"Joint Yale-Harvard-Tufts Sleep Conference COPD-OSA Overlap Syndrome" Omesh Toolsie (03.10.2021)

March 15, 2021

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00:14Alright, hello everybody.
00:17My name is Andres in check and I am
00:20from assistant professor at Yale
00:22School of Medicine and Work at the
00:26Sleep Center at Yale and so thank
00:28you very much for joining us for
00:31yet another edition of the joints.
00:33Yale, Harvard and Tufts Sleep Conference,
00:35and we're excited to have you back,
00:38and we have a special session
00:40today with Doctor Omesh Toolsie
00:42from the Tufts Medical Center is a
00:45fellow or first felt a presence.
00:47Princeton I think first hopefully of many,
00:50and I just also want to introduce
00:52Doctor already.
00:53Grover, who is from the Tufts Medical Center.
00:56Who is the medical director at the
00:58Central Sleep Medicine and a program
01:00director of the Sleep Fellowship at Tufts,
01:03and so she will kindly
01:04introduce Doctor Mitchell.
01:05See for the rest of the talk and
01:08just wanted to ask you to just
01:11keep in mind to mute yourself as
01:13the talk that progress is.
01:15If you wanted to ask a question or.
01:18Keep up,
01:18feel free to raise your hand or
01:20put your question in the chat and
01:22we can certainly stop talking
01:24and ask questions at the time.
01:26Or we can summarize things at the
01:28end and have a nice discussion then.
01:30So without further ado Doctor Eric Brewer.
01:36Hi good afternoon everyone. Thank you Andre.
01:41I again my name is Artie Grover.
01:45Like understood, I wear from
01:47Tufts Medical Center and.
01:51It's my pleasure to introduce
01:53the speaker for today.
01:54Doctor Omesh Toolsie,
01:56who's our Sleep Medicine fellow?
01:58I just to introduce
02:00Doctor Chelsea to briefly.
02:02He comes to us from New York after
02:05completing his pulmonary critical
02:06Care fellowship from the Monte Fiore.
02:09Albert Einstein,
02:10with the Bronx health care system
02:13Program combined program doctor
02:15Chelsea completed completed his
02:17residency program also at the
02:19Bronx Care Health System in New
02:21York and he completed his medical
02:23degree from University of West
02:26Indies in Trinidad and Tobago.
02:28Doctor tulsi.
02:29During his residency and
02:31fellowship has completed,
02:32several investigative research
02:33projects has been involved in
02:35many poster presentations.
02:37Oral presentations.
02:37In addition to many peer reviewed
02:40Journal articles as well as
02:42quality improvement initiatives
02:44during his fellowship this year,
02:46Doctor Chelsea has been very
02:48involved with the Fellowship in
02:50terms of teaching the residents
02:52and teaching at Ents residence
02:54in terms of sleep lectures.
02:56He has been very involved with.
02:59King lecture star.
03:00Sleep technologist.
03:01In a sleep lab as well and he's been
03:04integral part of our hypoglossal
03:07nerve stimulator program at
03:09Tufts Medical Center as well.
03:11Today he will be speaking
03:13about overlap syndrome.
03:14OSA COPD overlap syndrome,
03:16and he will be discussing
03:17the pathophysiology,
03:19clinical presentation management
03:20and morbidity and mortality
03:22associated with this disease.
03:24So, without further ado,
03:26I would like to introduce
03:28Doctor Chelsea for the talk.
03:31Thank you.
03:33So
03:34good afternoon everyone.
03:35I'm a mesh, very grateful for the
03:37opportunity to present at today's conference.
03:39So I was only able to kind of
03:41share the presentation in the
03:43traditional PowerPoint format,
03:45but nonetheless it will not take away from
03:47the essence of the presentation anyway,
03:50so there there are no Commission.
03:52There's no commercial support
03:53for this grand rounds.
03:55There are no conflicts of interest from
03:58me or any of my faculty here at Tufts.
04:02And to receive credit for.
04:04This afternoon's conference
04:05stood up to text 21610.
04:07To this number, 2034429435, OK,
04:09so I'd like to start today's conference
04:12by reviewing a case of a patient that's
04:15still being followed here at Tufts,
04:1757 year old female who was sent to
04:20us from a community health provider
04:22because of normal chest X Ray was done
04:25because she has some upper respiratory
04:28symptoms on the chest X Rays.
04:30She they saw her.
04:32Memory care physician so along module and
04:35sensor across two or pulmonary colleagues,
04:37she has medical morbidities
04:39including hypertension,
04:40diabetes,
04:40chronic kidney disease,
04:41she's obese and also has a
04:44history of hypothyroidism and
04:46while she's not a current smoker,
04:48she does have a significant
04:50smoking history of 35 pack years.
04:53So while speaking to our
04:55pulmonary colleagues,
04:55in addition to having some
04:58complaints of dyspnea on exertion
05:00and some intermittent cough.
05:02She also complained of feeling very sleepy,
05:04but after spending 10 or 12 hours
05:06in bed and she had just retired she,
05:09she worked in healthcare and while
05:11initially planning to retire at 60,
05:13she opted to retire now because of Kovid
05:15and she said that now but she has more time,
05:18which seems very sleepy during the day
05:20and she takes naps in the afternoon.
05:23So pulmonary colleagues center across
05:24to US phone evaluation in addition to
05:26ordering the see T chest on PFTS for
05:28evaluation of pulmonary complaints.
05:30So they Sleep Medicine clinic.
05:32We sort by one of our telehealth visits.
05:34She had never seen a Sleep
05:36Medicine specialist before now.
05:37How to sleep study before
05:39she complained of snoring.
05:41Nor witnessed.
05:41Apneas ducting said though she
05:43did not have a bad partner.
05:46She complained of some arousals at night,
05:48about four to five browsers at night,
05:51some of which she said were spontaneous
05:54or this triggered by cough.
05:55All this, triggered with the urge
05:58to to to to use the restroom.
06:00She very often woke up feeling tired,
06:03complaining of nonrestorative sleep,
06:05having headaches and some nights
06:07and efforts cause 12.
06:08Um, she said that while she,
06:10you know,
06:11in retrospect you noticed symptoms
06:13progressed over the past five years.
06:14It's only when she retired that she really
06:17began to appreciate these complaints.
06:19So as part of our investigation,
06:20of course, we ordered a sleep study,
06:23so while waiting for that sleep study,
06:25she had her CAT scan done.
06:27By the way,
06:28there was known audio to be found,
06:30but was found.
06:31As you may see on this axial cutter for
06:33see T chess is an exploratory film you
06:36can see basically different Shades of Grey.
06:38You can see some areas
06:40that are very hyper Lucent.
