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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4538_Библиотеки_им_академика_М_И_Перельмана
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Sleep Related Breathing Disorders
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FaustoFernandes
3.1 Classification
Sleep pathologies are prevalent and frequent.
The classication of disorders plays several vital roles in Medicine. First, they
are essential as a guide to clinicians in identifying the specic disease state. It provides them with information regarding numerous related factors, including pathogenesis, prognosis, course, heritability, and therapeutics necessary for precision
diagnosis and treatment.
It also serves to dene de domain of a given medical specialty.
The rst classication for sleep disorders was made by the American Disorders
Sleep Association in 1979. It was named the Diagnosis Classication of Sleep and
arousal diseases.
This classication was reviewed in 2011, and the third edition was performed
in 2014.
The concepts are based on the International Classication of Sleep Disorders,
AASM, ICSD 2014—Third Edition (Table3.1), [1] here we join the concepts of
The AASM Manual for Scoring of Sleep and Associated Events, 2.6
Version-2020 [1, 2].
These are the denitions adopted:
Apnea—There is a drop in the pick signal ≥90% of prevent signal, and last
≥10s (recommended).
Hypopnea—The pick signal excursion drop by ≥30% of pre-event base line is
≥10s, and PO2 desaturation ≥3% (recommended).
3
F. Fernandes (*)
School of Medicine, University of Minho, Braga, Portugal
Hospital Senhora da Oliveira-Guimarães-Portugal, Hospital da Luz Guimarães,
Guimarães, Portugal
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
P. M. Baptista et al. (eds.), Obstructive Sleep Apnea,
https://doi.org/10.1007/978-3-031-35225-6_3
43
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Table 3.1 Sleep-related breathing disorders
Obstructive sleep apnea disorders
Obstructive sleep apnea, adult
Obstructive sleep apnea, pediatric
Central sleep apnea disorders
Central sleep apnea with Cheyne–Stokes breathing
Central sleep apnea due to a medical disorder without Cheyne–Stokes breathing
Central sleep apnea due to a medication or substance
Central sleep apnea due to high-altitude periodic breathing
Primary central sleep apnea
Primary central sleep apnea of infancy
Primary central sleep apnea of prematurity
Treatment-emergent central sleep apnea
Sleep-Related Hypoventilation Disorders
Obesity hypoventilation syndrome
Congenital central alveolar hypoventilation syndrome
Late-onset hypoventilation with hypothalamic dysfunction
Idiopathic central alveolar hypoventilation
Sleep-related hypoventilation due to a medication or substance
Sleep-related hypoventilation due to medical disorder
Sleep-related hypoxemia disorder
Sleep-related hypoxemia
Isolated symptoms and normal variants
Snoring
Catathrenia
F. Fernandes
Obstructive—If it meets apnea criteria and is associated with continued or
increased respiratory effort through the entire period of absent airow
(recommended).
Central—If it meets apnea criteria and is associated with absent inspiratory
effort, throughout the entire period of absent airow (recommended).
Mixed—If it meets apnea criteria, in the initial portion of the event absent inspiratory effort, followed by the reasumption of inspiratory effort in the second period
of the event, without airow [2].
3.2 Classification
3.2.1 Sleep-Related Breathing Disorders
The sleep-related breathing disorders are characterized by abnormalities of respiration during sleep (Table3.1).
The disorders are:
Obstructive sleep apnea (OSA)
Central sleep apnea disorders
Sleep-related hypoventilation disorders
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Sleep-related hypoxemia disorder
Isolated symptoms and normal variants
Summary:
In general, patients have a combination of obstructive and central sleep apnea.
The diagnosis is often based on which disorder predominates; this may vary from
night to night, and over time in individual patients.
On the other hand, OSA is different in adults that in children.
These disorders are characterized by upper airway narrowing or closure during
sleep while respiratory effort continues.
We will essentially pay attention to the breathing disorders during sleep of the
adult that are the most frequent.
We will reference central apnea due to neurologic or medical condition and cite
a new entity—treatment-emergent central sleep apnea.
Sleep-related hypoventilation disorders are characterized by an abnormal
increase in arterial PCO2 during sleep (≥55 mm). Obesity hypoventilation syndrome is in this category.
A reference is made to the sleep hypoxemia disorders, which are characterized
by sustained periods of signicantly reduced oxyhemoglobin saturation during sleep.
