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XII
Contributors
FrankRalls Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine,
University of New Mexico School of Internal Medicine, Albuquerque, NM, USA
FRalls@salud.unm.edu
KannanRamar Center for Sleep Medicine, Mayo Clinic, Rochester, MN, USA
Department of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN, USA
Ramar.Kannan@mayo.edu
WilliamC.Scott Department of Otolaryngology, Vanderbilt University, Nashville, TN, USA
KatelynSmith Geisinger Health System Sleep Medicine Clinic, Port Matilda, PA, USA
katelyngr@gmail.com
AndrewR.Spector Department of Neurology, Duke University Medical Center, Durham, NC, USA
andrew.spector@duke.edu
JereyJ.Stanley Departments of Otolaryngology and Neurology, University of Michigan, Ann Arbor,
MI, USA
jjst@med.umich.edu
Kingman Strohl Case Western Reserve University, School of Medicine, University Hospitals Cleveland
Medical Center, Cleveland, OH, USA
kingman.strohl@case.edu
ChristopherViozzi Division of Oral Diagnosis and Oral and Maxillofacial Surgery, Mayo Clinic, Rochester,
MN, USA
Viozzi.christopher@mayo.edu
SamanthaD.Weaver Academy of Orofacial Myofunctional Therapy, Academy of Applied Myofunctional
Sciences, Los Angeles, CA, USA
samanthadweaver@gmail.com
LarryWolford Texas A&M University College of Dentistry, Baylor University Medical Center, Dallas, TX,
USA
lwolford@drlarrywolford.com
PratyushaYalamanchi Department of Otolaryngology, University of Michigan, Ann Arbor, MI, USA
ypratyus@umich.edu
AudreyJung-SunYoon Stanford Sleep Medicine Center, Department of Psychiatry and Behavioral Sciences,
Stanford University School of Medicine, Stanford, CA, USA
Department of Orthodontics, University of the Pacic Arthur A. Dogoni School of Dentistry, Stanford, CA,
USA
jungdds@gmail.com
SoroushZaghi The Breathe Institute, Los Angeles, CA, USA
Academy of Orofacial Myofunctional Therapy, Los Angeles, CA, USA
UCLA Health, Los Angeles, CA, USA
zaghimd@gmail.com
RocioZeballos-Chave Division of Pediatric Pulmonology, Department of Pediatrics, Saint Louis Univer-
sity School of Medicine, St. Louis, MO, USA
Rocio.zeballoschavez@health.slu.edu
1
Principles and
Fundamentals of OSA
Contents
Chapter 1 Classication of Sleep-Related Breathing Disorders–3
Katelyn Smith
Chapter 2 Pathophysiology of Obstructive Sleep Apnea (OSA) –11
Frank Ralls, Lisa Cutchen, and Lee K. Brown
Chapter 3 Health Consequences of Obstructive Sleep Apnea–23
Joseph Roland D. Espiritu
I
Chapter 4 Neurocognitive and Neuropsychological
Eects of OSA–45
Andrew R. Spector and Thomas J. Farrer
Chapter 5 Diagnostic Considerations in Metabolic Disease
Associated with Obstructive Sleep Apnea–57
Raymond E. Bourey
3
Classication ofSleep-Related
Breathing Disorders
KatelynSmith
Contents
1.1 Introduction – 4
1.2 Obstructive Sleep Apnea – 4
1.2.1 Obstructive Sleep Apnea, Adult – 4
1.2.2 Obstructive Sleep Apnea, Pediatric – 5
1.3 Central Sleep Apnea – 6
1.3.1 Central Sleep Apnea WithCheyne-Stokes Breathing – 7
1.3.2 Central Sleep Apnea DuetoaMedical Disorder Without
Cheyne-Stokes Breathing – 7
1.3.3 Central Sleep Apnea DuetoHigh-Altitude Periodic Breathing – 7
1.3.4 Central Sleep Apnea DuetoMedication or Substance – 7
1.3.5 Primary Central Sleep Apnea – 7
1.3.6 Treatment-Emergent Central Sleep Apnea – 7
1
1.4 Sleep-Related Hypoventilation Disorders – 8
1.5 Sleep-Related Hypoxemia Disorder – 8
1.6 Mixed Disorders – 8
1.7 Isolated Symptoms – 8
1.7.1 Snoring – 8
1.7.2 Catathrenia – 8
1.8 Summary – 8
References – 9
© Springer Nature Switzerland AG 2021
K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_1
4
RD
ApneaHypopneaRERA
Total sleep time
60
K. Smith
1
1.1 Introduction
The overarching term sleep-related breathing disorders
(SRBDs) is utilized to collect the various conditions in
