Respiratory JC016: A Fatigued And Sleepy Patient: Sleep And Breathing: Sleep Apnea Flashcards
Definition of sleep
Complex amalgam of physiological + behavioural process
2 physiological states:
1. Rapid eye movement (REM) sleep
2. Non-rapid eye movement (NREM) sleep
—> Characteristic brain wave activities
NREM and REM
- Enter sleep in NREM
- NREM and REM alternate —> 1 cycle 90 mins
NREM:
- 3/4 of sleeping time
- **↓ mental activities
- actively regulatory
- **body movable
Further divided into 4 stages according to EEG waves:
- Stages 1 and 2 (Light sleep)
- Stages 3 and 4 (Deep sleep): Slow wave sleep
REM:
- 1/4 sleep time
- increase in later hours of sleep (2nd phase of sleep)
- **dreaming
- **inhibit brainstem + motor neurons —> body paralysed, flaccid
Pattern of sleep
Factors affecting sleep patterns
- Age
- Prior sleep history (e.g. deprived of sleep —> REM rebound)
- Circadian rhythms
- Drug ingestion
- Pathological states
Control of breathing during sleep
- ***Respiratory centres
- **Chemical (O2, CO2 level), **Mechanical (respiratory muscle), CNS information
- ***Respiratory muscles (synchronised contraction)
- upper airway muscles
- diaphragm
- others
Sleep and Breathing
Sleep: ↓ Ventilation
NREM:
- ***↓ TV
- Similar rate
REM:
- **Unstable pattern
- **More shallow
—> If have lung disease —> even worse breathing pattern —> more hypoxaemia
In normal healthy lungs:
- Mild ↓ in blood O2 tension but still normal with no ↓ in SaO2
- Mild ↑ in blood CO2 tension but still normal
In diseased states e.g. COPD:
- Abnormal baseline —> worsen during sleep
Contributors for ↓ Ventilation in sleep
- ***↓ Muscle contraction from intercostal muscles (diaphragm relatively normal)
- **↓ Chemosensitivity to O2, CO2 with **↓ Ventilatory response to hypoxia and hypercapnia
- ***↓ Arousal response
- Recumbency (***Supine) with ↓ in Functional residual capacity (FRC) (∵ Diaphragm move up)
Primary sleep-related breathing disorders vs Respiratory diseases
Primary sleep-related breathing disorders:
- Breathing disorder occurs during sleep
- e.g. Sleep apnea
Respiratory diseases:
- Derangements in breathing pattern and gas exchange during sleep
- Changes in sleep pattern
Case:
- 45 male
- chronic smoker, social drinker
- sedentary lifestyle
- excessive fatigue 1-2 years but never dozed off during work
- wife notes he dozes off on buses / watching TV
- drives only on weekends, never dozed off but need loud music to keep awake
- heavy snoring for years
- weight gain 5kg in past few years
- no other systemic symptoms
- BP borderline high
History:
1. Sleep history
- duration
- ***quality
- Night time symptoms
- ***sleep choking (sense of suffocation during sleep)
- unusual body / limb movements - Daytime symptoms
- **sleepiness / fatigue (esp. during passive activity)
- assessment of sleepiness (subjective report using questionnaires in most daily settings, objective test too expensive)
—> **Epworth sleepiness scale
- “Do you think you will doze off in conditions where you should be keeping awake?” - Assess occupational / personal risks
- ***driving
- operation of mechanical devices
- home accidents - Other diseases
- ***hypertension
- stroke
- DM - Ask for medications
Physical examination
1. Body habitus: BMI, waist, neck circumference
- Craniofacial + Oropharyngeal features
- **chin structure (e.g. steep **thyromental plane)
- **enlarged tonsils (e.g. adenoid, palatine tonsils esp. in children)
- **uvula - BP, pulse
- Others
Common causes of Daytime sleepiness other than OSA
Daytime sleepiness: Cardinal symptom of OSA
Other causes:
- Insufficient sleep
- **Medications (e.g. opioids)
- Disturbance of sleep-wake cycle e.g. shift work
- **Central sleep apnea (mainly occur in people with certain disease)
- **Obesity hypoventilation syndrome
- Narcolepsy (cataplexy, sudden sleepiness)
- **Depression
- ***Fibromyalgia (Chronic fatigue syndrome)
- Idiopathic hypersomolence
- Periodic leg movement syndrome?
