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Central Sleep Apnea Pathophysiology and Treatment — Transcript

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0:00welcome everyone to the first of uh the
0:03Sleep uh Network for chest at the uh
0:06respiratory sleep section's uh webinars
0:09um today we have Dr cardu mol who will
0:13be speaking to us about Central sleep
0:15apnea um Dr mcau has her Bachelor's in
0:19music and Technology from University of
0:21Michigan in an arba Michigan uh she then
0:24did her interal Medicine Residency in
0:26the Bowmont hospital and then completed
0:28her uh pulmonary as well as her sleep
0:30medicine fellowships at uh um at the
0:33Mayo she's currently faculty there and
0:36is an invited speaker at chest ATS and
0:40sleep conferences and um I most recently
0:43heard her speak about Central sleep
0:44apnea in Hawaii and in chess uh was a
0:47fabulous talk um and so um welcome Dr um
0:52duri
0:54mcau right thank you thanks for having
0:57me I'm really excited to be uh doing
1:00this today um this is the first of
1:02hopefully many um webinars from the
1:05Sleep Network here so so if you're uh
1:07today I'm going to talk about Central
1:09sleep apnea uh including the
1:11pathophysiology and treatment it's one
1:12of my favorite things to talk about um
1:15I'm parly I'm from Mayo Clinic in
1:19Rochester um and I do have a disclosure
1:22to make I do some work for resp cardio
1:25who are the makers of the remedy system
1:27which is the frenic nerve stimulator for
1:28treatment of central sleep apum that's
1:30actually I'm going to be talking that
1:31today about that today so um just keep
1:34in mind that they have paid me money
1:37before um so today we're going to be
1:40talking about the group of disorders
1:42that is Central
1:44sleepapnea and talking about the
1:46pathophysiology of all of the different
1:47types of uh Central sleep apnea and then
1:51um you know using that knowledge to
1:53discuss what treatment options are
1:54available and which treatment options
1:56make sense for which types of central
1:58apnea
2:01um so the definition of a central apnea
2:04is a period where you have a absence of
2:08air flow and absence of effort and so on
2:12your sleeve study you'll see no air flow
2:15here and no effort here and then the
2:18syndrome of central seop is if you have
2:20this happening um repetitively over five
2:23times an hour with
2:25symptoms um we have a little bit of data
2:28about the epidemiology a lot of comes
2:30from the Sleep heart health study when
2:32you look at patients who are presenting
2:33to The Sleep Lab it's about 1% and then
2:38about half of those are going to be
2:39people with Shane Stokes
2:41breathing and in this data set people
2:44are more likely to be men who are older
2:46with a lower BMI and a lower upper
2:48sleeping scale than their Osa
2:51counterparts um important to note though
2:54in this study it suggested that
2:58obstructive sleep apnea was a lot more
2:59common than Central sleep apnea but if
3:02you look at other studies looking at
3:04patients with heart failure with with
3:06reduced ejection fraction um the actual
3:09incidence in that population is likely a
3:11lot higher um 25 to 50% are the the
3:14figures most often um in the Sleep heart
3:17health study it was self-reported heart
3:18failure so that's probably why that that
3:20was lower but anyway just um a point of
3:23interest in patients with heart failure
3:25this actually happens a
3:27lot the risk factors Central apnea or
3:31age um so probably due to increasing
3:34comorbidity as people age but could be
3:37due to the aging process itself um more
3:39common in men heart failure atrial
3:42fibrillation valvular disease stroke it
3:45can occur in the acute setting and it it
3:47can actually occur long term too
3:49depending on the location of the stroke
3:51and then Ral failure uh medications most
3:55commonly opioids but there's also a
3:57couple other ones that we'll talk about
3:59in then there's kind of other category
4:01so conditions including spinal cord
4:03injury acromag and neuromuscular
4:08disease there is primary central sleep
4:11apnea also known as idiopathic Central
4:13sleep apnea and that is where we don't
4:16have another reason for the presence of
4:19central sleep apnea and then there are
4:21many different causes of secondary
4:23Central sleep apnea so um th this
4:26illustrates why central sleep apnea is
4:28not really one thing it's it's a group
4:30of disorders and this is why treatment
4:33can be challenging because the central
4:35sleep apnea is sometimes occurring for
4:37very different reasons Patient to
4:38Patient and so there's no one-sized
4:40fitall approach that's going to work for
4:42everyone so when you have secondary
4:44sleep apnea that can come from chain
4:47soaks breathing people with heart
4:49failure um Central sleep apnea due to
4:51high altitude periodic breathing
4:53treatment emergent Central sleep apnea
4:55that comes about when people with Osa
4:57are in the sleep lab and we put p on
4:59them and we discover Central sleep
5:01apia um Central sleep apia due to a
5:04medical disorder without chain Stokes so
5:07this will be you know if you have a
5:09stroke and Central sleep AP as a result
5:11of that and it catches kind of all of
5:13those different medical disorders and
5:15then Central sleep apnea due to a
5:16medication or substance and these are
5:18from the icd3 so um you know this is how
5:21we code all of these different um sleep
5:25related breathing
5:27disorders um I read this really
5:29wonderful paper by shro javaheri and
5:32safan batter which describes Central
5:34sleep apnea based on the ideology and um
5:38after I read that paper I reorganized
5:41this talk because I think it makes so
5:43much sense to categorize things
5:45according to their ideology and then you
5:48know using that structure to think about
5:50how you would treat each of these types
5:51of patients so we have high Loop gain
5:56which is the primary or idopathic
5:58Central sleep apnea chain Stokes High
6:00Altitude periodic breathing and
6:02treatment emergence Central sleep apnea
6:04failure of rhythmogenesis
6:06which is typically going to happen due
6:08to medications or some sort of
6:11structural incident affecting the
6:13breathing centers and then other so
6:18Shane Stokes or I'm sorry Central subia
6:20due to a medical disorder without Shane
6:23Stokes and the others are typically
6:27going to fall into one of two categories
6:29either High Loop gain with high plant
6:31gain um so conditions associated with
6:34chronic
6:35hypercapnia and spinal cord injury and
6:38then pseudo Central sleep apnea um I
6:42like the term pseudo Central sleep apnea
6:44because uh in in this type of central
6:47sleep apnea the brain actually is
6:49sending a signal to breathe most of the
