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SLEE5102 > Module 3 - Central Breathing Disorders of Sleep > Flashcards

Module 3 - Central Breathing Disorders of Sleep Flashcards

1
Q

What is Central Sleep Apnea (CSA)?

A

CSA is a condition characterized by periodic breathing during sleep, influenced by complex and multifactorial mechanisms, particularly in individuals with heart failure (HF).

CSA is characterized by periods of apnea or hypopnea during sleep due to a lack of respiratory effort, distinguishing it from obstructive sleep apnea where airflow is blocked despite effort.

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2
Q

What is Loop Gain?

A

Loop gain is an engineering term that describes the tendency of a negative feedback loop to become unstable in response to a ventilatory disturbance. A high loop gain indicates a system’s propensity to fluctuate between underventilation and overventilation.

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3
Q

What are the components of Loop Gain in heart failure?

A

The components include increased arterial circulation time (mixing gain), enhanced chemoreceptor gain, and enhanced plant gain (e.g., decreased functional residual capacity).

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4
Q

How does increased arterial circulation time affect CSA in HF?

A

It delays the transfer of information regarding changes in Po2 and Pco2, potentially destabilizing the negative feedback system controlling breathing, making periodic breathing more likely.

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5
Q

How does the gain of chemoreceptors influence CSA?

A

Individuals with increased sensitivity to CO2 or O2 elicit large ventilatory responses to slight increases in Pco2 or decreases in Po2, leading to intense hyperventilation and subsequent central apnea.

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6
Q

What role does decreased functional residual capacity play in CSA?

A

It results in underdamping, where small changes in ventilation cause significant fluctuations in Po2 and Pco2 levels, destabilizing breathing patterns and increasing the likelihood of periodic breathing.

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7
Q

How does sleep affect Loop Gain and the development of CSA?

A

Sleep, especially in the supine position, leads to reductions in functional residual capacity, metabolic rate, and cardiac output, augmenting the likelihood of developing periodic breathing and CSA beyond wakefulness levels.

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8
Q

What is the significance of the apneic threshold in CSA?

A

The apneic threshold is the level of Pco2 below which rhythmic breathing ceases. A small Pco2 reserve, or a close proximity of prevailing Pco2 to the apneic threshold, increases the likelihood of CSA during sleep.

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9
Q

How does chemosensitivity below eupnea contribute to CSA in HF?

A

Increased chemosensitivity below eupnea means the prevailing Pco2 and the apneic threshold Pco2 are close together, which increases the likelihood of developing central apnea during sleep.

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10
Q

What predictive value does a low steady-state arterial Pco2 have for CSA?

A

A low steady-state arterial Pco2 (<35 mm Hg) has about an 80% predictive value for the occurrence of CSA in patients with HF, often due to increased pulmonary wedge pressure sensitizing chemoreceptors

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11
Q

What are the classifications of CSA?

A

CSA classifications include Cheyne-Stokes breathing, Primary CSA, High-altitude periodic breathing, CSA due to a medical condition without CSB, CSA due to medication or substance, and Treatment emergent CSA.

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12
Q

How does mechanical dysfunction contribute to CSA?

A

Mechanical dysfunction in CSA involves the collapsibility of the upper airway, impacting ventilatory stability due to imbalanced forces and muscle activity that maintain airway patency.

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13
Q

What neural mechanisms affect CSA?

A

Respiratory neurons, both inspiratory and expiratory, and the neural pathways they form, control ventilation and contribute to the development of CSA by affecting airway patency and respiratory rhythm.

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14
Q

How is ventilation controlled in CSA?

A

Ventilation in CSA is controlled through a complex feedback mechanism known as “loop gain,” which involves chemoresponsiveness and the effectiveness of CO2 excretion, contributing to ventilatory stability.

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15
Q

What factors influence the epidemiology of CSA?

A

The prevalence of CSA varies, influenced by factors such as age, gender, underlying medical conditions, and treatment for obstructive sleep apnea (OSA).

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16
Q

What genetic aspects are associated with CSA?

A

Congenital Central Hypoventilation Syndrome (CCHS) is linked to mutations in the PHOX2B gene, illustrating the genetic basis of some forms of CSA.

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17
Q

What is the impact of CSA on morbidity and mortality?

