is sleep sixth sense

Dr. Jayadev Kangila MD DNB.

SLEEP is a state of physical and mental inactivity

with profound physiological changes.



freshens mind and body, maintains normal neurohumoral homeostasis.



freshens mind and body, maintains normal neurohumoral homeostasis.

It’s importance is best understood by those who do not get it.

Is sleep sixth sense?

Is sleep sixth sense?Yes. It is probably so for the observer or the physician.

Is sleep sixth sense?Yes. It is probably so for the observer or the physician.

We can unravel many a complex states by understanding sleep. e.g.,Narcoanalysis.

Look at these persons

What do they have in common?

SLEEP DISORDERED BREATHING (SDB)

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.




* Hunter, Cheyne, and Stokes described SDB in 19th century.

* In 1976 Guilleminault had coined the term OSA.


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.


Apnea can be Obstructive, Central or Mixed.


Apnea can be Obstructive, Central or Mixed.

A majority of patients with obstructive sleep apnea (OSA) have both obstructive and mixed apneas.


Central Sleep Apnea (CSA) is less common and is characterized by transient cessation of rhythmic breathing. Occurs in CVA, CHF.


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.


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.

PATHOGENESIS OF OSA

PATHOGENESIS OF OSA

The pathogenesis of OSA involves both an anatomic and a neurologic component.

PATHOGENESIS OF OSA

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.

PATHOGENESIS OF OSA

PATHOGENESIS OF OSA

In a patient with sleep apnea, collapse of the upper airway occurs most commonly in the retropalatal and retroglossal regions.

PATHOGENESIS OF OSA

Anatomic Features That Predisposes to Apnea

PATHOGENESIS OF OSA


Upper airway caliber during wakefulness itself is smaller in patients with sleep apnea.

PATHOGENESIS OF OSA


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.

PATHOGENESIS OF OSA

PATHOGENESIS OF OSA

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.

PATHOGENESIS OF OSA

Neural Modulation of Upper Airway Patency

PATHOGENESIS OF OSA

Neural Modulation of Upper Airway Patency During sleep there is reduced upper airway dilator muscle activity.

PATHOGENESIS OF OSA

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.

PATHOGENESIS OF OSA

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.

Epidemiology of OSA

Epidemiology of OSAIncidence 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.



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.

LET’S HAVE A BREAK!

LET’S HAVE A BREAK!One day Penga comes to a Lab.

LET’S HAVE A BREAK!One day Penga comes to a Lab.

Finds his friend Ninga there, who is crying...

LET’S HAVE A BREAK!Penga: “Why are you crying”?

LET’S HAVE A BREAK!Ninga: “ I came for BLOOD

investigation and they CUT MY FINGER”!

LET’S HAVE A BREAK!At this, Penga bursts into cry.

LET’S HAVE A BREAK!Ninga: “Now why are you crying”?

LET’S HAVE A BREAK!Penga: “I came to get my URINE

examined”!

Risk Factors for Obstructive Sleep Apnea

Risk Factors for Obstructive Sleep Apnea• Gender (male/female 2:1)

Risk Factors for Obstructive Sleep Apnea• Gender (male/female 2:1)• Obesity (>120% ideal body weight)

Risk Factors for Obstructive Sleep Apnea• Gender (male/female 2:1)• Obesity (>120% ideal body weight)• Neck size (collar size > 17 inches in males, > 15 inches in females)

Risk Factors for Obstructive Sleep Apnea• Gender (male/female 2:1)• Obesity (>120% ideal body weight)• Neck size (collar size > 17 inches in males, > 15 inches in females)• Upper airway anatomy


- Macroglossia


- Macroglossia - Lateral peritonsillar narrowing


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate - Tonsillar hypertrophy


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate - Tonsillar hypertrophy - Nasal septal deviation


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate - Tonsillar hypertrophy - Nasal septal deviation - Retrognathia, micrognathia


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate - Tonsillar hypertrophy - Nasal septal deviation - Retrognathia, micrognathia - Narrowing of the hard palate


- Macroglossia - Lateral peritonsillar narrowing - Elongation/enlargement of the soft palate - Tonsillar hypertrophy - Nasal septal deviation - Retrognathia, micrognathia - Narrowing of the hard palate - Class III/IV modified Mallampati airway



• Specific genetic diseases, e.g., Treacher Collins, Downs syndrome etc.



• Specific genetic diseases, e.g., Treacher Collins, Downs syndrome etc.• Genetic factors



• Specific genetic diseases, e.g., Treacher Collins, Downs syndrome etc.• Genetic factors• Endocrine disorders - hypothyroidism, acromegaly, diabetes



• Specific genetic diseases, e.g., Treacher Collins, Downs syndrome etc.• Genetic factors• Endocrine disorders - hypothyroidism, acromegaly, diabetes• Alcohol, sedative or hypnotic use

Clinical Presentation of Obstructive Sleep Apnea


o Loud, habitual snoring


o Loud, habitual snoringo Witnessed apneas


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakening


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleep


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturia


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headaches


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headacheso Excessive daytime sleepiness


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headacheso Excessive daytime sleepinesso Automobile or work-related accidents


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headacheso Excessive daytime sleepinesso Automobile or work-related accidentso Irritability, memory loss, personality change


