208 Locke Sleep Apnea For Puln Fellows

208.1 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.

208.2 Slide outline

208.2.1 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 ### 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
Chemoresponsiveness
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 increased improvement after CPAP
(probably only severe & OHS for increased perioperative risk) ### Slide 26
TODO: No text extracted from this slide. ### Slide 27
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 28
TODO: No text extracted from this slide. ### Slide 29
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 30
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 31
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 32
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 33
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 34
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 35
TODO: No text extracted from this slide. ### Slide 36
Don’t screen for OSA: USPSTF
DO NOT HAVE PATIENTS SAY ‘AHHH’ WHEN ASSESSING MALLAMPATI ### Slide 37
Additional References ### Slide 38
Why is it so confusing to know what to do with OSA?
How could we possibly be designed to get so much sleep apnea?
https://www.sciencedirect.com/science/article/abs/pii/S138994570200237X?via%3Dihub ### Slide 39
From JAMA SR ### Slide 40
OSA pathophysiology ### Slide 41
TODO: No text extracted from this slide. ### Slide 42
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 43
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 44
[ 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 45
Who needs an inpatient sleep study? ### 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
Does the PaCO2 ‘set-point’ change?
For example, in OHS:
Loop gain terminology primarily describes tendency toward stability of ventilation. ‘Gain’ of the feedback loop.
Controller gain: ventilatory response to PO2 and PCO2 )
Plant gain: changes in pulm capillary blood PO2 and PCO2 in response to changes in vent
Mixing gain: effective circulation time – time which cap blood changes are sensed by controller
Many changes are known to influence chemoreflex sensitivity
Ventillatory long-term facilitation is the process that should keep things on track
Ventilatory long-term facilitation is the term for adaptation to chronic stimulus (ie. sustained hypercapnia should increase loop gain to re-establish a baseline, and if this goes wrong you get a ‘wandering baseline’) ### Slide 49
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 50
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
Separate out OHS? ### Slide 51
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 52
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 53
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 54
TODO: No text extracted from this slide. ### Slide 55
Reasons not to get a Sleep study (analogous to why not to get a TTE while most congested) ### Slide 56
TODO: No text extracted from this slide. ### Slide 57
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 ### Slide 58
Should you get a nocturnal oximetry to diagnose overlap syndrome in your patient with COPD? No https://pubmed.ncbi.nlm.nih.gov/31995805/ ### Slide 59
TODO: No text extracted from this slide. ### Slide 60
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 61
CPAP and OSA
https://journals.lww.com/cardiologyinreview/abstract/9900/effectofcontinuouspositiveairwaypressure.108.aspx
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7642642/ ### Slide 62
Is unexplained exertional intolerance a reason to look for OSA?
https://doi.org/10.1016/j.chest.2022.09.027
I think, not entirely clear? ### Slide 63
VCO2
even when at rest the cellular production of CO2 is
prodigious, approximating 10 mmol/min and yielding aVCO2
of about 0.2 liter/min for a fit 70 kg person. Any reduction in
the ability of the respiratory system to eliminate CO2 at the
lungs results in rapid acidification of the blood and tissues.
The situation becomes more profound with exercise. VCO2
can increase 30-fold with high-intensity exercise, reflecting
both the high rate of skeletal muscle CO2 production and acid
titration of CO2 stores.

208.3 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

208.4 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

208.5 Approach

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

208.6 Red flags / when to escalate

TODO: List red flags that require urgent escalation.

208.7 Common pitfalls

TODO: Capture common errors or missed steps.

208.8 References

TODO: Add landmark references or guideline citations.

208.9 Slides and assets

Presentations/Locke Sleep Apnea for Puln Fellows.pptx

208.10 Source materials

Presentations/Locke Sleep Apnea for Puln Fellows.pptx