Sleep. 19(9):S57-S60
© 1996 American Sleep Disorders Association and Sleep Research Society
How and Why Should We Stabilize the Upper Airway?
Victor Hoffstein
St. Michael's Hospital. University of Toronto, Toronto, Canada
Summary: This review focuses on the evidence for upper airway instability during sleep and on the methods
used to correct this instability. Upper airway patency during sleep is determined by the balance between the forces
tending to constrict the pharynx (i.e. negative suction force generated by the diaphragm) and those tending to dilate
the pharynx (i.e. force acting on the tongue, soft palate, and pharyngeal dilator muscles). The evidence for reduction
in genioglossus activity and tensor palatini activity, failure of compensatory mechanisms to maintain these activities,
and increase in upper airway resistance during sleep is reviewed. Coupled with abnormal pharyngeal anatomy to
start with, the above events lead to abnormal pharyngeal function and cause repetitive episodes of airway occlusion,
that is, sleep apnea. It is concluded that abnormal airway function in sleep apnea is a diffuse, rather than a localized
process, that may involve the entire airway from the nasopharynx to the larynx. Methods to improve abnormal
pharyngeal anatomy and pharyngeal function, such as nasal continuous positive airway pressure (CPAP), oral
appliances, posture, weight loss, medications, and surgery are discussed. Given the pathophysiology of sleep apnea,
that is, diffuse abnormality of the upper airway, it is reasonable to expect that only those approaches that exert a
beneficial effect on the entire upper airway, as opposed to the approaches that modify only a short segment of it,
may be expected to be of benefit in treatment of sleep apnea. Key Words: Sleep apnea-Upper airway patencyContinuous positive airway pressure-Abnormal pharyngeal anatomy-Oral appliances-Sleep position-Surgery-Electrical stimulation.
Why is the upper airway unstable?
Upper airway instability is the final common pathway leading to recurrent episodes of complete or partial airway obstruction during sleep. Stabilizing the upper airway will resolve sleep apnea. To understand the
rationale behind various techniques used to accomplish
this goal, we must first understand the mechanisms of
airway instability in patients with sleep apnea. Let us
briefly review this subject by considering first what
normally happens to the upper airway with the onset
of sleep.
Almost 20 years ago Sauerland and Harper (1) noted
a progressive reduction in the activity of the genioglossus muscle (which controls the tongue and is
therefore one of the important determinants of upper
airway patency) during sleep in normal subjects. This
means that the tongue relaxes and tends to fall backwards, thus occluding the upper airway. Tangel et al.
(2) noted a similar sleep-induced reduction in the activity of the tensor palatini muscle, meaning that the
soft palate tends to fall backwards. Consequently, the
pharyngeal airway becomes narrower during sleep, a
Accepted for publication July 1996.
Address correspondence and reprint requests to Dr. V. Hoffstein,
St. Michael's Hospital, 30 Bond Street, Toronto, Ontario M5B 1W8,
Canada.
fact noted by several investigators. For example, Hudgel et al. (3) showed that in normal sleeping subjects
the supraglottic (i.e. pharyngeal) airway resistance increases, that is, the pharynx becomes more narrow,
whereas the lower airway (i.e. laryngeal and lung) resistance is unchanged. This tendency to airway occlusion becomes more pronounced during inspiration.
Each negative swing of the intrathoracic pressure tends
to "suck" the tongue and the soft palate downward,
occluding the airway. Airway patency during normal
sleep is maintained because, on balance, the force acting to keep the airway open, that is, neuromuscular
force generated by the pharyngeal dilating muscles,
wins over the collapsing force generated by the negative suction of the thoracic pump, mainly the diaphragm (4,5).
Remmers et al. (6) hypothesized that this balance of
forces is disturbed in patients with sleep apnea. He
demonstrated that the genioglossus muscle, which controls the tongue, plays an important role in the pathogenesis of airway occlusion (6). During the occlusion,
negative intrathoracic pressure progressively increases,
genioglossus muscle activity is low, and there is a
burst of activity when the obstruction is released. This
peak in genioglossus muscle activity always coincides
with release of pharyngeal occlusion and opening of
the airway. High negative intrathoracic pressure, al-
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V. HOFFSTEIN
ways generated during episodes of airway occlusion,
exerts a retracting force on the passive tongue, forcing
it backwards and down. This force exceeds the dilating
force of the genioglossus, causing complete occlusion
of the pharynx. Contrary to what happens in normal
subjects, in patients with sleep apnea it is the airway
suction force, tending to constrict the pharynx, that
wins over the dilating forces of the pharyngeal muscles. This basic concept of airway instability, caused
by the imbalance between the constricting influence of
the negative intrathoracic pressure generated by the diaphragm and the dilating influence due to neural activation of the dilating muscles of the pharynx, remains unchallenged. Most of the research in this area
has been directed toward a better understanding of the
factors that perpetuate airway instability, tilting the
balance of forces toward pharyngeal collapse. The factors favoring airway occlusion can be broadly divided
into two categories: 1) abnormal airway structure and
2) abnormal airway function.
