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Sleep apnea is a the most prevalent breathing disorder in society. It is characterized by repeated breathing pauses in the flow as a result of partial obstruction (hypopnea) or complete (apnea) of the upper airway. This collapse is usually generated at the height of the throat section. This disease is carried out exclusively during sleep and its exact pathophysiology has not yet been medically cleared. The conditions, that favor the development of OSA due to different anatomical and functional abnormalities of the upper airway that predispose to occlusion. Because of its importance in sleep breathing disorders, the upper airway structure requires further analysis.
The UA is composed of both rigid structures such as soft tissue and depressive alternate functions of breathing, swallowing and phonation. This multifunctional nature of the UA requires a complex machinery to allow opening during respiration and ensure its closure or narrowing during speech and food intake.
This equipment is built around a complex network of muscles and structures that modify and adjust the size of the UA according to their functionality integrating ventilation, swallowing and phonation. In the breath of the upper airway patency depends on a stable balance of power between the inspiratory muscles (diaphragm and intercostal muscles) and the pharyngeal dilator muscles. Constrictor and dilator action must be seen simultaneously in time and with similar intensity. Any mismatch in this activation results in the collapse of the UA. During the vigil, in the absence of diseases, the airway resistance is low because the tone of the dilator muscles is sufficient to maintain patency. The intrinsic muscle weakness during sleep changes radically the balance of forces and affects the dilator muscles, while tonic activity of the diaphragm remains unchanged. This alteration causes a physiological increase of the airflowresistance during sleep that can lead to collapse and cause the cessation of breathing. The study of mechanical ventilation and the anatomy of the UA is a key in understanding the pathophysiology of OSAHS.