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Wake Up!
www.tnpj.com The Nurse Practitioner • June XXXXXXXXXX
Elizabeth Foster, RN, CDE, BSN
structive sleep apnea (OSA) is a form of sleep-
disordered
eathing characterized by repetitive
upper airway obstruction that often results in oxy-
gen desaturation and arousals from sleep.1 These occlusions
may be partial (hypopnea) or complete (apnea), and occu
despite continued respiratory effort. Sleep fragmentation
leads to significant nocturnal hypoxemia, as well as dimin-
ished amounts of slow wave sleep and rapid eye movement
(REM) sleep.2,3 The Seventh Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treat-
ment of High Blood Pressure recognizes sleep apnea as an
identifiable cause of hypertension.4
OSA has long been associated with a range of cardio-
vascular effects and an increase in cardiovascular mortality.5
Other adverse sequelae include obesity, excessive daytime
sleepiness, impaired concentration, and neuropsychological
dysfunction, as well as stroke, motor vehicle collisions, and
diminished quality of life.1,6-8 While obesity is a strong risk
factor for OSA, it is a misconception that OSA is purely a
weight-related phenomenon.2,9 Similarly, the belief that OSA
is uncommon in women is untrue.2 While the frequency is
higher in males, pre- and postmenopausal women are also
at risk, possibly due to hormonal changes.9
n Varying Criteria
It is estimated that more than 12 million Americans have
sleep apnea, although approximately 80% remain undiag-
nosed.10,11 Many with this disorder remain undiagnosed be-
cause they are unaware of the condition or they have not
sought medical attention.2 Women are less likely to be eval-
uated and diagnosed.8
A number of epidemiological studies have evaluated
the prevalence of OSA in diverse populations. Criteria
vary and may utilize an apnea/hypopnea index (AHI), ap-
nea index, or oxygen desaturation.1 In most population
studies, a polysomnogram is used to determine the num-
er of hypopnea and apnea events per hour of sleep. Events
occu
ing 5, 15, and 30 times per hour, with or without
excessive daytime sleepiness, are frequently used to cate-
gorize OSA as mild, moderate, or severe, respectively. In
the general population, researchers used the criteria of an
AHI of five or more events per hour and reported that the
estimated prevalence of OSA in 30 to 60 year olds was 9%
for women and 24% for men.12 Approximately one in five
adults has at least mild OSA, and 1 in 15 has moderate o
worse OSA.11 Population-based epidemiologic studies re-
veal that undiagnosed OSA is highly prevalent and dis-
plays a wide spectrum of severity. Even mild OSA is
associated with significant mo
idity. Strategies are
needed to reduce the high prevalence and associated mor-
idity of OSA, and primary care providers will play a cru-
cial role.8
While OSA is common in adults with type 2 diabetes
mellitus (T2DM), the direction of causality is unknown.
Studies suggest that T2DM and OSA commonly coexist and
that each condition exace
ates the other.13 These two con-
ditions share risk factors such as hypertension and obesity,
and are both associated with cardiovascular disease. In this
population, a recent study found that half of males and 20%
of females with diabetes had OSA.14 Diabetes was also re-
ported as more prevalent in patients with sleep disordered
eathing, and that this relationship is independent of othe
isk factors.15 Nonetheless, it is not clear that sleep disor-
dered
eathing causes the development of diabetes.
The risk of developing T2DM within the next 4 years
for patients with moderate to severe OSA was 62% highe
than in persons without OSA. Investigators hypothesized
that diabetes has an independent association with sleep dis-
ordered
eathing, and that the sleep abnormalities were
central rather than obstructive in nature.16 They concluded
that diabetes is associated with periodic
eathing, a respi-
O
2.0
CONTACT HOURS
Uncovering
Sleep Apnea
Misconceptions
www.tnpj.com24 The Nurse Practitioner • Vol. 33, No. 6
atory abnormality associated with abnormalities in the cen-
tral control of ventilation. The negative effects of diabetes
on central control of respiration may result in sleep distur-
ances. While obesity and other confounders may explain
the high prevalence of sleep apnea in diabetes, perhaps there
is a potentially treatable risk factor for cardiovascular dis-
ease in this population.16
There is an independent association between both sleep
disordered
eathing and insulin resistance,17-19 and sleep
disordered
eathing and impaired glucose tolerance.18,19
OSA is associated with a high frequency of T2DM and im-
paired glucose tolerance. The relationship between sleep
disordered
eathing and impaired glucose tolerance is in-
dependent of age and obesity.20 Furthermore, OSA is more
prevalent in patients who have both diabetes and autonomic
neuropathy than in controls with diabetes but without au-
tonomic distu
ances.21
n Pathophysiology
The pathophysiology of OSA is complex and not completely
understood. Upper airway patency depends upon the func-
tion of oropharyngeal dilator and abductor muscles, which
are normally activated in a rhythmic fashion during inspi-
ation. When negative airway pressure from inspiratory ac-
tivity of the intercostal muscles and diaphragm exceeds the
force produced by these muscles, the upper airway collapses.
Anatomical na
owing of the upper airway, loss of uppe
airway muscle tone, and defective upper airway protective
eflexes contribute to upper airway obstruction.3 Other air-
way abnormalities may include nasal obstruction secondary
to septal deviation, enlarged tu
inates, nasal polyps, or in-
flammation and congestion due to allergies. The soft palate
may be elongated, the uvula enlarged, or adenotonsillar hy-
pertrophy may be present.9 Loud snoring often accompa-
nies diminished airflow.
