Central sleep apnea

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Sleep sleep apnea ( CSA ) or central sleep apnea syndrome ( CSAS ) is a sleep-related disorder where attempts to breathing is reduced or absent, usually for 10 to 30 seconds either intermittently or in cycles, and is usually associated with decreased blood oxygen saturation. CSA is usually due to instability in the body feedback mechanism that controls respiration. Central sleep apnea can also be an indicator of Arnold-Chiari malformation.

Video Central sleep apnea

Signs and symptoms

Individuals without sleep apnea while "resting" as far as the cardiovascular workload is concerned. Regular breathing in healthy people during sleep, oxygen levels and carbon dioxide levels in the bloodstream remain constant: After respiration, blood oxygen levels decrease and increase in carbon dioxide. Gas exchange with fresh air lungs is needed to fill in oxygen and cleanse the carbon dioxide blood stream that is formed. Oxygen and carbon dioxide receptors in the bloodstream (called chemoreceptors) send nerve impulses to the brain, which then signals for the reflexive opening of the larynx (enlarging the opening between the vocal cords) and the muscle movement of the ribs and diaphragm. These muscles expand the thorax so that a partial vacuum is created inside the lungs and inlet air to fill it. In the absence of central apnea, any decrease in oxygen or excess carbon dioxide, even if small, strongly stimulates the respiratory center of the brain to breathe; The breathing impulse is so strong that even a conscious effort to hold your breath does not overcome it.

In pure central sleep apnea, the brain's respiratory control center, located in the region of the human brain known as the pre-Botzinger complex, is unbalanced during sleep and fails to give a signal to inhale, causing the individual to miss one or more breathing cycles. The neurological feedback mechanism that monitors the levels of carbon dioxide in the blood and in turn stimulates respiration to fail to react fast enough to maintain a flat breathing rate, allowing the entire respiratory system to cycle between apnea and hyperpnea, even for a short time after awakening during respiratory pauses. Sleeper stops breathing for up to two minutes and then starts again. No effort is made to breathe during the respiratory pause: no chest movement and no muscle is struggling, although when waking occurs in the middle of a pause, the inability to immediately operate the respiratory muscles often results in cognitive struggles accompanied by panic feeling compounded by feelings associated with excessive CO ₂ blood levels. Even in cases of severe central sleep apnea, the effect almost always results in pauses that make breathing irregular rather than causing an end to total respiration in the medium term. After episodes of apnea, breathing may be faster and/or more intense (hyperpnea) for a period of time, compensating mechanisms to remove exhaust residue, absorb more oxygen, and, when voluntary, allow return to the normal instinctive breathing patterns by returning oxygen to the respiratory muscles themselves.

Maps Central sleep apnea

Diagnosis

The diagnosis of sleep apnea requires clinical determination. The examination may require study of individuals in the sleep lab, although AAST has said two IHT (In Home Test) belts will replace PSG to diagnose obstructive apnea. There, the patient will be monitored at rest, and the period when the breathing stops will be measured with respect to the length and frequency. During PSG (sleep studies), a person with sleep apnea exhibits respiratory distress followed by a decrease/decrease in blood oxygen and elevated levels of carbon dioxide in the blood.

• In adults, the pause should take 10 seconds to be assessed as apnea. However, in small children, who usually breathe at a much faster rate than adults, a shorter pause may still be considered apnea.
• Hypopneas in adults is defined as a 30% reduction in airflow for more than ten seconds, followed by an oxygen saturation reduction of at least 3% or 4% per AASM stability. and/or EEG passion. The Apnea-Hypopnea Index (AHI) is expressed as the number of apnea or hypopnea per hour of sleep.

As mentioned above, in central sleep apnea, the cessation of airflow is associated with a lack of physical effort to breathe; Specifically, polysomnograms reveal a correlation between the absence of ribs and abdominal movement and the cessation of airflow in the nose and lips. Conversely, in obstructive sleep apnea, the pause is not correlated with the absence of effort to breathe and may even correlate with breathing more instinctive attempts to cope with the pressure on the patient's airway. If most apnea/hypopnea sufferers of sleep apnea are central, the condition is classified as central; Similarly, if the majority is obstructive, the condition is classified as obstructive.

Differential diagnosis

Although central and obstructive sleep apnea has some of the same signs and symptoms, others are present in one but none elsewhere, allowing differential diagnosis between the two types:

Signs and symptoms of sleep apnea are generally

• Alerts:

• Observed breathing stopped during sleep
• High carbon dioxide saturation of blood, especially right before awakening where a sufferer experiences an urgent need to breathe (see "Symptoms" below)
• Low blood oxygen saturation
Increased heart rate (response to hypercapnia and hypoxemia/hypoxia), unless there is also a problem with cardiac muscle or autonomic nervous system severe enough to make this compensatory increase impossible

• Symptoms:

• high frequency of urgent need to breathe when awake (symptoms created by hypercapnia), especially among the waking parts that occur at other times than normal for individual bedtime schedules and circadian rhythms

Signs and symptoms of central sleep apnea

• Alerts:

• Lack of abdominal and thoracic movements for 10 seconds or more during sleep and coincides with breathing stops

• Symptoms:

• Disability, whether complete or without excessive effort, to voluntarily operate the diaphragm and other thoracic muscles upon awakening

• The combination of these symptoms with high frequency of urgent need to breathe when waking is particularly specific because the joint presence of the last symptom distinguishes the presentation of central sleep apnea from sleep paralysis in general.

