Central sleep apnea (CSA) or central sleep apnea syndrome (CSAS) is a sleep-related disorder in which the effort to breathe is diminished or absent, typically for 10 to 30 seconds either intermittently or in cycles, and is usually associated with a reduction in blood oxygen saturation. CSA is usually due to an instability in the body's feedback mechanisms that control respiration. This type of sleep apnea can also be an indicator of Arnold–Chiari malformation.
Signs and symptoms In a healthy person during sleep, breathing is regular, so that the concentration of oxygen and carbon dioxide in the blood stays fairly constant: After exhalation, the blood oxygen falls and carbon dioxide rises. Exchange of gases with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of 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 in the lungs and air rushes in to fill it. In the absence of central apnea, 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 central sleep apnea, the brain's respiratory control centers, in pre-Botzinger complex, are imbalanced during sleep and fail to give the signal to inhale, causing the person to miss one or more cycles of breathing. The neurological feedback mechanism that monitors blood 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 apnea and hyperpnea, even for a brief time after an awakening during a breathing pause. The sleeper 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; 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 central sleep apnea, 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 apnea, breathing may be faster and/or more intense (hyperpnea) for a while; this is a compensatory effort 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 apnea or not, trigger additional effects on the body. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures, how short the interval is between failures to breathe, and the presence or absence of independent conditions whose effects amplify those of an apneic 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 central sleep apnea, 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 sleep apnea, 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 apnea 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 apnea 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 sleep apnea, breathing irregularities during sleep 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 sleep apnea to stop breathing altogether. Should these individuals have general anaesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea 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 sleep apnea; the recommendation, prevalent since the mid-1980s, of placing infants on their backs rather than their stomachs for sleep 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 central sleep apnea 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 apnea, medications that can cause respiratory drive depression are either not given to them or administered to them only under careful monitoring, with resuscitation equipment 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 apnea for preterm infants regardless of context.
Diagnosis AHIRating 5 to <15 apneas or hypopneas per hour of sleep Mild sleep apnea/hypopnea 15 to <30 apneas or hypopneas per hour of sleep Moderate sleep apnea/hypopnea A diagnosis of sleep apnea requires determination by a physician. The examination may require a study of an individual in a sleep lab, although the AAST has said a two belt IHT (In Home Test) will replace a PSG (polysomnography) (a sleep study) for diagnosing obstructive apnea. There, the patient will be monitored while at rest, and the periods when breathing ceases will be measured with respect to length and frequency. During a PSG, a person with sleep apnea shows breathing interruptions followed by drops/reductions in blood oxygen and increases in blood carbon dioxide level. In adults, a pause must last 10 seconds to be scored as an apnea. However, in young children, who normally breathe at a much faster rate than adults, shorter pauses may still be considered apneas. Hypopneas in adults are defined as a 30% reduction in air flow for more than ten seconds, followed by oxygen-saturation declines of at least 3% or 4% per the AASM standards. and/or EEG arousal. The Apnea-Hypopnea Index (AHI) is expressed as the number of apneas or hypopneas per hour of sleep.
As noted above, in central sleep apnea, the cessation of airflow is associated with the absence of physical attempts to breathe; specifically, polysomnograms reveal a correlation between the absence of rib cage and abdominal movements and cessation of airflow at the nose and lips. By contrast, in obstructive sleep apnea, pauses are not correlated with the absence of attempts to breathe and may even be correlated with more effortful breathing in an instinctive attempt to overcome the pressure on the affected person's airway. If the majority of a sleep-apnea patient's apneas/hypopneas are central, their condition is classified as central; likewise, if the majority are obstructive, their condition is classified as obstructive.
Criteria
CSA is divided into 6 categories: primary CSA; Cheyne–Stokes breathing (CSB); high-altitude periodic breathing; CSA due to a medical condition without CSB; CSA due to a medication or substance; treatment emergent central apnea (also called complex sleep apnea). The following symptoms are present in primary CSA: excessive daytime sleepiness, frequent arousals and awakenings during sleep or insomnia complaints, awakening short of breath, snoring, witnessed apneas.American Academy of Sleep Medicine (2014). International Classification of Sleep Disorders, 3rd edition. Darien, IL: American Academy of Sleep Medicine The patient's polysomnography shows ≥5 central apneas and/or central hypopneas per hour of sleep, representing at least 50% of total respiratory events in the apnea-hypopnea index. CSA with CSB is characterized by at least one of the criteria of primary CSA or the presence of atrial fibrillation/flutter, congestive heart failure, or a neurologic disorder. The patient's polysomnography looks like the primary CSA polysomnography with the addition of a ventilatory pattern compatible with CSB. High-altitude periodic breathing requires that the patient has recently been at least 2500 meters above sea level. In CSA due to a medication or substance, opioids or other respiratory depressants must have been taken. For CSA due to a medical condition without CSB, the criteria are the same as primary CSA, but the symptoms are caused by a disease. Treatment emergent CSA must appear only after treatment for obstructive respiratory events has begun.
Differential diagnosis
Although central and obstructive sleep apnea have some signs and symptoms in common, others are present in one but absent in another, enabling differential diagnosis as between the two types:
Signs and symptoms of sleep apnea generally Signs: Observed breathing pauses during sleep High carbon-dioxide saturation of blood, especially just before awakenings during which a patient experiences an urgent need to breathe (see "Symptoms" below) Low oxygen saturation of blood Heart rate increase (response to both hypercapnia and hypoxemia/hypoxia), unless there also exist problems with the heart muscle itself or the autonomic nervous system severe enough to make this compensatory increase impossible Symptoms: High frequency of urgent need to breathe upon awakening (symptom created by hypercapnia), especially among a subset of awakenings occurring at times other than normal for an individual's sleep schedule and circadian rhythms
Signs and symptoms of central sleep apnea Signs: Lack of abdominal and thoracic movement for 10 seconds or longer during sleep and coincident with breathing pauses Symptoms: Inability, either complete or without excessive effort, to voluntarily operate the diaphragm and other thoracic muscles upon awakening The combination of this symptom with a high frequency of urgent need to breathe upon awakening is especially specific in that the co-presence of the latter symptom differentiates central sleep apnea's presentation from that of sleep paralysis generally.
Signs and symptoms of and conditions associated with obstructive sleep apnea Signs: