Sleep disordered breathing encompasses a spectrum of breathing abnormalities during sleep ranging from primary snoring to obstructive sleep apnea. The main types are upper airway resistance syndrome, obstructive sleep apnea, and central sleep apnea. Risk factors include obesity, large neck circumference, and family history. Consequences of untreated sleep apnea include hypertension, diabetes, heart disease, and motor vehicle accidents due to daytime sleepiness. Diagnosis involves an overnight sleep study and treatment options include weight loss, continuous positive airway pressure, oral appliances, surgery, and in rare cases pharmacotherapy.
2. Function of sleepFunction of sleep??
⢠Humans spend almost 30% of their
lives sleeping
⢠Normal sleep has two distinct states:
â NREM (1/2-3/4âdelta sleepâ stages)
â REM with EEG activity similar to that in
wakefulness but muscle atony,
âdreaming and increased metabolic
activity of CNS â
Restorative!
3. Sleep deprivationSleep deprivation
⢠Cognitive deficits with impaired
creativity and rapidity of response to
unfamiliar situations
⢠Chronic sleep loss may contribute to:
â Recurrent viral illnesses,
â Diabetes, obesity, heart disease, and
other age-related chronic disorders and
â Depression.
An average adult needs 6-8 hours of
consolidated sleep/day
4. Sleep DisordersSleep Disorders
⢠Sleep disordered breathing (SDB)
⢠Insomnia
⢠Narcolepsy and other hypersomnias
⢠Restless legs syndrome / Periodic
Limb Movement Disorders
⢠Parasomnias
9. CLASSIFICATION OF SRBDCLASSIFICATION OF SRBD
⢠Intermittent snoring- no health sequelae
⢠UARS- upper airway resistance syndrome
⢠Mild OSA- AHI 5-15
⢠Moderate OSA- AHI 15-30
⢠Severe OSA- AHI >30
⢠CSA- central sleep apnea
10. SnoringSnoring
⢠Usually an inspiratory
sound, but it also may
be present in expiration
⢠Overall, it affects 19%
to 37% of the general
population and more
than 50% of middle-
aged men
⢠Male predominance
⢠Snoring usually occurs
in conjunction with a
disordered sleep pattern
11. Primary snoringPrimary snoring
⢠Some non apneic snorers may have objective
physiologic findings as high blood pressure,
cardiac disease, strokes, and endocrine diseases
such as diabetes or impaired insulin resistance.
⢠The patient may complain of snoring themselves,
a feeling of tiredness on waking, excessive
sleepiness during the day, poor work
performance, and difficulty with concentration.
⢠The International Classification of Sleep
Disorders: Diagnostic and Coding Manual defines
primary snoring (ICSD 780.53-1) as "loud upper
airway breathing sounds in sleep, without
episode of apnea or hypoventilationâ
12. Upper airway resistanceUpper airway resistance
syndrome âUARSsyndrome âUARSââ
⢠Repeated arousals due to upper airway
resistance âRespiratory effort-related
arousals (RERAs)â that lead to excessive
daytime sleepiness/fatigue
⢠Patients also may complain of difficulty with
concentration, morning headaches,
impotence, difficulty sleeping, or restless
sleep. They often report having repetitive
nightmares, such as choking or being buried
alive. Characteristically they may manifest
with psychosomatic disorders
13. UARSUARS
⢠Reduction in airway area is sufficient
enough to avoid hypopneas and apnea but
enough to increase upper airway
resistance.
⢠Unlike in OSAHS, there is no evidence of
oxygen desaturations
⢠Arousals is based on the generation of
negative intrathoracic pressure as
detected by various mechanoreceptors
located in the upper airway.
14. UARSUARS
⢠The prevalence of UARS in the general
adult population is unknown, yet it has
been estimated to be as high as 10% to
15% when the definition is applied to
adults that suffer from snoring and
excessive daytime sleepiness.
⢠It has been suggested that UARS occurs
in a less obese younger population and
more frequently in females than does
OSAHS.
15. Snoring and UARSSnoring and UARS
⢠This disorder often produces a snoring pattern
termed crescendo snoring .
⢠Recognition of UARS has led to a more conservative
use of the term snoring:
â Primary snorers: Patients who snore and have
no daytime symptoms or excessive daytime
sleepiness.