06:42On some areas that appear
06:44like normal long parent Kima,
06:45and that is really a radiological
06:47finding that we turn wiziq, music.
06:49Profusion or some people say mosaic
06:51attenuation in the right clinical context.
06:54What it basically means is that there is
06:56the presence of air trapping and there's
06:59certainly some areas of her long as well.
07:01They look hyper loose ends,
07:03especially along the power septal
07:05areas that look like it's probably
07:07emphysematous lung as well.
07:08So she then went on to get
07:11her PFTS here at Tufts.
07:13AF V1 FEC ratio,
07:14which is the marker obstruction for from
07:17for PFTS less than .70 or less than the
07:20lower limit of normal depending on.
07:22Your lab.
07:23Showed that she had evidence of
07:25obstruction and it was irreversible.
07:27Obstruction meaning that the LCD one
07:29did not improve after administration of
07:32bronchodilators that actually dropped,
07:33which means that would persistent
07:36respiratory effort hoefl who
07:37energy or the effort that it took
07:40to produce that forced expiatori
07:41flow in one minute actually.
07:43So so in addition to having
07:46irreversible obstruction,
07:47she was also found to have an increased
07:49total lung capacity and increased residual
07:52volume to total lung capacity ratio.
07:54So the residual volume is really
07:57volume of remaining A and lungs in the
08:00lungs after maximum forceful expiration.
08:02So what that ratio tells us is
08:04after you force everything out.
08:07This in very simple terms after you
08:09force everything out how much is left
08:12relative to total lung capacity.
08:14And for her it's 50%,
08:16which is very much elevated.
08:1835 to 37 really is the upper
08:20limit of what's accepted.
08:22So in addition to having this
08:25irreversible obstruction,
08:25she certainly has hyperinflation.
08:27So she came to get her sleep study here tops.
08:31She had a sleep efficiency of just 58%,
08:34about 2 hours after.
08:35You know she fell asleep, she was awake.
08:38She had very poor quality sleep,
08:40very limited amounts of sleep or REM.
08:43Duration was reduced to about 7.6%.
08:45She spent all the night in supine sleep,
08:49where she had 99 apneas and
08:52105 high partners.
08:54So that was calculated for age.
08:57I opting hypotony index of 41
09:00with an oxygen need year of 59%.
09:04And I took this out of the part
09:06of the hypnogram studies that
09:08we usually give patients,
09:09and you can see that Bahari artifacts.
09:12They are quite significant fluctuations
09:14in her oxygen saturation where
09:16it dips as low as the high 50s,
09:18low 60s.
09:18Around 1:10 you can actually actually
09:20went into REM sleep here,
09:22and you can see that that even after
09:24the significant drops in saturation,
09:26they don't actually recover to
09:28levels that she had during non REM *****.
09:30****** 3:00 AM was when she actually
09:33woke up and she just could not.
09:35All sleep after that I took a 10
09:37minute extra from her REM sleep
09:39to kind of demonstrated pointed.
09:41I'm trying to make that she goes down to 67%.
09:45She does not actually reach anyway above 91%,
09:48so the High Street which is 91% and
09:50that's why I took this 10 minute excerpt.
09:53As you can see, it's marked with significant
09:55amount of respiratory events as well,
09:57so you know at this point she has a diagram.
10:00This is officially off obstructive
10:02obstructive sleep apnea,
10:03moderate COPD and it's likely that
10:05these two conditions were present
10:07in her for sometime prior to the
10:10presentation and very much explained.
10:11Do we should present it before
10:13I kind of go into explaining the
10:16interplay of these two conditions.
10:18I do want to touch on a little bit about
10:21COPD just for those of US demeanor.
10:24Have a background in pulmonary
10:26medicine so COPD as defined by gold.
10:29Gold is the global initiative.
10:31For chronic obstructive pulmonary
10:32disease and they really is suited,
10:35standards of care that we follow.
10:37Every ending is yearly guidelines for us,
10:40and that defines the PD as a common,
10:44preventable and treatable disease that
10:46characterized by persistent respiratory
10:48symptoms and airflow limitation that is
10:50due to airway and valvular abnormalities
10:53usually caused by significant exposure
10:55to noxious particles of gases.
10:57I really couldn't have said it better.
11:01And you know those noxious particles
11:03in gases in the developed world
11:05tends to come from cigarette smoking
11:07in the developing world.
11:10It tends to come from the use of biomass
11:13fuels for heating and for cooking especially,
11:16and there's those noxious particles
11:18that attract large numbers of
11:20inflammatory cells like neutrophils
11:21and and macrophages that produces
11:23hydrogen peroxide and proteases.
11:25So these are proteolytic enzymes,
11:27the overwhelm the antiprotease
11:29activity of the long so.
11:31Aren't proteins activity towards responsible
11:33for the normal reparative processes of
11:36the longer these ideas cellular level?
11:39So then these proteolytic enzymes
11:41destroyed along parent Kima irreversibly.
11:43So this chronic inflammation from from
11:46these cells that are present in the
11:49long leads to small airway fibrosis.
11:52So what you have developing
11:54pathologically is emphysema and air
11:56trapping from small airway fibrosis.
11:58Clinically,
11:59it presents us dyspnea chronic cough.
12:02And chronic phlegm production,
12:03chronic phlegm production,
12:05I think,
12:05is one of the last things to present.
12:09But it's one of the most
12:11debilitating along with cough,
12:13and it tends to occur when
12:15chronic inflammation has really
12:17set in in these patients,
12:18not unlike asthma,
12:20which is a clinical diagnosis.
12:23It is a spirometric diagnosis,
12:25so as I was able to demonstrate
12:29in our patient,
12:30you do need spirometry to diagnose COPD,
12:33so we use.
12:34I'm sorry we used it in a criteria
12:37after a patient has shown and
12:40demonstrated irreversible obstruction
12:42to categorize the severity of theopedia
12:45is important clinically and it's
12:47important also for research purposes.
12:50So based on the Fe V1 there.
12:53Given spirometric classifications
12:54as mild as above 80,
12:56all the way down to very severe.
12:58This lesson 30 and his symptom
13:00categories based on two things,
13:02the severity of the symptoms and we
13:04just spoke about how it affects the
13:06quality of life and the frequency
13:08of exacerbation.
13:09So they get a gold severity grade
13:12and a category symptom grade an.
13:14Those things together help us to determine,
13:16for example, when you need to escalate
13:19therapy when you need to deescalate
13:21therapy when you need to get.
13:23Pulmonary rehab or when you
13:25need to consider even that long
13:27transplant for these patients.
13:29Now in respect to Theo PD and
13:32sleep irrespective of whether or
13:34not there is a sleep disorder,
13:36patients would still be tend to have.
