Ravi Gupta, S. R. Pandi-Perumal, Ahmed S. BaHammam - Clinical Atlas of Polysomnography (2018, Apple Academic Press)
Ravi Gupta, S. R. Pandi-Perumal, Ahmed S. BaHammam - Clinical Atlas of Polysomnography (2018, Apple Academic Press)
Ravi Gupta, S. R. Pandi-Perumal, Ahmed S. BaHammam - Clinical Atlas of Polysomnography (2018, Apple Academic Press)
POLYSOMNOGRAPHY
CLINICAL ATLAS OF
POLYSOMNOGRAPHY
By
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The front cover illustration was created by using the Starry Night (original was an oil on canvas by the Dutch post-impressionist painter Vincent van Gogh, 1889)
with a superimposed picture of a polysomnographic tracing.
CONTENTS
Dedication........................................................................................................................................................................................ vii
About the Authors.......................................................................................................................................................................... ix
List of Abbreviations...................................................................................................................................................................... xiii
Forewords......................................................................................................................................................................................... xvii-xx
Preface................................................................................................................................................................................................ xxi
Credits and Acknowledgments.................................................................................................................................................... xxv
1. Normal Sleep....................................................................................................................................... 1
2. Common Sleep Disorders................................................................................................................. 21
3. Introduction to Polysomnography.................................................................................................. 37
4. Basic Concepts of Polysomnography Channels........................................................................... 53
5. Preparations for the Sleep Study...................................................................................................... 115
6. Placement of Leads for the Sleep Study......................................................................................... 121
7. Starting and Closing the Study......................................................................................................... 145
8. Calibration and Biocalibration......................................................................................................... 179
9. Minimal Recording Parameters and Extended Montage........................................................... 197
10. Montages............................................................................................................................................... 221
vi Contents
To our families . . .
for their abundant support, patience,
understanding, and everlasting love and affection.
ABOUT THE AUTHORS
Ravi Gupta, MD, PhD, MAMS, Certified Sleep Physician (World Sleep Federation), is presently
working as Professor in the Department of Psychiatry & Sleep Clinic, Himalayan Institute of Medical
Sciences, Dehradun, India. He has contributed chapters to various high profile academic volumes.
He has also authored a book “Psychiatry for Beginners,” and has more than 100 published articles
in various peer-reviewed journals to his credit. He has received numerous awards and fellowships,
including the Young Psychiatrist Award from the Indian Psychiatric Society (2008), fellowships
from the World Psychiatric Association (2008) and from the Japanese Society of Psychiatry and
Neurology (2009), and membership of the Indian Academy of Medical Sciences, New Delhi (2015)
to name a few. In 2010, he received a Mini-Fellowship from the American Academy of Sleep Medi-
cine. This fellowship provided him a chance to refine his knowledge and skills in the area of Sleep
Medicine under able guidance of Dr. Jim Walker and Dr. Robert Farney at LDS Hospital, Salt Lake
City, Utah. Continuing with the legacy of his mentors, he is engaged in imparting knowledge of Sleep
Medicine to physicians from various streams through lectures, workshops, and training programs in
S. R. Pandi-Perumal, MSc, is the President and Chief Executive Officer of Somnogen Canada
Inc, a Canadian Corporation. He is a well-recognized sleep researcher, both nationally and inter-
nationally, and has authored many publications. His general area of research interest includes
sleep and biological rhythms. He is a well-known editor in the field of sleep medicine and has
edited over 20 volumes dealing with various sleep-related topics. He received an honorable men-
tion in the New York Times in 2004. The India International Friendship Society awarded him the
prestigious Bharat Gaurav award on January 12, 2013. The Bharat Gaurav Award is usually recog-
nition of a person who has made achievements in a particular field, which in turn will put a positive
Ahmed S. BaHammam, MD, FRCP (Lon), FRCP (Edin), ABIM, EDIC, FACP, FCCP, is a
tenured Professor of Medicine at King Saud University (KSU). Recognized as a leading expert
in the field of sleep medicine, both nationally and internationally, Prof. BaHammam established
the first academic sleep disorders center in Saudi Arabia and the first Sleep Medicine Fellow-
ship program and subsequently chaired the committee that established the Saudi regulation for
accreditation of sleep medicine specialists and sleep technologists. As a founding member of the
Saudi Thoracic Society and the Saudi Sleep Medicine community, Prof. BaHammam has orga-
been conducted in several countries in the Middle East. For his contribution to sleep medicine,
he was awarded the Lifetime Achievement Award (2016) by King Saud University. He has pub-
lished more than 200 scientific articles. He is a member of the editorial board of several interna-
system) pressure
blood plethysmography
blood SA sino-atrial
lars of sustainable health. Conversely, chronic lack of sleep or disturbed sleep is well known to produce
detrimental consequences for both physical and mental health. For instance, epidemiological studies
have shown strong associations between sleep loss and sleep disorders, on one hand, and increased risks
for cardiovascular and psychiatric disorders, premature cognitive impairments, and even mortality, on
the other hand. It may be no surprise then that sleep disorders have become a major public health issue
Polysomnography is the gold standard for measuring normal sleep and for diagnosing many sleep
disorders. It provides the most comprehensive and reliable assessment of multiple physiological param-
eters during sleep. Many of the discoveries in basic sleep and circadian research and in clinical sleep
medicine are the direct results of technological advances, particularly polysomnography. Just to note a
few examples, the discovery of rapid-eye movement (rem) sleep, the diagnosis ofsleep disorders such
as narcolepsy, sleep-related breathing disorders, and REM behaviordisorder, as well as the observation
of sleep state misperception in some forms of insomnia, could not have been made without polysom-
nography. Of course, polysomnography is only one tool among several assessment modalities of sleep.
Depending on whether the context of assessment is clinical or research, adding a clinical interview,
xviii Foreword
along with subjective sleep diaries, behavioral devices such as actigraphy, and a variety of patient-
questionnairesare likely to yield useful and complementary information and provide thecompleteas-
mation and graphical illustrations about everything that is needed to perform thepolysomnographic
assessment. From basic concepts about normal sleep and sleep disorders, technical information
about calibration, artifacts, and various montages, to practical recommendations for managing a
sleep laboratory, this atlas represents a superb referenceguide. The atlas is filled with useful illustra-
tions of actual records depicting standards for monitoring, artifacts recognition, and key findings
associated with different sleep pathologies. A compendium of review questions at the end of each
chapter is extremely handy for testing new learning. Although intended primarily for sleep technolo-
gists, this atlas will serve as a useful reference for any sleep clinician, researcher, or trainee wanting to
learn more about the technical and clinical aspects of evaluating sleep and sleep disorders.
The authors of this atlas, Drs. Ravi Gupta, S.R. Pandi-Perumal, and Ahmed BaHamman, are inter-
nationally known leading experts in sleep medicine and sleep research. Theyare to becommended
for compiling this essential tool for a better understanding normal sleep and diagnosing many sleep
disorders. This atlas is likely to remain a key reference in the field for years to come.
phy by Dr. Ravi Gupta, Dr. S. R. Pandi-Perumal, and Dr. Ahmed S. BaHammam. It is not so because I
am doing the same as the President of the Indian Society for Sleep Research and Asian Sleep Research
Society. The reason is something different. We, the leaders in Indian Society for Sleep Research, are
engaged in Sleep Medicine education across the country and across the spectrum for last ten years by
organizing courses for physicians and technicians and had envisioned the development of a book on
PSG for readers not only in India but also in Asia. We thought of a book that will be easy to understand
and comprehensive and that one can begin a career in sleep medicine by simply reading it. Now we do
not have to hunt for such a book. This long-cherished desire of the core group has been accomplished.
I thank all the authors for their tremendous effort and commitment to bring this unique book for the
Sleep disorders are now recognized as a major public health issue. Investigating sleep is the most
challenging medical investigation as it requires background knowledge of physiology and sleep medi-
cine and expertise in sleep technology. The Clinical Atlas on Polysomnography has everything that you
want to learn or teach on sleep technology. The physiological principles of respiration, gas exchange,
the genesis of electrical potentials with color illustrations make it easy to understand for technicians.
xx Clinical Atlas of Polysomnography
The beginners who are starting a career in Sleep Medicine will be immensely benefitted by this
book. It is not merely another book on polysomnography. It is something different. It begins with a
description of normal sleep, covers everything about polysomnography, and ends with career develop-
ment, sleep laboratory management, and financial viability of a sleep laboratory. You will find learning
objectives at the beginning of each chapter and some review questions to test your knowledge at the
end. The essence of a sleep technology book is quality of representative graphs capturing various physi-
ological and pathological events during sleep. This book offers the best. The authors have put extra
Recent developments in sleep data acquisition systems and analysis software, including automated
computing techniques, make the life of sleep technicians ever challenging. This book describes all the
major PSG machines available in the market with their software features.
No doubt the book is a stepping stone for starting a career in Sleep Medicine, and the authors pro-
vide the blueprint for future revisions and refinement with readers’ feedback.
Professor, Physiology
who had a keen interest in this area developed themselves as somnologists. Initially, Sleep Medicine
was focused towards research; however, as happens in science, with evolution of knowledge, pathologi-
cal conditions related to sleep (i.e., sleep-disorders) were also recognized. With this advancement of
knowledge, the practice and scope of Sleep Medicine extended from bench-side to clinics.
Polysomnography has always been a useful tool for understanding physiological and pathological
aspects of sleep. In the past 30 years, sleep laboratories have become places not only for research but
also for providing clinical care. The person in command in any sleep laboratory is often a sleep tech-
nologist who records and scores the data. He is expected to understand not only the machine and the
software that he handles but also to possess at least basic knowledge regarding electrophysiological,
Recording of data is of paramount importance and, thus, training and certification programs were
developed for sleep technologists. Well-structured training programs for sleep technologists also
helped to establish a minimum standard of care for patients, as trained sleep technologists must cross
the established benchmark of expected knowledge and skills in this area. However, in many parts of
xxii Preface
the globe, structured training programs for sleep technologists are not available. In those geographical
areas, despite the need felt by sleep physicians, sleep laboratories are difficult to be established and run
in the absence of trained sleep technologists. This present book is an attempt to fill that void and to
It was important to maintain consistency and comparability of data within and across sleep labora-
tories. To address this issue, rules for scoring the polysomnographic data were laid down by eminent
scientists. The American Academy of Sleep Medicine has been a forerunner in the development of sleep
technology courses and scoring rules and, most recently, on April 1, 2017, it produced the AASM Manual
for the Scoring of Sleep and Associated Events, version 2.4. These guidelines and rules are at present consid-
ered as standard globally, and this book follows the framework of same. However, this book is intended
to complement, not to substitute, for the AASM scoring manual, as many areas that are covered in the
This book provides basic information regarding normal sleep, sleep disorders, and electrophysiol-
ogy aspects of sleep that are outside of the scope of the AASM scoring manual. The book will guide
you through the fundamental aspects of, for example, types of overnight sleep studies, establishing a
sleep laboratory, preparing the patient for a sleep evaluation study, placement of electrodes and other
signal recording devices, and scientific aspects of recording of data. This book also includes chapters
on depicting real-time illustrations of sleep data as captured in the sleep laboratory, and the scoring of
recording data. Information regarding common montages, artifacts, and troubleshooting in the sleep
Preface xxiii
laboratory will facilitate your journey as a trainee sleep technologist. Graphical one-page representa-
tions of overnight recorded data (i.e., histograms) can provide a great deal of useful information. An
attempt has been made to explain the interpretation of histograms. It is prudent to summarize the data
and observations in a report that is not only comprehensive and informative but also is easy to under-
stand, even by physicians whose primary specialty is not Sleep Medicine. A chapter has been dedicated
to explain this in detail. Lastly, we have provided ready-made forms, questionnaires, and documents
We hope that our humble attempt will be welcomed and that readers will find this book useful!
— RG
SRP
ASB
CREDITS AND ACKNOWLEDGMENTS
This volume owes its final shape and form to the assistance and hard work of many talented people. We
would like to express our profound gratitude to the many people who have helped and also to some who
have contributed without realizing just how helpful they have been.
First of all, the authors would like to express their reverence towards all those scientists, physicians,
and sleep technologists whose dedication and contribution have evolved the area of Sleep Medicine
and who are still improving our understanding. This book is an attempt to collectively reflect their work.
Our sincere appreciation goes to Prof. Charles Morin and Prof. Hrudananda Mallick who are well
known figures in field of sleep medicine. They graciously agreed to write forewords for this book. We
know them as great scientists, successful leaders, acclaimed teachers, revered mentors and last but not
the least, as humble persons. Their testimonials mean a lot to us. We also would like to thank Prof. Jan
Ulfberg, an eminent scientist, a great physician and mentor for many persons in Sleep Medicine for
going through the book prior to the print and providing his insights. We are humbled to receive encour-
aging comments from him. We want to say him a big, “Thank you!”.
xxvi Credits and Acknowledgments
We gratefully acknowledge our corporate partners, namely Philips Respironics Inc., Cadwell Inc.,
and Somnomedics LLC, who kindly accepted our request to provide requested illustrations for this
volume.
The authors would also like to acknowledge several of our friends and colleagues—Dr. Abhishek
Goyal (Associate Professor, Department of Pulmonology, All India Institute of Medical Sciences,
Bhopal, India), Dr. Rajanish Sharma (Sleep Physician, Rudraksh Clinic, Jaipur, India), Dr. Supriy Jain
(Consultant Cardiologist, Jaipur, India), and Dr. Sourav Das (Sleep Physician, Somnos Sleep Clinic,
Kolkata, India)—for providing some illustrations for the book. The authors would also like to acknowl-
edge the technical help provided by the following colleagues: Divinagracia E. Gacuan, RPSGT; Smitha
George, RPSGT; and Karen Lorraine Acosta, RPSGT, from the University Sleep Disorders Center
at King Saud University, Riyadh, Saudi Arabia. Mr. MM Mathavan from the Himalayan Institute of
Medical Sciences, Dehradun, has contributed a chapter “Financial Viability for a Sleep Unit” and we are
The authors would also like to acknowledge the close co-operation we have received from each
No volume can be completed without the untiring efforts of many publishing professionals. Produc-
ing a volume such as this is a team effort and we acknowledge with gratitude the work of the editorial
department of Apple Academic Press. We are especially indebted to Mr. Ashish Kumar, the President
of Apple Academic Press, who was an enthusiastic and instrumental supporter from start to finish. Our
Credits and Acknowledgments xxvii
profound gratitude is offered also to Mr. Rakesh Kumar, Production Editor, whose equally dedicated
efforts promoted a smooth completion of this important project. They both provided unflagging dedi-
cation, invaluable help, and encouragement. We appreciate their intellectual rigor and personal com-
We also thank the Apple Academic Press production department colleagues for their meticulous
work. They all gave unstintingly of their time, energy, and enthusiasm. This talented and dedicated
team of copy and production editors strengthened, polished, trimmed, and conscientiously checked
Last, but certainly not least, we are most grateful to our wonderful wives, families and friends, who
provided love and support too valuable to measure. We owe everything to them; without their support
this work would have been not completed. With unwavering optimism and encouragement, they saw
the work through from the conception of an idea to the completion of an interesting project.
Without a whole host of dedicated individuals, this volume would never have come to completion.
We recognize these people individually and collectively for their contribution. To all these people goes
our sincere gratitude. Their willingness to contribute their time and expertise made this work possible,
and it is to them that the greatest thanks are due. They made our work possible and pleasurable.
LEARNING OBJECTIVES
1
Contents
A fter reading this chapter, the reader should be able to:
1.1 Sleep Across Age.......................................................................................2
1. Define sleep and changes in sleep across age.
1.2 Neurobiology of Sleep.............................................................................3
2. Discuss neurobiological mechanisms of sleep including the two-
SLEEP
3. Discuss different stages of sleep along with physiological changes.
1.5 Neurophysiology of EEG Rhythms from Wakefulness to Sleep...12
4. Discuss the neurobiology of EEG waves seen across different sleep
1.6 Atonia During REM Sleep....................................................................16
stages.
1.7 Concluding Remarks.............................................................................17
Further Reading................................................................................................19
are seen during this temporary unconsciousness, and from which the arousal is
Review Questions.............................................................................................19
Answer Key........................................................................................................19
2 Clinical Atlas of Polysomnography
possible in response to any internal or exter- anxiety or dyspnea. External stimuli are often A remarkable variation is seen in all these
nal stimuli. This definition has several impor- auditory or tactile in nature. However, these parameters across age. For example, total sleep
tant aspects that will help you understand the stimuli must be sufficiently intense to arouse the time of an infant is around 18–20 hours, which
physiology of sleep. First, it is a state of uncon- person, and their intensity also varies across the reduces as the child grows and comes to adult
sciousness that is reversible and this reversibility sleep stages. timing during mid-adolescence (6–8 hours), after
differentiates it from coma. Second, the person which it remains more or less stable. However, it
is not aware of the environment during sleep, starts declining in the fourth decade of a person’s
so he does not perceive (although he may sense 1.1 SLEEP ACROSS AGE life. During old age, it reduces to 5–6 hours/day.
it) most stimuli during sleep. Perception is dif- Regarding continuity, infants have fragmented
ferent from sensation – when a sensory stimu- Sleep has many important parameters, for sleep and they tend to wake up multiple times.
lus is consciously recognized it is considered as example, the total duration of sleep, mainte- It becomes consolidated into a single sleep as
perceived. This suggests that a sleeping person nance of sleep, and at what time of the day we the age grows. Children often go to bed early at
cannot take any conscious decision – rather he fall asleep. Electrophysiologically, sleep may be night, however, during adolescence, they develop
reacts on instinct. This explains why patients divided into two main stages: non-rapid-eye- a phase delay. Phase delay refers to delayed bed-
suffering from sleep-walking when aroused forc- movement (NREM) sleep and rapid-eye-move- time and wake time. On the other hand, the phase
ibly often commit violent acts. The third part of ment (REM) sleep. NREM sleep can be further is considered to be advanced in old age. Aging also
the definition says that a person may be aroused divided into three stages: N1 (light sleep), N2, influences the electrophysiology of sleep. Chil-
with any internal or external stimuli. Internal and N3 (deep sleep). dren have a high proportion of N3 (deep sleep),
stimuli that may arouse a person include pain, which reduces as the person grows old.
Normal Sleep 3
1.2 NEUROBIOLOGY OF SLEEP located close to the hypothalamus. The first is areas is modulated through another group of
the sleep-promoting area – the ventrolateral pre- neurons, the hypocretin neurons that are pres-
Sleep is dependent upon two processes: homeo- optic nucleus (VLPO), which sends inhibitory ent in the lateral and posterior hypothalamus.
static and circadian. These processes together signals through the GABAergic neurons to the Under normal conditions, the hypocretin neu-
decide when we will fall asleep and also the other wake-promoting area of the brain. Wakefulness rons modulate the activity of the other two areas
characteristics of sleep, such as depth, duration, is dependent upon the monoaminergic nuclei of the brain in such a manner that only one state
maintenance, and proportion of sleep stages. of the brain that are the part of the reticular acti- of consciousness, that is, wakefulness or sleep
The homeostatic (also known as “S”) pro- vating system (RAS). Monoaminergic nuclei prevails (Figure 1.1). Damage to the hypocretin
cess makes us feel sleepy depending upon the include serotonergic neurons (located in dorsal neurons leads to a condition known as narco-
duration of wakefulness. The longer the period and medial raphe nuclei), noradrenergic neurons lepsy. In this condition, a person is not able to
of wakefulness, the higher the sleep pressure; in (locus coeruleus), histaminergic neurons (tuber- maintain either states and experiences bouts of
other words, higher are the chances to fall asleep. omammillary nucleus) and cholinergic neurons sleepiness during wakefulness.
That is the reason why a person who is awake (located in pedunculopontine (PPT), laterodor- The circadian process (process “C”) is depen-
for a long time falls asleep even during the day. sal tegmental (LDT) nuclei, and basal forebrain dent upon environmental light. Certain other fac-
Moreover, this process regulates the proportion nuclei). In addition, there are glutaminergic neu- tors can also regulate this process, for example,
of deep sleep (N3 sleep) - the longer the period rons that are diffusely distributed throughout food, emotions, social activity, and exercise. These
of wakefulness, the higher the proportion of the RAS. When the VLPO sends GABArgic sig- factors are called “zeitgebers.” Among these, light
deep sleep. The homeostatic process is depen- nals to these neurons, sleep ensues. The activity is the strongest factor which can entrain the cir-
dent upon two major areas of the brain that are of both wake-promoting and sleep-promoting cadian rhythm. Environmental light falls on the
4 Clinical Atlas of Polysomnography
1.2).
Figure 1.2 Suprachiasmatic nucleus and its connections: Suprachiasmatic nucleus receives signals from retina and passes them to ventrolateral preoptic area (VLPO)
through dorsomedial hypothalamus. Dorsomedial hypothalamus has connections with other areas as well that regulate circadian rhythm of other biological functions
in addition to sleep.
6 Clinical Atlas of Polysomnography
(Figure 1.3).
waveforms in EEG . NREM sleep can further Figure 1.3 Relationship of process C and S in a normal individual: Normally process C and process S overlap
with each other so as to increase the propensity to fall asleep at night and propensity to stay awake during the
be divided into three stages: N1 sleep (charac- day. Any disruption in this overlapping disrupts the quantity as well as quality of sleep and appears in the form
of circadian rhythm sleep disorders.
terized by theta waves in EEG; slow eye move-
Figure 1.4 30 seconds epoch showing N1 sleep: This epoch shows mix EEG activity (alpha and theta) along with vertex waves (in circle).
8 Clinical Atlas of Polysomnography
Figure 1.5 30 seconds epoch showing N2 sleep: In this epoch K complex can be seen in the square box and sleep-spindle in circle. Background EEG activity is
in theta range.
Normal Sleep 9
Figure 1.6 30 seconds epoch showing N3 sleep: This epoch show delta activity. Delta waves are also known as slow waves with frequency of 0.5–2 Hz and amplitude of
more than 75 mV.
10 Clinical Atlas of Polysomnography
Figure 1.7 30 seconds epoch showing REM sleep: REM sleep is characterized by low voltage mixed frequency activity, rapid eye movements and atonia.
Normal Sleep 11
by low-voltage, mixed-frequency activity in sleep-pressure lowers, and in the second half of This has important implications as certain
EEG, rapid eye movement, and muscle atonia night minimal, if any, N3 sleep is seen. REM disorders are limited to one sleep stage and they
(Figure 1.7). sleep is regulated by the process “C” and it is are seen during that part of night. For example,
These stages follow a characteristic pattern predominantly seen during the second half of sleep-walking that occurs during N3 sleep is
in normal persons where NREM and REM the night. Thus, each episode of REM sleep seen more commonly before midnight while
sleep keep alternating at an interval of 90–120 shows progressive lengthening across the night REM sleep behavior disorder is more commonly
min. Sleep starts with NREM sleep, and after (Figure 1.8). reported close to the morning.
the night is characterized by a high propor- Figure 1.8 Hypnogram: Hypnogram depicts the sleep stages in relation with time. NREM sleep is maximum
in the first half of the night, while REM dominates the second half. As the night progresses, duration of N3
tion of N3 sleep. As more time is spent asleep, periods reduces and that of REM periods increases. NREM-REM has a cycle of around 90–120 min.
12 Clinical Atlas of Polysomnography
in the cortex of the brain that lies beneath the Fast-spiking activity of the cortical pyramidal interneurons fire at their natural frequency but
electrodes. The cortex is made up of various neurons through their interaction with the par- some of the pyramidal cells may have a longer
types of neurons that include pyramidal cells valbumin interneurons generates a gamma refractory period.
and interneurons, besides glial cells. Pyramidal rhythm in the EEG. It is thought to represent Unlike gamma and beta frequency waves,
cells are excitatory in nature and they remain the synthesis of information as gamma rhythms other waveforms of EEG are regulated by the thal-
in contact with other cortical neurons through appear during the sensory stimulation. These amocortical system. Thalamus has relay neurons
the fibers that they send to other cortical areas pyramidal neurons are glutaminergic and their which receive inputs from the peripheral sensory
(known as association fibers). They also send activity is regulated by the parvalbumin inter- system and also from the different monoaminer-
fibers to the subcortical nuclei and spinal cord neurons, which are GABAergic in nature. These gic neurons from the brainstem. These neurons
(known as projection fibers). These connec- interneurons have fast-spiking activity and they show tonic firing of action potentials. In other
tions are usually reciprocal and thus, other corti- rhythmically inhibit and disinhibit pyramidal words, they show depolarization at regular inter-
cal, subcortical nuclei and information coming neurons. Parvalbumin interneurons also get a vals. On the other hand, when these relay cells are
from the peripheral nervous system (through collateral from the pyramidal cells, thus, excita- in the state of hyperpolarization, they show bursts
spinal cord) regulate their activity in a complex tion of the pyramidal neurons excites the parv- of action potential followed by a period of quies-
manner. In addition, cortical interneurons that albumin interneurons, which in turn, inhibit the cence (Figure 1.9). Burst firing of the thalamocor-
are primarily inhibitory in nature also regulate pyramidal neurons. tical relay neurons is important for the generation
their activity. Beta waves also originate in the cortex and of various waveforms seen during NREM sleep.
During active wakefulness, EEG activ- they may either represent a slow gamma activ- Thalamic relay neurons receive afferents from
ity in the gamma or beta band is often visible. ity or it may be possible that the parvalbumin the periphery as well as the ascending reticular
14 Clinical Atlas of Polysomnography
1.10).
Figure 1.9 Tonic firing vs. burst firing in thalamic relay neurons: Different electrophysiological waves are eration of alpha activity is dependent upon the
produced by different electrical activity of thalamic relay neurons. (Adapted from Qiang Zhou, Dwayne W.
thalamocortical system, in addition to the cho-
Godwin, Donald M. O’Malley, Paul R. Adams. Visualization of Calcium Influx Through Channels That Shape
the Burst and Tonic Firing Modes of Thalamic Relay Cells. Journal of Neurophysiology Published 1 May 1997 linergic neurons from the brainstem. GABAergic
Vol. 77 no. 5, 2816-282.)
Normal Sleep 15
alpha and, thus, could be regulated by the brain- thalamus and cortex help in synchronization of 1.6 ATONIA DURING REM
stem cholinergic inputs. the two sources of delta waves while connections SLEEP
Sleep spindles are 10–14 Hz frequency sinu- between various cortical cells help to spread
soidal waves lasting for at least 0.5 seconds (Fig- them over widespread cortical areas. Profound muscle atonia develops during REM
ure 1.5). These are seen during N2 sleep and are REM sleep is characterized by low voltage sleep, leading to multiple ramifications that are
generated by burst firing of the thalamocortical mixed frequency activity and sawtooth waves clinically important. For example, by producing
relay neurons and reticular neurons. These sleep in EEG. REM sleep is modulated by laterodor- atonia in upper airway muscles, in particular, genio-
spindles are transmitted to the cortex through sal tegmental/ pedunculopontine tegmental glossus, it narrows the caliber of the upper airway
relay neurons. Connections between various (LDT/PPT) cholinergic nuclei situated in the and increases risks for hypopnea and apnea; when
pyramidal cells in the cortex spread them to the brainstem. These nuclei, depolarize thalamic it appears during wakefulness, it manifests as cata-
widespread cortical areas. Sleep spindles result neurons leading to cortical activation that is plexy, which is a sign of narcolepsy; lastly, absence
in hyperpolarization of relay neurons and thus important for generation of dreams. These cells of atonia during REM sleep leads to the REM sleep
prevent the peripheral sensations from reach- also activate GABAergic cells in ventomedial behavior disorder.
ing to the cortex. Thus, they help in maintaining medulla that secrete GABA and glycine on the It is produced by the glycine-mediated (gly-
sleep. anterior horn cells in spinal cord leading to pro- cineric) inhibition of the anterior horn cells in the
Delta waves seen during N3 sleep (slow-wave found atonia. spinal cord and the hypoglossal nerve by the REM-
sleep) have their origin both in the thalamus as Changes in brain’s electrical activity that on cells of the sub-dorsolateral tegmental nucleus.
well as the cortex. Connections between the occur during sleep are depicted in Figure 1.11.
Normal Sleep 17
1.7 CONCLUDING REMARKS tuning on each other to maintain one of the two responsible for the generation of various physi-
states. Sleep is regulated by the circadian as well ological characteristics that help to determine
Sleep and wakefulness are regulated by two inter- as the homeostatic processes. Throughout the the different sleep stages.
connected areas of the brain, which exert a fine sleep, neuronal activity keeps changing, which is
Figure 1.11 EEG, EOG, and chin EMG during various stages of sleep and wakefulness.
18 Clinical Atlas of Polysomnography
FURTHER READING B. first stage to appear is NREM sleep 5. Low voltage mixed activity is seen during:
1. Infant sleep is different from adult sleep as: C. interlaminar nucleus D. burst firing of cerebellar neurons
A. first stage to appear is REM sleep D. suprachiasmatic nucleus 8. Thermoregulation is impaired during:
Normal Sleep 19
A. N1 sleep
B. N2 sleep
C. N3 sleep
D. REM sleep
A. quiet Wakefulness
B. REM sleep
C. NREM sleep
D. active wakefulness
A. REM sleep
B. N2 sleep
C. quiet wakefulness
D. deep sleep
ANSWER KEY
1. A 2. C 3. B 4. D 5. A 6. B
7. C 8. D 9. B 10. A
2
COMMON SLEEP DISORDERS
LEARNING OBJECTIVES
Contents
After reading this chapter, the reader should be able to:
2.1 Obstructive Sleep Apnea (OSA)........................................................22
1. Discuss common sleep disorders as per the International Classifica-
2.2 Cheyne-Stokes Breathing (CSB)........................................................24
tion of Sleep Disorders-3.
2.3 Obesity Hypoventilation Syndrome (OHS)...................................26
2. Diagnose common sleep disorder seen in the sleep laboratory.
2.4 Narcolepsy...............................................................................................28
3. Understand basic management outlines of common sleep disorders.
2.5 Restless Leg Syndrome (RLS)............................................................29
Further Reading................................................................................................31
I n this chapter, we cover the most important sleep disorders that are impor-
Answer Key........................................................................................................35
2.1 OBSTRUCTIVE SLEEP 2.1.1 OSA Symptoms Several questionnaires have been developed
closures, which cause repeated apneas despite ing sleep, witnessed apnea, nocturia, mouth
2.1.2 Risk Factors for OSA
continued efforts to breathe. This, in turn, breathing with dry mouth and throat on awaken-
results in intermittent hypoxemia and frequent ing, excessive salivation during sleep, excessive Several risk factors have been associated with
arousals. Intermittent hypoxemia and arousals sweating, morning headache, nocturnal heart OSA, including:
cause an increase in sympathetic activity, which burn, nocturnal palpitation, unrefreshing sleep, • Obesity: approximately, 70% of OSA
increases the risk of cardiovascular complica- and excessive daytime sleepiness (EDS). In patients are obese. Nevertheless, severe
tions and arrhythmia. Frequent apneas during some occasions, OSA patients may present with OSA can be seen in non-obese subjects
sleep disturb the sleep architecture, resulting insomnia, particularly in women. In a subgroup with craniofacial abnormalities.
in poor sleep quality and daytime sleepiness. of patients, obstructive events may occur mainly • Increased neck circumference (>17 inches
The obstructive sleep apnea syndrome during REM sleep, and this is called REM- for men and >16 inches in women)
(OSAS) is defined as five or more abnormal related OSA. REM-related OSA is seen mainly • Gender: OSA is more prevalent in men
obstructed breathing events per hour of sleep in women, children and young adults. Usually, • Age: OSA is more prevalent in older
and sleepiness. Studies have reported a preva- patients with this disorder exhibit milder symp- people. The risk in women increases
lence of OSAS in 4% of middle-aged men and 2% toms; however, they may present with night- significantly post-menopause.
• Craniofacial abnormalities affecting 2.1.4 OSA Diagnosis index (the number of desaturations with a 4%
the jaw size: retro- and micrognathia (or 3%) drop in SpO2 compared of baseline/
The American Academy of Sleep Medicine
(appears as a small mandible and an hour of sleep) and time spent with SpO2 less
(AASM) considers polysomnography to be
overbite). than 90%.
routinely indicated “Standard” for the diag-
• Enlarged tonsils and adenoids particularly
nosis of sleep disordered breathing. Neverthe-
in children; nevertheless, occasionally it can 2.1.6 OSA Treatment
less, recent studies have shown that level-III
be seen in adults. The gold-standard treatment for OSA is the
portable studies (home sleep testing) can be
positive airway pressure (PAP) therapy applied
2.1.3 OSA Complications used in patients with high clinical likelihood of
non-invasively via an interfacing mask in the
moderate to severe OSA.
OSA can lead to EDS , which increases the risk
form of continuous positive airway pressure
of motor vehicle and other accidents. In addi-
(CPAP) or bi-level positive airway pressure
tion, there is a great link between OSA and car- 2.1.5 OSA Severity
(BPAP). The AASM considers PAP therapy
diovascular and cerebrovascular complications, The severity of OSA is determined by the num- as the treatment of choice for mild, moderate,
such as hypertension, ischemic heart disease, ber of apneas and hypopneas per hour of sleep. and severe OSA. PAP therapy results in signifi-
arrhythmias, heart failure pulmonary hyperten- That index is called the apnea hypopnea index cant improvement in the patient’s complaints.
sion, and stroke. New studies have linked OSA (AHI). Normal = AHI < 5/hour, mild = 5–15/ Several studies have shown that PAP therapy
with insulin resistance. In addition, OSA can hour; moderate = 15–30/hour; and severe = reduces cardiovascular complications of OSA.
cause depression, and decreased memory and >30/hour. Other parameters that may indi- PAP therapy side-effects are usually minor and
concentration. cate the severity of OSA include desaturation reversible. However, adherence to PAP therapy
24 Clinical Atlas of Polysomnography
remains a major obstacle. Therefore, patients increased morbidity and mortality and impaired Overnight PSG typically shows cyclical fluc-
should receive a systematic educational pro- quality of life. tuations in ventilation, with periods of central
gram to improve adherence and PAP usage apnea or hypopnea that alternate with periods
should be monitored objectively and regularly. of hyperpnea, which predominates during stages
2.2.1 CSB Diagnosis
N1 and N2 of NREM sleep.
It is usually difficult to differentiate symptoms of
acute pulmonary edema, advanced renal failure, and patients with atrial fibrillation. It is not uncom- 2.2.2.1 Pharmacological Therapy
and central nervous system lesions. The presence mon to find that patients with HF have co-existing Several drugs have been used to treat patients
of CSB in patients with HF is associated with OSA and CSB. with HF and CSB. Although these drugs
Common Sleep Disorders 25
frequently reduce sleep-related breathing dis- 2.2.2.3 Positive Airway Pressure improvement in both left ventricular ejec-
orders, they may cause undesirable side-effects (PAP) Support tion fraction and heart transplant-free survival.
and/or interactions with other drugs. Currently, Therefore, the investigators recommended that
CPAP has been shown to be an effective and safe
none of these drugs are recommended as a first- a one month trial of CPAP be continued only if
treatment for patients with acute pulmonary
line treatment to manage the CSB of patients it suppressed AHI significantly. Based on this
edema; however, its role in patients with CSB is
with HF. study, CPAP should not be routinely used to
not well-established. A multicenter trial (CAN-
manage CSB in patients with HF.
PAP) was conducted to evaluate the efficacy of
2.2.2.2 Oxygen Adaptive servo-ventilation (ASV) is a new
CPAP in reducing mortality and morbidity asso-
mode of automated pressure support that
The theory behind using oxygen supplementa- ciated with CSB in patients with HF. The study
performs breath-to-breath analysis and deliv-
tion is that oxygen will offset the hypoxic ven- revealed that CPAP had positive effects on oxy-
ers ventilatory needs accordingly, in order to
tilatory drive and, hence, suppress periodic gen saturation, left ventricular ejection fraction,
prevent the hyperventilation that drives CSB.
breathing. Several studies that have examined the and six-minute walk distance, and resulted in a
Numerous observational studies have demon-
role of home oxygen therapy have reported con- 53% reduction in AHI. However, no significant
strated the beneficial effect of ASV in CSB in
flicting results and no data are available regard- difference was found in transplant-free survival,
patients with HF. Nevertheless, randomized
ing long-term clinical outcome. For the present the rate of hospitalization, or quality of life. The
long-term controlled trials are needed to deter-
time, long-term oxygen therapy is not recom- study group advised against the routine use of
mine the long-term clinical efficacy of these
mended as a standard treatment for patients with CPAP in patients with HF and CSB. However,
devices. ResMed Company issued on May 2015
heart failure and CSB. in the posthoc analysis of the study, patients
a serious safety concern during the preliminary
with residual AHI < 15/hr on CPAP showed
26 Clinical Atlas of Polysomnography
primary data analysis from the SERVE-HF A. The presence of hypoventilation during in patients with OSA, such as excessive day-
clinical trial. The investigators reported an wakefulness (PaCO2> 45 mm Hg) as mea- time sleepiness, snoring, choking during sleep,
increased risk of cardiovascular death with ASV sured by arterial PCO2, end-tidal PCO2, or morning headaches, fatigue, mood disturbance,
therapy for patients with symptomatic chronic transcutaneous PCO2. and impairments of memory or concentration.
