?
comment: The brain needs a constant supply of oxygen to keep its cells alive and functioning. When the blood circulating to the brain cells is either cut off or is not receiving enough oxygen to adequately supply the brain cells, they essentially starve to death. The same happens when people have cardiac issues where blood is cut off to the heart and parts of the heart muscle die if too much time passes before oxygen flow is restored.
passages: However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory. If oxygen deprivation continues, cognitive disturbances, and decreased motor control will result. The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.
   Some examples of people that have returned from this apparent interruption of life lasting over half an hour, two hours, eight hours or more while adhering to these specific conditions for oxygen and temperature have been reported and analysed in depth, but these cases are not considered scientifically valid. The brain begins to die after five minutes without oxygen; nervous tissues die intermediately when a "somatic death" occurs while muscles die over one to two hours following this last condition.
   In severe cases it is extremely important to act quickly. Brain cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes.
  
  Section::::Prognosis.
  
  Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia; on the other hand, the outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.
   The term latent hypoxia strictly refers to the situation while the potential victim is still conscious, but is also loosely applied to the consequential blackout, which is a form of hypoxic blackout also referred to as blackout of ascent or deep water blackout, though deep water blackout is also used to refer to the final stage of nitrogen narcosis.
  
  Section::::Mechanism.
   Section::::Signs and symptoms.
  
  The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain's oxygen needs then no symptoms will result.
   Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial pressures, including underwater diving using compressed breathing gases, hyperbaric medicine, neonatal care and human spaceflight. These protocols have resulted in the increasing rarity of seizures due to oxygen toxicity, with pulmonary and ocular damage being mainly confined to the problems of managing premature infants.
   BULLET::::4. Cerebral infarction – A "stroke", caused by complete oxygen deprivation due to an interference in cerebral blood flow which affects multiple areas of the brain.
  
  Cerebral hypoxia can also be classified by the cause of the reduced brain oxygen:
   There are physiological and psychological disorders related to prolonged exposure to hypoxic conditions. For example, sleep apnea is a condition where there is partial, or complete, blockage of breathing during sleep. In addition, the respiratory system linked to central nervous system via base of brain. Thus, prolonged exposure to low oxygen concentration has detrimental effects on the brain.
  
  Section::::Relationship with other physiological systems.:Sensorimotor system.
   Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness. This may be followed by a tonic–clonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state). The onset of seizure depends upon the partial pressure of oxygen in the breathing gas and exposure duration. However, exposure time before onset is unpredictable, as tests have shown a wide variation, both amongst individuals, and in the same individual from day to day. In addition, many external factors, such as underwater immersion, exposure to cold, and exercise will decrease the time to onset of central nervous system symptoms. Decrease of tolerance is closely linked to retention of carbon dioxide. Other factors, such as darkness and caffeine, increase tolerance in test animals, but these effects have not been proven in humans.
   A lack of oxygen or chemical changes in the lungs may cause the heart to stop beating. This cardiac arrest stops the flow of blood and thus stops the transport of oxygen to the brain. Cardiac arrest used to be the traditional point of death but at this point there is still a chance of recovery. The brain cannot survive long without oxygen and the continued lack of oxygen in the blood combined with the cardiac arrest will lead to the deterioration of brain cells causing first brain damage and eventually brain death from which recovery is generally considered impossible. The brain will die after approximately six minutes without oxygen at normal body temperature, but hypothermia of the central nervous system may prolong this.
   Although the convulsions caused by central nervous system oxygen toxicity may lead to incidental injury to the victim, it remained uncertain for many years whether damage to the nervous system following the seizure could occur and several studies searched for evidence of such damage. An overview of these studies by Bitterman in 2004 concluded that following removal of breathing gas containing high fractions of oxygen, no long-term neurological damage from the seizure remains.
   BULLET::::- Ischemic hypoxia ( or "stagnant hypoxia") – Reduced brain oxygen is caused by inadequate blood flow to the brain. Stroke, shock, cardiac arrest and heart attack may cause stagnant hypoxia. Ischemic hypoxia can also be created by pressure on the brain. Cerebral edema, brain hemorrhages and hydrocephalus exert pressure on brain tissue and impede their absorption of oxygen.
  
  BULLET::::- Histotoxic hypoxia – Oxygen is present in brain tissue but cannot be metabolized by the brain tissue. Cyanide poisoning is a well-known example.
  
