Bowel sounds in shock

#KYJ Bowel sounds.

Understanding bowel sounds in a trauma patient does not need to be a complicated process that is difficult to interpret. 

Here is the thing, smooth muscles lining the intestines require a healthy blood flow to continue peristalsis (movement).  When well perfused, the bowel rhythmically contracts to move food chyme through the digestive system.  As it does, the movement is heard using the diaphragm of a stethoscope in all four quadrants of the abdomen.  These sounds of squelching, are called bowel sounds.

In trauma or sick medical/surgical patients, shock may reduce bowel sounds through a simple process of redistribution of blood volume to more vital organs.  When this happens, peristalsis ceases, thus bowel sounds stop being heard.

So let's apply the typical assessment of a patient in shock. As blood loss worsens, the vascular system starts shutting blood flow to non critical  organs .

First is skin (pale, cold and clammy skin is the symptom)

Next is the gut. Poor gut perfusion ceases gut peristalsis and subsequent bowel sounds.

Loss of bowel sounds is not necessarily a gut pathology, but most commonly a significant indicator of shock.

Opiates and constipation

#KYJ - How Morphine causes constipation.

#KnowingYourJargon or KYJ for short is the #ect4health contribution of free open access nurse education (#FOANed).  As a teacher of nurses, I get lots of questions on drugs and their side effects.

Nurse Glenda writes:

Rob, I've noticed that a drug we give at work, Targin (oxycodone/naloxone) has both an opiate and its antidote in it.  Why is this? Wouldn't one cancel out the other?

Well this is a great question.  The answer lies in understanding the opioid's effects and side effects.

Oxycodone, fentanyl, morphine, codeine and other opium derivatives all act as pain killers by attaching to two receptors in the central nervous system.  The Mu and the Delta receptors.  When activated these receptors reduce the perception of pain impulses that the patient feels.  They still have the cause of their pain (Cancer, inflammation, injury) but the brain doesn't interpret it as pain.  The Mu receptors specifically initiate a sense of happiness often desired as a high, or a floaty euphoric sensation, sought after by many who are opiate addicts. Heroin is a perfect example.

Now naloxone antagonises this by competing at the Mu receptor and deactivating morphine/oxycodone's ability to stimulate the sensors.  Hence, naloxone is thought to be an effective "reversal" of opioid overdosage.

This brings us to the question of why you'd put naloxone in a combination treatment with an opioid like morphine or oxycodone.  At the simplest reckoning, you'd think that it would stop the opioid from working but it has little effect on the pain killing effects of morphine and more inhibition of the side effects which are euphoria, drowsiness, respiratory depression, nausea and constipation.

Targin, and other combo drugs like it allow the analgesic effects but limit the negative side effects.  Resp depression, and constipation are the big ones.

So how exactly does morphine and its cousins cause constipation.  The bum is a long way from the central nervous system and brain, yeah?

Well here is the thing.  Mu and delta receptors also line the intestines.  Opiates that stimulate these in the brain, also stimulate them in the gut.  When they are stimulated they have a few effects:

1- Gastric motility slows causing more transit time and dehydration of faecal matter- hence constipation.

2- strength of rectal muscles (those used to poo) is reduced, so dry faeces, is harder and more difficult for drug weakened rectal muscles to push out.

3- the nerves in the anus that detect a stool, are desensitised, causing a full rectum to be less of a stimulus to have the urge for number Twos.

So given these three issues, all leading to less moisture, weak pushing, and reduced urge, all roads lead to constipation as a major side effect of opiates.

Now let's bring back the question of adding naloxone into the analgesic... Naloxone inhibits the Mu receptor effects of constipation, yet allows the analgesic effect to still offer comfort.

If you are enjoying these #KYJs, please let me know, share this post or consider attending one of our seminars which are full of this sort of stuff.

 

Specifically our Rusty Pills (pharmacology refresher for nurses) is booking solidly for later this year.  You need to get in and book now you you will miss out.  These seminars are capped to enhance the quality and intimacy of the face to face seminars.

http://www.ect4health.com.au/rustypills/

Inflammation - 1 of 5 Pain

#KYJ - Inflammation pain

Episode 1 of 5

In KYJ (#KnowingYourJargon) we explore those terms in health that we use commonly, yet often don't understand.

Think of KYJs as putting the science into your nursing artistry.

Inflammation

It starts with tissue damage and involves a storm of cellular chemicals that have 5 cardinal effects.

Dolor = Pain

Calor = heat

Rubor = Redness

Tumor = swelling

Loss of function = doesn't rhyme with the other four.

So let's look at why we see these symptoms.  In this episode- Pain

Pain is thought to be through multiple mechanisms.

Pain receptors (nociceptors) in your tissues fall loosely into two categories. 

Fast Delta-A fibres transmit sharp, burning pain messages to the spinal cord and brain for processing.

Slow C fibres transmit the dull ache of pressure/crushing, heaviness.  Pulsatile throbbing and crampy pain.

Both are stimulated directly by chemicals released during injury, but both are also stimulated by delayed manufacture of inflammatory chemicals made by the immune system eg bradykinin, and prostaglandins.

