Non-Invasive Ventilation

I could rehash the many excellent write-ups of non-invasive ventilation (NIV) that already exist on the internet, but I thought it would be more personal for me to tell how my son came to use it, explaining NIV along the way...

Bear in mind that these events took place over a period of 10 years and involved many medical professionals from various hospitals and clinics, although it may read as if it took just a few nights. 

A person's breathing might not be enough to sustain them for various reasons including:

• Illness (short term or long term)
• Injury (critical phases)
• Neuro-muscular issues

Sometimes a person will need respiratory support during these times. Sometimes it can be for a short while whilst in intensive-care or a high-dependency unit, other times it can be a life-long need, in which case they will likely have to have a tracheostomy tube fitted in order to leave their face free and unobstructed.

There are also people who only need respiratory support whilst they are asleep.

Due to changes in our respiratory drive and how our muscles respond during sleep our breathing undergoes many changes, this can even vary depending on the stage of sleep we are in. 

The following graphs contain information about how much air I was breathing per minute during the various stages of sleep (as scored by Zeo)...

I won't go into great detail about the why here, instead I want to concentrate on what can be done about the problems that these changes can cause.

At the time of writing, there is a good Wikipedia article about these changes entitled "Sleep & Breathing" 

When he was first paralysed, my son was on full time ventilation. This was considered to be a long-term and possibly a life-long situation and he was give a tracheostomy tube (a tube inserted through an opening in the neck and directly into the windpipe) to allow the ventilator to be connected to him.

10 years on, he is still paralysed but fortunately after several months of being in hospital the tracheostomy tube was able to be removed because the higher part of his spine had partially recovered. He had been slowly weaned off ventilation.

After the tube was removed his oxygen levels were continuously monitored and it was discovered that his oxygen saturations plummetted when he was asleep, but they always picked up again. We left hospital with a pulse-oximeter (a device that monitors pulse rate and blood oxygen saturations via a finger probe).

On some occasions his levels dropped as low as 65% (Generally speaking most people maintain a level of >92%). It was this that prompted me to buy the equipment to record his oxygen saturations so that I could show the relevant doctors involved in his care. Although, not a chart of the lowest that he dropped, this is a chart from early on (right) that is a good guide to what used to happen.

Each row is 4 hours of data (grey parts are when the machine was not monitoring due to him being awake).

Red = heart rate (bpm). Green = oxygen saturations (%) 

 

Left: How the chart should appear (taken from a fairly recent night when he was breathing oxygen via a mask)

 Right: His chart from a typical night

So why not just use oxygen, if it makes the graph all straight and pretty?

Well, oxygen is only one of the gasses involved in breathing, granted it's an important one, but Carbon Dioxide is also involved.

At school we were all taught that we breathe in air, use the oxygen then exhale carbon dioxide, but the carbon dioxide actually serves a purpose. It is used as a trigger to breathe. When the levels rise to a certain level, we breathe to remove the CO2.

If the "sense and control" mechanism in the brain is damaged, or if the muscles are not able to respond to its signal to breathe, then CO2 can build up in a condition known as hypercapnia.

That is what was going on while my son was using oxygen. We were able to see this by the use of a split cannula. It looks like a standard nasal cannula for oxygen delivery, but the tube to one nostril is used to deliver oxygen whilst the other is used to monitor the CO2 using an end-tidal CO2 monitor / Capnograph.

High CO2 can lead to other health issues, and it actually affects the Ph of your blood.

So my son was trialed on a type of ventilation known as Continuous Positive Airway Pressure (CPAP). This involves a constant pressure of air being delivered into your nose (or nose and mouth) via a mask. 

If you ask a child to blow a balloon up, then they will probably struggle, but if you "do the tricky bit" and start it off for them then they will probably be able to top up what you've started and finish inflating the balloon.

That's essentially the idea of CPAP. The airways are kept open by the pressure, leaving the user the task of inflating their lungs.

CPAP can be a great help when people suffer from Obstructive Sleep Apnoea. It can prevent the airway closing off, thus allowing the sleeper to breathe normally.

However, CPAP wasn't preventing my son's apnoeas.