HF with reduced ejection fraction (≤45%) B. Presence of obesity (BMI > 30 kg/m2). However, when compared to eucapnic OSA
and moderate to severe central sleep apnea C. Hypoventilation is not primarily due to lung patients, those with OHS tend to complain
syndrome (CSAS). Based on that, the AASM parenchymal or airway disease, pulmonary more often of shortness of breath.
recently published updated guidelines indicat- vascular pathology, chest wall disorder
ing that ASV targeted to normalize the AHI (other than mass loading from obesity), 2.3.1 Diagnosis
should not be used for the treatment of CSAS medication use, neurologic disorder, muscle
related to HF in adults with an ejection fraction weakness, or a known congenital or idio- OHS is a diagnosis of exclusion and, therefore,
≤45% and moderate or severe CSA predomi- pathic central alveolar hypoventilation many diagnostic tests should be carried out to
nant, sleep-disordered breathing. syndrome. distinguish OHS from other disorders in which
It is important to note that OSA often coexists hypercapnia is a common finding, such as pul-
2.3 OBESITY with OHS, in those cases, the diagnosis of both monary diseases, skeletal restriction, neuro-
HYPOVENTILATION OSA and OHS should be made. About 90% muscular disorders, hypothyroidism or pleural
SYNDROME (OHS) of patients with OHS have coexisting OSA; pathology. Tests should include ABG, pulmo-
therefore, symptoms and many of the physical nary function tests, chest imaging, laboratory
To diagnose OHS, the following criteria must be
findings of OHS patients are similar to those tests, electrocardiography (ECG), transthoracic
met:
Common Sleep Disorders 27
echocardiogram, and polysomnography. ABG level during sleep, compared with levels during pulmonary physiology and function including
sampling is a key test since hypercapnia is a fun- wakefulness. improvement in alveolar ventilation and noc-
damental feature of the disorder and is required turnal oxyhemoglobin saturation. However, it is
to make the diagnosis. Usually, ABG reveals low 2.3.2 Management of OHS important to realize that weight loss cannot be
PaO2 and a high bicarbonate level, which reflects Untreated OHS is associated with a high mortal- used as the sole initial treatment.
the chronic nature of the disease. ity rate, a reduced quality of life, and numerous
Pulmonary function tests (PFTs) are essen- 2.3.2.2 Positive Airway Pressure
morbidities, including hypertension, pulmonary
tial to exclude other causes of hypercapnia such Therapy (PAP)
hypertension, right heart failure, angina, and
as chronic pulmonary diseases. Although PFTs acute hypercapnic respiratory failure. Application of positive airway pressure is the
can be normal, they usually reveal mild -to-mod- Although there are no treatment guidelines mainstay of therapy for OHS. It seems reasonable
erate restrictive pattern due to obesity. for OHS, treatment approaches are based on to start with CPAP knowing that the majority of
Polysomnography in patients with OHS reversing the underlying pathophysiology of OHS patients have coexisting OSA. CPAP has
may show oxygen desaturation and hyper- OHS including the reversal of sleep-disordered- been shown to be effective in a group of patients
capnia during sleep not related to obstructive breathing, weight reduction, and treatment of with stable OHS, especially in those with severe
apneas and hypopneas periods. Hypoventila- comorbid conditions. OSA. There are no clear guidelines on when to
tion is usually more prominent during REM start or switch to bi-level PAP (BPAP); however,
sleep compared to NREM sleep. If PaCO2
2.3.2.1 Weight Loss
BPAP should be strongly considered in patients
can be monitored, it may also demonstrate an Significant weight loss is desirable in patients with OHS without OSA, and in patients with
increase of more than 10 mm Hg in the PaCO2 with OHS and will lead to improvement in OHS and coexisting OSA, if CPAP is insufficient
28 Clinical Atlas of Polysomnography
and hypercapnia persists despite being on long- hypoxemia on pulmonary vasculature and other in falling down. Full consciousness during
term CPAP, or if they fail to tolerate CPAP. In vital organs. However, it is important to keep in cataplexy. Cataplexy is pathognomonic
addition, BPAP should be used in patients with mind, that treatment with oxygen alone is inad- for narcolepsy and is not present in
OHS who experience acute-on-chronic respira- equate and is not recommended as it does not all narcolepsy patients. If cataplexy
tory failure. reverse hypoventilation or upper airway obstruc- is present, the patient has narcolepsy
Treatment of OHS with PAP improves blood tion on its own. type 1. A diagnosis of narcolepsy
ABG with an assessment of adherence to PAP. Narcolepsy is a relatively rare autoimmune REM phenomenology (hypnogogic
disease. It has pentad of clinical features hallucinations and sleep paralysis) but
2.3.2.3 Oxygen Therapy including: without cataplexy.
Patients with OHS commonly suffer from pro- • Irresistible attacks of sleep, which is usually • Hypnagogic hallucination: Vivid
longed episodes of hypoxemia during sleep, present in all patients. The other feature of dreams that occur at the transition from
in addition to daytime hypoxemia. Therefore, narcolepsy is not present in all patients. wakefulness to sleep (hypnagogic) or from
oxygen therapy is needed if hypoxemia per- • Cataplexy, characterized by sudden sleep to wakefulness (hypnopompic).
sists despite the relief of upper airway obstruc- bilateral loss of muscle tone brought on • Sleep paralysis: It is a temporary inability
tion and hypoventilation with PAP therapy, in by emotions, which can be limited to to move or speak that happens when the
order to prevent the long-term consequences of certain muscles or generalized, resulting patient is waking up or falling asleep.
Common Sleep Disorders 29
and dopamine antagonists have an association can use as needed. For severe persistent RLS,
2.5.1 Prevalence of RLS
with RLS. In some patients, RLS may worsen dopamine agonists, such as pramipexole or rop-
An RLS prevalence of 3.2–12% has been reported
with nicotine, alcohol, or caffeine. inirole can be used 1–2 hour before bedtime.
in different countries.
However, it is preferred that this class of drugs
Common Sleep Disorders 31
should be started by a sleep specialist to titrate symptoms persist, they can be treated based on 4. Oliveira, M. G., Garbuio, S., Treptow, E. C.,
the proper dose and avoid side effects. The their severity. Polese, J. F., Tufik, S., Nery, L. E., et al., (2014).
The use of portable monitoring for sleep apnea
problem with dopamine agonists is that a good
diagnosis in adults. Expert Rev Respir Med. 8(1),
proportion of RLS patients may develop tachy-
123–132. Epub 2013/12/07.
phylaxis to the drugs and, hence, augmentation FURTHER READING
5. Epstein, L. J., Kristo, D., Strollo, P. J., Jr., Fried-
of symptoms . Recently, the calcium channel 2δ man, N., Malhotra, A., Patil, S. P., et al. (2009).
1. Al-Jawder, S. E., & Bahammam, A. S., (2012).
ligands gabapentin and pregabalin have been Clinical guideline for the evaluation, manage-
Comorbid insomnia in sleep-related breathing
ment and long-term care of obstructive sleep
approved for the treatment of RLS. Augmenta- disorders: an under-recognized association. Sleep
apnea in adults. J Clin Sleep Med. 5(3), 263–276.
tion is lower with this class of drugs. Breath. 16(2), 295–304. Epub 2011/03/30.
Epub 2009/12/08.
Secondary RLS is dependent on the caus- 2. BaHammam, A. S., Al-Shimemeri, S. A., Salama,
6. AlDabal, L., & BaHammam, A. S. (2010).
R. I, & Sharif, M. M., (2013). Clinical and poly-
ative conditions, which once managed, RLS Cheyne-Stokes respiration in patients with
somnographic characteristics and response to
can be cured . Therefore, in RLS patients with heart failure. Lung. 188(1), 5–14. Epub 2009/
continuous positive airway pressure therapy in
12/04.
iron deficiency, pregnancy, and uremia, symp- obstructive sleep apnea patients with nightmares.
7. Carmona-Bernal, C., Ruiz-Garcia, A., Villa-Gil,
toms may remit after treatment or resolution Sleep Med. 14(2), 149–154. Epub 2012/09/11.
M., Sanchez-Armengol, A., Quintana-Gallego,
of these conditions. For patients with ferritin 3. Kushida, C. A., Littner, M. R., Morgenthaler, T.,
E., Ortega-Ruiz, F., et al. (2008). Quality of life
Alessi, C. A., Bailey, D., Coleman, J., Jr., et al.,
level <112 picomols/L (50 nanograms/mL), in patients with congestive heart failure and cen-
(2005). Practice parameters for the indications
iron treatment can be initially started and fer- tral sleep apnea. Sleep Med. 9(6), 646–651. Epub
for polysomnography and related procedures:
2008/01/22.
ritin levels monitored. If ferritin levels are an update for 2005. Sleep. 28(4), 499–521. Epub
8. Sin, D. D., Fitzgerald, F., Parker, J. D., Newton,
>112 picomols/L (50 nanograms/mL) and 2005/09/21.
G., Floras, J. S., & Bradley, T. D. (1999). Risk
32 Clinical Atlas of Polysomnography
factors for central and obstructive sleep apnea for Patients with Central Sleep Apnea and Heart Recommendations for the 2012 AASM Guide-
in 450 men and women with congestive heart Failure Trial (CANPAP). Circulation. 115(25), line: “The Treatment of Central Sleep Apnea
failure. American Journal of Respiratory and Criti- 3173–3180. Syndromes in Adults: Practice Parameters with
cal Care Medicine. 160(4), 1101–1106. Epub 12. Javaheri, S., Brown, L. K., & Randerath, W. J. an Evidence-Based Literature Review and Meta-
1999/10/06. (2014). Clinical applications of adaptive ser- Analyses.” Journal of clinical sleep medicine.
9. Vital, F. M., Ladeira, M. T. & Atallah, A. N. voventilation devices: part 2. Chest. 146(3), 858– JCSM: Official Publication of the American Acad-
(2013). Non-invasive positive pressure ven- 868. Epub 2014/09/03. emy of Sleep Medicine. 12(5), 757–761. Epub
tilation (CPAP or bilevel NPPV) for car- 13. ResMed. Important medical device warning. 2016/04/20.
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Epub 2013/06/04. wyg/ServeHFDoctorLetter.pdf. (2015). Relocation of CLIC1 promotes tumor
10. Bradley, T. D., Logan, A. G., Kimoff, R. J., Series, 14. Eulenburg, C., Wegscheider, K., Woehrle, H., cell invasion and colonization of fibrin. Mol Can-
F., Morrison, D., Ferguson, K., et al., (2005). Angermann, C., d’Ortho, M. P., Erdmann, E., et cer Res. 13(2), 273–280.
Continuous positive airway pressure for central al., (2016). Mechanisms underlying increased 17. Al Dabal, L., & Bahammam, A. S., (2009). Obe-
sleep apnea and heart failure. The New England mortality risk in patients with heart failure and sity hypoventilation syndrome. Ann Thorac Med.
Journal of Medicine. 353(19), 2025–2033. Epub reduced ejection fraction randomly assigned 4(2), 41–59. Epub 2009/06/30.
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11. Arzt, M., Floras, J. S., Logan, A. G., Kimoff, R. study: results of a secondary multistate model- cal characteristics, and predictors of obesity
J., Series, F., Morrison, D., et al., (2007). Sup- ling analysis. Lancet Respir Med. 4(11), 873–881. hypoventilation syndrome in a large sample
pression of central sleep apnea by continuous Epub 2016/11/02. of Saudi patients with obstructive sleep apnea.
positive airway pressure and transplant-free sur- 15. Aurora, R. N., Bista, S. R., Casey, K. R., Chow- Saudi Med J. 36(2), 181–189. Epub 2015/ 02/27.
vival in heart failure: a post hoc analysis of the dhuri, S., Kristo, D. A., Mallea, J. M., et al., 19. Bahammam, A. S., & Al-Jawder, S. E., (2012).
Canadian Continuous Positive Airway Pressure (2016). Updated Adaptive Servo-Ventilation Managing acute respiratory decompensation in
Common Sleep Disorders 33
the morbidly obese. Respirology. 17(5), 759–771. 25. BaHammam, A. S., Pandi-Perumal, S. R., & Neu- of restless legs syndrome: existing and emerg-
Epub 2011/11/05. bauer, D. N., (2015). Sodium Oxybate (Xyrem®): ing treatment options. Nat Sci Sleep. 2, 199–212.
20. Aaron, S. D., Fergusson, D., Dent, R., Chen, Y., A New and Effective Treatment for Narcolepsy Epub 2010/01/01.
Vandemheen, K. L., & Dales, R. E., (2004). Effect with Cataplexy. In: Guglietta A, editor. Drug 30. BaHammam, A., Al-Shahrani, K., Al-Zahrani,
of weight reduction on respiratory function and Treatment of Sleep Disorders: Milestones in S., Al-Shammari, A., Al-Amri, N., & Sharif, M.,
airway reactivity in obese women. Chest. 125(6), Drug Therapy. Switzerland: Springer Interna- (2011). The prevalence of restless legs syn-
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syndrome: a state-of-the-art review. Respiratory of the restless legs syndrome. The International 2011/05/21.
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failure complicating obesity hypoventilation: walder, C., Walters, A. S., & Montplaisi, J. (2003). of second generation antidepressants. J Psychiatr
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REVIEW QUESTIONS
perspective of an under-recognized disorder. Saudi Sleep Med. 4(2), 101–119. Epub 2003/11/01.
Med J. 27(9), 1352–1357. Epub 2006/09/05. 28. Salas, R. E., Gamaldo, C. E., & Allen, R. P., (2010). 1. OSA occurs because of:
24. Bahammam, A., (2007). Periodic leg movements Update in restless legs syndrome. Curr Opin Neu- A. reduction in the calibre of upper
in narcolepsy patients: impact on sleep architec- rol. doi, 10.1097/WCO.0b013e32833bcdd8. airway
ture. Acta Neurol Scand. 115(5), 351–355. Epub 29. Facheris, M. F., Hicks, A. A., Pramstaller, P. P., &
B. reduction in the calibre of lower airway
2007/05/11. Pichler, I. (2010). Update on the management
34 Clinical Atlas of Polysomnography
C. increased calibre of upper airway B. PAP therapy 7. Diagnosis of RLS is based on:
2. Cheyene Stokes breathing is characterized by: D. weight management B. the level of serum ferritin
D. no change in breathing pattern with D. at least 35. B. seen only in cases of RLS
central sleep apnea 6. Cataplexy is characterized by: C. seen only during childhood
3. Untreated OSA has been found to increase A. sudden loss of muscle tone during D. always diagnostic of RLS
severe OSA is: can’t be recovered for hours after a 10. Two or more sleep onset REM periods sug-
A. idiopathic hypersomnia
C. narcolepsy
ANSWER KEY
1. A 2. C 3. D 4. B 5. C 6. C
7. D 8. A 9. D 10. C
3
INTRODUCTION TO POLYSOMNOGRAPHY
LEARNING OBJECTIVES
Contents
After reading this chapter, the reader should be able to:
3.1 Why Is Polysomnography Required?................................................39
1. Discuss the principle and utility of polysomnography.
3.2 Types of Sleep Studies and Sleep Monitoring Devices..................40
2. Understand the basis of differentiating between various polysomnogra-
3.3 Advancement of the Machines............................................................45
phy techniques.
3.4 Advantages and Limitations of Various Sleep Studies...................45
3. Recognize various devices with their advantages and disadvantages.
3.5 Guidelines for the Use of Sleep Studies at Home/Out-of-Center... 46
4. Understand the indications and contraindications of Home Sleep
3.6 Concluding Remarks.............................................................................49
testing.
Further Reading................................................................................................49
Review Questions.............................................................................................49
F or a very long time, the human race has remained interested in the myster-
ies of sleep. Reference to sleep can be seen in the texts and scriptures across
diverse religions. Sleep has been described in ancient Hindu texts, such as Vedas,
Answer Key .......................................................................................................51
38 Clinical Atlas of Polysomnography
Upanishads, and Puranas; the ChristianBible could depict alpha activity during wakefulness Thus, it was recommended to include the EEG,
and in the Islamic text, Quran. These books rein- and slowing of waves during sleep. A group EOG, and EMG channels during polysomno-
forced the need for good sleep and described the of researchers from Harvard Medical School graphic recording.
omens of bad sleep. Thus, it appears that our and University of Chicago (USA) described In 1959, the Pickwickian syndrome was first
ancestors knew about the importance of sleep the features of NREM sleep between the years described using the EEG, breathing, and pulse.
and the adverse effects of sleep disorders. How- 1935–1938. At the same time, researchers kept In 1965, Kulho et al expanded our knowledge
ever, these religious scriptures discuss sleep dis- experimenting with the filters of the EEG to regarding the Pickwickian syndrome, using
orders in a cryptic manner with religious flavor get clearer signals and using different chan- the EEG, and respiratory movements monitor-
and thus, the ancient knowledge regarding sleep nels to record other bioelectrical potentials, ing via a belt, heart rate, and carbon-di-oxide
was difficult to decipher and transform to clinical such as electrocardiography, body movements, content during expiration. One year later, i.e.,
practice. and respiration along with EEG. However, it in 1966 apnea and sleep fragmentation were
A sleep study is used to objectively assess took another fifteen years to describe the REM described after monitoring the oro-nasal air-
changes in physiological parameters that occur sleep. Two researchers, Eugene Aserinsky and flow, chest wall movement, and EEG. Thus, you
during sleep. First, the objective monitoring of Nathanial Kleitman, developed the electroocu- can appreciate that the development of sleep
sleep became possible after the discovery of the logram and published their findings regarding medicine and polysomnography took a long
EEG by the German Psychiatrist, Hans Berger, REM sleep in 1953. Atonia during REM sleep time and both the fields are still evolving. As our
in 1924. He was the first person to record and was described by Michael Jouvet in 1959 in cats knowledge expanded, we kept including elec-
demonstrate the cortical electrical activity and, hence, it was proposed that an electromyo- trodes to obtain more data that would help us to
via electrodes applied to the human scalp. He gram should be recorded during sleep study. understand sleep physiology and the associated
Introduction to Polysomnography 39
pathological changes. It was in 1974, that the • Advantages and limitations of each of these stable, heart rate slows and peripheral muscle
term polysomnography (PSG) was used for the machines; and tone reduces. During REM sleep, respiration
first time to describe the simultaneous record- • Guidelines for the use of various devices. and cardiac activity become erratic, peripheral
ing of an EEG, EOG, EMG, and respiratory muscle tone is lost and periodic twitches appear
Since then, we have witnessed a great devel- 3.1 WHY IS the EEG as well. As the person drifts into sleep,
opment in the technology—size of the machines POLYSOMNOGRAPHY EEG activity begins to slow down and certain
has reduced to a great extent; specificity and REQUIRED? characteristic waveforms start appearing, for
sensitivity of the channels have improved owing example, vertex waves, sleep spindles, K com-
The functioning of almost all body systems,
to technical advancement; instead of the analog plexes, delta waves or low-amplitude, mixed-
such as brain, heart, respiratory system, gas-
paper and ink-pen based recording, we now have frequency EEG. These EEG waves, in addition
tro-intestinal system, genitor-urinary system,
computerized software-based recordings that to the information from muscle tone and eye
endocrinal system, and musculoskeletal tone,
allow us to get digital signals, and to tailor the channels, help us to determine sleep stages.
changes between two states of consciousness,
recording according to our need. At times, these physiological functions get
that is, wakefulness and sleep. Even during
In this chapter, we will discuss a few basic disrupted and give rise to different disease states.
sleep, the functioning does not remain static
issues: This disturbance may be limited to either state
and keeps changing, and it is influenced by/
• Need for polysomnography; of consciousness, that is, wakefulness or sleep,
gives rise to different sleep stages. For exam-
• Types of polysomnography machines or at times, may be seen during both stages. For
ple, during NREM sleep, respiration become
available; example, exercise-induced cardiac ischemia may
40 Clinical Atlas of Polysomnography
remain limited to the state of wakefulness. On sleep process, and in such a situation, it is termed useful research tool to understand the physiolog-
the other hand, some pathological processes as sleep disorder. ical changes occurring in various organs of the
are seen only during sleep. These conditions During polysomnographic recording, we body, for example, brain, cardiovascular system,
may, (i) interfere with the initiation or mainte- gather data regarding physiological parameters respiratory system, muscular system, and upper
nance of sleep, for example, insomnia; (ii) lead and try to detect any abnormality. Thus, poly- GI tract during sleep.
tions during sleep, for example, sleep apnea, different pathologies occurring during sleep. In
sleep-related laryngospasm; (iii) be associated addition, it also helps us in measuring the sever- 3.2 TYPES OF SLEEP
with movements during sleep, for example, rest- ity of some sleep disorders (sleep apnea using STUDIES AND SLEEP
less legs syndrome/periodic limb movement apnea-hypopnea-index or respiratory distur- MONITORING DEVICES
disorder, sleep seizure, night terrors, and REM bance index; periodic limb movement disorder
sleep behavior disorder; (iv) lead to excessive (PLMS) by measuring PLMS index) and treat- Depending upon the number of channels that
sleepiness, for example, narcolepsy, idiopathic ment of sleep disorders (for obstructive sleep record various physiological parameters and the
hypersomnia, and Kleine-Levine syndrome. apnea—positive airway pressure titration study). availability of a qualified sleep technician during
Lastly, some pathologies are present during Lastly, polysomnography may be used to mea- the recording, sleep studies may be divided into
wakefulness but further deteriorate during sleep, sure the effect of treatment in certain conditions, four major types:
for example, non-apnic hypoxemia during sleep for example, REM-sleep-behavior-disorder Level IV: This is the elementary machine
in COPD patients. The latter two entities that and sleep apnea. Besides offering medical help that contains only one or two channels for the
are seen during sleep interfere with the normal to patients, polysomnography is an extremely recording of at least one or two respiratory
Introduction to Polysomnography 41
parameters throughout the night. Thus, it • Nasal airflow • Electrocardiogram: At least 2 electrodes
records one of the following parameters during • Chest or abdominal movements that can record any of Leads I, II or III.
or both signals. The channel is mounted at the Level II: This type is also called comprehen- of EEG are present. Active electrodes are
appropriate place where it remains through- sive portable polysomnography. It contains all placed at either of the following positions:
out the night, and next day, the tracing can be channels that are recorded in the Level I sleep frontal, central, and occipital on both sides of
deduced from the data. This machine can be study, except for the video. However, a sleep study the head—right side and left side. They are
used for screening of obstructive sleep apnea. is not attended by a sleep technician and can be usually referred to the opposite mastoid area
However, it is not approved by the AASM for done at the patient’s home. These devices have and thus one electrode is placed on the right
diagnosing obstructive sleep apnea. EEG channels, electrooculogram, and chin elec- mastoid and the other on the left mastoid.
Level III: These devices have at least a mini- tromyogram; in addition to the respiratory moni- These channels are sufficient for the
mum of four channels including, ventilation (at toring channels and ECG. Thus, the total number determination of sleep stages and arousals.
least two channels of respiratory movement or of channels is at least seven and may be expended : However, most available monitoring devices
respiratory movement airflow), oxygen satura- • Pulse oximeter. provide an option for recording from other areas
tion respiratory effort, oxygen movement, and • Nasal airflow: recorded by either of the brain, for example, prefrontal and tem-
airflow), heart rate or ECG, and oxygen satura- thermistor, pressure transducer or both. poral. Thus, devices actually have provision for
tion (Figure 3.1). • Chest and abdominal movements: one belt 24–32 channels of EEG, and thus, they may be
Thus, they have following channels: for each. used for monitoring sleep-related seizures and
• Electro-occulogram: 2 electrodes; one for • Video recording that is synchronized to the • Esophageal pressure monitor: Its use is
the right eye and the other for the left eye. recording of other data. limited to the research purposes. It can
They are usually referred to the mastoid • Audio recording that is synchronized to the reliably differentiate between central and
electrode of the opposite side. recording of other data. obstructive sleep apnea.
• Electromyogram: At least 1 channel for In addition to the diagnosis of sleep disorders, Level II: Sleep studies are cumbersome and
recording chin electromyogram; two are this study type allows manual titration of positive impractical and, therefore, are used mainly in
placed on the anterior tibialis muscles of airway pressure therapy for patients with sleep- research.
each leg. related breathing disorders. Thus, it has a: According to the AASM (2007), portable
• Body position. • Channel for PAP machines that are utilized device must be capable of displaying the raw
• During these studies, Auto-PAP may be during manual titration of PAP in patients data for review by the clinician, in order to allow
used for the titration of PAP pressure in with sleep apnea. assessment of the quality of the data. Moreover,
patients with sleep apnea. The following are the optional channels that may portable sleep studies are approved for patients
Level I: This study is done using devices that be added depending upon the need: with high clinical likelihood of moderate to severe
are used in type II study. The only difference is that • Capnograph: End-tidal carbon dioxide or OSA. These devices are not approved to diagnose
level I sleep study is done in the sleep laboratory using finger capnograph. patients with central sleep apnea, obesity hypoven-
and a sleep technologist attends the whole study. • Channel for pH monitoring in the pharynx: tilation syndrome or other sleep disorders. Addi-
However, to gather more information than type II helps in detecting nocturnal gastro- tionally, they have not yet been approved for
study provides, the following channels are added: esophageal reflux disease (GERD). children and elderlies (>65 years) (Figure 3.2).
44 Clinical Atlas of Polysomnography
3.3 ADVANCEMENT OF THE 2011. This system classifies the devices based leads may fall off. Both the conditions result in loss
MACHINES upon the channels that they have and this has of data as well as limit the mobility of the patient.
been done specially for the home-sleep-testing. It Now, devices are available that offer telem-
In the past few years, considerable advances
is known as the SCOPER system where S stands etry recording of data. These machines improve
have taken place with regards to the devices and
for Sleep, C stands for Cardiovascular parame- the mobility of the patient and the data con-
their software. This has changed the classical
ters, O stands for Oximetry, P stands for Position, tinues to be recorded even when the patient is
definition of the devices. Now some devices fall
E stands for respiratory Effort, and R stands for mobile. Of course, with vigorous movements,
between type III and type II devices. For exam-
Respiratory flow. Then, each of these parameters leads may fall off, as happens with traditional
ple, some of the manufacturers have devices that
is rated between 1 and 5, depending upon the monitoring devices (Figure 3.3).
in addition to the above channels record the snor-
technique used for the collection of data.
ing or the ambient light, or have 1–2 EEG chan-
A considerable progress has been made in type
nels or the body position sensor. In addition, 3.4 ADVANTAGES AND
II and types I devices as well. Most of the devices
many devices have the facility for generating data LIMITATIONS OF VARIOUS
that are used for type I and II studies have a cable
from surrogate channels, for example, respiratory SLEEP STUDIES
connection between the head box and the central
movements from the electrocardiogram or snore
processing unit for storing the data. With traditional So far, it is clear that different types of sleep stud-
microphone or snoring from the nasal cannula.
machines, the cable has to be disconnected when the ies use different kinds of devices and they pro-
Based on the recent advancement in devices
patients want to go to the washroom; if the patient vide different information. Thus, each of them
and methods used to capture data, a new clas-
is making any vigorous movement during sleep, as has limitations and certain advantages. These are
sification system was proposed by the AASM in
we see in sleep-related seizures and parasomnias, the depicted in Table 3.1.
46 Clinical Atlas of Polysomnography
3.5 GUIDELINES FOR THE • Sleep physician must have access to the raw
having OSA.
The AASM has proposed guidelines for the use
• Patient is not bale to attend laboratory
of various types of sleep studies. According to the
because of immobility or any critical
guidelines, Level III studies, which are also known
illness.
as Home Sleep Testing (HST) or Out-of-center
• Patient has been educated regarding
(OCC) studies, can be done in high-risk patients
placement of sensors by a trained sleep
to verify the presence of sleep apnea. However,
physician or sleep technologist.
a negative test does not rule out OSA, and if the
HST/OCC cannot be used if:
clinical suspicion is high, patients should be sub-
• The patient has congestive heart failure,
jected to level I (in-lab attended) polysomnogra-
neuromuscular abnormalities. or severe
phy. However, when performing an HST, it must
COPD that may compromise the quality of
be ensured that:
data.
• A trained sleep physician has evaluated
• The patient has co-morbid or exclusively
the patient comprehensively. Report of
suffering from sleep disorders other than
Figure 3.3 Devices that do not fall in classical I-IV
the HST/OCC should be made in the
OSA.
level category: Alice PDX from Philips Respironics. background of the clinical evaluation.
Introduction to Polysomnography 47
• The machine does not provide raw data to FURTHER READING 5. Kapur, V. K., Auckley, D. H., Chowdhuri, S.,
be verified by a trained sleep technologist/ Kuhlmann, D. C., Mehra, R., Ramar, K., & Har-
1. Collop, N. A., Anderson, W. M., Boehlecke, B., rod, C. G. (2017). Clinical Practice Guideline for
sleep physician.
Claman, D., Goldberg, R., Gottlieb, D. J., Hud- Diagnostic Testing for Adult Obstructive Sleep
HST/OCC can be a good technique to:
gel, D., Sateia, M., & Schwab, R. (2007). Clinical Apnea: An American Academy of Sleep Medi-
• Monitor the progress of non-PAP therapies cine Clinical Practice Guideline. J Clin Sleep Med.
guidelines for the use of unattended portable mon-
for OSA. itors in the diagnosis of obstructive sleep apnea in Jan 31. pii: jc-17-00035.
3.6 CONCLUDING REMARKS monitoring for obstructive sleep apnea. Sleep REVIEW QUESTIONS
Medicine Clinics. 6(3), 261–386.
3. Collop, N. A., Tracy, S. L., Kapur, V., Mehra, R., 1. Gold standard for the sleep study is:
To summarize, polysomnography is a good method
Kuhlmann, D., Fleishman, S. A., & Ojile, J. M.
to assess sleep and sleep disorders. It is useful not A. level IV study
(2011). Obstructive sleep apnea devices for out-
only for the clinical diagnosis but for the research B. level III study
of-center (OOC) testing: technology evaluation.
as well. Choice of appropriate parameters and tech- J Clin Sleep Med. 7(5), 531–548. C. level II study
nology, along with the availability of trained sleep 4. Haba-Rubio, J., & Keriger, J. Evaluation Instru- D. level I study
ments for Sleep Disorders: A brief history of 2. For screening of obstructive sleep apnea fol-
technician and certified sleep physician, can bring
polysomnography and sleep Medicine. In: Intro-
a remarkable change in the quality of life of patients lowing may be used:
duction to Modern Sleep Technology. Chiang,
suffering from sleep disorders as well as help in the A. home sleep testing
R. P. Y., & Kand, S. C. (eds.). Springer; Nether-
advancement of knowledge in this field. lands: 2012, pp. 19–31. B. actigraphy
50 Clinical Atlas of Polysomnography
C. pulmonary function testing D. attended level I polysomnography with 7. To monitor the progress of PAP therapy
E. pulse oximetry 5. Home sleep testing is not accurate for A. level I PSG
3. End tidal CO2 is useful for the diagnosis of: assessment of OSA because: B. level II PSG
A. Cheyene Stokes breathing among A. it may give a false negative result or C. level III PSG
B. obesity hypoventilation syndrome B. it may give a false negative result or 8. Telemetry recording of data during PSG is
C. obstructive sleep apnea among C. it may give a false positive result or A. accurately depicting the EEG waves
D. daytime hyperventilation among D. it may give a false positive result or B. depicting the respiratory waveform dur-
4. For the patient with suspected parasomnia 6. Polysomnography is required to differenti- C. leg movements during PLMS
best sleep study will be: ate between: D. ECG during cardiac asystole
A. attended level I polysomnography A. obesity hypoventilation syndrome and 9. Synchronized audio-video recording helps in:
A. 4
B. 3
C. 2
D. 1
ANSWER KEY
1. D 2. A 3. C 4. C 5. B 6. D
7. C 8. A 9. B 10. D
4
BASIC CONCEPTS OF POLYSOMNOGRAPHY CHANNELS
LEARNING OBJECTIVES
Contents
After reading this chapter, the reader should be able to:
4.1 Electrical Potentials of the Neurons, Muscles, and Heart.............54
1. Discuss the electrical potentials of cells including resting membrane
4.2 Electrical Concepts................................................................................60
potential, Inhibitory post synaptic potential, excitatory postsynaptic
4.3 Concepts Related to Digitalized Recordings...................................77
potential, and action potential.
4.4 Physiology and Recording of Electrical Potentials.........................85
2. Discuss the mechanisms underlying the generation of various
4.5 Respiratory Data.....................................................................................98
potentials. 4.6 Body Position....................................................................................... 110
3. Discuss mechanism of synaptic and neuromuscular communication. 4.7 Video Data............................................................................................ 110
4. Define electricity, polarity, and the concept of dipole. 4.8 Carbon Dioxide Monitoring (PCO2)............................................. 111
5. Understand the principle of use of amplifier and filters during polysom- Further Reading............................................................................................. 112
a number of activities, some of them are electri- discussed with reference to neurons, muscles,
6. Discuss the importance of sampling
cal in nature and recorded as such, for example, and heart.
rate and bit resolution
EEG, EOG, EMG, and ECG; some of them are
7. Discuss the sources of EEG, EOG,
mechanical but converted into electrical activ- 4.1 ELECTRICAL POTENTIALS
EMG and EKG signals
ity during data acquisition, for example, respi- OF THE NEURONS, MUSCLES,
8. Differentiate between various mea-
ratory flow, chest, and abdominal movements AND HEART
sures used to monitor airflow and
during respiration and body position. Similarly,
respiratory efforts 4.1.1 Resting Membrane Potential
chemical changes occurring in the body (oxygen
9. Understand the concept of oximetry
saturation and end-tidal CO2) are converted into Grossly, we can divide the body into two com-
and capnography
electrical signals during the process of record- partments, intracellular and extracellular. Both
10. Discuss the mechanism of body posi-
ing. These changes are necessary to visualize compartments are separated by cell mem-
tion sensor
the data in clear waveforms/numbers for easier branes. Water and electrolytes are present in
11. Discuss the importance of audio-video
interpretation. our body, both inside the cell and outside the
recording during polysomnography
In this chapter, the basic concepts for each cell, but in different concentrations. The differ-
of these channels will be reviewed. To under- ent concentrations across the cell membrane of
S ince Level I polysomnography is the most stand some of the technical aspects of different the three main ions, Na+, K+, and Cl– create a
informative and gold-standard diagnostic concepts, one needs to be informed regarding potential that is known as the resting membrane
test for sleep disorders, we will focus our discus- certain physiological functions. Hence, in the potential. This resting membrane potential is
sion on it in this book. Polysomnography records initial section, an electrical potential will be present across all cells such as neurons (unit of
Basic Concepts of Polysomnography Channels 55
to make the organ properly function. For exam- Figure 4.1 Resting membrane potential across cell membrane: Resting membrane potential (RMP) is
produced by different concentrations of anions and cations across cell membrane. Each ion produces its
ple, neurons talk to each other whenever we potential difference and final RMP is sum of all potentials. In general three ions are most important owing to
their concentration and have maximum contribution to the RMP. These are sodium, potassium and chloride
learn, discuss, or recall. Similarly, when we make
ions. A pump known as sodium-potassium pump maintains the concentration of these ions across cell
any movement, signals from the motor area of membrane in a narrow range to maintain resting membrane potential.
interconnected through synapses while neurons membrane potential reaches to –70 mV from the action potential. However, all these events take
connect to muscles via motor end plates. resting membrane potential of –90 mV), it opens place during milliseconds, and the duration of one
When a neuron gets a signal from the preced- up the Na+ channels in the axon of neurons that action potential is between 0.5–1 msec. After the
ing neuron, neurotransmitters are released into are sensitive to changes in the membrane poten- action potential, Na+ and K+ are brought back to
the synapse from the axon of the preceding neu- tial, known as the voltage-sensitive Na+ channels. their normal concentration across the membrane
ron (Figure 4.2A). These neurotransmitters, for Then, more Na+ enters inside the neuron and the with the help of the Na+-K+ pump that is present
example, adrenaline, acetylcholine, glutamate, or membrane potential start rising (becomes less in the cell membrane. It sends three Na+ outside
GABA get attached to neurotransmitter-specific negative) with the opening of many voltage-sensi- the cell membrane along with bringing two K+
receptors containing ion channels on the postsyn- tive sodium channels. This change in the neuronal inside the cell to restore the resting membrane
aptic membrane and open them, which allows ions membrane potential is known as the depolariza- potential (Figure 4.2B).
to pass through the postsynaptic neuron and cre- tion phase of the action potential. However, the On the other hand, inhibitory neurotransmit-
ate a local potential. Excitatory neurotransmitters, neuron has to return back to its resting membrane ters such as GABA act on the GABA channels
such as acetylcholine and glutamate open chan- potential and to accomplish this, the voltage-sen- that allow Cl– to enter inside the neurons and,
nels that increase the flow of Na+ and Ca++ ions sitive K+ channels open, but with a slight delay hence, make the inside of the cell more nega-
inside the cell and make the resting membrane compared to the voltage-sensitive Na+ channels. tive. This is known as the inhibitory postsynaptic
potential less negative. This change in poten- This process allows K+ to move outside cells, thus potential (IPSP). Like EPSP, it also changes the
tial is called as excitatory postsynaptic potential reducing the positivity inside them, and leads to resting membrane potential towards more nega-
(EPSP). Once the EPSP reaches a threshold a fall back of potential towards the resting state. tive and by hyperpolarizing the cell, it inhibits
value, say +20 mV (in other words, neuronal This is known as the repolarization phase of the neurotransmission.
Basic Concepts of Polysomnography Channels 57
Figure 4.2A Steps in generation of action potential: 1. Action potential in the presynaptic neuron opens cess occurs in a small group of neurons, it will
the calcium channels in presynaptic axon. 2. Calcium ions move inside presynaptic axon. 3. Entry of calcium
produce a difference in the membrane potential
ions move vesicles filled with neurotransmitters to the end and makes them fuse with presynaptic membrane.
4 Neurotransmitters released in synaptic cleft. 5. Neurotransmitter attach to receptors on postsynaptic of that area relative to surrounding area form-
dendrites. 6. Attachment of neurotransmitters to its receptors brings a conformational change and open ion
channels. Movement of ions generates local postsynaptic potential that may be either excitatory or inhibitory. ing a dipole (see below). These changes can be
7. Excitatory postsynaptic potential opens channels in axon hillock and generate action potential that travels to picked at the surface during an EEG.
end of axon through movement of ions across cell membrane.
58 Clinical Atlas of Polysomnography
Figure 4.3 Muscle contraction in EMG: A single muscle contraction appears as multiple deflections; each deflection is produced by a small number of motor units.