To start to understand inflammatory pain, let's explore what happens at the site of injury.  A cut or splinter.

Direct skin cell injury causes destruction of the membranes that encapsulate cells.  This membrane you will remember from grade 9 science, is made of fat (lipids).  It is actually a phospholipid that you know better by its common name Cholesterol.

That's right, all cells are lined by cholesterol and our liver makes this constantly to build cells and repair dead tissue.

But that is a whole other post.

So ... Cells are damaged, the phospholipid membrane leaks into the interstitial fluids (Extracellular fluid) around all our cells.

An enzyme present in this fluid is called Phospholipase (foss-foe-lype-aze). Any enzyme you read about inside our bodies will end with the suffix "-ase".

Now this enzyme breaks down the phospholipids released during injury, and it converts them into an acid called Arachidonic Acid.

Another enzyme present in extracellular fluid called cyclooxygenase or COX for short , now acts on the newly created Arachidonic acid, and converts it into a pro-inflammation protein called prostaglandin.

Many prostaglandins are responsible for stimulating those pain receptors, hence pain.

Application.  Recognising pain is chemically induced by this injury cocktail of substances, let's briefly look at the two big families of anti-inflammatory drugs used for inflammatory pain.

Remember pain is stimulated by the ultimate production of prostaglandins.

Steroid drugs 

These include hydrocortisone, methylprednisolone , Dexamethasone, fluticisone, betamethasone, Prednisolone, and others you are likely familiar with.

These "sone" steroid drugs stop Phospholipase from converting phospholipid into Arachidonic acid.  This stops further stages of inflammation occuring... Including pain.

The other family of drugs is the Non steroidal antiinflammatory drugs.

Abbreviated to NSAIDs, these drugs include ibuprofen, nurofen, aspirin, indocid, naproxen, diclofenac (voltaren).

These drugs inhibit the COX enzyme converting Arachidonic acid into prostaglandins that cause inflammation and pain.

Are we done?   Questions ?

Consider sharing the KYJs.  Or better still, come to our seminars.  

Pink puffers and Blue Bloaters -COPD

#KYJ #pinkpuffers and #bluebloaters
I was teaching on COPD in Christchurch last week, and mentioned Pink Puffers and Blue Bloaters. It occurred to me that these old fashioned expressions may be jargon that not all nurses have heard.
So here goes another episode of #KnowingYourJargon
COPD or Chronic Obstructive Pulmonary Disease  (or Airways disease = COAD) is a chronic lung disease causing restriction and obstruction to the Bronchi, bronchioles and alveoli.
It is a collection of two or three diseases in one.
Emphysema where the alveoli air sacs undergo membrane degradation and alveoli septal wall disintegration.
Chronic Bronchitis which is degenerative inflammation to the larger bronchi, and chronic Asthma where there is narrowing of the smaller bronchioles.

Most people with COPD have a dominant illness.
Those with dominant Emphysema are often barrel chested, emaciated pink in colour and have reasonable sats. Their chest is often silent.  These people may be referred to as Pink Puffers, as the gas trapping they experience causes rapid shallow breathing, puffing.

Blue bloaters are usually those with chronic Bronchitis.  They are usually larger framed, obese, cyanosed and will cough frequently to clear continuous secretions from over active sputum producing cells in their bronchi and bronchioles.  They wheeze and cough.  Rattles and Rhonchi (low pitched wheezing) is common on auscultation.
They are frequently Hypoxaemic with sats below our normal 94%,  frequently hovering in the high 80s.
So there we have it. Blue bloaters with their bronchitis, and pink puffers with their emphysaema.
It's not too late to come to my Respiratory Failure seminar. Just check out our what's on page www.ect4health.com.au

Ross River Virus infection

After recent big rain and a cyclone in the South East of Qld, we find our selves on the cusp of an epidemic of Ross River Virus

This painful condition is spread by Mosquitos breeding in water dishes, puddles, pot plant trays, and any still sources of water around the home.  Easily recognised as small black Mosquitos with white dots on their torso and "magpie footy socks" the Aedes genus are also responsible for other diseases. 

The virus is harboured in kangaroos, wallabies and Flying foxes. Once bitten by the mozzie the virus is transmitted to humans when we are bitten.

Symptoms are awful.  Aching joints (polyarthritis), headache, fever and victim feel lethargic.  The incubation is 3-14 days and symptoms last on average 4-6 weeks and are debilitating.

There is no cure, it is not fatal, and all victims recover.

Only symptomatic treatment is available (anti-inflammatory medications. Rest and gentle joint movement is recommended.

Brisbane, Gold and Sunshine Coast, and the Darling downs are about to see huge numbers of infection.

Prevention of mozzie breeding and protection from being bitten is paramount. 

KYJ - Understanding Heart Failure

#KYJ. Understanding heart failures.

In a nut shell, heart failure is the condition diagnosed when your heart “fails” to pump an adequate volume/minute.  It is measured using Cardiac output and its components- stroke volume (the amount of blood your heart pumps each beat) x the heart rate.

CO = SVxHR

Normally your CO is 4.2-7litres /min.

