To counter the effects of high-altitude diseases, the body must return arterial p toward normal. Acclimatization, the means by which the body adapts to higher altitudes, only partially restores p to standard levels. Hyperventilation, the body’s most common response to high-altitude conditions, increases alveolar p by raising the depth and rate of breathing. However, while p does improve with hyperventilation, it does not return to normal. Studies of miners and astronomers working at 3000 meters and above show improved alveolar p with full acclimatization, yet the p level remains equal to or even below the threshold for continuous oxygen therapy for patients with chronic obstructive pulmonary disease (COPD). In addition, there are complications involved with acclimatization. Polycythemia, in which the body increases the number of red blood cells in circulation, thickens the blood, raising the danger that the heart can’t pump it.

In high-altitude conditions, only oxygen enrichment can counteract the effects of hypoxia. By increasing the concentration of oxygen in the air, the effects of lower barometric pressure are countered and the level of arterial p is restored toward normal capacity. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 4000 m, raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an altitude equivalent of 3000 m, which is much more tolerable for the increasing number of low-landers who work in high altitude. In a study of astronomers working in Chile at 5050 m, oxygen concentrators increased the level of oxygen concentration by almost 30 percent (that is, from 21 percent to 27 percent). This resulted in increased worker productivity, less fatigue, and improved sleep.

Oxygen concentrators are uniquely suited for this purpose. They require little maintenance and electricity, provide a constant source of oxygen, and eliminate the expensive, and often dangerous, task of transporting oxygen cylinders to remote areas. Offices and housing already have climate-controlled rooms, in which temperature and humidity are kept at a constant level. Oxygen can be added to this system easily and relatively cheaply.

A prescription renewal for home oxygen following hospitalization requires an assessment of the patient for ongoing hypoxemia.

When the pulmonary capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of carrying fluid away from the interstitial spaces perhaps as much as 10-fold. Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mm Hg have been measured without the development of lethal pulmonary edema.[Guytun and Hall physiology]

Hypoxia exists when there is a reduced amount of oxygen in the tissues of the body. Hypoxemia refers to a reduction in PO2 below the normal range, regardless of whether gas exchange is impaired in the lung, CaO2 is adequate, or tissue hypoxia exists. There are several potential physiologic mechanisms for hypoxemia, but in patients with COPD the predominant one is V/Q mismatching, with or without alveolar hypoventilation, as indicated by PaCO2. Hypoxemia caused by V/Q mismatching as seen in COPD is relatively easy to correct, so that only comparatively small amounts of supplemental oxygen (less than 3 L/min for the majority of patients) are required for LTOT. Although hypoxemia normally stimulates ventilation and produces dyspnea, these phenomena and the other symptoms and signs of hypoxia are sufficiently variable in patients with COPD as to be of limited value in patient assessment. Chronic alveolar hypoxia is the main factor leading to development of cor pulmonale—right ventricular hypertrophy with or without overt right ventricular failure—in patients with COPD. Pulmonary hypertension adversely affects survival in COPD, to an extent that parallels the degree to which resting mean pulmonary artery pressure is elevated. Although the severity of airflow obstruction as measured by FEV1 is the best correlate with overall prognosis in patients with COPD, chronic hypoxemia increases mortality and morbidity for any severity of disease. Large-scale studies of LTOT in patients with COPD have demonstrated a dose-response relationship between daily hours of oxygen use and survival. There is reason to believe that continuous, 24-hours-per-day oxygen use in appropriately selected patients would produce a survival benefit even greater than that shown in the NOTT and MRC studies.

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.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons.

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.

Long-term comas can have a significant impact on a patient's families. Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma. Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult. Treatment decision often involve complex ethical choices and can strain family dynamics.

Treatment of infants suffering birth asphyxia by lowering the core body temperature is now known to be an effective therapy to reduce mortality and improve neurological outcome in survivors, and hypothermia therapy for neonatal encephalopathy begun within 6 hours of birth significantly increases the chance of normal survival in affected infants.

There has long been a debate over whether newborn infants with birth asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

IH/BA is also a causitive factor in cardiac and circulatory birth defects the sixth most expensive condition, as well as premature birth and low birth weight the second most expensive and it is one of the contributing factors to infant respiratory distress syndrome (RDS) also known as hyaline membrane disease, the most expensive medical condition to treat and the number one cause of infant mortality.