Finally, a reference is made to hypoventilation syndrome, hypoxemias disorders,
and normal variants like snoring or catathrenia.
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3.3 Phenotypes andSleep andObstructive
Apnea Syndrome
Beyond the classication, we must pay attention to the purpose of treatment on
patient phenotypes. With these tools, we can do “tailor-made” treatment for the
patient with sleep disorder breathing (SDB) [3].
Three phenotypes have been identied—position-dependent OSA (POSA),
severe OSA in obese patients (OSA and Obese), and OSA and periodic limb movements (OSA PLM).
There are nine variables that should be looked for: (1) Body mass index (BMI),
(2) Systolic arterial blood pressure, (3) Daytime saturation of oxygen in the arterial
blood (SaO2), (4) partial carbon dioxide pressure in arterial blood (PaCO2), (5) partial oxygen pressure in arterial blood (PaO2), (6) apnea–hypopnea index (AHI), (7)
periodic limb movement index (PLMS), (8) supine AIH, and (9) nonsupine AHI.
POSA is the most frequent.
As we know, in our practice, many patients modify snoring and witnessed apneas
changing positions from supine to lateral decubitus.
The prevalence of OSA and PLM is not high, but strongly correlate with arousals
index and snoring and contributes to lower sleep quality. In this situation, OSA
treatment is a good solution for both problems.
The phenotypes vary signicantly when comparing specic anthropometric,
clinical, and polysomnographic ndings. However, these differences cannot be
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F. Fernandes
identied only by measuring only the AHI index. The phenotype classication is
completed classication with the AHI [3].
This is crucial for a complete diagnosis and treatment of OSA.
3.4 Obstructive Sleep Apnea Adult
The criteria diagnosis is in Table3.2.
OSA is characterized by repetitive episodes of complete (apnea) or partial
(hypopnea) upper airway obstruction, during sleep and can occur in any age group.
It often results in a reduction of blood oxygen saturation and are in general terminated by brief arousals from sleep. These events last a minimum 10s.
The partners report snoring, breathing interruptions, as well episodes of gasping
or choking.
Patients awaken in the morning feeling tired and unrefreshed.
This phenomenon may be exacerbated by the ingestion of alcohol or sedation
medication.
During the day, excessive sleepiness during activities as conversing, eating,
walking, or driving.
There is a direct relationship between frequency of AHI, and daytime symptoms,
and its impact on life quality, but is not well correlated with the degree of oxygen
desaturation.
A common nding in OSA is refractory hypertension, a risk factor, independent
of obesity or smoking.
Patients with OSA have coronary artery disease, atrial brillation, and stroke.
In severe forms, it can develop pulmonary hypertension and cor pulmonale.
Also, it is associated with common gastroesophageal reux symptoms, nocturia,
mood disturbance, and erectile dysfunction.
Table 3.2 Diagnosis criteria of adult sleep apnea syndrome
Obstructive sleep apnea adult
Diagnostic criteria
A+B or C
A—One or more of following:
1—Patient complaints of sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms
2—Patient wakes with breath holding, gasping or choking
3—Bed partner testimonies snoring or breathing interruptions
4—Patient with hypertension, mood disorder, cognitive dysfunction, coronary artery
disease, stroke, congestive heart failure, atrial brillation, or type 2 diabetes mellitus
+
B—Polysomnography (PSG) or Out of Center Sleep Testing (ambulatory) (OCST)
demonstrates:
Five or more predominantly obstructive respiratory events
OR
C—Polysomnography or OCST demonstrates:
Fifteen or more predominantly obstructive respiratory events (apneas, hypopneas, or
Respiratory-Effort Related Arousals (RERAs)) per hour
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Some questionnaires, as Epworth Sleepiness Scale, can measure daytime sleepiness and quality of life. From a clinical perspective, there is no difference between
patients that have predominantly apnea or hypopnea.
Patients with UARS (upper airway resistance syndrome) is a variant of OSA,
where there are obstructive events, which results in arousals, but minimal arterial
oxygen desaturation. In general, they snore and report daytime sleepiness [4].
Estimates of prevalence are dependent of how sleep-related respiratory events
are dened.