which a person experiences an aberration of respiration,
entirely or in part, during sleep. These disorders are
divided into several categories and detailed in the
International Classication of Sleep Disorders Third
Edition (ICSD3). The primary classications include
obstructive sleep apnea disorders, central sleep apnea
syndromes, sleep-related hypoventilation disorders, and
sleep-related hypoxemia disorders [2]. Of note, The
American Academy of Sleep Medicine Manual for the
Scoring of Sleep and Associated Events describes the
particulars of the specic respiratory events, which comprise these SRBDs, a portion of which will not be discussed here. Overall, the focus of this text will be on the
broader categories of SRBDs.
tion, whereas obstructive apneas (.
sidered complete. Hypopneas are also associated with
an oxyhemoglobin desaturation of at least 3% or 4%
(depending of the denition used) and/or an arousal at
the termination of the event. Additionally, respiratory
effort-related arousals (RERAs) are episodes of airway
obstruction in which there is attening of the inspiratory ow signal and/or amplied respiratory effort, followed by an arousal, which do not fulll the hypopnea
or apnea denitions.
These three different obstructive events (apneas,
hypopneas, and RERAs) all must last a minimum of
10seconds in adults and co-occur with continued respiratory effort [4]. It is believed that these obstructive
events share a fundamental pathophysiology, and all are
thought to contribute to the symptoms and sequelae of
OSA.Obstructions tend to be more severe during stage
R sleep, particularly while in the supine position.
Fig.1.2) are con-
Apneas, hypopneas, and RERAs are tallied and averaged per hour of sleep to arrive at the Respiratory
1.2 Obstructive Sleep Apnea
Disturbance Index (RDI) [2]. With certain insurance
companies and payers, RERAs are excluded, and the
1.2.1 Obstructive Sleep Apnea, Adult
criteria for hypopneas are more stringent. In this case,
the Apnea Hypopnea Index (AHI) is calculated, which
The most prevalent of the sleep-related breathing dis-
excludes RERAs.
orders is obstructive sleep apnea (OSA) [9]. In OSA,
there are partial and complete upper airway obstruc-
I
tions which occur in sleep. Obstructive hypopneas
(. Fig. 1.1) consist of an incomplete airow reduc-
. Fig. 1.1 This is a 60-second epoch showing an obstructive hypopnea meeting the criteria of at least a 30% drop in pressure signal from
the baseline for at least 10seconds with an associated 3% desaturation
A
ApneaHypopneaRERA
Total sleep time
60
Classication ofSleep-Related Breathing Disorders
5
1
. Fig. 1.2 This is a 60-second epoch showing an obstructive apnea meeting the criteria of at least a 90% drop in ow signal from the base-
line for at least 10seconds
HI
The RDI or AHI is then used to gage the severity of
OSA.The severity classication for adults is as follows:
5 Mild: RDI or AHI≥5 and <15
5 Moderate: RDI or AHI≥15 and <30
5 Severe: RDI or AHI≥30 [9]
If the RDI or AHI is in the mild range (<15 events per
hour), then there are other diagnostic criteria required
in addition to polysomnographic ndings to make the
diagnosis of OSA.These criteria include one or more of
the following:
1. Awakenings associated with gasping, choking, or
breath holding
2. Witnessed repeated episodes of snoring or pauses in
breathing
3. Comorbidities of mood disorder, cognitive
dysfunction, hypertension, coronary artery disease,
congestive heart failure, atrial brillation, stroke, or
diabetes mellitus type 2
4. Complaints of fatigue, sleepiness, insomnia, or unrefreshing sleep
Both in-lab polysomnography and home sleep apnea
testing (HSAT) may be used to evaluate for OSA.While
in-lab polysomnography is the rmly established goldstandard method of testing for sleep disorders, the