13:40Very much fragmented sleep because
13:42of some of these symptoms associated
13:45with UPD and also of course,
13:47because it could also be
13:49in certain phenotypes.
13:51Undiagnosed obstructive sleep apnea.
13:52So group of researchers from the
13:55Boltzmann Institute of COPD looked
13:57at this and they prospectively
14:00assessed about 50 or 52 patients with
14:02mild to moderate theopedia matched
14:04controls and administered TV stations.
14:06Sleep disorders.
14:07Question is reliable questionnaire
14:09it's a validated.
14:10Questionnaire on it uses about 175
14:13questions to categorize symptoms
14:15into four main sleep disorders,
14:17sleep apnea, narcolepsy, PLM,
14:19and psychiatric sleep disorders.
14:20So what they found was that patients
14:23with seal PD had hired higher
14:26where they complained more snoring.
14:29They complete more storing that
14:31disturbed others that these symptoms
14:34were worse if they were on their
14:36back or if they consumed alcohol.
14:39Not surprisingly, they were more smokers.
14:42These patients also week woke
14:44up more often during the night.
14:46They tended to have more in some way,
14:49and I think part of that,
14:51as well as contributed by concommitant
14:53use of stimulants like nicotine or
14:56even if there are nicotine replacements
14:58that may actually delay their
15:00sleep onset and lower the arousal
15:02thresholds very much similar to.
15:05To alcohol,
15:06and these patients tend to
15:07have more fragmented sleep,
15:09they tend to have increased wake
15:11after sleep onset periods as our
15:13patient demonstrated as well.
15:15So not surprisingly, then,
15:16they have reduced total sleep time.
15:18They have reduced REM sleep and
15:20you know they have reduced sleep
15:22efficiency so you know what you
15:25see happening then is a pattern of
15:27sleep deprivation and patients with
15:29COPD develop both the acute and
15:31chronic effects of sleep deprivation?
15:33The acute effects.
15:34Like in pair cognition,
15:36which can certainly have any effects
15:38on medication adherence or forgetting
15:40their clinic appointments or
15:42forgetting inhaler, technique use,
15:44and of course, the chronic.
15:46Effects of sleep deprivation,
15:48like systemic inflammation,
15:49altered immune function,
15:51puts them at increased risk of of infections,
15:54which which which obviously puts them
15:56an increased risk of exacerbation.
15:59So you're looking at the acute
16:01and chronic effects of sleep,
16:03adding to the burden of disease already
16:06present in COPDLCOPD affects the Physiology.
16:09The normal Physiology of normal ventilation,
16:11Physiology,
16:12and impatient with in in sleep
16:14in a very specific way,
16:16and I wanted to discuss that.
16:20A bit,
16:20but I just want to touch base
16:23very quickly on what is normal
16:26ventilation changes in sleep.
16:28So during sleep we have reduced wakefulness.
16:30You have reduced activity from the
16:33reticular activating system and
16:35that in itself can induce a physiologic
16:37ventilation of a physiologic hypoventilation.
16:40But you also have reduced metabolic rate.
16:43You have reduced chemosensitivity
16:44to oxygen to carbon dioxide,
16:46and you have increased airway resistance.
16:49So increased airway resistance
16:51is especially marked.
16:52During REM sleep,
16:53when you have respiratory muscle
16:56hypertonia and all of these factors
16:58can cause a physiologic hypoventilation
17:01as much as 1.5 liters per minute.
17:03Now those changes in a normal
17:05subject you know is is not going
17:08to be clinically significant,
17:10but there are certain factors
17:13in patients with COPD.
17:15Not really kind of exaggerates what
17:17you see in normal Physiology of sleep.
17:20So first of all you have increased
17:22load under respiratory system
17:24from increased airway resistance,
17:26which is further increased in patients
17:28with COPD and you have impaired
17:30ventilla Tori capacity on the implant.
17:33Surgery capacity.
17:34Steel especially during REM
17:35so patient with COPD.
17:37They needed the accessory muscles
17:39to help them breathe very often,
17:41especially the progress to
17:43chronic respiratory failure.
17:44That is when they become hypoxemic steel.
17:47CD's they do need the accessory
17:49muscles of respiration during REM
17:52sleep when you lose tone from the
17:54when you lose tone when you lose
17:57tone in your respiratory accessory
17:59muscles of respiration together with
18:02an inefficient flat and diaphragm
18:04that leads to reduce title volumes
18:06and reduced minute ventilations and
18:09that together with a blunted neural
18:11respiratory drive is going to cause
18:13profound alveolar hypoventilation and
18:15increased physiologic Dead Space there.
18:17So that translates.
18:18Altogether,
18:19two leading to A to causing us
18:22a clinical situation where you
18:24have profound hypoxemia,
18:25especially so in patients with with
18:27COPD and very often associated with
18:30hyperventilation as well or hypercarbia.
18:32Now,
18:33when you think about where
18:35patients with COPD,
18:36you know where they stand on the
18:39oxygen hemoglobin dissociation curve.
18:40You know they sit in a position where
18:43you know more drops in attention
18:46of oxygen or smaller drops in it.
18:49Partial pressure of oxygen is gonna
18:51cause a lot more rapid desaturations
18:53because of the allosteric effect
18:55of hemoglobin in the configuration
18:58of hemoglobin.
18:59The affinity for oxygen changes so
19:01much so that especially in REM sleep,
19:04they have more profoundly saturation.
19:06And I think that certainly.
19:10What we were able to see in our patients.
19:14So when you think about well,
19:16what is this overlap syndrome?
19:18It is this profound nocturnal
19:20desaturation that is seen in
19:22this condition that it might be
19:25otherwise present in COPDOS.
19:27Or is he alone,
19:28very often accompanied by hypercapnia.
19:30So this was first described by David Flynn,
19:34leads to Davis family was a
19:36professor of respiratory medicine
19:38from the University of Edinburgh.
19:40Gives also was a respiratory physiologist.
19:43On what he described in 1985,
19:45what was I what I like to think
19:47is just clinical suspicion,
19:50basically saying that in a
19:52patient with COPD who were tree?
19:54Who,
19:54who being hypoxemic is treated
19:56with nocturnal oxygen therapy,
19:58but then persistently has symptoms?
20:00Including headaches that these
20:03individuals should get a sleep study.
20:07To you know to rule out the coexistence
20:10of obstructive sleep apnea so patients
20:12with COPD with undiagnosed OSA of course.
20:14To run the risk of poor outcomes and it's
20:17still very much clinically applicable
20:19today so you know a group of researchers
20:22from the University of Washington.
20:24What they did is that they took
20:26the cohort that was used in the
20:29long term oxygen treatment trials.
