The central sleep apnea (CSA) is a heterogeneous group of disorders that is characterized by changes in respiratory drive without obstruction of the airways. Most of these diseases cause asymptomatic changes in breathing patterns during sleep. Diagnosis is based on clinical findings and, if necessary, confirmed by polysomnography. The treatment is symptomatic.
The central sleep apnea (CSA) is a heterogeneous group of disorders that is characterized by changes in respiratory drive without obstruction of the airways. Most of these diseases cause asymptomatic changes in breathing patterns during sleep. Diagnosis is based on clinical findings and, if necessary, confirmed by polysomnography. The treatment is symptomatic. Etiology patients with CSA are classified based on their CO2 levels and their respiratory drive into 2 groups. One group presents itself as hypercapnic reduced respiratory drive before. The causes include hypothyroidism and central lesions (z. B. brainstem infarcts, encephalitis, Arnold-Chiari syndrome). The other group presents with Eukapnie or Hypokapnia with increased respiratory drive but sleep induced apnea, periodic breathing or both before. Cheyne-Stokes respiration, a discrete pattern of this second form of the CSA, is suspected of it is produced by intrinsic properties of the respiratory control center in response to hypoxia and acidosis with hyperventilation, to reoxygenation and alkalosis caused, leading to hypoventilation performs hypopnea and apnea. Altitudes are another cause of recurrent CSA, which manifests itself with hypocapnia. Chronic use of opiates (z. B. patients on methadone, cancer patients with chronic pain) triggers a CSA from erratic with a frequency and depth of breathing, and apnea. The CSA may be “hypercapneic or hypocapneic”. The congenital central hypoventilation (a form of undine Bane syndrome) is a rare form of idiopathic CSA in neonates and may be associated with Hirschsprung’s disease. A mutation of the gene PHOX2 is responsible for 80-90% of cases. This mutation produces variable phenotypes and clinically manifest cases are inherited in a dominant pattern. Symptoms and complaints CSA is usually asymptomatic and is noticed by nurses or sleeping partners, which long strike respiratory pauses, shallow breathing, or restless sleep. Patients with hypercapnic variant can develop daytime sleepiness, lethargy and headaches in the morning. Diagnosis Clinical evaluation Often polysomnography The diagnosis is suspected on the floor of the medical history and confirmed by polysomnography. However, the study may not be necessary if the CSA does not cause symptoms or if it is due to a clearly identifiable cause. To find the causes of CSA, the Bilfgebung of brain or brainstem may be indicated. Therapy Supportive treatment The primary treatment is the optimal management of underlying causes and the avoidance of opiates and other sedatives. The secondary treatment of symptomatic patients may be in a tentative additional O2 administration or in patients with hypercapnic CSA having despite treatment symptoms consist in non-invasive continuous CPAP or bilevel positive airway pressure. In patients who CSA and Cheyne-Stokes respiration, have an ongoing CPAP may reduce the apnea and hypopnea, but the effects on clinical outcomes are not clear. Acetazolamide is effective in CSA by staying at high altitudes. Electrode stimulation of the phrenic nerve and / or the membrane is a possibility, as in children> 2 years with congenital central hypoventilation syndrome. More information American Sleep Apnea Association Stop Bang Questionnaire