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January 14, 1997
Non-REM (non-rapid eye movement) sleep is further subdivided into four stages, defined by patterns in the electroencephalogram (EEG). The four non-REM stages roughly parallel depth of sleep, with arousals easier in stage 1 and most difficult in stage 4.
REM (rapid eye movement) sleep is defined by EEG activation, muscle atonia, and bursts of rapid eye movements. The mental activity of REM sleep is associated with dreaming, based on dream recall after 80 percent of arousals from this state.
Stage 2 sleep is signaled by sleep spindles and/or K complexes on the EEG, following the first brief episodes of stage 1 and continuing for 10 to 25 minutes. More intense stimuli are required to produce an arousal.
As sleep progresses, there is a gradual appearance of high-voltage slow wave activity in the EEG. When this activity accounts for more than 20 percent but less than 50 percent of the EEG activity, stage 3 sleep occurs. Stage 3 lasts only a few minutes in the first cycle, and is transitional to stage 4, when slow wave activity is more than 50 percent of the record. Stage 4 lasts about 20 to 40 minutes in the first cycle. Again, the stimulus needed to arouse from these stages is increased compared to stages 1 and 2. Often, stage 3 and 4 sleep is combined and called slow wave, delta, or deep sleep.
Prior to the first REM episode, there is an ascension to the lighter non-REM stages. The REM sleep in the first cycle is usually short-lived (1 to 5 minutes).
Non-REM and REM sleep continue to alternate through the night in cyclic fashion. REM episodes generally become longer as the night proceeds; while stages 3 and 4 occupy less time per cycle, and may disappear altogether in later cycles, as stage 2 expands to occupy the non-REM portion of the cycle. The average period of the non-REM/REM cycle is approximately 90 to 110 minutes.
The following general statements can be made regarding sleep in the normal adult individual who is without sleep complaints:
Sleep apnea may be caused or exacerbated by obesity. Excessive weight on the chest wall and dysfunction of the diaphragm impair ventilatory effort during sleep. Additionally, fatty tissue in the throat and tongue decrease the diameter of the airway, predisposing the obese patient to premature closure of the airway when the muscle tissue is relaxed during sleep (154).
Nasal polyps or a deviated septum may also be a factor in OSA. The additional negative pressure needed to overcome the narrowing of the nasal passages may, on someone with poor muscle tone or narrow airways, be enough to close off the airway until the person begins mouth breathing. In children, especially, enlarged tonsils and adenoids narrow the airways enough to cause blockage and apnea.
Alcohol, muscle relaxants, antihistamines and sleeping tablets, all of which can be had very easily, may also exacerbate OSA and CSA through depression of the central nervous system.
Undiagnosed OSA also causes excessive daytime somnolence, and the patient may fall asleep at the drop of a hat. This may occur in a warm room, sitting and watching TV, while reading, or any sort of a quiet situation. The most dangerous time, of course, is when the patient is driving a car or truck. They may swerve off the road or into oncoming traffic, causing injury and death. Tim Hilchey reported in the New York Times that, in a study involving 159 commercial truckers, 78 percent suffered from OSA, three times higher than the general population. Many commercial trucking firms are now requiring their drivers to undergo sleep studies to determine if they suffer from OSA. It has been speculated that the accident at Chernobyl and the grounding of the Exxon Valdez were caused, at least in part, by sleep-related disorders.
Due to the decrease in SpO2, the heart is made to work harder, leading to hypertension. This may carry over into the daytime hours as well. According to the National Heart, Lung and Blood Institute, cardiac arrhythmias, usually bradyarrhythmias, have been associated with sleep apnea (1288). In addition, heart problems such as Cor Pulmonale, Congestive Heart Failure, and Cardiomyopathy, may be aggravated to the point of death of the patient.
