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. 

Pharmacology Refresher- Probenecid and Cephazolin

#KYJ - Pharmacology Refresher 1- Cephazolin and Probenecid combos

Over the last few days, I have been treating a significant number of people with machete, bush knife and other significant compound lacerations.  For the first 24-36 hours after wound closure these patients are given daily or BD IV Cephazolin with concomitant oral Probenecid.

I thought I'd share the rationale for using a common Gout drug, as a synergistic anti infective agent. 

Let's start with Probenicid.  This drug is a uricosuric drug that increases Uric Acid yexcretion in the urine. This is why it is primarily used in treating gout and high blood Uric acid.

But originally, Probenecid was developed to competitively inhibit renal excretion of some drugs, thereby increasing their plasma concentration and prolonging their effects.

Enter intravenous Cephalosporin drugs like Cephazolin.

Cephazolin is a renally excreted first generation Cephalosporin antibiotic which (like Penicillin) is categorised as a Beta-Lactam drug. This group of antibiotics works by inhibiting cell wall synthesis of the bacteria.  They stick to special proteins in the bacteria cell wall and cause it to disintegrate and die. They are bactericidal, meaning that they kill the targeted bacteria (as opposed to inhibiting reproduction as other bacteriostatic antibiotics do).

It makes sense then that if these antibiotics are excreted via the kidneys, then their bioavailability would be lessened with healthy renal function.  Enter Probenecid.  In a patient given probenecid which inhibits antibiotic excretion through the kidneys, the Cephazolin stays in circulation in higher bactericidal concentrations for much longer, effectively increasing the antibiotic's half life, bioavailability and duration of action. 

It's like levelling up in the game of Germ Warfare.

Fevers, paracetamol, Rigors

#KYJ -Rigors ( Hot shivers )

in a recent paediatric course that I was teaching, a nurse asked me about rigors (pron: rye-gores)

A rigor is  the uncontrolled shivering that a person with extremely high temperature often exhibits. It seems counterintuitive that somebody's temperature is very high they should shiver, but when you stop and look at the pathophysiology that causes this shivering, then it makes a whole lot more sense.  So start with, let's look at how fever is produced. 

The hypothalamus deep in the middle of your brain has a mechanism in it that regulates body temperature. It is a thermostat that maintains normal body temperature between 36 and 38°C. Older texts site 36.5 to 37.5°C.  Let's not split here's what's just say if your temperature is elevated above 38 then you have a fever, also called pyrexia.

Fevers are induced when White blood cells called macrophages release pyrogenic chemicals, as they enfulf dead infected cells, bacteria and viral destruction.   These pyrogens stimulate the release of the inflammatory markers known as prostaglandins particularly prostaglandin E (PGE).

When PGE is released in inflammation, this instructs the hypothalamus to raise the thermostatically set temperature, hence, fever.  As long as macrophages and neutrophils are actively fighting infection, they will continue to release the pyrogen is the cause prostaglandins to be formed.  Fever is therefore your body's natural response to fighting infection and enhances the immune system's ability to do its job.

Now let's have a look at how rigors occur.  When the hypothalamus reacts to PGE by raising body temperature, it actively causes the body to generate heat. This occurs a number of ways.  Reduction in heat loss, by pulling away blood vessels from the surface of the skin- vasoconstriction.  If this alone is not effective enough to bring body temperature up to the new thermostat set temperature,  then the brain initiates shivering which generates more heat thus reaching the new set point sooner. 

Therefore recognising this is a normal response in infective conditions, should a patient be experiencing shivering while febrile, despite seeming counterintuitive, nurses should actually put blankets on the rigoring patient to assist the body to increase temperature in accordance with its immune initiated goal.

Now this doesn't always sit well with us, because for years doctors and nurses have been taught to actively try and reduce temps. So putting a blanket on a febrile shivering person seems so silly, but when we grasp the concept that fever should be facilitated not inhibited, then we recognise that it makes for well informed care.  This issue of whether a fever should be treated or not is one that polarises nurses, doctors and parents. If you are game, you can view my thoughts on this here https://m.facebook.com/Ect4Health/posts/314445358696672

.

For now, I hope that you have a greater understanding of rigors and how they occur. 

#KYJ - Febrile Convulsion. The myths vs the truths.

Over the years, few of our #knowingyourjargon topics have sparked as much interest as fever and its treatment. Fever in children seems to be a cesspool for cultivation of strong opinions in nurses.  Well boy, are you gonna hate this post.

If you have experienced caring for a child with febrile convulsion, you will probably remember the fear, trepidation and shear anxiety in the eyes of the parents of that child at the time.  In this post we explore this explosive onset presentation and dispel a few myths. 

Myth 1

Febrile convulsion is caused by high fever in children.

Truth: Febrile convulsion manifests when a temperature in a child aged 6 months- 3 years (rarely up to 6 years), changes rapidly.  It relates to the speed of fluctuation not the height of a temp.  A child with a temp of 41.6 is no more likely to fit than a child with a temp of 38.6.

Additionally, many febrile convulsions are induced during the rapid drop in temp seen post tepid sponging, and administration of antipyretic medication... Yes the ones on TV ads claiming "nothing works faster for pain and fever". Those ads are telling the truth, they cause RAPID drop in temperature.   These drugs prevent the formation of prostaglandins which are those "healing" thermogenic chemicals released during infection and inflammation.  