Abnormal airway structure means anatomical narrowing of the airway; this can occur at any level in
the pharynx and may be present even during wakefulness. These anatomical abnormalities leading to upper airway narrowing may be quite gross and obvious
on physical examination. They include micrognathia,
macroglossia, tonsilar or adenoidal hypertrophy, etc.
In most patients, however, the anatomical abnormalities are subtle and can only be demonstrated using
specialized techniques. For example, we used acoustic
reflections to demonstrate that total pharyngeal area
(or volume) is lower in patients with obstructive sleep
apnea (OSA) than in control subjects (7). Other investigators, using various imaging techniques, have also
demonstrated reduction in upper airway area during
wakefulness or sleep in patients with OSA (8,9).
Whatever the reason for abnormal anatomy, it is
clear that the anatomically narrow airway is more vulnerable to collapse on inspiration than a wider airway,
because greater inspiratory pressures are required to
generate adequate airflow.
Abnormalities in pharyngeal function include increased collapsibility of pharyngeal walls and abnormal function of pharyngeal dilator muscles. "Floppiness" of pharyngeal walls in patients with sleep apnea
has been demonstrated using several techniques. For
example, we used acoustic reflections to measure pharyngeal area in response to applied pressure and found
that, for the same negative suction pressure, pharyngeal area is reduced to a much greater extent in patients with sleep apnea than in control subjects (10).
Schwartz et al. (11) defined pharyngeal collapsibility
as the critical pressure surrounding the collapsible part
of the pharyngeal airway; if this pressure is exceeded,
the airway will collapse. These investigators (11) demSleep. Vol. 19. No.9. 1996
onstrated that in normal subjects critical pressure
around the collapsible part of the airway is negative,
that is, the airway tends to stay open. In non-apneic
snorers the pressure is much less negative, implying
that their airway is more susceptible to collapse. In
patients with sleep apnea the critical pressure, measured during sleep at the time of apneas, is positive,
implying that the airway is occluded. During non-obstructed breathing the critical pressure is negative, and
therefore the airway is patent. This serves as another
illustration of airway instability during sleep.
Abnormal neuromuscular control of upper airway
dilating muscles has been demonstrated by many investigators. In patients with sleep apnea there is a failure of reflex activation of the dilator muscles in response to airway occlusion. There are multiple reasons
for this, including defects in ventilatory control, defects in arousal mechanism, abnormal delay in activation of dilator muscles, and others. An interesting
hypothesis to explain the failure of activation of pharyngeal dilator muscles in patients with OSA was proposed recently by Mezzanotte et al. (12). These investigators (12) showed that patients with sleep apnea
during wakefulness actually have a very strong pharyngeal dilator muscle activity; they interpreted this
finding as a compensatory mechanism required to keep
a narrow airway open. Non-apneic control subjects,
whose airway is larger, do not require increased dilator
muscle activity to keep it open. Once the need to keep
the airway open is abolished by administering nasal
continuous positive airway pressure (CPAP) to apneic
patients, the genioglossus muscle activity decreases. It
is possible that in patients with sleep apnea this strong
dilating compensatory mechanism may be lost during
sleep, and the narrow airway occludes passively in response to negative suction pressure.
These selected examples illustrate some of the reasons why patients with sleep apnea have an unstable
upper airway, perpetuating the vicious circle of alternating episodes of upper airway occlusion and patency.
How can we stabilize the upper airway?
How can we stabilize the upper airway and prevent
this sequence of pathological events? Remembering
that the basic factors responsible for upper airway occlusion are abnormalities in airway structure and function, it is clear that resolution of sleep apnea will depend on successful correction of these abnormalities.