A

CSA, especially CSA-CSB, can affect cardiac hemodynamics, increase hospital readmission rates, and is associated with conditions like cerebrovascular accidents and atrial fibrillation, impacting mortality.

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18
Q

How is CSA treated and what is its prognosis?

A

reatment varies by CSA subtype and may include CPAP, adaptive servo-ventilation, and addressing underlying conditions. The prognosis depends on the severity of the underlying condition and treatment efficacy.

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19
Q

What is the most important pathophysiologic feature of the non-hypercapnic central sleep apnea syndromes?

A

Reduced CO2 reserve in REM sleep

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20
Q

Which sleep stage are central apneas most common?

A

N1 and N2

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21
Q

What type of loop gain problem does obesity hypoventilation syndrome have?

A

Increased plant gain
Decreased controller gain

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22
Q

What type of loop gain problem does neuromuscular weakness have?

A

Increased plant gain

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23
Q

What type of loop gain problem does congenital central hypoventilation syndrome have?

A

Decreased plant gain

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24
Q

What type of loop gain problem does hypercapnic chronic obstructive pulmonary disease have?

A

Decreased plant gain

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25
Q

What type of loop gain problems does CSB have?

A

Increased controller gain
Increased mixing gain

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26
Q

What type of loop gain problem does high-altitude periodic breathing have?

A

Increased controller gain

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27
Q

What type of loop gain problem does treatment emergent central apnea have?

A

Increased controller gain

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28
Q

What type of loop gain problem does idiopathic pulmonary hypertension have?

A

Increased mixing gain

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29
Q

What is the awake cut-off differences for people with Hypoventilation or Hyperventilation?

A

Hypo: above 45
Hyper: below 40

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30
Q

For which diseases is hyperventilation (low CO2) a common indicator?

A

Stroker and heart failure

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31
Q

For which diseases is hypoventilation (high CO2) a common indicator?

A

Lung disease or muscle weakness, particularly relevant in REM sleep

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32
Q

What part of the brain detects changes in CO2 levels? (Central chemoreceptors)

A

Proton receptors in the retrotrapezoid nucleus

CO2 diffuses into the brainstem and converts to BCO3- and H+. There are receptors on the dendrites that detect protons.

Surrounded by astrocytes which release ATP

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33
Q

What types of cells surround the retrotrapezoid nucleus (where central chemoreceptors are found)?

A

Astrocytes, they release ATP

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34
Q

How is ATP related to central chemoreceptors?

A

Astrocytes surround the retrotrapezoid nucleus (central chemoreceptor location) so that ATP can be provided to the nucleus.

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35
Q

How is ATP and central apneas related?

A

Unsure, but changes to ATP can cause central apneas

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36
Q

What type of information are central and peripheral chemoreceptors sensitive to?

A

Central: CO2
Peripheral: O2 (mainly), CO2, pH, temperature and role in detecting glucose

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37
Q

What is the analogy for peripheral chemoreceptors and taste buds?

A

They are like taste buds, which taste the blood before it goes to the brain. Ensures quality.

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38
Q

Do peripheral chemoreceptors work all the time or in the background?

A

On always, but in the background. Only turn on more when hypoxic response occurs. Happens very suddenly.

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39
Q

What is the reflex response by peripheral chemoreceptors to oxygen?

A

Non-linear response between O2 levels and ventilation (pa not saturation).

O2 has to be very low (i.e. <70) to kick in.

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40
Q

What is the history of discovery of periodic breathing (central sleep) disorders?

A

John Hunter found people dying of heart failure would increase then decrease their breathing.
Cheyne-Stokes similarly discovered this in awake and asleep people.
In extreme cases, they would stop breathing all together.

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41
Q

What is the classical case of Central Sleep Apnea breathing?

A

Each increase and decrease (waxing/waning) cycle of breathing are identical and have a 20sec central apnea between them.

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42
Q

What is the cause of central sleep apneas?

A

Classic negative feedback control system due to:
- increased gain response (big reflex response) and/or
- slow time to respond to changes (delay getting back to controller)

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43
Q

When there is an upper airway obstruction, the increased effort that is noted in the trachea is driven by which chemoreceptor?

A

Carotid body (peripheral) because its sensitivity increases when O2 drops. Its sensitivity also increases (bigger response) when hypercapnic.

