2. is a state of physical and mental inactivity
with profound physiological changes.
3. is a state of physical and mental inactivity
with profound physiological changes.
freshens mind and body, maintains
normal neurohumoral homeostasis.
4. is a state of physical and mental inactivity
with profound physiological changes.
freshens mind and body, maintains
normal neurohumoral homeostasis.
It’s importance is best understood by
those who do not get it.
5.
6. Yes. It is probably so for the observer or the
physician.
7. Yes. It is probably so for the observer or the
physician.
We can unravel many a complex states by
understanding sleep. e.g.,Narcoanalysis.
19. SLEEP DISORDERED BREATHING (SDB)
* Sleep-disordered breathing is an extremely common
medical disorder associated with important morbidity.
20. SLEEP DISORDERED BREATHING (SDB)
* Sleep-disordered breathing is an extremely common
medical disorder associated with important morbidity.
* Recognition of its relevance in medicine is relatively
recent.
21. SLEEP DISORDERED BREATHING (SDB)
* Sleep-disordered breathing is an extremely common
medical disorder associated with important morbidity.
* Recognition of its relevance in medicine is relatively
recent.
* Hunter, Cheyne, and Stokes described SDB in 19th
century.
22. SLEEP DISORDERED BREATHING (SDB)
* Sleep-disordered breathing is an extremely common
medical disorder associated with important morbidity.
* Recognition of its relevance in medicine is relatively
recent.
* Hunter, Cheyne, and Stokes described SDB in 19th
century.
* In 1976 Guilleminault had coined the term OSA.
23. SLEEP DISORDERED BREATHING (SDB)
SDB is present when there are repetitive
episodes of cessations of respiration (apnea)
or decrement in airflow during sleep
(hypopnea), associated with sleep
fragmentation, arousal and reduction in SPO2.
25. SLEEP DISORDERED BREATHING (SDB)
Apnea can be Obstructive, Central or Mixed.
A majority of patients with obstructive sleep
apnea (OSA) have both obstructive and mixed
apneas.
26. SLEEP DISORDERED BREATHING (SDB)
Central Sleep Apnea (CSA) is less common
and is characterized by transient cessation of
rhythmic breathing. Occurs in CVA, CHF.
27. SLEEP DISORDERED BREATHING (SDB)
Central Sleep Apnea (CSA) is less common
and is characterized by transient cessation of
rhythmic breathing. Occurs in CVA, CHF.
Upper Airway Resistance Syndrome (UARS) is a
milder form of OSA without hypoxemia.
28. SLEEP DISORDERED BREATHING (SDB)
Obesity hypoventilation syndrome (OHS), or
the Pickwickian syndrome, is defined by morbid
obesity (BMI >40 kg/m2) and chronic
hypoventilation with hypercapnia
(PaCO2 >45 mmHg) during wakefulness.
29.
30. The pathogenesis of OSA involves both an
anatomic and a neurologic component.
31. The pathogenesis of OSA involves both an
anatomic and a neurologic component.
The upper airway is an extremely
complicated structure performing several
different physiologic functions, including
vocalization, respiration, and deglutition.
32.
33.
34. In a patient with sleep apnea, collapse
of the upper airway occurs most
commonly in the retropalatal and retroglossal
regions.
36. Anatomic Features That Predisposes to Apnea
Upper airway caliber during wakefulness itself is
smaller in patients with sleep apnea.
37. Anatomic Features That Predisposes to Apnea
Upper airway caliber during wakefulness itself is
smaller in patients with sleep apnea.
Patients with OSA have larger tongues and longer
soft palates and narrowing of the pharyngeal
lumen compared with normal subjects, whether
or not they are obese.
38.
39. Upper airway caliber during wakefulness is smaller in
patients with sleep apnea caused by larger tongues,
longer soft palates and generalized narrowing of the
pharyngeal lumen than normal subjects.
41. Neural Modulation of Upper Airway Patency
During sleep there is reduced upper airway
dilator muscle activity.
42. Neural Modulation of Upper Airway Patency
During sleep there is reduced upper airway
dilator muscle activity.
The neurotransmitters like serotonin,
noradrenaline, TSH, Substance p, and
aminobutyric acid are also influenced by sleep.
43. Neural Modulation of Upper Airway Patency
During sleep there is reduced upper airway
dilator muscle activity.
The neurotransmitters like serotonin,
noradrenaline, TSH, Substance p, and
aminobutyric acid are also influenced by sleep.
In REM sleep the airway dilator muscle activity
can be completely suppressed. Therefore,
apneas occur more commonly during REM
sleep.
45. Epidemiology of OSA
Incidence and prevalence rates depend upon study
pattern and population strata studied.
46. Epidemiology of OSA
Incidence and prevalence rates depend upon study
pattern and population strata studied.
The prevalence has been reported to be 4 to 9
percent in men and 2 to 4 percent in women
between the ages of 30 and 60.
47. Epidemiology of OSA
Incidence and prevalence rates depend upon study
pattern and population strata studied.
