Just the facts, ma’am (or, Everything you ever wanted to know about upper airway collapse but were afraid to ask…)

The following section may go into more detail than you may need regarding the mechanics of collapse of the upper airway. It should give you a much better understanding regarding what’s really going on with snoring and OSAS, though, so I recommend that you give it a try…

The airway collapse in snoring and sleep apnea can be better understood when you look at a couple simple anatomic facts and understand the physics of the throat. The airway can be roughly divided into the two parts: the lower airway, consisting of the trachea (windpipe) and bronchi (bronchial tubes); and the upper airway, consisting of the vocal cords and everything above them. When you breathe, the expansion of the chest generates negative pressure forces, which sucks the air into the lungs. This negative pressure, as well as the force of the air rushing through the airways, exerts pressure on the walls of the airways, which if unopposed would result in collapse of the walls.

The lower airway has an advantage over the upper airway, in that the trachea and bronchi are constantly held open by a rigid framework of cartilage. This keeps the lower airway from collapsing from the force of these negative pressures. The upper airway isn’t so blessed, however. Patency of the upper airway is largely dependent on the activity of a number of muscles, referred to as dilator muscles of the pharynx. During sleep (especially rapid eye movement or REM sleep), there is a generalized relaxation of the upper airway muscles, especially of these dilators. This decreased dilator muscle tone, in conjunction with the negative pressure changes resulting from breathing, can result in narrowing or obstruction of the airway.

This then starts a vicious cycle: because of the airway narrowing, the body needs to generate even more negative pressure in the chest to keep the air flowing adequately. This results in a faster velocity of the airflow through the airway. This increased velocity through an already narrowed tube further reduces the pressure within the airway (that’s called Bernoulli’s principle for you physics fans), which causes even further narrowing by sucking the walls in even more. This vicious cycle eventually can result in obstruction, or apnea, in susceptible people.

Patients with what is referred to as “disproportionate anatomy” of the airway are particularly prone to complete airway collapse during sleep, or sleep apnea. Sleep apnea is manifested by repeated cycles of obstruction. During these obstructive episodes, snoring ceases and the person’s chest and belly heave as they try to suck air in through a closed air passage in vain. As this process continues, oxygen stores in the bloodstream can drop to seriously low levels, which can be dangerous.

The apneic event is eventually terminated by a loud gasp, snort, sigh, or startle, which occurs as the body attempts to restore throat muscle tone and airway patency. Breathing then resumes, and the patient slips back into deeper sleep. The cycle of events is repeated, in some people up to several hundred of times per night.

So why am I falling asleep all the time?

Because sleep apnea can really screw up your sleep. It can prevent you from getting enough quantity and quality of sleep to feel rejuvenated the next morning.

The sleepiness of associated with sleep apnea is referred to in medical lingo as excessive daytime somnolence (EDS). EDS results from the repeated cycles of obstruction that occur throughout the night. As previously outlined, the apneic event is terminated by a gasp, snort, body jerk, etc., which can be quite dramatic to the bed partner.

What is most interesting, however, is what is going on in the brain at the instant of this resuscitative snort or gasp. In order for the brain to get the body to open up the throat, the person actually has to briefly arouse or awaken for a fraction of a second; such microarousals can be seen easily on sleep studies. Even though the person is not conscious enough to be aware that he is awake, for that brief instant he is no longer technically asleep. Once airflow is restored, however, the person slips back into sleep, and the cycle begins all over again. Even though this cycle may repeat itself hundreds of times a night, these repetitive awakenings are usually not recalled in the morning. Nevertheless, the level of alertness during the day following such a fragmented night of sleep can be as impaired as if there had been no sleep at all.

The reason for this simple. Though severe sleep apneics might be able to accumulate up to 8 hours or more of sleep per night, it is done so in exceedingly small fragments. Sleep researchers have repeatedly demonstrated that for sleep to be restorative, it needs to occur in uninterrupted units of at least several minutes—and probably at least 10 minutes—each. If sleep is interrupted for any reason before this amount of time has elapsed, that sleep has little or no restorative value. If the repeated cycles of apneas and/or hypopneas occur repeatedly through the night, the whole night of sleep might be wasted. It is no wonder that so many sleep apneics find it hard to stay awake during their daily activities, have concentration problems, experience mood alterations, etc.