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44
Q

How does the hypoxic response differ between people with OSA + hypercapnia and normocapnia?

A

Hypercapnic: no hypoxic response
Normocapnic: elevated response, due to repetitive hypoxia and increased gain of response

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45
Q

How does the carotid body’s response change when someone is hypercapnic (temporarily not always)?

A

Increased sensitivity

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46
Q

How does the body respond to ongoing increased CO2 levels?

A

You start to retain BCO3- to bring pH back to normal. This is how people with OSA get hypercapnic.

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47
Q

What happens when someone changes from obstructive to central apnea during sleep?

A

OSA are shorter events, so when they move to CSA the apneas are longer but CO2 falls.

Happens post-stroke

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48
Q

What are the risk factors for people with congestive heart failure to have central sleep apnea?

A

Age older than 60 years
male gender
presence of atrial fibrillation, and hypocapnia

49
Q

What are the risk factors for treatment-emergent central sleep apnea?

A

a high baseline AHI or arousal index
hypertension
opioid use
coronary artery disease
stroke
congestive heart failure

50
Q

What is the estimated prevalence of central sleep apnea?

A

5-10% of SDB

51
Q

What type of heart dysfunction makes cheyne-stokes breathing (CSA) more common?

A

left ventricular dysfunction regardless of the etiology (ischemic versus idiopathic), type (preserved or low ejection fraction), New York Heart Association (NYHA) class, and acuity of event (acute or chronic heart failure)

52
Q

What portion of patients with heart failure with a reduced ejection fraction (HFREF) and preserved ejection fraction have cheyne-stokes breathing at night?

A

69% ejection
27% preserved

53
Q

What portion of patients with systolic heart failure have cheyne-stokes breathing during wakefulness?

A

57%

54
Q

How common is primary CSA (or idiopathic CSA)?

A

Quite uncommon
within the sleep center population, the prevalence has been reported to be 4% to 7%

These individuals usually complain of excessive daytime sleepiness, insomnia, or difficulty breathing during sleep.

55
Q

How common is High-Altitude Periodic Breathing?

A

Despite considerable heterogeneity in the susceptibility to altitude illness, periodic breathing in the form of cyclic central apneas and hypopneas occurs in almost all individuals at a sufficiently high altitude.

56
Q

How common is Treatment Emergent Central Sleep Apnea?

A

When treatment emergent CSA (or “complex” CSA) is simply defined as the emergence of central apneas and hypopnea both during and after the application of PAP therapy in patients with OSA, its estimated aggregate point prevalence in the general sleep center patient population is 8% with the estimated range varying from 5% to 20%.

Treatment emergent CSA was found to be transient in 55.1% and persistent in 25.2% of patients after 13 weeks of CPAP initiation.

57
Q

What are risk factors for Treatment Emergent Central Sleep Apnea?

A

male gender, higher baseline AHI, and central apnea index at the time of diagnostic study

58
Q

How common is Central Sleep Apnea Due to a Medical Disorder?

A

CSA events were identified by PSG in 10.6% of a cohort

as a result of a variety of conditions, such as idiopathic pulmonary hypertension, chronic thromboembolic disease with pulmonary hypertension, chronic obstructive pulmonary disease, and interstitial lung disease

59
Q

How common is Opioid-induced CSA?

A

of 30% of patients in a methadone pain program or in cancer patients receiving opioids for pain

60
Q

How is age related to CSA-CSB?

A

Rare in children
More common in advanced age

61
Q

How is gender related to CSA-CSB?

A

CSA syndromes are overall much more common in men (7.8%) than in women (0.3%)

CSA is uncommon in premenopausal women, who are less susceptible to hypocapnic CSA than men. Although OSA is increasingly recognized in postmenopausal women, similar consistent data for CSA are lacking.

62
Q

How is race related to CSA-CSB?

A

Unknown

63
Q

What is the relationship between CSA and morbidity?

A

There are intermittent surges in blood pressure and heart rate which may cause poorer outcomes to HF with CSA as opposed to HF without it.

May be related to more readmissions (HF+CSA).

More cerebral hypoxia during CSA.

significantly associated with incident atrial fibrillation even after accounting for confounders, including cardiovascular risk and disease

64
Q

What is the relationship between CSA and mortality?

