Central Sleep Apnea And ASV: What Should I Know As A Tech?

Fall 2014 MeetingOctober 3-4, 2014Central Sleep Apnea and ASV:What should I know as a tech?Christopher E. Morgan, MDSleep Medicine/NeurologyMedical Director, Mercy Health St. Mary’s Sleep Center

Conflict of Interest Disclosures for SpeakersX1. I do not have any relationships with any entities producing, marketing, re-selling, ordistributing health care goods or services consumed by, or used on, patients, OR2. I have the following relationships with entities producing, marketing, re-selling, ordistributing health care goods or services consumed by, or used on, patients:Type of Potential ConflictDetails of Potential ConflictGrant/Research SupportConsultantSpeakers’ BureausFinancial supportOther3. The material presented in this lecture has no relationship with any of these potential conflicts, OR4. This talk presents material that is related to one or more of these potential conflicts, and the followingobjective references are provided as support for this lecture:1.2.3.

Objectives1) Understand the diagnosis and treatment strategiesfor central sleep apnea (CSA)2) Understand the different forms of central sleepapnea3) Describe how Adaptive/Automatic Servo‐Ventilation(ASV) works and treats central sleep apnea4) Describe the appropriate indications to use ASV

General Principles for Diagnosis1) Must have clinical symptoms or medical comorbiditiesto make diagnosisy Sleepiness, insomnia, snoring, apneas, awakening withSOBy A‐fib, CHF, or neurological disorder (such as stroke, MS)2) Central AHI 53) Central apneas and hypopneas 50% of total AHI4) Not better explained by another sleep disorder

Sleep Apnea and Comorbidities 86% of obese type 2 diabetics suffer from sleep apnea 65‐70% of stroke patients have Sleep DisorderedBreathing (SDB)

Prevalence of CSAy 6.5–15% of OSA patients suffer from complex sleepapnea syndromey 18% of heart failure patients with OSA developcomplex sleep apnea during CPAP titrationy 30% of heart failure patients have Cheyne–StokesRespiration (CSR)y 75% of patients on opioids for chronic pain have anAHI 5

CSA Pathophysiologyy CO2 falls below apneic thresholdy CO2 does not rise as much during sleepy CO2 levels during sleep closer to apneic thresholdy Arousals and transitional sleep lead tohyperventilationy Increased responsiveness of chemoreceptorsy Heightened ventilatory responses to arousals and CO2changesy Hyperventilation and lowering of CO2y Increased sympathetic toney High loop gain

CSA Pathophysiology (cont.)y Delay in circulation timey Leads to longer cycle length in CSBy Pulmonary irritant receptor stimulationy Pulmonary congestionySupine Position: Ç cardiac filling pressuresy CPAP over‐titrationy Central apneas usually increase through the nighty Due to increased pulmonary congestion during the nighty Mild airway obstruction possibly contributes

Supine Position‐ Ç cardiac filling pressures‐ Upper airway narrowingOver‐titrationof CPAP

Central Sleep Apnea Classificationy With Cheyne‐Stokes Breathing (CSB)y Due to a medical disorder without Cheyne‐Stokesy Due to high altitude periodic breathingy Due to medication or substancey Primary (Idiopathic)y Primary of Infancy or prematurityy Treatment‐Emergent (Complex SA)

CSA with Cheyne‐Stokesy Crescendo‐decrescendo patterny Cycle length 40 seconds (usually closer to 60seconds)y Systolic CHF – longer cycle lengthy May be a delay in desaturations – adjust when scoringy Arousals at top of hyperpnea

Cheyne‐Stokes, Delayed Desats

Timing of arousals CSB vs otherEckert,Chest 2007

CSA with Cheyne‐Stokesy Less commonly complain of daytime sleepinessy Often combination OSA and CSA, and CSA becomesmore prominent after CPAP initiatedy Usually absent or minimal in REM, minimal in N3y May be seen in 25‐40% of patients with chronic CHFand 26‐50% of those acutely following strokey Associated with A‐fib, renal failure, daytimehypocapnia

