Snoring is caused, fundamentally, by airway narrowing — causing high velocity airflow. This high velocity airflow imparts kinetic energy to the soft tissues of the upper airway, and eventually causes vibration of soft tissue (perceived as snoring). Therefore, snoring is an indicator of upper airway narrowing (anyone who snores, by definition, has upper airway narrowing).
As the airway lumen narrows, the air moving within the airway tube has to increase velocity in order to fill the lungs in the same amount of time as the normal respiratory cycle (in other words, people with airway narrowing do not take longer to inspire and expire than people without airway narrowing; lung volumes do not change — therefore, the air has to travel more quickly through these areas of anatomic upper airway narrowing in order to fill the lungs during the normal respiratory cycle).
Changes in airway pressures result (Venturi and Bernouli principles apply), and the high velocity airflow imparts kinetic energy to the soft tissues within the airway. This energy, over time, causes stretching or pulling of these soft tissues — eventually leading to secondary elongation of these various tissues (typically, the soft palate is the most unsupported or compliant portion of the upper airway, and that is why the soft palate typically becomes elongated first). Additionally, the lateral pharyngeal walls may also become stretched over time.
These elongated tissues eventually become very loose and floppy (ie: compliant), and when the inherent tissue resistance to movement is overcome by the ongoing kinetic energy, vibration results. This vibration is what is perceived as snoring — and can be measured in terms of both frequency and intensity.
People are not born with long soft palates (primary elongation); instead, palates become stretched-out over many years of rapid airflow (secondary elongation).
It is important to realize, however, that the primary source of airway narrowing in these cases is typically NOT at the level of the soft palate. Instead, in the vast majority of patients, it is the tongue-base region in which the primary site of narrowing often occurs (in other words, the elongated and unsupported soft palate vibrates as a result of high velocity airflow produced by airway narrowing at another site within the airway).
While primary sites of airway narrowing will vary from patient to patient, upstream narrowing (often occurring in the nasal region) may also contribute to downstream collapse of the airway (ie: nasal obstruction may often contribute to tongue-base collapse — so-called Starling Resistor Effect). This is why it is often important to deal with areas of nasal obstruction as a pretext for solving problems occurring lower in the airway. Similarly, massively enlarged tonsils and adenoids (particularly in the pediatric population) may serve to affect airway narrowing and high velocity airflow — as well as contribute to further downstream narrowing.
People who suffer from very slight airway narrowing (ie: just enough to cause enough rapid airflow to cause snoring without frank closure of the airway) have a diagnosis of Primary Snoring. As the airway continues to collapse, however (with further rapid airflow until frank obstruction), snoring persists. This is why it is generally impossible to discern — out of all people who snore — who actually has sleep apnea versus primary snoring (in other words, all of these patients will snore). This is also why each person who snores truly requires some type of sleep study in order to discern the severity of their airway problem, and to discern whether snoring represents possible obstructive apnea.
Based upon the above model, there are actually three fundamental ways to deal with snoring:
Expansion of the airway is the fundamental mechanism for both CPAP and oral appliance therapy (nonsurgical therapies), and most tongue-base surgical procedures (including jaw advancement and hyoid suspension.)
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