Another important concept to understand in regards to daytime sleepiness is that of “sleep debt.” It is well known that for each individual there is a specific amount of nightly sleep which is necessary to produce the same level of daytime alertness over successive days. Research has shown that every hour of restful sleep that an individual obtains less than that needed amount seems to be recorded in the brain as a debt, and this debt is precisely added up over time, much like a credit card balance. For example, if an individual who needs 8 hours of sleep per night only gets 6 hours a night for a week, the amount of lost sleep would add up to a sleep debt of 14 hours by the end of the week. This debt does not disappear on its own, but can only be repaid by getting extra sleep.

Most persons whose sleep has been significantly fragmented due to repeated apneic episodes feel sleepy the next day, though some individuals often do not feel sleepy even when they have accumulated sizable sleep debts. Yet all severely sleep deprived individuals develop a strong tendency to fall asleep, which could happen at almost any moment—in conferences, while driving, and during other sedentary or boring activities such as reading this website. As this sleep deprivation can drive the brain to sleep, the amount of the debt determines the level of risk that any person operating hazardous equipment or making crucial decisions may make a disastrous error.

It is important to note that excessive daytime sleepiness associated with significant snoring can occur even in the absence of classic apneic or hypopneic events. This is the case with an entity called upper airway resistance syndrome (UARS). UARS is significant snoring associated with increased airway resistance from partial airway collapse that doesn’t meet the criteria to be defined as true apnea or hypopnea on a sleep study. These people have airways that are narrowed enough to impede airflow, but not so much as to get diagnosed with true sleep apnea. In order to maintain airflow, though, they have to work hard enough that the increased effort results in frequent arousals, much like what is seen with true OSA. Because patients with UARS experience frequent arousals from this increased respiratory effort, they can be as sleep deprived as the most severe apneics, though they present with a normal or near-normal RDI.

What about sleepiness in the bed partner of the snorer? A study published in October of 1999 showed that the unlucky person sharing the bed of a significant snorer loses about an hour of sleep each night due to the buzzsaw noise—that is if the spouse is still in the same bed as the snorer!

And what if I don’t get my sleep apnea treated?

You could be in serious trouble. You could fall asleep while driving or operative heavy machinery. You could have a heart attack or stroke. You could develop high blood pressure. You could continue to get embarrassed by falling asleep in meetings, movies, or in the middle of dinner with that hot date you’ve finally gotten the nerve to ask out.

It is increasing recognized that OSAS can be implicated in a host of medical problems, including hypertension (high blood pressure), myocardial infarction (heart attack), angina (cardiac chest pain), and stroke. Though it can be difficult to prove a cause and effect relationship between OSAS and these conditions, many patients who undergo treatment of their OSAS show improvement in these conditions and mortality risks. It has been estimated that the cardiovascular consequences of untreated OSAS may contribute to 38,000 deaths and up to $2 billion of health care costs per year.

Keep your eye on this website in the near future when the results of a huge, multicenter study, the Sleep Heart Health Study, is published. This massive clinical study is investigating the links between sleep apnea and cardiovascular problems in much more depth.

The cumulative mortality rates associated with OSAS are thought to range from 11 to 13 %. In a landmark study published 1988, investigators studied the 8-year mortality rates in untreated vs. treated OSA patients. Those with a RDI < 20 had an overall mortality of 4%, vs. a 37% mortality in those with a RDI > 20. It is significant to note that no patients whose OSAS was corrected with tracheotomies died during the study.

Even when the OSAS is not severe enough to be associated with heart, lung, blood pressure or stroke problems or death, however, apneic patients may suffer significant consequences due to excessive daytime somnolence. As previously noted, this EDS is due to fragmented sleep and microarousals, and may lead to poor work performance and emotional disturbance due to impaired cognition and memory loss. It has been shown that reaction times in even moderate sleep apneics can be as impaired as people with blood alcohol contents of 0.08%. It is therefore understandable that the risk of automobile accidents in this population is up to 7 times that of non-apneics.

