Central Sleep Apnoea - Sleep Apnea | RealSleep

Central Sleep Apnoea

Dr Eric Livingston
Glasgow Royal Infirmary

Central Sleep Apnoea (CSA)

• Characterised by a lack of drive to breathe
during sleep, resulting in insuficient or absent
ventilation and compromised gas exchange

• It is defined by a lack of respiratory effort
during cessations of airflow (cf. OSA)



Manifestations of CSA

• There are many, including:

– Congenital Central Hypoventilation Syndrome
– High altitude-induced periodic breathing
– Idiopathic CSA
– Narcotic-induced CSA
– Cheyne-Stokes Breathing

Prevalence

• Varies greatly between the various forms of
CSA

• ICSA is uncommon (<5% of patients referred
to a sleep clinic)

• 37% of patients with LVEF <45%

Chemical control of breathing

• Chemoreceptors

– Central medullary neurons

• Responding to CO2 vis shifts in H+

– Carotid bodies

• Responding to PaO2 and PaCO2

• The ventilatory output to a given change in
PaO2 and PaCO2 can vary greatly between
individuals and with disease states

Chemical control of breathing

• Highly sensitive chemoresponses can place an
individual at risk for unstable breathing
patterns as these individuals over respond to
small changes in chemical stimuli

• The inherent delays in the negative feedback
loop controlling ventilation also contribute to
the risk for developing instability

– Loop gain

Classification of CSA

• Different classifications

– Primary or secondary
– Hypercapnic CSA or non-hypercapnic CSA

Hypercapnic CSA

• Sleep hypoventilation

• Impaired central drive (‘Won’t breathe’)

– Congenital central hypoventilation syndrome
– Opiate use

• Interesting evidence that sleep disruption worsens
physical pain, leading to intriguing hypothesis that
opiate induced CSA can increase opiate requirements

Hypercapnic CSA

• Impaired respiratory motor control (‘Cant’t
breathe’)

– Neuromucular conditions

• Myasthenia Gravis
• MND
• Kyphoscoliosis

Non-hypercapnic CSA

• Cheyne Stokes Breathing

– Commonly observed in patients with CCF
– Can also be seen post CVA
– May be due to prolonged circulation time

• Idiopathic CSA

– Thinner and snore less than OSA patients

• Complex sleep apnoea





Complex Sleep Apnoea

• Thought to be a form of central sleep apnoea
• Exhibit primarily obstructive or mixed apneas during

diagnostic study
• Identified by central apneas/hypopnoeas emerging

when treating obstructive apnoeas with a CPAP or
bilevel device

• Controversial as to whether actually a real entity
• Reduction in central apnoeas with time on CPAP

Physiologic factors likely to influence
CSA severity

• Hypoxia

– The depressive effects of hypoxia may further
increase disease severity

• Upper airway anatomy

– An individual with a narrow UA is extremely
reliant on neural drive to UA muscles to maintain
an open UA, in contrast to someone with an
anatomically larger UA



Therapeutic interventions

• Treat underlying cause

– Optimise treatment in CCF

• Cardiac resynchronisation devices
• Medical management

– Reduce opiate dose



Therapeutic interventions

• Oxygen therapy

– Non-hypercapnic CSA patients with heightened
chemosensitivity may benefit incl. CSB

• Carbon dioxide

– Studies have demonstrated that mild increases in
inspired CO2 can be effective in treating CSA

• Decreases AHI, without apparent acute cardiovascular
adverse effects, in patients with ICSA and CSB

Non-invasive ventilation

• Clear-cut in those with hypercapnic CSA
• Less clear in less severe forms of CSA

• CPAP

– CANPAP

• Reduces AHI, but no difference in survival or
hospitalisations

Non-invasive ventilation

• Bilevel ventilation

– Often used with a back-up respiratory rate in OHS
– If used without a back-up rate , may exacerbate

hyperventilation, hypocapnoea, and central
apnoea by augmenting tidal volume

Therapeutic interventions

• Adaptive Servo-ventilation (ASV)

– Provides a small, but varying, amount of
inspiratory pressure superimposed on a low level
of CPAP

– In a study looking at patients with CSA and CCF,
ASV more effectively suppressed central apnoeas
than CPAP

– Evidence for benefit in complex sleep apnoea

Respiratory Stimulants

• Acetazolamide

– Carbonic anhydrase inhibitor
– Leads to metabolic acidosis
– Shifts the hypercapnic ventilatory response, and

lowers the PaCO2 apnoea threshold
– Improves CSA in patients wih CCF and ICSA

Respiratory Stimulants

• Theophyllines

– Improves SDB via increasing central respiratory
drive and cardiac contractility

– Improves CSA in patients with CCF

• Progesterones

– Increases chemoresponsiveness and may lead to
improvement in daytime gas exchange in patients
with OHS