6:52time it's just that because of
6:54neuromuscular weakness or some sort of
6:56restriction in the thoracic cage you
6:59know the there's no respiratory movement
7:01happening so it will still look the same
7:03on a
7:04polysomnogram where you'll see you know
7:06no air flow and no effort but the reason
7:09why it's happening is a little bit
7:10different than some of the other types
7:12of central
7:16annea the clinical presentation of
7:18central sleep apnea um you know a lot of
7:21times we compare it to obstructive apnea
7:23and say that you know typically these
7:25patients are less sleepy um you know and
7:29have have less report of disorder
7:31Breathing by the bed partner which can
7:33be true but I think it's important when
7:35you're talking about the patient
7:36population that has Central sleep apnea
7:38and their um clinical presentations it
7:40can really be all over the board so um
7:43they can still have symptoms of sleep
7:45sleep fragmentation and excessive
7:47daytime
7:48sleepiness um and then they can also
7:52have you know shortness of breath at
7:53night I talked to a lot of people who
7:55will awaken during the hyperonic phase
7:58you know so they just had breathing
7:59pause and they awaken taking you know
8:01some deep breaths um some people awaken
8:04because they're short of breath so
8:06there's a a spectrum there and then as
8:09opposed to obstructive sleep apnea where
8:10you have you know loud snoring breathing
8:12pause loud snoring um a lot of times the
8:15bed partner will say oh they're actually
8:17really quiet when they sleep or I have a
8:19lot of people say yeah sometimes I have
8:21to reach over and poke them to see if
8:23they're still breathing so um you know
8:26it's not necessarily breathing pauses
8:28and sometimes I just ask you know have
8:29you noticed any abnormal breathing um in
8:33your bed partner um because it can be
8:35like I said a little bit um different
8:37than the description of OB struct of
8:39apnea um for diagnosis polysomnogram is
8:43the gold standard as always hope sleep
8:46apnea testing can detect Central sleep
8:50apnea um even the watch pet uh claims to
8:55have a good sensitivity and specificity
8:57but um I think we are maybe quite there
9:01uh getting a really really good accurate
9:03diagnosis of central sleep apnea in the
9:05home environment um but then the other
9:07reason that it's really helpful to have
9:08a polysomnogram is for the titration
9:11portion of it um as I mentioned there's
9:14all sorts of different reasons that
9:16people have Central sleep apnea and so
9:18one treatment that might work really
9:19well for one person won't work for
9:21another person um and also Insurance in
9:25many cases won't cover the treatment for
9:27Central sleep apnea unless you prove
9:28that in the sleep lab so still the best
9:31way to do this is with a polysomnogram
9:33to take advantage of the titration
9:35opportunity and of course for insurance
9:37reimbursement which unfortunately we do
9:39have to think
9:41about all right so now I'm going to talk
9:44about some more details about the
9:47different types of uh the pathogenesis
9:50of central sleep apnea so kyane is a
9:54term from the electronics World which
9:56describes how multiple inputs to a
9:59system affect the output in this case
10:02the output is homeostasis um respiratory
10:06homeostasis maintenance of pH and carbon
10:09dioxide and oxygen levels and then the
10:12inputs to that s system that we're going
10:14to be describing here are inputs from
10:16the heart the brain and the
10:18lungs so we have controller gain which
10:21is chemoresponsiveness
10:23and that relates to the peripheral and
10:26Central chemo
10:27receptors and then plant gain which
10:29relates to the lungs and uh some of this
10:33is uh stretch receptor activation uh and
10:37some of it is change in carbon dioxide
10:39level over change in alular volume and
10:43then the mixing time or the blood
10:45circulation time and so if any of these
10:49elements get out of balance then it can
10:52lead to a high Loop gain system and
10:54predispose the patient for Central sleep
10:56apnea
10:59and what happens during the respiratory
11:02cycle might look something like this
11:04where you know you have your
11:06CO2 somewhere above your apnet threshold
11:10there's some sort of respiratory
11:12stimulus that happens um oftentimes this
11:15will have something to do with the
11:16carbon dioxide but can also be oxygen
11:19and the patient will have a period of
11:21hyperia where they breathe a lot which
11:24will cause the carbon dioxide to go
11:26below the apnic threshold and then you
11:28will have a breathing pause and then
11:30during that breathing pause carbon
11:32dioxide's going to rise again and you
11:34know whatever stimulus that kicked off
11:36the whole thing is usually going to come
11:38back into the picture and then you're
11:39going to have another period of hypera
11:40and another breathing pause and so most
11:43of the time in central s apnea we see
11:45pretty high Ahi levels because once you
11:49get into this dysfunctional breathing
11:51cycle it's hard to break out of
11:58that uh so for idiopathic or primary
12:01central sleep apnea this is the
12:02diagnosis of exclusion so you really
12:04have to rule out all of the other causes
12:06of central sleep
12:08apnea it is prevalent in four to 7% of
12:12central sleep apnea patients refer to
12:14sleep medicine so it's less common to
12:16have the idopathic central sleep apnea
12:19and that's why it's important to do a
12:22little bit of a directed workup in this
12:24patient population there's actually a
12:26study that suggested 27% of people with
12:29quote unquote idopathic Central sleep
12:31AUM may have atrial fibrillation so I
12:34think it's important to at least do an
12:35echocardiogram if the patient has not
12:38had one recently because of the high
12:40instance of heart failure in this
12:42population and then you know at least in
12:44EKG a good physical exam and I usually
12:47question patients about any symptoms of
12:50you know intermittent shortness of
12:52breath palpitations things like that and
12:54if appropriate I've actually even
12:56ordered a halter monitor in the past if
12:57there's a high index of suspect
12:59obviously that would just be based on
13:00your clinical judgment
13:03though in Shain stes respiration you
13:06have to have an hi of at least five with
13:09over half of the events being Central in
13:11nature they have to have symptoms and
13:13the respiratory cycle length has to be
13:15at least 40 seconds so these are
13:17criteria from the
13:18icd3 and this is you know one of the the
13:23main ones um although I will say if you
13:25see this on a sleep study it's usually
13:27pretty easy to recognize
13:29um but this is the technical