Franklin, Nilsson, Sahlin and Naslund, in an article published in The Lancet, reported a study of ten men who reported nocturnal angina. Each of the ten had coronary artery disease. During the initial study, four patients were awakened by nocturnal angina; four of the attacks were preceded by apneas and one during a heart rate increase in REM sleep. During the second study, with CPAP (Continuous Positive Airway Pressure), none of the patients were awakened. Their results (1086) indicated that:
all patients examined with disabling coronary artery disease and nocturnal angina had sleep apnoea [sic]. Apnoea was the most common preceding factor of nocturnal ischaemia [sic] and ischaemic episodes decreased during treatment of nocturnal angina with continuous positive airway-pressure.
The prevalence of CSA in the general population is unknown; however certain patient groups have a higher predisposition, such as those with neuromuscular disorders, and there is also an increased prevalence in the elderly.
Central apneas are common during the transition from wakefulness to sleep, when the body regulates it's chemical balance. Hypercapnic ventilatory drive has been shown to be reduced in all stages of sleep, and especially pronounced during REM. Hypoxic respiratory drive is also demonstrated to be reduced to two-thirds of the wakening value, with further decrease during REM. In COPD patients, a low hypercapnic drive during wakefulness predisposes the patient to oxygen desaturation during sleep.
Patients with CSA are mostly normocapnic and without obvious disease, however their breathing instability during sleep can lead to major symptoms, with hypersomnolence and tiredness (DeBacker, 1372-1383).
Patients with PLMS usually complain of feeling unrested when they wake up in the morning. The leg movements cause arousals, and may prevent the patient from falling into deeper, more restful sleep. This, in turn, can lead to increased tiredness and fatigue during the day.
Large neck girth in both males (> 17 inches) and females (> 16 inches) in snorers is highly predictive of sleep apnea. Other signs and symptoms that can help identify patients at risk are listed in Fig. 1.
If a patient has a complaint of sleepiness, but does not exhibit other signs and symptoms, a review of the patient's sleep habits (e.g., how many hours of sleep the patient averages per night, recent lifestyle changes, or recent changes in schedule) may be helpful. If the patient is getting sufficient sleep, then other conditions, such as narcolepsy or depression, should be considered.
Other lifestyle factors which promote sleep-disordered breathing include cigarette smoking, which is a risk factor for snoring and may worsen the hypoxemia associated with sleep apnea; and consumption of alcohol or sedative drugs, which increase airway vulnerability to collapse by acting as muscle relaxants and reduce ventilatory responsiveness (Phillips 194).
Antidepressant drugs bring about immediate and often profound changes in sleep; most have the ability to suppress sleep. Neuroleptics do not have characteristic effects on sleep, although in therapeutic doses most tend to decrease wakefulness and increase slow wave sleep. Diuretics, while having very little effect on sleep, may have a profound effect on sleep patterns, such as the patient having to get up more frequently to urinate.
Patients at Risk for Sleep Apnea (Fig. 1)
SymptomsSigns
- Chronic, loud snoring.
- Gasping or choking episodes during sleep.
- Excessive daytime sleepiness (especially drowsy driving).
- Automobile or work-related accidents due to fatigue.
- Personality changes or cognitive difficulties related to fatigue.
- Obesity, especially nuchal obesity.
- Systemic hypertension.
- Nasopharyngeal narrowing.
- Pulmonary hypertension (rarely).
- Cor Pulmonale (rarely).
Epworth Sleepiness Scale (Fig. 2)Name: ___________________________________________ Date: _______________________ Age: ______________ Sex: ____________ How likely are you to doze off or fall asleep in the following situations, in contrast to feeling just tired? This refers to your usual way of life in recent times. Even if you have not done some of these things recently, try to work out how they would have affected you. Use the following scale to choose the most appropriate number for each situation: 0 = would never doze 1 = slight chance of dozing 2 = moderate chance of dozing 3 = high chance of dozing Situation Chance of Dozing Sitting and reading ______ Watching TV ______ Sitting inactive in a public place (theater, meeting) ______ As a passenger in a car for an hour without a break ______ Lying down to rest in the afternoon when circumstances permit ______ Sitting and talking to someone ______ Sitting quietly after a lunch without alcohol ______ In a car, while stopped for a few minutes in traffic ______ Thank you for your cooperation.