â UARS: Patients who snore and have daytime
sleepiness symptoms.
⢠Snoring, however is not a necessary feature of
UARS because the upper airway resistance is due
to a partial decrease in airway cross-sectional area;
therefore, the airway walls do not have to vibrate
to produce a snoring sound, Idiopathic
hypersomnia?!
16. Diagnosis of UARSDiagnosis of UARS
⢠Three essential clinical features:
â Excessive daytime somnolence;
â A normal respiratory disturbance index
(RDI) of less than five events per hour of
sleep.
â An elevated EEG arousal index more than
10 per hour of sleep, with the arousal
related to increased respiratory efforts
(usually made by use of nocturnal
oesophageal pressure monitoring).
)A dedicated polysomnographic study(
17. Obstructive sleep apnea/hypopneaObstructive sleep apnea/hypopnea
syndrome âOSAHSsyndrome âOSAHSââ
⢠Hypopneas are defined in adults as a 10-second
event during which there is continued breathing
but in which ventilation during sleep is reduced by
at least 50% from baseline.
⢠Apnea occurs due to total cessation of airflow for
at least 10 seconds.
â Obstructive: Cessation of airflow but with
continued respiratory effort, or
â Central: Airflow and respiratory effort are both
absent.
â Mixed: Central and obstructive
⢠Hypopnea can produce clinical sequelae similar to
those of apnea
18. RespiratoryRespiratory disturbancedisturbance indexindex
(RDI(RDI((
⢠The RDI (or AHI) is the number of apneas
plus hypopneas per hour of sleep.
⢠In individuals aged 30 to 60 years, 24% of
men and 9% of women had abnormal AHI
indices ( > five events per hour of sleep)
⢠An RDI greater than 15 events per hour
indicates possible OSAHS.
⢠Generally, as the RDI increases, the severity
of âapneaâ increases
19. Definitions of OSAHSDefinitions of OSAHS
⢠RDI>5
⢠RDI > 20 increases risk of mortality
⢠RDI 20-40=moderate, >40=severe
⢠Upper Airway Resistance Syndrome
âShares pathophysiology with OSA
âNo desaturation, continuous ventilatory
effort
⢠Snoring
20. Diagnosis of OSAHSDiagnosis of OSAHS
⢠History.
⢠Physical examination (Collar Size, Mallempeti Sign, BMI)
⢠Screening procedures (F/V Loop (saw), N-PSG)
⢠Radiographs.
⢠Pulse Oximetry (detect ODI ď no. of desaturations
(>4%) /hr sleep, if >15 begin titrating CPAP, if <15
continue full PSG)
⢠Polysomnogram (EEG, EOG, ECG, EMG, Oronasal
airflow, Thoraco-abdominal resp effort, Oximeter,
Optional)
21. Diagnosis of OSAHSDiagnosis of OSAHS
A) Excessive daytime
sleepiness that is not
explained by other factors
OR
B) Two or more of the
following that are not better
explained by other factors:
â Choking or gasping from sleep
â Recurrent awakenings from
sleep
â Feeling unrefreshed after sleep
â Daytime fatigue
â Poor concentration
C) Overnight monitoring
indicates five or more
obstructed breathing
events per hour
during sleep or 30
events per 6 hours of
sleep.
These events can be a
combination of OSA,
hypopnea, or RERAs
(resp events related arousals(
22. Nocturnal polysomnography.
From n.PSG we can obtain:
⢠Sleep architecture (REM and NON-REM).
⢠ECG (HR,PAC, PVC)
⢠AHI if > 10 â diagnosis of SAHS.
⢠Total no. And type of:
ďŽ Apneas
ďŽ Hypopneas
⢠Degree of desaturations during:
⢠Apneas & Hypopneas.
23. EpidemiologyEpidemiology
⢠Currently, the prevalence of OSAHS is
conservatively estimated to be 1% to 2% in
middle-aged men and half that, or approximately
0.5% to 1%, in middle-aged women.
⢠The disorder is more common among family
members suffering from OSAHS than in the
general population. This relationship seems to be
independent of familial obesity tendencies
⢠It is estimated that only 1% of OSAHS patients
are receiving appropriate treatment for their
disease.
