CO2 retention

#KYJ - CO2 retention

In our #Pirate seminar and #RespNursing we touch on CO2 retention.   It’s a commonly used term, and most nurses will recall hearing it, and associating it with end stage COPD.

That said, do you know what it means to be a carbon dioxide retainer?  Where is the CO2? Where does it come from? And; given that the patient is still breathing, why are they not just blowing it off?

Ok.   Take a deep breath...

Physiology refresh: cells burn glucose with oxygen to make energy (ATP).

Like all engines that burn carbon, (wood on a furnace, petrol in a car, diesel in a truck) so too, glucose in a cell produces   Carbon dioxide (CO2) as a waste gas.

Now stay with me ...

As cells produce CO2, this diffuses into the extra cellular fluid around the cells.   Now capillary blood in close proximity to those cells absorbs this CO2 and two things happen.

The capillary plasma pH drops (CO2 is acidic) so blood becomes acidic.  This also causes micro-vessel dilation.

Entrapped acidic blood in engorged dilated vessels now slows and saturates with CO2, red blood cells off load their oxygen, now freeing up space to absorb the CO2 and transport it to lungs to be blown off (expelled).

So a couple of things here.  

Oxygen binds to haemoglobin;

but so does CO2.  

As the blood cell carrying oxygen starts to off load the oxygen in these peripheral tissues, CO2 hops on because there is space in the RBC.

Think of a bus full of footballers arriving at the field, they get off the bus, and now there is space for the cheerleaders to get on the bus.  

Ok- enter the world of lung disease.  Chronic bronchitis, asthma and alveolar destruction called emphysema.  

Now slowly and insidiously over years, the person with lung disease reduces their oxygen carriage, and subsequently increases CO2 carriage.  They start accumulating more carbon dioxide in blood.  Now this blood should normally just release it’s CO2 in the lungs, but remember, these are the same chronically diseased lungs that had reduced oxygen exchange, so they also have diminished CO2 diffusion and off-gassing.

They start becoming slowly hypoxaemic (lower sats), and slightly CO2 retentive. Slightly more acidic-slightly more vasodilated.  As lower oxygen levels reach the tissues, cells now starving for oxygen (hypoxia), start burning more glucose (carbon) to attempt to make energy anaerobically (lacking oxygen).  

As more glucose is burned, then more carbon dioxide is produced.  This is the cause of increasing levels of carbon dioxide in tissues.  As tissue CO2  levels increase, then blood CO2 levels also increased.

Diseased lungs can’t off gas it, so it becomes retained in tissues and in blood. Now- acidic blood has another interesting property... it won’t carry oxygen.  So this is a downward spiral where the diseased lungs won’t in-gas oxygen, and acidic blood is reluctant to transport it.  Acidosis leads to hypoxia leads to CO2 retention leads to acidosis; and around it goes.

So we think that oxygenating these guys should help, but remember the bus?  If you fill it with footy players, there is no room to transport the cheerleaders.

CO2 retention is worsened by unnecessarily oxygenating end-stage COPD patients.  Allow SpO2 levels of 88-92% in these patients if not distressed. And if you must oxygenate them, just enough (1-2lpm via Nasal prongs) to get their sats into the 88-92% range.

For years we’ve taught the dogma of “Hypoxic Drive” in CO2 retainers; and cautioned clinicians against giving oxygen for fear the patient would stop breathing.  Well we had it wrong.  By all means withhold oxygen as a routine, but it is for worsening of CO2 retention, not loss of drive to breathe.

CO2 retention like the COPD disease pathophysiology is complex, and slow to develop, but one thing is certain, unnecessary oxygen exacerbates it.

#ECT4Health- check out our what’s on page What’s On

Statins and Number Needed to Treat (NNT)

#CageRattler #KYJ

Statins and NNT

The number needed to treat (NNT)  before one person gets any benefit is a pharmacology statistic that drug manufacturers use to to determine that a drug has efficacy (that it does the job it intends).

The same drug can have an NNT that is different depending on the end point you are measuring.  Eg if you measured morphine for the NNT before analgesia is achieved then it is probably about 1 in 3, but if I measured sedation as it’s end point then it might be closer to 1 in 30.

So with younger people being put on statins at an alarming rate (they are the highest selling group of drugs on the planet), the common question in my #CardiacSeminar and #RustyPills pharmacology refresher for Nurses and Paramedics is: “ what is the efficacy of #statin drugs ?”