A

As the oxyhemoglobin desaturations, arousals, increased sympathetic output, and negative intrathoracic pressure (during hyperpnea that follows central apnea in CSA-CSB) contribute to myocardial ischemia, CSA-CSB could contribute to excess mortality in patients with heart failure,

but - different results in studies and all without treatment in CSA with HF.

No difference in one study when CPAP was used in heart transplant patients.

65
Q

Why is it difficult to diagnose CSA in people with heart failure?

A

because obesity and habitual snoring, which are the two hallmarks of OSA are commonly absent in patients with HF and CSA

66
Q

Why is it difficult to suspect sleep apnea in patients with HF?

A
  • the prevalence of sleepiness is similar in HF patients with and in those without sleep apnea
  • the symptoms of HF and sleep apnea overlap
67
Q

What are the symptoms of heart failure and sleep apnea that overlap?

A

sleep-onset and maintenance insomnia
nocturia
waking up with shortness of breath (orthopnea, paroxysmal nocturnal dyspnea, hyperpnea resulting from periodic breathing)
unrefreshed sleep
daytime fatigue

68
Q

What signs would indicate someone with HF likely has CSA?

A

a high-numbered class in the New York Heart Association classification
low LVEF
low steady-state arterial P co 2
atrial fibrillation
and nocturnal ventricular arrhythmias

ven when there is no subjective daytime sleepiness, such patients score 10 or less on the Epworth Sleepiness Scale (ESS) when tested objectively by multiple sleep latency, short sleep latencies, even below 5 minutes, are observed

69
Q

What are the differences between patients with heart failure who have OSA vs CSA?

A

Patients with OSA were more obese and had a higher prevalence of habitual snoring than patients with CSA

70
Q

What can happen to people on PAP for their OSA in terms of central apneas?

A

treatment-emergent CSA (TE-CSA)

alleviation of obstructive apneas with positive airway pressure (PAP) amplifies a sensitive chemoreflex with resultant centrally mediated apneas and periodic breathing

71
Q

How is a CSA syndrome defined by PSG?

A

five or more central apneas and/or central hypopneas are present per hour, that is, a central apnea-hypopnea index (CAHI) of greater than 5, with CAHI comprising more than 50% of all respiratory events

72
Q

How can PSG help diagnose central hypopneas?

A

predominance during non–rapid eye movement (NREM) versus rapid eye movement (REM) sleep
arousal after and flow restoration pattern at hypopnea termination,
lack of thoraco-abdominal paradox.

73
Q

What pathophysiologic changes make someone more susceptible to central apneas/hypopneas during sleep?

A

(1) low CO 2 reserve (CO 2 reserve = Paco2 eupneic − Pa co 2 apneic)

2) abnormally high or low loop gain (a product of controller, plant, and mixing gains),

(3) sleep state and stage instability.

74
Q

What happens to CO2 reserve when metabolic acidosis vs akalosis and what does this mean in relation to loop gain?

A
  • alkalosis (inc plant gain): CO2 reserve decreased, promoting the risk for central apneas and ventilatory instability
  • acidosis (dec plant gain): increased CO2 reserve, which protects against central apneas
75
Q

What happens when oxygen is administered in sleep to support CSA? How does this impact loop gain?

A

reduces the hypoxic stimulus to breathing has been shown to decrease ventilation and responsiveness to Paco2 during sleep

This stabilizes breathing through reduction in controller gain and increase in Paco2 reserve, whereas hypoxia leads to opposite effects

76
Q

How does mixing gain impact central breathing?

A

inherent delays in the negative feedback loop controlling ventilation (mixing gain) increase loop gain.

This delayed recognition of blood gases by the controller (as in those with systolic CHF) predisposes to unstable and periodic breathing, which can abate with improvement in cardiac output.

77
Q

How do arousals in sleep affect ventilation?

A

can result in ventilatory instability, with the level of ventilatory response and arousal threshold playing important roles.

78
Q

What happens to someone’s ventilatory drive after a sudden arousal in sleep?

A

the sleep eupneic Pa co 2 (normally about 5 mm Hg higher than awake Pa co 2 ) is detected as hypercapnic by the aroused respiratory control center. This signal to increase ventilatory drive, combined with the removal of the upper airway (UA) resistance induced by sleep, results in increased ventilatory response and reduction in Pa co 2

79
Q

How can frequent arousals in sleep impact central apneas?