13:31specification and sometimes what
13:32differentiates it from other types of
13:33sleep of central sleep
13:35apnea with um chain Stokes you'll have
13:38increased chemosensitivity and increased
13:40mixing gain so increased time that the
13:42blood takes to to circulate through the
13:44body it's higher risk in heart failure
13:48with reduced ejection fraction as you
13:50might imagine but you can also see it in
13:52high heart failure of preserved ejection
13:54fraction although I will say that um I I
13:57don't think that I have seen this very
13:59often in heart failure with preserved
14:00dejection INF fraction I don't know if
14:02anyone else has another experience with
14:05that uh it can be exacerbated by
14:08pulmonary edema increasing the pulmonary
14:11capillary pressure which as I mentioned
14:13can increase lot gain and then that
14:15would stimulate respiration or hyperia
14:18and it's associated with a poor
14:21prognosis and so classically you'll see
14:23this waxing and waning Crescendo a
14:27crescendo pattern in your or respiratory
14:30air flow
14:34signal the next one is high altitude
14:36perodic breathing uh this is a picture
14:39of me and my friend when we were uh in
14:43Wyoming this is probably at about 9,000
14:45ft uh everyone was starting to
14:48experience symptoms and we were uh not
14:50smart this day and as soon as we
14:53ascendit altitude decided to go mountain
14:55biking up the mountain is not not the
14:57smartest thing I've ever done I'll be
14:59including this uh picture in my talk
15:02about high altitude ponary EMA I'm just
15:04kidding um so over 3,000 meters almost
15:09everyone develops high altitude periodic
15:11breathing but the presence and severity
15:12can
15:14vary uh this is caused by increased
15:16controller gain in response to a hypoxic
15:18environment and increase in carbon
15:20dioxide response so this one is actually
15:23usually triggered by hypoxia instead of
15:26carbon dioxide and so that's why oxygen
15:28works well for
15:30treatment this will usually manifest as
15:32a cluster pattern with several breaths
15:35and Then followed by an apnea so
15:36typically you will not see that waxing
15:38and waning pattern and typically it will
15:41have a shorter cycle duration than chain
15:43Stokes but PA patients will usually
15:46describe similar symptoms disrupted
15:48sleep sometimes waking up with um either
15:51dmia or
15:55hyperia treatment emerence Central seia
15:57is the next one then this C
15:59the
16:01incidence is about 12% on average but it
16:05varies depending on what study you look
16:07at so it's been reported between two and
16:1020% um based on the type of study that
16:12was performed and whether it was split
16:14night versus mul titration um and the
16:20risk factors for treatment emergence
16:21Central sleep apnea do overlap with risk
16:23factors for um Central sleep apnea in
16:26general so male gender if the patient
16:29has underlying severe obstructive sleep
16:31apnea they're more likely to have this
16:33if they have really high pressures on
16:34CPAP and then of course if they have any
16:36of these other conditions that
16:38predisposes to Central sleep
16:43apnea it's important to note also
16:45treatment emergent Central sleep apnea
16:47does not just happen in Pap therapy
16:50there is some data in the literature
16:52about a variety of other treatments for
16:54obstructive apnea in which treatment
16:56emergent Central sleep apnea has been
16:58reported
16:59including mandibular advancement devices
17:02hypoglossal nerve stimulation I did find
17:04a a pre prevalence report of 3% the
17:08tongue protrusion device I don't know a
17:11lot of people who use that because I've
17:12heard they're very uncomfortable um
17:14provent nasal epap this is not on the
17:17market anymore but there are other nasal
17:19epap devices so I would presume that it
17:21would be you know similar risk uh
17:24tracheostomy Mas facial surgery not
17:28albow relatively UNC commmon and then
17:29soft tissue surgery and some of these
17:31don't have incidence reports in the
17:36literature so the next category we have
17:38failure of rhythmogenesis
17:42the rhythm of Brea breathing originates
17:45in the pre-botzinger complex in the
17:47ventrolateral Medela so as I mentioned
17:50before if you have anything that is
17:51affecting that area you can get
17:53alterations in brething
17:57pattern the most common in this category
18:00is going to be opioids but there's case
18:03reports of other medications including
18:05bphen bpro acid and sodium oyate and a
18:08few others and actually I just recent
18:10had a recently had a patient who was on
18:12tanine who I really think that was a
18:15cause of his Central sleep app I'm going
18:16to write that up with one of our fellows
18:18um so this probably comes from a
18:21depression of the inspiratory neurons
18:23and the pre-botzinger
18:25complex um that area has opioid and
18:27gabber receptors
18:29and you can see a variety of different
18:31respiratory patterns but the classic one
18:33would be axic breathing and that's where
18:36you have a very um irregular breathing
18:39Rhythm and also uh irregular amplitudes
18:42of each
18:44breath one point of Interest
18:47tagore which is a platelet inhibitor
18:51causes moderate to severe Central sleep
18:53apnea and 30% of patients which I think
18:55is strikingly High um I'm still waiting
18:58for that sleep medicine referral where
19:01someone comes in and they're on tagore
19:03and I can look really smart by um
19:05telling everyone that the tagore is
19:06causing Central sleep apnea but that
19:08hasn't happened for me
19:11yet uh so structural reasons for Central
19:14sleep apnea uh can be in the form of K
19:18kii malformation which can compress the
19:20Medela and uh alter respiratory
19:22mechanics and chemon receptor function
19:25stroke depending on which area the
19:27stroke is in it can impair ventilation
19:30in different ways during sleep I
19:32actually have seen this I had a patient
19:34who had a stroke in the ponds and he had
19:35permanent Central sleep apnea after that
19:38and then of course
19:40tumors if they're compressing the
19:42breathing centers and also neurod
19:43degenerative
19:45disease um so as that Progressive as
19:48that progresses you can get impairment
19:50in the respiratory cers as
19:53well and then the other
19:56category so High Loop gain and high
20:00plant gain is one of these uh so this
20:03can happen in conditions associated with
20:05chronic hypercapnia and sometimes in
20:07spinal cord injury as well and part of
20:10the reason for this oops sorry is the uh
20:14location of the patient's Baseline
20:16carbon dioxide level on this carbon
20:18dioxide curve so you know normally the
20:21carbon dioxide level should be down here
20:23in a flatter P portion of the curve if