20:31That trial also a landmark trial
20:33in in pulmonary medicine,
20:34was published in 2016.
20:36It was basically aimed at looking at
20:38mortality benefit in patients with
20:40and without nocturnal oxygen pair.
20:42Empty and they took this quarter
20:44patients direct respectively
20:46applied a modified stock bond.
20:47Scores modified because there were
20:49no next to conference data for those
20:52individuals in this cohort on the
20:54classified patients in intermediate
20:56high risk and low risk of having
20:58undiagnosed obstructive sleep apnea.
21:00And then they looked at some quality
21:02of life indices in this individual.
21:05In these individuals and what they were
21:07able to demonstrate was that patients with
21:10intermediate to higher risk of having.
21:12Undiagnosed COPD,
21:13I'm sorry.
21:14Undiagnosed OSA in CPD had lower
21:16quality of life scores and higher
21:18scores on the Saint George Respiratory
21:21Questionnaire so that reps in Georgia.
21:23Respiratory questionnaire.
21:26It basically assesses overall health
21:27and perceived well being in patients
21:29with obstructive airway diseases,
21:31and So what they what they put forward
21:34as a conclusion for this study was that.
21:37There's there's high mobility
21:39in terms of quality of life from
21:41undiagnosed obstructive sleep apnea.
21:43In you know,
21:44the population of patients with
21:46COPDI think what is lacking?
21:48Go is Israel epidemiologic studies to
21:51see which particular phenotype or which
21:53population of patients with stupid
21:55you may or may not be an increased
21:58risk of getting obstructive sleep apnea.
22:00Now, when looking at the prevalence
22:02of the overlap syndrome,
22:04it really does depend on the
22:06population that you look at.
22:08This is really good.
22:09Meta analysis was done by a group of
22:12researchers from Australia and they
22:13looked at 27 studies and found that
22:16the prevalence ranged anywhere from
22:1811% to 66% and it really did depend
22:20on the population that you looked at.
22:23If you require a high hi for your study
22:26and your patience for a bit younger,
22:28the prevalence is about 11%.
22:30If you require a lower hi and you
22:32look at some older population,
22:34it was about 41% if your population was
22:37higher 67 average it was as high as 66%.
22:40So what they're basically implying
22:42by this is that the higher the age
22:46population that you look at is,
22:48the more likely that you want to find
22:51the overlap syndrome being present.
22:53Of course,
22:54there's no direct correlation with,
22:56I just want to add,
22:58like obstructive sleep apnea,
22:59though see OPD is is a heterogeneous disease.
23:02It's not, you know, One Cup fits all.
23:05It's it's.
23:06You have clinical,
23:07physiologic and radiologic subtypes
23:09of this disease, but.
23:11Even these New York subclassifications
23:15of phenotypes.
23:16Still can broadly be still can
23:18broadly be categorized under
23:19predominant emphysematous
23:21subtypes and predominant chronic
23:23bronchitic subtypes, and you know,
23:25these phenotypic classifications.
23:26Do you know they do?
23:28They do predict in some way,
23:31and they do have an effect on
23:34on which particular types of
23:36patients may be at more risk of
23:38developing obstructive sleep apnea.
23:41So, for example,
23:42patients with predominant emphysema subtypes.
23:44You know, these folks tend to have lower BMI.
23:48They tend to have more hyperinflation
23:50and they tend to have more dyspnea,
23:53and they have a lower likelihood
23:55of having obstructive sleep apnea.
23:57And now like I said,
23:59there's no epidemiological
24:01studies to support this,
24:02but there was a really good physiologic
24:05study that I found that looked at
24:08functional residual capacity and P crit,
24:10so functional residual capacity is a
24:13direct correlation correlator with with
24:15hyperinflation and unlike residual volume,
24:17it simply represents the amount of.
24:19Air left in your lungs after a normal
24:22expiration as opposed to a forced expiration,
24:25and of course P crit windows.
24:28Really the gold standard for measuring
24:30upper respiratory collapse ability so
24:32soapy create they measured the nasal
24:34pressure or where passive upper airway
24:37collapse occurs on airflow thesis.
24:39And So what you were able to find
24:41was a negative correlation with FRC,
24:45NP, crit,
24:45basically saying that the more
24:48hyper inflation that you had.
24:50The more negative your peak rate
24:52and the less likely you are to
24:55have upper airway obstruction,
24:56the mechanism that was proposed for this
24:59is that impatient with hyperinflation,
25:01they have more chordal traction,
25:03more quarter tracheal traction.
25:05During in inflation of the lungs,
25:07producing more stiffer and
25:09less collapsible upper airway.
25:10Now this is opposed to patients with
25:13chronic bronchitis with these individuals.
25:15I'm sorry these individuals tend
25:17to have higher BMI's,
25:19more comorbidities, right heart.
25:20Celia,
25:21they have rustrel fluid
25:22shift from peripheral edema.
25:24Rostral fluid shift is really where
25:27you have redistribution of edema.
25:30Where you have very pharyngeal Perry,
25:32laryngeal and pray pharyngeal
25:33edema developing,
25:34which of course can increase your
25:36risk of upper airway obstruction and
25:38they have a lower respiratory drives.
25:41And so these individuals had
25:42a higher likelihood.
25:43I thought I should say I thought
25:45to have a higher likelihood
25:47of obstructive sleep apnea,
25:49so the Theo PD gene investigators
25:51that did your original SEAL PD
25:53gene study and that's the OPD gene
25:55study was done to kind of establish
25:58any genetic susceptibilities.
25:59In general patient populations.
26:01UPD they took this data on the
26:04divided patients into having chronic
26:06bronchitis and those that did not have
26:09chronic bronchitis based on coughing,
26:11phlegm,
26:11production for at least two years,
26:14and they found that these individuals with
26:17chronic bronchitis had a significantly
26:19higher risk of developing sleep apnea.
26:22The thought behind this is that
26:24the pathophysiology of obstructive
26:26sleep apnea and chronic bronchitis
26:28specifically overlapped more
26:30so than they did.
26:31Those individuals with emphysema
26:33adopting said our patient had
26:35significant hyperinflation and was
26:37somewhere in between both categories.
26:39Of course you have.
26:41You definitely have variations of this.
26:44You know occurring in real life so you have
26:47factors that you know also a shared between
26:50these two conditions like risk factors.
26:52There's no established risk of smoking,
26:55at least that I was able to find directly
26:57being linked to obstructive sleep apnea,
27:00there are few animal studies that I did
27:03find that was positing that to be true,
27:05but of course smoke exposure can't contribute
27:08to every information which can narrow the
27:11upper Airways and predisposed to collapse.
27:14And obstructive events.