Abnormal anatomy may be corrected by 1) nasal
CPAp, 2) oral appliances, 3) changes in position, or 4)
surgery. Nasal CPAP (13) acts as a pneumatic splint,
making pressure inside the airway positive throughout
the respiratory cycle, thus increasing airway size. This
UPPER AIRWAY STABILIZATION
splinting of the airway and increase in its cross-sectional area have been demonstrated by many investigators using different techniques, such as computed
tomography (CT) scans (14), magnetic resonance imaging (MRI) (1S), acoustic reflections (16), etc. The
reason why CPAP is so effective in abolishing sleep
apnea is because it acts along the entire airway, rather
than only at an isolated segment. It splints the entire
airway, thus eliminating all potentially occluding segments.
Changes from a supine to a lateral position may
stabilize the airway simply by reducing the gravitational force on the tongue and soft palate, which fall
passively backwards against the posterior pharyngeal
wall. In some OSA patients the apnealhypopnea index
may be substantially reduced by assuming a lateral
rather than a supine posture (17).
Another way to stabilize the airway is with the help
of oral appliances. There are basically two main
types-the more commonly used mandibular advancement type and the less commonly used tongue-retaining type. These appliances are becoming more popular,
particularly since the introduction of the adjustable
mandibular advancement prosthesis. Such a prosthesis
can be better individualized for each patient, therefore
reducing the discomfort of wearing it overnight. There
is evidence that the mandibular advancement prosthesis increases upper airway size (18) and improves
sleep apnea in some patients.
Various surgical procedures are used to enlarge and
stabilize the airway. These include 1) elimination of
the specific deformity (e.g. deviated nasal septum, enlarged tonsils, etc.), 2) uvulopalatopharyngoplasty
(UPPP), 3) mandibular osteotomy with hyoid suspension, and 4) other maxillary/mandibular surgery. Surgery works best in cases of obvious abnormalities,
such as micrognathia, tonsilar hypertrophy, etc. It
works least well in procedures that modify only a
small segment of the airway, such as UPPp, particularly if the site of obstruction is located at the base of
the tongue or below, that is, at a position inaccessible
to surgery. Surgical procedures that can modify long
airway segment work best, particularly if the muscle
function can also be beneficially affected. Such procedures include osteotomy with hyoid advancement, or
maxillary/mandibular surgery (19,20).
To stabilize the airway by modifying its function,
that is, reducing pharyngeal collapsibility and increasing the muscle tone, is a much more difficult task, and
the results are inconsistent. The strategies available to
modify the function of the upper airway include 1)
nasal CPAP, 2) weight loss, 3) avoidance of muscle
relaxants, 4) medications, and S) nerve stimulators.
Nasal CPAP not only corrects abnormal anatomy,
but it also has a beneficial effect on pharyngeal func-
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tion. It stiffens the pharynx and makes it less susceptible to collapse (21).
Weight loss unquestionably helps sleep apnea and
snoring. The mechanism this benefit is probably due
to its reducing pharyngeal collapsibility, rather than
increasing airway area, as is suggested by our own
measurements of pharyngeal function using acoustic
reflections (22). These measurements revealed no
change in area before and after weight loss, but they
demonstrated a reduction in pharyngeal collapsibility
(22).
Generalized muscle relaxants, including alcohol,
will also relax upper airway muscles, thus increasing
their susceptibility to collapse. The effect of alcohol
on the upper airway has been particularly well studied.
Alcohol may preferentially suppress genioglossus activity without modifying diaphragmatic activity, thus
tilting the balance of forces in favor of airway occlusion (23). Alcohol increases upper airway resistance,
producing apneas in otherwise asymptomatic individuals (24), and it has been shown to worsen sleep apnea
(2S).
There are no medications that can stabilize the upper
airway. Over the years many different drugs have been
employed (26), such as protryptyline, progesterone,
strychnine, nicotine, theophylline, L-tryptophan, cilazapril, almitrine, naloxone, acetazolamide, bromocriptine, and others. The rationale for using these drugs
includes potential beneficial effects on control of ventilation and on pharyngeal muscles. Trials using these
medications, which at least on theoretical grounds or
based on animal experiments are thought to modify
the neuromuscular reflexes, have not confirmed their
usefulness for treatment of sleep apnea (27), however,
and pharmacological therapy is not useful in patients
with idiopathic OSA.
Nerve stimulators, which discharge an electrical impulse into the chin muscles in response to loud snoring
or cessation of airflow, should theoretically be useful
in increasing the genioglossus activity and thus stabilizing the airway. Although initial reports demonstrated a beneficial effect of these stimulators (28) on sleep
apnea, several subsequent studies did not confirm
those observations (29,30).
In conclusion, there is overwhelming evidence for
upper airway instability in patients with sleep apnea.
Successful strategies for treatment of this disorder
must be directed to overcoming this instability.
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