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

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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/

Croup

#KYJ - Croup.

Laryngotracheobronchitis, commonly called Croup is a mild viral upper respiratory tract infection which causes a characteristic Seal-like barking cough. 

Despite it being almost always viral, and mild, I need to make mention that rarely, some children  are very ill and airway compromise can be a cause of mortality.  In our not too distant past, the major cause of croup was diphtheria, which killed thousands of children until the advent of vaccination.

Today, the vast majority of croup is caused by a parainfluenza virus, and occasionally Respiratory Synctical Virus (RSV).

Patho

Croup causes inflammation of the  lower pharynx, larynx and trachea. This inflammation narrows the upper airway lumen (pipe) causing dyspnoea, cough and stridor.

Symptoms

The course is typically viral with a slow onset of miserableness, sore throat and runny nose (head cold symptoms).  It is accompanied by a fever that is mostly low grade (up to 39.5). There is often a cough, in the early morning or night time. This cough is not usually sputum producing, but characteristic in its seal barking tone.  At its worst, the child with croup has an inspiratory stridor which sounds like the child is choking.  This symptom is often the antecedent to ED presentation.

Assessment

Vital signs reveal tachycardia, and rapid Resp rate if the child is a little dehydrated. Important to note,  is no desaturation. This is not a lung condition, so gas exchange is not normally affected.  If there is low sats, then consider that this is not plain croup, but a secondary chest infection/pneumonia or asthma.

Points of difference

Chest infections are 45% mixed viral/bacterial in kids, (15% in adults), croup will have normal sats, but chest infections often desaturate.

Asthma and croup both cough, but asthma cough often demonstrates exploratory wheeze, whereas croup is dry cough with inspiratory stridor.

Both can coexist. Croup can trigger asthma in a susceptible child.

Treatment

Viral infections respond to time, rest, and oral fluids.  So there is no magic bullet.  Symptoms usually resolve in 5-6 days, and if they don't, invariably indicate concomitant opportunistic bacterial infection, or viral invasion to the bronchioles and lungs. Taking a timeline history is therefore important. 

There is a role in managing stridor  with steroidal anti-inflammatories.  In kids, Prednisolone (Predmix) is a favourite.  Alternatively inhaled corticosteroids eg Budesonide or Dexamethasone has been used.  These drugs are not curative, not antiviral, and can predispose the croup sufferer to a greater chance of opportunistic bacterial infection due to their strong immunocompromise effects.  That said, this is rare, and invariably will be used for severe stridor producing croups.  Note that they are slow to work (4-8 hours), so in extremis, when the kid is really working hard to breathe, a quick fix is needed.

As an ED nurse, my first line is adrenaline as a neb.  4mg neat, in the nebuliser and get it on that face.  This should be reserved for the exhausted patient who looks like they are really struggling.

Rarely is oxygen needed, and should not be used unless the sats are South of 95%.

Adrenaline is a vasoconstrictor, and immediately reduces swelling in the larynx and trachea.  Parenteral (subcutaneous or IM) epinephrine can also be used, but  last resort. 

I don't know if I've just been lucky in 25 years as an ED nurse or what, but I have never seen a pure croup need intubation.  In every case I've dealt with, those who crash are mixed URTI with some Asthma or pneumonia complication. 

These #knowingyourjargon  posts are our way to contribute to #FOANed and if you like and support these posts, please share, comment and like our page.  Of course if you want more, check out our courses. This material is covered in our Acute assessment seminars, acute Deterioration, and Respiratory seminars. 

 

The video linked is an example of a child with croup cough

http://youtu.be/Qbn1Zw5CTbA

Oxygen damaged cardiac cells

#KYJ - Lipid Peroxidation and why you want to know about it.

In 2010 most of the resuscitation councils in the universe made interesting changes to the use of oxygen for ischaemic chest pain and MI.  It was a final straw in the oxygen coffin culmination from 50 years of its use being complete dogma.  While the cardiology world and its protocols are largely on board with this global reluctance to apply oxygen to chest pain /MI patients, there exists a sense in nurses that we just go with the flow and just do what we are told without understanding the reasons for change.

So let's explore the three reasons oxygen is no longer "routinely" used, and I emphasise "routinely used", because we all know that there are clear indications eg hypoxaemia (Sats <94%).