Now the question is a poisonous chalice, and heavily loaded with misperceived  erroneous opinion about heart disease causes and inappropriate obsolete concepts of cholesterol and it’s evils.

Let’s set the record straight.

Fact: Cholesterol is made in your liver- it is not eaten.  Bacon and eggs for breakfast won’t raise your blood cholesterol like a Glass of fruit juice will raise your blood glucose.   The irony is that that same fruit juice is far far more likely to raise your cholesterol than a serve of pork belly with a butter glaze.... more on that later**.

Fact:  your liver is genetically programmed to produce cholesterol and a bunch of proteins (Lipoproteins) that transports the cholesterol around in your blood.  If you have familial high cholesterol (hypercholesterolaemia #scrabblewordoftheday), then nothing you eat will lower it.  Whether you have high cholesterol or not, your basal cholesterol level is preset genetically, and any attempt to reduce it will cause your liver to attempt to make more.  It does this even to the detriment of breaking down your muscle and fat stores to seek ingredients for your liver to to replenish what your body is programmed to make.

Fact:  Cholesterol is essential for three main functions.

1- it makes steroid hormones (oestrogen, progesterone, Testosterone, cortisol, and aldosterone)

2- it is the primary ingredient in bile which is used by the gut to emulsify fats in your diet preparing them for absorption in your small intestine.

3- and this is the Big one. Cholesterol is a chief ingredient in every (EVERY) cell in your body.  As surgery, injury, infection, trauma or wear and tear occurs in your body, those very cells need repair, so cholesterol is the bricks and mortar that the liver must make to fix you.  That is where lipoproteins like LDL and HDL come into play.   They transport cholesterol in the blood to the site of tissue repair. 

Think of your liver as Bunnings

Think of cholesterol as building materials

Think of low density lipoproteins (LDL) as the delivery trucks that transport the building supplies (cholesterol).

Fact:  if I had a blood vessel injury (coronary or cerebral as just one example), the walls of the blood vessel needs to be repaired.  Cholesterol production will be stimulated to facilitate this repair.  It often gets trapped and deposited in pockets of inflammation and over years and years of injury and reinjury, it’s accumulation develops the atheroma that you commonly call a plaque.   It is a cholesterol rich scar that is brittle and can rupture- stimulating a clot that becomes the blockage that is called a heart attack or stroke.

Phew!! 

Summarise: Cholesterol made not eaten, and used for really important things. It’s essential!

At the scene of every stroke or heart attack you will find cholesterol.

But ... at the scene of the building fire, you’re likely to find a firefighter.   The firefighter was there to help.  The fire fighter didn’t start the fire.

Cholesterol is there to repair injury, of course it’s there at the scene, but it didn’t cause the MI or stroke.

Ok... if you are still with us. 

NNT.

Statin drugs lower cholesterol - they are great at doing this job. So if cholesterol lowering is your end point, then they are the best we have.   But if they are being taken to reduce heart attack /stroke risk, is there enough efficacy to take them? 

Back to NNT.

If you believe, like some, that cholesterol causes the heart attack or stroke, then you will appreciate that cholesterol lowering statins might lower your risk of heart attack and stroke.

Do they? In short yes.  But enough? Well.... 

Well let’s look at the NNT data:

If you are under 50 these are the numbers for MI and CVA.

Preventing MI or stroke death 

Women - 1 in 5000 on statins will have their life saved.

Men - 1 in 1000 taking a statin will have their deaths avoided.

We must remember that the major decline of deaths from CHD occurred before the introduction of statins.

That said, most people with strokes and heart attacks don’t die first event.

So what about having a non-fatal heart attack or stroke?

Debilitating, but not deadly-

NNT for MI = 1 in 217.

NNT for CVA = 1 in 313

Can you see efficacy changes whether you are looking at death or non-fatal vessel events?  NNT also alters with age and previous history.

What remains is the balance between the costs and benefits of any medication you take.

Statins cause muscle pain (1:21 people on statins) and links to memory loss, impotence, early menopause and digestive upset... nothing fatal in that list, but lately a very sinister phenomenon has emerged in the literature with respect to statin induced type 2 diabetes.

These numbers are not small. 

0.5% or (1 in 200).

A one in 200 risk of getting diabetes (the #1 risk factor of Heart attack) taking a pill that give you a 1 in 217 chance of having a non fatal heart attack.... I’m going to leave that there for you to mull over.