60 Clinical Atlas of Polysomnography
potential. Similar to nerve fibers, it opens the volt- multiple motor units work together. Changes in (AC) where the current produces a sine wave
age gates Na+ channels and an action potential is the concentration of ions across the cell mem- with negative and positive polarities, and direct
generated. This action potential traverses inside brane produce a localized change in potential current (DC) where sine waves are not produced.
the myocyte through a structure called T-tubules, that can be picked up through a surface EMG. During DC flow, electrons move in a single direc-
which contain Ca++ in high concentration. The Since all motor units do not contract together, tion while during an AC current, electrons change
action potential opens the voltage-sensitive cal- multiple deflections are seen in an EMG during their direction with time resulting in oscillations.
cium channels in the T-tubules to release Ca++ a single contraction (Figure 4.3). These oscillations are measured as they occur in a
inside. This Ca++ binds with the actin and myosin unit time (second) and are expressed as frequency
to induce contraction. and measured in Hertz (Hz). This is an important
4.1.4 Potential Generation Across
It must be remembered that a motor (as well concept to understand the filter setting.
Cardiac Muscles
as sensory) nerve is made up of multiple nerve Further, the potential difference between
fibers, with each nerve fiber representing one The mechanism of cardiac muscles contraction two electrodes placed on any charged sur-
axon (or dendrite). In the muscles, one nerve is similar to that discussed for skeletal muscles. face is recorded in Volts (V). Since electrodes
fiber supplies many myocytes ranging from few are placed over the body, they are not able to
units to several hundred myocytes. Myocytes assimilate with the underlying surface. There-
4.2 ELECTRICAL CONCEPTS
that get stimulated by stimulation of one nerve fore, some resistance is always present dur-
fiber are called a motor unit because they con- 4.2.1 Basic Concepts of Electricity ing measurement of electrical activity in the
tract together upon stimulation of one nerve Current is represented as (I) in the electrical lit- underlying area. This resistance is denoted as
fiber. Thus, during contraction of a muscle, erature. It can be of two types: alternating current R and measured in Ohms (Ω). Voltage equals
Basic Concepts of Polysomnography Channels 61
current multiplied by resistance (V=IR). This the potential of –70 mV, B is considered posi- a factor of 1000 (or 1 μV of incoming potential is
means that increasing resistance will lower the tive relative to A (because it has +20 mV dif- amplified to a signal of 1 mV), then the gain, in this
potential difference (V) for a given current. It is ference as compared to A). As the electrical case, would be 1000. It is also expressed in decibels
important to remember this concept while plac- current flows from the negative to the positive (dB) in some literature. The sensitivity of an ampli-
ing leads. side, the direction of current will be from A to fier is calculated as the ratio of input voltage to the
The concept of resistance applies to the DC B. If we attach a galvanometer to these points, it vertical amplitude of waveform and is measured as
circuit. For some reasons, that may not appear will show a deflection. μV/mm. In other words, how many micro-volts are
AC circuit is denoted as impedance (Z) despite 4.2.3 Amplifiers As expected, the vertical waveform decreases in size
being measured in Ohms. Hence, for AC cir- These devices serve two purposes: amplification with increasing sensitivity. Sensitivity is chosen so
cuits the relationship between the three factors and differential discrimination. as different waveforms appear distinctly in leads, at
is displayed as V = IZ. As their names suggest, these are the devices the same time, waveforms from nearby channels do
that amplify the signals coming to them. This is not overlap with each other (Figure 4.4 A-E).
4.2.2 Dipole important because signals generating inside the
negative charge and the other has a positive them. This is quantified as amplifier gain, which is Differential discrimination refers to the capacity of
charge. Positivity of the other is relative to the denoted as the ratio between input and output volt- the amplifier to detect the potentials at two inputs
first. For example, if point A is having -90 mV age (Vout/Vin). Let us consider an example: an and to reject the potential that is identical at two
charge (electrical potential) and point B carries amplifier is set to increase the incoming voltage by places. The body is a conductive environment
62 Clinical Atlas of Polysomnography
Figure 4.4A Amplitude changes with sensitivity: Amplitude of the waveform in EEG is dependent upon the sensitivity. Lower the sensitivity, higher the amplitude. This
can be manually set in an epoch. This epoch shows EEG waves with sensitivity of 7 mV/mm.
Basic Concepts of Polysomnography Channels 63
of the wave in Volts) decreases as we go farther from Figure 4.5A Electrical potentials inside the body: Electrical potentials are generated by almost all cells in the
body. However, those of large amplitude traverse to distant areas. These potentials may produce artifacts in
the organ that is emitting that current. It results in
EEG. These may be seen as changes in EEG during muscle contraction and EKG artifacts.
the appearance of physiological artifacts in the elec-
Figure 4.5B ECG artifacts in the EEG derivations: ECG artifacts in the EEG and chin EMG derivations. They can be recognized by their regularity and synchronized
appearance with QRS complex in ECG derivations.
Basic Concepts of Polysomnography Channels 69
reference potential.
4.2.4 Polarity
put as either negative or positive. It depends on the Figure 4.7 Potential difference between two electrodes defines final output: Output potential is determined
by difference of the potentials between two points. One point acts as the reference and other as active electrode.
relative difference in the potential between two In this diagram A is the reference electrode and B is the active electrode.
electrodes from which recordings are acquired.
versa.
Basic Concepts of Polysomnography Channels 71
Depending upon the reference electrode Since machines are attached to an electrical electrode helps in finding out the unequal
used, channels may be either unipolar (better source for the power and patients are connected impedance.
termed referential) or bipolar. Unipolar elec- to machines through electrodes, any short-circuit
trode refers to the use of a distant electrode inside the machine may allow the current from an 4.2.6 Filters
as a reference electrode (e.g., scalp electrode external source to enter inside the patient’s body As the name implies, filters are used to attenuate
referred to an electrode outside an electrically and causing the injury. Hence, proper grounding the waves of a particular frequency from the trac-
active area viz., mastoid), and bipolar refers to of the machine is of paramount importance. ing. Notch filter helps in attenuating electrical
the measurement of the potential difference Another grounding, that is, (patient’s interference of 60 Hz that enters into the channel
between two electrodes that are placed on elec- grounding) helps in providing a common refer- (Figure 4.9A-C). Once it is turned on, it removes
trically active area, for example, frontal and cen- ence point to the machine to find out the actual electrical interference from all leads. However, it
tral. Because of the polarity, the output from potential difference between the two electrodes is important to realize that this filter should not
unipolar and bipolar electrodes will be different in question (see common mode rejection). be used routinely as it may obscure important sig-
(Figure 4.8 A and B). Hence, the ground electrode should be placed at nals. As we have discussed earlier, poor ground-
a site where we expect minimal endogenous elec- ing can cause the appearance of 60 Hz artifact in
4.2.5 Ground trical activity. One such site is the forehead and it the tracing. If the filter is kept turned on since the
Grounding is done for two purposes: to increase is usually placed at the FPz location. Placement outset, this information may be missed and we
the safety of the patient by grounding the of the ground electrode at this location lacks the may not obtain good quality data.
machine and to improve the quality of signal activity of the cerebral hemispheres. In addition, Filters are used to improve the display of
acquisition by grounding the patient. because of its proximity to the eyes, a ground waves of physiological interest and to minimize
72 Clinical Atlas of Polysomnography
Figure 4.8 Output of same epoch from referential (A) and bipolar (B) montages. A: referential montage all derivations are referred to Auricular electrode
of opposite side is shown in this illustration. Compare it with B on next page.
Basic Concepts of Polysomnography Channels 73
B: Bipolar montage: Adjacent channels are referred anteroposteriorly. In referential montage (A) waves are of high amplitude due to a large potential difference.
74 Clinical Atlas of Polysomnography
Figure 4.9A Due to high impedance electrical signals appear in O1 and PG2.
Basic Concepts of Polysomnography Channels 75
artifacts. Hence, filter setting varies according to usually kept at 0.35 Hz since we are interested in score data. A few other concepts that are unique to
the type of lead under consideration. This can be waves above this frequency, especially for sleep the digitalized data are discussed here.
understood by paying attention to the wave gen- staging. However, in certain cases where the The sampling rate is defined as the frequency at
erated during calibration (Figure 4.10). During sweating artifact is distorting the tracing, this fil- which an analog signal is captured and converted
calibration, a constant current is applied to the ter may be set a bit higher, for example, to 1 Hz to into a digital signal. A low sampling rate (i.e., less
filters and is usually of 50 μV. As a result, a sud- minimize the distortion (Figure 4.12 A-D). frequent acquisition of signal from the body) may
den deflection followed by a gradual diminution Similarly, high-frequency filter (HFF) induce malformed output (known as aliasing),
of the wave is seen. The time spent in falling back defines a cut-off frequency where waves having leading to incorrect reporting (Figure 4.13). Thus,
of the signal to 37% of its maximum amplitude a frequency higher than this cut-off frequency the sampling rate of 200Hz in the EEG means that
(peak) is known as “time constant,” and it has an will be attenuated to minimize their display in this signal will be captured 200 times in a second,
inverse relationship with low-frequency filters the tracing. Hence, waveforms of physiological before converting it to digital format. To obtain a
(LFFs) (Figure 4.11). Therefore, increasing the interest are displayed better. For an EEG, it is digital signal similar to the analog signal, it is rec-
low-frequency filter will reduce the time-con- usually kept at 70 Hz, although the AASM rec- ommended to capture the digital signal at least six
stant, and as a result, a waveform will die prema- ommends a setting of 35 Hz. times the frequency of the original signal. Aliasing
turely. LFFs diminish the low-frequency waves is difficult to recognize, hence, it is advised to keep
by nearly 30% in order to improve the display of 4.3 CONCEPTS RELATED TO the recommended settings of filters and signaling
waveforms of frequencies higher than that. That DIGITALIZED RECORDINGS rate before starting the recording. In the modern
is why it is also known as high-pass filter. For studies, aliasing may also emerge because of poor
These days most of the sleep laboratories are using
example, in EEG leads, LFF (high-pass filter) is resolution of the monitor. Monitor Aliasing refers
computer programs designed to gather, store, and
78 Clinical Atlas of Polysomnography
Figure 4.10 Waves generated through calibration: Waves generated during calibration.
Basic Concepts of Polysomnography Channels 79
Figure 4.11 Time constant: Time spent in falling back the signal to 37% of its maximum amplitude is known as “time constant” and it has inverse relationship with low
frequency filter. This figure has been taken from Figure 4.10.
80 Clinical Atlas of Polysomnography
Figure 4.12(A-D) Epochs showing EEG signals using different filters. A: N2 stage with HFF70 LF 0.3.
Basic Concepts of Polysomnography Channels 81
Figure 4.13 Waveforms depends upon the signal capturing rate: Low sampling rate can distort the signals digitalized form. For example, a system of 16 bits
while higher sampling rate improves the waveform.
means than 216 bits are available for represent-
4.4 PHYSIOLOGY AND electrode (local potential, that is, the sum of all information is transmitted from one neuron to
RECORDING OF ELECTRICAL inhibitory and excitatory potentials). Similarly, another via neurotransmitters. In response to the
POTENTIALS we see the sum of electrical changes induced by action potential, neurotransmitters released from
Electrical activity is recorded using surface elec- the heart in an ECG and from muscles in an EMG presynaptic neurons induce two kinds of poten-
trodes that are placed over the area of interest. (see Section 4.4.3). It must be remembered that tials in the postsynaptic neurons: an excitatory
To improve the contact between the surface and an electrode records the electrical signals gener- postsynaptic potential (EPSP) and an inhibitory
the electrode (which reduces impedance), a con- ated inside the body and, hence, during the study, postsynaptic potential (IPSP) (Figure 4.2A-
ductive gel is applied after scrubbing the area to we do not allow any external current to flow inside B). An excitatory neurotransmitter produces
remove the dead skin. During the recording of an the body. an EPSP while an inhibitory neurotransmitter
electrical activity, we actually measure the poten- produces an IPSP by opening different channels
tial difference between two electrodes and the (Na+ or Ca++ and Cl– or K+, respectively). These
4.4.1 Electroencephalogram (EEG)
result is displayed as a waveform. In contrast to potentials are the major source of EEG signals
4.4.1.1 Source of Electrical Signals owing to their slow activity. Pyramidal cells lie
what has been mentioned earlier in the section of
potentials, when electrical data are collected from The brain continues to discern stimuli from the in the outermost layer of the cortex. Their den-
the scalp (EEG), eye (EOG), muscles (EMG) external as well as the internal environment; drites are close to the outer side of the cerebral
and heart (ECG) during a sleep study, we do hence, neurons keep working. Working, in other cortex. Hence, postsynaptic potentials of the
not get the activity from a single cell. Rather, the words, refers to the cross-talk between the neu- pyramidal dendrites is the major source of EEG
EEG depicts the sum of electrical activity occur- rons to pass on the processed information. Neu- signals—non-synaptic activity, for example—
ring in all the cortical neurons that underlie the rons are interconnected through synapses and action potentials of neurons are fast enough to
86 Clinical Atlas of Polysomnography
amplitude of these waveforms depend on the pat- group. During the neuronal activity, stimuli from to delta. As the frequency of activity goes down
tern of discharge of afferent fibers. various sources increase and, thus, influence the (from beta to alpha to theta to delta), the ampli-
Depending upon the state of depolarization electrical state of the neuron. During the active tude of waveforms increases. It must be remem-
or hyperpolarization, the surface potential of the process, multiple neurons fire; however, some bered that activity in different areas of the brain
neuron changes. Because of this, electrical sig- may be depolarized while others may be hyper- could be specific to the state of wakefulness and
nals continue to appear in an EEG. However, polarized. Different electrical states occurring stages of the sleep that are regulated by a complex
their frequency and amplitude keep changing simultaneously in a group of neurons result in a process.
neurotransmitters and neuromodulators regulate the beta range. As a person closes eyes, informa- 4.4.1.2 Electrodes—Active and
the activity of an individual neuron. In general, tion reaching the occipital cortex reduces, while Reference
the reticular activating system (see Chapter 1) synchronized activity continues in this area, and
innervates most of the areas of the brain. Thus, this generates the alpha waves. As a person goes EEG records the sum of the electrical state
it helps in regulating the activity of a specific area into sleep, information reaching the brain from (depolarized or hyperpolarized) of the neurons
(neuron and group of neurons). In addition, each the external environment reduces, which results that lie under it. While recording data from
neuron receives signals from various neighboring in reduced firing of neurons. With reduced stimuli electroencephalography channels during poly-
neurons as well as those present at some distance from the environment, the activity of the cortico- somnography, we place six electrodes on the
(neuronal circuits, for example, thalamocortical subcortical circuits becomes more conspicuous. scalp, three on either side of the scalp, placed in
relay). Stimuli from these sources also influence Thus, the activity becomes more synchronized frontal, central, and occipital positions. These
the activity of a neuron, and in turn, the neuronal and it changes to theta and with deeper sleep, electrodes are the active electrodes. They
88 Clinical Atlas of Polysomnography
are referred to the opposite mastoid, that is, are essential for the recognition of sleep stages of the eyes and they are referred to the opposite
electrodes from the right side of the scalp are may disappear (Figure 4.8). mastoid. Eyeballs have a difference in the electri-
referred to the left mastoid (e.g., F2-M1; C2-M1 However, bipolar electrode placement is cal potential between the cornea and the retina
and O2-M1) and vice versa. Electrodes on the important when we are looking for nocturnal (Figure 4.15). The cornea of the eye is positive
scalp are considered as ‘active’ electrodes and seizures. During a seizure, one area of the brain relative to the retina. Thus, when the eyes move
they gather information regarding electrical becomes electrically different relative to the other towards the left, the cornea of the left eye having
potential from the underlying cortex. Reference areas. In such case, bipolar electrodes help in local- positive potential, comes close to the electrode
electrodes are chosen at a distant place to allow izing that area, since electrodes are placed on the placed near the outer canthus of the left eye and
for a maximum potential difference between scalp, which also contains muscles, contraction of this electrode will show a positive deflection.
the two points, as electrical activity is minimal the scalp muscles produces electrical potential, Since, the eyes have the conjugate movement,
in the mastoid area, which results in a good which may appear in these electrodes, causing sig- that is, both eyes move in one direction, the posi-
waveform. Additionally, a reference electrode nificant noise. Similarly, if any of these electrodes tively charged cornea of the right eye will move
from the scalp is chosen as a reference (e.g., F2– is placed over an artery, which carries the cardiac away from the electrode placed outside right can-
C2). As the potential difference between both electrical potentials, ECG artifacts may appear in thus, and the negatively charged retina will come
these areas may be small (as both are placed these leads (see the chapter on artifacts). closer to it, this electrode will show negative
above electrically active cortex), this combina- deflection. Thus, in the electrooculogram, an out-
tion will not produce a good waveform. More- 4.4.2 Electroocculogram (EOG) of-phase deflection will appear. Similar changes
over, because of the common mode rejection, This is used for recording eye movements. Two will be seen when eyes are moved up or down,
certain important characteristic waveforms that active electrodes are placed near the outer canthi however, during vertical movement, deflections
Basic Concepts of Polysomnography Channels 89
Figure 4.16C Waveform is also noticed in frontal derivations due to their proximity to the eye.
92 Clinical Atlas of Polysomnography
Figure 4.17 Rapid eye movements: Fast saccadic movements are seen during REM sleep.
Basic Concepts of Polysomnography Channels 93
tibialis muscles of both legs. However, in spe- innervated by single nerve fiber constitute 4.4.4 Electrocardiogram (ECG)
cial cases where a movement disorder is sus- one motor unit) become recruited. This
An ECG depicts the sum of the electrical
pected, an EMG may be recorded from the results in the enhancement of the electrical
activity of the heart during its pumping pro-
affected area, for example, masseter muscles potential, which can be picked by the EMG
cess. The heart has its own conduction system
during bruxism or arms in a suspected REM electrodes, and high amplitude signals appear
that is present below the endocardium. The
sleep behavior disorder. An EMG records the in the EMG recording (Figure 4.19). How-
conduction system of the heart is specialized
sum of electrical activity in the underlying ever, recruitment is random, hence, the signal
where impulses generated in the sino-atrial
muscles. is also random and not synchronized. As sleep
(SA) node traverse down to the atrioventricu-
Even during the resting state, muscle starts, basal tone reduces resulting in lower-
lar (AV) node and then to the ventricles. Upon
maintains a basal tone. In other words, myo- ing of the amplitude of the EMG signal. Dur-
activation of the conduction system, changes
cytes remain in the partially contracted state. ing REM sleep, profound physiological atonia
akin to the skeletal muscles occur that result in
As we have already discussed, contraction develops, leading to the diminution of signals
contraction and relaxation.
of a myocyte is brought by a change in the in the EMG.
The heart has four chambers, two atria, and
electrical potential. Thus, even at rest, some Signals from muscles are optimal if the dis-
two ventricles. They do not contract together.
activity can be observed in the EMG chan- tance between the muscles and the surface is
First, the conduction system depolarizes the
nels (Figure 4.18A and B). During a muscle minimal. However, the presence of subcutane-
atria (when the ventricles remain at resting
contraction, the firing frequency of the nerve ous fat increases the distances, hence, the ampli-
membrane potential), and after a few seconds, a
fibers supplying the myocytes increases and tude of the signals decreases.
depolarization wave proceeds to the ventricles
more and more motor units (many myocytes
94 Clinical Atlas of Polysomnography
Figure 4.19 Changes in muscle tone are dependent upon state of wakefulness and sleep, sleep stages and movement. A: As the sleep ensues, muscle tone reduces, with
complete atonia during REM and increment of tone with movement. This epoch depicts chin tone during N3.
Basic Concepts of Polysomnography Channels 97
from right to left, it will create a positive deflec- Figure 4.20 Thermistors and nasal cannula from various manufacturers.
A: Thermisters.
4.5 RESPIRATORY DATA
pressure transducer.
exhaled air. With that temperature change, these the ability to produce an electrical charge when the other hand, in AC channels, constant voltage
metals also change their property that generates pressure is applied to them. The electrical signal input will be filtered. This is important as dur-
the signals. Since they can detect a small change in produced by piezoelectric sensors is proportional ing flow limitations (hypopnea/apnea), airflow
the temperature, they are sensitive to detect apnea, to the degree of pressure applied; hence, these becomes constant for some time resulting in
where, by definition, air does not flow through the sensors provide a waveform that is concordant to a constant voltage output from the nasal trans-
oro-nasal passage. However, during hypopnea and the depth of respiration. Because of this quality, ducer. In AC channels, it will be filtered and will
during airflow limitation as seen during the upper pressure transducers are optimal for recording not produce any waveform. Hence, in machines
airway resistance syndrome, some air continues to airflow limitation. with AC channels, a low frequency filter is set to
flow causing temperature changes and generating 0.01 Hz that results in a time constant of approxi-
a signal that usually has an equal amplitude to that 4.5.1.1 Concepts of Aliasing, Filter mately 5 seconds. With this setting, waveforms
of a normal breath. In short, thermistors and ther- Setting, Sampling Rate, and Polarity in AC will appear similar to DC. Nowadays,
mocouples are not able to detect flow limitation These are applicable to the respiratory param- most of the machines come with DC inputs for
and hypopneas (Figure 4.21). eters as well. Hence, we need to define a sampling respiratory channels. For the high-frequency fil-
On the other hand, a pressure transducer rate, and LFF and HFF. Another important deci- ter, a decision has to be made whether recording
detects the changes in the pressure of air column, sion is to choose the signal recording from AC or of snoring is required embedded in the respira-
which is transmitted to a piezoelectric detector, DC input. tory flow waveform or not. Snoring is generated
which in turn generates an electrical signal. Piezo- In DC inputs, constant voltage input will pro- by partial resistance in the upper airway and this
electric sensors are based on the piezoelectric duce constant voltage out, so the input signals resistance can produce minor changes in the flow
principle. Certain materials (e.g., quartz) have are proportional to the output waveform. On (Figure 4.22A-B). If the HFF is set to 10–15 Hz,
100 Clinical Atlas of Polysomnography
Figure 4.21 Change in thermistor and nasal cannula signals during hypopnea: Hypopnea is defined as at least 30% reduction in amplitude of airflow. During hypopnea,
thermistor signals change minimally while signals in pressure transducer to a large extent.
Basic Concepts of Polysomnography Channels 101
snoring signals can be removed. The setting of apnea from central sleep apnea. It is important example, sometimes the position of the body
HFF is required in DC systems as well. since the pathophysiology and management of may limit the movement of the belt, and thus,
The respiratory waveform should be placed in both are different. because of inappropriate pressure transferred to
the correct polarity with the rounded up tip and For measuring the chest and abdominal the sensor, the movement may be missed or may
the sharp part at the bottom to get a clear idea movements, belts are tied around the chest and be exaggerated. Moreover, the output signal of
about flow (Figure 4.23A-B). Sampling rate has to around the abdomen. During inspiration, chest the piezo technology is not linear; therefore, it
be adjusted depending on the decision to record and abdomen both expand and during expira- cannot be used to assess hypopnea. Additionally,
snore signals in the airflow waveform or not. If tion, both deflate. Belts tied around the chest the piezo technology can produce a false para-
filtered signal (without snoring) is preferred, the and abdomen also sense a strain during expan- doxical breathing signal when tension is applied
sampling rate may be 10 Hz, however, for record- sion (inspiration) and come back to a normal to the belt during patient movements.
ing snoring, it needs to be increased to 200 Hz. state during exhalation. This is recorded through To overcome this limitation, another tech-
sensors attached to the belts. nology was adopted that uses the inductance.
4.5.2 Chest and Abdominal These elastic belts are made up of nylon and Faraday’s law states that when a current is
Movements they are connected to a small sensor from both passed through a loop of wire, it creates a mag-
With respiration, the volume of the chest and sides. The simplest type of sensor is a piezo- netic field around it. When the girth of this
abdomen changes, and measurement of the electric strain gauge that emits current when a loop is changed, it induces an opposing current
change of volume is known as plethysmography. change in the strain occurs in the belts during the that is directly proportional to the change in
Recording of the chest and abdominal move- respiratory movement. However, these strain girth (Lenz’s law). Thus, in respiratory induc-
ments help to differentiate obstructive sleep gauge sensors have important limitations. For tance plethysmography (RIP), small alternate
102 Clinical Atlas of Polysomnography
Figure 4.22A Snoring embedded in respiratory waveform: Snoring signals from the airflow waveform can be removed by appropriate filter setting. A: Setting high
frequency filter to 50 Hz derivations to appearance of snoring. In this illustration, respiratory waveform is flat as LFF has been mistakenly set as 1 Hz.
Basic Concepts of Polysomnography Channels 103
Figure 4.23A Polarity of the respiratory waveform. Correct polarity for respiratory flow wave is rounded up tip and sharp part at the bottom.
Basic Concepts of Polysomnography Channels 105
Figure 4.23B Incorrect polarity of respiratory flow waveform. This may be rectified by reversing the polarity through channel properties.
106 Clinical Atlas of Polysomnography
volume loops.
Basic Concepts of Polysomnography Channels 107
4.5.2.1 Concepts of Aliasing, Filter where it binds with the hemoglobin (Figure amount of infrared light and less of red lights
Setting, and Sampling Rate 4.25). One molecule of hemoglobin can carry (that is why it appears red), while the deoxyhe-
eight molecules of oxygen. Then blood enters moglobin possesses the opposite quality. Light-
To overcome aliasing, the sampling rate is set
the left side of the heart through the pulmonary emitting diodes in pulse oximeter emit lights of
at 10 Hz. Just like respiratory flow signals, when
veins from where it is pumped to the whole body these two wavelengths that are made to traverse
these belts are attached to an AC channel, LFF is
through the aorta. The aorta divides into small through the tissue (finger, nose, ear lobe). These
set to 0.1 Hz or lower while HFF is set to 35 Hz.
arteries, arteries into arterioles, and arterioles in are present on one side of the probe. On the
capillaries. Capillaries form the smallest part of other side of the probe, the amount of lights that
4.5.3 Oxygen Saturation
the vascular system and are present close to the has passed is sensed by a photodiode (Figure
In the body, oxygen is carried to the peripheral tis- cells in the peripheral tissues. This is how oxygen 4.26). Relative amounts of red and infrared lights
sues through hemoglobin. Oxygen of the inhaled (and other nutrients) is delivered (through diffu- are measured using a mathematical formula that
air diffuses through the alveoli of the lungs to sion) to the peripheral tissues. Areas of the body allows calculation of the concentration of oxygen
the capillaries. These capillaries carry the deoxy- like finger, nose, ear lobe, and forehead have rich bound to hemoglobin.
genated blood (hemoglobin in red blood cells vascularity; hence, they are the best sites to mea- Considering this principle, it is simple to deci-
(RBC) without oxygen) that is propelled by the sure oxygen concentration. pher that any condition that reduces the flow of
right ventricle of the heart through the pulmo- Pulse oximetry is based on the principle of dif- blood to peripheral tissues (such as congestive
nary artery. Because the concentration of oxygen ferential absorption of infrared (940 nm) and red heart failure, any kind of pressure on the artery
is higher in the inhaled air, it diffuses through (660 nm) lights by oxyhemoglobin and deoxy- supplying the area where probe is applied), any-
the alveolar wall and capillary wall into the RBC, hemoglobin. Oxyhemoglobin absorbs a greater thing that interferes with transmission of light
108 Clinical Atlas of Polysomnography
Figure 4.25 Oxygen exchange in lungs: Because of the concentration gradient, Atmospheric oxygen diffuses through the alveolar and capillary to enter the RBC. It has
high affinity for hemoglobin so it converts the deoxygenated hemoglobin to oxygenated hemoglobin. Reverse happens in the peripheral tissues.
Basic Concepts of Polysomnography Channels 109
therapy.
110 Clinical Atlas of Polysomnography
4.5.4 Record of Snoring the patient during the study, if a need arises but accurately gauge the true severity and appropriate
also supplements visual information recorded PAP titration. Body position sensor has a gyro-
As has been already discussed, snoring may be
during sleep. Signals from the microphone are scope that determines the position of the body. It
recorded through the pressure transducer. How-
synchronized with video recording and other sends different signals depending upon the body
ever, most modern machines have a microphone
data, hence, they play an important role in cases position: right, left, supine, prone, and upside.
or piezoelectric sensor that is placed on the lar-
of sleep seizures and parasomnias. Snoring can These different signals are then converted into a
ynx. This microphone sends the signals to the
also be recorded via nasal pressure cannula, waveform and depicted in the polysomnography.
software where these are shown in the form of
where the snoring signal can be seen superim- The body position sensor reports the position of
waveforms. The amplitude and duration of these
posed on the airflow waveform signal when the the sensor rather than the position of the human
waveforms vary according to the intensity and
signal from airflow sensor cannula is unfiltered. body; therefore, it is essential to assure that the
duration of snoring (or any other sound pro-
sensor is oriented correctly to the patient.
duced in close proximity to the probe). Thus, it
light is emitted from the camera, and its sensors ETCO2 and transcutaneous PCO2 are noninva- increasing local capillary perfusion, and measures
record the reflected infrared signals. The focus sive validated indirect methods to predict arterial the CO2 gas as it diffuses from the dermis across
and direction of the camera may be manipulated PCO2 (ETCO2 reflects exhaled CO2 at an end- a gas-permeable membrane. Currently available
from the monitoring room with the help of spe- tidal sample of exhaled gas. Infrared spectroscopy devices require less heating (42°C for adults and
cial software. With these manipulations, a sleep is the technique usually used to assess ETCO2 in 41°C for neonates); therefore, resulting in less dis-
technician can record even the smallest move- the exhaled gas. When the patient is being ven- comfort and less potential for skin damage. Never-
ment during any activity occurring in sleep. tilated using a closed circuit (e.g., endotracheal theless, the sensor may need to be repositioned at
tube), ETCO2 can be measured directly with good least once during a sleep study. The absolute value
4.8 CARBON DIOXIDE accuracy. However, during a sleep study, ETCO2 is of transcutaneous PCO2 is affected by skin thick-
MONITORING (PCO2) measured using a nasal cannula in a spontaneously ness and capillary density. Therefore, it is impor-
breathing patient; therefore, side-stream sampling tant to place the electrode at a site of high capillary
In pediatrics, end-tidal PCO2 (ETCO2) is consid- often occurs. When a patient is on a noninvasive density and thin skin. This presents no problem in
ered a standard practice during PSG monitoring. PAP device, the increased flow within the open cir- the newborn, in which these conditions are usually
On the other hand, in adult patients, the AASM cuit results in dilution of the exhaled gas. Therefore, present. However, in adults, there is greater varia-
recommends the use of arterial PCO2, ETCO2, or the numerical value or the displayed waveform of tion from site to site. The suggested locations for
transcutaneous PCO2 for detection of hypoventila- ETCO2 may not accurately reflect arterial PCO2. best transcutaneous measurements are the fore-
tion during a diagnostic sleep study, and the use of Mouth breathing may influence the displayed sig- head, forearm, chest, or abdomen. Transcutaneous
arterial PCO2 or transcutaneous PCO2 for detec- nal too. Transcutaneous PCO2 is obtained through PCO2 provides a good alternative to ETCO2 during
tion of hypoventilation during PAP titration. Both the skin where the electrode warms the skin surface, PAP titration to assess the response to treatment.
112 Clinical Atlas of Polysomnography
underlies electrode
1. Patil, S. P., (2010). What every clinician should 1. Resting membrane potential differs from B. electrical activity of a small group of
know about polysomnography. Respiratory Care
action potential as: neurons that underlie electrodes
55, 1179–1195.
A. it is not dependent upon the transmis- C. cumulative electrical activity of all the
2. Olejniczek, P. (2006). Neurophysiologic basis of
EEG. J Clin Neurophysiol. 23, 186–189. sion across synapse cortical neurons irrespective of elec-
3. Bucci, P., & Galderisi, S. (2011). Physiologic basis of B. it has smaller time duration than action trode placement
EEG signals. In: Standard Electroencephalography in potential D. cumulative electrical activity of all
Clinical Psychiatry: A Practical Handbook. Boutros,
C. not seen in muscles the subcortical neurons that underlie
N., Galderisi, S., Pogarell, O., Riggio, S. (Eds.).
D. mainly dependent upon the concentra- electrode
Wiley–Blackwell, Oxford Chichester, pp. 7–12.
4. Hall, J. E., & Guyton, A. C., (2011). Guyton and tion of calcium ions 4. During a muscle contraction:
Hall textbook of medical physiology. Philadel- 2. At the termination of action potential fol- A. all the motor units contract together
phia, PA, Saunders Elsevier. lowing pump bring the cell to pre-excitatory B. all the motor units contract sequentially
5. Chan, E. D., Chan, M. M., & Chan, M. M.,
stage: one after another
(2013). Pulse oximetry: understanding its basic
A. Na-Cl pump C. all the motor units contract in two
principles facilitates appreciation of its limita-
tions. Resp Med. 107, 789–799. B. Ca+2 pump divided parts
6. Kirk, V. G., Batuyong, E. D., & Bohn, S. G., C. Na+-K+ pump D. all the motor units contract so as they
(2006). Transcutaneous carbon dioxide moni- D. Cl– pump reach a peak followed by relaxation
toring and capnography during pediatric poly-
3. EEG waves depict: 5. Amplifiers works to:
somnography. Sleep. 12, 1601–1608.
Basic Concepts of Polysomnography Channels 113
A. amplify the frequency of electrical signals 8. Ventricular contraction in EKG is depicted by: D. positive charge in cornea and negative
B. amplify the resistance of electrical signals A. QRS complex charge in eye muscles
C. amplify the voltage of electrical signals B. P wave 11. Best measure for the hypopnea is:
A. accepting the identical potentials 9. Ideally, for higher amplitude, during EEG C. strain gauge
between two electrodes acquisition reference electrodes are placed at: D. thermistor
B. rejecting the identical potentials A. area that is electrically active 12. Pulse oximetry is important for:
C. accepting non-identical potentials C. area with frequent change of potentials B. scoring obstructive apnea
between two places D. area having equal potential to the active C. scoring hypoventilation
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, reader must be able to:
1. Understand the optimal environment and setting of a sleep laboratory. 5.1 Sleep Laboratory................................................................................. 116
2. Able to check the equipment for electrical safety. 5.2 Preparing the Machines..................................................................... 116
3. Prepare the patient for optimal recording of data during 5.3 Preparing the Patient.......................................................................... 117
polysomnography. Review Questions.......................................................................................... 118
4. Provide instructions to the patient for optimal recording. Answer Key..................................................................................................... 119
A good recording requires that the room, equipment, and patient are well-
prepared before the process of gathering data is initiated. These issues are
important as they may influence the quality of data and, thus, your conclusion and
116 Clinical Atlas of Polysomnography
as well as the safety of the patient. It is important television, and an attached bathroom. The room The laboratory must provide means for the
that you choose the correct machine (Chapters 3 size should be adequate enough to alley anxi- patient to communicate with the sleep tech-
and 9), and have correct montage (Chapter 10) ety in claustrophobic subjects. A couch must be nician anytime during the recording, without
for recording the data. Adequate measures to provided for a family member to stay with the reaching for the phone. For this, a microphone
prevent infection should be taken care of before patient. The room must be air-conditioned and and a speaker may be placed near the head-end
subjecting a patient to the sleep study (Chapter sound proof, and should have thick curtains to of the bed.
24). This chapter does not discuss topics that create a dark environment for daytime record-
have already been covered in other chapters. ings. Air-conditioning is necessary for multiple
reasons—it prevents dust from entering into the 5.2 PREPARING THE
room, which can interfere with signals, and it also MACHINES
5.1 SLEEP LABORATORY helps to maintain a comfortable temperature for
a good sleep. Many patients with OSA sweat a Polysomnography machines require electrical
The room in which a patient will stay for the lot because their work of breathing is increased. power for their working and so they are con-
recording plays an important role in the qual- This is one of the major reasons for falling off the nected to the electrical supply that usually has
ity of the study. The sleep laboratory should be electrodes and artifacts in the recording. Having 240 V current. These machines also have capaci-
situated away from a crowded and noisy area an adequate temperature of around 22°C mini- tors and transformers, in addition to the inte-
and its décor should be attractive and homely. mizes sweating. A blanket may be provided in grated circuits. Normally, these parts are placed
It must have adequate ventilation and provision case the patient feels cold. close to each other to enable the electric flow
for daylight. It should include a comfortable bed between them. This results in the generation
Preparations for the Sleep Study 117
of an electromagnetic field, which can generate “patient’s body” depends upon the relative resis- printed flyer with the patient explaining the rea-
“stray capacitance” and “stray inductance.” This, tance of each. If the resistance is lesser in the son and procedure of the study. The flyer must
in turn, can generate a small amount of current “earth,” the current will prefer this path. also depict the “Dos and Don’ts before the sleep
in the system that can flow through the leads, Hence, it is of utmost importance that study” to allow the patient to be better prepared
especially the leads that attach directly to the the “earth/ground” wire of the plug is work- for the procedure. It is also advisable to explain
body (e.g., EEG, EKG, and EMG) and may be ing properly and has minimal resistance. This the entire procedure to the patient using appro-
delivered to the patient’s body. Another source should be regularly checked by an electrical priate visuals to allay all fears and anxiety. A
of aberrant current is any short-circuit inside the engineer. change of place is another factor contributing to
polysomnography recorder that connects the the “first night effect.” A change in environment
patient directly to the power supply. prevents a patient from going to sleep. To mini-
To avoid both these unwanted scenarios, 5.3 PREPARING THE mize this, the patient should be advised to report
almost all manufacturers take optimal precau- PATIENT at least 8–10 hours ahead of the bedtime. Once
tions of “grounding” the machine. A wire is in the sleep laboratory, the patient may spend
attached to the chassis of the motherboard that Before conducting a sleep study, it is important time in some leisure activities in order to get
“sucks” unwanted current and delivers it to the to prepare the patient for it. If the patient is not acclimatized to the environment.
