Central sleep apnea

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 is the interval 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 against 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 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 apnea for preterm infants regardless of context.[9]

CSA is divided in 6 categories, Primary CSA, Cheyne–Stokes respiration, High-altitude periodic breathing, CSA due to a medical condition without CSB, Central sleep apnea due to a medication or substance and Treatment Emergent Central Apnea (also called Complex Sleep Apnea).[11] The following symptoms are present in the Primary CSA: excessive daytime sleepiness, frequent arousals and awakenings during sleep or insomnia complaints, awakening short of breath, snoring, witness apneas.[12] His 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.[12] CSA with Cheyne-Stokes breathing is characterized by at least one of the criteria of Primary CSA or the presence of atrial fibrillation/flutter, CHF, or a neurologic disorder.[12] His polysomnography looks like the Primary CSA polysomnography with the addition of a ventilatory pattern compatible with CSB.[12] High-Altitude Periodic Breathing requires that the patient has recently been at least 2500 meters.[12] In the CSA due to a medication or substance, opioid or respiratory depressants must had been taken.[12] For the CSA due to a medical condition without CSB, the criteria are the same as Primary CSA, but the symptoms are caused by a disease.[12] In the Treatment Emergent Central Apnea, there was firstly some obstructive respiratory events but after their disappearance, the CSA has appeared.[12]

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 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 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 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[13]

• Signs:

• Observably ineffective respiratory movements (observable lack of air flow despite observable muscle movements indicating efforts to breathe)
• Snoring (high-sensitivity but low-specificity)
• Observably dry mouth or throat (high-sensitivity but low-specificity)

• Symptoms:

• Sleepiness, fatigue, or tiredness, often rising to the level of excessive daytime sleepiness
• Frequent feelings of choking (airway and/or lung compression), as distinguished from mere feeling of suffocation nonspecific with respect to presence/absence of pressure, upon awakening

• Associated conditions:

• Opioid medication use
• Large neck circumference (>16" for females, > 17" for males) (frequent causal factor and possible indirect symptom; see "Obesity" below)
• Obesity (frequent causal factor and possible, albeit low-specificity, sign both direct and indirect): Obesity frequently involves accumulation of fat below the chin and around the neck, depressing the trachea when one is in the supine position, and central obesity can, depending on an individual's fat distribution, lead to increased direct pressure on the thoracic cavity and/or compressive anterior (headward) displacement of the abdominal organs, in the second case reducing space for and increasing difficulty of the motion of the diaphragm. Poor breathing during sleep a] reduces oxygen available for metabolism and may therefore depress basal metabolic rate during sleep, increasing the difference between supply of food energy and demand for it during that time and thereby promoting weight gain, and b] reduces sleep quality and recovery per time unit of sleep, resulting in sleepiness or fatigue that may prompt affected people to eat more in an attempt to increase short-term energy levels.
• Correlation with cardiac disorders:

• Atrial fibrillation (AF): A study in the medical journal Sleep found that the prevalence of atrial fibrillation among patients with idiopathic central sleep apnea was significantly higher than the prevalence among patients with obstructive sleep apnea or no sleep apnea (27%, 1.7%, and 3.3%, respectively). The study was based on 180 subjects with 60 people in each of the 3 groups. Possible explanations for the association between CSA and AF include a causal relationship in one direction or the other between the two conditions or a common cause involving an abnormality of central cardiorespiratory regulation.[14]
• Adults with congestive heart failure are at risk for a form of central apnea called Cheyne-Stokes respiration, which manifests itself both during sleep and during waking hours. Cheyne-Stokes respiration is characterized by periodic breathing featuring recurrent episodes of apnea alternating with episodes of rapid breathing. There is good evidence that replacement of the failing heart (heart transplant) cures central apnea in these patients. Temporary measures (e.g., those taken pending the availability of an organ donor) include the administration of drugs whose effects include respiratory stimulation, although these drugs are not universally effective in reducing the severity of Cheyne-Stokes apneas.

Congenital central hypoventilation syndrome (CCHS), often referred to by its older name "Ondine's curse," is a rare and very severe inborn form of abnormal interruption and reduction in breathing during sleep. This condition involves a specific homeobox gene, PHOX2B, which guides maturation of the autonomic nervous system; certain loss-of-function mutations interfere with the brain's development of the ability to effectively control breathing. There may be a recognizable pattern of facial features among individuals affected by this syndrome.[15]

Once almost uniformly fatal, CCHS is now treatable. Children who have it must have tracheotomies and access to mechanical ventilation on respirators while sleeping, but most do not need to use a respirator while awake. The use of a diaphragmatic pacemaker may offer an alternative for some patients. When pacemakers have enabled some children to sleep without the use of a mechanical respirator, reported cases still required the tracheotomy to remain in place because the vocal cords did not move apart with inhalation.

Persons with the syndrome who survive to adulthood are strongly instructed to avoid certain condition-aggravating factors, such as alcohol use, which can easily prove lethal.[16]

Central sleep apnea is common in preterm, newborn, and infancy stages but a decrease in risk is found with aging and maturity of the central nervous system. Underlying neurological disorders are the most common cause of CSA in full term infants. Of the apnea related events in preterm infants born at less than 29 weeks, 25% are central in origin.[21]

CSA is less common after 2 years of age. The prevalence of CSA in healthy children aging 10 to 18 years is 30%. Children with underlying medical conditions fall under a prevalence rate of 4-6%. For children diagnosed with Prader-Willi syndrome (PWS), CSA is more common and can occur in up to 53% of cases.[21]

Research shows that rates of sleep apnea are higher in adults over the age of 65 years,[20] due to older individuals having higher risks of developing CSA due to pre-existing medical conditions. Recorded prevalence in a cohort study of 2,911 men over the age of 65 was 7.5%.[19] There is reduced risk of CSA in women, and a higher incidence in men. One study showed the incidence of CSA in men was 7.8% and 0.3% in women, stating a difference in hormones have an effect on the apneic threshold (AT) for apnea.[20]