27:15So you have these factors,
27:17then President and CEO PD that may
27:20protect or that may pretend to
27:22getting obstructive sleep apnea.
27:25So steroids of course is is is is very
27:28often used in patients with stupid,
27:31especially during exacerbations.
27:34Very much the same way as they can
27:36cause proximal myopathy of you know
27:38they can also cause you know Upper
27:40Airways upper airway myopathy as
27:42well and may potentially lead to.
27:46Um may potentially lead to increased risk
27:48of having upper airway obstruction feel.
27:51Filing is thought to be protected
27:53because of its, you know,
27:54because of its central stimulatory effect
27:56on the respiratory centers of the brain.
27:59So when you, when you clinically
28:01assess a patient who you know you,
28:04you know who may have stupidly
28:06overlap syndrome.
28:07It's so important to have clinical suspicion,
28:09OK, because if you don't know that
28:12these two conditions can coexist,
28:13you won't look for it.
28:15So if you're.
28:16For example, in a sleep clinic,
28:18your patient is telling you,
28:20hey, you know I can't.
28:22You see Pop because of persistent
28:24cough or phlegm or congestion,
28:26and they have the appropriate
28:27clinical history.
28:28Then you want to consider referring
28:30them to pulmonologists or getting PFTS.
28:32If you have the capacity to do without.
28:35And of course if you're
28:36in a pulmonary clinic.
28:38If despite optimization of Sio PD patients
28:40persistently has you know symptoms,
28:42especially headaches,
28:42for example,
28:43then you off definitely want to
28:45consider getting a full night of.
28:47Full night PSG for these individuals,
28:50so in terms of the symptoms that patients
28:53develop with the overlap syndrome,
28:56they really can be linked to
28:58the underlying pathophysiologic
29:00changes that we see so morning
29:02headaches arising from hypercapnia.
29:04Hypoxemia commit to cyanosis
29:06and polycythemia and of course
29:09peripheral edema can result from
29:11from from chronic cor pulmonale E.
29:13So these individuals as well with
29:16Overlap syndrome specifically tend to.
29:18Fall under that OSC phenotype
29:21of older more comorbid HI,
29:23HI and less time or I should say more
29:27time with saturations of less than
29:3090% and wild hypoxemia and hypoxia
29:33certainly you know contributes
29:35clinically in terms of how these
29:38individuals present it contributes
29:40in a major way to the to the to the
29:44morbidity associated with this disease.
29:46By activation off the inflammatory pathways.
29:49It's very well established in.
29:51See OPD patients that you know that
29:55interleukin six neutrophils and
29:57fibrinogen values much higher in uncon.
30:00Trolls theopedia is associated with loss,
30:03survival and cause system wide
30:05inflammation in patients with COPD.
30:07But you know the pattern of hypoxia
30:10in COPD and the pattern of hypoxia
30:13in obstructive sleep apnea.
30:15Else is is not the same.
30:17So in patients with obstructive sleep apnea,
30:20these individuals tended to.
30:22These individuals tend to have, you know,
30:25tend to have intermittent type of hypoxia
30:28as opposed to patients with with COPD.
30:31They tend to have sustained hypoxia
30:33when the two conditions overlap.
30:36Sustained hypoxia tends to be the
30:38predominant type or the predominant
30:41pattern of hypoxia that you
30:43typically see in sleep studies.
30:46Interesting physiologic study that I saw.
30:49A done in 2005.
30:52This group of researchers that took
30:54it from pronouncing this correctly,
30:57he la cells and these are basically
30:59immortal cell lines typically used
31:01in in Cancer Research on the exposed
31:04these cells to sustained hypoxia and
31:07varying degrees of intermittent hypoxia,
31:09and they looked at two inflammatory pathways.
31:12Again,
31:13these are two separate inflammatory
31:15pathways in nuclear factor.
31:17Kappa Beta Pathway is a master
31:19regulator of TNF Alpha.
31:21The hypoxia induced factor 1 pathway.
31:24ENCODE for proteins like erythropoetin
31:26vascular endothelial growth factor,
31:27and nitric oxide synthase,
31:29so they do different things in terms
31:32of how they exert a inflammatory
31:34effects and what you know what
31:37they were able to prove,
31:39that intermittent hypoxia preferentially
31:40caused increased activation,
31:42increased activity in the nuclear factor.
31:44Kappa Beta partly as opposed
31:46to sustained hypoxia,
31:47which favored the hypoxia,
31:49induced one luciferase activity.
31:50Partly so of course,
31:52I'm not saying that that's directly
31:54transmissible.
31:55Or translated into a patient
31:57with overlap syndrome,
31:59but it does help us to understand that
32:02in patients with overlap syndrome with
32:04nocturnal with profound nocturnal oxygen,
32:07D saturation.
32:08You then have this exaggerated,
32:10profound activation of system
32:12wide information.
32:13Then you might not otherwise see in
32:15either conditions alone which directly
32:18causes endothelial dysfunction.
32:19Now you have to remember,
32:22endothelial dysfunction is one
32:23of those whole normals.
32:25Tell us which I was trying,
32:28so endothelial dysfunction will in
32:29turn lead to increased risk of Trumbo,
32:32SIS,
32:32increased arterial sclerosis,
32:34increased risk of developing accurate
32:36sclerotic plugs and of course all
32:38of the cardiovascular morbidity.
32:39That's what it comes with that
32:42and so you know,
32:43in terms of not just in terms of
32:46cardiovascular disease and mobility,
32:48but also in terms of pulmonary hypertension,
32:50is something that you see more commonly
32:53in patients with overlap syndrome, you know.
32:56In patients with pure overseeing.
33:00The the pulmonary hypertension
33:01that you typically see is not as
33:04severe that you would see in a
33:06patient with overlap syndrome,
33:08and when you think about the
33:10effect of pulmonary hypertension,
33:12you think about right ventricular remodeling.
33:14Chronic cor pulmonale.
33:15When you think about endothelial dysfunction,
33:17like I said,
33:18you think about arterial sclerosis
33:20so that you know,
33:22I found it very interesting.
33:24Single center study that looked at
33:26overlap patients overlap patients with
33:27overlap syndrome and assessing right
33:29ventricular remodeling using cardiac MRI,
33:31which is not as is not Goldstein.
33:34That is not a right heart cast,
33:37but it's pretty accurate and they were
33:39able to show that in patients with overlap
33:43syndrome there was significantly increased
33:45risk or increase in significantly increased
33:48presence of right ventricular remodeling
33:50than was present in matched controls
33:52facility must for severity of disease.
33:55This was not found to be
33:57correlated with FEV one values,
34:00but it was found to be correlated
34:02with oxygen D saturation indices,
34:05oxygen D saturation indices of course is.