Finally, it is estimated that the economic impact in the United States of EDS from all causes (when defined as the sum of injury and death from auto accidents and industrial accidents) is more than $20 billion per year. OSAS is thought to be a significant contributor to this figure.

Are there any risk factors for this problem?

There are several risk factors for OSAS, including the male sex, obesity, older age, certain facial bone skeletal abnormalities, and familial risks.

Eighty-five percent of obstructive apneics are male, and the disorder is most common in the fifth through the sixth decades; loud snoring and excessive sleepiness may precede the diagnosis of frank sleep apnea by many years. Obesity is a strong predictor of OSAS, as 2/3 of these patients are more than 20% above ideal body weight. Among those facial skeletal anomalies that may predispose to OSAS are the Pierre Robin Syndrome, Treacher Collins Syndrome, and any other instances of mandibular development problems. In addition, if you have a family history of OSAS, you have a relative risk of development of the syndrome of 1.5.

Other factors that can exacerbate OSAS are tranquilizer use, sedating medications such as antihistamines, alcohol use, and fatigue. It is therefore extremely important for snorers and especially sleep apneics to develop regular sleep habits and improve their sleep hygiene, avoid alcohol in the evening, and stay away from sedating medications.

Hey, I’m asleep when this is going on. How am I supposed to know how bad the problem is?

You very likely may not have any idea of bad the problem really is. But your bed partner may have a clue; just ask him or her. But even this isn’t necessarily enough.

Most snorers are unaware of their snoring, and self-reported snoring alone is not enough to accurately predict the presence of OSAS. It is important for physicians to be able to identify which snorers are at high risk of having OSAS. This is primarily done through a combination of the history, physical exam, and the polysomnogram (sleep study).

As discussed in other parts of this website, the clinical features that suggest a history of OSAS include a history of habitual snoring, nocturnal gasping, witnessed apneic episodes, and daytime sleepiness. When a new patient is evaluated for snoring or presumed OSAS, experienced physicians realize that the bed partner may have the most insight as to what is going on. It is therefore suggested that the bed partner accompany the patient to the initial appointment, so that he or she can be questioned as well. Such questions include information regarding the degree of social disruption caused by the snoring, duration and frequency of the snoring, effects of body position, and whether or not the patient has apneic episodes. The patient’s bed partner may also be the best judge of the patient’s degree of EDS. (This also allows the bed partner to vent and bitch to the physician about how annoying the problem is, but that’s another story.)

The sleep study

Though the history is of course extremely important in evaluating the snoring patient, the primary method of determining the presence of OSAS is the polysomnogram (PSG), or sleep study. There are several different levels of polysomnographic analysis, from the full 10 to 12-channel technician-attended study, to a variety of unattended or “ambulatory” studies that provide less information but which may be adequate in some instances and which are certainly less expensive. There is not a clear consensus yet among sleep clinicians regarding the role for these less-intensive studies, and this debate is beyond the scope of this website.

The full polysomnogram is performed in a sleep center, often associated with a hospital or medical clinic, though some sleep labs are free standing. They are generally performed at night, and should be done during your regular sleep hours. A technician hooks you to a slew of wires, electrodes, monitors, and gauges, and then monitors the information obtained by all that equipment while you sleep. Yes, it is possible to actually sleep with all that equipment hooked up. Though it may not be the best quality sleep you will ever have, as long as you get to sleep, adequate information can be obtained. Sleep centers actually try hard to make their sleeping rooms as comfortable as possible, and many include showers, televisions, etc. to make it as easy as possible.

There is an accreditation process by which American sleep disorders centers are certified for standards of care. The American Board of Sleep Medicine, the accrediting body in the US, has a list of certified sleep labs around the country.

Aside from being the most expensive night of sleep you will ever have, much important information is obtained during a PSG. These include information regarding the quality and depth of sleep, body positions during sleep, breathing patterns, blood oxygen levels, limb movements, presence of snoring, and sometimes other information, such as stomach acid reflux during sleep or esophageal pressure measurements. This information is derived from a variety of monitors, wires, and gauges.

