heart author" faq
Obstructive sleep apnea


There are three types of apnea: obstructive, central, and mixed; of the
three, obstructive is the most common. Despite the difference in the
root cause of each type, in all three, people with untreated sleep apnea
stop breathing repeatedly during their sleep, sometimes hundreds of
times during the night and often for a minute or longer.

Obstructive sleep apnea (OSA) is caused by a blockage of the airway,
usually when the soft tissue in the rear of the throat collapses and
closes during sleep.

In central sleep apnea, the airway is not blocked but the brain fails to
signal the muscles to breathe.

Mixed apnea, as the name implies, is a combination of the two. With each
apnea event, the brain briefly arouses people with sleep apnea in order
for them to resume breathing, but consequently sleep is extremely
fragmented and of poor quality.


Approximately 30 million Americans are victims of a sleep disorder
called obstructive sleep apnea. Many millions more are predisposed and
have a high risk of developing the illness. If you are an adult male,
the odds are about 50/50 that your breathing is not normal when you are
sleeping. It is imperative that anyone who might have this problem or is
predisposed, or knows someone they care about who has the problem,
should have the clearest possible understanding about it.


1. What is Obstructive Sleep Apnea (OSA)?

People with OSA experience recurrent episodes during sleep when their
throat closes and they cannot suck air into their lungs (apnea). This
happens because the muscles that normally hold the throat open during
wakefulness relax during sleep and allow it to narrow(osa-fig5). When
the throat is partially closed and/or the muscles relax too much, trying to inhale will suck the throat completely closed and air cannot pass at
all (osa-figures5,6,6b,6c). This is an obstructive sleep apnea episode

Figure5: Obstructive sleep apnea (OSA) is caused by the closing of the upper airway while asleep.
The uvula and soft pallet collapses on the back wall of the upper airway. Then the tongue falls backward, collapsing on the back wall of the upper airway, the uvula and soft pallet forming a tight blockage, preventing any air from entering the lungs. The effort of the diaphragm, the chest and the abdomen only cause the blockage to seal tighter. In order to breathe the person must arouse or awaken, causing tension in the tongue thereby opening the airway, allowing air to pass into the lungs.

Figure 6: Snoring showing a partially closed upper airway

osa-fig 6c: Abnormal airway during sleep.
Multiple sites of obstruction often occur in patients with obstructive sleep apnea. An elongated and enlarged soft palate impinges on the posterior airway at the level of the nasopharynx and oral pharynx. In addition, a retruding jaw pushes an enlarged tongue posteriorly to impinge on the hypopharyngeal space.

A cessation of breathing must last 10 seconds or more to be called an
apnea. Obstructive apnea episodes can last as long as two minutes and
are almost always associated with a reduction in the level of oxygen in
the blood. When an individual is in the midst of an obstructive sleep
apnea episode, as long as sleep continues, the apnea continues. It is
only terminated and the victim's life is saved by waking up. This
arousal instantly increases the activity of the muscles of the tongue
and throat muscles that enlarge the airway. The victim will be able to
breathe and to once again fill the lungs with life-giving oxygen. This
cycle may be repeated hundreds of times a night while the sufferer has
no idea it is happening.

2. What are the cardinal symptoms?

a) Fatigue and tiredness during the day.
b) Loud snoring; if the loud snoring is repeatedly punctuated by brief
periods of silence or choking sounds, the individual is certain to have
obstructive sleep apnea.

3. Other common features are:

a) Obesity
b) Small jaw, thick neck

osa-fig 6f. A 24-year-old woman with facial abnormalities that contribute toobstructive sleep apnea.

(Lower) The receding lower jaw provides inadequate support for the lower lip, resulting in lip curling and a deep mental-labial fold (curved arrow).
(Upper) Shortness of the lower one third of the face (arrows) contributes to inadequacy of the airway.

c) High blood pressure
OSA is now recognized to be an independent risk factor for daytime
hypertension (osa-fig4).

osa-Figure 4 Dose-response relationship between the severity of
obstructive sleep apnea based on apnea-hypopnea index and the adjusted odds ratio of hypertension, defined as blood pressure >140/90 mm Hg or current treatment with antihypertensive medications. Odds ratio was adjusted for baseline hypertension status, age, gender, habitus, and weekly alcohol and cigarette use. P= 0.002 for linear trend of the logistic regression coefficients.
data from Peppard et al.

