Non-REM Sleep

Non-REM sleep usually begins immediately after an individual dozes off. This phase consists of four separate stages, each progressing into a deeper sleep. During stages N1 and N2 the ventilatory rate and tidal volume continually increase and decrease, and brief periods of apnea may be seen. The electroencephalogram (EEG) shows increased slow-wave activity (slow-wave sleep) and loss of alpha rhythm. Alpha rhythm is defined as containing EEG signals at 8 to 13 Hz. Cheyne-Stokes respiration also is commonly seen in older male adults during non-REM sleep, especially at high altitudes.

During stage N3, ventilation becomes slow and regular. Minute ventilation is commonly 1 to 2 L/min less than during the quiet wakeful state. Typically, the Paco₂ levels are higher (4 to 8 mm Hg), the Pao₂ levels are lower (3 to 10 mm Hg), and the pH is lower (0.03 to 0.05 units) during stage N3. Normally, non-REM sleep lasts for 60 to 90 minutes. Although an individual typically moves into and out of all four stages during non-REM sleep, most of the time is spent in stage N2. An individual may move into REM sleep at any time directly from any of the three non-REM sleep stages, although the lighter stages (N1 and N2) are commonly the levels of sleep just before REM sleep.

REM Sleep

During REM sleep a burst of fast alpha rhythms occurs in the electroencephalographic tracing. During this period the ventilatory rate becomes rapid and shallow. Sleep-related hypoventilation and apnea frequently are demonstrated during this period. Apneic periods occur in normal adults as often as five times per hour. These apneas may last 15 to 20 seconds without producing any discernible effects. In the normal infant, apneas are shorter (approximately 10 seconds in length), although even these may be cause for concern. A marked reduction in both the hypoxic ventilatory response and the hypercapnic ventilatory response occurs during REM sleep. The heart rate also becomes irregular, and the eyes move rapidly. Dreaming occurs mainly during REM sleep, and profound atonia (paralysis) of movement occurs. The skeletal muscle paralysis primarily affects the arms, legs, and intercostal and upper airway muscles. The activity of the diaphragm is maintained during REM sleep.

The muscle paralysis that occurs during REM sleep can affect an individual’s ventilation in two major ways. First, because the muscle tone of the intercostal muscles is low during this period, the negative intrapleural pressure generated by the diaphragm often causes a paradoxic motion of the rib cage. In other words, during inspiration the tissues between the ribs move inward, and during expiration the tissues bulge outward. This paradoxic motion of the rib cage causes the functional residual capacity to decrease. During the wakeful state the intercostal muscle tone tends to stiffen the tissue between the ribs.

Second, the loss of muscle tone in the upper airway involves muscles that normally contract during each inspiration and hold the upper airway open. These muscles include the posterior muscles of the pharynx, the genioglossus (which normally causes the tongue to protrude), and the posterior cricoarytenoid (the major abductor of the vocal cords). The loss of muscle tone in the upper airway may result in airway obstruction. The negative pharyngeal pressure produced when the diaphragm contracts during inspiration tends to bring the vocal cords together, collapse the pharyngeal wall, and suck the tongue back into the oropharyngeal cavity.

REM sleep periods last 5 to 40 minutes and recur approximately every 60 to 90 minutes. The REM sleep periods lengthen and become more frequent toward the end of a night’s sleep. REM sleep constitutes about 20% to 25% of the total sleep time. Most studies show that it is more difficult to awaken a subject during REM sleep. Table 30-1 provides an overview of the electroencephalographic findings in the various stages of sleep.