“ground (earth)” through a large round pin in explained the procedure in advance, the equip- Some general precautions should be taken
the socket. In absence of this ground, the cur- ment and the web of wires could prevent his/ while a patient is in the sleep laboratory. These are
rent will flow towards the patient. Which path her sleep, leading to what is known as the “first listed in Table 5.1. Further, a patient also needs to
the aberrant current will prefer—“earth” or the night effect.” Hence, it is advisable to share a be prepared for effective monitoring, for example,
118 Clinical Atlas of Polysomnography
Table 5.1 Instructions to the Patients Before Sleep Study an abrasive gel needs to be applied to remove the
1. Keep your body clean. For the proper application of electrodes on your body, the skin should be
dead layers of the skin from the body. This is done
clean, dry and free of dirt and any grease. It is better that you take bath two hours before the start
of polysomnography and clean your hair with shampoo. If it does not interfere with your religious to reduce the resistance between the electrode and
practices/beliefs, men are requested to shave the beard. After this, please do not apply any kind of
the skin such that the EEG, EMG and EKG elec-
oil or cream on your skin/hair.
trodes are able to accurately capture the electrical
2. Cotton cloths are preferred during the test. Clothes made up of synthetic material may have elec-
trostatic discharges, which may interfere with the signal acquisition. signals from the body. However, the abrasive gel
3. You are advised to wear pajama and t-shirt. While choosing your clothes, please consider that
should not be applied to an inflamed area or any
sleep technician may enter the room in the night to replace the fallen electrode.
area where a breach in the skin is visible. Similarly,
4. Although the blanket/bedsheet/pillow is available in the sleep laboratory, however, if you prefer,
you may bring your own. the patient’s history should be studied in advance
5. Please do not bring any valuable item with you.
to identify any history of allergy to the gel, and if
6. Women should avoid wearing jewelry during the test.
found, the gel should be avoided.
7. Avoid taking nap in the day before your sleep study is planned.
8. Take your medications as you are taking on other days. However, please discuss them before with
your sleep physician before you come for the study.
9. It is advisable that you do not consume any substance of abuse before the test. Please consult your REVIEW QUESTIONS
sleep physician in this regard.
10. If you prefer to sleep with any particular object, for example, any toy (especially children), you
may bring it along with. 1. Following are the possible reasons that can
polysomnography, EXCEPT:
A. stray inductance
Preparations for the Sleep Study 119
B. double grounding of the machine 4. Following may interfere with oximetry data,
application of:
inductance
6
PLACEMENT OF LEADS FOR THE SLEEP STUDY
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Place sensors at correct position during a sleep study. 6.1 Electroencephalogram (EEG)......................................................... 122
2. Get the optimal output from the sensors. 6.2 Electrooculogram (EOG)................................................................. 129
3. Discuss why sensors are placed at that very position as suggested in 6.3 Electromyogram (EMG)................................................................... 131
manual from American Academy of Sleep Medicine. 6.4 Electrocardiogram (ECG)................................................................ 132
optimal data. If the sources of the signals are not placed at defined places,
the recording will be of suboptimal quality and the data captured would not be
Further Reading............................................................................................. 142
from two different persons. To counteract these 1. Frontal electrodes best pick the delta activ-
Box 1 EEG Derivations for the
issues, the AAMS has recommended appropriate ity (exhibit N3 sleep) Polysomnography Recommended by AASM*
places and methods of hooking up the patients. 2. Central electrodes best pick the Vertex Primary Backup
F4-M1 F3-M2
In this chapter, we will guide you on how to place waves, K complexes, spindles and sawtooth C4-M1 C3-M2
O2-M1 O1-M2
different sensors during a sleep study. waves (determine N1, N2 and REM stage)
*American Academy of Sleep Medicine, 2016
3. Occipital electrodes best pick the alpha
Figure 6.1 Malfunction of one electrode: F4-Avg does not show waves clearly due to poor contact between F4 and skin, but waveforms from frontal area can be
recognized in F3.
124 Clinical Atlas of Polysomnography
of these leads may obscure the waves and affect 2. Non-elastic measuring tape;
reporting. These cephalic electrodes should be ref- 3. Abrasive material to clean the area;
taminate the electrical signals. Rather, it increases First, identify the nasion on the front of the
the distance between the leads and amplifies the face. Nasion is the depressed area on the top of
electrical potential (see Chapter 4). the nose and between the eyes where it meets
To overcome the problem , EEG electrodes the frontal bone (Figure 6.2). Second, identify
should be placed according to the International the inion at the backside of the lowermost part Figure 6.2 Nasion (the depressed area where the
nose meets forehead between eyes).
10–20 system. The figures 10 and 20 denote of skull. Run your finger from the back of head
the distance between the electrodes that area towards the neck in the median plane. You will
measured in percentages (10% or 20%) of the feel a protuberance here. This is the inion (Fig-
length and breadth of the fixed anatomical ure 6.3). Using a non-elastic measuring tape,
points of the scalp. measure the distance between these two points.
tion of FPz
tion of Oz
10% = 2.8 cm
20% = 5.2 cm
5% = 2.4 cm
10% = 4.8 cm
Placement of Leads for the Sleep Study 127
on the right)
important.
Figure 6.6 Marking in the coronal plane: If you are doing sleep study where extended EEG montage (for In step 4, measure the distance between
seizure or parasomnia) is not required, only C3 and C4 markings are important.
F7-Fz and Fz-F8. Place a mark halfway (50%)
important.
Frontal: F3 and F4
Central: C3 and C4
Figure 6.7A Markings on the head circumference: If you are doing sleep study where extended EEG
montage (for seizure or parasomnia) is not required, only O1 and O2 markings are important. Occipital: O1 and O2
Mastoid: M1 and M2
6.2 ELECTROOCULOGRAM
(EOG)
Figure 6.7B Markings on the head circumference: If you are doing sleep study where extended EEG conductance.
montage (for seizure or parasomnia) is not required, only O1 and O2 markings are important. Placing one electrode above and below has
Figure 6.8 Markings for frontal and parietal electrodes: If you are doing sleep study where extended EEG Figure 6.9 A Placement of EOG electrodes: One
montage (for seizure or parasomnia) is not required, only F3 and F4 markings are important. EOG electrode is placed one cm above and other
one cm below to the outer canthi of eyes on opposite
sides. Placement of EOG electrodes: One EOG
electrode is placed one cm above and other one cm
below to the outer canthi of eyes on opposite sides.
Placement of Leads for the Sleep Study 131
in one direction whether is up, down, right or mentalis-submentalis muscle, which helps in
left unless the patient has a weak extra-ocular scoring of the sleep stage and another one to
muscle(s) or an artificial eye. Placing the EOG measure the periodic limb movements during
electrodes above and below to outer canthi of sleep (PLMS).
both eyes helps in detecting signals of opposite To measure the tone of mentalis-submentalis
polarity in both leads, which makes them easily muscles, electrodes are placed close to the chin.
recognizable during sleep (Figures 6.10–6.13). One electrode is placed in the midline, 1 cm
However, if, for some reasons these deriva- above the lower border of the mandible and the
tions cannot be placed, EOG electrodes on both other two are placed 2 cm below the lower edge
sides can be placed 1 cm below and 1 cm lateral of the mandible and two centimeters lateral to
to the outer canthi of the eyes. These are then the midline on either side (Figure 6.15).
referenced to Fpz instead of the opposite side of Placement of these electrodes is difficult in
the mastoid (Figure 6.14). bearded persons and they often fall off.
Figure 6.9 B Placement of EOG electrodes: One dle one-third of the anterior tibialis muscle. This
EOG electrode is placed one cm above and other 6.3 ELECTROMYOGRAM
may be identified by asking the patient to extend
one cm below to the outer canthi of eyes on opposite
(EMG)
sides. Placement of EOG electrodes: One EOG his/her lower limb and to dorsiflex the foot. As
electrode is placed one cm above and other one cm
below to the outer canthi of eyes on opposite sides. the person makes this movement, you will feel
Electromyogram is placed at two sites in
some muscle moving just lateral to the shin. This
the body. First is to measure the tone of the
132 Clinical Atlas of Polysomnography
6.4 ELECTROCARDIOGRAM
(ECG)
Figure 6.11 Eye movements during wake state-opposite phase: Eye movements during wakefulness. Waveform around each star represents one eye movement.
Appreciate that when signals of LEOG lead are moving up, signals in other REOG/ROC lead are moving in opposite direction. Thus, eye movements can be easily
recognized. In addition to the EEG signals, deflections in the frontal channels (in the circle depicting blinking) differentiate eye movements that occur during awake state
from those seen during REM sleep.
134 Clinical Atlas of Polysomnography
Figure 6.12 Eye movements during REM-opposite phase: Eye movements during REM sleep. Waveform around each star represents one movement. Appreciate that
when signals of one EOG lead are moving up, signals in other EOG lead are moving in opposite direction. Thus, eye movements can be easily recognized. Please see that
waveforms in EEG are different and blinking artifacts are absent.
Placement of Leads for the Sleep Study 135
Figure 6.13 Sometimes K complexes and delta waves may appear in eye derivations. These waves may be differentiated from true eye movements as true eye
movements are out of phase deflections while these are “in-phase” deflections (marked with star).
136 Clinical Atlas of Polysomnography
Figure 6.14 Acceptable EOG derivations: These derivations are referenced to the
Fpz instead of opposite mastoid. Since they are placed lying at same level, vertical
movements will appear “in-phase” while horizontal movements will appear “out of
phase.”
Figure 6.16 Placement of leg EMG electrodes.
Placement of Leads for the Sleep Study 137
6.5 PLACEMENT OF not have this kind of cannula, you may place the
Nasal airflow is measured using a thermistor Respiratory effort is measured by either an elastic
and a pressure transducer. Pressure transducer belt or an RIP belt which is placed over the chest
is usually attached to a cannula that is kept and abdomen. These belts should not be too
close to the nostrils (Figure 6.18 and 6.19A). loose or too tight. In the former case, they will fail
Cannula may have one end that is to be fixed to record the movement, while in the latter case,
on the sensor. In the laboratories, which are they will produce discomfort. A rule of thumb is
recording the end tidal CO2 as well, this can- to lengthen the belt to the two-third of the cir-
nula has two ends. Other end of the cannula is cumference of the chest and abdomen, and then
Figure 6.17 Placement of ECG electrodes. attached to the capnograph. The cannula must using its elastic property, tie it around the chest
be properly fixed on the face with tape so that it and abdomen. The belly should not be twisted
does not get misplaced during the study. Some as it will not only produce discomfort, but in case
companies supply cannula that has a provision of an RIP belt, also interfere with proper signal
ure 6.19B). This kind of cannula reduces the On the chest, it should be placed at the level
crowding of instruments in nostrils. If you do of nipples. Fixing the chest belt may be a bit
138 Clinical Atlas of Polysomnography
6.21).
6.5.3 Oxymeter
Figure 6.20 Placement of RIP belts: RIP belt for the chest is placed at the level does not fall off during sleep.
of nipples while that of abdomen is placed at the level of navel.
Figure 6.21 In females, placement of RIP belt over breasts generate notched waveform. Thus, in females, RIP belt may be placed just below the breasts.
142 Clinical Atlas of Polysomnography
plan.
Figure 6.23 Placement of body position sensor: Body position sensor should be placed in midline
and is usually mounted on the chest belt.
Placement of Leads for the Sleep Study 143
REVIEW QUESTIONS C. 1 cm lateral and then above and below 7. In patient with predominant oral breathing,
maximum
A. Forehead
B. Abdominal belt
patient sleeps
of neck in midline
ANSWER KEY
1. A 2. D 3. C 4. B 5. D 6. C
7. A 8. B 9. C 10. C
7
STARTING AND CLOSING THE STUDY
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to start and close
the recording in Level 1 polysomnography machines from various Steps at Starting and Closing the Sleep Study ........................................ 146
manufacturers. Review Questions.......................................................................................... 178
Answer Key..................................................................................................... 178
I n this chapter, we will discuss, step-by-step, how to start and close a sleep
Philips Respironics, Somnomedics, and Cadwell. This does not involve any tech-
nical information, hence, only illustrations are used for the understanding (Figures
7.1–7.31).
146 Clinical Atlas of Polysomnography
Figure 7.1 Handling Somnoscreen Software: On opening the software this page appears on the screen. Click on “New Study.”
Starting and Closing the Study 147
Figure 7.4 Enter details regarding recording and click on OK and Next.
150 Clinical Atlas of Polysomnography
Figure 7.6 Start Calibration (Chapter 8). Click again to end calibration.
152 Clinical Atlas of Polysomnography
Figure 7.7 At the end of calibration, these signals will appear on the page. This is real-time data.
Starting and Closing the Study 153
Figure 7.8 To close the study, click on the red box in the right-hand corner (see the arrow).
154 Clinical Atlas of Polysomnography
Figure 7.9 This dialogue box will appear. Click on Yes and Stop Device.
Starting and Closing the Study 155
Figure 7.10 Handling Philips Alice 5 Software: Click on the G3 icon on desktop.
156 Clinical Atlas of Polysomnography
Figure 7.11 This box will appear. Enter your information. Click OK.
Starting and Closing the Study 157
Figure 7.12 This page will appear. Click on Start Acquisition in the drop-down menu.
158 Clinical Atlas of Polysomnography
Figure 7.19 Choose the montage that you wish to record in and click on Start.
Starting and Closing the Study 165
Figure 7.20 This recording page will appear. Start Calibration (Chapter 8).
166 Clinical Atlas of Polysomnography
Figure 7.21 Click on this arrow in top right-hand corner to stop the study.
Starting and Closing the Study 167
Figure 7.23 This box will appear. Let the file transfer be completed.
Starting and Closing the Study 169
Figure 7.24 Handling Cadwell Software: Click on Easy III Record Data.
170 Clinical Atlas of Polysomnography
Figure 7.29 This page will appear. Start Calibration (Chapter 8).
Starting and Closing the Study 175
Figure 7.30 To stop the study, click here. (see arrow in top right-hand corner).
176 Clinical Atlas of Polysomnography
Figure 7.32 This box will appear. Click the appropriate command.
178 Clinical Atlas of Polysomnography
A. Impedance
B. Lighting of room
C. Oxygen saturation
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Discuss the needs for biocalibration. Steps of Biocalbration .................................................................................. 179
2. Can recognize the waveforms that appear during biocalibration. Further Reading............................................................................................. 194
3. Can perform the biocalibration during a sleep study. Review Questions.......................................................................................... 194
C alibration is done to check that all the channels are getting adequate infor-
mation and are free from artifacts. This should be done before every study.
Figure 8.1 A Location of Calibration Command varies among manufacturers. Here, we show how to get Calibration Command in machines from three major
manufacturers. A: Calibration Command in Somnoscreen.
Calibration and Bio-Calibration 181
For electrical calibration, we usually pass a 3. Ask the patient to look up and down 3 measurement of blood pressure during the
current of around 50 μV in the EEG channels times and then right and left 3 times with- start of the recording (Figure 8.9).
and look for the waveform. All the channels must out moving head (Figure 8.4). 10. Ask the patient to clench his/her teeth for
have similar waveform during calibration. This 4. Ask the patient to close eyes for 10 seconds 5 seconds (Figure 8.10).
should be done for at least 10 seconds (Figure and look for change in EEG (appearance 11. Ask the patient to speak something and
8.2). For optimal quality signals, the impedance of Alpha rhythm in occipital leads) (Figure make sure that you can hear his/her voice
of the electrode should be below 5 Kohms. 8.5). through a speaker (Figure 8.11).
After calibration, it is time to check that 5. Ask the patient to open his/her eyes. 12. Body position signals are calibrated by
all channels are working properly, that is, bio- 6. Now ask the patient to stop breathing for asking the patient to turn left and then turn
calibration. This should be done by providing 10 seconds (Figure 8.6). right in bed. He/She should remain in each
the commands to the patient and checking that 7. Ask the patient to resume breathing and position for at least 5 seconds.
the respective channels are working properly. produce a snoring sound (Figure 8.7). Also, check that signals are good in ECG
To do this, please give the following commands 8. Ask the patient to move his/her feet up leads, oximeter, capnograph, and video. Once
and look for the changes in the display on the and down (Figure 8.8). you are satisfied, you may start the study.
1. Record with eyes open and eyes closed for in real-time. In those machines, blood
Figure 8.2 Electrical calibration: During this a fixed voltage current is passed from the device to all the channels. This ensures that all the channels are working
normally.
Calibration and Biocalibration 185
Figure 8.3 Calibration of blinking: Blinking appears as positive wave in frontal derivations as positively charged cornea moves towards frontal derivations due to bells-
eye phenomenon during blinking.
186 Clinical Atlas of Polysomnography
Figure 8.4 Calibration of eye movement: Eye movements appear as darting signals, which are out of phase, i.e., move away from each other. In this epoch signals from
left EOG are shorter in amplitude compared to signals from right EOG. This is because of higher impedance in left EOG. Also appreciate spillage of eye movement signals
in frontal derivations due to bells-eye phenomenon.
Calibration and Biocalibration 187
Figure 8.5 Calibration for Alpha: Alpha waves appear in the occipital derivations during quiet wakefulness. However, about 10% individuals are not alpha producers.
See the low voltage mixed frequency activity during open eyes. Rapid eye movements suggest that patient is scanning the environment. Alpha appears as soon as he is
asked to close his eyes.
188 Clinical Atlas of Polysomnography
Figure 8.6 Calibration of respiratory signals: Flattening of signals in the flow and respiratory effort sensors appear during wishful breath holding. Look after
“Hold Breath.”
Calibration and Biocalibration 189
Figure 8.7 Calibration for microphone: Snoring usually appear as crescendo-decrescendo signals in microphone channel. See signals just before “Snore” in Snoring
Channel. Wishful snoring sound also creates signals in Chin EMG Channel.
190 Clinical Atlas of Polysomnography
Figure 8.8 Calibration of leg EMG signals: Patient is asked to flex each of his feet up and down without moving thighs or legs. Signals appear in Leg channel.
Calibration and Biocalibration 191
Figure 8.9 Calibration of blood pressure: Some PSG machines provide real time BP based upon the surrogate signals. In those machines, BP calibration is done by
measuring the blood pressure at the start of study and entering the values in software. Software then calibrates the signals itself and shows blood pressure over the duration
of study.
192 Clinical Atlas of Polysomnography
Figure 8.10 Calibration of teeth clenching: Teeth clenching appear as muscle artifacts in EEG derivations and as sustained muscle contraction in chin EMG.
Calibration and Biocalibration 193
Figure 8.11 Calibration of voice signals in microphone: This is done by asking the patient to speak something. Check that you can hear his voice in your room. This
ensures that the sound system is working properly. Signals are also seen on the microphone lead.
194 Clinical Atlas of Polysomnography
working properly
properly
Calibration and Biocalibration 195
A. Delta A. EEG
B. Theta B. EMG
C. Beta C. EKG
D. Alpha D. EOG
muscles 1. B 2. A 3. C 4. D 5. C
B. Hypopnea
9
MINIMAL RECORDING PARAMETERS AND
EXTENDED MONTAGE
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Discuss the minimum recordable parameters during an attended sleep 9.1 Optional Parameters........................................................................... 214
study. 9.2 Extended Parameters for Special Circumstances......................... 219
2. Reason the importance for including these parameters. Further Reading............................................................................................. 219
3. Enumerate the optional parameters and their utility. Review Questions.......................................................................................... 219
4. Discuss the extended parameters in special situations. Answer Key..................................................................................................... 220
plan. It translates into symptom resolution, limited parameters, other sleep disorders may 1. Electroencephalogram (EEG): EEG
improvement in the quality of life, and increased be missed, culminating in a compromised treat- must be recorded using at least six chan-
productivity of the patient. ment planning. nels. Three of these channels are placed on
Sleep disorders rarely occur in isolation and To overcome it, the AASM has proposed right side of the head and the other three
many times co-morbid disorders influence the that a minimal number of parameters must be on the left side. These channels are placed
courses of a sleep disorder, or at times, two-sleep recorded. These recommendations were made at frontal, central and occipital areas on
disorders are seen together. As a case point, considering that: both sides and are referred to the opposite
certain medical disorders, for example, chronic 1. Main sleep disorder and co-morbid disorder mastoid. These places are important as
renal failure and Parkinson’s disease increase the can be picked after the scoring. they help in picking specific waveforms to
risk for obstructive sleep apnea as well as the rest- 2. Optimal technology is used to pick the sig- score a sleep stage. Alpha waves that are
less legs syndrome. Thus, a patient who has been nals related to a given parameter. seen during quiet wakefulness, are best seen
referred for OSA may have co-morbid periodic 3. Signals should help the scorer/clinician to in the occipital area, hence, this area was
limb movement during sleep. Similarly, periodic reach a conclusion. chosen (Figures 9.1 and 9.2). Central leads
limb movement during sleep as well as insomnia, 4. Prevention of data that may be lost due to show vertex waves that characterize Stage 1
are not uncommon with obstructive sleep apnea; issues arising during sleep study, for exam- sleep, sleep spindles that characterize stage
certain parasomnias, for example, night ter- ple, falling leads, malfunction of channels. 2 sleep, and sawtooth waves seen during
rors and sleep-walking are common in patients The AASM has proposed that during a REM sleep (Figures 9.3–9.5). Similarly,
with obstructive sleep apnea. In such cases, if sleep study, the following parameters must be K-complexes of stage 2 sleep and delta
patients are subjected to home sleep testing with recorded: waves that characterize stage 3 sleep (deep
Minimal Recording Parameters and Extended Montage 199
Figure 9.1 Determination of active wakefulness: Active wakefulness can be determined by EEG, EOG, and chin activity together. EEG shows mixed alpha and beta
activity blinking artifacts (in the ellipse), rapid eye movements (waveforms around stars) and relatively high chin tone.
200 Clinical Atlas of Polysomnography
Figure 9.2 Alpha waves during wakefulness: During quiet wakefulness, alpha waves appear in occipital derivations (in box). In addition, eye movements are slower and
chin tone reduces. Thus composite data from all three gives an idea regarding sleep-wake state.
Minimal Recording Parameters and Extended Montage 201
Figure 9.3 Vertex waves in central derivations: Vertex waves (circle) are best seen in central derivations during stage 1 sleep.
202 Clinical Atlas of Polysomnography
Figure 9.4 Spindle activity in central derivations: Spindle activity of stage 2 is best seen in central derivations (circle).
Minimal Recording Parameters and Extended Montage 203
Figure 9.5 Sawtooth waves in central derivations: Sawtooth waves of REM sleep are best seen in central derivations (box).
204 Clinical Atlas of Polysomnography
sleep) are best seen in frontal leads (Figures loss in case of fall-off of lead but also clearly asleep . REM sleep is characterized
9.6 and 9.7). Electrodes are placed on both delineates the eye-movement. For the by profound atonia, however, in
sides of the head, corresponding to both reasons discussed in Chapter 3 (section on patients with REM sleep behavior
hemispheres of the brain. During the study, EOG), true eye movement is always in the disorder, this atonia is not seen.
the patient may turn in the bed, resulting in opposite phase, that is, if one channel deflects Submentalis muscle has been cho-
fall of one or more leads, resulting in loss of towards the negative side, the other deflects sen because it is a skeletal muscle,
signals. If the electrodes are placed on both towards the positive side (Figure 9.8). Since lies just beneath the skin, thus,
sides, data from the other side can still be these channels are placed close to the frontal provides good signals, and normally
scored to reach a conclusion. area, sometimes, delta waves may be spilled remains inactive during sleep, in
Some evidence suggests that a single EEG in these channels, giving the impression of contrast to other skeletal muscles
channel, that is, placement of central elec- eye movement (Figure 9.9). Eye movements, that may get activated episodically
trodes helps in optimal scoring of sleep along with EEG, help in scoring wakefulness, during sleep. To prevent data loss,
stages, still the placement of three chan- quiet wakefulness, and REM sleep. signals are recorded from sub-men-
nels (along with three back-up channels) 3. Electromyogram (EMG): talis/mentalis muscles of both sides.
is considered gold standard. a. Muscle tone: An EMG is required Along with EEG, these signals help
2. Electrooculogram (EOG): An EOG that to score the sleep stage as well as the in recognizing REM sleep stage and
records the movement of the eyeball is also abnormal movements during sleep. REM sleep without atonia.
recorded from both eyes. Having the data During wakefulness, muscles have b. Limb movements: To record the
from both eyes not only prevents the data a basal tone that reduces as well fall periodic limb movement during sleep
Minimal Recording Parameters and Extended Montage 205
Figure 9.6 K complexes in frontal derivations: K-complexes of stage 2 are best seen in frontal derivations (box).
206 Clinical Atlas of Polysomnography
Figure 9.7 Delta waves in frontal derivations: Delta waves (in broken box) of stage 3 sleep are best seen in frontal derivations.
Minimal Recording Parameters and Extended Montage 207
Figure 9.8 True eye movement: True eye movements are in opposite phase (see arrows).
208 Clinical Atlas of Polysomnography
Figure 9.9 Delta waves may be mistaken for eye movements: Frontal delta activity or K complexes may appear in eye channels, but these deflections are in-phase,
as opposite to true eye movements. In this epoch some of them appear out of phase (arrows), however, their waveform is similar to right and left frontal derivations
respectively.
Minimal Recording Parameters and Extended Montage 209
(PLMS), signals are recorded from discussed in chapter 3, the thermistor is absent. Though it can be measured using
anterior tibialis muscles of both legs. important for the diagnosis of apnea while strain gauges, RIP belts are considered supe-
To minimize data loss, signals are a pressure transducer helps in recognizing rior and are recommended for the measure-
recorded from both legs separately hypopnea, Cheyne-Stokes breathing, and ment of respiratory efforts (Chapter 3). In
(Figure 9.10). In addition, signals periodic breathing. addition, sum of the chest is abdominal efforts
from both sides should not be com- However, during titration with PAP is calculated and depicted as a waveform. Dur-
bined as it may reduce the detectable machine, signals must be taken from the ing obstructive apnea and hypopnea, the chest
numbers of limb movements. These PAP device, as placing a cannula or thermis- and abdomen breath “out of phase” and thus,
signals, along with the EEG, help in tor below the mask may not provide good their sum shows a flat line (figure out of phase
scoring PLMS-associated arousals. signal due to a continuous flow of air and also movement during apnea and sum showing
In addition, these signals also help in increase the leakage from the mask owing to flattening). Thus, the waveform of the “sum”
scoring “alternate leg muscle activity” incomplete sealing. of efforts makes the scoring of respiratory
(ALMA), Hypnogogic foot tremors 5. Respiratory Effort: Analysis of respiratory events easier (Figure 9.12).
(HFT), and excessive fragmentary effort is important for differentiating between 6. Oxygen Saturation: Oxygen saturation is
myoclonus (EFM). obstructive and central respiratory events measured using a pulse oximeter that provides
4. Respiratory Flow: Respiratory flow is an (both apneas and hypopneas). In obstructive a value that is an average of 3 seconds values
important signal to score apnea and hypop- sleep apnea and hypopnea, the respiratory (Figure 9.13).
nea. It is measured using a thermistor and efforts are present in absence of respiratory 7. Electrocardiogram: Some patients may
a pressure transducer (Figure 9.11). As flow, while in central apnea, the effort is also have arrhythmia during sleep, especially
210 Clinical Atlas of Polysomnography
Figure 9.10 EMG signals from legs: Signals from both legs are recorded separately.
Minimal Recording Parameters and Extended Montage 211
Figure 9.11 Measurement of respiratory flow: Respiratory flow is recorded using a thermistor and a cannula (in box).
212 Clinical Atlas of Polysomnography
Figure 9.12 Measurement of respiratory efforts: Respiratory effort is recorded from thorax and abdomen using RIP belt. In addition a sum of them should be displayed.
During apnea, paradoxical movement is seen between thorax and abdomen and thus the RIP shows flattening (in box).
Minimal Recording Parameters and Extended Montage 213
Figure 9.13 Recording of oxygen saturation: Oxygen saturation is recorded as 3 seconds averaged value during the sleep study (in box). Also shown is body position.
214 Clinical Atlas of Polysomnography
during obstructive sleep apnea, or may have the parasomnia and seizure activity. A when supplemental oxygen is administered
sleep-related asystole that worsens the sleep laboratory may choose to have the provi- (Figure 9.15).
quality, or may develop ischemia during sion for synchronized video recording 3. Snoring: Although snoring can be
sleep due to hypoxemia. Hence, cardiac using an infrared imaging camera (that recorded through pressure transducer
electrical activity has to be recorded. It is captures images in the dark as well) and as mentioned in Chapter 3, it is recom-
recommended that it uses at least two leads, audio recording by placing a microphone mended that it is recorded using a snore
preferably limb lead I and II (Figure 9.14). near the patient’s head end. With the help microphone that is placed on the neck
8. Body Position: A number of patients have of a microphone, one can also discern the close to the larynx (Figure 9.16). This
sleep apnea that is specific to a body posi- verbal content spoken during the study. microphone also helps in detecting sleep
tion, for example, supine-dependent. In such 2. Capnography: This is important for the talking and bruxism.
cases, at least theoretically, positional therapy diagnosis of hypoventilation during sleep. 4. Espohageal Manometery: This measures
may help to ameliorate the symptoms. One may choose to use the transcutaneous the esophageal pressure that changes dur-
Hence, recording of body position is recom- sensor, however, the value in the trans- ing the respiration and is the most reliable
mended throughout the study (Figure 9.13). cutaneous sensor lags behind by approxi- method to differentiate obstructive events
mately two minutes to that of PaCO2 and it from central events. However, being an
cannula, however, it may provide false low 5. Pharyngeal pH: This is measured in cases
1. Synchronized Audio-Video Recording:
values in cases of nasal obstruction and of nocturnal gastro-esophageal reflux
This will help to differentiate between
Minimal Recording Parameters and Extended Montage 215
Figure 9.14 Recording of electrical activity of heart: Two channels of electrocardiogram are recorded during the sleep study (in box).
216 Clinical Atlas of Polysomnography
Figure 9.15 Recording of End tidal CO2: Capnography signals as recorded during the sleep study (in box).
Minimal Recording Parameters and Extended Montage 217
Figure 9.16 Snoring signals in microphone: Snoring usually appear as crescendo-decrescendo signals in microphone channel.
218 Clinical Atlas of Polysomnography
Figure 9.17 Extended montage for seizures: Extended Seizure montage includes all the EEG channels.
Minimal Recording Parameters and Extended Montage 219
disease and helps in differentiating sleep- and masseter muscles. To record their REVIEW QUESTIONS
related laryngospasm from chocking during activity, additional leads may be placed on
obstructive sleep apnea. However, its use is these muscles with the EMG derivation 1. Determination of sleep wake stage is depen-
also limited to research purpose only. setting. Similarly, in cases of REM sleep dent upon all of the following EXCEPT:
EXCEPT:
transducer
belts
C. Pulse oximeter
D. Acoustic sensor
A. RIP belts
B. Esophageal manometry
C. Piezoelectric belts
D. Thermistor
10
MONTAGES
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Discuss various montages used during polysomnography. Configuration of Various Montages ......................................................... 221
L
Answer Key..................................................................................................... 234
ead or electrode refers to a sensor that captures electrical signals. Deriva-
potential difference between two areas. On the other hand, montage refers to the
provide some montages, still you may design your own montage in the software,
10.2)
10.3)
3. Seizure/parasomnia montage
Figure 10.2 Montage for diagnostic study: This montage contains all the data for diagnostic study except video. Signals from Video may be added to this montage to
make it complete.
Montages 225
Figure 10.3 Montage for titration study: Please note that upper panel shows sleep-wake state related data hence, epoch duration is set to 30 sec, while respiratory
parameters are depicted in lower panel. Epoch duration setting for this panel is 120 seconds data for better recognition.
226 Clinical Atlas of Polysomnography
Figure 10.4A Referential montage for seizures. Referential montage where right sided electrodes are referred to left mastoid and vice versa.
Montages 227
Figure 10.4B Bipolar montage for seizures. This montage helps in localizing the focus of seizure activity. Bipolar montage where adjacent electrodes are referred to
each other.
228 Clinical Atlas of Polysomnography
Figure 10.4C Referential montage for parasomnia. Parasomnia montage should include other parameters (respiratory, cardiac, movement) also so as to differentiate
between seizure and parasomnia.
Montages 229
Figure 10.5 Bipolar montage for parasomnia where sleep related breathing disorders have been ruled out.
230 Clinical Atlas of Polysomnography
Figure 10.6 Montage for scoring of sleep stages: EEG, EOG and chin EMG are important for scoring of sleep stages. Leg EMG has been added to score Limb
Movement related arousals.
Montages 231
REVIEW QUESTIONS 3. Localization of seizure activity can be done B. Include leg EMG in sleep
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
U sually, we record the 6–8 hours sleep data during the diagnostic study.
However, we cannot analyze whole of the data just at one glance. There
are many reasons for that—first, as we have mentioned, sleep consists of different
stages that give discrete appearance on an EEG (see below); second, such a large
raw data cannot be concise to a single page; third, transition between wakefulness
236 Clinical Atlas of Polysomnography
and sleep and among different sleep stages is Table 11.1 Standard Duration of An Epoch
S. No. Parameter to be scored Duration of epoch
gradual. Hence, we divide the data into small
1 Sleep stage 30 sec
parts called epochs. 2. EEG for seizures 15 sec
3. Respiratory 2 min
Most of the polysomnography machines pro-
4. Cheyne-Stokes breathing 5 min
vide the independence to set the epoch duration 5. Leg movements 5 min
6. EKG 15 sec
varying from as short as 5 seconds to as long as
FURTHER READING
Figure 11.1 Sleep stage in 15 seconds. This epoch allows to identify each waveform separately and clearly.
238 Clinical Atlas of Polysomnography
Figure 11.2 Sleep stage in 30 seconds: In 30 seconds epoch, various waveforms appears condensed but recognizable. 30 sec epoch has been chosen as it depicts most
of waveforms important for sleep-wake stage scoring clearly (compare with 60 sec epoch) and at the same time, reduces time spent in scoring the data (compare 15 sec
epoch).
The Concept of Epochs 239
Figure 11.3 Sleep stage in 60 seconds: In 60 seconds epoch, waveforms are so condensed that they cant be recognized.
240 Clinical Atlas of Polysomnography
Figure 11.4B OSA in 30 seconds. Only a part of OSA can be seen in the epoch.
242 Clinical Atlas of Polysomnography
Figure 11.5 Respiration in 60 seconds: Normal respiration in 60 seconds. It provides a better view than 30 seconds epoch.
The Concept of Epochs 243
Figure 11.6B OSA in 120 seconds. Breathing disorders are easy to recognize in 120 seconds. In this epoch, rhythm and amplitude of the respiration can be
recognized easily.
The Concept of Epochs 245
Figure 11.8 CSB in 60 seconds: In 60 seconds, appearance is better, still CSB cannot be assessed.
The Concept of Epochs 247
Figure 11.9 CSB in 300 seconds: 300 seconds epoch shows that central apnea/ hypopnea is actually the parts of Cheyne-Stokes breathing. This should be
differentiated from respiratory pattern seen in OSA in 300 seconds epoch (Figure 11.12).
248 Clinical Atlas of Polysomnography
Figure 11.10 Leg movement in 30 seconds: 30 seconds epoch help to differentiate between independent leg movement and those associated with respiratory events. If
a movement starts within 1 seconds of respiratory event, it is not scored as movement.
The Concept of Epochs 249
Figure 11.11 Leg movement in 120 seconds: 120 seconds epoch makes it easier to see the periodic limb movements series.
250 Clinical Atlas of Polysomnography
Figure 11.12 Leg movement in 300 seconds: 300 seconds epoch makes PLM series prominent.
The Concept of Epochs 251
A. EKG
B. Leg movement
12
ARTIFACTS
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
ther physiological nor pathological but still appears in the recording because
setting, etc.
Signals for sleep staging are picked through electrodes placed on the scalp,
face, and sub-mentalis muscles. EEG signals originate in the brain (cortex and
254 Clinical Atlas of Polysomnography
thalamocortial circuit) and before being picked 3. EKG artifact (Figure 12.3); 60 Hz artifact secondary to increased imped-
up by the electrode, they have to travel through 4. Movement artifact (Figure 12.4); ance, a pop artifact due to poor contact of
the skull, scalp and other anatomical structures in 5. Artifact due to physiological activities of the lead with skin). In addition, physiological
the vicinity. These signals are electrical in nature. orofacial structures (Figure 12.5); activities that involve the whole body often
Because of these issues, these are liable to alter in 6. Electrical artifact (Figure 12.6); produce widespread artifacts, for example,
a variety of situations. Many times, a number of 7. Muscle artifact (Figure 12.7); ECG artifact, sweating artifact or movement
artifacts may appear in any of the PSG channels. 8. Cardioballistic artifact (Figure 12.8). artifact.
The artifact is defined as any abnormal activ- The scorer must be able to differentiate the It is of paramount importance to recognize
ity appearing in any diagnostic aid that is not artifact from the true signals so that a definitive these artifacts while recording the study and also
pathognomic of any disease but can be ascribed conclusion may be reached. while scoring the recorded data. If they are recog-
to the alteration in the signals because of unde- As we have discussed above, the source of nized during data acquisition, they can be fixed
sired input from other sources. the signal may be the patient, the electrodes, to obtain a good quality recording (as in Level I
Commonly following artifacts may appear in head-box, or the amplifier. Artifacts arising polysomnography). Similarly, a scorer has to be
the PSG channels: secondary to the head-box or amplifier prob- vigilant of the artifacts should they remain unat-
1. Electrode pop artifact: because of poor lems are widespread. Localized artifacts are tended (as in Level II study or level III study) to
contact between electrode and skin (Figure either attributed to a patient’s physiological prepare a good quality report.
12.1); activity spilling in the channel (e.g., pulse arti- In this chapter, we will discuss how to recog-
2. Respiration artifact also is known as sweat- fact, chewing artifact) or to a problem local- nize them and fix them during data acquisition
ing artifact (Figure 12.2); ized to one or few leads (sweating artifact or and during scoring of data (Table 12.1).
