Obstructive Sleep Apnea

OSA is a disorder characterized by recurrent episodes of upper airway obstruction and a reduction in
ventilation. It is defined as cessation of breathing (apnea) during sleep usually caused by repetitive
upper airway obstruction. The estimated prevalence of OSA is approximately 26% of adults between the
ages of 30 and 70 years (Peppard, Young, Barnet, et al., 2013). It is believed that between 4% and 9% of
women and 9% and 24% of men in the United States have OSA, and that up to 90% are not diagnosed;
these increased rates have been linked to the increase in rates of obesity (Downey, 2015) (see Chapter
48). OSA interferes with people’s ability to obtain adequate rest, thus affecting memory, learning, and
decision making.

Risk factors for OSA include obesity, male gender, postmenopausal status, and advanced age. The major
risk factor is obesity; a larger neck circumference and increased amounts of peri pharyngeal fat narrow
and compress the upper airway. Other associated factors include alterations in the upper airway, such
as structural changes (e.g., tonsillar hypertrophy, abnormal posterior positioning of one or both jaws,
and variations in craniofacial structures) that contribute to the collapsibility of the upper airway
(Downey, 2015).

Pathophysiology
The pharynx is a collapsible tube that can be compressed by the soft tissues and structures surrounding
it. The tone of the muscles of the upper airway is reduced during sleep. Mechanical factors such as
reduced diameter of the upper airway or dynamic changes in the upper airway during sleep may result
in obstruction. These sleep-related changes may predispose to upper airway collapse when small
amounts of negative pressure are generated during inspiration.
Repetitive apneic events result in hypoxia (decreased oxygen saturation) and hypercapnia (increased
concentration of carbon dioxide), which triggers a sympathetic response. As a consequence, patients
with OSA have a high prevalence of hypertension. In addition, OSA is associated with an increased risk of
myocardial infarction and stroke (cerebrovascular accident), which may be mitigated with appropriate
treatment (Downey, 2015).
OSA is characterized by many apneic and hypopneic periods during the sleeping cycle. For OSA, the
definition of apnea is arrest of breathing for 10 seconds or longer and hypopnea is defined as ventilating
50% or less of normal.2 OSA occurs when the musculature of the pharynx and tongue relax during sleep,
obstructing ventilation. Many structures contribute to airway obstruction.4 (See An inside look at OSA.)
The lack of ventilation decreases oxygenation, activating the fight-or-flight response of the sympathetic
nervous system, which leads to an increase in heart rate, BP, respiratory rate, blood glucose levels, and
mental activity.2 These changes aren’t conducive to well rested sleep. Over time, the repeated episodes
put a strain on the cardiovascular system, leading to hypertension as well as daytime sleepiness,
nonrestorative sleep, fatigue, and difficulty concentrating

Clinical Manifestations
OSA is characterized by frequent and loud snoring with breathing cessation for 10 seconds or longer, for
at least five episodes per hour, followed by awakening abruptly with a loud snort as the blood oxygen
level drops. Patients with sleep apnea may have anywhere from five apneic episodes per hour to several
hundred per night.
Classic signs and symptoms of OSA include the “3S’s”—namely, snoring, sleepiness, and significant-other
report of sleep apnea episodes. Common signs and symptoms of OSA are presented in Chart 22-4.
Symptoms typically progress with increases in weight and aging (Downey, 2015). Patients are typically
unaware of nocturnal upper airway obstruction during sleep. They frequently complain of insomnia,
including difficulty in going to sleep, nighttime awakenings, and early morning awakenings with an
inability to go back to sleep, as well as chronic fatigue and hypersomnolence (daytime sleepiness). When
obtaining the health history, the nurse asks the patient about sleeping during normal activities such as
eating or talking. Patients with this symptom are considered to have pathologic hypersomnolence
(Downey, 2015).

Eventually, excessive daytime sleepiness and lack of concentration occur. Symptoms of daytime
sleepiness and impaired concentration may be so intense that they interfere with the patient’s ability to
function at work. Falling asleep at work, showing up late, not completing work on schedule, being
forgetful, and having mood changes may diminish an employee’s productivity. Work performance may
deteriorate so much that the patient is fired or laid off. Hypertension and choking during sleep, signs of
OSA, can increase the heart’s workload. Many signs and symptoms, including nocturia and restlessness
and fitful sleep, also interfere with sleep, increasing daytime sleepiness and inability to concentrate.
Libido changes can impair relationships at home.1,6 In children, behavioral signs and symptoms include
hyperactivity, irritability, and aggression as well as daytime sleepiness, snoring, and nocturnal enuresis.
Often the signs and symptoms of OSA are confused with attention-deficit hyperactivity disorder (ADHD).
Children may also experience difficulty in school and with relationships.

Assessment and Diagnostic Findings

The diagnosis of sleep apnea is based on clinical features plus a polysomnographic finding (i.e., sleep
study), which is the definitive test for OSA. The test is an overnight study, performed in a specialized
sleep disorders center, which continuously measures multiple physiologic signals while the patient
sleeps. These signals are analyzed as they are related to stages of sleep; measures include those taken
by electroencephalogram (EEG), electro-oculogram, and chin electromyogram (EMG). In addition,
cardiac rhythms and dysrhythmias are monitored with a single-lead electrocardiogram (ECG) and leg
movements are recorded by an anterior tibialis EMG. Airflow at the nose and mouth is monitored using
both a thermal sensor and a nasal pressure transducer, breathing effort is monitored using inductance
plethysmography, and hemoglobin oxygen saturation is monitored by oximetry. The breathing pattern is
analyzed for the presence of apneas and hypopneas. Characteristic findings consistent with OSA include
apneic episodes occurring in the presence of respiratory muscle effort, clinically significant apneic
episodes lasting 10 seconds or longer, and apneic episodes most prevalent during the rapid eye
movement (REM) stage of
1595sleep. Sleep disruption from automated patient arousal is usually seen at the termination of an
episode of apnea (Downey, 2105).

