central sleep apnea and asv: what should i know as a tech? 2014 meet… · objectives 1) understand...
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Central Sleep Apnea and ASV: What should I know as a tech?
Fall 2014 MeetingOctober 3-4, 2014
Christopher E. Morgan, MDSleep Medicine/Neurology
Medical Director, Mercy Health St. Mary’s Sleep Center
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Conflict of Interest Disclosures for SpeakersX 1. I do not have any relationships with any entities producing, marketing, re-selling, or
distributing health care goods or services consumed by, or used on, patients, OR
2. I have the following relationships with entities producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients:
Type of Potential Conflict Details of Potential Conflict
Grant/Research Support
Consultant
Speakers’ Bureaus
Financial support
Other
3. The material presented in this lecture has no relationship with any of these potential conflicts, OR
4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
1.
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3.
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Objectives1) Understand the diagnosis and treatment strategies
for central sleep apnea (CSA)2) Understand the different forms of central sleep
apnea 3) Describe how Adaptive/Automatic Servo‐Ventilation
(ASV) works and treats central sleep apnea4) Describe the appropriate indications to use ASV
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General Principles for Diagnosis1) Must have clinical symptoms or medical comorbidities to make diagnosis
Sleepiness, insomnia, snoring, apneas, awakening with SOBA‐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
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Sleep Apnea and Comorbidities• 86% of obese type 2 diabetics suffer from sleep apnea• 65‐70% of stroke patients have Sleep Disordered Breathing (SDB)
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Prevalence of CSA6.5–15% of OSA patients suffer from complex sleep apnea syndrome18% of heart failure patients with OSA develop complex sleep apnea during CPAP titration30% of heart failure patients have Cheyne–Stokes Respiration (CSR)75% of patients on opioids for chronic pain have an AHI > 5
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CSA PathophysiologyCO2 falls below apneic thresholdCO2 does not rise as much during sleep
CO2 levels during sleep closer to apneic thresholdArousals and transitional sleep lead to hyperventilationIncreased responsiveness of chemoreceptors
Heightened ventilatory responses to arousals and CO2 changes Hyperventilation and lowering of CO2 Increased sympathetic toneHigh loop gain
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CSA Pathophysiology (cont.)Delay in circulation time
Leads to longer cycle length in CSBPulmonary irritant receptor stimulation
Pulmonary congestionSupine Position: cardiac filling pressures
CPAP over‐titrationCentral apneas usually increase through the night
Due to increased pulmonary congestion during the nightMild airway obstruction possibly contributes
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Over‐titration of CPAP
Supine Position ‐ cardiac filling pressures‐ Upper airway narrowing
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Central Sleep Apnea ClassificationWith Cheyne‐Stokes Breathing (CSB)Due to a medical disorder without Cheyne‐StokesDue to high altitude periodic breathingDue to medication or substancePrimary (Idiopathic)Primary of Infancy or prematurityTreatment‐Emergent (Complex SA)
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CSA with Cheyne‐StokesCrescendo‐decrescendo patternCycle length >40 seconds (usually closer to 60 seconds)Systolic CHF – longer cycle lengthMay be a delay in desaturations – adjust when scoringArousals at top of hyperpnea
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Cheyne‐Stokes, Delayed Desats
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Timing of arousals CSB vs other
Eckert, Chest 2007
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CSA with Cheyne‐StokesLess commonly complain of daytime sleepinessOften combination OSA and CSA, and CSA becomes more prominent after CPAP initiatedUsually absent or minimal in REM, minimal in N3May be seen in 25‐40% of patients with chronic CHF and 26‐50% of those acutely following strokeAssociated with A‐fib, renal failure, daytime hypocapnia
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CSA from Medical DisorderUsually brainstem lesionStroke
May continue in 7% long termCan get Cheyne‐Stokes in bilateral lesions
Multiple SclerosisBrainstem plaques
TumorChiari MalformationMultiple System Atrophy
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CSA and Stroke
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Medullary Astrocytoma
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CSA from Medication or SubstanceSuppresses respiratory driveOpioids – Methadone, long acting opioids, Suboxone, fentanyl patches
Dose dependentMay improve somewhat over timeMay see ataxic breathing (Biot’s respirations)Can also cause hypoventilation and OSASleepiness often caused by substance, not CSA
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Primary (Idiopathic) CSAUsually have low normal CO2 levels at baselineHeightened ventilatory responses to arousals and CO2 changes – chemoreceptors more responsive
High loop gainFrequent arousals worsen central apnea ‐ usually lower arousal threshold
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Treatment‐Emergent (complex) CSAObstructive or mixed events on baseline, then predominantly central events on titrationOften resolved in REM and N3, prominent in N1‐N2.
Look in REM to see what pressure treats obstructionPrevalence: 2‐20% on first or second night with CPAP
Seen in 15% of SDB population in academic sleep centerSeen in 18% of CHF patientsCloser to 2% have persistent CSA on chronic CPAP therapy
About 50% of complex SA patients never have good clinical response to CPAP
Residual sleepiness, insomnia, arousalsCPAP intolerance: “tearing off mask”
Morgenthaler et al, Sleep, 2006
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Treatment‐Emergent (complex) CSAOften low arousal thresholdReducing upper airway resistance brings out centralsOver‐titration can bring out central apneasUnder‐titration can lead to events and arousals which lead to central eventsBi‐PAP often makes it worseArousals from mask leak Split night studies are more commonly associatedUnclear how much will resolve with time
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Treatment Options for CSAASVSupplemental oxygen
Trouble with reimbursementBiPAP with fixed backup rate (ST)
Usually only if ASV and oxygen not effectiveHypnotics – decrease arousalsPositional therapy? Acetazolamide (Diamox)Opioid induced – withdrawal of opioids
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When do I use ASV?
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ASV Indications – AASM Practice ParametersClearly for CSA in CHF
Initial treatment still optimization of medical therapy and CPAPNo long term dataShort term follow up shows improved outcomes
Improved survivalImproved cardiac functionDecreased cardiac eventsImproved exercise tolerance & quality of life
Increased cost
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ASV Indications (cont.)Insufficient evidence in opioid related SA, complex SA or primary CSA
Barely any outcomes studies for theseStudies on complex SA show good effectiveness of ASVMixed studies on effectiveness in opioid related CSA
Recent study showed good long term efficacy and compliance Mean 25 month f/u, usage 5.1 hrs, AHI 3.3, ESS decrease by 2
Controversial to use in opioid CSA without hypoxemia or desats
Javaheri S. J Clin Sleep Med. 2014 Jun 15;10(6):637‐43
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CSA in Opioid Use
Javaheri S. J Clin Sleep Med. 2014 Jun 15;10(6):637‐43
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ASV IndicationsDo not use if hypoventilation
Targets patient’s own ventilation, which is inadequate in patients with hypoventilation
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When To Switch To ASVVery severe central apnea on initial titration
To the point you feel may cause harm to patient if sent home on CPAP or BiPAPIf patient cannot tolerate CPAP or BiPAP
If after 1‐2 month follow up, high suspicion for persistent central sleep apnea
High AHI on downloadPatient having persistent insomnia, arousals or daytime sleepiness, despite adequate compliance
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CSA CMS GuidelinesMUST be aware of this if switching patients to ASV in middle of study – must meet criteria
Need to calculate central AHI if possibleCentral AHI >5
Can be on titration if complex sleep apneaCentral AHI >50% of total AHISymptoms of excessive sleepiness or disrupted sleepCPAP has been ruled out as effective therapy
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Transplant Free Survival in CHF Patients With CSA on CPAP
Artz, Circ2007CANPAP
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Effect of ASV on Survival in CHF
Takama and Kurabayashi, Circulation J, 2012
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How does ASV work???
