Draft

259  Sleep Apnea For Pulm Fellows

259.1 Summary

  • Control of Ventilation and Sleep Disordered-Breathing for Pulm Fellows
  • 90+% reduction in airflow with no respiratory effort throughout
  • Or, could wait and do nothing; or give oxygen
  • Central Apneas
  • Control of Respiration
  • Ventilation during sleep
  • Synthesis:
  • If these issues are so common, why don’t we see apneas all over the place inpatient?
  • Stage
  • Greater than 30 AHI CPAP just as effective, but faster, easier, cheaper.

259.2 Slide outline

259.2.1 Slide 1

  • Control of Ventilation and Sleep Disordered-Breathing for Pulm Fellows
  • SEEK Q #315 ### Slide 2
  • Control of Ventilation and Sleep Disordered-Breathing for Pulm Fellows
  • Brian Locke MD MSc
  • Not a sleep doc
  • (Chronic Vent. Failure @ Intermountain) ### Slide 3
  • TODO: No text extracted from this slide. ### Slide 4
  • TODO: No text extracted from this slide. ### Slide 5
  • 90+% reduction in airflow with no respiratory effort throughout
  • 30+% reduction in airflow; 3-4% desat OR cortical arousal ### Slide 6
  • TODO: No text extracted from this slide. ### Slide 7
  • Or, could wait and do nothing; or give oxygen
  • Central Apneas (Periodic Breathing)
  • Developed after OSA treatment TECSA ### Slide 8
  • Central Apneas
  • Hunter-Cheyne Stokes Respiration or Elevation depending on period length; high loop gain or low CO2 reserve
  • Respiratory Generator Impaired; Stroke, ICP, Herniation
  • Respiratory Generator Impaired; Opiates
  • Many causes ; high loop gain or low CO2 reserve ### Slide 9
  • Central Apneas
  • High Loop Gain
  • Narrow CO2 Reserve ### Slide 10
  • Control of Respiration
  • Chemoreflex –
  • Central: CSF pH, correlates to blood CO2 (slow, increases 45+)
  • Peripheral: CO2>41, O2 < 55, pH low. Fast.
  • Voluntary / supratentorial: rib movement censors
  • Metabolic drive – mediated by unknown mechanisms (e.g. how the Ve increases in CPET before blood gases change)
  • Wakefulness drive – disappears during sleep, such that a minor PaCO2 drop in the presence of normoxia produces a central apnea during sleep or anesthesia ### Slide 11
  • Ventilation during sleep
  • Wakefulness drive to breath a stimulus to keep breathing at some Ve even when the CO2 is below the apneic threshold (the flat part of the hockey stick)
  • Defined in absence… the hockey stick (a maintained low level of ventilation) goes away when you go to sleep.
  • Apneic threshold PaCO2 below which breathing stops during sleep.
  • ~33-35 mmHg at sea level; goes up faster than PaCO2 with hypercapnia
  • PaCO2 to terminate an apnea ~1-4 CO2 higher than PaCO2 to start an apnea
  • Difference between PaCO2 baseline and Apneic threshold called the CO2 reserve) ### Slide 12
  • Synthesis:
  • You want to induce apneas in someone, what mode would you set them in?
  • Why does oxygen reduce central apneas?
  • What happens if you send someone with new diagnosed OHS home with BPAP and no back-up? ### Slide 13
  • If these issues are so common, why don’t we see apneas all over the place inpatient?
    1. Pulse oximetry averages waveforms over 10 seconds
  • “HRPO” noc ox; average over 2 seconds for inpatient sleep
    1. All BPAP inpatient is BPAP S/T – always backup rates preventing apneas. ### Slide 14
  • Stage
  • Mechanics (Loads on the respiratory system)
  • Muscle Activity
  • Chemo-responsiveness
  • PaCO2
  • Awake
  • Upright-ish; open airway
  • Ok
  • Normal
  • CO2 stable across a huge range of VCO2 (30x in health)
  • NREM (1-3)
  • Supine (decreased FRC -> EELV), decreased UA tone increased resistance to flow
  • Reduced
  • Slight increases in PaCO2 (Decreased VCO2, but more decreased VE)
  • REM
  • Non-diaphragm muscles are paralyzed
  • Very reduced
  • Normal: increases up to 6 mmHg of CO2; pathologic 10+ (sleep hypoventilation)
  • When will obstructive apneas be the worst?
  • When will central apneas be the worth?
  • When will sleep hypoventilation be the worst, and in whom? ### Slide 15
  • TODO: No text extracted from this slide. ### Slide 16
  • Greater than 30 AHI CPAP just as effective, but faster, easier, cheaper.
  • 70% of patients with OHS have AHI > 30 ### Slide 17
  • Same question; but just diagnosed and on hospital discharge:
  • What do you prescribe?
  • VAPS-AE
  • BPAP-S
  • BPAP-ST
  • Nothing; sleep clinic referral ### Slide 18
  • Same question; but just diagnosed and on hospital discharge:
  • What do you prescribe?
  • VAPS-AE
  • BPAP-S
  • BPAP-ST
  • Nothing; sleep clinic referral ### Slide 19
  • OSA, some OHS
  • CSA
  • some OHS