20:26the patient has an elevated carbon
20:27dioxide at Baseline then small changes
20:30in ventilation can really cause uh you
20:33know large shifts in carbon dioxide
20:35level and sometimes shifts that below
20:37the apnic
20:41threshold and then pseudo CSA as I
20:45mentioned can be due to neuromuscular
20:47weakness or sub thoracic cage
20:49abnormality this is the opening slide
20:51that I used um so this is actually from
20:54a patient who when I saw him he had not
20:57been diagnosed with anything he had just
20:59some kind of
21:01non-specific um neuromuscular
21:03symptoms and a very abnormal bite a
21:07symmetry and so when we did his study
21:10you could see having Paradox in the shx
21:14and the abdominal bands um suggesting
21:19obstruction or in this case
21:20diaphragmatic dysfunction and then you
21:22know this this period where there is no
21:26air flow and then no respiratory
21:29effort um and then this is the hypnogram
21:33from his
21:35polysomnogram and I thought this was
21:36really interesting because on his ax
21:39symmetry we were just seeing these you
21:40know periodic episodes of oscillatory
21:43variability and decline in the Baseline
21:46oxygen saturation which really looked
21:47like it could be you know obstructive
21:50apan hypoventilation during Ram but then
21:52when we did the sleep study we realized
21:54that you know when he lost the function
21:57of the diaphragm that was really when
22:00all this Central sleep apno started
22:01occurring in REM sleep um so this one
22:04you have to look out for because
22:05classically we think that Central sleep
22:08apnea is associated more so with non-r
22:10sleep and it usually is but in certain
22:12cases you can see it um during real
22:14sleep especially in the pseudo CSA
22:20population all right so now we'll go on
22:22to talk about treatment and going to
22:25discuss treatment in each of these uh
22:29within each of these um pathogenisis
22:33groups and I have a question for
22:36everyone a 68-year-old female active
22:39smoker with a medical history
22:40significant for chronic pain on opioid
22:42therapy and heart failure with a
22:44junction protection of 40% underwent
22:46diagnostic sleep study with evidence of
22:48severe Central sleep apnea which of the
22:50following is considered a contra
22:52indication to ASV therapy for this
22:54patient is it the female gender tobacco
22:57use opioid use or for a protection of
23:0040% and you guys can put your answers in
23:04the chat box or just think about your
23:07answers if you want
23:13to and the answer to this one is the
23:17adjunction fraction of
23:1840% at least currently um based on
23:21existing
23:23data um so we had a study called the
23:28surf HF trial which came out in 2015
23:30that basically showed that people with
23:32injection protection of less than or
23:34equal to 45% have increased mortality on
23:37ASV and so we try not to use ASV in that
23:42population so for High Gain there's a
23:45bunch of different treatment options
23:47CPAP oxygen
23:49ASV pharmacologic therapy and Fric nerve
23:53simulation those are going to be the
23:54main
23:56treatments so there was a trial called
24:00the canpap trial that looked at use of
24:02CPAP in patients with heart failure um
24:07and it found that when they took the
24:12group of patients in which their Ahi was
24:14actually suppressed effectively there
24:16was actually a signal for increased
24:18transplant-free survival and a better
24:21left Andric ejection friction although
24:24I'm not sure that an increase of
24:263.6% would be clinically meaningful um
24:30but it's encouraging in that it doesn't
24:32seem to be um a bad thing for patients
24:35with heart failure so cpath is generally
24:38accepted as a reasonable treatment
24:39option but it doesn't always work well
24:44so uh at least in this study you know
24:46about half of people had their Ahi
24:47suppressed
24:49effectively and the rest of them had an
24:51elevated Ahi um and I would say this
24:54happens in the real world as well
24:55sometimes CPAP works really well and
24:56sometimes not so much
24:59supplemental oxygen therapy is also
25:01something that works really well but not
25:03in all cases uh there are multiple
25:05studies that date back to probably the
25:0880s um or even earlier that show
25:11reduction in the central apnea index in
25:13patients with heart failure with reduced
25:15ejection fraction um and some of them
25:19show reductions in ahi of at least 50%
25:22but it's not effective in all heart
25:24failure patients um I would say we use
25:28this most most often in heart failure
25:29patients because in people with
25:31idiopathic Central sleep apnea or some
25:33of the other types of sleep apnea you
25:34can't get it paid for because of
25:35Medicare you have to have a qualifying
25:37diagnosis for that um and uh I guess in
25:42my past experience sometimes it worked
25:43really really well and all the central
25:45ACO melts away and sometimes not uh and
25:49then as I mentioned before for high
25:51altitude periodic breathing this is
25:52actually the first line therapy and
25:53typically works
25:56well so of Servo ventilation I alluded
26:00to earlier in that question ASV is the
26:03resond device and autosv is the
26:05Respironics device this works for
26:09obstructive and Central sleep apnea
26:12there is an epap which stabilizes the
26:14airway and can treat obstructive apnea
26:17and this can be either um Auto adjusting
26:20or
26:21fixed and then the device looks at
26:24either a three or a 4 minute window
26:26depending on the brand of the device
26:28and it changes the ipap in the backup
26:31braate to uh even out the patient's
26:34ventilation and it aims to replicate uh
26:39the patient's Mina ventilation if it's
26:41the resond device or it operates more so
26:42on Peak flow if it's respirant
26:44device the ASB or Auto SB is reasonable
26:49to try in primary central sleep apnea
26:51treatment emergent Central sleep apnea
26:54people who have mixed obstructive and
26:56Central sleep apnea um you can use it in
26:59opioids as long as it doesn't as long as
27:01there's no significant hypoventilation
27:03and then there's some conflicting data
27:05for high altitude periodic breathing
27:06I've seen some studies that say that it
27:08works and I've seen some studies that
27:09say that it doesn't um at the most
27:13recent chest conference um that we had
27:17we did a procon debate or or just a
27:20discussion about some of the
27:21controversies in central sleep apia we
27:22were actually very fortunate to have a
27:25sleep Tech who worked at the Sleep Lab
27:27at the highest Elation level in the
27:29country and so I actually asked him if
27:31they use ASV in their lab and he says
27:34that they do and that they have success