1.  They are not Hypoxaemic.

Haemoglobin, that oxygen carrying protein in your red blood cells holds 4 molecules of oxygen.  When it does it is full, and can't hold more, it is what we call "100% Saturated".  In patients with cardiac chest pain their sats are normal (SpO2 94-100%), so their haemoglobin can't carry any more than it already has loaded. Ischaemic chest pain is ... Wait for it ... Ischaemic.  The hypoxia of cardiac tissue is caused by ischaemia  which means poor perfusion or blood flow.  The ischaemia is due to vessel spasm (angina) or a physical blockage of a coronary arteriole from a clot.  The blood dammed up behind the blockage is well oxygenated, it just can't get through.  If the Sats are fine, then oxygen is unnecessary, they already have all they need.

2.  Vessel size.

In chest pain management, the focus of interventions is placed on improving blood flow to the oxygen starved muscle (perfusion).  The GTN you give, the rest, the morphine and even the Aspirin all aims to relax the blood vessel walls that are restricting blood flow.  On the other hand, we have previously administered oxygen routinely, thinking that this is what they need, when we missed an important property of oxygen; it is vasoconstrictive.  During gas exchange in the lungs, oxygen saturates available haemoglobin sites, while dissolving into the plasma, exerting oxygen tensions higher that the 80-100mmHg normal.  In fact breathing oxygen from a simple face mask at 6-8 lpm is 3 x as concentrated than room air.  This high concentration of breathed oxygen increases plasma oxygen tension vasoconstrictive heights.  Doesn't it seem a bit dumb to give all these vasodilation, vessel relaxation, perfusion improving drugs, and at the same time, give oxygen which is profoundly vasoconstrictive? Yep... Dumb.

Counter productive in fact.

3.  Oxygen destroys cells

Big call I know, but in normal physiology, some oxygen we consume becomes radicalised. Oxygen is stable in its O2 configuration.  During metabolism some splits in to radically reactive single atoms which bind to other substances in your body to form damaging and corrosive molecules called "oxygen free radicals". An example is hydrogen peroxide formed when a single oxygen (O) binds to water (H2O).  The resulting H2O2 causes damage to cell membranes, especially previously hypoxic ones like heart and brain tissue.  Your cell membranes are made of fat (lipids).  Cell membranes are called a phospholipid bilayer, and if there is one thing H2O2 loves to attack, or "oxidise" it is cell membranes. The more oxygen you breathe, the more free radicals you make.  In chest pain management, this oxidisation of cell membranes targets ischaemic cardiac cells, and destroys them (necrosis).  It is called lipid peroxidation.

Filling up a patient with oxygen while waiting for the clot to be dissolved, allows for the formation of these reactive oxygen species (free radicals). Now the blockage is dissolved, and a flush of highly concentrated oxygen free radical blood floods the ischaemic tissue, causing a wave of destruction.  This is called an oxidative burst or more commonly, reperfusion injury.

There it is. Three reason to be weary of oxygen in chest pain.

1 they don't need it

2 it narrows and reduces flow

3 it damages cardiac tissue 

Be in formed. If you like these #knowingyourjargon topics, let me know, pass them round the station or the ward and most of all, share on your social media.  This is free open access nurse education #FOANed

Our seminars cover this and more. Check out our web site.

Epiglottitis

#KYJ - Epiglottitis

Twenty plus years ago the presentation of a child with upper respiratory tract infections (URTIs) was fraught with anxiety that the infection was a killer disease called Epiglottitis.  inflammation of the Epiglottis, a small flap like piece of anatomy that sits like a trap door over the trachea. 

As the Epiglottis becomes inflamed it loses its function as an airway protecting flap, and in children especially, becomes so engorged and top heavy, that is flops onto the trachea causing obstruction, and subsequent death.

The most common incidences are seen in adults or children who have not been immunised for Haemophylus influenzae type B (HIB).  Although other throat infection causing bacteria eg Strep Pyogenes, Moraxella, and Staph Aureus, are causative, HIB remains the most common cause, and is not caught per se, because it is a resident normal flora in our respiratory tree.

Children with epiglottitis are sick. I mean critically unwell, so airway assessment and security is the highest priority.

Classically they are hyperpyrexic with temps over 39.5C.

They are reluctant to swallow their own saliva causing a characteristic drooling, and because of airway obstruction, they will often tripod their position.

