Sleep Apnea Treatment

Causes

Sleep apnea has multiethiological character, that combines anatomical and functional factors, that converge in the development of the disease. An anatomical and functional alteration of upper airway disease is the epicenter, but the real cause of this syndrome still remains a mystery. With the current experience, we can only assume a wide range of conditioning factors, that are involved in diagnosed patients. But why at the same conditions, some subjects develop OSAHS and others not, is a question still unanswered. The development of OSAHS is caused by the convergence of neurological, anatomical, muscular and neuroventilatorious, that cause functional alterations, which trigger the disease. Although the pathogenesis is unknown, several hypotheses are envisaged to explain this mismatch between the functional theory of power imbalance and the imbalance of pressure, which shuffled neuromuscular and structural constraints potentially significant in the pathogenesis of OSAHS. All authors agree that the development of OSA is associated with anatomical, neuromuscular and neuroventilatorios agents.

Muscular factors
The relaxation or inactivity of the dilator muscles during sleep, predisposes to obstruction because it disrupts the forces junction opposed to the action of the diaphragm. An insufficient tone in the pharyngeal muscles lead to a distorted relationship between the dilator muscle function and action of the diaphragm, what due to neuromuscular dysfunction during sleep. In healthy subjects, the action of dilator muscles, the tensor palatine, the geniohyoid, sternohyoid, and mainly of the genioglossus, maintains the stability of the UA during sleep and their action is sufficient to counteract the negative pressure exerted by the diaphragm during inspiration. The studies suggest that OSAHS subjects present a dysfunction of the sensory receptors cause of the slow response of the dilator muscles against the pressure changes of the pharynx.

Anatomic Factors
The development of OSA is associated with anatomical changes. Morphological abnormalities involving the reduction of airway caliber influence an increased resistance and a predisposition to collapse. OSAHS is associatedto all the circumstances including morphological narrowing of the airways as tonsillar hypertrophy, retrognathia, macroglossia and patients with type II diabetes. Studies of patients with OSAHS have shown, that these awake patients have a smaller airway in diameter than those of healthy subjects. This observation would indicate a hypertrophy of the walls of the pharynx of OSAHS subjects common to favor the development of the disease, but whose cause is still unknown. As shown Carrera M. et al., the anatomical arrangement of pharyngeal light is representative in comparative studies of healthy subjects with OSA patients. The area does not differ in both groups, but it is not the same case in terms of shape and spatial arrangement, where differences are revealing. Noting the morphology of the pharynx in healthy subjects it has circular shape, however in OSAHS subjects, the anteroposterior diameter is less than the transverse and the pharynx acquires an oval or elliptical. The major axis in healthy subjects is coronal, and sagittal in patients with OSAHS. This has pathophysiological implications, because the pharyngeal dilator muscles (genioglossus, geniohyoid, sternohyoid, tensor palatine) are inserted into the anterior wall to tighten up, acting on its anteroposterior axis, increasing the diameter of the UA. In OSAHS patients , the predominant axis is anteroposterior, and the contraction of these muscles is not effective to dilate the caliber of the pharynx. Any anatomic obstruction, that reduces the size promotes pharyngeal collapse. Many of these alterations are common in OSA subjects and are easily detectable upon physical examination of the patient.

Neurological factors
The motor dysfunction of the muscles of the pharynx, as explained above, is essential in reducing the size of the upper airway, that causes the collapse in OSAHS persons. But the morphological conditions can not explain this collapse in them themselves and these anatomical changes producing a narrowing and predispose of the pharyngeal occlusion during sleep, are not of clinical importance in these same individuals during wakefulness. Therefore it is justified to defend, that the pathophysiology of OSAHS is intrinsically linked to the neurological mechanisms, that regulate sleep and adjust the tone of respiratory muscles to maintain steady the size of the UA. The investigations suggest, that subjects, which develop OSA, have some neurological disturbances. The activity of the respiratory system depend on extrinsic regulation of central nervous system. The breath acts sent from the central nervous system are stimulated by the central and peripheral chemoreceptors located in the brainstem, that are responsible for the automatic control of ventilation during sleep, in the absence of volunteer activity, settles in a "state" of vulnerability, which is responsible for sleep breathing disorders. Because of this fact the alterations in the central nervous system control, which regulates breathing and controls the dilator muscle tone, have a direct affect on the pathogenesis of sleep apnea.