27:37with it so again I think it's reasonable
27:39to
27:40try this is a picture from the rmed user
27:43manual about how it works and so um
27:46here's the patient flow we have a nice
27:49waxing and waning breathing pattern
27:52here and here's the minute ventilation
27:55you can see you know as the breathing
27:58pattern waxes and WS the minute
28:00ventilation increases and
28:02decreases uh so here's the point at
28:04which the ASB comes on in this example
28:08we have a fixed epap mode um so the epap
28:11is the same all the time but then in the
28:13periods where the patient is taking
28:15smaller breaths or not breathing the IEP
28:18will increase and possibly the
28:21respiratory of the backup rate can kick
28:23in and then when the patient is in a
28:25period of hyperpnea that eyad app can
28:28back off and so as not to encourage the
28:31hyperia and then you know over time this
28:33can even out their minute ventilation
28:36and their respiratory
28:40pattern but as I mentioned previously
28:43the surf agf trial happened in
28:462015 and they studied patients with
28:50heart
28:51failure um and discovered that people
28:55who were in The ASV group had increased
28:59all cause all cause mortality and so
29:01it's because of this study that we try
29:03not to use ASV and patients with
29:05interjection traction of less than or
29:07equal to
29:0845% although there has been a little bit
29:11more recent research that suggest that
29:14it might be okay but I'm going to get
29:16into that in a couple
29:18minutes so the medications that we use
29:22are typically acetazolamide is probably
29:26the most common one it has been shown to
29:28reduce the Ahi and daytime sleepiness
29:30and this can also be effective for high
29:32altitude periodic breathing a lot of the
29:33time people will only have high altitude
29:35periodic breathing until they acclimate
29:37and so it's not in commmon that I give a
29:40seide to people for use you know for the
29:42first several days that they're at
29:44altitude uh there's also data on filene
29:47although I have not typically used this
29:50in clinical practice it just has a very
29:53narrow therapeutic window and a lot of
29:55the time you're using this in people
29:56with cardiovascular comorbidities and so
29:58probably a potential for more side
29:59effects with be but anyone else has more
30:02experience with that i' be curious to
30:04hear about
30:05it um there's a couple more medications
30:08that uh there's a little bit of research
30:11about so buus perone is one of them
30:14there were a couple studies that have
30:15been done looking at very small numbers
30:17of patients and this particular study
30:20looked at the Ahi at night and during
30:24the day and found that the abuse brone
30:27was effective
30:28in treating um the Ahi like I said both
30:32at night and during the day so there are
30:34serotonergic neurons in the Medela that
30:37sense carbon dioxide and pH and there's
30:40been some studies in animal models that
30:42show that um beeron which is a receptor
30:46agones can stimulate respiration and
30:48shift the apnic threshold to a lower
30:50level of
30:51P2 and that reduces the ventilatory
30:54instability and so that's why it's not
30:57to work
30:58um there was also another study where
31:01they looked at buaron versus
31:04trazadone uh versus nothing and found
31:07that neither bupron nor trazadone were
31:10effective in reducing the central apnea
31:13index um that was also a very small
31:15study of I think seven patients and the
31:18reason that that might have been a
31:20different outcome than this study is
31:21because they used a lot lower dose for a
31:24shorter period of time but you know this
31:27is interesting data again these studies
31:30are so small that I think we need more
31:32data before we can you know confidently
31:35suggest this as a good treatment for
31:37Central
31:39fbm and then there's also a little bit
31:42of data again just very small studies uh
31:46I think just with triazolam and zadam
31:48looking at whether sleep consolidation
31:52is an effective means of controlling
31:54Central Sleek apnea so the theory behind
31:57this is that if you can increase sleep
32:00stability and lessen the amount of
32:02arousals from sleep that should lead to
32:05less oscillation in
32:06CO2 and with less you know periods of
32:10hyperia and oscillations of CO2 you
32:12should get less Central
32:14apnea um there's also a theory that
32:18zadam may decrease the ventilatory
32:21responsiveness during the arousals and
32:23so it would you know additionally reduce
32:25the hyperia and subsequent hypocapnia
32:28yeah um in the studies that were done on
32:30zadam they it did not change the
32:33obstructive hi for most patients but
32:34actually for a few patients it worsened
32:37the obstructive Ahi and then of course
32:40you know you would probably worry about
32:41the same thing with
32:43triazolam um it being a benzo aspine so
32:47there's certain patient populations in
32:49which you probably would not want to use
32:50these medications you know if someone
32:52has untreated of stretch of sleep apnea
32:54or hypoventilation um but you know I I
32:57think appropriate to consider in some
33:01patient
33:05populations all right so here is a
33:08question about frenic nerve stimulation
33:09before we get onto that topic which
33:12patient is an appropriate candidate for
33:13frenic nerve stimulation for the
33:14treatment of central sleep apnea so
33:1655-year-old man with mixed obstructive
33:18and Central apnea who is intolerant to
33:20Pap and has failed CPAP and ASV of
33:24search of apnea index is 28 and Central
33:26apnea index is 15
33:28b a 67y old woman with Central sleep
33:30apnea due to spinal cord injury C
33:3350-year-old woman with breast cancer who
33:35gets regular MRIs to monitor for
33:37recurrence and has reduced ejection of
33:4040% and hi of 30 or a 45-year old man
33:44with primary central sleep apnea with an
33:46Ahi of 48 all of them are Central who is
33:48intolerant to pth therapy I'll give you
33:51guys just a minute for to contemplate
33:54this answer
34:01so there's actually two correct answers
34:03I I left this and on uh this question
34:07was written a while ago um it used to be
34:10that D was only the only correct answer
34:13but now C is actually okay too because
34:16recently the remedy device did get
34:19approved for use of MRI so it is that it
34:22does have an MRI protocol um so C used
34:25to not be true but now it's not a
34:29barrier um so the reasons that amb are
34:34incorrect is that uh obstructive events
34:38must account for less than 20% of the
34:40total Ahi I of similar to
34:43inspire and then it's not appropriate
34:46for Central sleep apnea Sy syndromes
34:48with hypoventilation so it has not been
34:50studied in
34:52hypoventilation um and and then