The Sleep Lab at the Walla Walla VA uses a typical PSG montage, consisting of 3 electroencephalogram (EEG) channels, 2 electromyogram (EMG) channels, 2 electro-oculogram (EOG) channels, 3 respiratory parameters, 1 electrocardiogram (ECG) channel, oxygen saturation (SpO2), and a microphone to record snoring.
The EEG electrodes are placed on the scalp using the International 10-20 Electrode Placement System. For reporting sleep stages, there are 2 electrodes centrally placed in the C3 and C4 positions, and are referred to neutral leads placed at A2 and A1 respectively. These measure the difference in electrical activity between the leads, allowing the determination of the brain wave frequency. A third channel uses the occipital lead O1 referenced to A2 for determination of alpha waves. The electrodes are attached to the scalp using collodion.
The EMG channels used are chin movement and leg movement. The chin leads are placed with one on the tip of the chin and one on the mandible. This channel is especially important in determination of REM sleep. The leg leads are attached to the anterior tibial muscles on the left and right legs, and are used for determination of PLMS. The chin leads are attached with collodion, and the leg leads are standard Silver/Silver Chloride electrodes.
The EOG electrodes are placed on the outer canthi of each eye, with the right eye higher than the left eye. The electrodes are referenced to the opposite Auricular lead. The tracings appear as mirror images of each other. These leads are smaller Silver/Sliver Chloride electrodes.
The respiratory parameters used are nasal air flow, measured either using a thermistor placed under the nares or through the mask used during titration of Continuous Positive Airway Pressure (CPAP); and respiratory effort measured with pneumatic belts placed on the chest and abdomen. The ECG electrodes are placed in the Lead I position. The oxygen saturation is recorded using a finger probe/pulse oximeter. A piezo-electric microphone is placed on the throat to monitor snoring. Finally, a position sensor is placed on the thoracic effort belt to record when a patient is lying on either side, his back, or his stomach.
The patient is asked to come in to the Sleep Lab about 8:30 pm on the night of the test. Following his orientation to the Sleep Lab, he is then given instructions on what the testing is for, the electrodes are placed, and the patient is then put to bed.
The patient is monitored for at least 6 hours and 10 minutes. During that time, it is determined how quickly the patient falls asleep, the amount of time spent in each stage of sleep, and any respiratory or limb movements which disturb his sleep. The sleep study is scored in 30-second time periods, called epochs. The predominant EEG features in each epoch determines the level of sleep.
The patient took 11 minutes to achieve sleep onset, slightly longer than normal but within limits, especially for the initial night of study. He began snoring almost immediately, and within 20 minutes began having episodes of hypopnea and apnea, with resultant desaturations. These episodes, combined with leg movements, kept him in wake or stage 1 sleep for 45 minutes, when he converted to stage 2 sleep. He remained in stage 2 with frequent arousals to wake or stage 1 (with the exception of 3.5 minutes of stage 3 sleep) for approximately 2 hours and 20 minutes until the beginning of his only REM period of the evening, which lasted 35 minutes. He then returned to stage 1 and 2 sleep with frequent arousals for the remainder of the evening. Of 6.4 hours of sleep, his total sleep time was 4.7 hours, with 59 awakenings, for a sleep efficiency of 73.5 percent.
Throughout the evening, the patient had 57 apneic events, 55 of which were obstructive; and 289 hypopneic events. His total sleep time spent in apneas or hypopneas was 2.7 hours. He had 377 desaturation episodes of 4 percent or greater, with a basal oxygen level of 86.7% and a minimum value of 38%. 144 respiratory events resulted in arousals. His resulting RDI (Respiratory Disturbance Index, or the number of times he had a respiratory event per hour) was 74.