25. Clinical presentation ofClinical presentation of
OSAHSOSAHS
Night time
⢠Loud habitual snoring
⢠Witnessed apneas
⢠Gasping or chocking
episodes during sleep
⢠Nocturnal awakening
⢠Nocturia
Day time
⢠Unrefreshing sleep,
morning headaches
⢠Excessive daytime
sleepiness
⢠Automobile or work-
related accidents
⢠Irritability, memory
loss, personality change
⢠Decreased libido
⢠Impotence
26. Risk Factors for OSAHSRisk Factors for OSAHS
⢠Prevalence increases with increasing age and body
mass index (>28), family history(54% offspring),
african american, asian and hispanic,
⢠Neck circumference >17 inches in men and >16 inches
in women is risk factor
⢠Other conditions predispose i.e hypothyroidism,
rhinosinusitis
⢠Males affected twice as much as premenopausal
women
⢠Certain syndromes affecting anatomy of upper airway
are associated with SRDB in the young (Treacher
Collins, Pierre-Robin, Marfans, Alperts, trisomy 21 etc)
⢠Drugs: Alcohol, sedatives, tobacco smoke
27.
28. Sleep apnea should be suspected inSleep apnea should be suspected in
cases withcases with::
⢠Hypertension
⢠Nocturnal cardiac
arrythmias
⢠Myocardial infarction
⢠Cerebrovascular
accident
⢠Pulmonary
hypertension
⢠Obesity
⢠Type II diabetes
mellitus
⢠Driver involved in a
sleep-related
automobile crash
⢠Sexual dysfunction
⢠Preop anesthesia
evaluation.
Questions pertaining to sleep disorders
should be performed in the review of
systems of all patients
29. OSA Increases Co-Morbid Health RisksOSA Increases Co-Morbid Health Risks
â˘OSA is an independent risk factor for HTN & Type
II DMObesity
Depression
40%
Diabetes
50%
CHF
50%
50%
Stroke
50%
Hypertension
35%
Wolk et al 2003 Javaheri et al 1999,
Somers et al 2007
Einhorn ADA 2005
Sjostrom et al 2004Sandberg et al 2008Smith et al 2002,
Schroder et al 2005
⢠Left undiagnosed, OSA increases risk of stroke by 2X, risk of fatal
cardiovascular events by 5X, and risk of serious vehicular accidents
%DiseaseCo-morbiditywithOSA
= With OSA
Sources: Yaggi et al, NEJM 2005; Young et al, Sleep 2008; Teran-Santos, NEJM 1999
30. Central sleep apnea andCentral sleep apnea and
Cheyne-Stokes respirationCheyne-Stokes respiration
during sleepduring sleep
⢠Patients with CHF have a high incidence of
SDB (primarily central apneas)
⢠Cheyne-Stokes respiration is commonly
seen during sleep in patients with CHF
(NYHA class 3 or 4), primarily in stages 1
and 2 NREM
⢠The presence of this respiratory pattern
appears to be an important risk factor for
the progression of heart failure
31. Obesity hypoventilationObesity hypoventilation
syndromesyndrome
⢠Morbid obesity (BMI>40kg/m2
) and chronic
hypoventilation with hypercapnia (PaCO2
>45mmmHg) during wakefulness
⢠Nocturnal hypoventilation with at least 10
mmHg increment in PaCO2 during sleep
⢠Frequently coexists with OSA (Overlap
syndrome)
32. â..And on the box
sat a fat and red-
faced boy, in a
state of
somnolencyâ
33. Methods of TreatmentMethods of Treatment
Treatment options can be broadly
divided into:
â˘Behavioral interventions (wt loss,
smoking and alcohol cessation, change
position at sleep)
â˘Non-surgical options
â˘Surgical options.
34. NON-SURGICAL INTERVENTIONNON-SURGICAL INTERVENTION
Continuous positive airway
pressure (CPAP)
Functions as a pneumatic splint to maintain
upper airway patency throughout all phases
of sleep breathing
⢠It operates by means of a flow generator
which delivers pressure through air tubing
to a nasal or face mask worn overnight
36. Sullivan V Elite (flow
generator)
Mirage Mask
Humidifier (heated or
passover)
37. CPAPCPAP
CPAP
Pressure must be individually
titrated
Compliance is as low as 50%
Air leakage,
eustachian tube dysfunction,
noise,
mask discomfort,
claustrophobia
38. BI-LEVEL POSITIVE AIRWAY
PRESSURE (BiPAP)
⢠These machines allow independent
adjustment of inspiratory and expiratory
pressures rather than having a fixed
pressure as with CPAP
⢠A well-designed randomised study found no
advantage for bi-level support over CPAP in
straightforward OSAHS
⢠This mode of non-invasive ventilation may
be more appropriate for patients with
ventilatory failure.
