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Cerebral hypoxia is a form of hypoxia (reduced supply of oxygen), specifically involving the brain; when the brain is completely deprived of oxygen, it is called cerebral anoxia. There are four categories of cerebral hypoxia; they are, in order of increasing severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia , cerebral infarction ...
A number of effects are reported. [2] [3] [clarification needed] It is important to differentiate between physiological adaptations to mild hypoxia and re-oxygenation episodes (i.e., the IHT protocol) and frequent nocturnal suffocation awakenings produced by sleep apnea, which might result in various pathologies.
Targeted temperature management (TTM), previously known as therapeutic hypothermia or protective hypothermia, is an active treatment that tries to achieve and maintain a specific body temperature in a person for a specific duration of time in an effort to improve health outcomes during recovery after a period of stopped blood flow to the brain. [1]
Intermittent hypoxia (also known as episodic hypoxia) is an intervention in which a person or animal undergoes alternating periods of normoxia and hypoxia. Normoxia is defined as exposure to oxygen levels normally found in Earth's atmosphere (~21% O 2 ) and hypoxia as any oxygen levels lower than those of normoxia.
Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury. [34] [35] Oxygen deprivation can be hypoxic (reduced general oxygen availability) or ischemic (oxygen deprivation due to a disruption in blood flow) in origin. Brain injury as a result of oxygen deprivation is generally termed hypoxic injury.
Freediving blackout, breath-hold blackout, [1] or apnea blackout is a class of hypoxic blackout, a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold (freedive or dynamic apnea) dive, when the swimmer does not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it.
The main reason for the acute phase of ischemia-reperfusion injury is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced.
At a brain temperature of 14 °C, blood circulation can be safely stopped for 30 to 40 minutes. [3] There is an increased incidence of brain injury at times longer than 40 minutes, but sometimes circulatory arrest for up to 60 minutes is used if life-saving surgery requires it. [4] [5] Infants tolerate longer periods of DHCA than adults. [6]