This could have been because he needed much higher pressures, or because the apnoeas were "central" and not "obstructive" in nature.

A central apnoea is where the brain doesn't tell the sleeper to breathe.

Fortunately, the CPAP machine records the overnight data to an SD Card and can decide whether the apnoeas are obstructive (airway closed) or central (airway open but no flow).

It showed that he had mainly obstructive apnoeas with hypopneas, but also the odd central apneoa, along with many apnoeas tagged as "unknown".

The night above shows them towards the end of the night. This didn't fit with the pattern of oxygen desaturation that we saw begin around an hour after sleep onset, even whilst on CPAP, hence we weren't sure how much to trust the detected central apnoeas as they seemed few and far between. However, if someone has both obstructive and central apnoeas, CPAP can reveal those central ones after it has removed the clutter of obstructive apnoeas. 

The CPAP that he was prescribed was "Auto-titrating CPAP" this means that the machine decides which pressures are needed. You can see this in the graph above (the pressure line varies throughout the night). Intriguingly, the when the pressure is the highest there are no apnoeas, but he still desaturated.

The auto-pressure function can be set to choose between limits, or forced to give a constant set pressure. After many nights of alarms. We obtained a chart from a night at 6cmH20 (left) and a night at 15cmH20 (right) to see what was going on.

 6cmH20 had little effect. 15cmH20 was better, but still unacceptable and uncomfortable for him.

He would wake in the middle of the night and not be able to call out due to the mask over his nose and mouth. His heart rate would then increase and his alarm sound to alert me. I'd have to turn the CPAP off and it would have to be re-ramped again (start at a low pressure and build up over time, hoping that he was asleep before it delivered high pressure again). 

Because his blood-oxygen only dropped at certain times of the night rather than be low ALL night it was suspected that it had something to do with a particular stage of sleep. Below is a picture of a normal hypnogram (a graph detailing the stages of sleep, as shown on the Zeo entry of this blog) overlaid with a graph of his oxygen levels from one night.

Seeing this was a goosebump moment...

The pattern of his oxygen desaturations matched up really well with a standard hypnogram, so it was pretty certain that his condition was REM related. However, this wasn't a graph of his REM.  A way of working out and recording when he was in REM was needed.

New equipment was also needed...

Due to the possible presence of central apnoeas, it seemed unlikely that CPAP was going to be an effective solution, afterall there is little point in keeping the airway open if the brain isn't initiating a breath (or the muscles aren't able to respond to the signal to breathe). It was suspected that he would need Bi-level ventilation. Well known brand names for this are BiPAP and VPAP.

These are both Bi-level Positive Airway Pressure devices. Bi-level delivers two alternating pressures. The higher one is the IPAP (Inspiratory Positive Airway Pressure) and the lower one is the EPAP (Expiratory Positive Airway Pressure). The IPAP is essentially the breath, while the EPAP is the amount of pressure required in order to keep the airway open. Usually the breaths are triggered by the sleeper's breathing efforts, but to cover the possibility that he did indeed also have central apnoeas we used a BiPAP machine that could also be set to deliver "backup breaths" if my son didn't breathe a certain number of times a minute.

The CPAP / BiPAP was delivered via nasal pillows. These are fantastic as they allow the user to speak whilst using them. However, this left us with no way of being able to reliably monitor his CO2 using a capnograph.

CO2 monitoring is essential, without this it would be too easy to adjust the ventilator so that there were no oxygen desaturations, but actually be hyperventilating him, or worse causing trauma to his lungs and airways; so unless we could find a way to reliably monitor his CO2 we couldn't go any further. A different type of CO2 monitor was bought in...  A transcutaneous CO2 monitor.

The transcutaneous CO2 monitor gathers its data by way of a probe that is attached to the skin of the chest or arm. It then heats up the skin and evaluates the gasses given off. The probe needs to be removed after several hours and placed on a new site in order to reduce the risk of probe burns to the skin.

The titration process wasn't a one night affair, so we had the luxury of being able to record readings at home between appointments. However, at home we didn't have an EEG machine to record brainwave data, so we couldn't tell what stage of sleep he was in.