Perinatal asphyxia is the medical condition resulting from deprivation of oxygen (hypoxia) to a newborn infant long enough to cause apparent harm. It results most commonly from a drop in maternal blood pressure or interference during delivery with blood flow to the infant's brain. This can occur as a result of inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. There has long been a scientific debate over whether newborn infants with asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

For newborn infants starved of oxygen during birth there is now evidence that hypothermia therapy for neonatal encephalopathy applied within 6 hours of cerebral hypoxia effectively improves survival and neurological outcome. In adults, however, the evidence is less convincing and the first goal of treatment is to restore oxygen to the brain. The method of restoration depends on the cause of the hypoxia. For mild-to-moderate cases of hypoxia, removal of the cause of hypoxia may be sufficient. Inhaled oxygen may also be provided. In severe cases treatment may also involve life support and damage control measures.

A deep coma will interfere with body's breathing reflexes even after the initial cause of hypoxia has been dealt with; mechanical ventilation may be required. Additionally, severe cerebral hypoxia causes an elevated heart rate, and in extreme cases the heart may tire and stop pumping. CPR, defibrilation, epinephrine, and atropine may all be tried in an effort to get the heart to resume pumping. Severe cerebral hypoxia can also cause seizures, which put the patient at risk of self-injury, and various anti-convulsant drugs may need to be administered before treatment.

There has long been a debate over whether newborn infants with cerebral hypoxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

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").

Techniques for preventing damage to brain cells are an area of ongoing research. Hypothermia therapy for neonatal encephalopathy is the only evidence-supported therapy, but antioxidant drugs, control of blood glucose levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation. Hyperbaric oxygen therapy is being evaluated with the reduction in total and myocardial creatine phosphokinase levels showing a possible reduction in the overall systemic inflammatory process.

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.

"Hypoxemia" refers to low oxygen in the blood, and the more general term "hypoxia" is an abnormally low oxygen content in any tissue or organ, or the body as a whole. Hypoxemia can cause hypoxia (hypoxemic hypoxia), but hypoxia can also occur via other mechanisms, such as anemia.

Hypoxemia is usually defined in terms of reduced partial pressure of oxygen (mm Hg) in arterial blood, but also in terms of reduced content of oxygen (ml oxygen per dl blood) or percentage saturation of hemoglobin (the oxygen binding protein within red blood cells) with oxygen, which is either found singly or in combination.

While there is general agreement that an arterial blood gas measurement which shows that the partial pressure of oxygen is lower than normal constitutes hypoxemia, there is less agreement concerning whether the oxygen content of blood is relevant in determining hypoxemia. This definition would include oxygen carried by hemoglobin. The oxygen content of blood is thus sometimes viewed as a measure of tissue delivery rather than hypoxemia.

Just as extreme hypoxia can be called anoxia, extreme hypoxemia can be called anoxemia.

Generally, high-altitude pulmonary edema (HAPE) or AMS precede HACE. In patients with AMS, the onset of HACE is usually indicated by vomiting, headache that does not respond to non-steroidal anti-inflammatory drugs, hallucinations, and stupor. In some situations, however, AMS progresses to HACE without these symptoms. HACE must be distinguished from conditions with similar symptoms, including stroke, intoxication, psychosis, diabetic symptoms, meningitis, or ingestion of toxic substances. It should be the first diagnosis ruled out when sickness occurs while ascending to a high altitude.

HACE is generally preventable by ascending gradually with frequent rest days while climbing or trekking. Not ascending more than daily and not sleeping at a greater height than more than the previous night is recommended. The risk of developing HACE is diminished if acetazolamide or dexamethasone are administered. Generally, the use of acetazolamide is preferred, but dexamethasone can be used for prevention if there are side effects or contraindications. Some individuals are more susceptible to HACE than others, and physical fitness is not preventative. Age and sex do not by themselves affect vulnerability to HACE.

Patients with HACE should be brought to lower altitudes and provided supplemental oxygen, and rapid descent is sometimes needed to prevent mortality. Early recognition is important because as the condition progresses patients are unable to descend without assistance. Dexamethasone should also be administered, although it fails to ameliorate some symptoms that can be cured by descending to a lower altitude. It can also mask symptoms, and they sometimes resume upon discontinuation. Dexamethasone's prevention of angiogenesis may explain why it treats HACE well. Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.

If available, supplemental oxygen can be used as an adjunctive therapy, or when descent is not possible. FiO2 should be titrated to maintain arterial oxygen saturation of greater than 90%, bearing in mind that oxygen supply is often limited in high altitude clinics/environments.

In addition to oxygen therapy, a portable hyperbaric chamber (Gamow bag) can by used as a temporary measure in the treatment of HACE. These devices simulate a decrease in altitude of up to 7000 ft, but they are resource intensive and symptoms will often return after discontinuation of the device. Portable hyperbaric chambers should not be used in place of descent or evacuation to definitive care.