34:55obviously you know it works by
34:56stimulating the frenic nerve so the
34:57frenic nerve doesn't work then it
35:00probably will not give you a good
35:04outcome um so a little bit more about
35:07the remedy device the study that got it
35:10approval was of 151 patients and they
35:14had Central AP of different
35:16ideologies um mostly idiopathic and
35:19heart failure and and mostly heart
35:21failure actually
35:2264% and at 6 months 50% had an AGI which
35:26was decreased by at least 50% % compared
35:28to 11% in the control group uh the
35:30Adverse Events were actually rather high
35:32at 9% but most of them were minor and
35:34were able to be you know fixed rans
35:37through
35:37easily and then based on what we know so
35:41far it probably does not affect
35:44mortality uh might be you know valuable
35:47for decreasing hospitalizations and
35:49heart failure although you really can't
35:51make that claim with the existing data
35:54there is a signal for increased quality
35:56of life and we have fiveyear data for
35:59this device and so the treatment effects
36:01seem to be enduring for at least 5 years
36:04this is just a picture of what it looks
36:06like it's implanted by an EP
36:10cardiologist and so it um goes down here
36:15through the vein and you have a
36:18stimulation lead that's in the left
36:20pericardio frenic or R brachio falic
36:23vein and that stimulates the nearby
36:25frenic nerve
36:30and then this is what I was talking
36:31about so this is looking at patients
36:33with heart failure post analysis of that
36:36subgroup so you know maybe it would be
36:39helpful for hospitalizations um you know
36:42hopefully does not cause increased death
36:45um but like I said this the study was
36:48not designed to evaluate these outcomes
36:50so you really can't um you know say
36:53either of these things
36:54definitively and then as far as the
36:57treatment is concerned we do have the
37:00fiveyear data here that shows that this
37:03um reduction in ahi is maintained most
37:08of the hypop events left over are
37:10hypopneas and so we're actually trying
37:13to assess these sleep studies now to
37:16find out you know are these obstructive
37:17hypopneas that were there before the
37:18device got implanted or are these
37:20residual Central sleep apneas that are
37:22left over just as you know Central
37:25Central hypopneas that the device is not
37:27treating so in the future hopefully you
37:29know we can get a better handle on this
37:31might help for predicting outcomes and
37:33counseling patients about um what they
37:35can expect as far as the effect efficacy
37:37of the
37:39treatment for failure of rhythmogenesis
37:42ideally if it's due to a medication you
37:45would discontinue that medication but
37:47you know a lot of the times that's not
37:48possible and then of course if there's
37:50an underlying condition you know a tumor
37:53K malformation um a stroke uh sometimes
37:57it will get better with with time
37:59sometimes not and then other treatments
38:02for failure of rhythmogenesis are just
38:05based on presence or absence of
38:06hypoventilation in the clinical scenario
38:10um most of the time if a patient gets
38:12diagnosed with Central sleep apia and
38:14you know we're about to call it
38:16idiopathic an MRI can be a useful thing
38:19as well to rule out any of these
38:22findings um sometimes it's a challenge
38:25with insurance though because uh Central
38:28sleep apne is not a diagnosis that some
38:30insurances will reimburse
38:33for um so other Central sleep apnea
38:37which as I mentioned can be you know
38:39spinal cord injury people are
38:41hypoventilating um you muscular disease
38:45most of the time these are actually
38:46going to require non-invasive
38:48ventilation which can either come in the
38:51form of a pressure targeted therapy and
38:54mostly bip St um weuse the backup rate
38:58for the basically the same benefits that
39:00were described with ASE or faps which is
39:03a volume targeted mode um there some
39:06people have the thought which I think
39:08makes sense that vaps might be a little
39:10bit better to use in this
39:12scenario with biev st you have a fixed
39:15ipap and a fixed epap and so if a
39:18patient is having hyperia the pressures
39:21are just going to be the same and so it
39:22will you know could potentially
39:24encourage that hyperia and even lead to
39:26more Central events whereas with vaps
39:29you're targeting a volume and so if if
39:32the patient is taking huge breaths the
39:35iath is hopefully going to back off a
39:38bit
39:39um and we don't have any data about
39:43long-term use of these modalities in
39:45patients with Central apnea um you know
39:48some people wonder could could these
39:50cause increase in mortality too because
39:52it's a you know higher IAP and a lower
39:54epap and a backup rate similar to ASD
39:57but um as far as I know we don't have a
39:59lot of data on
40:01that um you know sometimes it might be
40:03appropriate to use a ventilator
40:04obviously if you're having a patient
40:05with ALS the gentleman that I previously
40:07mentioned ended up getting a ventilator
40:09because his respiratory situation was
40:11very imper even during the day um and
40:15then you know you'll notice that ASV is
40:17not included in a treatment for people
40:19who are hypoventilating and that's
40:21because the ASV targets the patients's
40:23own Minute ventilation or Peak flow and
40:26so if they have a crappy minute
40:28ventilation the ASV is going to create a
40:31crappy ventilation um sometimes you can
40:36kind of make the ASV do things that it's
40:39it's not necessarily designed to do you
40:42know you can give a pressure support of
40:44the the normal pressure support range is
40:453 to 15 um in the past if it's some sort
40:49of acute situation or you know this is
40:51the machine that the patient has at home
40:53or we're just trying to get them through
40:54a period where we're getting a new
40:55machine you know you can increase the
40:57minimum uh epap to 6 cm H2O and do a a
41:01pressure support of 6 to 15 to hopefully
41:04provide some ventilation but I try not
41:06to do that because that's not really
41:07what the machine is designed for so I
41:09would say typically just avoid ASV in
41:14case of hypo
41:16ventilation so I I have this nice slide
41:20about upcoming trials looking at various
41:23treatments for central sleep apia but
41:25unfortunately a couple of them have been
41:28uh discontinued so we had the Advent HF
41:32trial that was looking at the effects of
41:36ASV on survival and Hospital admissions
41:38and heart failure uh and then all of
41:40these secondary outcomes mortality newa
41:43FIB will be function BNP every later day
41:45six minute walk her fig stage and
41:48functional CL class Ai and quality of
