Week 3: Sleep Disordered Breathing

Question 1

Normal sleep architecture

Answer 1

• Goes through cycles of stage 1,2,3, Rem sleep
• as night progresses, there is more REM sleep
• stage 3=slow wave sleep/deep sleep, which there is more of in early night
• brain EEG: progression through the night-frequency decreases and amplitude increases
• beta, alpha, theta delta waves (from beta to delta, there is decreased frequency and increased amplitude)

Question 2

Changes in ventilation during sleep

Answer 2

• MV=TV x RR
• MV decreases, TV decreases, RR incresases during sleep
• End tidal O2 decreases, and end tidal CO2 increases
• SpO2 drops ~2%, PaO2 drops 3-10 mmHg, PaCO2 increases 2-8mmHG
• There is decreased CO2 production and decreased chemosensitivity (body tolerates greater CO2 in blood during sleep)

Question 3

Central sleep apnea

Answer 3

• means there is a problem with the sensor or central controller (in brainstem)
  1. Causes of sensor central sleep apnea: CHF (Cheynes Stokes breathing)
  2. Central controller sleep apnea
• respiratory depressant: narcotic, barbituates, benzodiazepines
• premature infants have immature brain stem-are treated with respiratory stimulant like caffeine or theophylline
• CCHS

Question 4

Describe respiratory pattern seen in CHF

Answer 4

• in heart failure there is a circulatory delay and increased CO2 sensitivity
• as a response to sensing greater pCO2, body will induce hyperpnea (deep and faster breathing)
• ventilation overshoots and generates opposite disturbance of decreased CO2 so is followed by period of apnea in response to the lowered CO2
• SpO2 has delayed response and desaturates at end of hyperpneic breathing

Question 5

Central vs obstructive sleep apnea seen in sleep studies

Answer 5

• both have airflow cessation
• in central apnea, there is no movement of chest and abdomen
• in obstructive there is effort seen in movement of chest and abdomen

Question 6

Upper airway changes during sleep

Answer 6

pharyngeal dilator muscles

• genioglossus: increased tone with inspiration, activated just before diaphragm contraction to stiffen the upper airway. decreased tone during sleep
• tensor palatini: tonic muscle contraction, reduced during sleep

Question 7

Mechanism of OSA

Answer 7

• negative pressure ventilation by diaphragm contraction
• extraluminal positive tissue pressure that is created by: fat deposition, small mandible/pharyngeal anatomy, enlarged tonsils and/or adenoids

Question 8

Risk factors for upper airway obstruction

Answer 8

• male
• post menopausal women
• age
• race: Asian>African american>hispanic>caucasian
• excess body weight
• large neck circumference
• craniofacial morphology: higher thyromental angle (between chin and neck), higher mallampati score (how much you can see through mouth), smaller thyromental distance (distance from chin to neck)
• familial, genetic predisposition

Question 9

Effects of repetitive apnea episodes

Answer 9

• Hypoxemia and reoxygenation injury: causing endothelial dysfunction, oxidative stress, inflammation, release of hypoxemia induced factor
• increased sympathetic stress associated with arousals during sleep: cardiac stress and insulin resistance
• multiple arousals leading to sleep deprivation

Question 10

Cardiovascular effects of sleep apnea

Answer 10

-associated with CV diseases: Afib, HTN (systemic and pulmonary), CV accident, CAD, CHF, insulin resistance

Question 11

Treatment options for OSA

Answer 11

• surgery: removal of parts of back of tongue, removal of tonsils/adenoids
• positive airway pressure: CPAP
• oral appliance/mandibular advancement device to pull the mandible/tongue forward