  • IVAPS (Resmed) vs
  • AVAPs (Respironics) ### Slide 20
  • RADs vs HMV
  • Respiratory Assist Device
  • Home Mechanical Ventilator
  • S / ST/ VAPS / PC modes
  • Required if you want AVAPS-AE
  • Titrates EPAP in addition to PS
  • (E0470 or E0471 are the DME codes)
  • Mouthpiece ventilation; High Flow O2, IPAP 30+
  • Sufficient for most patients; but difficult insurance requirements (next slide)
  • In patients who’s ventilatory needs are likely to be more complex over time (e.g. NMD)
  • Or a patient who MUST have on discharge
  • Comes with RT support from the DME
  • Rent to own; less expensive
  • $$$ (just rent; never own)
  • Battery Powered ### Slide 21
  • Qualification for RADs ### Slide 22
  • The disorder is likely to worsen during REM sleep.
  • Bilevel pressure, spontaneous mode, is an effective therapy.
  • The use of low-dose hypnotics is likely to exacerbate disease.
  • The addition of supplemental oxygen during sleep may decrease the frequency of events. ### Slide 23
  • The disorder is likely to worsen during REM sleep.
  • Bilevel pressure, spontaneous mode, is an effective therapy.
  • The use of low-dose hypnotics is likely to exacerbate disease.
  • The addition of supplemental oxygen during sleep may decrease the frequency of events. ### Slide 24
  • TODO: No text extracted from this slide. ### Slide 25
  • Just send to surgery.
  • Mild OSA is not associated with much of anything, except marginally improved QOL after CPAP
  • (probably only severe & OHS for increased perioperative risk) ### Slide 26
  • The definition of OSA is bad
  • OSA, as currently defined, is improbably common.
  • The definition does not discriminate well between people suffering adverse consequences and those who don’t.
  • AHI does not really represent what we care about
  • Just frequency of events; not duration, their impact, etc.
  • Why is 5(+sx) or 15 the cutoff?
  • NOT 95% range in healthy individuals as usual
  • Associated with increased risk of stroke at 15/hr in large cohorts
  • Prevalence of excess sleepiness in Prim Care? 1 in 4
  • Just because they ”have OSA” doesn’t mean they have OSA
  • Alternatives to AHI?
  • there are many, not ready for primetime ### Slide 27
  • TODO: No text extracted from this slide. ### Slide 28
  • The definition of a hypopnea in UT
  • Utah
  • Sea-level
  • Big event required at sea level for 3-4% oxygen desaturation
  • Small event required at elevation level for 3-4% oxygen desaturation
  • “Prevalence” in UT, by accepted definitions, would be absurdly high.
  • If you look, you will find it
  • You can’t use the presence of ”disease” as an indication for treatment ### Slide 29
  • A 45-year-old man is seen in your clinic for severe obstructive sleep apnea and was recently started on continuous positive airway pressure (CPAP) after an in-laboratory titration demonstrated adequate control of disease on 12 cm of water pressure using an oronasal mask interface. He presents complaining that the mask is too cumbersome, and requests a change to a nasal interface.
  • Which of the following will be most likely after the patient is transitioned to this new interface?
  • He will require a higher CPAP pressure for adequate control of disease with a nasal mask.
  • His average adherence, as measured in hours per night, will increase.
  • He will have more air leak from the system.
  • His Epworth Sleepiness Scale (ESS) score will improve. ### Slide 30
  • A 45-year-old man is seen in your clinic for severe obstructive sleep apnea and was recently started on continuous positive airway pressure (CPAP) after an in-laboratory titration demonstrated adequate control of disease on 12 cm of water pressure using an oronasal mask interface. He presents complaining that the mask is too cumbersome, and requests a change to a nasal interface.
  • Which of the following will be most likely after the patient is transitioned to this new interface?
  • He will require a higher CPAP pressure for adequate control of disease with a nasal mask.
  • His average adherence, as measured in hours per night, will increase.
  • He will have more air leak from the system.
  • His Epworth Sleepiness Scale (ESS) score will improve. ### Slide 31
  • SEEK