Signs and symptoms associated with obstructive sleep apnea

• Alerts:

• Ineffective breathing movements that can be seen (lack of visible airflow even if visible muscle movement indicates effort to breathe)
• Snoring (high sensitivity but low specificity)
• Dry mouth or throat that can be observed (high sensitivity but low specificity)

• Symptoms:

• Drowsiness, fatigue, or fatigue, often rises to excessive daytime sleepiness
• Frequent choking (compression of the airway and/or lungs), which is distinguished from just the feeling of suffocation is not specific with respect to the presence/absence of pressure, upon awakening

• Related conditions:

• Large neck circumference (& gt; 16 "for women, & gt; 17" for men) (frequent causal factors and indirect symptoms possible; see "Obesity" below)
Obesity often causes fat accumulation under the chin and around the neck, suppresses the trachea when a person is in the supine position, and the center of obesity can, depending on on the individual fat distribution, causing an increase in direct pressure in the thoracic cavity and/or anterior shift (toward the head) of the abdominal organs, in the latter case reducing the space for and increasing the difficulty of diaphragm movement. Bad breathing during sleep a ] reduces the oxygen available for metabolism and therefore can suppress basal metabolic rate during sleep, increasing the difference between food supply energy and demand for it during that time and thus increasing the increase weight, and b ] reduces sleep quality and recovery per unit of sleep time, resulting in drowsiness and/or fatigue which can cause the patient to eat more in an effort to increase short-term energy levels.
• Correlation with heart problems:

• 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 relationship between CSA and AF include causal relationships in one direction or another between two conditions or common causes involving cardiacpiratory central regulatory disorders.
• Adults suffering from congestive heart failure are at risk for central apnea called Cheyne-Stokes respiration, which manifests itself well during sleep and during waking hours. The Cheyne-Stokes respiration is characterized by periodic breathing that features recurrent episodes of alternating apnea with rapid breathing episodes. There is good evidence that failed heart replacement (heart transplant) cures central apnea in these patients. Temporary measures (eg, , taken while awaiting availability of organ donors) include administration of drugs whose effects include respiratory stimulation, although they are not universally effective in reducing the severity of Cheyne-Stokes apnea.

Congenital central hypoventilation syndrome

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

After almost a fatal uniform, CCHS can now be treated. Children who have it must have tracheotomies and access to mechanical ventilation on the respirator during sleep, but most do not need to use a respirator when awake. The use of a diaphragm pacemaker may offer an alternative to some patients. When a pacemaker allows multiple children to sleep without using a mechanical respirator, the reported cases still require tracheotomy to remain in place because the vocal cords do not move apart by inhalation.

People with syndrome who survive to adulthood are strongly instructed to avoid factors that aggravate certain conditions, such as alcohol use, which can be easily proven to be lethal.

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Secondary effects

The condition of hypoxia and hypercapnia, whether caused by apnea or not, triggers additional effects on the body. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe lasts, how short the interval between failure to breathe, and the presence or absence of an independent condition that affects the episodes of apnea.

• Brain cells need constant oxygen for life, and if blood oxygen levels remain low enough for long enough, brain damage and even death will occur. This effect, however, is rarely the result of central sleep apnea, which is a chronic condition whose effect is usually much lighter.
• Decreased levels of oxygen in the blood that are severe but not severe enough to trigger brain cells or death as a whole can trigger seizures even in the absence of epilepsy.
• In severe cases of sleep apnea, a more translucent area of ​​the body will show the bluish or blackish casts of cyanosis, the discoloration ("blue") produced by blood deoxygenation in the vessels near the skin./li>
• The effect of compounding the independent conditions:

• In people with epilepsy, hypoxia caused by apnea may be strong enough to trigger seizures even with the presence of drugs that control seizures well.
• In adults with coronary artery disease, severe blood oxygen depletion can cause angina, arrhythmias, or heart attack (myocardial infarction).
• Long and repeated episodes of apnea can, for months and years, have a cumulative effect of increasing blood carbon dioxide levels to the point where enough carbon dioxide dissolves in the blood to form carbonic acid in sufficient overall proportion to cause respiratory acidosis..
• In people who have one or both forms of sleep apnea, breathing disorder during sleep can be exacerbated harmfully by taking respiratory suppressants, especially sedatives that operate by suppressing the central nervous system in general; respiratory depressants including opiates, barbiturates, benzodiazepines, and, in large quantities, alcohol, the last three are broad-spectrum SSP depressants. The amounts that are usually considered safe can cause people with chronic sleep apnea to stop breathing altogether. If these people have general anesthesia, for example, they require prolonged monitoring after early recovery, compared with people who have no history of sleep apnea, because apnea may occur even with low drug levels in their system.
• Sudden infant death syndrome is sometimes theorized by sleep apnea; A conventional recommendation since the mid-1980s, putting babies on their backs rather than their stomachs to sleep is an attempt to prevent examples of breathing cessation caused by compressive obstruction.
• Premature babies with immature brains and high-risk reflex systems for central sleep apnea syndrome, even if these babies are healthy. Premature babies who have syndrome will generally grow up after they grow up, provided they receive careful monitoring and supportive care during infancy to survive. Because of the premature infancy of central apnea, drugs that may cause respiratory depression are not given to them or given to them only under careful monitoring, with equipment for immediate resuscitation available. Such precautions are routinely taken for premature infants after general anesthesia; caffeine has been found not only to assist in the maintenance of respiratory function after general anesthesia but to reduce apnea for premature infants without context.

src: circ.ahajournals.org

Treatment

Source of the article : Wikipedia