They can rarely lay flat, they are reluctant to talk and if they do, have a muffled voice.  They just look septic, often pale, listless, disinterested and frightened.

This illness is rapid in its onset; one case I nursed was a 4 year old boy who went from being a child picked up from daycare at 4pm to needing a surgical airway and helicopter retrieval inside 90 minutes.  It is most common in adults, but in children (unimmunised), it represents a high priority emergency and a triage category of at least 2.  HIB can also cause septicaemia, and pneumonia, so it is one serious disease. 

Whilst the immediate management is always airway security, and the preparation for endotracheal intubation, and urgent surgical airway needs to be made, the initial focus is on a de-stressing environment for the child and their parents.  Low lights, calm atmosphere, careful positioning, and no sudden surprises that startle or scare the family unit.  The child's anxiety is heightened if 'Mum' is stressed, so calm, soothing quiet movements are paramount.

Unless all difficult airway equipment is primed and ready, with a specialist anaesthetist at the ready, don't attempt to assess the throat of the child.  At any hint of distress the child may obstruct, making ETT impossible.

In adults it is a painful and miserable disease, but it is rarely fatal in this population.  That said George Washington was reported to have died from epiglottitis. 

Cephtriaxone is one of the common antibiotics of choice. Pre-empting it's use intravenously once airway is secured would be reasonable. In children,  where IV cannula insertion is very distressing, the liberal application of 'Emla' or AngelGel would be a sensible early intervention.

Differential diagnosis:

Croup a milder viral inflammation of the Larynx and Trachea,

Peritonsilar abscess (Quinsy)

Remember these kids are often drooling and have a rapid onset of symptoms.  Suspected Epiglottitis is an emergency.

Asthma Attack or Flare-up

#KYJ - Asthma Flareup

Just a quicky "knowing your jargon" this morning.

In 2013 most asthma councils around the western world changed the term "Asthma Attack" to "Asthma flare-up".

The change was in part due to the notion that the term 'attack' implies sudden and without provocation.  The Gurus in asthma wanted to make it clear that a 'well controlled' asthmatic doesn't have acute episode if they are well managed.

Provocative words, but the stance is... If you are an asthmatic and you use your "blue puffer (reliever) medication" more than once /week, then you have poor control of your asthma.

So, interesting and challenging concept. I wonder how many asthmatics out there using their Salbutamol 2-4 times each day to "stay well" , actually believe that they could be better controlled?

If an asthma flare up occurs, most Asthmatics will have a management plan ( often a written down list of "what to do instructions").

The Resus Council, and Asthma Council maintain that asthma flare up treatment includes the following:

4 puffs of salbutamol (1 puff with 4 breaths)

Always use a spacer- never place the puffer in your mouth.

Wait 4 minutes, then

Repeat the 4 puff regimen.

Don't use oxygen unless the patient's saturation is less than 94%.

Remember: 4 puffs, 4 breaths, 4 minutes and repeat. Puffers only hold 200 medicated doses, after that the puffer sprays a propellant gas, that to the patient feels and sounds and tastes like salbutamol. Don't be fooled. Use a new metered inhaler every time.

Bottom line is this is a disease of lower airway bronchoconstriction.

They need a bronchodilator more than anything else.

Steroids, including IV Hydrocortisone won't help an acute flare up, they take 4-6 hours to start working on oedema control.

We have to get air into their distal alveoli and into their bases.

It's all about the Base 😉

Wheezes Vs Stridors

#KYJ - Wheezes vs Stridor 

For many nurses, breath sounds are a difficult assessment. Perhaps it is that you weren't taught, perhaps you feel it is the doctors job, and perhaps you can do it, but because the culture of nursing inhibits this that you just don't; but for most nurses I teach, they agree that they just don't feel confident with the terminology. 

For this episode of KYJ, I just want to highlight two terms. 

Wheezes

Wheezes are polyphonic (multiple notes) of sound emitted when air is squeezed through narrow pipes.  In respiratory conditions, wheeze may be heard when smooth muscles strangle or constrict bronchioles.  Often heard in Asthma flare ups or exacerbations of COPD, a wheeze is the term for the sounds made during expiration.

Stridor 

Stridor is actually a wheeze also, accept it is used to describe inspiratory sounds.  Commonly a Stridor is heard when there is upper airway partial obstruction, eg a foreign body.