If you are a woman under 50 

5000 of you need to take a statin for one death to be prevented.

But 250 if you will get diabetes while hoping you are that one.

In all things, if risks are less than benefits then that medicine might be a good idea, but if risks are higher- go for a walk, eat some salad, enjoy your bacon, reduce your stress and ponder a little before blindly believing what we were told about cholesterol in the 1980s.

Cholesterol didn’t cause your fire... why on earth would you try and lower it?  Target the real cause of vessel injury, not the scapegoat trying to repair damage.

By now you might be thinking that statins are not that great; but let me remind you that they are the best at doing what they were designed to do- lower cholesterol production in the liver.    They never claimed to lower heart attack rates.

Now.  What can you do to slash your risk.  

Cut Sugar!  Remember that fruit juice**

Fructose in sweets and juice is not metabolised to fuel, it is stored as fat.  Not just the jiggly, wobbly fat, but visceral organ coating fat.

Glucose is used as fuel, and in high amounts, makes blood viscous, and red blood cells sticky. So sticky and abrasive that high HbA1c values (red blood cell sugar) cause the  erosion and vessel damage that stimulates cholesterol production.

If the food you eat converts to quickly to glucose, it is damaging vessels.  Any excess is (like fructose) stored as fat .  But it’s causing vessel injury along that journey.

Im off for some avocado and salmon for lunch.  I might even sauté in butter.  Mmmmm butter.

Fat is your friend

Deep breaths to improve Sats

#KYJ-Oxygen Saturations and Deep breaths.

Do you ask your patient to take a few deep breaths when the sats are being recorded?

You know the patient I'm talking about.  Old mate, lying there restfully in the bed, sats sitting at 91%, and you don't want to write that number on the colour coded obs chart; so you lean over, give him a nudge, and say...

"Mate, take 5 deep breaths for me"

....

Well stop it.

...

It doesn't work, its dishonest and it demonstrates that you believe that it puts more oxygen into the blood which is plain wrong.

... have I got your attention? 

Read on: 

The patient taking deep or fast breaths is breathing the same air you are breathing. The same air they were breathing 2 minutes before you woke him for obs.

21% or a fraction of inspired oxygen (fiO2) of 0.21.

This translates to roughly 100mmHg in his lungs, which diffused into his blood to saturate his haemoglobin.  Here’s the vid 

You cant increase blood oxygen unless you increase the concentration (fiO2) he is breathing. So take 5 breaths or 50 breaths, and it makes zero difference to his oxygenation.

So what does it do?

Why do you see the sats go up 1-2%?

Well takes few deep breaths, and you blow off CO2. In fact, the faster and deeper you breathe the more CO2 you rid from your blood. This does three things:

One: it raises your pH making your blood slightly alkalotic.

Alkalotic red blood cells (haemoglobin) binds to oxygen more readily raising the saturation.  It is temporary and lasts only 20-70 seconds. Before you finish the next patient's obs, old mate has desaturated right back to where he was at the beginning.

Two: Bohr's principle suggests that when decreasing 

CO2 bound in Red Blood cells, there is more room temporarily to transport more oxygen... again it it very very short lived.

Three: Taking deep breaths recruits more alveoli (the gas exchange air sacs).

This optimises ( not increases) diffusion. Here again it is temporary, and unless old mate continues to stay awake and rapidly deep breathe, his sats will base line out back at that number you didn't want to write in the chart.

So... what to do ?

Assess your patient.  Is he distressed? Does he have any other symptoms that could indicate respiratory discourse?

Triangulate your vital signs and talk to the patient. Normal is anything over 90% (93-96% ideal) when breathing room air.  Chronic lung disease patients may have an acceptable lower limit of normal for them (often 88-92%). But all of us when resting or sleeping drop, not just our sats, but also our resp rates, so take the data in context, investigate your patient, and stop bugging them to deep breathe just so your graph looks good.

Final word on deep breathing- its good to get all your patients to do this every hour. It prevents DVTs, pressure area ulcers, atelectasis/pneumonia, and helps clear pooled secretions in de-recruited lungs.

Be a part of our live OnlineEducation sessions

More: check out our Pirate (ARRR) seminar, Respiratory Failure seminar, or Advanced Physiology seminars.