HSAT may be adequate to evaluate for obstructive sleep
apnea. There are important stipulations regarding
which patients are appropriate for HSAT (discussed in
7 Chap. 8).
Oxyhemoglobin desaturations may result from the
obstructions and generally resolve after the obstructive event ends. However, if there are lengthy or particularly recurrent apneas and hypopneas or there is
underlying pulmonology disease, these desaturations
may persist. For example, it is not uncommon for OSA
and COPD to co-occur, and this dual contribution
from diverse pathologies can lead to more marked
desaturations in sleep and hypercapnia in wake.
Arousal may also result from obstructive events and
are included in the diagnostic criteria of hypopneas
and RERAs. The prevalence of obstructions may
increase with the ingestion of alcohol and sedatives, as
well as with weight gain [2].
1.2.2 Obstructive Sleep Apnea, Pediatric
However, if the RDI or AHI reaches or exceeds 15, then
the diagnosis is made even in the absence of additional
signs, symptoms, and comorbidities [2].
There are several differences in the classication and
diagnosis of Pediatric OSA and in the denition of
obstructive events. Rather than having a 10-second
6
K. Smith
duration requirement, in children the duration of
1
obstructive event must be at least the length of two
breaths [4]. The use of HSAT has not been validated in
children [14]. Diagnosis requires snoring, abnormal
breathing (e.g., paradoxical), or daytime symptoms such
as sleepiness or behavior issues.
Additionally, the child must have at least one
obstructive event per hour of sleep or meet criteria for
obstructive hypoventilation in addition to as associated
feature (i.e., paradoxical breathing, snoring, or attening of the inspiratory portion of the nasal pressure
waveform). The ICSD3 describes this obstructive
hypoventilation as spending at least 25% of the total
sleep time with arterial carbon dioxide levels greater
than 50mm of Hg.
under the CSA classication. There are a few unifying
themes within the fundamental elements. During the
central event, there is near or complete cessation of airow in tandem with an absence of respiratory effort
Fig. 1.3). Additionally, the central apneas tend to
(.
occur due to unstable central nervous system respiratory
controller mechanisms [8].
The ICSD3 further subdivides CSA into the following categories for adults: Cheyne-Stokes breathing
(CSB), CSA due to a medical condition without CSB,
CSA due to high-altitude periodic breathing, CSA due
to medication or substance, primary CSA, and
treatment- emergent CSA.When considering the pediatric population, this list also includes primary CSA of
prematurity and primary CSA of infancy.
To make the above adult diagnoses, clinical features
must be present. For all but CSA due to high-altitude
1.3 Central Sleep Apnea
periodic breathing and the pediatric diagnoses, the average of central respiratory events must be at least 5 per
Patients with central sleep apnea (CSA) often have multiple or even unknown contributing etiologies, which
lead to the wide variety of disease entities which fall
hour, and the majority of the respiratory events must be
central in nature. In general, the treatment options include
treating the underlying conditions and PAP therapy [2].
. Fig. 1.3 This is a 60-second epoch showing a central apnea meet-
ing the criteria of at least a 90% drop in the ow signal (orange waveform) for at least 10seconds with a complete cessation of respiratory
effort as displayed by the attening of the chest and abdominal signals (blue waveform)
Classication ofSleep-Related Breathing Disorders
7
1
1.3.1 Central Sleep Apnea With
Cheyne-Stokes Breathing
Central sleep apnea with Cheyne-Stokes breathing (CSACSB) is a subcategory of CSA in which periodic breathing is exhibited through a string of crescendo- decrescendo
breathing episodes in between central apneas and/or
hypopneas. CSA-CSB, as it is classied in the ICSD3,
requires specic symptomatology (e.g., snoring, sleepiness, or witnessed apneas) and/or comorbidity including
congestive heart failure, atrial utter/brillation, or
neurologic disorder [2, 16]. Additionally, the diagnosis
requires that the disordered breathing is not better
explained by another sleep disorder or medication or substance use. The polysomnogram should demonstrate at
least ve central breathing events per hour, the total number of which is >50% of the total apneic/hypopneic events
along with the CBS pattern of ventilation. Heart failure
and stroke may be underlying causes and should be evaluated for in a patient with a diagnosis of CSA-CSB [3, 12].