A
  • After a sudden arousal, the normal CO2 levels are seen as hypercapnia (as ~5mmHg higher) -> Increased ventilatory drive & with reduction of UA resistance -> increased ventilatory response and decrease CO2
  • Sleep starts again, that CO2 is seen as hypocapnic and often below the apneic threshold, resulting in central apnea.

Thus any process that leads to frequent sleep-wake transitions, such as sleep-maintenance insomnia, sleep apnea, maladaptation to continuous positive airway pressure (CPAP), or periodic limb movement disorder, can increase the propensity to ventilatory overshoots, periodic breathing, and CSAs , especially in a setting of high chemosensitivity

80
Q

What are common to CSA disorders & their arousals that are nonhypercapnic?

A

(1) normal or slightly low awake steady-state Paco2 and
(2) increased ventilatory responsiveness to Paco2 or hypoxemia (increased loop gain)

In the setting of arousals, CSAs are perpetuated because of the so-called “inertial” effect

81
Q

Why do people with heart failure develop CSB?

A

It is in part a consequence of increased loop gain resulting from a heightened chemoreflex (sensitive controller) and lack of the “normal” increase in Pa co 2 with sleep onset (decreased CO 2 reserve).

These are superimposed on prolonged circulation time from impaired cardiac output (increased mixing gain), resulting in cyclical ventilatory instability.

82
Q

What type of chemo reflexes are seen in periodic breathing?

A

hyperactive

83
Q

Why does periodic breathing at altitude occur?

A

The cycle time of periodic breathing at high altitude is short (probably because of elimination of the mixing gain defect).

The mechanism involves exposure to hypoxemia with resultant chemoreceptor-mediated hyperventilation during sleep.

84
Q

What happens to ventilation after 10 minutes of hypoxia in sleep?

A

tidal volumes oscillate in a waxing and waning pattern

tidal volumes oscillate in a waxing and waning pattern.

85
Q

Why does altitude breathing result in CSA?

A

The hypoxic environment of high altitudes triggers a chain of physiological responses that disturb the normal regulation of breathing, leading to the development of CSA-CSB. This is primarily due to the body’s attempt to balance the need for increased oxygen uptake with the need to prevent excessive loss of CO2.

  1. Reduced SaO2: At high altitudes, the ppO2 decreases. This hypoxic condition is sensed by peripheral chemoreceptors, primarily located in the carotid bodies, which then stimulate an increase in ventilation (hyperventilation) to improve oxygen uptake.
  2. Ventilatory Response to Hypoxia: The hyperventilation increases the elimination of CO2 from the body, which can lead to a state of hypocapnia.
  3. Apneic Threshold: During sleep, particularly in non-REM (rapid eye movement) sleep phases, the sensitivity to CO2 increases. A central apnea can occur below the threshold.
  4. Crescendo-Decrescendo Breathing Pattern: The cycle of hyperventilation followed by apnea and then a gradual resumption of breathing creates a characteristic breathing pattern known as Cheyne-Stokes Breathing.
  5. Increased loop gain resulting in reduced CO2 reserve and increased chemrsensitivity
  6. Periodic Breathing: The combination of hypoxia-induced hyperventilation, subsequent hypocapnia, and the body’s attempts to correct this imbalance can lead to periodic breathing. This is characterized by cycles of deep breathing alternating with apneas or hypopneas, common at high altitudes.
86
Q

Describe primary central sleep apnea

A

a rare disorder characterized by repetitive episodes of central apneas in NREM sleep, which are short and irregular (rather than periodic) and terminate with an abrupt, large breath, in contrast to CSA-CSB

87
Q

What ares the main pathophysiologic differences between primary CSA and other types of CSA?

A

increased hypercapnic ventilatory response during wakefulness

impairment of switching between expiration and inspiration has been found in these patient. It has been speculated that the long expiratory pause that typically occurs with these CSA events may be attributable to this impairment.

88
Q

How does hypercapnia CSA and non-hypercapnia CSA syndromes differ in sleep?