41:50life so I was really really excited for
41:53this one to come out because you know
41:55the thought was that our modern ASP is
41:58different than the one that they used in
42:00the survey je trial and and that maybe
42:03you know with the current machines that
42:04we're using we're not going to see that
42:06increase in
42:07mortality but the they were using bre
42:11bronic machines and then the Philips
42:12recall hit and so the trial had to be
42:16stopped and it has not started again
42:19there is some preliminary
42:21data and the preliminary data that they
42:24published one paper was about use
42:27and the point of that paper was just to
42:30say that the use that they saw during
42:32this trial was a little bit better than
42:34some of the other trials so the average
42:36Pap used for people with Osa was 4.6
42:39hours and for CSA it was 5.2 hours um
42:42only 177% stopped using ASV which was a
42:46lot less than during the serve HF
42:49trial and then they were not able to
42:52publish safety outcomes which I know is
42:54kind of the thing that most people want
42:56to know about they did have a data
42:58safety monitoring committee looking at
42:59the safety data every six months and
43:01there weren't any safety concerns so the
43:04serve HF trial you know was was stopped
43:07because there was that signal of
43:09increased mortality so it seems like
43:11they're not seeing that although like I
43:14said the the safety outcomes are not um
43:18available the other study that I was
43:20really excited for is uh this impact of
43:23lowf flow nocturnal oxygen therapy on
43:25Hospital admissions and mortality in
43:26patient with heart failure and Central
43:28sleep apnea so as I mentioned before we
43:31have some data to suggest that oxygen is
43:34effective in reducing the Ahi but it
43:36would be really helpful to know you know
43:39morbidity mortality hospital admission
43:41you know heart function um you know does
43:44oxygen impact any of these and so they
43:48were going to look at some of these
43:49outcomes measures but it was terminated
43:52early due to low feasibility of
43:55completion within the study Peri perod
43:57because they had slow participant acral
44:01so I don't know what is to become of
44:05that study um there's not a whole lot of
44:08other studies going on um with oxygen
44:11and Central sleep apnea according to
44:13clinical trials.gov
44:14but I really wish we had gotten some
44:17information from that study and then
44:20there's the rest study which is a
44:23prospective coht study evaluating some
44:25more out comes from people who are
44:28implanted with the remedy frenic nerve
44:30stimulator so and this is just kind of
44:33getting going but they're going to
44:34enroll up to 500 patients from multiple
44:36institutions and so hopefully that will
44:38give us a little bit more long-term data
44:41on the efficacy and safety of the remedy
44:46system and that's all I
44:48have so if anyone has any questions or
44:52discussion or comments I would love to
44:54hear
44:55it yeah just be sure to unmute uh so
44:59that you can you'll be
45:03heard
45:05Sara hey it's Lisa Wolf hi hey I just
45:09wanted to throw something out there for
45:11you I know that this is not something
45:13that people usually look at your
45:16question on the frenic nerve
45:18stimulation yeah was very remedy focused
45:22if you look at the other two frenic
45:24nerve stimulation devices on the market
45:27the Avery Pacemaker and the synapse
45:29pacemaker those actually are directly
45:32tested for hypoventilation and approved
45:34for
45:35hyperventilation okay
45:38um yeah those are the devices we use for
45:41things like spinal cord injury and
45:44Central congenital hypoventilation
45:47syndrome obviously for the people who
45:50are on here that are just looking at
45:53more traditional Central sleep apnea
45:55they've probably never heard of those to
45:57but I just wanted to throw it out there
46:01yes thank you um I as I mentioned I have
46:03a bias so um but yeah but the are are
46:08those those devices are not for Central
46:10sleep AP though correct or they're just
46:14for or well I mean look these are for
46:18people so let's say that you have
46:22cchs um cchs is Central
46:25hypoventilation so so to the degree that
46:28that's a form of central sleep apnea yes
46:31and in spinal cord injury same thing um
46:36like you said they're like pseudo
46:38Central right because like nothing but
46:41they have a backup rate and that backup
46:44rate on both of those devices is there
46:46to treat the central apnea so you know
46:50the question is would you ever use an
46:52Avery for somebody who had normal muscle
46:55function or normal brain
46:57function
46:59um I haven't done that I've only done it
47:03like I said for um spinal cord injury
47:07and
47:08cchs okay I I'm going to include that
47:11that's a good point Thank you for
47:13pointing that
47:14out obviously I don't know as much about
47:21those yeah that's called a day in Wolf
47:24Clinic
47:29and uh it does it looks like Ally Ally
47:31posted that uh there are some sleep
47:33medicine fellows from Northwestern who
47:35have presented a case at the Illinois
47:37sleep Society uh on uh I'm gonna butcher
47:41this name
47:42uhor yes into CSA thank you so much yeah
47:47we learned from them um I actually
47:49didn't know that until that summer so
47:51that was fun and to hear it here um and
47:55you know just why common question and
47:58just to kind of see what the group is
48:00doing but um I've had H quite a few
48:04patients where they have let's say it's
48:07opioid most of them are opioid related
48:09and they have a pretty significant
48:12combination of obstructive and centrals
48:15and actually hypoventilation that I put
48:17on vaps devices but I have to say the
48:20iaps with the intelligent backup R is a
48:22pain because the backup R tries to like
48:25stay out of the way which then what I
48:28tend to see is this High residual
48:30Central so I've been then switching them
48:33to the pressure support venation with
48:35the target safety water which is Al all
48:39you have to do is add three so like if
48:42you're using the intent um the the in
48:46ibr instead of the regular yeah um so
48:50like if normally you would put 12 make
48:52it 15 if you normally would do 15 do it
48:5518 all you have to do add three and it
48:57essentially turns off your ibr it turns
49:00it off yeah okay great because it's
49:04starting to higher back aak what do you
49:06the the other mode that is the pressure
49:09support ventilation with the targets
49:11like the safety F of volum because it's
49:13a such like like evap in
49:17it if you're I'm so sorry Cara do you
49:20want to answer no no please I I'm I'm
49:22learning also so no go ahead the problem
49:25the problem is going to be
