In a healthy person during<unk> , breathing is regular so oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gases with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. Oxygen and carbon dioxide receptors in the body (called chemoreceptors) send nerve impulses to the brain, which then signals for reflexive opening of the larynx (enlarging the opening between the vocal cords) and movements of the rib cage muscles and diaphragm. These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it. In the absence of central<unk> , any sudden drop in oxygen or excess of carbon dioxide, even if small, strongly stimulates the brain's respiratory centers to breathe; the respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. In pure<unk> , the brain's respiratory control centers, located in the region of the human brain known as the pre-Botzinger complex, are imbalanced during<unk>  and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. The neurological feedback mechanism that monitors blood levels of carbon dioxide and in turn stimulates respiration fails to react quickly enough to maintain an even respiratory rate, allowing the entire respiratory system to cycle between<unk>  and hyperpnea, even for a brief time following an awakening during a breathing pause. The<unk> er stops breathing for up to two minutes and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no muscular struggling, although when awakening occurs in the middle of a pause, the inability to immediately operate the breathing muscles often results in cognitive struggle accompanied by a feeling of panic exacerbated by the feeling associated with excessive blood CO2 levels. Even in severe cases of<unk> , however, the effects almost always result in pauses that make breathing irregular rather than cause the total cessation of breathing over the medium term. After the episode of<unk> , breathing may be faster and/or more intense (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases, absorb more oxygen, and, when voluntary, enable a return to normal instinctive breathing patterns by restoring oxygen to the breathing muscles themselves. Secondary effects The conditions of hypoxia and hypercapnia, whether caused by<unk>  or not, trigger additional effects on the body. The immediate effects of<unk>  on the body depend on how long the failure to breathe endures, how short is the interval between failures to breathe, and the presence or absence of independent conditions whose effects amplify those of an<unk> c episode. * Brain cells need constant oxygen to live, and if the level of blood oxygen remains low enough for long enough, brain damage and even death will occur. These effects, however, are rarely a result of<unk> , which is a chronic condition whose effects are usually much milder. * Drops in blood oxygen levels that are severe but not severe enough to trigger brain-cell or overall death may trigger seizures even in the absence of epilepsy. * In severe cases of<unk><unk> , the more translucent areas of the body will show a bluish or dusky cast from cyanosis, the change in hue ("turning blue") produced by the deoxygenation of blood in vessels near the skin. * Compounding effects of independent conditions: :* In persons with epilepsy, the hypoxia caused by<unk>  may be powerful enough to trigger seizures even in the presence of medication that otherwise controls those seizures well. :* In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). :* Longstanding and recurrent episodes of<unk>  may, over months and years, have the cumulative effect of increasing blood carbon-dioxide levels to the point that enough carbon dioxide dissolves in the blood to form carbonic acid in overall proportions sufficient to cause respiratory acidosis. :* In persons who have either or both forms of<unk><unk> , breathing irregularities during<unk>  can be dangerously aggravated by taking respiration-depressing drugs, especially sedative drugs that operate by depressing the central nervous system generally; respiratory depressants include opiates, barbiturates, benzodiazepines, and, in large quantities, alcohol, the last three of which are broad-spectrum CNS depressants. Quantities that are normally considered safe may cause the person with chronic<unk><unk>  to stop breathing altogether. Should these individuals have general anaesthesia, for example, they require prolonged monitoring after initial recovery, as compared against a person with no history of<unk><unk> , because<unk>  is likely to occur with even low levels of the drugs in their system. :* Sudden infant death syndrome is sometimes theorized to be attributable to<unk><unk> ; the recommendation, prevalent since the mid-1980s, of placing infants on their backs rather than their stomachs for<unk>  represents an attempt to prevent those instances of breathing cessation that are attributable to compressive obstruction. :* Premature infants with immature brains and reflex systems are at high risk for<unk>  syndrome, even if these babies are otherwise healthy. Premature babies who have the syndrome will generally outgrow it as they mature, provided that they receive careful enough monitoring and supportive care during infancy to survive. Because of premature infants' propensity toward central<unk> , medications that can cause respiratory drive depression are either not given to them or administered to them only under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia; administration of caffeine has been found not only to aid in maintenance of respiratory function after general anaesthesia but to reduce<unk>  for preterm infants regardless of context.
Central sleep apnea
Sleep apnea
Obstructive sleep apnea
Hyperventilation syndrome
Obesity hypoventilation syndrome
Central hypoventilation syndrome
Sleep-related breathing disorder
Shift work sleep disorder