CSA from Medical Disordery Usually brainstem lesiony Strokey May continue in 7% long termy Can get Cheyne‐Stokes in bilateral lesionsy Multiple Sclerosisy Brainstem plaquesy Tumory Chiari Malformationy Multiple System Atrophy

CSA and Stroke

Medullary Astrocytoma

CSA from Medication or Substancey Suppresses respiratory drivey Opioids – Methadone, long acting opioids, Suboxone,fentanyl patchesy Dose dependenty May improve somewhat over timey May see ataxic breathing (Biot’s respirations)y Can also cause hypoventilation and OSAy Sleepiness often caused by substance, not CSA

Primary (Idiopathic) CSAy Usually have low normal CO2 levels at baseliney Heightened ventilatory responses to arousals and CO2changes – chemoreceptors more responsivey High loop gainy Frequent arousals worsen central apnea ‐ usuallylower arousal threshold

Treatment‐Emergent (complex) CSAy Obstructive or mixed events on baseline, then predominantlycentral events on titrationy Often resolved in REM and N3, prominent in N1‐N2.y Look in REM to see what pressure treats obstructiony Prevalence: 2‐20% on first or second night with CPAPy Seen in 15% of SDB population in academic sleep centery Seen in 18% of CHF patientsy Closer to 2% have persistent CSA on chronic CPAP therapyy About 50% of complex SA patients never have good clinicalresponse to CPAPy Residual sleepiness, insomnia, arousalsy CPAP intolerance: “tearing off mask”Morgenthaler et al,Sleep, 2006

Treatment‐Emergent (complex) CSAy Often low arousal thresholdy Reducing upper airway resistance brings out centralsy Over‐titration can bring out central apneasy Under‐titration can lead to events and arousals whichyyyylead to central eventsBi‐PAP often makes it worseArousals from mask leakSplit night studies are more commonly associatedUnclear how much will resolve with time

Treatment Options for CSAy ASVy Supplemental oxygeny Trouble with reimbursementy BiPAP with fixed backup rate (ST)y Usually only if ASV and oxygen not effectivey Hypnotics – decrease arousalsy Positional therapyy ? Acetazolamide (Diamox)y Opioid induced – withdrawal of opioids

When do I use ASV?

ASV Indications – AASM PracticeParametersy Clearly for CSA in CHFy Initial treatment still optimization of medical therapy andCPAPy No long term datay Short term follow up shows improved outcomesyyyyImproved survivalImproved cardiac functionDecreased cardiac eventsImproved exercise tolerance & quality of lifey Increased cost

ASV Indications (cont.)y Insufficient evidence in opioid related SA, complex SAor primary CSAy Barely any outcomes studies for thesey Studies on complex SA show good effectiveness of ASVy Mixed studies on effectiveness in opioid related CSAyyRecent study showed good long term efficacy and compliancey Mean 25 month f/u, usage 5.1 hrs, AHI 3.3, ESS decrease by 2Controversial to use in opioid CSA without hypoxemia ordesatsJavaheri S. J Clin Sleep Med. 2014 Jun 15;10(6):637‐43

CSA in Opioid UseJavaheri S. JClin Sleep Med.2014 Jun15;10(6):637‐43

ASV Indicationsy Do not use if hypoventilationy Targets patient’s own ventilation, which is inadequate inpatients with hypoventilation

When To Switch To ASVy Very severe central apnea on initial titrationy To the point you feel may cause harm to patient if senthome on CPAP or BiPAPy If patient cannot tolerate CPAP or BiPAPy If after 1‐2 month follow up, high suspicion forpersistent central sleep apneay High AHI on downloady Patient having persistent insomnia, arousals or daytimesleepiness, despite adequate compliance

CSA CMS Guidelinesy MUST be aware of this if switching patients to ASV inmiddle of study – must meet criteriay Need to calculate central AHI if possibley Central AHI 5y Can be on titration if complex sleep apneay Central AHI 50% of total AHIy Symptoms of excessive sleepiness or disrupted sleepy CPAP has been ruled out as effective therapy

Transplant Free Survival in CHF PatientsWith CSA on CPAPArtz, Circ2007CANPAP

Effect of ASV on Survival in CHFTakama and Kurabayashi, Circulation J, 2012

How does ASV work?

