Clinical Polysomnography





Introduction


The assessment of patients for snoring and sleep apnea includes a comprehensive sleep history, physical examination, and a diagnostic sleep study. The compilation of this information allows for the formulation of a treatment plan that is tailored to the patient’s specific issues and needs.


There is much more information on a sleep study report than just the Apnea/Hypopnea Index (AHI) and Respiratory Disturbance Index (RDI). The purpose of this chapter is to present a practical approach to looking at sleep study reports to get the most information out of them in an attempt to allow individualized treatment recommendations for our sleep patients.


Sleep studies can be performed either in a sleep laboratory or at home. There are advantages and disadvantages to both. The decision to do a study in the laboratory versus at home is sometimes dictated by the expertise and comfort level of the physician, the desires of the patient, or, unfortunately at times, by the edict of the insurance company.


This chapter will focus on in-laboratory sleep studies. Chapter 5 will review home sleep apnea testing.





Data Acquisition for Polysomnography


The patient generally presents to the sleep laboratory in the evening. However, shift workers, who usually sleep during the day, are better served by having the test performed during the day in what would be their normal sleep period. After being checked in and changing into their sleep attire, a sleep laboratory technician will perform the setup by attaching all of the appropriate leads.


When ready, the patient will lie down and the technician will start the recording. The technician observes the data channel, for each lead, on a monitor in a different room. If a lead detaches during the study, the technician may enter the test room, at the appropriate time, and replace it. Generally, each technician will set up and monitor two patients during the course of a night.


The patients are being videotaped by a low-resolution video camera that serves three purposes. First, it allows the technician to record body position, that is, supine vs. nonsupine. Second, it allows monitoring of parasomnias, such as sleep walking, rapid eye movement (REM) behavior disorder (RBD) and seizures. Finally, it is there to protect both the patient and the sleep laboratory from inappropriate behaviors and/or accusations. There is also a microphone that allows patients to communicate with the sleep technician if they have any questions or concerns.


After the recording is finished in the morning, the raw data collected during the night will be “scored” by a respiratory polysomnography technologist. Scoring a sleep study generally entails analyzing all data channels on multiple passes. First, it is staged for wakefulness and sleep stages. Subsequently, it will be analyzed for respiratory, and other, events.





Sleep Staging


The leads that are used during a sleep study include those that measure electroencephalography (EEG), electrooculography (EOG), electromyography (EMG), electrocardiography (ECG), nasal pressure, airflow, effort (chest and abdomen), and pulse oximetry.


The top half of the recording of sleep data is usually EEG, EOG, and chin EMG. This helps us determine if a patient is awake or asleep and, if asleep, what stage of sleep they are in. The bottom half of the data allows us to visualize events, such as respiratory events, snoring, and limb movements. The ECG is usually in the top half of the screen, which is best seen in a 30-second window, similar to the best way to visualize the EEG. The channels at the bottom half of the screen are usually viewed in a 2-minute screen ( Fig. 4.1 ).




FIG. 4.1


Typical layout for sleep study data. The top third of the screen is in a 30-second window to allow visualization of the EEG and ECG. The lower two-thirds of the screen is a 2-minute window to allow a more global view of breathing and respiratory events. The left hand labels, from top to bottom, include EOG (two rows), EEG (six rows), chin EMG, ECG, leg EMG (two rows), snoring microphone, nasal pressure, airflow, chest and abdominal effort leads (three rows), pulse oximetry, heart rate, and body position.


There are three general states of being: wakefulness, non-REM sleep, and REM sleep. Normally, one proceeds from wakefulness into non-REM sleep and then into REM sleep. One cycles between non-REM and REM sleep approximately four to five times in a typical night before awakening in the morning.


As stated earlier, wakefulness and sleep on a sleep study are determined by EEG, EOG, and chin EMG leads.


Wakefulness and stages of sleep are artificially broken down into 30-second epochs. The epoch is scored as whatever stage of sleep or wakefulness makes up the majority of the 30 seconds. The chin EMG amplitude helps with the staging of sleep. It decreases from a high in wakefulness, decreases in non-REM sleep, down to a low in Stage REM.