1.3.2 Central Sleep Apnea DuetoaMedical
Disorder Without Cheyne-Stokes
Breathing
Central sleep apnea due to a medical disorder without
Cheyne-Stokes breathing (CSA w/o CSB) lacks the CSBpatterned breathing but comprises all other forms of CSA
thought to be caused by a medical diagnosis in adults.
While these medical diagnoses may range from respiratory
to cardiovascular to neurologic, the neurological causes
cover the vast majority of etiologies. Brainstem lesions,
stroke, and Chiari malformations are a few of the most
common neurological causes [7]. The diagnostic criteria
require symptomatology (i.e., snoring, sleepiness, awakening with dyspnea, difculty sleeping, or witnessed apneas)
if the patient is an adult and the absence of CSB on polysomnogram. The polysomnogram should display at least
ve central breathing events per hour, the total number of
which is >50% of the total of apneic/hypopneic events.
Additionally, the disordered breathing cannot be due to
substance or medication use. Sleep-related hypoventilation may also be present but is not required [2].
1.3.3 Central Sleep Apnea Due to
High-Altitude Periodic Breathing
Typically seen in altitudes of at least 2500meters but
also seen as low as 1500meters, this is a classication
of CSA wherein the body responds to a sudden
increase in altitude with manifestation of symptoms
and periodic breathing while asleep. The breathing
pattern is comprised of hyperpnea alternating with
central apnea in a cycle length between 12 and 40seconds [2, 5].
1.3.4 Central Sleep Apnea
DuetoMedication or Substance
Central sleep apnea due to medication or substance is a
secondary form of CSA caused by the use of a respiratory depressant substance or medication, most commonly an opioid. Morphine, oxycodone, fentanyl
patches, narcotic infusions, and suboxone are possible
culprits [2]. Opioids have multiple deleterious effects on
breathing while asleep in that they suppress the respiratory drive at a central level, increase the likelihood of
OSA by relaxing the patient’s airway, and induce
hypoventilation [10].
1.3.5 Primary Central Sleep Apnea
Primary central sleep apnea is rare and characterized by
the lack of other differentiating features. To establish
this diagnosis, there must not be Cheyne-Stokes breathing, daytime or nocturnal evidence of hypoventilation,
or the existence of a causal medical condition or use of
medication.
1.3.6 Treatment-Emergent Central
Sleep Apnea
Treatment-emergent central sleep apnea (TE-CSA) and
complex sleep apnea both describe the same clinical
phenomenon; this occurs when a patient displays CSA
while using a positive airway pressure (PAP) without a
backup rate to treat established OSA.A high number of
arousals persist on PAP treatment along with an AHI
that is higher during NREM than REM. Patients on
opioids are more likely to manifest TE-CSA than opioid
naive patients [13]. While some consider TE-CSA merely
a manifestation of OSA, the ICSD3 includes TE-CSA
as a discrete form of CSA in its diagnostic criteria. In
the available literature, TE-CSA is found in up to 20%
of patients with OSA who have initiated PAP therapy.
Fortunately, as treatment with PAP continues this percentage drops to around 2% [2].
8
K. Smith
1
1.4 Sleep-Related Hypoventilation
Disorders
shunting, ventilation-perfusion mismatch, diffusion
abnormalities, low atmospheric PO2, and increased dead
space [2, 6].
In the disorders of sleep-related hypoventilation (SRHV),
the essential element is a sustained aberrantly elevated
arterial partial pressure of carbon dioxide while asleep.