Information regarding the quality and depth of sleep (referred to as sleep staging) is obtained from monitoring your brain waves (via and electroencephalogram or EEG) and eye movements through the closed eyelids (via an electro-oculogram or EOG). There are several different stages of sleep, and for optimal rest, people need to spend a certain amount of time in each stage. These include Stages I, II, delta or slow wave sleep (stages III and IV), and rapid eye movement, or REM, sleep. REM sleep is the stage of sleep during which dreaming occurs and in which the person is most relaxed and motionless. Because of the generalized muscle relaxation of REM sleep, OSAS may be more frequent and/or more severe during this stage of sleep.

As the intensity and amount of snoring can vary significantly depending on sleep position (back, sides, or stomach), it is important to monitor body position with a position sensor during the PSG. As heart rate and rhythm can be affected by apnea, these are monitored by electrocardiogram electrodes, and blood oxygen levels are followed with an oximeter that painlessly clips to a finger.

A device called a thermister, placed at the nose or mouth measures airflow. A belt-like strain gauge is placed at the chest to detect the movements associated with breathing attempts. If those sensors show continued chest movements but the airflow thermister shows no airflow, you by definition are experiencing an obstructive apneic event. As stated earlier, that event must by definition last ten seconds to before it is counted during the sleep study. If chest movements and airflow both continue, but that airflow is significantly diminished over ten seconds, you are experiencing hypopnea.

At the conclusion of the PSG, the number of apneas and hypopneas is totaled, and divided by the number of hours of documented sleep to arrive at the respiratory disturbance index, or RDI. (Some sleep disorders instead refer to this number as the apnea-hypopnea index, or AHI, or the disordered breathing events index, or DBI, etc.)

The entity called periodic leg movements during sleep (PLMS) is defined by sudden and repeated leg jerks interfere with sleep. The presence of this problem is detected with leg electromyelogram (EMG) electrodes. Anther EMG electrode is generally placed under the chin during a PSG to detect the vibrations produced by snoring.

Other monitors used in some centers include an esophageal manometer to measure the intrathoracic pressures generated during breathing, helpful in detecting upper airway resistance syndrome (UARS), a snoring microphone, or an intrathoracic pH probe to detect gastroesophageal reflux.

In some instances, it is important to objectively quantify the degree of daytime sleepiness of the subject. This EDS is measured by performing a Multiple Sleep Latency Test, or MSLT. This test measures the average latency to Stage I of sleep for four consecutive naps on the morning following the PSG, utilizing much of the same equipment from the preceding night’s PSG. An average sleep latency of less than 10 minutes is abnormal, and is indicative of sleepiness. Sleep-onset REM periods are seen with narcolepsy and the MSLT is an important test in diagnosing this entity. Another test that is sometimes used in determining EDS is the Maintenance of Wakefulness Test, in which you would be told to try to stay awake in a non-stimulating environment.

What are some general guidelines for treatment of sleep apnea?

Certainly, it is possible to treat anyone with simple non-apneic snoring or minimal sleep apnea. But the important question is who needs to be treated from a medical standpoint? Unfortunately, there are no hard and fast guidelines for treatment, and the recommendations regarding treatment continue to change as new medical information is uncovered.

At present, though, there is a general consensus within the medical community to treat any person presenting with:

q Excessive daytime somnolence, especially when this interferes with the activities of daily living

q Twenty or more obstructive breathing events per hour of sleep, or pathologic EDS in selected cases with RDI < 20

q Significant oxygen desaturations, particularly when <85

q Arrhythmias associated with obstructive events

q UARS

Regardless of the type of treatment, follow-up is important. A post-treatment PSG should be obtained when significant OSAS has been treated, as self-reporting of symptoms is not enough. Likewise, CPAP compliance should be followed closely. A variety of new CPAP machine that can measure usage via built in computer chips makes objective measurement of compliance easy and reliable.

Treatment for snoring and sleep apnea can be either medical, or surgical, or both. The exact treatment plan for a specific person is dependent upon the severity of the problem, the patient’s desires and lifestyle, the relevant physical findings, the person’s overall health, and the presence of other contributing or complicating medical problems.

The remaining pages of this website will discuss the treatment of snoring and OSAS, beginning with proper sleep hygiene, and then following with medical treatment (including nasal CPAP, weight loss, and medications), dental appliances, and a thorough discussion of all available surgical options.