We needed to see when (and if) he achieved REM sleep while his settings were adjusted over the course of several nights. We also needed to make sure that the pressures weren't waking him up. Afterall, if he didn't have much REM (or his REM was disturbed) then his oxygen levels would look good and give the false impression that the settings were working. The Zeo was perfect for this.

This graph is from one of the first nights of BiPAP (when the settings were good but not optimal) and it shows a great correlation between his oxygen desaturations and Zeo's calculations of REM sleep. (The dips in the green oxygen line are a near perfect match for the green chunks of REM from Zeo), as are the rises in pulse rate and CO2.

This gave me a lot of confidence in the Zeo's decisions as REM is probably the hardest state to detect due to its similarity to being awake. In fact I'd even feel confident enough to say that the piece of missing data from the Zeo (headband was too loose) would have shown REM.

The result of a few nights adjustments during REM was that BiPAP at the correct pressures eliminated his oxygen desaturations completely and allowed him (and me) to sleep all through the night for the first time in a very long time.

It turned out that obtaining a machine that could provide additional "backup" breaths was a good investment... Pressures alone weren't enough to prevent his oxygen levels dropping, so a backup-rate was set of 13 breaths per minute.

This meant that if he didn't breathe 13 times a minute of his own accord, that the machine would make up the number of breaths. 

 

The graph on the left is with BiPAP pressures set to 18/10. This was fine for his oxygen requirements, but it still was uncomfortable for him (but tolerable). The high EPAP of 10cmH20 made it hard for him to exhale (remember that he has neuro-muscular issues).

The pressures were re-titrated but this time with a lower EPAP. This seems essential for him to be able to exhale effectively, and provides a more comfortable night.

These settings will be reviewed periodically by the medical professionals that have been involved in his care to see if they are still optimal.

He now loves the BiPAP machine and doesn't like sleeping without it, he doesn't sleep in until noon at the weekends, he doesn't fall asleep at school and can stay awake until long into the evening. He also has a ZQ of 137 which he likes to use to mock my awful average ZQ of 68.

5-HTP, Serotonin and Sleep

 

For the last 5 days I've been taking 5-HTP.

5-HTP is a precursor to serotonin (that is, it becomes serotonin once metabolised by the body).

I've previously used 5-HTP for experimenting with my sleep composition, and to try to reliably trigger lucid dreams. The dosage that I was taking then was 50 - 100mg at night.

This time I tried a brand that contained "co-factors". These are associated vitamins and minerals that help the body to metabolise the 5-HTP into serotonin. 

I decided on 200mg each night about 10 minutes before getting into bed. 100mg is the recommended maximum daily dose of this brand, although I have seen others that give a maximum daily dose as 300mg.

I have also seen medical literature that cites doses of 150mg-300mg as a daily dose (as a trial for treating depression), so toxicity at this dose seemed unlikely.

Why did I take 5-HTP?

The rather lazy answer is that (as I mentioned above) I've taken it before without ill effect, and that it is mentioned to have a positive effect on sleep, even being cited as having a positive effect on a severe case of insomnia 

A rather cheeky and over-simplified answer is that I have already shown that a depressant (alcohol) increases my AHI, so I wondered if something that has antidepressant properties would have the opposite effect and reduce my AHI.

I have also seen medical literature that suggests a link between depression and sleep apnoea (both as a cause and effect of sleep apnoea). 

Depression is more complicated that just having low serotonin levels, but low serotonin does play a part. Serotonin is a neurotransmitter (it is used in the body's sending and receiving of nerve impulses), so I wondered if increasing my levels would mean that I would have stronger signals to breathe during sleep and that the muscle tone in my airways would be that much "sharper".

Okay, so how did the 5 days go?

I noticed the following effects (sleep related and non-sleep related):

• I wasn't as tired in the evenings, so went to bed later
• I found it easier to wake up
• I didn't feel as hungry during the day, generally ate once at 2pm, then didn't eat in the evening.

Throughout these experiments, I go to bed when I am tired.

I calculated my average bedtime using the Zeo data. As I am doing these 5-day comparisons on weekdays (except the alcohol test - see separate blog for that), the time that I had to wake up was the same each day, hence later to bed meant less time in bed, which oddly with the 5-HTP didn't feel like a bad thing.