ASV in once sentence:Dynamically adjustspressure support andrespiratory rate to stabilizepatient’s breathing

Different Machines Work Differentlyy Respironics BiPAP Auto SV Advanced System Oney Peak flow measurement – 95% targety 4 minute moving windowy Auto adjusting EPAPyResponds to OA, OH, flow limit, snorey Biflexy EPAP decreases with excessive leaky ResMed VPAP Adapt Autoy Minute ventilation – 90% targety 3 minute moving windowy Now auto adjusting EPAP (ASV auto mode)yResponds to OA, flow limit & snorey “Easy‐breath” – syncs with patients breathingy no EPR availabley BR increases with excessive leak

BiPAP Auto SV Advanced estimates peak flowServo Ventilation Algorithm4 MinutesOn a breath by breath basis peak flow is capturedPeak flow is monitored over a moving 4 minute windowAs 1 breath is added, the initial breath falls offAt every point within this 4 minute period an Average Peak Flow is calculatedThe Peak flow target is established around that average and is based on thepatient’s needs

VPAP Adapt Estimates Minute Ventilationy Targets 90% of this calculationy It averages over a 3 minute moving windowy Peak flow may be the same although minuteventilation is different

BiPAP Auto SV Advanced – Auto EPAPy Increase 1 cm after 2 events (OA or OH) or 3 snoring eventsy Will wait at least 2 minutes before increasing EPAP againy Looks every 5 minutes at flow signal and increases EPAP by1 cm to see if makes a difference in flow limitation (ProActive Analysis)Sophisticated Three Layered Algorithm:Safety NetPrimary FunctionLeak TolerancePro ActiveAnalysis

Event classified as an Obstructed AirwayApneaNo FlowResponse!EPAP pressure increased (after 2‐OA’s)Backup Breaths

Obstructed Airway Apnea12.5 to 13.5

VPAP Adapt Auto EPAP Mode

Auto SV Advanced System One ParametersyyyyyyyEPAPmin: 4‐25 cm H2OEPAPmax: 4‐25 cmH2OPSmin: 0‐21 cmH2O (default 0)PSmax: 0‐21 cm H2O (PS min to IPAP 25)Max pressure: 25 cm H2ORate: Auto (8‐15), or fixed (4 – 30 BPM)Timed Insp (if rate fixed): 0.5 – 3.0 sec (default 1.2 secs)y Consider shorter inspiratory time for COPD patientsy Rise: 1 – 6 (100 – 600ms) – longer rise may help with comforty Bi‐Flex: set to patient comfort (0‐3)

ResMed VPAP Adapt Auto Parametersy EPAPmin: 4‐15 cm H2Oy EPAPmax: 4‐15 cm H2Oy PSmin: 0‐6 cm H2O (default 3) – previously was 3‐6y Default is 3, mainly for comfort, to assist with work ofbreathingy PSmax: 5‐20 cm H2O (PS min to IPAP 25)y Max pressure: 25 cm H2Oy Rate: Auto (15)y 15 is default, but adjusts down as low as 10 if patient meetingminute ventilation requirements in last 4‐6 breathsy Ramp time: 0‐45 miny Can’t input Inspiratory time or Rise time

ASV Effectivenessy Both Machines very effective in reducing AHI in CSAVPAP AdaptAuto SV Advanced706050403020100PSGCPAPautoSV autoSV Advanced

ASV Titrationsy CPAP and BiPAP titrations: only need to worry aboutEPAP and fixed pressure support for BiPAPadjustmentsy ASV has more settings to adjust, however, adjustmentsare not usually as frequent as CPAP and BiPAP

Auto SV Advanced System One Protocoly Usually start a few cm below CPAP pressure whicheliminated obstruction on the CPAP or BiPAP titration

y ASV is a SLOW titration – often recommended to wait20 minutes before a change, but use your best judgmenty Always keep an eye on what the machine is doing

VPAP ASV older titration guide