All our courses are here

Www.Ect4Health.Com.Au/whats 

Now Look at a video that discusses this 

Bronchial Thermoplasty

#KYJ Bronchial Thermoplasty

Have you lot heard much about this newish treatment.
I first heard about this treatment when I was teaching in our respiratory seminar and one of the nurses attending mentioned it. If you are listening nurse PW, thank you for getting the ball rolling.

Bronchial Thermoplasty- let's look at the word - bronchial, obviously means the Bronci and the larger bronchioles. Thermoplasty means the application of heat (Thermo) to create physical changes to tissue (plasty).

This is a procedure that can be performed under general anaesthesia for adults that meet certain severe asthma criteria. Usually requires a series of treatments a month apart each lasting about one hour.  I bronchoscoped is passed into the lungs, and a heating element is applied to the smooth muscle causing it to essentially scar and become hardened (stenosis).
This might sound like a bad idea but if you recall one of the fundamental pathophysiology's of asthma is that the smooth muscle surrounding the small airways undergo bronchospasm.  When stenosed, this is less likely.

For patients who have frequent asthma flareup, this treatment shows promise and reduces the number and severity of acute episodes. This treatment is not for everybody it's got a fairly hit and miss success rate the that is not that much better than (20-25%) placebo.  Interestingly, the research even demonstrated that up to 5% of asthmatic patients undergoing clinical trials, required more of their preventative medication after the treatment . This is no magic bullet, but if you were one of those patients in that success group, and it meant less asthma flareup and less preventative medication that arguably has its own problems; then I guess it's worth discussing treatment with your respiratory physician.

As you know it's asthma week this week.  If you have an opportunity to support research and treatment and ongoing knowledge in this field now would be a great time to surf over to the asthma Council of Australia website and the supporting foundations.  There is a lot to read, there is a lot to learn and that's all good for CPD.
For more information on Bronchial Thermoplasty and have a look at this link.
https://www.asthmaaustralia.org.au/national/about-asthma/manage-your-asthma/special-and-new-treatments

Link to AsthmaAustralia page

The Silent Chest - severe asthma

I had a colleague who asked me to post about the "Silent Chest" 

....

#KYJ Beware the silent chest. 

In the world of chronic disease, there exists, a classification or grading system that generally numbers Stage 1 through to stage 4 or 'End Stage'.

These grading or staging systems carry with them a set of typical symptoms that define the patients severity of disease.

Typically this staging system follows a predictable model of percentages of each stage.

35% with stage 1 illness generally have no obvious red flag symptoms, are often undiagnosed and live life ignorant of the fact they actually have chronic disease.

Stage two illness often recognise symptoms, and may flag these to their GP who diagnose disorders based on symptoms.  These patients make up another 35%.

Stage 3 patients will be well into recognition of their disease, will often be medicated, and perhaps experience frequent acute exacerbations of their chronic disease, which results in infrequent hospitalisations. These stage 3 people make up 20-25% of patients with the respective chronic condition.

Then there is the real sickies, stage 4 or End Stage patients, who make up 5-10%.

These patients are often in hospital or ED with acute exacerbation. They have lives that are limited in activity/ or ability to function too far from their specialist/GP or healthcare support network.

Unique to the end stage chronic disease patient is a unique symptom set, that by their very features, sets them apart from the other 90-95% of sufferers of their disease.

For the Chronic renal patient it may be the need for dialysis.

For the chronic Heart failure patient it might be frequent episodes of severe Pulmonary oedema.

For the COPD patient, it might be the development of CO2 retention and permanent home oxygen.

For Asthma, it is the frequent presentation of Asthma flare-ups, which often have a silent chest on auscultation.

Now a non wheezing asthmatic patient may be a red herring.

It might be nothing, but it might be significant.

The real danger, it can be misleading or distract an unsavvy clinician; but make no mistake, you want to assess your patient with a silent chest well.  Get this wrong, and your patient is making it to ICU if you (and they) are lucky.

Let's review wheeze.  Wheeze is the sound of air being squeezed through narrowed bronchi and bronchioles.  Say it aloud...slowly "squeeeeeezed"

Right in that word is "wheeeeze".

Frequently a symptom of mild to moderate asthma, a wheeze is audible when enough air is forced through bronchospastic airways.   In end stage, preterminal exacerbation, the severe asthma flare may not be physically moving enough or any air through their low airways, meaning that no vibration or sound is audible.