Artifacts 255
Figure 12.1 Electrode pop artifact: Electrode pop artifacts appear as sudden uprise of wave from the baseline (Channel C4). Electrode in question should be pasted
properly in this case.
256 Clinical Atlas of Polysomnography
Figure 12.2A Sweating artifacts or poor contact artifacts: Sweating artifacts appear due to poor contact between the skin and electrode owing to presence of sweat in
between. A: Note the undulating waves in F4 and O2 with respiration.
Artifacts 257
Figure 12.2B Sweating artifacts without respiratory waveform. In such cases, room should be cooled using an air conditioner.
258 Clinical Atlas of Polysomnography
Figure 12.2C If not fixed during recording of data, sweating artifacts can also be removed by increasing the LFF to 1 Hz from 0.3. However, it may compromise
appearance of slow waves in EEG.
Artifacts 259
Figure 12.3A EKG artifacts: EKG artifacts appear when an electrode is placed over a blood-vessel. Electrical activity from the heart is carried through blood-vessels.
They may be recognized by looking at the EEG and EEG simultaneously.
260 Clinical Atlas of Polysomnography
Figure 12.3B EKG artifacts: EKG artifacts appear when an electrode is placed over a blood-vessel. Electrical activity from the heart is carried through blood-vessels.
They may be recognized by looking at the EEG and EEG simultaneously.
Artifacts 261
Figure 12.3C EKG artifacts may be removed by changing the place of electrode or using the EKG filter in the software or referring the scalp electrodes to M1 and M2
simultaneously. This illustration shows that short-circuiting M1 and M2 to form an average reference has removed the EKG artifacts.
262 Clinical Atlas of Polysomnography
Figure 12.4 Movement artifacts: They appear as dangling EEG waves due to change in contact between electrodes and body.
Artifacts 263
Figure 12.5 Artifacts due to orofacial structures: Like any other organ, tongue is also a dipole and its movement inside the oral cavity changes the electrical potential
beneath some electrodes. In this epoch patient is talking during sleep (signals in microphone). Also shown that movement of tongue is showing deflections in EEG and
EOG derivations due to change in electrical potentials close to the electrodes.
264 Clinical Atlas of Polysomnography
Figure 12.6 Electrical artifacts: They appear due to poor grounding of the patient. In such cases, ground electrode should be removed, area should be cleaned again and
then electrode should be placed.
Artifacts 265
Figure 12.7 Muscle artifacts: In this epoch you can see muscle artifacts due to grinding of the teeth. Noise produced during teeth-grinding can be seen in the
microphone channel as well. This is rhythmic activity is and is known as Rhythmic Masticatory Movement Activity (RMMA).
266 Clinical Atlas of Polysomnography
Figure 12.8 Cardioballistic artifacts: They may create problem in scoring central sleep apnea. Due to heart beat, chest belt records some movements in this epoch
cardioballistic artifacts may be seen in THO channel..
Artifacts 267
FURTHER READING D. Replacing the electrode after cleaning C. Central Sleep Apnea
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Recognize and score sleep-wake stages in the recording of an adult 13.1 Scoring of Sleep Stage...................................................................... 270
patient. 13.2 Scoring of Respiratory Data............................................................ 340
2. Recognize and score respiratory events in the recording of an adult 13.3 Leg Movements................................................................................. 350
patient. 13.4 Bruxism............................................................................................... 363
3. Recognize and score leg movements in the recording of an adult 13.5 REM Sleep Behavior Disorder....................................................... 363
patient. 13.6 Rhythmic Movement Disorder...................................................... 363
4. Recognize and score cardiac rhythms. 13.7 Scoring of EKG Data........................................................................ 382
5. Recognize and score REM sleep behavior disorder, sleep-related brux- Further Reading............................................................................................. 382
ism and rhythmic movement disorder. Review Questions.......................................................................................... 382
Figure 13.1 Active wakefulness is characterized by electrical activity in EEG channels that is low voltage, mixed frequency (Gamma-beta-theta), Reading eye
movements (See Star) in opposite phase having initial slow phase followed by a rapid phase (LEOG and ROCA2) associated with eye blinks having frequency of 0.5–2
Hz (Frontal derivations) (see inside circle), and rapid eye movements, where initial deflection is less than 0.5 seconds (see Box) (30 seconds epoch).
272 Clinical Atlas of Polysomnography
Figure 13.2 Quiet wakefulness is characterized by alpha rhythm in occipital derivations for more than 50% of epoch, slow eye movements (Star) (30 seconds epoch).
Scoring of Data in Adults 273
Figure 13.3 Microsleep: Please note that transition from wakefulness is gradual. Before a scorable N1 epoch, few epochs of microsleep are seen. In these epochs, EEG
shows islands of theta rhythm (in the box) in between alpha. However, this epoch will be scored as Wake as alpha occupies more than 50% of epoch.
274 Clinical Atlas of Polysomnography
Figure 13.4 A Microsleep: Slow eye movements (star) are sinusoidal and duration of initial deflection is more than 0.5 seconds. They may persist during quiet
wakefulness as well as during N1. This epoch shows SEMs while a person is drifting into sleep. Shall be scored as Wake as alpha occupies more than 15 seconds of epoch.
Scoring of Data in Adults 275
Figure 13.4B N1 is scored when alpha activity in EEG is replaced by low voltage mixed frequency activity in theta range in more than half of the epoch (> 15 seconds
in an epoch of 30 seconds) and slow eye movements (satr). Chin tone goes down with N1. Vertex sharp waves (duration < 0.5 seconds and in circle) appear maximally in
central derivations. First scorable N1 epoch also marks the sleep onset (30 seconds epoch)
276 Clinical Atlas of Polysomnography
Earlier rules (R and K rules) proposed four are seen but also the scoring of the subsequent Wakefulness is scored when the epoch shows
different stages of normal NREM sleep – S1,S2, epoch, as we shall see. As we have already dis- blinking; rapid eye movements with high tone in
S3 and S4. In new rules, S1 has been replaced by cussed, sleep stages are scored in an epoch of chin EMG or saccadic eye movements are seen
N1, S2 by N2 while S3 and S4 together formed 30 seconds. Remember, if waveforms for two (Figure 13.1). Alpha activity (8–13 Hz) is seen
stage N3.. This change was brought as scientific different stages are seen in an epoch, the epoch during wakefulness if the subjects close their eyes
literature failed to show any advantage of divid- is assigned the stage whose waveforms occupy in the occipital leads, also known as posterior dom-
ing deep sleep (N3) into two stages (S3 and S4). more than 50% of the epoch. At times, waveforms inant rhythm (Figures 13.2 and 13.3). However,
With this information in the background, suggesting three or more stages may be seen in nearly 10% of individuals are not alpha producers
we can now proceed with the scoring of sleep an epoch. In such case, first, decide whether it and their EEG activity remains same during eyes
stages. represents “wake” or “sleep” depending upon open and eyes closed. Rules for scoring of N1 are
For the scoring of sleep staging, we depend the relative amount of respective waveforms in different between alpha producers and alpha-non-
upon the EEG, EOG, and chin EMG informa- the epoch. Once it is decided that it should be producers (Figures 13.4 A,B and 13.5 C-G).
tion. When we are scoring the sleep stage, we scored as “sleep,” assign the sleep stage (N1, N2, It must be remembered that in alpha produc-
need to determine arousals also (see section on N3 or REM) whose waveforms represent most of ers, vertex waves and slow eye movements, though
the scoring of arousals). These arousals can be the part of the epoch. During the study, patients generally seen during N1, are not required for
physiological, viz., at the transition of sleep stages, may be disconnected from the PSG as they may scoring of N1. In alpha producers, the only atten-
or pathological, for example, associated with the need to go to the washroom. However, recording uation of alpha to low-voltage, mixed-frequency
respiratory event or leg movement. These arous- continues during this period and this should be activity is sufficient for scoring of N1 (Figures
als determine not only the epoch in which they scored as awake. 13.5A and 13.8B). In alpha non-producers, N1 is
Scoring of Data in Adults 277
Figure 13.5 A Vertex waves in N1: Vertex waves are sharp waves that appear distinct to the background EEG in central derivations (Circle) and have duration less
than half a second. Slow eye movements are also seen (star) and background EEG activity is low voltage mixed frequency in theta range during whole of epoch. So this is
scored as N1.
278 Clinical Atlas of Polysomnography
Figure 13.5 B N1: Vertex waves are sharp waves that appear distinct to the background EEG in central derivations (Ellipse) and have duration less than half a second.
Background EEG activity is low voltage mixed frequency in theta range for more than 15 seconds. Though alpha is seen in the last part of epoch; but it occupies less than
50% of epoch, hence this epoch will be scored as N1.
Scoring of Data in Adults 279
Figure 13.5C–G Scoring of N1 in subjects that do not produce alpha as posterior dominant rhythm: This epoch shows low voltage mixed frequency activity with high
chin tone and slow eye movements. This is quiet wakefulness.
280 Clinical Atlas of Polysomnography
Figure 13.5D This epoch shows low voltage mixed frequency activity with high chin tone and slow eye movement. Last part of epoch shows eye blink artifacts,
movement artifacts and further increase in chin tone. EEG activity is just like previous epoch. This will be scored as wake.
Scoring of Data in Adults 281
Figure 13.5E This epoch does not show any change in EEG, however, eye movements are lesser pronounced. This will also be scored as wake.
282 Clinical Atlas of Polysomnography
Figure 13.5F This epoch shows slowing of background EEG activity compared to previous epoch with lowering of chin tone and reduction of eye movement. This
should be scored as N1.
Scoring of Data in Adults 283
scored when the EEG activity shows theta waves is seen during the first half of the present epoch Continue to score epoch with low volt-
(4–7.99 Hz) with slowing of background EEG or second half of the previous epoch, the pres- age mixed frequency activity as N2, till any
activity by 1 Hz or greater than the awake EEG ent epoch should be scored as N2. other sleep stage appears, even in absence of
activity, or vertex sharp waves appear, or slow A sleep spindle is a train of high frequency K-complexes and sleep spindles (Figure 13.12).
eye movements appear. Any one of these three (11–16 Hz) waveform having a duration of at Although eye movements are absent during N2,
features is sufficient to score N1 in alpha-non- least 0.5 seconds with maximum amplitude in sometimes they may be seen during N2 (Figure
producers (Figure 13.5 C-G). central derivations (Figure 13.8A and 13.8B). 13.13). A microarousal during N2 is shown in
The patient may have arousals during any K complexes are large waves that appear dis- Figure 13.14A. Majority of this epoch shows
stage of sleep. An arousal in NREM sleep is scored tinct from the background activity with initial waveforms suggesting N2, hence it will be scored
when the EEG activity abruptly shifts for at least negative followed by positive deflection having the as N2. End scoring N2, if an epoch of K-arousal
3 seconds to alpha or it becomes higher than the duration of at least 0.5 seconds and seen with maxi- in the first half appears (Figure 13.11) or an
earlier frequency. However, this must be differ- mum amplitude in frontal leads (Figure 13.9). An epoch of wakefulness appears (Figure 13.14 B),
entiated from sleep spindles as they may be pro- epoch having either sleep spindle or K complex in or an epoch of major body movement (Figures
longed. At least 10 seconds of stable sleep must be first half is scored as N2. If an epoch shows these 13.16; 13.17 A,B,C and 13.18 A, B) followed by
present before arousal (Figures 13.5B and 13.6). waveforms in second half, then subsequent epoch an epoch with slow eye movement appears (Fig-
If the arousal lasts more than 50% of the epoch, should be scored as N2, unless it confirms wave- ure 13.18 A, B) or N2 converts to N3 (Figure
that epoch is scored as wake (Figure 13.7). forms depicting any other sleep-wake stage (Fig- 13.19) or REM (Figure 13.20A).
Stage 2 (N2) sleep is characterized by ure 13.10). Any K complex associated with arousal Stage 3 (N3) sleep is scored when slow-wave
K-complexes and sleep spindles. If any of them is not considered as K complex (Figure 13.11). activity, defined as waveforms having frequency
Scoring of Data in Adults 285
Figure 13.6 Arousal in N1: An arousal in N1 is scored if the EEG activity shifts to alpha in the occipital and central derivations. To be scored as an arousal, the activity
must last at least 3 seconds but not more than 15 seconds. If it is more than half the epoch, score the epoch as wake. At least 10 seconds of uninterrupted sleep must be
present before an arousal.
286 Clinical Atlas of Polysomnography
Figure 13.7 N1 to wakefulness: If the arousal lasts more than 15 seconds in an epoch, score it as wake (60 seconds epoch) Subsequent epoch must be scored based
upon the waveforms present in epoch, as discussed in Figures 13.4 and 13.10.
Scoring of Data in Adults 287
Figure 13.8 A Distribution of Sleep spindles in EEG derivations: Sleep spindles (in box) are distinct waves of 11–16 Hz frequency that are seen most prominently in
central derivations, having duration of at least 0.5 seconds and are easily distinguishable from the background. In this epoch (30 seconds) they appear in first half, hence
this will be scored as N2.
288 Clinical Atlas of Polysomnography
Figure 13.8 B Sleep spindles in N2: Sleep spindles (in box) are distinct waves of 11–16 Hz frequency that are seen most prominently in central derivations, having
duration of at least 0.5 seconds and are easily distinguishable from the background. In this epoch (30 seconds) they appear in first half, hence this will be scored as N2.
Scoring of Data in Adults 289
Figure 13.9 K Complexes in N2: K complex are prominently seen in frontal derivations and sometimes in EOG as well due to their proximity to frontal area (Box).
Having a duration of more than half a second, they have initial negative deflection, followed by a positive deflection and the coming to baseline. They are quiet distinct
from the background.
290 Clinical Atlas of Polysomnography
Figure 13.10A Initiation of N2: If an epoch shows either of the two-sleep spindles or K-complex in the first half, that epoch should be scored as N2. If it is seen in later
half, score sleep stage in present epoch as that of previous epoch or whichever waveform dominates the present epoch. Here K complexes are seen in first half, no arousal
is seen, hence tis will be scored as N2.
Scoring of Data in Adults 291
Figure 13.10B Figure shows low voltage mixed frequency activity, however, K complex is seen only in second half, hence this will be scored as epoch previous to this,
i.e., N1. Epoch subsequent to this will be scored as N2, unless it is interrupted by arousal or shows waveforms confirming any other stage.
292 Clinical Atlas of Polysomnography
Figure 13.11 K arousal in first half of N2: If an arousal starts within 1 seconds of termination of K complex, it is not considered as K complex. Here K-arousal is
apparent in first half of epoch, and sleep spindle or K complex are not seen before or after K-arousal, hence it should be scored as N1. Change the scoring of subsequent
epochs to N2 according to Figure 13.10 A, B.
Scoring of Data in Adults 293
Figure 13.12 N2 scoring without spindle of K complex: Once started, scoring of N2 should be continued if low voltage mixed frequency activity is seen in EEG even in
absence of K complex or sleep spindles. However, the previous epochs must have been scored as N2 and did not have intervening arousals.
294 Clinical Atlas of Polysomnography
Figure 13.13 SEM during N2: Although eye movements are absent during N2, in some cases, slow eye movements may be seen during N2.
Scoring of Data in Adults 295
Figure 13.14 A Arousal in N2: An arousal in N2 is scored if the EEG activity shows an abrupt change to the higher frequencies- alpha, lasting for 3–15 seconds. If it
occupies more than half of the epoch, score as wake. If less, score as N2. See that theta activity appears after alpha at the end of epoch, following epoch shall be scored as
N1 anc continue to score N1 till an epoch with sleep spindle or K complex appears as mentioned in Figure 13.10.
296 Clinical Atlas of Polysomnography
Figure 13.14 B Change of N2-wakefulness: Since the alpha is seen for more than 50% of the epoch, this epoch will be scored as wake.
Scoring of Data in Adults 297
Figure 13.15 A–C Arousal in the later half of N2: A: This epoch shows arousal in second half. However, after arousal, waveforms suggestive of N1 are seen in last part.
Since largest part of the epoch is covered by waveforms suggestive of N2, this will be scored as N2.
298 Clinical Atlas of Polysomnography
Figure 13.15 B This epoch does not show K complexes or spindles, hence will be scored as N1.
Scoring of Data in Adults 299
Figure 13.15C This epoch shows K complex in the first half, hence, it will be scored as N2.
300 Clinical Atlas of Polysomnography
Figure 13.16 Body movement during N2: In this epoch body movement is followed by alpha but low voltage mixed frequency activity is present in most of the epoch,
and preceding epoch was N2, hence this will be scored as N2.
Scoring of Data in Adults 301
Figure 13.17 A–C Major body movement during N2: If a major body movement (defined as obscuring EEG beyond recognition in more than 50% epoch as in 13.17
B2) follows an epoch of undisputed N2 epoch (13.17 B1) and also follows an epoch of undisputed N2 (13.17 B3), epoch of movement will be scored as N2.
302 Clinical Atlas of Polysomnography
Figure 13.17 B Major body movement during N2: If a major body movement (defined as obscuring EEG beyond recognition in more than 50% epoch as in 13.17 B)
follows an epoch of undisputed N2 epoch (13.17 A) and also follows an epoch of undisputed N2 (13.17 C), epoch of movement will be scored as N2.
Scoring of Data in Adults 303
Figure 13.17 C Major body movement during N2: If a major body movement (defined as obscuring EEG beyond recognition in more than 50% epoch as in 13.17 B2)
follows an epoch of undisputed N2 epoch (13.17 B1) and also follows an epoch of undisputed N2 (13.17 B3), epoch of movement will be scored as N2.
304 Clinical Atlas of Polysomnography
Figure 13.18A–B Slow eye movement in N2 epoch following a major body movement: A: N2 epoch shows a major body movement in second half that continues in
first half of B.
Scoring of Data in Adults 305
Figure 13.18B After the major body movement, slow eye movements are seen (starred). A will be scored as N2 while B will be scored as N1.
306 Clinical Atlas of Polysomnography
Figure 13.19 Shifting from N2 to N3: N2 sleep may shift to N3. If the epoch has delta waves less than 6 seconds, continue with N2. If the epoch has delta waves for at
least 6 seconds, change the scoring to N3. In this epoch delta activity is seen in more than 20% (6 seconds) of epoch, hence, this will be scored as N3.
Scoring of Data in Adults 307
Figure 13.20 A Shift from N2 to REM: If the epoch has waveforms characterizing REM for more than 15 seconds, score as REM, otherwise continue scoring N2 In this
epoch see the rapid eye movements and sawtooth waves hence this will be scored as REM. Previous epoch was N2.
308 Clinical Atlas of Polysomnography
Figure 13.20 B1–B4 Shift from N2 to REM: Sometimes EEG makes it difficult to differentiate between N2 and REM. In such cases, scoring depends upon chin tone.
Start scoring REM if an epoch shows lowering of chin tone for more than 15 seconds, does not have K complex or spindle and subsequent epochs can be scored as REM.
In this series of epochs also appreciate that all the features of REM (Figure 13.24) do not appear simultaneously. In this series, EEG and EOG changes appeared first and
chin tone lowered much later. Since B4 has all the criteria for REM, this will be scored as REM and previous epochs will be scored as N2.
Scoring of Data in Adults 309
Figure 13.20 B4 Shift from N2 to REM. B4 has all the criteria for REM. This will be scored as REM, and previous epochs will be scored as N2.
312 Clinical Atlas of Polysomnography
Figure 13.20 C Shift from N2 to REM: Even if the chin tone drops in N2, continue scoring N2 till the last epoch where spindle is seen. Subsequent epoch may be
scored as REM, if it has all the characteristics of REM. In this epoch though chin tone is low and rapid eye movement is seen in second half, still this will be scores as N2 as
spindles are seen all over the epoch.
Scoring of Data in Adults 313
Figure 13.21A Appearance of N3: Score N3, if an epoch has slow wave for at least 6 seconds. Slow wave activity is best seen in frontal derivations, having a peak-to-
peak amplitude of 75 µV and frequency of 0.5–2 Hz. These are also known as delta waves. Unlike N2, for scoring of N3, it is immaterial whether delta waves are present in
first half or the second half of the epoch (sensitivity 12.5 µV/mm).
314 Clinical Atlas of Polysomnography
Figure 13.21B Sleep spindles in N3: Sleep spindles may persist along with delta waves. In this case, epoch should be scored as N3 (sensitivity 12.5 µV/mm).
Scoring of Data in Adults 315
of 0.5–2 Hz and peak-to-peak amplitude of at (Figure 13.31), or N2 (Figure 13.32) or N3. If REM epoch in the first half of the epoch, it
least 75 μV, is seen in frontal regions and occu- there is a major body movement during REM should be scored as N2.
pies at least 20% of the epoch (Figure 13.21). scoring of epoch, having major body movement 3. An epoch with K-complex or sleep spindles,
Scoring of REM sleep is based upon three and its subsequent epoch depends upon various meeting other criteria for REM and having
characteristics—low chin tone (lower than any characteristics (Figures 13.33 and 13.34). rapid eye movements should be scored as
other stage of sleep), low-voltage, mixed-fre- The transition from N2 to REM is especially REM even in presence of spindles/K com-
quency activity, and rapid eye movements (Fig- important and epochs between definite N2 plexes (Figure 13.20C)
ure 13.24). Sawtooth waves often accompany and definite REM may present some difficulty. Major body movements are defined as epochs
rapid eye movements and are best seen in cen- These epochs may be scored using the follow- where body movement and muscle arti-
tral derivations as serrated, triangular waves in ing rules: facts make the EEG incomprehensible to the
the frequency of 2–6 Hz (Figure 13.25). REM is 1. Between these epochs, an epoch that shows extent that staging cannot be done. If such an
also characterized by transient muscle activity, a drop of muscle tone to the level of REM in epoch shows alpha waves even for less than
usually seen in lower limbs, having a duration the first half, but in absence of sleep spindles 50% epoch, it should be scored as Wake. This
of less than 250 msec, and superimposed upon and K-complex, should be scored as REM. epoch should also be scored as Wake if the
lower muscle tone (Figure 13.26). Continue to Scoring of REM may continue till the previous or subsequent epoch can be scored
score REM, even in absence of rapid eye move- epochs showing definite REM. as Wake. In absence of these two features, it
ments (Figure 13.27 A,B). Stop scoring REM, 2. However, if an epoch shows K-complex or should be scored as the sleep stage of the fol-
if an epoch of wakefulness appears (Figure spindles in absence of rapid eye movements, lowing epoch.
13.34), or epoch shows characteristics of N1 but with low chin tone similar to definite
316 Clinical Atlas of Polysomnography
Figure 13.22 K complex as delta: When K complexes have characteristics of delta waves and are present in more than 20% epoch, epoch should be scored as N3.
Scoring of Data in Adults 317
Figure 13.23A–B N3 to REM transition: A: This epoch shows N3 in most of the part, hence it will be scored as N3.
318 Clinical Atlas of Polysomnography
Figure 13.23B This epoch has all characteristics of REM, hence, it will be scored as REM.
Scoring of Data in Adults 319
Figure 13.24 REM sleep: Score as REM if the epoch shows all three features of REM-low voltage mixed frequency activity, low chin tone and rapid eye movements
(usually lasting less than half a second) for at least 15 seconds.
320 Clinical Atlas of Polysomnography
Figure 13.25 Sawtooth waves in REM: Sawtooth waves characterize REM. They are triangular waves with sharp top and appears serrated. They have frequency of 2–6
Hz and maximum amplitude is seen in central derivations. They are usually associated with rapid eye movements.
Scoring of Data in Adults 321
Figure 13.26 Transient muscle activity in REM: REM is characterized by transient muscle activity, which is less than 0.25 seconds in duration along with low EMG
tone. This may be seen in any of the derivations (limb, chin, EOG, EEG) depending upon which muscle is involved. In this epoch transient activity is seen in Leg 1.
322 Clinical Atlas of Polysomnography
Figure 13.27 A-B Scoring REM: A: Once a epoch of REM is found, subsequent epochs should be scored as REM, even in absence of rapid eye movements unless
interrupted by any other sleep stage. However, the epochs must have EEG and EMG characteristic of REM as described in Figure 13.24.
Scoring of Data in Adults 323
Figure 13.27 B In between epochs of REM, epochs of N2 may appear. If an epoch has spindle of K complex even if preceding and following epochs can be scored as
undisputed REM, score as N2 if sleep spindles or K complex is seen, score as N2. In this epoch spindle is seen in first as well as second half.
324 Clinical Atlas of Polysomnography
Figure 13.28 Chin tone transiently increasing in REM: If chin tone increases during REM epoch change of scoring depends upon the duration of high tone. If it is less
than half the epoch continues scoring REM, however, if it is seen in more than half the epoch, change the score to N1, if other characteristics of N1 are seen or to wake
if all characteristics of wakefulness are seen. In this epoch, chin tone increased for more than a second, but lowers down, and is followed by slow eye movements; hence
subsequent epoch will be scored as N1. However, in this epoch, REM characteristics are present in more than 50% of epoch, hence, it will be scored as REM.
Scoring of Data in Adults 325
Figure 13.29A-F Arousal in REM: Arousal in REM is scored if the EEG changes suggest arousal (Figure 13.14) along with increased chin tone for at least for 1 seconds.
Change to W if EEG and Chin EMG suggestive of arousal persist for more than half the epoch. A: Epoch showing REM.
326 Clinical Atlas of Polysomnography
Figure 13.29B Scored as N1 SEM are seen and tone is increased for most of the epoch.
Scoring of Data in Adults 327
Figure 13.29C Following epoch will be scored as N1 as chin tone is still high.
328 Clinical Atlas of Polysomnography
Figure 13.29E This epoch will be scored as wake as chin tone is high in more than 50% epoch and alpha waves also appeared.
330 Clinical Atlas of Polysomnography
Figure 13.29F Though alpha is seen during REM, but chin tone does not increase and hence, arousal will not be scored.
Scoring of Data in Adults 331
Figure 13.30A-B Arousal in REM: If following arousal, chin tone again goes low and slow eye movement are not seen, continue to score REM A: Lowering of chin tone
after arousal and SEM not seen hence scored as REM.
332 Clinical Atlas of Polysomnography
Figure 13.30B This epoch show lowered tone in absence of SEM hence scored REM.
Scoring of Data in Adults 333
Figure 13.31A-B REM to N1: If an arousal during REM is followed by slow eye movements, score the epoch with SEM as N1. A: Arousal in later part of epoch.
334 Clinical Atlas of Polysomnography
Figure 13.31B Slow eye movements in the initial parts of the epoch. Continue to score N1 till another sleep stage (N2 or REM) appears.
Scoring of Data in Adults 335
Figure 13.32 REM to N2: Change scoring from REM to N2, if K complex or sleep spindle is seen in the first half of the epoch. If it is seen in the latter half of the REM
epoch, score present epoch as REM and subsequent epoch as N2 even in presence of low chin tone.
336 Clinical Atlas of Polysomnography
Figure 13.33 Movement during REM: If a major body movement makes the EEG and RMG findings indiscernible in an epoch, but previous and subsequent epochs
are REM, score present epoch as REM. This epoch shows a minor movement and REM occupies more than 50% of epoch, hence scored as REM.
Scoring of Data in Adults 337
Figure 13.34 Major movement during REM: If an epoch of major body movement during REM is followed by slow eye movements in an epoch, both epochs (with
movement and SEM) should be scored as N1.
338 Clinical Atlas of Polysomnography
Figure 13.35 N1 to REM: If an epoch following N1, shows characteristics of REM, score as REM.
Scoring of Data in Adults 339
Figure 13.36 Alpha during REM: Alpha may also be seen during REM, however, alpha during REM is usually 1–2 Hz slower than waking alpha.
340 Clinical Atlas of Polysomnography
13.2 SCORING OF best assessed using esophageal manometry, it is If there is a malfunction of cannula signals,
RESPIRATORY DATA not routinely used due to the invasive nature of this information may be obtained from alternate
the sensor. Hence, thoracoabdominal RIP belts signals, that is, RIP belts from thorax and abdo-
Respiratory data is gathered to look for abnor- are used to measure the respiratory efforts. men, RIP sum or RIP flow to score hypopnea
malities of breathing during sleep. These include Hypopnea is defined as at least 30% reduction (Figure 13.38C).
sleep apnea—obstructive, mixed, and central or in the amplitude of pressure transducer (cannula) Apnea is diagnosed when the thermal sensor
hypopnea. In addition, central apnea and central lasting for at least 10 seconds and desaturation of signals drop by at least 90% of the baseline value for
hypopneas may be associated with Cheyne-Stokes 3% or 4% from the baseline, depending on the def- at least 10 seconds (Figures 13.39–13.41). Note
breathing (CSB), which needs to be assessed. In inition of desaturation (Figure 13.38A). Duration that hypoxemia, though usually accompany apnea,
addition, periodic respiration and sleep-related of event is measured from the lowest point preced- they are not required to score an apnea. If there is
hypoventilation need to be assessed. Snoring is an ing the breath, this clearly reduces in amplitude to a malfunction of cannula signals, this information
important parameter associated with obstructive the first breath having a baseline amplitude. may be obtained from alternate signals, that is, RIP
sleep apnea and data must provide this information. If the hypopnea is associated with snoring, flat- belts from thorax and abdomen, RIP sum or RIP
As we have already discussed, thermistors or tening of inspiratory signal, and paradoxical move- flow to score hypopnea (Figure 13.38C).
thermocouples are used to score apnea and nasal ment in the chest and abdominal belts (resulting Depending upon the respiratory effort, apnea
cannula for the hypopnea along with oxygen satu- in a reduction of signal amplitude in effort sum), it is divided into obstructive, mixed and central
ration. Figure 13.37A depicts normal respiration is termed as obstructive hypopnea (Figure 13.38 apnea (Figures 13.41–13.43). During obstructive
during sleep and Figure 13.37B shows benign B). However, any hypopnea without these charac- apnea, respiratory flow ceases while effort contin-
snoring. Though the respiratory effort can be teristics is termed as central hypopnea. ues. Central apnea is characterized by cessation of
Scoring of Data in Adults 341
Figure 13.37A Normal Respiration during sleep: 2 min epoch showing normal respiration. See that flow in the thermistor and cannula is regular, rhythmic, and has
equal amplitude across the epoch. Chest and abdomen RIP belts show in phase movement and effort sum (RIP-Sum) does not show any change in amplitude. Oxygen
saturation is maintained throughout the epoch and microphone does not show any signal.
342 Clinical Atlas of Polysomnography
Figure 13.37B Snoring without sleep related breathing events: Tracing showing snoring (microphone channel) without the hypopnea or apnea.
Scoring of Data in Adults 343
Figure 13.38A Hypopnea is characterized by at least 30% reduction in the amplitude of nasal airflow (pressure transducer) with retained signals in thermistor and
regular breathing effort (chest and abdominal belts) and desaturation in oximetery channel (3% or 4% depending upon the criteria followed). Duration must be at least 10
seconds (Blue lines). In this epoch regular snoring is also visible.
344 Clinical Atlas of Polysomnography
Figure 13.38B Hypopnea is characterized by at least 30% reduction in the amplitude of nasal airflow (pressure transducer) with retained signals in thermistor and
regular breathing effort (chest and abdominal belts) and desaturation in oximetery channel (3% or 4% depending upon the criteria followed). Duration must be at least
10 seconds (horizontal blue arrows). In this epoch regular snoring is also visible. Also see in-phase breathing (red arrows)) during normal breathing and paradoxical
breathing (blue vertical arrows) and reduction in effort-sum (box).
Scoring of Data in Adults 345
Figure 13.38C Hypopnea and apnea during pressure transducer malfunction: In case of malfunction of pressure transducer, hypopnea and may be diagnosed using
signals from RIP belts. During Hypopnea sum of Chest and abdominal belts show paradoxical movement followed by desaturation with reduction in effort-sum signals,
whereas in apnea, signals from thermistor as well as effort-sum are flat.
346 Clinical Atlas of Polysomnography
Figure 13.39 Obstructive sleep apnea: If a part of hypopnea meets criteria for apnea (Figure 13.39: Red arrows), score the event as apnea. Note that in the latter part
thermistor signals showing flattening, hence this will be scored as apnea.
Scoring of Data in Adults 347
Figure 13.40 Obstructive sleep apnea: If a part of hypopnea meets criteria for apnea (Figure 13.39: Red arrows), score the event as apnea. Note that in the latter part of
thermistor signals showing flattening, hence this will be scored as apnea.
348 Clinical Atlas of Polysomnography
Figure 13.41 Obstructive sleep apnea: Obstructive apnea is characterized by absence of signals (for at least 10 seconds) in thermistor and pressure transducer. There is
usually reduction of signals in RIP belts and effort-sum followed by hyperpnoea (belts) and subsequent desaturation. However, desaturation is not necessary to diagnose
OSA. In this epoch you can appreciate paradoxical breathing (movement of chest and abdomen in opposite phase) during apnea.
Scoring of Data in Adults 349
Figure 13.42 Central sleep apnea is diagnosed with absence of flow and effort signals for at least 10 seconds. In this epoch central sleep apnea can be seen (Green Box).
350 Clinical Atlas of Polysomnography
respiratory flow as well as respiratory efforts, and Sleep-related hypoventilation is scored when 13.3 LEG MOVEMENTS
mixed apnea (Figure 13.43) is scored when the there is at least 10 mmHg increase in PaCO2
initial portion of an event shows morphology of during sleep (compared to wake supine value) Leg movement is defined as an increment of at least
central apnea and the latter part that of obstructive to at least 50 mmHg for 10 or more minutes or 8 μV in leg EMG signals from the resting signals for
apnea. During titration study, apnea and hypop- PaCO2 increases to 55 mmHg or more for at the duration of 0.5 to 10 seconds. The point where
nea are scored using signals from the PAP sensor. least ten minutes during sleep. During a diag- the voltage increases at least 8 μV is considered as
Respiratory effort related arousal (RERA) is nostic study, arterial PCO2 or transcutaneous the starting point of the leg movement and termi-
diagnosed when a progressively increased breath- PCO2 or end-tidal CO2 (EtCO2) may be used nates where this EMG remains increases by at least
ing effort is noticed for 10 or more seconds and for this purpose, however, end tidal CO2 value 2 μV for at least half a second (Figure 13.46).
culminates in an arousal but does not meet the cri- is not reliable during PAP titration because of For scoring periodic limb movement series
teria for hypopnea or apnea (Figure 13.44 A–E). dilution from the external air that is delivered (PLMS), at least four consecutive movements are
Cheyne-Stokes breathing is scored when 3 through PAP. However, transcutaneous CO2 or required separated by at least 5 seconds (consider-
or more central sleep apnea or hypopneas are EtCO2 does not represent arterial CO2. Trans- ing the time of onset) and maximally by 90 seconds
separated by crescendo-decrescendo breath- cutaneous CO2 values usually lag behind arterial (considering the time of onset). However, move-
ing and the cycle length is at least 40 seconds. values by at least 2 min and have to be routinely ment in different legs separated by less than 5 sec-
In such cases, central AHI should be at least 5 calibrated with PaCO2. Similarly, nasal secre- onds (considering the time of onset) is considered
along and the crescendo-decrescendo breath- tions, nasal obstruction, supplemental oxygen as one movement (Figures 13.47 and 13.48).
ing pattern must be seen for at least 2 hours and mouth breathing can provide spurious val- If a leg movement occurs within 0.5 sec-
during the study (Figure 13.45). ues of EtCO2. onds of the onset or offset of a hypopnea or
Scoring of Data in Adults 351
Figure 13.43 Mixed apnea: Initial part of the apnea meets criteria for central sleep apnea (Green arrows) and latter half that of obstructive sleep apnea (Maroon
Arrows). In this epoch chest resumes movement before apnea terminates in flow signals.
352 Clinical Atlas of Polysomnography
Figure 13.44A-B Respiratory event related arousal: A series of breaths with flattened waveform showing increased efforts to breath for at least 10 seconds and
associated with an arousal. These breaths do not meet criteria for hypopnea. A: All the breaths in the nasal cannula have nearly equal amplitude.
Scoring of Data in Adults 353
Figure 13.44C Normal amplitude of respiration appears with an arousal, later part of epoch shows progressive flattening.
Scoring of Data in Adults 355
Figure 13.44D Normal amplitude appears with an arousal. See in all epochs, oxygen desaturation does not fulfill criteria for the hypopnea.
356 Clinical Atlas of Polysomnography
Figure 13.45A Cheyne–Stokes breathing: A: Cheyne–Stokes breathing is characterized by three or more central apnea/hypopnea that are separated by crescendo-
decrescendo pattern of breathing and this cycle lasts at least 40 seconds. In addition central apnea/hypopnea index should be at least 5. In addition, crescendo-
decrescendo breathing should be present at least 2 hours of total sleep time.
358 Clinical Atlas of Polysomnography
Figure 13.45B This breathing pattern seen in obstructive sleep apnea should not be confused with CSB.
Scoring of Data in Adults 359
Figure 13.46 Leg movement: To be considered as movement, leg EMG must rise at least 8 µV above the baseline EEG and should last between 0.5 to 10 seconds. End
point of leg movement is marked where EMG remains elevated by at least 2 µV for at least half a second.
360 Clinical Atlas of Polysomnography
Figure 13.47 Leg movement: Leg movements in two limbs that are separated by less than 5 seconds are considered as one movement.
Scoring of Data in Adults 361
Figure 13.48A Periodic limb movement series: At least four or more leg movements where they are separated by at least 5 seconds and maxim by 90 seconds from each
other are termed as leg movement series.
362 Clinical Atlas of Polysomnography
Figure 13.48B Periodic limb movement series: At least four or more leg movements where they are separated by at least 5 seconds and maxim by 90 seconds from each
other are termed as leg movement series.