The prevalence has been reported to be 4 to 9
percent in men and 2 to 4 percent in women
between the ages of 30 and 60.
Around 80% of OSAs are not diagnosed, therefore
actual OSA prevalence could be about 34% of
general population.
82. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
83. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
84. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
85. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
86. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
o Excessive daytime sleepiness
87. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
o Excessive daytime sleepiness
o Automobile or work-related accidents
88. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
o Excessive daytime sleepiness
o Automobile or work-related accidents
o Irritability, memory loss, personality change
89. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
o Excessive daytime sleepiness
o Automobile or work-related accidents
o Irritability, memory loss, personality change
o Decreased libido
90. Clinical Presentation of Obstructive Sleep Apnea
o Loud, habitual snoring
o Witnessed apneas
o Nocturnal awakening
o Gasping or choking episodes during sleep
o Nocturia
o Unrefreshing sleep, morning headaches
o Excessive daytime sleepiness
o Automobile or work-related accidents
o Irritability, memory loss, personality change
o Decreased libido
o Impotence
94. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
95. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
96. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
97. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
o Pulmonary hypertension
98. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
o Pulmonary hypertension
o Type II diabetes mellitus
99. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
o Pulmonary hypertension
o Type II diabetes mellitus
o Nocturnal cardiac arrhymthmias
100. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
o Pulmonary hypertension
o Type II diabetes mellitus
o Nocturnal cardiac arrhymthmias
o Driver involved in a sleep-related automobile crash
101. Conditions in which Sleep Apnea Should be Suspected
o Systemic hypertension
o Obesity
o Myocardial infarction
o Cerebrovascular accident
o Pulmonary hypertension
o Type II diabetes mellitus
o Nocturnal cardiac arrhymthmias
o Driver involved in a sleep-related automobile crash
o Preoperative anesthesia evaluation
104. Cardiovascular and Cerebrovascular
Consequences
o OSA raises 24 hr mean BP by 5 – 10 mm Hg.
o Rise occurs due to arousal at apnea termination
and raised sympathetic tone.
o There is 20% risk increase in MI and 40% in CVA.
o There is evidence that treatment of OSA improves
stroke outcome.
106. Diabetes Mellitus and OSA
o Obesity is common in both.
o Increased Insulin resistance is independent of
obesity.
o OSA aggravates DM and treatment of OSA helps in
reducing the Insulin requirements.
110. Anaesthetic risks in OSA
o Increased perioperative risk.
o Upper airway may obstruct due to sedation.
o There is a correlation between patients with
difficult intubation and SDB. Therefore pre
anaesthetic work up must involve OSA also.
111. Anaesthetic risks in OSA
o Increased perioperative risk.
o Upper airway may obstruct due to sedation.
o There is a correlation between patients with
difficult intubation and SDB. Therefore pre
anaesthetic work up must involve OSA also.
127. Diagnosis of OSA
History and physical examination.
Obtained in one of three settings:
128. Diagnosis of OSA
History and physical examination.
Obtained in one of three settings:
1. Part of routine health maintenance
evaluation,
129. Diagnosis of OSA
History and physical examination.
Obtained in one of three settings:
1. Part of routine health maintenance
evaluation,
2. Part of an evaluation of symptoms of
obstructive sleep apnea,
130. Diagnosis of OSA
History and physical examination.
Obtained in one of three settings:
1. Part of routine health maintenance
evaluation,
2. Part of an evaluation of symptoms of
obstructive sleep apnea,
3. As part of the comprehensive evaluation of
patients at high risk for OSA.
132. Diagnosis of OSA
High-risk patients include those who are
• obese,
133. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
134. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
135. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
• treatment refractory hypertension,
136. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
• treatment refractory hypertension,
• type 2 diabetes, stroke,
137. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
• treatment refractory hypertension,
• type 2 diabetes, stroke,
• nocturnal dysrhythmias,
138. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
• treatment refractory hypertension,
• type 2 diabetes, stroke,
• nocturnal dysrhythmias,
• pulmonary hypertension,
139. Diagnosis of OSA
High-risk patients include those who are
• obese,
• congestive heart failure,
• atrial fibrillation,
• treatment refractory hypertension,
• type 2 diabetes, stroke,
• nocturnal dysrhythmias,
• pulmonary hypertension,
• high-risk driving populations (such as commercial
truck drivers), and those being evaluated for bariatric
surgery
140. Diagnosis of OSA
Questions to be asked during a routine health evaluation:
141. Diagnosis of OSA
Questions to be asked during a routine health evaluation:
• History of snoring and daytime sleepiness and
an evaluation for the presence of obesity,
retrognathia or hypertension.
142. Diagnosis of OSA
Questions to be asked during a routine health evaluation:
• History of snoring and daytime sleepiness and
an evaluation for the presence of obesity,
retrognathia or hypertension.
• Positive findings on this OSA screen should lead
to a more comprehensive sleep history and
physical examination.