 

I wondered if my body "needed" more sleep, afterall I am used to roughly an extra hour (and still crave more), but on two mornings of the week (Fri and Sat) I can have a bit of a lie-in if I need to but I didn't want to lie in when taking 5-HTP at night (It's Saturday and I'm typing this at 7am, after waking up at my normal weekday time of 6:30am)!

It is known that some anti-depressants can decrease the amount of REM sleep that you have, so I suspected that my percentage of REM would decrease.

As percentages, the figures do not show this. In fact they show an increase in the percentage of deep sleep, along with a slight increase in REM and wake...

However, as REM is more abundant at the end of the night, it follows that the less time one spends in bed, the less opportunity there is for REM sleep, hence my actual 5-day-mean time in REM fell by 11 minutes from my baseline of 98 minutes, although it put it more inline to the average for my age of 90 minutes.

My actual time in slow-wave sleep (deep) rose by a mean of 3 minutes.  My mean deep sleep (34 minutes) is still way below the average for my age (69 minutes) but within limits, so I am pleased with this small increase.

I'm not sure if these changes are actually significant, perhaps a longer trial may reveal more?

So, even if 5-HTP didn't affect my AHI, it still had positive effects on several aspects of my sleep composition. 

However, it did have a positive effect on my AHI and it was much more noticeable... 

I've graphed my 5-day-mean AHI alongside the other 5-day-mean AHIs for alcohol and my baseline.

It brings my mean AHI down to a level that puts me in the "normal" category (<5 AHI = normal). Maybe this is the reason for not wanting to sleep so early and finding it easier to wake in the mornings.

For the sake of showing that this is a consistent effect, I also graphed the data on a night by night basis... 

For now, this seems too good to be true: 

• Lower AHI
• Normal bedtimes
• Less time in bed
• Increase in slow-wave sleep

So what now? Keep on taking the tablets?

Based on my limited data, I wouldn't dare go so far as to claim that this is a effective treatment for mild (very mild) obstructive sleep apnoea, nor would I suggest that it would work for others, but it is intriguing and does need looking at further.

It leaves me wanting to know more about the mechanism behind this effect. Yes, it's good that it has helped me as far as my AHI is concerned, but I want to know how. In a previous post, I noted that my sleep apnoea seems to be REM related. Serotonin related activity drops dramaticaly during REM sleep, so maybe the higher levels due to 5-HTP reduced that effect?

Is my pseudo-science hypothesis correct, or is there more to it than that?

I'd be interested to see if this effect carried on, or if my body got used to the 5-HTP and the effect faded.

I'd also like to try this with a lower dose of 5-HTP (after all, why take a high dose if you don't need to)? I'd also like to see if sustained-release 5-HTP is more effective.

I was planning to try the mandibular advancement device next, but after such a positive effect, I think I'll stay with 5-HTP for a while and see if I can improve on the results even more. I'd like to bring my sleep latency (time to sleep onset) down.

Yes, this is good news but I can't help feeling a little like Lizzy in "Drop Dead Fred", she knows that she's taking a pill that will stop her seeing things that others can't. Will taking 5-HTP, increasing my serotonin levels and bringing my AHI down stop me from having sleep paralysis, lucid dreams and seeing/hearing the sleep-wake border imagery that I have grown so used to? 

I hope not.

I'll explain how and why I came to like sleep paralysis in an upcoming blog-post. Hopefully it may be of use to anyone that fears it as I used to.

I have to say that this is a test with a tiny sample size, and of limited duration. I am not suggesting that anybody should try this, and certainly not use it in place of recognised treatments. 

Update on Saturday, May 12, 2012 at 7:54PM by Hypnagogia Blog

I've also found that 5-HTP helped reduced residual snoring after lowering my AHI with positional therapy.

Snoring Remedies? Results for 5-HTP

Apnoeas, me? My Baseline AHI

I'm going to be exploring some of the sensible and not so sensible suggestions in order to bring down my AHI (see my post "What is an Apnoea?" for an explanation).

