Lecture 19 - Pathophysiology Of Sleep Apnoea Flashcards

1
Q

Apnoea definition

A
  • cessation of airflow at the mouth and nose for over 10 sec during sleep
  • reduction in the peak aiflow excursion on an oro-nasal thermal sensor of 90% of the pre-event baseline
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2
Q

Hypopnoea definition

A
  • reduction in amplitude of airflow or thoraco-abdominal wall movement of >30% of pre-event baseline measurement
  • the amplitude reduction is associated with either oxygen desaturation of 3% or an arousal
  • the duration of the 30% drop in signal excusrion lasts 10 sec +
  • at least 90% of the events duration must meet the amplitude reduction criteria
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3
Q

Respiratory effort related arousal

A
  • sequence of breaths lasting >10 sec characterised by increasing respiratory effort or by flattening of the inspiratory portion of the nasal pressure signal
  • event needs to lead to arousal from sleep
  • sequence of breaths does not meet criteria for an apnoea or hypopnoea
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4
Q

Central apnoea

A
  • apnoea accompanied by an absence of diaphragm EMG and thoraco-adominal wall movement
  • no effort to breathe, its a drive problem
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5
Q
  • Obstructive apnoea
A
  • apnoea with continued or raised EMG diaphragm activity and/or thoraco-abdominal wall movement
  • paradoxical thoraco-abodminal movement may occur
  • difficulty breathing
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6
Q

Mixed apnoea

A
  • apnoea with. Both central and obstructive componets, with central component for at least one respiratory cycle length
  • more related to obstructive
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7
Q

Obstructive sleep apnoea clinical syndrome

A
  • characterised by recurrent upper airway obstruction during sleep
  • spectrum: normal ->snoring -> OSA

Syndrome:

  • recurrent episode of apnoea and hypopnoea
  • respiratory disturbance index of over 5 events per hour of sleep
  • symptoms of functional impairment
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8
Q

OSA diagnostic criteria

A

1) Excessive daytime sleepiness unexplained by other factors
2) 2+ of choking during sleep, recurrent nocturnal awakening, unrefreshing sleep, daytime fatigue, impaired concentration, memory disturbances
3) overnight monitoring demonstrates 5+ apnoeas and hypopnoes per hour of sleep

  • must have 1 or 2, + 3
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9
Q

OSA consequences

A
  • fragmentation of sleep
  • hypersomnolence
  • cognitive dysfunction
  • memory loss
  • emotional disturbances
  • social disharmonhy
  • pulmonary and systemic hypertension
  • cardiac arrythmias, AF
  • myocardial infarction and stroke
  • decreased survival
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10
Q

Factors contributing to upper airway obstruction during sleep: pharyngeal airway

A
  • anterior wall has no body or cartilaginous support and depends on upper airway muscle activity to maintain patency
  • these muscles are normally activated in a rhytmical fashion during each inspiration
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11
Q

Balance of forces

A
  • upper airway patency depends on a balance of collapsing and dilating forces
  • collapsing forces: negative airway pressure generated by the inspiratory acrtivity of the diaphragm
  • dilating force: upper airway dilator muscle activity
  • collapse occurs when the force produced by the muscles, for a given cross-sectional area of the upper airways, is exceeded by the negative airway pressure
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12
Q

Causes of upper airway obstruction

A
  • anatomical narrowing of the upper airway
  • excessive loss of upper airway muscle tone
  • defective upper airway protective reflexes
  • increased loop gain promotes an unstable airway
  • frequent arousal destabilise airway
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13
Q

Site of airway obstruction

A
  • alway s between choanae and epiglottis
  • generally behind uvula and soft palate (nasopharynx)
  • also behind tongue (oropharynx)
  • collapse at the level of the epiglottis is unusual
  • multi-level collapse is usual`
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14
Q

Factors promoting OSA

A
  • Sex: males have higher pharyngeal resistance
  • Age: pharyngeal resistance increases with age, and so does risk of OSA
  • obesity: strong association between obesity and OSA, may relate to fat deposition in pharyngeal walls, neck or abdomen
  • Genetics: familial association exists
  • Ethanol reduces upper airway muscle tone, so it increases frequency and duration of apnoeas
  • Cranio-facial anatomy: retrognathia and enlarged tonsies
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15
Q

