OSA syndrome occurs when at least five apnea or hypopnea events per hour of sleep occur as the result of an obstruction in the upper airway. In the general population, between 3% and 7% of people have severe OSA.24 The incidence of OSA is believed to increase with age. Consequences include chronic hypoventilation syndrome; arousals that fragment sleep; cardiovascular changes such as hypertension, stroke, ischemic heart disease, insulin resistance, ventricular hypertrophy; and nocturnal angina.²⁵ Because of the cardiovascular complications and accidents caused by sleepiness, such as motor vehicle accidents, job related injuries, falls, and other non-intentional accidents related to lack of concentration, OSA is a significant condition that should be effectively evaluated.

The cause of OSA is not entirely understood; however, upper airway structure, hormonal balance, and neural control are implicated. Factors that contribute to OSA are (1) anatomic narrowing of the upper airway, (2) increased compliance of the upper airway tissue, (3) reflexes affecting upper airway caliber, and (4) pharyngeal inspiratory muscle function.²⁶ Computed tomographic studies of awake subjects have shown that patients with OSA have narrower airways than normal subjects do. The narrower the airway, the more easily it may become obstructed (Figure 5-1).

Upper airway patency is also affected by upper airway function, which is under the control of the respiratory motor neurons. During sleep, this control varies and causes decreased neural activity, thereby narrowing the airway. This effect is especially prevalent during REM sleep, when the motor neurons are hypotonic. Unstable control of the respiratory nerves of the diaphragmatic, intercostal, and upper airway muscles can cause sleep apneas.²³ Hypothyroidism can alter respiratory controls and thereby contribute to OSA. Other contributing disorders are exogenous obesity, kyphoscoliosis, and autonomic dysfunction.

The patient with OSA develops cycles of hypoxemia, hypercapnia, and acidosis with each episode of apnea until he or she is aroused and airflow resumes. Alveolar hypoventilation accompanies each episode of apnea and results in hypercapnia. Between episodes, alveolar ventilation improves so that overall there is no retention of carbon dioxide (CO₂).

With obstruction, inspiratory subatmospheric intrathoracic pressures are abnormally elevated. This leads to a tendency for airways to collapse, resulting in hemodynamic and electrocardiographic changes. The extremely elevated pressures that occur in individuals with OSA who have apneic episodes in REM and NREM stages cause systemic and pulmonary hypertension. Systemic pressures of 200/120 mm Hg (awake control: 130/80 mm Hg) and pulmonary artery pressures of 80/54 mm Hg (awake control: 30/20 mm Hg) have been reported.²⁷ Cardiac dysrhythmias associated with obstructive apnea include bradycardias, sinus arrest, and occasionally, second-degree heart blocks. After resumption of airflow, tachycardias commonly occur. Bradycardia-tachycardia syndrome is associated with OSA.²⁸

Careful monitoring of oxygen saturation and breathing patterns can help the critical care nurse identify patients with this syndrome and assist in its diagnosis and treatment. Patients at risk for OSA may have the following symptoms: snoring; obesity; short, thick neck circumference; cardiovascular disease; systemic hypertension; pulmonary hypertension; sleep fragmentation; gastroesophageal reflux; and an impaired quality of life. Apneas may occur in people whose throats are abnormally small or collapsible. Muscles that would normally hold the throat open relax while the patient is asleep. Snoring is caused when those soft tissues in the throat vibrate. Snoring often precedes the complaint of daytime sleepiness, and the intensity increases with weight gain and alcohol ingestion.26 Men with a collar size of 17 or greater and women with a size 16 or greater are thought to have an increased incidence of apnea. Friedman and others showed a clinical correlation between modified Mallampati grade (MMP), tonsil size, body mass index, and the severity of apnea. These assessments are used by anesthesiologists to determine intubation difficulty.²⁶ There is an increased incidence of sleep apnea among African Americans as well as Mexican Americans, and an increased incidence is observed among those with metabolic syndrome.

OSA episodes frequently end in brief EEG arousals. Patients may experience hundreds of arousals and not even realize they awaken hundreds of times during the night. These arousals cause sleep fragmentation and daytime sleepiness, which can lead to irritability, poor job performance, troubled relationships, depression, and impaired quality of life.

The definitive diagnosis of OSA syndrome is made with PSG during an overnight sleep study. PSG is used to determine the number and length of apnea episodes and sleep stages, number of arousals, airflow, respiratory effort, and oxygen desaturation.