49:27that your initial pressure support
49:30minimum if you're going to do something
49:32that is um not volume targeted but
49:35volume safety is going to have to be a
49:38lot higher so otherwise it's going to
49:42take too long to get to the Target so as
49:44long as your pressure support minimum is
49:47set higher closer to where you think
49:49you're going to need to be you can
49:52safety Target and you're fine otherwise
49:55you're better off looking at volume
49:58targeting and then just up in your
50:00Baseline respitory
50:02rate and the the I sorry I'm sorry I
50:06don't mean to go crazy here but the
50:09intelligent backup great then doesn't it
50:11like increases the backup rate to 18 at
50:14some point and then goes back down it
50:17kind of goes up in their own well I mean
50:21the the reality is when the intelligent
50:25backup rate is there it waits for the
50:28patient's endogenous rate to go down and
50:30then it kicks in but that can be
50:32uncomfortable for patients so by giving
50:35them the extra three it will kick in as
50:39necessary and then you don't have to
50:42have that
50:43problem okay I'll try it yeah
50:48sorry how me work with any of this the
50:53oh using using vaps for Central sleepout
50:57yet yeah um I think that especially I
51:01iaps sometimes has unpredictable um
51:05results um but a lot of times when I'm
51:09doing that this when I'm initiating iaps
51:12um we're on that Hospital Sleep Medicine
51:15service and so you know typically
51:18there's a lot more opportunities to just
51:20you know play with their settings and
51:22and alter you know increase the backup
51:23rate if needed and so um I'm sure that I
51:27could describe it as eloquently as Lisa
51:29does but yes increasing the backup rate
51:31is a good
51:32thing yeah the the only time that that
51:35intelligent backup rate is helpful is in
51:38COPD because it allows them to fall
51:40asleep without the intrusion of extra
51:44events but if you're in neuromuscular
51:47it's the opposite because the patient
51:49can't fall asleep without that support
51:51and so that's why you know in increasing
51:54that backup rate takes over for that
51:56problem but it's one of the big
51:59differences between COPD and neurom
52:07Masque and then Cara can I just throw
52:09one other thing out there yeah um the um
52:14the discussion that you had about drugs
52:16I love because you put backlin in
52:20there I just want to remind people that
52:23the biggest offense with backlin is
52:25backlift and pumps
52:27and frequently pumps don't get added to
52:29our med list because the patient doesn't
52:31have to take it daily right it's just
52:32there and pumping so reminding people to
52:36ask specifically about
52:39pumps yeah I've seen several cases of
52:42central sleep apnea which were at least
52:44in part due to backlin pump um I had a
52:48patient who had a morphine and a backlin
52:50pump Good Very badal sleep baby if you
52:53wanted them to never breathe again
52:54that's how you'd do it
52:58yeah I I you know I had a patient too
53:00which I I um was really curious about I
53:03you know I haven't really this was
53:05recently so I haven't really mentioned
53:06it to a lot of people but um he was on
53:09to zanine and came into the sleep lab
53:13you know for obstructive
53:15apnea um and then you know he was on
53:18there with on his iPad awake and was
53:22having just you know periodic breathing
53:25during the day and then of course he
53:26went to sleep and he did still have
53:28obstruction but you know there's
53:29definitely a central component and then
53:32the next time that he came in um he had
53:36stopped the
53:37tanine um because I could not figure out
53:40why he would have Central apnea during
53:43the day and I just was like will you do
53:46this experiment for me and he said I
53:48don't think the tanine is doing anything
53:50anyway and he came back and he he still
53:53had Central apnea when he was sleeping
53:55but it was gone when he was awake so I
53:58just found that
53:59very
54:04interesting yeah it's the Gaba function
54:06of the cine that's doing it and in the
54:09animal models um they take the little
54:12micro dialysis pipets and just put the
54:15Gaba blocker onto the brain stem and you
54:18can get horrible centrals if it's bad
54:22enough with a pump they're actually
54:24agnostic with breath holds rather than
54:27at exhalation and that can make it super
54:30hard to treat because if it's with
54:32breathhold what do you do with the p
54:34right like somebody would have to sit
54:36there and squeeze their chest rather
54:38than give them
54:47NIV does anyone else have any fun
54:49stories
54:52or any other questions
54:57okay I just have one other fun story
55:00yeah um have you guys ever heard of a
55:02FODMAP diet yes so one of the things
55:06about the FODMAP diet they use it a lot
55:08for like irritable bowel and that kind
55:10of thing um they change you so that you
55:13get all of these foods that eventually
55:15induce
55:17alkalosis and the
55:20alkalosis apparently helps the bowel but
55:23what it does is it closes the CO2 two
55:26Gap so that when you look at their
55:29ability to handle Loop gain it's
55:32significantly impaired so we have a guy
55:35who's gone on and off fod map and when
55:37he's on it he gets centrals and then
55:39when he's off it it goes
55:41away that is super interesting my mom is
55:44on a fod
55:50maath but no I hadn't heard that before
55:52and I I actually didn't even realize
55:54that it was me that it was meant is a
55:55design to induce alkalosis or is that
55:58just like a it it may just be part of
56:00the side effect of it it sounds like a
56:02horrible diet I I won't be doing
56:05that it it makes them very gassy
56:09too not
56:12fun but that's that's super interesting
56:14I'm gonna have to look that
56:22up I just saw sh comment yes yes yes
56:27um all right any anything
56:31else okay if there's uh no other
56:33questions thanks everybody for joining
56:35us today this is awesome I'm glad that
56:37uh we are getting more section uh
56:40content out there so thank you k for
56:43being our our guinea pig on our first
56:44sleep webinar uh more to come uh we will
56:48be editing this um I will drop it in uh
56:51to our Communications team and we'll
56:53post it on our sleep Network page so
56:56that so we can share it out to everyone
56:57else but thank you all for joining us
56:59today um if you have any other questions
57:03uh you can uh reply to the email that
57:07invited you and we can get those over so
57:09if Cara has any answers for you
57:11afterwards we can get those out as
57:13well all right thank you so much
57:15everybody I'm really um honored that I
57:19got to do the inaugural lecture so um
57:24thanks lot for having me

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