1.6 Mixed Disorders
There are two scenarios that would qualify an adult as
having sleep-related hypoventilation, the rst of which is
arterial carbon dioxide (CO2) levels of greater than
55 mmHg for at least 10 minutes of sleep. The second
possible scenario is an increase of at least 10 mmHg in
sleep when compared to supine wake if it exceeds
50mmHg for at least 10minutes. In children, sleep- related
hypoventilation is dened as arterial carbon dioxide levels
of greater than 50mmgHg [2] for at least 25% of the total
Central apneas and hypopneas may occur along with
the obstructive events. Generally, if the central events
are few and there is a relative preponderance of obstructive events, then the individual is still considered to have
OSA.However, there are those whose polysomnograms
meet criteria for both obstructive and central sleep
apnea; therefore, they are considered to have a mixed
disorder [2].
sleep time. Carbon dioxide may be monitored through
end-tidal CO2, transcutaneous PCO2, or ABG [4].
The ICSD-3 distinguishes six separate sub-
1.7 Isolated Symptoms
classications. The adult subtypes include obesity
hypoventilation syndrome, idiopathic central alveolar
1.7.1 Snoring
hypoventilation, disorders due to another medical disorder, and disorders due to a medication or substance.
In children, the subtypes include congenital central
alveolar hypoventilation syndrome and late-onset central hypoventilation with hypothalamic dysfunction [2].
While all the SRHV disorders may have hypoventilation during wake, only obesity hypoventilation disorder
requires it for diagnosis [15]. If hypoventilation is present
in wake, it will likely worsen in sleep. Briey, the foundation of SRHV disorders treatment is directed toward the
particular underlying etiology and often hinges on positive airway pressure therapy.
Essentially, snoring is a sound produced by respiration
while sleeping, most often in the inspiratory phase. A
designation of simple or primary snoring is given in the
absence of apnea or hypoventilation and when there is
no associated sleep disturbance or daytime sleepiness.
While sporadic snoring is extremely common, persistent
nocturnal snoring is less common and should be considered a potential symptom of OSA. Additionally, the
ICSD recommends PSG or HSAT for all patients with
cardiovascular disease who snore [2]. Adult men snore
more commonly than any other affected group, and
there is a strong correlation between snoring and obesity
[11]. In children who snore, adenotonsillar hypertrophy
1.5 Sleep-Related Hypoxemia Disorder
is strongly implicated. Smoking, alcohol, opiates, and
muscle relaxants can all increase the likelihood of
The dening characteristic of this classication is the
snoring [2].
disordered systemic hypoxemia which is not secondary
to hypoventilation. Hypoxemia is diagnosed through
PSG, HSAT, or continuous oximetry during sleep. The
1.7.2 Catathrenia
differentiation between sleep-related hypoventilation
and sleep-related hypoxemia depends upon the ability to
assess for nocturnal hypoventilation by monitoring CO
To qualify as sleep-related hypoxemia disorder, the arterial oxygen saturation needs to be 88% or less for at least
5 minutes in adults. In children, the arterial oxygen
saturation must be 90% or less for at least 5minutes. If
Catathrenia is the term used to describe a vocalization in
.
sleep during a prolonged expiration, typically in REM
2
sleep. It is also referred to as sleep-related groaning. The
clinical signicance of catathrenia is debated in the literature, and currently the phenomenon is seen chiey as
a social problem rather than a medical concern [1, 2].
the hypoxemia can be solely attributed to OSA or CSA,
it excludes the diagnosis of sleep-related hypoxemia or
hypoventilation. Conversely, while OSA and CSA may
1.8 Summary
be present, they do not necessarily preclude the diagnosis of sleep-related hypoxia disorder provided they are
not associated with the majority of the sleep time during
which hypoxemia is present. Conditions that may be
responsible for sleep-related hypoxemia include venous
The sleep-related breathing disorders are a collection of
several conditions, all of which include dysfunctional
respiration during sleep. The primary classications
include obstructive sleep apnea disorders, central sleep
Classication ofSleep-Related Breathing Disorders
9
1
apnea syndromes, sleep-related hypoventilation disorders, and sleep-related hypoxemia disorders. These classications are further broken down into subcategories.