CPAP via nasal mask is the treatment of choice. CPAP machines are simply pressure generators with the effective pressure being determined during the titration part of the PSG. This holds the airway open and prevents collapse. The patient wears a small, triangle-shaped mask over the nose or uses nasal pillows if the mask is not tolerated. CPAP treats the obstruction and the snoring, choking, and gasping that accompany it, and it provides cardiovascular benefits. Although CPAP is the treatment of choice, it is effective only if the patient is compliant with therapy. Regular attendance at CPAP clinics can improve patient compliance.29 If a patient cannot tolerate the continuous pressure of CPAP, bimodal positive airway pressure (BiPAP), which provides separate pressures for inspiration and expiration, may be tried. Refer to Box 5-1 for nursing care of the patient using CPAP.

Various surgical interventions are available for the treatment of apnea and snoring. Patients with mild OSA or snoring alone may undergo an outpatient procedure called laser uvulopalatopharyngoplasty (LAUP), which uses lasers to remove excess tissue at the soft palate level. For patients who snore but do not have apnea, somnoplasty may provide relief. Somnoplasty involves inserting a small electrode into the soft palate and heating the tissue, causing the area to shrink and tighten.³⁰

Uvulopalatopharyngoplasty (UPPP) was one of the earlier surgeries used to treat OSA. Essentially, a large tonsillectomy is performed and all redundant tissue is removed (Figure 5-2). Reports of success from UPPP vary widely, with 40% to 80% of patients experiencing sleep apnea improvement.^30,31 Complications include speech impairment, inability to eat, postoperative bleeding, and infection. Severe pain after UPPP is documented and may continue well into the postoperative period.³¹ Although tracheostomy was the original surgical procedure used to treat OSA, it is now used only in the most severe cases of apnea that do not respond to other treatments. Bariatric surgery is an effective means to facilitate weight loss and subsequent improvement in OSA.³²

Treatment of OSA with medication is usually a last resort and has proved to be very disappointing. Protriptyline has been shown to decrease apnea and reduce excessive daytime sleepiness by decreasing sleep apnea frequency that increases during REM sleep. Oxygen may be used to lower hypoxemia and nocturnal desaturations.

UPPP patients are not usually admitted to critical care areas because the postoperative recovery does not require intensive care.33 Postoperative monitoring after UPPP includes risk of aspiration, pain management, anxiety relief, patient education, and monitoring for respiratory complications, hemorrhage, infection, impaired speech, nutritional concerns, and sleep disturbance.

Central sleep apnea (CSA) can be seen on PSG as an absence of airflow and respiratory effort for at least 10 seconds. A complete loss of electromyographic activity by the respiratory muscles would be expected since CSA is defined as a pause in respiration without ventilatory effort.34

A chemoreceptor sensitive to the levels of CO₂ resides within the brain. When CO₂ levels become excessive, ventilatory efforts are increased to blow off the excess CO₂. This negative-feedback loop exists to provide a homeostatic balance in the carbon dioxide and oxygen levels of the body. Whereas OSA results from an obstructed or collapsed airway, patients with CSA suffer from a lack of ventilatory effort. This can be observed in patients with cardiopulmonary disease (e.g., COPD) or heart failure, because their chemoreceptors have become adjusted to an increased CO₂ level. It is not uncommon for a patient who experiences CSA to also have some obstructive events.

CSA may result from many physiological or pathophysiological events.³⁵ Possible causes of nonhypercapnic CSA include periodic breathing at high altitude, renal or metabolic disturbances, and idiopathic central apnea seen at sea level. Hypercapnic CSA can occur in many neuromuscular conditions such as spinal cord or brain injury, encephalitis, brainstem neoplasm or infarcts, muscular dystrophy, myasthenia gravis, bulbar poliomyelitis, and postpolio syndrome.

Because there are two types of CSA, there are two therapeutic approaches depending on the cause of the apnea. The hypercapnic patient who has worsening hypoventilation during sleep is best served by nocturnal ventilation. Most such patients experience some respiratory muscle failure. One treatment for nonhypercapnic or heart failure patients is nasal CPAP, which also may provide a beneficial cardiovascular effect. Nocturnal oxygen supplementation may be effective as well. If CPAP is not tolerated, pharmacologic management may be tried. Medroxyprogesterone, a respiratory stimulant, may improve ventilation in selected patients.34 Acetazolamide, a carbonic anhydrase inhibitor that can result in metabolic acidosis, also may decrease the frequency of apneic episodes.