Central sleep apnea


Central sleep apnea or central sleep apnea syndrome 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.
R/ SleepApnea

Signs and symptoms

In a healthy person during sleep, 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 send nerve impulses to the brain, which then signals for reflexive opening of the larynx and movements of the rib cage muscles and diaphragm. These muscles expand the thorax so that a partial vacuum is made within 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, located in the region of the human brain known as the pre-Botzinger complex, are imbalanced during sleep 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 apnea and hyperpnea, even for a brief time following 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, 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 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 for a while, 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 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 produced by the deoxygenation of blood in vessels near the skin.
  • Compounding effects of independent conditions:

Diagnosis

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 will replace a PSG 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 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:
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. 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 and symptoms of central sleep apnea
Signs and symptoms of and conditions associated with obstructive sleep apnea

Congenital central hypoventilation syndrome

Congenital central hypoventilation syndrome, 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.
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.

Treatment

After a patient receives a diagnosis, the diagnosing physician can provide different options for treatment. If central sleep apnea is medication-induced, reducing the dose or eventual withdrawal of the offending medication often improves CSA.
  • The FDA has recently approved a pacemaker-like implantable device called the remedē System for adult patients with moderate to severe central sleep apnea. After a commonly performed procedure, the device stimulates a nerve in the chest to send signals to the large muscle that controls breathing. It monitors respiratory signals during sleep and helps restore normal breathing patterns. The device is silent, activates automatically during the night, and does not require the patient to wear a mask.
  • Mechanical regulation of airflow and/or airway pressure:

Epidemiology

Central sleep apnea is less prevalent than obstructive sleep apnea. In one study, CSA is stated to have a prevalence of 0.9% in comparison to OSA.
There are many factors that increase the risk of developing CSA. Chronic opioid use produces a mean prevalence in central sleep apnea development of 24%. An estimate of 10% of chronic kidney disease patients have a CSA diagnosis. Cohort studies of stroke patients show a 70% development rate of CSA within 72 hours of the stroke event, although CSA was detected in less than 17% after 3 months of follow-up. Another cohort study from the Sleep Heart Healthy study showed the incidence of CSA in heart failure patients to be 0.9%.

Infancy

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.

Childhood

CSA is less common after 2 years of age. The prevalence of CSA in healthy children aged 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, CSA is more common and can occur in up to 53% of cases.

Adulthood

Research shows that rates of sleep apnea are higher in adults over the age of 65 years, 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%. 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 for apnea.