A

Hypercapnic: low loop gain (controller or plant) and worsening of hypoventilation and apneas during REM sleep

non-hypercapnia: nREM dominantD

89
Q

Describe Congenital Central Alveolar Hypoventilation Syndrome

A

a rare disorder of respiratory control and autonomic systems

Small tidal volumes and monotonous respiratory rates result in hypoventilation, and the wakefulness and behavioral stimuli supply the respiratory drive

With sleep onset, worsened hypoventilation, hypercapnia, and hypoxemia ensue because of the impaired automatic control system. In many cases, if not identified early, this leads to asphyxia and death

Mutations of the PHOX2B gene are disease-defining. This gene encodes a transcription factor responsible for the fate of early autonomic nervous system cells, including those in the respiratory control centers

90
Q

What does mutations of the PHOX2B gene relate to?

A

Disease defining for CCHS. This gene encodes a transcription factor responsible for the fate of early autonomic nervous system cells, including those in the respiratory control centers

91
Q

What is Pickwickian Syndrome

A

Obesity hypoventilation syndrome

92
Q

How do you diagnose Obesity hypoventilation syndrome?

A

obesity (body mass index [BMI] ≥30 kg/m 2 ) and daytime hypoventilation (Pa co 2 >45 mm Hg) be present without other causes for the latter

93
Q

What happens in sleep for people with Obesity hypoventilation syndrome?

A

progressive hypoventilation and hypoxemia during REM sleep and further impairment in NREM sleep

94
Q

What are the causes for sleep disruptions in Obesity hypoventilation syndrome?

A

(1) ventilatory abnormalities of obstructive sleep apnea (OSA, nearly universal in OHS
(2) obesity-related changes in the respiratory system (reduced lung volumes, impediment of diaphragmatic motion, ventilation/perfusion mismatch from intrinsic positive end-expiratory pressure)
(3) blunted chemosensitivity (decreased loop gain).

95
Q

How does chronic opioid use impact sleep?

A

hypoventilation and obstructive and central apneas can occur in a single patient, fulfilling diagnostic criteria for several disorders under the ICSD-3

Two unique patterns of breathing
(1) cluster breathing characterized by cycles of deep breaths with relatively stable tidal volumes, with interspersed central apneas of variable duration
(2) Biot breathing (ataxic breathing) with variable tidal volumes and rates

96
Q

How does treatment emergent CSA occur?

A

a disordered interplay between (1) UA collapsibility, (2) ventilatory system instability, and (3) a propensity for arousals (low threshold)

The relief of UA obstruction provided by CPAP, oral appliance, or tracheostomy is believed to “reveal” an elevated loop gain leading to hypocapnia with central apneas and short-cycle periodic breathing, similar to respiration at high altitude

97
Q

When is treatment emergent CSA more common?

A

TE-CSA is higher among patients with severe versus mild OSA

98
Q

What is complex sleep apnea?

A

the pathophysiologic coexistence of obstructive and nonobstructive pathophysiologic components, essentially high–loop gain OSA

TE-CSA is an outcome of targeting the UA alone in patients with high–loop gain OSA

The key feature of complex apnea and TE-CSA is NREM-dominant central hypopneas or periodic breathing with obstruction, resolving spontaneously during REM sleep.

99
Q

What is the key feature of complex apnea and TE-CSA?

A

NREM-dominant central hypopneas or periodic breathing with obstruction, resolving spontaneously during REM sleep.

A consistent feature of patients with treatment-emergent or complex sleep apnea is sleep fragmentation, which often persists despite reasonable respiration-targeted therapy. Because arousals amplify hypocapnic instability, inadequate cohesion of the NREM sleep–related network activity seems to be the core pathology in some of these patients

100
Q

How does CPAP modify chemo reflexes long term?

A

reduction in controller gain and increase in Pa co 2 reserve

101
Q

What is a potential treatment for TE-CSA and complex sleep apnea?

A

Stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most cases of OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output through moderate hypercapnia eliminates “obstructive” apnea in most patients with a wider range of chemosensitivity and CO 2 reserve.

Recent experiments suggest that in those with elevated loop gain and mild UA collapsibility, reducing chemosensitivity through hyperoxia may be effective.

102
Q

What are the key symptoms of CSA in nonhypercapnic patients?

A

Insomnia
Mild intermittent snoring
Awakenings (choking)
Normal body habits

103
Q

What are the key symptoms of CSA in hypercapnic patients?

A

Daytime sleepiness
Morning headache
Snoring
Respiratory failure
Normal or obese
Polycythemia
Cor pulmonale

104
Q

During what stage of sleep is nonhypercapnic central apneas more common?