General population-based studies indicate that OSA associated with daytime
sleepiness occurs in 3–7% of adult men and 2–5% of adult women. However,
because many individuals with OSA do not endorse daytime sleepiness, the incidence must be much higher. Some studies refer prevalence of AHI index >5/h as
24% in men and 9% in women, and the prevalence of OSA increases with age [5].
The ratio of men/women is approximately two to one.
Occurs in all racial and ethnic groups.
The major predisposing factor is obesity. About 60% of moderate or severe OSA
is attributed to obesity. The risk increases as the degree of weight gain increases,
with a high prevalence of morbid obesity. The BMI is vital. As weight increases,
OSA will become worse. Weight loss will improve the severity of OSA.
If the patient has normal weight and forms OSA, there is a need to check for
maxilla-mandibular malformation or adenotonsillar (mainly in children) enlargement, as well as neck enlargement (♂ >43cm; ♀ >39cm).
In women, menopause is a risk factor, and replacement therapy may be protective.
Anatomic characteristics of the head and neck either, either hereditary or
acquired, may inuence OSA (mandibular size, mandibular position, palatal height,
enlarged adenoids or tonsils, etc.).
Endocrine disorders such as acromegaly or hypothyroidism are also risk factors.
Children with Down syndrome have a high prevalence of OSA as well as patients
with neurologic disorders such as myotonic dystrophy.
Alcohol consumption and use of sedating drugs may worsen OSA.
However, there are no clear data if smoking is a risk factor for OSA.
Also, nasal obstruction due to rhinitis or anatomical anomalies (such as hypertrophic rhinitis or deviated septum or valve collapse) predispose to OSA.
As demonstrated by familial clusters, OSA can be a heritable condition.
First-degree relatives of OSA patients are twice as likely to have OSA, compared
to not familial affected. In addition, about one-third have hereditability obesity in OSA.
Genetics is essential in craniofacial morphology and ventilatory control.
However, a unique gene responsible for OSA heritability has not been
demonstrated.
Studies show that the severity of OSA measured by the AHI tends to progress
slowly time. Being more evident in men than women.
In middle-aged individuals, OSA is a signicant risk factor for refractory hypertension, coronary artery disease, congestive heart failure, stroke, atrial brillation
bradyarrhythmia or tachyarrhythmia, and premature mortality [6].
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F. Fernandes
It is an essential factor for developing type 2 diabetes mellitus, independent of
obesity? [7].
OSA increases the severity of depression, reduces job performance, causes
impaired familial relationships, reduces overall quality of life, and may accelerate
de onset of Alzheimer disease.
Also, the risk of vehicle accidents is signicantly augmented in drivers with OSA.
OSA can occur in any age or group and increases between young adulthood and
middle age, and the plateau is about age 65.
In PSG, OSA is documented by cessation of airow with ongoing respiratory
efforts. Oxygen saturation lowers from 1% or 2 to 40%.
Some events associated with the increased respiratory effort, and arousal, and
normal oxygen saturation, is an event dened as RERAs.
In isolated snoring, there are no apneas, hypopneas, or RERAs.
Other causes of sleepiness then OSA, should be kept in mind, such as narcolepsy,
idiopathic hypersomnia, and insufcient sleep [1].
3.5 Obstructive Sleep Apnea Pediatric
Above are the criteria for pediatric OSA (Table3.3).
In children, upper airway obstruction occurs predominantly during REM sleep.
Even short obstructive apneas may be associated with severe hypoxemia because
children have a lower functional residual capacity and a higher metabolic rate
than adults.
Snoring is usually loud with pauses and gasps.
They may sleep in unusual positions such as seated or neck hyperextended.
Excessive daytime sleepiness may be present.
These children have developmental, behavioral, and learning issues, including
attention decit, hyperactivity, moodiness, irritability, and impaired academic
performance.
The prevalence in children is estimated 1–4%. Predisposing and precipitating
factors are, adenotonsillar hypertrophy and obesity.