- Many medical conditions can cause “fatigue”
History and Physical examination of OSA
History:
1. Sleep history
- duration
- ***quality
- Night time symptoms
- ***sleep choking (sense of suffocation during sleep)
- unusual body / limb movements - Daytime symptoms
- **sleepiness / fatigue (esp. during passive activity)
- assessment of sleepiness (subjective report using questionnaires in most daily settings, objective test too expensive)
—> **Epworth sleepiness scale
- “Do you think you will doze off in conditions where you should be keeping awake?” - Assess occupational / personal risks
- ***driving
- operation of mechanical devices
- home accidents - Other diseases
- ***hypertension
- stroke
- DM - Ask for medications
Physical examination
1. Body habitus: BMI, waist, neck circumference
- Craniofacial + Oropharyngeal features
- **chin structure (e.g. steep **thyromental plane)
- **enlarged tonsils (e.g. adenoid, palatine tonsils esp. in children)
- **uvula - BP, pulse
- Others
Definitions of events
Apnea
- **complete cessation of airflow at nose and mouth lasting **>= 10 seconds
Hypopnea
- ↓ in airflow, usually needs O2 desaturation criteria (3-4% from baseline)
- ***>10 seconds per episode
- not complete closure of airway
**Apnea-Hypopnea index (AHI) / Respiratory disturbance index
- no. of apnoeic / hypopneic episodes per sleep hour
- normal: **<5 events per sleep hour (different for children / elderly) (some can be as severe as 100 episodes per hour)
- OSA: 5-15 times / hour (mild), 15-30 (moderate), >30 (severe) (from SC071)
2 mains types of sleep apnea
- Obstructive
- Central
One person may have both
- e.g. HF, Stroke
- NOT called “mixed apnea” —> refers to third type of apneic event
Obstructive Sleep Apnea
- Sleep-related breathing disorder
- Recurrent apneic / hypopneic episodes during sleep due to **Functional occlusion of upper airway
—> otherwise **patent during daytime - Apneic / hypopneic episodes will terminate eventually
- Wide range of severity
—> classified by conventional measurement of Apnea-Hyponea index
Categorisation for need of treatment:
- **Symptoms e.g. Daytime sleepiness
- **Sleep parameters e.g. Oxygen desaturation
***Mechanisms of obstruction
Anatomical + Non-anatomical factors
Non-anatomical factors:
1. **↓ Neuromuscular tone of upper airway during sleep
2. **Subatmospheric (negative) pressure in upper airway during inspiration (if airway more collapsible —> OSA)
3. Weight of soft tissue of neck
Anatomical abnormalities predisposing to functional obstruction:
1. **Micrognathia (small jaw)
2. **Enlarged tongue (falling back on supine posture)
3. ***Enlarged tonsils, adenoids (important factor in children)
4. Redundant pharyngeal tissue (fatty infiltration)
N.B. Acute infection / tumour can cause obstruction but not OSAS
***Investigations: Polysomnography (Sleep study)
- Full vs Limited sleep study
- In-laboratory (usually full study) vs Home study
- Non-invasive with multiple belts / leads
Aim:
1. Confirm presence + Define nature (obstructive / central) of apnea / hypopnea
2. Relation to other physiologic disturbances
—> O2 saturation (Multiple repeated dips: ↓ and then ↑)
—> HR, rhythm (***Tachy-Brady cycle)
—> Sleep architecture (sleep stages)
—> Body position (some only have OSA in supine position)
3. Look for Leg movements
Signs:
1. **Flow: episodic no flow (abdominal, thoracic belt moving in **opposite direction: one expand, one contract)
2. **EEG: disturbance in waveform after apneic episode
3. **Arousals
4. **Sleep fragmentation
5. **Intrathoracic pressure swings (∵ upper airway opening and closing) —> may cause strain on heart as well (worsen LV function)
6. **Intermittent hypoxia —> followed by Hypoxia-reoxygenation
7. **↑ BP during apneic episodes
Prevalence of OSA
- may occur in all age groups
- men > women
- ***sleepiness do NOT correlate well with numbers of events on sleep studies (i.e. Apnea-Hyponea index)
OSA syndrome (symptomatic OSA, usually defined as AHI >=5 / hour + Sleepiness):
- 4% men, 2% women
- but can be much higher if not take symptoms into consideration (many are asymptomatic)
- can be as high as 50% men with AHI >5
- updated prevalence expected to be much high due to obesity
- ***non-obese patients can have OSA!!! (esp. chinese ∵ unique cranio-facial features)
Symptomatology of OSAS
- ***Snoring
- ***Excessive daytime sleepiness
- Witnessed apneas
- ***Nocturnal choking (subclinical arousal)
- Restless sleep
- Unrefreshing sleep, ***morning headache
- Irritability, Intellectual deterioration, Poor concentration
- Decreased libido
- ***Enuresis / Nocturia
Risk factors for OSAS
- OSA patients very heterogenous
- multifactorial, unknown determinants
Risk factors:
- **Obesity / central obesity (major risk factor)
- Receding / **Small chin
- Thick neck
- Other medical diseases (esp. obesity-related)
—> HT
—> DM
—> **Metabolic syndrome etc.