A

Non-REM, particularly SWS

105
Q

Why does flow limitation occur in central sleep apneas?

A

fluctuating neural drive to the UA

106
Q

Which types of CSA syndromes are worse in non-REM vs REM sleep?

A

Non-REM: CCHS and opioid-induced CSA
REM: hypercapnia CSAs (+OSA) (e.g. Chemoreflex-Modulated Sleep Apnea)

107
Q

What are risk factors for people with HF to develop CSA?

A

age older than 60 years, male sex, atrial fibrillation, diuretic use, and daytime hypocapnia

108
Q

How do CHF patients present when they have CSA?

A

fatigue, and weakness rather than sleepiness

109
Q

What are the symptoms of CSA at high altitude?

A

restlessness, frequent brief arousals, and unrefreshing sleep

110
Q

What are the unique features of primary central sleep apnea?

A

resent with insomnia or frequent awakenings during the night, rather than daytime sleepiness, as seen in OSA.

Cycles of central apneas in idiopathic CSA are shorter (20– 40 seconds) and not as gradual as in CSA with CSB

111
Q

What pathophysiologic changes may be noticed in someone who has hypercapnia CSA?

A

locating the lesion along an anatomic pathway that could result in hypoventilation: corticobulbar tracts, brainstem, bulbospinal tracts to cervical spinal cord, anterior horn cells, lower motor neurons, neuromuscular junction, and diaphragmatic muscles.

Lung and chest wall abnormalities are generally apparent on examination

112
Q

How is CSA treated?

A

adaptive servo ventilation (ASV) and enhanced CPAP. Positive pressure ventilation can be used but is suboptimal

113
Q

How do adaptive servo ventilation (ASV) devices work to improve CSA and what are they most commonly used for?

A

provide expiratory support, inspiratory pressure support, and backup supportive responses guided by measures of ventilation or flow averaged over several minutes.

primarily designed for patients with elevated loop gain and thus nonhypercapnic CSA, but can be beneficial when hypoventilation is not the primary and sole abnormality

114
Q

How do you score respiratory events and efficacy of adaptive servo ventilation?

A

should use the pressure output signal from the ventilator. This is roughly equal and opposite to the patient’s respiratory output.

115
Q

How do you treat hypercapnia CSA?

A

bilevel ventilation with a backup rate, volume target pressure-support ventilation, or invasive volume ventilation through a tracheostomy

Volume-assured pressure support (VAPS) is an advance in the management of hypoventilation syndromes and hypercapnic CSA. VAPS is most effective if there is hypoventilation without CSA, but it can provide benefits if used cautiously in hypercapnic CSA.

Sufficient expiratory pressure support to prevent major obstructive events is critical.

116
Q

What is the problem of using positive pressure therapy in hypercapnia CSA?

A

of inducing relative hypocapnia and respiratory instability and associated sleep fragmentation by overly aggressive ventilation

There is a trade-off between improving ventilation and oxygenation versus sleep quality because excessive volume targets and the associated pressure rises can induce sleep fragmentation.

117
Q

What are some non-positive pressure therapies that can be used to treat CSA?

A

Phrenic Nerve Stimulation: activating the diaphragm during central apneas has been shown to markedly improve CAI and arousals in patients in CSA

Minimization of Hypocapnia: enhanced expiratory rebreathing space (EERS). EERS consisted of 50 to 150 mL of tubing and a nonvented mask (dead space) added to PAP therapy, which markedly improved AHI and sleep efficiency

Oxygen: Supplementary O 2 can reduce chemosensitivity and has a long history in treating CSA and periodic breathing without CSA.

Enhancing Sleep Consolidation: Sedatives can probably be used safely in minimally hypoxic, nonhypercapnic CSA and NREM-dominant apnea in general.

Carbonic Anhydrase Inhibition: Acetazolamide, a diuretic and carbonic anhydrase inhibitor, diminishes the ventilatory response of the peripheral chemoreceptors to hypoxia, decreases loop gain, and reduces the ventilatory response to arousals

A subset of CSA and TE-CSA patients appear very supine position dependent, and avoidance of the supine position can markedly improve treatment efficacy

118
Q
A

SLEE5102 (5 decks)

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