Obstructive sleep apnea

Sleep Disorders - obstructive sleep apnea

independent risk factors

• obesity

Index of Suspicion for OSA?

• Step 1: History 

• S: "Do you snore loudly, loud enough to be heard 

through a closed door?"

• T: "Do you feel tired or fatigued during the 

daytime almost every day?"

• O: "Has anyone observed that you stop breathing 

during sleep?“ Awakening with choking.

• P: "Do you have a history of high blood pressure

with or without treatment?"

Step 2 : Physical Exam

• B: BMI greater than 35; body habitus

• A: Age older than 50 years

• N: Neck circumference greater than 43 cm (17 in)

• G: Gender, male (postmenopausal female)

Conditions associated with OSA

• Hypothyroidism – elderly females
• Neurologic syndromes –
• muscular dystrophies
• Stroke – cause vs effect
• Acromegaly - macroglossia
• Environmental exposures –second-hand smoke, environmental irritants or allergens

Obesity Hypoventilation Syndrome (Pickwickian Syndrome)

Joe the Fat Boy

• Type 1 – typical OSA (90%) 

- decrease of functional lung volume - airway compromise, V/Q mismatch – decreased O2 sat, and cor pulmonale.

• Type 2 – chronic hypercapnia, decreased noc O2 sat without simultaneous apnea or hypopnea (10%)

Risk of OSA based on palate (Mallampati Score)

Sleep Studies

done during nl sleep period

• Sleep stages - EEG, 
• electro-oculogram, and chin electromyogram (EMG).
• Heart rhythm - singlelead ECG.
• Leg movements -
• anterior tibialis EMG.
• Breathing pattern analyzed for the presence of apneas and hypopneas
• O2 saturation.
• Breathing - airflow at the nose and mouth (thermal sensors, nasal pressure transducer), effort - chest wall and abdomen (inductance plethysmography)

Tx choices

• CPAP
• Tracheostomy
• Weight loss
• Oral appliance
• Surgery
• Supplemental Oxygen

USMLE – Benefits of CPAP

• Decreased RDI

• Improved sleep architecture

• Improved nocturnal O2 sat

• Improved driving, daytime sleepiness, neurocognitive fn

• Improved perceived health status

• Decreased mortality, arrhythmia, HTN, noc ischemia, health care visits

• Improved LVH in CHF 

Central Sleep Apnea (CSA) - no breathing effort 

• Primary central apnea is rare

• Most cases occur with OSA (mixed apnea)

• During polysomnography a central apneic event is defined as cessation of airflow for 10 seconds or longer without an identifiable respiratory effort

• Causes: drug use, high altitude, Cheyne-Stokes breathing , stroke, other rare medical conditions

• unstable ventilatory control during sleep is the hallmark, the pathophysiology and prevalence of various forms of CSA vary

Basic Pathophysiology - CSA

• Brainstem chemoreceptors (neurons responding to CO2 via shifts in H+ concentration) and peripheral chemoreceptors (carotid body via Pao2 and Paco2 ) play a key role in 

modulating ventilation. 

• ventilatory output to a given change in Pao2 or Paco2 varies between individuals and with disease status. Highly sensitive chemoresponders are at risk for unstable breathing patterns because they over-respond to small changes in chemical stimuli. 

• delays in the negative feedback loop controlling ventilation also contribute to the risk for developing instability. E.g. increased PaCO2 will result in increased ventilation; increased ventilation leads to reduced PaCO2 due to chemoreceptor response; low PaCO2

then leads to hypoventilation and potential apnea

• Sleep generally characterized by elevation of PaCO2 and a higher PaCO2 apneic threshold, (PaCO2 below which apnea occurs). Very small reduction of PaCO2 can result in apneas. 

• Central apneic events commonly occur during the transition between wake and sleep, a 

period during which the PaCO2 set point adjusts.

Eckert, et al, Chest. 2007 February; 131(2): 595–607 

Treatment

• Non-pharmacologic methods vary, depending on underlying conditions: O2

(CHF), CPAP (CheyneStokes), increased dead space

• Drugs: acetazolamide - causes bicarbaturia and metabolic acidosis, which presumably shifts the apneic threshold of PaCO2 to a lower level 

• Theophylline 

• benzos, newer sedative-hypnotics (eg zolpidem) – non-hypercapnic CSA, believed to work by consolidating the sleep pattern, thus minimizing the instability in ventilation induced by sleepwake transitions