39. Intra-oral devices (IODs) area range
of oral appliances designed to alter
upper airway patency
⢠Several techniques have been employed,
but mandibular advancement has gained
most acceptance
⢠Most mechanisms have a similar action in
producing anterior displacement of the
mandible, thus increasing upper airway
diameter in some appliances.
⢠The degree of mandibular protrusion can
be specified and subsequently adjusted
42. IODSIODS
⢠an appropriate therapy
for snorers and for
patients with mild
OSAHS with normal
daytime alertness
⢠appropriate alternative
therapy for patients
who are unable to
tolerate CPAP
44. Surgical InterventionSurgical Intervention
Many different surgical approaches have been used
in the treatment of OSAHS, all with the intention
of increasing pharyngeal caliber and reducing
pharyngeal resistance during sleep
⢠UVULOPALATOPHARYNGOPLASTY (UPPP)
⢠Laser-assisted Uvulopalatopharyngoplasty
(LAUP) ď both not recommended in OSAHS
⢠Lateral Pharyngeoplasty
⢠Tracheostomy ď for OSAHS
⢠Mandibular Advancement
⢠Bariatric or Nasal or Lingual surgeries
⢠Radiofrequency Ablation
45. SDB in childrenSDB in children
⢠Snoring affects 18-20% of infants, 7-13%
of 2-8 year-old children, and 3-5% of
older children.
⢠Adenotonsillar hypertrophy is a major
contributor to SDB
⢠Other contributing factors include obesity,
craniofacial genetics, and neural control
mechanisms of upper airway patency
46. The pathophysiology of SDB in children isThe pathophysiology of SDB in children is
still poorly understood but the spectrum ofstill poorly understood but the spectrum of
disease and awareness of morbiditydisease and awareness of morbidity
associated with it is expandingassociated with it is expanding
Neurobehavioral
⢠Nocturnal enuresis,
⢠Reduced somatic
growth,
⢠Learning and
cognitive deficits, and
⢠Behavioural problems
that resemble
attention deficit-
hyperactivity disorder.
Cardiovascular
⢠Pulmonary
hypertension,
⢠Systemic hypertension
Increased use of healthcare services (2.6 fold)
47. SDB in The ElderlySDB in The Elderly
⢠Both snoring and sleep-related breathing
disorders (both central and obstructive
apnea) increase in frequency with
advancing age, at least until age 60 years.
⢠Little to no relationship seems to exist
between sleep apnea and typical risk
factors such as excess weight and
increased airway resistance.
48. ⢠The mechanism is purportedly a gradual
increase in sleep instability
⢠The effect on general health in elderly
people appears to be minimal.
49. SDB in WomenSDB in Women
⢠The prevalence in males exceeds that of
females by 3 fold in middle age.
⢠In the subset of patients with severe
obstructive sleep apnea, men outnumber
women by 8 fold, (?testosterone)
⢠Apneas tend to cluster during REM sleep
⢠No sex difference exists before puberty,
and, after menopause, the differences again
become small.
50. Hormonal influenceHormonal influence??
⢠Menopause may be a significant risk factor
for SDB in women
⢠The prevalence of SDB in postmenopausal
women on HRT is significantly lower than
in postmenopausal women not on HRT
51. UnderdiagnosisUnderdiagnosis??
⢠Data from the Wisconsin sleep cohort
study of patients without obvious barriers
to health care access estimate that 93% of
women and 82% of men with moderate-
to-severe sleep apnea were undiagnosed
⢠Women present for therapy even less
often!
52. OverLap SyndromeOverLap Syndrome
Â
Both COPD and the sleep apnea hypopnea syndrome
(SAHS) are relatively common conditions. Thus, by chance
alone, the two conditions will coexist in some patients
(Douglas, 1986). The term âoverlap syndromeâ was introduced
by Flenley to describe the association of SAHS with COPD.