d) Restless sleep; the repeated struggle to breath can be associated
with a great deal of movement.
e) Depressed mood and/or irritability
f) Reduced sex drive and impotence
g) Snorting, gasping, choking during sleep

4. Not as commonly reported but may be present:

Feeling that sleep is strangely unrefreshing
Difficulty concentrating
A dry mouth upon awakening
Excessive perspiration during sleep
Heartburn(gastroesophageal reflux)
Rapid weight gain
Morning headaches
Change in personality
Memory lapses
Intellectual deterioration
Frequent nocturnal urination (nocturia)
Confusion and severe grogginess upon awakening
Specially in young children, large tonsils and adenoids.
There may be chest retraction during sleep (the sternum and the
spaces between ribs pull unnaturally inward when trying to inhale)

4. How serious is OSA?

Depending on the degree of severity, OSA is a potentially
life-threatening condition. Someone who has undiagnosed severe
obstructive sleep apnea is likely to have a heart attack, a stroke,
cardiac arrest during sleep, or a harmful accident(osa-fig.3)

Figure 3. Prevalence of obstructive sleep apnea (OSA) in patients with cardiovascular and cerebrovascular disease.

The figures used are approximations from published data and are unadjusted for baseline variables (1 to 4):

1. Parati G, Ongaro G, Bonsignore SIR, Glavina F, Di Rienzo M, Mancia G. Sleep apnoea and hypertension. Curr Opin Nephrol Hypertens 2002; 11:201-14;
2. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med.1999;160:1101-6;
3.Bassetti C., Alrich, Ms .Sleep apnea i acute cerebrovascular diseases:final report on 128 patients. Sleep 999;22:217-23;and
4.Peker Y. and others. An independent assoiation between obstructive sleep apnea and coronary artery disease.Eur.Respir.J 1999;14:179-84.

Sleep apnea has clearly been demonstrated to be an independent risk
factor for hypertension.More importantly,all published studies have
shown that a large proportion(40% to 80%) of stroke patients have
OSA, suggesting it may increase the stroke risk beyond direct effects on
blood pressure level and variability.
Patients with OSA have many features in common with the metabolic
syndrome, including systemic hypertension(osa fig.2), central obesity,and
insulin resistance(due to increased sympathetic nerve activity).

Figure 2 Sympathetic nerve activity increases through the obstructive apnea, resulting in marked vasoconstriction followed by increased systolic and diastolic blood pressure.

Continuous positive airway pressure (CPAP) stabilizes both sympathetic activity and blood pressure surges. BP = blood pressure (mm Hg); OSA = obstructive sleep apnea; REM = rapid eve movement; RESP = respiration; SNA = sympathetic nerve activation. permission.

The risk of experiencing angina or an acute coronary syndrome is
increased in the hours after waking from sleep.

Strong evidence of a link between snoring and stroke now exist from
case-controlled studies.

Arrhythmias and risk of causes of cardiovascular morbidity in OSA
patients appears related to the severity of sleep apnea.

Obstructive apnea is common in heart failure patients.40% of these
patients had CSA (central sleep apnea),which differs from OSA in that
there is periodic cessation of breathing with no "respiratory
effort",followed by hyperventilation.The key mechanisms of periodic
breathing in heart failure patients are enhanced chemoreflex
sensitivity,hypocapnia ,and unstable breathing control,especially
during sleep.
Patients with heart failure can have a combination of CSA and OSA.

Acute pulmonary hypertension changes during obstructive apneas are well
defined but the extent to which these tranlate into permanent daytime
PHT remains less certain.

In addition, awakening to breathe hundreds of times in a single night
causes the victim to become very sleep deprived. There is a constant
risk of serious accidents such as falling asleep while driving as well
as impaired function in the workplace and in personal relationships. All
of the negative consequences of OSA increase as severity increases.

Untreated OSA tends to progressively worsen and sooner or later will
result in partial or complete disability and death.