Wakefulness, with the eyes closed, is characterized by alpha waves making up >50% of the epoch and a high chin EMG ( Fig. 4.2 ). Non-REM sleep is made up of three stages: Stage N1, Stage N2, and Stage N3. If you are looking at an old sleep study report, you may notice mention of Stage 4 sleep. In a revision of sleep staging by the American Academy of Sleep Medicine (AASM), 2007, Stage 3 and Stage 4 were combined into Stage N3.




FIG. 4.2


Wakefulness (with alpha waves [within the green rectangle], in the frequency of 8 to 12 Hz, making up >50% of the epoch).


Stage N1 is the transition between wakefulness and deeper stages of sleep. It is a very light sleep. If someone taps you on the shoulder during Stage N1 sleep, you may awaken easily and respond. It is typically 2% to 5% of a night’s sleep. Increased Stage N1 sleep is seen with fragmented sleep where a patient has multiple awakenings. As they are frequently falling back to sleep, they may transition briefly through Stage N1. Stage N1 is characterized by low-amplitude, mixed-frequency EEG activity and alpha waves that make up <50% of the epoch ( Fig. 4.3 ).




FIG. 4.3


Stage N1 (light sleep with <50% of the epoch made up of alpha waves [within the green rectangles]).


Adults with normal sleep architecture generally spend more time in Stage N2 than in any other individual sleep stage. At times, it is a higher percentage of sleep than all of the other sleep stages combined. Normally, we spend 45% to 55% of the night in Stage N2. It is characterized by sleep spindles and K-complexes ( Fig. 4.4 ).




FIG. 4.4


Stage N2 (red rectangle demonstrates K-complex, and green rectangles show sleep spindles).


Stage N3 sleep is generally considered “deep sleep” and allows for “restorative sleep.” It is easy to recognize Stage N3 by its slow, rhythmic, high-amplitude delta waves ( Fig. 4.5 ). Delta waves are 1 to 4 Hz. Stage N3 sleep typically encompasses 3% to 20% of sleep. This stage of sleep slowly decreases as a percentage of sleep as we get older, more in men than in women.




FIG. 4.5


Stage N3 (high-amplitude, low-frequency delta waves are easy to see).


Obviously, the classic, feature and basis for naming of Stage REM is the rapid eye movements (see Fig. 4.6 ). This is documented by the EOG leads. The EEG during Stage REM is also characterized by intermittent saw tooth waves.




FIG. 4.6


Stage REM (conjugate rapid eye movements seen in the EOG leads [green rectangle] with very low chin EMG signal [thin green line above the ECG lead on the bottom]).


The classic physiologic finding of Stage REM, other than the eye movements, is atonia. The only muscles that work during Stage REM are of the diaphragm, eyes and heart. This atonia is a protective mechanism that allows us to dream in Stage REM without getting out of bed and acting out our dreams. On the other hand, obstructive sleep apnea (OSA) is generally worse in Stage REM than in non-REM sleep because of this atonia and the increased collapsibility of the airway.


Lack of atonia during Stage REM, which is pathologic, is seen in RBD. There is a higher incidence of RBD in patients with Parkinson disease than in the general population. In fact, RBD sometimes precedes the diagnosis of Parkinson disease by several years.





Categories


There are five categories of information that should be easily accessible on any sleep study report. How the information is presented depends on the software that is used to collect and analyze the data.


If you know what information to look for, and what it means, you will be in a good position to fully evaluate any sleep study report that comes your way. This will mean more comprehensive and effective treatment for your sleep patients.



Sleep Architecture


Sleep architecture describes the structure and pattern of sleep. What is considered normal sleep architecture changes with age. Normal sleep is clearly an evolutionary outcome that has been created by multiple selective pressures. Normal sleep architecture can be affected by various sleep disorders. These will be discussed further as this chapter progresses. Unless otherwise stated, this chapter will discuss sleep architecture in adults.


Sleep study reports will list the percentage of the night spent in each stage of sleep. Another way to get a sense of sleep staging, and a gestalt of what transpired during the night, is by looking at the hypnogram on a sleep study report. It is a graphic representation of the stages of sleep and wakefulness from the beginning of the night to the end. A normal hypnogram ( Fig. 4.7 ) and one from a patient with severe OSA and fragmented sleep look very different. In fact, you can sometimes have a good understanding of what transpired over the sleep period by just looking at the hypnogram.