146. Diagnosis of OSA
An evaluation of secondary conditions
hypertension,
stroke,
myocardial infarction,
cor pulmonale,
decreased daytime alertness, and
motor vehicle accidents.
The physical examination can suggest increased
risk and should include the respiratory,
cardiovascular, and neurologic systems.
147. Diagnosis of OSA
Particular attention should be paid to the presence of
148. Diagnosis of OSA
Particular attention should be paid to the presence of
obesity,
signs of upper airway narrowing or
the presence of other disorders that can
contribute to the development of OSA or to the
consequences of OSA.
150. Diagnosis of OSA
Features to be evaluated
increased neck circumference(>17” in men, >16” inches in women),
body mass index (BMI) ≥ 30 kg/m2,
Modified Mallampati score of 3 or 4
The presence of retrognathia,
lateral peritonsillar narrowing,
Macroglossia,
tonsillar hypertrophy
elongated/enlarged uvula,
high arched/narrow hard palate,
nasal abnormalities (polyps, deviation, valve abnormalities,
turbinate hypertrophy) and/or overjet.
152. Diagnosis of OSA
Objective testing:
The severity of OSA must be established in order to make
an appropriate treatment decision.
No clinical model is recommended to predict severity of
obstructive sleep apnea therefore objective testing is
required.
The two accepted methods of objective testing are
in-laboratory polysomnography (PSG) and
home testing with portable monitors (PM).
PSG is routinely indicated for the diagnosis of sleep
related breathing disorders.
155. Diagnosis of OSA
Polysomnography:
Requires recording the following physiologic signals:
electroencephalogram (EEG),
Electrooculogram (EOG),
Chin electromyogram,
Airflow,
Oxygen saturation,
Respiratory effort, and
Electrocardiogram (ECG) or heart rate.
body position and leg EMG derivations.
Anterior tibialis EMG is useful
to assist in detecting movement arousals
added benefit of assessing periodic limb movements.
156. Diagnosis of OSA
Polysomnography:
Requires recording the following physiologic signals:
electroencephalogram (EEG),
Electrooculogram (EOG),
Chin electromyogram,
Airflow,
Oxygen saturation,
Respiratory effort, and
Electrocardiogram (ECG) or heart rate.
body position and leg EMG derivations.
Anterior tibialis EMG is useful
to assist in detecting movement arousals
added benefit of assessing periodic limb movements.
157. Diagnosis of OSA
Polysomnography:
Requires recording the following physiologic signals:
electroencephalogram (EEG),
Electro-oculogram (EOG),
Chin electromyogram,
Airflow,
Oxygen saturation,
Respiratory effort, and
Electrocardiogram (ECG) or heart rate.
body position and leg EMG derivations.
Anterior tibialis EMG is useful
to assist in detecting movement arousals
added benefit of assessing periodic limb movements.
158. Diagnosis of OSA
Full night PSG:
Full-night PSG is recommended for the diagnosis of a
sleep related breathing disorder
A split-night study is an alternative to one full night of
diagnostic PSG.
The split-night study may be performed if an AHI ≥ 40/hr
is documented during 2 hours of a diagnostic study but
considered for an AHI of 20-40/hr based on clinical
judgment.
In patients where there is a strong suspicion of OSA, if
other causes for symptoms have been excluded, a second
diagnostic overnight PSG may be necessary to diagnose
the disorder.
159. Diagnosis of OSA
Confirmation of Diagnosis of OSA:
Number of obstructive events on PSG is greater than 15
events/hr or greater than 5/hour in a patient who reports any
of the following:
unintentional sleep episodes during wakefulness;
daytime sleepiness;
unrefreshing sleep;
fatigue;
insomnia;
waking up breath holding,
gasping, or
choking; or
the bed partner describing loud snoring, breathing
interruptions, or both during the patient's sleep.
160. Diagnosis of OSA
Confirmation of Diagnosis of OSA:
Number of obstructive events on PSG is greater than 15
events/hr or greater than 5/hour in a patient who reports any
of the following:
unintentional sleep episodes during wakefulness;
daytime sleepiness;
unrefreshing sleep;
fatigue;
insomnia;
waking up breath holding,
gasping, or
choking; or
the bed partner describing loud snoring, breathing
interruptions, or both during the patient's sleep.
OSA severity is defined as
mild for RDI ≥ 5 and < 15,
moderate for RDI ≥ 15 and ≤
30, and severe for RDI > 30/hr.
161. Diagnosis of OSA
Testing with Portable Monitors (PM):
PM for the diagnosis of OSA should be performed only in
conjunction with a comprehensive sleep evaluation.
Clinical sleep evaluations using PM must be supervised by a
practitioner with board certification in sleep medicine or
an individual who fulfills the eligibility criteria for the
sleep medicine certification examination.
A PM should, at a minimum record
airflow,
respiratory effort, and
blood oxygenation.
162. Treatment of OSA
Medical treatment of OSA by
Dr. Narayana Pradeep DTCD
Surgical treatment of OSA by
Dr. Adarsha Herale DLO, DNB.