Table 30-1

Stages of Sleep

Stage	Electroencephalogram (EEG)	Characteristics
Eyes open-wake (Stage W)		The EEG shows beta waves, and high-frequency, low-amplitude activity. The electrooculogram (EOG) looks very similar to REM sleep waves—low-amplitude, mixed-frequency, and saw-toothed waves. Electromyogram (EMG) activity is relatively high.
Eyes closed-wake (drowsy)		The EEG is characterized by prominent alpha waves (>50%). The EOG shows slow, rolling eye movements, and the EMG activity is relatively high.
Non-REM Sleep
Stage N1 (light sleep)		The EEG shows low amplitude alpha waves (8-13 Hz) that may be replaced by mixed frequency activity and theta waves (4-7 Hz). Vertex waves commonly appear. Vertex wave are sharp upward deflection EEG waves. The amplitude of many of the vertex sharp waves is greater than 20 µv. Vertex waves are usually seen at the end of stage N1. The EOG shows slow, rolling eye movements. The EMG reveals decreased activity and muscle relaxation. Respirations become regular, and the heart rate and blood pressure decrease slightly. Snoring may occur. If awakened, the person may state that he or she was not asleep.
Stage N2 (light sleep)		The EEG becomes more irregular and is composed predominantly of theta waves (4-7 Hz), intermixed with sudden bursts of sleep spindles (12-18 Hz), and one or more K complexes. Sleep spindles are a sudden burst of EEG activity in the 12-14 Hz frequency (6 or more distinct waves) with a duration of ≥ 0.5 to 1.5 seconds (not illustrated here). Vertex waves may also be seen during this stage. The EOG shows either slow eye movements or absence of slow eye movements. The EMG has low electrical activity. The heart rate, blood pressure, respiratory rate, and temperature decrease slightly. Snoring may occur. If awakened, the person may say he or she was thinking or daydreaming.
Stage N3 (slow wave sleep)		Slow wave activity 0.5 Hz-2.0 Hz and peak to peak amplitude > 75 µv. EOG shows little or no eye movement, and the EMG activity is low. Heart rate, blood pressure, respiratory rate, body temperature, and oxygen consumption continue to decrease. Snoring may occur, and there is no eye movement. Dreaming may occur, and the sleeper becomes more difficult to arouse.
(Deep sleep)		The EOG shows no eye movements, and the EMG has little or no electrical activity. The sleeper is very relaxed and seldom moves. The vital signs reach their lowest, normal level. Oxygen consumption is low. The patient is very difficult to awaken. Bed-wetting, night terrors, and sleepwalking may occur.
REM Sleep
		About 90 minutes into the sleep cycle, there is an abrupt EEG pattern change. The EEG pattern resembles the wakeful state with low-amplitude, mixed frequency EEG activity. Saw-toothed waves are frequently seen. Alpha waves may be seen. The respiratory rate increases, and respiration is irregular and shallow. The heart rate and blood pressure increase. Rapid eye movement occurs, and there is paralysis of most skeletal muscles. Most dreams occur during REM sleep.

Obstructive Sleep Apnea

It is estimated that more than 12 million people in the United States have OSA.

OSA is caused by an anatomic obstruction of the upper airway in the presence of continued ventilatory effort (see Figure 30-1). During periods of obstruction, patients commonly appear quiet and still, as though they are holding their breath, followed by increasingly desperate efforts to inhale. Often the apneic episode ends only after an intense struggle. A snorting sound called “fricative breathing” may be heard at the end of the apneic periods. In severe cases, the patient may suddenly awaken, sit upright in bed, and gasp for air. These events are called confusional arousals. Patients with OSA usually demonstrate perfectly normal and regular breathing patterns during the wakeful period.

In fact, a large number of patients with OSA demonstrate what is commonly called the Pickwickian syndrome (named after a character in Charles Dickens’s The Posthumous Papers of the Pickwick Club, published in 1837). Dickens’s description of Joe, “the fat boy” who snored and had excessive daytime sleepiness, included many of the classic features of what is now recognized as the sleep apnea syndrome. Box 30-1 provides common signs and symptoms associated with OSA. However, many patients with sleep apnea are not obese, and therefore clinical suspicion should not be limited to this group. Table 30-2 provides the more common risk factors associated with OSA.

Central Sleep Apnea

CSA occurs when the respiratory centers of the medulla fail to send signals to the respiratory muscles. It is characterized by cessation of airflow at the nose and mouth along with cessation of inspiratory efforts (absence of diaphragmatic excursions), as opposed to OSA, which is characterized by the presence of heightened inspiratory efforts during apneic periods.

CSA is associated with cardiovascular, metabolic, and central nervous system disorders. A few brief central apneas normally occur with the onset of sleep or the onset of REM sleep. CSA, however, is diagnosed when the frequency of the apnea or hypopnea episodes is excessive (more than 30 in a 6-hour period). Box 30-2 provides a listing of clinical disorders associated with CSA.

Mixed Sleep Apnea

Mixed sleep apnea is a combination of obstructive and CSAs. It usually begins as central apnea followed by the onset of ventilatory effort without airflow (obstructive apnea). Clinically, patients with predominantly mixed apnea are classified (and treated) as having OSA.

Figure 30-2 illustrates the patterns of airflow, respiratory effort (reflected through the esophageal pressure), and arterial oxygen saturation in central, obstructive, and mixed apneas.