Sleep Apnoea
Revisited- by Ian Neering PhD MSc
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This article and that
by Dr Colebatch in the June 2008 newsletter are reprinted from PPN NSW
Newsletter June 2004. These and other articles can be viewed on the PPN NSW
website www.post-polionetwork.org.au Long-time
member of the NSW PPN, Ian Neering was Associate Professor of Physiology and Pharmacology at
the article – it is imperative for polio survivors to have their particular causes of sleep apnoea correctly diagnosed and appropriately treated. |
Articles in the NSW - PPN Network News in 2004 prompted me to put
down my experiences with sleep apnoea as they might be of interest to some readers. Let me stress that these are my personal
experiences and people should not necessarily extrapolate from them to form any
sort of generalisation.
By way of background, I should say that I contracted polio in 1950 when
I was around 4 years of age. I was
completely paralysed and spent a good deal of time in an iron lung. Over the years, with the sort of therapies
most polio readers will know only too well, I made a pretty good recovery and
was able to lead quite an active life without any prostheses of any kind. I have quite a marked kyphoscoliosis with
significant deformity and associated low functional lung volumes.
At around the age of 40, I started to notice the signs of PPS and my
general condition started to deteriorate. I took to using a walking stick and
was forced to modify my life style significantly. When I had respiratory infections, they
lasted longer and were increasingly troublesome. I now need crutches to get around.
In 1993, a dose of flu saw me admitted to hospital with life-threatening
respiratory failure which basically means that my lungs could not function
sufficiently well to provide me with an adequate supply of oxygen. I was on a
ventilator for a few days but was fortunate enough to make a good
recovery. In the aftermath of my period
in intensive care, sleep studies were performed and sleep apnoea was
diagnosed. The respiratory specialist theorised
that cumulative fatigue of my respiratory muscles, partially as a consequence
of the sleep apnoea, was responsible for the respiratory failure and a C-PAP
device was prescribed
Let me tell you, I struggled with that machine! Let alone the fact that no mask seemed to fit around my nose properly
and jets of air burbled and squeaked from the poor seal around my face unless I
lay “just so” in bed and didn’t move a muscle. Not conducive to a good night as you can
imagine. I felt no improvement in my
overall well being after weeks of persevering and follow up visits to the doctors.
I’m afraid I have a general antipathy to the medical profession
not uncommon amongst old polios and a general mistrust of “blanket
treatments”. I, like many polios,
have become rebellious towards doctors’ prescriptions and prefer to find
my own bumbling way to the solutions that best suit me. At my wit’s end, I decided to take
matters into my own hands and here I have an advantage over most in that I am a
physiologist by training. I need to
digress for a moment here. Articles on
sleep apnoea don’t say very much about the sleep study used to
definitively diagnose the condition.
When you go in for an overnight study, you are fitted up with a number
of sensors. Cables are attached to your scalp for an EEG which records your
brain waves and allows the investigators to assess your level of sleep. A finger probe records oxygen saturation of
the blood which is the critical measure telling us if you are not receiving
sufficient oxygen as a result of the sleep apnoea.
A more sensitive measure of ventilation is that of carbon dioxide, but
not all sleep studies include this.
Wires are also attached to your chest so that the activity of the
respiratory muscles can be recorded. This is known as an EMG. It’s
important to understand that EMG records muscle activity only. A reduced EMG activity recording could be
caused by a reduced drive from the motor nerves controlling the muscle or from
a weakened muscle, unresponsive to nerve stimulation. There may be other sensors attached to
measure airflow, leg movements and so on.
A good sleep study will look at all of these parameters; an inadequate
ones don’t and may lead to a misdiagnosis
Now, there are two main types
of sleep apnoea: obstructive sleep apnoea and central sleep
apnoea.
In the former, the problem is mechanical in that respiratory muscles may
be working well but actual airflow into the lungs is restricted for any of a
variety of reasons. In the latter, there
is reduced respiratory drive from the brain to the muscles of respiration
resulting in a reduced or absent inspiratory effort. Weakness of respiratory
muscles will exacerbate both forms of apnoea.
Dr Joyner, in her classification, quite reasonably, has delineated a
category just for polios which contains aspects of both forms of apnoea though,
strictly speaking, does not add a third category to the two groups already
defined.