Scoring of Data in Adults 363
apnea or RERA or any other sleep disordered evidence of at least 2 episodes of teeth grinding (ETMA). ETMA is scored when any 5 of the
breathing, it is not scored as LM (Figure (but not with seizure) along with polysomnog- mini-epochs (created by dividing a 30 seconds
13.49). Similarly, if an arousal (start or termi- raphy during the study night, the reliability of REM epoch into 10 equal epochs) show phasic
nation) is within 0.5 seconds of the start of a scoring improves. For better signals, EMG elec- muscle bursts lasting 100 m seconds to 5 sec-
leg movement, they are considered associated trodes may be placed over masseter muscles. onds and at least four times higher than back-
with each other (Figure 13.50). Rhythmic masticatory movement activity ground EMG in chin EMG or leg EMG (Figure
13.4 BRUXISM
It is characterized by brief (at least three 13.5 REM SLEEP BEHAVIOR 13.6 RHYTHMIC MOVEMENT
sequential signals of 0.25–2 seconds duration) DISORDER DISORDER
or sustained (at least 2 seconds) elevation of
chin EMG, where chin EMG amplitude at least REM sleep behavioral disorder can be diag- RMD can be diagnosed when the EMG activity
doubles the background activity (Figures 13.51 nosed when at least half of the REM epoch increases at least twice the background activ-
and 13.52). To be considered different, two shows activity in chin EMG that is higher ity, movements occur at the frequency of 0.5–2
bruxism signals must be separated by at least than the minimum activity seen during REM Hz, and at least one cluster of four movements
3 seconds of baseline activity in chin EMG. In epoch in the same study (Figure 13.54), or is seen.
addition, if audio signals provide concomitant when excessive transient muscle activity is seen
364 Clinical Atlas of Polysomnography
Figure 13.49 Leg movements associated with respiratory events: Leg movement preceding or following a sleep related breathing disorder event by 0.5 seconds is not
considered as leg movement (A). However, if the start of leg movement is beyond 0.5 seconds, it is cored as leg movement (B).
Scoring of Data in Adults 365
Figure 13.50 Leg movement related arousals: If a leg movement and an arousal is separated by less than half a second, they are considered associated with each
other (box).
366 Clinical Atlas of Polysomnography
Figure 13.51 Bruxism: 2 seconds elevation in chin EMG suggesting sustained activity during bruxism.
Scoring of Data in Adults 367
Figure 13.52 Bruxism: Phasic elevation in chin EMG suggesting bruxism. See the teeth grinding in microphone channel.
368 Clinical Atlas of Polysomnography
Figure 13.53 Three episodes of sustained bruxism: Three episodes are three seconds apart, hence they will be considered as separate episodes of Brixusm.
Scoring of Data in Adults 369
Figure 13.54A REM sleep without Atonia. Sustained muscle activity is seen in this epoch throughout (chin EMG: Channel 1A-1R).
370 Clinical Atlas of Polysomnography
Figure 13.54B REM sleep without atonia: Most of epoch shows loss of muscle atonia in chin EMG during REM.
Scoring of Data in Adults 371
Figure 13.55 Excessive fragmentary transient muscle activity also suggests REMBD. It is scored by diving a 30 seconds epoch into 10 mini-epochs of 3 seconds
duration each.
372 Clinical Atlas of Polysomnography
Figure 13.56 ECG-left ventricular hypertrophy: Asymmetrical T wave inversion in both derivations I and II (Blue box). Also see in the long run in Lead II (Red Box).
In such cases, Physician’s opinion must be sough as this may be seen in a number of non-life threatening conditions, e.g., Left ventricular hypertrophy as well as potentially
life threatening conditions, e.g., Myocardial infarction. However, in myocardial infarction, inverted T waves are symmetrical.
Scoring of Data in Adults 373
Figure 13.57 T wave inversion: Symmetrical T wave inversion is seen in lead I. in such cases opinion from a physician should be sought immediately and complete 12
derivations ECG must be obtained.
374 Clinical Atlas of Polysomnography
Figure 13.58 Wide QRS complex: This ECG shows wide QRS complex (arrows) (duration >120 msec; line
segments) suggestive of bundle branch block.
Figure 13.59 This ECG shows short lasting Ventricular Tachycardia. In this ECG, P wave (red arrows) is independent of QRS complex even during tachycardia. Such
events are pathological and should be immediately reported to attending Physician.
Scoring of Data in Adults 375
Figure 13.60 2:1 heart block: This ECG shows 2:1 AV block. QRS complex (redline segment) appears after every two waves (blue stars).
376 Clinical Atlas of Polysomnography
Figure 13.61 VPC: This ECG shows ventricular premature beat (marked in box as V) in between normal beats (Marked as N). Look that VPC lacks P wave, hence,
ventricular in origin.
Scoring of Data in Adults 377
Figure 13.62 Asystole: This ECG shows cardiac asystole (Maroon box). The baseline is flickering giving appearance of AF. Asystole is followed by one QRS-T complex
(Blue box), which is functional in origin and P wave is absent. Last beat is QRS complex is preceded by P wave (red arrow).
378 Clinical Atlas of Polysomnography
Figure 13.63 Bradycardia: This ECG shows sinus bradycardia with PQRST waves but they are widely placed. One big square of ECG represents 0.2 seconds duration.
Heart rate is calculated by dividing 60 with the RR interval. In this case RR interval is 1.4 seconds. Hence, heart rate is 42/min..
Scoring of Data in Adults 379
Figure 13.64 Tachycardia: This ECG shows sinus tachycardia with PQRST waves but they are closely placed. Heart rate is 150/min.
380 Clinical Atlas of Polysomnography
Figure 13.65 Grade 1 AV block: This ECG shows prolonged PR interval. If it is longer than 0.2 seconds, it is considered as AV block. This ECG shows PR interval of
nearly 0.4 seconds which is equal duration throughout the strip and regular QRS complex following each P wave. Hence, this is first degree AV block.
Scoring of Data in Adults 381
Figure 13.66 Atrial fibrillation: In this ECG P wave can not be seen and heart rhythm is irregularly irregular. This is suggestive of atrial fibrillation.
382 Clinical Atlas of Polysomnography
FURTHER READING C. EEG shows alpha rhythm in posterior A. N2 even when spindle or K-complexes
B. Eye blinks are seen subsequent epoch shows low voltage mixed
REVIEW QUESTIONS
C. Chin tone is lowest frequency activity with chin EMG equal to
1. An epoch is scored the sleep wake stage D. Limb EMG shows no activity REM will be scored as:
that occupy at least following percent of the 4. In patients who do not produce alpha, N1 is A. N2
epoch: scored when: B. REM
A. 20% A. K-complexes appear C. N1
B. 50% B. Delta activity appear D. N3
Scoring of Data in Adults 383
7. If an epoch subsequent to N3 epoch do not C. K-complexes meeting criteria for delta B. REM
A. N2, unless it meets criteria for REM or 10. If an epoch of N2 is followed by an epoch 12. An epoch subsequent to an epoch of REM
wake with K-complex in first half but has low volt- with an arousal in second half, but without
B. N2, irrespective of waveforms age mixed frequency activity in most of the eye movements will be scored as:
C. N3, irrespective of waveforms epoch along with chin EMG to REM level, A. N1
C. N1 11. If an epoch of REM is followed by an epoch A. REM if subsequent epoch shows slow
D. REM that has high chin EMG and low voltage eye movement
9. Following may be seen during N3 sleep mixed frequency activity for more than 15 B. N1 irrespective of other waveforms in
A. Delta waves > 6 seconds K-complex in first half, epoch with high chin C. N1 if slow eye movement appears in
A. N2
384 Clinical Atlas of Polysomnography
D. Wake, irrespective of waveform in sub- A. Crescendo-decrescendo breathing 18. Leg movements are considered as a part of
14. If an epoch has REM waveforms in majority intervening central sleep apnea A. Their starting points are separated by
of epoch but has K-complex, will be scored as: C. Crescendo-decrescendo breathing with minimum 5 seconds and maximally by
B. REM central AHI at least five B. Their terminal points are separated by
15. Mixed apnea is scored when: central AHI at least five and this pattern C. Their starting points are separated by
A. Respiratory flow and effort show is seen for at least 2 hours minimum 10 seconds and maximally by
B. First half of the event shows CSA fol- movement when: D. Their terminal points are separated by
lowed by OSA A. They occur less than 5 seconds apart minimum 10 seconds and maximally by
C. First half of the event shows OSA fol- B. They occur more than 5 seconds apart 90 seconds
lowed by CSA C. Their starting points are separated by 19. A major body movement is scored when:
D. Respiratory flow shows flattening with less then 5 seconds A. EMG artifacts are seen in the epoch
regular efforts D. Terminal point of first is separated by B. EMG artifacts are seen in the epoch
16. For Cheyne-Stokes breathing following is less then 5 seconds from the starting to such an extent that staging is not
tive epochs
A. EKG
B. EMG
C. EOG
D. EEG
ANSWER KEY
1. A 2. C 3. A 4. D 5. B 6. C
19. B 20. D
14
USE OF VIDEO POLYSOMNOGRAPHY
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Discuss the importance of audio-video signals during a sleep study. Information Provided by Video ................................................................. 387
Any movement made by the patient causes disturbance in the ECG. In such
cases, absence of a video would make accurate diagnosis difficult. This is especially
For optimum results, it is essential to have movements usually favor seizures, especially if Different characteristics of the audio signals
an infrared camera that can capture pictures in associated with EEG changes. These movements have been used in recent years to detect snoring
the dark and also has a zoom facility. Besides, it may also be observed during sleep-related rhyth- and sleep apnea, however, this technique is not
should be possible to be maneuver the camera mic movement disorder, however, in that case, recommended by the AASM scoring manual.
through a console in the technician’s room. A they are not associated with the EEG changes
good camera would be able to capture even the seen during seizures.
most trivial movement, for example, lip smack- Without a video, it may be difficult to differ- FURTHER READING
ing during sleep. Thus, information captured on entiate between the “turning in bed” and having
1. Roebuck, A., Monasterio, V., Gederi, E., et al.
the video can help to arrive at a more accurate an abnormal movement. Sleep-related rhythmic
(2014). A review of signals used in sleep analy-
diagnosis. movement disorder, seizures, parasomnia and sis. Physiological measurement. 35(1), R1–57.
Video can be used to detect localized move- turning in bed, especially if brief, produce similar doi:10.1088/0967–3334/35/1/R1.
ment that may be suggestive of REM sleep behav- kinds of movement artifacts.
ioral disorder, for example, hand movement Audio forms an important part of the sleep
along with chin muscle atonia. Video recording study. Teeth grinding and sleep talking are two REVIEW QUESTIONS
may also be used to show the movement to the activities that produce similar kind of signals in
bed partners and to analyze whether the move- the microphone channel. However, the micro- 1. Synchronized video recording during sleep
ment observed in the sleep laboratory is simi- phone only provides visual signals. In such cases, study helps in recognizing:
lar to what happens at home ; in other words, having an external microphone may be helpful A. Sleep apnea
D. Hypersomnia seen
2. Requirement of light for video recording C. Focused on the legs of the patient
during sleep study is overcome by: D. Focused on the trunk of the patient
recording disorder
maneuvering
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Comment on sleep and sleep disorders looking at histogram and Interpretation of Histograms ..................................................................... 391
hypnogram. Review Questions.......................................................................................... 403
Answer Key..................................................................................................... 403
INTERPRETATION OF HISTOGRAMS
The graphical display of the sleep architecture, or sleep stages, along a time axis
stages, sleep-related events and other measured sleep parameters along a time axis,
392 Clinical Atlas of Polysomnography
is called histogram. Figures 15.1 and 15.2 shows all sleep stages in a normal pattern. It also bradycardia and tachycardia, secondary to the
hypnogram and histogram, respectively. shows the effect of PAP therapy on sleep obstructive events. The signal is more stable in the
A histogram is the end result of a scored sleep architecture. therapeutic part. The obstructive events (apneas
study. It provides a wealth of information and C. ECG and oximetry profile. This shows the and hypopneas) are represented by red and pink
enables the health care provider to access the effect of respiratory events on heart rate lines. The length of the lines represents the dura-
major findings of a sleep study on a single page. variability (bradycardia and tachycardia) tion of the events. During an REM sleep, the apnea
A histogram graphically depicts the progres- and oxygen saturation. and hypopnea duration is longer and is associated
sion of sleep stagees, and provides information D. Respiratory events and arousals. REM- with more desaturation. Desaturation is elimi-
on factors such as continuity of sleep, latency of related OSA can be easily detected in the nated at a pressure of 15 cm H2O; however, the
various sleep stages, major awakenings, respira- histogram (Figure 15.4). patient continues to snore associated with arous-
tory events, heart rate, and response to positive E. Body position. als, indicating RERA. Upon increasing the CPAP
airway pressure therapy. F. PAP therapy. pressure, snoring is eliminated. However, during
We propose a systematic approach to histo- Figure 15.5 demonstrates that there is no slow REM sleep, hypopneas reappears again; hence,
gram interpretation that includes: wave (N3) in the diagnostic part due to severe pressure is increased to eliminate OSA during
A. PSG type: The histogram tells us if the OSA. During the therapeutic part, sleep pro- REM sleep.
study is diagnostic, therapeutic, or split- gresses into N3 after eliminating the obstructive Figure 15.6 shows short REM latency with
night study (Figure 15.3). events, indicating a good subjective response to SOREM sleep. Causes of SOREM include, narco-
B. The flow of sleep stages: The hypnogram CPAP therapy. The ECG variability line is thicker lepsy, sudden withdrawal of REM suppressants,
shows if the patient has progressed into during the diagnostic part due to the alternating major depression, and sleep deprivation.
Use of Sleep Histogram 395
Figure 15.3 Three histograms showing: A: A diagnostic study; B: A therapeutic study; and C: A split-night study: Difference in the Histogram showing overnight
diagnostic study, overnight PAP titration and split-night study.
396 Clinical Atlas of Polysomnography
Figure 15.4 Histogram showing REM related OSA: Normal pattern of the sleep architecture as can be seen more N3 in the first half of the night. Frequent dips in
saturation that appear as darker oxygen saturation line due to the intermittent desaturation. Hypopneas are restricted to REM sleep only and occur even in the lateral
position during REM.
Use of Sleep Histogram 397
Figure 15.5 Histogram of a split night study: A split-night study of a patient with severe OSA and significant desaturation. There is no slow wave (N3) in the diagnostic
part due to severe OSA. During the therapeutic part, sleep progressed into N3 after eliminating the obstructive events indicating a good subjective response to CPAP
therapy. ECG variability line is thicker during the diagnostic part due to alternating bradycardia and tachycardia secondary to the obstructive events. The signal is more
stable in the therapeutic part. The obstructive events (apneas and hypopneas) are represented by red and purple lines. The length of lines represents the duration of the
events. During REM sleep, apnea and hypopnea duration is longer and is associated with more desaturation. Desaturation was eliminated at a pressure of 15 cm H2O;
however, the patient continues to snore associated with arousals indicating RERA. Upon increasing CPAP pressure, snoring was eliminated. However, during REM sleep,
hypopneas reappeared again; hence, pressure was increased to eliminate OSA during REM sleep.
398 Clinical Atlas of Polysomnography
Figure 15.6 Sleep onset REM: A diagnostic study of a patient who was referred for sleep study to rule out OSA. However, the study as can be seen showed sleep onset
REM (SOREM) with a REM sleep latency of 9.5 min. Causes of SOREM include, narcolepsy, sudden withdrawal of REM suppressants, major depression, and sleep
deprivation.
Use of Sleep Histogram 399
Figure 15.7 Position dependent OSA: A diagnostic sleep study showing position-related OSA. Obstructive events occur only during sleep in the supine position.
Obstructive apneas and hypopnea appear only in the supine position and are associated with desaturation.
400 Clinical Atlas of Polysomnography
Figure 15.8 Position and sleep stage dependent OSA: A diagnostic study showing position and REM-related OSA. Obstructive apneas and hypopneas occurred during
REM sleep in the supine position and are associated with desaturation. During REM sleep in the lateral position, there were no obstructive events or desaturation.
Use of Sleep Histogram 401
Figure 15.9 Split-night study with treatment emergent CSA (complex sleep apnea): A split-night study of a patient with severe OSA. It shows incorrect rapid CPAP
pressure build up. The rapid increase in pressure increases the chance in developing central apneas. This patient developed central apneas (CPAP emergent apneas)
associated with desaturation.
402 Clinical Atlas of Polysomnography
Figure 15.10(A,B) Hypnogram in a patient with insomnia: A: Hypnogram shows prolonged sleep latency
and middle insomnia; B: Multiple awakenings in patient with insomnia.
Use of Sleep Histogram 403
Histograms can help in detecting position- B. Helps in assessing the severity of sleep A. Reverse first night effect
related and sleep stage related OSA (Figures 15.7 disordered breathing B. Second night effect
Additionally, histograms provide a clear picture D. Provides the guidance to the D. Reverse second night effect
of PAP titration pattern and patient’s response to management 5. To explain to the patient regarding the ill-
therapy. Figure 15.9 shows incorrect rapid CPAP 2. Sleep stage related sleep apnea can best be ness, especially sleep disordered breathing
pressure build up. The rapid increase in pres- viewed in: use:
(CPAP emergent central apneas) associated with C. Tabular depiction of data C. Hypnogram
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Discuss changes in EEG seen during sleep among children. 16.1 Respiratory Events............................................................................ 408
2. Correlate EEG changes with the age among children. Further Reading............................................................................................. 415
3. Discuss the rules for respiratory scoring among children. Review Questions.......................................................................................... 415
are followed for scoring of sleep data among chil- slowly develops, 3.5–4.5 Hz at the age of 3–4 usually intermixed with posterior slow waves of
dren. These rules apply to children aging from 2 months post-term, 5–6 Hz by 5–6 months and youth (2.5–4.5 Hz bilaterally present slow waves
months post-term to adolescents. 7.5–9.5 Hz by 3 years of age. that block with eye opening and disappear with
Vertex sharp waves, similar to adults in Due to their small face, chin EMG elec- sleep seen between 8–14 years of age) or ran-
morphology, first appear at the age of 16 trodes in children are placed at a distance of 1 dom occipital slowing (<100 µV, 2.5–4.5 Hz
months post-term. Sleep spindles may be seen cm and EOG electrodes at a distance of 0.5 cm. activity lasting less than 3 seconds seen between
at the age of 4–6 weeks post-term and are usu- Among children, sleep stages are divided 1–15 years age). However, if alpha reactive to
ally seen in post-term 2–3 months old infants, as adults, that is, awake, N1, N2, N3 and REM eye opening or age-appropriate PDR is not seen,
but are often asynchronous over hemispheres. in addition to N (NREM) stage. N is scored eye blinks, reading eye movements and high chin
K complexes usually develop at the age of post- when all epochs of NREM sleep do not con- tone can be used to score wakefulness.
term 4–6 months. Slow waves usually appear tain characteristic waveforms, that is, K-com- N1 is scored when PDR is attenuated by low-
by the age of post term 2 months and are well- plex, spindle, or slow waves. However, epochs amplitude-mixed-frequency activity in more
developed at the post-term age of 4–5 months. that contain K-complex are scored as N2 and than half of the epoch. However, where PDR
N1, N2, and N3 can be diagnosed at the age epochs that show greater than 20% of slow- is not seen, any of the following is sufficient to
of post-term 4 months. Non-EEG signals, for wave activity are scored as N3. The rest of the score N1: 4–7 Hz activity, which represents 1–2
example, irregular respiration, atonia, rapid eye epochs are scored as N. Hz slowing compared to wake activity, slow eye
movements and transient muscle activity may Wakefulness is scored when more than 50% movements, vertex sharp waves, rhythmic ante-
help to differentiate between REM and NREM of the epoch contains age-appropriate posterior rior theta (5–7 Hz theta predominantly seen in
sleep. Similarly, posterior dominant activity dominant rhythm (PDR) (Table 16.1). PDR is frontal and/or central regions, appears at 5 years
Polysomnography in Children: Scoring Rules 407
of age and continues till adulthood), diffuse or and terminal points of the event are scored as in balloon or calibrated respiratory inductance
occipital predominant 3–5 Hz activity, or hyp- adults. plethysmography.
nagogic hypersynchrony (Figure 16.1). N2, N3, Mixed apnea is scored when the initial portion Hypopnea is cored when there is at least 30%
and REM are scored as in adults though waves of the event is characterized by a loss of respira- fall in amplitude of airflow signals for the dura-
gradually develop with age. In infants < 3 months tory effort but it is resumed before the end of the tion of at least two breaths and is associated with
post-term age, REM appears at sleep onset rather event. either an arousal (Figure 16.2A–C) or at least
than N1. Central apnea is diagnosed when the absence 3% oxygen desaturation (Figure 16.3).
of airflow is associated with an absent respira- Respiratory effort related arousal (RERA) is
tory effort of at least 20 seconds duration. If the scored when there is an increased respiratory effort
16.1 RESPIRATORY EVENTS duration of the event is less, then it should last or there is flattening of the nasal pressure wave-
the duration of at least two normal breaths, and form for the duration of at least two normal breaths
Obstructive apnea is scored as an apnea that should be associated with either an arousal or an or snoring, or an increase in EtCO2 or TransCO2
meets the duration of at least two normal awakening, or at least 3% oxygen desaturation to from the pre-event baseline. If the esophageal
breaths (duration calculated by the duration of be scored as central apnea. manometry is used, it should show progressively
two normal breaths) with more than 90% fall in Classification of apneas among chil- increased respiratory effort for the duration of at
signal amplitude for the duration of the event; it dren into subtypes should be avoided in the least two normal breaths and is associated with
is associated with continued respiratory efforts absence of quantitative assessment of respi- snoring, noisy breathing, increased respiratory
during the entire period of the event. Starting ratory efforts through either esophageal efforts, or increased EtCO2 or TransCO2.
Polysomnography in Children: Scoring Rules 409
Figure 16.1A Hypnogogic hypersynchrony is paroxysmal EEG activity of 75–350 µV, 3–4.5 Hz in frequency bisynchronous activity that is usually seen in frontal and/
or central derivations (30 sec epoch).
410 Clinical Atlas of Polysomnography
Figure 16.1B Hypnogogic hypersynchrony is paroxysmal EEG activity of 75–350 µV, 3–4.5 Hz in frequency bisynchronous activity that is usually seen in frontal and/
or central derivations (15 sec epoch).
Polysomnography in Children: Scoring Rules 411
Figure 16.2A Hypopnea among children can be diagnosed when with 30% reduction in amplitude of airflow for the duration of at least two normal breaths is associated
with an arousal.
412 Clinical Atlas of Polysomnography
Figure 16.2B Hypopnea among children can be diagnosed when with 30% reduction in amplitude of airflow is associated with an arousal.
Polysomnography in Children: Scoring Rules 413
Figure 16.2C Hypopnea among children can be diagnosed when with 30% reduction in amplitude of airflow is associated with an arousal.
414 Clinical Atlas of Polysomnography
Figure 16.3 Hypopnea among children can be diagnosed with 30% reduction in amplitude and at least 3% oxygen desaturation.
Polysomnography in Children: Scoring Rules 415
FURTHER READING A. Duration is longer than required in A. >2 central apneas each event lasting at
REVIEW QUESTIONS 3. In case oro-nasal thermal sensor goes dys- D. >5 central apneas each event lasting at
1. Duration of a respiratory event to be scores measure airflow among children is: is <40 seconds
as obstructive apnea among children is: A. Oximetry 5. Which of the following is important for
D. Duration equal to 4 normal breaths 4. Periodic breathing is scored among children B. Gestational age
A. Elderly
B. Adults
C. Children
D. Infants
REM among:
A. Children
B. Infants
C. Adults
D. Elderly
17
TEST PROTOCOLS
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to perform sleep studies
as per protocols to ensure recording of good quality data. 17.1 Protocol for the Diagnostic Sleep Study...................................... 418
17.2 Protocol for the Manual Titration with PAP.............................. 418
17.3 Protocol for the Multiple Sleep Latency Test (MSLT)........... 419
and manual titration with PAP. In some cases of severe OSA, split-night poly-
17.4 Protocol for the Maintenance of Wakefulness Test (MWT).... 420
during the day. In this chapter, we will present 6. The patient should have taken all the pre- 12. If any channel is malfunctioning, try to rec-
the protocols for these tests. scribed medications tify it before the start of the study.
7. Start the preparation at least 40–60 min 13. After calibration, let the patient sleep. Reas-
before the patient’s usual bedtime, as prepa- sure him/her that you are watching his/her
17.1 PROTOCOL FOR THE ration may take around 20–30 min. Any output and you are available in case of any
DIAGNOSTIC SLEEP STUDY deviation from this will cause spuriously emergency.
long or short sleep onset latency. This may 14. The patient should be woken up at his/her
1. The patient should be given time to get be checked by looking at the data from the usual wake time in the morning.
acclimatized to the room. Hence, it is bet- patient’s sleep diary 15. In the morning patient should be given the
ter that he/she is called at least 6–8 hours 8. Apply all the channels on the patient’s body, post-diagnostic study questionnaire.
before his/her usual bed time.
as discussed in Chapter 5.
2. Request the patient to fill the details in the 9. Fill all the details as requested by the
“Pre-sleep questionnaire.” software. 17.2 PROTOCOL FOR THE
3. Make sure that the scalp and face of the 10. Check for the impedance in the electrical MANUAL TITRATION WITH
patient are free of any grease/oil. channels and try to keep it below 5 Kilo PAP
4. The patient’s clothes must be comfortable Ohms.
and should not be synthetic. 11. Do the electrical calibration and follow it by 1. It should be done during the night after the
5. The temperature of the room should be bio-calibration. Make sure that all the chan- diagnostic polysomnography.
kept at around 22°C . nels are working properly.
Test Protocols 419
2. The patient should be informed about the lead to leakage. Instead, flow signals are 3. Get the sleep log for at least one week prior to
results of the diagnostic study and should acquired from the mask. the MSLT.
be given time to acclimatize with the mask. 6. Raise the pressure of PAP, as discussed in 4. Stimulant medications or medications that
3. For acclimatization, show the patient the Chapter 20. suppress REM should be withdrawn at least
PAP and mask during the day. Explain how 7. The patient should be requested to fill two weeks ahead of the test. Physician consul-
it works and give him/her the mask during the details in the “post-CPAP night tation should be done to avoid the influence
the day before the titration study. questionnaire.” of hypnotic medication on the day of the test.
4. Ask him/her to hold the mask in front of Vigorous physical activity, exposure to bright
the nose and breathe through it. For this, light, smoking, caffeine should be avoided on
the patient should be allowed to hold the 17.3 PROTOCOL FOR THE the day of the test as they may be counterpro-
mask in hand (this should not be strapped MULTIPLE SLEEP LATENCY ductive to the sleep. Any other measure to
at once). Request him/her to practice it TEST (MSLT) promote wakefulness should be terminated at
by keeping it in position for longer periods least 15 min prior to every nap opportunity.
during the day. 1. This should be done after the diagnostic study. Drug screening may be performed in selected
During the diagnostic study, sleep apnea and
5. Follow the steps 2–12 as mentioned in the cases.
any other cause that may lead to sleep disrup-
“diagnostic study” section above. How- 5. The test is started in the morning at least two
tion should be ruled out.
ever, during titration, nasal cannula and hours after waking up after a light breakfast.
2. Total sleep time during the night should be at
thermistor should not be placed as it may 6. Five opportunities for sleep are provided, 2
least 6 hours. hours apart during the day.
420 Clinical Atlas of Polysomnography
7. Sleep lab should be sufficiently dark and quit to 14. Recording should be done for 20 min. If the SOREM is defined as REM appearing within
promote the sleep. The temperature of the lab patient does not fall asleep during 20 min, 15 min of the sleep onset during a recording.
8. Make sure that the scalp and face of the patient 15. If the patient falls asleep during this 20 min, 17.4 PROTOCOL FOR
are free of any grease/oil. from the first epoch-defining sleep, another THE MAINTENANCE OF
9. The patient’s clothes must be comfortable and 15 min should be provided for REM sleep to WAKEFULNESS TEST (MWT)
should not be synthetic. appear. For example, if the epoch-defining
1. The test should be started at least 2–3 hours
10. Make sure the patient’s sleep is not disrupted sleep is seen at the 10th min, the test should be
after the night nap.
because of any other reason, for example, going terminated at the 25th min (10 min + 15 min)
2. Diagnostic polysomnography in the preced-
to the washroom. instead of the 20th min.
ing night and sleep logs are not mandatory
11. Apply the EEG electrodes, EOG electrodes, 16. After each nap, the patient should be asked
before MWT. They may be conducted
chin EMG, and EKG for the test. and information should be filled in the “MSLT
using clinical judgment.
12. Perform bio-calibration to assess alpha waves questionnaire.”
3. Light breakfast should be provided before
in the EEG, eye movement, and chin EMG. 17. Light lunch should be provided during noon.
the first recording.
Preferably, this should be done in every nap. 18. Report “start and stop time,” “sleep onset
4. Sleep lab should be sufficiently dark and
13. Instruct the patient “Please close your eyes and latency from lights out,” for each recording,
quit to promote sleep. The temperature of
try to fall asleep” before the nap and request “mean sleep latency,” and “number of sleep
the lab should be optimal.
him/her to lie down and be comfortable in onset REM (SOREM) out of five naps.”
5. Make sure that the scalp and face of the
bed.
patient are free of any grease/oil.
Test Protocols 421
6. The patient’s clothes must be comfortable 12. Instruct the patient “Please sit still and FURTHER READING
and should not be synthetic. look in front of you. Try to stay awake
7. Make sure the patient’s sleep is not dis- as long as possible,” before starting the 1. Littner, M. R., Kushida, C., Wise, M., Davila,
D. G., Morgenthaler, T., Lee-Chiong, T., et al.,
rupted because of any other reason, for recording.
(2005). Standards of Practice Committee of the
example, going to the washroom. 13. Four recordings are done, each lasting 40
American Academy of Sleep Medicine. Practice
8. The patient is not allowed to take any min (if no sleep occurs) and two hours parameters for clinical use of the multiple sleep
stimulant unless approved by the sleep phy- apart. latency test and the maintenance of wakefulness
sician. They are instructed to avoid using 14. A recording may be terminated earlier than test. Sleep 28(1), 113–121.
any other measure to stay awake, e.g., sing- 40 min if three consecutive epochs of N1
ing, etc. A drug screen may be performed in sleep are seen or one epoch of any other
B. Leak if large, may be managed for opti- C. Leave the choice to the patient
breathing event
A. MSLT
D. MWT
18
DOCUMENTATION
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Recognize the importance of proper documentation during sleep Various Documents and Questionnaires ................................................. 425
study monitoring. Review Questions.......................................................................................... 430
2. Enumerate names of records to be maintained in a sleep laboratory. Answer Key..................................................................................................... 430
3. Design their own document for recording the information.
a good quality sleep study that will assist the treating physician to reach accurate
424 Clinical Atlas of Polysomnography
Table 18.1 Examples of the Subjective and Objective Events that Need Documentation During PSG
Subjective Objective
diagnosis. Included in the technologist’s docu- Patient’s perception regarding sleep quality Sleep-wake patterns of patient’s sleep.
during the study.
mentation are all the events especially unusual Any unusual complaints, i.e., a headache, pain, Unusual events, i.e., short REM sleep latencies, leg move-
nightmares, etc. ments, hypopneas, apneas, sleep walking, parasomnias,
sleep-related events that were noted during the sleep talking, etc.
PSG, as well as, any medication taken by or given The subjective feeling when a PAP device titra- Artifacts
tion was implemented.
to the patient during the time of the study. Table Patient’s perception of PAP device therapy. Response to PAP device titration
ing PSG.
18.2–18.6).
Documentation 425
3. Did you fall asleep during this test? Yes/No Yes/No Yes/No Yes/No Yes/No
5. Did you dream during the nap? Yes/No Yes/No Yes/No Yes/No Yes/No
6. Did you fall asleep between two tests? Yes/No Yes/No Yes/No Yes/No Yes/No
8. Did you dream during that nap? Yes/No Yes/No Yes/No Yes/No Yes/No
Documentation 429
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader should be able to:
1. Identify and troubleshoot common problems encountered during Steps at Troubleshooting ............................................................................ 431
recording of polysomnography. Review Questions.......................................................................................... 436
Answer Key..................................................................................................... 437
hardware and software. In this case, it becomes prudent that the hardware can
support the platform that you are loading in the computer system to run other
which version of the platform you are using) of the computer system must also
432 Clinical Atlas of Polysomnography
support the software provided by the polysom- the connections is loose or compromised in any • All derivations with poor waveform
nography manufacturer. If any of these parts are other way (short-circuit, generation of local have a common reference
incompatible, the system will not work properly . electrical potential), an interference with either • All derivations showing poor waveform
This should be taken care of by the sleep technol- signal acquisition or signal quality will appear. are from one side of the scalp (right or
ogist at the time of purchasing the instrument. At These communication cables must be checked left)
times, the antivirus software of the computer sys- time-to-time. • Derivations with poor waveform don’t
tem can also interfere with the functioning of the Troubleshooting of the artifacts has been have anything in common.
polysomnography software. In such cases, the discussed in Chapter 12. Similarly, all manufac- If the derivations with poor waveform
PSG software does not open, or takes a long time turers provide the common trouble-shoots in have common reference (M1 or M2), check
while opening or may automatically shut down. their manual. The reader is advised to consult if the reference electrode is properly placed
In such cases, a trial may be given to turn off the those manuals for issues that may be specific and its impedance is within normal limits. If
antivirus software. to a particular machine. In this chapter, we will there is a problem, fix it.
Sensors placed on the body are connected to discuss other issues related to in-lab attended If derivations with poor waveform
the head-box; head-box is connected through polysomnography. belong to one side of scalp, see if their con-
cable to the base system, which, in turn, feeds 1. Some of the EEG derivations are showing tact with skin is improper. It may happen
the signals to the computer system. If a sensor dangling waves. when patient takes a turn in the bed during
is not generating signals (improper placement, This may be seen when the EEG elec- sleep. Fix them. If these derivations belong
high impedance, battery dead if it requires bat- trodes are in poor contact with the skin. to the side of scalp/head that is resting on
tery power for signal generation), or if any of To resolve this issue, look if: pillow, it may be possible that the patient is
Troubleshooting 433
the electrodes.
Figure 19.1 Software and hardware required in a polysomnography laboratory. 2. Waveform is attenuated in one of the EOG
channels.
this issue,
• See if the filter and sensitivity setting of Check whether signals are missing 5. Flow signals are not appearing during the
• Remove the electrode and place it both. During the titration study, flow signals
again after cleaning the underlying If they are missing from both sensors, are generated from the PAP device. If they
area. make sure that: are not apparent, make sure that:
• If this does not work, consider changing • Both sensors are connected to the right • The PAP device is working.
the electrode with a new one. slots in the head box. • Mask fitting is adequate and leakage is
3. Signals from chin EMG are distorted. • Patient is a nose breather and nasal within the prescribed limits.
Common issues that lead to distorted airway is patent. • The PAP device is connected with the
chin EMG signals include high imped- • If the patient is nose breather, sensors system, as depicted in the manual of PSG.
ance between the skin and electrode. are placed correctly. • If this is ok, look for the sensitivity and
This is especially common among • If sensors are correctly placed but filter setting in the software. If it is not
patients who wear a beard. If the patient signals generation require some elec- set as depicted in the AASM manual,
allows, an area large enough to place the trical current, make sure the battery is change the settings.
EMG electrodes may be cleaned using working. 6. Signals from chest and/or abdominal belts
curved scissors, and electrodes may be • If this is ok, look for the sensitivity and are not appearing.
placed after that. filter setting in the software. If it is not Please check if:
4. Flow signals are not apparent during diag- set as depicted in the AASM manual, • Belts are loose or too tight. Ide-
nostic study. change the settings. ally, an un-stretched RIP belt should
Troubleshooting 435
cover around two-third of the chest • It is connected to the hardware 9. Mask leakage too high.
• If the belts require battery to generate 8. Signals from the pulse oximeter are ting of the mask. Please ensure that an appro-
signals, it is not discharged. If there is a intermittent. priate mask has been chosen depending upon
problem, fix it. This can happen if there is an interfer- the shape of the face and other factors.
• Jack from the Z-RIP-module is placed ence with the transmission of light waves Poor mask fitting is seen when:
properly in the head box. If not, fix it. from one side to the other. • It is tied too tightly on the face. Tight
• Sensitivity and filter setting of the In such case, please ensure that: fitting will lose the cushioning effect of
waveform in the software is correct. If • Probe is placed correctly. A loose probe the mask and promote leakage.
not fix it. may lead to intermittent loss of signals. • Mask is lying loose on the face.
7. EtCO2 signals not coming up. Fix it. • The patient is not able to breathe
Please check if: • Fingernail is completely clean. If some through the mask as pressure is consid-
• Cannula is properly placed. If not, fix it. part of the fingernail is covered with any ered too high.