5. Risk Factors

a) The primary risk factor for OSA is excessive weight gain(see osa-fig 6b below). The accumulation of fat on the sides of the upper airway causes it to become narrow and predisposed to closure when the muscles relax.


osa-fig 6b An obese young woman with the short, thick neck typically seen in patients with obstructive sleep apnea.

b) Age is another prominent risk factor. Loss of muscle mass is a
common consequence of the aging process. If muscle mass decreases in the
airway, it may be replaced with fat, leaving the airway narrow and soft.

c) Men have a greater risk for OSA. Male hormones can cause structural
changes in the upper airway.

d) Other predisposing factors associated with OSA include:

e) Anatomic abnormalities, such as a receding chin

osa-Fig.6h.A 36-year-old woman with facial abnormalities that contribute to obstructive sleep apnea. Note the small, receding jaw (black arrows), as well as the moderate curling of the lower lip and the deep mental labial fold (white arrow).

f) Enlarged tonsils and adenoids, the main causes of OSA in children

osa-fig 6d Enlarged uvula resting on the base of the tongue (large arrow), along with hypertrophied tonsils (small arrows). The posterior pharyngeal erythema may be secondary to repeated trauma from snoring or gastroesophageal reflux

osa-fig 6e Elongated soft palate (arrows). In this patient, an increased anteroposterior dimension caused the soft palate to rest on the base of the tongue in the relaxed position.

g) Family history of OSA, although no genetic inheritance pattern has
been proven

h) Use of alcohol and sedative drugs, which relax the musculature in
the surrounding upper airway

i) Smoking, which can cause inflammation, swelling, and narrowing of
the upper airway

j) Hypothyroidism, acromegaly, amyloidosis, vocal cord paralysis,
post-polio syndrome, neuromuscular disorders, Marfan's syndrome, and
Down syndrome

k) Nasal congestion


If you suspect that you may have OSA, what should you do?

1) You must first become as knowledgeable as possible about OSA yourself.
2) You can also do a number of simple things that will convert your
suspicions into certainty.

3) The best first step is to involve your spouse or other family member. He
or she can audiotape or videotape you while you are sleeping. The sounds
and repeated silences and struggles to breath are highly characteristic.

4) When you have enough ammunition, make an appointment with your
physician specifically to get help for your OSA. Your spouse must
accompany you if at all possible.

5) Polysomnography is the "gold standard" diagnostic tool for assessing
sleep-disordered breathing.

It requires an overnight stay at a sleep laboratory, with monitoring of
oxygen saturation, heart rate, sleep stage by electroencephalography,
nasal airflow, oral airflow, jaw muscle tone by electromyography, sleep
position, and chest and abdominal

Measurement of these parameters allows diagnosis of the type
of sleep-disordered breathing and its severity. The apnea-hvpopnic index
(AHI)-the number of obstructive events per hour-is the most commonly
used measurement to quantify OSA:mild OSA = 5-15 events/h;moderate=15 to 30 events/h; and severe > 30 events/h.A "negative" polysomnographic
study does not exclude mild OSA,however,because there is night-to-night
variability in the frequency of obstructive events(osapolysomnography-Fig.1).

oaspolysomnograghy-figure 1 Polysomnography: an overnight summary.

The graphs from the top are:

1) hypnogram: the sleep stage report (MOV AWK = movement when awake; REM = rapid eye movement; 1 to 4 = non-rapid eye movement sleep);

2) arousals: each is a single mark;

3) SaO2 = percentage oxygen saturation;

4) apnea score: each is a single mark (Cn.A = central apnea; Ob.A -_- obstructive apnea; M4x.A = mixed apnea; Hyp = hypopnea; Uns =unscored);

5) PLMS=paroxysmal limb movements;

6) heart rate versus time(beats/min.);

7) body position: this subject remained on
his back throughout the study; and

8) time(h).

All patients with hypertension,obesity, or heart failure should be asked
routinely asked about OSA(see paragraphs 2-4 above describing cardinal
symptoms and referred for a sleep study if they are symptomatic.

The Epworth Sleep Scale standardizes these questions and these by
providing a rapid,validated method of screening for tiredness and is
useful in both clinical practice and research settings.

Table 1. Epworth Sleepiness Scale


Sitting and reading
Watching TV
Sitting in an inactive place (e.g., movie)
As a passenger in a car without a break for an hour
Lying down to rest in the afternoon when the circumstances permit

Sitting and talking to someone
Sitting quietly after lunch without alcohol
In a car, while stopped for a few minutes

Scale--------------------------------------------------- Score


No chance of dozing-----------------------------------0
Slight------------------------------------------------------ 1
Moderate------------------------------------------------- 2
High-------------------------------------------------------- 3
(Score for each situation is added to total)


<-6 = Less tired than average
7-8 = Average
<-9 = Tiredness requiring investigation

How is sleep apnea treated?

