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

Histamine- the why and why

#KYJ - Histamine and Mast cells. (H1)

In a course on Respiratory nursing last week I was asked about the role of Histamine. Specifically H1.  Not the H2 variety in gut.

So here is my analogy:  imagination needed.

Say there was a bad guy (Buggsy Peanuts) outside your house.  To deal with him you needed to get out of your house.

You are too big to fit out the window so but you you don't have a key to get out the door.

You are stuck inside with Basil, your frightened mate.  Buggsy the bad guy is outside.  Picture it?

Ok- your friend Basil, can't deal with the bad guy but does have a door key.   Basil opens the front door for you, and you you go and deal with Buggsy.

Specialised White blood cells called Basophils (Basil) possess a key that opens pores inside blood vessel walls.   That key is a protein called Histamine.

Ordinarily, large allergen or pathogen fighting phagocytes can't get out of the blood vessels to fight allergens or pathogens, so basophils inside blood vessels and Mast Cells in your tissues (mast cells are just basophils outside the blood stream), produce this Histamine key to make blood vessels porous to allow white blood cells out to attack invaders.

Think of histamine as a protein like insulin, but instead  of opening doors for Glucose to move , histamine opens doors for immune fighting cells to migrate to the tissues where the epic battle between Buggsy Peanut and the White knights of the immune system attack.

Now the downside to this histamine, is that its very action of Vasodilation and increased permeability, causes plasma and water attracting proteins (Albumin) to leak into tissues - Oedema is the result.

Engorgement of vessels close to the invasion causes the blood flow to increase giving rise to redness.

Now reflect on the last ant sting or mosquito bite.
It was red, hot , swollen and painful/itchy wasn't it.

Local histamine responses in skin causes these same symptoms.  They are called urticaria or hives, and are typical in allergies.

If histamine response is in the nasal mucosal or sinus tissues, then the swelling and congestion is called Allergic Rhinitis (Hay Fever), or in sinuses-sinusitis.

If the histamine response occurs in upper airway structures like Lips, tongue and throat, it is referred to as Angioneurotic oedema, or simply angiooedema.  This is a common symptom in a life threatening allergic reaction, and often compromises the patient's airway.   You will know it as the deadly symptom in Anaphylaxis.
When the response is in the lungs, and bronchial tissues become swollen then histamine is one player in the diseases of Asthma and Broncheolitis.

The above examples are all local effects
When the histamine release is systemic, the massive overwhelming release of histamine in all vessels, causes such vasodilation and capillary leakage, that the patient loses their circulating blood volume (hypovolaemia) and their distribution of blood between arteries and veins becomes critically imbalanced (maldistribution).   This is a complex and life threatening cause of shock.  In severe allergic response it is called anaphylactic shock, and in severe pathogenic responses, it is called Septic Shock.

Recap:
Anaphylaxis causes anaphylactic shock.
Infection causes septic shock.

Histamine is a potent vasodilator . And makes blood vessels engorge and leak.

Can you now see the role (in mild allergies) of drugs that block or inhibit histamine?  These are a family of Anti-cholinergic drugs called antihistamines.   Examples include Loratidine, Zadine, Clarityne, polaramine, Telfast and some of the older phenothiazine drugs like the Rock Star -Promethazine (Phenergan).

All antihistamines cause sedation but only if the drug can cross the blood-brain-barrier.  Phenergan and Polaramine are examples.

Any how- as usual, I digress.

The point is Basil (Basophils) holds the key (Histamine) to the door (vessel wall) so you (Phagocyte) can get out and kill Buggsy Peanut (pathogen or allergen).

If it was you who asked the histamine question, Thankyou for stimulating such a great topic for our #knowingyourjargon (KYJ) series.

Check out the blog for more. There is heaps of #FOANed

Autoimmune Hepatitis

#KYJ -  AIH -Autoimmune Hepatitis.

AIH is an ideopathic destruction of the liver by the body's own immune system.   In a similar vane to rheumatoid conditions where the immune system attacks joints and other connective tissues, AIH attacks the liver (Hepa*),leaving it inflamed (*itis)= hepatitis.
It is not related to viral hepatitis like HepA, B, C or other viral disease.
It is not related to alcohol use or drug taking like Cirrhosis of the Liver.
AIH has no known cause.  We just don't know why an otherwise normal immune system should turn on one of its own organs (the liver) and seek to destroy it.  That's what ideopathic means; "cause unknown".

All tissue that becomes injured, need to be repaired.  The repair process is called inflammation.  When injured, and subsequently inflamed, the tissues/organs that they form, stop doing the job they were built to do.
In encephalitis brain stops functioning
In arthritis, joints stop working.
In gastroenteritis the gut stops working.
Well as you probably guessed, in hepatitis, the liver ceases to function.

In hepatitis important enzymes and proteins can't be made.
The Liver converts brain damaging ammonia into a less toxic waste, preventing brain injury.
The Liver makes the blood proteins used for coagulation, with out these, bleeding occurs and clotting mechanisms in the body fail.
The Liver manufactures an important blood protein called Albumin which acts as a water magnet that stops your capillaries leaking into your body tissues (Oedema or swelling).
The Liver processes dead red blood cells (bilirubin) and converts this into bile for digestion.
The Liver makes cholesterol which is the building material for all cells in the body.  Without it the body can't repair or make hormones and bile.

Now if inflamed, the Liver can't do these jobs.  Hepatitis leaves toxic buildup of ammonia causing confusion and brain damage.
A toxic buildup of bilirubin stains the skin yellow (jaundice) and causes the hepatitis patient an incessant itch (Pruritus).
The hepatitis patient can't clot, and with less albumin, they develop swollen legs, and swollen abdomens (called ascites).  Occasionally the capillaries in the lungs will leak causing lungs to fill with fluid, breathlessness and reduction of oxygen delivery to all cells.

Hepatitis is a dangerous disease state, and when destroyed, the Liver can't regenerate fast enough to support life. The end stage treatment for AIH is transplant.  The gift of life allows restoration of function to a person with liver destruction.

I hope that this short KYJ on AIH and hepatitis was interesting, and helped you understand this rare liver condition.

More education in my face to face  seminars www.ect4health.com.au/whats
www.ect4health.com.au/whats

Love you to swing by our face book page too.  Www.facebook.com/ECT4Health