34:08Is the amount of time that you
34:10would spend below estate in Bill.
34:13It's it's a number of times per hour of
34:16sleep that a blood oxygen level would drop.
34:19The lowest integrate from baseline and disk.
34:21In this case they took.
34:23They took it as 3%.
34:25Another single sensor.
34:26Japanese study looked at overlap patients
34:28with overlap syndrome versus patients
34:30with just obstructive sleep apnea.
34:32Of course you see it is skewed
34:34towards patience with just two assay,
34:36but they looked at Brick Hill.
34:39Uncle Pathway Velocities,
34:40which is a direct surrogates were
34:42direct indicator of arterial stiffness
34:44right and after adjusting for
34:46even smoking status which was very
34:48interesting to be after adjusting the
34:50smoking status they were able to show
34:52that patient with overlap syndrome
34:54had significantly higher values.
34:56So this what these two studies show
34:58and even their single center studies.
35:01They were well conducted studies and
35:03they were able to show real end organ.
35:07Manifestations real end organ damage
35:08from everything that we talked about in
35:11terms of theoretical pathophysiology,
35:12and I think that has real clinical
35:14implications in terms of the mobility and
35:17attains of in terms of how aggressive
35:19we should be in ensuring that these
35:21patients are really managed properly.
35:23There are some new associations
35:25that have been looked at.
35:26I saw there was a group of researchers
35:28from the University of Buffalo and I
35:31think also with the system in Buffalo
35:33where the weather where they assessed
35:35the prevalence of atrial fibrillation.
35:37Impatients overlap syndrome as well.
35:39It was a retrospective study,
35:41but they looked at five years of data
35:44and they they they looked at patients
35:46with COPD who were then diagnosed with
35:49obstructive sleep apnea who were then
35:51diagnosed with Dean over a failed.
35:54They excluded patients with valvular disease.
35:56Included patients were diagnosed
35:57with a fit previously with other
35:59chronic respiratory disorders.
36:01Now they were not able to find a
36:03direct link between obstructive.
36:05I'm sorry, overlap syndrome and a firm.
36:08But how they reported their data
36:11was very interesting.
36:12Well,
36:12they reported was in patients with
36:15Overlap syndrome who will less adherent
36:17to CPAP that these individuals had
36:19a higher risk of developing each
36:22real fibrillation.
36:22Of course that's not surprising.
36:24CPAP we know reduces fluctuations
36:26and intrathoracic pressure.
36:27Of course, it mitigates hypoxemia.
36:29It will prevent right atrial remodeling,
36:32so there is an explanation for why they
36:35may have found why they may have had.
36:39That particular finding,
36:40so in terms of mortality,
36:43specifically in patients with
36:45overlap syndrome,
36:46and if there's any positive
36:49effect on pop therapy on
36:52mortality. This was look by
36:55list looks up at Joseph Moran.
36:57I think some University of Minnesota
36:59and it was a prospective study that was
37:02done to assess the relation of overlap
37:05syndrome to mortality and first time
37:07hospitalization due to stupid exacerbation.
37:09And then if see pub and had any
37:12effect on these major outcomes.
37:15Again, this was a prospective studies
37:17these individual these these research
37:19participants were followed for
37:21nights and average about nine years.
37:23So he categorized individuals into
37:26overlap syndrome treated with CPAP
37:28overlap syndrome not treated with CPAP,
37:32and then with and then theopedia individuals
37:35without obstructive sleep apnea.
37:37He found that there was increased all
37:40cause mortality in patients with with
37:44overlap syndrome and that exacerbation
37:47free survival and overall survival was
37:50lowest in patients with overlap syndrome.
37:53Who were not treated with CPAP and that
37:56there was a significantly increased
37:58survival in patients who were treated
38:01with CPAP in terms of you know,
38:04hypoxemic COPD as patients who with COPD
38:06you know to the progression of their
38:09disease requires supplemental oxygenation.
38:11You know this.
38:12This has also been studying.
38:14This was studied by a group
38:16of researchers from Brazil,
38:18and again this was a simple single
38:21center study was a prospective study.
38:23And they were able to demonstrate a,
38:26you know,
38:27increased survival in hypoxemic CPD
38:29patients who were treated with CPAP as well.
38:31Of course, this is patients with
38:34CPAP and oxygen therapy.
38:35So when assessing patients
38:36with the overlap syndrome,
38:38it's very,
38:39very important to think about.
38:42You know the clinical context in which in
38:44which these individuals are presenting.
38:47These patients should have,
38:48in love attended titration studies,
38:50and I think that's important because
38:52you need to have objective data and
38:54objective evidence that you are actually
38:56mitigating these significant hypoxemia
38:58that you're seeing in these individuals,
39:01that you may not get from an automated CPAP.
39:04Of course,
39:05you can do oximetry,
39:06but many times these patients also
39:09have concommitant hypoventilation that
39:11you may need to switch to buy popped.
39:13Before, during your titrations,
39:15if you have hypoventilation,
39:17Bipap or noninvasive ventilation
39:20is preferred.
39:21You know of course it's high pop Mia
39:24predominant OSA predominant CPAP,
39:26like we showed it certainly has mortality
39:28benefit and certainly will be good enough.
39:31Supplemental oxygen therapy is
39:33something you may be able to
39:35determine as necessary during your
39:37titration study as well in terms
39:39of optimization of CPD therapy.
39:41This is very,
39:42very important and I think you
39:44know in terms of the perspective
39:47of a Sleep Medicine physician,
39:49I think it's important for us.
39:51In these individuals to make sure they
39:54have established care with a pulmonologist,
39:56maybe assess their medication adherence
39:58if they have prescriptions for their Med.
40:00Patiens if they've been having
40:02frequent exacerbations,
40:03have been following up with
40:05their providers because we can be
40:07doing everything with regards to
40:09optimization of their sleep apnea,
40:11but this UPD is kind of left,
40:14you know, to its own devices,
40:17everything will be we were doing,
40:19could just be moved.
40:20I think from the perspective of a
40:22pulmonologist smoking cessation as
40:24well as pulmonary rehabilitation
40:26is certainly important.
40:28So pulmonary rehabilitation is
40:29basically where we subject tations
40:31to strength intensity exercises.
40:33But what it really does,
40:35it helps patients perception
40:36of dyspnea improve.
40:37And I think this could actually help.
40:41Their sleep quality a
40:43significantly so these two,
40:44you know, arms of management
40:46needs to be looked at together,
40:49so this is just my modified algorithm that
40:52I took from the sleep clinics or lecture.
40:55I think it's important for us
40:57to have clinical suspicion that
41:00COPD needs to be optimized.
41:02That these individuals then should have
41:04a pulmonary function tests anti SGS.
