SNORING and SLEEP APNEA

These terms describe parts of the continuum of airway collapsibility expressed as sleep-disordered breathing. This spectrum ranges from slight vibration of tissues at its mildest to death from asphyxiation at its severe extreme. Between lies pathologic snoring and periods of complete airway closure and breathing cessation called "apnea".

Some of the most serious chronic diseases of man have been associated with snoring and sleep apnea, including: stroke, hypertension (high blood pressure), myocardial infarction (heart attack), arteriosclerosis (hardening of the arteries), cardiac arrhythmias (irregular pulse), diabetes, gastro-esophageal reflux disorder (GERD), polycythemia vera (thickening of the blood) and others.

Sleep disordered breathing also disrupts the normal patterns of brain activity and relaxation, precluding restorative sleep. Overwhelming daytime sleepiness contributes to the risk of accident and injury from decreased attention span, judgment and reflex. The risk of automobile accident in the untreated sleep apnea patient is about 8 times that of the normal sleeper. Work productivity and safety suffer.

What happens?

During the increasing muscular relaxation of deepening sleep, the airway can become increasingly flaccid. The relaxing tongue falls back, sealing against the back of the throat during the sucking, negative pressure of the attempt to take a breath. Snoring is the vibration of the uvula, soft palate and throat walls against the tongue during the inspiratory phase of breathing, with reduced airflow due to increased resistance. As collapsibility increases, complete closure can occur.

In either narrowing (hypopnea) or closing (apnea) events, oxygen levels of the blood can drop precipitously triggering a response of the brain to prevent asphyxia. This "sympathetic discharge" of adrenaline, corticosteroids and other agents raise blood pressure, pulse rate, muscle activity and brain activity to protect the unconscious sleeper from death.