207 -Obstructive Sleep Apnoea Flashcards

1
Q

define obstructive sleep apnoea

A

the stopping or slowing of breathing during sleep due to closing of the upper airway. Sleep causes pharyngeal incompetence (muscles relax) causing a collapse of the upper airway. Incr. in PaCO2 causes the px to wake up causing broken sleep and daytime sleepiness.

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2
Q

what are the risk factors for OSA?

A
  • Obesity/lower facial shape *tonsil/nasal problems
  • hypothyroidism *alcohol/sedatives *smoking
  • being male *ty II DM *snorers *40-60 y/o
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3
Q

how might a px with OSA present?

A
  • Excessive daytime sleepiness - assess with Epworth Sleepiness scale
  • snoring
  • partner notices px stop breathing at night
  • morning headaches, dry throat, anxiety, poor concentration, irritability
  • sweats, reduced libido
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4
Q

how would you investigate suspected OSA?

A
  • overnight oximetry tracing - shows pattern of regular desaturation
  • measure nasal flow
  • measure throax/abdo movements
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5
Q

how would you manage a px with OSA?

A
  • treat underlying disorder - hypothyroidism, bariatric surgery
  • lifestyle changes - smoking, alcohol in eve, weight, posture
  • ventilation - Continuous positive airway pressure (CPAP) - continuously blows column of air down airway
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6
Q

what can untreated OSA lead to?

A
  • personality changes
  • sleepiness at work/job problems
  • relationship problems & sexual dysfunction
  • risk of sudden death and cardiac problems
  • commonest cause of 2ry hypertension
  • poor diabetic control
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7
Q

what ABG changes would you see in a px with type I respiratory failure?

A
  • PO2 low
  • PCO2 normal or low
  • pH normal or alkalytic
  • HCO3 normal or low
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8
Q

what ABG changes would you see in a px with type II respiratory failure?

A
  • PO2 low
  • PCO2 high
  • pH acidotic or normal
  • HCO3 high or normal
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9
Q

what FEV1 and FVC changes would you see in a px with restrictive lung disease

A

both FEV1 and FVC reduced and ration between them normal or incr. as full expiration achieved rapidly

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10
Q

what ABG changes would you see in a px with respiratory acidosis and why?

A

caused by incr. in CO2 so incr. PaCO2, decr. pH & incr HCO3. Acute - slight incr. in HCO3 as more CO2 for dissociation. compensated - kidneys compensate over time gently incr. HCO3 retention

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11
Q

what ABG changes would you see in a px with respiratory alkalosis and why?

A

caused by decr. in CO2 so decr. PaCO2, incr. pH & decr HCO3. Acute - slight decr. in HCO3 as more CO2 eliminated. compensated - kidneys compensate over time gently decr. HCO3 retention

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12
Q

what ABG changes would you see in a px with metabolic acidosis and why?

A

caused by incr. in H+ due to incr. lactic acid production/decr. H+ elimination (renal failure) so normal/decr. PaCO2, decr. pH & decr HCO3. Acute - marked decr. in HCO3 as used to buffer acid. compensated - further decr. HCO3 due to hyperventilation

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13
Q

what ABG changes would you see in a px with metabolic alkalosis and why?

A

caused by decr. in H+ due to loss of H+(vomit gastric acid)/excess bicarbonate infusion so normal/decr. PaCO2, incr. pH & incr HCO3. Acute - marked incr. in HCO3 as no acid to conjugate. compensated - further incr. HCO3 due to hypoventilation

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14
Q

where does the automatic rhythm of breathing originate and what does it act upon?

A

the medulla oblongata (lowest segment of brainstem). Impulses are sent down the spinal cord to phrenic nerve & intercostals & via CN12 to the pharynx larynx. Compression of medulla causes respiratory depression

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15
Q

what 3 medullary regions are responsible for impulses driving respiration?

A
  • Parafacial Respiratory Group (PFRG) - originate action potentials just before inspiration
  • Dorsal Respiratory Group (DRG) - action potentials during inspiration (stimulate muscles of insp)
  • Ventral Respiratory Group (VRG) - mostly action potentials during expiration
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16
Q

From where do the 3 medullary regions receive inputs from?

A
  • chemoreceptors - via CN9/10 - monitor arterial blood gas/acid conc.
  • higher CNS (cerebral cortex, hypothalamus) via Pontine Respiratory Group (PRG) in pons which fine tunes respiratory rhythm (sets vol when insp turns to exp)
17
Q

what ventilatory rhythm pacemaker models are there?

A
  • distributed network model
  • multiple oscillator models
  • single oscillator models
  • couple oscillator model - insp rhythm originates in pre botzinger complex (PBC) and exp in PFRG
18
Q

what is the group pacemaker hypothesis of signal generation?

A
  • beginning of cycle - all neurones hyperpolarised
  • recovery - some neurones recover and depolariseto cause Action potential
  • recurrent excitation - AP stimulate other neurones to depolarise
  • burst - incr. stimulation leads to all neurones to depolarise
19
Q

what innervates the muscles of respiration

A
  • phrenic nerve supplies diaphragm for C3/4/5

* intercostals supplied by respective thoracic segments

20
Q

where in the brain does voluntary control originate?

A

from cerebral cortex via pyramidal tracts direct to effector muscles - voluntary control bypasses the medulla (Px can still breathe if medulla damaged)
reflexes can also modify resp rhythm via vagus (sneeze/cough in U/LRT, pulmonary stretch receptors, irritant receptors in epithelial cells, j-receptors in alveolar walls)

21
Q

why is chemoreception important?

A

maintains PaO2 to maintian O2 supply to tissue

maintains PaCO2 to keep pH of tissues constant

22
Q

how do chemoreceptors affect ventilation during exercise?

A

ventilation incr with work as chemoreceptors sense incr. in PaCO2 (due ro CO2 production in metabolism) to keep PaO2 and PaCO2 constant

23
Q

which chemoreceptors sense CO2 and O2?

A

CO2 - both central and peripheral (main stimulus for breathing)
o2 - peripheral only (stimulates breathing when PaO2 <60mmHg)

24
Q

where are central chemoreceptors located and what stimulates them?

A
  • neurones on surface of ventro-lateral medulla (medullary raphe, retrotrapezoid)
  • stimulated by [H+} in CSF that bathes medulla (indirectly determined by PaCO2 as CO2 diffuses from cerebral arteries to CSF and some [H+]blood - central more sensitive to resp acidosis than metabolic but slow acting due to diffusion
25
Q

where are peripheral chemoreceptors located and what stimulates them?

A
  • carotid bodies
  • stimulated by PaO2 when <60mmHg and some PaCO2 & [H+] - glomus cells sense blood gas levels and send to medulla via vagus. Fast acting due to thin membrane between blood and cells