• Patient is a nose breather and nasal kind of opaque material, it may lead to • The patient is fiddling with the mask.
airway is patent. If the patient is mouth intermittent loss of signals. • The patient has taken turn in bed and
breather, you may switch to a cannula • Flow of blood is not obliterated in the mask has been drawn to one side of
that has a port for oral breathing as well. the arm in which the sensor is placed. the face. In such case, place the PAP in
• If you are using EtCO2 signals, the can- Intermittently, it may happen when the the back of the bed and place the hose
nula is free of moisture. patient is using this arm as a pillow. pipe loose and in such a manner that it
436 Clinical Atlas of Polysomnography
passes over the head. These maneuvers computer system. Poor feed from the video A. Checking the reference electrodes
will reduce the dragging of the mask and may be related to interference in the electri- B. Checking the ground electrode
improve its fitting. cal supply to camera or due to interference C. Checking the filter setting
• Cannula/thermistor is placed below the in the communication cable. At times, soft- D. Checking the individual electrode
mask. ware that runs the video may also malfunc- 2. If the flow signals from PAP show flattening
10. Study not downloading in the computer tion. Take the following steps: after optimal titration:
system. • Ensure that infrared lights are tuned on A. Look for the ground electrode
Some PSG machines store the data in a in the camera. For this, you may have B. Look for the oxygen saturation
base station and transfer it to the computer to go to the patient’s room. If lights are C. Look for the leakage
system when you close the study, for exam- turned on, electrical supply is OK. D. Look for the respiratory rate
ple, Alice 6. This transfer may be hampered • Look for the available disc space. If 3. If the signals from effort RIP Chest belt are
if the available disk space is inadequate. In space is low, waveforms may continue present intermittently, but from abdomen
such case, create some space in your com- to be recorded, but not the video. regularly:
puter system and then try to download the A. Check the battery of RIP module
data from the base station again. B. Check if the chest belt is loose or
This results from poor feed from the 1. If the signals in all EEG channels show elec- D. Check the filter settings
sible EXCEPT:
oximeter is placed
C. Oximeter is loose
headbox
20
MANUAL TITRATION WITH
POSITIVE AIRWAY PRESSURE
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader must be able to:
1. Understand the steps of manual PAP titration among adults and children.
20.1 Pressure Limits.................................................................................. 440
2. Select the proper mask for the patient.
20.2 CPAP Titration for OSA................................................................. 440
3. Discuss and recognize the quality of titration study.
20.3 When to Switch From CPAP to BPAP in Patients with OSA?... 441
C
Further Reading............................................................................................. 444
ontinuous positive airway pressure (CPAP) and bi-level positive airway
Review Questions.......................................................................................... 444
pressure (BPAP) are the gold standard and the most effective treatment
Answer Key..................................................................................................... 445
for OSA and other sleep-related breathing disorders. Non-invasively, positive air-
way pressure applied through a mask provides a continuous stream of air pressure
440 Clinical Atlas of Polysomnography
through the nose and/or mouth. Positive air the strap on their hand, for progressively longer maximum CPAP should be 15 cm H2O for patients
pressure prevents airway collapse, allowing the periods. Finally, have the patient try CPAP or <12 years, and 20 cm H2O for patients ≥12 years.
patient to breathe freely during sleep. BPAP for some time while awake, starting at a PAP should be increased until the following
The mask provides a bridge between patient very low setting (4–5 cm H2O) and titrate until obstructive respiratory events are eliminated (no
and device. It is an important component of a 10 cm H2O. This simple maneuver improves the specific order); apneas, hypopneas, respiratory
successful PAP therapy. compliance to titration at night. effort-related arousals (RERAs), snoring, or the
Usually, titration of the PAP device pressure PAP titration should aim for an AHI less than or recommended maximum CPAP is reached.
is done gradually under PSG monitoring. Prior to equal to 5/hr, SpO2 >88%, respiratory arousal index
PAP titration, all patients should receive adequate less than or equal to 5/hr, and to eliminate snoring.
20.2 CPAP TITRATION FOR
education about PAP, hands-on demonstration, The AASM has published Clinical Guidelines
OSA
careful mask fitting, and acclimatization prior to for the Manual Titration of PAP in Patients with
the process. The technician has to size and fit a OSA. In the coming section, we will summarize
• CPAP should be increased if at least 1
patient with proper mask size. Some laborato- those guidelines.
obstructive apnea is observed for patients
ries provide time for mask acclimatization to the
<12 years or at least 2 obstructive apneas are
patients. After selecting the correct mask, patients
20.1 PRESSURE LIMITS observed for patients ≥12 years.
are given the mask in the morning before the titra-
• CPAP should be increased if at least 1
tion study is planned, and they are asked to keep
The recommended minimum starting CPAP hypopnea is observed for patients <12 years
it on their nose and breathe normally. As they get
should be 4 cm H2O for pediatric and adult or at least 3 hypopneas are observed for
comfortable with the mask, the mask is fixed with
patients. On the other hand, the recommended patients ≥12 years.
Manual Titration with Positive Airway Pressure 441
• CPAP should be increased if at least 3 RERAs Table 20.1 The Titration Steps and Indications to BPAP. Figure 20.2 shows a hypnogram of
<12 years of age ≥12 years of age
are observed for patients <12 years or at least a patient who continues to have obstructive
≥1 OA ≥2 OA
5 RERAs are observed for patients ≥12 years. ≥1 Hypopnea ≥3 Hypopneas hypopneas on CPAP pressure of 20 cm
• CPAP should be increased if at least 1 ≥3 RERAs ≥5 RERAs H2O. Upon shifting the patient to BPAP, the
≥1 minute of loud ≥3 minutes of loud un-
minute of loud or unambiguous snoring is unambiguous snoring ambiguous snoring obstructive events disappeared .
OA: obstructive apnea; RERAs: respiratory effort-related
observed for patients <12 years or at least 3 arousals. • If the patient with OSA is uncomfortable or
minutes of loud or unambiguous snoring are intolerant of high pressures on CPAP, he/
observed for patients ≥12 years. one that the patient reports is comfortable she may be tried on BPAP.
• Increase CPAP pressure by at least 1 cm H2O enough to allow are turn to sleep.
with an interval no shorter than 5 minutes. Table 20.1 summarizes the titration steps and
• Make sure that the increment in CPAP indications. 20.4 BPAP TITRATION FOR
pressure is not done too fast, as this may OSA
result in central apneas (CPAP emergent
• If the patient awakens and complains that • If there are continued obstructive respiratory • The recommended minimum starting IPAP
the pressure is too high, the pressure should events at 20 cm H2O of CPAP during the should be 8 cm H2O for pediatric and adult
be restarted at a lower pressure chosen as titration study, the patient may be switched patients.
442 Clinical Atlas of Polysomnography
Figure 20.1 A hypnogram of a patient with OSA. Rapid titration resulted in PAP emergent central apneas.
Manual Titration with Positive Airway Pressure 443
Figure 20.2 A hypnogram of a patient who continues to have obstructive hypopneas on CPAP pressure of 20
cm H2O. Upon shifting the patient to BPAP, the obstructive events disappeared.
444 Clinical Atlas of Polysomnography
• The recommended maximum IPAP should • Good titration: It reduces RDI ≤10 or by to meet the AASM criteria (i.e., titration
be 20 cm H2O for patients <12 years, and 30 50% if the baseline RDI <15 and should duration should be >3 hr) (a consensus
cm H2O for patients ≥12 years. include supine REM sleep that is not con- agreement).
than 5 minutes. did not occur at the selected pressure (a apnea. Journal of Clinical Sleep Medicine. JCSM:
official publication of the American Association
The AASM has categorized the success of consensus agreement).
of Sleep Technologists. 4(2), 157.
PAP titration into several categories: • Unacceptable titration: It is one that does
• Optimal titration: It reduces the respira- not meet any one of the above grades (a
REM sleep at the selected pressure that is not be considered if the initial titration does
1. Titration with Auto-PAP is not recom-
continually interrupted by spontaneous arous- not achieve a grade of optimal or good
mended as:
als or awakenings (a consensus agreement). and, if it is a split-night PSG study, it fails
Manual Titration with Positive Airway Pressure 445
2. BPAP is recommended when: dren <12 years before increasing the pres-
A. CSB appears
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, the reader must be able to write an informative
report that can be understood by any medical person. Contents of an Informative PSG Report ................................................. 447
end user. Reports do come with superfluous amounts of data, which, fortu-
nately, can be customized according to the needs of the users. For in-depth analysis
and research purposes, a report can contain multiple tables, statistics, graphs, and
charts. On the other hand, if the report is mainly for clinical use, it usually includes
the patient’s demographic data, main findings of the sleep study, sleep study hyp-
nogram that reflects the summary of the sleep study, and the recommendations of
448 Clinical Atlas of Polysomnography
the treating physician. Important sleep parame- interpretation of the report. The physician thorax, abdomen, and RIP-sum. The respiratory flow
ters that must appear in the report include a sum- should be able to provide a clear opinion and was recorded using a thermistor and nasal cannula
mary of sleep architecture, respiratory events, modify his/her own treatment, if required. Sleep and overnight oximetry by oximeter placed at the
oxygen saturation levels, limb movements, study report generated in a standard performa right index finger with three seconds averaged value.
arousals, and heart rate. If a PAP device was used, often has multiple tables and a page that shows Snore microphone was placed to diagnose snoring.
the report should summarize the subjective and the graphical representation of data (Figure EtCO2 was recorded using a capnograph. Body posi-
objective response to therapy and the optimal 21.1). Based on observations at night and data tion sensor was used to ascertain body position and
setting of the device. The sleep technologists’ available in a tabulated and graphical format, one leg EMG was recorded from two channels from ante-
comments are important and can add further comprehensive summary should be provided rior tibialis. Synchronized video was also recorded.
insight into the study report as they stay around that clearly indicates your opinion. The patient was explained about the overnight
the patient during monitoring. Examples of A good report would be like this: sleep study in advance and was given time to get accli-
important technologists’ comments include an The patient was referred for the diagnostic sleep matized to the sleep lab. The recording was started at
account of the patient’s physical and emotional study with the suspicion of obstructive sleep apnea his usual bed-time (or earlier or later to that) and ter-
status during the study, unusual sleep-related due to his long history of systemic hypertension. The minated at his usual wake time (or earlier or later to
behavior or atypical findings that are not evident recording included three EEG channels—Frontal, that). The patient took (or was asked not to take) his
in the monitored sleep parameters. Central and Occipital, which were referred to the con- medications at his usual time which included (mention
While writing the report, it must be con- tralateral mastoid. Two channels from EOG and two here names as some medications may alter sleep-wake
sidered that a physician who does not special- channels from the submentalis were included. Respi- cycle and proportions of sleep stages). Morning report
ize in sleep medicine is able to understand the ratory effort was measured using RIP belts from the suggests that patient was comfortable (if not, mention
Writing an Informative Report 449
Figure 21.1A,B Histograms depicting graphical representation of the whole night data: A: Histogram showing diagnostic study B: Histogram shows that sleep related
breathing events improved after correction of mask fitting at same pressure.
450 Clinical Atlas of Polysomnography
the reason for discomfort) during the study and that No effect of sleep stage and body position could be 5. Sleep was interrupted by the urge to void,
he had his usual kind of sleep. Data generated from observed on RDI or desaturation index. Cheyne- which may be related to the sleep-disordered
the recording suggests total sleep time of 300 min with Stokes breathing, periodic breathing, and sleep-related breathing.
asleep efficiency of 80%. Sleep onset latency was 25 min hypoventilation were not observed during the study. 6. Moderately severe sleep apnea without any
that matches with sleep diary data, and hypnogram Frequent limb movements were observed with PLMS modification from body position and pres-
suggests that sleep was well-maintained except for 2–3 score of 24, however, they were not associated with ence of systemic hypertension suggests that
arousals to go to the washroom. However, he fell asleep arousals. EKG did not show any abnormality. the patient needs treatment for sleep-disor-
soon after each arousal. Total arousal index was 25 This report clearly indicated that: dered breathing.
which is higher than expected, and was mostly related 1. Sleep latency was within normal limits and 7. High PLMS score could be an incidental
to the sleep-disordered breathing events. Data suggests also he did not have difficulty in falling finding as patient does not have RLS.
that proportion of stage 1 was higher (12%), while asleep after waking up for the need to go to In summary, treatment of sleep-disor-
that of N3 lower (8%), again related to sleep-disor- the washroom, so insomnia can be ruled out. dered breathing would take care of most of the
dered breathing. Snoring started soon after sleep initia- 2. Adequate time was given to diagnose the complaints.
tion and many events of the respiratory-event-related condition in question, that is, sleep apnea.
arousals, hypopnea and obstructive sleep apnea were 3. The patient usually did not get deep sleep
observed with respiratory disturbance index (RDI) (low N3). REVIEW QUESTIONS
of 18.3. Average oxygen saturation was 92% with the 4. Sleep-disordered breathing was respon-
minimum saturation of 79% and desaturation index of sible for the non-refreshing sleep (multiple 1. If usual bed time and start time is not men-
22. Overnight oximetry showed sawtooth appearance. arousals). tioned in the report:
Writing an Informative Report 451
total RDI, but not the RDI achieved at the C. helps in diagnosing parasomnia
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, reader should be able to:
1. Decide when to institute oxygen therapy during sleep study. 22.1 Introduction....................................................................................... 453
2. Provide oxygen therapy using the AASM guidelines. 22.2 Oxygen Delivery Devices and Polysomnography...................... 454
22.3 Precautions......................................................................................... 454
In the sleep disorders center (SDC), desatu- 22.2 OXYGEN itself, it strongly enhances combustion. There-
ration events related to sleep-disordered breath- DELIVERY DEVICES AND fore, care should be practiced to ensure that
ing (SDB) are commonly seen. In most cases, POLYSOMNOGRAPHY flammable substances used in the SDC such as
the use of positive airway pressure is sufficient to collodion should not be used near oxygen. If
maintain a patient’s oxygen level within a normal During diagnostic polysomnography, airflow is oxygen cylinders are used, it should be realized
range. However, in certain cases such as patients usually monitored by using a thermistor, nasal that oxygen is stored in the cylinders under very
with co-existing lung or heart disease or patients pressure, and capnography. When oxygen is high pressure; hence, cylinders must be secured
with obesity hypoventilation syndrome, the supplied to the patient via a nasal cannula, oxy- from falling and must be stored away from heat-
need to increase FiO2 may arise and necessitate gen supplementation may interfere with airflow ing sources.
the addition of supplemental oxygen. Therefore, signal in the form of dampened flow signal. To
sleep technologists should be acquainted with overcome this problem, a cannula with a bifur-
the rules and regulations governing the adminis- cated access to each nostril can be used allowing 22.4 DEVICES FOR OXYGEN
tration of oxygen. both oxygen delivery and pressure monitoring. DELIVERY
In general, there should be clearly written
protocols and parameters to regulate oxygen A. High-flow devices: These delivery systems
administration in the SDC. As a general rule, 22.3 PRECAUTIONS deliver oxygen of precise concentration at
the least amount of oxygen to bring about the flow higher than the patient’s inspiratory
desired therapeutic effect, which is often defined Oxygen as a chemical substance has potential flow. An example of these devices is the
as a predetermined level of oxygen saturation. dangers. Although oxygen is not flammable by Venturi mask. High-flow oxygen is usually
Guidelines for Supplemental Oxygen 455
delivered through a facemask with humidi- • Be aware of the patient’s diagnosis and • Administer oxygen at 1 liter/min, and
fication. High-flow systems are not often any history of CO2 retention. increase it by 1 liter/min, with an inter-
used in the sleep center. • Document SpO2 of the patient while val no shorter than 15 min, until the
B. Low-flow devices: This method provides awake. SpO2 is between 88% and 94%.
100% oxygen at a rate that is less than the B. During Sleep Study Recording • Oxygen flow should not exceed 3 liters/
peak inspiratory flow rate of the patient. It • If obstructive respiratory events asso- min unless ordered by a physician.
is recommended to use humidification with ciated with SpO2 drop below 88%, • In general, each sleep disorders center
these systems. Examples of these systems start PAP therapy and assure that all should have clear policies about oxygen
include nasal cannulas and simple masks. respiratory events are corrected. Fig- administration.
Figure 22.1 OSA must be treated before starting oxygen therapy: 5 min epoch of patients with obstructive respiratory events associated with oxygen desaturation.
CPAP pressure should be increased to eliminate the obstructive events before adding oxygen.
Guidelines for Supplemental Oxygen 457
Figure 22.2 Oxygen saturation after elimination of OSA: If SpO2 stays below 88% for >5 min after elimination of respiratory events, then oxygen supplementation is
indicated.
458 Clinical Atlas of Polysomnography
D. 25 minutes
A. scoring of CSA
1. Before starting oxygen flow, ensure that:
B. scoring of OSA
A. all sleep disordered events are corrected
C. scoring of hypopnea
B. arterial PCO2 is below 45 mmHg
D. scoring of MSA
C. patient is sleeping
of (L/min)
23
INFECTION CONTROL
LEARNING OBJECTIVES
CONTENTS
After reading this chapter the learner should be:
1. Able to discuss the common sources of infection in sleep laboratory. Importance of Infection Control ............................................................... 459
2. Able to take optimal precautions for control of infections in sleep Review Questions.......................................................................................... 460
laboratory. Answer Key..................................................................................................... 461
I nfection control is an important issue during the sleep study . A patient has
are applied during the study, and these may transmit infection. In this chapter,
we will discuss the common modes of infection transmission and their prevention
measures.
460 Clinical Atlas of Polysomnography
The first source of infection could be the The second common source of infection is after every sleep study. Alcohol not only removes
room itself. This is an example of airborne the linen. All linen used in a case study should be the greasy conductive gel but also works as a
infection. If there is any seepage in the wall or thoroughly washed and dried and each patient disinfectant.
in the bathroom, fungal spores can grow and should be given fresh linen. This is because linen Respiratory belts seldom act as fomite as they
be a source of infection. It is therefore prudent may be a source of infection in case it contains are usually worn over the clothes. However, care
to inspect the room regularly and take correc- mites, ticks, lice, or any other arthropods. must be taken that the patient does not acci-
tive measures in case seepage is observed. It The other common sources of infection dently contaminate them. In case they are con-
is also good to get the room fumigated before include the nasal cannula, mask of PAP, and taminated, they must be washed thoroughly with
posting another patient for a sleep study. hosepipe of the PAP machine. It is essential soap.
Besides, one patient may also be a source of that the nasal cannula is changed after every For further details, please refer to the infec-
infection for another patient. It is advisable sleep study. Since the mask and the hosepipe tion control policy in Chapter 24.
not to take patients with an active respiratory are expensive items and cannot be discarded so
infection for a sleep study. Even otherwise, a often, they should be sent for autoclaving after
REVIEW QUESTIONS
person with an active upper or lower respira- each use. Mask straps can also transmit infection
tory infection may have spurious data so it is as they are applied directly to the patient’s skin/ 1. Electrodes are disinfected using:
best to avoid such patients. Also, it is impor- hair. They should also be washed after each use. A. soap
tant that the room is well-lit and ventilated, The EEG and EMG electrodes may also be B. collioiden
and there is a regular exchange of air to pre- infrequent sources of infection, and, therefore, C. medical spirit
vent infection. they should be thoroughly cleaned with alcohol D. water
Infection Control 461
B. ETO
C. soap
B. meningitis
C. gastrointestinal
D. urinary
A. it is well ventilated
A. electrode
B. nasal cannula
24
SLEEP LAB MANAGEMENT
CONTENTS 24.6 Policy for Quality Assurance.......................................................... 472
c. Thick curtains must be drawn on the k. Dustbins for disposal of recyclable waste
LEARNING OBJECTIVES windows l. Disposal facility for the consumables in
d. Must be sound attenuated sleep lab and sharp objects, if and when
After reading this chapter, the reader must
e. Must be well lit used
be able to:
f. Have an attached washroom with Gey- One polysomonography can be carried out
1. Able to logically formulate various
ser installed in one room. So the number of rooms required
policies for a sleep-laboratory.
g. Must have air-conditioning and a televi- varies depending upon the number of polysom-
sion with remote control facility nography machines one wishes to establish.
Sleep laboratory must be established in a calm j. Furniture required for the sleep lab c. Must be sound attenuated
and quiet place in the hospital. The place must i. King size bed with mattress, linen, d. Must be well-lit
1. Room and furniture for the sleep-lab iv. Platform for the PSG equipment g. Must have an area with running water to
a. Size of the room: At least 10 x 12 feet v. Couch/bed for the attendant along clean reusable items, for example, mask
h. Have a washroom close to the monitor- c. Real-time audio recording vi. Disinfectant
ing room d. Intercom between the sleep laboratory vii. Cotton Gauges
i. Must have a kitchenette for staff and monitoring room viii. Gloves and Mask
j. Furniture required for the monitoring e. CPAP/BiPAP instrument with remote 4. Equipment for the monitoring room:
(2) Cupboard for storage of accessories i. Full face c. Intercom with amplifier connected to
(3) Revolving chairs for sleep ii. Nasal mask sleep laboratory
Depending upon the number of beds in the g. Oxygen line in the sleep lab with e. Emergency kit: Medications used
facility, the storage room may be separated from humidifier for emergency; measures to secure
3. Equipment for the sleep laboratory laboratory 5. Documents that must be available in a
dard manufacturer with extended EEG i. Neuroprep Gel a. Inventory register, duly completed
b. Infrared video recording with maneu- iii. Electro-conductive gel b. Accounts and budget Register
ii. Organizational structure 1. Administration of the Sleep Clinic and laboratory in collaboration with
iii. Protocol for sleep study Laboratory shall be as follows: other members
Manual ii. Trainee Sleep Physicians (3) Review of the technical side of
vi. Protocols for various sleep iv. In-Charge Sleep Technologist the instruments to be purchased
vii. Trouble-shooting guides vi. Trainee Sleep Technologists improve the quality of work
viii. Emergency Contact Numbers vii. Manager Sleep Laboratory in the sleep clinic and sleep
The most recent version should be Sleep laboratory is fairly a busy place with (5) Expansion of services at the
g. AASM Scoring Manual: The latest ver- the responsibilities must be divided among (6) Building the team for multi-
b. Training and Research: (2) Networking with other physi- (5) Participation in various administra-
(1) Supervise the training programs cians in the geographical area tive works along with director/in-
physicians/short-term trainee (3) Running awareness campaigns (6) Completing the patients case sheet
(2) Periodic revision of the syllabus for the medical fraternity and at the time of admission
with the other members of the patients (7) Providing special instructions, if
team for trainees d. Clinical Care: any, in the case sheet before the
(3) Finding opportunities for the (1) Providing clinical care to the sleep study
further training of team members patients through sleep clinic/ (8) Monitoring the prescribed medi-
(4) Organizing departmental work- PAP clinic cations and mentioning them in
shops/training programs for the B. Sleep Physicians/Trainee Sleep the case report sheet at the time of
(5) Conducting and motivating the (1) Providing clinical care to the C. Sleep Technologists Including Trainee
duct research (2) Scoring the sleep study a. Administrative: One Sleep Tech-
c. Networking and Patient Education: (3) Conducting research in association nologist will be assigned the
(1) Develop the material for mar- with other members of the team administrative work by the local
keting and patient education (4) Participation in departmental edu- administration. He/She will be
along with team members cational programs responsible for the following duties:
468 Clinical Atlas of Polysomnography
(1) Looking after the administra- (2) Ensuring infection control 24.3 STAFF:
tion of the sleep lab in sleep laboratory, as men- QUALIFICATION, REGULAR
(2) Developing the inventory of the tioned in the protocol TRAINING, NUMBER AND
sleep lab and regularly main- section/section of infection WORKING HOURS
taining it control
(3) Refilling the consumables in the (3) Ensuring the quality of record- 24.3.1 Sleep Physicians Including
sleep lab at appropriate intervals ing of the study Director/In-Charge
(4) Keeping a record of the quality (4) Interacting with the sleep physi-
A. Qualifications:
of data recorded in the sleep lab cians for improving the services
(i) Preferably certification in sleep medicine
every day and patient care
by any international/national board after
(5) Ensuring that all the equipments (5) Participation in various activi-
graduate/post-graduate medical degree.
are functional in the sleep ties (for improving quality of
(ii) In case, board-certified person is not
(6) Communication with the bio- work, patient education) in the
available in the country, any physician
medical engineer, whenever sleep lab
having documented interest in sleep
required D. Manager - Sleep Laboratory:
medicine may be opted. In that case,
b. Clinical: a. Exploring new business
other minimum qualifications shall
(1) Recording and scoring the sleep opportunities
remain the same.
study as mentioned in the pro- b. Managing billing-related issues
B. Training:
tocol section
Sleep Lab Management 469
(i) Sleep physicians are expected to par- optimal care to the patients attending (iii) In such case, he shall undergo 6
ticipate in in-house and other training Sleep Clinic/Sleep Laboratory. months intensive training under the
programs at regular intervals to keep their (ii) In case of any emergency during supervision of Sleep Physician in the
C. Number of Sleep Physicians and Team expected to attend the patient at night as B. Training:
(i) At least one sleep physician should be participate in in-house and other train-
attached with each sleep laboratory. 24.3.2 Sleep Technologists ing programs at regular intervals to keep
(ii) Practice of sleep medicine requires multi- A. Qualifications: their knowledge updated.
disciplinary approach, and team com- (i) Preferably certification in sleep technol- (ii) Must be trained in basic life support
D. Working Hours: ogy may be opted. In that case, other for the night shift, the other for the day-
(i) Sleep physicians shall be working in 8 minimum qualifications shall remain shift, and the third, reliever, in case of
(ii) One sleep technologist will take care 24.4 WORKFLOW FROM department), the sleep physician is
of two sleep studies at a time (that SLEEP CLINIC TO SLEEP expected to thoroughly study the history,
includes one titration study) as recom- LABORATORY examine the patient and get any other
Sleep Medicine. 1. Sleep study is an elective procedure; hence, must be recorded and a provisional diagno-
D. Number of Working Hours: patients may be scheduled depending sis should be made. Provisional diagnosis
(i) Each night shift will be spanning 12 upon the number of beds in the facility and must include other comorbid illnesses as
hours starting at 20.00 to 8.00 AM for 5 patient load. However, at the same time, well.
days. In usual circumstances, no study Director/In-Charge of the facility should 4. Findings must be discussed with the patient
shall be recorded on Saturday and Sun- try to reduce the waiting period as far as and the reason for the sleep study should be
(ii) Sleep Technologists shall be given two 2. Patients may be given appointments after 5. Based on the provisional diagnosis, if any
days off after 5 working nights. a Sleep Physician has examined them. In intervention is required before the sleep
(iii) The daytime technicians would cases of patients referred from other physi- study, it may be done.
undertake tasks such as performing cians as well, it is best that the patients pay 6. In case, based upon his/her clinical
MSLT, MWT, Scoring, Teaching and at least one visit to the Sleep Physician, judgment, the sleep physician desires to
Training, and other administrative before the sleep study. discontinue some medications before
duties. 3. During the visit in the Sleep Clinic (which the sleep study, the patient should be
is usually situated in an outpatient’s informed.
Sleep Lab Management 471
7. Appointment should be scheduled according allowed to spend time in the sleep lab. This 16. All records must be kept as per the policy
to the local hospital policy (some hospitals will help in acclimatization. of the facility.
may require part payment in advance for 11. Before admitting the patient in the Sleep 17. In case of voluntary termination of a
scheduling an appointment; in case of medi- Laboratory, it is mandatory to take informed sleep study, appropriate protocol must be
cal insurance, a process has to be initiated consent in writing to conduct the sleep study. followed.
with the appropriate person of the facility). 12. After the diagnostic study, the patient 18. Report should be provided to the patient
8. Patient should preferably be given a pam- should be requested to fill the information within a week of the sleep study.
the study will be done, and what is expected 13. Before the CPAP study, the patient should
from him/her on the day of study. be handed over a clean and autoclaved 24.5 POLICY FOR
9. In general, two nights should be given to mask in the morning by the sleep technolo- ACCOUNTING AND
the patient: First for the diagnosis and, gist. The patient should be instructed to BUDGETING
second, for the intervention, if required. practice wearing it during the day so as to
However, the sleep physician may use facilitate acclimatization. 1. This should be done according to the policy
his/her clinical judgment for the split- 14. Take the informed consent in writing for of the facility, where the sleep laboratory is
10. On the day of the sleep study, the patient 15. After the sleep study, information must be 2. Sleep Physicians and sleep technologists
should be called at least 6–8 hours before obtained from the patient using appropri- musts obtain professional indemnity insur-
his/her usual bedtime and should be ate questionnaires. ance according to the policy of the facility.
472 Clinical Atlas of Polysomnography
Table 24.1 Format for the Accounting in a Sleep Laboratory feedback may help in improving the
Date Name of patient/purchased article Receipt Number Income Expenditure
standards.
b. Sleep Technologists:
3. In-Charge Sleep technologist of the facil- best serve the patients. To achieve this, the subject and that they are engaged
ity should maintain monthly record in the following must be ensured: in advancement of their knowledge
following format (Table 24.1). This must be a. By the In-Charge Sleep Technologist: by attending periodic trainings.
get signed by the Director/In-charge of the i. All the measures to prevent infec- ii. They must ensure that they stick
facility at the end of the month. tion control are taken in the sleep to the protocols developed by the
lab. facility.
ii. All t parts of the equipments are iii. If there is any mal-function in the
24.6 POLICY FOR QUALITY
working and consumables are equipments or if there is any patient-
ASSURANCE
refilled before their exhaustion. related issue, they should bring it to
iii. Hygiene is maintained in the sleep the notice of In-Charge Sleep Tech-
1. Assuring the quality of data is an important
laboratory and monitoring room. nologist and/or Director/In-Charge
parameter for the success of the sleep disor-
iv. Patients are providing informa- of the sleep clinic at the earliest.
ders center. A center should try to achieve
tion regarding their experience iv. They must ensure that their behav-
the highest standards of the quality so as to
before and after the test, as their ior with the patients is professional.
Sleep Lab Management 473
v. They must encourage the patient ii. In case some action for rectification The American Academy of Sleep Medicine
to provide post-test information in is required, they must ensure that has proposed some indicators for the quality
appropriate form. they take a prompt action. assurance. These are tabulated in Table 24.3.
vi. They should score the data as per iii. They must ensure that the record-
the latest guidelines from the Amer- ings are assessed daily for the qual-
ican Academy of Sleep Medicine. ity and that the sleep technologists 24.7 POLICY FOR
c. Sleep Physicians Including Director/ get the feedback (Table 24.2). MAINTAINING THE RECORDS
In-Charge: iv. They must ensure that they conduct a
Records in the Sleep Clinic and Sleep Laboratory
i. They are responsible for the overall monthly meeting with all staff members to
should be maintained for a minimum duration as
functioning of the sleep clinic and rectify all issues related to patients, equip-
advised by the local administration of the law of
sleep lab. They must ensure that they ments, quality of recordings, and overall
land. Two kinds of records are required in a sleep
get regular feedbacks from the staff. services of the facility.
laboratory—one for administrative purpose and Table 24.4 Format for the Inventory Register
S. Date Manufac- Equipment/ Num- Number Number of Signature Sign of
the others that are related to the patients.
No. turer Part number ber of of arti- articles/ of Sleep direc-
articles/ cles/parts parts dis- tech tor/In-
Administrative records include inventory
parts procured carded Charge
available of the
register (Table 24.4), appointment register
facility
(Table 24.5), service logs of the equipments
are provided here, although they may be modi- Table 24.5 Template for Appointment Register
Patient ID Name Age/Gender Contact Diagno- Type of Referred Special In-
fied for individual facility. Number sis Sleep by structions
Study for Sleep
Patient-related records are important not required Tech, if
any
only for future references but also for the medi-
local policy.
A. Case record form must be completed at the Table 24.6 Template for Service log
time of admission after obtaining written Date Problem in Equip- Recommenda- Equipment/component: Serviced Signatures
the equip- ment/part tion made serviced/Changed by of Sleep
informed consent. Case record form must ment/part inspected Tech
by
bear at least the following:
• Patient ID number
476 Clinical Atlas of Polysomnography
• Demographic data B. Raw data of sleep study: Raw data may be a. Gold Cup Electrodes are properly
• Contact number stored for variable duration, depending cleaned after every study.
• Informed consent for the sleep study upon the local policy. Some facilities may They must be cleaned using mild
and PAP choose to store the data for training and soap and water. A toothbrush with soft
• Medical history research purpose as well. bristles may be used to remove paste
• Findings of other laboratory investiga- 24.8 POLICY FOR INFECTION b. Sticking electrodes/Button electrodes
tions, if required CONTROL IN THE SLEEP LAB are to be disposed after every use.
h. Mask of the CPAP, hosepipe and straps E. Precautions to be taken by the Sleep A. Cardiac arrhythmias
are cleaned with lukewarm water after Technologists to Prevent Infection: B. Precordial chest pain
every study and then sent for Ethylene i. They must wear clean clothes. C. Seizures
Oxide Sterilization. ii. They must wear gloves while apply- D. Dyspnea
i. Do not apply the electrodes on the ing electrodes and other sensors on 2. Policy to handle such situations:
parts of skin where there is a breach in the patients. A. Sleep technologists must possess ade-
continuity. iii. If they have any active respiratory quate knowledge and skills to recognize
C. Maintenance of Hygiene in the Sleep Lab: infection, they must seek medical and handle such events.
a. Sleep lab technician along with the advice at the earliest and start treat- B. In countries where sleep technology
nursing in-charge of the ward will ment. If they have been allowed to certification is not available, sleep tech-
ensure that: handle patients by the physician, nologists must be trained to recognize
b. The bed linen/pillow-cover is changed they must wear a mask while in the and handle such events.
after every study. sleep lab. C. Such situations may require different
c. Area where machines are kept in the levels of experience, knowledge, and
sleep lab is clean and free of dust. 24.9 POLICY IN CASE OF skills. Hence, sleep technologist must
d. There is free circulation of air after ANY EMERGENCY DURING involve the nursing staff, trainee-phy-
every study. SLEEP STUDY sicians and sleep physician of the facil-
e. The washroom attached to the sleep lab ity while handling such a situation.
1. Common emergency situations that can
is clean and hygienic. D. Course of action in such cases:
arise during a sleep study:
478 Clinical Atlas of Polysomnography
In such cases, the sleep technolo- In such cases, the trainee-physician iv. Call the physicians/surgeons from
gist is expected to initiate the following is expected to take the following course other specialties, if required.
i. Inform the nursing staff in the i. Assess the gravity of the situation. if required.
facility ii. Provide optimal care to the patient. E. Once the patient is stabilized, sleep
ii. If dyspnea occurs during a titration iii. Work with the sleep technologist physicians and sleep technologists
study, remove the mask and turn off and attending nursing staff in the must review the event to uncover its
the PAP machine. benefit of the patient. possible reasons by examining the case
iii. Provide basic life support to the iv. Call the physicians/surgeons from record forms. The discussion must be
In such a case, nursing staff is expected to In such cases, the sleep physician on be ensured for future, if possible.
initiate the following course of action: call is expected to take the following
b. Please check the case record sheet for f. Ensure that the patient has taken 4. Placement of respiratory sensors:
special instructions, if any. medications, as prescribed by the a. RIP belts are to be placed on the thorax
2. Preparation of the patient: physicians and approved by the sleep and abdomen. Please adjust the belts so
a. Please ensure that hair and face of the physician. that the unstretched belt covers two-
patient are free of oil and grease. 3. Placing the electrodes on the patient’s third of the circumference for improving
b. In cases of males, please ensure that body: the signals and longevity of the belts.
the patient is shaven, unless he wears a a. Start placing electrodes (EEG/EOG/ b. Both thermister as well as cannula
beard for personal or religious practice. EMG/ECG) 45 min before the should be placed and fixed properly.
In that case, please ensure that the beard patient’s usual bed-time. c. Make sure the cannula is attached to the
is free of greasy material. b. Please clean the area and prepare it with Capnograph at the appropriate time to
c. Please ensure that the patient is Neuroprep gel. ensure EtCO2 signals.
comfortable and is wearing proper c. Use adequate amount of the conductive d. Place the oximeter properly so that it
d. Ensure that the air-conditioner is d. Electrodes are to be fixed as per the 5. Place the body position sensor over the
working properly and the temperature is AASM manual ver. 2.3 released in chest belt in the middle of the chest.
e. Blanket/sheet is to be made available to e. Please fix electrodes so as to minimize a. Please fill the name, age, gender, and ID
the patient. the chances of their falling off at night. of the patient.
480 Clinical Atlas of Polysomnography
b. Please fill the anthropometric data e. Please check that the oximeter and a. Please check all the signals periodically
(height/weight). capnograph signals are proper. and enter the signal quality at an interval
c. Please fill the name of the referring f. Please check that the body position is of 30 min in the patient’s file, till the end
d. Please choose the appropriate montage g. Please check that the video and audio b. Audio and video signals from the sleep
(Diagnostic/Seizure/Parasomnia). signals are working properly. lab are to be kept turned-on during the
7. Checking the signals and biocalibration h. If any of these signals are not whole study.
before lights off: appropriate, fix the electrode using c. Please make yourself available in case of
a. Please check the impedance from appropriate measures, as conveyed any assistance required by the patient
electrodes and make sure that it is below during your training. during the study.
5 K Ohms in the EEG/EMG/EOG i. Do the bio-calibration before every d. If any unusual behavior is seen, mention
leads. study. Put a note in the patient’s record it in the patient’s file along with the time
leads have good quality signals and are 8. If all the signals are adequate and have 10. Terminating the study:
free from artifacts. good quality, then start the record- a. Study to be terminated at the usual
c. Please check that the ECG signals are of ing and ask the attendants to turn off wake time of patient or at 7.00 AM.
good quality. the lights. Place a marker in the sleep b. Please ensure proper closure of the study.
d. Please check that the respiratory flow recording. c. Ensure that data has been transferred to
signals are appearing properly. 9. During the study: the computer system before turning off
11. After the study: beard for personal or religious practice. e. Please fix the electrodes so as to
a. Please remove the electrodes so as to In that case, please ensure that the beard minimize the chances of their falling off
b. Electrodes are to be cleaned after the c. Please ensure that the patient is com- 3. Placement of respiratory sensors:
study. fortable and is wearing proper clothes. a. RIP belts are to be placed on the thorax
c. Place all sensors at an appropriate place d. Ensure that the air-conditioner is working and abdomen. Please adjust the belts
so as to minimize damage. properly and the temperature is set at 22°C so that the unstretched belt covers
d. If data of a diagnostic study suggest e. Blanket/sheet is to be made available to two-third of the circumference for
that titration is required, please the patient. improving the signals and longevity of
provide mask to the patient with 2. Placing the electrodes on the patient’s the belts.
instruction to wear it during the day for body: b. Place fix the mask properly and make it
acclimatization. a. Start placing electrodes (EEG/EOG/ comfortable for the patient. Attach it to
1. Preparation of the patient: Neuroprep gel. 4. Place the body position sensor over the
a. Please ensure that hair and face of the c. Use adequate amount of the conductive chest belt in the middle of the chest
patient are free of oil and grease. gel. 5. Recording the study:
b. In cases of males, please ensure that d. Electrodes are to fixed as per the AASM
a. Please fill the name, age, gender and ID e. Please check that the oximeter signals b. Please check all the signals periodically
of the patient are proper. and enter the signal quality at an interval
b. Please fill the antropometric data f. Please check that the body position is of 30 min in the patient’s file, till the end
c. Please fill the name of referring g. Please check that the video and audio c. Please mention the PAP pressure in
Physician signals are working properly. the file at 30 min interval along with
d. Please choose appropriate montage h. If any of these signals are not number of hypopneas and apneas seen
(Titration) appropriate, fix the electrode using during the preceding 30 min.