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ASV in once sentence:
Dynamically adjusts pressure support and respiratory rate to stabilize patient’s breathing
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Different Machines Work DifferentlyRespironics BiPAP Auto SV Advanced System One
Peak flow measurement – 95% target4 minute moving windowAuto adjusting EPAP
Responds to OA, OH, flow limit, snoreBiflexEPAP decreases with excessive leak
ResMed VPAP Adapt AutoMinute ventilation – 90% target3 minute moving windowNow auto adjusting EPAP (ASV auto mode)
Responds to OA, flow limit & snore“Easy‐breath” – syncs with patients breathingno EPR availableBR increases with excessive leak
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Servo Ventilation Algorithm
4 Minutes
On a breath by breath basis peak flow is captured
Peak flow is monitored over a moving 4 minute window
As 1 breath is added, the initial breath falls off
At every point within this 4 minute period an Average Peak Flow is calculated
The Peak flow target is established around that average and is based on the patient’s needs
BiPAP Auto SV Advanced estimates peak flow
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VPAP Adapt Estimates Minute VentilationTargets 90% of this calculationIt averages over a 3 minute moving windowPeak flow may be the same although minute ventilation is different
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BiPAP Auto SV Advanced – Auto EPAP
Pro Active Analysis
Leak Tolerance
Sophisticated Three Layered Algorithm: Safety Net
Primary Function
Increase 1 cm after 2 events (OA or OH) or 3 snoring eventsWill wait at least 2 minutes before increasing EPAP again
Looks every 5 minutes at flow signal and increases EPAP by 1 cm to see if makes a difference in flow limitation (Pro Active Analysis)
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Event classified as an Obstructed Airway Apnea
EPAP pressure increased (after 2‐OA’s)
No Flow Response!
Backup Breaths
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Obstructed Airway Apnea
12.5 to 13.5
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VPAP Adapt Auto EPAP Mode
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Auto SV Advanced System One ParametersEPAPmin: 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)
Consider shorter inspiratory time for COPD patientsRise: 1 – 6 (100 – 600ms) – longer rise may help with comfortBi‐Flex: set to patient comfort (0‐3)
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ResMed VPAP Adapt Auto ParametersEPAPmin: 4‐15 cm H2OEPAPmax: 4‐15 cm H2OPSmin: 0‐6 cm H2O (default 3) – previously was 3‐6
Default is 3, mainly for comfort, to assist with work of breathing
PSmax: 5‐20 cm H2O (PS min to IPAP 25)Max pressure: 25 cm H2ORate: Auto (15)
15 is default, but adjusts down as low as 10 if patient meeting minute ventilation requirements in last 4‐6 breaths
Ramp time: 0‐45 minCan’t input Inspiratory time or Rise time
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ASV EffectivenessBoth Machines very effective in reducing AHI in CSA
VPAP Adapt Auto SV Advanced
0
10
20
30
40
50
60
70
PSG CPAP autoSV autoSV Advanced
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ASV TitrationsCPAP and BiPAP titrations: only need to worry about EPAP and fixed pressure support for BiPAP adjustmentsASV has more settings to adjust, however, adjustments are not usually as frequent as CPAP and BiPAP
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Auto SV Advanced System One ProtocolUsually start a few cm below CPAP pressure which eliminated obstruction on the CPAP or BiPAP titration
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ASV is a SLOW titration – often recommended to wait 20 minutes before a change, but use your best judgmentAlways keep an eye on what the machine is doing
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VPAP ASV older titration guide
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My Thoughts on ASV TitrationsUsually we are titrating based on hypopneas Always watch for high leaks, very common! – adjust maskFlow limitation, paradoxical breathing, snoring: min EPAP
Keep an eye on what machine is automatically doing with EPAP and PS: watch the pressure line
If none of above and breathing looks periodic, centrals occurring or PS maxing out: Max PSIf still ambiguous hypopneas:
Try backup rate: May be helpful for opioid related CSATry increasing Min PS: can help with patient comfort, decrease arousalsConsider adding supplement O2 (especially if low sats)
See how they look in the lateral positionIf arousals very frequent – try hypnotic
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Watch for Breath StackingPatient below had a sleeping baseline rate of 9‐10 bpm Switched to a backup rate of 12 and started breath stackingNeed to pick rate 1‐2 below baseline rate.