This is badness!

Lack of air movement is gas trapping and not only represents a massive risk of desaturation, but also a risk of pneumothorax .

Frequently, the silent chest is a symptom of the severest form of asthma flare... the Status Asthmaticus.

This pre-arrest condition often progresses to acute respiratory failure (PaO2<60mmHg), and imminent respiratory arrest.

With limited air reaching alveoli, the wheeze disappears, oxygenation decreases, CO2 is retained, and level of consciousness rapidly declines.  In adults, we have physiological reserves to keep struggling to breathe. We fight for our breaths using our developed chest and shoulder muscles (laboured breathing); but in children, especially those under 8, these kids die from shear exhaustion.

Until proven to be an irrelevant symptom, the silent chest must be regarded as a medical emergency.

So when is the silent chest, not a problem?

In a mild asthma presentation, the work of breathing is not markedly increased.  The patient may be coughing, but is not distressed, cerebrally irritated, or desaturated.

In the "I can hear you wheezing from across the room" type presentations, place your stethoscope over the patients throats before auscultation grandson their chest.  If the wheeze is heard in the throat, and not in the lung fields, then the presentation is likely to be anxiety induced vocal cord dysfunction, and not asthma.

The true asthmatic silent chest is as sick as an asthmatic can be.  Believe them! Look at sats, their work of breathing, and history of ICU admissions, to guide your index of suspicion that this patient is sicker than they sound.

It echoes, the sound, of silence.

Interested in more?

You could attend our Respiratory seminar.  http://www.ect4health.com.au/respiratory-failure-nursing-seminar/

Link to Seminar on Respiratory Failure Nursing

Vasculitis in diabetics

#KYJ - Vasculitis

Nurse M asks "can you do a blog on vasculitis and why it's a diabetic complication?"

So here we go...

Vessel disease and in particular, vasculitis has recently been found to be associated with fibromyalgia and related Neuralgia (nerve pain).

Literally, vasculitis means inflammation of the blood vessels.  It is just one of a myriad of Autoimmune disorders.

Think of it as rheumatoid arthritis inside blood vessels.   Some medical co-morbidities are often prerequisite. Perhaps the most well known is  Diabetes.

Diabetes is commonly associated with both microvascular (small vessel) and macrovascular  (large vessel) complications. Vessel hardening (sclerosis), endothelial injury from viscous blood, and fatty plaques (atheroma) all contribute to the vessel inflammation that is vasculitis.

Hypertension, frequently present in diabetics, accelerates the onset of vasculitis. Over the past 10-15 years, we have developed a good understanding of the underlying chemical changes in diabetic blood vessels. 

What we know, is that vasculitis is immune, mechanical (BP) and metabolic; and that these factors interact to stimulate the release of cytokines (cell communication proteins) and growth factors in branches of small blood vessels.  Eyes, kidneys, and hands/feet.

In diabetics a common factor is byproducts of glycated proteins in diabetic blood.  You better know of these proteins as HbA1C. The higher their HbA1C is, the more vasculitis and subsequent effects.

Two important substances over secreted in diabetics, is seen in the glomerulus, and the retina vessels. 

In the kidney, "transforming growth factor-beta" has been observed to be prosclerotic (causing hardening) in  renal arterioles.  This fuels and exacerbates the Renin-Angiotensin response which pushes up BP.

In the retina, vascular endothelial growth factor and its receptor, vascular endothelial growth factor R-2 are increased.  Gobbledygook I know, but these cytokines cause new blood vessel growth (angiogenesis). 

Ultimately, the cell changes caused by these cytokines stimulates inflammation- Vasculitis.

Now here is the clincher, inflammation inside blood vessels, traps the smallest cholesterol carrier proteins called LowDensity Lipoproteins (LDLs).  This is in essence, the formation of cholesterol deposits in arteries (atheromas), narrowing and hardening the vessels (atherosclerosis).

DM and cardiovascular disease are inextricably linked.

So the next time the diabetic you are looking after complains of fatigue and flu like aches, it may very well be vasculitis, and is contributing to kidney failure, blindness, small peripheral vascular disease (ulcers and slow healing), and a massive increase in risk of MI and CVA.

Keep those HbA1C levels in check, monitor vision, renal function and manage hypertension aggressively.

#ECT4Health 

#KnowingYourJargon posts are found on Facebook and our blogspot site 

Wee.