To do that I needed reliable data, so I decided on a 5 day mean with a few basic rules:

• No coffee after 3pm
• Monday - Friday monitoring only (to ensure routine sleep and wake times)
• No alcohol
• No other supplements known to affect sleep
• Begin sleep on my back (supine)
• Motion detection IR camera (for verification of events if needed)
• The same apnoea / hypopnea scoring criteria will be used throughout

I could use the IR camera to detect sleep position, but that would take a lot more time, so until I have a system that can detect that reliably then I won't include that data, and I may re-evaluate some weeks using that ability.

I did initially check the camera to see if I attempted to breathe when the system was detecting apnoeas. I did make some respiratory effort, so I will make the presumption (for now) that my apnoeas are obstructive in nature.

I also noticed that when the oxygen desaturations due to apnoeas were compared to the Zeo hypnogram, that like my son's, they were clustered around REM sleep.  

The top line is my oxygen level.

It does look like I'm awake for those periods, but the black line is a more detailed Zeo hypnogram (data calculated on a 30 second basis). Zeo has a scoring system and shows the highest scoring sleep stage as being the dominant one. "Wake" scores the highest; this makes sense, as being awake is probably the most important thing to show when you are supposed to be sleeping.

The 30 second graph shows why the main Zeo graph shows a lot of wakefulness during the night... I have oxygen desaturations which in turn wake me up, hence Zeo shows "wakefulness for the whole 5 minute epoch. However, when you see Zeo's calculations of time spent in each sleep stage, these are based on the more detailed 30 second data.

Sleep apnoea can run in families. Whether that is a factor or not, my diagnosis (albeit a self-diagnosis) doesn't surprise me. I sometimes snore, I wake up with headache a lot, and I could do with losing a bit of weight.

I have long suffered with sleep paralysis, and I suspect that being disturbed in REM sleep is a major factor in that, if not the sole cause.

So, how is this a problem?

My average AHI (number of apnoeas and hypopneas per hour) is 7, hence I am classified as having "Mild Obstructive Sleep Apnoea".

The classification ranges are:  

<5      -    Normal (unless symptomatic)
5-15   -    Mild
15-30 -    Moderate 
30+    -    Severe 

The REM element brings the name to "Mild REM-Related Obstructive Sleep Apnoea"

I will say that this "diagnosis" is an amateur one, it may not correlate with a professional one in a sleep lab, but if I use the same equipment throughout this experiment the results will still be valid, just relative to my original numbers.

So, what if I don't want to have that diagnosis, what if I want to be "normal" (says the man who sleeps with electrodes on his head, prongs up his nose and a camera watching him)?

Standard advice:

• Lose weight if you are overweight (even a small amount can make a difference)

That's all very well, and something that I will do, but that won't help me fix my sleep tonight will it?

Other advice includes:

• Prop the head of your bed up by 4-6 of inches (takes the weight off your neck)
• Cut down on alcohol (see this blog entry on alcohol)
• Quit smoking
• Use a mandibular advancement device (pushes the bottom jaw forward to hold the airway open)
• Use a CPAP device (see this blog entry on NIV)
• Avoid caffeine and heavy meals within two hours of bed
• Use a nasal dilator (keeps the nostrils open)
• Try a nasal saline spray
• Throat exercises
• Surgery

I'll evaluate some of these (plus a few more ideas that I have) and back up the findings with a 5 day mean AHI and sleep graphs.

Let's face it, we're all looking for quick-fix solutions, and I'm not trying to cut corners, but I am trying to help myself whilst on the journey to losing a bit of weight.

So that I don't confuse the issue I will not intentionally lose weight until I have tried some of the other methods.

So, in essence I am looking for some way of bringing my AHI down, along with the time that I spend awake at night.

...but before I do that, how about trying to INCREASE my AHI? Next blog post.

A nightcap - Alcohol and Apnoeas

 

A nightcap helps you sleep, right?

Well, yes but...

During my initial explorations with the flow-meter, I thought that I'd test my set-up by trying to INCREASE my AHI using a well known substance that makes sleep apnoea worse...

Alcohol.

A sleep experiment where I get to have a drink or three... it's tough, but I'll do it for science. 