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If pressure intolerance – patient complains, frequent arousals:Increase Min PSTry adjusting rise time or Biflex (on Respironics)Consider decrease Max PS (as long as central events controlled)
O2 sats low despite events being controlled: Min PS, consider O2Be careful: This may be a sign of hypoventilation or lung diseaseIf obstructive lung disease: backup rate with decreased I‐timeIf restrictive lung disease: backup rate with increased I‐time
If all else fails:Consider switching brand of ASV machine or trying BiPAP STConsider CPAP at lower pressures with supplemental O2 +/‐ hypnoticsConsider trying AVAPS (if suspicion for hypoventilation)
AVAPS not effective for CSB or periodic breathing
ASV Titrations (cont.)
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Note position and sleep stage differences
ASV started
Min EPAP increased
Central ApneasObstructive Apneas
Hypopneas
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Obstructive apneas on baseline
Central apneas on CPAP (absent in REM)
Down titration of CPAP did not improve centrals
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Obstructive & central apneas on CPAP
Central apneas on BiPAP
ASV started
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With CPAP
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With BiPAP
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With ASV
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ASV Follow Up Goals:
improve arousals, daytime sleepinessNo good evidence on this
Improve cardiac function & survival in CHF patientsProblems
Residual AHI ? Obstructive vs CentralFrequent arousals/insomnia – try hypnoticHigh leaks
Pressure intolerance ‐ try ramp, Biflex, adjust rise time, or decrease pressureHigh leaks – mask adjustment, pressure decreaseResidual sleepiness – look for other causes
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High Leak Causing Increase AHI
AHI better when leak better
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Summary/ConclusionsCSA is a prevalent disorder in certain populationsCan lead to worse outcomes in CHF, but not much data on long term outcomes in other forms of CSAASV often first line of treatment, improves outcomes in CHFSwitch to ASV for severe centrals or poor clinical response to CPAP/BiPAP on follow upThe 2 main ASV machines differ in mechanism, but both achieve good resultsASV titration is SLOW
Always watch for leaksWatch patient and machine closely to determine next step in titration
Watch for residual symptoms or elevated AHI on follow up
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Questions??
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Art Prize Beer Tour – Lets Go!!
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ReferencesInternational Classification of sleep disorders, Third Edition, 2014ResMed ASV slides – including titration protocolsRespironics ASV slides – including titration protocolsAntonescu‐Turcu A, Parthasarathy S. Respir Care. 2010 September ; 55(9): 1216–1229.Fernández J. Indian J Crit Care Med. 2013 Jan;17(1):16‐22.Kasai, et al. Circ Heart Fail. 2010;3:140‐148 Hastings et al. Int Journal of Cardiology 139(2010) 17‐24 Banno, et al. J Clin Sleep Med 2006;2(2):181‐186 Arzt, et al. CHEST 2008;134:61‐66 Randerath, et al. Sleep Medicine 9 (2008) 823‐830 Teschler, et al. Am J Respir Crit Care Med 2001;164:614‐19 Artz, et al. Circulation 2007;115;3173‐80Allam, et al. CHEST 2007;132:1839‐1846. Morganthaler, et al. SLEEP 2007;30(4):468‐475 Westhoff, et al. Sleep Breath On line 2/25/11 Brown, et al. J Clin Sleep Med 2011;7(2):187‐195. Javahari, et al. J Clin Sleep Med 2008;4(4):305‐310 Farney, et al. J Clin Sleep Med 2008;4(4):311‐319 Javaheri S. J Clin Sleep Med. 2014 Jun 15;10(6):637‐43David Wang. Sleep Breath (2014) 18:229–231Morganthaler, et al. Sleep. 2006 Sep;29(9):1203‐9.Oldenburg et al. SLEEP 2012 Poster and Abstract. Javaheri, S. et. al, ERS 2009, Session #52