  Section::::Treatment.
   The usual consequence, if the airway is not protected, is drowning. A breath-hold diver who has blacked out and has been promptly returned to the surface, will usually regain consciousness within seconds. While the diver is still unconscious underwater, they are at high risk of drowning. While unconscious the diver has lost voluntary bodily control, but still has protective reflexes that protect the airway. One of these is laryngospasm, which closes the larynx, to preventing water from entering the lungs. After some time a laryngospasm will relax and the airway will open, which may result in water ingress if the diver is still underwater. If the diver has reached the surface, and the divers face is kept above water, when the laryngospasm relaxes spontaneous breathing will often resume. The laryngospasm will eventually relax, and if the diver is still underwater then water will enter the airway and may reach the lungs which will cause complications if resuscitation is successful, and secondary drowning is possible. The time between loss of consciousness and death varies considerably depending on a number of factors but can be as little as two and a half minutes.
   Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial pressures, including underwater diving using compressed breathing gases. These protocols have resulted in the increasing rarity of seizures due to oxygen toxicity.
   Effect of oxygen on chronic obstructive pulmonary disease
  
  In some individuals, the effect of oxygen on chronic obstructive pulmonary disease is to cause increased carbon dioxide retention, which may cause drowsiness, headaches, and in severe cases lack of respiration, which may lead to death. People with lung ailments or with central respiratory depression, who receive supplemental oxygen, require careful monitoring.
  
  Section::::Signs and symptoms.
   Temporary exposure to high partial pressures of oxygen at greater than atmospheric pressure can lead to central nervous system toxicity (CNS). An early but serious sign of CNS oxygen toxicity is a grand-mal seizure, also known as a generalized tonic-clonic seizure. This type of seizure consists of a loss of consciousness and violent muscle contractions. Signs and symptoms of oxygen toxicity are usually prevalent, but there are no standard warning signs that a seizure is about to ensue. The convulsion caused by oxygen toxicity does not lead to hypoxia, a side effect common to most seizures, because the body has an excess amount of oxygen when the convulsion begins. The seizures can lead to drowning, however, if the convulsion is suffered by a diver still in the water.
   Oxygen (O) must be present in every breathing gas. This is because it is essential to the human body's metabolic process, which sustains life. The human body cannot store oxygen for later use as it does with food. If the body is deprived of oxygen for more than a few minutes, unconsciousness and death result. The tissues and organs within the body (notably the heart and brain) are damaged if deprived of oxygen for much longer than four minutes.
   BULLET::::2. Ischaemic hypoxia is caused by reduced blood flow to the brain arising from cerebral vasoconstriction brought on by low carbon dioxide following hyperventilation, or increased pressure on the heart as a consequence of (lung packing) which can reduce blood circulation in general, or both. If the brain used more oxygen than is available in the blood supply, the cerebral oxygen partial pressure may drop below the level required to sustain consciousness. This type of blackout is likely to occur early in the dive.
   If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate, but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death. Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.
   Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Biot's respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged.
   The second most common cause of coma, which makes up about 25% of cases, is lack of oxygen, generally resulting from cardiac arrest. The Central Nervous System (CNS) requires a great deal of oxygen for its neurons. Oxygen deprivation in the brain, also known as hypoxia, causes sodium and calcium from outside of the neurons to decrease and intracellular calcium to increase, which harms neuron communication. Lack of oxygen in the brain also causes ATP exhaustion and cellular breakdown from cytoskeleton damage and nitric oxide production.
   BULLET::::- Hypoxic hypoxia – Limited oxygen in the environment causes reduced brain function. Divers, aviators, mountain climbers, and fire fighters are all at risk for this kind of cerebral hypoxia. The term also includes oxygen deprivation due to obstructions in the lungs. Choking, strangulation, the crushing of the windpipe all cause this sort of hypoxia. Severe asthmatics may also experience symptoms of hypoxic hypoxia.
  
  BULLET::::- Hypemic hypoxia – Reduced brain function is caused by inadequate oxygen in the blood despite adequate environmental oxygen. Anemia and carbon monoxide poisoning are common causes of hypemic hypoxia.
   Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die due to an increasing acidity in the brain tissue (acidosis). Additionally, during the period of oxygen deprivation, materials that can easily create free radicals build up. When oxygen enters the tissue these materials interact with oxygen to create high levels of oxidants. Oxidants interfere with the normal brain chemistry and cause further damage (this is known as "reperfusion injury").
   Section::::Scope of risk.
   Bronchopulmonary dysplasia is reversible in the early stages by use of break periods on lower pressures of oxygen, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. One or two days of exposure without oxygen breaks are needed to cause such damage.
  