For obese subjects, including those with the metabolic syndrome, weight loss is a cornerstone of therapy, not only by reducing AHI ( apnea-hypopnic index - the number of obstructive events per hour), though seldom to
normal, but also by improving hypertension, lipid metabolism, and insulin
resistance. Patients with a normal BMI, severe OSA at diagnosis, or those
having difficulty losing weight require specific treatment of OSA, such
as nasal CPAP or an oral appliance. The mainstay of OSA therapy for the
past 20 years has been nasal CPAP. But an alternative or even first line treatment of mild and moderate OSA is the use of oral appliance therapy, which can also serve as therapy for severe OSA, where CPAP is not viable or tolerable (Personal communication from Dr. David J. Stern DDS, DABDSM, MSCC, MAAD, Member of Canadian Sleep Society).

As you are probably aware of the most recent guidelines, in the practice parameters established by the AASM has recomended Oral Appliance Therapy as a first line treatment of Mild and Moderate OSA and even as therapy for Severe OSA where Cpap is is not viable or tolerable. I sincerely believe your readers may benefit from this information and may be appreciative aware of more alternatives to treatment.
Kindest regards
David Stern
Doctor of Dental Surgery
Diplomate of The American Board of Dental Sleep Medicine
Member of The Canadian Sleep Society
Member of The American Academy of Cosmetic Dentistry

1. The most commonly prescribed treatment for obstructive sleep apnea is
continuous positive airway pressure (CPAP). The CPAP machine delivers
air pressure through a small nasal mask that the patient wears while
sleeping (osa-fig7).

Figure 7: CPAP flow generators develop a constant, controllable pressure to keep the upper airway open so that one can breath normally. CPAP is effective on 95% of the patients with OSA. The units are reliable, quiet and efficient and come in a variety of sizes and shapes.
Controlled pressure is induced through the nasal passage, holding the soft tissue of the uvula and soft palate and the soft pharyngeal tissue in the upper airway in position so the airway remains open while one descends into the deeper stages of sleep and REM sleep. The pressure acts much in the same way as a splint, holding the airway open.

The pressure acts as an "air splint" as noted above ,which keeps the
throat open ,eliminating obstructive apneas and allowing one to breathe normally all night long. Sleep becomes uninterrupted and restorative. For many patients, CPAP therapy dramatically improves their daytime functioning
as well as their general health. CPAP is not a cure, but a noninvasive
therapy for managing OSA.

There are typically three methods of inducing the pressure and airflow into the nasal cavity: nasal masks, nasal pillows and nasal seals. The most common used is the nasal mask. Nearly all CPAP manufactures make at least one style of nasal mask, most make two or three different ones. Nasal pillows are small, oval shaped latex rubber prongs that fit into the opening of the nostril. They are held in place by a shell that is attached to the headgear. When fit properly they are very comfortable and seldom leak. Nasal seals fit against the opening of the nostril and are held in place by a special frame attached to the headgear.
Compliance can be a problem, even in patients with severe symptomatic
OSA. some patients do not tolerate the therapy, and others find purchasing a machine financially prohibitive.Early followup when commencing CPAP therapy is important.Common concerns raised when initiating CPAP therapy include nasal congestion or dryness,which can usually be over come with a humidifier,and abrasions or mask leak,which respond to local measures.

Nursing support and intensive education programs have also been shown to improve compliance.Followup studies indicate,on the average,4 h of effective CPAP is administered per night,and even thie amount of CPAP treatment improves daytime tiredness.

The latest development in CPAP treatment is automated CPAP.These devices determine the prssure for each breath.Improved tolerability is particularly noticeable in patients who awake frequently,those with body dependent and rapid eye movement-related OSA.Detailed data logging of compliance and air l=eak by these devices also allows monitoring of the effectiveness of the treatment.

2. Sleep apnea can also be treated surgically. However, the costs and
success rates may vary greatly depending on which procedure is chosen
and the experience and skills of the surgeons. If one wishes to consider
surgical treatment of OSA, learning as much as one can about the various
surgical procedures is very highly recommended. One must also be certain
the surgeons are well qualified and have successfully treated many patients.