Pretty much as it does with people, alcohol relaxes the muscles in the airways making them more prone to flopping around all over the place and causing an obstruction.

When it comes to the rest of the practices, gadgets, fads and ideas that I'll be exploring I'll be testing them for 5 days in a row each. To be honest I'm not going to do that with alcohol as I can't afford a week of waking up sluggish and groggy. 

So, what I did was to take 5 non-consecutive days instead. I consumed alcohol and recorded my AHI on those nights along with my 5 day no-alcohol mean AHI for comparison (see previous blog).

Pretty conclusive.

Alcohol increased the number of times that I either stopped breathing or breathed so little that it was ineffective.  

Not only that, but it did it in quite a startling way. It took my 5 day mean AHI from 6.95 to 12.2.(max 15.3) To get that into perspective, that's nearly double the number of times PER HOUR that I had breathing problems.

As discussed on the post "My Baseline AHI", I went from just scraping in with a diagnosis of "Mild Obstructive Sleep Apnoea" to being firmly in the category!

Surely there was something positive to salvage from this bad news?

Yes. Annecdotally, in my mind alcohol helped me to get to sleep and I found that the Zeo data backed that up. Again, using a 5 day mean value, my time to sleep onset (or Zeo's "Time to Z") went from 28 minutes without alcohol down to 9 with alcohol.

That seemed to be the only significant difference in the data, so I haven't bothered to clutter the page with other measurements.

It may help you to get to sleep, but the chances are that the sleep will not be good sleep. The chances are that it will be disturbed sleep, the chances of having to go to the bathroom will increase, as will the likelihood of dehydration-related headaches and fragmented sleep towards the morning.

Not only would I wake up feeling slow and mildly hungover, but I'd be tired from being woken up up to 15 times an hour through apnoeas.

Don't misunderstand me, this isn't one of those damning posts about alcohol, but it is something to bear in mind if you already suffer with sleep apnoea, and it may even cause mild apnoea in people who don't have it.

Will I continue to drink alcohol? Of course, and that's the dilemma. So I guess the answer is "everything in moderation".

Zeo & CPAP / BiPAP

I've posted on a couple of CPAP boards (and read at more) and it's clear that there are a lot of us who like to see what the ventilators are doing overnight and how many apnoeas & hypopneas there are. Quite a few of us own pulse-oximeters too, so this data can also be included.

One problem is that each device has it's own printout making comparing them tricky.

I created an A4 page in Photoshop and found that it was then easy to align all the graphs as long as all the monitors were were started and stopped at the same time (or as close as you can manage).

You can either print all the various outputs to PDF files using either Adobe or the free CutePDF then open them in Photoshop or you can take a screenshot from each piece of software.

Then cut and paste each graph onto your A4 blank and stretch them so that the start and stop times align.

Below is an example of one from a night of my son's BiPAP data. 

It includes: 

• BiPAP output (Pressure, RR, flow rate, triggered breaths, apnoeas etc)
• Transcutaneous CO2 (actually a reprocessed photo of the onboard graph)
• Oximetry trend
• Pulse rate
• Zeo 30 second resolution hypnogram
• Zeo 5 minute resolution hypnogram

I then pasted bits of relevant data from Zeo and the oximeter around the edge.

This is from a night of making adjustments to the backup rate of breaths and is a good example of what aligning the data can reveal.

Take a look at the highlighted strip and work down from the top...

• The backup rate had been increased a couple of hours before. 
• Then in the highlighted part you can see that the number of breaths increased even more.
• However, there was a much higher increase in the number of breaths he was doing for himself

Why?

When you look down to the Zeo hypnogram it becomes clear. The extra breaths were waking him from sleep, hence his spontaneous respiratory rate increased even more.

The backup rate was too high, so I reduced it.

I have also tried the Zeo with CPAP on myself.

Here is a simple overlay of the Zeo hypnogram onto the ResScan report. (I pasted the hypnogram into a new layer in Photoshop and then made it semi transparent).

A correlation between minute ventilation and periods of being awake (actually broken REM according to the 30 second hypnogram) is easy to see.

Also the apnoea flags point to me losing deep sleep due to apnoeas.

More about that and what I plan to do about it in another post though.