Despite continued respiratory effort, loss of upper air-
way patency precludes or reduces ventilation. When the air-
way obstructs, ca
on dioxide levels rise and oxygen levels
fall, resulting in stimulation of chemoreceptors and trigger-
ing arousal. Airway muscle tone improves and unimpaired
ventilation resumes. While patients with OSA are generally
unaware of this sleep disruption, the resulting changes in
sleep architecture significantly contribute to excessive day-
time sleepiness,3 which may translate into impaired diabetes
self-care (see Understanding OSA).13
The likely mechanism that adversely affects glucose me-
tabolism is hypoxia and sleep fragmentation. This causes a
stress response resulting in increased sympathetic nervous
system activity, elevated levels of fatigue-causing cytokines,
and alterations in leptin levels that contribute to weight
gain.13, 22 Neuropeptide Y (NPY) and leptin are peptides that
assist in the regulation of body weight, energy balance, and
sympathetic tone.
One study investigated the independent role of apnea
events and obesity on NPY and leptin plasma levels. Re-
sults showed that in patients with OSA, these peptide lev-
Sleep Apnea
Understanding OSA
When
eathing is unobstructed, air flows normally. During an apneic event, the airway becomes blocked and ai
ceases to flow.
Normal airway
Uvula
Uvula
Soft palate
Soft palate
Nasopharynx
Oropharynx
Laryngopharynx
Tongue
Epiglottis
Epiglottis
Small or
eceding jaw
Tongue
Willard RM, Dreher M. Wake-up call for sleep apnea. Nursing. 2005;35(3):48.
Nocturnal obstruction
Ill
us
tra
tio
n
y
Ch
is
ty
K
am
es
Sleep Apnea
els are increased. The authors concluded that while NPY
appears independent of obesity, leptin is mostly associated
with obesity.6 Glucose transport and utilization through
effects on hypoxia-inducible factor 1, which induces the
expression of several genes that encode various glycolytic
enzymes and glucose transporters, may be influenced by
the intermittent hypoxia of OSA.22 Sleep loss and hypoxia
can independently contribute to glucose metabolism dis-
orders, and therefore may be causal in the pathway between
OSA and alterations in glucose metabolism.19 Possible
mechanisms that may explain how sleep apnea alters glu-
cose metabolism include stimulation of the sympathetic
nervous system and hypothalamic-pituitary-adrenal axis,
and the release of cytokines.
Obesity, elevated blood glucose levels, sleepiness and fa-
tigue, impaired cognitive function, depression, motor vehi-
cle collisions, atrial fi
illation, hypertension, myocardial
infarction, stroke, and mo
idity and mortality are associ-
ated with untreated OSA.1,2,5,8,9,18-20 Patients with T2DM are
already at elevated risk for cardiovascular disease and typi-
cally have various como
idities such as hypertension and
obesity. Treating the OSA is crucial in managing these asso-
ciated conditions and in reducing the risk of complications.
n Clinical Presentation
Patients may present with snoring, periods of apnea, and ex-
cessive daytime sleepiness. Other classic findings include ob-
served apnea, nonrestorative sleep, na
ow upper airway,
gastroesophageal reflux disease, and hypertension. Neck cir-
cumference over 17 inches in men or 16 inches in women
may predict OSA. Macroglossia may be a predisposing con-
dition.2 Other associated symptoms may include nocturia,
dry mouth, sleep-related headaches, poor concentration,
memory loss, and i
itability (see Symptoms of OSA and Risk
factors for OSA).9
It is important for providers to recognize that not all pa-
tients with OSA are male, obese, sleepy, and middle-aged,
nor do they all snore. Symptoms ought not be dismissed be-
cause the patient does not fit this profile. Patients with dia-
etes should be questioned about OSA symptoms.11
Screening patients for sleep apnea is not necessarily time-
consuming. Reports of snoring and of not feeling refreshed
after a full night’s sleep should arouse the clinician’s level of
suspicion for OSA. Self-administered questionnaires are ef-
fective screening tools and can quickly identify patients likely
to have OSA, and who should be refe
ed for polysomno-
gram for diagnosis. The most commonly used tools are the
Epworth Sleepiness Questionnaire23 and the Berlin Ques-
tionnaire,24 which are validated and easy to use. The Cleve-
land Adolescent Sleepiness Questionnaire, a new tool, may
e more useful in that population.25
n Diagnosis
The Institute for Clinical Systems Improvement lists the fol-
lowing symptoms as suspicious for OSA: cardiovascular dis-
ease, coronary artery disease, sleep complaints, recu
ent
atrial fi
illation, hypertension, obesity, T2DM, and large
neck circumference.26 Atypical or complicating symptoms
may wa
ant refe
al to a sleep specialist. Persons with a more
straightforward presentation can be refe
ed directly fo
polysomnogram. An in-home, unattended sleep test is an-
other option, although an in-lab, attended polysomnogram
is the gold standard. If OSA is diagnosed, severity of the con-
dition is determined, lifestyle modification is recommended,
and treatment commences.
Polysomnogram evaluates sleep characteristics, snor-
ing, respiratory effort and air flow, oximetry, heart rate,
electroencephalography, electro-oculography, electromyog-
aphy, electrocardiography, REM, limb movements, and
ody position7 in a monitored facility. During polysomno-
gram, apneas (cessation of air flow for more than 10 sec-
onds) and hypopneas (reduction of air flow by at least 50%
with an oxygen saturation drop