3. The following surgical procedures are available foe OSA in patients who cannot tolerate CPAP.Caution is necessary when prescribing these therapies,as apneas are rarely completely averted and less information is available on their effectiveness,particularly in patients with cardiac failure:

Genioglossus Tongue Advancement

Hyoid Suspension

Somnoplasty (Radio frequency or RF procedure)

Maxillomandibular Advancement

osa-fig. 6I and 6J Lateral skull radiographs of a patient before and after treatment.

(Lower) The patient has a retruding jaw and an attenuated posterior airway space of 6 mm (arrows).
(Upper) Maxillofacial surgery produces normal maxillary-mandibular occlusion and an adequate posterior airway diameter of 12 mm (arrows).

Laser Assisted Uvuloplasty (LAUP)

Uvulopalatopharyngoplasty (UPPP)

Tracheostomy,in extreme situations where OSA is severe and CPAP is not tolerated.

4. Finally, some patients try dental appliances. These appliances work by
bringing the lower jaw forward to increase the size of the airway. This
approach is usually reserved for milder cases of OSA or for individuals
who snore but don't obstruct. Relatively few well-designed studies exist
to show that these appliances work well, nor has patient compliance been
carefully evaluated.

How does Continuous Positive Airway Pressure (CPAP) therapy work?

In the last decade and a half, continuous positive airway pressure
(CPAP) machines have been the most effective way of treating obstructive
sleep apnea.

1. To use the machine, a small comfortable mask is fitted over
the nose leaving the mouth uncovered. Patients must sleep with their
mouths closed, aided by a chin strap, while the machine gently blows air
into the nose at a pressure slightly higher than the surrounding air
pressure. Most people get used to it quickly, some do not.

2. Literally within minutes of achieving the correct CPAP pressure to
maintain an open airway, patients with obstructive sleep apnea start
sleeping like people who have gone without sleep for many days. For the
first week or so after starting to use the machine, patients will spend
a great deal of time in deep sleep. Patients often report that there is
a dramatic increase of daytime alertness and energy in just a few nights
on CPAP.

3. Nasal CPAP is by now a very well established and safe treatment. Most
insurance companies will cover the cost of leasing or purchasing a
machine. Today, thousands of CPAP users are now happy after experiencing
a dramatic positive improvement in their daytime alertness and energy level.

There are three types of CPAP devices: Standard CPAP, Bi-level CPAP, and
Smart CPAP.

Who To Treat?

Treatment of OSA to relieve symptoms of daytime tiredness and to avoid somnolence-induced motor vehicle and work-related accidents is an established practice . Recently there has been increased interest in the role of CPAP to prevent cardiovascular disease and aid in controlling hypertension. Evidence for a dose-response relationship between AHI and daytime hypertension is strong, and small studies have shown improvements in blood pressure , baroreceptor sensitivity , and nitric oxide derivative production , and a reduction in sympathetic nervous system activation with treatment of OSA.
In heart failure patients, CPAP provides symptomatic relief and reduces the need for incubation during acute exacerbations . Small trials have demonstrated improved quality of life and exercise capacity with CPAP therapy. Improved left ventricular ejection fraction has also beenIn heart failure patients, CPAP provides symptomatic relief and reduces the need for intubation during acute exacerbations . Small trials have demonstrated improved quality of life and exercise capacity with CPAP therapy. Improved left ventricular ejection fraction has also been reported, with deterioration in left ventricular ejection fraction on withdrawal of therapy . Mechanisms by which CPAP therapy exerts its beneficial effect may include reductions in left ventricular afterload and sympathetic nerve activity . Currently, the Canadian Continuous Positive Airway Pressure Trial for Congestive Heart FailurePatients with Central Sleep Apnea (CANPAP) is underway, with the aim of further defining the role of CPAP in heart failure therapy .
Arrhythmia reduction and improved PHT have also been reported with CPAP. For many cardiovascular events, including acute coronary syndromes and sudden death, however, no treatment studies are available, so treatment decisions must be made empirically.

Figures osa 1, 2, 3, 4 from Lattimore, Jo-Dee L. and al. OSA and Cardiovascular Disease, Jaccvol.41, No.9.2003, May , 2003: 1429-37.

Figures osa 6D, 6F,6I, 6J from Sheldon Mintz, D.D.S., M.S., M.S., Dearborn, Mich.

Figures osa 6c, 6e from Lyle D. Victor, M.D., Department of Medical Education, Oakwood Hospital, 18101 Oakwood Blvd., Dearborn, MI 48124