The patient had a total of 492 leg movements, none of which were during REM sleep. 74 of those events resulted in arousals.
Impression: Severe OSA with baseline hypoxemia; moderate to severe Periodic Limb Movements.
Nasal reconstruction, to remove polyps or to correct septal deformities, is required for patients in which that is the cause of their upper airway obstruction. Nasal obstruction may also inhibit other treatment methods (710).
Uvulopalatopharyngoplasty (UPPP) is a procedure which removes a portion of the soft palate and uvula, as well as any residual tonsillar tissue. It is conducted on an inpatient basis. This potentially relieves any obstruction which may be present in the pharyngeal area. However, it is very uncomfortable for the patient, and is only about 40 percent effective in reducing OSA (710-714).
Laser-Assisted Uvulopalatoplasty (LAUP) differs from UPPP in both technique and setting (this can be done in the surgeon's office). A smaller part of the uvula and soft palate are excised, and it is more comfortable for the patient. However, as with UPPP, the relief of snoring may occur with no change in OSA (NHLBI 1293).
Base of tongue surgery may also be performed, to reduce the size of the base of the tongue as well as where it attached to the mandible. In patients where other medical and surgical treatments are ineffective, surgical advancement of the mandible my be required (Powell 714).
The most drastic surgical intervention is tracheostomy, a surgical opening in the trachea which completely bypasses the upper airway and any obstructions which may be present. This was a common form of treatment in the past; however, with the advancement of medicine, it has become relatively rare for treatment of OSA (NHLBI 1293).
CPAP is provided by a small blower device which provides a set level of positive pressure to the upper airway via a nasal mask. The level of pressure is determined during a PSG. Keeping the gentle pressure on the airway prevents the trachea from collapsing during inspiration, as well as keeping the tongue from falling back and obstructing the airway. As stated previously, where there is a nasal obstruction it must be cleared before CPAP will be effective. The development of a mask which fits over the mouth as well as the nose reduces the immediate need for surgery, however it is still not very effective in keeping an adequate seal, and a considerable loss of pressure may be experienced.
Some patients may require a higher pressure to eliminate obstructive events than to eliminate snoring. In these patients, BiPAP may be more effective. Similar in principle to CPAP, BiPAP provides a lower pressure during the exhalatory and resting phase of breathing, keeping the airway open and reducing the work of breathing. During the inhalatory phase, the higher pressure is given. Typically there is a pressure difference of 5 - 10 cmH2O (centimeters of water pressure) between the inhalatory and exhalatory pressures.
DPAP is a combination of CPAP and BiPAP. The theory behind it is that the only time a patient needs a higher pressure is during hypopneas (reduced air flow) and apneas. A low constant pressure is given to the patient until the unit determines that an event is occurring and reacts by increasing the pressure until the end of the event. A drawback is that the events and resultant drop in saturation have already occurred, and depending on the number of apneic and hypopneic episodes the patient has per hour a patient may be receiving the higher pressure constantly. This method is still undergoing testing.
In all three methods, the single most important factor is proper fitting of the mask. Without a proper seal, the pressures necessary may not be achieved. If a patient does not have front teeth to provide a rigid structure, a denture must be provided to rectify the situation. Leaking around the mask could lead to drying of the eyes. And if the mask is fitted too tightly, pressure sores and patient compliance become an issue (Sullivan and Grunstein 697).
Sleep onset occurred after 4.5 minutes. Once again, he began snoring almost immediately. With the onset of snoring, the CPAP pressure was increased to 7. This had the effect of eliminating many respiratory events, and the patient progressed to stage 2 sleep in 15 minutes, and began stage 3 and 4 sleep within a few minutes. Throughout the evening, the patient had 101 minutes of slow wave sleep, compared to 3.5 minutes during the previous test. The first REM sleep began 74 minutes from start of test, slightly ahead of normal, and lasted about 40 minutes, considerably more than normal. This could be caused by REM rebound, common when a patient has been deprived of his normal amount of REM sleep.