Reduced upper airway size leads to

A
  • increased upper airway resistance
  • more negative pharyngeal pressure during inspiration - can lead to collapse
  • increased transmural collapsing pressure
  • upper airway occlusion during sleep
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16
Q

Anatomical abmnormalities associated with OSA

A
  • adenotonsillar enlargment
  • micrognathia
  • infiltration of muslces and soft tissue: myxoedema in hypothyroidism, acromegaly, neoplastic processes, mucopolysaccharisosis
  • nasal obstriction -> icnreases negative pressure, but not a strong association with sleep apnoea
17
Q

Effect of NREM sleep on muscle activity

A
  • genioglossus and diaphragm maintain normal activity
  • palatoglossus, levator palatini and tensor palatini all reduce activity
  • tensor palatini has the most reduced activity and it is the most important muscle for OSA because it is the one that pulls the soft palate away from the tongue, opening up the airways
18
Q

Upper airway muscle and sleep in normal

A
  • upper airway remains patent in normal subjects despite decrements in upper airway muscle activity during sleep
  • upper airway muscle respond to negative airway pressure by reflex activation
  • during sleep, this reflex response to negative pressure is diminished or absent
19
Q

Upper airway muscle and sleep in OSA patients

A
  • during wakefulness, OSA patients compensate for inadequate airway anatomy by increasing pharyngeal dilator muscle activity
  • this neuromuscular compensation mechanism is driven by reflex responses to negative airway pressure
  • loss of neuromuscular compensation during sleep leads to airway occlusion in OSA patients
20
Q

Control of breathing and OSA

A
  • reduced hypercapnic ventilatory response in OSA
  • imbalance of upper airway muscle activity and diaphragm activity during sleep - favors upper airway collapse
  • hypoxia causes periodid breathing and may lead to hypocapnia, which predisposes to further apnoea
  • impaired resistive load detection in OSA patient
21
Q

Arousal and OSA

A
  • arousal from sleep is responsible for terminating obstructive events: airway occlusion, hypoxia and hypercapnia all play a part
  • arousal do not usuallylead to complete awakening
  • impaired arousal responses will lead to more profound and prolonged apnoeas
  • arousal may lead to hyperventilation post-apnoea, leading to hypocapnia and reduced ventilatory drive, predisposing to recurrent upper airway occlusion
22
Q

3 types of central apnoea

A
  • due to hyperventilation (low CO2)
  • due to hypoventilation (high CO2)
  • due to cheyne stokes respiration associated with cardiac failure
23
Q

Central apnoea due to hyperventilation

A
  • respiration during NREM is critically dependent on PaCO2
  • central apnoea results if arterial PaCO2 is lowered below ethe apnoeic threshould

EVENTS

  • stimulus induces hyperpnoea
  • hyperpnoea causes ventilatory overshoot and hypocapnia, causing central apnoea
  • central apnoea causes PaCO2 to rise, restoring rhtymic respiration with or without arousal
  • hyperpnoea, ventilatory overshoot, hypocapnia and further central apnoea follows
24
Q

Syndromes with hypercapnia

A
  • dominant central apnoea with no cardiac disease
  • more regular pattern of panoeas
  • abnormally. High awake ventilatory responses
  • disinhibition of brainstem respiratory reflexes may result in extreme sensitivity of the respiratory controller to CO2
  • may be precipitated by stroke and frontal lobe syndrome
  • may not be any identifiable neurological diseae
25
Q

Central apnoea due to hypoventilation

A
  • less common
  • occurs in patients with marginal ventilatory statys
  • wakefulness stimulus to breathe disappears during sleep, resulting in alveolar hypoventilation and cental pnoeas
  • ventilation is restored by arousal from sleep, but declines during sleep
26
Q

Syndromes with hypocapnia

A
  • alveolar hypoventilation in sleep
  • reduced tidal volume rather than discrete apnoeas
  • irregular pattern of decreased tidal volumes, central apnoea and arousal
  • abnormally low awake ventilatory response
27
Q

Syndromes with cardiac failure

A
  • congestive cardiac failure predisposes to central apnoea and Cheyne-stokes breathing
  • induces overall alveolar hyperventilation
  • up to 80% of patients may have sleep disordered breathing
  • delayed circulation time with fluctuation of arterial CO2 is thought to dominate the mechanism