Clinical forms of sleep apnea
Sleep apnea was classified into three types:
a) Obstructive sleep apnea;
In obstructive apnea, airflow ceases despite respiratory impulses, its cause oropharyngeal obstruction with persistent thoracic-abdominal respiratory movements; usually is accompanied by a reduction in oxygen saturation, followed by a micro-awakening and resume normal breathing temporarily.
The narrowing of the upper airway obstructive apnea is usually done at oropharyngeal muscle tone following the collapse of the pharyngeal dilators, whose contract ensures the maintenance of upper airway patency during inspiration. May be secondary to obstruction and mandibular malformation, tonsillar hypertrophy or alterations of pharyngeal teeth and soft tissues of acromegaly, myxedema, and obesity.
b) Central sleep apnea;
Central type apnea is characterized by the fact that the nervesresponsible for all respiratory muscles are temporarily abolished. This is a neuronal dysfunction while obstructive apnea is a mechanical lock, although the effects are similar. Recurrent episodes of apnea are not accompanied by respiratory effort, patients with a defect in breath control or neuromuscular function. Polysomnographic, during episodes of apnea central, does not register thoracic-abdominal respiratory movements.
Central apnea, although permeable airway is often accompanied by insomnia and can cause excessive daytime sleepiness. These unobtrusive apnea occurs in both elderly and in premature and newborn babies to term. Central apnea and oxygen desaturation producing cardiac arrhythmia episodes appear to be involved in sudden infant death syndrome.
Compared with obstructive apnea, the central origin are rarer. They occur more frequently during light-wave sleep and are based on alterations in metabolic regulation and control system of breathing.
c) Sleep apnea - mixed form
Mixed apnea, which consists of a central apnea followed by an obstructive component is a variant of obstructive sleep apnea. The two components of mixed apnea creates a complex picture symptomatic and functional consequences caused by humoral regular stop breathing. In the absence of respiratory movements most mixed apnea is central initial determination and ends as obstructive apnea. The sequence of events can be determined by polysomnographic recording.
Obstructive sleep apnea is significantly correlated with morbidity and mortality from cardiovascular disease was reaching 20-30% frequency at hypertensive. The prevalence of obstructive sleep apnea increases after age 40 years is about. 2% to 4% in men and women, with a marked increase in the prevalence in people who snore and obese. It is estimated that 8 of 11 snorting have obstructive sleep apnea. In men, the disease is 2 times more frequently than women.
Basic pathogenic element in obstructive sleep apnea syndrome, upper airway obstruction is usually the oropharynx. Resulting apnea causes a progressive asphyxia sudden awakening from sleep until after upper airway permeability and resume flow is restored. Patients fall asleep and sequences of events is repeated hundreds of times a night, resulting in fragmentation of sleep.
Upper airway obstruction during sleep alters both the control and regulation mechanisms of lung ventilation, and neuro-humoral bases of sleep-wake alternation. Metabolic imbalances and functional deterioration in sleep quality produce results accompanied by a wide range of pathological conditions associated, whose set is obstructive sleep apnea.
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