FIG. 4.7


Hypnogram in a patient with normal sleep and sleep architecture. Yellow represents Stage N1; green, Stage N2; blue, Stage N3; and maroon, Stage REM. Notice five cycles of non-REM and REM sleep during the course of the night with very few awakenings.


A typical pattern we see in patients with severe OSA is fragmented sleep demonstrated by an increased amount of Stage N1 and a decreased amount of Stage REM. The decrease in stage REM may be related to greater sleep instability of OSA patients in REM where more severe obstructions occur. Patients obstruct and transition out of Stage REM very quickly. The reason for the increased Stage N1 is the frequent transitions back through Stage N1 after multiple arousals from respiratory events ( Fig. 4.8 ).




FIG. 4.8


Hypnogram in a patient with very severe OSA. Notice markedly increased yellow Stage N1 61.6% (normal is 2%–5%) and no Stage REM (normal is 20%–25%).


A sleep study report will list the sleep efficiency. This is the percentage of the night, from the time the sleep technician says “lights out” until he or she says “lights on,” that the patient is actually sleeping. Normal sleep efficiency is >85%.


It is important to consider both sleep efficiency as well as the total sleep time (TST). The TST is how long the patient actually slept during the study. The TST and sleep efficiency are important numbers if they are way off. You do not want to walk into a patient examination room to discuss sleep study results and start talking about the AHI, only to be interrupted by the patient who says, “But I only slept for 30 minutes. How can you draw any conclusion from this?” If you had looked at the report and saw a sleep efficiency of 15% and a TST of 43 minutes, you could have started the conversation with, “I hope your night in the laboratory was not a typical night’s sleep for you.” Then, you would have their attention.


Two latencies are seen on a sleep study report. The sleep latency is how long it took from the time the technician says “lights out” until sleep onset. Sleep onset is defined as the first three consecutive epochs of Stage N1 or the first epoch of a deeper stage of non-REM sleep, whichever comes first. The other latency is the REM latency. This is the period of time from sleep onset until the first epoch of REM sleep.


A markedly decreased sleep latency, such as 2 minutes, may be a sign of hypersomnolence. Many patients are begrudgingly brought for evaluation by their significant other who complains of the patient’s snoring. The patients frequently say that they have no sleeping problems. In fact, they are quick to point out that they are such good sleepers that they fall asleep as soon as their head “hits the pillow.” We take this opportunity to inform the patient that such a short sleep latency may, in fact, be pathologic.


A significantly prolonged sleep latency of >30 minutes, while sleeping at home, may be suggestive of sleep-onset insomnia or a circadian rhythm disorder. However, it is difficult to make this diagnosis based on a single night’s sleep at the sleep center, given that the patient is sleeping in an unfamiliar environment and with multiple sensors attached.


Frequently, we will see the combination of a low sleep efficiency and an increased sleep latency during a patient’s first study in the sleep laboratory. This constellation of findings may be due to “first night effect” in the sleep laboratory.


A normal REM latency is 80 to 110 minutes. A mild to moderately decreased REM latency can be seen with depression, withdrawal from REM suppressant medications (such as certain antidepressants), and hypersomnolence.


A markedly decreased REM latency, such as 5 minutes, can be seen with narcolepsy . You may see a patient with severe excessive daytime sleepiness (EDS) and some snoring. The sleep study may not reveal significant sleep-disordered breathing (SDB). You do not want to miss a REM latency of 5 minutes and the possible diagnosis of narcolepsy.


To some degree, narcolepsy is the intermingling of two of the three states of being, wakefulness and REM sleep. As stated earlier, two of the main physiologic findings of Stage REM are dreaming and atonia. This helps explain three entities that can occur with narcolepsy.


Hypnogogic hallucinations occur as you are going to sleep. It is the awareness of dreaming even though you know you are still awake. This is a combination of the dreaming seen in Stage REM and wakefulness.


Sleep paralysis occurs upon awakening. It is when you open your eyes and know you are awake but cannot move a muscle. It can be quite frightening. This is a combination of atonia as seen in Stage REM and wakefulness.


Hypnogogic hallucinations and sleep paralysis can be seen in isolation without narcolepsy, but are more common in narcoleptics than the general population.