53. ⢠Sleep disturbances and disorders are common in
patients with COPD
⢠Treatable sleep problems in COPD patients:
â Hypoxemia
â OSA
â RLS
â Insomnia
⢠We miss opportunities to help these patients when we
donât ask about, evaluate, or treat sleep problems
⢠CPAP is useful in overlap
54. Have aHave a
Nice DayNice Day
Good day starts withGood day starts with
good sleepgood sleep
Editor's Notes
Optimum daytime performance altered metabolism of glucose with an insulin resistance pattern similar to that observed in elderly men
Sleep apnea and other sleep-related breathing disorders constitute the greatest number of sleep disordersSDB refers to a wide spectrum of sleep-related breathing abnormalities; those related to increased upper airway resistance include snoring, ----- Besides being a common disorder, SDB also has been associated with considerable morbidity. Therefore, a basic understanding of this prevalent disease state is essential for the practicing physician.
Sleep apnea and other sleep-related breathing disorders constitute the greatest number of sleep disordersSDB refers to a wide spectrum of sleep-related breathing abnormalities; those related to increased upper airway resistance include snoring, ----- Besides being a common disorder, SDB also has been associated with considerable morbidity. Therefore, a basic understanding of this prevalent disease state is essential for the practicing physician.
This concept suggests that an individual who snores may be exhibiting the first manifestation of SDB and that snoring should not be viewed as normal. A patient can move gradually through the continuum, for example, with weight gain and eventual development of Pickwickian syndrome. He or she also can move rapidly through the spectrum through alcohol or sedative use, which can cause an individual who snores to turn into a snorer with obstructive sleep apnea (OSA). Additionally, although continuous positive airway pressure may be effective in the treatment of apnea, the individual may be left with continued residual UARS or snoring. Therefore, the clinician must recognize the continuum state of this disease entity because patients may continue to suffer from symptoms due to one aspect of SDB while being treated for another aspect of SDB.
Loud upper airway breathing sounds in sleep
In the past, snoring generally had been considered a social nuisance without any consequence to the snorerâonly to the suffering bed partner. After sleep apnea syndrome was recognized, snoring began being viewed in a new lightâas an important clinical symptom. Although it is by far the most common symptom of sleep apnea and is usually the main reason for a patient visit, not all patients who snore have sleep apnea. Many nonapneic snorers present with a constellation of signs and symptoms similar to those found in OSAHS, including daytime somnolence, tiredness, difficulty with concentration, headaches, and reduced work performance. Therefore, separating the effect of primary snoring from apnea is difficult because both conditions are linked closely.
Lugaresi E, Cirignotta F, Coccagna G, Piana C. Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep. 1980;3:221-4.
Gavriely N, Jensen O. Theory and measurements of snores. J Appl Physiol. 1993;74:2828-2837.
Bloom JW, Kaltenborn WT, Quan SF. Risk factors in a general population for snoring. Importance of cigarette smoking and obesity. Chest. 1988;93:678-683.
This concept suggests that an individual who snores may be exhibiting the first manifestation of SDB and that snoring should not be viewed as normal. A patient can move gradually through the continuum, for example, with weight gain and eventual development of Pickwickian syndrome. He or she also can move rapidly through the spectrum through alcohol or sedative use, which can cause an individual who snores to turn into a snorer with obstructive sleep apnea (OSA). Additionally, although continuous positive airway pressure may be effective in the treatment of apnea, the individual may be left with continued residual UARS or snoring. Therefore, the clinician must recognize the continuum state of this disease entity because patients may continue to suffer from symptoms due to one aspect of SDB while being treated for another aspect of SDB.
A primary snorer is usually asymptomatic and does not suffer from cardiovascular disease. Snoring in this population is usually an annoyance to the bed partner, but the snorer may deny any symptoms of daytime somnolence or difficulty with concentration. In contrast, snoring also may occur in conjunction with a disordered sleep pattern and may be associated with a range of symptoms, including overt OSAHS. This raises the possibility that, even in the absence of sleep apnea, snoring may be a causative factor in the pathogenesis of these disorders
Bedpartners, family members, or friends who may have shared a room with the sleeping patient initially may complain of loud or disruptive noises. The patient may complain of snoring themselves, a feeling of tiredness on waking, excessive sleepiness during the day, poor work performance, and difficulty with concentration.