In our Assessment seminars we go into greater detail on breath sounds, auscultation and all the physiology.

Did you “refresh” your skills whilst reading this?

If so and you wish to “refresh” more, join us on the 8^th – 9^th December in Toowoomba for our Basic Nursing Assessment Skills Refresher Seminar.  Those lucky to attend can also join us for our Christmas Party afterwards.  

For further information or to enrol:

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Putting the science into the art of nursing

PF ratio and why we need it

#KYJ -  PF Ratio

In our respiratory seminar today we discussed PF ratio. I thought that is might be an interesting 'Knowing your jargon' topic.

PF ratio or P:F is a calculation to determine severity of lung injury.

The P stands for PaO2

The F stands for fiO2

So PaO2:fiO2

Normally on air, a persons PaO2 is 80-100 mmHg. Let's say 90.

The fiO2 on room air (21% oxygen) is 0.21

So a PF ratio of 90:0.21 is calculated as 90/0.21=428

Therefore a PF ratio of >400 is considered normal.  If a person develops an acute lung injury or acute Respiratory Distress Syndrome (ARDS), their PF Ratio is markedly diminished. 

The 100/50 rule is a diagnostic example. If a person's PaO2 is 100 while they are breathing 50% O2, then the PF is at the diagnostic point for ARDS.

(<200)

100mmHg / fiO2 of 0.5

100/0.5= 200

You would expect their PaO2 to be at least 200mmHg if breathing 50%. 

The PF ratio is a good way to determine if the ABG oxygen value is consistent with the concentration that the person is breathing.

Critical values

PF ratio >400 is normal

<300 = Acute lung Injury (ALI)

<200 = Acute Respiratory Distress Syndrome (ARDS).

Pathophysiology of Shock

#KYJ Pale, Cold 'n' Clammy

In this Knowing your jargon episode of #FOANed I look at arguably the most recognisable symptoms of shock and the Fight or flight response.

When many animals sense fear, threat or stress, they experience a neurohormonal response that aims at assisting the animal to stand and fight the threat (eg an attacking predator) or flee from it.  This is called fight n flight.  It manifests as tachycardia, adrenaline release, enhanced muscle strength, increased cardiac output/blood pressure, miscarriage, high blood sugar, pupil dilation, And our topic of the day "Pale, cold n clammy".  Let's look at these individually.

Pale

As the sympathetic nervous system is activated to cause increase in cardiac output, it achieves this in part, by constricting peripheral veins in arms, legs, feet, hands and skin. Given that our perfused skin takes on a pink tinge due to blood in the dermal vessels, vasoconstriction in skin leads to reduced blood, so reduced pink hues.  The skin looks pale to ashen in colour.  In dark skinned people, the palms and nail beds become pale.

Cold

For the same reason as pallor, reduced blood flow in skin causes the skin to feel cool to cold, to the touch. 

The vasoconstriction peripherally, redistributes blood away from tissues that ate not vital to immediate survival, and towards the core central circulation (heart,brain,lungs,kidneys).

Clammy

Perspiration or sweat is stimulated by the sympathetic nervous system activated during a stressful event or threat. This has its roots in evolutionary biology where at one time sweat contained many chemicals. Some were toxic to predators to ingest, some were foul tasting, dissuading the predator from eating you, and some, collectively called pheromones, are produced as a chemical attractant, or in the case of attack, as a repellant, offensive odour.  The Skunk is perhaps the most notable mammal that achieves this.   Clamminess it therefore an ancient symptom that serves little purpose in humans, but still seen as part of this fight n flight response of pale,cold n clammy.

Many intimate partners would attest to the fact that their partner's perspiration and scent is different when they are aroused, than when they are angry.  This is largely due to their being different sweat glands. Eccrine glands are the most abundant sweat glands that are all over our body, apocrine sweat glands are specialised and found around nipples, axilla, groin, genitalia and other areas. These produce scents usually associated with sexual arousal.

So there it is. Pale, cold and clammy =Shock (usually).  These symptoms represent a response to a physical or psychological threat.

Like, comment, tag  a nurse/paramedic, and I'd love you to share.  #FOANed is for you.

 

Methoxyflurane- The Green Whistle

#KYJ The Green Whistle.