Now SV is measured as the volume your left ventricle squirts out each pump.  It is about 70 mls.
That 70 mls is approximately 70% of what was in your full ventricle (100ml).

So... if you fill with 100 and pump out 70ml.  Then the efficiency of your Squirt is called Ejection Fraction (and it’s approx 70%)

Fall short and you have Left heart failure....

Causes could be a weak pump or a stiff ventricle wall, or low volume or injury to the left ventricle (commonly seen after MI)

Let’s recap our plumbing...
Blood in veins (returning blood to the heart) traveling to  the Arterial side of circulation must travel through three way points;
Right heart , lungs and left heart

When arterial blood pressure is too high (Hypertension), also referred to as "Afterload",  the left heart has difficulty with its forward traffic flow.  Traffic backs up in the Left heart causing it to fail. - left heart failure.

Once this happens, blood attempting to drain into the left heart can't, and and pressure builds in the pulmonary vessels; it's called pulmonary hypertension.

This leakage causes the spaces between capillaries and alveoli to fill with plasma leaking from the pulmonary capillaries-  it's called pulmonary Oedema and when severe the patient is breathless, wheezing, and may cough pink frothy sputum. Being caused by Left heart failure, this type of oedema is defined as Cardiogenic pulmonary oedema. Wet crackling lungs and desaturation leads to a respiratory failure on top of cardiac failure.

Right heart failure (Cor Pulmonale)
The venous network drains into the right heart.  The right heart then pumps relatively deoxygenated blood through the Lungs to become oxygenated.  When the Right heart fails to efficiently pump, blood backs up into the venous system causing venous congestion, engorgement, ankle and peripheral oedema, Jugular venous pressure elevation, and Ascites.

The Right heart will fail if you snore chronically.  When sleeping (obstructive sleep apnoea) is a major contributor of Right heart failure. It's the sequelae of untreated snoring (you don't have to just live with it!)
In fact any restrictive airway disease that is unmanaged, causes more pressure in the lungs (pulmonary hypertension), making the right heart have to work harder to pump blood through the lungs.  If you force an engine to work too hard for too long, it inevitably fails. Get that snoring looked at- especially if you see stricture marks on your legs after wearing socks.  If you have ankle swelling.  You are probably already experiencing the beginning of Right Heart Failure.

There is so much more to this.   Consider coming to one of our Cardiac days.
Book me to present to your crew.
Or check out our CPD seminars near you - here
Www.Ect4Health.Com.Au/whats  

Check out the latest Videos

KYJ- Recording CPD

Question I was asked.

What constitutes CPD for AHPRA if I was Audited.

Answer: any diarised active learning done that relates to 

1.  Your role

2.  Offers education towards your diarised learning plan that you have linked to one of the 10 nursing competency standards of NMBA.

When the day comes, and your number is randomly selected for audit, AHPRA are not interested in the certificates of attendance you collected, or the list of courses, workshops,conferences and seminars you went to;  they want your diary. This diary is called the professional portfolio.  It contains your personal CPD learning plan. Where you noted that one day you went to work, and identified that you needed to develop a new skill; or seek learning about a patient's presentation for which you were not previously familiar.  Perhaps you needed to brush up on a rusty procedure, or refresh your understanding of a professional aspect of practice.

What ever it is, you noted it in your portfolio, and documented that you needed to seek some education on your identified learning need.  You must review the NMBA standards and link that  learning to one of those standards.

Eg Sally was challenged by Joan about why she administered Ventolin via a puffer to her Asthma patient; and not a nebuliser.  Sally told Joan that as an RN she is allowed to give a Metered Aerosol of Salbutamol with out an order, but not a neb. Having recently moved from interstate, Joan did not realise this and noted that she will seek education on current drug legislation.  Joan reviewed the NMBA standards and found that standard 1 states that a nurse "complies with legislation relating to practice"

So, homework time.  

Do you have a Professional portfolio?

In it, do you have a "learning plan" that meets the Registration standard?

Do you know the NMBA competency standards? 

Here --> http://www.nursingmidwiferyboard.gov.au/documents/default.aspx?record=WD10%2F1342&dbid=AP&chksum=N5ws04xdBlZijTTSdKnSTQ%3D%3D

Nurses, this CPD can be gained anywhere. Of course I want you to read my blogs and attend my cruises and seminars, and claim the CPD to be had, but if you think AHPRA cares one bit about the wad is certificates you want to send them at audit time, you are sadly mistaken.  They don't even look at them. They are interested only in your Learning plan, and how you recorded your CPD. 

Final question :  Yes mandatory training is 100% acceptable as CPD.  Ref= section 8 of the NMBA registration standard.

This excerpt from the NMBA standards for registration
Documentation of CPD

7. Documentation of self-directed CPD must include dates, a brief description of the outcomes, and the number of hours spent in each activity. All evidence should be verified. It must demonstrate that the nurse or midwife has:
a) identified and prioritised their learning needs, based on an evaluation of their practice against the relevant competency or professional practice standards
b) developed a learning plan based on identified learning needs
c) participated in effective learning activities relevant to their learning needs
d) reflected on the value of the learning activities or the effect that participation will have on their practice. 
8. Participation in mandatory skills acquisition may be counted as CPD.