Diuretics may be helpful, but pose risks outside of a hospital environment. Sildenafil and tadalafil may help HACE, but there is little evidence of their efficacy. Theophylline is also theorized to help the condition.

Although AMS is not life-threatening, HACE is usually fatal within 24 hours if untreated. Without treatment, the patient will enter a coma and then die. In some cases, patients have died within a few hours, and a few have survived for two days. Descriptions of fatal cases often involve climbers who continue ascending while suffering from the condition's symptoms.

Recovery varies between days and weeks, but most recover in a few days. After the condition is successfully treated, it is possible for climbers to reascend. Dexamethesone should be discontinued, but continual acetazolamide is recommended. In one study, it took patients between one week and one month to display a normal CT scan after suffering from HACE.

If the alveolar ventilation is insufficient, there will not be enough oxygen delivered to the alveoli for the body's use. This can cause hypoxemia even if the lungs are normal, as the cause is in the brainstem's control of ventilation or in the body's inability to breathe effectively.

In-hospital monitors in the NICU typically measure respiratory movements, heartrate, and pulse oximetry. Central apnea can be detected quickly since it results in absence of respiratory movements. Obstructive apnea can be detected when the level of oxygen has declined in the blood and/or results in slowing of the heart rate.

Home apnea monitors (which must be distinguished from infant monitors that are designed only to allow parents to listen to the infant remotely) most frequently measure only respiratory movements and/or heart rate. They are generally used with premature infants who are otherwise ready for discharge, but who continue to require supplemental oxygen or medication for mild residual AOP. Home apnea monitoring is typically required for 6–12 weeks after discharge.

Compressive asphyxia (also called chest compression) is mechanically limiting expansion of the lungs by compressing the torso, hence interfering with breathing. Compressive asphyxia occurs when the chest or abdomen is compressed posteriorly. In accidents, the term traumatic asphyxia or crush asphyxia usually refers to compressive asphyxia resulting from being crushed or pinned under a large weight or force. An example of traumatic asphyxia includes cases where an individual has been using a car-jack to repair a car from below, and is crushed under the weight of the vehicle. Pythons, anacondas, and other constrictor snakes kill through compressive asphyxia. In cases of co-sleeping ("overlay"), the weight of an adult or large child may compress an infant's chest, preventing proper expansion of the chest. Risk factors include large or obese adults, parental fatigue or impairment (sedation by drugs or alcohol) of the co-sleeping adult and a small shared sleeping space (for example, both adult and infant sharing a couch).

In fatal crowd disasters, compressive asphyxia from being crushed against the crowd causes the large part of the deaths, rather than blunt trauma from trampling. This is what occurred at the Ibrox disaster in 1971, where 66 Rangers fans died; the 1979 The Who concert disaster where 11 died; the Luzhniki disaster in 1982, when 66 FC Spartak Moscow fans died; and at the Hillsborough disaster in 1989, when 96 Liverpool fans were crushed to death in an overcrowded terrace. In confined spaces, people push and lean against each other; evidence from bent steel railings in several fatal crowd accidents have shown horizontal forces over 4500 N (equivalent to a weight of approximately 450 kg, or 1014 lbs). In cases where people have stacked up on each other forming a human pile, estimations have been made of around 380 kg (838 lbs) of compressive weight in the lowest layer.

"Positional" or "restraint" asphyxia is when a person is restrained and left alone prone, such as in a police vehicle, and is unable to reposition himself or herself in order to breathe. The death can be in the vehicle, or following loss of consciousness to be followed by death while in a coma, having presented with anoxic brain damage. The asphyxia can be caused by facial compression, neck compression, or chest compression. This occurs mostly during restraint and handcuffing situations by law enforcement, including psychiatric incidents. The weight of the restraint(s) doing the compression may contribute to what is attributed to positional asphyxia. Therefore, passive deaths following custody restraint that are presumed to be the result of positional asphyxia may actually be examples of asphyxia occurring during the restraint process.

Chest compression is also featured in various grappling combat sports, where it is sometimes called wringing. Such techniques are used either to tire the opponent or as complementary or distractive moves in combination with pinning holds, or sometimes even as submission holds. Examples of chest compression include the knee-on-stomach position; or techniques such as leg scissors (also referred to as body scissors and in budō referred to as "do-jime"; 胴絞, "trunk strangle" or "body triangle") where a participant wraps his or her legs around the opponent's midsection and squeezes them together.

Pressing is a form of torture or execution that works through asphyxia e.g. burking.