The initial treatment of sleep-related hypoxemia and
many of the central sleep apnea disorders and sleeprelated hypoventilation disorders requires treatment of
the underlying conditions. One patient may have multiple SRBDs, and, in these cases, each disorder should be
addressed.
References
1. Abbasi AA, Morgenthaler TI, Slocumb NL, et al. Nocturnal
moaning and groaning catathrenia or nocturnal vocalizations.
Sleep Breath. 2012;16(2):367–73.
2. American Academy of Sleep Medicine. The international classication of sleep disorders, Third edition. Darien: American
Academy of Sleep Medicine; 2014.
3. Anker SD, von Haehling S, Germany R.Sleep-disordered breathing and cardiovascular disease. Indian Heart J. 2016;68(Suppl
1):S69–76.
4. Berry RB, Albertario CL, Harding SM, for the American Academy of Sleep Medicine, etal. The AASM manual for the scoring
of sleep and associated events: rules, terminology and technical
specications, version 2.5. Darien: American Academy of Sleep
Medicine; 2018, www. aasmnet. org.
5. Burgess KR, Lucas SJ, Shepherd K, etal. Worsening of central
sleep apnea at high altitude: a role for cerebrovascular function.
J Appl Physiol (1985). 2013;114(8):1021–8.
6. Casey KR, Cantillo KO, Brown LK.Sleep-related hypoventilation/hypoxemic syndromes. Chest. 2007;131(6):1936–48.
7. Dauvilliers Y, Stal V, Abril B, et al. Chiari malformation and
sleep related breathing disorders. J Neurol Neurosurg Psychiatry. 2007;78(12):1344–8.
8. Eckert DJ, Jordan AS, Merchia P, et al. Central sleep apnea:
pathophysiology and treatment. Chest. 2007;131(2):595–607.
9. Epstein LJ, Kristo D, Strollo PJ Jr, et al. Clinical guideline for
the evaluation, management and long-term care of obstructive
sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263–276.
10. Guilleminault C1, Cao M, Yue HJ, etal. Obstructive sleep apnea
and chronic opioid use. Lung. 2010;188(6):459–68. https://doi.
org/10.1007/s00408-010-9254-3. Epub 24 Jul 2010.
11. Kezirian EJ, Chang JL.Snoring without OSA and health consequences: the jury is still out. Sleep. 2013;36(4):613.
12. Lanfranchi PA, Braghiroli A, Bosimini E, etal. Prognostic value
of nocturnal Cheyne-Stokes respiration in chronic heart failure.
Circulation. 1999;99(11):1435–40.
13. Lehman S, Antic NA, Thompson C, etal. Central sleep apnea
on commencement of continuous positive airway pressure in
patients with a primary diagnosis of obstructive sleep apneahypopnea. J Clin Sleep Med. 2007;3(5):462–6.
14. Marcus CL, Brooks LJ, Draper KA, etal. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):e714–55.
15. Mokhlesi B.Obesity hypoventilation syndrome: a state-of-theart review. Respir Care. 2010;55(10):1347–62; discussion 1363-5.
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respiration. Proc Am Thorac Soc. 2008;5(2):226–236.
11
Pathophysiology ofObstructive
Sleep Apnea (OSA)
FrankRalls, LisaCutchen, andLeeK.Brown
Contents
2.1 History andIntroduction – 12
2
2.2 Airway Collapsibility and Pcrit (.
2.3 Instability ofVentilatory Control During Sleep – 14
2.4 Anatomical Factors (. Fig. 2.2) – 16
2.5 Gender, Genetics, and Pathogenesis (.
2.6 The Possible Role ofLeptin – 18
2.7 Summary – 18
References – 19
Fig. 2.1) – 12
Fig. 2.3) – 16
© Springer Nature Switzerland AG 2021
K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_2