Central Sleep Apnea in Adults: Causes and Treatment Timothy Daum MD Spectrum Health Grand Rapids
Rogers, R. Chest 2008;133:598
The majority of sleep apnea we see is obstructive in nature:
Central Sleep Apnea At most 10% of sleep study population Pathogenesis –Distinguishing characteristics Approach to management
Central Sleep Apnea Sleep transition central apnea Congenital Alveolar Hypoventilation –Ondine’s Curse CHF –Cheyne-Stokes Periodic Breathing Stroke or Other Neurologic Insult High Altitude Periodic Breathing Narcotics Treatment Emergent Central Apnea Complex Sleep Disordered Breathing
CSA: Symptoms Disrupted, unrefreshing sleep Many complain of insomnia Excessive daytime sleepiness
Sleep Transition Central Apnea Common with recurrent arousals –OSA, PLMS CO2 will climb from 40 to 45 in normal sleep Robust ventilatory response with arousal CO2 driven below ventilatory threshold Apnea with sleep onset
Sleep Transition Central Apnea
Sleep Transition Related Central Apnea
Congenital Alveolar Hypoventilation Ondine’s curse Due to recently recognized genetic abnormality Affected individuals have higher CO 2 set point Usually identified in infants –Milder cases found in adults Responds well to timed Bilevel Pressure
CSA and CHF Up to 40% of those with reduced LVEF Most common with: –More advanced age –Male –Atrial fibrillation Presence of CSA portends a worse prognosis
SDB in CHF Patients OSA CSA Level IVLevel IIILevel IILevel I Mixed Apneas New York Heart Association
CSA and CHF: Cheyne-Stokes Periodic Breathing Note period length of sec Note circulation time. Usually over 30 seconds in CHF.
CHF and CSA: Pathogenesis Dyspnea leads to hyperventilation and hypocapnea while awake With sleep onset, hypocapnea leads to apnea and hypoventilation With increased circulation time, hypercapnea becomes significant before blood gets from lungs to brain stem leading to marked hyperventilation Hyperventilation leads to hypocapnea Repeat
CHF and CSA: Treatment Main therapy is optimize medical management of CHF Positive airway pressure shown to: –Improve exercise tolerance –Improve LVEF –Decrease catecholamines –Quality of Life No proven benefit on mortality
CHF and CSA: Alternative Treatments Oxygen –May decrease dyspnea and hyperventilation Theophylline –Respiratory stimulant Adaptive Servo Ventilation
CSA and CVA Present in 26% of acute stroke patients Continues in 7% long term Remember the high incidence of OSA in stroke patients as well –Unclear if this precedes CVA
CSA and Narcotics Can be seen in up to 50% of chronic narcotic users. Prevalence almost certainly increasing.
Treatment Emergent Central Apnea Titration of CPAP beyond that needed to resolve obstructive events can lead to the development of central events with arousals. Important to differentiate from complex sleep apnea –Central events seen before obstructive events controlled
Complex Sleep Disordered Breathing Traditional classification is obstructive vs central sleep apnea Recently recognized group of patients who start out looking like mostly OSA but develop prominent CSA with CPAP Central apneas develop before obstructive events controlled
Complex SDB: Baseline
What Do We Know About CompSA? Prevalence: Estimated to be 15% of SDB population About 50% don’t ever respond to CPAP –Residual symptoms (fatigue, sleepiness, depression) –Intolerance to therapy Dramatic improvement during REM sleep (reverse of pattern seen in OSA) No distinguishing clinical profile Morgenthaler et al, Sleep, 2006
CSA: Treatment
Maximize medical therapy of underlying condition –Diuretics; afterload reduction; beta-blockers, biventricular pacers for CHF –Minimize narcotics and other sedatives Trial CPAP –Often unresponsive
Adaptive Servo Ventilation Servo: Any type of self-regulating feedback system or mechanism VPAP Adapt SV –ResMed BiPAP auto SV –Respironics
PAP Therapy ™
How Does it Work? Creates a Target Ventilation –The ASV algorithm monitors recent average minute ventilation (~3 min window) –It continuously calculates a target ventilation throughout the night (90% of recent average ventilation) Ventilates to the Target –Algorithm monitors patient ventilation and compares it to the target ventilation –Adjusts pressure support up or down as needed to achieve target
End Expiratory Pressure (EEP) EEP = EPAP Default EEP = 5 cm H 2 0 –May adjust in 1-2 cm increments to resolve any upper airway obstruction (for CHF patients wait 40 minutes before adjusting) EEP: manually titrate like CPAP to hold airway patent Time Pressure (cm H 2 0)
Pressure Support (PS) Pressure support = IPAP - EPAP Pressure support varies between limits –minPS (default 3 cm H 2 O) –maxPS (default 10 cm H 2 O) Values are adjustable but defaults work in almost all cases maxPS Time Pressure (cm H 2 0) minPS
Gives Support Only When Needed The ASV algorithm automatically adjusts the magnitude of pressure support breath by breath to: –Provide minimal, comfortable support during the over-breathing phase (hyperpnea) or during normal breathing –Increase support during under-breathing (hypopnea or apnea) Time Pressure (cm H 2 0) Central apnea (no spontaneous effort) Normal breathing effort
Support When Needed Effort Flow SpO 2 FG
Normalized Breathing: 10 Minutes Into Session Effort Flow SpO 2 FG
Greatest Reduction in Central Apnea Index 83% further reduction in CAI compared to CPAP 50% reduction compared to bilevel Teschler et al, AJRCCM, 2001
Normalizes Total Arousal Index Partial improvement with oxygen and CPAP Normalization with bilevel and ACS Teschler et al, AJRCCM, 2001
Significant Increase in Deep Sleep SWS+REM = % time spent in deep, restorative sleep Large increases in SWS+REM with ASV and bilevel but not with either O 2 or CPAP Teschler et al, AJRCCM, 2001
CMS Guidelines for CSA (E0471)
Conclusion By now, you should be able to: –List the ideal types of patients for VPAP Adapt SV –Describe how the VPAP Adapt SV treats patients –Discuss the results of studies using ResMed’s Adaptive Servo-Ventilation algorithm –List the keys to successful treatment –State the qualifying criteria and reimbursement guidelines for the VPAP Adapt SV