Myth 2

Febrile convulsion is dangerous.

Truth: a classic (or simple) febrile convulsion is one that follows three rules:

1- Short lived < 15 mins (92% less than 5 mins duration).

2- Convulsion onset is inside 24 hours from the onset of fever illness

3- Child will have only 1 convulsion during the illness.

The febrile convulsion that does not follow these rules is considered complex, and therefore sinister and  neurologically suspect.

Febrile convulsions do not harm the child and do not cause brain damage.  Whilst they are frightening to all who witness them, the hypoxic brain injuries associated with other convulsions and states of status epilepticus, are just not seen in children experiencing febrile convulsions. 

It is therefore safe to allow a febrile convulsion to ride itself out. It is not an emergency.

Myth 3

No antipyretic medication reduces the risk of febrile convulsion.

Truth:  antipyretic drugs (Ibuprofen and paracetamol) have been extensively studied for their prophylactic effects and found to be dismally ineffective.  In fact this is not new. It is a fact we've known since 1995, and was first proposed before many of our readers were born (pre 70s).

There is an interesting claim that they may even cause a convulsion.

Two mechanisms that induce fits.

Think about what neutrophils and macrophages are doing here.  Releasing chemicals to instruct the hypothalamus to raid the temperature. If paracetamol or ibuprofen is given and inhibits the prostaglandin message, more and more pyrogenic chemicals are being released by frustrated WBCs.  Now the antipyretic drug starts to wear off, massive amounts of pyrogenic chemicals released by WBCs now induce a burst of fever inducing prostaglandins, and the temp rapidly shoots up. 

The second mechanism is seen when a dose is given to a febrile child. The antipyretic shuts down prostaglandin production, resulting in a rapid fall of the fever. This in turn can induce the convulsion as they are caused by rapid fluctuation in temperature.

Myth 4

Febrile convulsions must be stopped.

Truth: they just don't.

While it is distressing to stand idle and do nothing, the only real benefit of stopping a febrile seizure is to alleviate the anxiety of the onlooker. So let's say you have a protocol or a mandate to treat, let's look at the standard management for convulsions.  Jurisdictions differ in their approach but always use one of two benzodiazepine drugs. Both are given mucosally, an IV cannula is not needed.

Midazolam is the favourite this month. Given intra-nasally via a mucosal atomisation device (MAD) pictured, the dose is 0.5mg/kg up to max 5mg.

It is a strong short acting sedative that may cause profound ALOC postictally (after the fit stops).  Therefore, lateral position, airway management, +/- oxygen if the kid's sats are below 95%

The other drug is Midazolam's older cousin, Diazepam.  This is usually given PR- low rectal.  10mg seems to be standard. Don't be pushing that stuff too high or it won't work!!  As a drug is administered low in the rectum it absorbed into systemic blood vessels and exerts immediate effect.  In fitting, this is desirable. If you ran it right up high in the rectum, the blood vessels drain first into the liver where diazepam is almost completely destroyed (read up on Hepatic First Pass).

Personally, I'm a fan of Midazolam, but that said, there is no evidence that a simple febrile convulsion needs to be stopped, and the irony here is that this family of drugs are also called anxiolytics, which is true when you think of the parents and nurses anxiety levels after the fit stops. 

Summary:

Febrile convulsions are caused by Rapid fluctuation of temp, not height of fever.

They are rarely harmful or even need to be stopped.

We have known for at least 20 years that antipyretic medications are not preventative.

More reading on this RCH site.

http://www.rch.org.au/kidsinfo/fact_sheets/Febrile_Convulsions/

Mean Arterial Pressure

#KYJ - MAP the Magic number 

In my classes, some nurses ask me what is the most important BP, the systolic or the diastolic. Of course the answer is somewhere in between. It's the Mean Arterial Pressure (MAP). 

Where systolic BP represents the peak pressure as a wave of blood pulses through arteries, the diastolic blood pressure represents the net pressure in the blood vessel during relaxation. 

The MAP represents perfusion of organs like brain heart kidneys etc. If a person is deteriorating, it is the MAP that is really the most important number.

MAP is a calculation of 1/3 of pulse pressure plus diastolic.

If bp is 110/68

Pulse pressure(PP) is S-D

So 110-68 = 42

PP=42.

MAP= 1/3PP+D

MAP= (42/3)+68

MAP= 14+68

MAP= 82

MAP normal range in adults is 65-120.  For the MAP to be too low means organs are not being adequately perfused with oxygen.

This lack of perfusion (hypoperfusion) is called ischaemia. 

That Magic MAP >65 is good.

In hypotension (low blood pressure), the MAP suffers. 

If the brain is poorly perfused the consequence is agitation, restlessness, confusion and worsening altered levels of consciousness.

If heart is poorly perfused the consequence is poor cardiac output, chest pain, ECG changes.

If kidneys are poorly perfused, renal output suffers.

All these are related to this mean arterial pressure.

So let's look at a low BP. 

80/50

MAP=1/3PP+D

PP=30

MAP= (30/3)+50

MAP= 10+50

MAP= 60 !!!

Can you see that this is substandard? Globally this person would not be perfuming their vital organs optimally.

This is just one of the topics I cover in our Basic Nursing Assessment Seminar. Check out our dates in my web page.

http://www.ect4health.com.au/nursing-assessment/