Obstructive Sleep Apnoea

Sleep Disorders Week

So I thought I'd do a quick #KYJ on Sleep Apnoea.

This is part 1 of 2.

There are two main types of Sleep Apnoea.  Central Sleep Apnoea (CSA), and 

Obstructive Sleep Apnoea (OSA).  As the name implies, OSA is a condition where soft tissues of the throat relax when sleeping, occluding or obstructing the airway. During periods of apnoea, oxygen levels in the blood fall (often dramatically -SpO2<75%).  While blood CO2 rises slightly, the effect of hypoxaemia is the most profound, and causes most of the acute sequelae. 

Let's just recap normal breathing stimulus.

Normally your brain stimulates you to take your next breath, based on a complex biofeedback mechanism.

When pH of the blood (and CSF) falls - acidosis; this is the primary trigger of breathing. Unlike you were probably taught, high CO2 isn't a direct stimulator of breathing, but it is secondary stimulant due to the fact that high plasma CO2 causes pH to fall (Carbonic or Respiratory Acidosis). So it is true to say high CO2 stimulates breathing, but indirectly through acidosis.

The second and more primitive stimulus to breathe is low plasma oxygen.  You were born with this mechanism, which you probably learned about when you were taught why a new born baby draws that first breath.   It is called "Hypoxic drive", but early in your infancy you switched to the high CO2/low pH trigger.  Called Hypercarbic drive, this mature lung, primary mechanism isn't in play during OSA, because CO2 doesn't dramatically rise.  You are asleep (or trying to), and at rest, you just don't make as much CO2.

So.  The Snorer is left with multiple obstructions, and apnoeas.  This leads to drop in plasma oxygen (hypoxaemia).  When oxygen falls low enough, the secondary hypoxic drive mechanism kicks in waking the snorer. They adjust position and inhale, restoring plasma oxygen levels.   The sleeper then drifts back to sleep with out realising that they woke up, and the whole cycle starts again.

Snoring is almost always present (even diagnostic).

Daytime tiredness morning headaches hunger and weight gain are common.

Poor concentration irritability and its extreme breathlessness on exertion, and ankle swelling which is the hallmark of right heart failure.

In its mildest form, people stop breathing every 5-12mins (5-14 episodes of apnoea/hour)

Moderate OSA is diagnosed at 15-30 Apnoea/hr

And severe OSA >30/hr.

That's an Apnoea every 1-2 mins.

Waking that often, causes the sufferer to feel like they are never well rested.  They may think they sleep all night, but realistically never completed important restorative sleep cycles, and this takes it toll on tissue healing, cell regeneration and hormone levels.

The body, in a constant state of stress, releases massive amounts of cortisol (our natural hydrocortisone) and Adrenaline driving up BP, and heart rate. While cortisol exerts its effects as glucose intolerance, insulin and leptin increase/resistance, obesity, atherosclerosis and T2 Diabetes, the adrenergic stress response contributes to the development of heart failure.

Just let that sink in for a minute.  Your snoring is causing your heart failure obesity and diabetes.

The age-old question of does a obesity cause OSA, or does OSA cause obesity is yet to be completely answered, but there is a biochemical body of evidence to suggest that poor sleep equals neurohormonal changes that lead to altered carbohydrate metabolism, and all the diseases linked to it.

You don't need to snore and snoring is the single most important feature of obstructive sleep apnoea. recognise it early nip it in the bud.   If you are sleeping next to that special someone who snores. Know this- it is not about your sleeplessness, it is about theirs.

Diagnosis :

Sleep studies are done to measure EEG , ECG and oxygen saturation, then when the moon is full a respiratory physician gazes at the cauldron of data and diagnoses OSA.

Treatment 

1. Surgery to remove or cauterise part of the soft palette.
2. Continuous positive airway pressure (CPAP) ,which blows air into the throat to splint the pharynx open. 
3. Jaw manipulation devices that thrust the lower jaw forward in an under-bite, while sleeping.  You remember from airway management courses that jaw thrust pulls tongue off the pharyngeal wall.
4. Tennis ball in a bum-bag.  Stops old mate rolling on his back and occluding his airway.

Big topic that we can't tackle comprehensively in one post.

Tomorrow (in our Sleep Week) we will look at Central Sleep Apnoea (CSA).

Hope you catch some zzzz! 

#ECT4Health 

ECT4Health