Cataplexy is pathognomonic for narcolepsy. Cataplexy is a loss of muscle tone that occurs during a state of excitement such as laughing. About 50% of narcoleptics do not have cataplexy, but if a patient has cataplexy, they have narcolepsy.



Respiratory


The respiratory summary is, for the most part, the main section of a diagnostic sleep study report. This is the section that gives the degree of OSA, which is the most common indication for sleep studies.


To understand the respiratory summary, one must first know the definitions of the terms that make up the all-important indices. An apnea is defined as a decrease in the airflow by >90% for at least 10 seconds ( Fig. 4.9 ).




FIG. 4.9


Obstructive apneas. Six consecutive obstructive apneas with several intervening breaths between each apnea seen best on airflow lead (red rectangle); persistent chest and abdominal effort as seen on effort belts (light blue rectangle); significant oxygen desaturations seen with each apnea (lower black rectangle); 5-minute window on lower two-thirds of screen; and 30-second window on upper third of screen.


Apneas can be divided into obstructive and central. An obstructive apnea, the one more commonly seen in the laboratory, is secondary to airway collapse with subsequent blockage of the upper airway during sleep. Central apneas are secondary to lack of signal from the brain to breathe. Central apneas are commonly seen in patients with congestive heart failure, people who are at high altitudes before acclimating, patients on narcotics, and patients with primary central sleep apnea (CSA).


The patient in the sleep laboratory has belts around the chest and abdomen to measure effort. During an obstructive event, the belt signal indicates that despite the fact that the patient is not breathing, he or she is trying to breathe ( see Fig. 4.9 ). During a central event there is no signal coming from the belts—that is, there is no inspiratory effort ( Fig. 4.10 ). This is an important distinction because OSA and CSA may be treated differently.




FIG. 4.10


Central apneas. Four consecutive central apneas with several intervening breaths between each apnea seen best on airflow lead (red rectangle); no chest or abdominal effort seen on effort belts (light blue rectangle); significant oxygen desaturations seen with each apnea (lower black rectangle); 5-minute window on lower two-thirds of screen; and 30-second window on upper third of screen.


There are two definitions for a hypopnea , which is the most common respiratory event seen in the sleep laboratory. The definition that the AASM recommends is a decrease in nasal pressure by >30% for at least 10 seconds with either a decrease in oxygen saturation by at least 3% or an arousal as determined by EEG ( Fig. 4.11 ).




FIG. 4.11


Hypopneas. Two consecutive hypopneas (black rectangles) with >30% decrease in nasal pressure and both arousals at the end of each event (red rectangles) as seen on EEG leads and >3% decrease in oxygen saturation as seen on salmon rectangles near the bottom of the page; 2-minute window on entire page.


The alternative definition that the United States Center for Medicare and Medicaid Services requires is a decrease in nasal pressure reading by >30% for at least 10 seconds with a concomitant decrease in oxygen saturation by at least 4%. The relevance of these two definitions is that a patient with Medicare or Medicaid insurance, who has to be scored by the 4% hypopnea rule, may have a lower AHI than a patient with commercial insurance despite the exact same recording. Therefore it is important to know which criterion was used in the scoring of the study before treating the patient based upon the study results. Hypopneas are inconsistently scored across centers and scorers.


The final respiratory event that can be included in degree of OSA is a respiratory effort related arousal, or RERA . This is an event that does not meet the criteria for an apnea or hypopnea but nonetheless demonstrates increased effort of breathing with a disruption in sleep, as evidenced by an arousal. To truly know that there is an increase in respiratory effort before an arousal, one would need to have an esophageal probe in place, and this may discourage many patients from undergoing polysomonography. However, a RERA can be extrapolated from the typical data collected. There are signs of increased respiratory effort on the parameters we do measure, such as flattening of the nasal pressure curve. RERAs are inconsistently measured between scorers and sleep centers.


The two main indices that are used to measure degree of OSA are the AHI and the RDI:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='AHI=(#of apneas+#of hypopneas)/total sleep time(TST)’>AHI=(#of apneas+#of hypopneas)/total sleep time(TST)AHI=(#of apneas+#of hypopneas)/total sleep time(TST)
AHI = ( # of apneas + # of hypopneas ) / total sleep time ( TST )

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Jun 10, 2019 | Posted by in OTOLARYNGOLOGY | Comments Off on Clinical Polysomnography

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