Since AOP is fundamentally a problem of the immaturity of the physiological systems of the premature infant, it is a self-limited condition that will resolve when these systems mature. It is unusual for an infant to continue to have significant problems with AOP beyond 42 weeks post-conceptual age.

Infants who have had AOP are at increased risk of recurrence of apnea in response to exposure to anesthetic agents, at least until around 52 weeks post-conceptual age.

There is no evidence that a history of AOP places an infant at increased risk for SIDS. However, any premature infant (regardless of whether they have had AOP) is at increased risk of SIDS. It is important that other factors related to SIDS risk be avoided (exposure to smoking, prone sleeping, excess bedding materials, etc.)

Respiratory stimulants such as nikethamide were traditionally used to counteract respiratory depression from CNS depressant overdose, but offered limited effectiveness. A new respiratory stimulant drug called BIMU8 is being investigated which seems to be significantly more effective and may be useful for counteracting the respiratory depression produced by opiates and similar drugs without offsetting their therapeutic effects.

If the respiratory depression occurs from opioid overdose, usually an opioid antagonist, most likely naloxone, will be administered. This will rapidly reverse the respiratory depression unless complicated by other depressants. However an opioid antagonist may also precipitate an opioid withdrawal syndrome in chronic users.

While there are no standard criteria for the diagnosis of Grinker's myelinopathy, neuroimaging can be an important diagnostic tool in ruling out other diagnoses. Magnetic resonance imaging (MRI) or computed tomography (CT) scans can be used to demonstrate a decrease in white matter density in the patient’s cerebral hemispheres, with the typical exception of overlying cortices. Unexplained, uniform demyelination of white matter can indicate acute onset Grinker's myelinopathy.

Disorders like congenital central hypoventilation syndrome (CCHS) and ROHHAD (rapid-onset obesity, hypothalamic dysfunction, hypoventilation, with autonomic dysregulation) are recognized as conditions that are associated with hypoventilation. CCHS may be a significant factor in some cases of sudden infant death syndrome (SIDS), often termed "cot death" or "crib death".

The opposite condition is hyperventilation (too much ventilation), resulting in low carbon dioxide levels (hypocapnia), rather than hypercapnia.

Those patients who survive initial hospitalization are likely to recover from Grinker's Myelinopathy, but may take up to a year or longer. Age seems to be a factor in the time for recovery, as one study indicated that the mean age of patients who recovered within one year was 10 years younger than that of patients who did not. For most patients, a recovery time of 3–6 months is typical. Even after recovering, however, some symptoms may persist, including cognitive deficits or Parkinsonian symptoms that can be treated separately.

Hypoxic hypoxia is a result of insufficient oxygen available to the lungs. A blocked airway, a drowning or a reduction in partial pressure (high altitude above 10,000 feet) are examples of how lungs can be deprived of oxygen. Some medical examples are abnormal pulmonary function or respiratory obstruction. Hypoxic hypoxia is seen in patients suffering from chronic obstructive pulmonary diseases (COPD), neuromuscular diseases or interstitial lung disease.

Inert gas asphyxiation is a form of asphyxiation which results from breathing a physiologically inert gas in the absence of oxygen, or a low amount of oxygen, rather than atmospheric air (which is largely composed of nitrogen and oxygen). Examples of physiologically inert gases, which have caused accidental or deliberate death by this mechanism, are: argon, helium, nitrogen and methane. The term "physiologically inert" is used to indicate a gas which has no toxic or anesthetic properties and does not act upon the heart or hemoglobin. Instead, the gas acts as a simple diluent to reduce oxygen concentration in inspired gas and blood to dangerously low levels, thereby eventually depriving all cells in the body of oxygen.

According to the U.S. Chemical Safety and Hazard Investigation Board, in humans, "breathing an oxygen deficient atmosphere can have serious and immediate effects, including unconsciousness after only one or two breaths. The exposed person has no warning and cannot sense that the oxygen level is too low." In the US, at least 80 people died due to accidental nitrogen asphyxiation between 1992 and 2002. Hazards with inert gases and the risks of asphyxiation are well established.

An occasional cause of accidental death in humans, inert gas asphyxia with gases including helium, nitrogen, methane, and argon, has been used as a suicide method. Inert gas asphyxia has been advocated by proponents of euthanasia, using a gas-retaining plastic hood device colloquially referred to as a suicide bag.

Nitrogen asphyxiation has been suggested by a number of lawmakers and other advocates as a more humane way to carry out capital punishment. In April 2015, the Oklahoma Governor Mary Fallin signed a bill authorizing nitrogen asphyxiation as an alternative execution method in cases where the state's preferred method of lethal injection was not available as an option.

Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor blood oxygenation in the lungs. It develops when arterial oxygen saturation drops to ≤85% or ≤75%.

Acute cyanosis can be as a result of asphyxiation or choking, and is one of the definite signs that respiration is being blocked.

Central cyanosis may be due to the following causes:

1. Central nervous system (impairing normal ventilation):

- Intracranial hemorrhage

- Drug overdose (e.g. heroin)

- Tonic–clonic seizure (e.g. grand mal seizure)

2. Respiratory system:

- Pneumonia

- Bronchiolitis

- Bronchospasm (e.g. asthma)

- Pulmonary hypertension

- Pulmonary embolism

- Hypoventilation

- Chronic obstructive pulmonary disease, or COPD (emphysema)

3. Cardiovascular diseases:

- Congenital heart disease (e.g. Tetralogy of Fallot, right to left shunts in heart or great vessels)

- Heart failure

- Valvular heart disease

- Myocardial infarction

4. Blood:

- Methemoglobinemia * Note this causes "spurious" cyanosis, in that, since methemoglobin appears blue, the patient can appear cyanosed even in the presence of a normal arterial oxygen level.

- Polycythaemia

- Congenital cyanosis (HbM Boston) arises from a mutation in the α-codon which results in a change of primary sequence, H → Y. Tyrosine stabilises the Fe(III) form (oxyhaemoglobin) creating a permanent T-state of Hb.

5. Others:

- High altitude, cyanosis may develop in ascents to altitudes >2400 m.

- Hypothermia

- Obstructive sleep apnea

In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in "Pa"CO. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

- Acute respiratory acidosis: HCO increases 1 mEq/L for each 10 mm Hg rise in "Pa"CO.

- Chronic respiratory acidosis: HCO rises 3.5 mEq/L for each 10 mm Hg rise in "Pa"CO.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

- Acute respiratory acidosis: Change in pH = 0.008 X (40 − "Pa"CO)

- Chronic respiratory acidosis: Change in pH = 0.003 X (40 − "Pa"CO)

Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.

Cyanosis is defined as the bluish or purplish discolouration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation. Based on Lundsgaard and Van Slyke's work, it is classically described as occurring if 5.0 g/dL of deoxyhemoglobin or greater is present. This was based on an estimate of capillary saturation based on a mean of arterial versus peripheral venous blood gas measurements. Since estimation of hypoxia is usually now based either on arterial blood gas measurement or pulse oximetry, this is probably an overestimate, with evidence that levels of 2.0 g/dL of deoxyhemoglobin may reliably produce cyanosis. Since, however, the presence of cyanosis is dependent upon there being an absolute quantity of deoxyhemoglobin, the bluish color is more readily apparent in those with high hemoglobin counts than it is with those with anemia. Also, the bluer the color, the more difficult it is to detect on deeply pigmented skin. When signs of cyanosis first appear, such as on the lips or fingers, intervention should be made within 3–5 minutes because a severe hypoxia or severe circulatory failure may have induced the cyanosis.

The name "cyanosis" literally means "the blue disease" or "the blue condition". It is derived from the color cyan, which comes from κυανός, "kyanós", the Greek word for "blue".

When humans breathe in an asphyxiant gas, such as pure nitrogen, helium, neon, argon, sulfur hexafluoride, methane, or any other physiologically inert gas(es), they exhale carbon dioxide without re-supplying oxygen. Physiologically inert gases (those that have no toxic effect, but merely dilute oxygen) are generally free of odor and taste. As such, the human subject detects little abnormal sensation as the oxygen level falls. This leads to asphyxiation (death from lack of oxygen) without the painful and traumatic feeling of suffocation (the hypercapnic alarm response, which in humans arises mostly from carbon dioxide levels rising), or the side effects of poisoning. In scuba diving rebreather accidents, there is often little sensation but euphoria—however, a slow decrease in oxygen breathing gas content has effects which are quite variable. By contrast, suddenly breathing pure inert gas causes oxygen levels in the blood to fall precipitously, and may lead to unconsciousness in only a few breaths, with no symptoms at all.

Some animal species are better equipped than humans to detect hypoxia, and these species are more uncomfortable in low-oxygen environments that result from inert gas exposure.

A 2008 bulletin from the World Health Organization estimates that 900,000 total infants die each year from birth asphyxia, making it a leading cause of death for newborns.

In the United States, intrauterine hypoxia and birth asphyxia was listed as the tenth leading cause of neonatal death.