Table 3.3 Diagnosis criteria of children obstructive apnea syndromes
Criteria A and B must be met:
A.The presence of one or more of the following:
1. Snoring
2. Labored, paradoxical, or obstructed breathing during the child’s sleep
3. Sleepiness, hyperactivity, behavioral problems, or learning problems
B.PSG demonstrates one or more of the following:
1. One or more obstructive apneas, mixed apneas, or hypopneas, per hour of sleep
C.A pattern of obstructive hypoventilation, dened as at least 25% of total sleep time with
hypercapnia (PaCO2 >50mmHg) in association with one or more of the following:
1. Snoring
2. Flattening of the inspiratory nasal pressure waveform
3. Paradoxical thoracoabdominal motion
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Craniofacial anomalies and Down syndrome, neuromuscular disease, cerebral
palsy, gastroesophageal reux, mucopolysaccharidosis, cleft palate treated with
pharyngeal ap, and environmental tobacco exposure, are predisposing factors to OSA.
There is evidence of an increased risk in children of families with OSA, but the
genetic factors are unknown.
Symptoms begin within the rst few years.
It is essential to treat early because of the behavioral and cognitive complications
the may occur together with a decit of the child’s development.
PSG demonstrates obstructive and mixed apneas, hypopneas, and periods of
obstructive hypoventilation, associated with desaturation and hypercapnia [1, 8].
3.6 Central Sleep Apnea Syndromes
These syndromes below described have the common criteria related in Table3.4.
The criteria to be classied as CENTRAL SLEEP APNEA SYNDROMES are
the ones in Table3.5.
Table 3.4 Central sleep apnea syndromes
Central Sleep Apnea Syndromes
Central apnea syndrome with Cheyne–Stokes breathing
Central apnea due to a medical disorder without CSB
Central sleep apnea due to medication or substance
Central apnea due to high-altitude periodic breathing
Primary central sleep apnea
Primary sleep apnea of infancy
Primary sleep apnea of prematurity
Treatment-emergent central sleep apnea
Table 3.5 Diagnosis criteria of central sleep apnea syndromes
Criteria Central Sleep Apnea Syndromes
A
1—Sleepiness
2—Difculty initiating or maintaining sleep, frequent awakenings or nonrestorative sleep
3—Awakening short of breath
4—Snoring
5—Witnessed apneas
B—PSG shows all the following:
1—5 or more central apneas or central hypopneas/hour of sleep
2—No. of central apneas >50% of total apneas or hypopneas
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3.6.1 Central Apnea Syndrome withCheyne–Stokes Breathing
This syndrome is characterized by a crescendo-decrescendo ventilation pattern
associated to central apnea–hypopnea. Heart failure is the primary cause of
CSA-CSB.
In association, patients have excessive daytime sleepiness, insomnia, or nocturnal dyspnea.
It is seen in subjects older than 60years, males.
It is observed in N1 and N2, and attenuated in REM.
Predisposing factors are congestive heart failure, stroke, and renal failure.
In general, there is subtle oxyhemoglobin desaturation [9].
3.6.2 Central Apnea DuetoaMedical Disorder
It is a consequence of a medical or neurological disorder.
Most patients have brainstem lesions of developmental, vascular, neoplastic,
degenerative, demyelinating, or traumatic.
Patients present with sleep fragmentation, excessive daytime sleepiness, or
insomnia.
The Chiari malformation appears during infancy. Older patients can suffer from
stroke [1].
3.6.3 Central Sleep Apnea DuetoaMedication or Substance
In this disorder, the patient is taking an opioid or another respiratory depressant, and
there is an absence of CSB.
The use of potent long-action opioid drugs may carry central apneas during
sleep, such as methadone, morphine, oxycodone, fentanyl, and suboxone.
If the patients are withdrawn from these drugs, the central apnea may resolve, but
the abuse can lead to death.
This appears in the non-REM sleep, mainly in N3 [10].
3.6.4 Central Sleep Apnea DuetoHigh-Altitude
Periodic Breathing
It is characterized by the criteria of CSA with history of recent ascent to high altitudes [7].
The clinic is comprises alternating periods of central apnea and hypopnea associated with a recent ascent to high altitude, over 2500 m, accompanied by dyspnea [11].
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3.6.5 Treatment-Emergent Central Sleep Apnea
This is a new entity. The diagnostic criteria are the same as CSA, but this pathology
emerges in patients treated with CPAP.
In some patients, CPAP use shows a signicant resolution of the obstructive
events. It entails the emergence, or persistence of central apnea or hypopnea, with a
number of central apneas or hypopneas above 50% of the total events.in a diagnostic
sleep study. During treatment with CPAP, CSA persists or emerges, despite signicant resolution of obstructive respiratory events, and any other CSA disorder [12].