A sleep study, by looking at the temporal relationship between the
activity in the respiratory muscles, air flow and oxygen saturation of the
blood, can determine what form of sleep apnoea you suffer from. The problem however is that getting to sleep
with all those wires attached to you, in what for many of us is an unpleasant
environment with unfortunate associations is not all that easy! The consequence is that we may not actually
reach the deepest form of sleep during which REM occurs. The investigating physician therefore will not
have a complete picture of what your breathing does during sleep.
Enough digression. I was lucky enough to be able to borrow (with
appropriate bribing and inducements) some bits of equipment and set up to
monitor my sleeping at home. I got hold
of an oximeter to measure blood oxygen saturation. Diaphragm EMG was measured
using a little battery operated portable device used by sports people. I measured airflow by taping a thermistor
(which measures temperature of the air) under my nose. Measuring EEG was beyond the range of my
ability to equip. It wasn’t really
necessary. The hardest part was logging
all the data. After all, I needed to be
able to record oxygen saturation, EMG and airflow over a period of at least 6
hours.
After fiddling with chart recorders and ending up almost buried in paper
upon waking, I ended up recording all the data continuously on my
computer. My partner was not
particularly impressed that I had turned our bedroom into a laboratory but I
soothed her with a vision of a well-rested husband who would not be snappy and
grumpy if he had a decent night’s sleep.
I can’t adequately describe my satisfaction to you when I finally
saw the definitive result.
Obstructive apnoea is characterised by an increased inspiratory
effort coincident with the decrease in airflow.
In other words, when the airway is obstructed, we try a whole lot harder
to breath in, at least initially, and you can see this in an increased response
in the tracing of the EMG from the muscles that help us inspire. In my tracing, respiratory effort just faded
away coincident with airflow, breathing stopped because the muscles were no
longer being asked to contract, a sign of a centrally mediated sleep apnoea.
My problem I now knew was that during sleep, the drive to my inspiratory
muscles, the messages from my brain telling my muscles to breath (respiratory
drive), was reduced. In fact it would
cease all together, causing blood oxygen content to fall until all those alarm
mechanisms that the body has to detect such a dangerous malfunction caused me
to wake up. It is known that respiratory
drive decreases during sleep even in normal individuals. Many polios have
weakened respiratory muscles. It seems
not unreasonable to suppose that for some polios the combined reduction in
respiratory drive from the brain and the weaker muscles could result in the
sleep apnoea. EMG recordings would be
unable to dissect out this scenario.
Remember, the EMG cannot distinguish between a reduction in nerve
impulses from the brain to the muscle, or a weakly contracting muscle. How did this new knowledge make a
difference?
Well, it meant that the C-PAP machine was quite inappropriate for my
needs. C-PAP is great for the
obstructive types of apnoeas where the positive air pressure from the machine “splints”
the airways in an open position and prevents their collapse during the
respiratory cycle. It’s a bit like
breathing in a gale. C-PAP won’t help you if you simply stop breathing
because its flow of air is continuous.
There’s no cycling.
Armed with my new data, I was able to show my respiratory physician that
a different form of therapy was required.
He promptly prescribed a Bi-PAP machine which is a bit like a ventilator
in that it cycles through an inspiratory and an expiratory phase. There is an obstructive component to my sleep
apnoea and the BIPAP machine will help against this also. That machine is now more than 10 years old
and has become an essential chattel of my life.
Since using sleep support, I have had fewer respiratory infections and
those I have had, have had a more benign outcome. Why have I felt the need to put all of this
down on paper? My main motivation is a
fear that some of you may go through the same misdiagnosis that I did. My message is: for those of us who had
respiratory paralysis during the acute phase of polio infection (and possibly
for others), C-PAP may NOT be the treatment of choice either because of
muscle weakness, reduction of central drive or a combination of both. I still have trouble with masks. Having spent
much time and effort making plaster casts of my face and attempting to mould
masks, cast masks, and experiment with various materials, I’ve found that
the “disposable” resuscitation masks sold by the St John’s
Ambulance people work as well as any.
Use of these with a fabric “gasket” and my partner’s design of head harness has enabled me to sleep relatively comfortably even allowing me to toss and turn as the dictates of comfort demand. One other fascinating aspect of these machines that I’ve not seen mentioned anywhere else, is the tendency, for me at least, to cause psychological dependence. This manifests as an inability to sleep at all without the machine. On occasion when I’ve been camping and my car battery fails, in a power outage, or when I have had to travel in an emergency without my machine, I simply can not sleep without it. On one occasion I had no sleep for two consecutive nights. On the third night, I was so exhausted I did manage to sleep fitfully. I wonder if others have noticed this effect?