41:06If hypercapnia is present by part,
41:09may be preferred if there is.
41:11You know,
41:12no evidence of hypoventilation
41:14CPAP may be sufficient,
41:15and if there is persistent hypoxia,
41:17you may want to consider.
41:19You may want to consider getting.
41:23These patients are nocturnal oxygen as well.
41:26Now,
41:26in terms of is their role for Eva.
41:31I put the slide up because
41:33I saw a few case reports.
41:34And we've actually prescribed one
41:36individual for a vast amounts,
41:38of course, is average volume assured
41:41pressure support the particular mode
41:44of a verbs that would be preferred
41:46in these individuals is a verbs AE.
41:48So if apps is basically a motor
41:51ventilation where you can,
41:53you know you can set a preset
41:56tidal volume that,
41:57with varying inspiratory pressures,
41:59that the machine through a feedback
42:01loop either will increase or
42:03decrease the inspiratory pressure.
42:05Breath breath over a minute.
42:07Not not to get that preset
42:10title volume the Evap's AE in
42:13addition to just changing I pop.
42:16Pressures can also adjust respiratory
42:18rate and also adjust the epoch as well.
42:20One of the things I particularly like
42:23about the AE mode is because in CRPS,
42:26patient specifically is that it looks
42:28at flow decelerations and flow patterns,
42:30so you prevent Brett talking in these
42:33individuals when the machine is able
42:35to to know when their cessation of flow
42:38and then deliver the subsequent breath.
42:40So there is some rule for this.
42:43Theoretically we have used it
42:45once from a patient we saw and.
42:47Impatient console that was discharged,
42:49we able to discharge an evil,
42:51but of course you need to
42:53know what your what your local
42:54coverage determinants might be.
42:56Of course,
42:57that's very important to
42:58know and that was also there.
43:00Was definitely some hoops to
43:01go through for that individual,
43:03so the potential benefits.
43:05Of course you can get the
43:07right pressure to right time.
43:09You know you can get consistency,
43:12CO2 elimination and it guarantees there
43:14should be an an average tidal volume
43:17and the other things that can spoke about.
43:20So getting back to our patients.
43:22So she came in.
43:24She had a titration study.
43:26This is who titration
43:28done about six weeks ago.
43:30You can see significantly
43:31improved sleep efficiency.
43:32Significantly reduced wake after sleep onset.
43:35I do want to mention that
43:37this is also a time.
43:39When she was optimized with
43:41regards to see OPD control.
43:43So the decision was made by
43:44pulmonary medicine to start up in
43:47a pulmonary rehab program earlier.
43:48Rather than later she was optimized
43:50with regards to a bronchodilator.
43:52So when we got it for this titration,
43:55she was fully optimized with regards
43:56to the COPD and I think that certainly
43:59helps in having more consolidated signal.
44:01She did not have as much REM
44:03sleep as we would have liked,
44:06but you can see significantly
44:08less variations in her oxygen.
44:10Saturation levels and we did not actually
44:12have to give a supplemental oxygen.
44:14This was her REM sleep.
44:16We did have to titrated to buy part.
44:18There was evidenced hypoventilation
44:20depression that we eventually
44:22settled on with 20 / 8.
44:23She started her therapy about.
44:25Three weeks ago, so the verdict is still out.
44:29That's how she does,
44:30but the titration study certainly
44:32is encouraging in that regard.
44:34So thank you guys.
44:36That's my presentation.
44:37I'm I very much appreciate
44:39the opportunity to present on
44:41this topic. Any questions?
44:46Great, thank you very much.
44:48A mesh for this eloquent presentation
44:51and two very common conditions that
44:53tend to overlap, and somebody know as
44:56as a overlap syndrome, and so there
44:59are several questions in the chat.
45:03Sorry, let me. I
45:04might start and I'll read it
45:06to you and help navigate,
45:09and so if there is a question
45:12from Karen Johnson from.
45:15Bay State and if you are only using
45:17entitle CO2, how do you know if
45:20there is still hypercapnia needing
45:21by apps versus C Pap with oxygen?
45:24We find the intitle SEO two is often
45:27artificially low in these patients
45:28and if you rely on it you may often
45:31under treat the hyperventilation.
45:33Yeah, I don't. I don't disagree with that.
45:37You know, there is certainly not instantly.
45:39I saw it's not especially in in in these
45:42patients with CPD where there's power in
45:44kymo long destruction there you could have
45:47a dissociation between what is the actual
45:49serum CO2 values and what is what is the
45:52value that you see on your end title.
45:54So you know I think it does
45:57depend a lot on your lab.
45:59You know we don't do routine abgs that
46:01would be ideally what you should do.
46:04Um, you know, um,
46:06under certain situations I can,
46:08for example, like Thomas just
46:10said like where you where we use,
46:12especially in pediatric populations we
46:14do using the adults about transcutaneous
46:16CO2 values in this individual
46:18that we did use entitles you to,
46:21and transcutaneous was not used.
46:22I don't disagree with that.
46:24I I I think that is a valid point.
46:30Sure, great, thank you.
46:32And so I I have a question
46:34and I think this might be open for
46:37discussion with you or whoever else
46:40wants to chime in and so is the.
46:43So PD Orsay overlap.
46:44Simply two conditions sort
46:46of occurring together?
46:47Or is there some unique part
46:49of pathophysiology and clinical
46:51presentation and outcomes that
46:52are unique to this as a syndrome?
46:55Potentially unique entity, so that.
46:57So that's a very good question,
46:59and I think that.
47:01I think I personally see a
47:03sum of both and I think that
47:05what you see specifically in
47:08patients with overlap syndrome,
47:10as I was able to demonstrate some of
47:13the cardiovascular comorbidities that
47:15you see is you know you get this more
47:18profound systemic inflammatory cysts on.
47:21You know this.
47:22This system wide inflammatory
47:24state that is much higher than you
47:26would see neither condition alone.
47:29I think these individuals also need.
47:32They tend to need more advanced
47:34types of ventilla Tori options
47:36because very often they do have
47:39hypoventilation present as well.
47:41But I think that specifically if
47:44there's any specific thing that is,
47:46you know that you see in
47:49patients with overlap syndrome.
47:51You know,
47:52I'm not particularly sure,
47:53but I think that what we see
47:55is just exaggerated multitudes.
47:59Great, thank you.
48:01Let's see, there's another question,
48:03so and. From Stuart men from
48:07Pacific Sleep Medicine Group,
48:08what is the mean Epworth Sleepiness
48:10Scale found in Group of patients with
48:12mild to moderate Sophie Dee without OSA.
48:14And so this is kind of getting
48:17up the question of how sleepy,
48:18yeah, the patients basically
48:20regardless of sleep apnea.