6. Checking the signals before lights off: appropriate measures as conveyed d. Audio and video signals from the sleep
a. Please check the impedance from during your training. lab are to be kept turned on during the
electrodes and make sure that it is below i. Perform bio-calibration before every study. whole study.
5 K Ohms in the EEG/EMG/EOG leads. Put a note in the patient’s record sheet. e. Please make yourself available in case of
b. Please check that the EEG/EOG/EMG 7. If all the signals are adequate and have any assistance required by the patient
leads have good quality signals and are good quality, then start the recording during the study.
free from artifacts. and ask the attendants to turn off the f. If any unusual behavior is seen, mention
c. Please check that the ECG signals are of lights. it in the patient’s file along with time
d. Please check that the respiratory flow a. Titrate the pressure of PAP as per 9. Terminating the study:
a. Study to be terminated at the usual a. This should be done after the diagnos- Any other measure to promote wake-
wake time of the patient or at 7.00 a.m. tic study. During the diagnostic study, fulness should be terminated at least
b. Please ensure proper closure of the study. sleep apnea and any other cause that 15 min prior to every nap opportunity.
c. Ensure that data has been transferred to may lead to sleep disruption should be Drug screening may be performed in
the computer system before turning off ruled out. selected cases.
the computer system. b. Total sleep time during the previous B. Starting the test:
10. After the study: night should be at least 6 hours. a. The test is started in the morning at
a. Please remove the electrodes so as to c. Get the sleep log for at least one week least two hours after waking up. The
cause minimum pain to the patient. prior to the MSLT. patient should be given a light break-
b. Electrodes are to be cleaned after the d. Stimulant medications or medications fast. Light lunch should be provided
c. Place all sensors at the appropriate place drawn at least two weeks ahead of the b. Five opportunities for the sleep are
so as to minimize damage. test. Physician consultation should be provided, 2 hours apart during the
d. Please hand-over the mask to the done to avoid the influence of hypnotic day.
in-charge of the ward for autoclaving. medication on the day of the test. Vigor- C. Preparing the patient and the lab:
ous physical activity, exposure to bright a. The sleep lab should be sufficiently
24.10.3 Protocol for the Multiple light, smoking, and caffeine should be dark and quiet to promote sleep. The
Sleep Latency Test (MSLT) avoided on the day of the test, as they temperature of the lab should be
b. Make sure that the scalp and face of nap and request him/her to lie down be filled in the “MSLT
the patient are free of any grease/oil. and be comfortable in bed. questionnaire.”
c. Patient’s clothes must be comfortable E. Duration of the each recording d. Report “start and stop time,”
and should not be synthetic. during the test: “sleep onset latency from lights out,”
d. Make sure that the patient’s sleep is a. Recording should be done for 20 min. for each recording, and “Mean
not disrupted because of any other If the patient does not fall asleep dur- sleep latency” and “number of
reason, for example, going to the ing 20 min, record sleep latency as 20 sleep onset REM (SOREM) out
e. Apply the EEG electrodes, EOG elec- b. If the patient falls asleep during this REM appearing within 15 min
trodes, chin EMG, and EKG for the 20 min, from the first epoch-defining of the sleep onset during a
b. Instruct the patient “Please close your min. 24.11.1 Forms, Questionnaires, and
eyes and try to fall asleep” before the c. After each nap, the patient should be Templates
asked and information should
Sleep Lab Management 485
1. Facility may carry out sleep study as mentioned above along with video-audio recording.
2. Facility may/may not use the data arising out of my investigation for the research/teaching purpose provided my identity is kept anonymous.
3. Facility may/may not use the audio-video data arising out of my investigation for the research/teaching purpose provided my identity is kept anonymous.
I, __________________ hereby declare that I have been explained in detail regarding my medical condition by Dr. __________________ on date.
I confirm that:
1. I have been advised to undergo sleep study/sleep study with PAP titration by my treating Physician.
2. I am not able to undergo the diagnostic sleep study/sleep study with PAP titration for the following reason: _________________ .
3. I am aware that not undergoing the sleep study/PAP titration may have adverse consequences on my health.
4. Despite knowing the possible adverse consequences, I am requesting the Sleep Technologist to terminate the sleep study.
5. If any untoward medical condition emerges in future, because of this reason (termination of sleep study on my request), I shall myself be responsible
for that.
Information to be filled by Sleep technologist during diagnostic sleep study at interval of 30 minutes
Study Started at ________ All information filled as mentioned in proto- Patient’s pre and posttest information Any other information you wish to pro-
col: Yes/No received and filed? Yes/No vide _______________
Body posi-
LEG EMG
Audio and
tory effort
tory Flow
Respira-
Respira-
Capno-
Video
graph
Time
SpO2
EOG
EKG
EEG
tion
Sleep Lab Management 489
Information to be filled by Sleep technologist during titration sleep study at interval of 30 minutes
Name: Gender: M/F
Age: …. years UHID: …………
Date of testing: ……….
Time PAP pressure Leak Apneas/Hypopneas Oxygen rate Sleep Stage Body position
EPAP IPAP observed
490 Clinical Atlas of Polysomnography
1. George, C. F. (1996). Standards for polysom- 4. American Academy of Sleep Medicine. Sleep
of the Canadian Sleep Society and the Canadian American Academy of Sleep Medicine, Wesches-
LEARNING OBJECTIVES
CONTENTS
After reading this chapter, reader should be able to:
1. Compute the financial viability of a sleep laboratory. 25.1 Revenue for Two Beds..................................................................... 500
25.2 Hospital-Owned/Academic/Medical College Programs........ 504
A good Sleep Center should have state-of-the-art sleep suites designed and
decorated for optimum patient comfort. Each suite should have its own
flat-panel television, queen-sized bed, and private bathroom. The manpower team
for a full range of sleep disorders, and certified physicians/specialists in sleep med-
icine to evaluate the test results, and prescribe an effective course of treatment so
There are three basic business structures for 25.1 REVENUE FOR TWO when managed optimally. Per Patient Revenue
physician-based sleep labs: BEDS for year 1 is considered at Rs. 15,000. A nominal
2. Independent diagnostic and testing facility; It is assumed that 300 patients can be accommo- revenue is considered.
and dated for one Sleep Lab (two beds, where one The breakeven for one sleep lab with the
3. Academic/medical college sleep programs. patient requires two nights of study; this calcula- assumed cost and revenue will happen in 4 years
A single trained technician can take care tion does not include split-night study) per year (Tables 25.4 and 25.5).
expenditure incurred.
25.2 HOSPITAL OWNED/ identified and adequately treated, health is a major priority for hospitals. If
ACADEMIC/MEDICAL costs and health-care utilization decrease. institutional leaders can be convinced
COLLEGE PROGRAMS • Identifying and treating sleep disorders that treatment of patients with sleep
improves comorbidities: Studies have apnea prevents readmission, they may
25.2.1 Raising Awareness of the indicated benefit from identification be more willing to support sleep center
“Unrecognized Benefits” of Having and treatment of sleep apnea, on programs. For example, patients with
a Sleep Center cardiovascular disease (hypertension, decompensated heart failure have both
arrhythmias, heart failure, and stroke) high risk for readmission and high
Given the current evolving environment of
and diabetes. Addressing sleep frequency of undiagnosed sleep apnea; for
health care, it is difficult to predict the level of prof-
apnea also likely improves symptoms such patients, Sleep Centers may be able
itability of sleep programs. As such, it becomes
associated with psychiatric illness. These to improve patient health and hospital
imperative for academic sleep centers to impress
improvements can decrease long-term, readmission rates simultaneously.
upon institutional leaders the vital role and
health-care costs. • Identifying and treating sleep apnea
“unrecognized benefits” of having an academic
• Identifying and treating sleep disorders is increasingly important to surgical
sleep center as part of their operations. Additional
improves quality of life: This too has been services: Growing data highlight the
outcomes research should be targeted to quantify
shown in a number of randomized trials. risk patients with sleep apnea face when
benefits and cost savings. Examples might include:
• Identifying and treating sleep disorders undergoing surgery, especially if sleep
• Identifying and treating sleep disorders
may help to reduce readmission rates: apnea is unexpected or undiagnosed.
saves health care costs: Numerous studies
Prevention of unnecessary readmission
have shown that once sleep apnea is
Financial Viability for a Sleep Lab 505
Identifying and treating these disorders for management of patients with sleep
could improve employee performance and disorders. This idea could require somewhat
outcomes as:
sleep disorders.
GLOSSARY
Active wakefulness: it is seen as mixed frequency Arousal index: the arousal index (ArI) is the specified in the hypopnea rules for adults.
EEG along with darting eye movements and total number of arousals per hour of sleep. The reduction in airflow must be accompa-
high muscle tone during a sleep study. Central apnea: it occurs when both airflow and nied by a ≥3% desaturation or an arousal or
Apnea: cessation of airflow or (≥90%) decrease ventilator effort are absent. a ≥4% desaturation.
in apnea sensor excursions compared to Cheyne-Stokes breathing (CSB): a breath- Hypoventilation: a specified period of increased
baseline of a minimum duration of ten ing rhythm with a specified crescendo and PaCO2 of >50 mmHg in children or >55
seconds in adults. Apneas are classified as decrescendo change in breathing amplitude mmHg in adults, or a rise of PaCO2 during
obstructive, mixed, or central based on the separating central apneas or hypopneas. sleep of ≥10 mmHg that exceeds 50 mmHg
pattern of respiratory effort. Desaturation: oxygen desaturation is a fre- for a specified period of time in adults.
Apnea hypopnea index: the apnea hypopnea quent consequence of apnea and hypopnea. Mixed apnea: it occurs when there is an interval
index (AHI) is the total number of apneas Several measures are used to quantify the during which there is no respiratory effort
and hypopneas per hour of sleep. severity of desaturation. (i.e., central apnea pattern) followed by an
Apnea index: the apnea index (AI) is the total Hypopnea: it is a reduction in airflow with interval during which there is obstructed
number of apneas per hour of sleep. the minimum amplitude and duration as respiratory efforts.
508 Clinical Atlas of Polysomnography
Obstructive apnea: it occurs when airflow is Respiratory effort related arousals: they are Respiratory events: the respiratory events are
absent or nearly absent, in the presence of the sequences of breaths characterized by defined as breathing abnormalities during
Posterior dominant rhythm: it is seen in the (PAP) device flow channel; or an increase in
occipital channels of EEG during quiet end-tidal partial pressure of carbon dioxide
Quiet wakefulness: it appears as slow eye from sleep. Respiratory effort related arousals
movement and alpha in the EEG and do not meet criteria for hypopnea and have a
Respiratory disturbance index: the respira- children. RERAs (>5 events per hour) associ-
tory disturbance index (RDI) is the total ated with daytime sleepiness were previously
number of events (e.g., apneas, hypopneas, called upper airway resistance syndrome
and RERAs) per hour of sleep. The RDI (UARS), which was considered a subtype
is generally higher than the AHI, because of obstructive sleep apnea (OSA). These
the RDI includes the frequency of RERAs, patients have abnormal sleep and cardiore-
while the AHI does not. spiratory changes typically found in OSA.
INDEX
A Alpha obstructive, 22, 27, 40, 41, 43, 47, 101, 198, 209, 214, 219,
rhythms, 14 340, 350, 351, 358, 394, 397, 400, 440, 441, 443, 448,
AASM scoring manual, 388
waves during wakefulness, 200 450, 455, 456, 507, 508
Abnormal sleep, 508
Alternate leg muscle activity, 209 hypopnea index, 23, 25, 26, 350, 440, 507, 508
Acceptable EOG derivations, 136
Alternating current, 60, 61, 99, 107 Arousal, 1, 270, 284–86, 290–292, 295, 297, 325, 330, 331, 333,
Acetylcholine, 15, 56, 58
American Academy of Sleep Medicine, 23, 24, 26, 41, 43, 45, 46, 350, 352, 354, 355, 363, 365, 408, 411–413, 440, 450, 507,
Action potential, 13, 53, 55–58, 60, 85
77, 111, 121, 122, 198, 270, 388, 434, 440, 444, 453, 466, 470, 508
Active
473, 479, 481, 482 index, 440, 450, 507
respiratory infection, 460, 477
Amplitude, 9, 12, 39, 61, 62, 67, 69, 73, 77, 79, 84, 87, 93, 94, 99, Arrhythmia, 22, 209
wakefulness, 199, 271, 507
100, 110, 186, 244, 284, 313, 315, 320, 340, 341, 343, 344, Arterial blood, 508
darting eye movements, 89, 507
352, 354, 355, 363, 406–408, 411–414, 507 gas analysis (ABG), 26–28
high muscle tone, 507
Annual maintenance contract (AMC), 502 Artifacts, 47, 48, 67, 68, 70, 77, 88, 116, 134, 179, 192, 194, 199,
Acute
Anterior tibialis muscle, 131, 132 253–262, 264–266, 280, 315, 388, 432, 480, 482
hypercapnic respiratory failure, 27
Anteroposteriorly, 73 cardioballistic artifact, 254
pulmonary edema. See PAP
Antihistamines, 30 EKG artifact, 254, 267
Adaptive servo-ventilation, 25, 26
Apnea, 16, 22–24, 26, 38, 40, 41, 43, 46, 47, 99, 101, 198, 209, electrical artifact, 254, 267
Adolescence, 2, 405, 406
212, 214, 219, 247, 266, 340, 342, 345, 346–351, 357, 358, electrode pop artifact, 254, 255, 267
Adrenaline, 56
363, 388, 394, 397, 401, 408, 419, 440, 441, 448, 450, 483, localized artifacts, 254
Advancement of the machines, 45
504, 507, 508 movement artifact, 254, 267
Airborne infection, 460
classifications muscle artifact, 254, 267
Air-conditioning, 116
central apnea, 340, 408, 507 physiological activities of orofacial structures, 254, 267
Airflow measures, 98
central based on the pattern of respiratory effort, 507 respiration artifact
Alcohol, 30, 425, 460, 476, 494
mixed, 507 sweating artifact, 254
Alice 6 from Philips Respironics, 44
510 Clinical Atlas of Polysomnography
Circadian Delta waves, 6, 9, 16, 39, 89, 135, 198, 204, 206, 208, 306, 313, filters, 71
clock, 4 314, 316 ground, 71
process, 3 frontal derivations, 91, 185, 186, 205, 206, 208, 289, 313, 407 polarity, 70
rhythm, 3, 5, 6, 30 Deoxygenated blood, 107 Electrical potential, 54, 61, 88, 93, 94, 124, 263, 432, 433
Coma, 2 Deoxyhemoglobin, 107 Electrical potentials of neurons, muscles, and heart, 54
Common mode rejection (CMR), 69, 71, 88 Depolarization, 13, 15, 56, 58, 87, 93 action potential of the neuron, 55
ratio (CMRR), 69 Depression, 23, 394, 398 communication between nerves and muscles, 58
Common sleep disorders, 21. See Obstructive sleep apnea Desaturation, 23, 27, 109, 340, 343–345, 348, 355, 394, 396, potential generation across cardiac muscles, 60
Concepts of aliasing, filter setting, sampling rate, 107 397, 399–401, 403, 408, 414, 450, 454–456, 507 resting membrane potential, 54
polarity, 99 Devices for oxygen delivery, 454 Electrical signals, 54, 74, 85, 87, 118, 124, 221
Concepts related to digitalized recordings, 77 Diabetes mellitus, 30 Electrocardiogram, 41, 45, 93, 132, 209, 215, 233
Continuous positive airway pressure, 23, 25, 27, 28, 394, 397, Diagnosis, 23, 24, 26–30, 43, 48, 49, 197, 209, 214, 267, 387, ECG, 26, 41, 54, 67, 68, 85, 88, 93, 94, 98, 132, 137, 183, 254,
401, 403, 419, 427, 439–441, 443, 455, 456, 465, 471, 474, 388, 424, 455, 470, 471, 475, 476, 485, 487 372–381, 387, 394, 397, 479, 480, 481, 482
477, 496, 501 Difference of polarity between cornea and retina, 89 EKG, 54, 67, 117, 118, 223, 236, 254, 259–261, 267, 382,
Contraction, 59, 60, 67, 88, 93, 94, 192, 219, 267 Dipole, 61 420, 421, 450, 473, 484, 488, 490
Coronal plane, 127 Direct current, 60, 61, 99, 101 Electrocardiography, 26, 38
Cortex, 4, 13–16, 85–88, 253 Dopamine agonists, 30, 31 Electrodes, 13, 38, 41, 43, 60, 70, 71, 85–89, 90, 93, 94, 116,
association fibers, 13 carbidopa-levodopa (sinemet), 30 118, 122, 124, 126, 128–132, 136, 137, 204, 221, 226, 227,
glial cells, 13, 86 pramipexole, 30 253, 254, 261–263, 363, 406, 420, 421, 432, 433, 434, 460,
interneurons, 13 ropinirole, 30 464, 476, 477, 479–484, 501
neurons, 13 Dorsomedial hypothalamus, 4, 5 Electroencephalogram, 1, 6–8, 11–13, 15–17, 38, 39, 41, 45, 54,
projection fibers, 13 57, 62, 67, 68, 70, 77, 80, 82, 85–87, 89, 117, 118, 122, 124–
pyramidal cells, 13, 14, 16 E 130, 133, 134, 183, 192, 194, 198, 199, 204, 209, 218, 230,
Cortical pyramidal neurons, 13 235, 236, 253, 258, –260, 262, 263, 270, 271, 273, 275–282,
Easy III device, 44
Crescendo-decrescendo breathing pattern, 350 284, 285, 287, 293, 295, 301–303, 308, 315, 321, 322, 325,
Efferents, 14
336, 359, 388, 405–407, 409, 410, 420, 421, 432, 448, 460,
Electrical calibration, 184
D 465, 469, 473, 479–482, 484, 488, 490, 501, 507, 508
Electrical concepts, 60
Electromagnetic field, 117
Daytime sleepiness, 22, 26, 28, 29, 508 amplifiers, 61, 69, 84
stray capacitance, 117
Decreased memory, 23 amplification, 61
stray inductance, 117
Deep sleep, N3, 2, 3, 6, 9, 11, 12, 16, 96, 122, 198, 270, 276, 284, differential discrimination, 61
Electromyogram (EMG), 17, 38, 39, 41, 43, 54, 59, 60, 67, 68,
306, 313, 314, 315, 316, 317, 394, 396, 397, 406, 407, 408, basic concepts of electricity, 60
85, 89, 93, 94, 95, 117, 118, 131, 136, 189, 190, 192, 194, 204,
450 dipole, 53, 57, 61, 86, 90, 94, 263
512 Clinical Atlas of Polysomnography
210, 219, 230, 276, 321, 322, 325, 350, 359, 363, 366, 367, F Histogram, 391, 393–395, 403
369, 370, 406, 420, 421, 434, 448, 460, 473, 479, 480–482, Homeostatic process, 3, 4, 16
Filters, 71
484, 488, 490, 501 brain, 3
Fomite, 460
Electrooculogram (EOG), 17, 38, 39, 41, 54, 85, 88–90, hypothalamus, 3–5
Forms, questionnaires, and templates, 484
129–131, 134, 136, 186, 194, 199, 204, 230, 263, 276, 289, Home sleep testing (HST), 23, 46, 49, 198
308, 321, 406, 420, 421, 433, 448, 473, 479–482, 484, 488, Hosepipe, 460, 477, 481
490, 501
G Hospital owned/academic/medical college programs, 504
Electrophysiological, 14, 221 GABA House Keeper, 501, 502
Electrophysiology aspects of sleep, 2 γ-aminobutyric acid, 4, 56 Human scalp, 38
Endocardium, 93 GABAergic neurons, 3, 14, 15 Hyperpolarization, 13, 16, 87
End tidal CO2 (ETCO2), 26, 54, 111, 216, 350 Gastroesophageal reflux disease, 43, 214 Hypertension, 23, 27, 448, 450, 504
Epochs, 235, 236, 273, 292, 293, 308, 311, 315, 322, 323, 336, Gastrointestinal (tract), 40 Hypnagogic
337, 355, 363, 371, 406, 421 General maintenance, 501, 502 hypersynchrony, 408
concepts, 235 Glutamate (Glu), 56 foot tremor, 209
EEG signals using different filters, 80 Grade 1 AV block, 380 hypersynchrony, 409, 410
Espohageal manometery, 214 Guidelines Hypnogram, 11, 270, 391, 392, 394, 402, 403, 441–443, 447,
Excessive supplemental oxygen, 453 450
daytime sleepiness (EDS), 22, 23, 26, 28 Hypocretin, 3
fragmentary myoclonus (EFM), 209 H Hypopnea, 16, 23, 24, 40, 99–101, 209, 245, 247, 340, 342–347,
salivation during sleep, 22 350, 352, 355, 357, 394, 397, 399, 408, 411–414, 440, 441,
Head circumference, 128, 129
sweating, 22 450, 507, 508
Heart
Excitatory postsynaptic potential, 53, 56, 57, 85, 124 Hypothyroidism, 26
failure, 23–27, 46, 107, 504
Extended Hypoventilation, 26–28, 43, 111, 214, 340, 350, 450, 454, 507
rate, 38, 39, 41, 270, 378, 394, 448
montage for seizures, 218 Hypoxemia, 22, 28, 40, 109, 214, 340
rate variability, 394
parameters for special circumstances, 219
bradycardia, 378, 394, 397
External stimuli, 2, 12 I
tachycardia, 374, 379, 394, 397
auditory, 2
Hemispheres, 71, 204, 406 Idiopathic central alveolar hypoventilation syndrome, 26
tactile in nature, 2
Hertz; a measure of frequency (cycles per second), 9, 12, 16, 60, Idiopathic hypersomnia, 40
Eye movements during
71, 77, 99, 101–103, 107, 254, 258, 267, 271, 276, 284, 287, Impedance, 61, 69, 70, 71, 74, 85, 183, 186, 253, 254, 267, 418,
REM-opposite phase, 134
288, 313, 315, 320, 339, 363, 406–410 432–434, 480, 482
wake state-opposite phase, 133
High-frequency filter, 77, 81–83, 99, 101, 103, 107 Infant, 2
High threshold bursting (HTB), 15 Infection, 116, 459, 460, 468, 472, 476, 477
Index 513
control, 459, 476 Low-frequency filter (LFF) (high pass filter), 77, 81–83, 99, titration study, 40, 223, 225, 350, 419, 434, 439–441, 444,
Informative report writing, 447 102, 107, 258, 267 470, 478
Inhibitory postsynaptic potential, 56, 57, 85 Lung parenchymal, 26 Morning headache, 22
Inion, 124 Multiple sleep latency test, 29, 48, 417, 419, 420, 428, 470, 474,
Insomnia, 22, 24, 40, 198, 402, 450 M 483–485, 497
Instructions to the patients before sleep study, 118 questionnaire, 428, 497
Maintenance of wakefulness test (MWT), 48, 417, 420, 470,
Insulin resistance, 23 Muscle
485
Internal stimuli, 2 contraction, 59, 60
Malfunction of one electrode, 123
anxiety, 2, 116, 117 tone, 6, 12, 28, 39, 96, 270, 315, 507
Management, 24, 27, 29, 463
dyspnea, 2, 24, 478 weakness, 26
OHS, 27
pain, 2, 424, 477, 481, 483 Myelination, 405
Manual titration with PAP, 418, 439, 440, 485
Interpretation of histograms, 391 Myocytes, 55, 58, 60, 93
Mastoid, 41, 43, 71, 88, 122, 124, 129, 131, 136, 198, 226, 267,
Iron deficiency, 30, 31 Mysteries of sleep, 37
448
Ischemic heart disease, 23
Medication use, 26
Methylphenidate, 29 N
J Microsleep, 273, 274 Narcolepsy, 3, 16, 28, 29, 40, 394, 398
Jaw size, 23 Mid-adolescence, 2 cataplexy, 28
Junction, 15, 132 Middle-aged women, 22 hypnagogic hallucination, 28
Mixed apnea, 351, 408, 507 interrupted fragmented sleep, 29
K Modafinil, 29 irresistible attacks of sleep, 28
Montage, 72, 73, 116, 125–130, 148, 164, 218, 221–224, sleep paralysis, 28
K complexes in frontal derivations, 205
226–229, 480, 482 Nasal
Kleine-Levine syndrome (KLS), 40
bipolar montage, 73, 227, 229 airflow, 137
diagnostic study, 224, 235, 350, 395, 398, 400, 417–419, 434, cannula, 45, 98, 100, 111, 138, 139, 214, 340, 352, 353, 419,
L 449, 471, 481, 483 448, 454, 460
Laboratory tests, 26 referential montage, 226, 228 oral airway, 98
Leg movements, 248–250, 350, 359, 360, 364, 365 scoring Nasion, 124
Lenz’s law, 101 electrocardiogram, 233 Neuro-biological mechanisms, 122
Level I polysomnography, 54 leg movement, 232 Neurobiology, 3
Limb movement, 40, 198, 204, 350, 361, 362 respiratory data, 231 basal forebrain, 3
Lithium, 30 sleep stages, 204, 230, 276 characteristics, 3
Locus coeruleus, 3 GABAergic neurons, 3, 14, 15
514 Clinical Atlas of Polysomnography
glutaminergic neurons, 3 N1 sleep, 2, 6, 7, 12, 15, 24, 122, 270, 273–279, 282–286, Out-of-center, 46, 49
hypocretin, 3 291, 292, 295, 297, 298, 305, 315, 324, 326, 327, 333, 334, Oxygen, 25, 28, 88, 107, 108, 122, 127–129, 209, 213, 256, 341,
laterodorsal tegmental, 3 337, 338, 406–408, 421 429, 453–455, 457, 465, 489
monoaminergic nuclei, 3 30 seconds epoch, 7–10 delivery, 454, 455
cholinergic neurons, 3, 14 N2 sleep, 2, 6, 8, 12, 15, 16, 24, 80, 122, 270, 276, 284, devices and polysomnography, 454
histaminergic neurons, 3 287–297, 299–313, 315, 323, 334, 335, 406–408 exchange in lungs, 108
noradrenergic neurons, 3 30 seconds epoch, 7–10 saturation, 25, 41, 54, 107, 209, 213, 340, 394, 396, 448, 450,
serotonergic neurons, 3 N3 sleep, 2, 3, 6, 9, 11, 12, 16, 96, 122, 270, 276, 284, 306, 454
pedunculopontine, 3 313, 314, 315, 316, 317, 394, 396, 397, 406, 407, 408, 450 supplementation, 25, 454, 455, 457
reticular activating system, 3, 4, 13, 86, 87 30 seconds epoch, 7–10 therapy, 25, 28, 109, 453, 456
sleep processes Norepinephrine, 29 Oxyhemoglobin, 27, 107
circadian, 3–6, 16, 30 Normal sleep, 40, 393 Oxymeter, 139
homeostatic, 3, 4, 16 Nostrils, 137
ventrolateral preoptic nucleus, 3 Nurse practitioner, 501, 502 P
Neurological disorders, 30
Parasomnia, 41, 45, 48, 110, 125–130, 198, 214, 219, 223, 228,
Neurologic disorder, 26 O 229, 387, 388, 424
Neuromuscular disorders, 26
Obesity, 22, 26 Parkinson’s disease, 30, 198
Neuronal membrane potential, 56
hypoventilation syndrome, 26–28, 43, 454 Partial pressure of CO2, 26, 27, 214, 350, 507, 508
Neurons, 3, 4, 13–16, 54–57, 85–87
Obstructive sleep apnea, 22–24, 26, 27, 40, 41, 43, 46, 47, 49, Partial pressure of O2, 27
thalamocortical system, 15
101, 109, 116, 198, 209, 214, 219, 241, 244, 247, 340, 348, Pedunculopontine tegmental nuclei, 3
Neurophysiology of EEG rhythms from wakefulness to sleep, 12
351, 358, 394, 396–401, 403, 408, 417, 439–442, 448, 450, Perception, 2
Neurotransmission, 56
456, 457, 508 Periodic limb movement, 40, 131, 198, 204, 209, 249, 350, 450
Neurotransmitter, 56, 57, 85, 87
complications, 23 Peripheral
Nicotine, 30
diagnosis, 23 nervous system, 13, 55
Nipples, 137
risk factors, 22 sensory system, 13
Nocturia, 22
severity, 23 Pharmacological therapy, 24
Nocturnal
symptoms, 22 Pharyngeal pH, 214
heart burn, 22
treatment, 23 Phase delay, 2
palpitation, 22
Obstructive sleep apnea syndrome, 22 Philips Respironics, 42, 44, 46, 145
seizures, 88, 387
Ohms, 60, 61, 418, 480, 482 Photodiode, 107
Non-rapid-eye-movement sleep (NREM), 2, 6, 11–13, 24, 27,
Optional parameters, 214 Physiological changes, 1, 12, 40
38, 39, 89, 270, 276, 284, 406
Oro-nasal airflow, 38 during normal sleep, 12
Index 515
Physiology and recording of electrical potentials, 85 scoring rules in children, 405 Protocols, 417, 466, 478
Pickwickian syndrome, 38 Position dependent OSA, 399 diagnostic sleep study, 418, 478
Piezoelectric principle, 99 Positive airway pressure (PAP)/titration, 23–25, 27, 28, 40, 43, maintenance of wakefulness Test, 420
Piezo technology, 101, 106 48, 49, 109–111, 209, 223, 350, 394, 395, 403, 417–419, 424, manual titration with PAP, 418
Placement of 427, 429, 434, 435, 439, 440, 442, 444, 448, 454, 455, 460, multiple sleep latency Test, 419, 483
body position sensor, 142 467, 471, 473, 474, 476, 478, 482, 485, 486, 489, 490, 496, titration sleep study, 481
ECG electrodes, 137 508 Pulmonary
EEG electrodes according to 10–20 systems, 124 adequate titration, 444 diseases, 26, 27
EOG electrodes, 130, 131 bi-level PAP, 23, 27, 28, 439–441, 443, 501 function tests, 26, 27
Measures of Respiration, 137 good titration, 444 vascular pathology, 26
nasal cannula, 138 optimal titration, 444 Pumping process, 93
oximeter, 142 PAP support, 25 Pyramidal neurons, 13, 14, 15
RIP belts, 140 PAP therapy, 27
thermistor, 138 questionnaire, 429 Q
Plethysmography, 101, 408 repeat PAP titration study, 444
Quality assurance indicators, 474
Pleural pathology, 26 unacceptable titration, 444
Quality of life, 24, 25, 27, 49, 198, 504, 505
Polarity, 70, 99, 104 Positive deflection, 88, 90, 98, 284, 289
Quartz, 99
Policy for Post CPAP night questionnaire, 427, 496
Quiet wakefulness, 272, 508
accounting and budgeting, 471 Post-diagnostic night questionnaire, 426, 495
case of any emergency during sleep study, 477 Posterior dominant rhythm, 276, 279, 406, 407, 508
infection control in the sleep lab, 476 Potassium ion, 54, 56, 85 R
maintaining the records, 473 Potential of hydrogen (pH), 43, 214 Rapid eye movements (REM), 2, 6, 10–12, 15, 16, 22, 27–29,
quality assurance, 472 Pre-auricular point, 126 38–40, 89, 92, 93, 96, 97, 122, 133, 134, 187, 198, 199,
Polysomnographic Precautions, 454, 477, 483 203, 204, 219, 269–271, 276, 284, 307–312, 315, 317–321,
data, 270 Pregnancy, 31 322–325, 328, 330–339, 363, 369, 370, 387, 388, 394, 396,
recording, 38, 40, 405 Preparing the machines, 116 397, 398, 400, 406, –408, 419, 420, 424, 444, 483, 484
Polysomnography (PSG), 12, 23, 24, 27, 29, 30, 37, 38, 39, 40, Preparing the patient, 117 Real time EMG data, 95
41, 46, 49, 53, 54, 67, 87, 110, 111, 115, 117, 118, 128, 145, Pre-sleep questionnaire, 425, 494 Recording, 116
172, 191, 197, 221, 223, 236, 253, 254, 270, 276, 363, 387, Pressure eye movements, 88
394, 417, 418, 420, 424, 431–434, 436, 440, 444, 454, 464, limits, 440 Record of snoring, 110
465, 473, 474, 485, 490, 501, 508 transducer, 41, 98–100, 110, 137, 194, 209, 214, 340, Recurring cost for two beds, 502
concepts, 53 343,–345, 348, 434 Red blood cells (RBC), 107, 108
516 Clinical Atlas of Polysomnography
Refractory period, 13 Respiratory flow, 41, 45, 54, 99, 104, 105, 107, 209, 211, 340, sensory stimulus, 2
Relationship of process C and S, 6 350, 448, 476, 480, 482 Sensory stimulation, 13
Relaxation, 93 Respiratory inductance plethysmography (RIP), 101, 106, 137, Serotonin, 29
REM sleep 140, 141, 194, 209, 212, 340, 341, 345, 348, 408, 434, 435, Serotonin-norepinephrine reuptake inhibitors, 29
30 seconds epoch, 7–10, 238, 242, 248, 271, 272, 275, 371 448, 479, 481 Setting HFF to 1 Hz removes snoring, 103
REM sleep behavior disorder, 11, 16, 40, 93, 204, 219, 269, 363, Respiratory waveform, 101, 102, 104, 257 Sino-atrial, 93
387 Resting membrane potential, 53–56, 58, 93, 94, 98 Skeletal myocytes, 55
Renal failure (uremia), 30 Restless legs syndrome, 29–31, 40, 198, 387, 450 Skeletal restriction, 26
Resistance, 23, 60, 61, 99, 117, 118, 508 creepy-crawly sensations, 29 Sleep across age, 2
Respiration, 12, 38, 39, 54, 99, 101, 214, 240, 242–244, 256, diagnosis, 23, 24, 26, 29, 30, 475, 487 Sleep and wake promoting areas in brain, 4
270, 340, 341, 354, 406 International restless legs syndrome study group, 29 Sleep architecture, 6, 22, 391, 394, 396, 448
Respiratory data, 98, 340 medical conditions associated with RLS, 30 Sleep disordered breathing (SDB), 23, 109, 363
Respiratory disturbance index (RDI), 40, 444, 450, 508 prevalence of RLS, 30 Sleep disorders, 6, 21, 38, 40, 43, 46, 48, 49, 54, 198, 391, 454,
apneas, 22–24, 27, 209, 394, 397, 399–401, 403, 408, 424, treatment, 30 455, 472, 499, 504, 505
440–442, 482, 507, 508 Reticular activating system, 3, 4, 13, 86, 87 Sleepiness, 3, 22, 26, 28, 29, 40, 48, 508
hypopneas, 23, 24, 27, 99, 109, 209, 340, 350, 394, 397, 400, Reticular neurons, 14 Sleep lab
424, 440, 441, 443, 482, 507, 508 Retinohypothalamic tract, 4 financial viability, 499
Respiratory effort related arousal (RERAs), 350, 356, 363, 394, Reversibility, 2 Sleep laboratory, 464, 466
397, 408, 440, 441, 508 Rheumatologic diseases, 30 Sleep laboratory setting, 116, 464, 466, 468, 469, 470–474, 501
abnormal sleep, 508 Rhythmic movement disorder, 363 Sleep latency and sleep onset REM, 29, 394, 398, 420, 484
cardiorespiratory changes, 508 Risk factors for OSA, 22 Sleep medicine, 23, 121, 122, 270, 469, 470, 473
obstructive sleep apnea, 22, 40, 41, 43, 47, 101, 198, 209, 214, Sleep onset rapid eye movement (SOREM), 29, 394, 398, 420,
219, 340, 351, 358, 448, 450, 508 S 484
partial pressure of carbon dioxide, 508 Sleep onset REM, 398
Saw tooth waves, 203, 320
pressure or positive airway pressure (PAP), 508 Sleep physician, 46, 49, 118, 421, 424, 425, 466–471, 473, 474,
central derivations, 203
upper airway resistance syndrome, 508 476–479, 494, 501, 502
SCOPER system, 45
Respiratory efforts, 41, 54, 137, 188, 209, 212, 340, 350, 408, Sleep-related seizure, 219
Scoring of
440, 441, 501, 507, 508 Sleep spindles, 6, 16, 39, 198, 284, 287, 288, 290, 293, 314, 315,
EKG data, 382
Respiratory events, 209, 248, 269, 364, 394, 408, 440, 441, 448, 323, 406, 407
respiratory data, 340
455–457, 508 Sleep stages, 1, 2, 3, 11, 16, 39, 41, 88, 96, 122, 204, 230, 236,
sleep stage, 270
breathing abnormalities, 508 270, 276, 391, 394, 406, 421, 448
Seizure, 40, 88, 110, 125–130, 214, 219, 227, 228, 363
See, Non-rapid-eye-movement sleep (NREM)
Sensation
Index 517
W
Wakefulness, 3, 4, 11–17, 26, 27, 28, 38–40, 204, 235, 270–274,
276, 279, 284, 286, 296, 315, 324, 406, 417, 419, 420, 483,
507, 508
Waveforms upon signal capturing rate, 84
Waves during eye movement, 132
Waves generated through calibration, 78
Weight loss/reduction, 27
Workflow from sleep clinic to sleep laboratory, 470
Y
Young adults, 22
Z
Zeitgebers, 3
Zig-zag, 106
Z-RIP-module, 435