- Predisposing diseases
—> **Acromegaly (∵ enlarged tongue)
—> **Hypothyroidism (∵ ↑ soft tissue)
—> Conditions with fluid retention
- **Adenotonsillar enlargement (esp. in children)
Co-morbidity / Consequences of OSA?
Consider:
1. Pathophysiology
2. Epidemiologic / Clinical associations, adjusting for confounding factors
3. Treat OSA —> look for improvement
Potential downstream pathophysiology:
Genetics / Non-genetics (diet, exercise, alcohol, smoking)
—> Fat
—> OSA
—> Intermittent hypoxia, Sleep fragmentation (—> Fat)
—> **Sympathetic activation + **Oxidative stress + ***Inflammation (e.g. adipocytokines)
—> Obesity, Insulin resistance, Glucose intolerance, Dyslipidaemia, NAFLD, Metabolic syndrome
***Potential consequences of OSA
- Excessive sleepiness
- car accidents
- other accidents - Neurocognitive impairment
- irritability
- poor concentration - Cardiometabolic diseases (suggested role in initiation / aggravation)
- **HT
- Atherosclerosis
- Ventricular dysfunction
- **HF
- Arrhythmia: AF
- ***DM - Chronic respiratory failure / Cor pulmonale
- uncommon in OSA only
- seen in ***Obesity-hypoventilation syndrome / presence of other condition e.g. COPD + OSA
—> very hypoxaemic —> Cor pulmonale
Aim of treatment of OSA
- Control symptoms
- Reduce long term sequelae
- Evidence based medicine
- evidence for long term clinical sequalae (e.g. HT)
- effects of treatment of OSA on these outcome measures
***Treatment of OSA
Consideration:
1. Which patients need treatment
2. Think about pathogenetic factors + pathophysiologic mechanisms
3. What treatment method can modify these pathogenetic factors / reverse pathophysiology
- Lifestyle modifications
- ***Weight reduction
- Avoid alcohol / hypnotics
- Sleep hygiene
- Sleep posture
- Avoid driving if not adequately treated
- Others: treat Rhinitis, Acromegaly, care after sedation / anaesthesia
- Must watch out for obesity-related conditions e.g. Metabolic syndrome, DM, HT - ***Nasal continuous positive airway pressure (nCPAP)
- positive pressure through nasal mask during sleep
- consistently effective but effects depends on compliance - Oral appliances
- advance mandible —> “enlarge” upper airway, modifies muscle collapsibility
- variable efficacy, usually not for severe OSA - Surgery
- children: removal of hypertrophied tonsils / adenoids
- adults: uvulopharyngoplasty, other faciomaxillary surgeries (for selected group, variable efficacy)
- bariatric surgery for reducing obesity - Newer devices
- neurostimulator for upper airway muscle
- sleep positioner - Pharmacological? Targeting:
- upper airway muscle tone
- obesity
- arousal threshold
- hypersomnolence
Obesity Hypoventilation Syndrome (OHS)
- Gross obesity
- Majority of OHS have severe OSA
- Hypoventilation evidenced by ***high daytime pCO2 —> sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness (“CO2 narcosis”)
- ***Chronic type 2 respiratory failure (may present as acute on chronic respiratory failure and CO2 narcosis)
- ***Cor pulmonale
- Excessive daytime sleepiness
- Respiratory failure respond well to treatment with nCPAP / Bi-level PAP (i.e. similar to non-invasive ventilatory support)
Central Sleep Apnea
Defect in:
- Central control: **lack of respiratory drive
- Efferent limb: **no muscle contraction (e.g. Muscular dystrophy / NMJ problem: Myasthenia gravis)
—> resulting in lack of effort to breathe
Sign:
- **Lack of abdominal / thoracic belt movement in polysomnography
- **Cheynes Stokes Breathing (CSR) (~ HF / LV dysfunction)
Cheynes Stokes Breathing
Characteristic form of breathing:
- ***wax and wane pattern
- may have central apnea at end of waning phase
- usually associated with HF / stroke
- CSR associated with worse prognosis in HF
- CSR likely caused by HF with circulatory slowing (may disappear if HF controlled)