  • A 56-year-old overweight woman with no medical history is referred to you for evaluation of OSA. She complains of loud disruptive snoring, excessive daytime sleepiness, and daytime fatigue. Her spouse is unwilling to sleep with her in the same room. Physical exam reveals a BMI of 28 kg/m2. Her oropharynx is crowded. The remainder of the physical exam is normal. Recently, her primary care provider ordered a sleep study that demonstrated mild OSA, with an apnea-hypopnea index of 12 events per hour. Treatment with nasal CPAP was initiated, but the patient could not tolerate CPAP, despite multiple mask changes and CPAP device adjustments with an experienced respiratory therapist, as well as discussions with a primary care provider with educational interventions emphasizing the importance of CPAP adherence. She remains very interested in treatment but simply cannot tolerate having a mask on her face. In fact, she finds CPAP more disruptive to her sleep. What would you recommend? ### Slide 32
  • Oral Appliance Therapy
  • The American Academy of Sleep Medicine and the American Academy of Dental Sleep Medicine produced a joint updated guideline in 2015: used in adults who are intolerant of CPAP or express a preference for OAT
  • AHI reduction of CPAP is superior, but degree of BP reduction and improvement in sleepiness is similar (perhaps from greater use) ### Slide 33
  • TODO: No text extracted from this slide. ### Slide 34
  • DO NOT HAVE PATIENTS SAY ‘AHHH’ WHEN ASSESSING MALLAMPATI ### Slide 35
  • Additional References
  • Questions?
  • brian.locke@imail.org ### Slide 36
  • Why is it so confusing to know what to do with OSA? Price to pay for speaking. ### Slide 37
  • PROBLEMS WITH THE AHI
  • AHI as the defining metric of OSA: driven by pragmatism and consensus but not by evidence:
  • Physiologic measurement / Disease status
  • “1 billion people have OSA” kinda bullshit ### Slide 38
  • From JAMA SR
  • Don’t screen for OSA: USPSTF. Also ### Slide 39
  • What are the things that diagnosing+treating sleep apnea improves?
  • Talk about effectiveness of CPAP in improving different health outcomes
  • Reasons to treat OSA, from strongest support to most dubious
  • [note AHRQ report - https://www.ahrq.gov/sites/default/files/wysiwyg/research/findings/ta/sleep-apnea/sleep-apnea-report.pdf ]
  • Sleepiness
  • HRQOL
  • MVAs
  • HTN
  • preventing exacerbations of OHS
  • to prevent post-op complications in mod-severe disease
  • ——
  • preventing exacerbations of COPD? Donovan
  • preventing CVAs
  • preventing heart attacks - https://jamanetwork.com/journals/jama/fullarticle/2810031 (note, with proper control, the role of sleepiness is
  • Preventing AFib ### Slide 40
  • problems with trials; equipoise etc.
  • [] - https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.202303-258ST fundamental problem for
  • — not very sleepy (if sleepiness is present, not ethical to withholds treatment) - however,
  • — not very much adherence.
  • ——> ways to get at this: aggregate under-powered trials into a meta-analysis, enrich the population (e.g. try to perform post-hoc analyses (though things like healthy adherer bias are hard to
  • Note: if this is the explanation, it must be either an issue of power, or a qualitative interaction. ### Slide 41
  • OSA pathophysiology ### Slide 42
  • TODO: No text extracted from this slide. ### Slide 43
  • Who needs an inpatient sleep study? ### Slide 44
  • TODO: No text extracted from this slide. ### Slide 45
  • Reasons not to get a Sleep study (analogous to why not to get a TTE while most congested) ### Slide 46
  • TODO: No text extracted from this slide. ### Slide 47
  • https://onlinelibrary.wiley.com/doi/full/10.1111/resp.12376
  • Hypoventilation occurs first during REM
  • But what to do with that?
  • Important for NMD.
  • Occurs in COPD/OHS , but the data is not there to say what we should do about it.
  • REM sleep neuromuscular control - > REM hypoventilation.
  • Sleep Hypoventilation very high prevalence in COPD ### Slide 48
  • OSA and pHTN
  • https://pubmed.ncbi.nlm.nih.gov/31682462/ 196 – both CPAP and NIV improved pHTN and LV diastolic dsfxn similarly
  • OSA alone probably does not cause (much) pulmonary hypertension.
  • Remember – sustained hypoxemia is a well established risk for pulmonary hypertension, and preventing it is the primary reason we give patients LOT
  • https://jcsm.aasm.org/doi/abs/10.5664/jcsm.10286 perhaps sustained desat is the more relevant parameter?
  • OHS has more phtn https://pubmed.ncbi.nlm.nih.gov/25370507/ ### Slide 49
  • OSA and pulmonary hypertension
  • PH related to OSA is generally mild in the absence of additional cardiopulmonary disease, with average mean pulmonary artery pressure between 25 and 30 mm Hg and rarely exceeding 35 mm Hg
  • There is NOT solid data that CO2 worsens it
  • NOT solid data for treating OSA in other pHTN ### Slide 50
  • Does OSA increase cardiovascular risk?
