Obstructive sleep apnea -consideration of its pathogenesis.

The pathogenesis of obstructive sleep apnea (OSA) is characterized not only by obstruction of the pharynx, but also by repeated obstruction. OSA onset is thought to involve four phenotypic traits: pharyngeal muscle responsiveness, respiratory center instability (loop gain), arousal threshold, and anatomical factors. Patients with lower muscle responsiveness are likely to have OSA, whereas those with higher responsiveness are not. When the loop gain is relatively high, reaction and suppression of the respiratory drive are repeated, decreasing ventilation and pharyngeal muscle activity and leading to mixed or central apnea events. Patients with a low arousal threshold tend to have frequent respiratory events and less severe respiratory efforts, whereas those with a high arousal threshold tend to have fewer respiratory events and more severe respiratory efforts. Pharyngeal muscle activity, as well as respiratory drive, increases during apnea and decreases after its release. Patients with a low arousal threshold have lower muscle responsiveness and instability of the respiratory center control, whereas those with a high arousal threshold have higher muscle responsiveness and relatively stable respiratory control. The overshoot and undershoot responses of the chemical drive and pharyngeal muscle tone characterize the periodic repetition of obstructive events, which are enhanced by the arousal response. The presence of certain anatomical factors is prerequisite for the onset of OSA. Also, not only volume and flow, but also stiffness and elasticity may contribute to the pathogenesis of OSA. Mouth breathing also plays an important role in the mechanism of pharyngeal collapse. These four factors influence each other, with the first three-muscle responsiveness, loop gain, and arousal threshold-in particular in a trinity. The era is already close in which not only anatomical treatment, but also treatments for other traits can be selected and combined according to the individual pathophysiological condition of each patient with OSA.