At the beginning of the first episode of REM, apneic episodes began, and the CPAP pressure was increased to 9. Obstructive events appeared once again at the beginning of the second REM episode, about 4.5 hours into the test. The CPAP pressure was increased to 10. This effectively eliminated all obstructive events as well as snoring.
Of 6.3 hours of sleep, the total sleep time was 5.9 hours, with 11 awakenings, for a sleep efficiency of 93.6 percent.
Throughout the evening, the patient had 3 apneic events, all obstructive; and 38 hypopneic events. His total sleep time spent in apneas and hypopneas was 0.3 hours. He had 43 desaturation episodes, with a basal oxygen level of 90.5% and a minimum value of 78.6%. 20 respiratory events resulted in arousals. His resulting RDI was 7.
The patient had a total of 616 leg movements, 4 of which were during REM sleep. 163 of those events resulted in arousals.
Impression: Successful CPAP titration at 10 cmH2O; persisting leg movements. Patient D was issued a CPAP unit set at the proper pressure, and referred back to his Primary Care Physician for drug therapy for the leg movements.
Given the prevalence of undiagnosed or untreated sleep disorders, especially sleep apnea, a public awareness program should be undertaken, including media advertising. Companies whose business can affect the public safety, such as merchandise transportation, the airline industry, and other public transportation industries, should be required to have their employees undergo screening for sleep apnea. Some companies are already doing this voluntarily.
Familiarity with the signs and symptoms of sleep disorders, proper and complete pre-screening, and sleep studies where indicated will help bring treatment to those who need it. It is up to us, as medical personnel, to ensure that sleep disorders are nothing to lose sleep over.
De Backer, W. A. (1995). Central sleep apnoea, pathogenesis and treatment: An overview. European Respiratory Journal, 8, 1372-1383.
Franklin, K. A., Nilsson, J. B., Sahlin, C., Naslund, U. (1995). Sleep apnoea and nocturnal angina. The Lancet, 29 April 1995, 1085-1087.
Guilleminault, C. (1994). Clinical features and evaluation of obstructive sleep apnea. In Dement, Kryger, and Roth (Eds.), Principles and Practices of Sleep Medicine (pp. 667-676). Philadelphia: Saunders.
Hilchey, T. (1995, 14 May). Sleep disorder may affect many truck drivers, researchers say. New York Times, sec. 1:28.
Lowe, A. A. (1994). Dental appliances for the treatment of snoring and obstructive sleep apnea. In Dement, Kryger, and Roth (Eds.), Principles and Practices of Sleep Medicine (pp. 722-734). Philadelphia: Saunders.
Lugaresi, E., Cirignotta, F., Montagna, P., and Sforza, E. (1994). Snoring: Pathogenic, clinical, and therapeutic aspects. In Dement, Kryger, and Roth (Eds.), Principles and Practices of Sleep Medicine (pp. 621-628). Philadelphia: Saunders.
National Heart, Lung and Blood Institute Working Group on Sleep Apnea. (1995). Sleep apnea: Is your patient at risk? Respiratory Care, 40(12), 1287-1298.
Phillips, B. (1996, March 15). Sleep apnea: Underdiagnosed and undertreated. Hospital Practice, 193-202.
Powell, N. B., Guilleminault, C., and Riley, R. W. (1994). Surgical therapy of obstructive sleep apnea. In Dement, Kryger, and Roth (Eds.), Principles and Practices of Sleep Medicine (pp. 706-719). Philadelphia: Saunders.
Sullivan, C. E., and Grunstein, R. R. (1994). Continuous positive airway pressure in sleep-disordered breathing. In Dement, Kryger, and Roth (Eds.), Principles and Practices of Sleep Medicine (pp. 694-704). Philadelphia: Saunders.
Thorpy, M. J., and Yager, J. (1991). The Encyclopedia of Sleep and Sleep Disorders. New York: Facts on File.
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