Although rare, systemic disease may lead to snoring through disruption or dysfunction of the upper airway anatomy; however, signs and symptoms of systemic disease should be carefully sought, including those for hypothyroidism or acromegaly. Some nonapneic snorers may have objective physiologic findings similar to patients with sleep apnea, including high blood pressure, cardiac disease, strokes, and endocrine diseases such as diabetes or impaired insulin resistance. This raises the possibility that, even in the absence of sleep apnea, snoring may be a causative factor in the pathogenesis of these disorders
25 2
The American Academy of Sleep Medicine Task Force published a report that notes the key role that RERA plays in the pathophysiology of UARS in the absence of apnea or hypopnea.27
there must be a pattern of progressively increased negative esophageal pressure that is terminated by a sudden change in the pressure to a less negative level and a sleep arousalCurrent literature supports that esophageal pressures greater than -10 cm H20 are abnormal
29there must be a pattern of progressively increased negative esophageal pressure that is terminated by a sudden change in the pressure to a less negative level and a sleep arousal. Furthermore, the event must last 10 seconds or longerCurrent literature supports that esophageal pressures greater than -10 cm H20 are abnormal
but, in general, apnea may be associated with a greater fall in oxygen saturations
This index has now become the standard by which to define and quantify the severity of OSAHS.
Because night-to-night variability can occur in mild cases of the disorder, misdiagnosis can occur. Therefore, a negative first night test is insufficient to rule out OSAHS in patients with a high clinical suspicion of the disease2The neck circumference should be measured at the level of the cricothryoid membrane.
The dominant symptoms of OSAHS are sleepiness and daytime somnolence. Other symptoms include difficulty with concentration, fatigue, unrefreshed sleep, nocturnal choking, nocturia, depression, and decreased libido. Bed partners may report snoring, apneas, restless sleep, or irritability
33 34 .8The site of the narrowing is usually at the level of the pharynx Genetics may play an important role in the pathophysiology of OSAHS.
Lifestyle modification should be addressed in all patients suffering from snoring, including reduction of risk factors such as obesity, alcohol consumption, and muscle relaxant use
Because many of the symptoms of OSA are nonspecific, the index of clinical suspicion for the presence of OSAHS needs to be high to make the diagnosis. polysomnography
patient needs optimization of anesthesia and postoperative management.The differential diagnosis for OSAHS should include primary snoring, chronic hypoventilation syndrome, and central sleep apnea and Cheyne-Stokes respiration.
45% of stable treated CHF have moderate to severe SDB javaheri s, parker tj, wexler l, et l occult sleep diusdrdered breathing in stable congestive heart failure ann inter med 122 487-492 1995 associated with arousals and desaturations respoinse to theophyllin Cheyne-Stokes respiration is characterized by a crescendo - decrescendo pattern of respiration and
1836 Charles DickensJoe, the fat boy
In recent years, it has become apparent that SDB and snoring are not as innocuous as previously thought- Failure to timely diagnosis and treat may prevent some of these morbid complications from being completely reversible, leading to long-lasting residual consequences. However, the point of transition between what constitutes pathology and what is normal remains to be defined.
As part of such phenotype delineation, development of more sensitive and accurate tools for definition of disease and morbidity are needed.
The mechanisms underlying sleep apnea in elderly people are purportedly be different, and they may reflect a gradual increase in sleep instability, which results in both central apnea and OSA.
The pattern of apnea in older persons having AHI greater than 5 resembles typical sleep apnea in regard to duration and degree of desaturation.
There are important sleep-related physiological differences in women, including timing of nocturnal growth hormone secretion and differential time course of delta activity across the night.
The hypothesis that healthy postmenopausal women not on HRT have more SDB compared to women on HRT has also been confirmed in a large population-based study.
significantly increased risk of motor vehicle accidents, with reports of a 7-fold increased risk in patients with an AHI greater than 5. in particular is associated with increased severity of sleep-related breathing disorders,. In men with OSA, apneas predominate in the supine position.
The increase in frequency of sleep-related breathing disorders in women who are postmenopausal may be related to decreases in progesterone levels.
Women present for therapy even less often than the prevalence numbers would suggest