  • They are definitely assocated
  • Burden of hypoxemia meiates CV? data reviewed here
  • https://www.atsjournals.org/doi/epdf/10.1164/rccm.202307-1243ED?roletab
  • Sleepy subtype? ### Slide 51
  • Lots of SDB in heart failure
  • CSA -> ASV?
  • HfPEF & SDB historical estimates, 37-58% [probably even higher in UT]; Artz et al ESC Heart Failure 2022 https://pubmed.ncbi.nlm.nih.gov/36052740/
  • n 3289 patients, used a threshold of AHI > 15. HSAT (not able to differentiate hypopnea)
  • Low prevalence in HFpEF vs HFrEF
  • Higher prevalence in Men.
  • Has [ ] good figure of OSA vs CSA
  • Agrawal AnnalsATS 2023 - https://pubmed.ncbi.nlm.nih.gov/36375082/
  • n 2961
  • People w/ and w/o failure with CSA have higher mortality than OSA.
  • —> particularly look for patients with low BMI
  • Explain ventilation control:
  • Controller Gain chemoresponsiveness
  • Plant gain amount of ventilation needed to reach the apnea threshold.
  • FACE HF
  • SERVE-HF increased CV mortality with ASVCAT-HF JACC 2017 subgroup with HFpEF benefitS? [ ] look into that
  • ADVENT-HF neutral ### Slide 52
  • Adherence
  • To be eligible for
  • long-termcoverage, CMSmandates that
  • beneficiaries use PAP 4 or more hours per
  • day for 70% of days over a continuous
  • 30-day period within the first 90 days of
  • receiving the device (37). These rules have
  • been widely adopted by other large insurance
  • carriers across the United States without any
  • validity testing. ### Slide 53
  • TODO: No text extracted from this slide. ### Slide 54
  • When should you send a noc ox?
  • Probably pretty much never
  • ——> talk about inpatient sleep testing.
  • Talk about the use of oxygen to treat sleep apnea etc. - it probably does actually have beneficial physiologic effects… but does this translate to meaningful benefits? probably not.
  • [NOTT]
  • (Presumably in the context of nocturnal hypoventilation: An Australian consensus statement recommends oxygen be entrained
  • when SpO2 is < 88% for 30% or more of the total sleep time.52
  • 52: Agency for Clinical Innovation Respiratory Network. Domiciliary Non-Invasive Ventilation in Adult Patients: A Consensus Statement. Australia:
  • Agency for Clinical Innovation Respiratory Network; 2012. ### Slide 55
  • Does O2 treat OSA? Yes and No
  • Yes: post-operative, and at elevation
  • No: we don’t know if that has any meaningful impact on anything important, and O2 is actually probably more expensive, even if better tolerated. ### Slide 56
  • Chest 2021 Noct o2 rev - DOI: https://doi.org/10.1016/j.chest.2021.02.017
  • 29-66 % of patients with COPD have OSA 37-41
  • Conflicting results about O2 effect OSA generally – no direct evidence to overlap
  • O2 therapy doesn’t seem to increase risk of hypercapnia - NSO therapy at 2 L/min reduced the episodes of desaturation per hour and the time spent in desaturation, but there were no differences between air and oxygen in episodes of SDB per hour, the duration of episodes of SDB, baseline sleeping PaCO2 , or PaCO2 during episodes of desaturation or SDB (https://www.sciencedirect.com/science/article/abs/pii/S0012369216310984) , 44. (Goldstein RS, Ramcharan V, Bowes G, McNicholas WT, Bradley D, Phillipson EA. Effect of supplemental nocturnal oxygen on gas exchange in patients with severe obstructive lung disease. N Engl J Med. 1984;310(7):425-429.)
  • In one study, elevated venous bicarbonate, a surrogate of hypercapnia, was noted in patients with OSA (not just overlap) receiving NSO - https://www.atsjournals.org/doi/10.1164/rccm.201802-0240OC

259.3 Learning objectives

  • Control of Ventilation and Sleep Disordered-Breathing for Pulm Fellows
  • 90+% reduction in airflow with no respiratory effort throughout
  • Or, could wait and do nothing; or give oxygen
  • Central Apneas
  • Control of Respiration

259.4 Bottom line / summary

  • Control of Ventilation and Sleep Disordered-Breathing for Pulm Fellows
  • 90+% reduction in airflow with no respiratory effort throughout
  • Or, could wait and do nothing; or give oxygen
  • Central Apneas
  • Control of Respiration

259.5 Approach

  1. TODO: Outline the initial assessment or decision point.
  2. TODO: Outline the next diagnostic or management step.
  3. TODO: Outline follow-up or escalation criteria.

259.6 Red flags / when to escalate

  • TODO: List red flags that require urgent escalation.

259.7 Common pitfalls

  • TODO: Capture common errors or missed steps.

259.8 References

TODO: Add landmark references or guideline citations.

259.9 Slides and assets

259.10 Source materials