48:21Yeah, so
48:22you know, I would tell you that I
48:24found studies where the update did
48:26not find any significant differences
48:28in effort scores between patients.
48:31You know with with with multi
48:33moderate COPD and it always.
48:35It does all depend on the
48:37study population that you use,
48:39but many of these studies and I looked
48:41at I didn't include it into talk.
48:44Did not really find significant differences.
48:46He mean efforts.
48:47I remember specifically ranged
48:49anywhere between 6668, I don't.
48:50I don't specifically remember but
48:52I found a lot of studies when no
48:55significance was actually found,
48:56but there was significant.
48:58In where overlap syndrome occurred.
49:02Sure, yeah, no, it's interesting.
49:04I think the other question I might ask is,
49:07you know how common is insomnia in
49:10patients with SAPIEN sleep apnea?
49:12Might that influence the OS? Certainly very
49:14common. I said so.
49:16That was sort of fun.
49:18Dives to insomnia is found to
49:20be significantly higher in that
49:21population for multiple reasons.
49:23Of course, one could be because
49:25you have undiagnosed OSA,
49:27but others other than that's the
49:29you know the symptoms of stupid
49:31cough with phlegm production.
49:33See the use of nicotine
49:35replacements to use of cigarettes.
49:37All of these stimulants that
49:39can't fragmented sleep and
49:40alter the arousal threshold,
49:42so insomnia certainly is
49:43significantly higher, sure,
49:45absolutely, and so you're mentioning
49:47altered arousal threshold,
49:48you're familiar with some data suggesting
49:51that residential may be altered in peace.
49:54Davis is those with OSA on. You know
49:57that is theoretical.
49:58I saw mentioned in some studies that I do.
50:00Have a title like directly to say that
50:03I was able to find that will certainly
50:05something I think is interesting
50:07to look at. Yeah, absolutely.
50:09I agree with you.
50:10I think there's some data from
50:12recent papers in looking at apnea,
50:14lengthening duration in patients
50:15and noticing that there is a direct
50:17correlation with shorter durations and
50:19those who have been prior smokers.
50:22And so that might suggest that
50:24because acne duration can be a
50:26surrogate of low arousal threshold,
50:28and I suggest that the lawyers that
50:30threshold like more common in those patients,
50:32so that would be an interesting question
50:34to study and see whether there is a
50:37relationship between arousability and so on.
50:39Yeah, that's more prevalent
50:40in those who have CBD in OSA.
50:43It's a great point.
50:44And so I there's another question
50:46here from Doctor Hilbert at Yale.
50:48And so she says thank you.
50:50It was an excellent talk and think she
50:52agrees that they traicion study is ideal,
50:54but. Occasionally not possible.
50:56For example, if you join the pandemic,
50:59our patient is in decline,
51:01and so and we have had to use
51:04limited APAP with downloads,
51:06oximetry and abgs.
51:07Are you aware of any data using
51:09such approaches in situations
51:11that might be constrained?
51:13Resource wise?
51:14No, I I don't think I actually came across
51:18anything for automated pop therapy.
51:21You know, I. I do agree with.
51:23I saw sided with some small studies that
51:26looked at that did actually looked at
51:29automated pap therapy in patients with.
51:31With overlap syndrome,
51:32but I I just did not include studies because
51:35of of how these studies were designed.
51:37What I will say is that I do agree with
51:39Doctor Hibbert that you need to have.
51:41I think it's not if you're
51:43going to do that approach,
51:44you really need to follow up very closely.
51:48And get their input on gather,
51:50download data and probably do get.
51:52Like she mentioned there in the
51:54comment abgs you'd have to follow
51:55those patients very very closely.
51:57For example,
51:58if they develop treatment emergent
52:00central apneas that this is a
52:03population that is on risk of that.
52:05So you'd have to follow those patients very,
52:07very closely to ensure that you know
52:09everything in the right direction.
52:11Sure, and so you know,
52:13I think we're hitting a nerve in the area
52:15of Sleep Medicine at this overlap topic,
52:18and so there's a lot of questions and
52:21another question has to do with reliability
52:23of figuring out food to test for OSA.
52:26And so questionnaires oftentimes may
52:28not be reliable in those with CPD,
52:30an OSA and so.
52:33What do you recommend as sort of
52:35the best way of who do you study?
52:38So screening questions in North,
52:39unreliable for oversea in stupid
52:41doesn't excellent. Excellent point.
52:43So that is absolutely correct and I think
52:46what we really need is short of getting,
52:49you know, good epidemiologic studies that
52:51tell us directly as to which phenotypes
52:54of stupidity maybe at more risk of OSA.
52:56Of course everything I presented was all
52:59physiologic studies and proposed hypothesis,
53:01but I think short of getting
53:03epidemiologic studies apart from getting
53:05a really good clinical history, I.
53:07You know, I I don't know if there's any just
53:10foolproof method to say that you plug in
53:12this questionnaire you plug in these risk,
53:15you know this.
53:16This calculates and you get a risk.
53:18I think it just just it just all comes
53:20down to having good clinical suspicion
53:22to look for either syndromes from
53:24either perspectives of a pulmonologist
53:25to a Sleep Medicine specialist.
53:27Great
53:28thank you. Thank you mesh and there's
53:31a couple of comments and in the in the
53:34chat and and so not as much questions
53:37and so some observations by Doctor
53:39Thomas and Doctor Johnson at yeah I saw
53:43you hypercapnic patients tend to have
53:45a deeper more amounts of N3 sleep and.
53:49Inexperience of Doctor Johnson that
53:51many of the hyperventilating patients
53:53that she takes care of no longer pursue
53:55and feel that sleep is much better
53:57and improve the quality of their life.
53:59And so I would that I wanted to thank
54:02everybody and specially you Umesh
54:04for doing a great job on the talk and
54:07thanks everybody for participating and
54:09asking all these wonderful questions
54:10before we leave.
54:11I just wanted to share a couple
54:14of announcements that we have our
54:15next weekly lecture,
54:16the Sleep Medicine grand rounds at Yale.
54:19It's going to be led by Magna Monster
54:22Connie from Mayo Clinic will be
54:24speaking about opioids and sleep,
54:26and so another highly relevant
54:28clinical topic is Sleep Medicine.
54:30And so again,
54:31if you wanted to obtain CME
54:33credit for today's session,
54:34please take a look in the chat
54:37and you can text a code 21610 to
54:39the telephone number provided,
54:41which is 2034429435 and wanted to
54:43thank again to all the participants
54:45and looking forward to seeing you
54:47again next week and resumption of
54:50the joint conference. In April.
54:52Thanks everybody.
54:54I think you guys. Thank you.