Finally, three rare clinical identities in CSA children and adults:
Primary central sleep apnea
Primary central sleep apnea of infancy
Primary central sleep apnea of prematurity
3.7 Sleep-Related Hypoventilation Disorders
The primary feature of these disorders is insufcient sleep-related ventilation,
resulting in abnormally high arterial partial pressure of carbon dioxide (PaCO2) during sleep.
Awake hypoventilation is dened as an arterial partial pressure of carbon dioxide
(PaCO2) ≥45mmHg.
The prevalence of these disorders is rare.
Hypoventilation generally results from impaired respiratory drive and CO2 and
O2 chemosensitivity.
There might also be hypoventilation with hypercapnia and hypoxemia [13].
3.7.1 Obesity Hypoventilation Syndrome (OHS)
It is a well-known disease. The old designation was Pickwick syndrome.
OHS is characterized by obesity and daytime hypercapnia (arterial PaCO2 >≥
45 mmHg), that cannot be fully attributed to an underlying cardiopulmonary or
neurologic disease.
Hypercapnia worsens during sleep and is often associated with severe arterial
oxygen desaturation. Hypoventilation is usually worse during REM sleep (Table3.6).
Table 3.6 Diagnosis criteria of obesity hypoventilation syndrome
Diagnostic criteria A–C must be met:
A—Presence of hypoventilation during wakefulness (PaCO2 ≥45mmHg) as measured by
arterial PCO2, end-tidal PCO2, or transcutaneous PCO
B—Presence of obesity (BMI >30kg/m2 in adults; for children >95th percentile)
C—Hypoventilation is not primarily due to lung parenchymal or airway disease, pulmonary
vascular pathology, chest wall disorder (other than mass loading from obesity), medication
use, neurologic disorder, muscle weakness, or a known congenital or idiopathic central
alveolar hypoventilation syndrome
2
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Most OHS patients have comorbid OSA (80–90%).
Patients with OHS commonly complain of hypersomnolence, morning headaches, fatigue, mood disturbance, and impairments of memory or concentration.
Physical examination may reveal cor pulmonale or circulatory congestion, such
as plethora, scleral injection, and peripheral edema.
Laboratory testing commonly shows polycythemia and elevated serum CO2 on
electrolyte testing (≈ serum bicarbonate), reduced forced vital capacity during pulmonary function testing, right heart strain, right ventricular hypertrophy and right
atrial enlargement on electrocardiography and ventricular dysfunction on
echocardiography.
Consequences of chronic hypercapnia and hypoxemia include pulmonary artery
hypertension, cor pulmonale, and neurocognitive dysfunction.
The prevalence of OHS in populations of patients with OSA varies across studies
but is often in the range of 10–15% of obese patients with OSA.
Although the prevalence of OHS is higher in men than women, the difference is
not as prominent as in OSA.Obesity is believed to be the primary pathophysiologic factor.
Central nervous system depressants, such as alcohol, anxiolytics, and hypnotics,
may further worsen respiratory impairment.
The serum bicarbonate level is usually elevated due to renal compensation for
chronic respiratory acidosis (hypercapnia) [14].
F. Fernandes
3.7.2 Congenital Central Alveolar Hypoventilation Syndrome
It is a syndrome of autonomic dysfunction. Primarily, there is the failure of automatic central control of breathing, due to a mutation of the PHOX2B gene.
It appears at birth and is rare.
It is associated with autonomic abnormalities, including Hirschsprung disease
(16% of patients), autonomic dysfunction (e.g., decreased heart rate variability or
hypotension), neural tumors (e.g., ganglioneuromas, swallowing dysfunction during the early years, and ocular abnormalities (e.g., strabismus) [1].
3.7.3 Late-Onset Central Hypoventilation
withHypothalamic Dysfunction
Patients are usually healthy until early childhood (often 2–3years of age); however,
they develop dysphagia and severe obesity, followed by central hypoventilation,
which often presents as respiratory failure.
There is hypothalamic dysfunction.
These patients often develop hypothalamic endocrine dysfunction: diabetes
insipidus, inappropriate antidiuretic hormone hypersecretion, precocious puberty,
hypogonadism, hyperprolactinemia, hypothyroidism, temperature dysregulation,
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