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headacheso Excessive daytime sleepinesso Automobile or work-related accidentso Irritability, memory loss, personality changeo Decreased libido


o Loud, habitual snoringo Witnessed apneaso Nocturnal awakeningo Gasping or choking episodes during sleepo Nocturiao Unrefreshing sleep, morning headacheso Excessive daytime sleepinesso Automobile or work-related accidentso Irritability, memory loss, personality changeo Decreased libidoo Impotence

Conditions in which Sleep Apnea Should be Suspected

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertension

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesity

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarction

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accident

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accidento Pulmonary hypertension

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accidento Pulmonary hypertensiono Type II diabetes mellitus

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accidento Pulmonary hypertensiono Type II diabetes mellituso Nocturnal cardiac arrhymthmias

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accidento Pulmonary hypertensiono Type II diabetes mellituso Nocturnal cardiac arrhymthmiaso Driver involved in a sleep-related automobile crash

Conditions in which Sleep Apnea Should be Suspectedo Systemic hypertensiono Obesityo Myocardial infarctiono Cerebrovascular accidento Pulmonary hypertensiono Type II diabetes mellituso Nocturnal cardiac arrhymthmiaso Driver involved in a sleep-related automobile crasho Preoperative anesthesia evaluation

Cardiovascular and Cerebrovascular Consequences

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.

Diabetes Mellitus and OSA

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.

Hepatic Consequences of OSA

Hepatic Consequences of OSA

o Hepatic dysfunction.

o Elevation of liver enzymes.

o Increased steatosis and fibrosis on liver biopsy.

Anaesthetic risks in OSA

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.

LET’S HAVE ANOTHER BREAK!

LET’S HAVE ANOTHER BREAK!Penga goes for his public exam.

LET’S HAVE ANOTHER BREAK!Penga goes for his public exam.

After writing a page, starts removing his shirt and pants.

LET’S HAVE ANOTHER BREAK!Examiner: “Penga, what are you doing?.

LET’S HAVE ANOTHER BREAK!Penga: “They have asked to write answers only in BRIEF”!

Diagnosis of OSA

Diagnosis of OSA

History and physical examination.

Diagnosis of OSA


Objective testing.

Diagnosis of OSA


Objective testing.

Polysomnography (PSG) and portable monitors (PM).

Diagnosis of OSA


Diagnosis of OSA

History and physical examination. Obtained in one of three settings:

Diagnosis of OSA


1. Part of routine health maintenance evaluation,

Diagnosis of OSA



2. Part of an evaluation of symptoms of obstructive sleep apnea,

Diagnosis of OSA



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.

Diagnosis of OSA High-risk patients include those who are


• obese,


• obese,• congestive heart failure,


• obese,• congestive heart failure, • atrial fibrillation,


• obese,• congestive heart failure, • atrial fibrillation,• treatment refractory hypertension,


• obese,• congestive heart failure, • atrial fibrillation,• treatment refractory hypertension,• type 2 diabetes, stroke,


• obese,• congestive heart failure, • atrial fibrillation,• treatment refractory hypertension,• type 2 diabetes, stroke, • nocturnal dysrhythmias,


• obese,• congestive heart failure, • atrial fibrillation,• treatment refractory hypertension,• type 2 diabetes, stroke, • nocturnal dysrhythmias, • pulmonary hypertension,


• 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

Diagnosis of OSAQuestions 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.


• 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.

Diagnosis of OSAA comprehensive sleep history

Diagnosis of OSAA comprehensive sleep history

evaluation for snoring,witnessed apneas, gasping/choking episodes, excessive sleepiness,total sleep amount,nocturia, morning headaches, sleep fragmentation/sleep maintenance insomnia,

and decreased concentration and memory

Diagnosis of OSAAn evaluation of secondary conditions

Diagnosis of OSAAn 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.

Diagnosis of OSAParticular attention should be paid to the presence of

Diagnosis of OSAParticular 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.

Diagnosis of OSAFeatures to be evaluated

Diagnosis of OSAFeatures to be evaluatedincreased neck circumference(>17” in men, >16” inches in women), body mass index (BMI) ≥ 30 kg/m2,Modified Mallampati score of 3 or 4The presence of retrognathia,lateral peritonsillar narrowing, Macroglossia,tonsillar hypertrophyelongated/enlarged uvula, high arched/narrow hard palate, nasal abnormalities (polyps, deviation, valve abnormalities, turbinate hypertrophy) and/or overjet.

Diagnosis of OSAObjective testing:

Diagnosis of OSAObjective 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.

Diagnosis of OSAPolysomnography:

Diagnosis of OSAPolysomnography: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.

Diagnosis of OSAPolysomnography: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.

Diagnosis of OSAFull 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.

Diagnosis of OSAConfirmation 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, orchoking; orthe bed partner describing loud snoring, breathing

interruptions, or both during the patient's sleep.

Diagnosis of OSAConfirmation 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, orchoking; orthe 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.

Diagnosis of OSATesting 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.

Treatment of OSA

Medical treatment of OSA byDr. Narayana Pradeep DTCD

Surgical treatment of OSA byDr. Adarsha Herale DLO, DNB.

is sleep sixth sense

Health & Medicine