ain a comprehensive health history, including a sleep history. The health history should include
questions about sleep hygiene such as these: • How many hours do you normally sleep each night? • Do
you wake up refreshed? • Do you feel sleepy during the day? • Are you fatigued during the day? • Do
you know if you snore? Assess sleepiness severity by asking the patient to complete the Epworth
Sleepiness Scale (ESS). The ESS will provide information about the impact of excessive sleepiness on
daily activities and quality of life.6,7 (The ESS was developed by Dr. Murray Johns. Individuals, including
clinicians and researchers, can obtain it for free from http://epworthsleepinessscale.com/. All other
users must have a license to use it. See the website for details.) The ESS, which is self-administered,
measures the chance of falling asleep in eight common scenarios. Scoring for each situation ranges from
0, not likely to fall asleep, to 3, highly likely to fall asleep. ESS scores have been found to correlate well
with sleep study results. Perform a thorough physical assessment. Obtain vital signs as well as height,
weight, and neck circumference. Pay special attention to the upper and lower respiratory systems.
Anatomic abnormalities that increase the risk of OSA include nasal obstruction as a result of septal
deviation and turbinate hypertrophy. Other factors that contribute to OSA include abnormalities of the
palate, uvula, tonsils, and tongue (including posterior placement and thickening of the palate, a thick or
long uvula, enlarged tonsils, and large tongue volume).6,8,9 Assess the cardiovascular system as well as
the thyroid gland. (See Risk factors for OSA.)

Assessing for Obstructive Sleep Apnea

Be alert for the following signs and symptoms of obstructive sleep apnea:
Excessive daytime sleepiness Frequent nocturnal awakening Insomnia
Loud snoring
Morning headaches
Intellectual deterioration
Personality changes, irritability Impotence
Systemic hypertension
Dysrhythmias
Pulmonary hypertension, cor pulmonale Polycythemia
Enuresis

Medical Management
Patients usually seek medical treatment because their sleeping partners express concern or because
they experience excessive sleepiness at inappropriate times or settings (e.g., while driving a car). A
variety of treatments are used. Weight loss, avoidance of alcohol, positional therapy (using devices that
prevent patients from sleeping on their backs), and oral appliances such as mandibular advancement
devices (MADs) are the first steps (American Sleep Apnea Association, 2015; Downey, 2015). When
applied correctly, an MAD advances the mandible so that it is slightly anterior to the upper front teeth,
preventing airway obstruction by the tongue and soft tissue during sleep. A randomized controlled trial
that compared the effectiveness of these devices among patients with OSA with the more conventional
therapy, continuous positive airway pressure(CPAP), found no difference in short-term outcomes
between MAD and CPAP, including daytime sleepiness and quality of life, suggesting that MAD is as
effective a treatment as CPAP in patients with mild-to- moderate OSA (White & Shafazan, 2013). In more
severe cases involving hypoxemia and severe hypercapnia, the treatment includes CPAP or bilevel
positive airway pressure (BiPAP) therapy with supplemental oxygen via nasal cannula. CPAP is used to
prevent airway collapse, whereas BiPAP makes breathing easier and results in a lower average airway
pressure. (The use of CPAP and BiPAP is discussed in more detail in Chapter 21.)

Surgical Management
Surgical procedures also may be performed to correct OSA. Simple tonsillectomy may be effective for
patients with larger tonsils when deemed clinically necessary, or when other options have failed or are
refused by patients (Morgan, 2015). Uvulopalatopharyngoplasty is the resection of pharyngeal soft
tissue and removal of approximately 15 mm of the free edge of the soft palate and uvula . Effective in
about 50% of patients, it is more effective in eliminating snoring than apnea. Nasal septoplasty may be
performed for gross anatomic nasal septal deformities. Maxillomandibular surgery may be performed to
advance the maxilla and mandible forward in order to enlarge the posterior pharyngeal region (Morgan,
2015). Tracheostomy relieves upper airway obstruction but has numerous adverse effects, including
speech difficulties and increased risk of infections. These procedures, as well as other maxillofacial
surgeries, are reserved for patients with concomitant cardiovascular disease and life- threatening
dysrhythmias or severe disability who have not responded to conventional therapy (Tierney et al., 2015).

Pharmacologic Therapy
Some medications are useful in managing symptoms associated with OSA. Modafinil (Provigil) has been
used to reduce daytime sleepiness (Downey, 2015). Protriptyline (Triptil) given at bedtime may increase
the respiratory drive and improve upper airway muscle tone. Medroxyprogesterone acetate (Provera)
and acetazolamide (Diamox) have been used for sleep apnea associated with chronic alveolar
hypoventilation; however, their benefits have not been well established. The patient must understand
that these medications are not a substitute for CPAP, BiPAP, or MAD. Administration of low-flow nasal
oxygen at night can help relieve hypoxemia in some patients but has little effect on the frequency or
severity of apnea.

Nursing Management
The patient with OSA may not recognize the potential consequences of the disorder. Therefore , the
nurse explains the disorder in terms that are understandable to the patient and relates symptoms
(daytime sleepiness) to the underlying disorder. The nurse also instructs the patient and family about
treatments, including the correct and safe use of CPAP, BiPAP, MAD, and oxygen therapy, if prescribed .
The nurse educates the patient about the risk of untreated OSA and the benefits of treatment
approaches.