10-2 CIS Sleep Apnea - Pate Flashcards
What did Dr. Pate mention about what is measured in a PSG?
- 17-channel polysomnography, including electroencephalogram, electrooculogram, submentalis electromyogram
- Airflow via pressure transducers
- Respiratory effort via chest and abdomen motion
- Arterial oxygen saturation via an oximeter
- Sleep score via EEG
What is the apnea index?
•Apnea index (per hour of sleep)
–>apnea = 10s absence of airflow and characterized as obstructive v. non-obstructive
- obstructive = respiratory effort in place
- non-obstructive = no respiratory effort, body isn’t trying to breathe at all
(Obstructive events can happen in REM, since there is still respiratory effort from the diaphragm.)
What is the hypopnea index?
•Hypopnea index (per hour of sleep)
–Reduced airflow for >10s accompanied by an oxygen desaturation >3%
What is the apnea-hypopnea index?
•(total # of events / total sleep time)
What is ataxic breathing?
•(AKA Biot’s respiration)
–Defined as irregular breathing pattern with central apneas. Measured during NREM sleep only
- breathing pattern and respiratory pattern is naturally erratic during REM due erratic innervation of the diaphragm
What is Cheyne Stokes respiration? Who has it?
periodic breathing (waxing and waning effort and air flow) over several minutes, with central apneas
Seen in visitors to high altitudes
Opioid use
How do opioids change the amount of sleep in the different stages?
increases stage 2
decreases stages 4 and REM
What are some potential causes of central sleep apnea (CSA)?
- Medications, especially opioids
- Congestive heart failure or stroke
- High altitude
- Patients with OSA who use CPAP
- Neurologic trauma
- Brain tumor
- Idiopathic
What are opioids used for? What is a common side effect?
- Opioid (narcotic) pain medication is used to treat moderate to severe pain that may not respond well to other medications, especially post-operative pain
- Respiratory depression may occur with opioid use
–Depends on a variety of other factors
•Some physicians are hesitant to prescribe due to the potential for respiratory depression, while others believe patients will overcome sleep-disordered breathing with prolonged use
What is the general mechanism for opioids?
- Opioid receptors are G-protein coupled receptors
- Receptors respond to ligand binding by initiating an intracellular signaling cascade that leads to decreased neuronal excitability
–Closing of voltage sensitive calcium channels
–Stimulation of potassium efflux
–Reduction of cAMP production
Where are opioid receptors found?
respiratory control centers of the brainstem,
in the carotid bodies,
in mechanosensory fibers from the lungs and airways
the anterior insula,
thalamus
anterior cingulate cortex
What effect do opioids have on respiratory drive? What areas of the brain?
•Opiates reduce respiratory drive from the:
medulla (ventral and dorsal respiratory group, pre-Botzinger complex) and
pons (Kolliker-Fuse, parabrachial nucleus, locus coeruleus)
Opioids reduce respiratory drive from the medulla and pons, what is the effect on motor neurons?
–Decreased efferent output to spinal motoneurons
•Decreased intercostal, abdominal, and diaphragm activity
–Decreased efferent output to cranial nerve motoneurons
Decreased upper airway muscle activity.
What effect do opioids have on airway diameter and resistance?
Decreased tone to CN nuclei will cause increased flaccidity of these mm, and will lead to collapse of the soft palate, tongue and other structures during sleep
- airway is narrower with less support from mm in mouth and upper airway
- airway is narrower, and much more prone to collapse because of this
Why do opioids lead to hypoventilation and central apnea?
Decreased effort to breathe
Increased propensity for airway to collapse
Decreased impetus to start/continue respiratory cycle
What respiratory changes with opiates?
•Leads to hypoventilation (due to decreased frequency and tidal volume), central apneas, increased upper airway collapsibility, hypercapnia, and hypoxemia
What do opiates do to central chemoreceptors?
Central chemoreceptors provide tonic drive to the respiratory motor output by sensing changes in pH
–Morphine may act directly on the brainstem (NTS receives input from carotid bodies) to blunt the hypoxic ventilatory response (HVR)
What is opiate’s effect on peripheral chemoreceptor?
•Peripheral chemoreceptors
–Cells (glomus cells) of the carotid bodies are sensitive to morphine
–Impulses from the carotid bodies travel in the glossopharyngeal nerve to the NTS in the dorsal medulla and modulate respiration
What is the effect of hypoxia on the pulmonary system? What pathology can it lead to?
–Hypoxic pulmonary vasoconstriction
•Pulmonary hypertension
What is the effect of hypoxemia on the kidneys?
•Renal release of EPO
–Increased hematocrit, blood viscosity
What is the cardiac effect of increased hematocrit and blood viscosity?
»Increased afterload of R ventricle
- R ventricular hypertrophy, potentially leading to cor pulmonale
- Increased R atrial volume
EPO has been made, and right atrium is now dilated. What hormone is secreted as a result, and how does it show up as a symptom?
- Secretion of ANP, suppression of ADH
- Nocturia - nocturnal polyuria frequently a symptom of sleep apnea
What is the effect of hypoxemia on the ANS? What pathology can this lead to?
•Repeated sympathetic activation
–Systemic hypertension, vascular remodeling
- Increased afterload of L ventricle
- Congestive heart failure
How does sleep apnea cause headaches?
–Dilation of cerebral blood vessels and increased cerebral blood flow
Why is paroxysmal nocturnal dyspnea frequently found with sleep apnea?
Intermittent suffocation will generally cause one to wake in transiently SOB
- apnea leads to changes in blood gases
- awakes to compensatory tachycardia, hyperpnea