In this short snipet we explore the drug Methoxyflurane marketed as Penthrox

This drug is a volatile anaesthetic analgesic, it was abandoned in general anaesthesia during the 1970s because of its association with hepatic and kidney failure, but in low doses is an effective safe analgesic.

Most nurses working in emergency departments will be familiar with the classic image of a patient sucking on what looks like a green whistle, being wheeled into a department by paramedics.  

The dose of 3ml of Penthrox is inserted into the "whistle" where it rapidly vaporises, is inhaled, and crosses the respiratory membrane diffusing into systemic circulation.  Being highly fat soluble, it crosses the Blood brain barrier and acts on the  

Pain relief begins after 6–8 breaths and continues for several minutes after stopping inhalation. Continuous use of methoxyflurane 3 mL provides analgesia for up to 25 minutes; a second 3 mL dose can be administered if required for up to 1 hour's analgesia. No more than 6 mL should be given in 1 day. 

It is a depressant which can cause euphoria, and drowsiness, and like most central nervous system analgesics, respiratory depression is likely.

Points to remember. 

• Methoxyflurane provides rapid-onset short-term analgesia for:
  — initial management of acute trauma pain
  — brief painful procedures such as wound dressing.
• The disposable, single-use inhaler device allows patients (including children) to self-administer the drug, under supervision.
• Avoid use in children aged under 5 years and those unable to self-administer.
• Only use methoxyflurane in conscious, haemodynamically stable patients.
• Methoxyflurane is nephrotoxic at high doses:
  — do not exceed maximum doses — 6 mL per day or 15 mL per week
  — do not use on consecutive days.
• Do not use in patients with renal impairment.

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http://www.nps.org.au/publications/health-professional/nps-radar/2010/may-2010/methoxyflurane

Hypoxia vs Hypoxaemia

#KYJ- Hypoxaemia vs Hypoxia

Often we get things mixed up a bit saying or documenting one thing but meaning another. In this KYJ ( #knowingyourjargon )we look at two old favourites.

 Cells need oxygen to make energy (ATP) from Glucose.  It is called aerobic metabolism; but when cells find themselves with less oxygen than they need, the cell is said to be hypoxic.

Hypoxia therefore means- reduced (low) oxygen.  Ischaemia is slightly different, and implies causation.  Ischaemia of tissue is Hypoxia but caused through a narrowing (constricted or spasming) blood vessel leading to said tissue, or a physical blockage in that vessel (clot/thrombus, air/fat/amnionic fluid bubble)   Perfusion means blood flow.

So pulling this together, tissue hypoxia, is also called tissue ischaemia but only when the problem is due to poor perfusion.

Enter another important cause of hypoxia; that is, lack of oxygen being carried in the blood.  This is called Hypoxaemia. It can occur for two main reasons, but when blood oxygen concentrations are low, hypoxaemia, then delivery of oxygen to cells is impaired causing hypoxia.

Technically hypoxaemia is oxygen pressures in arterial blood below 80mmHg breathing air, OR, oxygen saturations less than 94%.

Causes 

Diffusion v anaemia v noxious atmosphere.

Respiratory diseases may reduce the ability of oxygen to diffuse into blood when there is fluid, inflammation or thickening(fibrosis) to the lungs, or if air flow is impeded.  Blood oxygen levels may also be low if the blood has less than the adequate numbers of Red Blood cells (bleeding) or less haemoglobin than optimum (anaemia).

Finally, where a person is not breathing in adequate oxygen, or where there exists poisonous gases (carbon monoxide, cyanide, smoke, my brother after cabbage). In these situations, oxygen in our air may be in such low quantity (norm 21%), or unable to bind and be carried in blood, then hypoxaemia is diagnosed. 

The take home here is Hypoxaemic blood always causes hypoxia, but hypoxia doesn't always mean that blood is hypoxaemic.

The classic example of this is seen in ischaemia like Strokes and MI (heart attacks).  Blood oxygen levels are fine, but cells are hypoxic.

Phew!! Big topic.

It's more interesting with pics, diagrams, and my white board images, so why not jump to our page and look at one of our Acute Deteriorating Patient seminars coming up, or our newest course. Basic Nursing Assessment skills (Resp/cardiac/neuro) in December. Last seminar for the year.

Www.ect4health.com.au/courses